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MRCP PART 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Complications of Acromegaly?

A

In acromegaly there is excess growth hormone secondary to a pituitary adenoma in over 95% of cases.

Complications:
Hypertension
Diabetes (>10%)
Cardiomyopathy
Colorectal cancer

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2
Q

When to add a second drug for T2DM?

A

It’s worthwhile thinking of the average patient who is taking metformin for T2DM, you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%).

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3
Q

Drug causes of gynaecomastia?

A
  • Spironolactone (most common drug cause)
  • Cimetidine
  • Digoxin
  • Cannabis
  • Finasteride
  • GnRH agonists e.g. goserelin, buserelin
  • Oestrogens, anabolic steroids
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4
Q

What is the mechanism of action of sulfonylureas?

A

Sulfonylureas are oral hypoglycaemic drugs used in the management of type 2 diabetes mellitus. They work by increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells.

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5
Q

Hashimoto’s thyroiditis is associated with which malignancy?

A

Hashimoto’s thyroiditis is associated with the development of MALT lymphoma.
Mucosa-associated lymphoid tissue (MALT) lymphoma is a rare form of thyroid lymphoma it is associated with a previous history of Hashimoto’s thyroiditis and histology shows extranodal marginal B-cells.

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6
Q

Management options for stress incontinence?

A

If stress incontinence is predominant:

  • Pelvic floor muscle training
    NICE recommend at least 8 contractions performed 3 times per day for a minimum of 3 months.
  • Surgical procedures: e.g. retropubic mid-urethral tape procedures.
  • Duloxetine may be offered to women if they decline surgical procedures. A combined noradrenaline and serotonin reuptake inhibitor
    mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced contraction
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7
Q

Management for urge incontinence?

A

If urge incontinence is predominant:

  • Bladder retraining (lasts for a minimum of 6 weeks, the idea is to gradually increase the intervals between voiding).
  • Bladder stabilising drugs: Antimuscarinics are first-line: Oxybutynin (immediate release), Tolterodine (immediate release) or Darifenacin (once daily preparation)
  • Immediate release oxybutynin should, however, be avoided in ‘frail older women’
  • Mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patients
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8
Q

Mode of inheritance for MODY?

A

Autosomal dominant.

Patients with MODY often present with mild non-ketotic hyperglycemia that is often detected incidentally or during routine screening. It may also be discovered during pregnancy. Unlike Type 1 diabetes, patients with MODY usually do not present with diabetic ketoacidosis except under severe stress conditions, and unlike Type 2 diabetes, they are often of normal weight and do not exhibit signs of insulin resistance.

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9
Q

Complications seen in Type 1 Renal Tubular Acidosis?

A

Type 1 RTA (distal)
- Inability to generate acid urine (secrete H+) in distal tubule
Causes HYPOkalaemia.

Complications include nephrocalcinosis and renal stones.

Causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy.

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10
Q

Complication seen in type 2 RTA?

A

Type 2 RTA (proximal)
decreased HCO3- reabsorption in proximal tubule

Causes HYPOkalaemia.
Complications include osteomalacia

Causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate).

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11
Q

Features of type 4 RTA?

A

Reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion.
- Causes HYPERkalaemia
- Causes include hypoaldosteronism, diabetes.

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12
Q

Feature of MEN TYPE 1?

A

3 Ps

  • Parathyroid Hyperplasia
  • Pituitary Tumours (Prolactinoma)
  • Pancreatic Tumours (insulinoma, gastrinoma)

MEN1 Gene.

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13
Q

Features of MEN Type 2a?

A

2 Ps

  • Medullary Thyroid Cancer
  • Parathyroid Hyperplasia
  • Phaeochromocytoma

RET oncogene.

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14
Q

Features of MEN Type 2b?

A

1 P

  • Medullary Thyroid Cancer
  • Phaechromocytoma
  • Marfanoid body habitus
  • Neuromas

RET Oncogene.

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15
Q

Paraneoplastic syndrome associated with small cell lung cancer?

A

Small cell lung cancer associated paraneoplastic syndromes:

  1. ACTH - Cushings
  2. ADH - SIADH - Hyponatraemia
  3. Lambert Eaton
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16
Q

Causes of Primary Hyperaldosteronism?

A
  • Bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases.
  • Adrenal adenoma: 20-30% of cases
  • Unilateral hyperplasia
  • Familial hyperaldosteronism
  • Adrenal carcinoma
17
Q

Features of primary aldosteronism?

