Regarding medical ethics, if a man is discovered to be hepatitis B or C
positive, is it advisable for the physician to inform the wife or sexual
contact of the patient?

Is it unlawful in most countries to limit medical care, particularly
by rationing the usage of drugs? Surely rationing must be against
the oath we took as doctors to provide the best care available.

What is meant by QALYs? Is there a difference between quality and
quantity of life?

Are ‘Do not resuscitate’ orders illegal in most countries?

What is a living will?

I’ve heard of the Bolam principle but when I mentioned it to my lecturer
I was told it was out of date. Could you explain please?

Why is counselling required before an HIV test can be done on a patient?
We don’t counsel patients when we look for a tumour marker to
diagnose cancer, which is often more serious for a patient.

As a junior doctor, I have to attend many multidisciplinary team
meetings. I am concerned about the confidentiality of these meetings as
they are attended by a diverse group of healthcare workers.

Is the role of the advocate in a medical interview to help the patient or
the doctor?

We are always asked by our seniors to make sure that the patient has
signed the consent form. Isn’t verbal consent enough? Also, for what
procedures do I have to get consent, e.g. urinary catheterization in a
patient with retention?

As cells grow and regenerate, what mechanism does the body use to
get rid of the continuously dying cells? And what kind of cells can’t be
replaced once dead?

I cannot find out why some of the autosomal dominant diseases have a
male or female preponderance, e.g. I have never seen a female Marfans. I
was attributing it to imprinting but on reading about imprinting in detail
it cannot be the case.

We have been told that some tumours in the colon are associated with
microsatellite instability. What does this mean?

I understand that microarrays are being used to define the molecular
abnormality and the prognosis in some patients with leukaemia. What
are microarrays?

Why do mitochondrial diseases cause a myopathy?

Why do successive generations of patients with some genetic disorders
present earlier and with progressively worse symptoms.

Does a normal serum uric acid level exclude the diagnosis of
Lesch–Nyhan syndrome?

How is retinoblastoma an autosomal dominant disease if the mutation of
both RB genes is required to express the disease?

Please could you explain how lymphocytes (especially B) can maintain
receptors on their surfaces? Is this genetically related? If so, when the
lymphocytes are first exposed to the antigens, how could the antigen
receptor be synthesized?

Is there a mutation within the nuclei of these lymphocytes when they
learn to make the receptors? If there is, can you explain how this occurs?

I understand how nuclear factor-κB (NFκB) works in the inflammatory
response but what is the mechanism by which it causes cancer?

What are the diseases associated with hypocomplementaemia and which
complement deficiency in particular?

What is meant by ‘B lymphocytes are sensitive to clonal deletion’?

What are the immunological implications of ‘bare lymphocyte
syndrome’/MHC deficiency?

Please explain oligoclonal and monoclonal.

I was wondering if there is any study regarding cell culture techniques of
CD4 helper cells (stem cell culturing) and, if so, is it of any benefit to
HIV-infected patients?

How do you define autoimmune disease?

1. Why is dexamethasone not routinely used instead of prednisolone,
which is almost universally used routinely in autoimmune diseases, or
other indications for steroids? Is it because dexamethasone lacks the
mineralocorticoid activity seen with prednisolone and therefore does
not cause salt/water retention and hypertension?

2. Can high doses of dexamethasone be used in acute relapses of
multiple sclerosis (MS) in place of pulse methylprednisolone? If so,
what is the recommended dosage?

What is meant by ‘pus cell’ and is this term synonymous with
neutrophils?

Can dendritic cells migrate into lymph nodes? Immunology textbooks
state that these initial blood monocytes infiltrate inflamed tissue. Is the
professional antigen-presenting cell the dendritic cell that enters lymph
nodes?

1. How often should treatment with azathioprine be monitored with
liver enzymes and a full blood count?

2. What is the most specific liver enzyme or function test for monitoring
azathioprine therapy?

Do you agree or disagree that the dose of azathioprine should be
adjusted according to the dose that lowers lymphocytes to 0.8 × 109/L?

Which haematogenous infections (bacterial, fungal and protozoal) can
give rise to positive findings in the urine? What are the appropriate
microbiological investigations for each infection?

Could you please explain the term ‘zoonosis’.

What are soil transmitters?

Please explain the difference between bacteraemia and septicaemia.
Can the presence of toxins, fungi or viruses in the blood also be called
septicaemia?

