Gastro Flashcards

Question

What are the signs and symptoms of a/I hepatitis?

Answer 1

Hepatomegaly, Jaundice, encephalopathy , WL, fatigue, abdo discomfort, Nausea, fever, telangectasias, pruritus, splenomegaly, GI bleed

Answer 2

AST+ALT - RAISED TO 200-300 (ALD only raised by 30) ALP GGT bilirubin - mod - markedly raised Serum globulin - markedly raised if untreated PT/INR - prolonged ASMA, ANA - raised in type 1 CERULOPLASMIN - exclude wilsons

Answer 3

Metaplasia from oesophageal squamous epithelium to columnar epithelium.

Answer 4

GORD, FHx, FHx adeocarcinoma, Male, white, smoker, dec socio, obesity

Answer 5

No differentiating symptoms to GORD | Heartburn, chest pain, reflux, regurgitation, laryngitis, Hx aspiration pneumonia, cough, dysphagia

Answer 6

Upper GI endoscopy - only with biopsy can Barrett's be formally diagnosed

Answer 7

Metaplasia/mild dysplasia - Omeprazole / esomeprazole 20mg OD - Radiofrequency ablation - turns squamous - columnar Severe dysplasia - PPIs, + oesophageal mucosal resection / oesophagectomy Need 2yrly endoscopy

Answer 8

Acute gallbladder inflammation. 90% caused by gallstone obstruction at the gallbladder neck or cystic duct.

Answer 9

Main = gallstones Severe illness, severe dehydration, trauma, infection, ciclosporin and ceftriaxome = cause gallstones, low fibre diet, TPN - causes gallbladder hypomotility

Answer 10

RUQ pain + tenderness. Pain = severe + 30mins+ (can begin in epigastric region) +ve murphey's sign - resp cessation on palpation due to pain PAIN AFTER FATTY MEAL - WHEN GALLBLADDER CONTRACTS Jaundice 10% due to contiguous inflammation of biliary ducts N+V, Anorexia, Fever, right shoulder pain.

Answer 11

FBC - WCC high LFTs - ALP H, GGT H, Bilirubin H, (AST+ALT NORMAL) CRP - raised >28.6 USS - shows thickened gallbladder wall and distension. May elicit Murphy on USS.

Answer 12

If mild/no gangrene/no perforation Supportive - maintenance of BP, oxygen if going septic Cefuroxime IV + diclofenac (NSAID) + possible early laparoscopic cholecystectomy If perforation/gangrene/severe - pt may be too ill to operate on: ICU admission, Cefuroxime IV, + urgent cholecystostomy Then elective cholecystectomy (due to recurrence likelihood)

Answer 13

A systemic autoimmune disease triggered by the ingestion of the peptide gluten, which is found in wheat, rye and barley. It results in villus atrophy, hypertrophy of the crypts, and increased lymphocytes in the epithelium and lamina propria.

Answer 14

Stomach - cramps, pains, bloating, distension, diarrhoea, WL ID anaemia, failure to thrive, apthous stomatitis, dermatitis herpetiforms, easy bruising, alopecia, loss of dental enamel. Peripheral neuropathy, ataxia.

Answer 15

FBC - shows microcytic anaemia (ID) IgA/G tTG abs - titres above normal range Endomysial abs - titres above normal range Skin biopsy - granular IgA deposits Gluten challenge = 6 weeks eating gluten then histological sample

Answer 16

Herniation of mucosa through the muscular layer of the colonic wall, and may be due to SM overactivity.

Answer 17

Age >50, dec fibre in diet, obesity, coffee/alcohol NSAID

Answer 18

LLQ pain, guarding and tenderness, Diffuse abdo pain, bloating, diarrhoea, palpable mass in LLQ, fever, leucocytosis Bleeding = abrupt, profuse and painless

Answer 19

FBC - polymorpholeukocytosis CxR - exclude acute abdomen CT - show the mass/outpouching/streaky mesenteric fat Contrast enema/colonoscopy/sigmoidoscopy if profuse bleed.

Answer 20

Asymptomatic = no rx Symptomatic = increase soluble and insoluble fibre, reduce refined foods ie white bread which leave residues. Pain - paracetamol / tramadol 50-100mg orally Oral abc if infection - amoxicillin + clavulanic acid. Severe bleed = endoscopic haemostasis -> if fails surgery If abscess - drain

Answer 21

Pathogenic infection of the GI tract that occurs primarily through ingestion of contaminated food/water/surfaces. Predominantly E-Coli

Answer 22

ETEC - enterotoxic E. coli

Answer 23

Travel recently, extremes of age, immunodeficiency, contact with infected, animal contact

Answer 24

Diarrhoea, abdominal pain and discomfort, fever = usually low grade and resolves within 24-48hrs unless bacteraemia, N+V, anorexia, volume depletion, lethargy

Answer 25

FBC - WCC up / poss low Plts U+E - inc urea and creatinine due to volume depletion, hypokalaemia from diarrhoea Stool culture - growth of E. coli/organism Can do blood culture if severe CRP + ESR - HH Abdo x-ray/CT/MRI - ddx/if inconclusive

Answer 26

Histological presence of gastric mucosal inflammation, for which there are 5 main types: Acute erosive, acute non-erosive, erosive, phlegmonas, and a/i.

Answer 27

H pylori / peptic ulcers

Answer 28

NSAID used (chron) - increased risk of peptic ulcer/haemorrhage

Answer 29

Bile acid salt reflux

Answer 30

Other a/i conditions

Answer 31

Staph A, E. coli, enterobacter.

Answer 32

DONT GET DIARRHOEA Dyspepsia, epigastric discomfort, no features of malignancy N+V and dec appetite Acute abdo pain, fever (low grade),

Answer 33

WCC- increased with inc left shift, possibly dec plts H pylori breath test / stool antigen detection Look for parietal cell /IF a/bs - a/i Endoscopy - visualisation of the damage to the mucosa Review of medications Blood/fluid cultures if suspect phlegmonas

Answer 34

Triple treatment: Omeprazole, clarithromycin, amoxicillin. Can up the abx to metronidazole if not working

Answer 35

Stop NSAIDS, PPI/H2

Answer 36

Rabeprazole = badass PPI

Answer 37

ICU admission, aggressive tailored abx, adrenaline, possible gastrectomy

Answer 38

cyanocobalamine

Answer 39

A break in the mucosal lining of the duodenum or stomach that >5mm and extends to the submucosa. Also described as an imbalance between the promotors of damage - HCL, pepsin, nsaids, pylori, and the preventers of damage - prostaglandins, hco3, mucous, mucosal blood flow.

Answer 40

Nsaid use, smoking, alcohol, in age, h pylori, ICU pts, stress

Answer 41

Epigastric pain, abdo pain and discomfort that is related to eating/nocturnal. CAUTION - duodenal ulcers can radiate to the back N+V, diarrhoea, patient able to point to exact location of pain, shock Signs of anaemia/acute bleed

Answer 42

Stop NSAIDs FBC - inc WCC, possible microcytic anaemia H pylori breath/antigen testing Stool heme testing Upper GI endoscopy = poss - visualisation

Answer 43

Evidence of bleed - endoscopy with embolisation, blood transfusion, PPIs, Surgery if needed No bleed + H pylori Triple therapy or quadruple triple - PPI + Amox + clarith quad - bismuth subsalicylate, metronidazole, PPI, tetracycline ongoing - PPI

Answer 44

Inflammation of the peritoneum, the thin tissue that lines the abdomen and covers many of the organs.

Answer 45

Recent surgery, ascites, any abdominal pathology that can cause perforation ie gallbladder, peptic ulcer, IBD, diverticulitis, appendicitis... Alcoholism, liver disease, dec immune system,

Answer 46

Diffuse/focal tenderness - with guarding Pain = exacerbated by moving the peritoneum ie coughing, flexing hips BLUMBERG SIGN - pressing causes pain, but sudden release causes more pain as the peritoneum snaps into place Fever, tachycardia, N+V, bloating absent bowel sounds

Answer 47

Release of deep palpation causes more pain in peritonitis

Answer 48

A complication of ascites. >250cells per mic/l = suggestive

Answer 49

Often clinically, if perforation is suspected -> straight to surgery WCC - H >250ul cells in ascites aspirate if SBP Abdo X-ray - pneumoperitoneum Laparoscopic exploration+washout + rx of anatomical pathology that may have caused

Answer 50

Broad spectrum abx until culture found. Cocktail must be used as there are G+ve,-ve, and anaerobic species in the GI tract. Laparoscopic washout + rx of anatomical pathology SBP DOESNT BENEFIT SURGERY

Answer 51

Haemorrhoidal cushions = normal anatomical feature of the anal canal. Symptoms result when they protrude from the anal canal as they enlarge.

Answer 52

45-65, excessive straining, low fibre diet, constipation, hepatic insufficiency

Answer 53

Rectal bleeding - fresh blood only @ defecation Pain/discomfort peri-anally, pruritus perianally Tender anal protrusion felt

Answer 54

Anoscopic examination FBC - micro anaemia Colonoscopy - to rule out carcinoma Faecal occult - only really performed if haemorrhoid cannot be visualised

Answer 55

Dietary mods - increasing fibre in diet Topical corticosteroids reduce pruritus Sclerotherapy -> rubber band ligation -> haemorrhoidoplexy (stapling) -> haemorrhoidectomy

Answer 56

Inflammation of the colon resulting from infectious origin.

Answer 57

C-dif colitis | EH colitis caused by shiga toxin - e-coli0157H7/shigella dysentery

Answer 58

Abdo pain + distension Incontinence Bloody diarrhoea (recurrent) WL, fever <40.5, flatulence, fatigue, PUS in stool, loss of appetite

Answer 59

FBC WCC up Stool cultures - causative organisms Inflammatory markers UP +/- endoscopy/CT (often not required)

Answer 60

Acute/chronic processes that result from non occlusive and occlusive causes that result in decreased blood flow to the GI tract.

Answer 61

Embolism (50% of mes isch), thrombosis (15-20%), vasculitis, trauma, external pressure, VT, hypoperfusion (20-30% mes isch) Shock/hypotension

Answer 62

Malaena, stomach pains, WL, diarrhoea, bruits, tenderness, vasculitis.

Answer 63

FBC - anaemia/thrombocytopenia Chemistry - potentially in U+C if due to hypoperfusion ABD - met acidosis - underperfusion ECG - cardioembolic causes CXR - pneumoperitoneum potentially Abdo x-ray / CT Sigmoidoscopy - may see petechaie / haemorrhage nodules/ oedema / necrosis / gangrene Mesenteric angiography - visualisation of blockage

Answer 64

Obstruction in the flow of the GI tract resulting in emesis, diarrhoea and abdominal pain.

Answer 65

Old age. Neoplasms, crohns, appendicitis, hernias, PREV SURGERY Children - volvulus

Answer 66

Inability to pass stools, diarrhoea, abdo pain, emesis, tenderness (due to ischaemia), palpable mass, Possible - especially if complicated, fever tachycardia severe lethargy, hypotension

Answer 67

Abdo X-ray - dilated loops, absent rectal gas, FBC - WCC if comp U+E - inc urea if volume dep, hypokalaemia, hyponatraemia, metabolic alkalosis CT/MRI/Lapatomy possible

Answer 68

If complicated/strangulated/severe - Urgent laparotomy with abx prophylaxis gentamicin and amoxicillin. + supportive Surg contraindicated = NG decompression + analgesia + antiemetic + antispasmodics If mild mild - NG decompression -> failure after 48-72 hrs = treat as though complicated

Answer 69

A chronic condition characterised by bloating, abdominal pain and discomfort. The pain is relieved on defecation and there are NO structural abnormalities.

