Week 3 - Liver Failure Flashcards
What are the major constituents of bile?
Bile salts Phospholipids Bile pigment Cholesterol Inorganic ions
What does enterohepatic recycling look like?

What prevents bile from entering the duodenum?
Where does bile go when it cannot enter the duodenum?
What happens to this after a meal and why?
Sphincter of Oddi
Into the gallbladder
Relaxes - due to neural influences and CCK and gall bladder contracts
How does the liver fulfill its detoxification role?
+ enzyme systems, allowing modification of chemical structures
Increase their water solubilities
Mechanisms = oxidation, reduction, methylation, conjugation
What controls the muscular activity in the GI tract?
Myenteric plexus
Label this diagram?
What is the effect of para and sympathetic nerve activation on the GI smooth muscle?
Parasympathetic = + motility
Sympathetic = decreases motility
What stimulates motility in the GI tract?
What are the stimulatory and inhibitory hormones in the GI tract?
Vagal fibres releasing ACh
Stimulatory = gastrin (antrum) and motilin
Inhibitory = gastrin (proximal stomach), secretin, CCK and nitric oxide
What are the 2 types of muscular contractions in the intestines?
Segmenting contractions = occurs in circular muscle, moves chyme, increasing exposure to mucosal surface
Peristaltic contractions = longitudinal muscle, short distances
What controls the motility of the samll intestine?
Myogenic mechanisms
Myenteric plexus
Extrinsic nerves
Local chemicals
How is lower intestine motility controlled?
Ileo-caecal sphincter (ZEP)
Slow movement from haustral contractions
Powerful contractions after meal, prior to defecation
What happens during/prior to defecation?
Arrival of faecal material
Sensory nerve activation
Peristaltic colonic wave
Relaxation of anal sphincter
Parasympathetic spinal reflex + voluntary effort
What are the 3 main markers in lFTs?
Aminotransferases = hepatocellular
Alkaline phosphates and gamma-glutamyl transpeptidase = obstruction
Albumin and coagulation = synthetic function
What causes prehepatic jaundice?
Water insoluble unconjugated billirubin produced faster than liver can conjugate it
Usually due to haemolysis
Gilbert’s syndrome = reduced levels of UDP-glucuronosyl transferase which conjugates billirubin
What caises hepatocellular jaundice?
Transaminases leak
Liver cannot convert insoluble billirubin into water soluble (liver damage)
Jaundice and pale stools
What are the 2 causes of cholestasis?
Intrahepatic = caused by:
- primary biliary cirrhosis, hepatocellular damage and pregnancy
Extrahepatic = caused by:
- gallstones or cancer on head of pancreas
What happens during obstructive jaundice?
- Cholestasis
- Elevated GGT and ALP
- Liver cannot convert insoluble bilirubin
- Cannot excrete bilirubin in bile
- Water soluble bilirubin excreted in urine
- Pale stools and dark urine
What is cholestasis?
Inability to get bile into duodenum
What are commensals?
What are transients?
Species that don’t harm host when confined to their proper site
Microorganisms which reside for a short time in a particular site without damaging host
How are water-soluble, lipid-soluble, and volatile drugs metabolised?
Excreted by liver or kidney
Metabolised by liver/gut/bloos –> forms water-soluble metabolite
Excreted in the lungs
What is the importance on cytochrome P450?
What most drugs require for metabolism
What are the preicteric and icteric clinical presentations of viral hepatitis?
Preicteric:
Malaise, anorexia, nausea, abdominal discomfort, pyrexia
Icteric:
- Pale stools, dark urine, jaundice
What are the 4 anti-emetic drugs?
H1-receptor antagonists - act on vestibular nuclei and have anti-muscarinic actions
Anti-muscarinic agents
Dopamine antagonists - acts in chemoreceptor trigger zone, effect against anti-cancer drugs
5-hydroxytryptamine antagonists - block 5-HT and 5-HT3 receptors in gut and CNS
What 3 drugs are used to treat IBD?
5-aminosacylates
Corticosteroids
Immunosuppressants