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Preferred anticoagulant for a chemistry panel
What chemistry panel evaluates (6) (not tests)
- metabolic function
What you need for chemistry panel
serum or heparinized plasma.
- fluid portion of whole blood in which cells are suspended.
- 90% water, 10% dissolved proteins, carbohydrates, vitamins, hormones, enzymes, lipids, salt, waste, antibodies, ions, etc.
- plasma without fibrinogen.
- plasma proteins
- When blood clots, fluid that remains is serum.
tests on a chemistry panel
- Blood glucose
- Total Protein (no fibrinogen)
- Total Bilirubin
- Alkaline Phosphatase
- ALT (SGPT)
Methods to determine chemical composition of a fluid (3)
- dry reagent chemistry strips (whole blood, color change. Glucose is one)
- Spectrophotometry (clinical chemistry)
- Electrochemical (electrolytes)
- biologically synthesized proteins that catalyze reactions (decrease energy of activation), acts on specific substrate.
- Can be leakage or induced
normally present within cell, leaks across when cell is damaged.
Produced by cells irritated by inflammatory or toxic chemicals
Enzymes that are manufactured by several different organs, function identically but have variations of structure.
Effects of hemolysis on chemistry panel
color interference with spectrophotometric assays causes false increases (K+ in horses and cattle)
effects of lipemia on chemistry panel
- Happens in post-prandial
- visible turbidity, opaque to light, interferes with spectrophotometry
- false decrease due to dilution (electrolytes)
Hyperbilirubinemia and chemistry panels
increased bilirubin in serum interferes with spectrophotometry.
- Synthesis, storage and metabolism of fats, carbs and protein
- Formation and secretion of bile
- synthesis of most coagulation factors
- detoxification and excretion of waste, drugs and toxic substances
- Liver is highly vascular.
- Arterial blood from hepatic artery
- venous blood from portal vein (70-75% of blood flow)
70-75% of blood flow to liver comes from
portal vein, post-intestines
- secondary to metabolic disorders
- biliary disorders
- Infections and parasites
- neoplastic disorders
Liver diseases can be secondary to metabolic disorders such as:
- diabetes mellitus
- starvation (hepatic lipidosis)
circulatory diseases of the liver
Biliary disorders of the liver
cholangitis, obstruction, cholecysitis
infections and parasites of the liver
infectious canine hepatitis, feline infectious peritonitis, equine infectious anemia, leptospirosis, ascarid migration
Signs of liver disease
- abdominal pain
- ascites (lack of albumin stops pulling water into circulation so it goes into abdomen)
- persistent VD
- icterus, bilirubinemia, bilirubinuria
- results from the rupture or lysis of RBC WITHIN circulation
- hemolyzed intravascularly
- Hgb bound to haptoglobin, macrophage rapidly phagocytizes, hgb degraded
Extravascular hemolysis within macrophage
- iron, heme and globulin separated
- globulin and amino acids reutilized
- Iron stored in mononuclear phagocytic system or combines with plasma protein and re-used in bone marrow
- heme biliverdin reduced to bilirubin in macrophage
- bilirubin released into plasma, binds to albumin, goes to liver
extravascular hemolysis within liver
conjugation of bilirubin forms bilirubin glucuronide. Conjugated bilirubin secreted into bile to enter intestine
Extravascular hemolysis with bacteria in large intestine
reduce bilirubin glucuronide to urobilinogen, most excreted in feces, some returns to enterohepatic circulation. Most reexcreted into bile, some bypasses liver, enters general circulation and excreted in urine.
The flow of bile acids from liver to intestine to portal blood to liver and back to intestine is known as enterohepatic circulation
- aid in digestion and absorption of fats in jejunum
- not absorbed until reach ileum, travel vial hepatic portal vein to liver.
- Must enter hepatocyte to be recirculated
- HEPATIC UPTAKE REQUIRED for circualtion
Enterohepatic circualtion in the liver
- bile acids almost completely absorbed from portal blood
- no bile acids reach caudal vena cava. LOW concentration in systemic circulation
- very slight increase postprandial.
specific functions of liver
- bile synthesis
- albumin synthesis
- synthesis of clotting factors
- detoxification (metabolites, drugs, toxins)
- NH3 to urea
in cells, leak out when cells are damaged (alterations in plasma membrane). Rise very quickly after cell injury, like hit by car, much faster than induction enzymes.
overproduction of enzymes cells make. Usually make very little, increase in production caused by stimuli. Develops more slowly in blood than leakage.
Tissue specific enzymes
Enzymes made only in a few organs or tissues. Very important diagnostically.
- enzymes with similar catalytic abilities, produced in different places, but can vary in structure or half life. If trying to identify a particular enzyme, get an idea of its half life.
