Important abdominal presentations

Question 1

Hepatomegaly: examination findings and causes

Answer 1

Pallor/anaemia: haemolysis, chronic liver disease, malignancy, marrow failure, infective endocarditis.
Jaundice: haemolysis, chronic liver disease, hepatitis.
Lymphadenopathy: lymphoma, metastatic disease, leukaemia, myeloproliferative disorders, connective tissue disorders, TB, viral hepatitis, infectious mononucleosis.
Cachexia: malignancy, TB.
Petechial rash: thrombocytopaenia in cirrhosis, leukaemia.
Herpes zoster, oral candidiasis: immunocompromised state in leukaemia, lymphoma, TB.
Stigmata of chronic liver disease: spider naevi, palmar erythema, leukonychia, digital clubbing, gynaecomastia.
Peripheral oedema: cirrhosis, right heart failure, hypoalbuminaemia.
Raised JVP: right heart failure.

Question 2

Hepatomegaly: further examination of the abdomen

Answer 2

Look for visible masses, prominent veins, caput medusa.
Palpate in each quadrant for tenderness and masses.
Palpate specifically for the kidneys, gallbladder, and presence of ascites.
Auscultate for murmurs over the liver.

Question 3

Hepatomegaly: causes

Answer 3

Infective: EBV, CMV, hepatitis, liver abscess, malaria, leptospirosis, amoebiasis, hydatid cyst, actinomycosis.
Neoplastic: hepatocellualr carcinoma, metastasis, myeloma, leukaemia, lymphoma, haemangioma.
Metabolic: haemochromatosis, amyloidosis, glycogen storage diseases (e.g. Hunter’s syndrome, Gaucher’s disease, Niemann-Pick disease), fat.
Congenital: Riedel’s lobe, polycystic disease.
Other: alcohol, right heart failure, Budd-Chiari syndrome, sarcoidosis.

Question 4

Causes of mild hepatomegaly

Answer 4

Infection: hepatitis, HIV, EBV, hydatid disease.
Other: biliary obstruction, and the causes of moderate-massive hepatomegaly.

Question 5

Causes of moderate hepatomegaly

Answer 5

Haematological: lymphoma, myeloproliferative disorders.
Infiltration: amyloidosis.
Haemochromatosis, and the causes of massive hepatomegaly.

Question 6

Causes of massive hepatomegaly

Answer 6

Malignancy: HCC, metastasis.
Haematological: myeloproliferative disorders.
Vascular: right sided heart failure, tricuspid regurgitation.
Alcoholic liver disease and fatty infiltration.

Question 7

Causes of hepatomegaly with irregular surface

Answer 7

Malignancy e.g. HCC, metastasis.
Cirrhosis.
Hydatid cysts.
Amyloid.
Sarcoid granulomas.

Question 8

Causes of hepatomegaly with pulsatility

Answer 8

Vascular: tricuspid regurgitation, vascular malformation e.g. AVM.
Malignancy: HCC.

Question 9

Causes of hepatomegaly with tenderness

Answer 9

Infection: hepatitis, malaria, EBV, hepatic abscess.
Malignancy: HCC, metastasis (stretching of liver capsule).
Vascular: right-sided heart failure, Budd-Chiari syndrome.
Biliary obstruction.
Ascending cholangitis.

Question 10

Chronic liver disease: examination findings, general inspection

Answer 10

Pallor (anaemia).
Tattoos, needle track marks (may suggest viral hepatitis).
Digital clubbing.
Terry’s nails (proximal 2/3 of nail plate white with distal 1/3 red.
Muehrcke’s lines.
Palmar erythema.
Spider naevi (number and size correlate with severity).
Gynaecomastia.
Generalised muscle wasting.
Loss of body hair.
Testicular atrophy.
Evidence of alcohol misuse: Dupuytren’s contracture, parotid enlargement, cerebellar signs (past-pointing, ataxic gait).
Signs of decompensated liver disease: jaundice, purpura, asterixis.

Question 11

Chronic liver disease: examination findings, abdominal inspection

Answer 11

Distension (ascites; a paraumbilical hernia may be visible).
Caput medusa.
Look also for scars, drain sites.

Question 12

Chronic liver disease: palpation, percussion and auscultation

Answer 12

Palpate for hepatomegaly, splenomegaly.
Percuss for liver span, spleen, shifting dullness, fluid thrill.
Auscultate for either hepatic arterial bruit or venous hum (in portal hypertension; Cruveilheir-Baumgarten murmur).

