Gastrointestinal (4) Flashcards
Define volvulus
A twisting of a loop of bowel around itself and the axis of its surrounding mesentery. This can result in obstruction and ischaemia.
Mostly sigmoid, then caecal. Can have midgut volvulus neonatorum which occurs in neonates
Summarise the aetiology of volvulus
Pregnancy Constipation Long sigmoid colon Long mesentery Mobile caecum Adhesions Chagas disease Parasitic infections Malrotation (risk factor in neonates) Hirschsprung disease - causes severe consitpation
Summarise the epidemiology of volvulus
Sigmoid volvulus usually occurs in pregnant women or elderly patients
Caecal volvulus occurs in young adults
Midgut volvulus occurs in babies and young children due to malrotation of bowel - presents around 3 months
What are the presenting symptoms of volvulus?
Abdominal bloating/distension Severe colicky abdominal pain Constipation or absolute constipation Bloody stool Vomiting
What are the signs on physical examination of volvulus?
Palpable abdominal mass
Tinkling or absent bowel sounds
Abdominal distension
If perforation occurs: Fever Severe abdominal tenderness Lying very still Tachycardia Hypotension
Signs of dehydration:
Reduced skin turgor
Dry mucous membranes
What are the appropriate investigations for volvulus?
Erect CXR - check for perforation
AXR - coffee bean sign if sigmoid volvulus, foetus sign if caecal volvulus, see large or small bowel dilatation
Barium enema (CONTRAINDICATED IF RISK OF PERFORATION) - shows bird beak sign at site of obstruction
Sigmoidoscopy/colonoscopy
DRE
CT scan
Define primary biliary cirrhosis
An autoimmune chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis, fibrosis, and, ultimately, cirrhosis.
Summarise the aetiology of primary biliary cirrhosis
Autoimmune condition
Anti-mitochondrial antibodies (PDC-E2) attack the bile duct cells, leading to destruction and allowing bile to exit the ducts and move into the interstitium and blood
An environmental trigger may cause bile duct epithelial injury
This leads to a T-cell mediated AI response directed against bile duct epithelial cells
Summarise the epidemiology of primary biliary cirrhosis
More common in women 9:1
Peak age between 55-65
Affects middle aged women
What are the presenting symptoms of primary biliary cirrhosis?
Inisidious onset Fatigue Jaundice Pruritis Smelly, fatty, light coloured stool Weight loss Joint pain
Rarely, it may cause discomfort in the RUQ
May present with a complication of liver decompensation (jaundice, ascites, variceal haemorrhage)
May present with symptoms of associated conditions (e.g. Sjogren’s syndrome, arthritis, Raynaud’s phenomenon)
What are the signs on physical examination of primary biliary cirrhosis?
Early, there may be no signs Jaundice Skin pigmentation Scratch marks (indicates pruritis) Xanthomas (secondary to hypercholesterolaemia) Hepatomegaly Ascites Signs of chronic liver disease
What are the appropriate investigations of primary biliary cirrhosis?
LFTS:
Elevated conjugated bilirubin
Elevated ALP
Elevated GGT
ALT and AST - normally initially but will become abnormal as disease progresses
Albumin - decreased to indicate impaired liver function
PT - prolonged as impaired liver function
Anti-mitochondrial antibodies present
Polycloncal elevation of IgM and IgG
Hypercholesterolaemia
Abdo USS - shows no obstructive lesion within bile duct causing abnormal LFTs
Liver Biopsy:
Chronic inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes
Define viral hepatitis
Inflammation of the liver caused by one of the five hepatitis viruses.
Hepatitis A virus is an RNA virus, transmitted by the faecal-oral route. Prevalent in environments with improper hygiene and is common in travellers.
Hepatitis B virus is a DNA virus transmitted by percutaneous and permucosal routes - blood, bodily fluids and birthing.
Hepatitis C virus is an infectious, hepatotropic RNA virus belonging to the Flavivirus family.
Hepatitis D is transmitted by blood and body fluids and cannot be obtained without Hepatitis B infection.
