More Free USMLE , MCCEE ,MCQe and AMQ Flashcards
Right, left, quadrate (superior) and
Name the lobes of the liver. What caudate (inferior) lobe. The right and
divides the two lobes on the anterior left lobe is separated by the interlobar
surface? fissure which is an invisible line running
from the gallbladder to the IVC.

The liver is secured in its anatomic
How is the liver secured in its position
location by the attachment of the
in the thorax?
hepatic veins to the IVC.

The liver lies in the right
hypochondrium under the rib cage and
5th intercostal space
extends from the _______ intercostal
space at the ______ line to just below
the costal margin.
Both enter via the hilum.
Portal vein (60-70% of the blood to the
liver): formed by the union of the
The liver receives approximately 25% splenic vein (IMV joins splenic) and
of total cardiac output. What SMV
vasculature supplies the liver?
Hepatic artery (30-40%): is a branch off
the common hepatic artery which arise
from the celiac trunk (T12).
Portal hypertension will cause blood
within the portal vein to reverse its flow
and enter the IVC to return to the heart.
What portal-IVC anastomosis becomes The three main sites are:
clinically relevant when portal Esophageal varices: left gastric vein-
hypertension occurs and what are the esophageal vein.
clinical signs? Caput medusa: paraumbilical vein-
superficial and inferior epigastric veins.
Hemorrhoids (rectum): superior rectal
vein - middle and inferior rectal veins

Fundus (anterior portion), body, neck
What are the three divisions of the gall (posterior).
bladder? The cystic artery (a branch of the right
What is the blood supply to the hepatic artery) supplies the gallbladder.
gallbladder? Sensory: the greater thoracic
What nerve innervates the gallbladder? splanchnic nerve (T7-T10).
Motor: vagus (CNX).
The common bile duct passes posterior
to the pancreas and ends at the
The common hepatic duct is joined by
hepatopancreatic ampulla (ampulla of
the cystic duct to from the common bile
Vader), where it joins the pancreatic
duct. Where does the common bile
duct. The sphincter of Oddi controls
duct continue to?
bile flow into the 2nd portion of the

What hormone causes contraction of
the gallbladder? What hormone inhibits

The liver is classically divided into
hexagonal lobules oriented around a
central vein (terminal veins). Portal
tracts (artery, vein, bile duct) are
arranged at the periphery. The
What is the classical microarchitecture
hepatocytes are arranged in plates
of the liver?
around the central vein and are
separated by vascular sinusoids (blood
drains to central vein). Bile canaliculi
are channels between hepatocytes that
drain towards the portal triad.
A liver acinus is divided into zone 1
(periportal - closest to portal triad),
Describe a liver acinus. Which
zone 2 (midzonal), and zone 3
hepatocytes in the acinus are most
(centrilobular -closest to central vein).
susceptible to ischemic injury?
The centrilobular hepatocytes are most
remote from blood supply.

Ito cells are fat-storing cells found in
the space of Disse. Sinusoids are lined
by fenestrated endothelial cells. The
space between these endothelial cells
What are ito cells and where do they
and the hepatocytes make up the
reside in the liver?
space of Disse. Ito (stellate) cells play
a role in storage of vit A and they form
collagen producing myofibroblasts in
Kupffer cells are resident macrophages
found in the liver sinusoids. They
secrete proinflammatory cytokines:
TNF-a: cause cholestasis.
What are Kupffer cells?
IL-6: cause synthesis of proteins by
TFG-b: cause stellate cells to secrete
type I collagen.
Cholesterol, bilirubin glucuronide, bile
salts (cholic acid and chenodeoxycholic
What are the main components of bile? acid conjugated to tuarine or glycine),
phospholipids (lecithin), electrolytes,
water, IgA.
Splenic macrophages degrade heme to
unconjugated bilirubin (UCB). UCB-
albumin complex travels to
hepatocytes. UCB is conjugated by
Explain the metabolism of senescent UDP glucuronyl transferase to form
RBCs. bilirubin-glucuronide (conjugated,CB
and is water soluble). CB is converted
to urobilinogen (UBG) by bacteria in
the intestines. UBG is oxidized to
During fasting, liver glycogen stores Most important: glycerol (from TGs),
are used up. Gluconeogenesis (90% in lactate (during exercise), and
liver) can help maintain BGL. Name the glucogenic amino acids.
gluconeogenic precursors that can be Additionally, all the intermediates of
used to produce a glucose. glycolysis and the citric acid cycle.

6-Pase) to F-6-P. CO2. Bloob-borne glucose is converted by exercising muscle to lactate. GTP) to accomplish this. 3) F-1. loss of CO2. increasing cAMP. thus activating protein kinase A. Lactate is What is the Cori cycle? taken up by the liver and reconverted to glucose (lactate to pyruvate) Glucogenic amino acids are those Leucine and lysine. acid cyle.6-P (via F-1. carboxylase. Protein kinase A favors the phosphorylation of PFK- 2/FBP complex which activates How does glucagon regulate fructose bisphosphatase (FBP). . Insulin gluconeogenesis? favors dephosphorylation of the complex and activated phosphofructokinase (PFK). 2) Oxaloacetate (via PEP Name the four reactions that carboxykinase. What two amino acids are phenylalanine. Glucagon also inactivates pyruvate kinsae and activates PEP carboxykinase. which are both whose catabolism yields pyruvate or essential amino acids (obtained from one of the intermediates of the citric diet). isoleucine. gluconeogenesis? 1) Pyruvate (via p. Tyrosine. 4) G-6-P (via G-6-Pase) to glucose. Glucagon binds to adenylate cyclase. reactions that must be circumvented. PEP. Glycerol is converted by glycerol Where does glycerol enter kinase to glycerol phosphate which is gluconeogensis? oxidized (by dehydrogenase) to dihydroxyacetone phosphate (DHAP). ATP) to oxaloacetate. and tryptophan are ketogenic and do not participate in ketogenic and glucogenic. biotin. (Note: oxaloacetate is transported across Gluconeogensis has three irreversible mitochondrial membrane as malate).

G-6-P A deficiency of glucose 6-phosphatase. have on gluconeogenesis? Acetyl CoA: activates pyruvate Fructose 2. What are the regulated enzymes of these two pathways? In liver: Glycogen synthase: activated by G-6-P Glycogen phosphorylase: activated by glucagon and epinephrine and inhibited What factors control glycogen by G-6-P. AMP. glycogenolysis. Sever fasting hypoglycemia. F-2. hepatomegaly.6-BPase (inhibits AMP gluconeogenesis) Glucagon Glucagon: increases gluconeogenesis. epinephrine and inhibited by ATP. fatty liver. renal disease. growth retardation.6 bisphosphate carboxylase (gluconeogenesis). ATP. which is responsible for releasing free glucose that can be used to maintain What is Von Gierke disease? blood glucose levels. Glucose1-P is first Glycogen synthase regulates conjugated to UDP (uridine glycogenesis. Acetyl CoA AMP: inhibits F-1. Glycogenesis is the conversion of glucose to glycogen. diphosphate) then passed to a growing polysaccharide. etc. . in the body and what are they used for? Liver: glycogen is used to maintain the blood glucose concentration (early on in fasting). Skeletal muscle: serve as a fuel reserve for the synthesis of ATP during Where are the main stores of glycogen muscle contraction. glucose synthesis and degradations in the liver Muscle: and in muscle? Glycogen synthase: activated by G-6-P Glycogen phosphorylase: activated by Ca. Glycogenolysis is the Glycogen phosphorylase regulates breakdown of glycogen to glucose-1-P.6-BP: activates What effect does the follow molecules phosphofructokinase (glycolysis).

serum alkaline phosphatase (ALP) . glycolysis? Phosphoenolpyruvate (via pyruvate kinase) pyruvate. thus. Fructose 6-P (via phosphofructokinase) What are the irreversible reaction of to F-1. What effects of this in flushing. shunting these intermediates away from gluconeogenesis. MEOS (microsomal ethanol-oxidizing system) metabolizes EtOH using NADPH and P450. tachycardia. NADH How does alcohol ingestion cause favors the conversion of pyruvate to hypoglycemia? lactate and oxaloacetate to malate.6. This pathway is How is chronic ethanol intake dealt with inducible which accounts for tolerance by the liver? build up. hepatocytes? Which are produced in the cells that line the bile canaliculi? Bile canaliculi cells: gamma- glutamyltransferase (GGT). This drug causes accumulation of An alcoholic patient is started on acetaldehyde in the blood which results disulfiram. Glucose (via hexokinase) to G-1-P. Ethanol metabolism results in a massive increase of NADH. and nausea.BP. it produces excess oxygen free radicals (very dangerous). aspartate transaminase Which liver enzymes are produced in (mitochondria). Ethanol is converted to acetaldehyde How is alcohol normally metabolized in by alcohol dehydrogenase.. treatment can be expected? hyperventilation. the liver (hint: two oxidation reactions)? Acetaldehyde is oxidized to acetate by What drug inhibits the 2nd enzyme? aldehyde dehydrogenase. Acetate is the final product of EtOH Why does chronic alcohol intake result metabolism. Unfortunately. Hepatocytes: alanine transaminase (cytosol). Acetate is used to make in a fatty liver? fatty acids. It is also inhibited by disulfiram.

black pigment 4) Rotor's syndrome 4) (AR) same as D-J but without the black pigment . 2) Gilbert syndrome 3) (AR) genetic defect in secretion of 3) Dubin-Johnson syndrome bilirubin into bile duct. barbituates. causes of jaundice? conjugation. AST > ALT.). Generally. ALP. drugs (phenytoin. disorders: 2) Minor reduction in glucuronyl 1) Crigler-Najjar (type I and Arias) transferase activity. viral hepatitis. increased in urine bilirubin and urine UGB. and secretion. and bilirubin will be normal. absent urine UBG. cholestasis? Smooth endoplastic reticulum. 1) Deficiency of bilirubin glucuronyl What is the defect in the following transferase. ALT is greater than AST. What are the three broad categories of Mixed (CB 20-50%): defect in uptake. ALT and AST are elevated. but will rise later in the course of the disease. GGT is increased. What is the cellular organelle that GGT Therefore when the P450 system is (gamma-glutamyl transferase) is found increased. alcoholic hepatitis? EtOH also induces the P450 system which increases GGT. GGT. Unconjugated (CB<20%): increased production of UCB (increased urine UBG) or decreased uptake or conjugation of UCB (normal urine UBG). because ALT Which liver enzymes will be increased is a specific marker for liver cell in viral hepatitis? necrosis. because AST is present in the mitochondria of hepatocytes and What liver enzymes will be increased in EtOH uncouples the mitochondria. etc. Break in? down of alcohol. Obstructive (CB > 50): increase urine bilirubin. What liver enzymes are increased in ALP and GGT.

unconjugated bilirubin (UCB) Hemolysis of RBCs cause an increase conjugated bilirubin (CB) in AST. hepatobiliary circulation. G-6-P dehydrogenase deficiency.absent UCB in blood CB in urine .Baseline bilirubin in a patient is 1. malaria. UCB in blood and recycling of UBG. and UBG are all increased. urobilinogen (UBG) AST Viral hepatitis (mixed): liver dysfunction How does viral hepatitis effect these involving uptake and conjugation of substances: UCB.elevated (normally zero) UBG in urine UBG in bowel . Crigler-Najjar hemolysis. sickle cell anemia. You Fasting test to determine Gilbert ask a patient to fast for 24 hours and syndrome: unconjugated type of they come back and their bilirubin is hyperbilirubinemia. following substances: thus. What effect does extravascular hemolysis of RBCs have on the UCB.normal UBG in bowel CB in urine .normal UBG in urine . Diagnosis? Pyruvate kinase deficiency. jaundice in newborn. CB. most common now 2. CB in bowel UCB in blood . secretion of CB into bile ducts. can be due to an obstruction in the Dubin-Johnson and Rotor's syndrome.elevated CB in urine CB in bowel . Hyperbilirubinemia (causing icterus) Primary biliary cirrhosis. turning stool and urine darker. hereditary cause of jaundice.absent UBG in bowel UBG in urine .elevated How does an obstructive liver disease UCB in blood . syndrome (deficiency in glucuronyl transferase).normal (gallstones) effect these substances: CB in bowel . What are Decreased extrahepatic bile flow: some examples? gallstone in common bile duct or carcinoma of head of pancreas. Hemolytic disease of Name some causes of extravascular newborn (Rh or ABO).5 (more than double!). CB in urine UBG in bowel .absent UBG in urine Decreased intrahepatic bile flow. hereditary spherocytosis.elevated (normally zero): CB in bowel dark urine. Gilbert syndrome (defect in uptake of UCB). .

fulminant hepatitis (very rare)? What Transmitted via fecal-oral. a dsDNA. enveloped icosahedral What viral family does hepatitis B capsid. Transmission occurs contracted? via parenteral. of a carcinoma of head of the Examination reveal a palpable pancreas. increased ammonia indicates cirrhosis or Reye syndrome. sign). What of jaundice is the most likely diagnosis? Hepatitis B is from the hepadna viridae. what test can Blood urea nitrogen (BUN): urea cycle be used to access hepatocyte is in the liver. Prothrombin time (PT): factors II. decreased BUN indicates function? cirrhosis. painful Acute viral hepatitis. Hepatitis A is the hepatomegaly. An increased CA19-9 is the gallbladder (positive Courvoisier's gold standard tumor marker. This virus family is this virus in? does not cause chronic hepatitis. sexual. The intact virus is referred to as belong to and how is this virus the Dane particle. Hepatitis A virus (HAV) is a naked Which viral hepatitis is transmitted via icosahedral capsid (capsid is antigenic) fecal-oral route and can cause a with a positive ssRNA. Vaccine is available.VII. Picornaviridae. and elevated most common viral hepatitis and cause levels of liver function enzymes. History This patient has all the clinical features reveals the patient has pale stool. Patient presents with a fever. jaundiced. IX. Serum ammonia: ammonia is metabolized in the urea cycle. What is the gold standard test to diagnose this patient? Serum albumin: hypoalbuminemia indicates cirrhosis. epigastric pain and weight loss. breast feeding. Besides liver enzymes. Patient presents with jaundice. pregnancy. Lymphocytic infiltrate with destruction What microscopic changes could be of hepatocytes: apoptosis of found in acute viral hepatitis? hepatocytes (Councilman bodies). . X are synthesized by the liver.

