Pathoma 2019 pdf free download

Pathoma 2019 pdf free download

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About Pathoma Pdf Free Download Pathoma is a complete medical video tutorial that teaches you how to recognize diseases and not just memorize them. It provides a quick and 10/11/ · Widely acclaimed Pathology book called Fundamentals of Pathology – Pathoma is now available here and just as promised, for free. Just Follow this page to the bottom to Fundamentals Of Pathology Pathoma pdf Free Download Talk to an Admission Officer Fundamentals of Pathology is a unique page text that combine Dr. Husain A. Sattar’s 03/02/ · Pathoma pdf free download, of Pathology Pathoma PDF ebook file for the version. Click the download button to start downloading. Dummies 1st Edition PDF Free 03/01/ · Download Pathoma Fundamentals of Pathology Pdf k Views Download Pathoma Fundamentals of Pathology Direct Link Pdf Fundamentals of Pathology ... read more

Dying cell shrinks, leading cytoplasm to become more eosinophilic pink, Fig. Nucleus condenses and fragments in an organized manner. Apoptotic bodies fall from the cell and are removed by macrophages; apoptosis is not followed by inflammation. Apoptosis is mediated by caspases that activate proteases and endonucleases. Proteases break down the cytoskeleton. Endonucleases break down DNA. Caspases are activated by multiple pathways. Intrinsic mitochondrial pathway i. Cellular injury, DNA damage, or decreased hormonal stimulation leads to inactivation of Bcl2. Lack of Bcl2 allows cytochrome c to leak from the inner mitochondrial matrix into the cytoplasm and activate caspases. Courtesy of humpath. Extrinsic receptor-ligand pathway i. FAS ligand binds FAS death receptor CD95 on the target cell, activating caspases e. Tumor necrosis factor TNF binds TNF receptor on the target cell, activating caspases. FREE RADICAL INJURY I. Free radicals are chemical species with an unpaired electron in their outer orbit.

Physiologic generation of free radicals occurs during oxidative phosphorylation. Cytochrome c oxidase complex IV transfers electrons to oxygen. Pathologic generation of free radicals arises with 1. Ionizing radiation - water hydrolyzed to hydroxyl free radical 2. Inflammation - NADPH oxidase generates superoxide ions during oxygen- dependent killing by neutrophils. Metals e. Drugs and chemicals - P system of liver metabolizes drugs e. Free radicals cause cellular injury via peroxidation of lipids and oxidation of DNA and proteins; DNA damage is implicated in aging and oncogenesis. Elimination of free radicals occurs via multiple mechanisms. Antioxidants e.

Metal carrier proteins e. EXAMPLES OF FREE RADICAL INJURY A. Carbon tetrachloride CCl4 1. Organic solvent used in the dry cleaning industry 2. Converted to CCl3 free radical by P system of hepatocytes 3. Results in cell injury with swelling of RER; consequently, ribosomes detach, impairing protein synthesis. Decreased apolipoproteins lead to fatty change in the liver Fig. Reperfusion injury 1. Return of blood to ischemic tissue results in production of O2 -derived free radicals, which further damage tissue. Leads to a continued rise in cardiac enzymes e. Amyloid is a misfolded protein that deposits in the extracellular space, thereby damaging tissues. Multiple proteins can deposit as amyloid. Shared features include 1. ОІ- pleated sheet configuration 2. Congo red staining and apple-green birefringence when viewed microscopically under polarized light Fig.

Deposition can be systemic or localized. Amyloid deposition in multiple organs; divided into primary and secondary amyloidosis B. Primary amyloidosis is systemic deposition of AL amyloid, which is derived from immunoglobulin light chain. Associated with plasma cell dyscrasias e. Secondary amyloidosis is systemic deposition of AA amyloid, which is derived from serum amyloid-associated protein SAA. SAA is an acute phase reactant that is increased in chronic inflammatory states, malignancy, and Familial Mediterranean fever FMF. FMF is due to a dysfunction of neutrophils autosomal recessive and occurs in persons of Mediterranean origin.

Presents with episodes of fever and acute serosal inflammation can mimic appendicitis, arthritis, or myocardial infarction ii. High SAA during attacks deposits as AA amyloid in tissues. Clinical findings of systemic amyloidosis are diverse since almost any tissue can be involved. Classic findings include 1. Nephrotic syndrome; kidney is the most common organ involved. Restrictive cardiomyopathy or arrhythmia 3. Tongue enlargement, malabsorption, and hepatosplenomegaly E. Diagnosis requires tissue biopsy. Abdominal fat pad and rectum are easily accessible biopsy targets. Damaged organs must be transplanted.

