# migrations

dir: embeddings_queue
filename: 00001-embeddings.sqlite.sql
hash: d3755dfd232be8e8301f4d7fcfb3a486
sql:
CREATE TABLE embeddings_queue (
    seq_id INTEGER PRIMARY KEY,
    created_at TIMESTAMP NOT NULL DEFAULT CURRENT_TIMESTAMP,
    operation INTEGER NOT NULL,
    topic TEXT NOT NULL,
    id TEXT NOT NULL,
    vector BLOB,
    encoding TEXT,
    metadata TEXT
);


dir: sysdb
filename: 00001-collections.sqlite.sql
hash: 38352d725ad1c16074fac420b22b4633
sql:
CREATE TABLE collections (
    id TEXT PRIMARY KEY,
    name TEXT NOT NULL,
    topic TEXT NOT NULL,
    UNIQUE (name)
);

CREATE TABLE collection_metadata (
    collection_id TEXT REFERENCES collections(id) ON DELETE CASCADE,
    key TEXT NOT NULL,
    str_value TEXT,
    int_value INTEGER,
    float_value REAL,
    PRIMARY KEY (collection_id, key)
);


dir: sysdb
filename: 00002-segments.sqlite.sql
hash: 2913cb6a503055a95f625448037e8912
sql:
CREATE TABLE segments (
    id TEXT PRIMARY KEY,
    type TEXT NOT NULL,
    scope TEXT NOT NULL,
    topic TEXT,
    collection TEXT REFERENCES collection(id)
);

CREATE TABLE segment_metadata (
    segment_id TEXT  REFERENCES segments(id) ON DELETE CASCADE,
    key TEXT NOT NULL,
    str_value TEXT,
    int_value INTEGER,
    float_value REAL,
    PRIMARY KEY (segment_id, key)
);


dir: sysdb
filename: 00004-tenants-databases.sqlite.sql
hash: 048867ce8fcdefe4023c7110e4433591
sql:
CREATE TABLE IF NOT EXISTS tenants (
    id TEXT PRIMARY KEY,
    UNIQUE (id)
);

CREATE TABLE IF NOT EXISTS databases (
    id TEXT PRIMARY KEY, -- unique globally
    name TEXT NOT NULL, -- unique per tenant
    tenant_id TEXT NOT NULL REFERENCES tenants(id) ON DELETE CASCADE,
    UNIQUE (tenant_id, name) -- Ensure that a tenant has only one database with a given name
);

CREATE TABLE IF NOT EXISTS collections_tmp (
    id TEXT PRIMARY KEY, -- unique globally
    name TEXT NOT NULL, -- unique per database
    topic TEXT NOT NULL,
    dimension INTEGER,
    database_id TEXT NOT NULL REFERENCES databases(id) ON DELETE CASCADE,
    UNIQUE (name, database_id)
);

-- Create default tenant and database
INSERT OR REPLACE INTO tenants (id) VALUES ('default_tenant'); -- The default tenant id is 'default_tenant' others are UUIDs
INSERT OR REPLACE INTO databases (id, name, tenant_id) VALUES ('00000000-0000-0000-0000-000000000000', 'default_database', 'default_tenant');

INSERT OR REPLACE INTO collections_tmp (id, name, topic, dimension, database_id)
    SELECT id, name, topic, dimension, '00000000-0000-0000-0000-000000000000' FROM collections;
DROP TABLE collections;
ALTER TABLE collections_tmp RENAME TO collections;


dir: sysdb
filename: 00005-remove-topic.sqlite.sql
hash: b1367c826b8fba5f96f27befdc1d42d2
sql:
-- Remove the topic column from the Collections and Segments tables

ALTER TABLE collections DROP COLUMN topic;
ALTER TABLE segments DROP COLUMN topic;


dir: sysdb
filename: 00006-collection-segment-metadata.sqlite.sql
hash: 4eea7468935bf25d4604a0fed2366116
sql:
-- SQLite does not support adding check with alter table, as a result, adding a check
-- involve creating a new table and copying the data over. It is over kill with adding
-- a boolean type column. The application write to the table needs to ensure the data
-- integrity.
ALTER TABLE collection_metadata ADD COLUMN bool_value INTEGER;
ALTER TABLE segment_metadata ADD COLUMN bool_value INTEGER;


dir: metadb
filename: 00001-embedding-metadata.sqlite.sql
hash: 2b4cf52c4bb2676e21d6860a4409f856
sql:
CREATE TABLE embeddings (
    id INTEGER PRIMARY KEY,
    segment_id TEXT NOT NULL,
    embedding_id TEXT NOT NULL,
    seq_id BLOB NOT NULL,
    created_at TIMESTAMP NOT NULL DEFAULT CURRENT_TIMESTAMP,
    UNIQUE (segment_id, embedding_id)
);

CREATE TABLE embedding_metadata (
    id INTEGER REFERENCES embeddings(id),
    key TEXT NOT NULL,
    string_value TEXT,
    int_value INTEGER,
    float_value REAL,
    PRIMARY KEY (id, key)
);

CREATE TABLE max_seq_id (
    segment_id TEXT PRIMARY KEY,
    seq_id BLOB NOT NULL
);

CREATE VIRTUAL TABLE embedding_fulltext USING fts5(id, string_value);


dir: metadb
filename: 00002-embedding-metadata.sqlite.sql
hash: 12a570f7121b3a8ce750a2a7c36da20f
sql:
-- SQLite does not support adding check with alter table, as a result, adding a check
-- involve creating a new table and copying the data over. It is over kill with adding
-- a boolean type column. The application write to the table needs to ensure the data
-- integrity.
ALTER TABLE embedding_metadata ADD COLUMN bool_value INTEGER


dir: metadb
filename: 00003-full-text-tokenize.sqlite.sql
hash: f97ad6334aeaa8f419f01110b648b97a
sql:
CREATE VIRTUAL TABLE embedding_fulltext_search USING fts5(string_value, tokenize='trigram');
INSERT INTO embedding_fulltext_search (rowid, string_value) SELECT rowid, string_value FROM embedding_metadata;
DROP TABLE embedding_fulltext;


