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Intro to path > cellular adaptations I and II > Flashcards

cellular adaptations I and II Flashcards

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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

Study These Flashcards
A

epithelial

mesenchymal

23
Q

Barrett esophagus is example of

Study These Flashcards
A

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

24
Q

causes of cell injury and give examples of each

Study These Flashcards
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
Types of cell injury
reversible | irreversible
26
is swelling of ER and mitochondria, membrane blebs in a cell reversible or irreversible?
reversible
27
Differences btwn necrosis and apoptosis
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
reversible cell injury
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
necrosis morphology
increased eosinohpilia nuclear shrinkage, fragementation breakdown of plasma membrane and organelle membranes
30
coagulative necrosis
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
liquefactive necrosis
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
caseous necrosis
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
gangrenous necrosis
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
ex of gangrenous necrosis
discoloration of toes in diabetic | gangrenous bowel
35
fat necrosis
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
ex of fat necrosis
acute pancreatitis fat necrosis of breast in trauma
37
fibrinoid necrosis
deposition of immune complexes (antigens and antibodies) in vascular wall looks like fibrin, pink and fuzzy occurs in vasculitis syndromes
38
principal targets within a cell due to injury
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
what results from mitochondrial damage/ATP depletion?
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
what are the effects of increased intracellular calcium in cell injury?
membrane damage, nuclear damage, decreased ATP
41
effects of decreased oxygen on cell function?
membrane damage is an example
42
ischemia vs hypoxia
ischemia is worse because no delivery of substrates for glycolysis and no removal of metabolites by blood flow
43
specific examples of cell injury
ischemic vs hypoxic injury reperfusion injury chemical (toxic) injury-direct toxin or toxic metabolites
44
death induced by cytotoxic T lymphocytes is an example of what type of cell death
physiologic apoptosis
45
pathologic apoptosis examples
eliminating cells with DNA damage cell injury induced by viral infec accumulation of misfolded proteins organ atrophy with duct obstruction
46
morphology of apoptosis
cytoplasmic eosinophilia chromatin condesation and aggregation, eventually karyorrhexis cell shrinkage with cytoplasmic blebs and apoptotic bodies phagocytosis w/o inflammation
47
how does lipofuscin develop in heart muscle? clinical significance?
results from lipid peroxidation occurs with aging especially in heart, liver, brain
48
how does Lysosomal storage disease occur? significance?
lysosomal dysfxn in breaking down a molecule, so large amts accumulate
49
anthracosis in lung
carbon from air in lung
50
accumulation of cytoskeleton abnormalities occurs how?
due to toxins like alcohol or unknown causes
51
Hemosiderin accumulates how?
occurs locally when there's been hemorrhage | or systemic deposition with increased iron absorption, in anemias, w/many transfusions, etc.
52
dystrophic vs metastatic calcification?
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
cellular aging
dna damage decreased cellular replication defective protein homeostasis

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