Gastrointestinal Flashcards
Learning objectives
Answer
Define achalasia
- A condition in which the normal muscular activity of the oesophagus is disturbed (absent or uncoordinated) due to FAILURE OR INCOMPLETE REAXATION OF THE LOWER OESOPHAGEAL SPHINCTER.
- This leads to delay in the passage of swallowed material into the stomach
- Aetiology: it is caused by degeneration of the ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause
- NOTE: oesophageal infection with Trypanosoma cruzi seen in Central/South America produces a similar disorder (CHAGAS DISEASE)
Summarise the epidemiology of achalasia
- It may occur at any age (mainly 25-60 yrs)
- Affects both sexes equally
- Annual incidence 1/100,000
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 (because they are eating less)
Recognise the signs of achalasia on physical examination
• May show signs of complications:
o Aspiration pneumonia
o Malnutrition
o Weight loss
Identify appropriate investigations for achalasia
• CXR may show:
o Widened mediastinum
o Double right heart border (dilated oesophagus)
o Air-fluid level in the upper chest
o Absence of the normal gastric air bubble
• Barium swallow may show:
o Dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)
• Endoscopy to exclude malignancy (which could mimic achalasia)
• Manometry (used to assess pressure at the LOS) may show:
o Elevated resting LOS pressure (> 45 mm Hg)
o Incomplete LOS relaxation
o Absence of peristalsis in the smooth muscle portion of the oesophagus
• NOTE: you may do serology for antibodies against T. cruzi if CHAGAS DISEASE is a possibility (and blood film may detect parasites)
Define acute cholangitis
• Infection of the bile duct.
Explain the aetiology / risk factors of acute cholangitis
• There are several causes:
o Obstruction of the gallbladder or bile duct due to stones
o ERCP
o Tumours (e.g. pancreatic, cholangiocarcinoma)
o Bile duct stricture or stenosis
o Parasitic infection (e.g. ascariasis)
Summarise the epidemiology of acute cholangitis
- 9% of patients admitted to hospital with gallstone disease will have acute cholangitis
- Equal in males and females
- Median age of presentation: 50-60 yrs
- Racial distribution follows that of gallstone disease - fair-skinned people
Recognise the presenting symptoms of acute cholangitis
• Most patents present with Charcot's Triad of symptoms: o RUQ Pain o Jaundice o Fever with rigors • This list of symptoms has been extended to include the following two symptoms, forming the Reynolds' Pentad: o Mental confusion o Septic shock • Patients may also complain of pruritus
Recognise the signs of acute cholangitis on physical examination
- Fever
- RUQ tenderness
- Mild hepatomegaly
- Jaundice
- Mental status changes
- Sepsis
- Hypotension
- Tachycardia
- Peritonitis (uncommon - check for alternative diagnosis)
Identify appropriate investigations for acute cholangitis
• Bloods
o FBC: High WCC
o CRP/ESR: possibly raised
o LFTs: typical pattern of obstructive jaundice (raised ALP + GGT)
o U&Es: may be signs of renal dysfunction
o Blood cultures: check for sepsis
o Amylase: may be raised if the lower part of the common bile duct is involved
• Imaging
o X-ray KUB: look for stones
o Abdominal ultrasound: look for stones and dilation of the common bile duct
o Contrast-enhanced CT/MRI: good for diagnosing cholangitis
o MRCP: may be necessary to detect non-calcified stones
Generate a management plan for acute cholangitis
• Resuscitation: may be required if the patient is in septic shock
• Broad-spectrum antibiotics: given once blood cultures have been taken (select drugs that are effective against anaerobes and Gram-negative organisms: e.g. cefuroxime + metronidazole)
• Most patients respond to antibiotics but endoscopic biliary drainage is usually required to treat the underlying obstruction
• Management depends on severity:
o Stage 1 (Mild)
• Antimicrobial therapy
• Percutaneous, endoscopic or operative intervention for non-responders (depending on aetiology)
o Stage 2 (Moderate)
• Early percutaneous or endoscopic drainage
• Endoscopic biliary drainage is recommended
o Stage 3 (Severe)
• NOTE: severe cholangitis counts as including shock, conscious disturbance, acute lung injury, AKI, hepatic injury or DIC
• Treatment of organ failure with ventilatory support, vasopressors etc.
• Urgent percutaneous or endoscopic drainage
• Definitive treatment required once the clinical picture improves
Identify the possible complications of acute cholangitis
• Liver abscesses • Liver failure • Bacteraemia • Gram-negative sepsis • Septic shock • AKI • Organ dysfunction • Percutaneous or endoscopic drainage can lead to: o Intra-abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage
Summarise the prognosis for patients with acute cholangitis
• Mortality between 17-40%
Define alcohol withdrawal
The symptoms that may occur when a person has been drinking too much alcohol on a regular basis and suddenly stops drinking.
Explain the aetiology / risk factors of alcohol withdrawal
Chronic alcohol consumption suppresses the activity of glutamate (an excitatory neurotransmitter), so the body compensates by increasing sensitivity to glutamate
So, when alcohol consumption stops, you get increased glutamate activity leading to excitatory symptoms
Summarise the epidemiology of alcohol withdrawal
If untreated, 6% of alcohol-dependent patients develop clinically relevant symptoms of withdrawal
Up to 10% of them will delirium tremens
Recognise the presenting symptoms of alcohol withdrawal
History of high alcohol intake Mild Symptoms: o Insomnia and fatigue o Tremor o Mild anxiety/feeling nervous o Mild restlessness/agitation o Nausea and vomiting o Headache o Sweating o Palpitations o Anorexia o Depression o Craving alcohol More severe symptoms: o Hallucinations o Withdrawal seizures (generalised tonic-clonic) Delirium tremens DEFINITION: an acute confusional sate often seen as withdrawal syndrome in chronic alcoholics and caused by sudden cessation of drinking alcohol. It can be precipitated by a head injury or an acute infection causing abstinence from alcohol.
