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Pathoma > Inflammation & Wound Healing > Flashcards

Inflammation & Wound Healing Flashcards

1
Q

acute inflammation is characterized by

A

edema and neutrophils (innate immunity)

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2
Q

Toll-like receptors

A

on innate and adaptive immune cells

activated by pathogen-associated molecular patterns (PAMPs) –> upregulated NF-kB

ie CD14 — LPS

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3
Q

arachidonic acid is released by

A

phospholipase A2

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4
Q

cyclooxygenase produces

A

prostaglandins

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5
Q

5-lipoxygenase produces

A

leukotrienes

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6
Q

prostaglandins mediate

A

PGI2, PGD2, PGE2 mediate vasodilation of arterioles and post-capillary vascular permeability

PGE2 mediates fever

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7
Q

leukotrienes mediate

A

LTC4, LTD4, LTE4 cause vasoconstriction, bronchospasm, and increase vascular permeability

ie smooth muscle contraction

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8
Q

what attracts and activates neutrophils?

A

LTB4
C5a
IL-8
bacterial products

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9
Q

mast cells are activated by

A

tissue trauma
C3a, C5a
crossing linking by IgE antigen

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10
Q

classical pathway activation

A

C1 bings IgG or IgM bound to antigen

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11
Q

alternate pathway activation

A

microbial products directly activate complement

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12
Q

mannose-binding lectin pathway

A

MBL binds to mannose of microbes

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13
Q

mast cells immediately

A

release histamine

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14
Q

mast cells delayed response

A

produce leukotrienes

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15
Q

Hageman factor (factor XII) activates

A

1) coagulation and fibrinolytic systems
2) complement
3) kinin system (HMWK –> bradykinin)

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16
Q

redness and warmth due to

A

vasodilation

key mediators: histamine, prostaglandins, bradykinin

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17
Q

swelling due to

A

leakage of fluid from postcap venules

key mediators: histamine, tissue damage

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18
Q

pain due to

A

sensitized nerve endings

key mediators: bradykinin and PGE2

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19
Q

fever due to

A

pyrogens cause macrophages to release IL-1 and TNF –> increased cyclooxygenase activity in perivascular cells in hypothalamus

key mediators: PGE2

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20
Q

margination involves

A

vasodilation and cells flowing to the periphery

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21
Q

rolling involves

A

selectin on endothelial cells binding to sialyl Lewis X on leukocytes

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22
Q

P-selectin is released from

A

Weibel-Palade bodies, mediated by histamine

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23
Q

E-selectin is induced by

A

TNF and IL-1

24
Q

adhesion

A

interaction of CAMs and integrins

25
Q

integrins are upregulated by

A

C5a and LTB4

26
Q

CAMs are upregulated by

A

TNF and IL-1

27
Q

leukocyte adhesion deficiency

A

CD18 on integrins

clinically see delayed separation of umbilical cord, increased circulating neutrophils, increased bac infection w/ no pus

28
Q

neutrophils are attracted by

A

IL-8, C5a, LTB4

29
Q

phagocytosis is enhanced by

A

IgG and C3b

30
Q

Chediak-Higashi syndrome has

A

impaired phagolysosome formation

clinically: pyogenic infection, neutropenia, giant granules in leukocytes, defective primary hemostasis, albinism, peripheral neuropathy

31
Q

killing in phagolysosomes done by

A

HOCl

O2 –> O2- –> H2O2 –> HOCl
enzymes: NADPH oxidase, SOD, MPO

32
Q

Chronic granulomatous disease is characterized by

A

poor O2 dependent killing due to NADPH oxidase defect

clinically: infection with catalase (+) organisms
test with NBT dye: colorless = (+)

33
Q

MPO deficiency is characterized by

A

increased risk of Candida infections

34
Q

macrophage peak at

A

2-3 days after inflammation begins

kill via lysozymes

35
Q

anti-infammatory cytokines produced by macrophages

A

IL-10 and TGF-B = resolution and healing

36
Q

produced by macrophages to recruit more neutrophils

A

IL-8 = continued acute inflammation

37
Q

abscess is

A

acute inflammation surrounded by fibrosis

38
Q

macrophages produce chronic inflammation when

A

macrophages present antigen to CD4+ helper T cells

39
Q

chronic inflammation characterized by

A

presence of lymphocytes and plasma cells

40
Q

CD4 helper T cell activation

A
  1. MHC class II (antigen presenting cell) —- TCR complex (CD4 T-cell)
  2. B7 (antigen presenting cell) —- CD28 (CD4 T-cell)
41
Q

T-cell receptor complex is

A

TCR + CD3

42
Q

activated CD4 secrete

A

cytokines Th1 and Th2

43
Q

Th1 secretes

A

IFN-y which activates macrophages, IgM class switching from IgM to IgG, inhibits Th2

44
Q

Th2 secretes

A

IL-4 which promotes B-cell class switching to IgE, IL-5 causes eosinophil chemotaxis and switching to IgA, IL-13 which is similar to IL-4

45
Q

IL-4 promotes

A

B-cell class switching to IgE

46
Q

IL-5 causes

A

eosinophil chemotaxis and B-cell class switching to IgA

47
Q

IL-13 is similar to

A

IL-4

48
Q

CD8 cytotoxic T-cell activation

A
  1. MHC class I (on all nucleated cells) —– TCR complex (CD8 T-cell)
  2. IL-2 (CD4 Th1 cell)
49
Q

CD8 cytotoxic T-cells induce apoptosis by

A
  1. secretion of perforin and granzyme

2. expression FasL

50
Q

B-cell activation occurs via

A

either:
1. antigen binding to surface IgM or IgD
or
2. MHC class II (B-cell) —– TCR complex (CD4) and CD 40 (B-cell) —– CD40L (CD4 T-cell)

51
Q

key cell of a granuloma is

A

epithelioid histiocytes (macrophages w abundant pink cytoplasm)

52
Q

granuloma is surrounded by

A

giant cells and rim of lymphocytes

53
Q

noncaseating granulomas

A

lack central necrosis

ie sarcoidosis, beryllium exposure, Crohn dz, cat scratch dz

54
Q

caseating granulomas have

A

central necrosis

ie TB, fungal infection

55
Q

macrophages secrete IL-12 which induces

A

CD4 helper T cells to differentiate into Th1 subtype

56
Q

IFN-y helps convert macrophages into

A

epithelioid histiocytes and giant cells

Pathoma (3 decks)

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