Regal- Histamines and Anti-Histamines Flashcards Preview

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Flashcards in Regal- Histamines and Anti-Histamines Deck (32)
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1

Where is histamine synthesized?

nearly every tissue w/ highest concentration in the lungs and stomach

in mast cells or basophils
(any cells that contain L-his decarboxylase)

2

What does L-histadine decarboxylase do?

Converts histadine to histamine

Found in mast cells and basophils

3

What are the two pools of histamine?

Mast cell histmaine (mast cells and basophils)

Non-mast cell histamine (CNS nerve endings)

4

How is histamine degraded?

Inactivated by metabolic enzymes
N-methyltransferase
diamine oxidase
MOA-B
ribose

5

Where are the enzymes that degrade histamine located?

Widely distributed (small intestine mucosa, skin, kidney, liver thymus, WBC)

Intestinal bacteria convert it to N-actylhistamine

6

What are the three ways that histamine contributes to inflammation?

1. vasodilation--> redness/heat

2. increased vascular permeability--> swelling

3. bronchoconstriction

7

What happens to orally administered histamine?

Absorbed and inactivated by enzymes of intestinal wall/liver

8

What happens to intracutaneously administered histamine?

Triple response

vasodilation-->Localized redness (s/m)

nerves dilating neighboring arterioles--> diffuse redness (slower)


Increased capillary permeability--> localized edema

9

What are nasal sxs associated w/ intranasal histamine?

Intense itching
sneezing
hypersecretion
nasal blockage

10

Intravenous administration of histamine leads to....

vasodilation
decreased bp
tachycardia
bronchoconstriction
face flushing
HA
wheal and flare
stimulation of mucous secretion
stimulation of gastric secretion

11

What type of agonists are histamines?

Inverse agonists--reduce receptor activity below basal levels observed in absence of ligand (looks like a competitive antagonist)

12

What leads to the endogenous release of histamine?

Antigen interaction w/ IgE Ab on mast cells and basophils

13

Activation of H1 leads to:

rapid and short lived VASODILATION

bronchoconstriction
contraction of GI smooth muscle
increased capillary permeability (wheal)
pruritits and pain
release of catecholamines from adrenal medulla

14

Activation of H2 leads to:

Gastric acid secretion
SLOWER and SUSTAINED VASODILATON

15

Activation of H3 leads to:

Present on histaminergic nerve terminals

16

Activation of H4 leads to:

Present on immune cells

17

What is the triple response caused by histamine and what receptors does it effect?

vasodilation-H1, H2
flare-H1 (some 2)
wheal- H1, some 2
pain and itching- H1

18

What triggered histamine receptors lead to cardiac effects?

H1 and H2

Increased HR, force, arrythmias
Decreased AV conduction

19

What are the two first generation antihistamines?

Diphenhydramine- Benadryl
Chlorampheniramine

20

What is the MOA of first generations antihistamines?

Block:
H1
muscarinic
alpha adrenergic
5-HT receptors (cholinergic properties)

21

Where are antihistamines distributed?

A: oral

D: widely includes CNS

22

How are antihistamines eliminated?

A: liver inactives enzymes

E: renal

23

What are the major toxicities associated w/ antihistamines?

Sedation
Drying of secretions

GI disturbances

24

What receptor does Diphenhydramine act on?

H1 receptor antagonist

25

What is a antihistamine toxicity that is minized by using diphenhydramine?

Lowers incidence of GI SE

26

What is a unique property of diphenhydramine?

It's good if you want a sedative effect (children)

27

When is chlorepheniramine commonly used?

day time

28

What are the second generation antihistamines?

Cetirizine
Fexofenadine
Loratadine

29

What is the MOA of SG antihistamines?

Block H1 recetpors
MINIMAL anticholinergic propgerites

30

How are SG antihistamines distributed?

D: does NOT cross BBB->
NO sedation or drying secretions