Endo Flashcards

Question

Q: How should glucocorticoid and mineralocorticoid doses be adjusted during intercurrent illness?

Answer 1

A: The glucocorticoid dose should be doubled, while the fludrocortisone dose remains the same.

Answer 2

Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison's disease, Hypopituitarism) Adrenal haemorrhage (e.g., Waterhouse-Friderichsen syndrome, fulminant meningococcemia) Steroid withdrawal

Answer 3

Hydrocortisone 100 mg IM or IV 1 litre normal saline infused over 30-60 minutes, or with dextrose if hypoglycaemic

Answer 4

A: Continue hydrocortisone every 6 hours until the patient is stable.

Answer 5

A: High cortisol exerts a weak mineralocorticoid action, so fludrocortisone is not necessary.

Answer 6

A: Oral replacement may begin after 24 hours and should be reduced to maintenance over 3-4 days.

Answer 7

A: Bartter's syndrome is an inherited (usually autosomal recessive) condition causing severe hypokalaemia due to defective chloride absorption at the Na+ K+ 2Cl- cotransporter (NKCC2) in the ascending loop of Henle.

Answer 8

A: Bartter's syndrome is associated with normotension, unlike other endocrine causes of hypokalaemia, which are associated with hypertension.

Answer 9

A: Loop diuretics inhibit NKCC2, and Bartter's syndrome can be thought of as similar to taking large doses of furosemide, as it also impairs chloride absorption at the same transporter.

Answer 10

Usually presents in childhood (e.g., failure to thrive) Polyuria and polydipsia Hypokalaemia Normotension Weakness

Answer 11

A: Carbimazole is used in the management of thyrotoxicosis.

Answer 12

A: It is typically given in high doses for 6 weeks until the patient becomes euthyroid, after which the dose is reduced.

Answer 13

Agranulocytosis It crosses the placenta but may be used in low doses during pregnancy.

Answer 14

A: Hypomagnesaemia can cause hypocalcaemia and render patients unresponsive to treatment with calcium and vitamin D supplementation.

Answer 15

A: Magnesium is required for both PTH secretion and its action on target tissues.

Answer 16

A: Magnesium is the fourth most abundant cation in the body, with 50% stored in bone and the remainder in muscle, soft tissues, and extracellular fluid.

Answer 17

A: Decreased magnesium affects the permeability of cellular membranes to calcium, resulting in hyperexcitability.

Answer 18

A: CAH refers to a group of autosomal recessive disorders that impair adrenal steroid biosynthesis, leading to cortisol deficiency and compensatory overproduction of adrenocorticotropic hormone (ACTH), which increases adrenal androgen production.

Answer 19

A: 21-hydroxylase deficiency (90%), which impairs the conversion of 17-hydroxyprogesterone to 11-deoxycortisol, leading to cortisol deficiency and excess androgen production.

Answer 20

11-beta hydroxylase deficiency (5%), leading to hypertension due to excess deoxycorticosterone. 17-hydroxylase deficiency (very rare), resulting in mineralocorticoid excess with low androgen and estrogen levels.

Answer 21

Virilization: Female infants may present with ambiguous genitalia; male infants appear normal at birth. Salt-wasting crisis: Occurs in 75% of cases with 21-hydroxylase deficiency, characterized by dehydration, hypotension, and electrolyte imbalances. Precocious puberty: Early development of secondary sexual characteristics. Infertility: Due to hormonal imbalances. Height and growth abnormalities: Accelerated growth rates initially, but shorter adult stature.

Answer 22

Glucocorticoid replacement to reduce ACTH levels and minimize adrenal androgen production. Fludrocortisone is prescribed in cases of mineralocorticoid deficiency.

Answer 23

Virilization of female genitalia Precocious puberty in males 60-70% of patients have a salt-losing crisis at 1-3 weeks of age

Answer 24

Virilization of female genitalia Precocious puberty in males Hypertension Hypokalaemia

Answer 25

Non-virilizing in females Inter-sex in males Hypertension

Answer 26

Prolonged neonatal jaundice Delayed mental and physical milestones Short stature Puffy face and macroglossia Hypotonia

Answer 27

A: Children are screened at 5-7 days using the heel prick test.

Answer 28

Endocrine: Impaired glucose regulation, increased appetite/weight gain, hirsutism, hyperlipidaemia, Cushing's syndrome (moon face, buffalo hump, striae) Musculoskeletal: Osteoporosis, proximal myopathy, avascular necrosis of the femoral head Immunosuppression: Increased susceptibility to infections, reactivation of tuberculosis Psychiatric: Insomnia, mania, depression, psychosis Gastrointestinal: Peptic ulceration, acute pancreatitis Ophthalmic: Glaucoma, cataracts Other: Suppression of growth in children, intracranial hypertension, neutrophilia

Answer 29

A: Fluid retention and hypertension.

Answer 30

A: Patients on long-term steroids should have their doses doubled during intercurrent illness.

Answer 31

A: Abrupt withdrawal may precipitate an Addisonian crisis, as prolonged use suppresses natural production of endogenous steroids.

Answer 32

Gradual withdrawal should be considered if patients have: Received more than 40mg prednisolone daily for more than one week Received more than 3 weeks of treatment Recently received repeated courses

Answer 33

Impaired glucose regulation Increased appetite/weight gain Hirsutism Hyperlipidaemia

Answer 34

Moon face Buffalo hump Striae

Answer 35

Osteoporosis Proximal myopathy Avascular necrosis of the femoral head

Answer 36

Increased susceptibility to severe infection Reactivation of tuberculosis

Answer 37

Insomnia Mania Depression Psychosis

Answer 38

Peptic ulceration Acute pancreatitis

Answer 39

Glaucoma Cataracts

Answer 40

A: Suppression of growth

Answer 41

A: Intracranial hypertension and neutrophilia

Answer 42

Fluid retention Hypertension

Answer 43

A: Glucocorticoid therapy (steroid use) is the most common cause of exogenous Cushing's syndrome.

Answer 44

Cushing's disease (80%): Pituitary tumor secreting ACTH, leading to adrenal hyperplasia Ectopic ACTH production (5-10%): Often caused by small cell lung cancer

Answer 45

Iatrogenic (steroids) Adrenal adenoma (5-10%) Adrenal carcinoma (rare) Carney complex: A syndrome that includes cardiac myxoma Micronodular adrenal dysplasia (very rare)

Answer 46

A: Pseudo-Cushing's syndrome mimics Cushing's syndrome, often caused by alcohol excess or severe depression. It can cause false positive results in the dexamethasone suppression test or 24-hour urinary free cortisol.

Answer 47

A: The insulin stress test can be used to differentiate pseudo-Cushing's syndrome from true Cushing's syndrome.

Answer 48

Hypokalaemic metabolic alkalosis Impaired glucose tolerance Very low potassium levels (especially in ectopic ACTH secretion, e.g., small cell lung cancer)

Answer 49

Overnight (low-dose) dexamethasone suppression test 24-hour urinary free cortisol Bedtime salivary cortisol

Answer 50

A: In Cushing's syndrome, the morning cortisol spike is not suppressed by dexamethasone.

Answer 51

9am and midnight plasma ACTH (and cortisol) levels. Suppressed ACTH suggests a non-ACTH dependent cause (e.g., adrenal adenoma). Elevated ACTH suggests an ACTH-dependent cause (e.g., Cushing's disease or ectopic ACTH).

Answer 52

Not suppressed cortisol, suppressed ACTH: Likely adrenal cause (e.g., adrenal adenoma) Suppressed cortisol and ACTH: Likely Cushing's disease (pituitary adenoma) Not suppressed cortisol and ACTH: Likely ectopic ACTH syndrome

Answer 53

Pituitary source: Cortisol levels rise after CRH stimulation Ectopic/adrenal source: No change in cortisol levels after CRH stimulation

Answer 54

A: It may be used to differentiate between pituitary and ectopic ACTH secretion.

Answer 55

A: The insulin stress test.

Answer 56

Abdominal pain Polyuria, polydipsia, dehydration Kussmaul respiration (deep hyperventilation) Acetone-smelling breath ('pear drops' smell)

Answer 57

Urine dip for glucose and ketones Fasting glucose and random glucose HbA1c (less useful for T1DM) C-peptide levels (typically low in T1DM) Diabetes-specific autoantibodies (e.g., anti-GAD, ICA, IAA, IA-2A)

Answer 58

Fasting glucose ≥ 7.0 mmol/l Random glucose ≥ 11.1 mmol/l (or after 75g oral glucose tolerance test)

Answer 59

The above criteria (fasting ≥ 7.0 mmol/l or random ≥ 11.1 mmol/l) must be demonstrated on two separate occasions.