This is the gap between HBsAg disappearing and appearance When does the window phase or of Anti-HBsAg serologic gap occur in the timeline of a HBV infection? Chronic hepatitis (asymptomatic or symptomatic). . Polyarteritis nodosa. HBeAg+. assume neg. nodules. Persistence of HBsAg in serology for how long indicates chronic HBV? 4-5 months. needle sticks. Flavivirus: + ssRNA. Anti-HBeAg+. Anti-HBcAg between 4-5 months) IgG 5) HBsAg+. HBeAG. Membranous glomerulopathy. Cirrhosis: fibrosis. fulminant hepatitis. 4) Chronic HBV w/ low infectivity HBcAg IgG 5) Acute HBV 3) Anti-HBsAg+ 6) Window phase (serology gap 4) HBsAg+. What are possible complications of a Hepatocellular carcinoma: viral DNA hepatitis B infection? incorporates into hepatocyte DNA and triggers malignant growth. Serum sickness prodrome. and Anti- HBcAg are shown in the following patients (if not shown. Co-infection with hepatitis D virus. Anti-HBc IgM 6) Anti-HBc IgM When does hepatitis B surface antigen (HBsAg) appear after exposure in 2-8 weeks after exposure. Anti-HBeAg. 1) Chronic HBV w/ high infectivity What is the status of these patients: 2) Recovery from HBV 1) HBsAg+. sexual. enveloped icosahedral capsid. serology reports? 6 months. Anti-HBcAg IgG 3) Immunized from HBV 2) Anti-BsAg+. Anti. Serology studies of HBsAg.). Anti-HBeAg+. Anti- HBsAg. and across the placenta. What viral family does Hepatitis C come from and how is it transmitted? Transmitted via blood transfusion.

HCV RNA. is Immigrant from Mexico presents to transmitted via the fecal-oral route. patient had recently recovered from Hep C? Recovery: + RIBA and . Ascending cholangitis due most often to E. Why should because this protozoa can form a liver you also do a CT scan on this patient? abscess (right lobe). mucosa. with this infection are also at a risk of cholangiocarcinoma.yes Is Anti-HBV IgG protective? HBV . a protozoa.coli or Klebsiella. Is Anti-HCV IgG protective? HCV .yes Is Anti-HEV IgG protective? HEV . What playhelminth (flat worm) is contracted by the ingestion of fish and Clonorchis sinensis (Chinese liver infects the common bile duct? Patients fluke). Ascending GGT.no Is Anti-HAV IgG protective? HAV . your office with a recent history of Most patients are asymptomatic bloody diarrhea and abdominal pain. naked What viral family does Hepatitis E icosahedral.yes Entamoeba histolytica. belong to and how is it transmitted? Transmitted via fecal-oral route. right upper characterized by inflammation of the quadrant pain and jaundice. CT scan should be performed Cysts are also present. What test would determine that a Infection: + RIBA (recombinant patient is currently infective with Hep immunoblot assay) and + HCV RNA C? How would the results differ if the (via PCR). . Caliciviridae: + ssRNA. Liver bile ducts (cholangitis). This condition is Patient presents with fever. Bloody diarrhea occurs when Examination of the stool reveals RBC trophozoites penetrate the intestinal in the cytoplasm of a trophozoites. carriers. infection and enzymes also show raised ALP and bile duct obstruction. What's the most likely diagnosis? cholangitis is the most common cause of multiple liver abscesses.

. Rupture of these cysts can and that the cysts must be removed. a platyhelminth (flat worm). The eggs of shistosoma incite a fibrotic response in the portal vein causing cirrhosis. The intermediate host of this on the liver? helminth is fresh water snails. Multinucleated giant cells. Occurs mostly in a patient with autoimmune hepatitis? younger women: fever. This is an A biopsy of a liver in a neonatal idiopathic disease. Antinuclear antibody and anti-smooth What serum markers could be found in muscle antibodies.. cause a massive anaphylactic reaction. with infections or errors of metabolism. CT scan reveal large cysts This patient has sheepherder's in the liver. jaundince hepatosplenomegaly. You inform the patient that disease. encephalopathy and hepatomegaly (fatty change). What serum markers could be found in a patient with autoimmune primary Antimitochondrial antibody and serum biliary cirrhosis? IgM. that penetrates through the What effect does schistosomiasis have skin. result in granulomatous hepatitis? histoplasma capsulatum.. Infection with echinococcus his dog transmitted the disease to him granulosus. The mitochondria is age? damaged leading to an increase in serum ammonia and defective beta- What manifests clinically and whats the oxidation.. What was your diagnosis and why must the cysts be removed? Miliary spread of what bacteria can Mycobacterium tuberculosis. . Schistosomiasis is caused by shistosoma mansoni. Clinical findings include underlying pathology? vomiting.. Patient presents with abdominal pain. and biliary obstruction. palpable liver mass. It is also associated hepatitis patient would reveal. Reye syndrome often follows What triggers Reye's syndrome in chickenpox or influenza and children younger than four years of salicylates.

and hepatocellular present. low platelets (due to DIC). sometimes E and rarely A). acetaminophen. PT is markedly D. Acute liver failure with encephalopathy within 8 weeks of hepatic dysfunction. resulting in sinusoidal dilation. Define fulminant hepatic failure. What are the causes of this syndrome? . the liver. What are the commonest causes of Anabolic steroids. Liver cell necrosis around portal triads. causing bacillary multiple blood filled cysts throughout angiomatosis. His liver is rapidly shrinking. carcinoma. this rare vascular disease? Budd-Chiari syndrome (occlusion of the hepatic veins or IVC) results in a liver Hepatic vein-thrombosis: polycythemia which is grossly enlarged and tender. vera (most common). Liver becomes enlarged with a What is the most common cause of mottled red appearance: nutmeg liver. Causes: viral hepatitis (most common). oral and severe intractable ascites is contraceptive pills. elevated serum transaminases. Peliosis hepatis is characterized by Bartonella henselae. Patients high. with this condition? Combine LHF (decreased cardiac output) and RHF (back up of systemic blood). Name two syndromes that can occur Preeclampsia can lead to HELLP during pregnancy that results in liver syndrome: hemolytic anemia with disease? schistocytes. Acute fatty liver of pregnancy: defect in beta-oxidation. Reye syndrome. Patient presents confused and This is fulminant hepatitis (most jaundiced. in AIDS patients. and increased transaminases. and transaminases are falling. Fetus must be removed/delivered. jaundice. Liver is typically small. who fall into a common > 80% chance What is the mortality rate of patients of dieing. Heart failure signs are absent. centrilobular hemorrhagic necrosis? Clinical findings: painful hepatomegaly. commonly caused by hepatitis B and bilirubin is rapidly rising.

TG's accumulate in the liver. and perivenular fibrosis. . to the liver. Acetaldehyde (via aldehyde dehydregenase. Metabolism of alcohol results in the excess production of NADH which stimulates the conversion of dihydoxyactone phophate to glycerol-3- phosphate. The end product of EtOH How does alcohol consumption lead to metabolism (acetone) is made into fatty change? acetyl CoA which is used to make FA. This system produces radical oxygen species. Mallory bodies (damaged (2) Alcoholic hepatitis intermediate filaments in hepatocytes). What are the consequences of excess All the hangover symptoms and it also acetaldehyde in the body? directly damages hepatocytes. 1) Fatty accumulation in hepatocytes. no fever or neutrophilic leukocytosis What are the microscopic findings in: 2) Fatty change with neutrophil (1) Alcoholic fatty change infiltration. Blood in the bile in patients with trauma Define hematobilia. non-inducible enzyme) What systems are used in the liver to is broken down to acetone. protein production is reduced therefore apolipoproteins are not produced. The glycerol backbone and FA are combined to form TG's. Additionally. EtOH (via alcohol dehydrogenase) is broken down to acetaldehyde. breakdown alcohol? Acetaldehyde is also broken down by MEOS (an inducible system using P- 450).

methotrexate 4) Fibrosis 4) Amiodarone. What laboratory findings? Lab findings: CB > 50%. and light colored stool. cholesterol deposits in the skin. Intrahepatic: drugs (OC. primary sclerosing pericholangitis. It is predominantly a male sclerosing pericholangitis. extrahepatic biliary Name the common causes of atresia. methotrexate. neonatal hepatitis. liver diseases? distended with bile. Liver is enlarged. What are the disease (2:1) and 70% of patients will defining characteristics of primary also have ulcerative colitis. retinoic acid Extrahepatic: stones originating from the gallbladder. anabolic 2) Cholestasis steroids 3) Fatty change 3) Amiodarone. bilirubinuria. Primary sclerosing pericholangitis is Three major intrahepatic biliary tract characterized by obliterative fibrosis of disease are primary biliary cirrhosis. What clinical and findings could find in green-colored. and primary ducts. absent urine UBG. thorium causes of these liver tumors: dioxide 1) Angiosarcoma 2) Oral contraceptive pills 2) Liver cell adenoma 3) Aflatoxin due to aspergillus mold 2) Hepatocellular carcinoma 4) Thorium dioxide 4) Cholangiocarcinoma 1) Isoniazid.What are the most common drug/toxin 1) Vinyl chloride. Patients are sclerosing pericholangitis? at risk of cirrhosis and cholangiocarcinoma. pregnancy induced cholestasis (estrogen). What are the most common drug/toxin acetaminophen. cholestatic. malabsorption. halothane. methyldopa causes of these liver disease: 2) Oral contraceptive pills (estrogen 1) Acute hepatitis prevents bile secretion). both extrahepatic and intrahepatic. carcinoma head of pancreas. Bile ducts will be obstructive. intrahepatic and extrahepatic bile secondary biliary cirrhosis. arsenic. . anabolic steroids). Jaundice with pruritus. cholestatic liver disease. increase in serum ALP and GGT.

