What is the meaning of ‘opsoclonus’ and does it always indicate
malignancy?

Does a greatly elevated lactate dehydrogenase (LDH) denote
malignancy?

Does a normal erythrocyte sedimentation rate (ESR) exclude malignancy
in a patient complaining of feeling easily fatigued?

Why is folic acid supplementation given just after the day of
methotrexate administration? Can we give them simultaneously on the
same day?

Is hydroxyurea useful in the treatment of chronic myeloid leukaemia?

What is the treatment of choice of mucosa-associated lymphoid tissue
(MALT) lymphoma? Is the eradication of Helicobacter pylori enough?
Does the positivity of CD2 rule out MALT lymphoma?

Stage IIE Hodgkin’s lymphoma is the ‘involvement of one or more
lymph node regions plus an extralymphatic site’ and that stage IV is
the ‘involvement of one or more extralymphatic organs with or without
lymph node involvement’. What is the difference? Is ‘site’ different from
‘organ’ and, if so, what is ‘site’?

1. What is Hodgkin’s lymphoma?

2. What is the difference between Hodgkin’s and non-Hodgkin’s
lymphoma?

Why is serum calcium elevated in patients suffering from lymphoma?

In a patient with suspected multiple myeloma, with pains in the back
ribs, is the skull still the most sensitive site to observe bony lesions?

Please explain why the incidence of ovarian cancer (surface epithelial
type )/ carcinoma is low in women who take the oral contraceptive pill
and who have undergone tubal ligation, compared with the general
population?

What is the treatment of Kaposi’s sarcoma?

How effective is a paracetamol and codeine phosphate combination
in cancer pain therapy and ordinary pain therapy, and what is the
difference in using them in cancer pain therapy

What is meant by co-analgesic drugs in palliative care?

Is trastuzumab useful in all patients with metastatic breast cancer?

I have heard that Imatinib is useful in stromal cell tumours. Can you
explain the mechanism?

Does monoclonal gammopathy of unknown significance (MGUS)
progress to multiple myeloma?

Why do some cancers particularly metastase to bone?

What is the difference between lead time bias and length time bias.

Could lymphocytosis (lymphocytes: 4.4 109/L, representing 56%
of total lymphocytic count) and not accompanied by any other
haematological or systemic symptoms or signs except for mild weight
loss (5–10% previous body weight) some 12 years ago, with no
progression until now, be chronic lymphocytic leukaemia?

What is the sensitivity of a prostate-specific antigen (PSA) in detecting
prostatic carcinoma?

How can gabapentin and carbamazepine act with a cervical disc
prolapse?

Do patients with cervical spondylosis, experiencing neck pain and
stiffness, benefit from putting on a neck collar? If so, for how long should
the collar be worn?

What is indicated by a straightening of the lumbar spine with a
loss of normal lordosis, and is there any relation to ankylosing
spondylitis?
the collar be worn?

Can cervical spondylosis cause hypertonia in one upper limb?

Should a female patient, with mild congestive cardiac failure,
microalbuminuria and cervical spondylosis receive IV vitamin D/
analogues? Would this not increase the risk of calcium stones owing to
the mild renal impairment? Would oral vitamin D be preferable?

What is the recommended treatment for spinal canal stenosis? Do
carbamazepine or vasodilators have a role to play in its treatment?

What technique is used for injecting steroids locally in the case of carpal
tunnel syndrome?

In a patient who has sustained an anterior cruciate ligament (ACL) knee
injury and whose pain and swelling have subsided on conservative
treatment, what are the chances of complications (e.g. osteoarthritis,
fibrosis) from the torn ligament. Will the patient be able to lead a
normal life?

Is either gapapentin or carbamazepine effective in the treatment of
meralgia paraesthetica?

What is the clinical differentiation between Dupuytren’s contracture and
ulnar nerve palsy? Is it the absence of sensory deficit in the former? Are
there any other differentiating factors?

1. Is a local corticosteroid injection in the palm effective in the case of
Dupuytren’s contracture?

2. Can Dupuytren’s contracture occur in early or well-controlled
diabetes, or is it more likely to occur in uncontrolled diabetes?

Besides cirrhosis of the liver and diabetes mellitus (DM), what other
causes of Dupuytren’s contracture are there? What is the
pathophysiology behind it?

According to one of my lecturers, who is a very well-qualified doctor
and orthopaedic specialist, there is an indirect connection between
osteoarthritis and subclinical local infections (such as periodontal
abscesses), changing the pH of bodily fluids. Can you explain this
mechanism?

What do you mean by saying that in nodal osteoarthritis each joint is
affected one at a time? Is it that each proximal interphalangeal (PIP) or
distal interphalangeal (DIP) joint is affected alone, or that at any one time
PIP or DIP joints are affected together in one or both hands?

What are the criteria for diagnosing osteoarthritis (OA) of the knee joint
radiologically? Are changes to be expected with advancing age? To what
extent would I consider it significant in those below 50 years of age?
Would you give me some X-ray examples if possible?

