Abdomen Cases

Chronic Liver Disease

Q) What investigations would you request for this patient?
1. Routine Bloods:
● FBC: anaemia, thrombocytopaenia.
● U&Es: deranged electrolytes as a risk for decompensation, monitoring therapy if
on diuretics, risk of hepatorenal syndrome.
● LFTs (+ albumin to assess liver synthetic function).
● Clotting (INR): to assess liver synthetic function, and prior to ascitic taps.
● ESR, CRP: for infectious causes.
● Glucose: there is risk of hypoglycaemia, hemochromatosis is associated with diabetes.
2. Ascitic tap:
● For white cell count with differential, albumin and total protein, MC&S, cytology.
− SBP: neutrophil count >250 per ml.
− Serum albumin- ascites fluid albumin (SAAG): used to differentiate between:
o Transudative ascites (> 11g/L).
o Exudative ascites (< 11g/L).
3. Imaging:
● USS abdomen:
− It is used to assess liver and spleen size; look for cirrhosis, liver masses,
ascites; and assess portal pressures).
− Surveillance for HCC involves: 6-months AFP and abdominal USS.
4. If cirrhotic liver:
a) Liver screen blood tests:
− Virology (HBV/HCV).
− Autoimmune screen: ANA, anti-mitochrondrial antibodies, Anti-LKM
antibodies.
− Caeruloplasmin and 24 urinary copper level (for Wilson’s disease).
− Ferritin and transferrin saturation (for Hemochromatosis)
− AFP (for hepatocellular carcinoma).
− Alpha-1-antitrypsin.
b) Imaging:
− Endoscopy: surveillance for oesophageal varices.
− MRCP: It can could be done prior to ERCP if there are features of
obstruction on USS to rule out sclerosing cholangitis (PSC).
c) Liver biopsy (for staging and diagnosis).
Model answer:
- To investigate this patient further, I would like to send blood tests with a focus on assessing
the liver synthetic function and enzyme profile and include a screen for the possible causes
of chronic liver diseases (listed above).
- Send ascitic tap sample for cytology, microbiology and biochemistry (if ascites present).
- An abdominal ultrasound could confirm the presence of cirrhosis, focal liver
lesion, splenomegaly and ascites; whilst an endoscopic examination could confirm varices.
- A liver biopsy may be required to confirm or stage the disease in certain causes.
 Q) How would you manage this patient?
1. General measures:
● Education and counselling. Advice to stop alcohol, avoid hepatotoxic agents.
● Vaccination (against hepatitis A and B, pneumococcal and annual influenza).
● Refer to dietician, optimise nutrition, and salt restriction and vitamins
replacement.

2. Treatment the underlying disease if possible:

● NAFLD: Weight loss, bariatric surgery, diet control, diabetes control with GLP1, statin.
● Viral hepatitis: antiviral medications.
● Autoimmune hepatitis: immunosuppressive medications.
● Hemochromatosis: Venesection, iron chelators (desferrioxamine).
● Wilson’s disease: Avoid high copper-containing food, copper chelation (penicillamine).
● PBC: fat-soluble vitamins, ursodeoxycholic acid (improves LFTs), cholestyramine (pruritus).

3. Management of long-term complications

a- Medical therapy:
● Diuretics if ascites and oedema is present.
− Spironolactone: start with 100mg OD uptitrated to 400mg OD.
− Loop diuretics: can be added if further diuresis is still required.
o Aiming to achieve approximately 1kg of weight loss per day
with careful monitoring of renal function and electrolytes.
● Prophylactic agents:
− Propranolol if oesophageal varices is present.
− Prophylactic antibiotics following SBP.
− Rifaximin of experienced hepatic encephalopathy.
− Regular laxatives to avoid encephalopathy (aiming for 2 soft
stools/day).

b- Surgical/procedure options include:

● Serial therapeutic paracentesis.
● Trans-jugular intrahepatic portosystemic shunt (TIPS): this increases the
risk of encephalopathy.
● Liver transplant.

Model answer:
- Managing this patient would requires education and counselling, advice to cease alcohol or drug
abuse if relevant, vaccination against hepatitis A and B, and referral to a dietician to advise on low
salt diet.
- If possible, the underlying disease should be treated, and long term complications managed such
as diuretics and elective paracentesis for ascites, antibiotics as per local guidelines for SBP followed
by antibiotic prophylaxis, laxatives aiming for 2 soft stools a day, beta blockers if varcies are
present, and rifaximin if they’ve experienced encephalopathy.
- Surgical options include transjugular intrahepatic portosystemic shunt formation, although this
increases the risk of encephalopathy; or liver transplant if they meet eligibility criteria.
Q) What are the causes of chronic liver disease (or
cirrhosis)?

Mnemonics: MAANDI
The most common cause of CLD in
1- Metabolic: the United Kingdom are:
a. Haemachromatosis.
• Alcoholic liver disease.
b. Alpha1 Antitrypsin deficiency • Non-alcoholic liver disease.
c. Wilson’s disease. • Chronic viral hepatitis
d. Cystic fibrosis. (HBV, HCV).
2- Autoimmune:
a. Primary Biliary Cirrhosis {(PBC)
b. Primary Sclerosing Cholangitis (PSC)
c. Autoimmune hepatitis
3- Alcohol.
4- Non-alcoholic steatohepatitis.
5- Drugs:
a. Methotrexate
b. Isoniazid
6- Infectious: viral (HBV, HCV).

Q) What are the complications of CLD?

1- Portal hypertension, lead to: Mnemonics: ABCDE-ST
a- Esophageal varices / bleeding. • Ascites
b- Ascites. • Bleeding (variceal)
c- Hypersplenism/thrombocytopenia • Carcinoma (hepatocellular)
2- Liver dysfunction, leading to: • Different organ involvement
a- Coagulopathy (hepatorenal syndrome)
b- encephalopathy. • Encephalopathy
c- Hypoalbuminaemia • Spontaneous bacterial peritonitis
3- Infections (spontaneous bacterial peritonitis "SBP") • Thrombosis of the portal vein
4- Hepatocellular carcinoma

Q) What are the causes of decompensation in CLD?

1. Infection. Signs of decompensation of CLD
2. Spontaneous bacterial peritonitis. Mnemonics: JASE
3. Electrolyte disturbance (Hypokalaemia) • Jaundice
4. Gastrointestinal bleeding. • Ascites
5. Drugs (sedatives), alcohol. • Splenomegaly
6. Constipation. • Encephalopathy.

