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CRH II > Immune-Mediated Hemolytic Anemia > Flashcards

Immune-Mediated Hemolytic Anemia Flashcards

1
Q

what is the main difference in lab work between regenerative anemia due to hemorrhage versus hemolysis?

A

hemorrhage: decreased PCV AND total solids (protein lost too)
-PCV drop may not be immediately apparent, may need to wait until fluid volume restored

hemolysis: decreased PCV, NORMAL total solids

both are macrocytic, hypochromic, with reticulocytosis and polychromasia

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2
Q

what do the clinical signs of anemia depend on? (5)

A
  1. the degree of anemia
  2. the chronicity of anemia:
    -acute = more severe usually (less time to adapt)
  3. changes in circulating volume
  4. concurrent disorders
    -if anemic plus no platelets = can’t clot = worse
  5. extent of physical activity
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3
Q

what are the clinical signs of hypoxemia?

A
  1. lethargy
  2. weakness and collapse
  3. increased heart rate
  4. mild to moderate heart murmur
    -grade I-III, hemic/physiologic murmur, altered blood viscosity
  5. weak pulses
  6. hypotension
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3
Q

describe RBC parameters of regenerative anemia (3)

A
  1. macrocytosis or anocytosis
  2. polychromasia or hypochromasia
  3. nucleated red blood cells
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4
Q

describe regenerative anemia due to hemorrhage

A
  1. initially normocytic, normochromic, non-regnerative until eyrthropoitein concentrations increase
  2. regenerative response in 3-5 days, peak at 4-7 days
    -leukocytosis with a left shift
  3. will see anemia, panhypoproteinemia (albumin and globulin), and reticulocytosis
  4. canine reticulocytosis:
    -interpret in context of severity of anemia
    -mild: 110-150K, moderate: 150-300K, marked >500K
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5
Q

describe 4 causes of external blood loss

A
  1. GI tract: melena if upper GI tract bleed
    -due to endoparasites, NSAIDs, Addison’s, IBD, neoplasia
  2. urinary tract:
    -trauma, neoplasia, idiopathic renal hematuria
  3. respiratory tract:
    -epistaxis can be swallowed and turn into melena (hard to find actual source), hemoptysis (coughing up blood)
  4. skin: ectoparasites (very heavy flea load)

-most young animal are classified as anemic compared to the adult reference interval, their milk diet, growing, and endoparasites

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6
Q

describe chronic external blood loss

A
  1. microcytic, hypochromic
    -loss of iron decreases hemoglobin concentration in RBC precursors
    -erythrocytes undergo extra division in the presence of lower hemoglobin concentration = microcytic
  2. eventually becomes non-regenerative
  3. treatment:
    -treat underlying cause!
    -iron supplement: oral or IM injection
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7
Q

describe causes of internal blood loss

A
  1. body cavities:
    -thoracic, abdominal
    -pericardium, joints, CSF, subcutis
  2. coagulopathies:
    -congenital, hemophilia
    -acquired, rodenticide toxicosis
    -trauma
    -neoplasia

iron is recycled so not depleted!

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8
Q

describe physiologic/normal extravascular hemolysis

A

-normal destruction of senescent erythrocytes

-in spleen, bone marrow, liver

-also triggered by: antibody attachment, blood parasite attachment, oxidative damage, intrinsic defects of RBCs, membrane fragility

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9
Q

what are 4 causes of NON-immunologic hemolytic anemia?

A
  1. microangiopathic:
    -heartworm dz, hemangiosarc, schistocytes!
  2. phospholipases:
    -snake venom, spider bites, bee stings
  3. RBC intrinsic defect/fragility:
    -RBC enzyme deficiency: phosphofructokinase, pyruvate kinase
    -osmotic fragility
    -hypophosphatemia: refeeding syndrome or DKA
  4. oxidative stress:
    -onion or garlic
    -zinc
    -heinz bodies!
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10
Q

what must go wrong for autoimmune hemolytic anemia to occur?

A
  1. recognition of erythrocyte self-antigen
  2. loss of immunological tolerance
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11
Q

describe the diagnostic approach to IMHA

A
  1. diagnose anemia
  2. confirm that regenerative and/or hemolytic
    -exceptions: PIMHA, feline anemia of immune-mediated origin
  3. rule out secondary or associative causes
  4. primary or non-associative/idiopathic IMHA is a diagnosis of exclusion!
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12
Q

summarize the pathogenesis of IMHA

A
  1. predisposing factors: genetics (MHC issue), age (primary more common in younger dogs), environment (season), or neoplasia, or infection/vaccine/drugs
  2. cause immune dysregulation (primary) or immune response (secondary) to make autoantibodies against RBCs
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13
Q

what drugs can cause IMHA?