Answer 70

Hx sex abuse, Female, <50, stress, prev infections

Answer 71

Abdo discomfort, pain and bloating. Alternating bowel habits. Normal abdo exam (rarely a very very mild tenderness in the lower quadrants)

Answer 72

``` FBC - N CT - N CRP + ESR - N (rules out IBD) Anti tTG - rules out coeliacs - N Stool cultures - N Hydrogen breath test - N Faecal calprotectin - N (IBD unlikely) Sigmoidoscopy/colon N ```

Answer 73

Lifestyle mods - increase fibre, dec caffeine, Can give probiotics Constipated - laxatives ie lactulose -> lubiprostone + antispasmodics - hyoscamine Diarrhoea -> use antidiarrhoeals - ie loperamide

Answer 74

Purulent collections in the liver parenchyma as a result of bacterial, fungal or parasitic infections.

Answer 75

Age >50, MD, interventional procedures involving biliary tract/liver, any underlying liver disease - cirrhosis, transplantation, alcoholism, hepatitis Portal vein drains - IBD, pancreatitis, diverticulitis, appendicitis

Answer 76

Swinging fever, RUQ tenderness, hepatomegaly, fevers and chills, N+V, effusion possible, jaundice, ascites, abdo pain WL, SOB,

Answer 77

FBC - leucocytosis, left shift, eosinophilia, anaemia LFTs - ALP raised lots, mildly raised AST ALT, hypoalbuminaemia PT/APTT - NORMAL LUSS - visualisation Culture/aspiration antibody/stool PCR - amoebiasis

Answer 78

Broad spectrum - piperacillin/tazobactam IV 6hrly, supportive, drainage, IV fluids Step up to vancomycin

Answer 79

A tear or laceration near the gastro-oesophageal junction that presents with bleeding and spontaneously resolves in 80-90%.

Answer 80

Anything that increases abdominal pressure: | Coughing, retching, vomiting, hiccuping, heavy alcohol consumption. Primal scream therapy

Answer 81

Malaena/haemoptysis/emesis with coffee flecks - bright blood. Light headed ness, pallor, dysphagia, oydonophagia, anaemia, postural/orthostatic hypotension

Answer 82

``` FBC - mild anaemia, usually N LFTs - N Urea - high if severe / prolonged bleed CXR - N INR - N OGD flex = show tear / laceration ``` CONSIDER: CK, troponin, CKMB, ECG - N N N

Answer 83

Urgent evaluation - some do not seen anything - spon resolves Others: INR correction with phystomenidione (VIT K) OGD +/- haemoclip placement/thermocoagulation/band ligation Abx prophylaxis - erythromycin Ondansetron Somatostatin analogue - octeotride - reduces blood flow from portal vein 2 - surgical intervention

Answer 84

Microvesicular hepatic steatosis in individuals who do not drink levels of alcohol considered harmful.

Answer 85

Obesity = primary | Insulin resistance, dyslipidaemia, omental fat, HTN, metabolic syndrome, TPN, Wilson

Answer 86

Absence of alcohol drinking Fatigue /malaise, hepatosplenomegaly, RUQ pain Pruritus, telangectasias, spider naevi, dupuytrens, captured medusae, malaena, haematemisis, nail changes, hepatic encephalopathy, jaundice, petechiae, palmar erythema, peripheral oedema

Answer 87

``` FBC - Thrombocytopenia, anaemia Lipids - all deranged LFTs - all H H H PT/INR - H Albumin - L ASMA - variable USS/CT/MRI - fatty deposits Definitive diagnosis = liver biopsy ```

Answer 88

Diet and exercise WL Roux-en-y bypass If lipids abnormal - statins Liver transplant with ESLD Can do transjugular intrahepatic portosystemic shunt TIPS (Post transplant nash happens interestingly in 10-35%)

Answer 89

Acute pancreatitis

Answer 90

Gallstones women 50-70 Men - 20-40 (alcoholism) HIV (CMV panc), ERCP USE, hypertriglyceridaemia Drugs - azathioprine, thiazides diuretics, furosemide

Answer 91

Mid epigastric pain radiating to back, worse on movement, N+V, anorexia, abdo pain, tachycardia, Chvosteks Cullen's - blue discolouration on peri umbilical region Grey-turner - blue discolouration on flanks Foxs - inguinal ecchymosis

Answer 92

``` Serum lipase - HH Serum amylase - 3x normal limit lipase:amylase - ratio >5 Urinary amylase - >5k units AST/ALT - 3x norm Plain abdo - may see sentinal loop in 2/3rds USS - fluid MRCP ( no contrast but not therapeutic), or ERCP - stones FNA - if aspiration ```

Answer 93

``` Resus - fluid resus Morphine Anti emetic Calcium replacement - calcium gluconate Mg replacement - magnesium sulfate Insulin if needed ERCP - can perform cholecystectomy if fit, /sphincterotomy if gallstones Alcoholic - benzos (1-2 mg) - + thiamine, folic acid and cyanocobalamine Resect any necrotic tissue ```

Answer 94

Recurrent/persistent inflammation results in scarring, fibrosis and loss of function.

Answer 95

Alcohol, smoking, FHx, coeliac, high fat/protein diet.

Answer 96

Epigastric pain radiation to back, worse 30 mins after meal (inability to digest fat), type a = sharp pain, B = prolonged Results in steatorrhoea, N+V, WL, painful joints, SOB due to effusions

Answer 97

Faecal fat - HH Faecal elastase - LL Steatocrit - HH BG - may be HH due to dec insulin Ct/X-ray/USS 0 evidence of megaly/calcification Biopsy potentially

Answer 98

paracetamol-tramadol-morphine STOP ALCOHOL/CIGARETTES LOW FAT DIET Replace enzymes with PANCREATIN +omeprazole Octeotride s/c = given for pain ``` Surg options Decompress cyst Decompression of lumen Lithotripsy if calcified, Pancreatoduodenectomy/distal pancreatectomy. ```

Answer 99

Caused by forceful insertion of a hair into the natal cleft resulting in prolonged inflammation which forms an epithelialised sinus.

Answer 100

Swelling, pain, discharge, toxaemia, fever, skin maceration

Answer 101

Male 15-40, FHx, lots of body hair, stiff hair

Answer 102

Pre hepatic - Splenomegaly, hepatic artery thrombosis Hepatic - cirrhosis, PBC, fatty liver, chron panc, PSC, Post hepatic - RHF, portal vein thrombosis, IVC thrombosis, budd-chiari

Answer 103

Ascites, hepatomegaly, caput medusae, abdo pain and tenderness, haemorrhoids

Answer 104

HVP gradient >5mmhg = diagnostic, >12 = clinically sig | Usually not taken though until a biopsy for cirrhosis is performed

Answer 105

``` TIPS (inflow portal vein and outflow hepatic vein connection) Portosystemic shunt (splen and renal vein connection) ``` Paracentesis and diuretics for ascites

Answer 106

Chronic progressive disease of the small intrahepatic bile ducts characterised by inflammation and damage as a result of toxic bile acids. Thought to be autoimmune. 95% have abs

Answer 107

Women, 45-60, UTI, FHx, smoking

Answer 108

Hepatomegaly, itch, dry eyes and mouth, fatigue, sleep disturbance, postural dizziness, splenomegaly, jaundice, ascites, WL, xanthelasmata

Answer 109

ALP, BILI, GGT AAT - all up Albumin - L ANA, AMA, ASP100, AGP210, APD-E2 abs - present PT - prolonged

Answer 110

A chronic progressive cholestatic liver disease characterised by fibrosis and inflammation of intra/extrahepatic bile ducts that result in stricture formation

Answer 111

Main association = with IBD | male, IBD, FHx

Answer 112

40-50s, WL, jaundice, ascites, splenomegaly, abdo pain, epigastric pain, fever, steatorrhoea, encephalopathy,

Answer 113

``` ALP - H AST ALT - H but not markedly (<300) Bili - H GGT - H PT 0 H ANCA - +ve Albumin - L ABDO USS - definitive - abnormal bile ducts +/- cirrhosis/splenomegaly ERCP/MRCP - Strictures and dilatations ```

Answer 114

A type of IBD that characteristically involves the rectum and extends proximally along the colon.

Answer 115

FHx, HLAB27, infection, non-smoker / former smoker

Answer 116

Rectal bleeding - intermittent and insidious Mild diarrhoea - >4 small stools per day Blood on DRE Malnutrition, abdo pains (mild and crampy to severe) Erythema nodosum no pyoderma gangrenosum, WL, fever, pallor, uveitis

Answer 117

Stool studies - -ve for C did toxins AB, WBC H, FBC - varying leucocytosis ESR + CRP - H Colonoscopy = definitive - see loss of vascular markings, diffuse erythema, rectal-continuous involvement. Fistulas rare.

Answer 118

Vaccination - FLU, VCZ, HEPB, pneumococcal polysaccharide, HPV Non fulminant: Topical and oral mesalazines -> oral beclometasone -> IV Remission - mesalazines topical/oral Refractory - azathioprine/mercaptopurine Refractory = if symptoms return once medication stopped Colectomy IF severe = IV corticosteroids, (fluids, infliximab, and cyclosporin)

Answer 119

Toxic megacolon

Answer 120

Whereby a portion of the intestine loops around itself and the mesentery that supports it resulting in BO.

Answer 121

Preg, enlarged colon, intestinal malrotation, high fibre, hirshprungs, adhesions

Answer 122

Two patterns depending on location Sigmoid volvulus - constipation and abdo pain Caecal volulus - presents more like BO: N+V, lack of flatus/stool Sig guarding, fever potentially, May be necrosis -> academia -> death if severe obstruction Sigmoid > caecal

Answer 123

Plain x-ray - coffee bean appearance If in doubt - barium enema Can do CT - diverticulitis Endoscopy - 80% of BO result from carcinomas therefore to rule out

Answer 124

Protrusion of abdominal or pelvic contents through a dilated internal inguinal ring or attenuated inguinal floor into the inguinal canal and out of the external inguinal ring, causing a visible or palpable bulge

Answer 125

Processes vaginalis fails to regress

Answer 126

Internal ring gradual dilation | Direct weakness of posterior wall

Answer 127

Protrusion of the abdominal contents through an enlarged oesphageal hiatus of the diaphragm. Most commonly the stomach

Answer 128

Heartburn/gord, regurgitation, dysphagia, oydonophagia, wheezing, haematemesis, obesity, chest pain, SOB, non billous vomiting, cough

Answer 129

Cxr - lack of gastric bubble / retro cardiac bubble (can be normal) Upper GI series - stomach partially intra thoracic

Answer 130

If haemorrhage/ob/volvulus - urgent surgery Irreversible ischaemia = surgical resection Symptomatic - lap surg

Answer 131

The vowels hit your bowels - A and E

Answer 132

Tonfovir, pegunterferon a

Answer 133

Achalasia may occur at any age; however, incidence peaks in individuals over the age of 60 years. There is equal gender distribution; although, several series demonstrate a female predominance, this may be due to greater numbers of women, compared with men, in the older general population.

Answer 134

Awaiting definitive Rx: CCBs before meals: nifedipine, verapamil, isosorbide denitrate ACUTE: Pneumatic dilation Laparoscopic cardiomyomotomy Poor surgical candidate: CCBs Botox injection Gastrostomy

Answer 135

The most common aetiology of acute cholangitis is cholelithiasis leading to choledocholithiasis and biliary obstruction. Iatrogenic biliary duct injury, most commonly caused via surgical injury during cholecystectomy, can lead to benign strictures, which can in turn lead to obstruction (with or without secondary sclerosing cholangitis). Other causes of benign biliary stricture include chronic pancreatitis (with stenosis and stricture of the distal common bile duct, which has an intrapancreatic course), radiation-induced biliary injury, or biliary injury as a complication of systemic chemotherapy (e.g., fluorodeoxyuridine). Obstruction of the common bile duct initially results in bacterial seeding of the biliary tree, possibly via the portal vein, and when combined with bacterial contamination, can lead to acute cholangitis. Additionally, sludge forms, providing a growth medium for the bacteria. As the obstruction progresses, the bile duct pressure increases. This forms a pressure gradient that promotes extravasation of bacteria into the bloodstream. If not recognised and treated, this will lead to sepsis.

Answer 136

NICE CKS Appendicectomy (surgical removal of the appendix) is the treatment of choice in secondary care for people with appendicitis. This may be done by an open incision in the lower right part of the abdomen (open appendectomy or laparatomy) or through small incisions in the abdomen with the help of a camera (key hole surgery or laparascopy).

Answer 137

NICE CKS Arrange immediate hospital admission if appendicitis is suspected. Anyone with appendicitis if fit for surgery.

Answer 138

``` Peforation Generalised peritonitis Appendicular mass Abscess formation Adhesions Wound infection post Surg ```

Answer 139

Non-severe = monitor Symptomatic non-severe to severe: Corticosteroid therapy +/- Azathioprine +/- ciclosporin / mycophenolate mofetil Biliary involvement - ursodeoxycholic acid Decompensated = liver transplantation evaluation

Answer 140

SEs of corticosteroid infection HCC ES-liver disease Infections Cholestatic hepatitis due to azathioprine therapy Pancreatitis/skin rash/teratogenicity due to azathioprine therapy

Answer 141

The natural history of AIH reveals that untreated AIH has a poor prognosis with a 5-year survival rate of 50% and 10-year survival rate of 10%. Immunosuppressive therapy significantly improves survival. Approximately 65% of patients enter remission within 18 months of therapy and 80% within 3 years, with a mean duration of treatment to remission being 22 months.

