GI/Liver Flashcards
List 5 functions of the liver
Filtration of blood from GI tract
- Detoxification of blood eg. clears adrenal androgens
- Drug metabolism
- Bile production and excretion
Storage
- Storage of glycogen, minerals, proteins
Synthesis
- Lipid, protein and carbohydrate metabolism
- Protein synthesis eg. clotting factors, albumin
- Thrombopoietin production (TPO): stimulates platalet produciton
Activation
- Enzyme activation
Which areas of the abdomen is the liver predominantly in?
Right hypochondrium and epigastric
Describe the microscopic anatomy of the liver
- Hepatocytes are arranged into lobules (structual units)
- Each lobule is drained by a central vein which drains into the hepatic vein
At the periphery of each lobule: portal triad which lies in the portal tract
- Arteriole: branch of hepatic artery entering the liver
- Venule: branch of portal vein entering the liver
- Bile duct: branch of the bile duct leaving the liver
What are the two main types of liver disease
- Space-occupying lesions (masses, focal disease)
- Diffuse liver disease
List 5 causes of liver injury
- Drugs and toxins inc. alcohol
- Abnormal nutrition/metabolism (eg. obesity)
- Infection
- Obstruction to bile/blood flow
- Autoimmune liver disease
- Neoplasm
- Primary Biliary disease eg. primary biliary cholangitis
- Vascular disease eg. venous obstruction
- Genetics eg. haemochromatosis
Differentiate between acute and chronic inflammation
Acute inflammation: agent causes injury but is then removed
- Days to weeks
- Fulminant: defined as severe, acute inflammation rapidly progressing toward liver failure
Chronic inflammation: agent causes injury and then persists
- Months to years
- Liver disease: any abnormality in LFTs for >6 months
- Acute on chronic: chronic liver disease often presents with acute exacerbating plus evidence of underlying chronicity
What is the main target of liver injury?
What is the relationship between different hepatic structures in inflammation?
- Liver injury mainly affects parenchyma ie. hepatocytes
- Bile ducts or blood vessels are rarely the main target
- Parenchyma, bile ducts, blood vessels and CT are interdependent, so damage to one leads to damage to the others
What is the clinical approach to liver disease?
- History, symptoms and signs by examination
- Investigations: LFTs, viral and autoimmune serology, metabolic tests and radiology
^ usually yields diagnosis without biopsy, should at least differentiate space-occupying lesion with diffuse liver disease
- Avoid liver biopsies due to significant complication rates
List 4 histological patterns that can be seen with diffuse liver disease
- Acute hepatitis
- Acute cholestasis
- Fatty liver disease (steatosis and steatohepatitis)
- Chronic hepatitis
- Chronic biliary/cholestatic disease
- Genetic/Deposition disease
- Hepatic vascular disease
Define cholestasis
Reduction in bile flow due to impaired secretion from hepatocytes or obstruction of bile flow through intra- or extrahepatic ducts
What are the features of acute hepatitis and acute cholestasis
- Inflammation
- Acute bile stasis (more marked in cholestasis)
What are the features of acute hepatitis?
- Inflammation in and affecting the hepatocytes, causing damage
- Diffuse hepatocyte injury seen as swelling
- Looks very busy
- Some cells have died: ‘spotty necrosis’
- Inflammatory cell infiltrate in all areas (portal tracts, interface and parenchyma)
What are the causes of acute cholestasis (cholestatic disease)?
Describe it’s histology
- Extrahepatic biliary obstruction
- Drug injury eg. antibiotics
Histology: borwn bile pigment (bilirubin) +/- acute hepatitis
- Inflammation and acute bile stasis
How would you differentiate acute and chronic hepatitis clinically and histologically?
Clinically: chronic is >6 month history of abnormal LFTs
Histologically: chronic hepatitis would have presence of fibrosis
Define chronic liver disease
Any abnormality in LFTs for >6 months
Which histological patterns are most likely to develop fibrosis and progress to cirrhosis?
- Fatty liver disease
- Chronic hepatitis
- Chronic cholestatic disease
- Genetic/Deposition disease
Describe the pathology of Hepatitis B
What is it’s distinguishing feature?
- Looks like acute hepatitis with addition of fibrosis
- Specific feature: ground glass cytoplasm hepatocytes (accumulcation of surface antigen)
Where is the target for damage in chronic biliary/cholestatic disease?
What are the causes?
- What is the histology?
- Damage to the portal tracts, esp. the bile ducts
Causes:
- Primary biliary cholangitis: autoimmune disease resulting in slow, progressive destruction of small bile ducts of the liver
- Primary sclerosing cholangitis (PSC): long-term progressive disease of liver and gallbladder characterised by inflammation and scarring of bile ducts
Histology:
- Focal, portal-predominant inflammation and fibrosis
- Granulomas
What conditions cause genetic/deposition liver disease?
- Haemochromatosis: excess iron, stained blue, not normally seen
- Wilson’s disease
- Alpha-1-antitrypsin deficiency (it’s produced in the liver)
What are the aims of management for diffuse liver disease?
What are the treatment options?
- Reduce symptoms, reduce inflammation and prevent/slow progression of fibrosis
Treatment options:
- Specific treatment against cause eg. removal of alcohol/drug, optimal diabetic control. antivirals or immunosuppression
- Supportive treatment eg. for severe acute hepatitis or cirrhosis
What histological pattern(s) can drug-induced liver disease present as?
- Almost any pattern of liver disease
- Therefore, usually in differential diagnosis esp. with acute hepatitis and acute cholestasis
What are the types of space occupying lesions that cause liver disease?
Non-neoplastic:
- Degenerative/Developmental eg. cysts
- Inflammatory eg. abscess
Neoplastic:
- Benign or malignant
Describe the pathology of liver cysts
What is the clinical significance of a liver cyst?
What is the treatment?
- Developmental or degenerative in origin
- Most common: simple biliary hamartoma
- Found on the surface of the liver and can resemble metastases by naked eye in operation
Treatment: none
Fill in the blanks
- Types of liver neoplasms
What are the risk factors for a hepatic adenoma?
Young, women, often associated with hormone therapy
In which situation is hepatocellular carcinoma likely to arise?
What investigation would you do?
- Usually arises in cirrhosis
- Associated with elevated serum AFP (alpha feto-protein)
Define cirrhosis
- diffuse process characterised nodule formation and fibrosis
- End-stage liver disease
What are the signs of chronic liver disease?
- Spider naevi
- Palmar erythema
- Loss of male hair pattern
- Gynaecomastia (reduced clearance of adrenal androgens)
- Sarcopenia (muscle breakdown)
- Bruising ( inc. prothrombin time, platelets)
- Itch (buildup of bile salt under the skin)
What causes easy bruising and itch in chronic liver disease (CLD)?
