Term
| Name the clinical signs of immune-mediated hemolytic anemia |
|
Definition
| Depression, Weakness, Lethargy, Anorexia, Pale MM, bounding pulses, tachychardia, tachypnea, fever, icterus, dark red/yellow/brown urine, petechiae (with concurrent thrombocytopenia) |
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|
Term
| Sex, Age, and Breed for number-one signalment of IMHA in small animal? |
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Definition
| Female (spayed), middle-aged, cocker spaniels |
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|
Term
| Diagnostic tests for IMHA? (Name 5) |
|
Definition
| Coomb's test; autoagglutination (negates need for Coomb's test); presence of spherocytes; signs of intravascular hemolysis (hemoglobinemia, hemoglobinuria); Inflammatory leukogram |
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|
Term
| What's unique about diagnosing IMHA in cats? |
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Definition
| Difficult to recognize spherocytes in the cat, because their RBCs already lack central pallor |
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Term
| First treatment for IMHA in SA? |
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Definition
| Treat the underlying cause! (Primary or secondary) |
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|
Term
| Treatment options for IMHA? |
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Definition
| (Treat underlying disease!), IV fluids? (controversy), Cage rest, oxygen if needed, transfusion if indicated, immunosuppressive drugs (steroids), Heparin |
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|
Term
| What category of drugs is the mainstay treatment for IMHA? |
|
Definition
|
|
Term
| Which specific drug is good for maintenance with IMHA? |
|
Definition
|
|
Term
| When do we use Intravenous human immunoglobulin (hIVGG)? What is it exactly? |
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Definition
| We use it in IMHA when we have lack of results with other drugs (it's expensive though!). It is purified human IgG |
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|
Term
| When is a splenectomy used with IMHA? |
|
Definition
|
|
Term
| What are the 2 main complications of IMHA? |
|
Definition
| DIC, Thromboembolic disease |
|
|
Term
| What's the mortality of IMHA? |
|
Definition
| Moderate to high, 20-50%. |
|
|
Term
| Name some poor prognostic indicators (up to 8) |
|
Definition
| 1) High bilirubin (>5 mg/dl), 2) autoagglutination, 3) Intravascular hemolysis, 4) Hypoalbuminemia, 5) Thrombocytopenia 6) Lower PCV, 7) Low reticulocyte values, 8) rapid hemolysis |
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|
Term
| With kitten neonatal isoerythrolysis, what blood type does the queen, father, and neonate typically have? |
|
Definition
| Queen = type B, Father = type A, Neonate = type A |
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|
Term
| Do we need to worry about NI in cats if it's the queen's first litter? Why or why not? |
|
Definition
| Yes, because cats have naturally occurring anti-A alloantibodies. |
|
|
Term
| What is the hallmark sign of kittens with NI? |
|
Definition
| Dark, reddish-brown urine |
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|
Term
| Name the clinical signs of NI in kittens (6) |
|
Definition
| 1. Sudden death w/n 24 hours (due to anemia, DIC, acute renal failure) 2. Fading kitten syndrome 3. ** Dark, reddish-brown urine 4. Pale MM 5. Icterus 6. Tail-tip necrosis |
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|
Term
| Treatment options for kittens with NI? |
|
Definition
| 1. Separate affected kitten from mother for first 2-3 days after birth and use milk replacer 2. Supportive care 3. Blood transfusion if needed |
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|
Term
| How do you diagnose NI in kittens? Include during necropsy. |
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Definition
| Clinical signs. Positive slide agglutination test and positive Coomb's test. At necropsy, liver and splenic erythrophagocytosis and extramedullary hematopoiesis, nephropathy. |
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|
Term
| What type of cats are especially susceptible to NI? |
|
Definition
