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Pathophysiology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

acute inflammation

A

stereotyped response to recent injury or infection

-vasodilation (largely due to histamine) , increased capillary permeability, PNM main players

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2
Q

chronic inflammation

A

more variable response to ongoing injury or infection

-T helper cells main players, infiltration by monocytes, macrophages, lymphocytes, and plasma cells

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3
Q

signs

A

red, heat, pain, loss of function, swelling

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4
Q

margination

A

PNMs adhere to capillary walls; largely due to adhesion molecules

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5
Q

emigration (diapedesis)

A

PNMs pass through capillary walls; driven by C5a

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6
Q

chemotaxis

A

PNMs follow chemical signals to damage/infection; driven by C5a

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7
Q

phagocytosis

A

PNMs engulf pathogens and disease; opsonins C3b and IgG

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8
Q

degranulation

A

neutrophils release cytoplasmic granules: prostaglandins, leukotrienes, free radicals, lysosomal enzymeshistamine

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9
Q

histamine

A

responsible for vasodilation and capillary permeability; released from tissue in mast cells (connective tissue cell that degranulates and releases it) during injury or infection

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10
Q

bradykinin

A

sort of like histamine responsible for vasodilation and capillary permeability; formed from kinin system; causes pain

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11
Q

C3a/C5b

A

release histamine; together form anaphyltoxins (too much histamine cause anaphylactic shock)

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12
Q

C5a

A

chemotaxis

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13
Q

C3b

A

opsonin

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14
Q

C5-C9

A

membrane attack complex (punches hole in membrane); final result of cascade pathways

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15
Q

arachidonic acid metabolites

A

derivatives of phospholipids; cells liberate the phospholipase A2 liberates AA from cell membranes (inhibited by steroids)

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16
Q

cyclooxygenase

A

converts AA to prostaglandins (inhibited by NSAIDS)

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17
Q

5-lipoxygenase

A

converts AA to leukotrienes

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18
Q

thromboxane A2

A

prostaglandin that is produced by platelets; vasoconstriction, platelet aggregation

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19
Q

prostacyclin

A

prostaglandin that is produced by endothelial cells; vasodilation prevents platelet aggregation

20
Q

Prostaglandin E2

A

vasodilation, potentiates bradykinin (pain) and fever

21
Q

Leuktriene C4

A

increased capillary permeability, breaks down LTD4 to LTE4 (each causes smooth muscle contraction)

22
Q

Leukotriene B4

A

neutrophil and monocyte chemotaxis

23
Q

monokines

A

released from monocytes/macrophages; produce acute phase reaction; IL-1 and TNFs; usually what makes people feel sick

24
Q

acute phase reaction

A

change in metabolism that occurs in inflammation
-shift in hepatic protein synthesis (increased complement, clotting, C-reactive protein and decreased normal liver proteins) , increased rbc sedimentation rate (nonspecific marker for course of inflammation)

25
Q

c reactive protein

A

risk factor for coronary disease

26
Q

SIRS (systematic inflammatory response syndrome)

A

exuberant production of inflammatory mediators; multi system organ failure due to damage in normal tissues
must have 2 or more: temp >38 or <36C, HR > 90. RR >20, Pco2 less than 32mmHg, WBV 12,000 or 4,000 or more than 10% immature PNMs

27
Q

outcomes of acute inflammation

A

complete resolution, healing with scarring, abscess, progression to chronic inflammation

28
Q

granulomas

A

macrophages adhere to each other and wall off shut

29
Q

granulomatous diseases/disorders

A

foreign body, TB, deep fungal infections, sarcoidosis

30
Q

predominant cell in common bacterial infection

A

PNM

31
Q

predominant cell in viral infection

A

lymphocyte

32
Q

predominant cell in spirochete diseases

A

plasma cell

33
Q

predominant cell in TB and fungal infections

A

monocyte/macrophage

34
Q

worm infection

A

eosinophils

35
Q

outcomes of chronic inflammation

A

regeneration of functional cells or repair by connective tissue

36
Q

labile cells

A

continuous replicators (most epithelium)

37
Q

stable cells

A

discontinuous replicators, but replicate when stimulated (granular cells,fibriblasts, endothelium, osteoblasts, liver)

38
Q

permanent cells

A

non replicators (glia, neurons, heart)

39
Q

how scar formed

A

fibroblasts infiltrate and produce ground substances and collagen fibers, endothelial cells proliferate forming new, leaky vessels

40
Q

immature scar

A

granulation tissue

41
Q

maturing scar

A

type III collagen replaced by type I, fibroblasts contract and return to rest (causes cells to get smaller over time, vessels resorb

42
Q

primary intention (ideal)

A

little necrosis, no infection, edges approximated
within minutes, clotting cascade, 24 hours: PNMs enter, epithelial cells regerating edges; 3 days: macrophages enter, granulation tissue appears and epithelial cells cover surface, 5 days: granulation tissue fills entire wound, 2 weeks: fibroblasts multiply, collagen accumulates; 4 weeks: epidermis completes sans axdnexal structures, capillary involution and scar contraction occurring, red scar turns white

43
Q

secondary intention

A

no approximation, larger fibrin meshwork, more inflammation, possibly infection, more granulation tissue, spectacular would contraction, much longer to complete healing, deformity produces

44
Q

contracture

A

fibroblasts contract too much, can be crippling *burns, ugly surgery)

45
Q

hypertrophic scar

A

exuberant scar tissue formation (stays within margins, usually regress)

46
Q

keloids

A

exuberant scar tissue formation, goes beyond margins, darkly pigmented people, usually enlarge

47
Q

hinderance to healing

A

inadequate nutrition (protein, vitamin C, zinc), poor blood supply, foreign bodies, infection, glucocorticoid (steroid) therapy

Pathophysiology (3 decks)

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