High-Yield Facts in Pathology 2021

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High-Yield Facts in Pathology 1. CELL INJURY a. Reversible Cell Injury • swelling of cell organelles and entire cell • dissociation of ribosomes from endoplasmic reticulum • decreased ener... gy production by mitochondria • increased glycolysis  decreased pH  nuclear chromatin clumping b. Irreversible Cell Injury • irreversible damage to cell membranes and mitochondria • influx of calcium into mitochondria; forms dense bodies (flocculent densities in heart) • release of cellular enzymes (e.g., SGOT, LDH, and CPK after MI) • nuclear degeneration (pyknosis, karyolysis, karyorrhexis) • cell death 2. FATTY CHANGE OF THE LIVER (STEATOSIS; FATTY METAMORPHOSIS) a. Mechanisms 1. Increased delivery of free fatty acids to liver • starvation • corticosteroids • diabetes mellitus 2. Increased formation of triglycerides • alcohol (note: NADH > NAD) 3. Decreased formation of apoproteins • carbon tetrachloride • protein malnutrition (kwashiorkor) 1 Copyright © 2007 by The McGraw-Hill Companies, Inc. Click here for terms of use.2 Pathology 3. CELL DEATH a. Apoptosis 1. Characteristics • “programmed” cell death • single cells (not large groups of cells) • cells shrink  form apoptotic bodies • gene activation  forms endonucleases • peripheral condensation of chromatin with DNA ladder • no inflammatory response 2. Mechanisms/phases a) initiation phase  caspases are activated b) execution phase  cell death occurs i. two distinct pathways i) extrinsic  receptor-mediated pathway • mediated by cell surface death receptors  type 1 TNF receptor (TNFR1) and Fas (CD95) ii) intrinsic (or mitochondrial) pathway • increased permeability of mitochondria  example is cytochrome c released into cytoplasm via bax channels 3. Examples of apoptosis: a) physiologic • involution of thymus • cell death within germinal centers of lymph nodes • fragmentation of endometrium during menses • lactating breast during weaning b) pathologic • viral hepatitis • cytotoxic T cell–mediated immune destruction (type IV hypersensitivity) b. Necrosis 1. Characteristics • cause  hypoxia or toxins (irreversible injury) • many cells or clusters of cells • cells swell • inflammation presentHigh-Yield Facts 3 2. Examples of necrosis: • coagulative necrosis  ischemia (especially of the heart and kidney but not the brain) • liquefactive necrosis  bacterial infection (and brain infarction) • fat necrosis  pancreatitis and trauma to the breast • caseous necrosis  tuberculosis • fibrinoid necrosis  autoimmune disease (type III hypersensitivity reaction) • gangrene  ischemia to extremities  dry (mainly coagulative necrosis) or wet (mainly liquefactive necrosis due to bacterial infection) 4. TERMS a. Cellular Adaptation • hypertrophy  increase in the size of cells • hyperplasia  increase in the number of cells • atrophy  decrease in the size of an organ • aplasia  failure of cell production • hypoplasia  decrease in the number of cells • metaplasia  replacement of one cell type by another • dysplasia  abnormal cell growth b. Abnormal Organ Development • anlage  primitive mass of cells • aplasia  complete failure of an organ to develop (anlage present) • agenesis  complete failure of an organ to develop (no anlage present) • hypoplasia  reduction in the size of an organ due to a decrease in the number of cells • atrophy  decrease in the size of an organ due to a decrease in the size or number of preexisting cells 5. STEM CELLS (LOCATIONS ARE CALLED NICHES) • liver  oval cells in the canals of Hering of the liver • muscle  satellite cells in the basal lamina of myotubules • cornea  limbus cells in the canals of Schlemm • colon  base of the crypts • brain  dentate gyrus of the hippocampus4 Pathology 6. CARDINAL SIGNS OF INFLAMMATION • rubor  red vasodilation) • calor  hot (increased blood flow) • tumor  swollen (fluid accumulation) • dolor  pain (bradykinin, and the like.) 7. COMPLEMENT CASCADE a. Products • C3b  opsonin • C5a  chemotaxis and leukocyte activation • C3a, C4a, C5a  anaphylatoxins • C5–9  membrane attack complex b. Deficiencies • deficiency of C3 and C5  recurrent pyogenic bacterial infections • deficiency of C6, C7, and C8  recurrent infections with Neisseria species • deficiency of C1 esterase inhibitor  hereditary angioedema • deficiency of decay-accelerating factor  paroxysmal nocturnal hemoglobinuria 8. THROMBOXANE VS. PROSTACYCLIN a. Thromboxane (TxA2) • produced by platelets • causes vasoconstriction • stimulates platelet aggregation b. Prostacyclin (PGI2) • produced by endothelial cells • causes vasodilation • inhibits platelet aggregation 9. GRANULOMATOUS INFLAMMATION a. Caseating Granulomas • aggregates of activated macrophages(epithelioid cells) • tuberculosis b. Noncaseating Granulomas • sarcoidosis • fungal infections • foreign-body reactionHigh-Yield Facts 5 10. COLLAGEN TYPES a. Fibrillar Collagens • type I  skin, bones, tendons, mature scars • type II  cartilage • type III  embryonic tissue, blood vessels, pliable organs, immature scars b. Amorphous Collagens • type IV  basement membranes • type VI  connective tissue 11. EDEMA a. Exudates 1. Composition • increased protein • increased cells • specific gravity greater than 1.020 2. Cause • inflammation • increased blood vessel permeability 3. Examples • inflammatory edema of lung  bacterial pneumonia • inflammatory edema of pleural cavity  empyema b. Transudates 1. Composition • no increased protein • no increased cells • specific gravity less than 1.012 2. Cause  abnormality of Starling forces a) increased hydrostatic venous) pressure • congestive heart failure • portal hypertension b) decreased oncotic pressure  due to decreased albumin • liver disease • renal disease (nephrotic syndrome)6 Pathology c) lymphatic obstruction • tumors or surgery • filaria 12. CARCINOMAS a. Squamous Cell Carcinoma • skin cancer • lung cancer • esophageal cancer • cervical cancer b. Adenocarcinoma • lung cancer • colon cancer • stomach cancer [Show More]

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