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Regular review Appendicitis = Acute Suppurative Appendicitis Lifetime incidence = 6% Most common surgical emergency Incidence declining (? If no diarrhoea or vomiting then no immediate danger of dehydration If you diagnose it discount wellbutrin 300mg overnight delivery depression symptoms yawning, or if you dont discount wellbutrin 300 mg mastercard depression quotes pinterest, youll be wrong 50% of the time! Symptoms & Signs Very difficult to diagnose considerable variety in presentation Fever: 37 generic wellbutrin 300mg amex bipolar depression natural remedies. In a child generic wellbutrin 300mg on-line depression symptoms speech, look for tenderness and guarding not rebound wont let anyone touch them after that. Mucinous cystadenocarcinoma invading the peritoneum, fills with tenacious semisolid mucus. Pathology Macroscopic appearance: Begins in rectum and extends in continuity to left colon. Acute dilation of colon due to loss of muscle tone gas distension vascular occlusion necrosis. Key risk facts: How long have they had it (main one): 1% at 10 years, 30% at 30 years. Minimal with only rectal involvement How well controlled is the inflammation Aggressive flat lesions, infiltrates quickly into lymphatics in submucosa Perforation Fibromuscular strictures (check to exclude malignancy) Treatment Sulphasalazine +/- steroids (or azathioprine). Surgery for Colectomy = cure obstruction and abscess common Small Bowel Tumours Benign: Polyps (Peutz-Jeghers), Juvenile Polyps, Adenomas, Stromal tumours Malignant: Carcinoid tumours: Tumours arising from neuroendocrine cells Mainly midgut. Appendix and rectum better, ileal and colonic worse Carcinoid Syndrome: due to excess serotonin. Resembles those in the colon Colorectal Cancer Presentation Change in shape of stools significant (e. Referral to plan appropriate surveillance Incidence has been declining since 1950s (5. Normally removed as dont know which will become invasive Malignancy related to size: <1. Head has closely packed tubules/glands lined by non-differentiated neoplastic columnar cells. May secrete lots of mucous Juvenile polyps: Left side of large bowel of kids Cause rectal bleeding Grossly look similar to adenomas Microscopically not neoplastic. Cystically dilated mucous glands, inflammation of lamina propria, maybe ulceration Peutz-Jeghers Syndrome: Polyp containing mucin filled cysts and smooth muscle in the lamina propria. Either through turnover due to mucosal damage risk of gene match failure or directly genotoxic mechanism Presentation: Left sided: annular encircling napkin ring or apple core constriction. Later: obliterate precursor adenoma Microscopic appearance: Most are moderately differentiated, irregular glands with pleomorphic cells, usually lack mucin production. Try and predict who needs irradiation and do it pre-operatively Palliation: hospice + chemotherapy better quality of life than hospice alone Prognosis of Colorectal Cancer Invade into serosal fat, metastasise to regional lymph nodes then to liver and lungs. Neither sensitive nor specific Diverticular disease of the colon Aetiology & Epidemiology Dietary fibre stool weight and colonic transit colonic pressure 50% in > 70 years Symptoms & Signs: Most asymptomatic Uncomplicated disease (Diverticulosis): non-specific tender sigmoid colon, cramping lower abdominal pain (esp. If really nasty then Gentamycin, Amoxycillin and Metronidazole) Epidural would be good for pain but is contraindicated if risk of sepsis Usually settles with conservative management. If not, then resect affected colon: Hartmans procedure: Remove affected segment. Mass movements occur once or twice a day (usually after a meal) Faecal mass in rectum internal anal sphincter opens by reflex. Exercise to improve abdominal muscles Adequate fibre and fluid Laxatives: Hydrophilic bulk forming agents, eg Normacol, Metamucil. Not useful in palliative care (patients are too sick to eat it) Osmotic agents, eg lactulose or sorbitol not broken down in small bowel osmotic gradient water content. Eg docusate agents, Coloxyl (a detergent effect breaks up stool, may be hepatotoxic) and lubricants. Oil based lubricants (eg paraffin) can affect vitamin and drug absorption and be aspirated Stimulants and irritants peristalsis and net fluid secretion. Long term use of laxatives causes constipation by damaging the nerve supply of the gut Locally acting agents eg glycerol suppository at peak motility time. Can have osmotic and irritant agents Investigational agents such as cisapride (prokinetic agent) Rectal Laxatives: For faecal impaction On exam will either have a loaded rectum or ballooning of the rectum (dilated distally impacted further up) Types: Glycerine suppositories: soften stool by lubrication and osmosis Bisacodyl (Dulcolax) suppositories: Causes peristalsis Sodium Phosphate enemas Oil Enemas Fibre Dietary Fibre: the undigested and unabsorbed polysaccharide (cereal, fruit, vegetable) that remains at the end of the small bowel. Other Bowel Diseases Collagenous colitis: Chronic or episodic watery diarrhoea F > M, 30 + years, autoimmune association Macroscopic appearance: Looks normal at colonoscopy Microscopic appearance: subepithelial hypocellular collagen band (prevents H2O absorption) Anorectal problems Haemorrhoids: Dilated veins beneath the submucosa. Risk factors as for cervical cancer (number of partners, age of first intercourse, etc). Can check vomit with urine dipstick for blood Melaena (black/sticky foul smelling stools): stomach denatures haemoglobin black. If they rebleed and surgery is required, the surgeon will want to know where its from Endoscope for varices injection sclerotherapy (e. Check: Bilirubin: in acute hepatitis will be 50:50 direct and indirect Raised aminotransferases predominate. Excreted in urine, but saturated kinetics serum level Physiological: Bone: Growth and fractures. Took blood downstream of iv line 46 year old, enlarged nodes, protein 50, albumin 33 globulin gap ? Jaundice, itching Microscopic appearance: Diffuse liver cell injury with lobular disarray: loss of normal radial array Focal necrosis of hepatocytes with hepatocyte regeneration (mitotic figures, variation in cell size) Portal inflammation: lymphocytes & macrophages. Architecture preserved, no fibrosis, no hepatocyte necrosis Chronic active hepatitis: Progressive hepatic necrosis and fibrosis, potentially leading to cirrhosis Clinical course variable. Onset to death in 2 3 weeks (massive necrosis) to 3 months (submassive failure) Causes: Viral (60%), drugs/chemicals (30%, eg paracetamol poisoning), numerous other minor causes Macroscopic appearance: all/most of liver destroyed. If it extends to another portal tract then called bridging necrosis Is there inflammation/necrosis out in the lobule intralobular or focal necrosis Are there inflammatory cells in the portal tract portal inflammation How much scar tissue/fibrosis is there? Intracytoplasmic droplets coalescing to fill the cell, may rupture (no inflammation before rupture). Perivenular fibrosis Gastro-Intestinal 185 Outcome: Liver function may be normal. If no fibrosis then can be cleared Fatty liver can also be caused by toxic, metabolic and hypoxic conditions, and occurs in malnourished kids in the third world Alcoholic hepatitis: Acutely following heavy drinking Often superimposed on fatty change or cirrhosis Microscopic appearance: Similar to viral hepatitis Liver cell necrosis and inflammatory infiltrate Mallory bodies (alcoholic hyaline): intracytoplasmic collection of cyto-skeletal proteins. Looks like candy floss Fibrosis Alcoholic Cirrhosis: Causes 60 70% of cirrhosis. Often micro-macro nodular presentation Microscopic appearance: Early: delicate portal-central fibrosis, fatty parenchyma. Key issue is how much fibrosis has occurred before clearance First stage of clearance: E antigen seroconvesion. Often severe/fulminating Chronic D on Chronic B: endemic in many parts of the world. Better prognosis Cholangiocarcinoma Arises in intrahepatic biliary tree rd Associated with parasitic infestation (ie 3 world) Microscopic appearance: well to poorly differentiated adenocarcinoma. Associated with vinyl chloride (ie plastics manufacture) and arsenic Hepatoblastoma: In infants, can be epithelial or mixed, recapitulates foetal liver Benign Tumours of the Liver Bile duct adenoma: von Myenberg complex, 1 cm pale nodules composed of small ducts in fibrous tissue. Incidental finding at surgery Liver cell adenoma: Associated with oral contraceptives, pregnancy, anabolic steroids. Also causes osteoarthritis and diabetes Primary/idiopathic/genetic: Common autosomal recessive, usually males 40 60 years. Brown/grey skin Microscopic appearance: Initially golden brown periportal ferritin deposits in hepatocytes. Pearl stain: stains iron blue Monitoring: If transferrin > 45% or serum ferritin > 300 ng/ml then liver biopsy if > 39 years Hepatic Iron Index = hepatic iron concentration/age. Chemo ineffective Treatment of haemochromatosis: if regular venesection before organ damage then normal life expectancy. Lumen of central vein occluded + collagen deposition in Space of Disse Pre-hepatic disease: Portal vein obstruction due to cancer, peritoneal sepsis, pancreatitis, surgery, cirrhosis Gilberts Syndrome Normal variant in? Also worse when ill due to other causes (may present as a red hearing) Bilirubin rarely > 100 micromol/L Gastro-Intestinal 193 Is totally benign Neonatal Liver Disease Extrahepatic Biliary Atresia: destructive inflammation of bile ducts cirrhosis Neonatal Hepatitis: non-specific idiopathic response to neonatal hepatic insult (eg virus).

