Gastrointestinal

Question 1

What is achalasia?

Answer 1

An oesophageal motility disorder, characterised by loss of peristalsis and failure of relaxation of the lower oesophageal sphincter (LOS)

Question 2

What is the aetiology of achalasia?

Answer 2

• Degeneration of ganglion cells of the meyenteric plexus in the oesophagus due to an unknown cause.
• Oesophageal infection with Trypanosoma cruzi seen in Central and South America producers a similar disorder- Chaga’s disease

Question 3

What is the epidemiology of achalasia?

Answer 3

Usual presentation age: 25-60 years

Question 4

What are the presenting symptoms of achalasia?

Answer 4

Insidious onset and gradual progression of

• Intermittent dysphagia involving solids and liquids
• Difficulty belching
• Regurgitation (particularly at night)
• Heartburn
• Chest pain (atypical/cramping, retrosternal)
• Weight loss

Question 5

What are the signs of achalasia on examination?

Answer 5

May reveal signs of complications

Question 6

What are the investigations of achalasia?

Answer 6

• CXR: may show widened mediastinum and double right border (dilated oesophagus), an air-fluid level in upper chest and absence of the normal gastric air bubble
• Barium swallow: Dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)
• Endoscopy: To exclude malignancy which can mimic achalasia
• Manometry: Elevated resting LOS pressure (over 45mmHg), Incomplete LOS relaxation, Absence of peristalsis in the distal (smooth muscle portion) of the oesophagus

Question 7

What is acute cholangitis?

Answer 7

Ascending cholangitis

• Infection of the biliary tree, most commonly caused by obstruction.
• In its less severe form, there is biliary obstruction with inflammation and bacterial seeding and growth int he biliary tree

Question 8

What is the aetiology of acute cholangitis?

Answer 8

• Most common aetiology is cholelithiasis leading to choledocholithiasis and biliary obstruction.
• Iatrogenic biliary tract injury, most commonly caused via surgical injury cholecystectomy, can lead to benign strictures, which in turn can lead to obstructions
• Acute prancreatitis
• Malignant strictures

Question 9

What is the epidemiology of acute cholangitis?

Answer 9

• Relatively uncommon
• Male to female ratio is equal
• Median age of presentation is 50-60

Question 10

What are the presenting symptoms of acute cholangitis?

Answer 10

• Jaundice
• Fever
• Right upper quadrant pain
• Right upper quadrant tenderness

Question 11

What are the signs of acute cholangitis on examination?

Answer 11

• Alcoholic stools
• Pruritis
• Hypotension
• Mental status changes

Question 12

What are the investigations for acute cholangitis?

Answer 12

• FBC: Raised WBC, decreases platelets
• Serum urea: Raised in severe cases
• Serum creatinine: Raised in severe cases
• ABG: Metabolic acidosis
• LFT: Hyperbilinuraemia
• CRP: Raised
• Serum K & Mg: May be decreased
• Blood cultures: Bacteria usually gram negative, but gram positive bacteria and anaerobes are also implicated in cholangitis

Question 13

How is acute cholangitis managed?

Answer 13

• IV antibiotics (Piperacillin/Tazobactam
• Biliary decompression
• Opioid analgesics
• Lithotripsy

Question 14

What are the possible complications of acute cholangitis?

Answer 14

• Acute prancreatitis
• Inadequate biliary drainage following performance of endoscopy, radiology or surgery
• Hepatic abscess

Question 15

What is the prognosis of acute cholangitis?

Answer 15

• If adequate biliary drainage is quickly obtained, most patients experience rapid clinical improvement
• Outcome worse for patient’s with underlying medical conditions

Question 16

What is alcoholic hepatitis?

Answer 16

Inflammatory liver injury caused by chronic heavy intake of alcohol

Question 17

What is the aetiology alcoholic hepatitis?

Answer 17

One of the three forms of liver disease caused by excessive intake of alcohol, a spectrum that ranges from alcoholic fatty liver (steatisus) to alcoholic hepatitis and chronic cirrhosis
- In alcoholic hepatitis, the liver histopathology shows centrilobar ballooning degeneration and necrosis of hepatocytes, steatosis, neutrophilic inflammation, cholestasis, Mallory hyaline inclusions and giant mitochondria

Question 18

What is the epidemiology of alcoholic hepatitis?

Answer 18

10-35% of heavy drinkers develop this form of liver disease

Question 19

What are the presenting symptoms of alcoholic liver disease?

Answer 19

• May remain asymptomatic and undetected unless they present for other reasons
• Mild illness with nausea, malaise, epigastric or right hypochondrial pain
• Low grade fever

Question 20

What are the signs of acute hepatitis on examination?

Answer 20

• Signs of alcohol excess: Malnourishes, palmar erythema, Dupuytren’s contracture, facial telangiectasia, parotid enlargement, spider naevi, gynaecomastia, testicular atrophy, hepatomegaly, easy bruising
• Signs of severe alcoholic hepatitis: Febrile (50% pts), tachycardia, jaundice, bruising, encephalopathy, ascites, hepatomegaly, splenomegaly

Question 21

What are the investigations for alcoholic hepatitis?

Answer 21

• Blood: Decreased Hb, Increased MCV, Increased WCC, Decreased platelets. U&E: Urea and K low unless significant renal impairment. Clotting: Prolonged PT sensitive marker of sig. liver damage
• Ultrasound: For other causes of liver impairment (e.g. malignancies
• Upper GI endoscopy: Investigate for varices
• Liver biopsy: Percutaneous or transjugular may be helpful to distinguish from other causes of hepatitis
• Electroencephalogram: For slow wave activity indicative of encephalopathy

Question 22

How is alcoholic hepatitis managed?

Answer 22

• Acute: Thiamine, Vitamin C and other multivitamins. Monitor and correct K, MG and glucose abnormalities. Ensure adequate glucose output. Treat encephalopathy with oral lactose and phosphate enemas. Ascites manages by diuretics
• Nutrition: Oral and or nasogastric feeding important with increased caloric intake. Protein restricted to be avoided unless patient is encephalopathic. Nutritional supplementation and vitamins started parenterally and continues orally after
• Steroid therapy

Question 23

What are the possible complications of alcoholic hepatitis?

Answer 23

• Acute liver decompensation
• Hepatorenal syndrome (renal failure secondary to advanced liver disease
• Cirrhosis

Question 24

What is the prognosis of alcoholic hepatitis?

Answer 24

Morality in first months is 10%; 40% in first year

• If alcoholic intake continues, most progress to cirrhosis within 1-3 years
• Maddrey’s discriminant function. If less than 32, indicates more than 50% 30-day mortality
• Glasgow alcoholic score

Question 25

What is an anal fissure?

Answer 25

Split in the skin of the distal anal canal characterised by pain on defecation and rectal bleeding

Question 26

What is the aetiology of anal fissures?

Answer 26

- Passage of hard stool bolus may precipitate an anal fissure - Fissure may begin during episode of loose stool, or often occurs spontaneously with no obvious precipitating factor - Opiate analgesia is associated with constipation and a subsequence increased incidence of anal fissure - Hard stool tears the anal skin at pectin (at dentate line) - Pregnancy is risk factor

Question 27

What is the epidemiology of anal fissures?

Answer 27

- Equally common in men and women - Often affects young adults ages 15-40, but may be seen in older adults - May be seen in younger adults due to poor toileting

Question 28

What are the presenting symptoms of anal fissures?

Answer 28

- Pain on defecation - Tearing sensation on passing stool - Fresh blood on stool or on paper - Anal spasm

Question 29

What are the signs of anal fissures on examination?

Answer 29

- Sentinel pile | - Fissure visible on retraction of buttock

Question 30

What are the investigations for anal fissures?

Answer 30

- Clinical diagnosis - Anal manometry: Low resting pressure - Anal ultrasound: Defects in external or internal anal sphincter

Question 31

How are anal fissures managed?

Answer 31

- Conservative treatment alone: high fibre diet, adequate fluid intake, sitz baths and topical analgesia - Topical glyceryl trinitrate - Topical diltiazem Resistant fissures: - Botulinium toxin injection - Surgical sphincterotomy - Anal advancement flap

Question 32

What are the possible complications of anal fissures?

Answer 32

- Chronic anal fissure - Incontinence after surgery - Recurrence

Question 33

What is the prognosis of anal fissures?

Answer 33

- 60% achieve healing of fissure after 6-8 weeks - Some patients relapse - Some require surgery

Question 34

What is an appendicectomy?

Answer 34

Surgical removal of vermiform appendix | - Can be formed laparoscopically or as open operation

Question 35

What are the indications of appendicectomy?

Answer 35

- Appendicitis - Consider for patients with history of persistent abdominal pain, fever and clinical signs of localised or diffuse peritonitis especially if leucocytosis is present

Question 36

What are the possible complications of appendectomy?

Answer 36

- Bleeding - Wound infection - Infection, redness and swelling of belly can occur if appendix bursts during surgery (peritonitis) - Blocked bowels - Injury to nearby organs

Question 37

What is appendicitis?

Answer 37

- Acute inflammation of vermiform appendix, most likely due to obstruction of lumen of the appendix

Question 38

What is the aetiology of appendicitis?

Answer 38

- Obstruction is main cause | - Faecolith (hard mass of faecal matter), normal stool or lymphoid hyperplasia are main causes for osbtruction

Question 39

What is the epidemiology of appendicitis?

Answer 39

- One of the most acute abdominal surgical emergencies - Predominantly in 15-59 age group - Incidence lower in populations where high-fibre diet is consumed

Question 40

What are the presenting symptoms of appendicitis?

Answer 40

- Abdominal pain - Anorexia - Right lower quadrant tenderness - Nausea - Fever - Vomiting

Question 41

What are the signs of appendicitis on examination?

Answer 41

- Adolescence or early adulthood - Diminished bowel sounds - Rovsing's sign (Pressing left side of abdominal cavity and eliciting pain in lower right quadrant) - Psoas sign (Extending right thigh on left lateral position elicits pain in right lower quadrant) - Obturator sign (Pain elicited in RLQ of abdomen by internal rotation of the flexed right thigh)

Question 42

What are the investigations for appendicitis?

Answer 42

- FBC: Mild leukocytosis - Abdominal and pelvic CT scan: Abnormal appendix, more than 6mm diameter - Urinary pregnancy test: Negative

Question 43

How is appendicitis manage?

Answer 43

- Appendectomy and supportive care | - Intravenous antibiotic therapy: cefoxitin

Question 44

What are the possible complications of appendicitis?

Answer 44

- Perforation - Generalised peritonitis - Appendicular mass - Appendicular abscess - Surgical wound infection

Question 45

What is the prognosis of appendicitis?

Answer 45

- Good if patients treated in timely fashion | - Laparoscopic appendectomy shown to reduce incidence of overall complications

Question 46

What is autoimmune hepatitis?

Answer 46

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

Question 47

What is the aetiology of autoimmune hepatitis?

Answer 47

In genetically predisposed individual, environmental agent may lead to hepatocyte expression of HLA antigens which then become focus of principally T-cell mediated autoimmune attack

Question 48

What is the epidemiology of autoimmune hepatitis?

Answer 48

Type 1 occurs in all age groups (mainly in young women) | Type 2 generally a disease of girls and young women

Question 49

What are the presenting symptoms of autoimmune hepatitis?

Answer 49

May be asymptomatic discovered incidentally by abnormal LFT - Insidious onset: Malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis - Acute hepatitis (25%): Fever, anorexia, jaundice, nausea, vomiting, diarrhoea, RUQ pain. May also present with serum sickness (e.g. arthalgia, polyarthritis, maculopapular rash May be associated with keratoconjuctivitis sicca

Question 50

What are the signs of autoimmune hepatitis on examination?

Answer 50

- Stigmata of chronic liver disease e.g. spider naevi - Ascites, oedema and encephalopathy are late features - Cushingoid features e.g. rounded face, cutaneous striae, acne, hirsutism) may be present even before the administration of stoids

Question 51

What are the investigations for autoimmune hepatitis?

Answer 51

- Blood: Increased AST and ALT, Increased AlkPhos, Increase bilirubin, Decreased albumin, Increased PT, Decreased platelets and WCC from hypersplenism if portal hypertension present - Liver biopsy: Needed to establish the diagnosis, shows interface hepatitis or cirrhosis - Other: Rule out other causes of liver disease - Ultrasound, CT or MRI of liver and abdomen: Visualise structural lesions - ERCP: Rule out PSC

Question 52

How is autoimmune hepatitis managed?

Answer 52

Indications- aminotransferases raised, the upper limit of normal and symptomatic - Immunosuppression: with steroids e.g. prednisolone, followed by maintenance treatment with gradual reduction in dose. - Monitor: Ultrasound ever 6-12 months to detect hepatocellular carcinoma - Hep A and B vaccinations - Liver transplant: for pts with refractory to or intolerant of immunosuppressive therapy and those with end-stage disease

Question 53

What are the possible complications of autoimmune hepatitis?

Answer 53

- Fulminant hepatic failure - Cirrhosis and complications or portal hypertension (e.g. varices, ascites) - Hepatocellular carcinoma - Side-effects of corticosteroid treatment

Question 54

What is the prognosis of autoimmune hepatitis?

