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Pathophysiology > cpt 4: cell injury, aging and death > Flashcards

cpt 4: cell injury, aging and death Flashcards

1
Q

cellular swelling and the accumulation of excess substance within the cell is frequently seen with what cell inury?

A

Reversible cellular injury

early stages of irreversible cellular injury

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2
Q

cellular adaption

A

generally reversible
may be detrimental to cell
results in changing structure or function of cell

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3
Q

Necrosis

A

type of irreversible cell injury leading to death of tissue

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4
Q

gangrene

A

type of necrosis that can be described as wet, dry, or gas

determination based upon location and appearance.

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5
Q

proteasomes

A

degrade intracellular proteins

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6
Q

telomeres

A

get shorter with each cell division, leading to cell aging

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7
Q

normal intracellular substances that accumulate in injured cells (4)

A

lipids
carbohydrate
glycogen
protein

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8
Q

adaption response: swim team student with increased skeletal muscle mass

A

beneficial hypertrophy

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9
Q

adaption response: cardiovascular pt with BLE hair loss and skin thinning

A

pathologic ischemic atrophy

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10
Q

adaption response: ETOH addiction and hepatomegaly

A

pathologic hypertrophy

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11
Q

adaption response: development of breast in puberty

A

beneficial hypertrophy

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12
Q

adaption response: increase in RBC when training in high altitude mountains

A

beneficial hyperplasia

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13
Q

adaption response: epithelium changes in bladder as a result of chronic cystitis

A

pathologic hyperplasia

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14
Q

adaption response: calluses on hands

A

pathologic hyperplasia

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15
Q

adaption response: cervical cells with abnormal variations in size, shape, and arrangement

A

pathologic dysplasia

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16
Q

adaption response: conversion of bronchial ciliated columnar epithelium to stratified squamous epithelium in smoking pt.

A

pathologic metaplasia

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17
Q

types of tissue necrosis with examples: 4

A

coagulative: MI
liquefactive: abscess
fat: cyst after breast surgery
caseous: damaged lung from TB

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18
Q

Common etiologies of cellular injury (5)

A 
ischemia and hypoxic injury
nutritional injury
infectious and immunologic injury
chemical injury
physical and mechanical injury
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19
Q

Na/K pump failure to remove Na probable cause of

A

cellular swelling during early stages of cell injury

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20
Q

glandular tissues response to increased functional demand

A

hyperplasia

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21
Q

steps of coagulative necrosis (4)

A
  1. ischemic cellular injury
  2. plasma membrane unable to maintain electrochemical gradient
  3. influx of Ca and mitochondrial dysfunction
  4. degradation of plasma membrane and nuclear structures.
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22
Q

hypoxia due to ischemia results in (3)

A

lactic acidosis
hydropic swelling
reduced ATP production

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23
Q

hydropic swelling: malfunction of Na/K pump

A

accumulation of Na in cell, creating osmotic gradient for water.
pump needs ATP: decease ATP leads to dysfunction, leads to swelling

