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618 Cards in this Set
- Front
- Back
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Normal PCV in the dog
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37-55%
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Normal PCV in the cat
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28-45%
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Normal HCT in the dog
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61-62%
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Why can anemia cause heart murmur?
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Lower blood viscosity
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Clinical signs of anemia
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Weakness, exercise intolerance, tachypnea, lethargy, tachycardia, heart murmur, pale mm
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3 categories of icterus
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Prehepatic
Hepatic Posthepatic |
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Possible cause of an elevated MCH ("Hyperchromic RBC")
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Free hemoglobin in the blood from hemolysis
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How long after blood loss do reticulocytes appear in the blood?
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2-4 days after onset of anemia
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A dog was HBC 30 minutes ago and is brought in with hemoabdomen. His PCV is 45. How is this possible?
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Acutye hemorrhage cases may have normal PCV due to even loss of all blood components, and splenic contraction.
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What causes the PCV in an acute hemorrhage case to drop several hours after onset of bloos loss?
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Fluid shift into vasculature from other compartments dilutes out remaining RBC
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Refers to the size of the RBC
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MCV- Mean copuscular volume
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Measure of hemoglobin in the blood cells
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MCH- Mean corpuscular hemoglobin
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Measure of hemoglobin in red blood cells as a function of their volume
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MCHC- Mean corpuscular hemoglobin concentration
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This form of anemia tends to be microcytic and hypochromic
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Regenerative
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How is reticulocyte count corrected for degree of anemia?
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Reticulocyte % * (pt PCV/normal PCV)
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A corrected reticulocyte % over this level indicates a regenerative response
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Over 2%
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Absolute reticulocyte count that constitutes a regenerative anemia
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Over 60,000 in dogs, 50,000 in cats
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Which reticulocytes should be counted in the cat-- punctate or aggregate?
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Aggregate
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What else can the presence of nRBC's indicate besides regeneration?
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Lead toxicity
Bone marrow leakage or disease Splenic absence or disease |
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Life span of the normal canine RBC
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120 days
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Characteristics of a typical chronic nonregenerative anemia
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Normocytic, normochromic
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Pancytopenia is indicative of...
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Severe bone marrow disease
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Changes in blood smear that may be seen with anemia
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Anisocytosis
Polychromasia Spherocytes nRBC Erythrocyte parasites |
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RBC fragments and fibrin strands together on a blood smear are indicative of...
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DIC
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Hemoglobinemia and hemoglobinuria indicate this form of hemolysis
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Intravascular
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Are most cases of IMHA associated with intravascular or extravascular hemolysis?
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Extravascular
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List some causes of Heinz body anemia
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Oxidative damage
Onions, garlic, propylene glycol Acetaminophen |
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How does zinc cause hemolysis?
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Oxidative damage to RBC
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RBC changes seen with zinc toxicity
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Spherocytes, eccentrocytes, ghost cells, target cells, Heinz bodies
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Why in an event of zinc toxicity can you see band neutrophilia?
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Process of RBC production stimulates WBC production
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Most common cause of nonregenerative anemia
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Anemia of chronic disease
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List some extramarrow causes of nonregenerative anemia
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Anemia of chronic disease
Renal failure Endocrine diseases Acute hemorrhage (Pre-regenerative) Nutritional deficiency |
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Is ACD more severe in cats or dogs?
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Cats
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How does chronic disease cause anemia?
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Inflammation triggers release of hepcidin from the liver which causes iron sequestration by hepatocytes to increase so that it is unavailable for RBC synthesis (or pathogens)
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How does kidney disease cause anemia
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Decreased erythropoetin
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List some infectious diseases of the bone marrow that may cause nonregenerative anemia.
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Ehrlichiosis, FIV, FeLV
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List some afflictions of the bone marrow that may cause nonregenerative anemia.
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Infections, Toxins, drugs, chronic blood loss, immune mediated, marrow neoplasia, myelodysplasia, myelofibrosis
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Type of anemia seen with chronic blood loss
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Microcytic, hypochromic, non-regenerative
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Macrocytic, normochromic nonregenerative anemia may be seen with...
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FeLV
Folate and cobalamin deficiency |
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How high will blood bilrubin have to be in order to have an icteric animal?
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2.5 mg/dL
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Site of red blood cell destruction in extravascular hemolysis
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Liver and spleen
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Is IMHA more commonly associated with intravascular or extravascular hemolysis?
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Extravascular
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List some causes of secondary IMHA
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Drugs like TMS
Neoplasia Cross reaction with infectious antigens (Ehrlichia, Babesia, hookworms, etc) |
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CS seen with IMHA
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Usually acute onset
Anotexia, lethargy Tachypnea, weakness Pale mm Icterus Heart murmur Fever Splenomegaly, hepetomegaly |
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Laboratory findings seen with IMHA
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Regenerative anemia
Spherocytes Autoaggluutination in saline Leukocytosis +/- LS Thrombocytopenia |
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Blood chemistry findings seen with IMHA
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Hyperbilirubinemia (70% cases)
Elevated liver enzymes (bilirubin metabolism, hypoxia, DIC) Bilirubinuria +/- hemoglobinuria and hemoglobinemia if intravascular |
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A dog presents with regenrative anemia, spherocytosis, autoagglutination, and a positive Coomb's test. All of these are strong indicators of...
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IMHA
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Why is the Coombs' test not always done for diagnosis of IMHA?
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Not very specific--> Can also get + result from sencondary immune-mediated hemolysis
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Possible complications of IMHA
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Severe anemia--> organ dysfunction
Immune-mediated thrombocytopenia DIC Thromboembolism Tx complications (glucocorticoids increase hypercoagulability) |
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How is IMHA treated?
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Treat any inciting cause (neoplasia, infection, drug administration)
Immunosuppression with corticosteroids Supportive care (transfusions) Anticoagulants--> Heparin |
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Primary treatment for IMHA
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Prednisone, 2-4 mg/kg/day
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How long before you can expect to see results when treating IMHA with prednisone?
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3-10 days
Stable PCV, followed by gradual rise as pr |
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Prognosis for IMHA
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50% mortality, intensive treatment required
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Describe the prednisone treatment protocol for IMHA
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High dose (immunosuppressive) until PCV is 30-35% and evidence of hemolysis is gone
Gradually taper q 2 weeks by 25-30% as long as PCV is stable |
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When can prednisone treatment be stopped in an IMHA patient?
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When PCV normal for at least 4 weeks on low EOD dose
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Drug commonly used concurrently with prednisone to treat IMHA
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Azathioprine
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Se associated with azathioprine
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Myelosuppression at high dose, pancreatitis, liver toxicity
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Which drug is best suited for pairing with prednisone in managing IMHA: Azathioprine or cyclophosphamide?
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Azathioprine
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Method of action for cyclophosphamide
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Alkalizing chemotherapy agent
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Why pair prednisone with azathioprine to treat IMHA?
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Lets us taper prednisone more quickly
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When is splenectomy indicated for the treatment of IMHA?
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If a full response is not achieved with medical management
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Pros and cons of splenectomy in an animal with IMHA
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Pros: Prevents splenic engulfment of RBC
Cons: Risky in an anemic, immunosuppressed animal |
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Supportive treatments for IMHA include:
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RBC transfusion
Plasma transfusion (Tx DIC) Anticoagulants like heparin, warfarin Aspirin |
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Common, often fatal complication of IMHA
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Thromboembolism
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Is IMHA more common in cats or dogs?
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Dogs
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How does feline IMHA differ from canine IMHA?
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Nonregenerative anemia
Cyclophosphamide and chlorambucil often used from beginning Less thromboembolism |
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Why is neonatal isoerythrolysis rarely seen in dogs?
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Dogs do not have pre-formed alloantibodies to RBC
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Describe the process of neonatal isoerythrolysis in the cat
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Example: Type A kittens born to Type B queen.
Queen has Ab to Type A RBC Hemolysis after colostrum ingestion These kittens die in a day or two |
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Under what circumstances would you see neonatal isoerythrolysis in the dog?
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Bitch exposed to blood product of same type as puppies
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Rickettsial RBC parasite transmitted by blood sucking arthropods
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Mycoplasma haemofelis
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Mycoplasma haemofelis is seen most commonly in these groups
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Outdoor cats, immunosuppressed animals
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Number 1 rule out for hemolysis in cats
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Mycoplasma haemofelis
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Does M. haemofelis cause intravascular or extravascular hemolysis?
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Extravascular
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Two reasons that cats with hemobartonellosis undergo hemolysis
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Immune mediated and parasite induces
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True or false: M. haemofelis may be carried by an asymptomatic carrier for years
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Trye
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CS associated with M. haemofelis
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Lethargy, wt loss, anorexia
Episodic fever Regenerative anemia Splenomegaly Icterus +/- Postive Coomb's test |
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What % of cats with M. haemofelis also have FeLV?
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50%
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How is Mycoplasma haemofelis diagnosed?
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Parasite visualized in 50% cases
PCR test |
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How is M. haemofelis treated
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Doxycycline or tetracycline for 3 weeks
Enrofloxacin another choice Prednisone 5-7 days if severe anemia |
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True or false: Treatment for M. haemofelis is often successful the first time around, with complete clearance of the pathogen from the body.
