Platelets Flashcards
1
Q
Where are platelets made and from what pre-cursor?
A
- Made in Bone marrow
- from Megakaryocytes
2
Q
What is the hormonal stimulus for platelet production?
A
Thrombopoeitin
3
Q
3 Steps of Platelet Plug Formation (Details)
A
-
Adhesion
- Platelets stick to vWF in subendothelium
-
vWF sticks to GP Ib/IX on platelet
- also sticks to collagen in vessel wall
-
Aggregation
- Platelets stick to eachother via fibrinogen bridges
- Fibrinogen binds to platelet receptor GP IIb/IIIa
- activated by:
- Thrombin
- TxA2
- Collagen
- ADP
- Epinephrine
- Serotonin
-
Secretion
- platelets release granular secretions that promote clots
*
- platelets release granular secretions that promote clots
4
Q
Petichiae & Purpura are signs of what regarding platelets?
A
Plateley hypoperfusion
5
Q
Basis of pseudothrombocytopenia
A
- Some patients have a factor that makes their blot clot when exposed to the EDTA in test tubes
- If not considered, reported platelet count will be much lower than in vivo count
- NO CLINICAL SEQUELLAE
6
Q
Symptoms of pseudothrombocytopenia
A
- Mucocutaneous bleeding (“oozing and bruising”)
- **NO JOINT/MUSCULAR BLEEDS **
- these are more like hemophilia
- Classic primary hemostasis defects
7
Q
3 Categories of Thrombocytopenis DDx
A
- Underproduction
- Peripheral Destruction
- Splenic sequestration
8
Q
Platet Undreproduction Characteristics
A
- Hallmark: Decreased megakaryocytes in bone marrow
- Could be due to
- Marrow failure
- Marrow infiltration
- Marrow toxins
9
Q
Peripheral Destruction Mechanisms
A
- DIC
- TTP
- HUS
10
Q
DIffuse Intravascular Coagulation (DIC)
A
- Abnormal Coag. activation, thrombin generation, clotting factor consumption , platelet destruction
- Lab
- Increased PT
- Decreased platelets
- Decreased fibrinogen
- Increased fibrin degeneration products (D-Dimers)
- Schistocytes
- Etiologies
- Gram (-) sepsis
- Burns
- OB complications
- Leukemias
- Shock
- Venom
- Treatment
- Platelet transfusion
- clotting factors
- fibrinogen
11
Q
Thrombotic Thrombocytopenic Purpura (TTP)
A
- Abnormal platelet activation, vWF deposition, RBC and platelet destruction
- Diagnosis - THE PENTAD
- MAHA - MUST BE PRESENT
- Schistocytes - MUST BE PRESENT
- Low platelets
- Fever
- Neurologic manifestations
- Renal Manifestations
- “My Parents Never Forget Rent…but My Parents MUST BE PRESENT”
- Etiologies
- Antibody against ADAMTS-13, which processes vWF
- Drugs
- Quinine
- Cyclosporine
- tacrolimus
- increased chance with pregnancy or AIDS
- Treatment
- Plasma exchange (PLEX)
- Corticosteroids (will only work with PLEX)
- NO PLATELET TRANSFUSIONS
- Splenectomy
- RItuximab
12
Q
Hemolytic Uremic Syndrome (HUS)
A
- Overlaps with TTP
- Fewer Neuro, more renal symptoms
- Precipitated by diarrheal symptoms (E. Coli/Shigella)
- see more in children
- not as good response to PLEX
13
Q
Immune Mediated Thrombocytopenia
A
- Antibodies binding to platelets via Fc receptors (Ig mediated) and destroying them via RE System macrophages
- NO DIAGNOSTIC TEST like coombs for hemolysis
- Same 3 mechanisms for action for drug induced thrombocytopenia as for drug induced hemolysis
- Innocent bystander
- Hapten mechanism
- True Immune Mechanism
- Drugs that can cause this
- Beta lactam antibiotics
- Sulfa Drugs
- Quinine/quinidine
- Heparin
14
Q
Why is Heparin dangerous?
A
- Can cause paradoxical thrombosis
- starts off as decreased platelet count…if this happens STOP HEPARIN IMMEDIATELY
15
Q
Immune mediated/Idiopathic Thrombocytopenic Purpura (ITP)
A
- Diagnosis of exclusion
- Should see megakaryocytes in bone marrow
- Spontaneous remission in children
- Adults need treatment
- Corticosteroids
- IVIg if more severe
- Splenectomy - 2nd line
- Rituximab - 3rd line
