Gastrointestinal Flashcards
Define achalasia.
- Oesophageal motility disorder
- Loss of co-ordinated peristalsis
- Failure of relaxation of the lower oesophageal sphincter
Explain the aetiology / risk factors of achalasia.
- Degeneration of ganglion cells of myenteric plexus
- In oesophagus
- Cause = unknown
Risk factors
- Herpes
- Measles
- Autoimmune disease
- HLA Class I antigens
- Consanguineous parents
Summarise the epidemiology of achalasia.
- 1 in 100,000 (annual)
- 25-60 years
Oesophageal infection “Trypanosoma cruzi” in Central/South America produces similar disorder = Chages’ disease
Recognise the presenting symptoms of achalasia.
- Intermittent dysphagia (solids & liquids)
- Difficulty belching
- Regurgitation
- Heartburn
- Chest pain (atypical, cramping, retrosternal)
- Weight loss
Insidious onset & gradual progression.
Recognise the signs of achalasia on physical examination.
- CXR
- Barium swallow
- Endoscopy
- Manometry
CXR
- widened mediastinum, double right heart border –> dilated oesophagus
- Air-fluid level in upper chest
- Absence of gastric air bubble
Barium swallow
- Dilated oesophagus
- Tapers down to the sphincter –> beak shaped
Endoscopy
- Done to exclude malignancy, does mimic
Manometry
- Elevated resting lower oesophageal sphincter pressure (>45mmHg)
- Incomplete relaxation of lower oesophageal sphincter
- Absence of peristalsis in distal (smooth muscle) oesophagus
Identify appropriate investigations for achalasia and interpret the results.
- CXR
- Barium swallow
- Endoscopy
- Manometry
CXR
- widened mediastinum, double right heart border –> dilated oesophagus
- Air-fluid level in upper chest
- Absence of gastric air bubble
Barium swallow
- Dilated oesophagus
- Tapers down to the sphincter –> beak shaped
Endoscopy
- Done to exclude malignancy, does mimic
Manometry
- Elevated resting lower oesophageal sphincter pressure (>45mmHg)
- Incomplete relaxation of lower oesophageal sphincter
- Absence of peristalsis in distal (smooth muscle) oesophagus
Define acute cholangitis.
- Inflammation of the common bile duct
- Leads to obstruction
- Leads to conjugated bilirubin buildup –> jaundice
Explain the aetiology / risk factors of acute cholangitis.
- Due to infected stone in common bile duct
- Due to spread from infected gallbladder (cholecystitis)
Risk factors
- Age >50 yrs
- Cholelithiasis -
- Benign or Malignant stricture
- Post-procedure injury of bile ducts
- Primary or Secondary sclerosing cholangitis
Summarise the epidemiology of acute cholangitis.
1% of patients with cholelithiasis
Identify appropriate investigations for acute cholangitis and interpret the results.
Blood cultures - to establish the identity and antibiotic sensitivities of infective bacteria.
Generate a management plan for acute cholangitis.
- Blood cultures
- Antibiotics
- Endoscopic Retrograde Cholangiopancreatography (ERCP) drainage
- Monitoring
Blood cultures
- Establish the identity and antibiotic sensitivities of the infective bacteria
Antibiotics
- Broad-spectrum until exact sensitivities identified
ERCP Drainage
- Physical drainage
- Endoscope passed via oesophagus into duodenum
- Catheter passed via sphincter of Oddi and into common bile duct
- Pus is drained and sent for culturing
- Small basket trawled through common bile duct to remove obstructing calculi/sludge
- Sphincterotomy to aid further calculi/sludge passage
- If ERCP fails - percutaneous transhepatic cholangiography (PTC)
Monitoring
- Post-drainage keep in hospital
- Antibiotics
- Nil-by mouth
- IV fluids
- Analgesia
- Monitor vital signs for sepsis
Summarise the prognosis for patients with acute cholangitis.
- Infection is not confined to gallbladder
- Infection can spread up the common bile duct to the liver and systemic circulation
= ascending cholangitis
Untreated high mortality (10-30%)
ERCP only temporary fix - need elective cholecystectomy to prevent reoccurance.
Define alcohol withdrawal.
- Withdrawal on cessation of alcohol
- Tolerance
- Compulsion to drink, difficulty controlling termination or levels of use
- Persistent desire to cute down or control use
- Time spent obtaining, using or recovering from alcohol
- Neglect of other interests (social, occupational, recreational)
- Continued use despite physical and psychological problems
Explain the aetiology / risk factors of alcohol withdrawal.
- Genetic factors (twin & family history - 1 in 3 with parent)
- Cultural
- Parental
- Peer group influences
- Availability of alcohol
- Occupation - increased risk in publicans, doctors, lawyers
- Depression
- Anxiety
Summarise the epidemiology of alcohol withdrawal.
2-9% of US (2004)
Recognise the presenting symptoms of alcohol withdrawal.
CAGE
- Cut-down?
- Annoyed by criticism?
- Guilt?
- Eye-opener (wake up)?
Withdrawal
- Nausea
- Sweating
- Tremor
- Restlessness
- Agitation
- Visual hallucination
- Confusion
- Seizures
Recognise the signs of alcohol withdrawal.
- Duputreyn’s contracture
- Palmar erythema
- Bruising
- Spider naevi
- Tel
Recognise the signs of alcohol withdrawal.
- Dupuytren’s contracture
- Palmar erythema
- Bruising
- Spider naevi - spider veins with central red spot
- Telangiectasia - spider veins
- Facial mooning
- Bilateral parotid enlargement
- Gynaecomastia
- Smell of alcohol
Identify appropriate investigations for alcohol withdrawal and interpret the results.
- Bloods
- Acute Overdose
Blood
- Raised MCV
- Raised GGT
- Raised transaminases
- Raised uric acid, triglycerides, bilirubin, albumin, PT in liver
Acute Overdose
- Blood alcohol
- Glucose
- ABG - risk of ketoacidosis or lactic acidosis
- VBG
- U&E
- Toxic screen - e.g. barbiturates, paracetamol
Generate a management plan for alcohol withdrawal.
- I.V. Vitamin B complex (Pabrinex)
- Reducing doses of chlordiazepoxide
- Watch dehydration, electrolyte imbalances, infections
- Nutritional support (malnourishment)
- Lactulose & phosphate enemas - help encephalopathy
Identify the possible complications of alcohol withdrawal and its management.
- Fits
- Delirium tremors - coarse tremor, agitation, fever, tachycardia, confusion, delusions, hallucinations
- Cerebral atrophy
- Dementia
- Cerebellar degeneration
- Optic atrophy
- Peripheral neuropathy
- Myopathy
- Hepatic encephalopathy
- Thiamine deficiency
- Wernicke’s Encephalopathy
- Korsakoff’s Psychosis
Summarise the prognosis for patients with alcohol withdrawal.
Depends on complications.
Alcoholic fatty liver - reversible with abstinence.
5 year rate of alcoholic cirrhosis is 60-70% if stop drinking, <40% if continue.
Define Wernicke’s Encephalopathy.
- Nystagmus
- Ophthalmoplegia
- Ataxia
- Apathy
- Disorientation
- Disturbed memory
Treatment: Thiamine
Define Korsakoff’s Psychosis.
Profound impairment of retrograde and anterograde memory with confabulation, due to damage to mammillary bodies and hippocampus.
Irreversible.
Define alcoholic hepatitis.