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False. Animals often remain persistent carriers
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Concern with administering doxycycline po to a cat
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Esophageal stricture if not washed down with plenty of water
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Hematozoan parasite of canine RBC, seen in the Southern US
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Babesia canis and Babesia gibsoni
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How is Babesia transmitted?
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Ticks
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Breed predisposed to Babesia canis
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Greyhounds
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Breed predisposed to Babesia gibsoni
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Pit bulls
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Which species of Babesia may be transmitted by bite wounds?
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B. gibsoni
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How does Babesia cause disease?
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Parasitism of RBC
Hemolysis from parasite and immune response Sludging of blood flow Coagulation activation Tissue hypoxia and multiple organ dysfunction |
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CS of Babesiosis
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Hemolysis (intra and extravascular)
Fever, lethargy, vomiting, wt loss Lymphadenopathy, splenomegaly, icterus |
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How is Babesiosis diagnosed?
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ID organisms on blood smears of peripheral blood
Serology if not found on blood smear PCR available |
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Primary treatment for Babesiosis
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Imidocarb diproprionate
Supportive treatment |
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Protozoal parasite of cats, transmtted by ticks. Seen in the Southern and SE USA. Causes hemolytic anemia, inflammation, DIC, and microvascular damage
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Cytauxooan felis
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Clinical signs associated with Cytauxzooan felis
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Acute onset fever, dyspnea, lethargy
Icterus, dehydration Mild to moderate anemia Leukopenia and thrombocytopenia common |
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How is Cytauxzooan feliz treated?
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Demonstrate organisms is RBC, bone marrow, spleen, liver
Signet ring or safety pin appearance |
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What distinguishes C. felis from M. haemofelis on blood smear?
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C. felis has shape of safety pin
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Treatment for C. felis
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Imidocarb or diamenazene
Supportive care: Fluids, transfusion, treat DIC with heparin |
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Prognosis for C. felis
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Guarded, but aggressive tx can save many cats
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Reversible oxidation of Fe in hemoglobin is called.....
Blood may be chocolate brown |
Methemoglobinemia
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Most common cause of feline methemoglobinemia
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Tylenol ingestion
(Also may be caused by propylene glycol, garlic, etc.) |
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Is oxidation of hemoglobin reversible or irreversible?
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Irreversible
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Irreversibly denatured and precipatated Hb appears on a blood smear as...
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Heinz bodies
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These can cause Heinz body formation
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Foods with onions, garlic, propylene glycol
Acetaminophen Zinc Cats with various other disorders |
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Is it possible for there to be oxidative damage in the absence of Heinz body formation?
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Yes
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Most common cause of anemia
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Anemia of chronic disease
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In ACD, which species has a lower PCV- dog or cat?
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Cat
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How long does a disease take place before causing ACD?
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Cat: 1 week
Dog: 2 weeks |
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CS of ACD
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Related to primary disease
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Which anemia tends to be more severe: ACD or anemia of chronic renal failure?
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Anemia of chronic renal failure
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In anemia of chronic renal failure, when should erythropoetin therapy be instituted?
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PCV < 25% in dogs, < 20% in cats
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EPO protocol in animals with anemia of chronic renal failure
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100 IU SQ 3X week until PCV > 35% in dog and 30% in cat, then reduce to 1-2 times weekly
Concurrent Fe supplementation |
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Most common cause of iron deficiency anemia
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Blood loss from parasites, GI hemorrhage, epistaxis, melena
Most commonly blood loss from GI hemorrhage |
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Characteristics of iron deficiency anemia
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Microcytic, hypochromic once advanced (early on, normocytic, normochromic)
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Treatment for iron deficiency anemia
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Iron supplementation
Stop bleeding |
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Cause of immune-mediated nonregenerative anemia
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Immune response against RBC precursors
Causes severe anemia |
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In a bone marrow aspirate, you see no RBC precursors at all. This is called...
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RBC aplasia
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How is immune mediated nonregenerative anemia treated?
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Immunosuppression
Blood transfusion |
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Anemia resulting when bone marrow fails to make RBC at all. Often pancytopenia results.
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Aplastic anemia
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Causes of aplastic anemia include...
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Infections (FeLV, ehrlichiosis)
Drugs (chemotherapeutics, adverse rxns) Estrogens |
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How is aplastic anemia diagnosed?
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BM aspirate and cytology
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A patient presents with tachypnea, pale mm and a heart murmur. CRT is under 2 seconds and pulses are normal. What is a likely cause?
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Anemia
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Why do thoracic and abdominal rads in an animal with acute onset hemolytic anemia?
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Rule out neoplasia, chronic infection, and FB
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In the event of hemolytic anemia with normal hydration, what is the best transfusion product?
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Packed RBC
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This blood type is practically considered "universal donor" in dogs
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DEA 1.1 negative
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True or false: Transfusion with DEA 1.1 negative canine blood will not elicit immune reaction.
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False. Other minor alloantibodies may not match recipient and may have minor reaction
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Major crossmatching of blood types includes...
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Test patient serum for Ab to donor RBC
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Minor crossmatching of blood types includes...
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Test doror plasma for Ab to patient RBC
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When is crossmatching very important in the canine?
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In patients transfused for the 2nd time if over 3-5 days since last transfusion
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You transfused a patient and in two days his PCV drops dramatically. Why?
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Likely Ab reaction to donor RBC and hemolysis
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How long do transfused RBC usually last int he dog if there is no hemolysis?
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5-7 days
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How is the dosage determined for RBC transfusion
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(Desired PCV-Patient PCV)/PCV donor blood * normal PCV * kg
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2 ml/kg of blood (PCV 40%) will raise patient PCV by...
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1%
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Typical desired post-transfusion PCV is...
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15-20%
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How many cc of blood in 1 unit?
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450 cc
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Possible pretreatments for blood component administration
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Pre-treat with antihistamine +/- dexamethosone
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How should RBC be administered during transfusion?
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1/2 calculated rate for first 30 mins, check temp q 15 min to monitor for transfusion reaction
Then 5-10 mL/kg/hr |
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You should stop a blood transfusion if the patient's temperature increases
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1.5 F or more
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How should you respond if a patient's temp increases during blood transfusion?
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Stop until T returns to normal, then re-administer at slower rate
Administer diphenhydramine or dexamethosone |
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Possible transfusion reactions include...
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Temperature increase
Tachycardia, tachypnea Urticaria, facial swelling, pruritus, vomiting |
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Occurrence of transfusion reactions in dogs and cats
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3-13%
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CS of anaplylactic shock
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Peracute onset
Hypotension, tachypnea, bradycardia Vomiting, urination, defecation Seizures |
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Most common feline blood type in US
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Type A
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Rarer blood type found in purebred cats in USA and up to 50% of cats in Australia
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Type B
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Why are cats more susceptible to blood transfusion reactions?
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Preformed alloantibodies to RBC
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Which feline blood type has stronger alloantibodies to the other type: A or B?
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B versus A
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Describe primary hemostasis
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Endothelial injury
Platelet adhesion with von WIllebrand factor Platelet aggregation |
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Extrinsic system of secondary coagulation
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Factor 7
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Factor 7 is activated by
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Tissue factor
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Intrinsic system of secondary coagulation
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Factors 12, 11, 9 and 8
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Intrinsic clottign cascade initiated by...
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Thrombin formed by intrinsic system activation and other factors
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Common pathway of secondary coagualtion
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Factors 10, 5, prothrombin, fibrinigen
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Factor 10 is activated by...
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Factor 7 and factor 8
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Substances released by platelets when they degranulate
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Serotonin, ADP, thromboxane A2
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Damaged tissue released this clotting factor
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Factor 3
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Prothrombin activator is activated by...
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Factor 10, Factor 3, Ca, and PF3
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Converts prothrombin to thrombin
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Prothrombin activator
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Converts fibrinogen to fibrin
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Thrombin
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Factor that causes the formation of fibrin cross linking to form a blood clot
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Factor 8
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These compunds inhibit coagulation factors
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PT3
Protein C |
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This factor is deficient in DIC
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AT3
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Breaks down fibrin clots
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Fibrin
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Fibrin is broken down into...
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FDP's
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CS of primary coagulopathy
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Petechia
Mucosal hemorrhage Epistaxis Urinary hemorrhage Melena |
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CS of secondary coagulopathy
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Ecchymosis
Hemarthrosis (bleeding from joints) Body cavity hemorrhage GI bleeding Hypotension and anemia |
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Tests for primary coagulopathy
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Platelet count
BMBT Platelet function tests |
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Tests for secondary coagulopathy
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PT
PTT ACT Fibrinogen FDP's D-dimers AT3 |
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Used to measure degree of fibrinolysis
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D-dimer
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Most common cause of primary coagulopathy
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Thrombocytopenia
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Test that assesses function of platelets and endothelial factors
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BMBT
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True or false: Platelet count may be normal but primary coagulopathy may still exist.
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True
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PT tests which coag. cascades?