Question 13

Chronic liver disease: aetiology

Answer 13

Toxins: alcohol and other drugs, e.g. amiodarone, methotrexate.
Viral: hepatitis B and C, CMV, EBV.
Metabolic: non-alcoholic steatohepatitis (NASH), haemochromatosis, Wilson’s disease, alpha-1-antitrypsin deficiency.
Autoimune: autoimmune hepatitis, primary biliary cirrhosis, primary sclerosis cholangitis.

Question 14

Chronic liver disease: clinical spectrum of alcoholic liver disease

Answer 14

Alcohol withdrawal syndrome including delirium tremens.
Wernicke’s encephalopathy: confusion, ataxia, and ophthalmoplegia.
Alcoholic fatty liver: fatty liver on ultrasound, abnormal liver enzymes on biochemistry with good synthetic function.
Alcoholic hepatitis: jaundice, raised liver enzymes, coagulopathy, encephalopathy.
Cirrhosis with portal hypertension.

Question 15

Hepatic encephalopathy: overview

Answer 15

Neuropsychiatric disorder in patients with liver dysfunction (personality changes, intellectual impairment, reduced consciousness).
Diversion of portal blood into the systemic circulation via collaterals leads to a lack of hepatic detoxification.
Exposure of the brain to excessive concentrations of ammonia can cause neurotoxicity.
Severity can be graded by the West Haven classification.
Ammonia levels don’t always correlate with severity.
Other toxins implicated include mercaptans, short-chain fatty acids, and phenol.

Question 16

Hepatic encephalopathy: epidemiology and prognosis

Answer 16

In decompensated cirrhosis, the risk of developing HE is 20% per year.
At any time, 30-45% of people with cirrhosis exhibit evidence of HE.
Development of HE is associated with a poor prognosis and strongly predicts short-term mortality in acute liver failure.

Question 17

Hepatic encephalopathy: common precipitants

Answer 17

Increased nitrogen load: constipation, GI bleeding, blood transfusion, azotaemia, infection, hypokalaemia.
Decreased toxin clearance: dehydration (fluid restriction, diuretics, abdominal paracentesis, diarrhoea, vomiting), hypotension (bleeding, systemic vasodilatation), anaemia, portosystemic shunts.
Altered neurotransmission: benzodiazepines, psychoactive drugs.
Hepatocellular damage: continued alcohol use, hepatocellular carcinoma.

Question 18

Jaundice: examination, inspection

Answer 18

Inspect the sclera and conjunctiva.
Using the left thumb, pull on the patient’s lower eyelid and ask them to look towards the ceiling.
Inspect the soft palate with a pen torch in cases of doubt (bilirubin is avidly taken up by tissues rich in elastin).
Check for signs of chronic liver disease.
Look for body piercings and tattoos (hepatitis risk).

Question 19

Jaundice: examination, palpation

Answer 19

Palpate the abdomen for tenderness, masses, and organomegaly (including the gallbladder).

Question 20

Jaundice: examination, percussion

Answer 20

Percuss for the liver, spleen, and presence of ascites.

Question 21

Jaundice: examination, completion

Answer 21

Perform a digital rectal examination to look for pale stools (post-hepatic) or melaena (GI bleed complication).
Examine the external genitalia for hair growth and testicular size (atrophic in chronic liver disease).
Examine the hernial orifices.
Carry out a urinary dipstick test for bilirubin (post-hepatic).

Question 22

Jaundice: prehepatic causes (unconjugated hyperbilirubinaemia)

Answer 22

Overproduction: haemolysis; ineffective erythropoiesis.
Impaired hepatic uptake: drugs (contrast agents, rifampicin), congestive cardiac failure.
Impaired conjugation: Gilbert’s syndrome, Crigler-Najjar syndrome.

Question 23

Jaundice: hepatic causes (conjugated hyperbilirubinaemia)

Answer 23

Infection: viral hepatitis, leptospirosis, liver abscess, septicaemia.
Alcohol and toxins: carbon tetrachloride, fungi (Amanita phalloides).
Drug-induced hepatitis: paracetamol, anti-TB drugs (isoniazid, rifampicin, pyrazinamide), statins, sodium valproate, halothane.
Metabolic: haemochromatosis, alpha-1-antitrypsin deficiency, Wilson’s disease, Rotor syndrome.
Vascular: Budd-Chiari, right-sided heart failure.

