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
Cystine crystals
Proximal tubular defects
AA reabsorption
Leucine crystals
Liver disorders
impaired AA metabolism
Tyrosinemia
Liver disorders
impaired AA metabolism
Sulfonamide crystals
Due to Sulfa drugs
not pathological
can be linked to kidney stones
Indinavir crytals
HIV Meds
Normal crystals
Uric acid Ca oxalate Ca phosphate Ca carbonate Triple Phosphate Hippuric Ammonium Blurate
Abnormal Crystals
Bilirubin Cholesterol Cystine Leucine Tyrosine Sulfa Acyclovir Indinavir
Renal function is assessed by
Acid base and electrolyte balance
K, cl, Ca, Na, CO2, HCO3
BUN, Cr, GLU
Chem 20
Creatinine origin
Comes from creatine
produced in the skeletal muscle, kidney and pancreas
Then transported to the skeletal muscle and brain
Creatinine concentration in the blood
Inversely related to GFR
Creatinine clearance
Occurs in the kidney and is a suitable estimate of GFR
Universally accepted
Steady decline in GFR
Serve as precursor to end stage renal disease
GFR
The number of milliliters cleared by the kidneys per unit of time
People 18 and over
GFR calculation
Urine Cr / Serum Cr X Urine Volume / Collection time X 1.73 / Body surface area = Corrected GFR
GFR adjustments for gender and race
186(Serum Cr) -1.154 Exponent X Age -0.203 X F = eGFr
Females F = 0.742
African Americans F = 1.210
Stages of kidney damage
0 = >90 = Normal kidney function
1 = >90 = Kidney damage despite normal GFR
2 = 60-89 = Mild GFR decrease with kidney damage
3 = 30-59 = Mod decrease in GFR
4 = 15-29 = Sever decrease in GFR
5 = <15 = Renal failure = Dialysis/Transplant
Urea
Produced by liver
Looks at ammonia and nitrogen content
BUN
Urea measured in serum or plasma (not whole blood)
Affected by state of hydration, protein intake and presence of blood in GI tract
BUN can decrease with liver failure or malnutrition
leading to decreased urea production
What does BUN do if GFR decreases
BUN elevates
BUN / Cr ratio 20:1
If BUN alone or BUN and Cr are elevated and if BUN/Cr ratio is 20:1 = Prerenal azotemia
Prerenal Azotemia
Results from a reduction in GFR
while the kidney tubules are functioning
Causes of prerenal azotemia include Dehydration Hemorrhage Heart failure hypoalbuminemia
BUN / Cr ratio 10:1
BUN and Cr are elevated at 10:1
Renal azotemia (insufficient filtering)
(assuming a chronic urinary tract obstruction had been excluded)
If chronic, not likely dehydration
Proteinuria
Greater than 1 g per day is considered clinically significant
Greater than 3.5 g per day is consistent with nephrotic syndrome
Many causes which include
Primary and secondary cause
Primary causes include:
Glomerulonephritis, Neuropathy, Glomulerosclerosis
Secondary causes include:
Drug use, lupus, HIV, HBV, Syphilis, malaria DM, etc
Nephritis
Clinical syndrome of
Hypertension Mild edema mild proteinuria hematuria RBC casts
Protein in urine scale
Protein= (mg/dl) Negative trace = 10-20 \+1 = 30 \+2 = 100 \+3 = 300 \+4 = 1000-2000
Done with urine dipstick
or 24 hour urine
Albumin in urine
Minimal but persistent amounts of albumin in urine
are associated with
Diabetic nephropathy and hypertensive renal damage
Urinalysis
Examination of urine
Physical
Chemical
microscopic contents
UA should complement BUN and Cr testing
Urine color
Normal straw colored
Color produced by urobilin
Elevated bilirubin and urobilirubin
can be brown or green
Red urine = Blood, Beets, medications
Smokey or cloudy red brown = intact RBC ‘s in urine
Orange Urine = Rifampin, bilirubin, pyridinium
Black Urine = Alkaptonuria (when exposed to air)
Purple urine = UTI (P. aeruginosa, E. Coli, klebsiella, Providencia stuartii, enterococcus)
Cloudy urine = Crystals, phosphate, urates, RBC’s, WBC’s, Chyluria
Red urine =
Blood, Beets, medications
