- Q. What occurs in Addison’s disease? What signs and symptoms are seen?
Rare condition in which there is destruction of the entire adrenal cortex, 90% of cases are due to organ-specific autoantibodies causing hypoadrenalism. Associated with other autoimmune conditions e.g. autoimmune thyroid disease, pernicious anaemia, type 1 DM
Clinical presentation: insidious presentation - lethargy, depression, anorexia and weight loss, postural hypotension (due to salt/water loss)
Hyperpigmentation due to excess ACTH, there may be vitiligo and loss of body hair in women
- Q. How may severe hypoadrenalism present?
Addisonian crisis - vomiting, abdo pain, profound weakness, hypoglycaemia and hypovalemic shock
- Q. Name two causes of hypoadrenalism, how is it investigated? Treated?
Causes: Addison’s (autoimmune), adrenal gland tuberculosis, surgical removal, haemorrhage (meningococcal septicaemia, malignant infiltration)
Single cortisol measurement, the short ACTH test (demonstrates failure of ACTH to increase cortisol levels), plasma ACTH levels, long ACTH stimulation test (secondary or adrenal suppression by steroids), adrenal antibodies (in autoimmune), CXR (TB with calcified adrenals)
Primary hypoadrenalism = high ATCH with low cortisol
Secondary or tertiary hypoadrenalism = reduced ACTH and cortisol
Tx: life long steroid treatment with hydrocortisone - steroid and fludrocortisone - aldosterone (hydrocortisone is increased when patient is under stress e.g. trauma, surgery, infection), screening for osteoporosis should also happen
- Q. What is the most common cause of inappropriate ADH secretion? (SIADH), what symptoms are seen?
Cancer - small cell cancer of the lung
Also: meningitis, head injury, pneumonia, TB, lung abscess, alcohol withdrawal, opiates
Nausea, irritability, headache, mild dilutional hyponatremia
- Q. How is SIADH investigated and treated?
Dx: low serum sodium, high urine osmolality and low plasma osmolality, continused urinary sodiu excretion, absence of hypokalaemia, hypotension, hypovolaemia
Tx: water restriction, demeclocycline (inhibits vasopressin action on the kidney), tolvaptan (vasopressin antagonist - expensive, not widely used), hypertonic saline with furosemide to prevent circulatory overload
- Q. What does the parathyroid gland secrete? How does this affect calcium metabolism?
PTH and calcitonin
PTH - stimulates reabsorption of calcium from the kidney and resorption of calcium from the bone (osteoclasts), also helps activate vitamin D to (1,25-dihydroxyvitamin D) in order to increase absorption of calcium from the gut
Calcitonin - acts on gut, kidney and bones to decrease blood calcium levels
- Q. What are the most common causes of primary hypercalcaemia?
Primary hyperthyroidism common in elderly women- single parathyroid gland adenoma, hyperplasia and rarely carcinoma
Severe hypercalcaemia - usually caused by malignancy
Tertiary hypercalcaemia - development of autonomous parathyroid hyperplasia after longstanding hyperthyroidism, most often in renal disease, plasma calcium and PTH are both raised
- Q. What signs and symptoms are seen in hypercalaemia?
Mild hypercalcaemia corrects serum calcium < 3mmol is often asymptomatic
More severe = general malaise and depression, bone pain, abdo pain, nausea and constipation
Calcium deposition in renal tubules can cause polyuria and nocturia, may cause CKD
Very high levels can cause dehydration, confusion, clouding of consciousness and risk of cardiac arrest
- Q. How is hypercalaemia treated?
Treatment:
- Rehydrate with saline IV
- Bisphosphonate
- Measure U&Es, serum calcium
- Prednisolone – myeloma, sarcoidosis, vit D excess
- Prevent recurrence – treat underlying cause
Treatment of primary hyperparathyroidism: surgical removal of adenoma, or surgical removal of all four glands in hyperplasia
- Q. What is the most common cause of hypocalcaemia? Name two other causes
- Q. What is the most common cause of hypocalcaemia? Name two other causes
CSK is the most common cause - inadequate production of active vitamin D - and renal phosphate retention = micro precipitation of calcium phosphate in the tissues
Acute pancreatitis
Hypoparathyroidism: reduced PTH function, post-thyroidectomy and parathyroidectomy
Vitamin D deficiency - reduced exposure to UV light and malabsorption
Drugs - calcitonin, bisphosphonates
- Q. How does hypocalcaemia present?
Increased excitability of muscles and nerves, numbness around the mouth and in the extremities, followed by cramps, tetany, convulsions and death if untreated
Chvostek’s sign - tapping over the facial nerve in the region of the parotid gland causes twitching of the ipsilateral facial muscles
Trousseau’s sign - carpopedal spasm induced by infiltration of the sphygmomanometer cuff to a level above systolic blood pressure
Severe hypocalcaemia may cause papilloedema and prolonged QT interval on ECG
- Q. What is hypocalcaemia investigated and treated?
Ix. Hypocalcaemia (Serum corrected for albumin), PTH conc, 25-hydroxyvitamin D levels
Tx. 10ml of calcium gluconate
In vit d defciency - ergocaliferol (vitamin D2) or cholecalciferol (vitamin D3) orally
Hypoparathyroidism - alfacalcidol to maintain Ca conc
- Q. What may cause hypokalaemia? Clinical features?Mx?
AE: duiretic tx and hyperaldosteronism e.g. liver/heart/renal failure, cushing’s, conn’s
Usually asymptomatic though muscle weakness if severe, increased risk of cardiac arrhythmias, predisposes to digoxin toxicity
Mx: tx of underlying cause, slow KCL infusion with ECG monitoring
- Q. What may cause hyperkalaemia? Clinical features?Mx?
AE: renal impairment and drug interference with potassium excretion
Few SSs till levels are high enough to cause cardiac arrest
Impaired neuromuscular transmission including muscle weakness and paralysis - may be associated with metabolic acidosis causing Kussmaul’s respiration (low, deep, sighing inspiration and expiration)
May cause progressive ECG abnormalities: normal → tented T wave → reduced P wave with widened QRS complex → sine wave pattern (pre-cardiac arrest)
Mx: dietary management, restriction of certain drugs and a loop diuretic to increase urinary potassium
- Q. What is diabetic ketoacidosis? Who is at risk of it? Ix? Tx?
Features: Kussmaul breathing (metabolic acidosis). lethargy, polyuria, dehydration (reduced tissue turgor, dry tongue, low BP), confusion, coma, abdo pain, ketone smelling breath
Diagnosis: finger prick test glucose >11, urine stix analysis = increased ketones > 3mmol/L,, pH < 7.3 (nausea/vomiting), bicarb < 15mmol/L (high anion gap)
Tx: fluid balance and dehydration 0.9% saline IV, insulin, adjust KCL conc
- Q. What occurs in diabetic neuropathy? What may this lead to?
A. Burning pain, paraesthesia, hyperaesthesia
B. Autonomic: orthostatic hypotension, gastroparesis, diarrhoea, constipation, incontience, erectile dysfunction
C. Insensitivity: foot ulceration, infection, amputation, falls, (Charcot foot, weakening of bones → fracture → change in foot shape)
- Q. What can be done to help prevent diabetic complications?
A. Screening, education and proving orthotic shoes, MDT foot clinic, pressure relieving footwear, podiatry, revascularisation, antibiotics
B. Good glycaemic control
C. Tricyclic antidepressants/SSRis
D. Anticonvulsants