1. In a young patient with osteoarthritis, does long-term treatment with
paracetamol (acetaminophen) 500 mg/day, rather than ibuprofen
600 mg/day, lower the incidence of renal toxicity?
2. How great is the risk of renal toxicity with both these treatments?

In India, total knee replacements are being recommended for every case
of severe osteoarthritis, without considering factors such as age, weight
or medical condition. What are the correct indications for surgery?

Methotrexate therapy is usually begun in rheumatoid arthritis that
doesn’t respond to NSAIDs plus 40–120 mg methylprednisolone depot.
If a remission is then induced, how long should methotrexate therapy
be continued? Will the patient (now in remission) be given maintenance
therapy?

Methotrexate therapy is usually begun in rheumatoid arthritis that
doesn’t respond to NSAIDs plus 40–120 mg methylprednisolone depot.
If a remission is then induced, how long should methotrexate therapy
What is the dose and regimen for folinic acid rescue after methotrexate in
rheumatoid arthritis?

1. What are the indicators of remission in rheumatoid arthritis? Is it
normalization of erythrocyte sedimentation rate (ESR) or clinical
improvement?

2. Does the rheumatoid factor disappear during a remission of
rheumatoid arthritis?

What is the relationship between rheumatoid arthritis and weight loss?
Can treatment aid the weight loss at the same time as controlling the
disease?

What is the relationship between rheumatoid arthritis and weight loss?
Can oral folic acid (1 mg/day) be used for high-dose methotrexate
therapy with subsequent leucovorin rescue in the treatment of
rheumatoid arthritis?

Can oral folic acid (1 mg/day) be used for high-dose methotrexate
therapy with subsequent leucovorin rescue in the treatment of
rheumatoid arthritis?

In what percentage of patients with psoriatic arthritis does the arthritis
precede the onset of skin or scalp lesions?

1. Is reactive arthritis a synonym for Reiter’s syndrome?

2. It is said that Reiter’s disease has been related to Chlamydia trachomatis
infection. Is this correct?

1. Is the response of an acutely inflamed joint to colchicine
pathognomonic of gouty arthritis?

2. We are told that, other than clinical tests, joint fluid microscopy is
the specific diagnostic test for gout. What does joint fluid microscopy
reveal? Is it the same as a polarized light study revealing needleshaped urate deposits?

In the prevention of gout, should allopurinol be used for life in a patient
who is hypertensive, alcoholic and overweight?

Does a serum uric acid level of 5.7 mmol/L need treatment? Can it be
significant with cholesterol levels of 213 mg/dL (5.5 mmol/L)? What is
the treatment?

In the diet of patients suffering from gout, should tea, coffee or other
compounds containing methylxanthine products be restricted?

1. When do joints that appear slightly swollen, but not warm, need to be
tapped?

2. In what circumstances might an immunologically suppressed patient
not mount a fever or not have heat around a septic joint?

What is the cause of Pott’s disease?

One thing that often baffles me is that patients with systemic lupus
erythematosus often suffer recurrent thrombosis due to lupus
anticoagulants (antiphospholipid syndrome). How can an anticoagulant
cause thrombosis?

Are elevated homocysteine levels an independent risk factor for
progression of systemic lupus erythematosus (SLE)/scleroderma? Kindly
suggest some references if possible.

1. What are the indicators of remission in systemic lupus erythematosus
(SLE)? Is it the normalization of erythrocyte sedimentation rate (ESR)
and the disappearance of antinuclear antibodies (ANA) and other
antibodies, or is it clinical improvement?

2. During remission of SLE, do ANA and other antibodies disappear?

When should the use of cyclophosphamide in systemic lupus
erythematosus (SLE) be commenced? What is the correct and safe dosage
of cyclophosphamide?

1. Given the benefits of dexamethasone, which lacks any
mineralocorticoid activity, why is this not prescribed in your book for
diseases that require long-term steroid therapy, such as systemic lupus
erythematosus or giant cell arteritis?

2. Does dexamethasone have more serious adverse effects than
prednisolone? Why is it not generally preferred?

Would an elevated C-reactive protein (CRP) level, in association with a
high erythrocyte sedimentation rate (ESR) and in the absence of infection
and serositis, exclude the diagnosis of systemic lupus erythematosus?

How do steroids precipitate a crisis in patients with systemic sclerosis?

Are neck and face muscles commonly affected in poly- and
dermatomyositis? Does this differ from the muscles that are affected with
myasthenia gravis?

1. In dermatomyositis, what is the shawl sign?

2. How frequently is dermatomyositis associated with Gottron’s papules?

How can cranial arteritis be diagnosed in the absence of any physical
symptom or feature of the disease other than headache?

Do pulmonary manifestations in Behçet’s syndrome present with
pulmonary infiltrates in the upper zone of the lung?

