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Big Pharma > ANS and Cardiovascular Pharmacology > Flashcards

ANS and Cardiovascular Pharmacology Flashcards

1
Q
  1. Preganglionic neurons and parasympathetic postganglionic neurons are said to be (cholinergic? or adrenergic?) in nature because of the presence of (acetylcholine? or norepinephrine?) at their respective synapses.
A

Cholinergic, acetylcholine

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2
Q
  1. A drug that inhibits muscarinic cholinergic receptors will selectively decrease? Parasympathetic responses on peripheral tissues or sympathetic responses on peripheral tissues?
A

Muscarinic inhibition would decrease parasympathetic response in peripheral tissues.

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3
Q
  1. In most peripheral tissues, what kind of neurotransmitter is released from the sympathetic postganglionic neurons? What type of receptors do these directly bind to?
A

Most sympathetic postganglionic neurons use norepinephrine and are referred to as adrenergic. They bind to alpha or beta-adrenergic receptors.

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4
Q
  1. Alpha and beta receptors are two primary subcategories of what type of receptor class? Adrenergic? Muscarinic cholinergic? Nicotinic cholinergic?
A

Adrenergic

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5
Q
  1. Indirect-acting cholinergic stimulants increase activity at cholinergic synapses by inhibiting what enzyme?
A

Indirect-acting stimulants increase activity at cholinergic synapses by inhibiting the acetylcholinesterase enzyme.

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6
Q
  1. Which of these would cholinergic antagonists be useful in treating: Motion sickness? Tachycardia? IBS? Parkinson disease?
A

Cholinergic antagonists, or anticholinergic drugs, are useful in treating Parkinson’s disease, IBS, and motion sickness. They are used to treat symptomatic bradycardia, but not tachycardia

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7
Q
  1. What kind of effect on the peripheral arterioles will a drug that selectively stimulates the alpha-1 adrenergic receptors?
A

Smooth muscle contraction or vasoconstriction

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8
Q
  1. How does the stimulation of alpha 2 adrenergic receptors on spinal interneurons affect the excitability motor neurons supplied by these interneurons?
A

Decreases sympathetic discharge to the heart and vasculature.

Because of its effect on the spinal cord, it also has antispasticity effects.

Because of its effect on the postsynaptic alpha-2 receptors in the prefrontal cortex, clonidine can also be used to treat ADHD.

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9
Q
  1. To increase cardiac output what receptor on the heart should be selectively be stimulated?
A

Beta-1

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10
Q
  1. What type of adrenergic agonist (beta-1 or beta-2?) treats bronchospasm associated with respiratory ailments such as asthma, bronchitis, and emphysema?
A

Beta-2

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11
Q
  1. What cardiac diseases are adrenergic antagonist that are selective for beta-1 receptors useful in treating?
A

Hypertension

Angina

Arrhythmia

Prevent reinfarction

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12
Q
  1. Do diuretics increase or decrease the excretions of water in the kidney? How does this affect the reabsorption of sodium in the kidney?
A

Increases excretion, inhibits reabsorption of sodium

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13
Q
  1. What is an adverse side effect of taking too much of a diuretic medication?
A

Fluid depletion and electrolyte imbalance (hyponatremia, hypokalemia)

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14
Q
  1. What is the advantage of using beta blockers such as pindolol or acebutolol?
A

They have high levels on sympathomimetic activity meaning they can stimulate beta receptors and inhibit and oppose stimulating affects of catecholamines. This can lower BP while maintaining HR.

“Mimics sympathetic NS”

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15
Q
  1. What neurotransmitter in the heart do beta blockers effect?
A

Epi and norepi

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16
Q
  1. Why do nonselective beta blockers produce bronchoconstriction in asthma and chronic respiratory conditions?
A

Because they bind to both beta-1 receptors in the heart and beta-2 receptors in the lungs.

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17
Q
  1. What is a beta blocker that bind preferentially due to beta-1 receptor in the heart called?
A

Selective beta-blockers

Ex: Metoprolol and Atenolol

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18
Q
  1. What receptors do the sympatholytic agents prazosin and doxazosin block?
A

Alpha-1

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19
Q
  1. Alpha blocker agents may cause a sudden fall in blood pressure that results in a compensatory increase in heart rate. What is the name of this type of tachycardia? What drug class administered with the alpha blocker can treat this?
A

This compensatory increase in heart rate is called reflex tachycardia, and often alpha blockers are prescribed with a beta blocker to treat this.