Q) What predictive models do you know for determining severity and the
prognosis in CLD?
• The most commonly used models are:
1- Child–Pugh classification, which considers ascites, encephalopathy, INR, PT, bilirubin.
2- MELD score (model of end-stage liver disease), especially for possible candidates
for liver transplant.
 Liver Transplant
Q) How would you want to approach this patient?
Model answer:
− History: I would like to obtain a detailed history of the patient’s symptoms, including past
medical and drug history.
− Bedside: I would like to get a full set of bedside observations and to review the fluid chart.
− Investigations:
- I would like to do urine dipstick and send blood tests including, urea and electrolytes, liver
function tests (including albumin & INR), inflammatory markers, bone profile, lipids,
HbA1c and immunosuppressant levels.
- I would like to review any recent ultrasound imaging and biopsy results in records.

Q) How would you manage this patient?

• Patient requires regularly within an MDT that includes input from doctors, specialist
transplant team, psychologists and pharmacists; in order to assess graft function and
complications of therapy including increased risk of neoplasia and cardiovascular disease.
• I would ensure he/she is educated regarding:
1- Healthy diet and exercise
2- Avoidance of alcohol and smoking
3- Importance of medication compliance
4- Regular vaccinations (against hepatitis B, pneumococcal vaccines, COVID19)
5- Attendance at cancer screening programmes,
6- Avoiding over the counter or herbal remedies without seeking specialist advice
(i.e.: no P450 inhibitors if on sirolimus/tacrolimus/cyclosporine, Avoid NSAIDs),
7- I would advise to seek urgent specialist advice if there was evidence of graft
dysfunction.

Q) What features in chronic liver disease would warrant consideration of

transplantation?

1- Progressive jaundice
2- Diuretic-resistant ascites,
3- Hepatocellular carcinoma.

Q) What risk scores can be applied to stratify short-term prognosis in those

with chronic liver disease awaiting transplant?

• MELD (model for end-stage liver disease) score gives an indication of prognosis
without liver transplantation.

Q) What chronic liver conditions can recur post-transplant?

1- Hepatitis B and C. 3- Primary biliary cirrhosis.

2- Hepatocellular cancer. 4- Budd-chiari syndrome.
Q) What conditions would you think If there are scars of
both liver and renal transplants?

1- Initial liver transplant, and then developed renal failure secondary to calcineurin
inhibitor use.
2- Hepatitis C with cryoglobulinaemia.
3- Polycystic diseases (ADPKD, VHL).
4- Hepatorenal syndrome.
5- Paracetamol overdose can sometimes affect the liver and kidneys.

Q) What criteria are used to decide on liver transplantation in the emergency

setting?

• King’s College Criteria are used for super-urgent listings on the liver transplant
waiting lists (See criteria below).

1- Acute fulminant liver failure (Paracetamol overdose, Non-paracetamol ALF).

King’s College criteria for urgent referral:

2- Decompensated CLD with cirrhosis (progressive jaundice, diuretic resistant ascites).

3- Compensated cirrhosis (child Pugh class B and C) with MELD score more than 15.

4- HCC if fulfil following criteria:

- if one lesion less than 5 cm
- or maximum three lesions the sum of all less than 3cm with no vascular invasion.

5- PBC or PSC if fulfil following criteria:

- Refractory itchiness.
- Serum bilirubin > 100.
- Encephalopathy.
 Polycystic Kidney Disease
Q) What investigations would you request for this patient?

Urine: MCS and cytology.

Blood: Full haematological and biochemical profile, U&E, and bone profile.
Imaging: US, IVU, CT, and MRI.
Further tests: EPO and haematinics. • ADPKD1 in chromosome 16
Genetic studies. • ADPKD2 in chromosome 4

Q) How would you manage this patient?

Medical: Treatment of hypertension, hyperlipidaemia, infection, and pain.

Surgical: RTT +/- nephrectomy, nephrectomy alone (for recurrent complications).
Non-pharmacological: Education, support groups, genetic counselling, family screening, and
screen for associated conditions (ICA).

Causes of unilateral
enlargement
• Polycystic kidney disease
• Renal cell carcinoma
• Simple cysts
• Hydronephrosis
Discussion
Causes of bilateral enlargement Possible complications of
• Polycystic kidney disease. APKD
• Bilateral renal cell carcinoma. Mnemonics: CA3MP
• Bilateral hydronephrosis. Cysts (liver).
• Tuberous sclerosis Anaemia.
(angiomyolipomata and cysts). Abdominal pain.
• Von Hippel Lindau. Aneurysms in brain.
• Amyloidosis. Mitral valve prolapse.
Polycythaemia.

Diagnostic criteria in people with positive family history of ADPKD

 Model presentation

- The patient presented with abdominal pain and was found to have bilateral flank
masses on abdominal examination. These masses are ballotable, indicating the
possibility of fluid-filled cysts. Percussion notes above the masses were resonant. The
clinical findings are consistent with adult polycystic kidney disease (APKD). There is
no evidence of renal replacement therapy (RRT) such as arteriovenous fistulas,
tunnelled catheters, peritoneal dialysis, or transplanted kidneys. No hepatomegaly is
observed, suggesting the absence of hepatic cysts. The patient is euvolemic and does
not exhibit signs of anaemia or uraemic flap on outstretched hands.
- I would like to complete my examination by looking at the observation chart, check
the blood pressure, perform a urine dip and a complete cardiovascular and
neurological examination to search for extra-renal complications of her condition.
- The pain she presented with today may be due to intra-cyst haemorrhage or
infection, and I would like to investigate further for that.
 Renal Transplant and Dialysis
Q) What investigations would you request for this patient?

Routine tests:
• Urine dipstick (blood, protein, glucose)
• Blood pressure (Evaluated)
• Finger prick glucose (Evaluated)
• ECG (saddle-shaped ST elevation and PR depression)
Bloods:
• FBC (anaemia).
• U&Es (creatinine, urea and potassium may be high).
• Bone profile (hypo or hypercalcaemia, hyperphosphatemia).
• Glucose and HbA1C (raised).
• Iron stores/B12/folate (need to be adequately supplemented to optimise Hb).
• EPO (to determine if EPO).
• Vitamin D (low).
• PTH (high in secondary or tertiary hyperparathyroidism).
Imaging: USS renal tract +/- doppler studies (stenosis, obstruction, thrombosis, leaks).
Renal biopsy.