Inflammatory liver injury caused by chronic heavy intake of alcohol.
Explain the aetiology / risk factors of alcoholic hepatitis.
- Due to excessive intake of alcohol
- Centrilobular balooning degeneration and necrosis of hepatocytes
- Steatosis
- Neutrophilic inflammation
- Cholestasis
- Mallory hyaline inclusions - eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments
- Giant mitochrondria
Risk factors:
- Heavy alcohol intake (15-20 years)
- Female - more florid illness than men
- Trigger event (e.g. aspiration pneumonia, injury)
Summarise the epidemiology of alcoholic hepatitis.
10-35% of heavy drinkers.
Recognise the presenting symptoms of alcoholic hepatitis.
- Asymptomatic
- Mild Illness
- Nausea
- Malaise
- Epigastric or right hypochondrial pain
- Low grade fever - Severe Illness
- Jaundice
- Abdominal discomfort or swelling
- Swollen ankles
- GI bleeding
Recognise the signs of alcoholic hepatitis on physical examination.
- Febrile
- Tachycardia
- Jaundice
- Bruising
- Encephalopathy - e.g. hepatic foetor, liver flap, drowsiness, unable to copy 5 pointed star, disorientated
- Ascites
- Hepatomegaly
- Splenomegaly
Identify appropriate investigations for alcoholic hepatitis and interpret results.
- Blood
- Ultrasound Scan - for other causes - e.g. malignancy
- Upper GI Endoscopy - for varices
- Liver biopsy - percutaneous, transjugular to distinguish cause
- Electroencephalogram - for slow-wave activity (indicates encephalopathy)
Blood
- FBC - low Hb, high MCV, high WCC, low platelets
- LFT - high transaminases, high bilirubin, low albumin, high AlkPhos, high GGT
- U&E - low Urea & K+
- Prolonged PT
Generate a management plan for alcoholic hepatitis.
- Thiamine, Vit C, multivitamins (parenterally)
- Monitor and correct K+, Mg2+, glucose
- Ensure adequate urine output
Encephalopathy - treat with oral lactulose and phosphate enemas.
Ascites - diuretics (spironolactone, furosemide), therapeutic paracentesis (body fluid sampling using needle)
Hepatorenal Syndrome - glypressin, N-acetylcysteine
- Nutrition
- Oral or NG feeding
- Increased calories
- Avoid protein restriction (unless encephalopathic)
- Consider total enteral nutrition = decreased mortality - Steroid Therapy (severe hepatitis)
Identify the possible complications of alcoholic hepatitis and its management.
- Acute liver decompensation
- Hepatorenal syndrome
- Cirrhosis
Summarise prognosis for patients with alcoholic hepatitis.
1st month mortality - 10%
1st year mortality - 40%
Continue alcohol intake - 1-3 years before cirrhosis
Define amyloidosis.
Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils.
Systemic or Localised.
Explain the aetiology / risk factors of amyloidosis.
Amyloid fibrils - polymers of low-molecular-weight subunit proteins.
- Derived from proteins that undergo conformational changes to adopt an anti-parallel B-pleated sheet configuration
- Associated with GAGs and serum amyloid P-component (SAP)
- Deposition disrupts structure & function of normal tissue
Risk factors:
Type AA Amyloid (Serum Amyloid A protein)
- Chronic inflammatory diseases - e.g. RA, seronegative arthritides, Crohn’s
- Chronic infections - e.g. TB, bronchiectasis, osteomyelitis
- Malignancy - e.g. Hodgkin’s, renal cancer
Type AL Amyloid (Monoclonal Immunoglobulin Light Chains)
- Subtle monoclonal plasma cell dyscrasoas
- Multiple myeloma
- Waldenstrom’s macroglobulinaemia
- B-cell lymphoma
Type ATTR - familia, genetic-variant transthyretin
- Autosomal dominantly transmitted mutations in gene for transthyretin (TTR)
Summarise the epidemiology of amyloidosis.
AA - 1-5% incidence among chronic inflammatory disease patients
AL - 3000 U.S & 300-600 UK annually
Hereditary - 5% of patients with systemic amyloidosis
Recognise the presenting symptoms of amyloidosis.
Depends on the tissues and organs affected, and presence of risk factors.
Kidney Failure:
- Swelling (oedema)
- Tiredness
- Weakness
- Loss of appetite
Heart failure:
- Shortness of breath
- Oedema
- Arrhthmia
Others:
- Lightheaded
- Fainting
- Peripheral neuropathy (numbness & tingling)
- Nausea, diarrhoea, constipation
- Carpal tunnel syndrome - numbness, tingling, pain in wrist
- Enlarged tongue (AL)
Recognise the signs of amyloidosis on physical examination.
Renal - proteinuria, nephrotic syndrome, renal failure
Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
GI - macroglossia (AL) , hepatomegaly, splenomegaly, gut dysmotility, malabsorption, bleeding
Neuro - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
Skin - waxy skin, easy bruising, purpura around eyes (AL), plaques, nodules
Joints - painful asymmetrical large joints, shoulder pad sign
Haem - bleeding diathesis (Factor X binds to amyloid, decreased synthesis of coagulation factors)
Identify appropriate investigations for amyloidosis and interpret the results.
- Tissue Biopsy - to diagnose, identify amyloid fibril protein (good for AA, poor for AL)
- Urine
- Blood
- 123I-SAP Scan
- Bone marrow
- ECG
- DNA analysis
Urine
- Proteinuria
- Free Ig light chains in AL
Blood
- CRP
- ESR
- Rheumatoid factor
- Ig levels
- Serum protein electrophoresis
- LFTs
- U&E
- SAA (monitoring in AA)
123-I-SAP Scan
- Radiolabelled SAP localizes to deposits
- Enables quantitative imaging of organs
Define anal fissure.
A tear in the squamous lining of the distal canal canal characterised by pain on defecation and rectal bleeding.
90% are posterior. Anterior - follow parturition.
Explain the aetiology / risk factors of anal fissure.
Risk Factors/Causes
- Hard stool
- Pregnancy
- Opiate analgesia
Rare Causes
- Herpes
- Syphilis
- Trauma
- Crohn’s
- Anal cancer
- Psoriasis
Summarise the epidemiology of anal fissure.
Young to middle aged adults.
1 in 350 people.
Recognise the presenting symptoms of anal fissure.
- Pain on defecation
- Tearing sensation on passing stool
- Fresh blood on stool or on paper
Recognise the signs of anal fissure on physical examination.
- Sentinel pile
- Mucosal tag
- ?Groin nodes - suggest complicating factor (HIV, immunosuppression)
Identify appropriate investigations for anal fissure and interpret the results.
Anal manometry - if resistant fissures
Anal ultrasound - with suspected anal sphincter deficits
Generate a management plan for anal fissure.
5% lidocaine ointment + 0.2-0.4% GTN ointment
or
2% topical diltiazem
Dietary fibre
Fluids
Stool softener
Hygiene advice
2nd line - Botulinum toxin injection and 2% topical diltiazem = fever side effects
Identify the possible complications of anal fissure and its management.
Spasm may constrict the inferior rectal artery causing ischaemia and prolonged healing
Summarise the prognosis for patients with anal fissure.
If conservative methods fail, a lateral partial internal sphincterotomy is needed.
Define appendicectomy.
Surgical removal of the vermiform appendix.
Summarise the indications for an appendicectomy.
