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STEP 1 PATH 1

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lizamariereagan's version from 2015-05-05 20:46

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Phases of myocardial injury1
Gross appearance at 4-24 hours?dark mottling
At 1-3 days?mottling with yellow infarct center
At 3-7 days?yellow softening with hyperemic border
At 10-14 daysred-gray infarct borders
At 2-8 weeksgray-white scar
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LM at 4-24 hours ?contraction bands, coagulative necrosis
At 1-3 days?widespread coagulative necrosis with neutrophil migration
At 3-7 days?macrophage infiltration
At 10-14 days?well-developed granulation tissue
At 2-8 weeks?collagen scar formation
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Risk at 4 hours to 3 days?arrhythmia
At 3-7 days?free wall rupture, papillary muscle rupture, intraventricular septal rupture, cardiac tamponade
At 2-8 weeks?ventricular aneurysm
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CXR findings1
Cardiomegalyheart >1 hemithorax in size
Alveolar edemaincreased vascular shadowing
Pleural effusionblunting of costophrenic angles
Kerley b linesshort horizontal lines situated perpendicular to pleural surface that represent edema of the interlobular septa (heart failure)
Bilateral patchy airspace diseaseARDS
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Reticular net-like opacities involving lung basesidiopathic interstitial fibrosis
Hyperinflated lungs and flattened diaphragmCOPD
Enlargement of pulmonary arteries and RVprimary pulm hypertension
White visceral pleural line; pulm vessels not visible beyond boundary; mediastinum often shifted away from affected sidepneumothorax
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What are pro-apoptotic proteinsBAX and BAK
What are anti-apoptotic proteinBcl-2
How does Bcl-2 prevent cytochrome c release?by binding to and inhibiting Apaf-1
What is the function of Apaf-1normally induces activation of caspases
What receptor initiates the extrinsic pathFas
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What are the two pathways in the extrinsic pathligand receptor interactions (FasL binding to Fas [CD95]) and immune cell (cytotoxic T cell release of perforin and granzyme B)
What does FADD do?binds inactive caspases, activating them
What is the basis of autoimmune disorders?defective or mutations of Fas-FasL interaction
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What is the Fas-FasL interaction necessary for? :thymic medullary negative selection
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How does cytochrome c function in apoptosisactivates caspases and indirectly brings about cell death through intrinsic pathway apoptosis
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When do you see noncaseous granulomatous inflammation ?sarcoidosis
When do you see granulomatous reactionin mycobacterial infections
When do you see an inflammatory process in association with necrosis?necrosis (there is none in apoptosis)
Features of coagulative necrosisnot in brain; tissue architecture preserved ; occurs in tissues supplied by end arteries; leukocyte (like neutrophil, eosinophil, basophil) infiltrate; occurs after irreversible ischemic injury; cells become anucleated; proteins denature first, then enzymatic degradation
Features of liquefactive necrosisoccurs in brain (due to high fat content) or fungal/bacterial abscess; enzymatic degradation first
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Features of caseous necrosisoccurs in TB, systemic fungi and nocardia; cheesy appearance; surrounded by hitiocytes (macrophage or dendritic cells) and multinucleated giant cells
Fatty necrosis featuresenzymatic (pancreatitis/saponification; chalky-white deposits) and nonenzymatic (breast trauma); calcium deposits appear dark blue on staining ; get release of active pancreatic enzymes (lipases) →digests adipose cells and release free FA
Features of fibrinoid necrosisvasculitides (eg henoch –schonlein purpura, churg strauss syndrome), malignant hypertension, amourphous and pink on h and e
Features of gangrenous necrosisdry (ischemic coagulative) and wet (superinfection) ; common in limbs and gi tract
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Atp depletionreversible with oxygen
Nuclear pyknosis, karyorrhexis, karyolysisirreversible
Cellular/mitochondrial swelling (decreased ATP leads to decreased activity of sodium/potassium pumps)reversible with oxygen
Plasma membrane damage (degradation of membrane phospholipidirreversible
Nuclear chromatin clumpingreversible with oxygen
Lysosomal ruptureirreversible
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Decreased glycogenreversible with oxygen
Mitochondrial permeability/vacuolization; phospholipid –containing amorphous densities within mitochondriairreversible
Fatty changereversible
Ribosomal/polysomal detachment (decreased protein synthesis)reversible
Membrane blebbingreversible
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areas susceptible to ischemia1
BrainACA/MCA/PCA boundary areas
Heartsubendocardium (LV)
Kidneystraight segment of PT (medulla) and TAL (medulla)
Liverarea around central vein (zone iii)
Colonsplenic flexure, rectum
What areas of the brain are affected in hypoxic ischemic encephalopathypyramidal cells of hippocampus and purkinje cells of cerebellum
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Where do red (hemorrhagic) infarcts occurin loose tissues with multiple blood supplies (Red = REperfusion)
Examples of where red infarcts occurliver, lungs and intestine
Where do pale infarcts occursolid tissues with a single blood supply
Examples of where pale infarcts occurheart, kidney, spleen
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What is shockreally low BP
What is the first sign of shocktachy
What is considered distributive shockseptic, neurogenic and anaphylactic shock
What is the other category of shockcardiogenic/hypovolemic
When is something considered hypovolemic and normal BP and CO cannot be maintainedwhen it is greater than 10% loss
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What happens to TPR in distributive shockdecreases
What happens to CO in distributive shockincreases
What happens to venous return in distributive shockincreases
