การเปลี่ยนคีย์ ( Key ) หมายถึง การเปลี่ยนลำดับเสียงในการขับร้อง ให้เป็นไปตามบันใดเสียงต่างๆที่กำหนดไว้อาจเป็นสูงหรือต่ำ
แล้วแต่ความเหมาะสม ของระดับเสียงของผู้ขับร้อง
บันใดเสียงที่ใช้เป็นหลักในการไล่เสียงได้แก ่บันใดเสียงเมเจอร์ (Major Scale)
มีทั้งหมด 15 คีย์ดังนี้
1. Key C Major ไม่ติด ชาร์ป ติด แฟลต
2. Key F Major ติด 1 แฟลต คือ Bb
3. Key Bb Major ติด 2 แฟลต คือ Bb, Eb
4. Key Eb Major ติด 3 แฟลต คือ Bb, Eb, Ab
5. Key Ab Major ติด 4 แฟลต คือ Bb, Eb, Ab, Db
6. Key Db Major ติด 5 แฟลต คือ Bb, Eb, Ab, Db, Gb
7. Key Gb Major ติด 6 แฟลต คือ Bb, Eb, Ab, Db, Gb, Cb
8. Key Cb Major ติด 7 แฟลต คือ Bb, Eb, Ab, Db, Gb, Cb, Fb
9. Key G Major ติด 1 ชาร์ป คือ F#
10. Key D Major ติด 2 ชาร์ป คือ F#, C#
11. Key A Major ติด 3 ชาร์ป คือ F#, C#, G#
12. Key E Major ติด 4 ชาร์ป คือ F#, C# , G#, D#
13. Key B Major ติด 5 ชาร์ป คือ F#, C#, G#, D#, A#
14. Key F# Major ติด 6 ชาร์ป คือ F#, C# , G#, D#, A#, E#
15. Key C# Major ติด 7 ชาร์ป คือ F#, C#, G#, D#, A#, E#, B#
**(ข้อควรนำไปใช้) คีย์ที่ติด ชาร็ป-แฟลต มากๆ จะไม่นิยมนำมาใช้เพราะการอ่านและการบรรเลงจะยาก ทำให้เกิดความผิดพลาดได้ง่าย
วันศุกร์ที่ 13 พฤษภาคม พ.ศ. 2554
วันพุธที่ 11 พฤษภาคม พ.ศ. 2554
วันพฤหัสบดีที่ 5 พฤษภาคม พ.ศ. 2554
ANTI PHOSPHOLIPID SYNDROME
APS was the most likely diagnosis in this patient. APS may be associated with extensive arterial and/or venous thromboembolic disease, which did manifest in this case. Recurrent pulmonary thromboembolism can result in pulmonary hypertension, which is the most likely cause of this patient's progressive dyspnea. APS is known to be associated with thrombocytopenia, as was evident in this case. Recurrent miscarriages, which are thought to be secondary to derangements in clotting, can also be a component of this disease. Other diagnoses were considered but ultimately excluded. The patient was not febrile, had multiple negative blood cultures, and had no stigmata of endocarditis. TTP is characterized by microangiopathic hemolytic anemia, thrombocytopenia, fever, neurologic manifestations, and renal dysfunction. It is a fatal, progressive disease without treatment. The course of illness in this case did not fit that of TTP, and her anemia was not microangiopathic in nature. APS was confirmed by an immunologic profile that revealed the anticardiolipin immunoglobulin G (aCL IgG) was 65 GPLU/mL (normal range, up to 23 GPLU/mL) with a negative aCL IgM. Lupus anticoagulant (LA) was 180 seconds (normal range, 33-45 seconds). An antinuclear antibody test was positive, while an anti-double stranded DNA test was negative. The elevation of aCL IgG persisted after 6 weeks.
