Gastroenterology Flashcards
What is the step-wise progression on alcoholic liver disease?
- Alcohol-related fatty liver-> temporary + reverses in 2 weeks if stop
- Alcoholic hepatitis-> inflammation from binge drinking, mild usually reversible with permanent abstinence
- Cirrhosis-> irreversible formation of scar tissue, stopping can prevent further damage
What is the weekly recommended limit of alcohol?
14 units a week spread over 3+ days and <5 units a day
What is the CAGE questionnaire and what are its components?
Assessment of harmful alcohol use
- have you thought about Cutting down?
- do you get Annoyed when people comment on your drinking?
- do you feel Guilty about drinking?
- ever had to have a drink in the morning to help with a hangover or nerves (Eye opener)?
What are the complications of harmful alcohol use?
- Liver-> ALD, cirrhosis, hepatocellular cancer
- Dependence and withdrawal
- Wernicke-Korsakoff syndrome
- Pancreatitis
- Alcoholic cardiomyopathy
- Increased risk of breast, mouth and throat cancers
What is the AUDIT tool?
Alcohol Use Disorders Identification Test-> 8/10 or more indicates harmful use
What are some clinical signs of liver disease?
Jaundice, hepatomegaly, spider naevi, palmar erythema, gynaecomastia, bruising easily, ascites, asterixis, caput medusae (engorged superficial epigastric veins)
Investigations for alcoholic liver disease?
- Bloods-> FBC for macrocytic anaemia, deranged LFTs, high bilirubin in cirrhosis, high PTT, U+Es
- US-> fatty change
- Fibroscan-> elasticity + degree of cirrhosis
- CT + MRI-> fatty liver, cancers, complicatins
- Biopsy-> confirm diagnosis
Treatment for alcoholic liver disease?
- Detox + abstinence
- Thiamine
- High protein diet
- Steroids-> improve short term outcomes in severe
- Liver transplant-> must abstain for 3+ months
How does alcohol withdrawal present?
- 6-12 hours-> tremor, sweating, headache, cravings, anxiety
- 12-24 hours-> hallucinations
- 24-48 hours-> seizures
- 24-72-> delirium tremens
How is alcohol withdrawal assessed?
Clinical Institute Withdrawal Assessment (CIWA-Ar)
How is alcohol withdrawal treated?
- Chlordiazepoxide (benzo) oral reducing regime for 5-7 days
- Pabrinex-> IV high dose vitami B
- Thiamine-> low dose after pabrinex
What is delirium tremens?
Medical emergency associated with alcohol withdrawal
What is the pathophysiology of delirium tremens?
- Alcohol stimulates GABA receptors + inhibits NMDA (glutamate) receptors-> inhibitory
- Chronic use causes downregulation of GABA + upregulation of NMDA
- Remove alcohol-> causes under + over function
- Overall extreme excitability of the brain + excess adrenergic activity
What are the symptoms and signs of delirium tremens?
- Confusion, agitiation, delusions, hallucinations
- Tremor, tachycardia, hypertension, hyperthermia, ataxia, arrhythmias
What is Wernicke-Korsakoff syndrome?
Disease due to alcohol excess-> thiamine (B1) deficiency due to poor diet + alcohol causing poor absorption
How does Wernicke-Korsakoff syndrome present?
- Wernicke’s encephalopathy-> confusion + oculomotor disturbance + ataxia
- Korsakoff’s syndrome-> irreversible memory impairment + behavioural change
How is Wernicke-Korsakoff syndrome treated?
- Thiamine supplements
- Alcohol abstinence
What is the pathophysiology of liver cirrhosis?
Chronic inflammation-> damage-> replaced by scar tissue (fibrosis)-> nodules-> affect structure and blood flow-> increased resistance + portal hypertension
What are the causes of liver cirrhosis?
ALD, NAFLD, Hepatitis B or C, AI hepatitis, PBC, haemachromatosis, Wilson’s disease, CF, drugs (methotrexate, amiodarone, sodium valproate)
What are some investigations for liver cirrhosis?
