Endocrinology

Question 1

WHO diagnostic criteria for DM

Answer 1

If symptomatic: fasting glucose >=7.0mmol/L or random glucose >=11.1mmol/L

If asymptomatic the above criteria must be demonstrated on two separate occasions

OR:
HbA1c >= 6.5% (48) is diagnostic
HbA1c 6-6.5% ?prediabetes
HbA1c <6.0% DM excluded

Question 2

Side effects of insulin and MoA

Answer 2

Hypoglyaemia, weight gain, lipodystrophy (alternate injection sites)
Beta blockes reduce hypoglycaemic awareness

MoA: Glucose utilisation and glycogen synthesis, Inhibits lipolysis, Reduces muscle protein loss, Increases cellular uptake of K+ (NaKATPase)

Question 3

Side effects of metformin and mechanism of action

Answer 3

GI upset, lactic acidosis, cant use in eGFR <30

MoA: Increases insulin sensitivity, and decreases hepatic gluconeogenesis

Question 4

Side effects of sulfonylureas (gliclazide) and MoA

Answer 4

Hypoglycaemia, weight gain, hyponatraemia

MoA: Stimulates pancreatic beta cells to secrete insulin

Question 5

Side effects of thiazolidinediones (pioglitazone)

Answer 5

Weight gain, fluid retention (Contraindicated in HF)

Question 6

Side effects of SGLT-2 inhibitors (-gliflozins) and MoA

Answer 6

UTI, weight loss

MoA: Inhibits reabsorption of glucose in the kidney (hence UTI as a side effect)

Question 7

Side effects of GLP-1 agonists

Answer 7

N+V, pancreatitis, weight loss

Question 8

Management of T2DM

Answer 8

Lifestyle modification first.
Metformin first line drug.
If HbA1c still >7.5% (58), add a gliptin or sulfonylurea or pioglitazone or SGLT-2 inhibitor (dual therapy)
If still >7.5% (58) add another of the above drugs (triple therapy)
If still not effective use insulin.
Or:
If triple therapy not effective, not tolerated or if contraindicated AND BMI >35 do metformin + sulfonylurea + GLP-1 mimetic (eg. exenatide)

Question 9

Guidelines for monitoring T1DM

Answer 9

Check HbA1c every 3-6m, target <6.5%
Self monitor at least 4 times/day (before each meal and before bed) - monitor more if ill, having hypoglycaemic episodes, sport, pregnancy
Target 5-7mmol/L on waking and 4-7mmol/L before meals/other times of the day

Question 10

Management of T1DM

Answer 10

Multiple daily injection basal-bolus insulin regimen:
twice-daily insulin detemir is regime of choice, with rapid-acting insulin before meals (novorapid)

Consider adding metformin if BMI >= 25

Question 11

T2DM risk factor modification

Answer 11

BP: target <140/80 (or <130/80 if end-organ damage), ACE-i first line regardless of age

QRISK2 >10% (10year cardiovascular risk of >10%) should be offered 20mg atorvastatin OD (primary prevention)
If secondary prevention (known IHD/PAD) give atorvastatin 80mg OD

Question 12

Sick day rules in DM

Answer 12

Check BMs at least every 4 hours, drink at least 3L in 24h,  if unable to eat then drink sugary drinks, pt's should be able to check Ketone levels
Continue oral hypoglycaemics even if not eating (stress response increases BMs) - possible exception is metformin (risk of dehydration -> lactic acidosis -> AKI)
Continue insulin (risk of DKA if stopped)

Question 13

Presentation of diabetic foot disease

Answer 13

neuropathy: loss of sensation
Ischaemia: absent foot pulses, reduced ABPI, intermittent claudication
Calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene

Question 14

Diabetic foot disease sceening

Answer 14

At least annually. Palpate for both dorsalis pedis pulse and posterior tibial artery pulse
Use a 10g monofilament on various parts of the sole to check sensation

