Endocrine Flashcards
Summarise Cushing’s disease/ syndrome
Pathophysiology: Prolonged raised cortisol levels.
Disease = pituitary adenoma secretes ACTH –> Syndrome. But syndrome can have other causes.
Presentation: Moon face, buffalo hump, striae, thin, wasting limbs with central obesity, hypokalaemia, hypernatraemia, hyperglycaemia, depression, insomnia, OP, poor skin healing, bruising
Causes: Steroid use, Cushings disease, adrenal adenoma, paraneoplastic (e.g. SCLC)
Ix: Dexamethasone suppression test. Normal result is shown by ACTH and cortisol being suppressed. If they aren’t = Cushings syndrome. Then give higher dose of steroids to find the location. Adrenal cause means ACTH supressed but not cortisol. Cushings disease both suppressed. In paraneoplastic neither suppressed.
Others: 24 hr free cortisol, FBC, UE, MRI brain for pituitary adenoma, chest CT for SCLC, abdo CT for adrenal tumout
Mx:
1) Surgery to remove tumour
2) remove adrenals and replace steroids
Summarise Adrenal Insufficiency
Pathophysiology: Adrenal glands do not produce enough steroids (cortisol and adrenaline)
Causes:
Primary - adrenal insufficiency, usually autoimmune
Secondary -Pituitary damage, so inadequate ACTH e.g. Sheehans, infection, tumour, radiotherapy
Tertiary - Sudden withdrawal of steroids
Presentation: Fatigue, N+V, abdo pain, tanned (high ACTH), postural hypotension.
Ix: Low Na+, High K+, Low glucose.
Diagnosis with short synacthen test for adrenal insuffciency (Give synethetic ACTH and measure cortisol response)
ACTH levels (high primary, low secondary)
Scans pituitary/ adrenals
Mx: Hydrocortisone to replace cortisol, fludrocortisone to replace aldosterone. Sick day rules.
Addisonian crisis: LOC, hypotension, hypoglycaemia. ABCDE, IV hydrocortisone, IV fluids, correct hypoglycaemia and deranged electrolytes.
Summarise hyperthyroidism
Types:
Primary: Pathology in the thyroid
Secondary: Pathology in hypothalamus/ pituitary
Grave’s: Autoimmunne where TSH-R Ab, Antithyroid Peroxidase (anti-TPO) Antibodies, Antithyroglobulin Antibodies which attack thyroid
Toxic multinodular goitre: Nodules stimulate thyroid
De Quervain’s thyroiditis: Viral illness with fever, neck pain and tenderness –> Hyper f/u by hypo
Postpartum
Drug induced
Solitary nodule
Presentation:
anxiety; sweating; tachycardia; wt loss; fatigue; diarrhoea
Graves: Exophalmos, pretibial myxoedema, diffuse goitre
Toxic multinodular goitre: Over 50, firm nodules
Ix:
Radioisotope scan shows diffuse uptake in Graves, focal uptake in toxic multinodular goitre, low uptake in cancer
U/S used for cysts
TSH low, T3/4 high
Mx:
1) Carbimazole
2) Proylthiouracil
Radioactive iodine; propranolol; surgery
Summarise Hypothyroidism
Causes:
Hashimoto’s: Anti-TPO and antithyroglobulin Ab
Iodine deficiency
Drugs: lithium, amiodarone
Iatrogenic: Hyperthyroidism treatment
Secondary: Pituitary e.g. Sheehans, infection, tumour, radiation
Presentation: wt gain, fatigue, dry skin, coarse hair, fluid retention, irregular periods, constipation
Ix:
TSH (↑ primary ↓ secondary) and T4/3 (vice versa)
Mx:
Levothryoxine
Summarise T1DM
Pathophysiology:
Pancreas isn’t producing insulin -> Glucose cannot enter cells or be stored -> Body breaks down fatty acids instead -> ketones -> metabolic acidosis
High glucose -> draws water out of kidneys -> polyuria and dipsia
Presentation: Polyuria/dipsia, N+V, acetone breath, dehydrated, LOC
Ix:
>11 bld glucose; >3mmol blood ketones, <7.3 pH
Mx:
1L stat with 4L + K+ over 12 hrs
0.1/unit/kg/hr insulin
Monitor glucose and add dextrose if <14mmol
Monitor K+ and ketones 4hrly
Check for infections
Est patient is on long-acting insulin when stop
Long term:
Short and long acting insulin
Mx hypoglycaemia with biscuits and lucozade.
Mx CAD, stroke, htn, peripheral neuropathy, retinopathy, nephropathy, infections.
Summarise T2DM
Pathophysiology: Resistance to insulin
RF: Fhx, Wt, age, ethnicity, diet, exercise
Presentation: Polydipsia, polyuria, fatigue, wt loss, opportunisitic infections, slow healing, glucose in urine, ED
Pre-DM:
Hba1c: 42-48
Fasting glucose: 6.1-6.9
OGTT: 7.8-11.1
Mx:
Lifestyle (low glucose, high fibre diet); exercise; stop smoking; optomise CVD risk; monitor for complications
Targets:
<48mmol in new
<53 if on more than metformin
Summarise Acromegaly
Pathophysiology: Excessive GH from the anterior pituitary due to pituitary adenoma or neuroendocrine tumour
Presentation:
Bitemporal heminopia (Optic chiasm pressure - lose outer half of vision)
Headache, frontal bossing, large hands, large nose, macroglossia, protruding jaw, arthiritis, hypertrophic heart, htn, T2DM, OSA, Carpal tunnel, wide spaced teeth, prognathism
Ix:
1) IGF-1
2) OGTT whilst measuring GH as normally suppresses it
MRI for tumour
Mx:
Trans-sphenoid surgery to remove pituitary tumour.
