Term
| True or False, most serum chemistry assays measure the amount of an enzyme in the blood |
|
Definition
FALSE,
serum chemistry values are generally functional assays that measure the degree of enzymatic activity in the blood
*exception is TLI, plasma proteases inhibit trypsin/trypsinogen in the blood so this immunologic assay reflects the amount of trypsin/trypsinogen rather than it's functionality |
|
|
Term
| True or False, the enzymes measured in serum chemistry assays are not physiologically regulated |
|
Definition
| TRUE, these enzymes have no function in the blood and as such are not tightly regulated. Reference intervals can be wide and mild deviations from these intervals have little diagnostic significance |
|
|
Term
| What are the three mechanisms for enzyme elevation? |
|
Definition
1. release from damaged cells
2. increased production/induction
3. decreased clearance |
|
|
Term
| Cell blebbing arises from a depletion of _____. |
|
Definition
|
|
Term
| Tissue(s) of origin for alanine aminotransferase (ALT) |
|
Definition
hepatocytes (most)
skeletal myocytes (much less)
ONLY DOGS AND CATS |
|
|
Term
| what is the mechanism for increased alanine aminotransferase (ALT) |
|
Definition
cell damage
ONLY DOGS AND CATS |
|
|
Term
| What is the tissue(s) of origin for aspartate aminotransferase (AST)? |
|
Definition
Hepatocytes (high)
Skeletal myocytes (high)
Erythrocytes (very little, only see elevations with extreme hemolysis, and even then rare)
ALL SPECIES |
|
|
Term
| What is the mechanism for increased aspartate aminotransferase (AST)? |
|
Definition
|
|
Term
| What is the tissue(s) of origin for iditol dehydrogenase (SDH)? |
|
Definition
Liver (very specific)
LARGE ANIMAL ONLY |
|
|
Term
| What is the mechanism for increased iditol dehydrogenase (SDH)? |
|
Definition
cell damage
LARGE ANIMAL ONLY |
|
|
Term
| What is the tissue(s) of origin for creatine kinase (CK)? |
|
Definition
skeletal myocytes
cardiac myocytes
smooth muscle myocytes (minor)
ALL SPECIES |
|
|
Term
| What is the mechanism for increased creatine kinase (CK)? |
|
Definition
muscle damage
ALL SPECIES
this assay is VERY SENSITIVE, only SEVERE increases are indicative of primary muscle disease
i.e. IM injections can cause elevations in CK |
|
|
Term
| What is the tissue(s) of origin for alkaline phosphatase (ALP/SAP)? |
|
Definition
Hepatocytes
Biliary epithelium
Bone (osteoblasts) |
|
|
Term
| What is the mechanism for increased alkaline phosphatase (ALP/SAP)? |
|
Definition
| induction/increased production |
|
|
Term
| What enzyme(s) may be elevated in DOGS with hyperadrenocorticism or exogenous corticosteroid therapy? |
|
Definition
| alkaline phosphatase (ALP/SAP) and gamma glutamyl transferase (GGT) |
|
|
Term
| What enzyme will be elevated in young growing animals? |
|
Definition
alkaline phosphatase (ALP/SAP)
elevated ALP correlates to an increase in number and activity of osteoblasts |
|
|
Term
| How does elevated alkaline phosphatase (ALP/SAP) affect the prognosis of osteosarcoma in dogs? |
|
Definition
| negative prognostic indicator |
|
|
Term
| What category of disease is associated with elevated alkaline phosphatase (ALP/SAP) in cats? |
|
Definition
metabolic and endocrine diseases
i.e. hyperthyroidism, diabetes mellitus |
|
|
Term
| What liver enzyme is often elevated in equine patients with colic. |
|
Definition
| alkaline phosphatase (ALP/SAP) bystander effect on liver, possible intestinal source |
|
|
Term
| General interpretation of elevated alkaline phosphatase (ALP/SAP) in most species can be divided into three main categories which are: |
|
Definition
1. cholestasis (high levels of bile acids solubilize cell surface ALP)
2. induction by drugs (phenobarbitol) or hormones (corticosteroids)
3. increased osteoblastic activity (growing animals, bone diseases) |
|
|
Term
| What is the tissue(s) of origin for gamma glutamyl transferase (GGT)? |
|
Definition
biliary epithelial cells
hepatocytes
renal tubular epithelial cells (GGT released into urine, NOT serum)
colostrum |
|
|
Term
| What is the mechanism for increased gamma glutamyl transferase (GGT)? |
|
Definition
| induction/increased production |
|
|
Term
| True or False, neonates have elevated gamma glutamyl transferase (GGT) for only a narrow time frame following ingestion of colostrum |
|
Definition
TRUE,
ex. puppies that have ingested colostrum can have 100XURL, but only for about 10 days
also seen in calves and foals |
|
|
Term
| True or False, cats with hepatic lipidosis can have elevated alkaline phosphatase (ALP/SAP) and elevated gamma glutamyl transferase (GGT) |
|
Definition
FALSE,
cats with hepatic lipidosis have increased ALP and normal GGT (idiosyncratic) |
|
|
Term
| True or False, gamma glutamyl transferase (GGT)can be used to screen for general liver disease in LARGE ANIMALS |
|
Definition
|
|
Term
| True or False, reversibility of cell damage cannot be determined based on a single value |
|
Definition
TRUE,
pronosis should be made by considering trends towards worsening or normalizing values |
|
|
Term
| True or False, the magnitude of increase of a serum enzyme values can distinguish focal from diffuse cell damage |
|
Definition
FALSE
** marked focal hepatocellular damage can elevate ALT/AST to the same extent as mild diffuse damage, or moderate multifocal damage. |
|
|
Term
| What is the tissue(s) of origin of amylase? |
|
Definition
| Pancreas to a lesser degree intestine to a much lesser degree liver |
|
|
Term
| What two mechanisms could be responsible for elevated serum amylase in a dog? |
|
Definition
cellular damage (Pancreas>Intestine>Liver)
also decreased clearance secondary to decreased GFR |
|
|
Term
| measurements of serum amylase are generally only indicated for which species? |
|
Definition
|
|
Term
| Very large elevation of amylase in a dog is most likely a reflection of what pathologic process? |
|
Definition
| pancreatic acinar cell damage |
|
|
Term
| How many fold elevations of serum amylase would be consistent with decreased GFR in a dog? |
|
Definition
|
|
Term
| T/F: serum lipase values generally mirror amylase values, however this test is expensive and not commonly run on routine chemistry profiles |
|
Definition
TRUE
species specific immunologic assays (ex. cPLI (canine)) are in development but their diagnostic performance has not been fully characterized |
|
|
Term
| Decreases in which enzyme is a very sensitive indicator of exocrine pancreatic insufficiency? |
|
Definition
| Trypsin-Like Immunoreactivity (TLI) Trypsinogen is produced by the pancreatic acinar cells and converted into the active enzyme trypsin in the small intestine where it participates in protein digestion. Because the pancreas is the only organ that produces trypsinogen/trypsin the lack of this enzyme in circulation is consistent with decreased pancreatic function |
|
|
Term
| How is trypsin/trypsinogen detected in serum samples? |
|
Definition
| via immunologic assays that are species specific (small animal only), because trypsin/trypsinogen enzymatic activity is inhibited by plasma proteases in the blood so functional enyzme assays are not effective at quantifying circulating concentrations of trypsin/trypsinogen. |
|
|
Term
| Increased TLI is consistent with what pathologic processes? |
|
Definition
decreased GFR with decreased renal clearance
pancreatitis
+/- IBD/GI lymphoma
generally parallels amylase and lipase but still not entirely reliable |
|
|
Term
9yr DSH presenting with PU/PD, dehydrated, azotemic, isothenuric, pale MM, small firm kidneys on palpation and a history of vomiting.
