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Primary Hemostasis.
| Question | Answer |
|---|---|
| Damage to the wall is repaired by__________, which involves formation of a ___________ at the site of vessel injury. | Homeostasis, thrombus(clot) |
| What is primary hemostasis? | Primary hemostasis forms a WEAK platelet plug and is mediated by interaction between platelets and the vessel wall. |
| What is secondary hemostasis? | Secondary hemostasis stabilizes the platelet plug and is mediated by the coagulation cascade. |
| Mechanism behind primary hemostasis?Step1 | Edotheliel cells sit on top of the basement membrane. Step 1- Transient vasoconstriction of damaged vessel 1. Mediated by reflex NUERAL STIMULATION and ENDOTHELIN release from endothelial cells |
| Mechanism behind primary hemostasis?Step2 | Von Willebrand factor (vWF) binds exposed subendothelial collagen.Platelets bind vWF using the GPib receptor. |
| Where does vWF come from?? | vWF is derived from the WEIBEL-PALADE bodies of endothelial cells and A-GRANULES of platelets. |
| What does the WEIBEL PALADE bodies contain? | Von Willebrand factor (vWF) and P -selectin for speed bumps and stopping neutophils. |
| Mechanism behind primary hemostasis?Step3 | Adhesion - causes shape change and degranulation.- ADP is released from platelet dense granules; promotes exposure of GPIIb/IIla receptor on platelets. TXA2 is synthesized by platelet cyclooxygenase (COX) and released; promotes platelet aggregation |
| Mechanism behind primary hemostasis?Step4 | Platelets aggregate at the site of injury via GPIIb/IIIa using fibrinogen (from plasma) as a linking molecule; results in formation of platelet plug 2. coagulation cascade (secondary hemostasis) stabilizes it. |
| Types of Disorders of primary hemostsis? | Divided into quantitative: not a lot qualitative: a lot but not good |
| clinical presentation of primary hemostasis? | Mucosal and skin bleeding |
| What are the symptoms of mucosal bleeding | Nose bleed(most common), cough up blood GI bleeding, hematuria, and menorrhagia. Intracranial bleeding occurs with severe thrombocytopenia. |
| What are the symptoms of skin bleeding | Symptoms of skin bleeding include petechiae (pinpoint bleeding1-2 mm, ecchymoses (> 1 cm), purpura(> 3 mm), and easy bruising; petechiae are a sign of thrombocytopenia and are not usually seen with qualitative disorders. |
| Laboratory exhibition of primary hemostasis- platelet count | l. Platelet count-normal 150-400 K/~L; < 50 K/~L leads to symptoms. |
| Laboratory exhibition of primary hemostasis- Bleeding time | 2. Bleeding time-norma1 2-7 minutes; prolonged with quantitative and qualitative platelet disorders. You prick the pt. 3. Blood smear- used to assess number and size of platelets 4. Bone marrow biopsy-used to assess megakaryocytes, which produce platel |
| Laboratory exhibition of primary hemostasis- Blood smear | 3. Blood smear- used to assess number and size of platelets |
| Laboratory exhibition of primary hemostasis- bone marrow biopsy | 4. Bone marrow biopsy-used to assess megakaryocytes, which produce platelets |
| What are the two major diseases for primary hemostasis(QUANTITATIVE) | IMMUNE THROMBOCYTOPENIC PURPURA (ITP) MICROANGIOPATHIC HEMOLYTIC ANEMIA |
| What happens in IMMUNE THROMBOCYTOPENIC PURPURA (ITP) | Patients have IgG against the platelet(eg GP11b/111a). The antigen antibody complex is eatten up by macrophages=thrombocytopenia(low platelet count) Both antibodies and the macrophages eat the antibody+antigen complex in the speen |
| There are two forms of IMMUNE THROMBOCYTOPENIC PURPURA (ITP). what are they? | Acute and chronic form |
| There are two forms of IMMUNE THROMBOCYTOPENIC PURPURA (ITP). Describe the acute phase | Acute form = children weeks after a viral infection or immunization; selflimited, usually resolving within weeks of presentation |
| There are two forms of IMMUNE THROMBOCYTOPENIC PURPURA (ITP). Describe the chronic phase | Chronic form =adults, usually women of childbearing age. May be primary or secondary (Lupus). May cause short-lived thrombocytopenia in offspring since antiplatelet IgG can cross the placenta.Lupus they have antibodies against one thing- here platelets. |
| Lab findings for itp? | 1. low platelet count, often < 50 K/~L(platelets are being consumed) 2. Normal PT/PTT-Coagulation factors are not affected. 3. high megakaryocytes(hyperplasia) on bone marrow biopsy |
| Treatment for itp? | corticosteroids. Children 0k; adults ok but relapse. IVIG is used to raise the platelet-shirt lived. Macrophages to eat them rather than the IgG bound to the platelets. -if splenectomy- kils platelet making site+ site of destruction. |
| What happens in MICROANGIOPATHIC HEMOLYTIC ANEMIA | MICROANGIO= small blood vessels PATHIC= pathology HEMOLYTIC= rbc die ANEMIA Pathologic formation of platelet microthrombi in small vessels(consumes platelets)- RBC sheared as they pass aross making them schistocytes |
| complications of MICROANGIOPATHIC HEMOLYTIC ANEMIA are? | thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) |
| thrombotic thrombocytopenic(use up platelets) purpura(bleeding) (TTP) mechnaism is what? | Pathologic formation of platelet microthrombi in small vessels. TTP is due to decreased ADAMTS13(autoantibody), an enzyme that normally cleaves vWF multimers into smaller monomers for eventual degradation thusabnormal platelet adhesion=microthrombi. |
| hemolytic uremic syndrome mechanism is what? | Pathologic formation of platelet microthrombi in small vessels. l. Classically seen in children with E coli Ol57:H7 dysentery,-beef 2. E coli verotoxin damages endothelial cells resulting in platelet microthrombi.= tearing RBC. |
| ClinicAL FINDINS OF hus AND ttp | 1.Skin and mucosal bleeding=usin platelets 2. Microangiopathic hemolytic anemia 3. Fever 4. Renal insufficiency (more common in HUS)- Thrombi involve vessels of the kidney. 5. CNS abnormalities (more common in TTP)- Thrombi involve vessels of the CN |
| Lab findings for HUS and TTP | 1. low platelet count, more bleeding time 2. Normal PT/PTT-Coagulation factors are not affected. 3. high megakaryocytes(hyperplasia) on bone marrow biopsy 4. Ripped RBC |
| Treatment for ttp | plasmapheresis- remove plasma from the blood-low auto antibodies corticosteroids- low production of auto antibodies |
| What are the two major diseases for primary hemostasis(QUALITATIVE) | Bernard-Soulier syndrome Glanzmann thrombasthenia |
| Symptoms behind Bernard-Soulier syndrome | due to a genetic GPib deficiency; platelet adhesion is impaired. 1. Blood smear shows mild thrombocytopenia(not used.. destroyed)with enlarged platelets(immature platelets). |
| Symptoms behind Glanzmann thrombasthenia | Glanzmann thrombasthenia is due to a genetic GPIIb/IIIa deficiency; platelet aggregation is impaired. |
| How does Asprin and Uremia show qualitative primary hemostasis. | Aspirin irreversibly inactivates cyclooxygenase; lack ofTXA2 impairs aggregation. D. Uremia disrupts platelet function; both adhesion and aggregation are impaired. |
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atayal
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