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what is in the space of Disse? Kupfer cells, perisinusoidal stellate cells, microvilli of hepatocytes
cells of ito vitamin D
perisinusoidal stellate cells vitamin A absorption and storage in space of Disse
zone 1 is closest to? portal triad
zone 3 is closest to? central vein
where does inflammation start, in terms of zone? zone 1 (closest to blood supply)
what is the name of the hepatocytes lining the portal triad? limiting plate (impt in inflammation)
B: why are most liver problems insidious or clinically silent? they either go unnoticed and heal themselves without clinical detection, or they are insidious because the liver stores a lot of materials and can survive despite damage for awhile
B: what is steatosis? accumulation of fat droplets (triglyceride fat) in hepatocytes during damage
ischemic injury and toxic reactions often cause what, regarding the zones? centrilobular necrosis around the terminal hepatic vein (central vein); midzonal and periportal necrosis are RARE.
B: In cases of severe parenchymal disruption in the liver, what holds the cells capable of restitution? canal of hering
which enzymes come from within hepatocytes, measuring hepatocyte integrity? AST, ALT, LDH
What substances are normally secreted into bile, from normal biliary excretory function? serum bilirubin (total, direct, delta) urine bilirubin, serum bile acids
B: What are the biliary plasma mem enzymes, that if present, indicate biliary canaliculus damage? alkaline phosphatase, gamma-glutamyl transpeptidase, 5'-nucleotidase
what proteins do hepatocytes secrete into the blood? serum albumin, prothrombotic factors (5, 7, 9, 10, prothrombin, fibrinogen)
What can be measured as a result of hepatocyte metabolism? ammonia
Portal HTN from cirrhosis causes what? Hypertension from Cirrhosis Sucks Ass! Hemorrhoids, Caput medusae, Splenomegaly, Ascites
What are the characteristic signs of liver disease? [My Hepatocytes Have Gotten Hurt, Can Somebody Please Just Fix Her!] muscle wasting, hypoalbuminemia, hypogonadism, gynecomastia, hypoglycemia, cholestasis, spider angiomas, palmar erythema, jaundice, fector hepaticus, hyperammonemia
how much of the liver must be damaged before failure will ensue? 80-90%
B: Liver failure results from 3 major alterations to the liver? massive hepatic necrosis, chronic liver disease, hepatic dysfunction without overt necrosis
Of the hepatitis infections that can cause massive hepatic necrosis leading to liver failure, which one doesn't do this? Hep C (and HepB is more likely to do it than Hep A)
What is the main cause of massive hepatic necrosis? main cause of chronic liver disease? hepatic dysfunction without overt necrosis? acetaminophen, chronic hepatitis, Reye's syndrome
B: In liver failure, dysfunciton of hepatocytes also causes hyperestrogenemia. What does this cause? hypogonadism (which produces gynecomastia), spider angiomas (due to local vasodilation)
B: what is fector hepaticus? body odor (musty, sweet, sour) as a result of methionine metabolism which produces mercaptan, may result from portosystemic shunting, not always present
B: what causes palmar erythemia in liver failure hyperestrogenemia
B: Pt has asterixis, hyperreflexia, and rigidity after an acute GI bleed ontop of a cormorbid liver disease. what is happening, why? hepatic encephalopathy due to hyperammonemia is causing hyperreflexia, asterixis (nonrhythmic, rapid ext-flex movements of the head and extrem esp when palms are dorsiflexed). It is reversible if hepatic condition is fixed quickly.