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Extrinsic (7) and common
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PTT tests which coagulation cascades?
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Intrinsic and common
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ACT tests which coagulation cascades?
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Intrinsic and common
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Why are D-dimers a better gauge of fibrinolysis? than FDP's
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Released when mature clots are destroyed
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Inhibits coagulation by binding thrombin to prevent conversion of fibrinogen to fibrin
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AT3
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Low AT3 is seen in these conditions
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DIC, PLN, PLE
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4 major causes of thrombocytopenia
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Destruction
Consumption Sequestration Decreased production |
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Site of thrombocyte sequestration
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Spleen
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Spontaneous bleeding from thrombocytopenia is most likely when the count is under
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50,000/ uL
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CS of thrombocytopenia
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Petechia
Mucosal hemorrhage Epistaxis Urinary hemorrhage Melena |
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List two breeds that may naturally have fewer thrombocytes
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Greyhound
Cavalier King Charles Spaniel |
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Common cause of severe thrombocytopenia
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Primary immune-mediated thrombocytopenia
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Three causes of secondary thrombocytopenia
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Neoplasia
Drugs Infection |
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Breeds predisposed to idiopathic immune-mediated thrombocytopenia
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Cocker spaniel
Old English sheepdog Poodle |
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CS of idiopathic thrombocytopenia
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Spontaneous hemorrhage
Usually no other CS |
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Describe the thrombocytopenia seen in idiopathic cases
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Severe, usually under 10,000
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Evans' Syndrome describes
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Thrombocytopenia and IMHA together
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How is primary immune-mediated thrombocytopenia diagnosed?
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Exclusion of other causes
Clinical findings |
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Most common bone marrow finding with immune-mediated thrombocytopenia
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Megakaryocyte hyperplasia
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Infections that may cause immune-mediated thrombocytopenia
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Ehrlichiosis
FeLV Babesiosis RMSF Bartonella Toxoplasmosis Histoplasmosis Cytauxzoonosis Acute ciral infections |
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Ab may be seen on megakaryocytes in what % of iimmune mediated thrombocytopenia cases?
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50%
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How is immune mediated thrombocytopenia treated>
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Supportive care (treat anemia and hypovolemia)
Immunosuppression +/- Platelet transfusion (PRP, but short lived and not very available) nRBC transfusion |
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Immunosuppressive protocol for immune mediated thrombocytopenia
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Prednisone (M/C)
Vincristine may stimulate thrombepoesis in low doses |
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How long until you can expect prednisone to halt the process of immune-mediated thrombocytopenia?
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1 week
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Platelets present in normal numbers, but not functioning well-- this is called...
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Thrombocytopathia
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Most common congenital bleeding disorder in the dog
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Von Willebrand's disease
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Function of von Willebrand's factor
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Important for platelet adhesion to damaged endothelium
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Causes of acquired thrombocytopathia
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Drugs: NSAIDs, Ca channel blockers, Abx
Infections like ehrlichiosis, FeLV Neoplasia Hepatic disease |
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CS of von Willebrand's Disease
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Mucosal bleeding
Excessive bleeding after trauma |
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Diagnosis of von Willebrands' disease
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BMBT
Plasma von Willebrand factor concentration Genetic tests for some breeds |
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Treatment for von Willebrand's disease
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Replace deficient vWF (cryoprecipitate has high concentration of it)
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Hormone causing release of preformed von Willebrands' Factor
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DD AVP
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Besides cryoprecipitate, what is another alternative for treating von Willebrands' disease?
|
Fresh frozen plasma
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Acquired clotting factor deficiencies may be caused by
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Vitamin K antagonists
Liver failure Neoplasia DIC |
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How prevalent are congenital factor deficiencies in the dog and cat?
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Rare
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These clotting factors require vitamin K to be activated
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Factors 2, 7, 9 and 10
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Where does activation of clotting factors occur?
|
In the liver
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FIrst clotting factor to see the effect of a lack of Vitamin K
|
Factor 7 (shortest half life)
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Method of action of most rodenticides
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Vitamin K antagonists
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Duration of treatment for 1st generation Vitamin K antagonists (warfarin)
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2 weeks
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Duration of treatment for 2nd generation Vitamin K antagonists (brodifacoum and diphacinone)
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3-4 weeks
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CS of Vitamin K antagonist toxicity
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Ecchymoses
Body cavity hemorrhage Depression, anorexia, vomiting Signs of anemia or hypovolemia |
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First coagulation assay to become prolonged with Vitamin K antagonist toxicity
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Prolonged PT
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How is diagnosis of Vitamin K antagonist toxicosis treated?
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History of exposure
Prolonged PT (first) Prolonged PTT Mild thrombocytopenia |
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How is Vitamin K deficiency treated?
|
Coagulation factor replacement with FRESH FROZEN PLASMA
Vitamin K1 Supportive care |
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Which treatment for vitamin K deficiency will have the quickest effect on coagulation: Fresh frozen plasma or vitamin K?
|
Fresh frozen plasma
(immediate effect versus several hours to effect with vitamin K) |
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|
List some of the coagulation deficiencies seen in conjunction with liver disease
|
Inadequate synthesis of clotting factors by hepatocytes
Vitamin K deficiency DIC |
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Why is Vitamin K deficiency seen with liver disease?
|
Fat soluble vitamin that needs bile acids for proper absorption
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How is coagulopathy from liver disease diagnosed?
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Appears similarly to DIC
PT and PTT prolonged FDP and D-dimers elevated Thrombocytopenia if DIC |
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How is liver-associated coagulopathy treated?
|
Manage liver disease
Fresh or frozen plasma Vitamin K |
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Way in which mast-cell tumors can cause defects in secondary hemostasis
|
Degranulation and heparin release causes vasodilation and bleeding
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Describe process of DIC
|
Coagulation activated by endothelial damage or cytokines--> microthrombi affect organs
Fibrinolysis activated Anticoagulation factors are consumed by excessive coagulation Hemorragic tendency results |
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In DIC, is AT3 elevated or decreased?
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Decreased
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Degrades fibrin into FDP
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Plasmin
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Causes for hemorrhage in DIC
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Coagulation factor deficiency
Thrombocytopenia Thrombocytopathia Excessive fibrinolysis |
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Clinical signs of chronic DIC
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Often none
Mild hemorrhage May abruptly decompensate |
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Clinical signs of acute DIC
|
Severe form
Hemorrhage Hypotension Multiple organ failure Thrombosis of large vessels |
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How is DIC diagnosed?
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Clinical findings
Disease known to cause DIC (sepsis, etc) Laboratory abnormalities |
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Describe the laboratory abnormalities seen with DIC
|
Prolonged PTT, PT, ACT
Thrombocytopenia Fibrinogen decreased FDP elevated D-dimer positive AT3 decreased Schistocytes |
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In DIC, does PTT or PT decrease first?
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PTT
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Is D-dimer test a definitive diagnostic test for DIC?
|
No, may have false positives so take CS into account too
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An animal must have 3 of these 4 signs to have DIC:
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Abnormal PTT
Abnormal PT Low platelet count +D dimer |
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Key to treatment of DIC
|
RESOLUTION OF UNDERLYING ILLNESS
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Treatment for DIC
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Resolve underlying illness
Improve perfusion and oxygenation Coagulation factor replacement AT3 replacement Heparin to activate AT3? |
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Prognosis for chronic DIC
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Not usually life threatening
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Prognosis for acute DIC
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Life threatenting
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Virchow's triad of thrombosis includes...
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Endothelial damage
Abnormal blood flow Hypercoagulable state |
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List some means of endothelial damage that contribute to thrombosis
|
Sepsis
Vasculitis Neoplasia Heartworm disease IV catheter Atherosclerosis (hypothyroid dogs) |
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Causes of blood turbulence and potential thrombosis
|
Heart disease
Increased viscosity Shock Prolonged recumbency |
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List some causes of hypercoagulability that may contribute to thrombosis.
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Hemolytic anemia
Hyperadrenocoticism Glomerular disease DIC Sepsis Neoplasia Pancreatitis |
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Acute onset of respiratory distress caused by this blood disorder. May cause any range of radiographic change to lung
|
Pulmonary thromboembolism
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CS of aortic thromboembolism
|
Acute onset hind limb paresis
Painful, firm muscles Cool distal hind ends Lack of femoral pulse Most common in cats with cardiomyopathy and dilated LA |
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How is thomboembolic disease diagnosed?
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CS for specific location
Presence of underlying disease Imaging D-dimer |
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Three drugs used to treat thromboembolism
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Hepatin
Low MW heparin Warfarin |
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IN Adverse Possession, the "A" is for ?
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Actual – X, the adverse possessor, must actually possess the land to obtain title.
There are two exceptions – The following things are not required: [1] O, the true owner, does not have to know what’s going on. [2] X, the adverse possessor, does not have to think he owns it. |
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Neonatal isoerythrolysis is most commonly seen in these two frequently studied species
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Horse and cat
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This branch of the immune system requires little-to-no education and is fully functional when a foal hits the ground. Includes macrophages, dendritic cells, and PMNs
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Innate immunity
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Immune response that ncludes humoral and cell mediated immune responses
Improves with exposure |
Acquired immunity
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True or false: Foals are born with no functional immune system
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False: Have innate immunity that can respond to infection
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Small amount of this Ig present in newborn foal due to in-utero exposure
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IgM
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How long does it take for an acquired immune response to occur in the foal?
