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Diabetic neuropathy is thought to affect 1.9% of the world’s population and 50% of patients with a diagnosis of diabetes mellitus which would equate to 2.25 million people in the UK. The term diabetic neuropathy includes multiple distinct clinical entities that have been classified under the broad headings of focal and multifocal neuropathies and symmetrical neuropathies. Peripheral diabetic neuropathy, a chronic distal symmetrical predominantly sensory neuropathy, is the most common form of diabetic neuropathy. Most patients describe moderate to severe pain, using neuropathic descriptors such as burning, shooting or electric shocks. The common presentation is of painful symptoms originating in the feet, that then spread to the knees before involving the distal portion of the upper limbs in a ‘glove and stocking’ distribution. There are number of specific neuropathic pain assessment tools that can be readily used in a non-specialist setting in the community, such as the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) questionnaire. This combines five simple questions and two examination findings to give a dimensionless score for the pain out of 24, with a score ≥ 12 suggesting a neuropathic component is likely.

Fibroids are benign, hormone-dependent tumours of uterine smooth muscle and connective tissue. They are commonly asymptomatic, but can cause symptoms such as heavy menstrual bleeding and pelvic pressure symptoms. Between 20 to 30% of women with heavy menstrual bleeding have fibroids. Fibroids are most prevalent in women aged 30-50 years and there may be a genetic predisposition. They are more common in black women than white women. Other risk factors include obesity and nulliparity. Asymptomatic women should only be referred if their uterus is palpable abdominally, if fibroids distort the uterine cavity or the uterus is larger than 12 cm in length. Symptomatic women should be referred when heavy menstrual bleeding has not responded to medical treatment, if large fibroids are causing pressure symptoms or when fibroids are associated with fertility or obstetric problems. Malignant change (leiomyosarcoma) is rare in premenopausal women. Fast track referral is indicated for women with rapid onset and progressive symptoms or rapidly enlarging fibroids, as these symptoms are suspicious of leiomyosarcoma; postmenopausal women presenting with enlarging fibroids or vaginal bleeding; and women with fibroids with any other features of cancer e.g. abnormal bleeding or weight loss.

Acute pyelonephritis is suggested by the constellation of fever (temperature ≥ 38.5° C), flank pain (typically unilateral), nausea and vomiting, and costovertebral angle tenderness. Complaints typical of lower UTI are variably present. The severity of symptoms ranges from a mild pyrexial illness to life-threatening sepsis. The diagnosis of acute pyelonephritis should be suspected on the basis of the history and clinical examination. If the urine dipstick is negative for nitrites and leukocyte esterase this does not exclude the diagnosis, but it should prompt a re-evaluation of the clinical features and consideration of other potential diagnoses. Antibiotic therapy should be initiated without delay; this can be modified subsequently depending on the culture result. Antibiotics that are typically effective in lower urinary tract infections are frequently inadequate in acute pyelonephritis, and more prolonged therapy is necessary. Review of the clinical course and urine culture results is necessary to ensure that the patient is improving. Patients who have not improved within two days of commencing antimicrobial treatment should be referred to secondary care unless the infecting pathogen is not susceptible to the agent originally used, an alternative appropriate antibiotic is available, and the patient remains well enough for community care.

Nephrotic syndrome is defined by a triad of clinical features: oedema, substantial proteinuria (> 3.5 g/24 hours) and hypoalbuminaemia (< 30 g/L). It is often associated with hyperlipidaemia, thromboembolism and an increased risk of infection. Nephrotic syndrome develops following pathological injury to renal glomeruli. This may be a primary problem, with a disease specific to the kidneys, or secondary to a systemic disorder such as diabetes mellitus. The most common cause in children is minimal change glomerulonephritis. In white adults, nephrotic syndrome is most frequently due to membranous nephropathy whereas in populations of African ancestry the most common cause of nephrotic syndrome is focal segmental glomerulosclerosis. Diabetic nephropathy is the most common multisystem disease that can cause nephrotic syndrome. Patients typically present with periorbital oedema (most noticeable in the morning) or dependent pitting oedema (more common later in the day). Proteinuria should be documented by a quantitative measurement e.g. urine protein: creatinine ratio (PCR) or albumin: creatinine ratio (ACR). PCR > 300-350 mg/mmol indicates nephrotic range proteinuria. Urgent referral to a nephrologist (ideally within 2 weeks) is necessary and a renal biopsy is usually performed. This will establish what form of glomerular disease is responsible. Additional tests may be undertaken to assess if nephrotic syndrome is secondary to another disorder e.g. systemic lupus erythematosus or amyloidosis.

