Liver Flashcards
What are the general anatomical features of the liver?
- Large, lobulated exocrine and blood-processing gland, with vessels and ducts entering and leaving at the porta.
- Enclosed by a thin Collagen Tissue capsule, mostly covered by mesothelium – provide support
- Collagen tissue of the branching vascular system provides gross support.
Parenchymal cells are supported by fine reticular fibres.
What does the blood supply to the liver look like?
Organ receives venous and arterial blood – unique – dual blood
* Portal vein – brings food rich blood from the GI tract
* Hepatic artery – bring arterial blood
* Hepatic vein – collects the blood from the liver parenchyma
* Lymphatic system – sewage system of the body
* Hepatic duct - liver produces and secretes bile via the hepatic ducts - bile stored in the gallbladder
Note - Proportion of blood supply – 25% from hepatic artery (oxygenated blood) and 75% from portal vein (rich in nutrients)
What does the nerve supply to the liver look like?
Sympathetic and Parasympathetic supply to perivascular structures but very little at the sinusoidal level
Cut the nerve supply – liver works pretty well – how do we know this? – liver transplant works well lacking the nerve supply
Outline the structure of the liver lobules.
Histology of the liver
Hexagonal structure – liver lobule – pattern repeated – surrounded by loose connective tissue (portal tract)
Corners you have the portal triad, which is where the main vessels enter – branch of portal vein, branch of hepatic artery and bile duct
Organization – small channels called sinusoids (surrounded by hepatocytes – cells arranged in perforated plates one cell wide) that start at the portal triad and feed into the portal vein
Path – Blood from HA and PV mix creating highly oxygenated nutrient rich blood moves along the sinusoids towards the portal vein – as the blood moves through the hepatocytes take up, process and release back into the sinusoids – ultimately returns into circulation
In general terms, how do hepaotcytes filter the blood in a coordinated manner?
Blood flow from the portal triad to the central vein
Flow slows down – allowing for the exchange of molecules with the hepatocytes
Hepatocytes upstream able to sense levels of nutrients, signals to hepatocytes downstream – such that the levels of nutrients are appropriate when entering in the systemic circulation
In between cells you also have bile ducts – flows in the opposite direction toward bile duct into common bile duct, and subsequently stored in the gallbladder
Closer to portal triad – sensing role, further downstream – regulatory function
Outline how bloods leaves the liver from the central vein?
Blood collected in central veins goes to sublobular veins, then to collecting veins, and
then hepatic veins leaving the liver.
What is the liver acinus?
Change of perspective – use the portal triad as the central unit – not the central vein
Liver Acinus – comprises a functional unit that puts the portal triad in the centre – based on the position of the triad you have three zones.
These different regions exhibit different metabolic functions – e.g.
1. Zone 1 (periportal) stronger focus on sampling
2. Zone 2 (intermediate) changing the composition
3. Zone 3 (perivenous) blood gets enriched
Low blood sugar – zone 1 detect and send signals downstream – so that downstream hepatocytes break down glycogen releasing glucose
Where are stem cells located in the liver?
Stem cells – located in the periportal area
Population of undifferentiated cells located near the portal tract – differentiate when there is evidence of liver damage.
Outline how the liver sinusoid is organised.
Liver sinusoids – channels between portal triad to the central vein that carry blood at low pressure
- Fenestrated endothelial cells gate to the hepatocytes – not tightly attached to hepatocytes creating a space called the space of disse which is where plasma can enter and interact with the hepatocytes (front garden)
- Hepatocytes have microvilli to increase surface area.
- Up and down liver sinusoids – Kupffer cells – surveying - and signal to the rest of the immune system in response to foreign/anitgens
- Stellate cells – store vitamin A - can close the gates of the fenestrated endothelial lining when there is inflammation – unfavorable – increase pressure
Note - Some of this fluid in the space of disse may pass to the periphery of the lobule to be collected as lymph.
What are the functions of the sinusoidal wall?