| Devon rex (British origin), curly coats, and exotic short hairs |
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|
Term
|
Definition
| Hemoglobin in which the iron component of the heme group has been oxidized from the ferrous to the ferric state |
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|
Term
| What are the causes of methemoglobinemia? |
|
Definition
| 1. Increased production of methemoglobin by oxidants 2. Decreased reduction of methemoglobin due to a decrease in the RBC methemoglobin reductase enzyme (can be inherited) |
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|
Term
| Primary differentials for methoglobinemia? |
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Definition
|
|
Term
| Would oxygen help methoglobinemic patients? |
|
Definition
|
|
Term
| Clinical signs of methemoglobinemia? |
|
Definition
| May be inapparent. If there are signs: cyanotic MM, lethargy, tachycardia, tachypnea, ataxia, stupor/coma/death |
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|
Term
| Laboratory signs of methemoglobinemia? |
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Definition
| 1. Anemia (if oxidant drug) or mildly elevated PCV 2. Heinz bodies 3. Elevated BUN/ALT 4. Brown-colored blood (if methemooglobin >10% of total hemoglobin) 5. Can measure methemoglobin reductase activity in certain labs |
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|
Term
| How do you treat methemoglobinemia? |
|
Definition
| If mild or if inherited: no treatment. Discontinue any suspected oxidant drug. Fluids, supportive care. NOT oxygen. If due to oxidant drugs may use N-acetylcysteine and/or absorbic acid or methylene blue |
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|
Term
| What is the type of hypersensitivity in lupus? What is the pathogenesis? |
|
Definition
| Type 3 hypersensitivity. Immune antigen-antibody complexes deposit in the glomerular basement membrane, synovial membrane, skin and blood vessels. Immune complexes activate complement --> attracts neutrophils --> causes tissue damage via release of proteolytic/hydrolytic enzymes |
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|
Term
| Signalment with lupus: Species/Breeds/Age |
|
Definition
| Cat or dog; Collies/shelties/GSD; mean age 6 years but any age |
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|
Term
|
Definition
| Varies with signs, but most often neoplasia and infectious diseases |
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|
Term
|
Definition
| Waxing and waning! Varies with site of immune complex deposition (Lethargy, anorexia, shifting leg lameness/swollen joints, dermatological manifestations (ULCERS, alopecia, necrosis on ear tips, seborrhea, pruritis), fever, lymphadenopathy, hepatosplenomegaly, arrythmias/heart murmurs, muscle wasting |
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|
Term
| Diagnostic tests for lupus? |
|
Definition
| 1. Antinuclear antibody test (ANA) - often positive 2. Skip biopsy with direct immunoflorescence testing or peroxidase 3. Clinical signs |
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|
Term
| Does lupus have regenerative or nonregenerative anemia? |
|
Definition
|
|
Term
|
Definition
| Supportive care, Immunosuppressive drugs like IMHA (corticosteroids, azithiaprine, cyclosporine) |
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|
Term
| What are the laboratory results you will see with lupus? |
|
Definition
| Regenerative or non-regenerative anemia; leukocytosis or leukopenia and/or thrombocytopenia; proteinuria (which can cause muscle wasting); May have positive Coomb's test with IMHA |
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|
Term
| What are the causes of marrow toxicity? |
|
Definition
| 1. Infectious 2. Non-infectious (Toxins, irradiation) |
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|
Term
| How is Ehrlichia canis transmitted? Be specific. |
|
Definition
| By tick - esp. the brown dog tick (Rhipicephalus sanguineus) |
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|
Term
| How do you diagnose Ehrlichia canis? |
|
Definition
| 1. Serology (IFA, ELISA, intra-cytoplasmic morulae in monocytes - can check buffy smears, PCR, cell culture, Western immunoblotting) |
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|
Term
