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Paper 1 Questions

[1] Concerning cardiac failure . . . (c) Dresslers syndrome
(a) valvular disease is the most common cause in the UK (d) electromechanical disociation
(b) raised levels of atrial natriuretic peptide (ANP) are (e) left ventricular aneurysm
thought to be beneficial in heart failure
(c) a third heart sound is a common finding on [5] The following cardiac events are matched correctly
ausculation to the corresponding ECG changes . . .
(d) the heart looks small on plain postero-anterior (a) inferior infarct ST-segment depression in leads
chest radiograph II, III and aVF
(e) all diuretics used in treatment of cardiac failure (b) pericarditis downward-sloping ST-segment
potentially cause hypokalaemia depression in all anterior chest leads
(c) atrial fibrillation irregularly irregular P-waves
[2] Concerning hypertension . . . (d) first degree heart block broad QRS complexes
(a) approximately 50% of all cases of hypertension are (e) ventricular aneurysm persistent ST-segment
caused by renal dysfunction elevation in chest leads
(b) patients with Conns syndrome usually have a raised
[6] In peripheral arterial occlusive disease . . .
serum potassium level
(a) the relationship between radius of artery and flow
(c) hypothyroidism does not cause hypertension
within it is described by the Fick principle
(d) the Cushing reflex is an increase in systolic blood
(b) claudication means cramping in Latin
pressure that occurs secondary to Cushings
(c) Leriche syndrome is arterial occlusive disease below
the popliteal trifurcation
(e) malignant hypertension can be diagnosed on
(d) rest pain commonly occurs in the feet and
fundoscopy alone
metatarsal heads
(e) arterial ulcers are usually painless
[3] Acute myocardial infarction . . .
(a) causes chest pain not relieved by glyceryl trinitrate [7] Concerning aortic stenosis . . .
(GTN) (a) all aortic valve murmurs are heard best with the
(b) can be entirely painless in elderly diabetic patients patient on their left side with breath held in end-
(c) should prompt administration of intramuscular expiration
morphine to relieve pain (b) it causes hypertrophy of only the left ventricle
(d) can be diagnosed on the history alone (c) it causes a Waterhammer character in the radial
(e) first shows on ECG in the form of Q waves pulse
(d) it causes an ejection systolic murmur
[4] The following are recognized complications of (e) it is a common cause of atrial fibrillation
acute MI . . .
(a) Sheehans syndrome [8] Concerning atrial fibrillation (AF) . . .
(b) acute aortic regurgitation (a) it is commonly caused by dehydration

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4 Paper 1 MCQs

(b) when caused by high levels of circulating thyroid (e) it causes bats wing pulmonary oedema, upper lobe
hormone, it is always accompanied by thyroid eye diversion and Kerley-B lines on chest radiograph
(c) no P waves are present on the ECG [13] Concerning asthma . . .
(d) the QRS complex is broad (a) airway limitation is uniformly reversible in asthma
(e) class Ic antidysrhythmics (e.g. flecainide) are safe to (b) typical asthma attacks occur during exercise
give to most patients with atrial tachyarrhythmias (c) ACE inhibitors should not be given to asthmatic
[9] Concerning the respiratory organs of the body . . . (d) symptoms of asthma are usually worse at night
(a) the right main bronchus lies more vertically than (e) b2 adrenoceptor antagonists are commonly used in
the left treatment of asthma
(b) the lung is an organ with a single blood supply (i.e.
the pulmonary artery) [14] Tuberculosis . . .
(c) the alveolar lining of the lungs comprises mainly (a) is caused by the Gram-negative bacillus
type I pneumocytes M. tuberculosis
(d) only the right lung has an oblique fissure (b) is a recognized cause of apical lung fibrosis
(e) in healthy subjects, the strongest stimulator of (c) is classically associated with the presence of
ventilation is an increase in the arterial partial non-caseating granulomas
pressure of CO2 (PaCO2) (d) is diagnosed using one test with two different
names: Heaf and Mantoux
[10] On examination of the chest of a patient with a (e) is a recognized cause of erythema nodosum
unilateral tension pneumothorax . . .
(a) chest wall movements are decreased on both sides [15] Concerning palpation of the abdomen . . .
(b) the mediastinum is pulled towards the affected (a) in healthy, slim individuals, the liver is normally
side palpable in the right upper quadrant in deep
(c) the percussion note may be hyperresonant inspiration
(d) breath sounds may be decreased or absent on the (b) the normal liver extends superiorly to the 3rd
affected side intercostal space
(e) tactile vocal resonance will be increased on the (c) hepatic enlargement usually proceeds toward the
affected side left iliac fossa
(d) in healthy, slim individuals, the spleen is normally
[11] Concerning chronic obstructive pulmonary palpable on deep inspiration in the left
disease (COPD) . . . hypochondrium
(a) the airway obstruction is entirely irreversible (e) splenic enlargement occurs obliquely, toward the
(b) chronic bronchitis is believed to be due mainly to right iliac fossa
mucous gland hypertrophy
(c) patients commonly demonstrate asterixis [16] The following are recognized gastrointestinal
(d) cor pulmonale is defined as lung disease secondary causes of finger clubbing . . .
to ventricular hypertrophy (a) fibrosis
(e) it mainly leads to type II respiratory failure (b) coeliac disease
(c) PlummerVinson syndrome
[12] Concerning respiratory failure . . . (d) gastrointestinal lymphoma
(a) PaCO2 is, by definition, elevated in all types of (e) cystic fibrosis
respiratory failure
(b) the commonest cause of type II respiratory failure is [17] The following are recognized medical causes of
pneumonia abdominal pain . . .
(c) pulsus paradoxus is a sign commonly associated (a) diabetic ketoacidosis
with respiratory failure (b) myocardial infarction
(d) it always presents with dyspnoea (c) Addisons disease
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6 Paper 1 EMQs

Question 1 (a) Mitral stenosis
(b) Mitral regurgitation
Match the following examination findings to the most (c) Aortic regurgitation
accurate diagnosis: (d) Aortic sclerosis with atrial fibrillation
(e) Aortic regurgitation with left ventricular failure
(1) JVP Normal (f) Mitral stenosis with atrial fibrillation
Apex Tapping in character, not (g) Mitral regurgitation and stenosis
displaced laterally (h) Aortic stenosis
Auscultation Grade 3 mid-diastolic murmur (i) Aortic sclerosis
at apex, no pre-systolic (j) Mitral regurgitation with diastolic flow murmur
accentuation (k) None of these
Chest Clear
BP 155/82 mmHg
Question 2
(2) JVP Elevated Match the following case histories to the best diagnosis
Apex Displaced laterally, and thrust- given in the list below.
ing in character
Auscultation Pan-systolic murmur at apex (1) A 47-year-old woman presents with a history of re-
Chest Bi-basal end expiratory current headaches over 5 years. The pain is described as
crepitations unilateral, behind the eye and severe. She is well between
BP 143/65 mmHg episodes. There is no vomiting although she feels nau-
seated and has abdominal discomfort. The onset is typi-
(3) JVP Normal cally sudden. She occasionally has hazy disturbance of
Apex Tapping in character, not her vision. There are no abnormal features on systemic
displaced review. In the past she has had hypertension, but is cur-
Auscultation Grade 3 mid-diastolic murmur rently not taking treatment.She has three children.There
at apex, pre-systolic are no regular medications. On examination she has a
accentuation BMI of 29 and a BP recording of 170/95 mmHg. Other-
Chest Clear wise a full neurological examination was normal,includ-
BP 162/73 mmHg ing fundoscopy.

(4) JVP 8 cm (2) A 15-year-old girl presents with a 5-week history of

Apex Displaced, thrusting in character persistent headaches. These are described as all over the
Auscultation Short early diastolic murmur head. There is associated episodic blurring of vision and
Chest Few bi-basal crepitations dizziness. There is no history of head injury. These
BP 180/62 mmHg headaches occur throughout the day. There have been
several episodes of vomiting. In the past she has been fit
(5) JVP Normal and well. Her mother and sister have both suffered
Apex Heaving in character and episodes of migraine since childhood. She takes the oral
displaced laterally contraceptive pill as her only medication. On examina-
Auscultation Grade 3 crescendo-decrescendo tion she is obese and has a BMI of 32. She is normoten-
systolic murmur over whole sive. Cranial nerve examination is normal. Fundoscopy
precordium, not heard in reveals bilateral blurring of the optic disc margins.
carotid area There are no abnormal findings in the peripheral nerv-
Chest Few bi-basal crepitations ous system.
BP 110/93 mmHg
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Paper 1 EMQs 7

(3) A 52-year-old patient attends complaining of (e) Giant cell arteritis
episodic bouts of headache. He has no previous history (f) Space occupying lesion
of headaches. The pain is described as burning and se- (g) Chronic subdural haematoma
vere. The pain occurs behind the right eye, and is associ- (h) Epilepsy
ated with lacrimation, and running of the nostril on the (i) Cavernous sinus thrombosis
same side. Each episode lasts approximately 1 h and then (j) Viral meningitis
subsides. In the past he has suffered from diabetes and (k) Benign intracranial hypertension
angina. He smokes 20 cigarettes per day. His current (l) Cluster headache
medication includes metfomin and GTN spray for occa- (m)Referred pain
sional use. You happen to see him during an acute (n) Hypertensive encephalopathy
episode. He has conjunctival injection on the side of the (o) Acute encephalitis
pain. Cranial nerve examination and fundoscopy find- (p) None of these
ings are normal.
Question 3
(4) A 58-year-old female patient presents with her rela-
tives with a history of increasing headaches. The pain is Match the following chest examination findings to the
felt worse at the top of the head. These occur every day most likely diagnosis:
and improve towards the end of the day.In addition there
have been several reported episodes of irregular jerking (1) Respiratory rate 36 b.p.m.
of the left arm,each lasting around 5 min.There is no his- Central cyanosis Present
tory of head injury. There is a 10-year history of excessive Trachea Central
alcohol consumption, 30 units per day. She takes no Chest shape Normal
regular medication. On examination she is apyrexial. Expansion Equal
There is a bilateral coarse tremor. There is a single spider Percussion note Resonant bilaterally
naevus on the upper chest wall, but no jaundice or he- Auscultation Normal breath sounds
patomegaly. Cranial nerve examination reveals a right-
sided homonymous inferior quadrantanopia.
(2) Respiratory rate 32 b.p.m.
Central cyanosis Present
(5) A 19-year-old university student presents acutely
Trachea Deviated to the right
with a headache, vomiting and photophobia. He had
Chest shape Normal
been found confused, wandering around his hall of resi-
Expansion Reduced on left
dence looking for his room.He had been fit and well until
Percussion note Hyperresonant on left
a few hours ago. Prior to admission, in the ambulance, he
Auscultation Reduced breath sounds on
had been observed to have a grand mal fit, which has
responded to rectal diazepam. Past medical history
includes an admission for observation 6 months previ-
ously following a minor head injury after falling off his (3) Respiratory rate 16 b.p.m.
bike. He had received the meningitis C vaccine before Central cyanosis Absent
going to university. On examination he was pyrexial at Trachea Deviated to left side
38.7C. Confused and GCS 10/15. There was obvious Chest shape Depressed chest wall at left
neck stiffness and photophobia. There was no rash. Cra- apex
nial nerve examination was normal. The pupil size was Expansion Reduced in left upper zone
3 mm bilaterally and reactive and the optic discs were Percussion note Dull over left clavicle
thought to be normal. Auscultation Normal