Amyloid cannot be removed. Amyloid deposition usually localized to a single organ. Senile cardiac amyloidosis 1. Non-mutated serum transthyretin deposits in the heart. A, Congo red. B, Apple-green birefringence. Mutated serum transthyretin deposits in the heart leading to restrictive cardiomyopathy. Non-insulin-dependent diabetes mellitus type II 1. Amylin derived from insulin deposits in the islets of the pancreas. Alzheimer disease 1. AОІ amyloid derived from ОІ-amyloid precursor protein deposits in the brain forming amyloid plaques. Gene for ОІ-APP is present on chromosome Most individuals with Down syndrome trisomy 21 develop Alzheimer disease by the age of 40 early-onset. Dialysis-associated amyloidosis 1. ОІ2-microglobulin deposits in joints. Medullary carcinoma of the thyroid 1. Calcitonin produced by tumor cells deposits within the tumor 'tumor cells in an amyloid background'. I REMINDER Thank you for choosing Pathoma for your studies.

We strive to provide the highest quality educational materials while keeping affordability in mind. A tremendous amount of time and effort has gone into developing these materials, so we appreciate your legitimate use of this program. It speaks to your integrity as a future physician and the high ethical standards that we all set forth for ourselves when taking the Hippocratic oath. Unauthorized use of Patho ma materials is contrary to the ethical standards of a training physician and is a violation of copyright. Pathoma videos are updated on a regular basis and the most current version, as well as a complete list of errata, can be accessed through your account at Pathoma. Sincerely, Dr. Allows inflammatory cells, plasma proteins e.

Characterized by the presence of edema and neutrophils in tissue Fig. Arises in response to infection to eliminate pathogen or tissue necrosis to clear necrotic debris C. Toll-like receptors TLRs 1. Present on cells of the innate immune system e. Activated by pathogen-associated molecular patterns PAMPs that are commonly shared by microbes i. CD14 a co-receptor for TLR4 on macrophages recognizes lipopoly- saccharide a PAMP on the outer membrane of gram-negative bacteria. TLR activation results in upregulation of NF-ОєB, a nuclear transcription factor that activates immune response genes leading toproduction of multiple immune mediators.

TLRs are also present on cells of adaptive immunity e. Arachidonic acid AA metabolites 1. AA is released from the phospholipid cell membrane by phospholipase A2 and then acted upon by cyclooxygenase or 5-lipoxygenase. Cyclooxygenase produces prostaglandins PG. PGI 2, PGD 2, and PGE2 mediate vasodilation and increased vascular permeability. PGE2 also mediates pain and fever. LTB 4 attracts and activates neutrophils. LTC 4, LTD 4, and LTE 4 slow reacting substances of anaphylaxis mediate vasoconstriction, bronchospasm, and increased vascular permeability. Mast cells 1. Widely distributed throughout connective tissue 2. Activated by 1 tissue trauma, 2 complement proteins C3a and C5a, or 3 cross-linking of cell-surface IgE by antigen pathoma.

mediate vasodilation of arterioles and increased vascular permeability. Delayed response involves production of arachidonic acid metabolites, particularly leukotrienes. Complement 1. Proinflammatory serum proteins that "complement" inflammation 2. Circulate as inactive precursors; activation occurs via i. Classical pathway - C1 binds IgG or IgM that is bound to antigen. Alternative pathway - Microbial products directly activate complement. Mannose-binding lectin MBL pathway - MBL binds to mannose on microorganisms and activates complement. C5b complexes with C6-C9 to form the membrane attack complex MAC. C3a and C5a anaphylatoxins - trigger mast cell degranulation, resulting in histamine-mediated vasodilation and increased vascular permeability ii. C5a - chemotactic for neutrophils iii.

