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PATHOMA HUSAIN SATTAR PDF

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HUSAIN A. SATTAR, MD. Assistant Professor of Pathology. Associate Director of Clinical Pathophysiology and Therapeutics. The University of Chicago. Medical course and Step 1 review. Fundamentals of Pathology is a unique page text that combine Dr. Husain A. Sattar's extensive teaching experience with . This article contains Fundamentals of Pathology Pathoma PDF free download of Husain A Sattar MD who is the author of Pathoma Pathoma Pdf free.


Pathoma Husain Sattar Pdf

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This article contains Fundamentals of Pathology Pathoma PDF for free download. This book has been authored by Husain A. Sattar. FUNDAMENTALS OF PATHOLOGY BY HUSAIN A. SATTAR. PDF. Only for you time i decided to read Pathoma and i see now how couldnt see the important. Fundamentals of Pathology [Husain A. Sattar] on yazik.info *FREE* Fundamentals of Pathology by Hussain A,sattar (pathoma paperback &videos).

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Fundamentals of Pathology

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Cellular injury occurs when a stress exceeds the cell 's ability to adapt. The likelihood of injury depends on the type of stress, its severity, and the type of cell affected.

Neurons are highly susceptible to ischemic injury; whereas, skeletal muscle is relatively more resistant.

Slowly developing ischemia e. Common causes of cellular injury include inflammation, nutritional deficiency or excess, hypoxia, trauma, and genetic mutations. Low oxygen delivery to tissue; important cause of cellular injury I.

Oxygen is the final electron acceptor in the electron transport chain of oxidative phosphorylation. Decreased oxygen impairs oxidative phosphorylation, resulting in decreased ATP production. Lack of ATP essential energy source leads to cellular injury. Causes of hypoxia include ischemia, hypoxemia, and decreased 0 2-carrying capacity of blood. Ischemia is decreased blood flow through an organ. Arises with I.

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Decreased arterial perfusion e. Decreased venous drainage e. Shock- generalized hypotension resulting in poor tissue perfusion D. Arises with 1. Diffusion defect-PA0 2 not able to push as much 0 2 into the blood due to a thicker diffusion barrier e. Decreased 0 2-carrying capacity arises with hemoglobin Hb loss or dysfunction.

Examples include l.

Carbon monoxide poisoning Fig. Courtesy of motherchildnutrition. Reprinted with permission from orthopaedia. CO binds hemoglobin more avidly than oxygen-Pao2 normal; Sao2 decreased ii. Exposures include smoke from fires and exhaust from cars or gas heaters.

Classic finding is cherry-red appearance of skin.

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Early sign of exposure is headache; significant exposure leads to coma and death. Methemoglobinemia i. Seen with oxidant stress e. Classic finding is cyanosis with chocolate-colored blood. Hypoxia impairs oxidative phosphorylation resulting in decreased ATP.

Low ATP disrupts key cellular functions including 1.

Ca 2"' pump, resulting in Ca Aerobic glycolysis, resulting in a switch to anaerobic glycolysis. Lactic acid buildup results in low pH, which denatures proteins and precipitates DNA. The initial phase of injury is reversible. The hallmark of reversible injury is cellular swelling. Cytosol swelling results in loss of microvilli and membrane blebbing. Swelling of the rough endoplasmic reticulum RER results in dissociation of ribosomes and decreased protein synthesis.

Eventually, the damage becomes irreversible. The hallmark of irreversible injury is membrane damage.

Plasma membrane damage results in i. Cytosolic enzymes leaking into the serum e. Additional calcium entering into the cell 2. Mitochondrial membrane damage results in i. Loss of the electron transport chain inner mitochondrial membrane ii. Cytochrome c leaking into cytosol activates apoptosis 3. Lysosome membrane damage results in hydrolytic enzymes leaking into the cytosol, which, in turn, are activated by the high intracellular calcium.

The end result of irreversible injury is cell death. A, Gross appearance. C, Normal kidney histology for comparison. The morphologic hallmark of cell death is loss of the nucleus, which occurs via nuclear condensation pyknosis , fragmentation karyorrhexis , and dissolution karyolysis.

The two mechanisms of cell death are necrosis and apoptosis. Death of large groups of cells followed by acute inflammation B. Due to some underlying pathologic process; never physiologic C.

Divided into several types based on gross features III. Coagulative necrosis 1. Necrotic tissue that remains firm Fig. SA ; cell shape and organ structure are preserved by coagulation of proteins, but the nucleus disappears Fig. Characteristic of ischemic infarction of any organ except the brain 3. Area of infarcted tissue is often wedge-shaped pointing to focus of vascular occlusion and pale. Red infarction arises if blood re-enters a loosely organized tissue e.

Liquefactive necrosis l. Necrotic tissue that becomes liquefied; enzymatic lysis of cells and protein results in liquefaction.

Characteristic of i. Brain infarction-Proteolytic enzymes from microglial cells liquefy the brain. Abscess-Proteolytic enzymes from neutrophils liquefy tissue. Pancreatitis-Proteolytic enzymes from pancreas liquefy parenchyma.Each night he focused on what he needed to understand to get through the next day. You're still the highest bidder! Liquefactive necrosis l.

Kidney and Urinary Tract Pathology. Pathologic hyperplasia e. The likelihood of injury depends on the type of stress, its severity, and the type of cell affected.

Vascular Pathology. Cytochrome c leaking into cytosol activates apoptosis 3.