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Pathology Exam 1 > Lectures 6-11 > Flashcards

Lectures 6-11 Flashcards

1
Q

cellular infiltrate in acute inflammation

A

neutrophils

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2
Q

cellular infiltrate in chronic inflammation

A

monocytes/macrophages and lymphocytes

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3
Q

what do TLRs do when activated?

A

stimulate release of cytokines (TNF)

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4
Q

role of inflammasome

A

cytoplasmic complex recognizing parts of dead cells; triggers activation of caspase-1 which activates IL-1, which, in turn, triggers leukocyte recruitment

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5
Q

key difference between TLRs and inflammasome

A

TLR recognizes extracellular microbes while inflammasome recognizes products of dead cells and some microbes

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6
Q

what cytokines activation endothelium at initiation of inflammation, leading to leukocyte binding?

A

IL-1 and TNF

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7
Q

vasodilation is caused by what mediators?

A

histamine and nitric oxide

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8
Q

increased vascular permeability is caused by what mediators?

A

histamine, bradykinin

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9
Q

histamine: source, effect

A

mast cells and basophils; vasodilation, increased vascular permeability, smooth muscle contraction

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10
Q

nitric oxide: source, effect

A

endothelial cells; vasodilation

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11
Q

bradykinin: effect

A

vasodilation, increased permeability, pain

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12
Q

transudate: protein and cell content, inflammatory/non-inflammatory, specific gravity

A

hypocellular and low protein content; non-inflammatory; low specific gravity (<1.012)

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13
Q

exudate: protein and cell content, inflammatory/non-inflammatory, specific gravity

A

cellular and protein rich; inflammatory; high specific gravity (>1.020)

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14
Q

specific gravity in infection

A

high

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15
Q

selectins: location, mechanism

A

on endothelial cells, platelets, leukocytes, not present on cell surfaces until cell is activated by mediators; aid in rolling and loose attachment of leukocytes to endothelial cells

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16
Q

integrins: location, mechanism

A

on leukocytes, TNF and IL-1 secreted by macrophages at site of injury increase endothelial cell ligand expression; results in stable attachment of leukocytes

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17
Q

what chemokine drives diapedesis?

A

CD31 (PECAM1)

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18
Q

cytokines that cause fever

A

TNF and IL-1

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19
Q

types of acute inflammation

A

serous, fibrous, suppurative, ulcer

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20
Q

serous inflammation: describe, examples

A

outpouring of protein-poor fluid from plasma or serosal cavity linings; congestive heart failure, skin blister from burn

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21
Q

congestive heart failure, skin blister from burn are examples of what type of acute inflammation?

A

serous

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22
Q

fibrinous inflammation: describe, examples

A

secondary to more severe injury than serous, affects linings (meninges, percardium, pleura, peritoneum), may lead to scarring; pericarditis, pleuritis, peritonitis

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23
Q

suppurative inflammation: describe, examples

A

occurs with infections, pus formation, abscess; acute appendicitis, acute meningitis

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24
Q

type of acute inflammation seen with acute appendicitis, acute meningitis, acute bronchopneumonia

A

suppurative

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25
Q

local defect on surface of organ or tissue in patients with circulatory insufficiency or diabetes

A

ulcer

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26
Q

role of eosinophils in chronic inflammation

A

produce major basic protein which is toxic to parasites and epithelial cells

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27
Q

two major characteristics of chronic inflammation

A

angiogenesis and fibrosis

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28
Q

what type of inflammation is characterized by aggregates of epithelioid macrophages, multinucleated giant cells, fibrosis, and angiogenesis?

A

granulomatous inflammation (a type of chronic inflammation)

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29
Q

granulomatous inflammation: morphology

A

aggregates of epithelioid macrophages, multinucleated giant cells, fibrosis, and angiogenesis

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30
Q

three characteristics of systemic inflammation

A

fever, elevated acute-phase proteins, leukocytosis

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31
Q

acute phase proteins: source, 3 proteins, function

A

synthesized in liver, stimulated by IL-6; C-reactive protein, fibrinogen, serum amyloid A protein; aid in elimination of microbes, fibrinogen binds to RBCs causing stacks that sediment more rapidly than normal, causing increased ESR (erythrocyte sedimentation rate)

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32
Q

increased erythrocyte sedimentation rate: mechanism, what it is indicative of

A

fibrinogen binds to RBCs causing stacks that sediment more rapidly than normal; infection or autoimmune disease

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33
Q

what cytokines stimulate leukocytosis in systemic inflammation?

A

TNF and IL-1

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34
Q

neutrophilia is indicative of what? what is left shift?

A

bacterial infection; accelerated release of immature neutrophils

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35
Q

lymphocytosis is indicative of what?

A

viral infection

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36
Q

which stage of an immune response is clinically silent?