Decrease BUN. Hepatorenal syndrome. portal hypertension. cryptogenic cirrhosis. Describe the relationship betweeen Kuppfer cells and stellate cells during the inflammatory response that leads to cirrhosis. alpha-antitrypsin deficiency. hepatocellular carcinoma. (3) Disruption of the architecture of the entire liver. What are the complications that occur ascites. PT.g. Alcoholic liver disease (60-70%) Viral hepatitis (10%) Biliary diseases (e. Hepatic encephalopathy: reversible What are some common clinical metabolic disorder. (1) Bridging fibrous septae linking portal tracts and portal and tracts with hepatic veins. in cirrhosis? hyperestrinism. Hypoalbuminemia: pitting edema. galactosemia Hepatic failure. increase in findings in hepatic failure and what test ammonia. Hyperestrinism. . Coagulation defects: inability to synthesize coagulation factors. confirms these features? Portal hypertension: Ascites: portal htn and secondary hyperaldosteronism. primary biliary In terms of frequency. 5-10%) most common causes of cirrhosis? Primary hemochromatosis (5%) Wilson disease. What are the three defining (2) Parenchymal nodules containing characteristics of cirrhosis? proliferating hepatocytes encircled by fibrosis. what are the cirrhosis. Decrease albumin. hepatorenal syndrome.

and hypogonadism. anastomoses? Ascites: liver cannot metabolize ALD and doesn't produce albumin (decrease oncotic pressure). Clinical findings include: What are the clinical manifestations of gynecomastia. Ammonia characterized by altered mental status. . Antibodies: anti- mitochondrial and anti-IgM. GABA (inhibiotry) is this syndrome? raised. spider telangiectasia. hyperestrinism due to hepatic failure? female distribution of hair. Renal failure without renal parenchymal disease due to hepatic What is hepatorenal syndrome? failure. Primary biliary cirrhosis commonly occurs in women (6:1) between 40-50. and death. appears to cause neurotransmitter coma. asterixis. 1) Esophageal varices: left gastric vein . What is the cause of dysfunction. is a key toxin that accumulates and disordered sleep rhythms. What are the three main 4) Retroperitoneal hemorrhage: ?. Portal hypertensions (intrasinusoidal 3) Hemorrhoids: superior rectal vein - hypertension) results in anastomoses middle and inferior rectal veins. and ascites.esophageal vein. This condition is primarily due to a decrease in renal blood flow. Ammonia also causes astrocytes to swell leading to cerebral edema. What is the pathogenesis of primary It is an autoimmune granulomatous biliary cirrhosis? What is the destruction of the bile ducts in the epidemiology of this disease? portal triads. palmer erythema. Hepatic encephalopathy is due to the persistence of toxic substance because of decrease liver function and portal Hepatic encephalopathy is hypertension (anastomoses). Liver cannot degrade estrogen and 17- ketosteroids. 2) Caput medusa: paraumbilical vein - superficial and inferior epigastric veins.

Further test followed by jaundice. Patient presents generalized pruritus Primary biliary cirrhosis. are the main sites of deposition in the Skin: increases melanin production. Joints: degenerative joint disease.leading to malabsorption. What are some causes of secondary Alcohol abuse (EtOH increases iron hemachromatosis (hemosiderosis)? absorption). and could reveal anti-mitochondrial dark urine. of ________. Pancreas: (1) bronze diabetes - Iron cause free radical damage to damage beta cells. What is a non-autoimmue condition that autoimmune disorder could cause this presents the same. Well water (iron pipes) Liver: in hepatocytes. pale stools. body? Heart: restrictive cardiomyopathy. patients condition? This autosomal recessive disorder is Why are women less likely to show characterized by an increase in iron symptoms of hereditary retention. Wilson's disease. . Examination reveals antibodies. thus. Menses causes a loss of iron hemochromatosis until there elderly which provides protection from years? hemochromatosis. xanthomas. What pancreas . absorption of iron is at a max. HFE gene product is damaged. Secondary biliary cirrhosis hepatomegaly. Prussian blue-stained section of the liver. The defective HFE is maximally stimulated. (?). Autosomal recessive disorder of ceruloplasmin leading to Kayser-Fleischer ring are characteristic accumulation of copper. Hereditary hemochromatosis. HFE product facilitates the binding of What is the defect in hereditary plasma transferrin to Tf-receptor on hemachromatosis? intestinal cells. (2) exocrine tissue and subsequent fibrosis. Blood transfusions: sickle cell and beta-thalassemia patients.

Defective hepatocyte transport of copper into bile for excretion. What is your primary during pregnancy causing an concern? intraperitoneal hemorrhage. 60. develops a liver cell tumor that has a tendency to rupture adenomas. previously on oral This is a highly vascularized benign contraceptives. have a normal life expectancy. Patients with this excretion of biliruin glucuronides across syndrome will be asymptomatic and the canalicular membrane. Red granules. What are the consequences of the Decreased synthesis of ceruloplasmin. copper in cerebral cortex leads to dementia. Decrease in H&E of the liver. could lead to this? Dubin-Johnson syndrome. AAT builds up to cause cirrhosis? toxic levels in the hepatocytes causing liver damage. Female patient. mutation that occurs in Wilson's Ceruloplasmin binds 90%-95% of the disease? How does this disease total serum copper concentration. Alpha-antitrypsin deficiency. many years. History reveals she has had hepatitis B for Hepatocellular carcinoma. Diagnosis? . What hepatic circulatory disorder liver: Budd-Chiari syndrome. Female patient. Thrombosis of major hepatic veins has caused extreme blood retention in the Liver. presents with a fever and hepatomegaly. present clinically? CNS symptoms: deposits in putamen resembles parkinsonism. PiZZ (wild type = PiMM) variant leads to a defect in the packing and How does alpha-antitrypsin deficiency transporting of AAT. Periodic acid-Schiff stain of the liver. Lab work up shows elevated alpha fetoprotein.

oral What are the risk factors for this contraceptive pills. rapid weight loss. particular cholelithiasis? lipid-lowering drugs. Native Americans. Risk factors: female over 40. AAT deficiency. obesity. Present as abdominal What is a choledochal cysts? pain with intermittent jaundice. Primary sclerosing pericholangitis. Brown pigment stones (not These stones in the gallbladder are a pictured) are a sign of infection in the sign of what? common bile duct. alcoholic cirrhosis. Increased incidence of cholelithiasis. Increase risk of cholangiocarcinoma. Clonorchis sinensis (Chinese liver What are the risk factors for fluke). Autosomal recessive disease associated with polycystic kidney What is Caroli disease and what is the disease. cholangiocarcinoma? Thorium dioxide. Hep B and C. resected? Congenital dilations of the common bile duct. Caroli is characterized by inheritance? segmental dilation of intrahepatic bile ducts. . Aflatoxin (from aspergillus mold). What are the risk factors for Hemochromatosis. and cirrhosis. Yellow cholesterol stones with bile pigment staining the center. What is the most common liver tumor of young childhood that is fatal unless Hepatoblastoma. presenting most often in children < 10 years old. cholangiocarcinoma. Choledochal cyst and Caroli disease. Black pigment stones (calcium bilirubinate) are a sign of extravascular hemolysis. hepatocellular carcinoma? Primary biliary cirrhosis.

7) Congenital dilations of the common bile duct. 2) Presence of stones within the bile What portion of the bile duct system do ducts of the biliary tree. 1) Bacterial infection of the bile ducts (any part). Mucus hypersecretion traps the cholesterol crystals. Bile must be supersaturated with cholesterol (in excess of lecithin and bile salts). Acute cholecystitis. 4) Biliary atresia 5) Estrogen inhibits intrahepatic bile 5) Cholestasis of pregnancy secretion. What are they? Cholesterol nucleation. 90% of these cases are due to a stone in the cystic duct. The pain then radiates to also converted to lysolecithin which is the right scapula. and vomiting shortly ischemia to gallbladder wall. Patient presents with colicky epigastric Increased intraluminal pressure and pain. Mucosal ulceration can predispose to a infection (normally E. slight fever. what is the end-product of heme UCB (Unconjugated bilirubin) degradation in splenic macrophages? UCB(Unconjugated bilirubin) is soluble lipid soluble in what? . 1) Cholangitis 4) Obstruction of the lumen of the 2) Choledocholithiasis extrahepatic biliary tree within the first 3) Ascending cholangitis 3 months of life. these conditions involve (define them): 3) Infection of intrahepatic biliary ducts. coli). Lecithin is after a meal. Diagnosis? toxic. Formation of cholesterol gallstones Gallbladder hypomotility (excess free include four simultaneous defects. 6) Caroli 6) Segmental dilation of intrahepatic 7) Choledochal cysts bile ducts. cholesterol is toxic to the gallbladder).

CB(conjugated bilirubin). glucuronic acid makes bilirubin undergo what water soluble change? Intestinal bacteria convert CB -> ? UBG (urobilinogen) UBG (urobilinogen) 20% is recycled to liver and kidneys where? Urobilin causes what color change in color change to color of stool and urine UCB ? what is the most common cause of viral hepatitis jaundice? 2nd most common cause of jandice. Gilbert's disease = ? fasting unconjugated hyperbilirubinemia prodrome phases of acute hepatitis? jaundice recovery .

what increases steadily before jaundice serum transaminases occurs? what is the most common viral cause of Hepiatitus A virus (HAV) jaundice? HAV (Hepiatitus A virus) : anti-HAV-IgM indicates infection anti-HAV-IgM indicates ? anti-HAV-IgG indicates anti-HAV-IgG indicates ? recovery/vaccination ↑↑ UBG (urobilinogen) Extravascular hemolysis lab findings no UB (urine bilirubin) what is the first antigen to arrive and last one toleave with recovery in HBsAg Hepatitis B virus(HBV)? HBeAg (HBV B e antigen) and HBV- DNA infective particles are both what type of particles? what is the only marker present during anti-HBc-IgM window phase in HBV? (Anti-HBV core antibody IgM) .

HBV? anti-HBc-IgG HBsAg what are infective carriers in chronic HBeAg HBV? HBV-DNA anti-HBc-IgG Disease: Normal %CB: %CB(conjugated bilirubin)? AST: AST (aspartate aminotransferase)? ALT : ALT (alanine aminotransferase)? ALP : ALP (alkaline phosphatase)? GGT: GGT(γ-glutamyltransferase)? UB : Absent UB (urine bilirubin)? Urine UBG : ↑ Urine UBG (urobilinogen)? . Anti HBs work as antibodies in what immunixation or recovery form past capacity of the bodies workings? infection HBsAg > 6 months is defined as what chronic HBV type of HBV? what are healthy carriers in chronic HBsAg. HBV antibodies convert to which anti-HBc-IgG antibody by 6 months thye are protective antibodies .

Disease: Viral Hepatitis %CB: 20-50% %CB(conjugated bilirubin)? AST: ↑↑↑ AST (aspartate aminotransferase)? ALT : ↑↑↑↑ ALT (alanine aminotransferase)? ALP : ↑ ALP (alkaline phosphatase)? GGT: ↑ GGT(γ-glutamyltransferase)? UB : ↑↑ UB (urine bilirubin)? Urine UBG : ↑↑ Urine UBG (urobilinogen)? Disease: Alcohlic hepatitis %CB: 20-50% %CB(conjugated bilirubin)? AST: ↑↑ AST (aspartate aminotransferase)? ALT : ↑ ALT (alanine aminotransferase)? ALP : ↑ ALP (alkaline phosphatase)? GGT: ↑↑↑ GGT(γ-glutamyltransferase)? UB : ↑↑ UB (urine bilirubin)? Urine UBG : ↑↑ Urine UBG (urobilinogen)? Disease: Cholestasis %CB: >50% %CB(conjugated bilirubin)? AST: ↑ AST (aspartate aminotransferase)? ALT : ↑↑ ALT (alanine aminotransferase)? ALP : ↑↑↑ ALP (alkaline phosphatase)? GGT: ↑↑↑ GGT(γ-glutamyltransferase)? UB : ↑↑↑ UB (urine bilirubin)? Urine UBG : Absent Urine UBG (urobilinogen)? Disease: Extravascular hemolysis %CB: <20% %CB(conjugated bilirubin)? AST: ↑↑ RBC's AST (aspartate aminotransferase)? ALT : N ALT (alanine aminotransferase)? ALP : N ALP (alkaline phosphatase)? GGT: N GGT(γ-glutamyltransferase)? UB : Absent UB (urine bilirubin)? Urine UBG : ↑↑ Urine UBG (urobilinogen)? interpretation: -Earliest phase of acute HBV: Earliest phase of acute HBV HBsAg + HBsAg HBeAg HBV DNA -- HBeAg HBV DNA Anti-HBc-IgM -- Anti-HBc-IgM Anti-HBc-IgG -- Anti-HBc-IgG Anti-HBs -- Anti-HBs .

