Learning Objectives GI Flashcards

Question

What are clinical feature of Head of pancreas tumour (70%)? Tail of pancreas? What is your Differential diagnosis for Painless jaundice? (obstructive, hepatic, pre-hepatic) What investigations are needed for head of pancreas tumour? Why is the K10 screening tool for depression important in pancreatic cancer?

Answer 1

Head of pancreas tumour (70%) * Present earlier due to obstruction of CBD * Non-specific - weight loss, fatigue, nausea Specific * Painless obstructive jaundice with pruritus (characteristic) * Courvoisier's sign = palpable gall bladder (due to obstruction) + obstructive jaundice * Malabsorption syndrome- steatorrhea due to obstruction of pancreatic ductMay have vague constant epigastric pain Body or tail of pancreas (30%) * Vague epigastric pain radiating to the back * Non-specific - weight loss, fatigue Others * Depression * Significantly higher incidence in PaCa patients * Depression and anxiety may even precede symptoms or knowledge of the diagnosis * Migratory thrombophlebitis (Trousseau's sign) - inflammation of veins in the lower leg * Type 1 DM - B-cell destruction * Hepatomegaly - biliary obstruction DDx painless jaundice Obstructive * Head of pancreas tumour - until proven otherwise * Cholangiocarcinoma Hepatic * Chronic viral hepatitis, ALD, NAFLD, drugs, liver Ca, PBC, autoimmune, PBC, PSC Pre-hepatic * Haemolytic anemia, gilbert's syndrome

Answer 2

Risk factors * Migrants or traveller from a high risk area - most hep B in Australia is in migrants * IVDU * Tattoos * Sexual - MSM, unprotected, overseas, with paid workers etc. * Blood products before 1990s * ATSI * Imprisonment * Occupational exposure * Body building - steroids * Sharing razor & personal hygiene equipment with someone with hepatitis Etiology Viral causesInfective acute hepatitis * Hepatitis viruses A,B,C,D,E Other non-specific viral causes * CMV - immunocompromised or newborn * EBV - mild hepatitis common in the acute phase * Herpes simplex - rarely may cause hepatitis in newborn or immunosuppressed → may lead to necrosis * Yellow fever - major cause in tropical regions → hepatic apoptosis can be severe and extensive Risk of chronic hepatitis * HBV - 5% progress to chronic hepatitis * HCV - 85% progress to chronic hepatitis Non-viral causes * Bacterial - leptospirosis, brucellosis, Q feve

Answer 3

**Clinical features** Acute viral hepatitis Pre-icteric prodrome * Fever, weight loss, malaise, N&V, myalgia & arthralgia, diarrhoea, urticaria Icteric phase * RUQ tenderness * Jaundice (mixed hyperbilirubinemia) * Dark urine and pale stool (obstruction due to swelling) * Splenomegaly and cervical lymphadenopathy - minority of cases Chronic (HBV,HCV,HDV only) * Fatigue, malaise, loss of appetite, bouts of jaundice, hepatic tenderness * Asymptomatic carriers - HBV

Answer 4

Work-up of acute viral hepatitis Causes of acute hepatitis Infective * Viral - HAV, HBC, HCV * Bacterial - leptospirosis, Q fever * Acute alcoholic hepatitis * Drug induced - paracetamol overdose * Ischemic hepatitis * Autoimmune hepatitis - anti-smooth muscle antibodies (PBC & PSC present chronic) DDx acute hepatitis * GB - cholecystitis, cholangitis * RSHF * Pancreatitis * PUD Investigating acute hepatitis Bloods FBC * Leukocytosis, aplastic anemia (rare complication) LFTs * ALT/AST very high (\>1000) - DDx = viral, drug induced, autoimmune, ischemic * GGT/ALP mildly elevated Coagulation * Raised INR UECs * Urea & creatinine reduced Acute hepatitis panel * Anti-HAV Ab IgM * HBV serology - HBsAg, HBsAb, HBcAb * HCV - Hep C antibodies, HCV-RNA * EBV & CMV serology * If RFs present - HIV serology, syphilis * Lipase Other causes to consider (depending on presentation) * Paracetamol levels * Autoimmune hepatitis - anti-smooth muscle antibodies

Answer 5

Management of acute viral hepatitisIndications for hospitalisation * Coagulopathy * Hypoglycaemia * Encephalopathy * Severe vomiting Specific medical * Refer to gastroenterology - should be reviewed by gastroenterologist * Not usually required acutely (for chronic infections) Supportive (mainstay) * Nutrition - maintain * Fluids - hydrate * Analgesia * Anti-emetics Follow-up viral serology in 6 months to determine if developed chronic infection * Hep B - if Hep B Ag positive = chronic * Hep C - likely Closing * Give information * Referral - gastroenterologist, GP * Safety-net Follow-up - GP for treatment Pregnancy and chronic hepatitis * There is a risk of vertical transmission to baby if they have acute or chronic infection in pregnancy * Risk with HBV\>HCV * During lifespan they have a high risk of cirrhosis and hepatocellular carcinoma Preventing * 3rd trimester anti-viral * At birth give HBV vaccination PLUS shot of HBV Ig Advice * Not yet pregnant - pregnancy should not be advised until \>6 months after cessation of anti-viral therapy due to teratogenicity * Already pregnant - does not affect route of pregnancy, breastfeeding still encouraged Complications * Acute fulminant hepatitis * Cirrhosis and its complications * Hepatocellular carcinoma * Aplastic anemia - rare * Membranous glomerulonephritis - immune complex formation * Polyarteritis nodosa - immune complex formation

Answer 6

Hepatitis A Epidemiology * Very common WW in developing countries with poor hygiene * Main differential in acute hepatitis of returning traveller Clinical * N&V, diarrhoea, fatigue, arthralgia (common), jaundice, fever, RUQ pain, dark urine * Acute liver failure \<1% * 2-3 week course with no chronic state Diagnosis * LFTs * Anti-HAV IgM positive Prevention * HAV vaccine available for travellers - inactivated Hand hygiene * Safe travelling practices - bottled water, avoid washed fruit/veges, avoid undercooked meat Management * Supportive

Answer 7

Hepatitis B à DNA virus * Parenteral spread: Blood products, IVDU, sexual, direct contact **Risk factors** * IVDU * Sexual partners/carers of IVDU * People receiving blood transfusions eg haemophiliacs * Haemodialysis and ESRF * Babies of HBsAg +ve mothers * Immigrants from HBV endemic countries (eg Vietnam, East Timor, Africa) **Clinical features** _Prodrome_ before jaundice: * Flu-like symptoms = N+V, anorexia, headaches, fatigue, myalgia, low-grade fever * Arthralgia, urticaria _Clinical jaundice_ (only some progress this far) * Pale stools and dark urine preceding jaundice * Hepatomegaly, RUQ pain * Splenomegaly, cervical lymphadenopathy **Diagnosis** * HBV serology * HbsAg: active infection (acute or chronic) * HBeAg: present in acute infection * HBcAg: Positive for life after infection * Anti HBs: immunity (infection or vaccination) * HBeAb: no replication is occurring * AntiHBc IgM: recent acute infection * AntiHBc IgG: marker of past infection * HBV PCR for monitoring response to Tx Investigation - Bloods: FBC, LFTs, coag profile, AFP - Imaging: Liver USS Natural progression of chronic HBV infection Four phases of chronic HBV infection over the patient's lifetime: 1. Immune tolerance = 15-30 years, normal transaminases, high HBV DNA 2. Immune clearance = Deranged transaminases, if prolonged there is worse prognosis. - Risk of progression to cirrhosis and HCC 3. Immune control = Normal transaminases, low or undetectable HBV DNA 4. Immune escape = Deranged transaminases, - Risk of progression to cirrhosis and HCC

