Gastrointestinal Flashcards
What is the function of the liver?
Glucose and fat metabolism
Detoxification and excretion (bilirubin, ammonia, drugs/hormones/ pollutants)
Protein synthesis (albumin, clotting factors)
Defense against infection (R-E system)
What are the different types of liver injury?
Acute - can lead to recovery or liver failure.
Results in damage to and loss of cells. Cell death may occur by necrosis (associated with neutrophils), or apoptosis.
Chronic - can lead to recovery, cirrhosis, liver failure, varices, hepatoma.
Leads to fibrosis. Most severely cirrhosis – wide fibrous septa join the portal tracts and central veins, leaving nodules of liver cells to attempt regeneration if the causative insult has been removed.
What can cause acute liver injury?
Viral (A,B, E, EBV) Drug Alcohol Vascular Obstruction Congestion
What can cause chronic liver injury?
Alcohol
Viral (B,C)
Autoimmune
Metabolic (iron, copper)
How does acute liver injury present?
Malaise, nausea, anorexia, jaundice
Rarer: confusion, bleeding, liver pain, hypoglycaemia
How does chronic liver injury present?
Ascites, peripheral oedema, haematemesis (varices), malaise, anorexia, wasting easy bruising, itching, hepatomegaly, abnormal LFTs
Rarer: jaundice, confusion
What are serum ‘liver function tests’ and what do they tell us?
- Serum bilirubin, albumin, prothrombin time (give some index of liver function)
- Serum liver enzymes:
cholestatic: alkaline phosphatase, gamma-GT
hepatocellular: transaminases (AST, ALT)
(give no index of liver function)
What are the different types of jaundice?
Jaundice is rasied serum bilirubin
- Unconjugated - pre-hepatic due to Gilberts syndrome or Haemolysis
- Conjugated (Cholestatic) - hepatic or post hepatic due to liver disease (hepatic) or bile stone obstruction (post hepatic)
How does unconjugated and cholestatic jaundice present?
Unconjugated: normal urine and stools, no itching, normal liver tests
Cholestatic: dark urine, pale stools, may have itching, abnormal liver tests
Which might be some of the causes of liver disease?
Hepatitis - Viral, Drug, Immune, Alcohol
Ischaemia
Neoplasm
Congestion
What might be some of the causes of liver obstruction?
Gallstone from the bile duct or gallbladder
Area of malignancy, ischemia, inflammation
Blocked stent
What are the investigation done in jaundice?
Liver enzymes: Very high AST/ALT suggests liver disease, some exceptions
Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultrasound
Need further imaging: CT, Magnetic resonance cholangioram (MRCP), Endoscopic retrograde cholangiogram (ERCP)
What questions would you ask to identify the cause of jaundice?
Dark urine, pale stools, itching?
Biliary pain, rigors, abdomen swelling, weight loss?
Past history of biliary disease/intervention, malignancy heart failure, blood transfusion, autoimmune disease
Drug history: anything new?
Social history: potential hepatitis contact - travel, irregular sex, certain foods
Family history rarely helpful
What is characteristic of gallstones?
Most form in gallbladder
Very common: 1/3 women over 60
70% Cholesterol, 30% pigment+/- calcium
Risk factors: Female, fat, fertile, fifty
(liver disease, ileal disease, TPN, clofibrate…)
Most are asymptomatic
How do you manage gallstones?
Laporoscopic cholecystectomy (day case) Bile acid dissolution therapy (<1/3 success)
How do you manage bile stones?
ERCP with sphincterotomy and removal (basket or balloon), crushing (mechanical, laser) or stent placement
Surgery (large stones)
How common is drug-induced liver injury?
Onset usually 1-12 weeks of starting
30% of Acute Hepatitis
>65% of Acute Liver Failure
- 50% Paracetamol
- 15% idiosynchratic
Commonest reason for drug withdrawal from formularyWhat are the types of drug-induced liver injury?
Hepatocellular
Cholestatic
Mixed
What are the usual causes of drug-induced liver injury?
Antibiotics (Augmentin, Flucloxacillin, Erythromycin, Septrin, TB drugs)
CNS Drugs (Chlorpromazine, Carbamazepine Valproate, Paroxetine)
Immunosupressants
Analgesics/musculoskeletal (Diclofenac)
Gastrointestinal Drugs (PPIs)
Dietary Supplements
Polypharmacy
How can paracetamol cause liver damage?
