Paper 2 - incorrect MCQ Flashcards
Acute confusion
Which of the following routine blood tests is most likely to indicate a cause
of an elderly patient’s acute confusional state?
A Calcium
B C-reactive protein (CRP)
C Liver function tests
D Sodium
E Urea
B. C-reactive protein (CRP)
The most common cause of acute confusional state in elderly patients is
a chest or urinary tract infection. These may present atypically, without
overt symptoms or a temperature, so looking for a rise in CRP roughly
corresponding with the onset of confusion can suggest that performing a
septic screen (blood cultures, chest X-ray, urine dipstick and culture) would
be of use in fi nding the cause. Uraemia, liver failure, hyponatraemia, and
hyper- or hypocalcaemia can cause acute confusional state, but more rarely
than an infection in older patients.
HLA-B27
Which of the following conditions is not associated with HLA-B27?
A Crohn’s disease
B Psoriasis
C Scleritis
D Ulcerative colitis
E Uveitis
C. Scleritis
Inflammatory bowel disease is associated with HLA-B27, as is psoriasis.
Uveitis is inflammation of the iris and associated structures, and causes
acute pain with blurred vision and photophobia with reddening of the iris.
This is associated with both ankylosing spondylitis and HLA-B27. Scleritis
is infl ammation of the sclera, causing pain and a gritty sensation in the eye
with redness of the sclera. This is associated with connective tissue disorders
and rheumatoid arthritis. If left untreated this can cause perforation of the
eye. It is not associated with HLA-B27. Genetic testing for HLA-B27 can be
useful in difficult diagnostic cases for seronegative spondyloarthropathies
and in counselling patients regarding chances of their offspring developing
the same disease.
Heart failure (1)
A 69-year-old man presents with a range of signs and symptoms that give
the impression of heart failure.
Which of the following is not a feature of heart failure?
A Hepatomegaly
B Non-pitting oedema
C Pulsus alternans
D Raised jugular venous pressure
E Tricuspid regurgitation
B. Non-pitting oedema
Heart failure is a disease of chronic, insidious onset that can fi rst present
with shortness of breath, persistent cough or insomnia. The heart fails
to maintain adequate cardiac output for a variety of reasons; the harder
it tries, the faster it fails. Occasionally, the left ventricle will weaken to
the point where it cannot empty effi ciently. The subsequent raised enddiastolic
volume causes a pre-stretched ventricle, leading to a more forceful contraction (Starling’s law). This alternating strong–weak pattern can be
seen in the ECG as pulsus alternans (varying amplitudes of the R-wave).
A column of blood builds up proximal to the left ventricle, in the lungs,
causing pulmonary oedema. This creates afterload upon the right ventricle,
which can lead to tricuspid regurgitation. The bottleneck of blood can
extend further, through the right side of the heart and hence JVP is raised
(the heart is unable to pull all the blood from the jugular vein through the
lungs and the left ventricle). Furthermore, close to the right side of the heart,
the inferior vena cava remains full of blood, leading to oedema in the liver
(hepatomegaly). Ankle veins swell with blood as the heart fails to suck the
blood vertically against gravity. The increased hydrostatic pressure results in
fluid extravasation into tissues. The push of a finger is enough to displace
this tissue fluid, hence this ankle oedema is pitting. Causes of non-pitting
oedema include lymphoedema and pretibial myxoedema.
Scoring systems (1)
A 57-year-old man with a history of alcohol abuse presents with a 12-hour
history of severe central epigastric pain radiating through to the back.
Blood tests reveal a normal white cell count, amylase 2250 U/ml, LDH 530
IU/L, calcium 2.2 mmol/L, albumin 38 g/dl, urea 12 mmol/L and blood
glucose 14 mmol/L. An arterial blood gas reading demonstrates a pO2 of
10.2 kPa on room air.
What is his Glasgow score?
A 0
B 1
C 2
D 3
E 4
C. 2
The massively raised amylase with this clinical picture supports a diagnosis
of acute pancreatitis. Acute pancreatitis can be a life-threatening condition
for it is an unpredictable disease that can cause quick deterioration. To aid
management, the modified Glasgow criteria were devised to help prognosis
and triage patients to an appropriate level of care. The eight parts of the
Glasgow criteria are as follows (1 point for each):
Age >55 years
White cell count >15 × 103/μL
Urea >16 mmol/L
Glucose >10 mmol/L
Arterial pO2 <8 kPa
Albumin <32 mmol/L
Calcium <2.0 mmol/L
Lactate dehydrogenase >600 mmol/L
This man scores 2 for age and his raised blood sugar, which is a moderate
risk for pancreatitis. A score of 3 and above should indicate to the physician
the need to discuss the case with intensive care as these patients are more
likely to need invasive monitoring of their fluid balance. Patients should
ideally be re-scored 48 hours after admission.