Question 15

DKA diagnostic criteria

Answer 15

Glucose >11 or known DM
pH <7.3
Bicarb <15
Ketones >3 or urine ketones ++

Question 16

Management of DKA

Answer 16

Fluid replacement (approx 6-8L dehydrated)

Correct hypokalaemia - 1L 0.9% NaCl over first hour and then add KCl into subsequent bags
If K >5.5 in first 24hr dont add KCl into bags
If K 3.5-5.5 add 40mmol/L into bags
If K <3.5 seek senior help

IV fixed rate insulin: 0.1unit/kg/hr
When glucose <15 add 5% dextrose infusion

Long acting insulin should be continued, short acting insulin should be stopped

Question 17

Complications of DKA

Answer 17

Gastric stasis
VTE
Arrhythmias (hyperkalaemia, hypokalaemia)
Iatrogenic complications due to fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia)
ARDS
AKI

Question 18

Cerebral oedema and DKA

Answer 18

Due to IV fluid therapy too much too quickly
Children/young adults most vulnerable - 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology
Usually 4-12hrs following commencement of treatment
CT head and senior review
Mannitol or hypertonic saline

Question 19

DM and DVLA

Answer 19

If on insulin/sulfonylureas, pt can drive as long as: not had severe hypoglycaemia in prev 12m, driver has full hypoglycaemic awareness, regular BM monitoring at least BD and at times relevent to driving, no other debarring complications of DM

No need to inform DVLA if on tablets that don’t induce hypoglycaemia, or if diet-controlled DM

Question 20

Hyperosmolar hyperglycaemic state

• at risk population group
• where are they managed
• clinical features

Answer 20

Typically presents in the elderly with T2DM
Medical emergency - managed in HDU or ITU
Osmotic diuresis, severe dehydration, electrolyte deficiencies
Clinical features: fatigue, lethargy, N+V, altered consciousness, headaches, papilloedema, weakness, hyperviscosity (MI, stroke, peripheral artery thrombosis), dehydration, hypotnesion, tachycardia

Question 21

Complications of hyperosmolar hyperglycaemic state

Answer 21

MI, stroke, peripheral artery thrombosis

Less common: seizures, cerebral oedema, central pontine myelinolysis

Question 22

Pathophysiology of hyperosmolar hyperglycaemic state

Answer 22

Hyperglycaemia results in osmotic diuresis with associated loss of Na and K
Severe vol depletion -> raised serum osmolarity (>320mosmol/kg) -> serum hyperviscosity

Question 23

Diagnosis of hyperosmolar hyperglycaemic state

Answer 23

Hypovolaemia
Marked hyperglycaemia (>30) without significant ketones or acidosis
Significantly raised serum osmolarity (>320mosm/kg)

Question 24

Management of hyperosmolar hyperglycaemic state

Answer 24

Normalise osmolality gradually, replace fluids and electrolytes, normalise blood glucose gradually

Fluid losses estimated to be 100-220ml/kg (7-16L in 70Kg)
IV 0.9% saline is first line (rate depends on patient and comorbidities) - aim to replace 50% of losses in first 12hrs and the remaining in the next 12h

Vigorous fluid replacement alone will result in gradual decline in plasma glucose and serum osmolarity

Insulin should NOT be used because rapid decline in glucose may be harmful

Question 25

Causes of hypoglycaemia

Answer 25

Insulinoma Self administration of insulin/sulphonylureas Liver failure Addisons disease Alcohol Nesidioblastosis in children (beta cell hypertrophy)

Question 26

Insulinoma features - what is it - clinical features

Answer 26

Most common pancreatic endocrine tumour (islets of langerhans) Hypoglycaemia early in the morning or just before meal Rapid weight gain high insulin, raised proinsulin:insulin ratio High C peptide

Question 27

Diagnosis and treatment of insulinoma

Answer 27

Supervised, prolonged fasting (up to 72 hours) - hypoglycaemia and increased plasma insulin CT pancreas Treatment: surgical excision (diazoxide and somatostatin if not eligible for surgery)