Pegvisomant, somatostatin analogues (ocerotide), dopamine agonists (bromcriptide)
Summarise Hyperparathyroidism
Pathophysiology: PTH gland sits on thyroid, 4 of them, chief cells make PTH in resonse to hypocalcaemia.
Raises calcium –> increased osteoclasts activity, calcium absorption kidneys/ gut, vit D activity (works on GI tract)
Presentation:
“Renal stones, painful bones, abdominal thrones and psychiatric overtones”
Types:
Primary - Tumour causing PTH secretion
Secondary - Low Vit D/ CKD - low absorption –> hypocalcaemia —> PTH overreacts –> hypercalcaemia
Tertiary - Hyperplasia after secondary
Ix:
Primary: High PTH, High Ca
Secondary: High PTH, low/ normal Ca
Tertiary: High PTH, high Ca
Summarise hyperaldosteronism
Pathophysiology: Aldosterone (part of RAAS). Increase Na reabsorption and loss H+ and K+.
Causes:
Primary (Conns) - adrenal adenoma/ hyperplasia –> renin low as suppressed
Seconary - Renal artery stenosis/ HF –> Excess renin stimulated aldosterone
Ix:
Renin: aldosterone ratio
BP, Hypokalaemia, alkalosis
CT adrenals, renal doppler us for cause
Mx:
Aldosterone antagonists - eplerenone/ spironolactone
Treat cause - angioplasty for renal artery stenosis, remove tumour
Summarise SIADH
Pathophysiology: Excessive ADH causes water reabsorption at the collecting ducts –> hyonatraemia. Not enough to cause fluid overload, so is euvolaemic. The urine then becomes very concentrated (high osmalility)
Causes: Post-op Head injury Infection Neuroendocrine Drugs (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs)
Presentation:
Vague - Headache, fatigue, cramps, confused, if severe seizures and LOC
Ix:
Diagnosis of exclusion. Euvolaemic. Urine sodium and osmalility high.
Exclude Addisons, diuretics, D+V, burns, excessive fluid intake, CKD/ AKI
Mx:
Est. cause - rule out malignancy and infection with CSX
Correct sodium slowly to stop central pontine myelinolysis - <10mmol/l / 24 hr
Fluid restrict to 500ml - 1L
Vaptans (ADH blockers) - specialist use
Demeclocycline
central pontine myelinolysis: in long-term hyponatraemia brain adjusts by reducing solutes in the brain so water is balanced along BBB –> no oedema. BUT if you correct hyponatraemia too rapidly water will move out of brain into blood –> encephalopathy –> demyelination
Summarise diabetes insipidus
Pathophysiology: Lack ADH –> Urine becomes full of water, blood becomes concentrated.
Types:
Nephrogenic: Kidneys don’t respond to ADH. Due to lithium, congenital, hypokalaemia, hypercalcaemia
Cranial: No ADH produced. Due to tumours, head injury, infections, radiotherapy.
Presentation:
Polyuria, polydipsia, dehydrated, postural hypotension, hypernatraemia
Ix: Low urine osmalalilty, high serum osmalilty, water deprivation test (don’t drink, do urine osmalility. then given desmopressin aka synthetic ADH , remeasure osmalilty and see if responded to ADH - wont be able to in nephrogenic)
Mx: treat cause, desmopressin
Summarise Phaechromocytoma
Pathophysiology: tumour of adrenal gland - chromaffin cells secrete excessive adrenaline
Presentation: Occurs in bursts as adrenaline secreted by tumour in bursts. Anxious, sweaty, htn, headache, PAF
Ix: 24 hr urine catecholamines. Plasma metanephrines.
Mx: Alpha blockers (phenoxybenzamine), BB, remove tumour once sx under control to reduce anaesthetic risk
Summarise Congenital Adrenal Hyperplasia
Pathophysiology: AR deficiency in enzyme –> low aldosterone + cortisol and high androgens.
Presentation: Ambigious genitalia in females, hyponatraemia, hyperkalaemia, hypoglycaemoa, N+V, arrthymias, FTT. If mild may just have early puberty + masculine features in women, Masculine features with small testicles in men.
Skin hyperpigmentation due to high ACTH.
Mx: Relace cortisol and aldosterone with hydrocortisone and fludrocortisone. Sugery for genitals.
Summarise Androgen Insensitivty Syndrome
Pathophysiology: X linked recessive condition where cells don’t resond to androgen. Androgen is then converted to oestrogen. XY chromosome but female phenotype.
Presentation: lack male hair and muscle, infertile, no descention testes (may cause hernia), breast tissue, female external genitalia. but no female internal parts - so may be assigned female at birth but have primary amenorrhoea.
Ix:
Raised LH, Raised oestrogen.
Mx:
Bilateral orchidectomy, oestrogen therapy, vaginal surgery.
Summarise Galactorrhoea
Causes: Due to hyperprolactin NOT in pregnancy/ breastfeeding, due to: prolactinomas; hypothroid; PCOS; dopamine antagonists
Prolactinoma: Tumour pituitary gland so causes bitemp hemi + headaches.
Presentation: Milk produced from breasts; amenorrhoea; low libido; ED; gynaecomastia
Differentials: mammory duct ectasia, duct papilloma, pus from breast abscess
Ix: PREGNANCY test!!, prolactin, UE, TFT, LFT, MRI brain
Mx: Dopamine agonists e.g. bromocriptide/ cabergoline; trans-sphenoidal surgery
