Gastrointestinal Flashcards

Question

Define alcoholic hepatitis

Answer 1

• Inflammatory liver injury caused by chronic heavy intake of alcohol

Answer 2

• One of the THREE forms of liver disease caused by excessive alcohol intake - the spectrum consists of: o Alcoholic fatty liver (steatosis) o Alcoholic hepatitis o Chronic cirrhosis • Histopathological features of alcohol hepatitis: o Centrilobular ballooning o Degeneration and necrosis of hepatocytes o Steatosis o Neutrophilic inflammation o Cholestasis o Mallory-hyaline inclusions (eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments) o Giant mitochondria

Answer 3

• Occurs in 10-35% of heavy drinkers

Answer 4

• May remain asymptomatic and undetected • May be mild illness with symptoms such as: o Nausea o Malaise o Epigastric pain o Right hypochondrial pain o Low-grade fever • More severe presenting symptoms include: o Jaundice o Abdominal discomfort or swelling o Swollen ankles o GI bleeding • NOTE: a long history of heavy drinking is required for the development of alcoholic hepatitis (around 15-20 years) • There may be events that trigger the disease (e.g. aspiration pneumonia, injury)

Answer 5

``` • Signs of Alcohol Excess o Malnourished o Palmar erythema o Dupuytren's contracture o Facial telangiectasia o Parotid enlargement o Spider naevi o Gynaecomastia o Testicular atrophy o Hepatomegaly o Easy bruising • Signs of Severe Alcoholic Hepatitis o Febrile (in 50% of patients) o Tachycardia o Jaundice o Bruising o Encephalopathy (e.g. liver flap, drowsiness, disorientation) o Ascites o Hepatomegaly o Splenomegaly ```

Answer 6

• Bloods o FBC: • Low Hb • High MCV • High WCC • Low platelets o LFTs: • High AST + ALT • High bilirubin • High ALP + GGT • Low albumin o U&Es: • Urea and K+ tend to be low o Clotting: prolonged PT is a sensitive marker for significant liver damage • Ultrasound - check for other causes of liver impairment (e.g. malignancy) • Upper GI Endoscopy - investigate varices • Liver Biopsy - can help distinguish from other causes of hepatitis • EEG - slow-wave activity indicates encephalopathy

Answer 7

• Acute o Thiamine o Vitamin C and other multivitamins (can be given as Pabrinex) o Monitor and correct K+, Mg2+ and glucose o Ensure adequate urine output o Treat encephalopathy with oral lactulose or phosphate enemas o Ascites - manage with diuretics (spironolactone with/without furosemide) o Therapeutic paracentesis o Glypressin and N-acetylcysteine for hepatorenal syndrome • Nutrition o Via oral or NG feeding is important o Protein restriction should be avoided unless the patient is encephalopathic o Nutritional supplementation and vitamins (B group, thiamine and folic acid) should be started parenterally initially, and continued orally • Steroid Therapy - reduce short-term mortality for severe alcoholic hepatitis NOTE: hepatorenal syndrome - the development of renal failure in patients with advanced chronic liver disease • Thought to arise because of abnormalities in blood vessel tone in the kidneys • Blood vessels in the kidney constrict because of the dilatation of blood vessels in the splanchnic circulation (supplying the intestines), which is mediated by factors released by the kidneys • The splanchnic vasodilation leads to reduced effective volume of blood detected by the juxtaglomarular apparatus, leading to activation of the RAS and vasoconstriction of vessels in the kidney • This leads to kidney failure

Answer 8

* Acute liver decompensation * Hepatorenal syndrome * Cirrhosis

Answer 9

• Mortality: o First month = 10% o First year = 40% • If alcohol intake continues, most will progress to cirrhosis within 1-3 years

Answer 10

• Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils

Answer 11

• Amyloid fibrils are polymers of low-molecular-weight subunit proteins • These are derived from proteins that undergo conformational changes to adopt an anti-parallel beta-pleated sheet configuration • Their deposition progressively disrupts the structure and function of normal tissue • Amyloidosis is classified according to the fibril subunit proteins o Type AA - serum amyloid A protein o Type AL - monoclonal immunoglobulin light chains o Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin

Answer 12

* AA - incidence of 1-5% amongst patients with chronic inflammatory diseases * AL - 300-600 cases in the UK per year * Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis

Answer 13

* Renal - proteinuria, nephrotic syndrome, renal failure * Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina * GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding * Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome * Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules * Joints - painful asymmetrical large joints, enlargement of anterior shoulder * Haematological - bleeding tendency

Answer 14

``` • Tissue Biopsy • Urine - check for proteinuria, free immunoglobulin light chains (in AL) • Bloods o CRP/ESR o Rheumatoid factor o Immunoglobulin levels o Serum protein electrophoresis o LFTs o U&Es • SAP Scan - radiolabelled SAP will localise the deposits of amyloid ```

Answer 15

* A painful tear in the squamous lining of the lower anal canal * NOTE: 90% of anal fissures are posterior (anterior anal fissures tend to occur after childbirth)

Answer 16

* Affects 1/10 people during their life time * Both sexes are affected equally * Can occur at any age * Most cases occur in children and young adults: 10-30 yrs

Answer 17

* Most are caused by hard faeces * Anal sphincter spasm can constrict the inferior rectal artery, causing ischaemia and impairing the healing process * Rare causes: syphilis, herpes, trauma, Crohn's, anal cancer, psoriasis

Answer 18

* Tearing pain when passing stools * There may be a little bit of blood in the faeces or on the paper * Anal itching (pruritus ani)

Answer 19

• Tears in the squamous lining of the anus on examination

Answer 20

• Examine the anus

Answer 21

``` • Conservative o High-fibre diet o Softening the stools (laxatives) o Good hydration • Medical o Lidocaine ointment (local anaesthetic) o GTN ointment (relaxes the anal sphincter and promoted healing) o Diltiazem (relaxes the anal sphincter and promotes healing) o Botulinum toxin injection • Surgical o Lateral sphincterotomy o This relaxes the anal sphincter and promotes healing but it has complications (e.g. anal incontinence) so it is reserved for patients who are intolerant or not responsive to non-surgical treatments ```

Answer 22

• Chronic anal fissure

Answer 23

* In most people, the fissure will heal within a week or so | * Treatment revolves around easing pain by keeping the stools soft and relaxing the anal sphincter to promote healing

Answer 24

• Inflammation of the appendix

Answer 25

* The MOST COMMON surgical emergency * Can occur at any age * Most commonly occurs between 10-20 yrs

Answer 26

* Gut organisms invade the appendix wall after lumen obstruction (e.g. by lymphoid hyperplasia, faecolith or filarial worms) * This leads to oedema, ischaemic necrosis and perforation

Answer 27

* Periumbilical pain that moves to the right iliac fossa * Anorexia is an important feature * Vomiting (may occur after pain) * Constipation * Diarrhoea

Answer 28

• General Signs o Tachycardia o Fever o Furred tongue o Lying still o Coughing hurts o Foetor with/without flushing o Shallow breaths • RIF Signs o Guarding o Rebound and percussion tenderness o PR pain on the right side (sign of low-lying pelvic appendix) • Special Signs o Rovsing's Sign - palpation of the left iliac fossa causes more pain in the right iliac fossa than the left o Psoas Sign - pain on extending the hip (caused by retrocaecal appendix) o Cope Sign - pain on flexion and internal rotation of the hip (occurs if the appendix is in close proximity to the obturator internus) • Variations in clinical picture o Inflammation of retrocaecal/retroperitoneal appendix may cause flank pain or RUQ pain • The only sign may be tenderness on the right on DRE o A child may have vague abdominal pain and will not eat their favourite food o A shocked confused 80+ year old who is not in any pain

Answer 29

``` • Bloods o High WCC (mainly neutrophils) o High CRP • Ultrasound may help • CT - high diagnostic accuracy ```

Answer 30

``` • Prompt appendicectomy • Antibiotics: o Cefuroxime o Metronidazole • Laparoscopy - diagnostic and therapeutic advantages ```

Answer 31

• Perforation • Appendix mass o Occurs when the inflamed appendix becomes covered with omentum • Appendix abscess o May occur if appendix mass fails to resolve o Treatment involves drainage and antibiotics

Answer 32

* Uncomplicated appendicitis - most people recover with no long-term problems * Ruptured appendix - greater risk of complications/death

Answer 33

• Chronic hepatitis of unknown aetiology, characterised by autoimmune features, hyperglobulinaemia and the presence of circulating autoantibodies

Answer 34

• In a genetically predisposed individual, and environmental agent (e.g. viruses or drugs) may lead to hepatocyte expression of HLA antigens, which then become the focus of a principally T-cell-mediated autoimmune attack • The raised titre of anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (ASMA) and anti-liver/kidney microsomes (anti-LKM) are NOT thought to directly injure the liver • The chronic inflammatory changes are similar to those seen in chronic viral hepatitis with lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and, eventually, cirrhosis • TWO major forms of autoimmune hepatitis: o Type 1 (Classic) • ANA • ASMA • Anti-actin antibodies (AAA) • Anti-soluble liver antigen (anti-SLA) o Type 2 • Antibodies to liver/kidney microsomes (ALKM-1) • Antibodies to liver cytosol antigen (ALC-1)

Answer 35

* Type 1: occurs in ALL age groups (but mainly young women) | * Type 2: generally occurs in girls and young women

Answer 36

``` • May be asymptomatic and discovered incidentally through abnormal LFT • Insidiously present with: o Malaise o Fatigue o Anorexia o Weight loss o Nausea o Jaundice o Amenorrhoea o Epistaxis • Acute hepatitis (25%) presents with: o Fever o Anorexia o Jaundice o Nausea/Vomiting/Diarrhoea o RUQ pain o Some may present with serum sickness (e.g. arthralgia, polyarthritis, maculopapular rash) • NOTE: check for personal or family history of other autoimmune diseases • A full history is important to rule out other causes of hepatitis (e.g. viral, alcoholic) ```

Answer 37

* Stigmata of chronic liver disease (e.g. spider naevi) * Ascites, oedema and hepatic encephalopathy are late features * Cushingoid features may be present even before the administration of steroids

Answer 38

``` • Bloods: o LFTs: • High: AST, ALT, GGT, ALP and Bilirubin • Low: albumin (in severe disease) o Clotting: • High PT (in severe disease) o FBC: • Low Hb, platelets and WCC (if hypersplenism from portal hypertension) o Hypergammaglobulinaemia • Presence of ANA, ASMA and Anti-LKM antibodies • Liver Biopsy: o Needed to establish diagnosis and check whether hepatitis or cirrhosis • To rule out other causes of liver disease: o Viral serology o Urinary copper/caeruloplasmin o Ferritin and transferrin saturation o 1 antitrypsin o Anti-mitochondrial antibodies (PBC) • US, CT or MRI of liver and abdomen o Visualise structural lesions • ERCP o To rule out PSC ```

Answer 39

* Prolonged exposure of the normal squamous epithelium to refluxate of GORD leads to mucosal inflammation and erosion, leading to replacement of the mucosa with metaplastic columnar epithelium * Metaplastic change: Squamous ----> Columnar * MAIN PROBLEM: Barrett's could progress to oesophageal adenocarcinoma

Answer 40

* Reflux will occur if the cardiac sphincter is not working properly (most of the time it is unclear why it is not working properly) * Hiatus hernia make GORD more likely

Answer 41

* 1/10 adults have heart burn every day | * 3-5% of people with GORD will develop Barrett's oesophagus

Answer 42

``` • Patients are likely to experience symptoms of GORD: o Heartburn o Nausea o Water-brash (sour taste in the mouth) o Bloating o Belching o Burning pain when swallowing ```

Answer 43

• Look at symptoms

Answer 44

• OGD and Biopsy | o This will show the replacement of the squamous epithelium with columnar epithelium

Answer 45

• Pre-malignant/High grade dysplasia: o Oesophageal resection o Eradicative mucosectomy o NOTE: this is appropriate if the patients are young and fit • Other techniques: o Endoscopic targeted mucosectomy o Mucosal ablation by epithelial laser, radiofrequency (HALO) or photodynamic ablation (PD) • Low-grade dysplasia - annual endoscopic surveillance is recommended • No pre-malignant changes found: o Surveillance endoscopy and biopsy performed every 1-3 years o Anti-reflux measures (e.g. high dose PPI)

Answer 46

* MAIN COMPLICATION: development of oesophageal adenocarcinoma * Risk of dysplasia

Answer 47

* Barrett's oesophagus carries a 30-60 times higher risk of oesophageal adenocarcinoma than the general population * Most patients, however, do not develop oesophageal adenocarcinoma * 5-10% of those with Barrett's oesophagus will develop adenocarcinoma over 10-20 years

Answer 48

• Primary adenocarcinoma of the biliary tree

Answer 49

• UNKNOWN • Risk Factors o Ulcerative colitis + primary sclerosing cholangitis o Choledochal cyst (congenital conditions involving cystic dilatations of bile ducts) o Caroli disease (rare genetic condition in which you get dilatation of intrahepatic bile ducts) o Parasitic infection of biliary tract

Answer 50

* VERY RARE | * More common in the developing world due to the increased prevalence of parasitic infections

Answer 51

``` Obstructive jaundice symptoms o Yellow sclera o Pale stools o Dark urine o Pruritus ``` Abdominal pain or fullness Systemic symptoms of malignancy: weight loss, malaise, anorexia

Answer 52

``` • Jaundice • Palpable gallbladder o NOTE: Courvoisier's Law - in the presence of jaundice, a palpable gallbladder (that is non-tender) is unlikely to be due to gallstones (i.e. cancer of the pancreas or biliary tree is more likely) • Epigastric/RUQ mass • There may be hepatomegaly ```