Easy bruising:
- Reduced production of clotting factors VII - XII, therefore takes longer to activate thrombin ie. longer prothrombin time (PT)
- Reduced production of TPO (thrombopoietin) which stimulates differentiation of megakaryocytes into platlets
Itch: accumulation of bile salts under the skin
What are the signs of portal hypertension?
- Caput medusa: the appearance of distended and enlarged superficial epigastric veins, seen radiating from the umbilicus across the abdomen
- Hypersplenism: over-active spleen, regardless of size, due to inc. blood flow to the spleen. Causes thrombocytopenia and pancytopenia
Define decompensated cirrhosis
What are the signs of decompensated chronic liver disease?
= Acute deterioration in liver function in a patient with cirrhosis
- Jaundice
- Ascites
- Hepatic flap
- Peripheral oedema
- Encephalopathy
- Bleeding varices
- Hepatocellular carcinoma
- Deteriotating synthetic function: high bilirubin, low albumin, high PT
What are the two types of cirrhosis?
- Micronodular: regenerating nodules <3mm and the liver is involved uniformly. Often caused by ongoing alcohol damage or biliary tract disease
- Macronodular: nodules variable in size and normal acini seen with larger nodules. Often following hepatitis eg. HBV
Describe/Explain the progression of cirrhosis and portal hypertension
Cirrhosis leads to increased intrahepatic resistance therefore slower blood flow through the liver and raised portal pressure (portal hypertension) → hypersplenism
Portal HTN leads to porto-systemic shunting → oesophageal-gastric varices and encephalopathy
this shunting leads to vasodilatation causing splanchnic vasodilatation (futher raising portal pressure) and reduced effective circulating volume → hyperdynamic circulation
this leads to compensatory vasopressors (RAAS) causing Na retenion and renal vasoconstriction → ascites and hepato-renal syndrome respectively (progressive kidney failure)
Describe the histology of cirrhosis
- Results from the necrosis of hepatocytes followed by fibrosis and nodule formation
- Architecture is diffusely abnormal which interferes with liver blood flow and function
- Clinical perspective: some patients are very well (compensated) and some are very unwell (decompensated)
What are the main complications associated with cirrhosis?
- Ascites
- Encephalopathy
- Variceal bleeding
- Hepatocarcinoma
How does cirrhosis lead to encephalopathy?
Failure of the cirrhotic liver to remove toxins from the blood, which ultimately negatively impacts the brain function
What are the best indicators for determining liver function?
Best indicators look at synthetic function:
- Albumin, bilirubin and clotting factors (Prothrombin Time (PT))
How are ascited assessed?
Ascites = build-up of fluid in the abdomen
- Diagnostic tap of the fluid
Cell count
- WCC >500 or neutrophils >250 suggests spontaneous bacterial peritonitis
- Inflammatory conditions also inc. WCC
Albumin
- Low protein ascites: portal hypertension
How are ascites managed?
- No added salt diet
- Diuretics: spironolactone (blocks aldosterone) or frusemide (loop diuretic)
- Paracentesis
- transjugular intrahepatic portosystemic shunt (TIPSS)
- liver transplant
What is the class, indication and action of furosemide?
Class: loop diuretic
Indication: HTN, hyperkalaemia, HF, cirrhosis (fluid retention, ascites), nephrotic syndrome
Action:
- Na/Cl/K symporter antagonists
- Act on the thick ascending loop of Henle
- Increases secretion of Na, Cl, K and water
What are the 3 main causes of liver disease?
- Alcohol
- Obesity
- Viral hepatitis
Where are the following produced in the liver and are they produced anywhere else in the body?
Alanine Aminotransferase / Aspartate Aminotransferase
Alkaline Phosphatase
GGT
Bilirubin
Albumin
PT
ALT/AST: produced in hepatocytes, also produced in skeletal and cardiac muscle. ALT is more specific to the liver
ALP: produced in canaliculi, also produced from bone (growing bone, pregnancy, Paget’s disease, bone mets, recent fracture)
GGT: produced in all cells, also produced with alcohol/drug metabolism
Bilirubin: hepatocyte function (conjugated), also produced in haemolysis (unconj)
Albumin: hepatocyte synthesis (low in abnormality), also low in infection/inflammation/renal loss (acute phase protein)
Clotting factors: hepatocytes
What investigations determine liver function?
What combination of results suggested liver failure?
Function of the liver indicated by:
- Serum albumin: guide to severity of chronic liver disease (may be normal initially in acute liver disease)
- Prothrombin time (PT): short half-life therefore is sensitive to both acute and chronic liver disease
- Bilirubin: normally all unconjugated in serum. Determination of conj. and unconj. bilirubin only necessary in congenital disorders of bilirubin metabolism or to exclude haemolysis
A high bilirubin/PT and encephalopathy indicates <25% function
What are the differentials for abnormal LFTs?
MEDIC PINNE HAT
Metabolic
Endocrinological
Degenerative
Inflammatory/Infection (Viral Hep)
Congenital (inc. genetic)
Psychological
Idiopathic
Neurological
Neoplasm
Environmental (exposure to drug/toxin)
Haematological
Autoimmune
Traumatic
Describe the interpretation of LFTs
- Assess ALT and ALP
- ALT is raised x10 in hepatocellular damage
- ALP is raised x3 in cholestasis
(Possible to have a mixed picture of hepatocyte injury and cholestasis)
- Look at GGT
- If ALP is raised, it’s important to look at GGT
- Raised GGT can be a sign of epithelial biliary damage and bile flow obstruction
- Raised ALP with raised GGT: highly suggestive of cholestasis
- Raised ALP with normal GGT: think non-hepatobiliary pathology ie. anything increasing bone formation
- Isolated GGT elevation: think drug/alcohol cause - Assess synthetic function: bilirubin
- Isolated bilirubin elevation: think pre-hepatic ie. Gilbert’s disease or haemolysis
- Ask about urine and stool - Assess synthetic function: albumin and PT
How are urine and stool affected by bilirubin
Urine
- Unconjugated bilirubin = water insoluble therefore elevated levels don’t change urine
- Conjugated bilirubin = water soluble and makes the urine darker
Stool
- If bile and pancreatic lipases cannot reach duodenum (post-hepatic jaundice), fat can’t be absorbed and stool appears lighter
So..
- normal urine and normal stool = pre-hepatic jaundice/cause
- dark urine and normal stool = hepatic
- dark urine and pale stool = post-hepatic
Define jaundice
Yellowing of the skin due to excess bilirubin pigment, caused by obstruction to the bile duct, hepatocellular damage or increased haemolysis (RBC breakdown)
What investigations would help identify acute liver injury?
- History: days/weeks
- Ultrasound (cancer, bile ducts, blood vessels)
- Acute viral hepatitis screen: Hep A/B/C/E virus
- Autoimmune liver disease
- Check paracetamol levels
What investigations would help identify chronic liver disease?
