Endocrinology

Question 1

Pathophysiology of T1DM

Answer 1

autoimmune destruction of β-cells → absolute

insulin deficiency.

Question 2

Pathophysiology of T2DM

Answer 2

insulin resistance and β-cell dysfunction → relative insulin deficiency

Question 3

Presenting symptoms of diabetes mellitus

Answer 3

polyuria, polydipsia, ↓wt, lethargy

• T1DM - DKA

Question 4

Diagnosis of DM

Answer 4

Symptoms and 1 abnormal result
Fasting ≥7mM
Random ≥11.1mM
HbA1c ≥ 6.5% (T2DM)

Or 2 results at different times

Question 5

Secondary causes of DM

Answer 5

 Drugs: steroids, anti-HIV, atypical neuroletics, thiazides
 Pancreatic: CF, chronic pancreatitis, HH, pancreatic Ca
 Endo: Phaeo, Cushings, Acromegaly, T4
 Other: glycogen storage diseases

Question 6

Define Metabolic Syndrome

Answer 6

Central obesity (↑ waist circumference) and two of:  ↑ Triglycerides
 ↓ HDL
 HTN
 Hyperglycaemia: DM, IGT, IFG

Question 7

Lifestyle Modifications in DM

Answer 7

Diet - healthy, reduced refined CHO, avoid alcohol 
Exercise
Lipids (T2 - >40 - statin)
ABP - <130/80
Aspirin >50y/o
Yearly/6m check up 
- control, complications, competency, coping
Smoking cessation

Question 8

Examination for DM complications

Answer 8

Macro
Pulses
 BP
 Cardiac auscultation
Micro
 Fundoscopy
 ACR + U+Es
 Sensory testing plus foot inspection

Question 9

Medical management of T2DM

Answer 9

1) Metformin
2) + sulphonylura/Gliptin/ Pioglitazone
3) + another
4) + insulin

Question 10

Metformin - action, SE and CI

Answer 10

↑ cells sensitivity to insulin
SE - diarrhoea, abdo pain, vitamin b12 deficiency, lactic acidosis
CI - GFR<30, tissue hypoxia (sepsis, MI)

Question 11

Sulphonylureas - example action and SE

Answer 11

Gliclazide
↑ insulin release from β-cells

SE - weight gain, GI disturbances, ↑ risk hypoglycaemia

Question 12

Pioglitazone - Action and SE

Answer 12

binding PPAR- γ- upregulates genes that affect glucose and lipid metabolism
SE - weight gain, oedema, liver dysfunction, effects on bone metabolism

Question 13

Gliptins - example, action and SE

Answer 13

Sitagliptin - protect native GLP-1 from inactivation by DPP-4
SE - GI

Question 14

Sodium – Glucose Co-transporter 2 inhibitors - example, action and SE

Answer 14

Dapagliflozin - Inhibit SGLT2 (PT) in kidney- decrease glucose reabsorption.

SE - weight loss, Low risk of hypoglycaemia, polyuria and lower UTIs/ Thrush/Urosepsis

Question 15

Common Insulin Regimes

Answer 15

Biphasic - Twice daily pre-mixed

• Mixed intermediate and rapid acting insulin BD - before breakfast and dinner
• regular lifestyle: children, older pts.

Basal-Bolus Regime

• Bedtime long-acting + short acting before each meal
• allowing flexible lifestyle

Question 16

Insulin requirements when ill

Answer 16

Insulin requirements usually ↑ (even if food intake ↓)
 Maintain calories (e.g. milk)
 Check BMs ≥4hrly and test for ketonuria
 ↑ insulin dose if glucose rising

if in hospital and NBM - variable rate insulin infusion (check capillary blood glucose every 1-2 hours)
- stop when eating and drinking and and long acting insulin

Question 17

SE of Insulin

Answer 17

 Hypoglycaemia
- At risk: EtOH binge, β-B (mask symptoms), elderly
 Lipohypertrophy
- Rotate injection site: abdomen, thighs
 Wt. gain in T2DM

