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158 Cards in this Set
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- Back
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Define Hemostasis |
1. Formation and dissolution of thrombi (blood clots) 2. Maintain the fluid state of blood when the vessels are healthy |
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What are the major players of hemostasis? |
1. Platelets (forming a primary then secondary plug) 2. Coagulation (leading to secondary plug) 3. Vessels (leading to secondary plug) 4. Fibrinolysis (after coagulation and secondary plug) *All happening at cell surfaces, simultaneously |
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What are the players in the formation of the primary hemostatic platelet plug? |
1. Endothelium 2. Platelets 3. vWF (protein from endothelial cells and megakaryocytes/platelets) 4. Fibrinogen (from the liver) |
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What are the steps in the formation of the primary platelet plug? |
1. Collagen in the subendothelial Connective tissue is exposed in injury 2. vWF binds to collagen, changing vWF and leading to platelet activation 3. Platelet surface now open for coagulation enzyme binding 4. Platelets then recruit more platelets 5. Thrombin and collagen activates more platelets 6. Fibrinogen binding site open for platelet bridging and aggregation |
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What are the two things that must be present in order for you to have proper primary hemostasis? How can you test for each thing? |
1. Proper concentration of coagulation players- test by getting blood analyzed and by looking at smear (for clumps and/or fragments of platelets) 2. Proper function of coagulation players- test by doing Buccal mucosal bleeding time test *understand that this is INDEPENDENT from the coagulation cascade! |
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What occurs during secondary hemostasis? |
The use of coagulation enzymes to make fibrin and stabilize the primary platelet plug formed (making a secondary plug) *The coagulation factors are made in the liver and circulate as zymogens |
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What is special about factor V and VIII in the coagulation cascade? |
These are nonenzymatic factors, the activation of thrombin leads to a markedly increased activity of these factors. |
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Describe the in vitro coagulation cascade. What is the importance of Ca? |
1. Exposure of collagen = Intrinsic and common pathway Intrinsic -> 12,11,9,8 Common -> 10,5,2,1 (2=thrombin, 1=fibrin) *increase in 2 leads to an increase in 9,8 and 5 = more thrombin 2. Exposure of 3 (tissue factor) = Extrinsic pathway Extrinsic = 7,3 Certain steps have to have Ca present. Without Ca, leads to decreased clotting *animal will die of hypocalcemia before any changes in clotting is seen |
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How do many anticoagulants work in the coagulation cascade? |
They are Ca binding, leading to decreased clotting |
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What is the difference between the in vitro coagulation cascade and the in vivo cascade? |
In the in vitro assays, the TF activation of 9 is not recognized (alternate pathway) 1. In the TF-bearing cell, low thrombin produced 2. Activated platelets of 5,8 and 11 provide a surface for large amounts of thrombin to be formed |
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When taking a sample intended for secondary hemostasis testing, what important things must you keep in mind? |
1. need a clean venipuncture so no TF is exposed 2. Separate the plasma right away 3. Refrigerate up to 24 hours 4. When using a blue top tube (containing trisodium citrate), this is a Ca binder so you get no clotting. However, you must fill the tube all of the way. Underfilling the tube tends to increase clotting times. |
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What tests are available to test the intrinsic and the common pathways of coagulation? |
Activated clotting time- (ACT)- not as sensitive but can be run right at patient side Partial thromboplastin time- (PTT)- must add PL, Ca to run with an activator of FXII *both measure fibrin formation |
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What tests are available to test the extrinsic and the common pathways of coagulation? |
Prothrombin time (PT)- must add PL and Ca with a source of TF *FVII would be the first to change, due to its shortest half-life |
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What tests are available to test for functional fibrinogen? |
Thrombin Time (TT)- add in thrombin and Ca, measures fibrin formation *fibrinogen measurement on a CBC is not sensitive enough to tell you if there is really a hypofibrinogenemia |
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What is the one physiologic inhibitor of coagulation that we can actually test for? How does it work? What are the ways you can have disorders that are linked to this inhibitor? |
ATIII (antithrombin III) is made by the liver AT + Thrombin -> complexes filtered in the liver *requires heparin or heparin-like structures to bind the complexes Increased consumption from increased activation of coagulation, decreased production from liver failure, loss due to renal disease or certain protein losing enteropathies |