Model answer:
- To investigate this patient further, I will conduct a series of routine tests to further
investigate the case, including a urine dipstick test, blood pressure measurement,
finger prick glucose test, and electrocardiogram (ECG).
- Blood tests will involve a full blood count (FBC), urea and electrolyte (U&Es) testing,
bone profile evaluation, glucose and HbA1C tests, and assessment of iron stores, B12,
folate, EPO, vitamin D, and PTH levels.
- An ultrasound of the renal tract may be performed, and a renal biopsy could be
considered if necessary.
Q) How would you manage this patient?

General management:
• Smoking cessation.
• Dietary restrictions on sodium and potassium.
• Avoid alcohol consumption.
• Avoid excessive sun exposure.
• Avoid live vaccines.
Medical:
• Review the potential drug interactions.
• Sodium bicarb and loops for hyperkalemia.
• Sodium bicarb for acidosis.
• Phosphate binders for renal osteodystrophy.
• IV iron and/or EPO.
• Vitamin D supplementation and replace haematinics.
Surgical:
• Parathyroidectomy.

Model answer:
- The general management of renal failure involves lifestyle modifications such as
smoking cessation, dietary restrictions on sodium and potassium intake, limiting
alcohol consumption, minimizing sun exposure, and avoiding live vaccines. From a
medical standpoint, a thorough review of medications is necessary to ensure safety
and avoid interactions.
- Treatment approaches for specific complications include using sodium bicarbonate
and loop diuretics for hyperkalemia, phosphate binders for renal osteodystrophy, and
sodium bicarbonate for acidosis. Supplementation with vitamin D and replacement of
hematinics like iron may be required. In some cases, IV iron and/or EPO therapy may
be considered.
- Surgical intervention in the form of parathyroidectomy may be recommended for
complications related to hyperparathyroidism.

Q) What are the commonest causes of renal transplant in the UK?

Diabetes mellitus. Glomerulonephritis

Hypertension Polycystic kidney disease (ADPKD)

Q) What are common immunosuppressant medications in renal transplant?

Prednisolone Tacrolimus
Sirolimus Cyclosporin
Mycophenolate

Q) What are the indications for urgent dialysis?

Mnemonic: AEIOU
• Acidosis
• Electrolyte abnormalities (Refractory hyperkalaemia)
• substance Intoxication
• volume Overload
• Uremic symptoms or encephalopathy
Q) What are the complications of renal transplantation?
• Rejection: acute or chronic
• Infection secondary to immunosuppression: Success of renal transplantation
o Pneumocystis carinii • 90% 1-year graft survival
o CMV • 50% 10-year graft survival
• Increased risk of other pathology:
o Skin malignancy
o Post-transplant lymphoproliferative disease
o Hypertension and hyperlipidaemia causing cardiovascular disease
• Immunosuppressant drug side effects/toxicity:
o Ciclosporin and tacrolimus: Nephrotoxicity.
o Steroids: Cushingoid symptoms.

Q) Forms of renal replacement therapy.

1- Haemodialysis via AV fistula 2- Haemodialysis via venous catheter

3- Peritoneal dialysis

Example presentation:

- This middle-aged female patient is diagnosed with end-stage renal failure, most likely
due to diabetic nephropathy, indicated by finger prick glucose testing marks and the
presence of insulin at the bedside. Other possible causes considered include
hypertensive nephropathy, glomerulonephritis, autosomal dominant polycystic
kidney disease, obstructive and renovascular disease. She currently has a functioning
renal transplant in the right iliac fossa, with previous renal replacement therapies
including an AV fistula in the right forearm and peritoneal dialysis catheter insertion
scars on the abdomen. Complications of immunosuppression, such as Cushingoid
body habitus, gum hypertrophy, and dysplastic skin lesions, are also present.
- To further investigate the patient, a comprehensive set of bedside observations and a
review of the fluid balance chart would be performed. Key blood tests of interest
include hemoglobin, urea, creatinine, electrolytes, bone profile, lipids, and HbA1c.
Recent ultrasound imaging of the renal tract and renal biopsy results would also be
reviewed. Regular follow-up is necessary to monitor graft function and assess for
complications, particularly the increased risk of cardiovascular and neoplastic
diseases. Collaboration within a multidisciplinary team (MDT) involving the GP,
specialist nurse, psychologists, and renal pharmacists is essential.
- Patient education regarding a healthy diet, exercise, smoking cessation, reducing sun
exposure, medication compliance, and the avoidance of over-the-counter or
alternative therapies without specialist advice is crucial. Vaccination against hepatitis
B and pneumococcus is recommended, while live vaccines and contact with
individuals with infections like chickenpox should be avoided. Immunosuppression
typically involves steroids, calcineurin inhibitors, and sirolimus. Urgent specialist
advice should be sought if there are signs of deteriorating graft function.
 Splenomegaly

Q) What investigations would you request for this patient?

First: Ultrasound
For haematological causes:
• FBC, blood film
• CT CAP
• Bone marrow aspirate
• LN biopsy

For infectious causes:

• Thick and thin films
• Viral serology

What are the causes of hepatosplenomegaly?

Massive splenomegaly (>8cm):

• Myeloproliferative disorders (CML, myelofibrosis, and polycythemia vera)
• Infections (malaria, visceral leishmaniasis: kala-azar)
Moderate splenomegaly (4–8cm):
• Myelo/lymphoproliferative disorders
• Infiltration (Gaucher’s and amyloidosis)
Tip splenomegaly (<4cm):
• Myelo/lymphoproliferative disorders
• Portal hypertension
• Infections (EBV, infective endocarditis and infective hepatitis)
• Felty’s syndrome
• Haemolytic anaemia

Q) What are the indications for splenectomy?

Traumatic injury: Rupture spleen.

Haematological diseases: (ITP, hereditary spherocytosis, and thalassemia major)

Q) What precautions can be implemented to individuals after splenectomy?

• Vaccination against (Pneumococcus, Meningococcus, and H. influenzae).

• Prophylactic penicillin.
• Medic alert bracelet.
• Seek medical attention early in infection.
 Craggy Hepatomegaly
Q) What investigations would you request for this patient?

