Liver & GI Flashcards
How long does hepatitis persist for to be deemed chronic?
6 months.
What are the simple stages that precede liver failure?
Hepatitis → fibrosis → compensated cirrhosis → decompensated cirrhosis (end stage liver failure)
Give 3 infective causes of acute hepatitis.
Hepatitis A to E infection.
EBV.
CMV.
Toxoplasmosis.
Give 3 non-infective causes of acute and chronic hepatitis.
Alcohol.
Drugs.
Toxins.
Autoimmune.
Give 3 presentations of acute hepatitis.
- Malaise
- Nausea
- Anorexia
- Jaundice
Rarer:
1. Confusion
2. Bleeding
3. Liver pain
Give 3 infective causes of chronic hepatitis.
Hepatitis B (+/-D).
Hepatitis C.
Hepatitis E.
Give 3 presentations of chronic hepatitis
- Ascites
- Oedema
- Haematemesis (varices)
- Malaise
- anorexia
- wasting
- easy bruising
- itching
- hepatomegaly
Name 3 things that liver function tests measure.
- Serum bilirubin.
- Serum albumin.
- Pro-thrombin time.
What enzymes increase in the serum in hepatocellular liver disease?
Transaminases
What is jaundice
Raised serum bilirubin.
Can be prehepatic (unconjugated) ie haemolysis, Gilberts
Hepatic (conjugated) ie hepatitis: viral, drugs, immune, alcohol
Post-hepatic (conjugated) ie gallstone: bile duct, structure: malignant, ischaemic, inflammatory
Describe the urine, stools, itching, and liver in someone with pre-hepatic jaundice?
Urine and stools are normal. There is no itching and the LFT’s are normal.
Describe the urine, stools, itching, and liver in someone with post-hepatic jaundice?
Dark urine, stools may be pale. May be itching, abnormal LFT
Tests for jaundice?
Liver enzymes: very high AST/ALT suggests liver disease, some exceptions
Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultra sound
Need further imaging:
CT
MRCP
ERCP
Where are most gallstones formed?
Gallbladder
What are gallstones made up of?
70% cholesterol
30% pigment
+/- calcium
Risk factors for gallstones
5F’s
Female, fat, fertile, forty, Fair
Gallstones in gallbladder vs bile duct
Cholecystitis in gallbladder but not bile duct
Obstructive jaundice seen in bile duct and sometimes in gallbladder
Cholangitis seen in bile duct but not gallbladder
Pancreatitis seen in bile duct but not gallbladder
Gallstones management
If symptomatic:
Gallbladder stones:
- laparoscopic cholecystectomy
- Bile acid dissolution therapy (<1/3 success)
Bile duct stones:
- ERCP with sphincterotomy and removal crushing stent placement
- surgery (large stones)
What is isoniazid? What common side effect is there?
Isoniazid is commonly used to treat tuberculosis.
Common side effect: acute liver injury with jaundice
Drug induced liver injury is common. What question should you remember to ask in a patient history?
“What did you start recently?”
onset usually 1-12 weeks of starting
Name a drug that can cause drug induced liver injury.
- Augmentin.
- Flucloxacillin.
- Erythromycin.
- TB drugs.
- Acetaminophen
UK general practice DILI study: What drugs are found to be not involved in drug induced liver injury?
- Low dose aspirin
- NSAIDs other than Diclofenac
- Beta blockers
- HRT
- ACE inhibitors
- Thiazides
- CCBs
What enzyme is responsible for ‘mopping up’ reactive intermediates of paracetamol and so prevents toxicity and liver failure?
Glutathione transferase.
Management of paracetamol induced fulminant hepatic failure?
- N acetyl Cysteine (NAC)
- Supportive to correct
1. coagulation defects
2. fluid electrolyte and acid base balance
3. renal failure
4. hypoglycaemia
5. encephalopathy
What may indicate that paracetamol induced liver failure is severe?
Late presentation (NAC less effective >24 hours)
Acidosis (pH <7.3)
Prothrombin time >70 s
Serum creatinine > 300 umol/l
Consider emergency liver transplant: otherwise 80% mortality
What is ascites?
An accumulation of fluid in the peritoneal cavity that leads to abdominal distension.
Give 4 pathophysiological causes of ascites and an example for each.
- Local inflammation e.g. peritonitis.
- Leaky vessels e.g. imbalance between hydrostatic and oncotic pressures.
- Low flow e.g. cirrhosis, thrombosis, cardiac failure.
- Low protein e.g. hypoalbuminaemia.
Describe the pathogenesis of ascites.
- Increased intra-hepatic resistance leads to portal hypertension -> ascites.
- Systemic vasodilation leads to secretion of RAAS, NAd and ADH -> fluid retention.
- Low serum albumin also leads to ascites.
Ascites management?
- Restrict fluid and sodium
- Diuretics. - especially spironolactone +/- furosemide
- Drainage.
Stages of alcoholic liver disease?
- Drinking Alcohol leads to Steatosis (fatty liver, undamaged)
- Drinking more alcohol leads to inflammation
- Alcoholic hepatitis (with mallory bodies)
- Alcoholic Cirrhosis (micronodular)
- Hepatocellular carcinoma
What might be seen histologically that indicates a diagnosis of alcoholic liver disease?
Neutrophils and fat accumulation within hepatocytes.
What is non alcoholic steato-hepatitis (NASH)?
An advanced form of non-alcoholic fatty liver disease.
Give 3 causes of non-alcoholic fatty liver disease.
- Type 2 diabetes mellitus.
- Hypertension.
- Obesity.
- Hyperlipidaemia.
What is cirrhosis?
A chronic disease of the liver resulting from necrosis of liver cells followed by fibrosis. The end result is impairment of hepatocyte function and distortion of liver architecture.
Give 3 causes of cirrhosis.
- Alcohol!
- Hepatitis B and C.
- Any chronic liver disease e.g. autoimmune, metabolic, vascular etc.
What is the treatment of liver cirrhosis?
- Deal with the underlying cause e.g. stop drinking alcohol.
- Screening for HCC.
- Consider transplant.
Approximately what percentage of blood flow to the liver is provided by the portal vein?
75%
Portal hypertension can lead to varices. Explain why.
Obstruction to portal blood flow e.g. cirrhosis leads to portal hypertension. Blood is diverted into collaterals e.g. the gastro-oesophageal junction and so causes varices.
Give 3 causes of portal hypertension.
- Cirrhosis and fibrosis (intra-hepatic causes).
- Portal vein thrombosis (pre-hepatic).
- Budd-Chiari (post-hepatic cause).
What are the potential consequences of varices?
If they rupture ->haemorrhage.
What is the primary treatment for varices?
Endoscopic therapy - banding.
Why do patients with chronic liver disease ‘go off’?
Common causes:
1. Constipation
2. Drugs - sedatives, analgesics, NSAIDs, diuretics, ACE blockers
3. Gastrointestinal bleed
4. Infection
5. HYPO
6. Alcohol withdrawal
What is the commonest serious infection in those with cirrhosis?
Spontaneous bacterial peritonitis. It can also affect immunocompromised people and those undergoing peritoneal dialysis.
How can spontaneous bacterial peritonitis be diagnosed?
