Diabetes risks and complications 2010


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Diabetes risks and complications

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  • 60-70% deaths in diabetes due to heart disease
  • 89% of people with diabetes have modifible isk factos compared to 78% general population Smoking Cessation reduces cardiovascular risk by half after 1 year and after ten years the risk is the same as an individual who has never smoked
  • Several studies have shown that the risk of cardiovascular disease rises with increasing blood glucose levels. 1,2 Evidence from the UKPDS (see slides 33–38) has shown that glycaemia is continuously related to the risk of cardiovascular disease and other complications associated with Type 2 diabetes, 1 in particular, increases in HbA 1c have been associated with increases in diabetes-related death, fatal and non-fatal myocardial infarction, stroke and peripheral vascular disease, and microvascular complications such as retinopathy. 2 Epidemiological extrapolations from this study study show that a 1% higher HbA 1c is associated with a highly significant (p<0.0001): 2 21% increase in risk of diabetes-related deaths 14% increase in myocardial infarction 43% increase in peripheral vascular disease. Therefore, cardiovascular disease and microvascular complications of Type 2 diabetes may be reduced by stricter control of blood glucose levels and blood pressure. The benefit of tight glycaemic control is also seen in respect of microvascular complications, with a 37% increase in risk for every 1% increase in HbA 1c . 2 1. Coutinho M, Gerstein HC, Wang Y, Yusuf S. Diabetes Care 1999; 22: 233–40. 2. Stratton IM, Adler AI, Andrew H et al . BMJ 2000; 321: 405 – 12.
  • 12x RR increase if >20kg weight change in 14 years!!! 7x increase if 11-19.9kg This was in women but still probably translates to the weaker sex too
  • In a study by Haffner et al., d iabetic patients without previous myocardial infarction had as high a risk of myocardial infarction as non-diabetic patients with previous myocardial infarction. 1 The increased risk in diabetes is not simply due to the presence of hypertension or high cholesterol levels, which is common in these patients. 1 People with hypertension concomitant to diabetes have an almost 3-fold greater risk of cardiovascular mortality than non-diabetic patients across all blood pressure levels according to the Multiple Risk Factor Intervention Trial (MRFIT). 2 Similarly, MRFIT demonstrated that at each cholesterol level, coronary heart disease mortality rates were 3–4 times higher in people with diabetes. 2 Therefore, specific risk tables/charts for diabetic patients, such as those issued by the joint British societies, should be used to assess cardiovascular risk in these patients, rather than standard ones. 3 1. Haffner SM, Lehto S, Ronnemaa T et al . N Engl J Med 1998; 339: 229–34. 2. Stamler J, Vacaro O, Neaton O et al . Diabetes Care 1993; 16: 434–44. 3. British Cardiac Society, British Hyperlipidaemia Society, British Hypertension Society, British Diabetic Association. Heart 1998; 80 (suppl 2): S1 – S29.
  • Our current understanding of the pathophysiology of Type 2 diabetes plus evidence from the UKPDS has shown that the aim of treatment should be not only to provide tight and sustained control of blood glucose, but also to reduce the long-term morbidity and mortality associated with cardiovascular disease and microvascular complications. The UKPDS has demonstrated that for many patients this has not been achieved. Earlier intervention with combination therapy may be necessary to provide lasting glycaemic control for the majority of patients. 1 However, treatment aimed at reducing other cardiovascular risk factors, such as insulin resistance, may be required. 2 There is therefore a role for agents that target insulin resistance – such as the thiazolidinediones. 1. Turner RC, Cull CA, Frighi V et al . JAMA 1999; 281: 2005 – 12 . 2. Haffner SM, Miettinen H. Am J Med 1997; 103: 152–62.
  • The majority of patients first seek medical attention when they experience symptoms including extreme thirst, excessive urination, weight loss and fatigue. However, as many as 60% of patients ignore their symptoms and do not present to the doctor until their condition has progressed and complications have developed. These complications may include hypertension, coronary heart disease, circulatory disorders, nerve damage and kidney disorders. If left untreated, these complications can lead to heart attacks, blindness, lower-limb amputation and kidney transplantation. The effect of these complications are costly not only to the individual, but to society, as they not only result in severe disability but also restrict a patient’s mobility and ability to work. UKPDS Group. UK Prospective Diabetes Study 6. Complications in newly diagnosed type 2 diabetic patients and their association with different clinical and biochemical risk factors. Diabetes Research 1990;13:1–11.