Liver damage results not from paracetamol itself, but from one of its metabolites, N-acetyl-p-benzoquinone imine (NAPQI). NAPQI decreases the liver’s glutathione and directly damages cells in the liver by oxidative stress.
How to manage paracetamol induced hepatic failure?
N acetyl Cysteine (NAC) causes glutathione conjugation to give stable metabolites. Supportive treatment to correct: coagulation defects fluid electrolyte and acid base balance renal failure hypoglycaemia encephalopathy
When is paracetamol induced hepatic failure classed as severe?
Late presentation (NAC less effective >24 hr)
Acidosis (pH <7.3)
High prothrommbin time
High serum creatinine
Consider emergency liver transplant, otherwise 80% mortality
What are spider naevi?
Type of swollen blood vessels found slightly beneath the skin surface, often containing a central red spot and reddish extensions which radiate outwards like a spider’s web.
Allowed up to 5 spider naevi before there is concern
Compress, and then fill from the centre after pressure is released
What are the potential causes of ascites?
Chronic liver disease (mostly) +/- Portal vein thrombosis, Hepatoma, TB
Neoplasia (ovary, uterus, pancreas…)
Pancreatitis
Cardiac causes (heart failure)
How is ascites managed?
Fluid and salt restriction
Diuretics Spironolactone
\+/- Furosemide
Large-volume paracentesis + albumin
Trans-jugular intrahepatic portosystemic shunt (TIPS)What is Alcoholic Liver Disease?
Main cause of liver death in UK
However, only 10-20% of heavy alcohol drinkers drinkers get serious ALD
Often not alcohol dependent (‘alcoholics’)
25% will stop drinking and 25% will reduce
Poor outcome – 10 year survival 25%
What is portal hypertension?
An increase in the blood pressure within a system of veins called the portal venous system. Veins coming from the stomach, intestine, spleen, and pancreas merge into the portal vein, which then branches into smaller vessels and travels through the liver.
Increased hepatic resistance
Increased splanchnic blood flow
What causes portal hypertension?
Cirrhosis, fibrosis, portal vein thrombosis
What can portal hypertension cause?
Varices (oesophageal, gastric)
Splenomegaly
Should liver transplants be given to patients with alcoholic liver disease?
100 of total of 700 transplants/year in UK -limited by supply of livers
Negative public attitudes
But: post transplant survival similar to that for other liver diseases
Drinking relapse –variable; recurrent ALD uncommon
What are the potential consequences of chronic liver disease?
Constipation
Drugs - sedatives, analgesics
- NSAIDs, diuretics, ACE blockers
Gastrointestinal bleed
Infection (ascites, blood, skin, chest)
HYPO: natraemia, kalaemia, glycaemia
Alcohol withdrawal (not typically)
Other problems (cardiac, intracranial)
Malnutrition
Coagulopathy
Endocrine changesWhy are liver patients vulnerable to infection?
Impaired reticulo-endothelial function
Reduced opsonic activity
Leucocyte function
Permeable gut wall
What is Spontaneous bacterial peritonitis?
Commonest serious infection in cirrhosis
Vague symptoms
Based on neutrophils in ascitic fluid
Gram stain often neg; use blood culture bottles
After 1 episode patients should have antibiotic prophylaxis and consider liver transplantation
What are the potential causes of renal failure in liver disease?
Drugs: Diuretics, NSAIDS, ACE Inhibitors, Aminoglycosides Infection GI bleeding Myoglobinuria Renal tract obstruction
What is Hepatic encephalopathy?
A decline in brain function that occurs as a result of severe liver disease.
Consequences: infection, GI bleed, constipation, hypokalaemia, drug (sedatives, analgesics)
What bedside talking tests would you do for encephalopathy?
Serial 7’s WORLD backwards Animal counting in 1 minute Draw 5 point star Number connection test
What are the 2 different types of cirrhosis?
If these nodules remain small the result is a micronodular cirrhosis. If they are able to regenerate, they may become large, giving a macronodular cirrhosis. The constant replication of hepatocytes in this condition make them liable to replication errors, which may result in neoplasia developing. Hepatocellular carcinoma is a risk in patients with long-standing cirrhosis.