By looking for the presence of neutrophils in ascitic fluid.
What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important.
It is important to do an ascitic tap so you can rule out spontaneous bacterial peritonitis as soon as possible.
Describe the treatment for spontaneous bacterial peritonitis.
Cefotaxime and metronidazole.
Causes of renal failure in liver disease
Drugs:
1. diuretics
2. NSAIDs
3. ACE inhibitors
4. Aminoglycosides
Infection
GI bleeding
Myoglobinuria
Renal tract obstruction
Hepatic encephalopathy is a complication of liver failure. Describe the pathophysiological mechanism behind this.
The liver can’t get rid of ammonia and so ammonia crosses the BBB -> cerebral oedema.
Bedside tests for encephalopathy
Serial 7’s
WORLD backwards
Animal counting in 1 minute
Draw 5 point star
Number connection test
What 3 symptoms make up the triad of Wernicke’s encephalopathy?
- Ataxia.
- Opthalmoplegia.
- Confusion.
How can Wernicke’s encephalopathy be reversed?
Give IV thiamine.
What to do if a liver patient has ‘gone off’?
- ABC airways, breathing, circulation
- Look at chart - vital signs, O2, BM (glucose), drug chart
- Look at patient - focus of infection? Bleeding?
- Tests - FBC, U&E, blood cultures, ascitic fluid clotting, LFTs
What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?
IgG4.
How is autoimmune chronic pancreatitis treated?
It is very steroid responsive.
What is primary biliary cirrhosis?
An autoimmune disease where there is progressive lymphocyte mediated destruction of intra-hepatic bile ducts -> cholestasis -> cirrhosis.
Describe 2 features of the epidemiology of primary biliary cirrhosis.
- Females affected more than men.
- Familial - 10 fold risk increase.
Describe the pathophysiology of primary biliary cirrhosis.
Lymphocyte mediated attack on bile duct epithelia -> destruction of bile ducts -> cholestasis -> cirrhosis.
Give 3 diseases associated with primary biliary cirrhosis.
- Thyroiditis.
- RA.
3.Coeliac disease.
Lung disease.
(Other autoimmune diseases).
Give 5 symptoms of primary biliary cirrhosis.
- Itching.
- Fatigue.
- Dry eyes,
- Joint pains.
- Variceal bleeding.
What is the treatment for primary biliary cirrhosis?
Ursodeoxycholic acid; improves liver enzymes; reduces inflammation and portal pressure and therefore the rate of variceal development.
Treatment of cholestatic itch
Cholestyramine
UDCA, antihistamines - little help
Rifampicin effective - occasionally damages liver
Describe the pathophysiology of primary sclerosing cholangitis.
Inflammation of the bile duct -> strictures and hardening -> progressive obliterating fibrosis of bile duct branches -> cirrhosis -> liver failure.
Give 3 symptoms of primary sclerosing cholangitis.
- Itching.
- Rigor.
- Pain.
- Jaundice.
75% also have IBD.
What is biliary colic?
Gallbladder attack - RUQ pain due to a gall stone blocking the bile duct.
What can trigger biliary colic?
Eating a heavy meal especially one that is high in fat.
90% of people with haemochromatosis have a mutation in which gene?
HFE gene
Haemochromatosis is a genetic disorder. How is it inherited?
Autosomal recessive
Describe the pathophysiology of haemochromatosis.
Uncontrolled intestinal iron absorption leads to deposition in the liver, heart and pancreas -> fibrosis -> organ failure.
What protein is responsible for controlling iron absorption?
Hepcidin.
Levels of this protein are decreased in haemochromatosis.
How might you diagnose someone with haemochromatosis?
Raised ferritin.
HFE genotyping.
Liver biopsy.
Describe the mechanism by which alpha 1 anti-trypsin deficiency can lead to chronic liver disease.
Alpha 1 anti-trypsin deficiency results in protein retention in the liver -> eventually cirrhosis.
What is Budd-Chiari syndrome?
A vascular disease associated with occlusion of hepatic veins that drain the liver.
How does normal flora discourage infection?
- Inhibiting overgrowth of endogenous pathogens
- Preventing colonisation by exogenous pathogens.
What is normal flora?
The community of microorganisms that live on another living organism without causing disease.
Name 3 things that can increase the risk of intraluminal infections?
- Less gastric acid (drugs such as PPIs)
- Broad spectrum antibiotics
- Raised gastric pH
Is C. Difficile Gram positive or negative?
Gram positive spore forming bacteria
How is C. diff treated?
Metronidazole or oral vancomycin. Sometimes can be treated by faecal transplant
Name a complication of C. diff
Pseudomembranous colitis
Recurrence rate is 25%
Faecal transplant to restore normal flora
List 3 infective causes of diarrhoea
Campylobacter
Salmonella
HIV
bacterial or amoebic dysentery
cholera
Bacterial causes of watery diarrhoea?
Bacteria:
Vibrio cholerae
E.Coli (ETEC)
Clostridium perfringens
Bacillus cereus
Staph. aureus
Viral causes of watery diarrhoea
Virus:
Rotavirus
Norovirus
Parasitic causes of watery diarrhoea?
Parasites:
Giardia
Cryptosporidium
Bacterial causes of bloody, mucoid diarrhoea? List 3
Shigella
E.Coli (EIEC, EHEC)
Salmonella enteritidis
V.parahaemolyticus
Clostridium difficile
Campylobacter jejuni
Parasitic causes of blood, mucoid diarrhoea?
Entamoeba histolytica
In the UK what is the major cause of diarrhoea?
50-70% of diarrhoea caused by viruses - rotavirus, norovirus
Define diarrhoea
Three or more loose or unformed stools a day
Give 3 causes of traveller’s 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!
Which bacteria is the most common cause of traveller’s diarrhoea?
ETEC: enterotoxigenic E. coli
Which type of e.coli can cause bloody diarrhoea and has a shiga like toxin?
EHEC: EnteroHaemorrhagic
Which type of E. coli can cause dysentery like illness and is similar to Shigella?
EIEC: Enteroinvasive
Which E. colis’ are non invasive and cause watery diarrhoea due to adhesion to the luminal wall?
EPEC: EnteroPathogenic
EAEC: EnteroAggregative
DAEC: Diffusely Adherent
How would you describe cholera-related diarrhoea?
Profuse watery “rice water” diarrhoea up to 20L a day
How would you treat cholera infection?
Fluids and doxycycline
What is the gold standard for treating fluid loss as a result of acute diarrhoea?
Oral rehydration therapy
Name a helminth responsible for causing diarrhoeal infection.
Schistosomiasis.
List two stool tests a GP might request to help differentiate between the different causes of diarrhoea.
- Microscopy
- Stool culture
- PCR
- Ova, cysts, parasites
List 3 red flags of Diarrhoea?
Dehydration
Electrolyte imbalance
Renal failure
Immunocompromise
Severe abdominal pain
Cancer risk factors
Over 50
Chronic diarrhoea
Weight loss
Blood in stool
FH cancer
What can helicobacter pylori infection cause?
H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer.
How would you treat H. pylori infection?
Triple therapy: 2 antibiotics and 1 PPI e.g. omeprazole, clarithromycin and amoxicillin.