C3b - opsonin for phagocytosis iv. MAC - lyses microbes by creating a hole in the cell membrane E. Hageman factor Factor XII 1. Inactive proinflammatory protein produced in liver 2. Activated upon exposure to subendothelial or tissue collagen; in turn, activates i. Coagulation and fibrinolytic systems ii. Complement iii. Kinin system - Kinin cleaves high-molecular-weight kininogen HMWK to bradykinin, which mediates vasodilation and increased vascular permeability similar to histamine , as well as pain. Redness rubor and warmth calor 1. Due to vasodilation, which results in increased blood flow 2. Occurs via relaxation of arteriolar smooth muscle; key mediators are histamine, prostaglandins, and bradykinin. Swelling tumor 1. Due to leakage of fluid from postcapillary venules into the interstitial space exudate 2. Key mediators are 1 histamine, which causes endothelial cell contraction and 2 tissue damage, resulting in endothelial cell disruption.

Pain dolor 1. Bradykinin and PGE2 sensitize sensory nerve endings. •y v - t Fig. A, Acute inflammation with neutrophils. B, Chronic inflammation with lymphocytes and plasma cells. Inflammation, Inflammatory Disorders, and Wound Healing 13 D. Fever 1. Pyrogens e. Increased PGE2 raises temperature set point. Step 1 - Margination 1. Vasodilation slows blood flow in postcapillary venules. Cells marginate from center of flow to the periphery. Step 2 - Rolling 1. Selectin "speed bumps" are upregulated on endothelial cells. P-selectin release from Weibel-Palade bodies is mediated by histamine. E-selectin is induced by TNF and IL Selectins bind sialyl Lewis X on leukocytes. Interaction results in rolling of leukocytes along vessel wall. Step 3 - Adhesion 1. Cellular adhesion molecules ICAM and VCAM are upregulated on endothelium by TNF and IL Integrins are upregulated on leukocytes by C5a and LTB4• 3.

Interaction between CAMs and integrins results in firm adhesion of leukocytes to the vessel wall. Leukocyte adhesion deficiency is most commonly due to an autosomal recessive defect of integrins CD18 subunit. Clinical features include delayed separation of the umbilical cord, increased circulating neutrophils due to impaired adhesion of marginated pool of leukocytes , and recurrent bacterial infections that lack pus formation. Step 4 - Transmigration and Chemotaxis 1. Leukocytes transmigrate across the endothelium of postcapillary venules and move toward chemical attractants chemotaxis. Neutrophils are attracted by bacterial products, IL-8, C5a, and LTB4. Step 5 - Phagocytosis 1. Consumption of pathogens or necrotic tissue; phagocytosis is enhanced by opsonins IgG and C3b.

Pseudopods extend from leukocytes to form phagosomes, which are internalized and merge with lysosomes to produce phagolysosomes. Chediak-Higashi syndrome is a protein trafficking defect autosomal recessive characterized by impaired phagolysosome formation. Clinical features include i. Increased risk of pyogenic infections ii. Neutropenia due to intramedullary death of neutrophils iii. Giant granules in leukocytes due to fusion of granules arising from the Golgi apparatus iv. Defective primary hemostasis due to abnormal dense granules in platelets v. Albinism vi.

Peripheral neuropathy F. Step 6 - Destruction of phagocytosed material 1. O2-dependent killing is the most effective mechanism. HOCl generated by oxidative burst in phagolysosomes destroys phagocytosed microbes. H2O2 is converted to HOCl bleach by myeloperoxidase MPO. Chronic granulomatous disease CGD is characterized by poor O2-dependent killing. Due to NADPH oxidase defect X-linked or autosomal recessive ii. Leads to recurrent infection and granuloma formation with catalase-positive organisms, particularly Staphylococcus aureus, Pseudomonas cepacia, Serratia marcescens, Nocardia, and Aspergillus iii. Nitroblue tetrazolium test is used to screen for CGD. MPO deficiency results in defective conversion of H2O2 to HOCl. Increased risk for Candida infections; however, most patients are asymptomatic.

NBT is normal; respiratory burst O2 to H2O2 is intact. O2-independent killing is less effective than O2 -dependent killing and occurs via enzymes present in leukocyte secondary granules e. Step 7 - Resolution 1. Neutrophils undergo apoptosis and disappear within 24 hours after resolution of the inflammatory stimulus. Macrophages predominate after neutrophils and peak days after inflammation begins. Derived from monocytes in blood B. Arrive in tissue via the margination, rolling, adhesion, and transmigration sequence C. Ingest organisms via phagocytosis augmented by opsonins and destroy phagocytosed material using enzymes e.