Answer 142

Cholangiocarcinomas are cancers arising from the bile duct epithelium. These can be divided depending on their location in the biliary tree: intrahepatic or extrahepatic (perihilar and distal). Perihilar tumours involving the bifurcation of the ducts are also known as Klatskin's tumours. More than 95% are adenocarcinomas. Most are of the infiltrating nodular or diffusely infiltrating type. Purely nodular or papillary are less frequent subtypes. Painless jaundice, weight loss, and abdominal pain in patient >55 years old. Liver enzymes, blood levels of CA 19-9, CEA, CA-125; abdominal ultrasound, abdominal CT/MRI, MR angiography, and cholangiography (ERCP, MRCP, percutaneous transhepatic catheterisation) are used for evaluation. Surgical resection offers only potential cure. Chemotherapy has been shown to be relatively ineffective. Liver transplant is indicated in a small subset of patients.

Answer 143

Approximately two-thirds of cholangiocarcinomas occur in patients between 50 and 70 years of age, with a slight male predominance. High rates of biliary cancer are also seen in South American countries (Bolivia, Chile) and northern Japan. Intermediate rates are seen in many European countries, and low rates are observed in the US, the UK, India, Nigeria, and Singapore.

Answer 144

There is a close association between infection, inflammation, and cancer. See RFs

Answer 145

``` Age > 50 Cholangitis Choledocholithiasis Cholecysolithiasis Bile duct adenoma, biliary papillomatosis, choledochal cyst, and Caroli's disease (non-obstructive dilation of the biliary tract) UC PSC Cirrhosis Alc liv disease Liver fluke Chronic typhoid carrier Hep C HIV Hep B Thorium dioxide DM Cigarettes Male ```

Answer 146

``` Painless jaundice WL Abdo pain Pruritus Acute cholangitis presentation -charcots triad fever jaundice RUQ pain Palpable gallbladder Hepatomegaly Dark urine Pale stools ```

Answer 147

Serum bilirubin - conjugated = elevated (OB) ALP - High GGT - High AST ALT - high PT - high (Caused by prolonged obstruction of the common bile or hepatic duct and a subsequent reduction in fat-soluble vitamins (A, D, E, and K)) CA19-9 / CEA / Ca-125 - high CT/MRI/ERCP/MRCP Percutaneous transhepatic catheterisation (PTC) - An invasive procedure that is used when the tumour causes complete obstruction of the biliary tree, and ERCP is unable to assess the biliary tree proximal to the tumour.

Answer 148

Surgical resection +/- partial liver resection Pre-op portal vein embolisation or biliary drainage Ablative therapy / chemo +/- radiotherapy

Answer 149

Node-positive cholangiocarcinoma is a poor prognostic indicator of survival. Metastatic disease precludes resection and has a poor prognosis. The common early pattern of spread is to regional lymph nodes and to distant sites in the liver. The 5-year survival for surgical resection alone ranges from 20% to 43%.

Answer 150

Cholangitis Biliary leak Biliary obstruction

Answer 151

cholangiocarcinoma

Answer 152

The majority of colorectal cancers are adenocarcinomas derived from epithelial cells. About 71% of new colorectal cancers arise in the colon and 29% in the rectum. Less common types of malignant colorectal tumours are carcinoid tumours, GI stromal cell tumours, and lymphomas. Increasing age is the greatest risk factor for sporadic colorectal adenocarcinoma with 99% of cancers occurring in people aged 40 years or over. Third most common cancer in the Western world. Rare below 40 years of age. Symptoms are not specific and occur frequently in benign colorectal conditions. Surgical resection is the main curative treatment. Combined modality treatment (chemotherapy, radiotherapy, resection of metastases) has increased survival in selected cases.

Answer 153

Colorectal cancer is the third most common cancer in the Western world. Worldwide, the highest incidence rates for colorectal cancer are seen in Europe, North America, and Australasia and are lowest in Africa and Asia. The lifetime risk of developing colorectal cancer is 5.42% and it is the third leading cause of cancer deaths in the US in men and women.

Answer 154

The majority of colorectal cancers are sporadic rather than familial, but next to age, family history is the most common risk factor. Obesity confers a 1.5-fold increased risk of developing colon cancer compared with normal weight individuals and is also associated with a greater risk of dying from the disease. Large prospective studies with long follow-up periods have shown that a high intake of red and processed meat is associated with an increased risk of colorectal cancer risk.

Answer 155

``` STRONG Increased age APC mutation Lynch syndrome - HNPCC MYH-associated polyposis Hamartomatous polyposis syndromes IBD Obesity ``` WEAK Acromegaly Limited physical activity Lack of dietary fibre

Answer 156

``` Rectal bleeding Change in bowel habit Rectal mass Fix Abdominal mass Anaemia Male sex Abdominal pain WL + anorexia Abdo distension Palpable LNs ```

Answer 157

FBC - anaemia LFTs - normal (baseline) RFTs - normal (baseline) Colonoscopy - ulcerating or exophytic mucosal lesion that may narrow the bowel lumen Double contrast barium enema - mass lesion in the colon and/or as a characteristic 'apple core' lesion CT colonography - CT thorax/abdo/pelvis - colonic wall thickening, enlarged lymph nodes, liver metastases, ascites, lung secondaries Biopsy - confirms the diagnosis with characteristic pathological appearances; the degree of tumour differentiation (i.e., well, moderate, or poorly differentiated) will also be reported CEA - confirmation only

Answer 158

SUITABLE FOR SURGERY STAGE 1 - local/radical excision STAGE 2-3 - Radical resection + pre+post operative chemotherapy [fluorouracil+folinic acid or capecitabine] Stage 4 - possibly same as 2-3 NOT SUITABLE FOR SURGERY Chemotherapy Monoclonal antibodies - cetuximab, panitumumab, bevacizumab Stenting

Answer 159

Overall, 5-year survival rates for colorectal cancer are 93% to 97% for stage I disease, 72% to 85% for stage II disease, 44% to 83% (depending on nodal involvement) for stage III disease, and <8% for stage IV disease.

Answer 160

bone marrow suppression during chemotherapy oxaliplatin-associated hepatotoxicity chemotherapy-associated GI (diarrhoea, nausea, vomiting, abdominal pain) chemotherapy-associated alopecia cetuximab-associated rash radiotherapy-associated faecal incontinence bladder dysfunction after rectal excision erectile dysfunction after rectal excision low anterior resection syndrome after anterior resection l oxaliplatin-associated pulmonary fibrosis oxaliplatin-associated neuropathy

Answer 161

colorectal carcinoma

Answer 162

Cirrhosis is a diffuse pathological process, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules. It can arise from a variety of causes and is the final stage of any chronic liver disease. It leads to portal hypertension, liver insufficiency, and hepatic failure. In general, it is considered to be irreversible in its advanced stages. Cirrhosis is the pathological end-stage of any chronic liver disease and most commonly results from chronic hepatitis C and B, alcohol misuse, and non-alcoholic fatty liver disease. The main complications of cirrhosis are related to the development of liver insufficiency and portal HTN and include ascites, variceal haemorrhage, jaundice, portosystemic encephalopathy, hepatorenal and hepatopulmonary syndromes, and the development of hepatocellular carcinoma. Once a patient with cirrhosis develops signs of decompensation, survival is significantly impaired. The management of cirrhosis is aimed at treating underlying liver disease, avoiding superimposed injury, and managing complications. Timely referral for liver transplantation is the only curative treatment option for patients with decompensated cirrhosis. Chronic liver disease and cirrhosis are listed among the 10 leading causes of death in the US.

Answer 163

Cirrhosis is an important cause of morbidity and mortality. It is the 12th leading cause of hospitalisations and death in the US. In the UK, mortality from cirrhosis rose from 6 per 100,000 population in 1993 to 12.7 per 100,000 in 2000.

Answer 164

The various causes of cirrhosis are listed below. Chronic viral hepatitis: hepatitis C, hepatitis B (with or without coexisting hepatitis D). Alcoholic liver disease. Metabolic disorders: non-alcoholic fatty liver disease, obesity, haemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency, glycogen storage diseases, abetalipoproteinaemia. Cholestatic and autoimmune liver diseases: primary biliary cholangitis, primary sclerosing cholangitis, autoimmune hepatitis. Biliary obstruction: mechanical obstruction, biliary atresia, cystic fibrosis. Hepatic venous outflow obstruction: Budd-Chiari syndrome, veno-occlusive disease, right-sided heart failure. Drugs and toxins: amiodarone, methotrexate. Intestinal bypass: anastomosis of the jejunum to the ileum to shorten the length of the digestive tract in morbid obesity, or to bypass a diseased area or blockage. Indian childhood cirrhosis (environmental copper poisoning, now rare). Cryptogenic cirrhosis

Answer 165

``` STRONG Alcohol misuse IVDU Unprotected intercourse Obesity ``` WEAK Blood transfusion Tattooing

Answer 166

``` COMMON Abdo distension Jaundice + pruritus Coffee-ground vomit and black stool Leukonychia Palmar erythema Spider angioma Telangectasia, spider angiomata Caput medusa Hepatosplenomegaly Altered mental status Fatigue, weakness, and weight loss Lower extremity swelling Hepatic fetor Muscle wasting Peripheral oedema Increased infection Decreased libido Chest wall features Dyspnoea Chest pain Syncope ```

Answer 167

``` LFTs GGT Albumin Sodium PT time Platelet count Hep C abs Hep B abs ``` ``` OTHER ANA Iron studies ASMA AMA antibodies Ceruloplasmin a1 anti-trypsin Abdo US/CT/MRI Upper GI endoscopy Liver biopsy ```

Answer 168

Rx if cause Refrain from toxins If ascitic - furosemide, spironolactone Fluid restriction Liver transplantation

Answer 169

The 10-year survival rate in patients with compensated cirrhosis is approximately 90%, and the likelihood of transitioning to decompensated cirrhosis within 10 years is 50%. The median survival time in patients with decompensated cirrhosis is approximately 2 years.

Answer 170

``` Ascites Varices HCC SBP Hepatic hydrothorax Portosystemic encephalopathy Hepatorenal syndrome Hepatopulmonary syndrome Portopulmonary HTN Hypogonadism Hepatic osteodystrophy ```

Answer 171

Cholelithiasis is the presence of solid concretions in the gallbladder. Gallstones form in the gallbladder but may exit into the bile ducts (choledocholithiasis). Symptoms ensue if a stone obstructs the cystic, bile, or pancreatic duct. Most gallstones in developed countries (>90%) consist of cholesterol. Cholesterol gallstone formation begins with the secretion of bile supersaturated with cholesterol from the liver. Initiated by nucleating factors such as mucin, microscopic crystals then precipitate in the gallbladder where hypomotility provides time for stone growth. Gallstones are highly prevalent, but most (80%) are asymptomatic. Common risk factors include older age, female sex and pregnancy, obesity, rapid weight loss, drugs, and a family history. Abdominal ultrasound provides effective diagnostic imaging. Laparoscopic cholecystectomy represents definitive treatment for symptomatic patients. Complications such as cholecystitis, cholangitis, and pancreatitis develop in 0.1% to 0.3% of patients annually. Gallstones are the most common gastrointestinal disease that requires hospitalisation in developed countries.

Answer 172

10% to 15% of adults Age, obesity, and female sex hormones are important aetiological factors. Biliary pain, however, develops in 1% to 2% of previously asymptomatic individuals each year. Once biliary colic has developed, about 50% of patients will go on to experience recurrent pain while up to 3% are at increased risk of complications: acute cholecystitis, cholangitis, or acute pancreatitis

Answer 173

CHOLESTEROL / BLACK / BROWN Ninety percent of gallstones are composed of cholesterol; these form in the gallbladder. Cholesterol cholelithiasis transpires as a result of three principal defects: bile supersaturated with cholesterol, accelerated nucleation, and gallbladder hypomotility retaining this abnormal bile. Approximately 2% of all gallstones are black pigment stones. The pigment material consists of polymerised calcium bilirubinate. Patients with chronic haemolytic anaemia, cirrhosis, cystic fibrosis, and ileal diseases are at highest risk of developing black pigment stones. Brown pigment gallstones form de novo in bile ducts as a result of stasis and infection. They consist of calcium bilirubinate, calcium salts of long-chain fatty acids, cholesterol, and mucin (glycoproteins primarily from bacterial biofilms). Bacterial infection, biliary parasites ( Clonorchis sinensis , Opisthorchis species, and Fasciola hepatica ), and stasis (from partial biliary obstruction) are key factors, particularly in Asian people. In developed countries, brown pigment gallstones form more commonly as a result of stasis due to biliary strictures, either inflammatory or neoplastic.