Answer 53

``` Bloods o FBC o U&Es o LFTs (high ALP + GGT) o Clotting screen o Tumour markers • CA19-9 is a marker of pancreatic cancer and cholangiocarcinoma ``` Endoscopy o ERCP will allow bile cytology and tumour biopsy Ultrasound CT, MRI, Bone Scan - for staging

Answer 54

• Inflammation of the gallbladder

Answer 55

• Types of Stones o Mixed Stones (80%) • Contains cholesterol, calcium bilirubinate, phosphate and protein • Form due to an imbalance between bile salts, phospholipids, cholesterol, nucleation factors and gallbladder motility o Pure Cholesterol Stones (10%) o Pigment Stones (10%) • Black stones made of calcium bilirubinate • Form due to increased bilirubin (e.g. due to haemolysis) • Risk Factors o Age o Female o Fat o Diabetes mellitus o Drugs (OCP, octreotide) o Family history o Ethnicity (Caucasian) o Pigment Stone Risk Factors: haemolytic disorders (e.g. sickle cell anaemia)

Answer 56

* Very COMMON * UK prevalence of gallstone disease = 10% * 3 x more common in FEMALES * More common with increasing age

Answer 57

* Systemically unwell * Fever * Prolonged abdominal pain * Pain may be referred to right shoulder (due to diaphragmatic irritation)

Answer 58

* Tachycardia * Pyrexia * RUQ pain or epigastric tenderness * May be guarding or rebound tenderness * Murphy's sign positive

Answer 59

• Bloods o FBC - high WCC in cholecystitis and cholangitis o LFT - high ALP + GGT in ascending cholangitis o Blood cultures o Amylase (exclude pancreatitis) • Ultrasound o Shows gallstones o Increased thickness of gallbladder wall o Dilatation of biliary tree • AXR - but only 10% of gallstones are radio-opaque • Other imaging - to exclude differentials (e.g. erect CXR, ERCP)

Answer 60

``` • Conservative o If only mild biliary colic - follow a low-fat diet • Medical o NBM o IV fluids o Analgesia o Anti-emetics o Antibiotics (if infection is present) o NOTE: if symptoms persist despite antibiotic treatment, suspect a localised abscess or empyema, which would require drainage o If there is an obstruction, urgent biliary drainage by ERCP or via a percutaneous route is necessary • Surgical o Laparoscopic Cholecystectomy ```

Answer 61

``` • Stones within the gallbladder o Biliary colic o Cholecystitis o Gallbladder empyema o Gallbladder cancer (RARE) • Stones outside the gallbladder o Obstructive jaundice o Pancreatitis o Ascending cholangitis o Cholecystoduodenal fistula o Gallstone ileus o Bouveret syndrome (gallstones cause gastric outlet obstruction) o Mirizzi syndrome • Complications of cholecystectomy o Bleeding o Infection o Bile leak o Post-cholecystectomy syndrome o Port-site hernia ```

Answer 62

* Gallstones do NOT cause symptoms most of the time | * Surgery offers an excellent chance of cure if they were to become symptomatic

Answer 63

• End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes. • Cirrhosis is considered DECOMPENSATED if it becomes complicated by any of: o Ascites o Jaundice o Encephalopathy o GI bleed • Decompensation can be precipitated by infection, GI bleeding, constipation, high-protein meal, electrolyte imbalances, alcohol and drugs, tumour development or portal vein thrombosis

Answer 64

``` • Chronic alcohol misuse (most common in the UK) • Chronic viral hepatitis (hep B/C - most common worldwide) • Autoimmune hepatitis • Drugs (e.g. methotrexate, hepatotoxic drugs) • Inherited o 1-antitrypsin deficiency o Haemochromatosis o Wilson's disease o Galactosaemia o Cystic Fibrosis • Vascular o Budd-Chiari Syndrome o Hepatic Venous Congestion • Chronic Biliary Diseases o PBC o PSC o Biliary atresia • Unknown: 5-10% • Non-Alcoholic Steatohepatitis (NASH) o Associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia and drugs (e.g. amiodarone, tamoxifen) ```

Answer 65

``` • Early non-specific symptoms: o Anorexia o Nausea o Fatigue o Weakness o Weight loss • Symptoms due to decreased liver synthetic function: o Easy bruising o Abnormal swelling o Ankle oedema • Symptoms due to reduced detoxification function: o Jaundice o Personality change o Altered sleep pattern o Amenorrhoea o Galactorrhoea • Symptoms due to portal hypertension: o Abdominal swelling o Haematemesis o PR bleeding or melaena ```

Answer 66

• One of the top 10 causes of death worldwide

Answer 67

``` These are all signs of chronic liver disease • Asterixis • Bruises • Clubbing • Dupuytren's contracture • Palmar erythema • Jaundice • Gynaecomastia • Leukonychia • Parotid enlargement • Spider naevi • Scratch mark (from cholestatic pruritis) • Ascites • Enlarged liver (may be shrunken in the later stages) • Testicular atrophy • Caput medusae • Splenomegaly ```

Answer 68

• Bloods o FBC: low platelets + Hb = because of hypersplenism as a result of portal hypertension o LFTs - may be normal but often get: • High AST, ALT, ALP, GGT and bilirubin • Low albumin o Clotting: prolonged PT o Serum AFP (alpha-fetoprotein = tumour marker for liver cancer): • Raised in chronic liver disease • High levels may suggest hepatocellular carcinoma • Investigations to determine CAUSE o Viral serology o 1-antitrypsin o Caeruloplasmin • This is a copper-carrying complex that is LOW in Wilson's disease o Iron studies: serum ferritin, iron, total iron binding capacity (TIBC) - check for haemochromatosis o Anti-mitochondrial antibody (PBC) o ANA, ASMA (autoimmune hepatitis) • Ascitic Tap o MC&S - check for infection o Biochemistry (protein, albumin, glucose, amylase) o Cytology o IMPORTANT: ascitic tap with neutrophils > 250/mm3 = spontaneous bacterial peritonitis (SBP) • Liver Biopsy o Performed either: • Percutaneously • Transjugular - if clotting deranged or ascitic o Histopathological features of cirrhosis: • Periportal fibrosis • Loss of normal liver architecture • Nodular appearance o Grade - indicates degree of inflammation o Stage - degree of architectural distortion (from mild portal fibrosis --> cirrhosis) • Imaging o US, CT or MRI - to detect complications such as: • Ascites • HCC • Hepatic or portal vein thrombosis • Exclude biliary obstruction o MRCP (if PSC suspected) • Endoscopy o To examine varices • Child-Pugh Grading - score for estimating the prognosis in chronic liver disease/cirrhosis. It is based on 5 factors: o Albumin o Bilirubin o PT o Ascites o Encephalopathy • Cirrhosis can be divided into Classes using the Child-Push grading system: o Class A: 5-6 o Class B: 7-9 o Class C: 10-15

Answer 69

• Treat the CAUSE if possible • Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver • Nutrition is important • Enteral supplements should be given • NG feeding may be indicated • Treating Complications: o Encephalopathy • Treat infections • Exclude GI bleed • Use lactulose and phosphate enemas  Normally, the liver breaks down ammonia that is absorbed in the GI tract, however, in Cirrhosis the ammonia can go through the liver without being broken down and exert toxic effects on the brain  IMPORTANT: lactulose reduces the absorption of ammonia from the gut  This helps prevent encephalopathy caused by ammonia reaching the brain • Avoid sedation o Ascites • Diuretics (spironolactone with/without furosemide) • Dietary sodium restriction • Therapeutic paracentesis (with human albumin replacement) • Monitor weight • Fluid restrict if plasma sodium < 120 mmol/L • Avoid alcohol and NSAIDs o Spontaneous Bacterial Peritonitis • Antibiotics (e.g. cefuroxime and metronidazole) • Prophylaxis against recurrent SBP with ciprofloxacin o Surgical • Consider TIPS (transjugular intrahepatic portosystemic shunt) - this helps reduce portal hypertension  However, it may precipitate encephalopathy because it is providing a route for blood from the GI tract to bypass the liver • Liver transplantation is the only curative method

Answer 70

* Portal hypertension with ascites * Hepatic encephalopathy * Variceal haemorrhage * SBP * HCC * Renal failure (hepatorenal syndrome) * Pulmonary hypertension (hepatopulmonary syndrome)

Answer 71

• Depends on aetiology and complications • Generally poor prognosis o Overall 5 year survival = 50% o If ascites, 2 year survival = 50%

Answer 72

* An inflammatory disease caused by intolerance to GLUTEN, causing chronic intestinal malabsorption. * It leads to subtotal villous atrophy and crypt hyperplasia

Answer 73

* Due to sensitivity to the GLIADIN component of gluten * Exposure to gliadin triggers and immunological reaction in the small intestine leading to mucosal damage and loss of villi * 10% risk of first-degree relatives being affected * Clear genetic susceptibility associated with HLA-B8, HLA-DR3 and HLA-DQW2 haplotypes

Answer 74

* UK: 1/2000 * West Ireland: 1/300 * Rare in East-Asia

Answer 75

* May be asymptomatic * Abdominal discomfort, pain and distention * Steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away) * Diarrhoea * Tiredness, malaise, weight loss (despite normal diet) * Failure to 'thrive' in children * Amenorrhoea in young adults

Answer 76

• Signs of anaemia: pallor • Signs of malnutrition: o Short stature o Abdominal distension o Wasted buttocks in children o Triceps skinfold thickness gives indication of fat stores • Signs of vitamin/mineral deficiencies: osteomalacia, easy bruising • Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)

Answer 77

• Blood: o FBC (low Hb, iron and folate) o U&E o Albumin o Calcium o Phosphate • Serology: o IgG anti-gliadin antibodies, IgA and IgG anti-endomysial tranglutaminase antibodies can be diagnostic o NOTE: IgA deficiency is quite COMMON (1/50 with coeliac) so Ig levels should be measured to avoid false negatives • Stool: culture to exclude infection, faecal fat tests for steatorrhoea • D-xylose test: reduced urinary excretion after oral xylose indicates small bowel malabsorption • Endoscopy: allows direct visualisation of villous atrophy in the small intestine (mucosa appears flat and smooth) o Biopsy will show villous atrophy and crypt hyperplasia in the duodenum o The epithelium adopts a cuboidal appearance - there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria

Answer 78

* Advice: avoid gluten (wheat, rye and barley products) | * Medical: vitamin and mineral supplements. Oral corticosteroids if disease does not subside with avoidance of gluten

Answer 79

* Iron, folate and B12 deficiency * Osteomalacia * Ulcerative jejunoileitis * GI lymphoma (particularly T cell) * Bacterial overgrowth * Cerebellar ataxia (rarely)

Answer 80

* FULL RECOVERY in most patients who strictly adhere to a gluten-free diet * Symptoms usually resolve within weeks though histological changes may take longer * Gluten-free diet must be followed for life

Answer 81

``` • Malignant adenocarcinoma of the large bowel o Distribution: • 60% - rectum and sigmoid • 30% - descending colon • 10% - rest of colon ```

Answer 82

``` • Environmental and genetic • There is a sequence of genetic changes that go from normal bowel epithelium to cancer (e.g. APC, K-Ras) • Risk Factors o Western diet (e.g. red meat, alcohol) o Colorectal polyps o Previous colorectal cancer o Family history o IBD ```

Answer 83

* SECOND MOST COMMON cause of cancer death in the West * UK: 20,000 deaths per year * Average age of diagnosis: 60-65 yrs

Answer 84

• Depends on the size and location of the tumour Left-Sided Colon and Rectum o Change in bowel habit o Rectal bleeding (blood or mucus mixed with the stools) o Tenesmus (due to a space-occupying tumour in the rectum) ``` Right-Sided Colon o Presents later o Anaemia symptoms (lethargy) o Weight loss o Non-specific malaise o Lower abdominal pain (rare) ``` IMPORTANT: 20% of tumours will present as an EMERGENCY with pain and distension due to: o Large bowel obstruction o Haemorrhage or peritonitis due to perforation

Answer 85

* Anaemia * Abdominal mass If metastatic: o Hepatomegaly o Ascites (shifting dullness) • Low-lying rectal tumours may be palpable on DRE

Answer 86

Bloods o FBC - anaemia o LFTs o Tumour markers (CEA) Stools o FOBT - used as a screening test Endoscopy o Sigmoidoscopy o Colonoscopy o This can be used to biopsy the tumour Double-Contrast Barium Enema o May show 'apple core' strictures Contrast CT o For staging (Duke's staging)

Answer 87

• Chronic granulomatous inflammatory disease that can affect any part of the gastrointestinal tract. Grouped with ulcerative colitis and known, together, as inflammatory bowel disease.