Answer 54

- Older patients with type 1 autoimmune hepatitis are more likely to have cirrhosis at presentation but may be more likely to respond to treatment - 80% receive remission by 3 years

Question 55

What is Barrett's oesophagus?

Answer 55

Change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia - Associated with gastro-oesophageal reflux even if reflux is asymptomatic

Question 56

What is the aetiology of Barrett's oesophagus?

Answer 56

- Main aetiology is gastro-oesophageal reflux | - Evidence that combined bile and acid reflux are primary causative agents

Question 57

What is the epidemiology of Barrett's oesophagus?

Answer 57

- More common in men and white people - Rare in children - More prevalent with age

Question 58

What are the presenting symptoms of Barrett's oesophagus?

Answer 58

- Heart burn - Regurgitation - Dysphagia - Chest pain - Cough - SOB/wheezing

Question 59

What are the signs of Barrett's oesophagus on examination?

Answer 59

- Laryngitis | - History of aspiration pneumonia

Question 60

What are the investigations for Barrett's oesophagus?

Answer 60

- Upper GI contrast radiography: hiatal hernia and reflux | - Upper GI endoscopy with biopsy: Abnormal epithelium characteristic of Barrett's oesophagus

Question 61

How is Barrett's oesophagus managed?

Answer 61

- Proton pump inhibitor plus surveillance - Radiofrequency ablation - Anti-reflux surgery plus surveillance - Radiofrequency ablation

Question 62

What are the possible complications of Barrett's oesophagus?

Answer 62

- Adenocarcinoma - Oesophageal stricture - Quality of life deficit

Question 63

What is the prognosis for Barrett's oesophagus?

Answer 63

- Adenocarcinomas discovered while screening for Barrett's oesophagus are early-stage lesions and have good prognosis

Question 64

What is biliary colic?

Answer 64

When pain occurs due to a gallstone temporarily blocking the bile duct Can last hours, associated with nausea and vomiting

Question 65

What are the risk factors of biliary colic?

Answer 65

- Previous episode of biliary pain (50% have another episode within a year) - Older age - Female sex - Obesity - Rapid weight loss - Drugs - Symptomatic stones, pregnancy, smoking

Question 66

What is the epidemiology of biliary colic?

Answer 66

- Sudden onset, severe RUQ pain - Constant in nature - Nausea and vomiting - May last hours - Radiates to back or right scapula and jaundice - Jaundice is common but can develop with choledocholelithiasis - Pain worse after fatty meal If fever present, suggests complication such as cholecystitis, cholangitis or pancreatitis

Question 67

What are the signs of biliary colic on examination?

Answer 67

- Right upper quadrant and epigastric tenderness

Question 68

What are the investigations for biliary colic?

Answer 68

- Abdominal ultrasound: For symptomatic patients - CT follow up if unremarkable - MRCP

Question 69

How is biliary colic managed?

Answer 69

- Analgesia - Rehydration - NBM - Elective laparoscopic cholestystectomy

Question 70

What are the possible complications of biliary colic?

Answer 70

- Cholangitis - Sepsis - Pancreatitis - Hepatitis - Choledocholithiasis - Gallbladder perforation

Question 71

What is the prognosis for biliary colic?

Answer 71

Uncomplicated biliary colic has low mortality

Question 72

What is cholecystectomy?

Answer 72

- Surgical removal of gallbladder - Common treatment of symptomatic gallstones and other gallbladder conditions - Can be laparoscopic or open

Question 73

What are the indications for a cholecystectomy?

Answer 73

- Calcified gallbladder - Acute cholecystitis - Choledocholithiasis - Gallstone pancreatitis - Biliary pain - Biliary dyskinesia

Question 74

What are the possible complications of cholecystectomy?

Answer 74

- Bile leek - Bleeding - Blood clots - Infection - Pancreatitis - Pneumonia - Post-cholecystectomy syndrome

Question 75

What is cholecystitis?

Answer 75

Acute gallbladder inflammation caused by an obstruction at the cystic duct

Question 76

What are the causes of cholecystitis?

Answer 76

Acute: Stone or sludge impaction in the neck of the gallbladder Chronic: Chronic inflammation and colic

Question 77

What is the epidemiology of cholecystitis?

Answer 77

8% of >40yrs. | 5 Fs: Fat, Forty, Female, Fertile, Fair

Question 78

What are the presenting symptoms of cholecystitis?

Answer 78

- Patient systemically unwell - Fever - Prolonged upper abdominal pain that may be referred to right shoulder (due to diaphragmatic irritation)

Question 79

What are the signs of cholecystitis on examination?

Answer 79

- Tachycardia - Pyrexia - Right upper quadrant or epigastric tenderness - They may be guarding. With or without rebound - Murphy's signs is elicited by placing a hand at the costal margin in the RUQ and asking patient to breathe deeply - Patient stops breathing as the inflamed gallbladder descends and contacts the palpating fingers

Question 80

What are the investigations for cholecystitis?

Answer 80

- Ultrasound: image stones and assess CBD diameter | - MRCP: to find CBD stones

Question 81

How is cholecystitis managed?

Answer 81

- Cholecystectomy | - If US shows dilated GB with stones → ERCP and sphincterotomy before surgery

Question 82

What are the possible complications of cholecystitis?

Answer 82

- Perforation - Suppurative cholecystitis - Gangrenous cholecystitis - Bile duct injury due to surgery - Gallstone ileus

Question 83

What is the prognosis for cholecystitis?

Answer 83

Removing the gallbladder and the contained gallstones when biliary pain starts will prevent further biliary attacks and reduce the risk of developing cholecystitis. If the gallbladder perforates, mortality is 30%. Untreated acute acalculous cholecystitis is life-threatening and is associated with up to 50% mortality.

Question 84

What is cirrhosis?

Answer 84

End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes. Decompensated when there are complications such as ascites, jaundice, encephalopathy or GI bleeding

Question 85

What is the aetiology of cirrhosis?

Answer 85

- Chronic alcohol misuse - Chronic viral hepatitis - Autoimmune hepatitis - Drugs: e.g. methotrexate, hepatotoxic drugs - Inherited: haemochromatosis, Wilson's disease, galactosaemia, cystic fibrosis, a1-Antitrypsin deficiency - Vascular: Budd-Chiari syndrome or hepatic venous congestion - Chronic biliary diseases: Primary biliary cirrhosis (PBC), primary sclerosing cholangitis, biliary atresia - Cryptogenic - Non-alcoholic steatohepatitis (NASH)

Question 86

What is the epidemiology of cirrhosis?

Answer 86

Among the top 10 leading cause of deaths worldwide

Question 87

What are the presenting symptoms of cirrhosis?

Answer 87

Early non-specific symptoms: Anorexia, nausea, fatigue, weakness, weight loss - Symptoms caused by decreased liver synthetic function: Easy bruising, abdominal swelling, ankle oedema - Reduced detoxification function: Jaundice, personality change, altered sleep pattern, amenorrhoea - Portal hypertension: Abdominal swelling, haematemesis, PR bleeding or melaena

Question 88

What are the signs of cirrhosis on examination?

Answer 88

Stigmata of chronic liver disease: ABCDE - Asterixis (liver flap) - Bruises - Clubbing - Dupuytren's contracture - Erythema (palmar) - Jaundice, gynaecomastia, leukonychia, parotid enlargement, spider naevi, stretch marks, ascites (shifting dullness and fluid thrill), enlarged liver, testicular atrophy, caput medusae, splenomegaly

Question 89

What are the investigations for cirrhosis?

Answer 89

- Blood: Decreased Hb and platelets. LFTs may be normal. Prolonged PT. Serum AFP Increased in chronic liver disease - Other: to determine cause - Ascitic tap: microscopy - Liver biopsy: Percutaneous or transjugular if clotting deranged or ascites present - Imaging: US, CT or MRI - Endoscopy: Examine for varices, - Child-Pugh grading

Question 90

How is cirrhosis managed?

Answer 90

Treat cause if possible, avoid alcohol, sedative, opiates, NSAIDs and drugs that affect the liver. Nutrition important if intake poor Treat complications Encephalopathy- Treat infections Ascites: Diuretics

Question 91

What are the possible complications of cirrhosis?

Answer 91

- Portal hypertension with ascites - Encephalopathy or variceal haemorrhage - SBP - Hepatocellular carcinoma - Renal failure (hepatorenal syndrome) - Pulmonary hypertension (hepatopulmonary syndrome)

Question 92

What is the prognosis of cirrhosis?

Answer 92

- Depends on the aetiology and complications - Generally poor: Overall 5 year survival is 50% - In presence of ascites, 2 year survival of 50%

Question 93

What is coeliac disease?

Answer 93

Inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption

Question 94

What is the aetiology of coeliac disease?

Answer 94

- Sensitivity to gliadin component of the cereal protein, triggers an immunological reaction int he small intestine, leading to mucosal damage and loss of villi - 10% risk of first-degree relatives being affected and there is clear genetic susceptibility associated with HLA-B8, DR3 and DQW2 haplotypes

Question 95

What is the epidemiology of coeliac disease?

Answer 95

UK Prevalence is 1 in 2000 | - Rare in East Asia

Question 96

What are the presenting symptoms of coeliac disease?

Answer 96

- May be asymptomatic - Abdominal discomfort: pain and distension - 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

Question 97

What are the signs of coeliac disease on examination?

Answer 97

- Signs of anaemia: pallor - Signs of malnutrition: Short stature, abdominal distension and wasted buttocks in children. Triceps skinfold thickness gives an indication of fat stores - Signs of vitamin or mineral deficiencies (e.g. osteomalacia, easy bruising) - Intense, itchy blisters on elbows, knees or buttock (dermatitis herpetiforms)

Question 98

What are the investigations for coeliac disease?

Answer 98

- Blood: Decreased Hb, iron and folate, albumin, phosphate - Serology: Testing for IgG anti-gliadin, IgA, and IgG anti-endomysial translutaminase antibodies can be diagnostic. IgA deficiency is common - Stool: Culture to exclude in infection - D-xylose test: Reduced urinary excretion after an oral xylose load indicates small bowel malabsorption - Endoscopy: Direct visualisation shows villous atrophy in small intestine, giving mucosa a flat smooth appearance. Biopsy shows villous atrophy with crypt hyperplasia of the duodenum. Epithelium adopts a cuboidal appearance, there is inflammatory infiltrate of lymphocytes and plasma cells in lamina propria

Question 99

How is coeliac disease managed?

Answer 99

- Advice: Withdrawal of gluten from the diet, with avoidance of all wheat, rye and barley products. Education and expert dietary advice is essential. The Coeliac Society offer patient support and advice - Medical: Vitamin and mineral supplements. Oral corticosteroids may be used if the disease does not subside with gluten withdrawal

Question 100

What are the possible complications of coeliac disease?

Answer 100

- Iron, folate and Vitamin B12 deficiency - Osteomalacia - Ulcerative jejunoiletis - Gastrointestinal lymphoma (particular T cell) - Bacterial overgrowth - Rarely can cause cerebellar ataxia

Question 101

What is the prognosis for coeliac disease?

Answer 101

- Strict adherence to gluten-free diet, most patients make a full recovery - Symptoms usually resolve within weeks - Histological changes may take longer to resolve - A gluten-free diet needs to followed for life

Question 102

What is a colonoscopy?

Answer 102

An endoscopic examination of the large bowel and the distal part of the small bowel with a CCD camera or a fiber optic camera on a flexible tube passed through the anus - Can provide visual diagnosis (polyps, ulceration) and grants opportunity for biopsy or removal of suspected colorectal cancer lesions

Question 103

What are the indications for a colonoscopy?

Answer 103

- Gastrointestinal haemorrhage - Unexplained changes in bowel habit - Suspicion of malignancies - Diagnose colon cancer and IBD

Question 104

What are the possible complications of a colonoscopy?

Answer 104

- Gastrointestinal perforation - Bleeding: by cauterisation via the instrument. Delayed bleeding at site of polyp removal up to weak after procedure - Splenic rupture - Dehydration caused by laxatives usually administered during bowel preparation

Question 105

What is Crohn's disease?

Answer 105

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

Question 106

What is the aetiology of Crohn's disease?

Answer 106

Cause has not yet been elucidated, but thought to involve an interplay between genetic and environmental factors - Inflammation can occur anywhere along GI tract (40% involving the terminal ileum) and 'skip' lesions with inflamed segments of bowel interspersed with normal segments is not unusual

Question 107

What is the epidemiology of Crohn's disease?

Answer 107

- Prevalence is 50-80 in 100,000 | - Affects any age but peak incidence is in teen or twenties

Question 108

What are the presenting symptoms of Crohn's disease?

Answer 108

- Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction) - Diarrhoea (may be blood or steatorrhoea) - Fever, malaise, weight loss - Symptoms of complications

Question 109

What are the signs of Crohn's disease on examination?

Answer 109

Weight loss, clubbing, signs of anaemia - Aphthous ulceration of the mouth - Perianal skin tags, fistulae and abscesses - Signs of complications (eye disease, joint disease, skin disease)

Question 110

What are the investigations for Crohn's disease?

