Pharmacology 12: Vasodilators And Treatment Of Angina Pectoris

Front 1

Most common cause of stable angina?

Back 1

atherosclerotic obstruction

Front 2

Most common cause of Prinzmental angina?

Back 2

vasospasm

Front 3

What causes chest pain in angina?

Back 3

inability for oxygen/blood supply to meet muscle demand = ischemic pain

Front 4

Why would a calcium channel blocker help treat Prinzmental angina (caused by vasospasm)?

Back 4

blocking calcium channels inhibits activation of light chain myosin = no smooth muscle contraction

Front 5

Why is it beneficial to have drugs that shift metabolism from fatty acid degradation to carbohydrate degradation in angina treatment?

Back 5

normal cardiac muscle uses fatty acids for energy. during angina we are trying to lower the oxygen demand of the myocardium. it requires less oxygen to make ATP if carbs are used

Front 6

Why are sodium channel blockers helpful in treating angina?

Back 6

reduce strength of contractile force of the heart by reducing calcium influx during contraction

Front 7

Why are B-blockers important in treating angina?

Back 7

reduce the heart rate = reduce oxygen demand of the heart

Front 8

Increasing cGMP has what effect on smooth muscle?

Back 8

high cGMP= muscle relaxation = vasodilation

Front 9

Nitric oxide has what effect on cGMP levels?

Back 9

NO = guanylyl cylcase activation = more cGMP production = smooth muscle relaxation = vasodilation

Front 10

Why does increasing permeability of K+ channels help patients with angina?

Back 10

helps prevent depolarization of the smooth muscle (if K is leaking out, the resting potential will be lower and it will be harder to hit the threshold)= no smooth muscle contraction = vasodilation

Front 11

Why are B2 agonists NOT used in angina treatment?

Back 11

too much cardiac stimulation (from sympathetics) = higher oxygen demand = worse for angina

Front 12

High levels of cAMP have what effect on vascular muscle tone?

Back 12

cAMP= inactivation of myosin light chain = smooth muscle relaxation = vasodilation

Front 13

Calcium (bound to calmodulin) activates which enzyme, leading to vasoconstriction (smooth muscle contraction)?

Back 13

myosin light chain kinase is activated by intracellular calcium (bound to calmodulin). calcium channel blockers work to prevent this pathway

Front 14

Nitroglycerin has minimal effect on which 2 types of muscle?

Back 14

cardiac and skeletal. NO is only useful to modify smooth muscle

Front 15

After a dose of nitroglycerin, what happens to venous return?

Back 15

decrease. pre-load and cardiac output fall

Front 16

Why might tachycardia result after high nitroglycerin dosage?

Back 16

nitroglycerin vasodilates vessels = BP falls = heart rate increases to try to compensate and keep BP up

Front 17

Nitric oxide has what effect on platelets?

Back 17

increased cGMP (NO increases guanylyl cyclase activity) = less platelet adhesion

Front 18

Why is nitrite ion formation helpful in patients with cyanide poisoning?

Back 18

nitrite ion binds hemoglobin to form methemoglobin = methemoglobin has a higher affinity for CN than cytochrome oxidase (cyanide poisoning is caused by binding of CN to cytochrome oxidase). once CN is bound to methemoglobin, it can be excreted

Front 19

Why can high levels of nitrite lead to a cyanotic appearance?

Back 19

nitrite ion can bind to hemoglobin and form methemoglobin. met hemoglobin has a poor affinity for oxygen. there will be many deoxygenated RBCs/hemoglobin

Front 20

Erectile dysfunction drugs mostly increase nitric oxide levels by what mechanism?

Back 20

phosphodiesterase inhibitors. prevents cGMP from being degraded = more cGMP = more smooth muscle relaxation = vasodilation

Front 21

Why are erectile dysfunction drugs very dangerous when combined with nitroglycerin?