What is acute cholecystitis?
Inflammation of the gall bladder caused by blockage of the bile duct -> obstruction to bile emptying.
Give 3 symptoms of acute cholecystitis.
- Gallbladder inflammation
- cystic duct obstruction by gall stones
- RUQ or epigastric pain
- fever
- leucocytosis
How can acute cholecystitis be diagnosed?
Ultrasound
Treatment of acute cholecystitis
Treatment: IV fluids, analgesia and antibiotics
Surgery: Cholecystectomy
What is ascending cholangitis?
Obstruction of biliary tract causing bacterial infection. Regarded as a medical emergency.
Name the triad that describes 3 common symptoms of ascending cholangitis.
Charcot’s triad:
- Fever.
- RUQ pain.
- JAUNDICE (cholestatic)!
What investigations might you do in someone who you suspect might have ascending cholangitis?
Endoscopic retrograde cholangiopancreatography (ERCP)
Treatment of ascending cholangitis?
Prompt admission and IV antibiotics
ERCP
Cholecystectomy
What is the difference between ascending cholangitis and acute cholecystitis?
A patient with acute cholecystitis would not have signs of jaundice!
Where would the pain be located in someone with a liver abscess?
RUQ
Name a bacteria that can cause liver abscess?
Faecal flora eg E.coli, Klebsiella spp
Name an amoeba that can cause liver abscesses?
Entamoeba histolytica
Hydatid that can cause liver abscesses?
Echinococcus granulosus (dog tapeworm)
What is peritonitis?
Inflammation of the peritoneum often due to infection.
What can cause peritonitis?
- Bacterial infection due to a perforated organ; spontaneous bacterial peritonitis; infection secondary to peritoneal dialysis.
- Non-infective causes e.g. bile leak; blood from ruptured ectopic pregnancy.
Which bacteria causes enteric fever?
Salmonella (para)typhi
Where is the pain located in someone with enteric fever?
Generalised / R lower quadrant pain
Enteric fever symptoms
Generalised / R lower quadrant pain
High fever
“Relative bradycardia”
Headache and myalgia
Rose spots
Constipation/green diarrhoea
How is enteric fever diagnosed?
Through blood culture and bone marrow aspiration
Complications of enteric fever
GI bleed
Perforation/peritonitis
Myocarditis
Abscesses
Which organs count as upper GI
Oesophagus
Stomach
Duodenum
A patient presents with melaena for 3 days. What could this mean?
Melaena refers to the dark black faeces - associated with upper gastrointestinal bleeding.
What is haematemesis?
When a person begins to vomit blood
What is coffee ground vomiting?
As the name suggests, vomit that looks like coffee grounds. Can be a sign of internal bleeding
Likely causes of GI bleeding?
Peptic ulcer= most common (50%)
Oesophageal varices
Mallory-Weiss syndrome
Gastric carcinoma (uncommon)
How to manage patients with GI bleeds?
A B C D E
Airway
- is airway compromised
Breathing
- work of breathing
- need oxygen?
Circulation
- HR, BP
- Bloods
- IV fluids/blood transfusion?
Disability
- AVPU/GCS
- pupils
- blood sugar
Exposure
- active melaena/haematemesis
Do not forget to keep the patient nil by mouth
Scoring system for upper GI bleeds
Glasgow Blatchford Score
Score >0 means patient require admission for inpatient endoscopy
Score 0 means patient can be discharged
Most accurate in identifying risk patients in need of transfusion
How would you differentiate between variceal bleeds and non-variceal bleeds?
Variceal bleed:
1. suspect in patients with a history of liver disease of alcohol excess
2. antibiotics and Terlipressin reduces mortality
3. Endoscopy within 12 hours
Non-variceal bleed:
1. suspect in patients with a history of peptic ulcers, using certain medications; NSAIDs, anticoagulation or antiplatelets.
2. Consider proton pump inhibitors.
3. Endoscopy within 24 hours.
What is most important when it comes to GI bleeding?
Initial assessment and management rather than endoscopy in most cases
In the UK how often do you see upper GI bleeding?
Nearly one presentation every 6 minutes
= very common medical emergency
Endoscopy: How would you treat non variceal bleeds?
- Heater probe to cauterize it
- Hemoclip
Endoscopy: How would you treat variceal bleeds?
Banding - to cut the blood supply and stop bleeding
Name the 3 broad categories that describe the causes of intestinal obstruction.
- Blockage.
- Contraction.
- Pressure.
Intestinal obstruction: give 3 causes of blockage.
- Tumour.
- Diaphragm disease.
- Gallstones in ileum (rare)
Intestinal obstruction: what is thought to cause diaphragm disease?
NSAIDS.
Intestinal obstruction: give 3 causes of contraction.
- Inflammation.
- Crohn’s disease
- Diverticular disease - Intramural tumours.
- Hirschprung’s disease.
Describe how Crohn’s disease can cause intestinal obstruction.
Crohn’s disease -> fibrosis -> contraction -> obstruction.
Describe how Diverticular disease can cause intestinal obstruction?
Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction.
What is Hirschprung’s disease?
A congenital condition where there is a lack of nerves in the bowel and so motility is affected. This leads to obstruction and gross dilatation of the bowel.
What is small bowel obstruction?
Mechanical blockage of the small intestine.
Symptoms of bowel obstruction
- Pain
- Distension
- Vomiting
- Constipation
Causes of bowel obstruction
- Compression
- Occlusion
- Lack of peristalsis
Intestinal obstruction: give 3 causes of compression.
- Adhesions.
- Tumour
- Hernia
Intestinal obstruction: what are adhesions?
Adhesions often form secondary to abdominal surgery. Loops of bowel stick together and the bowel is pulled and distorted. 40% of intestinal obstructions are due to adhesions.
Intestinal obstruction: what causes adhesions?
Adhesions often form secondary to abdominal surgery.
Intestinal obstruction: give 3 luminal causes.
Growth - tumour
Foreign body - (digested or gallstone)
Structure - inflammatory, malignant, scarring
Intestinal obstruction: give 3 causes of lack of peristalsis
Drugs - opioids
Low electrolytes
Neurological
Severe illness / post operative
Signs of bowel obstruction upon examination
Distention
Tympanic
Tender
Hernias
Bowel sounds
Scars
PR
Consequences of bowel obstruction
Issues with:
Nutrition
GI viability
Gut barrier / translocation
Fluid loss
Investigations for bowel obstruction
Bloods
- FBC
- U&E
- CRP
- Lactate
Imaging
- AXR vs CT
Treatment for small bowel obstruction
Decompression
Fluid replacement
Electrolyte replacement
Nutrition
Stent
Surgery
Give 2 common causes of large bowel obstruction.
Colorectal malignancy.
2. Volvulus (especially in the developing world).
Give 5 symptoms of large bowel obstruction.
Tenesmus.
Constipation.
Abdominal discomfort.
Bloating.
Vomiting.
Weight loss.
What investigations might you do in someone who you suspect to have a large bowel obstruction?
Digital rectal examination.
Sigmoidoscopy.
Plain X-ray.
CT scan.
Describe the management for a large bowel obstruction.