| What cells do Ehrlichia canis infect? |
|
Definition
|
|
Term
| What are the drugs used to treat E. canis? Which one should you use if you aren't sure if it's Ehrlichia? |
|
Definition
| Can use Doxycycline or Imidocarb diproprionate (pre-treated with atropine or glycopyrollate). Use Imidocarb if you aren't sure if it's Ehrlichia. |
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|
Term
| What is the most consistent laboratory finding in E. canis? What are some other possible lab findings? |
|
Definition
| Thrombocytopenia. Also mild leukopenia, anemia, hyperglobulinemia (polyclonal gammopathy), hypoalbuminemia |
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|
Term
| How soon can you detect IgG antibodies after an Ehrlichia infection? |
|
Definition
|
|
Term
| Which disease that we discussed induces vasculitis? |
|
Definition
|
|
Term
| Treatment of Babesia canis vs. Babesia gibsoni? |
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Definition
| B. canis = Imidocarb, B. gibsoni = Atovaquone, Azithromycin or Clindamycin |
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|
Term
| What is the reservoir of Cytauxzoon felis? |
|
Definition
|
|
Term
| What is the treatment of Cytauxzoon felis? |
|
Definition
| Supportive care, possibly atovaquone? |
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|
Term
| How do you get rid of the carrier state in Babesia canis? |
|
Definition
|
|
Term
| How is Babesia gibsoni transmitted? |
|
Definition
| Fighting - blood transmission |
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|
Term
|
Definition
| Blood meal from tabadids, iatrogenic |
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|
Term
| What is the most common type of EIA infection? (AKA acute, chronic, subclinical, etc) |
|
Definition
| Subclinical! Most horses will look normal! |
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|
Term
| What type of virus is EIA? |
|
Definition
|
|
Term
| What are the clinical signs of acute EIA? |
|
Definition
| Fever, lethargy, anorexia, THROMBOCYTOPENIA, Petechial hemorrhages, +/- anemia, SUBCLINICAL, seroconversion after 40 days |
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|
Term
| When do you see thrombocytopenia in EIA? |
|
Definition
| Usually with each recurring febrile episode |
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|
Term
| What are the initial diagnostic tests for an anemic patient? |
|
Definition
| CBC, Evaulation of blood smear, Reticulocyte count |
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|
Term
| American cats are usually type ___ and British cats are usually type ___ |
|
Definition
| American = type A, British = type B |
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|
Term
| Where is Hemobartonella felis located in a blood smear? |
|
Definition
|
|
Term
| Where is Babesia canis located in a blood smear? |
|
Definition
|
|
Term
| What is the number one cause of zinc toxicity in dogs? |
|
Definition
| Ingestion then erosion of pennies post-1983 |
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|
Term
| What are the clinical signs of zinc toxicity? |
|
Definition
| Pale MM, vomiting, diarrhea, anorexia, hemoglobinuria, Hematuria, Icterus, cardiac arrythmias |
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|
Term
| What would you see in a blood smear of a dog with zinc toxicity? |
|
Definition
| Basophilic stipling, target cells, increased nRBCs |
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|
Term
| Heinz body anemia: dogs vs. cats? |
|
Definition
| Dog are more resistant to Heinz body formation than cats because the hemoglobin of cats is more easily oxidized |
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|
Term
| The most common cause of Heinz body anemia in is ______ in the cat and _______ in the dog |
|
Definition
| Oxidant drugs (esp. acetominophen) = cats, onion ingestion = dogs |
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|
Term
| How do you definitively diagnose Heinz body anemia in cats? |
|
Definition
| Heinz bodies and regenerative anemia (BOTH) |
|
|
Term
| Clinical signs in Heinz body anemia? |
|
Definition
| Sudden onset! Pale MM, weakness, anorexia, fever, hemoglobinemia/nuria, cyanosis w/ methoglobinemia |
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|
