Abdominal System

Abdominal Masses
Ascites
Cirrhosis
Crohn’s Disease
Haemochromatosis
Hepatomegaly
Primary Biliary Cirrhosis
Splenomegaly
Transplanted Kidney
Unilateral Palpable Kidney
Wilson’s Disease
 THE ILLUSTRATED MRCP PACES PRIMER

Abdominal Masses

Epigastric masses
Lymphadenopathy
Masses arising from stomach
Pancreatic masses
AAA

Right iliac fossa mass Left iliac fossa mass

L ymph nodes L ymph nodes
O vary (tumour) O varian cancer
C rohn’s C olonic – cancer
C aecal cancer Diverticular abscess, faeces
C arcinoid K idney (transplanted)
K idneys( transplanted or ectopic)
Amoebiasis

Actinomycosis
Abscesses (ileocaecal/ appendiceal)

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 ABDOMINAL SYSTEM

Ascites
Causes Features
Cirrhosis
Full flanks
CCF

Cancer (primary/ secondary)

Nephrotic

Constrictive pericarditis

TB

Budd–Chiari
NB: Separate into whether due to portal
Shifting dullness
hypertension or not on the basis of the
serum to ascites albumin gradient (SAAG)
if >11 mmHg then due to PHTN the
causes of which include cirrhosis/
Budd–Chiari, etc.

Complications
Respiratory problems
Spontaneous bacterial peritonitis

Management of ascites

Diuretic responsive ascites Diuretic resistant ascites

(NaFD) Paracentesis + albumin
Na: Sodium restriction (<88 mmol/day) Peritoneovenous shunt (LeVeen shunt)
F: Fluid restriction (if Na <120) TIPPS
D: Diuretics (spironolactone + frusemide) Extracorporeal ultrafiltration
Liver transplantation

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 THE ILLUSTRATED MRCP PACES PRIMER

Cirrhosis
= Fibrosis with abnormal regenerating nodules

Causes Head
A utoimmune (PBC/CAH) Jaundice
Encephalopathy
a L pha1 antitrypsin >5 spider naevi
chest
I atrogenic (methyldopa/ methotrexate/
amiodarone/ azathioprine)
V iral (Hep B)
M
MO
E xcess alcohol

R (haemochRomatosis/ Wilson’s)

Investigations that everyone Hand signs Abdomen

should get Clubbing Hepatosplenomegaly
Dupuytren’s (not always)
Bloods: FBC/ LFT/ PT Hep B/ Auto-Ab aFP/
contracture Caput medusae
Ferritin
Flap Testicular atrophy
Fluids: Ascites
Tattoos Ascites
Radiology: Liver USS
Excoriation marks Bruising

Complications TIPS
G lucose low Once you have found chronic liver disease signs, you
R enal failure know this patient has cirrhosis – now find a cause –
E ncephalopathy unkempt? (=EtOH), tattoos (=Hep B), massive
A scites hepatomegaly (+PBC). If there are no chronic liver
T hypoTension disease signs, consider pre- (most likely in the exam) or
post-hepatic causes of jaundice.
C oagulopathy Pre-hepatic causes can be separated into congenital
N utrition (haemoglobin defects, e.g. sickle cell, or membrane
G hypoGlycaemia defects, etc.) or acquired.
S epsis

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 ABDOMINAL SYSTEM

Crohn’s Disease
Features

Iritis

Clubbing

Multiple abdominal scars

Patient may be small (given steroids

as a child)

Erythema nodosum

Pyoderma gangrenosum

Associations
Hepatobiliary: gallstones, steatosis
Eye: iritis, episcleritis
Signs of nutritional deficiencies, e.g. angular cheilosis (B12), anaemia, dermatitis (zinc)
Renal: oxalate stones

Investigations Treatment
Endoscopy Metronidazole and ciprofloxacin
CT for abdominal masses Elemental diet (controversial)
Barium follow through Steroids
Steroid-sparing agents (azathioprine/ methotrexate)
TNF-alpha antagonists

