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T22 - Cell Injury I Flashcards

1
Q

What are physiologic adaptations?

A

response of cells to normal stimuli

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2
Q

What are pathologic adaptations?

A

response of cells to stress that allow them to modulate structure/function and escape injury

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3
Q

Give an example of a physiologic adaptation.

A

hormone-induced enlargement of uterus and breasts during pregnancy

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4
Q

Give an example of a pathologic adaptation.

A

reversible changes in number/size/metabolic activity of cells

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5
Q

What are the four primary morphologic adaptations to stress in cells?

A

hyperplasia

hypertrophy

metaplasia

atrophy

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6
Q

What cellular processes are associated with hyperplasia? (2)

A

DNA synthesis

mitosis

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7
Q

What cellular processes are associated with hypertrophy?

A

synthesis of cell components

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8
Q

What cellular processes are associated with metaplasia?

A

genetic reprogramming of stem cells

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9
Q

What cellular processes are associated with atrophy?

A

deeply eosinophilic cytoplasm

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10
Q

What is hyperplasia? (2)

A

increase in number of cells because of proliferation of differentiated cells by tissue stem cells

this is the response when cells are capable of division

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11
Q

What is hypertrophy?

A

cells can’t divide, so cells increase in size instead

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12
Q

What is metaplasia?

A

reversible change from one differentiated cell type to another (i.e. reprogramming of stem cells)

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13
Q

What is atrophy?

A

decrease in cell size because of loss of cell substance

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14
Q

Give an example of hormonal physiologic hyperplasia.

A

female breast enlargement at pregnancy and puberty

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15
Q

Give an example of compensatory physiologic hyperplasia.

A

liver regenerates after resection

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16
Q

Explain how hyperplasia differs from cancer.

A

if signal abates, hyperplasia disappears (hyperplastic responses remain controlled)

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17
Q

Give two examples of physiologic hypertrophy.

A

estrogen-stimulated smooth muscle hypertrophy in uterus during pregnancy

striated skeletal muscle hypertrophy in response to weightlifting

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18
Q

Give an example of pathologic hypertrophy.

A

left ventricle enlargement of heart (cardiomyocytes can’t divide) due to hypertension or aortic valve disease

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19
Q

What is the basis of metaplasia?

A

reprogramming of stem cells (not due to transdifferention)

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20
Q

Give three examples of metaplasia.

A

esophagus: stratified squamous → simple columnar
lungs: pseudostratified → stratified squamous
cervix: simple columnar → stratified squamous

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21
Q

What is the basis of atrophy?

A

decrease in cell size because of loss of cell substance

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22
Q

What system mediates the degradation associated with atrophy?

A

ubiquitin-proteasome pathway

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23
Q

Give two examples of physiologic atrophy that result from decreased work load.

A

immobilization of a limb (casts/arthritis)

space flight

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24
Q

What two factors can contribute to physiologic atrophy?

