Pharmacology-Anti-Anginal Drugs Flashcards Preview

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Flashcards in Pharmacology-Anti-Anginal Drugs Deck (22)
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What is happening during the time indicated in the image below?

Variant (Prinzemal) Angina. Note the elevated ST segments. This is a short period of chest pain caused by vasospam (accentuated by areas of atherosclerosis) that result in transient ischemia.


A 64 year old patient comes to your clinic complaining of chest pain lasting for an hour or more at a time that only gets better with nitroglycerine. It started about one month ago and has been getting more frequent and more severe. What is your diagnosis?

Unstable angina.


How does oxygen demand, oxygen supply, trigger, occlusion, symptoms, relief and necrosis therapy differ in variant angina, stable angina, unstable angina, NSTEMI (non-ST elevated MI) and acute MI?



How does our body regulate vascular tone?

NO, VG Ca Channel, Ligand-gated Ca release, Ca-dependent K+ channel


How does NO result in vasodilation?

Production of cGMP -> Myosin light chain phosphatase -> relaxation. Inhibits Ca-dependent K+ channel -> hyperpolarization. Inhibits Ca influx from extracellular space. 


What are the classes of anti-anginal drugs?



How does oral dinitrate get from your mouth to vasodilation?

Metabolized by the liver to form mononitrate -> enters mitochondria -> aldehyde reductase releases NO from mononitrate -> NO activates guanylyl cyclase which produces cGMP -> activates cGMP-dependent protein kinase -> inhibits ECM influx of Ca and activates mitochondrial uptake of Ca.


What are the different organic nitrates?



Why can you put mono nitrates directly under you tongue?

They do not need to be metabolized by the liver.


What do all organic phosphates except for sodium nitroprusside need to function?

The enzyme aldehyde reductase to release NO from the mononitrate.


How do organic nitrates 1) increase coronary blood flow, 2) decrease O2 demand, 3)prevent coronary steal and 4) decrease O2 consumption?

1) Systemic venule dilation decreases preload. This increases the pressure gradient from the aorta to the endocardium and increases coronary blood flow. 2) Reduction of preload decreases O2 demand. 3) Preferential dilation of large epicardial coronary vessels prevents coronary steal and 4) Declines in systolic BP (after load) decreases O2 consumption


What pathologies benefit from use of anti-anginal drugs?

Angina, CHF, hypertension and acute MI


A 44 year old factory worker comes to see you and while you are in the clinic he starts having severe chest pain radiating down his arm. You decide to administer sublingual nitroglycerine to dilate his blood vessels and perfuse the heart, but nothing happens. Why could this be?

The factory he works in may have exposed him to organic nitrates over a long period of time which caused him to develop a tolerance for them.


Why do organic nitrates have such a low bioavailability?

The liver has a reductase that converts it very easily.


What are the contraindications for taking organic nitrates?



How do calcium channel blockers decrease O2 consumption? O2 demand? Increase coronary blood flow?

Reduces afterload as it dilates arteries = decreases O2 consumption, Reduces contractility = decreases O2 consumption. Decreases the heart rate = decreases O2 demand. Decreases coronary resistance = increases coronary blood flow.


In what setting do you prescribe calcium channel blockers?

Angina (especially variant angina), acute MI, hypertension and as a vasodilator.


What drugs are contraindicated with variant angina?

Beta blockers.


What side effects come with calcium channel blockers?

Those that deal with AV node conduction.


How do beta blockers decrease oxygen consumption?

Reduction of heart rate, contractility and arterial blood pressure. This happens because beta blockers block sodium channels, funny sodium channels, VG calcium channels and SERCA uptake of calcium.


What are side effects of beta blockers?

Asthma, erectile dysfunction, depression and insomnia (inhibits melatonin secretion).


What condition causes secondary variant angina at rest?


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