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Flashcards in Get Ahead EMQs Deck (214)
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1

A 45-year-old woman collapses during a church service in summer. Her husband states that she turned pale and collapsed shortly after standing up. She did not jerk or lose urinary continence. She denies chest pain, shortness of breath and palpitations. She recovered after 30 seconds and now feels back to her usual self. All observations – including blood tests, ECG, and lying and standing blood pressure – are normal

A. Acute myocardial infarction
B. Cerebrovascular accident
C. Dissecting aortic aneurysm
D. Drug allergy
E. First-dose hypotension
F. Left ventricular failure
G. Ruptured abdominal aortic aneurysm
H. Stable angina
I. Stokes–Adams attack
J. Supraventricular tachycardia
K. Vasovagal syncope
L. Ventricular rupture
M. Wolff–Parkinson–White syndrome

K – Vasovagal syncope

Vasovagal syncope occurs when there is excessive activation of the parasympathetic nervous system in response to certain stimuli, such as heat, fear and stress. The parasympathetic activity causes systemic vasodilatation and bradycardia, which triggers profound hypotension and cerebral hypoperfusion. Collapse is often preceded by a feeling of faintness, nausea, sweating and ringing in the ears. Occasionally, witnesses may describe the patient twitching and a loss of urinary incontinence, which may be confused with seizure activity. Following collapse, cerebral perfusion is restored and recovery is rapid. Situational syncope describes the scenario when vasovagal episodes are triggered by specific actions, such as coughing, urinating or having blood taken.

In all cases of collapse, the patient should be questioned about the presence of chest pain, shortness of breath, urinary incontinence, tongue biting, palpitations, weakness and paraesthesia. A pre-/peri-/post-collapse history is essential, and should be supplemented by a collateral history from a witness when available. Routine investigation should always include ECG, capillary blood glucose, and lying and standing blood pressure.

2

A 72-year-old man attends the emergency department following a fall. On examination, there is bruising on the right upper arm and the man is unable to extend his metacarpals on the same side. There is loss of sensation over the lateral dorsal aspect of the hand.

A. Accessory nerve
B. Anterior interosseous nerve
C. Axillary nerve
D. Distal median nerve
E. Distal ulnar nerve
F. Long thoracic nerve
G. Lower brachial plexus
H. Posterior interosseous nerve
I. Proximal median nerve
J. Proximal ulnar nerve
K. Radial nerve
L. Upper brachial plexus

K – Radial nerve

The radial nerve runs in close proximity to the shaft of the humerus in the spiral groove. Common causes of radial nerve palsies include humeral shaft fractures (as in this scenario, in which case patients also suffer bruising to the upper arm), compression of the nerve in the arm with prolonged use of ill-fitting crutches, and elbow dislocations or Monteggia fractures. Damage to the radial nerve is also seen in people who fall asleep with their arm hanging over the back of a chair (‘Saturday night palsy’).

The radial nerve supplies the extensors to the forearm and wrist, and radial nerve palsy results in an inability to extend the wrist or metacarpophalangeal joints (wrist drop), forearm extensor wasting and a loss of sensation in the anatomical snuffbox. The anatomical snuffbox is the name given to the triangular region on the radial dorsal aspect of the hand at the level of the carpal bones. It is so called as this was the surface used since the 16th century for placing and snorting ‘snuff’ (powdered tobacco).

3

A 28-year-old man is involved in a motorcycle accident. He has fractured both his femurs and complains of pain in his neck. On examination, his right arm is hanging by his side, is fully extended at the elbow and is rotated inwards. There is loss of sensation on the outer edge of the right arm and forearm.

A. Accessory nerve
B. Anterior interosseous nerve
C. Axillary nerve
D. Distal median nerve
E. Distal ulnar nerve
F. Long thoracic nerve
G. Lower brachial plexus
H. Posterior interosseous nerve
I. Proximal median nerve
J. Proximal ulnar nerve
K. Radial nerve
L. Upper brachial plexus

L – Upper brachial plexus

Upper brachial plexus injuries, also known as Erb’s palsy, involve the C5 and C6 nerve roots (the brachial plexus is made of the roots C5–T1). They are commonly caused by traction injuries, such as motorcycle accidents or birth injuries (due to pulling on the baby’s arm). There is flaccid paralysis of the arm abductors, lateral rotators of the shoulder and supinators, so the affected arm hangs limp and is medially rotated, extended at the elbow and pronated, with the hand pointing backwards – the ‘waiter’s tip’ position. Paralysis is accompanied by loss of sensation over the lateral arm and forearm.

4

A 46-year-old type 1 diabetic man attends a routine follow-up clinic. A urine dipstick analysis demonstrates 3+ protein, 1+ blood, no nitrates and no leucocytes. His annual blood tests show a sodium of 135 mmol/L, a potassium of 4.9 mmol/L, a creatinine of 130 µmol/L and a urea of 8.9 mmol/L.

