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224 Cards in this Set
- Front
- Back
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what loss of liver finction is considered hepatic failure?
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75-80%
|
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what are two direct tests of liver function?
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1. bile acids
2. ammonia |
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what are five indirect tests of liver function?
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1. albumin
2. glucose 3. cholesterol 4. urea 5. coag (PT/PTT) |
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in which species is ALT liver-specific?
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dogs and cats
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which tissues produce AST as a leakage enzyme?
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liver and muscle
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which liver-specific enzyme is good for ruminants and horses?
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SDH
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which enzymes are increased with muscle injury?
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CK and AST
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what are the four isoforms of ALP and comment on species specificity?
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1. liver (L-ALP): made by liver
2. Bone (B-ALP): made by bone 3. Corticosteriod (C-ALP): Dog only; made by liver 4. Mammary: less important |
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which tissues make GGT?
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- liver and biliary epithelium
- also in milk and urine, but not in blood |
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which liver enzymes are indicative of cholestasis?
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L-ALP and GGT
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schematically describe the process of forming bilirubin and transport to liver
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1. HGB → heme + globin
2. heme → bilirubin + iron 3. bilirubin + albumin → liver |
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where in the liver is bilirubin secreted?
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canaliculi and biliary tract
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describe the process that makes urine yellow
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1. HGB/albumin in liver → conjugated bilirubin
2. conjugated bilirubin → biliary system → small instestine 3. conjugated bilirubin + bacteria → urobilinogen → portan vein → liver → blood → kidney 4. urobilinogen → urobilin (yellow) |
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what causes pre-hepatic hyperbilirubinemia?
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hemolysis (IVH and or EVH)
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what is the difference between direct and indirect bilirubin?
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- direct: conjugated and water soluble
- indirect: insoluble, so bound to albumin |
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what indicator of bilirubin do you see first with hemolysis?
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hyperbilirubinemia; indirect bilirubin must be conjugated before you see bilirubinuria
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what blood chemistry indicator do you see with IVH that you don't see with EVH?
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hemoglobinemia
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what UA indicator do you see with IVH that you don't see with EVH?
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hemoglobinuria
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what three basic disease processes cause hepatic and/or post-hepatic hyperbilirubinemia?
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1. decreased uptake of indirect bilirubin (hepatic)
2. decreased conjugation of indirect bilirubin (hepatic) 3. decreased excretion of conjugated bilirubin (hepatic and post-hepatic) |
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which liver induction enzymes usually accompany hyperbilirubinemia?
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ALP and GGT
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what two things are indicative of functional cholestasis?
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1. hyperbilirubinemia
2. INFLAMMATORY LEUKOGRAM |
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what non-pathologic process can cause hyperbilirubinemia in horses?
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anorexia (note: no elevation in liver enzymes)
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what molecule are bile acids made from?
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cholesterol
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what percentage of bile acids are reabsorbed from the GI tract?
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95%
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what three basic processes cause increased bile acids?
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1. altered blood flow (e.g. PSS)
2. decreased haptic function (direct liver function test) 3. biliary obstruction (cholestasis) |
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why are bile acid tests not indicated for obstructive cholestasis?
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because you will have hyperbilirubinemia, which tells you the same thing
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in which situation will you see increased bile acids, but not hyperbilirubinemia?
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PSS
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why does chronic liver disease cause an INCREASE in bile acids, rather than a decrease?
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because the lack of hepatic cells to re-uptake the bile acids are not present and you will get bile acid spillover into the blood
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what is the range of the following enzymes in the dog and cat that indicate pancreatic acinar cell damage?
- amylase - lipase |
- amylase: dog WRI > 10-fold; cats WRI < 3-fold
- lipase: dog WRI > 10-fold; cats WRI < 4-fold |
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what are two things that cause increased amylase?
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1. pancreatic acinar cell damage
2. decreased renal clearance |
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what are five things that cause increased amylase?
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1. pancreatic acinar cell damage
2. decreased renal clearance 3. pancreatic neoplasia 4. dexamethasone 5. widespread steatitis |
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what two things cause an INCREASE of TLI?
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1. pancreatic acinar cell damage
2. decreased renal clearance |
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what two things cause a DECREASE of TLI?