Recognise the signs of alcohol withdrawal
FEATURES: Anxiety Tremor Sweating Vivid and terrifying visual and sensory HALLUCINATIONS (usually of animals and insects) Can be FATAL
Identify appropriate investigations for alcohol withdrawal and interpret the results
NO investigations
Generate a management plan for alcohol withdrawal
Chlordiazepoxide - reduces symptoms of alcohol withdrawal
Barbiturates may be used if refractory to benzodiazepines
Thiamine (Pabrinex) - prevents progression to Wernicke-Korsakoff syndrome
Identify the possible complications of alcohol withdrawal and its management
Patients can have seizures and die if it is left untreated
Summarise the prognosis for patients with alcohol withdrawal
Delirium tremens has a mortality of 35% if untreated
Mortality is < 2% with early detection and treatment
Define alcoholic hepatitis
• Inflammatory liver injury caused by chronic heavy intake of alcohol
Explain the aetiology / risk factors of alcoholic hepatitis
• One of the THREE forms of liver disease caused by excessive alcohol intake - the spectrum consists of:
o Alcoholic fatty liver (steatosis)
o Alcoholic hepatitis
o Chronic cirrhosis
• Histopathological features of alcohol hepatitis:
o Centrilobular ballooning
o Degeneration and necrosis of hepatocytes
o Steatosis
o Neutrophilic inflammation
o Cholestasis
o Mallory-hyaline inclusions (eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments)
o Giant mitochondria
Summarise the epidemiology of alcoholic hepatitis
• Occurs in 10-35% of heavy drinkers
Recognise the presenting symptoms of alcoholic hepatitis
• May remain asymptomatic and undetected
• May be mild illness with symptoms such as:
o Nausea
o Malaise
o Epigastric pain
o Right hypochondrial pain
o Low-grade fever
• More severe presenting symptoms include:
o Jaundice
o Abdominal discomfort or swelling
o Swollen ankles
o GI bleeding
• NOTE: a long history of heavy drinking is required for the development of alcoholic hepatitis (around 15-20 years)
• There may be events that trigger the disease (e.g. aspiration pneumonia, injury)
Recognise the signs of alcoholic hepatitis on physical examination
• Signs of Alcohol Excess o Malnourished o Palmar erythema o Dupuytren's contracture o Facial telangiectasia o Parotid enlargement o Spider naevi o Gynaecomastia o Testicular atrophy o Hepatomegaly o Easy bruising • Signs of Severe Alcoholic Hepatitis o Febrile (in 50% of patients) o Tachycardia o Jaundice o Bruising o Encephalopathy (e.g. liver flap, drowsiness, disorientation) o Ascites o Hepatomegaly o Splenomegaly
Identify appropriate investigations for alcoholic hepatitis
• Bloods
o FBC:
• Low Hb
• High MCV
• High WCC
• Low platelets
o LFTs:
• High AST + ALT
• High bilirubin
• High ALP + GGT
• Low albumin
o U&Es:
• Urea and K+ tend to be low
o Clotting: prolonged PT is a sensitive marker for significant liver damage
• Ultrasound - check for other causes of liver impairment (e.g. malignancy)
• Upper GI Endoscopy - investigate varices
• Liver Biopsy - can help distinguish from other causes of hepatitis
• EEG - slow-wave activity indicates encephalopathy
Generate a management plan for alcoholic hepatitis
• Acute
o Thiamine
o Vitamin C and other multivitamins (can be given as Pabrinex)
o Monitor and correct K+, Mg2+ and glucose
o Ensure adequate urine output
o Treat encephalopathy with oral lactulose or phosphate enemas
o Ascites - manage with diuretics (spironolactone with/without furosemide)
o Therapeutic paracentesis
o Glypressin and N-acetylcysteine for hepatorenal syndrome
• Nutrition
o Via oral or NG feeding is important
o Protein restriction should be avoided unless the patient is encephalopathic
o Nutritional supplementation and vitamins (B group, thiamine and folic acid) should be started parenterally initially, and continued orally
• Steroid Therapy - reduce short-term mortality for severe alcoholic hepatitis
NOTE: hepatorenal syndrome - the development of renal failure in patients with advanced chronic liver disease
• Thought to arise because of abnormalities in blood vessel tone in the kidneys
• Blood vessels in the kidney constrict because of the dilatation of blood vessels in the splanchnic circulation (supplying the intestines), which is mediated by factors released by the kidneys
• The splanchnic vasodilation leads to reduced effective volume of blood detected by the juxtaglomarular apparatus, leading to activation of the RAS and vasoconstriction of vessels in the kidney
• This leads to kidney failure
Identify the possible complications of alcoholic hepatitis
- Acute liver decompensation
- Hepatorenal syndrome
- Cirrhosis
Summarise the prognosis for patients with alcoholic hepatitis
• Mortality:
o First month = 10%
o First year = 40%
• If alcohol intake continues, most will progress to cirrhosis within 1-3 years
Define amyloidosis
• Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils
Explain the aetiology/risk factors of amyloidosis
• Amyloid fibrils are polymers of low-molecular-weight subunit proteins
• These are derived from proteins that undergo conformational changes to adopt an anti-parallel beta-pleated sheet configuration
• Their deposition progressively disrupts the structure and function of normal tissue
• Amyloidosis is classified according to the fibril subunit proteins
o Type AA - serum amyloid A protein
o Type AL - monoclonal immunoglobulin light chains
o Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin
Summarise the epidemiology of amyloidosis
- AA - incidence of 1-5% amongst patients with chronic inflammatory diseases
- AL - 300-600 cases in the UK per year
- Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis
Recognise the presenting symptoms and signs of amyloidosis
- Renal - proteinuria, nephrotic syndrome, renal failure
- Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
- GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding
- Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
- Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules
- Joints - painful asymmetrical large joints, enlargement of anterior shoulder
- Haematological - bleeding tendency
Identify appropriate investigations for amyloidosis
• Tissue Biopsy • Urine - check for proteinuria, free immunoglobulin light chains (in AL) • Bloods o CRP/ESR o Rheumatoid factor o Immunoglobulin levels o Serum protein electrophoresis o LFTs o U&Es • SAP Scan - radiolabelled SAP will localise the deposits of amyloid
Define anal fissure
- A painful tear in the squamous lining of the lower anal canal
- NOTE: 90% of anal fissures are posterior (anterior anal fissures tend to occur after childbirth)
Summarise the epidemiology of anal fissures
- Affects 1/10 people during their life time