I want to know about the safety of antibiotics used in pregnancy in
different trimesters.

What are the uses and the side-effects of the antibiotic lincomycin?

I have a question that keeps troubling me. Is there any drug taken orally
that prevents penicillin hypersensitivity reactions?

Is there any replacement intravenous antibiotic for those patients who
have hypersensitivity to penicillin?

Is it correct to perform an intradermal skin sensitivity test before
administering penicillin or a cephalosporin?

Why are antibiotics not allowed in the treatment of rotaviruses?

Does aciclovir prevent the chances of developing herpes zoster (shingles)
when given during primary infection?

How long does it take after vaccination to become immunized against
chickenpox and therefore safe to work in infectious areas?

Is meticillin-resistant Staphylococcus aureus (MRSA) the only major
hospital-acquired infection?

Do you have to have antibiotics to get Clostridium difficile infection?

Why do some patients with rheumatic fever later progress to chronic
rheumatic heart disease?

What is the World Health Organization recommendation for the
prophylaxis of rheumatic fever after a streptococcal throat infection?

Does rheumatic fever have an infectious or an immunological aetiology?

Why is migratory polyarthritis found in rheumatic heart disease?

Are penicillins still the drug of choice in streptococcal infections
(particularly Strep. Pneumoniae)?

1. How long can the antistreptolysin-O (ASO) titre remain positive after
a streptococcal infection?

2. What is the effect of a suitable antibiotic on the ASO titre, if any?

What is the correct method of diagnosis of meningococcal septicaemia:
cerebrospinal fluid culture or blood culture?

Can Escherichia coli 0157 be spread by foods other than meats?

I have a question about a patient with brucellosis in whom, after
6 weeks of treatment with 600 mg rifampicin +200 mg doxycycline,
the agglutination test still shows a 1/320 titre. If, after stopping the
treatment, the patient begins to experience identical symptoms as
previously, how should treatment proceed? What is the best laboratory
test to show relapse?

Do steroids have a role in the treatment of dengue haemorrhagic fever, in
particular to prevent the further fall in the platelet count?

Please give me the mechanism of thrombocytopenia in dengue and
malaria.

What is the recommended procedure for the treatment of a case of
dengue fever?

What diseases can you get from tick bites?

Why has severe acute respiratory syndrome (SARS) not spread as widely
as was predicted?

Please explain the relation between recurrent typhoid fever and chronic
carrier, and the recommended treatment for both.

What is the single most confirmatory diagnostic test for typhoid?

Has human-to-human transmission of the H5N1 avian influenza virus
been described?

In brucellosis, is it possible to see a brucella agglutination test of more than
1/160 even for years after specific and successful therapy of brucellosis?

Please define the terms holoendemic, mesoendemic, and hyperendemic
in relation to malaria.

You only recommend malarone for malarial prophylaxis when there is a
significant chlorquine resistance. Isn’t malarone now widely used in
travellers going to areas with low resistance.

Parenteral vaccination with a killed suspension of Vibrio cholerae is
recommended by some – isn’t an oral vaccine better?

Please suggest possible reasons why Entamoeba histolytica infection
associated with bloody diarrhoea is not relieved by treatment with
ciprofloxacin and metronidazole 400 mg × 2 daily over a 3-week
period.

Is there a basis for treating patients for filariasis according to the
eosinophil count (except for cases of tropical pulmonary eosinophils;
TPE)? Filariasis is everywhere in my part of the world; a fluorescent
antibody test (FAT) might not be very useful – except when there are
very high values.

Why do patients who ingest eggs from a tapeworm in contaminated
food not develop tapeworms?

Why do patients who ingest eggs from a tapeworm in contaminated
food not develop tapeworms?

I have a query about one of the details in the book. You mention that
perihepatitis is a feature of gonorrhoeal infection, but other books say
that perihepatitis (Fitz-Hugh–Curtis syndrome) is a complication of
chlamydial infections. Is there a possibility of perihepatitis in
gonorrhoea? Thank you.

In the 7th edition of Kumar and Clark Clinical Medicine, you indicate that
there is no benefit in treating the male partner of a woman diagnosed with
bacterial vaginosis (BV). As many physicians use the 2 g × 1
metronidazole dose, is this unwarranted? Does it differ in women
experiencing frequent recurrences of infection?

Why is a caesarean section recommended for the delivery of HIV-positive
women?

Why is HIV not transmitted when delivering a baby through caesarean
section?