Answer 60

Ketosis Rapid weight loss Age of onset below 50 years BMI below 25 kg/m² Personal and/or family history of autoimmune disease

Answer 61

If T1DM is suspected but the clinical presentation includes atypical features such as: Age > 50 years BMI ≥ 25 kg/m² Slow evolution of hyperglycaemia or long prodrome

Answer 62

If the patient is over 40 years old Responds well to oral hypoglycaemic agents No need for further testing for T1DM unless there is doubt

Answer 63

Diagnosis: T1DM is confirmed with random serum glucose of 14 mmol/L (no further investigations needed).

Answer 64

Perform C-peptide levels and diabetes-specific autoantibodies due to atypical features (obesity, intermediate age).

Answer 65

T1DM is suspected due to symptoms, but due to age, further testing with C-peptide levels and diabetes-specific autoantibodies is recommended.

Answer 66

HbA1c ≥ 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus HbA1c < 48 mmol/mol (6.5%) does not exclude diabetes In asymptomatic patients, the test must be repeated for confirmation.

Answer 67

Haemoglobinopathies Haemolytic anaemia Untreated iron deficiency anaemia Suspected gestational diabetes Children HIV Chronic kidney disease Medications that may cause hyperglycaemia (e.g., corticosteroids)

Answer 68

Fasting glucose ≥ 6.1 but < 7.0 mmol/l.

Answer 69

Fasting glucose < 7.0 mmol/l and OGTT 2-hour value ≥ 7.8 but < 11.1 mmol/l.

Answer 70

An Oral Glucose Tolerance Test (OGTT) should be offered to rule out diabetes. A result between 7.8 and 11.1 mmol/l indicates Impaired Glucose Tolerance (IGT), not diabetes.

Answer 71

A: Metformin, which increases insulin sensitivity and decreases hepatic gluconeogenesis.

Answer 72

Insulin: Required for Type 1 DM and some poorly controlled Type 2 DM patients. Metformin: First-line for T2DM. Sulfonylureas: Stimulate insulin secretion. GLP-1 agonists and SGLT-2 inhibitors: Incretin mimetics and glucose reabsorption inhibitors.

Answer 73

A: GLP-1 (glucagon-like peptide-1) is a hormone released by the small intestine in response to oral glucose. It enhances insulin secretion and inhibits glucagon secretion, contributing to the incretin effect. In Type 2 diabetes (T2DM), this effect is impaired.

Answer 74

A: GLP-1 mimetics, such as exenatide and liraglutide, are drugs that mimic the action of GLP-1. They increase insulin secretion, inhibit glucagon secretion, and often result in weight loss, making them different from many other diabetes medications.

Answer 75

A: Exenatide is a GLP-1 mimetic that is administered by subcutaneous injection. It should be given 60 minutes before meals, twice daily. It helps increase insulin secretion and suppress glucagon secretion.

Answer 76

A: GLP-1 mimetics typically result in weight loss and are used in combination with other drugs like metformin or sulfonylureas. They are beneficial for patients with high BMI and may help with other comorbidities related to weight.

Answer 77

A: The main adverse effects include nausea and vomiting. Exenatide has also been associated with severe pancreatitis in some patients.

Answer 78

NICE suggests adding exenatide if: BMI ≥ 35 kg/m² in people of European descent with weight-related problems, or BMI < 35 kg/m², and insulin is not acceptable due to occupational reasons or weight loss benefits.

Answer 79

A: NICE recommends that GLP-1 mimetics should only continue if the patient achieves a >11 mmol/mol (1%) reduction in HbA1c and a 3% weight loss after 6 months.

Answer 80

A: DPP-4 inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins (GLP-1 and GIP) by inhibiting their breakdown, enhancing insulin secretion and suppressing glucagon without causing weight gain.

Answer 81

A: DPP-4 inhibitors are well tolerated, do not increase the incidence of hypoglycaemia, and do not cause weight gain, making them a preferable option for patients who need to avoid these side effects.

Answer 82

A: HbA1c should be monitored every 3-6 months. The target for adults is a level of 48 mmol/mol (6.5%) or lower, but individual factors like daily activities and history of hypoglycaemia should be considered.

Answer 83

A: Blood glucose should be tested at least 4 times a day, including before each meal and before bed. More frequent monitoring is recommended during illness, increased hypoglycaemia, exercise, pregnancy, or breastfeeding.

Answer 84

5-7 mmol/l upon waking 4-7 mmol/l before meals at other times of the day

Answer 85

A: A multiple daily injection basal-bolus insulin regimen is preferred, rather than a twice-daily mixed insulin regimen. Insulin detemir twice daily is the regime of choice, with once-daily insulin glargine or insulin detemir as alternatives.

Answer 86

A: Rapid-acting insulin analogues should be used before meals, rather than rapid-acting soluble human or animal insulins.

Answer 87

A: Metformin should be considered if the patient's BMI is ≥ 25 kg/m².

Answer 88

A: The target HbA1c is 48 mmol/mol (6.5%).

Answer 89

A: A second drug should be added if the HbA1c rises to 58 mmol/mol (7.5%).

Answer 90

A: The target is 48 mmol/mol (6.5%). For those on drugs that cause hypoglycaemia (e.g., sulfonylureas), the target is 53 mmol/mol (7.0%).

Answer 91

A: Metformin is the first-line drug of choice.

Answer 92

A: SGLT-2 inhibitors should be added if the patient has a high risk of cardiovascular disease, established cardiovascular disease, or chronic heart failure. Metformin should be established before introducing an SGLT-2 inhibitor.

Answer 93

A: If the patient has cardiovascular disease or chronic heart failure, use SGLT-2 monotherapy. If not, consider DPP-4 inhibitors, pioglitazone, or sulfonylureas.

Answer 94

Options include: Metformin + DPP-4 inhibitor Metformin + pioglitazone Metformin + sulfonylurea Metformin + SGLT-2 inhibitor (if criteria met)

Answer 95

Metformin + DPP-4 inhibitor + sulfonylurea Metformin + pioglitazone + sulfonylurea Metformin + (pioglitazone, sulfonylurea, or DPP-4 inhibitor) + SGLT-2 inhibitor (if criteria met)

Answer 96

A: GLP-1 mimetics should be added if BMI ≥ 35 kg/m² with obesity-related issues or if BMI < 35 kg/m² with potential benefits for weight loss or insulin therapy implications.

Answer 97

A: Start with human NPH insulin (isophane, intermediate-acting) at bedtime or twice daily according to need, while continuing metformin.

Answer 98

A: The target blood pressure is 140/90 mmHg in the clinic and 135/85 mmHg using ABPM or HBPM.

Answer 99

A: Statins (atorvastatin 20mg) should be prescribed if the patient has a 10-year cardiovascular risk > 10% (using QRISK2).

Answer 100

Do not stop insulin to prevent diabetic ketoacidosis. Check blood glucose every 1-2 hours, including through the night. Consider checking blood or urine ketone levels regularly. Maintain normal meal patterns if possible. If appetite is reduced, replace meals with carbohydrate-containing drinks (e.g., milk, milkshakes, fruit juices, sugary drinks). Aim for at least 3L (5 pints) of fluid a day to prevent dehydration.

Answer 101

Temporarily stop some oral hypoglycaemics. Restart medications once the person feels better and is eating and drinking for 24-48 hours.

Answer 102

A: Stop metformin if there is a risk of dehydration to reduce the risk of lactic acidosis.

Answer 103

A: Stop sulfonylureas if there is a risk of hypoglycaemia during illness.

Answer 104

Check for ketones. Stop SGLT-2 inhibitors if acutely unwell or at risk of dehydration, due to the risk of euglycaemic diabetic ketoacidosis (DKA).

Answer 105

A: Stop treatment if there is a risk of dehydration to reduce the risk of acute kidney injury (AKI).

Answer 106

A: Do not stop insulin therapy, as it is essential to prevent diabetic ketoacidosis.

Answer 107

A: Monitor blood glucose more frequently as necessary, particularly when ill or when there are changes in eating patterns or hydration.

Answer 108

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

Answer 109

Neuropathy: Loss of sensation. Ischaemia: Absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication. Complications: Calluses, ulceration, Charcot's arthropathy, cellulitis, osteomyelitis, gangrene.

