Secondary hypertension — viva

Stem

Practice viva. The examiner asks how you decide whom to screen for secondary hypertension, then works through primary aldosteronism, phaeochromocytoma, sleep apnoea, Cushing's syndrome and thyroid disease, and drug-induced hypertension.^[1][2]

Branch A — Whom do you screen?

Examiner: Which patients with hypertension do you screen for a secondary cause?^[1][2]

Strong answer:

• ESC 2024: patients presenting with suggestive signs, symptoms or medical history of secondary hypertension should be appropriately screened (Class I, Level B).^[1]
• ESC 2024: comprehensive screening for the main causes in adults diagnosed with hypertension before the age of 40 years, starting with an obstructive sleep apnoea evaluation in obese young adults (Class I, Level B).^[1]
• AHA/ACC 2025: screening for specific forms is recommended when clinical suspicion is present (COR 1, LOE C-EO); it lists stage 2 or treatment-resistant hypertension, sudden onset, rising BP after previous control, onset before 30 years, diastolic hypertension in older adults and disproportionate target organ damage as settings where secondary hypertension is more common.^[2]

Follow-up: What do the routine tests already screen for?^[1]

• ESC 2024 Table 8: blood sodium and potassium, haemoglobin and/or haematocrit, calcium and TSH screen for primary aldosteronism, Cushing's disease, polycythaemia, hyperparathyroidism and hyperthyroidism; creatinine, eGFR, urinalysis and the albumin-to-creatinine ratio include renoparenchymal and renovascular screening.^[1]

Branch B — Primary aldosteronism

Examiner: How do you screen for primary aldosteronism in someone already on treatment?^[2]

Strong answer:

• AHA/ACC 2025 recommends plasma aldosterone, renin activity and their ratio for initial screening (COR 1, LOE C-LD), continuing most antihypertensive medications other than MRAs (COR 1, LOE C-EO).^[2]
• ESC 2024 describes testing on current drugs and interpreting the result against them, or, for a clean screen, stopping interfering drugs where feasible and using long-acting CCBs and alpha-receptor antagonists, which do not interfere.^[1]
• Beta-blockers raise the ratio (false positive), and ACE inhibitors and ARBs lower it (false negative) (ESC 2024 Table 12).^[1]

Follow-up: The ratio is positive. What next?^[2]

• AHA/ACC 2025: after a positive screen, or with continued suspicion based on suppressed renin or disproportionate target organ damage, refer to a hypertension specialist or endocrinologist (COR 1, LOE C-EO); the diagnosis may require an aldosterone suppression test, and if confirmed and surgery is desirable, adrenal venous sampling decides between unilateral adrenalectomy and an MRA.^[2]
• The 2025 Endocrine Society guideline, from its abstract, suggests suppression testing when screening results show an intermediate probability of lateralising disease and the patient wants to pursue surgery, and CT plus adrenal venous sampling before choosing treatment when the probability is high.^[4]

Branch C — Phaeochromocytoma

Examiner: When do you suspect a phaeochromocytoma or paraganglioma, and how do you test?^[1]

Strong answer:

• ESC 2024: suspect with signs and symptoms of catecholamine excess, syndromic PPGL, a family history of PPGL, or a germline mutation in a PPGL-causing gene; metanephrines are preferred for screening because they are secreted constitutively, unlike the highly variable catecholamine secretion.^[1]
• The 2014 Endocrine Society guideline recommends initial testing with plasma free or urinary fractionated metanephrines, suggests CT for initial imaging (with MRI a better option in metastatic disease or when radiation exposure must be limited) and recommends considering genetic testing in all patients.^[5]

Follow-up: How do you prepare the patient for surgery?^[1][5]

• ESC 2024: identifying a single tumour mandates surgical excision after adequate pharmacological preparation; doxazosin or terazosin followed by a beta-blocker usually controls BP and adrenergic crises, and fluid administration should be carefully managed because of the risk of profound hypotension after excision.^[1]
• Endocrine Society 2014: preoperative blockade for all functional PPGLs, with a high-sodium diet and fluid intake to prevent postoperative hypotension.^[5]

Branch D — Sleep apnoea, Cushing's syndrome and thyroid disease

Examiner: How do you screen for these three?^[1]

Strong answer:

• Sleep apnoea: ESC 2024 Table 13 lists overnight ambulatory polysomnography; ESC 2024 says it should be suspected in all patients with resistant hypertension and grades severity by the apnoea–hypopnoea index (mild <15, moderate 15–30, severe >30).^[1]
• Cushing's syndrome: ESC 2024 Table 13 lists 24 h urinary free cortisol and a low-dose dexamethasone suppression test; AHA/ACC 2025 Table 10 screens with the overnight 1-mg dexamethasone suppression test and confirms with 24-h urinary free cortisol (preferably multiple) and midnight salivary cortisol.^[1][2]
• Thyroid disease: ESC 2024 Table 13 lists TSH; AHA/ACC 2025 Table 10 lists TSH and free thyroxine for both hypothyroidism and hyperthyroidism.^[1][2]

Follow-up: Which OSA rows does AHA/ACC 2025 give?^[2]

• Weight loss combined with CPAP can be effective in reducing SBP in adults with hypertension and OSA who are overweight or obese (COR 2a, LOE B-R), and CPAP can be useful in reducing BP in resistant hypertension with moderate-to-severe OSA (COR 2a, LOE B-R).^[2]

Branch E — Drug-induced hypertension

Examiner: Which drugs and substances do you ask about?^[2]

Strong answer:

• AHA/ACC 2025 Table 11 (not all inclusive) includes alcohol, caffeine, decongestants, herbal supplements, black licorice, NSAIDs, recreational drugs, clonidine withdrawal, amphetamines, antidepressants, atypical antipsychotics, cyclosporine, oral contraceptives, systemic corticosteroids, angiogenesis and tyrosine kinase inhibitors, and androgen deprivation therapy.^[2]
• ESC 2024: vascular endothelial growth factor inhibitors raise BP in 80%–90% of treated patients, and combined oestrogen-progesterone contraceptives are among the most common causes of drug-induced hypertension in young women.^[1]