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Med 103 > Cellular response to stress and noxious stimuli > Flashcards

Cellular response to stress and noxious stimuli Flashcards

1
Q

what are the properties of disease

A
  • etiology (cause, risk factors)
  • Pathogenesis
  • Morphologic changes
  • Clinical manifestations
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2
Q

what are the changes in response to physiological states (adaptations)

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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3
Q

what is the increase in the size of cells which

increases the size of the organ

A

hypertrophy

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4
Q

what is an example of hypertrophy

A

fat gaining in adipose tissue (weight gain)

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5
Q

what causes

a) Physiologic hypertrophy
b) Pathologic hypertrophy

A

a) hormones, growth factors

b) work overload e.g. exercise

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6
Q

what are the mechanisms of hypertrophy

A

✓Increased production of cellular proteins
✓Switch of adult to fetal or neonatal forms
✓Re-expression of some shut down genes

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7
Q

what is hyperplasia

A

increment in the number of cells in an organ or tissue in response to a stimulus

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8
Q

true or false, hypertrophy and hyperplasia cannot occur at the same time

A

false they can

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9
Q

what kind of cells does hyperplasia only take place

A

in a tissue with cells capable of dividing i.e. not in muscle or nerve cells

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10
Q

what are the mechanisms of hyperplasia

A

✓Growth factor dependent proliferation of mature cells

✓Increased output of new cells from stem cells

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11
Q

what is the opposite of hypertrophy

A

atrophy (reduction in size of an organ or tissue due to a decrement in cell size & number)

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12
Q

where is physiological atrophy usually seen

A

in fetuses

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13
Q

what are the types of pathological atrophy

A 
Disuse atrophy
Denervation atrophy
Senile atrophy
Undernourishement
Loss of endocrine stimulus
Continuous pressure
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14
Q

what are the mechanisms of atrophy

A
  • Nutrient deficiency or disuse

* autophagy (self-eating)

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15
Q

what are residual bodies

A

vesicles containing indigestible materials

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16
Q

what is example of residual bodies

A

Lipofuscin granules in brown atrophy

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17
Q

what is metaplasia

A

is a reversible change in which one differentiated cell type is replaced by another cell type which is better able to withstand the adverse environment

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18
Q

what are examples of metaplasia

A

✓Columnar epithelium → stratified squamous epithelium
✓Stratified squamous → mucinous epithelium
✓Connective tissue metaplasia

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19
Q

what are mechanisms of metaplasia

A

➢Reprogramming of stem cells
➢Reprogramming of mesenchymal cells in connective tissue
➢Cytokines, growth factors, extracellular matrix components causing gene expression and hence differentiation
➢Retinoic acid regulates progenitors derived from tissue stem cells

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20
Q

when does injury develop

A
  • limits of adaptive responses are exceeded
  • cells exposed to ınjurious agents, stress
  • cells are deprived of essential nutrients
  • compromised by mutations
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21
Q

what does reduction in oxidative phosporylation cause

A

→depleting energy stores (ATP)
→ ion pumps are affected then stop
→causing water influx
→ cells swell

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22
Q

what is hypoxia

A

Having low oxygen levels in your tissues

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23
Q

what can cause hypoxia

A
  • Decreased blood flow (ischemia)
  • Cardiorespiratory failure
  • decreased oxygen carrying capacity of the blood
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24
Q

what can cause cell injury and death

A 
oxygen deprivation 
physical agents
chemical agents 
infectious agents 
immunologic response
genetic derangements 
nutritional imbalance
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25
Q

what is the main change that occurs morphologically during reversible injury as seen on a light microscope

A

cellular swelling

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26
Q

what is vacuolar degeneration

A

cells show small clear vacuoles within the cytoplasm

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27
Q

what changes are seen on an electron microscope during reversible injury

A

▪Plasma membrane alterations; blebbing (protrusions of the cell membrane), blunting, loss of microvilli
▪Mitochondrial changes; swelling, small amorphous densities
▪Dilation of ER; detachement of polysomes, intracytoplasmic myelin figures
▪Nuclear alterations; disintegration of granular & fibrillary elements

28
Q

what is it called when cells are lethally injured

A

necrosis

29
Q

why do necrotic cells have a glassy homogenous appearance

A

because of loss of glycogen

30
Q

why do myelin figures appear during cell necrosis

A

due to enzymes digesting the organelles and dead cell is replaced by whorled phospholipid structures called myelin figures

