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Block 3 Found Sci > 2-Acute Inflammation > Flashcards

2-Acute Inflammation Flashcards

1
Q

inflammation

definition-general

A

local reaction of vascularized tissue to injury

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2
Q

inflammation by time

A

acute = 0-2 days
subacute = 2-14 days
chronic = 14+ days

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3
Q

acute inflamm cells

A
  1. neutrophils
  2. eosinophils if allergic reaction
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4
Q

subacute inflamm cells

A

neutrophils + monocytes + lymphocytes + plasma cells + fibroblastc elements + angioblastic elements

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5
Q

chronic inflamm cells

A

mononuclear cells - monocytes + lymphocytes
plasma cells, macrophages
granuloma cells- epithelioid cells + giant cells

monocyte @ vasculature > migrate to macrophage

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6
Q

eosinophils

A

predominant inflamm cell in allergic reaction and parasitic infestations

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7
Q

plasma derived molecular systems

A
  1. immune - Ab, C3, C5 frags
  2. kinin- bradykinin
  3. clotting - thrombin
  4. fibrinolytic - plasmin
  5. acute phase proteins - CRP, cereuloplasmin, haptoglobin
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8
Q

tissue derived molecular systems

A
  1. vasoactive amines- histamine, serotonin
  2. acidic lipids- prostaglandins, leukotrienes, lipoxins
  3. cytokines- IL1, TNF, chemokines (IL8, MCP1, MIP-1alpha, lymphotactin)
  4. others- PAF, NO, free radicals, lysosomal enzymes
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9
Q

inflamm protective response

A

to get rid of initial cause of cell injury aka microbes, toxins
or consequences of the injury aka necrotic cells and tissues

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10
Q

inflamm harmful response

A

if
-inflamm rxn underlies common chronic diseases
-uncontrolled lead to life threatening hypersensitivity rxns
-repair produces constrictive scarring and limb immobilization

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11
Q

6 cardinal signs

A
  1. heat aka inc blood flow to site
  2. redness- inc blood flow
  3. swelling- acc of water and cells
  4. pain- pressure of fluid and effect of mediators
  5. loss of function- secondary to 1-4
  6. systemic changes- release of humoral factors
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12
Q

causes of inflamm

A
  1. infection
  2. trauma
  3. physical injury (thermal extremes, radiation)
  4. chemical injury (poisons)
  5. immunologic injry
  6. tissue necrosis (inflamm arises in living tissue next to necrotic area)
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13
Q

serous inflamm

morphologic patterns

A

outpour of watery, protein poor fluid aka effusion

from serum or mesothelilal cell secretions (peritoneal, pleural, pericardial cavities)
OR from skin blisters from burns or viral infections

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14
Q

fibrinous inflamm

morphologic patterns

A

more severe injuries or inflamm of body cavities but may resolve

inc vascular permeability so leakage of larger molecules (fibrinogen) so extravascular fibrin acc
-if fibrin not completel removed then ingrowth of fibroblasts and blood vessles happen (organization process)

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15
Q

suppurative/purulent inflamm

morphological patterns

A

large amounts of pus (neutrophils + necrotic cells + edema fluid + microbes maybe) from pyogenic bacteria most likely

abscess is a collection of pus with central necrotic region surrounded by layer of preserved neutrophils
-can be walled off by fibroblasts in chronic

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16
Q

ulceration inflamm

morphologic patterns

A

local excavation by sloughing of inflamm necrotic tissue on/near a surface of skin and mucosa

most common @ mucosa mouth, GI tract, GU tract, LE

acute or chronic (fibroblasts in base of ulcer with chronic inflamm cells and scarring)

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17
Q

outcomes of acute inflamm

A
  1. resolution
  2. scarring after substantial tissue destruction or tissues that can’t regenerate
  3. abscess
  4. chronic
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18
Q

key events

A
  1. inc blood flow via vasodilation after initial constriction
  2. plasma proteins and leukocytes leave circulation, structual changes to microvasculature
  3. emigration of leukocytes from microcirculation to acc in focus of injury, activation to eliminate offending agent
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19
Q

hemodynamic changes

A
  1. vasoconstriction of arterioles, immediate and transient
  2. vasodilation of arterioles and venules, precapillary sphincters open, inc blood flow
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20
Q

transudate

A

formed when fluid leaks out of vascular bed from inc hydrostatic pressure or dec oncotic pressure

effusion characteristics- hypocellular/no cells so clear, low protein, low LDH,

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21
Q

exudate

A

vascular permeability inc as result of inc interendothelial spaces, lymphatic obstruction, inflamm, or malignancy

effusion character- cellular so cloudy, high protein and LDH

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22
Q

mechanisms of inc permeability

aka vascular leakage

A
  1. endothelial contraction to widen junctions, capillaries and post cap venules
  2. direct injury
  3. leukocyte injury
  4. new blood vessel leakage
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23
Q

leakage pathway

A
  1. leakage of fluid to interstitial space aka edema
  2. stasis of circulation resulting in inc blood viscosity
  3. dec absorption of fluid from interstitial space
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24
Q

lymphedema

A

is initially transudate and causes pitting edema but becomes more proteinaceous/exudate over time and usually fibrotic