A
  1. penicillins
  2. cephalosporins
  3. TMS
  4. methimazole

if give and causes a reaction, DONT give again (duh)

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14
Q

describe extravascular hemolysis and IMHA

A
  1. phagocytosis and RBC destruction, usually go to spleen (splenomegaly on rads)
  2. opsonization of erythrocytes = spherocytes!! (clue to immune-mediated attack)
  3. heme metabolized and excreted in canine kidneys, which can excrete conjugated bilirubin
    -small amounts of urinary bilirubin normal in healthy dogs
    -bilirubinuria is NOT normal in cats!!
  4. IMHA = excess hemoglobin enters bilirubin pathway
    -pre-hepatic cause of hyperbilirubinemia
    -will see icterus/jaundice when bilirubin >1.5-2 mg/dl
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15
Q

describe intravascular hemolysis and IMHA

A
  1. activation of complement = spontaneous lysis of RBCs
  2. release of hemoglobin into bloodstream = hemoglobinemia
    -hypercoagulable
  3. subsequent hemoglobinuria
    -red urine!!!
  4. typically a worse prognosis than extravascular hemolysis
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16
Q

what history is important to rule out other factors and rule in IMHA?

A
  1. diet: onion or garlic-containing foods?
  2. medications: including flea and tick preventatives
  3. bee stings, spider bites, snake venom
    -phospholipases can cause intravascular IMHA
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17
Q

describe the criteria for IMHA (4)

A
  1. PCV <25%
  2. spherocytes (dogs only, cats too small) or autoagglutination
  3. positive coomb’s test
18
Q

describe autoagglutination

A

macroagglutination
-hemoagglutination visible on blood tube
-do saline dispersion test (1 drop saline: 1 drop blood) to see if actually platelet clumping instead

microagglutination:
-visible when slide examined under microscope
-tap slide to differentiate from rouleaux

19
Q

describe coomb’s test/direct/serum antiglobulin test (DAT/SAT)

A

checks for anti-canine immunoglobulin antibody

20
Q

describe flow cytometry to detect IMHA

A

detects anti-canine immunoglobulin antibody (more senstive, newer test)

21
Q

describe diagnostic testing for IMHA on the patient side

A
  1. MM color, CRT, pulse quality, and blood pressure
  2. PCV/TS
    -hemorrhage vs hemolysis
    -serum icteric or hemolyzed?
  3. blood smear:
    -polychromasia, spherocytosis (dogs, can’t see in cats bc too small), nRBCs, hemoparasites
    -eval WBCs and platelets too
  4. saline agglutination test
  5. CBC
    -RBC indices, reticulocytosis, WBC, platelets
  6. chem:
    -albumin/globulin: hemolysis vs hemorrhage
    -renal parameters to detect CKD
    -liver disease: hepatic and post-hepatic hyperbilirubinemia
    -Na, K for Addison’s disease
    -phosphorous for refeeding or DKA
  7. UA:
    -USG to detect CKD
    -bilirubinuria
    -pigmenturia: hemoglobinuria, hematuria (spin down), myoglobinuria (rare in small animal)
    -sediment exam: may see evidence of neoplasia/TCC
22
Q

describe how to determine primary versus secondary IMHA

A
  1. screen for neoplasia and rule out zinc foreign body
    -thoracic and abdominal rads
    -+/- abdominal US or CT
    -+/- ECG and echo
  2. rule out infectious disease
    -antibodies/titers/serology (serum)
    -PCR, antigen within cells/plasma
    -blood smear: organisms not always visible
    -serology: mycoplasma hemocanis, babesia (not typically on a 4Dx SNAP test), lepto
    -snap tests: FeLV antigen/FIV antibody, mycoplasma hemofelis
    -PCR assay: M. felic and canis, babesia, leptospira, fresh feline bone marrow for occult FeLV
23
Q

describe poor prognostic factors for IMHA

A
  1. increased BUN
    -could indication pigment nephropathy or a GI bleed
  2. icterus:
    -indicates severity of hemolysis
  3. band neutrophils, petechiae
    -indicates severity of systemic inflammatory response

IMHA can also be seen with other immune-mediated diseases
-Evan’s disease: IMHA and ITP
-systemic lupus erythematous