A. Atherosclerosis
B. Autonomic neuropathy
C. Charcot’s joint
D. Connective tissue disease
E. Diabetes dermopathy
F. Lipoatrophy
G. Lipohypertrophy
H. Peripheral vascular disease
I. Neuropathic ulcer
J. Nephropathy
K. Necrobiosis lipoidica
L. Osteoarthritis
M. Venous ulce

J – Nephropathy

Diabetic nephropathy is an important cause of morbidity and mortality in the diabetic population, with up to 30% developing chronic renal failure during their lifetime. Diabetic nephropathy has a complex pathophysiology, which can be simplified into three important processes: glomerular involvement, ischaemia and infection. Important contributors to the development of diabetic nephropathy are poor glycaemic control, hypertension and renovascular disease (e.g. renal artery stenosis). The earliest detectable sign of nephropathy is microalbuminuria, i.e. the presence of trace amounts of albumin in the urine that are not detectable using standard dipstick analysis. If untreated, microalbuminuria can progress to intermittent albuminuria and then persistent albuminuria. It is thought that patients with persistent albuminuria are 5–10 years away from end-stage renal failure, even if their creatinine is normal. To reduce the risk of developing end-stage renal failure, all diabetic patients should have their kidney function and urine tested on a regular basis. Good glycaemic and blood pressure control are essential and must be communicated to the patient. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists have been shown to reduce the progression of microalbuminuria, and also contribute to blood pressure control.

5

A 37-year-old type 1 diabetic man presents to his GP complaining of a painless discoloured lesion over the lateral aspect of his right lower leg. It began as a well-circumscribed red nodule, but enlarged and flattened over time. The surface is brownish-yellow and scaly and has a number of telangiectatic vessels.

A. Atherosclerosis
B. Autonomic neuropathy
C. Charcot’s joint
D. Connective tissue disease
E. Diabetes dermopathy
F. Lipoatrophy
G. Lipohypertrophy
H. Peripheral vascular disease
I. Neuropathic ulcer
J. Nephropathy
K. Necrobiosis lipoidica
L. Osteoarthritis
M. Venous ulce

K – Necrobiosis lipoidica

Necrobiosis lipoidica diabeticorum is a rare dermatological complication of diabetes mellitus seen in approximately 1% of patients. It is most often occurs on the anterolateral aspect of the lower limb. The lesion usually begins as a small red nodule that increases in size and flattens over time. Eventually, the lesion becomes depressed, irregular, scaly or waxy, and develops a brownish-yellow discoloration. If the lesion is not ulcerated, topical steroids in association with appropriate dressings can be applied. If ulceration is present, immunosuppressive agents such as ciclosporin can be beneficial. Treatment is often unsuccessful.

Lipoatrophy describes a localized loss of fat tissue, which may occur in people with diabetes at the site of repeated subcutaneous insulin injections. The opposite condition is lipohypertrophy, the accumulation of fat at the point of repeated subcutaneous injections. Both of these conditions can be avoided by regularly rotating injection sites.

6

A 12-year-old boy is brought to the GP by his mother. Over the last couple of years, he has suffered from repeated chest infections, and his mother is worried that he is not putting on any weight. On examination, there are coarse crepitations throughout both lung lobes.

A. Asbestos-related lung disease
B. Asthma
C. Bronchiectasis
D. Chronic obstructive pulmonary disease
E. Cryptogenic fibrosing alveolitis
F. Cystic fibrosis
G. Extrinsic allergic alveolitis
H. Mesothelioma
I. Non-small cell lung tumour
J. Open pneumothorax
K. Sarcoidosis
L. Secondary lung metastases
M. Sleep apnoea
N. Small cell lung tumour
O. Tuberculosis

F – Cystic fibrosis

Cystic fibrosis (CF) is the commonest autosomal recessive condition in white populations in the UK, affecting 1 in 2500 live births. CF is caused by an abnormal gene coding for the cystic fibrosis transmembrane regulator protein (CFTR), located on chromosome 7. CFTR is a cAMP-dependent chloride channel blocker. The most common mutation in CF is the ∆F508 mutation. The poor transport of chloride ions and water across epithelial cells of the respiratory and pancreatic exocrine glands in CF results in an increased viscosity of secretions. The range of presentations is varied, including recurrent chest infections, failure to thrive due to malabsorption and liver disease. In the neonatal period, infants may present with prolonged neonatal jaundice, bowel obstruction (meconium ileus) or rectal prolapse.

The boy in this case has bilateral coarse crepitations. Given the history, these are a sign of bronchiectasis. Bronchiectasis is an abnormal dilatation of the bronchioles. Causes of bronchiectasis can be congenital (ciliary dyskinesia or CF) or acquired (whooping cough, measles or tuberculosis). Pus accumulates in the dilated bronchi, resulting in a productive cough that is worse in the morning and brought about by changes in posture. Bronchiectasis is associated with clubbing of the fingers. The best investigation to confirm bronchiectasis is CT. Management is by physiotherapy (postural drainage and chest percussion) and prompt antibiotics for respiratory tract infections.