Manage the next step of the inflammatory process. Outcomes include 1. Resolution and healing - Anti-inflammatory cytokines e. Continued acute inflammation - marked by persistent pus formation; IL-8 from macrophages recruits additional neutrophils. Abscess - acute inflammation surrounded by fibrosis; macrophages mediate fibrosis via fibrogenic growth factors and cytokines. Characterized by the presence of lymphocytes and plasma cells in tissue Fig. Delayed response, but more specific adaptive immunity than acute inflammation C. Stimuli include 1 persistent infection most common cause ; 2 infection with viruses, mycobacteria, parasites, and fungi; 3 autoimmune disease; 4 foreign material; and 5 some cancers.

Produced in bone marrow as progenitor T cells B. T cells use TCR complex TCR and CD3 for antigen surveillance. Inflammation, Inflammatory Disorders, and Wound Healing 15 2. TCR complex recognizes antigen presented on MHC molecules. Extracellular antigen e. TH1 subset secretes IFN-Оі activates macrophage, promotes B-cell class switching from IgM to IgG, promotes TH1phenotype and inhibits TH2 phenotype. T H 2 subset secretes IL-4 facilitates B-cell class switching to IgE , IL-5 eosinophil chemotaxis and activation, and class switching to IgA , and IL function similar to IL Intracellular antigen derived from proteins in the cytoplasm is processed and presented on MHC class I, which is expressed by all nucleated cells and platelets.

Cytotoxic T cells are activated for killing. Killing occurs via i. Secretion of perforin and granzyme; perforin creates pores that allow granzyme to enter the target cell, activating apoptosis. Expression of FasL, which binds Fas on target cells, activating apoptosis III. Immature B cells are produced in the bone marrow and undergo immunoglobulin rearrangements to become naГЇve B cells that express surface IgM and IgD. B-cell activation occurs via 1. Antigen binding by surface IgM or IgD; results in maturation to IgM- or IgD- secreting plasma cells 2. CD40 receptor on B cell binds CD40L on helper T cell, providing 2nd activation signal. Helper T cell then secretes IL-4 and IL-5 mediate B-cell isotype switching, hypermutation, and maturation to plasma cells.

Subtype of chronic inflammation B. Characterized by granuloma, which is a collection of epithelioid histiocytes macrophages with abundant pink cytoplasm , usually surrounded by giant cells and a rim of lymphocytes C. Divided into noncaseating and caseating subtypes 1. Noncaseating granulomas lack central necrosis Fig. Common etiologies include reaction to foreign material, sarcoidosis, beryllium exposure, Crohn disease, and cat scratch disease. Caseating granulomas exhibit central necrosis and are characteristic of tuberculosis and fungal infections Fig. TH1cells secrete IFN-Оі, which converts macrophages to epithelioid histiocytes and giant cells. DIGEORGE SYNDROME A. Developmental failure of the third and fourth pharyngeal pouches 1.

Due to 22q11 microdeletion B. Presents with T-cell deficiency lack of thymus ; hypocalcemia lack of parathyroids ; and abnormalities of heart, great vessels, and face II. Defective cell-mediated and humoral immunity B. Etiologies include 1. Cytokine receptor defects - Cytokine signaling is necessary for proliferation and maturation of B and T cells. Adenosine deaminase ADA deficiency - ADA is necessary to deaminate adenosine and deoxyadenosine for excretion as waste products; buildup of adenosine and deoxyadenosine is toxic to lymphocytes. Characterized by susceptibility to fungal, viral, bacterial, and protozoal infections, including opportunistic infections and live vaccines D.

Treatment is sterile isolation 'bubble baby' and stem cell transplantation. Complete lack of immunoglobulin due to disordered B-cell maturation 1. Pre- and pro-B cells cannot mature. Due to mutated Bruton tyrosine kinase; X-linked C. Presents after 6 months of life with recurrent bacterial, enterovirus e. Live vaccines e. Low immunoglobulin due to B-cell or helper T-cell defects Fig. A, Noncaseating. B, Caseating. Increased risk for bacterial, enterovirus, and Giardia lamblia infections, usually in late childhood C. Increased risk for autoimmune disease and lymphoma V. Low serum and mucosal IgA; most common immunoglobulin deficiency B. Increased risk for mucosal infection, especially viral; however, most patients are asymptomatic.