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What are the molecules responsible for fibrinolysis in the body? |
FDPs and D-dimers- breakdown products D-dimers are just cross-linked FDPs, requiring thrombin |
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What are the two general categories of hemostatic disorders? |
1. Thrombotic disease (due to increase production or decrease removal of thrombi) 2. Bleeding disorder (due to decreased formation or increased removal of thrombi) |
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What are the general categories of bleeding disorders? Are they most commonly congenital or acquired? |
Decreased vascular integrity, decreased platelet and vWF concentration and/or function, decreased coagulation factors or increased fibrinolysis Acquired is most common |
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What kind of clinical scenarios should you consider a bleeding abnormality in? |
Uncontrolled or excessive hemorrhage No explainable disease process that would lead to bleeding Widespread, multi-site hemorrhage |
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What are some of the clinical signs associated with a primary bleeding disorder? Secondary? |
Primary- bleeding from mucosal surfaces, hyphema (bleeding from the eye), petecchia, ecchymoses *petecchia and ecchymoses NOT seen with a vWF disorder Secondary- bruising, bleeding into body cavities and joints |
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Describe the pathogenesis of a bleeding disorder leading to hyperproteinemia |
1. Inflammation leads to the increased production of globulins (ex. fibrinogen) 2. Dehydration leads to fluid loss, leading to hemoconcentration |
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At what platelet amount would you expect to see spontaneous bleeding? |
25-30,000 (unless further complicated by other clotting disorder, then it would be more) |
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What are the general categories of causes of thrombocytopenia? |
Decreased production of megakaryocytes in the bone marrow Increased loss, consumption, destruction or redistribution (or could be pseudothrombocytopenia if platelet clumping was seen on a smear) |
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Describe the pathogenesis of thrombocytopenia caused by redistribution |
Any disease that causes splenomegaly and causes an increase in the size of the spleen leads to increased trapping and redistribution of the platelets into the spleen *this is NEVER a cause of severe thrombocytopenia on its own |
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How would you diagnose a thrombocytopenia caused by decreased production? What would you see on a CBC/diagnostic test to support this? |
Diagnose it with a bone marrow aspirate or biopsy Look at the biopsy- platelets larger than RBCs or an increase in mean platelet volume (on CBC) would support a rushed production and an increase in immature platelets |
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What are the two ways thrombocytopenia can be caused increased production? |
*usually associated with a SEVERE thrombocytopenia Immune mediated- either primary (idiopathic) or secondary (from drug, infection or neoplasia) Infections |
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Increased consumption of platelets causing thrombocytopenia is often associated with what other disease? |
Often affects multiple organ systems (as seen in DIC) *look for other abnormalities in other tests |
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When would you use a buccal mucosal bleeding test? |
When you have a suspected coagulation disease but you don't have a significant thrombocytopenia (will be prolonged with platelet defect or vWF defect) |
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What are the causes of thrombocytosis? |
(check for ghost cells or fragments, this can falsely increase the thrombocytes) If it is reactive- it can be responding to epinephrine or exercise (causing redistribution) or it can be increasing the production (from inflammation or anemia) *could also be a neoplasm |
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If the clotting time is hereditary, how many clotting factors would you expect to be prolonged? If it was acquired? |
Hereditary- 1 factor affected Acquired- more than one factor |
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What are all of the ways that you can get an acquired increase in clotting times? |
1. Vitamin K antagonism/deficiency 2. Hepatic disease (decreased functional mass) 3. Increased consumption by overwhelming clotting (DIC) 4. Circulating inhibitor (toxin or drug) |
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What are the different hereditary clotting factor deficiencies? Which ones cause clinical disease? |
Deficiency of 12- most common in cats, subclinical Deficiency of 11 or 7- subclinical or mild, not detected until it is challenged *Deficiency of 7 = hemophilia Deficiency of 9,8,10,5,2,1 - spontaneous bleeding *formation of 9/8 complex is critical! |
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Describe the pathogenesis behind vitamin K antagonism leading to increased clotting times |
