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CLINICAL PATHOLOGY > 4 – RBC 2 > Flashcards

4 – RBC 2 Flashcards

1
Q

When do you know you have a hemolytic anemia?

A
  • Regenerative
  • Macrocytic, hypochromic
  • Polychromasia/reticulocytosis
  • *hemoglobinemia/hemoglobinuria
  • *hyperbilirubinemia/bilirubinuria
  • *abnormal RBC morphology or parasites
  • Proteins WRI
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2
Q

Intravascular vs. extravascular hemolysis

A
  • May help determine etiology
  • Intravascular=poor prognosis
  • Extravascular=more common
  • *often both are present
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3
Q

Intravascular hemolysis

A
  • RBC destruction within blood vessels
  • Hemoglobinemia and hemoglobinuria
    o Increased MCH and MCHC(measuring free Hb and intact Hb in RBCs)
  • Over time: hyperbilirubinemia and bilirubinuria
  • **free Hb is bad=poor prognosis
    o Hemoglobinuric nephropathy and thrombosis
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4
Q

Extravascular hemolysis

A
  • RBC destruction by macrophages primarily in spleen
  • intracellular=normal process
  • does NOT cause hemoglobinemia or hemoglobinuria
  • usually have hyperbilirubinemia and bilirubinuria with pathologic extravascular hemolysis
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5
Q

Icterus in the big picture

A
  • RBC destruction is a normal homeostatic process
  • Aged RBC captured in spleen
  • Macrophages degrade heme into bilirubin
  • Bilirubin travels to liver for conjugation
  • Excreted into bile
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6
Q

What are the 2 ways that hyperbilirubinemia can develop?

A
  1. Hemolytic anemia
    a. Normal liver, but capacity overwhelmed by increased breakdown of RBC
  2. Liver disease
    a. Liver can’t handle normal daily turnover of RBCs
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7
Q

What is and what happens with pathologic hemolysis?

A
  • *accelerated RBC destruction
  • Intravascular or extravascular
  • Increased Hgb breakdown in macrophages=increased delivery of bilirubin to liver
  • *if liver can handle=wont see hyperbilirubinemia
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8
Q

What happens when there is an increased plasma [bilirubin]?

A
  • Increased urinary excretion
    o Bilirubinuria +/- bilirubin crystals
    o Bilirubinuria precedes clinical icterus (low renal threshold)
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9
Q

What are the many paths to destruction?

A
  • Immune-mediated
  • Infectious agents
  • Oxidative damage
  • Mechanical injury
  • (Defects in RBC metabolism)
  • (neoplasia)
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10
Q

What is the biggest cause of hemolytic anemia in dogs?

A
  • Immune-mediated
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11
Q

IMHA due to

A
  • Primary: auto-immune
  • Secondary
    o Drugs/toxins
    o Infectious agents
    o Neoplasia
    o Transfusion reaction
    o Neonatal isoerythrolysis
  • *initiating cause often undetermined (idiopathic)
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12
Q

Production of Ab with IMHA

A
  • Direct or indirect binding to RBC
  • Result in RBC destruction
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13
Q

What are the 2 ways RBC may be destroyed in IMHA?

A
  • Ab-coated RBC engulfed by macrophages
    o Extravascular
    o Spherocyte formation
  • Ab may fix complement=MAC formation
    o Intravascular hemolysis
    o Ghost cells
  • *extravascular hemolysis predominates
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14
Q

Spherocyte formation with RBC destruction

A
  • Piece of RBC membrane removed
  • Less SA, same volume
  • Spherical shape
  • Loss of central pallor
  • *Difficult to detect except in dogs
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15
Q

What is the problem with spherocytes?

A
  • NOT flexible
  • Trapped in spleen and macrophages will come along and ‘eat them’
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16
Q

Ab may fix complement with RBC destruction

A
  • Get a hole in membrane of RBC=all Hb leaks into circulation
17
Q

Coomb’s Test (direct antiglobulin test: DAT)

A
  • Confirm presence of bound Ab or C3 on RBC surface
  • *many false negatives
  • Not standardized
  • Often not needed
18
Q

What is seen in a classic case of IMHA?

A
  • Regenerative anemia
  • Spherocytes
  • Coomb’s +
  • Hyperbilirubinemia/bilirubinuria
  • Inflammatory leukogram
  • Might see
    o Agglutination
    o Ghost cells: intravascular
    o Thrombocytopenia: if concurrent IM destruction of platelets
19
Q

Infectious agents: what is one of the only things you will see in Canada

A
  • Hemotrophic Mycoplasma
    o Epicellular: on surface of RBC
    o Form invaginations
  • *cats, dogs, pigs, cattle, llamas, mice
  • Immune-mediated component to hemolysis
20
Q

What are some other examples of infectious agents?

A
  • Erythrocytic Anaplasma
  • Babesia: cattle, horses, dogs
  • Theileria
  • Leptospira, Clostridium, EIA virus
21
Q

What does oxidative damage result in?

A
  • Heinz body and/or eccentrocyte formation
    o May see keratocytes and blister cells
  • *onions in all species (except humans)
22
Q

What can cause oxidative damage in dogs?

A
  • Garlic
  • Acetaminophen
  • Zinc
  • Skunk spray
23
Q

What can cause oxidative damage in cats?

A
  • *acetaminophen
  • Propofol
24
Q

What can cause oxidative damage in horses?

A
  • Wilted red maple leaves
  • Garlic
25
Q

What can cause oxidative damage in cattle?

A
  • Brassica
  • Copper
  • Oak leaves
  • Acorns
26
Q

What are Heinz bodies?

A
  • Denatured Hg
  • See on New Methylene blue stain
27
Q

What are eccentrocytes?

A
  • Fused RBC membranes
  • All Hg content to one side
28
Q

What are the problems with Heinz bodies and eccentrocytes?

A
  • Can’t get through spleen
    o Eaten by macrophages
    o *extravascular hemolysis predominates
  • May have small component of intravascular hemolysis
29
Q

Cats are special: small, individual Heinz bodies can be seen in

A
  • Normal cats
  • Ill but not anemic
    o Diabetes mellitus
    o Hyperthyroidism
  • Anemic cats
30
Q

What is seen with mechanical injury? What can lead to it?

A
  • Schizocytes, keratocytes (maybe acanthocytes)
  • *direct lysis and shortened lifespan due to abnormal shape (trapped in spleen)
  • Due to:
    o Fibrin strand injury (ex. DIC)
    o Turbulent blood flow (ex. endocarditis)
31
Q

Acanthocytes: significance

A
  • **hemangiosarcoma
  • Splenic, hepatic, renal disorders
    o Due to change in membrane lipids
  • Mechanical injury
    o Seen with schizo/kerato
  • *irregularly irregular
32
Q

What are the 3 possibilities if you get 3+ for blood on a urinalysis?

A
  • Intact erythrocytes
  • Myoglobin
  • Hemoglobin
  • *if cystocentesis=likely where the RBC are coming from

CLINICAL PATHOLOGY (7 decks)

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