1. Is Behçet’s disease accompanied by an elevated erythrocyte
sedimentation rate (ESR)? If so, how often?

2. Can Behçet’s disease be diagnosed in a young adult with an ischaemic
stroke and a history of almost weekly mouth ulcers that heal quickly,
but with no other symptoms of Behçet’s disease?

Mouth ulcers are too common to be a cardinal feature in the diagnosis of
Behçet’s disease. Are there any distinguishing features other than mouth
ulcers that would confirm diagnosis?

Mouth ulcers are too common to be a cardinal feature in the diagnosis of
Please explain how to diagnose familial Mediterranean fever. Is a
diagnosis of exclusion still used or are there now more up-to-date tools
for the diagnosis?

Is a leucocytoclastic reaction in a tissue biopsy specific for
Henoch–Schönlein purpura or is it also associated with other problems?

What are the anatomical, histological and radiological differences
between:

1. physis

2. metaphysis

3. epiphyseal disc

4. epiphyseal line?

Why does the serum alkaline phosphatase increase in bone disorders and
in some other disorders?

What is the normal amount of calcium excreted in the urine in a 24-hour
period?

Does hydrochlorothiazide have a prophylactic effect against
osteoporosis?

How effective is parathyroid hormone in the management of
osteoporosis? Please explain the mechanism.

1. What is the recommended treatment for severe osteogenesis
imperfecta?
2. Where two siblings have already been born with severe osteogenesis
imperfecta, what is the risk of subsequent children of the same parents
being born with this condition?

Why does achondroplasia not affect the mandible (when all other bones
are affected)?

If an elderly patient with rheumatoid arthritis who has been taking
myocrisin (injectable gold) for several years presents with pancytopenia,
should the gold treatment be stopped? If so, what treatment should
replace it?

In a patient with dermatomyositis, what laboratory tests
should be ordered to exclude systemic lupus erythematosus
(SLE)?

What treatment is recommended for tarsal tunnel syndrome?

In a patient with documented antiphospholipid syndrome, should lupus
anticoagulant be investigated for? If it is found to be present, will this
necessitate the use of anticoagulants?

What are the findings to be looked for during routine fundus
examination in patients on long-term chloroquine or any other
antimalarial therapy for the treatment of systemic lupus erythematosus
(SLE)?

What is the sensitivity of plain X-ray in detecting ankylosing spondylitisrelated
spine lesions in both early and late disease, and is there a specific
diagnostic test for this?

It is reported by the Oxford Handbook of Clinical Medicine that glucosamine
and chondroitin sulphate have failed an NEJM trial for the treatment of
osteoarthritis? Is there still a valid use for these compounds?

Can high serum titres of C-reactive protein (CRP) with normal
erythrocyte sedimentation rate (ESR) indicate relapse of rheumatoid
arthritis in established rheumatoid arthritis which is in remission?

What is the positive predictive value of hyperuricaemia in the diagnosis
of gout?

What is Scheuermann’s disease? And is this a specific clinical or
radiological or haematological disease? What is the treatment for this
disease?

How do you calculate the plasma creatinine clearance value at the
bedside, by body weight?

Can you tell me whether administering low doses of dopamine to
increase renal blood flow is today considered obsolete?

Why does haemoglobinuria cause anuria?

I am confused over the use of a ‘high-protein diet’ in the management
of nephrotic syndrome. You say it confers no advantage, but the Oxford
Handbook of Clinical Medicine advocates its use and Davidson’s Principles
and Practice of Medicine says it is even dangerous as it could lead to renal
damage. Which one should I choose, assuming I see the question in
an MCQ?

Is albumin infusion contraindicated in nephrotic syndrome? If not, then
what are the indications?

Listed under the drug causes of nephrotic syndrome, it has been
stated that high doses of captopril can induce an immune-complex
mediated membranous glomerulonephritis. If a patient with nephrotic
syndrome has hypertension, is it detrimental to give captopril as a
treatment for his hypertension? Could this exacerbate the patient’s
nephrotic syndrome?

Please explain the pathophysiology of ascites in the nephrotic
syndrome?

Does the nephritic syndrome cause hyperkalaemia? I don’t seem
to be able to find a definitive answer in the textbooks that I have
consulted.

You say that the investigation of first choice for urinary tract infections
(UTIs) in males or children, or recurrent UTIs in females, is intravenous
urography (IVU); in Oxford Handbook of Clinical Medicine it is ultrasound
(US). Which is best?

1. Other than amoxicillin, what other orally administered drug is
recommended for the treatment of a urinary tract infection (UTI)
caused by enterococcus?

2. What is the recommended dosage for antibiotics in the prophylactic
treatment of recurrent UTI in pregnancy? Is amoxicillin clavulanic
acid safe to use during pregnancy?

What is the advantage of intermittent self-catheterization over an
indwelling catheter? How is bladder training done while on an
indwelling catheter?

Kindly tell me about the role of pulse wave velocity (PWV) in early
diagnosis of arteriosclerosis. How is it useful in cardiac, diabetic and
renal medicine?