What is the most likely explanation for mildly elevated amylase in this patient? |
|
Definition
Decreased GFR
isothenuria w/ dehydration suggesting azotemia is renal. Pale MM is secondary to anemia of chronic renal disease. |
|
|
Term
| If you see 1.5-2X increase in liver enzymes in the absence of clinical signs what should you do? |
|
Definition
1. look for other organ system abnormalities
2. review medical history for enzyme inducing drugs (ALP: corticosteroids(k9), phenobarbitol)
3. re-evaluate bloodwork in 2-4 weeks unless clinical signs develop |
|
|
Term
| What are the three main categories of liver disease? |
|
Definition
1. Hepatocellular damage
2. Cholestasis
3. Decreased liver function |
|
|
Term
| What enzyme elevations are expected in small animal patients with hepatocellular damage? |
|
Definition
elevated AST and ALT
*remember, these enzyme elevations do NOT usually define a specific cause for the hepatocellular injury |
|
|
Term
| What enzyme elevations are expected in large animals with hepatocellular damage? |
|
Definition
elevated AST, SDH +/- GGT (esp. in cattle with acute hepatic necrosis)
*remember, these enzyme elevations do NOT usually define a specific cause for the hepatocellular injury |
|
|
Term
| What serum chemistry abnormality is consistent with pre-hepatic cholestasis? |
|
Definition
hyperbilirubinemia due to increased destruction of RBC
(ie. the liver's ability to remove bilirubin for circulation is overwhelmed by the rate of production (heme is broken down into bilirubin in the liver)) |
|
|
Term
| What two processes other than decreased liver function can cause hepatic cholestasis in horses? |
|
Definition
sepsis and anorexia
via interference of receptor mediated uptake of bilirubin by hepatocytes |
|
|
Term
| Why are ALP and GGT not significantly elevated by pre- and intrahepatic cholestasis? |
|
Definition
| ALP and GGT are induced by accumulation of bile within the ducts so in cases of pre- and/or intrahepatic cholestasis you may only see hyperbilirubinemia with normal to slightly elevated liver enzymes |
|
|
Term
| Other than increased ALP/GGT what serum chemistry abnormalities are associated with post-hepatic cholestasis? |
|
Definition
| hyperbilirubinemia/icterus and hypercholseterolemia (cholestasis results in elevations in the rate limiting enzyme for cholesterol synthesis) |
|
|
Term
| hypoglycemia, hypoalbuminemia, hypocholesterolemia, hyperbilirubinemia, low BUN and prolonged PT/PTT are all associated with what pathology? |
|
Definition
|
|
Term
| T/F: liver must be functioning below 30% of its original capacity before synthetic function is compromised enough to produce abnormalities expected in serum chemistry |
|
Definition
|
|
Term
| T/F: you can use the relative magnitude of enzyme elevations to identify the primary disease processes in a patient |
|
Definition
|
|
Term
what are the primary disease processes in this canine patient?
10X ALP
10X GGT
WRI ALT/AST/glucose/albumin
0.5X cholesterol |
|
Definition
1. post hepatic cholestasis
2. corticosteroid induction |
|
|
Term
| What is the primary disease process in this K9 patient? low ALP WRI GGT/AST/glucose/albumin/cholesterol 6X ALT |
|
Definition
hepatocellular damage
*remember: low enzyme values are not diagnostically relevant and do not consistently occur in patients with liver failure <-- however; in patients with severe hepatocellular damage liver enzymes may be low to normal if so few viable hepatocytes remain that levels of enzymes released by damaged cells are not enough to elevate serum values beyond the reference intervals. |
|
|
Term
What are the primary disease processes in this k9 patient?
0.1X ALP/GGT
5X ALT
4X AST
WRI glucose, albumin, cholesterol |
|
Definition
1. hepatocellular damage
2. secondary cholestasis (ie. the magnitude of elevation of ALP/GGT is small compaired to ALT/AST) |
|
|
Term
What is the primary disease process in this k9 patient?