- Acute appendicitis
= persistent abdominal pain, fever, peritonitis, leukocytosis present
Identify the possible complications of an appendicectomy.
- Perforation - <1% mortality
- Elderly - 5% mortality
- Infection - high temperature, discharge from wound, hot to touch, vomiting, pain and swelling
- Shoulder pain - due to gas pumped into abdomen
- Constipation
- Haematoma
- Scarring
- Abscess
- Hernia
Define appendicitis.
Acute inflammation of the vermiform appendix.
Explain the aetiology / risk factors of appendicitis.
Gut organisms invade the appendix wall after lumen obstruction by lymphoid hyperplasia, faecolith or filiarial worms.
Leads to oedema ,ischaemia, necrosis and perforation.
Risk factors:
- <6 months of breastfeeding
- Low dietary fibre
- Improved personal hygiene
- Smoking
Summarise the epidemiology of appendicitis.
Most common surgical emergency.
Lifetime incidence 6%.
Highest incidence 10-20yrs.
Rare before 2 years old - cone shaped, wider lumen
Recognise the presenting symptoms of appendicitis.
- Periumbilical pain that moves to the right inferior flank
- Anorexia
- Nausea
- Vomiting
- Constipation
Recognise the signs of appendicitis on physical examination.
- Tachycardia
- Fever
- Peritonism
- Guarding and rebound
- Percussion tenderness in right inferior flank
- Pain during PR examination - suggests inflamed, low-lying pelvic appendix
- Rovsing’s sign - pain greater in right inferior flank than left inferior flank, if left inferior flank is pressed
- Psoas’s sign - pain on extending hip if retrocaecal appendix
- Cope sign - pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus
Identify appropriate investigations for appendicitis and interpret the results.
- Blood tests - FBC, reveal neutrophil leukocytosis, elevated CRP
- Abdominal CT - reduces -ve appendicectomy rate
- Abdominal ultrasound
- Urinalysis
- Pregnancy test
- Group and save
- Abdominal MRI
Generate a management plan for appendicitis.
- Appendicectomy
- Antibiotics - piperacilin / tazobactam 4.5g/8h, 1 to 3 doses IV starting 1h pre-op
Identify the possible complications of appendicitis and its management.
- Perforation - more common if faecolith present, young children
- Appendix mass - inflamed appendix covered in omentum
- Appendix abscess - if mass fails to resolve, enlarges further
Summarise the prognosis for patients with appendicitis.
Perforation - <1% mortality
- Elderly - 5% mortality
Define autoimmune hepatitis.
Chronic hepatitis characterised by autoimmune features, hyperglobulinaemia and presence of circulating autoantibodies.
Explain the aetiology / risk factors of autoimmune hepatitis.
- Genetic predisposition
- Virus’ or drugs trigger hepatocyte expression of HLA antigens
- T-cell mediated autoimmune attack
- Raised ANA, ASM, anti-liver/kidney microsomes do not injure liver directly
- Chronic inflammatory changes similar to chronic viral hepatitis –> lymphoid infiltration of portal tracts and hepatocyte necrosis
- Leads to fibrosis and cirrhosis
Type 1 - ANA, anti-smooth muscle antibodies (anti-SMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA)
Type 2 - antibodies to liver/kidney microsomes (ALKM-1 directed at CYP2D6 epitope), antibodies to liver cytosol antigen (ALC-1)
Risk factors:
- Female gender
- Genetic pre-disposition
- Immune dysregulation
- Measles virus
Summarise the epidemiology of autoimmune hepatitis.
Type 1 - all age groups (mainly women)
Type 2 - disease of girls and young women
Recognise the presenting symptoms of autoimmune hepatitis.
Insidious onset:
- Malaise
- Fatigue
- Anorexia
- Nausea
- Amenorrhoea
- Epistaxis - nose bleeds
Acute hepatitis (25%):
- Fever
- Anorexia
- Nausea
- Vomiting
- Diarrhoea
- RUQ pain
- Serum sickness
Recognise the signs of autoimmune hepatitis on physical examination.
Insidious onset:
- Weight loss
- Jaundice
Acute hepatitis (25%): - Jaundice
Others:
- Stigmata of chronic liver disease - e.g. spider naevi
- Ascites
- Oedema
- Encephalopathy
- Cushingoid features
Identify appropriate investigations for autoimmune hepatitis and interpret the results.
- Blood
- Liver biopsy - shows interface hepatitis or cirrhosis
- Ultrasound, CT, MRI of liver or abdomen - visualise structural lesions
- ERCP - rule out PSC
- Others
Blood
- LFT - high AST, ALT, GGT, AlkPhos, bilirubin, low albumin
- Clotting - high PT
- FBC - low Hb, platelets, WCC - from hypersplenism if portal hypertension is present
Others
- Rule out other causes of liver disease
- e.g. viral serology - Hep B & C
- e.g. caeruloplasmin and urinary copper - Wilson’s
- e.g. ferritin and transferrin saturation - haemochromatosis
- e.g. alpha-1-antitrypsin - deficiency
- e.g. antimitochondrial antibodies - PBC
Define Barrett’s oesophagus.
Metaplasia of oesophageal squamous epithelium and replacement with columnar epithelium.
Pre-malignant condition - increased risk of dysplasia and adenocarcinoma.
Explain the aetiology / risk factors of Barrett’s oesophagus.
- Chronic gastro-oesophageal reflux disease (GORD)
- Increased age
- Male sex
- White ethnicity
- Tobacco use
- Obesity
- Family history
Summarise the epidemiology of Barrett’s oesophagus.
Middle-aged older adults
Male
White ethnicity
8% prevalence - varies massively
Recognise the presenting symptoms of Barrett’s oesophagus.
- Heartburn
- Regurgitation
- Dysphagia
- Chest pain
- Laryngitis
- Cough
- Dyspnoea / wheeze
Recognise the signs of Barrett’s oesophagus on physical examination.
- Heartburn
- Regurgitation
- Dysphagia
- Chest pain
- Laryngitis
- Cough
- Dyspnoea / wheeze
Identify appropriate investigations for Barrett’s oesophagus and interpret the results.
- Biopsy - endoscopically visible columnarisation, record length using Prague classification
- Barium oespehagogram
Generate a management plan for Barrett’s oesophagus.
Detecting and preventing oesophageal adenocarcinoma.
Endoscopic surveillance ever 2-3 years (if more extensive disease).
If high-grade dysplasia, intramural carcinoma - endoscopic resection or mucosal radio-frequency ablation.
Low-grade dysplasia - confirm by repeat examination after 6 months.
Identify the possible complications of Barrett’s oesophagus and its management.
- Oesophageal adenocarcinoma - increase age, large length of oesophagus involved, dysplasia
Define cholangiocarcinoma.
Cancer arising from the bile duct epithelium.
Intrahepatic or extrahepatic.
[Perihilar or distal]
Perihilar - involves bifurcation of the left and right hepatic ducts = Klatskin’s tumours.
Define cholangiocarcinoma.
Cancer arising from the bile duct epithelium.
Intrahepatic or extrahepatic.
[Perihilar or distal]
Perihilar - involves bifurcation of the ducts = Klatskin’s tumours.
Slow growing.
Explain the aetiology / risk factors of cholangiocarcinoma.
Causes:
- Flukes
- Caroli’s disease
- Biliary cysts
Risk factors:
- 50 years +
- Cholangitis
- Choledocholithiasis
- Cholecytolithiasis
Summarise the epidemiology of cholangiocarcinoma.
