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Asthma/COPD Exam 3 > Antihistamines > Flashcards

Antihistamines Flashcards

1
Q

what is the important mediator in inflammation?

A

mast cells and basophils

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2
Q

in the metabolism of histamine all forms are found what?

A

inactive

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3
Q

in the localization of histamine releasing cells, histamine is complexed with what particular storage granule?

A

heparin sulfate

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4
Q

what is the mechanism of histamine release?

A

binding of antigen to antibody molecules causes increase in cytoplasmic Ca2+ concentration

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5
Q

what drugs prevent histamine release and their dosage forms?

A

Cromolyn sodium
–> Rx- mastocytosis (oral)
–> OTC- allergic rhinitis (nasal spray)

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6
Q

how many histamine receptors are there?

A

4

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7
Q

where are H1 receptors distributed?

A

throughout CV, respiratory systems G.I smooth muscle

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8
Q

where are H2 receptors distributed?

A

in the CV system and GI smooth muscle and stomach

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9
Q

describe the H1 and H2 colocalization:

A

H1 in vascular endothelium : Inc. NO and contraction of endothelial cells
H2 in vascular muscle: relaxation (vasodilation)

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10
Q

how are H3 receptors distributed?

A

located mainly in the CNS–> coupled to Gi/Go

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11
Q

what are H1 antagonists referred to as?

A

antihistamines

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12
Q

how are H4 cells distributed?

A

located in mast cells, basophils, and eosinophils–> coupled to Gi/Go

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13
Q

what are H2 antagonists referred to as?

A

acid blockers

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14
Q

h1 antagonists are predominately what?

A

inverse agonists

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15
Q

what are the 1st gen antihistamines and their class?

A
  1. Bropheniramine –> alkylamine
  2. Cyproheptadine –> piperadine
  3. Diphenhydramine –> ethanolamine
  4. Promethazine –> phenothiazine
  5. Hydroxyzine –> piperazine
  6. Pyrilamine –> elenediamine
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16
Q

what are the antocholinergic effects of H1 antagonists/

A

1, not very selective
2. anti-muscarinic (atropine-like)
3. more lipid soluble - inc. CNS access
4. anti-motion sickness and anti-emetic effects (promethazine/ diphenhydramine)
5. only 1st gen drugs
6. typical anticholinergic effects: dec. urination, dry mouth

17
Q

what are the other adverse effects of h1 antagonists?

A
  1. not very selective
  2. local anesthetic –> pyrilamine/ promethazine
  3. anti-serotonin –> cyproheptadine/ azatidine (headaches)
  4. adrenergic antagonism –> phenothiazines (hypotension)
  5. extrapyramidal –> phenothiazine/ promethazine (dystonia/ akathisia)
18
Q

what are the 2nd gen antagonists?

A

loratidine, desloratidine, fexofenadine, cetirizine, levocetirizine

19
Q

what do second gen antagonists do?

A
  1. dec. lipid solubility
  2. efflux from CNS by P-glycoprotein transporter
  3. little or no sedation
  4. no anti-muscarinic/ anti-emetic/ anti-motion sickness act
20
Q

what does allergic mean?

A

histamine indirectly stimulates mucus discharge via H1 receptors on nerve endings

21
Q

what does the common cold mean?

A

virus stimulates reflex independent of peripheral H1 receptors
1. 1st gen drugs act in the brain to inhibit rhinorrhea and sneeze
2. 2nd gen drugs may not be as effective

22
Q

where do H1 receptors act?

A

nerve

23
Q

where do H1 and M2/3 receptors act?

A

PSNS

24
Q

what are topical H1 antagonists and a common side effect?

A
  1. olopatadine –> Patanol (ED & NS)
  2. azestaline –> astelin (ED & NS)
  3. ketotifen –> zaditor (eye drops)
    ** all three can cause drowsiness if taken orally or as nasal spray **
    – systemic use approved in Europe –
25
Q

is there a relationship between sedation and peripheral antihistamines?

A

no relationship

26
Q

what are the uses and side effects for H2 antagonists and the drugs?

A

Uses: reduce gastric acid secretion, treat peptic ulcers & GERD
SEs: CNS dysfunction, antiandrogen, impotence, blood dyscrasias, hepatotoxicity

27
Q

what does budesonide/ fluticasone do in AR?

A
  1. NS in rx or OTC
  2. slow onset- max benefit may take several days
  3. Fluticasone-low systemic absorption from intranasal
  4. budesonide- 1/3 dose is absorbed < 1hr
    ** both may suppress HPA axis with prolonged, high doses
28
Q

what are the roles of T calls in AR?

A

after activation the TH2 cells are going to release a number of inflammatory mediators that can cause infiltration of different inflammatory cells (eosinophil, neutrphil, basophil, lymphocytes) and lead to inflammation and congestion

29
Q

what glucocorticoid mechanisms are more important in AR?

A
  1. Suppress Th2 cells –> dec. cytokine
  2. Mast cells –> dec. #, mediator, Cytokine, FceRI
    ** 1&2 nasal epithelium
  3. Glands/ Goblet cells –> dec. mucus secretion
    ** nasal epithelium

Asthma/COPD Exam 3 (9 decks)

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