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TOPNOTCHER PEDIA > CELLULAR RESPONSES TO STRESS > Flashcards

CELLULAR RESPONSES TO STRESS Flashcards

1
Q

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

A

HYPERTROPHY

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2
Q

Increase in NUMBER of cells

A

HYPERPLASIA

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3
Q

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

A

ATROPHY

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4
Q

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

A

METAPLASIA

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5
Q

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?

A

Myocardial infarction; Left ventricular hypertrophy; Pathologic hypertrophy

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6
Q

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?

A

Complex atypical hyperplasia; Pathologic hyperplasia

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7
Q

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?

A

Denervation atrophy; Pathologic atrophy

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8
Q

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?

A

DENERVATION ATROPHY; PATHOLOGIC ATROPHY

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9
Q

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?

A

Barrett esophagus; Intestinal metaplasia

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10
Q

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)

A

CELLULAR SWELLING

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11
Q

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

A

STEATOSIS

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12
Q

enlarged (swelling)

A. NECROSIS
B. APOPTOSIS

A

A.

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13
Q

pyknosis -> karyorrhexis -> karyolysis

A. NECROSIS
B. APOPTOSIS

A

A.

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14
Q

disrupted plasma membrane

A. NECROSIS
B. APOPTOSIS

A

A.

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15
Q

reduced (shrinkage)

A. NECROSIS
B. APOPTOSIS

A

B.

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16
Q

fragmentation into nucleosome-sized fragments

A. NECROSIS
B. APOPTOSIS

A

B.

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17
Q

intact plasma membrane
altered structure especially orientation of lipids

A. NECROSIS
B. APOPTOSIS

A

B.

18
Q

Intact cellular contents; maybe released in apoptotic bodies

A. NECROSIS
B. APOPTOSIS

A

B.

19
Q

No adjacent inflammation

A. NECROSIS
B. APOPTOSIS

A

B.

20
Q

often physiologic; may be pathologic

A. NECROSIS
B. APOPTOSIS

A

B.

21
Q

Enzymatic digestion; cellular contents leak out of cell

A. NECROSIS
B. APOPTOSIS

A

A. NECROSIS

22
Q

frequent adjacent inflammation

A. NECROSIS
B. APOPTOSIS

A

A.

23
Q

Invariably pathologic

A. NECROSIS
B. APOPTOSIS

A

A.

24
Q

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

A

Coagulative necrosis

25
Q

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

A

Liquefactive necrosis

26
Q

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

A

Gangrenous necrosis

27
Q

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

A

Caseous necrosis

28
Q

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

A

Enzymatic fat necrosis

29
Q

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

A

caseous necrosis

30
Q

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

A

Enzymatic fat necrosis

31
Q

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

A

fibrinoid necrosis

32
Q

acidophilic tombstone

A

coagulative necrosis

33
Q

types of apoptosis

initator pathways

A

intrinsic pathway

extrinsic pathway

34
Q

mitochondrial pathway

apoptosis

A

intrinsic (mitochondrial) pathway

35
Q

death receptor pathway

A

extrinsic receptor pathway

36
Q

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

A

coagulative necrosis

37
Q

form of necrosis from hypoxic death of cells within the CNS

A

liquefactive necrosis

38
Q

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

A

Intrinsic (mitochondrial) pathway

39
Q

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

A

Extrinsic (Death receptor) pathway

40
Q

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

A

Dystrophic calcification

41
Q

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

A

Metastatic calcification

TOPNOTCHER PEDIA (30 decks)

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