Answer 110

Ischaemia screening: Palpate for dorsalis pedis and posterior tibial pulses. Neuropathy screening: Use a 10 g monofilament on various parts of the sole of the foot.

Answer 111

A: All patients with diabetes should be screened for diabetic foot disease at least annually.

Answer 112

Low risk: No risk factors except callus alone. Moderate risk: Deformity, neuropathy, or non-critical limb ischaemia. High risk: Previous ulceration, amputation, renal replacement therapy, neuropathy and non-critical limb ischaemia together, neuropathy with callus/deformity, or non-critical limb ischaemia with callus/deformity.

Answer 113

A: All moderate or high-risk patients should be followed up regularly by the local diabetic foot centre.

Answer 114

Uncontrolled lipolysis, leading to excess free fatty acids that are converted into ketone bodies. Common precipitating factors: infection, missed insulin doses, and myocardial infarction.

Answer 115

Abdominal pain Polyuria, polydipsia, dehydration Kussmaul respiration (deep hyperventilation) Acetone-smelling breath ("pear drops" smell)

Answer 116

Fluid replacement: Most patients are depleted by 5-8 liters, starting with isotonic saline. Insulin: IV infusion at 0.1 unit/kg/hour. Once blood glucose is < 14 mmol/l, start dextrose infusion (10% dextrose at 125 mls/hr). Electrolyte correction: Serum potassium is often high initially but may drop with treatment, requiring potassium replacement. Long-acting insulin: Should continue, but short-acting insulin should be stopped.

Answer 117

0.9% sodium chloride 1L over 1st hour 0.9% sodium chloride 1L with potassium chloride over next 2 hours Continue 0.9% sodium chloride with potassium chloride at 1L every 2-4 hours as per need.

Answer 118

Potassium > 5.5 mmol/L: Nil replacement. Potassium 3.5-5.5 mmol/L: Add 40 mmol of potassium to the infusion. Potassium < 3.5 mmol/L: Senior review for additional potassium replacement

Answer 119

pH > 7.3 Blood ketones < 0.6 mmol/L Bicarbonate > 15.0 mmol/L Both ketonaemia and acidosis should resolve within 24 hours.

Answer 120

Gastric stasis Thromboembolism Arrhythmias from hyperkalaemia/iatrogenic hypokalaemia Iatrogenic complications (e.g., cerebral oedema*, hypokalaemia, hypoglycaemia) Acute respiratory distress syndrome Acute kidney injury (*Cerebral oedema is especially a risk in children/young adults and requires close monitoring.)

Answer 121

Sensory loss, typically in a "glove and stocking" distribution. The lower legs are affected first due to the length of the sensory neurons. Painful diabetic neuropathy is common in clinical practice.

Answer 122

First-line treatment: Amitriptyline, duloxetine, gabapentin, or pregabalin. If the first-line drugs are ineffective: Try another of the 3 first-line options. Rescue therapy: Tramadol for exacerbations of neuropathic pain. Topical treatment: Capsaicin for localized neuropathic pain (e.g., post-herpetic neuralgia). Pain management clinics may be helpful for patients with resistant problems.

Answer 123

Gastroparesis (delayed gastric emptying): Symptoms: erratic blood glucose control, bloating, vomiting. Management: Metoclopramide, domperidone, or erythromycin (prokinetic agents). Chronic diarrhoea: Often occurs at night. Gastro-oesophageal reflux disease (GERD): Caused by decreased lower esophageal sphincter (LES) pressure.

Answer 124

Karyotype: 46 XY (genotypically male). Cause: X-linked recessive condition with a defect in the androgen receptor, resulting in resistance to testosterone. Phenotype: Female external genitalia, rudimentary vagina, and testes (no uterus). Hormone levels: Elevated testosterone, oestrogen, and LH.

Answer 125

Karyotype: 46 XY (genotypically male). Cause: Autosomal recessive condition, inability to convert testosterone to dihydrotestosterone (DHT). Phenotype: Ambiguous genitalia at birth, common hypospadias. Virilization: Occurs at puberty due to increased DHT levels.

Answer 126

Karyotype: 46 XY. Cause: The individual has testes, but external genitalia are female or ambiguous. Example: Can be secondary to androgen insensitivity syndrome.

Answer 127

Karyotype: 46 XX. Cause: The individual has ovaries, but external genitalia are male or ambiguous. Example: Can be secondary to congenital adrenal hyperplasia.

Answer 128

Karyotype: 46 XX or 47 XXY. Cause: A rare condition where both ovarian and testicular tissue are present. Phenotype: Both male and female reproductive tissues.

Answer 129

Red blood cell lifespan: Longer lifespan = higher HbA1c. Average blood glucose concentration: Higher blood glucose = higher HbA1c.

Answer 130

Sickle-cell anaemia G6PD deficiency Hereditary spherocytosis Haemodialysis

Answer 131

Vitamin B12/folic acid deficiency Iron-deficiency anaemia Splenectomy

Answer 132

HbA1c should be checked every 3-6 months until stable, then 6 monthly.

Answer 133

Graves' disease is an autoimmune thyroid disorder where the body produces IgG antibodies against the TSH receptor. It is the most common cause of thyrotoxicosis, typically affecting women aged 30-50 years.

Answer 134

Weight loss Heat intolerance Tachycardia Tremor Increased appetite Anxiety Diarrhoea

Answer 135

Eye signs (30% of patients) Exophthalmos (bulging eyes) Ophthalmoplegia (eye movement abnormalities) Pretibial myxoedema (swelling of the lower legs) Thyroid acropachy: a triad of Digital clubbing Soft tissue swelling of the hands and feet Periosteal new bone formation

Answer 136

TSH receptor stimulating antibodies (90%) Anti-thyroid peroxidase antibodies (75%)

Answer 137

Diffuse, homogenous, increased uptake of radioactive iodine.

Answer 138

Anti-thyroid drugs (ATDs) like carbimazole Radioiodine treatment Surgery

Answer 139

Significant symptoms of thyrotoxicosis High risk of hyperthyroid complications, such as in elderly patients or those with cardiovascular disease

Answer 140

Propranolol is used to block the adrenergic effects of thyrotoxicosis, helping to control symptoms like tachycardia, tremors, and anxiety.

Answer 141

Carbimazole is started at 40 mg and gradually reduced to maintain euthyroidism. Treatment typically lasts 12-18 months. The major complication is agranulocytosis. An alternative regime is block-and-replace, where carbimazole is combined with thyroxine.

Answer 142

Patients on a titration regime (adjusting carbimazole dose to maintain euthyroidism) suffer fewer side effects compared to those on block-and-replace.

Answer 143

Relapse after ATD therapy Resistance to primary ATD treatment

Answer 144

Pregnancy (avoid for 4-6 months after treatment) Age < 16 years Thyroid eye disease (relative contraindication, as it may worsen)

Answer 145

The majority of patients will require thyroxine supplementation within 5 years due to hypothyroidism.

Answer 146

Proven growth hormone deficiency Turner's syndrome Prader-Willi syndrome Chronic renal insufficiency before puberty

Answer 147

It is given by subcutaneous injection.

Answer 148

Treatment should be discontinued if there is a poor response in the first year of therapy.

Answer 149

Headache Benign intracranial hypertension Fluid retention

Answer 150

Gynaecomastia is the abnormal growth of breast tissue in males, usually caused by an increased oestrogen:androgen ratio.

Answer 151

Galactorrhoea is caused by the action of prolactin on the breast tissue, not related to gynaecomastia.

Answer 152

Normal in puberty Syndromes with androgen deficiency: Kallman's syndrome, Klinefelter's syndrome

Answer 153

Testicular failure (e.g. mumps) Liver disease Testicular cancer (e.g. seminoma secreting hCG) Ectopic tumour secretion Hyperthyroidism Haemodialysis

Answer 154

Spironolactone (most common drug cause) Cimetidine Digoxin Cannabis Finasteride GnRH agonists (e.g. goserelin, buserelin) Oestrogens, anabolic steroids

Answer 155

Hashimoto's thyroiditis (chronic autoimmune thyroiditis) is an autoimmune disorder of the thyroid gland. It is typically associated with hypothyroidism but may have a transient thyrotoxicosis in the acute phase. It is 10 times more common in women.

