Professional Intermediate Skilled non-manual Skilled manual Partly skilled (manual) Unskill ed manual ! r e g n o l m e e s y l n i a t r e c \200\207Poor people living in North London (eg Tottenham Green) live 17yrs less than rich people (in Chelsea); their life expectancy (71yrs) is < that in Ec- uador, China and Beliz e (none has a national health service!). 236 Mortality rates are higher in social class V v s class I: In stillbirths, perinatal deaths, infant deaths, deaths in men aged 15 \200\2236 4 and women aged 20 \200\22359 this factor is 1.8, 2, 2.1, 2, and 1.95. Ditto for lung canc er (SMR1=1.98), heart disease (1.3) and stroke (1.9). Melanoma and Hodgkin \200\231s diseas e are exceptions. l l i w e f i l r i e h t : e r u s a e l p Eff ects of social class and geography are hard to tease apart: in the UK, city dwellers \200\231 mortality rates are 22% (95% con \201 dence interval: 19% \200\22325%) higher th an those in the most rural areas (especially for lung cancer and respiratory disease \200 \224and pollution is a likely cause of this). 237 y l n o s \200\231 e n o e m o s Within occupations the eff ect of social class is seen in a \200\230purer \200\231 way tha n when groups of many occupations are compared: in a study of >17,000 Whitehall civil serva nts there was a >3-fold diff erence in mortality from all causes of death (except genitouri nary disease) comparing those in high grades with those in low grades. Similarly in the arm y, there is a 5-fold dif- ference in mortality from heart disease between highest and lowes t ranks. d e v o m e r e v a h We know that illness makes us descend the social scale, but this eff ect is probably not bi g enough to account for the observed diff erences between classes. It is more likely that t he diff erences are due to smoking behavior, education, diet,2 poverty, stress, and overcro wding. Cognitive ability can partly explain socio-economic inequalities in health ( \200 \230intelligent people look after themselves \200\231 \200\224has some truth). Note that sm oking is 3-fold more com- mon in nurses than in doctors 238 and cognitive factors must play some part in this. This need not imply pessimism about attempts to break the chain that li nks socio-economic status and cognitive ability with health. During some life stages, envir onmental factors may be able to in \202 uence cognitive skills. Interventions can be targe ted in order to optimize these eff ects. 239 y a m u o y g n i k o m s g n i v o m e r y B 1 The SMR (standard mortality ratio) is the ratio of mortality rates in one class compared with the aver- age for the whole population. The whole population has an SMR of 1.00. 2 Low earners consume only a bit less wholemeal bread and more sugary drinks, processed meat and sugar than average, eg 2.5 portions of fresh fruit and vegetables, compared with the avera ge of 2.8. 240 Purchasers and providers Two sets of contrasting principles 1a He who pays the piper, calls the tune. 1b Priceless therapeutic assets cannot be bought or sold: compassion, conti- nui ty of care, and commitment. 2a My job is to spend, spend, spend, until all my patients are healthy. 2b The job of the Treasury is to squeeze, squeeze, squeeze, until all spending is within government targets. (The clarity of this dichotomy becomes turbid when the doctor is asked to do the squeezing.) 524 Never just ask how good a structure is without also asking how good it is at transforming i tself: that which cannot transform, dies. The UK National Health Service is the largest emp loyer in the Western world and for years the search has been on to \201 nd ways to contro l and transform this dear, mighty thing. The purchaser \200\223provider split is the most p owerful lever yet developed for this purpose. Purchasers commission care by drawing up cont racts with compet- ing providers, who deliver the care. The better the provider delivers se condary care (do not pause to ask what \200\230better \200\231 means: speculation on this point might ruin the argument) the more likely they are to get the contract next year. The catch is that all the extra eff ort the provider makes to out-perform a contract this year will probably be taken for granted next year. The same may hold true if purchasing is used for the imposition of guidelines ( \200\230evidence-based purchasing \200\231). What has be en created is a treadmill which goes faster and faster, while taking less and less account of individual patients \200\231 and doctors \200\231 legitimate but varying needs. Unless t he market is rigged, natural selection ensures that the \201 ttest and fastest providers survive. Patients and taxpay- ers bene \201 t \200\224until the point where cynicism and e xhaustion set in. There is no evidence that once the purchaser \200\223provider path is cho sen, then cynicism and exhaustion inevitably follow, and there is evidence at local level t hat bene \201 ts accrue, and services become more tuned to consumers \200\231 desires. (Co nsumers are not infallible judges of what constitutes health \200\224but they are the best judges we have.) \200\207If the State runs both supply (money from general taxa- tion) and demand (control of waiting lists etc), the rules of the market cannot operate and effi cie ncy is hard to achieve \200\224which is why NHS trusts are being freed from central NHS con trol. Controlling change from on top: an historical example from maternity: 1 Government se ts up an expert group (mothers, midwives, ministers, obste- tricians, and general practitio ners \200\224these are jokers in the pack, because they are simultaneously consumers, purch asers and providers). e r a c y r a m i r P 2 Issuing of objectives and indicators of success \200\224eg by 5 years: Women should have a named midwife to ensure continuity of care. \200 Women should be able to choose their place of delivery. Aim to achieve the outcome that she believes is best for her baby and herself. \200 \211 75% of women should know the person who is to deliver t hem in labor. \200 Midwives should have direct access to some beds in all maternity units. \200 \211 30% of women should have a midwife as the lead professional. 3 Fanfare phase: the group \200\231s attractive-looking report is issued (at great ex- pens e to taxpayers) to all groups and personnel involved (except mothers). 4 Lack of \201 nan ce is blamed when no improvements are detected at 5 years. 5 Later, the units are marked fo r closure and the cycle of hope, rising expecta- tions followed by despair and cynicism bec omes complete as the consulta- tion exercise proves to be a derisory exercise in making glo ssy reports. 241 Anatomy of change Ideals (woman-centered care) \200\203Speci \201 c polic y objective (all women to have the chance to discuss their care) \200\203Purchasers \200 \231 action point (set up maternity services liaison committee with lay chairperson) \200 \203Providers \200\231 action point (provide link-workers, and advocacy schemes for women w hose \201 rst language is not English). This type of activity may or may not lead to incr eased accountability and quality of services. 242 525 Referral statistics There is great variability in individual GPs \200\231 referral statisti cs, which leads purveyors of government strategy to the error of saying \200\234Why is the re a 4-fold diff erence in referral rates between GPs? Such variation is insupport- able; s ome doctors must be referring too much \200 \200\235 An advance is made when this issue i s reframed as: \200\234There is information contained in this variability \200\235. This i nformation can guide service development. 243 Understanding the intricacies of purchasing health care depends on un- derstanding referral patterns. If high-referring GPs refer needlessly, then the proportion of their referrals r esulting in further action will be smaller than that of practices with low-referring GPs. U sually, this is not the case. Those with high referral rates have high rates of interventio n. If I refer an ever- increasing number of my patients to a geriatric clinic, must a time come when admissions level off ? The idea of a \200\230leveling-off eff ect \200\231 is im portant. If the consultant is \200\230correct \200\231, and the GP \200\231s expectation a s to the outcome of referral are uniform (probably never true) then when a leveling-off eff ect is observed, it may be true that the average referral rate is optimal, and that low-re ferrers are under-treating, and high-referrers are wasting money. In fact, leveling- off ef f ects are rarely seen, except in general surgery. Other specialists may admit a \201 xed proportion of patients referred to them. There is evidence that this was true for ENT cons ultants and tonsillectomy. Another possibility is the Coulter \200\223Seagroatt hypothesis \200\224that consultants have a threshold of severity for admission (eg a claudication dist ance of 50 meters) and even the majority of patients from the high-referrers ful \201 l t his criterion. In this case (assuming the consultant is right), even the high-referrers are not referring enough. This may be true for angiography. But if the consultant is over-enth usiastic, and overstates treatment bene \201 ts, then the lower referrers are to be applau ded for limiting the excesses of the consultant. \200\207In general, only agree that a ref erral is inappropriate if the patient, the GP, and the consultant concur on its lack of uti lity. Each of these parties has diff erent motivations \200\224eg reassurance/explanation, medicolegal, as well as providing therapy. Despite the rhetoric, secondary care can be preo ccupied by its own agendas and may have little interest in the unique needs of referred pat ients. 