13 Inflammation Flashcards by Ryan Lee

what causes chronic granulomatous disease? what does it result in?

NADPH-oxidase system enzyme defect in PMNs. results in decreased superoxide radical formation

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what is the primary mediator of reperfusion injury?

PMNs

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what are the cellular defenses against oxidative species?

for superoxide anion radical, superoxide dismutase: converts to hydrogen peroxide.
glutathione peroxidase, catalase then break down hydrogen peroxide

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what are the oxidants generated in inflammation and what are the enzymes that caused it?

superoxide anion radical produced by NADPH oxidase. hydrogen peroxide generated from xanthine oxidase

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what does CXC chemokines stand for and what are they?

C = cysteine; X = another amino acid. IL-8 and platelet factor 4

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what do cxc chemokines do?

chemotaxis, angiogenesis, wound healing

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what does thyroid hormone do during injury or inflammation?

nothing

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what is the neuroendocrine response to injury?

afferent nerves from site of injury stimulate CrF, ACTH, ADH, growth hormone, epinephrine, and norepinephrine release

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where in the body are epinephrine and norepinephrine released?

adrenal medulla (neural response to injury)

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where in the nerve is norepinephrine released?

from sympathetic postganglionic neurons

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when do catecholamines peak after injury?

24-48h

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what does LTB4 do?

chemotactic for inflammatory cells

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what are the leukotrienes and what do they do?

LTC4, LTD4, LTE4. slow reacting substances of anaphylaxis. bronchoconstriction, vasoconstriction, followed by inc permeability (wheal and flare)

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where do prostaglandins come from?

arachidonic precursors

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where do leukotrienes come from?

produced from arachidonic precursors

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what does phospholipase do?

converts phospholipids to arachidonic acid

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how do steroids work?

inhibit phospholipase, which converts phospholipids to arachidonic acid –> inhibits inflammation.

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what does aspirin do? is it irreversible?

inhibits cyclooxygenase (irreversible), inhibits platelet adhesion by decreasing TXA2

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what do NSAIDs do? are they reversible?

inhibits cyclooxygenase (reversible)

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what prostaglandins cause vasodilation, bronchodilation, inc permeability, and inhibits platelets?

PGI2 and PGE2

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what factors are responsible for chemotaxis for inflammatory cells?

C3a and C5a

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what does opsonization do? mediated by what?

targets antigen for immune response, C3b and C4b

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what is the membrane attack complex and what does it do?

C5b-9b; causes cell lysis (usually bacteria) by creating a hole in the cell membrane

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what are the anaphylatoxins? what do they do?

C3a, C4a, C5a.

Increase vascular permeability
bronchoconstriction
activate mast cells and basophils

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what factors are activated in classic pathway?

C1, C2, C4 found only in classic pathway

what electrolyte is required for both pathways?

what factor is common to and is the convergence point for both common and alternative pathway?

what factors are activated in alternate pathway?

B, D, P found only in the alternate pathway

what are the activators in alternative pathway?

endotoxin, bacteria, other stimuli

what are the major molecules in classic pathway?

IgG or IgM: antigen-antibody complex activates complement

can you illustrate leukocyte recruitment?

illustration

where are ICAM, VCAM, PECAM, ELAM located? what do they do?

located on endothelial cells, bind beta-2 integrin moecules located on leukocytes and platelets. Also involved in transendothelial migration

what CD molecules are beta-2 integrins? where are they located? where do they bind? what do they do?

CD11/18 located on leukocytes bind ICAMs etc. they anchor adhesion

where are L-, E-, and P- selectins located?

leukocytes, endothelial, platelets

what do selectins do? what is the process?

cause rolling adhesion. L-selectins bind to E and P selectins

what are the cell adhesion molecules?

selectins, beta-2 integrins, ICAM, VCAM, PECAM, ELAM

what hepatic acute phase response proteins are decreased?