Management of hypercalcaemia
A 70-year-old man presents to the emergency department with a cough
productive of blood-stained green sputum and shortness of breath. A chest
X-ray demonstrates a suspicious lesion in the right lower zone associated
with consolidation. On further questioning, he admits to recent weight loss
and back pain. Blood tests show:
Na+ 137 mmol/L
K+ 3.8 mmol/L
Urea 14.5 mmol/L
Creatinine 160 μmol/L
Corrected Ca2+ 3.0 mmol/L
PO4 0.33 mmol/L
Alk Phos 450 mmol/L
Which of the following is NOT appropriate in the management of this
patient?
A Check patient’s urea and electrolyte level and serum calcium level twice
daily
B Consider starting intravenous bisphosphonate
C Consider starting loop diuretics
D Rehydration with intravenous normal saline
E Request an urgent isotope bone scan
E. Request an urgent isotope bone scan
The most common causes of hypercalcaemia are primary hyperparathyroidism
and malignant hypercalcaemia. Patients with hypercalcaemia
present with polyuria, polydipsia, renal colic, nausea, anorexia, lethargy,
dyspepsia, peptic ulceration, constipation, depression, drowsiness and impaired
cognition. Urgent fluid replacement with 0.9% saline is essential
(3–6 L over 24 hours) and the patient’s urea and electrolyte, and calcium
levels should be checked twice daily. Loop diuretics could aid renal clearance
of calcium. Intravenous bisphosphonate (e.g. pamidronate) could
cause a fall in calcium by causing bone reabsorption. Its effect is maximal
at 2–3 days and lasts a few weeks.
Nosebleeds
A 55-year-old man is referred to haematology with repeated nosebleeds,
malaise, weight loss and night sweats. Investigations show a raised white
cell count, mainly neutrophils and myelocytes, anaemia, increased urate
and increased alkaline phosphatase. On blood film there are no blast cells.
Genetic studies show a t(9:22) translocation encoding for the BCR-ABL gene.
What is his diagnosis?
A Acute lymphoblastic leukaemia
B Acute myeloid leukaemia
C Chronic lymphoblastic leukaemia
D Chronic myeloid leukaemia
E Non-Hodgkin lymphoma
D. Chronic myeloid leukaemia
The t(9:22) translocation (i.e. a translocation between chromosomes 9
and 22) encoding for the BCR-ABL gene is also known as the Philadelphia
chromosome and is the genetic mutation in over 90% of the cases of chronic
myeloid leukaemia. The mutation is a balanced translocation, which leads to
increased tyrosine kinase activity disturbing stem cell kinetics.
Chronic myeloid leukaemia (CML) is a myeloproliferative disorder. Its
peak incidence is 50–70 years and it is rare in children. There is excessive
proliferation of myeloid cells in the bone marrow. Patients typically have
massive splenomegaly, anaemia, bruising and infection on a background
of generalised illness. A blood film shows myeloblasts (granulocyte
precursors) and granulocytosis. Patients with CML but without the
Philadelphia chromosome have a worse prognosis compared to those with
the translocation. There are three stages of disease in CML: 1) the chronic
phase (which is responsive to treatment), 2) the accelerated phase (where
the disease is difficult to control) and 3) the blast crisis phase (where the
disease progresses into an acute leukaemia, usually AML). The median
survival rate is 5 years. Death usually occurs within months of blast
transformation (from bleeding and infection). Chemotherapy is often
used and allogeneic stem cell transplantation can provide a cure. Having
isolated the gene there is now an effective drug that can block the BCRABL
gene – imatinib mesylate – which can reverse the effects of the protein
and produce remission in 95% of patients with this mutation.
Failure to thrive
A 5-month-old girl presents with failure to thrive, pallor and mild
jaundice. The child has frontal bossing of the skull, prominent maxillae
and hepatosplenomegaly.
Which of the following is the most likely diagnosis?
A Congenital biliary atresia
B Congenital hypothyroid
C Hydrops fetalis
D Lead poisoning
E Thalassaemia major
E. Thalassaemia major
Beta-thalassaemia major is an autosomal recessive disorder in which there
is a complete lack of production of the haemoglobin chain beta-globin.
