AIHA Flashcards
Autoantibodies become active and attack red blood cells only at temperatures below normal body temperature. (4C)
Cold Autoimmune Hemolytic Anemia
Activation of **Complement system by IgM antibodies **resulting to cell lysis
Intravascular Hemolysis
Recognition of C3b resulting to hemolysis occuring in the liver
Extravascular Hemolysis
Caused by antibodies that optimally react at 4C
Cold Agglutinin Disease
**Occurs in older population; peak incidence >50 yrs old
Cold Agglutinin Disease
Can be caused by Mycoplasma pneumoniae or Infectious Mononucleosis
CAD
If complement system fails to form membrane attack complex, complement proteins deposit on RBC surface
Extravascular Hemolysis
IgM binds to polysaccharide region of glycoprotein on RBC surface complement system is triggered to lyse RBC
Intravascular Hemolysis
A clinical manifestation of cold agglutinin disease
Reynaud’s Phenomenon
Polychromasia,
Macrocytosis,
Spherocytosis,
Hyperbilirubinemia are laboratory findings in
Warm Autoimmune Hemolytic Anemia
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Reticulocytosis
* Positive DAT due to complement - Agglutinated RBCs, Poikilocytosis, Anisocytosis
Cold Agglutinin Disease
Aka secondary Cold AIHA.
Occurs as a transient disorder.
Secondary to infection.
Pallor and jaundice are characteristically present. Antibodies have anti-i specificity.
Cold Autoantibodies secondary to infxn.
Treatment drug for Cold Autoantibodies Secondary to Infection
Chlorambucil 10mg OD
often seen in children.
caused by **biphasic hemolysin. **
Anti-p specificity.
Donath Landsteiner antibody.
Paroxysmal Cold Hemoglobinuria
cold temp fixes complement, Warm temp lyses RBC.
Paroxysmal Cold Hemoglobinuria
Certain infections trigger antibody formation that reacts with the P antigen of RBC surface. After infection, polycolonal anti-P autoantibody binds to P antigen of RBC in cold temperature. When temperature is increased, complement system is activated and RBC is lysed.
Intravascular Hemolysis
Paroxysmal Cold Hemoglibinuria Treatment that is the only useful therapy
Protection from cold exposure
Following M. pneumoniae infection
CHD
Following viral infection
PCH
site of hemolysis of PCH
Intravascular
Positive Donath-Landsteiner Test
PCH
Treatment for PCH
Supportive
monophasic antibody class
CHD
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the autoantibodies attach to and destroy red blood cells at temperatures equal to or in excess of normal body temperature
It is the most common form of autoimmune hemolytic anemia
Warm Autoimmune Hemolytic Anemia
Associated with collagen disease, SLE, RA, Carcinoma, Pregnancy
Warm Autoimmune Hemolytic Anemia
Treatment for Warm Autoimmune Hemolytic Anemia when patient does not respond to prednisnone
Intravenous Immune Globulin (IVIG)
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Drug does not bind covalently to RBCs but rather complexes with drug antibody
Drug-Induced Hemolytic Anemia - Neo antigen type
occurs only when the patient receives massive doses of the antibiotic
Drug-Induced Hemolytic Anemia - Drug Adsorption Type
Most frequently encountered drug in Drug-induced Hemolytic Anemia - Drug Adsorption Type
Cefotetan
AIHA with variable complement activity
Warm-Reactive Autoantibody
has specificity to Anti-Rh precursor, **anti-common Rh, anti-LW, anti-U **
Warm-reactive autoantibody AIHA
site of RBC destruction wherein it is** predominantly in the spleen** with some liver involvement
Warm Reactive Autoantibody AIHA
Quinidine and Phenacetin are under what mechanism of drug-related antibodies
Immune complex
positive DAT only when drug is added to test system
Drug-induced hemolytic anemia - Autoimmune type