Functions of the sinusoidal wall
* Blood cleansing – acts as a filter – plasma only enters
* Hemopoiesis in embryo
* Brings plasma into intimate contact with hepatic cells for metabolic functions
What is the main functional cell of the liver?
Hepatocytes are the main functional cells of the liver and perform an astonishing number of functions. 80% of the mass of the liver is hepatocytes.
The cells are polygonal in shape and their sides are in contact either with sinusoids (sinusoidal face - microvilli) or neighbouring hepatocytes (lateral faces - low/no microvilli)).
A portion of the lateral faces of hepatocytes is modified to form bile canaliculi.
Hepatocyte nuclei are distinctly round, with one or two prominent nucleoli.
What role do stellate cells play in liver cirrhosis?
Liver Cirrhosis – disorganized liver structure – hepatocytes no longer receive the nutrients and oxygen – destroyed and replaced by collagen
Alcohol – most common cause of liver disease – activate of Kupffer cells – retrieves White blood cells – activates stellate cell – converts to a fibroblast – that produces collagen – seals the fenestrations – collagen deposition – increase blood pressure in the sinusoids – blood pressure increases enter the portal vein – start of liver cirrhosis
In what direction deos bile flow in the liver sinusoids?
Bile is produced by hepatocytes – flows in opposite direction into the bile duct via the bile canaliculi
Bile duct is formed by several bile canaliculi – become bigger and bigger to form the common bile duct – drains in towards the ampulla (sphincter of Oddi)
How is lymph formed in the liver?
Lymph is formed in the space of Disse – flows through the peri-portal lymphatic vessels – drain into the portal triad
What are the main veins that form the portal vein?
Blood from small intestine (superior mesenteric), large intestine (inferior mesenteric) and spleen – deoxygenated but nutrient rich
Bilirubin metabolism - Outline how bilirubin is formed, converted into bile and excreted?
Bilirubin – component of bile – break down product of RBC recycling (hemoglobin) – hemolysis
- Unconjugated bilirubin formed from RBC break down
- Transported into the hepatocytes and conjugated with glucuronic acid producing conjugated bilirubin
- Enters the biliary system and released into the small intestine.
- Conjugated bilirubin converted into urobilinogen by bacterial proteases
- Some urobilinogen is re-absorbed and enters the circulation and excreted by the kidney but most is secreted by the feces
Outline the liver’s role in regulating glucose metabolism?
Pancreas can regulate glucose via insulin/glucagon release - in harmony with liver
High blood sugar – insulin release – glucose converted to glycogen and gluconeogenesis is inhibited in the liver
Low blood sugar – glucagon released - glycogen catabolized and gluconeogenesis is activated – released into the blood
What roles does the liver play in detoxificaiton of the body?
Detox organ of the body - Cytochrome p450 system
Toxins go into the liver – steps to produces water soluble product that can then be excreted via the gall bladder or via the kidneys in urine
What are the main liver function tests performed?
Simple tests to see how healthy the liver is
- Bilirubin – high levels – likely some sort of blockage in the bile ducts – spilling over in the circulation – jaundice
- Aminotransferases - ALT (normally measured) and AST – enzymes within the hepatocytes – when the hepatocytes are dying, they are released into the bloodstream – measure of damage
- GGT and alkaline phosphatase (ALP) – go up when there is damage or blockage of the biliary system – these are released into circulation – note that GGT can also be elevated in response to certain drugs (anti-epileptics) and ALP can come from bone - so if in doubt check both.
- Albumin + clotting factors – synthetic function - liver responsible for their production – Low albumin levels or if prothrombin time decrease (marker of clotting), this indicates that the liver isn’t function properly
What is cholestasis and how is it related to jaundice?
CHOLESTASIS refers to high levels of bilirubin which then results in jaundice - due to a tumour, gall stones, lesion at the ampulla, etc.
