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Pathology Block 1 > Block 1 Acute Inflammation > Flashcards

Block 1 Acute Inflammation Flashcards

(51 cards)

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1
Q

Inflammatory response components

A

Vascular: increased flow, vessel structure changes for plasma protein & leukos to leave circulation
Cellular: emigration and accumulation of WBCs, activation of cells, cytokines, etc.

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2
Q

Stimuli of acute inflam

A

Infection, trauma, tissue necrosis (ischemia, phys/chem injury), foreign body, immune reaction (AI, hypersens rxn)

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3
Q

Toll-like receptor

A

In PM, endosomes; sense microbial products, recognize bacterial DNA and viral dsRNA, activate TFs (inflam mediators, interferons, lympho activation)

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4
Q

Inflammasome

A

Recognizes products of dead cells (uric acid, extracell ATP, crystals), activates caspase-1 to activate IL-1b -> recruit leukos

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5
Q

Cryoporin-associated periodic fever syndromes (CAPS)

A

Gain of function mutation in cryoporin (inflammasome component)

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6
Q

Signs of acute inflammation

A

Rubor, calor, tumor, dolor, loss of function

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7
Q

Causes of increased vascular permeability

A 
Contraction of venule endothelial cells (histamine, bradykinin, LKT, substance P) for 15-30 min
Cytoskeleton changes (TNF, IL-1) 4-6 hours for 24 hrs or more
Endothelial injury (trauma, microbe, neutro) -> delayed, prolonged leakage
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8
Q

Trancytosis

A

Fluid, protein through endothelial cells in venules via vesiculovacuolar organelle (channels ^ by VEGF)

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9
Q

Transudate

A

Serous ultrafiltrate of plasma with little cellular material, low protein, low specific gravity; can cause effusion; ex: blister, serositis

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10
Q

Exudate

A

Fibrinous fluid due to endothelial gaps in venules, contains cellular material, some protein, high specific gravity; converted to scar tissue in organization; ex: friction rub, adhesions

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11
Q

Pus/purulent/suppurative

A

Exudate with abundant neutros, bacterial infection (Staph); abscess is localized collection of purulent inflammatory tissue

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12
Q

Extravasation of WBCs

A

Margination, rolling, adhesion, transmigration (diapedesis), migration (chemotaxis)

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13
Q

Selectins

A

For rolling; E on endothelium, P on endothelium and platelets, L on leuko
Ligand: sialylated oligosaccharides with mucin-like glycoprotein backbone

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14
Q

Integrins

A

For adhesion: LFA-1, Mac-1 bind ICAM-1

VLA-4 binds VCAM-1

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15
Q

Leukocyte adhesion deficiency 1 and 2

A

1: Defect in B2 chain (LFA-1 and Mac-1) -> repeat bact infxn, poor healing, severe form needs bone marrow transplant
2: sialyl-Lewis X-ligand absence (for E- and P-selectins) -> lack fucosyl transferase enzyme, small stature, cog impairment, bact infxn

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16
Q

Transmigration proteins

A

PECAM-1/CD31 on endothelium and WBCs
Leukos invade BM with collagenases, adhere to ECM with integrins and CD44
Polys in 6-24 hr, mononuc in 24-48 hr

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17
Q

Chemotaxis chemoattractants

A

Exogenous: bact products (peptide with terminal N-formyl-methionine)
Endogenous: complement (C5a), AA pathway (LTB4), cytokines (IL-8)
Movement by actin polymerization

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18
Q

Causes of leuko activation

A

Microbes, ag/ab complexes, necrosis products, cytokines (INF-y)

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19
Q

Leukocyte activation responses

A

Increased cytosolic Ca2+, enzyme activation, AA metabolite production, cytokine secretion, degran of lysosomal enzymes, oxidative burst, modulation of adhesion molecules

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20
Q

Phagocytosis recognition, attachment, result

A

Mannose/scav receptors for LDL, opsonization by IgG (FcR on WBCs), C3b (CR1,3), plasma lectins/collectins (C1q)
Formation of phagocytic vacuole + lysosome = phagolysosome

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21
Q

Phagocytosis killing mechanisms

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A

Resp burst (H2O2)
Myeloperoxidase -> HOCl
NO -> peroxynitrite (free rad)
Neutrophil granules (enzymes/elastase, defensins, lysozyme, MBP)

