Case 16- Obesity Flashcards
Cushings Syndrome Sx
Facial plethora, fat redistribution, skin bruising and thinning, violaceous abdominal striae, proximal myopathy, HTN, impaired glucose tolerance, hypokalaemia, osteoporosis, acne, hirsutism
Investigations for suspected cushings
BP, FBC (WCC), UE (hypernatraemia, hypokalaemia, metabolic acidosis)
Salivary night time cortisol- 2 samples taken or 24 hour urinary free cortisol
Overnight Dexamethasone suppression test- gold standard for outpatient (inpatient- 24 hour urinary cortisol). If abnormal do one of the following;
Venous sampling for ACTH
MRI brain
Chest CT- SCLC
Abdominal CT for adrenal tumours
Investigations for hyperaldosteronism
BP- HTN
FBC, UE, ABG- hypokalaemia and alkalosis
Aldosterone/ renin ratio- high aldosterone low renin for Conn’s. Should be first line
High resolution CT abdomen and adrenal vein sampling
Ct angiogram kidneys
Investigations for adrenal insufficiency
BP- hypotension
FBC, UE- hyponatraemia, hyperkalaemia, metabolic acidosis (normal anion gap)
Early morning cortisol (between 100-500, do short synacthen test)
Short synacthen test- gold standard
Serum ACTH (primary-high, secondary-low)
Adrenal antibodies
CT abdomen- if adrenal damage
MRI head- if suspect pituitary pathology
Nephrogenic causes of DI
Lithium
Intrinsic kidney disease
Cranial causes of DI
Cerebral tumours
Head injury
Brain surgery
CNS infection eg. Meningitis
Investigations for diabetes insipidus
FBC UE- hypernatraemia
Urine osmolarity- low
Serum osmolarity- high
Water deprivation test- gold standard
CT head- if water test positive, may want to exclude a brain tumour
NB- no glucosuria
NB- essential to exclude hypercalcaemia due to hyperparathyroidism before progressing
to a water deprivation test
Aetiology of Cushing’s syndrome
Exogenous steroids (most common cause)
Cushings disease- pituitary adenoma releasing ACTH (most common endogenous cause)
Adrenal cushings- adrenal adenoma realising cortisol
Paraneoplastic cushings- ectopic ACTH from SCLC
NB- adrenal adenoma is the only primary hypercortisol cause as the others all increase ACTH
NB- pseudo cushings- due to alcohol excess or severe depression (mimics symptoms and lab results, including dexamethasone suppression test)
Nelsons syndrome
Symptoms arising many years after a a bilateral adrenalectomy, where there is a rapidly enlarging pituitary adenoma (has been trying to increase ACTH levels for many years and this predisposes to tumour development)
Sx of conns syndrome (primary hyperaldosteronism)
Usually asymptomatic, HTN, hypokalaemia (fatigue, muscle wasting, cramps, headaches, polyuria, polydipsia, palpitations)
NB- classically a young pt with hypokalaemia and drug resistant hypertension
Adrenal insufficiency
Adrenal glands don’t produce enough steroid hormones, esp. cortisol and aldosterone
Addison’s disease
Where adrenal glands have been damaged (autoimmune) resulting in decreased cortisol and aldosterone (primary adrenal insufficiency)
Secondary adrenal insufficiency
Inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release. Damage to the pituitary gland is most common cause (Sheehans syndrome)
Tertiary adrenal insufficiency
Inadequate CRH release by the hypothalamus. Usually when a patient is on steroids for numerous weeks then stops suddenly, the hypothalamus doesn’t reactivate quick enough and so endogenous steroids aren’t produced quickly enough
Sx Addison’s
Hypotension, weight loss, fatigue, myalgia, N & V, diarrhoea, salt cravings, loss of libido, loss of axillary and public hair, hyperpigmentation (increased ACTH), abdominal pain, hypoglycaemia, vitiligo
NB- hyponatraemia, hyperkalaemia
Sx of Diabetes Insipidus
Polyuria, polydipsia, nocturnal, signs of volume depletion eg. Hypotension, visual field defects (pituitary adenoma), hypernatraemia
Differentials for diabetes insipidus
Psychogenic polydipsia, diabetes mellitus, diuretic use
SIADH Sx
Hyponatraemia (anorexia, n and v, headache, cramps, lethargy), normotensive, euvolemic, absence of oedema
SIADH aetiology
Increased ADH secretion
Diseases of CNS- stroke, trauma, infection
Pulmonary disease- pneumonia, COPD
Drugs- SSRI
Endocrine disorders- glucocorticoid deficiency
Ectopic ADH- SCLC
Enhanced stimulation of ADH receptors in the kidney
SIADH Investigations
Fluid balance chart- check no excessive fluid intake
BP- normal (euvolemic)
Urinalysis- sodium and osmolarity increased