It occurs mainly in Mediterranean and Middle Eastern families and is
due to a point mutation on chromosome 11. Because patients with betathalassaemia
major have mutations on both alleles and cannot synthesise
any beta-globin, they cannot produce functioning adult haemoglobin
(HbA – α2β2). This condition typically presents within the first year of
life, when the production of fetal haemoglobin (HbF – α2γ2) begins to fall.
Affected children become generally unwell and fail to thrive secondary
to a severe microcytic anaemia. Ferritin levels are normal since there is
no iron deficiency. A compensatory increase in the synthesis of HbF and
haemoglobin A2 (HbA2 – α2δ2) occurs, which can be detected on serum
electrophoresis.
Clinical features include failure to thrive, lethargy, pallor and jaundice. On
examination there is often hepatosplenomegaly (secondary to extramedullary
haematopoiesis) with bossing of the skull, maxillary prominence and long
bone deformity (due to excessive intramedullary haematopoiesis). The
treatment of beta-thalassaemia major is with regular blood transfusions, aiming to maintain the haemoglobin concentration above 10 g/dL, or with
allogenic bone marrow transplant. Regular iron chelation therapy (with
desferrioxamine) is required to prevent iron overload and deposition in
vital organs such as the heart, liver and endocrine glands. If untreated, death
is inevitable in the first years of life.
Beta-thalassaemia minor describes people heterozygous for the beta-chain
chromosomal mutation. Affected persons have only mild anaemia and
are usually asymptomatic. Alpha-thalassaemia is common in South-East
Asia. There are four alpha genes, and therefore four variants of alphathalassaemia.
Affected patients can be asymptomatic (one gene corruption),
have mild hypochromic anaemia (two corruptions), have HbH disease
(three corruptions) or can die in utero (all four genes are corrupted). HbH
is a beta-chain tetramer that is functionally useless. Treatment options are
as for beta-thalassaemia.
Acute coronary syndrome (2)
A 52-year-old man presents to his GP with chest pain and is afraid he is
having a heart attack. His most significant symptom toward a diagnosis of
acute coronary syndrome (ACS) is:
A Chest pain located just under the left nipple, near the apex beat
B A past medical history of controlled angina
C A sharp chest pain
D Shortness of breath
E Tachycardia
B. A past medical history of controlled angina
ACS typically presents with a central/retro sternal chest pain of a crushing
character. Stable angina can evolve into the unstable angina of ACS.
Tachycardia and shortness of breath are more likely attributed to anxiety
in a patient who is scared. It should be noted that these symptoms should
never be ignored. Patients in the midst of real cardiac pain are also likely to
be anxious and may not necessarily offer textbook characterisations of what
they are experiencing. A brief admission to monitor troponin levels 8–12
hours after symptom onset is the correct course of action for any patient
presenting with possible cardiac chest pain.
Antibiotics (1)
From the following list of antibiotics and their predominant cover, which
is incorrect?
A Co-amoxiclav – broad-spectrum Gram-positive and -negative cover
B Flucloxacillin – Gram-positive cover
C Gentamicin – Gram-negative cover
D Metronidazole – anaerobic cover
E Vancomycin – Gram-negative cover
E. Vancomycin – Gram-negative cover
Vancomycin is a glycopeptide antibiotic that binds D-ala-D-ala peptide
sequences to prevent peptidoglycan cell wall synthesis, therefore it is active
against Gram-positive but not Gram-negative bacteria (the peptidoglycan
cell wall is a far more prominent and important feature in Gram-positive
bacteria). Co-amoxiclav has good Gram-positive and -negative cover as well
as much anaerobic cover, so is a widely used antibiotic in many scenarios,
however, its broad-spectrum characteristic means it disturbs the gut flora
and can predispose to Clostridium difficile infection. Flucloxacillin is a
narrow-spectrum antibiotic with only Gram-positive cover and is often
used in staphylococcal infections. Gentamicin has predominantly Gramnegative
cover although it has some Gram-positive cover. Metronidazole
has wide anaerobic cover and is often used in surgery due to the presence of
anaerobes in the bowel.
Topical steroids
A 25-year-old man presents with a severe outbreak of a dry erythematous
itchy rash that is now widespread, despite having used a steroid cream
prescribed by his GP. It appears to be eczema, and along with regular
emollients for the dryness, and antihistamines for the itch, you would like
to prescribe some very potent topical steroids for a brief period to attempt
get on top of the outbreak.