interpretation: -Acute infection: Acute infection HBsAg + HBsAg HBeAg HBV DNA + HBeAg HBV DNA Anti-HBc-IgM + Anti-HBc-IgM Anti-HBc-IgG -- Anti-HBc-IgG Anti-HBs -- Anti-HBs interpretation: -Window phase. or serologic gap: Window phase. or serologic gap HBsAg -- HBsAg HBeAg HBV DNA -- HBeAg HBV DNA Anti-HBc-IgM + Anti-HBc-IgM Anti-HBc-IgG -- Anti-HBc-IgG Anti-HBs -- Anti-HBs interpretation: -Recovered from HBV: Recovered from HBV HBsAg -- HBsAg HBeAg HBV DNA -- HBeAg HBV DNA Anti-HBc-IgM -- Anti-HBc-IgM Anti-HBc-IgG + Anti-HBc-IgG Anti-HBs + Anti-HBs interpretation: -Immunized: Immunized HBsAg -- HBsAg HBeAg HBV DNA -- HBeAg HBV DNA Anti-HBc-IgM -- Anti-HBc-IgM Anti-HBc-IgG -- Anti-HBc-IgG Anti-HBs + Anti-HBs interpretation: -"Healthy" carrier: "Healthy" carrier HBsAg + HBsAg HBeAg HBV DNA -- HBeAg HBV DNA Anti-HBc-IgM + Anti-HBc-IgM Anti-HBc-IgG + Anti-HBc-IgG Anti-HBs -- Anti-HBs interpretation: -Infective carrier: Infective carrier HBsAg + HBsAg HBeAg HBV DNA + HBeAg HBV DNA Anti-HBc-IgM -- Anti-HBc-IgM Anti-HBc-IgG + Anti-HBc-IgG Anti-HBs -- Anti-HBs .

sexual Hepatitis C (HCV) incubation: transmission? 2-26 weeks (avg. orally. breast feeding) Hepatitis B (HBV) incubation: transmission? 30-180 days incubation? prevention: prevention? immunization with recombinant vaccine % of cases? % of cases: 45% of all cases in US transmission: virus: Parenteral. vertical. transmission: Fecal-oral virus: incubation: Hepatitis A (HAV) 15-50 days (avrg 30 days) transmission? prevention: incubation? passive immunization (immunoglobulin) prevention? % of cases: % of cases? 37% of all cases of acute hepatitis in US transmission: Parental. virus: (pregnancy. 6-7 weeks) incubation? prevention: prevention? no preventive vaccine available % of cases? % of cases: 18% of all cases in US transmission: Parental. sexual. sexual virus: incubation: Hepatitis D (HDV) n/a transmission? prevention: incubation? immunization with recombinant vaccine prevention? for HBV % of cases? % of cases: 1%> of all cases in US virus: transmission: Hepatitis E Fecal-oral (water-born) transmission? Occurs in developing countries incubation? Only produces acute hepatitis prevention? Fulminant hepatitis may develop in % of cases? pregnant women .

fever. virus: nausea/vomiting. entecavir).. lamivudine. abdominal pain Hepatitis A (HAV) treatment: clinical? Passive immunization: immunoglobulin treatment? (passive transfer of antibodies) for pre- exposure prophylaxis and postexposure prophylaxis clinical: variable fever. liver transplant clinical: mild hepatitis (70-80% subclinical). liver transplant clinical: Chronic state less likely with coinfection (HBV and HDV exposure at virus: same time) than superinfection (HBV Hepatitis D (HDV) carrier exposed to blood containing clinical? HBV and HDV) treatment? Chronic infection develops in 60-85% of people infected treatment: virus: Occurs in developing countries Hepatitis E Only produces acute hepatitis clinical? Fulminant hepatitis may develop in treatment? pregnant women . virus: jaundice uncommon (80% anicteric) Hepatitis C (HCV) Treatment: early treatment of acute clinical? infection with pegylated IFN-α may treatment? prevent chronic infection. pegylated IFN-α also used in treating chronic HCV. clinical? polyarthritis. clinical: jaundice > 70%.g. painful hepatomegaly (87%). profound malaise. membranous treatment? glomerulopathy Treatment of chronic hepatitis: pegylated IFN-α. urticaria. nucleoside analogues that block viral replication (e. serum sickness prodrome (15-20%): virus: immunocomplex disease (HBsAg + Hepatitis B (HBV) antibody). vasculitis (PAN).

alkalosis. regenerative Cirrhosis = ? nodules Regenerative nodules = ? produce intrasinusoidal hypertension what is the most common cause of Alcoholic liver disease cirrhosis? reversible metabolic disorder. encephalopathy? portasystemic shunts . anitbiotics. irreversible fibrosis. ↑ serum ammonia Ammonia derives from amino acid Where does ammonia derive from? metabolism and urease-producing bacteria in bowel ↓ Ammonia = ? ↓ protein intake. sedatives. ↑ false Hepatic encephalopathy = ? neurotransmitters. lactulose Precipitating factors of ↑ protein.

connects portal shunt (TIPS) = ? vein with hepatic vein transudate due to alterations in Starling Ascites pressures. Hepatic encephalopathy alterations mental status. somnolence. most physiologic Splenorenal shunt = ? shunt Transjugular intrahepatic portosystemic ↓ portal vein pressure. pathogenesis? secondary aldosteronism . clinical findings? asterixis Portal vein = ? splenic vein superior mesenteric vein Portal vein hypertension due to intrasinusoidal hypertension is caused by? from regenerative nodule compression Shunts used in treating Portal shunts that bypass the liver can hypertension (PH)? precipitate encephalopathy does not bypass liver.

Ascites . Serum albumin .1g/dL = peritoneal origin reversible renal failure without Hepatorenal syndrome = ? parenchymal disease what is the only curative treatment for liver transplantation is the only curative Hepatorenal syndrome? treatment Hyperestrinism in males: cynecomastia. - Pathogenesis? destruction by CD8 T cells -antimitochondrial antibodies .liver vs. peritoneal: >1. spider telangiectasia clinical findings? Postnecrotic cirrhosis is most often chronic hepatitis HBV and HCV caused by? Primary biliary cirrhosis (PBC) autoimmune destruction of bile ducts in Epidemiology? triads -damage to mitochondrial proteins in Primary biliary cirrhosis (PBC) bile duct epithelium in triads.1g/dL = liver origin what is useful in distinguishing? <1.ascitic fluid albumin.

↓ total iron-binding capacity lab findings? (TIBC) -Serum ferritin is primarily used to follow therapy . Hemochromatosis ferritin. AMA. IgM laboratory findings? Secondary biliary cirrhosis cystic fibrosis Complications? -unrestricted reabsorption of iron in small intestine Hereditary Hemochromatosis: -missense mutations HFE gene on pathogenesis? chromosome 6 -Iron initiates synthesis hydroxyl free radicals Hemosiderosis causes what change in acquired iron overload disease iron? -"bronze diabetes" Hemochromatosis -malabsorption clinical findings? -restrictive cardiomyopathy -infertility ↑ serum iron. PBC -pruitus before jaundice clinical findings? -jaundice is a late finding PBC ↑: serum ANA. % saturation.

ceruloplasmin Lab findings? ↓ serum/ urine free copper Rx Wilson's disease penicillamine (copper chelator) treatment? (α1. renal disease Wilson's disease: ↓ total serum copper. Hemochromatosis % saturation best screen best test? ↓ incorporation copper into Wilson's disease: ceruloplasmin pathogenesis? ↓ excretion copper into bile enzyme synthesized in the liver that Ceruloplasmin = ? contains copper -Kayser-Fleischer ring: excess copper in Descemet's membrane of cornea Wilson's disease: -lenticular degeneration in central Clinical findings? nervous disease (CNS). movement disorder.Antitrypsin) AAT deficiency: M is the normal allele. dementia -hemolytic anemia. pathogenesis? Z and S are deficiency variant alleles .

AAT not Cirrhosis in AAT deficiency = ? secreted properly and accumulates in the liver ↓ serum blood urea nitrogen (BUN).vitamin D central stellate scar with radiating Focal nodular hyperplasia (FNH) = ? fibrous septae what is the most common type of Cavernous hemangioma. dysfunction. potential for benign tumor? intraperitoneal hemorrhage . which effects? ↑ PT ↓ serum albumin. Hypoglycemia in cirrhosis = ? ↓ glycogen stores cirrhosis causes severe liver ↓ serum albumin. Lab test abnormalities in Cirrhosis ? -lactic acidosis -hyponatremia -hypokalemia ↓ gluconeogenesis. ↑ serum ammonia. homozygous ZZ variant. Hypocalcemia in cirrhosis = ? ↓ 25(OH).

clinical findings? blood in ascitic fluid -↑ serum AFP. HCC: (Hepatocellular carcinoma) fever. rapidly increasing bloody ascites HCC (Hepatocellular carcinoma): -Ectopic hormones: lab findings? PTH-related protein. ↑ in ascites. Erythropoietin (EPO) . Liver cell adenoma OCPs causes? Produce intraperitoneal hemorrhage Metastasis . insulin-like factor. lung is the most common What is the most common liver cancer? primary site Hepatocellular carcinoma (HCC): pre-existing HBV or HCV cirrhosis most what is the most common risk factor? common risk factor HCC (Hepatocellular carcinoma) pre-existing cirrhosis causes? HCC: (Hepatocellular carcinoma) bile in neoplastic cells microscopic findings? pain.

phospholipid. biocarbonate what is the most common type of Cholesterol gallstones stone? . protein. free CH. exposure to vinyl chloride (plastic Liver angiosarcoma = ? pipes) what is the most common biliary tract Choledochal cyst: pain with intermittent cyst in children jaundice Cystic diseases have a increased risk cholangiocarcinoma for ? association with juvenile polycystic Caroli disease = ? kidney disease what is the most common cause for Primary sclerosing cholangitis cholangiocarcinoma? bile salts/acid. Components of Bile = ? CB. electrolytes.

Stone complications = ? acute pancreatitis ↑ CH in bile CH gallstones = ? ↓ bile salts and lecithin .Black pigment gallstone is a sign of sign of extravascular hemolysis. cancer. fertile ↑ high-density lipoprotein (HDL) and delivery of CH to liver. CH gallstones fat. risk factors? forty. what? calcium bilirubinate Brown pigment gallstone is a sign of sign of common bile duct (CBD) what? infection CH gallstones : ↑ CH in bile pathogenesis ↓ bile salts and lecithin female. CBD obstruction. How does Estrogen effect CH ↑ low-density lipoprotein (LDL) gallstones? receptors and HMG-CoA reductase activity cholecystitis.

Stone complications = ? acute pancreatitis ↑ CH in bile CH gallstones = ? ↓ bile salts and lecithin . cancer. CBD obstruction. How does Estrogen effect CH ↑ low-density lipoprotein (LDL) gallstones? receptors and HMG-CoA reductase activity cholecystitis. ↑ high-density lipoprotein (HDL) and delivery of CH to liver. cancer. Stone complications = ? acute pancreatitis ↑ CH in bile CH gallstones = ? ↓ bile salts and lecithin ↑ high-density lipoprotein (HDL) and delivery of CH to liver. CBD obstruction. How does Estrogen effect CH ↑ low-density lipoprotein (LDL) gallstones? receptors and HMG-CoA reductase activity cholecystitis.

+ Murphy sign. midepigastric colicky pain Stage 2: stone impacts in cystic duct. pain shift to right upper What are the stages of development of quadrant(RUQ). subsides if stone falls out Stage 4: perforation what is the pain radiation in acute right scapula/shoulder cholecystitis? what is the gold standard in diagnosis ultrasound of acute cholecystitis? What does HIDA (Hepatobiliary identifies stone in cystic duct and CBD iminodiacetic acid) scan do for stones? what is an indication for CBD jaundice exploration? what is the treatment for cholecysitis? surgery via laparoscope . Stage 1: stone ledges in cystic duct. radiation to right acute cholecystitis? (4 stages) scapular shoulder Stage 3: bacterial invasion GB wall.

porcelain GB cancer = ? GB ↑ risk for gallbladder cancer. speckled yellow cholesterolosis = ? mucosal surface chronic obstruction of cystic duct hydrops = ? treatment = ? treatment: surgery association with GB stones. immediate Porcelain gallbladder = ? surgery . what should be given for pain for meperidine not morphine cholecysitis? what is the most common symptomatic chronic cholecystitis disorder of gallbladder (GB)? chronic cholecystitis chemical inflammation pathogenesis? excess CH in bile.

Major pancreatic duct = ? stone blocking CBD causes acute pancreatitis What is the most common cause of Alcohol abuse acute pancreatitis? What is the most common cause of seat belt trauma pancreatitis in children? how do you describe the pain in a knife-like pain pancreatitis? fluid unavailable for maintenance of third space fluid in regards to volume in vascular compartment pancreatitis ? refers to the collection of fluid as the pancreas autodigests itself circulating phospholipase destroys hypoxemia = ? surfactant Grey-Turner sign = ? flank hemorrhage . empties into terminal part of CBD.