244 e r a c y r a m i r P Overall, referral rates are no more variable than admission rates, even in populations with similar morbidity. The reason may be that there is still a great deal of uncertainty under lying very many clinical decisions. We don \200\231t know who exactly should have knee repl acements, cholecystectomy, etc. 245 \200\207There is no known relationship between high or low referral rates and qual- ity of care. Here are 3 cautions in interpreting referrals. 1 Don \200\231t accept GP list size as a denominator (takes no account of diff ering workloads in a practice). Consultations/yr is a better denominator. 2 If a GP has a special interest, this will in \202 uence referral patterns. More knowledg e may lead to more referrals as partial knowledge leads to greater, not less, uncertainty. For example after a while all GPs with a spe- cial interest (GPSI) in dermatology will have been tricked by melanomas masquerading as seborrhoeic warts \200\224so their referrals for histology will be higher than GPs who have less experience and have never been so tricked. 3 Years of data are needed to compare referrals to rarely used units. Referral incentive sc hemes The foregoing shows that this is a complex and uncertain way to in \202 uence referr als. 246,247 But it is true that local educational in- terventions with secondary care spec ialists and structured referral sheets can impact on referral rates. 248 \200\230In-house \200\231 2nd opinions and other primary care based alternatives to outpatient referral are promising. 248 In 2011 referrals in England fell by 5% (to 3.7 \211\210 106) after a long period of rising. 249 The foregoing shows that there are many ways to interpret this statis tic (rationing is biting; patients are less demanding; GPs are more realistic about hospita l bene \201 ts). Fitness to drive,UK \202 y & do sport dvla.gov.uk/medical/ataglance.aspx Ordinary UK driv ing licenses issued by DVLA (driver & vehicle licensing agency) imply that You are required by law to inform Drivers Medical Branch, DVLA, Swansea SA99 1AT at once if you have any ph ysical or medical condition), that is, or may affect your \201 tness as a driver, unless you don \200\231t expect it to last more than 3 months. It is the responsibility of the dri ver to inform DVLA. It is the responsibility of doctors to advise patients that medical con ditions (and drugs) may aff ect their ability to drive and for which conditions patients sh ould inform the DVLA. Drivers should also inform their insurance company of any condition d isclosed to DVLA. \200\207If in doubt, ask your defense union. Vascular disease Uncomplica ted MI: don \200\231t drive for 4wks. Angioplasty or pacemaker: don \200\231t drive for 1wk post-op. Angina: no driving if symptoms occur at the wheel; DVLA need not be informed. Arr hythmias: driving may be OK if the cause is found, and controlled for >1 month if low risk of \200\201consciousness & \200\201motor power. Syncope: OK to drive 1wk after, if cause identi \201 ed and treated. If no cause is found, stop for \211 6 months. TIA/stroke: sto p for \211 1 month; no need to inform DVLA unless there is residual de \201 cit for >1 mo nth. Abdominal aortic aneurysm >6.5cm: Disquali \201 cation (if 6 \200\2236.4cm: inform DV LA; do annual review). Diabetes All on oral hypoglycaemics or insulin must inform DVLA (in general, stop driving for 1 month after starting insulin, to get stable; drivers must show satisfactory control, and must recognize hypoglycaemia). Check vision con- forms to require d standard (BOX). Avoid driving if hypoglycaemic risk \200\200 (eg meal delay; or after ex cess exercise). Carry rapidly absorbed sugar in vehicle and stop, turn off ignition and eat it if any warning signs. A card should be carried to say which drugs they are using, to ai d resuscitation if needed. If an accident is due to hypoglycaemia a diabetic driver may be charged with driv- ing under the in \202 uence of drugs. Advise patients to notify DVLA ( \200\230stop driving \200\231 advice) if limb or visual problems or impaired awareness o f hypoglycaemia. 250 CNS disorders Disabling giddiness, vertigo, and problems with movement s preclude driving. DVLA need to know about unexplained blackouts, multiple sclerosis, Park inson \200\231s (any \200\230freezing \200\231 or on \200\223off eff ects), motor neuron d isease, recurrent TIAs and strokes. In the latter the license is usually withheld for 3 mon ths depending on an examination by an independent doctor, and some- times a driving test. T hose with dementia should only drive if the condition is very mild (do not rely on armchair judgments: on-the-road trials are better). Encourage relatives to contact DVLA if a dement ing relative should not be driv- ing. GPs may desire to breach con \201 dentiality (the GM C approves) and inform DVLA of demented or psychotic patients (tel. 01792 783686UK). Many e lderly drivers ( 1 in 3) who die in accidents are found to have Alzheimer \200\231s. Epilep sy and brain surgery: If a seizure while awake, he must not drive for 1yr. If attacks are o ccurring only when asleep, driving may be possible, eg if after 3yrs no seizure has ever oc curred while awake. Contact DVLA. In any event, the driving by such a person should not be likely to cause a public danger. If a license holder/applicant can satisfy the above, a 3yr license is nor- mally issued. The \200\230till 70 \200\231 license may be restored if \201 t-free for 7yrs with drugs as needed (if no other disqualifying condition). Single sei zure: OK to drive after 6 months if specialist says so and no abnormal tests (eg CT, MRI, E EG). 