Vitamin K hydroquinone is required for the carboxylation of clotting factors 2,7,9 and 10 The carboxylation step is needed for Ca binding capabilities (to properly participate in clotting) Warfarin/Coumarin prevents the formation of vitamin K hydroquinone, leading to decreased carboxylation, increase in the number of inactive factors, leading to the decreased production of fibrin |
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What are the common CBC findings associated with rodenticide toxicity? |
Thrombocytopenia (due to increased consumption) Hyerfibrinogenemia (inflammation and decreased production) Increased FDPs (reason unknown) |
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Besides warfarin, what are the other causes of vitamin K antagonism? |
Coumarin (ingestion of moldy sweet clover) Cholestasis (decreased fat absorption leading to decreased vitamin K adsorption) Maldigestion/malabsorption leading to decreased absorption of vitamin K |
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What are the triggers seen with increased consumption of clotting factors (DIC) |
Widespread, uncontrolled activation of hemostatic pathways Endothelial damage Exposure of TF (most common)- destruction, sepsis or injury Inflammatory cytokines Circulating foreign debris |
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What clinical disorders can lead to DIC? |
Infection, tissue injury and neoplasia are the most common Heatstroke/fever Blood static disorders IMHA |
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What things do you need to have diagnosis of DIC? |
Clinical signs + at least 3 of the following Thrombocytopenia, Increased PT/APTT, Increased FDPs/D-dimers (due to increased fibrinolysis, hypofibrinogenemia, fragmentation of RBCs |
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What is the difference between an D-Dimer and an FDP? |
FDP- due to fibrinogen or fibrin, more global D-Dimer- cross-linked fibrin |
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When does hemostatic abnormalities as caused by liver disease usually manifest itself? |
It is common to have this problem but is subclinical until clotting is challenged/overwhelmed (DIC) With hepatic disease, you get increased clearance and decreased production of both pro and antithrombotic factors |
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How does liver disease contribute to an increased PT/PTT? |
Decreased hepatic function leads to decreased production of clotting factors Vitamin K antagonism can lead to cholestasis (from decreased fat absorption in the SI) Increased consumption from DIC |
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How does liver disease lead to hypofibrinogenemia? |
Decreased production from hepatocytes |
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An increase in FDPs and D-dimers is caused by hepatic disease in what pathophysiology? |
Decreased clearance from the hepatocytes DIC, leads to increased production |
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Liver disease leads to thrombocytopenia in what way? |
Portal hypertension -> splenomegaly -> increased sequestration Increased consumption in DIC |
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ATIII is decreased in liver disease. What causes this? |
Decreased production by the liver Increased consumption in DIC |
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BMBT would expect to be increased (with thrombocytopenia) in liver disease. Why? |
Increased FDPs impair platelet function, leading to an increased BMBT |
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Proteins are divided into what two general categories? Where are each of them made? |
Two groups- albumin and globulins (make up the oncotic pressure in vessels) The hepatocytes make albumin and globulins Lymphocytes and plasma cells make immunoglobulins |
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What is the difference between plasma and serum? |
Plasma has fibrinogen and clotting factors, serum does not have |
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What is the half-life of albumin/globulins What is the half-life of immunoglobulins? |
Albumin/globulins- 8 days (dogs), 3 weeks (cow, horse) Immunoglobulins- 1-4 weeks |
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Define Dysproteinemia What is the difference between selective and nonselective dysproteinemia? |
Dysproteinemia- abnormal concentrations of normal proteins or presence of abnormal proteins Selective- only some proteins affected Nonselective- all affected equally |
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Inflammation leads to what changes in the proteins in the body? |
Increase in + acute phase proteins (fibrinogen, haptoglobin, serum amyloid A, C-reactive protein) Decrease in - acute phase proteins (albumin) Delayed response proteins (immunoglobulins) |
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What CBC level marks inflammation on a large animal assay? |
Fibrinogen- *produced in hepatocytes with cytokines present |
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How do you measure pTP in a lab? |
Refractometer that is calibrated for protein Measures protein by bending light through the proteins. The more protein, the more light bending that happens. *Always confirm reading with a serum/plasma chem. test (blurret reaction)- more reliable than refractometry |
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What kind of things interfere with the pTP measurement on a refractometer? |
Lipids, glucose, urea and other solutes |
