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Serum cholesterol 20gr benzac with visa acne gel 03, blood pressure benzac 20gr fast delivery skin care zarraz, cigarette smoking benzac 20gr low cost acne keloid treatment, and death from coronary heart disease. Changes in cholesterol synthesis and excretion when cholesterol intake is increased. Effect of dietary egg on variability of plasma cholesterol levels and lipoprotein cholesterol. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men. Effects of dietary cholesterol on the regulation of total body cholesterol in man. Tissue storage and control of choles- terol metabolism in man on high cholesterol diets. Infant feeding and adult glucose tolerance, lipid profile, blood pressure, and obesity. Control of serum cholesterol homeostasis by choles- terol in the milk of the suckling rat. The role of orphan nuclear receptors in the regula- tion of cholesterol homeostasis. Genetic factors influence the atherogenic response of lipoproteins to dietary fat and cholesterol in nonhuman primates. U-shape relationship between change in dietary cholesterol absorption and plasma lipoprotein responsiveness and evidence for extreme inter- individual variation in dietary cholesterol absorption in humans. Is relationship between serum choles- terol and risk of premature death from coronary heart disease continuous and graded? Dietary palmitic acid results in lower serum cholesterol than does a lauric-myristic acid combination in normolipemic humans. The effect of increased egg consump- tion on plasma cholesteryl ester transfer activity in healthy subjects. Dietary fats and lung cancer risk among women: The Missouri Women’s Health Study (United States). Tzonou A, Kalandidi A, Trichopoulou A, Hsieh C-C, Toupadaki N, Willett W, Trichopoulos D. A prospective cohort study on dietary fat and the risk of postmenopausal breast cancer. Dietary oxysterols are incorporated in plasma triglyceride-rich lipoproteins, increase their suscepti- bility to oxidation and increase aortic cholesterol concentration of rabbits. Apolipoprotein A4-1/2 polymorphism and response of serum lipids to dietary cholesterol in humans. Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: A meta-analysis. Total and high density lipoprotein cholesterol as risk factors for coronary heart disease in elderly men during 5 years of follow-up. Egg yolk and serum-cholesterol levels: Impor- tance of dietary cholesterol intake. Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. Effect of dietary cholesterol on cholesterol synthesis in breast-fed and formula-fed infants. Dietary choles- terol, fat, and lung cancer incidence among older women: The Iowa Women’s Health Study (United States). Effect of egg choles- terol and dietary fats on plasma lipids, lipoproteins, and apoproteins of normal women consuming natural diets. Proteins also function as enzymes, in membranes, as transport carriers, and as hormones; and their component amino acids serve as precursors for nucleic acids, hormones, vitamins, and other important molecules. For amino acids, isotopic tracer methods and linear regression analysis were used whenever possible to deter- mine the requirements. The estimated average requirements for amino acids were used to develop amino acid scoring patterns for various age groups based on the recommended intake of dietary protein. Moreover, the constituent amino acids of protein act as precursors of many coenzymes, hormones, nucleic acids, and other molecules essential for life. Thus an adequate supply of dietary protein is essential to maintain cellular integrity and function, and for health and reproduction. Proteins in both the diet and body are more complex and variable than the other energy sources, carbohydrates and fats. The defining char- acteristic of protein is its requisite amino (or imino) nitrogen group. The average content of nitrogen in dietary protein is about 16 percent by weight, so nitrogen metabolism is often considered to be synonymous with protein metabolism. Carbon, oxygen, and hydrogen are also abundant elements in proteins, and there is a smaller proportion of sulfur. The structures for the common L-amino acids found in typical dietary proteins are shown in Figure 10-1. In the protein molecule, the amino acids are joined together by peptide bonds, which result from the elimination of water between the carboxyl group of one amino acid and the α-amino (or imino in the case of proline) group of the next in line. In biological systems, the chains formed might be anything from a few amino acid units (di, tri, or oligopeptide) to thousands of units long (polypeptide), corresponding to molecular weights ranging from hundreds to hundreds of thousands of Daltons. Polypeptide chains do not exist as long straight chains, nor do they curl up into random shapes, but instead fold into a definite three- dimensional structure. The chains of amino acids tend to coil into helices (secondary structure) due to hydrogen bonding between