Gastrointestinal Flashcards
Define achalasia
a oesophageal motility disorder, characterised by loss of peristalsis and failure of the lower oesophageal sphincter (LOS)
Explain the aetiology / risk factors of achalasia
Degeneration of ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause.
Oesophageal infection with Trypanosoma cruzi seen in Central and South America produces a similar disorder (Chagas disease).
Summarise the epidemiology of achalasia
Annual incidence: 1 in 100000.
Usual presentation age: 25–60 years.
Recognise the presenting symptoms of achalasia
Insidious onset and gradual progression of:
- intermittent dysphagia involving solids and liquids;
- difficulty belching;
- regurgitation (particularly at night);
- heartburn;
- chest pain (atypical/cramping, retrosternal);
- weight loss.
Recognise the signs of achalasia on physical examination
Signs of complications (e.g. cachectic)
Identify appropriate investigations for achalasia and interpret the results
1st Line:
- Barium swallow: Dilated oesophagus which smoothly tapers down to the sphincter (beak- shaped).
- Endoscopy: To exclude malignancy which can mimic achalasia.
- Manometry:
- -> Elevated resting LOS pressure (>45 mmHg);
- -> incomplete LOS relaxation;
- -> absence of peristalsis in the distal (smooth muscle portion) of the oesophagus.
Other Ix:
- CXR: widened mediastinum, double right heart border (dilated oesophagus), an air-fluid level in the upper chest and absence of gastric bubble.
- serology: for antibodies against T. cruzi
Define acute cholangitis
Infection of the bile duct; usually bacterial of duodenal source
Explain the aetiology / risk factors of acute cholangitis
Bile duct obstruction: usually caused by gall stones
- Can be benign structuring (tumour) or malignancy (pancreatic, gall bladder, bile duct)
- Iatrogenic: post-operative damage/altered structure of bile duct
Pathogenesis: increased pressure in bile duct brings bacteria in contact with blood, resulting in infection Risk Factors: age, female, cirrhosis
Summarise the epidemiology of acute cholangitis
15% have gallstones; 2-3% will develop acute cholangitis
Recognise the presenting symptoms of acute cholangitis
RUQ abdominal pain; fever, rigors, malaise
Recognise the signs of acute cholangitis on physical examination
Jaundice, RUQ tenderness
Charcot’s Triad: Abdominal pain, jaundice and fever (15-20% of cases)
Worsened condition => Reynold’s pentad (add septic shock and mental confusion)
Identify appropriate investigations for acute cholangitis and interpret the results
Bloods: FBC (raised WCC), CRP (raised); LFTs (obstructive picture: raised bilirubin, ALP), cultures
USS: distinguish between cholangitis and cholecystitis
MRCP: better imaging than USS
ERCP: gold standard test for biliary obstruction (but it is invasive)
Generate a management plan for acute cholangitis
Fluids, antiobiotics (ciprofloxacin, metronidazole), vasopressors
Unblock the bile duct: 24-48hrs after admission, once settled
- ERCP (dilation of duct/removal of stones)
- Lithotripsy: acoustic shock waves to break stones
- Cholecystectomy: removal of gall bladder
Identify the possible complications of acute cholangitis and its management
Recurrent biliary pain; jaundice; further episodes; death risk increased
Summarise the prognosis for patients with acute cholangitis
Risk of death (multiple organ failure); 10-30% mortality
Define alcoholic hepatitis
Inflammatory liver injury caused by chronic heavy alcohol abuse
Explain the aetiology / risk factors of alcoholic hepatitis
One of three alcoholic liver diseases (hepatitis; steatosis; cirrhosis)
Histopathology: centrilobular ballooning, DEGENERATION AND NECROSIS OF HEPATOCYTES; STEATOSIS, neutrophilic inflammation, cholestasis
Summarise the epidemiology of alcoholic hepatitis
10-35% of heavy drinkers
Recognise the presenting symptoms of alcoholic hepatitis
May remain asymptomatic and undetected; mild illness with nausea, malaise, epigastric or right hypochondrial pain
More severe: jaundice, abdominal discomfort/swelling, swollen ankles, GI bleed
Recognise the signs of alcoholic hepatitis on physical examination
Excess Alcohol: malnourished, palmar erythema, Dupuytren’s contracture, facial telangiectasia, parotid enlargement, spider naevia, gynaecomastia, hepatomegaly
Alcoholic Hepatitis: febrile, tachycardic, jaundiced, bruising, encephalopathy (e.g. liver flap), ascites, hepatomegaly, splenomegaly
Identify appropriate investigations for alcoholic hepatitis and interpret the results
BLOODS: FBC (reduced Hb, platelets; increased MCV and WCC), LFT (increased transaminases, bilirubin, GGT, ALP, reduced albumin) U&Es ( urea and K+ low), Clotting (prolonged PT)
USS: for other causes
Upper GI endoscopy: investigate varices
Liver biopsy: distinguish other causes of hepatitis Electroencephalogram: indicative for encephalopathy
Generate a management plan for alcoholic hepatitis
ACUTE:
- Thiamine, VitC, monitor electrolytes and glucose
- Treat encephalopathy (lactulose)
- Ascites: diuretics (spironolactone and furosemide)
NUTRITION:
- Oral/NG feeding
- Avoid protein restriction unless encephalopathic
Steroid Therapy: Reduce short-term mortality
Long Term: see alcohol dependence
Identify the possible complications of alcoholic hepatitis and its management
Acute liver decompensation; hepatorenal syndrome; cirrhosis
Summarise the prognosis for patients with alcoholic hepatitis
10% mortality in 30 days, 40% in 1 year; most progress to cirrhosis with continued alcohol intake Maddrey’s discriminant factor: (bilirubin/17) + (PT prolongation x 4.6) [>32 = > 50% 30 day mortality) Glasgow Alcoholic Gepatitis score (GAHS) if >9, >50% 30 day mortality
Define anal fissure
A break or tear in the skin of the anal canal (usually posterior midline)
Explain the aetiology / risk factors of anal fissure
Stretching of the anal mucosa beyond capability.
