Endocrinology Flashcards
Hormones from posterior pituitary and target tissue
Vasopressin - renal tubules
Oxytocin - breast and uterus
Hormones from anterior pituitary and target tissue
LH/FSH - ovaries and testis Growth hormone - lots of tissues TSH - thyroid Prolactin - breasts and gonads ACTH - adrenals to make steroids.
What is the function of the adrenal cortex
Make mineralocorticoids e.g. aldosterone, glucocorticoids e.g. cortisol and androgens e.g. DHEA
Difference between Cushing’s syndrome and Cushing’s disease
Syndrome = any cause of chronic excessive glucocorticoids. Disease = cause of excessive glucocorticoids is due to a pituitary adenoma
Causes of Cushing’s syndrome
STEROIDS USE (low ACTH) Other low ACTH, loss of negative feedback loop and hence 'ACTH-indpendent' causes = Adrenal carcinoma, adrenal nodular hyperplasia.
ACTH-dependent/high ACTH levels = Cushing’s disease/Pituitary adenoma, small cell lung cancer paraneoplastic syndrome/ectopic ACTH production.
S+S of Cushing’s syndrome
Weight gain Central obesity and moon face Proximal muscle weakness Bruises Acne Irregular menses, erectile dysfunction Mental change e.g. depression, irritability
O/E: Facial plethora, buffalo hump, supraclavicular fat pads. Hirsutism Purple striae on abdo Osteoporosis or unexplained fractures High BP Glucose intolerance/high BM.
Investigating for Cushing’s syndrome
Bloods = HbA1c, plasma ACTH levels, pregnancy test in females.
Other Lab = ∆ overnight dexamethasone suppression test (Failure to suppress cortisol <50nmol/L = +ve for Cushing’s) or 3x24hr urinary free cortisol (high). In secondary care can do a 48hr suppression test or higher-dose.
Imaging = pituitary MRI.
Mx of Cushing’s syndrome
If Cushing’s disease = transsphenoidal pituitary adenomectomy.
Stop steroids.
Metyrapone for symptomatic relief for ectopic ACTH.
Name 4 skin changes in Cushing’s
Purple striae
Easy bruising
Hirsutism
Acne
Normal cortisol level fluctuation
Diurnal - highest in morning and lowest at midnight.
Adrenal insufficiency causes
Primary adrenal insufficiency = Addison’s disease. Autoimmune destruction of adrenal cortex leading to glucocorticoids and mineralocorticoid deficiency. Primary insufficiency also caused by TB (globally most common cause!), lymphoma, adrenal mets from kidneys, breast, lung.
Secondary adrenal insufficiency = long-term steroid therapy (on withdrawal of steroids only)
S+S of Addison’s/Adrenal insufficiency
In adrenal crisis. Chronic symptoms: so vague 🤕 Fatigue Weight loss, anorexia, premature satiety. Nausea, vomiting, abdo pain, salt cravings. Muscle cramps and arthralgia Headache Polyuria and polydipsia
O/E:
Hyperpigmentation at scars, pressure points, palmar creases, mucus membranes.
Muscle weakness
Females loose pubic hair
Differentials for adrenal insufficiency
Anorexia - will have a potassium but in Addison’s its raised.
Investigating adrenal insufficiency
Primary care = MORNING serum cortisol (refer if less than 500nonomol/L, admit ASAP if less than 100), U+E (low Na, high K), BM low.
Secondary care = adrenocorticotrophic hormone stimulation test (Synacthen) which involves injection of an ACTH synthetic analogue and measuring serum cortisol. serology for 21-hydroxylase autoantibody, plasma renin (high) and aldosterone (low).
Exclusion = HbA1c.
Antibody common in Addison’s disease
21-hydroxylase autoantibody.
Management of confirmed adrenal insufficiency
Glucocorticoid replacement = hydrocortisone, prednisolone, dexamethasone. Resemble physiological release so higher dose in morning and then smaller doses at lunch and evening.
Mineralocorticoid replacement = Fludrocortisone
Safety net advise for features of an adrenal crisis. Increase steroids on sick days.
Who get Addison’s
Females on steroids
2 drugs for Addison’s
Hydrocortisone and fludrocortisone.
