Quantitative. Quantitative platelet defects produce either thrombocytopenia due to: 1) increased platelet destruction, utilization, or sequestration, or decreased platelet production, or 2) thrombocytosis from increased platelet production or release from tissue stores. Of these conditions, immune-mediated thrombocytopenia accounts for the majority of chronic cases. The immunological basis has been examined in humans and in the dog, cat, and horse. Primary immunological thrombocytopenia, of unknown etiology, has been termed idiopathic thrombocytopenic purpura (ITP), although the majority of cases appear secondary to a variety of underlying conditions such as infections, neoplasia, viral diseases, vaccine-associated reactions and drug use.

Qualitative. The major causes of qualitative platelet function defects include hereditary defects, various disease states, and a large number of drugs known to produce thrombopathias. Most drugs act by inhibiting the adhesion of platelets to subendothelium (aspirin, which blocks platelet cyclic endoperoxides) and/or the platelet release reaction (phenylbutazone, sulfonamides, non-steroidal antiinflammatory drugs, ticlopidine, promazine tranquilizers). Drugs that interfere with platelet function are contraindicated or must be used with caution in individuals with hemostatic disorders. Similarly, elective surgery should be avoided during the viremic phase (3Ð10 days) after live virus vaccination or viral exposure.

The most common diseases manifesting a bleeding tendency attributable to platelet dysfunction are renal failure and uremia and liver disease. Less common causes are the dysproteinemias such as myelomas and macroglobulinemias. The classic clinical case of uremic bleeding is tha of the old dog with compensated chronic interstitial nephritis which has inflamed gums and chronic periodontal disease. Dentistry on such a patient frequently results in excessive and prolonged gingival bleeding.

Thrombasthenia (Glanzmann's Disease)—an autosomal recessive bleeding disorder of humans and otterhound dogs in which there is little or no clot retraction. There may be low normal platelet counts or mild thrombocytopenia, and some bizarre giant platelets are seen in the ottherhound disorder. The bleeding diathesis is severe and of the purpuric type, and epistaxis is common and profuse. Bleeding episodes are triggered by stress events or surgery.

Thrombopathia. Hereditary animal thrombopathias have been recognized in fawn-hooded rats, basset hounds, spitz dogs, American cocker spaniels, Simmental cattle, and cats. The defect in fawn-hooded rats and American cocker spaniels is similar to that of human platelet storage-pool disease and Chediak-Higashi disease of mice and cats. These conditions produce a bleeding tendency primarily of mucosal surfaces and intrinsic to the platelet. Thrombopathic platelets fail to respond normally to very high concentrations of most physiologic agents that activate platelets.