M > F Prevalence Geography Five to ten per cent of young women in temperate cli- Much more common in Turkey generic 300 mg wellbutrin with amex anxiety night sweats, Iran generic wellbutrin 300 mg line depression nausea, China trusted 300 mg wellbutrin anxiety attacks, Korea and mates purchase 300mg wellbutrin fast delivery depression nos. Patients demonstrate pathergy (a gered autoimmune reaction in a genetically susceptible papule or pustule forms at sites of skin puncture) this individual. Clinical features Management Patients have recurrent oral aphthous or herpetiform ul- Corticosteroids and immunosuppressive agents are used cers. Colchicine may be of benet for ery- ular disease (uveitis), skin lesions (erythema nodosum), thema nodosum and arthralgia. A thin section a few mil- limetres around and underneath the resulting defect Nomenclature and description is taken, divided into pieces, and cut as a fresh frozen specimen. If tumour is seen at a particular margin re- The cornerstone of dermatological diagnosis is accu- section is continued at the appropriate margin, and rate observation and description of lesions and rashes. Dermatological procedures Skin grafts r Shaveortangential excision: This procedure slices a Skin grafts are sections of skin that are completely de- surface growth off using a blade, often to remove a tached and transferred to cover large areas of skin defect. The recipient site requires a good blood supply, as the r Punch biopsy: Under local anaesthesia a full thickness graft has no supply of its own. Ifaverylargedefectneeds are scraped off with a special tool and the area is cau- covering, the graft can be meshed. Repeated treatment may be take up a blood supply more easily than full thickness required. The area heals often leaving a small hypopig- grafts, but tend to shrink and have abnormal pigmen- mented mark. Lightfreezingcausesapeeling,moderate dermis, are used mainly in reconstructive surgery. They leave a donor site, which requires closure by su- r Mohs surgery: This is a technique used in the re- tures, limiting the size of the graft. Erythroderma Intense and widespread reddening of the skin due to dilation of blood vessels, often with exfoliation. Excoriation Stripping of the skin usually by scratching as a result of intense itching of the skin. May be a primary lichenoid disease or a secondary lichenication due to repeated excoriation as seen in chronic eczema. Macule Describes a skin lesion that is at, often well circumscribed with alteration of colour. Skin aps Geography Mayoccur anywhere, but higher incidence in urban Skin aps differ from skin grafts in that they are taken areas. The coverage can thus be thicker and stronger than grafts, and can be applied to avascularareassuchasexposedbone,tendonsandjoints. Aetiology/pathophysiology Flaps may be transferred whilst maintaining their orig- The term atopy is a disease resulting from allergic inal vascular attachments (pedicle aps), or may be re- sensitisation to normal environmental constituents anastamosed to local blood supply (free aps). The underly- ing cause and mechanisms in eczema have yet to be fully elucidated; however, dry skin (xerosis) is an important Scaly lesions contributor. There appear to be genetic and immuno- logical components to allergic sensitisation (see also page 498). Offspring of one atopic parent have a 30% risk of Atopic eczema being atopic, which rises to 60% if both parents are Denition atopic. Achronic inammatory skin disorder associated with r Chromosome studies suggest that atopic tendency atopy, causing dry, scaly, itchy lesions. More common in children with peak onset usually 218 Serum IgE is elevated in 85% of individuals and higher months. It is thought that the high frequency of secondary Sex infectionisacombinationofthelossofskinintegrityand M = F deciency of local antimicrobial proteins. These are erythematous and r Antibiotics are used for secondary bacterial