Jaundice – yellowing of the skin and sclera of the eye – due to accumulation bilirubin
Are the liver function tests a better reflection of damage or function? Are they sensitive or specific?
No blood test for telling you how well the liver is working – markers provide more insight into damage
Not sensitive or specific – can have patients with liver cirrhosis but will have completely normal liver function test
BUT clinically useful AND patterns give clues
Do hepatocytes and cells in the bile duct have HLA antigens? What implications does this have for transplantations?
Hepatocytes don’t have HLA antigens – consequence liver transplant don’t need to match – need to have the same blood group but not HLA antigens
Bile ducts do have HLA antigens – potential source of liver transplant rejection
What is the most common cause of a high bilirubin?
Most common cause of high bilirubin – Gilberts (1/20) - agenetic hereditary disorder where slightly higher than normal levels of bilirubin build up inthe blood, causing jaundice
Not always noticeable – jaundice is noticeable at 50 and evident at 100
Causes an isolated rise in bilirubin, all other LFTs is normal
How is unconjugated bilirubin transported in the blood?
Low solubility in aqueous solutions, so it binds to albumin to be transported to the liver.
What does the ALT/AST liver function tests tell us? What can we learn from the ratio of ALT:AST?
Test for damage/hepatocyte integrity
Hepatocyte dies – AST and ALT leak out into the blood – tells you the number of hepatocytes have died
Both have a short half life - hepatocyte death in the last 24 hours (acute) - chronic liver disease these may be normal as there aren’t many hepatocytes left.
ALT = 50 (or less) - normal
Ratios
Ratio of AST to ALT is only useful in NAFLD to distinguish the severity
* Healthy liver = equal ratio
* NAFLD (advanced) = AST increases more than ALT - AST is derived from the mitochondria and the higher levels are due to mitochondrial dysfunction.
Alcohol liver disease – AST is always higher than ALT
What do ALP and GGT tell us?
ALP and GGT - show damage in bile ducts – don’t tell us that the bile duct cells are dyeing rather that they are irritated.
Hence, if elevated tells us that something is wrong with the bile ducts – stones, autoimmune disease, etc.
Alkaline phosphatase – ALP – liver is the most common cause of raise ALP
Note - ALP can also be derived from bone, intestines and placenta - so check GGT is elevated.
GGT made by liver and biliary system - can also increase in response to alcohol, obesity, phenytoin, carbamazipine (last two - anti-epileptics) - so check ALP
In long standing NAFLD cirrhosis, what is potentially the only LFT abnormality that you might see?
NAFLD cirrhosis – quite common that GGT is the only abnormality
Early on in NAFLD ALT is typically also abnormal
What does an albumin LFT tell us? When does it normally change in cirrhosis?
Albumin - tells us about the synthetic function of the liver
Important to note that it can also be high in states of dehydration (concentrating) and low due to a state of dilution.
Often normal in cirrhosis until liver failing.
What does an prothrombin LFT tell us? Is it better at assessing short or long term changes?
Good marker of synthetic function of the liver.
Very good in acute liver failure - e.g. paracetamol poisoning – prothrombin time becomes very high – very useful test to tell us whether we should transplant someone
Rarely very abnormal in cirrhosis - usually no longer than 20 (normal is 10-12)
What condition(s) should you think of if bilirubin is the only abnromal LFT?
Bilirubin only – think gilbert’s or increased hemolysis
What condition(s) should you think of if ALT is midly elevated?
ALT mild (50-100) – common
* NAFLD
* HepC
* Alcoholic liver disease including alcoholic hepatitis
What condition(s) should you think of if ALT is significantly elevated?
ALT high – hepatitis – can be viral or drug induced damaged
What condition(s) should you think of if GGTP is only elevated?
GGTP only – induction – drug + alcohol or inactive cirrhosis (may be the only marker – as number of hepatocytes is low)
Commonly elevated in people that drink to excess (not damage – induction)
What condition(s) should you think of if ALP and GGTP are both elevated?
