Hypertension Flashcards
Why is controlling bp important
Reduction in CV damage Preservation of renal function Limit or reverse left ventricular hypertrophy PRevention of IHD Reduction in mortality due to strole/MIs
BP hypertension in clinic?
140/90
BP in home/ambukatory
130/85
What BP requires same day referral
> 180/120
When is renin released by kidney
When it detects low levels of sodium, and when it detects low blood pressure
What is the RAAS system
Renin turns angiotensin (formed by liver) into angiotensin 1. ACE then turns this into angiotensin 2.
Angiotensin 2 causes vasoconstriction and acts on adrenal gland to release aldosterone.
Aldosterone then acts on distal convuluting tubule of kidney and early collecting duct of the kidney to cause sodium retention and potassium loss. This then increases retention of water which increases circulating volume
Role of ACEI
Inhibit ACE. Therefore:
- Reduce arterial and venous vasoconstriction
- Reduced aldosterone production
Side effects of ACEI
Potentiate bradykinin which leads to cough
May increase Potassium (interaction with salt KCL substitute)
Angioedema (increased incidence in black patients)
When should ACEI be avoided
Renovascular disease (bilateral renal artery stenosis) -Renin-dependent hypertension. ACEI lead to renal underperfusion and severe hypotension
What should you monitor before and during treatment of ACEI
- eGFR
- K+
What is the best antihypertensive in patients with diabetes and why
ACEi
They’re effective in preventing nephropathy in DM
Action of AT1 receptor antagonists
Block the effect of angiotensin 2 which acts at the AT1 receptor to cause vasoconstriction
Do AT1 receptor antagonists give rise to cough
no
Two classes of calcium channel inhibitors
Rate limiting (e.g. verapamil): have greater effecrs on cardiac tissue
Dihydropyridines (e.g. amlodipine) more on vascular smooth muscle
Mechanism of action of calcium channel inhibitors
Inhibit voltage operated Ca2+ channels on vascular smooth muscle leading to vasodilatation and reduction in BP