WRI ALP/ALT/AST
slightly elevated GGT
decreased glucose/albumin/cholesterol |
|
Definition
| 1. decreased liver function (indicated by poor synthetic function without predictable changes in hepatocellular damage enzymes) |
|
|
Term
| What three tests are more sensitive to decreased liver function than evidence of decreased synthetic capacity (ie. hypoalbuminemia)? |
|
Definition
| serum bilirubin, serum bile acids, and blood ammonia |
|
|
Term
| How is the majority of bilirubin in the body produced? |
|
Definition
| degradation of red blood cell hemoglobin by macrophages |
|
|
Term
| How is bilirubin delivered from circulation to hepatocytes? |
|
Definition
| transported in the plasma bound to albumin |
|
|
Term
| How is bilirubin removed from the body? |
|
Definition
| bilirubin is conjugated by hepatocytes to make it water soluble and then excreted in the bile |
|
|
Term
| Why might you see bilirubinuria without bilirubinemia in a patient with renal failure? |
|
Definition
| glomerular dysfunction allows large amounts of albumin bound unconjugated bilirubin through the filtration barrier and into the urine |
|
|
Term
| T/F: decreased serum bilirubin indicates hepatocellular damage |
|
Definition
FALSE
decreased serum bilirubin is NOT diagnostically significant |
|
|
Term
| What other clinical abnormalities are expected in patients with hyperbilirubinemia secondary to hemolysis? |
|
Definition
hyperbilirubinemia can be mild to severe
+ regenerative anemia (due to RBC damage), and abnormal RBC morphology (spherocytes, agglutination, heinz bodies, RBC ghosts, schistocytes) |
|
|
Term
| hemolyzed plasma is consistent with _____ hemolysis |
|
Definition
|
|
Term
| icteric plasma is consistent with ________ hemolysis |
|
Definition
|
|
Term
| True or False: neonatal foals have a slightly higher reference interval for serum bilirubin and ALP than adult horses |
|
Definition
|
|
Term
| What magnitude of hyperbilirubinemia would be expected secondary ONLY to decreased liver function? |
|
Definition
mild to moderate hyperbilirubinemia
*would also expect low albumin, cholesterol, glucose, BUN, and prolonged PT/PTT |
|
|
Term
| What is the physiologic role performed by bile acids? |
|
Definition
facilitate fat digestion
cycle: Made from cholesterol in the liver --> conjugated and secreted in the bile --> excreted into the small intestine to facilitate fat absorption --> reabsorbed into portal circulation |
|
|
Term
| T/F: in health about 50% of bile acids are reabsorbed by hepatocytes from the portal circulation |
|
Definition
FALSE
in health almost all of the bile acids are reabsorbed by hepatocytes so only very low levels of bile acids should be present in peripheral blood |
|
|
Term
| How should you prepare a patient prior to drawing blood for bile acids in order to attain the greatest diagnostic sensitivity? |
|
Definition
Collect a post-prandial blood sample (exception: horses- have no gallbladder so small amounts of bile acids are continuously secreted into GI, no post-prandial effect)
*In fasted animals the minimal amounts of bile acids present in circulation may be cleared by a compromised liver; however, feeding induces secretion of large amounts of bile acids into the intestine, which are absorbed into the portal circulation and overwhelm functionally compromised hepatocytes resulting in elevated serum bile acids. |
|
|
Term
| Bile acids are not a very good test of liver function in what species? |
|
Definition
| Cattle (wide reference intervals decrease diagnostic value) |
|
|
Term
| elevated bile acids cannot be used to evaluate liver function with which concurrent disease process? |
|
Definition
cholestasis
*do not use bile acids to evaluate liver function in animals that are grossly icteric or have hyperbilirubinemia |
|
|
Term
| T/F: spontaneous gall bladder contraction can result in mild elevations in fasting serum bile acids |
|
Definition
|
|
Term
| List in order from most sensitive to least sensitive the serum chemistry abnormalities supportive of decreased liver function? |
|
Definition
| Bile acids > blood ammonia > decreased synthetic capacity |
|
|
Term
| T/F: elevated blood ammonia in large animals is always due to decreased liver function |
|
Definition
FALSE
Ruminants: dietary supplementation
Horses: colic (production by gut microflora + compromised gut wall) |
|
|
Term
| What technical issues associated with sample collection and handling complicate analysis of liver function via blood ammonia? |
|
Definition
RBC have a high ammonia content, as such complete serum separation from RBC, and absolutely no hemolysis is necessary in order to ensure the greatest accuracy
*preanalytical error is high |
|
|
Term
| T/F: low blood ammonia indicates decreased liver function |
|
Definition
FALSE
*The liver has a large reserve capacity for detoxifying ammonia from the blood into urea, and low blood ammonia is not diagnostically significant |
|
|
Term
| What are the four main mechanisms for increased serum bile acids? |
|
Definition
1. Decreased liver function
2. Cholestasis
3. Portovascular abnormality
4. Post-prandial (very mild in patients with normal liver function) |
|
|
Term
| What two plasma abnormalities can be noted in patients with concurrent liver disease? |
|
Definition
|
|
Term
| What three ways does glucose enter the blood? |
|
Definition
1. dietary sources
2. glycogenolysis
3. gluconeogenesis |
|
|
Term
| T/F: anorexia can cause significant deviations in levels of blood glucose |
|
Definition
FALSE
*glucose levels are tightly regulated by hormones (ie. insulin/glucagon) and as such only prolonged and/or extreme anorexia, often associated with poor BCS can be attributed to decreased blood glucose |
|
|
Term
| What 5 hormones can promote hyperglycemia? |
|
Definition
| glucagon, corticosteroids, catecholamines, growth hormones, thyroid hormone (T4) |
|
|
Term
| What is the main hormone responsible for decreasing blood glucose? |
|
Definition
Insulin
*binds to receptors on hepatocytes, myocytes, and adipocytes to promote uptake, use, or storage of glucose. |
|
|
Term
| What error in sample handling may result in artifactually lowered blood glucose? |
|
Definition
| failure to spin whole blood down in a serum separator tube will allow RBC to continue consuming glucose in vitro |
|
|
Term
| Which assay can be used to assess average blood glucose values over a period of 2-3 weeks? |
|
Definition
Fructosamine
*fructosamine is the result of non-enzymatic irreversible glycation of albumin during prolonged periods of hyperglycemia.
Hypoprotinemia may result in decreased fructosamine levels |
|
|
Term
| Liver failure, sepsis, neonates/toy breeds, exertion, hypoadrenocorticism, hypothyroidism, and bovine ketosis are associated with what abnormality in serum glucose? What is the mechanism for this abnormality? |
|
Definition
| hypoglycemia associated with inadequate glucose production |
|
|
Term
| failure to promptly separate serum from RBC following blood collection, insulin overdose, paraneoplastic (ex. insulinoma, IGF producing tumor), and sepsis are associated with what abnormality in serum glucose? What is the mechanism for this abnormality? |
|
Definition
| hypoglycemia associated with excessive cellular uptake or usage |
|
|
Term
| Stress, post-prandial, diabetes mellitus, hyperadrenocorticism, hyperthyroidism, pheochromocytoma (Adrenal tumor that produces epinephrine), pancreatitis, and colic are associated with what abnormality in serum glucose? What is the mechanism for this abnormality? |
|
Definition
| hyperglycemia associated with excessive production or decreased cellular uptake |
|
|
Term
| T/F: Ketone body formation in monogastrics occurs during times of relative glucose unavailability as an alternative energy source |
|
Definition
TRUE
*ruminants normally use ketones for energy |
|
|
Term
| What are the three main ketone bodies? |
|
Definition
| acetone, acetoacetic acid, and beta-hydroxybutyrate |
|
|