7

A 25-year-old man presents with facial and ankle swelling. He is found to have 3+ of protein in his urine on dipstick analysis. Blood tests reveal an albumin of 16 g/L.

A. Drug-induced glomerulonephritis
B. Focal segmental glomerulosclerosis
C. Goodpasture’s syndrome
D. IgA nephropathy
E. Membranous glomerulonephritis
F. Mesangiocapillary glomerulonephritis
G. Minimal-change glomerulonephritis
H. Post-streptococcal glomerulonephritis
I. Rapidly progressive glomerulonephritis
J. Rhabdomyolysis

E – Membranous glomerulonephritis

Membranous glomerulonephritis is the most common cause of nephrotic syndrome in adults. In this condition, immune complexes are formed when circulating antibodies bind to basement membrane antigens or antigens deposited in the glomerulus from the circulation. The immune complexes activate an immunological response that involves the complement cascade. This response damages the glomerular basement membrane, making it more permeable. Membranous glomerulonephritis is usually idiopathic (90%), but may be secondary to a number of disease processes, including systemic lupus erythematosus, hepatitis B, systemic infection and drugs.

Treatment is largely the same as for nephrotic syndrome in children (see above). The prognosis is variable. Approximately one-third of patients recover spontaneously, one-third will respond to immunosuppression and one-third will develop end-stage renal failure. Up to 5% of patients will develop renal vein thrombosis.

8

A 15-year-old girl presents to the GP 2 weeks after being diagnosed with tonsillitis. She is generally unwell and puffy and complaining of dark urine. Urine dipstick analysis shows 3+ of protein and 3+ of blood. She is found to have high titres of antistreptolysin O antibody.

A. Drug-induced glomerulonephritis
B. Focal segmental glomerulosclerosis
C. Goodpasture’s syndrome
D. IgA nephropathy
E. Membranous glomerulonephritis
F. Mesangiocapillary glomerulonephritis
G. Minimal-change glomerulonephritis
H. Post-streptococcal glomerulonephritis
I. Rapidly progressive glomerulonephritis
J. Rhabdomyolysis

H – Post-streptococcal glomerulonephritis

This form of glomerulonephritis is usually seen 1–2 weeks after an infection caused by a group A β-haemolytic streptococcus, e.g. tonsillitis or cellulitis. The pathophysiology involves immune complex deposition within the glomerular basement membrane. Patients present with acute nephritic syndrome, i.e. fluid retention, peripheral oedema, hypertension, proteinuria and haematuria. The urine is classically dark in colour and is sometimes referred to as ‘Pepsi urine’. Investigation usually reveals proteinuria, haematuria, elevated anti-streptolysin O titres and reduced complement (C3). In cases with a clear history and consistent initial investigation results, renal biopsy is often not required. Management is largely supportive with fluid restriction and antihypertensive medications.

9

A 45-year-old man is admitted with headache and neck stiffness. A lumbar puncture is performed and reveals the following results: clear fluid, lymphocytes 2/mm3, neutrophils 1/mm3, low glucose, high protein, positive India ink stain.

A. Cryptococcus neoformans
B. Haemophilus influenzae
C. Malignancy
D. Multiple sclerosis
E. Mumps
F. Mycobacterium tuberculosis
G. Neisseria meningitidis
H. Streptococcus pneumoniae

A – Cryptococcus neoformans (fungal)

10

A 43-year-old man with a long history of bipolar disorder presents to his GP complaining of weight gain, lethargy and feeling cold all the time. Blood tests show a low T 4 level and a high TSH level.

A. De Quervain’s thyroiditis
B. Graves’ disease
C. Hashimoto’s thyroiditis
D. Hypopituitarism
E. Hypothyroidism secondary to amiodarone therapy
F. Hypothyroidism secondary to lithium therapy
G. Sick euthyroid syndrome
H. Single toxic nodule goitre
I. Thyroid cancer
J. Toxic multinodular goitre

F – Hypothyroidism secondary to lithium therapy

Lithium, a drug used to treat bipolar disorder (manic depression), is one of a number of medications known to affect the thyroid gland. Lithium can cause goitre formation and inhibit T4 and triiodothyronine (T3) secretion from the thyroid gland. Therefore, prior to starting lithium, every patient should receive a neck examination and have their thyroid function checked. The majority of patients taking lithium become subclinically hypothyroid (i.e. are asymptomatic, with a normal T 4 level and a high TSH). Unless the patient is acutely unwell, it is usual practice to continue the lithium and start the patient on T4 replacement. After commencing therapy, thyroid function should be tested every 6 months.

