Flashcards
Endocrine hypertension
Cards in this deck (24)
- 1What are the causes of endocrine hypertension?1) Cushing's (due to high cortisol)
2) Hyperthyroidism
3) Acromegaly
4) Conn's (primary aldosteronism)
5) Pheochromocytoma
6) Renal artery stenosis - 2What are the zones of the adrenal gland and what do they produce?Adrenal cortex:
1) Zona reticularis - androgens
2) Zona fasciculata - glucocorticoids
3) Zona glomerulosa - mineralocorticoids
Adrenal medulla - noradrenaline and adrenaline (cholinergic innervation from the splanchnic nerve, cortisol increases PNMT expression, which converts noradrenaline to adrenaline) - 3Describe the blood supply to the adrenal glands1) 6-8 superior suprarenal arteries from the phrenic artery
2) Middle suprarenal artery from the aorta
3) Inferior suprarenal artery from the renal artery
Right suprarenal vein drains into the IVC, the left drains into the left renal - 4What is Conn's syndrome?Adrenal adenoma which produces aldosterone. Leads to sodium retention, hypokalaemia, metabolic alkalosis and high BP.
2/3rd of cases of primary aldosteronism - 5What else causes primary aldosteronism?1/3 of cases are due to bilateral hyperplasia of the adrenals.
Rarely:
Adrenal carcinoma
Glucocorticoid-remediable aldosteronism (GRA) - ACTH regulatory element binds to 11B hydroxylase so that aldosterone is under the control of ACTH - 6What causes secondary hyperaldosteronism?Due to high renin production in under perfusion of the kidneys e.g. renal artery stenosis, accelerated hypertension, diuretics, CCF or hepatic failure
- 7What are the actions of angiotensin II?1) Aldosterone release from adrenal cortex
2) Release of ADH (otherwise triggered by high serum osmolality or low blood volume by carotid baroreceptors)
3) Triggers sympathetic nervous system - 8How does the tubuloglomerular feedback mechanism work to increase GFR?1) Drop in GFR leads to a drop in Na+
2) Vasodilation of afferent arteriole relative to efferent causes an increase in glomerular filtration rate - 9How does Conn's present?Asymptomatic or signs of hypokalemia: weakness, cramps, paresthesia, polyuria, polydipsia, high BP
- 10When should you think of Conn's as a cause of hypertension?1) Hypertension associated with hypokalemia
2) Refractory hypertension e.g. despite more than 3 anti-hypertensives
3) Hypertension in anyone under the age of 40 - 11What tests are done in Conn's?U&E
Renin and aldosterone
Adrenal vein sampling
Do not rely on low K+ as ~20% are normokalemic
Genetic testing for GRA
MRI/CT to image adrenals - 12How is Conn's managed?Laparoscopic adrenalectomy - spironolactone for 4 weeks pre-op to stabilise BP and K+
- 13How is bilateral adrenal hyperplasia managed?Spironolactone or amiloride
- 14How is GRA managed?Dexamethasone for 4 weeks (should lower ACTH) if it does not normalise high BP then try spironolactone
- 15How are adrenal carcinomas managed?Surgery +/- post-op adrenolytic therapy with mitotane. Prognosis is poor.
- 16What are pheochromocytomas?Catecholamine-producing tumours, formed from sympathetic paraganglia cells (collections of chromaffin cells). If found outside the adrenal medulla they are called paragangliomas.
10% are malignant
10% are extra-adrenal
10% are familial
10% are bilateral - 17What are the genetic causes of pheochromocytomas?Thyroid, MEN-2a, MEN-2b, von Hippel-Lindau syndromes (will also cause tumours of the brain, spinal cord, eye, and vasculature)
- 18What is the classic triad associated with phaeochromocytomas?Intermittent headaches, sweating and tachycardia
There may be normal or high BP - 19What are the cardiac, CNS, psychological, gastric, and other symptoms associated with pheochromocytomas?1) Raised pulse, palpitations, VT, dyspnoea, faints, angina, MI, cardiomyopathy
2) Headache, visual disorders, dizziness, tremor, numbness, fits, horner's syndrome (paraganglioma), subarachnoid haemmorhage
3) Anxiety, panic, hyperactivity, confusion and episodic psychosis
4) D&V, abdominal pain over the tumour site, mass
5) High temperature, backache, sweats, heat intolerance, sweats/flushes - 20How are pheochromocytomas investigated?Biochemical - 24hr urinary metanephrines and look for raised WCC
Localisation - abdominal CT/MRI. Meta-iodobenzyleguanide can localise extra-adrenal sites - 21How are pheochromocytomas managed?Surgery - a-blockade pre-op with phenoxybenzamine (helps lower BP, always use before beta-blocker as B2 vasculature activity causes vasodilation)
Beta-blockers if there is heart disease or tachycardia
Do 24hr urinary metanephrine 2 weeks post op - 22How does a pheochromocytoma emergency present?Acute hypertensive crisis - pallor, pulsating headache, hypertension ('feels like I'm about to die'), pyrexial, ECG, signs of LVF, raised ST segment, VT, and cardiogenic shock
- 23How is a pheochromocytoma emergency managed?Take to ICU
Short acting alpha blocker to get BP under control (i.e. phentolamine 2-5mg IV)
When BP controlled, use long-acting alpha blocker e.g. phenoxybenzamine (30mg/12hr PO) to the point that BP is well-controlled but no significant postural hypotension
B1 blocker to control any tachycardia or cardiac disease
Elective surgery 4-6 weeks to make sure the alpha blockers have had time to work - 24How does renal artery stenosis cause hypertension?Reduced perfusion leads to release of renin. Renin leads to angiotensin II release which stimulates vasoconstriction, aldosterone and ADH.
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- Met3B (Endocrinology) Flashcards on Endocrine hypertension, created by Anna Hogarth on 08/03/2020.
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