Question 18

Macrovascular DM complications and Rx

Answer 18

 MI: May be “silent” due to autonomic neuropathy
 PVD: claudication, foot ulcers
 CVA

Rx: Manage CV risk factors
 BP (aim <130/80)
 Smoking
 Lipids
 HBA1c <6%
- regular fundoscopy, foot check

Question 19

Features of diabetic feet

Answer 19

ISCHAEMIA
 Critical toes
 Absent pulses (do ABPI)
 Ulcers: painful, punched-out, foot margins, pressure
points

NEUROPATHY
 Loss of protective sensation
 Deformity: Charcot’s joints, pes cavus, claw toes
 Injury or infection over pressure points
 Ulcers: painless, punched-out, metatarsal heads, calcaneum

Question 20

Management of diabetic feet

Answer 20

Conservative
 Daily foot inspection (e.g. ̄c mirror)
 Comfortable / therapeutic shoes
 Regular chiropody (remove callus)

Medical
 Rx infection: benpen + fluclox ± metronidazole

Surgical
 Abscess or deep infection 
 Spreading cellulitis
 Gangrene
 Suppurative arthritis

Question 21

Pathophysiology of nephropathy in DM

Answer 21

Hyperglycaemia → nephron loss and glomerulosclerosis

Question 22

Features of nephropathy in DM

Answer 22

 Microalbuminuria: urine albumin:Cr (ACR) ≥30mg/mM
 If present → ACEi / ARA
 Refer if UCR >70

Question 23

Pathogenesis of retinopathy in DM

Answer 23

 Microvascular disease → retinal ischaemia → ↑VEGF

 ↑ VEGF → new vessel formation

Question 24

Presentation of retinopathy of DM

Answer 24

 Retinopathy and maculopathy
 Cataracts
 Rubeosis iris: new vessels on iris → glaucoma
 CN palsies

Question 25

Stages of Diabetic retinopathy

Answer 25

Background Retinopathy  Dots: microaneurysms  Blot haemorrhages  Hard exudates: yellow lipid patches Pre-proliferative Retinopathy  Cotton-wool spots (retinal infarcts)  Venous beading  Haemorrhages Proliferative Retinopathy  New vessels  Pre-retinal or vitreous haemorrhage Maculopathy  ↓ acuity may be only sign  Hard exudates w/i one disc width of macula

Question 26

Pathophysiology of neuropathy

Answer 26

 Metabolic: glycosylation, ROS, sorbitol accumulation |  Ischaemia: loss of vasa nervorum

Question 27

Features of polyneuropathy in DM

Answer 27

 Glove and stocking: length-dependent ( feet 1st)  Loss of all modalities  Absent ankle jerks  Numbness, tingling, pain (worse @ night)

Question 28

Treatment of polyneuropathy of DM

Answer 28

 Paracetamol  Amitriptyline, Gabapentin, SSRI  Capsaicin cream  Baclofen

Question 29

Pathogenesis of DKA

Answer 29

Ketogenesis  ↓ insulin → ↑ stress hormones and ↑ glucagon  → ↓ glucose utilisation + ↑ fat β-oxidation  ↑ fatty acids → ↑ ATP + generation of ketone bodies. Dehydration  ↓ insulin → ↓ glucose utilisation + ↑ gluconeogenesis → severe hyperglycaemia  → osmotic diuresis → dehydration  Also, ↑ ketones → vomiting Acidosis  Dehydration → renal perfusion  Hyperkalaemia

Question 30

Precipitants of DKA

Answer 30

 Infection / stress ± stopping insulin  New T1DM  Alcohol

Question 31

Presentation of DKA

Answer 31

```  Abdo pain + vomiting  Gradual drowsiness/ confusion  Sighing “Kussmaul” hyperventilation  Dehydration  Ketotic breath ```

Question 32

Diagnosis of DKA

Answer 32

 Acidosis (↑AG): pH <7.3 (± HCO3 <15mM)  Hyperglycaemia: ≥11.1mM (or known DM)  Ketonaemia: ≥3mM (≥2+ on dipstix)

Question 33

Investigations for DKA

Answer 33