Answer 156

Features of hypothyroidism Goitre: firm, non-tender Anti-thyroid peroxidase (TPO) and anti-thyroglobulin (Tg) antibodies present

Answer 157

Associated with other autoimmune conditions such as: Coeliac disease Type 1 diabetes mellitus Vitiligo Associated with the development of MALT lymphoma (mucosa-associated lymphoid tissue lymphoma).

Answer 158

Primary hyperparathyroidism – most common in non-hospitalized patients. Malignancy – most common in hospitalized patients, including: PTHrP secretion by tumors (e.g. squamous cell lung cancer) Bone metastases Myeloma (due to osteoclastic bone resorption driven by cytokines like IL-1 and TNF)

Answer 159

Parathyroid hormone (PTH) levels – helps to distinguish between primary hyperparathyroidism and malignancy-related hypercalcaemia.

Answer 160

Sarcoidosis and other granulomatous diseases (e.g., tuberculosis, histoplasmosis) Vitamin D intoxication Acromegaly Thyrotoxicosis Milk-alkali syndrome Drugs: Thiazides Calcium-containing antacids Dehydration Addison's disease Paget’s disease of the bone – hypercalcaemia may occur with prolonged immobilization.

Answer 161

Hyperglycaemia → increased serum osmolality → osmotic diuresis → severe volume depletion.

Answer 162

Intercurrent illness Dementia Sedative drugs

Answer 163

Gradual onset (over days) compared to DKA (which presents within hours). Consequences of volume loss: Clinical signs of dehydration (e.g., dry mouth, reduced skin turgor) Polyuria Polydipsia Systemic: Lethargy Nausea and vomiting Neurological: Altered level of consciousness Focal neurological deficits Haematological: Hyperviscosity, which may lead to: Myocardial infarctions Stroke Peripheral arterial thrombosis

Answer 164

Hypovolaemia Marked hyperglycaemia (>30 mmol/L) Raised serum osmolality (>320 mosmol/kg), calculated as: 2 * Na+ + glucose + urea No significant hyperketonaemia (<3 mmol/L) No significant acidosis: Bicarbonate > 15 mmol/L or pH > 7.3 Acidosis may occur due to lactic acidosis or renal impairment.

Answer 165

Fluid replacement: IV 0.9% sodium chloride solution, typically at 0.5 - 1 L/hour Fluid losses are estimated to be 100-220 ml/kg Potassium levels should be monitored and added if necessary. Insulin: Only start when blood glucose stops falling with IV fluids. Venous thromboembolism prophylaxis: Patients are at risk due to hyperviscosity.

Answer 166

Vascular complications due to hyperviscosity: Myocardial infarction Stroke

Answer 167

Insulinoma: increased ratio of proinsulin to insulin Self-administration of insulin/sulphonylureas Liver failure Addison's disease Alcohol: causes exaggerated insulin secretion by affecting pancreatic blood flow Nesidioblastosis: beta cell hyperplasia

Answer 168

Hormonal response: Decreased insulin secretion Increased glucagon secretion Later, growth hormone and cortisol are released. Sympathoadrenal response: Increased catecholamine (adrenergic) and acetylcholine (cholinergic) neurotransmission.

Answer 169

Blood glucose <3.3 mmol/L causes autonomic symptoms (due to glucagon/adrenaline release): Sweating Shaking Hunger Anxiety Nausea Blood glucose <2.8 mmol/L causes neuroglycopenic symptoms (due to inadequate glucose supply to the brain): Weakness Vision changes Confusion Dizziness Severe features (uncommon): Convulsion Coma

Answer 170

Measure serum insulin and C-peptide levels. Insulin and C-peptide are released in equimolar amounts, so C-peptide is a marker of endogenous insulin production.

Answer 171

Initially, administer oral glucose (10-20g) in liquid, gel, or tablet form. Alternatively, use a proprietary quick-acting carbohydrate like GlucoGel or Dextrogel. HypoKit: A kit with a syringe and vial of glucagon for IM/SC injection may be prescribed for home use.

Answer 172

If the patient is alert, administer quick-acting carbohydrates (as above). If the patient is unconscious or unable to swallow: Subcutaneous or intramuscular glucagon. Alternatively, intravenous 20% glucose solution via a large vein.

Answer 173

Primary hypoparathyroidism is a condition where there is a decreased secretion of parathyroid hormone (PTH). Commonly seen secondary to thyroid surgery. It presents with low calcium and high phosphate levels. Treatment: Alfacalcidol (a form of vitamin D).

Answer 174

Tetany: Muscle twitching, cramping, and spasms. Perioral paraesthesia: Tingling around the mouth. Trousseau's sign: Carpal spasm induced by inflating a blood pressure cuff above systolic pressure. Chvostek's sign: Tapping over the parotid gland causes facial muscle twitching. Chronic symptoms: Depression, cataracts. ECG: Prolonged QT interval due to hypocalcaemia.

Answer 175

It is a condition where target cells are insensitive to PTH due to an abnormality in a G protein. Features include low IQ, short stature, and shortened 4th and 5th metacarpals. Laboratory findings: Low calcium, high phosphate, and high PTH. Diagnosis: Measure urinary cAMP and phosphate levels after PTH infusion. In hypoparathyroidism, both cAMP and phosphate levels rise. In pseudohypoparathyroidism type I, neither rises. In pseudohypoparathyroidism type II, only cAMP rises.

Answer 176

It has a similar phenotype to pseudohypoparathyroidism but normal biochemistry. The term is used to describe patients with the same physical characteristics but without the laboratory abnormalities seen in pseudohypoparathyroidism.

Answer 177

Although it results from a secondary cause (e.g., thyroid surgery), most medical textbooks classify it as primary hypoparathyroidism due to the loss of parathyroid hormone secretion from the glands.

Answer 178

Hashimoto's thyroiditis is the most common cause of primary hypothyroidism. It is an autoimmune disease often associated with insulin-dependent diabetes mellitus (IDDM), Addison's disease, or pernicious anaemia. It may cause transient thyrotoxicosis in the acute phase. Gender prevalence: 5-10 times more common in women.

Answer 179

Subacute thyroiditis (de Quervain's) Riedel thyroiditis After thyroidectomy or radioiodine treatment Drug therapy: e.g., lithium, amiodarone, or anti-thyroid drugs (e.g., carbimazole) Dietary iodine deficiency

Answer 180

Secondary hypothyroidism is much rarer and occurs due to pituitary failure, where the pituitary gland doesn't produce enough thyroid-stimulating hormone (TSH).

Answer 181

Down's syndrome Turner's syndrome Coeliac disease

Answer 182

Many causes of hypothyroidism may have an initial thyrotoxic phase, where there is excess thyroid hormone release before the gland becomes underactive.

Answer 183

Weight gain Lethargy Cold intolerance

Answer 184

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

Answer 185

Constipation

Answer 186

Menorrhagia (heavy menstrual bleeding)

Answer 187

Decreased deep tendon reflexes Carpal tunnel syndrome

Answer 188

Hoarse voice

Answer 189

Initial starting dose should be 25 mcg once daily, with dose titrated slowly. For patients over 50 years or with severe hypothyroidism, the BNF recommends this approach.

Answer 190

The initial starting dose should be 50-100 mcg once daily.

Answer 191

Thyroid function tests should be checked 8-12 weeks after a change in dose.

Answer 192

The therapeutic goal is normalization of the thyroid-stimulating hormone (TSH) level. Preferably aim for a TSH level in the range of 0.5-2.5 mU/L.

Answer 193

The dose should be increased by 25-50 mcg during pregnancy due to increased demands. The TSH should be monitored carefully, aiming for a low-normal value.

Answer 194

Hyperthyroidism (due to over-treatment) Reduced bone mineral density Worsening of angina Atrial fibrillation

Answer 195

Iron and calcium carbonate reduce the absorption of levothyroxine. They should be taken at least 4 hours apart from levothyroxine.

Answer 196

Insulin is composed of 51 amino acids with a molecular weight of 5808 Da. It consists of a dimer of an A-chain and a B-chain, linked by disulfide bonds.

Answer 197

Insulin is produced by the beta cells of the pancreas.

Answer 198

Pro-insulin is formed in the rough endoplasmic reticulum of pancreatic beta cells. Pro-insulin is cleaved to form insulin and C-peptide. Insulin is stored in secretory granules and released in response to Ca2+.

Answer 199

Secreted in response to hyperglycaemia. Promotes glucose utilisation and glycogen synthesis in liver and muscles. Inhibits lipolysis (fat breakdown). Reduces muscle protein loss. Increases cellular uptake of potassium via the Na+/K+ ATPase pump.