Hepatitis E is spread by the faecal oral route and occurs in entermic areas. In pregnant woman it can cause fulminant hepatitis.
Summarise the epidemiology of viral hepatitis
Hepatitis A - faecal oral route, travellers, contaminated food and water
Hepatitis B - transmitted through blood and bodily fluid - IVDU, unprotected sex, blood transfusions, birthing
Hepatitis C - blood and bodily fluid
Hepatitis D requires HBV infection
Hepatitis E - faecal oral route, causes fulminant hepatitis in pregnant women
What are the risk factors for hepatitis A and hepatitis B/C?
Risk factors for Hepatitis A:
Living in endemic regions
Personal contact with infected person
Risk factors for Hepatitis B/C: Recipients of blood products IV drug users Tattooing Sexual activity
Summarise the epidemiology of viral hepatitis?
Hepatitis A:
Endemic in the developing world and infection often occurs sub-clinically
Less common in the developed world due to better sanitation
Age of exposure is higher in developed world
Common in travellers
Hepatitis B:
Common, causing 1-2 million deaths annually
Hepatitis C:
Common, with different genotypes having different geographical prevalence
What are the presenting symptoms of viral hepatitis?
Incubation period of HAV and HEV: 3-6 weeks
Incubation period of HBV is 3-6 months
HCV: 90% of acute infections are asymptomatic, 10% get jaundiced with mild flu-like illness
Jaundice RUQ pain Fever Fatigue Pruritis Dark urine Light coloured stool Nausea and vomiting Malaise Anorexia Headache
Hepatitis C:
Causes extrahepatic manifestations eg cryoglobulinaemia causing headaches, palpable purpura, arthritis
What are the signs on physical examination of viral hepatitis?
Jaundice
Hepatomegaly
Pyrexia
Splenomegaly
Cervical lymphadenopathy (in 10-20% of patients)
Occasionally: urticaria and maculopapular rash
Hepatitis B and C may have signs of chronic liver disease or decompensation - asterixis, bruising, dupytren’s, palmar erythema etc
Absence of stigmata of chronic liver disease in HAV (although spider naevi may be present)
What are the appropriate investigations for viral hepatitis?
LFTs: high AST, ALT, ALP and bilirubin (ALT GREATER THAN AST)
High ESR
Low albumin + high platelets (if severe)
Prolonged PT and PTT if severe
Viral Serology:
Hepatitis A:
Anti-HAV IgM (acute)
Anti-HAV IgG (recovery phase and lifelong persistence)
Hepatitis B:
HBsAg, IgM anti-HBcAg, HBeAg, HBV DNA - acute
Anti-HBs, total antiHBc - chronic
Hepatitis C:
HCV IgM - acute
HCV IgG - chronic or past exposure
Hepatitis E:
Anti-HEV IgM (raised 1-4 weeks after onset)
Urinalysis: Positive for bilirubin and raised urobilinogen
Liver biopsy: in HBV and HCV to assess liver disease
What is the appropriate management for viral hepatitis?
Hepatitis A - fluids, bed rest, symptomatic treatment eg antipyretics, antiemetics, cholestyramine for severe pruritis, vaccination
Hepatitis E - fluids
Hepatitis B:
HEP B IS A NOTIFIABLE DISEASE
Acute: Symptomatic treatment (antipyretics, antiemetics and cholestyramine) and bed rest.
Chronic: interferon alpha (standard or pegylated) is given.
Hepatitis C: Pegylated interferon-alpha and ribavirin (guanosine nucleotide analogue).
What are the possible complications of viral hepatitis?