11

A 38-year-old man who is currently in hospital being treated for a severe chest infection is shown to have low T4 and TSH levels.

A. De Quervain’s thyroiditis
B. Graves’ disease
C. Hashimoto’s thyroiditis
D. Hypopituitarism
E. Hypothyroidism secondary to amiodarone therapy
F. Hypothyroidism secondary to lithium therapy
G. Sick euthyroid syndrome
H. Single toxic nodule goitre
I. Thyroid cancer
J. Toxic multinodular goitre

G – Sick euthyroid syndrome

Sick euthyroid syndrome describes abnormal thyroid function in the presence of systemic disease. There are many different subtypes of sick euthyroidism, but, as a general rule, the T3 and T4 levels are low, with TSH levels falling in more severe disease (i.e. everything is low). As the patient recovers from the underlying disease, the thyroid function usually returns to normal.

12

A 70-year-old man presents with a 6-month history of worsening forgetfulness and intellectual decline. He has, however, had frequent episodes of relative lucidness during this period. He tries to chase soldiers whom he thinks he sees in the garden, but his gait has markedly slowed down. His sleeping pattern is now irregular.

A. Alzheimer’s disease
B. Creutzfeldt–Jakob disease
C. Depression
D. HIV dementia
E. Huntington’s disease
F. Lewy body dementia
G. Normal-pressure hydrocephalus
H. Parkinson’s disease
I. Pick’s disease
J. Vascular dementia
K. Wernicke–Korsakoff syndrome

F – Lewy body dementia

Lewy body dementia is the second most common dementia after Alzheimer’s disease. Characteristic features of Lewy body dementia include day-today fluctuating levels of cognitive functioning, visual hallucinations, sleep disturbance, transient loss of consciousness, recurrent falls and parkinsonian features (tremor, hypokinesia, rigidity and postural instability). Although people with Lewy body dementia are prone to hallucination, antipsychotics should be avoided, as they precipitate severe parkinsonism in 60%. Lewy bodies are abnormalities of the cytoplasm found within neurons, containing various proteins and granular material. They are found in the cerebral cortex in patients with Lewy body dementia, and are also found in patients with Parkinson’s disease

13

A 52-year-old woman presents to the emergency department following her first-ever seizure. Her husband said that she had to leave her job because, over a period of 2 months, she rapidly lost the ability to cope with its intellectual demands. A previous cryptic crossword fanatic, she cannot even fill out the simplest tabloid grid. On further questioning, she admits to muscle weakness and difficulty walking.

A. Alzheimer’s disease
B. Creutzfeldt–Jakob disease
C. Depression
D. HIV dementia
E. Huntington’s disease
F. Lewy body dementia
G. Normal-pressure hydrocephalus
H. Parkinson’s disease
I. Pick’s disease
J. Vascular dementia
K. Wernicke–Korsakoff syndrome

B – Creutzfeldt–Jakob disease

Creutzfeldt–Jakob disease (CJD) is a rapidly progressive dementia caused by prions (infectious agents composed only of protein). The prion proteins can be transmitted by neurosurgical instruments and human-derived pituitary hormones. Features of CJD include rapid cognitive impairment, which may be preceded by anxiety and depression. Eventually, physical features become prominent, including muscle disturbance (rigidity, tremor, wasting, spasticity, fasciculations, cyclonic jerks and choreoathetoid movements). Convulsions may also occur. The EEG is characteristic (showing stereotypical sharp wave complexes). Death occurs within 6–8 months.

New variant CJD (nvCJD) occurs secondary to ingestion of bovine spongiform encephalopathy (BSE)-infected beef. It is more common in younger adults. The features are as for CJD, but decline is slower, with death occurring within 18 months. There are no typical EEG changes in nvCJD, although there is a characteristic feature on MRI (symmetrical hyperintensity in the posterior nucleus of the thalamus – the pulvinar sign).

14

A 69-year-old woman presents after a fall, having been unsteady on her feet for some time. She has severe memory loss, but is relatively well orientated. She has recently developed urinary incontinence. On examination, she has a wide-based gait.

A. Alzheimer’s disease
B. Creutzfeldt–Jakob disease
C. Depression
D. HIV dementia
E. Huntington’s disease
F. Lewy body dementia
G. Normal-pressure hydrocephalus
H. Parkinson’s disease
I. Pick’s disease
J. Vascular dementia
K. Wernicke–Korsakoff syndrome

G – Normal-pressure hydrocephalus

Normal-pressure hydrocephalus is characterized by the triad of dementia (mainly memory problems), gait disturbance and urinary incontinence. It is caused by an increased volume of CSF, but with only a slightly raised pressure (as the ventricles dilate to compensate). There is an underlying obstruction in the subarachnoid space that prevents CSF from being reabsorbed but allows it to flow from the ventricular system into the subarachnoid space. Diagnosis is by lumbar puncture (to demonstrate a normal CSF opening pressure) followed by head CT/MRI (showing enlarged ventricles). Treatment is with ventriculoperitoneal shunting.