ECG interpretation is an essential skill in the management of the acutely unwell patient and in addition to history taking and physical examination has been shown to have a significant effect on referral patterns to cardiologists. One of the basic initial steps in ECG interpretation is assessment for the presence of artefact which if present can dramatically influence the diagnosis. The most common sources of artefact are tremor e.g. in Parkinson’s disease, loose skin electrodes and electromagnetic interference from other medical devices and mobile phones. The Medicines and Healthcare products Regulatory Agency in the UK advises that mobile phones should be kept at least one metre away from equipment that is sensitive to electromagnetic interference. The possibility that artefact is the cause of the ECG appearance should always be considered if bizarre ECG changes are present particularly in an asymptomatic patient. The ECG should always be interpreted in the context of the patient’s condition. If artefact is thought to be the cause of the ECG appearance, then any contributory factors present should be corrected and the ECG should be repeated before invasive investigations are undertaken or treatment is administered.

Depression and dementia are both common conditions in older people, and they frequently occur together. Late life depression affects about 3.0-4.5% of adults aged 65 and older. Depression occurs in up to 20% of patients with Alzheimer’s disease and up to 45% of patients with vascular dementia. Rather than a risk factor, depression with onset in later life is more likely to be either prodromal to dementia or a condition that unmasks pre-existing cognitive impairment by compromising cognitive reserve. Depression can be a psychological response to receiving a diagnosis of dementia. The distinction between depression and early dementia may be particularly difficult. Detailed histories obtained from patients and their relatives as well as longitudinal follow-up are important. Cognitive testing can be very helpful. It is preferable to use a neuropsychological test that is sensitive to subtle cognitive changes and assesses all cognitive domains, such as the Montreal Cognitive Assessment. Older people with depression are at raised risk of dementia and this risk is increased if they have had symptoms for a long time, if their symptoms are severe, where there are multiple (vascular) comorbidities, and where there are structural brain changes including hippocampal atrophy and white matter abnormalities.

The greatest proportional increase in the number of people with diabetes by age group is predicted to occur in those aged 60 to 79. In older people living with diabetes, geriatric syndromes, which indicate frailty, are emerging as a third category of complications in addition to the traditional microvascular and macrovascular sequelae. Frailty is defined by the presence of three or more phenotypes (weight loss, weakness, decreased physical activity, exhaustion and slow gait speed). The presence of one or two phenotypes describes a pre-frail state, and the absence of phenotypes describes a non-frail person. Sarcopenia, or loss of muscle mass, is the muscular manifestation of frailty phenotype and is defined as a generalised loss of skeletal muscle mass and strength that leads to low physical performance. Persistent hyperglycaemia has been shown to be associated with poor muscle quality, performance and strength independent of age, race, sex, weight, height and physical activity. The coexistence of dementia and diabetes also increases the risk of frailty. There is evidence that midlife behaviours such as smoking, alcohol consumption, poor diet and low levels of physical activity are associated with frailty and dementia in later life. Frailty is a dynamic condition which can worsen or improve over time. Patients may progress from a non-frail to pre-frail or frail state. With timely intervention, there is a greater chance for an individual to recover from pre-frail to non-frail than to deteriorate into frailty. The progression of frailty is likely to be multifactorial, therefore multimodal intervention, including maintenance of adequate nutrition, physical exercise, and glycaemic control, may help to delay or prevent the development of frailty and to improve outcomes.

More than 200 hereditary cancer susceptibility syndromes have been described, and it is thought that they account for 5-10% of all cancers. Many have dermatological manifestations (usually lesions, occasionally rashes) which frequently precede other systemic pathology. Dermatological signs are usually non-specific and often trivial in appearance, making their significance easy to overlook and a clinical diagnosis challenging. Histological examination is often required to differentiate lesions. They are usually benign and pathologically unrelated to the primary tumours, with the exception of the atypical moles of the dysplastic naevus syndrome, and may present simply as a cosmetic problem for the patient. However, a number of cancer syndromes exhibit an increased risk of developing malignant skin lesions. For instance, Gorlin syndrome (nevoid basal cell carcinoma syndrome) which typically results in the development of multiple basal cell carcinomas, within the first few decades of life. The majority of cancer syndromes with skin signs are inherited in an autosomal dominant pattern demonstrating complete penetrance before the age of 70. Once a cancer syndrome has been diagnosed, the cornerstone of management is frequent surveillance for the early detection and treatment of malignancy. Genetic testing and counselling should be offered to family members.