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94 Cards in this Set

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204
204
How is the liver broken up
8 complete segments (instead of old lobes)
What is the ligament in the center of the liver
Falciform (w/ umbilical/paraumbilical channels)
What is the name of the liver capsule & what is it made out of?
Glisson's capsule – type 1 & 3 collagen
What is the blood supply to the liver?
Portal vein (from intestines) & hepatic artery
What comes out of the liver
Bile ducts & hepatic vein (R & L)
Components of portal triad
Hepatic artery, bile duct, portal Vein
Lobular vs Acinar arrangement of liver
Lobular – central vein in center. Acinar – portal triad in center (zone 1) vein in outside (zone 3)
Where is most detox in liver?
Near central vein (centrilobular)
Zonal necrosis
Ex = tylenol. Production of toxic by product results in necrosis of zone 3 cells.
Protein malnutrition – hepatic signs
Periportal fatty change in liver.
Nutmeg liver
CHF results in nutmeg appearance of liver.
Typical pattern of regeneration in liver:
Of neoplasm:
Regen: Two cell thick sinusoids
Neoplasm >2 cells (i.e. 3-6)
One cause of hepatization of pancreas
Deficinet copper diet.
NonPerenchymal liver cells & function (3)
Kupffer – macrophages. Endothelial.
Stellate (ito) – Store Vit A and pathologically act as myofibroblasts.
Where do kupffer cells live?
In the sinusoids of the liver.
Causes of NASH
(nonalcoholic steatohepatitis) –
Obesity
Diabetes Mellitis
Metabolic disturbances (Fatty acids)
“Syndrome X”
Direct vs indirect bilirubin testing
Direct: Water soluble(unconjugated).
Indirect: Fat soluble (conjugated)
Prehepatic jaundice
When more bilirubin is produced (from hemolysis) than the liver can conjugate.
Bilirubin pathway
Unconjugated Biliribin --> liver – conjugated --> portal blood --> systemmic circ --> kidney –conjugated out urine
205
205
Micro vs Macro nodular cirrhosis
Micro is < 3mm
Causes of macronodular cirrhosis
HCV, HBV, Toxic chemicals.
4 common complications of cirrhosis
(PILE)
Portal hypertension,
infection
liver cell carcinoma,
Endocrine changes
Budd Chiari syndrome
Hepatic vein thrombosis from any cause. Common causes – hypercoagulability, neoplasm, parasites. Clinical signs – Hepatomegaly, abdominal pain, ascites.
Portal hypertension – anastamoses
Gastroesophogeal (varices), Anorectal (hemorrhoids), periumbilical (spider angiomas)
Endocrine problems w/ cirrhosis
Peripheral conversion of testosterone and androstenedione into estrone and estradiol results in feminization. (Also, estrogen escapes the liver via anastomoses)
What happens to male repro system in cirrhosis?
Infertility due to loss of spermatogenic cells (don't know why)
206/207
206/207
Which hepatitises can be chronic?
B,C,D (also spread parenterally)
Hep B is in which body fluids?
Blood, semen, vaginal, saliva.
Dane Particle
Particle of HepB
Three hep B antigens
HBsAg - envelope of virus, cytoplasm of hep.
HBcAg - Nucleocapsid of virus, nucleus
HBeAg - nucleocapsid of virus, nucleus.
Ground Glass Cell
Hepatocyte with large glassy cytoplams. Indicative of HepB
Which of the Hep B antigens does NOT confer long term immunity?
HBeAg
Def of chronic Hep B
Persistance of HBsAg for more than 6 mos
HDV dependent on?
HBsAg from HepB
Two types of HDV infections
Coinfection (both at same time), Superinfection (serial infections)
HBsAg antigen/antibody significance
(as expected) Ag+Ab- = acute carrier, Ag-Ab+ = recovered
HBcAg antigen/antibody significance
Ag-Ab+ is EITHER carrier OR complete recovery
What indicates active, infectious HBV
HBeAg, or Dane particles.
What makes HCV so likely to be chronic?
Genome mutations (error prone viral polymerase)
How are hepatitises removed from the body?
Via destruction of affected hepatocytes (hence chronic causes liver damage)
Councilman bodies
Apoptic cells in the liver.
Histo features of CAH
1. Piecemeal necrosis,
2. Fibrous bridges,
3. Liver cell rosettes,
4. Groundglass cells
HBV vs HCV
See slide 73
210
210
Abnorm. Alkaline phosphatase is indicative of:
Bile duct damage
Murphy's sign
Sensitivity to pressure on gall bladder area.
