Endocrinology Flashcards
What are some common causes of primary hypothyroidism and what would TFTs typically show.
TFTs show high TSH and low T4.
Common causes are:
- Autoimmune (Hashimoto’s, atrophic)
- Iodine defiency
- thyroiditis
- Iatrogenic (cytotoxics, thyroidectomy, radioiodine)
What are some common causes of secondary hypothyroidism and what would TFTs typically show.
TFTs show low TSH and low T4
Pituitary insuffiency most likely cause and so MRI of gland neccesary
What is sick euthyroid syndrome and what would TFTs typically show.
TFTs show slightly low TSH and low T4.
Associated with systemic illness during which TFTs become deranged. Test should be repeated after recovery. T3 may be particularly low.
What is Graves Disease and what would TFTs typically show.
TFTs show low TSH, increased T3 and T4.
Most common cause of hyperthyroidism accounting for ~2/3. 9 times more common in females typically presented at age 40-60yrs.
Caused by circulating IgG autoantibodies binding to and activating thyrotropin receptors leading to smooth goitre and increased hormone production.
What are some causes of thyrotoxicosis?
- Graves Disease
- Toxic multinodular goitre
- Toxic adenoma
- ectopic thyroid tissue
- exogenous (iodine excess, levothyroxine)
- Subacute de Quervain’s thyroiditis
- drugs (amiodarone, lithium)
What is subacute deQuervain’s thyroiditis?
Self-limiting post viral hyperthyroidism followed with longer hypothyroid phase, with painful goitre, febrile, and typically increased ESR. low isotope uptake on scan. Managed with NSAIDs.
Describe insulinoma its tests and treatment
This often benign (90-95%) pancreatic islet cell tumour is sporadic or seen with MEN-1. It presents as fasting hypoglycaemia, with whipple’s triad:
- Symptoms associated with fasting or exercise
- Recorded hypoglycaemia with symptoms
- Symptoms relieved with glucose
Tests: Fasting hypoglycaemia (<2.5mmol/L) with elevated insulin
Proinsulin and C-peptide test (administration of insulin does not decrease levels)
MRI,CT
Treatment:
Initial management - immediate K+ replacement and dextrose administration
Surgical excision
Unresectable - eating frequent small meals with high starch and complex carbohydrate
Describe Diabetic Ketoacidosis, precipitating conditions, presentation, investigation, and management
A medical emergency.
Ketonaemia/ketonuria (2+ standard urine sticks)
Blood glucose >11mmol/L or known DM
Bicarbonate <15mmol or venous pH <7.3
Precipitating conditions - infection, discontinuation of insulin, inadequate insulin, CV disease, drugs (steroids, thiazides, SGLT2 inhibitors), physiological stress
Presentation: abdo pain, polyuria, polydipsia, vomiting, dehydration, altered mental state, coma
Weight loss, weakness, lethargy, Kussmaul respiration, acetone smell breath (‘pear drops’)
Investigations:
- cap blood glucose
- urine dipstick
- blood: FBC, glucose, ketones, U+E, ABG, cultures
- ECG
- CXR
Management:
- ABCDE
- fluid replacement with 0.9% NaCl (add KCl after 1st bag - correct hypokalaemia)
- Continuous infusion of insulin at 0.1unit/kg/hr.
- Once blood glucose is <15mmol/l, start 5% dextrose infusion
Describe Hyperosmolar Hyperglycaemic State (HHS),its symptoms, investigations, management.
- Dehydration
- Osmolality >320mosmol/kg
- Hyperglycaemia >30 mmol/L with pH >7.3, bicarbonate >15mmolL and no significant ketonenaemia <3mmol/L
Symptoms: Generalised weakness, leg cramps, visual disturbance, nausea and vomiting, delirium, seizures, focal neurological signs
Investigations
- Urinalysis, culture
- Cap glucose
- Bloods: U+E, FBC, CRP, culture, ABG
- ECG
- CXR
Management:
- ABCDE
- IV 0.9% NaCl (fall in blood glucose should be no more than 5mmol/L/hr)
- Low dose IV insulin (0.05units/kg/hr) if blood glucose no longer falling with IV fluids
- Encourage patient to drink as soon as safe
- Identify and treat underlying precipitants
Describe Cushing’s syndrome, it’s causes, investigations, and management.
Syndrome due to chronic glucocorticoid excess.