```  Urine: ketones and glucose, MCS  Cap glucose and ketones  VBG: acidosis + ↑K  Bloods: U+E, FBC, glucose, cultures  CXR: evidence of infection ```

Question 34

Treatment of DKA

Answer 34

- Fluids - Potassium replacement (if <5.5) - Insulin Infusion (actrapid) - 1 unit/kg/hr +- catheter; NGT; LMWH; find and treat precipitating factors

Question 35

Aims with DKA treatment

Answer 35

 ↓ ketones by ≥0.5mM/h or ↑HCO3 by ≥3mM/h  ↓ plasma glucose by ≥3mM/h  Maintain K in normal range  Avoid hypoglycaemia

Question 36

Resolution of DKA

Answer 36

 Ketones <0.3mM + venous pH>7.3 (HCO3 >18mM)  Transfer to sliding scale if not eating  Transfer to SC insulin when eating and drinking  Pt Education and action plan

Question 37

Hyperglycaemic Hyperosmolar State presentation

Answer 37

``` Usually T2DM, often new presentation  Usually older  Long hx (e.g. 1wk)  Marked dehydration and glucose >30mM/L  No acidosis (no ketogenesis)  Osmolality >320mosmol/kg ```

Question 38

Complications of HHS

Answer 38

Occlusive events are common: DVT, stroke, leg ischaemia | - Give LMWH

Question 39

Management of HHS

Answer 39

```  Rehydrate --> 0.9% NS over 48h - May need ~9L  Wait 1h before starting insulin - It may not be needed - Start low to avoid rapid changes in osmolality --> E.g. 1-3u/hr (to avoid cerebral oedema)  Look for precipitant - MI - Infection - Bowel infarct ```

Question 40

Symptoms of hypoglycaemia

Answer 40

``` Autonomic: 2.5-3  Sweating  Anxiety  Hunger  Tremor  Palpitations ``` ``` Neuroglycopenic: <2.5  Confusion  Drowsiness  Seizures  Personality change  Focal neurology (e.g. CN3)  Coma (<2.2) ```

Question 41

Causes of hypoglycaemia

Answer 41

 Usually insulin or sulfonylurea Rx in a known diabetic  Exercise, missed meal, OD  Exogenous drugs  Pituitary insufficiency  Liver failure  Addison’s  Islet cell tumours (insulinomas)  Immune (insulin receptor Abs: Hodgkin’s)  Non-pancreatic neoplasms: e.g. fibrosarcomas

Question 42

Investigations of hypoglycaemia

Answer 42

 72h fast ̄c monitoring |  Symptom: Glucose, insulin, C-peptide, ketones

Question 43

Management of hypoglycaemia

Answer 43

Conscious and able to help self --> Rapid acting: lucozade or 5-7 glucose tablets Conscious but unable to help self --> Dextrogel - wait 15 min and check; can repeat up to 3x If corrected then give long acting snack (toast) Unconscious (GET SENIOR HELP)and IV access --> 20% glucose 75ml in 15min (can repeat) Unconscious and no Iv access --> IM 1g Glucagon If responded long acting snack After snack check CBG in 30-60 mins then refer for hypoglycaemic education. Monitor CBG for 24-48 hours.

Question 44

Thyrotoxicosis symptoms

Answer 44

```  Diarrhoea  ↑ appetite but ↓ wt.  Sweats, heat intolerance  Palpitations  Tremor  Irritability  Oligomenorrhoea ± infertility ```

Question 45

Thyrotoxicosis signs

Answer 45

``` Hands  Fast / irregular pulse  Warm, moist skin  Fine tremor  Palmer erythema Face  Thin hair  Lid lag  Lid retraction Neck  Goitre or nodules Graves’ Specific  Ophthalmopathy  Exophthalmos  Ophthalmoplegia: esp. up-gaze palsy  Eye discomfort and grittiness  Photophobia and ↓ acuity  Chemosis  Dermopathy: pre-tibial myxoedema  Thyroid acropachy ```

Question 46

Investigations for thyrotoxicosis

Answer 46