(a) Trigeminal neuralgia

(b) Migraine
(c) Acute bacterial meningitis
(d) Tension headache
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8 Paper 1 EMQs

had run a cross-country race at school without prob-

(4) Respiratory rate 20 b.p.m.
lems. There is no family history of haemophilia or other
Central cyanosis Absent
bleeding disorder. On examination he was mildly pyrex-
Trachea Deviated to the right
ial at 37.5C and he appeared in pain. The right knee was
Chest shape Normal
hot, swollen and locally tender. The following investiga-
Expansion Reduced at right base
tions were obtained:
Percussion note Stony dull at right base
Hb 12.3 g/dL
Auscultation Reduced breath sounds at
WCC 5.6 109/L
right base
Platelets 354 109/L
PT 12 s (NR 1015 s)
(5) Respiratory rate 28 b.p.m.
APPT 72 s (NR 2535 s)
Central cyanosis Present
Bleeding time Normal
Trachea Central
Factor VIII:C 5% of normal
Chest shape Normal
Expansion Normal
Percussion note Dull at right base (2) A 34-year-old man presents with a swollen and
Auscultation Bronchial area at right base painful right knee. There is no preceeding history of
trauma. His brother had had similar problems in the
(6) Respiratory rate 28 b.p.m. past. The following investigations were obtained:
Central cyanosis Present Hb 14.7 g/dL
Trachea Central WCC 10.6 109/L
Chest shape Hyperinflated bilateral Platelets 373 109/L
Expansion Equal PT 14 s (NR 1015 s)
Percussion note Resonant equally left and APPT 79 s (NR 2535 s)
right sides Bleeding time Normal
Auscultation Diffuse polyphonic Factor VIII:C Normal
expiratory wheezing
(3) A 27-year-old female is investigated for heavy peri-
(a) Lung abscess ods. Her mother had similar problems. She had also no-
(b) Right lower lobe pneumonia ticed prolonged bleeding from simple cuts and after
(c) Right sided pleural effusion blood taking. She was on no medication. The following
(d) Old tuberculosis at right apex investigations were obtained:
(e) Acute pulmonary oedema Hb 10.2 g/dL
(f) Asthma WCC 9.6 109/L
(g) Tension pneumothorax on the right Platelets 175 109/L
(h) Left ventricular failure PT 11 s (NR 1015 s)
(i) Left apical lung fibrosis APPT 79 s (NR 2535 s)
(j) Right ventricular failure Bleeding time 18 min (normal <10 min)
(k) Pulmonary embolism Factor VIII:C 20% of normal
(l) Inhaled foreign body in right main bronchus
(m)None of these (4) A confused 78-year-old patient is admitted and
noted to have numerous bruises. Her relatives say she
takes a range of medications, but the details are not
Question 4
known and no reliable history can be obtained from the
From the following questions, choose the best diagnosis patient. In her bag is found a cardiology outpatients ap-
from the list below. pointment card. On examination she is confused and
drowsy with a GCS of 9/15. There are multiple large
(1) A 7-year-old boy presents with spontaneous onset of bruises of the skin. She has an enlarged right pupil that
swelling and pain, in his right knee. The previous day he reacts poorly to light. Her pulse is 52/min and irregularly
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Paper 1 Answers

[1] (a) F (b) F (c) T (d) F (e) F Ischaemic myocardial disease, coronary artery
[2] (a) F (b) F (c) F (d) F (e) F disease
[3] (a) F (b) T (c) F (d) F (e) F Cardiomyopathy (alcoholic, diabetic, drug-
[4] (a) F (b) F (c) T (d) T (e) T induced, idiopathic)
[5] (a) F (b) F (c) F (d) F (e) T Myocarditis
[6] (a) F (b) F (c) F (d) T (e) F Valvular heart disease
[7] (a) F (b) T (c) F (d) T (e) F Congenital heart disease with severe pulmonary
[8] (a) T (b) F (c) T (d) F (e) F hypertension
[9] (a) T (b) F (c) T (d) F (e) T Terminal ventricular septal defect or atrial septal
[10] (a) F (b) F (c) T (d) T (e) F defect
[11] (a) F (b) T (c) T (d) F (e) T Dominant diastolic heart failure
[12] (a) F (b) F (c) T (d) F (e) F Hypertension
[13] (a) F (b) F (c) F (d) T (e) F Severe aortic stenosis
[14] (a) F (b) T (c) F (d) F (e) T Hypertrophic cardiomyopathy
[15] (a) T (b) F (c) F (d) F (e) T Restrictive cardiomyopathy
[16] (a) F (b) T (c) F (d) T (e) T Ischemic myocardial disease, coronary artery
[17] (a) T (b) T (c) T (d) T (e) T disease
[18] (a) F (b) F (c) T (d) F (e) F Acute heart failure
[19] (a) F (b) F (c) F (d) T (e) F Acute mitral or aortic regurgitation
[20] (a) F (b) F (c) F (d) F (e) F Rupture of valve leaflets or supporting structures
[21] (a) F (b) F (c) F (d) T (e) T Infective endocarditis with acute valve
[22] (a) F (b) T (c) F (d) F (e) F incompetence
[23] (a) F (b) F (c) T (d) T (e) T Myocardial infarction
[24] (a) F (b) F (c) F (d) F (e) F (b) Atrial cells store and release the 28-amino-acid
atrial natriuretic peptide (ANP) in response to stretch
of the right atrium by increased central venous pressure.
The relative volume overload of the atria that occurs
[1] (a) F (b) T (c) T (d) F (e) F in heart failure causes levels of ANP to be high, leading
(a) Valvular disease only causes 7% of cases of heart to a variety of beneficial effects in heart failure, including
failure in the UK. The commonest cause of heart failure ...
in the UK is atherosclerotic ischaemic heart disease. In Increased sodium and water excretion by the kidney
general, the causes of low-output cardiac failure can be (natriuresis and diuresis)
split up depending on whether they cause predominant- Increased glomerular filtration, hence increased
ly systolic, predominantly diastolic or acute failure of the sodium excretion (by selective vasodilatation of
myocardium . . . renal glomerular afferents, and vasoconstriction of
Dominant systolic heart failure renal glomerular efferents)

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50 Paper 1 MCQs

Relaxation of vascular smooth muscle (vasorelaxa- tal convoluted tubule by binding to the chloride site of

tion of capacitance vessels) the electroneutral Na+/Cl co-transport system and in-
Increased vascular permeability hibiting its action. Potassium loss with these drugs is
Inhibition of release/action of several undesirable significant and can be serious. Excretion of uric acid
hormones which exacerbate heart failure (e.g. aldos- ( gout) and calcium is decreased, whereas that of
terone, angiotensin II, endothelin, ADH) magnesium is increased.
When it was first discovered, ANP was cast as the car- Loop diuretics (e.g. furosemide, bumetanide): inhibit
diovascular hero, standing opposed to the villainous in- transport of NaCl out of the lumen of the thick seg-
tents of vasoconstrictors such as angiotensin, ADH and ment of the ascending limb of the loop of Henle. These
endothelin in heart failure. Unfortunately, its potential are the most powerful of all currently used diuretics,
therapeutic use foundered with the discovery of its short potentially causing loss of up to 25% of the Na+ in the
plasma half-life. Subsequent attempts to devise ANP ag- filtrate by direct inhibition of the Na+/K+/2Cl carrier
onists or agents to block clearance of the endogenous in the luminal membrane.Again,these drugs cause sig-
peptide have been thus far unsuccessful. nificant K+ loss. There is an increase in the excretion of
(c) The third heart sound (S3) occurs in early diastole calcium and magnesium, and a decrease in the excre-
due to rapid ventricular filling as soon as the mitral and tion of uric acid ( gout).
tricuspid valves open. It can be normal in children and Potassium-sparing diuretics (e.g. spironolactone,
young adults, but is abnormal in others and represents amiloride): Spironolactone has a limited diuretic ac-
heart failure or volume overload of the heart (e.g. mi- tion. By acting as an aldosterone antagonist it inhibits
tral or aortic regurgitation). It is commonly referred to as Na+ retention and decreases K+ excretion. Similarly,
a distressed sound. amiloride has limited diuretic efficacy.By blocking Na+
The fourth heart sound (S4) occurs in late diastole in reabsorption in the collecting tubules and ducts, it
association with ventricular filling due to atrial systole, concomitantly decreases K+ excretion. Importantly,
and is related to reduced ventricular compliance. It is a drugs in this class are the only diuretics that do not
low-frequency oscillation that can be normal at older cause hypokalaemia.
ages owing to a physiological decline in ventricular com-
pliance,but is nearly always abnormal at younger ages es- [2] (a) F (b) F (c) F (d) F (e) F
pecially if it is of high intensity or is palpable. It is (a) Over 90% of all cases of hypertension arise due to no
common in ventricular hypertrophy, particularly with known cause, referred to as essential hypertension.
hypertension and aortic stenosis, and is almost invari- The remaining cases of hypertension that do have a de-
able in acute myocardial infarction.S4 may arise from the fined cause are known as secondary hypertension.
right ventricle, the left ventricle or both. It is commonly These are always important to consider because even
referred to as a stressed sound. though they are rare, they are frequently amenable to
(d) The chest X-ray in a patient with heart failure has a treatment.
classical pattern, comprising . . .
Cardiomegaly (greater than the width of one Secondary causes of hypertension
hemithorax) Renal causes: these account for >80% of cases of sec-
Upper lobe venous diversion ondary hypertension. They cause inappropriate re-
Kerley-B lines (fine peripheral septal lines; named tention of salt and water and inappropriate elevation
after Peter J. Kerley, an English radiologist who also of plasma renin levels. They may be split into:
described Kerley-A and Kerley-C lines on chest radi- Renovascular
ographs) Renal artery stenosis
Bats wing hilar oedema Renoparenchymal
Bilateral effusions Chronic glomerulonephritis
(e) Diuretics commonly used in the treatment of heart Chronic pyelonephritis
failure include . . . Diabetic nephropathy
Thiazide diuretics (e.g. bendrofluazide, metolazone): Adult polycystic kidney disease
decrease active reabsorption of Na+ and Cl in the dis- Chronic tubulointerstitial nephritis
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Paper 1 MCQs 51

Endocrine causes: there are eight . . . lessening chest pain in acute MI that they do in stable

Conns syndrome (excess mineralocorticoid) (b) angina, they are still able to noticeably lessen the pain of
Cushings syndrome (excess glucocorticoid) acute MI when given sublingually, buccally or intra-
Acromegaly (excess growth hormone) venously.
Adrenal hyperplasia (congenital) (b) So-called silent infarcts occur in the elderly,diabet-
Phaeochromocytoma ics and patients with a long history of hypertension.
Hyperthyroidism Instead of presenting with pain, these infarcts present
Hypothyroidism (c) with dyspnoea from development of acute pulmonary
Hyperparathyroidism oedema, syncope or coma from dysrhythmias, acute
Cardiovascular causes: the most important is coarcta- confusional states, diabetic hypoglycaemic crisis,
tion of the aorta (also polycythaemia rubra vera) hypotension or shock.
Pharmacological causes: including the oral contra- (c) Although administration of morphine (or more
ceptive pill, corticosteroids, monoamine oxidase correctly diamorphine) is an important early manoeu-
inhibitors (paroxysms when eating tyramine- vre in treating acute MI (since it produces analgesia and
containing foods), cocaine, amphetamines, vaso- lessens subjective distress from dyspnoea), it should be
pressin, etc. given intravenously (or orally if access is difficult) and
Pregnancy not intramuscularly. This is because should the patient
Raised intracranial pressure (ICP): an acute rise in later be thrombolysed, significant internal or external
ICP causes the Cushing phenomenon or reflex, bleeding can occur if intramuscular injections have been
which is essentially a rise in systemic blood pressure in recently given.
response to the increased intracranial pressure. Com- (d) Myocardial infarction should be suspected on the
monly occurs in head injury or intracranial haemor- history,but is should only be diagnosed in the presence of
rhage (d) either positive ECG findings, or a raised level of cardiac
To impress examiners with your knowledge of second- enzymes on testing the blood an appropriate interval
ary causes of hypertension, also mention GRA (gluco- after onset of symptoms.
corticoid remediable aldosteronism). In this condition (e) The first change of acute MI visible on the ECG is a
there is a crossover mutation and fusion of the adreno- point of contention, although it most certainly is not the
corticotrophic hormone (ACTH)-regulatory element of appearance of Q-waves.
the 11-b-hydroxylase gene and the aldosterone synthase ST-segment elevation is said to occur within minutes
gene, meaning that every time the body attempts to of the onset of acute MI and can persist for up to 2 weeks.
manufacture steroid, it instead produces aldosterone, If elevation persists over 4 weeks, this suggests formation
causing profound hypertension via salt and water reten- of a ventricular aneurysm.
tion. Once discovered, the treatment is simple: give ex- Occasionally T-wave inversion is said to be the first
ogenous dexamethasone to switch off the need for visible ECG change of acute MI. This tends to persist
endogenous steroid production, thereby switching off longer than ST-elevation, yet it is still usually only a tran-
inappropriate aldosterone production. sient change. T-wave inversion that occurs without
(e) Malignant hypertension is said to occur when the BP subsequent formation of Q-waves is typical of sub-endo-
rises suddenly and precipitously to levels above cardial infarction (non-Q-wave infarction).
140 mmHg diastolic. There is characteristic fibrinoid The final ECG change associated with acute MI is the
necrosis of vessel walls and rapid progression to renal appearance of pathological Q-waves. These are broad
failure. There are marked changes in retinal vessels, and (>1 mm), deep (>2 mm) negative deflections that start
grades 3 and 4 on the KeithWagener classification of the QRS complex. They occur physiologically in aVR, I
hypertensive retinopathy are diagnostic of malignant and III. Pathological Q-waves develop over hours or
hypertension, but only in the presence of a diastolic days,and are the hallmark of transmural infarct.They re-
BP > 140 mmHg. flect electrical silence of infarcted cardiac tissue, causing
a window through which the normal endo- to epicardial
[3] (a) F (b) T (c) F (d) F (e) F activation of the opposite,non-infarcted ventricular wall
(a) Although nitrates do not have the marked effect of is seen. They are almost always permanent.
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52 Paper 1 MCQs