1. Is HIV transmitted from mother to child during breastfeeding?

2. Is it possible to be infected with HIV through the ingestion of food
and drinks contaminated with the virus?

Is it true that some patients are resistant to HIV infection despite
repeated exposure to the virus?

With regard to live vaccination and HIV, can MMR be given to an
HIV-positive baby?

In a patient with meningitis: can the development of digital gangrene of
the thumbs and sudden dyspnoea with a respiratory rate of 40/min, with
intercostal, subcostal and suprasternal withdrawal, be attributed to
disseminated intravascular coagulation (DIC)?

1. What are the causes of anaemia in HIV infection?

2. What are the measures necessary to prevent the transfusion of
HIV-infected blood to an individual (please explain in light of the
window period)?

What is the recommended treatment for pulmonary anthrax?

What primary or specific tests should be performed before
giving a patient primaquine for the treatment of relapsing
malaria?

How sensitive is the polymerase chain reaction (PCR) test for herpes
simplex virus 1 (HSV-1) in the cerebrospinal fluid (CSF) for confirming
the diagnosis of HSV-1 encephalitis? And is herpes simplex virus 2
(HSV-2) usually tested for as well?

Herpes simplex is usually not associated with chronic infections such as
tuberculosis or typhoid fever. Why is this?

In my country, now that we know that the pin in the percussion reflex
hammer bottom and the pinwheel can transmit infections such as
hepatitis B from patient to patient, we prefer the use of wooden or
dispersible metal pins. Do the authors agree?

Can scorpion bite be complicated by ischaemic stroke? If so, how does
this occur?

Please give examples of red meat, white meat and lean meat.

What is lean body weight and how does it differ from routine
measurement?

Is the combination of drugs sibutramine and orlistat more effective in
reducing obesity than using these on their own?

Why does vitamin B12 deficiency cause glossitis?

Is a dosage of 2.5 mg/day of methyltestosterone, as a component in some
multivitamin formulae, safe in the long-term?

What is the effect of sodium/potassium imbalance on the microminerals?

What is the role of fluoride in healing?

In K&C 7e (Box 5.6, p. 239) it states ‘Do not drink [alcohol] during the
daytime’. Please explain why this is not recommended.

Could you please tell me about the aetiology of ‘refeeding syndrome’?

What is the Atkin’s diet?

What is meant by bariatric surgical procedures?

In a patient with marked obesity, is bariatric surgery better than a balloon
inserted into the stomach?

Does intravenous nutrition always have to be given via a central vein?

Why has there been an explosion of obesity in the young?

Are proteins mostly absorbed from the intestinal lumen into the blood as
amino acids?

What are ‘congeners’ in alcohol?

Cholesterol is synthesized in the body. What is the comparative
role of diet and endogenous production in the level of serum
cholesterol?

We frequently read of the severe but ‘rare’ side-effect of myositis with
statins. Do these drugs have more ‘common’ side-effects?

Is there a relationship between brain disease and alcohol intake? Does
alcohol have a proven toxic effect on the brain?

What is the difference between malabsorption and malnutrition and how
can these be differentiated clinically?

What are the health hazards of eating smoked foods such as meat or fish?

What are the benefits of royal jelly (from bees)

Please explain the role of the sympathetic nervous system in the
gastrointestinal tract.

What is the difference between a submandibular salivary gland swelling
and swelling of a salivary lymph node?

How does Barrett’s oesophagus develop?

Is it recommended to treat asymptomatic endoscopically diagnosed
reflux oesophagitis with acid suppression and/or antireflux
measures?

Is it recommended to give a young patient, diagnosed endoscopically to
have mild reflux oesophagitis, life-long proton pump inhibitors (PPIs) to
prevent the development of Barrett’s oesophagitis?

Is it safe to give a patient with reflux oesophagitis who is on proton
pump inhibitors (PPIs) for treatment of acid suppression, aspirin in
antiplatelet doses (75–325 mg per day)?

Does a combination of magnesium and aluminium hydroxide salts,
taken as antacid for reflux oesophagitis, have serious long-term adverse
effects?

In the treatment of reflux oesophagitis with a proton pump inhibitor
(PPI), should the PPI be life long or given for 4–8 weeks, as mentioned by
the drug manufacturers?

Would a patient who suffers with reflux oesophagitis as a result of a
hiatus hernia, and who is not responsive to proton pump inhibitors
(PPIs), benefit from a highly selective vagotomy?