- Longer half lives are more likely to appear in serum
leakage enzymes and severity of injury
- Not directly correlated. Dead cells can't leak but once. Sub-lethal injuries make many more leakage enzymes.
- necrosis or cirrhosis makes high serum enzymes, but less severe makes even higher.
Tests that detect hepatocyte injury through leakage enzymes (4)
- GLDH (or LDH)
- Hepatocellular damage, liver-specific enzymes.
- alanine aminotransferase, leakage enzyme
- liver specific in dog, cats and primates.
- Not liver specific in horses, ruminants, pigs, birds.
- Aspartate Aminotransferase, leakage enzyme.
- Comes from liver, skeletal muscle, cardiac muscle, kidney, pancreas, erythrocytes
- caused by: liver disease, muscle inflammation or necrosis, hemolysis
- sorbitol dehydrogenase, leakage enzyme.
- liver-specific in all domestic animals.
- Used in large animals because ALT can't be.
- sheep, horses, swine, goats, cattle).
- glutamate dehydrogenase, leakage enzyme
- cattle, sheep and goat hepatocytes.
- caused by hepatocellular damage or necrosis
- standardized test not available. Use SDH instead.
Induced enzyme tests for hepatocyte injury
- Increased production in cells that usually produce a small amount
- ALKP (ALP)
- Usually detecting cholestasis
Isoenzymes to ALKP
- alkaline phosphatase-like enzymes can come from
- osteoblast (bone)
- chondroblast (cartilage)
- intestine (short 1/2 life)
- placenta (short 1/2 life)
- renal (short 1/2 life)
- liver (hepatobiliary system, so evaluates cholestasis. Longer 1/2 life)
ALP or ALKP
- alkaline phosphatase
- cholestasis in dogs, mostly
- serum or plasma ALP indicates liver bone or corticosteroid isoenzymes
- Increase caused by: cholestasis, bone growth in young or cancer, corticosteroids in dogs, severe periodontal disease
Most common bloodwork abnormality
- ALP or ALKP
- comes from bone, liver, steriods
- common in young animals, stress, cushings, older dogs, cholestasis.
- Tested by ALP/ALKP, earliest indicator of biliary stasis in dog.
- degenerative, by necrosis or hepatocyte swelling
- metabolic, by diabetes or hyperadrenocorticism (cushings)
- neoplastic by pancreatic carcinoma or lymphoma
- inflammatory by pancreatitis
- toxic diseases
First indicator of biliary stasis in dogs
ALP. Serum ALP increases before serum bilirubin.
- gamma-glutamyltransferase, induced enzyme
- Liver is #1 source, found in several tissues.
- Increased indicates liver disease, especially obstructive.
- Increased with ALP in d/c indicates hepatobiliary disease
- Useful in detecting cholestasis in large animals, with SDH. More sensitive to large animals than ALP.
- Normal is <15, cholestasis = 200-300
tests of hepatic synthesis (3)
- clotting factors
Glucose in liver
- glucose absorbed by small intestine, to liver via portal, to hepatocytes, converted from glucose to glycogen.
- Hepatocytes can perform gluconeogenesis and glycogenolysis.
- Up or down in liver disease, used as test of liver synthesis
- Test of hepatic synthesis.
- Glucose can be up or down in liver disease
- increased glucose means decreased hepatic uptake, so prolonged postprandial hyperglycemia
- decreased glucose means reduced gluconeogenesis or glycogenolysis, most common in liver failure.
- test of hepatic synthesis
- If albumin in decreased in dogs, indicates 60%-80% loss of hepatic function.
- Less common in horses.
Clotting factors test
- test of hepatic synthesis.
- decreased clotting factors may present with bruising.
- Liver synthesizes most coagulation factors and activates Vit K.
- Blockage of bile flow reduces Vit K absorption and making of Vit K factors (2,7,9,10)
Prolonged PT and APTT with liver
problem if liver coagulation factors are less than 30% of normal. Can mean liver failure.
For gallbladder obstruction
treat with Vit K.
Tests of hepatic function (3)
- Bile Acids
- Must evaluate liver, determine cause of icterus and assess bile obstruction.
- From breakdown of hemoglobin by macrophage.
- Small amounts in urine normal in dog.
- Conjugated in the liver, secreted in bile. Can tell where problem is by conjugation etc, but rarely mentioned on tests.
accumulation of thick mucous bile from gallbladder inflammation
increase of bilirubin in serum. Hemolysis (HCT, CBC), hepatocellular disease (ALT) or biliary obstruction (ALP, GGT)
- increase of bilirubin in urine. Increased hemolysis, hepatocellular disease, biliary obstruction.
- Small amount common in dog, not in cat.
- increase of urobilinogen in urine. Clinically insignificant
- Unstable in urine, hard to detect.
