Endocrinology Flashcards
Describe the clinical features of hypoglycaemia
Autonomic – sweating, anxiety, hunger, tremor, palpitations, dizziness
Neuroglycopenic – confusion, drowsiness, visual trouble, seizures, coma
List common causes of hypoglycaemia
Main cause – insulin or sulfonylurea treatment in a diabetic
EXogenous drugs
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours
Non-pancreatic neoplasms
Describe investigations for hypoglycaemia
BM during attack & lab glucose if in hospital
Take a drug history & exclude liver failure
72h fasting, bloods – glucose, insulin, c-peptide & plasma ketones if symptomatic
Describe the treatment for hypoglycaemia
Conscious – 15-20g of quick-acting carbohydrate snack & recheck BM after 10-15 mins
Conscious but uncooperative – squirt glucose gel between teeth and gums
Unconscious patients – IVI glucose or give glucagon IV/IM
Describe the clinical features of hyponatraemia
Early – headache, nausea, vomiting, general malaise
Late – confusion, agitation, drowsiness
Acute severe – seizures, respiratory depression, coma & death -> requires urgent treatment under senior supervision
Describe investigations for suspected hyponatraemia
Full history & examination – drug history and hydration status
Urine osmolality, urine sodium, TFTs & assessment of cortisol reserve (0900 cortisol/synacthen test)
Describe the management of hyponatraemia
Correct underlying cause
Asymptomatic chronic hyponatraemia – fluid restriction is often sufficient
Acute/symptomatic hyponatraemia – cautious rehydration with 0.9% saline (do not correct rapidly as cerebral pontine myelinolysis may occur)
Vasopressor receptor antagonists – promote water excretion without loss of electrolytes & are effective in treatment hypervolaemic & euvolaemic hyponatraemia
Emergency – seek expert help, consider hypertonic saline
Describe the clinical features of hypernatraemia
Lethargy
Thirst
Weakness
Irritability
Confusion
Coma
List causes of hypernatraemia
Fluid loss without water replacement
Diabetes insipidus
Osmotic diuresis
Primary aldosteronism
Iatrogenic eg. incorrect IV fluid replacement
Describe the management of hypernatraemia
Give water orally if possible, if not give glucose
Use 0.9% saline IV if hypovolaemic
Describe the clinical features of hypokalaemia
Muscle weakness
Hypotonia
Hyporeflexia
Cramps
Tetany
Palpitations
Light-headedness
Constipation
Describe the treatment of hypokalaemia
Mild – give oral K+ supplement
Severe – give IV potassium, don’t give K+ oliguric
Describe the clinical features of hyperkalaemia
Fast irregular pulse
Chest pain
Weakness
Palpitations
Light-headedness
Describe the management of hyperkalaemia
Polystyrene sulfonate resin (calcium resonium) binds K+ in the gut, preventing absorption and bring K+ levels down over a few days
Emergency – calcium gluconate, insulin & glucose, salbutamol
Outline the different causes of hypercalcaemia
Primary hyperparathyroidism – hypercalcaemia with non-suppressed PTH until proved otherwise
Malignancy – hypercalcaemia with suppressed PTH
Describe the clinical features of hypercalcaemia
Asymptomatic
Tiredness, generalised aches & pains
Polyuria and polydipsia
Abdominal pain and constipation
Kidney stones
Describe the investigations done for hypercalcaemia
Ca2+
PTH
ALP – high ALP reflects increased bone turnover
Renal ultrasound – nephrocalcinosis
Describe the treatment of hypercalcaemia
Depends on the underlying cause
Hyperparathyroidism – parathyroidectomy if Ca2+ > 2.85 mmol/L, young; calcimimetic drugs (cinacalcet)
Describe the common causes of hypocalcaemia
1) Post-surgical hypoparathyroidism
2) Vitamin D deficiency
3) Hypomagnesaemia
Describe the clinical features of hypocalcaemia
Acute severe hypocalcaemia – laryngospasm, prolonged QT interval, seizures
Muscle cramps
Carpo-pedal spasm
Peri-oral and peripheral paraesthesia
Neuro-psychiatric symptoms
Describe the treatment for hypocalcaemia
Calcium replacement
Reverse the underlying cause
Hypoparathyroidism – treated with 1-alfacalcidol or calcitriol
Magnesium deficiency – precipitating drugs should be stopped and IV magnesium replacement started
Describe diabetes insipidus