You say that no convincing evidence was found that chronic
hyperuricaemia causes nephropathy and nor can it be corrected by
allopurinol. However, some patients we see have high serum uric
acid and creatinine, which both come down with allopurinol. Please
comment.

Can aspirin cause analgesic nephropathy? If yes, then how could we
justify its use in primary prevention of coronary artery disease (CAD),
even in high-risk patients? I have read that regular use of analgesics for
3 years could cause analgesic nephropathy.

What is the probability that a patient on a moderate daily dose of nonsteroidal
anti-inflammatory drugs (NSAIDs; ibuprofen 800 mg once daily
for tension headache) will develop analgesic nephropathy?

Do daily doses of paracetamol with the dosage range of 1 g/day cause
analgesic nephropathy. If so, after what length of time?

Allopurinol is used for the treatment of uric acid stones; it is also one
of the aetiologies of renal calculi. Could you please explain its actual
effect.

Why should we avoid angiotensin-converting enzyme (ACE) inhibitors
as hypertensive therapy in the presence of renal artery stenoses? How
can they lead to acute renal failure? What else can we prescribe for this
patient to regulate the hypertension?

Is the use of angiotensin-converting enzyme (ACE) inhibitors
contraindicated in cases of unilateral renal artery stenosis?

1. How effective is renal duplex in detecting renal artery
stenosis?

2. Is magnetic resonance angiography superior to renal duplex in
detecting renal artery stenosis?

How accurate is ultrasonography in detecting renal calculi?

Please explain the most effective way to manage a case of intrauterine
fetal unilateral hydronephrosis in the 32nd week of pregnancy.

In renal failure, why does oedema first occur in the periorbital area and
nowhere else?

How does sodium valproate decrease serum urea concentration and GI
bleed increases it?

1. What clinical information can be obtained by checking the blood urea
nitrogen (BUN) level that cannot be obtained by checking the blood
urea and serum creatinine alone?

2. What is the signifying difference between blood urea and BUN?

1. Does uraemia cause dysentery with blood and mucus mixed with the
stools?

2. Is it correct to use the term ‘uraemic dysentery’?

3. Does uraemia cause finger clubbing?

What are the causes of a low serum creatinine?

Why does oliguria occur in the early stages of acute tubular
necrosis (ATN)?

Is renal impairment induced by lithium therapy in bipolar affective
disorders irreversible? How often does it occur?

Can you please explain why a patient with chronic renal failure (CRF)
might present with either oliguria or polyuria?

What are uraemic frost conditions?

What is the role of terlipressin or novapressin in the management of
hepatorenal syndrome?

What is the rationale of angiotensin-converting enzyme (ACE) inhibitors
in chronic renal disease?

What procedure is recommended for post renal transplant if this is the
second graft?

Do the cysts in autosomal-dominant polycystic kidney disease (PCKD)
undergo malignant transformation and in what percentage?

In a 69-year-old patient with a 2-cm hard prostatic nodule on digital
rectal examination, what is the more appropriate way to make a
definitive diagnosis of prostate cancer: prostate biopsy or serum prostatespecific antigen (PSA)?

A 50-year-old patient complains from slight lower urological symptoms
(mild difficulty in urination). By digital rectal examination a mass of
(1) hypertrophy can be palpated. His family history contains cases of
prostate cancer (in some relatives). What is the next investigation to do in
this patient?
● Titration of serum prostate-specific antigen (PSA): Is it useful in such a
patient? Why?

● Transrectal ultrasound (TRUS)?
● TRUS-guided needle biopsy?

What are the causes of urinary incontinence in the elderly?

For how long could urinary retention persist after major gastrointestinal
tract surgery? Will cholinesterase inhibitors be of benefit in enhancing
emptying of the bladder?

1. What are the possible causes of a large, white kidney?

2. What is the physiological significance of a giant cell?

What is the amount of 24-hour urinary albumin excretion above which a
diabetic patient is said to have microalbuminuria?

How is forced diuresis induced in cases of prerenal failure?

1. Why do conditions that cause retention of sodium, such as cardiac
failure, result in low serum sodium?

2. What is meant by ‘free water’?

Why is there a difference in the pattern of oedema in nephrotic syndrome
and cardiac oedema? How is it related to the interstitial spaces and all
that? I am confused.

Why is there a difference in the clinical presentation of oedema due to
renal failure and oedema due to cardiac failure, and how is this related
to the loose nature of the interstitial tissue in the periorbital area? The
answer given was that it is because, in cardiac failure, there is orthopnoea
and the most dependent portion in this case is the legs, which is why the
oedema occurs there. You also mentioned that in renal failure there is no
orthopnoea and the patient doesn’t have to sit up, hence the difference.
This does not seem to take into account right ventricular heart failure
(RVF), where there is no question of orthopnoea. Pedal oedema is found in
right ventricular failure. Is the answer not that, in congestive heart failure
(CHF) there is pump failure (and the heart cannot pump blood against
gravity) hence oedema in the dependent areas, whereas in renal failure
there is no pump failure and the heart does not lose its capacity to pump
blood against gravity. The oedema in this case develops in those tissues
that have a loose interstitium, one such site being the periorbital area of the
face. This is the reason for the difference in clinical presentation.

