USMLE-First Aid : Adaptations, Inflammation and Neoplasm Flashcards
(174 cards)
Cellular Adaptations
Reversible changes that can be physiologic or pathologic. If stress is excessive or persistent, adaptations can progress to cell injury.
Hypertrophy
↑ structural proteins and organelles → ↑ in size of cells. Example: cardiac hypertrophy.
Hyperplasia
Controlled proliferation of stem cells and differentiated cells→ ↑ in number of cells.
Atrophy
↓ in tissue mass due to ↓ in size and/or number of cells (apoptosis).
Metaplasia
Reprogramming of stem cells → replacement of one cell type by another that can adapt to a new stress. Usually due to exposure to an irritant.
Dysplasia
Disordered, precancerous epithelial cell growth; not considered a true adaptive response. Characterized by loss of uniformity of cell size and shape (pleomorphism); loss of tissue orientation; nuclear changes
Coagulative Necrosis - Seen in :
Ischemia/infarcts in most tissues (except brain)
Coagulative Necrosis - Due to:
Ischemia or infarction; injury denatures enzymes → proteolysis blocked
Coagulative Necrosis - Histology:
Preserved cellular architecture (cell outlines seen), but nuclei disappear; ↑ cytoplasmic binding of eosin stain
Liquefactive Necrosis - Seen in :
Bacterial abscesses, brain infarcts
Liquefactive Necrosis - Due to:
Neutrophils/Microglia release lysosomal enzymes that
digest the tissue
Liquefactive Necrosis - Histology:
Early: cellular debris and macrophages
Late: cystic spaces and cavitation (brain)
Neutrophils and cell debris seen with
bacterial infection
Caseous Necrosis - Seen in :
TB, systemic fungi
Caseous Necrosis - Due to:
Macrophages wall off the infecting microorganism → granular debris
Caseous Necrosis - Histology:
Fragmented cells and debris surrounded
by lymphocytes and macrophages (granuloma)
Fat Necrosis - Seen in :
Enzymatic: acute pancreatitis (saponification of
peripancreatic fat)
Nonenzymatic: traumatic (eg, injury to breast tissue)
Fat Necrosis - Due to:
Damaged pancreatic cells release lipase,
which breaks down triglycerides; liberated fatty acids bind calcium → saponification (chalky white appearance)
Fat Necrosis - Histology:
Outlines of dead fat cells without peripheral nuclei; saponification of fat (combined with Ca2+) appears dark blue on H&E stain
Fibrinoid Necrosis - Seen in :
Immune vascular reactions (eg, Polyarteritis Nodosa)
Nonimmune vascular reactions
(eg, hypertensive emergency-Renal vessels, preeclampsia-Placenta)
Fibrinoid Necrosis - Due to:
Immune complex deposition (type III
hypersensitivity reaction) and/or plasma protein
(eg, fibrin) leakage from damaged vessel
Fibrinoid Necrosis - Histology:
Vessel walls are thick and pink
Gangrenous Necrosis - Seen in :
Distal extremity and GI tract, after chronic ischemia
Gangrenous Necrosis - Due to:
Dry: ischemia
Wet: superinfection
Gangrenous Necrosis - Histology:
Dry- Coagulative
Wet - Liquefactive superimposed on coagulative