side chain residues, and sections of the helices may fold on each other due to hydrophobic interactions between nonpolar side chains and, in some proteins, to disulfide bonds so that the overall molecule might be globular or rod-like (tertiary structure). Their exact shape depends on their function and for some proteins, their interaction with other molecules (quaternary structure). The most important aspect of a protein from a nutritional point of view is its amino acid composition, but the protein’s structure may also influ- ence its digestibility. Some proteins, such as keratin, are highly insoluble in water and hence are resistant to digestion, while highly glycosylated proteins, such as the intestinal mucins, are resistant to attack by the proteolytic enzymes of the intestine. Amino Acids The amino acids that are incorporated into mammalian protein are α-amino acids, with the exception of proline, which is an α-imino acid. This means that they have a carboxyl group, an amino nitrogen group, and a side chain attached to a central α-carbon (Figure 10-1). Functional differences among the amino acids lie in the structure of their side chains. In addition to differences in size, these side groups carry different charges at physiological pH (e. These side chains have an important bearing on the ways in which the higher orders of protein structure are stabilized and are intimate parts of many other aspects of protein function. Attractions between positive and negative charges pull different parts of the molecule together. Hydrophobic groups tend to cluster together in the center of globular proteins, while hydrophilic groups remain in contact with water on the periphery. The ease with which the sulfhydryl group in cysteine forms a disulfide bond with the sulfhydryl group of another cysteine in a polypeptide chain is an important factor in the stabilization of folded structures within the poly- peptide and is a crucial element in the formation of inter-polypeptide bonds.

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Environment The causative bacteria can live in the environment and tend to prefer damp areas with low pH order genuine benzac online acne prevention. How is the disease The most common route of infection is ingestion and large numbers of bacilli transmitted to animals? High densities of animals lead to build up of faecal material providing ideal conditions for the transmission of infection buy cheap benzac 20 gr on-line acne off. Aerosol inhalation either from a contaminated environment discount benzac 20gr free shipping skin care equipment suppliers, or directly from lesions in the respiratory tract of infected birds, has been suggested as the cause of pulmonary infections in domestic or captive birds, but this is relatively unusual. How does the disease Close proximity of susceptible groups of animals such as pigs and poultry allows spread between groups disease transfer and the feeding of poultry manure to domestic mammals of animals? Most typically there is chronic wasting with birds becoming emaciated often exhibiting a prominent keel. In late stages of the disease, abdominal distension as a result of liver enlargement and a build up of ascitic fluid can give an emaciated bird an unusual ‘bottom heavy’ appearance. Ceres and other areas of exposed skin may become progressively paler as the disease progresses. Alternatively birds may just be found dead or succumb to another cause of death before these clinical signs are apparent. Johne’s disease often presents as progressive weight loss and reduced milk production. In pigs, there are generally no obvious signs of disease with evidence of infection being found at slaughter in either or both the lymph nodes around the neck or those draining the intestine. Diagnosis In live birds the disease is difficult to diagnose, and diagnosis relies on a combination of laboratory tests such as abnormal blood cell counts and/or finding bacteria in the faeces. More often the diagnosis is reached at post mortem examination, based on the presence of acid-fast bacilli within tuberculous granulomatous lesions in affected tissues. Microscopy using a modified Ziehl Neelsen stain (see images below), or further laboratory tests (e. When this is not possible, the liver, kidneys and intestines or any other obviously affected tissues should be submitted to the diagnostic laboratory. At post mortem examination a shot pink-footed goose Anser brachyrhynchus is found to have typical tuberculous lesions in its liver. In a stained slide of a smear from the liver lesions, the causative bacteria show up as pink rods. The bacteria prefer a low pH and increasing this may help reduce environmental contamination e. Good surveillance ensures any problems can be dealt with quickly before infection becomes established. Diagnosis of the disease in poultry ideally should prompt a policy of culling of the flock. In addition, cleansing and disinfection is important, as subclinically infected animals and environmental