```  ↓TSH, ↑T4/↑T3  Abs: TSH receptor, TPO  ↑Ca, ↑LFTs  Isotope scan  ↑ in Graves’  ↓ in thyroiditis  Ophthalmopathy: acuity, fields, movement ```

Question 47

Management of thyrotoxicosis

Answer 47

Medical  Symptomatic: β-B (e.g. propranolol 40mg/6h)  Anti-thyroid: carbimazole (inhibits TPO)  Titrate according to TFTs or block and replace  In Graves’ Rx for 12-18mo then withdraw  ~50% relapse → surgery or radioiodine  SE: agranulocytosis Radiological: Radio-iodine  Most become hypothyroid  CI: pregnancy, lactation Surgical: Thyroidectomy  Recurrent laryngeal N. damage → hoarseness  Hypoparathyroidism  Hypothyroidism

Question 48

Features of thyroid storm

Answer 48

```  ↑temp  Agitation, confusion, coma  Tachycardia, AF  Acute abdomen  Heart failure ```

Question 49

Precipitants of thyroid storm

Answer 49

 Recent thyroid surgery or radio-iodine  Infection  MI  Trauma

Question 50

Management of thryoid storm

Answer 50

1. Fluid resuscitation + NGT 2. Bloods: TFTs + cultures if infection suspected 3. Propranolol PO/IV (counteracts peripheral effects of t3/4) 4. Carbimazole 5. Hydrocortisone (I. thyroid hormone synthesis) 6. Rx cause (e.g. Abx) 6. no change in 24h > thyroidectomy

Question 51

Signs of hypothyroidism

Answer 51

```  Bradycardic  Reflexes relax slowly  Ataxia  Dry hair and skin  Yawning (lethargy)  Cold hands  Ascites and Myxoedema  Round Puffy face  Depression and mental slowing  Intolerant to cold  Appetite ↓; ↑wt ``` ``` Other:  Constipation  Menorrhagia  CTS  Goitre  Myopathy, neuropathy ```

Question 52

Causes of hypothyroidism

Answer 52

Primary  Atrophic thyroiditis (commonest UK)  Hashimoto’s thyroiditis  Subacute thyroiditis (e.g. post-partum)  Post De Quervain’s thyroiditis  Iodine deficiency (commonest worldwide)  Drugs: carbimazole, amiodarone, lithium  Congenital: thyroid agenesis Post-surgical  Thyroidectomy  Radioiodine Secondary  Hypopituitarism (v. rare )

Question 53

Investigations for hypothyroidism

Answer 53

```  ↑TSH, ↓T3/T4  ↑MCV ± normochromic anaemia  ↑ triglyceride + ↑ cholesterol  Hyponatraemia (SIADH)  ↑ CK if assoc. myopathy  Abs: TPO, TSH ```

Question 54

Management of hypothyroidism

Answer 54

 Levothyroxine - Titrate to normalise TSH - Enzyme inducers ↑ thyroxine metabolism 0 Clinical improvement takes ~2wks  Check for other AI disease: e.g. Addison’s, PA

Question 55

Features of hashimoto's thyroiditis

Answer 55

 TPO +ve  Atrophy + regeneration → goitre  May go through initial thyrotoxicosis phase  May be euthyroid or hypothyoid

Question 56

Features of myxoedema coma

Answer 56

```  Looks hypothyroid  Hypothermia  Hypoglycaemia  Heart failure: bradycardia and ↓BP  Coma and seizures ```

Question 57

Precipitants of myxoedema coma

Answer 57

 Radioiodine  Thyroidectomy  Pituitary surgery  Infection, trauma, MI, stroke

Question 58

Management of myxoedema coma

Answer 58

 Bloods: TFTs, FBC, U+E, glucose, cortisol  Correct any hypoglycaemia  T3/T4 IV slowly (may ppt. myocardial ischaemia)  Hydrocortisone 100mg IV  Rx hypothermia and heart failure

Question 59

Complications of thyroid surgery

Answer 59

- haematoma - laryngeal oedema - recurrent laryneal nerve palsy - hypoparathyroidism - thyroid storm - hypothyroidism