- Bloods-> LFTs, albumin (low), PTT (high), hyponatraemia, urea, creatinine
- Alpha-fetoprotein-> hepatocellular marker checkec every 6 months in cirrhosis
- Viral markers + auto-antibodies
- Enhanced liver fibrosis (ELF) bloods-> for NAFLD + measured 3 markers (HA, PIIINP, TIMP-1)
- US-> enlarged portal vein etc
- Fibroscan-> every 2 years when high risk (for elasticity)
- Endoscopy, CT, MRI, biopsy
What is the Child-Pugh scoring system?
Assessment of liver cirrhosis
- 5 features-> bilirubin, albumin, INR, ascites, encephalopathy
- Each scored out of 3-> 5 minimum + 15 maximum
What is the MELD scoring system?
Model for End-stage Liver Disease-> predicts mortality after liver transplant + other interventions
- Looks at bilirubin, creatinine, INR, sodium and need for dialysis
- Done every 6 months in cirrhosis
How is liver cirrhosis managed?
- US + AFP + MELD score every 6 months
- Endoscopy every 3 years
- High protein low sodium diet
- Transplant
What diet do people with liver cirrhosis need to follow and why?
- Regular meals, low sodium, high protein, high calorie
- Due to increased use of muscle as fuel-> affects protein metabolism in liver + disrupts ability to store glucose
Why does portal hypertension and varices occur in liver cirrhosis?
Cirrhosis increases resistance of blood flow in the liver-> back pressure into portal venous system-> swollen + tortuous anasthamoses in systemic venous system (varices)
What does the portal system in the liver entail?
Superior mesenteric + splenic veins-> portal system-> blood to liver
Where do varices commonly occur in liver disease?
Gastro-oesophageal junction, ileocaecal junction, rectum, anterior abdominal wall (caput medusae)
How are stable varices in liver disease treated?
- Propanolol
- Elastic band ligation
- Inject sclerosant
- Transjugular intrahepatic portosystemic shunt (TIPS)-> stent from portal to hepatic vein to relieve pressure
How are bleeding varices treated in liver disease?
- Terlipressin-> vasopressin analogue
- Vitamin K + FFP for coagulopathies
- Broad spectrum antibiotics
- Urgent endoscopy + inject sclerosant
- Ligation
- Sengstaken-Blakemore tube
What is the pathophysiology behind ascites?
- Increased pressure in portal venous system-> fluid leaks from capillaries in the liver + bowel-> into the peritoneal cavity
- Circulatory volume drops-> reduced BP in kidneys-> RAAS activation-> sodium + fluid reabsorbed-> transudative (low protein) ascites
How is ascites managed?
- Low sodium diet
- Spironolactone (aldosterone antagonist)
- Paracentesis
- Prophylactic antibiotics for SPC (eg ciprafloxacin)
- Transjugular intrahepatic portosystemic shunt (TIPS)
What is spontaenous bacterial peritonitis?
Infection in ascitic fluid + peritoneal lining
What organisms typically cause spontaneous bacterial peritonitis?
E.coli, Klebsiella pneumoniae, gram +ve cocci (eg staph)
What are the symptoms and signs of spontaneous bacterial peritonitis?
Asymptomatic, fever, abdominal pain + tenderness, deranged bloods, ileus, hypotension
What is the management for spontaneous bacterial peritonitis?
- Ascitic culture
- IV cephalosporin-> eg cefotaxime
What is hepatorenal syndrome and what is its pathophysiology?
Hypertension in portal veins dilates blood vessels-> blood pools + causes loss of volume in kidneys-> RAAS activation-> renal vasoconstrction + low blood to kidney-> low function that can be fatal if not transplanted
What is hepatic encephalopathy and what is its pathophysiology?
