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POD > Path > Flashcards

Path Flashcards

1
Q

What are the types of cellular adaptation?

A

atrophy
hypertrophy
hyperplasia
metaplasia

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2
Q

What is atrophy? What is the mechanism? What is a clinical finding?

A

decrease in cell size and number due to autophagic vacuoles or ubiquitin-proteasome
find lipofusin-undigested lipid

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3
Q

What is hypertrophy? What is the mechanism? What are some examples?

A

increase in size of cells
due to growth factors
beta from myosin heavy chains and ANF when chronic HBP

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4
Q

What is hyperplasia? What are some examples?

A

increase in number of cells

endometrial hyperplasia, EPO in high altitude, breast development, HPV

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5
Q

What is metaplasia? What are some examples?

A 
replacement of fully differentiated cell type with another
acid reflux (squamous to glandular in Barrett's esophagus)
smoking-glandular to squamous
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6
Q

What are nondividing cells?

A

cardiac and neurons–>cannot undergo hyperplasia

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7
Q

What are quiescent cells?

A

liver and kidney

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8
Q

What is reversible injury? What is the mechanism?

A

swelling of ER and mitochondria
decrease in oxidative phoshorylation leads to decrease in ATP, decrease in Na/K ATPase, Na stays in cell and water follows it

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9
Q

What are the leading causes of cell injury?

A

hypoxia and ischemia

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10
Q

What is hypoxia?

A

low oxygen

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11
Q

What is ischemia?

A

low oxygen and nutrients

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12
Q

What is infarct?

A

localized area of coagulative necrosis

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13
Q

What is pyknosis?

A

nucleus condensed into clumps

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14
Q

What is karyohexis?

A

nucleus fragments

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15
Q

What is karyolysis?

A

nucleus fully lysed

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16
Q

What is coagulative necrosis? What is the pathological finding?

A

happens from ischemia to all parts except brain
coagulation of proteins
outline without nuclei

17
Q

What is liquefactive necrosis? What would cause it?

A

enzyme digestion into a viscous liquid

abscess due to bacterial infetion or hypoxia in brain

18
Q

What is caseous necrosis? When is it seen?

A

combination of liquefactive and coagulative

TB and fungal infections

19
Q

What is gangrenous necrosis?

A

no blood supply

20
Q

What is fat necrosis?

A

occurs in breast, pancreas, white chalky foci if from lipases

21
Q

What is saponification?

A

free fatty acids+calcium

22
Q

What are pro apoptotic proteins?

A

BAK BAX (allow leakage of cytochrome c)

23
Q

What are anti apoptotic proteins?

A

Bcl2, Bcl-xl, MCL1 (prevent leakage of cytochrome c)

24
Q

What does entry of calcium do to the cell?

A

activates enzymes and increases permeability

increased permeability can cause irreversible injury–>leaking of cytochrome c

25
Q

What are clinical markers of leaking enzymes?

A

CK-MB, Troponin, LDH

coagulative necrosis has occurred

26
Q

What is a reperfusion injury?

A

treat with tPA and blood flow returns but brings increased free radicals
increased oxidative stress

27
Q

What is steatosis?

A

accumulation of triglycerides in the liver due to increased esterification
causes-alcohol, malnutrition, diabetes mellitus, obesity, hypoxia

28
Q

What are xanthomas?

A

deposits of cholesterol in a macrophage

29
Q

What is an extracellular pigment deposition?

A

coal worker’s pneumononiosis

30
Q

What is dystrophic calcification?

A

deposition of calcium on dead tissues
due to atherosclerosis, calcified granulomas, aortic stenosis
normal calcium levels

31
Q

What is metastatic calcification?

A

calcification of normal tissues (lung, kidney, gastric mucosa)
elevated calcium levels
due to multiple myeloma, hyperparathyroidism, bone metastasis, hypervitaminosis D, sarcoidosis
calcium appears deep blue on H and E

POD (4 decks)

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