  • The benefits of tight glycaemic control have already been discussed, but the UKPDS also investigated the effects of tight blood pressure control. Patients with diabetes randomised to tight blood pressure control (mean achieved blood pressure 144/82 mmHg) had a lower risk of a range of endpoints. 1 Epidemiological extrapolation showed that overall, a 10 mmHg lower systolic blood pressure was associated with a reduction in the risk of myocardial infarction by 12%, stroke by 19%, heart failure by 15% and diabetes-related deaths by 17% and microvascular endpoints by 13%. 1,2 Diabetes UK treatment targets for the control of cardiovascular risk factors in people with diabetes now suggest that 140/80 mmHg represents good control of blood pressure, 3 another example of the UKPDS results directly influencing treatment guidelines. 1. UKPDS Group. BMJ 1998; 317: 703-13. 2. Adler IA, Stratton IM, Andrew H et al . BMJ 2000; 321: 412–19. 3. Diabetes UK. Recommendations for the management of diabetes in primary care . 2nd ed. London, October 2000.
  • These are some key points from NICE. This is the algorithm provided by NICE, there are a number of provisos identified (see previous slide or guidelines) a In young patients (under 55) whose BP may be managed on monotherapy, consider starting with a beta-blocker. b Patients at high risk have a strong family history of type 2 diabetes, have impaired glucose tolerance (FPG >– 6.5 mmol/l), are clinically obese (body mass index >– 30) or are of South-Asian or African-Caribbean ethnic origin. c Beta-blocker contraindications include asthma, coronary obstructive pulmonary disease and heart block. d Offer an angiotensin receptor blocker (ARB) if an angiotensin-converting enzyme inhibitor (ACEi) is not tolerated because of cough. Contraindications include known or suspected renovascular disease and pregnancy. e Only dihydropyridine calcium-channel blockers should be prescribed with a beta-blocker. Contraindications include heart failure. f Consider offering a beta-blocker or angiotensin-converting enzyme inhibitor (ACEi if not yet used), another drug or specialist referral. A beta-blocker and thiazide-type diuretic combination may become necessary in patients at high risk of developing diabetes if hypertension or CVD progresses.
  • Coster et al - HTA report 2000 HTA report concluded that self-monitoring is well established as a practice but that the evidence-base is weak Optimal use of the technique has not been established
  • Diabetes risks and complications 2010

    1. 2. Famous Diabetic people- Mae West, Jonny cash, Tommy Lee
    2. 3. Diabetes mellitus <ul><li>Syndrome with vascular, neuropathic and metabolic components. </li></ul><ul><li>Multiple aetiology- hyperglycaemia & glucose intolerance due to: Insulin deficiency, impaired insulin action or both. </li></ul><ul><li>5 mechanisms: Absolute insulin deficiency </li></ul><ul><li>Impaired release of insulin by pancreatic beta cells </li></ul><ul><li>Defective insulin receptors </li></ul><ul><li>Inactive insulin </li></ul><ul><li>Insulin is destroyed before it can carry out its actions </li></ul>
    3. 4. Several types <ul><li>Hall (2003) Type 2 can be treated with insulin but they are not reclassified- biochemical processes determine classification. </li></ul><ul><li>Type 1 and Type 2 </li></ul><ul><li>Gestational </li></ul><ul><li>Drug Induced- steroids and thiazides </li></ul><ul><li>Genetic syndromes- Down Syndrome </li></ul><ul><li>Pancreatic diseases- tumours, pancreatitis </li></ul><ul><li>Endocrinopathies- acromegaly. </li></ul>
    4. 5. MODY <ul><li>Maturity onset Diabetes of the young </li></ul><ul><li>Hyperglycaemia diagnosed before the age of 25yrs. </li></ul><ul><li>Treatable for 5 yrs without insulin if no markers for IDDM ( most prove to be). </li></ul><ul><li>Rare in caucasians, inherited as a dominant gene. </li></ul>
    5. 6. Types <ul><li>Type 1 </li></ul><ul><li>Insulin dependent </li></ul><ul><li><30yrs </li></ul><ul><li>Unplanned weight loss </li></ul><ul><li>Beta cell destruction-autoimmune- absolute lack of insulin </li></ul><ul><li>Immune mediated </li></ul><ul><li>Inherited- Asian, African </li></ul><ul><li>10% pos family history </li></ul><ul><li>Rapid onset </li></ul><ul><li>Type 2 75-80% </li></ul><ul><li>Non insulin dependent </li></ul><ul><li>>30yrs ( debated) </li></ul><ul><li>Over weight </li></ul><ul><li>Insulin resistance, insufficiency, high hepatic glucose output. </li></ul><ul><li>Linked to metabolic syndrome (X). </li></ul><ul><li>30% pos family history </li></ul><ul><li>insidious onset </li></ul>
