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Hemostasis and Throm

Clinical Medicine II

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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