Endocrine Flashcards

Question

What are the appropriate investigations for adrenal insufficiency?

Answer 1

Definite investigation is ACTH stimulation (synACTHen) test 9am serum cortisol may also be helpful

Answer 2

> 500 nmol/l makes Addison’s very unlikely < 100 nmol/l is definitely abnormal 100-500 nmol/l should prompt a ACTH stimulation test to be performed ACTH stimulation test should show an increase in plasma cortisol levels 30 minutes after giving Synacthen 250ug IM

Answer 3

1a. Bloods- Haematology (FBC for neutrophilic, CRP and ESR for infection) 1b. Biochemistry (U&Es for hyperkalaemia, hyponatraemia, hypoglycaemia and metabolic acidosis) 1c. Microbiology (blood cultures) 2. Urine- MCS

Answer 4

1. Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism) 2. Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia) 3. Steroid withdrawal

Answer 5

1. Hydrocortisone 100 mg im or iv 2. 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic 3. Continue hydrocortisone 6 hourly until the patient is stable (no fludrocortisone is required because high cortisol exerts weak mineralocorticoid action) 4. Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days 5. Treat the underlying cause e.g. Abx for sepsis

Answer 6

Replacement therapy of glucocorticoid and mineralocorticoid Combination of: 1.Hydrocortisone (usually given in 2 or 3 divided doses, 20-30 mg per day, with the majority given in the first half of the day) 2.Fludrocortisone Patient education: importance of not missing doses, MedicAlert bracelets, hydrocortisone injection for crisis Management of intercurrent illness: glucocorticoid dose should be doubled with fludrocortisone staying the same

Answer 7

Give hydrocortisone before thyroxine to avoid precipitating an Addisonian crisis

Answer 8

Hyperkalaemia Death during an Addisonian crisis

Answer 9

Adrenal function rarely recovers, but normal life expectancy can be expected if treated

Answer 10

A slow growing type of neuroendocrine tumour originating in the cells of the neuroendocrine system, but can metastasise

Answer 11

1. Usually occurs when metastases are present in the liver and release serotonin into the systemic circulation 2. May also occur with lung carcinoid as mediators are not 'cleared' by the liver

Answer 12

Fore, mid or hindgut tumours

Answer 13

1. Flushing (often earliest symptom) 2. Diarrhoea 3. Bronchospasm 4. Hypotension 5. Right heart valvular stenosis

Answer 14

ACTH and GHRH

Answer 15

1. Urinary 5-HiAA 2. Plasma chromogranin A y 3. Radiolabelled octreotide scans to detect carcinoid tumours as they express somatostatin receptors

Answer 16

1. Somatostatin analogues e.g. octreotide 2. Diarrhoea: cyproheptadine may help

Answer 17

The clinical manifestation of pathological hypercortisolism (chronic inappropriate elevation of free circulating cortisol) from any cause

Answer 18

Can be divided into exogenous and endogenous: exogenous causes of Cushing's syndrome (e.g. glucocorticoid therapy) are far more common than endogenous ones

Answer 19

1. ACTH-dependent (80%): a. Excess ACTH secreted from a pituitary adenoma: Cushing’s disease (80%). b. ACTH secreted from an ectopic source, e.g. small-cell lung carcinomas, pulmonary carcinoid tumours (20%) 2. ACTH-independent (20%): a. Excess cortisol secreted from a benign adrenal adenoma (60%) b. RARE: 1% of Cushing’s syndrome cases are caused by adrenal carcinoma BUT of this 1%, adrenal overproduction of cortisol is seen in 30% to 40% of adrenal carcinomas

Answer 20

1. Relatively uncommon 2. Exogenous Cushing's is more common than endogenous 3. Endogenous Cushing's is more common in women (x4) 4. Peak incidence is 20–40 years, although it can occur at any age

Answer 21

1. Weight gain and fatigue 2. Muscle weakness, myalgia 3. Thin skin 4. Easy bruising 5. Poor wound healing 6. Fractures (resulting from osteoporosis) 7. Hirsutism 8. Acne 9. Frontal balding 10. Oligo- or amenorrhoea 11. Depression or psychosis

Answer 22

Specific features: 1. Facial plethora: increased perfusion, redness, one of the earliest features of Cushing’s syndrome 2. Proximal muscle weakness 3. Bruises Other signs: 1. Facial fullness 2. Interscapular fat pad 3. Thin skin 4.Central obesity 5. Pink/purple striae on abdomen, breast, thighs 6. Kyphosis (due to vertebral fracture) 7. Poorly healing wounds 8. Hirsutism, acne, frontal balding. 9. Hypertension 10. Ankle oedema (salt and water retention as a result of mineralocorticoid effect of excess cortisol) 11. Pigmentation in ACTH-dependent cases

Answer 23

1. Overnight dexamethasone suppression test: a. most sensitive test and is now used first-line b. Patients with Cushing's syndrome do not have their morning cortisol spike suppressed 2. 24 hr urinary free cortisol

Answer 24

If ACTH is suppressed then a non-ACTH dependent cause is likely such as an adrenal adenoma

Answer 25

Used to localise the pathology resulting in Cushing's syndrome: Cushing's disease and ectopic ACTH secretion

Answer 26

Cushing's syndrome due to other causes (e.g. adrenal adenomas): a. Cortisol: Not suppressed b. ACTH Suppressed Cushing's disease (i.e. pituitary adenoma → ACTH secretion): a. Cortisol: Suppressed b. Cortisol: Suppressed Ectopic ACTH syndrome: a. Cortisol: Not suppressed b. ACTH: Not suppressed

Answer 27

Discontinue administration, lower steroid dose or use an alternative steroid-sparing agent if possible

Answer 28

Indication: Pre-operative or if unfit for surgery 1. Inhibition of cortisol synthesis with: a. metyrapone (competitive inhibitor of 11β-hydroxylation in the adrenal cortex inhibiting cortisol production) or b. ketoconazole (potent inhibitor of cortisol and aldosterone synthesis) 2. Treat osteoporosis and provide physiotherapy for muscle weakness

Answer 29

1. Pituitary adenomas, also known as Cushing’s disease: a. Trans-sphenoidal adenoma resection b. Hydrocortisone replaced until pituitary function recovers 2. Adrenal adenoma/carcinoma: Surgical removal of tumour (plus adjuvant therapy with mitotane for adrenal carcinoma)

Answer 30

Investigate lung tumour: chest x-ray, bronchoscopy, CT Treatment is directed at the tumour

Answer 31

A hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance

Answer 32

1. Diabetes 2. Osteoporosis 3. Hypertension 4. Pre-disposition to infections 5. Adrenal insufficiency secondary to adrenal suppression 6. Complications of surgery: CSF leakage, meningitis, sphenoid sinusitis, hypopituitarism

Answer 33

In the untreated, 5-year survival rate is 50%, mortality is mainly from cardiovascular disease Depression usually persists for many years following successful treatment

Answer 34

Characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)

Answer 35

Hypotonic polyuria (production of large quantities of dilute urine)

Answer 36

1. Idiopathic 2. Post head injury 3. Pituitary surgery 4. Craniopharyngiomas 5. Infiltrative: e.g. Sarcoidosis 6. Haemochromatosis 7. DIDMOAD: association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome)

Answer 37

1. Genetic: a. More common form affects the vasopression (ADH) receptor b. Less common form results from a mutation in the gene that encodes the aquaporin 2 channel 2. Electrolytes: a. Hypercalcaemia b. Hypokalaemia 3. Lithium: desensitizes the kidney's ability to respond to ADH in the collecting ducts 4. Tubulo-interstitial disease: e.g. obstruction, sickle-cell, pyelonephritis

Answer 38

1. Polyuria 2. Polydipsia

Answer 39

1. Both mechanisms result in the failure of activation of aquaporins channels and the luminal membrane of the collecting duct remains impermeable to water 2. This results in large volume hypotonic urine and polydipsia

Answer 40

Nocturia ± enuresis (involuntary urination) and sleep disturbances

Answer 41

1. Few signs if patients drink adequate fluids 2. Urine output is often >3 L/24 h 3. If fluid intake < fluid output: signs of dehydration may be present e.g. tachycardia, reduced tissue turgor, postural hypotension, dry mucous membranes 4. Signs of the cause: e.g. visual field defect bitemporal hemianopia from pituitary tumour

Answer 42

1. Bloods and urine analysis: high plasma osmolality, low urine osmolality (if urine osmolality of >700 mOsm/kg excludes DI) 2. Water deprivation test: 1. Water is restricted for 8 h 2. Plasma and urine osmolality are measured every hour over the 8 h 3. Weigh the patient (hourly) to monitor the level of dehydration (stop the test if the fall in body weight is >3%) 4. Desmopressin (2 mg IM) is given after 8 h and urine osmolality is measured

Answer 43

1. Water restriction causes a rise in plasma osmolality and increase in ADH secretion 2. This leads to increased water reabsorption in the collecting ducts 3. Urine is concentrated: (Urine osmolality > 600 mosmol/kg)