HYPER-IgM SYNDROME A. Characterized by elevated IgM B. Due to mutated CD40L on helper T cells or CD40 receptor on B cells 1. Second signal cannot be delivered to helper T cells during B-cell activation. Consequently, cytokines necessary for immunoglobulin class switching are not produced. Low IgA, IgG, and IgE result in recurrent pyogenic infections due to poor opsonization , especially at mucosal sites. WISKOTT-ALDRICH SYNDROME A. Characterized by thrombocytopenia, eczema, and recurrent infections defective humoral and cellular immunity ; bleeding is a major cause of death B. Due to mutation in the WASP gene; X-linked VIII. C5-C9 deficiencies-increased risk for Neisseria infection N gonorrhoeae and N meningitidis B. Cl inhibitor deficiency-results in hereditary angioedema, which is characterized by edema of the skin especially periorbital, Fig.

Characterized by immune-mediated damage of self tissues 1. Involves loss of self-tolerance 1. Self-reactive lymphocytes are regularly generated but develop central thymus and bone marrow or peripheral tolerance. Central tolerance in thymus leads to T-cell thymocyte apoptosis or generation of regulatory T cells. AIRE mutations result in autoimmune polyendocrine syndrome. Central tolerance in bone marrow leads to receptor editing or B-cell apoptosis. Peripheral tolerance leads to anergy or apoptosis of T and B cells. Fas apoptosis pathway mutations result in autoimmune lymphoproliferative syndrome ALPS. Regulatory T cells suppress autoimmunity by blocking T-cell activation and producing anti-inflammatory cytokines IL and TGF-ОІ.

CD25 polymorphisms are associated with autoimmunity MS and type 1DM. FOXP3 mutations lead to IPEX syndrome Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked. More common in women; classically affects women of childbearing age 1. Estrogen may reduce apoptosis of self-reactive B cells. Etiology is likely an environmental trigger in genetically-susceptible individuals. Association with certain HLA types e. Environmental triggers lead to bystander activation or molecular mimicry. Autoimmune disorders are clinically progressive with relapses and remissions and often show overlapping features; partially explained by epitope spreading II. Chronic, systemic autoimmune disease 1. Flares and remissions are common.

Classically arises in middle-aged females, especially African American and Hispanic women 1. May also arise in children and older adults less dramatic gender bias C. Antigen-antibody complexes damage multiple tissues type III HSR. Poorly-cleared apoptotic debris e. Antigen-antibody complexes are generated at low levels and taken up by dendritic cells. DNA antigens activate TLRs, amplifying immune response IFN-О±. Antigen-antibody complexes are subsequently generated at higher levels and deposit in multiple tissues causing disease. Deficiency of early complement proteins C1q, C4, and C2 is associated with SLE.

Almost any tissue can be involved. Fever, weight loss, fatigue, lymphadenopathy, and Raynaud phenomenon 2. Malar 'butterfly' rash Fig. Oral or nasopharyngeal ulcers usually painless 4. Serositis pleuritis and pericarditis 6. Psychosis or seizures 7. Renal damage i. Diffuse proliferative glomerulonephritis is the most common and most severe form of injury. Other patterns of injury e. Anemia, thrombocytopenia, or leukopenia type II HSR 9. Libman-Sacks endocarditis Antinuclear antibody ANA; sensitive, but not specific Anti-dsDNA or anti-Sm antibodies highly specific E. Antiphospholipid antibody is associated with SLE one-third of patients. Autoantibody directed against proteins bound to phospholipids Fig. Inflammation, Inflammatory Disorders, and Wound Healing 19 2. Important antiphospholipid antibodies include anticardiolipin false-positive VDRL and RPR syphilis screening tests , anti-ОІ2-glycoprotein I, and lupus anticoagulant falsely-elevated PTT.

Antiphospholipid antibody syndrome is characterized by hypercoagulable state due to antiphospholipid antibodies especially lupus anticoagulant. Results in arterial and venous thrombosis including deep venous, hepatic vein, placental recurrent pregnancy loss , and cerebral stroke thrombosis 2. Requires lifelong anticoagulation 3. Associated with SLE; however, more commonly occurs as a primary disorder G. Antihistone antibody is characteristic of drug-induced lupus. Procainamide, hydralazine, and isoniazid are common causes. ANA is positive by definition. CNS and renal involvement are rare. Removal of drug usually results in remission. First-line treatment includes avoiding exposure to direct sunlight and glucocorticoids for flares; other immunosuppressive agents are useful in severe or refractory disease.