Answer 110

- Blood: FBC (Decreased Hb, Raised platelets * WCC), U&E, LFT (low albumin), increased ESR, haematinics to look for deficiency states, ferritin, Vit B12 and red cell folate - Stool microscopy and culture: to exclude infective colitis - AXR: evidence of toxin megacolon - Erect CXR: If risk of perforation - Small bowel barium follow through: May reveal fibrosis/ strictures (string sign of Kantor), deep ulceration (rose thorn), cobblestone mucosa - Endoscopy and biopsy: May help differentiate between ulcerative colitis and Crohn's. - Radionuclide-labelled neutrophil scan

Question 111

How is acute exacerbation of Crohn's disease managed?

Answer 111

- Fluid resuscitation - IV or oral corticosteroids - 5-ASA analogues (e.g. mesalazine, sulfasalazine) may induce a remission in colonic Crohn's disease - Analgesia - Elemental diet may induce remission (more often used in children) - Parenteral nutrition may be necessary - Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin) - Assess for complications

Question 112

How is Crohn's disease managed in the long term?

Answer 112

- Steroids: For treating acute exacerbations - 5-ASA analogues (e.g. sulfasalazine, mesalazine) decreased relapses: useful for mild-moderate disease - Immunosuppression: Using steroid-sparing ages (e.g. azathioprine, 6-mercaptopurine, methotrexate) to reduce relapses - Anti-TNF agents (e.g. infliximab, adalimumab): Very effective agents in achieving and maintaining remission. Usually reserved for refractory cases

Question 113

What advice is given to patient's with Crohn's disease?

Answer 113

- Stop smoking - Dietician referral - Education and advice (e.g. from inflammatory bowel disease nurse specialists

Question 114

When is surgery for Crohn's disease indicated?

Answer 114

- When medical treatment fails - Failure to thrive in children or the presence of complications - Involves resection of affected bowel and stoma formation, although there is a risk of disease recurrence

Question 115

What are the possible GI complications of Crohn's disease?

Answer 115

- Haemorrhage - Bowel strictures - Perforation - Fistulae (between bowel, bladder, vagina) - Perianal fistulae and abscess - GI carcinoma (5% risk in 10 years) - Malabsorption

Question 116

What are the extraintestinal features of complications of Crohn's disease?

Answer 116

- Uveitis - Episcleritis - Gallstones - Kidney stones - Arthropathy - Sacroilitis - Ankylosing spondylitis - Erythema nodosum and pyoderma gangrenosum - Amyloidosis

Question 117

What is the prognosis of Crohn's disease?

Answer 117

- Chronic relapsing condition | - 2/3 will require will surgery at some stage and 2/3 of these have more than 1 surgical procedure

Question 118

What is diverticulosis?

Answer 118

Presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel

Question 119

What is diverticular disease?

Answer 119

Diverticulosis associated with complications e.g. haemorrhage, infection, fistulae

Question 120

What is diverticulitis?

Answer 120

Acute inflammation and infection of colonic diverticulae

Question 121

What is the aetiology of diverticular disease?

Answer 121

- Low fibre diet leads to loss of stool bulk - Consequently, high colonic intraluminal pressures must be generated to propel the stool, leading to herniation of the mucosa and submucosa through the muscularis

Question 122

What is the epidemiology of diverticular disease?

Answer 122

Common - 60% of people living in industrialised countries will develop colonic diverticula - Rare, under 40 years - Right sided diverticula are more common in Asia

Question 123

What are the presenting symptoms of diverticular disease?

Answer 123

- Often asymptomatic (80-90%) - PR bleeding - Diverticulitis: left iliac fossa or lower abdominal pain, fever - Diverticular fistulation into bladder: pneumaturia, faecaluria and recurrent UTI

Question 124

What are the signs of diverticular disease on examination?

Answer 124

Diverticulitis: - Tender abdomen - Signs of local or generalised peritonitis if perforation has occurred

Question 125

What are the investigations for diverticular disease?

Answer 125

- Blood: FBC, Raised WCC and CRP in diverticulitis, check clotting and cross match if bleeding - Barium enema: Demonstrates presence of diverticulae with a saw-toothed appearance of lumen, reflecting pseudohypertrophy of circular muscle - Flexible sigmoidoscopy and colonscopy: Diverticulae can be seen and other pathology can be excluded

Question 126

How is diverticular disease managed?

Answer 126

- Asymptomatic: Soluble high fibre diet. Probiotics and anti-inflammatories (mesalazine) - GI Bleed: PR bleeding managed with IV rehydration, antibiotics, blood transfusion if necessary. Angiography and surgery if severe - Diverticulitis: IV antibiotics and IV fluid rehydration and bowel rest. - Surgery: May be necessary with recurrent attacks or when complications develop e.g. perforation and peritonitis. Can be open (Hartmann's, one-stage resection) or laparoscopic

Question 127

What are the possible complications of diverticular disease?

Answer 127

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

Question 128

What is the prognosis for diverticular disease?

Answer 128

- 10-25% of patients will have one or more episodes of diverticulitis - Of these 30% will have a second episode

Question 129

Endoscopic retrograde cholangiopancreatography?

Answer 129

A technique that combines the use of endoscopy and fluoroscopy to diagnose and treat certain problems of the biliary or pancreatic ductal systems - Through the endoscopy, the physical can see the inside of the stomach and duodenum , and inject a contrast medium into the ducts in the biliary tree and pancreas so they can be seen on radiographs

Question 130

What are the indications for Endoscopic retrograde cholangiopancreatography?

Answer 130

- Obstructive jaundice - Gallstones with dilated bile ducts - Indeterminate biliary strictures and suspected bile duct tumours - Suspected injury to bile ducts either as a result of trauma or iatrogenic - Sphincter of Oddi dysfunction - Chronic pancreatitis

Question 131

What are the possible complications of Endoscopic retrograde cholangiopancreatography?

Answer 131

- Pancreatitis - Intestinal perforation - Risks associated with the contrast dye in patients who are allergic to compounds containing iodine - Oversedation can results in low BP, respiratory depression, nausea and vomiting - Cholangitis

Question 132

What is an endoscopy?

Answer 132

Refers to looking inside the body for medical reasons using an endoscope, an instrument used to examine the interior of a hollow organ or cavity of the body. Unlike most other medical imaging techniques, endoscopes are inserted directly into the organ.

Question 133

What are the indications for an endoscopy?

Answer 133

- Investigation of symptoms, such as symptoms in the digestive system including nausea, vomiting, abdominal pain, difficulty swallowing and gastrointestinal bleeding - Confirmation of diagnosis, most commonly by performing a biopsy to check for conditions such as anaemia, bleeding, inflammation and cancers of the digestive system - Giving treatment, such as cauterisation of a bleeding vessel, widening a narrow oesophagus

Question 134

What are the possible complications of an endoscopy?

Answer 134

- Infection - Over-sedation - Perforation - Tear of the stomach or oesophagus lining - Bleeding

Question 135

What is gastro-oesophageal reflux disease?

Answer 135

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

Question 136

What is the aetiology of gastro-oesophageal reflux disease?

Answer 136

- Disruption of mechanisms that prevent reflux (physiological LOS, mucosal rosette, acute angle of junction, intra-abdominal portion of oesophagus) - Prolonged oesophageal clearance contributes to 50% of cases

Question 137

What is the epidemiology of gastro-oesophageal reflux disease?

Answer 137

Common | Prevalence 5-10% adults

Question 138

What are the presenting symptoms of gastro-oesophageal reflux disease?

Answer 138

- Substernal burning discomfort or 'heartburn' aggravated by lying supine, blending or large meals and drinking alcohol - Pain relieved by antacids - Waterbrash - Regurgitation of gastric contents - Aspiration may results in voice hoarseness, laryngitis, nocturnal cough and wheeze & pneumonia - Dysphagia (caused by formation of peptic stricture after long-standing reflux)

Question 139

What are the signs of gastro-oesophageal reflux disease on examination?

Answer 139

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

Question 140

What are the investigations for gastro-oesophageal reflux disease?

Answer 140

- Upper GI endoscopy: Biopsy and cytological bushings: To confirm the presence of oesophagitis, exclude the possibility of malignancy (all patients over 45 years) - Barium swallow: To detect hiatus hernia, peptic stricture, extrinsic compression of oesophagus can be visualised - CXR: Not specifically for GORD. Incidental finding of hiatus hernia (gastric bubble behind cardiac shadow) - Twenty-four hour oesophageal pH monitoring: pH probe placed in lower oesophagus determined the temporal relationship between symptoms and oesophageal pH

Question 141

How is gastro-oesophageal reflux disease managed?

Answer 141

- Advice: Lifestyle changes, weight loss, elevating head of bed, avoid provoking factors, stopping smoking, lower fat meals, avoiding large meals late in the evening - Medical: Antacids and alginates, H2 antagonists (e.g. ranitidine) or proton pump inhibitors (e.g. Iansoprazole) are sufficient for most patients - Endoscopy: Annual endoscopic surveillance for Barrett's oesophagus, may be necessary for stricture dilation or stenting - Surgery: Antireflux surgery for those with symptoms despite optimal medical management or those intolerance of medication - Nissen fundoplication: (fundus of the stomach is wrapped around the lower oesophagus and held with sermuscular sutures) helps reduce any hiatus hernia and reduce hiatus

Question 142

What are the possible complications of gastro-oesophageal reflux disease?

Answer 142

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

Question 143

What is the prognosis of gastro-oesophageal reflux disease?

Answer 143

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

Question 144

What is gastroenteritis?

Answer 144

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

Question 145

What is the aetiology of gastroenteritis?

Answer 145

Can be caused by viruses, protozoa or toxins contained in contained in contaminated food or water - Viral: Rotavirus, adenovirus, astrovirus, calcivirus, Norwalk virus, small round structured viruses - Bacterial: Campylobacter jejuni, E coli, Salmonella, Shigella, V cholerae, Listeria, - Protozoal: E hystolycia, C parvum - Toxins: From S aureus, C bolutinum, C perfingens, mushrooms, heavy metals, seafood - Non inflammatory mechanisms: V cholerae - Inflammatory mechanisms: Shigella, E coli release cytotoxins and invade and damage the epithelium

Question 146

What is the epidemiology of gastroenteritis?

Answer 146

- Common - Often under-reported - Serious case of morbidity and mortality in the developing world

Question 147

What are the presenting symptoms of gastroenteritis?

Answer 147

- Sudden onset nausea - Vomiting - Anorexia - Diarrhoea (bloody or watery) - Abdominal pain or discomfort - Fever and malaise - Enquire about recent travel - Antibiotic use and recent food intake (how cooked, source and whether anyone ill)

Question 148

What are the signs of gastroenteritis on examination?

Answer 148

- Diffuse abdominal tenderness - Abdominal distension and bowel sounds are often increased- - If severe, pyrexia, dehydration, hypotension, peripheral shutdown

Question 149

What are the investigations for gastroenteritis?

Answer 149

- Blood: FBC, Blood culture (helps identification if bacteraemia present), U&E's (dehydration) - Stool: Faecal microscopy for polymorphs, parasites, oocytes, culture, electron microscopy (used to diagnose viral infections). Analysis for toxins, particularly for pseudomembranous colitis (C diff toxin) - AXR or ultrasound: To exclude other causes of abdominal pain - Sigmoidoscopy: Often unnecessary unless inflammatory bowel disease needs to be excluded

Question 150

How is gastroenteritis managed?

Answer 150

- Bed rest - Fluid and electrolyte replacement with oral rehydration solution (containing glucose and salt) - IV rehydration may be necessary in those with severe vomiting - Most infections are self limiting. Antibiotic treatment is only warranted if severe or the infective agent has been identified (e.g. ciprafloxacin against Salmonella, Shigella, Campylobacter - Botulism: Botulinum antitoxin IM and manage in ITU - Public health: Often a notifiable disease. Educate on basic hygiene and cooking.

Question 151

What are the possible complications of gastroenteritis?

Answer 151

- Dehydration - Electrolyte imbalance - Prerenal failure - Secondary lactose intolerance (particularly in infants) - Sepsis and shock (particularly Salmonella and Shigella) - Haemolytic uraemia syndrome is associated with toxins from E coli - Guillian-Barre syndrome may occur weeks after recovery from Campylobacter gastroenteritis - Botulism: Respiratory muscle weakness or paralysis

Question 152

What is the prognosis of gastroenteritis?

Answer 152

Generally good, as the majority of cases are self-limiting

Question 153

What is gastrointestinal perforation?

Answer 153

Hole in the wall of part of the gastrointestinal tract

Question 154

What is the aetiology of gastrointestinal perforation?

Answer 154

Underlying causes include: - Gastric ulcers - Duodenal ulcers - Appendicitis - Gastrointestinal cancer - Diverticulitis - Inflammatory bowel disease - Superior mesenteric artery syndrome - Trauma - NSAIDs - Typhoid

Question 155

What is the epidemiology of gastrointestinal perforation?

Answer 155

Children: blunt trauma Adults: Duodenal perforation more than gastric perforation

Question 156

What are the presenting symptoms of gastrointestinal perforation?

Answer 156

- History of penetrating issue - NSAID or aspirin use - Abdominal pain - Vomiting - Hiccuping - History of travel - Sharp severe sudden onset (perf peptic ulcer)

Question 157

What are the signs of gastrointestinal perforation on examination?

Answer 157

- External injury, abrasion, ecchymyosis | - Breathing pattern, distension, discolouration of abdomen

Question 158

What are the investigations for gastrointestinal perforation?

