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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
Q

reasons for accumulation of normal substances inside cell (2)

A

faulty metabolism: excess storage

absent enzyme: no breakdown

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26
Q

lipid accumulation: location and causes

A

liver
excessive alcohol intake
genetic disorders: enzymes needed to metabolize lipids is impaired.

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27
Q

carbohydrate accumulation: cause

A

lysosomal enzyme degradation of these is impaired

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28
Q

glycogen accumulation

A

common with diabetes, excess sugar is stored.

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29
Q

accumulation of protein cause

A

denatured proteins due to cellular stress, may cause dysfunction and death.
chaperones will try to correct defect

30
Q

ubiquitin

A

protein that binds with abnormal proteins creating a complex that enters a proteosome where proteins are digested into fragments.

31
Q

accumulation of pigments and inorganic particles (2)

A

endogenous: produced by body: hemosiderin, bilirubin
exogenous: introduced form outside: tar, mineral dust.

32
Q

atrophy

A

cells shrink and reduce their differentiated functions.

33
Q

disuse: reasoning and leads to

A

bedrest, casting

leads to atrophy

34
Q

denervation: reasoning and leads to

A

loss of nervous stimulation -> decrease muscle size

leads to atrophy

35
Q

ischemia

A

loss of blood supply

leads to atrophy

36
Q

nutrient starvation

A

poor intake, absorption, or distribution.

leads to atrophy

37
Q

cells attempt to minimize its energy and nutrient consumption by decreasing number of intracellular organelles and other structures

A

atrophy

cells shrink

38
Q

hypertrophy

A

increase in cell mass accompanied by an augmenting functional capacity
in response to increased physiologic or pathophysiologic demands

39
Q

hyperplasia

A

increase in number of cells.

40
Q

demand induced hyperplasia

A

increase in cells due to physiologic demand: increased RBC in high elevation

41
Q

pathologic hyperplasia

A

dysregulation of hormones or growth factors: thyroid or prostate enlargement.

42
Q

chronic irritation hyperplasia

A

calluses or corn

43
Q

metaplasia

A

replacement of one differentiated cell with another.

fully reversible when stimulus is removed.

44
Q

dysplasia

A

disorganized appearance of cells due to variations in size, shape, and arrangement.
carcinoma in situ

45
Q

necrosis

A

consequence of ischemia or toxic injury characterized by cell rupturing, contents spilling into extracellular fluid, and inflammation.

46
Q

indications of necrosis (7)

A 
general inflammatory response
malaise
fever
tachycardia
increased WBC
decreased appetite
intracellular proteins in bloodstream determine location and extent of death.
47
Q

gangrene

A

cellular death involving a large area of tissue

usually results from a major interruption of blood supply

48
Q

dry gangrene

A

form of coagulative necrosis
blackened, dry, wrinkled tissue
generally on extremites

49
Q

wet gangrene

A

form of liquefactive necrosis
typically found in organs
cold, black, and foul smelling

50
Q

gas gangrene

A

characterized by formation of bubbles of gas in damaged tissue
result of infection of necrotic tissue by anaerobic bacteria clostridium.

51
Q

apoptosis

A

organized cellular death

52
Q

fas ligand

A

extracellular signal that binds to cell and triggers death cascade in apoptosis

53
Q

internal activated apoptosis

A

mitochomial damage leaks cytochrome C in to cytoplasm with activates apoptosis pathway.

54
Q

caspases

A

degrades intracellular structures in apoptosis

55
Q

ischemia and hypoxic injury

A

insufficient amount of oxygen to produce ATP and survive

56
Q

re-perfusion injury

A

occurs after ischemia/hypoxic injury.

cellular damage occurring after blood supply to tissue is restored.

57
Q

re-perfusion injury cascade

A

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
Q

nutritional injury

A

excess or deficient nutrients:

lipids, proteins, carbs, vitamins and minerals.

59
Q

infectious and immunologic injury

A

bacteria and viruses

60
Q

bacteria affect on cell

A

from outside:
excrete digestive enzymes that digest cellular membrane and connective tissue
produce exotoxins which interfere with cellular functions

61
Q

gram negative bacteria affect

A

endotoxins in cell wall. When bacteria is killed endotoxins release causing
fever, malaise, shock

62
Q

infectious and immunologic injury from immune response

A

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
Q

virus affect on cells

A

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
Q

chemical injury

A

chemicals, posions, toxins

can cause direct cell injury or become injurious when metabolized.

65
Q

physical and mechanical injury

A 
extreme temp
abrupt changes in atmospheric pressure
mechanical deformation 
electricity
ionizing radiation
66
Q

cellular basis of aging

A

progressive decline in the proliferative and reparative capacity of cells along with exposure to environmental factors.

67
Q

programed senescence theory

A

aging is a result of an intrinsic genetic program

cells have a finite number of divisions

68
Q

somatic death

A

death of an entire organism

no immunologic or inflammatory response

69
Q

24-48 hours after death

A

tissue deterioration or putrefaction apparents

70
Q

brain dead

A

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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