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.

Actinic, or solar, keratosis is caused by chronic ultraviolet-induced damage to the epidermis. In the UK, 15-23% of individuals have actinic keratosis lesions. Risk factors include: advanced age; male gender; cumulative sun exposure or phototherapy; Fitzpatrick skin phototypes I-II; long-term immuno-suppression and genetic syndromes e.g. xeroderma pigmentosum and albinism. Actinic keratoses are regarded by some authorities as premalignant lesions that may transform into invasive squamous cell carcinoma (SCC) and by others as in situ SCC that may progress to an invasive stage. The risk of malignant change appears low; up to 0.5% per lesion per year. Up to 20-30% of lesions may spontaneously regress but in the absence of any reliable prognostic clinical indicators regarding malignant potential active treatment is considered appropriate. Actinic keratosis lesions may present as discrete hyperkeratotic papules, cutaneous horns, or more subtle flat lesions on sun-exposed areas of skin. The single most helpful diagnostic sign is an irregularly roughened surface texture: a sandpaper-like feel almost always indicates actinic damage. Dermatoscopy can be helpful in excluding signs of basal cell carcinoma when actinic keratosis is non-keratotic. It is always important to consider the possibility of SCC. The principal indication for referral to secondary care is the possibility of cutaneous malignancy. However, widespread and severe actinic damage in patients who are immunosuppressed is also a reason for referral.

Chronic hepatitis C (HCV) infection affects 0.8-1.0% of the UK population, with up to 70% having ongoing chronic infection. HCV is curable but if left untreated can progress to end stage liver disease and potentially hepatocellular carcinoma. HCV management options have changed dramatically over the past five years, with improvement in cure rates and tolerability; cure rates of more than 90% can now be achieved. The main risk factors for acquiring HCV infection in the UK are injecting drug use and sharing drug using equipment. Other risk factors include receipt of blood products in the UK before 1991; tattooing or acupuncture with non-sterile equipment; medical procedures; needlestick injuries and contact with blood from an infected person. Acute hepatitis C infection has mild symptoms only and is likely to go undiagnosed. The estimated diagnosis rate in England is 35%, suggesting that 65% of the total HCV-positive population remains undiagnosed. The most common method of detecting HCV is case finding in high- risk groups. Those who test positive for HCV antibodies should be tested for persisting viral presence through HCV PCR testing - a positive result confirms active infection. GPs can play a major role in identifying those at risk of the disease, which includes patients with known risk factors and those with unexplained abnormal liver function tests, providing information and arranging testing. Patients with confirmed active HCV infection should be referred to the local specialist hepatology or infectious disease service in accordance with locally agreed pathways.

Dermatophyte fungi are confined to the keratin layer of the epidermis and include three genera: Microsporum, Epidermophyton and Trichophyton. These infections can be transmitted by human contact (anthropophilic), from the soil (geophilic) and by animal (zoophilic) spread. Dermatophyte infections usually present as an erythematous, scaly eruption, which may or may not be itchy. Asymmetry is an important clinical clue to fungal infection, as is annular morphology. Examination under ultraviolet (Wood's light) can be helpful. The gold standard for diagnosing cutaneous fungal infections is microscopy and culture of scale, hair or nail, and a definite diagnosis is desirable before commencing treatment, especially with oral therapy. Any dermatophyte species affecting the body can affect the hands. The most common organism is T. rubrum. Tinea corporis infection affects the trunk mainly in children and adolescents, and all genera of dermatophyte can cause it. Tinea cruris infection involves the groin region and is more common in men than women. T. rubrum is the most common causative dermatophyte. The clinical features of tinea capitis include patchy hair loss with varying degrees of scale, erythema and pustules. Infected hairs tend to break at the base, leaving stubble. Occasionally, there is invasion of the visible epidermis, resulting in a boggy, painful swelling with associated alopecia and regional lymphadenopathy known as a kerion.

In around 85% of cases, multiple sclerosis (MS) starts with an acute neurological episode, a clinically isolated syndrome, which is considered to be the first clinical episode of relapsing-remitting MS (RRMS). It is characterised by the presence of acute relapses, after which there is normally good functional recovery. About 15-20 years after symptom onset, most patients develop secondary progressive MS, characterised by a gradual and irreversible neurological decline. MS affects women more frequently than men, with a ratio of 2-3:1. In RRMS the disease generally starts in the late 20s. Symptom onset in those with primary progressive MS occurs around the age of 40. Clinical relapses in RRMS reflect acute inflammation in the CNS, resulting in specific clinical syndromes including optic neuritis, myelitis, brainstem/cerebellum syndrome and supratentorial syndrome. In progressive MS, progression generally presents with gradual loss of power in the lower limbs, which may be asymmetric. It is often accompanied by sensory disturbances in the lower limbs, bladder and bowel symptoms. Investigations need to rule out conditions that can mimic an inflammatory-demyelinating disease of the CNS and determine the presence of dissemination in space and dissemination in time of the inflammatory-demyelinating disease. There is no confirmatory test for MS and it remains essentially a clinical diagnosis.