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Intro to path > cellular adaptations I and II > Flashcards

cellular adaptations I and II Flashcards

1
Q

What are the 3 proliferative capacities of tissues

A

continuously dividing cells (or labile cells)
stable tissues
permanent tissues

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2
Q

ex of continuously dividing cells/labile cells

A 
hematopoietic cells
surface epithelia (upper airway, GI, skin...)
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3
Q

definition of stable tissues

A

minimal replication usually
proliferate in response to injury
parenchyma of most solid organs like kidney, liver, pancreas
endothelial cells, fibroblasts, smooth muscle

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4
Q

definition of permanent tissues

A

non-proliferative

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5
Q

ex of permanent tissues

A

neurons

cardiac muscle cells

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6
Q

define hypertrophy

A

increase in size of cells, leading to increased organ size

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7
Q

what kinds of cells undergo hypertrophy?

A

cells that have limited or no capacity to divide

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8
Q

physiologic hypertrophy can occur due to

A

increased functional demand or hormonal stimuli

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9
Q

ex of physiologic hypertrophy

A

skeletal muscle hypertrophy in weight lifter

uterus in pregnancy

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10
Q

ex of pathologic hypertrophy

A

cardiac muscle hypertrophy in HTN

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11
Q

define hyperplasia

A

increased cell number

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12
Q

in what kind of cells does hyperplasia occur?

A

those that are able to divide (labile and stable)

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13
Q

ex of physiologic hyperplasia

A

female breast at puberty, pregnancy
compensatory hyperplasia in liver after partial resection
would healing-connective tissue

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14
Q

pathologic hyperplasia examples

A

excessive hormones–>endometrial hyperplasia

benign prostatic hyperplasia

skin warts and mucosal lesions associated with viruses (papilloma virus)

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15
Q

what differentiates pathologic hyperplasia from cancer?

A

pathologic hyperplasia cells respond to normal regulatory mechanisms (it’s just that there is excessive stimulation)
in cancer, abnormal regulation

however, pathologic hyperplasia increases the risk for cancer

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16
Q

enlargement of uterus in pregnancy is ex of

A

both hyperplasia and hypertrophy

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17
Q

atrophy definition

A

decrease in size of cell due to loss of cell matter

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18
Q

causes of atrophy include

A

physiologic and pathologic

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19
Q

ex of physiologic atrophy

A

endometrium at menopause (loss of hormones)

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20
Q

ex of pathologic atrophy

A

decreased function (broken arm in cast)
loss of innervation (trauma to nerve)
inadequate nutrition

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21
Q

metaplasia defintion

A

one adult cell type is replaced by another adult cell type (to better tolerate the stress)

  • is an adaptive process to chronic stress (ex. chronic smoking, chronic gastric acid reflux..)
  • stem cells differentiate through a new pathway
  • may be associated with greater chance of cancer
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22
Q

types of metaplasia

A

epithelial

mesenchymal

23
Q

Barrett esophagus is example of

A

epithelial metaplasia (squamous epithelium turns into glandular epithelium like that in stomach)

24
Q

causes of cell injury and give examples of each

A 
oxygen deprivation (hypoxia, ischemia)
physical agents (trauma, temperature, radiation)
chemical agents (chemicals like sodium and glucose, poisons, asbestos)
infectious agents
immunologic reactions (autoimmune diseases, hypersensitivity)
genetic (point mutations, polymorphisms)
nutritional imbalance (protein/calories, viatmin and mineral deficiency)
aging (lowered ability to repair damage)
25
Q

Types of cell injury

A

reversible

irreversible

26
Q

is swelling of ER and mitochondria, membrane blebs in a cell reversible or irreversible?

A

reversible

27
Q

Differences btwn necrosis and apoptosis

A

cell size: swelling for necrosis, shrinkage for apoptosis

nucleus:
necrosis-pyknosis (condensation of chromatin), karyorrhexis (fragmentation of nucleus), karyolysis (breakdown of nuclear membrane)
apoptosis-fragmentation into nucleosome-size fragments

plasma membrane:
necrosis-disrupted
apoptosis-intact

cellular contents
necrosis-enzymatic digestion and may leak out of cell
apoptosis-intact

adjacent inflammation

necrosis: frequent
apoptosis: none

physiologic or pathologic

necrosis: always pathologic
apoptosis: often physiologic to eliminate unwanted cells but myay be pathologic

28
Q

reversible cell injury

A

fatty change-lipid vacuoles in cytoplasm, primarily in cells depending on fat metabolism

cellular swelling-results from failure of membrane pumps to maintain homeostatis so get membrane blebs, vacuoles appear in cells corresponding to distended ER

