Respiratory Drugs

Question 1

asthma prevalance

Answer 1

8% of the population

Question 2

Asthma cascade

Answer 2

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

Question 3

Why can MDI doses be smaller?

Answer 3

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

Question 4

B2 agonists mechanism

Answer 4

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

Question 5

Beta 2 agonist ancilliary processes

Answer 5

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

Question 6

Beta 2 pharmacokinetics

Answer 6

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

Question 7

pharmacodynamics

Answer 7

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

Question 8

beta 2 agonists effects/toxicities

Answer 8

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

Question 9

Salmeterol: mech of action

Answer 9

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

Question 10

Salmeterol use

Answer 10

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

Question 11

MDIs

Answer 11

must be taken the right way. technique is important.

Question 12

Ipratropium bromide

Answer 12

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

Question 13

Ipratropium advere effects

Answer 13

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

Question 14

Tiotropium

Answer 14

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

Question 15

Corticosteroids

Answer 15

Fluticasone, Hydrocortisone, Prednisone, Methylprednisolone

Question 16

Corticosteroid uses

Answer 16

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

Question 17

Corticosteroids mechanism

Answer 17

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

Question 18

corticosteroids delivery

Answer 18

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

Question 19

corticosteroid adverse effects

Answer 19

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

Question 20

Leukotriene antagonists

Answer 20

Montelukast

Question 21

Leukotriene

Answer 21

LTC4 and LTD4 are the most potent bronchoconstrictors

Question 22

Montelukast-mechanism

Answer 22

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

Question 23

Motelukast-use

Answer 23

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

Question 24

Montelukast-pharmdynamics

Answer 24

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

Question 25

Montelukast-pharmkin

Answer 25

good oral absorption. hepatic CYP3A, food decreases bioavailablility

Question 26

Motelukast-adverse effects/indications

Answer 26

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

Question 27

Second line anti-asthma

Answer 27

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

Question 28

Absolute contraindications to asthmatics

Answer 28

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

Question 29

Disodium Cromoglycate

Answer 29

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

Question 30

Disodium cromoglycate- side effects

Answer 30

nasal stinging, headache, nausea. very safe

Question 31

Histamine

Answer 31

mediator released by mast cells.

Question 32

H1

Answer 32

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

Question 33

H1 receptor antagonists

Answer 33

diphenhydramine, fexofenadine

Question 34

H1 receptor antagonists

Answer 34

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

Question 35

H1 receptor antagonists side effects

Answer 35

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

Question 36

H1 receptor antagonist interactions,

Answer 36

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