Answer 8

**Treatment** *Acute* * Supportive * Simple analgaesia, IVF *Chronic* * Education and harm minimisation * Transmission prevention (body fluids, sexual contact, IVDU, tattoos) * Avoid EtOH * Weight management (prevent NAFLD) * Vaccinate against HepA * Vaccinate sexual contacts against HepB * Treatment should be considered in _chronic infection_ (immune clearance and immune escape phases). * Antiviral medications or pegylated interferon (at least 12-months) * Entecavir PO OR Tenofovir PO OR Pegylated IFN * Monitor for HCC * If evidence of chronic infection (↑AST/ALT and HBsAg +ve for \>6 months = chronic hepatitis) OR HBsAg in a risk group (Asian men \>40, Asian women \>50, cirrhosis, HCC FHx), do HCC surveillance: * Liver USS every 6-months **Prognosis** * Cirrhosis: 20-50% * HCC: ↑Risk with duration of infection (eg if infected as a child, higher risk of HCC in later life)

Answer 9

Hepatitis C * RNA virus. * ↑↑Develop into chronic infection (85%). * Blood-borne spread: IVDU, needle-stick injuries **Risk factors** * IVDU: Main RF * Blood transfusion before 1992 * Tattoos **Clinical features** * Clinical manifestations develop 6-8 weeks after exposure * Mild and non-specific features (fatigue, malaise, nausea) * Most people are asymptomatic **Diagnosis** * Suspected on basis of elevated ALT/AST and positive serum anti-HCV * Diagnosis: Serum PCR (HCV RNA) **Investigation** * Bloods: FBC, LFTs, coag profile, AFP, HCV serology, HCV genotype (has implications for response to Tx) * Imaging: Liver USS **Treatment** * Supportive * Simple analgaesia, IVF * Observe for spontaneous resolution of HCV infection * Tx with IFN * Significant SEs * +/- Pegylated interferon started within 12-wks of hepatitis onset for 24-wks of Tx

Answer 10

Further work-up after chronic hepatitis C diagnosed To be done before referral for treatment Bloods * HCV genotype * FBC - anemia, thrombocytopenia * LFTs - hypoalbuminemia, raised AST/ALT * Coagulation * Screen for other disease - HBV, HIV, syphilis Imaging (chronic) * USS & FibroScan - determine cirrhosis Management of chronic infection * Non-pharmacologicalCounsel * Now curable; requires treatment to prevent cirrhosis and HCC * Cure rates \>90% Lifestyle * Avoid alcohol * Vaccination - HAV, HBV * Avoid transmission - safe sex, no syringe sharing, don’t share personal equipment Refer ALL CHRONIC HEP C to specialist for anti-viral treatment New interferon-free regimens have revolutionised hep C (many drugs) * Became available in 2016 * \>90% success rate without significant side effects Cannot be used in pregnancy unlike Hep B Duration = 12 weeks then reassess Serology **HCV RNA --\> if undetectable = cured** **HCV antibodies - do NOT mean they are immune (can be reinfected)**

Answer 11

Autoimmune Hepatitis * Diagnosis of exclusion: rule out viruses, drugs, metabolic or genetic causes * Can be severe: 40% 6 month mortality without treatment * Extrahepatic manifestations * Sicca, Raynaud’s, thyroiditis * Hypergammaglobulinemia Drug-Induced Liver disease **Causes** * Acetaminophen: active ingredient in many over the counter medications e.g. paracetamol * Direct hepatotoxin * 10-15g in healthy adult, less in EtOH abuse * Saturates glucoronidase enzyme → reactive metabolites build up and not eliminated → damage to hepatocyte membrane * Blood levels of acetaminophen proportionate to severity of liver damage * Methotrexate * Amiodarone * Chlorpromazine, Isoniazid * Statins, phenytoin, PTU, sulfonamides, tetracyclines **Clinical features** * Acetaminophen: Fulminant liver failure (AST, ALT \>1000 then jaundice and encephalopathy) * Methotrexate: Cirrhosis * Amiodarone: Similar picture to alcoholic hepatitis * Chlorpromazine: Cholestasis, fever, rash, jaundice, pruritus, eosinophilia * Isoniazid: ↑AST, ALT **Investigation** Bloods: Serum paracetamol level, LFTs **Treatment** *Paracetamol poisoning* * Oral activated charcoal if \<1h after ingestion * Gastric lavage / emesis if \<2h after ingestion * N-acetylcysteine (NAC) PO or IV (best within 8-10h of ingestion) to promote hepatic glutathione regeneration

Answer 12

Haemochromatosis à Inherited disorder of Fe metabolism causing excessive Fe storage → multiorgan dysfunction (liver, pancreas, heart, joints, pituitary, adrenals, skin). **Epidemiology** * Northern European descent * Tends to present in middle-age * Men are more frequently and severely affected than women * Women tend to present with the disease 10yrs later than men (menstruations) **Aetiology** * Primary (hereditary) hemochromatosis * Hepcidin deficiency results in ongoing gut absorption of iron despite adequate iron stores * HFE gene found on chromosome 6 is the most common mutation. Incomplete penetrance. * Results in ongoing gut absorption of iron despite adequate iron stores   * Secondary hemochromatosis * Parenteral iron overload (e.g. transfusions) * Chronic haemolytic anaemia: thalassemia, pyruvate kinase deficiency * Excessive iron intake   **Clinical features** à Usually presents with trivial ↑ transaminases _Early_ * Asymptomatic * Tiredness, arthralgia (2nd and 3rd MCP joints, knee) * Erectile dysfunction _Late_ * Slate-grey skin (melanin) * Chronic liver disease (cirrhosis, HCC) * Dilated cardiomyopathy * Osteoporosis _Endocrinopathies_ * DM (bronze diabetes), hypogonadism (pituitary) **Investigations** * Bloods: ↑LFTs, FBC, AFP (6-monthly HCC screening if cirrhosis) * Fe studies - transferrin saturation \>45%, ↑ferritin * HFE gene testing * Imaging: Liver USS (6-monthly HCC screening if cirrhosis) * Liver biopsy in late stage to define degree of Fe overload and detect cirrhosis **Treatment** * Venesection * Once every 1-3 weeks returns life expectancy to normal if no permanent organ damage done. Continue for life. * Diet * Well balanced low-iron diet. Tea and coffee with meals to ↓Fe absorption. Limit vit C with meals as it ↑Fe absorption. * Screening * Monitor pt with LFTs, BSLs, HbA1cs * Genetic testing for 1st degree relatives for haemochromatosis * _Pharmgological:_ Desferrioxamine (Fe chelator) if intolerant of venesection or contraindicated

Answer 13

Alcoholic Liver disease * Fatty liver (all alcoholics): reversible if EtOH stopped. * Alcoholic hepatitis (35%): usually reversible if EtOH stopped. * Cirrhosis (10%): potentially irreversible **Pathophysiology** * Ethanol oxidation → acetalaldehyde * Impaired lipolysis * FAs and TGs accumulate in the liver * Necrosis and hepatic vein sclerosis * Immune reaction to acetaldehyde and by extension, hepatocytes **Clinical features** *Liver* * Fatty liver * Mildly tender hepatomegaly, jaundice rare * Mildly ↑transminases * Alcoholic hepatitis * Variable severity, mild to fatal * Jaundice, low grade fever, RUQ discomfort, ascites, ↑WCC * Cirrhosis (see below) *Other organs* * CVS: Arrhythmias, HTN, cardiomyopathy * CNS: Self-neglect, ↓memory/cognition, cortical atrophy, ataxia, neuropathy, Wernicke's encephalopathy, Korsakoff's dementia * GIT: Obesity, D+V, gastritis and gastric erosions, peptic ulcers, varices, pancreatitis, cancer, Mallory-Weiss tears, oesophageal rupture (Boerhaave's syn.) * Blood: Macrocytic anaemia **Investigations** * Bloods: FBC, U&Es, LFTs, coag profile * LFTs: AST \> ALT (2:1), ↑GGT * FBC: ↑MCV * Imaging: Liver USS * MCS: Ascitic tap **Treatment** _Non-pharmacological_ * EtOH cessation * Alcoholics Anonymous, disulfiram (↑acetaldehyde if drink), naltrexone, acamprosate (↓ cravings) * Optimise nutrition, high-protein diet * Daily weight, LFTs, U&Es, INR _Pharmacological_ * Thiamine PO/IM/IV and multivitamins * 100mg PO tds +/- * 200mg IM/IV for 3 days * Benzodiazepines (loading dose then maintenance) for EtOH withdrawal * Prednisolone 40mg daily for 4 wks if hepatic encephalopathy or severe liver disease * Lactulose PO to ↓ risk of hepatic encephalopathy