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1. EPI
2. > 90% reduction of acinar cells |
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what must cPLT/fPLI levels be to rule out decreased renal clearance as the sole cause?
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> 200 μg/L
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what causes decreased cPLI/fPLI?
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EPI
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what causes a decrease of Spec cPLI?
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nothing
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what are the thresholds of Spec cPLI for pancreatitis?
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- negative ≤ 200 μg/L
- grey zone: 201-399 μg/L - positive: ≥ 400 μg/L |
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what is the most sensitive and specific test for pancreatitis in the dog and cat?
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dog: cPLI; cat: fPLI
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what disease has the same clin path profile as pancreatitis?
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pancreatic adenocarcinoma
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how many pancreatic acinar cells are typically lost to cause maldigestion?
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> 90%
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what are three causes of a loss of panancreatic acinar cells?
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1. atrophy
2. chronic pancreatitis 3. dudonal resection |
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EPI:
- predisposed breed - clinical signs |
- German Shepherd
- weight loss, increased appetite, flatulance, loose stool, statorrhea |
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what are four tests to screen for EPI?
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1. TLI
2. PLI 3. cobalamin and folate 4. plasma turbidity test |
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what is the normal leukocyte density in a 10x field?
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18-52
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what percentage of Heinz bodies in cat blood is normal?
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5-10%
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on a 100x field, 1 platelet equals what concentration?
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15,000 / μL
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what is a normal platelet count for a dog at 100x field?
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10-25
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what tube type and color do you use for coagulation studies?
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citrate; blue top
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name the four tube types and corresponding septa colors?
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- red: serum (nothing added)
- green: heparin - blue: citrate (coagulation studies) - lavender: EDTA |
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how do you visulalize reticulocytes on a blood smear?
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incubate in NMB
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what must be in your tube when collecting blood to measure fibrinogen?
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antocoagulant
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what is the best way to dry a blood smear to minimize artifacts?
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air-dry quickly prior to staining
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if your blood smear comes out too thick, how do you spread it out more thinly on another blood smear?
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decrease the angle
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what is the appropriate method to dry a blood smear stained with Diff-Quik?
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air dry
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what is the correct method to incubate blood with NMB?
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1:1 = blood:NMB; incubate 15 minutes
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for stained specimens, where should the condenser be located?
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directly under the slide
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which species have prominent RBC central pallor?
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dog
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which species does not release reticulocytes into the blood?
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horse
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which species (cow, horse, goat, dog, cat) has the smallest RBC size?
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goat
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in which species is mild RBC anisocytosis normal?
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cow (bovine)
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in the cat, which type of reticulocytes should be counted and which should be skippped?
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count aggregate; skip punctate
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RBCs stacked like coins are what? What causes this?
|
Rouleaux; excess plasma proteins
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if lekuocytes appear at the feathered edge, how does this affect your leukocyte estimation at 10x?
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artificially decreased
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which species has elliptical RBCs?
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llama
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which species normally has nRBCs?
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avian spp.
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which leukocyte is large, hard to find, lobulated-to-oval nucleus, with blue-gray cytoplasm and round vacuoles?
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monocyte
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which granulocyte has a lobulated nucleus and bright pink to red cytoplasmic granules?
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eosinophil
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which is the primary lekuocyte in horses?
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neutrophil
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which granulocyte has a lobulated nucleus and has dark purple cytoplasmic granules?
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basophil
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which leukocyte has a round, dark purple nucleus with clumped chromatin?
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lymphocyte
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what is the primary leukocyte type in cattle?
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lymphocyte
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if there are 3 platelets per field at 100x, what is the estimated count?
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45000
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what is the lifespan of an erythrocyte?
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70-160 days (note dogs > cat)
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how long does it take to see new RBCs after EPO release from the renal cortex?
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2-3 days
|
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why are iron deficient RBCs microcytic?
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the rubricytes undergo an extra, 5th division
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what do you call a circulating reticulocyte that is stained with Diff-Quik?
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hypochromatocyte
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what are three things that can cause an elevated MCHC?
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1. intravascular hemolysis
2. poor sample handling (in vitro hemolysis) 3. Heinz Bodies |
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how long from stem cell to mature RBC?