Answer 44

1. Lack of ADH activity means that urine is unable to be concentrated by the collecting ducts (Urine osmolality < 400 mosmol/kg) 2. Cranial: Urine osmolality rises by >50%, following administration of desmopressin (due to deficiency in vasopressin) 3. Nephrogenic: Urine osmolality rises by <45%, following administration of desmopressin (resistance to vasopressin)

Answer 45

With desmopressin administration, there will be an increase in urine osmolality in patients with cranial DI (not in nephrogenic because are insensitive to it)

Answer 46

Cranial DI: desmopressin Nephrogenic DI: thiazides and a low salt/protein diet

Answer 47

Hypernatraemic dehydration: 1. Mild to moderate hypernatraemia may present with irritability, restlessness, lethargy, muscle twitching, spasticity, or hyper-reflexia 3. Severe hypernatraemia may present with delirium, seizures, or coma Excess desmopressin therapy may cause hyponatraemia

Answer 48

Variable depending on cause: 1. While DI is often a lifelong condition cranial DI may be transient following head trauma 2. Cure of cranial or nephrogenic diabetes insipidus may be possible on removal of cause, e.g. tumour resection, drug discontinuation

Answer 49

A chronic condition characterised by abnormally raised levels of blood glucose

Answer 50

1. Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system 2. This leads to an absolute deficiency of insulin resulting in raised glucose levels

Answer 51

Tends to develop in childhood/early adult life and typically present unwell, possibly in diabetic ketoacidosis

Answer 52

1. Caused by a relative deficiency of insulin due to an excess of adipose tissue 2. In simple terms there isn't enough insulin to 'go around' all the excess fatty tissue, leading to blood glucose creeping up

Answer 53

The most common cause of diabetes in the developed world

Answer 54

1. Prediabetes: used for patients who don't yet meet the criteria for a formal diagnosis of T2DM to be made but are likely to develop the condition over the next few years (require monitoring and advice) 2. Gestational: raised glucose levels during pregnancy (important to detect) 3. MODY: Maturity onset diabetes of the young, group of inherited genetic disorders affecting the production of insulin, results in younger patients developing symptoms similar to those with T2DM 4. Latent autoimmune diabetes of adults (LADA): a small group of patients who develop autoimmune diabetes later in life

Answer 55

1. Weight loss 2. Polyuria 3. Polydipsia 4. DKA: a. Abdominal pain b. Vomiting c. Reduced consciousness

Answer 56

1. Often picked up incidentally on routine blood tests 2. Polydipsia 3. Polyuria

Answer 57

1. Urine: dip for glucose (and ketones) 2. Fasting glucose and random glucose 3. C-peptide levels are typically low in patients with T1DM 4. Antibody testing: e.g. Antibodies to glutamic acid decarboxylase (anti-GAD), Islet cell antibodies, Insulin antibodies

Answer 58

1. Fasting glucose greater than or equal to 7.0 mmol/l 2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

Answer 59

Must be demonstrated on two separate occassions: 1. Fasting glucose greater than or equal to 7.0 mmol/l 2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

Answer 60

Atypical features e.g. age 50 years or above, BMI of 25 kg/m² or above, slow evolution of hyperglycaemia or long prodrome: measurement of C‑peptide and/or diabetes‑specific autoantibody titres

Answer 61

Diagnosis can be made from either a plasma glucose or a HbA1c sample

Answer 62

1. Fasting glucose greater than or equal to 7.0 mmol/l 2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

Answer 63

Demonstrated on two separate occasions: 1. Fasting glucose greater than or equal to 7.0 mmol/l 2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

Answer 64

Greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus

Answer 65

1. A HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes 2. In patients without symptoms, the test must be repeated to confirm the diagnosis 3. It should be remembered that misleading HbA1c results can be caused by increased red cell turnover e.g.: a. haemoglobinopathies b. haemolytic anaemia c. untreated iron deficiency anaemia d. CKD e. HIV f. Children g. People taking medication that may cause hyperglycaemia (e.g. corticosteroids)

Answer 66

42-47 mmol/mol (Or fasting glucose 6.1 -6.9 mmol/l)

Answer 67

1. Impaired fasting glucose = a fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies 2. Impaired glucose tolerance = fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

Answer 68

Type 1: 1. Typically presents < 20 years 2. Presents more acutely (hours-days) 3. Recent weight loss is typical 4. Features of DKA Type 2: 1. Typically presents > 40 years (can present in younger, obese patients) 2. Presents more slowly (weeks to months) 3. Obesity is a strong RF 4. Milder symptoms e.g. polyuria, polydipsia 5. Ketonuria is rare

Answer 69

1. Patients always require insulin to control the blood sugar levels 2. This is because there is an absolute deficiency of insulin with no pancreatic tissue left to stimulate with drugs 3. Different types of insulin are available according to their duration of action: short, immediate and long acting

Answer 70

Subcutaneous: direct replacement for endogenous insulin

Answer 71

1. Hypoglycaemia 2. Weight gain 3. Lipodystrophy

Answer 72

1. Majority of patients are controlled using oral medication (after lifestyle advice) 2. First-line drug for the vast majority of patients is Metformin 3. Second-line drugs include sulfonylureas, gliptins and pioglitazone 4. If oral medication is not controlling the blood glucose to a sufficient degree then insulin is used

Answer 73

1. Oral medication 2. Increases insulin sensitivity and decreases hepatic gluconeogenesis 3. First line medication 4. Not to be used in patients with an eGFR < 30ml/min

Answer 74

1. Gastrointestinal upset: should be slowly titrated up to minimise this 2. Lactic acidosis *If standard-release metformin is not tolerated then modified-release metformin should be trialled

Answer 75

1st: Metformin + SGLT-2 inhibitor (first line for patients with CVD/HF) Then: Metformin + gliptin/ sulphonylurea (only add a second drug if HbA1c > 58mmol/mol)

Answer 76

1. Oral medication, end in -gliptin 2. Increases incretin levels which inhibit glucagon secretion 3. Generally well tolerated, increased risk of pancreatitis 4. Good for patients with CKD

Answer 77

1. Oral medication 2. Stimulate pancreatic beta cells to secrete insulin 3. E.g. gliclazide and glimepiride 4. SE: Hypoglycaemia, weight gain, hyponatraemia

Answer 78

1. Oral medication 2. Inhibits reabsorption of glucose in the kidney 3. Typically results in weight loss 4. SE: UTI

Answer 79

Triple therapy: Metformin + sulfonylurea + gliptin/ SGLT-2 inhibitors

Answer 80

Metformin + sulfonylurea + GLP-1

Answer 81

1. SC medication in Type 2 DM 2. Incretin mimetic which inhibits glucagon secretion 3. Typically results in weight loss 4. SEs: Nausea and vomiting, pancreatitis

Answer 82

If Metformin in contraindicated and there is a risk of CVD/ HF

Answer 83

1. Individual targets should be agreed with patients to encourage motivation 2. HbA1c should be checked every 3-6 months until stable, then 6 monthly

Answer 84

1. Lifestyle alone: 48 mmol/mol (6.5%) 2. Lifestyle and metformin: 48 mmol/mol (6.5%) 3. Lifestyle and any drug that could lead to hypoglycaemia e.g. sulfonylurea: 53 mmol/mol (7.0%)

Answer 85

53 mmol/mol (7.0%)

Answer 86

1. Ecourage high fibre, low glycaemic index sources of carbohydrates 2. Control the intake of foods containing saturated fats and trans fatty acids 3. Discourage the use of foods marketed specifically at people with diabetes 4. Initial target weight loss in an overweight person is 5-10%

Answer 87

If they become unwell: 1. Increase frequency of blood glucose monitoring to four hourly or more frequently 2. Encourage fluid intake aiming for at least 3 litres in 24hrs 3. If struggling to eat they may need sugary drinks to maintain carbohydrate intake 4. It is useful to educate patients so that they have a box of 'sick day supplies' that they can access if they become unwell 5. Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis 6. If a patient is taking oral hypoglycaemic medication, they should be advised to continue taking their medication even if they are not eating much

Answer 88

Insulin, due to risk of DKA

Answer 89

Metformin due to potential impact on renal function

Answer 90

Depends on the blood glucose level

Answer 91

Autonomic symptoms due to the release of glucagon and adrenaline: 1. Sweating 2. Shaking 3. Hunger 4. Anxiety 5. Nausea

Answer 92

Neuroglycopenic symptoms due to inadequate glucose supply to the brain: 1. Weakness 2. Vision changes 3. Confusion 4. Dizziness

Answer 93

Convulsions and coma

Answer 94

1. Initially, oral glucose 10-20g should be given in liquid, gel or tablet form 2. Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel. 3. A 'HypoKit' may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home

Answer 95

1. If the patient is alert, a quick-acting carbohydrate may be given e.g. GlucoGel 2. If the patient is unconscious or unable to swallow, SC or IM glucagon may be given 3. Alternatively, intravenous 20% glucose solution may be given through a large vein

Answer 96

1. There has not been any severe hypoglycaemic event in the previous 12 months 2. The driver has full hypoglycaemic awareness 3. The driver must show adequate control of the condition by regular blood glucose monitoring (memory function monitors), at least twice daily and at times relevant to driving 4. The driver must demonstrate an understanding of the risks of hypoglycaemia 5. There are no other debarring complications of diabetes