HARD STOOLS, PREGNANCY, OPIATE ANALGESIA
- Constipation
- Passing large, hard stools
- Prolonged diarrhoea
- Childbirth trauma; sexual activity; Crohn’s Disease; Ulcerative Colitis
- Spasming of Internal Anal Sphincter: impaired blood supply to fissure, causing impaired healing
- STIs can cause breakdown of skin (syphilis, herpes)
Summarise the epidemiology of anal fissure
1:350; occur in 15-40 yrs, more common in men
Recognise the presenting symptoms of anal fissure
A tear or paper cut-like scar in the skin of the anal canal Pain on defecation
Recognise the signs of anal fissure on physical examination
Appearance of scar in midline, extending from the anal opening
Identify appropriate investigations for anal fissure and interpret the results
Investigate possible causes of fissure (proctoscopy, sigmoidoscopy or colonoscopy for CD or colorectal cancer)
DO NOT attempt DRE as it is painful
Generate a management plan for anal fissure
Non-surgical:
- gt ointment and lidocaine ointment, with diltiazem (calcium channel blocker)
- Topical anaesthetics, high-fiber diets and stool softeners
- 2nd line: botulinum toxin injection and topical diltiazem
Surgical: for those who have unsuccessfully tried non-surgical treatment for 1-3 months
- Lateral Sphincterectomy
Identify the possible complications of anal fissure and its management
Complications of treatment include Incontinence
Summarise the prognosis for patients with anal fissure
Most can be non-surgically treated
Define appendicectomy
Surgical removal of the vermiform appendix
Summarise the indications for an appendicectomy
acute appendicitis
Identify the possible complications of an appendicectomy
Wound infection, abscess, ileus
Contraindications of appendicectomy
Haemodynamic instability Lack of surgical expertise Severe abdominal distension Generalised peritonitis Severe pulmonary disease Pregnancy
Define amyloidosis
Extracellular deposition of amyloid fibrils; three types:
- AL (light chain)
- AA (serum A amyloid)
- ATTR (familial)
Explain the aetiology / risk factors of amyloidosis
Amyloid fibril deposition disrupts the structure and function of normal tissue; amyloidosis is classified according to fibril subunit:
- AL – monoclonal immunoglobulin light chains; associated with plasma cell disorders i.e. multiple myeloma
- AA – Serum amyloid protein A; associated with chronic inflammatory conditions (IBD and rheumatoid arthritis)
- ATTR – a genetic variant; autosomal dominant transmitted mutations
Summarise the epidemiology of amyloidosis
Primary - AL Amyloidosis: 3-600 annual cases
Secondary - AA Amyloidosis: 1-5% of those with chronic inflammatory conditions
Hereditary Amyloidosis: 5% of patients with systemic amyloidosis
Recognise the presenting symptoms of amyloidosis
Multi-systemic affects:
- Renal: renal failure, oedema
- Vascular: Periorbital Purpura
- PNS: pain/numbness in arms and legs
- GI: macroglossia, bleeding, weight loss, malabsorption
- Cardiac: angina, orthopnoea, PND
- Haematological: bleeding diathesis
- Neurological: carpal tunnel syndrome
- Dermatological: waxy skin, easy bruising
- Joints: painful joints
Recognise the signs of amyloidosis on physical examination
Multi-systemic Affects:
- Renal: proteinuria
- Cardiac: arrhythmias, heart failure
- GI: hepatosplenomegaly
- Neurological: sensory and motor neuropathy
- Skin: purpura around eyes
- Joints: tender, swelled joints
Identify appropriate investigations for amyloidosis and interpret the results
Tissue biopsy: congo red stain; to diagnose AA; poor diagnostic power for AL
Urine: proteinuria, free immunoglobulin light chains for AL
