Revise Notes Gastro

Question 1

Hepatitis E

Pathophysiology: RNA HEpEvirus

Transmission: FaEco-oral , prevalent in central and SE Asia, mexico, africa

Answer 1

Presentation: Presents with features of acute hepatitis – RUQ pain / jaundice

NO risk of chronic hep or HCC

Mortality is as high as 20% especially in pregnant patient populations

Question 2

Hepatitis D

Pathophysiology:

ssRNA virus, transmitted via blood/ bodily fluids
Requires the presence of Hep B sAg to complete replication

Answer 2

High risk of fulminant hepatitis / chronic hepatitis and cirrhosis

Investigation: Reverse PCR of Hep D RNA

Treatment: Interferon

Question 3

Hepatitis C

Organism: RNA Flavivirus, incubation period 6-10 weeks

Transmission: Blood borne (IVDU/needlestick/vertical/transfusion), bodily fluids (sex)

Presentation: 30% of patients will present with symptoms of flu, fatigue, and transaminitis/jaundice

Answer 3

Chronic hepatitis C:

Affects 85% of patients
Complications:
Hepatocellular carcinoma
Cryoglobulinaemia type 2
20% will develop liver cirrhosis
Sjogrens
Porphyria cutanea tarda
Management:

Protease inhibitor combination +/- ribavirin. For example:
Dactlatasvir + Sofosbuvir +/- ribavirin
Sofosbuvir + Simeprevir +/- ribavirin

Question 4

Hepatitis B Serology

Hepatitis B serology results are commonly examined.

The following should therefore be remembered:

HBsAG (surface antigen) +ve = Disease Present
Normally present in the acute phase (< 6 months)
If present > 6 months – indicates chronic hepatitis B

Answer 4

Anti-HBs = Immunity to Hep B
Suggests previous immunisation or previous acute infection cleared by immune system
Tip: Anti-HBs = anti-HBsafe

Anti-HBc = infected with hepatitis B - either previous or current
IgM – indicated acute/recent infection
IgG persists even if the virus has been cleared

Tip: Anti-HBc = Anti-HBcaught
HBeAG = a marker of infectivty - It is a breakdown product of core antigen from the liver cells

Question 5

Examples.. Try and work out the following Hep B serologies..

Anti-HBs +ve, all others negative?
Anti-HBc +ve but HBsAG -ve
Anti-HBc +ve and HBsAG +ve

Answer 5

Answers

Immune but never infected (i.e. vaccinated)
Previous infection which has been cleared
Previously caught HepB, remains positive - chronic hepatitis b

Question 6

Hepatitis B in pregnancy

Answer 6

All pregnant patients are offered screening for hepatitis B

If the mother has chronic hepatitis B or acute hepatitis B during the pregnancy treat baby with:

Vaccination course
Hepatitis B immunoglobulin
It’s safe to Breastfeed with Hep B (no risk of transmission)

Question 7

Hepatitis B

Organism: hepaDNAvirus

Transmission: bodily fluids/ blood

Complications

Chronic hepatitis– 10% “groundglass hepatocytes”

PAN – Hep B +ve in 30%, associated nerve palsy

Cryoglobulinaemia – Hep B + Purpuric rash
HCC

Answer 7

Immunisation

Given to al babies at 2, 3 and 4 months
Immunisation is also recommended for people at high risk of catching Hep B:

This includes: intravenous drug users, people with multiple sexual partners,

men who have sex with men,

people requiring regular blood transfusions, healthcare workers etc.

Question 8

Testing immunisation response

Limited indications, including (1) CKD or (2) Occupational risk
Antibody count:

> 100 = good response – perform booster after 5 yrs

10-100 = suboptimal response – 1 more vaccine required, no further testing

< 10 = non-responder – test for current/previous infection of Hep B

Repeat all 3 doses of immunisation regimen, and repeat test

Answer 8

Treatment

Confirmed Hep B: Pegylated IFN-alpha - given as a weekly injection for 48 weeks

Reduces viral replication by 30% and supports immune system response

Question 9

Hep B - Post-Exposure Prophylaxis

Answer 9

Immunisation with the hepatitis B vaccine should be given as soon as possible following exposure (e.g. needlestick injury),
and no later than seven days post-exposure.

Question 10

Hepatitis A

Organism: RNA PicornAvirus, fAeco-oral transmission

Answer 10

Clinical features:

Acute hepatitis - RUQ pain, flu-like symptoms, jaundice and deranged LFTs
No risk of chronic disease

Question 11

Acute Cholangitis
Key learning

Most commonly bacterial (E.coli) infection due to bile duct obstruction
Associated with gallstones
Often defined by Charcot’s triad (fever,

RUQ pain and jaundice), Reynold’s pentad (in addition hypotension and altered mental status) in severe cases

USS will show dilated CBD and bloods deranged LFTs
Management is with IV antibiotics and prompt ECRP/PTC to relieve obstruction followed often by cholecystectomy

Pathophysiology

Acute cholangitis results from bacterial infection due to bile duct obstruction
Most commonly due to E.coli
Epidemiology

More common in older adults

Answer 11

Causes

Most common:
Gallstones
Others:
Strictures
Tumours
Clinical Features

Charcot’s triad (fever, right upper quadrant pain, jaundice)
Reynolds’ pentad (Charcot’s plus hypotension, altered mental status) in severe cases.

Other symptoms include nausea/vomiting, lethargy, pale stools and dark urine

Investigations

Blood tests:
Elevated liver function tests (raised ALP and/or bilirubin)
Elevated inflammatory markers
Imaging:
1st line: Ultrasound- dilated common bile duct (>6mm)

Other imaging such as CT or MRI indicated if cause of cholangitis not clear

Question 12

Short bowel syndrome
Short Bowel Syndrome (SBS) is a malabsorption disorder resulting from significant surgical resection of the small intestine, leading to nutrient, fluid, and electrolyte deficiencies.

Aetiology

Significant surgical resections (typically > 50% of small bowel) due to Crohn’s disease, mesenteric ischemia, trauma, malignancies, or congenital defects like volvulus and necrotising enterocolitis in neonates.

Answer 12

Clinical features

Chronic diarrhoea +/- steatorrhea
Malnutrition, weight loss, dehydration
Anaemia
Electrolyte imbalances
Management

Nutritional Support

> 100 cm remaining Small Intestine:
Patients may manage with oral intake adjustments, including a high-calorie, high-protein, low-fat diet, and supplementation with vitamins and minerals.

<100 cm remaining Small Intestine: Total parenteral nutrition (TPN) is often necessary to meet nutritional needs and manage fluid and electrolyte balance.

Medication:
Anti-diarrhoeal agents, PPIs, bile acid sequestrants can help manage symptoms.

Glucagon-like peptide-2 analogues (e.g., teduglutide) can enhance intestinal absorption.

Surgical Interventions: Bowel lengthening or intestinal transplantation may be considered.