    6. 7. Metabolic syndrome <ul><li>Syndrome features- impaired insulin sensitivity, hyperglycaemia, dyslipidaemia, central obesity and hypertension- need 3 out of 5 for diagnosis. </li></ul><ul><li>Cluster of disorders leading to increased risk of Type 2 Diabetes. </li></ul><ul><li>? Due to central obesity as is linked to IR but IR only occurs in ½ of obese people so is IR primary? </li></ul><ul><li>There is an impaired response to insulin so get compensatory hyperinsulinaemia. But can’t last for long. </li></ul><ul><li>Hypertension due to increased sympathetic NS. </li></ul><ul><li>LIPGENE study – 5yr, European, impact of fat. </li></ul>
    7. 8. Insulin resistance <ul><li>Schwarzbein and Deville (1999) Due to the normal aging process everyone develops insulin resistance- normal for a 90yr old. </li></ul><ul><li>Lifestyle =Accelerated metabolic aging. </li></ul><ul><li>Insulin- hormone-chemical communicator </li></ul><ul><li>Insulin protects brain from cell destruction due to high glucose levels </li></ul>
    8. 9. Insulin resistance 3 <ul><li>Prolonged elevated insulin levels age the metabolism on a cellular level which results in disease. </li></ul><ul><li>Microvascular complications are less common than in type 1 but still occur. </li></ul><ul><li>Higher risk of large vessel atherosclerosis. </li></ul><ul><li>Precise mechanisms linking hyperglycaemia and vascular complications is unknown. </li></ul><ul><li>?high glucose=toxicity to endothelial cells, increasing permeability allowing influx of lipids to form plaques. </li></ul>
    9. 10. Control <ul><li>Women have poorer metabolic control- IHD higher in women and higher mortality. </li></ul><ul><li>Women perform less exercise </li></ul><ul><li>Men report greater social support </li></ul><ul><li>Men get greater emotional support from spouses </li></ul><ul><li>? Gender specific approaches. </li></ul>
    10. 11. Incidence <ul><li>Higher rate in men than women but women have higher mortality- UK- </li></ul><ul><li>6 times more common in adults of southern Asian descent. </li></ul><ul><li>3 times more common in Afro-caribbeans </li></ul><ul><li>Highest in Prima Indians </li></ul><ul><li>Type 2-More common in those from social classes 4&5 not type 1. </li></ul>
    11. 12. Wales <ul><li>Audit commission Diabetes Services (2003) </li></ul><ul><li>Identified 93,000 diabetics in Wales compared to 1,966,000 England & 167,000 for Scotland. </li></ul><ul><li>National Public health Service For Wales (2007) lower in north and higher in south- combined rate of 5.3% of population. </li></ul>
    12. 14. Ethnicity <ul><li>India highest 32 million- 14% of population </li></ul><ul><li>Asia and Africa- 4.5% have Diabetes 35% MSy </li></ul><ul><li>USA 35% of population have Met Syndrome </li></ul><ul><li>France 7%, Spain 28%, Greece 19% ( 44% of population overweight) 37% pop smokers, link-low educational level especially women- western diet </li></ul><ul><li>UK-1.3-2.5% 1.8 million have diabetes </li></ul><ul><li>80% 45-59 yr olds will become obese (James 2004) </li></ul><ul><li>Sweden 2-4% </li></ul><ul><li>Globally 10% school age children-obese </li></ul>
    13. 15. Ethnicity <ul><li>Mexico-Latham & Calvillo (2007) </li></ul><ul><li>Emotional experience ( susto- fright) San Antonia Heart Study (2006) marital stress n=2,900 doubled incidence: treatment = herbs, prayers, ethnic food. </li></ul><ul><li>Beliefs- fatalism-impacts ability to self care and take responsibility. </li></ul><ul><li>In women dietry education had no effect as being thin = illness. Health =slightly overweight. </li></ul><ul><li>Strong link with control of Diabetes and good family support : women had lower HBA1C- men had higher lipid levels ( Gleason- Kreig 2002) </li></ul>
    14. 16. Xiae Ke- chinese <ul><li>Yin and Yan disregulation- caused by diet, anxiety, fatigue. </li></ul><ul><li>Yin vacuity,dryness and heat. Liver depressions transforms fire damaging viscera of kidneys, lungs and spleen. Treatment- regulate liver and enrich kidneys </li></ul><ul><li>Chai hu, sheng di, shan Zhu yu, shan yoa: restore essence and yin ( Radix) </li></ul><ul><li>1 st man made insulin was made in china in 1969. </li></ul><ul><li>( Flaws 2002) </li></ul>
    15. 17. Hjelm et al (2006) Gestational diabetes- swedish V middle east <ul><li>13 swedish: 14 Middle East ( diab2-4% in sweden-)Migration =Stress= increases blood glucose levels and reduces control= increased perinatal mortality morbidity. </li></ul><ul><li>Ability to manage stress linked to social support. </li></ul><ul><li>Swedish women perceived as disease wanted knowledge & competence but ME viewed as normal life wanted caring and supportive attitude, had limited knowledge of body did not wish to make decisions of be empowered- followed advice- swedish were questioning and not satisfied with information given. </li></ul>
    16. 18. Diabetes Risk factors and complications Tracy Ross What do people die from? What do diabetic people die from?