Blood: CRP, ESR, rheumatoid factor, LFTs, U&Es
Define appendicitis
Inflammation of the appendix
Explain the aetiology / risk factors of appendicitis
Organisms of the gut invade the appendix
Summarise the epidemiology of appendicitis
very common
Recognise the presenting symptoms of appendicitis
pain in the umbilical region that migrates to the right iliac fossa region
Diarrhoea/constipation
Anorexia and vomiting (rare)
Recognise the signs of appendicitis on physical examination
Rovsing’s sign: pushing down on the LIF causes an increase in pain in the RIF
Psoas sign: pain on extending the hip
Cope sign: pain on flexion and internal rotation of the right hip
Rebound tenderness: when infection involves the peritoneum
Identify appropriate investigations for appendicitis and interpret the results
FBC: CRP, neutrophil leucocytosis
CT: high diagnostic accuracy (reduces –ve appendicectomy, but can cause delay)
USS: appendix not always visualised
Generate a management plan for appendicitis
Prompt appendicectomy
Antibiotics: metronidazole and cefuroxime
Identify the possible complications of appendicitis and its management
Perforation: more common if feacolith is present; young children
Appendix Mass: when inflamed appendix becomes covered in omentum (US/CT helps with diagnosis)
Appendix Abscess: can result in appendix mass also
Summarise the prognosis for patients with appendicitis
Most recover easily after surgery, between 10-28 day recovery
Define autoimmune hepatitis
Chronic hepatitis of unknown aetiology; characterised by autoimmune features, hyperglobulinaemia and the presence of circulating antibodies
Explain the aetiology / risk factors of autoimmune hepatitis
Genetically predisposed individual – environmental agent leads to hepatocyte expression of HLA antigens, which become focus of t-cell mediated attack
Type 1 (classic): ANA, anti-smooth muscle antibodies (ASMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA)
Type 2: antibodies to liver/kidney microsomes
Summarise the epidemiology of autoimmune hepatitis
Type 1: all age groups (mainly young women)
Type 2: generally disease of girls and young women
Recognise the presenting symptoms of autoimmune hepatitis
May be asymptomatic and discovered incidentally by deranged LFTs Insidious Onset: malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis Acute Hepatitis (25%): RUQ pain, fever, anorexia, jaundice, nausea, vomiting, diarrhoea Family history of autoimmune disease (e.g. T1DM, vitilgo)
Recognise the signs of autoimmune hepatitis on physical examination
Chronic Liver Disease Signs: spider naevi, gynacomastea, abnormal hair growth
Late Features: Ascites; oedema and encephalopathy
Cushingoid Features: round face, cutaneous striae, acne, hirsuitism
Identify appropriate investigations for autoimmune hepatitis and interpret the results
Bloods: LFTs (increase AST, GGT, ALT, AlkPhos, bilirubin)
Clotting (increase PT)
FBC (mild reduced Hb and platelets and WCC- hypersplenism in portal hypertension)
Liver Biopsy: needed for diagnosis; interface hepatitis or cirrhosis
Other: to rule out other causes e.g. viral serology, ferritin/trasnferritin
USS/CT/MRI: of liver and abdomen: visualise lesions
ERCP: rule out Primary Sclerosing Cholangitis
Define Barrett’s oesophagus
a change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia.
[Metaplasia of the squamous epithelium of the lower third of the oesophagus to columnar epithelium]
Mucosal inflammation and erosion, and replacement of mucosa with metaplastic columnar epithelium, in the lower third of the oesophagus.
