Gastrointestinal

Question 1

Define achalasia

Answer 1

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

Question 2

Explain the aetiology / risk factors of achalasia

Answer 2

Degeneration of ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause.

Oesophageal infection with Trypanosoma cruzi seen in Central and South America produces a similar disorder (Chagas’ disease).

Question 3

Summarise the epidemiology of achalasia

Answer 3

Annual incidence: 1 in 100000.

Usual presentation age: 25–60 years.

Question 4

Recognise 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

Recognise the signs of achalasia on physical examination

Answer 5

Signs of complications (e.g. cachectic)

Question 6

Identify appropriate investigations for achalasia and interpret the results

Answer 6

1st Line:

• 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 (>45 mmHg);
• -> incomplete LOS relaxation;
• -> absence of peristalsis in the distal (smooth muscle portion) of the oesophagus.

Other Ix:

• CXR: widened mediastinum, double right heart border (dilated oesophagus), an air-fluid level in the upper chest and absence of gastric bubble.
• serology: for antibodies against T. cruzi

Question 7

Define acute cholangitis

Answer 7

Infection of the bile duct; usually bacterial of duodenal source

Question 8

Explain the aetiology / risk factors of acute cholangitis

Answer 8

Bile duct obstruction: usually caused by gall stones
- Can be benign structuring (tumour) or malignancy (pancreatic, gall bladder, bile duct)
- Iatrogenic: post-operative damage/altered structure of bile duct
Pathogenesis: increased pressure in bile duct brings bacteria in contact with blood, resulting in infection Risk Factors: age, female, cirrhosis

Question 9

Summarise the epidemiology of acute cholangitis

Answer 9

15% have gallstones; 2-3% will develop acute cholangitis

Question 10

Recognise the presenting symptoms of acute cholangitis

Answer 10

RUQ abdominal pain; fever, rigors, malaise

Question 11

Recognise the signs of acute cholangitis on physical examination

Answer 11

Jaundice, RUQ tenderness
Charcot’s Triad: Abdominal pain, jaundice and fever (15-20% of cases)
Worsened condition => Reynold’s pentad (add septic shock and mental confusion)

Question 12

Identify appropriate investigations for acute cholangitis and interpret the results

Answer 12

Bloods: FBC (raised WCC), CRP (raised); LFTs (obstructive picture: raised bilirubin, ALP), cultures
USS: distinguish between cholangitis and cholecystitis
MRCP: better imaging than USS
ERCP: gold standard test for biliary obstruction (but it is invasive)

Question 13

Generate a management plan for acute cholangitis

Answer 13

Fluids, antiobiotics (ciprofloxacin, metronidazole), vasopressors

Unblock the bile duct: 24-48hrs after admission, once settled

• ERCP (dilation of duct/removal of stones)
• Lithotripsy: acoustic shock waves to break stones
• Cholecystectomy: removal of gall bladder

Question 14

Identify the possible complications of acute cholangitis and its management

Answer 14

Recurrent biliary pain; jaundice; further episodes; death risk increased

Question 15

Summarise the prognosis for patients with acute cholangitis

Answer 15

Risk of death (multiple organ failure); 10-30% mortality

Question 16

Define alcoholic hepatitis

Answer 16

Inflammatory liver injury caused by chronic heavy alcohol abuse

Question 17

Explain the aetiology / risk factors of alcoholic hepatitis

Answer 17

One of three alcoholic liver diseases (hepatitis; steatosis; cirrhosis)
Histopathology: centrilobular ballooning, DEGENERATION AND NECROSIS OF HEPATOCYTES; STEATOSIS, neutrophilic inflammation, cholestasis

Question 18

Summarise the epidemiology of alcoholic hepatitis

Answer 18

10-35% of heavy drinkers

Question 19

Recognise the presenting symptoms of alcoholic hepatitis

Answer 19

May remain asymptomatic and undetected; mild illness with nausea, malaise, epigastric or right hypochondrial pain
More severe: jaundice, abdominal discomfort/swelling, swollen ankles, GI bleed

Question 20

Recognise the signs of alcoholic hepatitis on physical examination

Answer 20

Excess Alcohol: malnourished, palmar erythema, Dupuytren’s contracture, facial telangiectasia, parotid enlargement, spider naevia, gynaecomastia, hepatomegaly
Alcoholic Hepatitis: febrile, tachycardic, jaundiced, bruising, encephalopathy (e.g. liver flap), ascites, hepatomegaly, splenomegaly

Question 21

Identify appropriate investigations for alcoholic hepatitis and interpret the results

Answer 21

BLOODS: FBC (reduced Hb, platelets; increased MCV and WCC), LFT (increased transaminases, bilirubin, GGT, ALP, reduced albumin) U&Es ( urea and K+ low), Clotting (prolonged PT)
USS: for other causes
Upper GI endoscopy: investigate varices
Liver biopsy: distinguish other causes of hepatitis Electroencephalogram: indicative for encephalopathy

Question 22

Generate a management plan for alcoholic hepatitis

Answer 22

ACUTE:
- Thiamine, VitC, monitor electrolytes and glucose
- Treat encephalopathy (lactulose)
- Ascites: diuretics (spironolactone and furosemide)
NUTRITION:
- Oral/NG feeding
- Avoid protein restriction unless encephalopathic
Steroid Therapy: Reduce short-term mortality
Long Term: see alcohol dependence

Question 23

Identify the possible complications of alcoholic hepatitis and its management

Answer 23

Acute liver decompensation; hepatorenal syndrome; cirrhosis

Question 24

Summarise the prognosis for patients with alcoholic hepatitis

Answer 24

10% mortality in 30 days, 40% in 1 year; most progress to cirrhosis with continued alcohol intake Maddrey’s discriminant factor: (bilirubin/17) + (PT prolongation x 4.6) [>32 = > 50% 30 day mortality) Glasgow Alcoholic Gepatitis score (GAHS) if >9, >50% 30 day mortality

Question 25

Define anal fissure

Answer 25

A break or tear in the skin of the anal canal (usually posterior midline)

Question 26

Explain the aetiology / risk factors of anal fissure

Answer 26

Stretching of the anal mucosa beyond capability. HARD STOOLS, PREGNANCY, OPIATE ANALGESIA - Constipation - Passing large, hard stools - Prolonged diarrhoea - Childbirth trauma; sexual activity; Crohn’s Disease; Ulcerative Colitis - Spasming of Internal Anal Sphincter: impaired blood supply to fissure, causing impaired healing - STIs can cause breakdown of skin (syphilis, herpes)

Question 27

Summarise the epidemiology of anal fissure

Answer 27

1:350; occur in 15-40 yrs, more common in men

Question 28

Recognise the presenting symptoms of anal fissure

Answer 28

A tear or paper cut-like scar in the skin of the anal canal Pain on defecation

Question 29

Recognise the signs of anal fissure on physical examination

Answer 29

Appearance of scar in midline, extending from the anal opening

Question 30

Identify appropriate investigations for anal fissure and interpret the results

Answer 30

Investigate possible causes of fissure (proctoscopy, sigmoidoscopy or colonoscopy for CD or colorectal cancer) DO NOT attempt DRE as it is painful

Question 31

Generate a management plan for anal fissure

Answer 31

Non-surgical: - gt ointment and lidocaine ointment, with diltiazem (calcium channel blocker) - Topical anaesthetics, high-fiber diets and stool softeners - 2nd line: botulinum toxin injection and topical diltiazem Surgical: for those who have unsuccessfully tried non-surgical treatment for 1-3 months - Lateral Sphincterectomy

Question 32

Identify the possible complications of anal fissure and its management

Answer 32

Complications of treatment include Incontinence

Question 33

Summarise the prognosis for patients with anal fissure

Answer 33

Most can be non-surgically treated

Question 34

Define appendicectomy

Answer 34

Surgical removal of the vermiform appendix

Question 35

Summarise the indications for an appendicectomy

Answer 35

acute appendicitis

Question 36

Identify the possible complications of an appendicectomy

Answer 36

Wound infection, abscess, ileus

Question 37

Contraindications of appendicectomy

Answer 37

``` Haemodynamic instability Lack of surgical expertise Severe abdominal distension Generalised peritonitis Severe pulmonary disease Pregnancy ```

Question 38

Define amyloidosis

Answer 38

Extracellular deposition of amyloid fibrils; three types: - AL (light chain) - AA (serum A amyloid) - ATTR (familial)

Question 39

Explain the aetiology / risk factors of amyloidosis

Answer 39

Amyloid fibril deposition disrupts the structure and function of normal tissue; amyloidosis is classified according to fibril subunit: - AL – monoclonal immunoglobulin light chains; associated with plasma cell disorders i.e. multiple myeloma - AA – Serum amyloid protein A; associated with chronic inflammatory conditions (IBD and rheumatoid arthritis) - ATTR – a genetic variant; autosomal dominant transmitted mutations

Question 40

Summarise the epidemiology of amyloidosis

Answer 40

Primary - AL Amyloidosis: 3-600 annual cases Secondary - AA Amyloidosis: 1-5% of those with chronic inflammatory conditions Hereditary Amyloidosis: 5% of patients with systemic amyloidosis

Question 41

Recognise the presenting symptoms of amyloidosis

Answer 41

Multi-systemic affects: - Renal: renal failure, oedema - Vascular: Periorbital Purpura - PNS: pain/numbness in arms and legs - GI: macroglossia, bleeding, weight loss, malabsorption - Cardiac: angina, orthopnoea, PND - Haematological: bleeding diathesis - Neurological: carpal tunnel syndrome - Dermatological: waxy skin, easy bruising - Joints: painful joints

Question 42

Recognise the signs of amyloidosis on physical examination

Answer 42

Multi-systemic Affects: - Renal: proteinuria - Cardiac: arrhythmias, heart failure - GI: hepatosplenomegaly - Neurological: sensory and motor neuropathy - Skin: purpura around eyes - Joints: tender, swelled joints

Question 43

Identify appropriate investigations for amyloidosis and interpret the results

Answer 43

Tissue biopsy: congo red stain; to diagnose AA; poor diagnostic power for AL Urine: proteinuria, free immunoglobulin light chains for AL Blood: CRP, ESR, rheumatoid factor, LFTs, U&Es

Question 44

Define appendicitis

Answer 44

Inflammation of the appendix

Question 45

Explain the aetiology / risk factors of appendicitis

Answer 45

Organisms of the gut invade the appendix

Question 46

Summarise the epidemiology of appendicitis

Answer 46

very common

Question 47

Recognise the presenting symptoms of appendicitis

Answer 47

pain in the umbilical region that migrates to the right iliac fossa region Diarrhoea/constipation Anorexia and vomiting (rare)

Question 48

Recognise the signs of appendicitis on physical examination

Answer 48

Rovsing's sign: pushing down on the LIF causes an increase in pain in the RIF Psoas sign: pain on extending the hip Cope sign: pain on flexion and internal rotation of the right hip Rebound tenderness: when infection involves the peritoneum

Question 49

Identify appropriate investigations for appendicitis and interpret the results

Answer 49

FBC: CRP, neutrophil leucocytosis CT: high diagnostic accuracy (reduces –ve appendicectomy, but can cause delay) USS: appendix not always visualised

Question 50

Generate a management plan for appendicitis

Answer 50

Prompt appendicectomy | Antibiotics: metronidazole and cefuroxime

Question 51

Identify the possible complications of appendicitis and its management

Answer 51

Perforation: more common if feacolith is present; young children Appendix Mass: when inflamed appendix becomes covered in omentum (US/CT helps with diagnosis) Appendix Abscess: can result in appendix mass also

Question 52

Summarise the prognosis for patients with appendicitis

Answer 52

Most recover easily after surgery, between 10-28 day recovery

Question 53

Define autoimmune hepatitis

Answer 53

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

Question 54

Explain the aetiology / risk factors of autoimmune hepatitis

Answer 54

Genetically predisposed individual – environmental agent leads to hepatocyte expression of HLA antigens, which become focus of t-cell mediated attack 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

Question 55

Summarise the epidemiology of autoimmune hepatitis

Answer 55

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

Question 56

Recognise the presenting symptoms of autoimmune hepatitis

Answer 56