The actual frequency of APS in the general population is unknown. Antiphospholipid antibodies (LA and aCL antibodies) are present in 1%-5% of the general population, and in about 50% of patients with systemic lupus erythematosus (SLE) and other autoimmune diseases.[1] There are 2 forms of APS. Primary APS involves thrombosis and/or obstetric complications in association with antiphospholipid antibodies, but without signs of connective tissue disease; secondary APS refers to those with SLE who also have antiphospholipid antibodies. Antiphospholipid antibodies may develop in patients receiving drugs such as phenytoin, chlorpromazine, dilantin, quinidine, procainamide, and some antibiotics. A miscellaneous group of patients with a variety of diseases, including malignancy, HIV, and other viral infections, may also be positive for antiphospholipid antibodies, although these patients are not at risk for thrombotic complications. There appears to be to be a correlation between the strength of the antiphospholipid (aPL) titer and the number of positive aPL serology tests; these tests include IgG and IgM antiphospholipid antibodies; LA, which manifests as a prolongation of the partial thromboplastin time that can be reversed with phospholipid neutralization; and anti-B2 glycoprotein (GP). A female predominance has been documented, particularly for secondary APS. This parallels the association of APS with SLE and other connective-tissue diseases, which also have a female predominance. APS is more common in young to middle-aged adults; however, it also manifests in children and elderly people. Disease onset has been reported in children as young as 8 months.[2]
Very recently, the discovery of shared peptide sequences between B2-GPI and some microorganisms, particularly Saccharomyces cerevisiae, has led to the hypothesis that at least some cases of APS may not be of primary autoimmune origin but instead may be molecular mimicry. B2-GPI also has complex interactions with the coagulation system that are poorly understood at present.[3]
APS can affect any system of the body, and the clinical picture may demonstrate many different sequelae of thromboembolic disease involving the peripheral venous system (deep venous thrombosis) and central nervous system (cerebrovascular accident, sinus thrombosis). Hematologic (thrombocytopenia, hemolytic anemia), pulmonary (pulmonary embolism, pulmonary hypertension), and dermatologic (digital cyanosis and gangrene, livedo reticularis, discoid rash and chronic ulcers) complications are common. Photosensitivity and cardiac (Libman-Sacks valvulopathy, myocardial ischemia), ocular (amaurosis, retinal thrombosis), adrenal (infarction/hemorrhage), and musculoskeletal (avascular necrosis of bone) manifestations may also occur.[4]
APS and LA are associated with pregnancy complications that include fetal loss, fetal growth restriction, preeclampsia, thrombosis, and autoimmune thrombocytopenia, and it is distinct from SLE and other connective tissue disorders.
The updated Sapporo APS classification criteria are commonly used for APS diagnosis. Based on these criteria, a diagnosis of APS requires both (1) thrombosis in any organ or tissue or pregnancy event (1 or more miscarriages after the 10th week of gestation, 3 or more miscarriages before the 10th week of gestation, or 1 or more premature deliveries before the 34th week of gestation because of eclampsia) and (2) a persistently positive aPL test (> 12 weeks apart in time), positive LA test, moderate-to-high titer anticardiolipin antibodies, or moderate-to-high titer B2-GPI antibodies.[5] There is debate whether or not testing for aPL can be undertaken in patients receiving anticoagulation, either from heparin or warfarin. Although false positive tests are common in some series (up to 10%), titers are usually quite low and do not persist.
An abnormal LA is the laboratory test result that confers the strongest risk for thrombosis. The postulated biologic effects mediated by human antiphospholipid antibodies include (1) reactivity with endothelial structures, which disturbs the balance of prostaglandin E2/thromboxane production, (2) interaction with platelet prostaglandins, with consequent upregulation of platelet aggregation, (3) dysregulation of complement activation, (4) interaction of aPL with phosphatidylserine exposed during trophoblast syncytium formation, which raises the possibility of a more direct effect of these autoantibodies on placental structures,[6] and (5) autoantibodies against the fibrinolytic receptor annexin 2.[7]
Rarely, patients with APS may present with acute multiorgan involvement, including signs and symptoms of encephalopathy, seizures, livedo reticularis, renal insufficiency, pulmonary failure, and multiple thrombi involving both large and small vessel occlusions. The term "catastrophic APS" and "Asherson syndrome" has been applied to this constellation, which is associated with high-titered antiphospholipid antibodies and a high mortality rate (approximately 50%).[8]
The international consensus statement is commonly used for establishing a diagnosis of catastrophic APS (CAPS). Based on this statement, a definite CAPS diagnosis requires (1) vascular thrombosis in 3 or more organs or tissues, (2) the development of manifestations simultaneously or in less than a week, (3) evidence of small vessel thrombosis in at least 1 organ or tissue, and (4) laboratory confirmation of the presence of aPL.[9]
The differential diagnosis of APS includes disseminated intravascular coagulation, infective endocarditis, TTP, heparin-induced thrombocytopenia, and inherited or acquired hypercoagulable states.