ALP + GGTP – biliary system e.g. stones, pancreatic cancer and primary biliary cholangitis
In practise, what happens if a GP has a patient with abnormal LFTs?
Abnormal LFTs triggers Liver Screen, looking at…
* Hepatitis viruses
* Autoantibodies – anti-nuclear Ab, anti-mitochondrial Ab, anti-smooth muscle Ab
* Ferritin – hemochromatosis
* Ceruloplasmin (Wilson’s disease) and alpha-1-antitrypsin – in young people with rare conditions
* Immunoglobulins – auto-immune liver disease
* Ultrasound
What role does the liver have in carbohydrate, fat and protein metabolism?
Carbohydrates
* Glucose metabolism: storage and release: glycogenesis, glycogenolysis, gluconeogenesis,
Lipids
* Fatty acid metabolism & synthesis of lipoproteins
Protein
* Protein synthesis: albumin, transport proteins, proteases, clotting factors, acute phase proteins
* Converts ammonia to urea
What role does the liver play in xenobiotic metabolism?
Liver plays an important role in drug metabolism, sometimes called xenobiotic metabolism, as it biotransforms less polar compounds into more polar compounds (water soluble) that can be excreted more easily.
Important to note that the kidney also plays a role in drug metabolism.
Drug metabolism - What processes take place in phase 1 and 2 reactions?
Phase 1 reactions – oxidation or hydrolysis - detoxification (can also activate drugs)
Phase 2 reactions – glutathione conjugation, sulphation, acetylation and glucuronidation - increased solubility
Note - Phase 3 is also possible - secretion (into bile) that is ATP mediated.
Outline how paracetamol is metabolised by the liver.
Paracetamol metabolism – most common cause of acute liver failure
Normally metabolised by the liver via conjugation with glucuronidation or sulphation
But another pathway is also present…
Paracetamol can be converted into (P450 – isoenzyme 2E1) NAPQI (toxic)
NAPQI needs to react with glutathione in order to form non-toxic products.
If glutathione is used up we get acute hepatocyte death – treatment is a NAC as it is a glutathione donor in order to increase levels
What is the definition of acute liver failure?
Definition: loss of liver function that occurs quickly in days or weeks in a person with NO pre-existing liver disease
Main causes are…
* Paracetamol
* Viral Hep B and A
* Drug Reactions
What are some early and later signs of acute liver failure?
Early non-specific; malaise, nausea, vomiting, abdominal pains, dehydration.
Later stages - fully developed syndrome manifests with acidosis, profound hypoglycaemia, coagulopathy and encephalopathy leading to coma. renal failure, multi-organ failure
Treatment outcome depends when they arrive into hospital
In general terms, outline the pathophysiology taking place in liver cirrhosis?
Pathophysiology of cirrhosis – scarring of the liver
Cirrhosis - Development of fibrotic tissue that disrupts the hepatic architecture coupled with disorganised hepatocyte regeneration.
Leads to nodules of hepatocytes surrounded by fibrosis - disrupting normal hepatocyte functioning.
Timeline…
* Sustained damage in the liver
* Activation of kuppfer cells
* Inflammatory cells come in destroying the hepatocytes
* Stellate cell activation which then start producing collagen.
* Fenestrations of the endothelial cells close up
* Increases the pressure in the sinusoids
* Pressure gradient is transmitted back into the portal vein, leading to portal hypertension.
What are the complications associated with liver cirrhosis?
Liver cirrhosis - portal hypertention leading to…
* Bleeding from varices
* Encephalopathy (flapping tremor, confusion, foetor hepaticus)
* Ascites
Ultimately leading to liver failure.
What biochemical changes do we see in liver failure?
Liver failure…
* low albumin
* prolonged PT
* low urea
* high ammonia
What is the treatment for end-stage liver disease?
Treatment of end stage liver disease –liver transplantation
Alcohol abstinence for 6 months important
How does portal hypertension result in esophageal varices?