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24
Q

organ enlargement

A

swelling of cells in a particular organ

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25
reasons for accumulation of normal substances inside cell (2)
faulty metabolism: excess storage | absent enzyme: no breakdown
26
lipid accumulation: location and causes
liver excessive alcohol intake genetic disorders: enzymes needed to metabolize lipids is impaired.
27
carbohydrate accumulation: cause
lysosomal enzyme degradation of these is impaired
28
glycogen accumulation
common with diabetes, excess sugar is stored.
29
accumulation of protein cause
denatured proteins due to cellular stress, may cause dysfunction and death. chaperones will try to correct defect 
30
ubiquitin
protein that binds with abnormal proteins creating a complex that enters a proteosome where proteins are digested into fragments.
31
accumulation of pigments and inorganic particles (2)
endogenous: produced by body: hemosiderin, bilirubin exogenous: introduced form outside: tar, mineral dust.
32
atrophy
cells shrink and reduce their differentiated functions.
33
disuse: reasoning and leads to
bedrest, casting | leads to atrophy
34
denervation: reasoning and leads to
loss of nervous stimulation -> decrease muscle size | leads to atrophy
35
ischemia
loss of blood supply | leads to atrophy
36
nutrient starvation
poor intake, absorption, or distribution. | leads to atrophy
37
cells attempt to minimize its energy and nutrient consumption by decreasing number of intracellular organelles and other structures
atrophy | cells shrink
38
hypertrophy
increase in cell mass accompanied by an augmenting functional capacity in response to increased physiologic or pathophysiologic demands
39
hyperplasia
increase in number of cells.
40
demand induced hyperplasia
increase in cells due to physiologic demand: increased RBC in high elevation
41
pathologic hyperplasia
dysregulation of hormones or growth factors: thyroid or prostate enlargement.
42
chronic irritation hyperplasia
calluses or corn
43
metaplasia
replacement of one differentiated cell with another. | fully reversible when stimulus is removed.
44
dysplasia
disorganized appearance of cells due to variations in size, shape, and arrangement. carcinoma in situ
45
necrosis
consequence of ischemia or toxic injury characterized by cell rupturing, contents spilling into extracellular fluid, and inflammation.
46
indications of necrosis (7)
``` general inflammatory response malaise fever tachycardia increased WBC decreased appetite intracellular proteins in bloodstream determine location and extent of death. ```
47
gangrene
cellular death involving a large area of tissue | usually results from a major interruption of blood supply
48
dry gangrene
form of coagulative necrosis blackened, dry, wrinkled tissue generally on extremites
49
wet gangrene
form of liquefactive necrosis typically found in organs cold, black, and foul smelling
50
gas gangrene
characterized by formation of bubbles of gas in damaged tissue result of infection of necrotic tissue by anaerobic bacteria clostridium.
51
apoptosis
organized cellular death
52
fas ligand
extracellular signal that binds to cell and triggers death cascade in apoptosis
53
internal activated apoptosis
mitochomial damage leaks cytochrome C in to cytoplasm with activates apoptosis pathway.
54
caspases
degrades intracellular structures in apoptosis
55
ischemia and hypoxic injury
insufficient amount of oxygen to produce ATP and survive
56
re-perfusion injury
occurs after ischemia/hypoxic injury. | cellular damage occurring after blood supply to tissue is restored.
57
re-perfusion injury cascade
calcium overload formation of reactive oxygen molecules: free radicals subsequent inflammation: free radicals stealing H atoms forming abnml molecular bonds causing more free radicals. damage cell membrane, denature proteins, and disrupt chromosomes increased inflammation
58
nutritional injury
excess or deficient nutrients: | lipids, proteins, carbs, vitamins and minerals.
59
infectious and immunologic injury
bacteria and viruses
60
bacteria affect on cell
from outside: excrete digestive enzymes that digest cellular membrane and connective tissue produce exotoxins which interfere with cellular functions
61
gram negative bacteria affect
endotoxins in cell wall. When bacteria is killed endotoxins release causing fever, malaise, shock
62
infectious and immunologic injury from immune response
WBC secrete enzymes and chemicals meant to kill invading organism normal body cells exposed immune cells produce free radicals which can attack host cell membranes.
63
virus affect on cells
genetic material able to gain access to cell uses host cell to replicate can live in cell a long time or cause rapid lysis
64
chemical injury
chemicals, posions, toxins | can cause direct cell injury or become injurious when metabolized.
65
physical and mechanical injury
``` extreme temp abrupt changes in atmospheric pressure mechanical deformation electricity ionizing radiation ```
66
cellular basis of aging
progressive decline in the proliferative and reparative capacity of cells along with exposure to environmental factors.
67
programed senescence theory
aging is a result of an intrinsic genetic program | cells have a finite number of divisions
68
somatic death
death of an entire organism | no immunologic or inflammatory response
69
24-48 hours after death
tissue deterioration or putrefaction apparents
70
brain dead
unresponsive, flaccidity, absence of brain stem reflexes, no respiratory effort, absence of brain waves, lack of cerebral blood flow.

Pathophysiology (80 decks)

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