Answer 88

* Cause unknown but thought to be due to interplay between genetic and environmental factors * Though inflammation can occur anywhere from mouth to anus, 40% involves the terminal ileum

Answer 89

* UK annual incidence: 5-8/100,000 * UK prevalence: 50-80/100,000 * Affects any age but peaks in teens, 20s and 40s

Answer 90

* Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction) * Diarrhoea (may be bloody or steatorrhoea) * Fever, malaise, weight loss * Symptoms of complications * Sometimes right iliac fossa pain due to inflammation of terminal ileum

Answer 91

* Weight loss * Clubbing * Signs of anaemia * Aphthous ulcers in mouth * Perianal skin tags, fistulae and abscesses * Uveitis, erythema nodosum, pyoderma gangrenosum

Answer 92

• Blood: o FBC - low Hb, high platelets, high WCC o U&Es o LFTs - low albumin o High ESR (suggests chronic inflammation) o CRP may be high or normal • Stool microscopy and culture: exclude infective colitis • AXR: could show evidence of toxic megacolon • Erect CXR: if there is a risk of perforation • Small bowel barium follow-through could show: o Fibrosis/strictures (string sign of Kantor - part of the intestine looks like a piece of string, showing incomplete filling of the intestinal lumen) o Deep ulceration (rose thorn ulcers) o Cobblestone mucosa • Endoscopy (OGD, colonoscopy) and biopsy may show: o Could help differentiate UC and CD o Useful for monitoring malignancy and disease progression o Can show mucosal oedema and ulceration with 'rose thorn fissures' (occurs when there is a cobblestone mucosa) o Fistulae and abscesses o Transmural chronic inflammation with infiltration of macrophages, lymphocytes and plasma cells o Granulomas with epithelioid giant cells may be seen in blood vessels and lymphatics • Radionucide-labelled neutrophil scan: can localise the inflammation (when other investigations are contraindicated)

Answer 93

• Acute Exacerbation o Fluid resuscitation o IV/oral corticosteroids o 5-ASA analogues (e.g. mesalazine and olsalazine) o Analgesia o Parenteral nutrition may be necessary o Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb • Long-Term o Steroids - for acute exacerbations o 5-ASA analogues - decreases the frequency of relapses (useful for mild to moderate disease) • NOTE: more commonly used in UC o Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine, methotrexate) reduces the frequency of relapses o Anti-TNF agents: (e.g. infliximab and adalimumab) - very effective at inducing and maintaining remission. Usually reserved for refractory Crohn's. • General Advice: o Stop smoking o Dietician referral (low fibre diet necessary if there are stricture present) • Surgery indicated it: o Medical treatment fails o Failure to thrive in children in the presence of complications o Involves resection of affected bowel and stoma formation - NOTE: there is a risk of disease recurrence

Answer 94

``` • GI: o Haemorrhage o Strictures o Perforation o Fistulae (between bowel, bladder, vagina) o Perianal fistulae and abscesses o GI cancer o Malabsorption • Extraintestinal Features: o Uveitis o Episcleritis o Gallstones o Kidney stones o Arthropathy o Sacroiliitis o Ankylosing spondylitis o Erythema nodosum o Pyoderma gangrenosum o Amyloidosis ```

Answer 95

* It is a chronic relapsing condition * 2/3 of patients will require surgery at some stage * 2/3 of these patients require more than 1 operation

Answer 96

• It is important to distinguish between the different terms used when discussing patients with diverticular disease o Diverticulosis: the presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel o Diverticular Disease: diverticulosis associated with complications e.g. haemorrhage, infection, fistulae o Diverticulitis: acute inflammation and infection of colonic diverticulae o Hinchey Classification of Acute Diverticulitis: • Ia: phlegmon • Ib and II: localised abscesses • III: perforation and purulent peritonitis • IV: faecal peritonitis

Answer 97

• Aetiology: o A low-fibre diet leads to loss of stool bulk o This leads to the generation of high colonic intraluminal pressures to propel the stool out o This, in turn, leads to the herniation of the mucosa and submucosa through the muscularis • Pathogenesis: o Diveticulae are most commonly found in the sigmoid and descending colon o However, they can also be right-sided o Diverticulae are NOT found in the rectum o Diverticular are found particularly at sites of nutrient artery penetration o Diverticular obstruction by thickened faeces can lead to bacterial overgrowth, toxin production and mucosal injury o Which can then lead to diverticulitis, perforation, pericolic phlegmon, abscess, ulceration and fistulation or stricture formation

Answer 98

* Diverticular disease is VERY COMMON * 60% of people living in industrialised countries will develop colonic diverticulae * Rare < 40 yrs * Right-sided diverticulae are more common in Asia

Answer 99

• Often ASYMPTOMATIC (80-90%) • Complications can lead to symptoms such as: o PR bleeding o Diverticulitis (causing LIF and lower abdominal pain and fever) o Diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)

Answer 100

• Diverticulitis - tender abdomen and signs of local or generalised peritonitis if a diverticulum has perforated

Answer 101

• Bloods: o FBC: increased WCC, increased CRP o Check clotting and cross-match if bleeding • Barium Enema (with or without air contrast): o Shows presence of diverticulae (saw-tooth appearance of lumen) o This reflects pseudohypertrohy of circular muscle o IMPORTANT: barium enema should NOT be performed in the acute setting because there is a high risk of perforation • Flexible Sigmoidoscopy and Colonoscopy: o Diverticulae can be visualised and other pathology (e.g. polyps and tumours) can be excluded • In ACUTE setting: CT scan for evidence of diverticular disease and complications may be performed

Answer 102

• Asymptomatic: o Soluble high-fibre diet (20-30 g/day) o Some drugs are under investigation for their use in preventing recurrent flares of diverticulitis (such as probiotics and anti-inflammatories) • GI Bleed: o PR bleeding usually managed conservatively with IV rehydration, antibiotics and blood transfusion if necessary o Angiography and embolisation or surgery if severe • Diverticulitis: o IV antibiotics o IV fluid rehydration o Bowel rest o Abscesses ma be drained by radiologically sited drains • Surgery: o May be necessary in patients with recurrent attacks or complications (e.g. perforation and peritonitis) o Open surgery: • Hartmann's procedure (proctosigmoidectomy leaving a stoma) • One-stage resection and anastomosis (risk of leak) - with or without defunctioning stoma o Laparoscopic drainage, peritoneal lavage and drain placement can be effective

Answer 103

* Diverticulitis * Pericolic abscess * Perforation * Faecal peritonitis * Colonic obstruction * Fistula formation (bladder, small intestine, vagina) * Haemorrhage

Answer 104

• 10-25% have one or more episodes of diverticulitis

Answer 105

``` • A functional bowel disorder defined as recurrent episodes of abdominal pain/discomfort (in the absence of detectable organic pathology) for > 6 months of the previous year, associated with two of the following: o Altered stool passage o Abdominal bloating o Symptoms made worse by eating o Passage of mucous ```

Answer 106

* UNKNOWN * Could be visceral sensory abnormalities, gut motility abnormalities, psychosocial factors (e.g. stress), food intolerance (e.g. lactose) and many more

Answer 107

* COMMON * 10-20% of adults * More common in females (2:1 ratio)

Answer 108

``` • 6+ months history of abdominal pain o Pain is often colicky o It is in the lower abdomen o Relieved by defecation or passing of flatus • Altered bowel frequency (> 3 motions per day or < 3 motions per week) • Abdominal bloating • Change in stool consistency • Passage with urgency or straining • Tenesmus ``` • MAKE SURE YOU SCREEN FOR RED FLAG SYMPTOMS: o Weight loss o Anaemia o PR bleeding o Late onset (> 60 yrs) o NOTE: if any of these are present then you must exclude colonic malignancy

Answer 109

* Usually NORMAL on examination | * Sometimes the abdomen may appear distended and be mildly tender on palpation in one or both iliac fossae

Answer 110

* Diagnosis is mainly from the history but organic pathology must be excluded * Blood: FBC (anaemia), LFT, ESR, CRP, TFT, anti-endomysial/anti-tranglutaminase antibodies (coeliac disease) * Stool examination: microscopy and culture for infective cause * Ultrasound: exclude gallstone disease * Urease breath test: exclude dyspepsia due to Helicobacter pylori * Endoscopy: if other pathologies suspected

Answer 111

• Advice: dietary modification • Medical: depends on the main symptoms affecting the patient o Antispasmodics (e.g. buscopan) o Prokinetic agents (e.g. domperidone, metaclopramide) o Anti-diarrhoeals (e.g. loperamide) o Laxatives (e.g. senna, movicol, lactulose) o Low-dose tricyclic antidepressants (may reduce visceral awareness) • Psychological therapy: o CBT o Relaxation and psychotherapy

Answer 112

* Physical and psychological morbidity | * Increased incidence of colonic diverticulosis

Answer 113

* Chronic relapsing and remitting course of disease | * Often exacerbated by psychosocial stresses

Answer 114

• Pain resulting from obstruction of the gallbladder or common bile duct, usually by a stone. The pain, which is very severe, is usually felt in the upper abdomen (in the midline or to the right) but can also be poorly localised due to its visceral nature.

Answer 115

``` • Occurs due to contractions of the biliary tree in an attempt to relieve an obstruction (e.g. due to a stone) • Risk factors of gallstones: o Fair (Caucasian) o Fat o Fertile o Forty o Female ```

Answer 116

* 10-15% of people in the adult Western world will develop gallstones * Biliary colic is the most common presentation of gallstone disease

Answer 117

* Crampy RUQ pain * Nausea and vomiting * Pain may radiate to the right scapula * The pain does NOT fluctuate and has a tendency to persist * Individuals may present with pain following ingestion of a fatty meal

Answer 118

• RUQ pain and epigastric tenderness

Answer 119

• Urinalysis, CXR and ECG to exclude other causes (e.g. basal pneumonia, inferior MI) • Ultrasound o Look for dilatation of the CBD o Gallbladder wall may be thickened • LFT • ERCP - useful diagnostically and therapeutically • CT - may be useful if other forms of imaging have been insufficient

Answer 120

``` • Analgesia • IV fluids • NBM • Surgical o Laparoscopic cholecystectomy • ERCP can also be used to help remove stones or stent a blocked bile duct ```

Answer 121

• Complications of surgery o Injury to the bile duct o Fat intolerance - due to inability to secrete a large amount of bile into the intestine because the patient no longer has a gallbladder o Post-cholecystectomy syndrome - presence of abdominal symptoms (e.g. dyspepsia, nausea/vomiting, RUQ pain) after the removal of the gallbladder

Answer 122

• GOOD prognosis with appropriate treatment

Answer 123

``` • Cancer of the stomach. Most commonly adenocarcinoma o Rarer causes of gastric cancer: • Lymphoma • Leiomyosarcoma • Stromal tumours ```

Answer 124

``` • UNKNOWN • Environment and genetics • Risk Factors o Smoked and processed foods o Smoking o Alcohol o Helicobacter pylori infection o Atrophic gastritis o Pernicious anaemia o Partial gastrectomy o Gastric polyps ```

Answer 125

* COMMON cause of cancer death worldwide * Highest incidence in JAPAN (and Asia in general) * 6th most common cancer in the UK * Usual age of presentation: > 50 yrs

Answer 126

* Often asymptomatic early * Early satiety * Epigastric discomfort * Systemic symptoms: weight loss, anorexia, nausea/vomiting * Dysphagia (in tumours of the gastric cardia) * Symptoms of metastases (e.g. ascites, jaundice)

Answer 127

* Epigastric mass * Abdominal tenderness * Ascites * Signs of anaemia * Virchow's Node (aka Troisier's sign) * Sister Mary Joseph's Nodule (metastatic node on the umbilicus) • Krukenberg's Tumour (ovarian metastases)

Answer 128

• Upper GI endoscopy * Bloods - FBC (check for anaemia), LFTs * CT/MRI - for staging * Endoscopic USS - assess depth of gastric invasion and lymph node involvement

Answer 129

• Inflammation of the oesophagus caused by reflux of gastric acid and/or bile.

Answer 130

• Caused by disruption of mechanisms that prevent reflux • Mechanisms that prevent reflux: o Lower oesophageal sphincter o Acute angle of junction o Mucosal rosette o Intra-abdominal portion of oesophagus (diaphragm acts as a sphincter) • Prolonged oesophageal acid clearance contributes to 50% of cases

Answer 131

* COMMON | * 5-10% of adults

Answer 132

• Substernal/epigastric burning discomfort or 'heartburn' • Aggravated by: o Lying supine o Bending o Large meals o Drinking alcohol • Pain is relieved by antacids • Waterbrash (regurgitation of an excessive accumulation of saliva from the lower part of the oesophagus often with some acid material from the stomach) • Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze • Dysphagia - caused by formation of peptic stricture after long-standing reflux

Answer 133

* Usually NORMAL | * Occasionally - epigastric tenderness, wheeze on chest auscultation, dysphonia

Answer 134

• Often a CLINICAL diagnosis • Upper GI endoscopy, biopsy and cytological brushings o Confirms presence of oesophagitis and can exclude malignancy • Barium Swallow can detect: o Hiatus hernia • NOTE: operation to repair hiatus hernia is called Nissen fundoplication o Peptic stricture o Extrinsic compression of the oesophagus • CXR: o This is NOT specific for GORD o However, a CXR can lead to the incidental finding of a hiatus hernia (gastric bubble behind the cardiac shadow) • 24 hr oesophageal pH monitoring: o pH probe places in lower oesophagus determines the temporal relationship between symptoms and oesophageal pH

Answer 135

• Advice: o Weight loss o Elevating head of bed o Avoid provoking factors o Stop smoking o Lower fat meals o Avoid large meals late in the evening • Medical: o Antacids o Alginates o H2 antagonists (e.g. ranitidine) o Proton pump inhibitors (e.g. lansoprazole, omeprazole) • Endoscopy: o Annual endoscopic surveillance - looking for Barrett's Oesophagus o May be necessary for stricture dilation or stenting • Surgery: o Antireflux surgery if refractory to medical treatment • Nissen Fundoplication: o Fundus of the stomach is wrapped around the lower oesophagus - helps reduce the risk of hiatus hernia and reduce reflux

Answer 136

* Oesophageal ulceration * Peptic stricture * Anaemia * Barrett's oesophagus * Oesophageal adenocarcinoma * Associated with asthma and chronic laryngitis

Answer 137

* 50% respond to lifestyle measures alone * In patients that require drug therapy, withdrawal is often associated with relapse * 20% of patients undergoing endoscopy for GORD have Barrett's oesophagus

Answer 138

• Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.

Answer 139

``` • Caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water (faecal-oral route) • Viral: o Rotavirus o Adenovirus o Astrovirus o Calcivirus o Norwalk virus o Small round structures viruses • Bacterial: o Campylobacter jejuni o Escherichia coli (particularly O157) o Salmonella o Shigella o Vibrio cholerae o Listeria o Yersinia enterocolitica • Protozoal: o Entamoeba histolytica o Cryptosporidium parvum o Giardia lamblia • Toxins from: o Staphylococcus aureus o Clostridium botulinum o Clostridium perfringens o Bacillus cereus o Mushrooms o Heavy metals o Seafood • Commonly contaminated foods: o Improperly cooked meat o Old rice o Eggs and poultry o Milk and cheeses o Canned food ```

