Thrombocytopenia - Revision history

Aesetholephews: /* Destruction/Consumption */

2022-10-21T05:29:13Z

Destruction/Consumption

Aesetholephews: /* Destruction/Consumption */

2022-10-21T05:27:32Z

Destruction/Consumption

Aesetholephews: 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..."

2022-10-21T05:26:20Z

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..."

New page

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?

@@ Line 10: / Line 10: @@
 * '''HIGH''' IPF%, Prolonged PT / aPTT
 * What happens to platelets after they help form a clot?
 * [[DIC]]
 * ITP
 * TTP

@@ Line 14: / Line 14: @@
 ** 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)
@@ Line 21: / Line 20: @@
 *** 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)
@@ Line 28: / Line 26: @@
 *** PT > 3s (1 pt), > 6s (2 pt)
 *** Fibrinogen < 1 g/L (1 pt)
 ** Treatments and Evidence Behind Them:
 *** Basically don't get it.
@@ Line 34: / Line 31: @@
 *** Treatment is lousy. Evidence behind treatment is likewise lousy.
 *** Platelets, cryo, FFP
 ** Morbidity/Mortality is 20-50%