S+S of Addisonian crisis
Abdo pain Tachycardia Hypotensive Low grade fever Oliguria Altered mental state/confused Hx of steroid use.
Precipitated by infection, trauma, surgery, missed replacement therapy.
Ix and Mx for Addisonian crisis
A to E resuscitation. Urgent Ix = serum cortisol, serum ACTH, U+E, BM, ECG IV Hydrocortisone IV fluid bolus Monitor and ween IV to oral steroids.
Adrenal cortex haemorrhage in a meningococcal septicaemia patient
Waterhouse-Friderichsen syndrome. Rx = Ceftriaxone + IV hydrocortisone.
Diabetes Mellitus Type 1 and Type 2 pathophysiology
T1 = Deficient insulin secretion due to destruction of beta-cells in pancreatic Islets of Langerhans, majority is autoimmune destruction. T2 = Insulin resistance/insensitivity as body is unable to respond to serum insulin and relative insulin deficiency as pancreas is unable to secrete enough insulin to compensate for resistance.
RFx for Type 2 DM
Obesity Inactivity FHx Asian, African or black ethnicity. Hx of gestational diabetes. PCOS Drugs = second generation antipsychotics, corticosteroids.
Micro and Macro - vascular complications of DM and other random complications.
Macro: CVD e.g. MI, stroke/TIA, peripheral arterial disease (intermittent claudication).
Micro: retinopathy, nephropathy (hyperfiltration), neuropathy (glove and stocking).
Other: depression, infections esp UTI, increased risk of dementia.
Genetic link in T1DM
HLA D3 and HLA D4.
Clinical features of diabetes (not hypo or DKA).
Rapid weight loss Lethargy Polyuria Polydipsia FHx Poor wound healing Recurrent thrush.
How could a T1DM present acutely
DKA!!
Investigating DM
- Random plasma glucose of ≥ 11.1mmol/L.
- Fasting plasma glucose concentration ≥7.0mmol/L.
- OGTT 2hr plasma glucose concentration ≥11.1mmol/L
- HbA1c ≥48mmol/mol (6.5%).
∆ if symptomatic + either random or fasting is +ve or is asymptomatic + both random and fasting are +ve.
Other Ix = urine dipstick (+ve protein in nephrotpathy), BP, fasting lipids
When not to use HbA1c
Children and suspected type 1 DM. Pregnancy Haemolytic anaemias Haemaglobinopathies Splenectomy patients Antiretroviral drug patients. quite a few others actually
Pre-diabetes
- HbA1c 42-47mmol/mol
- Fasting glucose 6.1 – 6.9 mmol/L
- OGTT 7.8 – 11.0 mmol/L.
Lifestyle advice and monitor annually for progression to diagnostic DM.
Non-drug treatment of DM
Lifestyle advice - healthy eating (low saturated fats, low sugar, higher starchy-carbohydrates), physical exercise.
Avoid alcohol on an empty stomach, have a carbohydrate snack pre drinking.
Annual influenza vaccine.
Group eduction e.g. DESMOND, DAPHNE
Screen for complications, foot care advice.
Treatment algorithm for T2 DM
Group eduction e.g. DESMOND, DAPHNE
- Metformin - monitor renal function.
- add a sulfonylurea/DPP4 inhibitor/SGLT-2 inhibitor/ thiazolidinedione,.
- triple therapy with a combo of metformin and 2 of above.
- Insulin.
Example of a
- Sulfonylurea
- DPP4 inhibitor
- SGLT 2 inhibiro
- Thiazolidinedione
- Gliclazide.
- Sitagliptin.
- Canagliflozin.
- Pioglitazone. Risk of HF and bladder cancer.
Target HbA1c in T2DM
48mmol/mol / 6.5%.
If on sulfonyurea or combo therapy aim for 53mmol/mol / 7.0%.
How does metformin work
Biguanide. Increase insulin sensitivity and helps control weight.
SE = GI upset (titrate dose up) and renal-toxic from lactic acidosis.
Target HbA1c in T1DM
48mmol/mol or 6.5%
Management of T1DM
Safety net advice for DKA/hypo
Basal-bolus insulin regimen - long-acting insulin (detemir) at night with short-acting insulin (Novorapid) to cover meals.
Sick day rules for DM
When pt is feeling unwell may need to adjust insulin = ‘sick days rules’.