Term
| Where are ketones produced and from what two substrates? |
|
Definition
| ketones are produced in the liver from fatty acids or/and ketogenic amino acids |
|
|
Term
| Elevated levels of ketones in the serum or urine of small animal patients is indivative of what disease process? |
|
Definition
metabolic stress usually manifest secondary to diabetic ketoacidosis
*in large animals anorexia/starvation |
|
|
Term
| How are lipids transported in the serum? |
|
Definition
| lipids are transported in the serum associated with proteins --> lipoproteins |
|
|
Term
| Where in the body is endogenous cholesterol produced? |
|
Definition
| the liver --> that's why decreased liver function is associated with hypocholesterolemia |
|
|
Term
| What enzyme is responsible for clearing lipids from circulation? What hormone activates this enzyme? |
|
Definition
| Lipoprotein lipase is activated by insulin and clears lipids from circulation by facilitating intraceullular uptake into adipocytes and hepatocytes. |
|
|
Term
| T/F: fractionation of cholesterol is not routinely performed in domestic species |
|
Definition
TRUE
*HDL is the predominant form of cholesterol in domestic animals |
|
|
Term
| T/F: hyperlipemia and hyperlipidemia are often used interchangeably and refer to non-specific elevation of lipids in the blood |
|
Definition
|
|
Term
| What does the term lipemia mean? |
|
Definition
| grossly turbid or opaque serum or plasma secondary to increased levels of lipids in the blood |
|
|
Term
| Liver failure, hypoadrenocorticism, protein-losing enteropathy, portosystemic shunt are all associated with what metabolic abnormality? |
|
Definition
|
|
Term
| T/F: many conditions associated with hypercholesterolemia are also associated with hyperglycemia |
|
Definition
TRUE
*exceptions: post-hepatic cholestasis and nephrotic syndrome are not reliably associated with hyperglycemia |
|
|
Term
| What abnormality of serum cholesterol is associated with hypothyroidism, hyperadrenocorticism, diabetes mellitus, pancreatitis, post-hepatic cholestasis, nephrotic syndrome, post-prandial, and familial syndomes? |
|
Definition
|
|
Term
| What may be the only abnormality on serum chemistry in dogs with hypothyroidism? |
|
Definition
hypercholesterolemia
(clinical exam findings may include bilaterally symmetrical alopecia, testicular atrophy, and lethargy) |
|
|
Term
| T/F: It is possible to have bilirubinuria in the absence of bilirubinemia |
|
Definition
TRUE
small amounts of bilirubin in the peripheral circulation is filtered and excreted by the kidney, which may result in bilirubinuria in the absence of bilirubinemia |
|
|
Term
| Which four rule outs can cause elevated ALP and cholesterol? |
|
Definition
post-hepatic cholestasis
pancreatitis
hyperadrenocorticism (cushings)
diabetes mellitus |
|
|
Term
| What is the most likely cause of hypoglycemia in an adult ferret with a history of collapse and seizure and no other chemistry abnormalities? |
|
Definition
| insulinoma (low BG --> collapse and seizure) |
|
|
Term
| What signalment and chemistry abnormalities are associated with bovine hepatic lipidosis/ketosis syndrome? |
|
Definition
| Postparturient overconditioned dairy cows develop a negative energy balance --> massive mobalization of peripheral stores of fat with accumulation in the liver --> elevated liver enzymes and FFA, liver biopsy is usually necessary to confirm Dx |
|
|
Term
| what is the pathophysiology behind hyperlipemia/hyperlipidemia syndrome in ponies and miniature horses? |
|
Definition
| decreased caloric intake relative to demand (often associated with gestation in overconditioned animals) --> mobalization of peripheral adipose with accumulation of lipid in the blood and liver |
|
|
Term
| What chemistry abnormalities can be seen secondary to excessive accumulation of fat within hepatocytes? |
|
Definition
| hepatocellular damage, post-hepatic cholestasis and in severe cases decreased liver function |
|
|
Term
| What is the difference between hyperlipidemia and hyperlipemia syndrome? |
|
Definition
hyperlipidemia is more mild, liver function and plasma color is normal, serum triglycerides are mildly elevated
hyperlipemia is severe and associated with grossly lipemic plasma, marked elevations in serum triglycerides, elevated liver enzymes and bilirubin, and decreased liver function (follows cholestasis) |
|
|
Term
| How does insulin deficiency affect glucose and fatty acid balance in the body? |
|
Definition
| insulin defficiency results in decreased tissue uptake and utilization of glucose and fatty acids --> hyperglycemia/hypercholesterolemia |
|
|
Term
| insulin causes intracellular translocation of what three serum analytes? |
|
Definition
| glucose, potassium, phosphorus |
|
|
Term
| What is the main mechanism responsible for polyuria in diabetic animals? |
|
Definition
Osmotic diuresis secondary to glucosuria.
Glucosuria increases the tonicity of the renal filtrate so that less water is reabsorbed --> dehydration and increased excretion of solutes (Na, K, Mg) |
|
|
Term
| What are the non-protein nitrogen compounds present in the blood? Are they a greater or smaller component of the blood than protein? |
|
Definition
| urea and amino acids represent non-protein nitrogen, which comprise only a small fraction of total blood nitrogen (ie. most of it is protein) |
|
|
Term
| What are the two major sites of synthesis for plasma/serum proteins? |
|
Definition
|
|
Term
| What is the most important function of serum proteins? |
|
Definition
| maintenance of colloid oncotic pressure |
|
|
Term
| What abnormalities in serum proteins are seen in neonatal animals? |
|
Definition
low globulins (secondary to immunologic inexperience)
low albumin (dilution effect as a result of high total body water content) |
|
|
Term
| What abnormalities in serum proteins are seen in geriatric animals? |
|
Definition
| elevated globulins (following lifetime antigenic exposure) with mild compensatory decrease in albumin |
|
|
Term
| What are the three major methods of measuring proteins in the blood? |
|
Definition
| refractometry, dye binding, electrophoresis |
|
|
Term
| Why is refractometry only an estimate of total serum protein? |
|
Definition
refractometry is influenced by all blood solutes, of which protein predominates, but also includes electrolytes, glucose, urea, and lipids
so the value you get from refractometry is Total Solids (includes ALL serum solutes) |
|
|
Term
| T/F: hyperbilirubinemia can cause falsely elevated values when assessing total protein with refractometry |
|
Definition
|
|
Term
| T/F: refractometry is a quick and accurate way to measure specific gravity of body fluids |
|
Definition
FALSE
SG scale is calibrated for URINE. Urea is the primary solute in urine and produces a smaller angle of refraction than protein, which is the major solute in body fluids. SG for body fluids with refractometry will be falsely elevated |
|
|
Term
| What method of quantifying serum protein is commonly employed by "wet" chemistry analyzers (ie. the big machines they have in the lab)? |
|
Definition
Dye binding
dyes are fairly species specific (ex. bromecresol blue gives different values for dogs and horses, and is completely unreliable for rabbits) |
|
|
Term
| What is the most sensitive and specific way to measure serum proteins? |
|
Definition
electrophoresis
esp. useful for identifying specific classes of immunoglobulins in cases of suspected lymphoid neoplasia (ex. multiple myeloma and/or lymphoma) |
|
|
Term
| T/F: albumin constitutes 35-50% of total serum proteins in our domestic species |
|
Definition
TRUE
(albumin is 60-70% of TP in primates) |
|
|
Term
| What is the only individual protein that can be detected by electrophoresis? |
|
Definition
|
|
Term
| Other than maintenance of colloid oncotic pressure what are the two most important functions of albumin? |
|
Definition
| transport amino acids labile storage pool of protein |
|
|
