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lab di final
| Question | Answer |
|---|---|
| two main functions of the liver | synthesizes substances, and proesses or breaks substances down into waste for elimination |
| what does the liver do with endogenous and exogenous compounds? | biotransformation, detox, and exretions |
| Bilirubin metabolism, starting with heme steps | Heme --> biliverdin --> bilirubin (water insoluble form,/unconjugated/indirect) |
| bilirubin is water ___ | insoluble |
| what is unconjugated bilirubin bound to? | albumin |
| unconjugated bilirubin cannot what, but can do what | it cannot be excreted in bile or urine, but does dissolve in lipid, crossing the BBB and placenta |
| What are the 3 phases the bilirubin must go thru in the liver? | UPTAKE by hepatocytes, CONJUGATION by hepatocytes and EXCRETION into bile. |
| What is the rate limiting step of bilirubin metabolism inthe liver? | excretion into bile |
| interference with any step in bilirubin metabolism in the liver results in what? | JAUNDICE |
| A lack of the enzyme glucuronyl transferase results in what? | jaundice (it conjugates bilirubin with glucuronic acid) |
| conjugated bilirubin is water _____, and therefore? | soluble! Therefore it can abnormally appear in the urine when plasma levels are increased |
| What does impaired excretion of conjugated bilirubin result in? | jaundice |
| What colors your POOP | stercobilin ( a metabolite of urobilinogen) |
| What creates urobilinogen? | reduction of conjugated bilirubin by anaerobic bacteria in the colon |
| What happens to 20% of the created urobilinogen? | Reabsorbed thru the colon wall, and returns to the liver via the enterohepatic circulation. |
| What happens to the other 80% of created urobilinogen? | excreted in urine, or in stool (stercobilin) |
| What happens to urobilinogen at the kidney? | oxidized to urobilin, which is excreted in the urine |
| What gives urine its color? | Urobilin (from kidney oxidizing urobilinogen) |
| What type of bilirubin can be found in urine? | direct (conjugated) bilirubin |
| where does excess bilirubin depoist in the eyes for jaundice? | in the conjunctiva, altho docs say yellow sclera |
| With jaundice name all the areas that get yellow | skin, sclera, gums, nail beds, tympanic membranes, and soft palate |
| what type of lighting is best to see jaundice? | natural light |
| in early jaundice what may appear yellow before the skin? | eyes |
| What else can bilirubin cause intensely in the skin? | intense pruritis and scratching |
| What are the 3 basic forms of jaundice | prehepatic hepatic post hepatic |
| What type of bilirubin is present in prehetpatic jaundice? | unconjugated (indirect) hyperbilirubinemia |
| What is the mechanism of prehepatic jaundice? | overproduction of indirect bilirubin, with typically normal liver function, usually caused by HEMOLYTIC ANEMIA of some form. |
| Due to increased indirect bilirubin in prehepatic jaundice, what else is therefore increased? | Increased conjugation @ the liver, and therefore increased direct bilirubin excreted into the GI tract, and therefore increased urobilingoen formed in GI tract. |
| What are the lab findings of prehepatic jaundice? | VERY elevated INDIRECT bilirubin, possibly elevated direct bilirubin, elevated urobilinogen. All of these levels depend on the severity of the underlying cause |
| What is the overall mechanism of hepatic jaundice? | problems @ the hepatocyte, could be trouble with conjugation, uptake, and excretion. |
| What disease could cause a problem with excretion, uptake, and conjugation, causing what tpye of jaudince? | Acute hepatitis, causing hepatic jaundice |
| What disease has decreased uptake and conjugation? | Gilberts dz (hepatic jaundice) |
| what dz has decreased conjugation only? | Crigler-Najjar syndrome (hepatic jaundice) |
| What type of dzs (mechanism) have impaired excretion of conjugated bilirubin? | any disorder that interferes with transport of conjugated bilirubin to the radiologically visible intrahepatic bile ducts. (ex: primary biliary cirrhosis) |
| normal pH of blood is? | 7.35-7.45 |
| leukomoid rxn number? | WBC count >50,000 |
| platlet count cutoff for spontaneous bleeding? | <20,000 |
| impaired fasting glucose range? | 110-126 mg/dl |
| threshold of glucose spilling into urine? | 180 mg/dl |
| normal cholesterol | <200 mg/dl |
| normal LDL cholesterol | <130 mg/dl |
| Normal HDL level | >45 mg/dl |
| Why would there be elevated direct bilirubin if there is impaired uptake and conjugation with hepatitis? | because liver still functions to some degree, some conjugation still occurs, but theres impaired excretion therefore conjugated bilirubin regurgitates into plasma |
| What are the lab findings of acute hepatitis with impaired uptake and conjugation? | increased levels of indirect bilirubin |