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2-5 days
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long does it take myeloid stem cells to proliferate?
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2-5 days
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how long does it take to see a full regenerative response to anemia?
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7-10 days
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how long after bleeding resolves does it take for reticulocytes to return to normal?
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1-2 weeks
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what are five signs of a regenerative anemia?
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1. macrocytosis (assuming many retics)
2. hypochromia (assuming many retics) 3. reticulocytosis 4. hypercellular bone marrow 5. metarubricytes (nRBCs) |
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what is the fancy name for a nucleated red blood cell?
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metarubricyte
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what type of poikilocyte do you see with iron deficiency?
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keratocytes, schistocytes, acanthocytes, microcytes
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why does epinephrine release cause lymphocytosis?
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because it stops circulating lymphocytes from getting into the lymph node
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what type of reticulocytes are counted and not counted in the cat when diagnosing regenerative anemia? Why?
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- aggregate - counted
- punctate - not counted - aggregate are 12-24 hours in the circulation and are indicative of regeneration; punctate have been 10-14 days in the circulation |
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what are seven causes of inappropriate metarubricytosis?
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1. severe hypoxia
2. lead toxicity (uncommon) 3. bone fractures 4. heat stroke 5. leukemia/infiltrative bone marrow disease 6. splenic disease or injury 7. marked extramedullary hematopoiesis |
|
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what two chemicals are made by the body to adapt to chronic blood loss?
|
1. EPO
2. 2,3-DPG |
|
|
what are three differentials for chronic GI hemorrhage?
|
1. parasites
2. neoplasia 3. ulcers |
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how does iron deficiency affect
- plasma protein? - platelet count? (why?) |
- panhypoproteinemia
- thrombocytOSIS (due to cytokine release) |
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what are the end products of hemoglobin that has been phagocytized?
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- hemoglobin → heme + globin
- globin → amino acids - heme → iron + bilirubin |
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how is unconjugated bilirubin made to be soluble?
|
bound to albumin
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where do the majority of the macrophages that phagocytose RBCs reside?
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in the SINUSOIDS of the spleen (not the BVs)
|
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what are three lab findings that suggest INTRAvascular hemolysis, rather than extravascular hemolysis?
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1. hemoglobinemia
2. hemoglobinuria 3. ghost cells |
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how do you test for autoimmune hemolytic anemia?
|
1. direct antiglobulin test
2. visualize autoagglutination on a slide |
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how will autoagglutination affect your CBC?
|
artificially ↓RBC and ↑MCV
|
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what are two specific RBC changes with oxidative damage and why do these changes occur?
|
1. Heinz Bodies - damage to hemoglobin
2. eccentrocytes - oxidative damage to the RBC cell membrane |
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how can oxidative damage cause intravascular hemolysis?
|
Heinz bodies weaken the RBC membrane, which may lyse in circulation, producing hemoglobinemia and ghost cells
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why is hemoglobinemia bad, other than it may be concurrent with anemia?
|
it damages renal tubules (horse >> dog, cat)
|
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what liver protein binds to free hemoglobin to scavenge it?
|
haptoglobin
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what is the difference between indirect and direct hyperbilirubinemia.
|
- Indirect: IVH → bilirubin in blood exceeds liver capacity; since the bilirubin is not conjugated and is albumin-bound, no bilirubinuria
- Direct: formation of conjugated bilirubin in liver → liver can't dump it into bile fast enough, so it spills into blood; bilirubinuria will occur |
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what are the four general causes of decreased RBC production?
|
1. anemia of chronic disease (most common)
2. renal failure (↓EPO) 3. generalized bone marrow disease (infiltrated by neoplasia, infection, fibrosis) 4. erythroid hypoplasia or aplasia |
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what are four causes of erythroid hypoplasia or aplasia?
|
1. destruction and/or apoptosis of RBC progenitors
2. chronic, late iron deficiency 3. endocrine disorders (hypothyroidism) 4. cobalamin or folate deficiency |
|
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how many functional nephrons are lost in CRF?
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> 75%
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what is the USG rang for isosthenuria?