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 THE ILLUSTRATED MRCP PACES PRIMER

Haemochromatosis
Clinical manifestations Treatment
Liver disease (worse with Hep C and EtOH) Bleed 1–2×/ week
Hepatocellular carcinoma (increased x200) Hct shouldn’t fall >20% of previous
Diabetes mellitus (selective for beta cell) level
Arthropathy – (squared-off bone ends and Aim for ferritin between 25-50 nh/mL
hook-like osteophytes in the Avoid Vit C/ uncooked seafood
metacarpophalangeal (MCP) joints,
particularly of the second and third
MCP joints)
Heart disease (15% of HH)
Hypogonadism (usually pituitary origin)
Hypothyroidism (deposition in thyroid)
Extrahepatic cancer (controversial)
Susceptibility to specific infections
(Listeria/ Yersinia (siderophage)/ Vibrio
Results
vulnificus (from uncooked seafood))
Improves everything except
Manifestations in heterozygotes (rarely due
• advanced cirrhosis
to HH alone)
• arthropathy
• hypogonadism
Secondary iron overload
Prognosis
Ineffective erythropoiesis (thalassaemia,
aplastic anaemia, red cell aplasia, SCD) Cardiac failure = bad sign
Chronic liver disease Survival normal if no diabetes/liver
Excessive medicinal iron damage
Parenteral iron overload If cirrhotic 70% 5-year survival
Porphyria cutanea tarda One-third of cirrhosis die from HCC

Investigations
Radiology
CT/MRI – liver is white/black respectively

Liver biopsy
To determine hepatic iron content

Familial things
Test all first degree relatives by PCR or
HLA typing (A3)
• Homozygote relative
12-monthly transferrin sats – venesect
if more than 45%
• Heterozygote relatives
Liver biopsies if LFTs abnormal.

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 ABDOMINAL SYSTEM

Hepatomegaly
Causes
H
CCF
I
Cirrhosis 3 Cs B
Cancer (1˚/2˚)
3Cs
Infiltration

Reticuloendothelial Causes of a normal

(e.g. leukaemia) palpable liver
Hepatoma (H) Diaphragmatic descent
Infections (EBV/Hep B) (I) Emphysema
Budd–Chiari (B) Thin
Palpable Riedel’s lobe
Right sided pleural effusion

Characteristics
Pulsatile liver Tricuspid regurgitation
Bruits EtOH or 1˚/ 2˚ cancer
Venous hum Portal hypertension
Friction rub Fitz–Hugh–Curtis syndrome

Tips
Hepatomegaly is most likely to be due to the 3Cs in the exam. Therefore

• look for the JVP for CCF

• look for lymphadenopathy/ cachexia/ rough liver edge in cancer
• look for signs of chronic liver disease in cirrhosis

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 THE ILLUSTRATED MRCP PACES PRIMER

Primary Biliary Cirrhosis

Associations Features
Glomerulonephritis Renal Middle-aged women
(M:F 1:15)
Hypertrophic
osteoarthropathy Icterus
Arthralgia
Sclerodactyly Rheum Xanthelasma
Raynaud’s
SLE Scratch marks

TP Derm Massive
Vitiligo hepatosplenomegaly

Thyroid disease Endocrine Clubbing

Addison’s

Phase Prognosis Histopathology

1. Increased AMA only >12 yrs 1. Biliary duct epithelial damage with
lymphocyte infiltration +/−
granulomas (fluid lesions)
2. Increased AMA and LFTs 8–12 yrs 2. Piecemeal necrosis
3. Increased AMA, LFTs and pruritis 5–10 yrs 3. Bridging fibrosis
4. Decompensated PBC 3–5 yrs 4. Cirrhosis

