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50 Cards in this Set

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Histamine is found in particularly high concentration in these three places?
Lung
Skin
GI tract
Three stages of inflammation
Immediate hypersensitivity
Delayed subacute phase
Chronic proliferative phase
Immediate hypersensitivity
vascular permability (H1&2)
smooth muscle contraction (H1)
vasodilation (H1 &2)
bronchospasm (H1)
pain and itiching (kinin's)
Delayed subacute phase
Infiltration of leukocytes and phagocytes
Chronic proliferative phase
Tissue degeneration and fibrosis or repair
How is histamine synthesized?

How is it inactivated?
histidine decarboxylase

methylation or oxidative deamination
Three methods of histamine release
Cell damage
Ca dependent exocytosis
Ca independent exocytosis (basic compounds like morphine and tubocurarine)
Inhibition of histamine release
Cyclimc AMP-linked receptor agonists (beta 2, H2, PGE 2)
Theophylline
Cromolyn sodium (lung mast cells)
H1 receptors
smooth muscle
endothelium
brain

linked to phospholipase C -> IP3, DAG
H2 receptors
gastric mucosa, mast cells, cardiac, brain

cAMP formation
H3 receptors
Brain
Myenteric plexus

Presynaptic
Receptor in endothelium
H1
Recetpor in myenteric plexus
H3
Receptor in gastric mucosa
H2
Receptor in brain
H1, H2, H3
Receptor in cardiac muscle
H2
Linked to phospholipase C
H1
Linked to cAMP
H2
Histamine effects this receptor to cause increased capillary permeability
H1
What is the difference between H1 and H2 vasodilation
H1 is rapid and short
H2 is slow, but sustatined
This receptor increass gastric acid secretion
H2
Increass gastirc acid motility
H1
Bronchial effects
H1
Two uses for histamine
Test gastirc acid secretion

Pheochromocytoma
Epinephrine as a histamine antagonist
smooth muscle relaxer

a physiological antagonist
Cromylyn Sodium as a H antagonist
inhibits mast cell degranulation
First generation antihistamines
Diphenhydramine
Chloropheniramine
Pyrilamine
Promethazine
Meclizine
Second generation antihistamines
Terfenadine
Astemizole
Fexofendaine
Loratadine
Are lipid soluble?
1st generation
Not sedative
2nd generation
Effective length of time for 2nd generation drugs
12-24 hours

terfenadine
astemizole
fexofenadine
loratadine
Penetrate the CNS
1st generation

diphenhydramine
chloropheniramine
pyrilamine
promethazine
meclizine
Effective time for 1st generation
4-6 hours

diphenhydramine
chloropheniramine
pyrilamine
promethazine
meclizine
Why do 1st generation drugs cause drowsiness
A central H1 receptor is involved in the control of wakefullness
CNS toxicity of H1 antagonist resembles?
Atropine poisioning
Two anti-H that cause serious cardia arrythmias
terfenadine
astemizole
Method of arrythmia in terfenadine and astemizole
Block delayed rectifier K channels
When are terfeanadine and astemizole a risk for causing arrythmia's?
In overdoes or with drugs that cause inhibition of cytochrome p450 (erthyromycin and antifungals)
Receptor that mediates antihistamines anti-emetic effects
M1 receptor
Two Anti-H's with local anesthetic activity
diphenyhydramine
promethazine
These have muscarinic cross reactivity
diphenhydramine
meclizine
promethazine
(and other 1st gen)
terfenadine
2nd generation antihistamine

Seldane
may cause cardiac arrythmias
diphenydramine
1st generation antihistamine

Bendadryl
Local anestehtic activity
Muscarinic cross reactivity
chloropheniramine
1st generation antihistamine

Chlor-trimeton
no antiemmetic effects
meclizine
1st generation antihistamine

Antivert
Muscarinic cross reactivity
primarily for motion sickness
fexofenadine
2nd generation antihistamine

Allegra 12 hours
No interaction with cyto p450 inhibiting drugs
loratadine
2nd generation antihistamine

Claritin 24 hours
pyrilamine
1st generation antihistamine

OTC cold and sleep aid
Promethazine
1st generation antihistamine

local anestehtic
muscarinic cross reactivity
alpha adrenocrecptor cross reactivity
anti emmetic
astemizole
2nd geneartion antihistamine

histamal
risk of cardiac arrythmias