- History: >6 months
- Ultrasound (cancer, bile ducts, blood vessels, portal hypertension) +/- CT/MRCP
- Liver screen: chronic viral hepatitis (HBV, HCV), autoimmune liver disease, metabolic liver disease
- Autoimmune liver disease:
IgG goes up with autoimmune liver disease, IgA goes up in alcohol, IgM goes up in primary biliary cholangitis
What are the stages of fatty liver disease?
1. Macro-vesicular steatosis with lipid vacuole filling the hepatocyte cytoplasm
- Steatosis aka fatty change, is abnormal retention of fat within a cell
2. Steatohepatitis: neutrophils and lymphocytes surrounding hepatocytes eith Mallory hyaline
- A type of fatty liver disease, characterised by inflammation of the liver with concurrent fat accumulation in liver
3. Pericellular fibrosis as well as bands of fibrotic tracts between portal tracts
What is the progression of alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD)
- Types of fatty liver disease
- Multifactorial
- Both can lead to end-stage liver disease or develop hepatocellular carcinoma
ALD: alcoholic steatosis > alcoholic hepatitis > alcoholic cirrhosis
NAFLD: steatosis > non-alcoholic steatohepatitis > NAFLD cirrhosis
How is fibrosis of the liver assessed?
Fibroscan (non-invasive testing)
What are the main associations with NAFLD?
How is it treated?
- Obesity
- T2DM
- Hyperlipidaemia
At higher risk of diabetes and CV death
Treatment: weight loss and reduce metabolic risks
How would ALD and NAFLD be differentiated clinically?
ALD: normal BMI and excessive drinking
NAFLD: elevated BMI and no history of alcohol excess
What are the characteristic features of alcoholic liver disease?
What are some of the essential features?
- Hepatomegaly +/- fever +/- leucocytosis +/- hepatic bruit (caused by narrowing of artery)
Also seen as disease progresses toward cirrhosis:
- Malaise, nausea, itch, jaundice, sepsis, encephalopathy, ascites, renal failure, death
Essential features:
- Excess alcohol within 2 months
- Bilirubin <80mmol/l for <2 months
- AST:ALT ratio >1.5
Compare NAFLD and ALD
NAFLD v ALD
Weight: elevated v variable
Fasting plasma glucose/HbA1c: usually elevated v normal
Reported daily alcohol: below daily v excess
ALT: elevated or normal in both
AST: normal v elevated
AST:ALT ratio: <0.8 v >1.5
GGT: elevated/normal v marked elevated
HDL-Cholesterol: low v elevated
Define acute hepatitis
Inflammation of the liver caused by infection with one of the five hepatitis viruses
- Inflammation begins suddenly and only lasts a few weeks
- Usually symptomatic (fever, flu, yellow sclera)
Define chronic hepatitis
- Inflammation of the liver for >6 months
- If viral chronic hepatits: virus has been present for >6 months
- Common causes: Hepatitis B and C virus (HBV/HCV)
- Usually asymptomatic by this stage
List 3 causes of acute hepatitis
- Infection: Hep A-E, Malaria, Syphilis,
- -* Toxins, drugs, alcohol
- Haemochromatosis
- Autoimmune
What are the laboratory findings to diagnose viral hepatitis?
Detection of specific immune responses (IgM or IgG)
- Look for antibodies against different viruses
- IgM: new/acute infection
- IgG: previous or chronic infection
Viral nucleic acid detection using PCR
What is Hepatitis A (HAV)?
Transmission
Clinical features
What: RNA virus
- Acute hepatitis
Transmission: faeco-oral with a human reservoir
- Virus can survive for months in contaminated water and sheds via biliary tree into gut
Clinical features:
- Jaundice, fever, diarrhoea
- Incubation period: 30 days
- Age: main determinant of severity (usually asymptomatic in <5yrs)
What is the diagnosis and treatment for HAV?
Are there any prevention strategies?
Diagnosis: IgM to Hepatits A or RNA in stool/blood
Treatment: self-limiting
- Maintain hydration, avoid alcohol
Prevention: vaccine
- inactivated vaccine, 2nd dose gives life protection
- Pre-exposure for travellers, MSM, IVDU, chronic liver disease
What is Hepatitis B Virus (HBV)?
Transmission
- DNA virus
- Chronic or acute
Transmission:
- Mother to baby transmission (most common)
- Blood and sex eg. transfusion, sex
- Organ and tissue transplantation
- Contaminated needles
What are the clinical features of acute hepatitis B?
What is the importance of the age of acquisition
- Incubation: 2-6 months
- Fever, jaundice
- Age at time of infection determines:
Severity of acute illness: younger people have weak immune system so weak immune response mounted therefore will be asymptomatic
Risk of developing chroniv hepatitis B (CHB)
- Infection at birth: asymptomatic but leads to chronic infection
- Infection in adults: usually symptomatic but is cleared
What are the complications of hep B?
- Weight loss
- Abdo pain
- Fever
- Cachexia (wasting and weakness of body due to severe chronic illness)
- Abdo mass
- Blood ascites
As it progresses:
- Liver failure
- Cirrhosis so higher risk of carcinoma (HCC)
- Decompensation
- Death
How is Hepatitis B diagnosed?
What do the results mean?
sAg - surface antigen, marker of current infection
sAb - surface antibody, marker of immunity (previously infected but not currently)
cAb - either been infected or currently infected, just know patient has come into contact with whole antigen (not from vaccine)
HBV DNA - determines viral load, patient currently infected
eAg - e-antigen, suggests high infectivity
eAb - e-antibody, suggests low infectivity
HBV infection diagnosed if sAg or DNA are detectable
Chronic HBV: sAg detectable for >6 months
Carriers divided into 2 groups:
eAg +ve (early disease): high viral load, high risk of CLD and HCC, highly infectious
eAg -ve (late disease): low viral load, low risk of CLD and HCC, less infectivity
What are the treatment options for acute and chronic hepatitis B?
Treatment:
Acute HBV: none (self-limiting)
Chronic HBV:
- Most don’t require treatment
- Only treat those with liver inflammation (LFT or biopsy) or fibrosis (fibroscan)
- Aim of treatment: suppress viral replication and prevent further liver damage
- Two types of treatment: immuno-modulatory (interferon) or suppress viral replication (Tenofovir)
- These aren’t curative but reduce risk of complications
Are there any prevention strategies for Hepatitis B?
- Education (safe sex, safe injecting)
- Immunisation (HBV sAg vaccine): included in immunisation schedule in UK
- Prevent mother-to-child transmission: HBV vaccine to newborn (6 doses in first year), Tenofovir during last trimester if high viral load
What is Hepatitis C (HCV)?