Question 28

Clinical features of thyrotoxicosis

Answer 28

Symptoms: diarrhoea, weight loss, increased appetite, swear, heat intolerance, palpitations, tremor, irritability, anxiety, oligomenorrhoea/infertility Signs: tachycardia/AF, warm moist skin, fine tremor, palmar erythema, thin hair, lid lag, lid retraction

Question 29

Causes of thyrotoxicosis

Answer 29

Graves, toxic nodular goitre, toxic adenoma, ectopic thyroid tissue, exogenous (levothyroxine overdose), acute phase of subacute (De Quervain's) thyroiditis, amiodarone

Question 30

Investigations of thyrotoxicosis

Answer 30

``` TSH down, T4 and T3 up Thyroid autoantibodies (anti-thyroid peroxidase antibodies, TSH receptor autoantibodies, thyroglobulin autoantibodies) ```

Question 31

Treatment of thyrotoxicosis

Answer 31

Beta blockers for rapid control of symptoms Carbimazole (SE: agranulocytosis, get urgent FBC if sore throat/infection) Radioiodone Thyroidectomy - risk of damage to recurrent laryngeal nerve (hoarseness) and hypoparathyroidism. Pt will become hypothyroid so levothyroxine required

Question 32

Features of thyroid eye disease

Answer 32

Exophthalmos, conjunctival oedema, optic disc swelling, ophthalmoplegia Inability to close the eyelids -> sore dry eyes -> exposure keratopathy NO SPECS 0. No signs or symptoms 1. Ocular irritation (dryness, FB sensation) 2. Soft tissue involvement (conjunctival chemosis/oedema) 3. Proptosis (exophthalmos) 4. Extraocular muscle fibrosis 5. Corneal exposure and ulceration if severe 6. Sight loss (due to corneal ulceration, compressive optic neuropathy or ↑ IOP)

Question 33

Management of thyroid eye disease

Answer 33

topical lubricants, steroids, radiotherapy, surgery | Smoking is the most important risk factor (stop smoking to prevent TED)

Question 34

TFT results for - thyrotoxicosis - primary hypothyroidism - secondary hypothyroidism - sick euthyroid syndrome - subclinical hypothyroidism - poor compliance with thyroxine - steroid therapy

Answer 34

- thyrotoxicosis: TSH low free T4 high - primary hypothyroidism: TSH high free T4 low - secondary hypothyroidism: TSH low free T4 low - sick euthyroid syndrome: TSH low free T4 low - subclinical hypothyroidism: TSH high free T4 normal - poor compliance with thyroxine: TSH high free T4 low - steroid therapy: TSH low free T4 normal

Question 35

Graves disease features

Answer 35

Commonest cause of thyrotoxicosis Typically seen in women aged 30-50y TSH receptor stimulating autoantibodies, and anti-thyroid peroxidase autoantibodies Typical features of thyrotoxicosis, plus: exophthalmos, ophthalmoplegia, pretibial myxoedema, thyroid acropachy

Question 36

Clinical features of thyroid storm

Answer 36

Fever >38.5, tachycardia, confusion, agitation, N+V, HTN, HF, abnormal LFTs (jaundice)

Question 37

Primary vs secondary vs congenital hypothyroidism

Answer 37

Primary - problem with the thyroid gland (eg. autoimmune disease affecting thyroid tissue) Secondary - disorder of the pituitary gland or lesion compressing pituitary Congenital - thyroid dysgenesis or thyroid dyshormonogenesis

Question 38

Clinical features of hypothyroidism

Answer 38

Weight gain, lethargy, cold intolerance, dry/cold/yellowish skin, non-pitting oedema, dry/coarse hair, constipation, menorrhagia, decreased deep tendon reflexes, carpal tunnel syndrome

Question 39

Subacute (DeQuervains) thyroiditis - precipitating event - investigations - management

Answer 39

- Following a viral infection - Ix: thyroid scintigraphy (globally reduced uptake of iodine-131) - Mx: usually self-limiting, thyroid pain may respond to aspirin/NSAIDs, steroids if severe or is hypothyroidism develops

Question 40

Causes of primary and secondary hypothyroidism

Answer 40

Primary: Hashimotos (Most common. Autoimmune. Women more common), DeQuervains thyroiditis, Riedel thyroiditis, after thyroidectomy/radioiodine, drug therapy (lithium, amiodarone, carbimazole), dietary iodine deficiency Secondary: Down's, Turner's, coeliac, pituitary failure (compression from external features or from pituitary itself)

Question 41

Management of hypothyroidism

Answer 41

Levothyroxine Check TFTs 8-12wks after thyroxine dose change Therapeutic goal is normalisation of TSH (0.5-2.5) Increase levothyroxine by 25-50mcg in pt who becomes pregnant (monitor carefully)

Question 42

Side effects and interactions of levothyroxine

Answer 42