Portal hypertension – high pressure in portal vein
Blood from the mesenteric system cannot go smoothly through the liver, so the blood takes a diversion via the coronary vein
This then results in the formation of collaterals (in the oesophagus and stomach), in order to allow the blood to return into systemic circulation.
Problematic as these varices can burst
What are the two main causes of fatty liver disease?
Fatty liver disease – excessive accumulation of fat
Two main causes
a) Alcohol
b) Metabolic syndrome – obesity and type 2 diabetes
How is alcohol metabolised by the liver? How does it result in fatty liver disease?
Alcohol metabolism
Alcohol converted into acetaldehyde (ALDH), which is converted into acetate, ultimately leading to acetyl CoA formation.
Results in high levels of oxidative stress (free radical production) and fatty acid formation (enhanced lipolysis, FFA release and esterification of FFA)
The end result is steatosis - macrovesicular with large droplets of fat accumulating within the hepatocyte.
What is the alcohol flush response? What causes it?
Alcohol flush syndrome - deficiency in ALDH-2 resulting in an accumulation of acetaldehyde – toxic
What histological mark points towards Alcoholic fatty liver?
Mallory’s hyaline bodies
What is MASLD?
Metabolic dysfunction associated liver disease (MASLD) - replaced NAFLD
Histological appearance is very similar to ALD.
But patients have Metabolic Syndrome - abdominal obesity, serum triglycerides, cholesterol, high BP and high blood sugar – any 3 of these used for metabolic syndrome diagnosis.
Who is most likely to suffer from MASLD?
MASLD - tightly linked to obesity and type 2 diabetes
Only a subgroup of MASLD patients have a normal BMI but have a genetic predisposition
Outline how MASLD can progress in disease severity?
Outline the underlying pathophysiology of MASLD.
In MASLD we see…
* Insulin resistance - peripheral and hepatic
* Dysregulated fatty acid metabolism - leading ROS production/oxidative stress by mitochondria
Inceased ROS can drive…
* Cell death
* Activate stellate cells - leading to fibrosis
* Drive an inflammatory response
Does adipose tissue secrete cytokines and hormones?
Adipose tissue is a physiological reservoir of hormones and cytokines
- Pro-inflamatory ( leptin, TNFa, IL-6 etc) - Leptin is raised in NAFL and correlated with degree of steatosis.
- Anti-inflammatory - adiponectin
Visceral fat rather than subcutaneous is responsible for secreting these cytokines.
What are the clinical features of MASLD?
- Can be asymptomatic
- Abnormal liver biochemistry on routine check up
- RUQ abdominal pain
- Fatigue
- Hepatomegaly
- Acanthosis nigricans (children) - skin condition that causes a dark discoloration in body folds and creases
What components make up bile?
Composed of…
* Bile acids primary (made in liver) and secondary (absorbed) - Allow digestion of dietary fats through emulsification
* Phospholipids
* Cholesterol
* Conjugated drugs
* Electrolytes: Na+, Cl-, HCO3- and copper
* Bilirubin
What are the stages of that lead up to cirrhosis?
- Simple steatosis
- Steatohepatitis - inflammation
- Fibrosis - In its initial stages, fibrosis is thought to be reversible to some degree, but in the late stages it is felt to be irreversible.
- Cirrhosis - distortion of hepatic architecture and the formation of regenerative nodules. It is traditionally believed to be an irreversible condition.
- Hepatocellular carcinoma
Outline the role of stellate cells in the development of cirrhosis.
- Liver injury
- Hepatocyte becomes injured releasing factors
- Drives an inflammatory response
- Stimulates stellate cells and kupffer cells
- Stellate convert into myofibroblasts and start to make collagen
- Blocks of the fenestrations increasing portal blood pressure and deprives hepatocytes of oxygen and nutrients leading to dysfunction.
What are the consequences of increased sinusoidal resistance?