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1.001 - 1.012
|
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what is the upper normal limit of USG for the
- dog? - cat? - horse, cow? |
- dog: 1.030
- cat: 1.035 - horse, cow: 1.025 |
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what protein is made to sequester iron in anemia of chronic disease? Where is it produced, and what stimulates its production?
|
hepcidin. Produced by the liver in response to inflammatory cytokines (IL-6 and others)
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what is a cause of primary absolute erythrocytosis?
|
polycythemia vera
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what causes secondary absolute erythrocytosis?
|
increased EPO. Appropriate from low oxygen (respiratory disease or high elevation); inappropriate from an EPO secreting tumor
|
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what are two causes of relative erythrocytosis?
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1. dehydration / hemoconcentration
2. splenic contraction (e.g. epinephrine release) |
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what is the preferred technique for a WBC differential?
|
manual
|
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what is the chemical mediator of a physiologic neutrophilia?
|
epinephrine (excitement)
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describe a physiologic ('excitement") CBC
|
- neutrophilia (no left shift)
- lymphocytosis - erythrocytosis - thrombocytosis |
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how long does physiologic/excitement neutrophilia last?
|
about 20 minutes
|
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describe a stress leukogram
|
- leukocytosis
- neutrophilia (± clinically insignificant left shift) - lymphopenia - monocytosis - ± eosinopenia |
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what are three causes for excess circulating corticosteroids and thus a stress leukogram?
|
1. severe physical or emotional stress
2. Hyper-A 3. Iatrogenic (e.g. prednisone) |
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what causes neutrophilia in a stress/corticosteroid leukogram?
|
1. ↓margination
2. ↑bone marrow release 3. ↓emigration to the tissue neutrophil pool |
|
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what comprises the neutrophil proliferation pool?
|
1. stem cells
2. myeloblast 3. progranulocyte 4. myelocytes |
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what comprises the neutrophil storage pool?
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1. metamyelocytes
2. bands 3. segs |
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how long does a neutrophil circulate in the blood?
|
10 hours
|
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how long does a neutrophil survive in the tissues?
|
2 days
|
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hypersegmented neutrophils are usually related to what?
|
cortisol (stress neutrophilia)
|
|
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how long does a stress neutrophilia last?
|
hours to days
|
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what is the normal ratio of marginal:circulating neutrophils?
|
- 1:1 in most animals
- 1:3 in cats |
|
|
how long from myeloid stem cell to:
- storage pool? - blood? |
- 2.5 days (five cell divisions in the proliferation pool)
- 5 days (proliferation pool → storage pool; no divisions in the storage pool) |
|
|
describe an acute inflammatory leukogram?
|
- note "acute" refers to inflammatory type, not time of insult
- neutrophilia - orderly left shift (bands > reference range; ± metamyelocytes) - ± lymphopenia (stress most likely reason) |
|
|
what cytokine stimulates the neutrophil proliferation pool
|
GM-CSF, secreted by T cells
|
|
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how long must inflammation persist before you start seeing myeloid hyperplasia?
|
> 2 days
|
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what is the difference between neutrophil toxic and degenerative change?
|
- toxic = cytoplasm change
- degenerative = nuclear change |
|
|
how do you interpret neutrophil toxic change without a neutrophilia or left-shift
|
inflammation
|
|
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what are four changes in neutrophil appearance?
|
1. Döhle bodies
2. cytoplasmic basophilia 3. cytoplasmic foamy vacuolization 4. retention of primary granules |
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what is a degenerative left shift?
|
bands > segs
|
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what neutrophil changes would you see with very severe inflammation?
|
1. degenerative left shift
2. leukemoid response 3. neutropenia (inflammatory; bone marrow disease; transient--endotoxemia) |
|
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how many neutrophils would you see in a leukemoid response?
|
> 50,000 (in the dog)
|
|
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what are three important types of neutropenia?
|
1. inflammatory - excessive tissue demand
2. endotoxemia - sequestration (margination) 3. decreased production (bone marrow) |
|
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what three effects on neutrophils does endotoxemia have?
|
1. ↑ neutrophil production
2. ↑ bone marrow release of neutrophils 3. ↑ tissue demand |
|
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decreased neutrophil production by bone marrow is called what?