Question 60

Features of cushing

Answer 60

``` Cataracts Ulcers Striae/ thin skin Hypertension/ Hirsutidsm Immunosuppresion/ INfection Necrosis of femoral head Glucose high Osteoporosis, obesity Impaired wound healing and bruising Depression ``` - Moon face and thin limbs - Proximal myopathy - Acne - hypokalaemia Interscapular and supraclavicular fat pad

Question 61

Causes of Cushing's

Answer 61

ACTH Independent causes - Iatrogenic steroids - Adrenal adenoma/ Ca - Adrenal nodular hyperplasia ACTH - dependent causes - Cushing's disease - Ectopic ATCH

Question 62

Ix for Cushings

Answer 62

1) 24h urinary free cortisol x 3 2) Dexamethosone suppression test - Suppression at high dose - cushing's disease (bilateral hyperplasia from ACTH secreting pituitary tumour) > MRI pituitary - No suppression - Adrenal cause/ Ectopic ACTH > CT thorax/ adrenals +- DEXA scan

Question 63

Treatment for Cushing's

Answer 63

- Iatrogenic steroids --> stop meds - Adrenal adenoma/ adrenal nodular hyperplasia --> adrenelectomy - Ectopic ACTH - - tumour excision +- metyropone - Cushing's disease - transphenoidal excision

Question 64

What is Nelson's syndrome

Answer 64

Rapid enlargement of a pituitary adenoma i fhave cushing disease following bilateral adrenelectomy

Question 65

Physical effects of Cushing's disease

Answer 65

- Bitemporal hemianopia (compresses optic chiasm) - hypopituitarism and hyperprrolactinaemia (compresses stalk and removes I) - Headache and double vision (invades cavernous sinus) - -> opthalmoplegia, Chemosis, Proptosis, Horners, CN sensory loss

Question 66

Features of Hyperaldosteronism

Answer 66

 Hypokalaemia: weakness, hypotonia, hyporeflexia, cramps  Paraesthesia  ↑BP

Question 67

Causes of hyperaldosteronism

Answer 67

PRIMARY  Bilateral adrenal hyperplasia (70%)  Adrenocortical adenoma (30%): Conn’s syndrome ``` SECONDARY  RAS  Diuretics  CCF  Hepatic failure  Nephrotic syndrome ```

Question 68

Treatment of hyperaldosteronism

Answer 68

 Conn’s: laparoscopic adrenelectomy  Hyperplasia: spironolactone, eplerenone or amiloride Ix

Question 69

Actions of Angiotensin 2

Answer 69

- ↑ADH (thirst centre and CD in kidney) - ↑ sympathetic activity - ↑ NAdr - ↑ Aldosteone = ↑ Na + Cl reabsorption + H20+K excretion - Arteriolar vasoconstriction - ↑ BP

Question 70

Pathophysiology of Addison's Disease

Answer 70

Destruction of adrenal cortex → glucocorticoid and mineralocorticoid deficiency

Question 71

Causes of Addison's

Answer 71

```  Autoimmune destruction: 80% in the UK  TB: commonest worldwide  Metastasis: lung, breast, kidneys  Haemorrhage: Waterhouse-Friedrichson  Congenital: CAH ```