Term
| T/F: unless you only have total protein on your chemistry panel it is much more valuable to interpret albumin and globulin separately |
|
Definition
|
|
Term
| What effect does pregnancy and lactationhave on serum albumin and globulin in large animals? |
|
Definition
albumin may decrease (dilutional effect secondary to water retention)
globulin may increase |
|
|
Term
| Protein deprivation must be severe (either marked starvation or nutritional deficiency coupled with increased losses) to result in decreases in serum protein. Which consistuent of serum protein is affected first? |
|
Definition
| albumin is affected before globulins in cases of nutritionally mediated hypoprotinemia |
|
|
Term
| What are three pathophysiologic mechanisms for selective hypoprotinemia manifested as hypoalbuminemia? |
|
Definition
-decreased liver function (also hypoglycemia, hypocholesterolemia, prolonged PT/PTT, low BUN)
-negative acute phase response to inflammation (mild hypoalbuminemia)
-increased loss through glomerulus (expect concurrent proteinuria) |
|
|
Term
| panhypoprotinemia is usually secondary to what mechanism? |
|
Definition
| increased non-selective losses (ex. GI, 3rd space- i.e. cavity effusions, external hemorrhage, cutaneous- i.e. burns) |
|
|
Term
| Hyperalbuminemia almost always occurs secondary to ______ |
|
Definition
| dehydration (the body rarely increases albumin production) |
|
|
Term
| hyperglobulinemia is likely secondary to what two processes? |
|
Definition
colostrum ingestion in neonates
increased production (usually secondary to inflammation and/or antigenic stimulation) |
|
|
Term
| inflammatory stimuli usually result in what type of gammopathy? |
|
Definition
polyclonal
(vs. monoclonal gammopathy, must be distinguished from paraneoplastic syndrome (ie. multiple myeloma or lymphoma)) |
|
|
Term
| How does albumin respond to inflammation? |
|
Definition
| mild decrease in albumin is associated with inflammation, negative acute phase response secondary to inflammatory cytokines |
|
|
Term
| What is the main route for solute and water excretion from the body? |
|
Definition
|
|
Term
| What sized particles are freely filtered through the glomeruli? |
|
Definition
|
|
Term
| What charge of particles are freely filtered through the glomeruli? |
|
Definition
| positive or neutrally charged particles are filtered because the basement membrane of the the glomerular endothelium is negatively charged |
|
|
Term
| What is the most important indicator of glomerular pathology? |
|
Definition
protinuria
*in the absence of lower UTI or hematuria |
|
|
Term
| What four physiologic factors influence the rate of GFR? |
|
Definition
-blood volume
-cardiac output
-number of functional glomeruli (remember fewer nephrons reduces total kidney GFR, but increases GFR for each remaining functional nephron (hypertrophy in response to increased workload))
-vascular tone of afferent and efferent glomerular arterioles (most commonly affected by drugs/toxins) |
|
|
Term
| What is the function of the renal tubular cells? |
|
Definition
| maintain electrolyte, acid/base, and mineral balance, and to conserve or excrete water from the urinary filtrate |
|
|
Term
| What SG values are considered isothenuric, what is the clinical significance of isothenuria |
|
Definition
1.008 - 1.012
isothenuria can indicate abnormal tubular function with an inability to concentrate or dilute the urinary filtrate
** isothenuria can be present in completely NORMAL animals depending on water consumption and time of day, so confim tubular dysfunction with the presence of persistant isothenuria through serial SG measurements and in light of hydration status/BUN/Creatinine |
|
|
Term
| T/F: marked protinuria is generally more indicative of glomerular damage than tubular dysfunction |
|
Definition
TRUE
*the renal tubular cells have the capacity to reabsorb small quantities of protein that may leak through normal glomeruli, but this mechanism is overwhelmed by marked protinuria as a result of glomerular disease |
|
|
Term
| How do the renal tubular cells respond to small amounts of glucose or protein in the urinary filtrate? |
|
Definition
normally renal tubular cells have the capacity to reabsorb small amounts of glucose and protein in the filtrate. In pathologic states where large amounts of glucose and protein are present in the urine this absorptive capacity is overwhelmed.
ie. glucosuria/protinuria are not necessarily an indicator of tubular dysfunction and may be the result of pre-renal overflow from the blood |
|
|
Term
| what solutes are responsible for generating the osmolality gradient in the renal medulla that allows for normal urinary concentration? |
|
Definition
urea, sodium, chloride
high osmolality of interstitial fluid of the renal medulla draws water out of the filtrate in the renal tubules resulting in urine concentration |
|
|
Term
| What are four possible mechanisms for failure of urine concentration? |
|
Definition
-No ADH (pretty rare)
-REVERSIBLE Poorly responsive tubular response to ADH (bacterial toxins (ex. pyometra), early/mild hypercalcemia)
-IRREVERSIBLE poor tubular response to ADH (tubular cell death <-- can be a result of severe or prolonged hypercalcemia with minieralization and renal vasoconstriction, also DAMNIT)
-Loss of medullary concentration gradient (either decreased tonicity of medullary interstitial fluid (low BUN/electrolytes, or disruption of vasa recta and countercurrent exchange)
OR
increased tonicity of the urinary filtrate (ex. glucosuria, osmotic diuretics like mannitol) |
|
|
Term
| What are three mechanisms for decreased urine concentrating ability in patients with renal failure? |
|
Definition
-fewer nephrons have to filter more fluid --> more solutes get through the initial glomerular filter, also overwhelms tubular reabsorption of electrolytes and water secondary to fluid dynamics
-tissue damage or abnormal blood flow impacts efficacy of counter current exchange in vasa recta --> loss of medullary hypertonicity
-damaged tubular cells have a diminished response to ADH |
|
|
Term
| Why might a normal animal have poorly concentrated urine? |
|
Definition
| recent large intake of water |
|
|
Term
| Hyperadrenocorticism AND hypoadrenocorticism can both cause poorly concentrated urine through different mechanisms, what are they? |
|
Definition
Hyperadrenocorticism: corticosteroids induce ADH resistance
Hypoadrenocorticism: mineralocorticoid defficiency --> no aldosterone --> decreased tubular reabsorption of sodium --> increased tonicity of urinary filtrate AND medullary washout |
|
|
Term
| What three mechanisms can induced ADH resistance? |
|
Definition
elevate corticosteroids
bacterial toxins (often associated with pyometra)
mild or transient hypercalcemia |
|
|
Term
| how can hypokalemia contribute to poorly concentrated urine? |
|
Definition
| secondary to abnormal vascular constriction, poorly concentrated urine can be reversible if hypokalemia is early/mild/transient |
|
|
Term
| T/F: patients with lymphoma often have lymphocytosis on CBC |
|
Definition
FALSE
*more commonly have peripheral lymphadenopathy +/- steroid leukogram secondary to stress of disease (lymphopenia**) |
|
|
Term
| When would you want to measure urinary GGT? |
|
Definition
| when you suspect acute tubular necrosis (usually associated with toxins) |
|
|
Term
| Why is horse urine normally turbid? |
|
Definition
| increased amounts of mucus and calcium carbonate crystals |
|
|
Term
| Why can bovine urine become turbid if the sample is allowed to stand? |
|
Definition
|
|
Term
| What is a more accurate method of quantifying proteinuria other than dipstick? |
|
Definition
| precipitation or protein/creatinine ratio |
|
|
Term
| Under what circumstances could you have proteinuria in the absence of hypoprotinemia? |
|
Definition
| pre-renal overflow secondary to elevated amounts of small proteins in the blood (usually immunoglobulins (paraneoplastic/colostrum), could also be hemoglobinemia/myoglobinemia) |