25
Q

leukocyte extravasation

A
  1. leukocyte activation
  2. endothelial activation
  3. chemotaxis

leukocyte exit from blood vessels at site of inflamm

26
Q

selectin family

general

A

calcium dependent lectins @ surface of endothelium, platelets, leukocytes

mediate rolling phase along endothelium at sites of inflamm but not firm adhesion just slow down

27
Q

selectin molecules

A
  1. P selectin = aka CD62P on endo binds with sialyl lewis X on glycoproteins on leuks
  2. E selectin = CD62E on endo binds sialyl lewis X on glyoproteins on leuks
  3. L selectin = CD62L on leuks bind with sialyl lewis X on glycoprotein on leuks
28
Q

immunoglobulin family

A

Ig family of moles with 3 endothelial adhesion molecules
1. ICAM 1 aka CD54 on endo for tight binding to integrins LFA1 and Mac 1 on neutrophils and macrophages
2. VCAM 1 aka CD106 on endo for tight binding to integrin VLA4 on lymphocytes, monocytes, eosins, basophils
3. PECAM1 aka CD 31 on endo and leuks to bind homophilic and diapedesis of leuk extravastion

29
Q

integrin family

A

group of adhesion moles with heterodimers alpha + beta subunits, transmembrane proteins linking exterior stimuli to cytoskeleton

30
Q

VLA-4

CD49a/CD29

A

beta1 integrin CD29 > heterodimer with alpha subunit CD49a

only on leuks to bind VCAM1 on endo

31
Q

LFA-1

CD11/CD18

A

beta2 integrin CD18 + CD11a mole = heterodimer

‘leukocyte fuction associated antigen-1’ on neutrophils and macrophages
-binds to ICAM-1 on endo with complement receptor 3 and 4 for extravasation

if deficient in beta2 then susceptible to infection

32
Q

functional responses leukocytes

A
  1. modulate leuk adhesion molecules
  2. activate oxidative burst and degranulation and secretion lysosomal enzymes
  3. produce arachidonic acid metabolites
  4. secrete cytokines
33
Q

phagocytosis

A
  1. recognition and attachment: enhanced by opsonins like IgG, C3b, mannonse-binding lectin
  2. engulfment: pseudopods surround object = phagosome that fuses with lysosome = phagolysosome
  3. kill microorganisms: oxygen dependent or independent
34
Q

aerobic pathway killing microorgansims

A

oxygen dependent aka respiratory burst
1. superoxide radical via NADPH oxidase
2. convert to hydrogen peroxide by superoxide dismutase
3. myelo-peroxidase from neutrophilic granules catalyzes rxn b/t Cl and hydrogen peroxide = hypochlorous acid powerful oxidant and antimicrobial

35
Q

oxygen independent pathway

killing microorgs

A

leukocyte granule proteins and enzymes

i.e. lysozymes, acid hydrolases, lactoferrin, cationic proteins

36
Q

mediators of inflamm rules

A
  1. og from plasma as precursor or tissue cells in granules or synthesized
  2. bind to specific receptors on target cells
  3. can stimulate release of other or same mediators from target cells
  4. short lived so quickly decay and inact by enz or inhibited
  5. potential to cause harmful effects
37
Q

vasoactive amines

A

aka histamine and serotonin
bind to H1 receptors on endo to cause inc permeability or postcap venules
-immediate but transient/quick effect
-stored in granules of mast cells, basophils, platelets

dilate ARTERIOLES but constrict LARGE ARTERIES

38
Q

mast cell release triggers

A
  1. trauma, cold, heat
  2. platelet aggregation
  3. C3a, C4a, C5a anaphylatoxins
  4. neuropeptides
  5. cytokines IL1 and 8
  6. histamine releasing proteins (cationic) from platelets and neutrophils
  7. IgE binding
39
Q

plasma protein systems

A
  1. complement system
  2. kinin system
  3. clotting system
  4. fibrinolytic system

