L20: Adrenal disorders Flashcards
What is the clinical presentation of cortisol deficiency?
Weakness, tiredness, weight loss, hypoglycaemic, nausea
What is the clinical presentation of mineralocorticoid deficiency?
Dizziness, low Na and high K, hypotension
What is the clinical presentation of androgen deficiency?
Mostly testosterone
No symptoms in men as not major testoterone producing organ
Women–> Hair loss, loss of libido
What is the clinical presentation of cortisol excess?
Weight gain
Features of Cushing syndrome
What is the clinical presentation of mineralocorticoid excess?
High BP and low K+
What is the clinical presentation of ACTH excess from pituitary?
Skin pigmentation–> Melanocyte stimulaton
What is the clinical presentation of adrenal medulla disease?
Excess adrenaline and NA Acute episodes Sweating Anxiety Palpitations High or low BP Collapse Can lead to sudden death
What biochemical assessment (tests) would you do for suspected adrenal hormone deficiency?
Electrolytes–> Na+ low, K+ high (low BP)
Basal cortisol (0900)–> low (should be high)
Stimulation test–> Inject synthestic ATCH (synatchen)–> see if cortisol levels increase
What biochemical assessment (tests) would you do for suspected adrenal hormone excess?
Electrolytes–> Na+ high, K+ low (high BP)
Midnight cortisol–> high (should be low)
24hr urine–> cortisol high
Suppression test–> failure to suppress cortisol
Androgens and derivatives high
What biochemical assessment (tests) would you do for the adrenal medualla?
24hr urine catecholamines –> adrenaline, NA, dopamine, 3-Methoxy-Tyramine
24hr urine metanephrines–> metabolites of adrenaline and NA–> metadrenaline and normetadrenaline
Plasma metanephrines–> more sensitive than 24hr urine
Before doing a biochemical assessment of adrenal medulla function what should be avoided?
Coffee, cake, bananas, chocolate and vanilla
What is Cushing’s syndrome?
Excess secretion of cortisol caused by hyperactivity of the adrenal cortex
What causes Cushing’s syndrome?
Adrenal adenoma–> tumour of the adrenal cortex
Pituitary adenoma–> Cushing’s disease–> tumour of the anterior pituitary–> increase ACTH secretion
Ectopic tumours secreting ACTH or CRH
Glucocorticoid treatment
What are the signs and symptoms of excess cortisol?
1) Thin arms and legs and muscle weakness–> muscle proteolysis
2) Abdominal fat, dorso-cervical fat pad, moon shaped face–> increased lipogenesis
3) Purple striae–> lower abdomen, upper arms and thighs–> catabolic effects–> protein breakdown–> easy bruising due to thinning of skin and subcutaneous tissue
4) High blood pressure and diabetes
- -> hyperglycaemia–> increased muscle proteolysis and hepatic gluconeogenesis–> polyuria and polydipsia
- -> mineralocorticoid effect of excess cortisol–> increased sodium and fluid retention
5) Osteoporosis–> thin bones –> disturbance in calcium metabolism
6) Plethoric (flushed) face
How is a suspected Cushing’s syndrome diagnosed?
Low dose dexamethasone test
Slight decrease in ACTH or Cortisol indicates Cushing’s syndrome
How can you differentiate between the causes of Cushing’s syndrome?
ACTH test
- -> Supressed= adrenal adenoma or glucocorticoid treatment
- -> Elevated= Cushing disease (pituitary tumour) or ectopic tumour
Differentiate between ACTH supressed–> Are they on glucocorticoids? –> yes glucocorticoid fault, no then adrenal ademona
High dose Dexamethosome test
- -> ACTH (therefore cortisol) levels decreased –> Pituitary tumour (Cushing’s disease)–> relatively insensitive to cortisol but a huge amount will have an effect
- -> ACTH level remains the same–> Ectopic tumour
How are adrenal adenomas treated?
Adrenalectomy Laproscopic ‘key hole surgery’
What do we call the disease that cause primary hyperaldosteronism?
Conn’s syndrome–> aldosterone-secreting adrenal adenoma
OR
Bilateral (idiopathetic) adrenal hyperplasia–> no discrete adenoma, increase in cell number
What does hyperaldosteronism lead to (signs and symptoms)?
Endocrine hypertension and hypokalaemia (low K+)
Elevated aldosterone despite the renin-angiotensin aldosterone system
Occasional muscular weakness and spasms
Tingling sensations
Excessive urination
(high BP, LV hypertrophy, stroke, hypernatraemia, hypokalaemia)
How is primary hyperaldosteronism diagnosed?
Clinical suspicion
Increase aldosterone with decreased renin
Scan–> confirm adrenal adenoma or bilateral hyperplasia
How does hyperaldosteronism lead to increased blood pressure?
Excess aldosterone
Increased Na+ reabsorption and K+ secretion
Increased blood volume and pressure
↑ BP–> increased renal perfusion–> ↓ renin
Normal ↓ renin–> ↓ aldosterone
However Conn’s syndrome–> ↑ aldosterone despite renin↓
What is congenital adrenal hyperplasia (CAH)?
Inherited disorder–> autosomal recessive
Deficiency in enzyme needed to synthesis corticosteroids from cholesterol
Lack of cortisol–> no negative feedback so ↑ACTH secretion–> enlargement of adrenal cortex (hyperplasia)
What is the most common enzyme deficiency in CAD? What does this deficiency result in?
Deficiency in 21-hydroxylase
Position means inhibits production of glucocorticoids and mineralocorticoid
No affect on adrogen synthesis
Therefore 17α hydroxylase precursor–> diverted to produce more androgens
What does increased androgen production result in in CAH?
Genital ambiguity in female infants–> look like boys–> clitoromegaly
Salt wasting crises–> high rate of Na+ loss in urine
Hypotension, hyponatraemia, hyperkalaemia, hypoglycaemia and virilisation (male characterisitcs)