Ampulla of Vater
Sphincter in the common bile duct
Sphincter of Oddi
Spincteer b/t common bile duct and duodenum
Primary Biliary Cirrhosis
(unknown etiology). Slow progressing cholestatic liver disease. More common in women. Elevated Alk Phosph, GGT. Often AMA pos. Lymphocytes around bile duct.
Functions (2) of bile salts
1. Detergent for fat dig/abs (and prevent bile stones).
2. Stim phosphatidylcholine change to bile.
Clin uses of Bile Salt therapy (ursodeoxycholic acid)
1. Treat cholestatic liver disease,
2. Treat pruritis ass. W/ cholestasis
3. Gallstone dissolution therapy
What enzyme conjugates bilirubin?
Bilirubin UDP-Glucoronysyltransferase (bUDP-GT)
Ntcp
Transporter for bilirubin – Involved in Estrogen induced cholestasis, Jaundice of sepsis
MRP2
Transporter for bilirubin – Involvied in Dubin -Johnson and Jaundice of sepsis
spgp/BSEP
Trasporter for bilirubin. Involve in Estrogen & Sepsis induced jaundice, gall stones, PFIC2
MDR3
Bilirubin transporter. Involved in PFIC-3
Fic1
Ibilirubin transporter in the Ileum. Involved in BRIC, PFIC1
Gilbert's disease
Failure of bUDP-GT (extra TA in TATA box) results in jaundice when sick/stressed.
Jaundice in newborns – cause, timeline
Caused by hemolysis, hematoma. (inc RBC breakdown). UDP-GT is activated at birth, so jaundice peaks at ~day 4-5, regardless of expecting date.
4 causes of hyperbilirubinemia
1. Inc production (via RBC breakdown)(unconj)
2. Decrease uptake or transport (unconj)
3. Defect in conjugation (unconj)
4. Defect in excretion (conjugated)
Kernicterus
Brain damage secondary to hyperbilirubinemia in newborn (unconj)
211
211
Sup Mesenteric Vein drains:
Righ colon, small int.
Inferior Mesenteric vein drains:
Left colon
Most common cause of portal hypertension
Schistosomiasis
Space of disse
Area under endothilial cells in liver capillaries. (Home of ito cells)
4 collateral circulations in portal hypertension
1. Azygous. 2. Umbilical. 3. Retroperitoneal 4. Rectal
Formula for surface tension
T = press*rad/width
Drugs to lower Portal inflow -
1. Beta Blockers 2. Vasopressin 3. Somatostatin
Drugs to lower portal resistance
Nitrates.
3 factors in ascites (cirrhotic)
1. Low albumin.
2. Hepatic outflow block
3. Portal hypertension
Hepatorenal syndrome
Progressive renal failure w/ advance cirrhosis/ascites
Hepatic encephalopathy
Asterixis, Abnormal EEG, impaired cerebral function in advanced liver disease
Asterixis
Loss of of postural control of hands.
4 stages of Hep Encephalopathy
1. Confusion
2. Drowsiness
3. Somnolence
4. Coma.
Lactulose
Initial treatment for hepatic encephalopathy (a non digestable disaccharide)
Three theories of hepatic encephalopathy
1. Ammonia (block glutamine rec) 2. Tryptophan (block monoamine trans) 3. GABA benzodiazepine (Inc GABA)
Underfill hypothesis of ascites
Transudation of fluid in ascites causes increased sodium reabs
Overfill hypothesis of ascites
Retention of Na --> vol expansion --> ascites
ALT
Aminotransferase in liver. Increased in nonalcoholic disease, decreased in alcoholic
AST
Aminotransferase found in most tissues. Relatively constant concentration in blood.
Normal ALT:AST
1
Alkaline phosphatase
Liver enzyme from plasma membrane. Marker of biliary tract disease
GGT
Liver enzyme, also sensitive for biliary tract.
What 2 things favor zone 1 necrosis?
Yellow phosphorous, and toxemia of pregnancy
Liver growth enzymes
HGF, TGF-a, EGF (require TNF, IL-6)
TGF-B
Negative regulator of hepatocyte growth.
2 death receptors on hepatocytes
Fas and TNF-R1
PPARa
Combustion - oxidizes fatty acids
PPARy
Conservation - stores fatty acids
Causes of micronodular cirrhosis
Alcohol, nutritional.