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LCRS Pharmacology and Therapeutics > Drugs and the cardiovascular system- the vasculature > Flashcards

Drugs and the cardiovascular system- the vasculature Flashcards

1
Q

What produces a raft of substances that can impact on smooth muscle tone?

A

Endothelial cells

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2
Q

What effect does the renin-angiotensin system have on CVS function?

A

Negative- Ang II promotes vasoconstriction and salt and water retention mainly via the stimulation of aldosterone secretion

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3
Q

What is the mechanism of action of aldosterone?

A

It passes through the cell membrane and binds to a mineralocorticoid receptor, it then upregulates production of sodium channels and production of Na+/K+ ATPase which means that you get more sodium reabsorption

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4
Q

What do ACE inhibitors inhibit?

A

Inhibit ACE which inhibits conversion of angiotensin I to angiotensin II

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5
Q

What are ACE inhibitors commonly used to treat?

A 
Hypertension
Heart failure
Post-MI
Diabetic nephropathy
Progressive renal insufficiency
Patients at high risk of cerebrovascular disease
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6
Q

How do ACE inhibitors reduce hypertension?

A

They reduce the AT1 dependent vasoconstriction which leads to a fall in TPR and a fall in blood pressure
It also reduces production of aldosterone which means you get a decrease in blood volume and decrease in venous return which is linked by starling’s law to contractility and cardiac output

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7
Q

What causes diabetic nephropathy?

A

Significant damage to the kidney glomerulus because of toxic products

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8
Q

In terms of diabetic nephropathy, what does high blood glucose lead to?

A

Production of oxygen free radicals

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9
Q

Why do you not want too much pressure in the glomerulus?

A

Allows toxic products to accumulate

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10
Q

What effect does ang II have around the glomerulus?

A

It constricts the efferent arteriole

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11
Q

What is the normal response at the glomerulus when your blood pressure falls?

A

The RAS will be stimulated and produce more Ang II which will constrict efferent arteriole and allow blood to flow more effectively and a cetain amount of pressure os maintained so the glomerulus can work

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12
Q

Why are ACE inhibitors used in diabetic nephropathy?

A

You don’t want the glomerular pressure to increase too much because of the toxic products, hence you don’t want Ang II mediated vasoconstriction of the efferent arteriole

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13
Q

What is the main unwanted effect of ACE inhibitors (and angiotensin receptor blockers)?

A

Cough (hyperkalaemia is also common)

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14
Q

Describe the process of smooth muscle contraction (4 steps)

A
  1. Membrane depolarisation opens voltage-gated calcium channels
  2. Ca2+ enters and binds to calmodulin (CaM)
  3. Ca2+-CaM complex binds to and activates myosin light chain kinase (MLCK)
  4. MLCK mediated phosphorylation -> smooth muscle contraction
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15
Q

What are dihydropyridines more selective for?

A

Blood vessels

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16
Q

Why don’t calcium channel blockers penetrate the plasma membrane to any great degree compared to the drugs that impact the heart?

A

They aren’t particularly liposoluble

17
Q

How do dihydropyridines have an effect?

A

They bind on the extracellular surface of the calcium channel and inhibit calcium entry into vascular smooth muscle

18
Q

What CCBs are most used in treating hypertension and why?

A

DHPs because they have a more powerful effect on vascular smooth muscle so a greater effect in reducing TPR

19
Q

What does the reduction in TPR by CCBs lead to?

A

Reflex tachycardia but massive reduction in TPR outweighs heart rate increase so bp decreases

20
Q

What is the most common cause of hypertension in younger patients?

A

Increased sympathetic drive

21
Q

How does increased sympathetic drive lead to hypertension?

A

Noradrenaline binds to B1 receptors and causes increased heart rate and force of contraction, it also binds to B1 receptors in kidneys increasing renin release

22
Q

What are beta blockers used to treat?

A 
Angina
Post MI
Cardiac dysrhythmias
Chronic heart failure
Hypertension
23
Q

Why have beta blockers been removed as first line treatment for hypertension?

A

They aren’t particularly effective on blood vessels- reduced TPR has the most profound effect on BP and beta blockers have their main effect on the heart

24
Q

What is now the first line treatment for hypertension?

A

CCBs and ARBs

25
Q

Why are mixed beta-alpha blockers now used?

A

Blockage of alpha 1 receptors allow the drugs to cause vasodilation

26
Q

What is the problem with alpha blockers?

A

You need one that is selective for alpha 1 because the alpha 2 receptor is the negative feedback receptor for SNS which needs to be stimulated to depress sympathetic function

27
Q

How does sumitriptan work?

A

It is a triptan which is an agonist at 5HT1D receptors which causes vasoconstriction of some large arteries and inhibits trigeminal nerve transmission

28
Q

What is sumitriptan used for?

A

Migraine attacks- painful stimuli is transferred by trigeminal and profound vasodilation is associated with migraine

29
Q

When is sumitriptan use contraindicated?

A

Patients with coronary disease

30
Q

Look at NICE treatment guidelines for hypertension in notes

A

Will do

31
Q

What is the first step in hypertension treatment in someone under 55 years?

A

ACE inhibitor or angiotensin receptor blocker

32
Q

What race is particularly at risk for hypertension?

A

Afro Caribbean

33
Q

What is the first step in hypertension treatment in someone over 55 years or Afro Caribbean of any age?

A

CCBs or thiazide-like diuretics

34
Q

What is spironolactone?

A

Aldosterone antagonist

35
Q

How does spironolactone work?

A

It blocks mineralocorticoid effects

36
Q

What is the definition of chronic heart failure?

A

Impaired cardiac function due to ischaemic heart disease, hypertension or cardiomyopathy that results in fluid retention, oedema and fatigue (serious condition with high mortality)

37
Q

What are the three main treatments for cardiac failure?

A

ACE inhibitors
Beta blockers
Angiotensin receptor blockers

LCRS Pharmacology and Therapeutics (33 decks)

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