# embeddings_queue

created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1ee-7265-11ef-87f9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 0, "chroma:document": "441 \u00a9 2 017 Indian Journal of Cancer | Pulished by Wolters Kluwer - MedknowCancer and cure: A critical analysis\nRoy PS, Saikia BJ\nDepartment of Medical Oncology, Dr. B. Borooah Cancer Institute, Guwahati, Assam, India\nCorrespondence to: Dr. Roy PS, E\u2011mail: drpsr.roy@rediffmail.com\nAbstract\nCancer is one of the most dreaded diseases of the 20th century and spreading further with continuance and increasing incidence in the 21st century. \nThe situation is so alarming that every fourth person is having a lifetime risk of cancer. India registers more than 11 lakh new cases of cancer \nevery year, whereas, this figure is above 14 million worldwide. Is cancer curable? The short answer to this question is \u201cYes.\u201d In fact, all cancers \nare curable if they are caught early enough. Cancer cells continue to grow unless one of four things occur: (1) The cancerous mass is removed \nsurgically; (2) using chemotherapy or another type of cancer\u2011specific medication, such as hormonal therapy; (3) using radiation therapy; or (4) the \ncancer cells shrink and disappear on their own.\nKey Words:  Cancer, carcinogenesis, targeted therapy\nIntroduction\nA hundred years ago, cancer was not so common; however, \nsince the last couple of decades, its incidence has been rising \nalarmingly , probably due to our changing lifestyle, habits, \nand increased life expectancy . Cancer is one of the most \ndreaded diseases of the 20th century and spreading further"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1ef-7265-11ef-9b73-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 0, "chroma:document": "since the last couple of decades, its incidence has been rising \nalarmingly , probably due to our changing lifestyle, habits, \nand increased life expectancy . Cancer is one of the most \ndreaded diseases of the 20th century and spreading further \nwith continuance and increasing incidence in the 21st century . \nThe situation is so alarming that every fourth person is \nhaving a lifetime risk of cancer.[1] India registers more than \n11 lakh new cases of cancer every year, whereas, this figure \nis above 14 million worldwide. We are constantly exposed \nto a variety of cancer causing agents, known as carcinogens.\nWhat is cancer? Put simply; cancer is the abnormal growth \nof cells. Cancers arise from any organ or body structure and \nare composed of tiny cells that have lost the ability to stop \ngrowing. Occasionally , cancer may be detected \u201cincidentally\u201d by \na laboratory test or radiological routine test or for an entirely \ndifferent reason. In general, cancer must reach a size of 1 \ncm, or be comprised of 1 million cells, before it is detected. \nAt this point, it may be referred to as a \u201c\u2018mass,\u201d a \u201cgrowth,\u201d \na \u201ctumor,\u201d a \u201cnodule,\u201d a \u201clump,\u201d or a \u201clesion.\u201d Exceptions \nto this general rule include cancers of the blood and bone \nmarrow (leukemia\u2019s and lymphomas) \u2013 which frequently do \nnot produce a \u201cmass,\u201d but will be evident on laboratory tests.\nTransformation of a normal cell into a cancerous cell is \nprobably not such a critical event in the genesis of cancer;"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f0-7265-11ef-9340-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 0, "chroma:document": "marrow (leukemia\u2019s and lymphomas) \u2013 which frequently do \nnot produce a \u201cmass,\u201d but will be evident on laboratory tests.\nTransformation of a normal cell into a cancerous cell is \nprobably not such a critical event in the genesis of cancer; \nrather it is the inability of immune cells of the body to \nidentify and destroy the newly formed cancer cells when \nthey are a few in numbers.[2] The risk of cancer is multiplied \nin those persons, whose immune system is suppressed due \nto any factor including chronic stress, old age, chronic \ndebilitating disease, previous use of chemotherapy , and abuse \nof drugs such as analgesics, antibiotics, and corticosteroids.\nMultidisciplinary Aspects\nCancer cells continue to grow unless one of four things \noccur:  (1) The cancerous mass is removed surgically; \n(2) using chemotherapy or another type of cancer -specific medication, such as hormonal therapy; (3) using radiation \ntherapy; or (4) the cancer cells shrink and disappear on their \nown. This last event, while extremely rare, can occur with \nsome melanomas or some kidney cancers.\nSurgery , radiotherapy , and chemotherapy from the \nconventional approaches are used to treat cancer. Surgery \nwas the first modality used successfully in the treatment of \ncancer. It is the only curative therapy for many common \nsolid tumors. The most important determinant of a successful \nsurgical therapy is the absence of distant metastases and \nno local infiltration. Chemotherapy is the administration"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f1-7265-11ef-ab49-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 0, "chroma:document": "cancer. It is the only curative therapy for many common \nsolid tumors. The most important determinant of a successful \nsurgical therapy is the absence of distant metastases and \nno local infiltration. Chemotherapy is the administration \nof cytotoxic agents (orally or intravenously , usually in \ncombinations) resulting in cytotoxicity to both resting and \ndividing cells. The objective of cancer chemotherapy is to \nprevent cancer cells from multiplying, invading, metastasizing, \nand killing the patient. Systemic chemotherapy is the main \ntreatment available for disseminated malignant diseases. \nRadiation therapy is a local modality used in the treatment of \ncancer. Other conventional techniques used in the treatment \nof cancer including bone marrow transplantation, peripheral \nstem cell transplantation, hormone therapy , photodynamic \ntherapy , cryosurgery , immunotherapy , and gene therapy .\nIs cancer curable? The short answer to this question is \u201cY es.\u201d In \nfact, all cancers are curable if they are caught early enough. That \nis the justification for screening tests (such as mammograms, \ncolonoscopies, and Pap smear examination). When cancers are \ncaught early , they tend to be smaller; they are thus either easier \nto remove surgically or more likely to shrink in response to \nchemotherapy or radiation therapy . When cancer is localized, it \ncan be totally removed by surgery but in most of the cases, it \nis practically impossible to detect cancer at such an early stage."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f2-7265-11ef-95eb-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 0, "chroma:document": "chemotherapy or radiation therapy . When cancer is localized, it \ncan be totally removed by surgery but in most of the cases, it \nis practically impossible to detect cancer at such an early stage. \nEarly detection is often the key to surviving any form of cancer.\nThe diagnosis and treatment of cancer have come a long way \nin the last 50 years. In the past, cancer, the \u201cC-word,\u201d was a \ndeath sentence. Today , we can treat and cure several types of \ncancer; however, it is evident that these cancers need to be \nfound at an early stage. More than 7 out of 10 children are \ncured of cancer. Testicular cancer, Hodgkin\u2019s lymphoma and \nHow to cite this article: Roy P, Saikia B. Cancer and cure: A \ncritical analysis. Indian J Cancer 2016;53:441\u20112.This is an open access article distributed under the terms of the Creative Commons \nAttribution\u2011NonCommercial\u2011ShareAlike 3.0 License, which allows others to remix, \ntweak, and build upon the work non\u2011commercially, as long as the author is credited \nand the new creations are licensed under the identical terms.\nFor reprints contact:  reprints@medknow.comReview \nArticle\nAccess this article online\nQuick Response Code:Website: \nwww.indianjcancer.com\nDOI: \n10.4103/0019\u2011509X.200658 \nPMID: \n***\nDownloaded from http://journals.lww.com/indianjcancer by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0\nhCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdgGj2MwlZLeI= on 12/03/2023"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f3-7265-11ef-abc7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 1, "chroma:document": "Roy and Saikia: Cancer and cureIndian Journal of Cancer | July-September 2016 | Volume 53 | Issue 3 442many cases of leukemia can all be cured in adults with current \ntreatments. Most skin cancers are cured with surgery . Moreover, \nmany cases of thyroid cancer and cancer of the larynx are cured \nwith radiotherapy . Many other types of cancer are also cured \nif they are found early enough  \u2013 for example, 75% of breast \ncancers found at an early stage. Of course, there is still a long \nway to go before we can cure most cancers. The difficulty is \nthat different cancers are caused by different things, so there \nis not one strategy that can prevent them. They also respond \nto different treatments, so not one kind of treatment can cure \nthem all. Even though we can cure several types of cancers, it \nis important to maintain vigilance about screening for cancer.\nSome forms of cancer are curable no matter when they \nare detected, and some are only curable if they are caught \nat any early stage. For example, acute leukemia and some \ntypes of lymphoma can be curable with chemotherapy . \nCertain lymphomas such as Hodgkin\u2019s disease require \nradiation therapy for a cure. Other common cancers such \nas colon cancer, breast cancer, prostate cancer, lung cancer, \nand pancreatic cancer are all curable, but only if they are \ndetected in early stages (Stage I or II).\nSome cancers have high survival rates with early detection. \nSix highly treatable cancers among others are \u2013 cancers of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f4-7265-11ef-8614-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 1, "chroma:document": "and pancreatic cancer are all curable, but only if they are \ndetected in early stages (Stage I or II).\nSome cancers have high survival rates with early detection. \nSix highly treatable cancers among others are \u2013 cancers of \nbreast, skin (nonmelanomas), colon, prostate, testes, and \ncervix. Most of the childhood malignancies (both solid and \nhematolymphoid) are curable.\nBreast cancer is the most common nonskin cancer among \nwomen, as one out of every eight women will be diagnosed \nin her lifetime. In patients whose breast cancer is detected \nwhile still in localized form have a 5-year survival rate of \n98%, compared with a survival rate of 72% by Stage III \nand just 22% by Stage IV .[3,4]\nSkin cancers (basal cell carcinoma and squamous cell \ncarcinoma) are the most common form of all human cancers, \nand if found early , skin cancer is nearly 100% treatable. \nLikewise, diagnosing cervical cancer while the lesions are \nprecancerous leads to a near 100% survival rate, but the \nrate drops to just 32% if diagnosed in Stage III and 16% if \ndiagnosed at Stage IV . Testicular cancer is treatable in 99% \nof the time when detected early , but only 73% are cancer -free \nafter 5 years if diagnosed in advanced stages. Similarly , 5-year \nsurvival rate when colon cancer is detected early is 90%, yet \nonly 39% of cases are diagnosed before cancer has begun to \nspread. According to the Surveillance, Epidemiology , and End \nResults Program, it is 98% survivable for 5 or more years"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f5-7265-11ef-a48d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 1, "chroma:document": "survival rate when colon cancer is detected early is 90%, yet \nonly 39% of cases are diagnosed before cancer has begun to \nspread. According to the Surveillance, Epidemiology , and End \nResults Program, it is 98% survivable for 5 or more years \nif prostate cancer diagnosed at stages when the disease is \nconfined to the prostate gland (Stage I and II).[1] The survival \nrate drops to about 28% if diagnosed at Stage IV .\nCancers cells not only have mutations that result in \ndysregulated expression of oncogenes and tumor suppressor \ngenes, but these changes result in the alteration of expression \nof hundreds of genes. Looking at this, we have various forms \nof \u201ctargeted\u201d therapy directed at specific single molecular \ntargets or a class of molecular targets in cancer cells. With \ntargeted therapy , the specific mechanism of action of the drug \nresults in an increase in its therapeutic index. Currently , the \ntwo major classes of targeted therapy are the small molecule tyrosine kinase inhibitors and monoclonal antibodies (MABs). \nImatinib, for instance, has been amazingly successful as a \ntargeted agent directed against several members of a class of \nenzyme known as tyrosine kinases, and by that mechanism, \nit has been phenomenally successful as a treatment of chronic \nmyeloid leukemia and gastrointestinal stromal tumors. \nTamoxifen is a targeted therapy directed at the estrogen \nreceptor (ER), and it still remains a mainstay of treatment for"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f6-7265-11ef-9d6f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 1, "chroma:document": "it has been phenomenally successful as a treatment of chronic \nmyeloid leukemia and gastrointestinal stromal tumors. \nTamoxifen is a targeted therapy directed at the estrogen \nreceptor (ER), and it still remains a mainstay of treatment for \nER-positive breast cancers, along with a newer class of drugs \nknown as aromatase inhibitors.\nCancer researchers work on developing new and more \neffective surgery techniques, radiotherapy and chemotherapy \ndrugs all the time. Biological therapies such as MABs, \ncancer vaccines, and gene therapies are all active areas of \nresearch. There are various anti-angiogenic drugs that can \nstop cancers from growing the blood vessels that they need. \nResearch is also looking into developing cost-effective ways \nof screening for the different common cancers so they can \nbe diagnosed early enough to be cured.\nAvoiding immune destruction is now considered a hallmark \nof cancer, and the immunotherapy arena has exploded \nwith the recent advances demonstrating an improvement \nin survival and a durability of response in patients with \ndifferent cancer types, like in melanoma, which translates \ninto an improved overall survival benefit.[5] To name those \nimmunotherapeutic strategies that include the adoptive \ntransfer of ex vivo activated T cells, immunomodulatory \nMABs, and cancer vaccines. Advances in molecular \npathology will provide the means to identify the targets \nand will be used to subtype tumors and will provide predict"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f7-7265-11ef-9a74-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 1, "chroma:document": "transfer of ex vivo activated T cells, immunomodulatory \nMABs, and cancer vaccines. Advances in molecular \npathology will provide the means to identify the targets \nand will be used to subtype tumors and will provide predict \nresponse to therapy and provide prognostic information.[6]\nConclusion\nUnfortunately , although we do fairly well  (and in some cases \nvery well) against early stage cancer, we do not do so well \nagainst Stage IV metastatic disease, particularly solid tumors. \nThere is still a long way to go before we can cure most cancers.\nFinancial support and sponsorship\nNil.\nCon\ufb02icts of interest\nThere are no conflicts of interest.\nReferences\n1. Mackay J, Jemal A, Lee NC, Parkin DM. The Cancer Atlas. Atlanta: \nAmerican Cancer Society; 2006.\n2. Hanahan D, Weinberg RA. Hallmarks of cancer: The next generation. Cell \n2011;144:646-74.\n3. Reeves GK, Beral V, Green J, Gathani T, Bull D; Million Women Study \nCollaborators. Hormonal therapy for menopause and breast -cancer risk \nby histological type: A cohort study and meta -analysis. Lancet Oncol \n2006;7:910-8.\n4. Cuzick J, DeCensi A, Arun B, Brown PH, Castiglione M, Dunn B, et al.  \nPreventive therapy for breast cancer: A consensus statement. Lancet \nOncol 2011;12:496-503.\n5. Couzin -Frankel J. Breakthrough of the year 2013. Cancer immunotherapy. \nScience 2013;342:1432-3.\n6. Bennett WP, Hussain SP, Vahakangas KH, Khan MA, Shields PG, \nHarris CC. Molecular epidemiology of human cancer risk: Gene -environment"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f8-7265-11ef-8e37-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\cancer_and_cure__a_critical_analysis.27.pdf", "page": 1, "chroma:document": "5. Couzin -Frankel J. Breakthrough of the year 2013. Cancer immunotherapy. \nScience 2013;342:1432-3.\n6. Bennett WP, Hussain SP, Vahakangas KH, Khan MA, Shields PG, \nHarris CC. Molecular epidemiology of human cancer risk: Gene -environment \ninteractions and p53 mutation spectrum in human lung cancer. J Pathol \n1999;187:8-18.\nDownloaded from http://journals.lww.com/indianjcancer by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0\nhCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdgGj2MwlZLeI= on 12/03/2023"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1f9-7265-11ef-9bbc-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 0, "chroma:document": "LECTURE NOTES \n \nFor Health Officers \n \n \n \n \nInternal Medicine \n \n \n \n  \n \n  \n \nEditors \nGetachew Tizazu, M.D. . \nJimma University \nTadesse Anteneh, M.D., M.P.H. \nHawassa University \n \n2006 \n \nIn collaboration with the Ethiopia Public Heal th Training Initiative, The Carter Center, \nthe Ethiopia Ministry of Health, and the Ethiopia Ministry of Education"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1fa-7265-11ef-8af6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 1, "chroma:document": "Funded under USAID Cooperative Agreement No. 663-A-00-00-0358-00. \n \n \nProduced in collaboration with the Ethiopia Pu blic Health Training Initiative, The Carter \nCenter, the Ethiopia Ministry of Health, and the Ethiopia Ministry of Education. \n   \n \n   \n \nImportant Guidelines for Printing and Photocopying Limited permission is granted free of charge  to print or photocopy all pages of this \npublication for educational, not-for-profit use by health care workers, students or faculty. All copies must retain all author credits and copyright notices included in the \noriginal document. Under no circumstances is it permissible to sell or distribute on a \ncommercial basis, or to claim authorship of, copies of material reproduced from this \npublication.  \n \u00a92006 by Getachew Tizazu, Tadesse Ante neh, Yoseph Mamo, Zenebe Assefa, \nAbere Bekela, Woldnecherkos Abebe, Fetih Mohammed, Tesfaye H/Tsion, \nGirma Tesfaye, and Dejuma Yadeta  All rights reserved. Except as expressly provided above, no part of this publication may \nbe reproduced or transmitted in any form or by any means, electronic or mechanical, \nincluding photocopying, recording, or by any information storage and retrieval system, without written permission of the author or authors. \n \n \n \n \nThis material is intended for educational use only by practicing health care workers or \nstudents and faculty in a health care field."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f1fb-7265-11ef-9402-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 2, "chroma:document": "i  \nPREFACE \n \nInternal medicine is a vast and complicated fiel d that is based on strong scientific and clinical \nfoundations. Moreover it is rapidly evolving and one needs periodic updating and catching up with the \nstate of the art knowledge.   \nProviding a comprehensive review of internal medici ne is not only difficult but almost impossible, as \nthe field is vast and extensive. Despite this limitation, the authors have tried to provide a basic \nframework for working knowledge of Internal medicine. Essential topics are included as much as possible, and some chapters and topics are dealt extensively, such as Infectious diseases in general and Acute febrile illnesses, Tuberculosis, and HIV/AIDS in particular, as these are known to be the commonest causes of morbidity and mortality in developing countries, like ours.  \nEven though a number of individuals have contributed in the original document of this lecture note, as \nmore than 3 years have elapsed, most of the topics are reviewed, and some topics are completely \nrewritten, to include new developments and the state of the art scientific knowledge. \nThis lecture note has been written primarily for Health officer students; however it can also be used by \nmedical students and all other health science students who deal with patients, who have medical \nillnesses. \n         G e t a c h e w  T i z a z u  \n & \n         Tadesse Anteneh"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 3, "chroma:document": "ii  \nACKNOWLEDGMENTS \n \nThe editors are very grateful to all the medical professionals from Jimma, Hawassa, and Haramaya \nUniversities, who have contributed in different ways to help develop this lecture note.  \nOur special thanks go to the contributing authors, who took time from their very tight schedules, to \nprepare the draft lecture notes, in different topics. We sincerely appreciate the effort of the reviewers who have given their valuable comments and inputs during the initial within University review, and the subsequent joint reviews conducted at the Carter center, in Addis Ababa. \nWe are mostly indebted to Dr. Akilu Azaje, Assistant professor of Internal medicine, in the department \nof Internal Medicine at the Medical faculty of A ddis Ababa University, who has reviewed the first draft \nlecture note, for his guidance and outstanding comments and valuable inputs. \nWe would like to thank Dr. Tekabe Abdosh, who reviewed some topics of this lecture note.  \nWe also thank all the staff of the Carter center, Ethiopia for their hospitable hosting and assistance \nduring the development of the lecture note.  \nLast but not least our deepest gratitude extended to Ato Aklilu Mulugeta, for his tremendous effort, \nclose follow-up and contribution in facilitating the completion of this lecture note.  \n         G e t a c h e w  T i z a z u ,  M . D .  \n          &           Tadesse Anteneh, M.D."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 4, "chroma:document": "iiiCONTRIBUTORS \n \nContributors   Chapters or Topics contributed  \nGetachew Tizazu, M.D. \nAssistant professor of internal medicine  \nFaculty of medical sciences,  Jimma University  ( Currently working for Columbia University ICAP \u2013 \nEthiopia Program) Infectious diseases \nDiseases of Metabolism and the Endocrine \nSystem \nDiseases of the connective tissue and  \nJoints \nDiseases of the Nervous system Diseases of the Cardiovascular system \nTadesse Anteneh, MD , MPH \nAssistant professor of Internal medicine ,  \nHealth sciences Faculty ,  \nHawassa University  Infectious diseases \nDiseases of the Respiratory system Diseases of the Gastrointestinal system \nHematologic diseases \nYoseph Mamo, M.D. \nAssociate professor of Internal medicine ,  \nFaculty of Medical sciences,  Jimma University  Diseases of Metabolism and the Endocrine \nSystem \n \nZenebe Assefa, M.D.  \nAssistant professor of Internal medicine ,  \nFaculty of Medical sciences ,  Jimma University  Diseases of the Nervous system  \nAbera Bekele, M.D. Assistant professor of Internal medicine ,  Faculty of Medical sciences ,  Jimma University  Diseases of the Kidneys"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 5, "chroma:document": "iv \nWoldecherkos Abebe, M.D. \nAssistant professor of Internal medicine ,  \nFaculty of Medical sciences ,  \nJimma University Diseases of the Cardiovascular System \nFetih Mohammed, M.D.  \nAssistant professor of Internal medicine ,  \nHealth sciences Faculty,  Jimma University  Disease of the Respiratory System Tuberculosis HIV/AIDS  \nTesfaye H/ Tsion M.D. \nLecturer in the department of  Internal medicine ,  \nFaculty of Medical sciences , Jimma University  Sexually transmitted Infections  HIV/AIDS \nGirma Tesfaye, M.D.  Lecturer in the department of  Internal medicine   Hematologic diseases \nDejuma Yadeta, M.D. \nLecturer in the department of Internal medicine ,  \nHealth sciences Faculty , Hawassa University Gastrointestinal diseases"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 6, "chroma:document": "vTable of Contents  \n \nPrefece ................................................................................................................... .... ......i \nAcknowledgement ............................................................................................................ii \nTable of Contents ............................................................................................................. i ii \nList of tables ................................................................................................................ ....vi \nAbbreviation .................................................................................................................. .. vii \nChapter I. Infectious diseases.............................................................................. .........1  \n1. Introduction  to infectious diaseses ......................................................... .........1 \n2. Acute Febrile Ilnesses ............................................................................. .........4 \n2.1.  Malaria  ......................................................................................... .........4  \n2.2. Typhoid (enteric) fever ................................................................... .......17  \n2.3. Relapsing fever  ............................................................................. .......22"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 6, "chroma:document": "2.2. Typhoid (enteric) fever ................................................................... .......17  \n2.3. Relapsing fever  ............................................................................. .......22 \n      2.4  Typhus fever  ................................................................................. .......29    3. Helmenthiasis and Parasitic Diseases..................................................... .......34 \n3.1 Intestinal Nematodes ...................................................................... .......34 3.2 Tissue Nematodes  ......................................................................... .......41 3.3 Filariasis & Related Infections ......................................................... .......43 3.4 Trematodes : Schistosomiasis  ....................................................... .......47 \n3.5 Cestodes ......................................................................................... .......53 \n3.6 Leishmaniasis ................................................................................. .......56 \n4 Tuberculosis ............................................................................................. .......64  5 Human Immunodeficiency Virus and AIDS............................................... .......79 \n6 Sexualy Transmited Diseases ................................................................. .....130"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 6, "chroma:document": "6 Sexualy Transmited Diseases ................................................................. .....130 \n7 Other infectious diaseses ......................................................................... .....145 \n7.1 Tetanus........................................................................................... .....145 7.2 Rabies ............................................................................................ .....150 7.3 Anthrax .......................................................................................... .....153 \n7.4 Brucellosis ...................................................................................... .....156 \n \nChapter II. Disease of the respiratory System .................................................... .....159 \n1. Common Symptoms of respiratory system ............................................ .....159 \n2. Upper Respiratory Tract Infection .......................................................... .....164"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 7, "chroma:document": "vi3. Pneumonia............................................................................................. .....169 \n4. Bronchial Asthma................................................................................... .....177 \n5. Chronic obstructive pulmonary diseases  ............................................. .....185 \n6. Suppurative lung diseases .................................................................... .....191  \n6.1 Bronchiectasis................................................................................. .....191 6.2 Lung Abscess ................................................................................. .....193 \n7. Pleurisy and pleural effusion.................................................................. .....195 8. Neoplasms of the lung .......................................................................... .....198 \n Chapter III. Diseases of the Cardiovascular System.......................................... .....203 \n1. Rhehumatic Fever ................................................................................ .....205 \n2. Congestive heart failure........................................................................ .....210"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 7, "chroma:document": "1. Rhehumatic Fever ................................................................................ .....205 \n2. Congestive heart failure........................................................................ .....210   \n3. Valvular Heart Diaseses ...................................................................... .....218 4. Infective Endocarditis .......................................................................... .....228 5. Cardiomypathies .................................................................................. .....238 \n6. Myocarditis .......................................................................................... .....246 \n7. Hypertension ....................................................................................... .....251 8. Pericarditis and Pericardial effussion .................................................. .....266 9. Ischemic Heart Diseases and Myocardial Infarction ............................ .....271 \n10. Cardiac Arrythemias ............................................................................ .....285 \n  \nChapter IV. Diaseses of the Kidneys .................................................................. .....292 \n1. Introduction to renal diseases ............................................................... .....292 \n2. Acute nephritic syndrome  .................................................................... .....297"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 7, "chroma:document": "1. Introduction to renal diseases ............................................................... .....292 \n2. Acute nephritic syndrome  .................................................................... .....297 \n3. Nephrotic Syndrome ............................................................................. .....301 4. Acute Renal Failure .............................................................................. .....305 5. Chronic Renal Failure ........................................................................... .....316 6. Urinary Tract Infection ........................................................................... .....327 \n \nChapter V. Disease of the Gastrointestinal system............................................ .....337 \n1. Approach to patients with GI disorders ....................................................... .....337 \n2. Gastritis and Peptic Ulcer Diseases ............................................................ .....342 \n3. Malabsorption ............................................................................................. .....354 \n4. Pancreatic Diseases ................................................................................... .....359 5. Hepatitis ...................................................................................................... .....365"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 8, "chroma:document": "vii 6. Chronic Liver Diseases Cirrhosis and Hepatoma ....................................... .....373 \n7. Diarrheal Diseases ...................................................................................... .....382 \n Chapter VI. Hematologic Diseases ...................................................................... .....389 \n1. Anemia ........................................................................................................ .....389 2. Lukemias ..................................................................................................... .....405 \n3. Lymphoma .................................................................................................. .....420 \n4. Disorders of Hemostasis ............................................................................. .....425 \n \nChapter VII. Disease of Metabolism and Endocrine System ............................ .....433 \n \n    1.  Introduction to Diseases of the Endocrine System ..................................... .....433     2. Diabetes Mellitus  ........................................................................................ .....435     3.  Thyroid diseases ......................................................................................... .....455     4.  Diseases of the Adrenal Gland ................................................................... .....474"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 8, "chroma:document": "5.  Diseases of the Pituitary Gland .................................................................. .....480 \n Chapter VIII. Diseases of the Nervous System ................................................... .....491 \n1. Headache .................................................................................................... .....491 \n2. Diseases of the Spinal Cord ........................................................................ .....500 \n3. Cerebrovascular diseases /Stroke .............................................................. .....507 \n4. Impairment of Consciousness and Coma.................................................... .....515 5. Seizures  and Epilepsy ................................................................................ .....523 6. Parkinson\u2019s diseases and other movement disorders ................................. .....536 \n7. Peripheral Neuropathy................................................................................. .....547 \n8. CNS infections : Meningitis and Encephalitis............................................... .....555 \n \nChapter XI. Connective Tissue Diseases and Diseases of Joints .................... .....562 \n1. Systemic Lupus Erythromatous ( SLE ) ....................................................... .....562 2. Rheumatoid Arthritis .................................................................................... .....566"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 8, "chroma:document": "1. Systemic Lupus Erythromatous ( SLE ) ....................................................... .....562 2. Rheumatoid Arthritis .................................................................................... .....566 \n3. Other connective tissue diseases : Systemic Sclerosis , Mixed connective \n      tissue disorders ........................................................................................... .....573 4. Gout ............................................................................................................ .....576"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 9, "chroma:document": "viiiLIST OF TABLES \nTableI-2.1-1 The basic characteristics of the two transmission types of malaria .... .........6 \nTable I-2.1-2 Types of plasmodium and their clinical features ............................... .........9 Table I-2.3 -1 The basic characteristics of the two types of borreliae...................... .......25 Table I-3.6-1: Important causes of cutaneous leishmaniasis................................... .......61 \nTable I- 4 -1: Tuberculosis Treatment Category...................................................... .......74 \nTable I- 4-2: Anti TB drugs are classified in to two groups ..................................... .......76 Table I-4-3: Side Effects of common Anti TB drugs and Treatment of side effects ......77  Table I-5-1. Manifestations of Tuberculosis in early and advanced HIV.................. .....100 \nTable I-5-2. Stages of ADIS dementia complex ...................................................... .....109 \nTable I-5-3. Revised classification system for HIV infection (CDC Classification)... .....122 Table I-5-4. WHO Clinical Staging System for HIV/AIDS ........................................ .....122 Table II-4-1 Comparison of the two major types of Asthma .................................... .....178 Table II-4-2. Step wise approach for managing Asthma in adults .......................... .....183 \nTable II-5-1 Summary of clinical manifestations of Chronic Bronchitis and Emphysema188"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 9, "chroma:document": "Table II-5-1 Summary of clinical manifestations of Chronic Bronchitis and Emphysema188 \nTable III -1-1 Jones criteria for the diagnosis of acute rheumatic fever ................... .....207 Table III -2-1:New York Heart Association Heart Failure Symptom Classification                         System.............................................................................................. .... .213 \nTable III-4-1: Frequencies of Occurrence of prominent Clinical and Laboratory                        Manifestations in Endocarditis........................................................... .....233 Table III -4-2  The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis ....234 Table III-5-1 Clinical classification of Cardiomyopathies ........................................ .....239 Table III-7-1 Classification of blood pressure for adults and older children ............ .....252 \nTable \u2013III-8-1.  Classification of Pericarditis ........................................................... .....267 \nTable V-1-1 Main differences between exudative and transudative ascetic fluids . .....339 Table V-2-1 Some differences in the clinical manifestations between DU and GU .....347 Table V-2-2 Regimens recommended for eradication of H. pylori infection ........... .....350 \nTable V -5-1 Comparisons of   some features of hepatitis A, B, and C .................. .....368"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 9, "chroma:document": "Table V -5-1 Comparisons of   some features of hepatitis A, B, and C .................. .....368 \nTable V-6-1 Stages of chronic hepatic encephalopathy and their manifestations .. .....379 Table VI-1-1 Criteria of anemia in adults at sea level ............................................. .....389 Table VI-1-2 Difference in between Cobalamine and Folate physiology and daily                      Requirement ....................................................................................... .....401  \nTable VI-2-1 Showing the main features of acute leukemic cells ........................... .....411 Table VIII-2-3 The treatment of acute leukemias (Cytotoxic drugs & phases of treatment)412"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 10, "chroma:document": "ix Table VI-4-1  Correlation of coagulation factor activity and severity in hemophiliac  \n                       and factor IX deficiency ................................................................... .....430 \nTable VI-4-2 Comparison between different coagulation disorders ........................ .....431 \nTable VII-2-1 Criteria for the Diagnosis of Diabetes Mellitus .................................. .... 440 Table VII-4- 2 Interpretations of Water deprivation test .......................................... .....489 Table VIII-3-1 Characteristic features of different types of stroke ........................... .....510 \nTable VIII-4-1 Glasgow coma Scale ....................................................................... .....517 \nTable VIII-5-1 Selection of antiepileptic drugs ........................................................ .....530 Table VIII-7-1 Etiologies of neuropathies based the predominant symptoms or signs .547   Table VIII-8-1 CSF analysis findings in different types of meningitis ...................... .....558"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 11, "chroma:document": "x ABBREVIATIONS AND ACRONYMS \n \nABC  \u2013 Airway, Breathing, and Circulation \nABG  - Arterial blood gas \nACTH \u2013 Adrenocorticotrophic hormone \nADH  \u2013 Antiduiretic hormone \nAFB \u2013 Acid fast bacilli \nAIDS  \u2013 Acquired Immunodeficiency Syndrome \nALT/SGPT  \u2013 Alanine aminotransferase \nAMI \u2013 acute myocardial infarction \nANC  \u2013 Antenatal care \nAPOC  \u2013 African Programme for Onchocerciasis Control \nARDS \u2013 Adult respiratory distress syndrome \nARF \u2013 Acute rheumatic fever/acute renal failure \nARTs  \u2013 Antiretroviral therapies \nASO titer  \u2013 Antistreptolysin O titer \nAST/SGOT  - Aspartate aminotransferase   \nAV - Atrioventricular or arteriovenous \nBCG \u2013 Bacille Calmette Guerin  \nBF \u2013 Blood film \nBID \u2013 Twice a day \nBLCM  \u2013 Below left costal margin \nBM \u2013 Bone marrow \nBMI \u2013 Body mass index \nBP - Blood pressure \nBPH - Benign prostatic hypertrophy \nBS \u2013 Blood sugar \nBUN \u2013 Blood Urea Nitrogen \nCAD \u2013 Coronary artery disease \nCBC  \u2013 Complete blood count \nCHF - Congestive heart failure \nCNS \u2013 Central nervous system"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 12, "chroma:document": "xi CPK  - Creatine phosphokinase   \nCR \u2013 Creatinine \nCRF - Chronic renal failure \nCRH \u2013 Corticotrophic hormone \nCSF \u2013 cerebrospinal fluid \nCT \u2013 Computerized Tomogram \nCTLs \u2013 Cytotoxic T Lymphocytes  \nCVD  \u2013 Cerebrovascular diseases \nCVS \u2013 Cardiovascular system \nCXR  \u2013 Chest x-ray \nDAT \u2013 Direct agglutination test \nDDI \u2013 Didanosine \nD4T- Stavudin \nDIC \u2013 Disseminated intravascular coagulopathy \nDirect IF  \u2013 direct Immunoflourescent  \nDKA  \u2013 diabetic ketoacidosis \nDM \u2013 diabetes mellitus \nDNA - Deoxyribonucleic acid   \nDOTS  \u2013 Directly Observed TB treatment Short course \nDW - dextrose in water \nEBV- Epstein-Barr virus  \nECF \u2013 Extracellular fluid \nECG  \u2013 Electrocardiogram \nEFV \u2013 Efavirenz  \nELISA  \u2013 Enzyme linked immunosorbent assay \nEPTB  \u2013 extrapulmonary tuberculosis \nESR - Erythrocyte sedimentation rate \nESRD \u2013 End stage renal disease \nETB \u2013 Ethambutol \nFBC \u2013 Full blood count \nFBS \u2013 Fasting blood glucose \nFSH \u2013 follicle stimulating hormone"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 13, "chroma:document": "xii GAS \u2013 Group A Streptococci \nGDM - Gestational onset diabetes mellitus \nGH \u2013 Growth hormone \nGHRH  \u2013 Growth hormone releasing hormone \nGI - Gastrointestinal \nGIT \u2013 Gastrointestinal tract \nGnTH  - Gonadotrophic hormone \nGTT - glucose tolerance test \nHAART  \u2013 Highly active antiretroviral treatment \nHAV  - Hepatitis A virus \nHBV \u2013 Hepatitis B virus \nHCV \u2013 hepatitis C virus \nHDL - high-density lipoprotein \nHgb \u2013 hemoglobin  \nHHV-8  \u2013 Human Herpes Virus-8 \nHIV \u2013Human Immunodeficiency Virus \nHx \u2013 Clinical history \nICF \u2013 Intracellular fluid \nICU \u2013 Intensive care unit \nIGT- Impaired glucose tolerance \nIHD \u2013 ischemic heart disease \nIM - Intramuscular \nINH \u2013 Isoniazid \nIV - intravenous \nIVDU  \u2013 Intravenous drug use \nJHR \u2013 Jarisch Herxheimer reaction \nJVP - Jugular venous pressure \nKS \u2013 Kaposi Sarcoma \nKUB \u2013Kidney Ureter Bladder \nLBRF \u2013 Louse borne relapsing fever \nLDH - Lactate dehydrogenase  \nLDL - low-density lipoprotein"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 14, "chroma:document": "xiiiLH - Luetenizing hormone \nLP \u2013 Lumbar puncture \nLVH \u2013 left ventricular hypertrophy \nMAC \u2013 Mycobacterium avium complex \nMDR \u2013 Multidrug resistance \nMODY 1, 2, 3  \u2013 Maturity onset diabetes of the young 1,2,3 \nMRI \u2013 Magnetic Resonant Imaging \nMTCT \u2013 Mother to Child transmission \nN/S \u2013 Normal saline   \nNCTs  \u2013 Nerve conduction test \nNK cells  \u2013 Natural killer cells \nNNN \u2013 Nichole MacNeal Novy medium \nNSAIDs  - Non-steroidal anti-inflammatory drugs \nOEPA \u2013 Onchocerciasis Eliminati on Programme for Americas \nOIs \u2013 Opportunistic infections \nOMs \u2013 Opportunistic malignancies \nP/E \u2013 Physical examination \nPaO2 \u2013 partial pressure of arterial oxygen \nPCP \u2013 Pneumocystis carinii pneumonia \nPCR  \u2013 Polymerase Chain Reaction \nPFT \u2013 pulmonary function test \nPLWHA  \u2013 People living with HIV/AIDS \nPML - Progressive multifocal leukoencephalopathy   \nPMTCT - prevention of Mother  to Child transmission \nPO \u2013 Per os (orally) \nPPD \u2013 Purified protein derivative \nPTB - pulmonary tuberculosis \nPTU - Propylthiouracil \nPZA - Pyrazinamide \nQD \u2013 once a day \nQID \u2013 four times a day \nR/O \u2013 rule out"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 15, "chroma:document": "xivRBC  - Red blood cells \nRF \u2013 relapsing fever/Rheumatic fever \nRHD \u2013 Rheumatic heart disease \nRIF - Rifampicin \nRNA \u2013 Ribonucleic acid \nRPR \u2013 Rapid  plasma reagin \nS1 - First heart sound \nS2 - Second heart sound \nS3 - third heart sound \nS4 \u2013 Fourth heart sound \nSC - Subcutaneously \nStat - Once \nSTDs  \u2013 Sexually transmitted diseases \nTB \u2013 Tuberculosis \nTBRF \u2013 Tick borne relapsing fever \nTID \u2013 Three times a day \nTLCP \u2013 TB leprosy control programme \nTRH \u2013 Thyroid releasing hormone \nU/S - Ultrasound \nUTI \u2013 Urinary tract infection \nVDRL  \u2013 Venereal Disease Research Laboratory \nWBC \u2013 white blood cells \nWHO \u2013 World Health Organization \nZDV \u2013 Zudovudine \nCMV  \u2013 cytomegalovirus \nUV-B  \u2013 Ultraviolet B \nUVA  \u2013 Ultraviolet A"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f211-7265-11ef-bf35-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 16, "chroma:document": "Internal Medicine \n \n 1CHAPTER ONE \nINFECTIOUS DISEASES \n \n1. Introduction to infectious diseases \n \nGenerally infectious diseases resu lt from bacteria, viruses, fungi, and parasites. Despite decades of \ndramatic progress in their treatment and prevention,  infectious diseases remain a major cause of \ndeath and are responsible for worsening the living conditions of many millions of people around the \nworld especially in the developing countries. Infecti ons frequently challenge the clinician\u2019s diagnostic \nskill and must be considered in the differential di agnosis of syndromes affecting a multitude of organ \nsystems. Infectious diseases often do not occur in isolated cases; rather they spread through a group exposed from a point source (e.g. a water supply cont aminated with cholera) or from individual to \nindividual (e.g. via respiratory droplets spreading tuberculosis). Many factors affect the likelihood of \nacquiring infections which include, host, environmental   microbial factors. \n \nHost and Environmental Factors     \nFor any infectious process to occur, the parasite and the host must first encounter each other. Factors \nsuch as geography (e.g. altitude and malaria), environment (e.g. mosquito breeding site and malaria), \ndisease vectors and host behavior (e.g. sexual behavior and sexually transmitted diseases) thus \ninfluence the likelihood of infection. Many Host Factors  such as age, immunization, prior illness,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d2f212-7265-11ef-9f76-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 16, "chroma:document": "disease vectors and host behavior (e.g. sexual behavior and sexually transmitted diseases) thus \ninfluence the likelihood of infection. Many Host Factors  such as age, immunization, prior illness, \nnutritional status, pregnancy, coexisting illnesses and emotional status all have some impact on the \nrisk of infection after exposure to a particular pathogen. \n \nMedical care itself can increase the patient\u2019s risk of acquiring an infection. This can occur in several ways: through contact with the pathogens during hospitalization, through injections, surgical incisions, via mucosal surfaces by end tracheal tubes and bladder catheters, through the introduction of foreign \nbodies, through alteration of the natural flora with antibiotics, and through treatment with suppressive \ndrugs such as steroids.\n \n \nMicrobial Factors    \nInfection involves complicated interaction of parasites and host and inevitably affects both. In most \ncases a pathogenic process consisting of several steps is required for the development of infections."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e72-7265-11ef-a5ea-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 17, "chroma:document": "Internal Medicine \n \n 2Since the competent host has a complex series of defense mechanisms in place to prevent infection, \nthe successful parasite must utilize specific strategies at each of these steps. The specific strategies used by bacteria, viruses, and parasites have some si milarities, but the details are unique not only for \neach class of organism but also for individual species within a class;                               \nInvasion;  \nMicroorganisms attached to mucosal surface use specific mechanisms to invade deeper structures. \nFor example, meningococci and gonococci penetrate  and traverse mucosal epithelial cells by \ntranscytotic mechanism. \nTropism; \nIn order to infect a host successfully, many pathogens occupy highly specific place within the host and \nthus are tropic to a particular body site or cell type. For example, malaria sporozoites are rapidly \ncleared from the blood into the hepatocyts, where they undergo maturation and release into the \ncirculation; trophozoites in turn can infect only the erythrocytes.  \nMicrobial virulence strategies;  \nMicrobes have developed a variety of strategies for escaping the immunity. For example, some \npathogenic organisms elaborate toxins and enzymes that facilitate the invasion of the host and are often responsible for the disease state and many bacteria are encapsulated with polysaccharides that allow them to invade and deposit in the absence of specific antibodies.\n \n \nImmune response:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e73-7265-11ef-82a7-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 17, "chroma:document": "Immune response:  \nIs a defense mechanism developed by the host for recognizing and responding to microorganisms.   It \nis divided I to two major classes. Innate and Acquired Immunity.  \nInnate immunity (Natural Immunity) :  \nIs first line of defense and serves to protect the host with out prior exposure to the infectious agent. \nThis immune response is nonspecific and has no memo ry. Examples of Innate immunity include skin \nand mucous mebrane, phagocytoses by macrophages and nutrophils, complement system etc \n \nAcquired (Adaptive) Immunity :  \nIs specific immune mechanism developed against a particular organism. It takes time to develop and \nit has long standing memory.  It has two major arms:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e74-7265-11ef-9cdb-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 18, "chroma:document": "Internal Medicine \n \n 3\u2022 Cellular immunity : comprising T- lymphocytes, NK cells  \n\u2022 Humeral Immunity : comprises of B-Lymphocytes and antibodies produced by plasma cells. \n \nLaboratory diagnosis \nThe lab diagnosis of infections requires the demonstration, either  \n1.  Direct microscopic visualization of pathogens in clinic al material (e.g. Plasmodium species in \nblood films) or the growth of microorganisms in the laboratory (e.g. culture) or \n2.   Indirect (e.g. antibody / serology test for HIV), of viral, bacterial, mycotic, or parasitic agents in \ntissues, fluids, or excreta of the host.  \nTreatment; \nOptimal therapy for infectious diseases requires a broad knowledge of medicine and careful clinical judgment. Life threatening infections such as bacteria l meningitis and sepsis require urgent   initiation \nof therapy often before a specific infective organism  is identified. Antimicrobial agents must be chosen \nempirically and must be against the range of potential infectious agents consistent with the clinical \ncondition. In contrast, good clinical judgment sometimes dictates withholding of antimicrobials in a self \nlimited process or until a specific diagnosis is made.  Certain infections (e.g. peritonitis, necrotizing \nfascitis, and abscess) require surgery as a primary m eans of cure; in these conditions, antibiotics play \nonly as an adjunctive role.  \nReferences: \n1. Kasper L., Braunwald E., Harrison\u2019s principles of  Internal medicine, 16th Edition, Intruducion to"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e75-7265-11ef-88b8-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 18, "chroma:document": "only as an adjunctive role.  \nReferences: \n1. Kasper L., Braunwald E., Harrison\u2019s principles of  Internal medicine, 16th Edition, Intruducion to \ninfectious diseases, pages 695-700."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e76-7265-11ef-adbb-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 19, "chroma:document": "Internal Medicine \n \n 42. Acute Febrile Illnesses \n \n2.1. Malaria \nLearning Objective :  At the end of this unit the student will be able to  \n1) Define Malaria  \n2) List the etiologies of the different types of malarias \n3) Describe the mode of transmission & the life cycle of malaria   \n4) Mention the epidemiology of malaria. 5) Explain the pathogenesis malaria 6) Identify the clinical features of the different malarial diseases 7) List the common complications of malaria. \n8) Describe the most commonly used tests for the diagnosis of malaria \n9) Make an accurate diagnosis of malaria 10) Treat malaria at the primary care level with  appropriate drugs   11) Design appropriate methods of prevention & control of malaria \n \nDefinition \nMalaria is a protozoal disease transmitted to man by the bite of the female anopheles mosquitoes. \nEtiology of Malaria \nMalaria is caused by the protozoan genus plasmodium . Four species are known to cause disease in \nman \nP. falciparum :  also called malignant malaria \nP. vivax            :  tertian malaria   \nP. ovale            :  tertian malaria \nP. malariae      :  quartan malaria \nN.B. Almost all deaths are caused by falciparum malaria \n Epidemiology of malaria \n\u2022 Malaria is one of the commonest infectious diseases of man having a global distribution with \nprevalence of 500 million people affected ever y year and about 2 million people die of \nmalaria/year.  40 % of the world population livi ng in tropical/subtropical climates are exposed"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e77-7265-11ef-8dbe-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 19, "chroma:document": "prevalence of 500 million people affected ever y year and about 2 million people die of \nmalaria/year.  40 % of the world population livi ng in tropical/subtropical climates are exposed \nto malaria. The prevalence of malaria is increasing because of the emergence of DDT \nresistant Anopheles mosquitoes, drug resistant plasmodia and global whether changes."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e78-7265-11ef-a33a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 20, "chroma:document": "Internal Medicine \n \n 5\u2022 Malaria is common in both low and high land areas and epidemics are commonly observed in \nthe latter with elevations between 1600 to 2150 meters during the months between September \nand December. The disease is prevalent in 75% of the country with over 40 million people at \nrisk.   \n\u2022 All human malarial parasites are found in Ethiopia, but P. falciparum and P. vivax  are the \ncommonest, accounting for 60% and 40% respectively. However P. ovale  and P . malariae  \naccount for less than 1% of all cases, \n\u2022 Endemicity of malaria is defined based on spleenic rates (palpable spleen) in children \nbetween 2 & 9 years.  Depending on this, region s are classified in to 4 endemicity areas:- \no Hypo endemic  - Where < 10% children have enlarged spleen \no Meso-endemic  - Where 10-50% children have enlarged spleen \no Hyper-endemic  - Where 51-75% of children have enlarged spleen \no Holo-endemic -   Where > 75% of children have enlarged    \" \n \n\u2022 In Holo - and H yper  endemic areas there is an intense transmission of P. falciparum people \ncan sustain more than one infectious mosquito bit per day \u2013 people are infected repeatedly in their lives. Is such places, morbidity and mortal ity are considerable during childhood. Immunity \nagainst disease is hard won and during adulthood most infections are asymptomatic. This frequent round-year transmission is termed Stable transmission ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e79-7265-11ef-8886-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 20, "chroma:document": "against disease is hard won and during adulthood most infections are asymptomatic. This frequent round-year transmission is termed Stable transmission .   \n\u2022 In Hypo  and Meso  endemic areas the transmission of malaria is low, erratic or focal, full \nprotective immunity is not acquired and symptomatic disease may occur at all ages .This is termed as Unstable transmission ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e7a-7265-11ef-b95a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 21, "chroma:document": "Internal Medicine \n \n 6   TableI-2.1-1 The basic characteristics of the two transmission types  of malaria   \n   \n Stable  Unstable  \nMosquito life  \nlong   \nshort \nMosquito bites Frequent Rare \n \nHuman immunity High Low \n \nEpidemics             No (only with rainy Season \n& migration of non- immunes to the area Yes \nEradication/ control Difficult  Possible \n Infant parasite rate  is percentage of infants with positive blood smears for malaria. It is the most \nsensitive index of transmission of malaria to a locality.  \n Transmission \n\u2022 Malaria is transmitted by the bite of the female anopheles mosquitoes or inoculation of \nblood.  The female anopheles mosquitoes carry the plasmodium parasite and discharge into human body during feeding on a blood meal.   \n \n\u2022 Transmission of malaria requires high environmental temperature and collected water \nbody, both of which are ideal conditions for breeding of mosquitoes.  Therefore, \ntransmission is common in lowlands during rainy season, especially with migration of non-immuned individuals to these areas. Rare cases of congenital transmission are known. \n \n  Life Cycle and Pathogenesis  \n\u2022 The life cycle of plasmodium is divided in to two, namely asexual and sexual cycles. \n\u2022 Sexual cycle occurs inside the  anopheles mosquitoes (definitive host)  \n\u2022 Asexual cycle occurs in human body which has two phases, namely  \n\u2010 Liver phase (pre & exoerythrocytic phase) and \n\u2010 Erythrocytic phase"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e7b-7265-11ef-8dd7-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 22, "chroma:document": "Internal Medicine \n \n 7\u2022 Human infection begins with inoculation of  plasmodium sporozoites by female anopheles \nmosquito   during blood meal. The sporozoites are transported to the liver by the blood \nwhere they invade liver cells and undergo as exual reproduction. In this phase a single \nsporozoite produces thousands (10,000 \u2013 30,000) of merozoites. The swollen liver cells rupture and discharge merozoites into the blood stream which then invade RBCs and multiply 6-20 fold every 48 to 72 hrs. When the parasites reach certain density in the \nblood, the symptomatic stage begins. In P. vivax  and P. ovale  some of these liver forms \nremain dormant (called hypnozoites) for months to years. These dormant forms \n(hypnozoites) are causes of relapses that characterize infection in these two species. \n\u2022 After entry into the blood stream, merozoites invade red blood cells and become \ntrophozoites. The trophozoites enlarge, develop pigment and then become amoeboid in shape and occupy most of the red cells consum ing nearly all hemoglobin by the end of 48 \nhr of life in the RBC. It is now called schizont .Then multiple divisions give rise to several \nmerozoites, which are released in to the blood stream when infected RBCs rupture and \nrepeat the same cycle by invading other new RBC.  This explains the anemia in malaria \nwhich is largely due to the destruction of RBC. \n\u2022 During this process the infected RBC & sometimes uninfected ones are removed from the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e7c-7265-11ef-990a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 22, "chroma:document": "repeat the same cycle by invading other new RBC.  This explains the anemia in malaria \nwhich is largely due to the destruction of RBC. \n\u2022 During this process the infected RBC & sometimes uninfected ones are removed from the \ncirculation by the spleen clearance function and contribute its share to the anemia. This immunologic function of the spleen causes enlargement of the organ. \n\u2022 In P. falciparum infected RBC containing mature forms adhere to small blood vessels \n(called cytoadherence ) and also with uninfected RBC forming rosettes ( called \nRosetting ) , both of which result in sequestration of RBCs in vital organs like the brain \nand the heart and interfere with the micro circulation and metabolism and contribute to its \nseverity. This makes detection of mature forms difficult, and only ring forms and \ngametocytes can be found on peripheral blood films. Sequestration is not a feature of other species of malaria and all stages of the parasite can be seen in the peripheral blood film.  \n\u2022 After a serious of asexual cycles some of the parasites develop in to morphologically \ndistinct, long lived sexual forms (gametocytes) that can transmit malaria.  During a blood meal gametocytes are taken by the female anopheles mosquito, the male and female gametocytes form zygotes, in the   insect\u2019s  midgut the zygotes mature in to ookinetes \nwhich then develop to oocystes and which divide to liberate several motile sporozoites."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e7d-7265-11ef-9b56-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 23, "chroma:document": "Internal Medicine \n \n 8Life Cycle of Parasite in Man \n \nLife cycle of the parasite in the \nMosquito"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e7e-7265-11ef-87af-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 24, "chroma:document": "Internal Medicine \n \n 9Clinical features  \nThe incubation period varies between 10-14 days in P. vivax , P. ovale, & P.falciparum, and \n18days to six weeks in P. malariae. \n \nTable I-2.1-2Types of plasmodium:and their clinical features  \nType of malaria Incubation period Pattern of fever Recurrence \nA) Benign form: \n \nPlasmodium malaria \n \nPl. vivax / ovale (dormant hypnocytes may stay in liver and cause later relapse)   21 \u2013 42 days \n \n10 \u2013 21 days   no fever for 2 days \n \nno fever for 1 day (both irregular at first)   no relapses \n \nrelapses possible for up to 5 years \nB) Malignant form: \nmay lead to death \nwithin days, causes almost all of deaths \ndue to malaria \nPl. falciparum 7 \u2013 20 days (Longer in 10 %) Irregular rhythm of fever due to unsynchronized replication of \nparasites no relapses \n\u2022 Early symptoms are non- specific- malaise, fatigue, headache, muscle pain and \nabdominal discomfort followed by fever, nausea and vomiting is common. \n\u2022 Classically malaria manifests in regular paroxysms of high grade fever, chills and \nrigor, occurring every 2 days in P. vivax and P.ovale, and every 3rd day in P. \nmalariae, but irregularly in P.falciparum. Malarial febrile paroxysms (which are due \nto rupture of schizonts and release of pyrogens) typically have 3 stages \n\u00be The \u201ccold stage\u201d the patient feels intensely cold & has shivering. This lasts \nfor 30 minutes to 1hour.It is characterized by vasoconstriction of vessels & the temperature rises rapidly."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e7f-7265-11ef-88d3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 24, "chroma:document": "\u00be The \u201ccold stage\u201d the patient feels intensely cold & has shivering. This lasts \nfor 30 minutes to 1hour.It is characterized by vasoconstriction of vessels & the temperature rises rapidly. \n\u00be The\u201d hot stage\u201d The patient feels hot & uncomfortable, & become delirious. \nThis stage lasts for 2-6 hours. \n\u00be The \u201csweating stage\u201d patient will have profuse sweating & become very \nmuch exhausted"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e80-7265-11ef-8c90-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 25, "chroma:document": "Internal Medicine \n \n 10Physical Findings \nUncomplicated infection has few physical findings except fever, malaise, and mild anemia, a \npalpable spleen and liver and mild jaundi ce e especially in children.  \n \nSevere and complicated Malaria \nIs defined as life threatening malaria caused by P. falciparum, and the asexual form of the parasite demonstrated in a blood film.  Clinical Criteria for diagnosing of sever and complicated falciparum malaria in adults (the \npresence of one criteria already defines a complicated malaria) \n\u2022 Cerebral malaria: is a state of unarousable coma lasting for more than 30 minutes and other causes of coma ruled out. \n\u2022 Change of level of consciousness less maked than unarousable coma \n\u2022 Generalized tonic clonic sezure  (> 2/day) \n\u2022 Severe Normocytic  anemia (Hgb < 5 g/dl) \n\u2022 Acute renal failure (Oliguria of < 400 ml/24 h and/or creatinine > 3 mg/dl) \n\u2022 Pulmonary edema or ARDS \n\u2022 Hypoglycaemia (BS < 40 mg/dl) is multi factorial \no The parasite consumes glucose \no Catabolic state increases glucose demand  of the host \no Anorexia associated with the illness \no Drugs like quinine can cause hypoglycaemia \n\u2022 Metabolic acidociis  (  lactic acidosis ) (pH < 7.25; plasma bicarbonate < 15 mmol/l) \n\u2022 Circulatory collapse, shock  ,septicaemia ( \u201c Algid Malaria \u201c ): systolic BP < 80 \nmmHg, core vs. skin temperature difference > 10\u00b0C) \n\u2022 Spontaneous bleeding / Disseminated Intravascular coagulation ( DIC) \n\u2022 Hemoglobinuria \n\u2022 Jaundice, bilirubine > 3 mg/dl"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e81-7265-11ef-a784-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 25, "chroma:document": "mmHg, core vs. skin temperature difference > 10\u00b0C) \n\u2022 Spontaneous bleeding / Disseminated Intravascular coagulation ( DIC) \n\u2022 Hemoglobinuria \n\u2022 Jaundice, bilirubine > 3 mg/dl \n\u2022 Hyperparasitemia (>5 % of erythrocytes affected by plasmodium or > 100.000 plasmodium/\u00b5l) \n\u2022 P. falciparum malaria in pregnant women is also considered as sever because it is \nassociated with adverse out comes to the mother and the foetus \nThese sever complications may occur singly, or, more commonly, in combination in the same patient"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e82-7265-11ef-98b6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 26, "chroma:document": "Internal Medicine \n \n 11Who is at risk of developing severe malaria in high transmission areas ? \no Young Children \no Visitors from non Endemic areas of any age \no Pregnant women \nLaboratory  \nSymptoms and signs of the disease are not specific to malaria, and resemble many types of \nfebrile illnesses. Therefore confirmation of infection with laboratory investigations is essential. \n1. Demonstration of the parasite by blood film  (thin & thick) stained by Giemsa or Wright\u2019s \nstain  \n\u2022 Thin blood film  is methanol fixed; you can see intact RBC with parasites inside it \nAdvantage : species identification is simple; percentage of RBC parasitized can be \nestimated  \n\u2022 Thick blood film,  not methanol fixed, RBC are lysed during staining, parasites are seen \nfree from RBC \nAdvantage : concentrates the parasite 20-40 times, this helps to determine parasite \nconcentration.  \nNOTE: A single blood film examination doesn\u2019t rule out malaria, and it should be repeatedly \ndone possibly during febrile episodes. However, studies have shown that BF can be negative in \nsmall percentage of patients with malarias \n \nOther Lab Tests  \n\u2022 Hemoglobin- anemia can be detected \n\u2022 Blood glucose \n\u2022 Peripheral morphology- Normocytic normochromic anemia - Low or normal WBC \n\u2022 LP and CSF analysis ( when indicated to R/O Meningitis )  \n\u2022 BUN/ Cr,  SGOT ,  SGPT , Serum electrolytes etc \n \nTreatment  \nDepends on the type of malaria and the severity of the diseases"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e83-7265-11ef-ae4b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 26, "chroma:document": "\u2022 LP and CSF analysis ( when indicated to R/O Meningitis )  \n\u2022 BUN/ Cr,  SGOT ,  SGPT , Serum electrolytes etc \n \nTreatment  \nDepends on the type of malaria and the severity of the diseases  \nA. Benign forms of malaria (Plasmodium malariae, vivax, ovale): \nChloroquine is effective  \nDose : Initial dose is 600 mg PO followed by 300mg after 6, 24 and 48 h subsequently."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e84-7265-11ef-82e2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 27, "chroma:document": "Internal Medicine \n \n 12N.B Cloroquine is no effect on the exoerythrocytic liver form (= reservoir). To protect \nfrom later recurrences, chloroquine therapy should be followed by:- \nPrimaquine:  (dose: 15 mg/day over 2 weeks), which is effective against liver forms \nand gametocytes. \n \nB. Treatment of P.Falciparum malaria  \n\u2022 The high treatment failure rates of chlor oquine for the treatment  of uncomplicated \nP.falciparum malaria as docum ented through a nationwide study conducted in 1997/98 in \nEthiopia, led to a treatment  policy change that recommends  the use of Sulfadoxine-\nPyrimethamine as first line drug for the treatment of uncomplicated falciparum malaria and \nchloroquine for the treatment of vivax malaria.   \n\u2022 In subsequent years, however, unpublished re ports from isolated st udies indicated higher \ntreatment failure rates. Accordingly, a nati onwide study on the therapeutic efficacy of \nSulfadoxine-Pyrimethamine for the treatment of uncomplicated falciparum malaria was \nconducted in 11 sentinel sites from October \u2013 December 200 3. Results obtained from the \nstudy showed a mean treatment failure rate of 35.9% on the 14-days follow-up and 71.8% on \nthe 28-days follow-up.  \n\u2022 This level of treatment failure rate is mu ch higher than the cut-off point recommended by \nWHO for a treatment policy change. In-vivo therapeutic efficacy and safety baseline study on \nartemether-lumefantrine was also  conducted in 4 sites by enro lling 213 subjects and after a"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e85-7265-11ef-bb38-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 27, "chroma:document": "WHO for a treatment policy change. In-vivo therapeutic efficacy and safety baseline study on \nartemether-lumefantrine was also  conducted in 4 sites by enro lling 213 subjects and after a \nfollow-up period of 14 days, no treatment failu re cases and drug side effects were reported \n \ni) Treatment of uncomplicated falciparum malaria : oral drugs are used can be used  \n In most tropical countries since resistance to chloroquine and Sulfadoxine-pyrimethamine is \nwell documented other drugs are recommended. \na) Aritemisinin and its derivatives  were developed originally in China, have proved to \nbe highly effective in adults and children. \nThere are different preparations like, Artes unate PO, or IV), Artemether (PO, IM)  \n\u2022 Artemether-Lumefantrine: (Coartem 20/120): is most widely used in Ethiopia.  \nTablet containing 20 mg Artemether plus 120 mg  Lumefantrine in a fix ed dose combination.  \nAdult Dosage:   < 35 kg: 3 tabs PO BID for 3 days  \n      > 35 Kg:  4 tabs PO BID for 3 days  \nSide effects: Dizziness and fatigue, anorexia, nausea, vomiting, abdominal pain, palpitations, \nmyalgia, sleep disorders, arthralgia, headache and rash."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e86-7265-11ef-aeec-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 28, "chroma:document": "Internal Medicine \n \n 13Contra-indications:  \n As malaria  prophylaxis either alone or in combination.  \n Persons with a previous history of reaction after using the drug  \n Pregnant women, mothers with infants less than three months of age and Infants less \nthan 5 kg  \nb) Quinine:  \nAdult dose :  600 mg PO TID for 5 \u2013 7 days alone or in combination with + Tetracycline 500 \nmg PO QID or Doxycycline 100mg PO /day for the same period \nSide effects: \n Cinchonism: Tinnitus, hearing loss, dizziness, tremor, nausea, resteleness, blurring \n Hypogycemia  : is the commonest adverse effect  \nc) Mefloquine  : Structurally ressembles Quinine. It is effective against all malarial specious \nincluding multi-drug resistant P.falciparum. Howe ver some resistance strains of P.falciparum \nfor Mefloquine are reported in some tropical countries. \nDose:   15mg/kg followed by second dose of 10mg/kg after 8-12 hr \nSide Effects : Nausea, abdominal cramp, vertigo, insomnia, sometimes acute psychosis and \nconvulsion  \nd) Sulfadoxine-pyrimethamine (oral) e.g. Fansidar -3 tablets stat as a single dose. (1 tablet = \n500mg sulfadoxine + 25 mg pyrimethamine). Cont raindicated in children less than one year. \nDue to high prevalence of resistance to this combination, it is not recommended for treatment of \nP.faciparum in most tropical countries including Ethiopia. \n\u20135 days (e.g 4 mg /kg for 3 days) in combination with Mefloquine 25 mg/kg \nTreatment of Severe and comp licated falciparum malaria:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e87-7265-11ef-8d60-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 28, "chroma:document": "P.faciparum in most tropical countries including Ethiopia. \n\u20135 days (e.g 4 mg /kg for 3 days) in combination with Mefloquine 25 mg/kg \nTreatment of Severe and comp licated falciparum malaria:   \nNB: Patients should be admitted and treated in a Hospital setting  A)  Drug Treatment: \ni) Quinine : is drug of choice for severe and complicated malaria. \nDosage and Adminstration:   \nWhere IV administration of quinine is possible  \nLoading dose:  Quinine 20 mg salt/kg of body weight by infusion over 4 hours, in 5 % \ndextrose in saline (5-10 ml/kg of body weight depending on the patient's overall fluid \nbalance).  \nMaintenance does: Twelve hours after the start of the loading dose, give quinine 10 mg \nsalt/kg of body weight in dextrose saline over 4 hours. Repeat the same dose of quinine \n(i.e. 10 mg salt/kg) every 8 hours until the patient can take oral medication."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e88-7265-11ef-8ddf-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 29, "chroma:document": "Internal Medicine \n \n 14  Wherever IV administration of quinine is not possible.  \nQuinine dihydrochloride 20 mg salt per kg loading dose intramuscularly divided in to two \nsites, anterior thigh). Then quinine dihydrochloride 10 mg salt per kg IM every 8 hours \nuntil patient can swallow. \nii) Artesunate injection (if available) : 2.4 mg/kg IV or IM stat followed by 1.2 mg/kg at 12 \nand 24 hrs and then daily.  \nB)  Supportive treatment:  \n\u2022 Bring down fever (cold sponges,  paracetamol)  \n\u2022 Administer glucose IV or PO to prevent hypoglycaemia and encourage early PO intake \nof food  \n\u2022 Ensure adequate fluid intake, check input and output and control water and electrolyte \nbalance (beware of pulmonary edema due to fluid overload).  \n\u2022 Consider transfusion in severe falciparum malaria with high parasitemia (> 20% of \nerythrocytes affected by plasmodium)  \n\u2022 Check renal function tests and blood sugar (beware of hypoglycemia).  \n\u2022 For  comatose or unconscious  patients proper nursing care is mandatory \n Position the patient on his/her sides; turn every 2 hours to avoid bed sores. \n Catheterize the bladder, monitor input-output. \n Avoid fluid overload \n Monitor blood glucose regularly \n Ensure adequate nutrition \nChronic Complications of Malaria \nTropical Splenomegaly Syndrome (Hyp erreactive malarial Splenomegaly) \nIt is a syndrome resulting from an abnormal immunologic response to repeated infection. Is \nseen is some residents of malaria endemic area in tropical Africa and Asia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e89-7265-11ef-8038-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 29, "chroma:document": "Tropical Splenomegaly Syndrome (Hyp erreactive malarial Splenomegaly) \nIt is a syndrome resulting from an abnormal immunologic response to repeated infection. Is \nseen is some residents of malaria endemic area in tropical Africa and Asia  \nIt is characterized by \n Huge spleen ( > 10 cm BLLCM ) with or with out hepatomegaly \n Hyperspleenism (anaemia, pancytopenia ) \n Marked elevation of serum IgM and anti malarial antibody \n Hepatic Sinusoidal lymphocytes  \n Peripheral B-Cell lymphocytosis \nClinical Feature:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e8a-7265-11ef-aad5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 30, "chroma:document": "Internal Medicine \n \n 15\n Abdominal mass or dragging sensation in the left upper quadrant and sometimes                        \nabdominal pan \n Anaemia and sometimes Pancytopenia  \u00c6 susceptibility to Infection \n The parasite may not be detected in peripheral blood film \nTreatment \n\u2022 Antimalarial prophylaxis for a long time , usually for the duration of malaria \nexposure.  \n\u2022 Drugs commonly used are chloroquine or mefloquine.  \n\u2022 The enlarged spleen and liver usually regress over a period of months with effective \nAntimalarial prophylaxis. \n\u2022 Splenectomy is only indicated for those with failure of antimalarial prophylaxis at least \ngiven for 6months. \nPrevention of Malaria  \nA. General measures  \nMechanical Barriers/Methods \n\u2022 Draining water collections and swampy areas \n\u2022 Use of chemical impregnated mosquito nets around beds \n\u2022 Wire mesh across windows \n\u2022 Staying indoors at night  \n\u2022 Use of long sleeved shirts and long trousers \n  Insecticides or Chemicals \n\u2022 Use insecticide spray aerosols (permethrin, deltamethrin and chlorinated \nhydrocarbons) \n\u2022 Application of insect repellents to exposed skin (e.g. diethyltoluamide) \n\u2022 DDT sprayed in the interior of houses is effective in killing the adult mosquito for many \nmonths. \n B. Drug prophylaxis  \nIt is indicated for   \n\u2022 Pregnant women in endemic areas because of   their increased risk of severe malaria \n\u2022 Children between 3 months and 4 years in endemic area (born to non-immune mother)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e8b-7265-11ef-8b70-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 31, "chroma:document": "Internal Medicine \n \n 16\u2022 Travelers to malarious areas \u0005 they should start taking drugs 1 week before traveling to \nthese areas & for 4 weeks after the individual left the endemic area. \n \nDrugs available for prophylaxis  \nIn Areas where there is chloroquine resistant P. falciparum \n\u2022 Mefloquine 250mg/week orally, effective against multi drug resistant p. falciparum, \nsafe during pregnancy \n\u2022 Doxycycline 100mg daily orally , not us ed for children < 8 years& during pregnancy \n\u2022 Maloprim (Pyrimethamine+ dapson) 1 tab orally/wk \n\u2022 Chloroquine+ proguanil combination alternative to mefloquine and doxycycline. \n \nIn areas where there is for chloroquine sensitive P.falciparum  and other\u201d benign\u201d malarias:                    \n\u2022 Chloroquine 2 tabs of 150 mg tablet orally every week  \n\u2022 Chloroquine+ proguanil combination can be used as an alternative \nReferences: \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nSalmonellosis, pages 1218-1232. \n2) Gordon c cook and Alimuddin Zumla, Manson\u2019s Tropical Diseases, 21st edition, 2003, \npages 937 \u2013 949. \n3)  Management of severe and complicated ma laria in Ethipoa , Federal MOH , 2005"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e8c-7265-11ef-b5be-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 32, "chroma:document": "Internal Medicine \n \n 172.2 Typhoid (Enteric) Fever \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define Typhoid fever    \n2. List the etiologies of typhoid fever    3. Describe the epidemiology of typhoid fever   . \n4. Explain the pathogenesis typhoid fever    \n5. Describe the clinical features of typhoid fever    6. List the common complications typhoid fever   . 7. Describe the most commonly used tests for the diagnosis of typhoid fever    8. Make an accurate diagnosis of typhoid fever    \n9. Treat typhoid fever with  appropriate antibiotics   \n10. Design appropriate methods of prevention and control of typhoid fever    \n \nDefinition:  Typhoid fever is a systemic infection characterized by fever and abdominal pain \ncaused by dissemination of Salmonella typhi and occasionally by S. paratyphi A and B and \nS.typhimarium, all of which are non capsulated, gram negative motile bacteria. \n \nEpidemiology \n\u2022 Human beings are the only hosts for S. typhi and S.paratyphi. Thus enteric fever is \ntransmitted only thorough close contact with acutely infected individuals or chronic \ncarriers through ingestion of contaminated food or water.  \n\u2022 Chronic carriers are the source of infection harboring the organisms in their gall bladder \n(especially in the presence of gall stones) and rarely at other sites.  It affects people of all ages and both sexes. Enteric fever is endemic in most developing countries."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e8d-7265-11ef-9534-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 32, "chroma:document": "(especially in the presence of gall stones) and rarely at other sites.  It affects people of all ages and both sexes. Enteric fever is endemic in most developing countries.  \n\u2022 Currently the disease is observed at a great frequency in AIDS  patients than the general \npopulation. \n \nPathogenesis \nFollowing ingestion of the organism in contaminated food or drink, Salmonella typhi passes the \ngastric barrier and reach the upper small inte stine where the bacilli invade the intestinal \nepithelium and they are engulfed by phagosoms which reside in the Peyer\u2019s patches. The bacilli multiply and enter the blood stream and cause transient bacteremia. At this stage the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e8e-7265-11ef-9086-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 33, "chroma:document": "Internal Medicine \n \n 18Salmonellae disseminate throughout the body in macrophages via lymphatic and colonize \nreticuloendothilial tissue (liver, spleen, lymph nodes, and bone marrow). Patients have relatively fewer or no signs and symptoms during this initial incubation period. Signs and symptoms, \nincluding fever and abdominal pain result when a critical number of bacteria have replicated. \nDuring weeks after initial colonization, further inflammation of the Peyer\u2019s patches may result enlargement and necrosis which may result intestinal hemorrhage and perforation. Infection may become persistent and invade the gall bladder. The clinical phase of the disease depends \non host defense and bacterial multiplication.  \n \nClinical Manifestation \nThe incubation period varies from 3-60 days.  The manifestation is dependent on inoculum size, \nstate of host defense and the duration of the disease. The Severity of the illness may range \nfrom mild, brief illness to acute, severe diseas e with central nervous system involvement and \ndeath.   \nFirst week   \n\u2022 Fever is high grade, with a daily increase in a step-ladder pattern for the 1\nst one \nweek and then becomes persistent.  \n\u2022 Headache , malaise , Abdominal pain \n\u2022 Initially diarrhea or loss stole followed by constipation in adults, diarrhea is dominate \nfeature in children \n\u2022 Relative bradycardia  \n\u2022 Splenomegally  Hepatomegaly   \n\u2022 \u201cRose spots\u201d not commonly seen in black pat ients. In whites it appears as small,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e8f-7265-11ef-a987-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 33, "chroma:document": "feature in children \n\u2022 Relative bradycardia  \n\u2022 Splenomegally  Hepatomegaly   \n\u2022 \u201cRose spots\u201d not commonly seen in black pat ients. In whites it appears as small, \npale red, blanching macules commonly over chest & abdomen, lasting for 2-3 days.  \n\u2022 Epistaxis \nSecond week \n\u2022 Fever becomes continuous \n\u2022 The patient becomes very ill and withdrawn confused, delirious and sometimes \nmay be even comatose"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e90-7265-11ef-9735-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 34, "chroma:document": "Internal Medicine \n \n 19Third Week \n\u2022 The patient goes to a pattern of \u201ctyphoidal state\" characterized by extreme toxemia, \ndisorientation, and \u201cpea-soup\u201d diarrhea and sometimes may be complicated by intestinal \nperforation and hemorrhage.  \nFourth Week \n\u2022 Fever starts to decrease and the patient may deferveresce with resolution of symptoms.  \nAt this point patient may lose weight.  \n\u2022 Relapse may occur in 10% of cases.  \n Complications  of Typhoid fever  \n\u2022 Gastrointestinal perforation and hemorrhage: are late complications that may occur in \nthe 3rd or 4th week. May develop despite c linical improvement. These complications are \nlife threatening and need immediate medical and surgical interventions \n\u2022 Other Less common complications  \n Hepatitis                                                  \n Meningitis                                             .  \n Arthritis, osteomyelitis \n Parotitis and  orchitis  \n Nephritis   \n Myocarditis  \n Bronchitis and pneumonia     \nN.B these complications can be prevented by prompt diagnosis and treatment \n \nChronic Carriers  \n\u2022 Approximately 1- 5 % of patient with Enteric fever become asymptomatic chronic carriers \n\u2022 They shed S.typhi  in either urine or stool for  > 1 year \n\u2022 Incidence of Chronic carriage is high in women and among patients with biliary \nabnormality (e.g. gall stone, carcinoma of gall bladder) and other GI malignancies.  \nDiagnosis \nCan be suggested by the presence of \n Persistent fever"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e91-7265-11ef-b09c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 34, "chroma:document": "\u2022 Incidence of Chronic carriage is high in women and among patients with biliary \nabnormality (e.g. gall stone, carcinoma of gall bladder) and other GI malignancies.  \nDiagnosis \nCan be suggested by the presence of \n Persistent fever \n Relative bradycardia, which was found to occur in 86% of Ethiopians. \n Rose spots, which occurs in 70% of whites and 20% of Ethiopians."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e92-7265-11ef-aa82-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 35, "chroma:document": "Internal Medicine \n \n 20\n Leucopenia \nBut definitive diagnosis of the disease requires laboratory tests. \n1. Isolation of the organism  by blood, stool or urine culture is diagnostic. \no The yield of recovery of the organism differs depending on the specimen cultured \nand the duration of clinical disease; \no Blood culture  -mostly (up to 90%) patients have positive culture in the 1st week, \nand only 50% by the 3rd week. The yield is much lower if patient has taken \nantibiotics prior to the test. \no Stool culture  is negative in the first week and becomes positive in 75% of \npatients in the 3rd week. Urine culture parallels stool culture. \nWidal test for O and H antigens \n\u2022 The O (somatic) antigen shows active infection whereas the H (flagellar) antigen could \nbe indicative of past infection or immunization for typhoid. \n\u2022 Widal test has certain limitations, and to make a diagnosis of current infection a 4X (fold) \nrise in titer on paired sera taken during the acute and convalescence phases is \nnecessary. \nLimitations of Widal test \n\u2022 It is non specific and a positive test could be due to \n Infection by other salmonellae (as the antigen used for the test is also \nshared by other salmonellae) \n Recent vaccination for typhoid \n Past typhoid (already treated)  \n\u2022 The demonstration of 4- fold rise in titer on paired sera is not useful for the treatment of \nacute cases, as this requires waiting for the convalescence phase of the disease and at"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e93-7265-11ef-b1c9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 35, "chroma:document": "Past typhoid (already treated)  \n\u2022 The demonstration of 4- fold rise in titer on paired sera is not useful for the treatment of \nacute cases, as this requires waiting for the convalescence phase of the disease and at \nthis stage if the patient is lucky recovery will occur.    \n \nTreatment   \nAntibiotic therapy is curative. These drugs can be given either orally or intravenous, depending on patient condition (able to take orally or not),  severity of the disease. One should note that \nfever may persist for 4-6 days despite effective antibiotic treatment"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e94-7265-11ef-8ef7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 36, "chroma:document": "Internal Medicine \n \n 21Oral drugs \nFirst Line  \nNowadays 4-amino quinolones are the drugs of choice because of their effectiveness on \nmultidrug resistant typhoid, and low relapse and carrier rates. Ciprofloxacin, norfloxacin, \nofloxacin, and pefloxacin are all equally effective. \n\u2022 Ciprofoxacin: 500mg PO BID for 10 days \n\u2022 Ceftriaxone 1-2 gm IM or IV for 10 -14 days  \n4- amino quinolones are not recommended for use in children and pregnant women because of \ntheir observed potential damaging effect on cartilage of the growing animals. However, in \nsevere infections especially by MDR strains,  we have to outweigh the benefits and the potential \nrisks. \n Alternative  \n\u2022 Azithromycine   1 gm PO daily for 5 days  \n\u2022 Chloramphenicol   500 mg Po QID for 14 days \n\u2022 Norfloxacin  400mg twice daily   for 10 days \nChloramphenicol is very cheap and also quit e effective with initia l doses of 3 - 4 g/d \nfor adults, with clinical response observed in  24 - 48hrs after initiation. Dose should \nbe reduced to 2g/d when fever starts to decrease (usually after 5 - 6 days), and \ncontinued to complete 2 weeks treatment.  \n Intravenous drugs  are recommended for critically sick patients who are admiited or for patients \nwho are unable to take oral drugs \n\u2022 Ceftriaxone 2-4gm once a day for 3 days and t hen 1- 2gm IV/IM for a total of 10- 14 \ndays. \n\u2022 Intravenous Chloramphenical  1gm IV QID for 2-3 days and then start PO medication"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e95-7265-11ef-a85f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 36, "chroma:document": "who are unable to take oral drugs \n\u2022 Ceftriaxone 2-4gm once a day for 3 days and t hen 1- 2gm IV/IM for a total of 10- 14 \ndays. \n\u2022 Intravenous Chloramphenical  1gm IV QID for 2-3 days and then start PO medication \nas soon as the patient can take oral medication.  This is a drug of choice for patients \nthat need parenteral therapy especially in Ethiopia (mainly for cost reason). \nProblems of antibiotic treatment \n\u2022 Multidrug resistant (MDR) S.typhi  is reported in different parts of the world, especially \nIndian subcontinent and Southeast Asia. Hence if resistance is suspected in an area, the preferred treatment would be with quinolones, azithromycin or third generation \ncephalosporins"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e96-7265-11ef-b4de-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 37, "chroma:document": "Internal Medicine \n \n 22\u2022 Early use of antibiotics is associated with high rate of relapse (up to 20%) as compared \nto untreated cases (where the relapse rate is 5 - 10%). This is due to inhibition of \nadequate development of immune response by early therapy. \n\u2022 Eradication of chronic carrier state  requires prolonged treatment with \n Ciprofloxacin for 4 weeks is effective and  much better than the other drugs  \n Ampicillin or Amoxicillin 100mg/kg/d ta ken with Probenecid 30mg/kg/day for 6 \nweeks. \n Co-trimexazole (160/800mg twice a day) plus Rifampicin 600mg orally/d for 6 \nweeks.. \n N.B. Drug treatment does not eradicate infection in 40% of the chronic carriers. Hence surgical \nresection of the gall bladder may sometimes be necessary. \n Prevention and  control \n\u2022 Improve environmental sanitation \n\u2022 Identification and treatment of Chronic carriers \n\u2022 Avoid food handling by chronic carriers \n\u2022 Vaccination for travelers to endemic areas \no Live oral vaccine (TY21a) 3 doses can be given to those over 6 years. Protective \nfor several years \no Purified Vi polysaccharide vaccine given in a single dose to those over 2 years \nand HIV positives, is as effective as live vaccine. \n References: \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nSalmonellosis, pages 897 - 902 . \n2) Gordon c cook and Alimuddin Zumla, Manson\u2019s Tropical Diseases, 21\nst edition, 2003, \npages 937 \u2013 949."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e97-7265-11ef-b571-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 38, "chroma:document": "Internal Medicine \n \n 232.3 Relapsing Fever \n \n Learning Objective :  At the end of this unit the student will be able to  \n1. Define relapsing fever  2. List the etiologies of the two major types of relapsing fever 3. Describe the mode of transmission relapsing fever \n4. Mention the epidemiology of relapsing fever \n5. Describe the pathophysiology of relapsing fever 6. Identify the different features of the two types of borrelia and their clinical manifestations  7. List the complications of relapsing fever 8. Describe the most commonly used tests for the diagnosis of relapsing fever \n9. Make an accurate diagnosis of relapsing fever \n10.  Manage relapsing fever at the primary care level with  appropriate drugs   11.  Design appropriate methods of prevention and control of relapsing fever \n \nDefinition \nRelapsing fever is an acute febrile illness caused by Borrelia species, presenting with \nrecurrence of characteristic febrile periods last ing for days alternating with afebrile periods.  \nRelapsing fever describes two distinct diseases: \n\u2022 Louse borne (Endemic) relapsing fever (LBRF):- transmitted by body louse Pediculus \nhumanis var corporis  \n\u2022 Tick borne (Epidemic) relapsing fever (TBRF)- transmitted by tick (Ornithodoros)  \n Etiology \nRelapsing fever is caused by Borrelia species,  which are spirochetal gram negative helical \nbacteria. \n\u2022 B. recurrentis  is the only species that cause LBRF \n\u2022 B. duttoni  is the commonest causes of TBRF in sub-Saharan Africa."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e98-7265-11ef-81f8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 38, "chroma:document": "Etiology \nRelapsing fever is caused by Borrelia species,  which are spirochetal gram negative helical \nbacteria. \n\u2022 B. recurrentis  is the only species that cause LBRF \n\u2022 B. duttoni  is the commonest causes of TBRF in sub-Saharan Africa. \nBorrelia  demonstrates remarkable antigenic variation and strain heterogeneity which help the \nparasite to escape the immune response of the host and result in recurrence of febrile episodes."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e99-7265-11ef-bcf9-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 39, "chroma:document": "Internal Medicine \n \n 24Transmission :  \nLBRF : Body lice become infected by B. recurrentis while  feeding  on spirochetemic human \nblood, the only reservoir of infection. Humans acquire infection when infected body lice are \ncrushed and their fluids contaminate mucous membrane or breaks in the skin (such as \nabrasions caused by scratching of pruritic louse bites)  LBRF is now an important disease only in the northeastern Africa, specially the highlands of \nEthiopia where an estimated 10,000 case occur annually. In Ethiopia the diseases affects \nmostly homeless men living crowded together in  very unhygienic circumstances especially \nduring rainy seasons. Some of the risk factors for LBRF are over crowding like in military \ncamps, civilian population disrupted by war and other disasters.  \nTBRF : Rodents are the primary hosts and vector ticks become infected when they feed \nspirochetemic rodents.  Ticks transmit the borreliae vertically over several generations. TBRF is \nmost highly endemic in sub-Saharan Africa  but also is found in Mediterranean and Middle \neastern countries.   \n \nPathophysiology \nIn humans, borreliae after entering the body multiply in the blood and circulate in great number \nduring febrile periods.  They are also found in  the spleen, liver, central nervous system, bone \nmarrow, and may be sequestered in these organs during periods of remission.  Severity is \nrelated to spirocheatal density in blood but systemic manifestations are related to release of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 39, "chroma:document": "marrow, and may be sequestered in these organs during periods of remission.  Severity is \nrelated to spirocheatal density in blood but systemic manifestations are related to release of \nvarious cytokines.  The disease is characterized by sub capsular and parenchymal hemorrhage with infarcts of \nspleen, liver, heart and brain is seen.  Thus, patients will have enlarged spleen and liver with \nvariable edema and swelling of brain, lung and kidneys. Relapsing fever in pregnancy can result abortion, still birth and fatal neonatal infection Death from TBRF is rare. In contrast fatality rate of LBRF may reach up to 20 % during out beaks mainly among malnourished and stressed population. \n \nClinical Features \n\u2022 The manifestation of both LBRF and TBRF are similar.   \n\u2022 Incubation period is 7 days (ranging from 2-18 days)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e9b-7265-11ef-878e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 40, "chroma:document": "Internal Medicine \n \n 25\u2022 The onset is sudden with high grade irregular fever, headache, chills, myalgias, \narthralgias, and insomnia.   \n\u2022 Patient will be withdrawn, disinterested to food and other stimuli and thirsty.  Patient will \nhave delirium associated with high grade fever, tachycardia and  dry tongue, injected \nconjunctiva and photophobia \n\u2022 Summation gallop , occasionally resulting from myocardial involvement \n\u2022 Upper abdominal tenderness with hepatosplenomegally,  \n\u2022 Scattered petechiae over the trunk, extremities and mucous membrane in 1/3 LBRF and \nfewer TBRF \n\u2022 Symptoms and signs of meningial irritation may be seen in some patients.   \n\u2022 Icteric sclera may be found in late stage of the disease.  \n Complications :-  \nLife threatening complications are unusual in otherwise healthy persons if the disease is diagnosed and treated early. Complications are common in late disease in untreated patients.  \n Epistaxis, blood streaked sputum other bleeding tendencies \n Neurologic manifestations like iridocyc litis, meningitis, coma, isolated cranial \nnerve palsies, \n Pneumonitis,  \n Myocarditis  \n Spleenic rupture of spleen etc.  . \n Without treatment, symptoms intensify over 2-7 days period and subside with spontaneous \ncrisis during which borrelia disappear from the circulation.  Such cycles of febrile periods alternating with afebrile periods may recur several times.   \nTable I-2.3-1 Basic characteristics of the two types of borreliae    \n    \n  \n    LBRF  TBRF"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e9c-7265-11ef-b3aa-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 40, "chroma:document": "crisis during which borrelia disappear from the circulation.  Such cycles of febrile periods alternating with afebrile periods may recur several times.   \nTable I-2.3-1 Basic characteristics of the two types of borreliae    \n    \n  \n    LBRF  TBRF  \nCauses B. recurrent is B. dutt oni + many others(all zoonotic \nParasite in the vector   Found in endolymph of  lice Found in all tissues, including  salivary \nglands & ovaries"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e9d-7265-11ef-b193-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 41, "chroma:document": "Internal Medicine \n \n 26 \nTransmission Contamination of mucous \nmembrane or breaks or abrasions \non the skin by body fluids of lice, \nreleased during crushing         -  \nNot transmitted by the bite of lice \nor inoculation of louse feces By bite of tick during blood meal  (organisms in the  saliva & coaxal fluid \nof borrelia) \nVertical transmission \n(Tran Ovarian) No Yes \nDistribution East Africa-Eth iopia Sub-Saharan Africa,  \nMediterranean littoral, middle east, Russia, India, China, USA \nOccurrence Epidemics are frequent in \nhomeless people living in \nunhygienic  crowded \ncondition \n Sporadic or in small often familial \nclusters \nVector longevity Short life span Lives over 10 Yrs \nJarisch \u2013 Herxheimer Reaction More sever Less sever \nEradication Easy Difficult because of: \n- the  night biting habit &  painless \nnature of the bite of ticks \n- vertical transmission/trans-ovarian/ \n-  long life span. \n \nDiagnosis \n\u2022 Diagnosis of relapsing fever is made based on demonstration of the organisms in blood, \nbone marrow, CSF etc  \nBlood Film:   \n\u2022 Giemsa or Wright stained peripheral blood smear is the most commonly done laboratory \ntest in Ethiopia, and an ideal test in the resource limited setting.   \n\u2022 Spiral organisms can be demonstrated on peripheral blood taken during febrile period \npreceding the crisis.  This is positive in more than 70% of LBRF and in lower percentage \nof patients with TBRF."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e9e-7265-11ef-aeea-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 42, "chroma:document": "Internal Medicine \n \n 27 Other Tests  \n\u2022 Dark field microscopy of unstained blood/CSF  \n\u2022 Serologic tests \n \nTreatment  \nRelapsing fever is treated with antibiotics.  In LBRF single dose of erythromycin, tetracycline, \ndoxycycline or chloramphenical, produces rapid clearance of borrelia from the blood & \nremission of symptoms.  TBRF is less sensitive to these antibiotics and requires a 7 days course of treatment. \n \n \n \nAdult Dosage  \nMedication     LBRF (single dose)  TBRF (7 day schedule) \nOral \n\u2022 Erythromycin  500mg   500mg every 6 hrs \n\u2022 Tetracycline  500mg   500mg every 6 hrs \n\u2022 Doxycycline  100mg   100mg every 12 hrs \n\u2022 Chloramphenicol  500mg   500mg every 6 hrs \nParenteral  \nPenicillin G (procaine)   600,000 I.M stat        600,000 IM daily \nDelousing of patients with Relapsing fever is important to prevent transmission and recurrence  \nJarisch- Herxheimer Reaction (JHR )  \n\u2022 Rapidly acting antibiotics regularly precipitate JHR within 1- 4 hrs of 1st dose \n\u2022 More sever in patients with LBRF than TBRF \n\u2022 It is more sever when high numbers of spirochetes are circulating in the blood \n\u2022 Jarisch- Herxheimer Reaction has three phases \nChill phase:-  lasts for 10- 30 minutes  \n\u2022 Rigor, hyperventilation, high cardiac output,  \n\u2022 High body Temperature ( > or = 41 Co)  accompanied by , agitation , confusion  \nFlush phase:  \n\u2022 Fall in body temperature, drenching sweating, Potential dangerous fall in Systemic blood \npressure  ( as  peripheral vascular resistance falls )"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31e9f-7265-11ef-944d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 43, "chroma:document": "Internal Medicine \n \n 28\u2022 Clinical and ECG evidence of myocarditis may be seen , S 3 gallop and prolonged QT \ninterval  \n\u2022 Vitals signs must be monitored closely during this time which usually lasts for <or = 8 hrs  \nRecovery (Deferverescence) phase \n\u2022 Vital signs slowly come to normal  \n\u2022 The Patients is exhausted ,  \nTreatment of JHR \n\u2022 Close monitoring of vital signs \n\u2022 Care full fluid management  \n\u2022 Control high body Temperature \n\u2022 Short term digoxin I.V administration in pat ients with evidence of myocardial dysfunction  \nPrevention and Control of Relapsing Fever \n\u2022 Avoiding over crowding  \n\u2022 Apply hygienic practices that reduce the number of body lice (washing clothes) \n\u2022 Elimination of ticks  \n\u2022 Health education  \n\u2022 Early case detection and treatment of infected persons and close contacts \n\u2022 In out breaks of LBRF, empirical single dose treatment with doxycycline  \n\u2022 Eradication of Rodents to control TBRF: ( Rodenticides )  \n \nReferences  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th  Edition, Relapsing \nfever, pages 991-994. \n2) Gordon c cook and Alimuddin Zumla, Manson\u2019s Tropical Diseases, 21st edition, 2003, \npages 937 \u2013 949 ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31ea0-7265-11ef-99fe-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 44, "chroma:document": "Internal Medicine \n \n 292.4 Rickettisial diseases: ( Epidemic and Endemic Typhus)   \n  \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define rickettsial diseases with Special Emphasis on Epidemic and Endemic Typhus 2. Classify  rickettsial diseases \n3. List the etiologies of the different types of rickettsial diseases   \n4. Describe the mode of transmission rickettsial diseases  5. Explain the epidemiology of rickettsial diseases 6. Describe the pathophysiology of rickettsial diseases 7. Identify the clinical manifestations of the different types of rickettsial diseases  8. List the complications of rickettsial diseases \n9. Describe the most commonly used tests for the diagnosis of rickettsial diseases \n10. Make an accurate diagnosis of rickettsial diseases  11. Refer complicated  cases of rickettsial diseases to hospitals for better management  12. Design appropriate methods of prevention and control of rickettsial diseases \n Definition:   \nRickettisiae are small intracellular bacteria that  are spread to man by arthropod vectors, namely \nhuman body lice, fleas, ticks & larval mites. Th e organisms inhabit the gastrointestinal tract of \nthese arthropods & spread to human host by the direct bite of the vector or the inoculation of the \norganism contained in the feces of the vector by bite induced body itching. These infections are \ncharacterized by persistence in the body, wides pread vasculitis (invading endothelial cells of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31ea1-7265-11ef-a6df-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 44, "chroma:document": "organism contained in the feces of the vector by bite induced body itching. These infections are \ncharacterized by persistence in the body, wides pread vasculitis (invading endothelial cells of \nsmall blood vessels) & multi-system involvem ent. Except in louse borne typhus humans are \naccidental hosts in most rickettisial diseases. \n \n Classification \nRickettsial diseases are classified into five general groups \n\u2022 Tick  and mite borne spotted fever group \n\u2022 Flea and louse borne typhus group \n\u2022 Chigger borne scrub typhus  \n\u2022 Ehrlichiosis \n\u2022 Q-fever"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d31ea2-7265-11ef-a789-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 45, "chroma:document": "Internal Medicine \n \n 30Etiology and Epidemiology of Epidemic and Endemic Typhus  :  \nEpidemic Typhus (Louse born ) : is caused by  R.prowazekii and  transmitted by human body \nlouse (Pediculus humanus corporis).  Lice acquire the rickettsia while ingesting a blood meal \nfrom an infected patient, the rickettsia multiply in the midgut epithelial cells of the louse and are \nexcreted via louse faeces. The infected louse defecates during a blood meal and the patient autoinoculates the organisms by scratching. It is commonly associated with poverty, cold \nweather, war and natural disasters. The disease is prevalent in mountainous areas of Africa, \nSouth America, and Asia. \n Endemic Typhus (Flea born) / Murine Typhus: is cause by R. thyphi which is transmitted by \nfleas. R.typhi  is maintained in mammalian host/flea cycles, with rats. Fleas acquire R.thyphi \nfrom rikettsemic rats and carry the organism th roughout the rest of their life span.  . Humans \nand rats are infected when rickettsia \u2013laden fleas are scratched in to pruritic bite lesions. \n \nPathophysiology \nIn man rickettsia multiply in the endothelial cells of capillaries causing lesions in the skin, brain, \nlung, heart, kidneys and skeletal muscles. Endothelial proliferation coupled with peri-vascular \nreaction causes thromboses and small hemorrhages. However, tissue and organ injury is"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 45, "chroma:document": "lung, heart, kidneys and skeletal muscles. Endothelial proliferation coupled with peri-vascular \nreaction causes thromboses and small hemorrhages. However, tissue and organ injury is \ncommonly due to increased vascular permeability with resulting edema, hypovolemia and organ ischemia. This leads to multi-system involvem ent with complications such as non-cardiogenic \npulmonary edema, cardiac dysrhythemia, encepha litis, renal and hepatic failure and bleeding.  \n \nClinical Features \nSigns and symptoms:   \n\u2022 Incubation period of 1 week \n\u2022 Abrupt onset of illness with prostration, severe headache and rapidly rising fever of 38.8 \nto 40.0 \u00b0C \n\u2022 Cough s seen in 70 % of patients , myalgia may also occur which may be severe \n\u2022 Rash, begins on upper trunk around 5th day and then becomes generalized, involving \nthe entire body except face, palms and soles;  at first, rash is macular, becoming \nmaculopapular, petechial and confluent without treatment, although in black people, rash \nmay be absent ( spotless epidemic typhus ) \n\u2022 Photophobia, with conjunctival injection and eye pain; frequent"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 46, "chroma:document": "Internal Medicine \n \n 31\u2022 Tongue may be dry, brown, furred \n\u2022 The signs of central nervous system involvement, commonly as meningo-encephalitis, \nappear towards the end of the 1st week progressing to seizure and coma .  \n \nBrill-Zinsser disease  (recrudescent typhus) : This is a mild form of epidemic typhus caused \nby reactivation of dormant R. prowazekii  in the body (in the lymph nodes) as a result of \nimmunosuppression or old age. Occurs after several years of acute infection .  The \nmanifestation of the disease is similar to  acute epidemic typhus but milder. The organisms \nmay infect other people in the presence of vectors (body lice).  \nEndemic typhus (Flea borne typhus)  \n\u2022 Epidemic typhus (also known as muri ne typhus) is a relatively milder.  \n\u2022 The incubation period is 1 - 3 weeks and followed by sudden onset of fever, \nrigors, frontal headache, pain in the back and limbs, constipation and cough (due \nto bronchitis). \n\u2022 The fever becomes constant after the third day and associated with conjunctivitis \nand orbital pain.  \n\u2022 Rash appears on the fifth day initially as blanching macules at the anterior axillary \nfolds, which subsequently spread to involve other parts of the body (sparing the face & the neck) and become purpuric.  \n\u2022 During the second week symptoms worsen and additional manifestations, such \nas sore lips, dry brown tremulous tongue, feeble pulse, enlarged spleen & delirium appear.   \nComplications of Endemic and Epidemic Typhus"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 46, "chroma:document": "\u2022 During the second week symptoms worsen and additional manifestations, such \nas sore lips, dry brown tremulous tongue, feeble pulse, enlarged spleen & delirium appear.   \nComplications of Endemic and Epidemic Typhus  \n Skin necrosis, gangrene of digits,  \n Venous thrombosis \n Interstitial pneumonia in severe cases \n Myocarditis   \n Oliguric renal failure  \n Parotitis  \nDiagnosis of rickettsial diseases is based on \nHistory, clinical course of the disease and epidemiologic of the disease may give a clue for \ndiagnosis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333e8-7265-11ef-a4a3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 47, "chroma:document": "Internal Medicine \n \n 32Laboratory investigations ;  \nSerologic tests :   \n\u2022 Indirect fluorescent antibody test \n\u2022 Weil-Felix agglutination test : This is widely used by many of the hospitals and the \nprivate clinics in this country, is not specific or sensitive. \nIsolation of the organism by inoculation  into laboratory animals is possible, it is time \nconsuming and technically demanding.  \n \nTreatment of rickettsial diseases \nEndemic Typhus  \n Doxycycline 100mg bid PO for 7-15 days \n Chloramphenicol 500mg QID PO for7-15 days \nEpidemic typhus \n Doxycycline 200mg as single dose  PO until the patient is afebrile for 24 hours.  \n Delousing louse borne typhus    \nSupportive Therapy \n Attention to fluid balance, prevention of bed sores,  \n Treat agitation with diazepam \n Steroid treatment (prednisolone 20 mg  daily for adults) in severe cases \n \nPrognosis:  Untreated disease is fatal in 7 to 40 % of cases, depending on condition of host. \nIn untreated survivors, renal insuffici ency, multiorgan involvement and neurologic \nmanifestations (12 %) are common.  However, endemic typhus has better prognosis with a \nmortality of only 1 \u2013 2%. Serious neurological, renal and other complications are unusual.  \n \nPrevention \nFor flea borne typhus \n Elimination of fleas on clothing & bedding using insecticides like 1% Malathion powder \n Apply residual insecticide powder on the floor & bedding to kill hatching fleas.  \n Rodent control using chemicals (e.g. warfarin) \nFor louse borne typhus"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333e9-7265-11ef-8c02-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 47, "chroma:document": "Elimination of fleas on clothing & bedding using insecticides like 1% Malathion powder \n Apply residual insecticide powder on the floor & bedding to kill hatching fleas.  \n Rodent control using chemicals (e.g. warfarin) \nFor louse borne typhus    \nEradicate all lice on clothing & bedding using insecticides (1% Malathion powder) \nincluding all family contacts. DDT is not useful as the lice are often resistant to it"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 48, "chroma:document": "Internal Medicine \n \n 33\n Wash the patient with soap and water & apply insecticides all over & disinfect clothing \nwith insecticides in a bag or sterilize by autoclaving. \n Protective wearing smeared with insect repellents is recommended for nurses and \nother attendants \nChemoprophylaxis: Doxycycline 100mg weekly will protect those at risk. \n \nReferences:   \n1) Kasper L., Braunwald E. , Harrison\u2019s principles of Internal medicine, 16th  Edition, \nRikettsial diseases, pages 999 - 1007 ."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 49, "chroma:document": "Internal Medicine \n \n 343. Helminthic Infections  \n\u2022 Intestinal Nematodes \n\u2022 Tissue Nematodes  \n\u2022 Filariasis and Related Infections \n\u2022 Schistosomiasis & Other Trematodes \n\u2022 Cestodes \n \n3.1 Intestinal Nematodes \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define intestinal nematodes  \n2. List the etiologies of intestinal nematodes \n3. Describe the mode of transmission of intestinal nematodes \n4. Mention the epidemiology of intestinal nematodes  5. Describe the pathophysiology of intestinal nematodes  6. Identify the clinical manifestations of intestinal nematodes \n7. List the complications of intestinal nematodes \n8. Describe the most commonly used tests to identify intestinal nematodes 9. Manage intestinal nematodes at the primary care level with appropriate drugs   10. Design appropriate methods of prevention and control of intestinal nematodes \n \nNematodes  are elongated, symmetric round worms.  These can be classified as intestinal or \ntissue nematodes. Some of the intestinal nematode species are Strongyloides stercoralis, \nEnterobius vermicularis, Trichuris trichuira, Ascaris lumbricoides, Necator americanus and \nAncylostoma  duodenale . More than a billion people worldwide are infected with one or more \nspecies of intestinal nematodes.  They are most common in regions with poor sanitation, \nespecially in developing countries.   \n \n3.1.1 Ascariasis \nDefinition:  Ascariasis is an infection caused by Ascaris Lumbricoides."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333ec-7265-11ef-a783-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 49, "chroma:document": "species of intestinal nematodes.  They are most common in regions with poor sanitation, \nespecially in developing countries.   \n \n3.1.1 Ascariasis \nDefinition:  Ascariasis is an infection caused by Ascaris Lumbricoides. \nEpidemiology  - Ascariasis has a worldwide distribution particularly in regions with poor \nsanitation.  Children frequently acquire ascariasis by the ingestion of embryonated eggs.   \nDevelopment:- The adult live in the lumen of the small intestine, especially in the jejunum.  \nEggs reach the external environment with the feces. After ingestion these eggs hatch in the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333ed-7265-11ef-9eee-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 50, "chroma:document": "Internal Medicine \n \n 35intestine, liberating minute larvae that rapidly penetrate blood or lymph vessels in the intestinal \nwall.  Some larvae reach the portal circulation & are carried to the liver; others pass through the thoracic duct.  They then reach the lung (lung phase), filtered out of blood stream.  After \nincreasing in size they migrate to the epiglottis and then down the esophagus to reach the \nintestine where mating takes place.  \n Clinical Features :  \n\u2022 During the lung phase patients may develop an irritating nonproductive cough and \nburning substantial discomfort. Fever is usual during this phase.  Chest x-ray may show evidence of pneumonitis (Leoffler's syndrome).  \n\u2022 In established infections, patients are often asymptomatic.  \n\u2022 In heavy infections, particularly in children, large bolus of worms may cause pain and \nsmall-bowel obstruction, or they could have chronic abdominal discomfort and growth retardation.  A large worm can enter and occlude the billiary tree, causing biliary colic, cholecystits & pancreatitis. \n Diagnosis:   Most cases of ascariasis can be diagnosed by the microscopic detection of \ncharacteristic Ascaris eggs in feces.  Treatment:  Mebendazole 100 mg twice daily for 3 days \nPiperazine 75mg/kg (max. 3.5g) single dos e daily for two days Pyrantel pamoate \nsingle dose of 10mg/kg Albendazole in a single dose of 400mg is also effective."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333ee-7265-11ef-ad65-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 50, "chroma:document": "Piperazine 75mg/kg (max. 3.5g) single dos e daily for two days Pyrantel pamoate \nsingle dose of 10mg/kg Albendazole in a single dose of 400mg is also effective.                        \nN.B Mebendazole and albendazole are contraindicated in pregnancy; but pyrantel pamoate and piperazine are safe. \n \n3.1.2 Hookworm \n \nDefinition:- It is infection caused by two hookworm species Ankylostoma duodenale  and \nNecator americanus . \nEpidemiology:  It is prevalent worldwide. But older children have the greatest incidence and \nintensity of hookworm infection. It is prevalent in  areas with poor sanitary conditions, particularly \nin relation to human waste disposal. Adults are usually infected when walking or walking bare"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333ef-7265-11ef-a49d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 51, "chroma:document": "Internal Medicine \n \n 36footed. Hookworm is one of the most common contributing factors for the development of iron \ndeficiency anemia in developing countries. \n \nEtiology and development :  The adults are pink or creamy white.  The oval buccal capsule \ncontains two pairs of fused teeth.  The male are 8-11mm long; the females, between 10 and 13mm.  The adult hookworms live attached to the mucosa of the small intestine.  Females liberate eggs into the lumen, which are eliminated with the feces.  Under optimum conditions of \nmoisture and temperature they hatch within 24 - 48 hours.  They then develop to become \ninfective (or filariform) larvae.  When these come into contact with unprotected human skin (usually bare foot), they penetrate the skin layers, enter the blood stream and are transported to the lungs.  Then they migrate up the bronchi and trachea and down the esophagus to reach the small intestine where maturity is attained. \nClinical features:   \n\u2022 Most hookworm infections are asymptomatic. \n\u2022 Infective larvae may provoke pruritic skin lesion at the site of penetration, as well as at \nsubcutaneous migration.  \n\u2022 Infected people may rarely present with mild transient pneumonitis.   \n\u2022 In the early intestinal phase, there may be epigastria pain, inflammatory diarrhea or \nother GI symptoms.   \n\u2022 The major consequence of chronic hookworm infection is iron deficiency because worms \nsuck blood from the intestine.  Anemia usual ly develops if there is preexisting iron"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f0-7265-11ef-a865-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 51, "chroma:document": "other GI symptoms.   \n\u2022 The major consequence of chronic hookworm infection is iron deficiency because worms \nsuck blood from the intestine.  Anemia usual ly develops if there is preexisting iron \ndeficiency states like malnutrition and pregnancy. \n \nDiagnosis:   Diagnosis is established by the finding of characteristic oval hookworm eggs in \nthe feces.  Eggs of the two species are not distinguishable.  Anemia of blood loss with Hypochromic microcytic picture is seen in hookworm disease. \n \nTreatment: Several drugs can be used to eradicate hookworm. Commonly used drugs are:  \n\u2022 Mebendazole 100mg twice daily for 3 days  \n\u2022 Albendazole 400mg in a single dose.    \n\u2022 Mild iron-deficiency anemia often can be treated with oral iron alone (ferrous \nsulphate tabs), until anemia is resolved."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f1-7265-11ef-b046-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 52, "chroma:document": "Internal Medicine \n \n 373.1.3 Strongyloidiasis \n \nDefinition:-   Strongyloidiasis is an infection by the nematode stronyloides stercoralis, the \nfemale of which usually is embedded in the mucosa of the small intestine of humans. \n \nEpidemiology:  Mainly distributed in tropical areas, particularly in South East Asia, sub-Saharan \nAfrica, and Brazil.  \nEtiology and development:   The parasitic adult female lays eggs that hatch in the intestine.  \nRhabditiform larvae passed in feces can transform in to infectious filariform larvae outside of the \nhost.  Humans acquire strongloidiasis when fila riform larvae in faecally contaminated soil \npenetrate the skin or mucous membranes.  The larvae then travel to the lungs from the blood \nstream to reach the epiglottis. They are then swallowed to the small intestine.  The minute \n(2mm-long) parasitic adult female worms reproduc e by themselves, parasitic adult males do not \nexist. \n Eggs hatch locally in the intestinal mucosa, releasing rhabditiform larvae that pass with the \nfeces into soil or the rhabditiform larvae in the bow el can develop directly into filariform larvae \nthat penetrate the colonic wall or perianal skin and enter the circulation to repeat the migration \nthat establishes internal re-infection, called autoinfection. This allows the infection to persist for decades.  \nClinical features : \n\u2022 Mild infections are usually asymptomatic.   \n\u2022 Recurrent urticaria, often involving the buttocks and wrists, is the most common"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f2-7265-11ef-9b84-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 52, "chroma:document": "Clinical features : \n\u2022 Mild infections are usually asymptomatic.   \n\u2022 Recurrent urticaria, often involving the buttocks and wrists, is the most common \ncutaneous manifestation.   \n\u2022 Adult parasites burrow into the duodeno-jejunal mucosa and can cause abdominal \n(usually midepigastric) pain, which resembles peptic ulcer pain.  Nausea, diarrhea, GI \nbleeding, mild colitis and weight loss can occur. \nThe autoinfection cycle of strongyloidiasis is normally contained by unknown factors of the \nhost's immune system.   Strongyloidiasis in immune compromised hosts  . \n\u2022 There will be hyper-infection with colitis, enteritis or mal-absorption."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f3-7265-11ef-aeab-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 53, "chroma:document": "Internal Medicine \n \n 38\u2022 In disseminated disease larvae invade not only the GIT and lung, but also the CNS, \nperitoneum, liver and  kidneys.   \n\u2022 Bacteremia may develop from enteric bacteria entering through the disrupted intestinal \nmucosa. \nDiagnosis:  In uncomplicated stongyloidiasis, the fi nding of rhabditiform larvae in feces is \ndiagnostic.  Serial stool examination may be necessary to detect the larvae.  Eggs are almost \nnever seen in stool because they hatch in the intestines. \n \nTreatment: -  Even asymptomatic patients should be treated.   \n\u2022 Thiabendazole , which is still the drug of choice, is given in a dose of 25mg/kg BID (max. \n3g/day) for 3 days. There are however common side effects like nausea, vomiting, \ndiarrhea, dizziness and neuropsychiatric disturbances.   \n\u2022 Ivermectin  200\u03bcg/kg as a single dose daily for 1 or 2 days is better tolerated.  \nDisseminated cases should be treated for 5-7 days. \n\u2022 Albendazole  400 mg can also be used in simple infections and produces 80% reduction \nin egg count and 200mg/day oral dose for 3 days gives 100% cure.. \n \n3.1.4 Trichuriasis (Whi p-worm infection) \n \nDefinition: Trichuriasis is an infection of the hum an intestinal tract caused by the nematode \nTrichuris trichiura. \nEpidemiology:- It is distributed worldwide, but is most abundant in the warm, moist regions of \nthe world, the tropics and subtropics. \nEtiology and development:- The parasites have a characteristic whip like shape.  The anterior"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f4-7265-11ef-840a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 53, "chroma:document": "Epidemiology:- It is distributed worldwide, but is most abundant in the warm, moist regions of \nthe world, the tropics and subtropics. \nEtiology and development:- The parasites have a characteristic whip like shape.  The anterior \nportion is long and thread like; the posterior portion is broader and comprises about 2/5 of the worm.  The females are slightly longer than the males, 35-50mm long. \nThe adult worms reside in the colon and caecum, the anterior portions threaded into the \nsuperficial mucosa.  Thousands of eggs are laid daily and pass with the feces.  They mature in the soil.  After ingestion, infective eggs hatch in the duodenum, releasing larvae that mature before migrating to the large bowel.  The adult worms may live for several years. \n \nClinical features: Most infections are asymptomatic.  Large worm burden may be associated, \nespecially in children, with diarrhea of long duration, dysentery, mucoid stools, abdominal pain"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f5-7265-11ef-86b6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 54, "chroma:document": "Internal Medicine \n \n 39and tenderness, dehydration, anemia, weight loss and weakness.  Rectal prolapse may occur, \nparticularly in children. Diagnosis: - Diagnosis is reached by demonstration of characteristic lemon-shaped whip \nworm eggs.  Adult worms, which are about 3-5cm long, can be seen on proctoscopy.  Treatment: -  Trichuriasis can be effectively treated with mebendazole or albendazol. \n Mebendazole 100mg twice daily for 3 days or \n Albendazole 4mg/kg as a single dose  \n \n3.1.5 Enterobiasis (Pinworm) \n \nDefinition:- Enterobiasis is an infection of the human in testinal tract by the pin worm Enterobius \nvermicularis. \nEpidemiology: Enterobiasis is found all over the world.  It is more common in temperate \ncountries than tropics. \nTiology and development:- Enterobius vermicularis is a spindle-shaped parasite of humans.  \nThe female is 8-13mm long; the male, 2-5mm.  Females lay embryonated eggs, which are \nflattened on one side. \n The gravid female worm migrates nocturnally out into the perianal region and releases upto \n10,000 immature eggs.  The eggs are rapidly in fective and are transmitted by hand-to-mouth \npassage.  The larvae hatch and mature entirely within the intestine.  Self-infection results from \nperianal scratching and transport of eggs to the hands or nails and then to mouth. Pinworm \ninfections are very common among family members."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f6-7265-11ef-a89a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 54, "chroma:document": "passage.  The larvae hatch and mature entirely within the intestine.  Self-infection results from \nperianal scratching and transport of eggs to the hands or nails and then to mouth. Pinworm \ninfections are very common among family members. \n \nClinical fearures: While pinworm infection may be asymptomatic, the most common symptom is the intense nocturnal pruritus ani.  This is because of the cutaneous irritation in the perianal region produced by the migrating gravid females and the presence of eggs.  Intense pruritus may lead to dermatitis, eczema and severe secondary bacterial infections of the skin.  Rarely, pinworms may invade the female genital tract, causing vulvovaginits and pelvic granulomas. \n \nDiagnosis:-  Eggs are not found in the stool because they are released in the perineum.  \nTherefore, eggs deposited in the perianal region are detected by the application of clear"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f7-7265-11ef-b9fb-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 55, "chroma:document": "Internal Medicine \n \n 40cellulose tape to the perianal region in the morning.  The tape is then transferred to slide to be \nseen under a microscope. Treatment: Keeping personal hygiene is part of the treatment; patients should keep their \nnails short and wash hands with soap and water after defecation. A single dose of mebendazole 100mg, or pyrantel pamoate10mg/kg, both repeated afte r 2 weeks is effective. An alternative is \npiperazine 65mg/kg for 7 days with repeat course after 2 weeks. It is advisable to treat all household contacts."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f8-7265-11ef-8987-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 56, "chroma:document": "Internal Medicine \n \n 413.2 Tissue Nematodes \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define tissue nematodes  2. List the etiologies of tissue nematodes 3. Describe the mode of transmission of tissue nematodes \n4. Mention the epidemiology of tissue nematodes \n5. Describe the pathophysiology of tissue nematodes 6. Identify the clinical manifestations of tissue nematodes  7. List the complications of tissue nematodes  8. Describe the most commonly used tests to identify tissue nematodes  \n9. Manage tissue nematodes at the primary care level with appropriate drugs   \n10. Design appropriate methods of prevention and control of tissue nematodes    \n \nTissue nematodes include Trichinosis , Visceral and Ocular larva migrans , Cutaneous larva \nmigrans , Cerbral angiostrogliasis  and Gnathostomiasis . \n \n3.2.1 Trichinosis  \nDefinition:- Disease caused by the parasite Trichinella spiralis,  characterized by an acute and \nrapid course with fever, gastrointestinal symptoms, myalgia and eosinophilia. Epidemiology:- It is widely spread throughout the temperate regions of the world wherever pork \nor pork products are eaten.  It is enzootic in wild life in Africa and man is involved sporadically by \neating fresh or inadequately cooked pork.  Etiology:- The trichina worm, T.spiralis is a white round worm just visible to the naked eye.  \nAdult male ranges from 1.4 - 1.6mm in length by 40 - 60 \u03bcm in diameter; the female is 3-4mm"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333f9-7265-11ef-809e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 56, "chroma:document": "eating fresh or inadequately cooked pork.  Etiology:- The trichina worm, T.spiralis is a white round worm just visible to the naked eye.  \nAdult male ranges from 1.4 - 1.6mm in length by 40 - 60 \u03bcm in diameter; the female is 3-4mm \nlong and about one and one - half times as broad as the male. Development:- The worm gains entrance to the digestive tract as larvae encysted in muscle \ntissue.  By the time they reach the small intest ine they are freed from their cysts, penetrate the \nduodenum epithelium and mature within a few days.  The female are fertilized and produce between 1000 and 1500 larvae during the 3-16 week period they parasitizes man.  The larva \ncirculates in the blood.  They then invade different tissues mainly the muscles. \nClinical features : -"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333fa-7265-11ef-b1f0-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 57, "chroma:document": "Internal Medicine \n \n 42Twenty-four hours following ingestion of larvae, signs of GI disturbance like nausea, vomiting, \ndiarrhea and abdominal pain may occur. With muscular infiltration there may be periorbital \nedema, myalgia and persistent fever up to 40.5oc.  The last stage is characterized by neurologic \nsymptoms and sometimes myocarditis.  \n Diagnosis:-  Blood eosinophilia develops in > 90% between 2-4 weeks after infection.  Serum \nlevels of IgE and muscle enzymes including creatine phosphokinase, lactate dehydrogenase \nand aspartate aminotransferase are elevated in most symptomatic patients.  A presumptive \ndiagnosis can be made based on fever, eosinophilia, periorbital edema and myalgias after a suspected meal.  Diagnosis is confirmed by incr easing titers of parasite specific antibody or \nmuscle biopsy demonstrating the larvae. Treatment:- Current antihelminthics are not effective.  Most lightly infected patients recover \nwith bed rest, antipyretics and analgesics.  Thia bendazole 25-50mg/kg/day for 2-5 days brings \ndown fever and eosinophilia. Mebendazole 300mg daily for 7 days is an alternative. Glucocorticoids (e.g. prednisolone 1mg /kg) are helpful for severe myositis and myocarditis.  \n3.2.2 Cutaneous Larva Migrans"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333fb-7265-11ef-82d7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 57, "chroma:document": "down fever and eosinophilia. Mebendazole 300mg daily for 7 days is an alternative. Glucocorticoids (e.g. prednisolone 1mg /kg) are helpful for severe myositis and myocarditis.  \n3.2.2 Cutaneous Larva Migrans \nCutaneous Larva Migrans (\"creeping eruption\") is skin eruption caused by burrowing larvae of animal hookworms, usually the dog and cat hookworm (Ancylostoma braziliense).  Larvae hatch from eggs passed in dog and cat feces and mature in the soil.  Humans become infected after skin contact with soil by penetration.  It is prevalent among children and in regions with warm humid climates. \n \nAfter larvae penetrate the skin, erythematous lesions form along the tortuous tracts of their migration through the dermal-epidermal junction.  The larvae advance several centimeters a day.  Intensely pruritic lesions occur any w here on the body.  The adult worm will die without \ntreatment in several weeks.   Diagnosis is readily made clinically.  \n \nTreatment  is with thiabendazole orally 25mg/kg bid or albendazol 200mg bid for 2 days or \ntopically petroleum jelly for 2-5 days."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333fc-7265-11ef-bac5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 58, "chroma:document": "Internal Medicine \n \n 433.3 Filariasis \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define filariasis 2. List the etiologies of filariasis 3. Describe the mode of transmission of filariasis  \n4. Mention the epidemiology of filariasis  \n5. Describe the pathophysiology of filariasis 6. Identify the clinical manifestations of filariasis  7. List the complications of filariasis 8. Describe the most commonly used tests to identify filariasis \n9. Manage filariasis at the primary care level with appropriate drugs   \n10. Design appropriate methods of prevention and control of filariasis \n \n3.3.1 Lymphatic filariasis \nLymphatic filariasis is caused by Wuchereria bancrofti , Brugia malayi  or Brugia timori .  While the \nlater two are found in Asia, the former is prevalent in the tropics and subtropics.  Therefore, \nW.bancrofti  is discussed below. \n \nDefinition: Filariasis (bancrofti) is due to the presence of adult W.bancrofti  in the lymphatic \nsystem or connective tissues of man.  Many species of Anopheles, Culex, Mansonia and Aedes \nare vectors. \n \nEpidemiology: It is widespread throughout much of the tropics and subtropics.  It is also found \nin some Far East countries.  Complete development of the larval forms has been found to occur in many species of mosquitoes.  Generally, W. bancrofti larvae are in lesser number (scarce) in \nthe peripheral blood by day and increase at night."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333fd-7265-11ef-83b2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 58, "chroma:document": "in some Far East countries.  Complete development of the larval forms has been found to occur in many species of mosquitoes.  Generally, W. bancrofti larvae are in lesser number (scarce) in \nthe peripheral blood by day and increase at night. \n Clinical features: The most common presentations of the lymphatic filariasis are asymptomatic \n(or subclinical) microfilaremia, hydrocel e, acute adenolymphangitis and chronic lymphatic \ndisease.  Most of infected individuals have few symptoms despite large numbers of circulating \nmicrofilaria in the peripheral blood.  But sub-clinical disease is common with microscopic \nhematuria and/or proteinuria and in men scrotal lymphangiectasia.  Only few patients progress"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 59, "chroma:document": "Internal Medicine \n \n 44to the acute and chronic stages of infection.  Patients may present acutely with high-grade \nfever, lymphangitis, and transient local edema.  Later patients may have lymphedema (upper and lower extremities) and scrotal swelling. \n \nDiagnosis:- Difficult because microfilaria may not easily be identified.  Definitive diagnosis is by \ndemonstration of microfilaria from blood, hydrocele fluid or other body fluids at night.  \nTreatment: Diethyl carbamazepine (DEC, 6mg/kg daily fo r 12 days is) the treatment of choice.  \nAlbendazol 400mg twice daily for 21 days has been shown to have microfilaricidal activity. \n \n3.3.2 Onchocerciasis \n \nDefinition: Onchocerciasis (\"river blindness\") is caused by the filarial nematode Onchocerca \nvolvulus.  Etiology:  The living parasites are white or cream colored and transparent.  The males are 19-\n42 mm long and the females 33 \u2013 50 cm. \n \nEpidemiology:- Infection in humans begins with deposition infective larvae on the skin by the \nbite of an infected black fly.  The larvae develop into adult in subcutaneous tissue and form nodules.  About 7 months to 3 years after infection the gravid female releases microfilariae that migrate out of the nodule and through out the tissues.  Infection is transmitted to other persons \nwhen a female black fly ingests microfilariae from the host\u2019s skin and these microfilariae then \ndevelop into infective larvae. \n \nClinical features:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d333ff-7265-11ef-81bd-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 59, "chroma:document": "when a female black fly ingests microfilariae from the host\u2019s skin and these microfilariae then \ndevelop into infective larvae. \n \nClinical features:  \n\u2022 Following the bite of an infected fly, there is an incubation period of several months \nbefore nodules appear. The subcutaneous nodules, onchocercomata,  are the most characteristic lesions of onchocerciasis. They usually app ear on coccyx, sacrum, thigh \nand bony prominences.     \n\u2022 But the most frequent manifestations of onchocerciasis are pruritus and rash."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33400-7265-11ef-9ce7-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 60, "chroma:document": "Internal Medicine \n \n 45\u2022 The skin lesions are characterized by wrinkling of skin and epidermal atrophy that can \nmore often lead to hypopigmentation than hyperpigmentation. Eczematous dermatitis \nand pigmentary changes are more common in the lower extremities.   \n\u2022 Visual impairment is the most serious complication of onchocerciasis.  This is due to \nintense inflammation that surrounds the dying mi crofilaria. Early lesions are conjuctivitis \nwith photophobia; sclerosing keratitis occurs in minority of patients, which leads to blindness. Inflammation in the interior eye cause iridocyclitis. \n\u2022 Patients could have enlarged inguinal lymph nodes (hanging groin). \n\u2022 Heavily infected patients could have severe wasting. \n \nDiagnosis:- Diagnosis depends on demonstration of the microfilariae in the skin snip or nodules. \nMicrofilariae are rarely found in blood smear, but may be seen in urine.  \nTreatment:  Chemotherapy is the main treatment.   \n\u2022 Ivermectin orally in a single dose of 150mg/kg, y early or semiannually is the treatment \nof choice.  No agent so far eradicates the adult worm.  The drug is microfilaricidal and \nhas many advantages: no severe ocular reaction and prevents blindness due to optic \nnerve disease by 50%, the drug is taken ora lly only once every 6 \u2013 12 months & inhibits \nthe production of microfilariae by adult female worms for some months. \n\u2022 Ivermectin is contraindicated if there is co-infection with loa loa, inn pregnant or lactating"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33401-7265-11ef-a31b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 60, "chroma:document": "the production of microfilariae by adult female worms for some months. \n\u2022 Ivermectin is contraindicated if there is co-infection with loa loa, inn pregnant or lactating \nwomen and children under the age of 5 years.  \n\u2022 Antihistamines should be given for the pruritus. \n \nPrevention \n\u2022 Personal exposure in endemic areas can be reduced by avoiding black fly localities and \nby protective clothing. Repellents are of value only for short periods as they are washed \noff by sweat. \n\u2022 Control programmes (2 in Africa and one in America) have covered over 99% of all \npopulation living in endemic areas.  \nThe control of onchocerciasis today is based on 2 strategies:  \n\u2022 Vector control by spraying insecticides. Onchocerciasis control Programme in West-\nAfrica used this strategy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33402-7265-11ef-9e0e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 61, "chroma:document": "Internal Medicine \n \n 46\u2022 Large scale Ivermectin chemotherapy is the ma in strategy being used by Onchocerciasis \nElimination Programme in the Americas (OEPA) and African Programme for \nOnchocerciasis control (APOC)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33403-7265-11ef-b548-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 62, "chroma:document": "Internal Medicine \n \n 473.4 Trematodes \n \nTrematodes or flatworms are a group of morphologically and biologically heterogeneous \nparasitic helminthes that belong to the phylum platyhelminthes.  Human trematode infections are classified according to the site they involv e; the adult flukes may in volve blood, biliary tree, \nintestines and lungs.  Blood flukes are schistosoma mansoni, S.haematobium, S.japonicum, S. \nintercalatum, and S. mekongi.  Biliary (hepatic ) flukes are opisthorchis viverini, clonorchs \nsinensis and fasciola hepatica.  Intestinal flukes are Fasciolopsis buski, and Heterophyes.  \nFinally, lung flukes are paragonimus westermani.  Because of its public health importance, only schistosomiasis is discussed here. \n \n3.4. 1 Schistosomiasis \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define schistosomiasis \n2. List the etiologies of the different types of schistosomiasis \n3. Describe the mode of transmission & the life cycle of schistosomiasis  4. Explain the risk behavior of transmission of schistosomiasis 5. Mention the epidemiology of schistosomiasis 6. Explain the pathogenesis of schistosomiasis \n7. Identify the clinical features of the different schistosomiasis \n8. List the common complications of schistosomiasis. 9. Describe the most commonly used tests for the diagnosis of schistosomiasis 10. Make an accurate diagnosis of schistosomiasis  \n11. Manage schistosomiasis at the primary care level with  appropriate drugs"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33404-7265-11ef-9984-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 62, "chroma:document": "11. Manage schistosomiasis at the primary care level with  appropriate drugs   \n12. Design appropriate methods of prevention & control of schistosomiasis  \n \nDefinition   \nSchistosomiasis (also known as Biliharziasis) is a group of diseases caused by the genus \nSchistosoma affecting mainly the gastrointestinal and genitourinary organs."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33405-7265-11ef-9bb0-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 63, "chroma:document": "Internal Medicine \n \n 48    Etiology and life cycle: Schistosomiasis  in man is caused by five species of Schistosoma  \n      S. mansoni \nS. haematobium \nS. japonicum- in southeast Asia \nS. makongi- in southeast Asia (makongi valley   Laos, Cambodia) S. intercalatum - endemic in Congo basin \nThe first three are common causes of schistosomiasis. S. haematobium is the cause of urinary \nschistosomiasis and all the rest cause intestinal schistosomiasis.  \nLife cycle \n \nMan is the definitive host where sexual reproduc tion takes place after cercarial entry by skin \npenetration and snails are intermediate hosts in which asexual regeneration continues. Each species of Schistosoma has a specific snail host i.e.   S. mansoni   -Biomphalaria species \nS. haematobium  - Bulinus species \nS. japonicum                - Onchomelania species \n \nLife cycle of Schistosomiasis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33406-7265-11ef-96c9-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 64, "chroma:document": "Internal Medicine \n \n 49Epidemiology \n \n\u2022 Distribution is world wide where appropriate snails are present. S. mansoni  is reported \nfrom Africa, Asia, Central and S. America and Europe, and S. haematobium  is endemic \nin most Africa and West Asia. The other three species have localized distribution. In \nEthiopia, only S. mansoni  and S . haematobium  are endemic. S. mansoni has a wider \ndistribution in the lower highland areas of Ethiopia between 1000- 2000 meter altitude. S. haematobium  is endemic in low lands of Ethiopia. \n\u2022 It is transmitted by cercarial skin penetration which requires contact with water bodies \ncontaining cercaria escaping from appropria te snail host. This is encouraged by limited \nsanitary facilities (lack of safe and adequate H\n2O supply and latrines) substandard \nhygienic practices, use of water for i rrigation, ignorance, poverty and population \nmovements. \n \nClinical manifestations \nIntestinal schistosomiasis is caused by all human Schistosoma except S. haematobium , \nwhich is the only cause for urinary schistosomiasis. It affects the large bowel, the liver(in the \nintestinal form), distal colon and  rectum, and manifestations are dependent on the stages of infection. The 1\nst two stages are the same for all species of Schistosoma:- \na) Stege1 . Swimmer\u2019s itch (stage of Invasion) : This is the first clinical sign of acute infection"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33407-7265-11ef-98e1-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 64, "chroma:document": "st two stages are the same for all species of Schistosoma:- \na) Stege1 . Swimmer\u2019s itch (stage of Invasion) : This is the first clinical sign of acute infection \nappearing soon after exposure, usually with in 24 \u2013 48 hrs, and characterized by itching at sites of cercarial entry commonly known as swimmer\u2019s itch . It is seen in new comers and \nnot common in indigenous people. \nb)  Stege2. Acute stage  (also called toxemia stage/ Katayama syndrome  in Asia)  \nIt is an early allergic manifestation to egg deposition (3 \u2013 l0 wks) in response to massive antigenic stimulus of eggs and include fever, headache, chills, myalgias malaise, profuse \ndiarrhea, nausea and vomiting. Patient may have generalized lymphadenopathy, hepatosplenomegally, urticaria and leucocytosis  with marked eosinophilia. Severity depends \non intensity of infection, and tends to be mild in indigenous population. \nc) Stage 3 &4  (Chronic stage ) occurs 3 months to several years later, coincides with \ndeposition of eggs in the tissues. The clinical picture represents the effect of the pathologic lesions caused by the eggs on the urinary and gastrointestinal systems. Thus urinary and \nintestinal Schistosomiasis are different in  their manifestations, as described below."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33408-7265-11ef-b77b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 65, "chroma:document": "Internal Medicine \n \n 50d) Stages 3&4 intestinal Schistosomiasis   \nThe disease is very light and symptom-less for months, and then presenting with recurrent \ndiarrhea with blood and lethargy. They may have intestinal polyps, and progressive fibrosis of \nthe intestinal wall leading to formation of strictures but intestinal obstruction is very rare. \nMoreover, granulomatous hepatitis followed by pr ogressive peri-portal fibrosis (also called \npipe stem fibrosis) may develop resulting in portal hypertension with associated splenomegally, ascites and esophageal varices that occasionally may bleed. \ne) Stages 3 and 4 urinary Schistosomiasis \nDeposition of eggs in the wall of the urinary bladder induces the formation of pseudo tubercles and epithelial hyperplasia, with subsequent fibrosis and calcification causing dribbling, incontinence, frequency, dysuria and hematuria. Chronic infection leads to obstructive uropathy, hydronephrosis, chronic pyelonephritis, renal failure and contraction of \nthe bladder. \nIn rare instances gonads, CNS (brain, spinal cord), lungs and endocrine organs can be involved. \n \nLaboratory Diagnosis   \n\u2022 Identification of the characteristic ova \nIn stool or urine by \n Direct smear method; easy but light infection can be missed  \n Sedimentation / Concentration method \n In rectal snip/bladder biopsy sample if it cannot be detected in the stool or urine. \n\u2022 Seroimmunological diagnosis lacks specificity,  \n  Clinical diagnosis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33409-7265-11ef-87a8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 65, "chroma:document": "Sedimentation / Concentration method \n In rectal snip/bladder biopsy sample if it cannot be detected in the stool or urine. \n\u2022 Seroimmunological diagnosis lacks specificity,  \n  Clinical diagnosis \n\u2022 For intestinal Schistosomiasis  \n Sigmoidoscopy and rectal snip identifies lesions and  ova of the parasite \n Ultrasound of liver and spleen to demonstrate  peri-portal fibrosis and  spleen \nenlargement \n Liver biopsy  \n\u2022 For urinary schistosomiasis \n Cystoscopy - demonstrates fibrosis and calcification of the bladder \n Bladder biopsy and histology demonstrates ova in biopsy sample \n Radiological"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3340a-7265-11ef-bb0d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 66, "chroma:document": "Internal Medicine \n \n 51o Plain abdominal X- ray may detect calcification of bladder \no Intravenous Pyelogram-to see for the presence of obstructive uropathy \no Ultrasound of the kidneys and ureter \n \nTreatment  \nDrug treatment is both safe and effective, \n\u2022 Praziquantel : has wide spectrum, effective against all species of Schistosoma, single \noral dose, has high cure rate  \n         Dose:     S. mansoni and S. haematobium = 40mg/kg orally once \n                      S. japonicum  = 60mg/kg orally once \n\u2022 Metrifonate  is effective against S. haematobium.  \n          Dose :  7.5 \u2013 10mg/kg in 3 doses at 2 wks interval  \n\u2022 Oxaminoquine  is effective against S. mansoni \n    Dose : 15mg/kg orally once for sensitive strains  \n                  In Ethiopia 40mg/kg orally once \n \nPrevention and control requires multidisciplinary approach  \n\u2022 Environmental sanitation avoidance of pollution of surface water \n Provision of latrine and sanitary waste disposal  \n Prevention of human contact with infected water \n Provision of safe and adequate water \n Protective clothing when contact is unavoidable \n Health education to reduce contact with infected water bodies \n\u2022 Elimination of the disease in the reservoir by chemotherapy \n Case finding and treatment and mass (community) treatment in selected \npopulation \n\u2022 Snail control  \n Physical control-alteration of habitat,eg removal of vegetation, drainage of   \nswamps etc \n Chemical control (moluscicides) Yuri min, Frescon, \u201cEndod\u201c (phytholacca"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3340b-7265-11ef-9993-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 66, "chroma:document": "population \n\u2022 Snail control  \n Physical control-alteration of habitat,eg removal of vegetation, drainage of   \nswamps etc \n Chemical control (moluscicides) Yuri min, Frescon, \u201cEndod\u201c (phytholacca \ndedocandra) \n Biological control- Fish or other snails that feed on vector snails"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3340c-7265-11ef-82d6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 67, "chroma:document": "Internal Medicine \n \n 52References: \n1. Schistosomiasis in Ethiopia , Patho Biology Department AAU \n2. Kasper L., Braunwald E. , Harrison\u2019s principles of Internal medicine, 16th  Edition, \nSchistosomiasis  , pages 1266-1271."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3340d-7265-11ef-b83e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 68, "chroma:document": "Internal Medicine \n \n 533.5 Cestodes \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define cestodes 2. List the types of cestodes and their etiologies  3. Describe the mode of transmission of cestodes \n4. Explain the risk behavior for the transmission of cestodes \n5. Mention the epidemiology of cestodes 6. Identify the clinical features of cestodes 7. List the common complications of infection by cestodes 8. Describe the most commonly used tests for the diagnosis of cestodes \n9. Make an accurate diagnosis of cestodes  \n10. Manage cestodes at the primary care level with appropriate drugs   11. Design appropriate methods of prevention and control of cestodes \n Cestodes or tapeworms are segmented worms .  The tapeworms can be divided into two.   \n\u2022 In one group the definitive hosts are humans, these include Taenia saginata, \nDiphyllobothrium, Hymenolepsis and Dipylidium Canium.   \n\u2022 In the other group, humans are intermediate hosts.  These are Echinococcosis, \nSparganosis and Coenurosis.   \n\u2022 Humans can be a definitive or intermediate host to T.solium. \n \n3.5.1 Taeniasis saginata \nDefinition:- Taeniasis saginata or beef tapeworm infection is caused by the presence of the \nadult beef tapeworm, T.Saginata, in the intestine of humans. \nDistribution:- It is found all over the world.  It occurs in all countries where raw meat is"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3340e-7265-11ef-a4ec-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 68, "chroma:document": "Definition:- Taeniasis saginata or beef tapeworm infection is caused by the presence of the \nadult beef tapeworm, T.Saginata, in the intestine of humans. \nDistribution:- It is found all over the world.  It occurs in all countries where raw meat is \ningested.  It is prevalent in sub-Saharan Africa and the Middle East. Ethiopia is one of the heavily affected countries. Etiology and Epidemiology: T.Saginata is a large tapeworm usually 5-10 meters in length.  \nThe scolex carries four round suckers.  Behind the scolex there is a short neck from which proglottids (segments) form.  As each proglottid ma tures, it is displaced further back from the \nneck by the formation of new, less mature segments.  Humans are the only definitive host.  Eggs deposited on vegetation can persist for months or years, until ingested by cattle.  Embryo"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 69, "chroma:document": "Internal Medicine \n \n 54from cattle intestine migrates to the muscle and transform into cysticercus.  When eaten raw or \nundercooked, this infects humans. Clinical features : Usually patients are asymptomatic.  Often infection is detected when \npatients pass proglottids with stool or alone.  Proglottids are motile and this causes perianal discomfort during discharge.  Mild abdominal pain, nausea, anorexia and weight loss can occur.  Diagnosis: The diagnosis is reached by demonstrating the eggs or proglottids in the stool. \nTreatment:  Treatment of choice is prazequantel 5 -10 mg/kg in a single dose. \n            Niclosamide as a 2 g single morning dose before breakfast is an alternative.  \n \n3.5.2 Taeniasis Solium:   \nIt is caused by T.solium from eating raw or undercooked pork. \nEtiology: The adult tapeworm resides in the upper jejunum, similar to taenia saginata.  Its \nscolex attaches to intestinal wall by both sucking disk and two rows of hooklets.  Life cycle is \nsimilar to beef tapeworm.  However, both the adult tapeworm and the larvae (Cysticerca) infect \npeople. Clinical features : Mostly patients are asymptomatic; but they could have epigastric discomfort, \nnausea and weight loss. Patients may note passage of proglottids.  When infected with \ncysticerica (cysticercosis), they are distribute d all over the body.  The major manifestations \ncome from the CNS with seizures, headache, raised intracranial pressure, mental changes etc."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33410-7265-11ef-9a83-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 69, "chroma:document": "cysticerica (cysticercosis), they are distribute d all over the body.  The major manifestations \ncome from the CNS with seizures, headache, raised intracranial pressure, mental changes etc. \nDiagnosis: The diagnosis of intestinal T.solium infection is made by the detection of eggs or \nproglottides.  Diagnosis is difficult in cysticercosis, which is done by different clinical and laboratory criteria. \nTreatment: Intestinal T.solium  infection is treated with a single dose of prazequantel 5-10 \nmg/kg, this treatment may be complicated by dev elopment of CNS inflammation if cysticercosis \nco-exist. If patients develop CNS symptoms, refer them to a hospital. \n \n3.5.3 Hymenolepis nana (Dwarf tapeworm) \nEtiology: Dwarf tapeworm is 25-40mm in length by 1mm in breadth.  The scolex bears four \nsmall suckers.   Epidemiology: It is distributed all over the world.  \nThis tapeworm doesn't require intermediate host.  Hatching of eggs occurs in the small intestine where they penetrate the villus and become cysticercoid."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33411-7265-11ef-ab50-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 70, "chroma:document": "Internal Medicine \n \n 55Eventually the parasites breakout in to the lumen of the gut and reach maturity.  Infection is \nprevalent in children. Clinical features: Most infections are asymptomatic.  Severe infections may manifest with \nabdominal pain, anorexia and diarrhea. Diagnosis: Diagnosis is based upon demonstration of the eggs in the stool. \nTreatment: -  The treatment of choice is praziquantel 25 mg/kg as single dose. \n  A course of niclosamide for 7 days is also effective. \n \n3.5.4 Diphyllobothriasis (fish tape worm):-  \nDiphyllobothriasis is infection caused by adult Diphyllobothrium latum. It is acquired from eating \nraw fish. Etiology: It is mostly found in Europe and Northern hemisphere.  It is the longest tapeworm \nreaching up to 25 meters. Clinical: Many people are asymptomatic.  But pati ents could have abdominal pain, loss of \nappetite, anorexia, nausea, diarrhea or loss of weight.  Since this tapeworm consumes a lot of vitamin B12 and interferes with its absorption, it can cause vitamin B12 deficiency; and some patients develop megaloblastic anemia. \n \nDiagnosis: Diagnosis is reached by demonstration of characteristic eggs in the stool. \nTreatment: \n\u2022 Praziquantel 5-10 mg/kg once is very effective.  \n\u2022 Vitamin B12 deficiency should be treated if present. \n \nN.B further reading Module on  intestinal parasitosis, by Health Science College, \nHawassa University"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 71, "chroma:document": "Internal Medicine \n \n 563.6 Leishmaniasis \n \n Learning Objective :  At the end of this unit the student will be able to  \n1. Define leishmaniasis \n2. Classify leishmaniasis 3. List the etiologies & animal reservoirs of the different types of leishmaniasis 4. Describe the mode of transmission leishmaniasis \n5. Explain the epidemiology of leishmaniasis \n6. Describe the pathophysiology of visceral leishmaniasis 7. Identify the clinical manifestations of the different types of leishmaniasis  8. List the complications of visceral leishmaniasis  9. Describe the most commonly used tests for the diagnosis of leishmaniasis \n10. Make a presumptive diagnosis of leishmaniasis  \n11. Refer suspected cases of leishmaniasis to hospitals for investigation & treatment  12. Design appropriate methods of prevention andcontrol of leishmaniasis \n \nDefinition : is an infectious disease caused by the protozoa called Leishmania \nClassification of leishmaniasis There are three major clinical forms of leishmaniasis : \n\u2022 Visceral leishmaniasis   \n\u2022 Cutaneous leishmaniasis   \n\u2022 Mucocutaneous leishmaniasis   \n \nEtiologic Agents \nThe different clinical forms of leishmaniasis (listed above) are caused by different species of \nleishmanial parasites which are listed under each of these diseases. The parasites are seen in \ntwo forms \n\u2022 Leishmanial form:-  ( amastogote )  this is non flagellate form seen in man and extra \nhuman vertebrate reservoir"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 71, "chroma:document": "leishmanial parasites which are listed under each of these diseases. The parasites are seen in \ntwo forms \n\u2022 Leishmanial form:-  ( amastogote )  this is non flagellate form seen in man and extra \nhuman vertebrate reservoir \n\u2022 Leptomonad forms (also called promastigotes) are flagellated forms  \nThe parasite is transmitted by the bite of vectors of the species phlebotomus, Sand flies"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 72, "chroma:document": "Internal Medicine \n \n 57Life Cycle of Leshimaniasis  \n\u2022 Transmitted by the bite of an infected female phlebotomine Sand fly, the leishmaniases \nare globally widespread diseases. Sand flies are primarily infected by animal reservoir \nhosts, but humans are also a reservoir for some forms. Animal Reservoirs: include \nRodents - Commonly in East Africa, Ethiopia, the Sudan and Kenya and Canines - Mediterranean and Asia. \n\u2022 The life-cycle starts when a parasitized female  sandfly takes a blood meal from a human \nhost. As the sandfly feeds, promastigote forms of the leishmanial parasite enter the human host via the proboscis. Within the human host, the promastigote forms of the parasite are ingested by macrophage where they metamorphose into amastigote forms \nand reproduce by binary fission. They increase in number until the cell eventually bursts, \nthen infect other phagocyctic cells and continue the cycle. \n\u2022 The infected host is bitten by another female sandfly. Parasites are picked up by the fly \nduring the blood meal. The parasites are transformed inside the fly and delivered to a \nnew host, and the life-cycle continues \n \nFig 3.6.1 Life cycle of Leshimania"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 73, "chroma:document": "Internal Medicine \n \n 58Visceral Leishmaniasis (Kala Azar) \n \nVisceral leishmaniasis is a chronic systemic disease caused by L. donovani.   It is characterized \nby chronic irregular fever, profound wasting, debility and hepatosplenomegally. \n Epidemiology  \nVisceral leishmaniasis affects many countries in Africa, mainly Ethiopia and the Sudan the \nMiddle East, Southern soviet union, India and S. America.  It is endemic in low land Ethiopia \nmainly North Western Ethiopia (Metema, Humera), Gikawo (Gambella), lower Omo river basin \nand in the south Woito and Segan river basin, Moyale and lower Genale river.  The disease is becoming a common opportunistic infection in HIV/AIDS.  \nTransmission \nThe commonest way of transmission is by inoculation of promastigotes into humans by the bite of sand flies which breed in termite hills and forests. The source of the aflagellate forms may be either humans or extra human vertebrate reservoirs, and the disease may have life cycles that involve humans and sand flies only, or humans, sand flies and extra human \nvertebrate reservoirs together. Rarely transmission may occur via blood transfusion and injections.  \nPathogenesis \nThe common site of entrance is the skin where primary cutaneous lesion appears at the sites of \nsand fly bite.  The lesion is tiny and may pass unnoticed.  This is also called primary"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 73, "chroma:document": "Pathogenesis \nThe common site of entrance is the skin where primary cutaneous lesion appears at the sites of \nsand fly bite.  The lesion is tiny and may pass unnoticed.  This is also called primary \nleishmanioma.  Here a cellular reaction by lymphocytes and plasma cells develop around the amasitigote-filled histiocytes in the dermis.  As immune response develops epitheloid and giant \ncells appear, to be followed in some by healing. \n \nIn others usually 4-6 months later amastigotes escape to the blood in macrophages, hematogeneous spread occurs and colonize the cells of reticuloendothelial system, where they multiply further and released after rupture of the cells and transported to new cells.  The cells affected include that of spleen, liver, bone marrow and lymphatic glands, where the parasite \nmultiplies and cause overcrowding of cells and as a result these organs are enlarged."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 74, "chroma:document": "Internal Medicine \n \n 59The spleen is grossly enlarged with smooth capsule initially, which become thickened & nodular \nas disease progresses.  The involvement of the bone marrow leads to the development of pancytopenia.  The liver with its Kuppfer cells packed with amastigotes is enlarged & progress \nto cirrhosis. The lymphatic glands are enlarged & congested especially the mesenteric group. \n \nClinical Features \n\u2022 Incubation period usually varies from weeks to months but can be as long as years.   \n\u2022 Visceral infections remain sub clinical or become symptomatic with acute, sub acute or \nchronic course.   \n\u2022 The onset is often gradual but can also be sudden with high grade fever (intermittent or \nremittent) lasting for 2-6 weeks and occasionally longer.  Waves of fever are separated \nby afebrile periods.   \n\u2022 In those with gradual onset in endemic areas discomfort below the left costal margin is \ncommon due to enlarged spleen and have cough, epistaxis and diarrhea.   \n\u2022 The patient will be markedly emaciated, with hepatosplenomegally, generalized \nperipheral lymphadenopathy and marked pallor in the late stage of the disease.   \n\u2022 Edema of the legs, brittle dry hair, hemorrhages from any site (gum, skin etc) with \npurpura and petechiae of the skin may occur. \n\u2022 Some patients develop post - Kala- Azar derma  leishmaniasis after months or years of \ntreatment for VL. \n \nDiagnosis \n\u2022 Definitive diagnosis is based on demonstration of the Parasite"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33418-7265-11ef-a8bc-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 74, "chroma:document": "purpura and petechiae of the skin may occur. \n\u2022 Some patients develop post - Kala- Azar derma  leishmaniasis after months or years of \ntreatment for VL. \n \nDiagnosis \n\u2022 Definitive diagnosis is based on demonstration of the Parasite \n- Giemsa stained smear of peripheral blood (in Indian form) and tissue touch \npreparation of organ aspirates and examined by light microscopy. \n- Culture of tissue aspirates taken from the spleen,  BM, liver or lymph node with \nthe corresponding yield of 95%, 85%, 75%, 60% respectively, using different media (NNN or Schneider insect media) \n\u2022 Serologic diagnosis  - ELISA or DAT, both 100% sensitive & specific \n\u2022 Montenegro skin test  - negative in visceral leishmaniasis, becomes positive 6-8 wks \nafter recovery. \n\u2022 CBC  - Pancytopenia (anemia, leucopoenia, thrombocytopenia)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33419-7265-11ef-82c7-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 75, "chroma:document": "Internal Medicine \n \n 60Management \nPatients need hospitalization for proper treatment and follow up. \n\u2022 Supportive treatment \n Blood transfusion to correct anemia \n Treat any additional infection \n Correct malnutrition \n\u2022 Definitive treatment \nPentostam / Sodium Stibogluconate :  IV, IM 20mg sb/kg per day for 28 days  \nFor relapse or incomplete cure the same drug can be used for 40-60 day \nIf resistant to the above drug use alternative drugs  \nAmphotercine B lipid formulation:   IV 2- 5mg/kg per day 5-25 weeks \nPetntamidine:  IV, IM 4 mg/kg per day for 3-4 weeks  \nPrevention measures should include  \n\u2022 Reduction of human contact with sand flies by using  \n Insecticide impregnated bed nets  \n Wearing protective clothing and covering as much skin as possible \n Chemical repellents applied on exposed skin before hours of sandfly activity \n(dusk and night) are effective. \n Combustion of permethrin containing mosquito coils is also effective \n   Screening windows and doors \n\u2022 Reduction of sand fly population by using insecticides  DDT, Malathion \n\u2022 Control of reservoir - dogs rodent \n\u2022 Construct huts and camps away from breeding sites (termite hills and forests).   \n\u2022 Destroy sand fly breeding sites \n \nCutaneous Leishmaniasis (oriental sore) \n \nThe skin is one of the organs commonly affected by leishmania. Following the bite of sand flies, \nleishmania multiply in the macrophages of the skin.  Single or multiple painless nodules occur"}