Answer 200

Insulin increases the cellular uptake of potassium by stimulating the Na+/K+ ATPase pump, which helps maintain potassium balance.

Answer 201

The insulin stress test is used to investigate hypopituitarism.

Answer 202

IV insulin is administered. Growth hormone (GH) and cortisol levels are then measured. With normal pituitary function, both GH and cortisol should rise in response to the insulin administration.

Answer 203

In a normal pituitary, both GH and cortisol should rise following the administration of IV insulin.

Answer 204

Epilepsy Ischaemic heart disease Adrenal insufficiency

Answer 205

Sweating Anxiety Blurred vision Confusion Aggression

Answer 206

Take 10-20g of a short-acting carbohydrate, such as: A glass of Lucozade or any non-diet drink Three or more glucose tablets Glucose gel

Answer 207

Glucagon kit for emergency use, to raise blood glucose in unconscious patients or those unable to ingest oral glucose.

Answer 208

Frequent hypoglycaemic episodes may lead to reduced awareness of symptoms. To restore awareness, allow glycaemic control to slip for a period of time. Beta-blockers can also reduce hypoglycaemic awareness.

Answer 209

Lipodystrophy presents as atrophy or lumps of subcutaneous fat at the injection sites. It can be prevented by rotating injection sites. If untreated, it can lead to erratic insulin absorption.

Answer 210

A neuroendocrine tumour mainly arising from pancreatic Islets of Langerhans cells. It is the most common pancreatic endocrine tumour.

Answer 211

50% of patients with multiple insulinomas have MEN-1 (Multiple Endocrine Neoplasia type 1).

Answer 212

Symptoms often occur early in the morning or just before meals, such as: Diplopia Weakness Other signs of hypoglycaemia.

Answer 213

High insulin levels Raised proinsulin:insulin ratio High C-peptide levels.

Answer 214

Supervised, prolonged fasting (up to 72 hours) to provoke hypoglycaemia and assess insulin response. CT scan of the pancreas.

Answer 215

Surgery (if feasible). If surgery is not possible, diazoxide and somatostatin can be used.

Answer 216

A cause of delayed puberty secondary to hypogonadotropic hypogonadism. Usually inherited as an X-linked recessive trait. It is caused by the failure of GnRH-secreting neurons to migrate to the hypothalamus.

Answer 217

Anosmia (lack of smell) in a boy with delayed puberty.

Answer 218

Delayed puberty Hypogonadism and cryptorchidism Anosmia Low sex hormone levels Inappropriately low/normal LH and FSH levels Normal or above-average height Cleft lip/palate and visual/hearing defects (in some patients).

Answer 219

Testosterone supplementation to induce puberty and secondary sexual characteristics. Gonadotrophin supplementation may be used to induce sperm production if fertility is desired later in life.

Answer 220

47, XXY karyotype.

Answer 221

Taller than average Lack of secondary sexual characteristics Small, firm testes Infertility Gynaecomastia (increased incidence of breast cancer) Elevated gonadotrophin levels but low testosterone.

Answer 222

Diagnosis is made by karyotype (chromosomal analysis).

Answer 223

Autosomal dominant.

Answer 224

Hypertension Hypokalaemic alkalosis Caused by disordered sodium channels in the distal tubules, leading to increased reabsorption of sodium.

Answer 225

Amiloride or triamterene.

Answer 226

A form of monogenic diabetes characterized by autosomal dominant inheritance, typically onset before 25 years of age, and insulin secretion impairment without major defects in insulin action.

Answer 227

Mild non-ketotic hyperglycemia Normal weight, no signs of insulin resistance No diabetic ketoacidosis, except under severe stress May be discovered incidentally or during pregnancy.

Answer 228

Suspected in individuals with persistent hyperglycemia before age 25, without typical features of Type 1 or Type 2 diabetes. Diagnosis confirmed by genetic testing.

Answer 229

Treatment varies by genetic subtype: MODY2 (GCK mutation): May not require treatment due to mild hyperglycemia. MODY3 (HNF1A mutation): Typically responds well to low-dose sulfonylureas. Insulin therapy may be needed, especially during pregnancy or if sulfonylureas are ineffective.

Answer 230

MEN is an autosomal dominant disorder that involves the development of tumors or hyperplasia in multiple endocrine glands.

Answer 231

MEN type I MEN type IIa MEN type IIb

Answer 232

3 P's: Parathyroid hyperplasia (95%): leading to hyperparathyroidism Pituitary tumors (70%) Pancreatic tumors (50%): e.g., insulinoma, gastrinoma (causing recurrent peptic ulceration) Also: adrenal tumors and thyroid involvement MEN1 gene mutation Most common presentation: hypercalcemia

Answer 233

2 P's: Parathyroid hyperplasia (60%) Phaeochromocytoma Medullary thyroid cancer (70%) RET oncogene mutation

Answer 234

1 P: Phaeochromocytoma Marfanoid body habitus Neuromas Medullary thyroid cancer RET oncogene mutation

Answer 235

RET oncogene

Answer 236

Myxoedema coma is a medical emergency caused by severe hypothyroidism, typically presenting with confusion and hypothermia.

Answer 237

Confusion Hypothermia Severe hypothyroidism symptoms.

Answer 238

IV thyroid replacement IV fluid IV corticosteroids (until coexisting adrenal insufficiency is excluded) Electrolyte imbalance correction Rewarming (sometimes)

Answer 239

Neuroblastoma is one of the top five causes of cancer in children, accounting for around 7-8% of childhood malignancies. It arises from neural crest tissue of the adrenal medulla (most common site) and sympathetic nervous system.

Answer 240

Abdominal mass Pallor and weight loss Bone pain, limp Hepatomegaly Paraplegia Proptosis

Answer 241

Raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels Calcification may be seen on abdominal X-ray Biopsy

Answer 242

BMI = weight (kg) / height (m)²

Answer 243

Underweight: < 18.49 kg/m² Normal: 18.5 - 25 kg/m² Overweight: 25 - 30 kg/m² Obese class 1: 30 - 35 kg/m² Obese class 2: 35 - 40 kg/m² Obese class 3: > 40 kg/m²

Answer 244

Conservative: Diet, exercise Medical: Orlistat, liraglutide Surgical

Answer 245

Orlistat is a pancreatic lipase inhibitor used to manage obesity. Adverse effects: Faecal urgency, incontinence, flatulence. Criteria for use: BMI ≥ 28 kg/m² with associated risk factors, or BMI ≥ 30 kg/m² Continued weight loss (e.g., 5% at 3 months) Typically used for < 1 year.

Answer 246

Liraglutide is a GLP-1 mimetic used in type 2 diabetes mellitus (T2DM) and obesity. Administered as a once daily subcutaneous injection. Weight loss noted in significant proportions of T2DM patients, leading to its use in obesity. NICE criteria for use: BMI ≥ 35 kg/m² Prediabetic hyperglycaemia (e.g., HbA1c 42-47 mmol/mol)

Answer 247

PTH: Elevated Ca2+: Elevated Phosphate: Low Urine calcium: creatinine clearance ratio: > 0.01

Answer 248

May be asymptomatic if mild Recurrent abdominal pain (pancreatitis, renal colic) Changes to emotional or cognitive state

Answer 249

Solitary adenoma (80% of cases) Multifocal disease (10-15%) Parathyroid carcinoma (< 1%)

Answer 250

PTH: Elevated Ca2+: Low or normal Phosphate: Elevated Vitamin D: Low

Answer 251

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

Answer 252

Parathyroid gland hyperplasia due to low calcium, often in chronic renal failure

Answer 253

Ca2+: Normal or high PTH: Elevated Phosphate: Decreased or normal Vitamin D: Normal or decreased Alkaline phosphatase: Elevated

Answer 254

Metastatic calcification Bone pain and/or fractures Nephrolithiasis (kidney stones) Pancreatitis

Answer 255

Ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, usually affecting all 4 glands

Answer 256

In benign familial hypocalciuric hypercalcaemia, the urine calcium: creatinine clearance ratio is < 0.01, unlike primary hyperparathyroidism, where it is > 0.01. Diagnosis is made by genetic testing.

Answer 257

Serum calcium > 1mg/dL above normal Hypercalciuria > 400mg/day Creatinine clearance < 30% Episode of life-threatening hypercalcaemia Nephrolithiasis Age < 50 years Neuromuscular symptoms Reduction in bone mineral density (T score < -2.5)

Answer 258

Bone pain Persistent pruritus Soft tissue calcifications

Answer 259

Allow 12 months to elapse after transplant, as many cases resolve. If an autonomously functioning parathyroid gland is identified, it should be excised. If unable to identify the culprit gland, total parathyroidectomy with re-implantation of part of the gland may be required.