Question 24

Jaundice: posthepatic causes (conjugated hyperbilirubinaemia)

Answer 24

Luminal: gallstones.
Mural: cholangiocarcinoma, sclerosing cholangitis, primary biliary cirrhosis, choledochal cyst.
Extra-mural: pancreatic cancer, lymph nodes at porta hepatis.
Drugs: antibiotics (flucloxacillin, fusidic acid, coamoxiclav, nitrofurantoin).

Question 25

Gallstones: background and epidemiology

Answer 25

Stones form due to the supersaturation of bile constituents, usually cholesterol.
Affects 10% of the population (and 2% of children).
Incidence increases with age (40% of women >80 years).
Male:female ratio roughly 1:2.
Typical patient: ‘5 Fs’ (female, forty, fair, fat, fertile).

Question 26

Gallstones: examination, inspection

Answer 26

There may be no signs of gallstones.
Look for risk factors and complications.
Jaundice?
Scars of open or laparoscopic cholecystectomy.
If the patient has recently had surgery, a T-tube and drain may be visible.
A flexible tube arising from the right upper quadrant.

Question 27

Gallstones: examination, palpation

Answer 27

Examine for a palpable gallbladder.

Question 28

Gallstones: Murphy’s test

Answer 28

Using 2 fingers, palpate just below the costal margin in the right upper quadrant and maintain the position whilst the patient takes a deep breath.
Note any tenderness.
Repeat the procedure in the left upper quadrant.
If the patient experiences tenderness only when the right side is palpated, the test is positive.
Indicates acute cholecystitis, ascending cholangitis, empyema.

Question 29

Gallstones: predisposing conditions

Answer 29

Haemolysis: sickle cell, hereditary spherocytosis, thalassaemia, pernicious anaemia, prosthetic heart valves.
Metabolic: diabetes, obesity, pancreatic disease, cystic fibrosis, hypercholesterolaemia, hyperparathyroidism, hypothyroidism, pregnancy.
Cholestasis: hepatitis, Caroli’s disease, parasitic infection, prolonged fasting (e.g. TPN), methadone use.
Malabsorption: (x10 risk of stone formation) IBD (especially Crohn’s), small bowel resection, bypass surgery.
Other: muscular dystrophy.

Question 30

Ascites: definition and aetiology

Answer 30

Ascites is more than 25mL of fluid within the peritoneal cavity.
Common causes: cirrhosis with portal hypertension, peritoneal carcinomatosis.
Less common causes: hepatocellular carcinoma, Budd-Chiari syndrome, congestive cardiac failure, pancreatitis, and TB.

Question 31

Ascites: complicating advanced cirrhosis

Answer 31

Ascites often marks the first sign of hepatic decompensation.
Occurs in >50% over 10 years of follow-up, worsens the course of disease, and reduces survival substantially.
If ascites becomes refractory to diuretics, 50% die within 1 year.
Spontaneous bacterial peritonitis is a frequent and serious complication of cirrhotic ascites and is defined as an ascitic neutrophil count >250 cell/mm^3.

Question 32

Ascites: examination, inspection

Answer 32

If there is gross ascites, the abdomen may be distended.
Look for bulging of the flanks in a supine patient (fluid accumulates in the paracolic gutters).
Look for signs of chronic liver disease.
- Hands: clubbing, leukonychia, bruising, palmar erythema, Dupuytren’s contracture, hepatic flap, scratch marks.
- Face: anaemia, jaundice, xanthelasma, parotid enlargement, glossitis.
- Neck: Troisier’s sign/Virchow’s node (intra-abdominal malignancy).
- Trunk: spider naevi, gynaecomastia.
- Abdomen: distended superficial veins, caput medusa.

Question 33

Ascites: examination, palpation

Answer 33

Palpate in each quadrant for tenderness and masses.

Palpation for organomegaly may be difficult in gross ascites.

Question 34

Ascites: examination, percussion

Answer 34

Percuss borders of the liver, spleen, bladder, and any masses.
Shifting dullness.
Fluid thrill test.

Question 35

Ascites: examination, completion

Answer 35

Examine the hernial orificies, lymph nodes and cardiovascular system (peripheral oedema and pleural effusion).