SE: hyperthyroidism, reduced bone mineral density, worsening angina, AF Interactions: iron and calcium carbonate -> reduce absorption of levothyroxine (give at least 4 hours apart)

Question 43

Congenital hypothyroidism - risks if not diagnosed - features - screening

Answer 43

If not diagnosed and treated within first four weeks it causes irreversible cognitive impairment Features: prolonged neonatal jaundice, delayed mental and physical milestones, short stature, puffy face, macroglossia, hypotonia Children are screened at 5-7 days using heel prick test

Question 44

Actions of PTH

Answer 44

Released in response to hypocalcaemia Acts on the bone to increase osteoclast activity -> bone releases calcium and phosphate into the blood Acts at the kidney to increase calcium reabsorption and increase phosphate excretion Also acts at the kidney to increase hydroxylation and activation of Vit D -> vit D then acts to increase calcium absorption from the intestine

Question 45

What is the difference between PTH and PTHrp

Answer 45

PTHrp has all the same effects as PTH however it cannot activate vitamin D

Question 46

Primary vs secondary vs tertiary vs malignant hyperparathyroidism (calcium and PTH levels)

Answer 46

Primary: increased calcium levels and increased PTH levels. Secondary: reduced calcium levels and increased PTH levels. Tertiary: increased calcium, significantly increased PTH. Malignant: increased calcium, and reduced PTH (PTHrp is not detected in PTH assay)

Question 47

Primary hyperparathyroidism - causes - presentation - tests - treatment

Answer 47

Causes: adenoma, hyperplasia, parathyroid cancer Presentation: often asymptomatic, detected with hypercalcaemia on routine tests Other signs/sx: tiredness, weakness, depression, pancreatitis, ulcers, bone pain, fractures, osteopenia/osteoporosis, dehydration, renal stones, abdo pain, thirsty, HTN Tests: increased calcium and PTH, reduced phosphate, increased ALP (bone activity), 24hr urinary calcium increased. Technetium-MIBI subtraction scan X-ray may show pepperpot skull. Check BP. Treatment: total parathyroidectomy is definitive Mx. Cinacalcet (calcimimetic) offered if surgery inappropriate (increased sensitivity of parathyroid cells to Ca)

Question 48

Secondary hyperparathyroidism - causes - treatment

Answer 48

Causes: reduced vit D intake, CKD. hypocalcaemia leads to excessive secretion of PTH Treatment: correct cause. Phosphate binders, vit D, cinacalcet, parathyroidectomy

Question 49

Tertiary hyperparathyroidism | -causes

Answer 49

Causes: occurs after prolonged secondary hyperparathyroidism, causing glands to become hyperplastic and release PTH regardless of calcium levels -> increased calcium, significantly increased PTH. Often seen in CKD.

Question 50

Cancers releasing PTH-rp

Answer 50

Squamous cell lung cancers Breast cancers Renal cell carcinomas

Question 51

Primary hypoparathyroidism - causes - presentation - tests - treatment

Answer 51

-causes: autoimmune gland failure, congenital (Di George) -presentation: hypocalcaemia, cramps, perioral numbness, Trousseau's sign (carpopedal spasm), Chvostek sign -tests: low calcium, high phosphate (or normal), normal ALP, low PTH Treatment: calcium supplements + calcitriol -tests

Question 52

Secondary hypoparathyroidism causes

Answer 52

Radiation, surgery (thyroidectomy, parathyroidectomy), hypomagnesaemia (Mg required for PTH secretion)

Question 53

Pseudohypoparathyroidism vs pseudopseudohypoparathyroidism

Answer 53

pseudo: Failure of target cells to respond to PTH. Short metacarpals, round face, short stature, calcified basal ganglia. pseudopseudo: morphological features of pseudo but with normal biochemistry

Question 54

Multiple endocrine neoplasia type 1 vs type 2a vs type 2b associated features (3Ps, 2Ps, 1P)

Answer 54

MEN1: hyperparathyroidism, pituitary tumours, pancreatic tumours (insulinoma, gastrinoma). Most common presentation is hypercalcaemia MEN2a: hyperparathyroidism, phaeochromocytoma (also medullary thyroid cancer) MEN2b: phaeochromocytoma (also medullary thyroid cancer and neuromas) MEN1 gene is a tumour suppressor gene, MEN2 gene is a proto-oncogene

Question 55

Cortisol negative feedback

Answer 55

Corticotropin releasing factor released from hypothalamus -> stimulates ACTH secretion from pituitary -> stimulates glucocorticoid (cortisol) production and androgen production by adrenal cortex

Question 56

Causes of Cushing's syndrome

Answer 56

