Module 4 L1-2 Flashcards

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
Q

Increased ROS leads to

A

Damaged lipids, proteins, DNA can break, abnormal folding, mutations

26
Q

Necrosis definition

A

Swell, rupture, and burst

27
Q

Apoptosis

A

cells destined to die enzymes incapable of degrading cells own dna, programmed destruction, dna damage, accumulation of misfolded proteins

28
Q

Intrinsic apoptosis pathway

A

Injury stressor injury to bcl2

29
Q

Extrinsic apoptosis pathway

A

receptor engaged by ligand

30
Q

Reversible cell injury leads to

A

necrosis

31
Q

Characteristics of reversible injury

A

Cellular injury and fatty change

32
Q

Characteristics of irreversible injury

A

Mitochondrial dysfunction and membrane dysfunction

33
Q

Mechanisms for OFRs and ROS

A

Superoxide dismutase, glutathione peroxidase, catalase, antioxidants, sequestration of free ionized iron and copper

34
Q

Defects in membrane permeability

A

mitochondrial membrane damage, plasma membrane damage, lysosomal membrane damage