Transmission
Clinical features
- RNA virus
- Acute or chronic
- Most common Hep virus in the UK
Transmission: blood-borne
- Shared needles, transfusion, transplant
Clinical Features:
- Incubation: 6-7 weeks
- Ususlly asymptomatic
What determines the progression from acute to chronic hepatitis C and on to cirrhosis?
Spontaneous resolution in 25% of acutely infected patients
Rate of progression related to:
- Male sex, age >40 at time of acquisition and alcohol >50g/week
Duration of infection:
- 20% risk of cirrhosis after 20yrs
- 50% risk of cirrhosis after 50years
How is hepatitis C diagnosed?
Diagnosis:
- Mostly diagnosed through screening high-risk groups (IVDU and immigrants from high prevalence countries) as usually asymptomatic
- Anti-hcv IgG (antibody) positive = chronic infection or cleared infection
PCR or antigen positive = current infection / viraemia
What is the treatment?
Are there any prevention strategies?
Spontaneous resolvement of acute HCV in 25% individuals
Treatment: aim to cure infection
- 8-12 weeks of oral treatment
- Direct Acting Antivirals (DAAs) inhibit different stages of the replication cycle
Prevention: no vaccine or exposure prophylaxis
- No reliable immunity after infection
What is Hepatitis D?
Transmission and acquisition
Complications
Treatment
- ssRNA virus
Transmission: requires HBV to replicate
- Blood and sex (same as HVB)
Acquisition:
- Co-infection with HBV
- Super infection of chronic HVB carriers
Complication: inc. risk of CLD
Treatment: Peg IFN (pegylated interferon (chemotherapy))
What is Hepatitis E (HEV)?
Transmission
Clinical features
- RNA virus
- Acute infection
Transmission: faeco-oral and pork products
Clinical features:
- Incubation period: 40 days
- Diarrhoeal illness (similar to Hep A)
- Neurological manifestations in some: Guillaine-Barre syndrome, encephalitis, ataxia, myopathy
What is the treatment for hepatitis E?
Are there any prevention strategies?
In what situations would Chronic Hep E arise?
Treatment: supportive
Prevention: none, no vaccine
Chronic Hep E develops in immunosuppressed patients or patients who’ve had a bone marrow transplant
Describe the biliary tree pathway
Bile drains through left and right hepatic ducts into common hepatic duct
This joins with the cystic duct from the gallbladder to form the common bile duct
Before it enters the duodenum, it joins with the pancreatic duct to form the ampulla of vater
Define cholelithiasis
The formation of gallstones
What can gallstones be composed of?
- Cholesterol
- Bile pigment
- Mixed (cholesterol, pigment, calcium)
Describe the pathophysiology of cholesterol gallstones
Cholesterol secreted into bile is not water soluble and kept in solution by micelles containing bile acids and phospholipid
- Excess cholesterol (in relation to bile salts) will crystallise out and form a gallstone
ie. supersaturated bile - This would occur if there was excess cholesterol secretion or decreased bile salt secretion
List 3 risk factors for formation of cholesterol gallstones
Fat (overweight)
Forty (near forty or above)
Female
Fertile (premenopausal therefore increased oestrogen levels which are thought to inc. cholesterol levels in bile and decrease gallbladder contractions
Fair (caucasians)
Others:
Things that inc. oestrogen: OCP, liver cirrhosis
Things that inc. cholesterol: diet, diabetes
Describe the pathophysiology of bile pigment gallstones
- bile pigment = bilirubin, a breakdown product of haemoglobin
- excessive bilirubin secretion (eg. haemolytic anaemia) can cause it’s precipitation in concentrated bile in the gallbladder
Explain the clinical features of gallstones depending on their location in the biliary system
80% gallstones are in gallbladder and are asymptomatic
Cystic duct/neck of gallbladder:
- RUQ pain, usually occuring after meals
- Crampy in nature
- no associated jaundice or fever
- Acute cholecystitis (inflam of GB)
Common bile duct: Biliary obstruction
- cholestatic jaundice
- bacterial infection and cholangitis
- severe RUQ pain
Pancreatic duct: can lead to pancreatitis (severe, constant abdo pain)
Rarely, can perforate through the wall of the inflamed GB into the intestine producing a fistula
Describe the pathophysiology and clinical features of acute cholecystitis
Pathophysiology:
- Initially, obstruction of the neck of the gallbladderor cystic duct by an impacted stone, leading to distension and inflammation
- Inflammation is usually sterile but within 24hours, organisms can grow there
- occassionly, the inflam subsides quickly leaving the gallbladder distended with mucus (mucocele): slight abdo pain with palpable gallbladder
- more commonly, inflam is more severe involves whole wall leading to localised perotinitis and acute pain
Clinical Features:
- severe RUQ pain
- continuous pain, increasing in intensity over 24 hours
- can radiate to shoulder and back
- nausea, vomiting
- fever and mild jaundice (20%)
- positive Murphy’s sign (right hypochondrium pain worse on inspiration)
What is lithogenic bile?
Bile that forms gallstones
- Excess cholesterol or
- Reduced bile salt or
- Excess bile pigment
List 3 complications of gallstones
- Inflamed gallbladder (cholecystitis)
- Blockage of common bile duct: severe pain, jaundice and cholangitis
- Blockage of the pancreatic duct: can lead to pancreatitis (intense, constant abdo pain)
- Gallbladder cancer
How are gallstones identified/diagnosed?
Abdominal Ultrasound
Endoscopic ultrasound (EUS)
- Helps identify smaller stones
MRCP (magnetic resonance cholangiopancreatography)
- Type of MRI
Operative cholangiogram
- Used to visualise bile ducts
ERCP (endoscopic retrograde cholangiopancreatography)
- gallstones diagnosed this way can also be removed in the same procedure
Bloods
- infection, jaundice, pancreatitis or other complications of gallstones
What are the treatment options for gallstones?
Asymptomatic: active monitoring
Keyhole cholcystectomy
- Removal of gallbladder, recommended if stone formation is frequent
ERCP to remove stones from bile duct
What LFT results would be seen in prehepatic , hepatic and post-hepatic jaundice?
Pre-hepatic: isolated rise in bilirubin (inc. RBC breakdown)
hepatic jaundice: rise in bilirubin, AST and ALT
Post-hepatic jaundice:
- Early: rise in ALP (bile ducts - cholestasis) and bilirubin
- Late: also get elevated AST/ALT due to back pressure
Define acute pancreatitis
Inflammation of the pancreas by enzyme-mediated autodigestion
List 4 causes of acute pancreatitis
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps/Metabolic
Autoimmune
Scorpian bites
Hyperlipidaemia, hypercholesterolaemia
ERCP
Drugs eg. OCP, azathioprine, HRT
List the symptoms seen with pancreatitis
List 3 examination findings
Severe epigastric pain, radiated to back
Worse lying flat
Nausea and vomiting
Fever (chills, temperature etc.)
