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Thrombocytopenia
Immune thrombocytopenias (ITP) – formerly known as immune thrombocytopenic purpura and idiopathic thrombocytopenic purpura
Splenomegaly
Gauchers disease
Familial thrombocytopenia
Chemotherapy
Babesiosis
Dengue fever
Onyalai
Thrombotic thrombocytopenic purpura
HELLP syndrome
Hemolytic–uremic syndrome
Drug-induced thrombocytopenic purpura (five known drugs – most problematic is heparin-induced thrombocytopenia (HIT)
Pregnancy-associated
Neonatal alloimmune associated
Aplastic anemia
Transfusion-associated
Pseudothrombocytopenia
Idiopathic thrombocytopenic purpura
Vaccine induced immune thrombocytopenia
Gilberts syndrome

Altered platelet function (thrombocytopathy)
Congenital
Disorders of adhesion
Bernard–Soulier syndrome
Disorders of activation
Disorders of granule amount or release
Hermansky–Pudlak syndrome
Gray platelet syndrome
ADP receptor defect
Decreased cyclooxygenase activity
Platelet storage pool deficiency
Disorders of aggregation
Glanzmanns thrombasthenia
Wiskott–Aldrich syndrome
Disorders of coagulant activity
COAT platelet defect
Scott syndrome
Acquired
Disorders of adhesion
Paroxysmal nocturnal hemoglobinuria
Asthma
Samters triad (aspirin-exacerbated respiratory disease/AERD)
Cancer
Malaria
Decreased cyclooxygenase activity

Thrombocytosis and thrombocythemia
Reactive
Chronic infection
Chronic inflammation
Malignancy
Hyposplenism (post-splenectomy)
Iron deficiency
Acute blood loss
Myeloproliferative neoplasms – platelets are both elevated and activated
Essential thrombocythemia
Polycythemia vera
Associated with other myeloid neoplasms
Congenital

Drugs affecting
Anti-inflammatory drugs
Some drugs used to treat inflammation have the unwanted side effect of suppressing normal platelet function. These are the non-steroidal anti-inflammatory drugs (NSAIDS). Aspirin irreversibly disrupts platelet function by inhibiting cyclooxygenase-1 (COX1), and hence normal hemostasis. The resulting platelets are unable to produce new cyclooxygenase because they have no DNA. Normal platelet function will not return until the use of aspirin has ceased and enough of the affected platelets have been replaced by new ones, which can take over a week. Ibuprofen, another NSAID, does not have such a long duration effect, with platelet function usually returning within 24 hours, and taking ibuprofen before aspirin prevents the irreversible effects of aspirin. Drugs that suppress platelet function
These drugs are used to prevent thrombus formation.
This event stimulates the coupled Gs protein to increase adenylate cyclase activity and increases the production of cAMP, further promoting the efflux of calcium and reducing intracellular calcium availability for platelet activation.ADP on the other hand binds to purinergic receptors on the platelet surface. Since the thrombocytic purinergic receptor P2Y12 is coupled to Gi proteins, ADP reduces platelet adenylate cyclase activity and cAMP production, leading to accumulation of calcium inside the platelet by inactivating the cAMP calcium efflux pump. The other ADP-receptor P2Y1 couples to Gq that activates phospholipase C-beta 2 (PLCB2), resulting in inositol 1,4,5-trisphosphate (IP3) generation and intracellular release of more calcium. This together induces platelet activation. Endothelial ADPase degrades ADP and prevents this from happening. Clopidogrel and related antiplatelet medications also work as purinergic receptor P2Y12 antagonists. Trigger (induction)
Platelet activation begins seconds after adhesion occurs. It is triggered when collagen from the subendothelium binds with its receptors (GPVI receptor and integrin α2β1) on the platelet. GPVI is associated with the Fc receptor gamma chain and leads via the activation of a tyrosine kinase cascade finally to the activation of PLC-gamma2 (PLCG2) and more calcium release.Tissue factor also binds to factor VII in the blood, which initiates the extrinsic coagulation cascade to increase thrombin production. Thrombin is a potent platelet activator, acting through Gq and G12. These are G protein-coupled receptors and they turn on calcium-mediated signaling pathways within the platelet, overcoming the baseline calcium efflux. Families of three G proteins (Gq, Gi, G12) operate together for full activation.