GASTRO Flashcards

Question

Define Anal Fissure

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

• Tears in the squamous lining of the anus on examination

Answer 6

Examine the anus

Answer 7

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

Answer 8

Chronic anal fissure

Answer 9

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

Answer 10

Inflammation of the appendix

Answer 11

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

Answer 12

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

Answer 13

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

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

• In a genetically predisposed individual, an environmental agent (e.g. viruses or drugs) may lead to hepatocyte expression of HLA antigens, which then become the focus of a principally T-cell-mediated autoimmune attack • The raised titre of anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (ASMA) and anti-liver/kidney microsomes (anti-LKM) are NOT thought to directly injure the liver • The chronic inflammatory changes are similar to those seen in chronic viral hepatitis with lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and, eventually, cirrhosis • TWO major forms of autoimmune hepatitis: o Type 1 (Classic) • ANA • ASMA • Anti-actin antibodies (AAA) • Anti-soluble liver antigen (antiMSLA) o Type 2 • Antibodies to liver/kidney microsomes (ALKM-1) • Antibodies to liver cytosol antigen (ALCM1)

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

• Bloods: o LFTs: • High: AST, ALT, GGT, ALP and Bilirubin • Low: albumin (in severe disease) o Clotting: • High PT (in severe disease) o FBC: • Low Hb, platelets and WCC (if hypersplenism from portal hypertension) o Hypergammaglobulinaemia • Presence of ANA, ASMA and Anti-LKM antibodies • Liver Biopsy: o Needed to establish diagnosis and check whether hepatitis or cirrhosis • To rule out other causes of liver disease: o Viral serology o Urinary copper/caeruloplasmin o Ferritin and transferrin saturation o alpha1 antitrypsin o AntiMmitochondrial antibodies (PBC) • US, CT or MRI of liver and abdomen o Visualise structural lesions • ERCP o To rule out PSC

Answer 25

Prolonged exposure of the normal squamous epithelium to reflux ate of GORD leads to mucosal inflammation and erosion , leading to replacement of the mucosa with metaplastic columnar epithelium - Metaplastic change: squamous --> columnar - Main problem: Barrett's could progress to oesophageal adenocarcinoma