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10-14 days
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True or false: The mare's hematochorial placenta allows afficient transfer of Ig's to the foal in utero
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False. Her epitheliochorial placenta prevents transfer of Ig's
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Maximum Ig absorption in the neonatal foal's gut occurs at...
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6 hours
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After how long is the foal's gut incapable of absorbing large proteins like Ig's?
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6-24h
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Failure of passive transfer is diagnosed if a foal has inadequate IgG at this age...
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24h
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IgG level indicating sufficient passive transfer in the foal
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800 mg/dL
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IgG level indicating partial FPT in the foal
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400-800 mg/dL
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IgG level indicating absolute FPT in the foal
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<400 mg/dL
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Most common cause of FPT
|
Fescue toxicosis and agalactia in the mare
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List some causes of FPT involving the mare
|
Fescue agalactia
Disease/death of mare Malnutrition of mare Poor colostrum quality |
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List some causes of FPT involving the foal
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Foal premature/dysmature and unable to stand
Foal disease/injury Foal rejection or separation Early maturation of the gut |
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Administering these drugs to a pregnant mare may cause premature maturation of the gut epithelium and FPT in the foal.
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Steroids
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Concentrations of serum IgG in the neonatal foal become detectable after this long...
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6 hours
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Concentrations of serum IgG in the neonatal foal peak after this long...
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18-24h
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Most common test used to measure serum Ig's in foal
|
Enzume immunoassay, stall-side SNAP test
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Most quantitatively accurate way to measure foal IgG levels
|
Single radial immunodiffusion
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How long does it take to get the results on a foal's radial immunodiffusion test for IgG's?
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24h
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A foal 3h old has yet to suckle. Describe treatment to prevent FPT.
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1-3L good quality colostrum
Feed 500 mL/hour for first 6-8 hours Bottle feed if foal can suckle-- otherwise pass NG tube |
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Maximal amount of colostrum that may be fed to a foal per hour.
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1 L
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Treatment for an FPT foal older than 6 hours
|
IV plasma therapy, 1-3 L
GIve 500 mL/kg over 10 mins, if no reaction, increase to 40 mL/kg |
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CS of a blood product reaction in a foal
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Elevated HR, temp
Agitation |
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Downside of IV plasma therapy in the foal
|
Expensive
Can cause future reactions to blood products |
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A healthy foal in a clean environment has partial FPT. What should be done?
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Monitor closely, possibly treat with abx
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A healthy foal in a contaminated environment has complete FPT. What should be done?
|
Transfuse with 1-3L of plasma
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A sick foal has FPT. What should be done.
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Transfuse with at least 2L of plasma, treat secondary illness
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In any case where a newborn foal is given a plasma transfusion, how soon should IgG be rechecked?
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6-24h after administration
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When transfusing an FPT foal, is it better to give the full dose all at once or to give small repeated doses?
|
All at once
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When is the mare exposed to foal RBC antigen?
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Parturition
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Is NI more common in the primiparous or multiparous mare?
|
Multiparous, foal from same stallion or paternal blood type
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Two most common equine blood types
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Qa and Aa
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Is a mare or a stallion more likely to be Qa/Aa positive?
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Stallion
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How long before CS of NI are seen in a foal?
|
12-24 hours (born healthy, adequate passive transfer)
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CS of NI in the foal
|
Lethargy, loss of interest in suckling
Hematuria Icterus Anemia Secondary complications |
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Treatment for neonatal isoerythrolysis in the foal
|
Transfuse if PCV under 15% with washed mare RBC or crossmatched donor
Supportive care--> Fluids, minimize stress |
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Foal plasma reaction with donor RBC
|
Major incompatablility
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Donor plasma reaction with foal RBC causes...
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Minor incompatability
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Px for neonatal isoerythrolysis
|
Based on severity of anemia and complications
If treated early and aggressively, foals often recover |
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Prevention of NI in the foal
|
Pre-breeding or pre-foaling cross-matching of mare and stallion
Presuckling Jaundiced Foal Agglutination test with colostrum Postsuckle Coomb's Test |
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If a mare is found to have Ab to her foal's RBC, what should be done?
|
Don't let foal suckle dam for 48h
Provide colostrum from another mare followed by milk replacer or other mare's milk Milk dam out during this time Keep foal and dam together but do not allow suckling |
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Condition that arises when mare's colostrum has Ab to foal's platelets
|
Alloimmune thrombocytopenia
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SIgns of alloimmune thrombocytopenia in the foal appear after...
|
12-24h
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|
Alloimmune thrombocytopenia is most frequent in these equines
|
Mules
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Tx for alloimmune thrombocytopenia
|
Keep foal quiet
Fresh plasma transfusion |
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Disease seen primarily in Arabian foals, caused by autosomal recessive trait preventing maturation of B and T cells and absence of humoral immunity
|
SCID
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CS of SCID
|
Normal post-birth if adequate PT
Recurring infections beginning at 4 weeks Improves with Tx, relapses when done with Tc Ultimately fatal from innocuous infections |
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SCID foal tend to get odd infections beginning at what age?
|
3-4 weeks
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In an SCID foal, the CBC will show...
|
Lymphocytes < 1000/uL
Panhypogammaglobulinemia |
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You are necropsying a n Arabian foal that died of pneumocystis carinii. The thymus is fatty and has few lumphocytes. The LN and spleen are grossly normal but have a lack of germinal centers and lymphocytes. What is the likely untimate cause of death?
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SCID
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Prognosis for SCID
|
Fatal, foals die by 5m
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How can SCID be prevented?
|
Genetic testing of at-risk breeding animals
Avoid breeding carriers, especially to each other |
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Congenital, fatal immunodeficiency, peripheral ganglionopathy, and anemia seen in Fell Ponies
|
Fell Pony syndrome
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Components of Fell Pony Syndrome
|
Anemia
Immunodeficiency Peripheral ganglionopathy |
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Cause of Fell-Pony Syndrome
|
Single autosomal recessive gene
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CS of Fell-Pony syndrome seen at this age
|
2-3 weeks of age
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CS of Fell Pony syndrome
|
Diarrhea, pneumonia, recurring infections
Decreased suckling, repeated chewing motions, progressive weakness Anemia, wt loss, death at 4-12 weeks |
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Signs of Fell Pony Syndrome seen at necropsy
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Absence of secondary lymphoid follicles and plasma cells
Erythroid hypoplasia in bone marrow Peripheral ganglionopathy |
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This species has small RBC's, which is why the normal PCV for this animal is lower.
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Goats
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Low PCV and low TP together are characteristic of...
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Blood loss
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Low PCV with normal TP is characteristic of what two causes of anemia?
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RBC destruction
Decreased production |
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Normal PCV with low TP is characteristic of...
|
Protein loss
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Hyperbilirubinemia is suggestive of this cause of anemia.
|
Hemolysis
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Most common form of anemia in ruminants
|
Anemia of chronic disease
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Normal equine PCV
|
28-45%
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A blood smear from this species will usually exhibit mild central pallor, mild anisocytosis, and rouleaux
|
Horse
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3 basic mechanisms of anemia
|
Blood Loss
Hemolysis Decreased erythropoesis |
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What proportion of erythrocytes lost in the equine abdomen/thorax will be autotransfused back into curculation within 24-72h?
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2/3
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The equine blood volume is approximately what % of the horse's body weight?
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8%
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How much of its blod volume can a horse lose acutely and survive?
|
1/3
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Hemoglobinemia and hemoglobinuria are associated with what form of hemolysis?
|
Intravascular
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Which form of hemolysis is associated with clear urine and plasma?
|
Extravascular
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How common is decreased erythropoesis in the horse?
|
Uncommon
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This species fails to release mature erythrocytes as a regenerative response to anemia.
|
Horse
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Why is melena less common in horses than small animals?
|
Gut flora breaks down digested blood before it can pass in feces
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Macrocytosis is associated with this form of anemia.
|
Regenerative
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Microcytosis is associated with this form of anemia.
|
Microcytic
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Hemoglobin should be what proportion of hematocrit?
|
1/3
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A horse has red urine and elevated serum muscle enzymes. This indicates that the red pigment is ...
|
Myoglobin
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A horse has red urine and pink serum. This indicates that the red pigment is ...
|
Hemoglobin
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|
Test that is used to diagnose neonatal isoerythrolysis.
|
Coombs' Test
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|
|
Test used to diagnose Equine Infectious Anemia
|
Coggins Test
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|
Why analyze the bone marrow of an anemic horse?
|
Evaluate erythroid regenerative response since reticulocytes not released into the blood
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|
3 sites for bone merrow aspiration in the horse
|
Sternum
Pelvis Ribs |
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|
Indications for blood transfusion in the horse include...
|
PCV < 20% over 12h period and ongoing hemorrhage
PCV < 12% over 1-2 day period Peracute hemorrhage |
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|
Transfused equine RBC will survive for how long in the recipient horse?
|
Under 1 week
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|
Fungus typically associated with guttural pouch mycosis
|
Aspergillus
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|
True or false: A horse has an episode of epistaxis associated with guttural pouch mycosis. It resolves on its own, so the horse is fine.
|
False. Usually fatal on 2nd or 3rd bleed.