Answer 14

Non-Alcoholic Fatty Liver Disease (NAFLD) à ↑ Fat deposition in hepatocytes (steatosis) +/- inflammation (steatohepatitis). à Spectrum of disorders characterized by macrovesicular hepatic steatosis   **Risk factors** * DM, dyslipidaemia, metabolic syndrome * Drugs (eg amiodarone, MTX, tetracycline) * Rapid weight loss/gain **Clinical features** * Often asymptomatic * Fatigue, malaise, vague RUQ discomfort * Mildly ↑transaminases (typically ALT\>AST) * Insulin resistance * ↑TGs, ↑cholesterol **Investigations** * Bloods: LFTs, lipids, coag profile, BSL/HbA1c * Imaging: Liver USS (echogenic texture) * Liver biopsy (rarely performed unless severe): diagnostic **Treatment** * Gradual weight loss is the best Tx * Modify risk factors (eg BSL, HTN, lipids etc) **Prognosis** * Most die from CVS or cerebrovascular disease * Risk of progression to cirrhosis \<25% , but ↑ if steatohepatitis

Answer 15

Acute Liver Failure à Liver failure either sudden onset (acute hepatic failure) or more often, decompensation of chronic liver disease (acute on chronic hepatic failure) * Fulminant hepatic failure is a clinical syndrome resulting from massive necrosis of hepatocytes → severe impairment of liver function. **Causes** * Infections * Viral hepatitis - Hep B, Hep C, CMV * Yellow fever, leptospirosis * Neoplasm * Vascular: Budd-Chiari syndrome * Drugs: Paracetamol overdose, isoniazid, EtOH * Metabolic * Haemochromatosis, *a*1-antitrypsin deficiency, Wilson's disease * Fatty liver of pregnancy, HELLP syndrome (haemolysis, elevated liver enzymes, low plts) **Clinical features** * Flu-like prodrome may precede jaundice by 1-2 weeks * N/V, anorexia, taste/smell disturbance, headaches, fatigue, myalgia, low-grade fever * Arthralgia and urticaria (especially HBV)  * Only some progress to icteric (clinical jaundice) phase, lasting days to weeks * Pale stools and dark urine 1-5 d prior to icteric phase * Hepatomegaly and RUQ pain * Splenomegaly and cervical lymphadenopathy (10-20% of cases) * Hepatic encephalopathy, hepatic asterixis, constructional apraxia (cannot copy a 5-pointed star) * +/- Signs of CLD (suggests acute-on-chronic hepatic failure) **Investigations** * Bloods: FBC, U&E, LFTs, coag profile, BGL * Paracetamol level * Serology - hepatitis, CMV, EBV * Fe studies, caeruloplasmin, a1-antitrypsin * Autoantibodies (ANA, AMA, SMA) * Imaging: Abdo USS, Doppler flow studies of portal vein, CXR * MCS: Blood cultures, urine, ascitic tap **Treatment** à Risk of sepsis, hypoglycaemia, GI bleeds/varices, encephalopathy _Non-pharmacological_ * Transfer to ICU, intubation, NG tube * IDC for fluid monitoring * Regular observations, daily weights * Optimise nutrition _Pharmacological_ * Treat cause (eg GI bleed, sepsis, paracetamol toxicity) * Thiamine PO/IM/IV and multivitamins * 100mg PO tds +/- * 200mg IM/IV for 3 days * Lorazepam (seizures) * Ascites * Restrict fluid, low salt diet * Diuretics: Spironolactone 100mg PO daily +/- frusemide PO * Bleeding * Vit K and platelets * FFP * +/- Endoscopy (varices) * Encephalopathy * Lactulose 30-50mL TDS aiming for 2-4 soft stools/day

Answer 16

Cirrhosis * Liver damage characterised by diffuse distortion of the basic architecture and replacement with scar tissue and nodular regeneration. * Stage 1 = cirrhosis is compensated and asymptomatic. Can last for 10-20yrs with almost normal life expectancy. * Stage 2 = cirrhosis is the onset of first decompensation, typically development of ascites, variceal bleeding, encephalopathy. **Aetiology** * Most often chronic EtOH abuse, HBV or HCV. * Other causes: * Metabolic - haemochromatosis, *a*1-antitrypsin def, Wilson's disease, NAFLD * Autoimmune - primary biliary cirrhosis, primary sclerosing cholangitis * Drugs - amiodarone, methotrexate **Clinical features** * May be asymptomatic with ↑LFTs * Leuconychia, half-and-half nails (Terry's nails), clubbing, palmar erythema * Dupuytren's contracture, parotid enlargement, xanthelasma * Spider naevi, gynaecomastia, testicular atrophy, loss of body hair * Hepatomegaly or small liver in late disease **Complications** **à VARICES** * Varices * Anaemia, pancytopenia * Renal failure, hepatopulmonary syndrome * Infection * Coagulopathy * Encephalopathy * Sepsis

Answer 17

**Investigations** * Bloods: LFTs (may be ↑ or normal in late stage), coag profile, FBC (↓WCC, ↓plts from hypersplenism) * Look for cause - Fe studies, antibody studies (ANA, AMA, SMA), AFP, caeruloplasmin, a1-antitrypsin deficiency * Imaging: Liver USS +/- Doppler flow studies * MCS: Ascitic tap (spontaneous bacterial peritonitis) * Liver biopsy: Gold standard, but not generally performed for diagnosis alone **Diagnosis** *Child-Pugh* à Used to assess the prognosis of chronic liver disease, mainly cirrhosis * Used to determine the prognosis as well as required strength of treatment and the necessity of liver transplantation * Scoring based on * Bilirubin * Albumin * Prothrombin time/INR * Ascites * Hepatic encephalopathy à Each measure given a score of 1 to 3 *Interpretation* Points Class One year survival Two year survival 5-6 A 100% 85% 7-9 B 81% 57% 10-15 C 45% 35% *MELD score – Model for End Stage Liver Disease* à Scoring system for assessing the severity of chronic liver disease * Useful in determining pronogis and prioritizing for receipt of liver transplant * Score based on * Serum bilirubin * Serum creatinine * INR *Interpretation* à Score required for possible transplantation: 15-30 à 3 month mortality * 40 or more — 71.3% mortality * 30–39 — 52.6% mortality * 20–29 — 19.6% mortality * 10–19 — 6.0% mortality * \<9 — 1.9% mortality **Treatment** * Symptomatic treatment * Cholestyramine for pruritus * Ascites: Fluid restriction, low-salt diet, spironolactone 100mg PO daily +/- frusemide PO * Prevent further complications * Hepatic encephalopathy: Lactulose 30-50mL PO tds aiming for 2-4 loose stools/day * Screen for HCC 6-monthly (AFP, liver USS) * Liver transplant is the definitive Tx *Treatment of varices* * Propranolol * Octreotide * Vasopressin * PPI * Surgery: banding + sclerotherapy *Managing complications of liver failure* * Seizures: Lorazepam * Bleeding: vitamin K, FFP +/- transfusion * Ascites * Mild: Spironolactone * Mod: add furusemide * Severe: paracentesis + albumin IV * Refractory: repeated paracetesis/TIPDS/transplant * Infection: ceftriaxone * Bleeding varices * Primary prevention: propranolol * Initial management of bleeding: octreatide (somatostatin anolouge – decreased sphlancnic blood flow + partial pressure) * + IV resuscitation – IVF + PRBC’s * + prophylactic antbiotiocs * Emergency endoscopy +/- banding/sclerotherapy * If this fails à Balloon tamponade * If ongoing, consider emergency TIPS * Hepatic encephalopathy * Recognise + treat: infection, constipation, reanl impairment, non-adherence, electrolyte disturbances, drugs * First line: lactulose * Consider empirical treatment of infection * Monitor for 2-4 stools/day * Cerebral oedema: mannitol *General meatures* * ICU and elevate head of bed * Protect the airway with intubation * NGT, IDC * Salt + water restriction * Determine Child’s Pugh score (A, B, C) – albumin, bilirubin, INR, encephalopathy, ascites