- Ammonia produced by intestinal bacterial when proteins broken down-> absorbed in gut
- Ammonia builds up due to bypassing the liver (as metabolism impaired + collateral vessels formed_
- Enters systemic circulation-> affects brain
How does hepatic encephalopathy present?
LOC, confusion, personality/memory/mood changes
What can precipitate hepatic encephalopathy?
Constipation, electrolyte disturbances, infection, high protein diet, medications (eg sedatives)
Management of hepatic encephalopathy?
- Laxatives to promote excretion
- Enemas
- Antibiotics eg rifaximin-> reduce intestinal bacterial producing ammonia
- Nutritional support
What is non-alcoholic fatty liver disease (NAFLD)?
Fat deposited in liver cells-> interfere with function-> can progress to hepatitis + cirrhosis
What are the 4 stages of non-alcoholic fatty liver disease (NAFLD)?
- non-alcoholic fatty liver disease (NAFLD)
- non-alcoholic steatohepatitis (NASH)
- fibrosis
- cirrhosis
What are the risk factors for non-alcoholic fatty liver disease (NAFLD)?
Same as diabetes + CVD
Investigations for non-alcoholic fatty liver disease (NAFLD)?
-When abnormal LFTs and no clear cause-> non-invasive liver screen
-Enhanced liver fibrosis (ELF) bloods-> 1st line
NAFLD fibrosis score-> age, BMI, liver enzymes, platelets, albumin, DM-> rule out fibrosis
-Fibroscan-> stiffness
-US liver-> can confirm
-Auto-antibodies for AI hep, PBC, PSC-> ANA, SMA, AMA, LMK-1
-Other-> hepatitis B/C serology, immunoglobulins (AI hep, PBC), ferritin + transferritin etc
Management for non-alcoholic fatty liver disease (NAFLD)?
- Weight loss, control co-morbidities, avoid alcohol
- Liver specialist-> may give pioglitazone or vitamin E
What is hepatitis?
Inflammation of the liver-> acute, chronic, severe etc
What can cause hepatitis?
Alcohol, NAFLD, viral, AI, drug induced
How might hepatitis present (in general)?
Asymptomatic, abdominal pain, fatigue, pruritis, muscle + joint aches, N+V, jaundice, fever
What might blood tests look like in hepatitis?
Deranged LFTs-> high AST/ALT (inflammation) + proportionally small rise in ALP + high bilirubin
What is the most common type of hepatitis worldwide?
Hepatitis A
How is hepatitis A transmitted?
Faecal-oral route-> food/water
What type of virus is Hepatitis A?
RNA virus
How does Hepatitis A present?
N+V, anorexia, jaundice, cholestasis, dark urine, pale stoold, moderate hepatomegaly
How is Hepatitis A managed?
- Often resolves spontaneously in 1-3 months
- Analgesia
- PHE notification
- Prevention with vaccine
What type of virus is Hepatitis B?
DNA virus
How is Hepatitis B transmitted?
- Blood + fluids-> sex, needles, toothbrushes, minor cuts
- Vertically-> mother to baby
What is the prognosis of Hepatitis B?
- Most recover in 2 months
- 10% become carriers as viral DNA in own DNA continue to produce proteins
How is Hepatitis B tested for?
- HBcAb-> core antibody, indicates previous infection when +ve
- HBsAg-> surface antigen, indicates active infection when +ve
- If these both positive then do others-> HBeAg, HBsAB, HBeAg, HBV DNA
What does a positive HBcAb test indicate when investigating Hepatitis B?
Core antibody-> previous infection
What does a positive HBsAg test indicate when investigating Hepatitis B?
Surface antigen-> active infection
What do the different tests for Hepatitis B mean?
- HBcAb-> core antibody-> previous infection
- HBsAg-> surface antigen-> active infection
- HBeAg-> e antigen-> marks viral replication so high level means high infectivity
- HBsAb-> surface antibody-> vaccination or past or current infection
- HBV DNA-> direct viral load
How is Hepatitis B managed?