• Bedside urine dipstick test: for hematuria (ADPCKD).

• Bloods: Full Blood Count (FBC), Liver Function Tests (LFTs), International Normalized
Ratio (INR), Electrolytes and Renal Function Tests (U&Es), ESR/CRP, virology
screening, and serological examination for echinococcus.
• Imaging: Abdominal USS (identify any mass lesions, assess for cirrhosis, cystic
lesions, and lymphadenopathy), CT CAP (to stage the condition and identify potential
biopsy sites).
• Special tests: Biopsy (If the diagnosis remains uncertain or cancer is suspected after
hydatid cysts excluded).

Q) What are the commonest causes of HCC?

1- Chronic liver disease:

• Chronic hepatitis B and C
• Alcoholism
• Hereditary haemochromatosis
• Primary biliary cirrhosis
2- Aflatoxins

Q) What primary sites metastasise to the liver?

GI tumor: stomach, pancrease, colon.
Others: lung, breast, ovarian and melanomas.
References:
- Hirschfield GM et al. Adult liver transplantation: what non-
specialists need to know. BMJ 2009. 338: b1670.
- Siddiky A et al. Management of arteriovenous fistulas. BMJ. 2014; 349.
- Thiruchelvam P et al. Renal Transplantation. BMJ. 2011; 343.
 Cardiology Cases
Absent Radial Pulse
Q) What are the causes of this condition?

If Symmetrical: (low output states e.g. Heart failure)

If Asymmetrical:
1. Anatomical
Congenital Malformation (coarctation of aorta) \ external compression proximally \
Masses \ Lymphadenopathy \ Unusual anatomic course \ Aortic dissection.
2. Iatrogenic
Local trauma by cannulation or ABG \ Previous surgical intervention (cardiac defects
repair).
3. Embolism (with Atrial Flutter)
4. Atherosclerosis (Associated with obesity, smoking, Hypertension, DM)
5. Vasculitis (Giant cell arteritis \ Takayasu’s arteritis)

Q) What investigations would you order for a patient with this condition?

Imaging:
• USS Doppler (sites of obstruction \ point to inflammation by showing wall edema)
• MR Arch Aortogram (if suspected proximal obstruction such as subclavian stenosis).

Q) What is subclavian steal phenomenon?

Obstruction or stenosis of subclavian artery proximal to origin of vertebral artery →

increased demand pulls blood from contralateral vertebral artery through their anatomical
connection → this diverts blood away from brain → Neurological symptoms + arm
claudication on use.
 Aortic Regurgitation
Q) What are the classic diseases associated with this condition?

• Mixed valve disease (Aortic stenosis).

• Connective tissue disorders
Marfan Syndrome (hypermobility, tall person, arachnodactyly).
Ehlers-Danlos Syndrome (hypermobility, hyperextensible skin, fish mouth scars).
Osteogenesis Imperfecta (blue sclerae, bony deformities).
pseudoxanthoma elasticum (plucked chicken skin appearance).
• Ankylosing Spondylitis (increased thoracic kyphosis with loss of lumbar lordosis and
compensatory extension and movement limitation of neck).
• Infective Endocarditis (Anemia, nail-bed hemorrhage, emboli, Osler nodes, Janeway
lesions, fever, ….).
• Syphilis (Argyll Robertson pupil).

Q) What investigations would you order for a patient suspected with this
condition?

• Bedside tests: Measure blood pressure (wide pulse pressure), ECG (LV hypertrophy,
conduction blocks), Temp. (↑ if IE), Urine dipstick (hematuria and proteinuria if IE),
Fundoscopy (Roth spots and retinal pulsations if IE).
• Blood: CBC (Anemia), CRP\ESR (↑if IE), Treponemal tests (specific {EIA \ TPHA} or non-
specific {VDLR \ RPR}).
• Imaging: Chest radiograph (Pulmonary edema, Pleural effusion), Echo (LV function,
valve anatomy and root size, vegetations).

Q) What is the management of this condition?

• Education.
• Pharmacological: Treat resultant HF + treat underlying cause (antibiotics for IE \
penicillin for syphilis).
• Surgical: Valve replacement regardless of symptoms severity to avoid LV dysfunction.

Austin flint murmur: Corrigan’s sign:

A mid-diastolic murmur at the Abrupt distension & quick
apex in a pt in w/ AR collapse of carotid a on pulsation

Q) what is its differential diagnosis of Corrigan’s sign?

• It is seen in Hyperdynamic circulation causes (e.g., PDA, sepsis, thyrotoxicosis,

anemia) and rarely in coarctation of aorta.
• Large jugular pulse will mimic this sign (pulsations within the venous system will not
be palpable and can be obliterated by pressure.)
Q) What are the indications for valve replacement?
Signs of severity:
Acute AR Complicated by HF • HF symptoms
Asymptomatic with: • Wide pulse pressure
• aortic root diameter >50mm or LVESD =55mm or EF • Austin Flint murmur
<50%. • Soft S2

Q) How would you monitor a patient with Marfan syndrome?

• Monitoring of aortic root size with annual transthoracic echo.

• β-blockers and angiotensin receptor blockers to slow aortic root dilatation.
• Surgical referral for pre-emptive aortic root surgery to prevent dissection and aortic
rupture when root is >5cm.
• Eye referral if necessary for Iridodonesis.
• Screen family members.

Q) How can you differentiate homocystinuria from Marfan’s?

Marfan> Autosomal dominant, associated with aortic root Marfan:

disease, lens dislocates upward and laterally. • Autosomal dominant
• Fibrillin-1 defect.
Homocystinuria> Autosomal recessive, associated with mental • Complete penetrance
retardation and thromboembolic events, lens dislocates • Variable phenotype
downward and medially.
 Aortic Stenosis
Q) What are the classic diseases associated with this condition?

• Co-arctation of aorta and bicuspid aortic valve (might be accompanied by physical

features of Turner’s syndrome or neurofibromatosis).
• Heyde’s syndrome: aortic stenosis, angiodysplasia, anemia.
• Williams syndrome: supravalvular aortic stenosis, Elfin facies, intellectual disability.