contamination may result in the disease becoming endemic. For poultry, keeping the age structure young and slaughtering early provides a powerful means by which to control the disease. The disease is often slow to progress and con-current infections or stress can allow activation or reactivation of subclinical infection, hence efforts should be made to reduce both of these contributory factors. High densities of wildlife represent a risk factor for this disease and practices such as supplemental feeding of wildlife can contribute to this risk. As for poultry, stress may play an important role in allowing a subclinical infection to develop into full-blown disease hence efforts should be made to mitigate against other stressors such as poor nutrition, pollution, con-current infections, disturbance etc. Humans General standards of personal hygiene are sufficient to reduce risk to most humans in and around wetlands and infected animals. However, it has been a problem for several threatened species such as the whooping crane Grus americana in North America, and the lesser flamingo Phoeniconaias minor in east Africa. It can be a problem where wild birds are attracted to wetlands where infected captive birds are maintained. Overall, efforts should be made to prevent infection becoming established in wild populations. Effect on livestock The greatest impact is on poultry flocks where control actions involve culling. Effect on humans Public health concerns are relatively limited although care should be taken if it is known that infection is present, to reduce potential for opportunist infections. Economic importance Where the disease is diagnosed in industrial units, and culling, cleansing and disinfection measures are required, economic losses can be significant. Within smaller flocks the loss of production and general unthriftiness of animals is of importance. Revue Scientifique et Technique de l’Office International des Epizooties, 20, 180–203. Revue Scientifique et Technique de l’Office International des Epizooties, 20, 204-218. This disease is typically spread to humans by inhalation of aerosols, or ingestion of contaminated unpasteurised milk (relatively rare). The disease has a broad host range and numerous wildlife species have been affected to varying degrees including kudu and African buffalo Syncerus caffer in southern Africa and bison and elk Cervus canadensis in Canada. The disease has also been described in wild felids, deer, elephants, rhinoceroses, hares, raccoons, bears, warthogs, primates, opossums, foxes, coyotes, mink, otters, seals, sea lions, deer, elk and some rodent species. In general the wetland manager should consider all wild mammals to be potentially susceptible to infection. Domestic species known to be susceptible include dogs, cats, pigs, ferrets, camelids, sheep, goats and horses. Although generally thought to be resistant there is little known about the susceptibility of birds to M. Geographic distribution Once found worldwide but now ‘kept at bay’ in domesticated animals in many countries due to control programmes. Eradication programmes are underway in some countries of Central and South America, the United States, Mexico, New Zealand, Japan and Europe. In cold, dark and moist conditions it can survive for several months and at 12-24°C (54-75°F), depending on the exposure to sunlight, survival time varies from 18 to 332 days. The bacterial agent may be carried on the clothing or shoes of personnel in contact with infected animals. The chief mode of transmission is exchange of respiratory secretions between infected and uninfected animals and ingestion of infected milk for calves. How does the disease Infection has been observed to spread in both directions between livestock and spread between groups wildlife, when both share the same environment and food. Potential routes of transmission include by aerosol, when in close proximity, and by ingestion when feeding in contaminated environments.

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They may rupture and cause an patients unable to maintain oxygen saturation above acute and severe upper gastrointestinal bleed purchase 20gr benzac visa acne breakout. Incidence/prevalence Further management: 30–50% of patients with portal hypertension will bleed r An upper gastrointestinal endoscopy should be per- from varices order benzac once a day acne 2000. Aetiology If banding is not possible purchase benzac acne practice, the varices should be in- Varicesresult from portal hypertension, the most com- jected with a sclerosant. Factorspredictingbleed- r If endoscopy is unavailable, vasoconstrictors, such as ing in varices include pressure within the varix, variceal octreotide or glypressin, or a Sengstaken tube may be size and severity of the underlying liver disease. Signs of r Infection may occur following a variceal haemorrhage chronic liver disease may be present (jaundice, pallor in cirrhotic patients resulting in significant morbidity spider naevi, liver