Term
| What are the clinical signs of acetaminophen toxicity? |
|
Definition
| Methemoglobinemia, dyspnea, FACIAL EDEMA, depression, hypothermia, vomiting |
|
|
Term
| How do you treat Heinz body anemia? How do you treat acetominophen toxicity specifically? |
|
Definition
| Remove source of oxidant (can do charcoal if ingested in last 2 hours); supportive care (oxygen, fluids); If acetominophen toxicity: N-acetylcysteine, ascorbic acid |
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|
Term
| What is the pathogenesis of hypophosphatemia? |
|
Definition
| Can cause ATP depletion and adversely affect high energy using cells such as RBCs (hemolysis), skeletal muscle cells (weakness, respiratory paralysis), and brain cells (seizures, altered mentation) |
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|
Term
| What are the clinical signs in hypophosphatemia? |
|
Definition
| (Varies with underlying cause). Pale MM, tachypnea or dyspnea, MUSCLE WEAKNESS, mental dullness |
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|
Term
| How do you treat mild hypophosphatemia? Severe? |
|
Definition
| If mild? Skim milk or sodium or phosphate supplements. If severe? IV balanced electrolyte solution for 6 hours (monitor P, Ca, K levels) |
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|
Term
| What are the breeds affected with pyruvate kinase deficiency? |
|
Definition
| #1 = basenjis, Westies, and beagles |
|
|
Term
| What are the clinical signs of PK deficiency? |
|
Definition
| BREED!! < 1 year, exercise intolerance, retarded growth, pale MM, tachycardia, hepatosplenomegaly, HIGHLY regenerative anemia |
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|
Term
| What is the breed associated with phosphofructokinase deficiency? |
|
Definition
|
|
Term
| How do you treat PK deficiency? |
|
Definition
|
|
Term
| How do you treat PFK deficiency? |
|
Definition
| Avoid situations inducing hyperventilation. Also, administer acetazolamide prior to anticipated episodes. |
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|
Term
| What are the clinical signs of PFK deficiency? |
|
Definition
| BREED, noticed at young age! Exercise intolerance and bilirubinuria which develop following episodes of hyperventilation accompanying exercise, excessive barking and elevated temperature (transient hemoglobinemia and hemoglobinuria, hepatosplenomegaly, anemia and icterus, bilirubinuria and reticulogytosis may persist, rarely muscle cramps) |
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|
Term
| What is the prognosis of PK deficiency? What is the prognosis of PFK deficiency? |
|
Definition
| PK = poor prognosis, PFK = fair to good prognosis |
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|
Term
| What is the breed associated with familial nonspherocytic anemia? |
|
Definition
|
|
Term
| How can you transmit Hemobartonella felis? |
|
Definition
| Ticks, blood transfusions, queen-to-kittens |
|
|
Term
| What are the most common blood types in horses? |
|
Definition
|
|
Term
| What are the differential dx for neonatal isoerythrolysis in horses? |
|
Definition
| SEPSIS, Hypoxic-ischemic encephalopathy, Meningitis, EHV-1, Hemorrhage |
|
|
Term
| How do you treat NI in horses? |
|
Definition
| Blood transfusion with a compatible donor (Aa and Qa negative) or dam with washed RBCs; Antimicrobials; Fluid/nutritional support; Nasal oxygen; Stall confinement; Oxyglobin; Seizure rx |
|
|
Term
| If it's a mare's first foal, do we need to worry about NI? |
|
Definition
| Not usually (Unlike cats!!!) |
|
|
Term
| What's the difference between acute and gradual NI in horses? |
|
Definition
| Acute involves hemolysins (and 80% of cases). Gradual involves agglutinins. |
|
|
Term
| When do clinical signs for NI in horses usually show up? |
|
Definition
|
|
Term
| What are the clinical signs of NI in horses? |
|
Definition
| Peracute hemolysis (shock, acute death), weakness/lethargy, icterus, tachycardia/tachypnea, pallor, anemia, pigmenturia, rare seizures |
|
|
Term
| According to Dr. Holbrook, what does a PCV of <20 usually mean? |
|
Definition
|
|
Term
| What test predicts the likelihood of NI in horses? |
|
Definition
| Jaundice foal agglutination test |
|
|
Term
| What are the top 2 hemolymphatic diseases in horses? |
|