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What tests can you use to test for albumin? |
Bromecresol green dye- binds albumin Bromecresol purple- (careful of falsely low values in dogs) |
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What test method do you use to test for fibrinogen? |
Heat-precipitant method- estimates fibrinogen by taking the difference between refractometer pTP before and after precipitation at 56 degrees. *Good for measuring increases NOT for decreases |
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Serum protein electrophoresis measures what? |
Runs serum through an electrified gel and the different types of proteins will separate into bands. The darker the band, the bigger the peak will be. Albumin is the most negative and also the biggest peak. IgG will travel the least Fraction % of each is area under the curve *No fibrinogen peak because this is measured on serum |
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Where are the ways that protein losses happen? |
Physiologic catabolism Hemorrhage Renal Disease Intestinal disease Exudation |
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Hyperproteinemia is caused by what two things? What other blood abnormalities are seen with each thing? |
*All causes hyperglobulinemia 1. Hemoconcentration- also causes hyperalbuminemia 2. Protein synthesis (inflammatory diseases and lymphocyte neoplasia of plasma cells or lymphocytes) |
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Inflammation is associated with what changes in plasma levels? What causes these changes? |
Increase in pTP, TP, Globulins (alpha and gamma) Decrease or no change in albumin *changes in globulins happen in a few days *severity of changes depends on degree and duration of inflammation Inflammation releases cytokines, cytokines react at the liver to lead to these protein changes |
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What does a polyclonal gammopathy look like on SPE? what is an example of a disease that causes this condition? |
Polyclonal gammopathy is a widened peak of several different kinds of globulins (ex. a wide peak of Beta globulins seen from ehrlichiosis) Ehrlichiosis- leads to increased pTP, TP, globulins, decrease in albumin |
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B lymphocyte neoplasias lead to what type of gammopathy? |
One type of neoplastic clone produces a lot of one Ig molecule, causes a monoclonal gammopathy. *Some infectious diseases can also cause a monoclonal gammopathy but, when you see this look hard for a tumor |
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What are the different causes of hypoproteinemia in the body? |
1. Increased loss from vasculature (blood loss, protein losing enteropathy and nephropathy) 2. Decreased synthesis (hepatic insufficiency, malabsorption/maldigestion, cachexia) 3. Failure of passive transfer |
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What overall changes in protein do you expect to see with a protein losing enteropathy? |
Decrease in PTP, TP, albumin and globulin *Albumin predominates |
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What overall changes in protein do you expect to see with a protein losing nephropathy? |
Decrease in pTP, TP, albumin No change or increase in globulins |
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What overall changes in protein do you expect to see with hemoconcentration? |
Increase in pTP, TP, albumin and globulin |
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What overall changes in protein do you expect to see with failure of passive transfer? |
Decrease in pTP, TP, globulin No change in albumin |
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What is the one major cause of hyperalbunemia? |
Hemoconcentration (would also see an increase in TP and Hct) |
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What are the causes of hypoalbuminemia? |
Decreased synthesis (inflammation, hepatic insufficiency, malabsorption/digestion, cachexia Increased loss (blood loss, protein losing enteropathy or nephropathy) Hemodilution |
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what are the causes of Hyperglobulinemia? |
Same reasons as a hyperproteinemia- inflammation, Hemoconcentration, B lymphocyte tumors |
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What are the causes of hypoglobulinemia? |
Decreased production, increased loss, failure of passive transfer *may also be seen with normoproteinemia |
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What are the causes of hyperfibrinogenemia? |
Increased fibrin synthesis, hemoconcentration (fibrinogen and TP increase the same degree) Inflammation (fibrinogen increases more than TP) |
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What are the three general functions of the urinary system? |
Glomerular filtration Tubular resorption (Glucose, amino acids, protein, Na, HCO3) *will see in urine with renal failure Secretion (K, acids, PO4, Creatinine, Urea *will see in blood with renal failure |
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What are the three components of the glomerular filtration barrier? Why doesn't albumin get through the barrier? |
Capillary endothelium/fenestrations, Glomerulus basement membrane, Podocytes Albumin is too large and too (-) charged to get through |
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What are the things that determine GFR? How can you measure GFR? |
