Cell Injury, Adaptations, and Death I and II Flashcards

1
Q

what type of stimuli can cells/organs respond to?

A

physiologic stimuli/stress (response of cells to normal stimuli ex. hormones during pregnancy); pathologic stimuli/stress (cells modify structure or function to decrease or avoid injury or death)

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2
Q

Proliferative capacities of tissues…what are the three groups of proliferative tissues?

A
  • continuoulsy dividing cells (labile; hematopoietic cells, surface epithelia- ex. linings of upper airways, GI tract, skin)
  • stable tissues (quiescent; liver, kidney pancreas, endothelia cells, fibroblasts, smooth muscle cells)
  • permanent tissues (neurons and cardiac muscle cells)
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3
Q

hypertrophy

A

increase in size of cells=increase of size of organ; increased amounts of proteins and organelles.
occurs in cells that have limited or no capacity to divide.

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4
Q

what are some examples of physiologic/pathologic hypertrophy?

A

physiologic: increased functional demand or hormonal stimulation ex. skeletal muscle hypertrophy in weight lifting athlete and uterus in pregnancy
pathologic: ex. cardiac muscle hypertrophy seen in hypertension, aortic valve stenosis

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5
Q

hyperplasia

A

increase in cell number; occurs in cells capable of division (labile and stable cells)

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6
Q

what are some examples of physiologic/pathologic hyperplasia?

A

physiologic: ex. hormonal hyperplasia of female breast in puberty and in pregnancy; compensatory hyperplasia of liver after partial resection; connective tissue response with wound healing
pathologic: excessive stimulation by growth factors or hormones; ex. hormonal imbalance stimulates endometrial hyperplasia-reversible. cells respond to normal regulatory mechanisms. Clinical significance-increases risk for cancer; another example: benign prostatic hyperplasia (BPH)-different than endometrial hyperplasia in that it is not associated with increased risk of prostate cancer; another example: skin warts and mucosal lesions associated with viral infections (papilloma viruses)

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7
Q

what is an example in which an organ/tissue can undergo hyperplasia and hypertrophy at the same time?

A

uterus during pregnancy!

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8
Q

atrophy

A

decrease in size of a cell due to loss of cell substance.
if severe=decreased organ size
decreased protein synthesis and increased degradation
decreased function, but NOT cell death

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9
Q

what are some examples of physiologic and pathologic atrophy?

A

physiologic: loss of hormonal stimulation; ex: endometrium at menopause
pathologic: decreased functional demand (ex. broken arm in cast); loss of innervation (ex. trauma to peripheral nerve); inadequate nutrition (ex. calorie or protein deficit)

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10
Q

in which condition can you see both skeletal muscle hypertrophy and atrophy?

A

myopathy!

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11
Q

Metaplasia

A
  • when one adult cell type is replaced by another adult cell type (that is better able to handle the stress)
  • adaptive process to chronic stress +/or persistent cell injury (ex. chronic smokers, chronic gastric acid reflux)
  • cells are “reprogrammed”
  • reversible
  • may be associated with risk of cancer
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12
Q

epithelial metaplasia

A
  • ciliated columnar epithelium becomes squamous epithelium (ex. trachea/bronchi of smokers)
    • stimulus that causes metaplasia may predispose to development of malignant neoplasm *in this case squamous cell carcinoma of lung)
  • squamous epithelium becomes gastric/intestinal type epithelium (ex. distal esophagus in those with reflux)
    • Barrett Esophagus: protects against reflux of stomach acid (predisposes to development of glandular carcinoma-adenocarcinoma)
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13
Q

mesenchymal metaplasia

A

bone formation in soft tissue (muscle/connective tissue) at sites of injury

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14
Q

what are some causes (etiologies) of cell injury?

A
  • oxygen depravation (hypoxia; ischemia)
  • physical agents (trauma, temperature extremes, radiation, etc.)
  • chemical agents (chemicals-sodium, glucose-, poisons, asbestos, etc.)
  • infectious agents (viruses, fungi, bacterial, parasites, etc.)
  • immunologic reactions (autoimmune diseases, hypersensitivity)
  • genetic derangements (point mutations, polymorphisms)
  • nutritional imbalances (protein/calorie imbalance, vitamin and mineral deficiencies, etc.)
  • aging (decrease ability to repair damage)
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15
Q

what defines irreversible cell damage? and what are two types of irreversible cell death?

A

inability to reverese mitochondrial dysfunction (lack of oxidative phosphorylation and ATP generation); disturbances of membrane function

necrosis and apoptosis

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16
Q
features of necrosis:
cell size?
nucleus?
plasma membrane?
cellular contents?
adjacent inflammation?
physiologic or pathologic role?
A

cell size=enlarged (swelling)
nucleus=pyknosis, karyorrhexis, karyolysis
plasma membrane=disrupted
cellular contents=enzymatic digestion: may leak out of cell
adjacent inflammation=frequent
physiologic or pathologic role=invariably pathologic

17
Q
features of apoptosis:
cell size?
nucleus?
plasma membrane?
cellular contents?
adjacent inflammation?
physiologic or pathologic role?
A

cell size=reduced (shrinkage)
nucleus=fragmentation into nucleosome-sized fragments
plasma membrane=intact: altered structure
cellular contents=intact: may be released in apoptotic bodies
adjacent inflammation=NO
physiologic or pathologic role=often physiologic: eliminating unwanted cells; may be pathologic

18
Q

morphology of reversible cell injury?

A

fatty change; cellular swelling-hydropic change or vacuolar degeneration

19
Q

what are some reasons as to why a fatty liver would develop?

A

accumulation due to any/all of the following (finish from pg 41/108)