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Pathology I > P2 - Cellular Injury Adaptation and Death > Flashcards

P2 - Cellular Injury Adaptation and Death Flashcards

1
Q

consequences of cell membrane injury (3 things)

A
  • loss of Na ion pump -> cell swelling
  • abnormal Ca influx -> decrease ATP production and apoptosis
  • injury to rough ER -> inhibition of protein synthesis
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2
Q

Free radicals (3)

A
  • O2
  • H2O2
  • OH
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3
Q

list the antioxidants used a defense mechanism against oxidative stress (5)

A
  • superoxide dismutase (SOD)
  • catalase
  • glutathione preoxidase
  • vitamin E
  • selenium
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4
Q

acute oxidative injury can cause (3 things)

A
  • nutritional myopathy
  • nutritional deficiency to vitamin E &/or selenium
  • demonstrates importance of antioxidative mechanisms
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5
Q

chronic oxidative injury can cause (3 things)

A
  • organ failure
  • accelerate aging
  • carcinogenesis and neoplastic disease
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6
Q

main functions of mitochondria (3 things)

A
  • fatty acid oxidation
  • citric acid cycle (Krebs cycle)
  • oxidatie phosphorylation
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7
Q

vulnerabilities of mitochondria

A
  • diminished ATP -> cell death

- leakage fo Ca -> apoptosis

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8
Q

main functions on nucleus (3 things)

A
  • storage of genetic information
  • maintenance of genetic information
  • transmission of genetic information
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9
Q

nuclear envelope can be damaged by

A

oxidative stress

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10
Q

DNA damage can occur by (4 things)

A
  • reactive oxygen and carbonyl species
  • chemical, drugs, radiation
  • random mutation and replication errors
  • DNA repair malfunction
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11
Q

causes of cell injury (9 things)

A
  • hypoxia
  • physical agents
  • infectious agents
  • nutritional deficiencies and imbalances
  • genetic derangement
  • workload imbalance
  • chemical, drugs, toxins
  • immunologic dysfunction
  • aging
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12
Q

inadequate tissue oxygenation (hypoxia) causes

A
  • reduced blood flow

- reduced oxygen saturation of blood

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13
Q

cell types that are most susceptible to hypoxic injury

A
  • have high metabolic demands

- have poor bloody supply

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14
Q

pathogenesis of hypoxia

A
  • lack of O2 inhibits oxidative phosphorylation -> reduction of ATP -> loss of Na/K pump -> influx of Ca, H2O, Na and efflux of K -> cell swelling
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15
Q

physical agents causing cell injury (6 things)

A
  • trauma
  • extreme cold
  • extreme heat
  • electricity
  • ionizing radiation
  • radiation
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16
Q

types of cellular response to injury (2 types)

A
  • reversible

- irreversible

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17
Q

hydropic degeneration (cell swelling) occurs with (2 things)

A
  • hypoxia

- cell membrane injury

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18
Q

pathogenesis of hydropic degeneration

A
  • injury -> hypoxia -> decreased ATP -> Na and H20 influx & K efflux -> osmotic pressure increases (push in) -> H2O moves into cell -> extensive vacuolation
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19
Q

hydropic degeneration is a ____ cellular response to injury

A
  • reversible
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20
Q

ballooning degeneration

A
  • severe cell swelling in epidermis

- indication of viral infection

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21
Q

cytotoxic edema

A
  • severe cell swelling that occurs in CNS
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22
Q

Necrosis is a _____ cellular response to injury

A
  • irreverisble
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23
Q

apoptosis is a _____ cellular response to injury

A
  • irreversible
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24
Q

oncotic necrosis

A
  • cell swelling beyond point of no return
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25
Q

pathogenesis of oncotic necrosis

A
  • inadequate ATP production -> cytosolic influx of Ca -> activation of destructive enzymatic cascade (proteases and phospholipase) -> self destruct
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26
Q

nuclear changes of necrosis (3 things)

A
  • pyknosis
  • karyolysis
  • karyorrhexis
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27
Q

pyknosis nuclear change

A
  • shrinkage
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28
Q

karyolysis nuclear change

A
  • lysis of nucleus
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29
Q

karyorrhexis nuclear change

A
  • fragmentation of nucleus
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30
Q

cytoplasmic changes of necrosis

A
  • increased eosinophilia and homogeneity
  • loss of cell boundaries - rupture
  • loss of cell adhesion
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31
Q

types of necrosis (4 types)

A
  • coagulation
  • caseation
  • liquefactive
  • gangrenous
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32
Q

types of injury that typically result in coagulation necrosis

A
  • sudden loss of blood supply resulting in severe acute hypoxic injury
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33
Q

is coagulation necrosis acute or chronic

A
  • acute
34
Q

morphologic features of coagulation necrosis

A
  • histologically - retention of cell outlines

- color change is white models surrounded by rim of red hemorrhage

35
Q

types of injury that typically result in caseation (caseous) necrosis

A
  • bacterial infection (intracellular)
36
Q

is caseation (caseous) necrosis acute or chronic

A
  • chronic
37
Q

morphologic features of caseation (caseous) necrosis

A
  • histologically - loss of cell outlines

- mass of granular material (friable and can be pulled apart)