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How is guttural pouch mycosis diagnosed?
|
Upper airway endoscopy
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|
How is guttural pouch mycosis treated?
|
Coil embolization of carotid artery under fluoroscopy.
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|
How are ethmoid hematomas treated?
|
Laser ablation
Formalin injection |
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|
3 arteries that can rupture during foaling
|
Middle uterine artery
Utero-ovarian artery External iliac artery |
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|
Most common BV to rupture during foaling
|
Middle uterine artery
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|
Typical presentation of a mare with post-foaling hemorrhage.
|
Multiparous mare presenting with colic < 48h after foaling and signs of hypovolemic shock
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|
Shock fluid rate in horses
|
20-45 ml/kg/h
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|
Treatment for post-foaling hemorrhage in the mare
|
1 L hypertonic saline or colloid
Crystalline fluid at shock rate Whole blood transfusion Oxytocin to involute uterus Flunixin Decrease fibrinolysis (aminocaproic acid) Naloxone to reduce CV derangements |
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|
What qualifies excessive post-castration bleeding in a horse?
|
Stream/fast drip > 15 mins
|
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|
Treatment for post castration hemorrhage in the horse
|
Drop horse again, re-emasculate, transfix bleeder, pack with gauze
Decrease fibrinolysis Treat for blood loss/shock with IVF and blood transfusion PRN |
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|
Horses that ear red maple leaves will develop anemia due to...
|
Oxidative RBC damage
|
|
|
CS of red maple toxicosis
|
Jaundice
Discolored urine, Coagulopathy Renal failure Laminitis Acute death |
|
|
Treatment of red maple toxicosis in the horse
|
Blood transfusion
Aggressive fluid therapy for kidneys Vitamin C via NG tube Vitamin E and selenium |
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|
Two agents that cause piroplasmosis in the horse
|
Babesia caballi
Theileria equi |
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|
CS of piroplasmosis in the horse
|
IP of 5-28 days
Fever Anorexia Incoordination Hemoglobinuria Death |
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|
How is piroplasmosis diagnosed in the horse?
|
ID organism on blood smear
ELISA IFAT Complement fixation |
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|
Treatment for equine piroplasmosis
|
Imidocarb
Tick control for prevention |
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|
Infectious agent that causes anaplasmosis
|
Anaplasma phagocytophilum
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|
|
Tick vector that spreads anaplasmosis
|
Ixodes
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|
Region in which Anaplasma is most common
|
East Coast USA
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CS of equine anaplasmosis
|
Fever
Icterus Edema Petechiation Ataxia Reluctance to move |
|
|
How is Anaplasmosis diagosed in the horse?
|
PCR when early fever
Cytoplasmic inclusions on PMN and eosinophils Seroconversion in weeks Leukopenia Thrombocytopenia Anemia |
|
|
Treatment for equine anaplasmosis
|
Recover on own in 2-3 weeks
Supportive care Otytetracycline to shorten disease course |
|
|
Disease AKA "Swamp Fever" in the horse
|
Equine infectious anemia
|
|
|
This disease of horses is transmitted by horseflies and causes necrotizing vasculitis
|
Equine infectious anemia
|
|
|
CS of acute EIA
|
Fever, anemia, icterus, edema, weight loss, depression, petechiation, abortion, death
|
|
|
CS of chronic EIA, if any
|
Depression
Weight loss Anemia Weakness Cyclic pyrexia |
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|
How is EIA diagnosed?
|
Coggins' Test (AGID)
PCR Coombs' + Anemia Thrombocytopenia |
|
|
Treatment for EIA
|
None. Euthanize or isolate.
|
|
|
How is EIA controlled when a reactor (+) horse is found?
|
Euthanasia or permanent ID by brand or tattoo
Isolation 200 yards from other horses Quarantine all horses within 200 yards of reactor and test every 30d until all negative for 60d |
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|
Cross matching donor RBC with patient serum is this kind of crossmatch
|
Major
|
|
|
Cross matching recipient RBC with donor serum is this kind of crossmatch
|
Minor
|
|
|
When crossmatching blood types, these signs indicate an incompatability
|
Hemolysis
Agglutination |
|
|
You are getting ready to transfuse a patient and find out that the donor blood has a minor incompatibility. What can you do?
|
Remove serum from donation and give washed RBC
|
|
|
Describe the immune system of a newborn foal or ruminant.
|
Immunocompetent: Able to make a response
Immunonaive: Immune system has no prior memory Required 10 days for acquired immunty to engage |
|
|
How long before a foal is able to have an acquired immune response?
|
10 days
|
|
|
Placenta of the mare is...
|
Epitheliochorial (6 tissue layers)
|
|
|
A newborn foal has small amounts of what antibody from in utero exposure
|
IgM
|
|
|
How long is a foal's gut epithelium capable of absorbing large proteins?
|
6 -24hours
|
|
|
Normal IgG levels for adequate passive transfer in the foal
|
>800mg/dL
|
|
|
IgG levels associated with partial FPT in the horse
|
400-800 mg/dL
|
|
|
IgG levels associated with absolute FPT in the horse
|
<400 mg/dL
|
|
|
Causes of FPT attributable to the mare
|
Fescue agalactia
Disease/death of the mare Malnutrition of mare Poor colostrum quality |
|
|
Causes of FPT attributable to the foal
|
Foal prematurity/dysmaturity
Disease of foal Foal rejection or separation Early maturation of the gut |
|
|
Administering these drugs to a pregnant mare may cause early maturation of the foal gut and FPT
|
Steroids
|
|
|
Serum IgG concentrations in the foal first become detectable at...
|
6 hours
|
|
|
Serum IgG levels in the foal peak at this age...
|
18-24 hours
|
|
|
Most quanititatively accurate test for FPT in the foal
|
Radial immunodiffusion
|
|
|
How long does it take to get data from a radial immunodiffusion test?
|
24 h
|
|
|
Most common semi-quantitiative test used to measure passive transfer in the foal
|
ELISA
|
|
|
How should a healthy foal under 3 hours old be handled if at risk of FPT?
|
Oral colostrum, 1-3 L good quality colostrum, feeding 500 mL hourly for first 6-8 hours
|
|
|
Specific gravity of "good quality" equine colostrum
|
1.060
|
|
|
How should a foal with FPT be managed if discovered over 6-12 hours of age?
|
IV plasma therapy, 1-3 L
(0.5 mL/kg over 10 mins, then gradually increase to 40 mL/kg/hr) |
|
|
Signs of a transfusion reaction in a foal
|
Elevated HR, temp, agitation
|
|
|
Long-term downside to plasma transfustion in an FPT foal
|
Cause future reactions to blood products
|
|
|
A healthy 45 kg foal with partial FPT is kept in a clean environment at low risk of contamination. How should he be managed?
|
Advise owner of increased risk of infection-- keep isolated and clean
Monitor closely for septicemia or other illness |
|
|
A healthy 45 kg foal in a high risk environment has absolute FPT. How should he be managed?
|
Transfuse with 1-3 L of plasma
|
|
|
A sickly 45 kg foal in a high risk environment has partial FPT. How should he be managed?
|
Transfuse with 2-3 L plasma
|
|
|
What follow-up monitoring is appropriate following a plasma transfusion in a foal?
|
Recheck IgG 6-24h after administration
|
|
|
Most likely blood antigen types to cause NI in a horse
|
Qa and Aa
|
|
|
If a mare that is Aa negative is mated to a stallion that is Aa positive, and the foal is Aa positive, there is a risk of this disease porcess occurring.
|
Neonatal isoerythrolysis
|
|
|
Describe the breeding history of a mare with an NI foal.
|
Multiparous
Previous dystocia, sick foal, or dead foal |
|
|
True or false: Foals who have NI often have adequate passive transfer
|
True
|
|
|
CS of neonatal isoerythrolysis
|
Lethargy, loss of interest in suckling
Hematuria Icteric Anemia Secondary complications |
|
|
Treatment for NI
|
If PCV < 15%, transfuse with either mare's washed RBC or a compatible donor
Supportive care, fluids and rest, minimize stress |
|
|
Prognosis for NI if caught early and treated aggressively
|
Most foals survive
|
|
|
How can NI be prevented pre-breeding/pre-foaling?
|
Blood type mare and stallion
|
|
|
How can NI risk be detected at the time of foaling?
|
Juandiced Foal Agglutination Test presuckling (tests for agglutination of foal RBC by mare colostrum)
Post suckling: Coombs' test |
|
|
If a mare is found to have anti-foal RBC antibodies, what should be done?
|
Don't allow foal to suckle dam for 48 hours.
