Inflammation

Question 1

acute inflammation

Answer 1

stereotyped response to recent injury or infection

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

Question 2

chronic inflammation

Answer 2

more variable response to ongoing injury or infection

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

Question 3

signs

Answer 3

red, heat, pain, loss of function, swelling

Question 4

margination

Answer 4

PNMs adhere to capillary walls; largely due to adhesion molecules

Question 5

emigration (diapedesis)

Answer 5

PNMs pass through capillary walls; driven by C5a

Question 6

chemotaxis

Answer 6

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

Question 7

phagocytosis

Answer 7

PNMs engulf pathogens and disease; opsonins C3b and IgG

Question 8

degranulation

Answer 8

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

Question 9

histamine

Answer 9

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

Question 10

bradykinin

Answer 10

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

Question 11

C3a/C5b

Answer 11

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

Question 12

C5a

Answer 12

chemotaxis

Question 13

C3b

Answer 13

opsonin

Question 14

C5-C9

Answer 14

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

Question 15

arachidonic acid metabolites

Answer 15

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

Question 16

cyclooxygenase

Answer 16

converts AA to prostaglandins (inhibited by NSAIDS)

Question 17

5-lipoxygenase

Answer 17

converts AA to leukotrienes

Question 18

thromboxane A2

Answer 18

prostaglandin that is produced by platelets; vasoconstriction, platelet aggregation

Question 19

prostacyclin

Answer 19

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

Question 20

Prostaglandin E2

Answer 20

vasodilation, potentiates bradykinin (pain) and fever

Question 21

Leuktriene C4

Answer 21

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

Question 22

Leukotriene B4

Answer 22

neutrophil and monocyte chemotaxis

Question 23

monokines

Answer 23

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

Question 24

acute phase reaction

Answer 24

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)

Question 25

c reactive protein

Answer 25

risk factor for coronary disease

Question 26

SIRS (systematic inflammatory response syndrome)

Answer 26

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

Question 27

outcomes of acute inflammation

Answer 27

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

Question 28

granulomas

Answer 28

macrophages adhere to each other and wall off shut

Question 29

granulomatous diseases/disorders

Answer 29

foreign body, TB, deep fungal infections, sarcoidosis

Question 30

predominant cell in common bacterial infection

Answer 30

PNM

Question 31

predominant cell in viral infection

Answer 31

lymphocyte

Question 32

predominant cell in spirochete diseases

Answer 32

plasma cell

Question 33

predominant cell in TB and fungal infections

Answer 33

monocyte/macrophage

Question 34

worm infection

Answer 34

eosinophils

Question 35

outcomes of chronic inflammation

Answer 35

regeneration of functional cells or repair by connective tissue

Question 36

labile cells

Answer 36

continuous replicators (most epithelium)

Question 37

stable cells

Answer 37

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

Question 38

permanent cells

Answer 38

non replicators (glia, neurons, heart)

Question 39

how scar formed

Answer 39

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

Question 40

immature scar

Answer 40

granulation tissue

Question 41

maturing scar

Answer 41

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

Question 42

primary intention (ideal)

Answer 42

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

Question 43

secondary intention

Answer 43

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

Question 44

contracture

Answer 44

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

Question 45

hypertrophic scar

Answer 45

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

Question 46

keloids

Answer 46

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

Question 47

hinderance to healing

Answer 47

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