What drugs would you prescribe in liver disease?
Analgesia: sensitive to opiates, NSAIDs cause renal failure, paracetamol safest
Sedation: use short-acting benzodiazepines
Diuretics: excess weight loss, hyponatraemia, hyperkalaemia,renal failure
Antihypertensives: avoid ACE inhibitors
Aminoglycosides: avoid
How would you treat the consequences of liver disease?
Malnutrition: naso-gastric feeding
Variceal bleeding: endoscopic banding, propranolol, terlipressin
Encephalopathy: lactulose
Ascites / oedema: salt / fluid restriction, diuretics, paracentesis
Infections: antibiotics
What are the causes of chronic liver disease?
Alcohol
Non Alcoholic Steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune: autoimmune hepatitis, primary biliary cirrhosis, sclerosing cholangitis
Metabolic: haemochromatosis, Wilson’s, antitrypsin deficiency…
Vascular: Budd-Chiari (rare condition that occludes the hepatic veins)
How would you investigate chronic liver disease?
Viral serology - hepatitis B surface antigen, hepatitis C antibody
Immunology - autoantibodies AMA, ANA, ASMA,coeliac antibodies, immunoglobulins
Biochemistry - iron studies, copper studies, 1-antitrypsin level, lipids, glucose
Radiological investigations - pelvic ultrasound / CT / MRI
What is autoimmune hepatitis?
Autoimmune hepatitis is liver inflammation that occurs when your body’s immune system turns against liver cells.
Can lead to cirrhosis and eventually liver failure.
70-75% women
ANA, ASMA- positive in about 70%
Aggressive disease, 30% have cirrhosis at presentation
90%: dramatic response to prednisolone and azathioprine
What is Primary Biliary Cholangitis/Cirrhosis?
A chronic disease in which the bile ducts in your liver are slowly destroyed.
90% women
Pathogenesis unknown
+ve AMA in 95% of patients
Many patients have progressive disease
Mayo Clinic prognostic score: uses bilirubin albumin and prothrombin time
What are the common symptoms of Primary Biliary Cholangitis/Cirrhosis?
Asymptomatic lab abnormalities Itching and/or fatigue Dry eyes Joint pains Variceal bleeding Liver failure: ascites, jaundice
How would you treat a cholestatic itch?
UDCA, antihistamines - little help
Cholestyramine helps in 50% of cases
Rifampicin effective; occasionally damages liver
Opiate antagonists
Also: ultraviolet light, plasmapheresis, liver transplantation
What effects does Ursodeoxycholic acid have in Primary Biliary Cholangitis/Cirrhosis?
Improvement in liver enzymes and bilirubin
Subtle reduction in inflammation; but not fibrosis
Reduced portal pressure and rate of variceal development
Modestly reduced rate of death or liver transplantation
No improvement in itching (may worsen it)
What is Primary Sclerosing Cholangitis?
Leads to strictures (areas of narrowing) ± gallstones
Over 50% have inflammatory bowel disease
Presents as itching, pain ± rigors, jaundice
Raised Alk phos and gamma-glutamyl transpeptidase
10% develop cholangiocarcinoma (bile duct cancer)
Ursodeoxycholic Acid: unclear benefits
Good results from Liver Transplantation
What is Haemochromatosis?
Genetic disorder
90% have mutations in HFE gene: C282Y, H63D
Autosomal recessive
Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas
Diagnosis suggested by raised ferritin and transferrin saturation, confirmed by HFE genotyping and liver biopsy
When cirrhosis present, increased risk of hepatocellular carcinoma
Iron removal may lead to regression of fibrosis
What are the signs and symptoms of Haemochromatosis?
Chronic fatigue Diabetes mellitus Melanoderma Skin dryness Joint pain Osteoporosis White, flat nails Hepatomegaly Cirrhosis Heptaocellular carcinoma
What is a1-antitrypsin deficiency?
Results in inability to export a1-antitrypsin from liver
Can lead to liver disease (protein retention in liver), emphysema (protein deficiency in blood)
Phenotypic expression is variable: neonatal jaundice, chronic liver disease in adults
No medical treatment
What is Hepatocellular carcinoma?