Brown or green urine
Elevated bilirubin and urobilirubin
Smokey or cloudy red brown urine =
intact RBC ‘s in urine
Orange Urine =
Rifampin, bilirubin, pyridinium
Black Urine
Alkaptonuria (when exposed to air)
Purple urine =
UTI
P. aeruginosa, E. Coli, klebsiella, Providencia stuartii, enterococcus
Cloudy urine
Crystals, phosphate, urates, RBC’s, WBC’s, Chyluria
Chyluria
Milky white fluid appearance in urine
results from leakage from lymphatic leakage into the kidneys
Urine Ph
Altered pH can be associated with
Metabolic acidosis or alkalosis
Fresh normal urine should be 5.0-6.5
pH over 8.0 suggests delayed analysis
Uncapped urine can lose CO2 raising pH
Urease producing organisms can cleave urea freeing ammonia that can raise urine pH
Exogenous causes of elevated urine pH
Uncapped urine can lose CO2 raising pH
Urease producing organisms can cleave urea freeing ammonia that can raise urine pH
Specific gravity
Urine specific gravity =
the weight of urine to the weight of an equal amount of water
Provides an assessment of capacity of the renal tubules
Normal should be 1.003 -1.035
Presence of glucose, protein, blood can elevate it
Specific gravity
failure to concentrate urine can indicate
tubular disease
central DI (ADH deficiency)
Nephrogenic DI (ADH resistance)
Drugs (i.e. Lithium)
Chronic Hypokalemia
Chronic Hypercalcemia
Urine Dipstick Test
Blood (Hemoglobin, RBC, myoglobin) Nitrites (bacteria) Glucose Bilirubin (hemolysis, biliary obstruct, liver dysfunction) Urobilirubin (Liver disease) Leukocyte esterase (WBC's) Ketones (DM)
BNG BULK
Unconjugated Hyperbilirubinemia
with hemolysis
Schistocytes present
Microangiopathic hemolytic anemia
(Rule out DIC, TTP, HUS)
Artificial heart valve
(history of valve replacement)
Autoimmune hemolytic anemia
(Prefer Coombs Test)
Unconjugated Hyperbilirubinemia
with hemolysis
Schistocytes are not present
Intra-marrow hemolysis
(Rule out B12 deficiency)
RBC Membrane defects
(Look for spherocytes/ elliptocytes)
RBC Enzyme defects
(Look for bite cells, Check G6PD)
Hemoglobinopathies
(Perform Hemoglobin analysis)
Tests for viral hepatitis
HAV
HAV total antibody = past, present infection or immz
HAV IGM = acute infection
Ammonia
Can be elevated in end stage renal disease
Tests for immune hepatitis
Positive for immune hepatitis
Anti-nuclear antibody
Anti-smooth muscle antibody
Anti-LMK1 auto antibody
Alpha fetoprotein
Positive for hepatocellular carcinoma
IGM antibodies
Acute infection
HDV antibody
Past or present infection
HCV Anitbody
Past or present infection
HBV Antibodies & Antigens
HBV surface antibody = chronic, past or immz
HBV e antibody = Chronic or past infection
HBV core total antibody= Present or past infection
HBV e antigen = Acute/chronic infection
(with increased infectivity)
HBV surface antigen = Acute/chronic infection
BAP Plate
Different types of strep
Beta hemolysis
Ring around colony
Alpha hemolysis
Green colonies
Gamma hemolysis
Red colonies
MacConkey plate
Selective
only lets gram negative to grow
CNA plate
selective
Only lets gram positive grow
Chocolate plate
Good for haemophilus and Neisseria
Mannitol salt agar plate
Staph
MTM plate
Meningitis
Neisseria
Gram positive color
Purple
Gram negative color
Pink
Catalase on gram positive
Means staph
(coagulase)
Catalase negative is strep
Gram positive cocci and negative catalase, with Beta hemolysis
Strep pyrogenes
Rheumatic fever
Strep throat
Strep agalactia
Endocarditis
Gram negative
oxidase positive
N. meningitis
Moraxella C.
Eye, ear, Resp, CNS, joint infections
Gram negative rods
Klebsiella
Lungs, brain, eyes, bladder, blood, wounds, liver
Proteus
UTI’s, catheters, Elderly
Serratia
Teeth, Resp, eyes, UTI, wound
Pseudomonas A. Hospital acquired Ventilator associated pneumonia Sepsis Resistant forms