|
myeloid hypoplasia / granulocytic hypoplasia
|
|
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what are five differentials for myeloid hypoplasia?
|
1. infection (e.g. parvovirus)
2. primary or metastatic bone neoplasia 3. toxicosis 4. necrosis 5. myelofibrosis |
|
|
what is myelophthisis?
|
bone marrow infiltrated and crowded out by neoplasia, fibrosis, etc.
|
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what is the lifespan of a platelet?
|
5-7 days
|
|
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what is a major difference between the leukogram of a small animal versus a ruminant?
|
lymphocytes > neutrophils 1:1 - 2:1
|
|
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why might you see neutropenia and a left shift in a ruminant with severe acute inflammation?
|
because they have a small neutrophil storage pool
|
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what can happen to the leukogram of a ruminant that has inflammation and stress?
|
N:L inversion (N > L)
|
|
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in a ruminant with an acute inflammatory neutropenia, how long would you expect a recovery of neutrophils if all is well?
|
4 days
|
|
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what are the major (-) and (+) acute phase proteins?
|
- (+) fibrinogen, globulin
- (-) albumin |
|
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what is a useful blood chemistry measurement to determine if inflammation or dehydration is present in a ruminant?
|
PP:fibrinogen ratio
|
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when is using the PP:fibrinogen ratio appropriate when evaluating the blood chemistry of a ruminant?
|
when they have HYPERfibrinogenemia
|
|
|
what are 2 causes for hyperfibrinogenemia?
|
1. dehydration (relative increase)
2. inflammation (absolute; positive APP) |
|
|
what four places produce lymphocytes?
|
1. lymph nodes
2. thymus 3. spleen 4. GALT |
|
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what are four causes of lymphopenia?
|
1. glucocorticoids (stress)
2. acute inflammation 3. loss or blocked flow of lymph (ruptured thoracic duct/PLE) 4. lymphoid hypoplasia/aplasia (congenital or acquired) |
|
|
why does stress produce a lymphopenia?
|
- glucocorticoids
1. lymphocytes trapped in the lymph nodes 2. redistribution to lymphocytes to bone marrow 3. chronic stress: lymphoid hypoplasia → ↓lymphopoiesis |
|
|
why does acute inflammation produce lymphopenia?
|
- cortisol
1. lymphocytes to inflamed tissue 2. lymphocytes to lymph node 3. lymphocytes stay in lymph node |
|
|
what are four causes of lymphocytosis?
|
1. chronic inflammation or antigenic stimulation
2. physiologic (epinephrine) 3. neoplasia 4. Hypo-A (mild; due to ↓glucocorticoids) |
|
|
what are three causes of monocytosis?
|
1. stress (cortisol; demargination)
2. inflammation (tissue demand for neutrophils) 3. compensatory to neutropenia ("the B team") |
|
|
how long do monocytes circulate in the blood?
|
10-12 hours
|
|
|
how long do eosinophils circulate in the blood?
|
10 hours
|
|
|
how long do eosinophils live in tissue?
|
> 2 days
|
|
|
what is the difference in the CBC between acute leukemia and chronic leukemia?
|
acute leukemia has many blast cells, where chronic leukemia has small cells that may look identical to non-neoplastic lymphocytes
|
|
|
what is the appearance of lymphoma on a lymph node biopsy?
|
mostly lymphoblasts; normal should be >90% small lymphocytes
|
|
|
what are the common locations for plasma cell tumors?
|
- cutaneous (usually benign)
- bone marrow - spleen |
|
|
number of platelets for
- spontaneous bleeding - induced bleeding |
- spontaneous: < 25,000
- induced: < 50,000 |
|
|
what are the factors for the intrinsic system?
|
12, 11, 9, 8
|
|
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what are the factors for the extrinsic system
|
7, 3
|
|
|
when does a prolonged ACT test not caused by a coagulation defect?
|
with severe (< 10,000) thrombocytopenia
|
|
|
what system does the ACT test?
|
intrinsic & common
|
|
|
what system does the PTT test?
|
intrinsic & common
|
|
|
what system does the PT test?
|
extrinsic & common
|
|
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what does a prolonged TT test indicate?
|
hypofibrinogenemia or excessive FDPs
|
|
|
what is a normal platelet range at 100X?