95%+ are adenocarcinomas.
Recognise the presenting symptoms of cholangiocarcinoma.
- Abdominal pain - right upper quadrant
- Fever
- Pruritus - itchy skin
- Malaise
Recognise the signs of cholangiocarcinoma on physical examination.
- Painless jaundice
- Weight loss
- Palpable gallbladder
- Hepatomegaly
Identify appropriate investigations for cholangiocarcinoma and interpret the results.
- Bloods - bilirubin, AlkPhos, gamma-GT, aminotransferase, PT time
- Abdominal ultrasound
- Abdominal CT, MRI
- MR angiography
- ERCP
Define cholecystectomy.
Surgical removal of the gall bladder.
Identify the possible complications of a cholecystectomy.
Early:
- Bleeding
- Bile leak
- Bile duct injury
- Infection
- Visceral injury
Late:
- Post-cholecystectomy syndrome
- Biliary stricture
- Port-site or incisional hernias
Identify the possible complications of a cholecystectomy.
Early:
- Bleeding
- Bile leak
- Bile duct injury
- Infection
- Visceral injury
Late:
- Post-cholecystectomy syndrome - persistant dyspeptic symptoms
- Biliary stricture
- Port-site or incisional hernias
Explain the aetiology / risk factors of cholecystitis.
Develops as a complication of cholethiasis/ gallstones.
- Complete cystic duct obstruction due to impacted gallstone in neck or cystic duct
- Bile thickening due to dehydration (inspissation)
- Bile stasis due to trauma or severe systemic illness
Risk Factors:
- Gallstones
- Physical inactivity
- Low fibre intake
- Severe illness
Summarise the epidemiology of cholecystitis.
10% of patients with symptomatic gallstones progress to acute cholecystitis.
Recognise the presenting symptoms of cholecystitis.
- Pain in the right upper quadrant
- Tenderness in the right upper quadrant
- Right shoulder pain
- Fever / chills
- Nausea
- Anorexia
Recognise the presenting symptoms of cholecystitis.
- Pain in the right upper quadrant
- Tenderness in the right upper quadrant
- Right shoulder pain
- Fever / chills
- Nausea
- Anorexia
Chronic:
“Flatulent dyspepsia” - vague abdominal discomfort, distension, nausea, flatulence, fat intolerance
Recognise the signs of cholecystitis on physical examination.
- Tachycardia
- Pyrexia
- Right upper quadrant or epigastric tenderness
- Possible guarding and rebound
- Palpable mass
- Murphy’s sign - lay 2 fingers over the right upper quadrant, ask the patient to breath in - pain & arrest of inspiration as inflamed gallstone impinges on your fingers (only a +ve if the same does NOT happen over the left upper quadrant)
- A Phlegmon - right upper quadrant mass of inflamed adherent omentum and bowel
Identify appropriate investigations for cholecystitis and interpret the results.
Bloods
- High WCC
Ultrasound
- Thick-walled, shrunken gallbladder
- Pericholecystic fluid
- Stones
- Common bile duct dilated (if >6mm)
Abdominal X-Ray
- Only shows 10% gallstones
- Porcelain gallbladder - increased risk of cancer
MRCP
- To find stones
ERCP + sphincterotomy before surgery
Generate a management plan for cholecystitis.
Nil by mouth. Avoidance of fat in diet. Pain relief. IV fluids. Antiemetics. Antibiotics. Laparoscopic cholecystectomy. Open if gallbladder perforates. Elderly/high risk - percutaneous cholecystostomy Obstruction - urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram (PTC)
Identify the possible complications of cholecystitis and its management.
- Cholangitis & obstructive jaundice as stone moves to common bile duct
- Fail to improve - localized abcess or empyema
- Predisposition to gallbladder cancer
- Porcelain gallbladder
Summarise the prognosis for patients with cholecystitis.
2% with gallstones develop symptoms annually - surgery is an effective treatment
Define cirrhosis.
End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.
Decompensated - ascites, jaundice, encephalopathy, GI bleeding
Identify the possible complications of cholecystitis and its management.
- ## Cholangitis & obstructive jaundice as stone moves to common bile duct
Explain the aetiology / risk factors of cirrhosis.
- Chronic alcohol misuse
- Chronic viral hepatitis
- Autoimmune hepatitis
- Drugs - e.g. methotrexate, hepatotoxic drugs
- Inherited - e.g. alpha-1-anti-trypsin deficiency, haemochromatosis, Wilson’s, galactosaemia, cystic fibrosis
- Vascular - Budd-Chiari syndrome or hepatic venous congestion
- Chronic biliary diseases - primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), biliary atresia
- Cryptogenic
- Non-alcoholic steatohepatitis (NASH) - associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia, drugs (e.g. amiodarone, tamoxifen)
Decompensation:
- Infection
- GI bleeding
- Constipation
- High-protein meal
- Electrolyte imbalances
- Alcohol and drugs
- Tumour development
- Portal vein thrombosis
Risk factors:
- Alcohol misuse
- IV drug use
- Unprotected sex
- Obesity
Recognise the presenting symptoms of cirrhosis.
Early:
- Anorexia
- Nausea
- Fatigue
- Weakness
- Weight loss
Reduced liver function:
- Easy bruising
- Abdominal swelling
- Ankle oedema
Reduced detoxification function:
- Jaundice
- Personality change
- Altered sleep pattern
- Amenorrhoea
Portal hypertension:
- Abdominal swelling
- Haematemesis (blood in vomit)
- PR bleeding
- Melanea (black stool)
Recognise the signs of cirrhosis on physical examination.
Chronic liver disease ABCDE:
A = Asterixis (liver flap) B = Briuses C = Clubbing D = Dupuytren's contracture E = Erythema (palmar)
- Jaundice
- Gynaecomastia
- Leukonychia
- Parotid enlargement
- Spider naevi
- Scratch marks
- Ascites - shifting dullness, fluid thrill
- Enlarged liver - shrunken in later stage
- Testicular atrophy
- Caput medusae - dilated superficial abdominal veins
- Splenomegaly - indicates portal hypertension
Identify appropriate investigations for cirrhosis and interpret the results.
- Bloods
- Ascitic tap
- Liver biopsy
- Others
- Imaging
- Endoscopy
- Child-Pugh Grading
Bloods
- FBC - low Hb, platelets
- LFT - normal or high transaminases, AlkPhos, GGT, bilirubin, low albumin
- Clotting - prolonged PT time, low synthesis of clotting factors
- Serum AFP - high in chronic disease, may suggest hepatocellular carcinoma
Ascitic Tap
- Microscopy, culture, sensitivity, biochemistry, cytology
- Neutrophils >250/mm^3 = spontaneous bacterial peritonitis (SBP)
Liver Biopsy
- Percutaneous or transjugular if clotting issues and ascites
- Periportal fibrosis
- Loss of normal liver architecture
- Nodular appearance
- Grade = degree of inflammation
- Stage = degree of architectural distortion
Others - determine cause
- Viral serology
- Alpha-1-antitrypsin
- Caeruloplasmin (Wilson’s)
- Iron studies - haemochromatosis
- Antimitochondrial antibodies - PBC
- Antinuclear antibodies - ANA
- SMA - autoimmune hepatitis
Imaging
- US, CT, MRI - detect complications of cirrhosis
- MRCP - if PSC suspected
Endoscopy
- Check for varices, portal hypertensive gastropathy
Child-Pugh Grading
- Class A, B or C
- Assess albumin, bilirubin, PT, ascites, encephalopathy
Generate a management plan for cirrhosis.