Provide colostrum from other dource, then milk replacer or nurse mare Milk out the dam while foal not allowed to suckle Keep mare and foal together but not suckling |
|
|
Disease in which mare colostrum contains Ab to foal platelets
|
Alloimmune thrombocytopenia
|
|
|
When do CS of alloimmune thrombocytopenia begin to show?
|
12-24h
|
|
|
CS of alloimmune thrombocytopenia
|
Petechia and bruising
Prolonged bleeding Signs of internal hemorrhage |
|
|
Treatment for alloimmune thrombocytopenia
|
Keep foal quiet
Provide fresh plasma from source other than mare |
|
|
Disease caused by an autosomal recessive trait that prevents maturation of B and T cells in Arabian foals.
|
Severe combined immunodeficiency
|
|
|
Recurring infections in SCID foals tend to begin at this age.
|
3-4 weeks
|
|
|
Cause of death in SCID foals, usually
|
Odd or innocuous respiratory infections like adenovirus or pneumocystitis carinii
|
|
|
Antemortem Dx of SCID is made by...
|
Lymphs < 1000/uL
Pan hypoglobulinemia Genetic testing |
|
|
Postmortem diagnosis of SCID is made based on...
|
Absence of lymphatic tissue
(Fatty thymus, lack of germinal centers in LN and sspleen) |
|
|
Prognosis for SCID
|
No cure-- foals die by 5 months
|
|
|
How can SCID be prevented?
|
Genetic testing of all breeding animals at risk
Avoid breeding carriers |
|
|
This breed of horse carries an autosomal recessive gene that causes a congenital fatal syndrome marked by anemia, immunodeficiency, and peripheral ganglionopathy.
|
Fell pony
|
|
|
Components of Fell Pony Syndrome include...
|
Anemia
Immunodeficiency Peripheral ganglionopathy |
|
|
Age at which Fell Pony Syndrome typically manifests.
|
2-3 weeks
|
|
|
CS of Fell Pony Syndrome
|
Decreased suckling, chewing, progressive weakness, anemia, wt loss, death at 4-12 weeks
|
|
|
Signs of Fell Pony Sundrome seen at necropsy
|
Absence of secondary lymphoid follicles
Lack of plasma cells Erythroid hypoplasia Peripheral ganglionopathy (trigeminal, cranial mesenteric, dorsal root ganglia) |
|
|
Most common form of anemia in ruminants
|
Anemia of chronic disease
|
|
|
Two major parasitic causes of blood loss in ruminants
|
Haemonchus
Coccidia |
|
|
Barber-poleworm that resides in the abomasum/C3 of ruminants/camelids, respectively
|
Haemonchus contortus
|
|
|
Why are Haemonchus so prevalent in alpacas?
|
Monthly deworming with Ivermectin for P. tenuis
|
|
|
Three drugs effective against Haemonchus
|
Fenbendazole
Moxidectin Levamisole |
|
|
Two blood abnormalities caused by Coccidia
|
Anemia and hypoproteinemia
|
|
|
In what food animal group is Coccidia typically a problem?
|
First month of fattening lambs
|
|
|
Treatment for Coccidia
|
Coccidiostats like monensin
Management |
|
|
Infestation of cattle with sucking lice is called...
|
Pediculosis
|
|
|
Conditions ideal for lice infestation in a cattle operation
|
Winter months with poor nutrition and crowding
|
|
|
Most common tick-borne infection of cattle worldwide
|
Anaplasmosis
|
|
|
Incidence of Anaplasmosis in cattle is highest in...
|
Late spring and summer
|
|
|
Primary determinant of CS severity seen with Anaplasmosis
|
Age of initial infection
|
|
|
Anaplasmosis is least severe in cattle aged...
|
Up to 6-9 months
|
|
|
Acute CS of anaplasmosis in adult cattle include
|
Fever
Anorexia Decreased milk Decreased rumination Dry muzzle Lethargy Staggering or aggressiveness (cerebral hypoxia) Constipation Abortion |
|
|
True or false: Cattle infected with Anaplasma clear the pathogen within a year of resolution of CS
|
False, they become persistent carriers
|
|
|
CS seen in a persistent carrier of Anaplasma marginale
|
None
|
|
|
Vectors responsible for transmission of Anaplasma marginale
|
Ixodidae (Dermacentor in US)
Flies Iatrogenic |
|
|
Incubation period for Anaplasma marginale in livestock
|
15-30 days
|
|
|
Diagnosis of Anaplasmosis in cattle is made on the basis of...
|
Falling Hct
Blood smear with NMB stain ELISA (not if acute) |
|
|
Treatment for Anplasmosis in cattle
|
Supportive care
Oxytetracycline |
|
|
Pathogen also known as "Epy" to some llama producers
|
Mycoplasma hemollamae
|
|
|
Samll bacteria lacking a cell wall, they reside on the durface of camelid RBC's
|
Mycoplasma hemollamae
|
|
|
Mycoplasma hemollamae is transmitted by...
|
Arthopods
Intrauterine |
|
|
CS of Mycoplasmosis
|
Anemia
Fever Depression Indertility Edema Poor growth |
|
|
Diagnosis of M. hemollamae is made based upon...
|
Blood smears
PCR |
|
|
Treatment for Mycoplasma hemollamae
|
Supportive care
Oxytetracycline to suppress infection |
|
|
Pathogen that causes an acute hemolytic syndrome in calves and lambs
|
Leptospira
|
|
|
CS of leptospirosis in ruminants
|
Fever
Lethargy Icterus Anemia Petechiae |
|
|
DIagnosis of Leptospirosis is based upon...
|
CS
Leukocytosis Hyperfibrinogenemia Leptospuria PCR Elevated Ab titer |
|
|
How is leptospirosis in ruminants treated?
|
Oxytetracycline
Penicillin Vaccination |
|
|
Tick borne intraerythrocytic disease in cattle
|
Babesiosis
|
|
|
Cattle infected up to this age may become asymptomatic carriers of Babesia
|
9 months
|
|
|
Babesia carriers are resistant to developing clinical disease for at least...
|
4 years
|
|
|
Agent that spreads Babesia among food animals
|
Ticks like Boophilus
(also Iatrogenic) |
|
|
Cause of anemia with Babesiosis
|
Intravascular hemolysis
|
|
|
CS of Babesiosis in ruminants
|
Acute: Fever, depression, icterus, anorexia, tachycardia, tachypnea, anemia, hemoglobinemia, hemoglobinuria, abortion, death
Also hyperexcitability, convulsions, opisthotonos, coma, and death |
|
|
How is Babesia diagnosed in food animals?
|
CS
Blood smears PCV dramatically drops in under 1 week Complement fixation and IFA |
|
|
How is Babesia prevented in food animals?
|
Eradication of Boophilus tick
Maintain endemic herd Vaccination (moderates disease) |
|
|
Agent responsible for bacillary hemoglobinuria (aka "red water")
|
Clostridium haemolyticum/novyi
|
|
|
Where in the US is bacillary hemoglobinuria endemic?
|
Poorly drained areas in the west
|
|
|
CS of Clostridium haemolyticum infection
|
Severe depression, anorexia, fever, hemoglobinemia, hemoglobinuria
|
|
|
Pathogen that seeds itself in the liver in areas damaged by migrating liver flukes
|
Clostridium haemolyticum
|
|
|
How does Clostridium haemolyticum cause disease?
|
Toxins cause hemolysis
|
|
|
la pena
|
pain; trouble; grief
|
|
|
Neurologic disorder commonly seen in milk-reared calves when first given free choice access to water
|
Water intoxication
|
|
|
Cause of CS in water intoxication
|
Volume overload causing drop in Na and Cl, and serum hypotonicity with hemolysis
|
|
|
CS of water intoxication in calves
|
Depression, convulsions, coma
Hemolytic anemia |
|
|
Treatment for water intoxication
|
Restrict water
Hypertonic saline Mannitol Corticosteroids |
|
|
Species most sensitive to copper toxicosis
|
Sheep
|
|
|
How does copper intoxication cause hemolysis?
|
Sequestered copper released from the liver in times of stress
Hepatocyte death Copper in blood causes RBC oxidation and hemolysis |
|
|
CS of copper intoxication
|
Asymptomatic until onset of hepatic necrosis
Inappetance, lethargy, weakness, pallor, tachycardia, tachypnea,hemoglobinuria, hypoxemia, anemia |
|
|
Treatment for coper intoxication
|
IV fluids
Oxygen Vitamin E Cuprimine to increase copper excretion Anhydrous Na sulphate Ammonium molybdate |
|
|
How can copper toxicosis in sheep be prevented?
|
Avoid sources of copper like cattle trace mineral, poulty or horse feed, copper fungicides
|
|
|
Bone marrow can begin to replace transfused RBC within...
|
5 days
|
|
|
Does a ruminant need to be cross-matched if it is his first blood transfusion?
|
No
|
|
|
How should a blood transfusion for a llama be administered?
|
Slowly at first, (0.1 cc/kg in 10 mins) then increase to 20 mL/kg
|
|
|
Normal blood volume of adult camelid
|
70 ml/kg
|
|
|
Blood volume that can be taken from a single donor camelid
|
~ 10 ml/kg
|
|
|
A camelid may show these adverse reactions to a blood transfusion
|
Tachypnea, dyspnea, restlessness, defecation, tachycardia, piloerection, muscle fasiculations, sudden collapse
|
|
|
Severe adverse reactions to camelid blood transfusions should be treated with...