1. What are the causes of belching and what appropriate drug can be
used?

2. What are the effects of smoking on the gastrointestinal tract and what
is its role in peptic ulcer disease?

Dear authors, why are gastric ulcers more common along the lesser
curve, near the pylorus of the stomach?

What is the best time of day to administer omeprazole, and why?

Is it safe to use the drugs omeprazole and ranitidine during pregnancy?

Are non-steroidal anti-inflammatory drugs harmful to the stomach when
taken parenterally, for example by intravenous or intramuscular routes?

Is it safe to give a patient with a past history of bleeding peptic ulcer
aspirin in an antiplatelet dose of 75–325 mg?

Is sulpiride effective in the treatment of a peptic ulcer or
gastrooesophageal reflux disease (GORD)?

Is clopidogrel gentle on the stomach?

Is there a drug interaction between non-steroidal anti-inflammatory
drugs (NSAIDs) and proton pump inhibitors (PPIs)?

Do antacids enhance mucosal resistance in the gastric mucosa? If so,
please indicate the mechanism.

Is there a drug interaction between antacids and H2-receptor blockers?

Does the combination of aluminium and magnesium hydroxide, given
as an antacid, decrease the absorption of omeprazole if these are
co-administered to help relieve heartburn quickly?

Should proton pump inhibitors be used with caution in patients with
renal impairment?

Has cisapride been withdrawn from the market because of the danger of
ventricular fibrillation?

In peptic ulcer disease:

1. What are the indications for an upper gastrointestinal endoscopy?

2. As this is an invasive procedure, is an oesophagogastroduodenoscopy
(OGD) or barium meal X-ray preferable?

Is telithromycin as, or more, effective than clarithromycin in the
treatment of Helicobacter pylori? If so, what is the recommended dosage
and how long should treatment be continued?

Currently favoured regimens for eradication of Helicobacter pylori are
triple therapy with a proton pump inhibitor along with two antibiotics
for 1 week. For example:

● Omeprazole 20 mg metronidazole 400 mg and clarithromycin
500 mg (all twice daily).
● Omeprazole 20 mg clarithromycin 500 mg and amoxicillin 1 g (all
twice daily).

Resistance to amoxicillin has not yet been demonstrated.

Previously, regimens such as omeprazole, metronidazole, amoxicillin
and clarithromycin were recommended; are these regimens no longer used?

The reason behind this question is the ‘sky-high’ cost of clarithromycin in
Pakistan, which is inversely proportional to patient compliance (that is,
low-cost regimens tend to have a higher rate of compliance).

What is the difference between the management of a gastric and of a
duodenal ulcer?

How does omeprazole suppress Helicobacter pylori?

Does omeprazole cause rebound hyperacidity? Does this also apply to
H2-blockers?

On (K&C 7e, p. 249), you state that the postsynaptic neurotransmitter that
inhibits the relaxation of lower oesophageal sphincter (LOS) is nitric
oxide (NO). I have understood NO to promote relaxation of LOS by
acting on the non-adrenergic, non-cholinergic (NANC) inhibitory
neurones, which inhibits the action of cholinergic excitatory neurones.
Could you please explain this paradox?

It is stated that nitric oxide (NO) inhibits the relaxation of the lower
oesophageal sphincter (LOS) and that sildenafil is given for treating
achalasia. As far as I know, sildenafil acts to increase the guanine
monophosphate (GMP), just as NO uses the same mechanism to relax the
LOS. Could you explain this paradox?

In Kumar and Clark Clinical Medicine you mention that auscultation
is not important in cases of gastrointestinal disorders, but Harrison’s
Principles of Internal Medicine gives this as being of equal importance
because succussion splash and bowel sounds can help in presumptive
diagnosis. Succussion splash indicates gastric obstruction (e.g.
gastroparesis) and likewise bowel sounds can help determine the status
of developing ileus. Would you agree that this is therefore a diagnostic
tool?

Is it hazardous to give aspirin in the antiplatelet doses (75–325 mg/day)
to a patient with a past history of haematemesis proved to be from a
peptic ulcer?

How can upper gastrointestinal (GI) bleeding be distinguished from
lower GI bleeding by using faecal analysis?

In upper gastrointestinal bleeding, without knowing the cause or
source of bleeding, why do we give proton pump inhibitors (PPIs,
e.g. omeprazole)? What is the role of these, if the source of bleeding is
not peptic or duodenal ulcer?

