Inflammatory Mediators Flashcards

1
Q

Histamine

Synthesis:

Degradation:

Biological Activities:

Receptors:

A

Histadine–> L-histadine decarboxylase–> histamine

?

Vasodilation (Redness, heat)
Increased vascular permiability –> edema
Airway constriction
Hypotension

H1
H2
H3
H4

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

Histamine H1 receptor:

A

Bronchoconstriction

Contraction of GI smooth muscle

Increased capillary permeability

Pruritis and pain

Release of catecholamines from adrenal medulla

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

Histamine H2 receptor:

A

Gastric acid secretion

Inhibition of IgE-mediated basophil histamine release

Inhibition of T-cell mediated cytotoxicity

Suppression of Th2’s and cytokines

Nasal mucous secretion

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

Histamine H3 and H4 receptors:

A

present on histaminergic nerve terminals (H3) and many immune cells (H4; eosinophils, dendrites, T-cells, neutrophils)

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

Mixed H1/2 histamine receptor response:

A

increased heart rate

increased force of cardiac contraction

increased arrhythmias

slows AV conduction (primarily H1)

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

Redness–vasodilation

A

histamine

PGE2

PGI2

Kinins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

swelling

increased vascular permeability

A

histamine

peptido leukotrienes (LTC4, LTD4, LTE4)

Kinins

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

Pain

A

PGE

PGI

LTB4

Kinins

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

Chemotaxis

A

LTB4 (neutrophils)

Peptido Leukotrienes (eosinophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fever

A

PGEs

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

Airway constriction

A

histamine

peptido leukotrienes

kinins

PGD2

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

hypotension

A

kinins

histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

platelets aggregation

vasoconstriction

A

TXA2

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

opposes platelet aggregation

vasodilation

A

PGI2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

chemotactic for PMNs

reduces pain threshold

A

LTB4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

VERY strong vasodilator –> hypotension

A

kinins

17
Q

Converts histidine to histamine

where is it located?

A

L-histidine decarboxylase

mast cells and basophils

18
Q

What is the “triple response”?

What causes it?

A

localized redness

flare

localized edema or wheal formation

**cause by histamine

19
Q

Phospholipids –> ___?_____ –> arachidonic acid

A

phospholipase A2

20
Q

Arachidonic acid–> ___?____ –> prostanoids (PG & TX)

A

cyclooxygenase COX 1/2

21
Q

Arachidonic acid –> ___?___ –> leukotrienes

A

lipoxygenase LOX

22
Q

Receptor for peptido leukotrienes causing:

BRONCHOCONSTRICTION

eosinophil chemotaxis and cytokine secretion

increased vascular permeability

increased mucous production

dendritic cell migration and maturation

smooth muscle proliferation

A

Cys LTR1

23
Q

Receptor for peptido leukotrienes causing:

endothelial cell migration and activation

fibrosis

A

Cys LTR2

24
Q

Cys LTR1 inhibitors?

A

Montelukast

Zafirlukast

25
Q

Enzyme converting AA to LTA4?

A

5-lipoxygenase

26
Q

Inhibitor of 5-lipoxygenase?

A

Zileuton

27
Q

Degrades bradykinin to prevent hypotension?

A

Angiotensin converting enzyme (ACE)

28
Q

How do kinins cause such severe hypotension?

A

vasodilation

29
Q

Which receptor do kinins interact with to cause vasodilation?

A

B2