- Screen high risk + other blood diseases
- Refer to specialist + test for complications (eg US + fibroscan)
- PHE notification + contact tracing
- Antivirals-> reduce progression + transmission
- Transplant
- Vaccine
How does the Hepatitis B vaccine work?
- Hep B surface antigen injected-> HBsAb tested to confirm
- 3 different doses in 6-in-1 vaccine at 8, 12 and 16 weeks
What type of virus is Hepatitis C?
RNA virus
How is Hepatitis C spread?
Blood + body fluids
What is the disease course of Hepatitis C?
- 1/4 fight off the infection
- 3/4 get chronic infection
How is Hepatitis C investigated?
- HepCAb-> screening
- HepC RNA-> confirm + calculate viral load
How is Hepatitis C managed?
- Low screening threshold + for other diseases
- Referral-> fibroscan + US
- Direct acting antivirals-> tailored to genotype + cures 90%
- PHE + education
- May need transplant
What are the complications of Hepatitis C?
Cirrhosis and hepatocellular cancer
What type of virus is Hepatitis D?
RNA virus
When is the only time that it’s possible to get Hepatitis D?
With current Hepatitis B infection-> attached to HBsAg
How is Hepatitis D managed?
- PHE notification
- No specific treatment
- Looks for complications-> can increase severity of Hep B
What type of virus is Hepatitis E?
RNA virus
How is Hepatitis E spread?
Faecal-oral route
How does Hepatitis E present and progress?
- Mild illness + clears within a month
- Rare progression to chronic + liver failure when immunocompromised
How is Hepatitis E treated?
None specific + needs PHE notification
What causes autoimmune hepatitis?
- Unknown
- Genetic + triggered by viral infection-> T cell response against liver cell
What is type 1 autoimmune hepatitis and how does it present?
- Mostly women in late 40s-50s
- Around menopause with fatigue + liver disease
- More chronic
What is type 2 autoimmune hepatitis and how does it present?
- In teens/early 20s
- Acute hepatitis
- Jaundice + high transaminases
What investigations are done for autoimmune hepatitis?
- Raised ALT, AST and IgG
- Type 1 auto antibodies-> ANA, anti-actin, anti-SLA/LP
- Type 2 auto antibodies-> anti-LKM1, anti-LC1
- Liver biopsy-> confirms
Treatment for autoimmune hepatitis?
- High dose prednisolone tapered over time
- Azathioprine immunosuppressant-> lifelong
- Transplant
What is haemachromatosis?
A genetic condition in which there are problems with iron storage leasing to excess total body iron + deposits in tissues
What is the inheritance pattern and genetic mutation of haemachromatosis?
- Autosomal recessive
- Human haemochromatosis protein (HFE) on chromosome 6-> regulates iton metabolism
What are the symptoms of haemochromatosis?
- Tired, joint pain, hair loss, erectile dysfunction, amenorrhoea, memory/mood problems
- Pigmentation-> bronze + slate-grey discolouration
- Usually symptomatic after age 40
- Presents later in females as menstruation regularly eliminates iron from the body
How is haemochromatosis diagnosed?
- Serum ferritin-> acute phase reactant so use with transferrin sats to distinguish between other disease (both high)
- Genetics-> if ferritin + transferrin high with no reason
- Liver biopsy + Perl’s stain-> iron concentration in parenchymal cells
- CT abdo-> high attenuation in liver
- MRI-> detailed iron deposits in liver + heart
What are the complications of haemochromatosis?
- T1DM-> iron affects pancreas functioning
- Deposits in pituitary and gonads-> endocrine + sexual dysfunction eg hypogonadism, impotence, amenorrhoea, infertility
- Deposits in organs-> cardiomyopathy, hypothyroidism, pseudogout, arthritis
Management of haemochromatosis?
- Venesection-> weekly blood removal to decrease iron
- Monitor ferritin
- Avoid alcohol
- Genetic counselling
- Monitor and treat complications
What is Wilson’s disease?
