Pathology Flashcards
1
Q
Cell adaptation
- hypertrophy
- hyperplasia
- atrophy
- metaplasia
- dysplasia
A
- increase in structural proteins and organelle which increases size of cell
- controlled proliferation of stem cells -> increase in amnt of cells
- decrease in tissue mass because decrease in size or number of cells
- reprogramming of stem cells causing replacement of one cell type to another because it is better at adapting to certain stressor
- disordered precancerous epi cell growth characterized by loss of uniformity of cell size and shape
2
Q
Injury
- reversible: ATP, ribosomes, membrane, nuclear, function
- irreversible: membrane, mito, lysosome, nuclear
A
- decrease in ATP -> decrease Ca activity and Na/K pmp -> cellular swelling; ribosomal detachment -> decrease protein synthesis; plasma membrane changes; nuclear changes; rapid loss of function
- breakdown of plasma membrane -> Ca into cell -> activates proteases; mito damage dysfunction -> loss of ETC -> low ATP; rupture of lysosomes -> autolysis; nuclear degradation
3
Q
Apoptosis
- intrinsic: what is it, regulated by, Function of apoptotic, Function of anti-apoptotic
- extrinsic: 2 pathways
A
- regulating factor is withdrawn from proliferating cell causing apoptosis; BCL2 family, BAX and BAK: form pores into mito membrane -> release of cyto C from inner mito membrane to cytoplasm -> activation of capases; BCL2: keep mito membrane impermeable
- ligand binding receptor (Fas-FasL or TNF-alpha) or immune cell mediated (CD8+ or NK)
4
Q
Types of Necrosis
- coagulative: seen in, due to, histo
- liquefactive
- caseous
- fat
- fibrinoid
- gangrenous
A
- ischemia / infarct; injury that denatures proteins; preserved cell architecture but nuclei disappear
- bacterial abcesses or brain infarcts; PMN release lysosomal enzymes that digest tissue; cellular debris and macro -> cystic spaces and cavitations
- TB, systemic fungi; macro wall off infecting organism -> granular debris; fragmented cells and debris surrounded by lymphocytes
- enzymatic: acute pancreatitis, non-enzymatic: trauma; damaged pancreatic cells release lipase which breaks down trigly and FFA binds to CA -> causing chalk white appearance of fat; outline of dead fat cell w/o peripheral nuclei
- immune vascular reaction; immune complex deposition and or plasma protein leakage from damaged vessel; vessel walls are thick and pink
- distal extremity and GI tract after chronic ischemia; Dry: ischemia, wet: super-infection; coagulative or liquefactive on top of coagulative
5
Q
Ischemia
- what is it
- mechanism
A
- inadequate blood supply to meet demand
- decrease arterial perfusion, decreased venous drainage, shock
6
Q
Type of infarct
- red
- white
A
- occurs in venous occlusions and tissues w/ multiple blood supplies and with re-perfusion
- occurs in solid organ with single blood supply
7
Q
Free radical injury
- function
- caused by
A
- damage cell membrane by lipid peroxidation
- radiation, meds, redox reactions, NO
- scavenging enzymes, spontaneous decay, anti-oxidant
8
Q
Type of calcification
- dystrophic: cell type, extent, etiology, serum Ca levels, associated conditions
- metastatic: cell type, extent, etiology, serum Ca levels, associated conditions
A
- in diseased tissue; localized; secondary to injury or necrosis; normal; TB, chronic abcess, fat necrosis, infarct
- in normal tissue; widespread; secondary to hyper Ca; abnormal; in interstitum of kidney, lung, GI mucosa,
9
Q
Lipofuscin
- what is it
- cause
- found in
A
- yellow-brown wear and tear pigment associated w/ normal aging
- oxidation and polymerization og autophagocytosed organellar membranes
- heart, colon, liver, kidney, eye of elederly on autopsy
10
Q
Amyloidosis
- what is it/ pathogenesis
- visualized w/
- location
A
- abnormal aggregation of proteins into beta pleated linear sheets -> insoluble fibrils -> cell damage and apoptosis
- congo-red stain
- glomerular mesangial areas
11
Q
Systemic amyloidosis
- primary: fibril protein, seen in
- secondary
- dialysis
A
- AL protein, seen in plasma cell disorders
- serum amyloid A, seen in chronic inflamm conditions
- B2 microglobulin, seen in pts with ESRD
12
Q
Localized amyloidosis
- Alzheimers: protein, from
- Type II DM: protein, cause
- Medullary thyroid CA: protein
- Isolated atrial amyloidosis: protein, pathogenesis, risk
- systemic senile amyloidosis: protein, location
A
- Beta amyloid protein; cleaved from amyloid precursor protein
- Islet amyloid polypeptide; caused by deposition of amylin in pancreatic islet cells
- calcitonin
- ANP, common in normal aging but puts at risk for a fib
- transthyretin, seen predominantly in cardiac ventricles
13
Q
Hereditary amyloidosis
- familial amyloid cardiomyopathy: protein, location, causes
- familial amyloid polyneuropathy: protein
A
- mutated transthyretin, ventricular endocardium -> restrictive cardiomyopathy
- mutated transthyretin -> caused by tranthyretin gene mutation
14
Q
Inflammation
- what is it
- signs
- acute phase
- fever
A
- response to eliminate cause of cell injury, remove necrotic cells and initiate tissue repair
- erythema / heat (histamine/ prostaglandin/ bradykinin causing increase in vasodilation), tumor / swelling (leukotrienes, hitamine, serotonin causeeing endothelial disruption allowing for leakage of proteins and increasing interstial oncotic pressure), pain (bradykinin, PGE2, histamine causing sensitization of nerve endings), loss of function
- fever, leukocytosis, increase in plasma acute phase protein produced by liver
- pyrogens cause macro to release IL-1 and TNF -> increase COX -> in pervacsular cells in hypothal -> increase PGE2 -> increase set point
- elevation of WBC count and type of cell depends on inciting agent
15
Q
Acute phase reactants
- ferritin
- fibrinogen
- serum amyloid A
- hepcidin
- CRP
- albumin
- transferrin
A
- upreg, binds and sequesters iron to inhibit microbial iron scavenging
- upreg, coag factor, promotes endo repain, correlates with ESR
- upreg, prolonged leads to amyloidosis
- upreg, decrease iron absorption and release
- upreg, opsonin
- down reg, conserves AA
- down reg, internalized by macrophages to sequester iron
16
Q
Erythrocyte sedimentation rate
- what is it
A
- RBC normally able to remain separated by neg charge but with inflammation fibrinogen will coat RBC and decrese negative charge -> increase in RBC aggregation