What treatment is recommended for recurrent attacks of generalized
swelling, with angio-oedema, in a middle-aged female patient?

Is an osmotic diuresis, due to hyperglycaemia for instance, a cause of
both hyponatraemia and hypernatraemia. Please explain how this can be
the case.

What is the mechanism of β2-agonists (albuterol) in correcting
hyperkalaemia in emergency? How does it cause a shift of potassium?

Why do we give sodium lactate along with sodium bicarbonate in
acidotic patients? How does sodium lactate then act?

How does hypochloraemia alone cause a metabolic alkalosis?

I have read the part concerning acid–base imbalances and I would like to
ask about two things:

1. Why is there a higher concentration of anions (18) on measuring the
anion gap while there is a high concentration of immeasurable anions?
I would have expected a higher concentration of cations because most
of them are measurable.

2. Could you explain to me in more details how NaCO3 loss or HCl
retention could lead to normal anion gap acidosis?

What is the exact formula for calculating the serum anion gap?

What is the role of IV saline in the management of a cirrhotic patient with
a serum sodium of 120 mmol/L?

Why do we give calcium gluconate to a patient with severe
hyperkalaemia?

Can you explain the respiratory alkalosis and metabolic acidosis in
salicylate poisoning?

In an elderly patient with oedema due to heart failure, which is the best
diuretic to start treatment with? Some books recommend thiazides
whereas others use loop diuretics.

What is the Bernheim effect and the reverse Bernheim effect?

Kindly explain why the left side of the heart is more prone to disease.

1. Is it always necessary to examine the cardiovascular system of a
patient in the 45° incline of the head end? Other than convenience for
examining the jugular venous pressure (JVP), does this position have
any other advantage?

2. If the JVP is not visible when the patient is in the upright position, can
one presume it is not raised?

The mitral area (of auscultation) normally corresponds with the apex
beat. When the heart is dilated and the apex beat is shifted laterally, will
the mitral area follow the apex beat to its new location or remain at the
place where the apex beat is normally situated?

Please explain in detail how to measure the pulsus paradoxus using
a sphygmomanometer.

What is the difference between dicrotic pulse and pulsus bisferiens?

1. Why does the radial pulse become more prominent when the hand is
lifted overhead?

2. Please explain the mechanism of a collapsing pulse. Which is the best
artery to elicit it: radial, brachial or carotid?

What is the mechanism of Durozier’s sign?

What effects do aortic stenosis, aortic regurgitation and coarctation of the
aorta have on systolic and diastolic blood pressure, and why do they
produce these effects?

In the section headed ‘Pulsus bisferiens’ (K&C 7e, p. 691) what do
‘percussion wave’ and ‘tidal wave’ mean? An illustration here would be
helpful.

When examining a patient’s carotid pulse, why should we not palpate
both carotids at once? Is it because it might block the blood supply to the
brain?

How can I differentiate between jugular and arterial pulsation in the neck
practically?

Can you please help me with this: ‘Thrusting due to mitral or aortic
regurgitation. Heaving due to aortic stenosis and systemic hypertension.
There is often confusion about the terms thrusting and heaving’.

Another book I read considers aortic stenosis and hypertension for
thrusting and mitral/aortic regurgitation for heaving. Who should I go
with? Thank you.

Where is the best place on the precordium to auscultate a split-second
heart sound?

What is the mechanism by which murmurs of mitral valve prolapse
(MVP) and hypertrophic cardiomyopathy (HC) are accentuated by
standing or the Valsalva manoeuvre?

What is the correct procedure for a fluoroscopy and why is this essential
for the insertion of cardiac catheter, pacemaker and prosthetic valve?

What is the role of amiodarone in the acute management of asystole or
pulseless electrical activity (PEA)?

1. Is there any contraindication to the use of microwaves or mobile
phones in patients with pacemakers?

2. What, if any, appliances should be avoided in a patient with
a pacemaker?

1. What is tachy-brady arrhythmia in the sick sinus syndrome?

2. How can it be managed?

Practically, how can we differentiate between a second-degree
atrioventricular (AV) block Mobitz I and Mobitz II? What is the meaning
of first-degree block? What is the difference between heart asystole, heart
arrest and third-degree AV block?

How can a complete atrioventricular (AV) block be diagnosed on an
electrocardiogram (ECG)?

Usually, we look for an RSR pattern for bundle branch block in the chest
leads. What does it mean if there is an RSR pattern in the limb leads?

What is Wolff–Parkinson–White syndrome?