Primary liver tumour
Most occur in patients with cirrhosis
Risk: highest for hepatitis B,C, haemochromatosis
lower: cirrhosis from alcoholic, autoimmune disease
Males >Females
May present with decompensation of liver disease, wt loss ascites, or abdominal pain
Treatment: Transplantation, resection or local ablative therapies, Sorafenib recently shown to prolong life
What is Non-alcoholic fatty liver (NAFL) disease?
Risk factors: Obesity, diabetes, hyperlipidaemia
Usually no symptoms; liver ache in 10%
Commonest cause of mildly elevated LFTs
Fat, sometimes with inflammation, fibrosis (NASH)
Need biopsy to distinguish NAFL from Nonalcoholic steatohepatitis
Still no effective drug treatments
Weight loss works- the more the better
What causes Hepatic vein occlusion?
Thrombosis (Budd-Chiari syndrome)
Membrane obstruction
Veno-occlusive disease (irradiation, antineoplastic drugs)
How might Hepatic vein occlusion present?
Abnormal liver tests
Ascites
Acute liver failure
How is Hepatic vein occlusion treated?
Anticoagulation
Transjugular intrahepatic portosystemic shunt
What are the symptoms of acute hepatitis?
None or non-specific, e.g. malaise, lethargy, myalgia (muscle aching)
Gastrointestinal upset, abdominal pain (right upper quadrant)
Jaundice + pale stools / dark urine
What are the signs of acute hepatitis?
Tender hepatomegaly ± jaundice
± signs of fulminant hepatitis (acute liver failure)
e.g. bleeding, ascites, encephalopathy
Raised transaminases (ALT/AST»_space; GGT/ALP) ± raised bilirubin
What are the infective causes of acute hepatitis?
Viral: Hepatitis A, B ± D, C & E Human herpes viruses e.g. HSV, VZV, CMV, EBV Other viruses Non-viral: Spirochaetes, e.g. leptospirosis, syphilis Mycobacteria, e.g. M. tuberculosis Bacteria, e.g. bartonella Parasites, e.g. toxoplasma
What are the non-infective causes of acute hepatitis?
Drugs Alcohol Other toxins / poisoning Non-alcoholic fatty liver disease Pregnancy Autoimmune hepatitis Hereditary metabolic causes
What are the signs and symptoms of chronic hepatitis?
Can be asymptomatic or have non-specific symptoms only
May have signs of chronic liver disease:
clubbing, palmar erythema, Dupuytren’s contracture, spider naevi, etc.
Transaminases (ALT/AST) can be normal
What are the different types of chronic hepatitis?
Compensated: liver function maintained
Decompensated: coagulopathy; jaundice (↑bilirubin); low albumin; ascites (± bacterial peritonitis); encephalopathy
Other complications: hepatocellular carcinoma (HCC); portal hypertension (varices, bleeding)
What are the infective causes of chronic hepatitis?
Hepatitis B ± D, C (& E)
What are the non-infective causes of chronic hepatitis?
Drugs Alcohol Other toxins / poisoning Non-alcoholic fatty liver disease Autoimmune hepatitis Hereditary metabolic causes
What are the clinical aspects of Hepatitis A?
Short incubation period: 15 to 50 days (mean 28 days)
Usually symptomatic in adults:
Pre-icteric phase: constitutional symptoms + abdominal pain
Icteric phase (few days to 1 week after pre-icteric phase) - jaundice
Self-limiting: no chronic disease
100% immunity after infection
How is Hepatitis A managed?
Supportive:
Monitor liver function (INR, albumin, bilirubin, etc.)
in the case of acute liver failure, liaise with hepatology / liver transplant centre
Management of close contacts
Primary prevention: vaccination
How does Hepatitis A spread?
Faeco-oral transmission:
Person-to-person contact
Ingesting contaminated food or water
Risk factors: Travel Household contact Sexual contact Injecting drug use
How does Hepatitis E spread?
Zoonotic reservoir (pigs) Undercooked meat products
Contaminated food & water
What are the clinical aspects of Hepatitis E?
> 95% cases asymptomatic
Usually self-limiting acute hepatitis
Occasional acute-on-chronic liver failure (high mortality)
Extra-hepatic manifestations, e.g. neurological
Risk of chronic infection in immunosuppressed patients
e.g. transplant recipients, HIV patients
Rapid progression to cirrhosis
How is Hepatitis E managed?