Cardiac output, blood volume, number of glomeruli and glomerular arterioles Measured by the clearance of Iohexol, creatinine, and serum SDMA |
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Describe how the osmalility of urine changes as it goes through the nephron of the kidney |
1. Stays the same in the glomerulus, only small proteins or non-proteins are filtered 2. Remains the same in the Pct- Water and H2O are absorbed at the same rate 3. Descending LOH- H2O resorbed, osmolality increases. Ascending LOH- H2O stays, solute absorbed, osmolality drops, creating hypertonicity 4. DT and CT- with ADH, osmolality spikes as H2O is resorbed. without ADH- osmolality stays the same |
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ADH is stimulated by what? |
Blood volume Blood pressure Hyperosmolality |
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Define isosthenuria hyposthenuria |
Isosthenuria- solute concentration in the urine is the same as when it started Hyosthenuria- urine has a lower solute concentration than when it started |
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The isosthenuric range of USG is what? |
1.007-1.013 (more concentrated when it gets larger, less concentrated as the number drops) *USG less than 1.007 shows the ability of the kidneys to dilute the urine, showing urine function, even in dehydration *USG reflects tubulointerstitial problems, not glomerular (problems with concentrating ability leads to decreased water resorption) |
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What is the definition of chronic renal failure? How much of the renal tubules must be non-functional in order to see these signs? |
Failure to concentrate/dilute urine, 2/3rds lost, you see PU and azotemia Failure to clear wastes, 3/4th lost, you see oliguria/anuria and azotemia |
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How is acute renal failure different than chronic? |
Acute- (from toxicants, infection, ischemia) No hypertrophy or compensation from the tubules is seen USG is variable, volume is usually reduced |
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Define
Azotemia Uremia |
Azotemia- the increase in nitrogenous compounds, increase in urea and/or creatinine Uremia- the clinical signs that are associated with azotemia |
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how does low urine flow rate (dehydration) affect urea? |
Can increase, would increase independently from creatinine |
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What are the three ways you can classify azotemia from decreased clearance? |
Pre-renal (decreased plasma flow from hypovolemia, decreased C.O or shock) Renal (loss of nephrons/decrease GFR/increase in interstitial/tubular pressures from inflammation, amyloidosis, toxicity, ischemia, congenital, hydronephrosis, neoplasia) Post-renal (obstruction or leakage of urine into tissues or peritoneal space) |
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What are the ways that azotemia can be caused by increased production? |
Hemorrhage Increase from diet Increased protein catabolism |
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What changes are seen in USG, Volume and other PE info with Prerenal Renal Post renal azotemia? |
Pre-renal: USG >1.030 (dog), >1.040(cat), >1.025(LA). Volume is decreased (increased with ADH), Decreased GFR, dehydration, hemorrhage, shock, decreased CO Renal: Post-renal: ? USG, Decreased volume, Dysuria, enlarged bladder, uroabdomen |
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If the cause of a urine concentration change was extra-renal, what could the cause be? |
1. If the distal nephron was unresponsive to ADH (diabetes insipidus) 2. Solute overload (osmotic diuresis 3. Decreased medullary hypertonicity (addison's, liver disease, prolonged diuresis) |
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50% interstitial tonicity is due to what? |
Urea (decreased urea, decrease concentration) |
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Urea and creatinine usually change together. What is different about this in horses and cattle? If you have an increase in Urea but no change in creatinine, what type of azotemia do you have? |
*creatinine is usually more affected by things because the urea has to be reabsorbed Creatinine is more sensitive in horse/cattle due to GI excretion of urea Pre-renal azotemia |
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On physical exam of urine, what 3 things do you want to evaluate? |
1. Color 2. Clarity 3. Solute concentration |
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What colors of urine would be more concerning than the normal yellow color? |
Red/brown- hematuria, hemoglobinuria, myogloinuria Orange- bilirubinemia *Color is usually a reflection of concentration, always check the color with a USG |
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Clarity is a reflection of what? How do you measure it? |
It is a measure of cloudiness- the amount of suspended particles in the urine (not glucose or proteins) Should be able to read print through the urine |
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How do you measure solute concentration in the urine? What can it vary depending on? |
Measured with USG or refractometer Can vary depending on hydration status of the animal as well as it can be falsely high up to 0.005 with very high protein or glucose. *only adjust for this if you are in a +++ range of protein or glucose on a dipstick |