526 e r a c y r a m i r P Epileptic drug withdrawal risks a 40% seizure rate in year 1. Those wish- ing to withdraw f rom medication should cease driving from the beginning of withdrawal and not recommence unt il 6 months after treatment has ceased. 527 Driving is prohibited in certain general categories \200 Severe mental disorder (includin g severe mental impairment). \200 Severe behavioral disorders \200\224or drug abuse/depen dency. \200 Alcohol dependency1 (including inability to refrain from drunken driving). \200 Psychotic medication taken in quantities that impair driving ability. Vision Acuity ( spectacles) must allow reading a 79.4mm-high number plate at 20.5 meters ( 6/10 on Snel len chart). Monocular vision is allowed if visual \201 eld is full. Binocular \201 eld of vision must be >120 . Diplopia isn \200\231t allowed un- less mild and eye-patch correc table. Diabetic retinopathy matters, but applicants/license holders may not need DVLA visua l \201 eld tests on a regular basis if vision meets required acuity and visual \201 eld standards, and a consult- ant con \201 rms that it is stable, eg: \200 Visual \201 el d shows no deterioration during the last yr. \200 No further laser use in the last year o r since their last license renewal. \200 No change in retinal signs in the last year or s ince renewal. 250 Drugs Driving or being in charge of a vehicle when under the in \202 uen ce (in- cluding side eff ect) of a drug is an off ence under the Road Traffi c Act 1988. Ma ny drugs aff ect alertness and driving ability (check Data-sheets), and many are potentiate d by alcohol, so warn patients not to drive until they are sure of side eff ects, not to dr ink and drive, not to drive if feeling unwell, and never to drive within 48h of a general a nesthetic. Old age DVLA says: \200\234progressive loss of memory, impairment in concentrat ion and reaction time with possible loss of con \201 dence, suggest consideration be given to cease driving. \200\235 This is vague, as when reapplying for a license (every 3yrs aft er 70) a driver simply signs to say \200\230no medical disability is present \200\231. 251 Fitness to \202 y: avoid hypobaric (high altitude) \202 ights if \200 \200 Climbing stairs causes troublesome dyspnoea (an easy screening test). \200 Gas- \201 lled dental caries (via putrifying bacteria): can cause severe tooth- e r a c y r a m i r P ache at altitude, and tooth damage may occur. Within 48h after diving below 50 feet (p814). Even at modest cabin alti- tudes death may oc cur. NB: barotrauma is worse on descent as the Eus- tachian tube is sucked \202 at by the low pressure in the middle ear, making the immediate equilibration of pressure more diffi cult. In uncontrolled cardiac failure, if O2 supplements used at sea-level, wean off before air t ravel, to help see if air travel is OK. These patients must travel with enough supplementar y O2 to give intermittent use, eg at 2L/min. \200 Confusional states and alcohol intoxica tion (synergistic with hypoxia). \200 Pneumothorax; pneumomediastinum; or <10 days post-o p to hollow organ. \200 Neonates <3 days old, or women in the last 4 weeks of pregnancy ( last 13 weeks if multiple pregnancy). See section on airlines, p8. Anemia (Hb <7.5g/dL); GI bleeding; any recent tissue infarctions. \200\207Encourage good h ydration and mobility; use aspirin & compression stockings on long-haul \202 ights \200 \224p16. NB: the list above is not exhaustive. See International Air Transportation Associa tion advice. Fitness to do sporting activities and cardiac rehabilitation GPs often have to advise on this. Ensure that those involved know you don \200\231t have a crystal ball. Com mon sense, and attention to warm-up exercise, is the key. If in an at-risk group, eg epilep sy + wanting to swim, or personal or family history of hypertrophic obstructive cardiomyopa thy + wanting to do heavy exercise, get help. In epilepsy, swim with a friend, only in life guard supervised pools. 252 In CCF, mild work with hand weights need not be banned. 