Q) What is the differential diagnosis? Causes of AS:

Congenital: Bicuspid valve
Acquired: age (senile degeneration and
• HOCM calcification); streptococcal (rheumatic)
• VSD, ASD
• Mitral regurgitation, Pulmonary stenosis
• Aortic sclerosis: normal pulse character and no radiation of murmur
• Aortic flow: high output clinical states e.g. thyrotoxicosis or anemia

Q) What investigations would you order for this patient?

• Bedside tests: ECG (LV hypertrophy, conduction problems), Temp. (↑if IE), urine dipstick
(haematuria if IE), Fundoscopy (Roth spots if IE).
• Imaging: CXR (cardiomegaly, pleural effusions, pulmonary edema, calcified valve, aortic
dilatation, exclude other diagnosis), Echo (confirm diagnosis, assess severity of valve
stenosis and LV dysfunction).
• Coronary angiography (exclude CAD and assess need for CABG to be done along with
valve replacement).

Q) What is the management of this condition?

• Asymptomatic > education, dental care, regular check up with echo.

• Symptomatic
⚬ Surgical
⚬ Aortic valve replacement +/− CABG
⚬ Percutaneous
⚬ Balloon aortic valvuloplasty (BAV)
⚬ Transcutaneous\Transfemoral aortic valve implantation (TAVI)
⚬ Medical
⚬ Manage co-existing CVS complications as HF.

Q) What would indicate severe AS clinically?

Narrow pulse pressure, soft S2, presence of S4, palpable thrill, late peak of murmur, and bi-
basal crepitations on auscultation of the lungs.

Life expectancy for each presentation of AS:

Angina >> 50% mortality at 5 years
Syncope >> 50% mortality at 3 years
Breathlessness >> 50% mortality at 2 years
Q) What are the complications of this condition?
LE2A2P

LV failure, Endocarditis, Emboli, Anaemia, Arrhythmias, Pulmonary hypertension.

Q) What are the indications for valve replacement in aortic stenosis?

Symptoms of angina/dyspnoea/syncope or EF <40% or pressure gradient >50mmHg.

Q) What are the causes of a pan systolic murmur at the apex in a patient in
whom you suspect aortic stenosis?

• Co-existent mitral valve disease (e.g.: rheumatic heart disease)

• Gallavardin phenomenon

Q) What is Gallavardin phenomenon?

A clinical sign found in patients with aortic stenosis described as dissociation of the murmur
of aortic stenosis, with the harsh bit heard at the aortic area and the musical bit transmitted
through to the apex.

Q) What is the effect of atrial fibrillation on JVP and the heart sounds?

• Absent ‘a’ wave in the JVP.

• No fourth heart sound to auscultation.

Key features of Williams syndrome:

• Autosomal dominant.
• Microdeletion of genes on chromosome 7.
• Hypercalcaemia and supravalvular aortic stenosis and intellectual disability.
• Short stature, depressed nasal ridge, prominent lips and small chin (elfin
facies).

Duke’s criteria for infective endocarditis

Major:
• Typical organism in two blood cultures
• Echo: abscess*, large vegetation*, dehiscence*
Minor:
• Pyrexia >38°C
• Echo suggestive
• Predisposed, e.g. prosthetic valve
• Embolic phenomena*
• Vasculitic phenomena (ESR↑, CRP↑)
• Atypical organism on blood culture
Diagnose if the patient has 2 major, 1 major and 2 minor, or 5 minor criteria.
Example presentation:

- During the patient assessment, I conducted various examinations. These included

measuring the patient's blood pressure and palpating their peripheral pulses, with a
focus on radio-femoral delay. Additionally, I performed assessments to identify
potential features of infective endocarditis, such as measuring the patient's
temperature, conducting a urine dipstick test to check for proteinuria and hematuria,
and performing a fundoscopy to look for Roth Spots.
- Underlying causes include degenerative aortic valve disease, bicuspid valve, and a
history of previous rheumatic fever. To gather more information, a detailed history
will be taken, focusing on symptoms like syncope, angina, and dyspnea. An
electrocardiogram will be performed to assess for left ventricular hypertrophy, left
axis deviation, and conduction abnormalities. Blood tests will evaluate hemoglobin
levels, cardiovascular risk factors (lipids, HbA1c), and renal function.
- The imaging modality of choice is an echocardiogram to assess valve area, gradient
(>40mmHg indicating critical aortic stenosis), accompanying valve lesions,
vegetations, and left ventricular function.
- Management involves counseling the patient, optimizing co-morbidities (such as
heart failure and hypertension), and cautious use of medications reducing afterload
(e.g., ACE inhibitors, GTN). Surgical options include open surgery for mechanical or
biological valve replacement, or transcatheter aortic valve implantation (TAVI).
Regular follow-up visits are emphasized.
 Aortic Valve Replacement
Q) What are the classic indications for aortic valve
replacement? Valves affection with IE:
1- Mitral
Rheumatic heart diseases. 2- Aortic

Q) What further investigations would you order for this patient?

§ Bedside tests: ECG (conduction abnormalities, LVH criteria), urine dipstick (proteinuria
and hematuria if IE), fundoscopy (Roth spots if IE).
§ Blood: FBC (anaemia), INR, CRP/ESR (infective endocarditis).
§ Imaging: CXR (heart failure), ECHO (valve and ventricular function).

Q) What are the complications of this procedure?

• Early:
Infective endocarditis, failure of the procedure (valve displacement).
• Late:
Infective endocarditis, heart failure, thromboembolus, bleeding (anticoagulants side
effect), hemolysis (and subsequent Jaundice).

Q) What are the common organisms associated with Infective endocarditis?

• Bacterial
Staph aureus (typically in tricuspid valve in IV drug users), Staph epidermidis (Early IE
(<2/12 post-op from skin), Strep viridans (late IE from hematogenous spread), HACEK
organisms.
• Fungal: Candida.

Q) Differentiate between the types of Prosthetic valves?

Valve type Indications Pros Cons

Bioprosthetic Aortic >65 years No need for Calcified after a
Mitral >70 years long-term while
anticoagulants
Mechanical Young Better durability Demand life-long
On warfarin, anticoagulant
e.g., for AF therapy
 Atrial Septal Defect
Q) What are the classic diseases associated with this condition?

Holt Oram Syndrome: upper limb deformities, ASD, heart block.

Down’s Syndrome: Short stature, low set ears, epicanthal folds, endocardial cushion defect.
Turner’s Syndrome: Female, short stature, webbed neck.
Iatrogenic: During balloon mitral valvuloplasty.