|
|
Term
| What is the most common form of protinuria? |
|
Definition
Post-renal associated with hemorrhage or inflammation anywhere in the genitourinary tract (including the kidney)
*WBC in the urine is supportive of post-renal proteinuria |
|
|
Term
| How is glucose handled by the kidney? |
|
Definition
| freely filtered and completely reabsorbed |
|
|
Term
| What is the most common cause of glucosuria? |
|
Definition
Marked hyperglycemia (>180-200 mg/dl) that overwhelms tubular resorptive capacity
*tubular dysfunction is a less common cause of glucosuria, which occurs in the absence of hyperglycemia (usually associated with acute tubular necrosis <-- toxins, thromboembolic disease, hypovolemic shock) |
|
|
Term
| T/F: ALL uremic patients are azotemia but, all azotemic patients are NOT uremic |
|
Definition
|
|
Term
| What is azotemia, what serum analytes are used to quantify azotemia? |
|
Definition
accumulation of nitrogenous wastes in the blood, measure BUN and creatinine
try to classify as pre, renal, or post |
|
|
Term
| What is uremia, what clinical signs are commonly seen in association with uremia? |
|
Definition
a constellation of clinical signs that result secondary to moderate or severe azotemia
include: lethargy, anorexia, mucosal ulceration, vomiting, diarrhea, weight loss, anemia, altered urine output |
|
|
Term
| How do serum chemistry abnormalities in cows with renal insufficiency differ from all other species? |
|
Definition
| normally BUN is elevated before creatinine; however, ruminants secrete large amounts of urea into their saliva where it is subsequently degraded by microbes so that creatinine may be elevated before BUN in cows with renal insufficiency |
|
|
Term
| How does fluid dynamics through the glomerulus affect urinary excretion of BUN? |
|
Definition
| BUN passively diffuses out of the renal tubules with water, low flow rates (ie. decreased GFR) result in increased resorption of urea out of the urinary filtrate and into the blood secondary to increased passage time through the renal tubules |
|
|
Term
| Elevated BUN can be indicative of what three processes? |
|
Definition
decreased GFR
high protein diet/ GI hemorrhage
Increased protein catabolism (starvation, extreme excercise, fever, corticosteroids) |
|
|
Term
| Why is creatinine a more specific test of renal function than BUN? |
|
Definition
| Creatinine is not affected by diet, rather it is produced at constant low levels from the muscle and is freely filtered with no tubular reabsorption. |
|
|
Term
| T/F: BUN and creatinine are relatively insensitive indicators of decreased renal function and become elevated in the blood in a non-linear relationship as GFR decreases |
|
Definition
TRUE
*75% of kidney function must be lost before appreciable elevations in BUN/Cr |
|
|
Term
| What can you NOT determine for BUN/creatinine? |
|
Definition
the cause of the azotemia
reversibility/prognosis
localization (pre, renal, post)
ARF vs. CRF |
|
|
Term
| In horses what has a greater effect on phosphorus levels, GFR or hormones? |
|
Definition
| Hormones --> phosphorus may be high, normal, or low, depending on calcium levels despite decreased GFR |
|
|
Term
| What effect does decreased GFR have on serum phosphorus levels in small animals? |
|
Definition
|
|
Term
| What effect does decreased GFR have on phosphorus in levels in horses? |
|
Definition
phosphorus may be high normal or low.
Phosphorus levels in horses is somewhat dependent on calcium values. If calcium is high PTH will override effects of decreased GFR resulting in normal to low serum phosphorus |
|
|
Term
| What effect does decreased GFR have on serum phosphorus levels in cattle? |
|
Definition
| unpredictable due to excretion of phosphorus in saliva and rumen |
|
|
Term
| How is magnesium affected by decreased GFR, what is the clinical significance? |
|
Definition
| hypermagnesemia, minor clinical significance |
|
|
Term
| What is the biologically active form of calcium in the blood? |
|
Definition
|
|
Term
| What abnormalities in serum potassium are associated with oliguric/anuric renal failure? |
|
Definition
| hyperkalemia secondary to failure of renal elimination of potassium |
|
|
Term
| What abnormalities in serum potassium are consistent with polyuric renal failure? |
|
Definition
| hypokalemia secondary to excessive renal losses of potassium |
|
|
Term
| What type of renal disease is most commonly associated with hypercholesterolemia? |
|
Definition
glomerular nephritis
*also hypoalbuminemia and protinuria |
|
|
Term
| What degree of increase in serum amylase is consistent with decreased GFR? |
|
Definition
2-3X URI
*this process predominantly occurs in DOGS and CATS |
|
|
Term
| What type of acid base disorder is common in ruminants with renal failure? |
|
Definition
metabolic ALKALOSIS ssecondary to abomasal stasis
*small animals and horses have acidosis secondary to decreased excretion of metabolic acids |
|
|
Term
| What type of acid base disorder is common in small animals and horses with renal failure? |
|
Definition
ACIDOSIS secondary to decreased renal clearance of metabolically generated acids (i.e. urermic acidosis)
*ruminants have alkalosis secondary to abomasal stasis secondary to renal failure |
|
|
Term
| What are the two most common precipitators of renal failure in horses? |
|
Definition
NSAID associated nephrotoxicity
secondary to an episode of hypoperfusion (often associated with colic/dehydration +/- shock/sepsis) |
|
|
Term
| What are the three most common causes of renal failure in cows? |
|
Definition
toxic, infectious, post-renal
*alkalosis (GI stasis), low electrolytes (increased renal excretion, GI stasis), hypocalcemia (reduced intake), hyperphosphatemia (reduced excretion in saliva secondary to anorexia and decreased GFR) |
|
|
Term
| plasma, interstitial fluid, lymph, transcellular fluid (i.e. 3rd space) are all elements of what total body fluid component? |
|
Definition
|
|
Term
| how does hyponatremia affect intracellular fluid volume? |
|
Definition
intracellular fluid volume will expand
**there is more sodium within the cells than the extracellular fluid, so water moves towards the region of greatest sodium concentration |
|
|
Term
| What are three situations that can result in hypovolemia without any fluid losses? |
|
Definition
| septic shock, anaphylactic shock, neurogenic shock ---> all of these mechanisms result in systemic vasodilation and increase the volume of the vasculature |
|
|
Term
| Where is most of the fluid in the body localized (intra or extracellularly)? |
|
Definition
40% of the body weight is due to the intracellular fluid volume
*20% due to extracellular fluid, 40 due to solid body matter (ie. bones) |
|
|
Term
| What are the four most common sources of fluid loss? |
|
Definition
| cutaneous (i.e. burns), renal, GI, 3rd space |
|
|
Term
| What is the stimulus for release of ADH (antidiuretic hormone) from the hypothalamus, and what is its mechanism of action? |
|
Definition
| ADH is release in response to hypertonicity or low blood pressure (ie. need to CONSERVE fluids) is induces thirst centrally and increased water resorption by the renal tubules |
|
|
Term
| How does angiotensin II contribute to the maintenance of tissue perfusion? |
|
Definition
enhances aldosterone secretion --> increased retention of sodium by the kidney
arteriolar vasoconstriction --> reduces volume of the vascular system |
|
|
Term
| What is the aldosterone's mechanism of action? |
|
Definition
receptor mediated increased in renal resorption of sodium in exchange for potassium and hydrogen
*that's why you see hyperkalemia in patients with mineralocorticoid defficient hypoadrenocorticism |
|
|
Term
| What is the stimulus for secretion of atrial natriuretic factor and what is its mechanism of action? |
|
Definition
secreted in response to hypotonicity, overhydration and high blood pressure.