Question 16

Acute Cholangitis mng

Answer 16

Management

Immediate:

IV fluids
Antibiotics- for example ceftriaxone and metronidazole
Definitive:

Early biliary decompression endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous transhepatic cholangiography (PTC) to relieve obstruction
Cholecystectomy can be planned later
Complications

Septic shock- therefore high mortality if left untreated
Liver abscess

Question 17

Angiodysplasia
Angiodysplasia refers to small vascular malformations in the gastrointestinal (GI) tract, often leading to intermittent bleeding.

Aetiology

Dilation and formation of fragile blood vessels in the mucosa and submucosa of the GI tract, primarily in the colon and small intestine.
Associated Conditions: Commonly associated with chronic kidney disease, aortic stenosis, and von Willebrand disease.
Clinical features

Occult GI bleeding - melaena or haematochezia.

Iron deficiency anemia - TATT etc.
Aortic stenosis - questions may make note of an ejection systolic murmur.

Answer 17

Investigations

Colonoscopy or upper GI endoscopy is the primary diagnostic tool, revealing characteristic red, flat or slightly raised lesions, ectatic vessels (spider-like appearance).

Capsule Endoscopy: Useful when initial endoscopies are inconclusive.
Angiography can help localise bleeding in actively bleeding patients

Management

First-line therapy includes endoscopic coagulation techniques/cautery.

Question 18

Primary Sclerosing Cholangitis

Pathophysiology

Inflammation of the intra AND extra hepatic bile ducts, with subsequent fibrosis
Associated conditions

ULCERATIVE COLITIS - 80% of patients with PSC have a diagnosis of UC
A big clue in questions!
HIV

Answer 18

Clinical features

RUQ pain
Obstructive jaundice, pruritus
Hepatosplenomegaly
Investigations

Labs: P-ANCA
imaging: ERCP/MRCP - Beaded appearance of ducts
Complications

Cholangiocarcinoma

Question 19

Autoimmune Hepatitis

Associations

MHCs - HLA-B8, HLA-DR3
Coeliac disease and other autoimmune disease
Most commonly - 5th-6th decade, Female
Clinical features

Can present as acute hepatitis
Deranged LTs - ALT/AST can be 5-10x upper limit of normal + jaundice, +/- inc. INR
Can present insidiously and non-specifically with TATT, secondary amenorrhoea, malaise etc.
Features of chronic liver disease
Bloods

Deranged LFTs - elevated ALT/AST
INR elevated
Antibodies as below
Hypergammaglobulinaemia

Answer 19

Subtypes

Type 1

Affects adults and children
Antibodies: SMA (smooth muscle antibody) +/- ANA
Type 2

Almost exclusively in children
Antibodies: Anti-Liver Kidney Microsomal (LKM) antibodies
Memory aid: LKM - Little Kids Mostly
Type 3

Affects middle aged adults
Antibodies: anti-soluble liver antigen antibodies
Commonly have a good response to prednisolone
Management

Prednisolone/steroids
Azathioprine/immunosuppressants
Transplant

Question 20

Autoimmune Hepatitis

Associations

MHCs - HLA-B8, HLA-DR3
Coeliac disease and other autoimmune disease
Most commonly - 5th-6th decade, Female
Clinical features

Can present as acute hepatitis
Deranged LTs - ALT/AST can be 5-10x upper limit of normal + jaundice, +/- inc. INR
Can present insidiously and non-specifically with TATT, secondary amenorrhoea, malaise etc.
Features of chronic liver disease
Bloods

Deranged LFTs - elevated ALT/AST
INR elevated
Antibodies as below
Hypergammaglobulinaemia

Answer 20

Subtypes

Type 1

Affects adults and children
Antibodies: SMA (smooth muscle antibody) +/- ANA
Type 2

Almost exclusively in children
Antibodies: Anti-Liver Kidney Microsomal (LKM) antibodies
Memory aid: LKM - Little Kids Mostly
Type 3

Affects middle aged adults
Antibodies: anti-soluble liver antigen antibodies
Commonly have a good response to prednisolone
Management

Prednisolone/steroids
Azathioprine/immunosuppressants
Transplant

Question 22

Bile acid malabsorption
Bile Acid Malabsorption (BAM) is a condition characterised by excessive bile acids in the colon, leading to chronic diarrhoea and other gastrointestinal symptoms.

Diagnosis is via the SeHCAT test, and management involves bile acid sequestrants (cholestyramine).

Aetiology

Primary BAM (Type 1): Often idiopathic, with no apparent underlying disease.
Secondary BAM (Type 2): Associated with conditions like IBD, coeliac, ileal resection, or cholecystectomy.

Type 3 BAM: Related to other gastrointestinal disorders, such as IBS or SBBOS

Answer 22

Clinical Features

Chronic, watery diarrhoea is the hallmark symptom, often leading to urgency and incontinence.
May be associated with bloating, abdominal pain, and steatorrhea.

Nutritional Deficiencies: Potential deficiencies in fat-soluble vitamins due to impaired fat absorption (Vitamin A, D, E, K malabsorption).
Investigations/Diagnosis

SeHCAT Test: The gold standard for diagnosis, measuring bile acid retention using a radiolabeled synthetic bile acid.
Management

Bile Acid Sequestrants: First-line treatment includes cholestyramine to bind bile acids and reduce diarrhoea.
Low-fat diet to reduce bile acid load in the intestines.

Question 24

Cholecystitis
Key learning

Inflammation of gallbladder most commonly due to gallstones
Tender RUQ and may be Murphy’s sign positive
Raised WCC/CRP

Management is initially supportive with analgesia, IV fluids and antibiotics
ERCP if stones in common bile duct
25-30% require surgery (cholecystectomy) or develop

complications

Epidemiology

10% of population will have an episode during lifetime
Causes

Gallstones- 90%
Risk factors- diabetes, inflammatory bowel disease, female, obesity
Acalculous- no gallstones, often functional cystic duct obstruction

Risk factors- associated sepsis, trauma, major surgery, burns, on TPN

Answer 24

Clinical Features

Biliary colic:
Occurs if obstruction is partial/short duration
Intermittent severe pain and tenderness RUQ
Acute cholecystitis:
Occurs if obstruction complete
Constant pain with or without guarding
Present for several hours

Referred pain may be felt in right shoulder or interscapular region
Associated- fever, nausea or vomiting, loss of appetite
Examination findings

RUQ tenderness
RUQ mass in a third of patients

Murphy’s sign- inspiration inhibited by pain on palpation when examiner’s hand positioned along costal margin)
Investigations

Abdominal ultrasound
Thickened gallbladder wall, gallstones or sludge in gallbladder or fluid around gallbladder
Bloods:

Raised CRP and WCC
Raised ALT, normal ALT

Amylase raised in pancreatitis
Bilirubin raised in Mirizzi syndrome
Consider MRCP to visualise biliary tree if diagnosis uncertain despite above