Why is the incidence of coeliac disease increasing in many countries?

Are small amounts of gluten harmful to a patient with coeliac disease?

I refer to the treatment of complications related to diverticular disease.
Under ‘bleeding’ you mention that ‘Persistent bleeding can often be
arrested by undertaking an “instant” barium enema, which acts to plug
the offending diverticulum’. When I mentioned this to my consultant he
said he had never heard of this. Could you clarify how this would work
and where I could obtain more information?

In children with abdominal pain and fever, does a white cell count help
establish a diagnosis of appendicitis?

I have always been taught that ulcerative colitis only affects the
large bowel with some associated proctitis. I read in your chapter on
gastrointestinal disease that it can cause mouth ulcers and am now
confused

In pseudomembranous colitis, what is the first treatment of choice,
metronidazole or vancomycin?

Is Crohn’s disease considered as an autoimmune disease. If it is, are there
other predisposing factors to it other than genetics? If it is not, what is its
nature?

Why does carcinoma of the ascending colon cause more anaemia than
obstruction, and carcinoma of the descending colon more obstruction
features and less anaemia?

Can you explain why a patient with colorectal carcinoma might present
with diarrhoea and abdominal pain?

What causes the blood to be altered in the presentation of melaena: is it
intestinal juice?

What is the differential diagnosis of multiple rectal ulcers in an 18-yearold female?

What is the best surgical technique in a chronic (2–3 years) painful anal
fissure that is located sagittally posteriorly?

Can I make a diagnosis of irritable bowel syndrome (IBS) in a 40-year-old
female patient without doing gastrointestinal investigations?

What is the cause of abdominal bloating, which is often a symptom in
patients with irritable bowel syndrome (IBS)?

1. Where is the Traub’s area situated anatomically?

2. What does it mean if it is dull on percussion?

3. What is the proper way to percuss this area?

In general, it is claimed that only water and some salts are absorbed
in the large gut, whereas the small gut is practically free of bacteria
(which are present only in the large gut). In a patient on broad-spectrum
antibiotics, bleeding can occur as a result of vitamin K deficiency. If the
flora synthesizing vitamin K is disturbed, how can vitamin deficiency
occur when the large gut is not supposed to absorb? How can this be due
to a change in bacterial flora?

Why does colonic cancer more commonly occur on the left rather than
the right side of the colon?

How much more likely are patients with reflux oesophagitis to develop
cancer of the oesophagus than normal people and does aggressive
treatment with H2-blockers or proton pump inhibitors nullify this
increased risk?

In Crohn’s disease localized to the ileum there are long-term side effects
and pros and cons of drug therapy. Is ileal resection a better option
(if Crohn’s disease is localized to the ileum) than long-term medicine
therapy which risks complicating lymphoma of the ileum?

Please could you tell me the normal range of values for the liver function
test serum alkaline phosphatase. The only mention of the parameters is
that a reading of 1000  serious liver condition.

What is the best single test of liver function to exclude liver cell failure in
the routine work-up of a patient with early dementia?

How valuable is the measurement of the liver span in a physical
examination?

Why has the term ‘chronic liver disease’ replaced terms such as ‘chronic
hepatitis’? What exactly does this new term mean and what conditions
does it cover?

Can jaundice occur early in schistosomal hepatic fibrosis and, if so, how?

My patient has been found to have a serum bilirubin of 34μmol/L
(2 mg/dL) on three occasions. The other liver tests are normal. He tells
me he has Gilbert’s disease; how can I prove this?

Why is urinary urobilinogen increased in haemolytic jaundice? If the
bilirubin in this condition is unconjugated, how does it reach the terminal
ileum to be converted into urobilinogen?

How does cholestatic jaundice affect the kidney?

What is the mechanism by which cholestatic jaundice causes
bradycardia?

Are ‘jaundice’ and ‘icterus’ one and the same? I was taught that icterus
is yellowing of the sclera, while jaundice is yellowing of the skin and the
mucous membranes. As a result, carotenaemia can produce jaundice but
not icterus: is this so? I would be grateful if you would clarify this for me.

I am a third-year student nurse and am currently researching a case
study based on the biopsychosocial history of a patient who suffers from
chronic hepatitis C, which initially occurred as a result of injecting drugs.
I am confused about the biological effect of hepatitis: how exactly does it
affect the liver?