Presence of goblet cells is necessary for diagnosis
Explain the aetiology / risk factors of Barrett’s oesophagus
Chronic inflammation: principal cause is GORD
RF: acid or bile reflux/GORD, male sex, age, white, family history of BO or oesophageal adenocarcinoma, obesity, smoking
Summarise the epidemiology of Barrett’s oesophagus
Men are 8x more at risk
Caucasian is at a higher risk
Recognise the presenting symptoms of Barrett’s oesophagus
Frequent heartburn, dysphagia, haematemesis, retrosternal pain, weight loss
Recognise the signs of Barrett’s oesophagus on physical examination
Diagnosis made in imaging
Identify appropriate investigations for Barrett’s oesophagus and interpret the results
Upper GI endoscopy with biopsy
barium oesophagram
Generate a management plan for Barrett’s oesophagus
If pre-malignant/high-grade dysplasia – oesophageal resection or eradicative mucosectomy
If no pre-malignancy or high-grade dysplasia: endoscopic surveillance + biopsy; every 1-3 years
- Anti-reflux measures: PPIs (omeprazole)
Identify the possible complications of Barrett’s oesophagus and its management
high risk of oesophageal cancer (oesophagogastric junctional adenocarcinoma)
Summarise the prognosis for patients with Barrett’s oesophagus
Risk of cancer is 1-7:1000; those with oesophageal cancer have low survival rates (most are <1 year)
Define cholecystitis
inflammation of the gallbladder
Explain the aetiology / risk factors of cholecystitis
Inflammation of the gallbladder – most commonly by gallstones. But can occur with blockage due to tumour or scarring
Risk Factors: age, female, pregnancy, oral contraceptives, obesity, diabetes mellitus
Calculous Cholecystitis: gallstones blocking flow; gallbladder can become infected (E. coli, Klebsiella). Can spread to diaphragm
Acalculous Cholecystitis: no stones; vasculitis, chemotherapy, major trauma or burns
Chronic Cholecystitis: repeated inflammations; may be asymptomatic
Summarise the epidemiology of cholecystitis
Accounts for 3-10% of abdominal pain; highest in 50-69 year olds
Recognise the presenting symptoms of cholecystitis
RUQ pain, worse on eating fatty foods, nausea and vomiting. Biliary colic preceding cholecystitis
Recognise the signs of cholecystitis on physical examination
Fever, tender abdomen, palpable gallbladder, jaundice
Murphy’s Sign: while pressing on RUQ, pain on inspiration and breath is terminated
Identify appropriate investigations for cholecystitis and interpret the results
Bloods: FBC (increased WCC), CRP (elevated), bilirubin (elevated)
USS: of RUQ, most commonly used to diagnose
CT: if complications (perforation, gangrene) are suspected
Generate a management plan for cholecystitis
Surgery: laparoscopic cholecystectomy (early has better prognosis)
Identify the possible complications of cholecystitis and its management
Gangrene, gallbladder rupture (abscess, peritonitis), empyema, fistula formation, gallstone ileus
Summarise the prognosis for patients with cholecystitis
Pre-complication prognosis is better, 25-30% develop complications
Define cirrhosis
End stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.
What is decompensated liver failure and what are the symptoms?
Compensated: Np symptoms of the disease
Decompensated: cirrhosis has progressed to the point that the liver is having trouble functioning and you start having symptoms of the disease
jaundice, ascites, encephalopathy or GI bleeding
Explain the aetiology / risk factors of cirrhosis
Most common: chronic alcohol misuse
Chronic viral hepatitis: Hep B+C most common worldwide
Autoimmune hepatitis
Drugs: e.g. methotrexate, hepatotoxic drugs
Inherited: α1-Antitrypsin deficiency, haemochromatosis, Wilson’s disease, galactosaemia, CF
Vascular: Budd-Chiari syndrome
Chronic biliary diseases: primary biliary cirrhosis, PSC, biliary atresia
Cryptogenic: 5-10%
Non-alcoholic steatohepatitis (NASH): associated with obesity, diabetes, parenteral nutrition, and drugs (amiodarone, tamoxifen)
Decompensation: infection, GI bleeding, constipation, alcohol, drugs
Summarise the epidemiology of cirrhosis
Top 10 causes of death
Recognise the presenting symptoms of cirrhosis
Early and non-specific: anorexia, nausea, fatigue, weakness, weight loss
Symptoms (decreased synthetic function): easy bruising, abdominal swelling, ankle oedema
Symptoms (reduced detoxification): jaundice, personality changes, altered sleep patterns, amenorrhoea
Symptoms (Portal Hypertension): abdominal swelling, haematemesis, PR bleeding or melaena
Recognise the signs of cirrhosis on physical examination
Chronic Liver Disease: ABCDE
- Asterixes (liver flap)
- Bruises
- Clubbing
- Dupuytren;s Contracture
- Erythema
- Other: jaundice, gynaecomastia, leukonychia, spider naevia, scratch marks, ascites, hepatomegaly, caput medusa, splenomegaly
Identify appropriate investigations for cirrhosis and interpret the results
BLOODS: FBC (lowered Hb, platelets [hypersplenism]) LFTs (can be normal, increased AlkPhos, reduced albumin) Clotting (prolonged PT), Serum AFP
Other: to determine cause (serology, α1 antitrypsin, caeruloplasmin {Wilson’s Disease])
Liver Biopsy: percutaneous (trans jugular if ascites or clotting deranged)
Imaging: USS, CT, MRI (detect complications, hepatocellular carcinoma, thrombosis), MRCP