In management of atrial fibrillation (AF), is the priority to control
ventricular rate or to restore cardiac rhythm?

Can digoxin be given in paroxysmal atrial fibrillation?

In a patient with atrial fibrillation and bronchial asthma, what is
the recommended treatment and do beta-blockers make the condition
worse?

What is the difference between atrial flutter and atrial tachycardia?

What are the possible causes of atrial extrasystoles, in a patient with
a normal echo, which last for several days and then disappear
spontaneously? Is treatment with anxiolytics recommended?

In the treatment of ventricular tachycardia, could lidocaine be used in the
absence of any other drug? How effective is lidocaine?

Why is an extremely low level of potassium in the blood sometimes
a cause of ventricular fibrillation?

How often does verapamil cause impotence and inhibit ejaculation?

Why does a patient with congestive cardiac failure have excessive
sweating?

What is cardiac asthma?

In a book, under the title ‘Heart failure’ I have seen the following phrase:
‘Cardiac failure occurs when, despite normal venous pressures, the heart
is unable to maintain sufficient cardiac output…’. Is it correct to say
‘normal venous pressures’? All protective and compensatory mechanisms
raise the venous pressure to maintain a sufficient cardiac output –
according to Frank–Starling law – and this is the case in heart failure, so
I think it was meant to say: ‘…despite high venous pressures…’.

I wanted to ask whether a third heart sound is present, or should be
present, in all cases of heart failure, whatever the underlying cause.

Why can left heart failure lead to right heart failure but not vice versa?
What is the physiology involved in this transition?

Could you explain the fetal gene program, activated in heart failure?

How safe is it to stop administration of carvedilol to a patient with
heart failure? Can the drug be tapered off? What are the effects/dangers
of stopping carvedilol suddenly? What, if any, are the reasons for
discontinuing carvedilol in patients with heart failure?

What are the advantages and disadvantages of furosemide in the
treatment of cardiac failure?

In heart failure, can furosemide be given once daily?

What are the clinical features of a ruptured sinus of Valsalva?

Does dobutamine (dose range 2.5–10μg/kg/min) cause significant
tachycardia?

Are beta-blockers indicated in heart failure; if yes, in all cases or in
selected cases?

Why does long-term treatment by digitalis cause gynaecomastia?

Why do toxic doses of digoxin (which cause a decrease in excitability of
cardiac tissue) cause arrhythmias, whereas therapeutic levels of digoxin
(which cause increase in excitability) cause no arrhythmias?

Hypokalaemia is one of the complications of digitalis. In treatment
we give K. How does the hyperkalaemia enhance the digitalis
toxicity?

Why should we measure serum potassium before we start digoxin?

The intravenous administration of loop diuretics such as furosemide
relieves pulmonary oedema rapidly. Is this due to arteriolar
vasodilatation reducing afterload which is an action that is independent
of its diuretic effect? I ask this because I have been told that this drug has
no effect on arterioles (except on efferent arterioles of the kidney), but
rather a venodilatatory effect. What could be the cause of such different
opinions?

There have been a number of recent publications concerning aspirin
versus warfarin trials. Would you recommend prescribing warfarin for
secondary prevention of coronary heart disease in patients suffering from
their first myocardial infarction (MI)?

Is it true that in future the ApoA : ApoB ratio will be used to predict
the risk of coronary artery disease more efficiently than low-density
lipoprotein (LDL)?

What is the exact link between C-reactive protein (CRP) and coronary
artery disease?

In angina pectoris, why does the chest pain get radiated to the left side,
i.e. left arm and back?

Please explain why thrombolytic therapy is not indicated in cases of
unstable angina and non-ST-segment elevation myocardial infarctions
(nSTE-MI) despite the fact that both nSTE-MI and ST-elevated MI
(STEMI) are caused by a thrombus for which thrombolytic therapy is
highly indicated? Could it be true that, in the case of unstable angina and
nSTE-MI has a higher incidence of intracranial haemorrhage than in the
case of ST-segment elevation MI?

Doesn’t the term ‘acute coronary syndrome’ include unstable angina, nonST-segment
elevation myocardial infarctions and ST-elevated MI (STEMI)?

Kindly mention the indications for clopidogrel in acute coronary
syndrome (ACS). Should it be used along with aspirin or alone if the
latter is contraindicated? Are there any studies that combine both
with either low-molecular-weight heparin (LMWH) or unfractionated
heparin? How long should clopidogrel be continued?

What role do IV fluids play in the management of acute inferior wall
myocardial infarction?

Is there any benefit in combining aspirin with clopidogrel in post-MI
angina and ischaemic stroke? A MATCH trial showed this combination
not to be of benefit – would you therefore recommend we stop using this
combination in our hospital unit?

In a patient with the typical chest pain of myocardial infarction (MI) and
no other criteria for thrombolysis would highly elevated cardiac enzymes
indicate thrombolysis?

I cannot figure out the role of an acetylcholinesterase inhibitor in postmyocardial
infarction from Conn’s Current Therapy and Swanson’s Family
Practice. Can you help?