Answer 97

ACE inhibitors are first line with a blood pressure target of < 140/90 mmHg for type 2 diabetics

Answer 98

1. Due to insulin deficiency, as is diabetic ketoacidosis, but patients are usually old and may be presenting for the first time 2. History is longer (e.g. 1 week) 3. There is marked dehydration, high Na + , high glucose (>35 mmol/ L), high osmolality (>340 mosmol/kg), BUT no acidosis and no ketones

Answer 99

1. Microvascular: a. Neuropathy b. Nephropathy c. Retinopathy 2. Macrovascular: a. Ischaemic heart disease b. Stroke c. Peripheral vascular disease

Answer 100

1. Diabetes typically leads to sensory loss and not motor loss 2. Sensory loss typically results in a 'glove and stocking' distribution, with the lower legs affected first due to the length of the sensory neurons supplying this area

Answer 101

1. First-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin 2. If the first-line drug treatment does not work try one of the other 3 drugs 3. Tramadol may be used as 'rescue therapy' for exacerbations of neuropathic pain

Answer 102

1. Gastroparesis: a. Symptoms include erratic blood glucose control, bloating and vomiting b. Management: metoclopramide, domperidone or erythromycin (prokinetic agents) 2. Chronic diarrhoea: often at night 3. GORD: decreased lower esophageal sphincter (LES) pressure

Answer 103

An important complication of diabetes mellitus which should be screen for on a regular basis

Answer 104

1. Neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot's arthropathy, dry skin 2. Peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia

Answer 105

1. Neuropathy: loss of sensation 2. Ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication 3. Complications: calluses, ulceration, Charcot's arthropathy, cellulitis, osteomyelitis, gangrene

Answer 106

All diabetic patients on at least an annual basis: 1. Screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse 2. Screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot

Answer 107

1. Low risk: no risk factors except a callus alone 2. Moderate risk: deformity or neuropathy or non-critical limb ischaemia 3. High risk: (should be followed up regularly) a. previous ulceration or b. previous amputation or c. on renal replacement therapy or d. neuropathy and non-critical limb ischaemia together or e. neuropathy in combination with callus and/or deformity or f. non-critical limb ischaemia in combination with callus and/or deformity

Answer 108

Common complication of diabetes mellitus, all patient should be screened annually: 1. Using urinary albumin:creatinine ratio (ACR) 2. Should be an early morning specimen 3. ACR > 2.5 = microalbuminuria

Answer 109

1. Dietary protein restriction 2. Tight glycaemic control 3. BP control: aim for < 130/80 mmHg 4. ACE inhibitor or angiotensin-II receptor antagonist (not both) should be started if urinary ACR of 3 mg/mmol or more 5. Control dyslipidaemia with statins

Answer 110

A serious complication or first presentation of type 1 diabetes mellitus (rarely type 2)

Answer 111

1. Uncontrolled lipolysis which results in the excess production of free fatty acids 2. These are ultimately converted to ketone bodies

Answer 112

1. Autoimmune disorder 2. Insulin producing beta-cells in the in the Islet of Langerhans in the pancreas are destroyed 3. Results in an absolute deficiency of insulin resulting in raised glucose levels

Answer 113

1. Abdominal pain 2. Of type 1: polyuria, polydipsia, dehydration 3. Kussmaul breathing: deep hyperventilation 4. Acetone-smelling breathing 5. Low GCS

Answer 114

1. Infection 2. Missed insulin doses 3. Myocardial infarction

Answer 115

1. A to E approach 2. Key investigations include VBG (pH, glucose) bloods for ketones, U&Es 3. Urine dip

Answer 116

1. Glucose > 11 mmol/L or known DM 2. pH < 7.3 3. Bicarbonate < 15 mmol/L 4. Presence of ketones: a. Ketones > 3mmol/L b. Urine ketones ++ on dipstick

Answer 117

MEDICAL EMERGENCY: A to E approach 1. Fluid resuscitation 2. Insulin 3. Correction of electrolyte disturbance 4. Long-term management e.g. insulin

Answer 118

1. Most patients with DKA will be deplete of 5-8 L 2. Isotonic saline is used initially (0.9% sodium chloride) 3. Bolus of 500ml over 10-15 minutes 4. Then replacement fluids: 100 ml/kg/day for the first 10kg, 50 ml/kg/day for the next 10kg, 20 ml/kg/day for weight over 20kg 5. Plus maintenance fluids

Answer 119

Cerebral oedema: 1. Children and young adults are particularly vulnerable 2. Slower infusion rates may be indicated 3. Presents with headache, irritability, visual disturbance, focal neurology 4. If suspicion: CT head and senior review

Answer 120

1. Start an IV infusion at 0.1unit/kg/hour 2. Once the blood glucose has been bought down to < 14mmol/L, continue the IV insulin and add 10% dextrose 3. Infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime

Answer 121

1. Serum potassium levels fall after the administration of insulin 2. Therefore may need to add potassium to the fluids 3. Of the rate of potassium infusion is > 20 mmol/hour then cardiac monitoring may be required

Answer 122

1. pH > 7.3 2. Blood ketones < 0.6 mmol/L 3. Bicarbonate > 15 mmol/L If the patient is eating and drinking at this point = switch to S/C insulin

Answer 123

The patient must be reviewed by a diabetes specialist nurse

Answer 124

1. Should resolve within 24 hours 2. If not, requires senior review from endocrinologist

Answer 125

Can be from DKA or the management of it: 1. Gastric stasis 2. VTE 3. Arrhythmias secondary to hyperkalaemia 4. Incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia 5. ARDS 6. AKI

Answer 126

Although a serious condition, mortality has decreased significantly due to improved understanding of pathophysiology and close monitoring of electrolytes

Answer 127

Classified as serum Total cholesterol, LDL-C, triglycerides, apolipoprotein B, or lipoprotein(a) concentrations above the 90th percentile for the general population

Answer 128

1. Primary causes: due to single or multiple gene mutations, resulting in a disturbance of LDL and triglyceride production or clearance (most commonly seen in children and young adults) 2. Secondary causes: caused by lifestyle factors or disorders that interfere with blood lipid levels over time such as obesity, CKD

Answer 129

1. Common, particularly in developing countries 2. Strong correlation between body mass index and coronary heart disease 3. Primary causes are common in children and young adults whereas secondary is seen more in adults

Answer 130

1. Excess body weight 2. PMH Diabetes Mellitus Type 2 or cardiovascular disease 3. Consumption of saturated fats 4. FH of early onset of coronary heart disease or Dyslipidaemia

Answer 131

1. Xanthelasmas: Yellow plaques that occur most commonly near the inner canthus of the eyelid 2. Tendinous xanthomas: Slowly enlarging subcutaneous nodules (on tendons or ligaments)

Answer 132

Lipid profile: 1. Total cholesterol (TC) >5.18 mmol/L (>200 mg/dL) 2. LDL-cholesterol >2.59 mmol/L (>100 mg/dL) 3. triglycerides >1.7 mmol/L (>150 mg/dL) 4. Fasting (12h) triglycerides: ≥2.3 mmol/L (200 mg/dL) Can also offer TFTs

Answer 133

Primary prevention: 20mg atorvastatin 1. 10-year cardiovascular risk > 10% 2. Type 1 DM 3. CKD, eGFR < 60ml/min Secondary prevention: 80mg atorvastatin 1. Known ischaemic heart disease 2. Cerebrovascular disease 3. Peripheral arterial disease

Answer 134

Combination of lifestyle changes to diet and exercise, medications, and dietary supplements 1. Lifestyle changes: dietary reduction in total and saturated fat, weight loss in overweight patients, aerobic exercise 2. Drug therapy: Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, a key enzyme in cholesterol synthesis, which leads to up-regulation of LDL receptors and increased LDL clearance

Answer 135

Due to atherosclerosis: 1. Ischaemic heart disease 2. Peripheral vascular disease 3. Acute coronary syndrome 4. Stroke 5. Erectile dysfunction (endothelial dysfunction)

Answer 136

The rate of adverse outcomes has been significantly reduced with the use of statins

Answer 137

1. An autoimmune thyroid condition associated with hyperthyroidism caused by TSH (thyroid-stimulating hormone) receptor antibodies 2. The most common cause of thyrotoxicosis

Answer 138

Typically seen in women aged 30-50 years

Answer 139

Autoantibodies: 1. TSH receptor stimulating antibodies (90%) 2. Anti-thyroid peroxidase antibodies (75%) These lead to stimulation of the thyroid and overproduction of thyroxine

Answer 140

1. Eye signs (30% of patients) a. exophthalmos b. ophthalmoplegia 2. Pretibial myxoedema 3. Thyroid acropachy, a triad of: a. digital clubbing b. soft tissue swelling of the hands and feet c. periosteal new bone formation

Answer 141

1. Diffuse, smooth enlarged goitre 2. Exophthalmos - bulging of the eye anteriorly 3. Signs of thyrotoxicosis

Answer 142

1. General: WL, manic, heat intolerance 2. Cardiac: palpitations, high-output HF 3. Skin: increased sweating, pretibial myxoedema, thyroid acropachy: clubbing 4. GI: diarrhoea 5. Oligomenorrhoea 6. Neuro: anxiety, tremor