31
Q

what forms in necrotic cells due to damaged membranes

A

calcium soaps causing calcification

32
Q

define these three forms of changes in the nucleus

a) Karyolysis
b) Pyknosis
c) Karyorhexis

A

a) basophilia of the chromatin fades & DNA is dissolved
b) nucleus shrinks, basophilia increases, chromatin condenses into solid shrunken basophilic mass
c) pyknotic (irreversible condensation of chromatin) nucleus undergoes fragmentation

33
Q

what are the types of necrosis

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. gangrenous necrosis
  4. caseous necrosis
  5. fat necrosis
  6. fibrinoid necrosis
34
Q

what is the localized area of coagulative necrosis called

A

infarct

35
Q

what happens to the architecture of dead tissues in coagulative necrosis

A

they are preserved

36
Q

how are necrotic tissues removed in coagulative necrosis

A

by leucocytes

37
Q

coagulative necrosis can affect everywhere except what organ

A

the brain

38
Q

what leads to coagulative necrosis

A

obstructed vessels leading to ischemia (restriction in blood supply to tissues)

39
Q

in coagulative necrosis how long does an anucleated cells persist

A

days or weeks

40
Q

what process is blocked during coagulative necrosis and hence what does it stain

A

proteinolysis (due to enzyme denaturing) , eosinophilic

41
Q

what does hypoxic death of cells within central nervous system often manifest as

A

liquefactive necrosis

42
Q

what forms during liquefactive necrosis and why

A

pus forms because of tissue digestion

43
Q

where does gangrenous necrosis usually occur

A

Seen usually in a limb which lost its blood supply

44
Q

what happens when bacteria superimpose and turn to a liquefactive necrosis

A

wet gangrene

45
Q

in which disease is caseous necrosis usually see

A

tuberculosis

46
Q

what necrosis is usually associated with trauma to the pancreas

A

fat necrosis

47
Q

how does fat saponification in fat necrosis occur

A

when fatty acid combines with calcium forming chalky deposits

48
Q

what happens during fibrinoid necrosis

A

antigen antibody complexes deposit in the arterial walls causing fibrin deposition

49
Q

what do does fibrinoid necrosis stain

A

bright eosinophilic

50
Q

what does response to injurious stimuli depend on

A

the nature of the injury
its duration
severity

51
Q

what causes hypoxia

A

Mechanical arterial obstruction

52
Q

what restores blood flow to ischemic tissue and promotes recovery but paradoxically may exacerbate the injury causing cell death

A

Ischemia-reperfusion

53
Q

what is a complement system

A

enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen’s cell membrane

54
Q

what is toxic injury

A

conversion to toxic metabolites or direct toxicity

55
Q

what is apoptosis

A

a tightly regulated suicide program within the cell

56
Q

what are apoptotic bodies

A

fragments containing portions of nuclear & cytoplasmic material formed during apoptosis

57
Q

what enzyme is mainly responsible for apoptosis

A

caspases

58
Q

what are the mechanisms of apoptosis

A
  1. intrinsic pathway

2. extrinsic pathway

59
Q

in the intrinsic pathway, what does cytochrome bind to in the cytosol

A

apoptosis activating factor1 forming an apoptosome which then binds to caspase-9 triggering a cascade of caspases

60
Q

during intrinsic pathway what happens when the outer cell membrane becomes more permeable

A

release of death inducing pro-apoptotic molecules into the cytoplasm

61
Q

what activates caspase 10 in the extrinsic pathway

A

Cytoplasmic domain intracellular apoptotic signals. the caspase 10 then activates caspase 8

62
Q

what happens during execution phase

A

caspase system cleaves cytoplasmic DNAse inhibitor hence cleaving DNA and leading to dead cell removal

63
Q

give 5 morphological changes during apoptosis

A

cell shrinkage
chromatin condensation
Formation of cytoplasmic blebs & apoptotic bodies
Phagocytosis of apoptotic cells by macrophages
Plasma membranes remain intact

64
Q

which type of necrosis has no inflammation

A

apoptosis

65
Q

what is another name for the extrinsic pathway

A

death receptor-initiated pathway of apoptosis

Med 103 (13 decks)

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