What are the admission criteria for a case of acute viral hepatitis?

I would like to know where I can find details on hepatitis B virus (HBV)
infection: chronic carrier, asymptomatic [normal liver function tests, HBV
DNA/real-time polymerase chain reaction (PCR)  240 copies/mL, core
less than 0.1]. Does a patient with such a profile need therapy or fine
needle aspiration (FNA) biopsy? What is the possibility of hepatocellular
carcinoma (HCC) in such a patient?

In chronic hepatitis B virus (HBV) infection, when anti-hepatitis B e
antibody (anti-HBe) develops (seroconversion), the antigen disappears
and there is a rise in alanine transferase (ALT). However, the graph in
your book (K&C 7e, p. 337, Fig. 7.16) seems to show a fall in ALT at this
point. Which is correct?

Interferon can be used in prophylaxis from hepatitis C after exposure.
Could you explain how this can be used, and what degree of success can
be expected as a result?

What is the latest recommended drug treatment for hepatitis C?

Can hepatitis C disease be treated in a carrier state completely by giving
interferon?

I am a carrier of hepatitis C (HCV) and am going to have antiviral
treatment soon. Are the side-effects of antiviral treatment for HCV bound
to occur? I am very worried.

Besides needle-pricks, how else is it possible to contract hepatitis C from
a hepatitis C (HCV)-positive patient? Are the patient’s skin/sweat (or
other bodily secretions) infectious?

What is the risk of infection with hepatitis C from blood splashed into
the eyes?

Hepatitis C (HCV): if results from the polymerase chain reaction (PCR)
examination are inconclusive, what does this mean? Should further
investigations be undertaken and, if so, will there be a risk of chronicity

In a patient with hepatitis C and autoimmune hepatitis, can
corticosteroids be prescribed for the autoimmune hepatitis?

We were told that the more vascular a structure is, the more antigen
(HLA/blood groups) matching is needed for transplantation, e.g. cornea
transplant needs no matching. However, the liver is a very vascular
organ; I don’t know why liver transplantation needs blood group
matching only but renal transplantation needs much more HLA
matching.

About steatohepatitis: please give me more information about the
occurrence of cirrhosis in such patients (non-alcoholic) and is there
any role and indication for lipotropic agents and hypocholesterolaemic
drugs?

I am working on non-alcoholic fatty liver disease (NAFLD) but I did not
find anything regarding it. Can you tell me about its relationship with
lipids?

Is NASH a valid term or not and what manifestation has it?

Is terlipressin better in controlling variceal bleeding than somatostatin?

Why is there a hyperdynamic circulation in cirrhosis?

Why is there an increased level of immunoglobulin G (IgG) in patients
with cirrhosis?

Cirrhosis of liver is reversible according to your book. What is the
progress and when will we be able to counteract the ‘tissue inhibitors
of metalloproteinases’ (TIMPs) and thus save the lives of our
patients?

What are the criteria for knowing the prognosis of cirrhosis (Child’s
criteria)?

What is the recommended treatment for cirrhosis of the liver?

Is there any role for liver dialysis in hepatic encephalopathy?

I have been asked to write an essay on ‘caring’ for a client who has been
an alcohol abuser for more than 10 years and is in the ‘recovery’ stage.
I am aware there are many different factors, such as length of abuse,
amount consumed, age, gender etc. . . .

My question is: how long will it take the liver to ‘recover’ or to
return to normal after stopping drinking?

I am especially interested in blood tests, fatty deposits and
gammaglutamyl transpeptidases (γ-GTs).

Can patients with liver cell failure suffer from myocardial infarction?

What is the definition of liver cell failure (decompensated liver
disease)?

Flapping tremors: why do we get flapping tremors and no other types of
tremor in liver failure? What is their mechanism and in which other
conditions do they occur?

In a patient with liver cell failure, can there be resting and action tremors
or parkinsonian features if it is confirmed that the patient does not have
Wilson’s disease?

Does the absence of any cirrhosis of the liver, together with normal liver
enzymes, in a 9-year-old boy complaining of chorea of a 5-year duration,
exclude Wilson’s disease?

Can Wilson’s disease be excluded in a patient complaining of movement
disorder for over 2 years, when there is an absence of cirrhotic liver change?

What drugs cause Budd–Chiari syndrome?

