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Pathophysiology I > Inflammation > Flashcards

Inflammation Flashcards

1
Q

acute inflammation is a response to

A

recent injury or infection

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2
Q

what is acute inflammation characterized by?

A

vasodilation
increased capillary permeability
neutrophils are main players

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3
Q

what is chronic inflammation a response to?

A

variable response to ongoing injury or infection

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4
Q

what is chronic inflammation orchestrated by?

A

t-helper cells

t-cells, b-cells, macrophages, eosinophils, fibroblasts may be involved

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5
Q

is inflammation infection? Immunity?

A

inflammation is not infection or immunity

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6
Q

what did Celsus describe?

A

manifestations of inflammation

-redness, heat, mass, pain

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7
Q

what did Virchow do?

A

added a fifth manifestation of inflammation

-loss of function

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8
Q

triple response of Lewis

A

red scratch
flare around scratch
swollen area around flare
1 & 3 mediated by histamine, 2 by autonomics

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9
Q

hallmarks of acute inflammation

A

vasodilation
increased capillary permeability
neutrophil infiltration

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10
Q

vasodilation-1

A

increased blood flow-redness and heat

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11
Q

increased capillary premeability-2

A

leakage of fluid and proteins
osmotic water loss-swelling
leakage of fibronigen leads to clotting

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12
Q

neutrophil infiltration-3

A

margination, emigration, chemotaxis
phagocytosis & degranulation-pain
monocytes/macrophages appear later

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13
Q

margination

A

neutrophils adhere to capillary walls

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14
Q

emigration (diapedesis)

A

neutrophils pass through capillary walls

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15
Q

chemotaxis

A

neutrophils follow chemical signals to damage/infection

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16
Q

phagocytosis

A

neutrophils engulf pathogens and debris

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17
Q

degranulation

A

neutrophils release cytoplasmic granules

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18
Q

what is due to histamine?

A

vasodilation and capillary permeability

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19
Q

what does margination depend on?

A

neutrophil and endothelial “adhesion molecules”

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20
Q

what drives diapedesis and chemotaxis?

A

C5a and various leukotrienes

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21
Q

what does phagocytosis rely on

A

opsonins IgG and C3b

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22
Q

what does degranulation release?

A

prostaglandins
leukotrienes
free radicals
lysosomal enzymes

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23
Q

what interferes with many aspects of neutrophil function?

A

steroids and diabetes

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24
Q

leukotrienes

A

act as chemotaxins

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25
Q

opsonins

A

enhance phagocytosis, make bacteria desirable to neutrophils

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26
Q

frustrated phagocytosis

A

lysosomes become extracellular when neutrophil can’t eat bacteria, spills out into cytoplasm

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27
Q

inflammatory mediators

A

chemicals responsible for aspects of inflammation

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28
Q

histamine

A

released from tissue mast cells during injury or infection

vasodilation & capillary permeability

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29
Q

bradykinin

A

formed from kinin system
vasodilation and capillary permeability
causes pain (bee venom)

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30
Q

complement system

A

collection of plasma proteins that under certain circumstances react with each other in a chain reaction-cascade

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31
Q

types of cascades

A

classical and alternate

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32
Q

classical and alternate cascades

A

two different chain reactions that ultimately lead to the same thing

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33
Q

C3a/C5a

A

stimulate mast cells to release histamine

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34
Q

what happens when you have an exaggerated amount of histamine?

A

you can go into anaphylaxis

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35
Q

C5a

A

acts as perfume, chemotaxin

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36
Q

C3b

A

opsonin, enhances phagocytosis

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37
Q

what is the end result of the complement system cascade-classical and alternate?

A

collection of complement proteins C5-C9 combine together to form membrane attack complex, punches holes in membranes

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38
Q

arachidonic acid metabolites

A

phospholipase A2 liberates AA from cell membranes

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39
Q

what is phospholipase A2 inhibited by?

A

steroids

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40
Q

cyclooxygenase

A

converts AA into prostaglandins

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41
Q

what inhibits cyclooxygenase?

A

aspirin and NSAIDs

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42
Q

5-lipoxygenase

A

converts AA into leukotrienes

43
Q

what does cyclooxygenase produce?

A

prostaglandins

44
Q

list prostaglandins

produced by cyclooxygenase

A

thromboxane A2
Prostacyclin (PGl2)
Prostaglandin E2

45
Q

thromboxane A2

A

produced by platelets

vasoconstriction, platelet aggression

46
Q

prostacyclin PGl2

A

produced by endothelial cells

vasodilation, prevents platelet aggression

47
Q

prostaglandin E2

A

vasodilation, potentiates bradykinin(pain), fever

48
Q

what does lipoxygenase produce?

A

leukotrienes

49
Q

list leukotrienes

produced by lipoxygenase

A

leukotriene C4

leukotriene B4

50
Q

leukotriene C4

A

increased capillary permeability
breaks down to LTD4 and LTE4
each causes smooth muscle constriction

51
Q

leukotriene B4

A

neutrophil and monocyte chemotaxis

52
Q

monokines

A

released from monocytes/macrophages

produce acute phase reaction

53
Q

what are included in acute phase reaction?

