Diagnostics Lab Exam 3 Flashcards
Two enzymes indicative of hepatocyte disease
AST
ALT
(also LD)
AST and ALT usually rise in tandem with liver disease
(Normally AST higher or equal)
Enzyme indicative of biliary tract disease
ALP (Can also come from bone)
also GGT and 5-NT
Major sources of ALT
Liver and kidneys
lesser amounts are from the skeletal and cardiac muscles
Chronic alcohol abuse Enzymes
AST (chronic liver disease)
Elevated to a greater extent than ALT (2 to 1)
(In the liver there is more AST but ALT is metabolized more slowly)
Lactate Dehydrogenase (LD or LDH)
LD 5 is the important one
Comes from Hepatocytes, Skeletal muscle & prostate
(when elevated, liver or skeletal, not really prostate)
LD is not favored for routine evaluation of liver
LD is released with injury of many different tissues
Enzyme marker of choice for skeletal muscle
CK
If CK is normal with elevated LD5,
skeletal muscle is not the source
What Viruses can LD be related to
SARS
MERS
Biliary tract disease
ALP for biliary tract disease
Greater increase than AST, ALT or LD
Other markers are
GGT and 5-NT
Used when there is technical difficulties with ALP
If bone is thought to be the source of the ALP
Use Bone ALP
BAP
GGT
(Gamma-Glutamyltransferase)
Sources
Sources are:
PCT of kidney
Liver
Pancreas
Intestines
GGT
(Gamma-Glutamyltransferase)
Elevated in
Alcohol use
Anticonvulsant use
(Not normally elevated in bone disease)
GGT
Gamma-Glutamyltransferase
ALP and GGT are compatible with
Biliary Tract disease
If ALP is elevated far higher than GGT
Sources such as bone should be looked at
ALT and AST
VS
ASP
Relative increases in ALT and AST
exceed the relative elevation of ASP
Acute reasons for liver disease
(Hepatocellular disease)
(Elevated AST & ALT)
Common Causes:
Viral hepatitis A. B & C
Alcoholic hepatitis
Toxic injury
Less common causes:
CMV
Epstein Barr virus
Autoimmune hepatitis (acute or chronic)
Other less common causes:
Viral hepatitis D, & E
Wilsons disease
Liver disease of pregnancy
Chronic reasons for liver disease (+ 6 months)
(Hepatocellular disease)
(Elevated AST & ALT)
Alcoholic Liver Disease Non alcoholic Fatty Liver Disease (NAFL) Inborn Errors Wilsons Disease Gaucher Disease
Other chronic causes: Viral Hepatitis B, C Drug toxicity Autoimmune Hepatitis Hemochromatosis Alpha 1 antitrypsin disease Glycogen storage disease
Gaucher Disease
chronic liver disease
Genetic disorder
Hepatomegaly
Splenomegaly
Bruising, Bleeding
Fatigue, anemia, low platelet count
Wilsons Disease
Chronic Liver Disease
Genetic disorder
Copper build up in body
Symptoms are related to brain and liver
Biliary Tract Disease
Elevated ALP (exceeds the elevation of AST/ALT)
Failure of formation of bile ducts
Obstruction or destruction of bile ducts
Compression of bile ducts
Biliary Tract disease
Major manifestation of obstruction
Jaundice from elevated bilirubin
Total bilirubin exceeds 2 to 3 mg/dl
Unconjugated bilirubin formation
Derived from Hemoglobin in normal break down of RBC’s
RBC’s are broken down by macrophages in the spleen
Phagocytes metabolize hemoglobin into biliverdin and then finally bilirubin
Unconjugated bilirubin (not soluble) enters the blood stream
the unconjugated bilirubin is transported to the hepatocytes bound to albumin
Unconjugated bilirubin is not excreted in urine
Bilirubin formation
Unconjugated bilirubin is in the hepatocytes:
Inside the hepatocyte, glucuronide molecules are conjugated to bilirubin, making the bilirubin water soluble.