Answer 18

Clinical Symptoms * Non-specific early symptoms - N&V, weight loss, anorexia, weakness, abdominal distention, jaundice * Often presents acutely with complications Exam * General - orientation (encephalopathy), jaundice, ascites, weight loss/wasting, SOB (pulmonary edema), if very sick consider spontaneous bacterial peritonitis * Vitals - tachypnoea, tachycardia, febrile (chronic) * Hands - clubbing (mostly biliary cirrhosis), koilonychia, leukonychia (white nails), muehrcke's lines (white lines parallel to lunula), dupyutren's contracture, tremor, palmer erythema, hepatic flap * Arms - bruising, scratch marks * Face - scleral icterus, conjunctival pallor, enlarged parotids, fetor hepaticus * Chest - spider naevi (\>3 is abnormal), gynaecomastia * Abdomen - distended ascites, caput medusa, palpate liver + percuss span, splenomegaly, percuss/shifting dullness, auscultate, DRE (haemorrhoids) * Legs - pedal edema, bruising * Others - CV (AF, alcoholic DCM), resp (pulmonary edema), neuro (peripheral neuropathy, Korsakoff's/Wernicke's) Ix Bedside * VBG - respiratory alkalosis, metabolic acidosis Bloods * Glucose - hypoglycaemia * FBC (anemia, thrombocytopenia, leukopenia) * Smear (target cells) * UECs (↓urea, hyponatremia, hepatorenal) * LFTs - AST/ALT may be normal, hyperbilirubinaemia, low albumin * Coagulation studies (↑INR) * Viral serology - HBV, HCV, HIV Imaging * Liver USS & FibroScan - shrunken, nodular (only good for advanced cirrhosis) * CT abdomen - varices, nodular liver, splenomegaly, ascites * Upper GI endoscopy \* - all cirrhosis for varices Haematological abnormalities * Macrocytic anemia - alcohol BM toxic, hypersplenism, bleeding, dietary folate deficiency * Thrombocytopenia - ↓thrombopoietin, hypersplenism * Leukopenia - hypersplenism, alcohol * ↑INR - relationship to bleeding is controversial as it doesn't measure altered fibrinolysis/prothrombotic factors also affected --\> therefor may not have bleeding diathesis * Hyponatremia - diuretics, renal impairment, water retention Cirrhosis complications = VARICES * Varices * Anemia/ascites (& SBT) * Renal failure (hepatorenal syndrome) * Infection & sepsis * Coagulopathy/Cancer (HCC) * Encephalopathy * Spleen (hypersplenism)

Answer 19

Primary Biliary Cirrhosis à Chronic inflammation and fibrous obliteration of intrahepatic bile ductules * Likely an autoimmune cause **Clinical features** * Often asymptomatic  * Initial symptoms: pruritus, fatigue  * Chronic: jaundice and melanosis (darkening skin) and other signs of cholestasis * End-stage: hepatocellular failure, portal HTN, ascites  * High incidence of osteoporosis   **Investigations** * Bloods * LFT: elevated ALP, GGT * Antibodies: anti-microbial antibodies (AMA) * Serum cholesterol: Mild decrease in LDL and large increase in HDL * Liver biopsy: confirms diagnosis and stages severity * MRCP: normal bile duct **Treatment** * Ursodiol +/- cochicine, methotrexate * Cholestyramine: pruritis, hypercholesterolaemia * Calcium and vitamin D for low bone density: bisphosphonates if osteoporosis severe * Monitor for thyroid disease * Liver transplant if disease severe, progressive Primary Sclerosing Cholangitis à Inflammation of the biliary tree (intra and/or extrahepatic bile ducts) → scarring and strictures. **Aetiology** * Primary = idiopathic * Associated with IBD (UC) * Secondary causes: * Long-term choledocholithiasis * Cholangiocarcinoma * Surgical/traumatic injury * Contiguous inflammatory process * Post-ERCP * Associated wit HIV/AIDS **Clinical features** * Fatigue and pruritus * Advanced disease: ascending cholangitis (biliary obstruction), cirrhosis, liver failure *Complications* * Repeated bouts of cholangitis may lead to complete biliary obstruction with resultant secondary biliary cirrhosis and hepatic failure * Increased incidence of Cholangiocarcinoma **Diagnosis** * ERCP shows narrowing & dilatations of bile ducts ("beading"), both intra- and extra-hepatic bile ducts **Investigation** * Bloods * LFTs: ↑ALP, mildly ↑AST * Autoantibodies: ↑ ANCA typical, elevated IgM * Imaging: ERCP, MRCP **Treatment** * Cholestyramine: Bile acid sequestrant * Abx for cholangitis * Surgery * Sphincterotomy, stenting * Liver transplant is definitive treatment

Answer 20

Portal hypertension à Pressure gradient between hepatic vein pressure and wedged hepatic vein pressure (corrected sinusoidal pressure) \>5 mmHg **Causes of portal HTN** * Pre-hepatic* * Thrombosis (portal or splenic vein) * Hepatic* * Cirrhosis (most common in developed countries), schistosomiasis (most common worldwide), sarcoid, myeloproliferative diseases * Post-hepatic* * Budd-Chiari syn, RVF, constrictive pericarditis **Investigations** *SAAG – Serum ascites albumin gradient* * Calculation used to determine cause of ascites * SAAG = Serum albumin – ascetic fluid albumin * High gradient (\>11g/L) indicates ascites is due to portal hypertension * This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system * Low gradient (\<11g/L) indicates causes of ascites are not associated with increased portal pressure * E.g. TB, pancreatitis, infections, serositis or nephritic syndrome **Complications** * GI bleeding from varices in oesophagus, less commonly in stomach, even less frequently from portal hypertensive gastropathy * ascites   * hepatic encephalopathy   * thrombocytopenia   * renal dysfunction   * sepsis   * arterial hypoxemia   **Treatment** * Control bleeding * Vasopressin * Octreotide * Flexible viewing tube: endoscope * Portosystemic shunting * If bleeding continues * Liver transplantation

Answer 21

Management Diverticulosis * Education * Lifestyle * Nutrition - high fibre diet + 2L water a day + Metamucil * Physical activity Diverticulitis DRSABCDE * DRS - gen surg * C - IVF replacement Admit if any 1 of: * Hx - severe pain or diffuse peritonitis, sepsis, significant comorbidities or immunocompromised, unable to tolerate PO intake * Workup - complicated diverticulitis on CT, high fever or leukocytosis Supportive * UO * NBM - clear fluids only until improve due to chance of surgery * IVFs * Analgesia * VTE prophylaxis Management depends on imaging * Diverticulitis with no complications is managed conservatively: * Consider none if systemically well * Antibiotics PO - gentamicin + amoxycillin + metronidazole * Cover - usual GIT flora (Gram -ve & anaerobic cover); particularly E.coli & Bacteroides Complicated diverticulitis * What - generalised peritonitis, abscess, fistula etc. * IV antibiotics - IV gentamicin + metronidazole + amoxycillin (triple therapy) Procedures * Abscess or fistula - percutaneous drainage or surgery to resect with anastomosis * Peritonitis (ruptured) - peritoneal washout + Hartmann procedure (bowel resection with colostomy --\> later re-anastomosis)