Excess copper accumulation as removal in the liver impaired
What is the inheritance pattern and gene mutation in Wilson’s disease?
- Autosomal recessive
- Wilson disease protein on chromosome 13
What organs are affected in Wilson disease and how can this present?
- Liver-> hepatitis + cirrhosis
- CNS/neuro-> dystonia, dysarthria, motor symptoms, Parkinsonism (basal ganglia), mild depression, psychosis
- Eyes-> Kayser-Fleischer rings (copper in corneal membrane)
- Blood-> haemolytic anaemia
- Kidney-> renal tubular acidosis
- Bones-> osteopaenia
What can Kayser-Fleischer rings be a sign of?
Wilson disease
How is Wilson disease diagnosed?
- Liver biopsy-> gold standard
- Serum caerulopasmin-> protein carrying copper in blood (will be low)
- 24 hour urine assay-> raised
- Serum copper (low)
- MRI brain
How is Wilson disease managed?
Copper chelation + penicillamine + trientene
What is alpha-1 antitrypsin deficiency and what does it cause?
- A genetic condition causing a deficiency in an enzyme that protects the liver and lungs against neutrophil elastase
- Mutant protein causes trapping of proteins in liver-> cirrhosis + cancer
- Excess protease attacks lung connective tissue-> bronchiectasis + emphysema
What is the inheritance pattern for alpha-1 antitrypsin deficiency?
Autosomal recessive
How is alpha-1 antitrypsin deficiency diagnosed?
- Low serum A1AT
- Liver biopsy + acid-Schiff-positive staiing globules
- Genetic tests
- High resolution CT of lungs
How is alpha-1 antitrypsin deficiency managed?
- Stop smoking to decelerate emphysems
- Symptom control
- Organ transplant
- Monitor for HC cancer
What is primary biliary sclerosis?
Autoimmune condition in which small bile ducts of the liver are blocked causing cholestasis and hence fibrosis + cirrhosis + liver failure
What is the pathophysiology of primary biliary sclerosis?
- 1st intralobal ducts ie small bile ducts of liver (Canals of Hering) attacked by immune system
- Obstruction of bile flow-> cholestasis + back pressure-> fibrosis + cirrhosis + liver failure
- Bile acids + bilirubin + cholesterol excretes from bile ducts to intestines-> obstruction + blood build up as not excreted
How does primary biliary sclerosis present and why?
- Fatigue
- Pruritis-> bile acid
- Jaundice-> bilirubin
- GI disturbance (greasy stools + fat malabsorption)-> as bile acids help digest
- Pale stools-> if lack bilirubin
- Xanthelasma + xanthomas-> cholesterol deposits
- Increased CVD risk-> hypercholesterolaemia
What is primary biliary sclerosis associated with?
- Middle aged women
- Autoimmune disease
- Rheumatoid (RA, SS)
How is primary biliary sclerosis diagnosed?
- ALP raised first then liver enzymes + bilirubin raised later
- Anti-mitochondrial antibodies
- Other-> ESR, IgM, liver biopsy
How is primary biliary sclerosis treated?
- Ursodeoxycholic acid-> reduced cholesterol absorption in intestine
- Colestyramine-> binds to bile acids + prevent absorption in gut
- Immunosuppression
- Liver transplant
How does primary biliary sclerosis progress?
- May be asymptomatic for decades
- Can get advanced cirrhosis + portal HTN
What are some of the complications of primary biliary sclerosis?
Pruritis, steatorrhoea (fatty stools), distal renal tubular acidosis, hypothyroidism, osteoporosis, HC cancer
What is primary sclerosing cholangitis?
- When the intrahepatic or extrahepatic ducts stricture and fibrose causing obstruction of bile outflow and imflammation
- Can’t get out of liver to intestines-> hepatitis, fibrosis + necrosis
What are the causes of primary sclerosing cholangitis?
- Genetic or environmental
- Associated with ulcerative colitis
- Risk factors-> male, aged 30-40, UC, family history
What are the symptoms of primary sclerosing cholangitis?