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topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 75, "chroma:document": "Cutaneous Leishmaniasis (oriental sore) \n \nThe skin is one of the organs commonly affected by leishmania. Following the bite of sand flies, \nleishmania multiply in the macrophages of the skin.  Single or multiple painless nodules occur \non exposed areas (mainly the face) within one week to 3 months of the bite.  The nodules may enlarge and ulcerate with erythematous raised border and overlying crust which may spontaneously heal over months to years.  Different clinical patterns are described depending on the etiologic agents as follows:-"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 76, "chroma:document": "Internal Medicine \n \n 61Table I- 3.6-1: Important causes of cutaneous leishmaniasis \n           \nIn the Old World \n  \nLeishmani\na Species  Distribution  Reservoir  Clinical Pattern  \nL.major & \nL.tropica Russia & Eastern Europe middle east, the \nMediterranean sub-Saharan& west Africa. \n           Desert rodent for \nL.major dog& \nhumans for L.tropica Spontaneous healing with \nscaring \nL. ethiopica Highlands of Ethiopia    & \nKenya Hyrax Spontaneous healing with \nin 6 mo \nIn the New World \n  \nL. amazonensis   Diffuse cutaneous \nleishmaniasis resembling \nlepromatous leprosy (but spares the nasal septum) \nL. peruviana Cooler climates( Andes)  Single or multiple \nulcers(Uta),heal \nspontaneously \nL. mexicana  Mexico, Guatemala  \nBrazil, Venezuela & \nPanama    Infection of Pinna \n(chiclero's ear) Causes destruction of Pinna lesion \npersisting for more  than \n20 yrs. \n \nInvestigation for Diagnosis \n\u2022 Giemsa staining of smear from a split skin :  This demonstrates leishmania in 80% of \ncases \n\u2022 Culture followed by smear"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 77, "chroma:document": "Internal Medicine \n \n 62\u2022 Leishmanin skin test is positive in over 90% of cases although it is negative in diffuse \ncutaneous leishmaniasis. \n \nTreatment  \nSmall lesions don't require treatment.  However la rge lesions or those on cosmetically important \nsites require treatment either \n\u2022 Locally - by surgery, curettage, cryotherapy or hyperthermia (40-420c) or \n\u2022 Systemic therapy:   with drugs like Pentostam.  \n N.B. Treatment is less successful than visceral leishmaniasis as antimonials are \npoorly concentrated in the skin L. ethiopica is resistant to antimonials. \n \nMucocutaneous Leishmaniasis  \n\u2022 It is caused by  L. braziliensis , and commly seen Latin America (Brazil, Ecuador. Bolivia, \nUruguay and Northern Argentina)  \n\u2022 In the early stage it affects the skin, but in secondary stage of the disease it involves the \nupper respiratory mucosa.  \n\u2022 Initially painful, itchy nodules appear on the lower limbs and then ulcerate with \nlymphangitis.  Tue lesion may heal spontaneously in 6 months.   \n\u2022 In about 40% of patients, secondary lesions appear several years later at the \nmucocutaneous junctions of nesopharynx.  This leads to nasal obstruction, ulceration, \nseptal perforations and destruction of the nasal cartilage called Espundia. \nDiagnosis  is difficult as there are a few leishmania in the lesions \n  \n\u2022 Leishmanin skin test is often positive \n\u2022 Antibody tests (DAT, ELISA) are often positive"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 77, "chroma:document": "septal perforations and destruction of the nasal cartilage called Espundia. \nDiagnosis  is difficult as there are a few leishmania in the lesions \n  \n\u2022 Leishmanin skin test is often positive \n\u2022 Antibody tests (DAT, ELISA) are often positive \n \nTreatment:  Requires systemic antimonials (Pentostam) but relapses are common.  \nAmphotericin is sometimes used. Death usually occurs from secondary  bacterial infection"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 78, "chroma:document": "Internal Medicine \n \n 63References:  \n1. Kasper L., Braunwald E. , Harrison\u2019s principles of Internal medicine, 16th  Edition, \nLeshimaniasis  , pages 1233-1237."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 79, "chroma:document": "Internal Medicine \n \n 644.  Tuberculosis \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define Tuberculosis \n2. List the etiologic agents for Tuberculosis 3. Describe the mode of transmission of Tuberculosis   \n4. Understand the epidemiology of Tuberculosis  \n5. Describe the pathophysiology of Tuberculosis  6. Identify the clinical manifestations of Tuberculosis   7. List the complications of  Tuberculosis  8. Describe the most commonly investigations for the diagnosis of Tuberculosis  \n9. Make an accurate diagnosis of Tuberculosis  \n10. Understand the different treatment categories of Tuberculosis be able to categorize any \ntype of Tuberculosis  \n11. Understand the different case definitions of tuberculosis \n12. Manage most cases of tuberculosis appropriately  \n13. Refer complicated  cases of Tuberculosis diseases to hospitals for better management  14. Design appropriate methods of prevention and control of Tuberculosis  \n Definition: Tuberculosis is a Chronic necrotizing disease caused by Mycobacterium \ntuberculosis complex.  It usually affects the lung s but almost all organs can be affected. Thus it \nis conveniently classified into:  \n\u2022 Pulmonary TB (PTB) : accounts for 80% of all TB cases. \nSmear-positive PTB: 75-80% of all PTB cases Smear-negative PTB: 20-25% of all PTB cases \n\u2022 Extra-pulmonary TB (EPTB) : accounts for 20% of all TB cases. \n Etiologic Agent:  Mycobacterium belongs to the myc obacteriaceae family.  The species"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 79, "chroma:document": "Smear-positive PTB: 75-80% of all PTB cases Smear-negative PTB: 20-25% of all PTB cases \n\u2022 Extra-pulmonary TB (EPTB) : accounts for 20% of all TB cases. \n Etiologic Agent:  Mycobacterium belongs to the myc obacteriaceae family.  The species \ncommonly involved are M. tuberculosis, M.bovis, M. africanum and M.microti.  But of all, \nM.tuberculosis is by far the commonest.  M. tuberculosis is a rod-shaped, non-spore-forming, \nthin aerobic bacterium measuring about 0.5 \u03bcm by 3\u03bcm.  The bacterium is demonstrated by acid \nfast staining technique."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33421-7265-11ef-99ce-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 80, "chroma:document": "Internal Medicine \n \n 65Epidemiology:- \n\u2022 Tuberculosis is one of the most prevalent diseases in the world.  About one-third of the \nworld\u2019s population is infected with tuberculosis and thus at risk of developing active \ndisease (TB). It is estimated that 8.4 million people develop active TB every year and 2.3 \nmillion die. More than 90 % of TB cases and deaths occur in developing countries and 75 % of cases are in the most economically productive age group. \n\u2022 TB has been recognized as major cause of morbidity and mortality in Ethiopia. \nAccording to a report from Ministry of health TB is 3\nrd leading cause of hospitalization \nand 1st leading cause of Hospital death. WHO Estimates Incidence of TB in Ethiopia is   \n356 per 100,000 /yr and the incidence Smear positive TB is 155 per 100,000/year. \n\u2022 In the year 2001 the TB leprosy control program (TLCP) registered 94,957 cases of TB \nfrom DOTS implementing areas.  \n\u2022 Coinfection with HIV significantly increases the risk of developing Active TB and HIV has \nbecome the most important risk factor to develop active TB. In HIV- infected persons the \nrisk of developing TB is increased by more than 10 times compared to those who are \nHIV negative. It is estimated that about 40% of adult TB cases in urban areas are HIV-positive. The incidence and prevalence of tubercu losis, in recent years has doubled or"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33422-7265-11ef-acb5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 80, "chroma:document": "HIV negative. It is estimated that about 40% of adult TB cases in urban areas are HIV-positive. The incidence and prevalence of tubercu losis, in recent years has doubled or \ntripled because of the HIV pandemic, especially in developing countries. It is also shown that active tuberculosis can result in rapid progression of HIV infection in a patient. \n\u2022 Multi-drug resistant TB which often results from poor management is becoming a serious \nconcern in many countries. \n \nTransmission  \nAdults with smear positive TB such as cavi tory TB and Laryngeal TB are the sources of \ninfection. Patients who are culture-negative pulmonary TB and extra pulmonary disease are not \ninfectious. \nM. tuberculosis is commonly transmitted from a patient with infectious tuberculosis to a healthy \nindividual through  \n\u2022 Inhalation of droplets excreted via coughing, sneezing or speaking.          \n\u2022 Un-boiled milk could also transmit M. bo vis, but the incidence seems to be decreasing \nbecause of health education on boiling or pasteurizing milk."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33423-7265-11ef-ae25-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 81, "chroma:document": "Internal Medicine \n \n 66Factors that facilitate transmission of pulmonary tuberculosis are \n\u2022 Infectivity of the contact  ( patients with heavy bacterial load) \n\u2022 Environment: overcrowding  \n\u2022 Duration of contact  ( prolonged exposure ) \n\u2022 Intimacy ( how close the source and the subject are )   \n \nPatients who acquire the infection may not develop the disease.  The rate of clinical disease is highest during late adolescence and early adulthood, but the reasons are not clear.  Especially young women are affected more than men.   \n The presence some disease conditions increase the likely hood of developing active TB \n(Clinically over disease).   \n\u2022 The commonest is co-infection with HIV, which suppresses cellular immunity.   \n\u2022 Hematologic and other malignancies : lymphoma, leukemia, malignancies,  \n\u2022 Chronic renal failure \n\u2022 Diabetes mellitus \n\u2022 Immune suppressive drugs like long-term corticosteroids (e.g. prednisolone)  \n\u2022 Old age because of decreased immunity.  \n\u2022 Malnutrition is a very important factor for the development of disease. \n \nPathogenesis  \nM. tuberculosis enters the body mostly via respiratory tract through coughed out droplets from \nan infectious patient."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 81, "chroma:document": "\u2022 Malnutrition is a very important factor for the development of disease. \n \nPathogenesis  \nM. tuberculosis enters the body mostly via respiratory tract through coughed out droplets from \nan infectious patient. \n \nM. tuberculosis interacts with host immune system immediately after entry.  Activated alveolar macrophages ingest the bacilli; after which they release chemicals to activate other immune system components and try to control the infection or multiplication of bacilli. This process will bring about cell - mediated immune response.  These activated cells aggregate around the \nlesion and the center becomes necrotic, soft cheese like material called caseous necrosis .  \nThe center, however, may still contain live bacteria that become dormant.  These bacteria will \nflare up and multiply when the person's immunity  is depressed. But if the bacteria inside the \nmacrophage multiply rapidly, they will kill the macrophage and are released but to be taken up"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 82, "chroma:document": "Internal Medicine \n \n 67by other macrophages again. If this process is not arrested, patients may develop disseminated \ninfection.  \nClinical Manifestations  \n Pulmonary Tuberculosis : - This can be classified as primary or post primary (Secondary). \nPrimary disease: Clinical illness directly after infection is called primary tuberculosis; this is \ncommon in children <4 years of age. Thus, it results from an initial infection.  \n\u2022 Frequently it involves the middle and lower lung zones.   \n\u2022 In the majority it heals spontaneously leaving a healed scar on the lung called Ghon \nlesion .  \n\u2022 It may be contained by immunity into dormant stage only to flare up in immuno-\ncompromised state.  \n\u2022 In children or in immune compromised individuals the disease is usually rapid involving \nthe lungs, pleura and mediastinal lymph nodes.  It may disseminate into the blood \nstream and cause milliary tuberculosis or TB meningitis that may be rapidly fatal. \n \nPost primary disease:  -If no clinical disease is developed after the primary infection, dormant \nbacilli may persist for years or decades before being reactivated, when this happens, it is called \nsecondary (or post primary) tuberculosis. There fore this is from endogenous reactivation of \nlatent infection.   \n\u2022 It is more common in adults, and typically in volves the apical lobes.  But any portion of \nthe lungs may be involved.  The disease could extend from small infiltrates to large"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 82, "chroma:document": "latent infection.   \n\u2022 It is more common in adults, and typically in volves the apical lobes.  But any portion of \nthe lungs may be involved.  The disease could extend from small infiltrates to large \ncavitory lesions.  Patients with cavitory lesion expectorate tuberculosis bacilli with \nsputum.   \n\u2022 Early in the course patients may have intermittent fever, night sweats, weight loss, \nanorexia and weakness.  Most patients have cough, which may be dry at first, but later \nbecomes productive of whitish sputum; it is frequently blood streaked.  Patients may have exertional dyspnea.   \n\u2022 Physical examination  may reveal a chronically sick patient with pallor and clubbing. \nInspiratory crepitations are seen in some cases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33427-7265-11ef-89c4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 83, "chroma:document": "Internal Medicine \n \n 68\u2022 Laboratory findings  may include raised ESR, anemia or leukocytosis. Sputum \nexamination may be positive for AFB. Chest x -ray findings are non-specific; infiltrations, \nconsolidation or cavitory lesions may be present. \n \nExtra-pulmonary Tuberculosis :-Commonly affected organs are lymph nodes, pleura, \nmeninges, genitourinary tract, bones and joints, and peritoneum. \n \nLymph-node tuberculosis (TB lymphadenitis):-   \n\u2022 It is seen more in HIV patients.   \n\u2022 The commonest sites are cervical and supraclavicular.  \n\u2022 Lymphnodes are typically matted and firm, sometimes pus may be discharging.  \n\u2022 The diagnosis is made by fine needle aspiration and/or lymph node biopsy.  \n Pleural tuberculosis:-   \n\u2022 Pleural involvement may be asymptomatic or  patients could have fever, pleuritic chest \npain and dyspnea.   \n\u2022 On physical examination, typically ther e will be decreased tactile fremitus, dullness and \ndecreased breath sounds on the affected side.   \n\u2022 Fluid should be aspirated from pleural space (thoracentesis) and analyzed.  \n\u2022 Chest x-ray is also helpful in diagnosis; it may show homogenous opacity with meniscus \nsign.  \n\u2022 Empyema (pus in the pleural space) may complicate tuberculosis occasionally. \n Genitourinary tuberculosis:   \n\u2022 It can involve any part of the system.   \n\u2022 Dysuria, intermittent hematuria and flank pain are common presentations.  But it may be \nasymptomatic for a long period of time."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33428-7265-11ef-83b8-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 83, "chroma:document": "Genitourinary tuberculosis:   \n\u2022 It can involve any part of the system.   \n\u2022 Dysuria, intermittent hematuria and flank pain are common presentations.  But it may be \nasymptomatic for a long period of time.   \n\u2022 Urinalysis shows pyuria and hematuria without bacteria in majority of cases (commonly \ncalled sterile pyuria). Diagnosis may be reached by culturing urine repeatedly for \nM.tuberculosis.   \n\u2022 It affects more females and may present as infertility or pelvic pain."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33429-7265-11ef-a22e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 84, "chroma:document": "Internal Medicine \n \n 69Skeletal Tuberculosis:-   \n\u2022 It is usually reactivation of hematogenous site  or extension from a nearby lymph node.  \nThe most common sites are spine, hips and knees.   \n\u2022 Spinal tuberculosis is called Pott's disease  or tuberculous spondylitis.  In adults, \nlower thoracic and lumbar vertebrae are commonly affected.  Patients may present with \nswelling and pain on the back with or without paraparesis or paraplegia due to cord compression.   \n\u2022 Tuberculosis in other bones or joints usually present with pain and swelling. \n\u2022 Joint tuberculosis: - Any joint can be affected but weight bearing joints; particularly the \nhip and knee joints are commonly involved. Patients present with progressive joint \nswelling, usually with pain and limitation of movement. If left untreated, the joint may be \ndestroyed.   \n Tuberculosis Meningitis:-   \n\u2022 It is commonly seen in children and immuno-compromised people particularly patients \nwith HIV.   \n\u2022 More than half have evidence of disease in the lungs.   \n\u2022 Patients with TB meningitis present with headache, behavioral changes and nuchal \nrigidity for about two weeks or more.  Patients may have cranial nerve paralysis and \nseizure.  \n\u2022 Cerebra spinal fluid analysis  is the most important modality to diagnose TB meningitis. \nCSF examination shows increased WBC c ount, predominantly lymphocytes, and high \nprotein and low glucose content. But any of theses could be normal in the presence of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3342a-7265-11ef-9f98-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 84, "chroma:document": "CSF examination shows increased WBC c ount, predominantly lymphocytes, and high \nprotein and low glucose content. But any of theses could be normal in the presence of \nthe disease. AFB can be seen in sediment CSF in only 20% of cases; this percentage increases if examined CSF volume is increased. Culture may be positive in about 80%, but it takes 4 to 6 weeks to grow.  \n\u2022 Patients should be referred to a hospital if TB meningitis is suspected.     \n Gastro Intestinal Tuberculosis:-  \n\u2022 Tuberculosis can affect anywhere from the mouth to the anus.   \n\u2022 Bacteria could reach GI by swallowing sputum, hematogenously or by ingesting raw \nmilk.  The commonest sites are terminal ileum and cecum."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3342b-7265-11ef-be97-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 85, "chroma:document": "Internal Medicine \n \n 70\u2022 Abdominal pain, diarrhea, symptoms of intestinal obstruction and hematochezia (frank \nblood on stool) may be the presenting symptoms.  There could be associated fever, \nnight sweats, weight loss and anorexia.  There could be a palpable mass in the abdomen.  Patient could have involvement  of the peritoneum, liver and spleen. \n\u2022 Tuberculos peritonitis  arises from ruptured abdominal lymph node or hematogenous \ndissemination. Patients usually present with abdominal swelling and pain, weight loss, fever and night sweating. Aspiration of perit oneal fluid (paracenthesis) reveals exudative \nfluid with many WBC, predominantly lympho cytes. AFB is rarely positive and culture \npositivity is very low. \n\u2022 Involvement of the liver and spleen is part of disseminated tuberculosis. Patients will \npresent with hepatomegaly and/or splenomegaly. There could be evidence of \ninvolvement of other organs.  \nPericardial Tuberculosis (TB pericarditis):   \n\u2022 It is frequently seen in patients with HIV.   \n\u2022 Patients usually present with fever, retro-sternal pain, cough, dyspnea and generalized \nedema because of pericardial effusion.  Cardiac tamponade may appear later  \n\u2022 Constrictive pericarditis may develop as a complication of TB pericarditis even after \ntreatment and patients can present with symptoms and signs of right sided heart failure. \n\u2022 Diagnosis is usually reached by analyzing the pericardial effusion, which is always done"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3342c-7265-11ef-acd5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 85, "chroma:document": "treatment and patients can present with symptoms and signs of right sided heart failure. \n\u2022 Diagnosis is usually reached by analyzing the pericardial effusion, which is always done \nin hospitals. It may show lymphocytos is, but yield for AFB is low.  \n\u2022 Chest x-ray may show enlarged heart shadow , which suggests effusion. Ultrasound \nshould be done when available and it demonstrates effusion.    \nMilliary tuberculosis: - \n\u2022 This is secondary to hematogenous dissemination of the bacilli.   \n\u2022 It is more common in children and immuno-compromised patients.   \n\u2022 Manifestations are nonspecific with fever, night sweats, anorexia, weakness, and weight \nloss.  Patients may or may not have respiratory symptoms.   \n\u2022 Physical examination findings include seriously sick patient with hepatomegaly, \nsplenomegaly and lymphadenopathy.   \n\u2022 Since symptoms and signs are not specific, high index of suspicious is required for the \ndiagnosis.   \n\u2022 Chest x-ray usually shows milliary pattern of infiltration bilaterally (milliate like lesions, \n\u201cdagussa\u201d in Amharic)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3342d-7265-11ef-b671-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 86, "chroma:document": "Internal Medicine \n \n 71Diagnosis \nClinical suspicion is very important for the diagnosis of tuberculosis.  Patients who have \nsuggestive symptoms and signs for tuberculosis should undergo further tests.   \n\u2022 AFB Microscopy : \nAFB is found on microscopy from specimens like sputum, pleural, peritoneal and cerebrospinal fluid and body discharges, but the yield is different. However, definitive diagnosis depends on detection of M. tuberculosis  from a culture of specimen.  \nSputum examination  is extremely important in patients who have sputum production.  \n AFB stain should be done 3 times in 2 consecutive days (spot - early morning - \nspot).  \n Sputum smear is said to be positive when at least 3 AFB are seen.  \n Smear positive TB is diagnosed when at  least 2 smears are positive or one \nsmear positive plus suggestive chest x-ray finding.  \n If all 3 sputum smears are negative and t he patient has suggestive clinical and \nchest x-ray findings, first the patient should be treated with broad spectrum antibiotics to rule out other bacterial causes. If the patient doesn\u2019t respond, \nsmear negative pulmonary TB can be strongly considered. \n\u2022 Mycobaterial culture  is the gold standard for making diagnosis. However the bacillus is \nslowly multiplying and it takes several weeks to grow the bacilli in a culture media. May \nbe used for drug sensitivity tests. \n\u2022 Chest x-ray  presentations of tuberculosis are varied.  Although any radiographic finding"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3342e-7265-11ef-9b3a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 86, "chroma:document": "slowly multiplying and it takes several weeks to grow the bacilli in a culture media. May \nbe used for drug sensitivity tests. \n\u2022 Chest x-ray  presentations of tuberculosis are varied.  Although any radiographic finding \nis possible, typically there will be nodular infiltrates and cavities in the upper lobe; pleural effusion is also common. Chest x-ray findings do not confirm diagnosis of TB.     \n\u2022 Raised ESR  is a very important clue for the diagnosis even though this is nonspecific. \nThere could also be anemia of chronic illness. \n\u2022 PPD skin  test is widely used to screen tuberculosis in developed countries where the \nprevalence of TB is low.   Positive reactions are obtained when patients have the infection but do not have active disease or they have received BCG for immunization.  \nTherefore, it is not a good method of screening in our country.   \n Standardized case Definition of Tuberculosis \nAfter making diagnosis of TB proper case Definition should be made to decide on appropriate \ntreatment. The definition of TB case depend on the following points"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3342f-7265-11ef-bac0-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 87, "chroma:document": "Internal Medicine \n \n 721. Site of TB ( Pulmonary Vs Extrapulmonary  ) \n\u2022 Pulmonary tuberculosis (PTB) refers to disease involving the lung parenchyma. \nTherefore tuberculous intrathoracic lym phadenopathy (mediastinal and/or hilar) or \ntuberculous pleural effusion, without radiographic abnormalities in the lungs, constitutes \na case of extrapulmonary TB. A patient with both pulmonary and extrapulmonary TB should be classified as a case of pulmonary TB.  Miliary tuberculosis is classified as pulmonary TB because there are lesions in the lungs. \n\u2022  Extrapulmonary tuberculosis (EPTB) refers to tuberculosis  of organs other than the \nlungs, e.g. pleura, lymph nodes, abdomen, genitourinary tract, skin, joints and bones, meninges. Diagnosis should be based on one cult ure-positive specimen, or histological \nor strong clinical evidence consistent with active EPTB, followed by a decision by a clinician to treat with a full course of tuberculosis  chemotherapy. The case definition of \nan extrapulmonary TB case with several sites affecte\nd depends on the site representing \nthe most severe form of disease . \n2. Bacteriology ( result of sputum smear ) : Smear positive Vs Smear negative \nIdentification of smear-positive cases is impor tant, because they are the most infectious \ncases and usually have higher mortality;"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33430-7265-11ef-a95e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 87, "chroma:document": "the most severe form of disease . \n2. Bacteriology ( result of sputum smear ) : Smear positive Vs Smear negative \nIdentification of smear-positive cases is impor tant, because they are the most infectious \ncases and usually have higher mortality;  \n\u2022 Pulmonary tuberculosis, sputum smear-positive (PTB+) a) Two or more initial sputum smear examinations positive for AFB, or b) One sputum smear examination positive for AFB plus radiographic abnormalities \nconsistent with active PTB as determined by a clinician, or \nc) One sputum smear positive for AFB plus sputum culture positive for M. tuberculosis.  \n\u2022 Pulmonary tuberculosis, sputum smear-negative (PTB-)  \nCase of PTB that does not meet the above definition for smear-positive TB. \nThis group includes cases without smear result, which should be exceptional in adults \nbut are relatively more frequent in children. \nNote . In keeping with good clinical and public health practice, diagnostic criteria for PTB-should \ninclude: \n\u2022 A at least three sputum specimens negative for AFB, and \n\u2022 A radiographic abnormalities consistent with active PTB, and  \n\u2022 No response to a course of broad-spectrum TB antibiotics, and \n\u2022 Decision by a clinician to treat with a full course of ant tuberculosis chemotherapy."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33431-7265-11ef-a0be-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 88, "chroma:document": "Internal Medicine \n \n 73\u2022 In health facilities where microscopy laboratory services are available and diagnostic \ncriteria are properly applied, PTB smear-positive cases represent at least 65% of the \ntotal of PTB cases in adults, and 50% or more of all TB cases. \n\u2022 Note that these proportions may be lower in high HIV-incidence populations. \n\u2022 It is apparent from the above definitions that in the absence of culture, standard chest \nradiography is necessary to document  cases of smear-negative PTB.  \n3. History of previous treatment of TB In order to identify those patients at increased risk of acquired drug resistance and to prescribe appropriate treatment, a case should be defined according to whether or not the patient has previously received TB treatment.  The following definitions are used: \n\u2022 New:  a patient who has never had treatment fo r TB or who has taken ant tuberculosis \ndrugs for less than 1 month.  \n\u2022 Relapse:  a patient previously treated for TB who has been declared cured or treatment \ncompleted, and is diagnosed with bacteriologically positive (smear or culture) tuberculosis.  \n\u2022 Treatment after failure: a patient who is started on a re-treatment regimen after having \nfailed previous treatment.  \n\u2022 Treatment after default. A patient who returns to treatment, positive bacteriologically, \nfollowing interruption of treatment for 2 months or more.  \n\u2022 Transfer in. A patient who has been transferred from another TB register to continue \ntreatment ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33432-7265-11ef-b9ec-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 88, "chroma:document": "following interruption of treatment for 2 months or more.  \n\u2022 Transfer in. A patient who has been transferred from another TB register to continue \ntreatment . \n\u2022 Other.  All cases that do not fit the above definitions. This group includes  \n Chronic case, a patient who is sputum-positive at the end of a re-treatment \n4. Severity of the diseases  \nBacillary load, extent of disease and anatomical site are considerations in determining TB \ndisease severity and therefore the appropriate treatment. Involvement of an anatomical site results in classification as severe disease if there is a significant acute threat to life (e.g. pericardial TB), a risk of subsequent severe handicap (e.g. spinal TB), or both (e.g. \nmeningeal TB). \nCase definitions  \n\u2022 Tuberculosis suspect. Any person who presents with symptoms  or signs suggestive of TB, in \nparticular cough of long duration (more than 2 weeks)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33433-7265-11ef-bf28-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 89, "chroma:document": "Internal Medicine \n \n 74\u2022 Case of tuberculosis. A patient in whom TB has been bacterio logically confirmed or diagnosed by a \nclinician.  \n\u2022 Definite case of tuberculosis: a patient with positive culture for the M.tuberculosis complex.  \nBased on the above criteria and case definitions, a TB patient falls in to one of the four \ncategories of treatment. This categorization helps in prioritizing patients and in selecting the type regime to be used in a patient. \n Table I- 4 -1: Tuberculosis Treatment Category  \nTB treatment \ncategory  \nPatients Recommended \nTreatment /Regimen \n Category  1  \u2022 New smear positive PTB \n\u2022 Smear \u2013ve PTB with extensive \nTB \n\u2022 Sever forms of extra \npulmonary TB   DOTs short course  HRZE/S for 2 months                +  \nHR 4 MO or HE 6 MO Or  H3R3 for 4 MO \n Category  2   \u2022 Relapse  \n\u2022 Treatment Failure  \n\u2022 Return after Default  Retreatment  2HRZES/ 1HRZE                +  \n            5ERH \n Category  3   \n  \n\u2022 Smear negative PTB with \nlimited  \n\u2022 EPTB less ever form \n\u2022 Children between 7 and 14 \nyears old with any type of \nTB, who are not seriously ill  \n  2HRZ or 2H3R3E3                  + \nHR 4 MO or HE 6 MO \nOr  H3R3 for 4 MO \n Category  4    \n\u2022 Chromic cases  2\nnd Line Anti TB drugs"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33434-7265-11ef-afe2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 90, "chroma:document": "Internal Medicine \n \n 75Anti Tuberculosis Chemotherapy \nAim of Treatment of Tuberculosis   \n\u2022 To cure the patient from the diseas es and prevent death and complications  \n\u2022 To decrease transmission of Tuberculosis  \nTreatment of tuberculosis has two phases, \n\u2022 The intensive (initial) phase : combination of 3 or more drugs is given for 2 \nmonths. In the retreatnment regimen it continued for 3 months. This is to decrease \nthe bacterial load and make the patient non-infectious rapidly. \n\u2022 Continuation phase:   Two or three drugs used for 4 -5 months.  This phase follows \nthe intensive phase and the aim is to achieve complete cure.   \n\u2666 During the intensive phase of DOTS, the drugs must be collected daily and must be \nswallowed under the direct observation of a health worker. During the continuation \nphase, the drugs must be collected every month and self-administered by the patient. \n\u2666 For category 2 pateints put on re-treatment, the whole duration of re-treatment, including \nthe continuation phase, the drugs must be taken under the direct observation of a health worker. Streptomycin should not be included in the re-treatment for pregnant \nwomen."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33435-7265-11ef-bbd2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 91, "chroma:document": "Internal Medicine \n \n 76Table I- 4-2: Anti TB drugs ar e classified in to two groups  \n \nFirst Line Drugs (Essential Anti \ntuberculosis drugs): There are five drugs \nin use currently  Second Line Drugs (reserve Anti TB drugs) are used only in Chronic case of \nTB  \n\u2022 Streptomycin (S) in 1gm vial : the \nonly drug given IM \n\u2022 Ethambutol  (E) in 400mg tablet,  \n\u2022 Isoniazeid (H) in 100mg and 300 \nmg tablet,  \n\u2022 Rifampicin (R) in 150mg and \n300mg tablets and  \n\u2022 Pyrazinamide (Z) in 500mg tablets. \nFixed drug combinations  \n\u2022 RIF , INH , PZA(RHZ) \n150/75/400mg \n\u2022 ETH and INH (EH) 400/150mg \n\u2022 RIF and INH (RH) 150/75mg \n\u2022 RIF, INH, PZA, ETB (RHZE) \n150/75/400/225  \u2022 AMINOGLYCOSIDES  \n Kanamycin and Amikacin \n Capreomycin (polypeptide) \n\u2022 THIOAMIDES  \n Ethionamide \n Protionamide \n\u2022 FLUOROQUINOLONES  \n Ofloxacin \n Ciprofloxacin \n\u2022 CYCLOSERINE (AND TERIZIDONE)  \n\u2022  P-AMINOSALICYCLIC ACID \nSide Efects of common Anti TB Drugs : Anti-tuberculosis drugs cause different side \neffects.  These may be Minor w here the drugs are continued or Major in which case the \ndrugs should be discontinued and the patient referred"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33436-7265-11ef-a1a6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 92, "chroma:document": "Internal Medicine \n \n 77Table I-4-3: Side Effects of common Anti TB drugs and Treatment of side effects  \n \n \nAnti TB Drug   \nSeverity of the \nadverse effect  \nSide Effects  \nTreatment of Side \nEffects \nMinor  Burning Sensation in the Feet  (Peripheral neuropathy) Pyridoxine 100 mg PO daily  \n Isoniazide  \nMajor  Jaundice /Hepatitis  Stop INH \nMinor  Orange or red discoloration of urine \nNausea , abdominal pain  Reassurance  \nTake drug with small \nmeal  \nRifampicine  \n \nMajor  Hepatitis , Acute renal failure shock , purpura  Stop Rifampcin \n \nMinor  None    \nEthambutol \nMajor  Optic neuritis : Visual impairment  Stop Ethambutol \n Minor  Mild skin rash  \nPerioral parasthesia Symptomatic treatment  \n Streptomycine  \n Major  Ototoxicity :  Vertigo and hearing impairment  Stop Streptomycin \nMinor  Joint pain  Analgesics like Aspirin \n  Pyrazinamide \nMajor  Hepatotoxicity / jaundice   Stop Pyrazinamide \n \nImportant points to consider in the treatment of tuberculosis: \n\u2022 Streptomycin should not be given to pregnant woman, and patients with renal \nfailure and ear problems.  It should be replaced by Ethambutol.  Streptomycin \ndose should not be more than 750mg if the patient's age is > 50 years. \n\u2022 Children who are 6 years or below should not be given Ethambutol because of \ndamage to the eyes and children may not complain of it. \n\u2022 Patients should be strictly followed after initiation of the drugs."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33437-7265-11ef-b793-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 93, "chroma:document": "Internal Medicine \n \n 78\u2022 All sputum-positive patients on DO TS must have one sputum specimen \nexamined at the end of the 2nd, 5th and 7th month. If sputum is negative at the \nend of 8 weeks, the continuation phase can be started. \n\u2022 Corticosteroids are added to the anti-TB in TB meningitis, pericarditis, and spinal \nTB. Adrenal TB patients should have replacement therapy. \nTuberculosis and HIV is dealt on HIV section \n \nRefernces: \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nTuberculosis, pages 953-965.    \n2) National TB Treatmnet guidline for Ethiopia  \n3) Treatment of Tuberculosis : Guidline for National programmes , Third edition , \nWHO- Geneva 2003 \n4) TB/HIV , a clinical manual , Second edition , WHO-Geneva , 2004"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 94, "chroma:document": "Internal Medicine \n \n 795. Human Immuno Deficiency Virus \u2013 HIV/AIDS \n \nLearning Objectives : At the end of the th is Unit the student will be able to  \n1. Define HIV disease and AIDS  \n2. Understand the basic virology of the etiologic agent  \n3. Describe the mode of transmission of HIV   4. Understand the epidemiology of HIV   5. Describe the pathophysiology of HIV/AIDS  \n6. Identify the clinical manifestations of HIV/AIDS    \n7. List the complications and Organ systems affected by HIV/AIDS  8. Describe the most commonly investigations for the diagnosis of HIV  9. Make an appropriate diagnosis of the common manifestations of HIV/AIDS  and different \nopportunistic infections  \n10. Make appropriate WHO clinical staging of HIV/AIDS   11. Manage common opportunistic infections  12. Understand the basics of Antiretroviral drugs and HAART including indications /eligibility \ncriteria for the initiation of ART  \n13. Initiate ART for most patients and follow patients on ART   14. Refer complicated  cases of HIV/AIDS  diseases to hospitals for better management  \n \nDefinition:  HIV disease is a chronic infe ctious disease caused by the Human Immuno \nDeficiency Virus, which is characterized by spec trum starting from primary infection, with or \nwithout the acute syndrome, followed by a relatively long period of asymptomatic stage after \nwhich in most patient\u2019s progress to advanced and life threatening disease (AIDS)  \n \nHistorical Back Ground"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 94, "chroma:document": "without the acute syndrome, followed by a relatively long period of asymptomatic stage after \nwhich in most patient\u2019s progress to advanced and life threatening disease (AIDS)  \n \nHistorical Back Ground  \n1981:  AIDS was first recognized in USA among Homosexual males \n PCP was seen among 5 homosexuals  \n Kaposi\u2019s sarcoma was diagnosed in 26 homosexuals with  1983: HIV virus was isolated from a patient with lymphadenopathy \n1984:  HIV virus was clearly demonstrated to be the causative agent for AIDS"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3343a-7265-11ef-a573-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 95, "chroma:document": "Internal Medicine \n \n 80Epidemiology  \n\u2666 According to UNAIDS report at the end of 2006 about 39.5 million people were living \nwith HIV/AIDS, out of which 2.3 million were children and 17.7 million were women. In \n2006 there were about 4.3 million new infections out of which 530, 000 were children < 15 years. There were about 2.9 million deaths out of which 380,000 were children. \n\u2666 Sub-Saharan Africa is the worst affected by the pandemic with 25.7 million living with \nHIV, Out of which 2.1 million are children < 15 years. The overall adult prevalence in this region is 5.9 %. There were about 2.1 million deaths due to HIV/AIDS in 2006. \n\u2666 Our country Ethiopia is the second most populous country in Sub-Saharan African \nsuffering from the brunt of HIV/AIDS. In Ethiopia HIV was first detected in collected sera in 1984. The first two AIDS cases were reported to the Ministry of Health in1986.  \n\u2666 National HIV prevalence rate according to AIDS in Ethiopia 6ht report is 3.5% (the \nprevalence is different in Urban and Rural areas 10.1 % and 1.9 % respectively.) There are about 1.3 million people living with HIV/AIDS out of which 134,586 were children. There were nearly 128, 988 new infections in 2006 of which 12, 9196 are children. There \nwere about 134, 450 deaths in 2006 among these 20,929 were children.  \n \nMode of Transmission of HIV  \n1. Sexual Transmission:  \n\u0083 Is the major mode of transmission worldwide ( 90 % )"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3343b-7265-11ef-8c1e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 95, "chroma:document": "were about 134, 450 deaths in 2006 among these 20,929 were children.  \n \nMode of Transmission of HIV  \n1. Sexual Transmission:  \n\u0083 Is the major mode of transmission worldwide ( 90 % ) \n\u0083 The virus is found in high quantities in the sexual fluids (seminal and vaginal \nfluid) of people with HIV infection  with in infected monocytes and in cell-free \nstate \n\u0083 Anal sex appears to be the sexual practice carrying the highest risk of \ntransmitting HIV. The reasons being rectal mucosa is thin and fragile and there are susceptible cells ( Langerhans cells  ) in the rectal mucosa  \n\u0083 Vaginal sex is also an effective from of transmission.   \n\u0083 The presence of other STDs like Syphilis , Gonorrhea etc increase the risk of \nacquiring or transmitting HIV infection by several fold, as the quantity of the virus in seminal or vaginal fluid significant ly increase and the number of infected \nmonocytes is high around the genital area in patients with STDs.. \n\u0083 Oral sex may have some risk however there are no reports so far attributable to \noral sex."