29
Q

necrosis morphology

A

increased eosinohpilia
nuclear shrinkage, fragementation
breakdown of plasma membrane and organelle membranes

30
Q

coagulative necrosis

A

due to hypoxic or anoxic injury due to ischemia

persistence of dead cells w/ intact outlines but with loss of cellular details

occurs in all solid organs except brain

31
Q

liquefactive necrosis

A

complete digestion of dead cells (tissue is semi-liquid) and no residual tissue architecture preserved

commonly seen with bacterial, fungal infec (WBCs release digestive enzymes, necrotic cells with acute inflammatory cells become pus)

exception: brain infarcts become liquefactive necrosis

32
Q

caseous necrosis

A

think TB
resembles cheese (crumbly)
fragmented and coagulated cells, loss of tissue architecture so no cell outlines
usually surrounded by border of inflammatory cells (granuloma)

33
Q

gangrenous necrosis

A

not a specific type of necrosis but used for ischemic coagulative necrosis of lower or upper extremity

can be wet or dry gangrene

also used for severe necrosis of other organs

34
Q

ex of gangrenous necrosis

A

discoloration of toes in diabetic

gangrenous bowel

35
Q

fat necrosis

A

usually seen in pancreas in acute pancreatitis b/c injury to pancreas releases lipase which liquefies fat (fatty acids combine with Ca2+ to make chalky white material)

also in trauma to fatty tissue with release of lipases and triglycerides

36
Q

ex of fat necrosis

A

acute pancreatitis

fat necrosis of breast in trauma

37
Q

fibrinoid necrosis

A

deposition of immune complexes (antigens and antibodies) in vascular wall

looks like fibrin, pink and fuzzy

occurs in vasculitis syndromes

38
Q

principal targets within a cell due to injury

A

mito (depletion of ATP and increased ROS)
calcium homeostatis (intracellular entry of Ca)
cellular membranes (increased permeability, also think lysosome)
DNA and cellular proteins (damage to DNA and protein misfolded)

39
Q

what results from mitochondrial damage/ATP depletion?

A

Na pump fxn decreases, get influx of calcium and sodium and water–leads to ER swelling, cellular swelling, loss of microvilli and blebs

increase anaerboic glycolysis leading to decreased pH and clumping of nuclear chromatin

production of ROS

40
Q

what are the effects of increased intracellular calcium in cell injury?

A

membrane damage, nuclear damage, decreased ATP

41
Q

effects of decreased oxygen on cell function?

A

membrane damage is an example

42
Q

ischemia vs hypoxia

A

ischemia is worse because no delivery of substrates for glycolysis and no removal of metabolites by blood flow

43
Q

specific examples of cell injury

A

ischemic vs hypoxic injury
reperfusion injury
chemical (toxic) injury-direct toxin or toxic metabolites

44
Q

death induced by cytotoxic T lymphocytes is an example of what type of cell death

A

physiologic apoptosis

45
Q

pathologic apoptosis examples

A

eliminating cells with DNA damage
cell injury induced by viral infec
accumulation of misfolded proteins
organ atrophy with duct obstruction

46
Q

morphology of apoptosis

A

cytoplasmic eosinophilia
chromatin condesation and aggregation, eventually karyorrhexis
cell shrinkage with cytoplasmic blebs and apoptotic bodies
phagocytosis w/o inflammation

47
Q

how does lipofuscin develop in heart muscle? clinical significance?

A

results from lipid peroxidation
occurs with aging
especially in heart, liver, brain

48
Q

how does Lysosomal storage disease occur? significance?

A

lysosomal dysfxn in breaking down a molecule, so large amts accumulate

49
Q

anthracosis in lung

A

carbon from air in lung

50
Q

accumulation of cytoskeleton abnormalities occurs how?

A

due to toxins like alcohol or unknown causes

51
Q

Hemosiderin accumulates how?

A

occurs locally when there’s been hemorrhage

or systemic deposition with increased iron absorption, in anemias, w/many transfusions, etc.

52
Q

dystrophic vs metastatic calcification?

A

dystrophic:

  • in damaged or dying tissue
  • normal serum calcium
  • gross apperance is white gritty deposits
  • microscopically looks basophilic

metastatic:

  • normal tissues
  • hypercalcemia
  • commonly in interstitial tissues
53
Q

cellular aging

A

dna damage
decreased cellular replication
defective protein homeostasis

Intro to path (15 decks)

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