palms, opaque nails, clubbing). All patients should receive a course of features of portal hypertension may be seen. Secondary prophylaxis following a variceal bleed in cir- Investigations rhosis: The diagnostic investigation is endoscopy, which may r Following control of active bleeding the varices also be therapeutic during an acute bleed. The varices should be eradicated using endoscopic band liga- must be confirmed to be the source of bleeding, because tion (sclerotherapy if banding unavailable). Following up to 20% of patients with varices also have peptic ulcers successful eradication of the varices repeated upper and/orgastritis. Thevaricesareseenastortuouscolumns gastrointestinal endoscopy is required to screen for in the lower third of the oesophagus. If they are used alone, it is recommended that childhood being common and adults universally im- hepatic venous pressure gradient is measured to con- mune. It is infec- Prognosis tious from 2 weeks before clinical symptoms until a few There is a 50% mortality in patients presenting for the days after the onset of jaundice. Prognosis atocyte necrosis is unclear; the virus is not cytopathic in is worse in patients with high Child–Pugh grading (see tissue culture. Without treatment to prevent recurrence two thirds of patients re-bleed whilst in hospital and 90% Clinical features re-bleed within a year. A history of contact/travel abroad may be found, al- Viral hepatitis thoughmanyasymptomaticcasesoccur. Patientspresent with a prodromal phase (malaise, anorexia, nausea, aver- Definition sion to fatty foods and cigarettes) lasting about a week. The term viral hepatitis usually refers specifically to the Jaundice appears after the prodromal phase and lasts diseases of the liver caused by the hepatotropic viruses, about 2 weeks. The liver may be palpably enlarged and which include hepatitis A, B, C, D, E (see Table 5. Other viruses such as the Epstein–Barr virus and cy- Complications tomegalovirus may cause acute hepatitis. Very occasionally fulminant hepatic The hepatotrophic viruses can cause a range of failure occurs. Chapter 5: Disorders of the liver 201 Infection Incubation Acute hepatitis (A,B,C) Asymptomatic Fulminant hepatic Self-limiting Chronic hepatitis failure (recovery) (B,C,D) Immunity Cirrhosis Asymptomatic carrier Hepatocellular carcinoma Figure 5. Prognosis Post exposure prophylaxis has reduced this transmis- Case fatality rate less than 1 per 1000. Nosocomial infections may Geography occur due to needle stick injuries or contaminated in- More common in the developing world with highest lev- struments. The virus is not cytopathic, the liver damage is immune- r Vertical transmission is the most common route in mediated by the cytotoxic T lymphocytes response to high endemic areas. It occurs at or after birth and is viral antigen expressed on the surface of liver cells dur- mostcommoninbabiesofe-antigenpositivemothers. The complete virion or Dane particle is spheri- Hepatitis B is diagnosed and followed using serological cal, 42 nm in diameter (see Fig. It has also sAg made in yeast cells) is given to at risk individuals been noted that patients who present with jaundice including health-care workers and in areas of high during the acute infection rarely convert to a carrier prevalence. The likelihood of these conditions depends on also used as post-exposure prophylaxis for needlestick the age of the patient: injuries. Less than 10% of patients have an acute flu-like illness with jaundice, the remainder are asymptomatic at the time of infection. Followinginfectionmostpatients developchronichepatitisC,whichpredisposestocirrho- Definition sis and hepatocellular carcinoma. Chronic hepatitis C is Hepatitis C is one of the hepatotrophic viruses, which oftenasymptomaticbutmaycausefatigue,myalgia,nau- predominantly causes a chronic hepatitis. Symptoms and signs of chronic liver disease occur years after initial Incidence/prevalence infection. Five per cent carrier rate in Far East; 1–2% in Mediter- Fatty change is seen in the hepatocytes, with little active ranean. It was discovered Chronic active hepatitis may be associated with autoim- in 1988 as being the most common cause of non-A, mune hepatitis, Sjogren’s syndrome, lichen planus, thy- non-B hepatitis, particularly in blood transfusion recipi- roiditis, membranous glomerulonephritis, polyarteritis ents. Quantification of the viral load may be of ing to an increased risk of rapidly developing cirrhosis use in tailoring treatment. Com- bination therapy with pegylated interferon α and rib- Management avirin is recommended for the treatment of people aged There is no vaccine for hepatitis D; however, vaccination 18yearsandoverwithmoderatetoseverechronichepati- against hepatitis B will prevent hepatitis D infection. In- tis C (histological evidence of significant scarring and/or terferon α can be used to treat patients with chronic significant necrotic inflammation). There is no Recovery from hepatitis B leads to clearance of