Fast the patient.
Supplement O2.
IV fluids to replace losses and correct electrolyte imbalance.
Urinary catheterisation to monitor urine output.
Give 3 consequences of untreated intestinal obstructions.
Ischaemia.
Necrosis.
Perforation.
What cells normally line the oesophagus?
What cells normally line the oesophagus?
What is Barrett’s oesophagus?
When squamous cells undergo metaplastic changes and become columnar cells.
What can cause Barrett’s oesophagus?
- GORD.
- Obesity.
Describe how Barrett’s oesophagus can lead to oesophageal adenocarcinoma.
GORD damages normal oesophageal squamous cells.
Glandular columnar epithelial cells replace squamous cells (metaplasia).
Continuing reflux leads to dysplastic oesophageal glandular epithelium.
Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
Give 5 symptoms of oesophageal carcinoma.
Dysphagia.
Odynophagia (painful swallowing).
People often present very late.
Vomiting.
Weight loss.
Anaemia.
GI bleed.
Reflux.
Give 3 causes of squamous cell carcinoma.
Smoking.
Alcohol.
Poor diet
What can cause oesophageal adenocarcinoma?
Barrett’s oesophagus
What can cause oesophageal squamous carcinoma?
Smoking.
Alcohol.
What investigations might you do in someone who you suspect to have oesophageal carcinoma?
- Barium swallow.
- Endoscopy.
Describe the 2 treatment options for oesophageal cancer.
Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery.
Medically unfit and metastases = palliative care. Stents can help with dysphagia.
Give 3 causes of gastric cancer.
Pickles.
H.pylori infection.
Smoked foods.
Pernicious anaemia.
Describe how gastric cancer can develop from normal gastric mucosa.
Smoked/pickled food diet leads to intestinal metaplasia of the normal gastric mucosa. Several genetic changes lead to dysplasia and then eventually intra-mucosal and invasive carcinoma.
Give 3 signs of gastric cancer.
Weight loss.
Anaemia.
Vomiting blood.
Melaena.
Dyspepsia.
A mutation in what gene can cause familial diffuse gastric cancer?
CDH1 - 80% chance of gastric cancer.
Prophylactic gastrectomy is done in these patients.
What investigations might you do in someone who you suspect has gastric cancer?
Endoscopy.
CT.
Laparoscopy.
What is the advantage of doing a laparoscopy in someone with gastric cancer?
It can detect metastatic disease that may not be detected on ultrasound/endoscopy.
What is the treatment for proximal gastric cancers that have no spread?
3 cycles of chemo and then a full gastrectomy. Lymph node removal too.
What is the treatment for distal gastric cancers that have no spread?
3 cycles of chemo and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too.
What vitamin supplement will a patient need following gastrectomy?
They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia.
Where in the colon do the majority of colon cancers occur?
In the descending/sigmoid colon and rectum.
Why do proximal colon cancers have a worse prognosis?
They have fewer signs and so people often present with them at a very advanced and late stage.
Describe the progression from normal epithelium to colorectal cancer.
Normal epithelium.
Adenoma.
Colorectal adenocarcinoma.
Metastatic colorectal adenocarcinoma.
What is the treatment for colorectal adenocarcinoma?
Surgical resection can be done when there is no spread. Remember to balance risks v benefits. The patient has a pre-op assessment.
What is the treatment for metastatic colorectal adenocarcinoma?
Chemotherapy and palliative care.
Give 5 risk factors for colorectal cancer.
Low fibre diet.
Diet high in red meat.
Alcohol.
Smoking.
A PMH of adenoma or ulcerative colitis.
A family history of colorectal cancer; FAP or HNPCC
What can affect the clinical presentation of a colorectal cancer?
How close the cancer is to the rectum affects its clinical presentation.
How does familial adenomatous polyposis (FAP) cause colorectal cancer? (only counts for 1% of colorectal cancer)
Adenomatous polyposis coli (APC) complex can normally bind to beta catenin and break it down.
Mutation in the APC gene means that the APC protein cannot break down the beta catenin protein. Beta catenin translocate to nucleus binds to DNA and upregulates genes for epithelial proliferation and adenoma -> colorectal cancer
How does hereditary nonpolyposis colorectal cancer HNPCC occur?
Abnormal DNA repair protein genes leads to no DNA repair protein produced, this leads to HNPCC.
Reasons for identifying HNPCC cancers
Risk of further cancers in index patient and relatives
Possible implications for therapy
- tolerance of 5-FU etc
- do not recognise DNA damage
- apoptosis not activated
Give 3 signs of rectal cancer.
PR bleeding.
Mucus.
Thin stools.
Tenesmus.
Give 2 signs of a left sided/sigmoid cancer.
Change of bowel habit e.g. diarrhoea, constipation.
PR bleeding
Give 3 signs of a right sided cancer.
Anaemia.
Mass.
Diarrhoea that doesn’t settle.
Describe the emergency presentation of a left sided colon cancer.
The LHS of the colon is narrow and so the patient is likely to present with signs of obstruction e.g. constipation; colicky abdominal pain; abdominal distension; vomiting.
Describe the emergency presentation of a right sided colon cancer.
The RHS of the colon is wide and so the patient is likely to present with signs of perforation.
What investigations might you do in someone who you suspect might have colorectal cancer?
Colonoscopy = gold standard!
It permits biopsy and removal of small polyps.
- Tumour markers are good for monitoring progress.
- Faecal occult blood is used in screening but not diagnosis.
What is diarrhoea?
Frequent loose or watery stools,
> 3 times per day or more frequently than normal
Non infective causes of diarrhoeal diseases (list 4)
Neoplasm
Inflammatory
Irritable bowel
Anatomical
Hormonal
Radiation
Chemical
Infective causes of diarrhoeal diseases
Non-bloody
Bloody (Dysentery)
Chain of infection
AGENT -> Mode of transmission -> Portal of entry -> HOST -> Person to person spread -> RESERVOIR -> Portal of exit
27 year old student just returned from backpacking holiday around South Asia.
Presents with frequent bouts of diarrhoea, flatulence, nausea and abdominal discomfort.
Likely diagnosis?
Vibrio cholerae
2 year old child presents with loose stools for 2 days. Miserable. Loss of appetite but drinking ok. No fever.
Attends nursery and playgroup.
Recently been to a petting zoo.
Likely diagnosis?
Animal contact -> likely Escherichia coli, Salmonella
87 year old resident of a care home presents with confusion, altered consciousness, dehydration and a history of diarrhoea.
Likely diagnosis?
Norovirus, rotavirus
When does norovirus usually occur?
In the winter
Where does norovirus usually occur?
Hospitals
Care Homes
Schools
Cruise ships
Families
36 year old man presents with bouts of low volume bloody stools.
He works in a take-away.
Likely diagnosis?
Shigella, Salmonella, E. coli,
What bacteria cause food poisoning through toxin production?
bacillus cereus
clostridium perfringens
A patient falls ill after 3-6 hrs of ingesting contaminated food. What is likely the culprit?
Toxin producing bacteria
eg bacillus cereus, clostridium perfringens
A patient falls ill after 12-24 hrs of ingesting contaminated food. What is likely the culprit?