- Both sexes are affected equally
- Can occur at any age
- Most cases occur in children and young adults: 10-30 yrs
Explain the aetiology / risk factors of anal fissure
- Most are caused by hard faeces
- Anal sphincter spasm can constrict the inferior rectal artery, causing ischaemia and impairing the healing process
- Rare causes: syphilis, herpes, trauma, Crohn’s, anal cancer, psoriasis
Recognise the presenting symptoms of anal fissure
- Tearing pain when passing stools
- There may be a little bit of blood in the faeces or on the paper
- Anal itching (pruritus ani)
Recognise the signs of anal fissure on physical examination
• Tears in the squamous lining of the anus on examination
Identify appropriate investigations for anal fissure
• Examine the anus
Generate a management plan for anal fissure
• Conservative o High-fibre diet o Softening the stools (laxatives) o Good hydration • Medical o Lidocaine ointment (local anaesthetic) o GTN ointment (relaxes the anal sphincter and promoted healing) o Diltiazem (relaxes the anal sphincter and promotes healing) o Botulinum toxin injection • Surgical o Lateral sphincterotomy o This relaxes the anal sphincter and promotes healing but it has complications (e.g. anal incontinence) so it is reserved for patients who are intolerant or not responsive to non-surgical treatments
Identify the possible complications of anal fissure
• Chronic anal fissure
Summarise the prognosis for patients with anal fissure
- In most people, the fissure will heal within a week or so
* Treatment revolves around easing pain by keeping the stools soft and relaxing the anal sphincter to promote healing
Define appendicitis
• Inflammation of the appendix
Summarise the epidemiology of appendicitis
- The MOST COMMON surgical emergency
- Can occur at any age
- Most commonly occurs between 10-20 yrs
Explain the aetiology / risk factors of appendicitis
- Gut organisms invade the appendix wall after lumen obstruction (e.g. by lymphoid hyperplasia, faecolith or filarial worms)
- This leads to oedema, ischaemic necrosis and perforation
Recognise the presenting symptoms of appendicitis
- Periumbilical pain that moves to the right iliac fossa
- Anorexia is an important feature
- Vomiting (may occur after pain)
- Constipation
- Diarrhoea
Recognise the signs of appendicitis on physical examination
• General Signs
o Tachycardia
o Fever
o Furred tongue
o Lying still
o Coughing hurts
o Foetor with/without flushing
o Shallow breaths
• RIF Signs
o Guarding
o Rebound and percussion tenderness
o PR pain on the right side (sign of low-lying pelvic appendix)
• Special Signs
o Rovsing’s Sign - palpation of the left iliac fossa causes more pain in the right iliac fossa than the left
o Psoas Sign - pain on extending the hip (caused by retrocaecal appendix)
o Cope Sign - pain on flexion and internal rotation of the hip (occurs if the appendix is in close proximity to the obturator internus)
• Variations in clinical picture
o Inflammation of retrocaecal/retroperitoneal appendix may cause flank pain or RUQ pain
• The only sign may be tenderness on the right on DRE
o A child may have vague abdominal pain and will not eat their favourite food
o A shocked confused 80+ year old who is not in any pain
Identify appropriate investigations for appendicitis
• Bloods o High WCC (mainly neutrophils) o High CRP • Ultrasound may help • CT - high diagnostic accuracy
Generate a management plan for appendicitis
• Prompt appendicectomy • Antibiotics: o Cefuroxime o Metronidazole • Laparoscopy - diagnostic and therapeutic advantages
Identify the possible complications of appendicitis
• Perforation
• Appendix mass
o Occurs when the inflamed appendix becomes covered with omentum
• Appendix abscess
o May occur if appendix mass fails to resolve
o Treatment involves drainage and antibiotics
Summarise the prognosis for patients with appendicitis
- Uncomplicated appendicitis - most people recover with no long-term problems
- Ruptured appendix - greater risk of complications/death
Define autoimmune hepatitis
• Chronic hepatitis of unknown aetiology, characterised by autoimmune features, hyperglobulinaemia and the presence of circulating autoantibodies
Explain the aetiology / risk factors of autoimmune hepatitis
• In a genetically predisposed individual, and environmental agent (e.g. viruses or drugs) may lead to hepatocyte expression of HLA antigens, which then become the focus of a principally T-cell-mediated autoimmune attack
• The raised titre of anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (ASMA) and anti-liver/kidney microsomes (anti-LKM) are NOT thought to directly injure the liver
• The chronic inflammatory changes are similar to those seen in chronic viral hepatitis with lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and, eventually, cirrhosis
• TWO major forms of autoimmune hepatitis:
o Type 1 (Classic)
• ANA
• ASMA
• Anti-actin antibodies (AAA)
• Anti-soluble liver antigen (anti-SLA)
o Type 2
• Antibodies to liver/kidney microsomes (ALKM-1)
• Antibodies to liver cytosol antigen (ALC-1)
Summarise the epidemiology of autoimmune hepatitis
- Type 1: occurs in ALL age groups (but mainly young women)
* Type 2: generally occurs in girls and young women
Recognise the presenting symptoms of autoimmune hepatitis
• May be asymptomatic and discovered incidentally through abnormal LFT • Insidiously present with: o Malaise o Fatigue o Anorexia o Weight loss o Nausea o Jaundice o Amenorrhoea o Epistaxis • Acute hepatitis (25%) presents with: o Fever o Anorexia o Jaundice o Nausea/Vomiting/Diarrhoea o RUQ pain o Some may present with serum sickness (e.g. arthralgia, polyarthritis, maculopapular rash) • NOTE: check for personal or family history of other autoimmune diseases • A full history is important to rule out other causes of hepatitis (e.g. viral, alcoholic)
Recognise the signs of autoimmune hepatitis on physical examination
- Stigmata of chronic liver disease (e.g. spider naevi)
- Ascites, oedema and hepatic encephalopathy are late features
- Cushingoid features may be present even before the administration of steroids
Identify appropriate investigations for autoimmune hepatitis
• Bloods: o LFTs: • High: AST, ALT, GGT, ALP and Bilirubin • Low: albumin (in severe disease) o Clotting: • High PT (in severe disease) o FBC: • Low Hb, platelets and WCC (if hypersplenism from portal hypertension) o Hypergammaglobulinaemia • Presence of ANA, ASMA and Anti-LKM antibodies • Liver Biopsy: o Needed to establish diagnosis and check whether hepatitis or cirrhosis • To rule out other causes of liver disease: o Viral serology o Urinary copper/caeruloplasmin o Ferritin and transferrin saturation o 1 antitrypsin o Anti-mitochondrial antibodies (PBC) • US, CT or MRI of liver and abdomen o Visualise structural lesions • ERCP o To rule out PSC