``` May be asymptomatic and discovered incidentally by deranged LFTs Insidious Onset: malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis Acute Hepatitis (25%): RUQ pain, fever, anorexia, jaundice, nausea, vomiting, diarrhoea Family history of autoimmune disease (e.g. T1DM, vitilgo) ```

Question 57

Recognise the signs of autoimmune hepatitis on physical examination

Answer 57

Chronic Liver Disease Signs: spider naevi, gynacomastea, abnormal hair growth Late Features: Ascites; oedema and encephalopathy Cushingoid Features: round face, cutaneous striae, acne, hirsuitism

Question 58

Identify appropriate investigations for autoimmune hepatitis and interpret the results

Answer 58

Bloods: LFTs (increase AST, GGT, ALT, AlkPhos, bilirubin) Clotting (increase PT) FBC (mild reduced Hb and platelets and WCC- hypersplenism in portal hypertension) Liver Biopsy: needed for diagnosis; interface hepatitis or cirrhosis Other: to rule out other causes e.g. viral serology, ferritin/trasnferritin USS/CT/MRI: of liver and abdomen: visualise lesions ERCP: rule out Primary Sclerosing Cholangitis

Question 59

Define Barrett’s oesophagus

Answer 59

a change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia. [Metaplasia of the squamous epithelium of the lower third of the oesophagus to columnar epithelium] Mucosal inflammation and erosion, and replacement of mucosa with metaplastic columnar epithelium, in the lower third of the oesophagus. Presence of goblet cells is necessary for diagnosis

Question 60

Explain the aetiology / risk factors of Barrett’s oesophagus

Answer 60

Chronic inflammation: principal cause is GORD | RF: acid or bile reflux/GORD, male sex, age, white, family history of BO or oesophageal adenocarcinoma, obesity, smoking

Question 61

Summarise the epidemiology of Barrett’s oesophagus

Answer 61

Men are 8x more at risk | Caucasian is at a higher risk

Question 62

Recognise the presenting symptoms of Barrett’s oesophagus

Answer 62

Frequent heartburn, dysphagia, haematemesis, retrosternal pain, weight loss

Question 63

Recognise the signs of Barrett’s oesophagus on physical examination

Answer 63

Diagnosis made in imaging

Question 64

Identify appropriate investigations for Barrett’s oesophagus and interpret the results

Answer 64

Upper GI endoscopy with biopsy | barium oesophagram

Question 65

Generate a management plan for Barrett’s oesophagus

Answer 65

If pre-malignant/high-grade dysplasia – oesophageal resection or eradicative mucosectomy If no pre-malignancy or high-grade dysplasia: endoscopic surveillance + biopsy; every 1-3 years - Anti-reflux measures: PPIs (omeprazole)

Question 66

Identify the possible complications of Barrett’s oesophagus and its management

Answer 66

high risk of oesophageal cancer (oesophagogastric junctional adenocarcinoma)

Question 67

Summarise the prognosis for patients with Barrett’s oesophagus

Answer 67

Risk of cancer is 1-7:1000; those with oesophageal cancer have low survival rates (most are <1 year)

Question 68

Define cholecystitis

Answer 68

inflammation of the gallbladder

Question 69

Explain the aetiology / risk factors of cholecystitis

Answer 69

Inflammation of the gallbladder – most commonly by gallstones. But can occur with blockage due to tumour or scarring Risk Factors: age, female, pregnancy, oral contraceptives, obesity, diabetes mellitus Calculous Cholecystitis: gallstones blocking flow; gallbladder can become infected (E. coli, Klebsiella). Can spread to diaphragm Acalculous Cholecystitis: no stones; vasculitis, chemotherapy, major trauma or burns Chronic Cholecystitis: repeated inflammations; may be asymptomatic

Question 70

Summarise the epidemiology of cholecystitis

Answer 70

Accounts for 3-10% of abdominal pain; highest in 50-69 year olds

Question 71

Recognise the presenting symptoms of cholecystitis

Answer 71

RUQ pain, worse on eating fatty foods, nausea and vomiting. Biliary colic preceding cholecystitis

Question 72

Recognise the signs of cholecystitis on physical examination

Answer 72

Fever, tender abdomen, palpable gallbladder, jaundice | Murphy’s Sign: while pressing on RUQ, pain on inspiration and breath is terminated

Question 73

Identify appropriate investigations for cholecystitis and interpret the results

Answer 73

Bloods: FBC (increased WCC), CRP (elevated), bilirubin (elevated) USS: of RUQ, most commonly used to diagnose CT: if complications (perforation, gangrene) are suspected

Question 74

Generate a management plan for cholecystitis

Answer 74

Surgery: laparoscopic cholecystectomy (early has better prognosis)

Question 75

Identify the possible complications of cholecystitis and its management

Answer 75

Gangrene, gallbladder rupture (abscess, peritonitis), empyema, fistula formation, gallstone ileus

Question 76

Summarise the prognosis for patients with cholecystitis

Answer 76

Pre-complication prognosis is better, 25-30% develop complications

Question 77

Define cirrhosis

Answer 77

End stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.

Question 78

What is decompensated liver failure and what are the symptoms?

Answer 78

Compensated: Np symptoms of the disease Decompensated: cirrhosis has progressed to the point that the liver is having trouble functioning and you start having symptoms of the disease jaundice, ascites, encephalopathy or GI bleeding

Question 79

Explain the aetiology / risk factors of cirrhosis

Answer 79

Most common: chronic alcohol misuse Chronic viral hepatitis: Hep B+C most common worldwide Autoimmune hepatitis Drugs: e.g. methotrexate, hepatotoxic drugs Inherited: α1-Antitrypsin deficiency, haemochromatosis, Wilson’s disease, galactosaemia, CF Vascular: Budd-Chiari syndrome Chronic biliary diseases: primary biliary cirrhosis, PSC, biliary atresia Cryptogenic: 5-10% Non-alcoholic steatohepatitis (NASH): associated with obesity, diabetes, parenteral nutrition, and drugs (amiodarone, tamoxifen) Decompensation: infection, GI bleeding, constipation, alcohol, drugs

Question 80

Summarise the epidemiology of cirrhosis

Answer 80

Top 10 causes of death

Question 81

Recognise the presenting symptoms of cirrhosis

Answer 81

Early and non-specific: anorexia, nausea, fatigue, weakness, weight loss Symptoms (decreased synthetic function): easy bruising, abdominal swelling, ankle oedema Symptoms (reduced detoxification): jaundice, personality changes, altered sleep patterns, amenorrhoea Symptoms (Portal Hypertension): abdominal swelling, haematemesis, PR bleeding or melaena

Question 82

Recognise the signs of cirrhosis on physical examination

Answer 82

Chronic Liver Disease: ABCDE - Asterixes (liver flap) - Bruises - Clubbing - Dupuytren;s Contracture - Erythema - Other: jaundice, gynaecomastia, leukonychia, spider naevia, scratch marks, ascites, hepatomegaly, caput medusa, splenomegaly

Question 83

Identify appropriate investigations for cirrhosis and interpret the results

Answer 83

BLOODS: FBC (lowered Hb, platelets [hypersplenism]) LFTs (can be normal, increased AlkPhos, reduced albumin) Clotting (prolonged PT), Serum AFP Other: to determine cause (serology, α1 antitrypsin, caeruloplasmin {Wilson’s Disease]) Liver Biopsy: percutaneous (trans jugular if ascites or clotting deranged) Imaging: USS, CT, MRI (detect complications, hepatocellular carcinoma, thrombosis), MRCP Endoscopy: examine for varices Child-Pugh Grading: Class A/B/C depending on score

Question 84

Generate a management plan for cirrhosis

Answer 84

Treat cause if possible Advice: avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver, ensure good nutrition Treat complications: - Encephalopathy: treat infections, exclude GI bleed, lactulose - Ascites: diuretics (spironolactone/furosemide), sodium restriction, fluid restriction - Spontaneous Bacterial Peritonitis: antibiotic treatment (cefuroxime and metronidazole) - Surgical: insertion of TIPS (relieve portal hypertension). Liver transplant

Question 85

Identify the possible complications of cirrhosis and its management

Answer 85

Portal hypertension with ascites, encephalopathy or variceal haemorrhage, SBP, hepatocellular carcinoma, peritonitis Renal failure

Question 86

Summarise the prognosis for patients with cirrhosis

Answer 86

Depends on aetiology: generally poor. 5 year survival at 50%, with ascites 2 year survival at 50%

Question 87

Define coeliac disease

Answer 87

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

Question 88

Explain the aetiology / risk factors of coeliac disease

Answer 88

Sensitivity to the gliadin component of the cereal protein, gluten – triggers an immunological reaction in the small intestine leading to mucosal damage and loss of villi 10% risk of first relatives being affected

Question 89

Summarise the epidemiology of coeliac disease

Answer 89

1:2000; more common in western society

Question 90

Recognise the presenting symptoms of coeliac disease

Answer 90

pain, tiredness,

Question 91

Recognise the signs of coeliac disease on physical examination

Answer 91

Anaemia: pallor Malnutrition: short stature, abdominal distension, wasted buttocks in children Vitamin/Mineral Deficiencies: osteomalcia, easy bruising Intense itchy blisters on elbows/knees/buttocks

Question 92

Identify appropriate investigations for coeliac disease and interpret the results

Answer 92

Bloods: FBC, iron, folate, U&Es, albumin, Ca2+ and phosphate Serology: testing for IgG anti-glandin, tissue transglutaminase (tTG) Stool: culture to exclude infection D-xylose test: reduced urinary excretion after oral xylose (small bowel malabsorption) Endoscopy: direct visualisation shows villous atrophy in small intestine (jejenum and ileum), giving smooth, flat appearance to mucosa. Biopsy: villous atrophy with crypt hyperplasia of duodenum

Question 93

Generate a management plan for coeliac disease

Answer 93

Advice: Withdrawal of gluten from the diet and educating on dietary advice Medical: vitamin and mineral supplements

Question 94

Identify the possible complications of coeliac disease and its management

Answer 94

Iron, folate and vitamin B12 deficiencies; osteomalacia; ulcerative jejunoileitis; bacterial overgrowth

Question 95

Summarise the prognosis for patients with coeliac disease

Answer 95

With strict adherence, most patients make a full recovery; symptoms resolving in weeks Life-long diet changes need to be made

Question 96

Define Crohn's disease

Answer 96

Chronic granulomatous inflammatory disease that can affect any part of the GI tract. Most commonly in ileum and colon

Question 97

Explain the aetiology / risk factors of Crohn's disease

Answer 97

Combination of environmental factors and genetic predisposition Genetics: siblings are 30x more likely to develop it; Immune system: impaired innate immunity Environmental Factors: smoking, oral contraceptives,

Question 98

Summarise the epidemiology of Crohn's disease

Answer 98

5-8:100,000; lower incidence in Asia and east Africa; bimodal onset at 15-30 and 60-80 years

Question 99

Recognise the presenting symptoms of Crohn's disease

Answer 99

Crampy abdominal pain; diarrhoea; fever/malaise/weight loss; symptoms of complications

Question 100

Recognise the signs of Crohn's disease on physical examination

Answer 100

Weight loss; clubbing; anaemia signs Aphthous ulceration of the mouth Perianal skin tags, fistulae and abscesses Signs of complications (eyes, joints or skin)

Question 101

Identify appropriate investigations for Crohn's disease and interpret the results

Answer 101

Blood: FBC, U&Es, LFTs, ESR, CRP (p-anca negative) Stool microscopy and culture: exclude infective colitis AXR: toxic megacolon Erect CXR: to see perforation Small-bowel barium follow-through; reveal fibrosis/strictures, rose thorn appearance Endoscopy (OGD, colonoscopy) and biopsy: differentiate between CD and UC. Will see granulomas in CD.

