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Pulmonology > Pharm - Histamine/ Histamine Antagonists > Flashcards

Pharm - Histamine/ Histamine Antagonists Flashcards

1
Q

Histamine is synthesized from what?

A

L-histadine

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2
Q

Name 2 most important sites of histamine synthesis? Key distinguishing difference between these sites and others within the body?

A

Mast cells and Basophils. These are the only 2 sites that can store large amounts of histamine. All others (epidermal cells, intestinal mucosa, CNS neurons, rapidly dividing cells) produce histamine as needed

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3
Q

Describe mechanism of time release that occurs with histamine?

A

Mast cells/basophils have granules that are - charged. These granules contain tons of histamine that are + charged. As granules fuse with mast cell membrane, the + charged histamine is slowly exchanged with Na+, essentially producing a long, slow release process.

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4
Q

What prevents histamine from having a systemic effect vs the local, regionalized effect it does have?

A

short 1/2 life of histamine.

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5
Q

Immunoglobulin associated with histamine? Mechanism?

A

IgE, binds to mast cells (along with allergen) triggers release of histamine

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6
Q

Histamine effect on capillary beds?

A

No effect, no histamine receptors

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7
Q

Increased “capillary” permeability via histamine occurs primarily at what sites?

A

Metarterioles, venules

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8
Q

Histamine binding to H1 receptors of arterioles and venules produces what effect?

A

rapid onset, short term dilation

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9
Q

Histamine binding to H2 receptors of arterioles and venues produces what effect?

A

slow onset, persistent dilation

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10
Q

Net effect of histamine on large vessels?

A

Vasoconstriction (via smooth muscles cells)

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11
Q

Net effect of histamine in lungs?

A

bronchoconstriction

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12
Q

Main MOA of histamine antagonists?

A

Histamine receptors occur in active and inactive confirmation. H antagonists simply bind to histamine receptors and increase # of inactive receptors, thus decreasing total receptor activity

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13
Q

Key difference(s) b/t 1st gen and 2nd gen H1 antagonists

  • structure?
  • 1/2 life?
  • dosing regimen?
  • sedation qualities?
  • Anti-cholinergic side effects?
A

1st generation
- based on structure of histamine
- short lived
- multiple dosing
- highly sedative
- anticholinergic side effects (which can be beneficial)
The last 3 are the key differences between 1st and 2nd generation H1 antagonists

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14
Q

1st generation H1 antagonists sedative effects due to what MOA? Key important fact about this?

A

H1 antagonists sedative effects ARE NOT due to antimuscarinic effects.
- sedative quality bc histamine antagonists cross BBB and act on H1 receptors in hypothalamus, causing sedative traits.

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15
Q

What key feature allows 1st gen H1 antagonists to have effect in brain.

A

Can cross BBB and evade p-glycoprotein (which is in charge of drug efflux)

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16
Q

1st gen H1 antagonist are contraindicated in what patients? Why?

A

Asthmatics, b/c these 1st gen drugs actually increase production of dry, thickened mucus secretions via anticholinergic effects.

17
Q

Cardiac effects of 1st gen H1 antagonists?

A

QT prolongation, ventricular arrhythmias

18
Q

Key point regarding selectivity of 1st gen H1 antagonists?

A

They can, in some cases, bind to other receptors besides H1, producing adverse effects (i.e. M receptors - hence the anticholinergic effects seen in 1st gen)

19
Q

1st gen H1 antagonists can produce antiemetic effects via what mechanism?

A

through anticholinergic effects, but can cause sedation as well. (he gives his story of working on a fishing vessel)

20
Q

Main structural difference b/t 1st and 2nd generation H1 antagonists? Why is this important? Hint: charge

A

2nd gen H1 antagonists have much greater + charge. Do not cross BBB as easily, thus do not have sedative effects. Key difference

21
Q

H1 blockade effects b/t 1st and 2nd generation antagonists?

A

Essentially the same, again main difference is lack of sedative effects seen with H2

22
Q

Asthmatics and 2nd generation H1 antagonists. Contraindicated? Why/Why not

A

Not contraindicated, 2nd gen doesn’t have anticholinergic effects. Won’t produce increased dry, thickened mucus (seen with 1st gen). Safe for asthmatics to take

23
Q

Which has greater duration of action, 1st or 2nd gen H1 antagonists?

A

2nd generation, much longer duration of action. single dosing.

24
Q

Main 2 goals of 3rd generation H antagonists

A
  1. Increase specificity and binding for H1 receptor (thus lower dose and more potent)
  2. Targe multiple receptor types in addition to anti-histamine functions (potentially having anti asthmatic function and histamine release inhibition)
25
Q

Allergic Rhinitis: 1st or 2nd/3rd generation H1 antagonists?

A

1st: ++

2nd/3rd: ++ (better compliance)

26
Q

Urticaria: 1st or 2nd/3rd generation H1 antagonists?

A

1st: ++

2nd/3rd: ++ (better compliance)

27
Q

Atopic dermatitis or itching dermatosis: 1st or 2nd/3rd generation H1 antagonists?

A

1st is better, Symptoms are due to adrenergic pathway effects (in which muscarinic receptors play a role)

28
Q

Asthmatics: 1st or 2nd/3rd generation H1 antagonists?

A

2nd/3rd better. No antimuscarinic effects (as seen with 1st)

29
Q

Anti-motion/antiemetics/appetite stimulation/insomnia: 1st or 2nd/3rd generation H1 antagonists?

A

1st is better. b/c of antimuscarinic effects

30
Q

List 1st generation H1 antagonists?

A 
Brompheniramine [Dimetane]
chlorpheniramine [Chlor-Trimeton]
Clemastine [Tavist]
cyclizine [Marezine]
Dimenhydrinate [Dramamime]
Diphenhydramine [Benadryl]
Hydroxyzine [Atarax]
Meclizine [Antivert]
Promethazine [Phenergan]
Tripolidine [Actidil]
31
Q

List 2nd generation H1 antagonists

A

Acrivastine [Semprex]
Cetirizine [Zyrtec]
Fexofenadine [Allegra]
Loratadine [Claritin]

32
Q

List 3rd generation H1 antagonists

A 
Azelastine [Astelin,Astepro]
Desloratidine [Clarinex]
Emedastine [Emadine]
Levocabastine [Livostin]
Mizolastine [Mistamine]
Olopatadine [Patanol]
33
Q

Main dif b/t loratadine (2nd gen) and desloratadine (3rd gen)

A

Desloratadine:

- 14-17x greater binding to H1 receptor

34
Q

Which 3rd gen drug is given ocularly for allergic rhinitis?

A

olopatadine

35
Q

Which 3rd gen drug inhibits release of histamine from mast cells?

A

olopatadine

36
Q

Olopatadine inhibits the release of what 2 mediators from inflammatory cells?

A

tryptase, PGD2

37
Q

Most specific 3rd gen H1 antagonist?

A

Levocabastine

38
Q

Azelastine key features

A
  1. inhibits histamine and leukotriene activity
  2. blocks Ca2+ and 5-lipooxygenase pathway
  3. Inibits PAF through receptor antagonism.

Pulmonology (31 decks)

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