What are some life threatening consequences of liver disease? multiple organ failure, coagulopathy (GI bleed/peticheal bleeds), hepatic encephalopathy, hepatorenal syndrome
B: asterixis is a sign of _____ life threatening hepatic encephalopathy
B:An older man comes in with alcoholic breath, complaining that he has "woman tits, some weird red bumps on his stomach." When looking at his stomach you notice he smells musty. On physical exam he is hyperreflexic and slow moving. What do you tell him? You're going to run liver tests. He has signs of gynecomastia, spider angiomas, fector hepaticus, and hyperammonemia
B: In end stage liver disease, cirrhosis is characterized by what characteristics? bridging fibrous septae (linking portal tracts with themselves or hepatic veins--which may redirect blood bypassing hepatocytes), parenchymal nodules (which encircle proliferating hepatocytes), and disruption of architecture of the ENTIRE liver
B: what are common etiologic factors in order of most to least freq for cirrhosis? alcohol liver ds (60-70%)>viral hepatitis>unknown>biliary ds>primary hemochromatosis>Wilson's> alpha-1-antitrypsin deficiency (other causes include childhood galactosemia/tyrosinosis; or drug-induced from methyldopa; or even CARDIAC cirrhosis
B: what is the pathogenesis of cirrhosis? architecture reogranized. Kupfer's release cytokines, stimulating collagen is lain down in the space of Disse by perisinusoidal stellate cells which causes the sinus to lose its fenestrations and blocking hepatic secretions of prothrombins and proteins
B: what is the major source of collagen in cirrhosis ? perisinusoidal stellate cells in the space of Disse
B: How does jaundice develop in cirrhosis? perisinusoidal stellate cells are stimulated by cytokines released from Kupfer cells, which lay down collagen which obliterate biliary channels
B: What is the ultimate mechanism of most cirrhotic deaths? progressive liver failure, a complication of portal HTN, or dvelopment of hepatocellular carcinoma
B: why does hepatic portal HTN develop? The collagen laid down by perisinusoidal stellate cells restricts blood flow
B: portal HTN may develop from three routes. Explain? COMMON CAUSES PREHEPATIC (thrombosis, obstruction of portal vein; splenomegaly shunting of blood thru splenic vein); INTRAHEPATIC (cirrhosis); POSTHEPATIC (right sided heart failure, constrictive pericarditis, hepatic vein outflow obstruction)
B: what are some less common causes of hepatic portal HTN schistosomiasis, massive fatty change, diffuse fibrosisng granulomatous disease (sarcoidosis), and miliary tb, and anything affecting portal circulation (nodular regenerative hyperplasia)
B: What are the 4 major clinical consequences of portal HTN? acites, portosystemic venous shunts, splenomegaly, hepatic encephalopathy
B: what do portosystemic shunts cause? hemorrhoids, esophagogastric varicies, abdominal wall collaterals extending from the umbilicus toward the ribs (caput medussae)
B: 2 functions of bile? fat emulsification and waste production
B: bile serves as the major pathway for excretion of what products? cholesterol, bilirubin, and xenobiotics
B: icterus? yellow coloring of eyes
B: if you notice an increase in free bilirubin in serum, what does this usually mean? bilirubin must travel with albumin in blood to travel to the liver. if bilirubin is free, then there's either excessive heme (hemolytic disease) or protein binding durgs are displacing bilirubin from albumin
B: what is the enzyme responsible for turning bilirubin into a form that can be transported in bile? UGT1A1
B: excess cholesterol can only be lost in the body via _____? fecal loss of bile acids (most bile acids are recycled though)
B: which form of bilirubin cannot be excreted in the urine, no matter how high blood levels are? unconjugated bilirubin (it requires albumin to be exreted)
B: kernicterus? unconjuagated bilirubin that diffuses into the brain tissue causing severe neurologic damage (erythroblastosis fetalis)
which form of bilirubin is excreted in urine? which is toxic? which can cause kernicterus? urine (conjugated bili), toxic (unconjugated bili), kernicterus (unconjugated bili)
B: what is the delta fraction? this is when conjugated bilirubin (which is pigmented) complexes with albumin, which is now soluble in water, causing a different type of bilirubin, the delta fraction
B: what are normal serum bilirubin levels? at what point do you get jaundice? 0.3-1.2mg/dL; jaundice occurs at levels above 2mg/dL
B: what are the causes of jaundice (hyperbilirubinemia)? 1) INCREASED BILIRUBIN (hemolytic anemia, etc), 2) decreased hepatic uptake 3) impaired hepatic conjugation 4) decreased hepatic output 5) biliary obstruction (intrahep/extrahepatic)
B: which causes of jaundice produce an unconjuaged bilirubinemia? increased bilirubin production (hemolytic anemia, GI bleed reabsorption), decreased hepatic uptake, and impaired conjugation (enzyme dysfunction UGT1A1