Answer 22

Ascites à Accumulation of excess fluid in the peritoneal cavity * Key factor: increased sodium (and water) retention by the kidney for reasons not fully understood * Types* * Refractory ascites: Ascites which cannot be mobilized by low sodium and maximal diuretics * Occurs in 5% of cirrhotic patients * Poor prognosis * Non-refractory ascites: Responds to low sodium and diuretics *Diagnosis* * Abdominal ultrasound * Physical exam * Bulging flanks, shifting dullness, fluid wave test positive * Most sensitive symptom: ankle swelling * Diagnostic paracentesis * Cell count * Chemistry * MCS, gram stain * Cytology *Treatment* * Non-refractory ascites * Na+ restriction * Diuretics: spironolactone, furosemide * Refractory ascites: Ascites which cannot be mobilized by low sodium and maximal diuretics * Therapeutic paracentesis with IV albumin Spontaneous Bacterial Peritonitis **à** Infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition à Defined by an ascitic fluid absolute neutrophil count \>250 cells/mm^3, whether or not there is culture growth. * One of the most frequently encountered bacterial infections in patients with cirrhosis, and most commonly seen in patients with end-stage liver disease. * Complicates ascites, but does not cause it * High risk in patients with GI bleed **Aetiology** * Infection of the ascetic fluid * Most common pathogens * E coli * S aureus * S pneumonia **Clinical features** * Patients are commonly minimally symptomatic, and may even be asymptomatic. * 1/3 of patients are asymptomatic * Fever, chills, abdominal pain, ileus, hypotension, worsening encephalopathy, acute kidney injury * Abdominal pain * Fever, vomiting * Altered mental status * GI bleeding * Diarrhoea * Hypothermia, hypotension, tachycardia **Investigations** * FBC: leukocytosis, anaemia * Ascitic fluid laboratory tests should include cell count and culture * Including an absolute neutrophil count (ANC) and gram stain * Bedside leukocyte esterase reagent strip testing can more rapidly rule in spontaneous bacterial peritonitis (SBP) but cannot rule it out. * Blood cultures * LFTs * INR **Diagnosis** * Absolute neutrophil count in peritoneal fluid \>0.25x10⁹ cells/L * Gram stain in only 10-50% of patients * Culture positive in \<80% of patients **Treatment** * Empiric antibiotic regimens that have been found to be equally efficacious include cefotaxime, ceftriaxone, fluoroquinolones, and ampicillin/sulbactam. * Albumin is indicated in the treatment of patients with renal dysfunction. * Continuous oral fluoroquinolone prophylaxis is indicated in patients with an ascitic fluid protein concentration Hepatic Encephalopathy à Potentially reversible neuropsychiatric syndrome secondary to liver disease. **Pathophysiology** * ↑ Systemic toxins due to portosystsemic shunting and reduced hepatocyte function. Especially ammonia from the gut, mercaptans, amino acids. These are believed to affect the brain. **Clinical features** Stages I to IV: 1. Altered mood/behaviour, sleep pattern disturbance, dyspraxia (5-point star drawing) 2. Drowsiness, confusion, slurred speech, personality change and inappropriate behaviour 3. Incoherent, restless, hepatic flap, stupor (rousable), hyperactive reflexes 4. Coma **Investigations** à Need to rule out other causes of acute confusion and behavioural changes * Bloods: FBC, U&Es, LFTs, coag profile, BSL * Imaging: CXR, CT head, EEG findings * MCS: Blood cultures, ascitic tap, urine * Clinical diagnosis: supported by laboratory findings and exclusion of other neuropsychiatric diseases **Treatment** * Treat precipitating factors * Renal impairment, GI bleeding, infections, medications (sedatives, opioids) * Lactulose 30mg PO * Hourly to 2 hourly initially * 3-4 times daily * Traps and binds ammonia in colon * Empirical Abx for infection until septic workup back * Ceftriaxone IV OR Cefotaxime IV OR Pip-taz IV *Severe encephalopathy and coma* * Endotracheal intubation * Respiratory support * Enteral nutrition

Answer 23

Liver tumours Clinical features - Hepatomegaly: smooth, hard, irregular - Look for signs of chronic liver disease: Abdominal mass, bruit - Evidence of decompensation: ascites, jaundice, hepatic encephalopathy, HRS, HPS Investigations - Blood: FBC, LFT, coags, U&E, ESR, alpha fetoprotein, hepatitis, serology - Imaging o USS/CT o MRI - Pathology: liver biopsy o Biopsy not required for diagnosis Management - HCC: resect solitary tumours \<3 cm: high recurrent rate o Liver transplant - Cholangiocarcinoma: very poor prognosis o Major hepectomy + Extrahepatic bile duct excision _ caudate lobe resection § Lots of post op complications o Stenting can provide temporary relief - Hemangiomas common: anabolic steroids, OCP, pregnancy o Only treat if symptomatic of \>5cm - Others: cysts