Cullen's sign = ? periumbilical hemorrhage persistent increase in serum amylase: consider pancreatic pseudocyst consider what condition? higher fever from gram-negative Pancreatic abscess = ? sepsis. ↑ amylase. CT shows bubbles Pancreatic ascites leaking pseudocyst caused by? is Amylase specific for pancreatitis? Amylase is not specific for pancreatitis acute pancreatitis increased clearance of amylase in what happens to the urine? urine serum lipase: more specific and lasts what is an excellent screen for acute longer than amylase in acute pancreatitis? pancreatitis .

what is an excellent screen for
serum immunoreactive trypsin
newborn cystic fibrosis?

what is the gold standard for pancreatic
CT scan

Plain radiograph of pancreatitis = ? sentinel loop; left-sided pleural effusion

what is the most common cause of
alcohol abuse
chronic pancreatitis?

what is the most common cause of
cystic fibrosis
chronic pancreatitis in children?

what is the most common cause of
chronic pancreatitis in developing malnutrition

chronic pancreatitis radiographic dyes show "chain of
pathogenesis? lakes" in major duct

Chronic pancreatitis malabsorption,
clinical findings? type 1 diabetes mellitus

Chronic pancreatitis
CT scan dystrophic calcification
lab findings?

Test for pancreatic insufficiency? secretin stimulation; bentiromide

what is the most common cause of smoking is the most common cause;
pancreatic carcinoma? chronic pancreatitis

signs of Carcinoma in head of jaundice, light-colored stools, palpable
pancreas? gallbladder

Pancreatic cancer
metastasis left supraclavicular node
lab findings?

what is the gold standard tumor marker
an increase of CA19-9 (tumor marker)
in diagnosing pancreatic cancer?

what is the best test for diagnosing
CT scan is the best test
pancreatic cancer?

What is UCB(Unconjugated bilirubin) heme degradation in splenic
the end product of? macrophages

yes. UCB is liquid soluble (indirect
UCB = liquid soluble?

glucuronic acid; and produces
UCB conjugates with _______ acid?
CB(direct bilirubin)

Intestinal bacteria converts CB → ? UBG (urobilinogen)

how much of UBG (urobilinogen) → to
liver and kidneys?

what color changes from urobilin? color of stool and urine

jaundice is most commonly caused by viral hepatitis ? what is 2nd most common cause of Gilbert's disease: fasting unconjugated jaundice? hyperbilirubinemia prodrome phases of acute hepatitis (3)? jaundice recovery transaminases peak before ? transaminases peak before jaundice what is the most common cause of Hepatitis A jaundice? anti-HAV-IgM indicates infection anti-HAV-IgM indicates? anti-HAV-IgG indicates anti-HAV-IgG indicates? recovery/vaccination Extravascular hemolysis = ? ↑↑ UBG(urobilinogen). no UB .

what is the first antigen to arrive and HBsAg(Hepatitis B surface antigen) last to leave with recovery? HBeAg (Hepatitis B e antigen) and HBV(Hepatitis B virus)-DNA are what infective particles type of particles? What is the only marker present during Anti-HBc-IgM (Anti-HBV core antibody the window phase in HBV? IgM) Anti-HBc-IgM is present after ___ 6 months months? Anti-HBs is a ___ antibody and is a a protective antibody marker from past infections? HBsAg (Hepatitis B surface antigen) > chronic HBV 6 months indicates? HBsAG what idnicates a "healthy" carrier? anti-HBc-IgG .

HBeAg. HBV-DVA. anti-HBc- what are infective carriers? IgG screen with EIA (enzyme immunoassay) HCV testing? confirm with RIBA(Recombinant immunoblot) and HCV RNA HCV RNA is what quality of test? the gold standard in testing HCV HCV. HDV = protective antibodies? no protective antibodies Viral hepatitis : -urine UBG urine UBG ++ -urine bilirubin urine bilirubin ++ increase/ decrease? what is the last enzyme to return ot serum ALT normal? what is the most common type of Autoimmune hepatitis hepatitis in the US? . HBsAg.

bilirubin. Autoimmune hepatitis : -serum ANA(antinuclear antibody) serum ANA ++ -anti-smooth muscle antibodies anti-smooth muscle antibodies ++ increase/decrease? Neonatal hepatitis: multifactorial. PT Reye syndrome: (prothrombin time). ↓ lab findings? glucose fatty liver of pregnancy: dysfunction in Reye syndrome regarding pregnancy? β-oxidation FAs. ammonia. fatal unless deliver baby . multinucleated giant cells biopsy shows ____? Reye syndrome is associated with ? aspirin and infection encephalopathy Reye syndrome: fatty change in liver pathogenesis? ↑ transaminases Reye syndrome: sleepy but respond → stuporous → clinical findings? obtundation → coma ↑ transaminasemia.

air in portal vein . HELLP syndrome Preeclampsia = ? (Hemolytic anemia ELevated serum transaminases Low Platelets) What is the most common cause of Fulminant hepatic failure viral hepatitis? Fulminant hepatitis is most commonly acetaminophen caused by what drug? Fulminant hepatic failure: ↓ transaminases lab findings? ↑ PT(prothrombin time) and ammonia Hepatic artery infarction is uncommon dual blood supply to liver due to? Hepatic artery infarction liver transplant rejection causes? PAN (polyarteritis nodosa) ascites. no hepatomegaly. periportal triad liver cell necrosis. Portal vein thrombosis = ? portal hypertension.

clinical findings? ascites complication of bone marrow Veno-occlusive disease = ? transplantation . hepatic vein thrombosis portal hypertension. causes? Bartonella henselae most common cause of hepatic vein polycythemia vera thrombosis? hepatomegaly.intrahepatic obstruction to blood flow is cirrhosis most often caused by ______? combined LHF and RHF Centrilobular necrosis = ? "nutmeg" liver (enlarged with mottled red appearance) Centrilobular necrosis may progress to cardiac cirrhosis ____? Peliosis hepatis anabolic steroids.

causes? methotrexate intrahepatic cholestasis OCP (oral contraceptive pills). Alcohol liver disease= ? hepatitis. microscopic changes? Mallory bodies intrahepatic fibrosis (fatty change) amiodarone. causes? anabolic steroids extrahepatic cholestasis: a stone in CBD (common bile duct) caused commonly by? . cirrhosis Alcoholic hepatitis: acetaldehyde damages hepatocytes acetaldehyde damages ____? fatty change. Alcoholic hepatitis: neutrophil infiltration. Hematobilia = ? blood in bile from liver trauma fatty change.

lab findings? urine bilirubin ++ effect of estrogen on intrahepatic bile secretion Cholestasis in pregnancy = ? (benign/ not dangerous to fetus or mother) extrahepatic biliary atresia : causes jaundice in newborns causes _____ in newborns PSC (Primary sclerosing cholangitis) = obliterative fibrosis intrahepatic and ? extrahepatic bile ducts PSC: strong association with ulcerative colitis strong association with ulcerative colitis > Crohn's disease > _____ disease PSC: cirrhosis. complications? cholangiocarcinoma ERCP (Endoscopic retrograde PSC (Primary sclerosing cholangitis) cholangiopancreatorgraphy) diagnostic. diagnosis? "beading" of bile ducts . Cholestasis absent urine UBG.

Rh and ABO HDN Increased production of UCB . black pigment in hepatocytes which disorders could have the following lab findings Rotor's syndrome: similar to Dubin- Johnson syndrome but without black CB >50% increase Urine Bilirubin..g. Normal normal macrophage destruction of fetal UBG. urobilinogen.. urobilinogen. pigment in hepatocytes absent UBG.g. absent Urine Bilirubin. Decreased extrahepatic bile flow Gallstone in common bile duct Carcinoma of head of pancreas . caused by UCB . jaundice occurs with fasting Crigler-Najjar syndromes: genetic which disorders could have the disorders with decreased to absent following lab findings conjugating enzymes Physiologic jaundice of newborn: Decreased uptake or conjugation of begins on day 3 of life. increase UBG. urobilinogen. Gilbert syndrome: common genetic defect in uptake/conjugation of UCB. describe Bilirubin metabolism which disorders could have the Extravascular hemolytic anemias: e. RBCs Decreased intrahepatic bile flow Drug- induced (e. following lab findings hereditary spherocytosis. absent Urine Bilirubin. OCP) Primary biliary cirrhosis Dubin-Johnson syndrome: genetic defect in secretion into intrahepatic bile ducts.

which components of bilirubin metabolism is the following Temporarily stored in the gallbladder Conguated Bilirubin is secreted into the Enters the duodenum via the common intrahepatic bile ducts. and then UCB is conjugated to produce onjugated bilirubin (CB). name the component of bilrubin metabolism combines with albumin in the blood Unconjugated bilirubin (UCB) name the compent of bilirubin metabolism UCB is taken up by hepatocytes. bile duct name the component of bilirubin metabolism Intestinal bacteria convert CB to which Intestinal bacteria convert CB to product urobilinogen (UBG). name the component of bilirubin metabolism Senescent red blood cells (RBCs) are phagocytosed by splenic macrophages. Unconjugated bilirubin (UCB) UCB is the end product of heme end product of heme degradation. . which product CB is water-soluble. is lipid-soluble. degradation. Jaundice is first noticed in the sclera. what causes jaundice and what are the signs Jaundice is due to an increase in UCB and/or CB.

or extrahepatic obstruction to bile Serum γ-glutamyl transferase (GGT) flow Induction of cytochrome P-450 system name the classic condition with component of the liver function test alcoholic liver increases GGT describe the component of the liver function test source of ALP other than liver (e. osteoblastic activity in bone) Normal GGT and increased ALP- Serum alkaline phosphatase (ALP) . name the component of the liver function test Serum alanine transaminase (ALT) Specific enzyme for liver cell necrosis Present in the cytosol name the condition with the following component of the liver function test viral hepatitis ALT >AST: name the component of the liver function test Serum aspartate transaminase (AST) Present in mitochondria Alcohol damages mitochondria name the condition in with the component of the liver function test indicates alcoholic hepatitis AST >ALT name the component of the liver function test Intra.g..

name the condition with component of the liver function test liver cholestasis Increased GGT and ALP: name the condition with component of the liver function test Bilirubinuria: viral hepatitis.or extrahepatic obstruction of bile ducts Urine bilirubin present in excess name the condition with component of Increased urine UBG: extravascular the liver function test hemolytic anemias. intra. viral hepatitis excess Urine UBG Absent urine UBG: liver cholestasis where is Albumin is synthesized liver where are the Majority of coagulation in the liver factors are synthesized what does increase Prothrombin time Increased PT: severe liver disease (PT) indicate where does the Urea cycle take place liver .

In which conditions is it associated with Anti-smooth muscle antibody is present Autoimmune hepatitis in which GI condition . what does a decrease in Blood urea cirrhosis nitrogen (BUN) indicate Ammonia is metabolized in the urea where is Ammonia metabolized cycle what does Increased serum ammonia cirrhosis. Reye syndrome indicate Serum IgM is increased in which GI Increased in primary biliary cirrhosis condition Antimitochondrial antibody is present in primary biliary cirrhosis which GI condition An antimicrosomal antibody is an antibody directed against Hashimoto's thyroiditis microsomes.

. painful hepatomegaly Serum transaminases increase Viral Hepatitis steadily. prisons. travelers to developing countries. bodies) what are they name the type of hepatitis and how it is transmitted No carrier state Hepatitis A .fecal /oral Does not lead to chronic hepatitis Occurs in day care centers. and male homosexuals (anal intercourse) . Peak just before jaundice occurs Atypical lymphocytosis what are the urine bilirubin and urine Increased urine bilirubin and urine UBG UBG findings in viral hepatitis Microscopic findings in acute viral Apoptosis of hepatocytes (Councilman hepatitis include councilman bodies.α-Fetoprotein (AFP) is a tumor marker Hepatocellular carcinoma for which GI condition name the condition Fever.

sexual Requires HBsAg to replicate Chronic state less likely with coinfection (HBV and HDV exposure at same time) than superinfection . vertical (pregnancy. type I MPGN. PCT Increased incidence of hepatocellular carcinoma name the type of hepatitis and how it is transmitted Carrier state may occur Hepatitis D Parenteral.name the type of hepatitis and how it is transmitted Carrier state may occur Chronic hepatitis in 10% of immunocompetent patients Hepatitis B Parenteral. sexual. membranous GN Increased incidence of hepatocellular carcinoma name the type of hepatitis and how it is transmitted Carrier state may occur Mild hepatitis. breast feeding) Serum sickness prodrome (5-10%): vasculitis (PAN). alcohol excess. sexual Associated with posttransfusion hepatitis. polyarthritis. jaundice uncommon Chronic hepatitis in >70% of cases Hepatitis C Parenteral.