Answer 140

* COMMON | * Serious cause of morbidity and mortality in the developing world

Answer 141

• Sudden onset nausea, vomiting, anorexia • DIARRHOEA (bloody or watery) • Abdominal pain or discomfort • Fever and malaise • IMPORTANT: enquire about recent travel, antibiotic use and recent food intake (how the food was cooked, sourced and whether anyone else is ill) • Time of Onset: o Toxins = early (1-24 hours) o Bacterial/viral/protozoal = 12+ hours • Pay attention to the other effects of toxins: o Botulinum causes paralysis o Mushrooms can cause fits, renal or liver failure

Answer 142

* Diffuse abdominal tenderness * Abdominal distension * Bowel sounds are often INCREASED * In SEVERE gastroenteritis: pyrexia, dehydration, hypotension and peripheral shutdown IMPORTANT: ANY DIARRHOEAL CONDITION CAN LEAD TO DEHYDRATION so assess and address the patient's hydration status immediately

Answer 143

* Bloods: FBC, blood culture (identify bacteraemia), U&Es (dehydration) * Stool: faecal microscopy and analysis for toxins (particularly for the toxin causing pseudomembranous colitis (C. difficile toxin) * AXR or ultrasound: exclude other causes of abdominal pain (e.g. bowel perforation) * Sigmoidoscopy: usually unnecessary unless inflammatory bowel disease needs to be excluded

Answer 144

* Bed rest * Fluid and electrolyte replacement with oral rehydration solution (contains glucose and salt) * IV rehydration may be necessary in those with severe vomiting * Most infections are self-limiting (so will go away with time) * Antibiotic treatment is only used if severe or if infective agent has been identified * NOTE: if botulism is present (due to Clostridium botulinum) treat with botulinum antitoxin (IM) and manage in ITU * NOTE: this is often a notifiable disease and is an important public health issue

Answer 145

* Dehydration * Electrolyte imbalance * Prerenal failure (due to dehydration) * Secondary lactose intolerance (particularly in infants) * Sepsis and shock * Haemolytic uraemic syndrome (associated with toxins from E. coli O157) * Guillain-Barre Syndrome may occur weeks after recovery from Campylobacter gastroenteritis * NOTE: botulism can lead to respiratory muscle weakness or paralysis

Answer 146

• Good prognosis because most cases are self-limiting

Answer 147

• Perforation of the wall of the GI tract with spillage of bowel contents

Answer 148

``` • Large Bowel o COMMON: • Diverticulitis • Colorectal cancer • Appendicitis o Others: volvulus, ulcerative colitis (toxic megacolon) • Gastroduodenal o COMMON: • Perforated duodenal or gastric ulcer o Others: gastric cancer • Small Bowel (RARE) o Trauma o Infection (e.g. TB) o Crohn's disease • Oesophagus o Boerhaave's perforation - rupture of the oesophagus following forceful vomiting • Risk Factors o Risk factors of cause (e.g. gastroduodenal - NSAIDs, steroids, bisphosphonates) ```

Answer 149

• Incidence depends on cause

Answer 150

• Depends on CAUSE • Large Bowel o Peritonitic abdominal pain o IMPORTANT: make sure you rule out ruptured AAA • Gastroduodenal o Sudden-onset severe epigastric pain - worse on movement o Pain becomes generalised o Gastric malignancy - may have accompanying weight loss and nausea/vomiting • Oesophageal o Severe pain following an episode of violent vomiting o Neck/chest pain and dysphagia develop soon afterwards

Answer 151

* Very UNWELL * Signs of shock * Pyrexia * Pallor * Dehydration * Signs of peritonitis (guarding, rigidity, rebound tenderness, absent bowel sounds) * Loss of liver dullness (due to overlying gas)

Answer 152

• Bloods o FBC, U&E, LFTs o Amylase - will be raised with perforation (but should not be astronomical (as seen in pancreatitis)) • Erect CXR ``` o Shows air under the diaphragm • AXR o Shows abnormal gas shadowing • Gastrograffin Swallow o For suspected oesophageal perforations ```

Answer 153

``` • Resuscitation o Correct fluid and electrolytes o IV antibiotics (with anaerobic cover) • Surgical o Large Bowel • Identify site of perforation • Peritoneal lavage • Resection of perforated section (usually as part of a Hartmann's procedure) o Gastroduodenal • Laparotomy • Peritoneal lavage • Perforation is closed with an omental patch ``` ``` • Gastric ulcers are biopsied • Helicobacter pylori eradication if positive for H. pylori o Oesophageal • Pleural lavage • Repair of ruptured oesophagus ```

Answer 154

* Large and Small Bowel - peritonitis | * Oesophagus - mediastinitis, shock, overwhelming sepsis and death

Answer 155

• Gastroduodenal o Gastric ulcers have higher morbidity and mortality than duodenal ulcers o POOR prognosis for perforated gastric carcinomas • Large Bowel o High risk of faecal peritonitis if left untreated o This can lead to DEATH from septicaemia and multiorgan failure

Answer 156

• An autosomal recessive disease in which increased intestinal absorption of iron causes accumulation of iron in tissues, which may lead to organ damage.

Answer 157

* Autosomal recessive * Caused be a defect in the HFE gene * NOTE: the genetic penetrance of haemochromatosis is complex - not everyone who is homozygous will develop the clinical disease

Answer 158

``` • Often ASYMPTOMATIC until the late stages of the disease • Symptoms usually start between 40-60 yrs • EARLY symptoms are vague: o Fatigue o Weakness o Arthropathy o Erectile dysfunction o Heart problems • May be an incidental finding (e.g. LFTs, serum ferritin) • LATE symptoms: o Diabetes mellitus o Bronzed skin o Hepatomegaly o Impotence o Amenorrhoea o Hypogonadism o Cirrhosis o Cardiac - arrhythmias and cardiomyopathy o Neurological and psychiatric problems ```

Answer 159

• Haematinics - serum ferritin (HIGH), transferrin (LOW), transferrin saturation (HIGH), TIBC (LOW) o NOTE: serum ferritin is NOT very specific because it is an acute phase protein o Serum iron concentration and transferrin saturation do NOT accurately reflect total body iron stores • Tests to exclude other causes of high ferritin: o CRP - inflammation o Chronic alcohol consumption o ALT - liver necrosis • LFTs • Other investigations for abnormal liver function (e.g. hepatitis serology) • Genetic testing • Liver biopsy (rarely required)

Answer 160

* Anal vascular cushions become enlarged and engorged with a tendency to protrude, bleed or prolapse in the anal canal * Classification of Haemorrhoids o Internal • Arise from the superior haemorrhoidal plexus • Lie ABOVE the dentate line o External • Lie BELOW the dentate line o NOTE: dentate line = a line that divides the upper 2/3 and the lower 1/3 of the anal canal and represents the hindgut-proctodeum junction • Degrees of Haemorrhoids o 1st Degree - haemorrhoids that do NOT prolapse o 2nd Degree - prolapse with defecation but reduce spontaneously o 3rd Degree - prolapse and require manual reduction o 4th Degree - prolapse that CANNOT be reduced

Answer 161

``` • Exact cause is disputed • Caused by disorganisation of the fibromuscular stroma of the anal cushions • Risk Factors o Constipation o Prolonged straining o Derangement of the internal anal sphincter o Pregnancy o Portal hypertension ```

Answer 162

* COMMON | * Peak age: 45-65 yrs

Answer 163

• Usually ASYMPTOMATIC • Bleeding o Bright red blood that is on the toilet paper and drips into the pan after passage of stool o Blood will NOT be mixed with the stool • ABSENCE of alarm symptoms (weight loss, anaemia, change in bowel habit, passage of clotted or dark blood, mucus mixed with the stool) • Other symptoms: o Itching o Anal lumps o Prolapsing tissue • NOTE: external haemorrhoids that have thrombosed can be very PAINFUL

Answer 164

• 1st or 2nd degree haemorrhoids are NOT usually visible on external inspection • Internal haemorrhoids are NOT normally palpable on DRE unless they are thrombosed • Haemorrhoids are usually visible on proctoscopy • Differential Diagnosis o Anal tags o Anal fissures o Rectal prolapse o Polyps o Tumours

Answer 165

• DRE • Proctoscopy • Rigid or flexible sigmoidoscopy o Important to exclude a rectal or sigmoid source of bleeding o IMPORTANT: haemorrhoids are common so the presence of haemorrhoids does NOT mean that you shouldn’t consider any other source of bleeding

Answer 166

• Conservative o High-fibre diet o Increase fluid intake o Bulk laxatives o Topical creams (e.g. local anaesthetics) • Injection Sclerotherapy o Induces fibrosis of the dilated veins • Banding o Barron's bands are applied proximal to the haemorrhoids o The haemorrhoid will then fall off after a few days o Higher cure rate but may be more painful than injection sclerotherapy • Surgery o Reserved for symptomatic 3rd and 4th degree haemorrhoids o Milligan-Morgan haemorrhoidectomy - excision of three haemorrhoidal cushions o Stapled haemorrhoidectomy is an alternative method o Post-operatively the patient should be given laxatives to avoid constipation

Answer 167

``` • Bleeding • Prolapse • Thrombosis • Gangrene • Injection Sclerotherapy Complications o Prostatitis o Perineal sepsis o Impotence o Retroperitoneal sepsis o Hepatic abscess • Haemorrhoidectomy Complications o Pain o Bleeding o Incontinence o Anal stricture ```

Answer 168

* Often CHRONIC * High rate of recurrence * Surgery can provide long-term relief

Answer 169

• Primary malignancy of the liver parenchyma

Answer 170

``` • Associated with: o Chronic liver damage • Alcoholic liver disease • Hepatitis C • Autoimmune disease o Metabolic disease • E.g. haemochromatosis o Aflatoxins • E.g. cereals contaminated with fungi ```

Answer 171

* COMMON * 1-2% of all malignancies * LESS common than liver metastases * High incidence in regions where hepatitis B and C are endemic

Answer 172

``` • Symptoms of Malignancy o Malaise o Weight loss o Loss of appetite • History of Exposure to Carcinogens o High alcohol intake o Hepatitis B or C (e.g. sexual activity, IV drug use) o Aflatoxins • Abdominal distention • Jaundice ```

Answer 173

``` • Signs of Malignancy o Cachexia o Lymphadenopathy • Hepatomegaly (may be nodular) • Jaundice • Ascites • Bruit over the liver ```

Answer 174

``` • Bloods o FBC o ESR o LFTs o Clotting o -fetoprotein - tumour marker for liver cancer o Hepatitis serology • Imaging o Abdominal US o CT/MRI - GOLD STANDARD for staging • Histology/Cytology o Ascitic tap my be sent for cytological analysis • Staging o CT scan (chest/abdo/pelvis) ```

Answer 175

• The abnormal protrusion of a peritoneal sac through a weakness of the abdominal wall in the inguinal region o Direct Inguinal Hernia • Protrusion of the hernial sac directly through a weakness in the transversalis fascia and posterior wall of the inguinal canal • Arises medial to the inferior epigastric vessels • Appear through Hesselbach's triangle (BORDERS: lateral border of rectus abdominis, inferior epigastric vessels, inguinal ligament) o Indirect Inguinal Hernia • Protrusion of the hernial sac through the deep inguinal ring, following the path of the inguinal canal o NOTE: if indirect and direct inguinal hernias coexist = pantaloon hernia

Answer 176

• Congenital - abdominal contents enter the inguinal canal through a patent processus vaginalis • Acquired - due to increased intra-abdominal pressure along with muscle and transversalis fascia weakness • Risk Factors o Male o Prematurity o Age o Obesity o Raised intra-abdominal pressure (e.g. chronic cough) o Constipation o Bladder outflow obstruction o Intraperitoneal fluid (e.g. ascites)

Answer 177

* COMMON * Peak age in adults: 55-85 yrs * 9 x more common in MALES

Answer 178

* Asymptomatic * Patient notices a 'lump in the groin' * May cause discomfort and pain * May be irreducible * May present because it has increased in size * May present because of complications (e.g. bowel obstruction)

Answer 179

• Groin lump that extends to the scrotum (males) or labia (women) • Distinguishing inguinal and femoral hernias: o Inguinal - superior and medial to the pubic tubercle o Femoral - inferior and lateral to the pubic tubercle • Check for cough impulse • Indirect hernias can be reduced and controlled by applying pressure over the deep inguinal ring • Auscultation - there may be bowel sounds over the hernia • Hernia may be irreducible • Tenderness if strangulated • Check for signs of complications o Bowel obstruction and systemic upset (pyrexia, tachycardia etc.)

Answer 180

• If ACUTE with painful irreducible hernia o Bloods • FBC • U&Es • CRP • Clotting • Group and save (if operation is likely) • ABGs - may show lactic acidosis from bowel ischaemia o Imaging • Erect CXR - check for perforation • USS - exclude other causes of groin lump • AXR - check for obstruction

Answer 181

• Surgical o Usually elective repair of uncomplicated hernias o Mesh Repair • The hernia is surgically reduced and a mesh is inserted to reinforce the defect in the transversalis fascia o Laparoscopic Mesh Repair o EMERGENCY • If obstructed or strangulated • Laparotomy with bowel resection may be indicated if the bowel is gangrenous

Answer 182

``` • Incarceration • Strangulation • Bowel obstruction • Maydl's hernia (image on the right - strangulated W-shaped loop of small bowel) • Richter's hernia (strangulation of only part of the bowel circumference) • Surgery Complications o Pain o Wound infection o Haematoma o Penile/scrotal oedema o Mesh infection o Testicular ischaemia ```