|
10-25
|
|
|
how do thrombopoietin (TPO) and platelet count relate?
|
- TPO adsorbs to platelet surface
- fewer platelets = more free TPO - more platelets = less free TPO - free TPO → megakaryocytic hyperplasia |
|
|
what are the four general causes of thrombocytopenia?
|
1. peripheral destruction
2. decreased production 3. consumption 4. sequestration (e.g. in spleen) |
|
|
what are three differentials for immune-mediated thrombocytopenia?
|
1. tick-borne diseases (e.g. A. phagocytophilum, E. canis, RMSF, Babesia, Bartonella)
2. drug reactions 3. paraneoplastic |
|
|
what are two major causes of consumption of platelets?
|
1. DIC (severe thrombocytopenia)
2. blood loss (mild to rarely moderate) |
|
|
what are four causes of acquires thrombopathia?
|
1. uremia
2. drugs (aspirin, NSAIDs) 3. hetastarch 4. supplements (e.g. ω-3 FA) |
|
|
what are four differentials for thrombocytosis?
|
1. excitement
2. chronic bleeding/iron deficiency 3. inflammation (IL-6) 4. essential thrombocytopenia (> 1+ million) |
|
|
describe two major coagulation abnormalities of the intrinsic pathway
|
- Hemophilia A - Factor 8 - x-linked
- Hemophilia B - Factor 9 - x-linked |
|
|
what is the most common extrinsic pathway inherited defect, and what breed is predisposed?
|
Factor 7 deficiency, reported in beagles
|
|
|
what are the three big differentials for a prolonged PT and PTT?
|
1. Vitamin K antagonism
2. hepatic failure 3. DIC |
|
|
what factors are dependent on Vitamin K?
|
2, 7, 9, 10
|
|
|
in early warfarin toxicosis, what test will indicate it first and why?
|
prolonged PT because factor 7 has the shortest half-life of all of the other factors
|
|
|
what are five indirect measures of liver function?
|
1. BUN
2. glucose 3. albumin 4. cholesterol 5. coagulation factors |
|
|
which coagulation factor is not produced by the liver?
|
8
|
|
|
what RBC abnormality will you commonly see with DIC?
|
schistocytes
|
|
|
which in vitro anticoagulant (tube top color) is used for
- CBCs? - coagulation testing? - chemistry panels |
- CBC: EDTA (purple top)
- coagulation: citrate (blue top) - chemistry: heparin (green top); or you can use red top |
|
|
what does heparin inhibit?
|
thrombin and 10a
|
|
|
what are three in vivo anticoagulants?
|
1. AT (ATIII)
2. Protein C 3. Protein S |
|
|
what does antithrombin inhibit?
|
thrombin (2a), 9a, 10a
|
|
|
why can protein-losing nephropathy cause a pro-coagulant state?
|
because antithrombin, being similar in size to albumin, is lost in the urine
|
|
|
what compound cleaves fibrin, fibrinogen, and cross-linked fibrin?
|
plasmin
|
|
|
what is the difference between plasma and serum?
|
plasma has fibrinogen, due to anticoagulants; serum is clotted, and has no fibrinogen.
|
|
|
what are four differentials for increased loss of albumin?
|
1. blood loss
2. renal loss 3. PLE 4. inflammatory exudate |
|
|
what are three differentials for decreased production of albumin?
|
1. hepatic failure
2. inflammation (negative APP) 3. severe malnutrition |
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what are two differentials for hypoglobulinemia in a foal?
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1. FPT
2. combined immunodeficiency |
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how do you differentiate coagulation from rouleaux?
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saline dispersion test
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what is a "Pelger Huet Anomaly"
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defect in Australian Shepherds and other dogs, where all granulocytes have ‘band’ or non-segmented nuclei with mature dark chromatin because they cannot normally segment
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what species normally have calcium carbonate crystals in their urine?
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horse, guinea pig, rabbit
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"coffin lid" shaped crystals in the urine are what?
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triple phosphate / struvite
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hexagonally shaped crystals in the urine are what?
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cystine (abonormal)
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what happens to cobalimin and folate in EPI?