Answer 158

- Bloods: WCC, CRP, Cultures, Group & Save, Cross Match, Amylase to rule out pancreatitis, ABG, LFT - Urinalysis - USS: Localised gas collection, thickens bowel loop - CT: If no delay - Plain AXR: Rigler's sign, Visible falciform ligament RUQ -> umbilicus - CXR if peritonitic or over 50: gas under diaphragm

Question 159

How is gastrointestinal perforation managed?

Answer 159

Laparoscopy | Laparotomy

Question 160

What are the possible complications of gastrointestinal perforation?

Answer 160

- Bleeding - Sepsis - Bowel infarction

Question 161

What is the prognosis of gastrointestinal perforation?

Answer 161

Chances of recovery improve with early diagnosis and treatment

Question 162

What is a haemorrhoidectomy?

Answer 162

Surgical excision of the hemorrhoid used primarily only in severe cases. - Associated with significant post-operative pain - Excisional haemorrhoidectomy (Milligan Morgan) - scalpel, laser, electrocautery - Stapled haemorrhoidopexy (if prolapsed) - ?less pain, shorter stay

Question 163

What are the possible complications of a haemorrhoidectomy?

Answer 163

- Anal fistula or fissure - Constipation - Excessive bleeding - Excessive discharge - Inability to urinate or have bowel movement - Excessive discharge of fluid from the rectum

Question 164

What are the indications for a haemorrhoidectomy?

Answer 164

- Prolapse | - Haemorrhoids

Question 165

What are haemorrhoids?

Answer 165

- Haemorrhoidal cushions are normal anatomical structures located within the anal canal, usually occupying the left lateral and right anterior and posterior positions - As they enlarge, they can protrude outside the anal canal and cause symptoms

Question 166

What is the aetiology of haemorrhoids?

Answer 166

- Excessive straining due to either chronic constipation or diarrhoea - Repetitive or prolonged straining causes downward stress on the vascular haemorrhoidal cushions, leading to the disruption of the supporting tissue elements with subsequent elongation, dilation, and engorgement of the haemorrhoidal tissues.

Question 167

What is the epidemiology of haemorrhoids?

Answer 167

- More common in white patients than black patients | - Presentation peaking between ages 45-65

Question 168

What are the presenting symptoms of haemorrhoids?

Answer 168

- Perianal pain/discomfort - Constipation - Rectal bleeding

Question 169

What are the signs of haemorrhoids on examination?

Answer 169

- Anal pruritus - Tender palpable anal lesion - Anal mass - Ascites

Question 170

What are the investigations for haemorrhoids?

Answer 170

- Anoscopic examination: haemorrhoids - Colonoscopy: Usually normal, may reveal other pathologies - FBC: May demonstrate microcytic/hypochromic anaemia - Stool for occult haem: Positive

Question 171

How are haemorrhoids managed?

Answer 171

- Dietary & lifestyle modifications - Topical corticosteroids - rubber band ligation or sclerotherapy or infrared photocoagulation or haemorrhoid arterial ligation or stapled haemorrhoidopexy

Question 172

What are the possible complications of haemorrhoids?

Answer 172

- Anaemia from continuous/ excessive bleeding - Thrombosis - Incarceration - Faecal incontinence - Pelvic sepsis - Anal stenosis

Question 173

What is the prognosis of haemorrhoids?

Answer 173

- Prognosis following treatment is good

Question 174

What are inguinal hernias?

Answer 174

- Protrusion of a viscus through an abnormal opening - Above and medial to pubic tubercle Indirect: Protrusion through internal inguinal ring passes along inguinal canal through abdominal wall, Failure of inguinal canal to close properly after passage of the testes in utero or during neonatal period Direct: Protrudes directly through a weakness in the posterior wall of the inguinal canal, Occurs in Hesselbach's triangle

Question 175

What are the risk factors of inguinal hernias?

Answer 175

- Infants, prematurity, male - Adults: male, obesity, constipation, heavy lifting, chronic cough, ascites, urinary obstruction, past abdominal surgery

Question 176

What is the epidemiology of inguinal hernias?

Answer 176

- More common in men - Direct: elderly - Indirect: common in children

Question 177

What are the presenting symptoms of inguinal hernias?

Answer 177

- Swelling in the groin (may appear with lifting and associated with sudden pain) - Indirect hernias are more prone to cause pain (dragging sensation) - Congenital hernias occur at birth - In older children and adults they develop gradually and can occur with episode of heavy lifting causing rupture

Question 178

What are the signs of inguinal hernias on examination?

Answer 178

- Appears above and medial to pubic tubercle - Ask to cough, increase in swelling, palpable - Reduces on lying - Reduce hernia and occlude internal ring. IF restrained= indirect

Question 179

What are femoral hernias?

Answer 179

- Bowel enters the femoral canal, below the inguinal canal - Point down the leg (not towards groin like inguinal) - Inferior and lateral to pubic tubercle

Question 180

What are the risk factors of femoral hernias?

Answer 180

- Women | - Middle aged and elderly

Question 181

What are the presenting symptoms of femoral hernias?

Answer 181

- Lump in groin, inferior and lateral to pubic tubercle

Question 182

What are the signs of femoral hernias on examination?

Answer 182

- Appears or swells on coughing - Reduces when lying - Cough impulse - Lower abdominal pain if incarceration occurs - May be possible to reduce

Question 183

What is an amyand hernia?

Answer 183

Inguinal hernia which occurs when the appendix is included in the hernial sac and becomes incarcerated

Question 184

What is a pantaloon hernia?

Answer 184

Direct inguinal hernia | Sac straddles the inferior epigastric vessels

Question 185

What is a paraumbilical hernia?

Answer 185

- Herniation through linea alba - Occurs just below or above the umbilicus - Risk factors= obesity and diabetes - Omentum or bowel herniates through defect

Question 186

What is an umbilical hernia ?

Answer 186

Congenital: Opening in muscle that allows umbilical cord to pass fails to close Acquired: Increased intra-abdominal pressure- pregnancy, obesity, heavy lifting

Question 187

What is an epigastric hernia?

Answer 187

Through linea alba above umbilicus

Question 188

What is an incisional hernia?

Answer 188

- Caused by incompletely healed surgical wound | - Open repair not easy if obese

Question 189

What is a spigelian hernia?

Answer 189

Occurs through linea semilunaris at the lateral edge of the rectus sheath below and lateral to the umbilicus

Question 190

What is an Obturator hernia?

Answer 190

- Through obturator canal - Pain on medial side of thigh in thin women - Howship Romberg sign: pain along medial sign on abduction, extension, internal rotation

Question 191

What is a gluteal hernia?

Answer 191

Through gluteal foramen or greater sciatic foramen

Question 192

What is a lumbar hernia?

Answer 192

Through inferior or superior lumbar triangles in the posterior abdominal wall 1) Petit hernia: Inferior lumbar hernia 2) Grynfeltt hernia: Superior lumbar hernia

Question 193

What is Richter's hernia?

Answer 193

- Involve the bowel wall only, not the whole lumen | - Features of strangulation without obstruction

Question 194

What is Littre's hernia?

Answer 194

Hernial sacs containing a strangulated Meckel's diverticulum

Question 195

What is Maydl's hernia?

Answer 195

Involving a herniating double loop of bowel | - Strangulated portion may reside as a single loop inside abdominal cavity

Question 196

What is a sciatic hernia?

Answer 196

- Passes through lesser sciatic foramen | - GI obstruction and gluteal mass

Question 197

What is a sliding hernia?

Answer 197

- Contains a partially extraperitoneal structure (caecum on right, signmoid colon on left) - Sac does not completely surround the contents

Question 198

What is a gastroschisis hernia?

Answer 198

Herniation through abdominal wall with no sac

Question 199

What is a omphalocele hernia?

Answer 199

Herniation through abdominal wall with sac

Question 200

What are the investigations for inguinal hernias?

Answer 200

- Clinical diagnosis - Groin ultrasound scan - CT of groin - Herniography - MRI of groin

Question 201

How are inguinal hernias managed?

Answer 201

- Open repair - Open mesh repair - Laparoscopic inguinal herniorrhaphy or open preperitoneal repair with mesh placement

Question 202

What are the possible complications of inguinal hernias?

Answer 202

- Urinary retention post-operative - Scrotal haematoma - Wound infection - Seroma - Paraesthesias - Numbness in groin

Question 203

What is the prognosis for inguinal hernias?

Answer 203

- Excellent prognosis after repair

Question 204

What is a hiatus hernia?

Answer 204

Protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm - Commonly contains variable portion of the stomach - Herniated contents usually contained within sac of peritoneum

Question 205

What are the risk factors of hiatus hernias?

Answer 205

- Obesity - Previous gastro-oesophageal procedure - Male - Elevated intra-abdominal pressure - Advanced age

Question 206

What is the epidemiology of hiatus hernias?

Answer 206

- 50% in western populations | - Lower prevalence in eastern populations

Question 207

What are the presenting symptoms of hiatus hernias?

Answer 207

- Heartburn - Regurgitation - Chest pain - Dysphagia - Shortness of breath - Cough

Question 208

What are the signs of hiatus hernias on examination?

Answer 208

May be asymptomatic - Bowel sounds in chest - Weight loss

Question 209

What are the investigations for hiatus hernias?

Answer 209

- Barium swallow - CXR: Air fluid level above the left hemi-diaphragm - Upper GI endoscopy visualises the mucosa - OGD

Question 210

How are hiatus hernias managed?

Answer 210

- Lose weight - Treat reflex - Surgery:

Question 211

What are the possible complications of hiatus hernias?

Answer 211

- Bloating following surgery - Gastric volvulus - Obstruction - Dysphagia following surgery - GI bleeding

Question 212

What is the prognosis of hiatus hernias?

Answer 212

Most patients with an uncomplicated sliding hiatal hernia will have adequate relief of symptoms (but not cure) with medical therapy.

Question 213

What is infectious colitis?

Answer 213

Large bowel inflammation with mucosal destruction and inflammatory exudates forming pseudomembranes on the bowel wall (raised yellow and white plaques) associated with toxin releasing C.difficile

Question 214

What is the aetiology of infectious colitis?

Answer 214

- C d.ifficile, a gram positive anaerobic bacillus. Colonic overgrowth of toxin forming bacteria associated with disturbance of gut microflora brought about by Abx use. In rare cases, occurs without prior Abx use

Question 215

What is the epidemiology of infectious colitis?

Answer 215

- Commonly carried asymptomatically in 2% | - Common in hospitals where there is both increased carriage and antibiotics use

Question 216

How does infectious colitis present?

Answer 216

1) Asymptomatic carrier state 2) Mild self limited diarrhoea 3) Pseudomembranous colitis 4) Fulminant colitis

Question 217

What are the presenting symptoms of infectious colitis?

Answer 217

- Water diarrhoea, may become bloody (loose stools to severe diarrhoea) - Absence of diarrhoea = paralytic ileus, toxic megacolon - Abdominal cramps - Fever - Rigors, septicaemia

Question 218

What are the signs of infectious colitis on examination?

Answer 218

- High temperature - Abdominal tenderness - In severe cases, toxic megacolon or perforation - Colitis: yellow adherant plaques on inflamed non-ulcerated mucosa

Question 219

What are the investigations of infectious colitis on examination?

Answer 219

Blood: FBC (high WCC, high CRP, U+E's, lactate, blood culture (excludes other organisms - Cytotoxic tissue culture assay (diagnostic standard) - Stool (Demonstration of C diff toxin by ELISA - Sigmoidoscopy/colonoscopy

Question 220

What is intestinal ischaemia?

Answer 220

Inflammation of the colon due to decreased colonic blood supply - Ischaemia leads to mucosal inflammation, oedema, necrosis and inflammation

Question 221

What is the aetiology of intestinal ischaemia?

Answer 221

- Thrombosis/embolism: occlusion of large vessels - Iatrogenic litigation: AAA surgery - Hypovolaemia - Younger patients: small vessel vasculitis, vasospasm (cocaine), hypercoagulable states - No specific cause

Question 222

What are the presenting symptoms of intestinal ischaemia?

Answer 222

May be acute or chronic - Crampy abdominal pain - Post-prandial (gut claudication) giving food fear - Fever - Nausea - Bloody diarrhoea 'current jelly stool'

Question 223

What are the the signs of intestinal ischaemia on examination?

Answer 223

- Abdominal distension and tenderness - Local peritonism (worse on left) - Fever - Tachycardia (depends on severity) - Proctoscopy shows normal rectal mucosa with blood from higher source

Question 224

What is the epidemiology of intestinal ischaemia?

Answer 224

- Elderly (60-80 years) | - Equal gender distribution

Question 225

What are the investigations for intestinal ichaemia?

Answer 225

``` FBC chemistry panel arterial blood gas/lactate level ECG erect CXR abdominal x-rays sigmoidoscopy or colonoscopy ```

Question 226

What is intestinal obstruction?

Answer 226

Obstruction to free passage of contents of the gut Ileus: Reduced bowel motility causes functional obstruction (no pain and bowel sounds present) - Simple obstructed bowel: One obstructing point, no vascular compromise - Closed loop obstructed bowel: Obstruction at 2 points forming a loop of grossly distended bowel at risk of perforation - Strangulated obstructed bowel

Question 227

What is the aetiology of intestinal obstruction?

Answer 227

``` Small bowel: - Hernias and adhesions - Malignancy - Volvulus Large bowel: - Colon cancer - Constipation - Diverticular stricture - Volvulus Rare: - Crohn's stricture - Gallstone ileus ```

Question 228

What is the epidemiology of intestinal obstruction?

