Primary Hypertension Part 2 Flashcards
what are “high risk” patients with hypertension
those with hypertension who are also over 50 WITH 1. clinical or sub clinical CVD
- chronic kidney disrase
- age >75%
- their estimated 10 year global cardiovascular risk is over 15%.
recommended office BP Treatment targets for those with high risk, low risk or with diabetes
Nonpharmacological therapy; if low risk and BP (140-159/90-99)
dietary and lifestyle
- sodium restriction to <2000mg
- high fruit and vegetable, high potassium
- low in saturated fat
- low in ethanol consumption
- physical activity
- weightloss of 10%
- waist <102cm
- cmoking cessation
how do non pharmacologic therapies for hypertension affect the equation BP=HRxSVxSVR or BP = COxSVR?
SV REDUCTION
- plasma volume reduction via dietary reduction of sodium, and dietary increases in potassium (improve sodium excretion through deacrivation of thiazide channels in the distal convoluted tubule
- weightloss
HEART RATE REDUCTION via better cardio, less stress and less etOH consumption
SVR RECUTION
- through exercsie
broad drug classes used to treat Htn
- diuretics particularly thiazides
- beta-blockers
- ace-inhibitors
- angiotensin receptor blockers
- calcium channel blockers
- alpha-blockers
- vasodilators
what two primary transporter channels are on the ascending loop of henle
- NaKCC channel
- the Mg2+ and Ca2+ transporter because of transepithelial potential difference
two primary channels on the distal convoluted tubule
the NaK2Cl co-transporter
and K+ channels that bring K+ into the filtrate.
thiazides inhibit ___ reabsorption. what is the end result?
inhibit sodium REABSORPTION. sodium cannot go back into the body, and water cannot follow. therefore, water is lost, reducing overall volume. good to reduce blood pressure.
why do thiazides also cause hypokalemia
because when the NKCC is blocked in the distal tubule, K+ and Cl- also cannot be reabsopred, and you pee these out too. causes K+ wasting and thushypokalemia
why are longer acting diuretics (thiazide-like) vs thiazides preferred?
because thiazide-like diuretics reduced coronary events and all-cause mortality.
2 main types of potassium sparing diuretics and their MOA
- aldosterone antagonists (spironolactone): inhibits mineralocorticoid receptors– used if aldosterone is in excess
- ENAC blockade (amiloride, triamerne): blocks Na channel/Na reabsorption. no effect on mineralocorticoids
usually these potassium sparing diuretics are add on to other diurtecs. they are not usually the first line therapy. they increases sodium wasting nad lowers potassium wasting.
primary side effects of beta blockers
impaired glucose tolerance, wheeze/bronchospasm, fatigue
where does aldosterone work in the kidney
recall; aldosterone is a potassium excretor– antagonists (potassium sparing diuretics) act on the collecting tubules and distal tubules.
how do calcium channel blockers work
they vasodilate arteries to create a general decrease in blood pressure
how do alpha blockers work
they block NE at post synaptic nerves, leading to vasodilation
single pill combinations can be used in people with hypertension without compelling indications. what SPC choices are there?
recommended SPC choices are those in which an ACE-i + CCB, ARB+CCB or ACEi/ARB+ diuretic
Specific conditions to AVOID 1 drug class over another:
management of Hypertensive URGENCY
- lower BP <160/100 over a matter of hours to days. oNly lower by 25-30% over 4 hours. Wanna try and get them to <140/90 long term.
- use shorter acting agents to avoid prolonged overshooting.
management of hypertensive URGENCY