| what are the lab findings of acute heptatis with impaired conjugation and excretion? | increased levels of direct bilirubin |
| What is Gilberts syndrome, and what are the lab findings? | common in men, causes a mild increase in unconjugated bilirubin d/t impaired uptake and conjugation. Worsened by fasting and alcohol. |
| What is Crigler-Najjar syndrome, and the lab finding with it? | impaired Conjugation due to deficiency of lack of UPD-glucuronyl transferase. Types I and II, genetic disoder, primary unconjugated hyperbilirubinemia |
| What is primary biliary cirrhosis and the lab findings? | Destruction of the interlobular bile ducts, resulting in impaired excretion (cholestasis), resulting in liver cirrhosis and increased conjugated bilirubin |
| What does the urine of a pt with acute hepatitis look like? | darkens/amber color |
| What is the mechanism of post-hepatic jaundice? | usually obstruction of the common bile duct by multiple causes, such as stones, tumors, spasms or strictures. |
| What usually causes obstruction in post-hepatic jaundice? | stones, tumors, spasms or strictures. |
| In post-hepatic jaudince what is not produced? | urobilinogen, because bilirubin does not get to the GI tract. |
| What are the lab findings of posthepatic jaundice? | very high direct (conjugated) bilirubin, and total bilirubin, and urine bilirubin. |
| Within 1-5 days of post hepatic jaundice what happens to the stool color? | white/clay colored stool (steatorrhea) |
| What can elevated Alk Phos indicate in the presence of liver dz? | can indicate bile duct obstruction |
| What enzyme is the most sensitive to chronic alcoholic liver dz? | GGTP, GTP, gamma-GTP |
| GGTP is also mildly elevated in what conditions? | kidney and biliary dz |
| If ALP elevated and GGTP elevated helps what? | confirm that the elevated ALP is from a liver problem, and not other cause |
| AST was once called what? | SGOT |
| AST elevated levels are ____ to liver damage, but not ___ | sensitive to liver damage, but not specific |
| AST might be elevated by how much? | many times nroaml depending on the condition - 1000s |
| ALT was once called? | SGPT |
| LDH 1 & 2 vs LDH 3 and LDH 5 | LDH 1&2 - RBCS, heart kidney, LDH 3 - lung LDH 5 - liver and skel mm |
| When does LDH elevate? and what is important? | in certain types of liver disorders, but the HX is essential to interpret and elevated LDH. |
| What elevates in pneumocystis carinii pneumonia>? | LDH |
| What should decrease in long standing liver dz? | albumin and cholesterol (b/c liver can't make it anymore) |
| In alcoholic liver dz what are the levels of AST and ALT? | AST is 2x ALT, 2:1 ratio |
| Alcohol inhibits ___ production | ALT |
| What enzymes are elevated in acute viral hepatitis | AST and ALT can increase up to 10-20 times ref range, total LDH elevates, ALP and GGTP can increase to 3 times ref ranges. |
| What are causes of hepatitis? | infection (usually viral), toxicity (alch, drugs), pharmacologic, and autoimmune |
| When is hepatitis considered acute? | if lasts <6 months, if more it's chronic |
| What is hepatitis? | hepatocellular injury and necrosis that can be focal or extensive |
| What are the viruses which cause acute viral hepatitis? | Hep A-G, CMV, and EBV. |
| What are some sx of acute viral hepatitis? | JOINT PAINS/ARTHRITIS, MYALGIAS, RUQ pain, naseau, jaundice, steatorrhea, bilirubinuria (dark urine which foams when shaken), headache |
| What are physical findings associated with viral hepatitis? | hepatomegally, splenomeg, jaundice, fever |
| What are lab findings of acute viral hep/ | AST, and ALT elevated 20X, ALP mildly elevated, Direct bilirubin moderately to highly elevated, indirect bilirubin normal to mildly elevated, urine bilirubin elevated. |
| Hep A AKA? | infectious hepatitis |
| Transmission of hep a? | poop-mouth. or sex. |
| What is the incubation of Hep a? | 2-6 weeks, can be mild to severe |
| Hep A infection never becomes... | chronic |
| What is a test for Hep a? | Anti-HAV IgM, Anti-HAV IgG |
| What is MC cause of cirrhosis and liver cancer worldwide? | Hep B |
| How is Hep B transmitted? | sex, blood transfusion, vertical (mom to infant), IV drug users, dialysis.....rarely pooop-mouthhhh |
| What is the incubation of Hep b? | 1-6 months |
| Hep B can develop into what? | carrier state or chronic state |
| What is the prognosis of chronic hepatitis based on? | the causative agent, the grade of injury and the degree, location, and amount of distortion of norm liver architecture. |
| What are tests for hep b? | HBV surface antigen (HBsAg), and Antibody to HBV core antigen (Anti-HBc) |
| Which Hep virus causes the most chronic hep? | Hep C (70-85% of cases) |
| How was Hep C transmitted? | transfusion, IV drug users, rarely tatoo needles, occasionally sex. |