- monitor BM more frequently (3-4hrs) and titrate insulin dose accordingly.
- consider ketone monitoring.
- try and maintain normal meal pattern even if appetite is reduced.
- Well hydrated.
Diabetic retinopathy
- Non-proliferative retinopathy = microaneurysm formation, leaky capillaries, macular oedema, cotton-wool spots.
- Preproliferaive retinopathy = increased as vascular tortuosity and haemorrhages.
- Proliferative retinopathy = retinal ischaemia, neovascularisation. Can lead to glaucoma, vitreous haemorrhage, retinal detachment and blindness.
Diabetic nephropathy
- Leading cause of CKD in developed world!! 🌎
- Thickening of basement membrane, increased gaps between podocytes, hyperfiltration.
- Proteinuria, albuminuria.
- Annual early morning urine sample for albumin:creatinine ratio. If raised Rx with ACE inhibitor (ramipril).
- Monitor eGFR, esp as Metformin increases risk of lactic acidosis.
Diabetic neuropathy
- Glove and stocking distribution. test sensation with monofilament fibre, lower limb reflexes and ‘Charcot’s foot’/rocker-bottom foot.
- Nocturnal diarrhoea = autonomic neuropathy.
Diabetic foot
Peripheral artery disease + neuropathy (no pain sensation to increased mechanical stress) +/- infection.
S+S = painless punched-out ulcers in area of thick callus/infection. Rocker-bottom feet, claw toes.
May need amputation.
Main cause of death in DM
Vascular disease e.g. MI. Prophylaxis statin (QRISK score).
DKA
Excess glucose, lack of insulin to take it up into cells and be metabolised. Body turns to starvation-like state of ketoacidosis to produce energy.
= Acidosis and hyperglycaemia.
S+S = drowsy/altered mental state, vomiting, abdo pain, coma, dehydration.
Ix = ABG pH <7.3, BM >11.0mmol/L or known DM patient, ketonaemia >3mmol/L or significant ketonuria.
Mx =
1. A to E resuscitation.
2. 500ml 0.9% saline STAT.
3. Order investigations e.g. ECG, ABG, urine dipstick, BM, serum ketones, U+E, FBC, CRP, CXR.
4. Mix soluble insulin with 0.9% saline to create a solution of 1unit/mol (e.g. 50 units in 50mls) and administer to patient at 0.1units/kg/hr.
5. Continue any sub-cut insulin the patient may be prescribed.
6. Monitor BM and ketones hourly.
7. Once BM is <14mmol/L administer Glucose 10% alongside 0.9% saline to avoid hypoglycaemia.
What is also needed in DKA fluids and why
0.9% saline may need potassium adding because hyperglycaemia can lead to hypokalaemia.
What is the ‘equivalent’ of DKA for T2DM
- Hyperosmolar hyperglycaemic state.
- Less acute prevention, develops over 1 week.
- Hypovolaemia, marked hyperglycaemia, high serum osmolality (>320mosmol/kg).
- S+S = Polyuria, polydipsia, weak, weight loss, TC, dry mucous membranes, poor skin turgor, hypotensive, dehydration, hypovolaemic shock.
- Ix = Urine dipstick +++glucose and +ketones, BM high, serum osmolarity >320mmol/L, ABG normal.
- Mx = IV 0.9% saline, only give insulin if failure to respond to fluids or signs of ketoacidosis, anticoagulation as increased risk of arterial or venous embolism (LMWH)
Complication of DKA/high BM
Cerebral oedema
Hypoglycaemia
- S+S = sweating, tachycardia, seizures, aggressive.
- 10g glucose oral = 2 teaspoons of sugar, 110ml if Lucozade + carbohydrate snack e.g biscuit.
- 1mg Glucagon either sub-cut or IM
- 20% glucose infusion + good flush.
Secondary causes of DM
Cushing’s disease
Steroids
Second generation anti-psychotics
Pancreatic surgery
Subtypes of hypothyroidism and causes of hypothyroidism
- Primary hypothyroidism = Overt primary hypothyroidism TSH levels high, Free T4 low. Subclinical primary hypothyroidism = TSH high, free T3 and T4 normal.
Causes include: iodine deficiency, autoimmune/Hashimoto’s thyroiditis, post-surgery, drugs e.g. carbimazole, congenital underdeveloped thyroid gland.