Define Barrett’s oesophagus
- Prolonged exposure of the normal squamous epithelium to refluxate of GORD leads to mucosal inflammation and erosion, leading to replacement of the mucosa with metaplastic columnar epithelium
- Metaplastic change: Squamous —-> Columnar
- MAIN PROBLEM: Barrett’s could progress to oesophageal adenocarcinoma
Explain the aetiology / risk factors of Barrett’s oesophagus
- Reflux will occur if the cardiac sphincter is not working properly (most of the time it is unclear why it is not working properly)
- Hiatus hernia make GORD more likely
Summarise the epidemiology of Barrett’s oesophagus
- 1/10 adults have heart burn every day
* 3-5% of people with GORD will develop Barrett’s oesophagus
Recognise the presenting symptoms of Barrett’s oesophagus
• Patients are likely to experience symptoms of GORD: o Heartburn o Nausea o Water-brash (sour taste in the mouth) o Bloating o Belching o Burning pain when swallowing
Recognise the signs of Barrett’s oesophagus on physical examination
• Look at symptoms
Identify appropriate investigations for Barrett’s oesophagus
• OGD and Biopsy
o This will show the replacement of the squamous epithelium with columnar epithelium
Generate a management plan for Barrett’s oesophagus
• Pre-malignant/High grade dysplasia:
o Oesophageal resection
o Eradicative mucosectomy
o NOTE: this is appropriate if the patients are young and fit
• Other techniques:
o Endoscopic targeted mucosectomy
o Mucosal ablation by epithelial laser, radiofrequency (HALO) or photodynamic ablation (PD)
• Low-grade dysplasia - annual endoscopic surveillance is recommended
• No pre-malignant changes found:
o Surveillance endoscopy and biopsy performed every 1-3 years
o Anti-reflux measures (e.g. high dose PPI)
Identify the possible complications of Barrett’s oesophagus
- MAIN COMPLICATION: development of oesophageal adenocarcinoma
- Risk of dysplasia
Summarise the prognosis for patients with Barrett’s oesophagus
- Barrett’s oesophagus carries a 30-60 times higher risk of oesophageal adenocarcinoma than the general population
- Most patients, however, do not develop oesophageal adenocarcinoma
- 5-10% of those with Barrett’s oesophagus will develop adenocarcinoma over 10-20 years
Define cholangiocarcinoma
• Primary adenocarcinoma of the biliary tree
Explain the aetiology / risk factors of cholangiocarcinoma
• UNKNOWN
• Risk Factors
o Ulcerative colitis + primary sclerosing cholangitis
o Choledochal cyst (congenital conditions involving cystic dilatations of bile ducts)
o Caroli disease (rare genetic condition in which you get dilatation of intrahepatic bile ducts)
o Parasitic infection of biliary tract
Summarise the epidemiology of cholangiocarcinoma
- VERY RARE
* More common in the developing world due to the increased prevalence of parasitic infections
Recognise the presenting symptoms of cholangiocarcinoma
Obstructive jaundice symptoms o Yellow sclera o Pale stools o Dark urine o Pruritus
Abdominal pain or fullness
Systemic symptoms of malignancy: weight loss, malaise, anorexia
Recognise the signs of cholangiocarcinoma on physical examination
• Jaundice • Palpable gallbladder o NOTE: Courvoisier's Law - in the presence of jaundice, a palpable gallbladder (that is non-tender) is unlikely to be due to gallstones (i.e. cancer of the pancreas or biliary tree is more likely) • Epigastric/RUQ mass • There may be hepatomegaly
Identify appropriate investigations for cholangiocarcinoma and interpret the results
Bloods o FBC o U&Es o LFTs (high ALP + GGT) o Clotting screen o Tumour markers • CA19-9 is a marker of pancreatic cancer and cholangiocarcinoma
Endoscopy
o ERCP will allow bile cytology and tumour biopsy
Ultrasound
CT, MRI, Bone Scan - for staging
Define cholecystitis
• Inflammation of the gallbladder
Explain the aetiology/risk factors of cholecystitis
• Types of Stones
o Mixed Stones (80%)
• Contains cholesterol, calcium bilirubinate, phosphate and protein
• Form due to an imbalance between bile salts, phospholipids, cholesterol, nucleation factors and gallbladder motility
o Pure Cholesterol Stones (10%)
o Pigment Stones (10%)
• Black stones made of calcium bilirubinate
• Form due to increased bilirubin (e.g. due to haemolysis)
• Risk Factors
o Age
o Female
o Fat
o Diabetes mellitus
o Drugs (OCP, octreotide)
o Family history
o Ethnicity (Caucasian)
o Pigment Stone Risk Factors: haemolytic disorders (e.g. sickle cell anaemia)
Summarise the epidemiology of cholecystitis
- Very COMMON
- UK prevalence of gallstone disease = 10%
- 3 x more common in FEMALES
- More common with increasing age
Recognise the presenting symptoms of cholecystitis
- Systemically unwell
- Fever
- Prolonged abdominal pain
- Pain may be referred to right shoulder (due to diaphragmatic irritation)
Recognise the signs of cholecystitis on physical examination
- Tachycardia
- Pyrexia
- RUQ pain or epigastric tenderness
- May be guarding or rebound tenderness
- Murphy’s sign positive
Identify appropriate investigations for cholecystitis
• Bloods
o FBC - high WCC in cholecystitis and cholangitis
o LFT - high ALP + GGT in ascending cholangitis
o Blood cultures
o Amylase (exclude pancreatitis)
• Ultrasound
o Shows gallstones
o Increased thickness of gallbladder wall
o Dilatation of biliary tree
• AXR - but only 10% of gallstones are radio-opaque
• Other imaging - to exclude differentials (e.g. erect CXR, ERCP)
Generate a management plan for cholecystitis
• Conservative o If only mild biliary colic - follow a low-fat diet • Medical o NBM o IV fluids o Analgesia o Anti-emetics o Antibiotics (if infection is present) o NOTE: if symptoms persist despite antibiotic treatment, suspect a localised abscess or empyema, which would require drainage o If there is an obstruction, urgent biliary drainage by ERCP or via a percutaneous route is necessary • Surgical o Laparoscopic Cholecystectomy
Identify possible complications of cholecystitis
• Stones within the gallbladder o Biliary colic o Cholecystitis o Gallbladder empyema o Gallbladder cancer (RARE) • Stones outside the gallbladder o Obstructive jaundice o Pancreatitis o Ascending cholangitis o Cholecystoduodenal fistula o Gallstone ileus o Bouveret syndrome (gallstones cause gastric outlet obstruction) o Mirizzi syndrome • Complications of cholecystectomy o Bleeding o Infection o Bile leak o Post-cholecystectomy syndrome o Port-site hernia
Summarise the prognosis for patients with cholecystectomy
- Gallstones do NOT cause symptoms most of the time
* Surgery offers an excellent chance of cure if they were to become symptomatic
Define cirrhosis
• End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.