253 Is this drug on the \200\230banned \200\231 list? See Sports Medicine in Mims Companion. medinet.co.uk/crit.htm 1 Alcohol & driving: anyone attempting to drive on a road, or public place (eg pub car park or a garage forecourt), may be required to give a breath test, to see if they are over the legal limit of alcohol: 35 g of alcohol/100mL of breath (or 80mg of alcohol/100mL of bloo d). The request must be made by a police offi cer. Chronic fatigue syndrome (CFS) CFS entails severe, disabling fatigue for >6 months, aff ect ing physical and men- tal functioning, present most of the time and feeling dreadful/relaps e after mild exertion. \200 : \200 \211\210 3 : 1. 254 Myalgia, sleep and mood disturban ce are common. Pre- disposing factors: Genetics; personality; anxiety/depression. 255 Preci pitating factors: Infections psychosocial stress. Perpetuating factors: Immunity \200 \201, poor skeletal muscle, cognitive ability, endocrine & cardiovascular homeosta- sis. 25 6 Physical correlates of CFS: Abnormal gene expression in 16 genes related to mitochondrial function (Epstein \200\223Barr or parvoviruses could switch on this ab- normal expression; this might form the basis for a diagnostic blood test). 257 Neu- trophil apoptosis is \200\200. 258 Electrodermal responses are somewhat characteristic. Diagnostic criteria/work -up for \200\230query chronic fatigue syndrome \200\231 The Ca- nadian criteria may be use d for research purposes (>60 areas are investigated; some are controversial, eg ataxia). 25 9 In practice, exclude anemia, TB, snoring, etc, with a history; physical exam; mental stat e (p324), urinalysis, FBC, U&E, TSH, ESR, LFT, glucose autoantibodies, creatine kinase, blood culture, and CXR. 528 e r a c THEN Pursue abnormalities (eg ?TB/HIV if weight \200\201; ?depression if anhedonia, p336). THEN ASK Does the pattern \201 t CFS? \200\224ie persistent or relapsing fatigue, not rel ieved by rest, and leading to substantial reduction in previous levels of activity. y r a m THEN ASK Are any exclusion criteria present? \200\224psychosis (p316), bipolar depression ( p354), dementia, anorexia (p348). THEN Are \211 4 of the following present for >6 months? \200 Unexplained muscle pain \200 Impaired memory/concentration unrelated to drugs or a lcohol use \200 Polyarthralgia (but swelling suggests a joint diagnosis) \200 Unrefresh ing sleep \200 Post-exertional malaise lasting over 24h \200 Persisting sore throat not caused by glandular fever \200 Unexplained tender cervical or axillary nodes. If criteri a met, call it CFS; if not fully met, call it \200\230idiopathic chronic fatigue \200\231. Co-morbid conditions are common, eg depression: consider diagnosing in a quanti \201 ed w ay using formal diagnostic instruments (eg Beck inventory). Treatment None is speci \201 c , and chronicity is common. 260 Aim for a therapeu- tic alliance with your patient. Some th erapists aim to prevent somatic \201 xa- tion: the strongest predictor of a poor prognosi s is a \201 xed belief that symp- toms are due only to physical causes. Allow non-threate ning discussion about psychological issues, keeping an open mind. Make it clear that psycho logical symptoms are not the same as malingering: \200\234Perhaps what starts as an illnes s may not be what keeps it going \200\235. Psychological factors aff ect outcome of many il lnesses: why should this be diff erent? Proven interventions: Graded exercise programs (not the same as \200\230pacing \200\2311);261,262 cognitive therapy (p374). i r P Treating associated anxiety/depression (p340) may be the best way to im- prove quality of l ife. 263 Also address family and work problems, and other per- petuating factors (above). T alking with other patients sounds sensible, but this could prolong symptoms. Slow recovery is the norm (faster in adolescents). 261 Trials of non-standard therapies Trials \201 nd modest bene \201 t from methyl- phenidate (20mg/d) 264 and nicotinamide adenine dinucleoti de (NADH). 265 When to get help \200 Children with CFS \200 Unresponsive to the above m easures \200 History of travel abroad \200 CNS signs \200 Walking diffi culty \200 Fevers \200 Suicidal. Prognosis Be optimistic. A key predictor of good outcome is emotion al pro- cessing (expressing, acknowledging, and accepting of emotional distress). 266 1 Pac ing is setting a realistic exercise routine and sticking to it to avoid \200\230boom and b ust \200\231 cycles. Proper rest between exercise (eg relaxation/meditation) is said to be vital. 267 Further reading: DoH CFS Working party. This page intentionally left blank Obesity See Healthy diets, OHCM p236 The prevalence of obesity (BMI >30kg/m2): USA 27%, UK 24%, Italy 10%. 268 Obe- sity is the commonest disorder of childhood and adolescence (see B MI charts, p227 and preventing adult diseases in childhood, p156). 269 530 Obesity shortens life expectancy 270 (MI; stroke; hypertension; dyslipidaemia/ metabolic sy ndrome, thromboembolism, diabetes) and contributes to gout, sleep apnoea, cognitive disease s, and gallbladder disease. 268,272 In Framingham studies, obesity alone accounted for 11% of heart failure in men (14% in women). Weight loss maintained for 2yrs, improves life expectancy and all the above complications. 