SJГ—GREN SYNDROME A. Autoimmune destruction of lacrimal and salivary glands 1. Lymphocyte-mediated damage type IV HSR with fibrosis B. Classically presents as dry eyes keratoconjunctivitis sicca , dry mouth xerostomia , and recurrent dental caries in an older woman years -"Can't chew a cracker, dirt in my eyes" 1. May progress to ulceration of corneal epithelium and oral mucosa C. Can be primary sicca syndrome or associated with another autoimmune disorder, especially rheumatoid arthritis 1. Rheumatoid factor is often present even when rheumatoid arthritis is absent. Anti-SSA and anti-SSB are associated with extraglandular manifestations e. Pregnant women with anti-SSA are at risk for delivering babies with neonatal lupus and congenital heart block. Anti-SSA and anti-SSB are also seen in a subset of patients with SLE screen pregnant patients E.

Lymphocytic sialadenitis on lip biopsy minor salivary glands is an additional diagnostic criterion Fig. Increased risk for B-cell marginal zone lymphoma, which presents as unilateral enlargement of the parotid gland late in disease course IV. Autoimmune disorder characterized by sclerosis of skin and visceral organs 1. Classically presents in middle-aged females years B. Fibroblast activation leads to deposition of collagen. Autoimmune damage to mesenchyme is possible initiating event. Endothelial dysfunction leads to inflammation increased adhesion molecules , vasoconstriction increased endothelin and decreased NO , and secretion of growth factors TGF-ОІ and PDGF.

Fibrosis, initially perivascular, progresses and causes organ damage. Limited type-Skin involvement is limited hands and face with late visceral involvement. Diffuse type-Skin involvement is diffuse with early visceral involvement. Any organ can be involved. Commonly involved organs include i. Vessels Raynaud phenomenon ii. GI tract esophageal dysmotility and reflux iii. Lungs interstitial fibrosis and pulmonary hypertension iv. Kidneys scleroderma renal crisis 3. Highly associated with antibodies to DNA topoisomerase I anti-Scl Autoimmune-mediated tissue damage with mixed features of SLE, systemic sclerosis, and polymyositis B.

Characterized by ANA along with serum antibodies to U1 ribonucleoprotein WOUND HEALING I. Healing is initiated when inflammation begins. Occurs via a combination of regeneration and repair II. Replacement of damaged tissue with native tissue; dependent on regenerative capacity of tissue B. Could you share with me the Pathoma book to my email? Best whishes. Need a link for downloading video lectures.. the one here is not working Also need download link of pdf of pathoma book Thank you! Your email address will not be published.

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No part of this publication may be reproduced, distributed, or transmitted in any form, or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without prior permission in writing from the publisher email: info pathoma. Disclaimer Fundamentals of Pathology aims at providing general principles of pathology and its associated disciplines and is not intended as a working guide to patient care, drug administration or treatment. Medicine is a constantly evolving field and changes in practice regularly occur.

It is the responsibility of the treating practitioner, relying on independent expertise and knowledge of the patient, to determine the best treatment and method of application for the patient. Furthermore, although care has been taken to ensure the accuracy of information present in this publication, the author and publisher make no representations or warranties whatsoever, express or implied, with respect to the completeness, accuracy or currency of the contents of this publication. This publication is not meant to be a substitute for the advice of a physician or other licensed and qualified medical professional. Information presented in this publication may refer to drugs, devices or techniques which are subject to government regulation, and it is the responsibility of the treating practitioner to comply with all applicable laws.

This book is printed on acid-free paper. Published by Pathoma LLC. com info pathoma. com Cover and page design by Olaf Nelson, Chinook Design, Inc. Growth Adaptations, Cellular Injury, and Cell Death пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ1 Chapter 2. Inflammation, Inflammatory Disorders, and Wound Healing пїЅ пїЅ пїЅ 11 Chapter 3. Principles of Neoplasia пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 23 Chapter 4. Hemostasis and Related Disorders пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 31 Chapter 5. Red Blood Cell Disorders пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 41 Chapter 6. White Blood Cell Disorders пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 53 Chapter 7.