Question 102

Generate a management plan for Crohn's disease

Answer 102

``` Acute Exacerbation: - Fluid rescus - IV or oral corticosteroids - 5-ASA Analogues (e.g. mesalazine) - Analgesia - Monitor activity markers Long Term: - Steroids: to treat acute exacerbations - 5-ASA analgoues (e.g. mesalazine) to reduce relapses - Immunosuppression: steroid-sparing agents (e.g. azathioprine) to reduce relapse - Anti-TNF agents (e.g. infliximab) to achieve and maintain remission Advice: - Stop smoking - Dietician referral - Education and advice Surgery: - Indicated by failure of medical treatment, failure to thrive in children or complications - Resection of bowel and stoma formation ```

Question 103

Identify the possible complications of Crohn's disease and its management

Answer 103

GI: Haemorrhage, bowel obstruction, perforation, fistulae, GI carcinoma Extra intestinal: uveitis; episcleritis; gallstones; kidney stones

Question 104

Summarise the prognosis for patients with Crohn's disease

Answer 104

Chronic relapsing condition; two thirds will require surgery eventually, and two thirds of these will have >1 procedure.

Question 105

Define diverticular disease

Answer 105

Diverticulosis: presence of diverticulae outpouchings of the colonic mucosa and submucosa throughout the large bowel Diverticular Disease: diverticulosis associated with complications (e.g haemorrhage, infection) Diverticulitis: acute inflammation and infection of the colonic diverticulae Hinchey Classification: - Ia: phlegmon - Ib and II: localised abscesses - III: perforation with purulent peritonitis - IV: faecal peritonitis

Question 106

Explain the aetiology / risk factors of diverticular disease

Answer 106

A low fibre diet can lead to loss of stool bulk, consequently high pressures are required to expel the stool, leading to herniations through the muscularis at weak points Pathogenesis: most common in sigmoid colon; can be obstructed with stool, leading to bacterial overgrowth, injury and diverticulitis

Question 107

Recognise the presenting symptoms of diverticular disease

Answer 107

``` Often asymptomatic (80-90%) Complications: PR bleeding, diverticulitis (LIF pain, fever) diverticular fistulation into the bladder (pneumaturia, faecaluria and recurrent UTIs) ```

Question 108

Recognise the signs of diverticular disease on physical examination

Answer 108

Diverticulitis: tender abdomen, signs of local/generalised peritonitis if perforation occurred

Question 109

Identify appropriate investigations for diverticular disease and interpret the results

Answer 109

Bloods: FBC, clotting, cross-match Barium Enema: demonstrated presence of diverticulae (not in acute; risk of perforation) Flexible sigmoidoscopy and colonoscopy: diverticulae can be seen Acute Setting: CT

Question 110

Generate a management plan for diverticular disease

Answer 110

Asymptomatic: soluble, high-fibre diet. [Anti-inflammatories (mesalazine) under investigation as preventions] GI Bleed: managed conservatively - IV hydration - Bowel rest Surgery: may be necessary with recurrent attacks or complications - Open or laparoscopic approaches - Open Hartmann’s (resection and stoma) - One-Stage resection and anastomosis - Laparoscopic drainage, peritoneal lavage and drain replacement can be effective

Question 111

Identify the possible complications of diverticular disease and its management

Answer 111

Diverticulitis, pericolic abscess, perforation, faecal peritonitis, colonic obstruction, fistula formation, haemorrhage

Question 112

Summarise the prognosis for patients with diverticular disease

Answer 112

10-25% will have >1 episode of diverticulitis

Question 113

Define gallstones and biliary colic

Answer 113

presence of solid concretions in the gallbladder. Gallstones form in the gallbladder but may exit into the bile ducts. Symptoms ensue if a stone obstructs the cystic, bile, or pancreatic duct. Biliary colic is right upper quadrant pain, radiating to shoulder

Question 114

Explain the aetiology / risk factors of gallstones and biliary colic

Answer 114

gallstones: 90% are made of cholesterol. form in the gall bladder, but can move into the ducts, where they can cause symptoms BC: Obstruction of common bile duct/cystic duct by a gall stone. Acute pain can be exacerbated by certain foods (high in fat) Risk Factors: age, female, family history, increased oestrogen exposure (pregnancy, birth control) diabetes mellitus, obesity, rapid weight loss, FHx

Question 115

Summarise the epidemiology of gallstones and biliary colic

Answer 115

high prevalence, usually symptomatic 2-3% risk of developing biliary colic

Question 116

Recognise the presenting symptoms of gallstones and biliary colic

Answer 116

Gallstones are highly prevalent, but most (80%) are asymptomatic. Pain: sharp RUQ pain, radiating to right shoulder/back, can follow high fat meals, lasts 30-120 minutes, nausea, vomiting, Other presentations Biliary colic: is characterised by steady, severe pain (intensity >5 on a scale of 1-10) in the right upper quadrant (RUQ) of the abdomen lasting more than 15-30 minutes. An attack of simple biliary colic commonly requires an analgesic but should resolve within 5 hours. Cholecystitis: biliary pain lasting more than 5 hours is accompanied by features of inflammation: fever, marked RUQ tenderness (Murphy's sign), and leukocytosis. Some patients progress to sepsis. Occasionally, stones can perforate the gallbladder, leading to intestinal obstruction (gallstone ileus). Choledocholithiasis: when stones obstruct the bile ducts, biliary-type pain is accompanied by cholestasis, which manifests as jaundice. More sinister is acute cholangitis, characterised by Charcot's triad of biliary pain, jaundice, and fever. Acute cholangitis represents a medical emergency. Acute pancreatitis: epigastric pain radiating to the back results from bile duct stones obstructing the pancreatic ducts. Inflammatory features include peritonitis.

Question 117

Recognise the signs of gallstones and biliary colic on physical examination

Answer 117

Biliary colic: Right upper quadrant or epigastric tenderness. Acute cholecystitis: Tachycardia, pyrexia, right upper quadrant or epigastric tenderness. There may be guarding +/- rebound. Murphy's sign is elicited by placing a hand at the costal margin in the RUQ and asking the patient to breathe deeply. Patient stops breathing as the inflamed gallbladder descends and contacts the palpating fingers. Ascending cholangitis: Pyrexia, right upper quadrant pain, jaundice.

Question 118

Identify appropriate investigations for gallstones and biliary colic and interpret the results

Answer 118

Bloods: usually normal, LFTs can show raised bilirubin and AlkPhos FBC, LFTs, serum lipase and amylase, abdominal ultrasound MRCP, endoscopic ultrasound scan, ECRP, abdominal CT scan

Question 119

Generate a management plan for gallstones and biliary colic

Answer 119

No treatment for asymptomatic cholecystolithiasis symptomatic cholecystolithiasis: Laparoscopic cholecystectomy cholelithiasis: ERCP, lithotripsy, papillary balloon dilation, stent Relief of symptoms and electrolyte/fluid imbalance - Anti-emetics (dimenhydrinate) - Pain: NSAIDs (diclofenac)

Question 120

Identify the possible complications of gallstones and biliary colic and its management

Answer 120

Cholecystitis, cholangitis, pancreatitis Delayed surgery can cause pancreatitis, empyema/perforation of gallbladder, cholecystitis, cholangitis, obstructive jaundice

Question 121

Summarise the prognosis for patients with gallstones and biliary colic

Answer 121

Good, dependant on development of complications The outlook for patients with symptomatic cholelithiasis managed by cholecystectomy is favourable. The same holds for patients with choledocholithiasis who undergo ERCP with biliary sphincterotomy and stone extraction, followed later by cholecystectomy.

Question 122

Define gastric cancer

Answer 122

Gastric malignancy, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma. cancer deriving from the stomach

Question 123

Explain the aetiology / risk factors of gastric cancer

Answer 123

50% involve pylorus 25% lesser curve 10% cardia 2-7% are lymphomas Most cases are probably caused by environmental insults in genetically predisposed individuals that lead to mutation and subsequent unregulated cell growth. Risk Factors: being >55, male, poor socio-economic status, • H.pylori infection; • atrophic gastritis; • diet high in smoked, processed foods and nitrosamines; low vegetable consumption • smoking • alcohol

Question 124

Summarise the epidemiology of gastric cancer

Answer 124

Common cause of cancer death worldwide, highest incidence in Asia (Japan). Sixth most common cancer in UK (annual incidence is 15 in 100000) Age>50 years. Cancer of the antrum/body is becoming less common, while that of the cardia and gastro- oesophageal junction is increasing.

Question 125

Recognise the presenting symptoms of gastric cancer

Answer 125

In early phases, it is often asymptomatic. Early satiety or epigastric discomfort. Weight loss, anorexia, nausea and vomiting. dyspepsia Haematemesis, melaena, symptoms of anaemia. Dysphagia (tumours of the cardia). Symptoms of metastases, particularly abdominal swelling (ascites) or jaundice (liver involvement).

Question 126

Recognise the signs of gastric cancer on physical examination

Answer 126

Physical examination may be normal. Epigastric mass. Abdominal tenderness. Ascites. Hepatomegaly, jaundice, ascites acanthosis nigricans Signs of anaemia. Many eponymous signs: Virchow’s node/Troisier’s sign: Lymphadenopathy in left supraclavicular fossa. Sister Mary Joseph node: Metastatic nodule on umbilicus. Krukenberg’s tumour: Ovarian metastases.

Question 127

Identify appropriate investigations for gastric cancer and interpret the results

Answer 127

Upper GI endoscopy: With multiquadrant biopsy of all gastric ulcers. Blood: FBC (for anaemia), LFT. CEA, Ca19-9, Ca72-4 CT/MRI: Staging of tumour and planning of surgery. Ultrasound of liver: Staging of tumour. Bone scan: Staging of tumour. Endoscopic ultrasound: Assesses depth of invasion and lymph node spread. Laparoscopy: May be needed to determine if tumour is resectable.