FBC UE- hyponatraemia
NB- if nothing found and someone has persistent hyponatraemia we do CT TAP- exclude malignancy
Pituitary gland hormones
Anterior- TSH, GH, ACTH, FSH, LH, PRL, endorphins
Anterior- Oxytocin, ADH
DM vs DI
Polyuria and polydipsia but no glucosuria in DI
DI vs SIADH
High urinary output vs low urinary output
Low ADH (or can’t respond to it) vs high ADH
Hypernatraemia vs hyponatraemia
Dehydrated vs hydrated
Lose too much fluid vs retain too much fluid
NB- both present with excessive thirst
Hypokalaemia and ADH
Hypokalaemia can cause a mild nephrotic diabetes insipidus
Kidneys don’t respond to ADH well in a hypokalaemia state
How are steroids prescribed
High dose in morning
2 smaller doses in late afternoon/ early evening
(Naturally levels are lower overnight)
Sx of Addisonian or adrenal crisis
Reduced consciousness
Hypotension
Hypoglycaemia hyponatraemia hyperkalaemia
Very unwell patients
Triggers for an adrenal crisis
Infection
Trauma
Acute illness
Surgery
Steroid withdrawal
adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcaemia)
In patients with established Addisons or long-term steroid use
Treat before looking for cause eg. IV hydrocortisone
Central pontine myelinolysis
When hyponatraemia is treated too quickly (or when too much insulin is given in HHS)
Sheehan Syndrome
Women who lose a life-threatening amount of blood in childbirth or who have severe low blood pressure during or after childbirth can deprive the pituitary gland of oxygen and damage it
Management of nephrogenic DI
Thiazides, low salt/protein diet
Cranial DI Management
Desmopressin (vasopressin analogue)
Causes of hypoadrenalism
Primary
Addisons disease (most common)
TB
Metastases (bronchogenic carcinoma)
Meningicoccal septicaemia (Waterhouse Friedrichsen syndrome)
HIV
Antiphospholipid syndrome
Secondary
Pituitary disorders eg. Tumour (non functioning), Sheehan’s syndrome, apoplexy
Exogenous glucocorticoid therapy
Management of Addison’s disease
Give both mineralocorticoids and glucocorticoids
Hydrocortisone (majority in 1st half of the day)
Fludrocortisone
Don’t miss doses, steroid cards, medic alert bracelets, hydrocortisone for injection during adrenal crisis
Management of inter current illness (not adrenal crisis) in Addison’s disease
Glucocorticoid dose doubled (hydrocortisone), fludrocortisone remains the same
Management of an adrenal or addisonian crisis
Hydrocortisone 100 mg IM (patients should have this in the community)
1 litre saline over 30-60 minutes
Oral replacement after 24 hours
Differentiate true cushings and pseudo cushings
Insulin stress test
Features of a pituitary adenoma
Excess hormone in secretory adenomas- cushings (ACTH), acromegaly (GH), amenorrhea or galactorrhoea due to excess prolactin
Depletion of hormones due to compression of functioning gland- non secretory tumours therefore present with generalised hypopituitarism
Stretched dura- headaches
Compression of chiasm- bitemporal hemianopia
Investigations for a pituitary incidentiloma
Pituitary blood profile- GH, prolactin, ACTH, FH, LSH, TFT
Formal visual field testing
MRI brain with contrast
Treatment of pituitary adenomas
Hormonal therapy (bromocriptine for prolactinomas)
Surgery eg. If incidental adenoma is increasing in size or if it is a functioning/secretory adenoma
Primary hyperaldosteronism
Bilateral idiopathic adrenal hyperplasia is most common cause
Unilateral adrenal adenoma- Conns syndrome (rarer)
Investigations for primary hyperaldosteronism
Plasma aldosterone/renin ratio (should show high aldosterone with low renin)
CT abdomen
Adrenal venous sampling (AVS) fir source of aldosterone excess-unilateral or bilateral
Management of primary hyperaldosteronism
Adenoma- surgery
Bilateral hyperplasia- spironolactone (aldosterone antagonist)
Causes of Addison’s disease
UK- autoimmunity
Worldwide- infection (TB)
Criteria for orlistat
Lipase inhibitor
BMI 30+ or BMI >28 with co morbidities
Criteria for bariatric surgery
BMI 40+, or 35+ and significant co morbidities
Secondary hyperaldosteronism
Renal artery stenosis or obstruction (renin and aldosterone raised)
ABG cushings disease
Hypokalaemic metabolic alkalosis
Corticosteroids
Fludrocortisone- min G, high M
Hydrocortisone- G, high M
Prednisolone- high G, low M
Dexamethasone, betmethasone- high G, no M
Glucocorticoids and neutrphils
They are immunosuppressive, but they can cause neutrophilia