Q) What are the types of septal defects in atria?

Ostium primum ASD (associated with Down syndrome, may involve mitral valve causing MR)
Ostium secundum ASD (most common)
Patent foramen ovale (unfused septa, no Eisenmenger’s).

Q) What are the complications of ASD?

RV dilatation (Eisenmenger’s syndrome), atrial arrythmia, paradoxical emboli.

Q) What investigations would you order if you suspect this condition?

• Bedside: Electrocardiogram (RBBB and RAD suggests secundum, RBBB and LAD
suggests primum).
• Blood: CBC (polycythemia).
• Imaging: Echocardiography (Doppler to study movement across the defect, right
heart pressures and function, associated valvular defects, shunt calculation,
amenability to closure), CXR (small aortic knuckle, pulmonary plethora, enlarged RA).
• Cardiac catheterization.

Q) What is the management of this condition?

• Education.
• Medical: treat co-existing morbidities.
• Surgical: defect repair before pulmonary hypertension.
Indications for closure: Contraindication for closure:
• Symptomatic: paradoxical systemic • Severe pulmonary hypertension
embolism, breathlessness. • Eisenmenger’s syndrome
• Significant shunt: Qp:Qs>1.5:1, RV
dilatation.

Q) What is Lutembacher’s syndrome?

An atrial septal defect complicated by or accompanied with mitral stenosis which can arise
due to co-existent rheumatic mitral valve disease or during balloon valvuloplasty of the
mitral valve.
 Co-arctation of the Aorta
Q) What investigations would you order for this patient?
1. Bedside tests: Blood pressure in both arms (reduced if origin proximal to LSA), ECG
(LVH, P mitrale), fundoscopy (Roth Spots if IE), urine dipstick (hematuria if IE), and
ankle-brachial pressure index.

2. Blood: CBC (Inflammation, anemia), CRP/ESR (↑in IE), and KFT (renal failure from
HTN).

3. Imaging: CXR (LVH, LSA dilation and aortic post-stenotic dilation form 3 shape, rib
notching) and Echo (LV function, Valves and other structural malformations)

4. Cardiac catheterization.

Q) How would you manage this patient?

• Education and counselling

• Cardiology referral, Obstetric consultation about conception.
• Continuous monitoring for BP, IE, HF
symptoms.
Complications after repair surgery?
• Surgical referral (Left subclavian artery flap
Re-coarctation. Dissections. Aneurysms.
repair, resection + end-to-end anastomosis,
balloon angioplasty and stenting).

Q) What are the other conditions commonly associated with this disease?

• Bicuspid aortic valve: 25-50% of patients with COA have bicuspid AV (characterized
by an opening click and aortic stenosis murmur).
• Other left-sided heart abnormalities, renal tract malformations.
• Turner's Syndrome.
• Vascular: Berry aneurysms, Hemangiomas and Hypertension (Often challenging to
treat due to reduced kidney blood flow, which activates the renin-angiotensin
system).

Q) Differential diagnosis of a reduced left radial pulse:

• Anatomical: Unusual anatomical course, absence or compression of arteries,

lymphadenopathy, or mass lesions.
• Iatrogenic: Trauma from medical procedures or surgical corrections of cardiac
defects.
• Atherosclerosis.
• Embolism: associated with Atrial fibrillation.
• Vasculitis: Giant cell arteritis and Takayasu's arteritis.
 Ebstein’s Anomaly
Q) What investigations would you order for this patient?

• Bedside tests: ECG (p pulmonale, RBBB).

• Imaging: Echo (confirm the diagnosis, look for associated defects).
• Electrophysiology (accessory conduction pathways).

Q) What is the management for this condition?

• Education.
• Medical: treat associated arrythmias and HF.
• Surgical: Valve repair or replacement, Fontan procedure (Bypass RV by shunting blood
straight to pulmonary artery).

Q) What is the underlying abnormality in Ebstein’s anomaly?

Other causes of tricuspid
A congenital abnormality affecting posterior and septal leaflets regurgitation?
of the tricuspid valve, leading to tricuspid regurgitation. Primary: IE, Rheumatic heart
It is characterized by a dilated right atrium and a right ventricle disease, Carcinoid syndrome.
hypoplasia. Secondary: Pulmonary HTN, PS,
MS.

Q) What are the risk factors for this anomaly?

Maternal use of certain teratogenic drugs such as Lithium and benzodiazepine.

Q) What is a special character of Ebestein’s Anomaly on jugular venous

pressure curve?

No prominent V wave of tricuspid regurgitation as the right atrium is enlarged and can
accept the regurgitant flow from RV and not transmit it up into Jugular vein.
 Eisenmenger’s Syndrome
Q) What is Eisenmenger’s Syndrome?

It is a condition where left-to-right shunts lead to pulmonary arterial hypertension. As the

shunt reverses to right-to-left over time, symptoms of cyanosis, breathlessness, and finger
clubbing appear.

Q) What investigations would you order for this patient?

• Bedside tests: ECG (rhythm and conduction abnormalities), urine dipstick, and
fundoscopy.
• Blood: CBC (↑RBCs secondary to hypoxia, ↓platelets), iron studies, KFT (renal failure is
common), coagulation profile (acquired VWF deficiency is common), and CRP/ESR (IE is
common).
• Imaging: CXR (enlarged pulmonary artery and trimmed peripherals), echocardiography
(ventricles size and function and other structural abnormalities) , and cardiac MRI.
• Cardiac catheterization.

Q) What is the management for this condition?

• Education and counselling about lifestyle specially conception (high mortality rate
associated) and Cardiology referral.
• Vaccinations (Pneumococcal, annual Influenza), Symptomatic management
(phlebotomy for hyperviscosity syndrome, HF management and iron supplementation if
necessary).
• Surgical: Combined heart-lung transplant.

Q) What are the complications of Eisenmenger’s Syndrome?

• Hyperviscosity: Headache, visual disturbance, impaired cognition, tingling sensation,

and tinnitus.
• Bleeding: Bruising, nosebleeds, gum bleeding, Menorrhagia, and Hemoptysis.
• Thrombosis: PE and paradoxical emboli.
• Ischemia: Stroke and TIA.
• Infections: IE and cerebral abscesses.
• Arrhythmias, renal failure, gout, and cholelithiasis.
• Impaired kidney function.
• Gallbladder stones.
• Gout.