[4] (a) F (b) F (c) T (d) T (e) T or or posterior MI; treated first with atropine, then

The complications of myocardial infarction can be with electrical pacing

thought of under five main headings . . . Atrioventricular blockade is also common; if
1. Further chest pain the infarction is an inferior one, the blockade is
A bruised sensation and musculoskeletal pain are often temporary and does not require treatment;
common within the first 48 h, especially if the pa- however, if the infarction is an anterior one and
tient has undergone CPR or repeated attempts at 2nd or 3rd degree block/bifascicular block arises,
DC cardioversion then prophylactic pacing is indicated
Pericarditis may develop in the first 13 days post- Ventricular ectopics post-MI have a poor progno-
MI; it is commoner with full thickness infarcts and sis as they frequently herald the development of
may cause an audible rub (like walking in fresh- ventricular tachycardia or fibrillation; there is no
laid snow); treat with high dose aspirin evidence that treatment of these alters prognosis,
Infarct extension may occur; look for further ST- but it may be prudent to correct PaO2, K+ and Mg2+;
elevation; treat with repeated thrombolysis or ur- if ectopics continue, a magnesium sulphate infu-
gent coronary angioplasty sion may be set up
It may simply be post-infarction angina; this usual- Ventricular tachycardia may arise, and it should be
ly develops within 10 days of the acute episode and treated in the usual way (Mg2+, lidocaine, amio-
can be treated with standard medical therapy, i.e. darone, synchronized DC shock). VT in the first
nitrates, b-blockers and Ca2+-channel antagonists 24 h post-MI has a less sinister prognosis than VT
2. Fever arising later in the post-MI course. Should ventric-
Fever commonly peaks 34 days post-MI and is due ular fibrillation develop from VT, prompt DC car-
to myocardial necrosis dioversion should be instigated
Other causes of fever must be considered, e.g. infec- 5. Hypotension and shock post-MI
tion, thrombophlebitis, venous thrombosis, drug Common in large MIs; treatment is with cau-
reaction, pericarditis, etc. tious plasma volume expansion (i.e. 100200 mL
Dresslers syndrome occurs weeks or even months colloid over 10 min), and then inotropes if the
after MI and consists of the triad of pericarditis, BP should remain low despite adequate filling
fever and pericardial effusion; it is actually an au- pressures
toimmune response to the damaged myocardium; Other complications of MI worth considering are
it may necessitate administration of anti-inflam- thromboembolism secondary to prolonged inactivity
matories. (c) or cardiac mural thrombus, left ventricular aneurysm
3. New systolic murmur (four to consider) formation (think persistent ST-elevation), heart failure
Pericardial friction rub secondary to inflamma- and, of course, death.
tion of the infarcted myocardium Sheehans syndrome is pituitary necrosis due to circu-
Long-standing murmur that was missed at presen- latory collapse following severe post-partum bleeds,
tation and is nothing to do with MI (a)
Ventricular septal defect: this classically occurs Acute aortic regurgitation is not a complication of
510 days post-MI and presents as sudden collapse, acute MI. It happens more often in dissecting aortic
pulmonary oedema and hypotension; usually diag- aneurysms or with valve destruction associated with
nosed on echo, where colour flow shows left to right the vegetations of bacterial endocarditis (b)
flow across the septum; requires emergent surgical Electromechanical dissociation (EMD) occurs when
repair the ECG is relatively normal and yet there is no
Acute mitral regurgitation occurs 210 days post- mechanical activity of the heart (normal ECG but no
MI due to infarction and rupture of papillary mus- output) (d)
cle; can cause torrential regurgitation and sudden The causes of EMD can be grouped into the 4 Hs and the
death, but if the patient survives, emergent surgical 4 Ts . . .
repair is vital H Hypothermia T Tension pneumothorax
4. Post-MI arrhythmias (four to consider) H Hypoxia T Thromboembolism
Sinus bradycardia is common, especially in inferi- (pulmonary)
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Paper 1 MCQs 53

H Hypovolaemia T Tamponade (cardiac) consumption by the difference in oxygen content

H Hypo- and T Toxins (i.e. drugs) of arterial and mixed venous blood. It is commonly
hyperkalaemia used in operating theatres to monitor cardiovascular
[5] (a) F (b) F (c) F (d) F (e) T (b) Claudication means limping, being derived from
(a) Inferior infarcts cause ST-segment elevation in the Latin claudicatio, to limp.
leads II,III and aVF. Remember: infarction causes eleva- (c) Leriche syndrome is aortoiliac occlusive disease,
tion, ischaemia causes depression. Inferior infarcts usu- which causes absent femoral pulses, lower extremity
ally reflect occlusion in the RIGHT coronary artery or claudication,wasting of buttock muscles and impotence.
one of its branches. It can be caused acutely by a saddle embolism at the bi-
(b) Pericarditis causes saddle-shaped ST-segment el- furcation of the aorta, but is more commonly seen in the
evation in all leads of the ECG. Downward-sloping ST- chronic setting of slowly progressive atherosclerosis.
segment depression indicates myocardial ischaemia, (d) Rest pain indicates advanced peripheral vascular
whereas upward sloping ST-segment depression is non- disease. It occurs most commonly in the toes and
specific. metatarsal heads on lying down at night. Temporary re-
(c) Atrial fibrillation causes the ECG to show fine oscil- lief can be obtained by dangling the legs over the side of
lations of the baseline (F-waves) and no clear P waves at the bed, or by standing up and walking, because this
all. The QRS segments occur in an irregularly irregular makes the feet dependent, increasing gravitational hy-
fashion, and at a rapid rate. The causes of AF can be re- drostatic pressure, increasing venous pressure and so
called by remembering that PIRATES were often dehy- temporarily enhancing oxygen delivery.Unlike claudica-
drated after long spells at sea . . . tion, which is caused by muscle ischaemia, rest pain is
Dehydration caused by nerve ischaemia, and it often corresponds to
P Pulmonary disease an ankle:brachial pressure index (ABPI) of <0.4. It
I Ischaemia, infarction should be differentiated from benign nocturnal cramps,
R Rheumatic heart disease which usually occur in the calf and are not associated
A Anaemia, atrial myxoma with impaired blood flow.
T Thyrotoxicosis (e) Arterial ulcers arise due to arterial insufficiency.They
E Ethanol tend to occur on the toes, heel or dorsum of the foot in
S Sepsis response to minor trauma and are exquisitely painful.
(d) First-degree heart block is manifest on the ECG as They have a punched-out appearance and a pale
simple prolongation of the PR-interval. In health, the necrotic base.
PR-interval should be between three and five small Venous ulcers usually occur at the medial or
squares on the ECG,i.e.0.120.2 s.If it is longer than this, lateral malleolus in response to venous pooling. They
then first-degree heart block is present. NB In first- often cause a brownish discoloration of the skin
degree heart block, the PR interval is constant even (haemosiderin deposition), have a granulating base and
though it is prolonged,and a QRS complex follows every whilst painful, do not cause anywhere near as much pain
P-wave. Broad QRS complexes suggest a rhythm of as arterial ulcers. They are associated with significant
ventricular origin OR a supraventricular rhythm with oedema. Treatment is usually conservative.
concomitant bundle branch block. Neuropathic ulcers are painless, and usually located on
(e) Ventricular aneurysm characteristically produces the plantar or lateral aspects of the foot. They are the di-
persistent ST-segment elevation in all leads for greater rect result of diabetic neuropathy and are often asso-
than 1 months duration. ciated with destruction of the ankle joint (Charcots
foot).Because of the nature of diabetes,these ulcers often
[6] (a) F (b) F (c) F (d) T (e) F co-exist with arterial ulceration.
(a) Flow rate within a vessel is, in fact, governed
by Poiseuilles law, which states that the flow within [7] (a) F (b) T (c) F (d) T (e) F
a vessel is proportional to the fourth power of the (a) Aortic stenosis is heard best in the aortic area (2nd
radius. The Fick principle is a means of indirectly right intercostal space) with the patient leaning forward
calculating cardiac output by dividing total body oxygen and the breath held in end-expiration (breathe in,
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54 Paper 1 MCQs

breathe out, hold it). Aortic regurgitation is best heard (b) Thyroid eye signs (i.e. retro-orbital swelling, prop-