Answer 260

A rare catecholamine-secreting tumour. 10% are familial and may be associated with MEN type II, neurofibromatosis, and von Hippel-Lindau syndrome.

Answer 261

Hypertension (around 90% of cases, may be sustained) Headaches Palpitations Sweating Anxiety

Answer 262

24-hour urinary collection of metanephrines (sensitivity 97%) This test has replaced 24-hour urinary collection of catecholamines (sensitivity 86%).

Answer 263

Surgery is the definitive management.

Answer 264

Alpha-blocker (e.g., phenoxybenzamine) should be given before a beta-blocker (e.g., propranolol) to stabilize the patient before surgery.

Answer 265

A benign tumour of the pituitary gland. Common (10% of all people), but often asymptomatic or found incidentally. Accounts for around 10% of adult brain tumours.

Answer 266

Size: Microadenoma: <1 cm Macroadenoma: ≥1 cm Hormonal status: Secretory/functioning adenoma: Excess hormone production. Non-secretory/functioning adenoma: No excess hormone production.

Answer 267

Prolactinomas: Most common, producing excess prolactin. Non-secretory adenomas: Next most common. GH-secreting adenomas: Produce excess growth hormone. ACTH-secreting adenomas: Produce excess ACTH (Cushing's disease).

Answer 268

Excess hormones (e.g., Cushing's disease, acromegaly, amenorrhea/galactorrhea). Depletion of hormones (due to compression of normal pituitary tissue). Non-functioning tumours: Present with generalised hypopituitarism. Dural stretching: Causes headaches. Optic chiasm compression: Causes bitemporal hemianopia.

Answer 269

Pituitary blood profile (GH, prolactin, ACTH, FSH, LSH, TFTs). Formal visual field testing. MRI brain with contrast.

Answer 270

Pituitary hyperplasia Craniopharyngioma Meningioma Brain metastases Lymphoma Hypophysitis Vascular malformation (e.g., aneurysm)

Answer 271

Medical therapy: Prolactinomas: Treated with dopamine agonists (e.g., cabergoline, bromocriptine). GH-secreting adenomas: Treated with somatostatin analogues (e.g., octreotide, lanreotide) and GH receptor antagonists (e.g., pegvisomant). ACTH-secreting adenomas: Treated with cortisol synthesis inhibitors (e.g., ketoconazole, metyrapone) and neuromodulators (e.g., pasireotide). Surgery: Transsphenoidal surgery is the primary treatment, especially for non-functioning adenomas, and ACTH- or GH-secreting adenomas. Surgery aims to remove the tumour, normalize hormone levels, and address compressive symptoms (e.g., visual problems). Radiotherapy: Indicated for residual or recurrent tumours post-surgery.

Answer 272

Lifestyle modification: Weight loss, increased exercise, and diet changes. Yearly follow-up with blood tests. NICE recommendations: Metformin for adults at high risk if blood glucose levels (fasting plasma glucose or HbA1c) show continued progression toward type 2 diabetes, despite intensive lifestyle changes.

Answer 273

Impaired Fasting Glucose (IFG): Due to hepatic insulin resistance. Impaired Glucose Tolerance (IGT): Due to muscle insulin resistance. IGT is more likely to progress to type 2 diabetes (T2DM) and cardiovascular disease than IFG.

Answer 274

Impaired Fasting Glucose (IFG): Fasting glucose ≥ 6.1 mmol/l but < 7.0 mmol/l. Impaired Glucose Tolerance (IGT): Fasting plasma glucose < 7.0 mmol/l and OGTT 2-hour value ≥ 7.8 mmol/l but < 11.1 mmol/l. IGT is diagnosed after an oral glucose tolerance test (OGTT). A result between 7.8 mmol/l and 11.1 mmol/l indicates IGT (not diabetes).

Answer 275

Increased thyroxine-binding globulin (TBG) levels in pregnancy cause an increase in total thyroxine levels. This increase in total thyroxine does not affect free thyroxine levels

Answer 276

Fetal loss Maternal heart failure Premature labour

Answer 277

Graves' disease is the most common cause. Transient gestational hyperthyroidism can also occur due to HCG activation of the TSH receptor.

Answer 278

Propylthiouracil (PTU) is traditionally used in the first trimester. PTU is preferred over carbimazole, which is associated with an increased risk of congenital abnormalities. Propylthiouracil is associated with an increased risk of severe hepatic injury, so careful monitoring is needed.

Answer 279

Keep maternal free thyroxine levels in the upper third of the normal reference range to avoid fetal hypothyroidism. Thyrotrophin receptor stimulating antibodies should be checked at 30-36 weeks gestation to assess the risk of neonatal thyroid problems. Block-and-replace regimes should not be used during pregnancy. Radioiodine therapy is contraindicated in pregnancy.

Answer 280

Thyroxine is safe during pregnancy. Serum thyroid-stimulating hormone (TSH) should be measured in each trimester and 6-8 weeks postpartum. Women often need an increased dose of thyroxine (up to 50% more) starting as early as 4-6 weeks of pregnancy. Breastfeeding is safe while on thyroxine.

Answer 281

Bilateral idiopathic adrenal hyperplasia (60-70% of cases) Adrenal adenoma (20-30% of cases) Other causes include unilateral hyperplasia, familial hyperaldosteronism, and adrenal carcinoma.

Answer 282

Hypertension (often treatment-resistant) Hypokalaemia (e.g., muscle weakness, though this occurs in only 10-40% of cases) Metabolic alkalosis Muscle weakness is more common with adrenal adenomas.

Answer 283

Plasma aldosterone/renin ratio High aldosterone with low renin levels (due to negative feedback from sodium retention) suggests primary hyperaldosteronism.

Answer 284

High-resolution CT abdomen: Identifies adrenal abnormalities. Adrenal vein sampling (AVS): Differentiates between unilateral adenoma and bilateral hyperplasia if CT is normal.

Answer 285

Adrenal adenoma: Surgery (laparoscopic adrenalectomy). Bilateral adrenocortical hyperplasia: Aldosterone antagonists (e.g., spironolactone).

Answer 286

85% of cases are caused by a solitary parathyroid adenoma.

Answer 287

"Bones, stones, abdominal groans, and psychic moans" Bones: Bone pain/fractures (osteitis fibrosa cystica) Stones: Renal stones Abdominal groans: Anorexia, nausea, constipation, peptic ulceration, pancreatitis Psychic moans: Depression, confusion Other symptoms: Polydipsia, polyuria, hypertension

Answer 288

Blood tests: Raised calcium Low phosphate PTH: May be raised or normal (inappropriately, given raised calcium) Technetium-MIBI subtraction scan X-ray findings: Pepperpot skull (due to cortical bone thinning) Osteitis fibrosa cystica

Answer 289

Total parathyroidectomy.

Answer 290

If calcium is less than 0.25 mmol/L above the upper limit of normal, the patient is >50 years old, and there is no evidence of end-organ damage.

Answer 291

Cinacalcet is a calcimimetic that mimics calcium's action on tissues, activating the calcium-sensing receptor. It may be used for patients not suitable for surgery.

Answer 292

Anterior pituitary

Answer 293

Stimulates breast development (initially and further hyperplasia during pregnancy) Stimulates milk production Decreases GnRH pulsatility at the hypothalamic level Blocks the action of LH on the ovary or testis to a lesser extent.

Answer 294

Thyrotropin-releasing hormone (TRH) Pregnancy Oestrogen Breastfeeding Sleep Stress Drugs: e.g., metoclopramide, antipsychotics

Answer 295

Dopamine Dopaminergic agonists

Answer 296

Dopamine Dopamine agonists (e.g., bromocriptine) can be used to control galactorrhoea.

Answer 297

Men: Impotence, loss of libido, galactorrhoea Women: Amenorrhoea, galactorrhoea

Answer 298

Prolactinoma Pregnancy Oestrogens Physiological: Stress, exercise, sleep Acromegaly (1/3 of patients) Polycystic ovarian syndrome Primary hypothyroidism (due to TRH stimulating prolactin release)

Answer 299

Metoclopramide, domperidone Phenothiazines Haloperidol Very rare: SSRIs, opioids

Answer 300

A prolactinoma is a type of pituitary adenoma (benign tumour) that produces an excess of prolactin.