Examination findings:
- tachycardic, hypotensive, pyrexia
Outline the pathophysiology of acute pancreatitis
(dependent on underlying cause)
- inflammation damages the pancreas and acini (exocrine functional units)
- acinar cells release digestive enzymes (protease/lipase/amylase) into surroundings rather than the pancreatic ducts causing further damage of surrounding structures and pancreatic tissue
- autodigestion
- amylase: measured for diagnosis
- lipase: fatty necrosis of pancreas
List investigations needed to diagnose acute pancreatitis and those to help with diagnosis
Need two of:
- clinical presentation
- LFTs
- Ultrasound (to exlucde/confirm gallstones): if positive may need ERCP
To aid diagnosis:
- FBC (leucocytosis), U&Es, LFTs
- CRP
- Amylase
- Ultrasound
- Glucose
What is the management for acute pancreatitis?
Treat underlying cause
Supportive treatment: 48hr monitoring for serious complications
- IV fluids
- oxygen
- analgesia
- nutritional support
List 3 acute and 3 chronic complications of acute pancreatitis
Acute:
- Fatty necrosis
- pancreatic abscess
- Haemorrhage (erosion of splenic artery)
- Portal vein thrombosis
- acute kidney infection
- acute respiratory distress syndrome
Chronic
- chronic pancreatitis
- exocrine failure and malnourishment
- endocrine failure and diabetes
- stones/strictures
Describe how fatty necrosis occurs following acute pancreatitis
= autodigestion
- enzymes (lipases) leak into the pancreatic tissue and abdominal tissue leading to fat necrosis
- yellow fat: damaged
- vessel necrosis leads to avascular tissue
List 3 different types of pancreatic cysts and state their ability to become malignant
Intraductal papillary mucinous neoplasm
- in continuity of main pancreatic duct or side branch
- dysplastic papillary lining secreting mucin
- risk of pancreatic cancer
Mucinous cystic neoplasm
- mucinous lining, ‘ovarian-type’ stroma
- small porportion can become malignant
Serous cystadenoma
- many small and some larger cysts
- no mucin production
- almost always benign
What is the most common cancer of the pancreas?
What is the pre-malignant stage?
Outline the pathology and prognosis
ductal adenocarcinoma (exocrine pancreatic cancer)
Pre-malignant stage: pre-malignant pancreatic intraepithelial neoplasm (PanIN) which is asymptomatic
Pathology: perineural invasion
Prognosis: common to present late as symptoms are vague and so 5yr survival is 5%
List two risk factors for development of pancreatic carcinoma
- smoking
- germline mutations eg. BRCA, but these are rare
List three signs and symptoms of ductal adenocarcinoma
- Painless obstructive jaundice
- New onset diabetes
- Abdo pain due to pancreatic insufficiency or nerve invasion
- Tumour in head may obstruct pancreatic and biliary duct - double duct sign on radiology
How are pancreatic carcinoma’s treated?
Whipple’s procedure: tumour in the head of the pancreas
- Removal of the head of the pancreas, duodenom, GB and bile ducts
- difficult to get clear resection margins
Neoadjuvant therapy
- improves margin status and may be associated with longer survival
List 3 cancers of the pancreas/biliary tract
Ductal adenocarcinoma
Pancreatic neuroendocrine tumour
Carcinoma of ampulla of Vater
Cholangiocarcinoma
Carcinoma of the GB
Outline the pathology of pancreatic neuroendocrine tumours
Outline the prognosis
- Sometimes secrete hormones (function tumours)
Commonest functional tumour: insulinoma
- Presents with hypoglycaemia
Prognosis:
- 90% are benign
- Malignant endocrine tumours have better prognosis than pancreatic carcinoma
What is a cholangiocarcinoma?
How does it present?
How is it classified?
How is it treated?
= Carcinoma of the bile ducts
Present: behave similarly to pancreatic cancers due to obstruction
Classification: intrahepatic/extrahepatic depending on origin
- intrahepatic cholangiocarcinoma needs distinguished from metastatic adenocarcinoma and HCC
Treatment: Whipple’s procedure to remove common bile duct
What is the biggest risk factor for carcinoma of the gallbladder?
Gallstones
outline the presentation of upper GI bleeds and how they correlate to the position of pathology in the GI tract
Haematemesis: vomiting blood
‘Coffee ground’ vomiting: presence of coagulated coffee
Melaena: dark tarry stool, usually diarrhoea
Location:
Oesophagus/Stomach: more likely to present with haematemesis
Duodenum/Below: Melaena
List 4 causes of upper GI bleed
Peptic ulcer
- Due to acid, H. pylori or NSAIDs
Oesophagitis
Gastritis
Duodenitis
Varices
Malignancy
Why do peptic ulcers need checked to ensure they’ve healed?
What is the aim of treatment of a bleeding peptic ulcer?
- Worried about malignancy
Aim: treat the ulcer but also need to find the bleeding vessel
What is the main cause of oesophagitis?
Gastric reflux
What is a mallory weiss tear?
How does it present?
= A tear of the mucous membrane, most common at the gastro-intestinal junction
Presentation: violet vomiting without blood then suddenly get vomiting with blood
- Non-variceal bleeding
Outline the management for upper GI bleeds
Resuscitate if required
- Pulse and BP
- IV access for bloods/fluids (more fluid resuscitation)
- Oxygen
Risk assessment and timing of endoscopy
Drug therapy and transfusion
What is involved in the risk assessment for upper GI bleeds?
To assess risk:
- Sometimes it’s obvious: severe upper GI bleed identified by clinical assessment (pulse, BP, age, co-morbidities)
- Endoscopic: rockall score
- Clinical: admission rockall score (pre-endoscopic score) or Glasgow Blatchford Score (more predictive of mortality and need for endoscopic intervention. GBS <1 identifies those at very low risk of poor outcome). GBS measures blood urea (goes up with GI bleed)
High Risk (haemodynamic instability or severe ongoing bleeding): emergency endoscopy
Moderate risk: admit and next day endoscopy. Most patients need endoscopy within 24hours)
Low risk: out-patient endoscope and management
What endoscopic therapy is available for upper GI bleeds?
