The Cardiovascular System and Sites for Drug Effects Flashcards

1
Q

Regarding adrenoreceptors:

Metaraminol’s main site of action is beta-1 receptors

A

False. Metaraminol affects alpha-1 receptors and has a purely vasoconstrictive mechanism of action.

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2
Q

Regarding adrenoreceptors:

Agonism of beta-1 receptors results in positive chronotropic and inotropic effects

A

True. Beta-1 receptors affect both contractility (inotropic) and heart rate (chronotrophic).

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3
Q

Regarding adrenoreceptors:

Clonidine is an example of an alpha-2 agonist

A

True. Clonidine stimulates centrally, activating alpha-2 receptors and reducing noradrenaline release and, as a result, decreasing sympathetic tone.

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4
Q

Regarding adrenoreceptors:

Noradrenaline only has effect on alpha-1 receptors

A

False. Although noradrenaline is predominantly a vasoconstrictor due to being an alpha-1 agonist, it also has some beta-1 agonistic effects and is a weak inotrope and chronotrope.

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5
Q

Regarding antagonists:

Doxazocin is an example of an alpha-1 blocker

A

True. Doxazocin binds to, and inhibits the action of, alpha-1 receptors, which in turn reduces systemic vascular resistance by inhibiting vascular smooth muscle contraction.

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6
Q

Regarding antagonists:

Beta-blockers all block the same receptor

A

False. Each beta-blocking drug has an affinity for a particular receptor.

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7
Q

Regarding antagonists:

Calcium channel blockers decrease systemic vascular resistance, myocardial contractility and cardiac output

A

True

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8
Q

Regarding indirect effects on the cardiovascular system:

Stimulation of the parasympathetic nervous system increases heart rate and contractility of the heart

A

False. Stimulation of the sympathetic nervous system increases contractility and heart rate. Stimulation of the parasympathetic nervous system reduces these.

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9
Q

Regarding indirect effects on the cardiovascular system:

Baroreceptors are receptors which are stimulated in response changes in the vessel walls

A

True. Baroreceptors are mechanoreceptors which are stimulated by stretch within the wall of the vessel they are found in.

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10
Q

Regarding indirect effects on the cardiovascular system:

Fibres from aortic and carotid sinus baroreceptors travel within the vagus nerve

A

False. Fibres from aortic baroreceptors travel within the vagus nerve (X), whereas fibres from the carotid sinus are within the glossopharnygeal nerve (IX).

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11
Q

Regarding indirect effects on the cardiovascular system:

Nitrates cause vasodilation via smooth muscle dilation

A

True. Nitric oxide binds to guanylyl cyclase, which converts GTP to cGMP, which activates protein kinase G. This then leads to a reduction in calcium levels and smooth muscle relaxation.

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12
Q

Regarding indirect effects on the cardiovascular system:

ACE inhibitors reduce blood pressure by affecting the renin angiotensin aldosterone system

A

True. They inhibit angiotensin converting enzyme from converting angiotensin-1 to angiotensin-2.

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13
Q

Match the effects to their vasopressin receptor (V1, V2 or V3):

Opens aquaporin channels in renal collecting ducts, thereby reducing urine volume, and releases von Willebrand factor

A

V2

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14
Q

Match the effects to their vasopressin receptor (V1, V2 or V3):

Previously categorized as V1b, mainly central nervous system (CNS) activity, including adrenocorticotropic hormone (ACTH) release

A

V3

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15
Q

Match the effects to their vasopressin receptor (V1, V2 or V3):

Vasoconstriction, especially in the gut, skin and skeletal muscle, and platelet aggregation

A

V1

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16
Q

Regarding the pharmacology of inotropes and vasoconstrictors:

α-adrenoceptor stimulation causes bradycardia in healthy individuals

A

True. The hypertension from increased systemic vascular resistance (SVR) causes a bradycardia through the baroreflex.

17
Q

Regarding the pharmacology of inotropes and vasoconstrictors:

Vasopressin is vasoconstrictive in all vascular beds

A

False. Vasopressin receptors are not found in the pulmonary vasculature.

18
Q

Regarding the pharmacology of inotropes and vasoconstrictors:

Noradrenaline is a powerful inotrope

A

True. Noradrenaline is a potent β1 agonist.

19
Q

Regarding the pharmacology of inotropes and vasoconstrictors:

A phosphodiesterase inhibitor usually increases blood pressure

A

False. PDE inhibitors increase cardiac output but the decrease in SVR usually leads to a reduction in blood pressure. They are often given in combination with noradrenaline.

20
Q

Regarding the pharmacology of inotropes and vasoconstrictors:

A slow bolus of levosimendan usually increases blood pressure in patients with cardiac failure

A

False. As with PDE inhibitors, the increase in cardiac output is insufficient to outweigh the reduction in SVR. This is especially obvious with bolus administration.

21
Q

A patient with pre-existing poor left ventricular function is very hypotensive after cardiopulmonary bypass and the heart is dilating. Appropriate immediate bolus drug therapy may include (select all those appropriate):

A. Adrenaline
B. Vasopressin
C. Noradrenaline
D. Milrinone
E. Levosimendan

A

A. True. There are times when this is the only drug that seems to help.

B. False. Vasoconstriction is not the aim here.

C. True. Noradrenaline is a potent β1 agonist, but adrenaline is a more likely choice.

D. False. A PDE inhibitor aggravates vasodilatation. It is likely to help cardiac contraction but the effect is not immediate.

E. False. As with PDE inhibitors, there is a reduction in SVR and the inotropic effect is not immediate.

22
Q

In the patient with pre-existing poor left ventricular function who was very hypotensive after cardiopulmonary bypass, the patient’s blood pressure responds to a bolus of adrenaline but is requiring significant doses to maintain adequate cardiac function. Appropriate supplementary drug therapy may include (select all those that apply):

A. Methylene blue
B. Vasopressin
C. Noradrenaline
D. Milrinone
E. Levosimendan

A

A. False. Vascular resistance does not seem to be the issue.

B. False. Vasoconstriction is not the aim here.

C. False. Noradrenaline is a potent β1 agonist, but adrenaline is already serving this function.

D. True. A PDE inhibitor enhances the response to adrenaline. Vasodilation may become a problem, in which case noradrenaline or vasopressin may become appropriate.

E. True. As with PDE inhibitors, there is a reduction in SVR but the unique inotropic effect warrants consideration.

23
Q

A septic patient in intensive care is becoming peripherally dilated and hypotensive.

Appropriate drug therapy may include (select all those that apply):

A. Adrenaline
B. Vasopressin
C. Noradrenaline
D. Milrinone
E. Levosimendan
F. Methylene blue

A

A. False. Adrenaline improves the numbers but not the outcome.

B. True. Vasoconstriction is exactly what is needed.

C. True. Noradrenaline is a potent drug to increase the SVR.

D. False. A PDE inhibitor aggravates vasodilatation.

E. False. As with PDE inhibitors, there is a reduction in SVR and the inotropic effect does not seem to be required.

F. False. Methylene blue may help in septic shock, but it is not first line treatment and would not be used at this stage. Similarly, it is a little early to start hydrocortisone.