38
Q

type of necrosis that occurs in tissues of CNS

A
  • liquefactive
39
Q

malacia

A
  • formation of gelatinous cavities
40
Q

encephalomalacia

A
  • gelatinous cavities in brain caused by liquefactive necrosis
41
Q

myelomaicia

A
  • gelatinous cavities in spinal cord caused by liquefactive necrosis
42
Q

is liquefactive necrosis (encephalomalacia) acute or chronic

A
  • acute
43
Q

liquefactive necrosis (suppurative inflammation) caused by

A
  • bacterial infection
44
Q

morphologic features of liquefactive necrosis (suppurative inflammation)

A
  • neutrophils resulting in pus
45
Q

liquefactive necrosis (suppurative inflammation) acute form

A
  • abscess
46
Q

liquefactive necrosis (suppurative inflammation) chronic form

A
  • inspissated with caseous texture
47
Q

types of liquefactive necrosis (2 types)

A
  • encephalomalacia - brain and spinal cord

- suppurative inflammation - everywhere else

48
Q

types of gangrenous necrosis (3 types)

A
  • dry
  • moist
  • gas
49
Q

gangrenous necrosis with no bacterial involvement

A
  • dry form
50
Q

are all gangrenous necrosis acute or chronic

A
  • chronic
51
Q

features of dry gangrenous necrosis

A
  • coagulation necrosis followed by mummification
52
Q

gangrenous necrosis with bacterial putrefaction

A
  • moist
53
Q

features of moist gangrenous necrosis

A
  • combination of coagulation and liquefactive necrosis
54
Q

gangrenous necrosis with hemorrhagic exudate with bubbles

A
  • gas
55
Q

features of gas gangrenous necrosis

A
  • necrosis followed by proliferation of anaerobic bacteria with gas production
56
Q

common pathogen of gas gangrenous necrosis

A
  • clostridium spp.
57
Q

programed cell death with cellular shrinkage and without inflammation

A
  • apoptosis
58
Q

apoptotic bodies

A
  • fragmentation of cell into small membrane-bound segments
59
Q

embryogenesis apoptosis

A
  • fetal development and remodeling
60
Q

immunology apoptosis

A
  • immune tolerance

- regulation of inflammatory responses to minimize associated tissue damage

61
Q

pathological apoptosis

A
  • hypoxia
  • withdrawal of growth factors or hormones
  • cell-mediated immune responses (cytokines and T-cells)
  • chemicals and cytotoxic drugs
62
Q

initiation phases of apoptosis (2 ways)

A
  • intrinsic (mitochondrial)

- extrinsic (death receptor-initiated)

63
Q

activation phase of apoptosis

A
  • caspase enzyme cascade
64
Q

chronic injury and cellular adaptation (6 things)

A
  • autophagocytosis
  • changes in cell size, number or appearance
  • pathological calcification
  • intracellular accumulations
  • extracellular accumulations
  • pigment accumulation
65
Q

autophagocytosis (autophagy) purpose

A
  • self digestion (removing junk in cell that isn’t needed)

- can be triggered by fasting

66
Q

autophagocytosis (autophagy) pathogenesis

A
  • damaged organelles enveloped by cell membrane to form autophagosomes that expelled by exocytosis or degraded by lysosomal fusion
  • some vacuoles may persist in cell forming residual bodies filled with ceroid lipofuscin
67
Q

atrophy

A
  • decrease in size of amount of cell, tissue or organ after normal growth
68
Q

hypertrophy

A
  • increase in tissue mass due to increase in individual cell size
69
Q

types of hypertrophy (2 types)

A
  • functional

- hormonal

70
Q

hyperplasia

A
  • increase in tissue mass due to increase in number of cells
71
Q

types of hyperplasia

A
  • physiologic
  • pathologic
  • idiopathic
72
Q

metaplasia

A
  • adaptive change from one adult cell type to another usually due to a chronic stimulus
73
Q

dysplasia

A
  • abnormal growth
74
Q

anaplasia

A
  • dedifferentiation
75
Q

types of pathological calcification (2 types)

A
  • dystrophic

- metastatic

76
Q

dystrophic pathological calcification

A
  • Ca deposition occurs locally at site of injury and necrosis
77
Q

metastatic pathological calcification

A
  • Ca deposition occurs in normal tissue and is secondary to hypercalcemia
78
Q

6 causes of hypercalcemia in vet med

A
  • renal failure leading to secondary hyperparathyroidism
  • primary hyperparathyroidism
  • paraneoplastic - PTH-related protein
  • Vit D toxicosis
  • destructive bone tumor
  • severe granulomatous disease
79
Q

serum calcium concentration in dystrophic calcification

A
  • normal
80
Q

serum calcium concentration in metastatic calcification

A
  • elevated

Pathology I (42 decks)

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