FA - Pathology Flashcards
(261 cards)
Apoptosis
- Intrinsic or extrinsically activated ATP-dependent process
- Results in activation of cytosolic caspases that mediate cellular breakdown
- No significant inflammation
Histologic features of apoptosis
Cell shrinkage, pyknosis, basophilia, membrane blebbing, nuclear fragmentation, formation of apoptotic bodies
Intrinsic pathway of apoptosis
Change in proportions of anti- and pro-apoptotic factors lead to increased mitochondrial permeability and cytochrome c release
Occurs when GF is withdrawn from a proliferating cell population or exposure to injurious stimuli
Extrinsic pathway of apoptosis
- ) Ligand receptor interactions (Fas ligand binding to Fas)
- ) Immune cell (cytotoxic T-cell release of perforin and granzyme B)
Necrosis
Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Inflammation occurs (cf. apoptosis)
Coagulative necrosis
Heart, liver, kidney
Liquefactive necrosis
Brain, bacterial abscess, pleural effusion
Caseous necrosis
TB, systemic fungi
Fatty necrosis
Peripancreatic fat (saponification via lipase)
Fibrinoid necrosis
Blood vessels
Gangrenous necrosis
Dry (ischemic coagulative) or wet (with bacterial); common in limbs and in GI tract
Reversible cell injury
Decreased ATP synthesis
Cellular swelling (no ATP –>impaired Na+/K+ pump)
Nuclear chromatin clumping
Decreased glycogen
Fatty change
Ribosomal detachment (decreased protein synthesis)
Irreversible cell injury
Nuclear pyknosis, karyolysis, karyorrhexis Ca++ influx -->caspase activation Plasma membrane damage Lysosomal rupture Mitochondrial permeability
Susceptible areas of ischemia: brain
ACA/MCA/PCA watershed areas
Susceptible areas of ischemia: heart
Subendocardium (LV)
Susceptible areas of ischemia: kidney
Straight segment of proximal tubule (medulla)
Thick ascending limb (medulla)
Susceptible areas of ischemia: liver
Area around central vein (zone III)
Susceptible areas of ischemia: colon
Splenic flexure, rectum
Hemorrhagic infarcts
Loose tissues with collaterals: liver, lungs, intestine, or following reperfusion
Pale infarcts
Solid tissues with single blodod supply: heart, kidney, spleen
Hypovolemic/cardiogenic shock
Low-output failure
Increased TPR
Low cardiac output
Cold, clammy patient (vasoconstriction)
Septic shock
High-output failure
Decreased TPR
Dilated arterioles, high venous return
Hot patient (vasodilation)
Inflammation
Rubor, dolor, calor, tumor, and functio laesa
Vascular component of inflammation
Increased vascular permeability, vasodilation, endothelial injury