Endoscopy: examine for varices
Child-Pugh Grading: Class A/B/C depending on score
Generate a management plan for cirrhosis
Treat cause if possible
Advice: avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver, ensure good nutrition Treat complications:
- Encephalopathy: treat infections, exclude GI bleed, lactulose
- Ascites: diuretics (spironolactone/furosemide), sodium restriction, fluid restriction
- Spontaneous Bacterial Peritonitis: antibiotic treatment (cefuroxime and metronidazole)
- Surgical: insertion of TIPS (relieve portal hypertension). Liver transplant
Identify the possible complications of cirrhosis and its management
Portal hypertension with ascites, encephalopathy or variceal haemorrhage, SBP, hepatocellular carcinoma, peritonitis
Renal failure
Summarise the prognosis for patients with cirrhosis
Depends on aetiology: generally poor. 5 year survival at 50%, with ascites 2 year survival at 50%
Define coeliac disease
Inflammatory disease caused by intolerance to gluten, causing chronic intestinal villous atrophy and malabsorption
Explain the aetiology / risk factors of coeliac disease
Sensitivity to the gliadin component of the cereal protein, gluten – triggers an immunological reaction in the small intestine leading to mucosal damage and loss of villi
10% risk of first relatives being affected
Summarise the epidemiology of coeliac disease
1:2000; more common in western society
Recognise the presenting symptoms of coeliac disease
pain, tiredness,
Recognise the signs of coeliac disease on physical examination
Anaemia: pallor
Malnutrition: short stature, abdominal distension, wasted buttocks in children
Vitamin/Mineral Deficiencies: osteomalcia, easy bruising
Intense itchy blisters on elbows/knees/buttocks
Identify appropriate investigations for coeliac disease and interpret the results
Bloods: FBC, iron, folate, U&Es, albumin, Ca2+ and phosphate
Serology: testing for IgG anti-glandin, tissue transglutaminase (tTG)
Stool: culture to exclude infection
D-xylose test: reduced urinary excretion after oral xylose (small bowel malabsorption)
Endoscopy: direct visualisation shows villous atrophy in small intestine (jejenum and ileum), giving smooth, flat appearance to mucosa.
Biopsy: villous atrophy with crypt hyperplasia of duodenum
Generate a management plan for coeliac disease
Advice: Withdrawal of gluten from the diet and educating on dietary advice
Medical: vitamin and mineral supplements
Identify the possible complications of coeliac disease and its management
Iron, folate and vitamin B12 deficiencies; osteomalacia; ulcerative jejunoileitis; bacterial overgrowth
Summarise the prognosis for patients with coeliac disease
With strict adherence, most patients make a full recovery; symptoms resolving in weeks
Life-long diet changes need to be made
Define Crohn’s disease
Chronic granulomatous inflammatory disease that can affect any part of the GI tract.
Most commonly in ileum and colon
Explain the aetiology / risk factors of Crohn’s disease
Combination of environmental factors and genetic predisposition
Genetics: siblings are 30x more likely to develop it;
Immune system: impaired innate immunity
Environmental Factors: smoking, oral contraceptives,
Summarise the epidemiology of Crohn’s disease
5-8:100,000; lower incidence in Asia and east Africa; bimodal onset at 15-30 and 60-80 years
Recognise the presenting symptoms of Crohn’s disease
Crampy abdominal pain; diarrhoea; fever/malaise/weight loss; symptoms of complications
Recognise the signs of Crohn’s disease on physical examination
Weight loss; clubbing; anaemia signs
Aphthous ulceration of the mouth
Perianal skin tags, fistulae and abscesses
Signs of complications (eyes, joints or skin)
Identify appropriate investigations for Crohn’s disease and interpret the results
Blood: FBC, U&Es, LFTs, ESR, CRP (p-anca negative)
Stool microscopy and culture: exclude infective colitis
AXR: toxic megacolon
Erect CXR: to see perforation
Small-bowel barium follow-through; reveal fibrosis/strictures, rose thorn appearance
Endoscopy (OGD, colonoscopy) and biopsy: differentiate between CD and UC. Will see granulomas in CD.
Generate a management plan for Crohn’s disease
Acute Exacerbation: - Fluid rescus - IV or oral corticosteroids - 5-ASA Analogues (e.g. mesalazine) - Analgesia - Monitor activity markers Long Term: - Steroids: to treat acute exacerbations - 5-ASA analgoues (e.g. mesalazine) to reduce relapses - Immunosuppression: steroid-sparing agents (e.g. azathioprine) to reduce relapse - Anti-TNF agents (e.g. infliximab) to achieve and maintain remission Advice: - Stop smoking - Dietician referral - Education and advice Surgery: - Indicated by failure of medical treatment, failure to thrive in children or complications - Resection of bowel and stoma formation
Identify the possible complications of Crohn’s disease and its management
GI: Haemorrhage, bowel obstruction, perforation, fistulae, GI carcinoma
Extra intestinal: uveitis; episcleritis; gallstones; kidney stones
Summarise the prognosis for patients with Crohn’s disease
Chronic relapsing condition; two thirds will require surgery eventually, and two thirds of these will have >1 procedure.
