Flashcards in 5. Hypertension Deck (15):
What is hypertension and how is it classified?
Sustained increase in BP.
Stage 1 hypertension:
- clinic BP = >140/90 mmHg
- ABPM/HBPM = >135/85 mmHg
Stage 2 hypertension:
- clinic BP = >160/100 mmHg
- ABPM/HBPM = >150/95 mmHg
- >180 systolic or >110 diastolic
- emergency significant rise in BP (rather than absolute value)
What is the difference between the 2 types of hypertension?
1. Primary hypertension (95% cases) = idiopathic or multifactorial. May be genetic or environmental factors. Pathogenesis unclear but recent evidence suggests dysfunction of dopamine Rs.
2. Secondary hypertension = cause can be defined, e.g. renovascular disease, chronic renal disease, hyperaldosteronism, Cushing's syndrome. Important to treat primary cause.
How does renovascular disease cause secondary hypertension?
Occlusion of renal artery (renal artery stenosis) causes fall in perfusion pressure in that kidney... increased renin production (thinks there is low BP)... activation of RAAS... vasoconstriction and Na+ retention at other kidney.
How does renal parenchymal disease (chronic kidney disease) cause secondary hypertension?
- Early stage: loss of vasodilatory substances - kidney loses sensitivity
- Later stage: Na+ and water retention due to inadequate glomerular filtration, i.e. volume-dependent hypertension
(causes kidney shrinkage)
Explain the adrenal causes of secondary hypertension.
- Conn's syndrome: aldosterone-secreting adenoma (benign kidney tumour)... hypertension and hypokalaemia
- Cushing's syndrome (steroids or adrenal gland tumour): excess secretion of glucocorticoid cortisol... at high concentrations acts on aldosterone Rs... Na+ and water retention
- Phaeochromocytoma (adrenal medulla tumour - some are extra-adrenal): secretes catecholamines (NA, adrenaline and dopamine)
Why is it important to treat hypertension?
Asymptomatic but associated with increased mortality rate and many vascular diseases. Affects brain, eyes, heart, arteries and kidneys.
Explain how hypertension causes organ damage.
1. Increases afterload (pressure against which heart must pump):
i) left ventricular hypertrophy... heart failure
ii) increased myocardial oxygen demand... myocardial ischaemia and MI
2. Arterial damage:
i) atherosclerosis (fat deposition and stiffening of BVs)... myocardial ischaemia and MI
ii) weakened vessels (+atherosclerosis):
- cerebrovascular disease stroke (cerebral haemorrhage but esp ischaemic)
- nephrosclerosis and renal failure
- retinopathy (90% mortality within 5 yrs if untreated)
What are the non-pharmacological approaches to treating hypertension?
2. diet: reduced Na+ intake
3. reduced alcohol intake
can have limited effect
What are the 4 main classes of hypertension medications?
1. targeting RAAS
How can the RAAS be targeted to treat hypertension?
1. ACE inhibitors (eg captopril, lisinopril, perindopril and enalpril): prevent conversion of AngI to AngII + block breakdown of bradykinin
2. AngII receptor antagonists
Blocking production or action of AngII has diuretic and vasodilator effects
Why can ACEi cause dry cough as a side effect?
build up of bradykinin causes lung vasodilation
How can vasodilators be used to treat hypertension?
- L-type Ca2+ channel blockers: reduce Ca2+ entry to vascular SM cells... vasodilation.
- In principle could also use alpha1 R blockers - reduce sympathetic tone (relaxation of vascular SM) - BUT can cause postural hypertension.
How can diuretics be used to treat hypertension?
Thiazide diuretics reduce circulating plasma volume by inhibiting Na/Cl co-transporter on apical membrane of cells in distal tubule.
Other diuretics (eg aldosterone antagonists like spironolactone) will also lower BP but not 1st line choice.
How can beta blockers be used to treat hypertension?
Blocking beta1 Rs in heart will reduce effects of sympathetic output: reduce heart rate and contractility.
But not used in hypertension alone due to side effects - would only use if other indications such as previous MI.