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29 Cards in this Set

  • Front
  • Back
What is histamine?
Histamine is a basic amine that is stored in mast cells & basophils. It is a chemical messenger that mediates a wide range of cellular responses, including allergic & inflammatory responses, gastric secretions and neurotransmission in parts of the brain.
How is histamine formed?
It is formed by decarboxylation of L-histidine by histidine decarboxylase.
What are the main actions of histamine?
Includes stimulation of gastric secretion, contraction of most smooth muscles (other than blood vessel smooth), cardiac stimulation, vasodilation & increased vascular permeability.
When injected intradermally, histamine causes “triple responses” which includes local vasodilation,wheal & flare.
What is histamine's two major pathophysical roles?
Stimulation of gastric secretion,which is tx’d with H2 antagonists & the mediation of type 1 hypersensitivity rxns such as urticara & hay fever, which is tx’d with H1Bs.
Where are histamine receptors located and what are their roles?
H1 - in bronchial muscle & linked to transduction systems that cause increased intracellular Ca which leads to muscle contraction;
H2 - in acid-secreting stomach cells & in the heart. Stimulation leads to gastric acid secretion & increased atrial rate. H2 receptors are linked to transduction system involved in the activation of adenylate cyclase & the increased production of cAMP.
H3 - related to neural tissue & found at presynaptic sites. Their stimulation causes the inhibition of neurotransmitter release.
Histamine release follows a distinct circadian pattern, the neurons being active by day and silent by night. How does H1 blockers affect this?
H1 receptors in the cortex and reticular activating system contribute to arousal and wakefulness, and H1Bs produce sedation.
Where is histamine found?
(1)Most tissue histamine is sequestered and bound in granules in mast cells or basophils (unbound histamine is biologically inactive). Many stimuli can trigger the release of mast cell histamine, allowing the free amine to exert its actions on surrounding tissues.
(2)Non-mast cell histamine is found in several tissues, including the brain, where it functions as a neurotransmitter.
(3)The enterochromaffin-like (ECL) cells of the fundus of the stomach release histamine, one of the primary acid secretagogues, to activate the acid-producing parietal cells of the mucosa.
How is histamine stored?
In storage granules containing histamine complexed with a sulfated polysaccharide, heparin or chondroitin sulfate, and an acidic protein.
How is histamine released?
The bound form of histamine can be released through several mechanisms:
(1)immunologic release -
degranulation leads to simultaneous release of histamine, ATP, and other mediators that are stored together in the granules.
Histamine released by this mechanism is a mediator in immediate (type I) allergic reactions.
(2) Chemical and mechanical release - certain amines, including drugs such as morphine and tubocurarine, can displace histamine from the heparin-protein complex within cells. Compounds 48/80, an experimental diamine polymer, specifically releases histamine from tissue mast cells by an exocytotic degranulation process.
The most important mechanism for histamine release is in response to an immunological stimulus. Describe the steps in this mechanism.
Mast cells, when sensitized by surface IgE antibodies, degranulate when exposed specific antigen,
releasing histamine(type I allergic reaction). 
Following local injury, histamine first produces a local vasodilation (reddening of the area) followed by an the release of acute inflammation mediators. 
Inflammatory cells involved in this process include neutrophils, eosinophils, basophils, monocytes & lymphocytes
Name the second messengers for each of the following histamine receptor subtypes:
H1, H2, H3 & H4.
H1 - Gq,↑IP3, DAG
H2 - Gs,↑cAMP
H3 - Gi,decrease cAMP
H4 - Gi,decrease cAMP
How does histamine affect the nervous system?
Histamine is a powerful stimulant of sensory nerve endings producing pain and itching, important components of the urticarial response and reactions to insect and nettle stings.
Presynaptic, neuronal H3 receptors are negatively coupled to release of several transmitters in the CNS.
They are constitutively active receptors on histaminergic neurons.
H3 antagonists, and inverse agonists increase synthesis and release of Histamine leading to increased wakefulness, vigilance, learning and memory.
H3 antagonists reduce the synthesis and release of Histamine, and release of NE, DA, 5-HT, and, in some studies, Ach in various areas of the brain.
How does histamine affect the CV system?
Effects are direct & indirect.
Stimulatory actions on the heart (H2) and a reflex tachycardia due to the vasodilator action (via H1/NO) on arteriole ECs ->
increased contractility & HR.
How does histamine affect edema in the body?
H1 receptors in the vessels of the microcirculation lead to separation of endothelial cells increasing permeability. This causes urticaria (surface)and angioedema (subdermal).
How does histamine affect the resp. system?
It causes bronchoconstriction (H1) especially, in asthma. This is the basis of the provocative test.
How does histamine affect the GI system?
Present on gastrointestinal tract smooth muscle (H1)
causes contraction.
Histamine is a powerful stimulant of gastric secretions via H2 receptors and to a lesser extent, gastric pepsin and intrinsic factor production.
How does histamine affect pregnancy?
Pregnant women suffering anaphylactic reactions may abort as a result of histamine-induced genitourinary tract contractions.
What is the main difference between first generation H1 blockers?
They are distinguished by the relatively strong sedative effect of most of the first generation drugs, which is determined by the degree of distribution of the drug into the CNS.
The first generation H1 receptor antagonists have many actions not ascribable to blockade of the actions of histamine. What accounts for these actions?
They results from the similarity of the general structure to the structure of drugs that have effects at muscarinic cholinoceptor, adrenoceptor, serotonin, and local anesthetic receptor sites
One of the effects of first generation H1 antagonists is sedation. This makes them
useful as “sleep aids.” At normal doses they have sedative effects on adults, how does this ocassionally differ in children?
At ordinary dosages, children occasionally manifest excitation rather than sedation.
Several first generation H1 antagonists have significant activity in preventing motion sickness. True or false? It is equally effective in treating motion sickness already present.
They are less effective against an episode of motion sickness already present.
What is histamine's antiparkinsonism effect due to?
Their anticholinergic effects.
True or false?
Diphenhydramine & promethazine (antihistamines) are more potent than procaine as local anesthetics.
They are occasionally used to produce local anesthesia in patients allergic to the conventional local anesthetic drugs.
What are clinical uses of H1 antagonists?
Tx allergic reactions,
motion sickness and vestibular disturbances &
nausea and vomiting of pregnancy.
What are common side effects of H1 blockers?
Drowsiness (mostly 1st generation),dry mouth, blurred vision, urinary retention, orthostatic hypotension
What are the possible food/dug interactions of H1Bs?
CYP3A4 inhibitors (2nd generation drugs),
antimicrobial agents (ketoconazole, itraconazole, or macrolide antibiotics),
grapefruit juice, CNS depressants (1st generation drugs)
Muscarinic and alpha-blocking agents (1st generation).
Promethazine is not recommended in children younger than 2 years of age. Why?
It can cause potentially fatal respiratory depression.
What are other considerations regarding the administration of promethazine in children?
Limit antiemetics to prolonged vomiting of known etiology.
Extrapyramidal symptoms d/t promethazine may be confused with the CNS signs of undiagnosed primary disease (e.g, encephalopathy, Reye syndrome).
In children who are acutely hydrated, there is an increased susceptibility to dystonias with the use of promethazine.
Promethazine may cause Neuroleptic Malignant syndrome (NMS). What is this?
A potentially fatal adverse effect associated with use of promethazine alone or in combination with antipsychotic drugs. Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, AMS, and evidence of autonomic instability (irregular & increased pulse or altered BP, diaphoresis & cardiac dysrhythmias).