A
  1. Hypertension
  2. Hypokalaemia
    e.g. muscle weakness
    this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients, and is more common with adrenal adenomas.
  3. Metabolic alkalosis
18
Q

Investigation for primary hyperaldosternism?

A

Plasma aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism.

It should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone).

Following this a high-resolution CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess.
If the CT is normal adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia

19
Q

Investigation for diabetes insipidus?

A

Water Deprivation Test

20
Q

Management for hypocalcaemia?

A

Severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement.

The preferred method is with intravenous Calcium Gluconate, 10ml of 10% solution over 10 minutes.

intravenous calcium chloride is more likely to cause local irritation.

ECG monitoring is recommended

21
Q

Chromosomal abnormality in Klinefelter’s syndrome?

A

Karyotype 47, XXY.

  • Often taller than average
  • Lack of secondary sexual characteristics
  • Small, firm testes
  • Infertile
  • Gynaecomastia - increased incidence of breast cancer
  • Elevated gonadotrophin levels but low testosterone
22
Q

Which diabetes medication causes weight gain?

A

Sulfonylureas - gliclazide

This is because they directly increase the amount of insulin secreted by the pancreas, which in turn stimulates cells to store glucose in the form of fat.

23
Q

Causes of primary hyperparathyroidism?

A

Primary hyperparathyroidism is caused by excess secretion of PTH resulting in hypercalcaemia. It is the most common cause of hypercalcaemia in outpatients and is often diagnosed following an incidental finding of an elevated calcium.

Causes of primary hyperparathyroidism:
1. Solitary adenoma
2. Hyperplasia
3. Multiple adenoma
4. Carcinoma

24
Q

Features of Addison’s disease?

A

Autoimmune destruction of the adrenal glands is the commonest cause of primary hypoadrenalism in the UK. This is termed Addison’s disease and results in reduced cortisol and aldosterone being produced.

Features:

  • Lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’.
  • Hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia.
  • Hyponatraemia and hyperkalaemia may be seen.

Crisis: collapse, shock, pyrexia

25
Q

Which medications cause hypercalcaemia?

A
  • Thiazide diuretics. (Bendroflumethiazide) is a thiazide diuretic which can cause hypercalcaemia by increasing renal tubular reabsorption of calcium.
  • Calcium containing antacids
26
Q

2 main causes of hypercalcaemia?

A
  1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients
  2. Malignancy: the commonest cause in hospitalised patients. This may be due to a number of processes:
  • PTHrP from the tumour e.g. squamous cell lung cancer
  • Bone metastases
  • Myeloma,: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
27
Q

Diagnostic criteria for DKA?

A
  1. Glucose > 11 mmol/l or known diabetes mellitus
  2. pH < 7.3
  3. Bicarbonate < 15 mmol/l
  4. Ketones > 3 mmol/l or urine ketones ++ on dipstick
28
Q

ECG feature in hypocalcaemia?

A

Prolonged QT interval.

29
Q

Definitive investigation for Addisons disease?

A

The definite investigation is an ACTH stimulation test (short Synacthen test).

30
Q

Electrolyte abnormalities seen in Addisons disease?

A
  • Hyponatraemia
  • Hyperkalaemia
  • Hypoglycaemia
  • Metabolic acidosis
31
Q

When should steroids be tapered?

A
  • Received more than 40mg prednisolone daily for more than one week.
  • Received more than 3 weeks of treatment
  • Recently received repeated courses
32
Q

Common drug cause of nephrogenic DI?

A

Lithium is a known iatrogenic cause of nephrogenic diabetes insipidus. Renal function must be monitored regularly in those taking lithium.

33
Q

Features of primary hyperaldosteronism?

A
  • Hypertension: increasingly recognised but still underdiagnosed cause of hypertension.
  • Hypokalaemia: e.g. muscle weakness, this is a classical feature in exams
  • Metabolic alkalosis
34
Q

Which type of thyroid cancer presents with invasive symptoms?

A

Anaplastic.

Anaplastic thyroid cancer is a highly aggressive, locally invasive tumour. It typically presents in older patients with a rapidly increasing mass or lymph node. Anaplastic tumours invades local surrounding tissues causing compression symptoms including: pain, shortness of breath and dysphagia. The aggression of the tumour often leads to lymphovascular invasion and subsequent bone and lung metastasis.

35
Q

Which biochemical abnormality is seen in Cushing’s syndrome?

A

Hypokalaemic metabolic alkalosis.

MRCP PART 1 (20 decks)

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