Jaundice, chronic RUQ pain, pruritis, fatigue, hepatomegaly
How is primary sclerosing cholangitis diagnosed?
- MRCP-> gold standard
- MRI of liver, bile ducts and pancreas-> strictures + lesions
- LFTs-> cholestatic picture (ALP high + may be some ALT/AST derangement)
- Autoantibodies> P-ANCA, ANA etc
What are some of the associations/complications of primary sclerosing cholangitis?
Acute bacterial cholangitis, cholangiocarcinoma, colorectal cancer, cirrhosis, liver failure, fat soluble vitamin deficiency
How is primary sclerosing cholangitis managed?
- ERCP to dilate/stend strictures + improve flow
- Colestyramine-> bind to bild acid + prevent absorption in gut
- Liver transplant
- Monitor complications
What are the different types of liver cancer?
- Hepatocellular (80% primaries)
- Cholangiocarcinoma (20% of primary)
- Secondary-> mets
What are the risk factors for hepatocellular liver cancer?
Hepatocellular-> hepatitis B+C, alcohol, NAFLD, chronic liver disease
What are the risk factors for Cholangiocarcinoma?
- Primary biliary cholangitis
- Over 50’s
How does liver cancer present?
- Asymptomatic for long time + presents late
- Weight loss, abdominal pain, anorexia, N+V, jaundice, pruritis
How does Cholangiocarcinoma present?
- Painless jaundice
- Weight loss, N+V, pruritis etc
What are the investigations for hepatocellular cancer?
- Alpha-feto protein
- Liver US
- CT/MRI
What are the investigations for Cholangiocarcinoma?
- CA19-9
- Liver US
- CT/MRI
- ERCP + biopsy/brushings
How is hepatocellular cancer managed?
- Resect or transplant in early disease can cure
- Kinase inhibitors eg sorafenib-> inhibit cell proliferation
- Usually resistant to chemo + radiotherapy
How is Cholangiocarcinoma managed?
- Can cure with early resection
- ERCP-> stent + allow drainage
- Resists chemo + radiotherapy
What is a haemangioma?
- Benign liver tumour + often incidental findings
- Usually no symptoms or treatment required
What is focal nodular hyperplasia and what causes it?
- Benign liver tumour of fibrotic tissue
- Often oestrogen related eg OCP
- Asymptomatic + no treatment usually needed
What are the different types of liver transplant?
- Orthotopic-> entire liver from deceased donor
- Living donor-> portion
- Split donation-> one liver to two donations
What are the indications for liver transplant?
- Acute failure-> viral hepatitis + paracetamol OD
- Chronic failure
What are the contraindications to a liver transplant?
- Severe CKD of HF
- Excess weight loss or malnutrition
- Active hepatitis B or C
- End stage HIV
- Active alcohol use-> needs 6 months abstinence
What scar is typical of a liver transplant?
Rooftop or Mercedez-Benz scar
What treatment/care is provided post-liver transplant?
- Lifelong immunosuppression-> steroids, azathioprine, tacrolimus
- Lifestyle-> avoid alcohol,
- Monitor disease recurrence + cancer + rejection
How might liver transplant rejection present?
- Fever + jaundice + fatigue
- Abnormal LFTs
What is the pathophysiology of gastro-oeseophageal reflex disease?
- Stomach acid through the lower oesophageal sphincter-> irritates the lining
- Squamous epithelial lining (more sensitive) turns to columnar epithelium in stomach (protective)
How does gastro-oeseophageal reflex disease present?
Dyspepsia (indigestion), heartburn, acid regurgitation, retrosternal/epigastric pain, bloating, noctural cough, hoarse voice
What symptoms alongside dyspepsia warrant a 2 week wait (urgent) endoscopy?
- Anaemia (iron deficiency) or low Hb
- Loss of weight
- Anorexia
- Recent onset of progressive symptoms
- Melaena/haematemesis
- Swallowing difficulty (dysphagia)
- Aged 55 or over
How is gastro-oeseophageal reflex disease managed?