Answer 143

Erythematous, oedematous lesions above the lateral malleoli

Answer 144

1. Thyroid function tests: High T3/4, low TSH 2. Autoantibodies: a. TSH receptor stimulating antibodies (90%) b. anti-thyroid peroxidase antibodies (75%) 3. Thyroid scintigraphy: diffuse, homogenous, increased uptake of radioactive iodine

Answer 145

1. Initial treatment 2. Anti-thyroid drugs: carbimazole 3. Radioiodine treatment 4. Surgery

Answer 146

Propranolol: used to help block the adrenergic effects

Answer 147

1. Carbimazole is started at 40mg and reduced gradually to maintain euthyroidism 2. Typically continued for 12-18 months 3. An alternative regime is termed 'block-and-replace': a. carbimazole is started at 40mg b. thyroxine is added when the patient is euthyroid c. treatment typically lasts for 6-9 months

Answer 148

Patients following atitration regime have been shown to suffer fewer side-effects than those on a block-and-replace regime

Answer 149

Agranulocytosis

Answer 150

1. Often used in patients who relapse following ATD therapy or are resistant to primary ATD treatment 2. The proportion of patients who become hypothyroid depends on the dose given, but as a rule the majority of patient will require thyroxine supplementation after 5 years

Answer 151

1. Pregnancy (should be avoided for 4-6 months following treatment) 2. Age < 16 years 3. Thyroid eye disease is a relative contraindication, as it may worsen the condition (e.g. exophthalmos, ophthalmoplegia, optic disc swelling, conjunctival oedema)

Answer 152

Alongside management of Grave's with Carbimazole: 1. Topical lubricants may be needed to help prevent corneal inflammation caused by exposure 2. Steroids 3. Surgery

Answer 153

Disorders of calcium metabolism, where the parathyroid hormone levels are elevated by different pathologies

Answer 154

1. Primary: high PTH and high calcium, most likely due to a solitary adenoma 2. Secondary: high PTH, low calcium, low Vitamin D, parathyroid gland hyperplasia as a result of low calcium due to CKD 3. Tertiary: high PTH, high/ normal calcium, occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder

Answer 155

Excess secretion of PTH resulting in hypercalcaemia, most commonly (85%) caused by a solitary adenoma of the parathyroid gland

Answer 156

80% of patients are asymptomatic (diagnosed on routine bloods)

Answer 157

'bones, stones, abdominal groans and psychic moans': 1. Polydipsia, polyuria 2. Depression 3. Anorexia, nausea 4. Constipation 5. Peptic ulceration 6. Pancreatitis 7. Bone pain/fracture 8. Renal stones 9. Hypertension

Answer 158

Hypertension and multiple endocrine neoplasia: MEN I and II

Answer 159

1. Bloods: a. High calcium, low phosphate b. PTH may be raised or (inappropriately, given the raised calcium) normal 3. Technetium-MIBI subtraction scan 5. X-ray findings: a. pepperpot skull b. osteitis fibrosa cystica

Answer 160

1. Definitive: total parathyroidectomy 2. Conservative: may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage 3. Patients not suitable for surgery: cinacalcet, a calcimimetic, 'mimics' the action of calcium on tissues by allosteric activation of the calcium-sensing receptor

Answer 161

1. Elevated serum Calcium > 1mg/dL above normal 2. Hypercalciuria > 400mg/day 3. Creatinine clearance < 30% compared with normal 4. Episode of life threatening hypercalcaemia 5. Nephrolithiasis: kidney stones 6. Age < 50 years 7. Neuromuscular symptoms 8. Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius (T score lower than -2.5)

Answer 162

Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure

Answer 163

1. May have few symptoms 2. Eventually may develop bone disease, osteitis fibrosa cystica and soft tissue calcifications

Answer 164

1. PTH = Elevated 2. Calcium = Low or normal 3. Phosphate = Elevated 4. Vitamin D levels = Low

Answer 165

1. Usually managed with medical therapy 2. Indications for surgery in secondary (renal) hyperparathyroidism: a. Bone pain b. Persistent pruritus c. Soft tissue calcifications

Answer 166

1. Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder 2. Hyperplasia of all 4 glands is usually the cause

Answer 167

1. Metastatic calcification 2. Bone pain and / or fracture 3. Nephrolithiasis: kidney stones 4. Pancreatitis Bloods: a. Calcium = Normal or high b. PTH = Elevated c. Phosphate levels = decreased/ normal d. Vitamin D = normal or decreased e. Alkaline phosphatase = elevated

Answer 168

1. Alow 12 months to elapse following renal transplant as many cases will resolve 2. The presence of an autonomously functioning parathyroid gland may require surgery 3. If the culprit gland can be identified then it should be excised - otherwise total parathyroidectomy and re-implantation of part of the gland may be required

Answer 169

1. IV fluids (often 4–6 in the first 24 h) 2. Conservative management: a. Avoid factors that can exacerbate hypercalcaemia including thiazide diuretics b. Maintain adequate hydration (at least 6–8 glasses of water per day), moderate calcium and vitamin D intake

Answer 170

Characterized by impairment of ovarian function

Answer 171

1. Gonadal dysgensis: Chromosomal abnormalities (e.g. Turner's syndrome), FMR1 gene pre-mutation carriers 2. Gonadal damage: Autoimmune, iatrogenic (chemotherapy, radiation, surgery)

Answer 172

1. Functional: Stress, weight loss, excessive exercise, eating disorders (anorexia nervosa, bulimia) 2. Pituitary/hypothalamic tumours and infiltrative lesions: Pituitary adenomas, craniopharyngiomas, haemochromatosis 3. Hyperprolactinaemia: Prolactinomas or tumours causing pituitary stalk compression 4. Congenital GnRH deficiency: Kallmann's syndrome, idiopathic

Answer 173

1. Secondary hypogonadism is a more common cause of anovulation and amenorrhoea than primary hypogonadism 2. Turner's syndrome occurs in up to 1.5% of conceptions,

Answer 174

Symptoms of oestrogen deficiency: 1. Night sweats 2. Hot flush 3. Vaginal dryness and dyspareunia (painful intercourse) 4. Reduced libido 5. Infertility Symptoms of the underlying cause e.g. prolactinomas

Answer 175

Divided into pre-pubertal hypogonadism or post pubertal hypogonadism

Answer 176

1. Delayed puberty: a. primary amenorrhoea b. absent breast development c. no secondary sexual characteristics 2. Eunuchoid proportions (e.g. long legs, increased arm span for height)

Answer 177

1. Regression of secondary sexual characteristics (loss of secondary sexual hair, breast atrophy) 2. Perioral and periorbital fine facial wrinkles 3. Signs of the underlying cause/associated conditions: a. Hypothalamic/pituitary disease: Visual field defects (bitemporal hemianopia) b. Kallmann's syndrome: Anosmia c. Turner's syndrome: Short stature, low posterior hairline, high arched palate, widely spaced nipples, wide carrying angle, short fourth and fifth metacarpals, congenital lymphoedema 4. Patients with autoimmune primary ovarian failure, signs of Addison's

Answer 178

1. Serum oestradiol: LOW 2. Serum FSH and LH: a. HIGH in primary hypogonadism (due to -ve feedback inhibition by ovarian oestradiol and inhibin). b. LOW or inappropriately normal FSH/LH in secondary hypogonadism 3. Investigating aetiology: a. Primary: Genetic testing/ Karyotype b. Secondary: Pituitary function tests (9 a.m. cortisol, TFTs, prolactin), pituitary MRI

Answer 179

A syndrome of reduced testosterone production, sperm production or both

Answer 180

1. Gonadal dysgensis: Klinefelter's syndrome (XXY), undescended testes (cryptorchidism) 2. Gonadal damage: Infection (e.g. mumps), torsion, trauma, autoimmune, iatrogenic (chemotherapy, surgery, radiation) 3. Rare causes: Defects in enzymes involved in testosterone synthesis, myotonic dystrophy

Answer 181

1. Pituitary/hypothalamic lesions 2. GnRH deficiency: Kallmann's syndrome (associated with anosmia) 3. Idiopathic 4. Hyperprolactinaemia 4. Systemic/chronic diseases 5. Rare causes: Genetic mutations, e.g. Prader–Willi syndrome: loss of a critical region on chromosome 15 causing obesity and short stature, small hands, almond-shaped eyes, learning difficulty/postnatal hypotonia

Answer 182

1. The prevalence of hypogonadism increases with age 2. Primary hypogonadism accounts for 30–40% of cases of male infertility; secondary hypogonadism accounts for 1–2% 3. Most common cause of primary hypogonadism is Klinefelter's syndrome

Answer 183

1. Delayed puberty (if the onset is before puberty) 2. Reduced libido, impotence, infertility 3. Symptoms of the underlying cause: Klinefelter's syndrome: intellectual dysfunction and behavioural abnormalities which cause difficulty in social interactions

Answer 184

Signs of delayed puberty: 1. High-pitched voice 2. Lack of pubic/axillary/facial hair 3. Small or undescended testes, small phallus 4. Gynaecomastia 5. Eunuchoid proportions (due to delayed fusion of the epiphyses and continued growth of long bones) Features of the underlying cause e.g. cryptorchidism, anosmia in Kallmann's syndrome

