练习观察。

Sarah Gray
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From this I gleaned: Twenty years previously, age 33, Tracey had developed menopausal flushes. Her mother had been prematurely menopausal in her 30s. No other explanation was identified and she was treated successfully with cyclical HRT. Sixteen years before, age 37, Tracey had changed to continuous combined hormone replacement therapy (HRT) in the form of 2mg estradiol þ1mg norethisterone (Kliofem , NovoNordisk). This was also effective and she had no obvious flushes or other menopausal symptoms. Three years before, age 51, Tracey had begun intermittently to bleed vaginally. This was more like discoloured discharge than a period but varied from pink to brown and occasionally red. The GP notes indicated that when examined her vagina had looked atrophic. Tracey had been advised to reduce the Kliofem and with that alteration, the blood loss had increased rather than reduced. An ultrasound at the time had revealed a uniform and thin endometrium with no structural anomaly. A month later, a gynaecology out patient letter noted both the ultrasound result and that Tracey had an atrophic vagina. An endometrial biopsy had been taken and reported as scanty and atrophic. Tracey had been advised to use vaginal estradiol 25 mg tablets (Vagifem , NovoNordisk) for six weeks and to plan to reduce the Kliofem. She had continued to use the vaginal tablets twice a week ever since and also to use the 2mg combination daily as any attempt to reduce the HRT had resulted in an increase in bleeding. At about the same time, Tracey had presented with symptoms of feeling hot and unwell, almost flu-like. She had developed low abdominal pain that varied but could be severe and debilitating. At one stage, this was bad enough that she had collapsed and an ambulance was called. When reviewed by her GP her urine had been positive for blood and leucocytes and she was treated for urinary tract infection though no positive culture was obtained on that or any other occasion since. The urologists had been involved noting blood and leucocytes on dipstick testing and proposing a ‘semiresistant bug’. Flexible cystoscopy was reported as normal, renal ultrasound was unremarkable and despite negative cultures prophylactic antibiotics were advised. After two years, she continued regularly to have symptoms summarized as back ache, suprapubic pain, a flu-like feeling but no dysuria. Bladder washes weekly for six weeks were tried without marked improvement. Two years after the first attempt, a gynaecological review occurred in a postmenopausal bleeding (PMB) clinic. The discharge summary noted the absence of endometrium on ultrasound (no thickness measured) and that no endometrium was obtained on endometrial (Pipelle ) sampling. No management advice was offered. As bleeding persisted, a third gynaecology appointment was considered as mention had been made of fitting a levonorgestrel IUS. 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Sixteen years before, age 37, Tracey had changed to continuous combined hormone replacement therapy (HRT) in the form of 2mg estradiol þ1mg norethisterone (Kliofem , NovoNordisk). This was also effective and she had no obvious flushes or other menopausal symptoms. Three years before, age 51, Tracey had begun intermittently to bleed vaginally. This was more like discoloured discharge than a period but varied from pink to brown and occasionally red. The GP notes indicated that when examined her vagina had looked atrophic. Tracey had been advised to reduce the Kliofem and with that alteration, the blood loss had increased rather than reduced. An ultrasound at the time had revealed a uniform and thin endometrium with no structural anomaly. A month later, a gynaecology out patient letter noted both the ultrasound result and that Tracey had an atrophic vagina. An endometrial biopsy had been taken and reported as scanty and atrophic. Tracey had been advised to use vaginal estradiol 25 mg tablets (Vagifem , NovoNordisk) for six weeks and to plan to reduce the Kliofem. She had continued to use the vaginal tablets twice a week ever since and also to use the 2mg combination daily as any attempt to reduce the HRT had resulted in an increase in bleeding. At about the same time, Tracey had presented with symptoms of feeling hot and unwell, almost flu-like. She had developed low abdominal pain that varied but could be severe and debilitating. At one stage, this was bad enough that she had collapsed and an ambulance was called. When reviewed by her GP her urine had been positive for blood and leucocytes and she was treated for urinary tract infection though no positive culture was obtained on that or any other occasion since. The urologists had been involved noting blood and leucocytes on dipstick testing and proposing a ‘semiresistant bug’. Flexible cystoscopy was reported as normal, renal ultrasound was unremarkable and despite negative cultures prophylactic antibiotics were advised. After two years, she continued regularly to have symptoms summarized as back ache, suprapubic pain, a flu-like feeling but no dysuria. Bladder washes weekly for six weeks were tried without marked improvement. Two years after the first attempt, a gynaecological review occurred in a postmenopausal bleeding (PMB) clinic. The discharge summary noted the absence of endometrium on ultrasound (no thickness measured) and that no endometrium was obtained on endometrial (Pipelle ) sampling. No management advice was offered. As bleeding persisted, a third gynaecology appointment was considered as mention had been made of fitting a levonorgestrel IUS. Tracey had done her research and thinking there may be a link between her problems asked to come to the menopause clinic. Her GP agreed and provided me with information. 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Practice observed.