Which of the following is classed as a very potent topical steroid?
A Betnovate
B Dermovate
C Eumovate
D Hydrocortisone
E Prednisolone
B. Dermovate
Topical steroids are categorised as mild, moderate, potent, or very potent.
The more potent the steroid, the more likely it is to have side effects such as
skin atrophy, striae and increased risk of infection. Subsequently, the more potent the topical steroid, the less time it should be used for. Hydrocortisone
is a mild steroid, eumovate a moderate steroid, betnovate a potent steroid,
and dermovate is a very potent steroid. Prednisolone is an oral steroid, and
if the dermovate does not get on top of the eczema, there may be a case for
using systemic oral steroids – although they are not normally used in eczema
and carry a greater risk of side effects when used: patients can become
cushingoid, hypertensive, diabetic, immunosuppressed, osteoporotic, and
may develop steroid-induced psychosis.
Skin lesion (2)
A 7-year-old boy presents with multiple erythematous patches, over both
sides of his face, head, neck, upper chest and left arm and shoulder, which
appear to be covered in a honey-coloured crust. His mother says that the
lesions have spread, over about a week, starting at the left neck and radiating
outwards. The child appears to be upset and the lesions are itchy. There is
no past medical history and no history of recent infections.
Which of the following diagnoses is most likely?
A Eczema
B Erysipelas
C Impetigo
D Psoriasis
E Staphylococcal scalded skin syndrome
C. Impetigo
Itchy erythematous skin could be due to a number of things, including
eczema and psoriasis, but two features another diagnosis. Firstly, the
spreading from a starting point, rather than patches appearing at the same
time or cropping up in unrelated positions over time, suggests infection.
Secondly, the honey or golden crust is a purulent discharge. Both features are
classical of impetigo. Impetigo is a contagious, superficial infection caused
most commonly by Staphylococcus aureus. The infection spreads when
lesions burst to release an exudate, which spreads the bacteria outwards and
leaves behind the crust. Swabs should be taken for microscopy, culture, and
most importantly sensitivities. In contained infections, topical antibiotics
can be prescribed, but in more widespread disease, systemic antibiotics
should be used. Antibiotics with good activity against Staphylococci, such
as flucloxacillin, should be used pending sensitivities. Antihistamines can
be prescribed to help with itching. Underlying skin disease, such as eczema,
can predispose.
Erysipelas is a superficial form of cellulitis with a well-demarcated edge to the
patch of warm, tender erythema. It can spread more rapidly. Staphylococcal
scalded skin syndrome follows infection with group 2 coagulase-positive
staphylococci, and a circulating toxin causes epidermal splitting in the
granular layer, leading to peeling of the epidermis in large sections. A focus
of infection should be sought, and systemic flucloxacillin should be started.
It normally develops over a period of hours to days.
Management of Parkinson’s disease (2)
A 75-year-old man has been recently diagnosed with Parkinson’s disease
and started on levodopa (L-DOPA), which has helped his tremor and
bradykinesia significantly. However, in the past week he had a fall shortly
after getting out of his chair, during which he briefly blacked out, and
afterwards was sweating and felt cold.
Which of the following side effects most likely explains the fall?
A Dyskinesia
B Hallucinations
C Nausea
D None, he actually has multiple system atrophy and not Parkinson’s disease
E Postural hypotension
E. Postural hypotension
The fall happened soon after he stood up, involved a brief loss of consciousness,
and he had an excess sympathetic discharge shortly afterwards. It certainly
sounds like an episode of postural hypotension. Standing up requires
a significant degree of autonomic nervous system function to detect and react to the intravascular volume redistribution. As L-DOPA is a precursor
in the synthesis of not only dopamine but also noradrenaline, excess
peripheral noradrenaline and dopamine can cause widespread autonomic
dysfunction, symptoms of which include nausea and postural hypotension.
Hallucinations can occur with L-DOPA but are unlikely to cause a fall,
and dyskinetic movements could cause a fall but don’t explain the loss of
consciousness. Multiple system atrophy (MSA), a Parkinson-plus syndrome,
indeed includes prominent autonomic dysfunction, however it is extremely
rare and would be less likely to respond well to L-DOPA therapy (as this
man has).
Management of skin lesions (2)
A 76-year-old man presents with a vesicular eruption on the left side of his
forehead only. It is severely painful and the vesicles have started to crust
over. On examination, the area affected is well-demarcated. You also note a
red eye with apparent conjunctivitis.