1-3 are cascade

40
Q

complement activation

A

critical step to cleave C3

  1. classic pathway: binding of antigen antibody (IgG or IgM) complex to C1
  2. alternate: C3 directly act by bacterial endotoxins, complex polysaccharides, aggregated globulins
  3. lectin: C1 act by binding mannose binding lectin to carbs on microbes
41
Q

important complement fragments

A
  1. C3-5a- anaphylatoxins, stim histamine from mast cells = inc vascular permeability and vasodilation
  2. C5a - chemotaxis of monocytes and granulocytes = inc surface expression of leukocyte CAM to activate lipoxygenase pathway in neutros and monocytes
  3. C3b - opsonize with recognition by receptors on neutrophils, macros, eosins
  4. C5-9 - membrane attack complex inserts into lipid bilayer to make pores to inc cell permeability = lysis
42
Q

hageman factor

A

aka factor XII of intrinsic clotting system

act by direct contact with activated platelets, endotoxins, collagen, or BM = kinin system and clotting system

will induce bradykinin, fibrin, fibrin split products, anaphylatoxins

43
Q

kinin system

A

hageman factor converts
prekallikrein into kallikrein:

amplifies act of hageman factor
cleaves high molecular weight kninogen = kinins like bradykinins
convert plasminogen to plasmin
chemoattractant for neutros and covert C5 to C5a (for leuks)
inc cell adhesion mole expression on endo

44
Q

bradykinin

A

short lived vasoactive peptide that

inc vascular permeability
dilates blood vessels
vontracts nonvascular smooth muscle
causes pain

short bc quickly inactivated by plasma kininase

45
Q

clotting and fibrinolytic system

A

cascade of reactions = fibrin clot dissolved by fibrinolytic system

46
Q

thrombin

A

protease that cleaves circulating soluble fibrinogen to generate insoluble fibrin by binding protease-activated receptors (PARs) on platelets. endo, smooth muscle,

connects coagulation system to inflammation

47
Q

effects of thrombin

A
  1. mobilize P selectin
  2. produce chemokines, PAF, NO
  3. stim endo adhesion mole formation
  4. induce COX2 and production of prostaglandins
  5. induce change in endothelial shape
48
Q

plasmin

A

lyses fibrin clots
formed by cleaving plasminogen by kallikrein or plasminogen activator released by endothelia and leuk

will activate hageman factor > cleave C3 to C3a > degrades fibrin to form fibrin split products that inc permeabilityin skin and lungs

49
Q

arachidonic acid metabolites

A

polyunsat fatty acid in cell membrane phospholipids that get released by phospholipases

either COX pathway or lipoxygenase LOX pathway

aspirin inhibits COX, glucocorticoids inhibit phospholipases

50
Q

COX products

A
  1. TXA2 aka thromboxane A2- potent platelet aggregator and vasoconstrictor
  2. PGI2- vasodilator and inhibit platelet agg
  3. PGE2- sensitizees skin to painful stimuli and play role in cytokine induced fever, will also vasodilate and agg
  4. PGD2, PGE2, PGF2a - vasodilation and potentiate edema
51
Q

LOX products

A

convert AA into luekotrienes and lipoxins
1. LT B4
2. LT C/D/E4

52
Q

LT B4

A

potent chemoattractant causing neutrophils to:
agg
adhesion to EC
generate ROS
release lysosomal enz

53
Q

LT C/D/E4

A

intense vasoconstriction
intense bronchospasm
inc vascular permeability without dilation

54
Q

lipoxins

A

inhibit leukocyte recruitment and cellular activities of inflamm

A4 and B4 inhibit neutros adhesion to endo and neutro chemotaxis

55
Q

platelet activating factor

PAF

A

from stimulated basophils, mast cells, neutrophils, macrophages, platelets, endo cells basically everything

causes platelet agg and release of platelet products (hist, serotonin)

vasoconstriction and bronchoconstriction BUT if low doses then vasodilation and inc venular permeability
-will also stim leuk oxidative burst, inc leuk adhesion to endo, leuk chemotaxis, stim prostaglandin and leukotriene syn

56
Q

cytokines/chemokines

A

polypeps like cellular hormones or locally acting cell to cell mediators
-participate in intricate network to achieve effect

strong chemotactic properties called chemokines

57
Q

cytokines of inflamm effects

A

IL1 and TNF from macrophages
1. acute phase proteins- induce fever, affect sleep and appetite, neutrophilia, hemodynamic effects in shock
2. endothelial- inc leuk adherence, stim PGI syn, inc procoagulant activity, inc syn of IL1/6/8, PDGF
3. fibroblasts- inc proliferation, collagen syn, and PGE syn, inc protease and collagenase production aka repair
4. leukocyte inc cytokine secretion IL1 and 6

58
Q

chemokines

A
  1. alpha or CXC - act on neutros, i.e. IL8
  2. beta or CC - attract other cells NOT neutros, i.e. MCP1, MIP1a, eotaxin for eosinophils
  3. gamma or C - specific for lymphocytes i.e. lymphotactin
  4. CX3C - fractalkine strong attractant for monocyte and T cells

Block 3 Found Sci (60 decks)

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