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Flashcards in Pathology Deck (14):

Types of Necrosis

Coagulative (Heart, liver, kidney; occurs in tissues supplied by end-arteries; inc cytoplasmic binding of acidophilic dye. Proteins denature first, followed by enzymatic degradation), Liquefactive (Brain, bacterial abscess; occurs in CNS due to high fat content. In contrast to coagulative necrosis, enzymatic degradation due to the release of lysosomal enzymes occurs first), Caseous (TB, systemic fungi, Nocardia) Fatty (Enzymatic (pancreatitis[saponification]) and nonenzymatic (e.g. breast trauma); calcium deposits appear dark blue on staining), Fibrinoid (Vasculitides (e.g., Henoch-Schonlein purpura, Churg-Strauss syndrome), malignant hypertension; amorphous and pink on H&E), Gangrenous (Dry (ischemic coagulative) and wet (infection); common in limbs and GI tract.)


Reversible Cell injury

ATP depletion
Cellular/mitochondrial swelling (dec ATP -> dec activity of Na/K pumps)
Nuclear chromatin clumping
dec glycogen
Fatty change
Ribosomal/polysomal detachment (dec protein synthesis)
Membrane blebbing


Irreversible Cell injury

Nuclear pyknosis, karyorrhexis, karyolysis
Plasma membrane damage (degradation of membrane phospholipid)
Lysosomal rupture
Mitochondrial permeability/vacuolization; phospholipid-containing amorphous densities within mitochondria (swelling alone is reversible)


Ischemia susceptible areas

Brain - ACA/MCA/PCA boundary areas (pyramidal cells of hippocampus and Purkinje cells of cerebellum)
Heart - Subendocardium (LV)
Kidney - Straight segment of proximal tubule (medulla). Thick ascending limb (medulla)
Liver - Area around central vein (zone III)
Colon - Splenic flexure, rectum


Distributive shock

Septic, neurogenic, and anaphylactic shock.
High-output failure (dec TPR, inc CO, inc Venous return), Dec PCWP, vasodilation (warm, dry skin), failure to inc blood pressure with IV fluids


Hyovolemic/Cardiogenic shock

Low-output failure (inc TPR, dec CO, dec venous return), inc PCWP in cardiogenic, dec PCWP in hypovolemic, vasoconstriction (cold, clammy patient), blood pressure restored with IV fluids



nodular collections of epitheloid macrophages and giant cells. Outcomes include scarring and amyloidosis


Leukocytes extravastation



Granulomatous diseases

Th1 cells secrete g-interferon, activating macrophages. TNF-a from macrophages induce and maintain granuloma formation. Anti-TNF drugs can, as a side effect, cause sequestering granulomas to breakdown, leading to disseminated disease. Always test for latent TB before starting anti-TNF therapy.


Erythrocyte sedimentation rate

Products of inflammation (e.g., fibrinogen) coat RBCs and cause aggregation. When aggregated, RBCs fall at a faster rate within the test tube. Increase ESR (most anemias, infections, inflammation (e.g. temporal arteritis), cancer (multiple myeloma), pregnancy, autoimmune disorders (SLE)). Decreased ESR (Sickle cell (altered shape), Polycythemia (inc RBCs "dilute" aggregation factors), CHF (unknown))


Disease conditions associated with neoplasms

FA 231


Oncogenes and tumor suppressor genes

FA 232


Psammoma bodies

Laminated, concentric, calcific spherules. Seen in Papullary carcinoma of thyroid, Serous papillary cystadenocarcinoma of ovary, Meningioma, Malignant mesothelioma


Common metastases

FA 236