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Bleeding Disorders
| Question | Answer |
|---|---|
| What are some physical examination findings that you see on patients with bleeding disorder? | Epistaxis, Petechiae, purpura, ecchymoses, edema, oral mucosal bleeding, Telangiectasia (spider veins), menorrhagia |
| What lab tests do you order for bleeding disorders? | CDC, Platelet function test, Coagulation Test, Protein Assays |
| 4 Steps of Coagulation | Resting -> Adhesion -> Activation -> Aggregation |
| What molecules are involved in Adhesion? | vWF, GP Ib + GP 9, collagen |
| Explain Glanzman Thrombasthenia | Autosomal recessive disorder in which platelets lack the GP IIb/ IIIa receptor on the cell surface |
| What is GP IIb/IIIa for? | They are proteins expressed on the platelet membrane that is important in platelet aggregation. (GP IIa/IIIb from 2 different platelets attach to 2 opposite ends of fibrinogen) |
| Explain Bernard-Soulier Disease | Disease that occurs when platelets lack GP Ib on their surface. These cells can't bind to vWF -> resulting in inability of adhesion |
| What is ITP? What are the two types? | ITP is a disease where autoantibodies are formed against platelets cause thrombocytopenia. The two types are Acute and Chronic |
| Explain Acute vs. Chronic ITP. Which age group is more likely to get Acute ITP? Chronic ITP? | Acute ITP has sudden onset of symptoms. Chronic ITP has gradual onset of symptoms from *IgG formed against GP IIa/IIIb*. Children (2-10) get mostly acute Teenagers and Adults get mostly chronic |
| How do you treat ITP? | Acute: Usually goes away on its own Chronic: 1) Steroids, IVIG 2) Splenectomy |
| How does Heparin-Induced Thrombocytopenia occur? | When Heparin is induced, heparin may bind to platelet factor 4 -> This creates heptan, which can be recognized as foreign antigen -> Body makes antibodies for it -> this *activates platelets* |
| What are some features of HIT? | Modest decline in platelet count, associated with arterial + venous thrombosis, excessive thrombi formation, NO excessive bleeding |
| What are the types of diseases under Thrombotic Microangiopathy (TMA)? | TTP, Hemolytic Uremic Syndrome, DIC |
| What protein defect cause TTP? | ADAMTS-13 -> required for cleaving vWF causing excess aggregation of platelets. |
| Symptoms of TTP are: | Excess thrombi formation, fever, renal failure, transient neurologic deficits |
| What is the name of the disease that is part of TMA and is caused by toxins from E. Coli? What is the toxin? | Hemolytic Uremic Syndrome. Toxin is called Shiga-like Toxins |
| Compare TTP with HUS. | They share symptoms of fever, anemia, thrombocytopenia (FAT) HUS patients present with more renal failure. (N) TTP patients present with more neurologic deficiency. (R) |
| What is DIC? | Constant deplete of platelets that is caused by large amounts of intravascular microthrombi. |
| What do you see in patients with DIC? | Depletion of platelets and clotting factors, widespread clot throughout body, excess bleeding (potentially hemorrhagic shock), *INCREASED level of D-Dimers* |
| Why do you see elevated D-Dimer in DIC? | The body is constantly forming plasmins to degrade the clot -> Giving very high levels of lysed products which are D-Dimers. |
| What causes DIC? | Sepsis Trauma Obstetric Complications Pancreatitis Malignancy (tumor) Nephrotic Syndrome Transfusion |
| Describe von Willibrand's Disease | Common autosomal dominant disorder that is caused from decrease or abnormal vWF Patient will have increased bleeding time (BT) and PTT. Abnormal ristocetin cofactor assay. |
| How are the two types of vWD different? | vWD Type 1 - vWF Ro: Ag ratio is >.7 -> Problem with vWF production vWD Type 2 - vWF Ro: Ag ratio is <.7 -> Problem with vWF function vWF Ag = immunoassay vWF Ro = function assay |
| What are the different types of Coagulation Tests? Describe each one. | PT - extrinsic factors = 8, 9, 10, 11, 12 aPTT - intrinsic factors - 7, 10 TT - fibrinogen - looks to see if fibrinogen can be turned into fibrin |
| Describe Hemophilia A | X-linked Recessive Disorder Decreased production of Factor 8 Prolonged aPTT, but normal PT and *BT* |
| Describe Hemophilia B | X-linked Recessive Disorder Decreased production of Factor 9 Prolonged aPTT, but normal PT and *BT* |
| Coagulation Factor Inhibitor mostly targets which factor? | CFI usually makes antibodies for Factor 8. The presentation is same as Hemophilia A, except that mixing with normal blood does not resolve the increase in PTT. |
| Which Vitamin deficiency leads to clotting problems? Why? | Vitamin K -> factors II, VII, IX, X and protein C and protein S are all dependent on Vitamin K |
| Why does liver disease/failure have possibility of resulting in coagulation dysfunction? | Almost all coagulation factors are created in the liver. |
| What does desmopressin do? | Increases the release of vWF by Weibel-Palade cells -> Good for vWD |
Created by:
soobyung92
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