Treatment of hypertension Flashcards
(12 cards)
explain hypertension treatment
blood pressure; the pressure exerted by blood on blood vessels thats essential for organ perfusion.
-BP= CO x TPR and flow= arterial BP/TPR
-short term regulation;
* baroreceptors
* neural; sympathetic and parasympathetic outflow
Long term regulation:
* hormonal (through Na+ balance, RAAS and ANP)
* control of blood volume via control of ECFV
What is high blood pressure or hypertension
-hypertension is defined according to increased risk
-hypertension is set at 140/90 because of studies done which found a very strong positive correlation between diastolic BP and storke/CAD.
-hypertension is a strong risk factor for; stroke ischemic heart disease, renal failure, retinopathy, left ventricular hypertrophy, cardiac failure
explain secondary (10%) and essential (90%) causes of hypertension
-secondary; known cause for high BP
-renal diseases
-vascular diseases
-hormonal abnormalities e.g. Conn’s syndrome, Cushing’s syndrome, Phaechromocytoma.
-drugs
-pregnancy
-myogenic genetic diseases
explain essential hypertension
-caused by a combination of genetic pre-disposition and environmental factors
-increased sympathetic nervous system stimulation
-increases RAAS
-obesity/insulin resistance
-endothelial dysfunction
-a reduction in capillary density (capillaries reduce resistance due to them being arranged in parallel)
-defect in smooth muscle contraction
-defects in renal Na+ handling, increased salt intake
-age
-ethnicity
-family history
Why treat hypertension
-a reduction in blood pressure level reduces the relative risk of consequences
-the goals of anti-hypertensive treatment are firstly adequate blood pressure control, preventing damage of target organ and controlling other CVS risk factors.
-there are three main treatment pathways;
* non-pharmacological
* pharmacologically
* surgically
explain non pharmacoloical treatment-lifestyle changes
-quit smoking
-weight control
-eat less salt
-regular exercise
-reduce alcohol intake
-behavioural therapies
explain pharmacological treatment: anti-hypertensive drugs
-ACE inhibitors
-Angiotension II receptor blockers
-Diuretics
-drugs acting on SNS
-Vasodilators
discuss ACE inhibitors and Angiotension II receptor blockers
-ACE inhibitors reduce the production of Ang II so less binds to the AT1 receptor. This causes less vasoconstriction and less aldosterone secretion. This reduces TPR and blood volume (causes a drop in CO and BP)
-Could get the same result as AT1 by using the antagonistic drug.
-side effects include;
* cough- decreased bradykinin (inflammatory agent that stimulates nerve fibres) breakdown
* hyperkaliemia leading to arrhythmias
* angioedema- high bradykinin levels cause vasodilation and swelling
explain duiretics and sympathetic nerve stimulation of CVS
Duiretics:
-increased Na+ and water excretion reducing blood volume, CVP, CO and BP.
-the duiretics can also produce a vasodilation, which can reduce TPR and also reduce BP.
Sympathetic nerve stimulation of the CVS:
-B1 receptors; increase HR and contractility which increases CO and BP
-beta blockers
-alpha 1 receptors will vasoconstrict arterioles to increase TPR and BP
Vasodilators: arterioles usually have a significant muscle tone so there’s scope for relaxation.
Explain K channel openers
-increased K+ channels open, K+ efflux
-VSMC hyperpolarization
-reduction in vgCa2+ activity
-reduction in [Ca2+]
-less MLCK activity, increased relaxation causing vasodilation
explain voltage dependent Ca2+ channel blockers and how to choose which drugs to use
Voltage dependent Ca2+ channel blockers:
-blocking VGCC activity in vascular smooth muscle cells will reduce the concentration of intracellular Ca2+
-this means less Ca2+ binds to calmodulin and there’s less MLCK activity. This causes relaxation and vasodilation.
So which drugs do we use:
-essential vs secondary hypertension
-evidence of efficacy
-side effects and drug interactions
-individual demographics
-co-existing diseases
-quality of life
-economic considerations
-complicated
