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Pharmacology > 14) Histamine 5HT Ergot Alkaloids > Flashcards

14) Histamine 5HT Ergot Alkaloids Flashcards

1
Q

Histamine synthesis and storage

A
  • Synthesized from istidine

- Stored in mast cells (enterochromaffin cells in the gut)

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2
Q

Histamine is metabolized by

A
  • Monoamine oxidase (MAO)

- Diamine oxidase

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3
Q

Excess production of histamine in the body (eg, in systemic mastocytosis) can be detected by

A
  • Measurement of its major metabolite (imidazole acetic acid) in the urine
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4
Q

Hitamine is released from mast cells in response to

A
  • IgE-mediated (immediate) allergic reactions

- Plays a pathophysiologic role in seasonal rhinitis (hay fever), urticaria, and angioneurotic edema

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5
Q

Histamine also plays a physiologic role in the control of

A
  • Acid secretion in the stomach

- As a neurotransmitter

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6
Q

Two receptors for histamine

A
  • H1 and H2
  • Mediate most of the peripheral actions
  • 2 others (H3, H4) have also been identified
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7
Q

The triple response

A
  • Demonstration of histamine effect on the skin
  • Mediated mainly by H1 and H2 receptors
  • This response involves a small red spot, an edematous wheal, which is surrounded by a red flare
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8
Q

H1 receptor distribution

A
  • Smooth muscle
  • Endothelium
  • Brain
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9
Q

H2 receptor distribution

A
  • Stomach
  • Heart
  • Mast cells
  • Brain
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10
Q

H3 receptor distribution

A
  • Nerve endings

- CNS

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11
Q

H4 receptor distribution

A
  • Leukocytes

- CD4 T-cells

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12
Q

5-HT1D/1B receptor distribution

A
  • Brain
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13
Q

5-HT2 receptor distribution

A
  • Smooth muscle
  • Platelets
  • Brain
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14
Q

5-HT3 receptor distribution

A
  • CNS

- Sensory and enteric nerves

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15
Q

5-HT4 receptor distribution

A
  • Gastro-intestinal tract
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16
Q

H1 and 5-HT2 post-receptor mechanisms

A
  • Gq; ↑ IP3 and DAG
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17
Q

H2 and 5-HT4 post-receptor mechanisms

A
  • Gs; ↑cAMP
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18
Q

H3, H4, and 5-HT1D/1B post-receptor mechanisms

A
  • Gi; ↓cAMP
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19
Q

5-HT3 post-receptor mechanism

A
  • Ligand-gated Na+/K+ channel
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20
Q

First generation H1 antagonists (blockers)

A
  • Very sedating
  • New subgroup prototyped by chlorpheniramine and cyclizine is less sedating
  • Half lives = 4–12 h
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21
Q

Second generation H1 antagonists (blockers)

A
  • Prototyped by loratadine
  • Great reduced sedation and autonomic effects
  • Half lives = 12–24 h
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22
Q

H1 blockers MOA

A
  • Competitive antagonists at the H1 receptor
  • No effect on histamine release from storage sites
  • More effective if given before histamine release occurs
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23
Q

Some (but not all) first-generation agents have

A
  • Anti-motion sickness effects (diphenhydramine, dimenhydrinate, cyclizine, meclizine….)
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24
Q

First generation H1 antagonists selectivity

A
  • Less selectivity to histamine receptors

- Anti-cholinergic activity

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25
Q

Second generation H1 antagonists selectivity

A
  • More selective to the peripheral histamine receptors

- Don’t cross the blood brain barrier (BBB) so they have less sedation side effects and less anticholinergic effects

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26
Q

H2 blocker prototype

A
  • Dimetidine

- Single dose DOA may be 12–24 h

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27
Q

H2 antagonist (cimetidine) MOA

A
  • Pharmacologic blockade of histamine H2 receptors
  • Relatively selective
  • No significant blocking actions at H1 or autonomic receptors
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28
Q

The only therapeutic effect of clinical importance (H2 receptor antagonist)

A
  • Reduction of gastric acid secretion
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29
Q

Cimetidine

A
  • Potent inhibitor of hepatic drug-metabolizing enzymes
  • May also reduce hepatic blood flow
  • Significant antiandrogen effects in patients receiving high doses (others don’t have this side effect)
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30
Q

H2 blockers (names)

A
  • Ranitidine
  • Famotidine
  • Nizatidine
  • Cimetidine
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31
Q

Serotonin production/storage

A
  • Produced from tryptophan

- Stored in vesicles in cells of the gut and neurons of the CNS and enteric nervous system

32
Q

After release, serotonin is metabolized by

A
  • Monoamine oxidase (MAO)
33
Q

Excess serotonin production in the body can be detected by

A
  • Measuring its major metabolite in the urine

- 5-hydroxyindole acetic acid (5-HIAA)

34
Q

After release from neurons, serotonin

A
  • Partially taken back up into the nerve ending by a serotonin reuptake transporter (SERT)
35
Q

Serotonin agonists in clinical use act at these receptors

A
  • 5-HT1D/1B
  • 5-HT2
  • 5-HT4
36
Q

Antidepressants

A
  • Selective serotonin reuptake inhibitors (SSRI)
37
Q

H1 receptor clinical outcome

A
  • Itching
  • Pain
  • Bronchoconstriction
  • Vasodilation, local edema
38
Q

H2 receptor clinical outcome

A
  • Gastric acid secretions
39
Q

H3 receptor clinical outcome

A
  • Appetite suppressant investigation
40
Q

5-HT2 receptor clinical outcome

A
  • In the CNS, mediate a reduction in appetite that has been used in the treatment of obesity
41
Q