at the left sternal border with the patient sitting forward tosis, exophthalmos, limitation of eye movements, visual
in end expiration. impairment due to optic nerve pressure) are only seen
(b) Aortic stenosis causes isolated hypertrophy of the in Graves disease. All causes of hyperthyroidism,
left ventricle. The left atrium does not become enlarged however, may cause atrial fibrillation, because it is the
or hypertrophied because the mitral valve is intact (un- high level of circulating thyroid hormone and not the
less there is mixed valvular disease). high levels of IgG (thyroid stimulating antibody) seen
(c) A water-hammer pulse describes a pulse with a in Graves that is responsible for precipitating atrial
forcible impulse but immediate collapse, and is charac- fibrillation.
teristic of aortic regurgitation. It is also known as a col- (c) Because there is no ordered contraction of the atria
lapsing pulse. The pulse character associated with aortic in AF (i.e. electrical activity does not start at and is not
stenosis is slow-rising because of the resistance encoun- propagated from the sino-atrial node), there are no P-
tered by the left ventricle when pushing blood past the waves visible on the ECG.
stenosed valve. (d) Anti-dysrhythmic agents are traditionally classified
The character of pulsation may also be described in into four groups according to the Vaughan-Williams
the following ways . . . classification . . .
Pulsus paradoxus: an exaggeration of the normal ten- Class 1: Membrane depressants
dency of the systolic pressure to fall on inspiration Class 1a: disopyramide, quinidine
(should be <10 mmHg in health,but is greater than this Class 1b: lidocaine
in pulsus paradoxus); characteristically seen in severe Class 1c: flecainide, propafenone
airway obstruction (e.g. acute severe asthma), cardiac Class 2: Antisympathetics
tamponade and constrictive pericarditis. e.g. b-blockers, the cardioselective (i.e. b-1 specific)
Pulsus alternans: alternating weak then strong (but ones being metoprolol and atenolol
regular) beats; characteristic of severe myocardial Class 3: Prolongers of the action potential
failure, indicating very poor prognosis. e.g. amiodarone, sotalol
Pulsus bigeminus: ectopic beats follow each sinus Class 4: Slowers of conduction in nodal tissue
beat, causing beats to occur in pairs; rhythm is not reg- e.g. the non-dihydropyridine calcium channel
ular. antagonistsverapamil, diltiazem
Pulsus bisferiens: an arterial pulse with palpable,sepa- Class 1c agents (like flecainide) and all other class 1 anti-
rated peaks; characteristic of hypertrophic, obstruc- dysrhythmics should only really be used in the treatment
tive cardiomyopathy (HOCM) and when aortic of intractable or life-threatening arrhythmias; they
stenosis co-exists with aortic regurgitation. should never be used where the patient has significant left
(d) The murmur caused by aortic stenosis is a diamond- ventricular dysfunction (e.g. heart failure), prior history
shaped ejection systolic murmur, best heard in the aor- of MI or acute coronary ischaemia.
tic area. It is said to be rough in quality, and is longer the (e) Treatment of AF can be approached in two ways:
more severe the stenosis. It radiates to the carotids. 1. Control the ventricular rate and ignore what the
A systolic ejection click may be heard when the valve atria are doing: this is usually achieved using an AV-
opens if it is calcified and has become immobile (severe nodal blocking drug (e.g. digoxin, b-blockers or
disease). There may be a prominent fourth heart sound verapamil).
(S4) if the left ventricle is hypertrophied and has become 2. Cardiovert in an attempt to stop the atria fibrillating:
stiff. this can be performed electrically (80% of patients
(e) Aortic stenosis alone is not associated with the devel- convert to sinus rhythm with synchronized DC car-
opment of AF as long as the mitral valve remains intact. dioversion) or medically (with an IV infusion of class
1a, 1c or 3 drug, usually amiodarone). Recurrent
[8] (a) T (b) F (c) T (d) F (e) F paroxysms can be prevented with prophylactic oral treat-
(a) Dehydration and hypovolaemia, whether acute or ment with a class 1a, 1c or 3 drug, again usually
chronic, are common causes of atrial fibrillation, espe- amiodarone.
cially in hospital patients. Amiodarone is one of a select number of drugs whose
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Paper 1 MCQs 55

side effect profile should be known for undergraduate of hydrogen ions in cerebrospinal fluid (CSF), stimulat-

final examinations . . . ing the brainstem respiratory centre. Sensitivity to in-
Sensitivity to sunlight (i.e. phototoxicity) creasing PaCO2 can be lost in chronic obstructive
Corneal microdeposits pulmonary disease (COPD) due to chronic over-expo-
Slate-grey skin discolouration sure of the brainstem to high levels of CO2, and in these
Peripheral neuropathy patients the chief stimulus to breathe becomes the partial
Hypo- or hyperthyroidism pressure of oxygen (PaO2), as detected by the carotid and
Pulmonary fibrosis (irreversible) aortic arch bodies. Patients with chronic type II respira-
tory failure should therefore not be administered high
[9] (a) T (b) F (c) T (d) F (e) T concentrations of oxygen because it abolishes their respi-
(a) The right main bronchus is wider,shorter and more ratory stimulus,and they would quickly have a respirato-
vertical than the left; this is why a swallowed foreign ob- ry arrest. Pyrexia, large doses of aspirin and the drug
ject or aspirated material is more likely to impact in the doxapram may directly stimulate the brainstem respira-
lower lobe of the right lung rather than the left. Material tory centre, whereas severe hypoxaemia and sedatives,
aspirated when a patient is lying flat is most likely to im- especially opioids, may depress it.
pact in the middle lobe of the right lung.
(b) The lung has a dual blood supply. The bronchi, [10] (a) F (b) F (c) T (d) T (e) F
connective tissue of the lung and the visceral pleura On examination of the chest in a patient with a unilateral
receive their blood supply from the bronchial tension pneumothorax . . .
arteries,which are branches of the descending aorta.The Chest wall movements will be decreased on the
alveoli on the other hand receive deoxygenated affected side only (a)
blood from the terminal branches of the pulmonary The mediastinum will be displaced away from the
arteries. affected side (b)
(c) The epithelial lining of the alveoli is mainly made up The percussion note will be hyperresonant on the
of type 1 pneumocytes. These form a thin barrier for gas affected side (c)
exchange. They are, however, derived from surfactant- Breath sounds will be decreased or absent on the affect-
producing type 2 pneumocytes, which are slightly more ed side (d)
in number but cover less surface area. Tactile vocal resonance will be decreased on the affect-
(d) Both lungs have oblique fissures, but only the right ed side (e)
has a horizontal fissure, hence there are three lobes in There are no added sounds
the right lung (upper, middle and lower) but only two in It is very useful for exams to be exactly sure of the chest
the left (upper, lower and the lingula a redundant seg- signs of the most common respiratory complaints. Re-
ment of pulmonary tissue anterior to the surface of the cent exams have contained MCQs and EMQs that tested
heart). precisely the candidates knowledge of such signs. A use-
(e) In health the strongest stimulation to ventilation is ful table to memorize is shown below, but there is no sub-
an increase in the arterial partial pressure of CO2 stitute for having seen/discovered such signs for yourself:
(PaCO2), which causes an increase in the concentration find patients with signs and examine them!

Pathological Chest wall Mediastinal Percussion Vocal

process movement displacement note Breath sounds resonance Added sounds

Consolidation Decreased None Dull Bronchial Increased Fine creps


Collapse Decreased Towards Dull Decreased or Decreased None

ipsilaterally absent or absent
Continued on p. 56
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56 Paper 1 MCQs

Pathological Chest wall Mediastinal Percussion Vocal

process movement displacement note Breath sounds resonance Added sounds

Fibrosis (general) Decreased None Normal Vesicular Increased Fine creps


Pleural effusion Decreased Away Stony dull Vesicular Decreased None

(>500 mL) ipsilaterally (decreased or or absent

Large Decreased Away Hyper- Decreased or Decreased None

pneumothorax ipsilaterally resonant absent or absent

Asthma Decreased None Normal Vesicular, with Normal Expiratory

bilaterally prolonged polyphonic
expiration wheeze

COPD Decreased None Normal Vesicular, with Normal Coarse creps

bilaterally prolonged plus expiratory
expiration polyphonic

11] (a) F (b) T (c) T (d) F (e) T coil of the lungs, decreased gas transfer, expiratory air-
(a) COPD describes airways obstruction that occurs flow limitation and air-trapping. Whilst bronchitis and
mainly in smokers or ex-smokers. The clinical distinc- emphysema are described as two separate clinical enti-
tion between COPD and asthma is blurred, because vir- ties, they usually co-exist in all patients with COPD.
tually all patients with COPD have a reversible element to (c) Patients with COPD commonly demonstrate aster-
their disease, and is the reason these patients are treated ixis, which is a coarse, flapping tremor due to chronic re-
with bronchodilators [(b-adrenoceptor agonists such tention of CO2. It is also seen in patients with hepatic
as salbutamol (Ventolin) and antimuscarinics such as encephalopathy (liver flap), although it can occur in a
ipratropium bromide (Atrovent)] and corticosteroids wide variety of metabolic and toxic encephalopathies.
(initially prednisolone orally, and if this is successful, CO2 retention also causes the hands to be warm (vasodi-
wean to inhaled beclamethasone). latation) and the pulse to be bounding (hyperdynamic
(b) Chronic bronchitis is defined on the basis of the his- circulation).
tory as cough productive of sputum on most days for at (d) Cor pulmonale is the term used to describe the
least 3 months of the year,for more than 1 year.This re- process of adaptation and failure the right side of the
flects the nature of the underlying condition: hypertro- heart undergoes as a result of lung disease. Normally
phy of the mucous-secreting glands of the bronchial tree the pulmonary vasculature responds to local hypoxia by
(mainly large bronchi). Emphysema, however, is defined arteriolar constriction. So, for example, in lobar pneu-
pathologically as dilatation and destruction of the monia, blood flow to the affected lobe is decreased, mi-
lung tissue distal to the terminal bronchioles. Thus, it nimizing the amount of poorly oxygenated blood
affects only the small airways, leading to loss of elastic re- reaching the systemic circulation. When the pneumonia
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Paper 1 MCQs 57

resolves, the vasoconstriction ceases and the flow returns called non-cardiogenic pulmonary oedema, where the

to normal. However, if hypoxia is widespread and irre- typical features are no upper lobe venous distension, no
versible, as is the case in COPD, the resultant arteriolar septal lines or pleural effusion, a normal heart size and
constriction is equally widespread and irreversible, thus the most reliable sign,which is peripheral alveolar shad-
causing pulmonary hypertension. Over time the right owing and/or an air bronchogram. The CXR in some-
atrium and ventricle hypertrophy, eventually the limit of one with suspected respiratory failure should also be
the hearts ability to adapt is reached, and the right heart checked carefully for pneumothorax, consolidation,
fails, leading to the typical signs and symptoms of right- bronchogenic cancer and oligaemia or wedge-shaped in-
sided cardiac failure. farcts (i.e. signs of PE). Localized oligaemia on CXR is
(e) Respiratory failure occurs when pulmonary gas ex- also known as Westermarks sign, and is usually indica-
change is sufficiently impaired to cause hypoxaemia tive of PE.
(PaO2 < 8 kPa) with or without hypercapnia The main causes of respiratory failure can be remem-
(PaCO2 > 7 kPa). There are two types of respiratory bered if you remember that A DIMPLE can cause res-
failure. piratory failure . . .
Type I respiratory failure acute hypoxaemic A Asthma, ARDS, aspirin
mainly due to ventilationperfusion mismatch D Drugs (opiates)
PaO2 low (<8 kPa) I Infection (pneumonia)
PaCO2 normal or low (<5 kPa) M Metabolic acidosis (e.g. diabetic ketoacidosis)
Common causes include pulmonary oedema, pneu- P PE, pneumothorax
monia, ARDS, pulmonary embolism (PE) L Left ventricular failure
Type II respiratory failure ventilatory failure E Effusions
PaO2 low (<8 kPa)
PaCO2 high (>7 kPa) [13] (a) F (b) F (c) F (d) T (e) F
Occurs when alveolar ventilation is insufficient to (a) Asthma is characterized by chronic inflammation of
excrete the volume of CO2 being produced by tissue the airways which normally presents with a classical triad
metabolism of symptoms . . .
Due to reduced ventilatory effort, inability to over- 1. Wheeze
come increased resistance, failure to compensate for 2. Nocturnal cough
increased dead space or CO2 production,or a combi- 3. Dyspnoea
nation of these Within the airways themselves, it has three main char-
Most common cause is COPD acteristics: bronchial inflammation (mainly involving
Other causes include chest wall deformity, respirato- eosinophils and mast cells with associated plasma exuda-
ry muscle weakness [e.g. GuillainBarr syndrome, tion, oedema, smooth muscle hypertrophy and mucus
motor neurone disease (MND)] and depression of plugging), airways hyper-responsiveness and re-
the respiratory centre (e.g. opioid excess) versible airflow limitation. It is important to realize,
however, that with chronic asthma, the airflow limita-
[12] (a) F (b) F (c) T (d) F (e) F tion does become irreversible to a certain degree. It
(a) PaCO2 is not elevated in type I respiratory failure. is also the case that aspects of the acute severe asthma
(b) The commonest cause of type II respiratory failure is that continues to kill young people are also irreversible
COPD. Pneumonia tends to cause type I respiratory (otherwise no-one would die from asthma as long as
failure. they were treated with the correct medications).
(c) Pulsus paradoxus is explained in the answers to (b) Typical asthma attacks occur after the conclusion
MCQ [7], above. of,and not during,exercise. Cold, dry air cools and dries
(d) Respiratory failure does not always present with the epithelial lining of the bronchi, precipitating attacks.
dyspnoea, e.g. opioid overdosage, GuillainBarr syn- (c) ACE-inhibitors are safe to give to asthmatic patients.
drome. Chronic retainers of CO2 may also present ACE-inhibitors should never, however, be given to pa-
drowsy and not obviously dyspnoeic. tients with renal artery stenosis as they block produc-
(e) The CXR described in the question is one of classical tion of angiotensin II and aldosterone, leading to a
heart failure. The CXR in respiratory failure is one of so- decrease in the already threatened renal perfusion, and
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64 Paper 1 EMQs

[24] (a) F (b) F (c) F (d) F (e) F (e) In paralytic ileus, there is characteristically no phys-

(a) The commonest cause of small bowel obstruction ical obstruction to passage of the luminal contents of the
worldwide is herniae, whilst the most common cause in bowel , i.e. it is functional. Causes of paralytic ileus
industrialized countries is postoperative adhesions. include . . .
(b) This is the description of an intussusception. A Sepsis (either within or adjacent to the peritoneal
volvulus occurs when a length of large bowel becomes cavity, e.g. pneumonia)
twisted on itself, using the mesentery as the axis about Drugs (e.g. opiates)
which it twists. Retroperitoneal haematoma
(c) In gallstone ileus, a large (>2.5 cm) stone passes Electrolyte abnormalities (e.g. hypokalaemia)
from gallbladder or common bile duct into the Physical inactivity
GIT through a fistula. The stones usually lodge in the Laparotomy
terminal ileum. Paralytic ileus classically demonstrates absent bowel
(d) Bowel sounds are characteristically infrequent, sounds, and may be definitively diagnosed from physical
high-pitched and tinkling in small bowel obstruction. obstruction by contrast studies and a history of less ab-
They would be absent in paralytic ileus. dominal pain.

