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25 Cards in this Set
- Front
- Back
Once activated, what morphological changes are seen in platelets?
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They spread out, forming a "fried egg" appearing patch
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Are platelets nucleated?
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NO
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What are the steps in platelets activating / clotting?
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1. Injury
2. Initiation: Exposed collagen fibrils and Vanwhilibrand Factor bind platelets as they travel past injury 3. Extension: platelets secrete ADP and TxA2 which aid in platelets sticking to each other 4. Stabilization |
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What 2 clotting reactions require the surface of platelets?
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1. The Ten-ase complex
2. The prothrombinase complex |
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What is the role of αIIbβ3?
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It is a transmembrane INTEGRIN heterodimer
- When activated, allows platelets to stick together |
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How are the platlet integrins activated?
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- Calcium Concentration increases
- calcium recruits Talin - Talin activates Integrin (αIIbβ3) |
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What is the role of TxA2?
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Helps to recruit platelets into the plug
Note: TxA2 is inhibited by Aspirin |
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What cell type produces platelets?
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Megakaryocyte
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What hormone drives platelet production?
Where is it produced? |
Thrombopoitin (TPO) via its receptor (MPL)
Produced CONSTITUTIVELY in the liver |
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What is the feedback cycle that regulates the level of platelets?
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As platelet count drops, less TPO is bound to circulating platelets, leaving more TPO to stimulate megakaryocytes in the bone marrow
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How long do platelets normally last in the blood?
What is a normal platelet count? |
~10 days
Normal Platelet count: 150,000-400,000 |
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What is an ecchymoses?
Petechiae? |
Ecchymoses: Bruise
Petechiae: Pin head sized bruises |
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What is thrombocytopenia?
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Low levels of Platelets
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What 4 symptoms are often seen in a platelet defects?
4 Symptoms from clotting defect? |
Platelet Defect
1. Petechiae and ecchymoses 2. Epistaxis (nose-bleed) and menorrhagia (heavy period) 3. Skin and Mucus membrane 4. "Immediate" bleeding from failure to form a platelet plug Clotting Defect: 1. Deep spreading hematoma 2. Hemarthroses (bleeding into joints) 3. Retroperitoneal Bleeding 4. "Delayed" bleeding when an inadequate fibrin clot breaks down prematurely |
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What is Glanzmann's thrombasthenia?
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Defect in αIIbβ3 integrin resulting in a failure of platelet aggregation
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What are the 2 main consequences of inappropriate platelet activation?
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1. Heart Attacks
2. Strokes |
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What are the 3 main causes of thrombocytopenia?
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1. Failure of Production
2. Reduced Survival 3. Increased Pooling (sequestration) |
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What are 2 main ways that decreased production of platelets in thrombocytopenia can be observed?
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1. Decreased Megakaryocytes
- Chemotherapy agents - Drugs - Marrow Disorders (aplastic anemia, leukemia) 2. Ineffective production - Vitamin Deficiencies (B12, Folate) - Marrow Disorders (pre-leukemia and leukemia) |
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What are the 2 main categories of decreased survival of platelets in thrombocytopenia?
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1. Immune
- ITP (immune thrombocytopenic purpura) - PTP (post-transfusion purpura) - Collagen-vascular disease (ie Lupus) - Drugs 2. Non-Immune - DIC (disseminated intravascular coagulation) - Sepsis - TTP (thrombotic thrombocytopenic purpura) - By-Pass Pumps |
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What is ITP?
What is caused by? |
Immune Thrombocytopenic Purpura
- Caused by anti-platelet antibodies that often attack the platelet integrin αIIbβ3 - Removal of antibody-coated platelets |
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What are the 4 ways that ITP can be treated?
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1. Inhibit phagocyte mediate clearance of Ab coated platelets
- steroids, splenectomy 2. Decrease AB production - Rituximab, steroids, immunosuppress 3. Impair T/B cell interactions - Steroids, rituximab 4. Enhance platelet production -Thrombopoetic agents, interleukin 11 |
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What is a mechanism for drug induced thrombocytopenia?
Drug example? |
- Drug sticks to glycoprotein on platelet surface
- AB recognizes drug/glycoprotein complex and attacks - Spleen removes platelets Example: Quinidine |
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What is the primary cause of thrombocytopenia via increased sequestration in the spleen?
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- Liver disease causes portal hypertension.
- That causes decreased outflow from spleen therby enlarging it |
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What is thrombocytosis?
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Elevated platelet counts
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What is thrombocythemia?
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Neoplastic thrombocytosis - JAK2 gain of function mutation, always active TPO receptor
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