Acute infection: Supportive
Monitor for fulminant hepatitis / acute-on-chronic liver failure:
Liaise with hepatology / liver transplant centre
Consider ribavirin
Chronic infection :
Reverse immunosuppression (if possible)
If persists, treat with ribavirin
How to prevent the spread of Hepatitis E?
Avoid eating undercooked meats
Vaccines in development
How does Hepatitis B spread?
Highly infectious blood-borne virus Blood Bodily fluids Transmission: Mother-to-child Sexual contacts Household contacts Iatrogenic Injecting drug use
How is Hepatitis B managed?
Supportive management
Monitor liver function (INR, albumin, bilirubin, etc.)
Rarely fulminant hepatitic failure: 0.1 to 0.5%
Oral nucleos(t)ide analogue (tenofovir, entecavir)
Liaise with hepatology / liver transplant centre
Management of close contacts - vaccinate!
What are the possible consequences of Hepatitis B?
Acute hepatitis B infection can spontaneously resolve (although may re-activate in immunosuppression)
Can lead to Chronic hepatitis B which can cause hepatocellular carcinoma or cirrhosis.
What are the treatment options for Hepatitis B?
Pegylated interferon-α 2a: immunomodulatory, weekly subcutaneous injection, 48 week long course, offers best chance of treatment-free control
Oral nucleos(t)ide analogues: Inhibit viral replication, One tablet once a day, High barrier to resistance, Minimal side effects, may be required lifelong
How can Hepatitis B be prevented?
Antenatal screening (HBsAg testing) of pregnant mothers
HBV vaccination administered to baby at birth and at 1, 2, 3, 4* and 12 months
Screening ± immunisation of sexual and household contacts
Universal childhood immunisation
Universal screening of blood products
Sterile equipment and universal precautions in healthcare
Immunisation of healthcare workers + other risk groups (e.g. MSMs, PWIDs)
What is hepatitis D?
Defective RNA virus: requires HBsAg to replicate
Transmitted via blood and body fluids
Can be acquired simultaneously with HBV
Alternatively acquired after HBV
- acute on chronic hepatitis
- accelerated progression to liver fibrosis
Test: Hepatitis D antibody: if positive, test HDV RNA
Treat: pegylated inteferon-α 48 to 96 weeks
What are Directly-acting antivirals?
Fixed dose combination of DAAs from 2 or 3 drug classes:
NS5A (-asvir), NS5B (-buvir) and NS3/4A protease (-previr) inhibitors
Sometimes co-administered with ribavirin (RBV)
High cure rates: >95% in non-cirrhotic patients
How can Hepatitis C be prevented?
No vaccine
Previous infection does not confer immunity, can be re-infected
Screening blood products
Universal precautions handling bodily fluids
Lifestyle modification, e.g. needle exchanges, etc.
Treatment and cure of “transmitters”, e.g. active PWIDs
What is the function of the gut bacteria?
- Bacterial enzymes deconjugate certain compounds within the enterohepatic circulation aiding reabsorption back across the intestinal wall (bilirubin, bile acids, cholesterol, drugs)
- Digestion of fibre
- Metabolism of certain vitamins (Vitamin K)
- Synthesis of Vitamin B12, folic acid & thiamine
- Interfere and compete with exogenous pathogens preventing infection
What is the gut microflora?
The intestinal microflora is a complex ecosystem
>400 species of bacteria
Predominantly anaerobes
Sparse microflora in the upper GI tract & luxuriant microflora in the lower GI tract.
How does the normal flora act as a protective measure against infection?
Stable normal flora produces antimicrobial substances (bacteriocins and short chain fatty acids) which discourage infection by:
Inhibiting overgrowth of endogenous pathogens
Preventing colonisation by exogenous pathogens.
Antibiotics can disrupt this balance increasing susceptibility to infections such as C.Difficile.
If normal barriers are breached - Peritonitis
What increases the risk of intraluminal infection?
Gastric acid kills most swallowed pathogens
The microbiome is protective against “alien invaders”, but is vulnerable to systemic antibiotics
Less gastric acid & use of broad spectrum antibiotics leads to increased risk of intraluminal infection
What are the main causes of diarrhoea?
Infective - Campylobacter, salmoella, HIV, bacterial or amoebic dysentry, cholera, systemic infections (sepsis, malaria..)