B: what can cause excessive production of bilirubin (leading to unconjugated hyperbilirubinemias)? hemolytic anemia, resoprtion of internal bleed, ineffective erythropoiesis syndromes (pernicious anemia, thalassemia);
B: what can cause reduced hepatic uptake causing unconjugated hyperbilirubinemias? drug interference with membrane carrier systems, Gilbert syndrome
B: what can cause impaired bilirubin conjugation in unconjugated hyperbilirubinemia? physiologic jaundice of the newbornd (decreased UGT1A1 activity), breast milk jaundice, Crigler-Najjar syndrome, genetic def; Filbert syndrome, diffuse hepatocellular disease
B: what can cause a predominant conjugated hyperbilirubinemia? deficiency of canalicular membrane transporters (Dubin Johnson syndrome, Rotor syndrome) or impaired bile flow
You have a pt that comes to you because they can't stop itching. She has many skin xanthomas. She is slightly jaundice and icteric. What labs would you expect to find abnormal? elevated serum alkaline phosphatase (an enzyme released from bile duct epithelium as a result of bile acid action on the lining--must verify hepatic isoenzyme); elevated gamma-glutamyl transferase (same process); may also see vita A, D, K deficiencies
B: what 2 enzymes are elevated as a result of bile acid stasis and damage to canalicular membranes? alkaline phosphatase and gamma-glutamyl transferase
B: why is it important to figure out if you have an intrahepatic or extrahepatic cholestasis? extrahepatic is ammenable to surgery, where intrahepatic is not
B: what are the infectious agents of hepatitis? [Students See Hepatic Microbes At Truman!] Salmonella, Staph bactermia, Hep (A thru E), Malaria, Amoebiasis, Tb (miliary)
what are the main functions of the liver? carb metab (glycogen storage, plasma glucose), fat metab (lipoprotein source), protein (albumin, coag, iron copper, acute phase), protein catab (urea prod), Bile syn, storage (glycogen, iron, KADE), detox (nitrogen, hormones, drugs)
clotting factors produced by liver? 2, 7, 9, 10
In liver failure, the accumulating bilirubin is mostly? conjugated
what gives unconjugated bilirubin that ability to cause kernicterus, etc? lipid soluble
What is a notable genetic defect in bilirubin conjugation that causes a mild unconjugated bilirubinemia in 5-10% of the population? Gilbert syndrome
Gilbert syndrome autosomal dominant, genetic, 5-10%, unconjugated hyperbilirubinemia, no cause identified, liver structure is normal
Crigler-Najarr syndrome genetic defect that causes hereditary loss of gluconoryl transferase (UGT1A1) causing impairment of bilirubin conjugation
How long do infants lack glucuronyl transferase? low in the first 2 weeks of life, neonatal jaundice
What are the major intrahepatic causes of conjugated hyperbilirubinemia? Dubin-Johnson and Rotor syndromes, Pregnancy, liver cell necrosis, drugs causing cholestasis
Dubin Johnson and Rotor Syndromes autosomal recessive, prevents release of conjugated bili from liver, intrahepatic cause
What are the common causes of extrahepatic sources of conjugated hyperbilirubinemia? bile stone in duct, obstruction due to a mass (LN) or inflammatory fibrosis, pancreatic carcinoma
alkaline phosphatase is elevated when? liver failure is due to biliary obstruction
major characteristics of HepA? RNA, fecal oral, seafood, no carrier, self-limited, short incubation, NO CANCER, icteric, immune for life, vaccine
characteristics of HepB? DNA, blood borne, sex, needles, carrier states, 60% subclinical, long incubation (>12 weeks), CANCER risk,
Dane particle capsid of Hep B virus
explain the order of seromarkers in HepB infection from the beginning? (1) surface Ag (2) IgM core Ab (3) IgG core Ab (4) surface Ab
Hep B surface Ag 1st to show up, acute phase
acute phase seromarkers in HepB surface Ag and IgM core Ab
IgM core Ab in HepB acute phase
surface Ab in Hep B resolved infx
A symptomatic pt in Hep will typically have which markers? surface Ag and IgM core ab
What percentage of Hep B infx go to chronic state? 10-20%
Hep C characteristics? RNA, parenteral, needles, sex, carrier, acute phase goes undetected, carrier increases risk for CA, long incubation >12 weeks, 60% go chronic
What % to chronic in Hep C? 60%
IgM and IgG markers in Hep C mean what? resolving
HCV+ indicates? acute phase
Autoimmune Chronic Hepatitis (leupoid hepatitis) 60% chronic, hard to dx, looks like B or C with no serology, ANTI-SMOOTH MUSCLE AB present, females, perimenopausal
What lab characteristics do you see in a pt with autoimmune hepatitis? abscense of markers, elevated serum IgG and gamma globulin, high serum titer of ANA, SMA, anti-LKM1, negative mitochondrial antibody
B: what is responsible for chronic hepatitis? HBV, HCV, (HBV+HDV), chronic alcoholism, Wilson's ds, alpha-1-antitrypsin def, drugs (isoniazid, methyldopa, methotrexate), and autoimmunity.
