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Inflammation Flashcards

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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

Study These Flashcards
A

pathogen lysis, opsonization, chemotaxis, mast cell degranulation

25
CRP
Marker for inflammation and infection. Opsonization, complement lysis,
26
Serum amyloid A
tissue repair via ECM, chemoattractant for monocytes/dendritic cells/lymphocytes/granulocytes
27
Coagulation factors
Prothrombin, factor VIII, von Willebrand factor, fibrinogen (increases ESR)
28
Ferritin
Sequesters iron away from microbes
29
Extravasation
Movement of leukocytes out of the blood vessels and into the tissues
30
Sialyl Lewis X
CD15. Is on neutrophils. Binds to e-selectin on endothelium
31
Leukocyte adhesion deficiency
Certain adhesion molecules are missing, so leukocytes cannot extravasate. Results in inability to form pus and impaired wound healing.
32
Deficiency of CD18 that makes up part of LFA1 results in what disease sate?
LAD1
33
Defective fucose metabolism preventing the sialyl-Lewis X results in what disease state?
LAD2
34
What is the purpose of respiratory/oxidative burst?
Generates reactive oxygen species to damage protein, lipids, and DNA
35
What enzyme reduces H2O2 to water/oxygen?
Catalase
36
What disease results in NADPH oxidase deficiency and repeat catalase-positive microbe infections?
Chronic granulomatous disease
37
What does the DHR test diagnose?
Chronic granulomatous disease
38
What are signs/symptoms of CGD?
Recurrent infections, pneumonia, skin and viscera abscesses, lymphadenitis
39
Complement
Group of serum proteins that act in cascade to do the following activities: lysis of Gram NEGATIVE bacteria, opsonization, Leukocyte chemotaxis/activation/degranulation
40
3 pathways of complement
Classical, lectin, alternative
41
What induces the classical complement pathway?
IgG, IgM, CRP
42
What induces lectin complement pathway?
Mannose residues
43
What induces alternative complement pathways?
When C3b binds to LPS on Gram NEGATIVE bacteria/zymosan on yeast
44
Which complements opsonize?
C3b > C4b
45
Which complements are inactivated by carboxypeptidase N and cause degranulation?
C5a>>C3a>C4a
46
What does reaction does histamine illicit?
(Released by mast cells/basophils/eosinophils) Induces smooth muscle contraction and increased capillary permeability (leads to local edema).
47
What complement is an activator/chemotaxin for all myeloid cells, induces PMN degranulation, and induces IL-1/IL-6 production in monocytes?
C5a
48
What complement in a chemotactic for eosinophils?
C3a
49
What does the membrane attack complex do?
Cause lysis of Gram-negative (NOT positive) bacteria
50
Classical complement pathway
C1q binds to CRP or Fc of IgM and IgG. Binding activates C1r molecules (Ca-dependent). C1r activates C1s molecules.
51
Lectin Pathway
MBL activates MASP1/2. | MASPs cleave C4 into a/b (C4a and C4b).
52
Alternative Pathway
C3b binds to LPS/endotoxin on Gram negative bacteria or zymosan in yeast
53
Terminal (Lytic) Pathway
MAC forms. A combination of the 3 pathwyas occurs to form C5b678. That complex inserts multiple C9s into the cell membrane, causing lysis
54
C1 esterase inhibitor (C1INH)
Disrupts C1qrs complex/MASP complex/C3bBb. Deficiency leads to hereditary angioedema. Edema worsens with stress/trauma/dental procedures
55
Decay-accelerating factor (DAF)
Binds to C4b. Is a GPI-anchored protein. Deficiency leads to paroxysmal nocturnal hemoglobinuria with red cell lysis (red urine in morning)
56
Membrane protein CD59
Interferes with MAC. | Deficiency leads to paroxysmal nocturnal hemoglobinuria.
57
C3 complement deficiency
Hard time fighting encapsulated bacteria (pneumococcus, influenzae, Neisseria)
58
MAC deficiency
Susceptible to Neisseria meningitidis/gonorrhoeae

Immunology (5 decks)

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