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Pathophysiology > Chapter 4 - Altered Cellular and Tissue Biology > Flashcards

Chapter 4 - Altered Cellular and Tissue Biology Flashcards

1
Q

Why does cellular injury occur?

A

cell unable to maintain homeostasis

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2
Q

two types of cell injury?

A

reversible (cell recover) & irreversible (cell die)

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3
Q

2 things that occur during cellular adaptation?

A

physiological - adaptive
pathogenic - causes disease

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4
Q

What are the five types of cellular adaptation? Explain each of them.

A

atrophy - decrease in cellular size

hypertrophy - increase in cellular size

hyperplasia - increase in number of cells

metaplasia - replacement of one cell type with another

dysplasia- deranged cellular growth.

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5
Q

what are the four cellular injury mechanisms?

A

hypoxic injury, free radicals and ROS, chemical injury, chemical agents including meds

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6
Q

what is the common cause of cellular injury?

A

hypoxic injury

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7
Q

what is ischemia? And what causes ischemia?

A

inadequate blood supply; hypoxia

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8
Q

what occurs in hypoxic injury?

A

reduced O2 production in mitochondria, therefore there is reduced production of ATP (1), meaning there is reduction of cellular energy.

(2)increase accumulation of H+ in mito = breakdown in mitochondrial membrane = increase in intracellular H+ = loss of membrane potential =necrosis.

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9
Q

what is ischemia reperfusion injury?

A

additional injury caused by restoration of blood flow and O2

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10
Q

what are the 3 mechanisms of ischemia reperfusion injury?

A

inflammation, oxidative stress, increased intracellular Ca

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11
Q

what are the cellular responses of ischemia-reperfusion injury?

A

decrease in ATP, leads to failure of Na-K pump and Na-Ca exchange (1) & cellular shrinking and swelling (2)

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12
Q

what are free radicals?

A

missing an electron, so they attack healthy atom to obtain a replacement electron.

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13
Q

what is the by-products of normal metabolism & created with metabolism of O2?

A

reactive oxygen species (ROS).

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14
Q

what causes oxidative stress?

A

not producing enough antioxidants to break down current free radicals (1)

major role in chronic and degenerative ailments (2)

too many free radicals = oxidative stress (cellular stress) = damage to cells)

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15
Q

what prevents damage to cell?

A

antioxidants

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16
Q

what causes free radicals and ROS

A

lipid peroxidation (1), alteration of proteins (2), alteration of DNA

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17
Q

what are xenobiotics?

A

substances foreign to body

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18
Q

some examples of xenobiotics?

A

lead, carbon monoxide, ethanol, mercury

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19
Q

where is the major injury ethanol impose?

A

liver

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20
Q

where is ethanol absorbed?

A

stomach

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21
Q

what shaped is the effect of alcohol consumption?

A

J-shaped

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22
Q

what is the mechanism for light to moderate drinkers?

A

low LDL levels, decreased b.p and decreased atherosclerosis

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23
Q

what xenobiotics recognized as a global threat to human and envrionmental health

A

mercury

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24
Q

this xenobiotics is the most common overexposure found in industry?

A

lead

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25
Q

what xenobiotics is odorless, colorless and nonirritating?

A

CO

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26
Q

CO ultimately causes hypoxic injury due to ____; CO attaches to mitochondria with a ______

A

O2 deprivation; higher affinity than O2

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27
Q

what is the leading cause of child poisonings?

A

medications

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28
Q

what are some hypersensitivity rxns from medications?

A

range from mild skin rashes to immune-mediated organ failure

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29
Q

activation of ___ metabolites is a drawback from chem agents including meds

A

toxic

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30
Q

how does chemicals and meds apply direct damage?

A

they injure cells by combining directly with critical molecular substances (1) & chemotherapeutic meds/drugs of abuse

31
Q

what is asphyxiation?

A

failure of cells to receive or use O2

32
Q

what causes asphyxiation?