Question 36

Primary biliary cirrhosis: overview

Answer 36

Autoimmune liver disease characterised by progressive destruction of intrahepatic bile ducts with cholestasis, portal inflammation and fibrosis.
May lead to cirrhosis, its complications, and eventually to liver transplantation or death.
Predominantly affects females in their 50s-70s.

Question 37

Primary biliary cirrhosis: history

Answer 37

Majority are asymptomatic.
Fatigue (multifactorial: autonomic dysfunction, sleep disturbance, and excessive daytime somnolence, depression).
Pruritus (typically precedes onset of jaundice by months to years, develops independently of degree of cholestasis and stage of disease).
Vague right upper quadrant pain.
Night blindness, bony pain, easy bruising, fat-soluble vitamin malabsorption (A, D, E, and K).

Question 38

Primary biliary cirrhosis: examination, inspection

Answer 38

Scratch marks.
Pigmentation.
Digital clubbing.
Arthropathy (involving small joints).
Xanthelasma.
Xanthoma.
Evidence of decompensated liver disease: jaundice, abdominal distension, dilated abdominal veins, hepatomegaly, splenomegaly, ascites, encephalopathy, asterixis.

Question 39

Primary biliary cirrhosis: associated autoimmune conditions

Answer 39

Look for evidence of rheumatoid arthritis, thyroid dysfunction, Sjögren’s syndrome, scleroderma, SLE, coeliac disease.

Question 40

Haemochromatosis: background

Answer 40

Autosomal recessive condition causing an abnormal accumulation of iron in the parenchymal organs, leading to organ toxicity.
Gene (HFE) for most genetic haemochromatosis (GH), lies on short arm of chromosome 6. The 2 major mutations are C282Y and H63D. Defective hepcidin (iron-regulatory hormone) gene expression or function may under most forms of non-HFE associated GH.
Carrier state ~1:10. Frequency of homozygosity ~1:200/400 but penetrance is low (higher with cofactors such as excess alcohol).
Male preponderance; menstruation has protective effect in females.

Question 41

Haemochromatosis: symptoms

Answer 41

Often vague and non-specific: weakness, fatigue, lethargy, apathy, weight loss.
Organ specific: arthralgia, abdominal pain (hepatomegaly), amenorrhoea, loss of libido, impotence (pituitary dysfunction, hepatic cirrhosis), shortness of breath (CCF).
Impaired memory, mood swings, and irritability.

Question 42

Haemochromatosis: examination findings

Answer 42

Hepatomegaly.
Cutaneous stigmata of liver disease (palmar erythema, jaundice, spider naevi).
Signs of portal hypertension (splenomegaly, ascites).
Arthritis and joint swelling: especially 2nd, 3rd metacarpophalangeal joints, wrists, hips, and knees.
Shortness of breath, oedema, raised JVP (dilated cardiomyopathy).
Arrhythmias (conduction abnormalities).
Altered pigmentation: bronzing or ‘slate-grey’ due to iron and melanin deposition.
Scars in cubital fossa (previous venesection).
Hair loss.
Hypogonadism (testicular atrophy, loss of axillary and pubic hair).
Increased blood and urine glucose levels (diabetes mellitus secondary to iron toxicity of pancreatic beta cells).
Signs of hypothyroidism.

Question 43

Wilson’s disease: definition and epidemiology

Answer 43

Wilson’s disease or hepatolenticular degeneration is a rare autosomal recessive inherited disorder of copper metabolism characterised by excessive deposition of copper in the liver, brain, and other tissues.
Affects about 1/30,000 people, often manifesting as liver disease in children and adolescents, and as a neuropsychiatric illness in young adults.

Question 44

Wilson’s disease: pathogenesis

Answer 44

The transport of copper by the P-type ATPase is defective due to one of several mutations (>300 identified) occurring within the ATP7B gene.
This gene has been mapped to chromosome 13q14.3.
Intestinal copper absorption and transport into the liver are intact, whilst incorporation into caeruloplasmin and excretion into bile are impaired.

Question 45

Wilson’s disease: clinical features, neurological

Answer 45

Dysarthria.
Dystonia.
Tremor.
Incoordination.
Parkinsonian symptoms (rigidity, bradykinesia).
Poor handwriting.
Abnormal eye movements.
Polyneuropathy.

Question 46

Wilson’s disease: clinical features, hepatic

Answer 46

Acute hepatitis, chronic active hepatitis.
Cirrhosis.
Fulminant hepatic failure.

