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Local health policy case studies. 7. Management of resources human, fiancial, infrastructural ; in health care. 8. Human resource management in health care. 9. The structure and function of social policy in Europe social insurance, pension systems etc. ; . 10 SPRING BREAK . 11 The practical aspects of social . policy. 12 Economic and societal . correlations of social and health policy: relationships of social support and health policy. 13 Social policy of high-risk . populations immigrants, ethnicities, unemployed, etc. ; . 14 Dilemmas in social and health . policy and their possible solutions. 15 The evaluation of the social and . health care reforms from the beginning of '90s world tendencies. NEUROLOGY 9th semester 15 weeks ; LECTURE 1 hr week ; a. Introduction. History of neurology. b. Physical examination. Neurological status. a. The organization of the sensory system. b. Pain. The organization of the motor system. Spinal cord. Neurological localization. Brainstem. Neurological localization. Cerebellum. Neurological localization. Cerebral cortex. Frontal lobe. Neurological localization. Temporal lobe. Neurological localization. AUTUMN BREAK a. Parietal and occipital lobes. Neurological localization. b. Vegetative nervous system. Cerebrospinal fluid. Diagnostic methods. Neurovascular system. Neurological localization. Extrapyramidal system. Neurologicallocalization. PRACTICE 2 hrs week ; Neurological investigation related to the lecture.

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Assessment of absolute cardiovascular risk is the starting point for all discussions with people who have cardiovascular risk factors measured. Reduction in cardiovascular risk is the goal of treatment. Risk assessment for most asymptomatic men is recommended from the age of 45 or from the age of 35 if they have risk factors ; . Risk assessment for most asymptomatic women is recommended from the age of 55 or from the age of 45 if they have risk factors ; . Mori should be assessed for cardiovascular risk 10 years earlier than non-Mori. There is an urgent need to focus intervention programmes on Mori, who bear the greatest burden of cardiovascular disease in New Zealand. The `outcome gap' between Mori and non-Mori is widening. A fasting lipid profile, fasting plasma glucose and two blood pressure measurements are recommended investigations for comprehensive risk assessment. People with known cardiovascular disease and those at high risk because of diabetes with renal disease, or some genetic lipid disorders, are clinically defined at very high risk. Cardiovascular mortality is high in people with impaired glucose tolerance IGT ; or diabetes and most will require intensive intervention. Particular attention is required for Mori who have a high rate of cardiovascular and renal complications from diabetes. Lifestyle change and drug intervention should be considered together. The intensity of intervention recommended depends on the level of cardiovascular risk: a life free from cigarette smoke, eating a heart healthy diet and taking every opportunity to be physically active is recommended for people at less than 10% 5-year CV risk lifestyle interventions for people at more than 10% 5-year CV risk are strongly recommended and this group should receive individualised advice using motivational interviewing techniques relating to smoking cessation if relevant, a cardioprotective diet and regular physical activity cardiovascular risk should be reduced in people at greater than 15% 5-year CV risk by lifestyle interventions, aspirin, blood pressure lowering medication and lipid modifying therapy statins ; . There should be a greater intensity of treatment for higher risk people more than 20 30% ; after myocardial infarction, comprehensive programmes that promote lifestyle change for people are best delivered by a cardiac rehabilitation team. Most people with angina or after myocardial infarction will be taking at least four standard drugs, low-dose aspirin 75 150 mg ; , a beta-blocker, a statin and an ACE-inhibitor virtually all ischaemic stroke and transient ischaemic attack survivors should be taking low dose aspirin, a combination of two blood pressure drugs and a statin.

Accepted for publication July 14, 1998. This study was supported by grants from the medical faculty of Goteborg University and the Medical Society of Goteborg, Goteborg, Sweden. We are grateful to Gorel Bergdahl for technical assis tance and Ann-Charlotte Wikstrom for help with prepara tion of the manuscript. Reprints: Lars Olaison, MD, PhD, Department of In fectious Diseases, Sahlgrenska University Hospital Ostra, Smorslottsgatan 1, S-416 85 Goteborg, Sweden e-mail: lars.olaison medfak.gu and fenofibrate.

Suspected before screening results were known. The ratio of males to females diagnosed with CAH in newborn screening programs is the expected 1: Causes of congenital adrenal hyperplasia: A number of separate genetic disorders comprise CAH, each one resulting from a defect in the activity of a distinct enzyme required for cortisol synthesis. The adrenal gland produces three classes of steroid hormones: glucocorticoids, principally cortisol; mineralocorticoids, principally aldosterone; and androgens. Depending on the location or severity of the enzymatic block, mineralocorticoid production may or may not be affected saltwasting or non-saltwasting forms ; , and androgen output could either be augmented or diminished virilizing or feminizing forms ; . The name of the condition derives from the fact that with low cortisol output, the pituitary gland secretes massive amounts of ACTH causing the adrenal glands to hypertrophy. There is a flow of precursor steroids into androgen-synthesizing pathways, which are unaffected by the enzymatic block. The most common form of CAH results from diminished activity of the 21-hydroxylase enzyme: 90% of cases result from this deficiency, and this is the only form detected by newborn screening methods. The cortisol precursor, 17-hydroxyprogesterone 17-OHP ; , accumulates to high levels because of the enzymatic block. Serum measurements of 17-OHP are generally used to diagnose 21-hydroxylase deficiency. A second form of CAH, accounting for less than 5% of cases, results from 11-hydroxylase deficiency; the precursor that accumulates to the highest levels in this disorder is 11deoxycortisol, also called compound S. Children with 11-hydroxylase deficiency tend not to waste salt, and may actually retain sodium and become hypertensive. Much rarer forms of CAH involve enzymatic steps that are crucial to the synthesis of androgen hormones. Rather than resulting in virilized female infants, these conditions result in male infants whose external genitalia are female or indeterminate because of inadequate testosterone production during critical periods in utero. These disorders are not detected in screening programs measuring 17-OHP such as those used in Tennessee. Treatment: Infants in adrenal crises require intensive management with intravenous fluids, glucose, and cortisol. Chronic management of infants with CAH is complex and should include the close involvement of a pediatric endocrinologist. Medical management includes provision of cortisol or other glucocorticoid, and in saltwasting individuals, a mineralocorticoid, 9 -flurocortisol Florin4f ; as well as supplemental sodium chloride. Treatment is lifelong. Salt craving characterizes many of these individuals their whole life. In situations of metabolic stress such as fever, major trauma, or the need for anesthesia, individuals with CAH will require a doubling or tripling of their daily glucocorticoid dose to compensate for the fact that they cannot generate the increased cortisol secretion that is required of normal adrenal glands under periods of metabolic stress. Although the uterus, ovaries, and fallopian tubes are present, the internal genitalia of affected female children are also altered by adrenal androgens, and reconstructive surgery may be required to generate an introitus for the vagina. Reconstruction of the external genitalia is often performed to restore female anatomy. Screening tests and confirmation.
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