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

• RUQ pain and epigastric tenderness

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

• GOOD prognosis with appropriate treatment

Answer 42

Inflammation of the gallbladder

Answer 43

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

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

``` • Chronic alcohol misuse (most common in the UK) • Chronic viral hepatitis (hep B/C - most common worldwide) • Autoimmune hepatitis • Drugs (e.g. methotrexate, hepatotoxic drugs) • Inherited o alpha1-antitrypsin deficiency o Haemochromatosis o Wilson's disease o Galactosaemia o Cystic Fibrosis • Vascular o Budd-Chiari Syndrome o Hepatic Venous Congestion • Chronic Biliary Diseases o PBC o PSC o Biliary atresia • Unknown: 5-10% • Non-Alcoholic Steatohepatitis (NASH) o Associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia and drugs (e.g. amiodarone, tamoxifen) ```

Answer 53

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

Answer 54

One of the top 10 causes of death worldwide

Answer 55

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

Answer 56

• Bloods o FBC: low platelets + Hb = because of hypersplenism as a result of portal hypertension o LFTs - may be normal but often get: • High AST, ALT, ALP, GGT and bilirubin • Low albumin o Clotting: prolonged PT o Serum AFP (alpha-fetoprotein = tumour marker for liver cancer): • Raised in chronic liver disease • High levels may suggest hepatocellular carcinoma • Investigations to determine CAUSE o Viral serology o alpha1-antitrypsin o Caeruloplasmin • This is a copper-carrying complex that is LOW in Wilson's disease o Iron studies: serum ferritin, iron, total iron binding capacity (TIBC) -check for haemochromatosis o AntiMmitochondrial antibody (PBC) o ANA, ASMA (autoimmune hepatitis) • Ascitic Tap o MC&S - check for infection o Biochemistry (protein, albumin, glucose, amylase) o Cytology o IMPORTANT: ascitic tap with neutrophils > 250/mm3 = spontaneous bacterial peritonitis (SBP) • Liver Biopsy o Performed either: • Percutaneously • Transjugular - if clotting deranged or ascitic o Histopathological features of cirrhosis: • Periportal fibrosis • Loss of normal liver architecture • Nodular appearance o Grade - indicates degree of inflammation o Stage - degree of architectural distortion (from mild portal fibrosis --> cirrhosis) • Imaging o US, CT or MRI - to detect complications such as: • Ascites • HCC • Hepatic or portal vein thrombosis • Exclude biliary obstruction o MRCP (if PSC suspected) • Endoscopy o To examine varices • Child-Pugh Grading - score for estimating the prognosis in chronic liver disease/cirrhosis. It is based on 5 factors: o Albumin o Bilirubin o PT o Ascites o Encephalopathy • Cirrhosis can be divided into Classes using the Child-Push grading system: o Class A: 5-6 o Class B: 7-9 o Class C: 10-15

Answer 57

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

Answer 58

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

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

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

Answer 63

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

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

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

Answer 69

Chronic granulomatous inflammatory disease that. can affect any part of the GI tract. Grouped with UC and known, together, as IBD

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

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

Answer 74

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

Answer 75

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

Answer 76

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

Answer 77

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

Answer 78

- Diverticulosis: presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel - Diverticular disease: diverticulosis associated with complications e.g. haemorrhage, infection, fistulae - Diverticulitis: actue inflammation and infection of colonic diverticulae - Hinchey Classification of Acute Diverticulitis : Ia: phlegm Ib and II: localised abscesses III: perforation and purulent peritonitis IV: faecal peritonitis

Answer 79

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

Answer 80

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

Answer 81

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

Answer 82

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

Answer 83

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

Answer 84

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

Answer 85

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

Answer 86

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

Answer 87

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

Answer 88

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

Answer 89

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

Answer 90

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

Answer 91

* Diffuse abdominal tenderness * Abdominal distension * Bowel sounds are often INCREASED * In SEVERE gastroenteritis: pyrexia, dehydration, hypotension and peripheral shutdown Very important to check hydration status immediately as any diarrhoeal condition can lead to dehydration

Answer 92

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

Answer 93

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

Answer 94

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

Answer 95

• Good prognosis because most cases are self-limiting

Answer 96

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

Answer 97

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

Answer 98

Incidence depends on cause

Answer 99

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

Answer 100

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

Answer 101

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

Answer 102

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

Answer 103

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

Answer 104

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

Answer 105

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

Answer 106

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

Answer 107

* COMMON | * 5-10% of adults

Answer 108

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

Answer 109

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

Answer 110

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

Answer 111

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

Answer 112

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

Answer 113

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

Answer 114

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

Answer 115

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

Answer 116

* COMMON | * Peak age: 45-65 yrs

Answer 117

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

Answer 118

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

Answer 119

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

Answer 120

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

Answer 121

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

Answer 122

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

Answer 123

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

Answer 124

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

Answer 125

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

Answer 126

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

Answer 127

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

Answer 128

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

Answer 129

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

Answer 130

``` • Incarceration • Strangulation • Bowel obstruction • Maydl's hernia (strangulated W-shaped loop of small bowel) • Richter's hernia (strangulation of only part of the bowel circumference) • Surgery Complications o Pain o Wound infection o Haematoma ```

