secondary hypertension

Question 1

secondary hypertension?

Answer 1

Renal Disease
Chronic renal disease
Renal artery stenosis (1-5%)

Endocrine Disease
Primary hyperaldosteronism (1%)
Phaeochromocytoma (0.5%)
Cushing’s disease, acromegaly

Other
Pregnancy
Drugs: e.g. Oral contraceptive, steroids
Coarctation

Question 2

who to investigate?

Answer 2

Suspicion on history and examination (all)
Accelerated (malignant) hypertension (>180/110)
Recent onset, or worsening hypertension
Resistant hypertension (not controlled by> 3 drugs)
Age < 30 years or requires treatment age 20-35
Abnormal screening tests
Hypokalaemia, increased creatinine
Proteinuria, haematuria
Specialist Referral

Question 3

causes of renal artery stenosis?

Answer 3

Causes
Atherosclerosis 90%
Proximal third of RA (and aorta)
Fibromuscular dysplasia 10% (young females)
Distal 2 thirds of RA

pathoogy

ecrease renal perfusion -> activation of renin angiotensin system angiotensin II -> aldosterone

Clinical
Hypertension Abrupt onset, young (<50)
Accelerated or Refractory
Abdominal bruit

Renal profile (Urea, creatinine and electrolytes)
 Unexplained renal dysfunction (can be induced by ACEI)
 Unexplained hypokalaemia

Imaging
Angiography
Duplex ultrasound

Management
Risk factors smoking, lipids, aspirin
Revascularization: Angioplasty (stenting)

Question 4

angioplasty?

Answer 4

Atheroma
Less in favour following recent trials–no long term improvement in renal function
- adverse events

Fibromuscular dysplasia
Improved rates of “cure” cf atheroma

Question 5

primary hyperaldosteronism?

Answer 5

(Conn’s Syndrome= adenoma)

Approx. 1% hypertensive patients
Adenoma 2/3rd
Hyperplasia 1/3rd
(Carcinoma) rare

Sodium and water retention

Symptoms due to hypokalaemia
not always present
muscle weakness, paraesthesia, polyuria and polydipsia

Question 6

aldosterone?

Answer 6

Adrenal cortex

Mineralocorticoid

Acts at distal renal tubule
Na+ uptake
K+ loss/ H+ loss

Question 7

if hyperaldosteronism suspected?

Answer 7

Suspect: Hypokalaemia (exclude diuretic as a cause)

Confirm: Aldosterone:Renin ratio
ensure adequate sodium and potassium intake
Stop spironolactone, oestrogen and ideally ACEI, b-blockers
Verapamil, alpha blockers and hydralazine ideally to ensure interpretable biochemistry

Localise
CT Scan, MRI scan
Selective venous sampling

Treatment
Adenoma - surgical
Hyperplasia - spironolactone

Question 8

phaeochomocytoma?

Answer 8

Catecholamine secreting tumours

Bilateral 10%+ ( esp familial forms)
Extra-adrenal ~20%
Hereditary ~25%
Mets <5% adrenal phaeos; ~33% extra-adrenal phaeos

Question 9

catecholamine synthesis?

Answer 9

Brain
Adrenal medulla
Sympathetic neurons

Question 10

catecholamine metabolism?

Answer 10

Question 11

phaeochromocytome clinical features?

Answer 11

Hypertension often severe, refractory

Paroxysmal attacks (55%)

Frequency: Variable, Usually 2-5/week

Symptoms: Headache
Hypertension
Sweating
Palpitations
Anxiety
Pain (epigastric, chest)

Other Hyperglycaemia, hypercalcaemia

Diagnosis = Biochemistry

Acidified 24-hour urine (2-3)

Metabolites (total): Metadrenaline, normetadrenaline

Catecholamines (free): Adrenaline
Noradrenaline
Dopamine

Localisation

Imaging:- CT Scan, MRI scan
MIBG scan
(Selective venous sampling)

treatment?

Control blood pressure
alpha blocker, followed by beta blocker

Surgery-
Experienced surgeon and anaesthetist

Follow-up
5% familial
Multiple endocrine neoplasia MEN2A/2B (RET)
Von Hippel-Lindau
Neurofibromatosis