Adrenaline injection: vasoconstriction, tamponade effect however this will wear off
Heat probe
Endoscopic clips: clip the artery
Haemostatic powders
Usually:
- Dual therapy of adrenaline with either heater probe or endoscopic clips
- Can follow up with a haemostatic powder
What is the pharmacological management for upper GI bleeds
IV PPIs
- Reduce rebleeding and mortality if given post-endoscopically (for 3 days) to high-risk patients who required endoscopic therapy
- not beneficial pre-endoscope
What advice is give to patients on:
Aspirin
NSAIDs
Clopidogrel
Warfarin
Aspirin: continue low dose aspirin once haemostasis is achieved and add PPI
NSAIDs: Stop
Clopidogrel: continue
Warfarin: difficult to achieve homeostasis therefore stop until haemostasis is achieved and then assess risks v benefit. Generally aim to restart as soon as possible
Define varices
Dilated veins in the distal oesophagus/proximal stomach caused by elevated pressure in the portal venous system (typically from cirrhosis). They may bleed but no other symptoms
Outline the pathophysiology of varices
With cirrhosis there is..
- The liver is scarred and therefore blood won’t flow as easily through it and increase pressure
- Also have increased portal inflow due to toxic excretions of the liver causing splanchnic vasodilation
- Increased pressure in the portal circulation ie. splenic, portal, superior and inferior mesenteric veins
- Portal vein drains into the liver which comes from splenic and mesenteric veins ie. the entire GI tract drains into the portal veins
- Poor flow through the portal vein and vasodilation increases portal pressure causing oesophageal veins to dilate (varices)
- Angiogenesis: production of more veins
How are varices diagnosed?
How are bleeding varices managed?
Diagnosis: upper endoscopy
Managed:
Primary prophylaxis: beta-blockers or band ligation
Acute bleeding:
- abx and terlipressin early in A&E
- Band ligation 1st line for oesophageal variceal bleeding
- TIPS for uncontrolled variceal bleeding
- Balloon tamponade (temporary salvage)
Prevention of rebleeding: beta-blocker and repeated band ligation
What is TIPS?
What does it do?
What is one risk of TIPS?
Transjugular Intrahepatic Portosystemic Shunt (TIPS
- A shunt between the portal vein and hepatic vein
- Without TIPS, blood has to pass through microcirculation of the liver and with all the scarring, the blood finds it difficult to flow through
Risk: encephalopathy
What is the classical presentation of upper GI cancers?
An ulcer which will not heal
- If an ulcer persists without definite, identifiable cause, think possible cancer
List the layers of the oesophagus
Mucosa: non-keratinising stratified squamous epithelium and muscularis muscosa
Submucosa
Muscularis propria (2 types of muscle orientation)
Adventitia
Outline the pathology of reflux oesophagitis
- acid and digestive enzymes injury squamous epithelium lining oesophagus
- inc. number of inflammatory cells- basal zone of the squamous epithelium is hyperplastic
List 2 infections and 2 inflammatory conditions that can occur in the oesophagus
Infections:
- Candida albicans (candida oesophagitis)
- Herpes Simplex virus
Inflammation:
- peptic oesophagitis / GORD (gastro-oesophageal reflux disease)
- pills (eg. iron, bisphosphonates) can get stuck in the oesophagus, causing damage/ulceration of the lining
Outline the pathology of candida oesophagitis
- Active chronic inflammation
- many neutrophils
Which 2 conditions affecting the oesophagus occur more commonly in immunosuppressed patients?
- Candida albicans
- Herpes Simplex Virus
Outline the histology/cytology of Herpes Simplex Virus in the oesophagus
- atypical squamou cells
- inflammatory exudate and cells slough
- multi-nucleared giant cells with ground-glass nuclei in epithelial cells
Define Barrett’s oesophagus
A pre-cancerous condition which is a complication of chronic GORD (gastro-oesophageal reflux disease) involving metaplastic changes to the epithelium that line the distal end of the oesophagus
Outline the pathology of Barrett’s oesophagus
- a metaplastic response to mucosal injury eg. from long-term GORD
- pre-cancerous condition
- squamous epithelium become glandular, usually intestinal with goblet cells
- associated with development of benign strictures but also with adenocarcinoma
- can progress to dysplasia then adenocarcinoma
- dysplasia can be defined as low- or high-grade
Outline the cell changes seen with low grade and high grade dyplasia as seen in Barrett’s oesophagus
Low grade
- Polarity lost
- nuclei are stratified
High grade
- polarity lost
- nuclei rounder and vesicular
- prominant nucleoli
- abnormal mitoses
- necrosis
What is the major complication of Barrett’s oesophagus?
Dysplasia can progress into adenocarcinoma
What is the diagnosis and treatment for Barrett’s oesophagus
Diagnosis: screening
- 4 biopsies taken
Treatment:
- radiofrequent ablation (endoscopic treatment)
What are the two cancer types seen in the oesophagus and list 2 risk factors for each
- Squamous carcinoma: smoking and alcohol
- Adenocarcinoma: GORD and obesity
List 3 causes of acute and 3 causes of chronic gastritis
Acute:
- Alcohol
- Medication eg. NSAIDs
- Severe trauma
- Burns (may cause systemic upset)
- Surgery
Chronic:
Autoimmune (destruction of parietal cells due to anutoantibodies to intrinsic factor therefore can’t absorb B12)
Bacterial (H. Pylori)
Chemicals eg. NSAIDs, bile reflux
Outline the pathophysiology of autoimmune gastritis
Autoimmune destruction of parietal cells due to autoantibodies against intrinsic factor and parietal cell antibodies in blood
Leads to:
- complete loss of parietal cells with pyloric and intestinal metaplasia
- Achlorhydria (HCl absence in gastric secretions) leading to bacterial overgrowth
- Hypergastrinemia (excess gastrin which stimulates HCl release) leading to endocrine cell hyperplasia / carcinoids (slow-growing neuroendocrine tumour)
- Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer
Outline the pathophysiology of H. Pylori infection
- H. pylori colonises gastric mucosa causing active chronic inflammation
- H. Pylori inhabits the gastric glands and produces large amounts of urease (turning urea into ammonium) therefore neutralising the acid
After exposire to H. Pylori, the resulting gastritis can occur in 2 patterns:
- Antral-predominant gastritis: hypergastrinemia, hyperchlordria and duodenal ulceration
- Pangastritis (more commonly seen with chronic infection): hypochlorhydria, multifocal atrophic gastritis, intestinal metaplasia, cancer
- In antral-predominant: the glands detect acidity to determine how much to secrete, and with H. pylori no longer detect acidity therefore more gastrin therefore HCl is produced, irritating the stomach and causing gastritis
- Patients with high IL-8 tend to get pangastritis
- Peptic ulceration is due to a combination of excess acid secretion and host effects: impaired mucosal defence (eg. NSAID interference with mucosal prostaglandin synthesis) and microbe factors
List 3 complicatoins of peptic ulceration
- haemorrhage
- perforation
- fibrosis (leading to stenosis)
- melena (black tarry stools)
Outline the pathophysiology of chemical gastritis
List 3 causes of chemical gastritis
- few inflammatory cells
- surface congestion oedema, elongation of gastric pits
- reaction hyperplasia/atypia, ulceration
- Seen in atrum
Causes:
- Bile reflux
- NSAIDs
- ethanol
- oral iron
What is the major complication of pangastritis and antral-predominant gastritis
Pangastritis: cancer
Antral-predominant: ulceration
What is the strong association with gastric cancer?
