Lecture 2 - hypertension Flashcards
What is hypertension
an elevation of systolic and/or diastolic blood pressure to the point where it increases risk of CVD. it gets worse with age
how does hypertension damage the CVD system
- high-pressure damages endothelium -> atherosclerosis
- hypertension increases afterload and this causes cardiac hypertrophy and ischaemia
- can lead to renal failure and stroke due to microcirculation affected
- in isolated systolic hypertension, a fall in diastolic pressure may compromise coronary blood flow to the wall of the left ventricle since this only occurs during diastole
midlife hypertension
mechanisms which regulate mean BP failure, are dysfunctional.
mean, systolic and diastolic BP rise associated with a rise in TPR
defect in Na+ excretion
neurohormonal abnormalities
old age hypertension
age-related arterial stiffening -> isolated systolic hypertension. systolic pressure rises but diastolic BP typically falls so only a small increase in mean BP
primary hypertension
no identifiable cause
polygenetic predisposition + environmental and lifestyle influences
secondary hypertension
the cause can be identified
renal, endocrine, identified monogenic syndromes
BP lowering
ANS/Baroreceptor reflex - short term, on heart and blood vessels
RAAS - long-term system - kidneys and blood vessels
natriuresis - acts on kidneys, and controls BP by regulating renal function
aorta stiffening
with age and hypertension, the aorta becomes stiffer and small arteries become constricted. as a result, pulse wave speeds up
BP lowering (2)
ANS/effector arm of baroreceptor reflex controls BP by regulating vascular tone and cardiac output
RAAS controls BP by regulating renal function , thereby stabilising blood volume, also influences vascular tone
natriuresis controls BP by regulating renal function, thereby stabilising blood volume
Ramipril - ACE inhibitor
blocks production and therefore effects of angiotensin 2
generally well tolerated but some adverse effects include
chronic dry cough, angioedema, hypotension, deterioration of renal function
ARBs - Losartan
block ang 2 receptros and therefore effects of ang 2
similar to ACE inhibitors but no cough - very well tolerated
renin antagonist - aliskiren
blocks binding of angiotensinogen therefore preventing ang 1 synthesis
not widely used
CCBs
Vascular selective CCBs inhibit constriction of arterioles by agonists by blocking voltage-gated Ca2+ channels thus decreasing TPR
Non selective CCBs inhibit constriction of arterioles by agonists and also cause negative inotropy and chronotropy which reduce CO
thiazide like diuretics - chlortalidone, metolazone
increase salt and water excretion by the kidneys, reduces blood volume and cardiac output
reduce Na+ absorption by blocking Na/Cl co transporter in distal tubule
TPR also falls via unknown mechanism