Viruses
eg norovirus, rotavirus
A patient falls ill after 2-3 days of ingesting contaminated food. What is likely the culprit?
Bacteria
eg Salmonella, E. coli, Shigella
84 year old patient at the Northern General Hospital presents with diarrhoea.
She is recovering from a surgical operation a few days ago.
Likely diagnosis?
Clostridium difficile
What does Clostridium difficile cause in hospitalised patients?
Antibiotic-associated diarrhoea
Antibiotic-associated colitis
Pseudomembranous colitis
Clostridium difficile prevention?
SIGHT
Suspect C diff as a cause of diarrhoea
Isolate the case
Gloves and aprons must be worn
Hand washing with soap and water
Test stool for toxin
Clostridium difficile management
Control antibiotic usage
Esp. Ampicillin, amoxicillin & cephalosporins
Standard infection control procedures
- Surveillance & case finding
Any patient with diarrhoea
- Isolate
- Enteric precautions
- Test stool samples
- Environmental cleaning
- Treat cases with metronidazole or vancomycin
Clostridium difficile investigation
Test stool samples for the toxin
Can also culture it (in order to identify which strain it is)
Tissue samples (histology) obtained at sigmoidoscopy
Don’t need to screen or treat asymptomatic carriers
59 year old patient presents with altered bowel motions, increased frequency and mucous content.
Symptoms for the past 6 months.
Some weight loss and he reports nightsweats.
Likely diagnosis?
Bowel cancer
Diarrhoeal Disease in Children
Frequent loose or watery stools,
> 3 times per day or more frequently than normal
most episodes are mild
Significant fluid loss can occur in children
if not replaced can lead to death
“What comes out must go in”
Wide range of causative organisms
Rotavirus contributes to 40% of hospital admissions
E. coli, Shigella, Campylobacter, Salmonella & Cryptosporidium
Package of Prevention and Treatment Measures (WHO-UNICEF, 2004)
Prevention package
1. Rotavirus and measles vaccinations
2. Promote early & exclusive breastfeeding + Vitamin A supplementation
3. Promote hand washing with soap
4. Improved water supply quantity & quality, including treatment & safe storage of household water
5. Community-wide sanitation promotion.
Treatment package
1. Fluid Replacement to prevent dehydration
2. Zinc treatment
Control Measures - Checklist for diarrhoea prevention (List 5)
Hand-washing with soap
Ensure availability of safe drinking water
Safe disposal of human waste
Breastfeeding of infants & young children
Safe handling and processing of food
Control of flies/vectors
Case management including exclusion
Vaccination
At risk groups for diarrhoeal disease?
A – Persons of doubtful personal hygiene or with unsatisfactory hygiene facilities at home, work or school
B – Children who attend pre school or nursery
C – People whose work involves preparing or serving unwrapped/uncooked food
D – HCW/Social care staff working with vulnerable people
Acute hepatitis symptoms?
Symptoms:
None or non-specific, e.g. malaise, lethargy, myalgia
Gastrointestinal upset, abdominal pain
Jaundice + pale stools / dark urine
Acute hepatitis signs?
Signs:
Tender hepatomegaly ± jaundice
± signs of fulminant hepatitis (acute liver failure), e.g. bleeding, ascites, encephalopathy
Acute hepatitis bloods?
Bloods:
Raised transaminases (ALT/AST»_space; GGT/ALP) ± raised bilirubin
Causes of acute hepatitis? (infection and non-infection)
Infection
Viral:
Hepatitis A, B ± D, C & E
Human herpes viruses, e.g. HSV, VZV, CMV, EBV
Other, e.g. influenza, SARS-CoV-2
Non-viral:
Spirochaetes, e.g. leptospirosis, syphilis
Mycobacteria, e.g. M. tuberculosis
Bacteria, e.g. bartonella
Parasites, e.g. toxoplasma
Non-infection
Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Pregnancy
Autoimmune hepatitis
Hereditary metabolic causes
Patient with chronic hepatitis signs and symptoms?
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
Compensated: liver function maintained
Decompensated: coagulopathy (↑PT, INR); jaundice (↑bilirubin); low albumin; ascites (± bacterial peritonitis); encephalopathy
Other complications: hepatocellular carcinoma (HCC); portal hypertension (varices, bleeding)
Causes of chronic hepatitis (infectious and non-infectious?)
Infection:
Viral
Hepatitis B ± D, C (& E)
Non-infection:
Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Autoimmune hepatitis
Hereditary metabolic causes
Hepatitis A transmission?
Faeco-oral transmission
Contaminated food & water
Linkage to access to safe drinking water & socioeconomic indicators
High income countries:
Travel
Sex (MSM)
Injecting drug use
Hepatitis A incubation period?
Short incubation period: 15 to 50 days (usually 14 to 28 days)
Hepatitis A symptoms?
Usually symptomatic in adults:
Pre-icteric phase: constitutional symptoms + abdominal pain
Icteric phase (few days to 1 week after pre-icteric phase)
Rarely fulminant hepatitis / acute liver failure (0.35%)
Hepatitis A immunity after infection?
100% immunity after infection
Hepatitis A serological response
In acute phase: anti-HAV IgM, then later on will develop anti-HAV IgG
Hepatitis A: Management
Supportive
- Monitor liver function (INR, albumin, bilirubin, etc.)
- Acute liver failure (“fulminant hepatitis”) in <1%
- liaise with hepatology / liver transplant centre - Management of close contacts (vaccine)
- Primary prevention: vaccination
e.g. travellers, MSMs, PWIDs
Hepatitis E transmission?
4 genotypes
Faeco-oral transmission:
G1 & 2: contaminated food & water
G3 & 4: undercooked meat (mammalian zoonotic reservoir, including pigs)
Blood and organ transplant recipients
Which type of Hepatitis E can lead to chronic infection?
G3 & 4
Hepatitis E symptoms?
> 95% cases asymptomatic
Usually self-limiting acute hepatitis
fulminant hepatitis 3.3%
increased risk in pregnancy with GT1/2, especially 2nd and 3rd trimesters
occasional acute-on-chronic liver failure (high mortality)
Extra-hepatic manifestations, e.g. neurological
Risk of chronic infection (GT3/4 only) in immunosuppressed patients
e.g. transplant recipients, HIV patients
rapid progression to cirrhosis
Hepatitis E: Management
Acute infection:
Supportive
Monitor for fulminant hepatitis / acute-on-chronic liver failure:
Liaise with hepatology / liver transplant centre
Consider ribavirin
Chronic infection (persistent HEV RNA > 6 months):
Reverse immunosuppression (if possible)
If HEV RNA persists, treat with ribavirin ≥ 3 months (2nd line: pegylated interferon-α)
Hepatitis E serological response?
Acute phase: anti-HEV IgM, then anti-HEV IgG
Anti-HEV IgG gives some immunity but not 100% unlike Anti-HAV IgG
HEV RNA test used instead, as serology test unreliable in immunosuppressed patients
Hepatitis E prevention?
Prevention:
Avoid eating undercooked meats (especially if immunocompromised)
Screening of blood donors
Vaccine available in China only (HEV 239 (Hecolin®) against HEV genotype 1
Hepatitis B ± D transmission?
