Lab Med Quiz 2

jmnies's version from 2017-03-22 17:04


Question Answer
2 blood supplies of liverHepatic artery and portal vein
Portal veingets blood from intestines, spleen, pancreas and brings nutrients, proteins, toxins to the liver, as well as meds, first pass effect
3 main functions of liversynthesis, processing of nutrients, and protection/clearance
Main products of liveralbumin, clotting factors, and bile salts (taken out via bile ducts)
Albumin is necessary for a lot of functions, big onemaintaining oncotic pressure
Clotting factors produced in the liver are dependent on thisVitamin K
Clotting is measured by thisthe PT and INR. The longer the bleeding time the higher the PT and INR (limited clotting factors to help clot)
Bile salts break down thisfats in intestines very important for fat and vitamin absorption (Vit. K is fat soluble)
Processing nutrientstakes glucose to glycogen (stores the glycogen)and back again to glucose if body needs energy, involved in lipids as well
Protection/clearancetoxins, etc. cleared by liver.
Kupffer cellsline capillaries and protects against enteric bacteria
Liver produces anti-oxidant thisglutathione, Tylenol rapidly depletes this and leads to liver failure
LFTsAST and ALT-ALT more specific to liver, liver (hepatocellular) injury not loss of function
Alcoholic liver disease ALT, AST findingsAST 8x AST higher than ALT, typically 2:1 ratio, also elevated GGT
Acute Viral HepatitisAST and ALT > 25x upper limit, ALT higher than AST
Acute Ischemic HepatitisAST/ALT > 50x higher than normal, LDH also very elevated
What has longer half life, AST or ALT?ALT (around 36 hours)
What is rule of thumb for ALTmore than 3x normal for pathologic elevation
Where ALT is elevatedAcute Viral Hepatitis, Non-alcoholic steatohepatitis
ALTused to monitor progression of liver disease, found predominantly in liver cells
ASTFound in highly metabolic tissues (brain, heart, skeletal muscle), indicates recent injury, sensitive but less specific
Cholestatic damage/injury to bile ductselevated Alkaline Phosphatase and GGT (see high GGT in ETOH as well as biliary problems)
Infiltrativeboth patterns with cholestatic usually dominating
Bilirubinbilirubin that is unconjugated comes from breakdown of RBC- taken to liver with the help of Albumin, after conjugation it goes into bile ducts and released into intestine (where it is worked on by bacteria and becomes urobili.)
What causes the highest levels of bilirubinObstruction in the bile ducts, gets backed up into bloodstream if can’t drain properly, this is conjugated bilirubin
AP, ALPcholestasis, bile duct obstruction, neoplastic, infiltrative and granulomatous liver disease
Released by hepatocytes in response to bile acid retentionALP (bone and liver)
Elevated ALPprimary, biliary cirrhosis, biliary obstruction
Highest concentration of GGT found inBiliary tract/gallbladder
Confirms elevation of ALP is due to biliary tract diseaseGGT
Elevated following ingestion of large amount of EtOH, chronic ingestionGGT
GGT clinical significancecholestatis, EtOH ingestion
In liver bilirubin is conjugated withglucuronic acid
Gilbert syndromeisolated elevation in bilirubin, usually mild, caused by genetic deficiency in UGT
Unconjugated bilirubin clinical significanceGilbert syndrome, Neonatal hyperbilirubinemia, Sepsis, anemia
Conjugated bilirubin clinical significanceAcute viral hepatitis, Cholelithiasis, drug induced cholestatis, chronic EtOH use
LDH 1 (heart) elevated > LDH 2 (most abundant)MI
LDH 5 elevatedHepatocellular injury
LDH 2 and 3Pulmonary injury or disease
Hepatic function determined byAlbumin and Prothrombin Time/INR
Decrease albuminindicates chronicity, chronic liver disease
Lack of clotting protein does what to PTprolongs PT/INR
Prothrombin indicatesseverity and prognosis
Protein measure of nutritionglobulins
What makes up total protein?albumin and globulin
Increased albuminDehydration
Decreased albuminMalnutrition, Pregnancy, Liver disease
Reflects hepatic capacity for synthesis of clotting factorsPT
Function of clotting factors depends on adequateVit K
Hepatocellular enzymesALT and AST
Markers of cholestasisAP and GGT
Tests of liver excretionBilirubin
Tests of liver synthetic functionAlbumin & PT/INR
Acute hepatocellular damageAST/ALT, AP, bilirubin, PT markedly elevated
Bile duct obstructionAST/ALT (mild) AP (marked) GGT (elevated) bilirubin (marked)
CirrhosisPT (elevated), albumin (decreased) AST/ALT/AP (normal or mild)
Predominace of ALT and AST suggesthepatocellular
Predominance of AP suggestcholestatic or infiltrative
Specific for pancreatitis, not sensitive due to other sourcesamylase
Specific for pancreatitis, more sensitive than amylaselipase