Hepatitis A:
Fulminant hepatic failure (more common in pregnant women)
Cholestatic hepatitis with prolonged jaundice and pruritus can develop after HAV infection
Post-hepatitis syndrome: continued malaise for weeks to months
Hepatitis B:
1% get fulminant hepatic failure
CHRONIC HBV INFECTION IN NEONATES (10% of adults, much higher in neonates)
CIRRHOSIS
EXTRAHEPATIC immune complex disorders (e.g. glomerulonephritis, polyarteritis nodosa)
Hepatocellular carcinoma
Hepatitis C: Fulminant hepatic failure Chronic carriage of HCV HEPATOCELLULAR CARCINOMA Less common: porphyria cutanea tarda, cryoglobulinaemia, glomerulonephritis
HEPATITIS E = FULMINANT HEPATITIS IN PREGNANT WOMEN
Summarise the prognosis of viral hepatitis
HAV: Recovery is usually within 3-6 weeks. Occasionally patients may relapse during recovery. There are no chronic sequelae.
Fulminant hepatic failure has a mortality of 80%.
HBV: 10% of infections become chronic. Of the chronic infections, 20-30% will develop cirrhosis.
HCV: 80% of exposed will progress to chronic carriage. Of these, 20-30% will develop cirrhosis over 10-20 years.
Define portal hypertension
An increased pressure in the hepatic portal vein - clinically significant when >10mmHg
Summarise the aetiology of portal hypertension
Restriction of blood flow through hepatic portal vein and into IVC causes back flow of blood and pressure build up
The most common cause is cirrhosis
Pre-hepatic causes: Blockage of hepatic portal vein due to: Congenital stenosis Portal vein thrombosis Splenic vein thrombosis Extrinsic compression
Hepatic:
Cirrhosis
Schistomiasis
Sarcoidosis
Post-hepatic:
Right heart failure
Constrictive pericarditis
Budd-Chiari syndrome
Summarise the epidemiology of portal hypertension
It is a common complication of cirrhosis
What are the presenting symptoms of portal hypertension?
Jaundice if due to cirrhosis Haematemesis Melana Distended abdomen Distended abdominal veins Abdominal pain and fever - spontaneous bacterial peritonitis
Symptoms of hepatic encephalopathy: Confusion Nausea Fatigue Changes in sleep
What are the signs on physical examination of portal hypertension?
Caput medusae
Ascites
Altered consciousness if hepatic encephalopathy
Splenomegaly
Signs of liver failure: Aterixis Bruising Clubbing Dupytren's contracture Palmar erythema Fetor hepaticus Gynaecomastia Spider naevi Jaundice Testicular atrophy
What are the appropriate investigations for portal hypertension?
Hepatic venous pressure gradient measurement
Upper GI endoscopy - eosophageal varices
Abdominal USS - liver and spleen size, portal blood flow, cirrhosis
Doppler USS
Liver CT/MRI - if other imaging methods inconclusive - ascites, cirrhosis, splenomegaly, IVC dilatation
Investigations to identify cause: Viral serology Autoantibodies - ANAs, ASMA for autoimmune hepatitis LFTs Clotting - prolonged PT is sign of liver failure Ferritin: haemochromatosis alfa1-antitrypsin levels Caeruloplasmin: Wilson's disease
Liver Biopsy if indicated
What is the appropriate management of portal hypertension?
Ascites - sodium restriction, diuretics
Treatment of oesophageal varices if present - sclerotherapy, variceal ligation, balloon tamponade, octreotide
Non-selective beta-blockers: reduces portal pressure and reduces risk of variceal bleeding
Terlipressin: can reduce portal venous pressure
Transjugular Intrahepatic Portosystemic Shunt (TIPS): surgical shunt placed between the hepatic portal vein and the hepatic vein to ease congestion in the portal vein
Liver transplant
What are the possible complications of portal hypertension?
Portosystemic shunts
Bleeding oesophageal varices - haematemesis
Bleeding rectal varices - meleana
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Ascites complications: hepatorenal syndrome, hepatic hydrothorax
Pulmonary complications:
Porto-pulmonary hypertension
Hepatopulmonary syndrome: triad hepatic dysfunction, hypoxaemia, extreme vasodilation (intrapulmonary vascular dilatation)
Liver failure
Cirrhotic cardiomyopathy
Summarise the prognosis of portal hypertension
Depends on the underlying cause
Variceal haemorrhages have a 1-year mortality of 40%
Define ulcerative colitis
A type of inflammatory bowel disease with a relapsing and remitting nature, involving mucosal and submucosal inflammation from the rectum moving proximally through the colon.