    17. 19. Deaths by cause in the general population, men aged 40-59 www.heartstats.org
    18. 20. Deaths by cause in people with diabetes, men aged 40-59, 1972/99, UK www.heartstats.org
    19. 21. Causes of Death in People with Diabetes Geiss et al., 200 5
    20. 22. Why Don ’ t many people die from Diabetes? <ul><li>Type 1- rapid onset- dramatic- seek help </li></ul><ul><li>Carry glucose </li></ul><ul><li>Education </li></ul><ul><li>Screening </li></ul><ul><li>Type 2- insiduous- symptoms similar to other illness ie dyspepsia </li></ul><ul><li>Don’t see rapid change until severe damage </li></ul>
    21. 23. Primary MVD Risk Factors <ul><li>Non-Modifiable Risks Modifiable Risks </li></ul>
    22. 24. <ul><li>89% of people with diabetes have modifiable risk factors - Hjelm et al (2003) Lifestyle disorder with some genetic susceptibility. </li></ul><ul><li>Smoking cessation reduces cardiovascular risk by half after 1 year & after 10years it is the same as an individual who has never smoked </li></ul>
    23. 25. Burden of Type 2 Diabetes <ul><li>Potential huge economic burden in terms of lost earnings </li></ul><ul><ul><li>(see T 2 ARDIS and CODE-2 UK papers on Diabetes UK website) </li></ul></ul><ul><li>Reduces life expectancy by around 7 to 10 years </li></ul><ul><li>Macrovascular disease causes greater than 70% of deaths - CVA, CHD, PVD </li></ul><ul><li>Microvascular disease immense cause of disability and suffering </li></ul><ul><ul><li>Retinopathy </li></ul></ul><ul><ul><li>Nephropathy and renal failure </li></ul></ul><ul><ul><li>Neuropathy + Metabolic complications </li></ul></ul>
    24. 26. Family history Relationship Type 2 Type 1 Mother 19% 2 Father 14% 9 Both 25% nil Sister &brother 75% 10% Twin 99% 50%
    25. 27. Risk Factors for Type 2 Diabetes <ul><li>Family history,age, Obesity - 80% Apples </li></ul><ul><li>Gestational Diabetes- 2-4% in UK- 40% </li></ul><ul><li>Social class 4&5 </li></ul><ul><li>Low birth weight </li></ul><ul><li>Gender- women disadvantaged in every way </li></ul><ul><li>(Whittemore et al 2005) incidence, management, support, depression, less exercise. </li></ul>
    26. 28. HbA 1c – relationship with CV risk 1% increase in HbA 1c 21% increase in diabetes-related deaths p<0.0001 14% increase in myocardial infarction p<0.0001 43% increase in peripheral vascular disease p<0.0001 Glycaemia increase Associated risk increase Stratton IM et al . BMJ 2000; 321: 405–12.