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↓cobalimin; ↑folate
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what happens to cobalimin and folate in SIBO?
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↓cobalimin; ↑folate
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how do you differentiate malabsorption from maldigestion in a plasma turbidity test?
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add enzymes; malabsorption will not cause plasma turbidity, whereas maldigestion will show turbid plasma after 2-3 hours
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describe folate and colbalimin levels with:
- duodenal malabsorption - ileal malabsorption |
- duodenal: low folate, normal cobalimin
- ileal: normal folate, low cobalimin |
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what is required for cobalimin absorption? Where is cobalimin abosorbed?
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- intrinsic factor
- absorbed in the ileum |
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which transporters are insulin sensitive?
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GLUT-4
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what is the affect on blood glucose and plasma lipids of:
- insulin? - glucagon? - cortisol? - GH? - epinephrine? - thyroxine? |
- insulin: ↓glucose, ↓plasma lipids
- glucagon: ↑glocose, ↑plasma lipids - cortisol: ↑glucose, ↑plasma lipids - GH: ↑glucose, ↓plasma lipids - epinephrine: ↑glucose, ↓plasma lipids - thyroxine: no affect on glucose, ↑plasma lipids |
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what are two advanced tests to diagnose long periods of hyperglycemia? What is the t1/2 of these compounds?
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- fructosamine: 2-3 weeks
- gHGB: 2-3 months |
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which non-weird animal that we have studied (e.g. no guniea pigs) does not utilize vitamin D to absorb calcium?
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horse
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what percentage of normal blood calcium is:
- free calcium - protein-bound - non-protein-bound |
- free: 50%
- protein-bound: 40% (albumin >>>> globulins) - non-protein-bound: 10% |
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which anticoagulant do you use to prepare blood samples for calcium measurement and why?
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heparin, because EDTA and citrate will bind calcium and screw up your test
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how does acidosis and alkalosis affect fCa?
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- acidosis ↑ fCa
- alkalosis ↓ fCa - in acid, H+ ions will compete for slots on the albumin to bind, so more calcium will be free; in base, less H+ is bound to albumin, so more is bound up and fCa will decrease |
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what is the net affect on calcium and phosphorous by inceasing:
- Vitamin D? - PTH? - calcitonin? - PTHrp? |
- ↑ Vitamin D leads to ↑Ca and ↑P (increases intestinal absorption)
- PTH leads to ↑Ca and ↓P (increases renal excretion) - ↑Calcitonin leads to ↓Ca and ↓P (↑kidney excretion and ↑ bone resorption of both) - PTHrp (from neoplasias) leads to ↑Ca and ↓P (increases renal excretion) |
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how do you differentiate milk fever from gras tetany?
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- milk fever: ↓Ca and ↑Mg
- grass tetany: ↓Ca and ↓Mg |
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why does lush grass cause hypomagnesemia? (grass tetany)
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because high K+ in the grass prevents Mg2+ aborsption in the gut
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what clin path chagnes are associated with hyperthyroidism?
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- ± erythrocytosis
- increased ALT, ALP (mild) |
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what are two clin path chagnes associated with hypothyroidism?
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1. anemia (ACD)
2. hypercholesterolemia |
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what is the most common cause of hypothyroidism?
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autoimmune thyroiditis
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what happens to TSH levels in the hypothyroid patient?
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they increase, and TRH increases as well
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what % thyroid hormone is protein-bound?
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99%
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what are two interpretations of a ↓ total T4?
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1. hypothyroidism
2. euthyroid sick |
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what are four causes of non-thyroidal illness and ↓tT4?
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1. concurrent illness
2. hypoalbuminemia 3. age (older dogs) 4. drug administration (many: glucocorticoids, phenobarb, sulfonamides, NSAIDs) |
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when is serum T3 or free T3 indicated?
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it is not
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what is the highest sensitivity and specificity test for true hypothyroidism?
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Free T4
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what is the gold standard test for autoimmune thyroiditis?
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TSH stimulation test
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what test, to evaluate a hyperthyroid cat, is not really done in reality? How does it work?
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T3 suppression test. Suppresses TRH and TSH, thus lowering T4 levels in euthyroid cats, but not affecting T4 levels in hyperthyroid cats.
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