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Heme/Onc > Hemolysis > Flashcards

Hemolysis Flashcards

1
Q

General Features of Hemolytic Anemia

A
  • Jaundice/Scleral icterus (excess bilirubin from free Hb degradation)
  • Dark Urine
  • Pigmented gallstones (excess bilirubin from free Hb degradation)
  • Ankle Ulcers
  • Splenomegaly
  • Aplastic Crises assoc. with Parvovirus B19
  • Increased Folate requirement
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2
Q

Functions of Spleen

A
  • Antibody factory
  • Blood quality control (macrophages)
  • WBC and platelet repository
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3
Q

Post Splenectomy Findings

A
  • Howell-Jolly Bodies
  • Target Cells
  • Acanthocytes
  • Schistocytes
  • Nucleated Red Cells (NRBCS) in plasma
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4
Q

Parvovirus B19

A
  • Non-encapsulated DNA virus
  • lyses RBCs in bone marrow
  • Not a problem for normal people because effects seen 7-10 days post exposure and normal RBC lifespan ~120 d
  • In hemolytic anemia patients, RBC life span is much shorter –> plumetting Hb values because current RBCs are lysing
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5
Q

Extravascular Hemolysis

A

Macrophages in Spleen, Liver, Marrow remove damaged or antibody coated cells

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6
Q

Intravascular Hemolysis

A
  • RBCs rupture inside vasculature
  • Release free Hb into circulation
  • Could potentially cause iron overload, other general features of hemolysis
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7
Q

Lab Features of Hemolytic Anemias

A
  • Increased RBC Production
    • Blood
      • Increased Rct (shows as polychromasia in smear)
      • Increased MCV (Rct larger than RBCs)
      • Circulating NRBCs
      • Increased RDW
    • Bone Marrow
      • Erythroid hyperplasia (increased prod. of RBC precursors)
      • Decreased M:E
    • Bone
      • Marow space expansion due to increased erythropoeisis
      • Frontal Bossing** **
  • Increased RBC Destruction
    • Decreased RBC lifespan
      • Increased LDH Levels
      • Increased unconj. bilirubin
    • Decreased serum Haptoglobin
    • Hemoglobinemia
    • Hemoglobinuria
    • Hemosiderinuria
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8
Q

Peripheral Smear Artifacts due to Hemolysis

A
  • Schistocytes
  • Sphereocytes
  • Bite/Blsiter cells
    • indicates Heinz Body hemolysis from oxidative damage
      • seen in G6PD deficiency
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9
Q

Classification of Hemolytic Anemias by Etiology

A
  • Congenital - membrane defects
    • Hereditary Spherocytosis
    • Enzymatic Defects
  • Immune Mediated Hemolysis
    • Warm Antibody HA
      • Drug Induced
    • Cold Antibody HA
  • Non-Immune Hemolytic Anemia
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10
Q

Hereditary Sphereocytosis

A
  • Congenital
  • Autosomal Dominant
  • Defect with Spectrin & Ankyrin - membrane skeleton proteins
  • lipid blebs @ surface from skeleton, pinched by macrophages inside splenic sinusoids
  • Over time = extravascular hemolysis
  • Clinical Features
    • Splenomegaly
    • Ankle Ulcers
    • Increased Osmotic fragility
  • Treatment
    • Folate
    • Splenectomy
      • will stop extravascular hemolysis, but spherocytes will remain
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11
Q

G6PD Deficiency

A
  • Shutdown of Aerobic glycolysis –> no energy for RBC to maintain biconcave shape
  • increases RBC susceptibility to ox. damage
  • anything that causes ox stress will percipitate hemolysis
  • No G6PD, nothing to stop Hb–>methemoglobin –> heinz bodies from methemoglobin percipitation –> bite cells
  • X-linked
  • Cells destroyed mainly by extravascular hemolysis
  • Clinical Features
    • Hemolysis
  • **Drugs that cause it **
    • Sulfa drugs
    • Dapsone
    • Vitamin K
    • Quinine
    • Cholorquinine
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12
Q

Ways Immune Mediated Hemolysis work

A
  • Ig coated RBCs interact with Fc Receptors on macrophages (extravascular hemolys)
  • C3 Coated RBCs
    • interact with C3 receptors on macrophages (extravascular hemolys)
    • complete complement cascade –> lysis (intravascular hemolys)
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13
Q

Hallmark of Autoimmune Hemolytic Anemias

A

Coomb’s Test

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14
Q

Coomb’s Test

A
  • Direct
    • looks for IgG OR C3 directly bound to RBC
  • Indirect
    • Looks for IgG ONLY in serum
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15
Q

Warm Antibody Hemolytic Anemia/Autoimmune Hemolytic Anemia (AIHA)

A
  • Antibodies react with RBCs at 37 degrees C
  • Do not agglutinate RBCs
  • IgG antibodies formed (indirect Coomb’s positive) and bind RBCs (direct Coomb’s positive) with or without completment deposition
  • both direct AND indirect Coomb’s will be positive
  • IgG will be +, C3 may or may not be positive
  • Associated with immune platelet destruction = Evan’s Syndrome
  • Clinical Features
    • Splenomegaly
    • Jaundice
  • Lab
    • Increased Rct
    • Increased Billirubin
    • Increased LDH
      • Coomb’s (direct & indirect)
    • **Spherocytes **on peri. smear
  • Treatment
    • Immune suppression
      • Corticosteroids (prednisone)
      • Splenectomy
      • Rituximab
    • Folate
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16
Q

Methods of Immune Suppression in Autoimmune Mediated Hemolyses

A
  • Corticosteroids (Prednisone)
  • Splenectomy
    • make sure to immunize against encapsulated organisms before doing this
  • Rituximab (immune suppression drug)
17
Q

General Mechanisms for Drug Induced Hemolyses

A
  • Innocent Bystander
    • Ab made against drug
    • Ab-drug complex form
    • Complexes deposit on RBC surface
    • Hemolysis
  • Hapten Mechanism
    • Drugs bind RBC
    • Ab form against Ab-RBC
    • Hemolysis
    • Ex: Penicillins & Cephalosporins
  • True Autoimmune Mechanism
    • Some drugs cause Ab to form against RBCs
    • once started, Abs form without drug present
    • Ex: alpha-methyldoa, L-Dopa, Procaindamide
18
Q

Cold Agglutinin Disease

A
  • Pathogenic bodies are usually IgM
  • DOES cause RBC agglutination
  • Fix complement for SURE
  • IgM falls off when RBCs return to warmer areas, but **complement stays on **
    • can cause **intravascular hemolysis **
    • OR can complete complement cascade in liver –> extravascular cascade
  • Treatment
    • Mycoplasma or Mononucleosis both associated with IgM
    • lymphoproliferative diseases
    • Keep patient warm
    • Immunosuppressors (Rituximab, chemo)
    • _***Steroids and Splenectomies are INEFFECTIVE_
19
Q

Non-Immune Hemolytic Anemia causes

A
  • Mechanical Traume to RBCs
  • Heart & large vessel abnormalities
  • March Hemoglobinuria
  • Infections
  • Drugs, Chemicals, Venom
20
Q

Microangiopathic Hemolytic Anemia (MAHA)

A
  • Shear damage do RBCs due to them passing by areas of endothelial damage
  • Schistocytes are hallmark
  • Etiologies
    • TTP/HUS
    • DIC
    • Hypertension
    • Vasculities

Heme/Onc (5 decks)

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