Define diverticular disease
Diverticulosis: presence of diverticulae outpouchings of the colonic mucosa and submucosa throughout the large bowel
Diverticular Disease: diverticulosis associated with complications (e.g haemorrhage, infection) Diverticulitis: acute inflammation and infection of the colonic diverticulae
Hinchey Classification:
- Ia: phlegmon
- Ib and II: localised abscesses
- III: perforation with purulent peritonitis
- IV: faecal peritonitis
Explain the aetiology / risk factors of diverticular disease
A low fibre diet can lead to loss of stool bulk, consequently high pressures are required to expel the stool, leading to herniations through the muscularis at weak points
Pathogenesis: most common in sigmoid colon; can be obstructed with stool, leading to bacterial overgrowth, injury and diverticulitis
Recognise the presenting symptoms of diverticular disease
Often asymptomatic (80-90%) Complications: PR bleeding, diverticulitis (LIF pain, fever) diverticular fistulation into the bladder (pneumaturia, faecaluria and recurrent UTIs)
Recognise the signs of diverticular disease on physical examination
Diverticulitis: tender abdomen, signs of local/generalised peritonitis if perforation occurred
Identify appropriate investigations for diverticular disease and interpret the results
Bloods: FBC, clotting, cross-match
Barium Enema: demonstrated presence of diverticulae (not in acute; risk of perforation) Flexible sigmoidoscopy and colonoscopy: diverticulae can be seen
Acute Setting: CT
Generate a management plan for diverticular disease
Asymptomatic: soluble, high-fibre diet. [Anti-inflammatories (mesalazine) under investigation as preventions]
GI Bleed: managed conservatively
- IV hydration
- Bowel rest
Surgery: may be necessary with recurrent attacks or complications
- Open or laparoscopic approaches
- Open Hartmann’s (resection and stoma)
- One-Stage resection and anastomosis
- Laparoscopic drainage, peritoneal lavage and drain replacement can be effective
Identify the possible complications of diverticular disease and its management
Diverticulitis, pericolic abscess, perforation, faecal peritonitis, colonic obstruction, fistula formation, haemorrhage
Summarise the prognosis for patients with diverticular disease
10-25% will have >1 episode of diverticulitis
Define gallstones and biliary colic
presence of solid concretions in the gallbladder. Gallstones form in the gallbladder but may exit into the bile ducts.
Symptoms ensue if a stone obstructs the cystic, bile, or pancreatic duct.
Biliary colic is right upper quadrant pain, radiating to shoulder
Explain the aetiology / risk factors of gallstones and biliary colic
gallstones: 90% are made of cholesterol. form in the gall bladder, but can move into the ducts, where they can cause symptoms
BC: Obstruction of common bile duct/cystic duct by a gall stone. Acute pain can be exacerbated by certain foods (high in fat)
Risk Factors: age, female, family history, increased oestrogen exposure (pregnancy, birth control) diabetes mellitus, obesity, rapid weight loss, FHx
Summarise the epidemiology of gallstones and biliary colic
high prevalence, usually symptomatic
2-3% risk of developing biliary colic
Recognise the presenting symptoms of gallstones and biliary colic
Gallstones are highly prevalent, but most (80%) are asymptomatic.
Pain: sharp RUQ pain, radiating to right shoulder/back, can follow high fat meals, lasts 30-120 minutes, nausea, vomiting,
Other presentations
Biliary colic: is characterised by steady, severe pain (intensity >5 on a scale of 1-10) in the right upper quadrant (RUQ) of the abdomen lasting more than 15-30 minutes. An attack of simple biliary colic commonly requires an analgesic but should resolve within 5 hours.
Cholecystitis: biliary pain lasting more than 5 hours is accompanied by features of inflammation: fever, marked RUQ tenderness (Murphy’s sign), and leukocytosis. Some patients progress to sepsis. Occasionally, stones can perforate the gallbladder, leading to intestinal obstruction (gallstone ileus).
Choledocholithiasis: when stones obstruct the bile ducts, biliary-type pain is accompanied by cholestasis, which manifests as jaundice. More sinister is acute cholangitis, characterised by Charcot’s triad of biliary pain, jaundice, and fever. Acute cholangitis represents a medical emergency.
Acute pancreatitis: epigastric pain radiating to the back results from bile duct stones obstructing the pancreatic ducts. Inflammatory features include peritonitis.