Question 47

Wilson’s disease: clinical features, psychiatric

Answer 47

Irritability or anger, emotional lability.
Hyperkinetic behaviour.
Mania, depression.
Psychosis.
Impaired concentration.
Personality changes.

Question 48

Wilson’s disease: clinical features, ophthalmic

Answer 48

Kayser Fleischer rings.
Deposition of copper in Descemet’s membrane at the limbus of the cornea.
Greenish gold-brown, may be readily visible with the naked eye or can be identified on slit-lamp examination.
Seen in nearly all with neurological signs of Wilson’s disease.
Sunflower cataracts (visible only with slit-lamp).

Question 49

Peutz-Jegher’s syndrome: background and epidemiology

Answer 49

Peutz-Jegher’s syndrome is due to germline mutations of the STK11 gene and is characterised by intestinal hamartomatous polyps and mucocutaneous melanocytic macules.
Autosomal dominant, with variable penetrance.
Incidence is estimated at between 1/50,000-200,000 live births.
The disease carries an increased risk of GI and other cancers, including pancreas, breast, cervix, ovary, uterus, lung, and testis.
Patients have a 93% cumulative risk of cancer by the age of 64.
~1/2 die from cancer by the age of 57.
Rapid increase in cancer risk >50 years.

Question 50

Peutz-Jegher’s syndrome: examination, inspection

Answer 50

Pigmented macules of 1-5mm in diameter.
Most commonly around the mouth, crossing the vermilion border of the lip.
Dark brown to black (like freckles).
May also be present on hands and feet, and around the umbilicus, genitalia, and anus.
Similar lesions often occur on the buccal mucosa.
A prolapsed rectal polyp may be seen.

Question 51

Peutz-Jegher’s syndrome: examination, other systems

Answer 51

Abdomen: inspect for scars (e.g. resulting from surgery for intussusceptions or malignancy).
A rectal mass due to a polyp may be palpable.
Testicular masses also occur: examine the testicles and check the chest for gynaecomastia (as a result of a Sertoli cell tumour).
In females, the breasts should be assessed for masses.

Question 52

Appendicitis: epidemiology

Answer 52

The diagnosis is clinical, therefore investigations are only needed to exclude other pathology.
Lifetime risk 7%.
Overall mortality 0.2-0.8%, but higher in >70yrs due to diagnostic delay.
After the first 36hrs, perforation risk is 16-36%, with 5% risk for every subsequent 12hrs.

Question 53

Appendicitis: examination, inspection

Answer 53

Fever.
Pain on movement.
Flexion of the right hip and a reluctance to extend it.
Flushed appearance.
Dry tongue.
Fetor oris.
Ask the patient to point to the site of pain with one finger- classically McBurney’s point (2/3 of the way along a line between the umbilicus and the right ASIS).

Question 54

Appendicitis: examination, palpation

Answer 54

Tenderness and guarding at the right iliac fossa.
Maximal tenderness may be over McBurney’s point.
Percussion tenderness in the RIF.
Rovsing’s test: press the left iliac fossa and ask the patient if and where they feel pain, if felt at the right iliac fossa, test is positive.

Question 55

Appendicitis: other tests

Answer 55

PR or PV examinations: tenderness on the right may indicate appendicitis, but examination may be normal.
Psoas sign: extension of the hip stretches the poses and is painful if irritated by a nearby inflamed appendix (especially retrocaecal).
Obturator sign: suprapubic pain on flexion and internal rotation of the right hip; due to obturator internus irritation by inflamed appendix.

Question 56

Ulcerative colitis: definition and epidemiology

Answer 56

UC is an idiopathic inflammatory bowel disease characterised by colonic mucosal inflammation and a chronic relapsing course.
UC extends uninterrupted from the anal verge to involve part or all of the colon.
Apart from backwash ileitis, the small bowel is not involved.
Bimodal distribution with peaks at 15-30 years and 60s.
3x more common in non-smokers (some relapse on quitting).

Question 57

Ulcerative colitis: associated conditions

Answer 57

Primary sclerosing cholangitis.
Cholangiocarcinoma.
Amyloidosis.
Uric acid renal stones.

Question 58

Ulcerative colitis: history

Answer 58

Depends on extent and activity of the disease.
Bloody diarrhoea.
Mucous discharge.
Faecal urgency.
Tenesmus.
Colicky abdominal pain.
Fever.
Malaise.
Anorexia.
Weight loss.