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Why is the chemical exam of urine said to be semiquantitative? |
Because it depends on the USG- with a low USG, the change of [solutes] becomes more significant |
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An alkaline urine can be due to what? |
Ammonium from bacteria OR a delay in analysis |
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Proteins show up on a reagent pad due to what property? How can a lab also report this? |
Proteins make the urine (-) charged and this charge is attracted to the reagent pad, making the color change seen. Sulfosalicylic acid can also precipitate out the urine and you can run this to determine the amount of protein *It is normal for a dog to have a 1+ urine |
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How does a proteinuria generally happen (how is it classified? |
Pre-renal (immunoglobulins, myoglobuli or hemoglobin) Glomerular Tubular- *Can only be mild proteinuria Hemorrhagic Inflammatory |
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Glucosuria can be falsely +/- in what situations? In order to have true glucosuria, what has to be surpassed? What are the two causes? |
Can be too high with H2O or bleach in the sample or too low with cold urine All glucose should be resorbed in health, and there is a renal threshold that marks the level of how much glucose can be resorbed. If that level is surpassed, you end up with glucosuria. 1. Cause 1- with hyperglycemia, the threshold was reached (diabetes mellitus) 2. Cause 2- normoglycemia (renal tubular disease) |
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Ketonuria is seen when what happens? what else is lost with ketones? |
Ketonuria should not be seen in good nutrition. It is caused when you have ketogenesis (due to increased lipid metabolism) *DM or starvation You also get a loss of Na and K |
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How is a heme + reaction measured on a dipstick? What are the different ways you can get a heme + reaction? |
Strip- measures the peroxidase activity of the urine (don't contaminate sample with peroxidases- H2O2 or Bleach) Hematuria - (Increased RBC seen), iatrogenic or pathologic increase in RBC Hemoglobinuria- (decreased Hct, pink/red plasma), intravascualr hemolysis Myoglobinuria- muscle damage |
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Billirubinuria is considered abnormal in dogs at what level? Cats? What does the reagent strip measure? What causes this? |
A 1+ is normal, it is a moderate reaction with a USG > 1.040 is abnormal It is ALWAYS abnormal in cats It measures conjugated billirubin but billirubin can also be destroyed in UV light, keep dark! Caused by hemolysis or heptobilliary disease *can see billirubinuria before hyperbillirubinemia |
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When using a urine dipstick, what things do you want to avoid exposing them to? |
No sunlight, touching the pads, volatile fumes, moisture Use before expiration date |
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Describe the pathophysiology of dehydration leading to pre-renal azotemia? |
Dehydration decreased the renal plasma flow This decreases GFR Increases urea resorption in the tubules Both lead to azotemia |
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How does dehydration change the USG? |
Dehydration decreases the blood volume This will increase ADH, increase aquaporins, increase water and Na resorption This increases USG (>1.025- horse, >1.040 cat, 1.030- dog) |
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How does azotemia develop from chronic renal failure? |
Loss of >75% of glomeruli, leads to decreased GFR, and decreased clearance of urea, creatinine and N wastes |
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Why is the USG within the isosthenuric range with chronic renal failure? |
With decreased clearance of solutes, you get more solute presented to the nephrons and less H2O is resorbed. By decreasing the medullary hypertonicity due to damaged interstitium and decreased resorption of Na and Cl in the LoH you get an overall effect of decreased water resorption. |
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How does decreased/no urine output lead to azotemia? |
An obstruction leads to increased vasoactive mediation and constriction of afferent arterioles. This will then lead to decreased GFR, and a decreased or no urine output |
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What are the steps that connect the clinical PU/PD with glucosuria seen on a urinalysis? |
Glucosuria leads to osmotic diuresis leading to PU/PD |
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How can diabetes mellitus lead to PU/PD and a USG or 1.025 or so? |
Increased glucose in the blood as it reaches the glomerulus means that the glucose threshold is surpassed in the tubules. Increased glucose being excreted in the urine leads to increased water excretion as the water follows. This leads to PU/PD |
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How does a bacterial infection end up in bacteruria/pyuria? |
The presence of bacteria leads to an inflammatory response leading to an increase in vascular permeability This allows WBCs and RBCs to leak into the urine = Pyuria/bacteruria |
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What are the causes of hyposthenuria? |