24
Q

describe treatment for IMHA

A
  1. acute stabilization
  2. anti-thrombotic and immunosuppressive drugs
  3. splenectomy/therapeutic plasma exchange
25
Q

describe volume support for IMHA

A

crystalloids:

  1. for deficiency + ongoing losses + maintenance
  2. canine maintenance approx 60ml/kg/day; feline approx 45ml/kg/day
  3. rate of replacement reflects disease timeline
  4. also helps with pigment nephropathy (bilirubin/Hb)
26
Q

describe use of blood products to treat IMHA

A
  1. only if indicated
    -use clinical signs (HR, RR), NOT absolute PCV% (but 15% is a trigger to look)
  2. ideally type canine donor and recipient for 1st transfusion
    -do not have to type dogs in an emergency but should crossmatch for next transfusion
  3. ALWAYS ALWAYS type feline donor and recipient for 1st transfusion!
27
Q

describe small animal blood typing

A
  1. visible hemaglutination
    -patient RBC surface antigen
    -known monoclonal or polyclonal antiserum
  2. can use card and ELISA
  3. if autoagglutination is already present, use sandwich or indirect ELISA
    -or a lateral flow test
28
Q

describe the method of blood transfusion

A
  1. screen donor for blood borne infectious diseases
  2. use filter to remove microclots
  3. give blood product over 4-6 hours
  4. monitor for transfusion reactions
    -HR, RR, temp, BP
    -fever, facial swelling, vomiting, tachypnea=bad
    -hemolysis indicated if see above
29
Q

describe anti-thrombotic drugs

A
  1. dogs with IMHA who survive the initial anemia die of thromboembolic complications (clots)
    -typically in the 1st 1-2 weeks of disease
    -mortality rates of up to 50%
  2. options:
    -clopidogrel (anti-platelet)
    -aspirin (low dose since giving with steroids, mixed efficacy)
    -rivaroxaban (anti Xa factor, parenteral and PO and pricey!)
    -heparin, parenteral
  3. when stop?
    -after 2 weeks or when discontinue prednisone
30
Q

describe use of corticosteroids to treat IMHA

A
  1. example is prednisone
  2. genomic and non-genomic mechanism of action
  3. affect multiple components of immunity:
    -lymphocytes, MOs, complement, neutrophils, NK cells, etc.
  4. very efficacious, work quickly, cheap
31
Q

describe prednisone/prednisolone

A
  1. prednisolone:
    -prednisone converted to prednisolone in the liver but some cats can’t do that so we usually just give cats prednisolone
  2. dosing per day:
    -DONT exceed 60 mg total per dog!!!
    -2-4mg/kg/day is the general dog dose for immunosuppression (much higher then physiologic or anti-inflammatory)

-alternate dosing is 40mg/m^2 if greater than 25-40kg dog

  1. goals:
    -aim for remission or PCV >30% for 2 weeks then taper 25-50% every 2-4 weeks, discontinue once dose 0.25-0.5mg/kg every 48 hours
    -complete withdrawal SHOULD take months
32
Q

describe use of dexamethasone to treat IMHA

A
  1. injectable formulation, if can’t take oral meds
    -is 7-10x more potent than prednisone!
    -MUST decrease dose from pred dose
33
Q

describe adverse effects of corticosteroids

A
  1. iatrogenic hypercortisolemia/Cuhsing’s
  2. acceptable side effects:
    -PU/PD
    -polyphagia
    -alopecia, muscle wasting
    -hepatomegaly, panting
  3. aim for once daily dosing, preferably in the morning: increases owner compliance and decreases nocturia
  4. unacceptable
    -GI bleeding: NEVER combine steroids with NSAIDs in dogs and cats!!!
    –give steroids with a meal for gastroprotection, consider gastroprotectants like omeprazole
34
Q

describe CBC and chem changes with IMHA and corticosteroids

A
  1. IMHA + high dose steroids often cause a leukemoid response
    -extreme leukocytosis
  2. prednisone medication
    -hypercortisolemia, expect a stress leukogram
    -SSMILED in dogs!
  3. CBC:
    -expect left shift to decrease with time
    -do NOT expect toxic changes (BAD if see; could indicate infection in immunosuppressed dog
  4. chemistry:
    -ALKP increases in dogs: steroid isoenzyme and cholestasis due to hepatocyte glycogen accumulation
    –do NOT expect to see an increased ALKP in cats on glucocorticoids (cats do not have this isoenzyme and ALKP half life is very short)
    -hyperlipemia, hypercholesterolemia
    -hyperglycemia (glucocorticoids)
35
Q

