1,022
edits
Changes
Jump to navigation
Jump to search
Created page with "Platelets come from megakariocytes and are produced in bone marrow and lung. Their development is stimulated by thrombopoeitin produced in liver and kidney. They are 2-3 um ac..."
Platelets come from megakariocytes and are produced in bone marrow and lung. Their development is stimulated by thrombopoeitin produced in liver and kidney. They are 2-3 um across. Platelet function follows the pattern: Adhesion -> Activation -> Aggregation. Platelet aggregation forms a platelet plug (primary hemostasis), which is stabilized by coagulation factors culminating in a fibrin mesh/net which stabilizes the platelet plug.
=Spurious=
* Clumping
=Sequestration=
* Hypersplenism
=Destruction/Consumption=
* '''HIGH''' IPF%, Prolonged PT / aPTT
* What happens to platelets after they help form a clot?
* [[DIC]]
** Most Common Etiologies
*** '''Bacterial sepsis''' (83%), '''Trauma''' (31%), '''Cancer''' (e.g. APML, 6.8%), placental abruption, preeclampsia, amniotic fluid embolism, burn, hyperthermia, rhabdomyolysis, infection, transfusion reaction (ABO incompatibility), snake venom, aortic aneurysm
** Pathogenesis
*** Expression of the transmembrane glycoprotein TF (which activates factor VII and the extrinsic pathway)
*** Consumption of clotting factors
*** Widespread micro and macrovascular thrombosis, depletion of fibrinogen and fibrin clot formation
*** Platelets are trapped in the clots
*** Plasminogen --> Plasmin also upregulated, leading to large increase in clot breakdown and release of [[FDPs]].
** Diagnostic Algorithm: Score of 5+ points strongly associated with DIC
*** Presence of a disease known to be associated with DIC (2 pts)
*** Platelets < 100k (1 pt), < 50k (2 pt)
*** Fibrin degradation products (FDPs) (e.g. d-dimer): moderate increase (2 pt), strong increase (3 pt)
*** PT > 3s (1 pt), > 6s (2 pt)
*** Fibrinogen < 1 g/L (1 pt)
** Treatments and Evidence Behind Them:
*** Basically don't get it.
*** Treat underlying condition
*** Treatment is lousy. Evidence behind treatment is likewise lousy.
*** Platelets, cryo, FFP
** Morbidity/Mortality is 20-50%
* ITP
* TTP
* HUS
* HIT
=Decreased Production=
* '''LOW''' IPF%
* Parvo
* Aplastic Anemia
* Cancer
* Chemotherapy
* Liver disease?
=Spurious=
* Clumping
=Sequestration=
* Hypersplenism
=Destruction/Consumption=
* '''HIGH''' IPF%, Prolonged PT / aPTT
* What happens to platelets after they help form a clot?
* [[DIC]]
** Most Common Etiologies
*** '''Bacterial sepsis''' (83%), '''Trauma''' (31%), '''Cancer''' (e.g. APML, 6.8%), placental abruption, preeclampsia, amniotic fluid embolism, burn, hyperthermia, rhabdomyolysis, infection, transfusion reaction (ABO incompatibility), snake venom, aortic aneurysm
** Pathogenesis
*** Expression of the transmembrane glycoprotein TF (which activates factor VII and the extrinsic pathway)
*** Consumption of clotting factors
*** Widespread micro and macrovascular thrombosis, depletion of fibrinogen and fibrin clot formation
*** Platelets are trapped in the clots
*** Plasminogen --> Plasmin also upregulated, leading to large increase in clot breakdown and release of [[FDPs]].
** Diagnostic Algorithm: Score of 5+ points strongly associated with DIC
*** Presence of a disease known to be associated with DIC (2 pts)
*** Platelets < 100k (1 pt), < 50k (2 pt)
*** Fibrin degradation products (FDPs) (e.g. d-dimer): moderate increase (2 pt), strong increase (3 pt)
*** PT > 3s (1 pt), > 6s (2 pt)
*** Fibrinogen < 1 g/L (1 pt)
** Treatments and Evidence Behind Them:
*** Basically don't get it.
*** Treat underlying condition
*** Treatment is lousy. Evidence behind treatment is likewise lousy.
*** Platelets, cryo, FFP
** Morbidity/Mortality is 20-50%
* ITP
* TTP
* HUS
* HIT
=Decreased Production=
* '''LOW''' IPF%
* Parvo
* Aplastic Anemia
* Cancer
* Chemotherapy
* Liver disease?