Answer 174

``` STRONG Increasing age Female Hispanic FHx Gene mutations - ABCG8 p.D19H, SULT2A1, GCKR, CYP7A1, UGT1A1, TM4SF4 Pregnancy Exogenous insulin Obesity DM metabolic syndrome Non-alcoholic liver disease Prolonged / rapid weightloss Total parental nutrition Octreotide Incretin based drugs Ceftriaxone (pigmented) Terminal ileum disease / resection (black pigmented) Haemoglobinopathy (black pigmented) ``` WEAK Low fibre

Answer 175

COMMON RUQ / epigastric pain >30mins Post-prandial pain (Constant pain typically increases in intensity and lasts for several hours (biliary colic). Dyspepsia, heartburn, flatulence, and bloating are common but are not characteristic features of gallstone disease.) UNCOMMON Nausea Jaundice - (Uncommon in simple acute cholecystitis except for Mirizzi syndrome (a rare complication in which a gallstone becomes impacted in the cystic duct or neck of the gallbladder, causing compression of the common bile duct or common hepatic duct, resulting in obstruction and jaundice). Jaundice develops primarily in patients with choledocholithiasis, and is characteristic of cholangitis.)

Answer 176

FBC - normal in simple (uncomplicated) biliary colic LFTs - cholelithiasis: normal; choledocholithiasis: elevated alkaline phosphatase, elevated bilirubin Lipase + amylase - elevated (>3 times upper limit of normal) in acute pancreatitis Abdominal US - may visualise stone Consider: MRCP (For suspected choledocholithiasis that is not confirmed by abdominal ultrasound.) ERCP (For suspected choledocholithiasis that is not confirmed by abdominal ultrasound - good for high-risk as offers therapy too) EUS - Patients who are unable to undergo an MRCP (e.g., those with implanted devices, or who are claustrophobic) can be evaluated using EUS. Abdo CT

Answer 177

Symptomatic cholelithiasis - cholecystectomy [laparoscopic] Choledocholithiasis - ERCP with biliary sphincterotomy and stone extraction is the treatment of choice. IF unsuccessful -> lithotripsy, papillary balloon dilation, and long-term biliary stenting. +/- cholecystectomy ASYMPTOMATIC cholelithiasis Observation (1-2% become symptomatic each year) - N.B Prophylactic cholecystectomy in asymptomatic individuals might be considered in two situations: a heightened risk of developing gallbladder carcinoma (either harbouring large gallstones [>3 cm] or possessing a partially calcified 'porcelain' gallbladder) or when the risk of gallstone formation and its complications are high (in those with sickle cell disease)

Answer 178

``` ERCP pancreatitis Iatrogenic bile duct injuries Post-sphincterotomy bleeding Bouveret syndrome - If a gallstone erodes through the gallbladder wall, a cholecystoenteric fistula can develop and lead to duodenal obstruction (Bouveret syndrome). Gallstone ileus Cholecystitis Ascending cholangitis Acute biliary pancreatitis Mirizzi syndrome - Occasionally, a large gallstone can become lodged in the cystic duct and compress or damage the common hepatic duct, resulting in biliary obstruction and jaundice. ```

Answer 179

The outlook for patients with symptomatic cholelithiasis managed by cholecystectomy is favourable. The same holds for patients with choledocholithiasis who undergo endoscopic retrograde cholangiopancreatography (ERCP) with biliary sphincterotomy and stone extraction, followed later by cholecystectomy. Recurrent choledochal problems Risk factors for recurrent choledochal problems are common with: bile duct dilatation to >15mm; a periampullary diverticulum; brown pigment stones; or the gallbladder being left intact.

Answer 180

Perforation of the gastrointestinal tract may be suspected based upon the patient's clinical presentation, or the diagnosis becomes obvious through a report of extraluminal "free" air or fluid collection on diagnostic imaging performed to evaluate abdominal pain or another symptom. Clinical manifestations depend somewhat on the organ affected and the nature of the contents released (air, succus entericus, stool), as well as the ability of the surrounding tissues to contain those contents. Intestinal perforation can present acutely, or in an indolent manner (eg, abscess or intestinal fistula formation).

Answer 181

``` Instrumentation/surgery Penetrating or blunt trauma Medications (NSAIDs, antibiotics, and potassium supplements), other ingestions, foreign body Violent retching/vomiting (Boerhaave syndrome) Hernia/intestinal volvulus/obstruction Inflammatory bowel disease Appendicitis Peptic ulcer disease Diverticular disease Cardiovascular disease Infectious disease — Typhoid, tuberculosis, and schistosomiasis can cause perforation of the small intestine Neoplasms Connective tissue disease Spontaneous intestinal perforation ```

Answer 182

Acute pain + tenderness - chest/abdo A subset of patients will present in a delayed fashion. These patients may present with an abdominal mass reflecting abscess formation, or fistula drainage, and some may present with abdominal sepsis. Cervical esophageal perforation can present with pharyngeal or neck pain associated with odynophagia, dysphagia, tenderness, or induration. Perforation of upper abdominal organs can irritate the diaphragm, leading to pain radiating to the shoulder. Retroperitoneal perforations often lead to back pain. Because the pH of gastric contents is 1 to 2 along the gastric luminal surface, a sudden release of this acid into the abdomen causes severe and sudden peritoneal irritation and severe pain. Sepsis — Sepsis can be the initial presentation of perforation. Organ dysfunction may be present, including acute respiratory distress syndrome, acute kidney injury, and disseminated intravascular coagulation NB - Sepsis in itself can contribute to the causation of perforation by reducing intestinal wall perfusion EXAM Tachypnoea/cardia, fever Signs of subcutaneous air, and auscultation and percussion of the chest for signs of effusion May be a mass (phlegmon or abscess)

Answer 183

Fullblood count (FBC), electrolytes, blood urea nitrogen (BUN), creatinine, liver function tests, amylase, and lipase. CRP Abdo XR - pneumoperitoneum/fluid US - free fluid/gas, reduced peristaltic activity in the intestines, and localized abscess CT - +/- contrast SEE FULL SIGNS ON IMAGING BELOW: Although demonstration of free intra-abdominal air on imaging studies is a sign of perforation, this may not be helpful in the postoperative period, particularly after laparoscopic surgery, because approximately 40 percent of patients will have more than 2 cm of free air at 24 hours postlaparoscopy, despite lack of any clinical evidence of bowel perforation. Free intra-abdominal air often may be seen on a radiograph up to a week postoperatively, but the volume should gradually decrease with time. Increasing amounts of intra-abdominal air during a period of observation is concerning, and a finding of increasing free intra-abdominal air suggests perforation until proven otherwise. FULL IMAGING SIGNS: •Pneumomediastinum (in the absence of tracheal injury). - The "V" sign of Naclerio is free air in the mediastinum outlining the diaphragm (image 1) and is seen in approximately 20 percent of cases [97]. - Ring-around-the-artery sign (image 2). - Widening of the mediastinum is sometimes seen with esophageal perforation. * Free air under the diaphragm on upright films (image 3). * Pleural effusion may represent leaked esophageal contents (image 4). * Pneumothorax is a rare finding in esophageal perforation and is thought to occur by the spread of gas along tissue planes (Macklin effect). * Subcutaneous emphysema may be seen in some cases. Free air under the diaphragm in upright abdominal films (image 3), air over the liver (right lateral decubitus) or spleen (left lateral decubitus), anteriorly on supine films (football sign). - Cupola sign (inverted cup) is an arcuate lucency over the lower thoracic spine [98]. - Rigler sign (double-wall sign) is seen as gas outlines the inner and outer surfaces of the intestine (image 5). - Psoas sign is air in the retroperitoneal space outlining the psoas muscle. - Urachus sign is air in the preperitoneal space outlining the urachus or umbilical ligaments. NBNB Other imaging studies include endoscopy (upper, lower), esophagography, upper gastrointestinal series, ultrasound, contrast enema, and dye studies [101]. It is important to note that for suspected perforation, barium should not be used initially as an oral contrast agent because it can produce granulomas in the tissues if it leaks out, and it can obscure abdominal findings on other imaging studies

Answer 184

Initial management of the patient with gastrointestinal perforation includes intravenous (IV) fluid therapy, cessation of oral intake, and broad-spectrum antibiotics. Drainage, gastrostomy, and feeding jejunostomy may be appropriate depending upon the level of the perforation. Monitoring should initially take place in an intensive care unit. The administration of intravenous proton pump inhibitors is appropriate for those suspected to have upper gastrointestinal perforation. Patients with intestinal perforation can have severe volume depletion. The severity of any electrolyte abnormalities depends upon the nature and volume of material leaking from the gastrointestinal tract. Surgical management of patients with free perforation should be expedited to minimize such derangements. Electrolyte abnormalities are common among those who have developed a fistula as a result of perforation (eg, metabolic alkalosis from gastrocutaneous fistula).

Answer 185

Infection of the colon caused by the bacteria Clostridium difficile . Characterised by inflammation of the colon and the formation of pseudomembranes. Occurs in patients whose normal bowel flora has been disrupted by recent antibiotic use. Also known as pseudomembranous colitis, CDI, or CDAD. This topic covers the diagnosis and management of adults only. Patients usually present with diarrhoea, abdominal pain, and leukocytosis, and a history of recent antibiotic use. Other common symptoms include fever, abdominal tenderness, and distension. Testing should be limited to patients with unexplained, new-onset diarrhoea (defined as 3 or more unformed stools in 24 hours). Molecular testing alone or as part of a multistep algorithm is recommended depending on local institutional protocols. May be evidence of pseudomembranes on sigmoidoscopy or colonoscopy in some patients. Treatment is to discontinue the inciting antimicrobial agent and start therapy with oral vancomycin or fidaxomicin. Surgery may be required in fulminant disease. About 5% to 50% of treated patients have recurrence after discontinuation of therapy, but most respond to a second course of therapy. Faecal microbiota transplantation may be recommended in patients with multiple recurrences.

Answer 186

The incidence of health care-associated infection was 92.8 per 100,000 persons, while the incidence of community-associated infection was 48.2 per 100,000 persons. White people, females, and patients aged 65 years and older had a higher incidence of infection. C difficile is responsible for 48% of health care-associated gastrointestinal infections in acute care hospitals across Europe.

Answer 187

Broad-spectrum antibiotics disrupt the normal bowel flora, the most common causative agents being ampicillin, cephalosporins, clindamycin, carbapenems, and fluoroquinolones. Clostridium difficile colonisation occurs after this disruption to bowel flora by ingestion of heat-resistant spores, which convert to vegetative forms in the colon. Transmission in the healthcare setting is most likely to be the result of person-to-person spread through the faecal-oral route (e.g., via the hands of healthcare workers), high-risk fomites (e.g., inadequately cleaned bedpans or rectal thermometers), or direct exposure to a contaminated environment. Patients with colonisation who are asymptomatic may also contribute to the spread. The incubation period is generally 2 to 3 days, but may be more than one week. Clostridium difficile are gram-positive, anaerobic, spore-forming rods that produce toxins A and B. These toxins cause an inflammatory response in the large intestine, leading to increased vascular permeability and pseudomembrane formation.

Answer 188

``` STRONG ABx Inc age Hospitalisation PMHx Acid suppressing drugs IBD Solid organ /haem stem cell transplants CKD HIV ``` WEAK Immunosuppressants / chemo GI surgery