Answer 183

* Slowly enlarge if left alone | * Surgical mesh repair has a GOOD outcome

Answer 184

• Prolapse of the upper stomach through the diaphragmatic oesophageal hiatus

Answer 185

``` • Congenital • Traumatic • Non-traumatic o Sliding - the hernia moves in and out of the chest o Paraoesophageal (rolling) - the hernia goes through a whole in the diaphragm next to the oesophagus o Mixed • Risk Factors o Obesity o Low-fibre diet o Chronic oesophagitis o Ascites o Pregnancy ```

Answer 186

* Common in WESTERN countries * Increased frequency with age * 70% of patients are > 70 yrs

Answer 187

• Most are ASYMPTOMATIC • Sliding hernias are more likely to cause symptoms • Patients may present with symptoms of GORD o Heartburn o Waterbrash • NO correlation between the size of the hernia and severity of the symptoms

Answer 188

• Usually NO SIGNS

Answer 189

• Bloods o FBC - check for iron deficiency anaemia • Radiology o CXR - gastric air bubble may be seen above the diaphragm o Barium swallow • Endoscopy

Answer 190

``` • Medical o Modify lifestyle factors (e.g. lose weight) o Inhibit acid production (e.g. PPIs) o Enhance upper GI motility • Surgical o Necessary in a MINORITY of patients o Usually performed in patients with complications of reflux disease despite aggressive medical treatment or pulmonary complications (e.g. aspiration pneumonia) o Nissen Fundoplication ``` • The stomach is pulled down through the oesophageal hiatus and part of the stomach is wrapped (360 degrees) around the oesophagus to make a new sphincter and reduce the likelihood of herniation o Belsey Mark IV Fundoplication • 270 degree wrap o Hill Repair • Gastric cardia is anchored to the posterior abdominal wall

Answer 191

``` • Oesophageal o Intermittent bleeding o Oesophagitis o Erosions o Barrett's oesophagus o Oesophageal strictures • Non-Oesophageal o Incarceration of hiatus hernia (only with paraoesophageal hernias) o This can lead to strangulation and perforation ```

Answer 192

* Generally GOOD | * Sliding hernias have a better prognosis than rolling hernias

Answer 193

• Obstruction of a mesenteric vessel leading to bowel ischaemia and necrosis

Answer 194

``` • Embolus (60%) • Thrombosis (40%) • Can be a consequence of: o Volvulus o Intussusception o Bowel strangulation o Failed surgical resection • Risk Factors o AF o Endocarditis (can throw emboli) o Arterial Thrombosis: hypercholesterolaemia, hypertension, diabetes mellitus, smoking o Venous Thrombosis: portal hypertension, splenectomy, septic thrombophlebitis, OCP, thrombophilia ```

Answer 195

* UNCOMMON | * More common in the ELDERLY

Answer 196

``` • Severe acute colicky abdominal pain • Vomiting • Rectal bleeding • History of chronic mesenteric artery insufficiency o Gross weight loss o Post-prandial abdominal pain • History of heart or liver disease ```

Answer 197

* Diffuse abdominal tenderness * Abdominal distension * Tender palpable mass (ischaemic bowel) * Bowel sounds may be absent * Disproportionate degree of cardiovascular collapse

Answer 198

``` • Diagnosis based on clinical suspicion or after laparotomy • AXR - thickening of small bowel folds and signs of obstruction • Bloods o ABG - lactic acidosis o FBC o U&Es o LFTs o Clotting o Cross-match • Mesenteric Angiography o Only if stable ``` NOTE: the 'watershed zone' (the area between the supply of the superior and inferior mesenteric arteries - near the splenic flexure) is most vulnerable to intestinal ischaemia

Answer 199

• Obstruction of the normal movement of bowel contents. Classified according to the site: o Small or Large bowel o Partial or Complete obstruction o Simple or Strangulated

Answer 200

``` • Extramural o Hernia o Adhesions o Bands o Volvulus • Intramural o Tumours o Inflammatory strictures (e.g. Crohn's strictures, diverticulitis) • Intraluminal o Pedunculated tumours o Foreign body (e.g. bezoars, gallstones) ```

Answer 201

* COMMON | * More common in the ELDERLY due to increasing incidence of adhesions, hernias and malignancy

Answer 202

* Severe gripping colicky pain with periods of ease * Abdominal distension * Frequent vomiting (it may be bile-stained or faeculent) * Absolute constipation

Answer 203

* Abdominal distension with generalised tenderness * May see visible peristalsis * Tinkling bowel sounds * Peritonitis - absent bowel sounds, guarding and rebound tenderness * Inspect for hernias * Look for abdominal scars - previous abdominal surgery increases the risk of adhesions * Inspect for abdominal mass (e.g. intussusception, carcinoma)

Answer 204

• AXR o Assists diagnosis and localisation o Check for valvulae conniventes (small bowel) or haustra (large bowel) • Water-Soluble Contrast Enema • Barium follow through

Answer 205

• General o Gastric aspiration via NG tube if the patient is vomiting o IV fluids o Electrolyte replacement o Monitor vital signs, fluid balance and urine output • Surgical o Emergency laparotomy in acute obstruction

Answer 206

* Dehydration * Bowel perforation * Peritonitis * Toxaemia * Gangrene of ischaemic bowel wall

Answer 207

* Variable | * Dependent on the general state of the patient and the prevalence of complications

Answer 208

* Abscess: liver infection resulting in a walled off collection of pus * Cyst: liver infection resulting in a walled off collection of cyst fluid

Answer 209

``` • Pyogenic (producing pus) o Escherichia coli o Klebsiella o Enterococcus o Bacteriodes o Streptococci o Staphylococci o 60% are caused by biliary tract disease (e.g. gallstones, strictures, congenital cysts) o 15% have unknown cause • Amoebic abscess o Caused by Entamoeba histolytica • Hydatid cyst: o Caused by tapeworm Echinococcus granulosis • Other causes: TB ``` NOTE: hydatid = a cyst containing watery fluid

Answer 210

* Pyogenic is the most common type of liver abscess in the industrialised world * Amoebic liver abscess - most common WORLDWIDE * Hydatid cysts - common in sheep-rearing countries

Answer 211

* Fever * Malaise * Nausea * Anorexia * Night sweats * Weight loss * RUQ/epigastric pain that may be referred to the shoulder (due to irritation of the diaphragm) * Jaundice * Diarrhoea * Pyrexia of unknown origin * IMPORTANT: make sure you ask about foreign travel

Answer 212

``` • Fever - continuous or spiking • Jaundice • Tender hepatomegaly (right lobe affected more than left) • Right lung base: o Dullness to percussion o Reduced breath sounds o Due to reactive pleural effusion ```

Answer 213

``` • Bloods o FBC • Mild anaemia • Leukocytosis • High eosinophils (if hydatid disease) o LFTs • High ALP • High bilirubin o High ESR and CRP o Blood cultures o Amoebic and hydatid serology • Stool MC&S - for E. histolytica • Liver US or CT/MRI - localises structure of mass ``` • CXR - check for right pleural effusion or atelectasis, raised hemidiaphragm • Aspiration and culture of the abscess material o Most pyogenic liver abscesses are polymicrobial o Amoebic abscesses have fluid of necrotic hepatocytes and trophozoites

Answer 214

• Severe liver dysfunction leading to jaundice, encephalopthy and coagulopathy • It is classified based on the time interval between the onset of jaundice and the development of hepatic encephalopathy o Hyperacute = < 7 days o Acute = 1-4 weeks o Subacute = 4-12 weeks • Acute-on-Chronic Liver Failure = acute deterioration (decompensation) in patients with chronic liver disease

Answer 215

• Viral o Hepatitis A, B, C, D and E • Drugs o Paracetamol overdose o Idiosyncratic drug reactions • Less common causes o Autoimmune hepatitis o Budd-Chiari syndrome o Pregnancy-related o Malignancy (e.g. lymphoma) o Haemochromatosis o Mushroom poisoning (Amanita phalloides) o Wilson's disease • Pathogenesis of the manifestations of liver failure o Jaundice - due to decreased secretion of conjugated bilirubin o Encephalopathy • Nitrogenous products (e.g. ammonia) is absorbed in the gut and goes via the portal circulation to the liver • A normal liver would be able extract these harmful substances • However, if the liver is failing, these toxic products can go through the liver and reach the brain and exert its effects o Coagulopathy • Reduced synthesis of clotting factors • Reduced platelets • Platelet functional abnormalities associated with jaundice or renal failure

Answer 216

• Paracetamol overdose counts for 50% of acute liver failure in the UK

Answer 217

* May be asymptomatic * Fever * Nausea * Jaundice (not always)

Answer 218

* Jaundice * Encephalopathy * Asterixis * Fetor hepaticus * Ascites and splenomegaly (less common if acute or hyperacute) * Bruising or bleeding * Signs of secondary causes (e.g. bronze skin colour, Kayser-Fleisher rings) * Pyrexia - may indicate infection or liver necrosis

Answer 219

``` • Identify the cause o Viral serology o Paracetamol levels o Autoantibodies (e.g. ASM, Anti-LKM) o Ferritin (haemochromatosis) o Caeruloplasmin and urinary copper (Wilson's disease) • Bloods o FBC • Low Hb (if GI bleed) • High WCC (if infection) o U&Es • May show renal failure (hepatorenal syndrome) o Glucose o LFTs • High bilirubin • High AST, ALT, ALP, GGT • Low albumin o ESR/CRP o Coagulation screen o ABG - to determine blood pH o Group and save • Liver US/CT • Ascitic Tap o Send for MC&S o If neutrophils > 250/mm3 = spontaneous bacterial peritonitis • Doppler scan of hepatic or portal veins - check for Budd-Chiari syndrome • EEG - monitor encephalopathy ```

Answer 220

• Resuscitation - ABC • Treat the cause if possible: o N-acetylcysteine - treatment for paracetamol overdose • Treatment/prevention of complications (invasive ventilation and cardiovascular support is often required) o Monitor - vital signs, PT, pH, creatinine, urine output, encephalopathy o Manage encephalopathy: lactulose and phosphate enemas o Antibiotic and antifungal prophylaxis o Hypoglycaemia treatment o Coagulopathy treatment - IV vitamin K, FFP, platelet infusions o Gastric mucosa protection - PPIs or sucralfate o AVOID sedatives or drugs metabolised by the liver o Cerebral oedema - decrease ICP with mannitol • Renal Failure o Haemodialysis o Nutritional support • Surgical - liver transplant

Answer 221

* Infection * Coagulopathy * Hypoglycaemia * Disturbance of electrolyte balance and acid-base balance * Disturbance of cardiovascular system * Hepatorenal syndrome * Cerebral oedema (causing raised ICP) * Respiratory failure

Answer 222

• Depends on severity and aetiology

Answer 223

• Tearing of the lining of the oesophagus around the junction with the stomach as a result of violent vomiting or straining to vomit.

Answer 224

``` • Caused by prolonged violent vomiting • Risk Factors o Chronic alcohol abuse o Bulimia o Other causes: trauma, intense coughing, gastritis ```

Answer 225

• Quite rare

Answer 226

* Most cases do not cause any symptoms * Abdominal pain * Severe vomiting * Haematemesis * Involuntary retching * Black/tarry stools * Symptoms of hypovolaemia if SEVERE blood loss (e.g. light-headedness)

Answer 227

* Melaena | * See above

Answer 228

* OGD | * Bloods - FBC to check for anaemia

Answer 229

• 80-90% of the time, the bleeding from a Mallory-Weiss tear will stop on its own • Surgery may be necessary if the bleeding does NOT stop o Injection sclerotherapy o Coagulation therapy o Arteriography • NOTE: transfusions may be required if blood loss has been severe • Anti-reflux medications may also be prescribed

Answer 230

• Boerhaave's perforation

Answer 231

• GOOD prognosis

Answer 232

• A term used to describe a range of conditions caused by the build-up of fat in the liver due to causes other than excessive alcohol use.