Answer 131

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

Answer 132

Prolapse of the upper stomach through the diaphragmatic oesophageal hiatus

Answer 133

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

Answer 134

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

Answer 135

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

Answer 136

usually NO signs

Answer 137

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

Answer 138

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

Answer 139

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

Answer 140

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

Answer 141

Inflammation of the colon due to bacteria, parasites or viruses

Answer 142

``` • Infection leads to inflammation of the colon • Risk Factors o Lack of sanitation o Drinking contaminated water o Antibiotic use ```

Answer 143

• Quite COMMON

Answer 144

* Diarrhoea * Blood and mucus in the stools * Lower abdominal pain * Malaise * Low-grade fever

Answer 145

* Diagnosis is largely CLINICAL | * Stool culture may be used to identify the causative organism

Answer 146

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

Answer 147

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

Answer 148

* UNCOMMON | * More common in the ELDERLY

Answer 149

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

Answer 150

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

Answer 151

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

Answer 152

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

Answer 153

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

Answer 154

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

Answer 155

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

Answer 156

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

Answer 157

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

Answer 158

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

Answer 159

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

Answer 160

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

Answer 161

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

Answer 162

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

Answer 163

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

Answer 164

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

Answer 165

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

Answer 166

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

Answer 167

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

Answer 168

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

Answer 169

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

Answer 170

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

Answer 171

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

Answer 172

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

Answer 173

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

Answer 174

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

Answer 175

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

Answer 176

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

Answer 177

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

Answer 178

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

Answer 179

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

Answer 180

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

Answer 181

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

Answer 182

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

Answer 183

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

Answer 184

• Depends on severity and aetiology

Answer 185

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

Answer 186

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

Answer 187

• Quite rare

Answer 188

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

Answer 189

Malaena (and clinical presentation)

Answer 190

* OGD | * Bloods - FBC to check for anaemia

Answer 191

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

Answer 192

• Boerhaave's perforation

Answer 193

Good prognosis

Answer 194

A term used to describe a range of conditions caused by the buildup of fat in the liver due to causes other than excessive alcohol use

Answer 195

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

Answer 196

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

Answer 197

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

Answer 198

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

Answer 199

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

Answer 200

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

Answer 201

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

Answer 202

• 20% with NASH will develop cirrhosis

Answer 203

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

Answer 204

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

Answer 205

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

Answer 206

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

Answer 207

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

Answer 208

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

Answer 209

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

Answer 210

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

Answer 211

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

Answer 212

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

Answer 213

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

Answer 214

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

Answer 215

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

Answer 216

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

Answer 217

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

Answer 218

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

Answer 219

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

Answer 220

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

Answer 221

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

Answer 222

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

Answer 223

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

Answer 224

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

Answer 225

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

Answer 226

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

Answer 227

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

Answer 228

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

Answer 229

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

Answer 230

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

Answer 231

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

Answer 232

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

Answer 233

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

Answer 234

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

Answer 235

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

Answer 236

• High recurrence rate without complete excision

Answer 237

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

Answer 238

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

Answer 239

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

Answer 240

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

Answer 241

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

Answer 242

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

Answer 243

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

Answer 244

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

Answer 245

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

Answer 246

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

Answer 247

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

Answer 248

* COMMON | * Affects 0.7% of young adults

Answer 249

* Painful natal cleft * Discharging swelling * Often recurrent

Answer 250

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

Answer 251

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

Answer 252

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

Answer 253

* Pain * Infection * Abscess * Recurrence

Answer 254

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

Answer 255

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

Answer 256

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

Answer 257

• A common consequence of cirrhosis

Answer 258

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

Answer 259

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

Answer 260

• Bloods o LFTs o U&Es o Blood glucose o FBC o Clotting screen (prolongation of PT is one of the earliest signs of liver failure) • Specific Tests o Ferritin - haemochromatosis o Hepatitis serology o Autoantibodies (e.g. anti-smooth muscle antibodies in autoimmune hepatitis) o alpha1-antitrypsin levels o Caeruloplasmin - Wilson's disease • Imaging o Abdominal ultrasound - check liver and spleen size and assess portal blood flow o Doppler ultrasound - assess direction of blood flow in vessels o CT/MRI - if other imaging methods are inconclusive o Endoscopy - to check for oesophageal varices • Measure hepatic venous pressure gradient (HVPG) • Liver Biopsy - if indicated

Answer 261

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

Answer 262

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

Answer 263

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

Answer 264

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

Answer 265

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

Answer 266

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

Answer 267

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

Answer 268

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

Answer 269

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

Answer 270

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

Answer 271

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

Answer 272

• Usually presents between 25-40 years of age

Answer 273

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

Answer 274

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

Answer 275

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

Answer 276

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

Answer 277

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

Answer 278

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

Answer 279

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

Answer 280

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

Answer 281

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

Answer 282

Chronic relapsing and remitting inflammatory disease affecting the large bowel

Answer 283

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

Answer 284

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

Answer 285

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

Answer 286

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

Answer 287

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

Answer 288

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

Answer 289

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

Answer 290

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

Answer 291

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

Answer 292

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

Answer 293

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

Answer 294

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

Answer 295

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

Answer 296

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

Answer 297

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

Answer 298

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

Answer 299

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

Answer 300

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

Answer 301

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

Answer 302

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

Answer 303

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

Answer 304

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

Answer 305

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

Answer 306

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

Answer 307

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

Answer 308

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

Answer 309

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

Answer 310

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

Answer 311

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

Answer 312

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

Answer 313

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

Answer 314

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

Answer 315

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

Answer 316

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

Answer 317

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

Answer 318

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

Answer 319

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

Answer 320

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

Answer 321

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

Answer 322

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

Answer 323

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

Answer 324

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

Answer 325

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

Answer 326

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

Answer 327

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

Answer 328

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

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