infection. Lesionsmayweepand r Wetwraps consist of the application of topical agents have tender tiny blisters termed vesicles especially when under bandages to facilitate absorption. The distribution is age depen- may be administered in this way or coal tar may be dent: used as a keratolytic in lichenied skin. If steroids are r Babies develop eczema predominantly on the face and appliedunderwetwrapsthedose/potencymustbede- head; this may resolve or progress by 18 months to the creased as increased absorption may result in systemic childhood/adult pattern. Complications r Topical tacrolimus, an immunosuppressant, is being Staphylococcus aureus is found on the skin of 90%, which increasingly used in children prior to the use of high- may result in acute infection (impetigenised eczema). Pimecrolimus is under study as a the young may cause dehydration and is life-threatening. Prognosis Eczemahasauctuatingcoursewithapproximately50% Management resolving by 18 months, and few have problems beyond There is no curative treatment. In ba- bies it may be appropriate to either test for cows milk allergy or to perform a therapeutic trial with a cows Contact dermatitis milk protein free formula. Denition r Generalised dry skin (xerosis) requires regular fre- Contact dermatitis is an allergic or irritant-induced der- quent use of emollient moisturisers especially af- matitis arising from direct skin exposure to a substance. Cream preparations are water based with emulsiers and preservatives and they tend Age todrytheskin. A balance has to be struck between application of sufcient grease and cosmetic satisfaction. Geography The lowest potency that is effective should be used Exposure is most common in the home or industrially and higher potency reserved for resistant cases. In babies a Oncetheepidermalbarrierisdamagedasecondaryin- widespread lesion of the scalp (cradle cap) is seen, and ammatory response occurs. Psoriasis Denition Clinical features Psoriasisisachronic,non-infectious,inammatorycon- Contact dermatitis often affects the hands or face. Le- dition of the skin, characterised by well-demarcated ery- sions may also affect the legs of patients with chronic thematous patches and silvery scaly plaques. Management Age The allergens can be identied by patch testing (see page Peak of onset in teens and early 20s and late onset 5560 467) and avoided. Seborrhoeic The aetiology is not fully understood but genetic en- dermatitis is a chronic scaly inammatory eruption af- vironmental and immunological components are sug- fecting areas rich in sebaceous glands. There is concor- rum ovale,ayeast that colonises the skin of patients with dance in monozygotic twins and a suggestion of genes seborrhoeic dermatitis; however, it is unclear if this is the located within the major histocompatibility complex cause or effect of the condition. The lesions appear pinkish due to mild erythema and r There is a suggestion of environmental components. Dilated capillaries are and damage (the Koebner phenomenon) and certain seen in the oedematous papillary dermis. Management Psoriasis is a chronic disorder that is managed rather Pathophysiology than cured. Treatments are chosen on the basis of dis- The epidermis is thickened with increased epidermal ease pattern and severity, patient preference and clinical stem cells and keratinocytes. There is a thick silvery scale, which when lifted off char- is a risk of rebound psoriasis on stopping treatment. These treatments are tiple small psoriatic lesions on the trunk often in a expensive and increase the risk of skin cancer. An al- child or young adult with no previous history of pso- ternative may be the use of a high-energy laser that riasis. There is acute onset of diffuse retinoids all of which have systemic toxicity requiring erythema and scaling with sheets of supercial non- monitoring. If the entire skin is affected, it is termed erythrodermic (the von Zumbusch variant).