- Treat the cause
- Avoid alcohol, sedatives, opiates, NSAIDs, drugs affecting liver
- Nutrition - dietitian review, enteral supplements, NG feeding
Complications:
- Encephalopathy - treat infections, exclude GI bleed, lactulose, phosphate enemas, avoid sedation
- Ascites - diuretics, dietary sodium restriction, therapeutic paracentesis, monitor weight daily, fluid restriction if sodium >120mmol/L, avoid NSAIDs and alcohol
- SBP - antibiotics, prophylaxis against recurrent SBP with ciprofloxacin
- Surgical - insertion of TIPS (Transjugular intrahepatic portosystemic shunt) to relieve portal hypertension (if recurrent variceal bleeds or diuretic-resistant ascites), liver transplant
Identify the possible complications of cirrhosis and its management.
- Ascites
- Hepatocellular carcinoma
- Hepatic or portal vein thrombosis
- Portal hypertension
- Encephalopathy
- Variceal haemorrhage
- SBP
- Renal failure - hepatorenal syndrome
- Pulmonary hypertension - hepatopulmonary syndrome
Summarise the prognosis for patients with cirrhosis.
Depends on aetiology and complications.
Generally poor - 50% 5 year survival
With ascites, 50% 2 year survival.
Define coeliac disease.
Inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption.
Explain the aetiology / risk factors of coeliac disease.
- Sensitivity to gliadin component in cereal = gluten
- Triggers immunological reaction in SMALL intestine
- Mucosal damage
- Loss of villi
Risk factors:
- Family history - 10% of 1st degree relatives affected
- Genetic - HLA-B8, DR3, DQW2
- IgA deficiency
- Type 1 diabetes
- Autoimmune thyroid disease
Summarise the epidemiology of coeliac disease.
European population - 1%
Recognise the presenting symptoms of coeliac disease.
- Abdominal discomfort
- Abdominal pain
- Abdominal distention
- Steatorrhoea - pale bulky stool, offensive smell, difficult to flush
- Diarrhoea
- Tiredness
- Malaise
- Weight loss
- Failure to thrive in children
- Amenorrhoea in young adults
Recognise the signs of coeliac disease on physical examination.
- Anaemia - pallor
- Malnutrition - short stature, abdominal distension, wasted buttocks, triceps skinfold thickness assessment (fat stores)
- Vitamin deficiencies - osteopenia, osteomalacia, easy bruising
- Itchy blisters on elbows, knees, buttocks = dermatitis herpetiformis
Identify appropriate investigations for coeliac disease and interpret the results.
- Bloods
- Serology
- Stool
- D-xylose test
- Endoscopy
Bloods
- FBC (low Hb), iron, folate, U&E, albumin, Ca2+, phosphate
Serology
- IgG anti-gliadin (AGA)
- IgA and IgG anti-endomysial transglutaminase
- IgA deficiency common so measure Ig levels
Stool
- Culture to exclude infection
- Faecal fat tests for steatorrhoea
D-xylose test
- Reduced urinary excretion after oral xylose load indicates small bowel malabsorption
Endoscopy
- Villous atrophy in small intestine (jejunum ,ileum)
- Smooth, flat mucosa
- Crypt hyperplasia of duodenum
- Cuboidal epithelium
- Inflammatory infiltrate of lymphocytes and plasma cells in lamina propria
Generate a management plan for coeliac disease.
Advice
- Withdrawal of gluten from diet
- Avoidance of wheat, rye, barley
Medical
- Vitamin and mineral supplements
- Oral corticosteroids (if gluten withdrawal doesn’t improve symptoms)
Identify the possible complications of coeliac disease and its management.
- Iron, folate and VitB12 deficiency
- Osteomalacia
- Ulcerative jejunoileitis
- GI lymphoma (T-cell)
- Bacterial overgrowth
- Cerebellar ataxia
Summarise the prognosis for patients with coeliac disease.
Full recovery if adhere to gluten-free diet for life
Symptoms - recover in weeks
Histological changes - longer
Define colonoscopy.
Enables visual inspection of the entire large bowel from distal rectum to cecum.
Summarise the indications for a colonoscopy.
Diagnostic:
- Rectal bleeding
- Iron-deficiency anaemia
- Persistent diahorrea
- Positive faecal occult blood test
- Assessment of suspicion of IBD
- Colon cancer surveillance
Therapeutic:
- Haemostasis - by clipping vessel
- Bleeding angiodysplasia lesion - argon beamer photocoagulation
- Colonic stent deployment (cancer)
- Volvulus decompression (flexi sig)
- Psuedo-obstruction
Identify the possible complications of a colonoscopy.
- Abdominal discomfort
- Incomplete examinatioon
- Haemorrhage after biopsy or polypectomy
- Perforation (<0.1%)
Define colorectal carcinoma.
Malignant adenocarcinoma of the large bowel.
Explain the aetiology / risk factors of colorectal carcinoma.
Sequence from epithelial dysplasia to adenoma and carcinoma - involves oncogenes (APC, K-ras) and tumour suppressor genes (p53, DCC).
Risk factors:
- Increasing age
- Adenomatous polyposis coli (APC) mutation
- Lynch syndrome - hereditary non-polyposis colorectal cancer
- MYH-associated polyposis
- Chronic bowel inflammation - e.g. IBD
Summarise the epidemiology of colorectal carcinoma.
60% in rectum and sigmoid colon.
20% in ascending colon
20% in transverse and descending colon
3rd most common cancer in western world.
4th leading cause of cancer deaths in the US.
Rare below 40yrs.
Recognise the presenting symptoms of colorectal carcinoma.
Depends on locations.
Left-sided colon and rectum:
- Change in bowel habit
- Rectal bleeding
- Blood / mucous in stool
- Tenesmus - sensation of incomplete emptying after defecation
Right-sided colon:
- Later presentation
- Symptoms of anaemia, weight loss and non-specific malaise or lower abdominal pain
Recognise the signs of colorectal carcinoma on physical examination.
- Anaemia only sign in right-sided lesions
- Abdominal mass
- Low-lying tumours palpable on rectal examination
Metastatic disease:
- Hepatomegaly
- Shifting dullness of ascites
Identify appropriate investigations for colorectal carcinoma and interpret the results.
- Blood
- Stool
- Endoscopy
- Barium contrast studies
- Abdominal ultrasound scan
Blood
- FBC - for anaemia
- LFT
- Tumour markers - CEA and CA-19-9 to monitor treatment and reoccurance
Stool
- Occult or frank blood in stool
- Screening
Endoscopy
- Sigmoidoscopy
- Colonoscopy
- Visualisation & biopsy
- If small isolated carcinoma, perform polypectomy
Barium Contrast Studies
- Apple core stricture on barium enema
Abdominal Ultrasound Scan
- For hepatic metastases
- CXR, CT, MRI, endorectal ultrasound
Define Crohn’s disease.
Chronic granulomatous inflammatory disease that can affect any part of the gastrointestinal tract.
Grouped with UC - together IBD.
Explain the aetiology / risk factors of Crohn’s disease.
Unknown cause - genetic and environmental factors.
Inflammation anywhere along the GI tract - 40% involving terminal ileum.
Skip lesions with inflamed segments of bowel interspersed with normal segments.