15

A 26-year-old woman presents with a 3-month history of general malaise, fever and weight loss. Over the last week, she has developed an intermittent cramping pain in her right arm. On examination, the upper limbs appear normal, but the radial pulses are not palpable.

A. Behçet’s disease
B. Churg–Strauss syndrome
C. Giant cell arteritis
D. Kawasaki’s disease
E. Microscopic polyangiitis
F. Polyarteritis nodosa
G. Polymyalgia rheumatica
H. Takayasu’s arteritis
I. Wegener’s disease

H – Takayasu’s arteritis

Vasculitis is an inflammation of the blood vessels. Takayasu’s arteritis (also known as ‘pulseless disease’) is a rare granulomatous inflammation of the aorta and its major branches. This results in poor blood flow to the peripheries and a lack of distal pulses. It is commonest in Japanese women. Patients present with systemic illness (malaise, fever and weight loss) and arm claudication. A third of patients suffer visual disturbance. Examination reveals absent pulses and arterial bruits. Diagnosis is by angiography, which demonstrates the inflamed constricted major vessels. Treatment is with steroids, but surgery may be required to bypass significantly stenosed or obliterated vessels.

16

A 32-year-old man presents with shortness of breath. He feels that it is similar to the asthma that he had as a child. He has also developed hayfever recently, which he has never had before. On examination, a palpable, purple rash is seen on the legs.

A. Behçet’s disease
B. Churg–Strauss syndrome
C. Giant cell arteritis
D. Kawasaki’s disease
E. Microscopic polyangiitis
F. Polyarteritis nodosa
G. Polymyalgia rheumatica
H. Takayasu’s arteritis
I. Wegener’s disease

B – Churg–Strauss syndrome

Churg–Strauss syndrome is a rare systemic vasculitis that is associated with eosinophilia and asthma. The disease may be triphasic, with a prodromal period (rhinitis and allergies), eosinophilia (asthma or eosinophilic gastroenteritis) and finally a systemic vasculitis. Churg–Strauss syndrome is associated with perinuclear antineutrophil cytoplasmic antibodies (pANCAs). Treatment is with steroids.

17

A 29-year-old man complains of recurrent painful ulceration in his mouth and on his genitals. The ulceration is clearly seen on examination. Swab cultures are taken and found to be negative for herpes simplex virus.

A. Behçet’s disease
B. Churg–Strauss syndrome
C. Giant cell arteritis
D. Kawasaki’s disease
E. Microscopic polyangiitis
F. Polyarteritis nodosa
G. Polymyalgia rheumatica
H. Takayasu’s arteritis
I. Wegener’s disease

A – Behçet’s disease

Behçet’s disease (pronounced ‘beh-chet’) is a chronic vasculitis most common in Turkey and the eastern Mediterranean. There is a strong association with HLA-B5 and disease is more severe in males. Behçet’s disease is characterized by an occlusive vasculitis and venulitis. The diagnosis is based on the clinical features, which include recurrent oral and genital ulceration, recurrent iritis, skin lesions, and thrombophlebitis. The pathergy reaction (where red papules >2 mm develop after 48 hours at sites of needle pricks) is pathognomonic of Behçet’s disease.

18

A 65-year-old woman presents with a pain in her shoulders. The pain came on suddenly this morning, and now she is barely able to move her arms. She is otherwise well. On examination, shoulder movement is limited by stiffness bilaterally

A. Behçet’s disease
B. Churg–Strauss syndrome
C. Giant cell arteritis
D. Kawasaki’s disease
E. Microscopic polyangiitis
F. Polyarteritis nodosa
G. Polymyalgia rheumatica
H. Takayasu’s arteritis
I. Wegener’s disease

G – Polymyalgia rheumatica

Polymyalgia rheumatica is not a vasculitis but is found in 50% of people with temporal arteritis (below). It is commonest in females over 50 years. Patients present with abrupt-onset proximal muscle pain (shoulder and hips) and stiffness without weakness. (The lack of weakness helps distinguish polymyalgia rheumatica from polymyositis.) Symptoms are worse in the morning. Treatment is with corticosteroids, and the response is prompt and dramatic.

Giant cell arteritis (temporal arteritis) is an inflammatory vasculitis of the cranial branches arising from the aorta. It is most common in the over-50s and is twice as frequent in females. Clinical features include general malaise, temporal headache, scalp tenderness and jaw claudication. Eventually, visual disturbance or visual loss can occur due to ischaemic optic neuritis caused by arteritis of the posterior ciliary artery and branches of the ophthalmic arteries. On examination, an enlarged, tender, non-pulsatile temporal artery is seen on the affected side. Temporal artery biopsy is the definitive investigation (showing patchy granulomatous inflammation), but skip lesions may be present and investigation should not delay treatment. Management is with prednisolone.

