Histamine & Antihistamine Flashcards
Histamine exerts its effects by what receptor type
G protein coupled membrane receptors
Histamine is what type of neurotransmitter
monoamine
name to other neurotransmitters in the same class as histamine
Ach & Serotonin
Histamine is stored
mast cell (skin, lungs, and GI tract), and basophils in a complex with heparin
The highest to lowest histamine content can be found where
LSNS(AS)S
Lungs>skin(face)>nasal mucosa>stomach/Duodenum>skin (abdomen)>spleen
What three factors cause histamine to be released
Antigen-antibody complex (Mast/Baso–IgE>degranulation>release of Heparin
Drugs & Chemicals (tissue damage, dextran, Epi, Morphine, Meperidine, Succin, d-Tubocurarine)
Physical agents (Touch, Cold, Heat)
Name two pathways of histamine metabolism
***Methylation>degradation via monamine oxidase
Oxidation
How many Histamine receptors exist
four (H1, H2, H3, H4)
Which Histamine receptors are most important
H2>H1>H3>H4
H2 receptor stimulation by histamine results in
increased cAmp Increase Gastric acid secretion CNS stimulation Increase cardiac output coronary vasodilation bronchodilaiton
H1 receptor stimulation by histamine results in
Increased cGmp bronchoconstriction coronary vasoconstriction decreased cardiac output **pruitis and sneezing
H3 receptor stimulation is thought
inhibit release of histamine
*blocade of H3 receptros cause increase in histamine
Local Histamine response results in
Triple response of Lewis
Triple response of Lewis is characterized by
Red spots (dilation of cap.)
Flare (arteriolar dilation)
Wheal (edema, capillary leaking)
True or False, Histamine blockers of H1 receptors can treat bronchoconstriction and hypotension
False it is effective in treating edema and pruitis only
Is ACUTE anaphlylaxis managed with antihistamines
NO! Epinephrine is effective in tx
H1 and H2 receptor ANTAGONIST act by
occupying receptors on effector cell membranes, WITHOUT initiating a response
*competitive inhibition and reversible
Do ANTIHISTAMINEs inhibit the release of histamine
NO, they attach to receptors and prevent responses mediated by histamine
H1-receptor antagonists are classified as
first generation and second generation antagonists
H1-first generation antagonists exert what type of effects
sedation
anticholinergic
serotonin activation
alpha-adrenergic activation
H1-receptor antagonist and CNS
Don’t use in children with seizure disorders
can potentiate ETOH
Good for motion sickness
H1-antagonist chemical class include:
Ethanolamine (Diphenhydramine, Dimenhydrinate)- EDD
Piperazine ( Hydroxyzine-antichol,sedative)
Phenothiazine (promethazine- sedative, N/V)
Name the therapeutic uses of H1-receptor antagonist
allergic rhinoconjunctivits, common cold, hay fever, anaphylaxis (itching, edema), motion sickness, sedative, pre-blood transfusions, N/V
True or False, 1st generation H1-receptor antagonists have most of the side effects profile than 2nd generation H1-receptor antagonists
True
Side effects of 1st gen. H1-recep. antagonists
CNS- decr. alertness
Anticholinergics- Dry mouth, blurred vision, urinary retention, impotence
CV- Tachy, prolonge QTc, heart block, dysrrhymias
H2-receptor antagonists MOA
competitively and selectively inhibits binding of histamine to H2 receptors which decreases cAmp and gastric parietal cell activity (dec. hydrogen ions)
Does H2-receptor antagonist influence pH of gastric fluid already present in stomach
No
What happens when chronic H2-receptor antagonists are discontinued
rebound hypersecretion of gastric acid
does H2-receptor antagonist effect lower esophageal sphincter tone or gastric emptying
No
What are the three therapeutic uses of H2-receptor antagonists
Preop- increase pH of gastric fluid prior to induction (give 30 min before induction)
Duodenal ulcer dx
OTC acid reflux
Cimetidine (Tagament) DOA
6 hours
Cimetidine precautions
Inhibits P450
Decreases hepatic blood flow
Dysrhythmias and hypotension with rapid injection
Cross BBB- confusion, agitation, seizures
**Don’t give to pregnant or breast feeders
Ranitidine (Zantac) DOA and precautions
10 hours give 60 minutes before induction 10x more potent than cimetidine decreases hepatic blood flow DOES NOT inhibit P450
**Famotidine (Pepcid) DOA and precautions
10 hours
give 60 minutes prior to induction
30x more potent than cimetidine
