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
What are clinical markers of leaking enzymes?
CK-MB, Troponin, LDH | coagulative necrosis has occurred
26
What is a reperfusion injury?
treat with tPA and blood flow returns but brings increased free radicals increased oxidative stress
27
What is steatosis?
accumulation of triglycerides in the liver due to increased esterification causes-alcohol, malnutrition, diabetes mellitus, obesity, hypoxia
28
What are xanthomas?
deposits of cholesterol in a macrophage
29
What is an extracellular pigment deposition?
coal worker's pneumononiosis
30
What is dystrophic calcification?
deposition of calcium on dead tissues due to atherosclerosis, calcified granulomas, aortic stenosis normal calcium levels
31
What is metastatic calcification?
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