Risk factors:
- White ancestry
- Age 15-40 or 60-80
- Family history of Crohn’s
- Cigarette smoking
Summarise the epidemiology of Crohn’s disease.
UK Incidence annually is 5-8 in 100,000.
UK Prevalance is 50-80 in 100,000.
Recognise the presenting symptoms of Crohn’s disease.
- Cramping abdominal pain
- Diarrhoea - bloody or steatorrhoea
- Fever
- Malaise
- Weight loss
- Symptoms of complications
Recognise the signs of Crohn’s disease on physical examination.
- Weight loss
- Clubbing
- Signs of anaemia
- Aphthous ulceration of the mouth
- Perianal skin tags
- Fistulae
- Abscesses
- Signs of complications - e.g. eye disease, joint disease, skin diseases
Identify appropriate investigations for Crohn’s disease and interpret the results.
- Bloods
- Stool microscopy and culture - to exclude infective colitis
- Abdominal X-Ray - for evidence toxic megacolon
- Erect Chest X-Ray - if risk of perforation
- Small bowel barium follow-through
- Endoscopy (OGD, colonoscopy) and biopsy
- Radionuclide-labelled neutrophil scan - localisation of inflammation
Blood
- FBC - low Hb, high platelets, WCC
- U&E
- LFTs - low albumin
- High CRP - high or normal
- High ESR
- Haematinics - look for deficiency states in ferritin, VitB12, red cell folate
Small Bowel Barium Follow-Through
- May reveal fibrosis or strictures - e.g. string sign of Kantor
- Deep ulceration - rose thorn
- Cobblestone mucosa
Endoscopy & Biopsy
- Differentiate between UC and Crohn’s
- Monitoring malignancy and disease progression
- Mucosal oedema and ulceration with rose thorn fissures (cobblestone mucosa)
- Fistulae
- Abcesses
- Transmural chronic inflammation with infiltration of macrophages
- Lymphocytes and plasma cells
- Granulomas with epithelioid giant cells may be seen in blood vessels or lymphatics
Generate a management plan for Crohn’s disease.
Acute exacerbation:
- Fluid resuscitation
- Corticosteroids (oral or IV)
- 5-ASA analogues - e.g. mesalazine, sulfasalazine
- Analgesia
- Elemental diet
- Parental nutrition
- Monitor markers of activity - e.g. fluid balance, ESR, CRP, platelets, stool frequency, Hb, albumin
- Assess for complications
Long Term:
- Corticosteroids
- 5-ASA analogues
- Immunosuppression using steroid sparing agents - e.g. azathioprine
- Anti-TNF agents - e.g. infliximab
Advice:
- Stop smoking
- Dietitian referral
- Education & advice - e.g. from IBD nurse specialist
Surgery:
- Failure of medical treatment
- Failure to thrive in children
- Presence of complications
- Resection of affected bowel and stoma formation
Identify the possible complications of Crohn’s disease and its management.
GI
- Haemorrhage
- Bowel strictures
- Bowel perforation
- Fistulae - between bowel, bladder, vagina
- Perianal fistulae and abscess
- GI carcinoma
- Malabsorption
Extra-intestinal Features:
- Uveitis
- Episcleritis
- Gallstones
- Kidney stones
- Arthropathy
- Sacroilitis
- Ankylosing spondylitis
- Erythema nodosum
- Pyoderma gangrenosum
- Amyloidosis
Summarise the prognosis for patients with Crohn’s disease.
Chronic relapsing condition
2/3rd need surgery, of those 2/3 >1 procedure.
Define diverticular disease.
The presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel, associated with complications - e.g. haemorrhage, infection, fistulae
Explain the aetiology / risk factors of diverticular disease.
- Low-fibre diet –> loss of stool bulk
- High colonic intraluminal pressures generated to propel stool
- Leads to herniation of mucosa and submucosa through muscularis
- Sigmoid and descending colon
- Sites of nutrient artery penetration
Proposed Diverticular Obstruction:
- By inspissated faeces
- Bacterial overgrowth
- Toxin production
- Mucosal injury & diverticulitis
- Perforation
- Pericolic phlegmon
- Abscess
- Ulceration
- Fistulation
- Stricture
Summarise the epidemiology of diverticular disease.
60% of people living in industrialised countries develop colonic diverticula, rare <40yrs
Right-sided diverticula more common in Asia.
Recognise the presenting symptoms of diverticular disease.
80-90% asymptomatic
- PR bleeding
- Diverticulitis
- Left iliac fossa or lower abdominal pain
- Fever
Fistulation into bladder:
- Pneumaturia - air bubbles passing in the urine
- Faecaluria
- Recurrent UTI
Recognise the signs of diverticular disease on physical examination.
- Tender abdomen
- Signs of local or generalised peritonitis if perforation has occurred
Identify appropriate investigations for diverticular disease and interpret the results.
- Bloods
- Barium enema
- Flexible sigmoidoscopy and colonoscopy
Bloods
- FBC - high WCC, CRP
- Check clotting and cross-match if bleeding
Barium enema
- Saw-tooth appearance of lumen
- Reflects psuedohypertrophy of circular muscle
Flexible Sigmoidoscopy and Colonoscopy
- Exclude polyps and tumours
- See diverticulae
Acute setting:
- Don’t perform barium enema
- CT scan to check for disease and complications
Generate a management plan for diverticular disease.
1 . Asymptomatic
- GI bleeding
- Diverticulitis
- Surgery
Asymptomatic
- Soluble high fibre diet - 20-30g/day
- Probiotics
- Anti-inflammatories - e.g. mesalazine
GI Bleed
- IV rehydration
- Antibiotics
- Blood transfusion
- Angiography, embolization or surgery if severe
Diverticulitis
- IV antibiotics
- IV fluid rehydration
- Bowel rest
- Radiologically sited drains if there are localised collections or abscesses
Surgery
- With recurrent attacks or complications
- Open or laparoscopic
- Hartmann’s procedure - resection and stoma
- One-stage resection and anastomosis and defunctioning stoma
- Drain placement
- Periotoneal lavage
Identify the possible complications of diverticular disease and its management.
- 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% of patients have 1+ episodes over diverticulitis
- 30% of those will have a second episode
Define endoscopic retrograde cholangiopancreatography (ERCP).
A technique that uses a combination of luminal endoscopy and fluoroscopy imaging to treat conditions associated with the pancreatobiliary system.
The endoscopic portion of the examination uses a side-viewing duodenoscope that is passed through the oesophagus and stomach and into the second portion of the duodenum.
Identify the possible complications of endoscopic retrograde cholangiopancreatography (ERCP).
- Pancreatitis
- Bleeding
- Cholangitis
- Perforation
- Mortality <0.2% overall, 0.4% if performing stone removal
Summarise the indications for an endoscopy.
Diagnostic Indications:
- Haematemesis/ melaena
- Dysphagia
- Dyspepsia - >55yr, alarm symptoms, treatment refractory
- Duodenal biopsy
- Persistent vomiting
- Iron deficiency (
Define endoscopy.
A procedure that uses an endoscope to examine the interior of a hollow organ or cavity of the body.
Define feeding (enteral & parenteral).
Enteral feeding - a mode of feeding that uses the GI tract, such as oral or tube feeding.
Parenteral feeding - a mode of feeding that delivers specialist nutritional products to a person intravenously, bypassing the usual process of eating and digestion.
