Endocrinology 1/6/20 Flashcards
causes of hyponatraemia (with urine Na osmolarity >20mmol/L)
euvolaemic patient
- SIADH
- hypothyroidism
hypovolaemic patient
> Addison’s disease
> renal failure
> diuretics (thiazides/loop diuretics)
causes of hyponatraemia (with urine Na osmolarity <20mmol/L)
hypovolaemic patient
> diarrhoea, vomiting
> burns
oedematous patient
> secondary hyperaldosteronism (heart failure, liver cirrhosis, renal artery stenosis)
> nephrotic syndrome
> IV dextrose
> psychogenic polydipsia
mild, mod, sev hyponatraemia serum Na values
normal blood sodium = 135-145mmol/L
mild = 130-134 mmol/l mod = 120-129 mmol/l sev = <120 mmol/l
symptoms of hyponatraemia
mild + mod:
Non-specific symptoms such as headache, lethargy, nausea, vomiting, dizziness, confusion, and muscle cramps
sev:
- seizures
- coma
- respiratory arrest
management of mild hyponatraemia (130-134 mmol/L)
- fluid restriction (<800ml/day)
- loop diuretics (eg. furosemide)
management of moderate hyponatraemia (120-129mmol/L)
- hypertonic saline in first 4 hrs (to raise Na)
- fluid restriction (<800ml/day)
- loop diuretics (eg. furosemide)
management of severe hyponatraemia (<120mmol/L)
- bolus of hypertonic saline until symptom resolution
- may add conivaptan/tolvaptan to inhibit ADH (can be hepatotoxic)
other management concerns for hyponatraemia
Fluids restriction in the following patients:
- Oedematous states like heart failure and cirrhosis
- SIADH
- Renal failure
- Psychogenic polydipsia
Central pontine myelinolysis is a risk in correcting severe hyponatraemia too quickly - leads to irreversible neuro damage, can lead to locked in syndrome
causes of hypernatraemia
- dehydration
- osmolar diuresis eg. hyperosmolar hyperglycaemic state (HHS)
- diabetes insipidus
- excess IV saline
hyperosmolar hyperglycaemic state (HHS) features
Often confused with DKA - check ketones/pH (HHS more common in DM2, while DKA usually DM1)
General Nervousness Harms Hearts
General:
polyuria, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia
diagnosis of hyperosmolar hyperglycaemic state (HHS)
- hypovolaemia
- marked hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
- significantly raised serum osmolarity (> 320 mmol/kg) gives features of hyperviscosity
management of hyperosmolar hyperglycaemic state (HHS)
treat underlying cause
- Normalise the osmolality (gradually)
- Replace fluid (normal saline or 0.45% saline if not reducing in osmolarity sufficiently as is more hypotonic) and electrolyte losses
- Normalise blood glucose (gradually)
prophylactic anticoagulation
iatrogenic causes of siADH
- carbamazepine
- thiazides
- SSRIs and tricyclics
- vincristine and cyclophosphamide
- oxytocin and vasopressin
management of siADH
correction must be done slowly to avoid precipitating central pontine myelinolysis
- fluid restriction
- demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH (can cause photosensitive rash)
- ADH receptor antagonist eg. conivaptan/tolvaptan
non-drug causes of siADH
- malignancy - particularly SCLC but also pancreatic and prostate
- neurological - stroke/SA or SD haemorrhage/meningitis or encephalitis or abscess
- infections - TB or pneumonia
diagnosis of siADH
diagnosis of exclusion, must fill the folowing criteria:
- low plasma sodium concentration <135 mmol/l
- high urinary sodium concentration >30mmol/L
- patient euvolaemic
- absence of adrenal and thyroid dysfunction
- no diuretic use (recent or past)
causes of hypercalcaemia
- primary hyperparathyroidism (PHPT): commonest cause in non-hospitalised patients
- malignancy: the commonest cause in hospitalised patients, may be due to a number of processes, including bone metastases, myeloma, PTHrP from squamous cell lung cancer
- other (<10% cases):
> vit D intoxication
> granulomas eg. sarcoidosis/TB
> drugs (thiazides, calcium antacids, lithium, dietary calcium)
> Addison's
> thyrotoxicosis
features of hypercalcaemia
- bones, stones, thrones (polyuria + constipation), abdo groans (stones, peptic ulcer, constipation, nausea) and psychiatric moans (confusion, mood change)
- polyuria + polydipsia
- anorexia/weight loss
- corneal calcification
- shortened QT interval
normal adjusted calcium
Adjusted calcium range = 2.20-2.60 mmol/L
management of hypercalcaemia
generally correct underlying cause and do an ECG and urine calcium (consider BMD scan)
- give saline IV
- bisphosphonate IV
- surgery in mets/PHPT
primary adrenal insufficiency (Addisons) site of disease
adrenal cortex dysfunction
secondary adrenal insufficiency site of disease
pituitary or hypothalamus dysfunction
tertiary adrenal insufficiency site of disease
chronic glucocorticoid administration
causes of primary adrenal insufficiency
- autoimmune “Addison’s” (destruction of adrenal glands)
- trauma
- TB
- malignancy (eg. bronchial carcinoma)
- meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
causes of secondary adrenal insufficiency
pituitary or hypothalamus disorders (e.g. tumours, irradiation, infiltration)
causes of tertiary adrenal insufficiency
- glucocorticoid suppression
- post treatment of Cushing’s
features of adrenal insufficiency
- lethargy, weakness, anorexia, nausea & vomiting, weight loss, hypotension, ‘salt-craving’
- skin/gum changes (in primary addison’s - hyperpigmentation (especially palmar creases), vitiligo, loss of pubic hair in women (due to reduced androgens)
- hypoglycaemia, hyponatraemia and hyperkalaemiac metabolic acidosis may be seen
investigations for adrenal insufficiency
ACTH stimulation test (short synacthen test)
- plasma cortisol is measured before and 30 minutes after giving synacthen 250ug IM
- adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated in Addison’s
if not readily available eg. general practice, can use a 9am serum cortisol blood test
history and examination can rule out secondary/tertiary
management of Addison’s
glucocorticoid and mineralocorticoid replacement therapy (double in illness to prevent crisis)
- hydrocortisone
- fludrocortisone
patient education
management of Addisonian crisis
- hydrocortisone 100 mg IM or IV
- 1000ml normal saline IV (with dextrose if hypoglycaemic)
- continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
- oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
role of PTH
increases:
- Ca2+ reabsortion in kidney
- hydroxylation of 25 OH vit D in kidney
- Ca2+ release from bone remodelling
- Ca2+ gut absorption via 25 OH vit D
decreases:
- phosphate reabsorption by kidney
hypoparathyroidism features (symptoms of hypocalcaemia)
symptoms due to hypocalcaemia:
- tetany: muscle twitching, cramping and spasm
- perioral paraesthesia
- Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
- Chvostek’s sign: tapping over parotid causes facial muscles to twitch
- if chronic: depression, cataracts
- ECG: prolonged QT interval