Answer 233

``` • A liver may initially become fatty due to alcohol abuse, however, these fatty deposits tend to resolve over a matter of days • If the fat persists, it can cause inflammation and fibrosis (steatohepatitis) • NASH also increases the risk of: o Diabetes mellitus o MI o Stroke • Risk Factors o Obesity o Type 2 diabetes mellitus o Hypertension o Hypercholesterolaemia o Age > 50 yrs o Smoking ```

Answer 234

* MOST COMMON liver disorder in developed countries | * 1/3 people in the UK have the early stages of NASH

Answer 235

• Usually NO SYMPTOMS in the early stages • Usually found as an incidental finding • Occasional symptoms include: o Dull or aching RUQ pain o Fatigue o Unexplained weight loss o Weakness • Symptoms of cirrhosis will be experienced in the most advanced stages of NASH

Answer 236

* RUQ pain/tenderness | * Signs of cirrhosis (e.g. jaundice, ascites, pruritus - in advanced stages of NASH)

Answer 237

* LFTs - showing elevated AST and ALT * Liver Ultrasound - may show steatosis * Liver Biopsy

Answer 238

``` • Conservative - controlling risk factors: o Blood pressure o Diabetes o Cholesterol o Lose weight o Stop smoking o Exercise regularly o Reduce alcohol consumption (although it is NOT caused by excessive alcohol, drinking can make it worse) ```

Answer 239

``` • CIRRHOSIS o Ascites o Oesophageal varices o Hepatic encephalopathy o Hepatocellular carcinoma o End-stage liver failure ```

Answer 240

• 20% with NASH will develop cirrhosis

Answer 241

• Malignant tumour arising in the oesophagus. There are TWO major histological types: o Squamous cell carcinoma o Adenocarcinoma

Answer 242

``` • Squamous Cell Carcinoma o Alcohol o Tumour o Plummer-Vinson syndrome o Achalasia o Scleroderma o Coeliac disease o Nutritional deficiencies o Dietary toxins (e.g. nitrosamines) • Adenocarcinoma o GORD o Barrett's oesophagus ```

Answer 243

* 8th most common cancer * 3 x more common in MALES * Squamous cell carcinoma is more common in DEVELOPING COUNTRIES * Adenocarcinoma is more prevalent in the WESTERN WORLD

Answer 244

* Often ASYMPTOMATIC * Progressive dysphagia (initially worse for solids) * Regurgitation * Cough * Choking after food * Voice hoarseness * Odynophagia (painful swallowing) * Weight loss * Fatigue (due to iron deficiency anaemia)

Answer 245

``` • There may be NO SIGNS • Metastatic disease may cause: o Supraclavicular lymphadenopathy o Hepatomegaly o Hoarseness o Signs of bronchopulmonary involvement ```

Answer 246

* Endoscopy - brushings and biopsy * Imaging - barium swallow and CXR * Staging - CT chest and abdomen * Other - bronchoscopy, lung function tests and ABGs

Answer 247

• Malignancy arising from the exocrine or endocrine tissues of the pancreas

Answer 248

``` • UNKNOWN • 5-10% are hereditary (e.g. MEN, HNPCC, FAP, Von-Hippel Lindau syndrome) • Risk Factors o Age o Smoking o Diabetes mellitus o Chronic pancreatitis o Dietary (low intake of fresh fruit and vegetables) ```

Answer 249

* Increasing incidence * 2 x more common in MALES * Peak age: 60-80 yrs

Answer 250

* Initial symptoms are often NON-SPECIFIC * Anorexia * Malaise * Nausea * Epigastric pain * Weight loss * Diabetes mellitus * Jaundice

Answer 251

* Weight loss * Epigastric tenderness or mass * Jaundice and a palpable gallbladder (Courvoisier's law - a palpable gallbladder with painless jaundice is unlikely to be due to gallstones) * If metastatic spread --> hepatomegaly * Trousseau's Sign of Malignancy - superficial thrombophlebitis

Answer 252

``` • Bloods o CA 19-9 o CEA is also elevated o Obstructive jaundice features: • High bilirubin • High ALP • Deranged clotting • Imaging o Ultrasound o CT with/without guided biopsy o MRI/MRCP o ERCP - may allow biopsy, bile cytology and stenting ```

Answer 253

• An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems. • It can be classified as: o Mild: minimal organ dysfunction and uneventful recovery o Severe: organ failure and/or local complications such as necrosis, abscesses and pseudocysts

Answer 254

``` • An insult will result in the activation of pancreatic proenzymes within the pancreatic duct/acini leading to tissue damage and inflammation • Causes of Pancreatitis: GET SMASHED o Gallstones o Ethanol o Trauma o Steroids o Mumps/HIV/Coxsackie o Autoimmune o Scorpion Venom o Hypercalcaemia/hypercalcaemia/hypothermia o ERCP o Drugs (e.g. sodium valproate, steroids, thiazides and azathioprine) ```

Answer 255

``` • COMMON • UK Annual Incidence: 10/10,000 • Peak age: 60 yrs • Most common cause in: o Males = alcohol o Females = gallstones ```

Answer 256

* Severe epigastric pain * Radiating to the back * Relieved by sitting forward * Aggravated by movement * Associated with anorexia, nausea and vomiting * IMPORTANT: check whether the patient has a history of high alcohol intake or gallstones

Answer 257

``` • Epigastric tenderness • Fever • Shock (includes tachycardia and tachypnoea) • Decreased bowel sounds (due to ileus) • In severe pancreatitis: o Cullen's sign (periumbilical bruising) o Grey-Turner sign (flank bruising) ```

Answer 258

• Blood: o VERY HIGH SERUM AMYLASE (this does not correlate with severity) o High WCC o U&Es (to check for dehydration) o High glucose o High CRP o Low Calcium (saponification - calcium binds to digested lipids from the pancreas to form soap) o LFTs (may be deranged if gallstone pancreatitis or alcohol) o ABG (for hypoxia or metabolic acidosis) • USS: check for evidence of gallstones in biliary tree • Erect CXR: may be pleural effusion. Also to check for bowel perforation • AXR: exclude other causes of acute abdomen • CT Scan: if diagnosis is uncertain or if persisting organ failure

Answer 259

• Assessment of severity has TWO main scales: o Modified Glasgow Score (combined with CRP (> 210 mg/L) o APACHE-II Score o NOTE: In the USA, the Ranson score is often used (this is specific for alcoholic pancreatitis) • Medical Management: o Fluid and electrolyte resuscitation o Urinary catheter and NG tube if vomiting o Analgesia o Blood sugar control o HDU and ITU care o Prophylactic antibiotics may be useful in reducing mortality • ERCP and Sphincterotomy: o Used for gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct o Ideally performed within 72 hours o All patients presenting with gallstone pancreatitis should undergo definitive management of gallstones during the same admission or within 2 weeks • Early detection and treatment of complications: o For example if there are persistent symptoms or > 30% pancreatic necrosis or signs of sepsis --> image guided fine needle aspiration for culture • Surgical: o Necrotising pancreatitis should be managed by specialists o Necresectomy (drainage and debridement of necrotic tissue) may be necessary

Answer 260

``` • Local: o Pancreatic necrosis o Pseudocyst (peripancreatic fluid collection lasting > 4 weeks) o Abscess o Ascites o Pseudoaneurysm o Venous thrombosis • Systemic: o Multiorgan dysfunction o Sepsis o Renal failure o ARDS o DIC o Hypocalcaemia o Diabetes • Long-Term: could result in chronic pancreatitis ```

Answer 261

* 20% follow severe fulminating course with high mortality * Infected pancreatic necrosis has a 70% mortality * 80% follow a milder course (but this still has 5% mortality)

Answer 262

• Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain.

Answer 263

• ALCOHOL - 70% • Idiopathic - 20% • RARE: recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism • EXTRA information about pathology/pathogenesis: o Chronic pancreatitis is caused by disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atrophy, ductal dilation and cyst and stone formation o Pain is associated with raised intraductal pressures

Answer 264

* Annual UK incidence: 1/100,000 * Prevalence: 3/100,000 * Mean age: 40-50 yrs (in alcohol-associated disease)

Answer 265

* Recurrent severe epigastric pain * Pain radiates to the back * Pain relieved by sitting forward * Pain can be aggravated by eating or drinking alcohol * Over many years --> weight loss, bloating and steatorrhoea

Answer 266

* Epigastric tenderness | * Signs of complications e.g. weight loss, malnutrition

Answer 267

• Bloods: o High glucose (endocrine dysfunction) - glucose tolerance test may be performed o Amylase and lipase usually normal o High Ig (especially IgG4 in autoimmune pancreatitis) • Ultrasound • ERCP or MRCP: o Early changes that can be seen include main duct dilatation and stumping of branches o Late manifestations include duct strictures with alternating dilatation • Abdominal X-Ray: o May show pancreatic calcification • CT Scan: o May show pancreatic calcification and pancreatic cysts • Tests of pancreatic exocrine function: o Faecal elastase (reflects pancreatic exocrine function)

Answer 268

• General: o Treatment is mainly symptomatic and supportive (e.g. dietary advice, stop smoking/drinking, treat diabetes, oral pancreatic enzyme replacement, analgesia) o Chronic pain management may need specialist input • Endoscopy Therapy: o Sphincterotomy o Stone extraction o Dilatation and stenting of strictures o Extracorporial shock-wave lithotripsy (ESWL) is sometimes used to fragment larger pancreatic stones before removal • Surgical: o May be indicated if medical management fails o Lateral pancreaticojejunal drainage (modified Puestow procedure) o Pancreatic resection (pancreaticoduodenectomy or Whipple's procedure) o Limited resection of pancreatic head (Beger procedure) o Combining opening of the pancreatic duct and excavation of the pancreatic head (Frey procedure)

Answer 269

``` • Local: o Pseudocysts o Biliary duct stricture o Duodenal obstruction o Pancreatic ascites o Pancreatic carcinoma • Systemic: o Diabetes o Steatorrhoea o Chronic pain syndromes o Dependence on strong analgesics ```

Answer 270

* Difficult to predict * Surgery improves symptoms in 60-70% but results are often not sustained * Life expectancy may be reduced by 10-20 years

Answer 271

• Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin. Peptic ulcers are most commonly gastric and duodenal (but they can also occur in the oesophagus and Meckel's diverticulum).

Answer 272

• Caused by an imbalance between the damaging action of acid and pepsin penis and the mucosal protective mechanisms • There is a strong correlation with Helicobacter pylori • COMMON CAUSES of peptic ulcer disease and gastritis: o Helicobacter pylori o NSAIDs • RARE cause: Zollinger-Ellison syndrome (a condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas cause overproduction of gastric acid, resulting in recurrent peptic ulcers)

Answer 273

``` • COMMON • Annual incidence: 1-4/1000 • More common in males • Mean age: o Duodenal ulcer: 30s o Gastric ulcers: 50s • Helicobacter pylori is usually acquired in childhood and prevalence is roughly equal to age in years ```

Answer 274

• Epigastric pain • Relieved by antacids • Symptoms have a variable relationship to food intake: o Gastric - pain is worse soon after eating o Duodenal - pain is worse several hours after eating • Patients may present with complications e.g. haematemesis, melaena

Answer 275

* There may be NO physical findings * Epigastric tenderness * Signs of complications e.g. anaemia

Answer 276

• Bloods: o FBC (for anaemia) o Serum amylase (to exclude pancreatitis) o U&Es o Clotting screen o LFT o Cross-match if active bleeding o Secretin test (if Zollinger-Ellison syndrome suspected) - IV secretin causes a rise in serum gastrin in ZE patients but not in normal patients) • Endoscopy: o Biopsies of gastric ulcers can be taken to rule out malignancy o Duodenal ulcers do NOT need to be biopsied • Rockall Scoring: o Scores the severity after a GI bleed o Score < 3 carries good prognosis o Score > 8 carries high risk of mortality • Testing for H. pylori: o C13-urea breath test : • Radio-labelled urea is given by mouth • C13 is detected in the expelled air o Serology: • IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication o Campylobacter-like organism (CLO) test: • Gastric biopsy is placed with a substrate of urea and a pH indicator • If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red

Answer 277

• Acute: o Fluid resuscitation needed if the ulcer is perforated or bleeding (IV colloids/crystalloids) o Close monitoring of vital signs o Endoscopy o Surgical treatment o NOTE: patients with upper GI bleeding should be treated with IV PPIs at presentation until the cause of bleeding is identified • Endoscopy: o If the ulcer is bleeding, haemostasis can be achieved with: • Injection sclerotherapy • Laser coagulation • Electrocoagulation • Surgery: o Indicated if the ulcer has perforated or if the bleeding ulcer can't be controlled • Helicobacter pylori eradication: o Triple therapy for 1-2 weeks o Various combinations may be recommended - usually a combination of 2 antibiotics + PPI (e.g. clarithromycin + amoxicillin + omeprazole) • If peptic ulcer disease is NOT associated with H. pylori: o Treat with PPIs or H2 antagonists o Stop NSAID use o Use misoprostol (prostoglandin E1 analogue) if NSAID use is necessary

Answer 278

• Rate of major complication = 1 % per year • Major complications: o Haemorrhage (haematemesis, melaena, iron-deficiency anaemia) o Perforation o Obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)

Answer 279

* Overall lifetime risk = 10% | * Outlook is generally good because peptic ulcers associated with H. pylori can be cured by eradication

Answer 280

* Perineal Abscess: a pus collection in the perineal region * Perineal Fistula: an abnormal chronically infected tract communicating between the perineal skin and either the anal canal or the rectum

Answer 281

• Bacterial infection • Fistulae develop as a complication of an abscess • Fistulae can develop as a complications of Crohn's disease o The development of multiple perineal fistulae in Crohn's disease is called pepper pot perineum • Risk Factors o IBD o Diabetes mellitus o Malignancy

Answer 282

• COMMON

Answer 283

* Constant throbbing pain in the perineum * Intermittent discharge (mucus or faecal staining) near the anal region * Personal or family history of IBD

Answer 284

• Localised tender perineal mass (may be fluctuant) • Small skin lesion near the anus (opening of the fistula) • DRE o A thickened area over the abscess/fistula may be felt o DREs are not always possible due to pain and anal sphincter spasm • Goodsall's Law o This is a rule that allows you to correlate the location of the internal fistula opening based on the location of the external fistula opening o If the external fistula opening is ANTERIOR to the anal canal (i.e. lies anterior to the transverse anal line), the fistula runs radially and directly into the anal canal o A fistula that is 3 cm away and any fistula that has an external fistula opening lying posterior to the transverse anal line will follow a curved path and open internally in the posterior midline

Answer 285

``` • Bloods o FBC o CRP o ESR o Blood culture • Imaging o MRI • Endoanal Ultrasound o Less useful than MRI ```

Answer 286

• Requires SURGICAL treatment • Open Drainage of Abscess • Laying Open of Fistula o A probe is inserted to explore the fistula o A dye can be inserted into the external opening to allow you to find the internal opening o Low Fistula • Fistulotomy • Care must be taken to prevent damage to the anal sphincter o High Fistula • Fistulotomy would cause INCONTINENCE so is NOT performed • Seton - a non-absorbable suture that is threaded through the fistula and allows drainage • Antibiotics

Answer 287

* Recurrence * Damage to internal anal sphincter * Incontinence * Persisting pain

Answer 288

• High recurrence rate without complete excision

Answer 289

• Inflammation of the peritoneal lining of the abdominal cavity. It can be localised to one part of the peritoneum or generalised.