Can thrombolytic therapy for myocardial infarction (MI) be started
in patients who have cardiac pain and raised cardiac markers? Can
streptokinase be given irrespective of electrocardiogram (ECG) changes
(according to some books, ST elevation has to be present)?

Can carvedilol be used in an elderly patient who developed left
ventricular failure after a very recent myocardial infarction, or should it
wait until the condition becomes stable?

I have seen some patients with chronic rheumatic heart disease with no
obvious evidence of rheumatic fever (i.e. they could not recall if there
was an episode of severe infection with subsequent fever and joint pain).
So, actually, how is chronic rheumatic heart disease diagnosed?

If a young patient presents with hemiparesis and rheumatic atrial
fibrillation and is already on oral anticoagulant, with an international
normalized ratio (INR)  3 and a normal computed tomography (CT)
scan done 2 hours after onset, should he receive heparin for prophylaxis
against further embolism? Should aspirin be combined with oral
anticoagulant later, or should target INR be increased?

When treating mitral stenosis using a balloon valvotomy, how come no
thrombus develops at the site of the atrial septum or at the separated
commissure of the valve leaflets?

Why does a mitral stenosis produce a loud S1?

Why is the mitral valve more affected than any other valve in the heart in
most valvular diseases?

What is William’s syndrome (supravalvular obstruction)? Why does
hypercalcaemia occur with this syndrome?

Kindly tell me all the causes postulated for the collapsing pulse seen in
aortic regurgitation.

Does pulmonary stenosis cause pulmonary hypertension?

Under what conditions would a pulsatile liver be found and what is its
clinical significance?

Can we use warfarin during pregnancy or during menstruation in
a patient with a prosthetic valve? Is anticoagulation necessary in a
patient with a corrected ventricular septal defect (VSD) or corrected
coarctation of aorta?

I want to ask about Duke criteria in diagnosing infective endocarditis.

Is Staphylococcus aureus the most frequent causative agent of acute
bacterial endocarditis? And is this typical of acute bacterial endocarditis?

Please explain the mechanism of the mycotic aneurysm in infective
endocarditis.

Why are the right valves more commonly affected in infective
endocarditis when the microbes enter through the IV route, for example
with IV drug users?

You have said that in IV drug users the microbes go directly to the right
ventricle, thus causing endocarditis in the right heart. But in dental
procedures the microbes also go through the veins to the right heart first,
so why are the left heart valves more commonly affected?

What causes splenomegaly in infective endocarditis?

We know that Janeway lesions appear with infective endocarditis, but is
there any other disease that can cause it?

Patent ductus arteriosus (PDA) is also called duct-dependent circulation.
What is the meaning of this phrase and do any other conditions present
with a similar condition? What is the implication of this condition to the
human body?

What is the recommended treatment for a child with both congenital and
valvular heart disease?

Can you describe a few instances that might cause a case of tetralogy
of Fallot to go into congestive cardiac failure, even though this is an
unlikely occurrence? Please explain how this happens.

Is a single ventricle disease associated with any syndrome? If so, what is
its name and what are its characteristics?

What is the cause of splitting of the second sound in breathing and why
is it wide and fixed in atrial septal defect (ASD)?

Why are deep-sea divers considered a ‘high-risk’ group if they have an
atrial septal defect (ASD)?

Is it prognostically beneficial to start treatment of impending cor
pulmonale in a case of chronic obstructive pulmonary disease (COPD)
with no symptoms of failing heart but with investigational evidence
(electrocardiogram and chest X-rays)?

What would be the ideal investigation for a suspected pulmonary
embolism according to the protocol in a UK hospital?

Can the apical pulsation in right ventricular enlargement be
hyperdynamic?

Please explain concentric and eccentric left ventricular hypertrophy.
When the hypertrophied ventricle dilates and the wall thins out, is it still
called a hypertrophied ventricle?

What is viral pericarditis?

I want to know why thrombolytic therapy is contraindicated in acute
pericarditis.

Why would sitting bring pain relief to, and lying aggravate, a patient
with acute pericarditis?

How do you determine whether a patient is in a ‘hypertensive
condition’? And what is wide pulse pressure?

I have a question about hypertension. Every textbook that I’ve come
across places the greatest emphasis on the systolic blood pressure;
it seems that diastolic pressure is often a figure that ‘just happens to
be there’. My question is: What is the clinical importance of a diastolic
pressure? And what problems might arise if a patient has a too high/low
diastolic blood pressure?

What causes hypertension in children?

Is haemochromatosis a cause of hypertension?

What are the most recent advancements in management of hypertensive
crisis? Is there any new approach or method under trial?

Why does hypertension not cause headache, and why does only the
accelerated hypertension cause headaches. You say in ‘coarctation of
aorta’ that there is headache and epistaxis from hypertension.

Why is a headache one of the signs and symptoms of hypertension?