Central diabetes insipidus- Hypothalmic/pituitary disorders, hyperadrenocorticism) Renal diabetes insipidus- hypercalcemia, hypoadrenocorticism, hyperadrenocorticism, pyometra, liver failure, hypokalemia |
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How does central diabetes insipidus lead to a decreased USG (of about <1.015) |
Hypothalmic or pituitary disorder means no ADH can be released. Leads to a decreased amount of inserted aquaporins, decreasing water resorption This will lead to a decreased USG |
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A very high protein:creatinine means what? What causes this? |
Glomerular disease Causes: glomerular proteinuria nephrotic syndrome, hypoalbuminemia, hypercholesterolemia, effusion/edema *protein losing nephropathies can lead to renal failure over time |
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What is cylinduria? What causes it? What are they made up of? |
Cylinduria- the presence of large tubule mold casts found in the tubular epithelium Caused by renal tubular disease or proteinuria Made up of protein, cells and cellular debris wrapped in mucoprotein |
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What level of pyuria is considered significant? What are the causes? |
>5/hpf reasons depend on collection method UTI- infection anywhere from glomeruli to urethra (infectious or non-infectious causes) GTI- prostate or urethra infection- only seen with a voided sample |
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How can you tell a significant pyuria from a contaminated pyuria? |
Very hard to tell debris from bacteria. Do an air dried stained prep to determine if the bacteria is contaminant bacteria or a significant bacteria. |
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What is the cause of epithelial cells seen in urine? |
Squamous, transitional or renal epithelium Caused by neoplasia, trauma or hyperplasia If +++ and in large clusters, do air-dried preparation evaluation for cancer |
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When dealing with a possible case of leptospirosis, how do you want to handle the urine? |
Carefully, wear gloves |
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What are the different methods for collecting urine? Which one is generally preferred? |
Cystocentesis- generally preferred, unless you are suspicious of a prostate/ureter disorder or if you are measuring hematuria, for neoplasia Voided Catheterization (generally not preferred) Off surfaces (don't do- increased contamination) |
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From collection to looking at a microscope, what are the steps taken to ensure a good urinalysis? |
1. If analysis has to be delayed, refrigerate. Before analyzing, bring it too room temperature (30-60min) 2. Mix urine and then dip dipstick in, perform chemical analysis by comparing color changes to bottle, after the alotted time has passed 3. Take 5mL of urine and spin down (unless it's really bloody. If bloody, spin first then dipstick) at 500-700g, for 5min. 4. Discard supernant. Then mix urine and measure solutes on refractometer *measure BEFORE fluid therapy 5. Place drop of remaining urine on slide and put coverslip on to evaluate |
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What do you look for on the microscope when evaluating urine? |
1. Lower condenser to look at urine properly 2. Evaluate the urine for epithelium, casts and crystals on low power 3. Evaluate for WBC, RBC, Bacteria, Sperm and Fat/hpf on high power *if you stain them, you can look for cells. But, staining is bad for looking at bacteria |
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The longer arrows are pointing to what? The shorter arrows? |
Longer- RBCs Shorter- WBCs |
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What is the amount/hpf that is considered few, moderate and many? |
1-10- few 11-40- moderate 41-60- many 60+- too many to count |
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What do you look for to identify bacteriuria? How do you confirm this? |
Look for rods and casts Confirm with a stained, air-dried slide |
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These strings are what? |
Fungal hyphae *wider than bacteria, have septae |
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This cast is what type? Caused by? |
Cellular casts caused by renal disease that involves the tubules |
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This is what type of cast? |
Granular cast |
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This is what type of cast? |
Hyaline cast |
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What type of cast is this? What causes this? |
This is a waxy cast, caused by chronic renal failure |
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What is this in this image? |
Transitional epithelial cells (rounded) |
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What is seen in this image? |
Squamous epithelial cells (more sharp pointed, oblique) |
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What type of crystals are seen in this image? |
Calcium Oxalate, of the Dihydrate form |
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What type of crystals are seen in this image? |
Calcium Oxalate, of the monohydrate form |
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What type of crystals are seen in this image? |
Struvite Crystals |