- Lifestyle-> reduce caffeine + alcohol, weight loss, avoid smoking, smaller meals + avoid food before bed, stay upright after meals
- Acid-neutralising medications-> gaviscon + rennies
- PPIs-> omeprazole/lansoprazole to reduce acid secretion
- H2 receptor antagonists-> ranitidine
- Laparoscopic fundoplication-> fundus of stomach around lower oesophagus to narrow lower sphincter
What is the pathophysiology of H.pylori infection?
- Gram negative bacteria living in stomach
- Damages epithelial lining cells via chemicals produced
- Avoids acid by forcing way into gastric mucosa + breaks it creates exposes epithelial cells under to acid
- Produces ammonia which neutralises acids-> ammonia directly damaged cells
- Causes gastritis, ulcers, increased stomach cancer risk
How is H.pylori infection investigated?
- Offered to anyone with dyspepsia-> have to e off PPIs for 2 weeks
- Urea breath test-> radiolabelled carbon 13
- Stool antigen test
- Rapid urease test ie campylobacter-like organism test-> biopsy during endoscopy and add urea-> converts to ammonia so alkaline pH test
How is H.pylori treated?
- Triple therapy with PPI + 2 antibiotics (eg amoxicillin + clarithromycin) for 7 days
- Urea breath test-> can use to see if eradicated
What is Barrett’s oesophagus?
- Metaplasia from squamous to columnar epithelium due to constant acid in lower oesophagus
- Premalignant-> risk factor for adenocarcinoma of the oesophagus
What can Barrett’s oesophagus put you more at risk of?
Adenocarcinoma of the oesophagus
How does Barrett’s oesophagus present?
Reflux symptoms then improvement
How does Barrett’s oesophagus transition to malignancy?
Barrett’s-> low grade dysplasia-> high grade-> adenocarcinoma
How is Barrett’s oesophagus treated?
- PPIs
- Ablation-> photodynamic, laser, cryotherapy to destroy epithelium + replace with normal cells
What is the pathophysiology behind peptic ulcers?
- Stomach/duodenum mucosa prone to breakdown of protective layer and increased stomach acid (eg stress, alcohol, caffiene, smoking, spicy food)
- Mucous and bicarb secreted from mucosa-> broken down by meds (steroids + NSAIDs) or H.pylori
What can increase the amount of stomach acid?
stress, alcohol, caffiene, smoking, spicy food
How do peptic ulcers present?
- Epigastric pain/discomfort, N+V, dyspepsia, iron deficiency anaemia, haematemesis, melaena
- Eating-> worsens pain (gastric) or improves (duodenal)
What type of peptic ulcer is most common?
Duodenal
What type of peptic ulcer is worsened by eating?
Gastric
What type of peptic ulcer is improved upon eating?
Duodenal
How are peptic ulcers managed?
- Endoscopy, rapid urease test (for H.pylori) + biopsy (malignancy)
- Treatment-> high dose PPI
- Monitoring-> endoscopy to ensure healing
What are the complications of peptic ulcers?
- Bleeding
- Perforation-> acute abdomen + peritonitis
- Pyloric stenosis due to scarring + stricture of muscles-> hard to empty contents
How does pyloric stenosis present and when can it occur in adults?
- Difficulty emptying contents-> abdo pain, distention, N+V after eating
- Can be a complication of peptic ulcers
What are the features of Chron’s disease?
Crows NESTS
- No blood or mucous (less common)
- Entire GI tract
- Skip lesions on endoscopy
- Terminal ileum (most affected) + transmural (full thickness inflammation)
- Smoking is a risk factor
- Others-> weight loss, strictures, fistulas, diarrhoea, abdominal pain
What are the features of ulcerative colitis?