22
Q

Chronic granulomatous disease of childhood

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A

Deficiency of NAPDH oxidase = impaired phagocytosis and resp burst

23
Q

Myeloperoxidase deficiency

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A

Candida infections

24
Q

Chediak-Higashi syndrome

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A

AR defect in LYST (lyso transfer to phago vacuole) -> infection susceptibility, albinism due to abnormal melanocytes, giant granules in leukocytes

25
NETs (neutro extracellular traps)
Extracellular framework of nuclear chromatin & embedded granule proteins, response to bact/fungi & inflam mediators -> physical barrier, high conc antimicrobials -> death of neutro (nuc ag in AI?)
26
Histamine
Preformed in mast cells, basos, platelets Trauma, ab (IgE), C3a/5a, IL-1,8 Binds H1-R -> dilation arterioles, increased venule perm Inact by histaminase
27
Serotonin
Preformed in platelets, enterochromaffin cells, neurons -> vasoconstriction
28
Steroids
Inhibit phospholipase -> no AA, LKT, LX, PG, TX
29
COX-1,2 inhibitors
Inhibit COX = no PG, TX but AA, LKT, LX allowed
30
Platelet activating factor
Platelets, basos, neutros, mast, MF, endothelium; vasodilation, bronchoconstriction, increased vasc perm, increased WBC adhesion, chemotaxis, degran, ox burst
31
Nitric oxide
Endothelium, MF, neutros; vasodilation, inhibits WBC recruitment, mast cell induced infam, derivatives = microbicidal
32
TNF and IL-1
MF, mast -> endothelium, WBCs, fibros, marrow Systemic acute phase rxn with IL-6 TNF: lipid, protein mobilization, dec appetite, cachexia IL-1: mutation upregulates genes for caspases = more IL-1 (fam Med fever), activated by urate crystals (gout)
33
IL-17
From T-lymphs to promote neutro recruitment
34
ROS
Endothelium damage = ^ perm, protease activation, injury to RBC, parenchyma, inactivated by SD, CAT, GSH peroxidase, ceruloplasmin, transferrin
35
Leukocyte granules
Specific: lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, alkaline phosphatase Azuro: myeloperoxidase, lysozyme, defensin, acid hydrolase, elastase, cathepsin G, collagenases
36
Seurm proteases that counteract leukocyte granular contents
a1-antitrypsin (inh neutro elastase) & a2 macroglobulin
37
Substance P
Neuropeptide from sensory nerves, WBCs; fibromyalgia
38
Complement pathways: C3 cleavage
Classical: ag/ab fixation Alt: microbial surface molecuels Lectin: plasma mannose-binding lectin binds microbes
39
Complement factors
C3a, C5a: anaphylatoxins C5a: WBC adh, chemotaxis, activation C3b: opsonin for phagocytosis C5-9: MAC for cell lysis
40
Hageman factor (XIIa)
Clotting, fibrinolysis, kinin, complement system trigger
41
Thrombin (IIa)
Coagulation protease, binds PARs -> mobilize P-sel, chemo, cytokines, inc adh molecules, induces complement and AA pathway
42
Kinins
Vasoactive peptides from plasma proteins (kininogens) by proteases (kallikreins - autocatalytic activator of Hageman) Bradykinin: inc vasc perm, dilates vessels, pain
43
Acute inflammation lab tests
Elevated WBC with left shift (15-20k, mostly neutrophils, toxic granulations), elevated erythrocyte sedimentation rate, SPEP elevated alpha-1,2 fractions, increased CRP
44
SPEP
Serum protein electrophoresis
45
Normal WBC count
7-9k per uL
46
ESR & what does elevated mean?
Erythrocyte sedimentation rate More rapid sed with inc fibrinogen >100 mm/hr = AI, neoplastic, infection
47
Normal values for ESR
Male: age/2 Female: (age + 10)/2
48
SPEP alpha-1,2 fractions
a1: antitrypsin, TBG, transcortin a2: haptoglobin, ceruloplasmin, a2 macroglobulin
49
CRP
C-reactive protein: acute phase reactant, increase x1000 in acute inflam, opsonin or fixes complement, non-specific, helpful in acute appendicitis, ? useful assessment cardiac risk
50
Histopathology of acute, chronic inflammation
Acute: stasis, vascular congestion, fluid/protein exudate = edema, margination, emigration neutros Chronic: mononuclear cells, angiogenesis, tissue destruction via proteases/ROS, fibrosis
51
5 R's of acute inflammation
``` Recognize injurious agent Recruit leukos Remove agent Regulate response Resolution ```

Pathology Block 1 (12 decks)

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