I recently saw a patient with pyrexia of unknown origin (PUO). He was
not particularly unwell and not jaundiced. But 1 week later he was found
to have a liver abscess on ultrasound. How can one make the diagnosis
earlier?

What is the most recent management of HCC (hepatocellular carcinoma)?
What is radiofrequency ablation? What is its role in the management of
HCC and its prognosis?

How do you differentiate haemorrhagic ascitic fluid due to malignancy
and accidental rupture of blood vessel while withdrawing the fluid?

Is there any place for the medical treatment of gallstones with
ursodeoxycholic acid?

n a case of common bile duct stones, where it is acknowledged that
spontaneous passage within 24 hours is observed in approximately 50%
of patients provided the stone is small, and that in these cases there is no
need for a sphincterotomy, is the use of antispasmodics, e.g. Buscopan
(active ingredient hyoscine-N-butylbromide), recommended? Surely these
will reduce the pain and improve the chance of a spontaneous release of
obstruction without surgical procedure?

What is sphincter of Oddi dysfunction?

I would like to know: what is the role of lysosomal hydrolases (cathepsin
B) in the pathogenesis of acute pancreatitis?

What is the role of octreotide in management of acute pancreatitis?

Why does paralytic ileus occur in pancreatitis?

How sensitive is the increase in serum lipase levels in the case of acute
pancreatitis?

What is the association between chronic pancreatitis and peripheral
vascular disease (PVD)?

Please, can you explain to us the mechanism of pancreatitis in
hypertriglyceridaemias?

Is there any role for chemotherapy in carcinoma of the pancreas?

1. How should portal hypertension be managed in patients with
bronchial asthma, where beta-blockers are contraindicated?

2. How should diuretics for these patients with hypertension be added?

Is cirrhosis a prerequisite for the development of hepatocellular
carcinoma (HCC) in hepatitis B (HBV)?

Should therapy with interferons in the treatment of hepatitis C (HCV)
and hepatitis B (HBV) commence when the polymerase chain reaction
(PCR) is positive, irrespective of serum glutamyl pyruvate transaminase
(SGPT) levels?

What is the degree of sensitivity of the CA19-9 as a marker of cancer in
the head of the pancreas?

What are the benefits and drawbacks of silymarin in the treatment of
liver cell failure? (This treatment is widely used in my country.)

If using zinc in the treatment of Wilson’s disease, should the salt used to
treat the disease be zinc acetate, or is any zinc-containing salt such as zinc
sulphate sufficient?

Is alkaline phosphatase of value in the differential diagnosis of jaundice?
If so, in what type is this raised?

What is favism?

What is the haemoglobin content of reticulocytes and how can this be
measured or determined?

We are told that an erythrocyte sedimentation rate (ESR) above
100 mm/h has a limited differential diagnosis, mainly vasculitis,
malignancy and granulomatous diseases. Could you explain whether
that applies to an ESR after one hour or two?

What causes a raised erythrocyte sedimentation rate (ESR)?

What are the causes of very raised erythrocyte sedimentation rate (ESR)?
I mean an ESR 100 mm/h. Is this test diagnostic in any disease besides
polymyalgia rheumatica and giant cell arteritis?

1. Does the erythrocyte sedimentation rate (ESR) rise with age?

2. Can an ESR of 50 mm/h in an 80-year-old female with no evidence of
systemic disease be considered normal?

1. What is a ‘normal’ erythrocyte sedimentation rate (ESR)? Is the
equation of a normal ESR  age  10, correct?

2. Would a normal ESR exclude a vasculitic cause in the case of stroke?

In which conditions is C-reactive protein (CRP) more informative than
the erythrocyte sedimentation rate (ESR)?

What is the management of an isolated high ferritin (without any signs,
symptoms or changes in the other blood investigations)?

Is the mean corpuscular volume (MCV) useful? What is the RDW and
when is it used?

What is the significance of renal disease with respect to anaemia, if any?

Can anaemia be a differentiating point between muscle wasting and
cachexia owing to another systemic disorder?

Anaemia of chronic disease does not respond to iron therapy, but there
are trials studying the use of iron and erythropoietin (EPO). Could you
tell me where to find more detailed information about these trials, and
whether there have since been any further developments?

Is the deoxyuridine test helpful?

The Schilling test is very rarely performed. Why is this?

There is no extramedullary haematopoiesis in aplastic anaemia, why?

Why is the anaemia in aplastic anaemia, macrocytic?

