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16 Cards in this Set
- Front
- Back
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What is the progenitor cell of platelets? How long do platelets live?
Normal platelet count? |
Megakaryocyte= mother of platelet
Lives for 8-10 days in blood (removed by macrophages) Normal= 150K-350K |
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Four major steps of making a blood clot?
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1. Vasoconstriction (↓ blood loss)
2. Primary hemostasis = platelet adhesion & aggregation 3. Secondary hemostasis= blood coagulation (mesh to stop bleeding) 4. Fibrinolysis=shave off blood clot |
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What do platelets contain in their granules?
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Factors that promote clotting, ex:
ADP, serotonin, TXA2, Platelet factors, and Factor 4 |
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Thrombocytopenia is defined as platelet count below ____.
What happens clinically at a count of >100,000? <40,000? <20,000? <10,000? What consequence of bleeding do you fear the most? |
<150k= thrombocytopenia
<100,000 - still no abnormal bleeding <40,000- bleeds with TRAUMA <20,000- bleeds SPONTANEOUSLY (petichiae and brusing) <10,000- severe spontaneous bleeding * severe consequence = Intracranial Hemorrhages |
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Describe the steps in Primary Hemostasis.
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1. Injury to vessels exposes tissue factor/ collagen
2. Collagen binds to the platelets 3. Platelets get activated (i.e. "adhere") 4. Then they undergo shape change and release ADP, TXA2, and activate Gp2b3a 5. Platelets aggregate with each other. |
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What clinical findings suggest bleeding from Thrombocytopenia?
What clinical findings suggest bleeding from lack of clotting proteins? |
Thrombocytopenia --> mucosal surface bleeds, petechiae and purpura, nose and mouth (epistaxis, gingiva), menses
Clotting factor deficiency --> deep muscle bleeds, joint bleeds |
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Examples of Acquired disordered of Platelet dysfunction?
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1. Liver disease
2. Renal disease (uremia) 3. Cardiopulmonary bypass *liver and kidney clear toxins that interfere with platelet function. Cardiopulm bypass machine can cause damage to platelets. |
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A patient comes in feeling completely fine but their platelet count is ridiculously low. What could be going on?
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Pseudothrombocytopenia
Clumping of platelets (subjects who make antibodies to EDTA which is an anticoagulant). Clumping of platelets results in artificially low levels. |
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Describe the pathogenesis of ITP?
How do you make the diagnosis? |
Isolated thrombocytopenia but otherwise normal CBC and normal peripheral smear with GIANT platelets. Diagnosis of EXCLUSION (rule out all other possibilities, meds, infections, etc.)
ITP- B cells make antibodies that destroy a patient's platelets. Unknown why. |
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What is the treatment for ITP? (there are 6 total)
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1. Prednisone (suppress immune system)
2. IV IgG- Fc portion on antibody binds to Macrophage and macrophage destroys this instead of the platelet. 3. Anti-D antibody- Antibody against Rh antigen on RBC that causes destruction of RBC instead of spleen 4. Rituximab- antibody against B cells so they can't produce antibodies to platelets 5. Splenectomy (↓ ability to destroy platelets) 6. Romiplostim and Eltrombopag- TPO receptor antagonist (stimulate megs to make platelets) |
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What are common drugs that induce Thrombocytopenia?
What is the Innocent bystander reaction and what drug does this occur in? |
*remember, can occur with any drug!
- Antibiotics (TMP/SMX, Vancomycin, Penicillin, Acyclovir- antiviral) - H2 blockers (pepcid) Quinidine (Innocent bystander rxn.--.> antibody binds drug and activates complement which damages platelets) |
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Type I vs. Type II, Heparin Induced Thrombocytopenia (HIT)?
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Type I: Not clinically significant, occurs couple days after heparin exposure --> slight decrease in counts that then rise. BENIGN
Type II: Occurs 4-10 days after exposure, rapid decrease in counts. Associated with THROMBOSIS (not bleeding). |
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What is the pathophysiology of HIT type II? How does it cause Thrombosis?
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Heparin binds platelet membrane --> antibody forms to this complex. This antibody then ACTIVATES platelet to release more factor 4 causing --> causes Thrombosis.
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Testing for HIT Type II?
What treatment is important to initiate in these patients? |
1) ELISA (test for the antibody against heparin/platelet complex)
2) Serotonin-release assay (take antibody from patient and see if it stimulates serotonin release from platelet) * Gold standard Treatment = STOP Heparin + GIVE ANTICOAGs (Argatroban a direct thrombin inhibitor, or Lepirudin) |
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What is the pathophysiology of TTP (thrombotic thrombocytopenic purpura)?
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Loss of ADAMTS13 protein that usually breaks up vWF. Large VWF are bound to platelets which can clog up microvasculature
leads to endothelial damage and fibrin formation --> causes thrombi in vessels --> multi-organ failure. |
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What is the treatment of TTP?
What are some etiologies of this condition? |
Treatment= PLASMA EXCHANGE (you take out high molecular weight von wildebrand Protein, and you take out antibody to ADAMTS 13 if it exists)
Etiologies include: Shiga toxin, Cancer, Chemo, Pregnancy/post partum, drugs, infectious (viral) |