- hemolysis, mammal's with hepatic or biliary disease sometimes.
increase fecal urobilin
hemolysis, dark orange stool.
decrease in fecal urobilin
- biliary obstruction.
- Clay colored stools. No bile, so no dark color.
Hemolysis liver results
- increase of bilirubin in serum/blood (icterus)
- increase in urine bilirubin (orange urine)
- increase in fecal urobilin (orange stool)
- hyperkalemia (false increase, leakage)
- hemoglobinuria (intravascular)
hepatocellular disease liver results
- increased bilirubin in blood (icteric)
- increased urine bilirubin (orange urine)
- NO orange stool due to not converting urobilogen
- Increase of bile acids in serum
biliary obstruction liver results
- increase bilirubin in blood (icterus)
- increase urine bilirubin (orange urine)
- decrease urine urobilinogen
- decrease fecal urobilin (clay stools)
- Increase of bile acids in serum
Ammonium with liver
- aka blood ammonia (NH3, plasma form NH4)
- produced in intestines by digestion of proteins or metabolism of bacteria
- enters liver through hepatic artery or portal vein, enters hepatocyte, converted into urea amino acids and protein (BUN) to be excreted by kidney.
Increased ammonium in test of hepatic function
- not removing from portal.
- Hepatocellular disease, decreased production of urea (decreased BUN)
- portosystemic shunt (intrahepatic in large breed or extrahepatic in small breed)
- portosystemic shunt
- congenital or acquired, abnormal blood vessel allowing blood to bypass liver.
- NH4 and toxins not cleared from portal blood.
- Intrahepatic, inside liver, in large breed dogs
- extrahepatic, outside liver, in small breed dogs.
Treatment of PSS
- antibiotics to decrease bacteria which produce NH4
- lactulose to change pH to trap toxins and NH4 in feces and speed stool transit time
- Low protein diet to reduce substrates for ammonia
- surgery with ameroid ring closing over 6 weeks.
- aid in fat absorption and digestion
- synthesized by hepatocytes from cholesterol, conjugated, sent to duodenum.
- reabsorbed by ileum, back into portal.
- 90-95% reabsorbed in ileum, rest in feces
- Very efficient normally.
Increase in bile acids postprandial
- should be very small.
- hepatocellular disease, shunts, biliary obstruction
Hepatocellular disease in bile acids
- decrease in reuptake and secretion
- more in circulation
- increase of acids in serum.
Acquired shunt results
- Caused by severe cirrhosis, collateral circulation.
- increased serum bilirubin
- normal to increased bile acids
- normal to increased blood ammonia
- normal to decreased blood glucose
- normal to decreased BUN
- normal to decreased Albumin serum
- prolonged coagulation test
congenital shunt results
- Increase in bile acids in serum. >100
- normal or slight increase in leakage enzymes
- normal ALP and GGT
- normal bilirubin
- normal to increased ammonia
- normal to decreased albumen, BUN, glucose, cholesterol
- possible liver atrophy or microcytic anemia eventually
biliary obstruction bile acids results
- lower bile acid excretion and subsequent regurgitation into systemic circulation--leakage from bile duct or gallbladder due to cholestasis
- increase of bile acids in serum.
BART for d/c
- Bile Acids Response Test
- Gold standard for liver function.
- d/c 2 samples, 2 hours apart. 1st after 12-hour fast, 2nd 2 hours after high-fat meal.
- normal is <5 pre and <15.5 post.
- If icteric with hemolysis, no need for BART
BART test results
- detects liver disease before clinical icterus, not specific for type or severity.
- decrease in BA, ileum not absorbing (cats)
- increase in BA, liver disease in d/c (>20 pre and >25 post)
BART in horses, ruminants and llamas
- single sample, normal is a pretty wide range.
- Increase suggests liver disease, but assess in conjunction with other symptoms
- only way to definitively diagnose liver disease
- Use open laparotomy, laparoscopy (preferred, less invasive and can control bleeding), ultrasound-guided needle biopsy (tiny and can't see bleeding)
decreased functional liver mass
- hypoalbuminemia (less production from less area)
- decreased BUN (less urea to remove ammonia)
- increased or decreased glucose
- glucose increased or decreased, often decreased due to fewer cells to perform
- lactate dehydrogenase, leakage enzyme.
- Marker of hepatic damage in all species. Also increased by muscle damage or hemolysis.
Gallbladder obstruction results
- increased ALP and GGT
- increased serum bilirubin
- increased urine bilirubin
- decreased urobilinogen in urine
- decreased fecal urobilin and clay stool
- increased bile acids
- increased ALT and AST (due to pressure)
- If advanced, albumin, ammonia, BUN, cholesterol, coagulation tests, glucose involved.