Question 25

Cholecystitis

Answer 25

Management Admit to hospital Supportive Intravenous fluids Antibiotics Analgesia ERCP if stones in common bile duct 25-30% require surgery (cholecystectomy) or develop complications Complications Necrosis of gallbladder wall (gangrenous cholecystitis) Gallbladder perforation (10% of acute cholecystitis, up to 30% mortality) Abscess/fistula Sepsis Jaundice Mirizzi Syndrome- stone in Hartmanns pouch or cystic duct causes compression of adjacent common hepatic duct (and therefore causes obstructive jaundice)

Question 26

Irritable bowel syndrome Clinical features Symptoms should be present for 6 months and include… Abdominal pain relieved by defecation or associated with a change in bowel habit And is accompanied by Altered stool passage (straining, urgency) Bloating Mucus Worse after eating Ensure there are no red flag/alarm symptoms

Answer 26

Management Abdominal pain 1st line: Antispasmodics – mebeverine / hyoscine 2nd line: tricyclic antidepressant – low dose amitriptyline (5-10mg) Constipation 1st line: Laxative (NOT lactulose – worsens bloating) Linaclotide if > 12 months of severe constipation Diarrhoea Loperamide:1st Line antimotility agent for diarrhoea in IBS. Reduce fibre intake Reduce caffeine, carbonated drinks Other strategies Trial low FODMAP diet CBT

Question 27

Coeliac Disease & IBS Coeliac disease Pathophysiology A chronic autoimmune disease of the GIT. Exposure to gluten results in villus atrophy, resulting in malabsorption Clinical features The most common age of diagnosis is 40-60 years of age, though symptoms can present at any age. Diarrhoea Abdominal bloating/distension Features of malabsorption Failure to thrive in children Symptoms of anaemia, TATT

Answer 27

Associations HLA-DQ2 [95%] Dermatitis herpetiformis Type 1 diabetes mellitus Complications Folate, B12, iron deficiency --> anaemia Hyposplenism Osteoporosis Investigations 1st line: IgA anti-TTG antibodies (IgA levels must be co-measured as deficiency could result in false negative). Other: IgA anti-EMA antibodies Duodenal (or jejunal) biopsy: Villous atrophy, lymphocytic infiltrates Management 1st line: Gluten free diet Other: Pneumococcal vaccine every five years due to functional hyposplenism

Question 28

Constipation in Adults Clinical Features Infrequent bowel movements (fewer than 3 times a week) Straining during defecation Hard or lumpy stools Sensation of incomplete evacuation Management Short-duration constipation (less than 3 months) Investigate and address underlying causes – e.g. medication-induced, secondary conditions. Lifestyle measures: Increase dietary fibre Ensure adequate fluid intake Increase physical activity 3. Phramacological management: 1st line: Bulk-forming laxatives (e.g. ispaghula) – ensure adequate hydration. 2nd line: If stools remain hard, add/switch to an osmotic laxative (e.g. macrogol). If macrogol is ineffective or not tolerated, offer lactulose. If stools are soft but difficult to pass: Add a stimulant laxative (senna).

Answer 28

Chronic constipation (> 3 months) Investigate secondary causes and manage similarly with a stepped approach. Further management considerations: Opioid-induced constipation: Avoid bulk-forming laxatives. Use osmotic laxative and stimulant laxative (or docusate). Faecal Impaction: Hard stools: Start with high-dose macrogol, add stimulant if needed. Soft stools: Consider bisacodyl suppository or mini enema if oral treatment fails.

Question 29

Gastrointestinal Infections Gastroenteritis Inflammation of the lining of the stomach and intestines, most commonly of infectious aetiology. Clinical features Abdominal pain Vomiting Diarrhoea Fever Flu-like symptoms

Answer 29

Common causes and exam ‘buzzwords’ E.Coli Most common cause of traveller’s diarrhoea Key features: Common, loose/watery stools +/- crampy abdominal pain Giardiasis Key features: Prolonged history of greasy diarrhoea associated with flatulence. Non-bloody. Cholera Key features: Uncommon in travellers. Associated with significant watery diarrhoea with resultant severe dehydration. Shigella Key features: Bloody diarrhoea Amoebiasis Key features: Bloody diarrhoea, classically associated with formation of a liver abscess – RUQ pain, fever, deranged LFTs. Staphylococcus aureus Key features: Severe vomiting with short incubation period after eating contaminated food Campylobacter jejuni Key features: History of uncooked poultry (e.g. BBQ) flu-like prodrome, followed by cramping abdominal pain, pyrexia and loose stools which (may be bloody). Management: If severe/immunocompromised - clarithromycin Bacillus Cereus Key features: After eating reheated/ takeaway rice – vomiting < 6 hours, or diarrhoea > 6hrs

Question 30

Clostridium Difficile Pathogen Gram positive rod Releases exotoxins causing pseudomembranous colitis Clinical features History of recent antibiotics (esp. cephalosporins, clindamycin), PPIs Abdominal pain, distension, foul-smelling watery diarrhoea, can result in toxic megacolon Investigation C. diff stool TOXIN (NOT antigen testing)

Answer 30

Management (guidance updated June ‘23): First episode of mild, moderate or severe c.diff: 1st line: PO Vancomycin 125mg QDS (10 days) 2nd line: PO Fidaxomicin 200mg BD (10 days) If considered life-threatening, specialist may offer: PO Vancomycin + IV metronidazole Further episodes of c.diff Within 12 weeks of symptom resolution (relapse): PO Fidaxomicin More than 12 weeks of symptom resolution (recurrence): PO Fidaxomicin OR Vancomycin

Question 31

Small Bowel Bacterial Overgrowth Syndrome (SBBOS) Clinical features Diarrhoea, flatulence Abdominal pain and bloating Typical risk factors: scleroderma, diabetes mellitus, GI malformations

Answer 31

Investigations Initial test: H+ breath test Gold standard: Small bowel aspirate + culture Management Antibiotics - Typically rifaximin Alternatives: co-amoxiclav/metronidazole

Question 32

Whipples Pathogen: Tropheryma Whippelei Risk factors: HLA-B27 predisposition Clinical features - A multi-system disorder with symptoms of: Malabsorption (weight loss) Arthralgia Pleurisy and pericarditis (chest pain) Lymphadenopathy

Answer 32

Investigation: Jejunal biopsy – deposition of macrophages with periodic acid-schiff (PAS) granules, and villous atrophy Management: Prolonged course of antibiotics - Commonly IV penicillin followed by PO co-trimoxazole for 1 year

Question 33

Tropical Sprue Infection results in small bowel malabsorption Investigation: Jejunal biopsy shows villous atrophy with mononuclear cell infiltrates

Answer 33

Treatment: 6 months of tetracyclines + treat B12/folate deficiencies

Question 34

Giardiasis Pathogen: Protozoan Giardia Lamblia Clinical features: Bloating Chronic greasy diarrhoea (non-bloody) Malabsorptive symptoms