Blood-borne virus
Transmission via blood and body fluids:
Mother-to-child***
Household contact
Blood products
Iatrogenic
Occupational
Sexual
Injecting drug use
Hepatitis B natural history (immunocompetent adults)
Acute HBV infection (95% spontaneous resolution) -> Chronic HBV infection -> Cirrhosis -> Decompensated cirrhosis + Hepatocellular carcinoma
How does hepatitis B natural history differ in adults vs neonates and infants?
Only 10% spontaneous resolution in neonates and infants. 90% chance that it will progress to chronic HBV infection
Hepatitis B serological response
Acute phase: Anti-HB core IgM
Anti-HB core IgG develops later on
If hepatitis B surface antigen present, it means that there is current HBV infection
Acute Hepatitis B incubation period?
Incubation period: 30 to 180 days (mean 75 days)
Acute Hepatitis B management
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 (HBV vaccine if non-immune)
Hepatitis B clearance
95% of adults will clear Hepatitis B
Will develop core and surface anti-HB antibodies
If develop chronic Hepatitis B
Will not develop anti-HB surface antibodies and Hepatitis B surface antigens will remain
Chronic hepatitis B treatment
Treatment option 1: pegylated interferon-α 2a
Treatment option 2: oral nucleos(t)ide analogues
Inhibit viral replication
HBV DNA polymerase
One tablet once a day
High barrier to resistance
Minimal side effects
Renal monitoring (TDF)
May be required lifelong
What two phases of chronic hepatitis B would you treat?
The immune reactive phase and immune escape phase
Hepatitis B: Prevention (List 4)
- Antenatal screening (HBsAg testing) of pregnant mothers
HBV vaccination administered to baby at birth and at 1, 2, 3, 4* and 12 months
HBIG given to baby at birth if mother e-antigen positive and/or has high HBV DNA levels or baby birth weight <1.5kg
tenofovir given to mother in pregnancy if high HBV DNA levels - Universal childhood immunisation
UK since 1st August 2017: hexavalent vaccine* at 8, 12 and 16 weeks - Immunisation of healthcare workers + other risk groups (e.g. MSMs, PWIDs)
- Screening ± immunisation of sexual and household contacts
- Barrier contraception, PrEP (Tenofovir/Emtricitabine)
- Universal screening of blood products
- Sterile equipment and universal precautions in healthcare
Hepatitis D transmission?
Blood-borne virus
Transmission via blood and body fluids:
Mother-to-child
Household contact
Blood products
Iatrogenic
Occupational
Sexual
Injecting drug use
Hepatitis D test?
Test: Hepatitis D antibody: if positive, test HDV RNA
Hepatitis D treatment
Treat: pegylated inteferon-α 48 weeks; buleviritide (Hepcludex®)(pending NICE)
Hepatitis C transmission?
Blood-borne virus
Transmission via blood and body fluids:
Mother-to-child
Household contact
Blood products
Iatrogenic
Occupational
Sexual (MSM)
Injecting drug use***
Tattoos, piercings, etc.
Hepatitis C natural history (immunocompetent adults)
Acute HCV infection (30% spontaneous resolution) -> Chronic HCV infection -> Cirrhosis -> Decompensated cirrhosis + Hepatocellular carcinoma
Hepatitis C testing
HCV antibody* -> Reflex testing of
positive samples -> HCV RNA -> Reflex testing of positive samples -> HCV genotype
RNA testing is important as it allows you to see whether there is a current infection
Hepatitis C treatment
Directly-acting antiviral (DAA) therapy
Glecaprevir/Pibrentasvir (Maviret®)
Elbasvir/Grazoprevir (Zepatier®)
Hepatitis C: Prevention (List 5)
No vaccine
Previous infection does not confer immunity: can be re-infected
Screening blood products (in UK since 1991)
Universal precautions handling bodily fluids
Sterile medical equipment + safe disposal
Opiate addiction treatment (OAT), e.g. methadone, buprenorphine
Provision of sterile injecting equipment
Treatment and cure of “transmitters”, e.g. active PWIDs
Safe sex, e.g. condoms
Mr JB is a 24 year old man who initially presented to primary care with diarrhoea for 6 months. He has announced that he was allergic to gluten and blood tests were performed in primary care:
FBC: Hb 95 ↓
UE: Normal
LFT: Normal
IgA: Normal
IgA tTG: 69 (0-7) ↑
Seeing these results, what further procedure should be undertaken?
gastroscopy - remove tissue for biopsy
Villous atrophy indicates indicates celiac disease
What is coeliac disease?
An autoimmune enteropathy caused by ingestion of gluten
Which gene is linked with coeliac disease?
HLA type
Coeliac disease management (list 3)
Gluten free diet - strict and lifelong
Dietitian review
Bone density assessment
Coeliac UK information
Prescription for gluten free foods - variable dependent upon location
Immunisations
Risks of coeliac patients not going for a gluten free diet? (List 4)
Enteropathy associated T-cell lymphoma
Small bowel adenocarcinoma
Vitamin deficiencies
Osteoporosis
Hyposplenism
Malnutrition
Depression
Delayed puberty
Anaemia
Iron deficiency
What conditions are commonly associated with coeliac disease?
Dermatitis herpetiformis (v common)
T1DM
Hashimoto’s thyroiditis
Name 6 things that can break down the mucin layer in the stomach and cause gastritis.
- Not enough blood - mucosal ischaemia.
- Aspirin, NSAIDS.
- Increased acid - stress, H. pylori.
- Bile reflux - direct irritant.
- Alcohol.
- Helicobacter infection
How would you treat gastritis caused by mucosal ischaemia?
- reverse the mucosal ischaemia
- reduce the acid - H2 blocker/proton pump inhibitor
How would you treat gastritis caused by aspirin/NSAIDS?
Enteric coated aspirin
How would you treat gastritis caused by Helicobacter infection?
Antibiotics
Give 5 broad causes of malabsorption.
- Defective intra-luminal digestion.
- Insufficient absorptive area.
- Lack of digestive enzymes.
- Defective epithelial transport.
- Lymphatic obstruction.
Malabsorption: what can cause defective intra-luminal digestion?
- Pancreatic insufficiency due to pancreatitis, CF.
- Defective bile secretion due to biliary obstruction or ileal resection.
- Bacterial overgrowth.
Malabsorption: what can cause insufficient absorptive area?
- Coeliac disease.
- Crohn’s disease.
- Extensive parasitisation.
- Small intestinal resection.
Malabsorption: give an example of when there is a lack of digestive enzymes.
- Lactose intolerance - disaccharide enzyme deficiency.
- Bacterial overgrowth - brush border damage
Malabsorption: what can cause defective epithelial transport.
- Abetalipoproteinemia
- Primary bile acid malabsorption - mutations in bile acid transporter protein
Malabsorption: What can cause lymphatic obstruction?
- Lymphoma
- Tuberculosis
Which hormone causes the release of bile into the small intestine?
Cholecystokinin
List 4 conditions associated with bile stones
- Biliary colic
- Gallstone ileus
- Cholecystitis
- Choledocholithiasis
- Cholangitis
- Mirrizzi syndrome
- Pancreatitis
Gallstones: signs and symptoms of someone who has biliary colic?