Answer 301

Amenorrhoea Infertility Galactorrhoea Osteoporosis

Answer 302

Impotence Loss of libido Galactorrhoea

Answer 303

Headache Visual disturbances: Bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia Symptoms of hypopituitarism

Answer 304

MRI is used to diagnose a prolactinoma.

Answer 305

Medical treatment: Dopamine agonists (e.g., cabergoline, bromocriptine) to inhibit prolactin release Surgery: If the patient cannot tolerate or fails to respond to medical therapy, trans-sphenoidal surgery is typically performed (unless there is significant extra-pituitary extension).

Answer 306

PTH is a polypeptide hormone secreted from the parathyroid glands. It plays a vital role in calcium homeostasis by maintaining blood calcium levels within a narrow range.

Answer 307

Calcium enters the body through the intestines and exits through urine and faeces. The main calcium reservoir is the bone. In the blood, calcium exists in three forms: Free calcium (physiologically active) Calcium bound to albumin Calcium complexed with anions

Answer 308

PTH is a single-chain polypeptide containing 84 amino acids. It is secreted by the chief cells of the parathyroid glands in response to low blood calcium levels. Function: In the bone: Increases osteoclast activity, causing bone resorption and releasing calcium and phosphate into the blood. In the kidney: Increases activation of vitamin D, which promotes calcium absorption. Increases calcium reabsorption from the renal tubules and increases phosphate excretion.

Answer 309

Negative feedback loop: Low calcium levels are detected by the parathyroid glands. PTH is secreted into the blood, causing calcium release from bones and reabsorption in the kidneys. Calcium levels rise and are detected by the parathyroid glands, which then reduce PTH secretion.

Answer 310

A condition where the parathyroid glands are overactive, leading to excessive secretion of PTH and resulting in hypercalcaemia. Common causes include hyperplasia, adenomas, or malignancies. Symptoms include renal calculi, constipation, polyuria, abdominal pain, and low mood. Treatment: Surgical removal of the glands.

Answer 311

A polypeptide that has a similar structure to PTH and can be secreted by cancer cells (e.g., squamous cell bronchial carcinoma). It causes hypercalcaemia but cannot activate vitamin D, unlike PTH.

Answer 312

A rare cause of hypothyroidism. Characterized by dense fibrous tissue replacing the normal thyroid parenchyma.

Answer 313

Hard, fixed, painless goitre on examination. Hypothyroidism symptoms (e.g., fatigue, weight gain, cold intolerance).

Answer 314

Retroperitoneal fibrosis (fibrous tissue growth in the retroperitoneal space).

Answer 315

They reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule. This reduces glucose reabsorption and increases urinary glucose excretion.

Answer 316

Urinary and genital infections (due to glycosuria). Fournier's gangrene (rare but severe). Normoglycaemic ketoacidosis. Increased risk of lower-limb amputation (close monitoring of feet is needed).

Answer 317

Weight loss is often seen, which can be beneficial for managing type 2 diabetes mellitus.

Answer 318

A condition where thyroid function tests are altered during systemic illness. It is characterized by low levels of thyroxine (T4) and T3, but the TSH is often inappropriately normal (higher than expected given the low T4 and T3).

Answer 319

TSH is often within the normal range, but may be inappropriately normal given low T4 and T3 levels. T4 and T3 levels are typically low.

Answer 320

No treatment is usually required. Changes in thyroid function are typically reversible upon recovery from the underlying systemic illness.

Answer 321

Substrate mobilization Muscle protein loss Sodium and water retention Suppression of anabolic hormones Activation of the sympathetic nervous system Immunological and hematological changes

Answer 322

Growth hormone Cortisol Renin ACTH Aldosterone Prolactin Antidiuretic hormone Glucagon

Answer 323

Insulin Testosterone Thyroid-stimulating hormone (TSH) Luteinizing hormone (LH) Follicle stimulating hormone (FSH)

Answer 324

Increases skeletal muscle protein breakdown Stimulates lipolysis Exhibits an anti-insulin effect Has mineralocorticoid effects Anti-inflammatory effects

Answer 325

Insulin release is inhibited by stress, leading to insulin resistance. Initially, there is functional insulin deficiency, contributing to hyperglycemia.

Answer 326

Decreased thyroid hormone production post-surgery, inversely correlated with sympathetic activity. Recovery occurs within a few days after surgery.

Answer 327

Initially, protein anabolism is inhibited, followed by enhanced catabolism in severe stress. Skeletal muscle protein is mainly affected. Amino acids released are used for gluconeogenesis.

Answer 328

Increased catecholamine, cortisol, and glucagon secretion promotes lipolysis and ketone body production.

Answer 329

Opioids suppress hormone secretion but may prolong recovery and increase ventilatory support needs. Spinal anaesthesia reduces hormone and glucose changes but does not alter cytokine responses. Nutrition (enteral feeding) improves recovery and mitigates adverse effects. Growth hormone and anabolic steroids may improve outcomes. Normothermia reduces the metabolic response.

Answer 330

Subacute thyroiditis (also called De Quervain's thyroiditis) is a condition believed to be triggered by a viral infection, often presenting with hyperthyroidism.

Answer 331

Phase 1 (3-6 weeks): Hyperthyroidism, painful goitre, elevated ESR (erythrocyte sedimentation rate). Phase 2 (1-3 weeks): Euthyroid (normal thyroid function). Phase 3 (weeks to months): Hypothyroidism. Phase 4: Return to normal thyroid structure and function.

Answer 332

Thyroid scintigraphy: Globally reduced uptake of iodine-131.

Answer 333

Self-limiting: Most patients do not require treatment. Pain relief: Aspirin or other NSAIDs may help with thyroid pain. In severe cases, steroids may be used, especially if hypothyroidism develops.

Answer 334

Subclinical hyperthyroidism is defined as: Normal serum free thyroxine (T4) and triiodothyronine (T3) levels A TSH (thyroid-stimulating hormone) level below the normal range (usually < 0.1 μU/L).

Answer 335

Multinodular goitre, especially in elderly females Excessive thyroxine (e.g., from overuse of thyroid hormone replacement therapy) can cause a similar biochemical picture.

Answer 336

Cardiovascular risk: Increased risk of atrial fibrillation. Bone health: May lead to osteoporosis. Quality of life: Can impact quality of life and may increase the risk of dementia.

Answer 337

Observation: TSH levels often revert to normal on their own. Treatment is considered only if levels remain persistently low. Therapeutic trial: A trial of low-dose antithyroid agents (e.g., methimazole) for 6 months may be considered to try and induce remission.

Answer 338

TSH is raised, but T3 and T4 are normal. Patients often have no obvious symptoms.

Answer 339

Progression to overt hypothyroidism: Risk is 2-5% per year, higher in men. Thyroid autoantibodies: Presence of these increases the risk of progression.

Answer 340

TSH > 10 mU/L with normal free thyroxine: Consider offering levothyroxine if TSH is > 10 mU/L on 2 separate occasions 3 months apart. TSH between 5.5 - 10 mU/L with normal free thyroxine: < 65 years: Offer a 6-month trial of levothyroxine if TSH is in this range on 2 separate occasions and there are symptoms of hypothyroidism. > 80 years: A 'watch and wait' strategy is often used. If asymptomatic, observe and repeat thyroid function in 6 months.

Answer 341

Sulfonylureas increase pancreatic insulin secretion. Effective only if functional beta cells are present. They bind to an ATP-dependent K+ (KATP) channel on the cell membrane of pancreatic beta cells.

Answer 342

Hypoglycaemic episodes (more common with long-acting preparations like chlorpropamide). Weight gain.

Answer 343

Hyponatraemia (due to syndrome of inappropriate ADH secretion). Bone marrow suppression. Hepatotoxicity (typically cholestatic). Peripheral neuropathy.

Answer 344

Avoid use in pregnancy and breastfeeding.

Answer 345

A: Thiazolidinediones are a class of agents used in the treatment of type 2 diabetes mellitus.

Answer 346

A: They are agonists of the PPAR-gamma receptor and reduce peripheral insulin resistance.

Answer 347

A: Weight gain and liver impairment (monitor LFTs).

Answer 348

A: They cause fluid retention, and the risk is increased if the patient also takes insulin.

Answer 349

A: No, they are not commonly seen as thyroid malignancies rarely secrete thyroid hormones.