    27. 29. UKPDS (1998) <ul><li>For every % point decrease in HBA1C = 40% reduction in the risk of complications but despite the evidence many patients never achieve this due to the demand between self management demands V preferred lifestyle. </li></ul><ul><li>Internal V external locus of control </li></ul>
    28. 30. Clinical guidelines by RCP,RCN, RCGP (2000) <ul><li>The presence of raised urine albumin levels and serum creatinine in type 2 Diabetes is predictive of premature cardiovascular events and increases the risk of end stage renal failure. </li></ul><ul><li>Mortality is increased 4 fold in those with microalbinuria and 8 fold in those with proteinurea. 32% are dead within 5 yrs. </li></ul><ul><li>Microalbinuria is not present in those without Diabetes. </li></ul>
    29. 31. Risk of developing Type 2 diabetes with weight change Colditz GA, et al. Ann Intern Med 1995; 122: 481-486 (from Medicine 2003;31)
    30. 32. Type 2 diabetes – impact on CV risk Non-smoker, age 60 years 1. British Cardiac Society, British Hyperlipidaemia Society, British Hypertension Society, British Diabetic Association. Heart 1998; 80 (suppl 2): S1 – S29. CHD risk 15 – 30% over next 10 years CHD risk <15% over next 10 years CHD risk >30% over next 10 years No diabetes Diabetes SBP SBP TC: HDL TC: HDL 3 4 5 6 7 8 9 10 11 110 120 130 140 160 170 180 190 150 3 4 5 6 7 8 9 10 11 110 120 130 140 160 170 180 190 150
    31. 33. Smoking cessation for the secondary prevention of coronary heart disease J   Critchley and S   Capewell: The Cochrane Database of Systematic Reviews 2006 Issue 2 <ul><li>Twenty studies were included. </li></ul><ul><li>Patients with a diagnosis of coronary heart disease (including previous M.I. or angina). There was a 36% reduction in crude relative risk (RR) of mortality for those who quit smoking compared with those who continued to smoke (RR 0.64, 95% confidence interval (CI) 0.58 to 0.71). </li></ul>
    32. 34. Exercise and Diabetes <ul><li>BDA (2002) 30 minutes brisk walking 5 times per week- minimum, build it up, allow recovery. </li></ul><ul><li>Within personal capability & as part of normal routine and assess first for risk (WAG 2008). </li></ul><ul><li>Realistic, purposeful ie building something, gardening, housework, painting. </li></ul><ul><li>Do it to music, with others, cool down, warm up. </li></ul><ul><li>Choose options ie stairs,walking to school, work, fun. Pain is not gain. </li></ul><ul><li>Vary activities to exercise different muscle groups </li></ul>
    33. 35. Exercise 2 <ul><li>Strength, stamina and flexibility </li></ul><ul><li>Specificity- concentrating on 1 area not recommended </li></ul><ul><li>Cross training- total fitness-mix </li></ul><ul><li>Talk test </li></ul><ul><li>Sing- you could work harder </li></ul><ul><li>Talk- just right </li></ul><ul><li>Gasp- slow down </li></ul>
    34. 36. Exercise 3 <ul><li>Plan and monitor- BM pre and post </li></ul><ul><li>Do not use injection site areas. </li></ul><ul><li>Take fast acting carbohydrate snacks </li></ul><ul><li>Meal adjustments and bedtime snacks can prevent delayed hypos, check for ketones- should not exercise. </li></ul><ul><li>REST if ill. If viral do not exercise for 24hrs post recovery. If in doubt, wait it out. </li></ul>
    35. 37. Dyslipidaemia <ul><li>Women 10 yrs behind men in terms of risk due to oestrogen- higher total but HDL </li></ul><ul><li>Lipids not soluble so bind to proteins </li></ul><ul><li>Types: cholesterol made by liver & ingested- cell membranes </li></ul><ul><li>Fatty acids- saturated, mono and polyunsaturated. 3 fatty acids+ glycerol = triglyceride- pancreatitis </li></ul><ul><li>Cholesterol + triglycerides bind to protein= lipoprotein- LDL and HDL </li></ul>
    36. 38. lipids <ul><li>Low density lipoproteins- large take cholesterol from intestine to tissues-so ^ atheroma </li></ul><ul><li>High density lipoproteins- small take cholesterol back to the liver- benefitial </li></ul><ul><li>Familial Hyperlipidemia 1:500 xanthelasma </li></ul><ul><li>Targets NICE (2008) </li></ul><ul><li>Total cholesterol <4mmls, LDL <2mmols, HDL> 1 in males 1.2 females Triglycerides <1.77mmols </li></ul>