Hepatitis B e antigen (HBeAg) and what are the serological findings in HBV-DNA Acute infection of Hepatitis B Infective particles Appear after HBsAg and disappear before HBsAg 3. Hepatitis B surface antigen (HBsAg) 2. Anti-HBV core antibody IgM (anti- HBc-IgM)-Nonprotective antibody Remains positive in acute infections what is the First marker of infection with Hepatitis B and when does it appear after infection Hepatitis B surface antigen (HBsAg) Appears within 2 to 8 weeks after exposure Anti-HBV core antibody IgM (anti-HBc- Converts to anti-HBc-IgG in 6 months IgM) converts to what in 6 months . hepatitis B surface antigen only 1.name the type of hepatitis and how it is transmitted No carrier state or chronic hepatitis Hepatitis E Fecal-oral (waterborne) Fulminant hepatitis may develop in pregnant women Occurs in developing countries what are the finding in Earliest phase of acute HBV HBsAg.

or serologic gap of Heptatis B contains which marker Anti-HBV core antibody IgM (anti-HBc- IgM) ONLY Nonprotective antibody what serological marker provides that Protective antibody against Hepatitis B Anti-HBV surface antibody (anti-HBs) which marker would indicate immunization after HBV vaccination Anti-HBV surface antibody (anti-HBs) ONLY what seroligical marker would indicate 1. anti-HBc-IgG. and hepatitis B. anti-HBc-IgG what serological marker would indicate "Healthy" carrier if HBsAg >6 months Presence of HBsAg and anti-HBc-IgG and Absence of DNA and e antigen what serological markers would indicate Infective chronic carrier of Presence of HBsAg. Window phase. Anti-HBV surface antibody (anti- Recovered from HBV HBs) and 2. what is the pt at increased infective particles (DNA and e antigen) risk for developing Increased risk for postnecrotic cirrhosis and hepatocellular carcinoma .

true. recovery and protective antibody Anti-HEV-IgG indicates recovery (protective antibody). how does conjugated bilirubin gain CB gains access to blood via damaged access to blood to increase the content bile ductules. Screen with enzyme immunoassay Presence of anti-HCV-IgG indicates infection or recovery. uptake. and uring bilirubin gain access to urine . It is not a protective antibody. HCV is confirmed Confirmatory tests with which modality Recombinant immunoblot assay (RIBA) HCV RNA using polymerase chain reaction FALSE. IgG is not a protective antibody. How does urine UBG redirected to the kidneys.anti-HCV-IgG indicates t/f anti-HCV-IgG a protective antibody. false. infection or recovery. Hepatitis C virus (HCV) is Screened with which modality.Hepatitis D virus (HDV) t/f Presence of anti-HDV-IgM or IgG Presence of anti-HDV-IgM or IgG indicates a protective antibody. Increased urine UBG and urine bilirubin CB is water-soluble and is filtered in is present in Viral hepatitis: defect in the kidneys.Hepatitis E virus (HEV) Presence of anti-HEV-IgM indicates t/f Presence of anti-HEV-IgM indicates active infection. conjugation of UCB and UBG recycled back to inflamed liver is secretion of CB. indicates active infection.

larvae enter common bile duct and become adults May produce cholangiocarcinoma .. right upper quadrant pain Most common cause of multiple liver abscesses name the pathogen that produces the following Infectious Diseases of the Clonorchis sinensis (Chinese liver Liver fluke) Contracted by ingesting encysted larvae in fish. coli from concurrent biliary infection and duct obstruction (e.g. name the pathogen that causes the following Infectious Diseases of the Entamoeba histolytica Liver Usually right lobe abscess name the pathogen of Infectious Diseases of the Liver Inflammation of bile ducts (cholangitis) e. stone) Triad of fever. jaundice.

jaundice. hepatosplenomegaly Autoimmune hepatitis Laboratory findings Positive serum antinuclear antibody (ANA) test Anti-smooth muscle antibodies name the condition Usually develops in children younger than 4 years of age Reye syndrome Often follows a chickenpox or influenza infection . and esophageal varices name the condition Clinical findings Fever. ascites. human is (sheepherder's disease) intermediate host Rupture of cysts can produce anaphylaxis name the pathogen that produces the following liver disease Eggs incite a fibrotic response in the portal vein ("pipestem cirrhosis") Schistosoma mansoni Complications of cirrhosis: portal hypertension. name the pathogen that produces the following infectious disease of the liver Single or multiple cysts containing larval forms Echinococcus granulosus Dog is definitive host.

convulsions Hepatomegaly name the condition Hypertension. dependent pitting edema in third trimester Preeclampsia Liver cell necrosis around portal triads Increased serum transaminases Hemolytic anemia with schistocytes Elevated serum transaminases describe the HELLP syndrome Low platelets-Due to disseminated intravascular coagulation name the condition Fulminant hepatic failure Acute liver failure with encephalopathy within 8 weeks of hepatic dysfunction Wrinkled capsular surface due to loss of hepatic parenchyma what are the Gross . Fulminant hepatic failure Increase in PT and ammonia . proteinuria. name the condition Microvesicular type of fatty liver. coma.Small cytoplasmic globules without nuclear displacement Reye syndrome Clinical findings Encephalopathy Cerebral edema. microscopic and Dull red to yellow necrotic parenchyma clinical findings in Fulminant hepatic with blotches of green (bile) failure Clinical findings Hepatic encephalopathy and jaundice Decrease in transaminases-Liver what are the Laboratory findings in parenchyma is destroyed.

Occurs in AIDS Potential for intraperitoneal hemorrhage name the condition and give 2 Posthepatic obstruction to blood flow examples Hepatic vein thrombosis Obstruction of blood flow out of the liver Veno-occlusive disease . because of a dual blood supply: Hepatic artery and portal vein why is Liver infarction is uncommon tributaries normally empty blood into the sinusoids ("nutmeg" liver). The liver has a mottled cut surface. name the condition Sinusoidal dilation due to blood Causes Anabolic steroids Peliosis hepatis Bartonella henselae causing bacillary angiomatosis . Dark areas represent congested central veins and sinusoids. Most often due to left-sided heart failure (LHF) and right-sided heart failure (RHF) LHF decreases cardiac output causing which condition can lead to this hypoperfusion of the liver. presentation in the liver Causes ischemic necrosis of hepatocytes located around central Centrilobular hemorrhagic necrosis vein RHF causes a back-up of systemic venous blood into the central veins and sinusoids.

arsenic. Mallory bodies. thorium dioxide (radioactive contrast material) . ascites. Alcohol-related disorders Due to acetaldehyde damage to hepatocytes describe the pathogenesis of Alcoholic Stimulation of collagen synthesis hepatitis around the central vein Perivenular fibrosis 1.or drug-induced liver disease Angiosarcoma Vinyl chloride. Fatty change with neutrophil infiltration what are the 3 Microscopic findings in 2. Hepatocellular carcinoma.Damaged Alcoholic hepatitis cytokeratin intermediate filaments in hepatocytes 3. painful liver Portal hypertension.Invades splenomegaly hepatic vein High mortality rate Complication of bone marrow name a condition that would lead to transplantation Veno-occlusive disease producing Posthepatic obstruction to blood flow Collagen develops around the central veins. list 3 causes of Hepatic vein thrombosis leading to Posthepatic Polycythemia vera obstruction to blood flow causing: Oral contraceptive pills Enlarged. Perivenular fibrosis name the tumor or disease associated with Chemical. why is Fatty liver change is the most Substrates of alcohol metabolism are common type of disease seen in used to synthesize liver triglyceride.

or drug-induced liver disease Liver cell adenoma or Cholestasis Oral contraceptive pills name the tumor or disease associated with Chemical. Mallory bodies and progression to cirrhosis). electron tubes. anabolic steroids name the tumor or disease associated with Chemical. halothane.or drug-induced liver disease Cholangiocarcinoma Thorium dioxide-used as a stabilizer in tungsten electrodes in TIG welding.or drug-induced liver disease Hepatocellular carcinoma Aflatoxin (due to Aspergillus mold) name the tumor or disease associated with Chemical. methyldopa name the tumor or disease associated with Chemical. and aircraft engines name the tumor or disease associated with Chemical. methotrexate .or drug-induced liver disease Fatty change or fibrosis in the liver Amiodarone (resembles alcoholic hepatitis.or drug-induced liver disease Cholestasis Oral contraceptive pills (estrogen interferes with intrahepatic bile secretion).name the tumor or disease associated with Chemical. acetaminophen.or drug-induced liver disease Acute hepatitis Isoniazid (caused by toxic metabolite).

Intrahepatic cholestasis what is the difference between Blockage of the intrahepatic bile ducts Intrahepatic cholestasis and Extrahepatic cholestasis Extrahepatic cholestasis Blockage of common bile duct (CBD) Drugs (e. anabolic steroids. oral contraceptive pills.. Primary sclerosing pericholangitis. descibe Bile salts do not enter the small why intestine. what causes Pruritus due to bile salts deposited in the jaundice skin the Clinical findings of obstructive liver Malabsorption disease include Malabsorption. Extrahepatic biliary Extrahepatic cholestasis atresia and Carcinoma head of pancreas most likely produce which Type of cholestatic liver disease the Clinical findings of obstructive liver Jaundice with pruritus disease include jaundice. Neonatal hepatitis Pregnancy-induced cholestasis Intrahepatic cholestasis (estrogen) produce which Type of cholestatic liver disease Stone usually originating from the gallbladder. the Clinical findings of obstructive liver disease include Light-colored stools.g. Due to a lack of urobilin why CB >50% what are the Laboratory findings in Bilirubinuria obstructive liver disease Absent urine UBG Increase in serum ALP and GGT .

Alcoholic liver disease (most common) 2. HCV) 3. name the condition Obliterative fibrosis of intrahepatic and extrahepatic bile ducts Male dominant Associated with ulcerative colitis Primary sclerosing pericholangitis Clinical findings Jaundice Cirrhosis Increased incidence of cholangiocarcinoma name the condition Cirrhosis Irreversible diffuse fibrosis of the liver with formation of regenerative nodules Hepatocyte reaction to injury -diffuse micronodular surface of the liver. Autoimmune disease (primary biliary list 4 causes of this type of liver cirrhosis) 4. Postnecrotic cirrhosis (HBV. Lack normal liver architecture Lack of portal triads and sinusoids Surrounded by bands of fibrosis describe the gross appearance of this Compress sinusoids and central veins cirrhotic liver Intrasinusoidal hypertension Reduction in the number of functional sinusoids Increase in hydrostatic pressure in portal vein 1. galactosemia . Metabolic disease: Hemochromatosis. Wilson's disease α1-Antitrypsin deficiency.

g. Increase in serum ammonia Due to a defective urea cycle that cannot metabolize ammonia Alterations in the mental status Somnolence and disordered sleep rhythms what are the Clinical findings in hepatic encephalopathy due to hepatic failure Asterixis (i. inability to sustain posture. Due to inability to synthesize why does hepatic failure lead to coagulation factors Multiple coagulation defects Produces a hemorrhagic diathesis why does hepatic failure produce Hypoalbuminemia from decreased dependent pitting edema and ascites synthesis of albumin 1. spider angioma (telangiectasia) on the cheek of a patient with cirrhosis. desribe the common condition that produce this symptom Multiple spider angiomas are common in cirrhosis and pregnancy. tyrosine. phenylalanine.e.g. tryptophan).. Increase in aromatic amino acids (e.. gamma encephalopathy aminobutyric acid) in hepatic failure 2..Converted into false what cause the Hepatic neurotransmitters (e. flapping tremor) Coma and death in late stages Resistance to intrahepatic blood flow due to intrasinusoidal hypertension describe the Pathogenesis of portal hypertension Anastomoses between portal vein tributaries and the arterial system .

Congestive splenomegaly- Increased hydrostatic pressure in splenic vein. 1. Hypersplenism with various cytopenias may occur describe 5 Complications of portal hypertension 3. periumbilical venous collaterals (caput medusae) Liver cannot degrade estrogen and 17- what cause the Hyperestrinism in ketosteroids (e. EARLY finding well before jaundice appears Hepatomegaly Primary biliary cirrhosis (PBC) Jaundice. name the condition Autoimmune disorder Granulomatous destruction of bile ducts in portal triads Primary biliary cirrhosis (PBC) Occurs more often in women between 40 and 50 years of age Progresses from a chronic inflammatory reaction to cirrhosis name the condition Pruritus.LATE finding after most of the bile ducts have been destroyed Cirrhosis with portal hypertension Increased risk for hepatocellular carcinoma ..Deposition of bile salts in skin. Ascites 2. Esophageal varices 4.g. Hemorrhoids. androstenedione). males Androstenedione is aromatized into with liver cell failure estrogen in the adipose cell. 5.

