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Pathophysiology > chapters 3 + 9 > Flashcards

chapters 3 + 9 Flashcards

1
Q
  • loss of structure, shrinkage, reduction in cell number
  • gradual decline in effectiveness or vigor due to: disuse, denervation, loss of endocrine stimulation, inadequate nutrition, or ischemia/decreased blood flow
A

atrophy

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2
Q
  • an increase in cell size and often tissue mass
  • can be due to biochemical stress or neurohumoral factors
A

hypertrophy

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3
Q

an increase in the number of cells in an organ or tissue

A

hyperplasia

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4
Q

a reversible change in whcih one adult cell type is replaced by another adult cell type

A

metaplasia

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5
Q

characterized by deranged cell growth of a specific tissue that results in cells that vary in size, shape, and organization

A

dysplasia

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6
Q

stressed cells may fill up with…

A
  • normal body substances such as lipids, proteins, pigments, carbs, bilirubin, melatonin
  • abnormal endogenous substances–metabolic products–glycogen, lipids resulting form inborn errors of metabolism
  • abnormal exogenous substances–pigments that cannot be broken down by the cell
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7
Q

physical injurious agents

A

trauma, heat, cold, electricity

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8
Q

radiation injurious agents

A

ionizing, ultraviolet, nonionizing

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9
Q

chemical injurious agents

A

drugs, lead, mercury

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10
Q

biological injurious agents

A

bacteria, viruses, parasites

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11
Q

nutritional injurious agents

A

imbalances of fats, minerals, vitamins, and amino acids

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12
Q

involves the substitution of fibrous connective tissue that cannot be repaired via regeneration

A

scar tissue repair

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13
Q

both pathways of apoptosis are carried out by _______, which are present in the cell as procaspases and are activated by the cleavage of an inhibitory portion of their polypeptide chain

A

caspases

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14
Q

the ability of tissues to repair damage depends on

A

the body’s ability to replace parenchymal cells and to organize them as they were originally

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15
Q

any class of polypeptide immunoregulatiory substances that are secreted by cells, usually of the immune system, that affect other cells

A

cytokine

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16
Q

tissue death

A

infarction

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17
Q

creates H2S bubbles in the muscle

A

gas gangrene

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18
Q

lack of venous flow lets fluid accumulate in tissue (cold, swollen, pulselesss, moist, black, odor)

A

wet gangrene

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19
Q

lack of arterial blood supply but venous blood flow can carry fluid out of tissue (dry, skin wrinkles, dark brown/black)

A

dry gangrene

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20
Q

when a considerable mass of tissue undergoes necrosis

A

gangrene

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21
Q
  • cell death in an organ tissue that causes a loss of cell membrane integrity and enzymatic breakdown of cell parts and triggers the inflammatory process
  • unregulated cell death caused by injury to cells
  • cells swell and rupture causing inflammation
  • liquefaction, coagulation, and caseous this
  • infarction
A

necrotic cell death

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22
Q

a type of necrosis which results in a transformation of the tissue into liquid viscous mass (often associated w/ infectious agents)

A

liquefactive necrosis

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23
Q

a type of cell death that occurs when blood flow to cells stops or flows (ischemia) or during infarction; can occur anywhere except for the brain

A

coagulative necrosis

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24
Q

a type of cell death that causes tissues to becaome “cheese-like” in appearance (ex: tuberculosis)

A

caseous necrosis

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25
Q

the act of enfolding, entangling, or turning inward

A

involution

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26
Q

required to convert amino acids to procollagen, if not sufficient fibroblasts cannot secrete procollagen

A

vitamin C

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27
Q

most injurious agents exert their damaging effects through

A
  • uncontrolled free radical production
  • impaired oxygen delivery or utilization
  • destructive effects of uncontrolled intracellular calcium release
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28
Q

most important factors affecting wound healing (6)

A
  • blood flow/oxygen (most important)
  • age
  • nutrition–protein, carbs, fats, and vitamins
  • immune status
  • infection
  • presence of foreign bodies
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29
Q

major causes of hypercalcemia

A
  • hyperparathyroidism
  • primary or secondary to phosphate retention in renal failure
  • increased mobilization of calcium from bone as in Paget’s disease
  • cancer w/ metastatic bone lesions or immobilization
  • vitamin D intoxication
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30
Q

involves the abnormal tissue deposition of calcium salts, together w/ smaller amounts of iron, magnesium, and other minerals