acts as a weak antagonist to angiotensin II, aldosterone and sympathetic stimulation (ie. vasoconstriction) --> promotes sodium wasting and has diuretic effects |
|
|
Term
| What serum electrolyte abnormalities are expected in situations where the patient is losing water without electrolytes (hypotonic loss)? |
|
Definition
elevated serum electrolyte levels
*elevated PCV/TP is supportive of hypotonic fluid loss as an explanation for elevated serum electrolytes |
|
|
Term
What serum electrolyte abnormalities are expected in situations where the patient is losing water with proportional losses of electrolytes (isotonic loss)?
acutely?
chronically? |
|
Definition
Acutely: serum electrolytes are normal
Chronically: ADH is released in response to low blood volume/hypoperfusion resulting in water retention and dilution of existing serum electrolyte concentrations |
|
|
Term
| What serum electrolyte abnormalities are expected in situations where the patient is losing electrolytes in excess of water (hypertonic loss)? |
|
Definition
serum electrolytes will be decreased
*replacement of blood volume by water retention will result in even more extreme dilution of serum electrolyte values |
|
|
Term
| What is the best way to assess dehydration? |
|
Definition
PHYSICAL EXAM (esp. body weight)
also loss of skin elasticity, dry mucous membranes, sunken eyes, prolonged capillary refill time |
|
|
Term
| What are two physiologic states that are commonly associated with increased total body water? |
|
Definition
pregnancy
neonatal animals |
|
|
Term
| What are two pathologic states associated with water retention? |
|
Definition
congestive heart failure
oliguric/anuric renal failure |
|
|
Term
| What are the two potential mechanisms for hypernatriemia? |
|
Definition
decreased water intake (no access or absence of thirst)
lost of water in excess of sodium (hypotonic loss): panting, +/- renal/GI
*increased intake is not a likely mechanism |
|
|
Term
| What body fluids contain large amounts of chloride? |
|
Definition
GI fluid
sweat (equine only)
saliva (ruminants) |
|
|
Term
| When serum chloride levels change independently of serum sodium levels what kind of disorder must by assessed? |
|
Definition
acid-base
(elevated HCO w/ low Cl --> alkalosis)
(low HCOW w/ elevated Cl --> acidosis)
(HCO and Cl in the same direction --> mixed acid base disorder) |
|
|
Term
| What can be a source of analytical error resulting in hyperchloremia? |
|
Definition
| KBr interferes with the electrode that measures serum Cl --> falsely elevated value |
|
|
Term
| Where is the majority of the body's potassium located? |
|
Definition
|
|
Term
| What are the two major mechanisms for regulation of serum potassium? |
|
Definition
exchange for hydrogen with intra/extracellular translocation of potassium in response to acidosis or alkalosis
balance between intake and renal excretion (potassium is not closely regulated by the kidney so changes in urine output have a big impact on serum potassium)
*additionally, since a large majority of the body's potassium is intracellular massive cell damage like heatstroke, trauma, multi-organ failure can result in hyperkalemia) |
|
|
Term
| What are three mechanisms of hypokalemia? |
|
Definition
decreased intake (often in combination with increased losses): anorexia
increased losses: GI, renal, 3rd space, cutaneous
intracellular shift: alkalosis, insulin |
|
|
Term
| What are two mechanisms of hyperkalemia? |
|
Definition
failure of elimination/renal retention: hypoadrenocorticism (secondary to aldosterone defficiency), oliguria/anuria, post-renal obstruction
extracellular shift: acidosis, insulin deficiency/resistance, massive muscle necrosis (cell damage) |
|
|
Term
| If ALL serum electrolytes are ELEVATED what two mechanisms should you consider? |
|
Definition
free water loss or decreased water intake(panting/H20 deprivation)
iatrogenic oversupplementation |
|
|
Term
| If ALL serum electrolyes are DECREASED what two mechanisms should you consider? |
|
Definition
hypertonic fluid loss (sweating/renal/GI)
isotonic fluid loss (hemorrhage/GI) with dilution of serum electrolytes secondary to free water replacement |
|
|
Term
| What three diseases/processes can present with decreased sodium and chloride and elevated potassium? |
|
Definition
hypoadrenocorticism (loss of aldosterone --> renal excretion of sodium and retention of potassium)
uroabdomen/oliguric-anuric renal failure (renal retention)
rarely, chronic or severe cavity effusion or diarrhea |
|
|
Term
| What is the best way to fully evaluate acid-base disorders? |
|
Definition
| arterial blood gas analysis |
|
|
Term
| What is the mechanism for increased bicarbonate/TCO2? |
|
Definition
loss of acid, usually renal or GI (vomit)
=alkalemia |
|
|
Term
| Decreased bicarbonate/TCO2 with a high anion gap could be the result of what three mechanisms? |
|
Definition
=acidosis
excessive acid generation (ketones, lactic acid)
toxicity (salicylic acids, ethylene glycol)
decreased renal excretion (uremic acidosis) |
|
|
Term
| Decreased bicarbonate/TCO2 with normal anion gab is secondary to what mechanism? |
|
Definition
| increased bicarbonate losses, usually GI (diarrhea) could also be renal |
|
|
Term
| What is the most common cause of a low anion gap? |
|
Definition
| hypoalbuminemia (albumin is the greatest negatively charged component of the blood) |
|
|
Term
| If the patient is acidotic but the anion gap is normal what is the likely cause of the acidemia? |
|
Definition
| loss of bicarbonate (GI-diarrhea or renal) |
|
|
Term
| If the patient is acidotic and the anion gap is elevated what is the likely cause of the acidemia? |
|
Definition
| accumulation of anionic acids (lactic, ketone, uremic, toxins) |
|
|
Term
| If sodium and chloride are changing disproportionately, and bicarbonate is elevated while chloride is decreased what kind of acid base disorder is occuring? The likely cause? |
