Drugs on vessels Flashcards
How is muscle contraction triggered (Basic)?
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.
How are ion levels in myocytes maintained?
ATPases drive majority of Ca2+ back into SR
Ca2+/Na+ transporters remove excess Ca2+
Na+/K+ ATPases remove excess Na+
What is considered hypertension?
140/90 mmHg OVER MULTIPLE MEASUREMENTS (OVER TIME)
What the common categories of anti-hypertensives?
ACE inhibitors (E.G Enalapril)
Calcium channel blockers (E.G Amlodipine)
Angiotensin receptors blockers (E.G Losartan)
Alpha blockers
Diuretics
Beta blockers
What are the ‘stages’ of hypertension treatment?
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
Why are ACEi and ARBs not first line in over 55s and afro Caribbean’s?
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.
Why is it good to give ACE I or ARB alongside diuretics?
Diuretics cause drop in Na+, this causes compensatory rise in RAS activity that is counteracted by ACE I and ARBs.
What is a side effect of ACE inhibitors?
Cough – 25% patients present with it. Occurs due to inhibition of bradykinin breakdown which is ordinarily performed by ACE.
What is a side effect of ACE Is and ARBs?
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)
What are the anti-hypertensive effects of ACE inhibitors?
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
How does Lorsartan work?
Competetively antagonises AII at AT1 (Angiotensin II type 1) receptor, converted into more potent metabolite that acts as an insummountable AII antagonist