Answer 185

1. Lack of Pubic/axillary/facial hair 2. Soft and small testes 3. Gynaecomastia 4. Fine perioral wrinkles 5. Features of the underlying cause e.g. visual field defects due to a pituitary tumour, signs of systemic/chronic illness

Answer 186

1. Serum total testosterone: Check between 6 a.m. and 8 a.m. ideally -less than 10.4 nanomol/L (<300 nanograms/dL) = as hypogonadism Results: a. Primary: LOW Testosterone, HIGH LH and FSH (due to -ve negative feedback) b. Secondary: LOW Testosterone, LOW or inappropriately normal LH and FSH levels 2. Secondary causes: Pituitary function tests, pituitary MRI

Answer 187

1. An X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype 2. Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome

Answer 188

1. 'primary amenorrhoea' 2. Undescended testes causing groin swellings 3. Breast development may occur as a result of conversion of testosterone to oestradiol

Answer 189

buccal smear or chromosomal analysis to reveal 46XY genotype

Answer 190

1. Counselling - raise child as female 2. Bilateral orchidectomy (increased risk of testicular cancer due to undescended testes) 3. Oestrogen therapy

Answer 191

The inadequate production of one or more of the hormones secreted by the pituitary gland

Answer 192

Compression of the pituitary gland by non-secretory pituitary macroadenoma

Answer 193

1. Pituitary apoplexy 2. Sheehan's syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage 3. Hypothalamic tumours e.g. craniopharyngioma 4. Trauma 5. Iatrogenic irradiation 6. Infiltrative e.g. hemochromatosis, sarcoidosis

Answer 194

GH FSH/LH Prolactin ACTH TSH

Answer 195

Vasopressin (ADH) Oxytocin

Answer 196

Relatively rare

Answer 197

Which hormones are deficient

Answer 198

1. Tiredness 2. Postural hypotension

Answer 199

1. Amenorrhoea 2. Infertility 3. Loss of libido

Answer 200

1. Feeling cold 2. Constipation

Answer 201

Problems with lactation

Answer 202

1. Pituriary macroadenoma → bitemporal hemianopia 2. Pituitary apoplexy → sudden, severe headache

Answer 203

1. Pituitary function tests: 9am hormone profile testing 2. Imaging: MRI or CT to show pituitary masses, vascular lesions 3. Visual field testing

Answer 204

1. Treatment of any underlying cause (e.g. surgical removal of pituitary macroadenoma) 2. Replacement of deficient hormones

Answer 205

1. Hydrocortisone: 20 mg in morning, 10 mg in evening (double oral dose for febrile illnesses, IM hydrocortisone at times of surgery). Should be provided with Medicalert bracelet and steroid card! 2. Levothyroxine: 100 mg daily (always taken after hydrocortisone to avoid Addisonian crisis) 3. Sex hormones: Testosterone/ Oestrogen and progestogerone 4. Growth hormone: SC 1.2 unit/day in adults, children require specialist supervision

Answer 206

Effectively lead to cranial DI: Desmopressin (vasopressin analogue) 10–20 mg/day intranasally

Answer 207

1. Adrenal crisis 2. Hypoglycaemia 3. Myxoedema coma: severe hypothyroidism leading to decreased mental status, hypothermia, and slowing of function in multiple organs- it is a medical emergency with a high mortality rate 4. Infertility 5. Osteoporosis; dwarfism (children)

Answer 208

1. Optic chiasm compression 2. Hydrocephalus (third ventricular compression) 3. Temporal lobe epilepsy

Answer 209

Good with lifelong hormone replacement

Answer 210

The clinical syndrome resulting from insufficient secretion of thyroid hormones

Answer 211

Reduced thyroid hormone production (high TSH, low T3/T4)

Answer 212

1. Acquired: a. Autoimmune (Hashimoto's) thyroiditis (cellular and antibody-mediated) b. Iatrogenic (post-surgery, radioiodine, Lithium, medication for hyperthyroidism e.g. carbimazole) c. Severe iodine deficiency or iodine excess (Wolff–Chaikoff effect) d. Thyroiditis 2. Congenital: a. Thyroid dysgenesis b. Inherited defects in thyroid hormone biosynthesis

Answer 213

Pituitary or hypothalamic disease resulting in reduced TSH, therefore low T3/T4

Answer 214

Uncommon, <5% of cases: Pituitary or hypothalamic tumours resulting in low TSH, pituitary failure

Answer 215

Affects around 1-2% of women in the UK and is around 5-10 times more common in females than males

Answer 216

Hashimoto's thyroiditis: 1. Autoimmune disease 2. Associated with T1DM, Addison's or pernicious anaemia 3. May cause transient thyrotoxicosis in the acute phase 4. 5-10 times more common in women

Answer 217

Into system e.g. general, skin, GI Overall: 1. Cold intolerance 2. Lethargy 3. Weight gain 4. Constipation 5. Dry skin 6. Hair loss

Answer 218

1. Weight gain 2. Lethargy 3. Cold intolerance

Answer 219

1. Dry (anhydrosis), cold, yellowish skin 2. Non-pitting oedema (e.g. hands, face) 3. Dry, coarse scalp hair, loss of lateral aspect of eyebrows

Answer 220

Constipation

Answer 221

Menorrhagia

Answer 222

1. Decreased deep tendon reflexes 2. Carpal tunnel syndrome

Answer 223

1. Hands: Bradycardia, cold hands 2. Head/Neck/Skin: a. Pale puffy face b. Oedema c. Hair loss d. Dry skin e. Vitiligo 3. Chest: Pericardial or pleural effusions 4. Abdomen: Ascites 5. Neurological: Slow relaxation of reflexes, signs of carpal tunnel syndrome

Answer 224

Thyroid function tests: 1. Primary: Low T4/T3 and High TSH (due to negative feedback) 2. Secondary: Low T3/T4 and Low or inappropriately normal TSH

Answer 225

General bloods: including anti-thyroid peroxidase (TPO) for Hashimoto's Imaging: MRI/ CT head to identify pituitary/ hypothalamic tumours

Answer 226

Levothyroxine replacement therapy: 1. Star on a dose of 50-100mcg od 2. Following a change in thyroxine dose TFTs should be checked after 8-12 weeks 3. The therapeutic goal is 'normalisation' of TSH levels, aim for a value 0.5-2.5 mU/

Answer 227

Patients with cardiac disease, severe hypothyroidism or patients over 50 years (this can then be slowly titrated up)

Answer 228

Should have their dose increased 'by at least 25-50 micrograms levothyroxine' due to the increased demands of pregnancy - the TSH should be monitored carefully, aiming for a low-normal value

Answer 229

1. Hyperthyroidism: due to over treatment 2. Reduced bone mineral density 3. Worsening of angina 4. Atrial fibrillation

Answer 230

Iron, calcium carbonate: Absorption of levothyroxine reduced, give at least 4 hours apart

Answer 231

Severe hypothyroidism usually seen in the elderly: 1. Hypothermia 2. Hypoventilation 3. Hyponatraemia 4. Heart failure 5. Confusion 6. Coma

Answer 232

1. Oxygen 2. Rewarming 3. Rehydration 4. IV T4/T3 5. IV hydrocortisone (in case hypothyroidism is secondary to hypopituitarism) 6. Treat the underlying disorder e.g. infection

Answer 233

1. Myxoedema coma 2. Mxoedema madness: psychosis with delusions and hallucinations or dementia in severe hypothyroidism (may be seen in the elderly after starting levothyroxine treatment)

Answer 234

80% mortality rate

Answer 235

Good, lifelong levothyroxine therapy is required

Answer 236

Incidental finding of high TSH but normal T3/4, often no obvious symptoms

Answer 237

1. Risk of progressing to overt hypothyroidism is 2-5% per year (higher in men) 2. Risk increased by the presence of thyroid autoantibodies

Answer 238

1. Not all patients require treatment 2. Depends on TSH and free thryoxine level

Answer 239

Consider offering levothyroxine if the TSH level is > 10 mU/L on 2 separate occasions 3 months apart

Answer 240

1. If < 65 years: consider offering a 6-month trial of levothyroxine if: the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart PLUS there are symptoms of hypothyroidism 2. In older people (especially those > 80 years) follow a 'watch and wait' strategy is often used 3. In asymptomatic people, observe and repeat thyroid function in 6 months

Answer 241

1. The permanent cessation of menstruation due to reduced levels of female hormones, principally oestrogen 2. Caused by the loss of follicular activity 3. Clinical diagnosis: when a woman has not had a period for 12 months

Answer 242

The period prior to the menopause where women may experience symptoms, as ovarian function starts to fail

Answer 243

1. Changes in periods 2. Vasomotor symptoms 3. Urogenital changes 4. Psychological changes 5. Longer term complications

Answer 244

1. Change in length of menstrual cycles 2. Dysfunctional uterine bleeding may occur

Answer 245

Affect up to 80% of women: Usually occur daily and may continue for up to 5 years: 1. Hot flushes 2. Night sweats