Back 21

nitroglycerin and phosphodiesterase inhibitors are both working to vasodilate (keep cGMP levels high). if both are taken together, there may be extreme vasodilation and BP can fall to induce shock

Front 22

Sildenafil, alprostadil, tadalafil, vardenafil are all what class of drugs?

Back 22

erectile dysfunction drugs/ phosphodiesterase inhibitors

Front 23

Why might very high doses of nitroglycerin actually make angina worse?

Back 23

too much nitro = excess vasodilation = BP drop = tachycardia to compensate = increased oxygen demand from heart = angina is worsened

Front 24

Nitroglycerin can lead to a lower venous return as systemic filling pressure drops. How does this help stable angina?

Back 24

we are now reducing the cardiac oxygen demand since the myocardium can pump slower and less forcefully (there isn't a high atrial pressure and overwork form high venous return)

Front 25

Most calcium channel blockers used in the treatment of angina block which calcium channels?

Back 25

L-type channels

Front 26

What class of calcium channel blockers have greatest effect on the blood vessel vasodilation?

Back 26

dihydropyridines (like amlodipine). verapamil and diltiazem have more effects on the heart

Front 27

Calcium channel blockers have what effect on BP?

Back 27

decrease BP by the vasodilation. less intracellular calcium = unable to activate myosin kinase = no contraction = relaxation

Front 28

Which calcium channel blockers have a greater cardiac effect, rather than smooth muscle effect?

Back 28

verapamil and diltiazem

Front 29

Why do calcium channel blockers not have a large effect on skeletal muscle?

Back 29

skeletal muscle usually stores large amounts of calcium intracellularly and doesn't rely on movement of calcium into the cell. calcium channel blockers don't have an effect if the calcium is already in the muscle

Front 30

Why is nifedipine helpful in treating stroke (cerebrovascular accident) patients?

Back 30

it is a calcium channel blocker that acts well on cerebral vessels for vasodilation

Front 31

The SA and AV nodes are most affected by which calcium channel blockers?

Back 31

verapamil and diltiazem

Front 32

Why do B-blockers help angina?

Back 32

decrease heart rate by blocking sympathetic innervation = lower contractility/heart rate = less oxygen demand

Front 33

How do pFOX inhibitors help angina?

Back 33

shift metabolism from fatty acids to carbs (which need less Oxygen to form ATP). this lowers oxygen demand

Front 34

How does the drug pentoxifylline help treat peripheral artery disease?

Back 34

works as a blood thinner to increase flow/decrease viscosity

Front 35

How does Cilostazol help peripheral artery disease?

Back 35

phosphodiesterase inhibitor = more cGMP/cAMP = myosin kinase inactivation = smooth muscle relaxation = vasodilator

Front 36

How does the drug ivrabradine reduce heart rate?

Back 36

inhibits sodium channels activated by hyperpolarization = neurons are more hyperpolarized = harder for action potential to fire = less muscle contraction

Front 37

Why are statins helpful in treating angina?

Back 37

prevent LDL formation = less atherosclerosis = less occlusion = less stable angina

Front 38

If nitrates are combined with Beta or calcium blockers, what effect is seen on the heart rate?

Back 38

decreased heart rate

Front 39

If nitrates are combined with Beta or calcium blockers, what effect is seen on the BP?

Back 39

decrease BP

Front 40

If nitrates are combined with Beta or calcium blockers, what effect is seen on the end-diastolic volume?

Back 40

decrease (lower systemic filling pressure), or no effect

Front 41

If nitrates are combined with Beta or calcium blockers, what effect is seen on the ejection time and contractility?

Back 41

none.

Front 42

Nitrates have what effect on end diastolic volume?

Back 42

decreases; lower filling pressure of the atria = less blood back to the heart = less blood in he ventricles after diastole

Front 43

Nitrates have what effect on heart rate?

Back 43

no direct effect, but if BP falls too low heart rate can increase (perhaps nitroglycerin overdose)