Summarise the aetiology of ulcerative colitis
Aetiology unknown
Genetic factors - often family history present - HLA-DRB1
Environmental factors eg diet, stress often involved in flares
T cell destruction of large intestinal lining cells
Often associated with pANCA and primary sclerosing cholangitis
Summarise the epidemiology of ulcerative colitis
Often affects young women
More common in Caucasians and Eastern European Jews
Uncommon before the age of 10 years
Peak onset: 20-40 years
Equal sex ratio up to the age of 40 years (higher in males from then on)
What are the presenting symptoms of ulcerative colitis?
Bloody diarrhoea Weight loss Mucous diarrhoea Fatigue Fever LLQ pain Cramping Bloating Tenesmus Feacal urgency
Extraintestinal symptoms: Uveitis Episcleritis Pyoderma gangrenosum Erythema nodosum Arthritis
What are the signs on physical examination of ulcerative colitis?
Pallor Erythema nodosum LLQ tenderness Abdominal distension Fever Dehydration Clubbing Tachycardia Blood, mucus and tenderness on PR examination
What are the appropriate investigations for ulcerative colitis?
FBC - macrocytic, megaloblastic anaemia Iron studies - iron deficiency anaemia ESR/CRP - elevated Albumin - decreased Faecal calprotectin - elevated Stool studies - negative culture AXR - rule out toxic megacolon
Colonoscopy and biopsy: Crypt abscesses Neutrophils Ulcers Paneth cells in descending colon Lead pipe colon NO granulomas Mucosal and submucosal inflammation
Barium Enema: Shows mucosal ulceration with granular appearance and filling defects (due to pseudo polyps). Narrowed colon and loss of haustral pattern – leadpipe appearance. Colonoscopy and barium enema may be DANGEROUS during an acute exacerbation - risk of perforation.
What is the appropriate management of ulcerative colitis?
Depends on severity of disease
Acute Exacerbation: IV rehydration, IV corticosteroids and bowel rest Parenteral feeding may be necessary Antibiotics If toxic megacolon - proctocolectomy
Mild Disease:
Oral or rectal anti-inflammatories - 5-ASA derivatives (e.g. mesalazine, olsalazine, sulphasalazine) and/or rectal steroids.
Moderate to Severe Disease:
Oral steroids
Oral 5-ASA
Immunosuppression (with azathioprine, cyclosporine, 6-mercaptopurine OR biologics - infliximab (anti-TNF monoclonal antibody)
Advice:
Patient education and support.
Treat complications
Regular colonoscopic surveillance
Surgical: If medical treatment fails, presence of complications or to prevent colonic carcinoma - colectomy
What are the possible complications of ulcerative colitis?
Toxic megacolon Strictures Colorectal cancer - adenocarcinoma Perforation Infection Pseudopolys Primary sclerosing cholangitis GI haemorrhage
Extra-gastrointestinal Manifestations: Uveitis, renal calculi, arthropathy, sacroiliitis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, osteoporosis (from chronic steroid use), amyloidosis
Summarise the prognosis of ulcerative colitis
Only colectomy is curative
Colonic adenocarcinoma develops in 3-5% of population
Most common cause of death is toxic megacolon
Normal life expectancy
Poor prognostic factors: Low albumin (< 30 g/L) PR blood Raised CRP Dilated loops of bowel 8+ bowel movements per day Fever
Define Wilson’s disease
An autosomal recessive disease of ATP7B, leading to impaired transport and biliary excretion of copper, leading to copper deposition particularly in the brain, liver and cornea.
Summarise the aetiology of Wilson’s disease
An autosomal recessive mutation in the ATP7B protein on the long arm of chromosome 13 prevents (copper transporting protein in hepatocytes)
Prevents copper transport into bile for excretion