19

A 42-year-old man presents with a 2-month history of recurrent nosebleeds. More recently, he has started coughing up blood as well. On examination, there is a deformity in the bridge of his nose.

A. Behçet’s disease
B. Churg–Strauss syndrome
C. Giant cell arteritis
D. Kawasaki’s disease
E. Microscopic polyangiitis
F. Polyarteritis nodosa
G. Polymyalgia rheumatica
H. Takayasu’s arteritis
I. Wegener’s disease

I – Wegener’s disease

Wegener’s disease is a granulomatous necrotizing vasculitis characterized by a classic triad of involvement: upper airway pathology (epistaxis, saddle nose deformity, rhinitis, deafness and proptosis), respiratory disease (pulmonary nodules and pulmonary haemorrhage) and renal disease (glomerulonephritis). It is associated with cytoplasmic antineutrophil cytoplasmic antibodies (cANCAs) in 90% of cases. Treatment is with steroids and immunosuppressants

20

A 54-year-old woman with end-stage liver failure secondary to primary biliary cirrhosis is noticed to have a rising serum creatinine and urea, and is passing only small volumes of urine each day.

A. Clotting factor deficiency
B. Hepatic encephalopathy
C. Hepatorenal syndrome
D. Hypoalbuminaemia
E. Hypoglycaemia
F. Lower gastrointestinal bleed
G. Ruptured oesophagus
H. Seizure
I. Spontaneous bacterial peritonitis
J. Thrombocytopenia
K. Upper gastrointestinal bleed

C – Hepatorenal syndrome

Hepatorenal syndrome is seen in up to 20% of patients with cirrhosis and portal hypertension. In hepatorenal syndrome, the patient develops acute renal failure despite having histologically normal kidneys. It is thought to arise secondary to the release of vasoactive substances that cause dilatation of the splanchnic vasculature and constriction of the renal cortical vasculature. This combination of events reduces the glomerular filtration rate. The treatment of hepatorenal syndrome involves restoring the intravascular volume with human albumin solution and reversing the splanchnic dilatation with potent arterial vasoconstrictors such as terlipressin. Severe and refractory disease may require liver transplantation for cure.

21

A 34-year-old woman presents with multiple painful lesions over her body. On examination, each of these lesions is soft and mobile and 2cm in size. She has no other symptoms.

A. Cavernous haemangioma
B. Deep capillary naevus
C. Dercum’s disease
D. Ganglion
E. Granuloma annulare
F. Kaposi’s sarcoma
G. Neurofibroma
H. Pyogenic granuloma
I. Sebaceous cyst
J. Seborrhoeic keratosis
K. Superficial capillary naevus

C – Dercum’s disease

These woman’s lesions are lipomas – soft, mobile lesions composed of fatty tissue that are usually painless. However, the presence of multiple painful lipomas is known as Dercum’s disease (or adiposis dolora). This occurs most commonly in obese middle-aged women, and may be accompanied by headaches, amenorrhoea and reduced sweating. Simple lipomas can be removed by excision for cosmetic reasons.

22

A 5-year-old girl was admitted to the emergency department with a seizure. On examination, she has a well-demarcated, purple, flat lesion over her right cheek and forehead. Her parents say that this has been present since birth.

A. Cavernous haemangioma
B. Deep capillary naevus
C. Dercum’s disease
D. Ganglion
E. Granuloma annulare
F. Kaposi’s sarcoma
G. Neurofibroma
H. Pyogenic granuloma
I. Sebaceous cyst
J. Seborrhoeic keratosis
K. Superficial capillary naevus

B – Deep capillary naevus

A deep capillary naevus (or port-wine stain) is a malformation of the capillaries in the deep and superficial dermis. These are congenital malformations that can occur anywhere in the body but are most often found unilaterally on the face. Occasionally, a port-wine stain is associated with seizures, learning difficulties and eye abnormalities (glaucoma and optic atrophy) due to underlying cranial malformations. This is known as Sturge–Weber syndrome and is usually associated with a port-wine stain in the distribution of the ophthalmic or maxillary division of the trigeminal nerve.

Superficial capillary naevi (also known as salmon patches) are small, flat, pink patches of skin with poorly defined borders. They are commonly found on the forehead (‘angel’s kiss’) or on the nape of the neck (‘stork mark’). Most superficial naevi disappear in the first year of life

23

An 18-month-old boy is brought to the GP by his parents with a red lesion on his forehead. This was not present at birth, but has been growing for 3 months. On examination, the lesion is 3 cm, bright red and well defined. There are no other symptoms.