CLOSEUP
- Continuous inflammation
- Limited to colon + rectum
- Only superficial mucosa affected
- Smoking is protective
- Excrete blood + mucus
- Use amino-salicylates
- Primary sclerosing cholangitis
- Others-> diarrhoea, abdominal pain, passing blood, weight loss
How is inflammatory bowel disease investigated?
- Bloods-> FBC (anaemia + infection), TFTs, U+Es, LFTs, CRP (raised when active)
- Faecal calprotectin-> released when intestines inflamed
- Endoscopy-> OGD + colonoscopy (diagnostic)
- Imaging-> US, CT, MRI etc for complications
How is Chron’s managed (to induce remission)?
- 1st line-> steroids ie oral prednisolone of IV hydrocortisone
- 2nd line (ie doesn’t work)-> azathioprine, methotrexate, infliximab etc
How is Chron’s managed (to maintain remission)?
- Azathioprine or mercaptopurine
- Some others can be used if doesn’t work
- Surgery-> resect distal ileum if only disease there, for strictures + fistulas if present etc
How is ulcerative colitis managed in a mild to moderate flare?
- 1st line-> aminosalicylates eg mesalazine
- 2nd line-> prednisolone
How is ulcerative colitis managed in a severe flare?
- 1st line-> IV hydrocortisone
- 2nd line-> IV ciclosporin
How is ulcerative colitis managed (maintaining remission)?
- Mesalazine, azathioprine or mercaptopurine
- Panproctocolectomy-> remove rectum + colon, ileostomy or J-pouch created
What is a J pouch?
Ileo-anal anastamosis-> ileum folded into rectum like structure
What is irritable bowel syndrome?
Abnormal bowel dysfunction with no organic cause
Who is IBS most common in?
- Women
- Young adults
What are the symptoms of IBS?
- Diarrhoea, constipation, fluctuating bowel habit, abdominal pain, bloating
- Symptoms worse after eating + improved after opening bowels
What is the diagnostic criteria for IBS?
- 2+ of abnormal stools, bloating, worsens after eating, PR mucous
- Abdominal pain relieved when open bowels
Exclude other pathology
- Bloods-> FBC, ESR, CRP
- Faecal calprotectin-> IBD
- Anti-TTG antibodies-> coeliac
- Cancer
How is IBS managed?
- Reassurance
- Healthy diet + exercise (eg FODMAP)
- Probiotic trial for 4 weeks
- Loperamine for diarrhoea
- Laxatives
- Antispasmodics-> Buscopan
- Tricyclic antidepressants or SSRIs
- CBT-> coping + distress
What is coeliac disease?
Inflammatory bowel caused by gluten
What is the pathophysiology of coeliac disease?
- Anti-tissue transglutaminase (anti-TTG) + anti-endomysial (anti-EMA) autoantibodies-> more active in active disease
- Target epithelial cells of intenstine
- Atrophy of intestinal villi + crypt hypertrophy (mainly in jejunum)-> malabsorption of nutrients + cause symptoms
What are the symptoms of coeliac disease?
- May be asymptomatic
- FTT, diarrhoea, fatigue, weight loss, mouth ulcers
- Anaemia-> iron, B12, folate deficiencies
- Dermatitis herpetiformis-> itchy blistering rash on abdomen
- Often linked with T1DM
- Rare neuro symptoms-> peripheral neuropathy, cerebellar ataxia, epilepsy
How is coeliac disease diagnosed?
-Should stay on gluten diet during investigation to detect antibodies
-Raised anti-TTG + anti-EMA
-Total IgA-> exclude deficiency
-
What conditions are associated with coeliac disease?
T1DM, thyroid disease, AI hepatitis, PBC, PSC
What are the complications of untreated coeliac disease?
Vitamin deficiencies, anaemia, osteoporosis, ulcerative jejunitis
-Cancers-> Non-Hodgkins lymphoma, enteropathy-associated T-cell lymphoma (EATL) of intestine, small bowel cancer
How is coeliac disease managed?
- Lifelong gluten free diet
- Check antibodies (monitoring)
