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HLSC 222 > Ch. 4 > Flashcards

Ch. 4 Flashcards

(105 cards)

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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
Oxidative Stress
when not enough antioxidants occur to break down current free radicals
26
Oxidative Stress major role
in chronic and degenerative ailments
27
Oxidative Stress are ok
if we have enough antioxidants to fix free radicals
28
Oxidative Stress too many free radicals
oxidative stress (cellular stress) = damage to cells
29
Antioxidants
prevent damage to cells
30
ROS is
a subset of free radicals that contain O2
31
Free radicals and ROS
electrically uncharged atom or groups of atoms having an unpaired electron that causes 3 pathological effects
32
Pathological effects of Free radicals and ROS
-Lipid peroxidation -Alteration of proteins -Alteration of DNA
33
Lipid peroxidation
Free radicals attack lipids
34
Alterations of proteins
Denaturation of proteins
35
Alteration of DNA
Mutations
36
Chemical injury
Chemicals damaging the body
37
Xenobiotics
Substances foreign to the body
38
Lead
-most common over exposure in industry -in old paint -Pb dust inhaled attacks BBB in fetus resulting in Pb poisoning
39
Carbon Monoxide
-Odorless, Colorless, Nonirritating -Ultimately caused hypoxic injury due to O2 depravation -CO attaches to hemoglobin in blood with a higher affinity than O2
40
Ethanol (Alcohol)
-Major injury: liver damage -Nutritional Deficiencies; Magnesium, Vit B6 -Absorbed in stomach then distributed to rest of body -J shaped effect
41
J Shaped Effect
-Light to moderate drinkers have lower mortality than non-drinkers -Heavy drinkers have high mortalitym
42
Mechanism for light to moderate drinkers
-Decreased LDL levels -Decreased BP -Decrease in atherosclerosis
43
Mercury
Recognized as a global threat to human and environmental health
44
Chemical Agents including medications
-over the counter and prescribed medications
45
Limitation to medication therapy
Chemical injury
46
Leading cause of child poisioning
medications
47
Direct damage (on-target toxicity)
-Chemicals and medications injure cells by combining directly with critical molecular substances -Activation of toxic metabolites
48
Hypersensitivity reactions
-Range from mild skin irritations to immune-mediated organ failure -Big issue
49
Chemotherapeutic medications/drugs of abuse
Direct damage to cells
50
Asphyxiation
Failure of cells to receive or use O2
51
Suffocation
-Systemic hypoxia -no air exchange
52
Strangulation
-Compression -closure of airway -causes cerebral hypoxia
53
Drowning
-Fluid fills lungs -no O2 exchange -fluid can pass through alveolar/capillary interface = massive fluid and electrolyte changes in blood
54
Chemical
-prevention of O2 delivery to cells or its utilization
55
Chemical Asphyxiation examples
-Carbon Monoxide -Cyanide
56
CA Carbon Monoxide
-Binds to Hb in same position as O2 - Treatment: hyperbaric chamber
57
CA Cyanide
-Blocks utilization of O2 at electron transport chain = Cardiac arrest
58
Jones Town
Cult members forced to drink cyanide laced fluid- 900 died
59
Contusion
-Crushing injury to muscle -Mild = bruising
60
Laceration
-Irregular cut from tearing -Irregular edges
61
Incision
-Sharp strait wound
62
Fracture
-Broken or shattered bones
63
Incised wound
-wound is longer then it is deep
64
Stab wound
-wound deeper then it is long
65
Puncture wound
-Sharp point, not sharp edges
66
Infectious injury
-Invasion of a pathogen -bacterium, virus, or other microorganism that cause disease
67
Disease-producing potential of pathogen infection
-Invasion and destruction -Toxin production -Production of hyper immune reactions
68
Cellular Death
-Apoptosis -Autophagy
69
Apoptosis
-Cell death that occurs as normal controlled part of an organisms death
70
What happens in Apoptosis
-Cell breaks up into sections/taken away by immune system
71
Autophagy
-Consumption if cells own contents for fuel to oppose starvation and certain diseases
72
"Auto"
Self
73
"Phag"
Consumption
74
Necrosis
-Swelling and bursting of cell membrane
75
What causes necrosis
-due to disease, injury, failure of blood supply
76
Necrosis occurs
at the cellular level
77
Look at cell death image
78
Types of necrosis
-Coagulative -Caseous -Liquefactive -Fatty -Gangrenous -GAS Gangrene
79
Coagulative Necrosis occurs
in kidneys and heart
80
Coagulative Necrosis cause
Ischemia or infarction (obstruction of blood supply causing death of cell)
81
Ischemia can be revived
if O2 is supplied within 20min
82
Coagulation is a result of
protein denaturation
83
Caseous Necrosis occurs
lungs
84
Caseous Necrosis
Dead tissue resemble clumped cheese (Soft and granular)
85
Caseous Necrosis cause
TB (Mycobacterium tuberculosis)
86
Caseous Necrosis Danger
-dead cells enveloped by other cells
87
In Caseous Necrosis
increased cell mass = decreased lung space
88
Liquefactive Necrosis occurs
-brain, ischemic injury to neurons and glia cells -bacterial infection: streptococci/E. coli
89
Liquefactive Necrosis cause
infarction (Blockage of blood supply causing death of cell)
90
Liquefactive Necrosis
transforms tissue into liquid
91
Fatty Necrosis occurs
breasts, abdominal organs
92
Fatty Necrosis cause
-Action of lipases
93
Fatty Necrosis danger
-Usually harmless -Often left alone and let body absorb it
94
Gangrenous Necrosis
-severe hypoxic injury often to major arteries in lower leg -Becomes a medium for bacterial growth (anaerobic bacteria)
95
GAS Gangrene cause
-clostridium (anaerobic bacteria) sp. infection -clostridium enters wound + produces gas
96
GAS Gangrene danger
-fatal if enters blood -diminished O2 carrying capacity of RBC
97
Oncosis
Cell death due to swelling
98
Look at images on oncosis slide
99
Cellular Aging
Atrophy: decreased function and loss of cells
100
Tissue and systemic aging
-Progressing stiffness and rigidity -sarcopenia
101
Sarcopenia
progressing/generalized loss of skeletal muscle mass and strength
102
"sarco"
flesh
103
"penia"
decreased/deficient
104
Frailty
-Mobility -Balance -Muscle strength -Motor activity -Cognition -Nutrition -Endurance -Falls -Fractures -Bone density
105

HLSC 222 (9 decks)

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