These findings will also be seen in pulmonary hyper-
Answer 1
tension due to other causes (e.g. congestive cardiac fail-
(1) Mitral stenosis with atrial fibrillation ure, COPD, chronic lung pathology, primary pulmonary
On examination the patient may have a malar flush and hypertension).
be in atrial fibrillation. There may be evidence of a cere-
brovascular accident (hemiplegia, facial weakness). An Causes of mitral stenosis
opening snap is followed by a rumbling mid-diastolic Rheumatic fever (a common cause)
murmur, localizing (often very localized) over the tap- Congenital
ping apex beat (palpable first heart sound). Listen with Calcification
the patient in the left lateral position with the bell of the
stethoscope in several positions over the apex. If difficult
to hear, the murmur may be accentuated by asking the Complications (often the patient is
patient (if this is possible) to sit up and lie down five times asymptomatic)
so raising the cardiac output.There is pre-systolic accen- Recurrent chest infections (wet lungs)
tuation only if the heart is in sinus rhythm and is due to Atrial fibrillation and embolization (stroke)
atrial systole. Pulmonary hypertension and pulmonary oedema
In addition if pulmonary hypertension has devel- Right ventricular failure
oped there may be a . . . Tricuspid regurgitation
Left para-sternal heave (right ventricular Bacterial endocarditis
Loud second heart sound over the pulmonary area The severity of the mitral stenosis is
Possible murmur of pulmonary regurgitation (Gra- indicated by:
ham Steell) Signs of pulmonary hypertension (see above)
Murmur of tricuspid regurgitation [systolic murmur Close proximity of the opening snap after the second
at lower left sternal edge plus large V waves in the JVP heart sound
(jugular venous pulse)] The length of the mid-diastolic murmur (directly pro-
Right ventricular failure (elevated JVP, he- portional, however, very tight lesions lead to quiet
patomegaly, ascites and peripheral oedema) murmurs)
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Paper 1 EMQs 65

ECG findings There may be a third heart sound (volume overload)

Atrial fibrillation and a diastolic flow murmur due to the re-entry of the re-
P mitrale (bifid M shaped P waves best seen in lead II) gurgitated blood back into the left ventricle.
Clinically the main differential will be aortic stenosis
CXR appearances causing an ejection systolic murmur, a ventricular septal
Prominent left atrium may be the only abnormality defect or tricuspid regurgitation which both cause pan-
Calcification of the valve ring systolic murmurs.
Possible features of congestive cardiac failure Tricuspid regurgitation, however, will result in promi-
Kerley-B lines nent V waves in the JVP, a murmur that increases during
Upper lobe venous diversion inspiration and possible hepatic pulsations.
Bilateral effusions
Cardiomegaly Causes of mitral regurgitation
Bats wing oedema spreading from the hilar areas Myocardial infarction (acute presentation following
an acute MI due to rupture of the chordae tendineae)
Management Rheumatic fever (acute or old)
Diuretics for symptoms of breathlessness Left ventricular dilatation
Anticoagulation and digoxin if atrial fibrillation Severe hypertension
develops Left ventricular failure
Prophylactic antibiotics for dirty procedures to pre- Cardiomyopathy
vent valve infection (dental procedures or pelvic sur- Bacterial endocarditis
gery). Check the British National Formulary for the Connective tissue diseases
current recommendations SLE
Surgical relief of stenosis if secondary pulmonary hy- Elastic tissue disorders
pertension develops Marfans syndrome
Open surgery can be avoided in those unfit for a EhlersDanlos syndrome
general anaesthetic by percutaneous trans-septal bal- Prolapsing mitral valve; floppy mitral valve. This oc-
loon valvotomy. Here a balloon catheter is passed via a curs in young women. Embolic events and atypical
peripheral vein into the right atrium. The atrial sep- chest pain (localized over the apex) may occur. A mid-
tum is then perforated and the balloon is passed across systolic click is heard.
the mitral valve and inflated. Mitral regurgitation is an The severity of mitral regurgitation can be assessed by
inevitable consequence. Patients most suitable for this the presence of a . . .
approach include those with: Third heart sound
Minimal mitral regurgitation Mid-diastolic flow murmur
Mobile valves (no calcification) Left ventricular enlargement
Minimal subvalvular disease Thrill
Patients more suitable for formal valve replacement in-
clude those with: (3) Mitral stenosis
Significant mitral regurgitation Here the patient is not in atrial fibrillation so there is pre-
Extensive valve calcification systolic accentuation of the murmur.
Thrombus in the left atrium
(4) Aortic regurgitation with left ventricular
(2) Mitral regurgitation failure
The patient may be in atrial fibrillation (left atrial dilata- The patient has a wide pulse pressure on measuring the
tion). The JVP may be elevated if associated with right blood pressure. The pulse is collapsing when the left
ventricular failure (secondary to pulmonary hyperten- brachial artery palpated with arm elevated. The apex
sion). The apex is displaced and thrusting (a dynamic beat is displaced (state the location) and is thrusting in
low-pressure movement indicating volume overload). character, indicating volume overload.
The first heart sound is soft. There is a pan-systolic With the patient sat forward and the breath held in
murmur heard at the apex radiating to the left axilla. end expiration, a short early decrescendo murmur radi-
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66 Paper 1 EMQs

ating down the left sternal edge is heard (listen in to replace the valve before irretrievable ventricular dys-

several positions down the left sternal edge with the di- function occurs as indicated by an enlarging heart on
aphragm). The longer and louder the murmur, the echocardiography. Once the end systolic diameter of
more severe the regurgitation. the left ventricle has reached 55 mm, then surgery is
In this case, left ventricular failure is suggested by the recommended.
elevated JVP, displaced apex and bi-basal crepitations.
There may be an additional ejection systolic murmur in (5) Aortic stenosis
the aortic area due to increased flow across the aortic This patient has a slow rising pulse and a blood pressure
valve. The aortic regurgitant jet can cause interference that has a narrow pulse pressure. The apex is displaced
with the anterior mitral valve cusp resulting in a mid- and heaving indicating pressure overload. There may be
diastolic murmur to be heard at the apex (Austin Flint a thrill felt with the ulnar border of the palm over the aor-
murmur). tic area (indicating at least a grade 4 murmur and often
Inspect the patient for Marfans body habitus, anky- reflects a pressure gradient across the valve of at least
losing spondylitis (kyphosis of the spine) features of 40 mmHg). An ejection click may be heard over the left
rheumatoid arthritis and the small, irregular Argyll sternal border indicating the stenosis is occurring from
Robertson pupils (which react to accommodation but the valves (and not subvalvular or supravalvular in
not to light) of syphilis. origin) and is due to opening of the valve. A click is espe-
cially heard in bicuspid aortic stenosis. Note that clicks
Causes of aortic valve regurgitation may also be heard in pulmonary stenosis or with a pro-
Aortic root dilatation lapsing mitral valve.
Severe hypertension An ejection systolic (rough, sawing, diamond
Connective tissue disorders: shaped) murmur is heard all over the precordium, but
Marfans syndrome especially in the aortic area and possibly radiating to
Rheumatoid arthritis the carotids. The second heart sound is quiet. The
Ankylosing spondylitis differential diagnosis includes mitral regurgitation,
Aortic aneurysm hypertrophic obstructive cardiomyopathy and aortic
Dissection of the aorta sclerosis.
Syphilis Aortic sclerosis is simply a noisy valve due to calcifica-
Valve disruption tion frequently seen in the elderly, and has no abnormal
Congenital (e.g. bicuspid valves) increase of the pressure gradient across the valve. Thus in
Rupture of the sinus of valsalva aortic sclerosis the patient has a normal pulse character, a
Endocarditis normal pulse pressure (blood pressure) and a normal
Rheumatic fever apex beat position and character.
Ventricular septal defect (loss of support)
Clinical features of aortic stenosis
Associated eponymous signs Palpitations due to arrhythmias (ventricular)
Corrigans sign: vigorous arterial pulsations in Syncope due to arrhythmias
neck Chest pain (angina)
De Mussets sign: head nodding with arterial Dyspnoea (left ventricular failure)
pulsations Sudden death (1020%)
Quinkes sign: visible nail bed capillary pulsations. In aortic stenosis the ventricular function is relatively
Partially compress the nail bed and look for pulsations well preserved, unlike in aortic regurgitation. However
in the subungual capillaries with significant stenosis exercise fails to improve cardiac
Duroziers sign: partially compress the femoral artery output leading to ischaemia and cardiac arrhythmias.
in the inguinal area with a digit and listen proximally For this reason exercise tolerance tests are avoided in
for a regurgitant murmur as blood turbulently flows these patients. In patients with aortic stenosis symptoms
back under the stenosis during diastole are a good indication of the disease severity.
Patients with aortic regurgitation may have few symp- Aortic stenosis is especially prone to bacterial endo-
toms until left ventricular failure occurs. It is important carditis as it is a high-pressure valve lesion.
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Causes of aortic stenosis avoid using a leading question when asking about ex-