-Secondary = insufficiency production of bioactive TSH due to pituitary or hypothalamic disorder.
Causes include: pituitary adenoma, Sheehan’s syndrome, gliomas, brain trauma or surgery.
Transiet thyroiditis
Subacute = de Quervain’s thyroiditis. Painful swelling of gland due to viral infection.
Postpartum thyroiditis is also transient.
S+S of hypothyroidism
Symptoms = Fatigue, weakness, arthralgia, myalgia Cold intolerance Weight GAIN Constipation Menorrhagia Low mood, poor concentration. Dry skin, sparse eye brows, brittle nails and hair. Hoarse voice
O/E = Coarse dry hair and hair loss. Eyelid oedema, ascites, puffy round face Goitre on palpation Cold hands Bradycardia Diastolic hypertension Reflexes are slow to relax
Some associated diseases with hypothyroidism
Turner's syndrome Down's syndrome Carpel Tunnel Syndrome Other autoimmune diseases e.g. DMT1, primary biliary cholangitis. Being treated for hyperthyroidism
Investigating hypothyroidism
- Serum TSH and free T4 and free T3.
- FBC
- HbA1c
- Serum lipid profile
- Serum thyroid peroxidase antibodies
Antibodies in Hashimioto’s thyroiditis
Thyroid peroxidase antibodies
Mx of hypothyroidism
If secondary = treat cause
Overt primary = Levothyroxine.
Subclinical primary = monitor TFT, if TSH >10 but FT4 is normal then can start treatment with Levothyroxine.
Myxoedema coma
S+S = hypothermia, hyporeflexia, low BM, bradycardia, hypotension, cyanosis, ileus/GI obstruction coma.
Mx = will need ITU. A-E resuscitation. High-flow oxygen. Correct hypoglycaemia if present. Warming blankets.
- SLOW IV T3 (liothyronine)
- IV hydrocortisone.
Ix to order = ABG, TSH high low FT4 and FT3, FBC (anaemia), BM, high CK, U+E (low Na)
Diffuse goitre ∆∆
Grave’s disease
Hashimoto’s thyroiditis
Nodular goitre ∆∆
Adenoma
Carcinoma
Toxic multinodular goitre
Painful goitre ∆∆
de Quervain’s transient thyroiditis.
Causes of hyperthyroidism
Grave’s disease = anti-TSH IgG autoantibodies stimulate TSH and cause thyroid enlargement and increased T3 production.
Toxic multinodular goitre = benign follicular adenomas, seen in elderly and iodine deficient.
Toxic adenoma
Ectopic thyroid tissue associated with cancers
Drugs = iodine, amiodarone, IV contrast.
RFx for hyperthyroidism
MORE COMMON IN FEMALES
Smoking = increased adenoma risk and Grave’s disease.
FHx = Grave’s disease
Hx of autoimmune diseases e.g. DMT1
S+S of hyperthyroidism
Malaise Insomnia, anxiety Palpitations Exercise intolerance Heat intolerance or excessive sweating Increased appetite + weight LOSS Diarrhoea Oligo/A -menorrhoea
O/E: Fine tremor Warm moist skin and palmar erythema Tachycardia, AF, HF. Goitre on palpation Proximal myopathy Brisk reflexes
Signs only really seen in Grave’s disease
- Thyroid acropachy = onycholysis, clubbing, swollen fingers.
- Eye signs = mostly asymmetrical, increased tear production, decreased acuity, diplopia, lid lag, lid retraction, ophthalmoplegia, exophthalmos, gritty eyes, loss of colour vision, conjunctival oedema.
- Pretibial myxoedema
Investigating hyperthyroidism
TSH - low, FT4 and FT3 raised in overt hyperthyroidism but can be normal in subclinical. Increased ESR in thyroiditis Increased Calcium Increased LFT Thyroid USS Radionuclide thyroid uptake scan
TSH autoantibody for Grave’s disease.
CT/MRI if eye signs present.
Management of hyperthyroidism
- Beta-blockers - symptomatic treatment (propranolol).
- Antithyroid meds - carbimazole (FBC as can cause agranulocytosis), in pregnancy use propylthiouracil.
- Radioiodine to kill thyroid cells, can cause hypothyroidism.
