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Immunology > 54-Breakdown of Homeostasis > Flashcards

54-Breakdown of Homeostasis Flashcards

1
Q

What is homeostasis

A

normal steady state

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2
Q

What happens when cells encounter physiologic stress

A

They must adapt, get injured, or die

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3
Q

What is the most crucial event in evolution of disease

A

Cell death

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4
Q

What happens after prolonged or severe injury

A

Cell death-necrosis or apoptosis

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5
Q

What are the cellular adaptations to stress

A

Atrophy
Hypertrophy-physiologic or pathologic
Hyperplasia-physiologic or pathologic
metaplasia

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6
Q

What is atrophy

A

Shrinking of cell to preserve function and survive

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7
Q

What is hypertrophy

A

Cell enlarges, limited capacity to divide

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8
Q

What is hyperplasia

A

More cells are produced if they are capable of replication

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9
Q

What is metaplasia

A

Differentiation from one adult cell type to another

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10
Q

What happens to skeletal muscle when it loses its innervation

A

denervation-atrophy, become small and angular

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11
Q

What causes atrophy

A 
Decreased workload
loss of innervation
Diminished blood supply
Inadequate nutrition
Loss of endocrine
aging
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12
Q

what is an example of pathologic hypertrophy

A

Hypertension and enlargement of heart

Muscular Dystrophy

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13
Q

What is an example of physiologic hypertrophy

A

Pregnancy from estrogen

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14
Q

What is an example of physiologic hyperplasia

A

Pregnancy and proliferation of breast tissue

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15
Q

What is the difference between hyperplasia and cancer

A

Hyperplasia is tightly controlled

Cancer has uncontrolled growth

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16
Q

What is an example of metaplasia

A

Chronic smokers
Change of epithelium in branches from columnar to squamous

Gain survival, but loss of protection like mucous secretion and cilia

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17
Q

Why does metaplasia occur

A

One cell type is sensitive to stress and is replaced by a type that can withstand the stress to try to survive

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18
Q

What causes cell injury

A

EVERYTHING
Intrinsic-genetic
Acquired-everything else

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19
Q

What does cell response to injurious stimuli depend on

A

Type, duration, severity

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20
Q

What are the consequences of injurious stimulus

A

Cell type, status, adaptability, genetic make up

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21
Q

Where are the sites of vulnerability for cell injury

A

Mitochondria, calcium, membrane, protein and DNA integrity

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22
Q

What are the morphologic changes from injury

A

Biochemical changes

They are time dependent

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23
Q

What does mitochondrial damage lead to

A

ATP depletion and increase ROS, necrosis and apoptosis

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24
Q

ATP depletion is due to what

A

Decreased oxygen, reduced nutrients, mitochondrial damage, toxins

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25
Q

If you have ATP depletion what can you test for

A

Lactic acidosis in serum blood test

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26
Q

Increase ROS leads to what

A

Damaged lipids, proteins, DNA

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27
Q

How does reduced ATP affect cells

A

Reduced ATP dependent sodium and calcium pumps, anaerobic glycolysis (lactic acid production and decreased pH), disruption of protein synthesis

28
Q

How are ROS formed

A

Produced normally during redox reactions

Produced by phagocytic leukocytes (neutrophils and Macs) for destroying microbes

29
Q

How does ROS contribute to disease

A 
Cancer-mutation from free radicals
atherosclerosis-plaque formation
Aging-accumulative damage
Toxicology-acetaminophen toxicology
hypoxia
30
Q

What are the sources of calcium

A

mitochondria, ER, extracellular space

31
Q

What does increased calcium do

A 
activate enzymes which leads to:
Membrane damage
Nuclear damage
Decreased ATP
trigger apoptosis
32
Q

Most important sites of membrane damage are

A

Mitochondrial, lysosomal, plasma

33
Q

What does damage to lysosomal membranes do

A

leak enzymes and digest cell components

34
Q

What does damage to DNA and proteins lead to

A

Accumulation of damaged DNA, misfolded proteins.

35
Q

What happens when damage exceeds repair mechanisms

A

apoptosis

36
Q

What is ischemia

A

Decreased blood flow leading to loss of oxygen and nutrients

37
Q

Does ischemic or hypoxic lead to faster injuries

A

ischemia

38
Q

What is hypoxia

A

Decreased oxygen delivery, use anaerobic glycolysis as result

39
Q

What happens to oxygen deprived cells

A

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

40
Q

What happens during the sequence of changes in cell injury

A 
Quickly lose cell function, but still reversible injury
Death and irreversible, biochemical alterations
ultrastructural changes (EM)
Light microscope changes (AP)
Gross morphological changes
41
Q

How can you reverse cell injury

A

During early stages if damaging stimulus is removed

42
Q

What are the 2 morphological correlates in reversible injury

A

Cell swelling

Fatty change

43
Q

What causes cell swelling in reversible injuries

A

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

44
Q

What happens in reversible cell swelling

A

Loss of microvilli, swollen mitochondria, membrane blebbing

45
Q

What happens in fatty change

A

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

46
Q

What 2 characteristics cause irreversibility

A

Cannot correct mitochondria dysfunction

Profound disruption of membranes

47
Q

What are the common early changes in necrosis

A

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

48
Q

What are the later changes in necrosis

A

Coagulation and liquefaction

49
Q

What is coagulative necrosis

A

autolysis-intrinsic source

Preservation of cell outlines

50
Q

What is a type of coagulative necrosis

A

Myocardial infarction, ischemic injury

51
Q

What is liquefactive neccrosis

A

heterolysis-extrinsic source

Loss of cell outline

52
Q

What is a type of liquefactive necrosis

A

Bacterial abscess

53
Q

What is caseous necrosis

A

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

54
Q

What is fat necrosis

A

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

Microscopically-shadowy outline with basophilic calcium deposits

55
Q

What is fibrinoid necrosis

A

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

56
Q

What is dystrophic calcification

A

Calcification in dead or dying tissues, seen in plaques

57
Q

What causes intracellular accumulation

A

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

58
Q

What are some intracellular accumulations

A

Lipids, proteins, glycogen, pigments

59
Q

What accumulates in Alzheimer’s

A

tau proteins

60
Q

Is necrosis physiologic or non physiologic

A

ALWAYS PATHOLOGIC

61
Q

What are the 2 ways to initiate apoptosis

A

Mitochondrial/intrinsic

Death receptor/extrinsic

62
Q

nonmorphologic characteristics of necrosis

A

Pathologic, no gene transcription, unregulated, no energy, lysosome disruption, cell membrane leakage

63
Q

Non morphologic characteristics of apoptosis

A 
Physiologic and non physiologic
Gene transcription
Highly regulated
Needs energy
Cleave chromatic
Lysosome intact
cell membrane intact
64
Q

Morphologic characteristics of necrosis

A 
Death of groups
karyolysis and karyorrhexis
organelles destroyed
Swelling
Inflammatory response
65
Q

Morphologic characteristics of apoptosis

A 
Death in individual cells
Chromatic clumping
Organelles preserved
Cell shrinkage
No inflammation
66
Q

Biochemical pathway that can be manipulated by pharmacology

A

Apoptosis-cancer

Immunology (19 decks)

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