Summarise the indications for feeding (enteral and parenteral).
Enteral Nutrition:
- Functioning GI tract
- Stroke - impairs ability to swallow
- Cancer - may cause fatigue, nausea, vomiting
- Critical illness or injury - reduces energy or ability to eat
- Failure to thrive or inability to eat in young children
- Serious illness - places body in state of stress
- Neurological or movement disorders that increase caloric requirements while making it more difficult to eat
- GI dysfunction or disease although this may required parenteral instead
Identify the possible complications of feeding (enteral & parenteral).
Enteral Nutrition:
- Aspiration - food into the lungs
- Refeeding syndrome - dangerous electrolyte imbalances
- Infection of tube or insertion site
- N&V results from too large and too fast feeds
- Skin irritation at tube insertion site
- Diarrhea due to liquid diet or medications
- Tube dislodgement
- Tube blockage if not flushed properly
Parenteral Nutrition:
- Sepsis - e.g. staphylococcus epidermidis, staphylococcus aureus, candida pseudomonas , infective endocarditis
- Thrombosis
- Metabolic imbalance - e.g. electrolyte abnormalities, deranged plasma glucose, hyperlipidaemia, deficiency syndromes, acid-base disturbance
- Mechanical - e.g. pneumothorax, embolism of IV line tip
Define functional dyspepsia & irritable bowel syndrome (IBS)
Functional dyspepsia - when your upper digestive tract shows symptoms of upset, pain or early or prolonged fullness for a month or longer
IBS - A functional bowel disorder defined as recurrent episodes of abdominal pain/discomfort for >6 months of the previous year associated with 2 of the following:
- Altered stool passage
- Abdominal bloating
- Symptoms made worse by eating
- Passage of mucous
Explain the aetiology / risk factors of functional dyspepsia & irritable bowel syndrome (IBS)
Absence of detectable organic pathology - unknown cause.
- Visceral sensory abnormalities
- Gut motility abnormalities
- Psychosocial factors (stress)
- Food intolerance (e.g. lactose)
Summarise the epidemiology of functional dyspepsia & irritable bowel syndrome (IBS)
Common - 10-20% of adults
M:F 2:1
Recognise the presenting symptoms of functional dyspepsia & irritable bowel syndrome (IBS)
- > 6 months abdominal pain (colicky in lower abdomen and relieved by defecation or flatus)
- Altered bowel frequency with >3 bowel movements daily or <3 motions weekly
- Abdominal bloating
- Change in stool consistency
- Passage with urgency or straining
- Tenesmus - feeling of incomplete defecation
NB: Screen for red flag:
- Weight loss
- Anaemia
- PR bleeding
- Late onset (>60 yrs)
Recognise the signs of functional dyspepsia & irritable bowel syndrome (IBS) on physical examination.
Nothing normally on examination
Distended abdomen and mildly tender to palpate in one or both iliac fossa.
Recognise the presenting symptoms of functional dyspepsia & irritable bowel syndrome (IBS)
- > 6 months abdominal pain (colicky in lower abdomen and relieved by defecation or flatus)
- Altered bowel frequency with >3 bowel movements daily or <3 motions weekly
- Abdominal bloating
- Change in stool consistency
- Passage with urgency or straining
- Tenesmus - feeling of incomplete defecation
NB: Screen for red flag:
- Weight loss
- Anaemia
- PR bleeding
- Late onset (>60 yrs)
Risk factors:
- Physical and sexual abuse
- PTSD
- Age <50yrs
- Female sex
Generate a management plan for functional dyspepsia & irritable bowel syndrome (IBS)
Advice:
- Explain and support with establishment of doctor-patient relationship
- Dietary modification - reducing insoluble fibre
- Exclusion diets
- Probiotics
Medical:
- Antispasmodics - e.g. mebeverin, buscopan
- Prokinetic agents - e.g. domperidone, metocloparamide
- Antidiarrhoeals - e.g. loperamide
- Laxatives - e.g. lactulose
- Low dose tricyclic antidepressants - reduces visceral awareness
Psychological
Identify the possible complications of functional dyspepsia & irritable bowel syndrome (IBS)
- Physical and psychological morbidity
- Increased incidence of clonic diverticulosis
Generate a management plan for functional dyspepsia & irritable bowel syndrome (IBS)
Advice:
- Explain and support with establishment of doctor-patient relationship
- Dietary modification - reducing insoluble fibre
- Exclusion diets
- Probiotics
Medical:
- Antispasmodics - e.g. mebeverin, buscopan
- Prokinetic agents - e.g. domperidone, metocloparamide
- Antidiarrhoeals - e.g. loperamide
- Laxatives - e.g. lactulose
- Low dose tricyclic antidepressants - reduces visceral awareness
Psychological therapies:
- CBT, relaxation, psychotherapy
Define gallstones and biliary colic.
Gallstones - stone formation in the gallbladder
Biliary colic - sudden onset, severe right upper quadrant or epigrastric pain, constant in nature associated with the formation of stones in the gallbladder
Explain the aetiology / risk factors of gallstones and biliary colic.
3 types of stone: Mixed stones, Pure cholesterol stones, Pigment stones
Mixed stones:
- Contain cholesterol, calcium bilirubinate, phosphate and protein
- Risk factors: older age, female, obesity, parenteral nutrition, drugs (OCP, ocreotide), family history, ethnicity (Pima Indians), interruption of the enterohepatic recirculation or bile salts (e.g. Crohn’s), terminal ileal resection
Pure Cholesterol Stones:
- Risk factors: older age, female, obesity, parenteral nutrition, drugs (OCP, ocreotide), family history, ethnicity (Pima Indians), interruption of the enterohepatic recirculation or bile salts (e.g. Crohn’s), terminal ileal resection
Pigment Stones:
- Black stones of calcium bilirubinate - high bilirubin secondary to haemolytic disorders, cirrhosis
- Brown stones - bile duct infestation by liver fluke Clonorchis sinesis
- Risk factors: Haemolytic disorders - e.g. sickle cell, thalassaemia, hereditary spherocytosis
Summarise the epidemiology of gallstones and biliary colic.
Very common UK prevalence = 10%
Older age
3x more females in younger population
Equal sex ratio after 65yrs
Recognise the presenting symptoms of gallstones and biliary colic.
90% Asymptomatic.
Recognise the presenting symptoms of gallstones and biliary colic.
90% Asymptomatic.
Biliary colic:
- Sudden onset, right upper quadrant or epigastric pain
- Constant
- Right scapula radiation
- Precipitated by fatty meal
- Nausea & Vomiting
Acute Cholecystitis:
- Patient systemically unwell
- Fever
- Prolonged upper abdominal pain
- Referred to right shoulder due to diaphragmatic irritation
Ascending Cholangitis
- Right upper quadrant pain
- Jaundice
- Rigors
- Hypotension
- Confusion
(1st 3 = Charcot’s triad, +last 2 = Reynold’s pentad)
Recognise the signs of gallstones and biliary colic on physical examination.
Biliary colic:
- Right upper quadrant pain
- Epigastric tenderness
Acute Cholecystitis:
- Tachycardia
- Pyrexia
- Right upper quadrant or epigastric tenderness
- Guarding +/- rebound
- Murphy’s sign - upon placing a hand at the costal margin in the right upper quadrant and asking the patient to breath in deeply
Ascending Cholangitis:
- Pyrexia
- Right upper quadrant pain
- Jaundice
Identify appropriate investigations for gallstones and biliary colic and interpret the results.