Iron stimulates the production of hydroxyl free radicals-Free radicals damage tissue and cause fibrosis. name the condition Laboratory findings Antimitochondrial antibodies (>90% of Primary biliary cirrhosis (PBC) cases) Increase in IgM name the condition Complication of chronic extrahepatic bile duct obstruction Secondary biliary cirrhosis Example-cystic fibrosis. The amount of endocytosed transferrin iron determines how much mucosal cell iron is released into the plasma. 1. Mutations involving hereditary hemochromatosis gene (HFE) describe the pathogenesis of hereditary hemochromatosis 3. . describe the The normal function of the this pic-Liver biopsy stained with HFE gene produc Prussian blue in a patient with hereditary hemochromatosis. where bile is dehydrated No increase in antimitochondrial antibodies or IgM to facilitate the binding of plasma transferrin (binding protein of iron) with its mucosal cell transferrin receptor so that transferrin can be endocytosed by intestinal cells. The hepatocytes are filled with blue iron granules. This is an early stage before parenchymal damage and fibrosis develop. Unrestricted reabsorption of iron in the small intestine 2.

Malabsorption. Destruction of β-islet cells 3. Gene mutation. "Bronze diabetes". Increased risk of hepatocellular carcinoma 2. degenerative joint disease 6. Cirrhosis.Destruction of hereditary hemochromatosis (6) exocrine pancreas 5. Decreased synthesis of ceruloplasmin (binding protein for copper in blood) describe the pathogenesis of this 2. joints. pancreas. skin. Hyperpigmentation. Restrictive cardiomyopathy. and ferritin Transferrin synthesis is decreased why is there a Decreased in total iron.Iron deposits primarily in hepatocytes . percent saturation. .Defective hepatocyte transport of copper into bile for excretion. Increased serum iron.AR.Type I diabetes mellitus. when iron stores are increased binding capacity in pt with hereditary hemochomatosis 1. Liver. heart. in which organs does iron from pituitary hereditary hemochromatosis deposit other than The hepatocytes are filled with blue iron granules 1.Iron deposits in skin and increases melanin production describe the clinical findings in pt with 4. Unbound copper eventually disorder accumulates in blood Loosely attached to albumin Copper deposits in other tissues causing a toxic effect.

Produces dementia Decreased serum ceruloplasmin what is Useful in diagnosing Wilson's disease in its early stages Increased serum and urine free copper what is Useful in diagnosing Wilson's disease in the later stages name the condition and describe the α1-Antitrypsin (AAT) deficiency pathogensis Alleles are inherited codominantly Neonatal hepatitis with intrahepatic (each allele expresses itself). Copper deposits in the putamen Produces a movement disorder resembling parkinsonism Copper deposits in the subthalamic what causes the Central nervous nucleus. cholestasis Normal genotype is PiMM. Due to free copper deposits in Descemet's membrane in the cornea The gene defect in Wilson's disease affects a copper transport system that what causes the Kayser-Fleischer ring produces a dual defect-decreased in Wilson's disease synthesis of ceruloplasmin in the liver and decreased excretion of copper into bile. Increased risk for hepatocellular Production of a mutant protein that carcinoma cannot be secreted into blood Accumulation of AAT in hepatocytes Young adults with panacinar causes liver damage. Most common abnormal allele is Z.Produces hemiballismus system symptoms in Wilson's Copper is toxic to neurons in the cerebral cortex. emphysema . Most common cause of cirrhosis in PiZZ variant has decreased AAT levels children in serum.

Increased risk for hepatocellular Production of a mutant protein that carcinoma cannot be secreted into blood Accumulation of AAT in hepatocytes Young adults with panacinar causes liver damage. what causes the Decreased serum Due to disruption of the urea cycle in blood urea nitrogen (BUN) and the liver increased serum ammonia in cirrhosis name the condition and describe the α1-Antitrypsin (AAT) deficiency pathogensis Alleles are inherited codominantly Neonatal hepatitis with intrahepatic (each allele expresses itself). emphysema what causes the Fasting hypoglycemia Defective gluconeogenesis and in cirrhosis decreased glycogen stores what causes the Decreased serum Due to disruption of the urea cycle in blood urea nitrogen (BUN) and the liver increased serum ammonia in cirrhosis Toxic products from hepatic what cause the Chronic respiratory dysfunction overstimulate respiratory alkalosis in cirrhosis center what causes the Fasting hypoglycemia Defective gluconeogenesis and in cirrhosis decreased glycogen stores . Most common cause of cirrhosis in PiZZ variant has decreased AAT levels children in serum. Most common abnormal allele is Z. cholestasis Normal genotype is PiMM.

AAT deficiency list 3 causes . PBC. Aflatoxins (from Aspergillus mold in large. with the remaining liver. hemorrhagic tumor masses are grains and peanuts) present in the liver. Multiple 2. chronic HBV and HCV Hepatocellular carcinoma. what causes the Lactic acidosis in Liver dysfunction in converting lactic cirrhosis acid to pyruvate Toxic products from hepatic what cause the Chronic respiratory dysfunction overstimulate respiratory alkalosis in cirrhosis center Benign tumor of hepatocytes Usually occur in women of childbearing in what pt population is Liver (hepatic) age cell adenoma most commonly seen and why Associated with the use of oral contraceptive pills what causes the Lactic acidosis in Liver dysfunction in converting lactic cirrhosis acid to pyruvate Benign tumor of hepatocytes Usually occur in women of childbearing in what pt population is Liver (hepatic) age cell adenoma most commonly seen and why Associated with the use of oral contraceptive pills 1. There is also diffuse infiltration of tumor blending in 3. alcoholic cirrhosis. Hereditary hemochromatosis.

characteristic finding is the presence of bile in neoplastic cells. or thorium dioxide increases the risk for which type of cancer name the cystic disease most common cyst in biliary tract in children younger than 10 years old Choledochal cyst Clinical findings Abdominal pain with persistent or intermittent jaundice . Production of ectopic hormones Erythropoietin (secondary list 3 important Laboratory markers for polycythemia) heptocellluar carcinoma Insulin-like factor (hypoglycemia) Lung most common metastatic site what is the most common site for metastasis of a hepatocellular carcinoma Exposure to vinyl chloride (most Angiosarcoma common cause). 1. what is the characteristic microscopic finding in Hepatocellular carcinoma. arsenic. Increased α-fetoprotein (AFP) 2.

The wall of the gallbladder is scarred name the type of gallstone Pigment stones Black and brown pigment stones Some are radiopaque. name the cystic condition AR Segmental dilatation of intrahepatic bile ducts Caroli disease Clinical findings Association with polycystic kidney disease Increased incidence of cholangiocarcinoma name the condition Most common malignancy of bile ducts Clinical findings Cholangiocarcinoma Obstructive jaundice Palpable gallbladder (Courvoisier's sign) 1. Choledochal cyst and Caroli disease (80% of cases) Gallstones (cholelithiasis) Yellow cholesterol stones with centers They are radiolucent containing entrapped bile pigments. Primary sclerosing pericholangitis Most common cause in United States 2. Clonorchis sinensis (Chinese liver fluke) name 4 cause of Causes of cholangiocarcinoma 3. Thorotrast (thorium dioxide) 4. .

. name the type of gallstone Black and brown pigment stones Some are radiopaque.g. Use of oral contraceptive pills what are the risk factors Estrogen increases cholesterol in bile.. use of lipid-lowering drugs Native Americans (e.g. sickle cell anemia) Excess bilirubin in bile produces calcium bilirubinate describe the pathogenesis Brown pigment stones Sign of infection in the Collecting Bile Dut 4 F's Female over 40 years old Obesity Cholesterol is increased in bile. Pima and Navajo Indians) . Pigment stones Supersaturation of bile with cholesterol Decreased bile salts and lecithin describe the pathogenesisi Both normally solubilize cholesterol in bile black pigment stones -Sign of chronic extravascular hemolytic anemia (e. Rapid weight loss.

belching. Associated with small bowel Annular pancreas obstruction . name the condition Fever with nausea and vomiting Usually 15 to 30 minutes after eating Initial midepigastric colicky pain Acute cholecystitis Pain eventually shifts to the right upper quadrant. minor inflammation and bloating name the condition Gallbladder with dystrophic calcification Gallbladder adenocarcinoma Dominant in elderly women Poor prognosis name the condition Dorsal and ventral buds form a ring around the duodenum. Pain is constant and dull Pain may radiate to right scapula Ultrasound is the gold standard what is the GOLD standard for testing for gall stones Radionuclide scan identifie name the condition Chronic cholecystitis Severe. persistent pain 1 to 2 hours postprandially Pathogenesis Cholelithiasis with repeated attacks of Recurrent epigastric distress.

describe how the Major pancreatic duct and CBD are confluent in their terminal part Both empty their contents into the duodenum via the ampulla of Vater describe the Important in the Stone(s) obstruct terminal part of the pathogenesis of acute pancreatitis CBD → Increased back-pressure refluxes bile into the major pancreatic duct → Bile activates pancreatic proenzymes causing acute pancreatitis t/f an increase in amylase is specific for false.increase in amylase is not pancreatitis specific for pancreatitis what are the 2 major causes of acute Alcohol abuse and gallstones are the pancreatitis major causes what are the 2 major causes of acute pancreatitis Alcohol abuse and gallstones are the major causes .

Alcohol thickens ductal secretions Also increases duct permeability to describe the pathogenesis of acute enzymes pancreatitis d.g. Obstruction of the main pancreatic duct or terminal CBD b.Chemical injury of acinar cells Examples-thiazides.. triglyceride (>1000 mg/dL) e. . Must be activation of pancreatic proenzymes (inactive enzymes)- Activation leads to autodigestion of the pancreas Mechanisms of activation of proenzymes a. Gallstones c. Infectious injury of acinar cells Examples-CMV. alcohol. posterior penetration of duodenal ulcer Metabolic activation of proenzymes (e. Mechanical injury of acinar cells Examples-seat belt trauma. coxsackievirus f. hypercalcemia. ischemia. mumps. shock) Trypsin is important in the activation of proenzymes.

Loss of surfactant produces atelectasis what causes the Hypoxemia in acute and intrapulmonary shunting. pancreatitis Acute respiratory distress syndrome (ARDS) may occur. what causes the Hypoxemia in acute Acute respiratory distress syndrome pancreatitis (ARDS) may occur. what are Grey-Turner's signand Cullen's sign (periumbilical Cullen's sign in acute pancreatitis hemorrhage) Hypocalcemia is caused by enzymatic fat necrosis. Calcium binds to fatty acids leading to what causes the Tetany in acute a decrease in ionized calcium. Due to hemorrhage and loss of enzyme-rich fluid around the pancreas (called "third spacing") what causes the shock in acute pancreatitis Circulating pancreatic phospholipase destroys surfactant. pancreatitis . Grey-Turner's sign (flank hemorrhage). name the condition fever. nausea and vomiting Severe. Loss of surfactant produces atelectasis and intrapulmonary shunting. boring midepigastric pain with radiation into the back acute pancreatitis Radiation into back is due to its retroperitoneal location. Circulating pancreatic phospholipase destroys surfactant.

pancreatitis Is not excreted in urine Computed tomographic (CT) scan is the gold standard for pancreatic imaging. children. Alcohol abuse is the most common known cause. and cause in children. . serum amylase longer than 10 days describe thise pseudocysts Amount of amylase in the fluid surpasses renal clearance of amylase. list the common causes of Chronic Cystic fibrosis is the most common pancreatitis in adults. Plain abdominal radiograph what is the gold standard for pancreatic Sentinel loop in subjacent duodenum imaging. Increased serum lipase More specific for pancreatitis Serum levels return to normal in 3 to 5 what lab findings are specific for acute days. where the bowel does not demonstrate peristalsis Left-sided pleural effusion containing amylase (10% of cases) Collection of digested pancreatic tissue around pancreas Complications of acute pancreatitis Abdominal mass with persistence of include Pancreatic pseudocyst. developing countries Malnutrition is the most common cause in developing countries. or transverse colon (cut-off sign) Localized ileus.

Pancreatic calcifications (CT scan best Chronic pancreatitis study) Clinical findings Severe pain radiating into the back Malabsorption Type 1 diabetes mellitus Pancreatic pseudocyst Smoking (most common cause) what causes Exocrine pancreatic Chronic pancreatitis cancer Hereditary pancreatitis Association with K-RAS gene mutation Mutation of suppressor genes (TP16 describe the Pathogenesis of exocrine and TP53) pancreatic cancer Most occur in the pancreatic head (65% of cases) Often blocks CBD causing jaundice what is the location of most exocrine Remainder occur in the body and tail pancreatic cancers . name the condition Radiographic dyes show a "chain of lakes" appearance in the pancreatic major duct.