ACTH dependent causes
- Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
- ectopic ACTH production (5-10%): e.g. small cell lung cancer
ACTH independent causes
- iatrogenic: steroids
- adrenal adenoma (5-10%)
- adrenal carcinoma (rare)
- Carney complex: syndrome including cardiac myxoma
- micronodular adrenal dysplasia (very rare)
Investigations:
Bloods: FBC, U+E
24 hour urinary free cortisol
- 9am and midnight ACTH and cortisol level (if ACTH suppressed –> non-ACTH dependent cause)
- High-dose dexamethasone suppression test
–if pituitary source then cortisol suppressed
–if ectopic/adrenal then no change in cortisol
-CRH stimulation
–if pituitary source then cortisol rises
–if ectopic/adrenal then no change in cortisol
MRI of pituitary
Chest abdo CT
Management:
- Treat cause
- Cushing’s disease: excision (transphenoidal), bilateral adrenectomy
- Adrenal adenoma or carcinoma: adrenectomy. Radiotherapy and adrenolytic drugs
- Ectopic ACTH: metyrapone, ketoconazole, fluconazole - preop or awaiting effects of radiotherapy
Describe primary adrenocortical insufficiency (addisons disease), it’s symptoms, tests and treatment
Rare but fatal
Destruction of adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency.
80% - autoimmune in UK,
TB is commonest world wide
Symptoms:
lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases), vitiligo, loss of pubic hair in women, hypotension
crisis: collapse, shock, pyrexia
Tests: U+E (hyponatreaemia, hyperkalaemia, uraemia), glucose (decrease), calcium (increased) FBC (eosinophilia, anaemia.) 9am serum cortisol ACTH stimulation test 21-hydroxylase adrenal autoantibodies
Treatment:
Hydrocortisone (in 2 or 3 divided doses; 20-30mg/day) and fludrocortisone
Education - not missing, MedicAlert bracelet and steroid cards, double glucocorticoid dose during illness
Describe secondary adrenal insufficiency
Commonest cause is iatrogenic due to long term steroid therapy leading to suppression of the pituitary adrenal axis.
Other causes: Pituitary disorders (tumours, irradiation, infiltration) Mineralocorticoid production remains intact and there is no hyperpigmentation
Describe male hypogonadism it’s features and causes
Hypogonadism is the failure of testes to produce testosterone, sperm or both.
Features: small testes, decreased libido, erectile dysfunction, loss of pubic hair, decreased muscle bulk, increased fat, gynaecomastia, osteoporosis, mood disturbance.
Primary hypogonadism causes:
•testicular failure from trauma, torsion, radiotherapy
•post-orchitis e.g mumps
•renal failure, liver failure or alcohol excess
•chromosomal abnormalities e.g. Klinefelters syndrome
Causes of secondary hypogonadism:
•hypopituitarism
•prolactinoma
•kallman’s syndrome (isolated GnRH deficiency often with anosmia and colour blindness
•systemic illness
•Laurence-moon-biedl and prader-willi syndromes
Describe the symptoms and causes of hyperprolactinaemia
Prolactin is secreted by the anterior pituitary and release is inhibited by dopamine produced in the hypothalamus.
Causes:
- excess production from the pituitary e.g. prolactinoma
- disinhibition, by compression of the pituitary stalk e.g. pituitary adenoma, or hypothalmic disease
- dopamine antagonist e.g. anti-emetics, anti-psychotics
Symptoms:
- females = amenorrhoea, oligomemorrhea, infertilty, galactorrhoea, also decreased libido, increased weight and dry vagina.
- males = erectile dysfunction, decreased facial hair, galactorrhoea.
Investigations: TFT, exclude pregnancy, basal serum prolactin (normal <400mU/L) Visual testing Pituitary imaging Assessment of pituitary function
Management
Rx underlying cause
Prolactinoma - Dopamine agonist (bromocriptine/cabergoline), surgery, radiotherapy
Prevent osteoporosis
Describe Diabetes insipidus, its symptoms, causes and tests.
This is the passage of large volumes of dilute urine due to deficiency of antidiuretic hormone, ADH, (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
Symptoms: polyuria, polydipsia, dehydration, irritability, confusion.
Causes of cranial DI:
- Idiopathic
- congenital defects in ADH gene (DIDMOAD)
- tumour (may present with DI + hypopituitarism) - craniopharyngiomas
- Trauma
- Infiltration e.g. sarcoidosis
- vascular e.g. haemorrhage
- infection e.g. menigoencephalitis
Causes of nephrogenic DI:
- inherited
- metabolic e.g. hypokalaemia, hypercalcaemia
- drugs e.g. lithium, demeclocycline
- tubulo-interstitial disease: obstruction, sickle cell, pyelonephritis
- post-obstructive uropathy
Tests: serum and urine osmolalities and water deprivation test.