From that time onwards wellbutrin 300 mg on-line mood disorder resources, the due to long hospitalization generic wellbutrin 300mg visa depression knowledge test, diagnostic pathogenesis of diabetes still has not 1-5 tests purchase wellbutrin 300 mg otc mood disorder statistics, e discount wellbutrin 300mg with visa depression disability. Furthermore, over worldwide will reach 333 million in 2025 the last decades much progress in 1-5 from 135 million in 1995. Regarding outcome of diabetes mellitus treatment western world Diabetes mellitus is one of has been within the field of self the most common chronic since in 2007, management and care. Indeed, the it was estimated that there were 246 reports of patients who lived 40-50 years million people with diabetes compared to without some severe complications 1 194 million in 2003. This significant following "treatment ", indicated that increase is expected to take place both the key-element to confront the disease in developing and developed countries is the effective management of 1-5 and is mainly attributed to the modern diabetes. Furthermore, it has been administration, b) relieve the symptoms acknowledged that treatment of the of the disease or handle with disease is more related to lifestyle and emergencies and disease-related less related to the quality of the provided exacerbations, c) prevent and manage 6-10 health care and services. However, the roles that education is held responsible for patients prefer in making medical frequent re-hospitalizations, disease decisions (i. Not passive roles) appear to be related to the surprisingly, these patients do not level of participation (active or not) in follow lifestyle modifications suggested decision-making about their treatment. Therefore, actively engaged in self-managing their 13 enhancing active patient participation in diabetes. However, Educated patients can positively affect education should be delivered as soon as the outcome of the disease. It is worth noting that strategies appear to be necessary for the design of educational intervention patients with a longer diabetic duration requires an overall approach including to achieve meaningful diabetic involvement of health professionals, education. Other important parameter that education is setting a realistic goal of need to be integrated in the contents of behavior changing. Patients should not the curriculum is accurate and elaborate be trapped into unrealistic expectations, informing about possible complications. The choice of scientific terms that depends on method depends on staff and individuals personality and environment availability, and patients comprehension ability. Information should be important factors for education success presented through written materials, are appropriate learning environment audio-visual media and physical objects. In particular, The use of media, where the student has the learning environment should be quiet the opportunity to see the techniques for ensuring greater understanding of the and skills required for an effectively instructions, and avoidance of management contributes to a better attendance distraction. The teaching methods are individual Educational interventions delivered by a approach and structured group single educator, in less than ten months, education approach. Although the with more than 12 hours and between 6 individual approach predominates over and 10 sessions give the best results but the group for the reason that it is more research is needed to confirm this. A well-designed program demands solving acute problems or handling signs regular reinforcement involving follow- and symptoms of complications etc. For all threat of severe and devastating diabetic the above reasons, annual attendance of complications or bothersome symptoms reinforcement education including a throughout their lives. Reinforcement of education ensures At the other side of the spectrum, long-term blood glucose control, as the comorbid chronic illness (e. As a the close involvement of patients and matter of fact the same education care givers is encouraged. Effective progamme delivered by different persons communication has been shown to in the same settings might not give the 1-4 influence patient decisions about their same results. Influence of Health Science Journal, 2010;4(4):201- the Duration of Diabetes on the 202. Structured clinic Patient Understanding of Diabetes Self- program for Canadian primary care. Prevention : development and Randomized controlled trial of implementation of a European Guideline structured personal care of type 2 and training standards for Diabetes diabetes mellitus. Impact of a program to guidelines for type 2 diabetes in primary improve adherence to diabetes guidelines care. Self-management Journal, 2011;5(1):15-22 education programmes by lay leaders for 17. These guidelines are also intended to enhance Website diabetes prevention efforts in Canada and to reduce the burden of diabetes complications in people living with this disease. As per the Canadian Medical Association Handbook on Clinical Practice Guidelines (Davis D, et al. It is incumbent upon health-care professionals to stay current in this rapidly changing eld. Unless otherwise specied, these guidelines pertain to the care of adults with diabetes. Two chapters Type 1 Diabetes in Children and Adolescents and Type 2 Diabetes in Children and Adolescents are included to highlight aspects of care that must be tailored to the pediatric population. Suggested Citation To cite as a whole: Diabetes Canada Clinical Practice Guidelines Expert Committee. Diabetes Canada 2018 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada. Diabetes