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20
Q
  1. Presynaptic adrenergic inhibitors decrease peripheral arteriole resistance by inhibiting the release of what neurotransmitter?
A

Norepinephrine

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21
Q
  1. Centrally acting sympatholytic drugs decrease blood pressure by inhibiting the sympathetic discharge from what part of the CNS?
A

a central inhibitory effect on the brainstem, decreased renin release from CNS

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22
Q
  1. What type of drug should be used to treat an autonomic hypertensive crisis, a life-threatening sudden increase in blood pressure?
A

Alpha antagonists

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23
Q
  1. What is the mechanism of action of nitric oxide?
A

Induces vasodilation

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24
Q
  1. How do angiotensin-converting enzyme inhibitors work to reduce blood pressure?
A

(ACE) prevent angiotensin 2 from being made, which is a substance that narrows blood vessels

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25
Q
  1. Patients on this type of medication should be cautioned about prolonged hot tub use?
A

Vasodilators

26
Q
  1. High renin angiotensin activity can cause increase production of this enzyme? What does this cause the vascular smooth muscle to do?
A

Increases enzyme angiotensin 2, causes vascular smooth muscle to vasoconstrict

27
Q
  1. How do calcium channel blockers reduce blood pressure?
A

They decrease calcium entry into vascular smooth muscle, leading to vasodilation and decreased vascular resistance.

28
Q
  1. What changes in blood pressure are patients on blood pressure medications most at risk of with positional changes?
A

Orthostatic hypotension

29
Q
  1. How do ACEI reduce hypertension?
A

ACE inhibitors decrease the hypertensive effects of angiotensin II by inhibiting the enzyme that converts angiotensin I to angiotensin II

30
Q
  1. What affect does nitroglycerin have on the myocardial oxygen demand thus relieving angina pectoris? What vasculature does it vasodilate?
A

Nitroglycerin decreases O2 demand on the heart. It decreases cardiac work by decreasing preload and afterload.

It vasodilates the peripheral arterioles.

31
Q
  1. Patients are directed to used nitroglycerine patches 12 hours on and then a 12-hour nitroglycerine free period, what does this prevent?
A

Drug dependency, prevents decreased tolerance to the drug

32
Q
  1. How can nitroglycerin be administered to avoid the first pass effect?
A

Sublingual, buccal

33
Q
  1. How do beta blockers reduce angina pectoris in patients?
A

BB reduce HR & myocardial contractility, which reduces myocardial O2 consumption

34
Q
  1. What is the best drug class to treat variant angina that causes coronary artery vasospasm?
A

Calcium channel blockers

35
Q
  1. Why is aspirin used for angina pectoris?
A

Decreases risk of clots, increasing BF to the heart

36
Q
  1. What medications can be used to treat the sudden rupture of atherosclerotic plaques that can cause chest pain and be potentially lethal?
A

(Beta blockers)

Combination of drugs.

Anticoagulants in early stages with antiplatelet drugs being continued indefinitely to prevent coronary occlusion.

ACE inhibitors can help protect the heart and vasculature in acute coronary syndromes, and lipid lower drugs such as statins can provide long term nad immediate beneficial effects in preventing coronary occlusion in patients with unstable angina

37
Q
  1. What drugs are used to treat cardiac arrhythmias?
A

Sodium channel blockers, beta blockers, drugs that prolong repolarization, and calcium channel blockers

38
Q
  1. Why are beta blockers effective in treating certain cardiac arrhythmias? Hint: how is the excitatory effects of the heart affected? What neurotransmitter in the heart is affected?
A

Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and norepinephrine and epinephrine on the heart. This effect decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.

39
Q
  1. Why are calcium channel blockers useful in treating certain cardiac arrhythmias?
A

Calcium channel blockers can alter the excitability and conduction of cardiac tissues. They decrease the rate of discharge of the SA node and inhibit conduction velocity through the AV node therefore are more effective in treating arrhythmias caused by atrial dysfunction.

40
Q
  1. Why can antiarrhythmic drugs controlling one type of arrhythmia exert proarrhythmic effects?
A

In the process of treating one type of arrhythmia, antiarrhythmics may aggravate or initiate other abnormalities in the cardiac rhythm and lead to a different arrhythmia.