- Thyroidectomy, can nick parathyroid so do U+E to check calcium.
Complications of
- hypothyroidism
- hyperthyroidism
- Coronary heart disease, heart failure, reduced fertility, angina.
- AF, heart failure, osteoporosis, pregnancy problems e.g. miscarriage, vision loss.
Thyrotoxic storm
S+S = Pyrexia, agitation, tachycardia, hypertensive, AF, acute abdo pain, D+V, confusion, jaundice, coma.
Mx = A-E resuscitations, IV fluids, anti-emetic/NG tube, cooling/fan, paracetamol.
- Propranolol (unless CV unstable/asthmatic).
- Carbimazole + Lugol’s iodine (give this 4hrs post carbimazole)
- Hydrocortisone (prevents peripheral conversion of T4 to T3).
Ix = TSH, free T4 and T3. Exclude differentials (sepsis 6).
Precipitants for a thyrotoxic storm or myeodema coma
Thyroid surgery, infection, MI, trauma, stroke.
Function of parathyroid horome
- Secreted in response to low serum calcium.
- Effects mainly at bones, kidneys and small intestine.
- Promotes synthesis of active vitamin D, increases calcium reabsorption, reduction in phosphate reabsorption in kidneys.
- Release of calcium and phosphate from bones via osteoclasts and resorption of bones.
- Active vit D increases calcium absorption in small intestine.
Types of hyperparathyroidism and their causes
Primary = abnormal parathyroid gland. Adenoma, hyperplasia of parathyroid gland. Secondary = Compensatory over secretion of PTH in response to pathologically caused low serum calcium. Chronic renal failure, vitamin D deficiency. Tertiary = continued high PTH after resolution of the precipitating condition of secondary hyperparathyroidism.
S+S of hyperparathyroidism
- Hypercalciaemia = boney pain, depressed, polyuria, polydipsia, renal calculi, abdo pain, muscle cramps, memory loss.
- Osteoporosis/osteopenia
- Hypertension
- FHx or symptoms of MEN-1.
Who gets primary hyperparathyroidism
Females over the age of 50 with a FHx
Could be in lithium treatment.
Post-menopause
Extreme osteoporosis in hyperparathyroidism complication
Osteitis fibrosa cystica - salt and pepper pot skull.
Investigating hyperparathyroidism
- Serum total calcium and calculation of corrected calcium with albumin.
- 25-hydroxyvitamin D level
- Serum PTH levels
- Serum phosphorus levels
- Urine calcium
- LFT (raised ALP in bone activity)
- Non contrast CT for renal calculi.
- DEXA bone mineral density. Skull x-ray = pepper pot.
- Parathyroid and neck USS.
- Secondary cause. If secondary blood results may show low 21-hydroxy vit D, low calcium, high phosphorus, high PTH
- Tertiary = High PTH, high Ca, high PO4
Management of hyperparathyroidism
PRIMARY = Vit D supplements e.g. calciferol, bisphosphonate e.g. alendronic acid, Cinacalcet, good fluid intake.
If no target organ damage and no indications for surgery then annual monitoring (DEXA, serum calcium and creatinine), if indications for surgery (e.g. over 50, CKD, serum calcium >1mg/dL above normal range, renal calculi) then parathyroidectomy.
SECONDARY = treat cause, if low vit D = UV radiation exposure, vitamin D supplements (calciferol), calcium supplement.
TERTIARY = cinacalcet, parathyroidectomy.
What drug, used in hyperparathyroidism, lowers serum calcium and serum PTH.
Cinacalcet.
Complications of hyperparathyroidism
Osteoporosis and bone fractures.
Recurrent laryngeal nerve injury post-parathyroidectomy = hoarse voice.
Post-parathyroidectomy hypoparathyroidism.
Nephrolithiasis.
Types and causes of hypoparathyroidism
- Primary = parathyroid gland failure
- Secondary = post parathyroidectomy, radiation
- Pseudohypoparathyroidism = target cells unresponsive to PTH, genetic cause.
- Pseudopseudohypoparathyroidism = phenotype of psuedohypoparathyroidism but normal biochemistry, genetic cause.
S+S of hypoPTH
Hypocalcaemia: Anxious Diarrhoea and malabsorption Muscle cramps and twitches Numbness, tingling and paraesthesia Poor memory and slowed thinking Brittle, dry hair.