This is now conjugated bilirubin
It is then transported across the plasma membrane into the bile canaliculi.
Normally bilirubin is not excreted in the urine
Bilirubin concentration elevation
If the concentration of either conjugated or unconjugated gets too high
Skin & eyes can turn a yellow color
Jaundice or icterus
Pathologic elevation of conjugated (Water soluble) bilirubin can lead to bilirubin in the urine turning it yellow-brown or green-brown
Classifying hyperbilirubinemia
Conjugated
or
Unconjugated
When conjugated is 0.4 greater
it is conjugated hyperbilirubinemia
Unconjugated Hyperbilirubinemia
with hemolysis
Schistocytes present
Microangiopathic hemolytic anemia
Artificial heart valve
Autoimmune hemolytic anemia
Schistocytes are not present Intra-marrow hemolysis RBC Membrane defects RBC Enzyme defects Hemoglobinopathies
Schistocytes = Hemolyisis or heart valve
Non schistocytes = RBC Defects
unconjugated hyperbilirubinemia
without hemolysis
Newborns Transient Physiological jaundice Breast milk jaundice Crigler-najjar syndrome Types 1 & 2
Exam 3 topics
Topics for exam 3
Know the microorganisms and tests that we discussed. Be able to pick out the organisms based on the tests we discussed as well as the types of infections they cause.
Know the tests we discussed for liver disease including hepatocellular and biliary causes
Be able to diagnose conditions based on urinalysis results
Know the chronic liver diseases we discussed including patient symptoms.
Know the fate of bilirubin as discussed in class
Know tables 16-5 and 16-8
Know the different types of casts and crystals as discussed in class
Know the different substances that can be found in urine and what the causes are for their presence. Also, what tests are used to measure these substances
Understand BUN and GFR
????
Hepatitis B Virus HBV
HBV surface antigen HBsAG
followed by HBV e Antigen HBeAG
Then HBV IgM antibody
During recovery HBsAG & HBeAG disappear
— HBcIGM converts to negative
HBV Antibodies
All negative = never infected, no immz
HBsAG & T-anti-HBc = Chronic
HBsAG & T-HBC & IgM anti-HBC = Acute
T-anti-HBC & anti-HBs = recovered
In acute hepatic failure how much does AST/ALT increase
100 fold increase for acute liver failure
Clotting factors and Liver failure
Liver produces clotting factors
Liver failure can result in prolonged PT
Vitamin K deficiency
Liver failure does what to BUN/Creatinine
Elevates them
decreased urine output
Cirrhosis
Ethanol abuse is the most common cause of cirrhosis in the western world
60-70%
Cirrhosis
Ethanol abuse is the most common cause of cirrhosis in the western world
60-70%
Some can have end stage liver disease
Kidney (renal disease indications)
malaise, headache, visual disturbances, N/V
Flank pain that radiates to the groin
Reduction in urine (<500 QD), Anuria (<100 QD)
Hematuria, RBC casts, WBC casts, proteinuria, Protein casts, Pyuria
discolored or odorous urine
> BUN/Cr
Electrolyte abnormalities
Bleeding, acidosis, anemia fractures, Malar rash, HTN
Hyaline casts
Not indicative of Renal disease
Cellular casts are most commonly the result of
ischemia
infarction
nephrotoxicity
Acute tubular injury
Casts are named after the cells they come from
Granular casts
Breakdown of other cells
Can’t distinguish between RBC or WBC
Red blood cell casts
from when there is intrarenal hemorrhage and the RBC’s get caught up in the Tamm-Horsfall matrix
Fatty casts
Identified by the presence of refractile lipid droplets
Thought to represent tubular degeneration
Waxy casts
Final stage of cast degeneration
Indicate tubular injury of a more chronic nature
likely associated with low urine flow
These are always of pathological significance
Bilirubin in urine
Must be conjugated
Pseudo gout
Calcium crystals
affects knees
Cholesterol Crystals
Nephrotic syndrome