Answer 189

``` COMMON RFs Diarrhoea - May range from loose stools to severe diarrhoea; absence of diarrhoea may be related to toxic megacolon or paralytic ileus. Abdo pain Fever Tenderness ``` UNCOMMON N+V Abdo distension Shock Sx - Systemic symptoms of shock including hypotension and tachycardia with severe abdominal pain and tenderness suggest fulminant colitis.

Answer 190

FBC - WBC increased Faecal occult blood - positive for occult blood Stool PCR - positive Stool immunoassay for glutamate dehydrogenase - positive Stool immunoassay for toxins A+B - positive Abdo X-ray - air in bowel, colonic dilation Consider: CT - colonic dilation and diffuse colonic thickening Possible to do sigmoid/colonoscopy but usually not needed

Answer 191

Initial episode non-severe/severe Vancomycin 125mg QTD or Fidaxomicin200mgBD or Metronidazole 500mgTDS DISCONTINUE AGENT INFECTION CONTROL Patients should be evaluated for fluid status initially, especially if they are hospitalised. If necessary, hydration and electrolyte replacement should be instituted. Fulminant episode: Combination ABx IVIG - 150-400 mg/kg intravenously as a single dose Early diagnosis and treatment are essential for a good outcome, and early surgical intervention should be considered in patients who are unresponsive to medical therapy or who have rising WBC count or lactate level. The surgical procedure of choice is a subtotal colectomy with preservation of the rectum. Diverting loop ileostomy (with colonic lavage followed by antegrade vancomycin flushes) is an alternative approach. ONGOING episodes - retreat with ABx - Faecal transplant `

Answer 192

Ileus - Abdominal x-ray shows small bowel dilation. Nasogastric tube insertion and supportive therapy is indicated until ileus resolves. Perforation + peritonitis Toxic megacolon - (>6cm) Patients may require intravenous, nasogastric, or rectal therapy with either metronidazole or vancomycin (or both). In severe cases, colectomy may be necessary.

Answer 193

The expected response to treatment is rapid resolution of fever and diarrhoea within 4 to 6 days. The majority of patients respond to initial treatment. Recurrence rates vary depending on the presentation, immune function, severity of disease, and treatment type and duration. Recurrence rates have been reported to vary from 5% to 50%.

Answer 194

C-Dif Symptoms can range from isolated mild diarrhoea to copious watery diarrhoea with severe abdominal pain and high peripheral white blood cell count (WBC). Life-threatening colitis can develop, especially in older people. A sudden rise in WBC in a patient with diarrhoea and a history of recent antibiotic use may be an indicator of impending fulminant colitis.

Answer 195

Crohn's disease (CD) is a disorder of unknown aetiology characterised by transmural inflammation of the gastrointestinal (GI) tract. CD may involve any or all parts of the entire GI tract from mouth to perianal area, although it is usually seen in the terminal ileal and perianal locations. Unlike ulcerative colitis (UC), CD is characterised by skip lesions (where normal bowel mucosa is found between diseased areas). The transmural inflammation often leads to fibrosis causing intestinal obstruction. The inflammation can also result in sinus tracts that burrow through and penetrate the serosa, thereafter giving rise to perforations and fistulae. Common presenting symptoms include chronic diarrhoea, weight loss, and right lower quadrant abdominal pain mimicking acute appendicitis. Diagnosis confirmed by colonoscopy with ileoscopy and tissue biopsy. Specialist input is required from the time of diagnosis, as treatment regimens require frequent monitoring of clinical response, knowledge of common side effects, and expertise in managing potential serious adverse events. The overall treatment goals are to induce and maintain remission plus prevent relapse or recurrence. Complications include extra-intestinal involvement, intestinal obstruction, abscess formation, sinuses, and fistulae.

Answer 196

0.3% The highest incidence of CD is in northern climates and in developed countries, and the lowest in southern climates and less developed areas. Onset peaks 14-40, 60-80 It is more common in white people and Ashkenazi Jews. Smokers

Answer 197

1. Genetic - NOD2 CARD15 2. Environmental factors Include: smoking, oral contraceptive pill, diet high in refined sugar, nutritional deficiencies (especially zinc), and infectious agents (measles virus, and a possible association with Mycobacterium avium paratuberculosis ). Some studies have indicated a possible role of NSAIDs in the development of CD. Correlation between acute gastroenteritis and subsequent risk of CD has also been suggested.

Answer 198

COMMON Abdominal pain (Right lower quadrant and peri-umbilical regions are common locations if ileitis present. May be partially relieved by defecation.) Diarrhoea (can be bloody) Perianal lesions Up to 20% to 30% of patients with CD may have perianal lesions including skin tags, fistulae, abscesses, scarring, or sinuses

Answer 199

FBC - anaemia; leukocytosis; may be thrombocytosis Iron studies - N / IDA B12 - N/L Folate - N/L Metabolic Panel - hypoalbuminaemia, hypocholesterolaemia, hypocalcaemia CRP ESR - High Stool testing - C.dif rule out Yersinia enterocolitica serology - Negative Plain abdo films - small bowel or colonic dilation; calcification; sacroiliitis; intra-abdominal abscesses CT abdomen - may show skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae MRI pelvis - skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae Colonoscopy consider +/- tissue biopsy - aphthous ulcers, hyperaemia, oedema, cobblestoning, skip lesions Capsule endoscopy - aphthous ulcers, hyperaemia, oedema, cobblestoning, skip lesions Biopsy - transmural involvement with non-caseating granulomas POSITIVE ASCA NEGATIVE pANCA ABs

Answer 200

Mildly active-mod ileocaecal disease: 1) Observe with monitoring OR budesonide (taper with cessation), mesalazine. 5-ASAs are contraindicated if there is hypersensitivity to aspirin 2) Azathioprine / mercapto OR Methotrexate + folic acid 1mg 3) Add biologic therapy - adalimumab, infliximab, ustekinumab, vedolizumab Severe: Hospitalisation and early consideration of biologic therapy ABx consideration Colonic disease not-fistulating + MILD 1) 5-ASA +/- rectal hydrocortisone 2) Oral corticosteroids Moderate or severe: Same 1+2 3) Surgery if there is a risk of perforation, obstruction, and development of a toxic megacolon. ``` EXTENSIVE = >100cm of bowel affected 1) oral corticosteroids + immunomodulators + Nutritional therapies + Biologics + consider surgical resection ``` UGI disease: Same Rx aside from + PPI May need surgery or dilation if strictures / fistulae Perianal fistulae: Loose seton (cord threaded through tract to keep it open) + drainage of perianal abscess + metro + cipro ONGOING - Maintenance therapy Considerations on choosing long-term treatment for remission include: course and extent of CD; effectiveness and tolerance of treatments previously used; presence of biological or endoscopic signs of inflammation; and potential for complications. Smoking cessation Antispasmodic agents Antidiarrhoeal agents - loperamide / colestyramine

Answer 201

Typically patients with CD have intermittent exacerbations followed by periods of remission, with 10% to 20% of patients experiencing a prolonged remission after the initial presentation. Many patients with CD require surgical treatment for the complications of their disease. Patients with isolated ileocolic disease are likely to undergo surgery, with some studies reporting up to 90% having surgery by 10 years. Of these people, 50% will never require further surgery. Predictors of a relatively severe disease include age <40 years, the presence of perianal disease, and initial requirement for corticosteroids. CD is associated with a decrease in life expectancy. The mortality rate of CD patients increases with the duration of the disease, higher comorbidity score, lower socioeconomic status, and in the 30 days post gastrointestinal surgery. Colon cancer is the leading cause of disease-related death, and other causes include non-Hodgkin's lymphoma, digestive diseases, pulmonary embolism, and sepsis.

Answer 202

``` Obstruction Complications in pregnancy Intra-abdominal sepsis Sinuses Toxic megacolon Anaemia Short bowel syndrome Malignancy Renal stones Methrotrexate ass. hepatotoxicity + pulmonary fibrosis + myelosuppression Malaborption Metabolic bone disease ``` ``` Extra-intestinal complications: Cholelithiasis PSC Hepatic steatosis Liver abscess Granulomatous hepatitis Arthropathy Ocular - uveitis, iritis, and episcleritis Erythema nodosum and pyoderma gangrenosum. ```

Answer 203

Case history #2 Atypical presentations depend on sites of inflammation and extra-intestinal manifestations: musculoskeletal (arthritis, polymyositis); skin (fissures, fistulae, erythema nodosum, pyoderma gangrenosum, 'metastatic CD'); hepatobiliary (primary sclerosing cholangitis [PSC], bile duct carcinoma, autoimmune hepatitis, pericholangitis, gallstones); pancreatic (acute pancreatitis); ocular (uveitis, episcleritis, scleromalacia, corneal ulcers, retinal vascular disease); blood (anaemia, thrombocythaemia secondary to inflammation, thrombocytopenic purpura); renal (urinary calculi, amyloidosis); neurological (peripheral neuropathy, myelopathy, myasthenia gravis); bronchopulmonary (pulmonary fibrosis, bronchitis, laryngotracheitis); cardiac (pericarditis, myocarditis); hypercoagulability (thrombophlebitis, thromboembolism, vasculitis); thyroid (Hashimoto's thyroiditis).

Answer 204

Treatment for sigmoid volvulus may include sigmoidoscopy. If the mucosa of the sigmoid looks normal and pink, a rectal tube for decompression may be placed, and any fluid, electrolyte, cardiac, kidney or pulmonary abnormalities should be corrected. The affected person should then be taken to the operating room for surgical repair. If surgery is not performed, there is a high rate of recurrence For people with signs of sepsis or an abdominal catastrophe, immediate surgery and resection is advised. In a cecal volvulus, the cecum may be returned to a normal position and sutured in place, a procedure known as cecopexy. If identified early, before presumed intestinal wall ischemia has resulted in tissue breakdown and necrosis, the cecal volvulus can be detorsed laparoscopically. Laparotomy for other forms of volvulus, especially anal volvulus.

Answer 205

``` Strangulation Gangrene Perforation Faecal peritonitis -> sepsis Recurrent volvulus ```

Answer 206

Due to the high risk of recurrence, a bowel resection within the next two days is generally recommended.

Answer 207

Haemochromatosis is a multisystem disorder of dysregulated dietary iron absorption and increased iron release from macrophages. Advanced cases may present with life-threatening complications that include cirrhosis, hepatocellular cancer, diabetes, and heart disease. The mutation associated with haemochromatosis is highly prevalent in white populations but the disorder has variable penetrance. An autosomal-recessive disorder; common presenting features include fatigue and arthralgias. Fasting transferrin saturation is the phenotypic hallmark of the disorder, and diagnosis is confirmed by genetic testing. The main goal of treatment is to avoid iron overload in early-stage disease and remove excess iron from body stores by phlebotomy in late-stage disease. Complications may include cirrhosis, hepatocellular cancer, arthropathy, diabetes, and heart disease.

Answer 208

northern European descent The major HFE mutation (C282Y) is common in the US: 1 in 10 white people is heterozygous for this mutation, while 1 in 200 is a C282Y homozygote. The frequency of C282Y homozygosity is much lower in other ethnicities including Hispanic people (0.27 per 1000), Pacific Islanders (0.12 per 1000), and black people (0.14 per 1000).[5] Globally, the frequency of this mutation may vary and other genetic mutations may predominate

Answer 209

The most common mutations of the haemochromatosis gene (HFE) are C282Y and H63D The HFE gene is on the short arm of chromosome 6

Answer 210

``` STRONG Middle age Male White FHx Supplemental iron ```

Answer 211

``` COMMON Fatigue Weakness Lethargy Arthralgia Hepatomegaly DM Impotence in males Loss of libido Skin pigmentation - May begin as a bronzing of the skin but then progress to grey or brown with slate-grey patches in the mouth. Changes are usually generalised, but most frequently occur on the face, neck, extensor aspects of the lower forearms, dorsum of the hands, lower legs, genitals, and in old scars. ``` UNCOMMON Congestive heart failure Arrhythmias Porphyria cutanea tarda

Answer 212

TF Saturation - >45% Ferritin - raised; >674 picomols/L (>300 nanograms/mL) in men; >449 picomols/L (>200 nanograms/mL) in women CAN DO MUTATION ANALYSIS BUT NOT NEEDED

Answer 213

Stage 0 - observe + 3yr FU Lifestyle mod - Vitamin C or vitamin C-containing supplements should also be avoided, as vitamin C can lead to increased intestinal absorption of dietary iron. Hep A+B vaccination Stage 1 = 1yrly FU Stage 2-4 = phlebotomy (TF sat >45% + ferritin >674) IRON CHELATION - Reserved for patients with a contraindication to phlebotomy (i.e., anaemia, severe heart disease, or severe problems with venous access).

Answer 214

In a study of 251 patients followed for over 33 years, the mean survival was 21 years. Overall, patients with haemochromatosis had an increased risk of dying from cancer (11%), especially hepatocellular carcinoma (7%), diabetes mellitus (2%), cardiomyopathy (2%), myocardial infarction (2%), and liver cirrhosis (6%). Life expectancy in subjects without diabetes or cirrhosis at the time of diagnosis was virtually identical to that of age- and sex-matched controls.

Answer 215

``` Cirrhosis DM CCHF HCC Hypogonadism Bone loss Infection ```

Answer 216

haemochromatosis Patients are often asymptomatic at diagnosis, having been identified by screening performed because of a relative with haemochromatosis or following routine blood tests showing raised serum ferritin or transferrin saturation.