Answer 34

Giardiasis Pathogen: Protozoan Giardia Lamblia Clinical features: Bloating Chronic greasy diarrhoea (non-bloody) Malabsorptive symptoms Investigation: String test- a string containing capsule is swallowed whilst tied proximally to cheek. After 4-6 hours it can be pulled back up and sent for MCS. Management: Metronidazole

Question 35

H.Pylori Pathophysiology A gram negative bacteria which burrows into the mucosa of the stomach. Produces ammonia, proteases and cytotoxins which results in gastritis and the formation of gastroduodenal ulcers. Complications Peptic ulcer disease (Duodenal ulcers (95%) > gastric ulcers) Gastric cancer Gastric B cell MALT lymphoma

Answer 35

Investigations Urea breath test – patient must avoid antibiotics for 4 weeks and PPI for 2 weeks prior The patient consumes a drink containing 13C urea The H. pylori urease metabolises this into 13CO2 which can be measured in breath Sensitivity 95%, specificity 98% Can be used to check for successful eradication of HP CLO test – biopsy sample is mixed with urea Gold standard - Gastric biopsy with culture Management: 7 day course of: (1) PPI + (2) Amoxicillin + (3) Metronidzole or clarithromycin Pen allergic: PPI + Metronidazole + Clarithromycin

Question 36

Gilbert's Disease There are 4 main causes of inherited jaundice Unconjugated: Gilbert's syndrome, Crigler-Najjar Syndrome Conjugated: Dubin-Johnson syndrome, Rotor syndrome Inheritance: All 4 – Autosomal recessive

Answer 36

Gilbert's syndrome Pathophysiology: Mild deficiency in UDP-glucuronyl transferase (UDP-GT) Prevalence: 1% population Presentation: Jaundice during illness. Investigations: Bilirubin - not in urine (unconjugated) Diagnosis: Increased bilirubin after fasting or IV nicotinic acid

Question 37

Inflammatory Bowel Disease Crohn’s disease and ulcerative colitis are chronic inflammatory diseases of the gastrointestinal tract, of autoimmune aetiology. Crohn's disease Pathology The whole gastrointestinal tract can be affected – mouth to anus Transmural - all layers of bowel wall Skip lesions present Worst disease in terminal ileum Clinical features Weight loss Abdominal pain - typically RIF Mouth ulcers O/E: Right iliac fossa mass, perianal disease (ulcers/tags)

Answer 37

Investigations Stool – elevated faecal calprotectin Bloods Anaemia, Low B12 (due to involvement of terminal ileum) Elevated CRP/WCC during flare Endoscopy: Cobblestone appearance due to the combination of skip lesions with intermittent deep ulcers Histology: Transmural inflammation with granulomas and increased goblet cells Management Flare: First line: Glucocorticoids +/- consider enteral feeding with elemental diet. Second line: 5 ASA (mesalazine) Maintaining remission First line: azathioprine or mercaptopurine – assess TPMT first Second line: methotrexate Consider infliximab for refractory disease Surgery - Stricturing terminal ileal disease often requires ileocecal resection

Question 39

Crowns complication

Answer 39

Complications Obstruction secondary to adhesions, fistulas GI malignancy: Small bowel cancer – RR 40, colorectal cancer – RR 2 Osteoporosis (steroid use, vitamin D deficiency) Perianal disease - Metronidazole may help

Question 40

Ulcerative colitis Pathology Inflammation most commonly starts at the rectum and works its way proximally. Inflammation is continuous (NO skip lesions)and never passes proximally to the ileocecal valve Clinical features Bloody diarrhoea Left iliac fossa pain Tenesmus Complications Colorectal cancer Primary sclerosing cholangitis RUQ pain, obstructive jaundice, pruritus

Answer 40

Investigations Barium enema: loss of haustra with a drainpipe appearance of colon Endoscopy: Pseudopolyps, mucosa is raw in appearance and bleeds easily Histology: SUB MUCOSAL inflammation with reduced goblet cells and crypt abscesses present Managing Flares Classifying Severity Mild: < 4 stools/day, systemically well Moderate 4-6 stools/day Severe: > 6 stools /day with blood +/- pyrexia, tachycardia, abdominal pain, anaemia Management of mild-moderate flare - Depends on the site of inflammation Proctitis: topical aminosalicylate (e.g. rectal mesalazine) Extensive disease: Topical ASA + PO ASA 1st line If ineffective, consider PO ASA and PO Steroids

Question 41

uC severe flare

Answer 41

Management of Severe flare Admit to hospital for intravenous steroids If there's no improvement add intravenous ciclosporin or consider surgery Maintaining remission ASA are 1st line (mesalazine/sulphasalazine). PO if extensive disease. Topical if distal. Severe relapse or more than two flares in one year - oral azathioprine or mercaptopurine Risk of colorectal cancer Colonoscopy surveillance should be performed for all patients (crohn’s and UC), the frequency of which dependens on risk stratification

Question 43

Extra-intestinal features of IBD include… Oligoarthritis Erythema nodosum Episcleritis, uveitis Primary sclerosing cholangitis Pyoderma gangrenosum

Answer 43

Extra-intestinal features of IBD include… Oligoarthritis Erythema nodosum Episcleritis, uveitis Primary sclerosing cholangitis Pyoderma gangrenosum

Question 44

Amoebiasis Cause Entamoeba Histolytica (protazoan, faeco-oral transmission) - 10% of the world are chronically infected Can cause dysentry, liver abscess Amoebic dysentery Presentation: profuse bloody diarrhoea Stool microscopy: trophozoites (stool sample is required) Management: metronidazole

Answer 44

Amoebic Liver Abscess Typically affects the right lobe of the liver Presentation: fever, right upper quadrant pain O/E: Mass in RUQ – on drainage contents are classically described as ‘anchovy sauce’ like in nature Investigations: serology positive for amoebiasis Management: Drainage and ABx Following treatment of amoebiasis, it is important to give a luminal amoebicide to get eradicate cysts which are resistant to metronidazole

Question 45

Liver abscesses Most common causative organisms Children- Staphylococcus aureus Adults- E.Coli Amoebiasis – suggested by history of bloody diarrhoea

Answer 45

management IV Cefotaxime Prophylaxis Consider if ascites AND either: Previous SBP or Ascitic protein < 15g/l / HRS / Child Pugh > 9 Prophylactic Abx – oral ciprofloxacin/norfloxacin

Question 46

Spontaneous Bacterial Peritonitis Bacterial infection of the ascitic fluid within the peritoneum Diagnosis Ascitic tap – neutrophil count > 250cells/uL Causative organism: In ALD the most common cause is E. Coli Nb. – in peritoneal dialysis related SBP the most common is staphylococcus epidermidis

Answer 46

management IV Cefotaxime Prophylaxis Consider if ascites AND either: Previous SBP or Ascitic protein < 15g/l / HRS / Child Pugh > 9 Prophylactic Abx – oral ciprofloxacin/norfloxacin