``` Oral steroids Cushings disease (pituitary adenoma -> increased ACTH) Ectopic ACTH (SCLC, carcinoid tumours) Adrenal adenoma/hyperplasia McCune-Albright syndrome ```

Question 57

Signs and symptoms of Cushings syndrome

Answer 57

Symptoms: weight gain, mood change (depression, irritability, psychosis), hirsutism, irregular menses, erectile dysfunction, acne, proximal weakness, recurrent achilles rupture Signs: central obesity, plethoric, moon face, buffalo hump, supraclavicular fat distribution, skin and muscle atrophy, bruises, purple striae, osteoporosis, hypertension, hyperglycaemia, infections, poor healing Signs of a cause (eg. abdo mass)

Question 58

Cushings syndrome investigations

Answer 58

Overnight dexamethasone suppression test (dex 1mg PO at midnight, serum cortisol measured at 8am) Normal: suppressed cortisol Cushings syndrome due to oral steroids: cortisol not suppressed by low dose dex Cushings disease: cortisol not suppressed by low dose dex, but suppressed by high dose dex Ectopic ACTH: not suppressed by low or high dose dex 24hr urinary free cortisol Other results: Hypokalaemic metabolic alkalosis Impaired glucose tolerance HTN

Question 59

Treatment of Cushings syndrome

Answer 59

- treat underlying cause - cushings disease: remove pituitary adenoma (trans-sphenoidally) - adrenalectomy

Question 60

What is addison's disease

Answer 60

Primary adrenocortical insufficiency, caused by destruction of adrenal cortex leading to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency

Question 61

Clinical features of addisons disease

Answer 61

lethargy, weakness, anorexia, N+V, weight loss, salt craving, hyperpigmentation of palmar creases, vitilligo, loss of pubic hair in women, low BP, hypoglycaemia, hyponatraemia, hyperkalaemia

