Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular 2018 > Drugs affecting control of blood pressure > Flashcards

Drugs affecting control of blood pressure Flashcards

1
Q

In vascular smooth muscle cell contraction describe how the intracellular concentration of calcium is increased?

A

Through the opening of L-type Ca channel bu numerous depolarizing mechanisms and GPCR receptor coupled to Gq/11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In vascular smooth muscle cell contraction what does intracellular calcium couple to?

A

calmodulin to form Ca-CaM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What role does Ca-CaM play in vascular smooth muscle cell contraction ?

A

It activated Myosin Light Chain Kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does active MLCK do in vascular smooth muscle cell contraction ?

A

It phosphorylates the myosin light chain and causes contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the role of cGMP in vascular smooth muscle cell relaxation?

A

It activates Protein Kinase G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the role of PKG in vascular smooth muscle cell relaxation?

A

Activates myosin-lc phosphatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the role of myosin-lc phosphatase in vascular smooth muscle cell relaxation?

A

It dephosphorylates the myosin light chain, causing relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do organic nitrates do to VSM?

A

Relax it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What organic nitrates do at clinical doses?

A

Venorelaxation
Increased coronary blood flow
Arteriolar dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does venorelaxation cause?

A

Reduced preload, then SV but CO is maintained by increased HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the benefit of organic nitrates to patients with angina?

A

Decreased myocardial oxygen requirement

1) decreased preload
2) decreased after load
3) improved perfusion of the ischaemic zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the effect of motivate on the coronary circulation?

A

dilate the collateral vessels, ensuring blood flow to the myocardium is increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of endothelin in vascular smooth muscle tone

A

when endothelin is produced as a result of altered gene expression through adrenaline, angiotensin II, ADH or NO, natriuretic peptides or sheer stress it will agonise the Eta receptor, and through numerous signalling pathways including Gw/11 increase intracellular calcium and cause contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the clinical use of organic nitrates?

A

used in stable and ACS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the main organic nitrates used in ACS?

A

GTN and isosorbide mononitrate (occasionally isosorbide dinitrate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the action of GTN?

A

Short acting- excessive first pass metabolism (this is why it is given as a spray or sublingual)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is GTN given in unstable angina?

A

IV infusion with aspirin to prevent a thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What method can GTN be administered for a long lasting effect?

A

Transdermal patch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the action on isosorbide mononitrate like?

A

Longer acting as it is resistant to first pass metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is isosorbide mononitrate administered?

A

Orally for prophylaxis of angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is associated with repeated administration of organic nitrates?

A

Reduced effect- tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name some unwanted side effects of organic nitrates?

A

Postural hypotension

Headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the Eta targeted in?

A

Pulmonary hypertension by bosentan and ambrisentan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What causes increased renin release?

A

increased Renal sympathetic nerve activity

decreased Renal perfusion

reduced glomerular filtration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does the AT1 (GPCR) cause

A

Increased release of noradrenaline from sympathetic nerves

Growth in the heart and arteries as a result of altered gene expression

aldosterone release from the adrenal cortex
cousin tubular Na reabsorption and salt retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where is ACE present?

A

On endothelial cells particularly the cells of the lung

27
Q

Where are AT1 receptors present?

A

Terminal sympathetic neurons which innervate VSM and VSM cells

28
Q

What do AT1 receptors in the adrenal cortex cause?

A

synthesis and release of aldosterone which acts to increase salt retention

29
Q

What does ACE do?

A

Convertes inactive angiotensin I to angiotensin II

Inactivates bradykinin (vasodilator)

30
Q

What do ACE inhibitors do?

A

block the conversion of angiotensin I to angiotensin II

31
Q

What do AT1 receptor antagonists do?

A

Block the action of angiotensin II at AT1 receptors in a competitive manner

32
Q

What do ACEI do do MABP?

A 
Decrease it 
venous dilatation (decreased preload) and arteriolar dilatation (decreased afterload and decreased TPR) decreasing arterial blood pressure and cardiac load
33
Q

What affect do ACEI have on cardiac contractility?

A

none

34
Q

What do ACEI do to aldosterone release?

A

Reduce (not abolish) the release of aldosterone (decrease in circulating levels of aldosterone promotes loss of Na+ and H2O)

35
Q

Where do they have the greatest effect and on whom?

A

much larger effect in hypertensive patients (especially if renin secretion is enhanced – e.g. as a consequence of diuretic therapy)

angiotensin-sensitive vascular beds (brain, heart, kidney)

36
Q

What is the additional effect of angiotensin II on the heart and vasculature?

A

Causes growth

37
Q

What are the adverse effects of ACEI?

A

hypotension

dry cough

38
Q

What is an essential difference between ARBs and ACEi?

A

ARBs do not inhibit the metabolism of bradykinin

39
Q

When are ACEI and ARBs contraindicated?

A

Pregnancy

bilateral renal artery stenosis

40
Q

What are the clinical uses of ARBs and ACEi?