Recognise the signs of gallstones and biliary colic on physical examination
Biliary colic: Right upper quadrant or epigastric tenderness.
Acute cholecystitis: Tachycardia, pyrexia, right upper quadrant or epigastric tenderness. There may be guarding +/- rebound. Murphy’s sign is elicited by placing a hand at the costal margin in the RUQ and asking the patient to breathe deeply. Patient stops breathing as the inflamed gallbladder descends and contacts the palpating fingers.
Ascending cholangitis: Pyrexia, right upper quadrant pain, jaundice.
Identify appropriate investigations for gallstones and biliary colic and interpret the results
Bloods: usually normal, LFTs can show raised bilirubin and AlkPhos
FBC, LFTs, serum lipase and amylase, abdominal ultrasound
MRCP, endoscopic ultrasound scan, ECRP, abdominal CT scan
Generate a management plan for gallstones and biliary colic
No treatment for asymptomatic cholecystolithiasis
symptomatic cholecystolithiasis: Laparoscopic cholecystectomy
cholelithiasis: ERCP, lithotripsy, papillary balloon dilation, stent
Relief of symptoms and electrolyte/fluid imbalance
- Anti-emetics (dimenhydrinate)
- Pain: NSAIDs (diclofenac)
Identify the possible complications of gallstones and biliary colic and its management
Cholecystitis, cholangitis, pancreatitis
Delayed surgery can cause pancreatitis, empyema/perforation of gallbladder, cholecystitis, cholangitis, obstructive jaundice
Summarise the prognosis for patients with gallstones and biliary colic
Good, dependant on development of complications
The outlook for patients with symptomatic cholelithiasis managed by cholecystectomy is favourable. The same holds for patients with choledocholithiasis who undergo ERCP with biliary sphincterotomy and stone extraction, followed later by cholecystectomy.
Define gastric cancer
Gastric malignancy, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma.
cancer deriving from the stomach
Explain the aetiology / risk factors of gastric cancer
50% involve pylorus
25% lesser curve
10% cardia
2-7% are lymphomas
Most cases are probably caused by environmental insults in genetically predisposed individuals that lead to mutation and subsequent unregulated cell growth.
Risk Factors: being >55, male, poor socio-economic status,
• H.pylori infection;
• atrophic gastritis;
• diet high in smoked, processed foods and nitrosamines; low vegetable consumption
• smoking
• alcohol
Summarise the epidemiology of gastric cancer
Common cause of cancer death worldwide, highest incidence in Asia (Japan). Sixth most common cancer in UK (annual incidence is 15 in 100000)
Age>50 years.
Cancer of the antrum/body is becoming less common, while that of the cardia and gastro- oesophageal junction is increasing.
Recognise the presenting symptoms of gastric cancer
In early phases, it is often asymptomatic. Early satiety or epigastric discomfort.
Weight loss, anorexia, nausea and vomiting.
dyspepsia
Haematemesis, melaena, symptoms of anaemia. Dysphagia (tumours of the cardia).
Symptoms of metastases, particularly abdominal swelling (ascites) or jaundice (liver involvement).
Recognise the signs of gastric cancer on physical examination
Physical examination may be normal.
Epigastric mass. Abdominal tenderness. Ascites. Hepatomegaly, jaundice, ascites
acanthosis nigricans
Signs of anaemia.
Many eponymous signs:
Virchows node/Troisiers sign: Lymphadenopathy in left supraclavicular fossa.
Sister Mary Joseph node: Metastatic nodule on umbilicus.
Krukenbergs tumour: Ovarian metastases.
Identify appropriate investigations for gastric cancer and interpret the results
Upper GI endoscopy: With multiquadrant biopsy of all gastric ulcers.
Blood: FBC (for anaemia), LFT. CEA, Ca19-9, Ca72-4
CT/MRI: Staging of tumour and planning of surgery.
Ultrasound of liver: Staging of tumour.
Bone scan: Staging of tumour.
Endoscopic ultrasound: Assesses depth of invasion and lymph node spread.
Laparoscopy: May be needed to determine if tumour is resectable.
Define gastro-oesophageal reflux disease
Inflammation of the oesophagus caused by reflux of gastric acid and/or bile
Explain the aetiology / risk factors of gastro-oesophageal reflux disease
Disruptions of mechanisms that prevent reflux (physiological etc.)
Risk Factors: obesity, pregnancy (increase in abdominal pressure), smoking, diet, hiatus hernia, increase in age, FHx
Summarise the epidemiology of gastro-oesophageal reflux disease
Common, 5-10% of adults
Recognise the presenting symptoms of gastro-oesophageal reflux disease
Substernal burning discomfort or ‘heartburn’, aggravated by supine position, bending, large meals and drinking alcohol
acid regurgitation
Waterbrash
Aspiration results in voice hoarseness, laryngitis, nocturnal cough and wheeze
dysphagia, bloating, early satiety
Recognise the signs of gastro-oesophageal reflux disease on physical examination
Usually normal.