- post prandial colicky pain , worse with fats, right upper quadrant/epigastrium
- nausea/vomiting
Gallstones: signs and symptoms of someone who has cholecystitis?
- constant pain
- fever, rigors
Gallstones: signs and symptoms of someone who has choledocholithiasis?
Jaundice
Gallstones: signs and symptoms of someone who has cholangitis?
- Jaundice
- Fever > 39 °C
What investigations might you do in someone who you suspect has gallstones?
Ultrasound!
Bloods: FBC, LFT, Coag, U+E, Amylase/lipase
ERCP
MRCP
What is Mirizzi’s syndrome?
Obstruction of the common bile duct by external compression from multiple or a single large impacted gallstone in the Hartman’s pouch.
Causes of pancreatitis
IGETSMASHED
I - Idiopathic
G - Gallstones
E - Ethanol
T - Trauma
S - Steroid use
M - Mumps
A - Autoimmune
S - Scorpions
H - Hypertriglyceridaemia/calcaemia
E - ERCP
D - Drugs
Pancreatitis symptoms and signs
- Severe central pain going to back
- Nausea and vomiting
- Fever
- Oliguria
- Jaundice
- Cullen’s and Grey turners
Complications of pancreatitis?
Auto digestion
- Haemorrhage
- Pseudoaneurysm
- Portal thrombosis
- Necrosis
- Infected necrosis
- Pseudocyst
Systemic inflammatory response system
- ARDS
- MOF
Pancreatitis treatment?
- ANALGESIA!
- Catheterise and ABC approach for shock patients.
- Drainage of oedematous fluid collections.
- Antibiotics.
- Nutrition.
- Bowel rest.
Give 2 potential complications of acute pancreatitis.
- Systemic inflammatory response syndrome.
- Multiple organ dysfunction.
What is chronic pancreatitis?
Chronic inflammation of the pancreas leads to irreversible damage.
What is the difference between ulcerative colitis and Crohn’s disease? Distribution
UC: continuous, starts distally from the rectum and extends proximally (pancolitis), only affects large bowel
CD: Patchy, anywhere from mouth to rectum, common in terminal ileum and right colon
What is the difference between ulcerative colitis and Crohn’s disease? Mucosal inflammation
UC: superficial, continuous, denuded
CD: Transmural, patchy
What is the difference between ulcerative colitis and Crohn’s disease? Histology
UC: cryptitis, crypt abscess
CD: 50-70% granulomas
What is the difference between ulcerative colitis and Crohn’s disease? Fistula
UC: /
CD: Perianal, enteric
What causes IBD?
Abnormal inflammatory response to gut bacteria in genetically susceptible individuals
Management of ulcerative colitis?
- Resuscitate
- Prophylactic LMWH **
- IV steroids (hydrocortisone 100mg 4x a day) **
- Monitor BM
- Stool cultures: exclude infections **
- Stool chart
- AXR
- Flexible sigmoidoscopy
Which criteria is used to assess ulcerative colitis?
Truelove and Witts criteria
What type of medication is infliximab and ciclosporin?
What do they act on?
Anti-TNF Monoclonal antibodies used to treat IBD
Acts on transmembrane insoluble TNF and prevents them from binding to TNF receptors, reducing inflammation
What surgery is done on patients with UC?
Subtotal colectomy.
- colon removed
- end ileostomy
- rectum remains
Management of Crohn’s disease?
- Resuscitate
- Prophylactic LMWH**
- IV steroids (hydrocortisone 100mg 4x a day) **
- Monitor BM
- Stool cultures: exclude infections**
- Stool chart
- AXR/MRE/CT AP
- Triage: gastroenterology ward
What surgery is done on patients with CD?
Right hemicolectomy
- remove diseased small bowel
- remove right side of colon
What are Functional Gastrointestinal Disorders (FGIDs)?
Chronic GI symptoms in the absence of organic disease to explain the symptoms.
What are the 2 most common FGIDs?
IBS (bowel)
Functional dyspepsia (stomach)
What GI symptoms are associated with FGIDs?
- Visceral hypersensitivity
- Motility disturbances
- Altered mucosal & immune
function - Altered CNS processing
- Altered gut microbiota
IBS symptoms
- Chronic frequent abdominal pain
- Altered bowel habit
- Bloating commonly associated
Differential diagnosis for IBS?
- IBD
- Coeliac disease
- Chronic GI infections ie Giardiasis
- Colorectal cancer
- Ovarian cancer
Endoscopies cannot be carried out for everyone with FGIDs why?
- IBS and functional dyspepsia are very common
- Endoscopies are invasive with appreciable risks
- The diagnostic yield of serious pathology is low
- Limit to those with alarm
features
When might you carry out further investigations for patients presenting with FGID symptoms?
Alarm features!
* Age >45 years
* Short history of symptoms
* Documented unintentional weight loss
* Nocturnal symptoms
* Family history of GI cancer/IBD
* GI Bleeding
* Palpable abdominal mass or lymphadenopathy
* Evidence of iron deficiency anaemia on blood
testing
* Evidence of inflammation on blood/stool testing
What steps would you take to diagnose someone with functional dyspepsia?
- Characteristics symptoms – chronic upper GI symptoms
- Exclusion of organic pathology
– History
– Examination
– 1st line investigations
FBC,CRP, LFT, coeliac serology
Stool Helicobacter pylori
– 2nd line investigations in a subset with alarm features
e.g.Upper GI endoscopy (OGD), Ultrasound abdomen
CT scan (if suspect cancer)
What steps would you take to diagnose someone with IBS?
- Characteristics symptoms – chronic lower GI symptoms
- Exclusion of organic pathology
– History
– Examination
– 1st line investigations
FBC,CRP, coeliac serology
Stool faecal calprotectin
Stool M,C & S
Ca-125 in women (if appropriate)
– 2nd line investigations in those with alarm features
e.g. Lower GI endoscopy (Colonoscopy), CT scan (if suspect cancer
What useful test can be used to differentiate between IBD and IBS?
Faecal calprotectin - sensitive marker that indicates GI inflammation = IBD
What is the largest Cavity in the human body ?
Peritoneal Cavity
Which organs are retroperitoneal organs?
SAD PUCKER:
S = Suprarenal (adrenal) Glands.
A = Aorta/IVC.
D =Duodenum (except the proximal 2cm, the duodenal cap)
P = Pancreas (except the tail)
U = Ureters.
C = Colon (ascending and descending parts)
K= Kidneys.
E = (O)esophagus.
Function of Peritoneum normally
In health:
Visceral lubrication
Fluid & particulate absorption
Function of peritoneum in disease
Pain perception.
Inflammatory and immune responses
Fibrinolytic activity
Among the visceral and parietal peritoneum, which one is more sensitive to pain?
Parietal peritoneum - mores sensitive to pain
What is peritonitis
Inflammation of peritoneum
How can peritonitis be classified?
