Antihistamines Flashcards
1
Q
What is the role of histamine in immune modulation?
A
-
Vasodilation →capillaries become permeable → allows for WBC to move into site of “threat”
- leads to facial flushing and edema
- separation of endothelial cells → urticaria
- Induces fluid secretion
- Gives rise to classic allergic symptoms
- runny nose, watery eyes etc.
2
Q
Morphine is a good example…..5/16
A
3
Q
2nd gen H1 antihistamines
- Indication?
- Selective for?
- BBB penetration.. yes or no?
- Onset of action/duration of action?
- DOC for ?
A
- Indication?
- allergic symptoms only
- Selective for?
- highly selective for H1 receptors with no other receptor effects
- BBB penetration.. yes or no?
- Limited BBB penetration (b/c these drugs are less lipophilic)
- Onset of action/duration of action?
- Rapid onset of action (1 hr); longer duration of action
- DOC for elderly pts
4
Q
- Available H2 receptor anatagonist?
- ADR’s?
- DDI’s?
A
- Ranitidine
- Cimetidine
- Nizatidine
- Famotidine
ADR’s:
- Most common are CNS related
- HA, dizzy, fatigue, confusion
- These are increased in elderly and renal impairment
- HA, dizzy, fatigue, confusion
-
Dose related gynecomastia occurs with cimetidine
- b/c cimetidine is also a weak androgen
DDI’s
- Drugs that need acid for proper absorption (b/c this is acid suppressive therapy)
- Ketoconazole, itraconazole, protease inhibitors
- Cimetidine inhibits most CYP450 enzyme pathways so it has a TON of DDI’s
5
Q
2nd gen. H1 antihistamines
- Agent available?
- Clinical notes?
A
6
Q
Histamine Receptors:
- Receptor types?
- which one has the widest distribution through out the body?
- Location of receptors?
- Action of receptors?
A
7
Q
- Histamine is stored and found in?
- Large amounts of histamine is released in?
A
1.)histamine=vasoactive amine derived from the amino acid histadine– “vasoactive” has effects on our blood vessels
- Mast cells, basophils
- defends against allergic (immune) rxn’s
- CNS
- acts as neurotransmitter
- Gut regulates gastric acid production
2.) *at any given time we have small amounts of histamine our body b/c it rapidly inactivated by our body
- allergic/hypersentsitivity rxn
- tissue injury
- direct mast cell destruction (drugs/chemicals)
8
Q
- ) Which Histamine receptors are in the CNS?
- ) effects of histamine in each “place” of the brain?
- ACh release →?
- Alertness→ ?
- Serotonin→?
- Food intake→?
- Emesis center→?
A
- ) H1 and H3 and some H2
- )
- ACh release → learning and cognition
- Alertness→ sleep-wake cycle: makes you alert
- Serotonin→ mood
- Food intake→ supression of appetite
- Emesis center→ N/V
- why antihistamine is useful in treatment for motion sickness
9
Q
Four facts about 1st generation H1 antihistamines
A
- Used to treat allergic symptoms, motion sickness and insomnia
- available OTC and Rx
-
Poor Receptor selectivity
- Often interact with other receptors of other amines
-
Anti-muscarinic - tachycardia, constipation, dry mouth
- Not preferred in elders
- Anti-alpha adrenergic and anti-serotonin
-
Anti-muscarinic - tachycardia, constipation, dry mouth
-
Highly lipophilic
- crosses BBB to interfere with histaminergic transmission
- leads to many ADR’s limiting use
- crosses BBB to interfere with histaminergic transmission
- Often interact with other receptors of other amines
10
Q
Explain the process of an allergic rxn?
A
- B-cells converted to active plasma cells
- produce IgE
- IgE binds to surface of mast cells
- Allergen binds to IgE antibodies on primed mast cells
- Degranulation of mast cells causes histamine to be released
- leads to allergic symptoms
11
Q
What histamine anatagonists do we have available? What affect do they have?
A
- Epinephrine
- smooth muscle relaxation
- stimulate alpha and beta receptors
- leads to increased BP as well as bronchdilation
- Cromolyn sodium -“histamine antagonist”
- takes a couple weeks to kick in so it would be used as an adjunct with pts. with severve allergies or allergic asthma
- stabilizes mast cells to prevent degranulation (the release of histamine
- Antihistamines
- H1 blockers
- tx allergies, insomnia, motion sickness- 1st and 2nd generation
- H2 blockers
- tx GERD/PUD
- H1 blockers
12
Q
- What H2 receptor antagonists are more effective than others?
- What is their absorption like? Can anything effect their absorption?
- Bioavailability of these drugs?
A
- All equally effectived and interchangable
- Well absorbed- BUT can be delayed with combined with antacid
- Bioavailability of cimetidine and ranitidine can be reduced with high doses of antacid
13
Q
ADE’s of 1st generation H1 antihistamines
A
14
Q
1st generation H1 blockers
- Agent name
- Anti cholinergic effect (is it + or ++ or +++) +++ means strongest
- Clinical Use and side effects/notes
A
15
Q
- What are the cardiovascular effects of histamine?
- Cardiovascular effects of histamine in pts with preexisting structural heart disease or reg. heart disease such as arrythmias, cardiomyopathy?
A
- Mast cells present in normal cardiac tissue→ Histamine released during anaphylatic state→enhances influx of Ca2+ into cardiac myocytes →increases contractility (pos. inotrope) → hypotension secondary to vasodilation →tachycardia (compensatory response to hypotension)
- These patients have increased expression of mast cells so more histamine would lead to more extreme systemic rxn to the histamine
17
Q
Histamine in the parietal cells
Gastric acid secretion (HCL) is mediated by? How does the process work ?
A
20
Q
Antihistamine actions
- H1
- Effects of histamine agonism?
- Effects of histamine antagonism?
- H2
- Effects of histamine agonism?
- Effects of histamine antagonism?
A