What happens to PCWP in distributive shockdecreases
Is there vasodilation or constriction in distributive shock ?dilation (warm/dry skin)
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If you give IV fluids in distributive shock what happens?fail to increase blood pressure
What kind of output failure is distributive shockhigh output
What kind of output failure is hypovolemic/cardiogenic shocklow output
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What happens to TPR in hypovolemic/cardiogenic shock? Increases
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What happens to CO in hypovolemic/cardiogenic shockdecreases
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What happens to venous return in hypovolemic/cardiogenic shockdecreases
What happens to PCWP in cardiogenic shock?increases
What happens to PCWP in hypovolemic shockdecreases
Do you get vasoconstriction/dilation in hypovolemic/cardiogenic shockconstriction (cold and clammy patient)
What happens if you give IV fluids in hypovolemic/cardiogenic shock ?blood pressure restored
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Does HR increase or decrease in septic shock? increase
Does HR increase or decrease in cardiogenic shockdecrease
Does HR increase or decrease in hypovolemic shockincrease
In happens to BP in septic, cardiogenic and hypovolemic shock?decreases
What happens when you lose more than 10% of volume?sym NS activates → constriction of arteriolar and venous beds and activation of heart
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Constriction of arteriolar beds leads toincreased TP; maintanence of end organ pressure; shunts blood away from extremities and skin toward vital organs
Constrition of venous beds leads toincreased blood return to heart, so helps maintain preload
What happens if you give vasopressors in hypovolemic shock?since intravascular volume is low and SNS already maximally activated, giving vasopressor is of little help
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What is inflammation characterized byrubor, dolor, calor, tumor and function laesa (loss of function)
What cells mediate acute inflammationneutrophils, eosinophils and antibody mediated
What cells mediate chronic inflammationmononuclear cells (lymphocytes (b and t and nk cells), monocytes or macrophages), and fibroblasts
What is chronic inflammation characterized by?blood vessel proliferation, fibrosis, granulomas
Outcomes of chronic inflammationscarring and amyloidosis
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Outcomes of acute inflammationcomplete resolution, abscess formation and progression to chronic inflammation
What is chromatolysisprocess involving the cell body following axonal injury
What changes do you see in chromatolysisround cellular swelling, displacement of nucleus to the periphery and dispersion of nissl substance throught cytoplasm
What do the changes in chromatolysis reflectincreased protein synthesis in effort to repair damaged axon
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What is dystrophic calcificationcalcium depostition in tissues secondary to necrosis
What is metastatic calcificationwidespread (diffuse) deposition of calcium in normal tissue secondary to hypercalcemia
When would you see metastatic calcificationprimary hyperparathyroidism, sarcoidosis, hypervitaminosis D or high calcium phosphate product (eg chronic renal failure + secondary hyperparathyroidism, long term dialysis , calciphylaxis, warfarin )
What does dystrophic calcification look like ?fine, gritty, white granules or clumps
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How does dystrophic calcification appear on hematoxylin and eosin staindeposits appear dark-purple, sharp edged aggregates
When do you see dystrophic calcificationTB, liquefactive necrosis of chronic abscesses, fat necrosis, infarct, thrombi, schistosomiasis, monckebery arteriolosclerosis, congenital CMV and toxoplasmosis, psammoma bodies
What is the calcium level in patients with dystrophic calcificationnormal!
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Where does leukocyte extravasation predominantly occur?postcapillary venules
What are the 5 steps of leukocyte extravasation?margination, rolling, activation, tight binding and transmigration
What is decreased in leukocyte adhesion deficiency type 2sialyl-lewis x
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What is at play during margination and rolling?e and p selectin on endothelial cells, glycam 1, CD34; sialyl lewis and l-selectin on leukocytes
What is defective in leukocyte adhesion deficiency type 1tight binding ; decreased CD18, integrin subunit
What is at play during tight binding?Icam and VCAM on endothelial cell and LFA-1 on leukocytes
What is at play during diapedesisPECAM on both endothelial cells and leukocytes
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When cells in heart, brain or skeletal muscle damaged, what leaks into circulation?creatine kinase
How can inflammatory macrophages in intima decrease plaque stabilityby secreting metalloproteinases which degrade collage
Who secretes PDGFactivated locally adherent platelets and macrophages and endothelial cells
What does PDGF doinduces vascular remodeling and smooth muscle cell migration from media into intima and their subsequent proliferation
What does PDGF stimulatefibroblast growth for collagen synthesis
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What does FGF dostimulate all aspects of angiogenesis
What does EGF dostimulates cell growth via tyrosine kinases (eg EGFR, as expressed by ERBB2)
What does TGF-beta doangiogenesis, fibrosis, cell cycle arrest
What does VEGF do?stimulates angiogenesis
What do metalloproteinases dotissue remodeling
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What are the three phases of wound healing and what is their time framesinflammatory (immediate), proliferative (2-3 days after wound), remodeling (1 week after wound)
Who mediates the immediate inflammatory stageplatelets, neutrophils, macrophages
What are the characteristics of the immediate inflammatory stageclot formation, increased vessel permeability, and neutrophil migration into tissue; macrophages clear debris 2 days later
What mediates the proliferative stagefibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages
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