Q) What is the differential diagnosis of this condition?

• Primary Pulmonary hypertension. Classic case:

• Septal defects without reversal of shunts. ASD with fixed wide S2
• Tetralogy of Fallot. splitting.
 Tetralogy of Fallot
Q) What are the underlying abnormalities in Tetralogy of Fallot?

• RV outflow obstruction \ Pulmonary stenosis.

• RV hypertrophy.
• Overriding Aorta.
• VSD.

Q) What is the principle of Blalock-Taussig shunt operation of TOF?

Partially corrects the Fallot’s abnormality by anastomosing the
subclavian artery to the pulmonary artery.
(will result in weak or absent radial pulse, harder to obtain
BP and lateral thoracotomy scar).
No longer the operation of choice
as it is palliative not curative.
Waterson anastomosis = Blalock but
used aorta instead of subclavian.

Q) What is the principle of the total repair operation of TOF?

The VSD is corrected using a mesh, which relieves the obstruction in the right ventricle
outflow tract.
(Can lead to different levels of pulmonary regurgitation\tricuspid regurgitation and
increased strain on the right ventricle with resultant elevated JVP and peripheral edema.
Midline sternotomy scar).

Q) What are the possible complications for this condition?

• HF.
• Eisenmenger’s syndrome
• IE.
• Emboli: Stroke, Brain abscess.

Q) What investigation would you conduct for a patient with this condition?

• Bedside tests: ECG (LVH, abnormal conduction, arrythmia), urine dipstick, temperature
and fundoscopy, pregnancy testing (High mortality rate).
• Blood: CBC (anaemia, infection), CRP/ESR.
• Imaging: CXR (boot shaped heart, ↑RV cavity size, right sided aortic arch, reduced
pulmonary vasculature), Echo (pressure gradients across valves, ventricular function and
other abnormalities), cardiac MRI (for further assessment).
 Ventricular Septal Defect (VSD)
Q) What are the types of VSD?

• Membranous (Most common, spontaneous closure possible).

• Muscular (typical presentation is 1-3 days following MI with rapid hemodynamic
collapse).
• Infundibular.
• Atrioventricular.

Q) What is the differential diagnosis of VSD?

• Mitral regurgitation.
• Tricuspid regurgitation.
• Hypertrophic obstructive cardiomyopathy.

Q) What are the common associations with VSD?

• Congenital: Other heart defects (TOF, Co-arctation of aorta, pulmonary\tricuspid atresia,

aortic regurgitation), part of genetic abnormalities (Down syndrome, Turner’s
syndrome).
• Acquired: as a complication of MI (septal rupture), traumatic, post-surgical.

Q) What are the investigations for this condition?

• Bedside tests: ECG (LVH, left axis deviation, conduction abnormalities).

• Blood: CBC (↑RBCs secondary to Eisenmenger’s).
• Imaging: CXR (dilated pulmonary arteries with trimming of peripherals), Echo (site and
size of the defect, ventricular function, other structural abnormalities, shunt direction
with doppler).
• Cardiac catheterisation.

Q) What is the treatment for this condition?

• Education and counselling.

• Medical: symptomatic for HF \ IE
• Surgical: Surgical (pericardial patch) or percutaneous (Amplatzer® device) closure of
hemodynamically significant defects.

Q) What is maladie de roger?

A loud murmur resulting from a small VSD because of high Maladie de roger doesn’t usually
degree of turbulence with normal cardiac examination. require treatment as it is
hemodynamically stable and
most likely closes spontaneously.
 Neurology Cases
Horner’s Syndrome
Q) What are the causes of Horner’s syndrome? Clinical signs: 'PEAS'
• Ptosis
• Congenital: Birth trauma (sympathetic chain injury in • Enophthalmos
Klumpke’s paralysis), hereditary. • Anhidrosis
• First order (hypothalamus to spinal cord): Trauma, • Small pupil (miosis)
tumor, Wallenberg syndrome, multiple sclerosis, and
syringomyelia.
• Second order (spinal cord to the neck): Trauma, Pancoast tumor, and aneurysm.
• Third order (neck to the face): internal carotid artery dissection, carotid cavernous
fistula, cluster or migraine headache.

Q) What investigations would you request for this patient?

Review old photos to clarify the time of onset.

Bloods: a full blood count (FBC), liver function tests (LFTs), and bone profile can be
considered to investigate malignancy if it is a second-order cause.
Imaging:
• MRI brain for first-order (ischemia, demyelination, or tumors).
• Chest radiograph and/or CT thorax for second-order (Pancoast's syndrome).
• MRA and/or carotid doppler for second and third-order (vascular abnormalities).
• MRI for third-order (cavernous sinus abnormalities).

Special tests:
• Apraclonidine test: Confirms Horner syndrome by causing dilation of the affected
pupil and, in some cases, resolving ptosis.
• Cocaine test: Confirms Horner syndrome by inducing dilation of the normal pupil
while the affected pupil remains unchanged.
• Hydroxyamphetamine test: Confirms the site of the lesion as normal dilation of the
affected eye suggests a first or second-order lesion, while absent or poor dilation
indicates a third-order lesion.

The treatment involves patient education and correcting the underlying cause, either medically or surgically.

Q) What is Wallenberg syndrome?

• Wallenberg syndrome, also known as lateral medullary syndrome, is characterized
by a posterior inferior cerebellar artery infarct.
• It presents with several symptoms, including dysphagia (difficulty swallowing),
sensory loss affecting the ipsilateral face and contralateral trunk and extremities,
ipsilateral cerebellar ataxia (uncoordinated movements), and rotatory nystagmus
(involuntary eye movement).
• The damage to the trigeminal spinal nucleus results in the impairment of ipsilateral
facial sensation.
Q) What is Klumpke’s paralysis?

Birth trauma → damages C8 and T1 → weakness, anaesthesia, and clawing of the hand.

Q) In a patient with Horner's syndrome who presents with neck or face pain,
which diagnosis should be considered?
Carotid artery dissection → Urgent CT or MR angiography.
 Seventh Cranial Nerve Palsy
Q) What investigations would you request for this patient?

