Cell Injury Flashcards

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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
Q

what are some physiological reasons for apoptosis?

A
  • thymus gland after infanthood
  • endometrial shedding with menstrual cycle
  • death of inflammatory cells after inflamation
  • deletion of autoreactive T cells in thymus
26
Q

what is the mechanism of apoptosis?

A

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
Q

What are the controlling factors of apoptosis?

A

inhibitors = growth factrs, cell matrix, sex steroids etc

inducers = growth factor withdrawal, loss of matrix attachment, glucocorticoids, some viruses, free radicals etc

28
Q

what internal signal leads to apoptosis?

A

mitochondrial damage

29
Q

what external signal leads to apoptosis?

A

surface suicide receptor ( FAS CD95) is stimulated

30
Q

dystrophic calcificaiton is what?

A

calcium level is normal in blood but the tissue is abnormal

ex) in cardiology= calcification of coronary arteries, breast calcificaiton due to breast carcinoma