hepatitis available vaccine. Any patient at risk of Geography hepatitis B is at risk of hepatitis D, particularly intra- Cause of water-borne epidemics in the Indian subconti- venous drug users. Hepatitis r WhenhepatitisBandDsimultaneouslyinfectthehost E, like hepatitis A, is transmitted via the faecal–oral route aco-infectionoccurs. It causes a able severity, but is more likely to cause fulminant self-limiting acute hepatitis, with no chronic or carrier hepatic failure. Liver cell membranes may become immunogenic resulting in a lymphocyte-mediated cytotoxic response against Other liver diseases the liver cells. Alcohol-induced liver disease Clinical features Definition Differing patterns are seen: r Acute alcoholic hepatitis resembles acute viral hepati- Liver disease caused by alcohol range from a fatty liver to hepatitis and cirrhosis. Microscopy Aetiology There are three main patterns of liver damage: The risk of developing chronic disease is related to quan- r Alcoholic hepatitis is focal necrosis of hepatocytes, tity, types of beverage, drinking pattern (see page 521), with neutrophil infiltration. Characteristically Mallory’s bodies composed of cytoskeletal fragments Pathophysiology andubiquitin,aheatshockproteinthatlabelsproteins r Any alcohol ingestion causes changes in liver cells, as being damaged and targets them for breakdown. Alcoholic It appears as bright eosinophilic amorphous globules hepatitis refers to alcohol-induced liver injury visible within hepatocytes. This form of change is seen in those ingesting more than 80 g alcohol per day (6 units, 1 bottle of wine or 3 pints of beer). Steatosis r Cirrhosis: Repeated damage has led to fibrosis, with damage to the normal architecture upon which func- Steatohepatitis tion is dependent.

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Rupture into the subarachnoid space may cause r Cerebral infarction particularly in the elderly buy generic benzac from india acne laser. There may be a Jacksonian March cheap benzac online master card skin care x, with the epilepsy progressively involving more of a limb generic 20 gr benzac otc skin care product reviews, e. Complex partial (impaired conciousness) May begin as a simple partial then become complex, or be complex from the start. Secondary generalised Partial seizures (simple or complex) can progress to secondary generalised seizures. Generalised seizures Nonconvulsive (absence) Impaired conciousness but without falling, although there may be involuntary movements. Atonic (drop attacks) Loss of muscle tone causing patient to fall to ground The main terms used to describe seizures are: gitis, stroke etc which may need urgent treatment. It is Partial (focal, localised seizure) also important to decide if the patient is likely to have r A partial seizure may be simple (no loss of con- further seizures. Status epilepticus Management This is defined as a prolonged single attack or continuing With a first seizure, it is important to exclude any under- attacks of epilepsy without intervals of consciousness. Sodium valproate Gabapentin r Lorazepam or diazepam are first-line treatment Lamotrigine Topiramate r If no response, intravenous phenytoin loading dose Tiagabine Levetiracetam of 15 mg/kg is given. However, if Neurosurgery is rarely undertaken except in selected attacks only occur whilst asleep and this pattern is es- patients, with persistent, frequent seizures where there is tablished for 3 years, patients can drive even if seizures a significant adverse impact on quality of life, with poor continue. Proce- injury, stroke, cranial surgery but excluding drugs or al- dures include local resection, lobectomy, hemispherec- cohol, the suspension may be shorter. The management of epilepsy should include the discussion of social is- Acute confusional state (delirium) suessuchassupportathome,relationships,employment andpsychologicalissuessuchasdepression. Womenwho Definition wish to become pregnant need special advice, but there Rapid onset of global but fluctuating confusion with an is no reason why they should not have children. There underlying toxic, vascular, ictal (seizure) or metabolic are support groups available. Chapter 7: Disorders of conciousness and memory 311 Aetiology Adetailed history including pre-morbid cognitive state, r Predisposing factors: The very young and very old, alcohol and drugs is essential, fluctuation helps sep- hearing loss or visual difficulty, those with diffuse arate delirium from dementia, examination should brain disease such as dementia or taking drugs with look for focal neurological signs and any evidence anticholinergic properties such as tricyclic antidepres- of other illness. Consider saving r Disorientation and impaired conscious level – urine for toxicology screen. Management r Motoractivity may be increased but is often purpose- r Detection of the underlying cause of the confusional less. Severe cases may require benzodiazepines, Toxic Alcohol intoxication, withdrawal haloperidol or one of