Appropriate procedures to evaluate specific thrombotic events differ according to the clinical situation and the vascular location involved. These include CT scanning or MRI of the brain (for the identification and characterization of cerebrovascular accident), CT angiography of the chest (pulmonary embolism), and CT scanning of the abdomen with contrast to identify thromboembolic disease in the intestinal or hepatic circulation (Budd-Chiari syndrome). Doppler ultrasound studies are recommended for detecting deep vein thrombosis. Two-dimensional echocardiography findings may demonstrate asymptomatic valve thickening, vegetations, or valvular insufficiency; aortic or mitral insufficiency is the most common valvular defect found in persons with Libman-Sacks endocarditis.
Treatment for APS depends largely on the clinical scenario and the severity of disease. Patients with active thrombotic disease should be on appropriate anticoagulation with an international normalized ratio (INR) goal of 2-3 if warfarin anticoagulation is used. Hydroxychloroquine has been shown in several studies to have intrinsic antithrombotic effects and may be considered in patients who have had a history of clot. Aspirin is added to most treatment regimens although evidence supporting its use is meager. Similarly, clopidogrel has been used in place of and in addition to aspirin.
The patient in this case started corticosteroid therapy at a dose of 40 mg/day aiming to elevate her platelet count before beginning anticoagulation. At a platelet count of 50,000/μL, anticoagulation therapy was started in the form of low-molecular-weight heparin (LMWH), and warfarin was added 5 days later. LMWH was discontinued when her INR was 3.0. Low-dose aspirin was added. Nifedipine was added at a dose of 80 mg/day and there was gradual improvement in the patient's dyspnea. A low-dose thiazide diuretic was also added, and the patient continues to be followed at monthly follow-up appointments.
The actual frequency of APS in the general population is unknown. Antiphospholipid antibodies (LA and aCL antibodies) are present in 1%-5% of the general population, and in about 50% of patients with systemic lupus erythematosus (SLE) and other autoimmune diseases.[1] There are 2 forms of APS. Primary APS involves thrombosis and/or obstetric complications in association with antiphospholipid antibodies, but without signs of connective tissue disease; secondary APS refers to those with SLE who also have antiphospholipid antibodies. Antiphospholipid antibodies may develop in patients receiving drugs such as phenytoin, chlorpromazine, dilantin, quinidine, procainamide, and some antibiotics. A miscellaneous group of patients with a variety of diseases, including malignancy, HIV, and other viral infections, may also be positive for antiphospholipid antibodies, although these patients are not at risk for thrombotic complications. There appears to be to be a correlation between the strength of the antiphospholipid (aPL) titer and the number of positive aPL serology tests; these tests include IgG and IgM antiphospholipid antibodies; LA, which manifests as a prolongation of the partial thromboplastin time that can be reversed with phospholipid neutralization; and anti-B2 glycoprotein (GP). A female predominance has been documented, particularly for secondary APS. This parallels the association of APS with SLE and other connective-tissue diseases, which also have a female predominance. APS is more common in young to middle-aged adults; however, it also manifests in children and elderly people. Disease onset has been reported in children as young as 8 months.[2]
Very recently, the discovery of shared peptide sequences between B2-GPI and some microorganisms, particularly Saccharomyces cerevisiae, has led to the hypothesis that at least some cases of APS may not be of primary autoimmune origin but instead may be molecular mimicry. B2-GPI also has complex interactions with the coagulation system that are poorly understood at present.[3]
APS can affect any system of the body, and the clinical picture may demonstrate many different sequelae of thromboembolic disease involving the peripheral venous system (deep venous thrombosis) and central nervous system (cerebrovascular accident, sinus thrombosis). Hematologic (thrombocytopenia, hemolytic anemia), pulmonary (pulmonary embolism, pulmonary hypertension), and dermatologic (digital cyanosis and gangrene, livedo reticularis, discoid rash and chronic ulcers) complications are common. Photosensitivity and cardiac (Libman-Sacks valvulopathy, myocardial ischemia), ocular (amaurosis, retinal thrombosis), adrenal (infarction/hemorrhage), and musculoskeletal (avascular necrosis of bone) manifestations may also occur.[4]
APS and LA are associated with pregnancy complications that include fetal loss, fetal growth restriction, preeclampsia, thrombosis, and autoimmune thrombocytopenia, and it is distinct from SLE and other connective tissue disorders.
