Add caption Background Inflammation of the brain. Causes Viral (50% of cases): Commonest (in order): herpes simplex (HSV1 > HSV2), VZV, EBV. Others: CMV, HIV seroconversion, measles, mumps, arboviruses (West-Nile, Japanese, tick-borne, St Louis), rabies. Autoimmune (20% of cases): Often affects the medial temporal lobes, when it is known as 'limbic encephalitis'. Often paraneoplastic. Antibodies (and associations): anti-Hu (small cell lung cancer), anti-Ma2 (germ cell tumour of testes), anti-NMDAR (50% have ovarian tumour), anti-LGI1 (formerly 'anti voltage-gated potassium channel'; only 20% have cancer). Other causes: Idiopathic (30% of cases). Any bacterial meningitis can become a meningoencephalitis. Spirochetes:  Listeria , Lyme, syphilis. TB Protozoa: malaria,  Toxoplasma . Fungal:  Aspergillus ,  Cryptococcus . Epidemiology Annual incidence: 1/20,000. Commonest under 1 years old or over 65. Signs and symptoms Initially non-specific: fever, headache, nausea, v

Background Definition and classification Inflammation of the glomeruli. This page discusses primary glomerulonephritides, but glomerular disease can also be secondary to diabetes and multi-system autoimmune or infiltrative diseases. Can be classified by whether they typically present with nephrotic syndrome – minimal change disease, membranous GN, membranoproliferative GN, FSGS – or haematuria/nephritic syndrome – IgA nephropathy, post-streptococcal GN, rapidly progressive GN. However, presentation is often non-specific and asymptomatic. Presentation Can be an incidental finding in an asymptomatic individual e.g. with hypertension, proteinuria or haematuria on dipstick, abnormal renal function test, anaemia. Symptomatic presentations include oedema (nephrotic syndrome), frank haematuria, or generally unwell (uraemia, anaemia). Management See  chronic kidney disease (CKD)  and/or  acute kidney injury (AKI)  for general management of renal impairment. BP control (SBP <130) and ACEi/AR

Investigations A complete developmental history and examination is important: not just social/emotional, but also speech, hearing, or cognitive problems, which can also cause behavioural problems. Learn the ABC of the problems: A ntecedents B ehaviour C onsequence Separation anxiety Anxiety about separation from main caregiver. Part of normal development from 6-8 months. By 2 years it usually reduces as they can extend attachment to others, and by school age they can normally tolerate hours away from parents. Its persistence or re-emergence beyond this time may be pathological, and known as separation anxiety disorder. Temper tantrums Common when kids reach an age where they have to comply with demands. School refusal Definition Inability to attend school due to overwhelming anxiety, which can be either parental separation anxiety, school phobia, or both. The anxiety is disproportionate i.e. not explained by rational fear of bullying or learning problems. Signs and symptoms Anxiety Hyp

Definition ↓Growth in infancy, falling across 2 centile lines and manifest in poor weight gain. May also have proportionally small height and head circumference, though more acute causes tend to affect weight only. If height also low, may suggest constitutionally small child, so check parental heights. Initial loss of up to 10% in first 3-4 days is normal (likely fluid loss), but this should be regained by 3 weeks. Thereafter, there should be an average weekly gain of 150-200 g in normal children, with weight doubling by 4 months and tripling by 12 months. Faltering growth is both an indicator of underlying disease and can itself can cause long-term problems of ↓growth and ↓IQ. Causes Non-organic/environmental (>90%). Inadequate intake due to: Feeding problems (common): unskilled feeding (breast or bottle), insufficient breast milk, infant difficult to feed (e.g. low appetite, weak suck). Maternal problems: neglect, postnatal depression. Organic: GI: IBD, coeliac disease, cow milk p

Background Familial (primary) dyslipidaemia Due to gene mutation(s). Should be suspected in patients with premature IHD (age <55 in men, <60 in women). WHO classifies them type 1-5 (T1-5). Acquired (secondary) dyslipidaemia Most cases of dyslipidaemia are acquired in later life. Obesity, sedentary lifestyle, and diabetes are common risk factors, though many cases are essentially idiopathic. Other causes: Endocrine: hypothyroidism, hypopituitarism. Hepatic: alcohol excess, cholestasis. Renal: nephrotic syndrome, chronic kidney disease. Others: pregnancy, anorexia, gout, antipsychotics. Signs and symptoms Usually detected through CVD risk assessment, or when presenting with complications such as IHD or stroke. The only specific sign is lipid deposits (xanthomas). Their presence and extent are a sign of disease severity. Locations: Eyelids: xanthelasma (also seen in smoking). Eyes: corneal arcus and retinal deposits. Tendon xanthoma: achilles (run finger and thumb along to feel for