Answer 290

• Localised Peritonitis o Appendicitis o Cholecystitis o Diverticulitis o Salpingitis • Primary Generalised Peritonitis o Bacterial infection of the peritoneal cavity without an obvious source • Could be via haematogenous or lymphatic spread or ascending infection from the female genital tract) o Risk Factors • Ascites • Nephrotic syndrome • Secondary Generalised Peritonitis o Caused by bacterial translocation from a localised focus o Could be non-bacterial due to spillage of bowel contents, bile and blood (e.g. perforated peptic ulcer)

Answer 291

* Primary peritonitis is RARE * Primary peritonitis is usually seen in adolescent females * Localised and secondary generalised peritonitis is COMMON in surgical patients

Answer 292

* Do a full SOCRATES for peritonitis * Inflammation of the parietal peritoneum is usually continuous, sharp, localised, exacerbated by movement and coughing * Symptoms may be vague in those with liver disease and ascites (due to confusion caused by encephalopathy)

Answer 293

• Check vital signs and look for signs of dehydration or compromised perfusion (e.g. due to sepsis or hypovolaemia) • Localised Peritonitis o Tenderness on examination o Guarding o Rebound tenderness • Generalised Peritonitis o Very unwell o Systemic signs of toxaemia or sepsis (e.g. fever, tachycardia) o The patient will lie still o Shallow breathing o Rigid abdomen o Generalised abdominal tenderness o Reduced bowel sounds (may be absent due to paralytic ileus) o DRE may show anterior tenderness (suggests pelvic peritonitis)

Answer 294

``` • Bloods o FBC o U&Es o LFTs o Amylase o CRP o Clotting o Group & Save or Cross-match o Blood cultures o Pregnancy test o ABG • Imaging o Erect CXR (check for air under the diaphragm) o AXR (check for bowel obstruction) o USS or CT abdomen o Laparoscopy • If Ascites o Ascitic tap and cell count o SBP = > 250 neutrophils/mm3 o Gram stain and culture ```

Answer 295

• Localised Peritonitis o Depends on CAUSE o Some causes may require surgery (e.g. appendicitis) o Some causes can be treated with antibiotics (e.g. salpingitis) • Generalised Peritonitis o Patient may be at risk of DEATH from sepsis or shock o IV fluids o IV antibiotics o Urinary catheter o NG tube o Central venous line (to monitor fluid balance) o Laparotomy • Remove the infected or necrotic tissue • Treat cause • Peritoneal lavage o Primary Peritonitis - should be treated with antibiotics • Spontaneous Bacterial Peritonitis (SBP) o Quinolone antibiotics OR o Cefuroxime + Metronidazole

Answer 296

``` • Early o Septic shock o Respiratory failure o Multiorgan failure o Paralytic ileus o Wound infection o Abscesses • Late o Incisional hernia o Adhesions ```

Answer 297

* Localised peritonitis usually resolves with treatment of the underlying cause * Generalised peritonitis has a much higher mortality (30-50%) * Primary peritonitis has a good prognosis with antibiotic treatment * SBP has a mortality > 30% if diagnosis and treatment is delayed

Answer 298

• An abnormal epithelium-lined tract filled with hair that opens onto the skin surface, most commonly in the natal cleft

Answer 299

• Caused by shed or sheared hairs penetrating the skin and inciting and inflammatory reaction and sinus development • Intermittent negative pressure will draw in more hair and perpetuate the cycle • Risk Factors o Hirsutism o Spending a long time sitting down o Occupational (e.g. hairdressers may develop interdigital pilonidal sinus)

Answer 300

* COMMON | * Affects 0.7% of young adults

Answer 301

* Painful natal cleft * Discharging swelling * Often recurrent

Answer 302

* Midline openings or pits between the buttocks * Hairs may protrude from the swelling * If infection or abscess, the swelling will become tender * It may be fluctuant and discharge pus or blood-stained fluid on compression

Answer 303

• NONE needed • Bloods - to check for signs of infection o Raised WCC o Fasting glucose (diabetics are at risk)

Answer 304

``` • Acute Pilonidal Abscess o Incision and drainage • Chronic Pilonidal Sinus o Excision under general anaesthesia with exploration • Prevention o Good hygiene o Shaving ```

Answer 305

* Pain * Infection * Abscess * Recurrence

Answer 306

* Good with drainage * Shaving will cure in most cases * Usually resolves by the age of 40

Answer 307

• Abnormally high pressure within the hepatic portal vein. | o NOTE: clinically significant portal hypertension is defined as a hepatic venous pressure gradient > 10 mm Hg

Answer 308

``` • CIRRHOSIS is the most common cause • Other causes can be divided as follows: o Pre-Hepatic - blockage of the portal vein before the liver • Congenital stenosis • Portal vein thrombosis • Splenic vein thrombosis • Extrinsic compression o Hepatic • CIRRHOSIS • Chronic hepatitis • Schistosomiasis • Myeloproliferative disease o Post-Hepatic - blockage of hepatic veins or venules • Budd-Chiari syndrome (hepatic vein obstruction) • Constrictive pericarditis • Right heart failure ```

Answer 309

• A common consequence of cirrhosis

Answer 310

• Features of Liver Disease (likely to coexist with portal hypertension) o Jaundice o History of alcohol abuse o Risk factors for viral hepatitis (e.g. tattoos, unprotected sex, IV drug use, travel abroad and blood transfusion) o Family history (e.g. haemochromatosis) • Complications of Portal Hypertension o Haematemesis or melaena o Lethargy, irritability, changes in sleep (hepatic encephalopathy) o Abdominal distension (ascites) o Abdominal pain and fever (spontaneous bacterial peritonitis) o Pulmonary involvement

Answer 311

``` • Signs of Portal Hypertension o Caput medusae o Splenomegaly o Ascites • Signs of Liver Failure o Jaundice o Spider naevi o Palmar erythema o Confusion o Asterixis o Fetor hepaticus o Enlarged or small liver o Gynaecomastia o Testicular atrophy ```

Answer 312

• Bloods o LFTs o U&Es o Blood glucose o FBC o Clotting screen (prolongation of PT is one of the earliest signs of liver failure) • Specific Tests o Ferritin - haemochromatosis o Hepatitis serology o Autoantibodies (e.g. anti-smooth muscle antibodies in autoimmune hepatitis) o 1-antitrypsin levels o Caeruloplasmin - Wilson's disease • Imaging o Abdominal ultrasound - check liver and spleen size and assess portal blood flow o Doppler ultrasound - assess direction of blood flow in vessels o CT/MRI - if other imaging methods are inconclusive o Endoscopy - to check for oesophageal varices • Measure hepatic venous pressure gradient (HVPG) • Liver Biopsy - if indicated

Answer 313

• Difficult to treat portal hypertension specifically • Treatment is mainly focused on treating the underlying cause where possible • Conservative o Salt restriction o Diuretics • Treatment of oesophageal varices if present • Non-selective beta-blockers - reduces portal pressure and reduces risk of variceal bleeding • Terlipressin - can reduce portal venous pressure • Transjugular Intrahepatic Portosystemic Shunt (TIPS) - surgical shunt placed between the hepatic portal vein and the hepatic vein to ease congestion in the portal vein • Liver transplant

Answer 314

``` • Bleeding from oesophageal varices • Ascites + complications of ascites: o Spontaneous bacterial peritonitis o Hepatorenal syndrome • DEFINITION: a life-threatening condition that consists of a rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure o Hepatic hydrothorax • DEFINITION: a transudative pleural effusion in patients with portal hypertension without any underlying primary cardiopulmonary cause • Pulmonary complications o Portopulmonary hypertension o Hepatopulmonary syndrome - triad of: • Hepatic dysfunction • Hypoxaemia • Extreme vasodilation (intrapulmonary vascular dilatation) • Liver failure • Hepatic encephalopathy • Cirrhotic cardiomyopathy ```

Answer 315

* Depends on the underlying CAUSE | * Variceal haemorrhages have a 1-year mortality of 40%

Answer 316

• A chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis, and, ultimately, cirrhosis

Answer 317

* UNKNOWN * Likely to be autoimmune * Genetic and environmental factors are involved * An environmental trigger may cause bile duct epithelial injury, which then leads to a T-cell mediated autoimmune response directed against bile duct epithelial cells

Answer 318

• Mainly affects middle-aged women (9:1 female: male)

Answer 319

• May be an incidental finding on blood tests • Insidious onset with vague symptoms such as: o Fatigue o Weight loss o Pruritis • Rarely, it may cause discomfort in the RUQ • May present with a complication of liver decompensation (e.g. jaundice, ascites, variceal haemorrhage) • May present with symptoms of associated conditions (e.g. Sjogren's syndrome, arthritis, Raynaud's phenomenon)

Answer 320

``` • Early - may be no signs • Late: o Jaundice o Skin pigmentation o Scratch marks o Xanthomas (secondary to hypercholesterolaemia) o Hepatomegaly o Ascites o Signs of chronic liver disease ```

Answer 321

• Bloods o LFT: • High ALP + GGT • Bilirubin may be high or normal • ALT and AST are normal initially but will increase as the disease progresses and cirrhosis develops o Clotting: prolongation of PT o Typical features of PBC: • Antimitochondrial antibodies (typical feature of PBC) • High IgM • High Cholesterol o TFTs - because PBC is associated with autoimmune thyroid disease • Ultrasound o Exclude extrahepatic biliary obstruction (e.g. gallstones) • Liver Biopsy o In PBC, it will show chronic inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes

Answer 322

``` • A chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts • Pathology/Pathogenesis o Periductal inflammation with periductal concentric fibrosis o Portal oedema o Bile duct proliferation o Expansion of portal tracts o Progressive fibrosis o Development of biliary cirrhosis ```

Answer 323

* UNKNOWN * Possible immune and genetic predisposition with environmental triggers * Close association with inflammatory bowel disease (especially ulcerative colitis) * IMPORTANT: ulcerative colitis is present in about 70% of patients with PSC

Answer 324

• Usually presents between 25-40 years of age

Answer 325

• May be asymptomatic and diagnosed after persistently raised ALP • May present with: o Intermittent jaundice o Pruritis o RUQ pain o Weight loss o Fatigue • May present with episodes of fever and rigors caused by acute cholangitis (but this is less common) • IMPORTANT: check for a history of ulcerative colitis

Answer 326

* May have no signs * Jaundice * Hepatosplenomegaly * Spider naevi * Palmar erythema * Ascites

Answer 327

• Bloods o LFTs: • High ALP + GGT • Mildly elevated ALT + AST • Low albumin + high bilirubin (later stages) • Serology o IgG high in children o IgM high in adults o ASMA and ANA present in 30% o Anti-mitochondrial antibodies (AMA) usually ABSENT o Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) present in 70% • ERCP o Shows stricturing and interspersed dilation of intrahepatic and (occasionally) extraheptic bile ducts o Small diverticuli on the common bile duct may be seen • MRCP o Enables non-invasive imaging of the biliary tree • Liver Biopsy o Confirm diagnosis and allows staging

Answer 328

• The abnormal protrusion of the full thickness (or only the mucosal layer) of rectum through the anus

Answer 329

``` • Straining • Abnormal rectal anatomy or physiology (e.g. pelvic floor weakness, poor fixation of rectum to sacrum or reduced anal sphincter pressure) • Risk Factors o Constipation o Causes of increased straining o Cystic fibrosis (in children) o Previous trauma to the anus/perineum o Neurological conditions (e.g. cauda equina syndrome, MS) ```

Answer 330

* Relatively COMMON | * Most commonly affected: CHILDREN (< 3 yrs) and the ELDERLY

Answer 331

* Protruding anal mass * Initially associated with defecation * May require digital replacement * Constipation * Faecal incontinence * PR mucus or bleeding * May be an EMERGENCY - irreducible or strangulated prolapse

Answer 332

* Prolapse may be seen on straining * May be ulcerated or necrotic if the vascular supply is compromised * Reduced anal sphincter tone

Answer 333

``` • Imaging o Proctosigmoidoscopy o Defecating proctogram or barium enema • Other o Anal sphincter manometry o Pudendal nerve studies • Sweat Chloride Test o Performed in children to test for cystic fibrosis ```

Answer 334

• Chronic relapsing and remitting inflammatory disease affecting the large bowel

Answer 335

• UNKNOWN • Possible genetic susceptibility • Other factors involved: immune response to bacterial or self-antigens, environmental factors, altered neutrophil function and abnormality in epithelial cell integrity • Positive family history - 15% of patients • Associations: o pANCA o Primary sclerosing cholangitis (70% of patients with PSC have UC)

Answer 336

``` • Higher prevalence in: o Ashkenazi jews o Caucasians • Uncommon before the age of 10 yrs • Peak onset: 20-40 yrs • Equal sex ratio up to the age of 40 yrs (higher in males from then on) ```

Answer 337

* Bloody or mucous diarrhoea (stool frequency depends on severity of disease) * Tenesmus and urgency * Crampy abdominal pain before passing stool * Weight loss * Fever * Extra-GI manifestations (e.g. uveitis, scleritis, erythema nodosum, pyoderma gangrenosum)

Answer 338

* Signs of iron deficiency anaemia (e.g. conjunctival pallor) * Dehydration * Clubbing * Abdominal tenderness * Tachycardia * Blood, mucus and tenderness on PR examination * Extra-GI manifestations (listed above)

Answer 339

• Bloods o FBC: • Low Hb • High WCC o High ESR or CRP o Low albumin o NOTE: X-match if there is severe blood loss • Stool o Infectious colitis is a differential diagnosis so a stool culture maybe useful o Faecal calprotectin allows differentiation of IBS from IBD • It is raised in inflammatory processes (i.e. IBD) • Both IBS and IBD can present with long-term diarrhoea • AXR o Rule out toxic megacolon • Flexible Sigmoidoscopy or Colonoscopy (and biopsy) o Determines severity o Histological confirmation o Detection of dysplasia • Barium Enema o Shows mucosal ulceration with granular appearance and filling defects (due to pseudopolyps) o Narrowed colon o Loss of haustral pattern - leadpipe appearance (right) o Colonoscopy and barium enema may be DANGEROUS during an acute exacerbation - risk of perforation

Answer 340