Question Answer
2 main lipidscholesterol and TG
Transported by lipoproteinsLDL (carries cholesterol), VLDL (primarily carries TG), HDL, IDL
Apolipoproteins on surfaceAPO A on HDL (“good cholesterol”) and APO B on LDL
APO B prolongs life ofLDL- makes it available to macrophages- leads to foam cells which are atherogenic
If LDL is in fluffy type Athen less atherogenic
If LDL in pattern B (small and sticky)then more likely to cause plaques
APO B is surrogate for LDL particle sizeif high APO B then lots of LDL particles
LDL-C can’t be calculated when triglycerides are over400
HDL is good because it takes cholesterol from bloodstream and plaques and puts it back into the liver(reverse transport)
High TG is a marker for metabolic problems in the bodymetabolic syndrome, pre-diabetes, insulin resistance
Total cholesterol/HDL ratio better marker for risk of atherosclerosis thanLDL-C
Lpa isatherogenic and pro-inflammatory- genetic
Cardiac markers BNPheart failure
Cardiac markers D-DimerPE/DVT (high sensitivity, low specificity)
Uric acidpro-inflammatory and increases cardiovascular risk
C-reactive proteinmarker for inflammation but not specific to heart disease (can be elevated in other conditions)
LDL primarily carriescholesterol
VLDL primarily carriesTG
Lack of this allows TG and cholesterol to build up in bloodlipoprotein lipase
Allows HDL to “dock” on cells that have excess cholesterolApo A
Allows LDL to “dock” on cells that need cholesterolApo B
Predominates on HDLApo A
Predominates on LDLApo B
APO B is surrogate for LDLparticle size
APO A is surrogate forHDL size


Question Answer
Useful for risk stratification in patients with unstable anginaTroponins
VERY high specificity for myocardial cell injury, T and ITroponins
Elevated soon (2-3 hours) after MITroponins
CK-MMtotal CK present in skeletal muscle and heart muscle, if elevated indicates skeletal muscle injury , amount varies with muscle mass
CK-BBpresent in brain tissue and smooth muscle, if elevated indicates brain injury
CK-MBpresent mostly in heart muscle, specific to cardiac muscle
CK-MBUseful for quantifying the degree of cardiac muscle injury (high levels indicate significant infarction has already occurred), timing of MI for clinical decision making about thrombolytics
LDH Cardiacelevation of LDH-1 > LDH-2, rises w/in 24-48 hours after an MI
Oxygen-binding protein found in cardiac and skeletal muscleMyoglobin
BNPreleased primarily from the ventricles-correlates well to LV pressure
Helps with evaluation of patients with dyspnea when diagnosis of HF is uncertainBNP
RiskyHigh CRP/low LDL Cholesterol


Question Answer
Specific gravity a marker ofhydration status ( the higher the # the more concentrated the urine= less water in the urine= the body is trying to hold onto water) This is elevated in dehydration states or when the body is producing too much ADH
Dilute UAlow specific gravity- see this in over-hydration and diabetes insipidus (not enough ADH or kidney can’t respond to ADH)
Leukocytesmarker of WBC in UA. Can be from infection or from contamination from genital tract. Need to look under the microscope to see if WBC are present and in what amount
Nitrates are usually seen withgram negative bacteria
Glucose in UAtypically means high in blood-need to confirm with a blood test
Proteincan be trace and still be normal. Protein in higher concentration is abnormal. Can get transient proteinuria from vigorous exercise- check 1st am catch after resting from exercise for 2 weeks
Ketonesfat metabolism. See in dehydration and diabetic ketoacidosis
Bloodcan be hemolyzed from RBC breakdown or non-hemolyzed
Dysmorphic RBC in urine typically indicative ofcancer in urinary tract or glomerulonephritis
Blood and protein in urine will indicatekidney disease/disorder
Clue cells indicatebacterial vaginosis
Trichomonas can be distinguished from WBC bytheir flagella
low ADHdilute urine
High ADHconcentrated urine
A degradation product of bilirubin formed by intestinal bacteriaUrobilinogen
Positive test indicates present of WBCs either as whole cells or as lyzed cellsLeukocyte Esterase
A positive test indicates that bacteria in significant numbers may be present in the urineNitrite
Ketonesdiabetic ketosis (DKA), alcoholic ketoacidosis (AKA) or some other form of calorie deprivation (starvation)
(microscope exam) squamous cellsIndicates contamination from vaginal secretions
(microscope exam) transitional cellsMen from skin surface or from outer urethra
Casts are formed in theDCT or the collecting duct (distal nephron)
Hyaline castscomposed of Tamm-Horsfall protein shown as green dots with a hyaline cast in the collecting duct (green)
Liver Damage (UA)Bilirubin, urobilinogen
Kidney Disease (UA)protein, blood, casts

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