- Chronic gastritis: H. Pylori or autoimmune
Outline the morphology of gastric cancer
- Atrophic musoca
- Chronic inflammation
- Intestinal metaplasia
- Dysplasia
Classified into intestinal and diffuse
- Diffuse: individual malignant cells with mucin vacuoles
Outline 3 conditions that can be categorised under the umbrella term irritable bowel disease (IBD)
Ulcerative colitis
- causes long-lasting inflammation and ulcers in the innermost lining of the colon (restricted to the colon)
Crohn’s disease
- inflammation of the GI tract, anywhere from mouth to anus
UC and Crohn’s are both inflammatory colitis
Other forms of colitis eg. infective, ischaemic colitis
Outline the epidemiology of IBD
Peak incidence: 16-24
Second peak in older generation
What is the aetiology of irritable bowel disease
Combination of:
- environment factors eg. diet
- genetic disposition eg. inflammatory conditions
- gut microbiome
- host immune responses (innate, adaptive)
Outline the presentation of infective colitis
Identify 2 clues in a patient’s history that may suggest infective colitis
- short history of diarrhoea +/- vomiting
- abrupt onset +/- resolution of synptoms
- systemic upset and predominant fever
History:
- travel
- unwell contacts
- immunocompromised
Outline the investigations and treatment required for a patient with suspected infective colitis
Infections: stool culture (need 4 samples for 90% sensitivity)
Treatment:
- clears spontaneously
- treatment usually conservative if immunocompetent
Outline the presentation of ischaemic colitis
- Abrupt onset of pain and bloody diarrhoea +/- systemic inflammatory response syndrome (SIRS)
SIRS: two of
- WCC <4 or >12
- Temp <36 or >38
- RR >20
- HR >90
Hypoperfusion > embolic
- Hypoperfusion causes segmental colitis
- blood supply is compromised (usually @ splenic flexure)
Outline the investigation and treatment for suspected ischaemic colitis
Investigation:
- CT may show segmental colitis in watershed areas (regions of body receiving dual blood supply from most distal branches of 2 large arteries eg. splenic flexure
Define acute severe colitis
What investigation is essential for severe colitis
>6 stools per day and systemic upset
Investigations: AXR and Endoscopy
AXR
- Helps assess extent as severity
- Megacolon: dianeter >5.5cm
- Toxic megacolon: perforation / about to perforate. Megacolon and signs of systemic toxicity
Endoscopy
- flexible sigmoidoscopy is safer and can still diagnose
- useful for biopsies
- need to be carried out within 72hrs (ideally 24hrs)
Outline the acute and chronic changes with chronic IBD
Acute:
- acute inflammation: inflammatory infiltrate helps determine if UC or Crohn’s
- Ulceration (and depth of ulceration)
- Loss of goblet cells
- Crypt abscess formation
Chronic:
- Architectural changes: shorter villi, doesn’t invade muscularis layer, can split dilate, brach
- Paneth cell metaplasia: red granular cytoplasm
- Chronic inflammatory infiltrate in lamina propria: plasma cells normally distributed superficially in mucosa, but with IBD there is loss of the gradient and plasma cells are seen throughout. Removes idea of infective colitis
- Neuronal hyperplasia
- Fibrosis
Outline the clinical presentation of ulcerative colitis
- Diarrhoea: often with blood/pus
- Fever
- Abdominal pain and cramping
- Rectal pain and bleeding
- Urgency to defecate
- Weight loss and poor appetite
- Fatigue
Outline the histology of ulcerative colitis
- inflammation confined to the mucosa
- active component: prominent crypt abscess formation
- degranded gland architecture, gland drop-out, dilation and branching
- inflamed lamina propria: diffuse inc. in plasma cells and lymphocytes
Outline the macroscopic and microscopic features of ulcerative colitis
Macroscopic:
- Diffuse involvement of the colon
- terminal ileum can be involved but generally only in severe cases where whole bowel inc. caecum is involved
Microscopic:
- Crypt architectural changes generally very marked
- little/no fibrosis
- no granulomas
Outline the treatment for ulcerative colitis
1st line - mesalazine (5-ASA)
- effective in inducing remission
- high dose controls UC quickly
- topical or oral
2nd line - Azathioprine
- used for severe relapse/freq. relapsing
- requiring 2+ corticosteroid courses within 12m period
Outline the treatment for acute severe ulcerative colitis
Treated with high-dose IV corticosteroids eg. methylprednisolone or hydrocortisone
- Start early, don’t need to wait for stool culture
If stool freq >8/day or >3/day with CRP >45 - need colectomy or infliximab / ciclosporin
- Infliximab: TNF-a monoclonal antibody
Identidy 3 complications of ulcerative colitis
Malignancy (colorectal tumour)
Local complications:
- haemorrhage
- toxic dilation (ie. toxic megacolon)
Systemic complications:
- Skin: erythema nodosum, pyoderma gangrenosum
- Liver: cholangiitis
- Eyes: iriitis, uveitis
- Ankylosing spondylitis
What is the commonest colorectal cancer?