Answer 350

A: Papillary thyroid cancer, accounting for 70% of cases, often in young females with an excellent prognosis.

Answer 351

A: 20%; it may appear macroscopically encapsulated, but microscopic capsular invasion is seen. Vascular invasion predominates.

Answer 352

A: It is a cancer of parafollicular (C) cells, secretes calcitonin, and is part of MEN-2 syndrome.

Answer 353

A: 1%; it is not responsive to treatment and can cause pressure symptoms. Treatment is resection where possible, with palliation through isthmusectomy and radiotherapy.

Answer 354

A: Lymphoma, which is rare.

Answer 355

A: Total thyroidectomy followed by radioiodine (I-131) to kill residual cells, with yearly thyroglobulin levels to detect early recurrent disease.

Answer 356

A: Anaplastic carcinoma, with local invasion being a common feature.

Answer 357

A: It is thought to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor, leading to retro-orbital inflammation and resulting in glycosaminoglycan and collagen deposition in the muscles.

Answer 358

A: Smoking

Answer 359

A: Radioiodine treatment may increase inflammatory symptoms, with around 15% of patients with Graves' disease developing or having worsening of eye disease. Prednisolone may help reduce the risk.

Answer 360

A: Exophthalmos, conjunctival oedema, optic disc swelling, ophthalmoplegia, and inability to close the eyelids which may lead to sore, dry eyes and risk of exposure keratopathy.

Answer 361

A: Smoking cessation, topical lubricants, steroids, radiotherapy, and surgery.

Answer 362

A: Exposure keratopathy is caused by eyelid retraction and proptosis (exophthalmos) leading to corneal exposure, dryness, irritation, and corneal ulceration.

Answer 363

A: Foreign body sensation, pain, photophobia, and in severe cases, corneal scarring and vision impairment.

Answer 364

A: Optic neuropathy is a serious complication of thyroid eye disease where enlarged extraocular muscles compress the optic nerve, leading to reduced visual acuity, color vision deficits, and visual field defects.

Answer 365

A: Fibrosis and enlargement of extraocular muscles can result in restrictive strabismus, causing misalignment of the eyes and double vision (diplopia), affecting visual function and quality of life.

Answer 366

A: Unexplained deterioration in vision, change in color vision quality, eye 'popping out' (globe subluxation), obvious corneal opacity, cornea visible when eyelids are closed, and disc swelling.

Answer 367

A: TSH: Low, Free T4: High. In T3 thyrotoxicosis, the free T4 will be normal.

Answer 368

A: TSH: High, Free T4: Low.

Answer 369

A: TSH: Low, Free T4: Low. Replacement steroid therapy is required before thyroxine.

Answer 370

A: TSH: Low (sometimes normal), Free T4: Low. T3 is particularly low in these patients. This is common in hospital inpatients.

Answer 371

A: TSH: High, Free T4: Normal.

Answer 372

A: TSH: High, Free T4: Normal.

Answer 373

A: TSH: Low, Free T4: Normal.

Answer 374

A: The primary aim is to exclude thyroid cancer, which accounts for around 5% of all nodules depending on the patient demographic.

Answer 375

A: Multinodular goitre, thyroid adenoma, Hashimoto's thyroiditis, cysts (colloid, simple, or hemorrhagic).

Answer 376

A: Papillary carcinoma (most common malignant cause), follicular carcinoma, medullary carcinoma, anaplastic carcinoma, lymphoma.

Answer 377

A: Thyroid function tests should be checked in all patients.

Answer 378

A: Ultrasonography is the first-line imaging of choice, which may help determine if the nodule has features suspicious of malignancy.

Answer 379

A: Thyroid storm is a rare but life-threatening complication of thyrotoxicosis, typically seen in patients with established thyrotoxicosis, and is rarely seen as the presenting feature.

Answer 380

A: Thyroid or non-thyroidal surgery, trauma, infection, acute iodine load (e.g., CT contrast media).

Answer 381

A: Fever >38.5ºC, tachycardia, confusion and agitation, nausea and vomiting, hypertension, heart failure, abnormal liver function tests (jaundice).

Answer 382

A: Paracetamol (for fever) and treatment of the underlying precipitating event.

Answer 383

A: Beta-blockers (typically IV propranolol), anti-thyroid drugs (e.g., methimazole or propylthiouracil), Lugol's iodine, and dexamethasone (blocks the conversion of T4 to T3).

Answer 384

A: Dexamethasone blocks the conversion of T4 to T3.

Answer 385

A: Graves' disease, accounting for around 50-60% of cases.

Answer 386

A: Graves' disease, toxic nodular goitre, acute phase of subacute (de Quervain's) thyroiditis, acute phase of post-partum thyroiditis, acute phase of Hashimoto's thyroiditis, amiodarone therapy, and contrast use.

Answer 387

A: Amiodarone can cause thyrotoxicosis, particularly in elderly patients with pre-existing thyroid disease (e.g., multinodular goitre, Graves'). It can cause hyperthyroidism due to a large iodine load on the thyroid.

Answer 388

A: TSH is low, and T4 and T3 are elevated.

Answer 389

A: Thyroid function tests (TSH, T4, T3), thyroid autoantibodies, and isotope scanning if needed. Other investigations are not routinely done.

Answer 390

A: Weight loss, 'manic' behavior, and restlessness, as well as heat intolerance.

Answer 391

A: Palpitations, tachycardia, and high-output cardiac failure, which may occur in elderly patients. A reversible cardiomyopathy can rarely develop.

Answer 392

A: Increased sweating, pretibial myxoedema (erythematous, oedematous lesions above the lateral malleoli), and thyroid acropachy (clubbing).

Answer 393

A: Diarrhoea.

Answer 394

A: Oligomenorrhea.

Answer 395

A: Anxiety and tremor.

Answer 396

A: Toxic multinodular goitre is a condition where a thyroid gland contains several autonomously functioning thyroid nodules, leading to hyperthyroidism.

Answer 397

A: Patchy uptake.

Answer 398

A: Radioiodine therapy.

Answer 399

A: The water deprivation test is used to evaluate patients with polydipsia.

Answer 400

A: The patient is prevented from drinking water, asked to empty their bladder, and urine and plasma osmolalities are measured hourly.

Answer 401

A: Starting plasma osmolality: Normal, Final urine osmolality: >600, Urine osmolality post-DDAVP: >600.

Answer 402

A: Starting plasma osmolality: Low, Final urine osmolality: >400, Urine osmolality post-DDAVP: >400.

Answer 403

A: Starting plasma osmolality: High, Final urine osmolality: <300, Urine osmolality post-DDAVP: >600.

Answer 404

A: Starting plasma osmolality: High, Final urine osmolality: <300, Urine osmolality post-DDAVP: <300.

Answer 405

review by senior

Answer 406

sulfonylurea

Answer 407

thiazolidinediones

Answer 408

GLP 1 mimetic

Answer 409

add liraglutide

Answer 410

OGTT + serial GH measurements

Answer 411

hypogonadotrophic hypogonadism

Answer 412

Test sensation using a 10 g monofilament

Answer 413

reduce but neutrophils increase

Answer 414

PTH super high, moderately raised calcium

Answer 415

an infusion of 10% dextrose should be started at 125 mls/hr in addition to the saline regime

Answer 416

sulfonylurea

Answer 417

Causes of raised prolactin - the p's pregnancy prolactinoma physiological polycystic ovarian syndrome primary hypothyroidism phenothiazines, metoclopramide, domperidone

Answer 418

Bi temporal superior quadrantanopia into bitemporal hemianopia

Answer 419

Bi temporal inferior quadrantanopia into bitemporal hemianopia

Answer 420

EXPLAIN Exogenous drugs (typically sulfonylureas or insulin) Pituitary insufficiency Liver failure Addison's disease Islet cell tumours (insulinomas) Non-pancreatic neoplasms

Answer 421

1) hypoglycaemia with fasting or exercise, 2) reversal of symptoms with glucose, and 3) recorded low BMs at the time of symptoms is hallmark for an insulinoma

Answer 422

super high glucose rather than super low

Answer 423

Not sure if this will help anyone but one of the consultants in the hospital described hyperthyroidism as everything going up besides weight and periods (i.e. heart rate, diarrhoea etc.) and hypothyroidism as everything going down besides weight and periods

Answer 424

primary hyperaldosteronism

Answer 425

pituitary adenoma (non functioning)

Answer 426

Split with the majority in the first half of the day

Answer 427

secondary - pituitary tertiary - hypothalamic