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What type of crystals are seen in this image? What form is this? |
Bilirubin crystals, the typical form is on the top, the flashlight variety is in the middle and on the bottom |
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What type of crystals are seen in this image? |
Ammonium Biurate (thorn apple variant) *can also be in a spheroid form, like in this image (on the right) |
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What type of crystal is seen here? What causes these crystals? |
These are cystine crystals. These are relatively rare but when they are seen, they are caused by a defect in tubular resorption of certain amino acids |
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What type of crystals are seen in this image? What species are these seen in? |
Calcium Carbonate crystals (can be different forms) Horses, rabbits, guinea pigs |
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What type of crystals are in this image? |
These are calcium phosphate crystals *note that when on their side, they are flat ended, not "coffins" like struvite crystals |
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What are these crystals? |
Amorphous crystals, no recognizable form |
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What is this type of crystal? What causes this? |
Sulfa crystal Seen in an animal on sulfa drugs |
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What is displayed in this image? |
Yeast (note the budding) |
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What is the dark purple stained material in this image? |
Blastomyces- fungal infection seen in this urine sample |
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What is this organism? |
Capillaria Plica *note the offset caps, unlike trichuris |
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What is this organism? |
Dioctophyma renale ova, kidney worm |
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What are these? |
Lipid droplets *usually in a different plane than everything else |
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What is seen on this slide? |
Spermatozoa |
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What is this large object on this slide? |
Mucous strand |
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This artifact is what? |
Starch granules, most likely from gloves |
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What levels of each are worrisome/"unacceptable on a UA? WBC/RBC Epithelial cells Casts Others? |
>5/hpf WBC or RBC Many or clumps of epithelial cells Mod to many hyaline or granular casts ANY cellular, waxy or Hgb casts Any cystine, bilirubin or tyrosine Ova Microfilaria Bacteria or fungi |
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What are considered normal levels in a UA for a dog? Cat? |
Dog- trace or 1+ protein, small-moderate bilirubin, 5.5-7.5pH, 1.015-1.050 USG Cat- trace protein, 5.5-7.5pH, 1.035-1.060 USG |
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What is the function of the ECF? When sampling, what is it representative of? What electrolytes is it high in? |
ECF transports substances from the ICF to the plasma When sampled, it represents the same electrolytes that are in the tissues High in Na and Cl, low in K |
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Where is ICF most abundant? What electrolytes is it rich in? Exception? |
Must abundant in muscles Rich in K, phosphates and Proteins, lower in Na *Exception- RBCs in dogs and cats where K is lower K in serum > plasma (platelets release K in clotting) |
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What is osmolality? What happens to cells when you have hypertonic fluid loss, hypotonic or isotonic fluid loss? |
Osmolality- concentration (number) of solute particles, causes water movement With hypertonic fluid loss- more electrolytes are lost than water, results in hypotonic ECF, water shift into the cells and cell shifting. *don't replace with hypotonic fluid- worsens problems Hypotonic fluid -> hypertonic ECF -> shrinking isotonic loss -> no change in ECF |
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How is Na regulated in the body? What is Na needed for? |
Na is needed for H2O regulation, blood volume and tonicity regulation it is regulated by the Na/K pump and, Cl and H2O follows Na The kidneys sense changes in osmolality and blood volume which will then change how much Na is resorbed in the renal proximal tubules |
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What changes are seen in Na regulation when the body senses hypervolemia? Hyperosmolality? |
Hypervolemia- ANP (atrial natriuretic peptide) released by kidney, this shuts down the Na channels in the kidney, increasing water release from the body Hyperosmolality- increase thirst, ADH and increases renal absorption |
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What are the three general causes of hypernatremia? |
1. H20 loss > Na loss 2. Not enough H2O intake or hypertonic fluid administration 3. Excess Na Gain |
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What are the causes of hypernatremia due to H2O loss more than Na loss? |
Decreased intake- CNS lesion decreasing thirst response or water deprivation Increased loss with no replacement- panting, fever, central diapetes insipidus, lack of renal response to ADH, hypotonic fluid losses (GI, renal, skin losses) |