Question 47

Hepato-renal syndrome Definition A severe complications of advanced liver cirrhosis associated – high mortality rate

Answer 47

Pathophysiology Vasoactive mediators released in liver disease cause splanchnic vasodilation which decreases effective circulating volume and results in renal hypoperfusion. The juxtaglomerular apparatus increases activation of RAAS in response resulting in: Systemic and renal vasoconstriction --> HRS Renal sodium avidity --> worsening ascites

Question 48

Ascites Classification of ascites: The SAAG or Serum: Ascites Albumin Gradient. SAAG > 1.1g/dl = Portal hypertensive ascites SAAG < 1.1 = Non portal hypertensive ascites Causes of portal hypertensive ascites (SAAG > 1.1) Liver cirrhosis Alcoholic hepatitis Acute liver failure Budd chiari / portal vein obstruction Spontaneous bacterial peritonitis (SBP) Heart failure

Answer 48

Causes of NON portal hypertensive ascites (SAAG < 1.1) Nephrotic syndrome Hepato-renal syndrome Protein losing enteropathies Peritoneal carcinoma or TB

Question 49

Hepatic Encephalopathy Pathophysiology Cerebral accumulation of toxins, including ammonia + glutamine, cerebral oedema occurs. Clinical features

Answer 49

Clinical features Confusion Drowsiness Agitation, personality changes Myoclonus Constructional apraxia (e.g. unable to draw a 5-point star) Management 1st Line: Lactulose Other treatments: Rifaximin, phosphate enemas

Question 51

Complications of Liver Cirrhosis Oesophageal Varices Management of Acute Variceal Bleed A-E, FFP + Vit K Terlipressin - arteriolar vasoconstriction in splanchnic circulation, reducing portal/collateral blood flow IV antibiotics – quinolones commonly used Endoscopy – variceal band ligation Other management options Sengstaken-Blakermore tube TIPPS – a last resort – classically complicated by hepatic encephalopathy

Answer 51

Prophylaxis Patients with oesophageal varices should be managed with: Beta-blockers – Propranolol Endoscopic variceal band ligation with PPI

Question 52

Wilson’s Disease Genetics Autosomal recessive - mutation on ATP7B gene on chromosome 13 Mnemonic: Wilson is ATP – At The Pub on his 13th Pint Pathophysiology The ATP7B gene controls the protein transporter facilitating copper excretion into bile, and out of the body. Impaired excretion results in copper accumulation. Excess copper deposits around the body, especially within the brain (basal ganglia), liver and cornea.

Answer 52

Clinical features Classically a young patient (teens to early thirties) with neurological disease and signs of liver disease. Signs include: Neurological: parkinsonism (basal ganglia deposition) chorea, ataxia, dementia, tremor, dysarthria, personality changes Liver: cirrhosis, ascites, jaundice, pruritus, hepatitis Blue nails, Keyser-flesher rings Investigations Reduced serum caeruloplasmin (a ferroxidase enzyme which is the major copper-carrying protein in blood)s Reduced total copper levels (due to reduced serum caeruloplasmin) Increased 24-hour urinary excretion of copper Management Penicillamine, trientine - copper chelating agents

Question 53

Non-alcoholic fatty liver disease Pathophysiology Steatosis - excess fat accumulation within the liver Can result in non-alcoholic steatohepatitis (NASH), where fatty infiltration co-exists with inflammation. NASH can lead to cirrhosis. Occurs in the context of metabolic syndrome/insulin resistance. Clinical features Suspect in patients with persistent elevation of ALT for > 3/12 in the absence of excess alcohol (ALT > AST) Associations: T2DM/ obesity/ dyslipidaemia are suggestive in question vignette

Answer 53

Diagnosis NICE - use 1st line non-invasive tool to assess level of fibrosis Fibrosis-4 (FIB-4) score NAFLD fibrosis score (NFS) Other - Enhanced liver fibrosis test Imaging: Ultrasound is 1st line Specialist/secondary care invx may include: Fibroscan (transient elastography) Biopsy is gold standard Management Lifestyle advice – weight loss, dietary advice, exercise, improve diabetic control etc.

Question 55

Liver Cirrhosis Causes Alcoholic liver disease (ALD) Non-alcoholic fatty liver disease (NAFLD) Viral hepatitis – hepatitis C & B Investigations Bloods - Deranged LFTs, raised INR, thrombocytopenia, hypoalbuminaemia Screening for cirrhosis: Fibroscan (transient elastography) +/- biopsy confirmation Further investigations: OGD 6 monthly US abdomen +/- AFP – HCC screening

Answer 55

Prognostication Child Pugh Scoring Classifies cirrhosis according to its severity from A to C. Calculated from ABCDE = Albumin, Bilirubin, Clotting (PT), Drainable (ascites), Encephalopathy MELD score Determines the risk mortality. Criteria includes bilirubin, creatinine, INR

Question 56

Acute liver failure

Answer 56

Acute liver failure Key features: decompensated liver disease (jaundice, encephalopathy, ascites etc.) Common causes of ALF Paracetamol overdose Alcohol access Viral hepatitis (hepatitis A/ hepatitis B) Acute fatty liver of pregnancy

Question 57

Alcoholic hepatitis Causes: Prolonged alcohol abuse, or a return to alcohol use following abstinence Labs: AST > ALT Reduced liver synthetic function (INR/Plts/Albumin) Management: Glucocorticoids can be used if indicated according to Maddrey’s discriminant function

Answer 57

Ischaemic hepatitis Pathophysiology: Acute hypoperfusion of the liver. Often associated with AKI/ end organ damage Causes: septic shock, cardiac arrest Labs: AST/ALT significantly raised – often > 1000

Question 58

Hepatomegaly and Hepatosplenomegaly Hepatomegaly Liver malignancy/ metastasis – Hard, irregular edge Right heart failure- tender, smooth edge +/- Pulsatile Other causes: Abscess/ haemochromatosis/ PBC/ infection/ malignancy Hepatomegaly + Dupytren’s + Parotitis = Alcoholic liver disease Hepatosplenomegaly Liver cirrhosis with portal hypertension Lymphoma/ leukaemia Infections: Epstein Barr virus/ hepatitis/ malaria Amyloidosis

Answer 58

Alcoholic Liver Disease Definition: A spectrum of liver disease occurring secondary to alcohol excess including alcoholic fatty liver disease, alcoholic hepatitis, alcoholic liver cirrhosis Labs AST: ALT ratio > 2 (if > 3 suggests acute alcoholic hepatitis) GGT is typically raised