Valvular acerbating factors
Rheumatic fever Progressively getting worse
Calcification No days off : relentless daily symptoms suggest a pos-
Congenital (e.g. bicuspid valve) sible serious cause
Supravalvular New onset in middle life (i.e. uncharacteristic, no pre-
Williams syndrome (supravalvular aortic dia- vious history of headaches)
phragm, mental retardation and hypercalcaemia) Risk factors for intracranial bleeding: e.g. anticoagu-
Subvalvular lation, alcoholism, old age
Diaphragm below the aortic valve Trauma: recent falls/head injury (frequently the
Septal trauma is forgotten)
Hypertrophic obstructive cardiomyopathy
Examination alarm features
The severity of aortic stenosis is indicated by: Any reduction in the Glasgow Coma Scale
A narrow pulse pressure on blood pressure recording Confusion (reduction in abbreviated mental test scor-
Reverse splitting of the second heart sound (i.e. pul- ing)
monary before aortic) Focal neurology: motor/sensory/coordination/visual/
A soft second heart sound meningeal irritation
A fourth heart sound (indicating ventricular stiffness Seizures
due to left ventricular Hypertrophy) Purpuric rash
A thrill Signs of meningeal irritation
A heaving apex beat Fever
The ECG may show signs of left ventricular hyper- Papilloedema
trophy (R wave in V6 plus S in V2 summate to more than Severe hypertension
35 mm) plus signs of ventricular strain (ST depression The diagnosis of headache is made largely on the
and T wave inversion) in the leads, which look at the left history. A good history will pick out those where there
ventricle (leads I, AVL, II,V5 and V6). should be heightened concern.
The chest radiograph may show post-stenotic dilata-
tion. There may be calcification of the aortic valve. (1) Migraine
Alternatively there may be feature of congestive cardiac The features of migraine may be classical in (only) 20%,
failure. presenting with a prodrome of visual auras (e.g. flashing
In the management, valve replacement is indicated lights or zig-zag lines due to cerebral vasospasm) often
for all patients with symptoms and where the pressure taking a stereotypical pattern for a given patient. This is
gradient across the valve exceeds 50 mmHg. Balloon followed by a severe unilateral headache with photopho-
valvotomy is reserve for those unfit for surgery or as a bia and phonophobia (intolerance of noise). Nausea and
temporary measure. Antibiotic prophylaxis is required abdominal pain may occur along with focal neurology,
for surgery. e.g. dysphasia, hemiplegia, sensory symptoms.
However, some of these features may be lacking in
common migraine and differentiation from tension
Answer 2 headaches (the main differential) can be difficult. The
approach to first-line treatment is with paracetamol or
Know the features for patients with a serious cause for ibuprofen (or both) used together with an anti-emetic,as
headaches: gastric stasis during migraine can impair absorption.
Codeine is avoided due to its predisposition to cause
History alarm features analgesicheadache, in addition to the risk of dependen-
Morning headache: improving after getting up cy and side effects such as constipation and drowsiness.
Morning vomiting Asking about triggers (food, stress, menstruation) and
Pain exacerbated by coughing, straining or bending: avoidance of these is helpful. Note that there is often a
note that this occurs in many headaches to a degree, so family history in migraine sufferers.
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(2) Benign intracranial hypertension Memory/intellect deterioration


A classical history. The problem is a recirculation disor- Primitive reflexes return (Plantar response, grasp
der of CSF. There is no focal neurology and the CT scan is and suck reflex)
normal without ventricular dilatation. Prominent papil- Expressive dysphasia (Brocas area)
loedema is found on examination. Enlargement of the Anosmia
blind spot on testing the visual fields occurs; if untreated, Parietal lobe
blindness can occur. A CT scan is required, however, to Apraxias (learned movements).
exclude mass lesions and other causes of raised intracra- Asteriognosis (shape recognition)
nial pressure. Treatment involves stopping any causative Homonymous inferior quadrantanopias
drugs (e.g. steroids or oral contraceptives), weight loss Extinction (sensory inattention for stimuli on the af-
and thiazide diuretics. Repeated lumbar puncture and fected side when both sides stimulated)
shunt operations are second line therapy. Temporal lobe
Receptive dysphasia (Wernickes area)
(3) Cluster headache Memory loss
Typically a pattern of recurrent headaches for a few Cortical deafness
days or weeks followed by temporary remission occurs. Homonymous superior quadrantanopias
20% of cases are chronic. The male:female ratio is 5:1. Occipital lobe
The exact cause is unknown; however, alcohol may pre- Cortical blindness
cipitate an attack. Sufferers are more commonly smok- Homonymous hemianopias
ers. The episodes may be brief (up to an hour) but are
recurrent in bouts, often with periods of remission last- Causes of cerebral mass lesions
ing several months. Severe pain occurs behind the eye. A Tumour
partial Horners syndrome may occur along with vaso- Secondary > Primary lesions
motor dysfunction causing lacrimation and nasal dis- Malignant > Benign
charge. The treatment is similar to migraine and 5HT Abscess
(serotonin) antagonists (e.g. sumatriptan) are often Pneumonia
helpful. In addition 100% oxygen (which may abort Skin sepsis
attacks), verapamil, lithium or methysergide are ENT sepsis
alternatives. Treatment can be very difficult (like some Haemorrhage
migraine). Extradural haemorrhage
(4) Space occupying lesion Subdural haemorrhage
This is a worrying history. The progression of focal neu- Subarachnoid haemorrhage
rology and seizures suggest an expanding mass lesion. Granulomatous
The exact neurological presentation depends on the Cerebral sarcoidosis
location; however, common patents of presentation Vascular
include; AV malformations
Features of rising intracranial pressure (headache, Hydrocephalus
Neurological deficit (see patterns below) (5) Acute bacterial meningitis
Epilepsy From the given history it may seem difficult to separate
Oedema around the lesion may exaggerate the picture. viral from bacterial meningitis. However, the lack of any
An urgent CT scan is indicated. Remember the approach viral prodromal illness and the importance of not miss-
to neurology: Where is the lesion? Then, what is ing acute bacterial meningitis, make this the best answer.
the lesion? The main other differential diagnoses include encephali-
tis, subarachnoid haemorrhage, severe migraine, cere-
Localizing mass lesions bral abscess, subdural and extradural haemorrhage.
Frontal lobe Immediate management includes antibiotics, which
Personality change should not be delayed awaiting investigations or even ad-
Disinhibition mission to hospital as this is associated with an adverse
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outcome. Penicillin V 1.2 g should be given immediately. Focal neurological signs are possible. Infarction or

A CT scan should ideally be performed before a lumbar false localizing signs due to raised ICP (C III, CVI palsy
puncture ideally to exclude raised intracranial pressure or hemi-paresis)
and other differential diagnoses. If meningococcal dis- Shock (septicaemic)
ease is suspected a lumbar puncture is avoided due to the Bleeding (due to DIC) e.g. bleeding from venepunc-
high risk of coning because of the prevalence of associat- ture sites
ed cerebral oedema. Blood cultures (several sets) should Note that many of these features may be absent in certain
be taken. The organism can also be looked for on PCR of patients with meningitis and that the disease may present
blood or CSF. General resuscitation measures (IV fluids in a non-acute and non-specific manner.
and oxygen) are required for septic shock, as well as close
monitoring and support usually in intensive care. De- Which blood tests?
spite optimum management overall mortality is still FBC/U and Es/CRP/PT/APTT/FDPs (fibrin degrada-
around 10%. Early recognition of symptoms is therefore tion products), blood cultures.
Which antibiotics?
Presentation of acute bacterial meningitis Penicillin V (2.4 g i.v. or 1 g i.m. stat if no IV access) and
Headache (bursting, gradual or abrupt onset) Cefotaxime (2 g/8 h i.v.).Usually hospitals will have their
Pyrexia own policy.
Signs of meningeal irritation, e.g. neck stiffness,
Kernigs sign Why CT scan?
Photophobia (a non-specific feature for meningitis) Helps exclude other causes,e.g.IC bleed/subarachnoid
Rash: A non-blanching purpuric rash due to dissemi- haemorrhage/cerebral abscess
nated intravascular coagulation (DIC) occurs in Ideally prior to lumbar puncture to exclude raised ICP
meningococcal meningitis only.The lesions may occur
anywhere, and the patient should be completely in- Lumbar puncture patterns
spected as even a single lesion may be significant Normal opening pressure: <16 cm manometric height of
Global cerebral dysfunction (cerebral oedema, water.
toxaemia): confusion/drowsiness/convulsions/vacant In general the following apply (for exam purposes):

Bacterial Viral TB Normal

Appearance Cloudy Clear Clear Clear

Cells Neutrophils Lymphocytes Lymphocytes <5/mm3
Glucose <1/3 levels in blood Normal <1/2 blood levels 1/22/3 blood levels
Protein >1 g/L <1 g/L >1 g/L 0.20.4 g/L

Answer 3 Haemoptysis
Chest pain (pleuritic type; a late feature)
(1) Pulmonary embolism Sudden collapse (cardiac arrest)
The diagnosis of pulmonary embolism relies on a com-
bination of the following . . . An assessment of the risk factors for
An assessment of the clinical symptoms Plaster casts/immobility*
Shortness of breath of abrupt onset (occasionally
gradual onset occurs with multiple small emboli)
Cough *Major risk factors
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70 Paper 1 EMQs

Postoperative/trauma* (hypercoaguable state, An assessment of basic investigations


dehydration) White cell count; to help exclude infection from the

Previous deep vein thrombosis (DVT)/PE* differential diagnosis
Pregnancy* Arterial blood gases; type I respiratory failure pattern
Poorly (major illness)* (hypoxia with normal or reduced CO2)
Oral contraception/oestrogens ECG
Obesity Tachycardia is the most frequent finding
Smoking Right axis deviation
Carcinoma The classic S1Q3T3 is far less common
Travel D-dimer
Old age (PE is rare under the age of 40 years without Sensitive but not specific
risk factors) Good for excluding PE if normal
Hereditary thrombophilic states: Should not be performed if there is strong clinical
Protein S deficiency suspicion
Protein C deficiency Chest radiograph
Antithrombin III deficiency Often normal
Factor V Leiden (fails to bind Protein C) Wedge-shaped infarction (opacity) which may cavi-
Secondary to other medical conditions: tate after several days
Nephrotic syndrome (renal loss of anti-thrombin
III) Assessing the probability of PE
Diabetic ketoacidosis (dehydration) This is assessed by scoring the above as follows . . .
Antiphospholipid syndrome (poorly understood No other likely diagnosis on the basis of the above
mechanism; antibodies to phospholipids involved in clinical findings and the basic investigations?
coagulation occur, the APTT is prolonged in vitro 1 point
but in vivo thrombosis occurs) Presence of a major risk factor (as above in bold)?
Homocystinuria 1 point
Paroxysmal nocturnal haemoglobinuria
Behets disease (arterial and venous thromboses) Definitive tests
V/Q scan
An assessment of the clinical findings Helical CT scanning
Tachycardia (sensitive sign) Pulmonary angiography (the most accurate test)
Tachyopnoea (sensitive sign) Following the diagnosis of PE anticoagulation is com-
Cyanosis menced with warfarin by giving a loading dose of
Chest findings (often normal): 510 mg for 2 days, followed by a dose adjusted to give an
Pleural rub INR between 2 and 3 normal. Warfarin is continued
Reduced air entry
Clinical evidence of DVT (frequently lacking) *Major risk factors

2 points 1 Point 0 points

Action (high risk) (medium risk) (low risk)

Heparinize? Yes Yes Wait

Arrange definitive tests? Urgent Soon Possibly
Alternative diagnosis? Possible Likely Very likely
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for 36 months.If the PE is a recurrent episode,consider- pleuritic on closer questioning. Diaphragmatic pleural

ation is given to lifelong warfarin treatment. Following pain may radiate to the epigastrium and cause con-
massive PE with collapse, intravenous thrombolysis is fusion with an acute abdomen. Pneumonia is an
given using rtPA or streptokinase. inflammation of the lung. The causes may be divided
into . . .
(2) None of these Infective
Tension pneumothorax on the left pushing all the medi- Bacterial, viral, fungal
astinal structures over to the right. Patients with tension Allergic
pneumothorax have respiratory compromise, frequent- e.g. allergic bronchopulmonary aspergillosis
ly extreme and rapidly progressive as the valve type leak Physical agents
causes further compromise with each breath. The im- Chemical; aspiration of vomit or caustic material
pedance of venous return to the right side of the heart Radiotherapy
leads to reduced cardiac output (tachycardia and hy- Remember the right lower lobe as the most likely loca-
potension) and an elevated JVP. The management in- tion of a pneumonia following aspiration.
volves urgent release using a green needle followed by
insertion of an intercostal drain. (See also OSCE 12, (6) Asthma
p. 244) Beware similar but late acute asthma with respiratory
failure and silent chest. Know the blood gases patterns in
(3) Left apical lung fibrosis acute asthma;
Type I respiratory failure early with low PaO2 and
Causes normal (or even elevated) PaCO2 progressing to fa-
Old TB tigue and eventual;
Silicosis Type II respiratory failure and rising PaCO2 and low
Sarcoidosis PaO2. In asthma, acidosis is an indication that urgent
Aspergillosis respiratory support (ventilation on ITU) is needed im-
Extrinsic allergic alveolitis mediately, so call for anaesthetic help. (See EMQ An-
Ankylosing spondylitis swers Q24 (4), p.158 and OSCE 1, p. 219.)