    37. 39. Treatments <ul><li>CVD Risk assessment ( 10 yr risk>20%), Diet modification. </li></ul><ul><li>Statin 40mgs daily ( Simvastatin or Pravastatin)- check LFT- increase to 80mgs if needed- block cholesterol production in the liver. </li></ul><ul><li>Fibrate ( Benzafibrate)- reduce triglycerides and raise HDL </li></ul><ul><li>Ezetimibe: Cholesterol absorption inhibitor ( ? Small risk of cancer- inconclusive evidence) </li></ul><ul><li>Bile acid sequestrants- colestipol- increase cholesterol conversion to bile </li></ul><ul><li>Nicotinic acid ( can affect glycaemic control) </li></ul><ul><li>All contraindicated in those with abnormal LFT </li></ul>
    38. 40. Influence of Multiple Risk Factors * on CVD Death Rate in Diabetics & Non-Diabetic Men <ul><li>* Systolic BP >120 mm Hg - Smoking - Serum Cholesterol > 200 mg/dl </li></ul>Stamler et al., 1993
    39. 41. <ul><li>Managing blood glucose is important, but in isolation it is not the key to preventing morbidity and mortality </li></ul><ul><li>MeReC Bulletin 2004; 15: 1-4 </li></ul>
    40. 42. Treating Type 2 diabetes Treat Reduce: Cardiovascular risk Microvascular complications Hyperglycaemia to achieve tight glycaemic control Insulin resistance – a root cause of Type 2 diabetes
    41. 43. Criticism- very medical- ? holism <ul><li>Whittemore et al (2005)- Increased risk of psychosocial distress and depression- results in poor self management and metabolic control. More common in women (Anderson et al 2001) </li></ul><ul><li>Hjelm et al (2003) </li></ul>
    42. 44. Management goals <ul><li>Holism </li></ul><ul><li>Team effort with patient and family </li></ul><ul><li>Increase internal LOC </li></ul><ul><li>Self management does not work for all </li></ul><ul><li>Move from sickness focus to prevention. </li></ul><ul><li>Culturally sensitive </li></ul>
    43. 45. Chronic Complications of Diabetes Nephropathy 16% of all new patients needing renal replacement therapy have diabetes Erectile Dysfunction May affect up to 50% of men with long-standing diabetes Retinopathy Most common cause of blindness in people of working age Macrovascular and Cerebrovascular Disease 2–3 fold increased risk of coronary heart disease and stroke Foot Problems 15% of people with diabetes develop foot ulcers; 5–15% of people with diabetic foot ulcers need amputations The Audit Commission. Testing Times. A Review of Diabetes Services in England and Wales, 2000.
    44. 46. Findings in the UKPDS 50% of newly presenting patients with type 2 diabetes already have one or more complications at diagnosis Retinopathy : 21% Hypertension : 35% Stroke or TIA: 7% Absent f oot pulses: 13% Intermittent claudication: 3% Ischaemic skin changes to feet: 6% Erectile dysfunction: 20% Plasma creatinine >120  mol/l: 3% Myocardial Infarction: 1% Abnormal ECG: 18% UKPDS Group. Diabetes Research 1990;13:1–11.
    45. 47. Retinopathy <ul><li>5% of world blindness & leading cause of avoidable blindness (WHO 2007).Retina is the seeing part of the eye& direct continuation of brain- connected by optic nerve. </li></ul><ul><li>Has highest O2 consumption than any other tissue </li></ul><ul><li>Why? Glucose causes membrane to thicken preventing the flow of nutrients entering and exiting cells. These damaged cells then release chemicals that encourage the formation of new vessels that are weak and leak fluids. </li></ul>
    46. 48. Eye Retina
    47. 49. Light sensitive tissue at back of eye <ul><li>Weakened blood vessels have incompetent vascular walls which become permeable & leak preventing nerve cells transmitting images to brain. New vessels grow around optic nerve & bleed. </li></ul>
    48. 50. 3 types <ul><li>Background - microaneurysms-red dots on Retina, proteins leak and form yellow patches at back of eye- may see slight bulging- need no treatment. </li></ul><ul><li>Maculopathy - Retina swells and leaks blood- first signs- difficulty reading small print- normally no treatment- ? Laser. </li></ul><ul><li>Proliferative - severe vitreous bleeding, fibrous strands grow, form scar tissue and contract pulling Retina off. Appears like a black cloud , difficulty seeing faces, painless, dark streaks, poor night vision. Permanent damage. </li></ul>
    49. 52. Treatments <ul><li>National screening programme as part of NSF (2003)- at diagnosis, then annual, plus visual acuity testing or if any sudden drop in acuity </li></ul><ul><li>Laser- In proliferative- Targets outer retina,burns abnormal vessels to prevent growth, only destroys vessels deprived of O2 so doesn’t restore vision but prevents deterioration. </li></ul><ul><li>Scatter laser- Panretinal Photocoagulation- hundreds of small laser burns from center- lose peripheral vision but saves center. Can cause reduced colour and night vision. </li></ul>