Question 62

Malignancies - Lower GIT Colorectal cancer Colorectal cancer (CRC) is the 3rd most common cancer in the UK (following breast and lung), it is the 2nd most common cause of cancer deaths. Pathophysiology Adenocarcinoma most common – rectal adnenocarcinoma (40%), sigmoid (30%) Most cases of colorectal cancer arise from adenomatous polyps which undergo malignant transformation. Screening can identify these polyps, enabling excision prior to transformation Sporadic CRC 95% of cases. Caused by a series of genetic mutations. APC TSG most common, K-ras, P53, DCC

Answer 62

Hereditary non-polyposis colorectal cancer (Lynch syndrome) 5% of cases of CRC Inheritance: Autosomal dominant Mutation: DNA mismatch repair genes – most commonly MSH2 (60% cases) 90% develop malignancies – proximal CRC or endometrial carcinoma Consider a diagnosis of HNPCC according to the Amsterdam criteria (3, 2, 1) 3 or more family members have a diagnosis of CRC.. Across 2 generations.. With 1 or more at < 50 yrs age

Question 63

Malignancies - Lower GIT Colorectal cancer Colorectal cancer (CRC) is the 3rd most common cancer in the UK (following breast and lung), it is the 2nd most common cause of cancer deaths. Pathophysiology Adenocarcinoma most common – rectal adnenocarcinoma (40%), sigmoid (30%) Most cases of colorectal cancer arise from adenomatous polyps which undergo malignant transformation. Screening can identify these polyps, enabling excision prior to transformation Sporadic CRC 95% of cases. Caused by a series of genetic mutations. APC TSG most common, K-ras, P53, DCC

Answer 63

Hereditary non-polyposis colorectal cancer (Lynch syndrome) 5% of cases of CRC Inheritance: Autosomal dominant Mutation: DNA mismatch repair genes – most commonly MSH2 (60% cases) 90% develop malignancies – proximal CRC or endometrial carcinoma Consider a diagnosis of HNPCC according to the Amsterdam criteria (3, 2, 1) 3 or more family members have a diagnosis of CRC.. Across 2 generations.. With 1 or more at < 50 yrs age

Question 64

Familial adenomatous polyposis <1% cases Inheritance: Autosomal dominant Mutation: APC gene - TSG on chromosome 5 Management: Preventative total colectomy with ileo-anal pouch during 20’s Associated with Gardeners syndrome: FAP, osteomas of the skull, epidermoid cysts, retinal pigmentation, thyroid cancer

Answer 64

Screening for colorectal cancer The current CRC screening program in the UK consists of a combination of faecal immunochemical testing (FIT test) + a one-off flexible sigmoidoscopy FIT Who? Men and women aged 60-74 years When? Every 2 years send 1 sample Positive FIT: Invitation for colonoscopy 50% of those scoped are normal, 40% polyps, 10% have CRC Flexible sigmoidoscopy Who? Invitation at 55 years (can accept up to age 60) One off flexi-sig to identify and remove polyps to reduce malignant transformation

Question 65

Suspected lower GI cancer NICE updated their guidance in August 2023 to include FIT testing. Step 1: Check FIT Step 2: Refer for 2WW suspected cancer pathway if they have a FIT result of at least 10 micrograms of haemoglobin per gram of faeces. NICE advises: Offer faecal immunochemical testing (FIT) to guide referral for suspected colorectal cancer in adults:

Answer 65

with an abdominal mass or with a change in bowel habit or with iron-deficiency anaemia or aged 40 and over with unexplained weight loss and abdominal pain or aged under 50 with rectal bleeding and either of the following unexplained symptoms: abdominal pain weight loss or aged 50 and over with any of the following unexplained symptoms: rectal bleeding abdominal pain weight loss or aged 60 and over with anaemia even in the absence of iron deficiency. People with a rectal mass, an unexplained anal mass or unexplained anal ulceration do not need to be offered FIT before referral is considered. Refer adults using a 2WW/suspected cancer referralif FIT is 10 micrograms of haemoglobin per gram of faeces or more. If FIT is < 10, safety net and consider referral to secondary care if ongoing strong clinical concern of cancer.

Question 66

Management lower git malignancy Surgical excision Chemotherapy – 5-fluorouracil +/- oxiplatin is a common regimen Monitoring: CEA levels can monitor treatment response or identify recurrence Associated conditions

Answer 66

Associated conditions Peutz-Jeghers syndrome Inheritance: Autosomal dominant Mutation: STK11 (LKB1) gene Key Features Characteristic freckles on face/lips/palms and soles of feet Development of many hamartomatous polyps in GIT Complications Intussusception GI bleeding 50% mortality by age 60 due to gastrointestinal malignancy

Question 67

NICE. Quantitative faecal immunochemical testing to guide colorectal cancer pathway referral in primary care. [August 2023]

Answer 67

Cowden’s syndrome Mutation: PTEN tumour suppressor gene Key Features: Development of hamartomatous polyps within the GIT Mucocutaneous lesions including oral mucosal papillomas, palmoplantar keratosis, trichilemmomas Thyroid dysfunction NICE. Gastrointestinal tract (lower) cancers - recognition and referral:Scenario: Referral for suspected gastrointestinal tract (lower) cancer. Available

Question 68

Malignancy upper git

Answer 68

Malignancies - Upper GIT Referral guidance for suspected cancer (2WW) Suspected gastric/Oesophageal cancer Refer patients for a 2 week wait appointment including OGD if they fulfil the following Dysphagia (any age) Age > 55 years with weight loss and one of the following: Upper abdominal pain Reflux Dyspepsia Upper abdominal mass Consider non-urgent referral for patients who are > 55 years and present with Treatment resistant dyspepsia IDA + upper abdominal pain Thrombocytosis + upper GI symptoms Nausea/vomiting + dyspepsia or weight loss Haematemesis

Question 69

Suspected gallbladder/liver cancer Refer patients for a 2 week wait appointment including abdominal US if Palpable gallbladder Palpable liver mass

Answer 69

Suspected pancreatic cancer Refer patients for a 2 week wait appointment if Age > 40 years with jaundice Age > 60 years with weight loss and one of the following: Abdominal/back pain Persistent nausea/vomiting New diagnosis of diabetes mellitus Constipation or diarrhoea/steatorrhoea

Question 70

Oesophageal cancer Pathophysiology Adenocarcinoma of lower 1/3rd oesophagus - most common in the UK Squamous cell carcinoma of upper 2/3rds oesophagus - more common in the rest of the world Clinical features Dysphagia, anorexia, weight loss etc.

Answer 70

Investigations 1st line: OGD + biopsy Staging: CT-TAP Nb. For local staging – endoscopic US is more reliable, providing accurate information about tumour invasion depth and lymph node involvement Management Surgery – e.g. Ivor-Lewis oesophagectomy

Question 71

Figure 144: Barium swallow X-ray film- oesophageal malignancy (‘Bird beak’ appearance). Netha Hussain, Barium swallow of malignancy oesophagus 01, CC BY-SA 3.0 Gastric cancer Pathophysiology Adenocarcinomas most common Histology Signet ring cell appearance Risk factors: Lifestyle: Smoking, Salty/spicy diets PMHx: Pernicious anaemia, H. pylori infection

Answer 71

Clinical Features Dyspepsia, weight loss, dysphagia, nausea/vomiting Investigations 1st line: OGD + biopsy 2nd line: Staging – endoscopic US > CT for local staging, CT TAP Gastric MALT lymphoma Gastric mucosa associated lymphoid tissue (MALT) lymphoma is most commonly associated with H.pylori infection (accounting for 95% of cases). Management If H.pylori associated, then eradication of H pylori is 1st line resulting in regression in 80% of cases.