Differential on CXR of apical opacity

Pancoast tumour Answer 4
Pneumonia Notes
Klebsiella Extrinsic pathway: utilizes factor VII. Tissue factor
Pneumocysti initiates coagulation
Fibrosis (as above) Intrinsic pathway: utilizes factors VIII, IX and XI. Tis-
sue factor/factor VII complex activates
(4) Right-sided pleural effusion Common pathway: Factor X dependent
Stony dull percussion. Normal respiratory rate and The PT (prothrombin time) measures factors II,
lack of cyanosis makes pneumonia less likely. Know V, VII, and X, i.e. the extrinsic and common
causes of effusions (exudates and transudates), CXR ap- pathways
pearances of and basic management. (See OSCE 26, APTT (activated partial thromboplastin time) meas-
p. 271.) ures VIII, X and XI, i.e. the intrinsic and common
(5) Right lower lobe pneumonia See diagram overleaf.
The patient is breathless, cyanosed with evidence of
right lower lobe consolidation. Other clinical features
might include pyrexia, tachycardia, herpes labialis.
The patient might complain of chest pain that is
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72 Paper 1 MCQs



Tissue thromboplastin Factors XII, XI, IX, VI

(expressed on surface of) (activated by blood coming into
perivascular tissue cells contact with a non-endothelial
+ surface)
Factor VII Platelet phospholipid
Factor VIII

Factor X
Factor V

Prothrombin Thrombin

Fibrinogen Fibrin

Vitamin K is a co-factor required for the gamma car- Bleeding into mucus membranes
boxylation of factors II, VII, IX and X, and proteins S Heavy periods
and C. This is required so that these factors can bind Prolongation of the bleeding time
calcium in the normal process of coagulation. The in- Note that the platelet count must drop below around
trinsic and extrinsic system will thus be affected by 50 109 before any bleeding disorder is likely to occur.
deficiency of vitamin K. Warfarin inhibits the reduc-
tion of Vitamin K epoxide to Vitamin K. As Vitamin K Therefore:
is a fat soluble vitamin (along with vitamins A, D and (1) Haemophilia A
E) deficiency may arise with cholestatic jaundice.Vita- Prolongation of the APTT with normal PT and bleeding
min K deficiency can also affect the newborn (haemor- time. Although the inheritance is X linked recessive, one
rhagic disease of the newborn) due to poor placental third of haemophilia A cases are spontaneous mutations
transfer of the vitamin. For this reason vitamin K is without family history.There is a range of severity.Factor
given immediately after birth VIII:C levels less than 5% are associated with sponta-
Coagulation disorders produce: neous haemarthrosis and bleeding into muscles. Restor-
Bleeding into muscles and joints ing factor VIII:C levels to 30% of normal is required in
Large bleeds into the skin the management.
Small cuts stop spontaneously but larger deeper cuts
do not (2) Haemophilia B, factor IX deficiency
Healing is delayed (Christmas disease)
Platelet disorders produce: As for Haemophilia A, there is prolongation of the APTT,
Multiple small areas of bleeding into the skin (pur- with normal PT and bleeding time. Factor VIII:C levels
pura/petechiae) are normal, however. There is identical inheritance and
Prolonged bleeding of smaller cuts (which depend presentation to Haemophilia A, but the condition is 20%
on platelet adhesion more than coagulation) as common as Haemophilia A.
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(3) Von Willebrands disease most certainly be investigated for both these possibilities.

Deficiency in factor VIII:WF. Three types occur (Types I Note that pregnancy does not contraindicate emergency
and II are dominant; Type II is recessive and produces a radiography. Other investigations include urgent blood
severe form of the disease). Chromosome 12. The com- cultures, FBC, U and Es, and arterial blood gases. Intra-
monest coagulation disorder.VIII:WF binds platelets, so venous fluids and road spectrum antibiotics (e.g. ce-
deficiency behaves like platelet problem. Confusingly furoxime 1.5 g t.d.s., plus erythromycin 50 mg q.d.s.) are
factor VIII:C (haemophilia A) may (or may not) also be required. Inatropic support may be required on ICU.
low,with a resultant prolongation of the APTT.However,
haemarthrosis is rare. Ristocetin (an antibiotic) normal- (3) Epidemic myalgia (Bornholms disease)
ly clumps platelets, but fails to do so in Von Willebrands Coxsackie B virus. A typical history. A seasonal illness
disease and so forms the basis of a the diagnostic test. often occurring in late summer. The pain may be unilat-
eral and severe (the devils grip). There are no signifi-
(4) Warfarin medication cant clinical findings on examination. Symptomatic
Although Vitamin K deficiency will produce the same treatment is all that is required and resolution occurs
pattern. The raised PT and APTT in this case are sugges- spontaneously.
tive of warfarin therapy given the clinical scenario.
The normal bleeding time counts against liver disease, (4) Aortic dissection of the thoracic aorta
which causes a coagulopathy via . . . The patient has a history of hypertension, which is a
Impaired protein synthesis; fibrinogen/coagulation major risk factor. Often a history of a valsalva type ma-
factors noeuvre (e.g. lifting, bending) before the event is ob-
Malabsorbtion of fat soluble vitamin K due to tained. The pain is usually very severe and described as
cholestasis ripping or tearing classically. Two thirds are of the as-
Hypersplenism; consumes platelets cending aorta, one third are in the descending aorta.
DIC Clinical examination is frequently normal, the diagnosis
Functional platelet abnormalities. Also seen in being made from the history and absence of the acute
uraemia/myeloma/scury/antiplatelet drugs/essential ECG changes of myocardial infarction (the major differ-
thrombocythemia/leukaemia/congenital conditions ential diagnosis).

(5) Easy bruising syndrome Risk factors for aortic dissection

Common and benign. Reassurance required. Similar to Hypertension
senile purpura in that vessel fragility is to blame. All Coarctation of the aorta (Turners Syndrome; XO)
measurements of coagulation are normal. Marfans syndrome
Giant cell arteritis
Answer 5 Major thoracic trauma

(1) Tietzes syndrome Complications for dissection of the aorta

Costochondritis of the sterno-costal junctions. The Inferior MI (occlusion of the right coronary artery ori-
aetiology is uncertain. Symptomatic treatment and gin)
reassurance is all that is required. Aortic regurgitation (causing cardiac failure)
Cardiac tamponade (retrograde dissection)
(2) Lobar pneumonia Dissection of the major arteries coming off the aortic
The main differential being pulmonary embolism, given arch leading to strokes and limb ischaemia.
the patients clear major risk factors for thrombosis. Rupture of the false lumen back into the aorta or
There has been no haemoptysis (although this does not externally (usually resulting in death). In this case
exclude a PE) and septic features dominate the clinical pulmonary haemorrhage had occurred
picture. In addition the prodromal symptoms and the
gradual onset of breathlessness make pneumonia Investigations
the more likely diagnosis. She is clearly very unwell given ECG: non-specific changes e.g. tachycardia, left ven-
the hypotension (septic shock) and in practice would al- tricular strain, possible inferior MI
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OSCEs 229

Q. What are the causes of an enlarged kidney?

OSCE station 3 A.
Q. What are the causes of a mass in the right iliac fossa? Renal carcinoma
A. Hydronephrosis
Carcinoma of the caecum Hypertrophy of a solitary kidney
Crohns disease (usually an underweight, frequently Adult polycystic kidney disease
young patient with scars from previous resections) May have had a previous nephrectomy (for a painful
Appendix mass or abscess non-functioning kidney) so that only one kidney is
Lymphoma palpable
Ileocaecal TB Cysts develop from all segments of the nephron dur-
Ovarian tumour (NB ovarian tumours often rise out of ing adolescence. Patients present with renal pain,
the pelvis centrally) treatment resistant hypertension, haematuria and
Transplanted kidney stone symptoms
(Amoebiasis) Renal failure occurs later in life (10% of chronic renal
(Schistosomiasis) failure)
(Carcinoid tumour) Various associations exist [see EMQ Answers 19 (2),
p. 142]
Q. What would be your next investigation for this right
iliac fossa mass? Q. What are the symptoms and signs of uraemia?
A. A.
Plain abdominal radiograph, looking for . . . Clinical features of uraemia . . .
Obstruction (air/ fluid levels) Symptoms
Calcification (tuberculosis) Nausea, vomiting
Bowel wall oedema thickening (CD) Diarrhoea
Chest radiograph Fatigue
TB Breathlessness:
Metastatic disease Anaemia
Abdominal ultrasound scan Pleural effusion
Abdominal CT scan Pericardial effusion
Small bowel meal and follow through for Crohns Impaired ventricular function
disease Weakness
Diagnostic laparoscopy Itching
Q. What are the causes of a mass in the left iliac fossa? Pallor (anaemia)
A. Scratch marks (pruritus)
Colonic carcinoma Bruising
Diverticular mass Pericarditis (pericardia rub or effusion)
Transplanted kidney Hypertension
Ovarian tumour Oedema
Faeces Confusion
Muscle weakness
Q. What are the causes of an epigastric mass? Fistula (for dialysis)

Hepatomegaly (see OSCE 4, p. 230)

Gastric malignancy
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230 OSCEs

Hepatitis A, B (D), C
OSCE station 4 Leptospirosis (Weils disease)
Q. What are the causes of hepatomegaly (without Infectious mononucleosis
splenomegaly)? Others:
A. TB, syphilis, brucellosis
Malignancy Tropical infections, e.g. malaria, kala-azar
Secondary tumours mainly Haematological malignancy:
Primary hepatocellular carcinoma CML* and CLL*
Lymphoma Polycythemia vera
Leukaemias: Myelofibrosis*
CML Lymphoma
CLL Haemolytic anaemias (splenic filtration)
Myelofibrosis Others
Cirrhosis Connective tissue disease:
NB Late alcoholic cirrhosis causes a small fibrotic SLE
liver RA
Blood Sarcoidosis
Cardiac failure Amyloidosis
Tricuspid regurgitation (pulsatile liver)
Budd Chiari syndrome (hepatic vein thrombosis) Q. What are the causes of hepatosplenomegaly?
NB Hepatic engorgement can give abnormal LFTs A.
(obstructive picture) As above; however, haematological malignancy and in-
Bile fections feature more prominently.
Primary biliary cirrhosis
Common bile duct obstruction: Q. How can you differentiate an enlarged spleen from an
Stones enlarged liver?
Strictures A.
Tumours There is a mass in the left/ right hypochondrium extend-
Lymph nodes ing down towards the pelvis. It moves with respiration. It
Infections is resonant to percussion (over lying air filled bowel).The
Viral hepatitis A, B (D), C upper border can be palpated (unlike a spleen or
Leptospirosis liver which have their upper pole under the ribs).You can
Infectious mononucleosis ballot the mass bimanually assessing the size, shape and
Others: consistency.Look for abdominal scars (?nephrectomy on
TB, syphilis, brucellosis the opposite side). Look also for an AV dialysis fistula
Tropical, e.g. malaria, kala-azar over the distil radius.
Sarcoid Kidney Spleen
Wilsons disease
Haemachromatosis Enlarges? Inferiorly To RIF
Glycogen storage diseases Ballotable? Yes No
Resonant? Yes No

Q. What are the causes of splenomegaly? Get above? Yes No

Portal hypertension (late cirrhosis with a small liver)
Busy spleen *Cause massive splenomegaly (as likely to be found in an
Infections: examination)
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OSCEs 231

Have you noticed any changes in your vision?