41
Q
  1. What channel does Lidocaine excite causing an antiarrhythmic effect?
A

Sodium channels

42
Q
  1. What node in the heart does a drug effect if it causes tachycardia although it is being used for bradycardia? What kind of effect does digitalis have to treat cardiac failure?
A

SA node

Digitalis typically increases cardiac output at rest and during exercise, and exercise tolerance often increases because the heart is able to pump blood more effectively.

43
Q
  1. What extracellular element’s concentration is increased by cardiac glycosides to increase the pumping ability of the heart?
A

Inhibition of the sodium-potassium pump causes sodium to accumulate inside the cell. This increase in sodium causes an increase in calcium.

44
Q
  1. Digitalis inhibits the sodium-potassium pump causing what kind of intracellular sodium concentrations?
A

Digitalis causes an increase in intracellular sodium concentration.

45
Q
  1. What is the potentially fatal side effect of digitalis toxicity?
A

Common adverse cardiac effects include arrhythmias such as premature atrial and ventricular contractions, paroxysmal atrial tachycardia, ventricular tachycardia, and high degrees of atrioventricular block. As toxicity increases, severe arrhythmias such as ventricular fibrillation can occur and may result in death.

46
Q
  1. What is the mechanism of action of the phosphodiesterase inhibitors?
A

By blocking the phosphodiesterase (PDE) enzymes from breaking down cAMP & cGMP, increase of these leads to increased intracellular calcium, this causes vasodilation & force of contraction w/in myocardial cells

47
Q
  1. What drugs will decrease the cardiac workload in individuals with heart failure?
A

ACE inhibitors, ARBs, direct renin inhibitors, beta-blockers, diuretics, and vasodialators

48
Q
  1. What are the best drugs in heart failure to reduce excessive sympathetic stimulation of the failing heart? Reducing fluid accumulation and congestion in the lungs and peripheral tissues?
A

Beta blockers (lols)

Diuretics (ides) for reducing fluid/congestion

49
Q
  1. A patient with life-threatening digoxin toxicity should be treated with what drug?
A

Serious or life-threatening digitalis toxicity can be treated by IV administration of digoxin immune Fab (Digibind, DigiFab)

Consists of antibody fragments that attach to digitalis glycosides and sequester the drug and terminate its toxic effects on the heart and other organs

50
Q
  1. Why are low molecular weight heparins preferred to traditional heparins?
A

Produce a more predictable anticoagulant response

Less risk of hemorrhage & heparin-induced thrombocytopenia

Can be injected subcutaneously in the fat

Only inhibit factor Xa & not also IXa with it

51
Q
  1. Warfarin decreases the production of clotting factors by interfering with the regeneration of this in the liver?
A

Vitamin K

52
Q
  1. Traditionally in DVT treatment, patients will start on this parental medication and converted to what orally?
A

Heparin IV and warfarin orally

53
Q
  1. Aspirin’s anticoagulant properties and antiplatelet properties can be useful for treating what types of acute disease?
A

Angina

Acute phase MI

Stroke

DVT

54
Q
  1. What drugs will inhibit platelet-induced clots?
A

Antiplatelet drugs:
COX inhibitors (aspirin, NSAIDs)

GPIIb/IIIa inhibitors

P2Y12 inhibitors

Phosphodiesterase inhibitors

55
Q
  1. What medication should be administered immediately for a patient with MI due to thrombus formation?
A

Fibrinolytics

56
Q
  1. What type of stroke is appropriate for treatment with a thrombolytic agent?
A

Acute ischemic stroke

57
Q
  1. What is appropriate pharmacologic treatment of hemophilia?
A

Replacing the missing clotting (coagulation) factor

58
Q
  1. How do HMG-CoA reductase enzymes inhibitors (statins) work?
A

Decrease plasma cholesterol concentrations by blocking the key enzyme of cholesterol biosynthesis

59
Q
  1. What is a common complaint from patients taking HMG-CoA reductase inhibitors (statins)?
A

Muscle pain (myalgia)

60
Q
  1. What type of drug has been discovered to possibly improve cognition and memory in Alzheimer’s disease?
A

Statins

Big Pharma (3 decks)

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