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Pharmacology > Respiratory Drugs > Flashcards

Respiratory Drugs Flashcards

1
Q

asthma prevalance

A

8% of the population

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2
Q

Asthma cascade

A

irritant stimulates mast cells. Immediatly release histamine causing vasospasm. Secondary release of leukotirenes, leading to a narrowing of the bronchus due to inflammatory exudate. Tertiary is stimulus of chemotactic factors leading to cellular infliltrate which occludes the bronchioles

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3
Q

Why can MDI doses be smaller?

A

because therapy is targeted, gets into the respiratory tree. small dose causes fewer side effects

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4
Q

B2 agonists mechanism

A

agonists binds to receptor, which phosphorylates GTp and activates cAMP and PKA. PKA phosphorylates Ca channels reducing Ca influx and thus relaxing smooth muscles.

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5
Q

Beta 2 agonist ancilliary processes

A

mucolilliary clearance, decrease musculovascular permeability by then, suppress inflammatory cell mediator release.

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6
Q

Beta 2 pharmacokinetics

A

reasonable oral absorption, Metabolized by COMT/MAO 15-70% bioavailability,. t(1/2) = 6-8 hours
8-15% of dose reaches systemic circulation,

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7
Q

pharmacodynamics

A

oral_30-60 minutes, peak 1-3 hours. Inhaled: onset minutes, peak 15-30 mmin duration, 4-6h. b2 selectivity reduced at higher dose, tolerance and tachyphylaxis

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8
Q

beta 2 agonists effects/toxicities

A

tachy, palpitations, flushing, exacerbation of angina/arrthymias, vasodilation pulm artery. CNS” tremor/anxiety+headache+insomina, hypokalemia,hyperglycemia

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9
Q

Salmeterol: mech of action

A

binds to beta receptor, and then side chain dips into receptor to dual binding. this prolongs the effect, as both don’t come off at the same time. Take twice a day

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10
Q

Salmeterol use

A

does not give immediate release 30 minute onset, peak is 3 hours. give twice a day. prescribe with an inhaled steroid

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11
Q

MDIs

A

must be taken the right way. technique is important.

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12
Q

Ipratropium bromide

A

anticholinergic. about an hour to get to the peak, slower onset than beta2 agonists. 8-15% reach bronchi, 6-8 hours

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13
Q

Ipratropium advere effects

A

bitter taste, Ach effects (rare), drying of secretions does not occur.

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14
Q

Tiotropium

A

same as ipratropium, except longer half life. can get exagerated half life.

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15
Q

Corticosteroids

A

Fluticasone, Hydrocortisone, Prednisone, Methylprednisolone

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16
Q

Corticosteroid uses

A

systemic: acute severe asthma, chronic maintenance. Inhaled, prophylaxis in mild refractory asthma, combined with systemic steroids in chronic asthma.

17
Q

Corticosteroids mechanism

A

binds to receptor, turns off of genes promoting inflammation, turns on inflammatory genes. produce effect on transcription factors. change in genes involved in inflammation

18
Q

corticosteroids delivery

A

10% dose bronchi, 90% of oropharynx, metabolism hepatic CYP3A, low systemic concentrations

19
Q

corticosteroid adverse effects

A

thrush, horse voice. systemic is HPA-axis suppression, bruising, cataracts, inhibit bone growth, a concern in children, behavioral disturbances, hypokalemia.

20
Q

Leukotriene antagonists

A

Montelukast

21
Q

Leukotriene

A

LTC4 and LTD4 are the most potent bronchoconstrictors

22
Q

Montelukast-mechanism

A

antagonist to the CysLT1. decrease the ability to the LTDs to bind to receptors.

23
Q

Motelukast-use

A

prophylatic and chronic maitenance, used in combination with other drugs, not as good as beta2, used for asprin induced asthma.

24
Q

Montelukast-pharmdynamics

A

bronchodilation in 1-2 hours, duration of receptor blockade in 10-14 hours

25
Q

Montelukast-pharmkin

A

good oral absorption. hepatic CYP3A, food decreases bioavailablility

26
Q

Motelukast-adverse effects/indications

A

GI, mild headaches, hepatits, transaminitis, Churg-Straus vasculits.

27
Q

Second line anti-asthma

A

H1 blockers, steroid sparing: Methotrexate, Azathioprine, monoclonal antibody-omalizumab.

28
Q

Absolute contraindications to asthmatics

A

beta antagonists, cholinergic agents, adenosine, aspirin/NSAIDS. Carefule about use of ACE inhibitors, due to cough.

29
Q

Disodium Cromoglycate

A

allergic rhinite, conjuntivits, asthma. Inhibits chloride channels and calcium flux and reduces release of perfromed cytonkine from T cell and eosinophils.

30
Q

Disodium cromoglycate- side effects

A

nasal stinging, headache, nausea. very safe

31
Q

Histamine

A

mediator released by mast cells.

32
Q

H1

A

g protein receptor, phospholipas c increases IP3 and DAG, increases Ca2+, smooth muscle contraction

33
Q

H1 receptor antagonists

A

diphenhydramine, fexofenadine

34
Q

H1 receptor antagonists

A

allergic reactions, anti emetics, anti motion sickness. competitve H1 antagonist.

35
Q

H1 receptor antagonists side effects

A

1st generation: CNS, GI. 2nd, GI

36
Q

H1 receptor antagonist interactions,

A

can inhibit metabolism, prolong qtcto VT. Increased sedation with ETOH.

Pharmacology (7 decks)

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