Consider secondary causes of hypertension Flashcards
Red flag
Symptomatic HTN (headache, visual disturbance)
The vast majority of people with HTN have
Essential (or primary) HTN
This is by definition HTN without an identifiable cause.
Thought to result from genetic predisposition and various environmental influences that are not completely understood.
Risk factors include:
- increased weight
- ageing
- lack of regular exercise
- dietary factors such as high salt intake (including soy sauce)
- excessive liquorice consumption.
Resistant hypertension
If a pt’s clinic blood pressure remains over 140/90 mmHg after a treatment regimen of an ACE inhibitor or an ARB, plus a calcium channel blocker and a diuretic, then the HTN is considered to be resistant.
Patient adherence to treatment should be re-examined
and an added emphasis placed on;
- weight loss,
- exercise,
- reduced salt intake,
- moderation of alcohol intake,
- stress reduction and
- minimisation of other medicines that may increase HTN, e.g. NSAIDs and OCP.
Secondary causes of HTN should also be assessed and consultation with a Nephrologist or Cardiologist considered.
Ambulatory monitoring of blood pressure should be conducted, where possible, to exclude a white-coat cause for the HTN and to accurately assess the effects of future and current treatment.
People may benefit from further examination of possible secondary causes of HTN and a more detailed assessment of potential end organ damage
- aged under 40 years
- with stage one (mild) HTN
- and no evidence of target organ damage, CVD, kidney disease or diabetes .
- If BP is high to control with > 2 agents
This is because short-term risk assessment (5yr predictive risk) can underestimate the lifetime risk of CV events in these people
Secondary causes of HTN include:
High alcohol intake
Obstructive sleep apnoea
Medicines, e.g. OCP and corticosteroids, NSAIDs, ciclosporin and decongestants, e.g. phenylephrine
Drug misuse, e.g. amphetamine or cocaine use
Renal parenchymal disease, including glomerulonephritis, suggested by a history of urinary tract infection or obstruction, haematuria, analgesic misuse, or family history of polycystic kidney disease
Renal artery stenosis
Primary hyperaldosteronism (Conn’s syndrome) suggested by significantly raised BP in otherwise well people, hypokalaemia and a Fhx of the syndrome in some people
Cushing’s syndrome – excessive cortisol production
Phaeochromocytoma – a rare adrenal gland tumour
Secondary hypertension investigation
Should be discussed first with an Endocrinologist
Measurement of blood renin, aldosterone, cortisol
Plasma aldosterone-renin ratio – for primary aldosteronism.
- Advise pt to have breakfast and be ambulatory for at least 1 hour before test.
- If possible, ensure test occurs before initiating beta blockers, diuretics, ACEi, or ARB.
If suspected phaeochromocytoma; palpitations, hot flushes and great flactuation of BP, then check plasma-free metanephrine and/or 24‑hour urinary metanephrine
24‑hour urinary cortisol or 1 mg overnight dexamethasone suppression test – for Cushing syndrome.
Echocardiogram – for left ventricular hypertrophy (LVH) and dilation of the ascending aorta
- Waiting list of one year in Auckland.
If suspected investigate as per OSA in Adults.
If renal artery stenosis is suspected, seek advice according to DHB as per Ultrasound Renal Doppler.
If FHx of kidney disease, palpable kidneys, suspected urinary obstruction, raised creatinine, investigate and request non-acute nephrology assessment.
If asymptomatic carotid bruit, carotid ultrasound is not indicated.
New techniques for treating hypertension
Renal sympathetic nerve denervation
- is a catheter-based technique showing promise in reducing BP in pts with resistant HTN.
After two years, in pts with SBP > 160 mmHg, there was an average BP reduction of 32/14 mmHg.
Blood glucose levels were also shown to improve.
The procedure does not appear to be associated with significant adverse effects.
Pts who may benefit from this technique should be discussed with a Cardiologist.