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HLSC 222 > Ch. 4 > Flashcards

Ch. 4 Flashcards

1
Q

Cellular Injury

A

Occurs if a cell is unable to maintain homeostasis

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2
Q

Types of cell injury

A

-Reversable
-Irreversible

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3
Q

Reversable

A

Cells recover

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4
Q

Irreversible

A

Cells die

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5
Q

Cell adaptation

A

-Physiological (Adaptive)
-Pathogenic (Disease causing)

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6
Q

Atrophy

A

Decrease in cell size

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7
Q

Hypertrophy

A

Increase in cell size

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8
Q

Hyperplasia

A

Increase in number of cells

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9
Q

Metaplasia

A

-Replacement of one cell type with another
-“After/Behind”

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10
Q

Dysplasia

A

-Deranged cell growth
-“Bad”

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11
Q

What causes metaplasia

A

chronic injury or irritation

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12
Q

What causes dysplasia

A

Persistent severe injury or irritation

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13
Q

Cellular Injury Mechanisms

A

-Hypoxic Injury
-Free Radicles and Reactive Oxygen Species
-Chemical Injury
-Chemical agents + Medications

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14
Q

ROS

A

Reactive Oxygen Species

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15
Q

Hypoxic Injury

A

Most common cause of cellular injury

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16
Q

Ischemia definition

A

Inadequate blood supply

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17
Q

What is Ischemia

A

-Most common cause of hypoxia

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18
Q

What happens during Ischemia

results

A

-Reduced O2 to mitochondria
-reduced ATP production/reduced cell energy

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19
Q

Ischemia breakdown

What is caused

A

-Increased accumulation of H+ in mitochondria = breakdown in mitochondrial membrane = increased intracellular H+ = loss of membrane potential = necrosis

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20
Q

Ischemia-reperfusion injury

A

additional injury caused by restoration of blood flow + O2

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21
Q

Mechanisms of Ischemia-reperfusion injury

A

-Oxidative stress
-Increased intracellular calcium
-Inflammation

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22
Q

Cellular response to Ischemia-reperfusion injury

A

-Decrease ATP, cause failure of Na/K pump and Na/Ca exchange
-Cellular swelling /shrinking

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23
Q

Free Radicals

A

-Missing an electron
-will attack a healthy atom to obtain a replacement electron

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24
Q

Free Radicals include

A

-ROS
-By product of normal metabolism

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25
Q

Oxidative Stress

A

when not enough antioxidants occur to break down current free radicals

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26
Q

Oxidative Stress major role

A

in chronic and degenerative ailments

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27
Q

Oxidative Stress are ok

A

if we have enough antioxidants to fix free radicals

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28
Q

Oxidative Stress too many free radicals

A

oxidative stress (cellular stress) = damage to cells

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29
Q

Antioxidants

A

prevent damage to cells

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30
Q

ROS is

A

a subset of free radicals that contain O2

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31
Q

Free radicals and ROS

A

electrically uncharged atom or groups of atoms having an unpaired electron that causes 3 pathological effects

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32
Q

Pathological effects of Free radicals and ROS

A

-Lipid peroxidation
-Alteration of proteins
-Alteration of DNA

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33
Q

Lipid peroxidation

A

Free radicals attack lipids

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34
Q

Alterations of proteins

A

Denaturation of proteins

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35
Q

Alteration of DNA

A

Mutations

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36
Q

Chemical injury

A

Chemicals damaging the body

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37
Q

Xenobiotics

A

Substances foreign to the body

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38
Q

Lead

A

-most common over exposure in industry
-in old paint
-Pb dust inhaled attacks BBB in fetus resulting in Pb poisoning

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39
Q

Carbon Monoxide

A

-Odorless, Colorless, Nonirritating
-Ultimately caused hypoxic injury due to O2 depravation
-CO attaches to hemoglobin in blood with a higher affinity than O2

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40
Q

Ethanol (Alcohol)

A

-Major injury: liver damage
-Nutritional Deficiencies; Magnesium, Vit B6
-Absorbed in stomach then distributed to rest of body
-J shaped effect

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41
Q

J Shaped Effect

A

-Light to moderate drinkers have lower mortality than non-drinkers
-Heavy drinkers have high mortalitym

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42
Q

Mechanism for light to moderate drinkers

A

-Decreased LDL levels
-Decreased BP
-Decrease in atherosclerosis

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43
Q

Mercury

A

Recognized as a global threat to human and environmental health

44
Q

Chemical Agents including medications

A

-over the counter and prescribed medications

45
Q

Limitation to medication therapy

A

Chemical injury

46
Q

Leading cause of child poisioning

A

medications

47
Q

Direct damage (on-target toxicity)

A

-Chemicals and medications injure cells by combining directly with critical molecular substances
-Activation of toxic metabolites