Answer 217

haemochromatosis Patients are often asymptomatic at diagnosis, having been identified by screening performed because of a relative with haemochromatosis or following routine blood tests showing raised serum ferritin or transferrin saturation.

Answer 218

An inguinal hernia is a protrusion of abdominal or pelvic contents through a dilated internal inguinal ring or attenuated inguinal floor into the inguinal canal and out of the external inguinal ring, causing a visible or easily palpable bulge. Protrusion of abdominal or pelvic contents, through a dilated internal ring or attenuated inguinal floor in the inguinal canal. Presents with visible or easily palpable swelling in the groin, often with discomfort during strenuous exercise or heavy lifting. Complications are rare but include incarceration, bowel obstruction, and strangulation. Diagnosis is usually clinical; imaging may be helpful where there is doubt about diagnosis, but also identifies many clinically insignificant apparent hernias. Surgical repair remains the mainstay of therapy, although watchful waiting is reasonable in adults with minimally symptomatic or asymptomatic inguinal hernia.

Answer 219

In general, inguinal hernia affects all ages, but the incidence increases with age. The lifetime risk of inguinal herniation is approximately 27% for men and 3% for women. Inguinal hernia is bilateral in up to 20% of affected adults. Family history of inguinal hernia is associated with increased risk

Answer 220

Congenital forms of indirect hernia occur because the processus vaginalis fails to undergo regression. Acquired defects occur because of degeneration and fatty changes in the wall of the inguinal floor. Progressive myopectineal degeneration leads to weakness, resulting in dilation of the internal ring (an opening in the transversalis fascia) and/or direct weakness of the posterior wall of the inguinal canal. Patients with inguinal hernia have been shown to have abnormal collagen metabolism and decreased collagen levels.

Answer 221

``` STRONG Male Old age Smoking Fix Prematurity AAA Previous RLQ incision Defective transversals fascia Chronic bronchitis/emphysema Marfan / Ehlers-danlos Lathyrsism ``` ``` WEAK Heavy lifting Pregnancy Ascites BPH Urethral stricture ```

Answer 222

Groin discomfort Pain with bulge Groin mass Acute abdomen Mid-abdominal discomfort or pain that is poorly localised and associated with an inguinal bulge, but which improves when the bulge is reduced, is indicative of small bowel stretch in the hernia sac Midpoint of PSIS and Pubic S is deep ring (indirect) Direct enters distal to the deep ring

Answer 223

Most inguinal hernias are diagnosed clinically by observation and palpation. Additional investigations are not usually required. Imaging may be useful when there is diagnostic uncertainty (e.g., in a very obese patient, or other complex cases). Possible to do an USS

Answer 224

Incarcerated / strangulated = surgical repair + prophylactic ABx Small + asymptomatic = watchful waiting Large or symptomatic = open mesh or laparoscopic repair Non-Surgical candidate - A truss (or a wearable device that compresses the tissues over the inguinal canal) may be used for patients in whom surgical intervention represents a very significant risk, whose life expectancy is limited, or who refuse repair.

Answer 225

Prognosis is excellent after surgical repair. Patients often report an improvement in their quality of life he incidence of recurrent hernia with mesh repair is reported to be less than 2% Moderate to severe chronic groin pain is reported to occur in 10% to 12% of patients after inguinal hernia repair.

Answer 226

Post op urinary retention - may be the result of pre-existing urinary dysfunction, spinal or general anaesthesia, opioid medication, and/or vagolytic medications Wound seroma post op Inguinal or scrotal haematoma ``` Division of vas deferent Incisional hernia Bowel obstruction Dysejaculation post op Pelvic adhesions Groin pain/ numbness Mesh infection post-op ```

Answer 227

inguinal hernia in adults Some patients will complain of a burning sensation in the groin associated with an inguinal bulge. This is indicative of stretching of the peritoneal lining of the hernia sac. A strangulated inguinal hernia may present acutely with a tender, reddish, irreducible lump causing severe colicky abdominal pain, vomiting and abdominal distension. In this situation, the cough impulse is absent and bowel sounds may be absent. This is a surgical emergency.

Answer 228

Femoral herniae are relatively uncommon but are are an important problem due to their high rate of strangulation (because of their narrow neck). Femoral hernia occur when abdominal viscera or omentum passes through the femoral ring and into the potential space of the femoral canal.

Answer 229

Femoral hernias account for 5% of abdominal hernias and are more common in women than men (ratio 3:1), because of the wider anatomy of the female bony pelvis. It is very rare for a femoral herniation to occur in a child.

Answer 230

The femoral canal (Fig. 1) is an anatomical compartment, located in the anterior thigh. It contains lymphatic vessels, lymph nodes and some loose connective tissue. The superior border of the femoral canal is the femoral ring, which is covered by the femoral septum (a connective tissue layer). The rigidity of the borders of the femoral ring, especially the concave margin of the lacunar ligament, results in femoral hernias being very prone to complications requiring urgent surgical intervention.

Answer 231

The main risk factors for developing a femoral hernia include: Female Pregnancy (higher incidence in multiparous women) Raised intra-abdominal pressure (e.g. heavy lifting, chronic constipation) Increasing age

Answer 232

Femoral hernias will commonly present as a small lump in the groin. Whilst a femoral hernia is usually asymptomatic (aside from the lump) at presentation, due to the anatomy of the femoral canal, around 30% of femoral hernia cases will present as an emergency (either obstruction or strangulation). It is important to identify the exact location of the lump in the groin in order to decide which type of hernia is present although often, particularly in obese patients, it is not clear. Femoral hernia – found infero-lateral to the pubic tubercle (and medial to the femoral pulse) Inguinal hernia – found supero-medial to the pubic tubercle A femoral hernia can roll up superiorly and in front of the inguinal ligament and are often misdiagnosed as inguinal The tightness of the femoral ring means that the hernia is unlikely to be reducible.

Answer 233

All patients with a femoral hernia need surgical intervention (as discussed below), hence routine pre-operative investigations should be performed if possible. Radiological Whilst the diagnosis can be made clinically, additional imaging is often required. Ultrasound scanning can demonstrate a femoral hernia (Fig. 2) but these are operator dependent and a high index of suspicion is necessary. A CT abdomen-pelvis scan will also demonstrate a femoral hernia, as well as delineate any differential diagnosis. If there is significant doubt in the diagnosis or evidence of complications, then the lump should be surgically explored.

Answer 234

All femoral hernias should be managed surgically, ideally within 2 weeks of presentation, due to the high risk of strangulation. Two different approaches can be taken with the femoral hernia surgical reduction: Low approach – the incision is made below the inguinal ligament, which has the advantage of not interfering with the inguinal structures but does result in limited space for the removal of any compromised small bowel High approach – the incision is made above the inguinal ligament is the preferred technique in an emergency intervention due to the easy access to compromised small bowel The operation involves reducing the hernia and then narrowing the femoral ring with sutures medially between the pectineal and inguinal ligaments or with a mesh plug .

Answer 235

The risk of strangulation of femoral hernias increases with time following initial diagnosis; after 3 months the risk of strangulation is 22% and reaches 45% after 21 months. As with any hernia, there is also a risk of becoming obstructed. An acute presentation of femoral hernia carries an increased morbidity and 20 times higher mortality than that of elective surgery, as well as the associated risks of bowel resection, wound infection, and cardiorespiratory complications.

Answer 236

Ischaemic bowel disease encompasses a heterogeneous group of disorders caused by acute or chronic processes, arising from occlusive or non-occlusive aetiologies, which result in decreased blood flow to the gastrointestinal tract. The clinical course may range from transient and reversible to fulminant. Intestinal ischaemia can be classified into three types: acute mesenteric ischaemia, chronic mesenteric ischaemia, and colonic ischaemia. Acute mesenteric ischaemia may also be further subdivided into embolic mesenteric ischaemia, thrombotic mesenteric ischaemia, and venous mesenteric ischaemia. Colonic ischaemia is the most common type and has the most favourable prognosis. It may present clinically in a number of ways, including transient reversible ischaemia, chronic irreversible ischaemia, or acute fulminant ischaemia. Mesenteric venous thrombosis may lead to acute or subacute intestinal ischaemia and may also present across a spectrum of severity. Long-term complications of ischaemic bowel disease depend on the location and nature of the underlying pathology. Possible complications include stricture formation, short bowel syndrome, and food fear leading to malnutrition.

Answer 237

Colonic ischaemia frequently occurs in older people with co-existing morbidities. Acute mesenteric ischaemia accounts for approximately 0.1% of hospital admissions. It also occurs more commonly in those with comorbidities, most notably atrial fibrillation, myocardial infarction, and atherosclerosis. Non-occlusive mesenteric ischaemia (NOMI) accounts for 20% to 30% of acute mesenteric ischaemia. NOMI may also occur in patients receiving enteral nutrition in intensive care following surgery or trauma

Answer 238

``` Embolism Thrombosis Vasculitis External compression Venous thrombosis Hypoperfusion (i.e., non-occlusive ischaemia): ie shock, HF, AAA repair, dialysis ```

Answer 239

``` STRONG Old age Hx smoking Hypercoagulable states AF MI Structural heart defects Hx vasculitis ``` ``` WEAK Recent CV surgery Shock Congestive HF Atherosclerosis ``` ``` Previous ileostomy IBS Colonic Carcinoma Constipation Long term laxative use Use of vasopressors ```

Answer 240

COMMON Pain Malaena / fresh blood Diarrhoea Tenderness - perceived pain may be out of proportion to tenderness appreciated on physical examination. WL - This is a notable feature of chronic mesenteric ischaemia, which is usually related to sitophobia (food fear) in these patients. Physical examination may reveal an epigastric bruit in 48% to 63% of patients with bowel ischaemia, indicative of turbulent flow through an area of vascular narrowing. UNCOMMON Vasculitis Light-headedness, pallor + dyspnoea

Answer 241

CT is the current first-line investigation of choice when acute ischaemia is suspected and should be obtained early. - bowel wall thickening, bowel dilation, pneumatosis intestinalis, portal venous gas, occlusion of the mesenteric vasculature, bowel wall thickening with thumb-printing sign suggestive of submucosal oedema or haemorrhage Colonoscopy/sigmoido - The best test to establish the diagnosis of colonic ischaemia, assess severity, and exclude alternative causes of colonic inflammation. May be repeated to follow disease progression or resolution. FBC - On admission, approximately 75% of patients with acute mesenteric ischaemia have a leukocytosis >15,000 cells/mm³ and about 50% have metabolic acidaemia. May reveal anaemia (often as a result of repeated episodes of melaena) that exacerbates ischaemia. Lactate - HIGH Acidosis, uraemia, elevated creatinine, amylasaemia COAG PANEL - in case cause is thrombo - check for hyper coag] ECG - atrial fibrillation, arrhythmia, acute myocardial infarction Erect CXR - free air if perforation present Abdo Xray - free air if perforation present

Answer 242

Evidence of infarction, perforation, or peritonitis - resus, supportive + emergency surgery (lapscop-or-otomy) SMA embolus - Endovascular surgery or embolectomy or resection Heparin if thombosis Papaverine to reduce spasms Non occlusive - correct medical cause +/- bowel resection Vasculitic cause - steroids CHRONIC mesenteric ischaemia -> angioplasty + stenting Colonic ischaemia - segmental colectomy

Answer 243

Acute mesenteric ischaemia results in mortality rates of between 60% and 100% in several large series. Chronic mesenteric ischaemia Mortality rates for surgical re-vascularisation tend towards the lower end of a range from 0% to 16%, with success rates of >90%, and recurrence rates generally <10% Colonic ischaemia Colonic ischaemia carries the most favourable prognosis of the varying forms of bowel ischaemia; nevertheless, 20% will develop chronic ulcerating ischaemic colitis

Answer 244

Sitophobia Stricture Short bowel syndrome - This results in a loss of surface area for fluid, nutrient, and medication absorption, causing an inability to maintain protein-energy, fluid, electrolyte, or micro-nutrient balance when ingesting a conventionally accepted, normal diet.

Answer 245

ischaemic bowel disease Up to 6.7% of patients who have undergone open or endovascular cardiac or major vascular procedures develop colonic ischaemia, and the mortality may be as high as 67% in this population.[2][3] These patients typically present with crampy abdominal pain and watery diarrhoea within a few days of surgery. Factors that may underlie these figures include emboli arising from cross-clamping of the aorta, a risk of intestinal hypoperfusion in the postoperative period, and a relatively high incidence of heart failure in these patients.

Answer 246

ischaemic bowel disease Up to 6.7% of patients who have undergone open or endovascular cardiac or major vascular procedures develop colonic ischaemia, and the mortality may be as high as 67% in this population.[2][3] These patients typically present with crampy abdominal pain and watery diarrhoea within a few days of surgery. Factors that may underlie these figures include emboli arising from cross-clamping of the aorta, a risk of intestinal hypoperfusion in the postoperative period, and a relatively high incidence of heart failure in these patients.

Answer 247

From inferior mesenteric artery (leading to left colic artery, marginal artery and sigmoid artery)

Answer 248

Superior mesenteric artery (leading to middle colic artery, right colic artery and ioliocolic artery)

Answer 249

Increased morbidity is associated with increasing age, shock, ICU admission, bacteraemia, multiple comorbidities, cirrhosis, chronic renal failure, cancer, jaundice, fungal infection, biliary origin of the abscess, acute respiratory failure, inadequate antibiotic therapy, and increased severity of illness.

Answer 250