| What is the incubation of hep c? | 15 weeks, but SX may not appear until 20-30 years after exposure. |
| What are tests for HCV? | ANTI-HCV. |
| what is the progression of alc liv dz? | fatty liver (reversible) --> alc hepatitis (may or may not be revers) --> cirrhosis (irreversible) |
| Findings with fatty liver | pt may have RUQ pain, jaundice is rare, ALT and AST may be mildly elevated, as well as GGTP. |
| how is damage of fatty liver reversible? | if pt stops boozin |
| What are SX and Phyiscal findings of alcholic hep? | sx: anorexia, nausea, vom, wt loss, RUQ pain. Phys findings: hepatomeg, fever, splenomeg, jaundice |
| What occurs within the liver in cirrhosis? (4 things) | repeat hepatocellular regeneration (forms nodules), fibrous scarring with adhesions, and distortion of normal architecture. The vascular bed becomes distorted leading to portal HTN |
| What is the mc cause of cirrhsis in the western world? | alc and HCV |
| what is the mc cause of cirrhosis in the 3rd world countries? | HBV |
| What are the features of cell dysfunction in cirrhosis? | jaundice, spider angiomas, palmar erythema, mantiitttties, body hair loss, testicular atrophy, dupuytren's contracture, mm wasting, bruising, fetor hepaticus (mercapten breath), signs of encephalopathy. |
| What are the features of portal tension d/t cirrhosis | splenomeg, ascites, caput medusae, bleeding esophageal varices. |
| What are the lab findings of cirrhosis? | hyperbilirubinemia, hypoalbuminemia, prolonged bleeding time, prolonged prothrombine time, elecated ammonia, decreased vit K, decreased cholesterol, often Macrocytic anemia in alcoholic pt. |
| Why would a pt bruise easily with cirrhosis? | damage to extrinisic pathway |
| Why does one with cirrhosis develop man boobage | liver can't process sex hormones |
| what is hepatic cancer associated with? | a hx of hep B or C, also may be mets |
| sucessful passing of a gallstone | cholelithiasis |
| Most gallstones are composed of what? | cholesterol |
| how do cholesterol stones form? | from supersaturation of bile with cholesterol in the gall bladder (saturation increased by estrogens, obesity, terminal ileum dz, mult pregnancies |
| Where is the usual site of trouble when stones either transiently obstruct the duct or lodge there? | the cystic duct |
| What are other names for acute cholelithiasis? | acute biliary colic, acute gallstone attack, gall bladder attack |
| What is acute cholelithiasis from? | from transient cystic duct obstruction |
| What are some sx of acute cholelithiasis? | RUQ AND/OR EPIGASTRIC PAIN, which lasts mins to 6hrs, PAIN RADIATES TO RT SHOULDER, RT INFRASCAP REGION, OCCASIONAL RLQ, AND SOMETIMES SPINE. Often naseua and vomitting, may occur after eating |
| What are physical findings and lab findings of acute cholelithiasis? | usually absent! |
| what is the imaging of acute cholelithiasis? | ultrasonography, sometimes x-rays. |
| Where is the mercedes benz sign seen? | in acute cholelithiasis |
| unsuccessful passing of a stone | cholecystitis |
| Sx of acute cholecystitis? | Low grade FEVER, possibly High Grade Fever and shaking and chills (gangrene of gallbladder), pain patterns the same in both cholecystitis and cholelithiasis |
| Physical findings of acute cholecystitis? | palpable gall bladder, but hard to do betcause Murphys sign exists. |
| Lab findings with acute cholecystitis? | Mild leukocytosis, mild elevation in total bilirubin, serum amylase, ALP, ALT, and AST. |
| Ultrasound of acute cholecystitis? | shows lodged stone in cystic duct |
| Radionuclide imaging of acute cholecystits shows? | if common bile duct is visualized but the gall bladder is not, there is likely an obstruction. This is the most accurate method for cholescystitis. |
| What is choledocholithiasis? | gallstone in the common bile duct |
| Where are choledocholithiasis from? | most from the gall bladder, but some form de novo in the biliary tree apart from the gall bladder. |
| If the common bile duct is completely obstructed there may be secondary ______, which is what? | secondary cholangitis, which is infection of the CBD, and is life threatening condition |
| What is charcots triad? | fever, jaundice, and biliary pain - suggestive of infection from obstruction cholangitis. |
| What do the lab studies of choledocholithiasis show/ | Elevated ALP AST ALT, bilirubin, and pssible amylase levels. |
| What is the best study for choledocholithiasis | endoscopic retrograde cholangiopancreatography (ERCP), which shows CBD stones and can iamge the pancreatic duct. |
| What is porcelain gallbladder a precursor to? | to carcinoma of the gall bladder, d/t calcification of the gall bladder wall from crhonic inflamm and scarring |
Created by:
margaretrhager
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