ITPdue to antibodies made after viral infection.
mucocutaneous bleeding (epistaxis, hematuria, ecchymosis, petechiae)
↑BT (normal PT & PTT)
normal/ slightly ↑ size
observe only if mild (cutaneous bleeds, PLT ≥30,000)
Steroids/IVG/anti-D if severe (bleeding or PLT<30,000)
Test for HCV & HIV
TTPhereditary/ acquired
Antibody against ADAMTS13 → uncleared vWF multimers → PLT trapping & activation
fever, neuro sx, renal failure
↓PLT with hemolysis (↑LDH, ↓haptoglobin, ↓RBC, schistocytes)
↑BT (normal PT & PTT)
plasma exchange/ steroids/ rituximab
replenishes ADAMTS13 & removes antibodies
HIT-1heparin activates PLT directly → ↓PLT count within the first 2 days of use. Then PLT normalizes. Milder than HIT-2
HIT-2auto-immune: antibodies against PLT factor 4 (PF4) complex with heparin. Seen 5-10 days after starting heparin with ≥50% drop in PLT. Massive clots → stroke/ PE/ Limb ischemia. Serotonin release assayStop all heparin. Argatroban (direct thrombin inhibitor) or fondaparinux.
Once PLT>150,000, switch to warfarin
DIC↑tissue factor (TF) from endothelial damage from TF release by cancers/ etc → over activated coagulation cascade → consumptive coagulopathy. Lipopolysaccharide (sepsis) →DIC↑PT, ↑PTT, ↓PLT, ↓fibrinogen, ↑D-dimertreat cause
appropriate blood products (eg massive bleed gets pRBC, PLT, FFP)
Hemophilia AXR, factor 8
↑PTT (normal PLT, PT)Desmopressin
Factor 8 replacement;
if inhibitor present give activated factor 7 or activated prothrombin complex
Hemophilia BXR, factor 9
↑PTT (normal PLT, PT)factor 9 replacement
Hemophilia Cfactor 11
vWDfactor 8
Vitamin K deficiencyfactor 2,7,9, 10, protein C&S
↑PT first then ↑PTT if severeVitamin K
Factor V Leiden mutationmost common hereditary hypercoagulability
Prothrombin mutation2nd most common
Antithrombin deficiencyinherited: rare
acquired: DIC, cirrhosis, nephrotic syndrome
Protein C/S deficiency↓inactivation of factor Va & VIIIa
warfarin-induced skin necrosis (protein C only)