CARDIO- treatment of hypertension Flashcards
outline the classification of hypertension
optimal - 120 / 80
normal - 130/85
high normal - 130-139 / 85- 89
grade 1 hypertension - 140 - 159 / 90-99
Grade two hypertension (moderate) - 160-179/ 100-109
Grade three hypertension (severe) - >180/>110
Isolated systolic hypertension (grade 1) - 140-159/<90
Isolated systolic hypertension (grade 2) - >160/<90
hat are the causes of essential / primary hypertension
genetic / environmental factors increases SNS increased RAAS obesity / insulin resistance defects in vascular smooth muscle contraction defects in renal Na handling, increased salt intake age ethnicity
what are the causes of secondary hypertension
hormonal abnormalities (Conn’s syndrome (excess aldosterone)
Cushing’s syndrome (excess mineralocorticoids)
genetic conditions (Liddle’s disease (increase in NA/H2O absorption in the kidney))
what are the benefits of treating hypertension
10 millions deaths per year associated with HBP
dropping BP reduces risk of cardiovascular disease mortality and morbidity
goals of treatment are to lower it to reduce risk but not too much
outline non-pharmacological treatments to reduce hypertension
quitting smoking weight control eat less salt regular excercise reduce alcohol intake behavioural therapies
surgery - treat the cause if known e.g., Cushing’s syndrome
outline the mechanism of action of RAAS modulation as a treatment for hypertension
ACE inhibitors
reduce the production of angiotensin II
act in lung endothelium
block ACE
angiotensin II receptor blockers
act as competitive antagonist at ATI receptors reducing effect of Ang II
both work by reducing Ang II induced vasoconstriction and aldosterone actions
what are side effects and contraindications of RAAS modulation for treatment of hypertension
ACE breaks down bradykinin (inflammatory molecule) - presents as a dry cough via stimulation of sensory neurones
angioedema
hyperkalaemia (reduction of aldosterone reduces NA reabsorption but increases K reabsorption by the kidney)
contraindications - pregnancy (foetal problems) - renal stenosis
outline the mechanism of action of calcium channel blockers as a treatment for hypertension
block calcium channels in vascular smooth muscles (selective)
lower rise in Ca inside the cell - calcium calmodulin pathway is not activated - decrease in myosin light chain kinase activity - prevents contraction
causes vasodilation and relaxation - reduces TPR
what are some side effects / contraindications from using calcium channel blockers to control hypertension
increased HR - response to lowering BP - arrythmias
headaches / ankle swelling - excessive vasodilation
contraindications
HF - need a calcium influx in the heart to produce contraction of cardia muscle - could exacerbate the problem
outline the mechanisms of action of loop diuretics in controlling hypertension
increase NA and H2O excretion from the kidneys
reduces blood volume - reduces cardiac output - reduces blood pressure
also produces vasodilation
what are the side effects of using diuretics to control hypertension
hypokalaemia - loos salt and potassium
lipid abnormalities
glucose intolerance / hyperglycaemia - decrease in insulin release
what are the effects of clonidine
acts at alpha 2 receptors in the brain decrease sympathetic nervous system output
what are the effects of trimethaphan - NIC blocker
blocks the ganglion
what are the effects of alpha 1 and beta -1- adrenoreceptor blockers
prazosin - alpha 1 - relaxation of smooth muscle
atenolol - beta -1- reduced CO and renin release