Given the most likely diagnosis, which of the following treatments is the
most appropriate?
A Intravenous aciclovir
B Oral aciclovir
C Topical aciclovir
D Topical antibiotic
E Topical steroids
B. Oral aciclovir
This patient has herpes zoster infection. Herpes zoster is caused by
the varicella zoster virus, which is responsible for chickenpox. After an
episode of chickenpox, the virus resides in dorsal root ganglia and can
be transported retrogradely along the sensory axons to emerge and cause
herpes zoster, most commonly in a dermatomal distribution (although it
can be diffuse, usually in immunosuppressed patients). It appears most
commonly on the trunk and is called “shingles”, however it can affect
branches of the trigeminal nerve, most commonly the ophthalmic, where
it can also cause conjunctivitis, keratitis or iridocyclitis. Concurrent illness
or immunosuppression can trigger zoster, and it is more common in the
elderly. Many episodes will resolve spontaneously after around 2 weeks so the decision to treat depends on severity. Oral aciclovir is usually the first port
of call, although intravenous aciclovir can be used in disseminated zoster.
Topical acyclovir or steroids are unlikely to help, and topical antibiotics are
not indicated unless there is concurrent bacterial infection.
Management of asthma (2)
A 28-year-old woman with a past medical history of asthma has been using
her inhaled salbutamol more frequently of late. She is currently on an
inhaled short-acting beta-2 agonist and an inhaled steroid 800 μg/day. She
has been compliant.
What should you do?
A Add inhaled long-acting beta-2 agonist
B Add leukotriene receptor antagonist
C Add oral steroid
D Increase dose of inhaled steroid
E Prescribe inhaled short-acting beta-2 agonist as regular therapy
A. Add inhaled long-acting beta-2 agonist
The pharmacological management of chronic asthma follows a stepwise
approach. There are five steps in the management. In step 1, patients with
mild intermittent asthma are prescribed an inhaled short-acting beta-2
agonist. If there has been an exacerbation of asthma in the last 2 years, if
patient uses inhaled beta-2 agonists three times a week or more, or if patient
reports symptoms three times a week or more, then inhaled corticosteroids
should be added on. In step 3, if the patient‘s asthma control remains poor,
an add-on therapy should be considered such as a long-acting beta-2 agonist.
If the long-acting beta-2 agonist is not working, addition of other therapies
such as leukotriene receptor antagonists or theophylline can be considered.
In step 4, the inhaled corticosteroid can be increased to 2000 μg/day as
well as the addition of a fourth drug (e.g. leukotriene receptor antagonist,
theophylline) if symptoms persist. The final step involves continuous or
frequent use of oral prednisolone. Osteoporosis can be prevented by using
bisphosphonates. Once asthma control is established, the dose of the inhaled
or oral corticosteroid should be titrated to the lowest dose at which effective
control can be achieved.
Diagnosis of abdominal pain (2)
A 56-year-old man with a long history of alcohol abuse presents to the
emergency department with abdominal pain. On examination he has a
distended abdomen with shifting dullness and has a temperature of 38.2°C.
What is the most likely diagnosis?
A Bowel obstruction
B Liver cirrhosis
C Mallory–Weiss syndrome
D Perforated peptic ulcer
E Spontaneous bacterial peritonitis (SBP)
E. Spontaneous bacterial peritonitis (SBP)
Patients with ascites are at risk of developing SBP, which usually presents
with severe generalised abdominal pain, worsening ascites, vomiting, fever
and rigors. The most common causative organisms are Gram-negative
bacilli such as Escherichia coli and Klebsiella spp., which enter the systemic
circulation from the intestinal lumen and colonise the ascitic fluid. SBP can
lead to rapid decompensation of liver disease causing hepatic encephalopathy
and death. The diagnosis of SBP is confirmed by paracentesis, which involves
taking a sample of ascitic fluid from the abdomen using a needle. The
aspirated ascitic fluid is analysed for white cell count, glucose and protein.
In addition, the fluid should be sent to microbiology for culture and Gram
staining. If the white cell count is above 250 cells/mm3 the patient requires
intravenous antibiotics (e.g. cefotaxime or ceftriaxone). Some patients
also require human albumin solution to restore their intravascular fluid
volume. Patients who have had a previous episode of SBP, and patients who
are considered to be at high risk of developing SBP, should be considered for prophylactic oral antibiotics (e.g. norfloxacin or ciprofloxacin). The
development of spontaneous bacterial peritonitis corresponds to a poor
long-term prognosis.