O/E:
+ve Chvostek’s sign (tap fail nerve and ipsilateral upper lip twitches)
+ve Trousseau’s sign (pain and carpel spasm when BP cuff is inflated above pt’s systolic BP).
Irregular HR, tachycardia
Cataracts
Investigations for hypoPTH
Serum total and corrected calcium (low)
Serum parathyroid hormone (low, unless pseudo where it is high)
Phosphorus (high)
25-hydroxy vitamin D, urine calcium, magnesium (low in secondary)
ECG = long QT interval in hypocalcaemia.
Management of hypoPTH
- Calcium, if severe symptoms = IV calcium gluconate, otherwise oral calcium carbonate.
- Calcitriol in primary hypoPTH.
- Consider magnesium replacement in secondary hypoPTH.
Describe a hereditary tumour syndrome
- Multiple endocrine neoplasia.
- Type 1 and 2 are autosomal dominant.
- Genes include MEN1 (associated with type 1) and RET porto-oncogene (associated with type 2).
- MEN type 1 commonly has parathyroid adenomas (hyperparathyroidism!!!!), pituitary adenomas, CNS tumours, neuroendocrine or carcinoid tumours, lipomas and some others.
- MEN type 2 (Sipple’s syndrome) commonly have thyroid cancer, pheochromocytoma, Hirschsprung’s, multi parathyroid adenomas. Prophylactic thyroidectomy in childhood.
Causes of hypercalcaemia
Hyperparathyroidism Ectopic PTH from squamous cell lung cancer Bony metastasis Phaemochromocytoma Calciferol and vitamin D supplements Thiazide diruetics Granulomatous diseases e.g. TB, sarcoidosis. Familial hypocalciuric hypercalcaemia
Clinical features of hypercalcaemia
Polyuria and polydipsia Anorexia Constipation Confusion, depression, poor memory Renal calculi/nephrolithiasis Peptic ulcers Muscle weakness Renal impairment Short QT interval on ECG
Management of acute hypercalcaemia
Ix = adjusted calcium (+albumin), PTH, phosphate, U+E.
- High Ca and high PTH = primary or tertiary hyperparathyroidism.
- High Ca and low PTH = malignancy or other rarer causes
Mx =
- 0.9% saline 500Ml STAT
- IV bisphosphonate e.g. Zoledronic acid.
- get endocrine help
S+S of hypocalcaemia
Digital paraesthesia
+ve Chvostek’s sign (tap fail nerve and ipsilateral upper lip twitches)
+ve Trousseau’s sign (pain and carpel spasm when BP cuff is inflated above pt’s systolic BP).
Prolonged QT interval on ECG
Most common cause is hypoparathyroidism. Also can be due to post parathyroidectomy, magnesium deficiency, large blood transfusion, pancreatitis, rhabdomyolysis
Ix and mx for severe hypocalcaemia
Ix = Adjusted serum calcium (+albumin), Phosphate, PTH, U+E, Vitamin D, Magnesum.
Mx =
- IV calcium gluconate in 5% dextrose.
Causes of decreased anterior pituitary hormone secretions
- From hypothalamus = Kallman’s syndrome, hypothalamic ischaemia, meningitis, CNS TB.
- From pituitary stalk = Trauma to stalk, surgical complication.
- From pituitary gland itself = adenoma, inflammation, autoimmunity, ischaemia (apoplexy, Sheehan’s, DIC).
S+S of hypopituitarism according to hormone.
Growth hormone = central obesity, dry wrinkly skin, weakness, poor balance, decreased exercise tolerance, hypoglycaemia, osteoporosis.
FHS/LH = oligo/a menorrhoea, infertility, low libido, erectile dysfunction, low muscle bulk.
TSH = constipation, depression, cold intolerance, weight loss, bradycardia.
ACTH = hyperpigmentation of skin, weight loss, anorexia, depression.
Prolactin = absent lactation post-partum.
Can get functional pituitary adenomas which secrete a hormone and cause Cushing’s, prolactinaemia, acromegaly.
Headache from raised ICP. Visual field defects in pituitary adenomas compressing on optic chasm.