Question 62

Causes of hypoadrenalism

Answer 62

``` Addisons disease TB Mets Meningococcal septicaemia HIV Antiphospholipid syndrome Pituitary disorders (tumour, irradiation, infiltration) -> secondary hypoadrenalism Long term exogenous gluocorticoid therapy ```

Question 63

Investigations for addisons disease

Answer 63

Synacthen test: plasma cortisol measures before and 30 mins after giving synthetic ACTH. No reponse in addisons because the ACTH has no where to act (due to adrenal destruction). Alternative: 9am serum cortisol (low in addisons but not diagnostic) Other results: hyperkalaemia, hyponatraemia, hypoglycaemia, met acidosis, hypercalcaemia, uraemia, anaemia, eosinophilia

Question 64

Treatment and follow up for addisons disease

Answer 64

A combination of hydrocortisone and fludrocortisone (PO) Wear a steroid bracelet Add 5-10mg hydrocortisone before exercise Double steroids in illness Follow up: yearly BP, yearly U+E, watch for other autoimmune diseases

Question 65

Addisonian crisis - causes - presentation - management

Answer 65

Causes: sepsis, surgery, adrenal haemorrhage, steroid withdrawal Presentation: shock (tachycardia, hypotension, vasoconstriction, oliguria, weak, confused, comatose), hypoglycaemia Management: hydrocortisone 100mg IM/IV, normal saline fluid boluses or with dextrose if hypoglycaemia, continue hydrocortisone 6 hourly until patient is stable Convert to oral after 24 hours and reduce back to maintenance over 3-4 days

Question 66

Causes of primary hyperaldosteronism

Answer 66

Conn's syndrome (adrenal adenoma) | Bilateral idiopathic adrenal hyperplasia

Question 67

Clinical features of primary hyperaldosteronism

Answer 67

Hypertension Hypokalaemia (muscle weakness, cramps, paraesthesia, polyuria, polydipsia) Alkalosis

Question 68

Investigations for primary hyperaldosteronism

Answer 68

First-line: plasma aldosterone/renin ratio (high aldosterone alongside low renin = diagnosis) High resolution CT abdomen and adrenal vein sampling used to differentiate between unilateral and bilateral sources of aldosterone excess

Question 69

Management of primary hyperaldosteronism

Answer 69

Adrenal adenoma: surgery | Bilateral adrenocortical hyperplasia: aldosterone antagonist (spironolactone)

Question 70

Phaeochromocytoma - what is it - associations - features - tests - management

Answer 70

- Rare catecholamine secreting tumour - 10% are familial, associated with MEN type 2, neurofibromatosis, and von Hippel-Lindau syndrome - Features: HTN, headaches, palpitations, sweating, anxiety - tests: 24hr urinary colection of metanephrines, and CT abdo - Mx: surgery is definitive, but pt should be medically stabilised first with alpha blocker (phenoxybenzamine) followed by a beta blocker (propranolol)

Question 71

Features of Klinefelters

Answer 71

``` Primary hypogonadism (47XXY) Tall Small, firm testes Lack of secondary sexual characteristics Infertile Gynaecomastia Elevated gonadotrophin levels but low testosterone ``` Diagnosed by karyotype