Vascular Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 65 Chapter 8. Cardiac Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 73 Chapter 9. Respira espiratory ory Tr Tract act Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 85 Chapter Gastroin astrointtestinal P Paathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 99 Chapter Exocrine Ex ocrine Pancr Pancreas eas,, Gallbladder Gallbladder,, and Liver Liver P PaathologyпїЅ.

пїЅ пїЅ пїЅ Chapter Kidney idney and Urinary Urinary Tract act Pa Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ Chapter Female Genital System and Gestational PathologyпїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ В» Chapter Male Genital System Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ Chapter Endocrine Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ Chapter Breast Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ Chapter Central Nervous System Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ Chapter Musculoskeletal Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ Chapter Skin Pathology пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ Index.

To this effect, the organization of this book follows that of most primary texts in the field and parallels the syllabus used in pathophysiology courses in medical schools throughout the United States. Ample space is provided for students to make notes during course study and while viewing the online videos that cover each section of the text www. We recommend that students use Fundamentals of Pathology during their medical courses, taking notes in the margin as pertinent topics are covered. When exam time comes around, these notes will likely be invaluable.

For examination preparation, we suggest students read the material first, then listen to the online lecture, and then reread the material to develop a solid grasp of each topic. One should not become disheartened if they are not able to retain all the information contained herein. This deceptively slim volume covers a tremendous amount of material, and repetition will be a key aid as you progress in your studies. An effort has been made to emphasize concepts and principles over random facts, the forest rather than the trees. Attention to the same by the student will provide a deeper, more meaningful understanding of human disease. We must always remind ourselves that ultimately our goal is to learn, to share, and to serve. Fundamentals of Pathology was developed with this goal in mind.

Husain A. To begin with, I would like to acknowledge Shaykh Zulfiqar Ahmad, whose clear vision has guided me to horizons I would never have known. My family is to be acknowledged for their limitless sacrifice, in particular the constant encouragement and support of my wife Amina, who has proved through the years to be the wind under my wings. Thomas Krausz, MD and Ali ya Husain, MD both Professors of Pathology at the University of Chicago deserve particular mention for their valuable advice and guiding vision, both in the development of this book as well as my career.

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Pathoma - Fundamentals of Pathology Edition Husain Sattar. FCB Husain Sattar. FOR THE® USMLE STEP 1 FIRST AID YASH CHAVDA, DO KIMBERLY 05/05/ · Fundamentals of Pathology Pathoma PDF or simply Pathoma Pdf is the preferred pathology assessment ebook amongst medical college students in the USA and all 03/01/ · Download Pathoma Fundamentals of Pathology Pdf k Views Download Pathoma Fundamentals of Pathology Direct Link Pdf Fundamentals of Pathology View Details. Request a review. Learn more 10/11/ · Widely acclaimed Pathology book called Fundamentals of Pathology – Pathoma is now available here and just as promised, for free. Just Follow this page to the bottom to About Pathoma Pdf Free Download Pathoma is a complete medical video tutorial that teaches you how to recognize diseases and not just memorize them. It provides a quick and ... read more

Red Blood Cell Disorders пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ пїЅ 41 Chapter 6. Transferrin transports iron in the blood and delivers it to liver and bone marrow macrophages for storage. Original PDF Format Pages: Series: Fundamentals of Pathology Pathoma Files size : 36 MB Students Pathoma reviews direct download : Five Stars Pathoma Videos, PDF Books, Study Note and slides Collection Download Pathoma PDF. Subtype of chronic inflammation B. CNS and renal involvement are rare. TH1cells secrete IFN-Оі, which converts macrophages to epithelioid histiocytes and giant cells. Sir kindly request to send pathoma PDF to my email [email protected] as I have started now in preparing usmle..

Peripheral tolerance leads to anergy or apoptosis of T and B cells. Abscess - Proteolytic enzymes from neutrophils liquefy tissue. Inflammation, pathoma 2019 pdf free download, Inflammatory Disorders, and Wound Healing пїЅ пїЅ пїЅ 11 Chapter 3. hello sir! I kindly request you to share Pathoma link with me, thanks. Classically presents as dry eyes keratoconjunctivitis siccadry mouth xerostomiaand recurrent dental caries in an older woman years -"Can't chew a cracker, dirt in my eyes" 1. Adenosine deaminase ADA deficiency - ADA is necessary to deaminate adenosine and deoxyadenosine for excretion as waste products; buildup of adenosine and deoxyadenosine is toxic to lymphocytes.