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What is Warm antibody autoimmune hemolytic anemia and explain in detail?
Warm antibody autoimmune hemolytic anemia (WAIHA) is the most common form of autoimmune haemolytic anemia. About half of the cases are of unknown cause, with the other half attributable to a predisposing condition or medications being taken. Contrary to cold autoimmune hemolytic anemia (e.g., cold agglutinin disease and paroxysmal cold hemoglobinuria) which happens in cold temperature (28–31 °C), WAIHA happens at body temperature.

Causes
AIHA may be:

Idiopathic, that is, without any known cause
Secondary to another disease, such as an antecedent upper respiratory tract infection, systemic lupus erythematosus or a malignancy, such as chronic lymphocytic leukemia (CLL)

Medications
Several medications have been associated with the development of warm AIHA. These medications include quinidine, nonsteroidal anti-inflammatory drugs (NSAIDs),  alpha methyldopa, and antibiotics such as penicillins, cephalosporins (such as ceftriaxone and cefotetan), and ciprofloxacin.

Pathophysiology
The most common antibody isotype involved in warm antibody AIHA is IgG, though sometimes IgA is found.  The IgG antibodies attach to a red blood cell, leaving their FC portion exposed with maximal reactivity at 37 °C (versus cold antibody induced hemolytic anemia whose antibodies only bind red blood cells at low body temperatures, typically 28-31 °C).  The FC region is recognized and grabbed onto by FC receptors found on monocytes and macrophages in the spleen.  These cells will pick off portions of the red cell membrane, almost as if they are taking a bite.  The loss of membrane causes the red blood cells to become spherocytes.  Spherocytes are not as flexible as normal RBCs and will be singled-out for destruction in the red pulp of the spleen as well as other portions of the reticuloendothelial system