Question 72

Clinical features of Addison's

Answer 72

```  Wt. loss + anorexia  n/v, abdo pain, diarrhoea/constipation  Lethargy, depression  Hyperpigmentation: buccal mucosa, palmer creases  Postural hypotension → dizziness, faints  Dry mouth and reduced skin turgor  Hypoglycaemia  Vitiligo  Addisonian crisis  Sparse axillary and pubic hair ```

Question 73

Symptoms of Addison's

Answer 73

Tired - fatigue and weakness Tanned - hyperpigmentation Tearful - apathy and depression Thin - weight loss/ n+v+d/ anorexia +/- abdo pain

Question 74

Investigations for Addison'

Answer 74

Bloods - ↓Na/↑K (as ↓ mineralocorticoid) ↓glucose (↓ cortisol); ↓Ca, (+- uraemia - dehydration)  Anaemia Differential  Short synACTHen test - Cortisol before and after tetracosactide (should stimulate adrenals to produce cortisol) - Exclude Addison’s if ↑ cortisol; ↑ 9am ACTH (usually low) ``` Other  21-hydroxylase Abs: +ve 80% AI  Plasma renin and aldosterone  CXR: evidence of TB  AXR: adrenal calcification  CT/MRI of adrenals ```

Question 75

Treatment of Addison's

Answer 75

Replace  Hydrocortisone  Fludrocortisone - emergency hydrocortisone injectino kit Advice  Don’t stop steroids suddenly  ↑ steroids during intercurrent illness, injury  Wear a medic-alert bracelet and steroid card F/up  Watch for AI disease e.g. pernicious anaemia  yearly BP/ UE

Question 76

Causes of secondary adrenal insufficiency

Answer 76

hypothalamo or pituitary failure  Chronic steroid use → suppression of HPA axis  Pituitary apoplexy / Sheehan’s  Pituitary microadenoma - No pigmentation as low ACTH

Question 77

Presentation of an Addisonian Crisis

Answer 77

 Shocked: ↑HR, postural drop, oliguria, confused  Hypoglycaemia Usually known Addisonian or chronic steroid user

Question 78

Precipitants of an Addisonian Crisis

Answer 78

 Infection  Trauma  Surgery  Stopping long-term steroids

Question 79

Management of an Addisonian Crisis

Answer 79

```  Bloods: cortisol, ACTH, U+E, cultures  ECG - ↑ K+  Check CBG: glucose may be needed  Hydrocortisone 100mg IV/IM 6hrly - oral after 72h and ween off dose  IV fluid bolus  Septic screen  Treat underlying cause ```

Question 80

What is a pheochromocytoma

Answer 80

Catecholamine-producing tumours arising from sympathetic paraganglia Usually found in adrenal medulla Extra-adrenal phaeo’s found by aortic bifurcation

Question 81

Presentation of a pheochromocytoma

Answer 81

Triad: episodic headache, sweating and tachycardia ```  ↑BP, palpitations  Headache, tremor, dizziness  Anxiety  d/v, abdo pain  Heat intolerance, flushes ``` May have precipitant  Straining, abdo palpation  Exercise, stress  β-B, IV contrast, TCAs, GA

Question 82

Investigations for pheochromocytoma

Answer 82

 Plasma + 24h urine metadrenaline and normetadrenaline  Also vanillylmandelic acid  Abdo CT/MRI  MIBG (mete-iodobenzylguanidine) scan

Question 83

Management of pheo

Answer 83

Medical: Chemo or radiolabelled MIGB Surgery: adrenelectomy  α-blocker first, then β-blockade pre-op  Avoids unopposed α-adrenergic stimulation  Phenoxybenzamine = α-blocker Monitor BP post-op for ↓↓BP and 24hr urine 2 weeks post up follow up is lifelong

Question 84

Hypertensive crisis features

Answer 84

``` Pallor Pulsating headache Feeling of impending doom ↑↑BP ↑ ST and cardiogenic shock ```

Question 85

Management of a hypertensive crisis

Answer 85

Phentolamine 2-5mg IV (α-blocker) or labetalol 50mg IV - Repeat to safe BP (e.g. 110 diastolic) Then α-blocker PO with elective surgery 4-6 weeks latere

Question 86

Causes of raised prolactin

Answer 86

``` Pregnancy Prolactinoma Physiological PCOS Primary hypothyroidism Pheothiazine/ metochlopramide ```

Question 87

Symptoms of hyperprolactinaemia

Answer 87

``` High PRL --> ↓ LH/FSH  Amenorrhoea  Infertility  Galactorrhoea  ↓ libido  ED  Mass effects from prolactinoma - headache; bitemporal hemianopia; CN 3,4,5,6 palsy; DI; CSF rhinorrhoea ```

Question 88

Treatment of hyperprolactinaemia

Answer 88

prolactinoma (Prolactin 100,000 iU/L) --> treated medically (dopamine agonist e.g. bromocryptine) Non-functioning adenoma (Prolactin 1,500 iU/L) --> treated surgically transphenotelectomy (or if visual/ pressure symptoms)

Question 89

Causes of Acromegaly

Answer 89

 Pituitary acidophil adenoma in 99% |  Hyperplasia from GHRH secreting carcinoid tumour

Question 90

Symptoms of Acromegaly

Answer 90