describe urinalysis changes with corticosteroids

A
  1. decreased USG
  2. pollakuria
  3. if UTI:
    -+/- bacteria: very dilute urine
    -+/- pyuria (WBCs), hematuria (RBCs), anti-inflammatory action
36
Q

describe “unacceptable” adverse effects of corticosteroids

A
  1. short term:
    -infections: skin, urinary tract
    -soft tissue catabolism: decreased wound healing, ligament rupture
    -aggression
    -Na retention: cardiac disease, careful in cats!
    -insulin resistance: diabetics: more careful in cats than dogs!
  2. long term:
    -uroliths: calcium oxalate
    -gall bladder mucoceles
    -calcinosis cutis
37
Q

describe using immunosuppressive drugs

A
  1. start with prednisone, lower dose
  2. when to use an adjunctive therapy:
    -to spare prednisone effects in larger dogs
    -IMHA with autoagglutination
    -intravascular IMHA
    -to spare prednisolone in cats (risk of diabetes mellitus)
38
Q

describe cyclosporin

A
  1. mainly affects T lymphocyte function
    -binds calcineruin and stops clonal expansion
    -VERY potent immunosuppression, be careful, esp if using with steroids!
  2. takes days to effect, expensive, microemulsified for predictable absorption but liquid and oral capsule forms available
    -DONT use compounded if can avoid! less reliable
  3. adverse effects:
    -GI V/D: put in the freezer, give with food or anti-emetics to control GI signs
    -dogs: gingival hyeprplasia and hirsuitism
    -cats: toxoplasma reactivation
39
Q

describe mycophenolate mofetil

A
  1. inhibits purine synthesis in B and T lymphocytes
  2. parenteral (injectable) and oral forms available
  3. takes days to effect, expensive!!!
  4. adverse effects mainly GI (V/D)
    -decrease with time, probiotics, +/- metronidazole if very severe
40
Q

describe azothioprine

A
  1. purine antagonist
  2. delayed clinical efficacy (3+ weeks), cheap
  3. but hepatotoxic and myelosuppressive
    -should monitor CBC and liver enzymes every 2-4 weeks
  4. teratogenic (tell owner to wear gloves)
  5. DO NOT USE IN CATS!!!!! NEVER!!!!!
41
Q

describe tapering/using immunosuppressive drugs

A
  1. reassess PCV/Hct before taper
  2. taper one drug at a time unless fulminant infection
    -typically taper prednisone first due to side effects
    -if money is more of an issue, taper adjunctive drug first
    -25-50% every 2-4 weeks
  3. can decrease steroid to physiologic dose if an emergency
    -0.25mg/kg/day
  4. if disease relapses:
    -add in second immunosuppressive drug if only on steroid monotherapy or go back up one step
    -taper more slowly: decrease taper mg increments and/or increase interval
  5. if using a second drug to spare effects of pred, taper pred more rapidly than if monotherapy
  6. remember concurrent disease!
    -might influence drug handling (hepatic or renal)
    -diabetes mellitus, cardiac disease, OA, NSAIDs
  7. these are NOT benign meds!
    -monitor for hematological + biochemical effects
    -secondary infections might kill your patient
    -most are teratogenic!! tell owners to wear gloves!!
42
Q

describe splenectomy and therapeutic plasma exchange to treat IMHA

A

splenectomy:
1. salvage option for unresponsive patients
-try to avoid triple immunosuppressing patients

  1. screen for tick-born disease
    -especially Babesia since risk of reactivation
  2. will have decreased wound healing
    -modify anti-platelet drug doses in peri-operative period

therapeutic plasma exchange:
1. removes antibodies
2. need specialized equipment and is expensive!

43
Q

describe precursor IMHA (PIMHA)

A
  1. immune response is aimed at RBC precursors
    -so anemia is NON-regenerative!
    -spherocytes and agglutination much less common
    -may need a bone aspirate/biopsy to diagnose
  2. anemia is chronic
    -patients can be stable with severe anemias (PCV <10%)
  3. treatment similar to classic IMHA
    -blood products and supportive care
    -anti-platelet drugs
    -immunosuppression
  4. may take months to respond, or become transfusion dependent
    -patients often euthanized due to money issues or drug adverse effects
    -splenectomy may be an effective alternate treatment: beware of the impact of steroids on wound healing, must stop anti-platelet drug 3-7d prior to surgery

CRH II (26 decks)

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