Module 4 L1-2 Flashcards

(34 cards)

1
Q

How cells respond to injury

A

Homeostasis, Adaptation, Cell injury, Cell Death

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2
Q

Hypertrophy definition

A

Increase in size

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3
Q

Hypertrophy occurs in what cells

A

Cells incapable of dividing - striated cells skeletal muscle and heart

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4
Q

Hypertrophy causes

A

Increased workload, uterus in pregnancy, hypertension, aortic valve, adrenergic hormones, stretching

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5
Q

Hyperplasia definition

A

Increase in number

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6
Q

Hyperplasia physical examples

A

Boob growth, compensatory hyperplasia (regeneration of liver)

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7
Q

Hyperplasia pathologic examples

A

excessive hormonal growth or growth factor stimulation, hyperplastic tissue may eventually become malignant

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8
Q

Atrophy definition

A

decrease in size

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9
Q

Atrophy causes

A

Decreased workload, loss of innervation, reduced blood supply, inadequate nutrition, aging, increased protein degradation, reduced protein synthesis

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10
Q

Metaplasia definition

A

one adult cell type is replaced by another, reversible change

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11
Q

Metaplasia examples

A

Ciliated cells in trachea to clear mucous, in smokers baretts esophagus

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12
Q

Cancerous cell adaptations

A

Metaplasia, Dysplasia, Hyperplasia

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13
Q

Dysplasia definition

A

Vary in size, shape, number, organization

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14
Q

Dysplasia examples

A

chronic irritation and inflammation, metaplastic squamous epithelium in respiratory tract and uterine cervix, reversible, pap smear

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15
Q

8 Causes of cell injury

A

Oxygen deprivation, chemical agents, infectious agents, immunological reactions, genetic defects, physical agents, nutritional imbalances, aging

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16
Q

Hypoxia

A

inadequate oxygenation of blood (pneumonia)

17
Q

Ischemia

A

loss of oxygen supply

18
Q

Astherosclerosis

A

blockage of coronary arteries

19
Q

Aging

A

accumuation of damage by ROS loss of telomerase function

20
Q

Ischemia death times

A

Non contractile 1-2min
Cell death 20-30min
Dead by electron microscopy 2-3hrs
Dead by light microscopy 6-12hrs

21
Q

Mechanisms of Cell injury

A

atp deletion, mitochondrial damage, membrane damage, calcium influx, increased ROS

22
Q

How to increase calcium influx

A

release from intracellular calcium stores or calcium influx across plasma membrane

23
Q

Plasma membrane damage

A

loss of osmotic balance, influx of fluids and ions

24
Q

Lysosomal membrane damage

A

leakage of enzymes into the cytoplasm and activation of acid hydrolases in acidic intracellular pH of the injured cells

25
Increased ROS leads to
Damaged lipids, proteins, DNA can break, abnormal folding, mutations
26
Necrosis definition
Swell, rupture, and burst
27
Apoptosis
cells destined to die enzymes incapable of degrading cells own dna, programmed destruction, dna damage, accumulation of misfolded proteins
28
Intrinsic apoptosis pathway
Injury stressor injury to bcl2
29
Extrinsic apoptosis pathway
receptor engaged by ligand
30
Reversible cell injury leads to
necrosis
31
Characteristics of reversible injury
Cellular injury and fatty change
32
Characteristics of irreversible injury
Mitochondrial dysfunction and membrane dysfunction
33
Mechanisms for OFRs and ROS
Superoxide dismutase, glutathione peroxidase, catalase, antioxidants, sequestration of free ionized iron and copper
34
Defects in membrane permeability
mitochondrial membrane damage, plasma membrane damage, lysosomal membrane damage