5-HT3 receptor clinical outcome

A
  • Sspecially in the chemoreceptive area and vomiting center

- Antagonists have anti-emetic effects

42
Q

5-HT4 receptor clinical outcome

A
  • Intestinal motility
43
Q

Prototypic H1 antagonists

A
  • Diphenhydramine

- Loratadine

44
Q

Prototypic H3 antagonists

A
  • Clobenpropit
45
Q

Prototypic H4 antagonists

A
  • Thioperamide
46
Q

Prototypic 5-HT1D/1B agonists

A
  • Triptans: Sumatriptan,….
47
Q

5-HT2 prototypic agonists

A
  • Loracserin
48
Q

5-HT2 prototypic antagonists

A
  • Ketanserin
49
Q

5-HT3 prototypic antagonists

A
  • Ondansetron
50
Q

5-HT4 prototypic agonists

A
  • Tegaserod (partial agonist)
51
Q

5-HT4 prototypic antagonists

A
  • Tegaserod (partial agonist)
52
Q

5-HT1D/1B agonists (names)

A
  • Sumatriptan
  • Almotriptan
  • Eletriptan
  • Frovatriptan
  • Naratriptan
  • Rizatriptan
  • Zolmitriptan
53
Q

5-HT1D/1B agonists indication

A
  • Acute migraine

- Cluster headache

54
Q

5-HT1D/1B agonists side effects

A
  • Paresthesias
  • Pain
  • Dizziness
  • Coronary vasospasm
55
Q

5-HT2 agonists indication

A
  • Treatment of obesity
56
Q

5-HT3 agonists indication

A
  • Especially in the chemoreceptive area and vomiting center

- Antagonists have anti-emetic effects

57
Q

5-HT4 agonists indication

A
  • Chronic constipation
58
Q

5-HT4 agonists side effects

A
  • Cardiovascular toxicity
59
Q

5-HT2 antagonist names/MOA

A
  • Ketanserin, cyproheptadine are competitive antagonists

- Phenoxybenzamine is an irreversible blocker

60
Q

5-HT2 antagonist indication

A
  • Treatment of carcinoid tumor (neoplasm that secretes large amounts of serotonin and peptides)
  • Causes diarrhea, bronchoconstriction, and flushing
61
Q

5-HT2 antagonist side effects

A
  • Ketanserin, phenoxybenzamine: cause α-blockade thus have α-blockade SE
  • Cyproheptadine: causes H1-blockade thus has H1-blockade SE
62
Q

5-HT3 antagonists (names)

A
  • Ondansetron
  • Granisetron
  • Dolasetron
  • Alosetron
63
Q

5-HT3 antiemetic actions

A
  • Vomiting associated with cancer chemotherapy and postoperative vomiting
64
Q

Alosetron (5-HT3 antagonist) is used in the treatment of

A
  • Women with irritable bowel syndrome associated with diarrhea
65
Q

5-HT3 antagonist side effects

A
  • Diarrhea

- Headache

66
Q

Dolasetron (5-HT3 antagonist) side effects

A
  • Has been associated with QRS and QTc prolongation in the ECG
67
Q

Alosetron (5-HT3 antagonist) side effects

A
  • Causes significant constipation

associated with fatal bowel complications

68
Q

Serotonin and drugs with 5-HT agonist effects are associated with

A
  • Hyperthermia (high fever)
  • Hyperreflexia and tremors (skeletal muscle effects)
  • Cardiovascular abnormalities (hypertension)
  • Hyperactive bowel syndrome; diarrhea
  • Mydriasis
  • Agitation and coma that can be life-threatening
69
Q

Precipitating drugs

A
  • SSRI
  • Sumatriptan
  • Ondansetron
  • Not sure how and if true
70
Q

Mild Serotonin Syndrome symptoms

A
  • Mydriasis
  • Shivering
  • Sweating
  • Tachycardia (mild)
71
Q

Moderate Serotonin Syndrome symptoms

A
  • Altered mental status
  • Autonomic hyperactivity
  • Neuromuscular abnormalities
72
Q

Life threatening Serotonin Syndrome symptoms

A
  • Delirium
  • Hypertension
  • Hyperthermia
  • Muscle rigidity
  • Tachycardia
73
Q

Ergot alkaloid clinical effects on vessels

A
  • Migraine treatment
  • α-adrenoceptor–mediated vasoconstriction
  • Overdose can cause ischemia and gangrene of the limbs or bowel
74
Q

Ergot alkaloid clinical effects on uterus

A
  • Reduce post-partum bleeding
  • Powerful and long-lasting contraction that reduces bleeding
  • Contract the uterus especially near term (delivery) - Ergonovine is the prototype
  • In pregnancy, the uterine contraction is sufficient to cause abortion or miscarriage
75
Q

Ergot alkaloid clinical effects on the brain

A
  • Bromocriptine has been used to reduce prolactin secretion (dopamine is the physiologic prolactin release inhibitor) in Hyperprolactinemia and parkinsonism
76
Q

Hallucinations may be prominent with

A
  • Naturally occurring ergots
  • Lysergic acid diethylamide (LSD)
  • Uncommon with the therapeutic ergot derivatives
77
Q

In the pituitary, some ergot alkaloids are

A
  • Potent dopamine-like agonists and inhibit prolactin secretion
  • Bromocriptine are among the most potent semisynthetic ergot derivatives

Pharmacology (27 decks)

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