the newer anti-psychotics such Drugs Prescribed/illicit drugs, including as risperidone or olanzapine. The prognosis is dependent Hepatic failure on the underlying cause and co-morbid features. Hypoxia Hypoxia and/or hypotension Vitamin deficiency Vitamin B12 Thiamine (Wernicke–Korsakoff) Coma Intracrania Definition Trauma Head injury Coma is a state of unrousable unconsciousness. Vascular Transient ischaemic attack, stroke, any intracranial bleed or space- occupying lesion Aetiology Epilepsy May be post-ictal (after a seizure) or The causes are mainly those of acute confusional state nonconvulsive status (see Table above), although there are other causes as well. No response 1 Best verbal response Management Orientated 5 Following resuscitation treatment of the underlying Disorientated 4 Inappropriate words 3 cause is the main priority. In at-risk patients such as alco- Best motor response holics and in pregnancy, intravenous thiamine should Obeys verbal commands 6 be given prior to any intravenous glucose as there Localizes painful stimuli 5 Withdrawal to pain 4 is a small risk of precipitating irreversible Wernicke– Flexion to pain 3 Korsakoff’s syndrome. No response 1 r Empirical use of naloxone (reverses opiates), flumaze- nil (reverses benzodiazepines) should be considered. Head Injury Definition Head injury is one of the most common causes of death Clinical features and disability in young men, mainly due to road traffic It is important to establish the level of consciousness. Incidence 1 The first priority is resuscitation – stabilise airway, Common;basedonhospitalattendancesandadmissions breathing and circulation and check the glucose level the incidence is ∼250 per 100,000 population. Hypoxia, hypoglycaemia or hypotension are reversible causes of coma and will exacerbate any Age other cause. Chapter 7: Disorders of conciousness and memory 313 r Penetrating trauma: Penetration of the skull by an ex- swelling of the brain. Pathophysiology The pathology of head injury can be divided into two groups: Complications r Primary brain damage: Short term: Vascular, e. Subarachnoid and intracerebral ticularly on the side of the trauma (coup lesion) and haemorrhage may also occur. Long term: ii Diffuse axonal injury due to shearing forces caus- r Posttraumatic epilepsy. Patients r Chronic traumatic encephalopathy (the punch drunk who survive such injury may have severe brain syndrome seen in professional boxers). Ifneckinjuryissuspected,thepatientshould cal treatment, whereas primary brain damage occurs be immobilised until a spinal cord injury or unstable at the time of injury and therefore can only be in- cervical spine has been excluded. Followingtrauma,thebrainismuch Coma Scale, and full neurological and general exami- more susceptible to hypoxia and hypotension due to nation. The decision to admit for observation is based disruption of autoregulation and impaired vascular on the history and assessment at presentation. Osmotic diuretics such as mannitol Clinical features may also be used to reduce brain oedema. In more severe injuries, there is persistent post- mission to intensive care for intracerebral pressure traumatic amnesia. Patients All patients require close monitoring to check for devel- may have other injuries depending on the nature of the opment of complications that require urgent treatment. Over a period of several hours there is oozing of r the patient is difficult to assess, e. Apathy and/or depression are common, there may be Prognosis disturbances of sleep, confusion of day & night, with Recovery may take weeks to months. Other neurological signs with a persisting disability or impairment is 100 such as hemiparesis, seizures tend to occur very late in per 100,000. Generally, in the early stages, the patient is aware of a loss of their memory and may become very frus- Dementia trated and anxious. They lose the ability to function in daily life grad- Definition ually, and in later stages they become more apathetic, Asyndromeofacquiredcognitiveimpairment,withpro- with little spontaneous effort and therefore require full gressive global loss of cognitive function in the context personal care such as feeding, washing, dressing and of normal arousal. Acollateral history from a relative or close carer who Incidence has known the patient for a long time is essential. The 1% of those aged 65–74 years, 10% of those over 75 and carer is often the one most emotionally affected by the 25% of those over 85 years. Aetiology There are numerous causes of dementia, including Investigations r Alzheimer’s disease (most common >60%). These are to exclude any treatable causes of chronic con- r multi-infarct dementia caused by multiple small in- fusion. Management The specific management strategies are covered under Clinical features specific causes but general treatment includes the fol- See also under specific causes of dementia. Patients may lowing: have impairment of the following cognitive functions: r Multidisciplinary assessment.