    50. 53. Virectomy <ul><li>Surgery under local-for vitreous bleeding- vitreous is removed and replaced with a saline solution. </li></ul><ul><li>Neovascular Glaucoma- abnormal blood vessels grow into the iris ( coloured part that controls how much light enters) disrupts the flow of fluids causing rise in pressure- causes permanent damage to the optic nerve. </li></ul>
    51. 54. Hypertension <ul><li>Prevalence of hypertension in type 2 diabetes is higher than that in the general population </li></ul><ul><li>Hypertension (>140/90 mmHg) is present in over 70% of people with type 2 diabetes </li></ul><ul><li>Hypertension increases the already high risk of cardiovascular disease associated with type 2 diabetes </li></ul>UKPDS 38. British Medical Journal 1998;317:703  713 British Hypertension Society. Journal of Human Hypertension 1999;13:569  592
    52. 55. What BP targets? <ul><li>NICE: </li></ul><ul><li>No proteinuria - below 140/80mmHg </li></ul><ul><li>Microalbuminuria/proteinuria – below 135/75mmHg </li></ul><ul><li>BHS: </li></ul><ul><li>No proteinuria – below 130/80mmHg </li></ul><ul><li>Microalbuminuria/Proteinuria – below 125/75mmHg </li></ul><ul><li>QoF: </li></ul><ul><li>90% of people with diabetes with a record of their BP within the past 15 months = 3 points </li></ul><ul><li>55% with BP ≤ 145/85 mmHg = 17 points </li></ul>
    53. 56. UKPDS – benefits of tight blood pressure control – risk of complications reduced? UKPDS 36. BMJ 2000; 321: 412 – 19. 10 mmHg lower systolic blood pressure 12% lower risk of myocardial infarction 19% lower risk of stroke 15% lower risk of heart failure 17% lower risk of diabetes-related deaths
    54. 57. Which Agent? NICE hypertension guidelines June 2006 <ul><li>Drug therapy should normally begin with a low-dose thiazide-type diuretic </li></ul>Where possible, recommend once-daily drugs Prescribe generics, where appropriate, and minimise costs
    55. 58. The UK Prospective Diabetes Study UKPDS- A pragmatic trial <ul><li>1977 through to 1991, 23 study centres. Stopped 1997 </li></ul><ul><li>Recruited 5,102 newly diagnosed diabetics, aged 25 to 65 (Fasting BG > 6mmol/l) </li></ul><ul><li>Initially treated for 3 months with diet and advice </li></ul><ul><li>Three main components: </li></ul><ul><ul><li>UKPDS 34 – Overweight patients and metformin </li></ul></ul><ul><ul><li>UKPDS 33 - Blood glucose control </li></ul></ul><ul><ul><li>UKPDS 38 - Blood pressure control </li></ul></ul>
    56. 59. Why do Patients With Type 2 Diabetes Develop Cardiovascular Disease? Hypertension Obesity Raised LDL cholesterol Low HDL cholesterol Hypertriglyceridaemia       Type 2 Diabetes Cardiovascular Disease Risk
    57. 60. Insulin resistance <ul><li>Prolonged elevated insulin levels age the metabolism on a cellular level which results in disease. </li></ul><ul><li>Microvascular complications are less common than in type 1 but still occur. </li></ul><ul><li>Higher risk of large vessel atherosclerosis. </li></ul><ul><li>Precise mechanisms linking hyperglycaemia and vascular complications is unknown. </li></ul><ul><li>?high glucose=toxicity to endothelial cells, increasing permeability allowing influx of lipids to form placques. </li></ul>
    58. 61. Clinical guidelines by RCP,RCN, RCGP (2000) <ul><li>The presence of raised urine albumin levels and serum creatinine in type 2 Diabetes is predictive of premature cardiovascular events and increases the risk of end stage renal failure. </li></ul><ul><li>Mortality is increased 4 fold in those with microalbinuria and 8 fold in those with proteinurea. 32% are dead within 5 yrs. </li></ul>
    59. 62. Role of statins in type-2 diabetes? <ul><li>Benefits appear to be around a 20-30% relative risk reduction regardless of age, gender, lipid levels. </li></ul><ul><li>Which statin: </li></ul><ul><ul><li>Evidence is for simvastatin 40mg/day or atovastatin 10mg/day </li></ul></ul><ul><ul><li>NICE recommends the most cost effective statin i.e. simvastatin </li></ul></ul><ul><ul><li>Safety concerns with rosuvastatin </li></ul></ul>
