Anatomy
What spinal level does the celiac trunk originate from?
T12
What is the functional unit of the liver known as?
Hepatic lobule
What are the components of the portal triad?
Portal vein
Hepatic artery
Bile duct
What are 2 risk factors for pancreatic carcinoma?
Any 2 of these
- smoking
- chronic pancreatitis
- Alcohol
- Peutz Jegher syndrome (a genetic disease where the patient has increased intestinal polyps).
What are the three impressions of the spleen and their major relationship?
Gastric - Stomach
Renal - Left kidney
Colic - splenic flexure
What is the function of kupfer cells? And where are they found?
Kupfer cells are phagocytic in function, they remove portal blood particulate matter.
They are found in hepatic sinusoids.
What are the left and right triangular ligaments formed by?
Formed when coronary ligaments of the liver meet.
What is Zollinger Ellison syndrome, and what type of diarrhoea is this?
Gastrin-producing Pancreatic tumor, which increases acid production leading to increased gastric motility.
Type: Secretory
What are the three major branches of the celiac trunk, and name one arterial branch of each of these.
Left gastric artery
- Arteries to the esophagus (ascending arteries supply lower esophagus).
Splenic artery
- Left gastro-omental
- Pancreatic branches
- Short gastric branches
Common hepatic artery
- Left hepatic artery
- Right hepatic artery
- Cystic duct artery
- Right gastric artery
- Superior pancreatoduodenal arteries
- Right gastro-omental artery
What is meant by the 3 functional zones of the portal acinus?
Portal acinus is a grouping of hepatocytes by the arterial blood supply.
Zone 1 - Peripheral region of the lobule, and this is the best perfused.
Zone 2 - middle zone.
Zone 3 - Lowest perfusion due to its distance from portal triad. Plays a large role in metabolism.
What is the new passageway called when the main pancreatic duct and the common bile duct merge? And what is the associated sphincter called?
Hepato-pancreatic ampullae (ampullae of Vater)
Sphincter = Hepatopancreatic sphincter (Sphincter of Oddi)
What 4 antibodies are produced by plasma cells in coeliac disease?
1. Anti-gliadin antibodies antibody
2. Anti-de-aminated gliadin antibody
3. Anti-tissue-transglutaminase antibody
4. Anti-endomysium antibody
Explain the course of the sensory innervation fibres from the gall bladder
Sensory innervation from the gallbladder travles along the cystic artey and then fibres continue with the right phrenic nerve.
This explains why some patients report right shoulder pain.
What is the function of stellate cells, where are they found and what can they do in response to liver injury?
Functions: Storage of vitamin A (as retinol ester) and also a source of key growth factors
Found in the space of Disse
Response to liver injury: Stellate cells can become activated and turn into myofibroblasts and particpate in fibrogenesis and release cytokines to recruit more stellate cells.
What is a hydatid cyst? and what is the cause of this?
3 layered cysts on the liver with a daughter cyst within.
Cause: tapeworms in larval or cystic stage (Echinococcus granulosus).
What are the 5 risk factors for gallstones?
5 Fs
- Female (Female>Male)
- Fertile (OCP or pregnancy)
- Forty (>40 years old)
- Fatty (obesity)
- Fair (fair skin)
What are the 5 contents of the porta hepatis?
Hepatic portal vein
Hepatic artery
Hepatic ducts
Hepatic pluxus (SNS - coeliac and superior mesenteric plexuses and PNS - vagus nerve)
How is bilirubin formed from fragile RBCs to excretion?
Fragile RBCs are broken into heme through the reticuloendothelial system. Heme is then converted to biliverdin (through the action of heme oxygenase). Bilverdin is rapidly converted to unconjugated bilirubin. This is uptaken by the liver into hepatocytes and is converted to conjugated bilirubin. Then through the action of bacteria, it is converted to urobilinogen which is soluble. It undergoes oxidation either to become urobilin (excreted in urine) or stercobilin and is excreted in feces.
Explain the pathophysiology of coeliac disease
1. Gluten metabolism to gliadin by brush border enzymes at the mucosal surface. Gliadin comes into contact with sensitive epithelial cells.
2. These cells produce IL-15 which activates cytotoxic T cells and accumulates intra-epithelial lympocytes.
3. Cytotoxic T cells damage non-sensitive epithelial cells.
4. As the non-sensitive cells are damaged, gliadin moves into lamina propria.
5. Gliadin is de-aminated into de-aminated gliadin through the action of tissue transglutaminase.
6. De-aminated gliadin is uptaken by antigen-presenting cells
7. APC presents de-aminated gliadin to CD4+ T cells.
8. The T helper cell secretes INF-gamma which damages mucosa.
9. INF-gamma also converts B cells to plasma cells to produce antibodies.
Explain the metabolic and secretory defects in fatty liver disease.
Metabolic defect
- High levels of NADH due to increased ethanol metabolism cause impaired fat catabolism which causes increased fat accumulation in hepatocytes.
- Excessive biosynthesis of lipids.
Secretory defect
- Impaired secretion of lipoproteins, which furthers fat accumulation in hepatocytes.