Inflammation Flashcards

1
Q

What are acute inflammatory reactions?

A

Increased blood supply/capillary permeability, WBC migration. Neutrophils are the first to the site of inflammation

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2
Q

What cells are typically present in chronic inflammation?

A

Macrophages, epithelioid cells, lymphocytes

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3
Q

What is the classic triad of inflammation?

A

Pain, heat, redness

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4
Q

What is the chemical on the microbes used to signal the immune system?

A

Pathogen-associated molecular patterns (PAMPs)

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5
Q

What to PAMPs bind to on phagocytes?

A

Pattern Recognition Receptors (PRRs)

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6
Q

What PRR-PAMP interaction is chemotactic for macrophages and neutrophils?

A

fMet-Leu-Phe (and receptor)

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7
Q

What is the PAMP of the outer membrane of Gram NEGATIVE bacteria?

A

LPS (endotoxin)

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8
Q

What PRR does LPS bind to?

A

TLR4 and CD14

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9
Q

What PAMP is a part of Gram-POSITIVE bacterial cell wall?

A

Lipoteichoic Acid

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10
Q

What PRR does Lipoteichoic acid bind to?

A

TLR2 and CD14

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11
Q

What color does gram-positive bacteria stain?

A

purple

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12
Q

What do NLRs bind to?

A

DAMPs and PAMPs

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13
Q

Where are NOD-like receptors found?

A

The cytosol of leukocytes and other cell types

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14
Q

What can help to active IL-1β?

A

NLRs assembled into inflammasomes

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15
Q

RIG-I-like receptors (RLRs)

A

Cytoplasmic RNA helices that induce interferon α/β production in response to a viral infection

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16
Q

What it the result of pro-inflammatory cytokines IL-1?

A

Fever and Up-regulation of adhesion molecules

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17
Q

What is the major result of pro-inflammatory cytokine TNF α?

A

Septic shock and up-regulation of adhesion molecules

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18
Q

What is the major result of pro-inflammatory cytokine IL-6?

A

Acute phase protein release from the live

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19
Q

Septic shock symptoms

A

Drop in BP, hyper/hypothermia, weakness, tachypnea, tachycardia

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20
Q

Exogenous pyrogens of Gram positive bacteria

A

Lipoteichoic acid

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21
Q

What synthesis does IL-1 induce?

A

PGE2 (central=raise in hypothalamic set point, peripheral= myalgia/arthralgias)

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22
Q

What is a negative acute phase protein? (APP)

A

Albumin

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23
Q

What do APPs do?

A

Aid host defense via opsonins, clots, tissue repair

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24
Q

Complement

A

pathogen lysis, opsonization, chemotaxis, mast cell degranulation

25
Q

CRP

A

Marker for inflammation and infection. Opsonization, complement lysis,

26
Q

Serum amyloid A

A

tissue repair via ECM, chemoattractant for monocytes/dendritic cells/lymphocytes/granulocytes

27
Q

Coagulation factors

A

Prothrombin, factor VIII, von Willebrand factor, fibrinogen (increases ESR)

28
Q

Ferritin

A

Sequesters iron away from microbes

29
Q

Extravasation

A

Movement of leukocytes out of the blood vessels and into the tissues

30
Q

Sialyl Lewis X

A

CD15. Is on neutrophils. Binds to e-selectin on endothelium

31
Q

Leukocyte adhesion deficiency

A

Certain adhesion molecules are missing, so leukocytes cannot extravasate. Results in inability to form pus and impaired wound healing.

32
Q

Deficiency of CD18 that makes up part of LFA1 results in what disease sate?

A

LAD1

33
Q

Defective fucose metabolism preventing the sialyl-Lewis X results in what disease state?

A

LAD2

34
Q

What is the purpose of respiratory/oxidative burst?

A

Generates reactive oxygen species to damage protein, lipids, and DNA

35
Q

What enzyme reduces H2O2 to water/oxygen?

A

Catalase

36
Q

What disease results in NADPH oxidase deficiency and repeat catalase-positive microbe infections?

A

Chronic granulomatous disease

37
Q

What does the DHR test diagnose?

A

Chronic granulomatous disease

38
Q

What are signs/symptoms of CGD?

A

Recurrent infections, pneumonia, skin and viscera abscesses, lymphadenitis

39
Q

Complement

A

Group of serum proteins that act in cascade to do the following activities: lysis of Gram NEGATIVE bacteria, opsonization, Leukocyte chemotaxis/activation/degranulation

40
Q

3 pathways of complement

A

Classical, lectin, alternative

41
Q

What induces the classical complement pathway?

A

IgG, IgM, CRP

42
Q

What induces lectin complement pathway?

A

Mannose residues

43
Q

What induces alternative complement pathways?

A

When C3b binds to LPS on Gram NEGATIVE bacteria/zymosan on yeast

44
Q

Which complements opsonize?

A

C3b > C4b

45
Q

Which complements are inactivated by carboxypeptidase N and cause degranulation?

A

C5a»C3a>C4a

46
Q

What does reaction does histamine illicit?

A

(Released by mast cells/basophils/eosinophils) Induces smooth muscle contraction and increased capillary permeability (leads to local edema).

47
Q

What complement is an activator/chemotaxin for all myeloid cells, induces PMN degranulation, and induces IL-1/IL-6 production in monocytes?

A

C5a

48
Q

What complement in a chemotactic for eosinophils?

A

C3a

49
Q

What does the membrane attack complex do?

A

Cause lysis of Gram-negative (NOT positive) bacteria

50
Q

Classical complement pathway

A

C1q binds to CRP or Fc of IgM and IgG.
Binding activates C1r molecules (Ca-dependent).
C1r activates C1s molecules.

51
Q

Lectin Pathway

A

MBL activates MASP1/2.

MASPs cleave C4 into a/b (C4a and C4b).

52
Q

Alternative Pathway

A

C3b binds to LPS/endotoxin on Gram negative bacteria or zymosan in yeast

53
Q

Terminal (Lytic) Pathway

A

MAC forms.
A combination of the 3 pathwyas occurs to form C5b678.
That complex inserts multiple C9s into the cell membrane, causing lysis

54
Q

C1 esterase inhibitor (C1INH)

A

Disrupts C1qrs complex/MASP complex/C3bBb.
Deficiency leads to hereditary angioedema.
Edema worsens with stress/trauma/dental procedures

55
Q

Decay-accelerating factor (DAF)

A

Binds to C4b.
Is a GPI-anchored protein.
Deficiency leads to paroxysmal nocturnal hemoglobinuria with red cell lysis (red urine in morning)

56
Q

Membrane protein CD59

A

Interferes with MAC.

Deficiency leads to paroxysmal nocturnal hemoglobinuria.

57
Q

C3 complement deficiency

A

Hard time fighting encapsulated bacteria (pneumococcus, influenzae, Neisseria)

58
Q

MAC deficiency

A

Susceptible to Neisseria meningitidis/gonorrhoeae