A

pathologic calcification

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31
Q
  • components of calcium deposits derived rom dead or dying cells as well as from the circulation and interstitial fluid
  • represents the macroscopic deposition of calcium in injured tissue–occurs in dead/dying tissue
A

dystrophic calcification

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32
Q

occurs in normal tissues as a result of increased serum calcium levels

A

metastatic calcification

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33
Q
A
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34
Q
  • cell usually maintains low cytosolic …
  • acts as a second messenger to turn on intracellular enzymes
  • can damage the cell
A

calcium

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35
Q
  • death receptor independent
  • activated by conditions such as DNA damage, ROS, hypoxia, decreased ATP levels, cellular senescence, and activation of the p53 protein by DNA damage
A

intrinsic pathway of apoptosis

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36
Q
  • death receptor dependent
  • end result includes activation of endonucleases that fragment DNA and cause cell death
  • primary signaling molecules: TNF-related apoptosis-inducing ligand, cytokind IL-1 (interleukin-1), LPS (lipopolysaccharide)
A

extrinsic pathway of apoptosis

37
Q
  • chemicals with an unpaired electron in the valence shell
  • extremely unstable and reactive
  • can react w/ normal cell components
  • normally removed from the body by antioxidants
A

free radicals

38
Q

a type of cell damage that occurs when cells swell due to an influx of water

A

hydropic change

39
Q
  • IR
  • microwaves
  • laser
  • doesn’t ionize but creates thermal agitation of biological molecules, i.e., HEAT, burns most common, skin and subQ
A

non-ionizing radiation injury

40
Q
  • dose-related
  • mutations in DNA, cancer
  • tissue w/ highest mitotic turnover (normal)
A

ionizing radiation injury

41
Q
A
42
Q

frequencies ABOVE visible, wavelengths BELOW visible (e.g., UV and above)

A

ionizing radiation

43
Q

frequencies BELOW visible, wavelengths ABOVE visible), e.g., IR and below

A

nonionizing radiation

44
Q
  • an innate automatic response to cell injury that neutralizes harmful agents, removes damaged and dead tissue, generates new tissue, promotes healing
  • cells present include: basophils, eosinophils, lymphocytes, platelets, neutrophils, monocytes, mast cells, collagen fibers, elastin, fibroblasts, macrophages, proteoglycan filaments
A

inflammation

45
Q

acute phase response steps (5)

A
  1. change in plasma protein concentration
  2. increased RBC sedimentation rate
  3. increased WBC and skeletal muscle catabolism
  4. fever
  5. negative nitrogen balance
45
Q
A
46
Q

components of granulomas

A
  • lymphocytes
  • fibroblasts
  • macrophages
  • epithelioid cell
  • multinucleated giant cell
  • fibrous connective tissue
47
Q

basic tissue or element of an organ as distinguished from supporting or CT or elements

A

parenchyma

48
Q

the supporting matrix of an organ as distinguished from its element

A

stroma

49
Q

describes the process by which tissue is replaced w/ cells of a similar type or function

A

regeneration

50
Q

cells that continuously divide and multiply throughout life

A

labile cells

51
Q

cells that have a long lifespan and divide slowly but can be sstimulated to enter the cell cycle when needed

A

stabile

52
Q

phases of tissue regeneration

A
  1. inflammatory
  2. proliferative
  3. remodeling
53
Q
  • increased capillary permeability
  • diapedesis
  • release of vasoactive/inflammatory mediators
  • coagulation, fibrin
A

inflammatory phase of tissue regeneration

54
Q
  • organized regeneration
  • budding capillaries
  • influx of macrophages
  • influx of fibroblasts, collagen
A

proliferative phase of tissue regeneration

55
Q

regenerated tissue function/strength is near, but probably doesn’t exceed, original tissue

A

remodeling phase of tissue regeneration

56
Q

builds on the granulation tissue framework of new vessels and loose extracellular material via
* emigration and proliferation of fibroblasts into the site of injury
* deposition of ECM by these cells

A

scar formation

56
Q
A
57
Q
  • organized regeneration
  • budding capillaries
  • influx of macrophages
  • influx of fibroblasts, collagen
A

proliferative phase of tissue regeneration

58
Q

complications to wound healing

A
  • contracture
  • adhesions
  • dehiscence
  • keloids
  • proud flesh
59
Q
A
60
Q
  • excess granulation tissue
  • can interfere with surface restoration
A

proud flesh

61
Q
  • wound breaking open
  • by pressure applied to healing tissues
  • common site: abdominal wall–high pressure
A

dehiscence

62
Q
  • excess TGFs
  • excess fibroblast production
  • common on upper body
A

keloids

63
Q
  • due to extensive damage, collagen displays exaggerated wound contraction
  • limits mobility (burns)
  • limits lumen of organ
A

contracture

64
Q
  • union of serous membranes
  • restricts movement: heart, lung, and digestive
A

adhesions

65
Q
  • barriers to entry
  • intact skin
  • commensal organisms
  • saliva
  • mucus
  • tears
  • chemical substances (lysozyme)
A

first line of immune defense

66
Q
  • non-specific immunity
  • antimicrobial substances
  • phagocytic WBCs
  • inflammatory response
  • NK cells
A

2nd line of immune defense

67
Q
  • specific immunity
  • T and B cells
A

3rd line of immune defense

68
Q

granulocytes involved in inflammation

A

eosinophils, basophils, neutrophils, mast cells

69
Q

agranulocytes involved in inflammation

A

monocytes –> macrophages, T lymphocytes, B lymphocytes –> plasma cells

70
Q

characteristics of inflammation

A
  1. redness
  2. swelling
  3. pain
  4. heat
  5. loss of function
71
Q

phases of inflammation

A
  1. vascular phase–exudation
  2. cellular phase
  3. leukocyte activation and phagocytosis
72
Q
  1. extravascular influx of fluid with increased concentration of proteins, salts, and WBCs
  2. fluid dilutes injurious chemicals
  3. fluid brings antibodies and chemotactic substances to injured area
  4. during acute phase, leaked out proteins set up a gradient that pulls water out of plasma and increases blood viscosity to allow clotting and containment of pathogens (cellular phase begins)
A

vascular phase of inflammation

73
Q
  1. adhesion and diapedesis; starts within 1 hr as blood viscosity increases
  2. chemotaxis (movement of WBCs because of chemical signals)
  3. phagocytosis
A

cellular phase

due to movement of neutrophils

74
Q
  1. opsonization of microbes
  2. phagocytosis
A

leukocyte activation and phagocytosis

75
Q

stages of tissue repair (2)

A
  1. replacement of destroyed tissue w/ scar tissue (collagen), which fills in lesion and restores tensile strength, but cannot carry out physiological functions of destroyed tissue
  2. scar-produced by fibrosis
76
Q
  • angiogenesis
  • granulation tissue
  • formed by fibroblasts and vascular endothelial tissue
  • contains new capillaries, proliferating fibroblasts synthesize collagen macrophages
A

tissue revascularization

77
Q

pink/granular appearance as new blood vessels form

A

granulation tissue

77
Q
  • incision, severing
  • duration of phases fairly predictable
A

primary intention tissue repair

78
Q
  • wound edges not closely opposed, process depends on extent of injury and healing environment environment
  • more granulation tissue
  • wound contraction
A

second intention tissue repair

79
Q

effects of histamine

A
  • dilates blood vessels
  • increase flow
  • increase capillary permeability
80
Q
  • fractured bone edges correctly positioned = “reduced”
  • osteoblasts –> osteoid “soft callus”
  • ossification forms “hard callus” (weak)
  • remodeling takes place using osteoclasts and osteoblassts
A

bone healing process

81
Q

epithelial cells are

A

labile

82
Q

glandular tissue is

A

stabile

83
Q

remaining tubules go through hypertrophic changes to compensate for nephron loss (tubules regenerate, nephrons do not)

A

kidneys

84
Q
  • permanent
  • neuroglia go through reactive gliosis
A

neuroglia

85
Q

skeletal and cardiac muscle are

A

permanent

86
Q

smooth muscle is

A

stabile

Pathophysiology (7 decks)

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