Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology Block 1 > Block 1 Acute Inflammation > Flashcards

Block 1 Acute Inflammation Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Stimuli of acute inflam

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Inflammasome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cryoporin-associated periodic fever syndromes (CAPS)

A

Gain of function mutation in cryoporin (inflammasome component)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Signs of acute inflammation

A

Rubor, calor, tumor, dolor, loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Trancytosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Transudate

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pus/purulent/suppurative

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Extravasation of WBCs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Integrins

A

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

VLA-4 binds VCAM-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of leuko activation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Phagocytosis killing mechanisms

A

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

22
Q

Chronic granulomatous disease of childhood

A

Deficiency of NAPDH oxidase = impaired phagocytosis and resp burst

23
Q

Myeloperoxidase deficiency

A

Candida infections

24
Q

Chediak-Higashi syndrome

A

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

25
Q

NETs (neutro extracellular traps)

A

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
Q

Histamine

A

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
Q

Serotonin

A

Preformed in platelets, enterochromaffin cells, neurons -> vasoconstriction

28
Q

Steroids

A

Inhibit phospholipase -> no AA, LKT, LX, PG, TX

29
Q

COX-1,2 inhibitors

A

Inhibit COX = no PG, TX but AA, LKT, LX allowed

30
Q

Platelet activating factor

A

Platelets, basos, neutros, mast, MF, endothelium; vasodilation, bronchoconstriction, increased vasc perm, increased WBC adhesion, chemotaxis, degran, ox burst

31
Q

Nitric oxide

A

Endothelium, MF, neutros; vasodilation, inhibits WBC recruitment, mast cell induced infam, derivatives = microbicidal

32
Q

TNF and IL-1

A

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
Q

IL-17

A

From T-lymphs to promote neutro recruitment

34
Q

ROS

A

Endothelium damage = ^ perm, protease activation, injury to RBC, parenchyma, inactivated by SD, CAT, GSH peroxidase, ceruloplasmin, transferrin

35
Q

Leukocyte granules

A

Specific: lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, alkaline phosphatase
Azuro: myeloperoxidase, lysozyme, defensin, acid hydrolase, elastase, cathepsin G, collagenases

36
Q

Seurm proteases that counteract leukocyte granular contents

A

a1-antitrypsin (inh neutro elastase) & a2 macroglobulin

37
Q

Substance P

A

Neuropeptide from sensory nerves, WBCs; fibromyalgia

38
Q

Complement pathways: C3 cleavage

A

Classical: ag/ab fixation
Alt: microbial surface molecuels
Lectin: plasma mannose-binding lectin binds microbes

39
Q

Complement factors

A

C3a, C5a: anaphylatoxins
C5a: WBC adh, chemotaxis, activation
C3b: opsonin for phagocytosis
C5-9: MAC for cell lysis

40
Q

Hageman factor (XIIa)

A

Clotting, fibrinolysis, kinin, complement system trigger

41
Q

Thrombin (IIa)

A

Coagulation protease, binds PARs -> mobilize P-sel, chemo, cytokines, inc adh molecules, induces complement and AA pathway

42
Q

Kinins

A

Vasoactive peptides from plasma proteins (kininogens) by proteases (kallikreins - autocatalytic activator of Hageman)
Bradykinin: inc vasc perm, dilates vessels, pain

43
Q

Acute inflammation lab tests

A

Elevated WBC with left shift (15-20k, mostly neutrophils, toxic granulations), elevated erythrocyte sedimentation rate, SPEP elevated alpha-1,2 fractions, increased CRP

44
Q

SPEP

A

Serum protein electrophoresis

45
Q

Normal WBC count

A

7-9k per uL

46
Q

ESR & what does elevated mean?

A

Erythrocyte sedimentation rate
More rapid sed with inc fibrinogen
>100 mm/hr = AI, neoplastic, infection

47
Q

Normal values for ESR

A

Male: age/2
Female: (age + 10)/2

48
Q

SPEP alpha-1,2 fractions

A

a1: antitrypsin, TBG, transcortin
a2: haptoglobin, ceruloplasmin, a2 macroglobulin

49
Q

CRP

A

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
Q

Histopathology of acute, chronic inflammation

A

Acute: stasis, vascular congestion, fluid/protein exudate = edema, margination, emigration neutros
Chronic: mononuclear cells, angiogenesis, tissue destruction via proteases/ROS, fibrosis

51
Q

5 R’s of acute inflammation

A 
Recognize injurious agent
Recruit leukos
Remove agent
Regulate response
Resolution

Pathology Block 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions