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Pharmacology Exam 1 > Antihistamines > Flashcards

Antihistamines Flashcards

1
Q

Distribution of mast cells

A

high numbers in skin, nose, mouth, lungs, intestinal mucosa

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2
Q

storage granules of mast cells

A

histamine is complexed with sulfated-polysaccharides, heparin sulfate, chondroitin sulfate, and proteases

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3
Q

what are some non-mast cells with histamine

A

nerve terminals in some areas of the brain (neurotransmitter)

fundus of the stomach - specialized cells store histamine for stimulation of acid secretion

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4
Q

Causes of histamine release from mast cells and basophils

A

Antigen mediated-binding of antigen (allergens) to antibodies bound to cell surface (IgE)

Non-antigen mediated - thermal or mechanical stress, cytotoxic agents - venoms, various drugs (e.g. high dose morphine)

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5
Q

what other inflammatory agents are released from mast cells after antigen mediated binding to allergens?

A

Aside from histamie, kinins, serotonin, leukotrienes, prostaglandins

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6
Q

number of different types of histamine receptors

mechanism of downstream activation

A

four histamine receptor subtypes

all are G-protein coupled

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7
Q

Distribution of H1 receptor

A

throughout CV, respiratory systems, GI smooth muscle

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8
Q

H1 receptor is linked to what sort of GPCR downstream activity in smooth muscle

A

linked to phosphoinositol pathway, contracts GI smooth muscle

H1+histamine->Gq->PLC->IP3+DAG->ups Ca2+->ups Ca2+-calmodulin->phospho MLC

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9
Q

H1 receptor in vascular endothelial cells

A

Hist+H1->ups NO release->NO diffuses to vascular smooth muscle->ups cGMP->drops Ca2+

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10
Q

How is H1 receptor linked to stimulation of sensory nerves

A

Hist+H1 (in cutaneous or nasal mucosal nerve endings) -> sneezing and itching

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11
Q

Distribution of H2 receptor

A

CV system, GI smooth muscle, stomach

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12
Q

function of H2 receptor

A

linked to relaxation of vascular smooth muscle and gastric secretion

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13
Q

Downstream activation of H2 Rs

A

Histamine+H2-> Gs->ups adenylate cyclase->ups cAMP

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14
Q

H1 and H2 colocalization

A

H1 in vascular endothelium -> ups NO, ups contraction of endothelial cells

H2 in vascular muscle -> relaxation

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15
Q

H3 distribution

A

mainly in CNS

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16
Q

histamine’s use in the CNS

A

auto-receptor in neurons that use histamine as a neurotransmitter

linked to inhibition of NT release

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17
Q

downstream mechanism of H3 R activation

A

histamine+H3-> downs Ca2+ influx through voltage-gated channels

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18
Q

H4 distribution

A

mast cells, basophils, and eosinophils

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19
Q

function of H4 R

A

linked to histamine-induced chemotaxis

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20
Q

possible future for H4 R drugs

A

promising target for future antiinflammatory drugs

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21
Q

histamine’s affects on cardiovascular system

A

heart-moderate increase in HR & contraction force (H2 increases in SA conduction; reflex tachy)
Vasodilation - (H1 in endothelium; H2 in smooth muscles)

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22
Q

histamine’s affects on respiratory

A

H1 mediated constriction of bronchial smooth muscle

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23
Q

histamine’s affect on acid release on the stomach

A

H2 mediated release from parietal cells in stomach

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24
Q

histamine’s role in anaphylaxis

A

hypotension and loss of fluid to the interstitial space, drops effective blood volume; swelling

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25
Q

histamine’s effects are (increased/decreased) when both H1 and H2 Rs are targeted

A

histamine blockage increases when both H1 and H2 are blocked

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26
Q

Triple response

A
  1. Red spot at point of injection (immediate)
  2. Red flare radiating ~1cm from injection site (~10s)
  3. Wheal (raised welt)@ site of injection (1-2min)
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27
Q

skin pathologies caused by histamine

A

urticaria-hives, rash, edematous welts
dermatographia-redness/welt w/mechanical stim
flushing(erythema)-redness due to vasodilation

28
Q

how many different H1 R antagonists are there

A

23-24 different compounds

120 products including combos

29
Q

antihistamines

A

H1 antagonists

DO NOT bind H2 Rs

30
Q

acid blockers

A

H2 antagonists

DO NOT bind H1 Rs

31
Q

Mechanism of action of H1 R antagonists

A

competitive inhibition

32
Q

First generation antihistamines

A

alkylamines, ethanolamines, ethylenediamines, phenothiazines, piperadines, piperazines

33
Q

eg of alkylamine

A

brompheniramine

34
Q

eg of piperadine

A

cyrpoheptadine

35
Q

eg of ethanolamine

A

diphenhydramine

36
Q

eg of phenothiazine

A

promethazine

37
Q

eg of piperazine

A

hydroxyzine

38
Q

eg of ethylanolamine

A

pyrilamine

39
Q

uniform characteristic of all H1 R antagonists

A

all lack amidazole group in H1

40
Q

side effects of H1 R antagonists

A

sedative effects
CNS stim @ high doses
paradoxical excitation in kids at normal dose

41
Q

most sedative H1 R antagonists

A

ethanolamines & phenothiazines

e.g. diphenyhydramine, promethazine

sedatives of others vary

42
Q

are 2nd gen antihistamines sedative

A

limited to no CNS affects

43
Q

do peripheral antihistamines have sedatvive effects

A

no relationship (2nd gen antihistamines are not sedative)

44
Q

OTC sedatives commonly contain

A

diphenhydramine

eg Sominex & Nytol contain diphenhydramine

45
Q

reason for 1st gen antihistamines being sedative

A

accumulate in CNS -> drowsiness

46
Q

how selective are 1st gen H1 R antagonists

A

not very selective

47
Q

what types of autonomic effects do H1 R antagonists have

A

anti-cholinergic effects

  • lipid solubility -> ups CNS penetration
  • imparts anti-motion sickness/vertigo effect & anti-emetic effect
  • NOT SEEN with clinical doses of 2nd gen drugs
48
Q

which 1st gen H1 R antagonists have local anesthetic effect

A

pyrilamine & promethazine, especially

49
Q

which 1st gen H1 R antagonists have anti-serotonin effects

A

cyproheptadine & azatadine

50
Q

which 1st gen H1 R antagonists have weak alpha-adrenergic antagonism

A

phenothiazines

51
Q

general side effects of 1st gen H1 R antagonists aside from sedation

A

headaches & hypotension

52
Q

2nd gen H1 R antagonists

A 
loratadine (claritin)
desloratidine (clarinex)
fexofenadine (allegra)
cetirizine (zyrtec)
levocetirizine (xyzal)
53
Q

sedative effects of 2nd gen H1 R antagonists

A

little or no sedation

54
Q

reason for little/no sedation of 2nd gen H1 R antags

A

decreased lipid solubility

Efflux from CNS by P-glycoprotein transporter

55
Q

compare extra activities between 1st gen and 2nd gen H1 R antags

A

2nd gen do not have anti-emetic, anti-muscarinic, ant-motion sickness

1st gen does

56
Q

origin of the 2nd gen H1 R antags

A

active metabolites of 1st gen, metabolites are not sedative

eg Terfenidine -> Fexofenadine

hydroxyzine->cetirizine

57
Q

cell processes that 2nd gen H1 R antags may also block

A

LTC4
neutrophil migration
eosinophil infiltration

58
Q

topical H1 R antags

A

Olopatadine (eye drops/nasal spray)
azelastine (eye drops/nasal spray)
Ketotifen (eye drops)

59
Q

when are topical H1 R antags used

A

indicated for tx of seasonal allergic rhinitis +/- conjunctivitis

60
Q

what is another use for Ketotifen (H1 R topical antag)

A

chronic asthma prevention in Europe

61
Q

H1 R antags are used in adjunct with epinephrine to treat

A

anaphylaxis

62
Q

1st gen H1 R antags’ sedative effects may interact with

A

alcohol, anxiolytis, antipsychotics

63
Q

1st gen drugs & (des)loratidine are contraindicated in

A

urinary retention, narrow angle glaucoma,

64
Q

promethazine (a phenothiazine) is structured similarly to ______ and can cause what sxs

A

promazine (antipsychotic drug)

can cause extrapyramidal effects

  • dystonia
  • akathisia (agitation)
  • Parkinsonian rigidity
65
Q

mechanism for H1 R antag CNS depression

A
  1. gains entry to CNS
  2. H1 R in thalamic relay cells have depolarized membrane potential, low freq. action potentials -> Wakefullness
  3. H1 antags block Rs-> hyperpolarization-> bursts of APs-> SLEEP
66
Q

noted effect of sedation from H1 R antags

A

tolerance to sedation can occur over time

Pharmacology Exam 1 (7 decks)

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