Question 59

Ulcerative colitis: general inspection

Answer 59

Physical examination is often unremarkable, unless the patient is presenting acutely.
Aphthous ulcers.
Glossitis.
Pallor (anaemia is common).
Peripheral oedema.
Digital clubbing.
Ocular inflammation (uveitis, episcleritis, scleritis).
Cushingoid features (if steroid use).
Enteropathic arthropathy (large joint arthritis, seronegative spondyloarthropathy: sacroiliitis, ankylosing spondylitis).
Erythema nodosum (15%).
Pyoderma gangrenosum (1-2%).

Question 60

Ulcerative colitis: inspection, abdomen

Answer 60

May be surgical scars (e.g. from hemicolectomy).
Stomas or healed stoma sites.
Abdominal drains or healed drain sites.

Question 61

Ulcerative colitis: palpation

Answer 61

May find distended, tense abdomen.

Question 62

Ulcerative colitis: percussion

Answer 62

Hyper-resonance (if abdomen distended).

Question 63

Ulcerative colitis: auscultation

Answer 63

Tinkling bowel sounds (in obstruction).

Question 64

Crohn’s disease: definition and epidemiology

Answer 64

Idiopathic inflammatory bowel disease characterised by transmural, granulomatous inflammation anywhere from mouth to anus (most common at ileocaecum).
It has a chronic, relapsing/remitting course.
Age of onset is bimodal with peaks at 15-30 and 60-80 years.
Smoking increases risk x3-4.

Question 65

Crohn’s disease: intestinal complications

Answer 65

Malnutrition.
Fistulae.
Colorectal adenocarcinoma (Crohn’s colitis).
Short bowel syndrome (following surgical resection).

Question 66

Crohn’s disease: extra-intestinal complications

Answer 66

Hepatic: fatty change, chronic active hepatitis, cirrhosis, amyloidosis.
Biliary tract: gallstones, sclerosing cholangitis, cholangiocarcinoma.
Renal: uric acid stones, oxalate stones.
Musculoskeletal: enteropathic arthropathy, osteoporosis.
Ocular: uveitis, episcleritis, scleritis.
Dermatological: erythema nodosum, pyoderma gangrenosum.
Haematological: anaemia (Fe, B12 and folate deficiency), thrombosis.

Question 67

Crohn’s disease: history

Answer 67

Abdominal pain.
Diarrhoea.
Weight loss.
Fever.
Malaise.
Anorexia.

Question 68

Crohn’s disease: general inspection

Answer 68

Aphthous ulcers.
Glossitis.
Pallor (anaemia is common).
Peripheral oedema.
Digital clubbing.
Ocular inflammation (uveitis, episcleritis, scleritis).
Cushingoid features (if steroid use).
Enteropathic arthropathy (large joint arthritis, seronegative spondyloarthropathy: sacroiliitis, ankylosing spondylitis).
Erythema nodosum (15%).
Pyoderma gangrenosum (1-2%).

Question 69

Crohn’s disease: inspection, abdomen and perineum

Answer 69

Multiple surgical scars.
Stomas or healed stoma sites.
Enterocutaneous fistulae.
Perianal skin tags, fissures, ulceration, sinuses.
Abdominal drains or healed drain sites.

Question 70

Crohn’s disease: palpation

Answer 70

May find distended, tense abdomen, mass (especially in right iliac fossa), hepatomegaly.

Question 71

Crohn’s disease: percussion

Answer 71

Hyper-resonance (if abdomen distended).

Question 72

Crohn’s disease: auscultation

Answer 72

Increased bowel sounds (in acute exacerbations).

Question 73

Perianal disease: haemorrhoids

Answer 73

Hypertrophied endoanal cushions (causing symptoms).
Acute prolapse and inflammation with associated perianal lump, soreness and irritation.
May bleed.
Chronic = bleeding and pruritus ani.
Sites: primary (3, 7, 11 o’clock in the supine position- the locations of the main anal blood vessel pedicles.
Lord’s classification: 1st degree = bleeding, no prolapse; 2nd degree = prolapse, spontaneous reduction; 3rd degree = prolapse, digital reduction.