Increasing medical specialization has undoubtedly resulted in better outcomes for patients with defined conditions. The converse to this is the lack of a generalist opinion for the presentation that is less obvious. One of the functions of the menopause clinic is to stand back and look at the bigger picture: to make an experienced analysis of a multisystem presentation. We routinely integrate risks and benefits affecting different bodily systems and in this respect differ from most other specialities. Just under a year ago, I was asked by her general practitioner (GP) to think about Tracey who was 54. I was given selected hospital correspondence and results from the previous three years and Tracey had written reams about what had happened to her. I take the view that in such situations the more information the better. From this I gleaned: Twenty years previously, age 33, Tracey had developed menopausal flushes. Her mother had been prematurely menopausal in her 30s. No other explanation was identified and she was treated successfully with cyclical HRT. Sixteen years before, age 37, Tracey had changed to continuous combined hormone replacement therapy (HRT) in the form of 2mg estradiol þ1mg norethisterone (Kliofem , NovoNordisk). This was also effective and she had no obvious flushes or other menopausal symptoms. Three years before, age 51, Tracey had begun intermittently to bleed vaginally. This was more like discoloured discharge than a period but varied from pink to brown and occasionally red. The GP notes indicated that when examined her vagina had looked atrophic. Tracey had been advised to reduce the Kliofem and with that alteration, the blood loss had increased rather than reduced. An ultrasound at the time had revealed a uniform and thin endometrium with no structural anomaly. A month later, a gynaecology out patient letter noted both the ultrasound result and that Tracey had an atrophic vagina. An endometrial biopsy had been taken and reported as scanty and atrophic. Tracey had been advised to use vaginal estradiol 25 mg tablets (Vagifem , NovoNordisk) for six weeks and to plan to reduce the Kliofem. She had continued to use the vaginal tablets twice a week ever since and also to use the 2mg combination daily as any attempt to reduce the HRT had resulted in an increase in bleeding. At about the same time, Tracey had presented with symptoms of feeling hot and unwell, almost flu-like. She had developed low abdominal pain that varied but could be severe and debilitating. At one stage, this was bad enough that she had collapsed and an ambulance was called. When reviewed by her GP her urine had been positive for blood and leucocytes and she was treated for urinary tract infection though no positive culture was obtained on that or any other occasion since. The urologists had been involved noting blood and leucocytes on dipstick testing and proposing a ‘semiresistant bug’. Flexible cystoscopy was reported as normal, renal ultrasound was unremarkable and despite negative cultures prophylactic antibiotics were advised. After two years, she continued regularly to have symptoms summarized as back ache, suprapubic pain, a flu-like feeling but no dysuria. Bladder washes weekly for six weeks were tried without marked improvement. Two years after the first attempt, a gynaecological review occurred in a postmenopausal bleeding (PMB) clinic. The discharge summary noted the absence of endometrium on ultrasound (no thickness measured) and that no endometrium was obtained on endometrial (Pipelle ) sampling. No management advice was offered. As bleeding persisted, a third gynaecology appointment was considered as mention had been made of fitting a levonorgestrel IUS. Tracey had done her research and thinking there may be a link between her problems asked to come to the menopause clinic. Her GP agreed and provided me with information. At that point her treatment consisted of generic estradiol 2mgþ norethisterone 1mg with estradiol 25 mg vaginal tablets twice a week. She was using no complementary menopause therapies but emptied out a
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