A

sensitization stage (primary response)

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37
Q

spring allergen, summer allergen, fall allergen

A

tree, grass, weed

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38
Q

early phase (15-30 min.) of type 1 hypersensitivity is marked by what?

A

tryptase

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39
Q

degranulation mechanism

A

mast cells and basophils express FcRI (high affinity receptor for IgE), and when IgE binds and the receptor is crosslinked, the mast cell/basophil degranulates, releasing preformed mediators

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40
Q

single best marker of mast cell degranulation

A

tryptase

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41
Q

role of IL-4 and IL-13

A

class switching to IgE

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42
Q

role of IL-3, IL-5, and GM-CSF

A

survival and activation of eosinophils

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43
Q

cytokines responsible for class switching to IgE

A

IL-4 and IL-13

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44
Q

cytokines responsible for survival and activation of eosinophils

A

IL-3, IL-5, and GM-CSF

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45
Q

leukotrienes: source, role in type 1 hypersensitivity reactions

A

mast cells; eosinophil migration, smooth muscle contraction, vascular permeability, mucus hypersecretion

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46
Q

elevated eosinophils is an indication of what?

A

NAACP mnemonic: neoplasia, asthma, allergy, connective tissue disease, parasitic disease

47
Q

how do eosinophils get to the site of inflammation?

A

they have CCR3, a receptor for eotaxin, which is a chemokine found at sites of allergic inflammation

48
Q

effects of corticosteroids on eosinophils

A

steroids induce rapid apoptosis of eosinophils; steroids inhibit the production of IL-5, causing decreased release of eosinophils form the marrow; this effect is mediated by steroid binding to GR-alpha and inhibiting AP-1 and NFkappaB

49
Q

major basic protein: source, function

A

eosinophil; mast cell activation, helminthotoxic

50
Q

eosinophil cationic protein (ECP): function

A

mast cell activation, helminthotoxic, neurotoxic

51
Q

platelet activating factor (PAF): source, function

A

eosinophil; bronchoconstriction, activates platelets

52
Q

LTC4 (leukotriene C4): source, function

A

eosinophil; bronchoconstriction, mucus hypersecretion, edema

53
Q

allergic rhinitis: mechanism

A

symptoms due to crosslinking of IgE in nasal mucosa and ocular conjunctiva with specific antigen exposure

54
Q

asthma: differential diagnoses

A

vocal cord dysfunction (localized obstruction), COPD (generalized obstruction)

55
Q

asthma: components in inflammatory cell infiltrate

A

eosinophils and lymphocytes

56
Q

asthma: mechanism

A

symptoms are due in part by IgE-mediated disease in lower airways: wheezing, shortness of breath due to increased airway constriction (prevents exhalation), increased mucus secretion and production

57
Q

mediators of anaphylaxis

A

histamine, leukotrienes, nitric oxide

58
Q

histamine function via H1

A

smooth muscle contraction, vascular permeability

59
Q

histamine function via H2

A

vascular permeability

60
Q

histamine function via H1+H2

A

vasodilation, pruritus

61
Q

what antibodies are involved in type 2 hypersensitivity?

A

IgG and IgM

62
Q

how do some drugs induce an antibody response?

A

they become antigenic when bound to RBCs or platelets

63
Q

basis of type 3 hypersensitivity

A

production of IgG against a soluble antigen –> immune complex forms and activates complement

64
Q

where do immune complexes preferentially deposit?

A

sites with increased vascular permeability, sites of increased antigen

65
Q

serum sickness: what is it, what type of hypersensitivity, when does it happen and why

A

systemic reaction from injection of large quantities of foreign (non-human) protein; type 3; occurs 7-10 days after first exposure to antigen (this time is needed to switch from IgM to IgG –> form complexes)

66
Q

serum sickness: sequence of events

A
  1. IgM is made and clears some of the foreign serum proteins 2. IgM is class-switched to IgG and antigen-antibody complexes start to form and cause symptoms 3. when antigen becomes limited, complexes do not form and symptoms go away
67
Q

farmer’s lung: what type of hypersensitivity, what happens

A

type 3; alveolitis (destruction of alveolar wall) due to type 3 reaction against hay dust or mold spores –> impairment in gas exchange

68
Q

usual target organ of type 4 hypersensitivity

A

skin

69
Q

IFNgamma: source, role in type 4 hypersensitivity

A

T cells; induces expression of adhesion molecules and activates macrophages

70
Q

TNF and lymphotoxin: source, role in type 4 hypersensitivity

A

T cells; local tissue destruction, induces expression of adhesion molecules

71
Q

IL-3 and GM-CSF: source, role in type 4 hypersensitivity

A

T cells; stimulates monocyte production from bone marrow

72
Q

what cell mediates a tuberculin response?

A

TH1

73
Q

Rhus dermatitis: mechanism

A

chemical from poison ivy leaf bind with self proteins and generates extensive macrophage-mediated inflammation

74
Q

is antigen soluble or cell-associated for each hypersensitivity reaction?