Definition
|
|
Term
| What is the most common immunodeficiency in horses? |
|
Definition
| Failure of Passive Transfer |
|
|
Term
| What is your #1 concern with FPT? |
|
Definition
| Risk of sepsis!! Treat as if there is sepsis! |
|
|
Term
| What can cause agalactia in horses and thus FPT? |
|
Definition
|
|
Term
| What are the causes of FPT? |
|
Definition
| Inadequate colostral intake, Leaking prior to parturition, Agalactia (fescue toxicity), Poor quality, Poor absorption |
|
|
Term
|
Definition
| Snap test ELISA; (IgG less than 800 mg/dl at 24 hours) |
|
|
Term
| How do you treat FPT (AND SEPSIS!!!)? |
|
Definition
| In first 24 hours = oral colostrum, EARLY INTERVENTION; Broad spectrum antimicrobials, fluid support, pressor support (dopamine, dobutamine, NE, vasopressin), Nutritional support (IV PPN or TPN) |
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|
Term
| What are the clinical signs of SCID? |
|
Definition
| At 1-3 months: failure to thrive, recurrent infections |
|
|
Term
| What is the signalment of SCID in horses? |
|
Definition
| Arabian, Foals 2-4 months of age |
|
|
Term
| What are the lab results in SCID? |
|
Definition
| Lymphopenia (B and T cells), Low immunoglobulins (IgM absent if sample is presuckle or it decreases over 2-4 weeks) |
|
|
Term
| How can you diagnose SCID? |
|
Definition
| Genetic testing, PCR and southern blotting, whole blood |
|
|
Term
| When is the clinical onset of IgM deficiency? |
|
Definition
| 2-8 months of age OR 2-5 years of age |
|
|
Term
| What is the classic clinical sign of selective IgM deficiency in foals? |
|
Definition
| Pneumonia! (esp. doesn't respond to antimicrobials) May develop sepsis. Many die by 2 years |
|
|
Term
| What is the classic clinical sign of selective IgM deficiency in adults? |
|
Definition
| Lymphoma! (Lymphadenopathy, weight loss) |
|
|
Term
| What is the age and sex of those affected by X-linked aggammaglobulinemia? |
|
Definition
|
|
Term
| What is missing in X-linked aggamaglobulinemia? |
|
Definition
| Lack B cells and plasma cells, No IgM, No IgA (IgG declines with age, post-colostral) |
|
|
Term
| Which is more common in DIC in horses: hypercoagulation or bleeding? |
|
Definition
|
|
Term
| What is DIC most commonly associated with? |
|
Definition
| Severe endotoxemia/sepsis |
|
|
Term
| What are the common causes of hemolysis in horses? |
|
Definition
|
|
Term
| How do you treat red maple toxicosis? |
|
Definition
| Remove source, Charcoal to exposed, fluid support, blood transfusions, VITAMIN C |
|
|
Term
| Which is higher in oxidative injury? Fe+2 or Fe+3? |
|
Definition
|
|
Term
| What are the clinical signs of red maple toxicosis? Laboratory signs? |
|
Definition
| Pigment nephropathy, laminitis, acute death, colic/diarrhea. In the lab: hemoglobinuria, bilirubinemia, bilirubinuria, Heinz bodies |
|
|
Term
| How do you treat equine piroplasmosis? |
|
Definition
|
|
Term
| What are the clinical signs of lymphosarcoma in horses? |
|
Definition
| Lethargy, weight loss, ventral edema, organ dependent signs |
|
|
Term
| What is the clinical pathology of lymphosarcoma in horses? |
|
Definition
| VARIABLE! Chronic inflammation, Often low IgM, normal to low lymphocytes, (RARE: leukemia, neoplastic cells) |
|
|
Term
| For horses to enter OK, how current does their health certificate need to be? Negative cELISA? Negative EIA? |
|
Definition
| 10 days, 14 days, 12 months |
|
|
Term
| What are the main clinical signs of hemolysis in the horse? |
|
Definition
| Hemoglobinemia/hemoglobinuria, Hyperbilirubinemia (indirect), pale MM or icteric, tachycardia |
|
|
Term
| What are the clinical signs of CHRONIC EIA? |
|
Definition
| Recurrent fever, weight loss, ventral edema, anemia |
|
|
Term
| What are the differential dx for weight loss in a horse? |
|
Definition
| Decreased intake, Maldigestion/malabsorption, Increased rate of loss, chronic organ failure |
|
|
Term
| How does EIA cause ventral edema? What does this lead to? |
|
Definition
| Vasculitis (increased permeability). This is what causes thrombocytopenia |
|
|
Term
|
Definition
| Don't treat - usually euthanize or quarantine |
|
|
Term
|
Definition
| AGID, c-ELISA, Ab (be aware of passive immunity in foals but pregnant mares can pass it on) |
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