Answer 246

Affects up to 35% of women: 1. Vaginal dryness and atrophy 2. Urinary frequency

Answer 247

1. Anxiety and depression may be seen - around 10% of women 2. Short term memory impairment

Answer 248

1. Osteoporosis 2. Increased risk of ischaemic heart disease

Answer 249

Three categories: 1. Lifestyle modifications 2. Hormone replacement therapy (HRT) 3. Non-hormone replacement therapy

Answer 250

1. Hot flushes: regular exercise, weight loss and reduce stress 2. Sleep disturbance: avoiding late evening exercise and maintaining good sleep hygiene 3. Mood: sleep, regular exercise and relaxation 4. Cognitive symptoms: regular exercise and good sleep hygiene

Answer 251

Hormone replacement therapy: 1. If the woman has a uterus then it is important not to give unopposed oestrogens as this will increase her risk of endometrial cancer: therefore oral or transdermal combined HRT is given 2. If the woman does not have a uterus then oestrogen alone can be given either orally or in a transdermal patch

Answer 252

1. Current or past breast cancer 2. Any oestrogen-sensitive cancer 3. Undiagnosed vaginal bleeding 4. Untreated endometrial hyperplasia

Answer 253

1. VTE: a slight increase in risk with all forms of oral HRT, but NO increased risk with transdermal HRT 2. Stroke: slightly increased risk with oral oestrogen 3. Coronary heart disease: combined HRT may be associated with a slight increase in risk 4. Breast cancer: there is an increased risk with all combined HRT although the risk of dying from breast cancer is not raised 5. Ovarian cancer: increased risk with all HRT

Answer 254

1. Vasomotor symptoms: fluoxetine, citalopram or venlafaxine 2. Vaginal dryness: vaginal lubricant or moisturiser 3. Psychological symptoms: self-help groups, CBT or antidepressants 4. Urogenital symptoms: a. if suffering from urogenital atrophy vaginal oestrogen can be prescribed (even on HRT) b. vaginal dryness can be treated with moisturisers and lubricants (can be offered alongside vaginal oestrogens if required)

Answer 255

Hereditary tumours of variable neoplastic patterns and characterised by the development of multiple endocrine tumours

Answer 256

Tnherited as an autosomal dominant disorder: MEN type 1: 3Ps MEN type 2a: 2Ps MEN type 2b: 1P

Answer 257

1. Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia 2. Pituitary (70%) 3. Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)

Answer 258

1. Parathyroid (60%) 2. Phaeochromocytoma Important: Medullary thyroid cancer (70%)

Answer 259

Phaeochromocytoma (may have Marfanoid body habitus, neuromas, Medullary thyroid cancer)

Answer 260

Hypercalaemia (from hyperparathyroidism from parathyroid hyperplasia)

Answer 261

Relatively rare In MEN type 1: at least 90% of patients develop primary hyperparathyroidism

Answer 262

1. Facial lesions (angiofibromas) 2. Irregular menses/ infertility/ erectile dysfunction 3. Visual changes 4. Clinical features of acromegaly 5. Clinical features of thyrotoxicosis 6. Heat intolerance

Answer 263

1. Episodic triad of sweating, palpitations and headaches 2. Palpable thyroid nodule (medullary thyroid cancer) 3. Unexplained flushing 4. GI bleeding 5. Hepatomegaly: if there are liver metastases

Answer 264

Type 1: 1. Fasting serum gastrin: raised 2. Serum chromogranin A: raised 3. Serum prolactin: raised 4. Insulin-like Growth Factor 1 (IGF-1): raised 5. Pituitary MRI: adenoma Type 2: 1. Serum calcitonin: raised (medullary thyroid cancer) 2. Plasma metanephrines: elevated levels suggest phaeochromocytoma 3. 24h urine metanephrines and catecholamines

Answer 265

Can be defined as a chronic adverse condition due to an excess amount of body fat

Answer 266

Caused by calorie intake, over time, is greater than the calorie expenditure Other factors: 1. Genetic predisposition 2. Behavioural dynamics (portion sizes) 3. Hormonal disturbances

Answer 267

1. Calculate BMI: (weight/height2) 2. Waist circumference 3. Co-morbidities such as type 2 diabetes, cardiovascular disease, hypertension, hyperlipidaemia

Answer 268

Usually a clinical diagnosis, can consider: 1. ECG: Routine screen for signs of heart disease if suspected 2. TFTs: Routine screen if hypothyroidism is suspected 3. Abdominal ultrasound: Routine screen for fatty liver, steatohepatitis

Answer 269

Underweight: < 18.49 Normal: 18.5 - 25 Overweight: 25 - 30 Obese class 1: 30 - 35 Obese class 2: 35 - 40 Obese class 3: > 40

Answer 270

1. Conservative: diet, exercise 2. Medical: a. Orlistat b. Liraglutide 3. Surgical

Answer 271

1. A pancreatic lipase inhibitor 2. Adverse effects: faecal urgency/incontinence and flatulence 3. A lower dose version is now available without prescription ('Alli') 4. It should only be prescribed as part of an overall plan for managing obesity in adults who have: a. BMI of 28 kg/m^2 or more with associated risk factors, or b. BMI of 30 kg/m^2 or more continued weight loss e.g. 5% at 3 months 5. Orlistat is normally used for < 1 year

Answer 272

1. A glucagon-like peptide-1 (GLP-1) mimetic that is used in the management of T2DM 2. Given as a once daily SC injection 3. For use in a person with: a. BMI of at least 35 kg/m² b. prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)

Answer 273

1. Primarily restrictive operations: a. laparoscopic-adjustable gastric banding (LAGB) b. Sleeve gastrectomy c. Intragastric balloon 2. Primary malabsorptive operations: biliopancreatic diversion with duodenal switch 3. Mixed

Answer 274

Softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content (rickets in children)

Answer 275

Vitamin D deficiency: 1. Malabsorption 2. Lack of sunlight 3. Diet

Answer 276

1. Chronic kidney disease 2. Drug induced e.g. anti-convulsants 3. Inherited: hypophosphatemic rickets 4. Liver disease: e.g. cirrhosis 5. Coeliac disease

Answer 277

1. Bone pain 2. Bone/muscle tenderness 3. Fractures: especially femoral neck 4. Proximal myopathy: may lead to a waddling gait

Answer 278

1. Bloods: a. Low vitamin D levels b. Low calcium, phosphate (in around 30%) c. Raised alkaline phosphatase (in 95-100% of patients) 2. X-ray: translucent bands (Looser's zones or pseudofractures)

Answer 279

1. Vitamin D supplementation: a loading dose is often needed initially 2. Calcium supplementation if dietary calcium is inadequate

Answer 280

1. Bossing of frontal and parietal bones- unusually prominent forehead 2. Swelling of costochondral junctions (upper ribs) (rickety rosary) 3. Bow legs in early childhood, knock knees in later childhood 4. Short stature

Answer 281

1. Bone deformities 2. Hypocalcaemia may cause epileptic seizures 3. Cardiac arrhythmias 4. Hypocalcaemic tetany: spasms of the hands and feet, cramps, spasm of the larynx and overactive neurological reflexes 5. Depression

Answer 282

1. Trousseau's sign: Inflation of the sphygmomanometer cuff to above the systolic pressure for >3 min causes tetanic spasm of wrist and fingers. 2. Chvostek's sign: Tapping over the facial nerve causes twitching of the ipsilateral facial muscles

Answer 283

1. Symptoms and radiological appearances improve with vitamin D supplementation 2. Bone deformities in children tend to be permanent

Answer 284

A complex skeletal disease characterised by low/reduced bone density and micro-architectural defects in bone tissue, resulting in: 1. Increased bone fragility 2. Susceptibility to fracture

Answer 285

<2.5 standard deviations below peak bone mass achieved by healthy adults

Answer 286

Advancing age and female sex

Answer 287

The prevalence of osteoporosis increases from 2% at 50 years to more than 25% at 80 years in women

Answer 288

1. History of glucocorticoid use 2. Rheumatoid arthritis 3. Alcohol excess 4. History of parental hip fracture (FH) 5. Low BMI 6. Current smoking 7. CKD 8. GI disease: IBD, coeliac disease 9. Endocrine: hyperthyroidism, hypogonadism, DM

Answer 289

Often asymptomatic until characteristic fractures occur: 1. Femoral neck fractures (commonly after minimal trauma) 2. Vertebral factures (loss of height or stooped posture or acute back pain after lifting) 3. Colles' fracture of the distal radius after fall onto outstretched hand

Answer 290

Often no signs until complications develop: 1. Tenderness on percussion (over vertebral fractures) 2. Thoracic kyphosis-roundback (if multiple vertebral fractures) 3. Severe pain with leg shortened and externally rotated (in a femoral neck fracture)

Answer 291

A screening tool in osteoporosis to assess the 10-year risk of a patient developing a fragility fracture

Answer 292

If a patient is diagnosed with osteoporosis or has a fragility fracture further investigations may be warranted: 1. History and physical examination 2. Blood cell count, ESR, CRP, serum calcium 3. LFTs: albumin, creatinine, phosphate, alkaline phosphatase and liver transaminases 4. TFTs 5. Bone densitometry (DXA)