|
Definition
=alkalosis
usually due to vomiting/upper GI stasis (loss/sequestration of fluid with high HCL content) |
|
|
Term
| If sodium and chloride are changing disproportionately, and bicarbonate is decreased while chloride is increased what kind of acid base disorder is occuring? The likely cause? |
|
Definition
=acidosis
need to evaluate anion gap -->
normal=GI/renal loss of bicarb
increased: keto/lactic/uremic/toxic |
|
|
Term
| If sodium and chloride are changing disproportionately, and bicarbonate and chloride are changine in the SAME direction what kind of acid base disorder is occuring? |
|
Definition
| Mixed <-- evaluate with blood gas |
|
|
Term
| What two substances affect intestinal absorption of calcium and phosphorus? |
|
Definition
Vitamin D (increases)
corticosteroids (decrease calcium absorption) |
|
|
Term
| How does the kideny handle filtered calcium and phosphorus? |
|
Definition
| reabsorbs most of the filtered calcium and phosphorus (exception=horses excrete a lot of calcium in the urine as calcium carbonate crystals) |
|
|
Term
| What three substances affect renal handling of calcium and phosphorus? |
|
Definition
Parathyroid hormone (increase calcium, decrease phosphorus)
Calcitonin (decrease calcium and phosphorus)
Vitamin D (increase calcium and phosphorus) |
|
|
Term
| How does parathyroid hormone respond to low serum calcium levels? |
|
Definition
| increases osteolysis, increases renal tubular reabsorption of calcium, increases formation of active form of Vit D --> increased calcium absorption for the GI tract |
|
|
Term
| How does parathyroid hormone affect serum phosphorus? |
|
Definition
| decreases serum phosphorus by decreasing renal tubular reabsorption |
|
|
Term
| Calcitonin is release in response to what abnormality in serum calcium? What is its mechanism of action |
|
Definition
| Calcitoning is released in response to high serum calcium levels --> inhibits osteolysis, inhibits formation of active Vit D (also inhibits renal reabsorption of phosphorus) --> decreased serum calicum and phosphorus |
|
|
Term
| What three things stimulate vitamin D activation? What is the major action of activated Vit D? |
|
Definition
PTH, low calcium, low phosphorus
activated Vit D increases intestinal absorption of calcium and phosphorus |
|
|
Term
| What is the mechanism of glucocorticoid mediated hypocalcemia? |
|
Definition
| glucocorticoids block intestinal vitamin D receptors --> net decrease in serum calcium and phosphorus |
|
|
Term
| T/F: serum of phosphorus is predominantly inorganic |
|
Definition
TRUE
most of the phosphorus in the body is organic and located intracellularly <-- not measured on serum chem |
|
|
Term
| How is ionized calcium (i.e. biologically active) affected by acidosis? |
|
Definition
| ionized calcium is increased by acidosis because H+ competes for calcium binding sites on proteins (i.e. albumin) |
|
|
Term
| What is the function of the protein-bound calcium? |
|
Definition
storage pool/emergency reserve
protein-bound calcium = 40-45% of total |
|
|
Term
| How are calcium and phosphorus levels different in younger animals? |
|
Definition
calcium and phosphorus are elevated, especially in large animals and large breed dogs due to active bone remodeling
*ALP is also elevated |
|
|
Term
| Which ion changes more consistently in disease states, calcium or phosphorus? |
|
Definition
| calcium, phosphorus is more likely to deviate from the expected pattern |
|
|
Term
| What is the most common cause of hypocalcemia in a dog? |
|
Definition
| hypoalbuminemia (protein bound clacium pool is 40-45% of total serum calcium) |
|
|
Term
| Other than hypoalbuminemia what is another possible cause of hypocalcemia with normophosphatemia in dogs and cats? |
|
Definition
acute pancreatitis with fat saponification
(phosphorous may be elevated if there is concurrent decreased GFR) |
|
|
Term
| What can be a cause of hypocalcemia in horses? |
|
Definition
colic (mediated by decreased intestinal absorption)
*phosphorus may be elevated if GFR is concurrently decreased |
|
|
Term
| What is the disease associated with hypocalcemia and hyperphosphatemia? |
|
Definition
hypoparathyroidism (secondary to lymphocytic parathyroiditis)
marked decrease in total and ionized calcium +/- elevated phosphorus (PTH normally promotes renal excretion of phosphorus)
+/- hypomagnesemia (Mg deficiency may inhibit release of PTH) |
|
|
Term
| What toxic susbstance can cause hypocalcemia and hyperphosphatemia? |
|
Definition
| ethylene glycol <-- calcium oxalate crystals chelate ionized calcium, initially hyperphosphatemia is secondary to high levels of phosphorus in anti-freeze, later it develops secondary to acute renal failure with decreased renal excretion of phosphorus |
|
|
Term
| What mechanism is associated with hypocalcemia and hypophosphatemia? |
|
Definition
decreased intestinal absorption secondary to malabsorptive GI disease (also panhypoprotinemia and hypocholesterolemia)
anorexia/ileus/colic in large animals |
|
|
Term
| What disease is associated with hypercalcemia and normo to hypophosphatemia? |
|
Definition
hyperparathyroidism (usually secondary to benign functional parathyroid tumor)
in addition to hypercalcemia (total and ionized) high levels of PTH and low phosphorus (PTH promotes renal excretiotion of phosphorus) <-- may be normal if concurrent decreased GFR |
|
|
Term
| What types of neoplasia can cause hypercalcemia of malignancy? |
|
Definition
| lymphosarcoma, apocrine anal sac adenocarcinoma, sometimes squmous cell carcinoma |
|
|
Term
| What are expected calcium and phosphorus abnormalities associated with hypoadrenocorticism? |
|
Definition
hypercalcemia (reduction in levels of corticosteroids promotes intestinal and renal absorption of calcium to protein bound pool <-- ionized calcium is unchanged)
hyperphosphatemia secondary to decreased GFR |
|
|