OSCE station 5
I do occasionally suffer a bit of double vision, mainly
A 48-year-old female sits in front of you in your OSCE. when Im tired.
You are asked to take a thyroid-based history from her. Have you noticed any changes in your periods?
Yes, theyre becoming much more infrequent. Very
Q. What questions would you ask her? hit-and-miss. But I suppose Im at that time of life,
A. arent I?
Has your weight changed recently?
Oh yes, Ive lost over a stone in the last 3 months You are asked to perform a thorough examination of the
alone. persons thyroid status.
Have you been trying to lose weight?
No. From the end of the bed you note a thin-looking woman
Has your appetite changed? who is very jittery and fidgets incessantly with her hands.
It has.I eat like a horse and yet I continue to lose all this You ask her to hold her hands out straight in front of her
weight. In fact, Im getting a bit concerned, as this is and close her eyes.You place a sheet of paper on top of her
what happened to my mother shortly before she was hands to accentuate the very fine tremor that is present.
diagnosed with cancer. Her hands are warm and her palms are flushed. There is
Have you noticed any change in your behaviour? neither clubbing, swollen fingers nor periosteal bone
Not really, but my husband says that Ive changed of formation. You palpate her pulse, and note a rate of
late; that Im crabby and irritable all the time. I just 98/min, irregularly irregular. Blood pressure is 161/91.
thought it was the change, you know. He also says JVP is not raised. In her face you note exophthalmos,
that Im unable to sit still and I suppose hes right and to confirm this you stand behind the patient, look-
about that really. I just like to keep active. ing down from on top of their forehead to check that
Have you noticed any weakness of your muscles? there is genuine protrusion if the eyeballs. You check
Not as such, though in saying that, I have noticed that for lid lag and there is none present. There is no clear
of late Ive found it a bit of a trial climbing up the stairs, loss of acuity, ophthalmoplegia or conjunctival oedema,
especially if Im carrying the washing. and no goitre in the neck. The apex beat is normally
Have you noticed any trembling of your fingers or located, but it is hyperdynamic. Heart sounds are nor-
hands? mal and the chest is clear. There is no peripheral oedema,
Its strange you should say that, because just the although there is evidence of a rash on both shins. Com-
other day I was writing a letter and I noticed that I prehensive neurological examination reveals question-
couldnt stop my hand trembling. Now Im beginning able wasting of the limb girdle musculature, and
to notice it more and more, even when Im holding a decreased power in both pectoral and pelvic muscles
cup of tea. (MRC grade 4).
Have you had any palpitations?
All the time. But thats nothing new, Ive had them for Q. What is the cause of this womans clinical situation?
years. Ive got an irregular heart beat, you know. A.
Are you as a rule a hotor a coldperson? This woman is hyperthyroid and is displaying nearly all
Im always red hot. And sweat? I could sweat for Eng- of the characteristic signs and symptoms.Like all types of
land, even when everyone else in the room is perfectly thyroid disease, hyperthyroidism is more common in fe-
happy with the temperature. males, patients with autoimmune disease and those with
Have you noticed any change in your bowel habit over a family history of thyroid disease.
the last year or so?

Well I am a bit looser than I used to be in that Q. What are the common causes of hyperthyroidism?
department. A.
Have you noticed any change in your appearance? The commonest cause of hyperthyroidism, and the only
Well my son says that my eyes are goggly, but I dont one associated with thyroid eye disease, is Graves dis-
really see any change. ease. It is due to autoantibodies directed at the TSH re-
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ceptor. It typically causes a fluctuating clinical picture, Q. What investigations would you perform to confirm
with alternating relapse and remission. your diagnosis?
Other causes of hyperthyroidism include . . . In all cases of primary hyperthyroidism, TSH will be
Toxic multinodular goitre: difficult to treat,tradition- suppressed, and this is the initial investigation of choice.
al antithyroid drugs rarely successful When this is combined with a raised serum T3 or T4,
Single toxic adenoma (Plummers disease): similarly then the diagnosis of hyperthyroidism is made. TSH-
difficult to treat receptor autoantibodies will be present in cases of
Iatrogenic hyperthyroidism (excessive levothyroxine Graves disease, but these are not commonly measured.
replacement) Surprisingly, the microsomal and thyroglobulin autoan-
Drug-induced hyperthyroidism (e.g. due to lithium, tibodies associated with hypothyroidism are also often
amiodarone) found in Graves disease.
Transient thyroiditis (e.g. de Quervains viral-medi- In very rare situations, a pituitary tumour will be the
ated transient thyroiditis, post-partum thyroiditis) cause of hyperthyroidsim, and TSH will be raised. The
Thyrotoxicosis factitia (patient takes thyroxine, but differing laboratory findings in thyroid diseases are sum-
attempts to conceal this) marized in the table below . . .

Thyroid state Thyroxine (T4) Triiodothyronine (T3) TSH (pituitary) TRH (hypothalamus)

Graves disease Raised Raised Decreased Decreased
Toxic multinodular goitre Raised Raised Decreased Decreased
Pituitary tumour Raised Raised Raised Decreased

Primary Decreased Decreased Increased Increased
Secondary Decreased Decreased Decreased Increased
Tertiary Decreased Decreased Decreased Decreased

Q. What are the treatment options available? neoplastic causes of hyperthyroidism because of the
A. morbidity, expense and free availability of alternative ef-
Treatment of hyperthyroidism is complex, and depends fective treatments. The procedure of choice is a sub-total
on the underlying cause and the clinicians choice. In thyroidectomy, and this should only be performed in pa-
general, however, it can be split into three options . . . tients rendered euthyroid with antithyroid drugs. The
1. Radioiodine: a safe treatment option that usually drugs should be stopped 2 weeks before surgery and
leads to euthyroidism in 36 months. I-131 is given and it potassium iodide given to reduce the vascularity of the
accumulates in the thyroid,destroying the gland.The pa- gland
tient should be rendered euthyroid before treatment is
given, with anti-thyroid medicaitons Whatever treatment option is chosen b-blockers are a
2. Antithyroid drugs, e.g. carbimazole, propylth- useful adjunct to treatment because they block the sym-
iouracil, methimazole: if these are going to work, they pathetic side effects that are so distressing in hyperthy-

will usually restore a euthyroid state in 412 weeks. They roidism. Propranolol also has the ability to block
are less likely to lead to permanent remission than either peripheral conversion of T4 to T3.
of the other main treatment options, and long-term
therapy may be necessary. Side effects can be severe, and Q. What is thyroid storm?
include hepatotoxicity, vasculitis and agranulocytosis A.
3. Surgery: the least favoured treatment option of non- This is also known as thyrotoxic crisis, and is a condition
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OSCEs 233

with a 2050% mortality, despite optimal management. to push in on her hips to tense the pectoralis
It occurs as an exaggerated manifestation of hyperthy- musculature
roidism, and is precipitated by major stressors, such as With the patient leaning forward slightly
infection, trauma, major surgery, diabetic ketoacidosis, On inspection you are looking for a number of
MI, CVA, PE and withdrawal of thyroid medications. It things . . .
presents with an overactivated sympathetic nervous Obvious lumps or masses
system (palpitations, tachycardia, tachyarrhythmia, car- Scars (previous neoplastic, augmentative or reduc-
diac failure, anxiety, agitation), and typically a very high tive surgery)
fever. Jaundice is a late and ominous sign. Sinuses
Bruising (old fine needle aspiration site)
Diagnosis should be made clinically, as thyroid function Inflammatory changes in skin (peau dorange)
tests often fail to be grossly deranged. Treatment is . . . Colour of skin (if darkened, may suggest previous
ALS stabilization of airway, breathing and circulation radiotherapy)
Commencement of an intravenous fluid infusion Irregular skin thickening
b-blocker infusion to block adrenergic effects Retraction
Cooling blankets Dimpling
Paracetamol Asymmetry
Propylthiouracil to block production of new T4 Nipple changes [e.g. indrawing, eczema (Pagets dis-
Iodine to block release of pre-formed T4 ease), differing directions, inversion]
Do not give the iodine until the propylthiouracil has Fungation or ulceration
had chance to work (90 min) otherwise there is a risk of Move on to palpation of the breast tissue itself. The
making the thyroid storm worse. Treat any precipitating best position to have the patient in is supine, with the
factors that may be present. hand behind the head.
There are a number of ways to palpate the mass of the
breast; which one you use does not matter as long
as you cover the whole of the breast tissue. Expect
OSCE station 6
the palpation of a single breast to take 3 minutes.
You arrive at an OSCE station and are asked to examine a Either . . .
patients breasts (this will almost always be on a dummy; Split the breast into four quadrants and palpate each
hence, you would be expected to both show what you quadrant in turn using small circular movements
would do and describe what you would do because the with the pads of the fingers, about the size of a 50
limitations of the model mean that you cannot physically pence piece; or . . .
demonstrate what you would like the patient to do). Start just anterior to the axilla and circle around the
Introduce yourself to the patient,stating full name and periphery of the breast in an ever-decreasing circle;
grade or . . .
Explain what it is that you propose to do,and that there Start just anterior to the axilla and palpate circularly
will be a nurse chaperone present at all times up and down the breast tissue moving from lateral to
Gain consent medial
Give the patient time to get undressed in private if she is If you find any abnormality you must describe its . . .
not already de-robed Site on the breast (and on which breast): often giving
Ensure that you have a female nurse chaperone a time in the oclock form helps; also site within the
Once undressed, uncover the patient from lower ribs breast (superficial or deep)
upward Size in cm

Begin with inspection: inspect in a number of ways Shape (circular, ovoid, elongated)
... Surface (regular or irregular)
With the patient sitting comfortably at rest with her Consistency (soft or hard)
arms by her sides Tender or non-tender
With the patients hands in the air above her head Overlying skin (tethered or mobile)
With the patients hands on her hips; ask the patient Underlying fascia (tethered or mobile)
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234 OSCEs

Temperature (any evidence of inflammation) starting as high in the axilla as you can, palpate the
Transillumability (can you shine a light through it medial and lateral axillary walls, attempting to trap
or not) any nodes against the chest wall or medial humerus
Once you have completely described it,move on to pal- respectively as you do so. Warn the patient that this
pate the rest of the breast tissue from where you left off; part of the examination may be the least comfortable
just because you have found one abnormality does not Describe any abnormalities found in the same way as
mean there are not more to find (there usually are in for a breast lump
the OSCE)! Complete your palpation by feeling for any enlarged
Describe each abnormality in the same way supraclavicular lymph nodes from behind
Once you reach the nipple, you must bi-manually pal- Immediately cover the patient up, thank them and
pate it by placing two fingers either side and gently turn to the examiner to present your findings
rocking the nipple, with the specific purpose of palpat-
Be aware that you may get asked to examine a patient who
ing any masses behind the nipple, and also of express-
has had a previous mastectomy. Do not panic! Begin by
ing any abnormal secretions or galactorrhoea from the
inspecting the mastectomy scar and axilla, looking for
nipple itself
signs of masses or nodularity. Note especially the colour
Move on the axilla (it is best to sit the patient up again
of the skin (radiation) and the presence of lymphoedema
to do so) . . .
(impaired lymph drainage post-surgery). Move on to
Begin with inspection, looking for signs of masses,
palpation: palpate gently along the scar (it is often exquis-
infection (hidradenitis suppuritiva), rashes or un-
itely tender), and then move on to the rest of the chest
usual skin pigmentation (acanthosis nigricans)
wall in a similar way as if the breast was still present.
Palpate any breast tissue you suspect to be deep in the
Take special care in palpating the axilla, looking for
axilla (do not forget that the axillary tail of Spence
can reach far into the axilla in some women)
Then palpate for lymph nodes. Support the arm of The way to differentiate between the most common three
the patient with your non-examining hand, and, breast masses is shown in the table below . . .

Breast cyst (breast mouse) Carcinoma

Age of patient Early middle age, aged Young, aged 1530; rare after Older, aged 35100+; usually
3550 years; uncommon age 50 years patient is >50 years
post-menopause except in
women on HRT

Shape of lesion Spherical Spherical, discoid or lobular Irregular

Consistency of lesion Soft Firm Hard

Surface of lesion Delineated from Delineated from surrounds NOT delineated from
surrounds surrounds

Tender or not Usually Rarely Rarely

Tethering Moderately mobile Very mobile Commonly tethered to skin


or fascia

Number of lesions Commonly multiple Can be multiple, but usually Usually single
at one time single