Canada 2018 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada: Pharmacologic Glycemic Management of Type 2 Diabetes in Adults. Can J Diabetes 42 (2018) S1S5 Contents lists available at ScienceDirect Canadian Journal of Diabetes journal homepage: www. In 2017, the The guidelines represent a summary of material and do not name of the Canadian Diabetes Association was changed to Dia- provide in-depth background clinical knowledge which is typi- betes Canada to reect the seriousness of diabetes, and to increase cally covered more comprehensively in medical textbooks and review perception of the organization as being committed to helping all articles. They are not meant to provide a menu-driven or cook- Canadians with diabetes, as well as to ending the disease. In addition, they are unable to provide guidance in all circumstances and for all people with diabetes. People with dia- betes are a diverse and heterogeneous group; treatment decisions must be individualized. Guidelines are meant to aid in decision making by providing recommendations that are informed by the best available evidence; however, therapeutic decisions are made at the level of the relationship between the health-care provider and the individual with diabetes. Evidence-based guidelines try to weigh the tes prevention efforts in Canada; and reduce the burden of diabe- benet and harm of various treatments; however, patient prefer- tes complications. The intended users are all health-care ences are not always included in clinical research and, as a result, professionals that are involved in the management of people with patient values and preferences must be incorporated into clinical diabetes and those at risk of developing diabetes, with a particu- decision making (2). For some clinical decisions, strong evidence lar focus on primary care or usual care providers. The guidelines is available to inform these decisions, and these are reected in the are also intended for people living with diabetes. However, there are many key messages directed at people living with this chronic disease have clinical situations where strong evidence is not currently avail- been added to each chapter. It is also important to note that clinical practice guide- have then incorporated the evidence into revised diagnostic, prog- lines are not intended to be a legal resource in malpractice cases nostic and therapeutic recommendations for the care of Canadi- as their more general nature renders them insensitive to the par- ans living with diabetes, as well as recommendations to delay the ticular circumstances of individual cases (1). The grading of all recom- mendations has been stringently reviewed by an Independent Methods Committee (see Methods chapter, p. Key Changes The guidelines are meant to improve the quality of care and healthcare outcomes of Canadians living with diabetes. A primary A number of changes have occurred with the development of purpose is to address clinical care gaps that exist, i. The guidelines also summarize key research ndings and Expansion of the Expert Committee to include 135 health- make clinical decisions more transparent. They are meant to reduce care professional volunteers from across Canada with broader representation from more allied health/interprofessional stake- Conict of interest statements can be found on page S5. Expert Committee members bring expertise from 1499-2671 2018 Canadian Diabetes Association.

Presents with It is also associated with reux nephropathy order wellbutrin 300mg on-line depression zoloft side effects, focal rapidly progressive glomerulonephritis wellbutrin 300 mg lowest price depression symptoms zoloft. Prognosis There is a poor response to treatment a trial of immunosuppression is often given if there is progres- sive renal dysfunction purchase 300mg wellbutrin amex depression definition nz. Renal involvement is usually seen in Wegeners granulomatosis and microscopic polyangiitis order wellbutrin 300 mg mastercard depression symptoms ehow. Typic- Aetiology ally, there is a focal proliferative glomerulonephritis, often with necrosis and crescent formation. Renal disease 167 but may develop following transplantation of a Prognosis normal kidney into a patient with Alport syndrome. The signicance of membranous change (class V) is There is an acute renal failure caused by a rapidly unclear. Pulmonary haemor- or cyclophosphamide can slow progressive renal rhage (in smokers) causes breathlessness and hae- damage. The disease usually responds to plasma exchange (to remove the autoantibody) combined with steroids Clinical features and cytotoxic therapy (usually cyclophosphamide). Oliguria, oedema, hypertension, haematuria and Recovery of renal function is rare once anuria or renalimpairmentfollow23weeksafterinfectionwith dialysis dependence has occurred. Investigations Systemic lupus ThroatorskinculturesmayshowgroupAstreptococci erythematosus if penicillin has not been given. Urine osmolality decreased and urine sodium tissue turgor and postural hypotension. In severe decreased: depletion, mental confusion, hypotension and shock diabetes insipidus (p. Urine osmolality increased and urine sodium in- Check serum osmolality and urine sodium. Serum osmolality is decreased and urine sodium is can be given orally or as intravenous 5% dextrose. Serum potassium decreased (hypokalaemia) Management Aetiology Salt depletion is corrected with NaCl, either orally (slow sodium tablets) or as intravenous normal sa-. Renal loss: diuretic therapy (thiazides, loop diuretics) Serum sodium increased mineralocorticoid excess. Renin secreted by the (hypernatraemia) juxtaglomerular apparatus in the kidney converts