Question 72

Kallmann's syndrome

Answer 72

``` Secondary hypogonadism (hypogonadotrophic hypogonadism) X-linked recessive (males) Lack of smell Delayed puberty Hypogonadism Sex hormones low LH and FSH levels inappropriately low/normal normal/above average height ``` Cleft lip/palate and visual/hearing defects may be seen

Question 73

Congenital adrenal hyperplasia - inheritance pattern - what is it

Answer 73

A group of autosomal recessive disorders affecting adrenal steroid biosynthesis Different types: 21-hydroxylase deficiency (90%), 11-beta hydroxylate deficiency, 17-hydroxylase deficiency CAH affects adrenal steroid biosynthesis -> in response to resultant low cortisol levels the anterior pituitary secretes high levels of ACTH -> adrenal androgen production -> virilisation in females and precocious puberty in males

Question 74

Indications, administration and side effects of GH therapy

Answer 74

Indications: proven GH deficiency, Turners, Prader-Willi, chronic renal insufficiency before puberty Administration: SC SE: headache, benign intracranial HTN, fluid retention

Question 75

Acromegaly causes

Answer 75

Excess GH secondary to a pituitary adenoma (95% of cases), or due to ectopic GHRH or GH production by tumours (eg. pancreatic tumour)

Question 76

Acromegaly features

Answer 76

Coarse facial appearance, spade like hands, increased shoe size, large tongue, prognathism (jaw protrusion), interdental spaces, excessive sweating, oily skin, raised prolactin (galactorrhoea) Pituitary tumour features (hypopituitarism, headache, bitemporal hemianopia) Some patients also have MEN-1

Question 77

Complications of acromegaly

Answer 77

HTN, diabetes, cardiomyopathy, colorectal cancer

Question 78

Acromegaly investigations

Answer 78

Serum IGF-1 levels are first-line (raised in acromegaly) If IGF-1 levels are raised, diagnosis can then be confirmed by doing OGTT test (GH should be suppressed in hyperglycaemia, in acromegaly there is no suppression of GH following OGTT) (IGF-1 = insulin-like growth factor 1) Pituitary MRI may show a pituitary tumour

Question 79

Acromegaly management

Answer 79

Trans-sphenoidal surgery is first-line in majority of patients Somatostatin analogue (octreotide) inhibits release of GH (may be used as surgery adjunct) Dopamine agonists (bromocriptine) effective in some patients

Question 80

Pituitary adenoma investigations

Answer 80

Pituitary blood profile (GH, prolactin, ACTH, FH, LSH, TFTs) Formal visual field testing MRI brain with contrast there are different types of pituitary adenomas - prolactinoma is the most common, followed by non-secreting adenomas

Question 81

Pituitary adenoma DDx

Answer 81

Pituitary hyperplasia, craniopharyngioma, meningioma, brain mets, lymphoma, hypophysitis, vascular malformation (eg. aneurysm)

Question 82

Management of pituitary adenoma

Answer 82

Hormonal: bromocriptine/dopamine agonist (first line for prolactinoma), octreotide/somatostatin analogue Surgery (trans-sphenoidal transnasal hypophysectomy) Radiotherapy

Question 83

Features of excess prolactin in men vs. women

Answer 83

Men: impotence, loss of libido, galactorrhoea Women: amenorrhoea, galactorrhoea

Question 84

Causes of raised prolactin

Answer 84

Prolactinoma, pregnancy, oestrogens, physiological (stress, exercise, sleep), acromegaly, PCOS, primary hypothyroidism Drugs: metoclopramide, domperidone, phenothiazines, haloperidol, SSRI, opioids Dopamine inhibits prolactin release, therefore dopamine antagonists promote prolactin secretion

Question 85

Side effects of glucocorticoids

Answer 85

- Head: insomnia, mania, depression, psychosis, intracranial HTN - Eyes: glaucoma, cataracts - Blood/immuno: neutrophilia, immunosuppression (infections, reactivation of TB) - MSK: growth suppression in children, osteoporosis, proximal myopathy, avascular necrosis of femoral head - GI: peptic ulcer, acute pancreatitis - Endocrine: DM, weight gain, hirsutism, hyperlipidaemia, Cushing's syndrome

Question 86

nephrogenic vs cranial diabetes insipidus - causes of nephrogenic - causes of cranial

Answer 86

Passage of large volumes of dilute urine due to impaired water absorption by the kidney, because of: Nephrogenic: impaired response of the kidney to ADH -causes: inherited, hypokalaemia, hypercalcaemia, lithium, demeclocycline, CKD, post-obstructive uropathy Cranial: reduced ADH secretion from the posterior pituitary -causes: idiopathic, congenital, tumour, mets, trauma, hypophysectomy, sarcoidosis, haemorrhage, meningoencephalitis

Question 87

Symptoms of diabetes insipidus

Answer 87

polyuria, polydipsia, dehydration, hypernatraemia

Question 88

Tests for diabetes insipidus

Answer 88

U+E (hypernatraemia, hypokalaemia), hypercalcaemia, glucose (exclude DM), serum and urine osmolalities Diagnosis: 8-hour water deprivation test (no drink for 8 hours -> measure urine osmolality -> should increase in the presence of dehydration, but doesnt if DI) Can then differentiate between cranial and nephrogenic by giving desmopressin at the end of the 8 hours -> if osmolality then increases (=cranial), if it doesnt (=nephrogenic)

Question 89

Management of diabetes insipidus

Answer 89

Cranial: desmopressin (synthetic ADH) Nephrogenic: treat cause. If it persists trial bendroflumethiazide