|
Epinephrine
|
|
|
Mild adverse reactions to camelid blood transfusions should be treated by...
|
Slow transfusion
+/- Corticosteroids or flunixin |
|
|
Autosomal recessive disorder of Holstein cattle that causes calves to be predisposed to recurrent bacterial infections.
|
Bovine leukocyte adhesion deficiency--> BLAD
|
|
|
Prevalence of BLAD in Holstein calves
|
6%
|
|
|
How does BLAD cause disease?
|
Lack of glycoproteins on neutrophils so they cannot migrate into tissue
|
|
|
CS of BLAD
|
Calf normal at birth but develop chronic, recurrent bacterial infections in first few months
Fever, pneumonia, stomatitis, gengivitis, diarrhea, dermatitis Death commonly before 1 year |
|
|
Calves with this genetic problem have persistent neutrophilia without left shift, lymphocytosis, and monocytosis. PMN not typically seen in infected tissue.
|
BLAD
|
|
|
How is BLAD definitively diagnosed?
|
PCR test available from Holstein Association of America
|
|
|
Autosomal recessive disorder of Shorthorn cattle, characterized by a defect of lymphocyte maturation and impaired cellular immunity.
|
Inherited deficiency of lymphocyte maturation (IDLM)
|
|
|
Calves with this condition have reduced intestinal absorption of zinc and a high metabolic requirement for zinc.
|
IDLM
|
|
|
Initial CS of IDLM in calves
|
Dermatologic disease at 1-2 months: Exanthema, alopecia, hyperkeratosis of head, neck, and limbs
|
|
|
Progression of IDLM
|
Dermatologic disease at 1-2 months
Untreated animals lose wt, develop pneumonia, and die before 4 months age |
|
|
Test used to diagnose IDLM in calves antemortem
|
Lymphocyte blastogenesis
|
|
|
Post mortem lesions accociated with IDLM
|
Acanthosis and hyperkeratosis
Lack of lymphocytes in lumphatic tissues |
|
|
How is IDLM treated?
|
Lifelong administration of zinc oxide
|
|
|
Autosomal recessive disorder of Hereford and Brangus cattle. Lysosomal storage disorder that decreases functionality of leukocytes and platelets.
|
Chediak-Higashi Syndrome
|
|
|
Calves affected with this genetic disorder have decreaced bacteriocidal activity and coagulopathy.
|
Chediak-Higashi syndrome
|
|
|
CS of Chediak-Higashi syndrome.
|
Partial albinism
Oculocutaneous hypopigmentation Photophobia Lacrimation Septicemia and death before 1 year of age |
|
|
Calves with this disorder have cytoplasmic granules in leukocytes, decreased leukocyte bacteriocidal activity, and decreased platelet function
|
Chediak-Higashi syndrome
|
|
|
How is Chediak-Higashi syndrome diagnosed?
|
SIgnalment, history, results of physical exam, and hematologic abnormalities
|
|
|
How does pregnancy affect the immune system of a pregnant cow?
|
Compromises it
|
|
|
What branch of the bovine immune system is suppressed during pregnancy and early postpartum?
|
Cell mediated immunity
|
|
|
How does pregnancy suppress the bovine immune system?
|
Increase in glucocorticoid activity in periparturient cow decreases PMN bacteriocidal activity and increases susceptibility to infections
|
|
|
IgG level required for adequate passive transfer in the calf
|
1,000 mg/dL
|
|
|
IgG level required for adequate passive transfer in the camelid
|
1,500 mg/dL
|
|
|
"Gold standard" test for diagnosing FPT in the calf.
|
Radial immunodiffusion
|
|
|
This test uses quantification of total serum protein as indicator of passive transfer of immunity
|
Refractometry
|
|
|
Total serum protein level indicating APT in the calf
|
> 5.0 g/dL
|
|
|
Total serum protein level indicating FPT in the calf
|
< 4.5 g/dL
|
|
|
Disadvantage of refractometry for diagnosis of FPT in the calf
|
False positive (APT) in dehydrated calf possible
|
|
|
This test uses ZnSO4 to precipatate IgG in calf serum.
|
Zinc sulfate turbidity test
|
|
|
In a ZnSO4 turbidity test, does turbidity or clarity indicate APT?
|
Turbidity
|
|
|
Cause of false positive on ZnSO4 turbidity test
|
Hemoglobinemia
|
|
|
Cause of false negative on ZnSO4 turbidity test
|
Poor reagent quality
|
|
|
This test uses NaSO3 to precipitate IgG in calf serum at varying concentrations.
|
Sodium sulfite precipatation test
|
|
|
In NaSO3, will calf serum with APT precipatate IgG at 14%, 16%, or 18% concentration?
|
All three
|
|
|
If a Na SO3 precip test on calf seum is turbid at 18%, this indicates what IgG level?
|
<500 mg/dL
|
|
|
If a Na SO3 precip test on calf seum is turbid at 18% and 16%, this indicates what IgG level?
|
500-1500 mg/dL
|
|
|
If a Na SO3 precip test on calf seum is turbid at 18%, 16%, and 14%, this indicates what IgG level?
|
>1,500 mg/dL
|
|
|
Disadvantages of NaSO3 test in diagnosing FPT in the calf.
|
False negative if bad reagent
False positive if hemolysis FPT cutoff falls in the intermediate result range |
|
|
IgG level at which glutaraldehyde will cause coagulation of calf serum.
|
600 mg/dL
|
|
|
Disadvantage of glutaraldehyde coagulation test for diagnosing FPT in calves.
|
May have FPT but be over the 600 mg/dL coagulation point = false +
|
|
|
Why is GGT measured as a gauge of FPT in bovines?
|
Mammary epithelial cells secrete large numbers of GGT during colostrogenesis--> calf should take in GGT with colostrum
|
|
|
GGT level that indicates APT in a calf
|
> 200 IU/L
|
|
|
GGT level that indicates FPT in a calf
|
< 50 IU/L
|
|
|
Treatment of calf under 12h of age with FPT
|
Colostrum at 10% BW in first 12h
Administer by bottle, OG or NG tube Colostral substitute or replacement possible |
|
|
Treatment of calf over 18h of age with FPT
|
IV bovine plasma (20-40 mL/kg)
Usually 2-4 L plasma in 40 kg calf |
|
|
Specific gravity of good quality bovine colostrum
|
1.050
|
|
|
How should frozen colostrum be stored?
|
Frozen in 1 gal plastic containers or 2qt Ziploc bag
|
|
|
How should frozen colostrum be thawed?
|
Gradually thaw in warm water or microwave at 60% with stirring
|
|
|
These species tend to have distinct large individual lymph nodes.
|
Ruminants
Carnivores |
|
|
These species tend to have many small lodes arranged in clusters.
|
Porcine
Equine |
|
|
All lymph passes through... before entering the blood stream.
|
Lymph node
|
|
|
Two reasons that lymph passes through the nodes before entering the blood stream.
|
Recruits lymphocytes against exposed antigens
Exposed to phagocytes to remove pathogens |
|
|
Locations where tonsils (unencapsulated lymph tissue) may be found
|
Pharyngeal, palatine, laryngeal, intestinal, preputial, vaginal areas
|
|
|
Lymph nodes associated with the blood stream. Most obvious in sheep.
|
Hemal node
|
|
|
CS of lymphatic disease
|
Peripheral swelling
Enlarged lymph nodes Lethargy Lameness Fever |
|
|
Occurs probably when bacteria diffuses into the tissue around lymph vessels.
|
Lymphangitis
|
|
|
Also known as "fat leg," or "big leg"
|
Lympangitis
|
|
|
Possible rule outs for a swollen horse limb that is very lame.
|
Fracture
Septic joint Lymphangitis |
|
|
Treatment for lymphangitis in the horse
|
Broad spectrum antibiotics
Analgesics Antiinflammatories Walking Pressure wraps Cold therapy |
|
|
How long does it take for lymphangitis to resolve?
|
Several weeks
|
|
|
Equine disease caused by Histoplasma capsulatum farciminosum, a dimorphic fungus
|
Epizootic lymphangitis
|
|
|
Epizoototic lymphangitis is endemic in these regions
|
Mediterranean, Africa, India, Pakistan, and Japan
|
|
|
How is epizootoic lymphangitis (Histoplasma) transmitted?
|
Through wounds, especially those contacted by fomites
|
|
|
Incubation period for epizootic lymphangitis
|
Weeks to months
|
|
|
How long can Histoplasma capsulatum survive in the environment?
|
Months in moist warm conditions
|
|
|
CS of epizootic lymphangitis
|
Painless intradermal nodules emerging on the extremities, chest, face, and neck.