Answer 228

- Most are small bowel obstruction | - Many colorectal malignancies will present with obstruction

Question 229

What are the presenting symptoms of intestinal obstruction?

Answer 229

- Vomiting, nausea and anorexia - Colicky pain - Constipation: absolute if no flatus passed - Distension

Question 230

What are the signs of intestinal obstruction on examination?

Answer 230

- Severe tenderness suggesting ischaemia or perforation - Dehydration, poor peripheral perfusion, tachycardia, hypotension - Tinkling bowel sounds, absent bowel sounds in ileus - Distension - Visible peristalsis - Hernias may be present - Fever

Question 231

What are the investigations for intestinal obstruction?

Answer 231

- Erect CXR: for intestinal perforation - AXR Small bowel: central gas shadows, no gas in large bowel - AXR Large bowel: Gas shadows proximal to obstruction, not in rectum, large bowel haustra

Question 232

How is intestinal obstruction managed?

Answer 232

- Drip & Suck: NG tube and IV fluids | - Analgesia

Question 233

What are the possible complications of intestinal obstruction?

Answer 233

- Tissue death | - Infection

Question 234

What is the prognosis of intestinal obstruction?

Answer 234

- Proper diagnosis and early treatment, good outcome | - 15% of partial small bowel obstructions need surgery

Question 235

What is irritable bowel syndrome (IBS)?

Answer 235

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

Question 236

What is the aetiology of IBS?

Answer 236

Unknown - Visual sensory abnormalities, gut motility abnormalities, psychosocial factors (particularly stress) food intolerance (e.g. lactose) are all implicated

Question 237

What is the epidemiology of IBS?

Answer 237

- Common - Prevalence 10-20% of adults - More common in females (2:1 ratio to males)

Question 238

What are the presenting symptoms of IBS?

Answer 238

- More than six months of abdominal pain (often colicky, in the lower abdomen and relieved by defecation or flatus - Altered bowel frequency with more than 3 bowel motions daily or less than 2 weekly - Abdominal bloating - Change in stool consistency - Passage with urgency or straining. Tenesmus - Screen for 'red flag' alarm symptoms ( Weight loss, anaemia, PR bleeding, late onset 60 years)

Question 239

What are the signs of IBS on examination?

Answer 239

- Normally nothing on examination | - In some cases the abdomen ma appear distended and be mildly tender to palpation in one or both iliac fossa

Question 240

What are the investigations for IBS?

Answer 240

Diagnosis mainly from history but may be vital to exclude organic pathology - Blood: FBC (for anaemia), LFT, ESR, CRP, TFT - Stool examination: microscopy and culture for parasites - Ultrasound: To exclude gallstone disease - Hydrogen breath test: To exclude dyspepsia associated with Helicobacter pylori - Endoscopy: Upper GI endoscopy, sigmoidoscopy

Question 241

How is IBS managed?

Answer 241

- Advice: Explanation & support with establishment of a positive doctor-patients relationship. Dietary modification (e.g. reducing dietary insoluble fibre) may help with constipation, other approaches include exclusion diets and use of probiotics - Medical: According to predominant symptoms (Antispasmodics, Prokinetic agents, Antidiarrhoeals, Laxatives) - Psychosocial therapies

Question 242

What are the possible complications of IBS?

Answer 242

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

Question 243

What is the prognosis of IBS?

Answer 243

A chronic relapsing and remitting course, often exacerbated by psychosocial stresses

Question 244

What is laparoscopic abdominal surgery?

Answer 244

Surgical technique in which operations are performed far from their location through small incisions (usually 0.5-1.5cm) elsewhere in the body - Used to see and biopsy

Question 245

What are the indications of abdominal laparoscopic surgery?

Answer 245

- Varices - Malignancy - Ulcers - Dyspepsia - Appendicits - Ruptured AAA - Ruptured spleen - Bowel obstruction

Question 246

What are the possible complications of abdominal laparoscopic surgery?

Answer 246

- Trocar injuries - Abdominal wall hematoma - Umbilical hernia - Umbilical wound infection - Penetration of blood vessels or small or large bowel

Question 247

What are liver abscesses and cysts?

Answer 247

Liver infection resulting in a walled off collection of pus or cyst fluid

Question 248

What is the aetiology of liver abscesses and cysts?

Answer 248

- Pyogenic: E. coli, Klebsiella, enterococcus, bacteroides, streptococci, staphylococci - Amoebic: Entamoeba hystolytica - Hydatid cyst: Tapeworm Echnicoccus granulosis - Other: Tuberculosis

Question 249

What is the epidemiology of liver abscesses and cysts?

Answer 249

- Pyogenic: Incidence 0.8 in 100,000, mean age 60, most common liver abscess in industrialised world - Amoebic: Most common type worldwide - Hydatid disease: Common in sheep-rearing countries

Question 250

What are the presenting symptoms of liver abscesses and cysts?

Answer 250

- Fever, malaise, nausea, anorexia, night sweats, weight loss - RUQ pain or epigastric pain, which may be referred to shoulder (diaphragmatic irritation) - Jaundice, diarrhoea, pyrexia of unknown origin - Ask about foreign travel

Question 251

What are the signs of liver abscesses and cysts on examination?

Answer 251

- Fever (continuous or spiking), jaundice - Tender hepatomegaly, right lobe affected more commonly than left - Dullness to percussion and reduced breath sounds at right base of lung, caused by reactive pleural effusion

Question 252

What are the investigations for liver abscesses and cysts?

Answer 252

- Blood: FBC (mild anaemia, leukocytosis, raised eosinophils in hydatid disease, LFTs, raised ESR, raised CRP - Stool microscopy, cultures: For E. histolytica or tapeworm eggs - Liver ultrasound or CT/MRI: Localises structure or mass - CXR: Right pleural effusion or atelactasis, raises hemidiaphragm - Aspiration and culture of the abscess material

Question 253

What is liver failure?

Answer 253

Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy - Hyperacute liver failure: Jaundice with encephalopathy occurring in less than 7 days - Acute: Jaundice with encephalopathy occurring from 1 to 4 weeks of onset - Subacute: Jaundice with encephalopathy occurring within 4-12 weeks of onset - Acute-on-chronic: Acute deterioration (decompensation) in patients with chronic liver disease

Question 254

What is the aetiology of liver failure?

Answer 254

- Viral: Hepatitis A, B, D, E, 'non-A-E hepatitis' - Drugs: Paracetamol overdose, idiosyncratic drug reactions - Less common: Autoimmune hepatitis, Budd-Chiari syndrome, pregnancy-related, malignancy (e.g. lymphoma), hemochromatosis, mushroom poisoning, Wilson's disease

Question 255

What is the pathogenesis of the manifestations of liver failure?

Answer 255

- Jaundice: Reduced secretion of conjugated bilirubin - Encephalopathy: Increased delivery of gut-derived products into the systemic circulation and brain from reduced extraction of nitrogenous products by liver and portal systemic shunting. Ammonia may play a part - Coagulopathy: Reduced synthesis of clotting factors, reduced platelets (hypersplenism if chronic portal hypertension) or platelet functional abnormalities associated with jaundice or renal failure

Question 256

What is the epidemiology of liver failure?

Answer 256

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

Question 257

What are the presenting symptoms of liver failure?

Answer 257

- May be asymptomatic | - Fever, nausea and possibly jaundice

Question 258

What are the signs of liver failure on examination?

Answer 258

- Jaundice, encephalopathy, liver asterixis, fetor hepaticus - Ascites and splenomegaly - Bruising or bleeding from puncture sites or GI tracts - Look for secondary causes (e.g. bronze skin colour, Kayser-Fleischer rings) - Pyrexia may reflect infection or liver necrosis

Question 259

What are the investigations for liver failure?

Answer 259

- Identify the cause: Viral serology, paracetamol levels, autoantibodies (e.g. ASM, LKM antibody, immunoglobulins) ferritin, caeruloplasmin and urinary copper - Blood (in addition to above): FBC: Reduced Hb in GI bleed, Raised WCC if infection. U&E: renal failure. Glucose, LFT, group and save - Ultrasound liver, CT scan: image liver - Ascitic fluid: Tap ascites and send for microscopy, culture, biochemistry - Doppler screening of hepatic or portal veins: To exclude Budd-Chiari syndrome - Electroencephalogram: To monitor encephalopathy

Question 260

How is liver failure managed?

Answer 260

- Resuscitation: (According to airway, breathing, circulation): ITU care and specialist unit support essential - Treat the cause if possible: N-acetylcysteine for paracetamol overdose - Treatment/prevention of complications: Monitor, Manage encephalopathy, Antibiotic and antifungal prophylaxis, Hypoglycaemia treatment, Coagulopathy treatment, Gastric mucosa protection, Avoid sedatives or drugs metabolised by liver

Question 261

What are the possible complications of liver failure?

Answer 261

- Infection - Coagulopathy - Hypoglycaemia - Disturbances of electrolyte acid-base and cardiovascular system, hepatorenal syndrome, cerebral oedema, raised intracranial pressure, respiratory failure

Question 262

What is the prognosis of liver failure?

Answer 262

Depends on severity and aetiology of liver failure | - Traditional prognostic score for surgical mortality is the Child-Pugh score

Question 263

What is a Mallory-Weiss tear?

Answer 263

Characterised by a tear or laceration at or near the gastro-oesophageal junction Patients present with non-variceal upper-GI bleeding

Question 264

What is the aetiology of a Mallory-Weiss tear?

Answer 264

- Coughing, retching, vomiting, straining, hiccups, close-chested pressure or cardiopulmonary resuscitation, acute abdominal blunt trauma, primal scream therapy, alcohol, medications (aspirin, NSAIDs), chemotherapeutic agents and oesophageal instrumentation associated with MWT - Hiatus hernia present in 40-100% of MWT cases

Question 265

What is the epidemiology of Mallory-Weiss tears?

Answer 265

- MWT represents 3-15% of cases of upper GI bleeding - More common in me than in women, ratio of 3:1 - No racial predilection - Most common in people ages 30-50

Question 266

What are the presenting symptoms of a Mallory-Weiss tear?

Answer 266

- Haematemesis - Light-headedness/dizziness - Postural/orthostatic hypotension - Dysphagia

Question 267

What are the signs of a Mallory-Weiss tear on examination?

Answer 267

Notice blood in vomit

Question 268

What are the investigations for a Mallory-Weiss tear?

Answer 268

- FBC - Urea: high in patients with ongoing bleeding - Flexible OGD

Question 269

How is a Mallory-Weiss tear managed?

Answer 269

- Urgent evaluation plus monitoring - Endoscopy with or without intervention - Supportive treatment, angio and embolise if unstable

Question 270

What are the possible complications of a Mallory-Weiss tear?

Answer 270

- Vasopressin infusion-related abdominal pain - Re-bleeding - MI

Question 271

What is the prognosis for a Mallory-Weiss tear?

Answer 271

- Most cases bleeding is self-limiting, bleeding would have stopped in most patients at the time of endoscopy - Prognosis excellent in pts without associated disease or complications

Question 272

What is nasogastric tube insertion?

Answer 272

- Gastric intubation via the nasal passage | - Provides access to the stomach for diagnostic and therapeutic purposes

Question 273

What are the indications for nasogastric tube insertion?

Answer 273

- Evaluation of upper gastrointestinal GI bleeding - Aspiration of gastric fluid content - Identification of the oesophagus and stomach on a chest radiograph - Administration of radiographic contrast to the GI tract - Feeding - Bowel irrigation - Gastric decompression

Question 274

What are the possible complications of nasogastric tube insertion?

Answer 274

- Pneumothorax caused by tube entering lungs - Oesophagus perforation - Tube entering brain - Tracheobronchial trauma

Question 275

What is non-alcoholic steatohepatitis (NASH)?

Answer 275

Clinico-histopathological entity that includes that includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis in those who do not consume alcohol in amounts generally considered harmful to the liver - With NASH, there is inflammation and liver cell damage along with fat in liver

Question 276

What is the aetiology of non-alcoholic steatohepatitis?

Answer 276

- Medications - Surgical procedures - Total parenteral nutrition - Obesity

Question 277

What is the epidemiology of non-alcoholic steatohepatitis?

Answer 277

- 20-40% in Western world - Asian and Pacific regions less affected - 40-60 years majority

Question 278

What are the presenting symptoms of non-alcoholic steatohepatitis?

Answer 278

- Fatigue and malaise - Hepatosplenomegaly - Truncal obesity - Absence of significant alcohol use

Question 279

What are the signs of non-alcoholic steatohepatitis on examination?

Answer 279

- RUQ abdominal discomfort - Pruritis - Jaundice - Nail changes - Palmar erythema

Question 280

What are the investigations of non-alcoholic steatohepatitis?

Answer 280

- Serum AST and ALT: Elevated - Total bilirubin: elevated - Alkaline phosphatase: elevated - FBC: Anaemia or thromocytopenia - Serum albumin: Decreased

Question 281

How is non-alcoholic steatohepatitis managed?

Answer 281

- Diet and exercise - Weight loss pharmacotherapy - With diabetes: insulin sensitiser - With dyslipidaemia: lipid lowering therapy

Question 282

What are the possible complications of non-alcoholic steatohepatitis?

