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.

Ischaemic stroke is rare in premenopausal women but risk increases with advancing age and doubles in the ten years following the menopause. Up to the age of 75 years men have a 25% higher risk of suffering a stroke compared with women. However, the increased life expectancy of women ultimately results in a higher overall incidence. Twice as many women die from stroke compare with breast cancer. Women with cerebrovascular disease are more likely to present with atypical symptoms than men. Altered mental status (including unresponsiveness, confusion and behavioural change) is the most common nonconventional symptom, and is reported by 23% of women compared with 15% of men. Other nonconventional symptoms reported more commonly by women include face or hemibody pain, lightheadedness and headache. Atrial fibrillation (AF) and hypertension, although less common than in men, are more potent risk factors for stroke in women. Compared with men with AF, women with AF are at increased risk of ischaemic stroke (6.2% versus 4.2% per year). This increased risk persists in anticoagulated patients with a relative risk ratio of 2.0. Pregnancy is a unique risk factor for stroke in women. The risk is highest in the third trimester and peripartum period. Women with hypertension in pregnancy, whether secondary to pre-existing disease, preeclampsia or eclampsia have a six-to nine-fold increased risk of stroke compared with normotensive women. Preeclampsia doubles the risk of stroke in later life. Gestational diabetes is also associated with higher risk of stroke extending beyond childbearing years.

Rheumatoid arthritis (RA) is a common, chronic systemic inflammatory disease of unclear aetiology leading to synovial hypertrophy and joint inflammation. It typically presents with symmetrical polyarthritis of small joints of the hands or feet, but can also involve larger joints, and have associated extra-articular manifestations. Diagnosis is based on duration of symptoms, joint distribution, level of inflammatory markers and autoantibodies i.e. rheumatoid factor(RhF) and anty-cyclic citrullinated peptide (CCP) antibodies. The presence of synovitis or effusion, either clinical or subclinical, seen on ultrasound or MRI, is essential for diagnosis. RA can sometimes present with a large joint monoarthritis or oligoarthritis. Although this is an atypical presentation, a diagnosis can be made in the presence of suggestive serology and/or histology. In cases presenting with monoarthritis, careful assessment for differential diagnoses is needed, particularly in the elderly population where other conditions such as gout, calcium pyrophosphate deposition disease and osteoarthritis are common. Early referral of patients with suspected synovitis via the rapid access early inflammatory arthritis clinic results in significant improvements in long-term outcomes. Hence it is important to consider early referral for individuals with synovitis, particularly if this is affecting small joints.

There has been a rapid rise in the number of people diagnosed with dementia in England from 232,000 in 2008 to 850,000 in 2014. Currently, it is estimated that the prevalence of mild cognitive impairment in adults aged 65 and over is 10-20%. It is likely that this figure will increase in line with trends in dementia diagnosis. In some cases, mild cognitive impairment may be a prodrome for dementia, and my be caused by any of the dementia pathology subtypes. The relationship between depression in the elderly and mild cognitive impairment is difficult to tease out as they are frequently comorbid conditions and both have been found to be independent risk factors for subsequent dementia: about 10% convert to dementia each year, compared with 1-2% of the general elderly population. It is important to obtain a history of cognitive changes over time, as well as information about the onset and nature of cognitive symptoms, confirmed by a reliable informant, if available. To confirm the diagnosis objective evidence of cognitive impairment is required. However, there are no specific neuropsychological tests for patients with mild cognitive impairment. On neuropsychological tests, individuals with mild cognitive impairment typically score 1-15 SD below the mean for their age and education, although these ranges are guidelines and not cut-off scores. GPs should consider referring people who signs of mild cognitive impairment for assessment by specialist memory assessment services to aid early identification of dementia, because more than 50% of people with mild cognitive impairment later develop dementia.

It is estimated that up to 80% of patients with Parkinson's disease will eventually develop cognitive impairment over the course of their illness. Even at the time of diagnosis, cognitive impairment has been reported in 20-25% of patients. Commonly affected cognitive domains are executive function, visuospatial ability and attention control. In addition, patients with Parkinson's disease dementia may present with deficits in language function and verbal memory. Psychosis may occur in approximately 40% of patients with Parkinson's disease, and is associated with an increased risk of developing cognitive impairment. Studies have shown that patients with Parkinson's disease with a history of visual hallucinations had an increased risk of developing dementia, four to eight years following diagnosis of the disease. Other clinical risk factors associated with cognitive decline in patients with Parkinson's disease include older age of onset, severe motor symptom burden and in particular akinetic-rigid subtype and olfactory dysfunction. Patients with Parkinson's disease who present with symptoms of cognitive decline, behavioural changes or psychotic symptoms should be referred for further investigation.

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.

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.

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.

In general practice palpitations are reported in around 8 per 1,000 persons per year. The differential diagnosis includes cardiac and psychiatric causes, as well as numerous others e.g. anaemia, hyperthyroidism, prescribed medication, caffeine and recreational drugs. Factors that point towards a cardiac aetiology are male sex, irregular heartbeat, history of heart disease, event duration > 5 minutes, frequent palpitations, and palpitations which occur at work or disturb sleep. Other clues suggesting a cardiac origin are abrupt onset and termination of palpitations, positional palpitations, and accompanying symptoms such as dizziness and presyncope. Cardiac arrhythmias are the result of enhanced automaticity, triggered activity or re-entry. The latter mechanism is responsible for the majority of clinically relevant arrhythmias, such as atrial fibrillation and supraventricular tachycardias. The prevalence of supraventricular tachycardia in the general population is around 2-3 per 1,000 persons. AV nodal re-entry tachycardia (AVNRT) is the most common paroxysmal supraventricular tachycardia, accounting for nearly two-thirds of all cases. The typical clinical presentation of AVNRT is a sudden onset of palpitations (98%) and/or dizziness (78%). Patients may present at any age and are more frequently female than male.

Androgens play a crucial role in bone, muscle and fat metabolism, erythropoiesis and cognitive health. In men aged 40-79 years the incidence of biochemical deficiency and symptomatic hypogonadism is 2.1-5.7%. Decreased libido or reduced frequency and quality of erections, fatigue, irritability, infertility or a diminished feeling of wellbeing may be presenting complaints. However, a significant proportion of men with androgen deficiency will be identified when they present for unrelated concerns. Important factors to elicit from the history in addition to the presenting complaint include: a medical history of obesity, type 2 diabetes, systemic diseases or metabolic syndrome which all impact on testosterone physiology. A comprehensive medical review will identify agents which can cause low testosterone levels such as statins, steroids, opioids, dopamine antagonists and 5-alpha reductase inhibitors. Alcohol, anabolic steroids and illicit substance use such as marihuana can impact on testosterone levels and non-prescribed drug use should be routinely discussed. The mainstay of treatment in persisting androgen deficiency is to restore normal physiological levels of testosterone by using exogenous testosterone. It may take at least three to six weeks to notice any clinical improvement in symptoms. Men receiving testosterone supplementation should be followed closely and have their testosterone, haematocrit and PSA levels checked at three, six and twelve months after initiation of testosterone replacement therapy. Men should then be reviewed at least annually thereafter.