Investigating hypopituitarism
Basal test = Morning cortisol and ACTH levels, TFT, Morning testosterone, LH and FSH, Serum prolactinSerum IGF-1 (low). U+E
Dynamic test = Short Synacthen test, dexamethasone suppression test.
MRI scan to look for lesion or tumour.
Management of hypopituitarism
Treat cause.
If adenoma = transphenoidal adenoectomy.
If apoplexy = IV hydrocortisone (emergency so do A-E stuff too).
Hormone replacement = levothyroxine, corticosteroids recombinant human growth factor, COCP.
Pituitary adenomas.
Headache
Bilateral temporal hemianopia due to optic chiasm compression.
Diabetes insipidus.
S+S of hypopituitarism.
Ix = MRI, screening hormone level test (Synacthen, ACTH, IGF-1 etc etc) Mx = steroids + levothyroxine, trans-sphenoidal surgery + hormone replacement.
Visual field defect seen in pituitary adenoma
Bilateral temporal hemianopia.
Most common functional pituitary adenoma and Mx
Prolactinoma. Increase prolactin - decrease LH and FSH, decrease osegotren and testosterone.
Headache and bitemporal hemianopia from compressing meningitis and optic chiasm.
Females = amenorrhoea, weight gain, low libido, dry vagina, osteoporosis form low oestrogen.
Males = gynaecomastia, erectile dysfunction, loss of facial hair, presents later in life.
Mx = dopamine agonist e.g. Cabergoline.
Severe headache, nausea + vomiting, third nerve palsy (down and out pupil, ptosis), low visual acuity and bi-temporal hemianopia, fever, neck stiffness, reduced consciousness ∆∆
Pituitary apoplexy = haemorrhage and infarction of pituitary gland tumour.
Differentals = SAH, meningitis, carvernous sinus thrombosis.
Urgent Ix = U+E, FBC, renal function, LFT, clotting profile.
Mx = IM hydrocortisone bolus.
Excessive growth hormone disease and clinical features.
Acromegaly due to pituitary somatotroph adenoma.
S+S =
- symptoms of pituitary tumour (headache, bi-temporal hemianopia).
- enlarged hands and feet, frontal bossing, thickened nose, coarse facial features.
- macroglossia = OSA.
- darker, thickened oily skin, increased sweating.
- arthralgia as bones over-grow, jaw pain.
- acroparesthesia in extremities.
- glucose intolerance.
- carpel tunnel syndrome
- Fatigue, hypertension, hepatomegaly, cardiomegaly, increased appetite.
Ix for acromegaly
Bloods = Serum IGF-1, random serum growth hormone (can be raised in other conditions and secretion is pulsatile), OGTT (growth hormone decreases with insulin release to glucose), raised calcium, raised phosphorus.
Imaging = MRI of pituitary, echocardiogram, ECG.
Visual field testing
Managing acromegaly
Trans-spenoidal surgery to remove tumour.
1. Somatostatin analogues
2. Dopamine agonist
Monitor for complications (BP, ECG, BM).
Complications of acromegaly
Carpel tunnel syndrome Increased risk of colon cancer Obstructive sleep apnoea Diabetes mellitus Cardiac = arrhythmias, LV hypertrophy, ischaemic heart disease. HTN
Disorder of hyperaldosterone
Primary = excess production due to hyperplasia of adrenal zone glomerulosa = Conn’s syndrome.
Secondary = excess RAAS activation e.g. renal artery stenosis, ectopic renin production from tumour.
S+S = asymptomatic.
- Symptoms of hypertension = fatigue, headache, polyuria, polydipsia.
- Symptoms of low potassium and high sodium = mood disturbance, paraesthesia, muscle cramps and weakness, palpitations.
- Metabolic alkalosis.
Ix = U+E (low K, high Na), Aldosterone: renin ratio (low renin, high aldosterone, ratio >30ish), fludrocortisone suppression test (no decrease), CT of adrenal glands, adrenal vein sampling.
Mx = Spironolactone. Adrenalectomy in Conn’s.
Tumour causing excessive adrenaline
Phaeochromocytoma. Tumour of the chromaffin cells in adrenal medulla that secretes unregulated and excessive amounts of adrenaline.
Episodic headache, sweating, tachycardia.
Also get palpitations, angina, faints, dizziness, tremor, numbness, anxiety, confusion, D+V, sweats and flushes and loads and loads of symptoms.
