1️⃣ Cell death Flashcards
(23 cards)
What are key morphological features of necrosis?
↑ eosinophilia, vacuolation, ER/mitochondrial swelling, myelin figures, membrane discontinuity, pyknosis, karyorrhexis, karyolysis.
Describe coagulative necrosis with example.
Denaturation > digestion, tissue architecture preserved; occurs in solid organ ischemia except brain.
Describe liquefactive necrosis with example.
Digestion > denaturation, complete breakdown; seen in infections and ischemic brain infarcts (→ cyst).
Describe caseous necrosis with example.
Fragmented cells and amorphous debris; characteristic of tuberculosis.
Describe fat necrosis with example.
Fat cell destruction → saponification; seen in acute pancreatitis.
Describe fibrinoid necrosis with example.
Immune-complex-mediated damage with fibrin leakage; occurs in vasculitis.
Describe gangrenous necrosis with example.
Widespread coagulative necrosis across tissue planes; becomes wet gangrene if infected (e.g., limb ischemia).
What are morphological features of apoptosis?
Cell shrinkage, eosinophilic cytoplasm, chromatin condensation/fragmentation, apoptotic bodies, no inflammation.
Outline the intrinsic apoptosis pathway.
DNA damage or GF withdrawal → BH3-only proteins inhibit BCL2 → BAX/BAK activation → cytochrome c release → caspase cascade → apoptosis.
Outline the extrinsic apoptosis pathway.
Death receptor activation (Fas-FasL, TNF) or perforin/granzyme → adaptor proteins → caspase cascade → apoptosis; eliminates infected or autoreactive T cells.
Describe key events in the caspase cascade.
Initiator caspases activate executioner caspases, leading to DNA fragmentation, cytoskeleton breakdown, apoptotic bodies → phagocytosis.
What is necroptosis?
A programmed, caspase-independent cell death with necrotic morphology (swelling, ROS, rupture).
What is ferroptosis?
Iron-dependent, ROS-driven lipid peroxidation leading to cell death.
What is pyroptosis?
IL-1–mediated, inflammatory cell death that induces fever.
What is autophagy?
A survival mechanism involving stress-induced recycling of damaged organelles and proteins.
What causes intracellular accumulations?
Overproduction, folding/transport defects, enzyme deficiencies, exogenous material uptake.
Describe water accumulation and effect.
↑ membrane permeability or pump failure → hydropic swelling (pale, vacuolated cytoplasm).
Describe triglyceride accumulation and effect.
Fat metabolism dysfunction (liver injury) → steatosis (fatty liver).
Describe cholesterol accumulation and effect.
Macrophage lipid ingestion → foam cells → atherosclerotic plaques → heart disease.
Describe exogenous pigment accumulation.
Carbon from air pollution → anthracosis (lung discoloration).
Describe lipofuscin accumulation.
ROS damage and lipid peroxidation → yellow-brown granules with aging.
Describe hemosiderin accumulation.
Excess iron (hemochromatosis) → golden-brown granules in liver and other tissues.
Describe protein aggregation accumulation.
Misfolded proteins aggregate → proteinopathies like neurodegenerative diseases.