Question 128

Define gastro-oesophageal reflux disease

Answer 128

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

Question 129

Explain the aetiology / risk factors of gastro-oesophageal reflux disease

Answer 129

Disruptions of mechanisms that prevent reflux (physiological etc.) Risk Factors: obesity, pregnancy (increase in abdominal pressure), smoking, diet, hiatus hernia, increase in age, FHx

Question 130

Summarise the epidemiology of gastro-oesophageal reflux disease

Answer 130

Common, 5-10% of adults

Question 131

Recognise the presenting symptoms of gastro-oesophageal reflux disease

Answer 131

Substernal burning discomfort or ‘heartburn’, aggravated by supine position, bending, large meals and drinking alcohol acid regurgitation Waterbrash Aspiration results in voice hoarseness, laryngitis, nocturnal cough and wheeze dysphagia, bloating, early satiety

Question 132

Recognise the signs of gastro-oesophageal reflux disease on physical examination

Answer 132

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

Question 133

Identify appropriate investigations for gastro-oesophageal reflux disease and interpret the results

Answer 133

Upper GI Endoscopy, biopsy: confirm presence of oesophagitis, exclude malignancy Barium Swallow: detect hiatus hernia, peptic stricture CXR: incidental hiatus hernia findings 24 hour oesophageal pH monitoring: determines temporal relationship to symptoms

Question 134

Generate a management plan for gastro-oesophageal reflux disease

Answer 134

Advice: - Lifestyle changes, weight loss, elevating head - Avoid provoking factors, stopping smoking, lower fat meals Medical: - Antacids - PPIs (e.g. lansoprazole) - H2 antagonists (e.g. ranitidine) Endoscopy: - Annual endoscopic surveillance for Barrett’s Oesophagus Surgery: - Anti-reflux surgery

Question 135

Identify the possible complications of gastro-oesophageal reflux disease and its management

Answer 135

Oesophageal ulceration; peptic stricture; anaemia; Barrett’s; oesophageal adenocarcinoma

Question 136

Summarise the prognosis for patients with gastro-oesophageal reflux disease

Answer 136

50% respond to lifestyle changes alone

Question 137

Define gastroenteritis

Answer 137

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

Question 138

Explain the aetiology / risk factors of gastroenteritis & infectious colitis i.e. name some of the pathogens

Answer 138

``` Viral: - Rotavirus, astrovirus, calcivirus Bacterial: - Campylobacter jejuni, Escherichia coli, Salmonella, Shigella Protozoal: - Entamoeba histolytica Toxins: - From Staphylococcus aureus, Clostridium botulinum ``` Commonly contaminated foods: improperly cooked meats, old rice, eggs, poultry CHESS organisms - Campylobacter - Haemorrhagic E. Coli - Entamoeba histolytica - Shigella - Salmonella

Question 139

Summarise the epidemiology of gastroenteritis

Answer 139

Common, often under-reported

Question 140

Recognise the presenting symptoms of gastroenteritis

Answer 140

Sudden onset nausea, vomiting, anorexia Diarrhoea, abdominal pain/discomfort, fever, malaise Enquire: recent travel, antibiotic use and recent food intake Time: toxins (1-24 hours), bacterial (12 hours)

Question 141

Recognise the signs of gastroenteritis (&IC)

Answer 141

Diffuse abdominal tenderness, abdominal distension and bowel sounds are increased Severe: pyrexia, dehydration, hypotension, peripheral shutdown

Question 142

Identify appropriate investigations for gastroenteritis & infectious colitis and interpret the results

Answer 142

Bloods: FBC, culture, U&Es Stool: faecal microscopy AXR/USS: exclude other causes Sigmoidoscopy: only if IBD needs to be excluded INFECTIOUS COLITIS Bloods: FBC, CRP, ESR Stool: MC&S

Question 143

Generate a management plan for gastroenteritis & infectious colitis

Answer 143

Bed rest, fluids and electrolyte replacement (advise increase oral fluid intake to compensate for the water lost from diarrhoea and vomiting) IV rehydration may be required in severe cases. Don;'t conventionally give antibiotics unless a bacteria has been isolated. Botulism: botulinum antitoxin IM, manage in ITU

Question 144

Identify the possible complications of gastroenteritis & infectious colitis and its management

Answer 144

Dehydration, electrolyte imbalance, prerenal failure, sepsis, shock Botulinum: respiratory muscle paralysis

Question 145

Summarise the prognosis for patients with gastroenteritis & infectious colitis

Answer 145

Generally good, majority are self-limiting

Question 146

Define infectious colitis

Answer 146

An inflammation of the large bowel, with an infective cause

Question 147

Summarise the epidemiology of infectious colitis

Answer 147

Rare, in those with lower hygiene levels, and contaminated food

Question 148

Recognise the presenting symptoms of infectious colitis

Answer 148

Bloody diarrhoea, generalised abdominal pain, vomiting

Question 149

Recognise the signs of infectious colitis on physical examination

Answer 149

Tenderness | DRE: bloody stool

Question 150

Define gastrointestinal perforation

Answer 150

A hole in the wall of the gastrointestinal tract

Question 151

Explain the aetiology / risk factors of gastrointestinal perforation

Answer 151

Gastric ulcers, duodenal ulcers, appendicitis, gastrointestinal cancer, diverticulitis Iatrogenic: abdominal surgery

Question 152

Summarise the epidemiology of gastrointestinal perforation

Answer 152

10-15% of patients with acute diverticulitis

Question 153

Recognise the presenting symptoms of gastrointestinal perforation

Answer 153

Sudden pain in epigastrium (duodenal ulcer), burning pain in epigastrium (gastric ulcer) Pain starts at perforation site, then spreads Severe abdominal pain, nausea, vomiting and hematemesis

Question 154

Recognise the signs of gastrointestinal perforation on physical examination

Answer 154

Severe abdominal tenderness and rigidity | Fever, silent bowel sounds, distended abdomen, tachycardia, dyspnoea

Question 155

Identify appropriate investigations for gastrointestinal perforation and interpret the results

Answer 155

Bloods: FBC, CRP, ESR, U&Es, LFTs AXR: gas under diaphragm CT Abdomen: may visualise location of perforation

Question 156

Generate a management plan for gastrointestinal perforation

Answer 156

``` Surgical Intervention: peritoneal wash and anatomical repair Conservative: - IV fluids - Antibiotics - Nasogastric aspiration and bowel rest ```

Question 157

Identify the possible complications of gastrointestinal perforation and its management

Answer 157

Peritonitis, bleeding, bowel infarction, sepsis, shock

Question 158

Summarise the prognosis for patients with gastrointestinal perforation

Answer 158

Depends on size and location; worse prognosis in older patients with existing bowel disease

Question 159

Define haemochromatosis

Answer 159

Deficiency of hepcidin, resulting in an accumulation of iron

Question 160

Explain the aetiology / risk factors of haemochromatosis

Answer 160

Defects of the HFE gene

Question 161

Summarise the epidemiology of haemochromatosis

Answer 161

Rare

Question 162

Recognise the presenting symptoms of haemochromatosis

Answer 162

Early: vague and nonspecific (fatigue, weakness) Late: diabetes, bronzing of the skin, impaired memory, depression

Question 163

Recognise the signs of haemochromatosis on physical examination

Answer 163

Hepatomegaly, diabetes mellitus, arrhythmias,

Question 164

Identify appropriate investigations for haemochromatosis and interpret the results

Answer 164

Bloods: serum iron, serum ferritin, transferrin saturation, LFTs Genetic testing: HFE testing Liver biopsy: rarely required

Question 165

Define haemorrhoids

Answer 165

Abnormally enlarged vascular mucosal cushions in the anal canal. They are either internal (above the dentate line) or external (below the dentate line) Internal Haemorrhoids: classified according to the degree of prolapse - First Degree: do not prolapse - Second Degree: prolapse on straining, reduce spontaneously - Third Degree: prolapse on straining, can be reduced manually - Fourth Degree: permanently prolapsed, cannot be reduced They are painless unless strangulated External Haemorrhoids - Can be painful and itchy - May be visible on external examination

Question 166

Explain the aetiology / risk factors of haemorrhoids

Answer 166

Caused by 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. Other conditions can contribute to the formation of haemorrhoids: an increase in intra-abdominal pressure in pregnancy or ascites. Risk Factors: constipation, prolonged straining, increased abdominal pressure (pregnancy, ascites, childbirth), heavy lifting, chronic cough

Question 167

Summarise the epidemiology of haemorrhoids

Answer 167

13-36% of population

Question 168

Recognise the presenting symptoms of haemorrhoids

Answer 168

May be asymptomatic Bright red, painless rectal bleeding with defecation, not mixed with stool. Anal itching or irritation Feeling of rectal fullness, discomfort or incomplete evacuation Strangulated: intensely painful

Question 169

Recognise the signs of haemorrhoids on physical examination

Answer 169

Non-prolapsed haemorrhoids are not evident on external examination, difficult to feel in DRE Local perianal irritation can be seen in chronic discharge Asking patient to strain can make haemorrhoids visible Thrombosed: purple, swollen, acutely tender, perianal lumps

Question 170

Identify appropriate investigations for haemorrhoids and interpret the results

Answer 170

Bloods: FBC, CRP Proctoscopy: should be carried out to aid diagnosis Flexible sigmoidoscopy/colonoscopy: exclude other pathology

Question 171

Generate a management plan for haemorrhoids

Answer 171

Depends on degree of prolapse Prevention and management of constipation: - Fluids and fibre intake Pain and symptom relief: - Simple analgesia e.g. paracetamol - Topical therapies: topical anaesthetics or corticosteroids Non-Surgical: - Rubber band ligation: band cuts off blood supply, necrotising the haemorrhoid and it falls off - Good for Grade II haemorrhoids Surgical: - Haemorrhoidectomy: painful, performed under GA Thrombosed Haemorrhoids: - Extremely painful, treat conservatively with analgesia

Question 172

Identify the possible complications of haemorrhoids and its management

Answer 172

Skin tags, ischaemia, perianal sepsis, thrombosed haemorrhoids can ulcerate

Question 173

Summarise the prognosis for patients with haemorrhoids

Answer 173

Generally good, 10% may need surgery

Question 174

Define hepatocellular carcinoma

Answer 174

Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver. Mostly occurs in those with chronic liver disease cancer of the hepatocytes

Question 175

Explain the aetiology / risk factors of hepatocellular carcinoma

Answer 175

- Chronic liver damage (e.g. alcoholic liver disease, hepatitis B, hepatitis C, autoimmune disease, primary biliary cirrhosis), - metabolic disease (e.g. haemochromatosis), and - aflatoxins (Aspergillus flavus fungal toxin found on stored grains or biological weapons).

Question 176

Summarise the epidemiology of hepatocellular carcinoma

Answer 176

common makes up 1-2% of malignancies very common malignancy in areas where Hepatitis B and C are endemic, i.e. Asia and sub-Saharan Africa ( 500 in 100,000/year). Not common in the west.

Question 177

Recognise the presenting symptoms of hepatocellular carcinoma

Answer 177

Symptoms of malignancy: Malaise, weight loss, loss of appetite. Symptoms of chronic liver disease: Abdominal distension, jaundice, RUQ pain. Pruritus, bleeding oesophageal varices History of carcinogen exposure: High alcohol intake, Hepatitis B or C, aflatoxins.

Question 178

Recognise the signs of hepatocellular carcinoma on physical examination

Answer 178

Signs of malignancy: Cachexia/weight loss, lymphadenopathy. Hepatomegaly: Nodular (but may be smooth). Deep palpation may elicit tenderness. There may be bruit heard over the liver. Signs of chronic liver disease: Jaundice, ascites, RUQ pain, confusion (see Cirrhosis).