Answer 24

Inflammatory bowel disease (IBD) à Crohn's disease (CD) and ulcerative colitis (UC) **Pathophysiology** * Unknown. * Genetic susceptibility + abnormally high immune responsiveness (lack of down-regulation) → * Sustained autoimmune response * Lack of appropriate down-regulation of immune responsiveness **Crohn’s Disease** **Ulcerative Colitis** Location Any part of GIT: skip lesions Colon and rectum: Continuous Macroscopic Thin, deep fissures ‘cobblestone’ Narrowing and proximal dilation of normal tissue, broad oedematous pseudopolyps Wide, shallow fissures with psuedopolyps Chronic inflammation à atrophy: smooth flat mucosa Microscopic Deep crypt abscess with lymphocytes and granuloma Shallow crypt abscess with lymphocytes but no granuloma Rectal bleeding Uncommon Very common Diarrhoea Occasional Frequent small stools Abdominal pain Colicky Less common Fever Common Uncommon Palpable mass Frequent: RLQ Rare Dermatologic manifestations Erythema nodosum Pyoderma gangrenosum Psoriasis Crohn’s plaques Perianal skin tags Mucosal ulcers Erythema nodosum Pyoderma gangrenosum Psoriasis Radiologic features Cobblestone mucosa Frequent strictures and fistualae AXR: bowel wall thickening ‘string sign’ Lack of haustra Rheumatology Arthritis more common Ankylosis spondylitis Sarcoilitis Arthritis less common Sacroilitis Hepatobiliary Cholelithiasis Fatty liver Primary sclerosing cholangitis Cholelithiasis Fatty liver Urology Calculi: Most Common Fistula: due to deep penetrating ulcer Calculi Ocular Uveitis :More common Uveitis Complications Fistula, Anorectal disease Toxic megacolon Strictures, adhesions, perforation, peritonism, abscess, malabsorption, anaemia Colon cancer Risk increased if \>30% bowel involved Risk increased Crohn's disease à Chronic inflammatory GI disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus * Terminal ileum and proximal colon most commonly affected. Skip lesions (unaffected bowel) between areas of active disease **Epidemiology** * F \> M * Presentation mostly 20-40yrs * Associated with smoking (↑risk) **Clinical features** * Usually presents with recurrent episodes of abdominal cramps, diarrhoea and weight loss * Diarrhoea/urgency * ↓Weight / FTT (children) * Fever, malaise, anorexia * Ileitis can mimic acute appendicitis * Presents with post-prandial pain, vomiting and RLQ mass * Perianal skin tags and fissures, fistulae, abscesses * Extra-intestinal manifestations of IBD more common *Complications* * Bowel obstruction, perforation * Deep fissures with risk of perforation into contiguous viscera * Abscesses: Perianal, abdominal, pelvic * Fistulae: Colovesical, colovaginal, perianal * Enteric fistulae may communicate with skin, bladder, vagina, bowel * Rectal bleeding, colon cancer **Diagnosis** Diagnosed if typical features are seen in a combination of endoscopic, histological and radiological investigations. **Investigation** * Bloods: FBC, U&Es, LFTs, ESR/CRP, Fe studies, vitamin B12, folate, coag profile, bacterial cultures * CRP elevated in most new cases, useful to monitor treatment response * Colonoscopy, endoscopy (less frequent) * Stool: MCS (rule out C. difficile, Campylobacter, E. coli) * Imaging: AXR, MRI (fistulae, abscesses, strictures) **Treatment** * Aims of drug therapy are to induce remission in active disease, maintain corticosteroid-free remission and prevent relapse * The severity of disease and the site(s) of affected bowel determine which drugs and route of administration may be used *Acute* * Admission if severe exacerbation * NBM * IVF * Induce remission * Mild to moderate CD * High dose oral steroids: Prednisone 40-50mg PO daily until response * Wean down steroids over 8-12 wks * +/- Metronidazole or Ciprofloxacin * Severe CD * IV steroids: Hydrocortisone 100mg IV QID * Generally given for 3-7 days * Surgery * Metronidazole or Ciprofloxacin * +/- Infliximab IV or Adalimumab SC (anti-TNF) * Antibiotics do not have a role unless transmural complications (e.g. abscess) *Chronic* _Non-pharmacological_ * Smoking cessation * Diet change * During exacerbation low fibre may help control diarrhoea and pain related to food intake * 2˚ lactose intolerance * Correct micronutrient deficiencies with appropriate supplements * Iron, zinc, vitamin B12, calcium, magnesium, folic acid, Vitamin D _Pharmocological_ * Maintain remission * Azathioprine PO (immunosuppressant) * Methotrexate plus Folic acid IV 8-weekly (immunosuppressant) * If Azathioprine not tolerated * Infliximab IV (anti-TNF alpha) * Steroids should _not_ be used as maintenance therapy * Perianal and fistulising disease * Metronidazole or Ciprofloxacin PO bd * Azathioprine * Infliximab IV or Adalimumab SC Ulcerative colitis à Inflammatory disease affecting the colonic mucosa anywhere from the rectum (always involved) to the caecum * It 'never' spreads proximal to the ileocaecal valve (except for backwash ileitis). * Pseudopolyps (oedematous intact mucosa) on colonoscopy. **Epidemiology** * More common than CD. * Presentation mostly 15-30yrs. * More common in non-smokers. **Clinical features** * Rectal bleeding * Episodic or chronic diarrhoea +/- blood, mucus * Crampy abdominal pain * Tenesmus, urgency, incontinence * Fever, malaise, anorexia * ↓ Weight * Extraintestinal manifestations less common in UC *Complications* * Perforation * Haemorrhage * Toxic megacolon (colonic diameter \>6cm) * Colon cancer **Investigation** * Bloods: FBC, U&Es, LFTs, ESR/CRP * Stool: MCS * Rule out C. difficile, Campylobacter, E. coli, Salmonella, Shigella * Imaging: AXR (dilated colon from toxic megacolon), erect CXR (perforation) * Sigmoidoscopy or colonoscopy with biopsy plus exclusion of infectious causes: diagnostic ![]() **Treatment** *Acute* * Active proctitis/distal colitis * Mesalazine/5-aminosalicyclic acid (5-ASA) suppository * Hydrocortisone or prednisolone * If 5-Aminosalicylates are ineffective * Surgery * Needed in ~20% of UC patients, higher mortality if performed as an emergency * Procoto-colectomy, terminal ileostomy *Chronic* * Maintain remission * Mesalazine/5-aminosalicyclic acid (5-ASA) * Active form of sulfasalazine and contains [sulfapyridine](https://en.wikipedia.org/wiki/Sulfapyridine) and mesalazine * Immunomodulators * Azathioprine PO or Mercaptopurine PO or Methotrexate + Folate * Infliximab * Surveillance colonoscopy for bowel cancer * Every 2-4 yrs

Answer 25

Gallbladder Ascending Cholangitis à Infection of the biliary tree * Stasis in the biliary tract due to obstruction or stricture * Infection originates in the duodenum or spreads haematogenously from the portal vein * Bacteria * E coli, Klebsiella, enterobacter, enterococcus * Co-infection with bacteroides and clostridia **Clinical features** * Charcot’s triad: fever, RUQ pain, jaundice * 50-70% of patients * Reynolds pentad: Charcot’s triad, hypotension, altered mental status **Investigations** * Bloods * Increased WBC * Increased ALP, ALT, bilirubin * Blood culture * Imaging: abdominal US - CBD dilation, stones **Treatment** * Drainage via ERCP * If not possible: percutaneous biliary or surgical routes * Antibiotic therapy: broad spectrum to cover gram-negatives, enterococcus, anaerobes * Pip-taz, ampicillin, sulbactam

Answer 26

Pancreas Pancreatic Enzyme Abnormalities **Increased serum amylase** * Pancreatic disease * Pancreatitis, pancreatic duct obstruction, pseudocyst, abscess, ascites, trauma, cancer * Non-pancreatic abdominal disease * Biliary tract disease, bowel obstruction, perforated or penetrating ulcer, ruptured ectopic pregnancy, aneurysm, chronic liver disease, peritonitis * Non-abdominal disease * Cancer, salivary gland lesions * Macroamylasemia **Increased serum lipase** * Pancreatic disease * Non-pancreatic abdominal disease * Non-abdominal disease: macrolipasemia, renal failure Acute pancreatitis **Aetiology** à I GET SMASHED * Idiopathic * Gallstones * Ethanol * Tumours * Scorpion stings * Microbiological * Bacterial: mycoplasma, campylobacter, TB, legionella, leptospirosis * Viral: mumps, rubella, varicella, viral hepatitis, CMV, EBV, HIV, Coxsackie virus * Parasites * Autoimmune: SLE, polyarteritis nodosa, Crohn’s disease * Surgery/trauma * Hyperlipidemia, hypercalcaemia, hypothermia * Emboli or ischaemia * Drugs/toxins **Pathophysiology** * Activation of proteolytic enzymes within pancreatic cells, starting with trypsin, leading to local and systemic inflammatory response   * In gallstone pancreatitis, this is due to mechanical obstruction of the pancreatic duct by stones   * In ethanol-related pancreatitis, pathogenesis is unknown   * In rare genetic diseases, mutations prevent the physiological breakdown of trypsin required  normally to stop proteolysis (e.g. mutant trypsin in hereditary pancreatitis or mutation in SPINK 1 gene which normally inhibits activated trypsin); may be model for ethanol-related pancreatitis   **Clinical features** * Pain: epigastric, constant * Can radiate to back * Jaundice: compression or obstruction of bile * May improve when leaning forward (Inglefinger’s sign) * Tender rigid abdomen; guarding  * N/V  * Abdominal distention from paralytic ileus * Fever: chemical, not due to infection * Cullen’s/Grey-Turner’s signs  * Tetany: transient hypocalcemia  * Hypovolemic shock: can lead to renal failure * Acute respiratory distress syndrome  * Coma **Investigations** * Bloods * Increased WBC, glucose * Decreased Ca2+ * Increased serum pancreatic enzymes: amylase, lipase * LFT: ALT * Imaging * X-ray: sentinel loop/dilated proximal jejunum * US: useful for evaluating biliary tree * CT scan with IV contrast * ERCP or MRCP **Treatment** * IV fluids * Analgesia: Morphine, fentanyl *Severe pancreatitis* * Nasogastric tube * Early enteral nutrition * Treatment of hyperglycaemia * Treatment of symptomatic hypocalcaemia * Imaging of the biliary tree with MRCP to confirm biliary obstruction and guide ongoing management Chronic pancreatitis à Irreversible damage to pancreas characterised by pancreatic cell necrosis, inflammation and fibrosis. **Causes** * EtOH (most common) * CF * Severe protein-calorie malnutrition * Idiopathic **Clinical features** * Recurrent attacks of severe abdo pain (upper abdo and back) * May be chronic painless pancreatitis * Malabsorption syndrome → steatorrhoea * Diabetes * Weigth loss *Complications* * Pseudocyst * Diabetes * Biliary obstruction * Gastric varices * Pancreatic cancer **Investigations** * Bloods: Glucose, LFTs, lipase and amylase * Imaging: AXR (pancreatic calcifications), USS or CT abdo (calcification, pseudocysts) * Other: 72h faecal fat test, faecal elastase **Treatment** *Chronic* _Non-pharmacological_ * Lifestyle modification * Abstain from EtOH * Low fat diet, high in protein * Vit ADEK supplementation _Pharmacological_ * Analgaesia * Coeliac-plexus blocks * Insulin * Pancreatic enzyme replacement * Creon * Surgery * Resistant pain * Opiate abuse * Blocked pancreatic duct