Question 74

Perianal disease: fissure in ano

Answer 74

A superficial linear tear in the anoderm distal to the dentate line commonly caused by passage of hard stool.
Almost always in the midline: 90% posterior, 10% anterior.
Identified on inspection, often too painful to perform PR.
Causes acute, severe, localised ‘knife-like’ pain during defaecation with associated deep throbbing pain for minutes or hours after (pelvic floor spasm).
Blood is often seen on the paper when wiping.

Question 75

Perianal disease: perianal abscess

Answer 75

Abscess within the soft tissues surrounding the anal canal.
Gradual onset, constant localised perianal pain.
Associated swelling with tenderness and possible discharge.

Question 76

Perianal disease: fistula in ano

Answer 76

Abnormal communication between the anorectal lining and the perineal or vaginal epithelium.
Nearly always caused by a previous anorectal abscess.
Other less common causes include trauma, Crohn’s disease, carcinoma, radiation therapy, and TB.
Perianal or perineal pain.
Swelling and erythema of perianal skin.
Fever.
Tachycardia.
Discharge.
Goodsall’s rule: if the external opening is posterior to a line drawn transversely through the anus (in the supine position), the opening will be in the midline and thus have a curved tract; if the opening is anterior to this line it will have a radial tract.

Question 77

Perianal disease: rectal prolapse

Answer 77

Protrusion of either the rectal mucosa or the entire wall of the rectum (complete prolapse).
Mainly occurs in the elderly and young children.
Obvious, large perineal lump, dark red/blue with surface mucosa and, occasionally, some surface ulceration.
Pain, constipation, faecal incontinence, mucous discharge, or rectal bleeding may occur.

Question 78

Nephrotic syndrome: clinical diagnosis

Answer 78

Proteinuria >3g/24hrs.
Oedema.
Hypoalbuminaemia.
Hyperlipidaemia.

Question 79

Nephrotic syndrome: common causes in adults

Answer 79

Minimal change disease (MCD).
Membranous nephropathy.
Focal segmental glomerulosclerosis.
Diabetic glomerulosclerosis.

Question 80

Nephrotic syndrome: other causes

Answer 80

Renal amyloidosis.
Lupus nephritis.
Mesangiocapillary glomerulonephritis.
Collapsing glomerulopathy (HIV-associated nephropathy).
Light chain deposition disease.

Question 81

Nephrotic syndrome: other causes of bilateral swollen legs

Answer 81

Right ventricular failure.
Lymphoedema.
Hypoalbuminaemia.
Hepatic failure.

Question 82

Nephrotic syndrome: complications

Answer 82

Increased risk of thromboembolism (loss of anticoagulant factors in the urine).
Those with albumin <20g/L are often anticoagulated with warfarin.
Renal vein thrombosis: suspect if the patient develops loin pain, haematuria, and an acute deterioration in their renal function.
Pulmonary emboli.
Infection (loss of immunoglobulin and complement).
Hypercholesterolaemia.

Question 83

Nephrotic syndrome: examination findings

Answer 83

Extensive oedema.
Periorbital swelling: typically worse in the morning.
Bilateral pitting oedema of the lower limbs: usually symmetrical, may extend up to the abdomen.
Also look for evidence of: pulmonary oedema, pleural effusion, ascites.

Question 84

Chronic kidney disease: common causes in the UK

Answer 84

Diabetes mellitus.
Glomerulonephritis, e.g. IgA nephropathy.
Reflux nephropathy.
Obstructive uropathy.
Renovascular disease.
Hypertension.
Polycystic kidney disease.

Question 85

Chronic kidney disease: other causes

Answer 85

Myeloma.
Renal amyloidosis.
SLE.
Vasculitis.
Tubulointerstitial nephritis.
Scleroderma.
Other inherited renal disease, e.g. Alpert's disease, oxalises, cystinosis.

Question 86

Chronic kidney disease: history

Answer 86

Many patients with CKD are asymptomatic.
Symptoms usually develop at an advanced stage.
Fatigue, weakness (secondary to anaemia).
Breathlessness (due to fluid overload, acidosis).
Anorexia, vomiting, metallic taste in mouth (due to uraemia).
Pruritus.
Restless legs.
Bone pain.
Leg swelling.

Question 87

Chronic kidney disease: examination findings

Answer 87

Pallor (due to chronic anaemia).
A lemon tinge to the skin (due to uraemia).
Scratch marks from pruritus.
Hypertension.
A pericardial rub (uncommon, due to uraemia).
Pleural effusions.
Palpable kidneys (causes include polycystic kidney disease, hydronephrosis).
Bilateral lower limb oedema (fluid overload or heavy proteinuria).
Distended bladder?