A

suffocation: systemic hypoxia/ no air exchange (1), strangulation: compression/ closure of airway/ causes cerebral hypoxia (2) & drowning: fluid fill lungs/ no O2 exchange (3)

33
Q

what chem preven O2 delivery to cell or its utilization?

A

CO and cyanide

34
Q

what chem binds to Hb in same position as O2? treatment?

A

CO; hyberbaric chamber

35
Q

what chemical blocks utilization of O2 at electron transport chain? cause of death?

A

cyanide; cardiac arrest

36
Q

what is contusion?

A

crushing injury to muscle; mild = bruising

37
Q

laceration?

A

irregular cut from tearing/ irregular edges

38
Q

incision?

A

sharp strait wound

39
Q

fracture?

A

broken or shattered bones

40
Q

incised wound?

A

wound is longer than it is deep

41
Q

stab wound?

A

wound is longer than it is deep

42
Q

puncture wound?

A

sharp point but not sharp edges

42
Q

what is infectious injury?

A

invasion of pathogen.

43
Q

what might occur from disease-producing potential of pathogen infection?

A

invasion and destruction (1), toxin production (2) & production of hyper immune rxn (3)

44
Q

what are the 3 types of cellular death?

A

necrosis, apoptosis, autophagy

45
Q

which cell death occurs as a normal controlled part of an organism’s growth and development?

A

apoptosis

46
Q

this is the consumption of a cell’s own contents for fuel to oppose starvation and certain diseases

A

autophagy – i.e., self-consumption

47
Q

the swelling and bursting of cell membrane & due to disease, injury, failure of blood supply?

A

necrosis.

48
Q

Necrosis occurs at _____

A

cellular level

49
Q

what is the cause of coagulative necrosis?

A

ischemia or infarction – obstruction of blood supply causing death of cell

50
Q

what organs linked to coagulative necrosis?

A

kidney and heart

51
Q

till when ischemic cells can be revived if O2 is supplied?

A

20 minutes

52
Q

Coagulation is a result of protein _____

A

denaturation

53
Q

what type of necrosis is due to dead tissue resemble clumped cheese?

A

caseous necrosis

54
Q

what organ does caseous necrosis affect?

A

lungs

55
Q

what causes caseous necrosis?

A

tuberculous

56
Q

what is the danger imposed by caseous necrosis?

A

dead cell enveloped by other cells/ increased mass= decreased lung space

57
Q

this type of necrosis is due cause by ischemic injury to neurons and glia cells & infarction?

A

liquefactive necrosis

58
Q

organ affected by liquefactive necrosis?

A

brain

59
Q

what is the bacterial infection in liquefactive necrosis?

A

streptococci/ E.coli

60
Q

this necrosis is usually harmless and often left alone and let body absorb it?

A

fatty necrosis

61
Q

organ affected of fatty necrosis?

A

breasts and abdominal organs

62
Q

in fatty necrosis, action of _____ occurs?

A

lipases

63
Q

this is severe hypoxic injury often to major arteries in lower leg?

A

gangrenous necrosis

64
Q

gangrenous necrosis is susceptible for what bacterial growth?

A

anaerobic bacteria

65
Q

this type of necrosis is due to clostridium speices infection?

A

gas gangrene

66
Q

As clostridium enter wound in gas gangrene, what does it produce?

A

gas

67
Q

how is gas gangrene fatal?

A

if it enters blood and diminishes O2- carrying capacity of RBC

68
Q

what is the process of cell death due to swelling?

A

oncosis

69
Q

what happens in aging?

A

cellular aging, tissue and systemic aging and frailty

70
Q

what is cellular aging

A

atrophy, decreased function and loss of cells

71
Q

what happens in tissue and systemic aging

A

progressive stiffeness and rigidity

72
Q

what is sarcopenia

A

progressive/ generalized loss of skeletal muscle mass and strength

73
Q

what happens in frailty

A

mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance, falls, fractures and bone density

Pathophysiology (20 decks)

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