Answer 293

T-score: based on bone mass of young reference population > -1.0 = normal -1.0 to -2.5 = osteopaenia < -2.5 = osteoporosis

Answer 294

1. Vitamin D and calcium supplementation should be offered to all women 2. Bisphosphonates: Alendronate is first-line 3. If cannot tolerate alendronate (upper GI problems): should be offered risedronate or etidronate

Answer 295

1. Alendronate is first line 2. The T-score criteria for risedronate or etidronate are less than the others implying that these are the second line drugs 3. If alendronate, risedronate or etidronate cannot be taken then strontium ranelate or raloxifene may be given based on quite strict T-scores (e.g. a 60-year-old woman would need a T-score < -3.5) 4. The strictest criteria are for denosumab

Answer 296

Disease of increased but uncontrolled bone turnover

Answer 297

Thought to be primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity

Answer 298

Common (UK prevalence 5%) but symptomatic in only 1 in 20 patients

Answer 299

1. Increasing age 2. Male sex 3. Northern latitude 4. Family history

Answer 300

The skull, spine/pelvis, and long bones of the lower extremities

Answer 301

Only 5% of people are symptomatic: 1. Stereotypical presentation: older male with bone pain and an isolated raised ALP 2. Bone pain (e.g. pelvis, lumbar spine, femur)

Answer 302

Bowing of tibia and bossing of skull

Answer 303

1. Bloods: a. raised ALP b. Normal calcium and phosphate (hypercalcaemia may occasionally occur with prolonged immobilisation) 2. Other arkers of bone turnover include: a. procollagen type I N-terminal propeptide (PINP) b. serum C-telopeptide (CTx) 3. X-rays: a. Osteolysis in early disease → mixed lytic/sclerotic lesions later b. Skull x-ray: thickened vault, osteoporosis circumscripta 4. Bone scintigraphy: increased uptake is seen focally at the sites of active bone lesions

Answer 304

1. Bone pain 2. Skull or long bone deformity 3. Fracture 4. Periarticular Paget's

Answer 305

Bisphosphonate: either oral risedronate or IV zoledronate

Answer 306

1. Deafness: cranial nerve, vestibulocochlear entrapment 2. Bone sarcoma: 1% if affected for > 10 years 3. Fractures 4. Skull thickening 5. High-output cardiac failure

Answer 307

A rare catecholamine secreting tumour

Answer 308

About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome

Answer 309

1. Usually arises from chromaffin cells of the adrenal medulla 2. Bilateral in 10% 3. Malignant in 10% 4. Extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)

Answer 310

Rare condition

Answer 311

Typically episodic: 1. Hypertension (around 90% of cases, may be sustained) 2. Headaches 3. Palpitations 4. Sweating 5. Anxiety

Answer 312

24 hr urinary collection of metanephrines (sensitivity 97%) - this has replaced collection of catecholamines

Answer 313

1. Stabilisation with medical: a. alpha-blocker (e.g. phenoxybenzamine), given first b. Then given a beta-blocker (e.g. propranolol) 2. Surgical = definitive

Answer 314

Pituitary adenomas that do not cause a characteristic hormone hypersecretion syndrome

Answer 315

1. Exact aetiology is unknown 2. FH of multiple endocrine neoplasia type1 (MEN1) and Familial pituitary adenomas

Answer 316

1. Pituitary adenomas are the third most common intracranial neoplasms 2. Account for about 10% of all intracranial tumours in adults

Answer 317

1. Prolactinomas 2. Non-secreting adenomas 3. GH secreting adenomas 4. ACTH secreting adenomas

Answer 318

1. Depletion of hormones 2. This is due to compression of the normal functioning pituitary gland 3. Therefore, present with generalised hypopituitarism

Answer 319

Generalised hypopituitarism: 1. Headaches 2. Decreased visual acuity- bitemporal hemianopia 3. Adrenal insufficiency: Nausea and vomiting, weakness, anorexia 4. Hypogonadism: Gynaecomastia, erectile dysfunction, amenorrhoea, infertility 5. Hypothyroidism:, Weight gain, cold intolerance, fatigue 6. GH deficiency: Similar to above plus increased central adiposity and reduced muscle mass

Answer 320

1. Pituitary blood profile: a. GH, FSH/LH, TSH, ACTH b. Prolactin levels: exclude prolactinomas 2. Pituitary MRI with gadolinium contrast 3. Formal visual field testing

Answer 321

1. Pituitary hyperplasia (if secreting hormone (s)) 2. Craniopharyngioma 3. Meningioma 4. Brain metastases 5. Lymphoma 6. Hypophysitis (inflammation of pituitary) 7. Vascular malformation (e.g. aneurysm)

Answer 322

May include a combination of: 1. Surgery (e.g. transsphenoidal transnasal hypophysectomy): if progression in size 2. Radiotherapy

Answer 323

A complex condition of ovarian dysfunction characterised by: 1.Oligomenorrhoea/amenorrhoea 2. Hyper-androgenism (clinical symptoms or biochemical)

Answer 324

Obesity, insulin resistance and an increased risk of developing type 2 diabetes

Answer 325

Not fully understood: combination of environmental factors (related to diet and development of obesity) and genetic determinants

Answer 326

1. FHx of PCOS 2. Premature adrenarche 3. Weaker risk factors: obesity, low birth weight

Answer 327

PCOS is the most common cause of infertility in women, thought to affect between 5-20% of women of reproductive age

Answer 328

1. Subfertility and infertility 2. Menstrual disturbances: oligomenorrhoea and amenorrhoea 3. Hirsutism, acne (due to hyperandrogenism) 4. Obesity 5. Acanthosis nigricans (due to insulin resistance)

Answer 329

1. Pelvic ultrasound: multiple cysts on the ovaries 2. Baseline investigatons: FSH, LH, prolactin, TSH, testosterone, sex hormone-binding globulin (SHBG): a. raised LH:FSH ratio is a 'classical' feature but is no longer thought to be useful in diagnosis b. Prolactin may be normal or mildly elevated c. Testosterone may be normal or mildly elevated - however, if markedly raised consider other causes d. SHBG is normal to low in women with PCOS 3. Check for impaired glucose tolerance

Answer 330

If 2 of the following 3 are present: 1. Infrequent or no ovulation (menstruation) 2. Clinical and/or biochemical signs of hyperandrogenism (e.g. hirsutism, acne, or elevated levels of total or free testosterone) 3. Polycystic ovaries on ultrasound scan: a. defined as the presence of ≥ 12 follicles in one or both ovaries and/or increased ovarian volume > 10 cm³ b. Follicles measuring 2-9 mm in diameter

Answer 331

1. Weight reduction if appropriate 2. If a women requires contraception then a combined oral contraceptive (COC) pill may help regulate her cycle and induce a monthly bleed

Answer 332

1. A COC pill may be used help manage hirsutism a. Third generation COC which has fewer androgenic effects or co-cyprindiol which has an anti-androgen action b. An increased risk of VTE with these 2. If doesn't respond to COC then topical eflornithine may be tried 3. Spironolactone, flutamide and finasteride may be used under specialist supervision

Answer 333

1. Weight reduction if appropriate 2. Should be supervised by a specialist. 3. Options include metformin, clomifene or a combination to stimulate ovulation 4. Some evidence showed clomifene was the most effective treatment- but potential risk of multiple pregnancies with anti-oestrogen therapies such as clomifene 5. Metformin is also used, either combined with clomifene or alone, particularly in patients who are obese 6. Gonadotrophins

Answer 334

1. Work by occupying hypothalamic oestrogen receptors without activating them 2. This interferes with the binding of oestradiol and thus prevents negative feedback inhibition of FSH secretion

Answer 335

Characterized by autonomous aldosterone overproduction from the adrenal gland with subsequent suppression of plasma renin activity

Answer 336

1. Bilateral idiopathic adrenal hyperplasia: 60-70% 2. Adrenal adenoma, also known as Conn's syndrome: 20-30% 3. Unilateral hyperplasia 4. Familial hyperaldosteronism 5. Adrenal carcinoma

Answer 337

Excess aldosterone results in: 1. Increased Na+ and water retention causing hypertension 2. Increased renal K+ loss and hypokalaemia 3. Suppression of renin because of NaCl retention

Answer 338

1. The prevalence in hypertensive patients is 1–2% 2. Aldosterone producing adenoma (Conns) occurs more commonly in women and in younger patients (<50 years) 3. Bilateral adrenal hyperplasia occurs more commonly in men and usually presents at an older age

Answer 339

1. Hypertension: increasingly recognised but still underdiagnosed cause of hypertension 2. Hypokalaemia e.g. muscle weakness, is more common with adrenal adenomas 3. Can also present with metabolic alkalosis

Answer 340

Patients with: 1. Hypertension with hypokalemia 2. Treatment-resistant hypertension

Answer 341

Plasma aldosterone/renin ratio: 1. Should show high aldosterone levels alongside low renin levels 2. This because of negative feedback due to sodium retention from aldosterone

Answer 342

1. High-resolution CT abdomen to differentiate between unilateral and bilateral sources of aldosterone excess 2. If the CT is normal: adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia

Answer 343

1. For adrenal adenoma: surgery (laparoscopic adrenalectomy) 2. For bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