Bedside tests: Otoscopy (tympanic membrane vesicles, House Brackmann scale:

cholesteatoma, and otitis media), Finger prick glucose Assess severity of the paralysis:
(diabetes), Urine dipstick (glycosuria and proteinuria), Blood 1 = normal to 6 = total paralysis.
pressure, ECG (AF).
Bloods: Fasting glucose and HbA1c (diabetes), Lipids, FBC (anemia, ↑ WBCs), and ESR/CRP.
Imaging: MRI head or auditory meatus (signs of cerebellopontine angle involvement,
bilateral/recurrent facial nerve palsy).
Special tests: Autoimmune screen(RF, ANA, anti-dsDNA, ANCA, complement, and
cryoglobulins, as well as ACE levels), Serology (HIV, Lyme's disease, and hepatitis), Blood
film/LDH (lymphoma), and Lumbar puncture (infection or meningeal infiltration from
malignancy).
Anti-ganglioside antibodies are
sometimes seen.
Q) How would you manage this patient?

• Re-assurance, eye care.

• Medical: Eye drops/ointments, early prednisolone, and analgesia.
• Surgical: Facial nerve decompression and cosmetic surgery.

Q) How to know the level of fascial nerve injury?

Level Cause Associations

Pons MS and stroke +VI palsy and long tract signs
Cerebellar-pontine angle Tumor (acoustic neuroma) +V, VI, VIII and cerebellar
signs
Auditory/facial canal Cholesteatoma and abscess +VIII
Neck and face Tumor and trauma Scars, parotid mass

Q) What are the causes of fascial nerve palsy?

Unilateral: Bell’s palsy:

• Bell’s palsy • Ramsay–Hunt syndrome • Rapid onset (1–2 days)
• Mononeuropathy due to diabetes or Lyme disease • HSV-1 is implicated
• Tumor/trauma • MS/stroke • In pregnancy outcome is worse

Bell’s phenomenon: eyeball rolls

Bilateral: upwards on attempted eye closure.
• Guillain–Barré • Myasthenia gravis
• Sarcoidosis • Bilateral Bell’s palsy Ramsay Hunt Syndrome:
• Lyme disease • LMNL of fascial nerve due to HZV
• Ear pain, vesicles on the tympanic
membrane and/or mouth.
 Sixth Cranial Nerve Palsy
Q) What investigations would you request for this patient?

Bedside tests: Finger prick glucose (diabetes), Urine dipstick (glycosuria and proteinuria),
Blood pressure, ECG (AF).
Bloods: Fasting glucose and HbA1c (diabetes), Lipids, FBC (anemia, ↑ WBCs), and ESR/CRP.
Imaging: CT or MRI head (brainstem lesions, inflammatory changes in the nerve, or causes
of raised intracranial pressure).
Special tests: Autoimmune screen (RF, ANA, anti-dsDNA, ANCA, complement, and
cryoglobulins, as well as ACE levels), Serology (HIV, Lyme's disease, and hepatitis).

Q) How would you manage this patient?

• Non-pharmacological interventions: patching, using fresnel prism glasses (which

resemble regular glasses but have visible ridges on the lenses), seeking ophthalmology
review, considering occupational therapy, and addressing DVLA regulations.
• Medical approaches: optimizing the control of cardiovascular disease (CVD) risk factors,
such as managing diabetes, hypertension, and hypercholesterolemia, in conjunction
with appropriate lifestyle modifications.
• Surgical options: If underlying cause can be corrected with surgery.

Commonest cause of an isolated 6th nerve palsy → Diabetes mellitus.

Commonest cause of diplopia in adults → 6th cranial nerve palsy.

Q) What are the causes of 6th nerve palsy?

• Brainstem lesion (stroke, aneurysm, tumors, or inflammation).

• Mononeuropathy (diabetes, vasculitis (ANCA-associated, rheumatoid arthritis, systemic
lupus erythematosus, cryoglobulinemia), sarcoidosis, or infections like Lyme's disease,
HIV, or leprosy).
• Raised intracranial pressure (tumors, idiopathic intracranial hypertension,
hemorrhages, or cerebral edema).
• A cavernous sinus lesion (infection from sources like teeth, central face, or sinuses (e.g.,
Staphylococcus aureus), thrombosis, or Tolosa Hunt Syndrome).

First nerve to be affected in cavernous sinus lesion is the 6th CN, then the 3rd and 4th CNs.

Q) What is an internuclear ophthalmoplegia (INO)?

• Internuclear ophthalmoplegia (INO) impairs lateral eye movement due to damaged medial
longitudinal fasciculus (MLF), often caused by multiple sclerosis or mid-brain ischemia.
• The right eye fails to adduct when looking left, left eye shows nystagmus when abducting.
 Third Cranial Nerve Palsy
Q) What investigations would you request for this patient?

Bedside tests: finger prick glucose (for diabetes), urine dipstick (glycosuria, proteinuria), and
blood pressure (hypertension).
Blood tests: fasting glucose (for diabetes), HbA1c (for diabetes), lipids (for cardiovascular
disease assessment), FBC (for anaemia, infection, or inflammation), CRP/ESR (for infection
or inflammation), and serology (HIV, syphilis, Lyme's).
Imaging: CT head (to check for bleeding or mass lesion) and CT or MR angio (to detect
aneurysms).
Special tests: catheter angiography (the gold standard for aneurysm detection, although
MRA can usually suffice for aneurysms of 2-3mm).

Q) How would you manage this patient?

• Re-assurance (improve within 3 months).

• Medical: analgesia, underlying cause.
• Surgical: Clip or coil an aneurysm.

Q) What are the causes of 3rd nerve palsy?

Medical (4Ms) Surgical (3Cs)

Mononeuritis multiplex (DM)
Midbrain infarction: Weber’
Midbrain demyelination (MS)
Migraine
Communicating artery aneurysm
(posterior)
Cavernous sinus abnormalities: thrombosis,
tumor or fistula. (IV, V and VI affected)
Cerebral uncus herniation

What is Weber’s Syndrome?

Medial midbrain stroke causing third nerve palsy & contralateral hemiparesis (cerebral
peduncle lesion)

What is Benedikt’s Syndrome?

Lateral midbrain stroke causing third nerve palsy & contralateral tremors (red nucleus
lesion).

What is Nothnagel’s Syndrome?

Third nerve palsy & ipsilateral ataxia (superior cerebellar peduncle lesion).

What ocular muscles does the 3rd nerve supply?

Superior, inferior, medial rectus and inferior oblique.