Question 72

VIPoma Pathophysiology A tumour with autonomous secretion of VIP, 90% pancreatic in origin High VIP results in low gastric acid secretion, and increased pancreatic secretions

Answer 72

Clinical Features Large volume diarrhoea, dehydration, and weight loss Labs Hypochlorhydria Hypokalaemia

Question 73

Zollinger-Ellison Pathophysiology Zollinger-Ellison syndrome occurs in the presence of a gastrinoma – a tumour with autonomous secretion of gastrin resulting in high levels of gastric acid 30% of cases occur in the context of MEN1 (3Ps - hPTH, pituitary, pancreatic) Clinical Features

Answer 73

Multiple gastro-duodenal ulcers Epigastric pain, diarrhoea, malabsorption Investigations First line: Fasting gastrin levels Alt: Secretin stimulation test (secretin normally suppresses gastrin) Management Surgery If non-operable: Octerotide + IFN + Chemotherapy

Question 74

Hepatocellular Carcinoma HCC is the 3rd most common cancer worldwide Causes Hepatitis B - commonest cause in the world Hepatitis C - commonest cause in Europe Clinical features Decompensated liver disease - jaundice, ascites Right upper quadrant pain Weight loss Hepatomegaly with irregular, hard liver border Screening

Answer 74

Patients at risk of HC should have regular screening (every 6 months) with US abdomen + AFP Indications: hepatitis B, hepatitis C, Alcoholic liver cirrhosis, haemochromatosis, primary sclerosing cholangitis Management Surgery, transplant Medication: Sorafenib (multikinase inhibitor)

Question 75

Pancreatic cancer Pathophysiology Adenocarcinoma of the head of the pancreas account for the majority of cases Clinical Features Painless jaundice New onset diabetes Steatorrhoea – impaired exocrine function Palpable gall bladder in the context of painless jaundice is not secondary to gallstones - Courvoisier’s law Trousseau's migratory thrombophlebitis

Answer 75

Investigations 1st line: CT pancreas - investigation of choice “double-duct sign” - dilatation of the CBD and pancreatic ducts Other: US abdomen Bloods: Ca-19-9 Management 80% inoperable - Palliative stenting may be considered Surgery inc. whipple's procedure (pancreaticoduodenectomy)

Question 76

Malnutrition in Adults Key learning Definition: BMI < 18.5, BMI < 20 with >5% weight loss in 3-6 months, or >10% weight loss in 3-6 months. Causes: Older adults, self-neglect/low mood, malabsorption (e.g., chronic pancreatitis, liver cirrhosis, Coeliac disease), anorexia nervosa. Screening: MUST score on hospital admission Management: Admit if severe electrolyte imbalance, monitor for re-feeding syndrome, address underlying causes, and consider safeguarding for neglect concerns.

Answer 76

Definition Any one of: BMI < 18.5 BMI < 20 and unintentional weight loss > 5% in last 3-6 months Unintentional weight loss > 10% over 3-6 months Causes Often older adults Self-neglect/low mood- poor dietary intake Malabsorption- i.e. chronic pancreatitis, liver cirrhosis, Coeliac disease Anorexia nervosa Screening MUST score completed on hospital admission for adults Risk-stratifies patients based on: BMI Recent weight loss Effect of acute disease High risk patients can then be highlighted at an early stage during hospital stay

Question 77

Malnutrition in Adults

Answer 77

Investigations Low WCC Low albumin Decreased electrolytes/urea Vitamin deficiencies i.e. B12, D Management Admit if severe electrolyte derangement- start slow and monitor for re-feeding syndrome Patient education to adapt diet Dietician support if high-risk- want to increase food as opposed to purely oral nutritional supplements Safeguarding if concerned r.e. neglect Treat underlying cause i.e. gluten free diet in Coeliac disease

Question 78

Melanosis coli Melanosis coli is a benign condition identified by dark pigmentation of the colonic mucosa, typically resulting from prolonged use of anthraquinone-containing laxatives, such as senna (including cases of laxative abuse). Aetiology Chronic use of anthraquinone laxatives (senna) leads to the accumulation of pigment-laden macrophages in the colon, causing the characteristic pigmentation.

Answer 78

Clinical features Often asymptomatic - often discovered incidentally during colonoscopy. The pigmentation is typically diffuse, ranging from light brown to black, affecting all or part of the colon. May present with diarrhoea due to laxative abuse. There may be a history of eating disorder/bulimia. Management Discontinue offending laxative. Reassure - benign nature, no malignant potential.

Question 79

Microscopic colitis Microscopic colitis is a condition characterised by chronic, watery diarrhoea without visible abnormalities on colonoscopy. Clinical Features A triad of: Watery diarrhoea Normal colonoscopy (hence microscopic) Inflammation of the lamina propria on biopsy with intraepithelial lymphocytosis. Causes The exact cause of microscopic colitis is unknown, but several factors may contribute, including: Autoimmune disorders Drugs - NSAIDs, PPIs, SSRIs Infections

Answer 79

Diagnosis Colonoscopy - normal Biopsy - microscopic changes - inflammation of the lamina propria on biopsy with intraepithelial lymphocytosis Management Stop causative medications. Most commonly.. PPIs NSAIDs Cimetidine Steroids - Budesonide is commonly used 1st line for moderate-severe cases

Question 80

Oesophageal Disorders Achalasia Pathophysiology Achalasia is caused by degeneration of the ganglia of Auerbach’s plexus, with two main consequences: Loss of oesophageal peristalsis – the oesophagus becomes dilated Increased tone at the LOS – unable to relax and allow food to pass into stomach

Answer 80

Clinical Features Dysphagia to both solids and liquids which classically develops simultaneously, from the onset Regurgitation Investigation 1st line: Oesophageal manometry – increased LOS tone Barium swallow: “birds beak” appearance +/- a fluid level within a dilated oesophagus Management Pneumatic balloon dilatation is commonly used first line Alternatives: Heller cardiomyotomy Botox - esp. in patients considered at high risk of surgical complications

Question 81

Pharyngeal pouch Pathophysiology Posteromedial herniation of the pharynx through Killian’s dehiscence (a triangular area of weakness in the wall of the pharynx located between the cricopharyngeus and thyropharyngeus). Clinical features

Answer 81

Clinical features Chronic cough Halitosis Regurgitation May have a history of aspiration +/- pneumonia On examination – a midline “gurgling” lump might be present if the pouch is large Management Surgery

Question 82

Eosinophilic oesophagitis Pathophysiology Allergic inflammation of the oesophagus Clinical features Risk factors: Atopy Dysphagia and vomiting Investigations Bloods: Eosinophilia Endoscopy: oesophageal strictures – biopsy of which demonstrates eosinophilc infiltrates

Answer 82

Management 1st line: Dietary modification 2nd line: Topical steroids if dietary modification alone does not improve symptoms

Question 83

Plummer-vinson Plummer–Vinson syndrome describes the formation of an oesophageal web above the aortic arch as a result of iron deficiency in women. The condition is premalignant and can lead to the development of carcinoma in the cricopharyngeal region. Clinical Features: A triad of: Dysphagia caused by the presence of oesophageal webs Iron deficiency anaemia Glossitis (plus koilonychia, angular stomatitis etc.)