angiotensinogen to angiotensin. Angiotensin sti- Aetiology mulates aldosterone secretion from the adrenal cortex which causes urinary sodiumretention and Too much sodium or too little water. Inchronickidneydiseaseacidosiscanbecorrected Management with oral bicarbonate or dialysing against a bicarbon- ate-based dialysis uid. In severe vomiting), potassium is given intravenously: 2g/l acidosis bicarbonate is sometimes replaced as 8. This should be rapid (give 50100ml) following sus- Serum potassium increased tained cardiac arrest as arrhythmias are difcult to (hyperkalaemia) revert in the presence of acidosis. In distal renal tubular acidosis (type 1) there is a Aetiology failure of hydrogen ion secretion in the distal tubule. Intravenous dextrose and in- eration, as in hyperaldosteronism, elevated cor- sulinmovespotassium into the intracellularcompart- ticosteroids or severe hypokalaemia ment. Fanconi syndrome glycosuria, aminoaciduria, phosphaturia, renal Aetiology tubular acidosis). Serum uric acid increased Hypomagnesaemia Causes Magnesium isthesecondmostabundantintracellular. The patient should be advised to Headache avoid excessive analgesic use, but a small dose of Headache is the most frequently reported neurolog- amitriptyline taken at night may help. The clinicians challenge is Migraine to exclude a treatable underlying intra- or extracranial Migraine is episodic and affects approximately 10% of secondary cause (Table 15. Itisthreetimes should ascertain: more common in women and there is often a family. Prodromal sensory phenomena (aura) have been attributed to vasoconstriction within intracerebral Primary headache vessels, although a wave of depolarisation spreading across the cerebral cortex may account for this early syndromes phase. Thereafter, vasodilatation of extracerebral ves- Tension headache (chronic daily sels correlates with the onset of headache. Clinical presentation Aetiology remains unclear but may be musculoskel- etal in origin. It is most common in middle-aged Classical migraine with aura women, but may occur at any age and in either sex, Characteristically migraine starts with a sense of ill especially in the context of stress or depression. Standard an- scotomata) usually in the eld opposite to the side of algesics are reported to be ineffective and continuous the succeeding headache and lasting up to 1h. In analgesic use may exacerbate the situation, especially severe cases the patient may develop a homonymous when the effects of medication wear off (so-called hemianopia or even complete blindness. Neurological examination is hypertension and must be used cautiously in those usually within normal limits, and between episodes with vascular risk factors. Hemiplegic and ophthalmoplegic migraine Prophylaxis Rarely focal neurological features may persist for sev- Precipitating causes should beidentied and avoided. Preventative treatment for migraine should be considered for patients who suffer: Investigation. Neurology 173 Cluster headache raised intracranial pressure (false-localising sign). They may occur several times mone and corticosteroids), systemic lupus erythema- a day, often waking the patient from sleep. In injection) is the treatment of choice for cluster more chronic cases, medical therapy with acetazol- headaches simple analgesics are rarely effective in amide, other diuretics or corticosteroids may be tried this condition. High-ow oxygen and corticosteroids but surgical intervention (lumboperitoneal shunt or have also been reported to be efcacious in some optic nerve sheath decompression) is often required patients. Prophylaxis with verapamil or lithium may torelievesymptomsand/orprotectvisionprolonged be tried (methysergide is reserved for refractory cases raised intracranial pressure predisposes to optic and,aswithmigraineprophylaxis,mustbeusedunder atrophy. Meningeal irritation Irritation of the meninges (meningism) occurring in meningitis or following subarachnoid haemorrhage characteristically produces a triad of symptoms: Secondary causes. Raised intracranial pressure In meningitis the headache evolves over minutes to hourswhereasinsubarachnoidhaemorrhageitisabrupt Usually secondary to an intracranial tumour, haema- in onset and may be followed by loss of consciousness. It improves Post-concussion 12h after rising and is exacerbated by coughing, sneezing, straining and bending down. Visual func- Similar to tension headache but usually associated tion may be preserved despite papilloedema, but with dizziness (not vertigo) and impaired concentra- other neurological symptoms and signs related to the tion, post-concussion headache persists for months primary lesion are usually evident. The pain often and there may be a history of inadequate recovery responds to simple analgesics. Occasionally, bilateral Trigeminal neuralgia predominantly affects those over sixth cranial nerve palsies are present and reect 50 years of age. It reects compression of the sensory 174 Neurology root of the trigeminal nerve (e. Eachyearasmallnumberofindividualswith Theagonisingsharppainisconnedtothedistribution this condition (12 per 100,000) die prematurely as a of the trigeminal nerve on one side, commonly the consequence of status epilepticus (see below), acci- maxillaryormandibulardivisions. It tends to get worse with age, and even- tually a continuous background pain may develop if Classication left untreated. Physical examination is usually normal but may reveal neurological signs inthe presence of an Partial seizures underlying mass lesion. These have a single focus of activity, which may be Simpleanalgesicsaregenerallyineffective.

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