• Cirrhosis is considered DECOMPENSATED if it becomes complicated by any of:
o Ascites
o Jaundice
o Encephalopathy
o GI bleed
• Decompensation can be precipitated by infection, GI bleeding, constipation, high-protein meal, electrolyte imbalances, alcohol and drugs, tumour development or portal vein thrombosis
Explain the aetiology/risk factors of cirrhosis
• Chronic alcohol misuse (most common in the UK) • Chronic viral hepatitis (hep B/C - most common worldwide) • Autoimmune hepatitis • Drugs (e.g. methotrexate, hepatotoxic drugs) • Inherited o 1-antitrypsin deficiency o Haemochromatosis o Wilson's disease o Galactosaemia o Cystic Fibrosis • Vascular o Budd-Chiari Syndrome o Hepatic Venous Congestion • Chronic Biliary Diseases o PBC o PSC o Biliary atresia • Unknown: 5-10% • Non-Alcoholic Steatohepatitis (NASH) o Associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia and drugs (e.g. amiodarone, tamoxifen)
Recognise the presenting symptoms of cirrhosis
• Early non-specific symptoms: o Anorexia o Nausea o Fatigue o Weakness o Weight loss • Symptoms due to decreased liver synthetic function: o Easy bruising o Abnormal swelling o Ankle oedema • Symptoms due to reduced detoxification function: o Jaundice o Personality change o Altered sleep pattern o Amenorrhoea o Galactorrhoea • Symptoms due to portal hypertension: o Abdominal swelling o Haematemesis o PR bleeding or melaena
Summarise the epidemiology of cirrhosis
• One of the top 10 causes of death worldwide
Recognise the signs of cirrhosis on physical examination
These are all signs of chronic liver disease • Asterixis • Bruises • Clubbing • Dupuytren's contracture • Palmar erythema • Jaundice • Gynaecomastia • Leukonychia • Parotid enlargement • Spider naevi • Scratch mark (from cholestatic pruritis) • Ascites • Enlarged liver (may be shrunken in the later stages) • Testicular atrophy • Caput medusae • Splenomegaly
Identify appropriate investigations for cirrhosis
• Bloods
o FBC: low platelets + Hb = because of hypersplenism as a result of portal hypertension
o LFTs - may be normal but often get:
• High AST, ALT, ALP, GGT and bilirubin
• Low albumin
o Clotting: prolonged PT
o Serum AFP (alpha-fetoprotein = tumour marker for liver cancer):
• Raised in chronic liver disease
• High levels may suggest hepatocellular carcinoma
• Investigations to determine CAUSE
o Viral serology
o 1-antitrypsin
o Caeruloplasmin
• This is a copper-carrying complex that is LOW in Wilson’s disease
o Iron studies: serum ferritin, iron, total iron binding capacity (TIBC) - check for haemochromatosis
o Anti-mitochondrial antibody (PBC)
o ANA, ASMA (autoimmune hepatitis)
• Ascitic Tap
o MC&S - check for infection
o Biochemistry (protein, albumin, glucose, amylase)
o Cytology
o IMPORTANT: ascitic tap with neutrophils > 250/mm3 = spontaneous bacterial peritonitis (SBP)
• Liver Biopsy
o Performed either:
• Percutaneously
• Transjugular - if clotting deranged or ascitic
o Histopathological features of cirrhosis:
• Periportal fibrosis
• Loss of normal liver architecture
• Nodular appearance
o Grade - indicates degree of inflammation
o Stage - degree of architectural distortion (from mild portal fibrosis –> cirrhosis)
• Imaging
o US, CT or MRI - to detect complications such as:
• Ascites
• HCC
• Hepatic or portal vein thrombosis
• Exclude biliary obstruction
o MRCP (if PSC suspected)
• Endoscopy
o To examine varices
• Child-Pugh Grading - score for estimating the prognosis in chronic liver disease/cirrhosis. It is based on 5 factors:
o Albumin
o Bilirubin
o PT
o Ascites
o Encephalopathy
• Cirrhosis can be divided into Classes using the Child-Push grading system:
o Class A: 5-6
o Class B: 7-9
o Class C: 10-15
Generate a management plan for cirrhosis
• Treat the CAUSE if possible
• Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver
• Nutrition is important
• Enteral supplements should be given
• NG feeding may be indicated
• Treating Complications:
o Encephalopathy
• Treat infections
• Exclude GI bleed
• Use lactulose and phosphate enemas
Normally, the liver breaks down ammonia that is absorbed in the GI tract, however, in Cirrhosis the ammonia can go through the liver without being broken down and exert toxic effects on the brain
IMPORTANT: lactulose reduces the absorption of ammonia from the gut
This helps prevent encephalopathy caused by ammonia reaching the brain
• Avoid sedation
o Ascites
• Diuretics (spironolactone with/without furosemide)
• Dietary sodium restriction
• Therapeutic paracentesis (with human albumin replacement)
• Monitor weight
• Fluid restrict if plasma sodium < 120 mmol/L
• Avoid alcohol and NSAIDs
o Spontaneous Bacterial Peritonitis
• Antibiotics (e.g. cefuroxime and metronidazole)
• Prophylaxis against recurrent SBP with ciprofloxacin
o Surgical
• Consider TIPS (transjugular intrahepatic portosystemic shunt) - this helps reduce portal hypertension
However, it may precipitate encephalopathy because it is providing a route for blood from the GI tract to bypass the liver
• Liver transplantation is the only curative method
Identify the possible complications of cirrhosis
- Portal hypertension with ascites
- Hepatic encephalopathy
- Variceal haemorrhage
- SBP
- HCC
- Renal failure (hepatorenal syndrome)
- Pulmonary hypertension (hepatopulmonary syndrome)
Summarise the prognosis for patients with cirrhosis
• Depends on aetiology and complications
• Generally poor prognosis
o Overall 5 year survival = 50%
o If ascites, 2 year survival = 50%
Define coeliac disease
- An inflammatory disease caused by intolerance to GLUTEN, causing chronic intestinal malabsorption.