A

decreased work load

aging

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25
Give an example of aging-induced physiologic atrophy.
postmenopausal atrophy of breast and vaginal tissue because of decreased hormone stimulation
26
What two factors contribute to pathologic atrophy?
loss of innervation endocrine stimulation
27
Give two examples of pathologic atrophy resulting from loss of innervation.
neuromuscular disease spinal trauma
28
Give an example of pathologic atrophy resulting from endocrine stimulation.
adrenal cortical atrophy secondary to exogenous steroids
29
What are the two primary causes of cellular injury?
hypoxia ischemia
30
What is hypoxia?
oxygen deficiency due to interference with aerobic oxidative respiration
31
What is the most common cause of cell injury/death?
hypoxia
32
What is ischemia?
loss of blood supply in tissue due to impeded arterial flow or reduced venous drainage
33
What causes hypoxia? (3)
ischemia pneumonia (inadequate oxygenation of blood) reduction in oxygen-carrying capacity of blood
34
What are the histological changes observed following reversible cell injury? (2)
cellular swelling: failure of ion pumps in plasma membrane fatty change
35
What are the electron microsocope changes observed following reversible cell injury? (4)
ER swelling mitochondrial swelling membrane blebs clumped chromatin
36
What is coagulative necrosis? (3)
cell is dead, but underlying tissue architecture intact affected tissue is firm characteristic of infarcts in all solid organs except brain
37
What are three subtypes of coagulative necrosis?
gangrenous dry gangrene wet gangrene
38
What is gangrenous coagulative necrosis?
type of coagulative necrosis applied to necrosis of distal limb
39
What is dry gangrene?
results from loss of blood supply (common in DM patients)
40
What is wet gangrene?
gangrene involving bacterial infection that has "wet" appearance due to release of bacterial enzymes and associated neutrophil response
41
Define pyknosis.
irreversible condensation of chromatin in nucleus of cell undergoing necrosis or apoptosis
42
Define karyorrhexis.
fragmentation of nucleus of dying cell in which chromatin irregularly distributed throughout cytoplasm
43
Define karyolysis.
complete dissolution of chromatin of dying cell due to enzymatic degradation by endonucleases
44
Where is caseous necrosis most commonly observed?
caseous necrosis most commonly seen in foci of tuberculosis infection
45
Describe the histologic presentation of caseous necrosis. (2)
tissue architecture lost and replaced with amorphous pink material surrounded by epithelioid cells and giant cells (granuloma)
46
What is liquefactive necrosis?
transformation of the tissue into a liquid viscous mass, often in response to focal bacterial or fungal infection
47
Define homeostasis.
ability of organism/cell to maintain internal equilibrium by adjusting physiological processes
48
Describe the events that occur in liquefactive necrosis. (2)
microbes attract neutrophils neutrophilic enzymes digest (liquefy) tissue, producing pus
49
Hypoxic death in the brain is typically attributed to what cell adaptation?
liquefactive necrosis
50
What is fat necrosis?
focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into peritoneal cavity and mesenteric fat
51
Give two examples of diseases/events that can result in fat necrosis.
acute pancreatitis motor vehicle accidents
52
In a gross specimen of the pancreas, what features indicate fat necrosis?
chalky white lesions scattered throughout tissue
53
Describe the process of fat necrosis on a cellular level. (4)
lipases split TGs in adipocytes liberated fatty acids combine with calcium results grossly in chalky white areas (saponification of fat) results histologically in basophilic calcium deposits
54
What is fibrinoid necrosis?
immune reactions with deposition of antigen-antibody complexes in blood vessels
55
Describe how fibrinoid necrosis is observed.
can only be observed histologically immune complexes with fibrin that's leaked from blood vessels produces _bright, pink_ amorphous appearance absence of nuclear material
56
What is dystrophic calcification? (2)
serum calcium is normal deposition of calcium in degenerating of necrotic tissue
57
Give an example of dystrophic calcification.
deposition of calcium in arotic valve of person with left ventricular failure [*note: in the image, an antecedent bacterial infection damaged the valve*]
58
What is metastatic calcification?
serum calcium abnormal ectopic calcification in setting of elevated serum calcium, caused by increased parathyroid hormone
59
Give three examples of diseases/conditions that can lead to metastatic calcification.
primary parathyroid tumor parathyroid related hormone (malignant tumors) renal failure (phosphate retention causes secondary parathyroid hormone)
60
What is the relationship between dystrophic and metastatic calcification?
metastatic calcification can _exacerbate_ dystrophic calcification
61
What are the symptoms of benign prostatic hyperplasia?
problems with urinary retention or urinating, caused by urinary obstruction
62
What causes benign prostatic hyperplasia?
problem with the 5-alpha reductase enzyme, which converts testosterone to dihydrotestosterone
63
What are the histologic changes associated with benign prostatic hyperplasia?
increase in glandular areas caused by papillary infoldings intervening stroma that is smaller than normal
64
What is the relationship between hypoxia and ischemia?
ischemia, a reversible injury, is the _most common cause_ of hypoxia
65
What are the two mechanisms that can lead to cardiac hypertrophy?
mechanical triggers, such as stretching trophic triggers, such as growth factors or adrenergic hormones
66
Describe how trophic triggers lead to cardiac hypertrophy. (4)
turn on genes → stimulate protein synthesis → more myofilaments → increased contractility to meet demand
67
What are the histological changes observed following irreversible cell injury? (4)
disruption of cell membranes (leakage, dissolution) pronounced eosinophilia (more eosin binding to cytoplasmic proteins) changes to nucleus (shrinkage, breakdown) inflammatory response (lysosomal enzymes)
68
What are the electron microscope changes observed following irreversible cell injury? (3)
breaks in plasma membrane/organelle membranes large amorphous densities in mitochondria marked mitochondrial swelling
69
(T/F) Pyknosis, karyorrhexis and karyolysis occur in sequence.
**False**. They do not happen in sequence. The order in which they occur depends on the injury and on time.
70
What are the five common patterns of necrosis?
coagulative caseous liquefactive fat fibrinoid
71
Necrosis most commonly results from (2)
metabolic failure depletion of ATP
72
What is an abscess?
inflammatory response to an infectious agent
73
Caseous necrosis is most commonly observed in which organ?
lung
74
Which forms of necrosis occur most commonly in the lungs? (2)
coagulative necrosis caseous necrosis
75
Which kind of necrosis commonly occurs in the brain?
liquefactive necrosis

Tissues (23 decks)

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