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Flashcards in 54-Breakdown of Homeostasis Deck (66)
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31

What does increased calcium do

activate enzymes which leads to:
Membrane damage
Nuclear damage
Decreased ATP
trigger apoptosis

32

Most important sites of membrane damage are

Mitochondrial, lysosomal, plasma

33

What does damage to lysosomal membranes do

leak enzymes and digest cell components

34

What does damage to DNA and proteins lead to

Accumulation of damaged DNA, misfolded proteins.

35

What happens when damage exceeds repair mechanisms

apoptosis

36

What is ischemia

Decreased blood flow leading to loss of oxygen and nutrients

37

Does ischemic or hypoxic lead to faster injuries

ischemia

38

What is hypoxia

Decreased oxygen delivery, use anaerobic glycolysis as result

39

What happens to oxygen deprived cells

Decreased ATP, mitochondrial damage, accumulation of ROS, Ca influx

40

What happens during the sequence of changes in cell injury

Quickly lose cell function, but still reversible injury
Death and irreversible, biochemical alterations
ultrastructural changes (EM)
Light microscope changes (AP)
Gross morphological changes

41

How can you reverse cell injury

During early stages if damaging stimulus is removed

42

What are the 2 morphological correlates in reversible injury

Cell swelling
Fatty change

43

What causes cell swelling in reversible injuries

Failure of energy ion pumps, inability to maintain ionic and fluid homeostasis

44

What happens in reversible cell swelling

Loss of microvilli, swollen mitochondria, membrane blebbing

45

What happens in fatty change

Clear lipid vacuoles in cells participating in fat metabolism, caused from chronic alcohol use

46

What 2 characteristics cause irreversibility

Cannot correct mitochondria dysfunction
Profound disruption of membranes

47

What are the common early changes in necrosis

hypereosinophilia-really pink
vacuolization
Nuclear changes (pkynosis, karyorrhexis, karyolysis, disappearance)

48

What are the later changes in necrosis

Coagulation and liquefaction

49

What is coagulative necrosis

autolysis-intrinsic source
Preservation of cell outlines

50

What is a type of coagulative necrosis

Myocardial infarction, ischemic injury

51

What is liquefactive neccrosis

heterolysis-extrinsic source
Loss of cell outline

52

What is a type of liquefactive necrosis

Bacterial abscess

53

What is caseous necrosis

TB infection!!
Cheese like appearance
Aggregate of granular pink material
tissue architecture obliterated

54

What is fat necrosis

Fat destruction from release of pancreatic lipases, liquefy membranes of fat cells

Microscopically-shadowy outline with basophilic calcium deposits

55

What is fibrinoid necrosis

Immune reaction with antigens and antibodies in walls of arteries
Bright pink appearance

56

What is dystrophic calcification

Calcification in dead or dying tissues, seen in plaques

57

What causes intracellular accumulation

Abnormal metabolism
Abnormal protein folding and transport
enzyme defect
Incomplete lysosomal degradation

58

What are some intracellular accumulations

Lipids, proteins, glycogen, pigments

59

What accumulates in Alzheimer's

tau proteins

60

Is necrosis physiologic or non physiologic

ALWAYS PATHOLOGIC