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Cardiology > Drugs affecting the vascualature and BP > Flashcards

Drugs affecting the vascualature and BP Flashcards

1
Q

Describe the role of the endothelium in vascular smooth muscle tone

A
  • Vasodilating substances Increase CA in endothelial cell.
  • This combines with calmodulin which activates an enzyme endothelial nitric oxide synthase.
  • ENOS catalyses the conversion of eNOS to NO and citrulline.
  • NO arrives at the vascular smooth muscle cells and activates soluble guanylate cyclase which converts GTP to cGMO which activates protein kinase G to facilitate relaxation.

-Organic nitrates like GTN will donate NO into the smooth muscle, NO arrives at the vascular smooth muscle cells and activates soluble guanylate cyclase which converts GTP to cGMO which activates protein kinase G to facilitate relaxation

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2
Q

What do organic nitrates do?

A
  • Cause venorelaxation. This reduces the amount of blood in veins.
  • This decreases the pressure in right atrium or central venous pressure.
  • Preload on heart is reduced. –This means work of heart is reduced and the oxygen necessity is reduced.
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3
Q

Do organic nitrates affect arterial pressure?

A

No

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4
Q

What normally occurs when coronary arteries are blocked?

A

Collateral vessels form between healthy vessels and diseased vessels at a region below the blocked artery in coronary artery disease.

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5
Q

What are the effects of organic nitrates do upon coronary circulation?

A

dilate the collateral vessels to increase the blood flow to the ischemic myocardium. Organic nitrates don’t dilate all the vessels as they are mostly healthy and therefore already dilated enough.

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6
Q

What is meant by first pass metabolism?

A

When a drug is fully metabolised by the liver. These drugs aren’t therefore suitable for oral use.

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7
Q

What form does GTN come under?

A

Inhaled or dissolvable tablet for sublingual use.

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8
Q

What are organic compounds usually given with?

A

antiplatelet drug ie aspirin in unstable angina

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9
Q

What are the two main used organic nitrates?

A

GTN and Isosorbide mononitrate

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10
Q

Which organic nitrate is resistant to first pass metabolism?

A

Isosorbide mononitrate

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11
Q

What are the negative effects of organic nitrates?

A
  • postural hypotension
  • headaches (initially)
  • formation of methaemoglobin (rarely)
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12
Q

What is the role of endothelin 1 in vascular smooth muscle tone?

A

Endothelin 1 activates Eta receptor which activates numerous signalling pathways including Gq/11 which leads to vascular smooth muscle contraction.

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13
Q

What does Enhanced gene expression of endothelin result from?

A

agents that cause vasoconstriction such as adrenaline

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14
Q

What does reduced gene expression of endothelin result from?

A

agents that cause vasodilation such as nitric oxide

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15
Q

What do these changes in gene expression result in?

A

changes in the amount of endothelin precursors which gets converted to endothelin 1. Therefore changes in gene expression results in reduced or increased contraction of vascular smooth muscle

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16
Q

Pharmacologically, how does renin cause increased MAP and blood volume?

A
  • Renin cleaves angiotensinogen to angiotensin 1.
  • Angiotensin 1 is converted to the pharmacologically active species angiotensin II by angiotensin converting enzyme (ACE)
  • Angiotensin II causes increased noradrenaline to be released by activation of AT1 receptors.
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17
Q

What is the role of the ACE inhibitors?

A

ACE inhibitors block conversion of angiotensin I to angiotensin II. Blocks vasoconstrictor and increased the ability of a vasodilator bradykinin.

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18
Q

What do angiotensin converting enzyme inhibitors do?

A

?cause venous dilation (reduced preload) and arteriolar dilation (decreased afterload). This decreases arterial blood pressure and cardiac load

19
Q

What are some of the side effects of angiotensin converting enzyme inhibitors?

A
  • hypotension

- dry cough

20
Q

When are the sue of Angiotensin receptors blockers used?

A

use in patients who find the dry cough produced by ACEIs intolerable

21
Q

When are ACEIs and ARBs contraindicated?

A

in pregnancy and in bilateral renal artery stenosis

22
Q

What are the clinical uses of ACE inhibitors and ARBs?

A
  • hypertension
  • cardiac failure
  • following myocardial infarction
23
Q

Why are beta blockers used in stable and non stable asthma?

A

They block the sympathetic drive to reduce HR and SV in order to reduce oxygen consumption to the heart.
-Beta blockers also increase the time the heart spends in diastole and decreases the time spent in systole to improve coronary circulation

24
Q

Re beta blockers high or low in the list of medications used to treat hypertension?

A

Low

25
Q

How do b blockers treat hypertension?

A

Either:

  • re setting the total peripheral resistance
  • reducing renin release from the kidneys
  • reduce sympathetic activity
26
Q

How are B blockers good in the treatment of heart failure?

A

B blockers block excess sympathetic drive. Used at a low dose in heart failure

27
Q

How do L type calcium channels work?

A

membrane depolarisation causes channels to open which allows calcium to enter from cardiac muscle cells or vascular smooth muscle which causes contraction

28
Q

Where are L type channels found?

A

heart and vasculature

29
Q

How do calcium antagonists work in the heart?

A

They block L type channels thereby decreasing the rate of action potential and slows the delay at the AV mode. This reduces the amount of calcium entering the cell which reduces the force of contraction

30
Q

What are the three main types of calcium antagonists?

A
  • verapamil
  • amolodipine (dihydropyradine)
  • diltiazem
31
Q

Which calcium antagonist blocks the channel directly?

A

Veapamil blocks the channel directly

  • Dihydropyradine have an allosteric effect and reduce the probability of channel opening.
  • diltiazem has intermediate selectivity
32
Q

Why is Dihydropyradine used in treating hypertension?

A

Of its selective action on vascular smooth muscle and has very little effect on the heart

33
Q

What is Dihydropyradine also used in treating?

A

angina, dysrhythmias and isolated systolic hypertension

34
Q

Why is Dihydropyradine used in treating angina?

A
  • Used to prevent angina not treat
  • decrease afterload via peripheral arterial dilation
  • decrease in force of contraction
35
Q

What is the K ATP channel regulated by?

A

Intracellular concentration of ATP

36
Q

What is the effect of ATP on potassium channels?

A

ATP closes potassium channels

37
Q

How do potassium channel openers work?

A
  • when ATP is antagonised potassium leaves the cell
  • Causing hyperpolarisation
  • moving resting potential away from threshold at which voltage activated CA channels open
  • thereby stopping calcium entering cell
  • educing relaxation
38
Q

What are two examples of potassium channel openers?

A
  • minoxidil

- nicorandil

39
Q

What is so good about nicorandil?

A

Opens potassium channels and also has NO donor activity

40
Q

What do a1 adrenoreceptor receptor antagonists do?

A

block a1 adrenoceptors and therefore reduce sympathetic transmission and MAPB

41
Q

What are two examples of a1 adrenoreceptor receptor antagonists

A

prazosin and doxazosin

42
Q

When would a1 adrenoceptors blockers be extremely recommended?

A

Treating old people with for example benign prostatic hyperplasia who also have hypertension

43
Q

What is the main adverse effect of a1 adrenoceptors blockers

A

treating old people with for example benign prostatic hyperplasia who also have hypertension

44
Q

What is the main adverse effect of a1 adrenoceptors blockers?

A

postural hypotension

Cardiology (32 decks)

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