A

interleukin-1 and tumor necrosis factor alpha (cachectin, TNF-a)

54
Q

acute phase reaction

A

“sick” from inflammatory illness
shift in hepatic protein synthesis, more complement, clotting, c-reactive protein
-increased erythrocyte sedimentation rate (“sed rate”)

55
Q

sed rate

A

nonspecific marker for course of inflammation

56
Q

c-reactive protein

A

risk factor for coronary disease

57
Q

what does SIRS stand for?

A

systemic inflammatory response syndrome

58
Q

what is SIRS?

A

exuberant production of inflammatory mediators

59
Q

what does SIRS result in?

A

multisystem organ failure due to normal tissue damage

60
Q

who is affected by SIRS?

A

super sick people in ICU

61
Q

what is the outcome of acute inflammation where neutrophils win?

A

complete resolution with no tissue damage

62
Q

what is the outcome of acute inflammation where neutrophils win but there are civilian casualties?

A

healing by scarring

63
Q

what is the outcome of acute inflammation where neutrophils cannot destroy but wall off?

A

abscess formation-“put” in a confined space other than a body cavity

64
Q

what is the outcome of acute inflammation where neutrophils and mediators cannot remove the noxious agent?

A

progression to chronic inflammation

65
Q

what is chronic inflammation defined as?

A

infiltration of mononuclear cells

-monocytes, lymphocytes, plasma cells

66
Q

does chronic inflammation include immune?

A

some crossover into immune system activation may be present

67
Q

what can chronic inflammation produce?

A

granulomas-macrophages adhere to each other and wall off stuff

68
Q

granulomatus diseases/disorders

A

foreign bodies
tuberculosis
deep fungal infections
sarcoidosis

69
Q

what is the predominant cell in infections by common bacteria (staph, strep, gram-negative rods)?

A

neutrophil

70
Q

what is the predominant cell in spirochete diseases (syphilis and Lyme)?

A

plasma cell

71
Q

what is the predominant cell in tuberculosis and fungal infections?

A

monocyte/macrophage

72
Q

what is the predominant cell in infections caused by worms?

A

eosinophil

73
Q

how could there be no inflammatory reaction?

A

depending on agent and host

example-diabetic on steroids

74
Q

what are the 2 courses following inflammation for damaged tissue?

A

regeneration of functional cells

repair by fibrous tissue (“scar”)

75
Q

labile cells

A

continuous replicators

ex. epithelium

76
Q

stable cells

A

discontinuous replicators
don’t normally regenerate but have capacity
glandular cells, fibroblasts, endothelium, osteoblasts, liver regeneration

77
Q

permanent cells

A

non-replicators

glia, neurons, heart

78
Q

repair-does damaged epithelium keep free edge?

A

No, cannot tolerate.

rapid re-epithelization by regeneration

79
Q

what replaces damaged cells?

A

connective tissue replaces permanent cells

80
Q

how does connective tissue replace permanent cells?

A

fibroblasts proliferate
-produce ground substance & collagen fibers
endothelial cells proliferate
-form new, leaky vessels
both invade and eventually displace the clot

81
Q

what is an immature scar?

A

granulation tissue

82
Q

what happens in maturing scars?

A

enough collagen to fill the void
re-epithelization completes
type III collagen replaced by type I
fibroblasts contract & return to rest
Most new vessels resorb
Never attains strength of original tissue

83
Q

what is the ideal situation for wound healing?

A

primary intention

84
Q

what does a surgical would healing by primary intention look like?

A

little necrosis
no infection (hopefully)
edges approximated

85
Q

primary intention: minutes

A

clotting cascade activated, stops the bleeding

86
Q

primary intention: 24 hours

A

neutrophils enter, epithelial cells are regenerating from the edges

87
Q

primary intention: 3 days

A

macrophages enter, granulation tissue appears, epithelial cells now cover the wound surface

88
Q

primary intention: 5 days

A

granulation tissue fills the entire wound

89
Q

primary intention: 2 weeks

A

fibroblasts multiply, collagen accumulates

90
Q

primary intention: 4 weeks

A

overlying epidermis complete sans adnexal structures, capillary involution & scar contraction occurring, red scar turns white

91
Q

what does secondary intention mean?

A

wound that can’t be closed or won’t be due to high risk of infection, heavily contaminated

92
Q

what does secondary intention look like?

A

no approximation

93
Q

what happens in secondary intention?

A

larger fibrin meshwork (scab), more inflammation, possibly infection, more granulation tissue, spectactular wound contraction

94
Q

what happens after complete re-epithelization in secondary intention?

A

scab is pushed off

95
Q

how long does it take for secondary intention to heal?

A

much longer than primary intention

96
Q

what does secondary intention produce?

A

always a deformity

97
Q

contracture

A

fibroblasts contract too much, can be crippling

98
Q

what causes contracture?

A

burns, ugly surgery

99
Q

hypertrophic scar

A

exuberant scar tissue formation

100
Q

does hypertrophic scar go beyond wound margins?

A

no, stays within wound margins

101
Q

does hypertrophic scar regress?

A

yes

102
Q

keloids

A

exuberant scar tissue formation

103
Q

do keloids go beyond wound margins?

A

yes, usually enlarge

104
Q

hindrances to adequate healing

A 
NOT OLD AGE
inadequate nutrition-protein, vitamin C, zinc
poor blood supply
foreign bodies
infection
glucocorticoid (steroid) therapy

Pathophysiology I (10 decks)

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