```  Acroparaesthesia  Amenorrhoea, ↓libido  Headache  Snoring  Sweating  Arthralgia, back ache  Carpal tunnel (50%)  Change in shoe size ```

Question 91

Signs of Acromegaly

Answer 91

``` Hands  Spade-like  Thenar wasting  Boggy sweaty palms (if active)  ↑ skin fold thickness  Carpal tunnel: ↓ sensation + thenar wasting ``` ``` Face  Prominent supraorbital ridges  Scalp folds: cutis verticis gyrata  Coarse face, wide nose and big ears  Prognathism/ Macrognathia  Macroglossia  Widely-spaced teeth  Goitre  Hirsutism ``` ``` Other  Puffy, oily, darkened skin skin  Acanthosis Nigricans  Tolling gait with bowed legs  Proximal weakness + arthropathy  Pituitary mass effects: bitemporal hemianopia ```

Question 92

Investigations for Acromegaly

Answer 92

- GH response to OGTT (failure to suppress GH) - MRI pituitary - Plasma IGF1 Blood - TSH+T4, prolactin, FSH + LH, GH - Visual fields and acuity

Question 93

Treatment of acromegaly

Answer 93

1st line: trans-sphenoidal excision 2nd line: re – octreotide 3rd line: GH antagonist – pegvisomant 4th line: radiotherapy

Question 94

Effects of GH on the body

Answer 94

Direct - carbohydrate metabolism - ↑ blood glucose - Fat metabolism - ↑ breakdown and release Indirect - -> LIVER --> IGF1 - ↑ cartilage formation & skeletal growth - ↑ protein synthesis, cell growth + proliferation

Question 95

Complications of Acromegaly

Answer 95

 Impaired glucose tolerance (40%)  DM (15%)  ↑BP  LVH/ HF Cardiomyopathy  ↑ IHD and ↑ stroke  ↑ risk of CRC

Question 96

Symptoms of Diabetes Insipidus

Answer 96

 Polyuria  Polydipsia  Dehydration  Hypernatraemia: lethargy, thirst, confusion, coma

Question 97

Causes of DI

Answer 97

``` Cranial - inadequate ADH secretion  Idiopathic: 50%  Congenital: DIDMOAD / Wolfram Syndrome  Tumours  Trauma  Vascular: haemorrhage (Sheehan’s syn.)  Infection: meningoencephalitis  Infiltration: sarcoidosis ``` ``` Nephrogenic - failure of kidneys to respond to ADH  Congenital  Metabolic: ↓K, ↑Ca  Drugs: Li, demecleocycline, vaptans  Post-obstructive uropathy ```

Question 98

Investigations for DI

Answer 98

Bloods: U+E, Ca, glucose  Urine and plasma osmolality - Exclude DI if U:P osmolality >2 - Water deprivation test +/- desmopressin trial

Question 99

Management for DI

Answer 99

If mild (3-4L) - no treatment Cranial- Find cause: MRI brain and Desmopressin PO (SE - hyponatraemia and worsen myocardial ischaemia) Nephrogenic - Treat cause +- bendroflumethiazide

Question 100

Causes of Hirsutism

Answer 100

- familial - idiopathic - increased androgens (PCOS; Cushings; Adrenal Ca; Steroids)

Question 101

Causes of gynaecomastia

Answer 101

- Cirrhosis - Hypogonadism - Hyperthyroidism - Hypopituitary - oestrogen/ HCG - producing tumour - Drugs - spiro/ oestrogen

Question 102

Causes of erectile dysfunction

Answer 102

- smoking - alcohol - DM - Endo - hypogonadism, hyperthyroidism - Neuro - MS; autonomic neuropathy; cord lesion - Pelvic surgery - bladder; prostate - Peyronie's disease