Caused by vasopressin deficiency (cranial DI) or vasopressin resistance (nephrogenic DI)
Leads to passing of large volumes of dilute urine with profound unquenchable thirst
Describe investigations to do for suspected diabetes insipidus
Low urine osmolality
High serum osmolality
Water deprivation test (measures urine osmolality):
1) cranial diabetes insipidus: low after deprivation, high after ADH
2) nephrogenic diabetes insipidus: low after deprivation, low after ADH
3) primary polydipsia: high after deprivation, high after ADH
Describe the management for diabetes insipidus
If possible, treat underlying cause
Mild cases can be treated conservatively
Desmopressin (synthetic ADH) can be used in:
1) CDI to replace ADH
2) NDI in higher doses under close monitoring
Describe Addison’s disease
Primary adrenal insufficiency
Arises as a result of destruction of the adrenal gland OR genetic defects in steroid synthesis
Describe the clinical presentation of Addison’s disease
Non-specific – fatigue, weakness, anorexia, weight loss, nausea
Glucocorticoid loss – hypoglycaemia & increased pigmentation
Mineralocorticoid loss – dizziness and postural hypotension
Androgen deficiency – reduced libido and loss of axillary and pubic hair
Describe the investigations for suspected Addison’s
Hyponatraemia, hyperkalaemia, raised urea, hypoglycaemia & mild anaemia
Confirmatory tests – low 9am cortisol & simultaneously raised ACTH concentration -> Synacthen test is needed for confirmation
Describe the management for Addison’s
Lifelong glucocorticoid and mineralocorticoid replacement
-hydrocortisone and fludrocortisone
Should double dose of glucocorticoid at times of illness
Provided steroid emergency card
Describe the clinical features of Cushing’s syndrome
Central obesity
Dorso-cervical fat pad
Increased roundness of the face
Plethora (red face)
Thin skin
Easy bruising
Describe investigations to do for suspected Cushing’s
24 hour urine free cortisol – elevated
Low dose dexamethasone suppression test – failure to suppress cortisol
Overnight dexamethasone suppression test – failure to suppress cortisol
Describe the different causes of Cushing’s syndrome
3 potential causes are pituitary, adrenal or ectopic ACTH
1) ACTH is low, adrenal tumour is likely -> negative feedback by high cortisol levels
2) If ACTH is normal or high, diagnosis is pituitary or ectopic
High dose DST leads to some cortisol suppression in Cushing’s disease but not in ectopic
Describe the management of Cushing’s syndrome
Adrenal tumour – laparoscopic adrenalectomy
Ectopic ACTH – appropriate treatment of the underlying malignancy and medical control of cortisol levels
Cushing’s disease – trans-sphenoidal removal of the pituitary adenoma
List common causes of hyperthyroidism
Graves’ disease – autoimmune disease & due to presence of TSH receptor stimulating antibodies
Nodular hyperthyroidism – autonomous secretion of T3/T4 either from a solitary toxic nodule/numerous nodules situated within a toxic multi-nodular goitre
Thyroiditis – inflammation causing a release of thyroxine
Outline common clinical manifestations of hyperthyroidism
Weight loss with increased appetite
Insomnia
Irritability
Anxiety
Heat intolerance
Palpitations
Tremor
List investigations to do for suspected hyperthyroidism
TFTs – increased T3, T4 & undetectable TSH
Thyroid ultrasound
Nuclear imaging (iodine uptake isotope scan)
1) Graves’ = uniform increased uptake
2) Nodular disease = increased uptake only in the autonomous nodule
3) Thyroiditis = absent uptake
Describe the management for hyperthyroidism
Medication – carbimazole & propylthiouracil (NB: can cause agranulocytosis – urgent FBC if unexplained fever or sore throat)
Surgery
Radioactive iodine
List the common causes of hypothyroidism
Hashimoto’s thyroiditis
Pregnancy/post-partum
Drugs – amiodarone & lithium
Describe the common clinical features of hypothyroidism
Weight gain
Cold intolerance
Depression
Constipation
Fatigue
List investigations done for suspected for hypothyroidism
TFTs – low T3/T4 & increased TSH
TPO antibodies – strongly positive in Hashimoto’s thyroiditis
Describe the treatment options for hypothyroidism
Thyroxine replacement