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3343c-7265-11ef-bf8e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 96, "chroma:document": "Internal Medicine \n \n 812. Transmission through blood and blood products  \n\u0083 IV drug abusers who share needles and syringes have high risk .This is the main \nmode of transmission in Eastern Europe. \n\u0083 Blood or blood products transfusion from infected donors (the risk of infection is \n90-100 %). Currently the risk is very minimal as blood and blood products are \nscreened carefully using antibody and p24 antigen testing to identify donors in the widow period. \n\u0083 Transmission through sharp instruments, injection needles etc. There may be a \nrisk of transmission from one patient to another or from an infected patient to health care provider  \n3. Mother to Child Transmission  \n\u0083 Without any intervention, the risk of mother to child  transmission is  30-45%  in \nthe developing world and 15-30% in the developed world , \n\u0083 HIV may be transmitted from infected mothers to children during  \ni. Pregnancy:-10 % before the 3\nrd Trimester  \nii. Labor and Delivery:- 70 % late pregnancy and during labor \niii. Breast Feeding :- 10-15 % \n\u0083  MTCT is by far the largest source of HIV infection in children under 15 \n \nFactors Influencing MTCT \nMaternal Factors \n\u0083 Maternal viral Load: The higher the viral load, the higher is the risk of MTCT  \n\u0083 Woman becomes infected with HIV during pregnancy \n\u0083 Severe immune deficiency  \n\u0083 Clinical and immunological state \n\u0083 Use of ART during pregnancy and postpartum to mother and newborn"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3343d-7265-11ef-ae34-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 96, "chroma:document": "\u0083 Woman becomes infected with HIV during pregnancy \n\u0083 Severe immune deficiency  \n\u0083 Clinical and immunological state \n\u0083 Use of ART during pregnancy and postpartum to mother and newborn \n\u0083 Viral, bacterial, and parasitic placental infection (especially malaria)  \n\u0083 Nutritional status, particularly vitamin A \n \n Labor and Delivery \n\u0083 Prolonged rupture of membranes (>4 hours) \n\u0083 Acute chorioamnionitis  \n\u0083 Invasive fetal monitoring or delivery techniques"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3343e-7265-11ef-b6c4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 97, "chroma:document": "Internal Medicine \n \n 82\u0083 Mixing of maternal and fetal body fluids \n\u0083 Episiotomy \n\u0083 First infant in a multiple birth \nFetal Conditions \n\u0083 Premature delivery \n\u0083 Immature immune status  \n\u0083 First-born twin \nInfant Feeding Practices/Breastfeeding \n\u0083 Mother becomes infected with HIV while breastfeeding (risk increases up to 20%)  \n\u0083 Mixed feeding (breast milk and other foods) increases risk \n\u0083 Breast pathologies (lesions, infections) \n\u0083 Advanced disease in the mother \n\u0083 Poor maternal nutritional status \n\u0083 Breastfeeding during the first 4\u20136 months  \n\u0083 The longer mother breastfeeds, the greater the risk \n\u0099 HIV is not spread via non-sexual everyday casual contact between people like kissing, \nhugging and sharing common utensils, baths etc. \n\u0099 HIV infected people are considered most infectious soon after acquiring the infection and \nduring the AIDS (symptomatic) phase.  However, remember that it is possible to transmit HIV any time during the disease.\n \n \nEtiologic agent: \nHIV is a retrovirus which belongs to the sub family of lente virus. HIV virus is cytopathic virus. There are 2 main Types of the virus  HIV- 1:   is the most common cause of HIV Disease throughout the world and  it has several \ngroups and subtypes; \n\u0083 M group  which comprises 9 subtypes: A,B,C,D,F,G,H,J,K, as well as growing \nnumber of major circulating recombinant forms   ( CRFs )  e.g. AE ,  AG etc  \n\u2022 O group (outliers) : relatively rare seen in Cameron and Gambia  \n\u0083 N group:  (reported only in Cameroon)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3343f-7265-11ef-a1bf-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 97, "chroma:document": "number of major circulating recombinant forms   ( CRFs )  e.g. AE ,  AG etc  \n\u2022 O group (outliers) : relatively rare seen in Cameron and Gambia  \n\u0083 N group:  (reported only in Cameroon)   \nGlobal Pattern of HIV -1 distribution \n\u2022 Africa:  > 75 % of strains recovered to date have been subtypes A, C and D with C \nbeing the most common \n\u2022 Europe and Americas : subtype B is the predominant strain"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33440-7265-11ef-9303-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 98, "chroma:document": "Internal Medicine \n \n 83\u2022 Asia: recombinant forms such AE account of the infections in south East Asia while \nsubtype C is prevalent in India. Subtype B is also seen in Asia.  \nHIV - 2:  Was first identified in West Africa and it is mostly confined to West Africa, however a \nnumber of cases which can be traced to West Africa are found worldwide. \n \nMorphology of the Virus  \n \n \n\u2666 HIV is Spherical shaped virus. The most important parts of the virus are:- \n\u0083 Its viral envelop has many small spikes  which consists of two important \nglycopropteins gp41 and gp120 which play an important role when the virus \nattaches to its host cells \n\u0083 The viral capsid ( core )  which contains two single stranded viral RNA and an \nimportant enzyme for the virus called reverse transcriptase enzyme  \n\u0083 The reverse transcriptase enzyme plays an important step in the life cycle of the \nvirus. It converts the single stranded viral RNA into double stranded DNA  ( this \nprocess is called reverse transcription ) \n Characteristics of HIV \n\u0083 HIV infect cells that express CD4 receptor molecules \n\u0083 The CD\n4 receptors are present on various types of blood cells including \nlymphocytes, macrophages, monocytes, tissue cells (e.g. Dendirtic cells in the genital tract and ano-rectal region) and glial cells of brain Successful entry of the virus to a target cell also requires cellular co-receptors  \n\u0083 A fusion co-receptor is designated CXCR5 for T-cell tropic stain and CCR4 for \nmonocyte -macrophage tropic strains"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 99, "chroma:document": "Internal Medicine \n \n 84\u0083 The receptor and co-receptors of CD4 cells interact with HIV\u2019s gp-120 and gp-41 \nproteins during entry into a cell  \n \nLife Cycle of HIV: Replication \n1) Attachment /binding  and fusion of the virus to the host cells \n\u0083 The receptor and co-receptors of CD4 cells interact with HIV\u2019s gp-120 and gp-41 \nproteins during entry into a cell \n2) Uncoatting  of the viral capsid and release of Viral RNA into the cytoplasm of the host \ncell \n3) Reverse transcription:  Viral RNA is concerted in to Double stranded DNA by reverse \ntranscriptase enzyme \n4) Translocation :  viral DNA is Imported to cell nucleus \n5) Integration of proviral DNA to host-cell DNA \n6) Cellular activation causes transcription (copying) of HIV DNA back to RNA \n\u0083 Some RNA translated to HIV proteins \n\u0083 Other RNA moved to cell membrane \n7) Viral Assembly  :HIV assembled under cell membrane and buddes from cell \n8) Maturation :  viral Proteases enzymes cleave longer proteins in to important viral \nproteins and help to convert immature viral particle into and  infectious HIV \n  \n \n \nLife cycle of the virus and Sites of action for antiretroviral drugs"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33442-7265-11ef-846a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 100, "chroma:document": "Internal Medicine \n \n 85Pathogenesis :  \nCD 4 positive T-Lymphocytes (also known as T helper  cells) play central role in the defense \nmechanism of the body against infection. They mainly coordinate the Cell mediated immune \nsystem and also assist the antibody mediated immune system .  \n \n\u2666 HIV virus has special affinity to CD 4 T-cells and infects them \n\u2666 HIV infection is  characterized by a pr ofound immunodeficiency from progressive decline \nof T-helper cells \n\u2666 The pathogenetic mechanism of HIV disease is multi-factorial and multiphasic and it \ndiffers in different stage of the disease \n \nMechanism of CD 4 Cell Depletion  \n\u2022 HIV-mediated direct cytopathicity (single cell killing) \u2013 infected CD 4 cells die \n\u2022 HIV-mediated syncytia formation \n\u2022 Defect in CD4 T-cell regeneration in relation to the rate of destruction \n\u2022 Maintenance of homeostasis of total T-lymphocytes (decreased CD4, increased \nCD8) \n\u2022 HIV-specific immune response (killing of virally infected and innocent cells) \n\u2022 Auto-immune mechanism \n\u2022 Programmed cell death (apoptosis) \n  Qualitative abnormalities (even the existing CD4 cells are dysfunctional)  \n\u2022 Impaired expression of IL-2 \n\u2022 Defective IL-2 and INF-Alfa production \n\u2022 Decreased help to B-cells in production of immunogloblins \n Peculiar Characteristics of HIV and reasons for Persistent Viremia   HIV is a unique infection in that, though the body reacts by producing antibodies to destroy the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33443-7265-11ef-ac75-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 100, "chroma:document": "\u2022 Decreased help to B-cells in production of immunogloblins \n Peculiar Characteristics of HIV and reasons for Persistent Viremia   HIV is a unique infection in that, though the body reacts by producing antibodies to destroy the \nvirus, the virus is not cleared, except partially in the early period of infection A chronic infection is established, and it persists with varying degrees of viral replication. Viral replication is continuous in all stages (early infection, during the long period of clinical latency, and in advanced stage.)  There is no virological latency."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33444-7265-11ef-9d2e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 101, "chroma:document": "Internal Medicine \n \n 86 \nDespite robust immune reaction, HIV evades elim ination by the immune system and a chronic \ninfection is established. Some of the mechanisms are: \n\u0083 High level of viral mutation \u2013 HIV has an extraordinary ability to mutate \n\u0083 Large pool of latently infected cells that cannot be eliminated by viral-specific CTLs \n\u0083 Virus homes in lymphoid organs, while antibody is in the circulation  \n\u0083 Exhaustion of CD8 T-lymphocytes by excessive antigen stimulation  \n\u0083 HIV attacks CD-4 T-cells, which are central to both humeral and-cell mediated immunity \n\u0083 HIV seeds itself in areas of the body where sufficient antibodies might not reach, e.g., \nthe central nervous system \n \nProgression of HIV is different in different individuals  \nRapid progressors: After the initial infection patients progress fast and develop OIs and die \nwithin 2-3 years. Account for 15 % of all patients  \nNormal Progressors: After the initial primary infection patients remain health for 6- 8 years \nbefore they start having overt clinical manife stations: account for 80 % of all patients  \n \nLong term survivors: Patients who remain alive for 10-15 years after initial infection. In most \nthe diseases might have progressed and there may be evidences of immunodeficiency. \n \nLong term non progressors: This is individuals who have been infected with HIV for > 10 \nyears. Their CD4 count may be in the normal range and they may remain clinically stable for \nseveral years"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33445-7265-11ef-a2cf-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 101, "chroma:document": "Long term non progressors: This is individuals who have been infected with HIV for > 10 \nyears. Their CD4 count may be in the normal range and they may remain clinically stable for \nseveral years  \n What affects disease progression in HIV Infected individuals  \n\u0083 Viral set point: The level of steady-state viremia (set-point) at six months to one year \nafter infection, has an important prognostic implication for progression of HIV disease \no Those with a high viral set-point have faster progression to AIDS, if not treated \n\u0083 Immune response \no High CD8 slow progression  \no Low CD8 rapid decline  \n\u0083 Viral type ; HIV 2 slow course  \n\u0083 Concomitant conditions \no Malnutrition hastens the progression of HIV"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33446-7265-11ef-96de-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 102, "chroma:document": "Internal Medicine \n \n 87o Chronic infectious conditions e.g. Tuberculosis  \n \nDiagnosis and Laboratory monitoring of HIV  \n1. Serologic Tests :  \na. HIV antibody tests :- detect antibodies formed by the immune system against \nHIV \ni. ELISA : used to be standard screening test for HIV  \n\u0083 Tests for a number of antibody proteins in combination \n\u0083 A very sensitive  test ( . 99.5 % ), but not very specific \n\u0083 A positive result  needs to be confirmed by Western blot for confirmation  \n\u0083 The test need skilled personnel  , takes several hours  \nii. Western blot: is an excellent confirmatory test. \n\u0083 It has high specificity but relatively poor sensitivity   \n\u0083 It should not be used for screening purpose \niii. Rapid HIV antibody testes  \nAdvantages:  \u0083 Rapid tests have reasonably good sensitivity and specificity ( >99 % ) \n\u0083 Easy logistically , does not need continuous water or electric supply \n\u0083 Can be done by less skilled personnel and the interpretation of results is \neasy \n\u0083 Test result can be made available in < 30 minutes \n Because of these advantages of rapid tests WHO has recommend a serious of Rapid HIV antibody testes to be done to diagnose HIV infection."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33447-7265-11ef-9630-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 103, "chroma:document": "Internal Medicine \n \n 88 \n \n \n \n \n   \n \n  \n  \n \n   \n \n\u2022 When the 1\nst test is non-reactive, then the client can receive negative HIV result  \n\u2022 When both tests are reactive, the final HIV result is positive.  Test Sample: \n \nNEGATIVE:  \nClient receives \nnegative result POSITIVE:  \nDo 2nd confirmatory \ntest \nNEGATIVE:  \nUse 3rd test to \nconfirm POSITIVE:  \nClient receives Positive result \nNEGATIVE  \nClient receives negative result  \n POSITIVE:  \nClient receives positive\n result   Test Al gorithm for HIV Dia gnosis\nPre Test counseling  \n1st Screening test  \n \nDetermine\u00ae:  \n3rd    Tie breaker test  \n \nUni-Gold \u00ae 2nd Confirmatory test  \n \nCApillus \u00ae"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33448-7265-11ef-a644-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 104, "chroma:document": "Internal Medicine \n \n 89\u2022 If one test is reactive and the other is non-reactive, then a third test known as a \ntiebreaker is performed.  \n\u2022 The tie-breaker determines the final result \u2013 if the tiebreaker is reactive, then the \nfinal HIV result is positive; if the tiebreaker is non-reactive, then the final HIV result \nis negative.  \n        \nb. HIV antigen assays ( Tests ) \ni. P24 antigen capture assay: this test detects p24 viral protein in the blood of HIV \ninfected individuals. This viral protein can be detected during early infection, before seroconversion. Thus this test is us ed to detect blood donors during the Window \nperiod  \n2. DNA \u2013 PCR : Viral replication  \n\u0083 Is an extremely sensitive test -can detect 1-10 copies of HIV proviral DNA per ml of \nblood  \n\u0083 It uses PCR technology to amplify proviral DNA  \n\u0083 This test is costly and needs sophisticated instruments and highly skilled \nprofessional  \n\u0083 It is highly sensitive and the chance of false positivity is high. hence it should not be used for making initial diagnosis of HIV infection  \n\u0083 It is often used  \ni. To make early diagnosis of HIV in HIV exposed infants as serology tests are \nunable to diagnose HIV till the infant is 18 months old \nii. To diagnose or confirm virologic failure in patients who are not responding to ART \niii. When there is indeterminate serology  \n3. CD\n4  T cell count : as CD4 cells play a crucial role in the body defense mechanism ,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33449-7265-11ef-af6e-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 104, "chroma:document": "ii. To diagnose or confirm virologic failure in patients who are not responding to ART \niii. When there is indeterminate serology  \n3. CD\n4  T cell count : as CD4 cells play a crucial role in the body defense mechanism , \nmeasuring the amount of CD4 cells is an important indicator of the level of immune \nsuppression  that a patient infected with HIV has  \n The average CD4 count of a normal person is in the range of 1000-1200 \n/mm3.  Studies have shown the average CD4 count of normal Ethiopians is \nlow \n In patients with HIV CD4 count drops by an average of 50 - 100 cells per \nyear  \n Tells you the level of immune damage inflicted by HIV"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3344a-7265-11ef-bfc6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 105, "chroma:document": "Internal Medicine \n \n 90\n It should never used to make diagnosis of HIV \n CD4 count may be variable depending on circumstances \no Diurnal variation; High evening low at midnight \no Inter current infection, use of steroids and stress could affect CD4 \ncount  \n Following the trend in CD4 count is us full in clinical decision  making  \n Percentage of CD4 count is useful in children below 6 years \n Importance\u2019s  of CD4 count  \no To decide eligibility of a patient for ART \no To follow the progress of a patient on ART \no To diagnose immunologic failure in patients who are not responding \nwell to ART  \n4. Additional  tests  that should be done is patients with HIV infection include:  \n\u0083 HBV , HCV  \n\u0083 FBP and ESR \n\u0083 SGOT/AST and  SGPT/ALT \n\u0083 Serum Creatinine \n\u0083 Syphilis serology: RPR  \n\u0083 AFB chest X-Ray where possible \n\u0083 Stool examination for parasites \n\u0083 Malaria blood slide \n\u0083 Pregnancy test for women in child bearing age  \n \nNatural History and Clinical Manifestations of HIV infection  \nThe clinical consequences of HIV infection encompass a spectrum ranging from an acute syndrome associated with primary infection to a prolonged asymptomatic state to advanced \ndisease \n \n1. Primary HIV Infection : Acute HIV syndrome and Seroconversion  \n2. Asymptomatic stage \u2013 Clinical latency 3. Early Symptomatic Diseases \u2013 mild immunodeficiency 4. AIDS defining illnesses : Advanced immunodeficiency"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 106, "chroma:document": "Internal Medicine \n \n 91\n \n \n1. Primary HIV Infection : Acute HIV syndrome and Seroconversion  \nAcute HIV syndrome: \n\u2022 Some patients are asymptomatic but 50 \u2013 70% of HIV infected individuals experience \nan acute clinical syndrome 3 \u2013 6 weeks after primary infection \n\u2022 A flue like syndrome in which symptoms persist from 1 \u2013several weeks and gradually \nsubside  \n\u2022 The typical clinical features includes  \n Fever \n Pharyngitis, lymphadenopathy,  \n Headache, artheralgia, myalgia, malaise,  \n GI symptoms : Anorexia, nausea vomiting, diarrhea,  \n Erythematous maculopapular rash and mucocutaneous ulceration \n Neurological symptoms: HIV in CSF, aseptic meningoencephalitis \nEncehphalitis, peripheral neuropathy  \nMost patients (> 90%) recover spontaneously 10 % manifest a fulminate course of immunologic \nand clinical deterioration  \n 2. Asymptomatic stage \u2013 Clinical latency  \n In most  ( 90 ) of patients, primary infection with or without the acute syndrome is \nfollowed by a prolonged period of clinical latency"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 107, "chroma:document": "Internal Medicine \n \n 92\n The length of time from initial infection to the development of clinical disease varies \ngreatly (median is 7-10 years.) \n Viral replication continues during this period of clinical latency. So there is no \nvirologic latency  \n The rate of disease progression is directly correlated with HIV RNA levels.  Patients \nwith high levels of HIV RNA progress to symptomatic disease faster than do \npatients with low levels of HIV RNA \n The CD 4 cell count fall progressively during this stage at an average rate of 50 \ncells/\u03bcl/year,  \n3. Early Symptomatic Diseases \u2013 mild immunodeficiency   \n Patients begin to develop sign and symptoms of clinical illness , when CD 4 cell \ncount falls below 500/ \u03bcl,  \n Most of the manifestations are due to minor opportunistic infections ( not AIDS \ndefining illnesses )  or direct effect of long standing HIV  \nThe clinical findings include: \na) Generalized lymphadenopathy  \no Definition: enlarged lymph nodes (> 1cm) in  \u2265 2 extra-inguinal sites for more than 3 \nmonths without an obvious cause. \no It is often the earliest symptom of HIV infection after primary infection \nb) Oral lesions: \n\u2022 Are usually indicative of fairly advanc ed immunologic decline, generally occurring in \npatients with CD4 count < 300 / \u03bcl.                                                                       \n            i. Oral thrush: \no Appears as a white, cheesy exudates, often on an erythematous mucosa"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3344d-7265-11ef-a209-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 107, "chroma:document": "patients with CD4 count < 300 / \u03bcl.                                                                       \n            i. Oral thrush: \no Appears as a white, cheesy exudates, often on an erythematous mucosa \n(most commonly seen on the soft palate) which gives an erythematous or \nbleeding surface on scraping  \no When it involves the esophagus, patients complain of difficulty and/or pain \non swallowing  \no Is due to Candida infection  \no Confirmatory diagnosis is by direct examination of a scraping for \npseudohyphal elements  \no Treatment  -   Apply 0.25% Gential Violet BID and/or \n         Nystatin tablets or suspension 500,000 IU every 6 hr"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 108, "chroma:document": "Internal Medicine \n \n 93If pharynx or esophagus involved; Ketoconazole 200 mg PO BID for 2 \nweeks or Miconazole oral gel. \n            ii. Oral hairy leukoplakia: \no Appears as a filamentous white lesion, generally along the lateral borders of \nthe tongue. \no Is presumed due to Epstein \u2013 Barr virus infection \n            iii.   Apthous ulcer: \no Ulcer on the oral cavity or pharynx of unknown etiology \no Usually are painful and may interfere in swallowing  \n  c)  Herpes zoster (shingles) \no Seen in 10 \u2013 20% of patients with HIV infection \no It is a reactivation syndrome of varicella zoster virus  \no Indicates a modest decline in immune function and is often the first clinical \nindication of immunodeficiency \no Lesions are usually localized to a single dermatome, but may extend over \nseveral dermatomes and frank cutaneous dissemination may be seen. \no It has a relapse rate of 20% \n      d) Thrombocytopenia: \no Thrombocytopenia in HIV infection has immunologic base (is due to auto \nimmune destruction of platlets).  \no It is very similar to IPT (idiopathic thrombocytopenic purpura) \no Since most patients have platelet count of >50,000/ \u03bcl serious clinical \nproblem are seen rarely.  \no In some patients, when the platelet count falls < 10,000/ \u03bcl, clinical symptoms \nsuch as bleeding of the gums, extremity petechiae, and easy bruisability are \ncommon presenting features. \no Bone marrow examination is normal or may show increased \nmegakaryocytes"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3344f-7265-11ef-9206-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 108, "chroma:document": "such as bleeding of the gums, extremity petechiae, and easy bruisability are \ncommon presenting features. \no Bone marrow examination is normal or may show increased \nmegakaryocytes  \n       e)  Other clinical conditions seen in patients during early stage of HIV: \no Molluscum contagiosum  \no Recurrent bouts of oral or genital herpes simplex \no Condylomata accuminata."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 109, "chroma:document": "Internal Medicine \n \n 94HIV/AIDS associated illnesses affecting different Organ Functions  \n \nOpportunistic infections: are infections that develop as a result of HIV \u2212inflicted damage \nto the immune system. \n\u0083 OIs are leading causes of morbidity and mortality in HIV-infected persons \n\u0083 Most of the common OIs are preventable as well as treatable \n\u0083 In resource-limited settings, it may be difficult to diagnose and manage OIs \n\u0083 Most opportunistic infections and complications of HIV develop when the CD4 count \ndrops below 200cells /ml \n Opportunistic malignancies: are neaoplastic conditions which tend to occur more \nfrequently in patients with underlining immunodeficiency.  \n \nDisease of the Respiratory system associated with HIV infection \n\u2666 The Respiratory system  is the most common site of HIV-associated \ncomplications/illnesses. \n\u2666 Respiratory problems are the leading cause of morbidity & mortality in persons \ninfected with HIV. \n\u2666 Many of the respiratory problems are both Preventable & Treatable. \n\u2666 Therefore, Prevention, evaluation, and treatment of pulmonary disease is an \nessential part of managing patients with HIV infection \nThere is a wide spectrum of Pulmonary Manifestations. \nOpportunistic Infection  \n\u0083 Bacterial: Streptococal, H.infleunza, gram negatives , Staphylococcal \n\u0083 Mycobacterial: M. tuberculosis, M. kansasi, M. aveum intracellularie  \n\u0083 Fungal: PCP, Cryptococcus neofrmans, Histoplasmosis, Coccidiodeoco \nmycosis, Aspergillosis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33451-7265-11ef-80e9-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 109, "chroma:document": "\u0083 Bacterial: Streptococal, H.infleunza, gram negatives , Staphylococcal \n\u0083 Mycobacterial: M. tuberculosis, M. kansasi, M. aveum intracellularie  \n\u0083 Fungal: PCP, Cryptococcus neofrmans, Histoplasmosis, Coccidiodeoco \nmycosis, Aspergillosis \n\u0083 Viral: Cutomegaovirus, Herpes simplex infection  \n\u0083 Parasitic pathogens: Toxoplasmosis, Strongliodosis  \nOpportunistic Malignancies    \n\u0083 Pulmonary Kaposi\u2019s sarcoma \n\u0083 Non Hodgkin\u2019s Lymphoma \n\u2666 The type of OIs or OMs that a patient develops depend on the degree of \nimmunosupression i.e. each of the OIs and OMs typically develop at or"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33452-7265-11ef-a73b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 110, "chroma:document": "Internal Medicine \n \n 95below a characteristic CD4 cell count range. Therefore CD4 cell count is an \nexcellent indicator of the risk of developing a specific OI or OM. \n\u2666 Knowing the stage of the disease will be useful in limiting the differential \ndiagnosis. \n\u2666 In the advanced stage of HIV infection, a person may be infected by more \nthan one pathogen.  \nRespiratory manifestations which may occur at any CD4 level \n\u0083 Upper respiratory tract infection (URI) :Sinusitis , Pharyngitis \n\u0083 Acute bronchitis \n\u0083 Bacterial pneumonia \n\u0083 Tuberculosis \n\u0083 Non-Hodgkin's lymphoma               \nRespiratory manifestations which may occur when CD4 level is <500/mm3 \n\u0083 Bacterial Pneumonia \n\u0083 Pulmonary TB \nRespiratory manifestations which may occur when CD4 level is <200/ mm3 \n\u0083 Pneumocystis carinii pneumonia \n\u0083 Cryptococcus neoformans pneumonia \n\u0083 Bacterial pneumonia (associated with bacteremia/sepsis) \n\u0083 Disseminated or extrapulmonary tuberculosis  \nRespiratory manifestations which may occur when CD4 level is <100/ mm3 \n\u0083 Pulmonary Kaposi's sarcoma \n\u0083 Bacterial pneumonia (Gram-negativ e bacilli and   Staphylococcus \naureus increased) \n\u0083 Toxoplasma pneumonitis  \nRespiratory manifestati ons which may occur wh en CD4 level is <50/  mm3 \n\u0083 Disseminated Histoplasma capsulatum \n\u0083 Disseminated Coccidioides immitis \n\u0083 Cytomegalovirus pneumonitis \n\u0083 Disseminated Mycobacterium avium complex \n\u0083 Disseminated mycobacterium (nontuberculous) \n\u0083 Aspergillus species pneumonia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33453-7265-11ef-b0b2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 111, "chroma:document": "Internal Medicine \n \n 96Knowledge of the relative frequencies of these pulmonary diseases is IMPORTANT. \nBacterial Pneumonia \n\u0083 Common etiological agents: S. pneumoniae \n\u0083 As the degree of immunosuppressioin worsens pneumonia may be recurrent  and \nassociated with sepsis  \n\u0083 Clinical presentation: Abrupt onset with fever, cough, production of purulent \nsputum, dyspnea, and pleuritic chest pain \n\u0083 Recommended Investigations : Chest X-ray, blood culture, FBC, gram stain of \nsputum, sputum culture and sensitivity \n\u0083 Common findings: X-ray may show pneumonic consolidation, infiltrates, or pleural \neffusion; leukocytosis; blood cultures may be positive \n\u0083 Treatment: \nAntibiotics : Penicillin (procaine Pen/Crystalinne Pen), Amoxicillin \nfluoroquiolones Supplemental Oxygen \n \nPneumocystis carinii Pneumonia (P . jiroveci  pneumonia)  \nEtiologic agent: P. jiroveci  is fungus which is the etiologic agent for PCP \n Epidemiology \n\u0083 One of the commonest OIs in industrialized countries. However the incidence has \ndeclined over the years due to HAART and use of CPT Prophylaxis \n\u0083 Used to be considered rare in Africa ( Early studies in 1990s showed  4-15% \nprevalence , however recent studies show a prevalence of 25-52% \n\u0083 In Ethiopia: though PCP is commonly seen in clinical practice there is only limited \npublished information. Study done by G. Aderaye (et al AIDS 2003, 17: 435-440) \nshows  30.3% prevalence of P. carinii among expectorated sputum samples of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d33454-7265-11ef-8236-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 111, "chroma:document": "\u0083 In Ethiopia: though PCP is commonly seen in clinical practice there is only limited \npublished information. Study done by G. Aderaye (et al AIDS 2003, 17: 435-440) \nshows  30.3% prevalence of P. carinii among expectorated sputum samples of \nHIV+/PTB- Pts. This suggests that  PCP may be an important differential diagnosis \namongst HIV + patients \n\u0083 50% of patients experience at least one bout of PCP during the course of their Life \ntime.  \n\u0083 Transmitted from human to human, or fr om environmental reservoirs to human"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 112, "chroma:document": "Internal Medicine \n \n 97Clinical Presentation \n Mode of presentation- PCP has indolent course characterized by weeks of vague \nsymptoms prior to presentation or diagnosis.  Median duration of symptom is 28 \ndays.  \n Dyspnea and fever are cardinal symptoms  \n Cough with scanty sputum in > 2/3 of cases \nSigns:  Findings on physical examination are minimal, and the usual findings for \npneumonia may not be noted.  \n Respiratory distress \u00b1 Cyanosis  \n Little abnormality on chest examination rhonchi or wheeze may be heard, \nespecially in patients with some other underlying pulmonary disease, findings of \nconsolidation are usually absent. \n P. carinii appears to be capable of hematogenic spread and seeding a variety of \norgan systems as well as causing a primary infection of the ear. \n Diagnostic Work-up \n1) Chest x-ray is helpful \nCould be normal. Diffuse bilateral alveolar/interstitial infiltrates is the usual findings \n2) LDH is elevated in > 90% of cases : Has a very high negative predictive value i.e. if \nLDH level is low in a patient the diagnosis of PCP is less likely  \n3) Definitive Dx  \u2013demonstration of the trophozoite or cyst from the organisms in \nsamples obtained from Induced sputum in which the yield is 60% or Brocho-alveolar \nlavage in which the yield is 95% . Staining: Wright-Giemsa, Methenamine silver, \nDirect IF, nPCR \n4) Other tests: Gallium 67 Scan, PFT, ABG \n Management (Treatment)  \n1) Antibiotics :"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35c6a-7265-11ef-a43c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 112, "chroma:document": "lavage in which the yield is 95% . Staining: Wright-Giemsa, Methenamine silver, \nDirect IF, nPCR \n4) Other tests: Gallium 67 Scan, PFT, ABG \n Management (Treatment)  \n1) Antibiotics :  \no The gold standard for therapy of PCP at present is co-trimoxazole IV/PO  \no It is effective in > 90% of patients.  \no Usual dose, 15 mg/kg/day (trimethoprim) in 3-4 divided doses (3-4 480 mg \ntabs 4X/day) \no Duration of Rx - 21 days ( 3 weeks )"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35c6b-7265-11ef-8e91-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 113, "chroma:document": "Internal Medicine \n \n 98o The major disadvantage is the relatively high incidence of side effects rash, \nfever, leucopenia 10% (HIV -ve) Vs 50% (HIV +ve) \no Response to treatment may not occur until the end of first week and the \npatient may get worse during the first few days owing to the inflammatory \nresponse resulting from the death of large number of organisms in the lungs. \n\u2666 Alternative Regimens : \n\u2022 Clindamycin 600 mg IV q8h or 300-400 mg PO q6h + primaquine 15-30 \nmg base/day x 21 days \n\u2022 Pentamidine 4mg/kg/day IVX21 days \n\u2022 Atovaquone 750 mg PO bid with meal x 21 days \n2) Adjuvant Treatment:  \no Supplemental O 2      \no Steroids:  reduces mortality by 50% and the need for mechanical ventilation. \nSteroids reduce the inflammatory response and its adverse clinical consequences.  Start within 72 hours of presentation \n\u2666 Indications are if the patient is in: \n\u2022  Moderate / severe respiratory distress or cyanotic \n\u2022 Pa O\n2   < 70mmHg \nDose : Prednisone 40 mg PO bid x 5 days \n40 mg daily for 5 days \n20 mg daily for 11 days \nPCP - preventive therapies \nPrimary Prophylaxis is strongly recommended for HIV infected person with \nevidence of significant immune deficiency:  \n\u2666 CD4+ count < 200/ \u03bcl (CD 4 cell percentage of less than 15% in \nchildren ) \n\u2666 HIV associated thrush \n\u2666 Unexplained fever \nSecondary prophylaxis  is indicated for patients with prior episode of PCP \nPCP - preventive therapies drugs/regimens: \no TMP-SMX two tablets/day (single strength)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35c6c-7265-11ef-850f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 113, "chroma:document": "children ) \n\u2666 HIV associated thrush \n\u2666 Unexplained fever \nSecondary prophylaxis  is indicated for patients with prior episode of PCP \nPCP - preventive therapies drugs/regimens: \no TMP-SMX two tablets/day (single strength) \no TMP-SMX two tablets three times per week"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35c6d-7265-11ef-9820-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 114, "chroma:document": "Internal Medicine \n \n 99Alternative regimens: \n\u2666 Dapsone 100 mg PO daily \n\u2666 Dapsone 50 mg PO daily, plus pyri methamine 50 mg PO weekly, plus \nleucovirin25 mg Po weekly \n\u2666 Aerosolized Pentamidine 300 mg monthly via nebulizer \n\u2666 Atovaqoune 1500 mg daily \nN.B. The prevention of PCP may also be beneficial in reducing the risk of having other HIV \nassociated infections such as CNS toxoplasmosis and other bacterial infections.  \n \nHIV and Tuberculosis \nTB is the leading OI in developing countries  \nHIV             TB \n \nImpact of HIV on tuberculosis  \nHIV affects almost all aspects of TB. \n \nEffect of HIV on Epidemiology of TB \n\u2666 Increases incidence and prevalence of TB .Life time risk of developing TB is \n50%among HIV positives compared to 5-10% in HIV negative patients \n\u2666 HIV is the most potent factor known to increase risk of progression from M. \ntuberculosis  infection to active disease. \n\u2666 The seroprevalence of HIV among TB patients may range from 30 % - 60 % \n Effect of HIV Clinical Manifestations of TB and it Diagnosis: \nClinical Presentation depends on degree of immunosupression"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 115, "chroma:document": "Internal Medicine \n \n 100Table I-5-1. Manifestaions of Tunerculosis in early and advanced HIV \n \n \n \n Early stage of HIV \nInfection :when CD 4 \ncount >200 cells/mm3 \n Late stage of HIV Infection  when CD\n4 \ncount <200 cells/mm3 \n \n Clinical \nPresentation  Similar to non HIV infected \nwith  productive cough  \nPulmonary manifestations \ndominate  Atypical presentation :  \nExtrapulmonary TB is more \ncommon  \nTB tends to be disseminated \n(involving different organs like \nmeningitis, pleura, pericardium, \nLymph nodes etc)  \nLaboratory \nDiagnosis  Sputum smear   \nPPD  \nOften positive  \n \nOften reactive with >10mm  Often negative  \n \nOften negative or annergic  \n \nChest X-ray  \nIn the setting of an \nHIV epidemic, it is \nno longer possible \nto look at a CXR \nand say that it is TB \nor it is not TB! \n Typical CXR findings of TB \nUpper lobe and or bilateral \ninfiltrates \nCavitations \nPulmonary fibrosis \n Atypical CXR findings  \nCXR may show interstitial infiltrates especially in lower zones \nwith no features of cavitation and \nfibrosis \nNegative CXR can be associated \nwith sputum AFB+ (12% with \npulmonary disease) \nIn the setting of an HIV epidemic, \nit is no longer possible to look at a \nCXR and say that it is TB or it is \nnot TB!  \n \nTreatment of TB in HIV infected patients  \n\u2666 When TB and HIV are coexisting TB is more life threatening and it should be treated \nfirst and patients should be stabilized  \n\u2666 The same Combination anti-TB drugs are given  based on the treatment category"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f14-7265-11ef-9b07-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 116, "chroma:document": "Internal Medicine \n \n 101\u2666 Close follow-up of patients on DOTs is required   \n\u2666 Complete cure from TB may be achieved in six to eight months \n \nMost patients who have TB-HIV co infection are eligible for ART  \nWhen to start ART in patients on Anti Tb Medication depends on CD4 count and the clinical condition of the patient  \n\u0083 CD4 < 50 /mm\n3: start ART as soon as the patient tolerates the Anti Tb medication  \n\u0083 CD4 count between 50 \u2013 200 mm3  start anti TB after completion of intensive phase \nof DOTs \n\u0083 CD4 > 200 mm3 ART can be initiated after compilation of Anti-TB treatment  \n \nChallenges / Problems in treatment of TB/HIV co infected patients  \n\u0083 Increased morbidity, mortality and high case fatality rate \n\u0083 Increased drug toxicity \n\u0083 Decreased Drug absorption \n\u0083 High pill burden which may decrease adherence to treatment  \n\u0083 Drug Interaction between Anti TB drugs and ARTs  \n \nImpact of TB on HIV \n\u0083 TB hastens the rate of HIV progression. \n\u0083 Tuberculosis is the leading cause of illness and death among PLWHAs. \n \nINH Preventive Therapy \n\u0083 Rationale: Life time risk  of having active TB in patients with HIV is  50%  with Annual \nrisk  of 7 - 9% ( compared to only 5-10 % life time risk in non HIV infected ) \n\u0083 It is advisable to give INH prophylaxis for HIV infected patents  \n\u0083 Patients should be screening for active TB before they are given preventive therapy  \n \nTreatment  \n\u0083 INH 300mg/d for 6-9 months. \n\u0083 Alternatively, Rifampicin for 4 months can be used"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 117, "chroma:document": "Internal Medicine \n \n 102Neurological Manifestations of HIV/AIDS \n    \n\u2022 The nervous system is the second commonl y affected organ system by HIV next to \nthe respiratory system  \n\u2022 Common cause of Morbidity & Mortality \n\u2022 Occur at any stage of HIV infection  \n\u2022 All levels of the neuro-axis are involved \n\u2022 Clinical manifestations are variable  \n \nPathogenetic Mechanisms for Neurologic manifestations  \n1. Directly related to HIV \n\u2022 Aseptic Meningitis \n\u2022 AIDS dementia complex \n\u2022 Myelopathy \n\u2022 Peripheral Neuropathy: AIDP( Acute demy linating distal polyneuropathy), MNM ( \nmononuritis multiplex ), DSPN ( distal sensory ply neuropathy ) \n\u2022  Myopathy \n\u2022  Vasculitis  \n2. Secondary to Immunodeficiency  \nA. Opportunistic Infections \n\u2022 CNS Toxoplasmosis \n\u2022 Cryptococcal Meningitis \n\u2022 Tuberculos Meningitis/Tuberculoma \n\u2022 PML \n\u2022 Neuro-syphilis \n\u2022 CMV polyradiculopathy/Encephalitis \nB. Opportunistic Malignancies \n\u2022 Primary CNS Lymphoma \n \n3. ART related \n\u2022 Peripheral Neuropathy :d4T, DDI \n\u2022 Myopathy :ZDV \n\u2022 EFV related \u2013 Psychiatric Manifestations"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 118, "chroma:document": "Internal Medicine \n \n 103Epidemiology \nHigh incidence of neurological disease among HIV patients:  \n\u2022 7-20% of initial AIDS diagnoses,  \n\u2022 30-70% prevalence among inpatients \n\u2022 >90% in post mortem studies \n \nAseptic meningitis:   \n\u2022 It may occur at any time in the course of HIV infection, most commonly at the \ntime of acute HIV infection. However it becomes increasingly rare following the \ndevelopment of AIDS. \n\u2022 Patients experience a syndrome of headache, photophobia, sometimes frank-\nencephalitis and cranial nerve involvement,  (commonly VII cranial nerve is affected ) \n CSF findings -    lymphocyte pleocytosis 10-100 cells/ \u03bcl \n                -   Increased protein level protein< 100mg/dl,  \n                   -   Normal glucose level \n The syndrome usually resolves spontaneously with in 2-4 weeks.              \nDiagnosis of HIV :  HIV serology may be negative if it occurs during the primary HIV infection. \nTo confirm the diagnosis of HIV p24 atg or DNA PCR may be done or Repeat HIV serology after \nfew weeks \n \nCNS TOXOPLASMOSIS  \nEtiology:  Toxoplasmosis is caused by protozoa, Toxoplasma gondii \nEpidemiology \n\u0083 Zoonotic infection cats are the definite hosts and excrete the oocysts in their feces and \ncan be transmitted from animals to humans.  \n\u0083 T. gondii cysts are also found in under-cooked meat. \n\u0083 Prevalence of latent Toxoplasma infection in the general population is high - 80% in \nEthiopia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f17-7265-11ef-972d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 118, "chroma:document": "can be transmitted from animals to humans.  \n\u0083 T. gondii cysts are also found in under-cooked meat. \n\u0083 Prevalence of latent Toxoplasma infection in the general population is high - 80% in \nEthiopia \n\u0083 Toxoplasmosis gondii is the most common cause of secondary CNS infection in patients \nwith AIDS."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f18-7265-11ef-a1e2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 119, "chroma:document": "Internal Medicine \n \n 104\u0083 It is generally a late complication of HIV infection and usually occurs when the CD 4 cell \ncount is less than 100/mm3. \n\u0083 It is thought to represent a reactivation syndrome of prior infection. \n \nClinical Features \n\u2022 Onset - Subacute \n\u2022 Fever, Headache, Hemiparesis, Seizures and altered mentation \n\u2022 Over 90% present with Focal neurologic deficits  \n\u2022 10% of patients present with encephalitis picture \u2013 confusion or comma and become \nmore toxic  \n\u2022 Commonly  affected areas \u2013 Basal ganglia, brain stem and cerebellum \n\u2022 Extra-cranial manifestation: \no Retinitis \no Myocarditis  \no Pneumonitis (lung) \n \nDiagnosis \nClinical (Hx + P/E) + Neuro-imaging + Therapeutic Trial +/--Histology - Biopsy \nNeuroimaging (CT/MRI):  \n\u2022 Multiple ring enhancing lesions are the findings in most patients (90%) with mass \neffect and edema \n\u2022 Preferential location: basal ganglia, grey-white junction, white matter \nSerologic assays: Limited value, a negative toxoplasma antibody test makes the diagnosis less likely Histology: brain biopsy \u2013 In patients with treatment failure (not possible in our country) \n \nTreatment Regimen 1  \nLoading dose of pyrimethamine 50-75mg/ day for 2-3 days, followed by \nPyrimethamine 25-50 mg/day, plus sulfadiazine 2 - 4 gm/d in divided doses, PO, plus folinic \nacid 10-20mg/d Regimen 2  \nPyrimethamine and leucovorin plus clindamycin 450 mg q8hrs"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 120, "chroma:document": "Internal Medicine \n \n 105Duration of Rx: 6 weeks, or 3 weeks after complete resolution of lesions on CT \nContinue suppressive Rx for life: pyri methamine 25mg/day + sulfadiazine2g/day + \nfolinic acid 5-10mg/day  \nHigh rate of adverse reactions \nRegimen 3 \nFansidar PLUS Folinic Acid ( Pyrimethamine 25 mg +Sulfadoxin 500mg ) \nN.B. As the other preparations are not available in Ethiopia, Fansidar is a drug which is widely \nused  \nDose:  Fansidar 525 mg tabs 2 tabs PO BID for 2 days and then 1 tab PO/day \nIf the patient is very critical, add Doxycycline 100mg PO BID \nSide effects: \n\u0083 Leukopenia is the main side effect of the treatment. A higher dose of fansidar (2 \ntab/day) has been found to be associated with frequent incidence of fatal \nhemorrhage.  \n\u0083 Check for bleeding tendency such as gum bleeding, epistaxis, hematuria  \n\u0083 Do Hgb, WBC and platelet count once per week.  \n\u0083 To prevent these side effects, give folinic  10mg PO per day or advice to take cream \ncake daily. \n\u0083 If there is bleeding tendency, stop Fansider and start Doxycycline 100mg PO BID.   \n\u0083 Alternatives:  \nCo-trimoxazole, or Clindamycin+Pyrimethamine/Primaquine,  \n\u0083 Azithromycin,Clarithromycin,      \nDoxycycline \nIndication for Steroids and dose :  \n\u0083 Evidence of marked increase in Intra cranial pressure and altered mentation \n\u0083 Dose : administer Dexamethasone 8 mg IV stat and then 4 mg IV QID till the  \nSuppressive/Maintenance therapy: Fansidar 1 tab per day should be continued."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f1a-7265-11ef-8d3b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 120, "chroma:document": "\u0083 Evidence of marked increase in Intra cranial pressure and altered mentation \n\u0083 Dose : administer Dexamethasone 8 mg IV stat and then 4 mg IV QID till the  \nSuppressive/Maintenance therapy: Fansidar 1 tab per day should be continued. \n\u2022 Suppressive therapy (secondary prophylaxis ) can be stopped when the CD4 \ncount is more than 200 for 6 months  \nPreventive Therapy Indications:  \n CD4+ count < 100cells/ \u03bcl \nRegimens \n TMP-SMX two tablets per day"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f1b-7265-11ef-95c7-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 121, "chroma:document": "Internal Medicine \n \n 106 TMP-SMX two tablets 3 times per week \nAlternative Regimens  \n Dapsone plus Pyrimetham ine plus leucovirin \nN.B. Primary prophylaxis can be stopped if CD4 count >200cells/ml for more than three months \nfollowing HAART \n \nCryptococcal Meningitis \nEtiology:  Cryptococcus neoformans, which is yeast - like fungus. \nPigeon droppings commonly contain serotypes A or D  \nInfection is acquired through inhalation  \nEpidemiology: \n\u0083 Is the leading cause of meningitis in patients with AIDS  \n\u0083 Is the initial AIDS defining illness in 2 % of patients \n\u0083 Particularly common in patients with AIDS is Africa \nClinical Features \n\u0083 Occurs late in the course of HIV/AIDS \u2013 when CD4 count is, 100/mm3  \n\u0083 CNS and meningial involvement is seen in 67-85 % of patients  \n\u0083 Low grade fever n nausea , vomiting , headache  ,  \n\u0083 Both fever and nuchal rigidity are often mild or lacking  \n\u0083 Papilledema is seen in one third of patients \n\u0083 Neck stiffness , Photophobia \u2013 Meningial signs are seen in 30% of patients  \n\u0083 Late manifestations : Confusion , altered state of consciousness \u00c6 comma  \nOther organ systems affected  \n\u0083 Extra cranial manifestations : Occasionally appears as pulmonary or disseminated \ndisease that includes the skin (10%). \n\u0083 Cutaneous Cryptococcosis: centrally umblicated multiple lesions on the face (look very \nmuch like Molluscum contagiosum.) \n\u0083 Pulmonary disease \n\u0083 Fungemia \n\u0083 Lymphadenopathy \n\u0083 The prostate gland may be a reservoirs for smoldering infection"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 122, "chroma:document": "Internal Medicine \n \n 107Diagnosis \nLP \u2013 CSF Analysis \n\u0083 Opening pressure is high  \n\u0083 WBC with differential, Protein, Glucose  is normal in 1/3 of patients  \n\u0083 Indian Ink \u2013 Positive in 60-80% \n\u0083 CSF Cryptococcal Antigen \u2013 Positive in   95-99% \n\u0083 Cryptococcal Culture \u2013 Gold Standard  \nTreatment \nInduction \nAmphotericin B (with or without flucytosine) \n 0. 7-1 mg/kg for two to three weeks followed by consolidation. \nConsolidation \nFluconazole 400 mg, PO, daily for 8-10wks OR until CSF is sterile \nMaintenance :( suppressive ) \nFluconazole, 200 mg, PO, daily life long \nAdjunct treatment   \n\u2022 Management of raised intracranial pressure ; \no If CSF opening pressure- CSF drainage until CSF pressure is < 200 mm \nH2O; repeat LP daily until stable OR CSF pressure normalizes  \n\u2022 There is no place for  Dexamethsone  \n\u2022 Discontinue maintenance or secondary prophylaxis when CD4 count rises to > 200 \n/mm3 for more than 6 months after completion of treatment following in patients who are taking HAART \n \nProgressive Multifocal Leukoencephalopathy (PML) \nEpidemiology of PML \n\u0083 Reactivation of JC Virus It is seen in 2-4% of AIDS Pts \nClinical presentation \n\u2022 Occurs late in the course of HIV when the CD4 counts< 100/ \u03bcl  \n\u2022 Subacute onset  \n\u2022 The patient is afebrile, alert no headache \n\u2022 Multifocal neurologic deficit \n\u2022 Variable presentation: \u201cClassic triad\u2019: dementia, hemiparesis, and hemianopsia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f1d-7265-11ef-987d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 123, "chroma:document": "Internal Medicine \n \n 108\u2022 Serology: 90% adults are seropositive for JC virus \nDiagnosis - PML \n\u0083 CSF is often non-diagnostic , JCV PCR or brain biopsy may help to make diagnosis c \nPML Treatment \nNo effective treatment. But initiation of HAART increases survival to  \n \nPrimary CNS Lymphoma \nClinical Presentation Occurs late in the course of HIV when the CD4+ counts: < 100/ \u03bcl \nOccurs in 2-4% of AIDS patients \nSymptoms and signs \n - Confusion, lethargy, memory loss; 57% \n - Hemiparesis or aphasia 40%  - Seizures 14%  - Cranial nerve palsy 9%  - Headaches only 3% \n - No fever  unless concomitant infection \nNeuroimaging \n\u0083 CT/MRI: multiple lesions as frequent as single lesion. (Irregular and solid enhancement, \nsubependymal enhancement more specific, variable mass effect. Localization mainly periventricular \nCSF : Epstein-barr virus DNA PCR \u2013 CSF ( sensitivity: 85-100% ,specificity: 98-100% ) \nHistology: Diffusely infiltrating, multicentric tumor of B cell lineage with the presence of EBV \ngenome in ~100% Treatment \n\u0083 Cytotoxic chemotherapy is not effective  \n\u0083 Radiotherapy can help some patients \n\u0083 Response to steroids variable \n \nHIV- associated Dementia Co mplex /HIV encephalopathy / HIV-1 associated \nDementia Complex \n\u0083 First AIDS defining illness in up to 5-10% \n\u0083 Major cause of dementia in young people"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 124, "chroma:document": "Internal Medicine \n \n 109\u0083 A major feature of this entity is the development of dementia, which is defined as a \ndecline in cognitive ability from a previous level. \n\u0083 TRIAD : cognitive, motor and behavioral dysfunction \n \nTable I-5-2. Stages of ADIS dementia complex  \n \n \n  Cognition   Behavior   Motor \nEarly Inability to \nConcentrate Altered personality  \n Middle Mental Slowing Forgetfulness \n Social \nwithdrawal Poor coordination \nLate  Global dementia  Apathy    Paraparesis \nDiagnosis : \n\u0083 Neuropsychological tests \n\u0083 Mini-mental test \n\u0083 It is often a diagnosis of  Exclusion  \nTreatment: \n\u0083 HAART \u2013 most patients improve with HAART with possible benefit from ARV agents \nthat penetrate the CNS (AZT, d4T, ABC, Nevarpine)  \n\u0083 Supportive care \n \nPeripheral Neuropathies \nOccurs in 1/3 of pts with AIDS \nType: \n\u0083 Mono neuropathy e.g. Bell\u2019s palsy \n\u0083 Mononuritis multiplex  \n\u0083 Distal sensory peripheral polyneuropathy (DSPN) \nDSPN: Is the most common.  \n\u0083 It may be cause by HIV infection or ART mainly d4T and DDI"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f1f-7265-11ef-acb8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 125, "chroma:document": "Internal Medicine \n \n 110\u0083 It presents with symmetric bilateral painful burning sensation parasthesia and  tingling of  \nthe feet and lower extremities ,  \nDiagnosis: Clinical, Nerve conduction study, Exclusion of other causes \nTreatment: Symptomatic treatment and discontinuation or changing the drug which is causing it \nwhen symptoms are sever, \n \nSeizure \n\u0083 Seizure is a relatively frequent complication of HIV infection. \n\u0083 May be a consequence of opportunistic infections, neoplasms, or HIV encephalitis.  \n\u0083 The seizure threshold is often lower than normal in patients with HIV infection owing to \nthe frequent presence of electrolyte abnormalities. \n\u0083 It may be the presenting clinical symptom of HIV disease. \nCommon causes of Seizure in HIV patients  \n\u0083 CNS toxoplasmosis 15-40 % of patients  \n\u0083 Primary CNS lymphoma15-35% of patients  \n\u0083 Cryptococcal meningitis 8% of patients  \n\u0083 HIV encephalopathy 7-50 % of patients  \nTreatment  \n\u0083 Most of the time patients will have 2 or more seizures suggesting that anticonvulsant \ntherapy is indicated in all patients with HIV infection and seizures, unless a rapidly \ncorrectable cause is found. \n\u0083 While Phenytoin (100 mg PO TID) remains the initial treatment of choice, Phenobarbital \n(100mg PO every night) or Valproic acid are also alternatives. \n \nGastrointestinal diseases in p atients infected with HIV \n \nCandidiasis \nCaused by Candida albicans \nOral Candidiasis Oral thrush:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 125, "chroma:document": "(100mg PO every night) or Valproic acid are also alternatives. \n \nGastrointestinal diseases in p atients infected with HIV \n \nCandidiasis \nCaused by Candida albicans \nOral Candidiasis Oral thrush: \n\u0083 Appears as a white, cheesy exudates, often on an erythematous mucosa (most \ncommonly seen on the soft palate) which gives an erythematous or bleeding surface on \nscraping"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 126, "chroma:document": "Internal Medicine \n \n 111\u0083 Erythematous Form : there is predominantly erythema rather that white patches \nEsophageal Candidiasis \n\u0083 Usually coincides with CD4 count of < 50 /\u00b5l \n\u0083 Causes substantial pain or a sense of obstruction on swallowing \n\u0083 Most lesions occur on the distal third of the esophagus and appear on endoscopy as \nredness, edema and focal white patches or ulcers \n\u0083 If and HIV infected person has oral thrush and substernal pain up on  swallowing  \npresumed diagnosis of Esophageal Candidiasis can be made s \n\u0083 Endoscopy would prove the diagnosis, but is unnecessary if the patient responds to \nantifungal therapy \n\u0083 Linear ulcerations of the esophagus may be seen on barium x-ray. \n \nTreatment \nOral candidiasis  \n\u0083 Nystatin IU/ml suspension 2.5-5 ml gargled 5X   daily \n\u0083 2% Miconazole oral gel applied 2-3 x daily \n\u0083 Amphotericin B lozenges \n\u0083 Fluconazole 100mg \u2013200mg PO /day for 7-14days in severe and persistent cases \n\u0083 Oral hygiene, discontinue  steroids and antibiotics if the patient is taking any  \n \nEsophageal Candidiasis   \nFirst line : Fluconazole 200mg/day PO ( up to 400mg/day) for 14-21 days \nAlternately  \n\u0083 Ketoconazole 200-400mg for 14-21 days \n\u0083 Itraconazole 200mg/day for 14-21 days \n \nDiarrhea in HIV positive patients \n\u0083 Is a common clinical condition in HIV infected patients (>50%) \n\u0083 May be acute or chronic , watery , mucoid or  bloody \n\u0083 May or may not be associated with fever  \n\u0083 Spectrum may depend on the degree of immunodeficiency state"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 126, "chroma:document": "\u0083 Is a common clinical condition in HIV infected patients (>50%) \n\u0083 May be acute or chronic , watery , mucoid or  bloody \n\u0083 May or may not be associated with fever  \n\u0083 Spectrum may depend on the degree of immunodeficiency state \n\u0083 Pathogens may be: Bacterial, Viral, Protozoal, Fungal  ,Spirochetal ,Mycobacterial \n,Metazoal , Others (malignancies)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 127, "chroma:document": "Internal Medicine \n \n 112Mechanism of diarrhea \n\u0083 Adhesion to mucosal surface \n\u0083 Enterotoxin  \n\u0083 Entero-invasion \n\u0083 Atrophy of mucosal surface \n \nChronic Diarrheas \nDefinition \u2013 Diarrhea lasting for more than two weeks with a single watery bowel motion and or \nthree or more loose stools per day \n\u0083 Diarrhea occurs in 30-90% HIV-positive cases in Europe and USA and in 90% of cases \nin the developing countries \n\u0083 Frequency of diarrhea increases as the CD4 count falls \n\u0083 With HAART, incidence of chronic diarrhea decreases  \n \nProtozoa that cause chronic Diarrhia in HIV patients:   \n\u0083 Cryptosporidia \n\u0083 Isospora belli  \n\u0083 Microsporidium  \nHIV enteropathy: (AIDS enteropathy) \n\u0083 Chronic diarrheal syndrome for which no etiologic agent other than HIV can be identified  \n\u0083 It is most likely a direct result of HIV infection  \n \n Clinical features  \n\u0083 Early stage : intermittent self limiting diarrhea however in advanced stage, persistent life \nthreatening diarrhea  \n\u0083 Copious amount of stool several times per/day associated with abdominal cramp. \nnausea and vomiting may also be present  \n\u0083 Significant weight loss ( wasting ) may occur due to the associated malabsorption  \n\u0083 Fluid and electrolyte depletion  \nDiagnostic investigation  \n\u0083 Stool Microscopy \n\u0083 Culture \n\u0083 Intestinal biopsy \n\u0083 Special stains: Modified AFB stain"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 128, "chroma:document": "Internal Medicine \n \n 113Treatment  \n1. General treatment of chronic diarrhea \n\u0083 Hydration: oral , parentaral with electrolyte replacement  \n\u0083 Symptomatic treatment : Anti-diarrheal agents \n Loperamide 2-4 mg QID \n Lomotil 5 mg QID \n Tincture of opium 0.3 ml QID \n Codeine tablets \n2. Specific treatment  \n Cryptosporidium \n\u0083 Nitazoxanide 0.5 \u2013 1.0 gm bid or  \n\u0083 Paromomycin 1 gm bid + azithromycin 600 mg qd \nIsospora  \n\u0083 Cotrimoxazole 2 tabs   QID for x 10 d, then bid for 3 weeks OR Pyrimethamine 75 mg + \nfolinic acid 10 \n\u0083 Chronic suppression (secondary prevention): Cotrimoxazole 2 tabs /day OR \npyrimethamine 25 mg + folinic acid 5 mg qd \nProblem:  malabsorption of drugs \nStrongyloidias  \n\u0083 Parasitic infection caused by Strongyliod stercolaris  \n\u0083 Acquired through skin penetration of its larva form  \n\u0083 Auto infection is common  \n\u0083 In its life cycle there is transition via the lungs and settles in the GI tract, primarily small \nintestine free-living or parasitic \n\u0083 Usually a mild disease in immunocopetent individuals \n\u0083 Disseminated infection common in immuno-compromised hosts, \n\u0083 Systemic manifestation may mimic sepsis \nClinical Manifestation \n\u0083 Asymptomatic to mild symptoms in i mmuno-competent indivi duals with occasional \nsevere pruritis .It may manifest with mild diarrhea, epigastric pain  \n\u0083 In Immunocopromised patients large amount of filariform larva are released and may \ninvade : \no GI tract : causing enteritis with severe diarrhea and malabsorption"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f25-7265-11ef-9644-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 128, "chroma:document": "severe pruritis .It may manifest with mild diarrhea, epigastric pain  \n\u0083 In Immunocopromised patients large amount of filariform larva are released and may \ninvade : \no GI tract : causing enteritis with severe diarrhea and malabsorption \no Lungs:  manifest with cough, shortness of breath 9 Loffler\u2019s\u2019 pneumonia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 129, "chroma:document": "Internal Medicine \n \n 114o CNS , peritoneum and liver may also be invaded  \n\u0083 Severe systemic symptoms are comm only seen in disseminated infections \n\u0083 May be complicated by Gram negative sepsis \n \nDrug Treatment \n\u0083 Ivermectine 200 \u00b5g 1-2 days  \n\u0083 Thiabendazole 75 mg/kg bid for 3 days \n\u0083 Albendazole 400mg/day for 5 days \n \nSkin Manifestations of HIV  \n\u0083 80-90 % of HIV patients have skin manifestation \n\u0083 Skin problems could be the first organ system affected  \n\u0083 Various type of skin disease occur \nClassification of cutaneous conditions associated with HIV/AIDS  \n\u0083 INFECTIONS: Bacterial  infections   \n\u0083 INFESTATIONS \n\u0083 INFLAMMATORY CONDITIONS \n\u0083 MALIGNANCY \nStaphylococcus auresus \nA common pathogenic causes infection  \nCommon manifestations are  \n\u0083 Bullous Impetigo Ecthyma      \n\u0083 Folliculitits \n\u0083 Furuncle  \n\u0083 Carbuncle  , Cellulitis  \n \nTreatment:  \nTopical Antibiotics or Systemic antibiotics depending on severity of the diseases  \n \nSyphilis (Treponema pallidum)in HIV infected patients  \n\u2022 Syphilis has atypical presentations in HIV patients  \n\u2022 Primary chancre usually painless can be tender \n\u2022 Latent period before development of meningovascular syphilis is shorter"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 130, "chroma:document": "Internal Medicine \n \n 115\u2022 Rapidly progresses to tertiary syphilis \n\u2022 Relapses without re-exposure \n\u2022 Pleomorphic skin lesions reported \n\u2022 VDRL can be negative-due to high titer antibody level \nDIAGNOSTIC TESTS  \n\u2022 Screening Tests-VDRL/RPR \n\u2022 Specific Test- FTA-ABS -fluorescent treponemal antibody absorption \nTreatment \n\u2022 Benzathin penicillin 2.4 mega unit IM weekly three doses \n\u2022 Penicillin IV / 2 to 4 mega unit every 4 hours for 10 to 14 days.(with CNS involvement) \n\u2022 Azithromycin + Benzathin penicillin + Amoxicillin \n\u2022 Follow up at intervals of 1, 2, 3, 6, 9 and 12 months. \nViral disease associated with HIV  \n\u2022 Herpes simplex \n\u2022 Varicella-zoster virus \n\u2022 Human papiloma virus \n\u2022 Moluscum contagiosum \nHerpes simplex virus \n\u2022 Is due to reactivation of latent virus \n\u2022 The usual manifestations are grouped vesicle with erythematous base \n\u2022 In HIV infected patients however : \no Atypical presentation \no Chronic non healing deep ulcer \no Verrucous erosion \no Mixed infection are common  \no High frequency of reactivation \no Widespread local extension \no Higher incidence of dissemination \no Viremic spread to visceral organs, which is life threatening \nTreatment \n\u2022 Systemic acyclovir 2oo mg.5 X a day 5-10 days \n\u2022 Acyclovir 50 mg /kg every 8 hours where absorption is poor \n\u2022 Acyclovir 400 mg 2 X a day in frequent relapse"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 131, "chroma:document": "Internal Medicine \n \n 116\u2022 Famcyclovir 125 mg 2 x daily for 5 days \n\u2022 Valacyclovir 1 gm 2 x daily for 10 days \n \nVaricella-zoster virus (HZ) \n\u2022 There is increased incidence of HZ in patients with HIV infection  \n\u2022 It is one of the earliest opportunistic infection to occur  \n\u2022 The clinical presentations are atypical presentation \no Hemorrhagic necrotic lesion \no Chronic verrucous lesion \no Multiple dermatomal involvement \no Tendency to be generalized \no It may occur recurrently \n \nTreatment \nPrimary varicella -acyclovir IV 10mg /kg ev ery 8 hours for 7 to 10 days \nHerpes zoster \n\u2022 Acyclovir 800 mg 5 X a day for 7 \u2013 10 days \n\u2022 Famcyclovir 500 mg 5 x /day for 7 days \n\u2022 Valacyclovir 1 gm 3 x a day for 7 days \n \nHumna papiloma virus \nWart is common infection in HIV \nIt is refractory to treatment \nComplications are neoplastic changes and increased risk of cervical carcinoma Treatment \n\u2022 Podophyllin 20 % or 5-Fluorouraacil \n\u2022 Cryotherapy or Excision of big tumors \n \nMoluscum contagiosum(MC) \nCause by pox virus \nIt occurs in HIV patients with low CD4 count \nAtypical presentations are common  \n\u2022 It is commonly seen in children but can infect immunocopromised adults"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 132, "chroma:document": "Internal Medicine \n \n 117\u2022 It tends to be Generalized \n\u2022 Giant Moluscum contagiosum  \n\u2022 Secondary infection \nTreatment \n\u2022 Cryosugery or  Curettage or Electrosurgery \n\u2022 Podophyllin or Cantaridine or 5-fluorouracil \n \nPruritic papular eruption (PPE) \n\u2022 It Chronic itchy condition commonly seen in HIV infected patients  \n\u2022 Symmetrical non-follicular papules on trunk and extensors of extremities \n\u2022 The most common cutaneous manifestation in HIV- prevalence 11-46 % \n \nDiagnosis : Biopsy \nTreatment  \nTopical : Antipruritic lotion, Corticostroid, Oatmeal bath \nSystemic: Antihistamin, coricosterroid, Phototherapy, UV-B, UVA + Psoralen \n \nCytomegalovirus (CMV)  \n\u2022 Cytomegalovirus (CMV) \n\u2022 Herpes virus \n\u2022 High incidence  \no 30 - 40% in general population are positive antibody for CMV \no 90% or more in IV Drug abusers have positive antibody for CMV \no 20-30 % of patients with AIDS had CMV reactivation prior to the era of HAART \n\u2022 Able to establish a latent infection that can reactivate \n\u2022 Late-stage AIDS illness (CD+4 < 100) \nClinical manifestations : retinitis, esophagitis, colitis \nCMV Retinitis;  \n\u2022 Clinical presentation:Visual disturbances \u2013 floaters , flashes of light photophobia and \nblurring of vision ,painless, gradual loss of vision  ,usually bilateral \nDiagnosis confirmed by retinal exam  \nCMV GI Disease Esophageal ulcers"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 133, "chroma:document": "Internal Medicine \n \n 118\u2022 Pain and difficulty in swallowing \n\u2022 Diagnosis by tissue biopsy \nColitis \n\u2022 Abdominal pain, watery diarrhea, sometimes bloody, rarely perforation \n\u2022 Fever \n\u2022 Diagnosis by tissue biopsy \nHepatitis and acalyculus cholecystitis  \nTreatment for CMV  \n\u2022 Valganciclovir  (PO) \n\u2022 Ganciclovir (IV)  \n\u2022 Ganciclovir Intra-ocular Implant  \n\u2022 Foscarnet (IV) \n\u2022 Cidofovir (IV) \n18% in IV Ganciclovir   \n \nVisceral Leishmaniasis and HIV Co-infection  \n\u2022 Visceral Leishmaniasis is Caused by L.donovanii  \n\u2022 VL has become an important OI among persons infected with HIV-1 \n\u2022 Most co-infected patients with clinically evident leishmania have CD4 cell less than \n200/\u00b5l. \n\u2022 The infections affect the same cell lines, causing cumulative deficiency of the immune \nresponse  \n\u2022 Leishmania parasite suppresses Th1 activity  \n\u2022 Visceral Leishmaniasis Clinical Manifestation  \n\u2022 Patients present with fever, organomegaly, anemia or pancytopenia  \n\u2022 Presentation could be atypical, but VL should be suspected in those with travel history to \nendemic areas \nDiagnosis \n\u2022 Serology less sensitive in immunocompromised  \n\u2022 Parasite could be detected in peripheral blood in immuno -compromised patients  \n\u2022 Bone marrow aspirate \n\u2022 Splenic aspirate most sensitive"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 134, "chroma:document": "Internal Medicine \n \n 119Treatment \nFirst line \u2013 Pentavalent antimonials (Sb) \nAlternatives- Pentamidine, Amphotericin B  \nRelapse and toxicity are common in patients co-infected with HIV  \nOpportunistic Malignancies  \n\u2022 Kaposi\u2019s Sarcoma  \n\u2022 Lymphoma  \n\u2022 Cervical cancer \n \nKaposi\u2019s sarcoma  \nEtiology/pathogenesis: multi-factorial \n\u2022 Vascular neoplasm affecting skin and mucosa \n\u2022 Immunosuppression increases risk of KS 400-500 times higher than general population \n\u2022 Presence of Human Herpes Virus 8 (HHV8) found in all types of KS \n\u2022 HIV virus Tat protein potentiates the milieu conducive to KS growth \nTransmission \n\u2022 Studies have shown that HHV-8 which is the etiologic agent for KS is believed to be \ntransmitted sexually. The risk factors are multiple partners, history of STD, and being \nHIV positive.  \n\u2022 More common in homosexual men  \n\u2022 Multiple heterosexual contacts is a risk factor for HHV-8 in Africa \n\u2022 Parentral: frequent IVDU \n\u2022 Oral: via saliva: HHV-8 titers 2-3 times higher in saliva than in semen, anorectal or \nprostate fluid samples \n Epidemiology \n\u2022 Is the most  common Opportunistic malignancy among  HIV positive patients  \n\u2022 With use of HAART, KS incidence has declined by 66%  \nClinical Manifestations \u2022 Can affect almost any organ system \n\u2022 Most common sites include"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f2c-7265-11ef-aee7-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 135, "chroma:document": "Internal Medicine \n \n 120o Skin: flat to nodular lesions; can progress to significant infiltration of skin and \nnecrosis \no Oral cavity: flat to invasive lesions \no GI tract: can have KS anywhere in GI tract, which can cause intestinal blockage and \nbleeding \no Pulmonary: can spread along bronchi and vessels. \nDiagnosis \n\u2022 Skin and oral lesions can be diagnosed by visual exam even though skin biopsy is most \naccurate to make diagnosis \n\u2022 Lung and GI-tract lesions would need endoscopy and biopsy for accuracy \n\u2022 Resolution of skin lesions with HAART can give a presumptive diagnosis \n\u2022 Testing for HHV-8 is more research than clinically applicable \n \nTreatment Primary treatment  is antiretroviral drugs (HAART). Lesions significantly regress with HAART  \nLocal therapy for skin lesions \n\u2022 Alitretinoin gel (35-50% response),Local radiation (20-70% response) \n\u2022 Intralesional vinblastine/vincristine (70-90% response) \n\u2022 Cryotherapy (85% response), Photodynamic therapy or Surgical excision \n \nSystemic Treatment :  \nImmunotherapy -interferon-alfa: immunomodulatory antiviral and antiangiogenic. This treatment \nmay have superior efficacy if combined with HAART. \nChemotherapy : Indicated for rapidly progressive oral or visceral disease \n\u2022 Liposomal doxorubicin/daunorubicin is superior to conventional chemo with less toxicity  \n \nLymphomas  \n\u2022 Lymphomas occur with increased frequency in immunoi deficiency states and there are \n120X increased incidence of Lymphoma among HIV patients."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f2d-7265-11ef-b93e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 135, "chroma:document": "Lymphomas  \n\u2022 Lymphomas occur with increased frequency in immunoi deficiency states and there are \n120X increased incidence of Lymphoma among HIV patients. \n\u2022 6% of all AIDS patients develop lymphoma at sometime in the course of their illness \n\u2022 As HIV diseases progress the risk of Lymphoma increases. \n\u2022 The incidence of lymphoma hasn\u2019t shown dram atic decrease even after HAART is being \nwidely used by HIV patients worldwide."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f2e-7265-11ef-972a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 136, "chroma:document": "Internal Medicine \n \n 121\u2022 It is a late manifestation which often occurs when the CD4count falls below 200/mm3 \n \nThree main categories seen with HIV \n\u2022 Grade III or IV Immunoblastic lymphoma (60%) \n\u2022 Burkitt\u2019s lymphoma(20%)- associated to EBV \n\u2022 Primary CNS lymphoma \n Treatment \n1. In patients with high  CD4 count \u2013 Intensive Chemotherapy \nIn patients with low Cd4 count \u2013 low dose Chemotherapy  \n2. Palliative measures : to decrease the size of the lesion and associated edema  \n\u2022 Radiotherapy \n\u2022 Glucocorticoides  :  \n \nCervical cancer \n\u2022 There is a five-fold risk of developing cervical c.a. in women with AIDS \n\u2022 Is associated with human papilloma virus infection \n\u2022 Invasive c.a. of the Cervix is an AIDS defining illness. \n\u2022 Abnormal PAP smear is seen in 60%of HIV infected women \n\u2022 Anorectal c.a. may also be seen in homosexual men \nClinical Staging of HIV/AIDS \n There are different types of staging systems.  The most common are: \n\u2022 The WHO clinical staging system  \n\u2022 The CDC staging system \n WHO Clinical Staging System for HIV/AIDS \n\u2022 It is a system designed for estimating the degree of immuno-suppression on clinical \ncriteria \n\u2022 Intended for use in patients known to have HIV (i.e. HIV+ antibody test) \n\u2022 It is widely used in recourse limited settings to make decisions as to when to start \npatients on ART \n\u2022 According to this staging system there are 4 clinical stages"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 137, "chroma:document": "Internal Medicine \n \n 122Table I-5-3. Revised classification system for HIV infection ( CDC Classification) \n \nClinical category \n  \nCD4 category \n \nAsymptomatic /Primary HIV Symptomatic Not A or C conditions  AIDS indicator conditions \n1.  > 500/mm3\n A1 B1 C1 \n2.  200-499 \n/mm3    \n  \nA2 B2 C2 \n3.  < 200 /mm3\n A3 B3 C3 \n \nThe shaded portion indicates the expanded AIDS surveillance case definition. \nComparison: WHO vs. CDC Classification \n\u2022 WHO classification does not require CD4 count and hence is more appropriate to use in \nresource limited settings with high HIV prevalence. \n\u2022 CDC clinical categories more dependent on expensive laboratories and the staging is \nnot adapted to resource poor settings \n \nTable I-5-4. WHO Clinical Staging System for HIV/AIDS \n \n \nStage 1 Asymptomatic \n Stage 2 Minor Symptoms \n Stage 3 Moderate Symptoms \n \nStage 4 AIDS defining illnesses"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 138, "chroma:document": "Internal Medicine \n \n 123Clinical Stage 1 \n\u2022 Asymptomatic  \n\u2022 Persistent generalized lymphadenopathy (PGL)(PGL-is defined as the presence of \nlymph node  > 1cm, in two extra inguinal sites and persisting for more than three \nmonths)  \nClinical Stage 2 s \n\u2022 Unexplained moderate weight loss  ( < 10 % of body weight ) \n\u2022 Recurrent upper respiratory tract infections ( sinusitis , tonsillitis , otitis media , and \npharyngitis ) \n\u2022 Minor mucocutaneous manifestations (seborrheic dermatitis, fungal nail infections, \nrecurrent oral ulcerations, angular chelitis) \n\u2022 Herpes zoster within the past 5 years (single dermatome) \nClinical Stage 3  \n\u2022 Unexplained sever weight loss (>10% of body weight ) \n\u2022 Unexplained chronic diarrhea longer than 1 month \n\u2022 Unexplained prolonged fever > 1 month \n\u2022 Persistent Oral candidiasis (thrush) \n\u2022 Oral hairy leukoplakia  \n\u2022 Pulmonary tuberculosis  \n\u2022 Severe bacterial infection (pneumonia, pyom yositis, empyema, meningitis, bateremia) \n\u2022 Acute necrotizing ulcerative stomatitis, ginigivitis, or periodentitis  \n\u2022 Unexplained anemia (< 8 gm/dl), neutropenia 500/mm3, and or chronic \nthrombocythopenia ( < 50, 000/mm ) \nClinical Stage 4 \n\u2022 HIV wasting syndrome \n\u2022 Pneumocystis carinii pneumonia \n\u2022 CNS toxoplasmosis \n\u2022 Cryptosporidiosis or Isosporosis related  watery diarrhea > 1 month ,  \n\u2022 Extrapulmonary cryptococcosis  \n\u2022 Cytomegalovirus (CMV) disease of an organ other than liver, spleen, or lymph nodes \n(e.g. retinitis)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 138, "chroma:document": "\u2022 CNS toxoplasmosis \n\u2022 Cryptosporidiosis or Isosporosis related  watery diarrhea > 1 month ,  \n\u2022 Extrapulmonary cryptococcosis  \n\u2022 Cytomegalovirus (CMV) disease of an organ other than liver, spleen, or lymph nodes \n(e.g. retinitis) \n\u2022 Chronic Herpes simplex ( HSV) infection \u2013 orolabial, genital anorectal lasting for more \nthan 1 month"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 139, "chroma:document": "Internal Medicine \n \n 124\u2022 Any disseminated endemic mycosis (e.g. histoplasmosis, coccidiodomycosis) \n\u2022 Esohagial Candidiasis ( involving  esophagus, trachea, bronchi or lungs ) \n\u2022 Recurrent Bacterial pneumonia \n\u2022 Recurrent septicemia  \n\u2022 Disseminated atypical mycobacterium \n\u2022 Extrapulmonary tuberculosis \n\u2022 Lymphoma ( cerebral or B- cell Non Hodgkin\u2019s lymphoma ) \n\u2022 Invasive cervical carcinoma \n\u2022 Kaposi\u2019s sarcoma \n\u2022 HIV encephalopathy \n\u2022 Symptomatic HIV associated neuropathy. \n \nAntiretroviral Drugs (ARTs) \nARTs are the corner stone of medical management of HIV infection.  \nClasses of Antiretroviral Drugs \n1) Nucleoside reverse transcriptase inhibitors  ( NRTIs)  \nLamivudine (3TC)   Stavudine ( d4t ) \nZidovudine (AZT     Abacavir ( ABC)  \nDidanosine (DDI )   Zalcitabin ( DDC )  \nEmtricitabine (FTC)   Tenofovir (TDF ),  \nMechanism of Action : Structurally these drugs resemble naturally occurring nucleosides and \nbreak the formation of viral DNA by breaking the chain ( chain breakers ) \nZidovudine (AZT )  \n\u2022 Dosage :300mg PO  BID  \n\u2022 Side effects : Anemia, Myalgias, bone Marrow Suppression  \n Lamivudine (3TC): \n\u2022 Dosing : 150mg BID or 300mg QD \n\u2022 Side effects :Headache , occasional nausea \nStavudine (d4T) \u2022 Dosing : 40 mg BID for weight > 60 kg , 30 mg BID for weight < 60 kg  \n\u2022 Side effects  :Peripheral Neuropathy (5-15%)  ,Lactic acidosis, Pancreatitis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 140, "chroma:document": "Internal Medicine \n \n 125Abacavir (ABC) \n\u2022 Dosing : 1 x 300mg tablet BID \n\u2022 Toxicity:  Allergic reaction (Hypersensitivity reacti on) which occurs within first 6 weeks of \ninitiation of therapy. Never re challenge the patient again with ABC \nTenofevir (TDF ):  is a ctually, a nucleoTIDE  \nDosing:  1 x 300mg tablet QD \nToxicity : Headache, Nausea, Diarrhea, Lactic acidosis \nDidanosine (ddI) \nDosing  \n1 x 400mg enteric coated capsule QD (if <60kg: 250mg QD) \nOr  \n2 x 100mg buffered tab BID or 4 x 100mg QD (if <60kg: 125 mg BID or 250mg QD) \nNOTE : If use buffered tablets, 2 or more tablets must be used at each dose to provide adequate \nbuffer . \nOr   \n250mg of reconstituted buffered powder BID (if <60kg: 167mg BID) \nDidanosine (ddI) (2) \nFood Interactions: take on empty stomach  Toxicity : Peripheral Neuropathy, Nausea, abdominal pain, Pancreatitis, Lactic acidosis \n2) Non-nucleoside reverse transcriptase inhibitors ( NNRTIs)  \n\u2022 Nevirapine (NVP, Nevipan\n\u00ae) \n\u2022 Efavirenz (EFV, Stocrin\u00ae) \n\u2022 Delavirdine (DLV, Rescriptor\u00ae), rarely used  \nMechanism of Action:  inhibit the active site of Reverse transcriptase enzyme  \nNevirapine (NVP, Nevipan\u00ae) \nDosing:  200 mg QD x 2 weeks, then 200 mg BID  \nToxicity : \n\u2022 Skin rash (17%)   may be  \no Milder form (dry rash )  : erythematous, maculopapular rash  \n\u0083 Treatment: continue medication with close observation antihistamins may be \nadministered \no Severe form (wet rash) : with mucous membrane involvement, Steven\u2019s Johnson"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 140, "chroma:document": "o Milder form (dry rash )  : erythematous, maculopapular rash  \n\u0083 Treatment: continue medication with close observation antihistamins may be \nadministered \no Severe form (wet rash) : with mucous membrane involvement, Steven\u2019s Johnson \nSyndrome and Toxic epidermal necrolysis (TEN) \n\u0083 Rx:- Discontinue medication, never re-challenge"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 141, "chroma:document": "Internal Medicine \n \n 126\u2022 Hepatitis : \nEfavirenz (EFV, Stocrin\u00ae) \nDosing : 3 x 200mg capsules or 600mg P.O. /d \nFood Interactions : Take with low-fat meal because high-fat meals increase absorption by 50% \n\u00c6 increases side effects  \nToxicity \n\u2022 CNS Changes  (52%) - Insomnia, nightmares, poor concentration, mood change, dizziness, \ndisequilibrium, depression, psychosis  \n\u2022 Skin Rash  (15-27%)- usually does not require discontinuation \n\u2022 Nausea \nCONTRAINDICATED DURING PREGNANCY  \n3) Protease Inhibitors \nLopinavir + Ritonavir (Kaletra\u00ae)    Nelfinavir (Viracept\u00ae) \nSaquinavir-SGC (Fortovase\u00ae)    Saquinavir-HGC (Invirase\u00ae) Indinavir (Crixivan\u00ae)    Amprenavir (Agenerase\u00ae) Fosamprenavir (Lexiva\u00ae)    Atazanavir (Reyataz\u00ae) \nRitonavir (Norvir\u00ae)   \nMechanism of Action : Inhibit viral assembly by blocking the  \n\u2022 PIs are mainly used as second line drugs in recourse limited settings as these drugs are \nexpensive and most formulations need refrigeration. \nCommon side effects of PIs  \u2022 Glucose intolerance (in some patients may cause Diabetes mellitus ) \n\u2022 Lipid abnormalities :hypertriglyceridemia , low HDL and  high LDL \n\u2022 Lipodystrophy-\u2013 Morphologic Changes ,fat accumulation in the lower part of the body and \natrophy of facial fat   \nGoals of ART: (HAART  = Highly Active Antiretroviral Therapy) \n1) Improve the length and quality of the patient\u2019s life 2) Increase total lymphocyte count (TLC) and CD4 cell count, allowing preservation or \nimprovement of immune function"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 141, "chroma:document": "Goals of ART: (HAART  = Highly Active Antiretroviral Therapy) \n1) Improve the length and quality of the patient\u2019s life 2) Increase total lymphocyte count (TLC) and CD4 cell count, allowing preservation or \nimprovement of immune function \n3) HIV RNA < 400 copies/ml or \u201cundetectable\u201d    within 4-6 months of ART initiation  \n4) Reduce HIV-related morbidity and mortality \n\u0099 Is not a cure for HIV. If treatment is stopped, the virus will continue to replicate  \n\u0099 It cannot eliminate HIV completely from the body."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 142, "chroma:document": "Internal Medicine \n \n 127What does HAART require to be effective ?  \n\u2022 Strict adherence to this regimen \n\u2022 Proper monitoring of side effects and disease progression \n\u2022 Recognition and treatment of co-morbidities \n\u2022 Recognition of drug interactions \nThe Baseline Assessment before initiation of HAART \n\u0099 Baseline medical history \n\u0099 Physical examination \n\u0099 Clinical staging \n\u0099 Laboratory testing \n\u0099 Development of the patient care plan \n \nWHO Criteria to Initiate ART in Adults and adolescents  \n \n \nWHO clinical \nstage  \nCD4 testing not available   \nCD4 testing available \n \n1  \nDon\u2019t treat \n \n2  \nART may be started if TLC is < \n1200/mm3  Start ART only  if CD4 \ncount is < 200/mm3  \n \n3  \nIf symptomatic initiate ART \nirrespective of TLC Start ART if CD4 is< \n350/mm3 and initiate \nbefore CD4 drops \n<200/mm3 \n \n4 Start ART irrespective of TLC Start ART irrespective of \nCD4 count  \n \nNote: ART should be initiated in WHO clinical stage 3 patients with CD4 <350/mm3 if patients \nhave: \no Pulmonary TB \no Sever bacterial infections"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f38-7265-11ef-8d8d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 143, "chroma:document": "Internal Medicine \n \n 128o Oral candidiasis  \nDo not start ARVs if: \n\u2022 The patient is not motivated \n\u2022 Without intensive counseling \n\u2022 If treatment cannot be continued \n\u2022 If asymptomatic and no information about CD4+ count \n\u2022 If the patient has active OI ( first treat the OI which may be an immediate danger to the \nlife of the patient before initiating ART ) \n\u2022 If the patient has serious psychiatric illness and there is no care giver  \n  \nFirst-Line ARV Regimen for Ethiopia  \n  \n \n \n \n   \n \n       \n \nFour combinations can be made from these first line drugs  \n\u2022 AZT/3TC/NVP or \n\u2022 AZT/3TC/NVP or \n\u2022 D4T/3TC/EFV or \n\u2022 D4T/3TC/EFV  \n \nSecond Line drugs for Ethiopia  \nABC or TDF or ZDV (if not taken)/+ Didianosin (ddI) + Kaletra\u00ae LPV/r or SQV/r or NFV          The indications for changing from First line to Second line regime is when there is evidence of \ntreatment failure  Zidovudine \n(AZT ) \nEfavirenze  \n(EFV )Stavudine \n (d4t) Nevirapine  \n( NVP )\nLamivudine \n(3TC)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f39-7265-11ef-887e-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 144, "chroma:document": "Internal Medicine \n \n 129\u2022 Clinical failure \n\u2022 Immunological failure \n\u2022 Virological failure  \n \nReferences :  \n1) Anthony S. Fauci, Harrison\u2019s Principles of Internal Medicine, Volume 1 pages 1076 -\n1139 \n2) WHO case definition of HIV for surveillance and Revised Clinical staging, 2006 \n3) WHO, Antiretroviral therapy for HIV infection for adolescents and adults in resource -\nlimited setting, 2006.  \n4) Hoffman Ch., HIV medicine, 2006. \n5) AIDS in Ethiopia, Federal MOH Ethiopia, June 2006"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f3a-7265-11ef-bb9a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 145, "chroma:document": "Internal Medicine \n \n 1306.  Sexually transmitted Infections \n \nLearning objectives: At the end of this lesson students are expected to  \n1. Define Sexually transmitted diseases ( STDs or STIs )  \n2. Understand the common etiologic agent for STIs 3. Understand the epidemiology of different STIs    \n4. Describe the pathophysiology of common STIS  \n5. Identify the clinical manifestations of different STIs     6. List the complications and Organ systems affected by STIs  7. Describe the most commonly investigations for the diagnosis of STIs   8. Make an appropriate diagnosis of Different STIs   \n9. Understand the syndromic approach for the management of different STIs  \n \nDefinition: \nSexually transmitted diseases (STD\u2019S) are a di verse group of infections, caused by different \ntypes of microbial agents, that are frequently transmitted by sexual contact, and for which \nsexual transmission is epidemio logically important, are considered sexually transmitted \ndiseases. \u201cSexual\u201d includes the full range of he terosexual or homosexual behavior, including \ngenital, oral-genital, oral-anal, and genital-anal contact.  \n\u2022 At present there are more than 20 known causes of STD. No single STD can be \nregarded as an isolated problem because multiple infections are common and because the presence of one STD denotes high-risk sexual behavior that is often \nassociated with other, more serious infection.  \n\u2022 Most STDs are rarely if ever transmitted by fomites, food, flies, or casual contact."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f3b-7265-11ef-a8c3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 145, "chroma:document": "associated with other, more serious infection.  \n\u2022 Most STDs are rarely if ever transmitted by fomites, food, flies, or casual contact.   \n\u2022 At least one sexual partner is always infected; the apparent exceptions usually can \nbe attributed to prolonged sub-clinical infection in one or both partners.  