Eventually they rupture. Cording of lymphatics. Local LN enlargement Ulcerative lesions partially heal then reopen. |
|
|
How is epizootic lymphangitis diagnosed?
|
CS of non-healing skin nodules and corded lymphatics
|
|
|
List two reportable equine lymphatic diseases.
|
Epizootic lymphangitis
Glanders |
|
|
How long does definitive culture of Histoplasma capsulatum take?
|
2-8 weeks
|
|
|
This dimorphic fungus appears on an impression smear as a Gram positive, pleiomorphic, and ovoid structure. Causes epizootic lymphangitis.
|
Histoplasma capsulatum var. farciminonsum
|
|
|
Treatment for epizootic lymphangitis
|
IV sodium iodide
Amphotericin B Surgical excision of lesions OR Quarantine and euthanasia |
|
|
Agent responsible for glanders
|
Burkholderia mallei
|
|
|
How long does definitive culture of Histoplasma capsulatum take?
|
2-8 weeks
|
|
|
This dimorphic fungus appears on an impression smear as a Gram positive, pleiomorphic, and ovoid structure. Causes epizootic lymphangitis.
|
Histoplasma capsulatum var. farciminonsum
|
|
|
Treatment for epizootic lymphangitis
|
IV sodium iodide
Amphotericin B Surgical excision of lesions OR Quarantine and euthanasia |
|
|
Agent responsible for glanders
|
Burkholderia mallei
|
|
|
This reportable equine lymphatic disease is caused by a short gram-negative aerobic rod bacteria called Burkholderia mallei.
|
Glanders
|
|
|
Where is glanders endemic?
|
Eastern Europe, Asia, and North Africa
|
|
|
Incubation period of glanders
|
Few days to a month
|
|
|
Risk factors for glanders
|
Poor sanitation, crowding, immunosuppression
|
|
|
How is glanders transmitted?
|
Through mucous membranes, contaminated feed and water
|
|
|
Which equine disease survives in the environment: Epizootic lymphangitis or glanders?
|
Epizootic lymphangitis
|
|
|
This lymphatic disease of horses may present with nodules developing into crater-like buds with exudates. These are called "Farcy buds"
|
Glanders
|
|
|
List the different forms of glanders
|
Cutaneous form (Farcy)
Nasal form Respiratory form |
|
|
How may glanders be diagnosed?
|
Mallein (LPS) hypersensitivity test
Serologic test Strauss test (Guinea pigs) |
|
|
Treatment for glanders
|
Euthanasia
|
|
|
A common fungal saphrophyte that can cause formation of non-painful cutaneous nodules that ulcerate and drain in the horse.
|
Sporothrix
|
|
|
Incubation period of Sporothrix
|
3-5 weeks
|
|
|
CS associated with sporotrichosis in the horse
|
Lymphangitis
Cutaneous nodules that ulcerate Corded lymphatics |
|
|
How is sporotrichosis diagnosed?
|
CS
Histopathology (budding spherical-cigar shaped yeasts) Culture |
|
|
Treatment for sporotrichosis
|
IV sodium iodide, then orally
Treat 4 weeks beyond resolution of CS Also may try antifungals |
|
|
Prognosis for sporotrichosis in the horse
|
Good to excellent
|
|
|
How long should you treat a horse for sporotrichosis
|
4 weeks beyond resolution of CS
|
|
|
Intracellular, facultative anaerobic G+ bacteria prevalent in the Southwest . Tends to live inside abscesses.
|
Corynebacterium pseudotuberculosis
|
|
|
Nitrate negative Corynebacterium pseudotuberculosis is what biovar?
|
Ovis
|
|
|
Nitrate positive Corynebacterium pseudotuberculosis is what biovar?
|
Equi
|
|
|
Which biovar of Corynebacterium pseudotuberculosis infects cattle?
|
Either ovis or equi
|
|
|
Biovar of Corynebacterium pseudotuberculosis that infects small ruminants
|
Ovis
|
|
|
Most common presentation of Corynebacterium pseudotuberculosis
|
External abscessation
|
|
|
How long may Corynebacterium pseudotuberculosis reside in the soil?
|
8 months
|
|
|
How long may Corynebacterium pseudotuberculosis live in hay and shavings?
|
2 months
|
|
|
How may Corynebacterium pseudotuberculosis enter the host?
|
Wounds or abrasions contaminated by flies, fomites, or other infected wounds
|
|
|
Incubation period for Corynebacterium pseudotuberculosis
|
3-4 weeks
|
|
|
What time of the year does Corynebacterium pseudotuberculosis typically present with external abscessation?
|
Late summer to early fall
|
|
|
Does Corynebacterium pseudotuberculosis replicate intracellularly or extracellularly?
|
Intracellularly
|
|
|
What two factors facilitate the intracellular survival of Corynebacterium pseudotuberculosis?
|
Bacteria cell wall lipids
Phospholipase-D exotoxin |
|
|
Function of phospholipase-D exotoxin in Corynebacterium pseudotuberculosis.
|
Inactivates complement
Increases vascular permeability |
|
|
This pathogen causes "pigeon fever" in the horse.
|
Corynebacterium pseudotuberculosis
|
|
|
Where is the most common site of external abscessation in the horse with Corynebacterium pseudotuberculosis?
|
Pectoral region and ventral midline
|
|
|
Case fatality in equines with Corynebacterium pseudotuberculosis internal abscessation.
|
30-40%
|
|
|
CS of internal abscessation associated with Corynebacterium pseudotuberculosis in the horse
|
Depressed appetite, fever, lethargy, weight loss, respiratory disease, abdominal pain
|
|
|
How is Corynebacterium pseudotuberculosis diagnosed in the horse
|
CS in endemic area
Culture or exudate from abscesses Serology for synergistic hemolysis inhibition |
|
|
Why ultrasound abscesses associated with Corynebacterium pseudotuberculosis?
|
Examination of external abscesses
Dx of internal abscesses Documentation of affected organs Collecting FNA or biopsy Monitoring Tx results |
|
|
Two drugs effective against C. pseudotuberculosis internal infection in the horse
Also duration of treatment |
Penicillin
TMS (+/- rifampin) Treatment for 1-6 months, until titer < 256 |
|
|
Disease caused by Corynebacterium pseudotuberculosis in small ruminants and camelids
|
Caseous lymphadenitis
|
|
|
CS of Corynebacterium pseudotuberculosis in cattle
|
Cutaneous granulomas, mastitis, visceral infection, mixed infection
|
|
|
This disease, caused by Corynebacterium pseudotuberculosis, causes abscesses of large superficial lymph nodes in small ruminants
|
Caseous lymphadenitis
|
|
|
Main CS of internal abscessation associated with Corynebacterium pseudotuberculosis in small ruminants
|
Chronic weight loss
|
|
|
Tx for caseous lymphadenitis in small ruminants
|
Allow abscess to mature, establish drainage, lavage with antiseptic solution, possibly excise under general anesthesia
|
|
|
How is caseous lymphadenitis prevented
|
Isolation of infected animals
Fly control Sanitation Careful shearing practices Disinfection of contaminated fomites Culling of infected animals |
|
|
How effective do vaccines against CLA tend to be?
|
Effective at reducing incidence and severity of disease
|
|
|
Gram positive cocci responsible for causing strangles
|
Streptococcus equi ss. equi
|
|
|
Virulence factors associated with Strep. equi
|
HA capsule inhibits PMN
M-proteins prevent phagocytosis |
|
|
How is Strep equi transmitted?
|
Direct or indirect contact with purulent discharge
|
|
|
Animals infected with Strep. equi usually shed the organism for how long?
|
4-6 weeks
|
|
|
Where in a carrier horse is Strep. equi sequestered?
|
Chondroids in guttural pouch
|
|
|
After S. equi enters the pharynx, how does it get to the lymph nodes?
|
Through tonsils and follicular lymphoid tissue.
|
|
|
CS of strangles
|
Fever
Mucopurulent nasal discharge Submandibular and retropharyngeal lymphadenopathy Depression, anorexia Dysphagia Upper airway obstruction |
|
|
% of horses with strangles that develop complications
|
20%
|
|
|
Describe "Bastard strangles"
|
Metastatic abscessation of the lung, mesentery, liver, spleen, kidneys, and/or brain following a typical infection with Strep. equi
|
|
|
Prognosis for bastard strangles
|
Guarded
|
|
|
Type III hypersensitivity reaction in which immune complexes with Strep equi are deposited in the vascular endothelium
|
Purpura hemorrhagica
|
|
|
CS of purpura hemorrhagica
|
Vasculitis: Edema, petechiae, and ecchymoses
|
|
|
How is Strep equi diagnosed?
|
Culture of nasal swab or wash
PCR Serology Endoscopy |
|
|
How is S. equi treated?
|
Drainage of abscesses
Lavage of guttural pouches Antibiotics if febrile or internal abscesses |
|
|
Uncomplicated cases of S. equi may shed the bacteria for how long past the resolution of clinical signs?
|
4-6 weeks
|
|
|
How is ACh synthesized and stored in the presynaptic terminal?
|
Synthes:
In Presynaptic Terminal: Choline acetyltransferases (e) catalyzes Acetyl CoA + Choline ----> to form ACh Storage: ACh stored in SYNAPTIC VESICLES W/ ATP and proteoglycan for later use |