Question 179

Identify appropriate investigations for hepatocellular carcinoma and interpret the results

Answer 179

Bloods: FBC, LFTs, clotting, alpha fetoprotein, AFP CT/MRI: imaging and staging Biopsy: cytology

Question 180

Define hernias (femoral)

Answer 180

``` A herniation of the contents of the abdomen through the femoral canal Femoral canal: - Anterior border: inguinal ligament - Posterior border: pectineal ligament - Medial border: lacunar ligament - Lateral border: femoral vein ```

Question 181

Explain the aetiology / risk factors of hernias (femoral, inguinal, miscellaneous)

Answer 181

Weakening of abdominal wall allows hernias to protrude through in an increase of intra-abdominal pressure RF: old age, smoking, FHx, gender (female=femoral, male=inguinal), prematurity, pregnancy, weight lifting, constipation, weight gain, chronic cough and previous abdominal surgery/trauma

Question 182

Summarise the epidemiology of hernias (femoral)

Answer 182

Account for 5% of abdominal hernias

Question 183

Recognise the presenting symptoms of hernias (femoral)

Answer 183

Femoral: - Lump in groin, lateral and inferior to pubic tubercle - Appears/swells on coughing, and reduces on relaxation or supination - May be possible to reduce hernia Strangulated: tender, colicky abdominal pain, distension, vomiting

Question 184

Recognise the signs of hernias (femoral) on physical examination

Answer 184

Hernias: reducible, irreducible, obstructed or strangulated Strangulated: lump becomes red and tender

Question 185

Identify appropriate investigations for hernias (femoral, inguinal, miscellaneous) and interpret the results

Answer 185

Diagnosis is largely clinical | Imaging: USS is first line, followed by CT/MRI

Question 186

Generate a management plan for hernias (femoral)

Answer 186

Surgical repair in elective surgery: dissection of the sac, reduction of its contents, completed with sac ligation

Question 187

Identify the possible complications of hernias (femoral) and its management

Answer 187

risk of strangulation at 22%

Question 188

Summarise the prognosis for patients with hernias (femoral, inguinal, miscellaneous)

Answer 188

Good prognosis, mortality for strangulated hernias lies at 2-13%

Question 189

Generate a management plan for hernias (inguinal)

Answer 189

- If small, may only need reassurance | - Elective surgery: dissection of sac, reduction of contents, ligation of sac

Question 190

Identify the possible complications of hernias (inguinal) and its management

Answer 190

recurrence, wound infection, bladder injury, intestinal injury

Question 191

Define hiatus hernias

Answer 191

A herniation of part of the abdominal contents through the oesophageal aperture of the diaphragm Sliding (90%):Gastro-oesophageal junction slides up in to thoracic cavity Rolling (10%): Gastro-oesophageal junction remains in place but a part of the stomach herniates into chest

Question 192

Explain the aetiology / risk factors of hiatus hernias

Answer 192

One or more of three mechanisms: - Widening of diaphragmatic hiatus - Pulling up of the stomach due to oesophageal shortening - Pushing up of the stomach by increased intra-abdominal pressure Risk Factors: increased abdominal pressure (obesity, pregnancy, ascites), age, previous hiatus operation.

Question 193

Recognise the presenting symptoms of hiatus hernias

Answer 193

Sliding: - Can be asymptomatic, retrosternal burning/heartburn, GORD, dysphagia Rolling: - Can be asymptomatic, chest pain, epigastric pain or fullness, nausea May be asymptomatic or may present with heartburn, dysphagia, odynophagia, hoarseness, asthma, shortness of breath, chest pain, anaemia or haematemesis, or some combination of these.

Question 194

Recognise the signs of hiatus hernias on physical examination

Answer 194

See symptoms: tender abdomen

Question 195

Identify appropriate investigations for hiatus hernias and interpret the results

Answer 195

Contrasted upper gastrointestinal series (also known as an upper GI or as a barium oesophagram) is the key investigation. CXR endoscopy

Question 196

Generate a management plan for hiatus hernias

Answer 196

Lifestyle: avoid factors that increase intra-abdominal pressure Pharmacological: PPIs, H2 receptor antagonists Surgical: not asymptomatic sliding hernias, laparoscopic fundoplication Uncomplicated sliding hiatus hernias are treated symptomatically with medical therapy, although some patients may select surgical therapy. Complicated hiatus hernias (those with bleeding, volvulus, or obstruction) have a stronger indication for surgical repair.

Question 197

Identify the possible complications of hiatus hernias and its management

Answer 197

obstruction, bleeding, volvulus with and without strangulation or necrosis, and Barrett's oesophagus Side effects of bloating and dysphagia, recurrence

Question 198

Summarise the prognosis for patients with hiatus hernias

Answer 198

Gain symptomatic relief with medical/surgical treatment, morbidity and mortality higher in >70

Question 199

Define intestinal ischaemia

Answer 199

Impaired blood transfusion to the intestine, resulting in ischaemia of the bowel wall

Question 200

Summarise the epidemiology of intestinal ischaemia

Answer 200

Mainly >50

Question 201

Recognise the signs of intestinal ischaemia on physical examination

Answer 201

tenderness and rebound | cachexia

Question 202

Explain the aetiology / risk factors of intestinal ischaemia

Answer 202

Conditions causing arterial emboli or thrombosis ``` Risk Factors: • old age • history of smoking • hypercoagulable states • atrial fibrillation ```

Question 203

Recognise the presenting symptoms of intestinal ischaemia

Answer 203

sudden severe pain, N&V | Colicky/constant and poorly localised abdominal pain

Question 204

Identify appropriate investigations for intestinal ischaemia and interpret the results

Answer 204

AXR: rule out other causes Angiography: to show blockage ECG: leucocytosis and possible anaemia (if bleeding)

Question 205

Define intestinal obstruction

Answer 205

Mechanical obstruction of the bowel lumen (extrinsic or intrinsic) causing blockage of the intestines

Question 206

Explain the aetiology / risk factors of intestinal obstruction

Answer 206

``` Small Bowel: - Adhesions from prior operations - Malignancy Large Bowel: - Colorectal malignancies Sigmoid/caecal volvulus Paralytic Ileus Postoperative ileus ``` ``` Risk factors • previous abdominal surgery • malrotation • Crohn's disease • hernia ```

Question 207

Summarise the epidemiology of intestinal obstruction

Answer 207

Most are small bowel

Question 208

Recognise the presenting symptoms of intestinal obstruction

Answer 208

``` Diffuse, central colicky pain Vomiting (higher obstruction) [Progression is faster in small bowel] Abdominal distension Progressive constipation and bloating failure to pass flatus or stool ```

Question 209

Recognise the signs of intestinal obstruction on physical examination

Answer 209

Abdominal distension, tympany, high pitched, tinkling bowel sounds Pyrexia – suggests perforation or infarction of bowel

Question 210

Identify appropriate investigations for intestinal obstruction and interpret the results

Answer 210

Bloods: FBC, U&Es, creatinine, group and save Fluid charts Plain AXR & CT

Question 211

Generate a management plan for intestinal obstruction

Answer 211

``` Surgery: - Laparotomy, if no clear diagnosis - Required if signs of peritonitis Non-Surgical treatment: - Drip and suck (bowel decompression) Volvulus: - Can be treated conservatively unless decompression fails/perforation ```

Question 212

Identify the possible complications of intestinal obstruction and its management

Answer 212

Any carcinoma causing obstruction is already advanced | Perforation can cause peritonitis and ischaemia

Question 213

Summarise the prognosis for patients with intestinal obstruction

Answer 213

Small bowel: mortality at 25% with delayed surgery >36 hours; drops to 8% at <36 hours

Question 214

What is functional dyspepsia?

Answer 214

also known as non-ulcer dyspepsia or indigestion, is a term used to describe a group of symptoms affecting the GI tract, including stomach pain or discomfort, nausea, bloating and belching characterised by troublesome early satiety, fullness, or epigastric pain or burning. It can be overlooked as the symptoms overlap with GORD and IBS a chronic disorder of sensation and movement (peristalsis) in the upper GI tract. The cause is unknown; however, several hypotheses could explain this condition. Excessive acid secretion, inflammation of the stomach or duodenum, food allergies, lifestyle and diet influences, psychological factors, medication side effects (from NSAIDs and aspirin), and H.pylori infection have all had their proponents.

Question 215

Define irritable bowel syndrome (IBS)

Answer 215

A functional bowel disorder defined as recurrent episodes of abdominal pain and discomfort for >6 months, associated with >2 of the following: - Altered stool passage - Abdominal bloating - Worsening on eating - Passage of mucous

Question 216

Explain the aetiology / risk factors of functional dyspepsia & irritable bowel syndrome (IBS)

Answer 216

Unknown, psychological factors

Question 217

Summarise the epidemiology of irritable bowel syndrome (IBS)

Answer 217

Common, 10-20% of adults, females 2x more than men

Question 218

Recognise the presenting symptoms of functional dyspepsia & irritable bowel syndrome (IBS)

Answer 218

>6 month history of abdominal pain (colicky in lower abdomen, relieved with defecation/flatus) >3 bowel motions daily or <3 a week Abdominal bloating, change in stool consistency - diarrhoea and constipation Screen for ‘red flag’: weight loss, anaemia, PR bleeding, late onset (>60 years)

Question 219

Recognise the signs of irritable bowel syndrome (IBS) on physical examination

Answer 219

Normally absent signs on examination – can be distended and mildly tender in iliac fossae

Question 220

Identify appropriate investigations for irritable bowel syndrome (IBS) and interpret the results

Answer 220

Diagnosis made by history, investigations used to exclude pathology Bloods: FBC, LFTs, ESR, CRP, TFT Stool examination: MC&S USS: excludes gallstones Hydrogen Breath Test: exclusion of H pylori infection

Question 221

Generate a management plan for irritable bowel syndrome (IBS)