- It leads to subtotal villous atrophy and crypt hyperplasia
Explain the aetiology/risk factors of coeliac disease
- Due to sensitivity to the GLIADIN component of gluten
- Exposure to gliadin triggers and immunological reaction in the small intestine leading to mucosal damage and loss of villi
- 10% risk of first-degree relatives being affected
- Clear genetic susceptibility associated with HLA-B8, HLA-DR3 and HLA-DQW2 haplotypes
Summarise the epidemiology of coeliac disease
- UK: 1/2000
- West Ireland: 1/300
- Rare in East-Asia
Recognise the presenting symptoms of coeliac disease
- May be asymptomatic
- Abdominal discomfort, pain and distention
- Steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away)
- Diarrhoea
- Tiredness, malaise, weight loss (despite normal diet)
- Failure to ‘thrive’ in children
- Amenorrhoea in young adults
Recognise the signs of coeliac disease on physical examination
• Signs of anaemia: pallor
• Signs of malnutrition:
o Short stature
o Abdominal distension
o Wasted buttocks in children
o Triceps skinfold thickness gives indication of fat stores
• Signs of vitamin/mineral deficiencies: osteomalacia, easy bruising
• Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)
Identify appropriate investigations for coeliac disease
• Blood:
o FBC (low Hb, iron and folate)
o U&E
o Albumin
o Calcium
o Phosphate
• Serology:
o IgG anti-gliadin antibodies, IgA and IgG anti-endomysial tranglutaminase antibodies can be diagnostic
o NOTE: IgA deficiency is quite COMMON (1/50 with coeliac) so Ig levels should be measured to avoid false negatives
• Stool: culture to exclude infection, faecal fat tests for steatorrhoea
• D-xylose test: reduced urinary excretion after oral xylose indicates small bowel malabsorption
• Endoscopy: allows direct visualisation of villous atrophy in the small intestine (mucosa appears flat and smooth)
o Biopsy will show villous atrophy and crypt hyperplasia in the duodenum
o The epithelium adopts a cuboidal appearance - there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria
Generate a management plan for coeliac disease
- Advice: avoid gluten (wheat, rye and barley products)
* Medical: vitamin and mineral supplements. Oral corticosteroids if disease does not subside with avoidance of gluten
Identify the possible complications of coeliac disease
- Iron, folate and B12 deficiency
- Osteomalacia
- Ulcerative jejunoileitis
- GI lymphoma (particularly T cell)
- Bacterial overgrowth
- Cerebellar ataxia (rarely)
Summarise the prognosis for patients with coeliac disease
- FULL RECOVERY in most patients who strictly adhere to a gluten-free diet
- Symptoms usually resolve within weeks though histological changes may take longer
- Gluten-free diet must be followed for life
Define colorectal carcinoma
• Malignant adenocarcinoma of the large bowel o Distribution: • 60% - rectum and sigmoid • 30% - descending colon • 10% - rest of colon
Explain the aetiology / risk factors of colorectal carcinoma
• Environmental and genetic • There is a sequence of genetic changes that go from normal bowel epithelium to cancer (e.g. APC, K-Ras) • Risk Factors o Western diet (e.g. red meat, alcohol) o Colorectal polyps o Previous colorectal cancer o Family history o IBD
Summarise the epidemiology of colorectal carcinoma
- SECOND MOST COMMON cause of cancer death in the West
- UK: 20,000 deaths per year
- Average age of diagnosis: 60-65 yrs
Recognise the presenting symptoms of colorectal carcinoma
• Depends on the size and location of the tumour
Left-Sided Colon and Rectum
o Change in bowel habit
o Rectal bleeding (blood or mucus mixed with the stools)
o Tenesmus (due to a space-occupying tumour in the rectum)
Right-Sided Colon o Presents later o Anaemia symptoms (lethargy) o Weight loss o Non-specific malaise o Lower abdominal pain (rare)
IMPORTANT: 20% of tumours will present as an EMERGENCY with pain and distension due to:
o Large bowel obstruction
o Haemorrhage or peritonitis due to perforation
Recognise the signs of colorectal carcinoma on physical examination
- Anaemia
- Abdominal mass
If metastatic:
o Hepatomegaly
o Ascites (shifting dullness)
• Low-lying rectal tumours may be palpable on DRE
Identify appropriate investigations for colorectal carcinoma and interpret the results
Bloods
o FBC - anaemia
o LFTs
o Tumour markers (CEA)
Stools
o FOBT - used as a screening test
Endoscopy
o Sigmoidoscopy
o Colonoscopy
o This can be used to biopsy the tumour
Double-Contrast Barium Enema
o May show ‘apple core’ strictures
Contrast CT
o For staging (Duke’s staging)
Define Crohn’s disease
• Chronic granulomatous inflammatory disease that can affect any part of the gastrointestinal tract. Grouped with ulcerative colitis and known, together, as inflammatory bowel disease.
Explain the aetiology/risk factors of Crohn’s disease
- Cause unknown but thought to be due to interplay between genetic and environmental factors
- Though inflammation can occur anywhere from mouth to anus, 40% involves the terminal ileum
Summarise the epidemiology of Crohn’s disease
- UK annual incidence: 5-8/100,000
- UK prevalence: 50-80/100,000
- Affects any age but peaks in teens, 20s and 40s
Recognise the presenting symptoms of Crohn’s disease
- Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction)
- Diarrhoea (may be bloody or steatorrhoea)
- Fever, malaise, weight loss
- Symptoms of complications
- Sometimes right iliac fossa pain due to inflammation of terminal ileum
Recognise the signs of Crohn’s disease on physical examination
- Weight loss
- Clubbing
- Signs of anaemia
- Aphthous ulcers in mouth
- Perianal skin tags, fistulae and abscesses
- Uveitis, erythema nodosum, pyoderma gangrenosum
Identify appropriate investigations for Crohn’s disease
• Blood:
o FBC - low Hb, high platelets, high WCC
o U&Es
o LFTs - low albumin
o High ESR (suggests chronic inflammation)
o CRP may be high or normal
• Stool microscopy and culture: exclude infective colitis
• AXR: could show evidence of toxic megacolon
• Erect CXR: if there is a risk of perforation
• Small bowel barium follow-through could show:
o Fibrosis/strictures (string sign of Kantor - part of the intestine looks like a piece of string, showing incomplete filling of the intestinal lumen)
o Deep ulceration (rose thorn ulcers)
o Cobblestone mucosa
• Endoscopy (OGD, colonoscopy) and biopsy may show:
o Could help differentiate UC and CD
o Useful for monitoring malignancy and disease progression
o Can show mucosal oedema and ulceration with ‘rose thorn fissures’ (occurs when there is a cobblestone mucosa)
o Fistulae and abscesses
o Transmural chronic inflammation with infiltration of macrophages, lymphocytes and plasma cells
o Granulomas with epithelioid giant cells may be seen in blood vessels and lymphatics
• Radionucide-labelled neutrophil scan: can localise the inflammation (when other investigations are contraindicated)
Generate a management plan for Crohn’s disease
• Acute Exacerbation
o Fluid resuscitation
o IV/oral corticosteroids
o 5-ASA analogues (e.g. mesalazine and olsalazine)
o Analgesia
o Parenteral nutrition may be necessary
o Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb
• Long-Term
o Steroids - for acute exacerbations
o 5-ASA analogues - decreases the frequency of relapses (useful for mild to moderate disease)
• NOTE: more commonly used in UC
o Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine, methotrexate) reduces the frequency of relapses
o Anti-TNF agents: (e.g. infliximab and adalimumab) - very effective at inducing and maintaining remission. Usually reserved for refractory Crohn’s.