Onset:
- Acute: sudden onset
- Chronic: gradual onset
Source of origin:
- Primary: no source
- Secondary: bowel perforation, appendicitis
Peritonitis causes (list 5)
- Bacterial, gastrointestinal and non-gastrointestinal
- Chemical, e.g. bile, barium
- Traumatic, e.g. operative handling
- Ischaemia, e.g. strangulated bowel, vascular occlusion
- Miscellaneous, e.g. familial Mediterranean fever
Paths to Peritoneal Infection (list 4)
- Gastrointestinal perforation, e.g. perforated ulcer, appendix, diverticulum
- Transmural translocation (no perforation), e.g. pancreatitis, ischaemic bowel, primary bacterial peritonitis
- Exogenous contamination, e.g. drains, open surgery, trauma, peritoneal dialysis
- Female genital tract infection, e.g. pelvic inflammatory disease
- Haematogenous spread (rare), e.g. septicaemia
Microorganisms in peritonitis (list 4)
Gastrointestinal source
- Escherichia coli
- Streptococci I Enterococci
- Bacteroides spp. I Clostridium spp.
- Klebsiella pneumoniae
Other sources
- Chlamydia trachomatis I Neisseria gonorrhoeae
- Haemolytic streptococci IStaphylococci I
Streptococcus pneumoniae
- Mycobacterium tuberculosis and other species
- Fungal infections
Signs and symptoms of localised peritonitis
- Pain
- Nausea and vomiting
- Fever
- Tachycardia
- Localised guarding
- Rebound tenderness
- Shoulder tip pain ( subphrenic)
- Tender rectal and / or vaginal examination (pelvic peritonitis).
Signs and symptoms of diffuse (generalised) peritonitis - early
- Abdominal pain ( worse by moving or breathing)
- Tenderness
- Generalised guarding
- Infrequent bowel sounds àcease ( paralytic ileus)
- Fever
- Tachycardia
Signs and symptoms of diffuse (generalised) peritonitis - late
- Generalised rigidity
- Distension
- Absent bowel sounds
- Circulatory failure
- Thready irregular pulse
- (Hippocratic face)
- Loss of consciousness
Investigations for suspected peritonitis
- Urine dipstix for urinary tract infection.
- ECG if diagnostic doubt (as to cause of abdominal pain) or cardiac history.
- Bloods I U&Es I Full blood count (WCC)
- Serum amylase (acute pancreatitis/ others like perf DU)
- Group and save.
Management of peritonitis
- Correction of Fluid Loss & Circulating Volume
- Antibiotics
- Urinary Catheterisation I Gastric Decompression
- Analgesics
Surgical treatment of cause when appropriate
What is ascites?
Effusion and accumulation of serous fluid in the peritoneal cavity
How is ascites classified?
Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
Stage 2 easily detectable but of relatively small volume.
Stage 3 obvious, not tense ascites. (moderate)
Stage 4 tense ascites. (Large)
What can cause exudative ascites?
Increased vascular permeability secondary to infection; inflammation (peritonitis) or malignancy
What can cause transudative ascites?
Increased venous pressure due to cirrhosis, cardiac failure or hypoalbuminaemia.
Give 2 signs of ascites.
- Flank swelling.
- Dull to percuss and shifting dullness.
What investigations might you do in someone who you suspect has ascites?
- Ultrasound.
- Ascitic tap.
Describe the treatment for ascites.
Restrict sodium.
Diuretics.
Drainage.
Duke’s staging system: Duke’s A
Dukes’ A
The cancer is in the inner lining of the bowel. Or it is slightly growing into the muscle layer.
Duke’s staging system: Duke’s B
The cancer has grown through the muscle layer of the bowel.
Duke’s staging system: Duke’s C
The cancer has spread to at least 1 lymph node close to the bowel.
Duke’s staging system: Duke’s D
Advanced bowel cancer
The cancer has spread to another part of
the body, such as the liver, lungs or bones.
A 19 year old woman presents with abdominal pain and loose stool. Which of the following features suggest that she has irritable bowel syndrome?
A: Anaemia
B: Nocturnal diarrhoea
C: Abdominal pain relieved by defecation
D: Weight loss
E: Blood in stool
C: Abdominal pain relieved by defecation
A 35 year old woman with a 6 month history of epigastric pain and fullness after meals. No history of weight loss or vomiting. She is a non smoker and does not drink alcohol. She was treated with PPI with no benefit. Upper GI endoscopy was normal including biopsies. What is the most likely diagnosis?
Functional dyspepsia
What is the SAFE level of alcohol consumption?
0!
14 units is the advised units of alcohol that you shouldn’t exceed per week
A 25 year old man presents to the hospital with abdominal pain and diarrhoea. CT scan shows inflammation in the transverse colon and terminal ileum. What is the most likely diagnosis?
Crohn’s disease
A 71 year old man was admitted to hospital with pneumonia. He was treated with a week of Augmentin (Co-amoxiclav) for his pneumonia. On day 7 of his admission, he started having diarrhoea 10 times a day without any blood. He feels unwell and dehydrated. What is the likely organism responsible for his diarrhoea?
Clostridium difficile - commonly linked with antibiotic use. No blood.
52 year old woman was referred by GP with fatigue and deranged LFTs (raised ALT and ALP). Normal ultrasound liver. Hepatitis screen negative, antimitochondrial antibodies +ve. What is the most likely diagnosis?
Primary biliary cholangitis.
(if you see antimitochondrial antibodies in question will almost ALWAYS be PBC)
A 45 year old man with known alcohol related liver cirrhosis presents to hospital with 5 day history of black stools. He is apyrexial, oriented but jaundiced. Blood shows new anaemia and raised urea. Which treatment is likely to reduce his mortality risk?
- tranexamic acid
- omeprazole
- co-amoxiclav
- metoclopramide
- iron infusion
- co-amoxiclav
Patient likely to have varices
- bloody stool
- liver cirrhosis
Best drug to give to patient would be Terlipressin which stops GI bleed. Co-amoxiclav is an antibiotic which prevents bacteria -> sepsis (thus reducing mortality risk)
40 year old man was admitted to the hospital with a fever and abdominal pain. He drinks 50 units of alcohol per week. On examination he is jaundiced and having tremors, and his abdomen is soft but distended and slightly tender. What is the most likely diagnosis?
50 units of alcohol per week -> liver cirrhosis
Likely spontaneous bacterial peritonitis
A 32 year old woman complains of a 6 month history of bloating and diarrhoea. What is the most likely diagnosis if her villi is flat upon histology?
Celiac disease
a 75 year old man presents with pain in RUQ with rigors and fever. On examination he has RUQ tenderness but negative Murphy’s sign. Blood tests show high CRP and bilirubin. What is the next most appropriate test?
abdominal ultrasound
What might RUQ pain indicate?
Just RUQ pain -> symptomatic gallstone
RUQ pain + fever -> acute cholecystitis
RUQ pain + jaundice -> common bile duct stone
RUQ pain + jaundice + fever -> ascending cholangitis
A 43 year old man with a history of renal transplant presented with deranged LFTs after eating raw pork meat while on holiday. What is the most likely cause of his deranged LFTs?
Hepatitis E
Dysplasia vs metaplasia?
Dysplasia: Morphological changes seen in cells in the progression to becoming cancer
Metaplasia: The change in differentiation of a cell from one fully-differentiated cell type to another