A. Cavernous haemangioma
B. Deep capillary naevus
C. Dercum’s disease
D. Ganglion
E. Granuloma annulare
F. Kaposi’s sarcoma
G. Neurofibroma
H. Pyogenic granuloma
I. Sebaceous cyst
J. Seborrhoeic keratosis
K. Superficial capillary naevus

A – Cavernous haemangioma

A cavernous haemangioma (or strawberry naevus) is a condition that appears in the first months of life as a bright-red lesion on the face or trunk that grows rapidly. Occasionally, these lesions bleed or ulcerate. Cavernous haemangiomas eventually regress and disappear spontaneously, so intervention is required only if lesions persist beyond a few years of age. Cavernous haemangiomas may rarely be associated with thrombocytopenia and haemolytic anaemia secondary to trapping and destruction of platelets and erythrocytes within the lesions. This is known as Kasabach–Merritt syndrome.

24

A 15-month-old boy is brought to the emergency department with a grossly swollen right knee. His parents claim that he has had several episodes of bleeding into his joints and muscles over the previous 6 months. A clotting screen was requested and showed a significantly prolonged APTT with a normal PT and bleeding time. The full blood count showed a mild microcytic anaemia.

A. Acquired haemophilia
B. Antibiotic side-effect
C. Complication of warfarin therapy
D. Congenital haemophilia
E. Disseminated intravascular coagulation
F. Global reduction in clotting factor synthesis
G. Heparin overdose
H. Hereditary haemorrhagic telangiectasia
I. Hypofibrinogenaemia
J. Pancytopenia
K. Thrombocytopenia
L. Von Willebrand’s disease

D – Congenital haemophilia

Haemophilia A is an X-linked recessive disorder of coagulation in which the patient cannot synthesize clotting factor VIII due to a gene mutation. Haemophilia B (also known as Christmas disease) is caused by an inability to synthesize factor IX and is clinically indistinguishable from the much more common haemophilia A. Although usually familial, a significant proportion of cases are caused by sporadic mutations. Factors VIII and IX are essential in the extrinsic clotting cascade, meaning that patients with haemophilia have a prolonged APTT. The intrinsic pathway does not require factors VIII or IX, and is therefore unaffected by haemophilia – shown by a normal PT. The bleeding time is also normal. Symptoms usually begin when the patient becomes mobile, i.e. when they begin to crawl or walk. Patients with haemophilia typically suffer painful recurrent bleeds into the joints and soft tissues (haemarthrosis), which may eventually lead to crippling arthropathy and neuropathy.

25

Six months after her original diagnosis, Mrs X (80 y/o, diagnosed with chronic heart failure) visits her GP because she still gets very short of breath, especially when she lies down. Her current medications include enalapril, atenolol, zopiclone, aspirin and furosemide. What additional treatment should the doctor prescribe her?

A. Angiotensin II receptor antagonist
B. Angiotensin-converting enzyme inhibitors
C. Amlodipine
D. β-Blockers
E. Brain-type natriuretic peptide
F. Digoxin
G. Lipid profile
H. Loop diuretics
I. Myoglobin
J. Potassium-sparing diuretics
K. Spironolactone
L. Thiazide diuretics
M. Thyroid function tests
N. Transoesophageal echocardiography
O. Transthoracic Doppler echocardiography
P. Troponin I

K – Spironolactone

Spironolactone is an aldosterone antagonist; therefore it causes increased sodium secretion and reduced potassium excretion. Because it does not cause hypokalaemia (unlike the thiazide and loop diuretics), spironolactone is known as a potassium-sparing diuretic. Amiloride is another example of such a drug. Spironolactone is indicated in patients with severe symptomatic disease that is not controlled by optimal medical therapy to improve symptoms and mortality. Since this medication reduces potassium excretion by the kidneys, it should not be given to patients with a potassium level over 5.0 mmol/L or to patients taking potassium supplements. Patients should have their serum potassium measured prior to prescription and at regular intervals thereafter in order to detect hyperkalaemia. Other well-known side-effects of spironolactone include hyponatraemia, gynaecomastia and menstrual disturbance.

26

A 45-year-old woman presents to the GP complaining of a new rash. There are multiple, light-brown, depressed lesions on her shins, each around 2 cm in size. She has diabetes mellitus, but is otherwise well.

A. Acanthosis nigricans
B. Alopecia
C. Diabetic dermopathy
D. Eruptive xanthomas
E. Erythema ab igne
F. Hyperhidrosis
G. Necrobiosis lipoidica diabeticorum
H. Paget’s disease
I. Pretibial myxoedema
J. Thrombophlebitis migrans
K. Tylosis
L. Xanthelasma

C – Diabetic dermopathy

Diabetic dermopathy describes the presence of depressed pigmented scars in the shin. It is associated with diabetic microangiopathy. Other skin features of diabetes include necrobiosis lipoidica diabeticorum (shiny, atrophic, yellowish-red plaques on the shins), cheiroarthropathy (a sclerodermalike thickening of the skin of the hands), granuloma annulare (small, papular lesions arranged in a ring and found on the back of the hands or feet) and acanthosis nigricans.