• General Advice:
o Stop smoking
o Dietician referral (low fibre diet necessary if there are stricture present)
• Surgery indicated it:
o Medical treatment fails
o Failure to thrive in children in the presence of complications
o Involves resection of affected bowel and stoma formation - NOTE: there is a risk of disease recurrence
Identify the possible complications of Crohn’s disease
• GI: o Haemorrhage o Strictures o Perforation o Fistulae (between bowel, bladder, vagina) o Perianal fistulae and abscesses o GI cancer o Malabsorption • Extraintestinal Features: o Uveitis o Episcleritis o Gallstones o Kidney stones o Arthropathy o Sacroiliitis o Ankylosing spondylitis o Erythema nodosum o Pyoderma gangrenosum o Amyloidosis
Summarise the prognosis for patients with Crohn’s disease
- It is a chronic relapsing condition
- 2/3 of patients will require surgery at some stage
- 2/3 of these patients require more than 1 operation
Define diverticular disease
• It is important to distinguish between the different terms used when discussing patients with diverticular disease
o Diverticulosis: the presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel
o Diverticular Disease: diverticulosis associated with complications e.g. haemorrhage, infection, fistulae
o Diverticulitis: acute inflammation and infection of colonic diverticulae
o Hinchey Classification of Acute Diverticulitis:
• Ia: phlegmon
• Ib and II: localised abscesses
• III: perforation and purulent peritonitis
• IV: faecal peritonitis
Explain the aetiology/risk factors of diverticular disease
• Aetiology:
o A low-fibre diet leads to loss of stool bulk
o This leads to the generation of high colonic intraluminal pressures to propel the stool out
o This, in turn, leads to the herniation of the mucosa and submucosa through the muscularis
• Pathogenesis:
o Diveticulae are most commonly found in the sigmoid and descending colon
o However, they can also be right-sided
o Diverticulae are NOT found in the rectum
o Diverticular are found particularly at sites of nutrient artery penetration
o Diverticular obstruction by thickened faeces can lead to bacterial overgrowth, toxin production and mucosal injury
o Which can then lead to diverticulitis, perforation, pericolic phlegmon, abscess, ulceration and fistulation or stricture formation
Summarise the epidemiology of diverticular disease
- Diverticular disease is VERY COMMON
- 60% of people living in industrialised countries will develop colonic diverticulae
- Rare < 40 yrs
- Right-sided diverticulae are more common in Asia
Recognise the presenting symptoms of diverticular disease
• Often ASYMPTOMATIC (80-90%)
• Complications can lead to symptoms such as:
o PR bleeding
o Diverticulitis (causing LIF and lower abdominal pain and fever)
o Diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)
Recognise the signs of diverticular disease on physical examination
• Diverticulitis - tender abdomen and signs of local or generalised peritonitis if a diverticulum has perforated
Identify appropriate investigations for diverticular disease
• Bloods:
o FBC: increased WCC, increased CRP
o Check clotting and cross-match if bleeding
• Barium Enema (with or without air contrast):
o Shows presence of diverticulae (saw-tooth appearance of lumen)
o This reflects pseudohypertrohy of circular muscle
o IMPORTANT: barium enema should NOT be performed in the acute setting because there is a high risk of perforation
• Flexible Sigmoidoscopy and Colonoscopy:
o Diverticulae can be visualised and other pathology (e.g. polyps and tumours) can be excluded
• In ACUTE setting: CT scan for evidence of diverticular disease and complications may be performed
Generate a management plan for diverticular disease
• Asymptomatic:
o Soluble high-fibre diet (20-30 g/day)
o Some drugs are under investigation for their use in preventing recurrent flares of diverticulitis (such as probiotics and anti-inflammatories)
• GI Bleed:
o PR bleeding usually managed conservatively with IV rehydration, antibiotics and blood transfusion if necessary
o Angiography and embolisation or surgery if severe
• Diverticulitis:
o IV antibiotics
o IV fluid rehydration
o Bowel rest
o Abscesses ma be drained by radiologically sited drains
• Surgery:
o May be necessary in patients with recurrent attacks or complications (e.g. perforation and peritonitis)
o Open surgery:
• Hartmann’s procedure (proctosigmoidectomy leaving a stoma)
• One-stage resection and anastomosis (risk of leak) - with or without defunctioning stoma
o Laparoscopic drainage, peritoneal lavage and drain placement can be effective
Identify the possible complications of diverticular disease
- Diverticulitis
- Pericolic abscess
- Perforation
- Faecal peritonitis
- Colonic obstruction
- Fistula formation (bladder, small intestine, vagina)
- Haemorrhage
Summarise the prognosis for patients with diverticular disease
• 10-25% have one or more episodes of diverticulitis
Define IBS
• A functional bowel disorder defined as recurrent episodes of abdominal pain/discomfort (in the absence of detectable organic pathology) for > 6 months of the previous year, associated with two of the following: o Altered stool passage o Abdominal bloating o Symptoms made worse by eating o Passage of mucous
Explain the aetiology/risk factors for IBS
- UNKNOWN
- Could be visceral sensory abnormalities, gut motility abnormalities, psychosocial factors (e.g. stress), food intolerance (e.g. lactose) and many more
Summarise the epidemiology of IBS
- COMMON
- 10-20% of adults
- More common in females (2:1 ratio)
Recognise the presenting symptoms of IBS
• 6+ months history of abdominal pain o Pain is often colicky o It is in the lower abdomen o Relieved by defecation or passing of flatus • Altered bowel frequency (> 3 motions per day or < 3 motions per week) • Abdominal bloating • Change in stool consistency • Passage with urgency or straining • Tenesmus
• MAKE SURE YOU SCREEN FOR RED FLAG SYMPTOMS:
o Weight loss
o Anaemia
o PR bleeding
o Late onset (> 60 yrs)
o NOTE: if any of these are present then you must exclude colonic malignancy
Recognise the signs of IBS on physical examination
- Usually NORMAL on examination
* Sometimes the abdomen may appear distended and be mildly tender on palpation in one or both iliac fossae
Identify appropriate investigations for IBS
- Diagnosis is mainly from the history but organic pathology must be excluded
- Blood: FBC (anaemia), LFT, ESR, CRP, TFT, anti-endomysial/anti-tranglutaminase antibodies (coeliac disease)
- Stool examination: microscopy and culture for infective cause
- Ultrasound: exclude gallstone disease
- Urease breath test: exclude dyspepsia due to Helicobacter pylori
- Endoscopy: if other pathologies suspected
Generate a management plan for IBS
• Advice: dietary modification
• Medical: depends on the main symptoms affecting the patient
o Antispasmodics (e.g. buscopan)
o Prokinetic agents (e.g. domperidone, metaclopramide)
o Anti-diarrhoeals (e.g. loperamide)
o Laxatives (e.g. senna, movicol, lactulose)
o Low-dose tricyclic antidepressants (may reduce visceral awareness)
• Psychological therapy:
o CBT
o Relaxation and psychotherapy
Identify the possible complications of IBS
- Physical and psychological morbidity
* Increased incidence of colonic diverticulosis
Summarise the prognosis for patients with IBS
- Chronic relapsing and remitting course of disease
* Often exacerbated by psychosocial stresses
Define biliary colic
• Pain resulting from obstruction of the gallbladder or common bile duct, usually by a stone. The pain, which is very severe, is usually felt in the upper abdomen (in the midline or to the right) but can also be poorly localised due to its visceral nature.