Occasionally, epigastric tenderness, wheeze on chest auscultation, dysphonia.
Identify appropriate investigations for gastro-oesophageal reflux disease and interpret the results
Upper GI Endoscopy, biopsy: confirm presence of oesophagitis, exclude malignancy
Barium Swallow: detect hiatus hernia, peptic stricture
CXR: incidental hiatus hernia findings
24 hour oesophageal pH monitoring: determines temporal relationship to symptoms
Generate a management plan for gastro-oesophageal reflux disease
Advice:
- Lifestyle changes, weight loss, elevating head
- Avoid provoking factors, stopping smoking, lower fat meals
Medical:
- Antacids
- PPIs (e.g. lansoprazole)
- H2 antagonists (e.g. ranitidine)
Endoscopy:
- Annual endoscopic surveillance for Barrett’s Oesophagus Surgery:
- Anti-reflux surgery
Identify the possible complications of gastro-oesophageal reflux disease and its management
Oesophageal ulceration; peptic stricture; anaemia; Barrett’s; oesophageal adenocarcinoma
Summarise the prognosis for patients with gastro-oesophageal reflux disease
50% respond to lifestyle changes alone
Define gastroenteritis
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort
Explain the aetiology / risk factors of gastroenteritis & infectious colitis
i.e. name some of the pathogens
Viral: - Rotavirus, astrovirus, calcivirus Bacterial: - Campylobacter jejuni, Escherichia coli, Salmonella, Shigella Protozoal: - Entamoeba histolytica Toxins: - From Staphylococcus aureus, Clostridium botulinum
Commonly contaminated foods: improperly cooked meats, old rice, eggs, poultry
CHESS organisms
- Campylobacter
- Haemorrhagic E. Coli
- Entamoeba histolytica
- Shigella
- Salmonella
Summarise the epidemiology of gastroenteritis
Common, often under-reported
Recognise the presenting symptoms of gastroenteritis
Sudden onset nausea, vomiting, anorexia
Diarrhoea, abdominal pain/discomfort, fever, malaise
Enquire: recent travel, antibiotic use and recent food intake
Time: toxins (1-24 hours), bacterial (12 hours)
Recognise the signs of gastroenteritis (&IC)
Diffuse abdominal tenderness, abdominal distension and bowel sounds are increased
Severe: pyrexia, dehydration, hypotension, peripheral shutdown
Identify appropriate investigations for gastroenteritis & infectious colitis and interpret the results
Bloods: FBC, culture, U&Es
Stool: faecal microscopy
AXR/USS: exclude other causes
Sigmoidoscopy: only if IBD needs to be excluded
INFECTIOUS COLITIS
Bloods: FBC, CRP, ESR
Stool: MC&S
Generate a management plan for gastroenteritis & infectious colitis
Bed rest, fluids and electrolyte replacement (advise increase oral fluid intake to compensate for the water lost from diarrhoea and vomiting)
IV rehydration may be required in severe cases. Don;’t conventionally give antibiotics unless a bacteria has been isolated.
Botulism: botulinum antitoxin IM, manage in ITU
Identify the possible complications of gastroenteritis & infectious colitis and its management
Dehydration, electrolyte imbalance, prerenal failure, sepsis, shock
Botulinum: respiratory muscle paralysis
Summarise the prognosis for patients with gastroenteritis & infectious colitis
Generally good, majority are self-limiting
Define infectious colitis
An inflammation of the large bowel, with an infective cause
Summarise the epidemiology of infectious colitis
Rare, in those with lower hygiene levels, and contaminated food
Recognise the presenting symptoms of infectious colitis
Bloody diarrhoea, generalised abdominal pain, vomiting
Recognise the signs of infectious colitis on physical examination
Tenderness
DRE: bloody stool
Define gastrointestinal perforation
A hole in the wall of the gastrointestinal tract
Explain the aetiology / risk factors of gastrointestinal perforation
Gastric ulcers, duodenal ulcers, appendicitis, gastrointestinal cancer, diverticulitis
Iatrogenic: abdominal surgery
Summarise the epidemiology of gastrointestinal perforation
10-15% of patients with acute diverticulitis
Recognise the presenting symptoms of gastrointestinal perforation
Sudden pain in epigastrium (duodenal ulcer), burning pain in epigastrium (gastric ulcer) Pain starts at perforation site, then spreads
Severe abdominal pain, nausea, vomiting and hematemesis