How do you tell the difference between autoimmune hepatitis and primary biliary cirrhosis on serology? PBC is AMA + (90-95%)
Primary Biliary Cirrhosis? autoimmune, women in their 40s, destroys bile ducts, zone lympho infiltrate, portal HTN, no serology, hallmark AMA+
Primary Sclerosisng Colangitis bile ducts present, onion skinning of ducts (due to fibrosis), esophageal varicies, hemorrhoids, and capit mudusae from portal HTN; dx: radiologically
how do you tell primary biliary cirrhosis from primary sclerosing cholangitis? DUCTS (PBC destroy) (PSC keeps)
What is the difference in dx bewteen primary biliary cirrhosis and primary sclerosing cholangitis PBC--AMA+, destroyed ducts; PSC (radiologic dx, ducts present)
Because alk phosph can be elevated in growing bones and placenta, how do you confrim? GGTP elevation
When the liver is _____% damaged you start getting hypoalbuminemia. 50%
ballooning degeneration? toxic or immunologic insult, reversive
feathering degeneration? cholestatic liver injury, retained biliary material results in foamy apearance.
hepatocyte with council bodies? indicates liver cell necrosis
In Hep B infection, zone ___ is necrotic? 1
What happens to the liver architecture during Hep B infection? piecemeal/briding necrosis: portal triad areas bridging and making connections with one another/necrotic triads, fibrotic triads; SYNONYMOUS WITH HEP B INFX
piecemeal (bridging) necrosis synonymous with Hep B infex
zonal necrosis fulminant hep B infex, good example
massive necrosis? rare in US, can see in Hep B/C, fulminant infex, usually caused by acetaminophin overdose
what commonly causes microvesicular fatty change? tetracycline and salicylates
B:ground glass hepatocytes chracteristics of Hep B viral infection
Not all cirrhosis is from alcohol. Other causes? parasite, hepatitis, inborn error of metabolism
alcohol causes what type of faty change? macrovesicular
cenrtrilobular necrosis? acetaminophen, rifampin
diffuse or massive necrosis? acetominophen, methyldopa, mushroom toxin
drug induced granuloma formation? methyldopa, allopurinol, sulfonamides
cholestasis--drug induced? anabolic steroids, oral contraceptives
macrovesicular fatty change--drug induced? alcohol and methotrexate
haloethane is a drug that causes what type of change in the liver? diffuse or massive necrosis
methotrexate causes what type of drug-induced change in the liver? macrovesciular fatty change
How does alcohol cause cirrhosis? it's directly toxic to hepatocytes causing breakdown of intermediate filaments and causes Mallory Bodies (Mallory hyalinization), hepatocytes swell, neutrophil infiltration, steatosis (fatty change), cirrhosis develops over time
what are the 4 characteristics of alcoholic cirrhosis? develops over time, Mallory bodies, swelling of hepatocytes (neutrophils), steatosis (fatty change)
what 3 ways does alcohol cause disease in liver? alcoholic hepatitis, hepatic steatoiss, cirrhosis
B: Hepatic steatosis (fatty liver), what happens? small microvesicular lipid droplets accumulate in hepatocytes, leads to macro with continue drinks, displace nucleus to periphery
B: Is hepatic steatosis reversible? yes
B: ALCOHOLIC HEPATITIS? hepatocyte swelling and necrosis, (ballooning), Mallory bodies (accum of cytokeratin), neutrophilic reactions (esp around Mallory bodies), fibrosis (perivenular, satellites in sinusoids, periportal)
B: MALLORY BODIES characteristic but dx for alcoholic liver ds (also found in primary biliary cirrhosis, Wilsons, chronic cholestatic syndromes and hepatocellular tumros),
B: Is Alcoholic hepatitis reversible? yes, with abstinence
what is the irrversible form of damage due to alcohol? alcoholic cirrhosis
B: In the picture in the book, what is growing at the lower left tip of the alcoholic cirrhotic liver? hepatocellular carcinoma
Who is more susceptible to developing alcoholic cirrhosis? M/W? women
B: why does alcohol cause hepatocellular steatosis? enzymes are shunting toward lipid biosynthesis which accumulate
B: why does alcohol cause impaired hepatic functin of metabolism? it decreases intrahepatic glutathione levels, sensitizing liver cells to oxidative injury. GSH is a antioxidant.