Inflammatory - Crohn’s disease, Ulcerative colitis
Loss of absorptive area - coeliac disease, bowel resection
Pancreatic disease - pancreatitis, cancer
Drugs - anitbiotics, magnesium, digoxin
Colon cancer
Systemic disease - Thyrotoxicosis, uraemia, carcinoid
Others - IBS, Gastrectomy
When trying to identify the cause of diarrhoea, what should you consider?
Onset/duration Characteristics of stool (blood, mucus, watery, fat content) Food/drink Travel/vaccinations Immunocompromised Occupation Hobbies (e.g fresh water swimming) Animal exposure Medications Unwell contacts
What causes viral diarrhoea?
50-70% of cases of diarrhoea in the UK are caused by viruses
Rotavirus (Children)
Norovirus (All age groups, major epidemics)
Rotavirus vaccine aged 8 & 12 weeks has led to a 70% reduction in cases!
Other causes: Campylobacter, shigella, salmonella, c.perfringens, staph aureus, e.coli, c. diff, parasites
What affect does the virus have on the gut in viral diarrhoea?
Damage mucosal architecture:
Shortening & damage to villi
Hyperplasia of crypts
Inflammatory exudate
What are the different types of bacterial diarrhoea?
Enterotoxin-mediated (Vibrio cholera, Enterotoxigenic E.coli):
Bacteria typically colonise the upper bowel
Produce enterotoxins, increases intracellular AMP, mucosal cells secrete fluid, watery voluminous diarrhoea & dehydration
Mucosal architecture remains intact
Invasive:(Shigella and campylobacter)
Typically affect the colon (shigella/campylobacter) or lower ilium (salmonella).
Penetrate the intestinal mucosa causing bloody mucoid stools.
Colitis marked by tenesmus (need to go but empty bowels)
What are the characteristics of cholera?
Vibrio cholerae, gram negative bacteria
Contaminated food and water (faecal-oral spread)
Cholera toxin causes profuse watery ‘rice water’ diarrhoea, vomiting and rapid dehydration.
15-20L faecal output daily
Tx: Doxycycline and fluids!
What is E coli?
Escherichia coli
1% of local GI microbiota in humans
Most serotypes harmless, some are pathogenic
Classified based on O, H & K antigens in the outer membrane, flagella & capsule (e.g. O157:H7)
What does E coli cause in a patient?
ETEC: EnteroToxigenic - LT and ST enterotoxin, Non invasive watery diarrhoea
EHEC: EnteroHaemorrhagic - Shiga-like toxin
Can cause Haemolytic Uraemic Syndrome (HUS)
EIEC: EnteroInvasive - Dysentry like illness
Similar to Shigella
EPEC: EnteroPathogenic
EAEC: EnteroAggregative
DAEC: Diffusely Adherent
LAST THREE: Watery diarrhoea due to adhesion to luminal wall, Non invasive
What is travellers diarrhoea?
Most common travel related illness
Bacteria (most common), viruses, protozoa
High risk destinations: Asia, Middle east, Africa, Mexico, Central and South America (>20% travellers affected)
3 or more unformed stools in 24hrs
+/-
Fever/nausea/ vomiting/cramps/bloody stools
(During or within 10 days of return from foreign travel)
What causes travellers diarrhoea?
Enterotoxigenic e.coli (30-70%) Campylobacter (5-20%) Shigella (5-20%) Non-typhoidal Salmonella (5%) V.parahaemolyticus (shellfish) Viral (10-20%) Protozoal (5-10% more chronic) Cholera
How would you investigate travellers diarrhoea?
Bloods
Inflammatory markers
Blood cultures
Stool tests Microscopy Culture Ova, cysts, parasites Toxin detection
How do you effectively manage diarrhoea?
Barrier nursing: side room, gloves and apron
Fluids
Electrolyte monitoring and replacement
Eg oral rehydration sachets, IV replacement
(↓potassium, ↕sodium, ↓magnesium, ↓phosphate)
Antiemetics
What are some of the red flags in diarrhoea?
Dehydration Electrolyte imbalance Renal failure Immunocompromise Severe abdominal pain
THINK OF CANCER Over 50 Chronic diarrhoea Weight loss Blood in stool FH cancer
What is Helicobacter pylori?