A

1: soluble 2: cell (or matrix) associated 3: soluble 4: soluble for TH1 cells and cell associated for CD8 CTLs

75
Q

components of repair (3)

A

remnants of injured tissue, endothelial cells, fibroblasts

76
Q

what kind of cells repair by connective tissue (scar)?

A

non-dividing cells

77
Q

asymmetric replication

A

with cell division, a daughter cell differentiates, but the other daughter cell remains a stem cell

78
Q

what growth factors induce angiogenesis?

A

VEGF and FGF

79
Q

what growth factors produce ECM proteins?

A

PDGF and TGF-beta

80
Q

PDGF and TGF-beta: source, functions

A

platelets, macrophages, epithelium, and smooth muscle cells; produce ECM proteins

81
Q

two basic forms of ECM and where each is synthesized

A

interstitial matrix: fibroblasts basement membrane: mesenchyme and epithelium

82
Q

provides scaffold essential for healing without scar

A

ECM

83
Q

Ehlers-Danlos syndrome: mechanism, clinical presentation

A

genetic defects in collagen synthesis; hyperextensible skin, hypermobile joints and ligaments, rupture of internal organs and large arteries

84
Q

hyperextensible skin, hypermobile joints and ligaments, rupture of internal organs and large arteries

A

Ehlers-Danlos syndrome

85
Q

Marfan syndrome: mechanism, clinical presentation

A

mutation affecting fibrillin (major component of ECM abundant in aorta, lens, ligaments); aneurysm and dilatation of aorta, dislocated lens, long legs, arms, fingers

86
Q

aneurysm and dilatation of aorta, dislocated lens, long legs, arms, fingers

A

Marfan syndrome

87
Q

4 sequential steps of repair by connective tissue

A

angiogenesis, fibroblast migration and proliferation, scar formation, remodeling

88
Q

granulation tissue: when does it appear

A

present by 3-5 days

89
Q

growth factors responsible for fibroblast migration and proliferation

A

TGF-beta, PDGF, FGF

90
Q

what growth factor is necessary for both angiogenesis and fibroblast migration/proliferation?

A

FGF

91
Q

remodeling of scar is accomplished by what?

A

matrix metalloproteinases (MMP) containing zinc degrades collagen and other ECM proteins

92
Q

matrix metalloproteinases (MMP): role

A

degrades collagen and other ECM proteins = remodeling of scar

93
Q

healing by first intention: when are neutrophils replaced with macrophages

A

by day 3

94
Q

how do hormones affect healing?

A

steroids inhibit TGF-beta and decreases fibrosis

95
Q

raised scar due to excess collagen

A

keloid

96
Q

keloid

A

raised scar due to excess collagen

97
Q

protrudes above surrounding skin without skin covering

A

exuberant granulation

98
Q

wound healing: when does a thin layer of epithelial cells cover wound?

A

48 hours

99
Q

wound healing: when is epidermis at full thickness?

A

day 5

100
Q

wound healing: when is granulation tissue present?

A

day 3 to second week

101
Q

wound healing: when is there connective tissue remodeling?

A

after one month

102
Q

wound healing: when is wound strength 70-80%?

A

by three months

103
Q

rank HIV transmission risk: mom-baby (without prophylaxis), IVDU, percutaneous (blood), receptive vaginal intercourse, receptive anal intercourse

A

IVDU > mom-baby > receptive anal intercourse > percutaneous (blood) > receptive vaginal intercourse

104
Q

window period: what is it, and how long

A

HIV can be detected in blood but antibodies to HIV are not present; 6-8 weeks

105
Q

HIV: when do signs and symptoms begin?

A

1-4 weeks after exposure

106
Q

HIV: how long do symptoms last?

A

<14 days

107
Q

HIV: when is viral load the highest?

A

first 2-3 months

108
Q

immune reconstitution inflammatory syndrome: when does it develop?

A

within 8 weeks of starting antiretroviral treatment

109
Q

microbial translocation in HIV: mechanism

A

massive mucosal CD4 T cell depletion results in increased gut permeability –> increased plasma LPS levels; gut permeability increases over time

110
Q

main difference between direct and indirect alloantigen recognition

A

direct: graft APCs indirect: host APCs

111
Q

major players in chronic rejection (3)

A

CD4 T cells, macrophages, cytokines

112
Q

what are minor histocompatibility antigens?

A

cleaved and processed endogenous proteins that occupy the binding groove of MHC class I and II

113
Q

GVHD: mechanism

A

incoming donor T cells recognize host APCs, become activated, attack tissues of recipient and cause immediate tissue damage

114
Q

what can exacerbate the symptoms off GVHD?

A

preconditioning can cause tissue damage that allows LPS to cross the gut barrier or cytokines to be released by damaged tissues –> activated macrophages amplify the function of donor T cells

Pathology Exam 1 (4 decks)

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