Explain the aetiology/risk factors of biliary colic
• Occurs due to contractions of the biliary tree in an attempt to relieve an obstruction (e.g. due to a stone) • Risk factors of gallstones: o Fair (Caucasian) o Fat o Fertile o Forty o Female
Summarise the epidemiology of biliary colic
- 10-15% of people in the adult Western world will develop gallstones
- Biliary colic is the most common presentation of gallstone disease
Recognise the presenting symptoms of biliary colic
- Crampy RUQ pain
- Nausea and vomiting
- Pain may radiate to the right scapula
- The pain does NOT fluctuate and has a tendency to persist
- Individuals may present with pain following ingestion of a fatty meal
Recognise the signs of biliary colic on physical examination
• RUQ pain and epigastric tenderness
Identify appropriate investigations for biliary colic
• Urinalysis, CXR and ECG to exclude other causes (e.g. basal pneumonia, inferior MI)
• Ultrasound
o Look for dilatation of the CBD
o Gallbladder wall may be thickened
• LFT
• ERCP - useful diagnostically and therapeutically
• CT - may be useful if other forms of imaging have been insufficient
Generate a management plan for biliary colic
• Analgesia • IV fluids • NBM • Surgical o Laparoscopic cholecystectomy • ERCP can also be used to help remove stones or stent a blocked bile duct
Identify possible complications of biliary colic
• Complications of surgery
o Injury to the bile duct
o Fat intolerance - due to inability to secrete a large amount of bile into the intestine because the patient no longer has a gallbladder
o Post-cholecystectomy syndrome - presence of abdominal symptoms (e.g. dyspepsia, nausea/vomiting, RUQ pain) after the removal of the gallbladder
Summarise the prognosis for patient with biliary colic
• GOOD prognosis with appropriate treatment
Define gastric cancer
• Cancer of the stomach. Most commonly adenocarcinoma o Rarer causes of gastric cancer: • Lymphoma • Leiomyosarcoma • Stromal tumours
Explain the aetiology/risk factors of gastric cancer
• UNKNOWN • Environment and genetics • Risk Factors o Smoked and processed foods o Smoking o Alcohol o Helicobacter pylori infection o Atrophic gastritis o Pernicious anaemia o Partial gastrectomy o Gastric polyps
Summarise the epidemiology of gastric cancer
- COMMON cause of cancer death worldwide
- Highest incidence in JAPAN (and Asia in general)
- 6th most common cancer in the UK
- Usual age of presentation: > 50 yrs
Recognise the presenting symptoms of gastric cancer
- Often asymptomatic early
- Early satiety
- Epigastric discomfort
- Systemic symptoms: weight loss, anorexia, nausea/vomiting
- Dysphagia (in tumours of the gastric cardia)
- Symptoms of metastases (e.g. ascites, jaundice)
Recognise the signs of gastric cancer on physical examination
- Epigastric mass
- Abdominal tenderness
- Ascites
- Signs of anaemia
- Virchow’s Node (aka Troisier’s sign)
- Sister Mary Joseph’s Nodule (metastatic node on the umbilicus)
• Krukenberg’s Tumour (ovarian metastases)
Identify appropriate investigations for gastric cancer
• Upper GI endoscopy
- Bloods - FBC (check for anaemia), LFTs
- CT/MRI - for staging
- Endoscopic USS - assess depth of gastric invasion and lymph node involvement
Define GORD
• Inflammation of the oesophagus caused by reflux of gastric acid and/or bile.
Explain the aetiology/risk factors of GORD
• Caused by disruption of mechanisms that prevent reflux
• Mechanisms that prevent reflux:
o Lower oesophageal sphincter
o Acute angle of junction
o Mucosal rosette
o Intra-abdominal portion of oesophagus (diaphragm acts as a sphincter)
• Prolonged oesophageal acid clearance contributes to 50% of cases
Summarise the epidemiology of GORD
- COMMON
* 5-10% of adults
Recognise the presenting symptoms of GORD
• Substernal/epigastric burning discomfort or ‘heartburn’
• Aggravated by:
o Lying supine
o Bending
o Large meals
o Drinking alcohol
• Pain is relieved by antacids
• Waterbrash (regurgitation of an excessive accumulation of saliva from the lower part of the oesophagus often with some acid material from the stomach)
• Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze
• Dysphagia - caused by formation of peptic stricture after long-standing reflux
Recognise the signs of GORD on physical examination
- Usually NORMAL
* Occasionally - epigastric tenderness, wheeze on chest auscultation, dysphonia
Identify appropriate investigations for GORD
• Often a CLINICAL diagnosis
• Upper GI endoscopy, biopsy and cytological brushings
o Confirms presence of oesophagitis and can exclude malignancy
• Barium Swallow can detect:
o Hiatus hernia
• NOTE: operation to repair hiatus hernia is called Nissen fundoplication
o Peptic stricture
o Extrinsic compression of the oesophagus
• CXR:
o This is NOT specific for GORD
o However, a CXR can lead to the incidental finding of a hiatus hernia (gastric bubble behind the cardiac shadow)
• 24 hr oesophageal pH monitoring:
o pH probe places in lower oesophagus determines the temporal relationship between symptoms and oesophageal pH
Generate a management plan for GORD
• Advice:
o Weight loss
o Elevating head of bed
o Avoid provoking factors
o Stop smoking
o Lower fat meals
o Avoid large meals late in the evening
• Medical:
o Antacids
o Alginates
o H2 antagonists (e.g. ranitidine)
o Proton pump inhibitors (e.g. lansoprazole, omeprazole)
• Endoscopy:
o Annual endoscopic surveillance - looking for Barrett’s Oesophagus
o May be necessary for stricture dilation or stenting
• Surgery:
o Antireflux surgery if refractory to medical treatment
• Nissen Fundoplication:
o Fundus of the stomach is wrapped around the lower oesophagus - helps reduce the risk of hiatus hernia and reduce reflux
Identify the possible complications of GORD
- Oesophageal ulceration
- Peptic stricture
- Anaemia
- Barrett’s oesophagus
- Oesophageal adenocarcinoma
- Associated with asthma and chronic laryngitis
Summarise the prognosis of patients with GORD
- 50% respond to lifestyle measures alone
- In patients that require drug therapy, withdrawal is often associated with relapse
- 20% of patients undergoing endoscopy for GORD have Barrett’s oesophagus
Define gastroenteritis
• Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.