``` CNS infection / haem spread Sepsis Abscess rupture Subphrenic absecc Pleuropulmonary fistula Hepatobronchial fistulae Hepatic artery pseudoaneurysm Abdominal or hepatic venous thrombosis Liver failure Acute pancreatitis Abscess recurrence Organ fistula ```

Answer 251

liver abscess The most common presenting symptoms of liver abscess are fever, chills, and RUQ pain. Right-sided pulmonary symptoms may also occur. Liver abscess can present in an insidious manner. The symptoms can be non-specific and of variable duration. Therefore, absence of abdominal pain and tenderness does not exclude the diagnosis. Clinical manifestations in older patients are similar to those in younger patients.

Answer 252

Wilson's disease is an autosomal-recessive disease of copper accumulation and copper toxicity caused by mutations in the ATP7B gene, which is part of the biliary excretion of copper pathway. Patients are usually aged 10 to 40 years and present with either hepatic disease or a movement disorder neurological disease. Siblings of a patient have a 25% chance of being affected, and family work-up allows the diagnosis to be made in those who do not yet have symptoms. An autosomal-recessive disease of copper accumulation and toxicity caused by a defect in an enzyme involved in the biliary excretion of excess copper. Affects up to 1 in 40,000 people. Diagnosis often missed; should be considered in patients aged 10 to 40 years with hepatitis, cirrhosis, hepatic decompensation, and symptoms suggestive of movement or psychiatric disorders. Screening and diagnostic tests: 24-hour urine copper measurement, ophthalmological slit-lamp examination for Kayser-Fleischer (KF) rings, blood ceruloplasmin levels, and liver biopsy with measurement of quantitative copper. Unlike many genetic disorders, it is treatable. Hepatic presentations are treated with a combination of trientine and zinc (liver transplantation if liver failure severe). Neurological presentations are treated with zinc. Maintenance and pre-symptomatic therapy: zinc. If zinc-intolerant, trientine next best choice for maintenance.

Answer 253

The worldwide incidence of Wilson's disease is in the order of 30 cases per million. Wilson's disease affects around 1 in 30,000 to 1 in 40,000 births. The disease does not favour a particular sex and all ethnic groups are affected equally. Clinical disease usually appears from about the age of 10 to 40 years

Answer 254

Wilson's disease is an autosomal-recessive disease caused by mutations in the ATP7B gene. The gene product of ATP7B is involved in excretion of excess copper in the bile and subsequent elimination in the stool. A normal diet contains about 1.0 mg/day of copper, and about 0.25 mg of this is excess.

Answer 255

STRONG ATP7B mutation WEAK Non-vegetarian diet

Answer 256

``` COMMON Hx hepatitis Behavioural abnormalities Tremor Dysarthria Dystonia Incoordination Sloppy / small handwriting Dysdiadochokinesia Esotropia (in-turning of the eyes), abnormal ocular pursuit, abnormal saccadic (rapid, intermittent) eye movements, diplopia (double vision) and distractibility of gaze and fixation. Normal sensation, strength and reflexes ``` ``` UNCOMMON Hx GI bleed Jaundice Liver tenderness Spider angiomata Gynaecomastia Ascites Peripheral oedema Bruising HJ reflux Encephalopathy Dysphagia ``` IE cirrhosis Sx

Answer 257

LFTs - abnormal - Liver function tests (LFTs) are always abnormal in hepatic presentation. May have raised aminotransferases and raised bilirubin if the patient has jaundice. May have lowered albumin if in liver failure. 24hr urine copper - >100 micrograms Blood Ceruloplasmin - <180 mg/L (18 mg/dL) Blood free copper - Copper levels have been found to be elevated at least 6-fold in Wilson's disease Possible to DNA test

Answer 258

zinc: children >10 years of age: 25 mg orally three times daily; adults: 50 mg orally three times daily zinc: children >10 years of age: 25 mg orally three times daily; adults: 50 mg orally three times daily Zinc is completely effective in causing a negative copper balance and preventing copper re-accumulation and copper toxicity and has a much better safety profile than available alternatives: namely, trientine and penicillamine. Rx liver disease

Answer 259

In general, if the treatment begins early enough, the outlook is good. If liver failure is only mild to moderate (Nazer scores of 1 to 9), liver function recovers to normal in 6 to 12 months. Unless the liver receives further insult (viral hepatitis, drug damage, etc.), and if the patient complies with therapy, liver function will probably be adequate for a normal life span.

Answer 260

Wilson's disease Liver disease may present as acute hepatitis, which will relapse if the disease remains undiagnosed. However, the liver involvement may remain subclinical with no jaundice, and patients can present with cirrhosis or complications of cirrhosis, such as variceal bleeding. Occasionally patients present with acute, severe, liver failure as their first manifestation of the disease. If haemolysis is also present, the diagnosis is almost certain to be Wilson's disease. Neurological presentation may be dominated by a single symptom, such as tremor, that has been present for years. Alternatively the patient may exhibit a range of movement disorder symptoms as an acute presentation. About half of the patients who present neurologically have had significant behavioural symptoms for some time (2-3 years). Wilson's disease may be clinically mistaken for Parkinson's disease if there is facial rigidity and difficulty initiating movement, such as walking.

Answer 261

Liver failure Oesophageal varices Aspiration

Answer 262

Liver failure Oesophageal varices Aspiration

Answer 263

Primary sclerosing cholangitis (PSC) is a chronic progressive cholestatic liver disease, characterised by inflammation and fibrosis of the intrahepatic and/or extrahepatic bile ducts, resulting in diffuse, multi-focal stricture formation. It is often associated with inflammatory bowel disease. Complications include dominant biliary strictures (focal areas of tight narrowing of the extrahepatic biliary tree that develops in 40% to 50% of patients as a result of progressive structuring), cholangitis, cholangiocarcinoma, and end-stage liver disease (due to chronic progressive biliary fibrosis). Cholestatic liver disease causing continued destruction of the bile ducts, cirrhosis, and end-stage liver disease. Predominantly affects young and middle-aged men, often with underlying inflammatory bowel disease. Patients may be asymptomatic at diagnosis but develop symptoms of pruritus and jaundice. Diagnosis involves laboratory tests and cholangiography. No effective medical therapy is available. Liver transplantation is the only treatment option for patients with advanced disease. Liver failure and cholangiocarcinoma are the leading causes of death.

Answer 264

5.58 per 100,000 in the UK It is more common in men than in women, with a male-to-female ratio of 2:1 Typically presents during the fourth or fifth decade of life, with a mean age of 40 years at the time of diagnosis Can occur at any age About two-thirds of patients with PSC have associated inflammatory bowel disease (typically ulcerative colitis)

Answer 265

The aetiology is not well understood. The frequent presence of serum auto-antibodies Inflammation and injury of the medium- and large-sized bile ducts, leading to fibrosis and multi-focal stricturing of the ducts, characterise the pathological process. Obstruction of the medium- and large-sized bile ducts leads to progressive fibrosis and ultimately obliteration of the smaller ducts (ductopenia) and bile stasis (cholestasis). Bile stasis above strictures predisposes patients to primary bile duct stones and retained bile salts may further contribute to bile duct damage. The biliary strictures of PSC, both intrahepatic and extrahepatic, contribute to jaundice, pruritus, episodes of bacterial cholangitis, and progression to biliary cirrhosis. Ongoing injury and continued destruction of the bile ducts results in secondary parenchymal damage, fibrosis, cirrhosis, and end-stage liver disease.

Answer 266

COMMON Male IBD Genetic predisposition

Answer 267

``` COMMON Male sex Hx IBD 40-50 Abdominal pain - RUQ/epi Pruritus Fatigue WL Fever Jaundice ``` ``` UNCOMMON Steatorrheoa Splenomegaly Ascites Encephalopathy ```

Answer 268

ALP - normal or elevated (>3x upper limit of normal) GGT - elevated AST ALT - mild to moderate elevation (typically <300 international units/L) Serum bilirubin - normal or elevated, predominantly conjugated Albumin - may be low FBC - normal or thrombocytopaenia ± anaemia, leukopaenia PT - normal or prolonged ANCA - positive or negative AMA - negative (PBC) Abdo USS - abnormal bile ducts (± cirrhotic liver, ascites, splenomegaly) BEST TEST MRCP / ERCP - normal or multi-focal intrahepatic and/or extrahepatic strictures and dilations ± dominant biliary stricture IgG4 raised in 12%

Answer 269

Asymptomatic patients only require observation and general lifestyle changes (including maintaining a healthy diet and weight, and limiting alcohol use). ITCHINESS colestyramine: children >6 years of age: 80 mg/kg orally three times daily; adults: 4-16 g/day orally given in 2 divided doses May need to Rx osteoporosis / osteopenia Patients with dominant biliary strictures (strictures of the extrahepatic biliary tree) who are acutely ill (rapidly worsening jaundice and pruritus, acute bacterial cholangitis, deteriorating liver function tests) require endoscopic retrograde cholangiopancreatography (ERCP), and balloon dilation of the stricture.

Answer 270

Age, bilirubin, and histological stage are the most consistently identified independent predictors of survival Life expectancy is reduced primarily by death from liver failure and hepatobiliary malignancies (cholangiocarcinoma in particular). The median survival from the time of diagnosis to death or liver transplantation is 7 to 14 years.