Answer 221

``` Advice: - Dietary modification Medical: - Antispasmodics e.g. buscopan - Prokinetic agents e.g. metoclopramide - Antidiarrhoeals e.g. loperamide - Laxatives e.g. lactulose - Tricyclic antidepressants Psychological Therapies - CBT/relaxation for stress ```

Question 222

Identify the possible complications of irritable bowel syndrome (IBS) and its management

Answer 222

Increase risk of colonic diverticulosis

Question 223

Summarise the prognosis for patients with irritable bowel syndrome (IBS)

Answer 223

Chronic, and relapsing condition – can be exacerbated by stress

Question 224

Define liver abscesses

Answer 224

Abscesses found on the liver (localised infection of liver parenchyma)

Question 225

Summarise the epidemiology of liver abscesses

Answer 225

Caused by bacterial, parasitic or fungal organisms

Question 226

Recognise the presenting symptoms of liver abscesses

Answer 226

Multiple abscesses tend to present more acutely | RUQ pain, tenderness, night sweats, nausea and vomiting, anorexia, dyspnoea

Question 227

Recognise the signs of liver abscesses on physical examination

Answer 227

Hepatomegaly, jaundice, pyrexia

Question 228

Identify appropriate investigations for liver abscesses and interpret the results

Answer 228

Bloods: FBC, ESR, CRP, LFTs USS: shows abscess

Question 229

Explain the aetiology / risk factors of liver cysts

Answer 229

Thought to be congenital

Question 230

Recognise the presenting symptoms of liver cysts

Answer 230

Usually asymptomatic, | Can cause RUQ pain and bloating symptoms

Question 231

Recognise the signs of liver cysts on physical examination

Answer 231

Jaundice, RUQ tenderness

Question 232

Identify appropriate investigations for liver cysts and interpret the results

Answer 232

Bloods: FBC, LFTs Imaging: USS/CT/MRI to show cyst anatomy

Question 233

Summarise the epidemiology of liver cysts

Answer 233

11% incidence

Question 234

Define liver failure

Answer 234

Severe liver dysfunction, causing jaundice, encephalopathy and coagulopathy Hyperacute: <7 days Acute: 1-4 weeks Sub-acute: 4-12 weeks Acute-on-chronic: acute deterioration in chronic liver disease patients

Question 235

Explain the aetiology / risk factors of liver failure

Answer 235

Drugs: paracetamol Viral: Hep A/B/D/E Other: autoimmune liver failure; Budd-Chiari syndrome Pathogenesis: - Jaundice: decreased conjugated bilirubin - Encephalopathy: increased delivery of gut products to systemic circulation - Coagulopathy: decreased clotting factor synthesis ``` Risk Factors • chronic alcohol abuse • poor nutritional status • female sex • age >40 years ```

Question 236

Summarise the epidemiology of liver failure

Answer 236

Paracetamol overdose accounts for 50% of all liver failures

Question 237

Recognise the presenting symptoms of liver failure

Answer 237

Can be asymptomatic Fever, nausea, jaundice abdominal pain, nausea and vomiting

Question 238

Recognise the signs of liver failure on physical examination

Answer 238

Jaundice, encephalopathy, liver asterixis, fetor hepaticus Ascites and splenomegaly, bruising, bleeding Pyrexia

Question 239

Identify appropriate investigations for liver failure and interpret the results

Answer 239

Identify Cause: - Viral serology, paracetamol levels, autoantibodies Bloods: FBC, LFTs, U&Es, glucose, coagulation, ABG, group and save USS/CT: image liver Ascitic fluid: MC&S Doppler: exclude Budd-Chiari syndrome

Question 240

Generate a management plan for liver failure

Answer 240

Resuscitation: ABC Treat Cause: paracetamol overdose Treat/Prevent Complications: - Monitor: vital signs - Manage encephalopathy: lactulose - Antibiotic and antifungal prophylaxis - Hypoglycaemia treatment - Coagulopathy treatment: IV Vitamin K - Gastric mucosa protection: PPI - Avoid: sedatives or liver metabolised drugs - Cerebral Oedema: decrease ICP using mannitol

Question 241

Identify the possible complications of liver failure and its management

Answer 241

Infection, coagulopathy, hypoglycaemia, cerebral oedema, raised ICP

Question 242

Summarise the prognosis for patients with liver failure

Answer 242

Depends on severity

Question 243

Define Mallory-Weiss tear

Answer 243

Mucosal lacerations in the upper gastrointestinal tract; usually at gastro-oesophageal junction or gastric cardia

Question 244

Explain the aetiology / risk factors of a Mallory-Weiss tear

Answer 244

Can be caused by a sudden increase in intragastric pressure | Risk factors: excess alcohol, hyperemesis gravidarum, bulimia, hepatitis, chronic cough

Question 245

Summarise the epidemiology of a Mallory-Weiss tear

Answer 245

Account for 4-8% of upper GI bleeds

Question 246

Recognise the presenting symptoms of a Mallory-Weiss tear

Answer 246

Haematemesis, following a bout of retching or vomiting | Melaena, light-headedness, dizziness, syncope

Question 247

Recognise the signs of a Mallory-Weiss tear on physical examination

Answer 247

Bloods: FBC, clotting screening, U&Es, creatinine, group & save, cardiac enzymes ECG

Question 248

Identify the possible complications of a Mallory-Weiss tear and its management

Answer 248

Vomiting: electrolyte imbalances Bleeding: hypovolaemic shock and death Comorbidities: MI, hepatitis

Question 249

Summarise the prognosis for patients with a Mallory-Weiss tear

Answer 249

Prognosis usually excellent, tears heal rapidly within 48-72 hours; re-bleeding in 8-20% of cases

Question 250

Define NASH

Answer 250

non-alcoholic steatohepatitis

Question 251

Define NASH

Answer 251

non-alcoholic steatohepatitis - An accumulation of fat in the liver, associated with inflammation, not due to excessive alcohol intake

Question 252

Explain the aetiology / risk factors of non-alcoholic steatohepatitis (NASH)

Answer 252

An accumulation of triglycerides and other lipids within hepatocytes Risk Factors: T2DM, polycystuc ovary syndrome, HepB/C HIV, Drugs (amiodarone, tamoxifen), metabolic disorders (Wilson’s)

Question 253

Summarise the epidemiology of non-alcoholic steatohepatitis (NASH)

Answer 253

Most common cause of deranged LFTs

Question 254

Recognise the presenting symptoms of non-alcoholic steatohepatitis (NASH)

Answer 254

Most are asymptomatic – but may report fatigue, malaise or RUQ pain Can present with symptoms of cirrhosis (ascites, oedema and jaundice)

Question 255

Recognise the signs of non-alcoholic steatohepatitis (NASH) on physical examination

Answer 255

Hepatomegaly, splenomegaly, signs of chronic liver disease (spider naevi, ascites, oedema, ABCDE)

Question 256

Identify appropriate investigations for non-alcoholic steatohepatitis (NASH) and interpret the results

Answer 256

Definitive diagnosis can only be made with biopsy Bloods: LFTs, FBC, lipids Imaging: USS/CT Biopsy: only way to diagnose

Question 257

Generate a management plan for non-alcoholic steatohepatitis (NASH)

Answer 257

Advice: • Adequate diet • Weight loss, and control of comorbidities

Question 258

Identify the possible complications of non-alcoholic steatohepatitis (NASH) and its management

Answer 258

Can progress to cirrhosis and liver failure

Question 259

Summarise the prognosis for patients with non-alcoholic steatohepatitis (NASH)

Answer 259

Depends on the stage of disease

Question 260

Define oesophageal cancer

Answer 260

Cancer derived from oesophageal cells

Question 261

Explain the aetiology / risk factors of oesophageal cancer

Answer 261

Majority are SCC and adenocarcinomas Risk Factors: smoking, alcohol, Caucasian, Barrett’s Oesophagus UK: usually adenocarcinoma (as a result of Barrett's oesophagus) Smoking, some Mediterranean/Chinese foods: squamous cell carcinoma

Question 262

Summarise the epidemiology of oesophageal cancer

Answer 262

Common, aggressive tumour

Question 263

Recognise the presenting symptoms of oesophageal cancer

Answer 263

Dysphagia, vomiting, anorexia and weight loss, symptoms of GI blood loss

Question 264

Recognise the signs of oesophageal cancer on physical examination

Answer 264

Lymphadenopathy, weight loss

Question 265

Recognise the signs of oesophageal cancer on physical examination

Answer 265

Lymphadenopathy, weight loss

Question 266

Identify appropriate investigations for oesophageal cancer and interpret the results

Answer 266

Bloods: CEA, Ca19-9, FBC, U&Es, LFTs, glucose, CRP Endoscopy: with biopsy of any lesions CXR: metastases

Question 267

Define pancreatic cancer

Answer 267

Cancer deriving from pancreatic tissue

Question 268

Explain the aetiology / risk factors of pancreatic cancer

Answer 268

11th most common cancer, 5th most common cause of cancer death

Question 269

Summarise the epidemiology of pancreatic cancer

Answer 269

Risk Factors: smoking, diet (high BMI, read meat, low vegetables), diabetes, alcohol

Question 270

Recognise the presenting symptoms of pancreatic cancer

Answer 270

Presents quite late Progressive painless jaundice Late symptoms: abdominal pain, acute pancreatitis, weight loss, haematemesis

Question 271

Recognise the signs of pancreatic cancer on physical examination

Answer 271

Courvoisier’s sign, abdominal tenderness, jaundice

Question 272

Identify appropriate investigations for pancreatic cancer and interpret the results

Answer 272

Bloods: Ca19-9, FBC, LFTs, glucose Imaging: USS, abdominal CT, Endoscopic ultrasound

Question 273

What is Courvoisier’s sign?

Answer 273

gallbladder that’s enlarged due to bile buildup (can usually see or feel it) no pain jaundice not caused by a gallbladder stone, usually a tumour 'in the presence of a palpably enlarged gallbladder which is non-tender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones.'

Question 274

Define acute pancreatitis

Answer 274

autodigestion of the pancreatic tissue

Question 275

Explain the aetiology / risk factors of acute pancreatitis

Answer 275

caused by alcohol abuse and gallstones

Question 276

Explain the aetiology / risk factors of acute pancreatitis

Answer 276

caused by alcohol abuse and gallstones

Question 277

Summarise the epidemiology of acute pancreatitis

Answer 277

common, but usually not severe

Question 278

Recognise the signs of acute pancreatitis on physical examination

Answer 278

cullens and grey-turners mass tender epigastric region

Question 279

Recognise the signs of acute pancreatitis on physical examination

Answer 279

cullens and grey-turners mass tender epigastric region

Question 280

Identify appropriate investigations for acute pancreatitis and interpret the results

Answer 280

bloods: hypocalcaemia (fat necrosis), FBC, CRP,

Question 281

Generate a management plan for acute pancreatitis

Answer 281

- initial fluid resuscitation (+ oxygen. analgesia and anti-emesis if necessary) - Choledocholithiasis without cholangitis - cholecystectomy Cholecystectomy should be delayed in patients with severe/necrotising acute pancreatitis. - gallstone pancreatitis with cholangitis - ERCP within 24 hours - Alcohol-induced pancreatitis: counselling intervention during admission. may need pharmacological treatment for alcohol withdrawal. Vitamin, thiamine and folic acid replacement - with infected pancreatic necrosis: IV ABs, catheter and surgery?

Question 282

Identify the possible complications of acute pancreatitis and its management

Answer 282

Local: pancreatic necrosis, pseudocyst Systemic: MODS, sepsis, renal failure, ARDS Long Term: chronic pancreatitis

Question 283

Summarise the prognosis for patients with acute pancreatitis

Answer 283

20% run severe course with 70% mortality, 80% run milder with 5% mortality

Question 284

Define chronic pancreatitis

Answer 284

Chronic pancreatitis is inflammation due to irreversible changes to the pancreatic structure, like fibrosis, atrophy and calcification. Healthy tissue is replaced by misshaped/stenosed ducts (caused by fibrosis of the ducts), (acinar) atrophy and calcification. This leads to adrenal insufficiency. Chronic inflammatory disease of the pancreas resulting in irreversible parenchymal atrophy and fibrosis, causing, in turn, impaired endocrine and exocrine function and recurrent abdominal pain