In a hypertensive hypercholesterolaemic patient, is it contraindicated to
use a bisoprolol–hydrochlorothiazide combination to control the patient’s
hypertension if it is not controlled on bisoprolol alone?

Should a hypertensive patient with recurrent ischaemic strokes, a total
cholesterol of 200 mg/dL (5.2 mmol/L), low-density lipoprotein (LDL)
cholesterol of 120 mg/dL (3.12 mmol/L) and high-density lipoprotein
(HDL) cholesterol of 35 mg/dL (1 mmol/L), have a statin therapy?

Has Tenormin any advantage over other beta-blockers in the control of
hypertension?

Is the use of sublingual captopril 25 mg/h, in combination with IV
furosemide 40 mg/h to a maximum of 120 mg, safe to lower greatly
elevated blood pressure?

Is ACEI superior to calcium channel blockers in the treatment of
hypertension, in terms of prognosis and of the prevention of
complications?

Are angiotensin-converting enzyme (ACE) inhibitors more effective
than beta-blockers in reducing the risk of stroke in hypertensive
patients?

Do non-steroidal anti-inflammatory drugs (NSAIDs) affect the
antihypertensive effect of angiotensin-converting enzyme (ACE)
inhibitors? If so, how?

What antihypertensive is recommended for a patient with aortic stenosis
(AS) and hypertension, as a mono- and combination therapy?

Impotence is a common side-effect of antihypertensive drugs. How can
I solve this problem in young hypertensive patients?

In the treatment of hypertension, is it recommended to commence
treatment with two drugs containing a thiazide (if elderly) or a betablocker (if young)?

1. Following a stroke, both haemorrhagic and ischaemic, in previously
hypertensive and normotensive patients, can you explain precise
blood pressure control and the desired blood pressure levels?

2. In the case of a hypertensive emergency, with a blood pressure of
220/130 with acute myocardial infarction, what immediate measures
should be taken?

On lowering blood pressure, to what extent can heart failure secondary
to chronic hypertensive heart disease be reversible?

Is the use of amlodipine or furosemide recommended to normalize blood
pressure in a case of hypertensive heart failure? If so, which is most
effective?

How can diabetes cause endothelial dysfunction? What are the roles of
ACE inhibitors in the kinin–kallikrein system? What are the mechanisms
by which a decrease in the level of nitric oxide causes endothelial
dysfunction?

Can sublingual nifedipine be given to a patient with malignant
hypertension/accelerated hypertension? It seems to be a controversial
issue with some favouring it and some against it.

Is the diagnosis of malignant hypertension based only on the basis of the
retinopathy (even in the presence of a normotensive state)? Labetalol,
parenterally, is suggested as a treatment for malignant hypertension.
What other more readily available preparations (besides sodium
nitroprusside) are recommended in addition to this drug? Parental
labetalol is not available in Pakistan!

Patients at medium risk of DVT and pulmonary embolism are usually
given specific prophylaxis with low-dose heparin at a dose of 5000 units
subcutaneously every 8–12 hours until the patient is ambulatory. Is the
first dose given immediately after, say, extensive varicose vein surgery of
small and great saphenous veins?

‘Anticoagulants are not necessary, as embolism does not occur from
superficial thrombophlebitis’ (K&C 7e, p. 809). Why?

Can we use enoxaparin for deep vein thrombosis (DVT) prophylaxis
in the immediate postoperative period and in a case of cerebral
haemorrhage? Wouldn’t it increase the risk of haemorrhage in
either case?

Can external jugular vein thrombosis cause tingling numbness over
the earlobe and adjoining part of the lower face?

For how long does a patient have to stay in bed to be labelled as
bedridden and to merit low-molecular-weight heparin (LMWH) as
prophylaxis for deep vein thrombosis?

Is an inferior vena cava filter an alternative treatment for a patient with
a history of recurrent deep vein thrombosis on lifelong anticoagulation
with warfarin?

Can you explain why a decrease in serum lipid levels follows an acute
myocardial infarction (MI)? For how long does this decrease last and
how is it known whether the patient has hyperlipidaemia in such a case?

In patients with myocardial infarction, why is aspirin to be taken
chewed, and not by any other method?

Must beta-blockers prescribed for hypertension be stopped if the heart
rate falls below 60 beats per minute?

How can aspirin resistance in patients with recurrent ischaemic stroke
be assessed; is the clotting time a factor? Does the substitution of aspirin
with clopidogrel solve this problem?

In a patient with heart failure and atrial fibrillation on warfarin who
experiences frequent transient ischaemic attacks, will the patient benefit
from having aspirin prescribed?

Is there a role for anticoagulation in inoperable carotid stenosis 70%?

What is the upper limit of serum creatinine reflecting renal damage from
hypertension above which thiazides should not be prescribed?

a. How is blood pressure measured?

b. Where should both cuff and stethoscope be placed in cases where the
patient is suspected of having coarctation of the aorta?