273,274 (Less certainty with obesity-associated depression, cata- racts, fatty liver diseas e, osteoarthritis, and benign intracranial hypertension.) Obesity and cancer: Obesity is as sociated with \200\200death rates from cancer of esophagus, colon, rectum, gallbladder, pa ncreas, and kidney, independent of smoking. It also \200\200 risk of death from stomach an d prostate cancer in \200 and breast, cervical and ovarian cancer in \200 . This could be from increased in \202 am- matory state in obesity. Risk of death correlates with BMI bey ond 25kg/m2. 272,275 Mother/child: Obesity \200\200 risk of pre-eclampsia ( \211\2102), di abetes ( \211\2104), thromboem- bolism, and maternal mortality. Rates of congenital deformi ties such as spina- bi \201 da and heart defects also increases. 276 Hormonal changes in o besity Interactions between gut, brain, circulating metabolites and adipose tissue are all integrated to regulate food intake and attempt to maintain weight. 277 Cholecystokinin, GLP -1, ghrelin, and peptide YY, are examples of gut hormones with eff ects on brainstem, hypot halamus, or hippocampus, regulating hunger \200\223satiety drive, food behavior, and mood.1 278 e r a c y r a m i r P Increased visceral fat enhances the degree of insulin resistance associated with obesity an d hyperinsulinaemia. Together, hyperinsulinaemia and insulin resistance enhance the risk of the co-morbidities described above. 272 Other endocrine changes include increased: leptin, TSH, insulin, IGF-1, andro- gens, proges terone, cytokines (IL-6), ACTH/cortisol, and decreased: GH, adipo- nectin279 and parasympat hetic activity. 280 Typical needs Women: 2079Kcal/d ( \200 \211\210 2605); most eat \200 \20610% more than needed. Once weight goes up, physical activity lessens, and weight increa ses further. Measuring obesity BMI is still useful, but waist circumference (midway bet- we en lower ribs and iliac crest at the end of gentle expiration) correlates better with risk of complications even if BMI nor- mal. 281 Reference intervals for obesity are lower in Asi an people (obese=BMI >27.5) because their central fat is increased. 281 Management The main problem is maintaining lost weight. Non-pharmacological: There is strong evidence that com bining a behavioral approach with more traditional dietary and activity advice leads to imp roved short-term weight loss and is currently the best lifestyle approach. 282,283 Behavior al therapy: Setting goals, self-monitoring, family/friend/group (eg weight watchers), cogni tive restructuring, problem solving, assertiveness. \200 284 Diet/exercise example: 1000Kc al/day and 30min of moderate activity every day ( \211 5 days/wk) 285,286 adapted to mainta in the weight loss. 283,286 500kcal/day reduction without any change of activity leads to 0.45kg of weight loss/wk. Easy! One may as well ask someone to hold their breath for a week . Waist circumference for central obesity \200 \211 94cm \200 \211 80cm Europeans South (S.) Asians \200 \211 90cm \200 \211 80cm \200 \211 90cm \200 \211 80cm Chines e \200 \211 85cm \200 \211 90cm Japanese S. & central Americans: use S. asian data pr o tem Africans + Middle East: use European pro tem 1 Increasing ghrelin levels, through injections or calorie restriction in mice, gives anxio lytic- and anti- depressant-like responses in forced swim tests. Ghrelin may defend against stress-induced depression. 287 Ghrelin \200\200GH & cortisol secretion (and, in men, prom otes restorative slow-wave sleep). 288 531 \200\234Doctor, I want to lose weight \200 \200\235 \200 Is it you who wants to lose we ight or have you been sent by someone else? \200 Any plans? What have you tried? What is/ was your maximum weight? \200 Are you on anything that increases weight (pioglitazone; an tipsychotics)? \200 Your motivation is \200 eg to decrease BP medication or NSAIDs for O A (p689)? \200 Would you accept a speci \201 c goal, eg \200\230lose 0.5kg/week eg with high-protein low-calorie, low carbohydrate diet? \200\224or go to a weight-watchers group? \200\231 \200 Can you change your obesogenic environment (eg less food stimuli)? 268,289 \200 Can you commit to increase your exercise to maintain weight loss? \200 Can you us e a pedometer, join a gym, or do home-based exercise programs? \200 Are you prepared to r ecord food intake and energy expenditure? 290 \200 Are you wanting a speci \201 c remedy (BELOW), if indicated (and no CI, eg BP \200\200)? 7 questions for weight-loss programs to answer (Mayo Clinic ) 1 Is there proof that it works (ask for evidence of long-term result s)? 2 Any quali \201 ed dietician or specialist in behavior modi \201 cation employed? 3 Is the recommended intake nutritionally balanced? 4 Does the patient have to buy special pr oducts? 5 Will the patient receive advice on starting safe, moderate exercise? 