Answer 27

Irritable bowel syndrome (IBS) à Functional bowel disease. Usually a diagnosis of exclusion. **Cause** * Unknown. * Altered bowel motility, visceral hypersensitivity and psychosocial factors. **Clinical features** Rome III criteria for IBS * ≥12 wks in the past 12 months of abdominal discomfort that is either: * Relieved by defecation OR * Associated with change in frequency or consistency of stool Suggestive features: * Abnormal stool frequency, consistency * Mucus * Bloating * Abnormal stool passage (straining, urgency, feeling of incomplete emptying) Diagnosis less likely in presence of red flag features * Weight loss * Fever * Nocturnal defecation * Anaemia * Blood or pus in stool * Abnormal gross findings on flexible sigmoidoscopy **Investigation** * Bloods: FBC, TFT, LFTs, CRP/ESR, tTG serology (coeliac) * Stool MCS, O&P (ova and parasite) * Faecal calprotectin: rule out IBD * Imaging: +/- Sigmoidoscopy * Colonoscopy **Treatment** *Chronic* * Reassurance, education * Tx has low success rate so aim to make symptoms more tolerable, no drugs are very effective * Symptomatic treatment * ↑ Fibre (but can also worsen bloating/flatulence) * +/- Anti-diarrhoeal medications (eg Loperamide) * +/- Laxatives

Answer 28

Appendicitis Clinical features * Lying still, dehydrated, shallow breaths * Tachycardia, hypotensive, fever * Furred tongue, fetor, flushing * Guarding, rigidity, rebound and percussion tenderness * Rovsing’s, Psoas, Obturator sign * PR painful on right side Investigations * Bedside: glucose, ABG, urinalysis, pregnancy test * Bloods: FBC, CRP elevated, LFT, ESR, lipase * Imaging: USS, CT Management * Admit to general surgery for prompt appendectomy * Antibiotics: metronidazole 500mg/8hour + cefuroxime * Emperical antibiotics: gentamycin, amoxicillin, metronidazole * Rehydrate * Pain relief

Answer 29

Lower GIT Bleeding à Bleed distal to the ligament of Treitz **Aetiology** à CHAND * Colitis: Radiation, infectious, ischemic, IBD (UC \> CD) * Haemorrhoids/fissure  * Angiodysplasia  * Neoplastic  * Diverticular disease **Clinical features** * Haematochezia * Anaemia  * Occult blood in stool  * Rarely melena Carcinoid tumours à Tumours of neural crest origin (enterochromaffin cells) that produce serotonin (5HT) * Can be part of MEN-1 syndrome **Common sites** * Appendix, ileum, rectum * Less commonly anywhere along the GIT, ovary, testes, bronchi. **Clinical features** * Initially few symptoms * GI tumour: Appendicitis, intussusception, obstruction * Hepatic metastases: RUQ pain * Carcinoid syndrome (5%) * Bronchoconstriction * Paroxysmal flushing * Tachycardia * Diarrhoea * CHF (pulmonary stenosis → pulmonary HTN → tricuspid regurgitation) **Diagnosis** * CXR + CT chest/abdo/pelvis to locate primary tumours * 24h urine 5HIAA (5HT metabolite) **Treatment** * Octreotide (somatostatin analogue) blocks release of tumour mediators * Surgery: Gold standard - only cure * +/- Loperamide for diarrhoea **Carcinoid crisis** * When a tumour outgrows it blood supply mediators escape * Results in life-threatening vasodiltation, hypotension, tachycardia, bronchoconstriction and hyperglycaemia * Treated with high dose octreotide

