CELLULAR RESPONSES TO STRESS Flashcards by Sam James

Increase in SIZE of cells resulting in increased size of organ; cellular adaptation of non-dividing cells e.g. myocardial fibers

HYPERTROPHY

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Increase in NUMBER of cells

HYPERPLASIA

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REDUCTION in cell SIZE and NUMBER resulting in decreased size of organ

ATROPHY

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A REVERSIBLE change wherein one differentiated cell type is replaced by another cell type

METAPLASIA

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55/M, with long-standing history of hypertension, eventually expired from myocardial infarction. Autopsy: increased thickness of the left ventricular wall with large areas of fibrotic scars. What is the diagnosis, and what cellular adaptation is seen in this case?

Myocardial infarction; Left ventricular hypertrophy; Pathologic hypertrophy

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47 G0, with granulosa cell tumor, presented with menorrhagia. UTZ showed thickened endometrium. Patient underwent diagnostic curettage. Biopsy shows back-to-back endometrial glands with nuclear atypia. What is the diagnosis (for the endometrium), and what cellular adaptation is seen in this case?

Complex atypical hyperplasia; Pathologic hyperplasia

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35/M, with history of poliomyelitis, presented with disproportionately thinner right lower extremity. Muscle Biopsy shows decrease in size of skeletal myocytes. What is the cellular adaptation seen in this case?

Denervation atrophy; Pathologic atrophy

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DENERVATION ATROPHY; PATHOLOGIC ATROPHY

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39/F, with long-standing history of heartburn and water brash. Endoscopy showed multiple pinkish-tan areas at the GEJ. Biopsy shows fragments with simple columnar epithelium with goblet cells. What is the diagnosis, and what specific cellular adaptation is seen in this case?

Barrett esophagus; Intestinal metaplasia

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The first manifestation of almost all forms of injury to cells; change is due to influx of ions (and consequently, water) due to failure of energydependent ion pumps (Na + -K + -ATPase)

CELLULAR SWELLING

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Appearance of lipid vacuoles in the cytoplasm; often seen in cells participating in fat metabolism (liver, heart)

STEATOSIS

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enlarged (swelling)

A. NECROSIS
B. APOPTOSIS

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pyknosis -> karyorrhexis -> karyolysis

A. NECROSIS
B. APOPTOSIS

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disrupted plasma membrane

A. NECROSIS
B. APOPTOSIS

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reduced (shrinkage)

A. NECROSIS
B. APOPTOSIS

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fragmentation into nucleosome-sized fragments

A. NECROSIS
B. APOPTOSIS

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intact plasma membrane
altered structure especially orientation of lipids

A. NECROSIS
B. APOPTOSIS

Intact cellular contents; maybe released in apoptotic bodies

A. NECROSIS
B. APOPTOSIS

No adjacent inflammation

A. NECROSIS
B. APOPTOSIS

often physiologic; may be pathologic

A. NECROSIS
B. APOPTOSIS

Enzymatic digestion; cellular contents leak out of cell

A. NECROSIS
B. APOPTOSIS

A. NECROSIS

frequent adjacent inflammation

A. NECROSIS
B. APOPTOSIS

Invariably pathologic

A. NECROSIS
B. APOPTOSIS

a form of necrosis wherein component cells are dead but the basic tissue architecture is PRESERVED

Coagulative necrosis

Digestion of dead cells, resulting in transformation of the tissue into a viscous liquid mass

Liquefactive necrosis

The term reserved for ischemic coagulative necrosis of the limbs (dry); may have superimposed bacterial infection with liquefactive necrosis (wet)

Gangrenous necrosis

Cheese-like gross appearance of necrotic areas; often seen in tuberculous infections; tissue architecture is NOT PRESERVED

Caseous necrosis

Focal areas of fat destruction, typically seen in acute pancreatitis; foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits (saponification), surrounded by an inflammatory reaction

Enzymatic fat necrosis

Cheese-like gross appearance of necrotic areas; often seen in tuberculous infections; tissue architecture is NOT PRESERVED

caseous necrosis

typically seen in acute pancreatitis; foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits (saponification), surrounded by an inflammatory reaction

Enzymatic fat necrosis

Seen in immune reactions involving blood vessels; deposits of immune complexes, together with fibrin that have leaked out of vessels, result in a bright pink and amorphous appearance

fibrinoid necrosis

acidophilic tombstone

coagulative necrosis

types of apoptosis | initator pathways

intrinsic pathway | extrinsic pathway

mitochondrial pathway | apoptosis

intrinsic (mitochondrial) pathway

death receptor pathway

extrinsic receptor pathway

form of necrosis seen in ischemic injury to most solid organs (heart, spleen, kidney)

coagulative necrosis

form of necrosis from hypoxic death of cells within the CNS

liquefactive necrosis

Inactivation of anti-apoptotic BCL2 protein that leads to activation of BAX/BAK channel, allowing cytochrome c to leak out of the mitochondria, activating apoptosis

Intrinsic (mitochondrial) pathway

Activation of "death receptors" by appropriate ligands that leads to activation of apoptosis

Extrinsic (Death receptor) pathway

Calcium deposition occurring in dead tissues, in the absence of calcium metabolic derangements

Dystrophic calcification

Calcium deposition in normal tissues occurring in the setting of hypercalcemia; example: Calcinosis

Metastatic calcification