A

hypertension
cardiac failure
post MI

41
Q

What is the mechanism by which ACEi and ARBs are used in the treatment of hypertension?

A

benefit derives from

1) reduced TPR and MABP
2) possible suppression of proliferation of smooth muscle cells in the media of resistance vessels

42
Q

What is the mechanism by which ACEi and ARBs are used in the treatment of cardiac failure?

A

is associated with inappropriate activation of the RAAS.

ACEIs

1) decrease vascular resistance improving perfusion
2) increase excretion of Na+ and H20
3) cause regression of left ventricular hypertrophy

43
Q

What is the function of alpha1 adrenoreceptors?

A

constrict

44
Q

What is the function of B1 adrenoreceptors?

A

increase HR
increase force of contraction
increase AV node conduction velocity

45
Q

What is the role of B2 adrenoreceptors?

A

bronchorelaxation

vasodilatation

46
Q

Why are B blockers useful in the treatment of angina pectoris?

A

decrease myocardial O2 requirement (decreased HR & decreased SV = decreased work = decreased O2)

counter elevated sympathetic activity associated with ischaemic pain

increase the amount of time spent in diastole (decreased HR), improving perfusion of the left ventricle

47
Q

Why are B blockers useful in the treatment of hypertension?

A

No longer first line
BUT

reducing cardiac output (MABP = CO x TPR) (However, CO returns to normal over time but MABP remains depressed by ‘resetting’ of TPR at a lower level – mechanism uncertain)

reducing renin release from the kidney

a CNS action that reduces sympathetic activity

48
Q

Why are B blockers useful in the treatment of heart failure?

A

In combination with other drugs to suppress adverse effects associated with elevated activity of the sympathetic nervous system and RAAS (Start low, go slow)

49
Q

What do calcium antagonists do?

A

prevent the opening of L-type channels in excitable tissues in response to depolarization and hence limit intracellular calcium

50
Q

What are L type channels responsible for?

A

upstroke in the AP in the SA and AV nodes- Ca2+ antagonists can reduce rate and conduction through the AVN

phase 2 of the ventricular AP- Ca2+ antagonists can reduce the force of contraction

51
Q

How do a1 adrenoreceptors function in VSM cells?

A

a1-adrenoreceptors couple to Gq/11 and open the cation selective channels (Na channel) which allows calcium entry into the cell

52
Q

what are the three main types of calcium antagonists?

A

“verapamil: selective for cardiac L-type channels
o physically blocks the L-type channel

amlodipine: selective for L-type channels in VSM

diltiazem: intermediate selectivity from cardiac and VSM cells
o act allosterically

53
Q

What are the clinical uses of calcium antagonists?

A

Hypertension
angina
dysrythmias

54
Q

What is the mechanism whereby calcium antagonists work in hypertension?

A

reduced Ca entry= arteriolar dilatation= reduce TPR & MABP

55
Q

What is the mechanism whereby calcium antagonists work in angina?

A

prophylactic treatment used with GTN (particularly if B blockers are contraindicated)

peripheral arteriolar dilatation- decreasing afterload and myocardial oxygen requirement

coronary vasodilatation

amlodipine: little effect on cardiac muscle

diltiazem and verapamil: negative inotropic effects. some of reduction in cardiac force is compensated by sympathetic system

56
Q

What is the mechanism whereby calcium antagonists work in dysrythmias?

A

Ventricular rate in rapid atrial fibrillation reduced by suppression of conduction through the AV node

Verapamil is usually used, but avoid in heart failure, particularly in combination with a b-block

57
Q

How do potassium channel openers function?

A

ATP closes the ATP type potassium channels, potassium channel openers have the opposite effect (opens K-ATP channels in VSM- causing the cell to hyperpolarise, moves membrane potential away from threshold- supressing the opening of voltage activated calcium channels- causing relaxation)

58
Q

What is minoxidil used for?

A

last resort in severe hypertension (causes reflex tachycardia- can be prevented by administration of a B-blocker) causes salt and water retention (alleviated by a diuretic). restores hair in balding men when applied topically.

59
Q

What is nicorandil used for?

A

opens ATP type potassium channels

60
Q

How do a-1 adrenoreceptor antagonists work?

A

Cause vasodilatation by blocking vascular a1-adrenoceptors. Reduced sympathetic transmission results in decreased MABP

61
Q

What are the most commonly used a-1 adrenoreceptor antagonists?

A

prazosin and doxazosin - both are competitive antagonists

62
Q

When do a-1 adrenoreceptor antagonists get moved up the prescribing list?

A

when patient is suffering from benign prostatic hyperplasia, this is because the muscle tone in the prostate is in part modified by -1 adrenoreceptor and noradrenaline and therefore blockers may relieve some of the effects

63
Q

Adverse effect of a-1 adrenoreceptor antagonists?

A

postural hypotension

Cardiovascular 2018 (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions