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Hemostasis and Throm
Clinical Medicine II
| Question | Answer |
|---|---|
| What is primary hemostasis | platelets activated, form a plug, with its phospholipid surface |
| What is secondary hemostasis | coag factors generate thrombi, fibrin mesh forms, holds plug in place |
| What stops hemostasis | regulatory proteins, shut off thrombin generation, controls clot size |
| Four steps of blood clots | primary hemostasis: platelets activated→plug , secondary hemostasis: fibrin mesh forms, hemostasis stops: shut off thrombin generation, fibrinolysis: clot dissovles when injury healed |
| What happens w/ thrombosis | hemostasis doesn’t shut off |
| What are we testing with INR and PT | the secondary hemostasis, fibrin mesh formation from the plasma factors |
| What do we test w/ primary hemostasis | platelet count and stickiness |
| Where are coag factors made | in the liver and circulate as inactive proteins |
| What are factors I, II, III and IV called | I: fibrinogen, II: prothrombin IIa: thrombin III: tissue factor IV: calcium, always called by names not numbers |
| What converts II to IIa | Va |
| How do we test an INR in a tube | Ca+ plus Phosphilpid (PTTP) + tissue factor |
| What are clotting factors that accelerate clotting cascade | V and VIII |
| Factors that shut off hemostasis | protein APC and S stop or inactivate Va and VIIIa |
| What happens if we don’t have protein C or S | huge clots will form from the result of injury |
| What is another way to inhibit clotting | anti-thrombin factors |
| What accelerates anti-thrombin pathway | heparin |
| What does antithrombin II shut off | thrombin, Factors Xa, IXa, Xia |
| Two common examples of bleeding d/o | hemophilia and von Willebrand dz |
| What do we ask for bleeding problems w/ pt hx | life long vs recent, and a constellation of bleeding sxs |
| What surgical histories should we remind them of | circumcision, dental extractions, tonsillectomy, surgical procedures, trauma, childbirth, menstrual periods, hysterectomy d/t heavy bleeding in past |
| Specific signs and sxs for bleeding | bruising, petechiae, epistaxis, gingival bleeding, hemoptysis, hematememis, hematureia, hematochezia melena, hemarthroses, soft tissue hemorrhages |
| Primary hemostasis | issues w/ platelets or vonwildbrands don’t stop bleeding initially, |
| Secondary hemostasis | issues w/ building fibrin clots, initial clot, but bleed like crazy later |
| Clinical features for primary hemostasis | prolonged initial bleeding, petechiae, mucosal bleeding, bruising-eccymoses, soft tissue bleeding can also happen |
| Bleeding problems commonly seen in secondary hemostasis | late re-bleeding, hemarthroses, ecchymoses, soft tissue bleeding |
| Labs for primary hemostasis | CBC (platelet count), platelet fxn testing, Von Willebrand panal |
| Labs for secondary hemostasis | PT/INR, aPTT, fibrinogen, mixing studies, factor levels |
| What factor may not be detected in inr/pt tests | factor XIII deficiency |
| What other factors can we detect | fibrinolysis and Ehlers-danlos syndrome |
| Ehlers-danlos syndrome | very flexible joints (stretchy collegen) |
| MC inherited bleeding d/o | von WIllebrand dz |
| Fxns of vWb factor | platelet adhesion to endothelial injury, plasma carrier of factor VIII |
| Inheritance pattern of vwb factor | autosomal dominant (males and females affected equally) |
| Types of Von willebrand dz | Type I: deficiency II: dysfunctional III: complete deficiency, homozygous gene for this |
| Common vWB dz sxs | epistaxis, dental bleeding, bruising, menorrhagia that doesn’t stop well |
| Tests for vWB dz | abnl platelet fxn closure time cuz they don’t stick together, vWB panal: low vWB antigen, low factor VIII, low ristocetin cofactor activity (how well it works-Type II) |
| Why is factor VIII low in vWB | it is a plasma carrier of factor VIII |
| How do we detect type II vWB | test for low ristocetin cofactor activity which is how well vWB works |
| What are tx’s of vWB dz | avoid drugs inhibit platelet fxn, desmopressin, antifibrinolytics, plasma derived VIII and cryoprecipitate |
| What does desmopressin do | synthetic ADH analog, releases stored vWF from endothelium |
| What do we need to be careful about when prescribing desmopressin | the concentration sue stimate (1.5mg/ml) while DDVAP is for bed wetting |
| What is amicar | oral antifibrinolytic: stops step for (fibrinolysis inhibition) |
| What is cryoprecipitate used for | rich in vWF and VIII but non viral inactivated |
| Congenital bleeding d/o caused by deficiency of coag factor VIII or IX | hemophilia |
| Inheritance pattern of hemophilia | x-dominant, females carriers, males affected |
| Two types of hemophilia | A: factor VIII deficiency (classical) , B: IX deficiency (christmas) |
| Dx of hemophilia | nl INR, prolonged PTT, nl platelet, measure factor VIII and IX (one or the other) |
| Classifications of hemophilia | mild >5%: dx adulthood sometimes, moderate 1-5%, occasional spontaneous bleeding severe <1%: made in early childhood, percentages of factors in the blood |
| Signs of hemarthrosis | large, cant move joints, hurts a lot, warm, squishy |
| Complications of recurrent joint bleeds | pseudotumors, severe destruction of joints, deep soft tissue bleeds, psoas bleeds, cranial bleeds, nerve palsies d/t n. compression |
| Hemophilia tx | avoid drugs that impair platelet fxn, factor VIII or IX concentrations either plasma derived or recombinant |
| Types of factor replacement | demand vs. prophylactic, demand won’t prevent joint destruction, prophylaxis 3 times/week, VERY expensive but better than joint replacement later. 8yo and teach them to inject themselves |
| Pathological hemostasis | thrombosis |
| Virchow triad | intimal injury, stasis, hypercoagubility state |
| Common but weak RFs for clotting | factor V leiden, prothrombin gene mutation |
| Causes of bleeding disorders in general | combination of genetic factors, diseases, medications |
| Arterial and venous thrombosis | A: stroke, MI (more common) Veins: DVT and PE |
| What is a large RF for VTE | age 1/10,000 befor age 40, 1/100 over 75 yo |
| Mechanisms and RF’s for arterial and venous clots | A: underlying vascular dz, (smoking, DM, HTN, ↑ lipids, bad Fhx, and excess platelet activation V: stasis (slow flow), failure to regulate thrombin generation |
| Tx of Arterial and Venous clots | A: RF modification, anti-platelet drugs (aspirin), V: prophylaxis w/ “blood thinners” (heparin, warfarin) |
| Clots in arterial clots and venous clots | A: lots of platelets and some fibrin V: lots of fibrin some platelets |
| Inherited thrombophilic conditions are exclusively associated w/ | venous thromboembolism |
| Signs for phlebitis vs. DVT | phlebitis: focal, over muscles, tx w/ NSAID for inflammation, DVT: whole limb, under muscles, tx with thrombolytics or anticlotting |
| Causes of venous thromboembolism | genetic predisposition + acquired triggers causes thrombosis |
| Why is Fhx so crucial w/ clotting | only 50% blood tests show clotting tendencies, there are many causes we don’t know |
| What are 5 common genetic thrombophilia | factor V leiden, prothrombin, protein C and S deficiency, antithrombin –III deficiency |
| Strong RF’s for clotting | def of C, S, and AT-III: many mutations, uncommon, strong Fhx of clots |
| Weak RF’s for clotting | Factor V leiden, Prothrombin: single pt mutations, Very common, many asymptomatic carriers |
| Failure to control thrombin generation | Factor V leiden, prothrombin gene mutation, protein C and S deficiency |
| Impaired neutralization of thrombin | antithrombin-III deficiency |
| Mechanisms of Factor V leiden | keeps making clots, doesn’t respond to C or S to shut off the clotting cascade |
| Mechanism of prothrombin gene mutations + excess thrombin making | |
| Mechanism w/ protein C and S deficiency | can’t shut off factors VIII and IX so continues to clot |
| Acquired triggers for thrombosis | immobilization, surgery, trauma, pregnancy/postpartum, estrogens (OCPs, HRT) older |
| What ↑ risk for clots | factor V and oral contraceptive use, 35 times risk, pregnancy also get closer to their later pregnancies, |
| Dx VTE | s/s: pain swelling, tenderness, discoloration, warmth, asymmetry, dyspnea, CP, anxiety, cough, hemoptysis, sudden death, D-dimer, V/Q, compression US, CT scan, Venography pulmonary angiography |
| What does a + d-dimer mean | could be a clot, but could be cancer, infx, trauma, surg, preg, inflamation if -, no clot possible, will stay elevation 3-6 weeks |
| How does a compression dvt US work | w/o clot, vein will collapse, w/o, won’t compress |
| Who do we work up for thrombosis management | young <45 yo, recurrent, Fhx, clots w/ no provocation (surgery), unusual locations, 3 or more unexplained spontaneous abortions |
| Tx of asymptomatic carriers | prophlaxis at times of ↑ risk, avoid OCPs |
| Tx of first thrombotic event | std low MW heparin, warfarin for 6m, life long anticoag not indicated |
| Indication for indefinite anticoagulation | unprovoked event, recurrent, life thretning, factor V homozygote, combined thrombophilias, persistent anti-PL abs |
| RF modifications | no smoke, exercise/wt lose, control BP, cholesterol, DM |
| Anti-platelete medications | aspirin, clopidogrel, dipyriamole, aspirin/dipyridamole combo |
| What is fondaparinux | factor Xa inhibitor |
| Initial short term txs | heparin, low MW heparin, factor Xa inhibitor, direct thrombin inhibitors |
| Long-term of VTE | warfarin (Coumadin/jantoven) |
| Whats wrong w/ warfarin | narrow therapeutic window, high variable in dose-response, requires frequent monitoring, many drug intx, not a direct anticoag |
| Disadvantages to new oral anticoagulants | no antidote, no measuring area, renally excreted, LT SE’s?? |
| New oral anticoagulants | Dabigatran: not available in U.S. , Rivaroxaban |
| Tx of arterial and venous clots | prevent it from formt |
| Does aspirin prevent VTE | no, only some arterial effects |
| Effects of heparin and warfarin | prevent clot from growing, do not dissolve the clots directly |
Created by:
becker15
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