Question 285

Explain the aetiology / risk factors of acute pancreatitis

Answer 285

Severe epigastric pain, radiating to the back, relieved by sitting forward Aggravated by movement, exacerbated by eating or drinking alcohol. Weight loss, bloating and steatorrhea Associated with anorexia, nausea and vomiting IMPORTANT: check whether the patient has a history of high alcohol intake or gallstones

Question 286

Recognise the signs of acute pancreatitis on physical examination

Answer 286

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

Question 287

Identify appropriate investigations for acute pancreatitis and interpret the results

Answer 287

Bloods: glucose, amylase, lipase, hypocalcaemia, CRP ERCP/MRCP: early changes are duct dilatation and stumping of branches; late changes are duct strictures with alternating dilatation AXR: pancreatic calcification

Question 288

Generate a management plan for acute pancreatitis

Answer 288

General: - Mainly symptomatic treatment and supportive Endoscopic therapy: - Sphincterotomy, stone extraction - Extracorporeal shock-wave lithotripsy used for fragmentation prior to endoscopic removal Surgical: - Indicated if conservative management failed

Question 289

Identify the possible complications of acute pancreatitis and its management

Answer 289

Local: - Pseudocysts, duodenal obstruction, pancreatic ascites Systemic: - Diabetes, steatorrhea, reduced quality of life

Question 290

Summarise the prognosis for patients with acute pancreatitis

Answer 290

Difficult to predict, life expectancy reduced by 10-20 years

Question 291

Define peptic ulcer disease and gastritis

Answer 291

Ulcerations in the GI tract caused by exposure to gastric acid and pepsin.

Question 292

Explain the aetiology / risk factors of peptic ulcer disease and gastritis

Answer 292

Imbalance of damaging pepsin and gastric acid with protective mucosal mechanisms. Common: Very strong association with H pylori (95% of duodenal, 80% of gastric), NSAID use Rare: Zollinger-Ellison syndrome: gastrin secreting pancreatic tumour RF: H.pylori, smoking (increases acid production), age, NSAIDs, burns and head trauma can increase ulcer development Pain- caused by breakdown reaches nerves Bleeding- breakdown reaches blood vessels

Question 293

Summarise the epidemiology of peptic ulcer disease and gastritis

Answer 293

Common, more in men, and annual incidence of 1-4:1000, with duodenal ulcers being more common in younger people Duodenal ulcers are 4x more common than gastric

Question 294

Recognise the presenting symptoms of peptic ulcer disease and gastritis

Answer 294

Epigastric pain, which is relieved by antacids Variable relationship to food: - If worse straight after eating, gastric - If worse hours later/relieved after eating or drinking milk, duodenal May have melaena and haematemesis May have weight loss, but more common in gastric ulcers. Pointing signs: they can point to where the pain is localised H.pylori: epigastric pain that worsens with eating, postprandial belching and epigastric fullness, early satiety, fatty food intolerance, nausea, and occasional vomiting

Question 295

Recognise the signs of peptic ulcer disease and gastritis on physical examination

Answer 295

May be no physical findings | Epigastric tenderness and signs of complications

Question 296

Identify appropriate investigations for peptic ulcer disease and gastritis and interpret the results

Answer 296

Bloods: FBC, amylase, U&Es, clotting, LFT, cross-match, Secretin test (ZE) Endoscopy: (over 55, or alarm symptoms) four quadrant ulcer biopsies to rule out malignancy, no need to biopsy duodenal ulcers Rockall Scoring: for severity after GI bleed H Pylori testing: (If under 55, with no alarm symptoms) - C13-urea breath test - Serology - Stool antigen testing

Question 297

Generate a management plan for peptic ulcer disease and gastritis

Answer 297

Acute: - Resuscitation if perforated/bleeding - IV PPI (omeprazole) Endoscopy: - Haemostasis by electrocoagulation, laser Surgery: - If perforated or bleeding uncontrolled H pylori Eradication: - Tripe Therapy (clarithromycin, amoxicillin + PPI) for 1-2 weeks If non-H pylori: - Treat with PPIs or H2 antagonists, stop NSAID use

Question 298

Identify the possible complications of peptic ulcer disease and gastritis and its management

Answer 298

Haemorrhage, perforation

Question 299

Summarise the prognosis for patients with peptic ulcer disease and gastritis

Answer 299

Lifetime risk is 10%, usually good as can be cured with H pylori eradication

Question 300

Define perineal abscesses

Answer 300

Collection of pus in the anal/rectal region

Question 301

Define perineal fistulae

Answer 301

an abnormal chronically infected tract communicating between the perineal skin and either the anal canal or the rectum

Question 302

Explain the aetiology / risk factors of perineal abscesses and fistulae

Answer 302

Caused by bacterial infection of anal fissure, STIs or blocked anal glands Fistulae develop as a complication of an abscess Fistulae can develop as a complications of Crohn's disease Risk Factors: IBD Diabetes mellitus Malignancy

Question 303

Summarise the epidemiology of perineal abscesses and fistulae

Answer 303

High risk groups include diabetes, immunocompromised, anal sex common

Question 304

Recognise the presenting symptoms of perineal abscesses and fistulae

Answer 304

Painful hardened tissue in perianal area, constant throbbing pain in the perineum Discharge of pus, lump/nodule, tenderness at anus edge, fever, constipation Personal or family history of IBD

Question 305

Recognise the signs of perineal abscesses and fistulae on physical examination

Answer 305

Lump/nodule, tenderness, discharge Small skin lesion near the anus (opening of the fistula) A thickened area over the abscess/fistula may be felt

Question 306

Identify appropriate investigations for perineal abscesses and fistulae and interpret the results

Answer 306

DRE confirms the presence of the fissure | MRI: shows fistular tracts/deep abscesses

Question 307

Generate a management plan for perineal abscesses and fistulae

Answer 307

ABSCESS: Prompt surgical drainage Pain relief Antibiotics usually not necessary FISTULA: Laying Open of Fistula A probe is inserted to explore the fistula. Dye can be inserted into external opening to help find internal opening Low Fistula - Fistulotomy. Care must be taken to prevent damage to the anal sphincter High Fistula - Fistulotomy would cause INCONTINENCE so NOT performed. Seton - a non-absorbable suture that is threaded through the fistula and allows drainage Antibiotics

Question 308

Identify the possible complications of perineal abscesses and fistulae and its management

Answer 308

Systemic infection, fissure, recurrence, scarring Damage to internal anal sphincter Incontinence Persisting pain

Question 309

Summarise the prognosis for patients with perineal abscesses and fistulae

Answer 309

Abscess: Good if treated promptly – 31% can develop a fistula Fistula: High recurrence rate without complete excision

Question 310

Define peritonitis

Answer 310

Inflammation of the peritoneum, can be primary or secondary, localised or generalised

Question 311

Explain the aetiology / risk factors of peritonitis

Answer 311

UGIT: malignancy, trauma, peptic ulcer, iatrogenic LGIT: ischaemic bowel, diverticulitis, hernia, appendicitis Hepatobiliary system: cholecystitis, malignancy, pancreatitis Genitourinary tract: pelvic inflammation, malignancy

Question 312

Recognise the presenting symptoms of peritonitis

Answer 312

Abdominal pain, worsening | Anorexia, nausea and vomiting

Question 313

Recognise the signs of peritonitis on physical examination

Answer 313

Patient appears unwell and distressed; fever; tachycardia Tenderness, guarding and rebound tenderness Patient may lie with knees flexed to avoid abdominal movement

Question 314

Identify appropriate investigations for peritonitis and interpret the results

Answer 314

Bloods: FBC, U&Es, LFTs, MC&S Imaging: AXR, erect CXR, USS, CT, MRI

Question 315

Generate a management plan for peritonitis

Answer 315

Medical: Third-generation cephalosporin, Surgical: Exploratory surgery

Question 316

Identify the possible complications of peritonitis and its management

Answer 316

Sepsis, death

Question 317

Summarise the prognosis for patients with peritonitis

Answer 317

Main prognostic factor is renal dysfunction

Question 318

Define pilonidal sinus

Answer 318

A small hole, or tunnel, that develops at the top of the buttocks An abnormal epithelium-lined tract filled with hair that opens onto the skin surface, most commonly in the natal cleft

Question 319

Explain the aetiology / risk factors of pilonidal sinus

Answer 319

Abnormal hair growth, that grows into the skin rather than out of it (caused by shed or sheared hairs penetrating the skin) inciting and inflammatory reaction and sinus development ``` Risk Factors sedentary life-style, obesity, friction Hirsutism Spending a long time sitting down Occupational (e.g. hairdressers may develop interdigital pilonidal sinus) ```

Question 320

Summarise the epidemiology of pilonidal sinus

Answer 320

COMMON | Affects 0.7% of young adults

Question 321

Recognise the presenting symptoms of pilonidal sinus

Answer 321

Boil-like lump, pain, swelling, redness, pus discharge Painful natal cleft Often recurrent

Question 322

Recognise the signs of pilonidal sinus on physical examination

Answer 322

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

Question 323

Identify appropriate investigations for pilonidal sinus and interpret the results

Answer 323

No real investigation, diagnosis made on examination

Question 324

Generate a management plan for pilonidal sinus

Answer 324

Advice: • Should be kept dry and clean, and area kept hair-free Medical: • Antibiotics: If there is pus or an abscess Surgical: • Incision and drainage, under general anaesthetic (acute) • Excision: removing the skin around the sinus (chronic)

Question 325

Identify the possible complications of pilonidal sinus and its management

Answer 325

Pain Infection Abscess Recurrence

Question 326

Summarise the prognosis for patients with pilonidal sinus

Answer 326

Good, simply needs to be treated

Question 327

Define portal hypertension

Answer 327

Abnormally high pressure in the hepatic portal vein; an hepatic venous gradient pressure of >12mmHg

Question 328

Explain the aetiology / risk factors of portal hypertension

Answer 328

Pre-Hepatic: - Congenital atresia or stenosis - Portal vein thrombosis; splenic vein thrombosis - Extrinsic compression e.g. tumours Hepatic: - Cirrhosis; chronic hepatitis - Schistosomiasis; granulomata Post-hepatic: - Budd-Chiari syndrome (hepatic vein obstruction) - Constrictive pericarditis; right heart failure Other: - Increased hepatic blood flow (splenomegaly) - Idiopathic Left-sided portal hypertension - Rare, confined to left side of portal system; presents as gastric varices bleeding

Question 329

Summarise the epidemiology of portal hypertension

Answer 329

Common in liver disease

Question 330

Recognise the presenting symptoms of portal hypertension

Answer 330

For Liver disease: - History of jaundice, alcohol consumption, blood transfusion (hep B or C susceptibility), family history For complications: - Malaena, lethargy, abdominal distension, abdominal pain and fever

Question 331

Recognise the signs of portal hypertension on physical examination

Answer 331

Dilated veins in anterior abdominal wall and caput medusa Venous hum, loudest in inspiration Splenomegaly; ascites ``` Signs of Portal Hypertension - Caput medusae - Splenomegaly - Ascites Signs of Liver Failure - Jaundice - Spider naevi - Palmar erythema - Confusion - Asterixis - Fetor hepaticus (breathe of the dead) - Enlarged or small liver - Gynaecomastia - Testicular atrophy ```

Question 332

Identify appropriate investigations for portal hypertension and interpret the results

Answer 332