The updated Sapporo APS classification criteria are commonly used for APS diagnosis. Based on these criteria, a diagnosis of APS requires both (1) thrombosis in any organ or tissue or pregnancy event (1 or more miscarriages after the 10th week of gestation, 3 or more miscarriages before the 10th week of gestation, or 1 or more premature deliveries before the 34th week of gestation because of eclampsia) and (2) a persistently positive aPL test (> 12 weeks apart in time), positive LA test, moderate-to-high titer anticardiolipin antibodies, or moderate-to-high titer B2-GPI antibodies.[5] There is debate whether or not testing for aPL can be undertaken in patients receiving anticoagulation, either from heparin or warfarin. Although false positive tests are common in some series (up to 10%), titers are usually quite low and do not persist.
An abnormal LA is the laboratory test result that confers the strongest risk for thrombosis. The postulated biologic effects mediated by human antiphospholipid antibodies include (1) reactivity with endothelial structures, which disturbs the balance of prostaglandin E2/thromboxane production, (2) interaction with platelet prostaglandins, with consequent upregulation of platelet aggregation, (3) dysregulation of complement activation, (4) interaction of aPL with phosphatidylserine exposed during trophoblast syncytium formation, which raises the possibility of a more direct effect of these autoantibodies on placental structures,[6] and (5) autoantibodies against the fibrinolytic receptor annexin 2.[7]
Rarely, patients with APS may present with acute multiorgan involvement, including signs and symptoms of encephalopathy, seizures, livedo reticularis, renal insufficiency, pulmonary failure, and multiple thrombi involving both large and small vessel occlusions. The term "catastrophic APS" and "Asherson syndrome" has been applied to this constellation, which is associated with high-titered antiphospholipid antibodies and a high mortality rate (approximately 50%).[8]
The international consensus statement is commonly used for establishing a diagnosis of catastrophic APS (CAPS). Based on this statement, a definite CAPS diagnosis requires (1) vascular thrombosis in 3 or more organs or tissues, (2) the development of manifestations simultaneously or in less than a week, (3) evidence of small vessel thrombosis in at least 1 organ or tissue, and (4) laboratory confirmation of the presence of aPL.[9]
The differential diagnosis of APS includes disseminated intravascular coagulation, infective endocarditis, TTP, heparin-induced thrombocytopenia, and inherited or acquired hypercoagulable states.
Appropriate procedures to evaluate specific thrombotic events differ according to the clinical situation and the vascular location involved. These include CT scanning or MRI of the brain (for the identification and characterization of cerebrovascular accident), CT angiography of the chest (pulmonary embolism), and CT scanning of the abdomen with contrast to identify thromboembolic disease in the intestinal or hepatic circulation (Budd-Chiari syndrome). Doppler ultrasound studies are recommended for detecting deep vein thrombosis. Two-dimensional echocardiography findings may demonstrate asymptomatic valve thickening, vegetations, or valvular insufficiency; aortic or mitral insufficiency is the most common valvular defect found in persons with Libman-Sacks endocarditis.
Treatment for APS depends largely on the clinical scenario and the severity of disease. Patients with active thrombotic disease should be on appropriate anticoagulation with an international normalized ratio (INR) goal of 2-3 if warfarin anticoagulation is used. Hydroxychloroquine has been shown in several studies to have intrinsic antithrombotic effects and may be considered in patients who have had a history of clot. Aspirin is added to most treatment regimens although evidence supporting its use is meager. Similarly, clopidogrel has been used in place of and in addition to aspirin.
The patient in this case started corticosteroid therapy at a dose of 40 mg/day aiming to elevate her platelet count before beginning anticoagulation. At a platelet count of 50,000/μL, anticoagulation therapy was started in the form of low-molecular-weight heparin (LMWH), and warfarin was added 5 days later. LMWH was discontinued when her INR was 3.0. Low-dose aspirin was added. Nifedipine was added at a dose of 80 mg/day and there was gradual improvement in the patient's dyspnea. A low-dose thiazide diuretic was also added, and the patient continues to be followed at monthly follow-up appointments.
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