- Portal hypertension - Portosystemic collaterals - forming varices that are at higher risk of bleeding
- Reduced venous return to the heart - drives Na+ retention and vasocontriction - increased cardiac output - increasing portal hypertension further.
- Portal hypertension + fluid retention - resulting in ascites - fluid accumulation in the peritoneal cavity.
- Portal hypertension - back pressure results in spleen enlargement
- Portal hypertension - Less blood going to the liver - less ammonia/ammonium is processed - hepatic encephalopathy
What are the some physical features of compensated and decompensated liver cirrhosis?
Compensated - Xanthelasmas, Spider naevi, gyno, liver enlargement, clubbing, xanthamos and purpura (skin hemorrhages)
Decompensated - Jaundice, neurological (encephalopathy, disorientation, drowsy, hepatic flap - hand tremor), ascites, dilated veins in abdomen (variceal bleeding) and oedema.
What is the definition of acute liver failure? What LFTs associated with acute liver injury, severe acute liver injury and acute liver failure?
Acute liver failure - Rapid onset (less than 2-3 months) + no underlying chronic liver disease
- Acute liver injury (most common) – damage to hepatocytes – causing a high ALT
- Severe acute liver injury (uncommon) – high ALT + jaundice/coagulopathy
- Acute liver failure – rare – high ALT + jaundice/coagulopathy and encephalopathy
General terms, what is the structure of a virus particle?
Viruses - require host cell machinary to replicate and survive
Structure:
* Single stranded or double stranded DNA or RNA
* Single stranded – can be + or – stranded
* DNA or RNA within a virus-encoded protein coat (nucleocapsid)
* Sometime an outer-most host cell membrane-derived envelope - those that have an envelope are more sensitive to detergents
* Viruses receptors and glycoproteins on the outside - determine species and tissue specificity
* Matrix proteins – can be viral proteins or human proteins
What are the clinical symptoms of hepatitis?
How can you group the hepatitis viruses (A-E) in terms of transmission?
Hepatitis B, C and D
* Are transmitted parenterally (not via the gut) – sexual contact, blood and blood products
* Often cause chronic diseases - virus is not eliminated after the initial infection and stays around.
* Treatments are available for Hep C and B – drugs are particularly good for hep C – treat up to 90% of patients with Hep C
* Envelope viruses
Hepatitis A and E
* Transmitted fecal-orally
* Fecal-oral viruses do not have an envelope – need to be more resistant to the environment
Note - Hep D – can only infect someone that is hep B positive
What can you tell me about hepatitis A incubation period, who it primarily affects, mode of transmission, onset, impact on liver function, mortality, chronicity and treatment?
Incubation - All Hepatitis viruses typically have a long incubation time - Hep A – 10-50 day incubation period
Primarily affects - children and young adults
Mode of transmission - fecal-orally - contaminated water infects food (vegetables or shellfish) - ingested
Onset - abrupt onset, commonly with pyrexia (fever)
Liver - results in high LFTs (1000s units/per ml of blood)
Morality - Fatality rate is relatively high – acute liver failure – increasing age morality goes up – e.g. over 50 mortality increases above 2%
Chronicity - resolves spontaneously (without chronicity – ie, no carrier state) followed by life-long immunity
Treatment - Prevention - Inactivated virus vaccine and immunoglobulins. Treatment is supportive
Where is hepatitis A most prevelant around the world?
Distribution of hepatitis viruses
Hep A – sub-Saharan Africa, India and south-east Asia
What are the outcomes for Hepatitis A infection in adults and children?
Children is typically subclinical and asymptomatic
A lot rarer in adults – usually gets jaundice = icteric disease + higher fatality rate
What can you tell me about hepatitis B incubation period, who it primarily affects, mode of transmission, onset, impact on liver function, mortality, chronicity and treatment?
