Cell Injury Flashcards

(30 cards)

1
Q

what are some responses to cellular response to stress and injury

A

atrophy

hypertrophy

hyperplasia

metaplasia

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2
Q

what is atrophy?

A

decrease in the size of cells due to loss of cell substance

either physiological or pathological

  • decreased workload
  • loss of innervation
  • diminished blood supply
  • inadequate nutrition
  • loss of endocrine stimulation
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3
Q

what is hypertrophy?

A

increase in the size of the cells resulting in an increase in the size of an organ

reflects increased production of cellular protein

occurs in cells incapable of division

physiological: skeletal muscle in exercise, uterus in pregnancy
pathological: left ventricular hypertrophy in hypertension

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4
Q

what is hyperplasia?

A

increase in the number of cells - usually also the size of the organ

physiologically: breast during pregnancy, after a partial hepatectomy
pathologically: excessive hormonal/growth factor

controlled process but fertile soil for cancer

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5
Q

columnar epithleium is better for what?

A

it is more adapt for acid, bile etc - contains goblet cells which produce mucous

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6
Q

squamus cell epithelium is better adapt for

A

physical strenghth, like skin, doesn’t produce mucous

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7
Q

what is the greatest factor of malnutrition in our country?

A

obesity

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8
Q

cellular response depends on …?

A

on the injury

  • type
  • severity
  • duration
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9
Q

consequences of cellular injury depends on …?

A

The cell

  • type
  • state
  • adaptability
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10
Q

which cell systems are most vulnerable to injuries?

A
  • mitochondria
  • cell membrane- requires energy to maintain
  • synthetic apparatus - proteins and enzymes
  • cytoskeleton
  • genetic apparatus (DNA)
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11
Q

what mechanisms occur with cell injury?

A
  • inhibition of aerobic respiration = ATP depletion
  • generation of oxygen species (free radicals)
  • defects in membrane permeability (ion depletion)
  • disruption of calcium homeostasis (calcium influx)
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12
Q

PET scan detects what?i

A

it shows the activity of cells

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13
Q

describe what occurs when there is a decreased oxidative phosphorylation within the mitochondria?

A
  • decreaed ATP
  • increased anaerobic glycolysis
  • reduced activity of sodium pump
  • increased cytosolic free calcium - activates enzymes
    • ATPase- decreased ATP
    • phospholipase - decreased phospholipids
    • endonuclease - nuclear chromatin damage
    • protease- disruption of membrane and cytoskeletal proteins
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14
Q

normal function of lysozomes?

A

degradation of proteins

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15
Q

what ion, in high concentration, leads to necrosis?

A

calcium

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16
Q

How are free radicals degraded?

A
  • spontaneous decay
  • inactivation by enzymes
  • antioxidants
17
Q

how do free radicals cause cell injury?

A
  • lipid peroxidation of membranes - react with membrane to produce highly reactive lipid peroxide
  • oxidative modification of proteins
  • react with DNA and cause mutation
  • generally cells irreversibly damaged by free radicals are deleted by apoptosis (by gaurdian of the genome = P53)
18
Q

what are the morphological changes associated with reversible cell injury?

A

cellular swelling (liver swells up after a three day drinking binge)

ultrastructural changes: plasma membrane alteration, mitochondrial swelling, dilation of ER with retachment of ribosomes, nuclear alterations

19
Q

what is the definition of necrosis?

A

a live organism experiencing tissue death

so you couldn’t find necrosis on a dead person… becuase all of their tissue is dead

this is important b/c it generates an infection in the surrounding tissues

20
Q

what nuclear changes are associated with necrosis?

A
  • nucleus becomes pale = karyolysis
  • nucleus become small and dense= pyknosis
  • fragment/breakdown of the nucleus = karyorrhexis
21
Q

what is coagulative necrosis?

A

preservation of the structural outlines, with necrosis

characteristic of hypoxic cell death except in the brain

22
Q

what is liquefactive necrosis?

A

transformation of solid tissue into a liquid mass

  • complete digestion of the dead cells leads to a complete loss of the tissue

characteristic of bacterial and some fungal infection , and hypoxic cell death in the CNS and the brain due to very little connective tissue stroma

23
Q

what is fat necrosis?

A

necrosis due to lipases = common in breast

creates a hard mass and is a symptom of malignancy

24
Q

what is gangrenous necrosis?

A

not a distinctive pattern of cell death - but infective in nature

ischaemia with secondary bacterial infection

  • wet gangrene
  • gas gangrene
  • dry gangrene
25
what are some physiological reasons for apoptosis?
* thymus gland after infanthood * endometrial shedding with menstrual cycle * death of inflammatory cells after inflamation * deletion of autoreactive T cells in thymus
26
what is the mechanism of apoptosis?
energy dependent using various genes to regulate plasma membrane remains intact, therefore inflammation is not induced involved in morphogenesis and control of organ size
27
What are the controlling factors of apoptosis?
inhibitors = growth factrs, cell matrix, sex steroids etc inducers = growth factor withdrawal, loss of matrix attachment, glucocorticoids, some viruses, free radicals etc
28
what internal signal leads to apoptosis?
mitochondrial damage
29
what external signal leads to apoptosis?
surface suicide receptor ( FAS CD95) is stimulated
30
dystrophic calcificaiton is what?
calcium level is normal in blood but the tissue is abnormal ex) in cardiology= calcification of coronary arteries, breast calcificaiton due to breast carcinoma