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A 2000-VA 230/115-V transformer has been tested to determine its equivalent circuit The results of the tests are shown below Open-circuit test Short-circuit test VOC = 230 V VSC = 132 V IOC = 045 A ISC = 60 A POC = 30 W PSC = 201 W All data given were taken from the primary side of the transformer (a) Find the equivalent circuit of this transformer referred to the low-voltage side of the transformer (b) Find the transformer s voltage regulation at rated conditions and (1) 08 PF lagging, (2) 10 PF, (3) 08 PF leading (c) Determine the transformer s efficiency at rated conditions and 08 PF lagging SOLUTION (a) OPEN CIRCUIT TEST:



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This is a rare autosomal recessive intrinsic platelet disorder causing bleeding Platelets are unable to aggregate because of lack of receptors (containing glycoproteins IIb and IIIa) for fibrinogen, which form the bridges between platelets during

Factor VIII Antigen or N or N or N 0 or N N Ristocetin Cofactor Activity or N 0 or N 0 or N N Factor VIII Coagulant Activity or N or N or N 0 N Abn Abn Abn N





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aggregation Clinically, it is manifested chiefly as mucosal (epistaxis, gingival bleeding, menorrhagia) and postoperative bleeding The defect is of variable severity but may be severe Platelet numbers and morphology are normal, but the bleeding time is markedly prolonged Platelets fail to aggregate in response to typical agonists (ADP, collagen, thrombin) but aggregate normally in response to ristocetin, which causes platelet clumping by a separate mechanism Patients are treated with platelet transfusions when necessary Platelet transfusion therapy is limited by the tendency of these patients to develop multiple alloantibodies

proportionate to the degree of renal insufficiency Bleeding is most commonly mucosal and gastrointestinal and may occasionally be severe Dialysis is effective in reducing the bleeding tendency but may not completely eliminate it Patients respond to DDAVP, 03 mcg/kg every 24 hours

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All the myeloproliferative disorders can produce abnormalities in platelet function A number of biochemical abnormalities are present in these platelets, but the cause of the bleeding tendency is unclear The severity of the bleeding tendency correlates roughly with the height of the platelet count, although conditions causing reactive thrombocytosis of normal platelets are not associated with abnormal function Bleeding decreases when the platelet count is controlled with myelosuppressive therapy In cases of life-threatening bleeding with high platelet counts, plateletpheresis may be necessary

Figure 14-35

This is a rare autosomal recessive intrinsic platelet disorder causing bleeding Platelets cannot adhere to subendothelium because they lack receptors (composed of glycoprotein Ib) for von Willebrand factor, which mediates platelet adhesion This is often a severe bleeding disorder with mucosal and postoperative bleeding Thrombocytopenia may be present, and platelets on smear are abnormally large The bleeding time is markedly prolonged Platelet aggregation is normal in response to standard agonists (collagen, ADP, thrombin), but platelets fail to aggregate in response to ristocetin Measurements of von Willebrand factor in the plasma are normal Patients are treated with platelet transfusion when necessary

045 A = 0001957 S 230 V P 30 W = cos 1 OC = cos 1 = 7315 (230 V )(045 A ) VOC I OC YEX = GC jBM = 0001957 7315 S = 0000567-j 0001873 S 1 = 1763 RC = GC 1 = 534 XM = BM YEX = GC jBM =

Aspirin causes a mild bleeding tendency by irreversibly acetylating cyclooxygenase, an enzyme that participates in platelet aggregation The effect lasts for the life of the platelet and may be manifest for 7 10 days, although the major effect lasts 3 5 days The effect is not dose dependent, and 65 mg of aspirin is sufficient Aspirin by itself does not cause significant bleeding, but it may unmask bleeding disorders such as mild von Willebrand s disease or mild thrombocytopenia Certain antibiotics (ticarcillin, some cephalosporins) cause a mild bleeding tendency, presumably by coating the surface of platelets Nonsteroidal anti-inflammatory drugs cause an aspirin-like effect that disappears when the drug leaves the system Patients with autoantibodies against platelets may have prolonged bleeding times even in the absence of thrombocytopenia Platelet-associated IgG levels should be high, and the bleeding tendency responds quickly to modest doses of prednisone, eg, 20 mg/d Acquired storage pool disease refers to the circulation of exhausted platelets that have been stimulated to release their granule contents and hence are no longer functional Such granule release occurs in response to cardiopulmonary bypass and severe vasculitis

Noris M et al Uremic bleeding: closing the circle after 30 years of controversies Blood 1999 Oct 15;94(8):2569 74 [PMID: 10515859]

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