Is vitamin B12 absorbed passively from the jejunum?

What role does ‘R’ binder play in the absorption of vitamin B12?

In pernicious anaemia, investigation of the serum shows an elevated
level of gastrin. Why is it so?

1. Please explain the term Coombs’ positive (direct and indirect) and
negative haemolytic anaemia.

2. What are the principles of the Coombs’ test?

How often is Aldomet (alpha methyldopa) associated with autoimmune
haemolytic anaemia or hepatitis? Is a normal person, with a positive Coombs’
test owing to previous treatment with this drug, safe to donate blood?

What is the mechanism of priapism in sickle-cell anaemia?

Is sickle-cell disease associated with any of the glomerular disorders?

What is the acute chest syndrome?

Patients with thalassaemia intermedia have recurrent leg ulcers and
recurrent infections. What is the mechanism of this?

What is the mechanism of iron absorption from iron polymaltose
complex and carbonyl iron?

Iron overload in patients with thalassaemia major should be checked by
measuring the serum ferritin and hepatic iron stores. How are the hepatic
iron stores measured? By liver biopsy? And does not the measurement of
serum ferritin suffice?

In the investigation for paroxysmal nocturnal haemoglobinuria (PNH),
are the sucrose haemolysis test and Ham’s acid serum test commonly
done? What are the principles behind these tests?

Why isn’t the blood of polycythaemia vera patients, after repeated
phlebotomies, used for transfusion purposes? Although it is a
premalignant condition, the red cells do not contain a nucleus and thus
transfusion of only pure red blood cells (RBCs) would be a great benefit.

What investigations are necessary to exclude secondary polycythaemia?

What is the management plan in a patient with secondary polycythaemia
presenting with transient ischaemic attacks (TIA)?

Why do patients with polycythaemia vera have a tendency to bleed, even
though 50% of them have an elevated platelet count?

In hyposplenic patients, what precautions are necessary for patients who
intend to travel to Saudi Arabia for the Haj?

What is the mechanism of development of splenomegaly in chronic
leukaemia?

In idiopathic thrombocytopenic purpura (ITP), thrombocytes are mainly
destroyed in the spleen owing to an immune mechanism. Why, therefore,
is there no splenic enlargement as there is with other diseases?

Where exactly is the Traub’s space? How exact is the percussion of the
Traub’s space as a sign indicating the size of the spleen?

Can you please tell me the indications and complications of blood
transfusion.

Several times I have read the phrase ‘white blood cells elevated with a
left shift’. I am wondering what ‘left shift’ or ‘left deviation’ stands for.

What is the clear definition of ‘bleeding time’ and ‘clotting time’? And
what are the applied differences between them?

What is the meaning of the international normalized ratio (INR) blood test?

What is the cause of moderate thrombocytopenia in Bernard–Soulier
syndrome? It is a qualitative defect not a quantitative platelet disorder.

What is new about thrombopoietin?

What is the rationale behind the use of desmopressin in bleeding
disorders?

What effect does the contraceptive pill have on the blood fibrinogen level
and on blood coagulability?

Does standard (unfractionated) heparin in doses of 10 000–15 000
units/day need monitoring?

Is there an antidote for low-molecular-weight heparin (LMWH)? Can
Enoxaprin be used?

1. What is the mechanism of the action of aprotinin?

2. What is the therapeutic window for aprotinin?

3. In a case of haemorrhagic stroke, how many days should aprotinin be
prescribed for and what is the recommended dosage?

My question is, what are thrombophilia scan tests? Can we use these in
patients on anticoagulant therapy?

In thromboembolic disorders, how is clopidogrel superior to aspirin?

What are the definitions for prothrombin time (PT) and partial
thromboplastin time (PTT), and how are they different?

1. Why, in chronic disease anaemia, are serum iron and the total ironbinding capacity (TIBC) low?

2. Why, in sideroblastic anaemia with increased levels of serum iron, is
the TIBC normal?

What is the red cell distribution width (RDW) value above which
anisocytosis can be diagnosed?

Is anisocytosis diagnostic of iron deficiency anaemia?

In the case of a patient who has been treated with streptokinase and has
bleeding complications in the form of haematemesis, haemoptysis or
similar, how can the effect of streptokinase on the coagulation system be
reversed, and can tranexamic acid help?

We know that salmonella infection is a common complication in patients
with sickle cell anaemia. Is this true for patients with thalassaemia major
and, if so, why?