Question 88

Chronic kidney disease: evidence that the patient is being prepared for dialysis

Answer 88

An arteriovenous fistula either at the wrist or in the antecubital fossa (usually non-dominant arm) for haemodialysis.
A peritoneal dialysis catheter situated in the abdomen.

Question 89

Transplanted kidney: overview

Answer 89

A renal transplant is the most favourable and desired form of renal replacement therapy for patients with end-stage renal disease.
Simultaneous pancreas-kidney transplants are performed in patients with type 1 diabetes and stage 5 CKD.
Following a renal transplant, patients are required to take life-long immunosuppression to prevent graft rejection.
Transplanted kidneys may be from a deceased or living donor.
A transplanted kidney will lie in either the left or right iliac fossa.

Question 90

Transplanted kidney: examination, inspection

Answer 90

Look around the bedside for clue that the patient has diabetes.
There may be lipoatrophy or lipohypertrophy at insulin injection sites.
Look for other complications of severe diabetes including signs of visual impairment due to diabetic retinopathy and peripheral vascular disease.

Question 91

Transplanted kidney: examination, abdomen

Answer 91

A firm mass palpable deep to a diagonal scar.
It is possible that a patient may have had more than 1 transplant and could have a transplanted kidney in each iliac fossa.
An extended Lanz incision in either iliac fossa is called a Rutherford-Morrison incision.
The renal artery is usually anastomosed to the internal or external iliac artery and the renal vein to the external iliac vein.
The ureter is attached separately to the patient’s bladder.
Look for scars of previous nephrectomy (midline, chevron, or loin).

Question 92

Transplanted kidney: evidence of end-stage renal disease

Answer 92

An arteriovenous fistula either at the wrist or in the antecubital fossa.
Small scars near the umbilicus consistent with previous peritoneal dialysis catheter placement.
Small scars beneath the clavicle on either side of the chest which might suggest previous tunnelled dialysis catheter placement.
A scar at the base of the neck consistent with parathyroidectomy (for advanced renal bone disease).

Question 93

Adult polycystic kidney disease: overview

Answer 93

Adult polycystic kidney disease (APKD) is the commonest inherited form of renal disease with a prevalence of ~1/1000.
APKD is autosomal dominant.
25-40% of patients will have no family history.

Question 94

Adult polycystic kidney disease: history

Answer 94

Flank or loin pain from enlarged or infected cysts.
Nocturia and polyuria (loss of urinary concentrating ability).
Hypertension.
Low grade proteinuria, persistent microscopic haematuria ± frank haematuria.
Uraemia symptoms if the patient presents late.

Question 95

Adult polycystic kidney disease: examination findings

Answer 95

Bilaterally enlarged kidneys with irregular surfaces.
Ballotable flank masses which move caudally with inspiration and the examining hand can ‘get above’.
There may also be an enlarged liver with an irregular, lobulated edge.
Look for evidence of end-stage renal disease.

Question 96

Adult polycystic kidney disease: evidence of advanced or end-stage renal disease

Answer 96

A scar in the iliac fossa and a mass consistent with a renal transplant.
An arteriovenous fistula either at the wrist or in the antecubital fossa for haemodialysis.
A peritoneal dialysis catheter situated in the abdomen or a scar consistent with previous catheter placement.
A scar at the base of the neck consistent with parathyroidectomy (for advanced renal bone disease).
Small scars beneath the clavicle on either side of the chest which might suggest previous tunnelled dialysis catheter placement.

Question 97

Adult polycystic kidney disease: APKD associations

Answer 97

Cysts of other organs notably the liver, spleen, and pancreas.
Cardiac abnormalities: mitral valve prolapse, aortic regurgitation.
Intracranial aneurysms which on rupture present as subarachnoid haemorrhage- patients are screened for these if there is a strong positive family history of intracranial bleeding.
Colonic diverticula, abdominal and inguinal hernias.

Question 98

Causes of bilateral renal enlargement

Answer 98

Adult polycystic kidney disease.
Bilateral hydronephrosis.
Amyloidosis (hepatosplenomegaly).
Tuberous sclerosis (adenoma sebaceous or shagreen patches?).
Von Hippel-Lindau disease.