Respiratory and Cardiovascular Pharmacology

Question 1

Albuterol mechanism

Answer 1

Question 2

Fluticasone

Answer 2

Inhaled corticosteroid. Transcriptionally represses genes associated with inflammatory response, and so can be used as a preventative medication in asthma. Reduces histamine production and secretion.

Question 3

Lovastatin

Answer 3

HMA-CoA-Reductase inhibitor

Decreases endogenous cholesterol synthesis and increases LDL-R expression on the liver, causing uptake of LDL and reducing serum levels. This decreases rate of atherosclerotic plaque buildup.

Question 4

Aspirin

Answer 4

aka acetylsalicylic acid

Irreversible acetylates COX-1 and COX-2. Prevents production of many arachadonic acid metabolites, except increases production of D series resolvins (makes aspirin generate 17-HpDHA from DHA, the same product as 15-LOX)

Question 5

DHA metabolism

Answer 5

Question 6

Metoprolol

Answer 6

Beta 1 blocker. Prevents activation of adenylyl cyclase and downstream PKA effects in cardiac myocyte (increased contractility from L-type channels, increased compliance from phospholamban, increased HR from SA node action)

Question 7

Montelukast

Answer 7

Cysteinyl leukotriene receptor antagonist. Prevents LTC4, LTD4, LTE4 from binding and exerting proinflammatory effects (bronchoconstriction, mucus production, etc)

Question 8

Nitroglycerin

Answer 8

Converted to NO within tissues. NO activates guanylate cyclase, and increased cGMP inhibits calcium release and activates myosin light chain phosphatase, both producing smooth muscle relaxation and vasodilation.

Selectively more venodilatory at low doses. The major use of nitrates is in the treatment of angina pectoris through venodilation, leading to reduced left ventricular preload.

Question 9

Salmeterol

Answer 9

Long-acting beta 2 agonist

Question 10

Tiotroprium

Answer 10

anti-cholinergic. Prevents activation of Gq, which would otherwise oppose PKA and allow smooth muscle contraction to go on uninhibited

Question 11

Diltiazem

Answer 11

Non-Dihydropyridine calcium channel blocker

Impede the influx of Ca++ through L-type channels in cardiac and smooth muscle. Relaxes smooth muscle. Reduces the rate of sinus firing and AV nodal conduction.

Greater affinity for heart targets (inotropic effects) than vascular targets

Question 12

Nifedipine

Answer 12

Dihydropyridine calcium channel blocker

Impede the influx of Ca++ through L-type channels in cardiac and smooth muscle. Relaxes smooth muscle. Reduces the rate of sinus firing and AV nodal conduction.

Greater affinity for vascular targets than targest in the heart, so primarily used to reduce blood pressure or perfuse coronaries.