Answer 271

``` Liver failure Complications of liver disease Cholangiocarcinoma Osteoporosis Fat soluble deficiencies ADEK Acute / ascending cholangitis Gallstones Colon cancer/gallbladder ```

Answer 272

PSC About half of patients are symptomatic at presentation. Symptoms include pruritus, upper abdominal pain, fatigue, and/or intermittent jaundice. Patients with overlapping autoimmune hepatitis often have significantly higher serum levels of aminotransferases (ALT 357 IU/L vs. 83.7 IU/L) and IgG (25.6 g/L vs. 12.9 g/L). Patients who present with sudden and marked deterioration in clinical status and biochemical tests (e.g., worsening pruritus, fevers, and jaundice) may have a complication of PSC such as a dominant stricture or cholangiocarcinoma. A minority of patients present initially with complications of end-stage liver disease, such as ascites (2%), variceal bleeding (3%), or bacterial cholangitis (6%). At the time of diagnosis, a dominant bile duct stenosis may be present in up to 36% of patients.

Answer 273

Primary biliary cholangitis (PBC) is a chronic disease of the small intrahepatic bile ducts that is characterised by progressive bile duct damage (and eventual loss) occurring in the context of chronic portal tract inflammation. Fibrosis develops as a consequence of the original insult and the secondary effects of toxic bile acids retained in the liver, resulting ultimately in cirrhosis. The almost universal presence of autoantibodies in PBC patients (classically anti-mitochondrial antibodies) has led to the widely held view that the disease has an autoimmune component to its aetiology. The prevalence of primary biliary cholangitis (PBC) is up to 35/100,000 in US populations, with a distribution that is heavily skewed towards women (10:1 female-to-male distribution) and those over 45 years of age. The combination of elevation of serum alkaline phosphatase and a PBC-specific autoantibody (typically anti-mitochondrial antibody) is sufficient for diagnosis in most patients, with no need for biopsy confirmation. PBC is progressive in most patients; although, in many people, the rate of progression can be so slow that it may not be clinically relevant. Cirrhosis and its typical complications arise in the end stage. Symptoms (typically pruritus and fatigue) can significantly lower the quality of life, even in patients with a very slowly progressive disease. These symptoms warrant treatment in their own right using specific regimens. Progression of the disease can be slowed by therapy with ursodeoxycholic acid. Obeticholic acid is recommended in patients with an inadequate response to ursodeoxycholic acid. Transplantation is an effective treatment for those patients who develop end-stage liver disease with PBC.

Answer 274

35 per 100,000 It is significantly more common in women than in men (up to a 10-fold difference). Peak age for the diagnosis of PBC is between 55 and 65 years

Answer 275

The classic pathophysiological process in PBC is damage to, and progressive destruction of, the biliary epithelial cells lining the small intrahepatic bile ducts PBC is conventionally thought to be an autoimmune disease There is a very high incidence of autoantibodies, most characteristically directed against mitochondrial antigens (antimitochondrial antibody). These antibodies, which are present in over 95% of patients, are principally directed against pyruvate dehydrogenase complex E2 subunit (PDC-E2), although reactivity is also seen, to a lesser degree, against other PDC components and the E2 subunits of related enzyme complexes. PBC patients also have a lower incidence of autoantibodies directed at disease-specific nuclear antigens (ANA)

Answer 276

STRONG Female 45-60 WEAK FHx AI Smoking UTI

Answer 277

``` COMMON Hypercholesterolaemia Itch Fatigue Postural dizziness/blackouts Hepatomegaly Jaundice Xanthelasmata ``` Ascites + splenomegaly May be associated with Sjogren's WL associated with advanced liver disease / coeliacs

Answer 278

``` AMA = main boi ANA Anti- pyruvate dehydrogenase E2 Anti M2 Anti glycoprotein 210 Anti sp100 ``` USS - excludes obstructive lesion within visible bile ducts MRCP - excludes obstructive lesion within visible bile ducts ``` ALP - H GGT - H Bili - H ALT - H Albumin - decreased ```

Answer 279

ACUTE Ursodeoxycholic acid: 12-16 mg/kg/day orally given in 3 divided doses Immunomodulatory therapy 1. Steroids 2. Steroids + AZA or MMF Antipruritic: colestyramine: 4 g orally once to twice daily Or rifampicin or naltrexone ESLF - transplant Check PT / liver complications

Answer 280

PBC is a slowly progressive condition in the majority of patients. Given the age of presentation with the disease, many patients die of other causes before reaching end-stage liver disease. There is approximately a doubling of risk of liver-related death in PBC patients compared with in relevant comparator populations.

Answer 281

``` Complication Hypercholesterolaemia Osteoporosis Portal HTN secondary to cirrhosis Hepatoma ```

Answer 282

PBC Although most PBC patients present early in the disease process with abnormal liver biochemistry (with or without the symptoms of itch or fatigue), occasionally patients will present with advanced liver disease. In these patients, the clinical features of cirrhosis would be more prominent than the features of PBC. Possible features would include ascites, splenomegaly, skin thinning, weight loss, and variceal bleeding. Jaundice may be significantly more prominent than would be expected in people with cirrhosis of different aetiologies. The disease can present from the 20s onwards and there is increasing evidence to suggest that it is more severe in nature and less responsive to first-line therapy in younger patients.

Answer 283

A perianal abscess is a collection of pus within the subcutaneous tissue of the anus that has tracked from the tissue surrounding the anal sphincter.

Answer 284

Epidemiology They are the most common form of anorectal abscess, making up around 60% of cases; They are more common in men (M:F 2:1); The average age of patients is around 40 years.

Answer 285

Features Patients may describe pain around the anus, which may be worse on sitting; They may have also discovered some hardened tissue in the anal region; There may be pus-like discharge from the anus; If the abscess is longstanding, the patient may have features of systemic infection.

Answer 286

Causes They are generally colonised by gut flora such as E. coli; Those caused by organisms such as Staph. aureus are more likely to be an infection of the skin rather than originating from the digestive tract.

Answer 287

Investigations Most perianal abscesses can be detected through inspection of the anus and digital rectal examination; When querying the underlying cause, colonoscopy and blood tests such as cultures and inflammatory markers may be of use; Imaging such as MRI and transperineal ultrasound can be useful tools, with the former being the gold standard in imaging anorectal abscesses. They are however rarely used except for cases where the abscess has complications or is part of a more serious underlying process such as IBD.

Answer 288

Associated conditions Any anorectal abscess can be caused by an underlying inflammatory bowel disorder, especially Crohn's; Diabetes mellitus is a risk factor due to its ability to affect wound healing; Underlying malignancy can cause these abscesses as well as other anorectal lesions due to the risk of bowel perforation.

Answer 289

Treatment Treatment is usually surgical, with incision and drainage being first line, usually under local anaesthetic. The wound can then either be packed or left open, in which case it will heal in around 3-4 weeks; Antibiotics can be of use, but are only usually employed if there is systemic upset secondary to the abscess, as they do not seem to help with healing of the wound after drainage.

Answer 290

As stated above 'perianal abscess' refers to a simple abscess of the subcutaneous tissue. There are numerous other anorectal abscesses which can be classified by the layers and planes that they occupy. Ischiorectal abscesses are found between the obturator internus muscles and the external anal sphincter; Supralevator abscesses form when infection tracks superiorly from the peri-sphincteric area to above the levator ani; Intersphincteric abscesses are rare (2-5% of cases) and as their name suggests are sited between the internal and external anal sphincters; The pelvis is notorious for the presence of potential spaces, which can become sites of infection. One such incidence of this is the formation of a horseshoe abscess, a reference to their shape. These are found in a potential space between the coccyx and the anal canal, and can be the result of complication of another type of anorectal abscess, such as a supralevator abscess.

Answer 291

Haemorrhoidal tissue is part of the normal anatomy which contributes to anal continence. These mucosal vascular cushions are found in the left lateral, right posterior and right anterior portions of the anal canal (3 o'clock, 7'o'clock and 11 o'clock respectively). Haemorrhoids are said to exist when they become enlarged, congested and symptomatic

Answer 292

Clinical features painless rectal bleeding is the most common symptom pruritus pain: usually not significant unless piles are thrombosed soiling may occur with third or forth degree piles Pain often worst at end of the day

Answer 293

External originate below the dentate line prone to thrombosis, may be painful Internal originate above the dentate line do not generally cause pain

Answer 294

Grade I Do not prolapse out of the anal canal Grade II Prolapse on defecation but reduce spontaneously Grade III Can be manually reduced Grade IV Cannot be reduced

Answer 295

Management soften stools: increase dietary fibre and fluid intake topical local anaesthetics and steroids may be used to help symptoms outpatient treatments: rubber band ligation is superior to injection sclerotherapy surgery is reserved for large symptomatic haemorrhoids which do not respond to outpatient treatments newer treatments: Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy

Answer 296

Acutely thrombosed external haemorrhoids typically present with significant pain examination reveals a purplish, oedematous, tender subcutaneous perianal mass if patient presents within 72 hours then referral should be considered for excision. Otherwise patients can usually be managed with stool softeners, ice packs and analgesia. Symptoms usually settle within 10 days

Answer 297

Anal fissures are longitudinal or elliptical tears of the squamous lining of the distal anal canal. If present for less than 6 weeks they are defined as acute, and chronic if present for more than 6 weeks.

Answer 298

Risk factors constipation inflammatory bowel disease sexually transmitted infections e.g. HIV, syphilis, herpes

Answer 299

Features painful, bright red, rectal bleeding around 90% of anal fissures occur on the posterior midline. if the fissures are found in alternative locations then other underlying causes should be considered e.g. Crohn's disease

Answer 300

Management of an acute anal fissure (< 6 weeks) dietary advice: high-fibre diet with high fluid intake bulk-forming laxatives are first-line - if not tolerated then lactulose should be tried lubricants such as petroleum jelly may be tried before defecation topical anaesthetics analgesia topical steroids do not provide significant relief Management of a chronic anal fissure (> 6 weeks) the above techniques should be continued topical glyceryl trinitrate (GTN) is first-line treatment for a chronic anal fissure if topical GTN is not effective after 8 weeks then secondary care referral should be considered for surgery (sphincterotomy) or botulinum toxin

Answer 301

Management of a chronic anal fissure (> 6 weeks) the above techniques should be continued topical glyceryl trinitrate (GTN) is first-line treatment for a chronic anal fissure if topical GTN is not effective after 8 weeks then secondary care referral should be considered for surgery (sphincterotomy) or botulinum toxin Management of an acute anal fissure (< 6 weeks) dietary advice: high-fibre diet with high fluid intake bulk-forming laxatives are first-line - if not tolerated then lactulose should be tried lubricants such as petroleum jelly may be tried before defecation topical anaesthetics analgesia topical steroids do not provide significant relief

Answer 302

Enterocutaneous These link the intestine to the skin. They may be high (>500ml) or low output (<250ml) depending upon source. Duodenal /jejunal fistulae will tend to produce high volume, electrolyte rich secretions which can lead to severe excoriation of the skin. Colo-cutaneous fistulae will tend to leak faeculent material. Both fistulae may result from the spontaneous rupture of an abscess cavity onto the skin (such as following perianal abscess drainage) or may occur as a result of iatrogenic input. In some cases it may even be surgically desirable e.g. mucous fistula following sub total colectomy for colitis. Suspect if there is excess fluid in the drain. Enteroenteric or Enterocolic This is a fistula that involves the large or small intestine. They may originate in a similar manner to enterocutaneous fistulae. A particular problem with this fistula type is that bacterial overgrowth may precipitate malabsorption syndromes. This may be particularly serious in inflammatory bowel disease. Enterovaginal Aetiology as above. Enterovesicular This type of fistula goes to the bladder. These fistulas may result in frequent urinary tract infections, or the passage of gas from the urethra during urination.

Answer 303

Enterocutaneous These link the intestine to the skin. They may be high (>500ml) or low output (<250ml) depending upon source. Duodenal /jejunal fistulae will tend to produce high volume, electrolyte rich secretions which can lead to severe excoriation of the skin. Colo-cutaneous fistulae will tend to leak faeculent material. Both fistulae may result from the spontaneous rupture of an abscess cavity onto the skin (such as following perianal abscess drainage) or may occur as a result of iatrogenic input. In some cases it may even be surgically desirable e.g. mucous fistula following sub total colectomy for colitis. Suspect if there is excess fluid in the drain.

Answer 304

Enteroenteric or Enterocolic This is a fistula that involves the large or small intestine. They may originate in a similar manner to enterocutaneous fistulae. A particular problem with this fistula type is that bacterial overgrowth may precipitate malabsorption syndromes. This may be particularly serious in inflammatory bowel disease.

Answer 305

Enterovesicular This type of fistula goes to the bladder. These fistulas may result in frequent urinary tract infections, or the passage of gas from the urethra during urination.

Answer 306

Some rules relating to fistula management: They will heal provided there is no underlying inflammatory bowel disease and no distal obstruction, so conservative measures may be the best option Where there is skin involvement, protect the overlying skin, often using a well fitted stoma bag- skin damage is difficult to treat A high output fistula may be rendered more easily managed by the use of octreotide, this will tend to reduce the volume of pancreatic secretions. Nutritional complications are common especially with high fistula (e.g. high jejunal or duodenal) these may necessitate the use of TPN to provide nutritional support together with the concomitant use of octreotide to reduce volume and protect skin. When managing perianal fistulae surgeons should avoid probing the fistula where acute inflammation is present, this almost always worsens outcomes. When perianal fistulae occur secondary to Crohn's disease the best management option is often to drain acute sepsis and maintain that drainage through the judicious use of setons whilst medical management is implemented. Always attempt to delineate the fistula anatomy, for abscesses and fistulae that have an intra abdominal source the use of barium and CT studies should show a track. For perianal fistulae surgeons should recall Goodsall's rule in relation to internal and external openings.

Answer 307

Anterior resection or abdomino-perineal excision of the colon and rectum. Total mesorectal excision is now standard of care. Most resections below the peritoneal reflection will require defunctioning ileostomy. Most patients will require preoperative radiotherapy.

Gastro Flashcards

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