``` Bloods: LFTs, U&Es, FBC, glucose, clotting Portal Hypertension Measurement: HVPG Scans: USS, Doppler, CT/MRI Endoscopy: for oesophageal varices Biopsy: if indicated ```

Question 333

Generate a management plan for portal hypertension

Answer 333

Difficult to treat, except by treating cause Drug: - Beta Blockers (carvedilol) reduces portal pressure - Nitrates reduces portal pressure - Vasoactive drugs (terlipressin and octreotide) to assist in acute bleeding Endoscopy: - To detect, monitor and treat varices Transjugular intrahepatic portosystemic shunt (TIPS) - Using a shunt to connect portal and hepatic veins, decompressing the portal system - Ascites, oesophageal varices and gastric varices Surgery: - Surgical portosystemic shunts

Question 334

Identify the possible complications of portal hypertension and its management

Answer 334

Bleeding, ascites, pulmonary problems, liver failure, hepatic encephalopathy, cirrhotic cardiomyopathy

Question 335

Summarise the prognosis for patients with portal hypertension

Answer 335

Depends on underlying disease, Child-Pugh score determines prognosis

Question 336

Define primary biliary cirrhosis

Answer 336

Chronic inflammatory liver disease of the bile system, leading to cholestasis and cirrhosis

Question 337

Explain the aetiology / risk factors of primary biliary cirrhosis

Answer 337

Unknown, autoimmune aetiology is likely

Question 338

Recognise the presenting symptoms of primary biliary cirrhosis

Answer 338

Can be an incidental finding (from detecting high ALP) Insidious onset fatigue, weight loss and pruritus Discomfort in the RUQ (rarely) Can present with a complication, or associated conditions

Question 339

Recognise the signs of primary biliary cirrhosis on physical examination

Answer 339

Early: no signs Late: jaundice, skin pigmentation, excoriation marks, xanthomas, xanthomata, hepatomegaly, ascites - Liver disease signs (palmar erythema, spider naevi, clubbing)

Question 340

Identify appropriate investigations for primary biliary cirrhosis and interpret the results

Answer 340

Bloods: LFT (increased AlkPhos, GGT and bilirubin) Anti-mitochondrial antibodies are hallmark feature USS: exclude extrahepatic biliary obstruction Liver Biopsy: chronic inflammatory cells and granulomas around intrahepatic bile ducts

Question 341

Define primary sclerosing cholangitis

Answer 341

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

Question 342

Explain the aetiology / risk factors of primary sclerosing cholangitis

Answer 342

Unknown, possible genetic predisposition with toxic/infective triggers

Question 343

Summarise the epidemiology of primary sclerosing cholangitis

Answer 343

more common in males (60% affects all ages associated with IBD

Question 344

Recognise the presenting symptoms of primary sclerosing cholangitis

Answer 344

Can be asymptomatic and diagnosed after an incidental finding of increased AlkPhos Intermittent jaundice, pruritus, RUQ pain, weight loss and fatigue Episodic fever, rigors, is less common History of UC and symptoms of complications

Question 345

Recognise the signs of primary sclerosing cholangitis on physical examination

Answer 345

May have no signs | Evidence of: jaundice, hepatosplenomegaly, spider naevi, palmar erythema and ascites

Question 346

Identify appropriate investigations for primary sclerosing cholangitis and interpret the results

Answer 346

Bloods: LFTs (increased AlkPhos, GGT, bilirubin and transaminases, decreased albumin) Serology: immunoglobulin levels (increased IgG (children) and IgM (Adults)) ERCP: structuring and interspersed dilation of bile ducts MRCP: non-invasive imaging Liver Biopsy: confirm diagnosis, and allows staging

Question 347

Summarise the epidemiology of primary biliary cirrhosis

Answer 347

more common in females | onset mostly at middle age

Question 348

Define rectal prolapse

Answer 348

The protrusion of either the rectal mucosa or the entire wall of the rectum Partial: only mucosa involvement Complete: all layers of the rectal wall

Question 349

Explain the aetiology / risk factors of rectal prolapse

Answer 349

Risk Factors: increased intra-abdominal pressure, previous surgery, pelvic floor dysfunction

Question 350

Summarise the epidemiology of rectal prolapse

Answer 350

Uncommon

Question 351

Recognise the presenting symptoms of rectal prolapse

Answer 351

Due to a lax sphincter, prolonger straining, and related to chronic neurological and psychological disorders. Risk Factors: increased intra-abdominal pressure, previous surgery, pelvic floor dysfunction

Question 352

Recognise the signs of rectal prolapse on physical examination

Answer 352

Protruding mass at anus, possible tenderness

Question 353

Identify appropriate investigations for rectal prolapse and interpret the results

Answer 353

Barium enema/colonoscopy: evaluate entire colon prior to surgery Other investigations to assess underlying conditions (e.g. stool microscopy)

Question 354

Define ulcerative colitis

Answer 354

Chronic relapsing and remitting inflammatory condition affecting the large bowel

Question 355

Explain the aetiology / risk factors of ulcerative colitis

Answer 355

Unknown, suggested genetic susceptibility, family history component inappropriate immune response in a genetically susceptible individual

Question 356

Summarise the epidemiology of ulcerative colitis

Answer 356

1:1500, common in Ashkenazi Jews and Caucasians 15-30s onset smoking increases risk NSAIDs may exacerbate

Question 357

Recognise the presenting symptoms of ulcerative colitis

Answer 357

Bloody diarrhoea, or mucous, tenesmus and urgency Weight loss, fever, abdominal pain before passing stool

Question 358

Recognise the signs of ulcerative colitis on physical examination

Answer 358

Iron-deficiency anaemia, dehydration, clubbing, abdominal tenderness, tachycardia DRE: blood, mucous, tenderness

Question 359

Identify appropriate investigations for ulcerative colitis and interpret the results

Answer 359

Bloods: FBC, ESR, CRP, LFTs (p-anca positive) Stool: culture (exclude infectious colitis) AXR: exclude toxic megacolon Flexible sigmoidoscopy: determines severity, histological confirmation Barium enema: mucosal ulceration with granular appearance

Question 360

Generate a management plan for ulcerative colitis

Answer 360

Observe activity markers: - Haemoglobin, albumin, ESR, CRP and diarrhoea frequency Acute Exacerbations: - IV rehydration, IV corticosteroids, antibiotics - Bowel rest, parenteral feeding, DVT prophylaxis - Mild disease: topical/oral 5-ASA derivatives e.g. mesalazine/sulphasalazine - Moderate/Severe disease: oral steroids and oral 5-ASA (sulphasalazine) and immunosuppression (azathioprine, cyclosporine) Advice: - Patient education and support - Treatment of complications Surgical: - Indicated if failure of medical treatment - Proctocolectomy with ileostomy or an ileo-anal pouch formation

Question 361

Identify the possible complications of ulcerative colitis and its management

Answer 361

GI: haemorrhage, toxic megacolon, perforation, colonic carcinoma Extra-GI: uveitis, arthropathy, renal calculi

Question 362

Summarise the prognosis for patients with ulcerative colitis

Answer 362

Relapsing and remitting condition: normal life expectancy Poor Prognosis: ABCDE; albumin <30, blood PR, CRP raised, dilated loops of bowel, eight or more bowel movements per day, fever

Question 363

Define viral hepatitis

Answer 363

Inflammation of the liver, due to a viral cause

Question 364

Explain the aetiology / risk factors of viral hepatitis

Answer 364

Causes are hepatitis viruses, HAV, HBV, HCV, HDV, HEV, EBV, CMV, (malaria, Q fever, syphilis, yellow fever) Hep A spread by faecal-oral route or shellfish Hep B spread by blood products, IV drug abused and physical or sexual contact Hep C spread by blood: transfusion, IV drug abuse, sexual contact. RF: male, older, high viral use, alcohol use, HIV, HBV

Question 365

Summarise the epidemiology of viral hepatitis

Answer 365

Incidence is declining Hep A endemic in africa and S.America. Hep B endemic in Far East, Africa and mediterranean

Question 366

Recognise the presenting symptoms of viral hepatitis

Answer 366

Acute Infection: • Nausea and vomiting; myalgia, fatigue, malaise • RUQ pain; change in smell or taste • Photophobia and headache Chronic infection: • May be asymptomatic Can lead to chronic hepatitis, cirrhosis and HCC

Question 367

Recognise the signs of viral hepatitis on physical examination

Answer 367

RUQ tenderness, fever, hepatomegaly | Later: Jaundice, hepatosplenomegaly, arthralgia, urticaria

Question 368

Identify appropriate investigations for viral hepatitis and interpret the results

Answer 368

Bloods: FBC, U&Es, LFTs, clotting factors, serology Imaging: USS/CT/MRI to assess cirrhosis

Question 369

Generate a management plan for viral hepatitis

Answer 369

``` HAV: • Mainly symptomatic; avoid alcohol HBV: • Advice: avoid unprotected sex, education • Treat acute infection: mainly symptomatic HCV: • Largely symptomatic; avoid excess alcohol • Drug therapy: peginterferon HDV: • Pegylated interferon alpha • Liver transplant HEV: • Mainly supportive, as HAV ```

Question 370

Identify the possible complications of viral hepatitis and its management

Answer 370

Cirrhosis, liver failure, Guillian-Barre syndrome, hepatitis, HCC

Question 371

Summarise the prognosis for patients with viral hepatitis

Answer 371

Poor without treatment, especially fatal in the elderly

Question 372

What type of bacteria is H.pylori?

Answer 372

helical-shaped gram-negative

Question 373

Define volvulus

Answer 373

Rotation of a loop of small bowel around the axis of its mesentery that results in bowel obstruction and potential ischaemia. The areas usually affected: - Sigmoid colon - 65% - Caecum - 30% - VOLVULUS NEONATORUM - occurs in neonates and typically affects the midgut Long, and twisted colon, usually in the sigmoid colon

Question 374

Explain the aetiology / risk factors of volvulus

Answer 374

Full bowel twists on its mesenteric pedicle to create a closed-loop obstruction Risk Factors: elderly, chronic constipation, megacolon ``` Risk Factors Adults - Long sigmoid colon - Long mesentery - Mobile caecum - Chronic constipation - Adhesions - Chagas disease - Parasitic infections Neonatal - Malrotation ```

Question 375

Summarise the epidemiology of volvulus

Answer 375

Leading cause of obstruction in lesser developed countries

Question 376

Recognise the presenting symptoms of volvulus

Answer 376

Sudden onset severe colicky pain, associated with a distended abdomen, complete/absolute constipation Vomiting There may be a history of transient attacks in which spontaneous reduction of the volvulus has occurred Neonatal volvulus presents around 3 months

Question 377

Recognise the signs of volvulus on physical examination

Answer 377

Distended abdomen, non-tender, palpable mass may be present ``` Signs of bowel obstruction with abdominal distension and tenderness Absent or tinkling bowel sounds Fever Tachycardia Signs of dehydration ```

Question 378

Identify appropriate investigations for volvulus and interpret the results

Answer 378

AXR: shows signs of volvulus (coffee bean or embryo) | May need barium enema - show obstruction

Question 379

Define Wilson's disease

Answer 379

An autosomal recessive disorder characterised by a reduced biliary excretion of copper, and accumulation in the liver and brain, especially in the basal ganglia

Question 380

Explain the aetiology / risk factors of Wilson's disease

Answer 380

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

Question 381

Summarise the epidemiology of Wilson's disease

Answer 381

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

Question 382

Recognise the presenting symptoms of Wilson's disease

Answer 382

Liver: (may present with hepatitis, liver failure or cirrhosis;) jaundice, easy bruising, variceal bleeding, encephalopathy Neurological: dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia Psychiatric: conduct disorders, personality changes and psychosis

Question 383

Recognise the signs of Wilson's disease on physical examination

Answer 383

Liver: hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia Neurological: (same as symptoms) dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia Eyes: green/brown Kayser-Fleischer rings in the corneal limbus, sunflower cataract

Question 384

Identify appropriate investigations for Wilson's disease and interpret the results

Answer 384

Bloods: LFTs, copper 24-hour urinary copper levels: increased Liver biopsy: increased copper content Genetic analysis: no simple genetic test to diagnose