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COM MOD > Robbins Chapter 2 Morphology > Flashcards

Robbins Chapter 2 Morphology Flashcards

1
Q

First manifestation of almost all forms of injury to cells

A

cellular swelling

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2
Q

Appearance when there is cell injury to many cells

A

pallor, increased turgor, increase in weight of organ

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3
Q

Nonlethal injury pattern- distended and pinched off vacuoles in cytoplasm

A

hydropic change or vacuolar degradation

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4
Q

Ultrastructural changes of reversible cell injury

A

plasma membrane alterations
mitochondrial changes
dilation of the ER
nuclear alterations

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5
Q

Plasma membrane alterations in ultrastructural changes of reversible injury

A

blebbing, blunting, loss of microvilli

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6
Q

Mitochondrial changes in ultrastructural changes of reversible injury

A

swelling, small amorphous densities

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7
Q

Dilation of ER in ultrastructural changes of reversible injury

A

detachment of polysomes, myelin figures

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8
Q

Nuclear Alterations in ultrastructural changes of reversible injury

A

disaggregation of granular and fibrillar element

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9
Q

Necrotic cell appearance on histo slide

A

increased eosinophilia in H and E stain due to loss of
cytoplasmic RNA
more glassy homogeneous appearance
myelin figures

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10
Q

Myelin figures

A

large, whorled phospholipid masses that replace dead cells

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11
Q

Characteristics of a necrotic cell

A

discontinuities in plasma and organelle membranes, dilation of mitochondria, large amorphous densities, myelin figures, debris, fluffy denatured proteins

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12
Q

Nuclear changes of necrotic cell (3)

A

karyolysis
pyknosis
karyorrhexis

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13
Q

Karyolysis

A

change the reflects loss of DNA due to enzymatic degradation by endonuclease

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14
Q

Pyknosis

A

nuclear shrinkage and increased basophilia

chromatin condenses into solid, shrunken basophilic mass

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15
Q

Kayorrhexis

A

pyknotic nucleus undergoes fragmentation

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16
Q

Coagulative necrosis

A

architecture of dead tissue is maintained

localized area of coagulative necrosis is called an infarct

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17
Q

Liquefactive necrosis

A

digestion of dead cells
turns tissue into liquid viscous mass
pus can be secreted which contains dead leukocytes

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18
Q

Gangrenous necrosis

A

limb that has lost blood supply and undergone necrosis

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19
Q

Caseous necrosis

A

tuberculous infection most commonly seen
friable white appearance
“cheese-like”

20
Q

Granuloma on microscopic exam

A

caseous necrosis

structureless collection of fragmented or lysed cells

21
Q

Fat necrosis

A

focal areas of fat destruction usually from pancreatic lipase
“chalky white” appearance from fatty acids combining with calcium

22
Q

Fibrinoid necrosis

A

seen in immune reactions involving blood vessels

see immune complexes with antigen and antibodies

23
Q

Necroptosis appearance

A

resembles necrosis morphologically

resembles apoptosis mechanistically as programmed

24
Q

What triggers necroptosis

A

ligation of TNFR1

viral proteins of RNA and DNA viruses

25
Q

What signals are used in necroptosis

A

RIP1 and RIP3

caspase independent

26
Q

Function of RIP1 and RIP3

A

reduce mitochondrial ATP generation
produce ROS
permeabilize lysosomal membranes
cause cellular swelling and membrane damage (necrosis)

27
Q

How does inflammation occur in necroptosis

A

by releasing the cellular contents of the cell

28
Q

When does pyroptosis occur in a cell

A

when a cel is infected by a microbe

29
Q

What is activated in pyroptosis

A

caspase 1 which cleaves the precursor of IL-1 to make IL-1 active

30
Q

What caspases cause death of the infected cell in pyrotosis

A

1 and 11

31
Q

What happens during autophagy

A

sequestration of cellular organelles into autophagic vacuoles (autophagosomes)
fuse with lysosomes
digest the enclosed material

32
Q

What is autophagy

A

adaptive response that is enhanced during nutrient deprivation causing the cell to cannibalize itself to survive

33
Q

What can occur with dysregulation of autophagy

A

disease- cancer, inflammatory bowel diseases, neurodegenerative diseases

34
Q

What accumulates during abnormal deposition of lipids- fatty change

A

free triglycerides in cells from defective transport or excessive intake

35
Q

What accumulates during abnormal deposition of lipids- cholesterol deposition

A

cholesterol from defective catabolism or excesseive takes

36
Q

When is accumulation of cholesterol deposition seen

A

in macrophages and smooth muscle of vessel walls in atherosclerosis

37
Q

What occurs during abnormal deposition of proteins

A

reabsorb proteins in kidney tubules

immunoglobulins in plasma cells

38
Q

Where is deposition of glycogen seen?

A

in macrophages of patients with defect in lysosomal enzymes that break down glycogen

39
Q

How does deposition of pigments occur?

A

through indigestible pigments - carbon lipofuscin or iron

40
Q

What is lipofuscin?

A

breakdown product of lipid peroxidation

41
Q

Dystrophic calcification

A

deposition of calcium at sites of cell injury and necrosis

42
Q

Metastatic calcification

A

deposition of calcium in normal tissues caused by hypercalcemia

43
Q

4 causes of cellular aging

A

accumulation of DNA damage
replicative senescence
defective protein homeostasis
nutrient sensing system

44
Q

How does accumulation of DNA damage cause cellular aging?

A

defective DNA repair systems

caloric restriction activates DNA repair– prolongs aging

45
Q

How does replicative senescence cause cellular aging?

A

reduced capacity of cells to divide secondary to progressive shortening of telomeres

46
Q

How does defective protein homeostasis cause cellular aging?

A

impaired chaperone and proteasome functions

47
Q

How does the nutrient sensing system cause cellular aging?

A

caloric restriction increases longevity

mediators may be reduced by IGF-1 signaling and increasing sirtuins

COM MOD (21 decks)

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