Answer 282

- Ascites - Variceal haemorrhage - Portosysemic encephalopathy - Hepatorenal syndrome

Question 283

What is the prognosis for non-alcoholic steatohepatitis?

Answer 283

- NASH associated with increased overall mortality, result of CVD and lesser extent liver-related causes - Progress to cirrhosis 9-20 % of time

Question 284

What is acute pancreatitis?

Answer 284

Acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems

Question 285

What is the aetiology of acute pancreatitis?

Answer 285

Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation Most common: Gallstones, alcohol (80% of cases)

Question 286

What is the epidemiology of acute pancreatitis?

Answer 286

- Common - Peak age is 60 yrs - Alcohol induced in more common in males while in females, principle cause is gallstones

Question 287

What are the presenting symptoms of acute pancreatitis?

Answer 287

- Severe epigastric or abdominal pain (radiating to back, relieved by sitting forward, aggravated by movement) - Associated with anorexia, nausea and vomiting - May be history of gallstones or alcohol intake

Question 288

What are the signs of acute pancreatitis on examination?

Answer 288

- Epigastric tenderness, fever - Shock, tachycardia, tachypnoea - Reduced bowel sounds (due to ileus) - If severe and haemorrhagic, Turner's sign (flank bruising) or Cullen's sign (periumbilical bruising)

Question 289

What are the investigations for acute pancreatitis?

Answer 289

- Blood: Increased Amylase, FBC (Increased WCC), U&E's, Raised glucose, CRP, Decreased Ca - USS: for gallstones or biliary dilatation - Erect CXR: May be pleural effusion, mainly for excluding other causes - AXR: To exclude other causes of acute abdomen. Psoas shadow may be lost - CT

Question 290

How is acute pancreatitis managed?

Answer 290

- Medical: Fluid and electrolyte resuscitation, urinary catheter and NG tube if vomiting. Analgesia and blood sugar control - ERCP and sphincterotomy - Surgiccal: patient with necrotizing pancreatitis should be managed in a specialist unit

Question 291

What are the possible complications of acute pancreatitis?

Answer 291

- Local: pancreatic necrosis, pseudocyst, abscess, ascites, pseudoaneurysm or venous thrombosis - Systemic: Multiorgan dysfunction, sepsis, renal failure, ARDS< DIC, hypocalcemia, diabetes - Long term: Chronic pancreatitis

Question 292

What is the prognosis of acute pancreatitis?

Answer 292

- 20% follow severe fulminating course with high mortality (infected pancreatic necrosis associated with 70% mortality)

Question 293

What is chronic pancreatitis?

Answer 293

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

Question 294

What is the aetiology of chronic pancreatitis?

Answer 294

Alcohol (70%), Idiopathic in 20% Rare: Recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism, hypertiglycidaemia

Question 295

What is the epidemiology of chronic pancreatitis?

Answer 295

Mean age- 40-50 years in alcohol-associated disease | 1/100000, Annual UK incidence

Question 296

What are the presenting symptoms of chronic pancreatitis?

Answer 296

- Recurrent severe epigastric pain, radiating to back, relieved by sitting forward, can be exacerbated by eating or drinking alcohol - Over many years, weight loss, bloating and pale offensive stools (steatorrhoea)

Question 297

What are the signs of chronic pancreatitis on examination?

Answer 297

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

Question 298

What is the pathogenesis of chronic pancreatitis?

Answer 298

- Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atropy, ductal dilatation, cyst and stone formation - Pancreatic stellate cells are thought to play a role, converting from quiescent fat storing cells to myofibroblast-like cells forming extracellular matric, cytokines and growth factors in response to injury - Pain is associated with raised intraductal pressures and inflammation

Question 299

What are the investigations for chronic pancreatitis?

Answer 299

- Blood: Glucose (increase indicates endocrine dysfunction, glucose tolerance test. Raised immunoglobulins, especially IgG4 in autoimmune pancreatitis - USS: percutaneous or endoscopic, can show hyperechoic foci with post-acoustic shadowing - ERCP or MRCP: Early changes include main duct dilatation and stumping of branches. Late manifestations are duct strictures with alternating dilatation - AXR: Pancreatic calcification may be visible - CT: Pancreatic cysts, calcification - Tests of pancreatic exocrine function: Faecal elastase

Question 300

How is chronic pancreatitis managed?

Answer 300

- General: Mainly symptomatic and supportive tx, e.g. dietary, abstinence from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacements - Endoscopic therapy: Sphincterotomy, stone extraction, dilatation or stenting of strictures - Surgical: May be indicated if medical management has failed. Later pancreaticojejunal drainage, resection or limited resection of the pancreatic head

Question 301

What are the possible complications of chronic pancreatitis?

Answer 301

- Psuedocytsts - Biliary duct stricture - Duodenal obstruction - Pancreatic ascites - Pancreatic carcinoma

Question 302

What is peptic ulcer disease?

Answer 302

Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin - Most commonly gastric and duodenal (can also occur in oesophagus and Meckel's diverticulum)

Question 303

What is the aetiology of peptic ulcer disease?

Answer 303

Cause is an imbalance between damaging action of acid an pepsin and mucosal protective mechanisms. Strong correlation with Helicobacter pylori infection, but it is unclear how to organism causes formation of ulcers Rare: Zollinger-Ellison syndrome

Question 304

What is the epidemiology of peptic ulcer disease?

Answer 304

- Common - More common in males - Duodenal ulcers have mean age in thirties, gastric ulcers mean age in fifties

Question 305

What are the presenting symptoms of peptic ulcer disease?

Answer 305

- Epigastric abdominal pain, relieved by antacids - Symptoms have a variable relationship to food - If worse soon after eating, most likely to be gastric ulcer - If worse several hours later, more likely to be duodenal - May present with complications (e.g. haematemesis, melaena)

Question 306

What are the signs of peptic ulcer disease on examination?

Answer 306

- May be no physical findings - Epigastric tenderness - Signs of complications (e.g. anaemia, succession splash in pyloric stenosis)

Question 307

What are the investigations for peptic ulcer disease?

Answer 307

- Blood: FBC (for anaemia, amylase (to exclude pancreatitis). U&E's, clotting screen , LF T - Endoscopy: Four quadrant gastric ulcer biopsies to rule out malignancy - Rockall scoring: for severity after a GI bleed, less than 3 carries good prognosis - Testing for H pylori - Histology of biopsies

Question 308

What is peptic ulcer disease managed?

Answer 308

- Acute: Resuscitation if perforated or bleeding, close monitoring of vital signs and proceeding endoscopic or surgical treatment - Endoscopy: Haemostasis by injection sclerotherapy, laser or electrocoagulation - Surgery: If perforated or ulcer-related bleeding cannot be controlled

Question 309

What are the possible complications of peptic ulcer disease?

Answer 309

- Rate of major complication is 1% per year including haemorrhage (haematemesis, melaena, iron deficiency anaemia), perforation, obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)

Question 310

What is the prognosis of peptic ulcer disease?

Answer 310

- Overall lifetime risk | - Generally good as peptic ulcers associated with H pylori can be cured by eradication

Question 311

What is gastritis?

Answer 311

Histological presence of gastric mucosal inflammation | - Broader term gastropathy encompasses lesions characterised by minimal or no inflammation

Question 312

What is the aetiology of gastritis?

Answer 312

- Acute non-erosive gastritis commonly due to H pylori infection

Question 313

What is the epidemiology of gastritis?

Answer 313

Prevalence of H pylori infection higher in developing countries and is impacted by multitude of factors, including geography, age, strain, virulence, environmental factors and socio-economic status

Question 314

What are the presenting symptoms of gastritis?

Answer 314

- Dyspepsia/epigastric discomfort - No suspicious features of malignancy - Nausea, vomiting and loss of appetite

Question 315

What are the signs of gastritis on examination?

Answer 315

- Acute abdominal pain - Glossitis - Cognitive impairment

Question 316

What are the investigations for gastritis?

Answer 316

- H pylori urea breath teat - H pylori faecal antigen test - FBC: May be reduced Hb and Hct and increased MCV in autoimmune gastritis. Leukocytosis with left shift in phlegmonous gastritis

Question 317

How is gastritis managed?

Answer 317

- H pylori eradication therapy | - Cyanocobalamin (autoimmune)

Question 318

What are the possible complications of gastritis?

Answer 318

- Achlorhydria - Vit B12 deficiency - Peptic ulcer disease - Gastric carcinoma

Question 319

What is the prognosis of gastritis?

Answer 319

Dependent on underlying aetiology and type | - With H pylori, good prognosis

Question 320

What is a perineal fistula?

Answer 320

A type of anorectal malformation that involves a misplaces anal passage that is often narrowed

Question 321

What is a perineal abscess?

Answer 321

Collection of pus outside the anus

Question 322

What is the aetiology of aperineal abscess?

Answer 322

Bacteria enters through a tear in the lining of anus or rectum Most often occurs between internal and external sphincters

Question 323

What is the epidemiology of perineal abscesses?

Answer 323

Common | Mean age is 40 years

Question 324

What are the signs of perineal abscesses on examination?

Answer 324

- Rectal exam may confirm presence of an anorectal exam

Question 325

What are the investigations for a perineal abscess?

Answer 325

Proctosigmoidoscopy

Question 326

How are perineal abscesses managed?

Answer 326

- Prompt incision and drainage of abscess - Deeper abscesses may require surgery - Antibiotics

Question 327

What are the possible complications of perineal abscesses?

Answer 327

- Systemic infection - Anal fistula formation - Recurrence - Scarring

Question 328

What is the prognosis for perineal abscesses?

Answer 328

Good following prompt treatment

Question 329

What is peritonitis?

Answer 329

Inflammation of the peritoneum

Question 330

What is the aetiology of peritonitis?

Answer 330

- Perforation of part of the gastrointestinal tract (perforation of distal oesophagus, stomach etc) - Disruption of peritoneum - Spontaneous bacterial peritonitis - Pelvic inflammatory disease - Leakage of sterile body fluids into peritoneum such as blood - Sterile abdominal surgery - History of alcoholism - Liver disease

Question 331

What are the presenting symptoms of peritonitis?

Answer 331

- Abdominal pain - Abdominal tenderness - Fever - Nausea - Vomiting - Bloating

Question 332

What are the signs of peritonitis on examination?

Answer 332

- Blumberg sign (rebound tenderness) | - Abdominal guarding

Question 333

What are the investigations for peritonitis?

Answer 333

- FBC: Leukocytosis, hypokalaemia, hypernatraemia, acidosis - Abdominal X-ray: dilated, edematous intestines - CT: differentiate causes of abdominal pain

Question 334

How is peritonitis managed?

Answer 334

- Supportive: IV rehydration - IV antibiotics - Laparotomy

Question 335

What are the possible complications of peritonitis?

Answer 335

If untreated, almost always fatal

Question 336

What is the prognosis of peritonitis?

Answer 336

Mortality rises to 40% in elderly people

Question 337

What is a pilonidal sinus?

Answer 337

- Caused by forceful insertion of hairs into the skin of the natal cleft in the sacrococcygeal area - Promotes chronic inflammatory reaction, causing an epithealised sinus

Question 338

What is the aetiology of a pilonidal sinus?

Answer 338

- Hair in the natal cleft and is more common in hirsute people - Risk may depend on hair type, the force of insertion created within the natal cleft, and the vulnerability of the tissues of the natal cleft to hair insertion

Question 339

What is the epidemiology of pilonidal sinus?

Answer 339

- Common - Affects men more than women - Mean age of presentation of 20 years

Question 340

What are the presenting symptoms of pilonidal sinus?

Answer 340

- Sacrococcygeal discharge - Sacrococcygeal pain and swelling - Fever

Question 341

What are the signs of pilonidal sinus on examination?

Answer 341

- Sacrococcygeal sinus tracts - Skin maceration - Hx of prior rupture of fluid into natal cleft

Question 342

What are the investigations for pilonidal sinus?

Answer 342

Clinical diagnosis: Pilonidal sinus or abscess

Question 343

How are pilonidal sinuses managed?

Answer 343

- Local hair removal - Antibiotic treatment - Pain relief

Question 344

What are the possible complications of a pilonidal sinus?

Answer 344

- Necrotising fasciitis | - Suppurative, post-operative collection deep to sutures

Question 345

What is the prognosis of a pilonidal sinus?

Answer 345

Depending on the surgical technique chosen, recurrence rates are variable and average 6.9%.

Question 346

What is portal hypertension?

Answer 346

Increase in blood pressure in the portal venous system

Question 347

What is the aetiology of portal hypertension?

Answer 347

- Cirrhosis of the liver - Blood clots in the portal vein - Schistosomiasis - Focal nodular hyperplasia

Question 348

What is the epidemiology of portal hypertension?

Answer 348

It is thought to account for 5 to 10 percent of patients with portal hypertension in developed countries and up to a third of patients in developing countries (because of an increased frequency of infectious complications that predispose to PVT)

Question 349

What are the presenting symptoms of portal hypertension?

Answer 349

- Ascites

Question 350

What are the signs of portal hypertension on examination?

Answer 350

- Splenomegaly - Oesophageal varices - Caput medusae - Haemorrhoids - Encephalopathy

Question 351

What are the investigations for portal hypertension?