albumin, prealbumin, transferrin

what hepatic acute phase response proteins are increased??

``` CRP amyloid A and P fibrinogen haptoglobin ceruloplasmin alpha-1 antitrypsin C3 (complement) ```

what is the most potent stimulant of hepatic acute phase response proteins?

IL-6

what type of protein is CRP?

an opsonin, activates complement

what do interferons do?

activate macrophages, natural killer cells, cytotoxic T cells. they inhibit viral replication

what releases interferons?

lymphocytes, in response to viral infections and other stimulants

what does IL-6 do?

increase hepatic acute phase proteins via c-reactive protein, amyloid A

how does atelectasis cause fever?

alveolar macrophages release IL-1

how do NSAIDs decrease fever?

reduce PGE2 synthesis

how does IL-1 cause fever?

through PGE2 mediated in hypothalamus, raising thermal set point, causing fever

what are the effects of IL-1?

similar to TNF-a and synergizes TNF-a | responsible for fever

what is the main source of IL-1?

macrophages

what is the major producer of TNF-a?

macrophages

is TNF-a a procoagulant or anticoaculant?

procoagulant

what does TNF-a do to pts with cancer?

cachexia

what does high concentrations of TNF-a do?

cause circulatory collapse and multisystem organ failure

what does TNF-a do?

recruits macrophages increases adhesion molecules activates neutrophils and macrophages --> more cytokine production, cell recruitment

what cytokine are initially released to injury and infection?

TNF-a and IL1

what substance causes the opposite effect of nitric oxide?

endothelin. (causes vascular smooth muscle constriction)

what is the other name for nitric oxide?

endothelium-derived relaxing factor

what does nitric oxide do?

activates guanylate cyclase and increases cGMP, resulting in vascular smooth muscle dilation

what amino acid is the substrate in the nitric oxide precursor? what is the enzyme?

arginine. nitric oxide synthase

what does angiotensin-converting enzyme (ACE) do? where is ACE located?

inactivates bradykinin. located in lung

what does bradykinin do?

peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction

what is the primary effector in type I hypersensitivity reactions?

histamine

what does histamine do?

vasodilation, tissue edema, postcapillary leakage

what is the primary cell type in type I hypersensitivity reactions?

mast cells

where are basophils found?

blood. not tissue

in what infections are eosinophils increased?

parasitic infections

what does major basic protein do?

stimulate basophils and mast cells to release histamine

how do eosinophils work?

have IgE receptors that bind to allergen, release basic science protein

what cells are involved in type I hypersensitivity reactions?

eosinophils, basophils, mast cells, histamine, bradykinin, ACE

what do TXA2 and PGI2 do?

what cells are involved in antibody production?

B cells

what cells are involved in chronic inflammation?

T cells

how long do platelets last?

7-10d

how long do PMNs last in the tissue? in blood?

1-2d. 7d in blood

what are the chemotactic factors for fibroblasts?

PDGF EGF FGF

what are the epithelialization factors?

PDGF

what are the angiogenesis factors?

PDGF EGF FGF IL-8

what are the chemotactic factors for inflammatory cells?

``` PDGF IL8 LTB-4 C5a, C3a PAF ```

what does FGF do?

- fibroblastic growth factor - chemotactic and activates fibroblasts (collagen and ECM proteins). - angiogenesis, epithelialization

what does EGF do?

epidermal growth factor chemotactic, activates fibroblasts, angiogenesis epithelialization

what generates PAF? is it stored? what makes it? what type of molecule is it?

phospholipase in endothelium. not stored. is a phospholipid.

what does PAF do?

platelet activating factor: chemotactic for inflammatory cells, increase of adhesion molecules

what cells migrate toward pdgf using chemotaxis?

inflammatory cells, fibroblasts, smooth muscle cells

what does PDGF do?

chemotacticm activates inflammatory cells, fibroblasts, angiogenesis, epithelialization, accelerates wound healing

what happens during the macrophages phase?

release of important growth factors (PDGF) and cytokines (IL-1 and TNF-a)

which cytokines are released during the macrophage phase?

IL-1 and TNFa

what cell plays a the dominant role in wound healing?

macrophages

what happens during the platelets bind collagen phase?

release growth factors (platelet-erived growth factor [PDGF]); leads to PMN and macrophage recruitment

what happens during the injury phase?

leads to exposed collagen, platelet activating factor release, and tissue factor release from endothelium

what are the inflammation phases?

injury, platelets bind collagen, macrophages