Drugs on vessels Flashcards

1
Q

How is muscle contraction triggered (Basic)?

A

Ca2+ enters via T-tubule, once threshold reached activates Ryanodine receptor, causing influx (70% of needed Ca2+) of Ca2+ from sarcoplasmic reticulum – Ca2+ causes contraction.

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2
Q

How are ion levels in myocytes maintained?

A

ATPases drive majority of Ca2+ back into SR
Ca2+/Na+ transporters remove excess Ca2+
Na+/K+ ATPases remove excess Na+

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3
Q

What is considered hypertension?

A

140/90 mmHg OVER MULTIPLE MEASUREMENTS (OVER TIME)

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4
Q

What the common categories of anti-hypertensives?

A

ACE inhibitors (E.G Enalapril)
Calcium channel blockers (E.G Amlodipine)
Angiotensin receptors blockers (E.G Losartan)
Alpha blockers
Diuretics
Beta blockers

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5
Q

What are the ‘stages’ of hypertension treatment?

A

1 – ACEi or ARB for under 55s / CCB or thiazide diuretics for over 55 AND afro Caribbean

2 – ACEi ARB group add CCB or Thiazide diuretic, CCB Diuretic group add ARB

3- Further addition of same drugs

4- Resistant hypertension – consider adding low-dose spironolactone/alpha or beta blocker

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6
Q

Why are ACEi and ARBs not first line in over 55s and afro Caribbean’s?

A

Plasma renin is low in these groups but is less of a determinant in Aii or BP – the treatments are therefore less effective in these groups.

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7
Q

Why is it good to give ACE I or ARB alongside diuretics?

A

Diuretics cause drop in Na+, this causes compensatory rise in RAS activity that is counteracted by ACE I and ARBs.

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8
Q

What is a side effect of ACE inhibitors?

A

Cough – 25% patients present with it. Occurs due to inhibition of bradykinin breakdown which is ordinarily performed by ACE.

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9
Q

What is a side effect of ACE Is and ARBs?

A

Hyperkalaemia – Less aldosterone is produced, less Na+/K+ proteins in membrane – K+ retained

Renal failure if given with pre-existing renal artery stenosis as glomerular pressure for filtration not achieved. (They cause efferent arteriole dilation)

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10
Q

What are the anti-hypertensive effects of ACE inhibitors?

A

They reduce the production of angiotensin II, which is a potent vasoconstrictor It also reduces the production of aldosterone, thus reducing salt and water retention This means that there is a decrease in blood volume, hence a decrease in venous return

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11
Q

How does Lorsartan work?

A

Competetively antagonises AII at AT1 (Angiotensin II type 1) receptor, converted into more potent metabolite that acts as an insummountable AII antagonist

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