A gram negative bacteria found in stomach of over half the worlds population. Transmission is faecal oral, gastro/oral and oral/oral.
It lives within the mucus layer releasing virulence factors such as ureas which converts urea -> CO2 and ammonia which neutralizes stomach acid. Virulence factors released also damage the epithelial cells causing gastritis and ulceration.
Acquisition usually asymptomatic (but can cause nausea, vomiting and fever)
Ongoing symptoms – dyspepsia, epigastric pain, loss of appetite
What is acute cholangitis?
Bacteria infection of the biliary tract due to obstruction
Obstruction of common bile duct - stasis of bile - invasion of bacteria from duodenum eg e.coli - bacteraemia
Can be obstructed by stone, cancer, stricture, parasite (ascaris). Also infection can be introduced through intervention eg ERCP
Clinical diagnosis based on Charcot’s triad: jaundice, right upper quadrant pain, fever
What are the causes of a liver abscess?
Bacterial : Faecal flora eg E.coli, Klebsiella spp etc
Amoebic: Entamoeba histolytica
RUQ pain, fever, “PUO - pyrexia of unknown origin”
Seen on ultrasound or CT
Antibiotics and drainage
Hydatid: Echinococcus granulosus (dog tapeworm)
Insidious RUQ pain, eosinophilia
Rupture - anaphylactic shock!
Albendazole and PAIR (puncture-aspiration-injection-reaspiration)
What are the causes of peritonitis?
Medical – SBP (spontaneous bacterial peritonitis), PID (pelvic inflammatory disease), dialysis related, TB
Surgical – perforation of GIT eg trauma, appendicitis, cancer
Intestinal flora are prime cause of infection in the perioneal cavity when intestinal wall breached
Sterile – endometriosis, pancreatitis, FMF (familial Mediterranean fever), porphyria, hereditary angioedema
What is Enteric fever?
Systemic, potentially life threatening febrile illness common in areas of poor sanitation (faeco-oral spread).
High incidence in South Asia
Generalised/RLQ pain, high fever, bradycardia,
headache, myalgia, rose spots, constipation or
green diarrhoea.
Diagnosis: Blood culture/bone marrow aspiration
What are the complications of enteric fever?
GI bleed
Perforation / peritonitis
Myocarditis
Abscesses
What are the two major consequences of salmonella?
TYPHOIDAL: Causes Typhoid Fever & Paratyphoid Fever. Salmonella Typhi & Salmonella Paratyphi A, B & C
NON-TYPHOIDAL: Causes Gastroenteritis and food poisoning. All other salmonella serotypes.
How would you treat enteric fever?
Emergency surgery
Antibiotics! (IV Ceftriaxone)
Mortality reduced from 20% to less than 1% with antibiotics!
Typhoid Vaccine!
How can the bowel become obstructed?
In the lumen
In the wall of the bowel - contracting down on itself
Outside the wall of the gut - squashing it
What could cause intraluminar bowel obstruction?
Tumour – carcinoma – lymphoma Diaphragm disease Meconium ileus Gallstone ileus
How can the location of a bowel tumour effect the likelihood of obstruction?
Some can stay in the wall, others invade into the lumen.
Tumours on the right side of the colon = faeces is more liquidy, less likely to obstruct
Tumours on the left side of the colon = faeces is more solid, more likely to obstruct
How can diaphragm disease increase the risk of bowel obstruction?
An uncommon gastrointestinal abnormality typical of nonsteroidal anti-inflammatory drug (NSAID)-induced injury.
The disease is characterized by circumferential lesions of short length (<5 mm), located most commonly in the small intestine, causing multiple stenosis of the lumen.
What is Gallstone Ileus?
Gallstone in the small bowel causing obstruction
Gallbladder is inflamed and erodes through, allowing gallstones to pass into the bowel (not through the bile duct)
What could cause intramural bowel obstruction?
Inflammatory – Crohn’s disease – Diverticulitis Tumours Neural – Hirschsprung’s disease
How can Crohn’s disease cause obstruction?
Can affect anywhere from the mouth to the anus
Distinct granulomas
Fibrosis and squeezing down of the bowel which causes the obstruction
How can Diverticular disease cause obstruction?
Causes lots of inflammation and fibrosis
Barium enema can be used to visualise
Diverticula can go into the fat and cause obstruction
With a low fibre diet, increased pressure, weaknesses in the mucosa mean that they push through. Faeces can get stuck there. They can get inflamed and rupture.
If it ruptures you can get faecal peritonitis.
What could cause extraluminar bowel obstruction?
Adhesions
Volvulus
Tumour
– peritoneal deposits
How can Hirschsprung’s disease increase the risk of bowel obstruction?
Developmental disorder is a neurocristopathy (abnormal migration, differentiation, division or survival of neural crest cells) and is characterised by the absence of the enteric ganglia along a variable length of the intestine.
Causes obstruction as the stool cannot move through the bowel as it normally would.
How can adhesions increase the risk of bowel obstruction?
Bowel adhesions are irregular bands of scar tissue that form between two structures that are normally not bound together. The bands of tissue can develop when the body is healing from any disturbance of the tissue that occurs secondary to surgery, infection, trauma, or radiation.
Can cause adhesive small bowel obstruction.
Can be surgically cut.
How can volvulus increase the risk of bowel obstruction?
Volvulus occurs when a loop of intestine twists around itself and the mesentery that supports it, causing a bowel obstruction. Due to the high risk of recurrence, a bowel resection within two days is generally recommended. If the bowel is severely twisted or the blood supply is cut off, emergent surgery is required.
How can a peritoneal tumour increase the risk of bowel obstruction?
Optimal conditions for tumour growth and spread across the peritoneum.
Can cause extrinsic intestinal compression, endoluminal obstruction, intramural infiltration, or extensive mesenteric infiltration.
What are the symptoms of intestinal obstruction?
Anorexia Nausea Vomiting Distension Abdominal Pain Altered Bowel Habits - Constipation - Obstipation
What is the pathophysiology of mechanical obstruction in the small bowel?
Proximal dilatation: Increased secretions and swallowed air (small bowel) or bacterial fermentation (large bowel).
More dilatation leads to decreased absorption and therefore mucosal wall oedema.
Increased pressure means that intramural vessels compressed leading to ischaemia
What is the pathophysiology of mechanical obstruction in the large bowel?
The colon proximal to obstruction dilates
Increased colonic pressure leads to decreased mesenteric blood flow
Mucosal oedema - transudation of fluid and electrolytes - lumen.
The arterial blood supply compromised which can lead to mucosal ulceration and full thickness necrosis
Bacterial translocation – sepsis
If ileocaecal valve competent – The caecum - usual site of perforation
If ileocaecal valve incompetent –faeculent vomiting
What are the clinical signs of mechanical obstruction in the small bowel?
Increased secretions and distension
Anorexia, nausea, vomiting / distension with pain
Fluid and electrolyte imbalance- hypovolemia
Bacterial overgrowth faeculent vomiting
Untreated obstruction leads
- Ischaemia
- Necrosis
- Perforation
What is a colonic volvulus?
Axial rotation – at mesenteric attachments:
A 360° twist -a closed loop obstruction is produced.
Fluid and electrolyte shifts into the closed loop
Increase in pressure and tension - impaired colonic blood flow
Ischaemia, necrosis, and perforation of the loop of bowel
What aspects of abdominal pain should you consider?
Site Onset Character Radiation Association Time Course Exacerbation / Relieving factors Severity
What aspects of vomiting should you consider?
NATURE Forceful Regurgitation CONTENT Bilious Faeculent Coffee Ground / Altered Blood
How does large bowel obstruction present?
Less common -25% Intestinal obstruction - Functional obstruction (due to abnormal intestinal physiology) - Mechanical can be partial or complete Acute presentation (5 days of symptoms) - abdominal pain and obstipation, Chronic - a progressive change in bowel habits.
What is the epidemiology of small bowel obstruction?
60 to 75% of Intestinal Obstruction
0.1 to 5% - No previous surgery
60% - previous surgery
Inflammatory bowel disease – Crohns -25%
0.5% in first 2 year of life
What are the potential causes of large bowel obstruction?
Age and Race dependent - US/Europe – 90% colorectal malignancy - Age 70y ; Men and women equal 30% colorectal malignancy 5% Volvulus 3% strictures 2% rare causes – foreign bodies, hernia, abscess
African countries – 50% Volvulus
Children: Anatomical development, Imperforate anus, Hirshsprung disease