Answer 351

- Hepatic venous pressure gradient= less than equal than 5mmHg - Liver biopsy for suspected cirrhosis

Question 352

How is portal hypertension managed?

Answer 352

- Postsystemic shunts - Non specific B blockers - Diuretics - Antibiotics

Question 353

What are the possible complications of portal hypertension?

Answer 353

- Intestinal ischaemia - Septic portal vein thrombosis - Portal cholangiopathy

Question 354

What is the prognosis for portal hypertension?

Answer 354

ival rates according to Child-Pugh class are: one-year survival in class A is 100%; class B 81%; class C 45%.

Question 355

What is primary biliary cirrhosis?

Answer 355

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

Question 356

What is the aetiology of primary biliary cirrhosis?

Answer 356

- Unknown - Autoimmune aetiology is likely - Genetic and environmental factors have also been proposed - An environmental trigger (possibly infection, chemical or toxi) may cause bile epithelial injury - In susceptible individuals, leads to a T-cell mediated autoimmune response directed against bile duct epithelial cells

Question 357

What is the epidemiology of primary biliary cirrhosis?

Answer 357

- Prevalence in 10-20 in 100,000 in UK | - Usually affects middle-aged women. Ratio if 9:1, women:men

Question 358

What are the presenting symptoms of primary biliary cirrhosis?

Answer 358

- May be an incidental finding on blood tests (e.g. raised AlkPhos, raised cholesterol) - Insidious onset. Fatigue, weight loss and pruritis - Discomfort in the RUQ of the abdomen (rarely) - May present with a complication of liver decompensation (e.g. jaundice, ascites, variceal haemorrhage) - Symptoms of associated conditions, e.g. Sjogren's syndrome (dry eyes and mouth), arthritis, Raynaud phenomenon

Question 359

What are the signs of primary biliary cirrhosis?

Answer 359

- Early: May be no signs - Late: Jaundice, skin pigmentation, scratch marks, xanthomas (secondary to hypercholesterolaemia), hepatomegaly, ascietes and other signs of liver disease may be present Signs of chronic liver disease, e.g. palmar erythema, clubber and spider naevi

Question 360

What are the investigations for primary biliary cirrhosis?

Answer 360

- Blood: LFT (raised AlkPhos, GGT, bilirubin may be normal or raised in later stages. Transaminases initially normally, raised with disease progression and cirrhosis. Raised IgM and cholesterol are typical. - Ultrasound: To exclude extrahepatic biliary obstruction (e.g. by gallstones or strictures) - Liver biopsy: Chronci inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes. Repeat liver biopsies whilst on treatment

Question 361

What is primary sclerosing cholangitis?

Answer 361

Chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts

Question 362

What is the aetiology of primary sclerosing cholangitis?

Answer 362

- Unknwon - Postulated immune and genetic predisposition and toxic or infective triggers - Close association with IBD, especially UC - About 5% of those with UC will develop PSC

Question 363

What is the epidemiology primary sclerosing cholangitis?

Answer 363

Usually presents between 25 and 40 years

Question 364

What are the presenting symptoms of primary sclerosing cholangitis?

Answer 364

- May be asymptomatic and diagnosed after persisently increased AlkPhos - May present with intermittent jaundice, pruritis, RUQ pain, weight loss and fatigue - Episodes of fever and rigors caused by acute cholangitis are less common - History of UC - Symptoms of complications

Question 365

What are the signs of primary sclerosing cholangitis on examination?

Answer 365

May have no signs of evidence of jaundice, hepatosplenomegaly, spider naevi, palmar erythema or ascites

Question 366

What is the pathogenesis of primary sclerosing cholangitis?

Answer 366

Periductal inflammation with periductal concentric fibrosis, portal oedema, bile duct proliferation and expansion of portal tracts, progressive fibrosis and development of biliary cirrhosis

Question 367

What are the investigations for primary sclerosing cholangitis?

Answer 367

- Blood: LFT (raised AlkPhos, GGT, transaminases). In later stages, reduced albumin and raised bilirubin - Serology: Immunoglobulin levels (raised IgG in children, IgM in adults - ERCP: Stricturing and interspersed dilation of intrahepatic and occasionally extrahepatic bile ducts, small diverticular on the common bile duct may be seen - MRCP: Enables non-invasive imagining of the biliary tree - Liver biopsy: Confirms diagnosis and allows staging of disease

Question 368

What is rectal prolapse?

Answer 368

- Rectal walls have prolapsed to a degree where they protrude out the anus and are visible outside the body

Question 369

What is the aetiology of rectal prolapse?

Answer 369

- Chronic constipation or chronic diarrhoea - Long term history of straining during bowel movements - Older age - Weakening of the anal sphincter - Prior injury to the anal or pelvic areas - Damage to nerves

Question 370

What is the aetiology of rectal prolapse?

Answer 370

- More common in elderly women

Question 371

What are the presenting symptoms of rectal prolapse?

Answer 371

- Pain - Constipation - Faecal incontinence - Mucous discharge - Rectal bleeding

Question 372

What are the the signs of rectal prolapse on examination?

Answer 372

- Concentric rings of mucosa= differentiation of haemorrhoids - Rectal ulcer - Decreased anal sphincter tone

Question 373

What are the investigations for rectal prolapse?

Answer 373

- Sigmoidoscopy/colonoscopy - Videodefecography - Colonic transit studies - Anorectal manometry

Question 374

What is ulcerative colitis?

Answer 374

Chronic relapsing and remitting inflammatory disease affecting the large bowel

Question 375

What is the aetiology of ulcerative colitis?

Answer 375

- Unknown - Suggested hypotheses include genetic susceptibility, immune response to bacterial or self-antigens , environmental factors, altered neutrophil function

Question 376

What is the epidemiology of ulcerative colitis?

Answer 376

- Higher prevalence in Ashkenazi Jews, Caucasians - Uncommon before age of 10 yrs, peak onset age 20-40 yrs - Equal sex ratio up to age of 40, then higher in males

Question 377

What are the presenting symptoms of ulcerative colitis?

Answer 377

- Bloody or mucous diarrhoea (stool frequency related to severity of disease) - Tenesmus and urgency - Crampy abdominal pain before passing stool, weight loss, fever - Symptoms of extra-Gi manifestations

Question 378

What are the signs of ulcerative colitis on examination?

Answer 378

- Signs of iron-deficiency anaemia, dehydration - Clubbing - Abdominal tenderness, tachycardia - Blood, mucous and tenderness on PR examination - Signs of extra GI manifestation

Question 379

What are the investigations for ulcerative colitis?

Answer 379

- Blood: (decreased Hb, Raised WCC, ESR, CRP, decreased albumin - Stool: Culture as infectious colitis is a differential diagnosis. Faecal calprotectin-marker for disease severity - AXR: To rule out toxic megacolon - Flexible sigmoidoscopy: Determines severity, histological confirmation, detection of dysplasia - Barium enema: Mucosal ulceration with granular appearance and filling defects. Colonoscopy and barium enema may be dangerous in acute exacerbations (risk of perforation)

Question 380

How is ulcerative colitis managed?

Answer 380

- Markers of activity - Acute exacerbation: IV rehydration, IV corticosteroids, antibiotics, bowel rest, parenteral feeding may be necessary and DVT prophylaxis. Monitor fluid balance and vital signs - Mild disease: oral or rectal 5-aminoslicyclic acid derivatives e.g. sulphasalazine and/or rectal steroids - Moderate to sever: oral steroids and oral 5-ASA - Advice - Surgical

Question 381

What are the possible complications of ulcerative colitis?

Answer 381

- Gastrointestinal: haemorrhage, toxic megacolon, perforation, colonic carcinoma, gallstones and PSC - Extra-gastrointestinal manifestations: Uveitis, renal calculi, arthropathy, sacroliitis, ankylosing spondulitis, erythema nodosum, pyoderma gangrenosum, osteoporosis, amyloidosis

Question 382

What it the prognosis of ulcerative colitis?

Answer 382

Relapsing and remitting condition, with normal life expectancy - Poor prognostic factors (ABCDEF): Albumin, blood PR, CRP raised, dilated loops of bowel, eight of more bowel movements per day, fever

Question 383

What is viral hepatitis?

Answer 383

Liver inflammation due to viral infection, may present in acute or chronic forms

Question 384

What is the aetiology of viral hepatitis?

Answer 384

The most common causes of viral hepatitis are the five unrelated hepatotropic viruses Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E. In addition to the nominal hepatitis viruses, other viruses that can also cause liver inflammation include Cytomegalovirus, Epstein–Barr virus, and Yellow fever. Up to 1997 there has been also 52 cases of Viral hepatitis caused by Herpes simplex virus

Question 385

What is the epidemiology of viral hepatitis?

Answer 385

There is the opportunity to prevent or treat the most common types. Hepatitis A and hepatitis B can be prevented by vaccination. Effective treatments for hepatitis C are available but expensive. In 2013 about 1.5 million people died from viral hepatitis. Most deaths are due to hepatitis B and hepatitis C.East Asia is the region of the world most affected.

Question 386

What are the presenting symptoms of viral hepatitis?

Answer 386

- Jaundice - Low grade fever - Headache - Muscle aches - Fatigue - Loss of appetite - Nausea - Vomiting

Question 387

What are the signs of viral hepatitis on examination?

Answer 387

- Hepatomegaly - Splenomegaly - Palmar erythema - Spider naevi - Spider angioma

Question 388

What are the investigations for viral hepatitis?

Answer 388

- Liver function tests (AST and ALT elevated out of proportion to alkaline phosphatase, usually with hyperbilirubinemia) - Viral serologic testing - PT/INR measurement - Seriology - Biopsy

Question 389

How is viral hepatitis managed?

Answer 389

Supportive care No treatments attenuate acute viral hepatitis. Alcohol should be avoided because it can increase liver damage. Restrictions on diet or activity, including commonly prescribed bed rest, have no scientific basis. Most patients may safely return to work after jaundice resolves, even if AST or ALT levels are slightly elevated. For cholestatic hepatitis, cholestyramine 8 g po once/day or bid can relieve itching. Viral hepatitis should be reported to the local or state health department.

Question 390

What are the possible complications of viral hepatitis?

Answer 390

- Acute or subacute hepatic necrosis. - Chronic active hepatitis. - Chronic hepatitis. - Cirrhosis. - Hepatic failure. - Hepatocellular carcinoma (HCC) in patients with HBV or HCV infection.

Question 391

What is the prognosis of viral hepatitis?

Answer 391

Virtually all patients with acute infection with hepatitis A and most adults (greater than 95%) with acute hepatitis B recover completely

Question 392

What is volvulus?

Answer 392

Loop of intestine twists around itself and the mesentery that supports it

Question 393

What is the aetiology of volvulus?

Answer 393

- Midgut volvulus occurs in people who are predisposed because of intestinal malrotation - Segmental volvulus occurs because of abnormal intestinal contents or adhesions - Volvulus of the cecum, transverse colon, or sigmoid colon occurs, usually in adults, with only minor predisposing factors such as redundant (excess, inadequately supported) intestinal tissue and constipation

Question 394

What is the epidemiology of volvulus?

Answer 394

Sigmoid volvulus is a leading cause of acute colonic obstruction in South America, Africa, Eastern Europe and Asia but is rare in developed countries such as the USA, UK, Japan and Australia. Sigmoid volvulus is the third leading cause of colon obstruction in adults but is rare in infants and children.

Question 395

What are the presenting symptoms of volvulus?

Answer 395

- Nausea or vomiting - Abdominal tenderness - Bloody or dark red stool - Constipation - Distended abdomen

Question 396

What are the signs of volvulus on examination?

Answer 396

- Abdominal examination reveals a tympanitic, distended (but usually non-tender) abdomen and a palpable mass may be present. - Empty rectal ampulla on rectal examination

Question 397

What are the investigations for volvulus?

Answer 397

- Plain abdominal X-ray: single grossly dilated sigmoid loop commonly reaching the xiphisternum. - May need limited barium enema without bowel preparation (can result in decompression itself). - CT scanning is the least invasive imaging technique that allows assessment of bowel wall ischaemia

Question 398

What is Wilson's disease?

Answer 398

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

Question 399

What is the aetiology of Wilson's disease?

Answer 399

- Gene responsible is on chromosome 13, and codes for a copper transporting ATPase in hepatocytes - Mutations interfere with transport of copper into the intracellular compartments for incorporation into caeruloplasmin (and secreition into plasma) or excretion in the bile. Excess copper damages hepatocyte mitochondria, causing cell death and release of free copper into plasma, which is subsequently deposited in other tissues

Question 400

What is the epidemiology of Wilson's disease?

Answer 400

Liver disease may be present in children over 5 | - Neurological disease usually presents in young adults

Question 401

What are the presenting symptoms of Wilson's disease?

Answer 401

- Liver: May present with hepatitis, liver failure or cirrhosis. Jaundice, easy bruising, variceal bleeding, encephalopathy - Neurological: Dyskinesia, rigidity, tremor, dystonia, dysarthia, dysphagia, drooling, dementia, ataxia - Psychiatric: Conduct disorder, personality change, psychosis

Question 402

What are the signs of Wilson's disease on examination?