Investigations Treatment
cholestyramine ursodeoxycholate
Cholestatic LFTs
Clotting (until late stages) Pruritis
Cholesterol increased naloxone
rifampicin
AMA E2 – specific to PBC so often no propofol
need for liver biopsy
tacrolimus
Complications azathioprine
steroids PBC
Vit ADEK deficiency
methotrexate
Metabolic bone disease (osteoporosis ciclosporin
plus malacia) colchicine
Hypercholesterolaemia and ADEK – stops bone problems (as per osteoporosis)
xanthomas Lipid lowering – no need
Malabsorption (due to decreased bile UDCA – 30% RR decrease to ALF
salt secretion) Liver transplantation = 50% 5-year survival
Hypothyroidism (in 20%) Monitoring = 6/12 alpha fetoprotein + USS
Anaemia Can recur
Azathioprine/steroids – marginal improvement

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 ABDOMINAL SYSTEM

Splenomegaly
Massive Moderate Mild
All the Ms Cirrhosis
Lymphoproliferative
Myeloproliferative
Malaria
Myelofibrosis I
+ Gaucher’s
+ Kala-azar

I Inflammatory
(Sarcoid/ SLE/ Rheumatoid arthritis)

Infection
(hepatitis/ EBV/ bacterial
endocarditis)

Haematological
(ITP/ spherocytosis/ PAU)

Causes of asplenia Reasons for splenectomy

Congenital Haematological disorders Malignancies
Acquired
After splenectomy Idiopathic Hodgkin's/
Sickle cell disease thrombocytopenic Non-Hodgkin's
Hereditary spherocytosis purpura (ITP) lymphoma
Hereditary spherocytosis Hairy cell leukaemia
Asplenia precautions Idiopathic autoimmune Lymphoproliferative
haemolytic anaemia disorders
At risk of: Felty's syndrome
Neisseria meningitidis Thalassaemia Miscellaneous
Strep. pneumoniae Sarcoidosis
Haemophilus influenzae B Sickle cell disease Splenic artery aneurysm
Babesiasis Gaucher's disease Splenic cysts/ abscesses
Malaria Congenital and acquired Trauma
hemolytic anaemia
Vaccination required Thrombotic
thrombocytopenic
Pneumococcal vaccine purpura
HiB
Meningococcal A and C

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 THE ILLUSTRATED MRCP PACES PRIMER

Transplanted Kidney
Causes of chronic renal Examination
failure (and therefore need
for transplantation)
G lomerulonephritis
P yelonephritis
C ystic disease
H ypertension
D iabetes mellitus
A myloidosis Tacrolimus tremor
M yeloma AV fistula (?bruit/ ?recently punctured?)
Laparotomy scar
Iliac fossa mass

Matching
considerations Contraindications
For donors For recipients
HLA DR>B>A
ABO
I
Complications
UG I
of renal ?
transplant
Coronary artery disease Pre-existing renal disease No infections (I)
Opportunistic infections Disease of unknown
Hypertension aetiology ? Normal uro-genital
Lymphoma and skin Ischaemic heart disease system (UG)
cancer Hypertension with Significant GI disease
Glomerulonephritis end-organ damage controlled (GI)
Steroid complications Autoimmune disease
quiescent (I)

Post transplant medications Causes of rejection

Steroids Opportunistic infection
Tacrolimus Premature CAD
MMF Hypertension
Azathioprine Lymphomas and skin cancer
Ciclosporin Glomerulonephritis
Steroid complications

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 ABDOMINAL SYSTEM

Unilateral Palpable Kidney

Causes
Adult polycystic kidney disease/ renal cyst

Renal cell cancer

Hydronephrosis (wide pelvis on picture)

Hypertrophied solitary functioning kidney

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 THE ILLUSTRATED MRCP PACES PRIMER

Wilson’s Disease
By 15 years about 50% will have clinical
manifestations

Also affects kidneys/ joints/ haemolytic

anaemia
?

Phases
IV. Progressive neurological
disease

III. Copper accumulates in

brain

II. Systemic disease

I. Copper accumulates in
liver

Treatment Investigations
D Penicillamine (for life) a. Copper stain on liver biopsy (not very
Trientine sensitive)
Maintenance with dietary zinc b. Increased serum Cu (body coloured
These can improve neurological in picture)
problems c. Increased urine excretion Cu
d. Caeruloplasmin decrease
Genetic counselling

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