How are liver cells damaged by alcohol? fat accum impairs, decr'd intrahepatic glutathione predisp to oxid injury, CYP2E1 is upreg converting drugs to toxins (esp acetaminophen), it directly affects mitochondrial membrane fxn, acetylaldehyde disrupts cytoskeleton, new epitopes for autoimmunity
B: what is typically the first sign of alcoholic cirrhosis? portal HTN with secondary esophageal varicies
B: HCC develops in alcoholics ____ % of the time? 6-9%
B: what are the genetic causes of cirrhosis? hemochromatosis, Wilson's ds, alpha1-antitrypsin deficiency
B; Non-alcoholic fatty liver disease? M=W, strong association with obesity, dyslipidemia, hyperinsulinemia and insuline resistence overt Type 2 DM, diagnosis of exclusion
Hemochromatosis? excessive accumulation of body irion, most depositied in organs such as the liver and pancreas
B: How does hemochromatosis develop? either genetically (from genetic defect of iron absorption) or by parenteral heavy administration
brown heart, heat failure, DM Hereditary hemochromotosis
Intra-acinar causes of cholestasis? viral hep, drugs (chlorapromazine, estrogens), alcoholic liver ds, pregnancy related, septicemia
extra-acinar causes of cholestasis? primary biliary cirrhosis, sclerosis cholangitis, polycystic liver ds, tumors in the liver
Where does iron typically accumulate in hemochromatosis? liver, heart, (pancreas)
What are the typical finding in Hereditary hemocrhomotosis? brown heart, heart failure, DM (due to obliteration of pancreas), AR, 6p, RARE, M>F
B: what is the most common cause of secondary hemochromotosis? hemolytic anemia (transfusions or increased absorption)
B: what are the morphologic associations with hemochromotosis? deposition of hemosiderin in liver, pancreas, myocardium, pituitary, adrenal, parathyr, joints, skin), CIRRHOSIS, and PANCREATIC FIBROSIS
B: Hereditary hemochromotosis ptc? 40 yo, Males, hepatomegaly, abd pain, slate-gray skin pigmentation, glucose problems, cardiomyopathy, atypical arthritis or impotence or decreased libido
B: what is the "classic triad" in hereditary hemochromatosis? pigmented cirrhosis with hepatomegaly, skin pigmentation, and DM
B: A significant cause of death in Hereditary Hemochromotosis is? cardiac dysfunction and HCC
Wilson's Disease? AR, abn accumulation of COPPER, possible brain malfunction, Kaiser-Fleisher rings in eyes, (deposition of copper in basal ganglia can cause dyskinesias), rarely manifests before age 6, marked urinary excretion of copper
B: pigmented cirrhosis with hepatomegaly, skin pigmentation, and DM Hereditary Hemochromotosis
Wilson's Disease can mimick chronic hepatitis (cirrhosis and inflammation) so how would you dx? grind up liver and weight it for copper
B: what is the biochemical diagnosis of Wilsons? How to treat? decrease in serum ceruloplasmin, increase in hepatic copper content, and increased urinary excretion of copper; D-penicillamine which chelates copper
B: acute or chronic liver disease in a patient with parkinsonian-like symptoms? investigate Wilson's Disease
Alpha1-antitrypsin deficiency causes what? pulmonary emphysema and liver disease (esp in young and neonates)
B: most commonly diagnoses genetic liver disease in infants and children *due to it's early presentation? alpha1antitrypsin deficiency
alpha1antitrypsin is a _____. protease inhibitor
B: what is the chief mechanism of cell injury involving alpha1AT deficiency? autophagocytosis of mitochondria in liver cells, due to ER accumulation of misfolded protein
B: In the liver, you see round to oval cells with red cytoplasmic globular inclusions in hepatocytes with PAS positive globules, dx? alpha1antitrypsin deficiency
Why is true infarction of the liver rare? dual blood supply
True infarction of the liver can occur in? surgeries, preeclampsia, bacterial endocarditis, polyarteritis nodosa
what are the most common causes of portal HTN? liver disease, schistosomiasis, idiopathic, polycystic liver ds
Budd-Chiari syndrome? occlusion of the hepatic vein
Budd-Chiari syndrome may occur in? HCC, oral contraceptive use, pregnancy, polycythemia,
which Hep viruses can be asymptomatic? A thru E
Which hep viruses can cause anicteric hepatitis? A thru E
which hep viruses can cause icteric hepatits? A thru E
types of hep viruses that form chronic states? B,C, D
hep viruses---carrier state? B, C, D
Bante syndrome? portal vein occlusion
portal vein compromise? Bante syndrome
protein C and S deficiency causes? Budd-Kiare syndrome
what can casuse veno-occlusive disease, a central vein fibroisis? GVHD and bone marrow transplants, due to toxic injury to sinusoidal epithelium
HELP syndrome? a subclinical sign that liver problems are going on in preeclampsia;seen in preeclampsia and eclampsia: hemolysis, elevated liver enzymes, and decreased platelets
Created by: HSF2