    60. 64. NICE Inherited Clinical Guideline Management of blood glucose – general (Sept 2002) <ul><li>Measure HbA1c 2-to-6 monthly (depending on control, changes to Rx etc.) </li></ul><ul><li>Set target between 6.5% and 7.5% </li></ul><ul><ul><li><6.5% hypoglycaemia risk may outweigh benefits </li></ul></ul><ul><ul><li>>7.5% sig. risk of macrovascular complications </li></ul></ul><ul><li>Self-monitoring BG if “integrated self-care” </li></ul><ul><li>Encourage weight loss and increased physical activity (in overweight), find approaches to lifestyle which are most likely to work! </li></ul><ul><li>Importance of patient education </li></ul>
    61. 65. Challenging blood glucose testing in Type 2 Diabetes. See MeReC Bulletin 2002; 13: 1-4 <ul><li>The ideal frequency of testing is not known </li></ul><ul><li>No evidence that blood testing is better than urine testing: </li></ul><ul><ul><li>Urine testing is easier and often preferred by patients with type-II diabetes </li></ul></ul><ul><li>Those with type-I seem to prefer blood glucose testing to give them a sense of control of their illness </li></ul><ul><li>HbA1c may be more relevant to outcome </li></ul>
    62. 66. NSF Diabetes 12 Standards <ul><li>Prevention of Type 2 </li></ul><ul><li>Identification of people with diabetes </li></ul><ul><li>Empowering people with diabetes </li></ul><ul><li>Clinical care of adults with diabetes </li></ul><ul><li>Children </li></ul><ul><li>Smooth Transition of young people </li></ul><ul><li>Management of Diabetic emergencies </li></ul><ul><li>Care of people with diabetes during admission to hospital </li></ul><ul><li>Diabetes & Pregnancy </li></ul><ul><li>Detection & mgt long term complications </li></ul><ul><ul><li>Surveillance </li></ul></ul><ul><ul><li>Treatment </li></ul></ul><ul><ul><li>All people with diabetes requiring multi-agency support will receive integrated health & social care </li></ul></ul>
    63. 67. Aspirin <ul><li>HOT study </li></ul><ul><ul><li>Aspirin 75 mg once daily </li></ul></ul><ul><ul><li>Reduced CVD by 15% </li></ul></ul><ul><li>Reduced MI by 36% </li></ul><ul><li>In patients with Diabetes Mellitus there was a 51% reduction in target group <80 mmHg </li></ul>Hansson L, et al. Lancet 1998;351:1755  1762
    64. 68. Conwy and Denbighshire Guidance <ul><li>Treat all people with type 2 diabetes as secondary prevention. </li></ul><ul><li>Initiate simvastatin 20mg or 40mg at night </li></ul><ul><li>New BHS guidelines have no separate risk charts for people with diabetes. </li></ul>
    65. 69. Anti-platelets <ul><li>Aspirin 75mg dispersible should be given to people with type 2 diabetes if they are: </li></ul><ul><ul><li>aged over 50 or </li></ul></ul><ul><ul><li>have had DM for >10 years, </li></ul></ul><ul><li>plus controlled systolic BP (<145). </li></ul>
    66. 70. Clopidogrel in people with diabetes? MeReC Briefing August 2004; 26 <ul><li>There are no trials specifically studying clopidogrel in patients with diabetes, particularly in the primary prevention of CVD. </li></ul><ul><li>There is no evidence to suggest that clopidogrel has any advantages over aspirin in a diabetic population. </li></ul><ul><li>Clopidogrel should not be used routinely in patients with type 2 diabetes who require antiplatelet treatment. </li></ul><ul><li>It is more expensive than aspirin, and should only be considered if people are truly intolerant of aspirin. </li></ul>
    67. 71. Summary <ul><li>Think CV risk, not blood glucose </li></ul><ul><li>Treating blood pressure is more important than worrying about drug choice. </li></ul><ul><ul><li>Low dose thiazides are safe and well tolerated (ALLHAT). </li></ul></ul><ul><ul><li>ACE inhibitors also a reasonable first choice. </li></ul></ul><ul><ul><li>Many will need combinations to achieve target BP </li></ul></ul><ul><ul><li>Is the emphasis on tight blood glucose control justified by the evidence? </li></ul></ul><ul><ul><li>Metformin in everyone with Type-2 DM? </li></ul></ul><ul><ul><li>Do patients really need to self monitor their blood glucose as often as they do? </li></ul></ul><ul><li>Manage overall risk (which is close to that with established CHD) </li></ul><ul><li>Polypharmacy is the norm! (and needs support) </li></ul>
    68. 72. Inpatients with Diabetes Figs from menu audit of one week 2003. C&D Trust pop. 240,000
    69. 73. W.H.O Diagnostic Criteria for Diabetes <ul><li>Random plasma glucose 11.1mmol/l </li></ul><ul><li>Fasting plasma glucose 7.0mmol/l </li></ul><ul><li>2hour plasma glucose 11.1mmol/l </li></ul><ul><li>Confirm by venous samples -medical & legal implications </li></ul><ul><li>Do not use Hba1c </li></ul>