Therefore, \nrisk assessment (including elicitation of a sexual history) and management of sexual partners are of paramount importance. \nEpidemiology of STIs \n\u2022 STIs are major public health problems in all countries, but are especially in developing \ncountries where access to adequate diagnostic and treatment facilities is very limited or \nnonexistent. There is limited information on the incidence and prevalence of STIs is"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f3c-7265-11ef-84e3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 146, "chroma:document": "Internal Medicine \n \n 131Ethiopia. FMOH compiled 58,632 and 27,947cases from all regions in 2002 and 2003 \nrespectively. \n\u2022 A large proportion of STIs are symptomatic  and most symptomatic patients seek \ntreatment from traditional healers , pharmacists , drug vendor shops and market places \n\u2022 STDs can be classified and managed in two different ways ( approaches ) \n1. Etiologic approach  \n\u2022 Advantages:  Accurate diagnosis, accurate treatment, proper use of antibiotics \n(decreases over treatment and antibiotic resistance). It is the better way to diagnose and treat asymptomatic infections  \n\u2022 Disadvantages : Needs lab support and expertise , expensive (cost may be \nincurred due to lab tests ) and it is time consuming \n2. Syndromic approach   \n\u2022 Advantages:   Treatment can be given immediately, mixed infection may exist \nand may be adrsessed, there is no need for laboratory diagnosis and the treatment can be given by middle level health professionals. Hence this approach may be a good alternative for in resource limited settings. \nDisadvantages:  over treatment with antibiotics, there is risk of creating antibiotic \nresistance and decreased compliance. There is also increased cost of drugs. Moreover asymptomatic infection missed. \nN.B \u2013 In general, an overall approach to the management of a patient with sexually \ntransmitted disease begins with \n \nRisk assessment of : \n\u2022 Sexual orientation and practice \n\u2022 Number of recent and current sexual partners \n\u2022 History"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f3d-7265-11ef-8cb1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 146, "chroma:document": "N.B \u2013 In general, an overall approach to the management of a patient with sexually \ntransmitted disease begins with \n \nRisk assessment of : \n\u2022 Sexual orientation and practice \n\u2022 Number of recent and current sexual partners \n\u2022 History\n of STD in the patient  \n\u2022 Recent history  of STD of the partner \n\u2022 Sociodemographic and other markers of high risk   \nClinical assessment : elicitation of information on specific current symptoms and signs of \nSTDs. \n Laboratory tests : If available, confirmatory diagnostic or screening tests may then be ordered."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f3e-7265-11ef-bbe5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 147, "chroma:document": "Internal Medicine \n \n 132Comprehensive Case Management : is vital approach for controlling STIs. So health care \nproviders should undertake the following measures besides treating individual patients   \n1. Partner notification and management  \n2. Condom promotion and supply \n3. Health education and risk reduction counseling  4. Linkage with HIV counseling and testing  5. Follow-up visits for patients with STI \nSTI Syndromes \n\u2022 Urethral discharge Syndrome \n\u2022 Vaginal discharge \n\u2022 Genital ulcer \n\u2022 Inguinal bubo \n\u2022 Scrotal swelling \n\u2022 Lower abdominal pain \n\u2022 Neonatal conjunctivitis \n \n1. Urethral discharge : \nUrethral discharge is the most common presenting compliant of men with STD.  In urethral \ndischarge, exudate is present in the anterior urethra and the discharge is often accompanied \nby dysuria or urethral discomfort. It may lead to epididymitis and complications such as infertility and urethral stricture.  \nEtiology \nFor practical purposes, STD-related urethritis is divided into  \n\u2022 Gonococcal urethritis: caused by  Nisseria gonorrhea \no Has a short incubation period (2-3days \no Vast majority of cases present with abundant and purulent discharge \no Tend to produce more severe urinary tract infection symptoms like \ndysuria, urgency and frequency. \n\u2022 Nongonococcal urethritis (NGU):  usually caused by Chlamydia trachomatis or \nU.urealyticum. \no Has scanty to moderate, white, mucoid or serous discharge. \no Mild urinary tract infection symptoms"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f3f-7265-11ef-80d4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 147, "chroma:document": "dysuria, urgency and frequency. \n\u2022 Nongonococcal urethritis (NGU):  usually caused by Chlamydia trachomatis or \nU.urealyticum. \no Has scanty to moderate, white, mucoid or serous discharge. \no Mild urinary tract infection symptoms \no Has long incubation period (1-3 weeks)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f40-7265-11ef-a10e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 148, "chroma:document": "Internal Medicine \n \n 133The quantity and appearance of the discharge can be used to distinguish accurately gonococcal \nand nongonococcal urethritis in about 75-80% of patients who have not urinated recently.  It can\u2019t, of course, be used to diagnose dual infection with N.gonorrhea and C.trachomatis. Milking \nof the urethra may be necessary to get a good amount of discharge sample. \nLaboratory  \n\u2022 Microscopy of urethral discharge stained with methylene blue or safranin or Gram\u2019s \nstain shows pus cells with characteristic intracellular coffee bean shaped diplococci \n\u00c6 N.gonorrhea. \n\u2022 Pus cells without intracellular diplococci = NGU. \nTreatment: When the accurate etiologic diagnosis is made  \n\u2022 Gonococcal Urethritis :   \nCeftriaxone 250mg IM stat  \nOR  \nCiprofloacin 500mg PO stat  \nOR  \nSpectinomycin 2mg IM stat. \n\u2022 NGU : Doxycycline 100mg PO BID for 7 days or Tetracycline 500mg PO QID for 7 days \nOR Erythromycin 500mg PO QID for 7 days if the patent has contraindication for TTC.. \nWhen there is no Etiologic diagnosis: Treatment should cover both gonococccal and \nchlamydial infections (combine the above treatments)  \n \n2.  Vaginal Discharge:  \n Etiology \n1. N.gonorrhea  \n2. Chlamydia trachomatis  \n3. Trichomonas vaginalis,  \n4. Gardnerella vaginalis  5. Candida albicans 6. Vaginal anaerobes (\u201cbacteria vaginosis\u201d) \n\u2022 The first three are sexually acquired and the last three are endogenous infections. \n\u2022 The first two cause cervicitis while the last four cause vaginitis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f41-7265-11ef-b31c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 149, "chroma:document": "Internal Medicine \n \n 134\u2022 Bacterial vaginosis  (Gardnerella vaginalis) is the leading cause of vaginal discharge \nin Ethiopia followed by Candidiasis, Trichomoniasis, and Gonococcal and Chlamydial \ncervicitis.  \n\u2022 As urethritis in males, co-infection with C.trachomatis is common in women with \ngonorrhea (~ 50%). \nClinical feature: \nMany women have a small amount of vaginal discharge (physiologi c leukorrhea), which is clear \nand odourless. It becomes abnormal if the woman notes a change in  the amount , colour or \nodour of the discharge . In general, most women with this syndrome will complain of: \n\u2022 Excessive secretions and soiling of undergarments  \n\u2022 Changes in colour and/or odour of discharge \n\u2022 Associated itching, dysuria, dysparunia \n\u2022 Redness of vulva \n\u2022 Sometimes may be accompanied by lower abdominal pain \nThe initial assessment of a patient who has vaginal discharge includes risk assessment and clinical evaluation with spec ulum examination to determine the site of infection. \n \nVaginitis : bacterial vaginosis, vaginal candidiasis and /or trichomoniasis are the usual causes \nof vaginitis.  \n\u2022 Bacterial vaginosis and trichomoniasis are more frequent among sexually active women \nwhile vaginal candidiasis occurs when there is impairment of local or systemic defense \nmechanism. \n\u2022 The discharge in bacterial vaginosis is homogenous with a typical fishy odour due to the \npresence of volatile amines and this may e apparent during examination or when the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f42-7265-11ef-a0a9-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 149, "chroma:document": "mechanism. \n\u2022 The discharge in bacterial vaginosis is homogenous with a typical fishy odour due to the \npresence of volatile amines and this may e apparent during examination or when the \ndischarge is mixed with 10 % KOH.  \n\u2022 Trichomonads present with profuse, runny, mal-odorous discharge. Yeasts (Candida) \noften present with white, curd-like discharge and pruritus. \nSpeculum examination : in isolated vaginitis the cervix looks healthy and discharge is not \ncoming from the cervical opening. \nCervicitis:  The presence of purulent exudates from the cervical os indicates infection with \nN.gonorrhea  and C.trachomatis. \nRisk factors for STI related cervicitis in Ethiopia ( one or more of the following ) \n\u2022 Multiple sexual partners in the last 3 months"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f43-7265-11ef-a051-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 150, "chroma:document": "Internal Medicine \n \n 135\u2022 New sexual partners in the last 3 months  \n\u2022 Age less than 25 years  \n\u2022 Having ever traded sex  \nCervicitis is frequently asymptomatic. It may be detected on routine pelvic examination or during \nevaluation of a patient with vaginal discharge  \nComplications of Cervicitis and Vaginitis  \n\u2022 PID \n\u2022 Premature rapture of membrane  \n\u2022 Preterm labour  \n\u2022 Infertility  \n\u2022 Chronic pelvic pain  \nLaboratory:  \nIt is used mainly for the diagnosis of trichom oniasis, bacterial vaginosis and candidiasis \nT.vaginalis : characteristic jerky motility of the parasite with many leukocytes. \nB.vaginosis : \n\u2022 The typical fishy odour will be enhanced by the addition of 1- 2 drops of KOH to the \nspecimen of vaginal discharge (\u201csniff test\u201d) \n\u2022 Number of epithelial cells per microscopic field exceeds the number of leukocytes.  \n\u2022 \u201cClue cells\u201d =cornified squamous epithe lial cells covered by coccobacilli.  \nCandidiasis:  Look for yeast (10% KOH may improve diagnostic sensitivity). \nN.B. In general, Gram stains are not helpful in diagnosing gonorrhea in females (low sensitivity). \nTreatment  \n When accurate Diagnosis is made  \nT.vaginalis  : Metronidazole 2gm PO stat \nB. Vaginosis  \n\u2022 Only symptomatic women need treatment. \n\u2022 Metronidazole 500mg PO BID for 7 days or Metronidazole 2 gm as single dose \nand repeat after 48hr. \n \nVulvovaginal candidiasis \nTopical antifungal agents:  Nystatin 100,000-1,000, 000 IU, intravaginally daily for 14 days."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f44-7265-11ef-b0ba-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 150, "chroma:document": "\u2022 Metronidazole 500mg PO BID for 7 days or Metronidazole 2 gm as single dose \nand repeat after 48hr. \n \nVulvovaginal candidiasis \nTopical antifungal agents:  Nystatin 100,000-1,000, 000 IU, intravaginally daily for 14 days. \n                Miconazole or clotrimazole 200mg intravaginally daily for 3 days                      \nMucopurulent discharge from the cervix  : treat for gonorrhea and chlamydial infection."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f45-7265-11ef-8b15-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 151, "chroma:document": "Internal Medicine \n \n 136When Specific diagnosis could not be made manage as vaginal discharge syndrome \n \n \nRecommended treatment for Vaginal Discharge  \nRisk Assessment Positive  Risk Assessment Negative  \nCiprofloxacin 500 mg PO stat Or \nSpectinomycin 2gm IM stat  \nPlus \nDoxycycline 100 mg PO BID for 7 \ndays  \nPlus \nMetronidazole 500mg Po ID for 7 days  \n Metronidazole 500mg Po ID for 7 \ndays  \nPlus \nClotrimazole vaginal tabs 200mg \nat bed time for 3 days  \n \n3. Genital Ulcer: \nA genital ulcer is a loss of continuity of the skin of the genitalia. Genital ulcers may be painful or painless and are frequently accompanied by inguinal lymphadenopatly. \nCommon Etiology agents: \n\u2022 Treponema pallidum (syphilis) \n\u2022 Haemophilus ducreyi (chancroid) \n\u2022 Calymmatobacterium granulomatis (granuloma inguinale) \n\u2022 C.trachomatis serovar L\n1-L3   (Lymphogranuloma venereum or LGV) \n\u2022 Herpes virus 1 or 2 (Herpes simplex virus or HSV) \nSyphilis  \n\u2022 Genital ulcer occurs in the primary stage of the diseases \n\u2022 It starts as a small popular lesion that rapidly ulcerates to produce a non tender \nindurated lesion with a clean base and raised margins known as chancre \n\u2022 Chancres may appear at any point of contact :genitals, anus, mouth, lips \n\u2022 Heal without treatment in 1 to 6 weeks \n\u2022 Swollen lymph nodes may appear"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f46-7265-11ef-8962-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 152, "chroma:document": "Internal Medicine \n \n 137Complications  \no Secondary syphilis \no Aortitis with valvulitis  \no Neurosyphilis \nGenital Herpes: \n\u2022 HSV virus has two types \no HSV-2 causes dominantly genital disease \no HSV-1 causes dominantly oral disease \n\u2022 Worldwide the most common cause of genital ulcer \n\u2022 Latency and frequent recurrence characterizes genital herpes , producing a lifelong \ninfection /persistent \n\u2022 Herpetic ulcers  \no Are usually painful and multiple \no Starts as clear vesicle and becomes pustule, which later erodes to an ulcer and \nthen crusts \no Heals spontaneously after 2-3 weeks  \no Recurrence possible but milder (number of vesicles are fewer)  \n\u2022 It tends to be aggressive in HIV patients with extensive tissue involvement and chronic \nulceration. It may also be dissemination to CNS, skin etc \nComplications: \no Recurrence  \no Aseptic meningitis and enchephalitis  \nChancroid \n\u2022 Caused by Haemophilus ducreyi   \n\u2022 Is one of the commonest causes of genital ulcer in most developing countries, however it \nwas not found to be a common cause of genital ulcer in Ethiopia. \n\u2022 Incubation period: 3 -15 days \n\u2022 Ulcer on the penile shaft or prepuce  \n\u2022 It is painful progressing from a small papule to pustule and then ulcer with soft margins \ndescribed as soft chancre  , yellow gray exudative covering and erythema \n\u2022 Inguinal adenopathy that becomes necrotic and fluctuant ( bubo ) follows the ulcer within \n1-2 weeks  \nComplication :  penile autoamputaion"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 153, "chroma:document": "Internal Medicine \n \n 138Lymphogranuloma Venereum (LGV) \n\u2022 Caused by L1, L2 and L3 serovars of Chlamydia trachomatis  \n\u2022 There is little evidence on the prevalence of LGV in Ethiopia \n\u2022 Major pathology occurs in the lymphatic system  \n\u2022 Primary stage  is marked by a painless vesiculo-papular ulceration at the site of \ninoculation  \n\u2013 Located in the penis in men  \n\u2013 On the labia and posterior vagina in women. \n\u2022 Primary lesion usually not noticed. \n\u2022 The secondary stage  is described as the inguinal syndrome \no  A painful inguinal lymphadenitis with constitutional symptoms   \no In men infection usually spreads through the lymphatics causing inguinal and \nfemoral lymphadenitis. \no In women upper vaginal and cervical infection results in enlargement of the \nobturator and iliac nodes. (sometimes pelvic nodes) \n\u2022 Inguinal adenopathy is usually unilateral (2/3 of cases) \n\u2022 Nodes initially discreet later becomes fluctuant and suppurative developing multiple \ndraining fistulas \n\u2022 Bubo may be grooved by the inguinal ligament (\"groove sign\" of LGV)  \n\u2022 External genitalia may be oedematous and swollen  \n\u2022 May lead to anatomical distortion and irregularity, particularly of the penis  \n\u2022 Spontaneous healing after several months possible  \nLate complications include  \no Genital elephantiasis  \no Adhesion \no Stricture and fistula of the penis,  urethra and the rectum \n \nGranuloma Inguinale (Donovanosis) \n\u2022 Chronic: progressively destructive bacterial infection of the genital region without"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f48-7265-11ef-8760-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 153, "chroma:document": "o Genital elephantiasis  \no Adhesion \no Stricture and fistula of the penis,  urethra and the rectum \n \nGranuloma Inguinale (Donovanosis) \n\u2022 Chronic: progressively destructive bacterial infection of the genital region without \nsystemic symptoms \n\u2022 Etiology: Calymmatobacterium granulomatis  a gram-negative intra-cellular bacteria \n\u2022 Transmission \u2013sexual and non-sexual contact"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 154, "chroma:document": "Internal Medicine \n \n 139\u2022 Distribution \u2013mainly in Australia, Caribbean, India, and southern Africa. Little information \nabout its prevalence in Ethiopia \nClinical Manifestation \n\u2022 Incubation period \u2013 usually1 to 4 weeks may be as long as a year \n\u2022 The patient usually presents with a non suppur ative genital lesion which develops from a \nsmall firm papule to painless ulcer with a beefy-red appearance and non-purulent base  \n\u2022 Lesion bleeds easily, expand gradually  \n\u2022 Extra inguinal in 6% of cases \n\u2022 50% women have lesion on cervix  \nComplications  \no Genital pseudo-elephantiasis of labia \no Adhesion  \no Urethral , vaginal or rectal stenosis  \nManagement of Genital Ulcer \n1. When specific Etiologic diagnosis is made \nSyphilis: \n\u2022 Benzanthine penicillin 2.4million IU IM stat OR  \n\u2022 Procaine penicillin 1.2milli on IU daily IM for 10 days. \n\u2022 In penicillin allergic patients, doxycycline 100mg PO BID for 15 days or Tetracycline 500mg \nPO QID for 15 days. \nGenital Herpes: \n\u2022 Acyclovir 200 mg 5X per day for 10 days or Acyclovir 400 mg Po TID for 10 days  \nTreatment of chancroid: \n\u2022 Ceftriaxone 250mg 1M stat or \n\u2022 Erythromycin 500mg PO TID for 7 days  \nTreatmen  of LGV: \n\u2022 Doxycycline 100mg PO BID for 14 days or  \n\u2022 Tetracycline 500mg PO QID for 14 days \nTreatment  of Granuloma inguinale  \n\u2022 Cotrimoxazole 02 tab PO BID for 14 days  \n      N.B \u2013 Tetracycline is contraindicated during pregnancy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f4a-7265-11ef-858b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 155, "chroma:document": "Internal Medicine \n \n 1402. When specific Etiologic diagnosis is not made \u2013 Syndromic approach  \nRecommended treatment for non-vesicular genital ulcer \nBenzanthine penicillin 2.4million IU IM stat  \nOr (in penicillin allergic patients) \nDoxycycline 100mg PO BID for 14 days \nPlus  \nCiprofloxacin 500 mg PO for 3 days or \nErythromycin 500mg PO QID for 7 days  \n        Recommended treatment for Vesicular, multiple or recurrent genital ulcer \nAcyclovir 200 mg 5X per day for 10 days or \nAcyclovir 400 mg Po TID for 10 days  \n       Recommended treatment for  \n Recurrent Infection : Acyclovir 400 mg Po TID for 5 days  \n Suppressive therapy : Acyclovir 400 mg PO BID continuously \n \n4. Lower abdominal pain: \nLower abdominal pain in women is associated with pelvic inflammatory disease (PID).PID \ndenotes pelvic infections in women (e.g. salphingitis, endometritis, parametritis, oopheritis) \ncaused by microorganisms which generally ascend from the lower genital tract to invade the \nendometrium, fallopian tubes, ovaries, other adjacent tissues and peritoneum \nEtiology:  \n\u2022 Commonly N.gonorrhea and C.trachomatis which are sexually transmitted  \n\u2022 PID if often polymicrobial and may be associated with Mycoplasma , Bacteriods , \nStreptococcus , E.Coli , H .Influenza which may or may not be sexually transmitted  \nRisk factors : \n\u2022 The occurrence of vaginal discharge may be an antecedent event  \n\u2022 STD \n\u2022 postpartum and postabortal ascending infections \n\u2022 Intra uterine device ( IUD)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f4b-7265-11ef-94a8-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 156, "chroma:document": "Internal Medicine \n \n 141Clinical feature:  \n\u2022 Mild to severe bilateral lower abdominal pain is the most common complaint, which may \nfirst be noticed during or shortly after the menses and which is sometimes associated \nwith fever.  \n\u2022 The presence of vaginal discharge supports the diagnosis of PID and pain during \nintercourse or urination may also be present \nPhysical examination  \n\u2022 Lower abdominal and adenexal tenderness toget her with cervical excitation tenderness \nmay be indicative of PID. \n\u2022 A tender pelvic mass together with fever, nausea or vomiting can also be detected. \n\u2022 Vaginal discharge, genital ulcer, presence of IUD, open cervix (abortion tissue seen or \nfelt) support the diagnosis of PID. \nDiagnosis :  \n\u2022 Is often difficult. Over diagnosis and treatment may be justified in order to prevent \ncomplications. \n\u2022 Rule out other cause of lower abdominal pain in women such as appendicitis , ectopic \npregnancy and Cholecystitis \nLaboratory : Direct wet mount microscopy of a vaginal specimen is necessary.  The presence of \npus cells in numbers exceeding those of epithelial cells suggests infection of the lower genital \ntract. Complications   \n\u2022 Peritonitis and intra-abdominal abscess \n\u2022 Adhesion and Intestinal obstruction  \n\u2022 Ectopic Pregnancy \n\u2022 Infertility  \nTreatment Most patients with mild to moderate PID can be treated as an out patient  \nSome patients need hospital admission: Indications for admission are  \n Uncertain diagnosis  \n Pelvic abscess suspected"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f4c-7265-11ef-b98d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 156, "chroma:document": "\u2022 Ectopic Pregnancy \n\u2022 Infertility  \nTreatment Most patients with mild to moderate PID can be treated as an out patient  \nSome patients need hospital admission: Indications for admission are  \n Uncertain diagnosis  \n Pelvic abscess suspected \n Pregnant patients  \n Co infection with HIV"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f4d-7265-11ef-99ce-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 157, "chroma:document": "Internal Medicine \n \n 142\u2022 As the infection is poly-microbial in nature instead of single, combination of antibiotics \nshould be prescribed. The spectrum of activity of the antimicrobial agents should cover \nthe following organisms: N.gonorrhea, C. trachamatis, aerobic and anaerobic bacteria.  \n\u2022 Antibiotics should be initiated empirically even before the microbiological report is \navailable.   \n \n Recommended treatment for PID \nOut patient   In patient  \nCiprofloxacin 500 mg PO stat \nOr \nSpectinomycin 2gm IM stat  \nPlus \nDoxycycline 100 mg PO BID for 14 days  \nPlus \nMetronidazole 500mg Po ID for 14 \ndays  \n \nAdmit the patient if there is no improvement within 72 hours  Metronidazole 500mg Po ID for 7 days  \nPlus \nClotrimazole vaginal tabs 200mg \nat bed time for 3 days  \n \nNon Specific : Adequate bed rest, analgesic,  \n If there are any obstetric or surgical complications, refer the patient as early as possible. \n5. Inguinal bubo: \n\u2022 Inguinal bubo is an enlargement of the lymph glands in the groin area. \n\u2022 Etiology: The common sexually transmitted pathogen associated with Inguinal bubo \ninclude  \no C.trachomatis serovar L 1-L3   (Lymphogranuloma venereum or LGV) \no Haemophilus ducreyi (chancroid) \no Calymmatobacterium granulomatis (granuloma inguinale) \no Treponema pallidum (syphilis) may sometimes cause inguinal bubo"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f4e-7265-11ef-8d48-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 158, "chroma:document": "Internal Medicine \n \n 143\u2022 Except in case of LGV, a bubo is rarely a sole manifestation of STD and is usually found \ntogether with the etiologically related genital ulcer.  Non-sexually transmitted local or \nsystemic infections can also  cause inguinal lymphadenopathy.  \nClinical feature: \n\u2022 Usually patients complain of unilateral or bilateral painful swelling in the groin, but \nbuboes can be painless. \n\u2022 It is important to ask for any history of associated genital ulcer. \n Treatment: \n \nRecommended treatment for Inguinal Bubo \nCiprofloxacin 500 mg PO BID  for 3 days  \n                                PLUS Doxycycline 100 mg PO BID for 14 days OR Erythromycin 500 mg PO BQID for 14 days   \n \n\u2022 Fluctuant buboes require aspiration through adjacent healthy skin (don\u2019t incise for \ndrainage). \n\u2022 If genital ulcers are present, treat with the etiologically related cause of the ulcer. \n \n6. Scrotal Swelling Syndrome \nThe cause of scrotal swelling depend on the age of the patient \nFor those younger than 35 years  \n\u2022 N.gonorrhoeae \n\u2022 C.tracomatis  \nFor those older than 35 years  \n\u2022 Gram negative organisms \n\u2022 Tuberculosis \n\u2022 Other cause include : Brucellosis , Mumps , Onchocerciasis , Wuchereria \nbuncrofti  \nIt is important to exclude other causes of scrotal swelling which may require urgent surgical \nevaluation and management"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f4f-7265-11ef-ad11-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 159, "chroma:document": "Internal Medicine \n \n 144\u2022 Testicular Torsion  \n\u2022 Trauma   \n\u2022 Incarcerated inguinal hernia  \n \nComplications of Scrotal Swelling: caused by STI include  \n\u2022 Epididymitis \n\u2022 Infertility  \n\u2022 Impotence  \n\u2022 Prostatitis  \nTreatment of Scrotal swelling suspected of STI origin is similar to Urethral discharge. \n \n Recommended treatment for Scrotal swelling  \nCiprofloxacin 500 mg PO stat OR Spectinomycin 2gm IM stat                                  PLUS \nDoxycycline 100 mg PO BID for 7 days OR Tetracycline 500 \nmg PO QID for 7 days  \n \nSupportive Treatment : Analgesia and scrotal support may be indicated if the patient has \nsevere pain   References: \n1. National guideline for Syndromic aproch of Sexualy transmited infections, Federal MOH, \n2005. \n2. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Sexualy \ntransmited diseases, overview, pages 762-774"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f50-7265-11ef-b071-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 160, "chroma:document": "Internal Medicine \n \n 1457. Other Important Infectious Diseases  \n \n7.1. Tetanus \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define tetanus  \n2. Classify tetanus \n3. Mention the etiology of tetanus 4. Describe the mode of transmission of tetanus 5. Explain the epidemiology of tetanus 6. Describe the pathophysiology of tetanus \n7. Identify the clinical manifestations of tetanus \n8. Describe the most commonly used method for the diagnosis of tetanus 9. Make a diagnosis of tetanus 10. Refer cases of tetanus to hospitals for better care and close follow up \n11. Design appropriate methods of prevention for tetanus  \n \nDefinitions \nTetanus is a neurologic disease characterized by increased muscle tone and spasms caused by \ntoxin released from the bacteria Clostridium tetani.  \n \nEtiologic Agent \n\u2022 Clostridium tetani  is an anaerobic, motile Gram-positive rod that forms an oval, colorless, \nterminal spore, which looks like a tennis racket or a drumstick.  It is found worldwide in soil. \n\u2022 Spores may survive for years in  soil.  They are also resistant to different disinfectant and \neven to boiling for less than 20 minutes. \n \nEpidemiology \n\u2022 Tetanus occurs sporadically and almost always affects non-immunized persons.  \nPartially immunized persons or fully immunized individuals who fail to maintain adequate immunity are also affected. \n\u2022 Tetanus is more prevalent in developing countries like India, Bangladesh, Pakistan,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f51-7265-11ef-b714-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 160, "chroma:document": "Partially immunized persons or fully immunized individuals who fail to maintain adequate immunity are also affected. \n\u2022 Tetanus is more prevalent in developing countries like India, Bangladesh, Pakistan, \neastern Mediterranean, South America and Africa including Ethiopia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f52-7265-11ef-a2d6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 161, "chroma:document": "Internal Medicine \n \n 146\u2022 Tetanus is more common in rural areas where there is frequent contact with soil.  It also \noccurs more frequently in warmer climates, during summer months and in males.  \nNeonates and young children are affected more in developing countries where immunization programs are not comprehensive.  Development of severe illness is seen more in the elderly.  Most cases of tetanus follow injuries especially during farming, gardening or other outdoor activities.  Tetanus may also be associated with surgery, \notitis media, abortion or delivery. \n \nPathogenesis  \n\u2022 Although C. tetani frequently contaminates wounds, germination and toxin production, \nhowever, takes place in wounds with necrotic tissue, foreign bodies or infection that is active. Often the wound is trivial or could seem to be healed from outside. \n\u2022 Tetanospasmin, a toxin produced by the bacteria in the wound binds to peripheral motor \nneuron terminals, enters the axon and is taken to spinal cord and brainstem by \nretrograde transport.  The toxin then inhibits release of inhibitory neurotransmitter and \u03b3-\naminobutyric acid (GABA) with diminished inhibition, there will be increased excitation \nspasm and rigidity.  Tetanospasmin may also block neurotransmitter release at the \nneuromuscular junction and produce weakne ss or paralysis.  Generalized tetanus \noccurs when toxin enters into blood stream and lymphatic to affect distant nerve \nendings. \n  Clinical Manifestations"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f53-7265-11ef-afa9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 161, "chroma:document": "neuromuscular junction and produce weakne ss or paralysis.  Generalized tetanus \noccurs when toxin enters into blood stream and lymphatic to affect distant nerve \nendings. \n  Clinical Manifestations \n\u2022 The incubation period  (time between the injury and first symptom) of tetanus is about 7 \n\u2013 10 days but it may range from 1 day to 2 months.  \n\u2022 The period of onset  (time between the first symptom and spasm) ranges 1 \u2013 7 days.  \nThe shorter the incubation period and period of onset, the more severe the disease becomes. There are different forms of tetanus: neonatal, generalized and localized tetanus.  The most common form is generalized tetanus.  \n \nGeneralized Tetanus  \n\u2022 The median time of onset after injury is seven days; but could occur as early as with in \nthree days. Usually the fist symptom is increased tone in the masseter muscle (trismus, or lockjaw) and patient is unable to open his mouth."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f54-7265-11ef-9d50-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 162, "chroma:document": "Internal Medicine \n \n 147\u2022 Immediately after this the patient develops dysphagia, stiffness in the neck and back. \n\u2022 Then the patient develops contraction of facial muscles to produce rhesus sardonicus  \n(sneer or grimace). \n\u2022 There may be arched back (opisthotonos), generalized muscle spasm triggered by \nstimulus such as light or noise.   \n\u2022 Deep tendon reflexes may be exaggerated.   \n\u2022 There may be dysphagia or paralytic ileus. \nLocalized tetanus:  is a rare form of tetanus.  \n\u2022 It presents with rigidity and spasm around the portal of entry.  \n\u2022 While most localized tetanus have good prognosis, cephalic tetanus has high mortality. It \ncomes after head injury, injury to the face or ear infection. \nPatients may come with wide ranges of wound severity, although most have trivial or healed \nwound. In fact 15% \u2013 20 % of patients may not give history of injury. Neonatal tetanus :  \n\u2022 Occurs in neonates of non-immunized mother and those delivered in unhygienic \ncondition. \n\u2022 It is a very severe form of tetanus with more than 90% mortality. \n\u2022 Neonates should be referred urgently to a near-by hospital if there is suspicion of clinical \ntetanus. \nTetanus may be graded according to severity. Grading is helpful in prognosis and \nmanagement . \n\u2022 Grade I (mild) : moderate trismus, generalized spasticity \n\u2022 Grade II (moderate)  : Moderate trismus, mild to moderate but short lasting spasms, \ntachypnea \u2013 RR 30-35/min and mild dysphagia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f55-7265-11ef-8c09-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 162, "chroma:document": "management . \n\u2022 Grade I (mild) : moderate trismus, generalized spasticity \n\u2022 Grade II (moderate)  : Moderate trismus, mild to moderate but short lasting spasms, \ntachypnea \u2013 RR 30-35/min and mild dysphagia  \n\u2022 Grade III (severe)  : Severe trismus, generalized spasticity, prolonged spasms, \nrespiratory embarrassment RR >40/min, apnoeic spells, tachycardia >120/min and \nsevere dysphagia \n\u2022 Grade IV (very severe)  : Features of grade III plus severe autonomic disturbance of \nCVS. It includes episodes of hypertension and tachycardia alternating with relative hypotension and bradycardia or severe persistent hypertension (DBP >110 mmHg) or \nsevere persistent hypotension (SBP <90mmHg)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f56-7265-11ef-a2e6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 163, "chroma:document": "Internal Medicine \n \n 148Poor prognostic factors in Tetanus : \n\u2022 Patients with higher grades \n\u2022 Short incubation period and period of onset \n\u2022 Cephalic tetanus and  \n\u2022 Patients with comorbidities have poor prognosis.     \nDiagnosis \nThe diagnosis of tetanus rests entirely on clinical grounds.  But wounds should be cultured for \nC.tetani or superinfection. CSF analysis is normal. \nTreatment \nThe goals of treatment are  \n\u2022 To eliminate source of toxin \n\u2022 Neutralize unbound toxin and  \n\u2022 Prevent muscle spasm. \nGeneral measures :  \n\u2022 Patients should be admitted to a quiet room in an ICU, where frequent monitoring is \npossible.   \n\u2022 If there are wounds, they should be explored and cleaned. \n\u2022 Respiratory care:   Intubation and tracheostomy may be required and should be done \nas early as possible if indicated.  Thes e procedures are required for hypoventilation \ncaused by laryngospasm or over sedation or to avoid aspiration. \n\u2022 Autonomic dysfunction : No definitive treatment has so far been outlined.  But \nhypotension requires fluid expansion and vasopressor agents. \n\u2022 Other measures:   hydration should be maintained.  Naso-gastric tube can be inserted \nfor nutrition.  Physiotherapy should be instituted as soon as possible to avoid \ncontracture.  Input and output should be monitored.  Bedsores and other infections \nshould be prevented.  Recovering patients should start active immunization against tetanus. \nSpecific Treatment ;"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f57-7265-11ef-9161-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 163, "chroma:document": "contracture.  Input and output should be monitored.  Bedsores and other infections \nshould be prevented.  Recovering patients should start active immunization against tetanus. \nSpecific Treatment ; \nAntibiotic treatment : This helps to eradicate the vegetative bacteria, not the toxin.  \n\u2022 Crystalline penicillin 3 million units IV 6X a day for 10 days is used but metronidazole \n500mg every 6 hrs or 1g every 12 hours can also be used.  Erythromycin and \nclindamycin are alternatives in patients allergic to penicillins. \nAntitoxin:  - This neutralizes only circulating toxins which are not bound."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f58-7265-11ef-99c3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 164, "chroma:document": "Internal Medicine \n \n 149\u2022 Human tetanus immune globulin (TIG) is the choice and if available should be given \nearly.  \n\u2022 But tetanus antitoxin (TAT), which is available in our setup, can be given in doses of \n10,000 IU intravenous and 10,000 IU intra-muscular. \nControl of muscle spasms :  \n\u2022 Diazepam and Chlorpromazine are given 6 hourly, alternatively.   \n\u2022 If spasms are not controlled by the above medication, neuromuscular blockers and \nmechanical ventilation can be used. \n \n \nReferences: \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Tetanus,  pages 840-841"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f59-7265-11ef-8223-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 165, "chroma:document": "Internal Medicine \n \n 1507.2. Rabies \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define rabies  2. Mention the etiology of rabies 3. Describe the mode of transmission of rabies \n4. Explain the epidemiology of rabies  \n5. Describe the pathophysiology of rabies  6. Identify the clinical manifestations of rabies 7. Describe the most commonly used method for the diagnosis of rabies  8. Make a diagnosis of rabies  \n9. Refer people who were bitten by rabied animals to hospitals for post exposure \nprophylaxis \n10. Design appropriate methods of prevention and control of rabies \n \nDefinition:  Rabies in an acute central nervous system  disease that is caused by rabies virus, \nan RNA virus, which is transmitted by infected secretions. Etiology : - The rabies virus is a single stranded RNA virus which belongs to the rhabdovirus \nfamily. \n Epidemiology:   \n\u2022 Rabies is found in animals in most regions of the world.  Source of infection could be \ndomestic or wild animals.  \n\u2022 Human infection occurs through contact with un-immunized domestic animals or \nexposure to wild animals in the periphery. Humans are occasionally infected by wild \nanimals like foxes and bats, but domestic dogs are responsible for more than 90% of \nhuman cases worldwide. \n\u2022 The incubation period of rabies is very variable, which ranges from as early as 7 days to \nas late as more than one year, but the mean incubation period is 1 to 2 months."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f5a-7265-11ef-bf57-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 165, "chroma:document": "human cases worldwide. \n\u2022 The incubation period of rabies is very variable, which ranges from as early as 7 days to \nas late as more than one year, but the mean incubation period is 1 to 2 months. \n \nPathogenesis:   Rabies virus enters the body through skin or mucous membrane.  There is \ninitial replication of virus at the muscles around port of entry.  The virus then ascends to the \nCNS through the neuromuscular junction.  Once in the CNS, the virus replicates in the gray"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f5b-7265-11ef-9daf-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 166, "chroma:document": "Internal Medicine \n \n 151matters.  The virus then passes to other organs like kidneys, salivary glands, heart, and skin, \nfollowing the autonomic nervous system. Passage of the virus into salivary gland facilitates further transmission. \n \nClinical manifestations:   \nClinical manifestations can be divided into four stages. \n\u2022 Prodromal stage:  usually it lasts less than 4 days; it is manifested by fever, headache, \nmalaise, and anorexia and vomiting.  \n\u2022 Encephalitis phase:  starts with excitation and agitation but later there will be confusion, \nhallucination, aggressive behavior, muscle spasms, meningismus, opisthotonus, seizure and focal paralysis.  Patients may have fever, irregular pupils, salivation, perspiration and postural hypotension. \n\u2022 Brainstem dysfunction:  begins soon after the encephalitis phase.  There will be \nmultiple cranial nerve deficits. Excessive salivation and inability to swallow results drooling of saliva.  Hydrophobia is seen in about 50% of cases. \n\u2022 Death:  Patients rapidly develop coma and death is usually caused due to respiratory \nfailure (by apnea).  \n \nLaboratory Findings:   Early in the course, routine investigations are normal.  Later the white \ncell count is usually moderately elevated, but it may as well be normal. \nHowever, the diagnosis of rabies rests on identification of the virus or serologic tests. \nTreatment \nOnce clinical disease appears, mortality is almost 100%. So far only 6 cases have recovered"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f5c-7265-11ef-ba45-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 166, "chroma:document": "However, the diagnosis of rabies rests on identification of the virus or serologic tests. \nTreatment \nOnce clinical disease appears, mortality is almost 100%. So far only 6 cases have recovered \nfrom disease in the world. Therefore anyone with history of domestic or wild animal bite should \nbe taken seriously.   \nPost exposure prophylaxis:  should be considered in people who had physical contact with \nsaliva or secretions of infected animals or bitten by unprovoked animal e.g. a dog may likely have rabies.  Post exposure pr ophylaxis of rabies includes: \n\u2022 Rigorous cleansing and treatment of the wound  \n\u2022 Administration of rabies vaccine together with anti-rabies immunoglobulin.   \n\u2022 As the incubation period of rabies is variable, post exposure prophylaxis should be \ninitiated as long as there is no clinical evidence of rabies."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f5d-7265-11ef-9878-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 167, "chroma:document": "Internal Medicine \n \n 152Pre-exposure Prophylaxis:  people who are at risk of contact with rabies like veterinarians, \nlaboratory workers and animal handlers should receive pre exposure prophylaxis. \n \nReference \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Rabis \nvirus,  pages 1155-1160"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f5e-7265-11ef-9753-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 168, "chroma:document": "Internal Medicine \n \n 1537.3. Anthrax \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define anthrax  2. Classify anthrax 3. Mention the etiology of anthrax \n4. Describe the mode of transmission of anthrax  \n5. Explain the epidemiology of anthrax  6. Describe the pathophysiology of anthrax   7. Identify the clinical manifestations of anthrax  8. Describe the most commonly used tests for the diagnosis of anthrax  \n9. Make a diagnosis of anthrax  \n10. Treat anthrax at the primary care level \n11. Design appropriate methods of prevention and control of anthrax   \n Definition:  anthrax is an infection that is caused by Bacillus anthracis. It mainly affects \nherbivorous animals but humans are infected by contact with the causative agent from infected \nanimals, by contact, ingestion or inhalation. \nEtiology:  Bacillus anthracis  is a large, aerobic, spore-forming, gram-positive rod, which is \nencapsulated and non-motile. Epidemiology:  Anthrax is more common in herbivorous animals like cattle, sheep and goats.  \nThey are infected while grazing on contaminated grass.  Humans may acquire anthrax from agricultural sites through contact with animals like butchering and feeding or industrial sites through exposure to contaminated hides, wool or bones. \nPathogenesis:    \n\u2022 Cutaneous anthrax is initiated when spores of B. anthracis  are introduced through \nabrasions of the skin or insect bite."}