27

A 45-year-old woman presents to the GP complaining of a new rash. There is a dark-brown, lacy rash over the front of both of her shins. She has recently started treatment for an underactive thyroid, but is otherwise well.

A. Acanthosis nigricans
B. Alopecia
C. Diabetic dermopathy
D. Eruptive xanthomas
E. Erythema ab igne
F. Hyperhidrosis
G. Necrobiosis lipoidica diabeticorum
H. Paget’s disease
I. Pretibial myxoedema
J. Thrombophlebitis migrans
K. Tylosis
L. Xanthelasma

E – Erythema ab igne

Erythema ab igne is a brown lacy rash seen on skin that has been exposed to heat for long periods of time. It classically develops in hypothyroid patients who are cold and spend a lot of time in front of the fire. Excessive hot water bottle use can also result in the rash.

Other cutaneous features of hypothyroidism include alopecia (especially loss of the outer third of the eyebrows), dry coarse hair, puffy yellow skin, periorbital oedema, xanthomas and a malar flush on an otherwise pale face (‘strawberries and cream’ appearance).

28

A 34-year-old woman has been suffering from profuse diarrhoea and vomiting for 4 days. She is now complaining of extreme muscle weakness and muscle cramps.

A. 3rd-degree heart block
B. Atrial fibrillation
C. Atrial flutter
D. Bifid P-waves
E. Delta wave
F. J-waves
G. Sinus arrhythmia
H. Sinus tachycardia
I. Tented T-waves
J. U-waves

J – U-waves

The 4-day history of diarrhoea and vomiting followed by the development of severe muscle weakness and cramps suggests hypokalaemia secondary to excessive gastrointestinal potassium loss. Other causes of reduced total body potassium include diuretic use, Conn’s syndrome, excessive sweating and burns. Potassium can also be redistributed from the extracellular compartment into the intracellular compartment, resulting in a reduction in bioavailable potassium despite there being normal total body potassium levels. Causes of potassium redistribution include β2-antagonist use (e.g. salbutamol), excess insulin administration and alkalosis. The clinical features of hypokalaemia become evident with serum potassium levels less than 2.5 mmol/L. These include lethargy, polyuria, profound muscle weakness, muscle cramps, palpitations and arrhythmia. ECG changes in hypokalaemia include U-wave formation (upward deflections following the T-waves), flattened T-waves, ST-segment depression, and atrial and ventricular arrhythmias. Treatment of hypokalaemia involves correcting the underlying cause and replacing the lost potassium. Patients with potassium levels above 2.5 mmol/L can usually be managed with oral potassium supplements.

29

An 85-year-old man with dementia is brought to the emergency department by the ambulance after escaping from his care home during the night. He was found wandering on the local moors by a farmer in the early hours of the morning. He is shivering and confused. His core temperature is 31°C.

A. 3rd-degree heart block
B. Atrial fibrillation
C. Atrial flutter
D. Bifid P-waves
E. Delta wave
F. J-waves
G. Sinus arrhythmia
H. Sinus tachycardia
I. Tented T-waves
J. U-waves

F – J-waves

This patient is hypothermic secondary to prolonged environmental exposure. Severe hypothermia can lead to coagulopathy, bradycardia, heart failure, arrhythmia and death. The ECG in severely affected patients may show an upward deflection following the R-wave of the QRS complex (J-wave). Patients with hypothermia should be re-warmed slowly at a rate no greater than 0.5°C/h, as rapid re-warming can cause vasodilatation, hypotension and circulatory collapse. Methods of re-warming include removal of wet clothing, supplying warmed humidified oxygen, applying a bear hugger device and infusing warm saline intravenously. More invasive methods of re-warming include peritoneal, pleural and bladder lavage with warmed fluid. Due to the risk of arrhythmia, hypothermic patients should be managed on a cardiac and blood pressure monitor.

30

This serological marker would indicate chronic hepatitis B infection if detected 6 months after the original infection.

A. α-Fetoprotein
B. Alanine aminotransferase
C. Hepatitis B core antibody (HBcAb)
D. Hepatitis B core antigen (HBcAg)
E. Hepatitis B e antigen (HBeAg)
F. Hepatitis B surface antibody (HBsAb)
G. Hepatitis B surface antigen (HBsAg)
H. Hepatitis B RNA titre

G – Hepatitis B surface antigen (HBsAg)

If HBsAg is still detected in the serum 6 months after an acute HBV infection, the patient has become a chronic carrier of the virus. The risk of developing chronic HBV infection is related to age at the time of infection. The majority of infected neonates develop chronic infection, whereas only 5–10% of adults do so. Patients with chronic hepatitis B are at risk of developing cirrhosis, liver failure and hepatocellular carcinoma. The treatment of chronic hepatitis B can involve interferon-α, peginterferon-α2a, lamivudine and (in some patients) eventual liver transplantation.