Incubation - All Hepatitis viruses typically have a long incubation time - Hep B – 60-90 day incubation period
Primarily affects - babies and young adults
Mode of transmission - parenteral, vertical (mom to fetous in pragnancy) and sexual
Onset - insidious onset (gradual) and apyrexial
Liver - Virus remains in hepatocytes for life and may re-active under immunosuppression
Morality - Up to 2% fatality rate in icteric cases.
Chronicity - Chronic infection* (carrier state) develops in 5-10% of adults (but >95% of neonates) and is associated with hepatocellular cancer.
Treatment - Prevention - HepB vaccine and immunoglobulins. Treatment is Interferon alpha OR antivirals.
Vaccine (Hepatitis surface antigen) is effective – 95-98% - good but not perfect for healthcare providers – means that you have 2-5% of non-responders
Where is hepatitis B prevelant in the world?
Sub-Saharan Africa, South east Asia, Russia
How do outcomes from Hep B infection differ between newborn/infants, young children and teenagers/adults?
Newborns and young children – infection is severe and have a high rate of chronic infection
Adults/teenagers – recovery rates are much higher and rates of chronic infection are a lot lower
Where is hepatitis C prevelant across the world?
Distribution is occurs everywhere.
What does the prevelance of HepD look like?
Specific countries with high prevelance.
How does alcohol influence paracetamol metabolism?
Competition between acetaminophen and alcohol in the liver
* Acutely taken together – might be protective
* Long term alcoholism – lowers glutathione – lower dose of paracetamol needed
Explain what this diagram is showing.
Most of the bilirubin comes from hemoglobin and myoglobin - break down product is called unconjugated bilirubin (not water soluble) – needs to transported with albumin
Liver takes up unconjugated bilirubin – processed in the liver – becomes conjugated (glucuronic acid) making it water soluble – excreted into bile
Enterohepatic reabsorption – bacteria process it, allowing for reabsorption
Bilirubin in the colon gets processed even further forming stercobilin – makes stool go brown
What are the different types of malignancy that can cause post-hepatic jaundice?
- Hilar of the liver or distal cholangiocarcinoma
- Compression from nodes (patient with colorectal cancer or lymphoma) – hilar lymphadenopathy
- Pancreatic tumours
- Ampullary tumours
What surgical procedure can be undertaken if someone presents with a distal cholangiocarcinoma, ampullary tumour or pancreatic tumours?
Whipples Procedure - Taking out the gall bladder, distal bile duct, duodenum and part of the stomach
High complication rate
How is endoscopic retrograde cholangiopancreatography (ERCP) used in the treatment of post-hepatic jaundice?
- Sometimes we can’t resect liver mets or lung mets – so an endoscope can be used to place a stent into the common bile duct to prevent blockage and improve symptoms.
- Benign disease – if gall stones are present in the common bile duct we can also do an ERCP – inflate balloon above the stone and pull it out
Outline the structure of the biliary system.
- Common hepatic duct (left and right branches)
- Cystic ducts (to/from gall bladder)
- Common bile duct - forms part of portal triad
Blood supply - Cystic artery – comes from the right hepatic artery
What are the different ways that gallstones may clinically present?
Clinic presentation
1. Biliary colic - fatty food followed by pain – right sides colicky pain 30-60 minutes after eating – most common presentation – gall stones getting trapped in the narrowing (Hartman’s pouch) resulting in spasms and colicky pain
2. Acute cholecystitis – inflammation of the gall bladder and sometimes infection – pain may start colicky but becomes constant + temperature – treatment with antibiotics – sometimes emergency operations to remove gall bladder
3. Obstructive jaundice – gall stones entering the bile duct causing jaundice – ERCP – drag down gall stone into duodenum
4. Acute pancreatitis – acute inflammation – pressure changes in the pancreatic duct – causes back pressure
What is the management for gallstones?
- Pain killers
- Antibiotics (infection)
- Percutaneous drainage (people not fit for general anesthetic – ask radiology to stick a drain in)
- ERCP (removal of gall stones)
- Surgery - e.g. Laparoscopic cholecystectomy