Answer 402

- Liver: Hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia - Neurological - Eyes: Green or brown Kayser-Fleischer ring at the corneal limbus, sunflower cataract (copper accumulation in the lens, seen with slit lamp)

Question 403

What are the investigations for Wilson's disease?

Answer 403

- Blood: LFT (Raised AST, ALT and AlkPhos), serum caerulolasmin and copper (may be low but may provide false negatives as caeruloplasmin is an acute phase protein) - 24h urinary copper levels: Increased - Liver biopsy: Increased copper content - Genetic analysis: Wide variety of mutations in the gene cause the disease, so there is no simple genetic test and sequencing requires specialist genetic advice

Question 404

What is autoimmune hepatitis?

Answer 404

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

Question 405

What is the aetiology of autoimmune hepatitis?

Answer 405

- In a genetically predisposed individual, an environmental agent (e.g. viruses or drugs) may lead to hepatocyte expression of HLA antigens which then become the focus of principally T-cell-mediate autoimmune attack - 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

Question 406

What are the types of autoimmune hepatitis?

Answer 406

- Type 1 (classic): ANA, anti-smooth muscle antibodies (ASMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA) - Type 2: Antibodies to liver/kidney microsomes, antibodies to liver cytosol antigen

Question 407

What is the epidemiology of autoimmune hepatitis?

Answer 407

- Type 1 hepatitis occurs in all age groups (although mainly in young women) - Type 2 is generally a disease of girls and young women

Question 408

What are the presenting symptoms of autoimmune hepatitis?

Answer 408

- May be asymptomatic and discovered incidentally with abnormal LFT - Insidious onset: Malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis - Acute: Fever, anorexia, jaundice, nausea, vomiting, diarrhoea, RUQ pain. Some present with serum sickness (e.g. arthralgia, polyarthritis, maculopapular, rash) - May be associated with keratoconjunctivitis sicca - Personal or Fhx of autoimmune disease e.g. T1DM and vitiligo. Important to take full history to rule out potential causes of liver disease (e.g. alcohol, drugs)

Question 409

What are the signs of autoimmune hepatitis on examination?

Answer 409

- Stigmata of chronic liver disease e.g. spider naevi - Ascites, oedema and encephalopathy are late features - Cushinhoid features (e.g. rounded face, cutaneous striae, acne, hirsuitism) may be present even before the administration of steroids

Question 410

What are the investigations for autoimmune hepatitis?

Answer 410

- Blood: LFT (raised AST, ALT, GGT, Alkphos, bilirubin. Low albumin if severe) Clotting (Raised PT if severe). FBC Mild reduced Hb and platelets). - Hypergammaglobulinaemia is typical with presence of ANA ASMA or anti-LKM autoantibodies - Liver biopsy: Needed to establish the diagnosis. Shows interface hepatitis or cirrhosis - Other investigations: Rule out other cases of liver disease - US, CT, MRI of liver & abdo: visualise structural lesions - ERCP: Rule out PSC

Question 411

How is autoimmune hepatitis managed?

Answer 411

- Indicated if aminotransferases more than 10x upper limit of normal - Immunosuppression: with steroids e.g. prednisolone. Azathioprine or 6-mercaptopurine can be used in maintenance phase as steroid-sparing agent with frequent monitoring of LFT & FBC - Monitor: US and a-fetoprotein level every 6-12 months in pts with cirrhosis - Hep A & B vaccinations - Liver transplant: For pts who are refractory to or intolerant of immunosuppressive therapy and those with end-stage disease

Question 412

What are the possibly complications of autoimmune hepatitis?

Answer 412

- Fulminant hepatic failure - Cirrhosis and complications of portal hypertension (e.g. varices, ascites) - Hepatocellular carcinoma - Side effects of corticosteroid treatment

Question 413

What is the prognosis for autoimmune hepatitis?

Answer 413

- Older pts with type 1 are more likely to have cirrhosis at presentation but may be more likely to respond to treatment - Approx 80% achieve remission y 3 years - 50% require lifelong maintenance

Question 414

What is viral hepatitis A & E?

Answer 414

Hepatitis caused by infection with the RNA viruses, hep A (HAV) or hep E virus (HEV), that follow an acute course without progression to chronic carriage

Question 415

What is the aetiology of viral hepatitis A & E?

Answer 415

- HAV is picornavirus and HEV is a calcivirus: Both are small-non enveloped single stranded linear RNA viruses with transmission by the faecal-oral route - The viruses replicate in hepatocytes and are secreted into bile - Liver inflammation and hepatocyte necrosis is caused by the immune response with targeting of infected cells by CD8+ T cells and NK cells

Question 416

What is the epidemiology of viral hepatitis A&E?

Answer 416

- HAV is an endemic in the developing world, infection often occurs subclinically - HEV endemic in Asia, Africa and Central America

Question 417

What are the presenting symptoms of viral hepatitis A & E?

Answer 417

Incubation period for HAV and HEV is 3-6 weeks - Prodromal period: Malaise, anorexia (distaste for cigarettes in smokers), fever, nausea and vomiting - Hepatitis: Prodrome followed by dark urine, pale stools and jaundice lasting approx. 3 weeks. Occasionally, itching and jaundice last several weeks in HAV infection

Question 418

What are the signs of viral hepatitis A & E on examination?

Answer 418

- Pyrexia, jaundice, tender hepatomegaly, spleen may be palpable (20%) - Absence of stigmata of chronic liver disease, although a few spider naevi may appear, transiently

Question 419

What are the investigations for viral hepatitis A & E?

Answer 419

- Blood: LFT (raised AST, ALT, bilirubin, Alkphos) Raised ESR, if severe, low albumin and raised platelets - Viral seriology 1) Hep A: Anti HAV IgM, anti HAV IgG 2) Hep E: Anti HEV IgM, anti HEV IgG. Hep B an C serology to rule out these - Urinalysis: Positive for bilirubin, raised urobilinogen

Question 420

How is viral hepatitis A & E managed?

Answer 420

- No specific management. Bed rest and symptomatic treatment (e.g. antipyretics, antiemetics) Colestyramine for servere pruritis - Prevention and control 1) Public health: safe water, sanitation, food hygiene standards 2) Immunisation: Passive immunisation with IM human immunoglobulin only effect for short period

Question 421

What are the possible complications of viral hepatitis A & E?

Answer 421

- Fulminant hepatic failure develop in some cases, but increased in pregnant women - Cholestatic hepatitis with prolonged jaundice and pruritis may develop after HAV infection - Post-hepatitis syndrome: Continued malaise for weeks to months

Question 422

What is the prognosis for hepatitis A & E?

Answer 422

- Recovery usually within 3-6 weeks - Occasionally, a relapse during recover - No chronic sequelae - Fulminant hepatic failure has 80% mortality

Question 423

What is viral hepatitis B & D?

Answer 423

- Hepatitis caused by infection with HBV which may follow an acute or chronic (viraemia and hepatic inflammation continuing more than 6mths) course - HDV, a defective virus, may only co-infect HBV or superinfect persons who are already carriers of HBV

Question 424

What is the aetiology of hepatitis B & D?

Answer 424

- HBV is an enveloped partially double stranded DNA virus. Transmission is by sexual contact, blood and vertical transmission. Various viral proteins are produced, - HDV is single stranded RNA virus - Antibody and cell mediated immune responses to viral replication lead to liver inflammation and hepatocyte necrosis

Question 425

What are the risk factors for Hep B?

Answer 425

- IB drug abuse, unscreened blood and blood products, infants of HbeAg pos mothers and sexual contact with HBV carriers - Risk of persistent HV varies with age, with younger individuals, especially babies, more likely to develop chronic carriage

Question 426

What is the epidemiology of Hep B & D?

Answer 426

- Common - Common in Southeast Asia, Africa and Mediterranean countries - HDV found worldwide - Uncommon in UK

Question 427

What are the presenting symptoms of Hep B & D?

Answer 427

Incubation period 3-6 months - 1-2 weeks prodrome of malaise, headache, anorexia, nausea, vomiting, diarrhoea and RUQ pain - May experience serum-sickness type illness (e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash - Jaundice develops with dark urine and pale stools - Recovery is usual within 4-8 weeks. - Chronic carriage may be diagnosed after routing LFT

Question 428

What are the signs of Hep B & D on examination?

Answer 428

- Acute: Jaundice, pyrexia, tender hepatomegaly, splenomegaly and cervical lymphadenopathy in 10-20%. Occasionally urticarial/maculopapular rash - Chronic: May have no findings, signs of chronic liver disease or decompensation

Question 429

What are the investigations for Hep B & D?

Answer 429

- Viral serology: Acute HBV (HbsAg positive, IgM anti- HbcAg) Chronic HBV (HbsAG positive, IgG anti-HBcAg, HbeAG positive or negative). HDv : detected by IgM or IgG against HDV - PCR: for detection of HBV DNA - LFT: Raised AST & ALT, bilirubin, alkphos - Clotting: raised PT in severe disease - Liver biopsy: Percutaneous or tranjugular if clotting is deranged or ascites is present

Question 430

How is Hep B & D managed?

Answer 430

- Prevention: Blood screen, instrument sterilisation, safe sex practices - Passive immunisation: Hep B immunoglobulin following acute exposure to neonates born to HbeAg-pos mothers - Active immunisation: Recombinant HbsAg vaccine for individuals at risk and neonates born to HBV-positive mothers. Immunisation against HBV protects against HDV

Question 431

How is Acute HBV hepatitis managed?

Answer 431

- Symptomatic treatment with bed rest, antiemetics, antipyretics and cholestyramine for pruritis - Notification to consultant in communicable disease control

Question 432

How is chronic HBV managed?

Answer 432

- Indications for tx with antivirals: HbeAg-pos or Hbe-AG neg chronic hepatitis, compensated cirrhosis and high HBV DNA, decompensated cirrhosis and detectable HBV DNA by PCR - Pts may be treated with interferon alpha or nucleos/tide analogues - Interferon alpha is cytokine which augments natural antiviral mechanisms. Side-effects include flu-like symptoms, fever, chills, myalgia, headaches, bone marrow suppression and depression, necessitating discontinuation in 5-10% pts

Question 433

What are the possibly complications of hep B & D?

Answer 433

- Fulminant hepatic failure - Chronic HBV infection - Cirrhosis and hepatocellular carcinoma - Extrahepatic immune complex disorders including glomerulonephritis, polyarteritis nodosa - Superinfection with HDV may lead to acute liver failure or rapidly progressive disease

Question 434

What is the prognosis of hep B & D?

Answer 434

- In adults, 10% infections become chronic and of these 20-30% develop cirrhosis

Question 435

What is viral hepatitis C?

Answer 435

Hepatitis caused by infection with HCV, often following a chronic course

Question 436

What is the aetiology of viral hepatitis C?

Answer 436

- Small enveloped single-stranded RNA virus of the flavivirus family. - Transmission occurs via parenteral route, and at-risk groups include recipients of blood and blood products prior to screening, IV drug users, non-sterile acupuncture and tattooing, those on haemodialysis and health care workers.

Question 437

What is the epidemiology of viral hepatitis C?

Answer 437

- Common | - 0.5-2% prevalence in developed countries, higher rates in areas because of poor sterilisation practices

Question 438

What are the presenting symptoms of viral hepatitis C?

Answer 438

- 90% of acute infections are asymptomatic with less than 10% becoming jaundiced with mild flu-like illness - May be diagnosed after incidental abnormal LFT or in older individuals with complications of cirrhosis

Question 439

What are the signs of viral hepatitis C on examination?

Answer 439

- May be no signs or may be signs of chronic liver disease in long-standing infection - Less common extra-hepatic manifestations include: - Skin rash, caused by mixed cryoglobulinaemia causing a small-vessel vasculitis and - Renal dysfunction, caused by glomerulonephritis

Question 440

What are the investigations for viral hepatitis C?

Answer 440

- Blood: HCV serology (Anti-HCV antibodies, wither IgM (acute) or IgG (past exposure or chronic)). Reverse-transcriptase PCR: Detection and genotyping of HCV DNA. LFT: Acute infection causes raised AST and ALT, mild raised bilirubin. Chronic infection causes 2-8x raised levels - Liver biopsy: Assess degree of inflammation and liver damage

Question 441

How is viral hepatitis C prevented?

Answer 441

- Screening of blood, blood products and organ donors - Needle exchange schemed for IV drug abusers - Instrument sterilisation - No vaccine currently available

Question 442

How is viral hepatitis C managed medically?

Answer 442

- No specific management and mainly supportive (e.g. antipyretics, antiemetics, cholestyramine) - Specific antiviral treatment can be delayed for 3-6 months

Question 443

How is chronic hepatitis C managed?

Answer 443

Combined treatment with pegylated-interferon-alpha (augments natural antiviral mechanisms) and ribavirin - Monitoring of HVC viral load is recommended after 12 weeks of treatment to determine efficacy of tx - Regular US of liver may be necessary if pt has cirrhosis

Question 444

What are the possible complications of hepatitis C?

Answer 444

- Fulminant hepatic failure in acute phase - Chronic HCV carriage - Cirrhosis and hepatocellular carcinoma - Less common are porphyria cutanea tarda, cryoglobulinaemia and glomerulonephritis

Question 445

What is the prognosis for hepatitis C?

Answer 445

- Approx 8% of exposed progress to HCV infection | - Of these 20-30% develop cirrhosis over 10-20 years