6 How will t he program reward and monitor progress? 7 Is there support and follow-up for after the form al program ends? Speci \201 c therapies for obesity Drug therapy Bene \201 ts are \200 \200weight loss (4 \200\2236kg added to diet alone), maintain- ing weight loss, improve vas cular risks with weight reduction. \200 284 Generally, stop if weight loss <5% at 12wks (l ess strict if diabetic). \200 284,291 Orlistat 120mg/8h PO. Intestinal lipase inhibitor; i nduces 5 \200\22310% weight loss in 50 \200\22360% which maintains for 4yrs. Explain to eat <60g fat/day otherwise stea- torrhoea occurs. SE: oily spotting, \202 atus with discharg e, fecal urgency \200 284,290 CI: chronic malabsorption, cholestasis, breastfeeding (see B NF). Bariatric surgery If all of these criteria are ful \201 lled: \200 BMI \211 40kg/m 2 or 35 \200\223 40kg/m2 and co-morbidities \200\200risk. \200 All appropriate nonsurgic al measures have been tried for >6 months \200 Involvement of a specialist obesity servic e. \200 No over-riding personality/behavioral problem. \200 284,292 Long term effects: I ron, vi- tamin, and protein de \201 ciencies; gallstones, weight regain. 292 Types of bari atric surgery: intragastric balloons, gastric banding (variable tightening); gastric bypass . NB: the morbidly obese are ghrelin and leptin hyporesponders with lesser intragastric bal loon treatment effi ciency. 293 Bariatric surgery in some cases can cure diseases caused by obesity such as type 2 diabetes. Are we in a passive-dependent relationship with our obesi ty genes? meta-analysis ) 294 So, at Exercise reduces the eff ect of FTO genes on obesity b y 27%.(Ruth Loos 2011 least to some extent, we can encourage our patients to take control. e r a c y r a m i r P 1 Websites for help with weight loss www.weightlossresources.co.uk www.eating4health.co.uk www.toast-uk.org (Obesity Awareness Trust). www.whi.org.uk www.weightlossresources.co.uk 2 Genetic testing may be counter-productive: one study showed that people who were told they had \200\200genetic susceptibility to obesity increased their dietary fat intake. We thank Dr Hamid Mani for his help with this topic. What to do for the best? Doctors are called on to make decisions about every patient they m eet: few are curable at once, so making a plan for what to do for the best is the secret of success at the bedside. The aim here is to explain this secret, to enable you to \202 ou rish in the clinical world, and to keep you out of lawyers \200\231 offi ces. 532 Let us look at the steps of the history, physical, or mental examination, and investigations. By the end of taking the history, you need to have acquired 3 things: 1 Rap port with the patient. 2 A diagnosis or diff erential diagnosis. 3 The placement of the dia gnosis in the context of the patient \200\231s life. Rapport: Consultations are shorter whe n rapport is good. 295(N=116) The patient is con \201 dent that he or she is getting the f ull attention of the doctor, and these patients are more understanding, and more forgiving when things go wrong. Doctors are far from infallible, so we need to have con \201 dence t hat the patient will feel able to come back if things are not right, tell us what has happe ned, agree on an adjustment of the treatment, and, by giving feedback, improve our clinical acumen. Diagnosis: Studies have shown that skilled physicians have made a provision- al di agnosis soon after the consultation starts, and they spend the rest of the history in con \201 rming or excluding it. What happens if you are not skilled, and you have no hint as to the diagnosis? You need to get more information. \200 Pursue the main symptom: \200\234 tell me more about the headache \200 \200\235 \200 Elicit other symptoms \200\224eg chan ge of weight or appetite, fevers, fatigue, un- e r a c y r a m i r P explained lumps, itching, jaundice, or anything else odd? Get help from a colleague or even a diagnostic system \200\224eg Mentor, p502. \200 Check you still have rapport with the patient. Are you searching for a physi- cal diagnosis when a psychological diagnosis would be more appropriate? Here you might ask questions such as \200\234How is your mood? \200\235 \200\234What would your wife or partner say is wrong? \200\235 \200\234Would they say you are depressed? \200\235 \200\234What would have to ch ange for you to feel better? \200\235. \200\207Do not proceed to the physical examination until you have a working diagno- sis: the answer is rarely found there (<10%). Placing the diagnosis in the context of the patient \200\231s life: If you do not do this, you will not know what will count as a cure, and, more speci \201 cally, dif- ferent patients need dif f erent treatments \200\224see p241. Some factors to focus on might be: the motivation of t he patient to get better ( \200\234I \200\231ve got to get my knee better so that I stay st rong enough to lift my wife onto the