48
Q

Hypersensitivity reactions

A

-Range from mild skin irritations to immune-mediated organ failure
-Big issue

49
Q

Chemotherapeutic medications/drugs of abuse

A

Direct damage to cells

50
Q

Asphyxiation

A

Failure of cells to receive or use O2

51
Q

Suffocation

A

-Systemic hypoxia
-no air exchange

52
Q

Strangulation

A

-Compression
-closure of airway
-causes cerebral hypoxia

53
Q

Drowning

A

-Fluid fills lungs
-no O2 exchange
-fluid can pass through alveolar/capillary interface = massive fluid and electrolyte changes in blood

54
Q

Chemical

A

-prevention of O2 delivery to cells or its utilization

55
Q

Chemical Asphyxiation examples

A

-Carbon Monoxide
-Cyanide

56
Q

CA Carbon Monoxide

A

-Binds to Hb in same position as O2
- Treatment: hyperbaric chamber

57
Q

CA Cyanide

A

-Blocks utilization of O2 at electron transport chain = Cardiac arrest

58
Q

Jones Town

A

Cult members forced to drink cyanide laced fluid- 900 died

59
Q

Contusion

A

-Crushing injury to muscle
-Mild = bruising

60
Q

Laceration

A

-Irregular cut from tearing
-Irregular edges

61
Q

Incision

A

-Sharp strait wound

62
Q

Fracture

A

-Broken or shattered bones

63
Q

Incised wound

A

-wound is longer then it is deep

64
Q

Stab wound

A

-wound deeper then it is long

65
Q

Puncture wound

A

-Sharp point, not sharp edges

66
Q

Infectious injury

A

-Invasion of a pathogen
-bacterium, virus, or other microorganism that cause disease

67
Q

Disease-producing potential of pathogen infection

A

-Invasion and destruction
-Toxin production
-Production of hyper immune reactions

68
Q

Cellular Death

A

-Apoptosis
-Autophagy

69
Q

Apoptosis

A

-Cell death that occurs as normal controlled part of an organisms death

70
Q

What happens in Apoptosis

A

-Cell breaks up into sections/taken away by immune system

71
Q

Autophagy

A

-Consumption if cells own contents for fuel to oppose starvation and certain diseases

72
Q

“Auto”

A

Self

73
Q

“Phag”

A

Consumption

74
Q

Necrosis

A

-Swelling and bursting of cell membrane

75
Q

What causes necrosis

A

-due to disease, injury, failure of blood supply

76
Q

Necrosis occurs

A

at the cellular level

77
Q

Look at cell death image

A
78
Q

Types of necrosis

A

-Coagulative
-Caseous
-Liquefactive
-Fatty
-Gangrenous
-GAS Gangrene

79
Q

Coagulative Necrosis occurs

A

in kidneys and heart

80
Q

Coagulative Necrosis cause

A

Ischemia or infarction (obstruction of blood supply causing death of cell)

81
Q

Ischemia can be revived

A

if O2 is supplied within 20min

82
Q

Coagulation is a result of

A

protein denaturation

83
Q

Caseous Necrosis occurs

A

lungs

84
Q

Caseous Necrosis

A

Dead tissue resemble clumped cheese (Soft and granular)

85
Q

Caseous Necrosis cause

A

TB (Mycobacterium tuberculosis)

86
Q

Caseous Necrosis Danger

A

-dead cells enveloped by other cells

87
Q

In Caseous Necrosis

A

increased cell mass = decreased lung space

88
Q

Liquefactive Necrosis occurs

A

-brain, ischemic injury to neurons and glia cells
-bacterial infection: streptococci/E. coli

89
Q

Liquefactive Necrosis cause

A

infarction (Blockage of blood supply causing death of cell)

90
Q

Liquefactive Necrosis

A

transforms tissue into liquid

91
Q

Fatty Necrosis occurs

A

breasts, abdominal organs

92
Q

Fatty Necrosis cause

A

-Action of lipases

93
Q

Fatty Necrosis danger

A

-Usually harmless
-Often left alone and let body absorb it

94
Q

Gangrenous Necrosis

A

-severe hypoxic injury often to major arteries in lower leg
-Becomes a medium for bacterial growth (anaerobic bacteria)

95
Q

GAS Gangrene cause

A

-clostridium (anaerobic bacteria) sp. infection
-clostridium enters wound + produces gas

96
Q

GAS Gangrene danger

A

-fatal if enters blood
-diminished O2 carrying capacity of RBC

97
Q

Oncosis

A

Cell death due to swelling

98
Q

Look at images on oncosis slide

A
99
Q

Cellular Aging

A

Atrophy: decreased function and loss of cells

100
Q

Tissue and systemic aging

A

-Progressing stiffness and rigidity
-sarcopenia

101
Q

Sarcopenia

A

progressing/generalized loss of skeletal muscle mass and strength

102
Q

“sarco”

A

flesh

103
Q

“penia”

A

decreased/deficient

104
Q

Frailty

A

-Mobility
-Balance
-Muscle strength
-Motor activity
-Cognition
-Nutrition
-Endurance
-Falls
-Fractures
-Bone density

105
Q
A

HLSC 222 (9 decks)

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