Answer 344

Complications of hypertension: 1. Heart failure 2. Coronary artery disease and MI 3. Cerebrovascular accident 4. Peripheral vascular disease 5. Thomboembolism 6. Retinopathy 7. Renal failure

Answer 345

Surgery may either cure hypertension (in about 50-60%) or make it more amenable to anti-hypertensive therapy in those who are not cured (usually the elderly or those with long-standing hypertension)

Answer 346

1. A type of pituitary adenoma 2. A benign tumour expressing and secreting prolactin

Answer 347

1. The majority of prolactinomas occur sporadically 2. A small percentage of patients may have multiple endocrine neoplasia syndrome type 1 (MEN-1) or familial isolated pituitary adenoma (FIPA)

Answer 348

1. Prolactinomas are the most common type of pituitary adenoma, constituting about 40% of these tumours 2. More frequent in women, mainly during the child-bearing years, with a peak incidence between 20-30s 3. Women and men of 10:1 but once over 50, frequency of prolactinomas is similar in men and women

Answer 349

1. Size (a microadenoma is <1cm and a macroadenoma is >1cm) 2. Hormonal status: a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess

Answer 350

Women: 1. Amenorrhoea 2. Infertility 3. Galactorrhoea 4. Osteoporosis Men: 1. Impotence 2. Loss of libido 3. Galactorrhoea

Answer 351

1. Headache 2. Visual disturbances: classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia 3. Symptoms and signs of hypopituitarism

Answer 352

Pituitary MRI (plus pituitary hormone profile, specifically Prolactin)

Answer 353

1. Medical: a. Majority of cases b. Dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland c. Result in prolactin normalisation, tumour shrinkage or disappearance, and rapid visual improvement 2. Surgery: a. Performed for patients who cannot tolerate or fail to respond to medical therapy b. A trans-sphenoidal approach is generally preferred

Answer 354

1. Visual field impairment 2. Cabergoline associated (at high doses) valvular disease 3. Pituitary apoplexy: due to acute haemorrhage into or ischaemic infarction of a large pituitary prolactinoma 4. From Trans-sphenoidal surgery: anterior pituitary failure/ diabetes insipidus

Answer 355

Characterised by continued secretion of ADH, despite the absence of normal stimuli for secretion (i.e. increased serum osmolality or low blood volume)

Answer 356

Hyponatraemia secondary to the dilutional effects of excessive water retention

Answer 357

1. Malignancy: a. Small cell lung cancer b. Pancreas, prostate 2. Neurological: a. Stroke b. Subarachnoid haemorrhage c. Subdural haemorrhage d. Meningitis/encephalitis/abscess 3. Infections: a. TB b. Pneumonia 4. Drugs: 1. sulfonylureas* 2. SSRIs, tricyclics 3. carbamazepine 5. Other causes: a. positive end-expiratory pressure (PEEP) b. porphyrias

Answer 358

Hyponatraemia is the most common electrolyte imbalance seen in hospitals <50% of all severe hyponatraemia are due to SIADH

Answer 359

1. Mild hyponatraemia (Na+ : 125–135 mmol/L) may be asymptomatic 2. Headache 3. Nausea/vomiting 4. Muscle cramp/weakness 5. Irritability 6. Confusion, drowsiness 7. Convulsions 8. Coma 9. Symptoms of the underlying cause

Answer 360

Mild hyponatraemia: No signs Severe hyponatraemia: Reduced reflexes, extensor plantar reflexes (Babinski reflex)

Answer 361

Diagnosis of exclusion: 1. Bloods: a. Serum sodium: low, <135 mmol/L b. Serum osmolality:low, <280 mmol/kg (hypotonic) 2. Urine: 1. Urine osmolality: elevated, >100 mmol/kg H2O -2. Urine sodium: elevated, >40 mmol/L The presence of the above and absence of hypovolaemia/hypotension, oedema, renal failure, adrenal insufficiency and hypothyroidism are required for a diagnosis of SIADH

Answer 362

1. Correction must be done slowly to avoid precipitating central pontine myelinolysis 2. Fluid restriction 3. Demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH 4. ADH (vasopressin) receptor antagonists have been developed

Answer 363

Rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells Presents with: quadreparesis, respiratory arrest, fits

Answer 364

Convulsions, coma, death

Answer 365

1. If the underlying cause is found and treated successfully, SIADH typically resolves 2. High morbidity and mortality with [Na+] <110 mmol/L 3. Up to 50% mortality with central pontine myelinolysis

Answer 366

The most common endocrinological malignancy and 4 types account for more than 98% of thyroid malignancies: 1. Papillary 2. Follicular 3. Anaplastic 4. Medullary

Answer 367

Genetic alterations are thought to underlie thyroid cancers (Family history is a strong RF)

Answer 368

1. Neck lump 2. Hoarseness 3. Dyspnoea 4. Dysphagia

Answer 369

1. Palpable thyroid nodule (most common in early adulthood) 2. Tracheal deviation: enlarged goitre 3. Cervical lymphadenopathy suggestive of neck metastasis

Answer 370

1. 70% of cases 2. Often young females 3. Excellent prognosis 4. Usually contain a mixture of papillary and colloidal filled follicles 5. Lymph node metastasis predominate

Answer 371

1. 20% of cases 2. Usually present as a solitary thyroid nodule 3. Malignancy can only be excluded on formal histological assessment

Answer 372

1. 5% of cases 2. Part of MEN-2 3. Cancer of parafollicular (C) cells, secrete calcitonin

Answer 373

1. 1% of cases 2. Most common in elderly females 3. Local invasion is a common feature 4. Not responsive to treatment, can cause pressure symptoms 5. Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy

Answer 374

1. TFTs: TSH often normal 2. Ultrasound neck: micro-calcifications, a more-tall-than-wide shape, hypervascularity, marked hypoechogenicity, or irregular margins 3. Fine needle biopsy: cytology of malignant features (variations in appearance), anapaestic (poorly differentiated) 4. Laryngoscopy: paralysed vocal cord is highly suggestive of malignancy

Answer 375

1. Total thyroidectomy 2. Followed by radioiodine (I-131) to kill residual cells 3. Yearly thyroglobulin levels to detect early recurrent disease

Answer 376

Solid or fluid-filled lumps that form within the thyroid (majority are not serious. and do not cause symptoms)

Answer 377

Benign: 1. Multinodular goitre 2. Thyroid adenoma 3. Hashimoto's thyroiditis 4. Cysts (colloid, simple, or hemorrhagic) Malignant: 1. Papillary carcinoma (most common malignant cause) 2. Follicular carcinoma 3. Medullary carcinoma 4. Anaplastic carcinoma 5. Lymphoma: rare, Hashimoto's thyroiditis

Answer 378

1. Most thyroid nodules don’t cause signs or symptoms 2. Neck lump 3. Cause dyspnoea or dysphagia (suggestive of malignancy) 4. Can cause hypo or hyperthyroidism features

Answer 379

1. Bloods: Thyroid function test, FBC 2. First line: ultrasonography: to determine if the nodule has features suspicious of malignancy

Answer 380

1. An autoimmune-mediated lymphocytic inflammation of the thyroid gland resulting in a destructive thyroiditis with release of thyroid hormone and transient thyrotoxicosis (hyperthyroidism) 2. This is frequently followed by a hypothyroid phase and full recovery

Answer 381

1. Hashimoto's thyroiditis (chronic autoimmune thyroiditis): most common cause of hypothyroidism 2. Postpartum thyroiditis 3. Subacute thyroiditis (also known as De Quervain's thyroiditis): following viral infection and typically presents with hyperthyroidism

Answer 382

Features of hyperthyroidism: 1. Heat intolerance 2. Nervousness 3. Palpitations 4. Weight loss 5. Excessive fatigue

Answer 383

1. Thyrotoxicosis 2. Hypothyroidism 3. Normal thyroid function (but high recurrence rate in future pregnancies)

Answer 384

Thyroid peroxidase antibodies

Answer 385

1. Thyrotoxic phase: a. Propranolol is typically used for symptom control b. Not usually treated with anti-thyroid drugs as the thyroid is not overactive 2. Hypothyroid phase: usually treated with thyroxine

Answer 386

1. Phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR 2. Phase 2 (1-3 weeks): euthyroid 3. Phase 3 (weeks - months): hypothyroidism 4. Phase 4: thyroid structure and function goes back to normal

Answer 387

Thyroid scintigraphy: globally reduced uptake of iodine-131

Answer 388

1. Usually self-limiting - most patients do not require treatment 2. Thyroid pain may respond to aspirin or other NSAIDs 3. In more severe cases steroids are used, particularly if hypothyroidism develops (phase 3)

Answer 389

1. Arrhythmias: AF 2. Exacerbation of co-morbidities particularly ismchaemic heart disease and congestive heart failure (lower risk) 3. More likely to develop permanent hypothyroidism 4. Can also develop Graves’ disease, recurrent hyperthyroidism

Answer 390

Most patients recover normal thyroid function, but: 1. 6% remain permanently hypothyroid 2. 1/3 have persistent goitre or thyroid peroxidase (TPO) antibodies 3. Recurrent episodes are common postnatally (69%) but may also occur in up to 11% of patients with sporadic disease