commode \200\235); their general health; social situat ion; drugs (not forgetting nicotine and alcohol); is help available at home; work (yes/no; type)? At the end of the history, occasionally there is enough information to start treatment. Usu ally you may be only, say, 70% sure of the diagnosis, and more information is needed before treatment is commenced. Fig 1. It is time for the physical examination. This aims to gain evidence to con \201 rm or exclude the hypothesis, to de \201 ne the extent of some process, or to assess the prog ress of known disease. At each step, ask \200\234What do I need to know? \200\235 Followin g the examination the diagram may look like this: 533 Fig 2. Investigations If the action threshold has not been crossed, further informa- tion i s need. Action thresholds vary from doctor to doctor, and from disease to disease. When the treatment is dangerous, the action threshold will be high (eg leukemia). In self-limiting illnesses, eg pharyngitis, the action threshold will be lower. Note that \200\230action \200\231 may be that, in agreement with such a patient, only symptomatic treatment is neede d, and future episodes could be man- aged without medical input. e r a c y r a m i r P Similarly, it may be important to move the probability of a serious but un- likely disease beyond the exclusion threshold. Once the probability of a disease passes the action threshold, treatment can commence, if the patient wishes. Fig 3. Supposing neither the action threshold nor the exclusion threshold is exceed- ed, th en more information is needed, eg from pathology, imaging, or the pas- sage of time. Time i tself is an investigation: it may reveal sinister causes or the benign nature of the diseas e. To use time this way, you need to be reasonably sure that immediate treatment is not req uired. If there is still not enough certainty to initiate management, get further in- formation, e g from books, computers, colleagues, further tests \200\224or you may feel it appropriate t o refer the patient at this stage. Or go round the process again, starting with the history \200\224from a diff erent viewpoint. Once above the action threshold, it is time to decide what to do for the best. This is a de cision shared by the doctor and the patient. It entails informed consent and consideration of: 296 \200 The probability of the diagnosis. \200 The likelihood of the diff erent po ssible outcomes. \200 The costs and side-eff ects of treatment. \200 The hope and value s of those aff ected, particularly the patient. \200 What is possible, considering the sk ills, resources, and time available. Finally, tell your patient how they will know if they are on the path to improve- ment or relapse, and if so, at what point to seek help (critica l action threshold, below; record this in the notes) \200\224eg if your peak \202 ow fall s by 40%, start this prescription for prednisolone, and come and see me. Fig 4. 7 Ear, nose and throat diseases \200 Prevalence of ENT symptoms 536 ENT examination 536 The ear 538 Hearing tests audiology 540 \200\2231 Painful ears 542 Discharging ears 544 Fluid in the middle ear 546 Who to refer wi th glue ear? 547 Childhood deafness 548 Issues with cochlear implants 549 Deafness in adult s 550 Tinnitus 552 Acoustic neuroma 553 Dangers of excessive noise 553 Vertigo 554 Rhinosin usitis & Nasal polyps 556 \200\2237 The paranasal sinuses 558 Nasal injury & foreign bodies 560 Nosebleed (epistaxis) 562 Throa t infections 564 Tonsillar tumors 564 \200 Stridor 566 Hoarseness 568 Laryngeal nerve pals y 569 Head & neck cancers 570 Dysphagia 572 (OHCM p233) Facial palsy 574 Lumps in the neck 576 The salivary glands 578 Dry mouth (xerostomia) 579 Dentistry for doctors 580 Transmitter Receiver Oval window Vestibular apparatus Round window External ear Multiple electrodes Tympanic membrane Sound processor attached by magnet Cochlea z 3000 H Fig 1. An electrode from a cochlea implant is strug- gling to reach the core of the cochlea \200\231s spiral, but un- less it negotiates the ever tightening bends, lower tones (encod ed near its core) are unheard, and speech will be distorted. 1 \200\2233 Its spirals vary a mong mammals depending (per- haps!) on how much low-fre- quency sounds in their habi- tat m ost need ampli \201 cation via the whispering chamber eff ect ( \201 g 3, whereby sound t raveling along a curved wall in a big room remains strong enough to be well- heard on its o pp osite side). Hz 00 2 0 0 5 0 Fig 3. Why is the coch- lea \200\231s spiral (blue) dif- ferent to sim ple spirals based on Fib onacci se- quences (black)? Low-tone hearing rang- es from mice to whales in step with the pitch of the spiral; the tighter it is, the more sound en- ergy in low-frequency waves is forced against the cochlea \200\231s outer wall. Trials show that this \200\230whisper ing chamber eff ect \200\231 augmen t s low- freq uency sound by 20dB.5-7 0 H z