``` • Markers of disease activity o Decreased Hb o Decreased albumin o Increased ESR and CRP o Diarrhoea frequency: • < 4 = mild • 4-6 = moderate • 6+ = severe o Bleeding o Fever • Management of an Acute Exacerbation o IV rehydration o IV corticosteroids o Antibiotics o Bowel rest o Parenteral feeding may be necessary o DVT prophylaxis o If toxic megacolon - the patient is likely to need a proctocolectomy because toxic megacolon has a high mortality • Management of Mild Disease o Oral or rectal 5-ASA derivatices (e.g. mesalazine, olsalazine, sulphasalazine) and/or rectal steroids • Management of Moderate to Severe Disease o Oral steroids o Oral 5-ASA o Immunosuppression (with azathioprine, cyclosporine, 6-mercaptopurine or infliximab (anti-TNF monoclonal antibody)) • Advice o Patient education and support o Treat complications o Regular colonoscopic surveillance • Surgical o If medical treatment fails, presence of complications or to prevent colonic carcinoma o Procedures: • Proctocolectomy with ileostomy ``` • Ileo-anal pouch formation

Answer 341

``` • Gastrointestinal Complications o Haemorrhage o Toxic megacolon o Perforation o Colonic carcinoma o Gallstones o Primary sclerosing cholangitis • Extra-gastrointestinal Manifestations o Uveitis o Renal calculi o Arthropathy o Sacroiliitis o Ankylosing spondylitis o Erythema nodosum o Pyoderma gangrenosum o Osteoporosis (from chronic steroid use) o Amyloidosis ```

Answer 342

``` • Normal life expectancy • Poor prognostic factors: o Low albumin (< 30 g/L) o PR blood o Raised CRP o Dilated loops of bowel o 8+ bowel movements per day o Fever ```

Answer 343

• Hepatitis caused by infection with the RNA viruses, hepatitis A or hepatitis E virus, that follow an acute course without progression to chronic carriage

Answer 344

• HAV = picornavirus • HEV = calicivirus • Transmission = faecal-oral route • Both viruses replicate within hepatocytes and are secreted into bile • Liver inflammation and hepatocyte necrosis is caused by the immune response • Infected cells are targeted by CD8+ T cells and NK cells • Histological features: o Inflammatory cell infiltration of portal tracts o Zone 3 necrosis o Bile duct proliferation

Answer 345

* HAV is endemic in the developing world * Infection often occurs sub-clinically * Better sanitation in the developed world means that it is less common, age of exposure is higher and, hence, patients are more likely to be symptomatic * HEV is endemic in Asia, Africa and Central America

Answer 346

``` • Incubation period of HAV and HEV: 3-6 weeks • Prodromal period symptoms: o Malaise o Anorexia o Fever o Nausea and vomiting • Hepatitis symptoms: o Dark urine o Pale stools o Jaundice lasting around 3 weeks o Occasionally, itching and jaundice may last several weeks in HAV infection ```

Answer 347

* Pyrexia * Jaundice * Tender hepatomegaly * Spleen may be palpable * ABSENCE of stigmata of chronic liver disease (although some spider naevi may appear transiently)

Answer 348

• Bloods o LFTs - high AST, ALT, ALP and bilirubin o High ESR o Low albumin + high platelets (if severe) • Vital Serology o Hepatitis A: • Anti-HAV IgM (during acute illness, disappears after 3-5 months) • Anti- HAV IgG (recovery phase and lifelong persistence) o Hepatitis E: • Anti-HEV IgM (raised 1-4 weeks after onset) • Anti-HEV IgG • Urinalysis o Positive for bilirubin o Raised urobilinogen

Answer 349

• There is no specific management other than bed rest and symptomatic treatment (e.g. antipyretics, antiemetics or cholestyramine (for severe pruritus)) • Prevention and Control o Public Health - safe water, sanitation and food hygiene o These are notifiable diseases o Immunisation is available for HAV • Passive immunisation with IM human immunoglobulin (effective for a short time) • Active immunisation with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas and high-risk individuals

Answer 350

* Fulminant hepatic failure (in a very small proportion of patients but is more common in pregnant women) * Cholestatic hepatitis with prolonged jaundice and pruritus can develop after HAV infection * Post-hepatitis syndrome: continued malaise for weeks to months

Answer 351

* Recovery is usually within 3-6 weeks * Occasionally patients may relapse during recovery * There is no chronic sequelae * Fulminant hepatic failure has a mortality of 80%

Answer 352

• Hepatitis caused by infection with hepatitis B virus (HBV), which may follow an acute or chronic course o Chronic is defined as viraemia and hepatic inflammation continuing for > 6 months • Hepatitis D virus (HDV) is a defective virus, that may only co-infect with HBV or superinfect people who are already carriers of HBV

Answer 353

• HBV is an enveloped, partially double-stranded DNA virus • Transmission: sexual contact, blood and vertical transmission (from mother to baby) • Various viral proteins are produced such as: o Core antigen (HBcAg) o Surface antigen (HBsAg) o e antigen (HBeAg) • This is a marker of high infectivity • HDV is a single-stranded RNA virus coated with HBsAg • Antibody and cell-mediated immune response to viral replication leads to liver inflammation and hepatocyte necrosis • Histology can show mild to severe inflammation and changes to cirrhosis • Risk Factors o IV drug use o Unscreened blood and blood products o Infants of HBeAg-positive mothers o Sexual contact with HBV carriers o Younger individuals (particularly babies) are more likely to become chronic carriers o Genetic factors are associated with varying rates of viral clearance

Answer 354

* Common * 1-2 million deaths annually * Common in Southeast Asia, Africa and Mediterranean countries * HDV is also found worldwide

Answer 355

``` • Incubation period: 3-6 months • 1-2 week prodrome consisting of: o Malaise o Headache o Anorexia o Nausea and vomiting o Diarrhoea o RUQ pain o Serum-sickness type illness (e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash) • Jaundice develops with dark urine • Recovery: 4-8 weeks • 1% develop fulminant liver failure • Chronic carriage may be diagnosed after routine LFT testing or if cirrhosis or decompensation develops ```

Answer 356

• Acute o Jaundice o Pyrexia o Tender hepatomegaly o Splenomegaly o Cervical lymphadneopathy (in 10-20% of patients) o Occasionally: urticaria and maculopapular rash • Chronic o May be no findings o May have signs of chronic liver disease or decompensation

Answer 357

``` • Viral Serology o Acute HBV: • HBsAg positive • IgM anti-HBcAg o Chronic HBV: • HBsAg positive • IgG anti-HBcAg • HBeAg positive or negative o HBV Cleared or Vaccinated against HBV: • Anti-HBsAg antibody positive • IgG anti-HBcAg o HDV infection: • Detected by IgM or IgG against HDV • PCR is used for detection of HDV • LFTs o High: AST, ALT, ALP, bilirubin • Clotting o High PT (in severe disease) • Liver Biopsy ```

Answer 358

• Prevention: blood screening, safe sex, instrument sterilisation • Passive immunisation o Hepatitis B immunoglobulin following acute exposure and to neonates born to HBeAg-positive mothers (in addition to active immunisation) • Active immunisation o Recombinant HBsAg vaccine for individuals at risk and neonates born to HB • Acute HBV Hepatitis o Symptomatic treatment (antipyretics, antiemetics and cholestyramine) and bed rest o Notifiable disease • Chronic HBV o Interferon alpha (standard or pegylated) • Side-effects: flu-like symptoms such as fever, chills, myalgia, headaches, bone marrow suppression and depression o Nucleoside/nucleotide analogues (adefovir, entecavir, telbivudine, tenofovir)

Answer 359

* 1% get fulminant hepatic failure * Chronic HBV infection (10% of adults, much higher in neonates) * Cirrhosis * HCC * Extrahepatic immune complex disorders (e.g. glomerulonephritis, polyarteritis nodosa) * Superinfection with HDV may lead to acute liver failure or more rapidly progressive disease

Answer 360

* Adults: 10% of infections become chronic | * Of the chronic infections, 20-30% will develop cirrhosis

Answer 361

• Hepatitis caused by infection with hepatitis C virus (HCV), often following a chronic course (in 80% of cases)

Answer 362

• HCV is a small, enveloped, single-stranded RNA virus • RNA viruses have poor fidelity of replication and mutation rates are high • So, there are lots of HCV genotypes (which can co-exist in a single patient) • Transmission: PARENTERAL o Sexual transmission o Vertical transmission • At risk patients: o Recipients of blood and blood products o IV drug users o Non-sterile acupuncture o Tattooing o Haemodialysis o Health care workers • Pathology/Pathogenesis of HCV o The virus is not thought to be directly hepatotoxic o It is the humoral and cell-mediated responses to the viral infection that leads to hepatic inflammation and necrosis o Liver biopsy shows: • Chronic hepatitis • Lymphoid follicles in portal tracts • Fatty change • Cirrhosis may be present

Answer 363

* COMMON | * Different genotypes of HCV have different geographical prevalence

Answer 364

* 90% of acute infections are ASYMPTOMATIC * 10% become jaundiced with mild flu-like illness * May be diagnosed after incidental abnormal LFT

Answer 365

• May be NO SIGNS • There may be signs of chronic liver disease (if long-standing HCV infection) • Extra-hepatic manifestations (rare) include: o Skin rash o Renal dysfunction (due to glomerulonephritis)

Answer 366

• Bloods o HCV Serology • Anti-HCV antibodies - IgM (acute) or IgG (past exposure or chronic) o Reverse-transcriptase PCR • Allows detection and genotyping of HCV o LFT • Acute infection: High ALT, AST and bilirubin • Chronic infection: 2-8 x elevation of AST + ALT (often fluctuates over time) • Liver Biopsy o Assess the degree of inflammation and liver damage o NOTE: transaminase (AST and ALT) levels bear little correlation to histological changes o Useful for diagnosing cirrhosis

Answer 367

• Prevention o Screen blood, blood products and organ donors o Needle exchange schemes for IV drug users o Instrument sterilisation o NO VACCINE AVAILABLE • Medical o Acute - mainly supportive (antipyretics, antiemetics, cholestyramine) o Chronic • Pegylated interferon- • Ribavirin (guanosine nucleotide analogue) • Duration:  HCV Genotype 1 or 4: 24-48 weeks  HCV Genotype 2 or 3: 12-24 weeks o Regular US of the liver may be needed if the patient has cirrhosis

Answer 368

* Fulminant hepatic failure * Chronic carriage of HCV * Hepatocellular carcinoma * Less common: porphyria cutanea tarda, cryoglobulinaemia, glomerulonephritis

Answer 369

* 80% of exposed will progress to chronic carriage | * Of these, 20-30% will develop cirrhosis over 10-20 years

Answer 370

• Rotation of a loop of small bowel around the axis of its mesentery that results in bowel obstruction and potential ischaemia. • The areas usually affected: o Sigmoid colon - 65% o Caecum - 30% o Volvulus Neonatorum - occurs in neonates and typically affects the midgut

Answer 371

``` • Anatomical factors (e.g. long mesentery) • Risk Factors o Adults • Long sigmoid colon • Long mesentery • Mobile caecum • Chronic constipation • Adhesions • Chagas disease • Parasitic infections o Neonatal • Malrotation ```

Answer 372

* Severe colicky abdominal pain and swelling * Absolute constipation * Vomiting * There may be a history of transient attacks in which spontaneous reduction of the volvulus has occurred * Neonatal volvulus presents around 3 months

Answer 373

* Signs of bowel obstruction with abdominal distension and tenderness * Absent or tinkling bowel sounds * Fever * Tachycardia * Signs of dehydration

Answer 374

``` • AXR • Erect CXR - if perforation is suspected • Water-soluble contrast enema o Shows site of obstruction • CT Scan ```

Answer 375

• An autosomal recessive disorder characterised by reduced biliary excretion of copper and accumulation of copper in the liver and brain, especially in the basal ganglia. Also known as hepatolenticular degeneration.

Answer 376

* Mutation in a gene on chromosome 13 that codes for copper transporting ATPase (ATP7B) in hepatocytes * This interferes with the transport of copper into the intracellular compartments for incorporation into caeruloplasmin (copper containing complex) * Caeruloplasmin is normally secreted into plasma or excreted in bile * Excess copper damages the hepatocyte mitochondria, leading to cell death and release of free copper into the plasma * This free copper then gets deposited in tissues and impairs tissue function

Answer 377

* Liver disease may present in children | * Neurological disease usually presents in young adults

Answer 378

``` • Liver o May present with: hepatitis, liver failure, cirrhosis o Symptoms: • Jaundice • Easy bruising • Variceal bleeding • Encephalopathy • Neurological o Dyskinesia o Rigidity o Tremor o Dystonia o Dysarthria o Dysphagia o Drooling o Dementia o Ataxia • Psychiatric o Conduct disorder o Personality change o Psychosis ```

Answer 379

``` • Liver o Hepatosplenomegaly o Jaundice o Ascites/oedema o Gynaecomastia • Eyes o Kayser-Fleischer Rings ``` o Sunflower cataract (copper accumulation in the lens, seen with a slit lamp)

Answer 380

• Bloods o LFTs: high AST, ALT, ALP o Low serum caeruloplasmin • NOTE: caeruloplasmin is an acute phase protein so may give false-negatives if there is an underlying infectious/inflammatory process o Serum copper • 24 hour urinary copper levels - increased in Wilson's disease • Liver biopsy - increased copper content • Genetic analysis - Wilson's is caused by a wide variety of gene mutations so there isn't a simple genetic test that can be done