Epigastric pain with weight loss Signs of CBD obstruction (carcinoma of head of pancreas) Jaundice (CB > 50%) Light-colored stools (absent UBG) what are the clinical and lab findings of exocrine pancreatic cancer Palpable gallbladder (Courvoisier's sign) Superficial migratory thrombophlebitis (see Chapter 8) Increased CA19-9 Gold standard tumor marker What is the end product of heme Unconjugated bilirubin degradation? Unconjugated bilirubin is _____ soluble Lipid UCB combines with what in the blood? albumin Conjugated Bilirubin is ____ soluble. Water .

ABO mismatches). <20% Crigler-Najjar syndrome. Physiologic Jaundice of a newborn Name the diseases associated with CB Viral Hepatitis 20-50% . What converts CB to urobilinogen? Intestinal bacteria Color of urine is due to? urobilin Jaundice is first noticed in the ______? Sclera Second most common cause of Gilbert's Syndrome jaundice? Most common cause of jaundice? Viral hepatitis Hemolytic anemias (hereditary Name the disease associated with CB spherocytosis.

Name the diseases associated with CB Dubin-Johnson syndrome. Carcinoma of head of Pancreas ALT Specific enzyme for liver cell necrosis Present in the mitochondria thus ETOH AST damages mitochondrea AST>ALT Indicates alcoholic hepatitis gamma glutamyl transferase: Intr a or GGT extrahepatic obstruction to bile flow Alkaline Phosphatase:Obstruction to ALP bile flow Serum Albumin Prothrombin time Hepatocyte Function Markers Blood Urea Nitrogen Serum Ammonia . Obstructed: Primary Biliary Cirrhosis. Gallstones > 50% in common bile duct.

Antimitochondrial Antibody is seen in? Primary biliary cirrhosis Antinuclear antibody is seen in? Autoimmune hepatitis What is the tumor marker for Alpha-Fetoprotein (AFP) hepatocellular carcinoma? Persistence of HBsAg for longer than What makes one have chronic HBV? 6months What makes one a "Healthy" chronic Presence of HBsAG. HBcIgG and carrier of HBV? absence of DNA and e antigen What makes one a "Infective" chronic Presence of HBV-DNA and HBVe carrier? antigen Autoimmune hepatitis occurs most Young woman often in? .

varicies. obstruction of portal vein or hepatic hemorrhoids. splenomegaly) artery blood present like? NO NUTMEG LIVER . What antibody would you find in a Anti-nuclear and anti-smooth muscle person with autoimmune hepatitis? Prehepatic obstruction to blood flow Hepatic artery and Portal vein includes what arteries or veins? Hepatic artery thrombosis is the dual blood suppy uncommon bc? Hepatic artery and portal vein tributaires normally empty blood into sinusoids the ____. What would cause an obstruction of the Liver transplant rejection or Vasculitis hepatic artery? due to polyarteritis ndosa Pylephlebitis (inflammation of the portal What would cause an obstruction to the vein) due to appendicitis portal vein? Polychythemia Vera (too many RBC) Hepatocellular Carcinoma What would the clinical finding of an Portal HT (ascites.

Centrilobular hemorrhagic What are the top 3 reasons for Necrosis (LHF or RHF). peliosis(anabolic steriods) LHF decreases CO causing How does LHF cause centrilobular hypoperfusion of the liver(via hepatic hemorrhagic necrosis? artery) thus causing an ischemic necrosis RHF causes a back up of systemic How does LHF cause centrilobular venous blood into the central vein and hemorrhagic necrosis? sinusoids What is the most common reason for Cirrhosis Intrahepatic liver obstruction? Sinusoidal dilation due to anabolic What is Peliosis hepatis? steriods What are ppl. with Peliosis hepatis at Intraperitoneal hemorrhage risk for? .Intrahepatic obstruction to blood flow is Blocked sinusoidal Blood flow caused by what? Cirrhosis. Sickle cell Intrahepatic obstruction? disease.

What is the main reasons for
Hepatic Vein Thrombosis or Veno-
Posthepatic obstruction of blood flow
occlusive disease
from the liver?

What is hepatic vein thrombosis
Budd-Chiari syndrome?

What is the 2 main reasons for Budd- Oral contraceptive and Polycythemia
Chiari syndrome? vera

What would the clinical finding be for
Portal HT (Ascites,Spleenomegaly,
someone who has Post hepatic
varices, hemorrhoids, Caput Madusae),
Obstruction of blood flow from the
Nut meg liver(hepatomegaly)

What is the main reason for veno- Collagen develops around the central
occlusive disease of the hepatic vein? vein

Blood in the bile in patients with trauma
What is hematobilia?
to the liver

Most common cause of hepatic vein
Polycythemia Vera

Alcoholic hepatitis is due to? Acetaldehyde damage to hepatocytes

Fatty infiltrate, Fibrosis, and
What four microscopic finding are
neurtophilic leukocytosis and mallory
indicative of alcoholic cirrhosis?

Painful hepatomegaly, Fever,
What are the clinical findings of
Neutrophilic leukocytosis, Ascites,
someone with Alcoholic hepatitis?
hepatic encephalopathy,

What are the 2 types of obstructive
Intrahepatic or extrahepatic
(cholestatic) liver disease?

Intrahepatic is most commonly caused Drugs: Oral contraceptive pills and
by what? anabolic steriods

Blockage of the CBD by a stone, biliary
Extrahepatic cholestasis is most
atresia, carinoma in the head of the
commonly caused by what?

Macroscopically what would a Enlarged, green gallbladder with the
cholestatic liver problem look like? bile ducts distended

light colored stool (no sterobilin), Puritis
(bile salts being deposited under the
What are some clinical findings of
skin), malabsorption (bile salts are not
someone suffering from a cholestatic
present in the small int. to help with
liver disease?
absorption of fats, and jaundice (back
up of CB)

Obstructive Bile
Absent UBG in urine
Increase ASP and GGT

Fibrosis of inttrahepatic and
What is Primary sclerosing extrahepatic bile ducts
pericholangitis? Male Dominant
Associated with ulcerative colitis

What is primary sclerosing
Ulcerative Colitis
pericholangitis associated with?

Irreversible diffuse fibrosis of the liver
What is cirrhosis?
with formation of regenerative nodules

Regenerative nodules of someone with
cirrhosis lacks what important Portal triads and sinusoids
anatomical features?

The bands of fibrosis in someone with Compression of sinusiods and central
cirrhosis cause what? veins leading to intrasinusoidal HT

Occurs What is primary biliary cirrhosis? most often in woman 40-50years of age What antibodies are found in primary Antimitochondria biliary cirrhosis? When does the jaundice present in late in the disease someone with primary biliary cirrhosis? Hereditary hemochromatosis is? Autosomal recessive. Name the complications of Cirrhosis? muscle wasting. esophageal varices. Icterus. Pitting edema. increased Prothrombin time. hemorroids. hypoalbuminemia. hyperammonium. hepatic encephaolopathy. spider angioma. Alcohol. Decreased immune funtction. Hepatitis Virus B or C. Name the most common reasons for Autoimmune (PBC). Gynecomastia. jaundice. male dominant . peptic ulcers An autoimmune disorder that destroys the bile ducts in portal triads. Female hair growth pattern. Metabolic one to get cirrhosis? (hemochromatosis or wilson's disease Ascites.

When do woman get After menopause bc menses causes a hemochromatosis? loss of iron unrestricted reabsorption of iron in the What is hemochromatosis? small intestines Free radicals that damage tissue and Iron stimulates the production of ? cause fibrosis What are the 3 main places that Iron Liver. pancreas and skin deposits in? How does iron cause Iron increases melanin production hyperpigmentation? How does Iron cause diabetes? Destruction of the Beta-Islet cells A liver biopsy must be stained with Prussian blue _______ for the iron to show up blue? .

subthalamic nuclues deposit? and cerebral cortex Lesion of the putamen causes? Parkinsonism movement disorders . Hemochromatosis will have an increase or decreased total iron binding decrease capacity? Autosomal recessive that causes a defect in hepatocytes ability to Wilson's Disease? transport copper into bile for excretion and decrease the synthesis of ceruloplasmin by the liver What binds Copper in the blood? Ceruloplasmin Copper deposits in the cornea is called Kayser-Fleisher ring what? Will the total serum copper be Decreased bc of the decrease increased or decreased in Wilson's production of ceruloplasmin disease? Where in the brain does copper like to In the putamen.

Lesion of the subthalamic nucleus Hemiballismus (wild flinging of arms) causes? Lesion of the cerebral cortex causes? Dementia Decrease BUN Increase Ammonia Lactic acidosis laboratory test Abnormalities in Hyponatremia cirrhosis? Hypokalemia Increased PT Hypocalcemia Vitamin D Deficiency Cavernous hemangioma' Name 2 Benign Liver tumors? Hepatic cell adenoma What is the most common benign Cavernous hemangioma tumor of the liver? Which benign tumor is highly vascular Hepatic cell adenoma and tend to rupture during pregnancy? Most common cancer of the liver is? Metastasis from the lung .

How can you tell if a cancer is from It's has multiple nodular masses metastasis? What is the most common primary liver Hepatocellular carcinoma cancer? What is the most common cause of Hep B and C heptocellular carcinoma? Hepatocellular carcinoma always Cirrhosis comes from a prexisiting ? Hepatocelluar carcinoma peaks Males 60y/o around? What is characteristic of HC Presence of bile in neoplastic cells carcinoma? Will you find blood in the ascites of someone with hepatocellular Yes carcinoma .

What is the most common metastatic Lung site for hepatocellular carcinoma? What protein will be increased in Alpha fetoprotein hepatocellular carcinoma? The most common malignancy of the cholangiocarcinoma bile ducts is What disease predisposes a person to Primary Sclerosing pericholangitis cholangiocarcinoma? What is Courvoisier's Sign Palpable gallbladder What color are cholesterol stones? yellow and radiolucent What color are pigment stones? Black and radiopaque .

This What is the most common leads to increase in intraluminal pathogenesis for acute cholecystitis? pressure and then to ischemia of the gallbladder wall then to ulceration. Fair skin. Pain that starts in the midepigastric and is colicky then moves to the RUQ Gallbladder disease radiating to the right scapula What is the gold standard for identifying a stone in the common bile Ultrasound duct? . CBD obstruction. Fat. What are the risk factors for Forty. oral gallstones? contraceptive pills Supersaturation of Cholesterol or How do cholesterol stones form? decreases bile salts Extravascular hemolysis (calcium Black pigment gallstones are a sign of? bilirubinate) What are 3 common complications of Cholecystitis. Female. acute pancreatitis Obstruction of cystic duct by a stone leading to the congestion of bile. gallbladder stones? gallbladder concer.

The Enzymes then causing acute pancreatitis? activate the proenzymes in the pancreas leading to it's destruction ETOH thickens the secretions thus What is the pathogenesis of a ETOH back flow of pancreatic enzymes back causing acute pancreatitis? into the pancreas and activation of trypsinogen and others Epigastric pain that radiates to the Pancreatitis back? What is the most common cause of Seat belt trauma pancreatitis in children? What is the most common cause of Alcohol acute pancreatitis in adults? . the bile then backs up into What is the pathogenesis of a gallstone the pancreas. Dorsal and ventral buds form a ring What is an annular Pancreas? around the duodenum that causes an obstruction of the small bowel What are the 2 major causes of acute ETOH and gallstone pancreatitis? The gallstone obstructs the Common bile duct.

What 2 enzymes are elevated in acute Amylase and Lipase pancreatitis? What is the gold standard for CT-bc pancreas is behind the stomach diagnosing Pancreatitis Sentinel loop(air in the duodenum) What would a plain radiograph show of because of localized ileus. What is a pancreatic pseudocyst? collection of digested around pancreas What is the most common cause of Idiopathic chronic pancreatitis? What is the most common cause of Alcohol then cystic fibrosis known chronic pancreatitis? . a person with acute pancreatitis? Inflammation around duodenum stops peristalsis What is a complication of pancreatitis that presents with an abdominal mass Pseudocyst with persistence of serum amylase longer than 10 days.

Type 1 diabetes . What is a radiographic hint that Calcium deposits inside the pancreas someone has chronic pancreatitis? What are some clinical finding of Severe pain radiating into the back. someone with chronic pancreatitis? Malabsorption.