Answer 83

Management: Iron replacement (e.g. ferrous sulphate) improves the anaemia, which improves the web. If symptoms do not improve adequately with iron, balloon dilatation of the web may be required

Question 84

Oesophagitis Presents with odynophagia (pain is a key), but otherwise well with no significant weight loss. Might be associated with a history of or reflux/GORD.

Answer 84

Oesophageal candidiasis Clinical features Immunosuppression - HIV, steroid inhaler use

Question 85

Systemic sclerosis Clinical features Calcinosis Raynaud’s Esophageal dysmotility Sclerodactyly Telangiectasias

Answer 85

Globus Hystericus Clinical features Suggested by a history of anxiety Dysphagia is painless and symptoms may come and go. Systemically well.

Question 86

Oesophageal cancer Unintentional weight loss Progressive dysphagia

Answer 86

Boerhaave’s syndrome Boerhaave’s syndrome follows an episode of severe retching or vomiting which results in a complete transmural oesophageal rupture. This most commonly affects the left lower oesophagus. CXR: pneumomediastinum Urgent surgical management required.

Question 87

Mallory-Weiss Severe retching/vomiting results in painful tears in the mucosa of the gastro-oesophageal junction (GOJ) Clinical features: Haematemesis

Answer 87

GORD Indications for UGI endoscopy = ALARMS A - Age > 55 at onset L - Loss of weight A - Anaemia (IDA) R - Relapsing symptoms (>4 weeks) / Resistant to treatment M - Melaena S - Swallowing difficulty (dysphagia) Investigations If OGD if negative consider 24-hour oesophageal pH monitoring (gold standard)

Question 88

Barrett’s oesophagus Pathology Barrett’s describes the metaplasia of the lower oesophageal mucosa from squamous epithelium to columnar epithelium Complications Risk of oesophageal adenocarcinoma = up to 100x increased Management

Answer 88

Management Endoscopic surveillance Metaplasia – repeat OGD every 3-5 yrs Dysplasia – endoscopic intervention – resection/radiofrequency ablation High dose PPI

Question 89

Peptic Ulcer Disease Key learning Collectively gastric and duodenal ulcers are known as peptic ulcer disease Most common causes are H.pylori infection and NSAID use Gastric ulcers worse on eating, duodenal improves with eating If H.pylori confirmed then triple therapy

Answer 89

Pathophysiology Breach in epithelium of gastric or duodenal mucosa Epidemiology Present in 13% of those with dyspepsia who undergo endoscopy 90% duodenal ulcers 75% gastric ulcers Risk factors Most commonly due to Helicobacter pylori infection Drugs- NSAIDs use, aspirin, SSRI, steroids, bisphosphonates Smoking Alcohol Stress Zollinger-Ellison syndrome- see separate note Hypersecretory state associated multiple peptic ulcers, weight loss, hypercalcaemia

Question 90

Clinical Features Dyspepsia Reflux Nausea and vomiting Epigastric pain Gastric ulcer- exacerbated by eating Duodenal ulcer- relieved by eating

Answer 90

Investigations Test for H/pylori Carbon-13 urea breath test of stool antigen test False negatives if taken PPI in previous 2 weeks or antibiotics in past 4 weeks Peptic ulcer confirmed through endoscopy Management General: Lifestyle modification- weight loss, avoid trigger foods, stop smoking, reduce alcohol Address stressors Medication review- ideally stop offending medications (commonly NSAIDs or aspirin)

Question 91

Specific: If H.pylori positive: Eradication therapy for 7 days (PPI and 2 antibiotics- commonly amoxicillin and clarithromycin or metronidazole) If H/pylori positive and NSAID use: Full dose PPI for 2 months followed by H.pylro eradication therapy If H.pylori negative but proven peptic ulcer on endoscopy: Full dose PPI for 4-8 weeks If gastric ulcer confirmed on endoscopy: Repeat endoscopy and re-testing of H.pylori 6-8 weeks after commencing treatment For all: Offer long term as required low dose PPI or standard dose histamine receptor antagonist (H2RA)

Answer 91

Complications Risk of recurrence 80% if remains H.pylori positive or 5% following eradication GI haemorhage- 10% mortality GI perforation - 25% mortality Gastric outlet obstruction Gastric malignancy- increased risk in H.pylori positive gastric ulcer disease

Question 92

Short bowel syndrome Short Bowel Syndrome (SBS) is a malabsorption disorder resulting from significant surgical resection of the small intestine, leading to nutrient, fluid, and electrolyte deficiencies. Aetiology Significant surgical resections (typically > 50% of small bowel) due to Crohn's disease, mesenteric ischemia, trauma, malignancies, or congenital defects like volvulus and necrotising enterocolitis in neonates. Clinical features Chronic diarrhoea +/- steatorrhea Malnutrition, weight loss, dehydration Anaemia Electrolyte imbalances

Answer 92

Management Nutritional Support >100 cm remaining Small Intestine: Patients may manage with oral intake adjustments, including a high-calorie, high-protein, low-fat diet, and supplementation with vitamins and minerals. <100 cm remaining Small Intestine: Total parenteral nutrition (TPN) is often necessary to meet nutritional needs and manage fluid and electrolyte balance. Medication: Anti-diarrhoeal agents, PPIs, bile acid sequestrants can help manage symptoms. Glucagon-like peptide-2 analogues (e.g., teduglutide) can enhance intestinal absorption. Surgical Interventions: Bowel lengthening or intestinal transplantation may be considered.

Question 100

NICE. Quantitative faecal immunochemical testing to guide colorectal cancer pathway referral in primary care. [August 2023]

Answer 100

Cowden’s syndrome Mutation: PTEN tumour suppressor gene Key Features: Development of hamartomatous polyps within the GIT Mucocutaneous lesions including oral mucosal papillomas, palmoplantar keratosis, trichilemmomas Thyroid dysfunction NICE. Gastrointestinal tract (lower) cancers - recognition and referral:Scenario: Referral for suspected gastrointestinal tract (lower) cancer. Available