- Bloods
- US Scan
- Abdominal X-ray
- Others
Bloods
- FBC - high WBC in cholecystitis and cholangitis
- LFT - high AlkPhos, bilirubin in cholangitis, transaminases
- Blood cultures
- Amylase - risk of pancreatitis
USS
- Gallstones - acoustic shadow within gallbladder
- Increased thickness of gallbladder wall
- Dilatation of biliary tree = obstruction
Others
- Erect CXR - perforation
- CT, MRCP, ERCP
Generate a management plan for gallstones and biliary colic.
Mild Symptoms:
- Conservative
- Avoid fat in diet
Severe Biliary Colic:
- Admission
- IV fluids
- Analgesia
- Antiemetics
- Antibiotics
- If do not improve, check for abscess or empyema - drain by cholecystostomy and pigtail catheter
- If obstructed, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram
Surgery:
- Laparoscopic cholecystectomy +/- on table cholangiogram
- Acute - within 72hrs or after weeks to let inflammation settle \
Generate a management plan for gallstones and biliary colic.
Mild Symptoms:
- Conservative
- Avoid fat in diet
Severe Biliary Colic:
- Admission
- IV fluids
- Analgesia
- Antiemetics
- Antibiotics
- If do not improve, check for abscess or empyema - drain by cholecystostomy and pigtail catheter
- If obstructed, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram
Surgery:
- Laparoscopic cholecystectomy +/- on table cholangiogram
- Acute - within 72hrs or after weeks to let inflammation settle
Identify the possible complications of gallstones and biliary colic and its management.
Stones within the gallbladder:
- Biliary colic
- Cholecystitis
- Mucocoele
- Gallbladder empyema
- Porcelain gallbladder
- Predisposition to gallbladder cancer
Stones outside the gallbladder:
- Obstructive jaundice
- Pancreatitis
- Ascending cholangitis
- Perforation
- Pericholecystic abscess
- Bile peritonitis
- Cholecystenteric fistula
- Gallstone ileus
- Mirizzi Syndrome - common hepatic duct obstruction by an extrinsic compression from an impacted stone in the cystic ducts
- Bouveret’s Syndrome - gallstones causing gastric outlet obstruction
Of cholecystectomy:
- Bleeding
- Infection
- Bile leak
- Bile duct injury (0.3% lap, 0.2% open)
- Post-cholecystectomy syndrome - persistent dyspeptic symptoms
- Port-site hernias
Define gastric cancer.
Gastric malignancy, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma.
Explain the aetiology / risk factors of gastric cancer.
Environmental insult in genetically predisposed individuals –> mutation, unregulated cell growth
Risk factors:
- H.pylori infection
- Atrophic gastritis
- Diet high in smoked, processed foods, nitrosamines
- Smoking
- Alcohol
Summarise the epidemiology of gastric cancer.
Common cause of death worldwide
Highest incidence - Asia, Japan
6th most common cancer in UK
UK annual 15/100,000.
M:F 2:1
Age >50 yrs
Reducing incidence of cancer of antrum/body
Cardia and GI/Oesophageal increasing.
Recognise the presenting symptoms of gastric cancer.
Early - asymptomatic
- Early satiety
- Epigastric discomfort
- Weight loss
- Anorexia
- N&V
- Haematemesis
- Melaena
- Symptoms of anaemia
- Dysphagia - tumours of the cardia
- Symptoms of metastases - e.g. abdominal swelling, jaundice
Recognise the signs of gastric cancer on physical examination.
- May be normal
- Epigastric mass
- Abdominal tenderness
- Ascites
- Signs of anaemia
- Virchow’s node/Troisier’s sign - lymphadenopathy in left supraclavicular fossa
- Sister Mary Joseph node - metastatic nodule on umbilicus
- Krukenber’s tumour - ovarian metastases
Identify appropriate investigations for gastric cancer and interpret the results.
- Upper GI endoscopy - multiquadrant biopsy of gastric ulcers
- Blood - FBC (anaemia), LFT
- CT/MRI - staging of tumour, surgery
- US of Liver - staging of tumour
- Bone scan - staging of tumour
- Endoscopic Ultrasound - assess depth of invasion, lymph node spread
- Laparoscopy - determine if resectable
Define gastro-oesophageal reflux disease.
Inflammation of the oesophagus caused by the reflux of gastric acid and/or bile.
Explain the aetiology / risk factors of gastro-oesophageal reflux disease.
Disruption of mechanisms that prevent reflux - e.g. physiological lower oesophageal sphincter, mucosal rosette, acute angle of junction, intra-abdominal portion of oesophagus, prolonged oesophageal clearance
Explain the aetiology / risk factors of gastro-oesophageal reflux disease.
Disruption of mechanisms that prevent reflux - e.g. physiological lower oesophageal sphincter, mucosal rosette, acute angle of junction, intra-abdominal portion of oesophagus, prolonged oesophageal clearance
Risk factors:
- Family history of heartburn or GORD
- Older age
- Hiatus hernia
- Obesity
Recognise the presenting symptoms of gastro-oesophageal reflux disease.
- Substernal burning discomfort or ‘heartburn’
- Aggrevated by lying supine, bending, large meals, alcohol
- Pain relieved by antacids
- Waterbrash
- Regurgitation of gastric contents
- Aspiration –> voice hoarseness, laryngitis, nocturnal cough, wheeze, pneumonia (rare)
- Dysphagia - due to peptic stricture after long-standing reflux
Recognise the signs of gastro-oesophageal reflux disease on physical examination.
- Epigastric tenderness
- Wheeze on chest auscultation
- Dysphonia
Identify appropriate investigations for gastro-oesophageal reflux disease and interpret the results.
- Upper GI endoscopy, biopsy, cytological brushings - confirm oesophagitis, exclude malignancy (>45yrs)
- ## Barium swallow - e.g. hiatus hernia, peptic stricture, extrinsic compression of oesophagus
Identify appropriate investigations for gastro-oesophageal reflux disease and interpret the results.
- Upper GI endoscopy, biopsy, cytological brushings - confirm oesophagitis, exclude malignancy (>45yrs)
- Barium swallow - e.g. hiatus hernia, peptic stricture, extrinsic compression of oesophagus
- CXR - hiatus hernia (gastric bubble behind cardiac shadow)
- 24hr oesophageal pH monitoring - pH probe in lower oesophagus to determine temporal relationship between symptoms and oesophagus pH
Generate a management plan for gastro-oesophageal reflux disease.
Advice
- Lifestyle changes
- Weight loss
- Elevating head of bed
- Avoid provoking factors
- Stopping smoking
- Lower fat meals
- Avoiding large meals late in the evening
Medical
- Antacids
- Alginates
- H2 Receptor Antagonists - e.g. ranitidine
- PPI - e.g. lansoprazole
Endoscopy
- Annual surveillance for Barrett’s oesophagus
- Stricture dilating
- Stenting
Surgery
- Anti-reflux surgery for those with symptoms despite optimal medical management
Nissen fundoplication
- Fundus of stomach wrapped around lower oesophagus and held with seromuscular sutures to reduce hiatus hernia and reflux
Identify the possible complications of gastro-oesophageal reflux disease and its management.
- Oesophageal ulceration
- Peptic stricture
- Anaemia
- Barrett’s oesophagus
- Oesophageal adenocarcinoma
- Asthma
- Chronic laryngitis
