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Pathoma Study Set – Questions & Solutions (Pass!)
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Pathoma Study Set – Questions & Solutions (Pass!)
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Pathoma Study Set – Questions & Solutions (Pass!)Hypoxia Right Ans - Ischemia, Hypoxemia, Dec. O2-carrying capacity
ischemia Right Ans - dec. blood flow through organ: block arterial flow to,
or venous flow from
budd-chiari syndrome Right Ans - thrombosis of hepatic vein => infarction
of hepatic parenchyma (1 - poly-cythemia very, or 2 - lupus anticoagulant)
hypoxemia Right Ans - PaO2 < 60, or SaO2 < 90
FiO2 dec: high altitude
PAO2 dec: high PACO2 (hypoventillation, OCPD), interstitial fibrosis
Dec. O2-carrying capacity Right Ans - anemia (PaO2 & SaO2 normal), CO
poisoning, methemoglobinemia (tx. IV methylene blue)
hypoxia => low ATP => cellular injury Right Ans - Low ATP => Na/K pump
(cell swell), Ca pump, anaerobic glycolysis
reversible cellular injury Right Ans - cellular swelling
microvilli swell, membrane blebbing, swelling of ER
irreversible cellular injury Right Ans - membrane damage
plasma membrane pops (Ca comes in), mitochondrial membrane (Cyt C),
lysosome membrane (Ca-activated, trash cell)
cell death Right Ans - loss of nucleus: pyknosis, karyorrhexis, karyolysis
necrosis Right Ans - coagulative, liquefactive, gangrenous, caseous, fat,
fibrinoid
coagulative necrosis Right Ans - ischemic infarction (except brain)
wedge-shaped & pale (except when red)
hemorrhagic infarction => red
liquefactive necrosis Right Ans - enzymatic lysis: brain infarct (microglial
cells), abscess (neutrophils), pancreatitis (pancreatic enzymes)
,gangrenous necrosis Right Ans - dry gangrene = like coag necrosis;
ischemia of lower limb (DM) & GI tract
wet gangrene = dry, but necrotic tissue becomes infected
caseous necrosis Right Ans - liquefactive w/something mixed in to thicken
the soup: TB or fungus
fat necrosis Right Ans - suponification = fatty acids released, binds Ca
trauma to breast & peri-pancreatic fat
fibrinoid necrosis Right Ans - damage to blood vessel wall
vasculitis and malignant HTN (can be seen in pre-eclampsia, necrosis of
placenta)
apoptosis Right Ans - endometrial shedding, durng embryogenesis
(webbed feet), CD8+ killing
apoptotic bodies removed by macrophages
mediated by caspases (activate proteases & endonucleases)
apoptosis activation Right Ans - intrinsic mitochondrial pathway (cell injry,
DNA damage, dec. hormone stimulation) => Bcl2 knocked out, Cyt C released,
activates caspases
extrinsic receptor-ligand pathway = FAS ligand binds FAS death receptor on
target cell (negative selection in T cell maturation)
cytotoxic Cd8+ = secrete perforin & granzymes (activate caspases)
free radical basics Right Ans - Cyt C oxidase transfers electrons to O2
during oxidative phosphorylation, accepts 4 electrons O2 => O2- => H2O2 =>
OH- => H2O
pathologic generation of free radicals Right Ans - ionizing radiation (H2O
=> OH- most damaging radical)
inflammatio (neutrophils oxygen dependent killing: makes HOCl)
metals (Cu & Fe, Fenten rxn => OH-... Wilson's & Hemocromatosis (=> cirrosis
of liver))
drugs/chemicals (tylenol by liver P450 => free radicals; CCl4)
free radical making enzymes Right Ans - O2 => O2- = NADPH oxidase
O2- => H2O2 = superoxide dysmutase (SOD)
,H2O2 => HOCl = myeloperoxidase
H2O2 => H2O + O2 (catalase)
OH- => H2O (glutathione peroxidase)
elimination of free radicals Right Ans - antioxidants: Vit A, C, E
metal carrier proteins: transferrin carries Fe in blood; Ferratin binds Fe in
liver (so radicals not produced)
enzymes SOD, catalase, glutathione peroxidase
free radical injury Right Ans - CCl4 dry cleaning industry
liver P450 converts CCl4 = CCl3-, damaged hepatocyes
cellular swelling, RER swell, lose ribosomes => fail to synthecize protein
(apolipoprotein) => fat can get in, but can't get out (function of liver) => fatty
change of liver
reperfusion injury
MI, cells die. cath lab, O2 returns => hits inflammatory cells, make free radicals
=> further damage to cardiac myocytes
amyloid Right Ans - usually beta-pleated sheet
amyloid pics up Congo red stain, reveals apple-green birefringence under
polarized light
systemic amyloidosis Right Ans - primary amyloidosis: deposition of AL
(light chain) amyloid; plasma cell dyscrasia diseases => overproduction of
light chain => deposits into tissue
secondary amyloidosis: depositoin of AA (acute phase reactant) amyloid; SAA
= acute phase reactant => AA... in chronic inflammation, malignancy, familial
mediterranean fever (dysfunctional neutrophils
kidney most involved organ => nephrotic syndrome (> 3.5 g/24 hr
proteinuria)
restrictive cardiomyopathy (amyloid => less compliant heart wall)
localized amyloidosis Right Ans - senile cardiac amyloidosis: non-mutated
serum transthyretin
familial amyloid cardiomyopathy: mutated serum transthyretin => restrictive
cardiomyopathy (5% blacks)
, DM II: byproduct of insulin is amylin, deposits in islets of pancreas => burns
out pancreas => insulin-dependent DM II
alzheimer disease: Abeta amyloid (beta-amyloid precursor protein Chr 21)
dialysis-associated amyloidosis: beta2-microglobulin (amyloid) structural
support for MHC I... gets filtered poorly => deposits in joints
medullary carcinoma of thyroid: tumor cells overproduce calcitonin, deposits
=> amyloid (thyroid cancer in amyloid backgroudn = medullary carcinoma)
acute inflammation Right Ans - edema + neutrophils
infection & tissue necrosis
acute inflammation factors Right Ans - Tol-like Receptors (TLRs)
Arachidonic acid
Mast cells
Compliment
Hageman factor
TLRs Right Ans - Tol-like receptors: recognize PAMPs, e.g. CD14 on
macrophages recognize LPS of gram neg bact => activate
macrophage/dendritic cell =>immune reponse
arachadonic acid Right Ans - from phospholipase A2; acted upon by 1 of 2
pathways
COX pathway => prostaglandins => vasodilation & inc. vascular permeability
(PGE2 => pain & fever)
5-lipooxygenase pathway => leukotrienes => vasoconstriction, bronchospasm,
& inc. vascular permeability (pericytes within vessel endothelial cells) (LTB4
attacts & activates neutrophils
mast cells Right Ans - distributed throughout CT of body
activated by (1) tissue trauma, (2) compliment proteins C3a & C5a, (3)
crosslinking of cell-surface IgE by antigen
immediate response: dumping of preformed histamine granules (vasodilation
& inc. vascular permeability)
delayed response: produciton of arachidonic acid metabolits, esp leukotrienes
=> maintenance of acute inflammatory response)
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