adenocarcinoma
Outline how an adenoma can develop into a carcinoma
Adenoma - benign tumour of glandular tissue
- In hollow organs, the adenoma grows into the lumen: adenomatous polyp
Progressive acquisition/accumulation of mutations
- Loss/mutation of TSGs occur early eg. TP53 (gene coding for P53)
- P53 can stall the cell cycle at checkpoints allowing for DNA repair or to initiate apoptosis
- Mutations of TSGs; point mutations or deletions
- Activation of proto-oncogenes (eg. RAS genes)
- Defective DNA repair: mismatch repair genes (eg. MSH2 and MSH6) can be mutated
Outline high-grade and low-grade adenomatous dysplasia
High grade: characterised by very abnormal architecture with complex glands (joined, fused, brnached)
Low grade: abnormal nuclei, abnormal, mitotic cells with chromatin all bundled together
What are the categories used to describe the architecture of adenomas
- Villous (>80% mucosa is villous)
- Tubulovillous
- Tubular (<20% of mucosa is villous)
List 3 risk factors for developing colorectal carcinoma
- Presence of adenoma (size, number, villous)
- History of IBD esp. ulcerative colitis
- Family history eg. polyposis syndromes
outline the histology of colon cancer
- ulcerated surface
- irregular gland architecture
- pink, inflammatory material at the surfave
Outline the features of bowel screening
qFIT testing (stool sample)
50-74yr olds every 2 years
+ve result goes to colonscopy
- Helps pick up polyps before they progress to cancer
List 2 risk factors for developing Crohn’s disease
- smoking: stopping smoking reduces relapse rate, need for immunosuppression and surgery
- peak incidence: 15-24yrs
Outline the clinical presentation of crohn’s disease
- abdominal pain
- diarrhoea (watery > bloody)
- weight loss
- fistulae, abscesses (could be oropharyngeal, gastroduodenal)
- fatigue
- mouth ulcers
Identify 3 extra-intestinal symptoms of crohn’s disease
Eyes: uveitis, episcleritis
Joints: sacroiliitis, inflammatory arthropathy
Skin: erythema nodosum, pyoderma gangrenosum
More complications than UC but less likely to develop cancer
Outline the investigations for Crohn’s disease
Faecal calprotectin (useful to differentiate between IBD/IBS and assess activity in IBD)
MR/CT enterography (extraluminal activity)
Ileocolonoscopy and biopsy
Outline the pathology of Crohn’s disease
GRANULOMAS
- Significant proportion don’t have granulomas, but if present, it’s highly suggestive of crohn’s
Microscopy: transmural inflammation (loss of the 5-layer structure)
- Inflammatory cells infiltrate from mucosa right through the muscularis layer
Outline the treatment for Crohn’s
Azathioprine (DMARD)
- maintenance of control
- reducing course of corticosteroid
Methotrexate
- induces remission, can be used for maintenance
Biologics
- TNF-a antagonists: infliximab
Surgery
- 70% lifetime risk of surgery
- non-curative
Compare and contrast the pathology of ulcerative colitis and crohn’s disease
Crohn’s: small and large bowel inflammation
UC: only large bowel involvement
Crohn’s: tends to involve prox. large bowel
UC: tends to extend from rectum and involve LHS of bowel
Crohn’s: patchy inflammation resulting in macroscopic ‘skip lesions’
UC: confluent, diffuse inflammation
Crohn’s: transmural, deeply ulcerating inflammation
UC: inflammation centred on mucosa
Crohn’s: granuloma’s present
Outline the assessment of LFTs
- Look at ALP and ALT
- elevated x10 ALT: hepatocellular injury
- elevated x3 ALP: marker of cholestasis (produced from bile canaliculi) - Look at GGT
- Suggests biliary epithelial damage and bile flow obstruction
- Elevated in response to damage or alcohol and drugs
- ALP elevation in absence of elevated GGT: increased bone breakdown - Jaundiced patient with normal LFTs
- Isolated bilirubin elevation
- Suggestive of pre-hepatic jaundice eg. Gilbert’s syndrome or haemolysis
Outline the pathway of bilirubin following haem breakdown
Haem is broken down into iron and unconjugated bilirubin
- Unconj. bilirubin is lipid soluble and transported to the liver to be conjugated (water soluble)
- this then is taken to the colon where it becomes urobilinogen
- 90% of urobilibogen is converted to stercobilin (brown) and excreted in faeces
- 10% of urobilinogen is taken back to the liver and converted to urobilin (yellow) and excreted in urine
Identify 2 causes of pre-hepatic jaundice and outline the changes of bilirubin and how this affects stool and urine
Pre-hepatic jaundice = increased RBC breakdown
- Overwhelms conjugation process in the liver therefore have increased unconjugated bilirubin
- Unconj. bilirubin isn’t water soluble therefore cannot enter urine so elevated levels have no affect on urine ie. normal urine
- No bile obstruction (which would cause poor fat breakdown) therefore normal stool (rather than fatty, pale stools)
Causes: Gilbert’s syndrome and haemolytic anaemia
Outline hepatic jaundice, the changes seen in bilirubin levels and the changes seen in stool and urine
Give two causes
Hepatic jaundice: hepatic injury (dysfunction of hepatocytes) therefore lose conjugation ability
- Increase in unconjugated bilirubin
In cirrhotic livers, there is compression of intrahepatic portions, causing a degree of obstruction
- Therefore, increase in inconjugated and conjugated bilirubin
- Inc. in conjugated bilirubin - dark urine
- Bile obstruction (only if cirrhosis) - fatty, pale stools
Causes: alcoholic liver disease
- hereditary haemachromatosis
- alcoholic hepatitis
- hepatocellular carcinoma
Outline post-hepatic jaundice, the changes seen in bilirubin levels and the changes seen in stool and urine
Give two causes
Post-hepatic jaundice: obstruction to biliary drainage
- inc. in conjugated bilirubin - dark urine
- bile obstruction - pale, fatty stools
Causes:
- gallstones
- cholangiocarcinoma
- pancreatic cancer
What causes dark urine and pale, fatty stools
Dark urine: increase in conjugated bilirubin
Pale, fatty stools: bile obstruction causing poor fat breakdown
What is a procelain gallbladder and what is it’s primary cause?
Porcelain gallbladder: calcification of the gallbladder
Cause: excessive gallstones (the exact cause is unclear)
What is Chilaiditi syndrome?
A rare condition in which a portion of the colon is abnormally located between the liver and diaphragm
What is the pathopneumonic sign of colitis on CXR?
Thumbprinting
Define pneumoperitoneum
What is it’s pathopneumonic sign?
Air in the peritoneual cavity
Pathopneumonic sign: Rigler’s sign (double-walled sign)
What would calcification outside of the kidney suggest on CXR?
- Calcified lymph node (TB)
- Calcification of faecal material
Outline the risk factors for a porcelain gallbladder
Fat
Forty
Fertile
Female
Fair (caucasian)
How do you differentiate between Chilaiditi syndrome and pneumoperitoneum?
Both are seen as air under the right hemidiaphragm
Chilaiditi syndrome: air is held within a specific space (the colon) and is confined
Pneumoperitoneum: looks free and not within a particular space
What is a hernia and how would it present
Hernia: abnormal protrusion of bowel through a weak spot in the abdominal muscles
Presentation:
- a buldge that is painful, especially on coughing, bending over, laughing
How do look for perforation radiologically?
CXR - 80% sensitive for free gas
CT used to confirm diagnosis and look for cause
How do you look for bowel inflammation radiologically?
AXR useful for colitis
US for cholecystitis
CT first choice otherwise
Define uroperitoneum
urine leakage into the peritoneal space
What is the most common cause of free air in the abdomen?
Perforated ulcer
If an obscured psoas muscle is identified on CXR, what would you want to think about?
- Burst aneurysm (haemorrhage pushing on the psoas muscle)
How would you look for obstruction radiologically?
How would the history help identify location of obstruction
Radiologically:
- AXR
- CT to look for cause
History:
- More distal: pain, constipation and more distension
- More proximal: pain, vomiting and less distension
Identify 3 common causes of bowel obstruction
- sigmoid volvulus (twists around it’s own mesentery
- hernia
- colon cancer
- gallstone that erodes through GB into intestine
What is the 1st choice imaging modality for ischaemia?
CT
