Endocrinology Flashcards
What is primary adrenal insufficiency?
Adrenal glands are damaged
Reduction in secretion of cortisol and aldosterone
Commonest cause: autoimmune
Also called Addison’s
What is secondary adrenal insufficiency?
Inadequate ACTH
Low cortisol release
Loss or damage to pituitary
Fun fact: Sheehan’s syndrome is where massive blood loss during childbirth leads to pituitary gland necrosis
What is tertiary adrenal insufficiency?
Inadequate CRH release by the hypothalamus
Cause: long term oral steroids -> hypothalamus suppression. Long term steroids need to be tapered slowly for the adrenal axis to regain normal function
What are the symptoms of adrenal insufficiency?
Fatigue
Nausea
Cramps
Abdo pain
Reduced libido
What are the signs of adrenal insufficiency?
Bronze hyperpigmentation (ACTH stimulates melanocytes to produce melanin), particularly in skin creases
Hypotension (particularly postural hypotension)
What do investigations show in adrenal insufficiency?
Hyponatraemia
Hyperkalaemia
Early morning cortisol
Short synacthen test
ACTH
Adrenal cortex antibodies and 21-hydroxylase antibodies
Consider:
CT/MRI adrenals
MRI pituitary
What is the short synacthen test?
Give synacthen (synthetic ACTH)
Blood cortisol is measured at baseline, 30 and 60 minutes after administration. Cortisol should normally at least double - if not = primary adrenal insufficiency
What are the replacement steroids for adrenal insufficiency?
Hydrocortisone for cortisol
Fludocrotissone for aldosterone
What are the symptoms of an Addisonian crisis?
Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia
Hyperkalaemia
What is the management of an Addisonian Crisis?
IV hydrocortisone 100mg stat and then 100mg every 6 hrs.
IV fluid resus
Correct hypoglycaemia
Monitor electrolytes and fluid balance
Where in the adrenal cortex is aldosterone made?
Zona glomerulosa
What does aldosterone do?
Regulates BP
Regulates blood volume
Increases Na+ reabsorption by kidneys
What causes an increase in secretion of aldosterone?
Low BP
High levels of angiotensin II or K+ in the blood or ECF
What causes a decrease in the secretion of aldosterone?
High Na+ in blood or ECF
How does aldosterone work?
Increases no. of Na+/K+ pumps on the principle renal tubule cells and ENaC channels.
Increases the reabsorption of sodium and increases excretion of potassium
This increases the fluid volume and blood pressure in the capillaries.
Also increases H+ secretion
What are the symptoms of Conn’s syndrome (primary aldosteronism)
Benign tumour in the zona glomerulosa cells
Hypokalaemia
Mild metabolic alkalosis
Increase in blood volume -> increased BP
Decreased plasma renin levels
Muscle weakness due to low levels of ECF K+
What are the management options for hyperaldosteronism?
Tumour removal
Spironolactone: aldosterone antagonist
What does ADH do?
Stimulates water reabsorption from eh collecting ducts in the kidneys
What can cause SIADH?
Posterior pituitary secreting too much
Small cell lung cancer secreting ADH
Also:
Post-op
Infection such as atypical pneumonia and lung abscesses
Head injury
Medications: (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs)
Malignancy
Meningitis
What does SIADH cause?
Dilution of sodium in the blood: euvoleumic hyponatraemia
More concentrated urine with him urine sodium
What are the symptoms of SIADH?
Non-specific
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia: seizures and reduced consciousness
How do you diagnose SIADH?
Exclusion of other causes of euvolaemic hyponatraemia (synacthen test, no diuretics, no D&V, no excessive water intake, no CKD or AKI)
How do you manage SIADH?
Establish and treat the cause
Why is important to correct sodium slowly?
To prevent central pontine myelinolysis (a change in sodium of less than 10 mmol/L per 24 hrs
You correct sodium by:
Fluid restriction
Tolvaptan (ADH receptor blockers) - but this can cause a rapid increase so only specialist use
What happens in central pontine myelinolysis?
Water moves rapidly out of the brain cells and into the blood
The brain cells have become used to a low osmolality due to long term severe hyponatraemia
First phase: encephalopathic and confused +/- headache, nausea and vomiting
Second phase: demyelination: spastic quadriparxsis, psudobulbar palsy and cognitive and behavioural changes. Significant risk of death
What can cause secondary acromegaly?
Ectopic GHRH or GH from lung or pancreatic cancer
What types or organ dysfunction can GH cause?
Hypertrophic heart
Hypertension
T2DM
Colorectal cancer
What are the investigations for acromegaly?
Insulin-like Growth Factor 1 (IGF-1) = raised
Oral glucose tolerance test whilst measuring GH = high glucose normally suppresses growth hormone but not in acromegaly
MRI brain
Formal visual field testing
What medication can be used in the treatment of acromegaly?
Pegvisomant (GH antagonist given subcutaneously and daily)
Somastatin analogues to block GH release
Dopamine agonists to block GH release (e.g. bromocriptine)
What do juxtaglomerular cells in the afferent arteriole of the kidney do?
Sense blood pressure and if low, they secrete renin.
Where is angiotensinogen made?
Liver
What does renin do?
Converts angiotensinogen to angiotensin I
Where is angiotensin I converted to angiotensin II?
The lungs with the help of angiotensin converting enzyme (ACE).
What does angiotensin II do?
Stimulates the release of aldosterone from the adrenal glands
What is the most common cause of primary hyperaldosteronism?
Bilateral adrenal hyperplasia
What causes secondary hyperaldosteronism?
Excessive renin stimulating the adrenal glands to produce more aldosterone.
What can cause high renin levels?
Renal artery stenosis (often in patients who are atherosclerotic)
Renal artery obstruction
Heart failure
What investigation for hyperaldosteronism?
Renin and aldosterone levels so that you can calculate a renin/aldosterone ratio
What is the management for renal artery stenosis?
Percutaneous renal artery angioplasty
A patient with high blood pressure that is not responding to treatment should be considered for investigation for what?
Hyperaldosteronism