Answer 30

Gastrointestinal Examination **Introduction, Vital Signs** **General inspection** Consider: stool charges, medications, if patient is in isolation bay Body habitus Cachexia Malignancy Malabsorption Cirrhosis Obesity Fatty liver: non-alcoholic steatohepatitis Colour Jaundice Hyperbilirubinemia: Pre-hepatic, hepatic or hepatic Pallor Abnormal skin pigmentation Haemochromatosis Excess iron à Haemosiderin stimulates melanocytes to produce melanin Slate grey discolouration of the skin Malabsorption Sunkissed pigmentation Mostly of nipples, palmar creases, pressure areas and mouth Confused/drowsy Hepatic encephalopathy due to decompensated advanced cirrhosis Features depend on aetiology and precipitating factors Patients eventually become stuporous and comatose Caused by the combination of hepatocellular damage and porto-systemic shunting Fulminant hepatitis (acute liver failure) Pain/anxiety Patient lying very still Parietal irritation Patient can’t get comfortable Visceral irritation Nephrolithiasis **Hands/Arms** Nails Clubbing: Not very common Chronic liver disease, cirrhosis Inflammatory bowel disease Coeliac disease Capillary refill Leuconychia: white in nails (may cover all but near end of nail) Hypoalbuminemia due to chronic liver disease Muehrcke’s lines: transverse white lines Koilonychia: Spoon nails Iron deficiency Palms Sweaty/dry Erythema of the palmar creases à Affects the thenar and hypothenar eminences Chronic liver disease Thyrotoxicosis Rheumatoid arthritis Polycythaemia: excess Hb in blood Can be a normal finding, particularly in pregnancy Pallor of the palmar creases Anaemia Dupuytren’s contracture: tendon-like appearance at base of finger – often ring finger and bilateral Alcoholism Manual workers – often familial Arms Hepatic flap/Asterixis à Arms stretched out in front with fingers separated and wrists extended for 15 seconds à Positive if jerk, irregular flexion extension movement at the wrist and metacarpophalangeal joints, often accompanied by lateral movements of the fingers, usually bilateral Hepatic encephalopathy Cirrhosis Wilson’s disease Opiate overdose Bruising/petichiae Large bruises (echymoses): clotting abnormalities Hepatocellular damage Obstructive jaundice Petichiae: chronic excessive alcohol consumption, splenomegaly Scratch marks Cholestatic jaundice: causes itchiness Primary biliary cirrhosis Spider naevi à Central arteriole from which radiate numerous small vessels, vary in size, occasionally bleed profusely, blanching à Number can vary depending on stage in underlying condition à Only occur in the upper part of the body Alcohol Cirrhosis Pregnancy Acanthosis nigricans in axilla: Black to brown velvety elevations of the epidermis due to confluent papillomas Skin marker of GIT malignancy **Face** Eyes Xanthelasma Primary biliary cirrhosis Scleral jaundice Bitot’s spots: yellow keratinised areas of the sclera Severe vitamin A deficiency Conjunctival pallor * Liver disease * Wilson’s disease Kayser-Fleischer ring: Brown ring on edge of iris * Wilson’s disease Iritis: red eyes Inflammatory bowel disease Cheeks Parotid gland enlargement à Ask patient to clench jaw: gland felt behind masseter and in front of ear Alcoholism * Due to fatty infiltration, perhaps secondary to alcohol toxicity +/- malnutrition Mouth Angular stomatitis Deficiency of iron, folate and B12 Brown-black lesions around mouth Peutz-jeghers syndrome * Lesions associated with hamartomas of the small bowel and colon * Can be present with bleeding or intussusception (inversion of a portion of the intestine) * Increases risk of GIT adenocarcinoma Telangiectasia around mouth Hereditary haemorrhagic telangiectasia * Multiple small telangiectasias occur * Often present on lips and tongue but may be found anywhere on the skin Fetor hepaticus: Sweet smell of breath Portal hypertension Late sign of liver failure/hepatocellular disease Mucosal petichiae and ulcers Crohn’s disease Coeliac disease Tongue Leukoplakia Premalignancy Causes * Smoking * Spirits * Sepsis * Syphilis Glossitis: inflammation of tongue à causes a smooth appearance and may be erythematous Deficiency of iron, folate and B12 Hydration **Neck and chest** Supraclavicular lymph nodes Virchow’s node: Enlarged left supraclavicular node * Secondary to gastric malignancy When enlarged and palpable: named Trosier’s sign Gynaecomastia in males Chronic liver disease Medication: E.g. Digoxin, cimetidine Spider naevi \>5 = abnormal: Cirrhosis **Abdomen** à Remember to watch patients face whilst palpating à During palpation palmar surfaces of the fingers are used but during palpation of the edge of organs the lateral surface of the index finger is used To decrease voluntary guarding: draw patients knees up, encourage deep breathing, engage patient in conversation Inspection Scarring Previous surgery or trauma Skin lesions * Herpes zoster: radicular pattern, localised to one side of the abdomen * Striae: Stretching of abdominal wall, results in pink linear marks with a wrinkled appearance. Caused by ascites, pregnancy, recent weight gain or Cushing’s syndrome Stomata * Colostomy, ileostomy, ileal conduit Prominent veins Caput medusa: Around umbilicus with blood flowing away towards legs (very rare) * Portal hypertension IVC obstruction: Blood flows towards head Due to a tumour, thrombosis or tense ascites Pulsations * AAA Visible peristalsis Intestinal obstruction * Pyloric obstruction: peptic ulceration or tumour Normal in very thin people Generalised distension Causes: * Fat: Gross obesity * Fluid: Ascites * Foetus * Flatus: Gaseous distension due to bowel obstruction * Faeces Tumour: ovarian tumour, hydatid cyst Discolouration Cullen’s sign: around umbilicus * Faintly bluish hue * In cases of extensive haemoperitoneum or acute pancreatitis * Rare Grey-turner’s sign: in flanks * Acute pancreatitis * Rare Visible masses à Look at abdomen squatting down and watch for any asymmetrical movement * Enlargement of one of the abdominal/pelvic organs * Hernia * Congenital abdominal wall defect * Chronically increased intrabdominal pressure Palpation Light palpation: 9 quadrants Feel for any tenderness or lumps Deep palpation: 9 quadrants Detect deeper masses and characterise masses already found Guarding: tending of abdominal wall muscles Voluntary, involuntary Rigidity: constant involuntary contraction of abdominal muscles Peritoneal irritation Rebound tenderness/Blumberg’s sign If patient winces = rebound test positive Peritoneal irritation Liver palpation If edge is felt note: * Regular/irregular * Consistency * Tender/non-tender * Pulsatile/non-pulsatile Gallbladder palpitation Felt as a bulbus, focal, rounded mass which moves downwards on inspiration Spleen palpation Splenomegaly Wilson’s disease Kidney palpation/blotting Occasionally the kidney can be felt * The lower pole of the right kidney may be palpable in thin, healthy people Aorta * Pulsation from the abdominal aorta may be present, usually in the epigastrium, in thin healthy people * Aortic aneurysm: pulsation is expansile, enlarges more in systole, large than 5cm Percussion Liver \* Do if liver was palpated Normally liver border begins at 6^th rib Liver is usually 8-13cm Ascites Presence of fluid in abdomen * When ascites is gross, the abdomen distends, the flanks bulge, umbilical eversion occurs and dullness is detectable closer to the midline Shifting dullness à If ascites is present If there is shifting dullness = ascites * Shifting dullness is present if the area of dullness has changed to become resonant, this is because the peritoneal fluid moves under the influence of gravity to the right side of the abdomen when this is the lowermost point Fluid thrill à If ascites is present * Occurs mostly with massive ascites * May also occur if there is a massive ovarian cyst or pregnancy with hydroaminos Auscultation Bowel sounds à Place diaphragm of stethoscope below the umbilicus Present/absent * Absent for \>4 minutes: Paralytic ileus, obstruction * Tinkling: obstruction * Hypoactive: gastroenteritis, diarrhoea, peritonitis, ileus * Hyperactive: obstruction, diarrhoea, increased peristalsis, malabsorption Liver friction rub * Indicate an abnormality of the parietal and visceral peritoneum due to inflammation * Rough, creaking or grating noise is heard as the patient breathes Carcinoma Liver infarct, abscess, recent biopsy Chlamydial perihepatitis Spleen friction rub Infarct Bruit Renal, liver, spleen * Liver: high pitched than a venous hum, it not continuous and is well localised * Liver: Hepatocellular cancer, alcoholic hepatitis, post-liver biopsy * Renal: renal artery stenosis, Venous hums: à Heard between xiphisternum and umbilicus Portal hypertension * Continuous, low pitched soft murmur that may become louder with inspiration and diminish when more pressure is applied * Caused by large volumes of blood flowing in the umbilical or paraumbilical veins in the falciform ligament are responsible *Special tests* Appendicitis Rovsing’s test à Press fingers in LIQ and quickly withdraw Pain in right iliac fossa during left side pressure = positive Rovsing’s sign Psoas sign à Place your hand above the patients right need and ask patient to raise thigh against your hand Increase pain = positive psoas sign Obturator sign à Flex patient’s right thigh at the hip and the knee bent, then internally rotate the leg at the hip Right hypogastric pain = positive obturator sign MacBurney’s sign: MacBurney’s point is 4-5cm along a line from the anterior superior iliac spine to the umbilicus Deep tenderness here is a sign of acute appendicitis Cholecystitis Murphy’s sign à Place right hand in right costal margin just lateral to lateral border of the rectus abdominis muscle On taking a deep breath the patient catches his breath when an inflamed gall bladder presses on the patients hand Renal tenderness Murphy’s punch à Tap on costovertebral angle Tenderness = positive **Legs** * Check of bruising, oedema and changes noted in the arms \* A hernia, rectal, vaginal and external genitalia examination is essential to a GIT examination \* Note: CVS, RS and CNS examinations may be helpful in patients with hepatomegaly

Answer 31

Clinical * Intermittent abdominal pain related to defecation * Bowel dysfunction - constipation & diarrhoea * Change in stool consistency * NO BLOOD IN STOOL IN IBS Exam * Systems exam * In the absence of gynaecological or perianal symptoms, neither pelvic examination nor rectal examination would be routinely indicated on initial investigation InvestigationsLabs (1st line for IBS) * FBC - anemia a red flag * IgA TTG Ab - rule out Coeliac * CRP - investigate for IBD Imaging * Not indicated in the absence of red flags * Any red flags --\> ?CT or USS depending on provisional diagnosis Assessment Red flags * Anemia * Loss of weight * Age \>50 at onset * Radiates to back * Melaena or haematochezia * Nocturnal with waking at night * Family history of CRC or IBD