Ix = 24hr urine catecholamines, plasma free metanephrines. Abdo CT. Rx = alpha blockade and adrenalectomy.
ECG of hyperkalaemia
Tall, tented T waves
Broad QRS complex
Prolonged PR interval
Flattening and progressive loss of P waves
Bradycardia, AV block.
Sine wave pattern = NEED TO INTERVENE THIS IS BAD, death is imminent.
S+S of hyperkalaemia and causes
Causes = CKD, AKI, adrenal insufficiency, rhabdomyolysis, potassium-sparing diuretics, mannitol, metabolic acidosis, hyperglycaemia. S+S = hypertension, depressed tendon reflexes, flaccid paralysis, fatigue and weak, palpitations
Action of vasopressin
Bonds to V2 receptor and inserts aquarporin 2 into luminal membrane of distal convoluted tubule and collecting duct. Increases water resorption.
Condition where body is unable to concentrate urine
Diabetes insipidus. Large amounts of urine which is not concentrated.
Causes of diabetes insipidus
Deficiency of vasopressin (cranial DI) = defected ADH gene, Craniopharyngiomas, trauma to pituitary stalk, haemorrhage, CNS infection, autoimmune hypophysitis.
Resistance to vasopressin (nephrogenic DI) = hypokalaemia, hypercalcaemia, lithium, CKD.
S+S of diabetes insipidus
Polydipsia and chronic thirst
Polyuria, nocturia - more than 3L/day
Dehydration
S+S of hypernatraemia = lethargy, weak, confused.
Ix for diabetes insipidus
Plasma and urine osmolality, urine:plasma.
24hr urine volume
U+E, serum calcium, serum glucose.
∆ Water deprivation test and desmopressin trial. Cranial DI: >50% increase in urine osmolality following desmopressin. Nephrogenic DI: no or <50% increase in urine osmolality following desmopressin.
MRI of pituitary.
Mx of diabetes insipidus
Cranial DI = desmopressin.
Nephrogenic = review medications, ensure adequate hydration in response to thirst, sodium restriction or use drugs such as thiazide diuretics to lower sodium.
Syndrome of inappropriate ADH secretion pathology, causes and presentation.
Causes = CNS (stroke, haemorrhage, infection, trauma), Malignancies (SCLC secretion), drugs (carbamazepine, SSRI), pulmonary (pneumonia, TB, resp failure), hereditary. S+S = hyponatraemia and low CSF osmolality. Nausea, vomiting, malaise, headache, seizures, coma.
Complication of rapid correction of low sodium
Central pontine myelinolysis.
Heart failure
No more than 10mmol/L per 24hrs.
ECG of hypokalemia
T wave invertion
Elevated U wave
Long QT
DM with need to control HTN
ACE inhibitor e.g. ramipril.
Indicated with evidence of micro-vascular disease
Aim 130/80
Ix for SIADH
- Rule out adrenal insufficiency with short synacthen test.
- Serum U+E - euvolaemic hyponatraemia. Serum osmolality - low.
- Urine sodium and urine osmolality both high.
- Identify cause e.g. CXR, medication review.
- Renal function, LFT, BM.
- Ensure examination has no signs of dehydration (must be euvolaemic hyponatraemia!).
Mx for SIADH
- Correct low sodium SLOWLY (change of less than 10mmol/L per 24hrs). If acute can uses hypertonic saline e.g. 3%NaCl.
- Fluid restrict, furosemide.
- ADH receptor blockers e.g. Tolvaptan (need 6hrly sodium levels).
Actions of aldosterone
Mineralocorticoid.
Increase sodium reabsorption from the distal tubule.
Increase potassium secretion from the distal tubule.
Increase hydrogen secretion from the collecting ducts.
What hormone prevents prolactin secretion
Dopamine
breathing in DKA
Kassmauls - eliminate acid.
Drug for CKD induced hyperparathyroidism
Sevelamer = non-calcium based phosphate binder = reduces hyperphosphataemia..
Changes in blood and vessels due to hyperglycaemia
change in blood flow: microthrombus and occlusion.
change in blood composition: increased viscosity and platelet aggregation.
change in blood vessel wall: loss of anti-thrombotic nature of epithelium.
