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Metabolic syndrome
- 1. RIFT VALLEY UNIVERSITY ABICHU CAMPUS DEPARTMENT OF MATERS OF ADULT HEALTH NURSING TOPIC: METABOLIC SYNDROME PRESENTER: GETU ENJIGU DEBELA SUBMITTED TO INST. DANIEL January 2021, ADDIS ABABA, ETHIOPIA
- 3. Definition …. The metabolic syndrome is a constellation of interrelated abnormalities that increase the risk for cardiovascular disease and type 2 diabetes. clustering of at least three of the following five medical conditions: abdominal obesity, high blood pressure, high blood sugar, high serum triglycerides, and low serum high-density lipoprotein (HDL)
- 4. Definition Diagnostic criteria: A. World Health Organisation, 1998 Diabetes or impaired fasting glycemia or impaired glucose tolerance or insulin resistance, Plus any two of the following: Obesity Dyslipidaemia Hypertension Microalbuminuria
- 5. Definition…Diagnostic criteria: B. National Cholesterol Education Program's Adult Treatment Panel III (NCEP: ATP III), 2001 Any 3 of the following: Central obesity (abdominal obesity) Hypertriglyceridaemia: triglycerides ≥ 150mg/dl Low HDL cholesterol: < 40mg/dl (male), 50mg/dl (female) Hypertension: blood pressure ≥ 135/85 mm Hg or medication Fasting plasma glucose ≥ (100 mg/dl)
- 6. Definition…Diagnostic criteria: C. International Diabetes Federation, 2005 Central obesity, Plus any two of the following: Raised triglycerides > 150mg/dl, or specific treatment for this lipid abnormality Reduced HDL (< 40mg/dl for male, <50mg/dl for female)or specific treatment for this lipid abnormality Raised blood pressure: SBP ≥ 130mmHg or DBP ≥ 85 mmHg Raised FPG ≥(100mg/dl), or previously diagnosed diabetes mellitus
- 7. Definition…Diagnostic criteria: D. European group for the study of insulin resistance (EGIR): Insulin resistance defined as the top 25% of the fasting insulin values among nondiabetic individuals AND two or more of the following: Central obesity: waist circumference ≥ 94 cm or 37 inches (male), ≥ 80 cm or 31.5 inches (female) Dyslipidemia: TG ≥ 2.0 mmol/L and/or HDL-C < 1.0 mmol/L or treated for dyslipidemia Blood pressure ≥ 140/90 mmHg or antihypertensive medication Fasting plasma glucose ≥ 6.1 mmol/L
- 8. pathophysiology 1, Insulin resistance Most accepted hypothesis That is why metabolic syndrome is also known as the insulin resistance syndrome A defect in insulin action results in hyperinsulinemia, hyperglycaemia, hypertension, increased FFA
- 9. Pathophysiology… Insulin resistance Expanded adipose tissue mass ˃ circulating free fatty acids (FFA) ˃ insulin resistance In muscle: FFA inhibits insulin-mediated glucose uptake ˃ reduces insulin sensitivity ˃ increase circulating glucose ˃ hyperinsulinemia In the liver: FFA increases the production of glucose, triglycerides, and secretion of very-low-density lipoproteins (VLDL) ˃ increase lipid accumulation
- 10. Pathophysiology… 2. Increased waist circumference (visceral obesity) Increase adipose tissue and abdominal subcutaneous fat ˃ increase adipokines (TNFα and IL-6) and decreases Adiponectin releases ˃ insulin resistance and vascular dysfunction. The RAS is also activated in adipose tissue, leading to hypertension and insulin resistance.
- 11. Pathophysiology… 3. Dyslipidaemia high plasma TG levels, low HDL cholesterol levels and an increase in LDL Insulin resistance and visceral obesity are associated with dyslipidemia impaired insulin signaling increases lipolysis, resulting in increased FFA levels. In the liver, FFAs serve as a substrate for synthesis of TGs. FFAs also stabilize the production of apoB, the major lipoprotein of very-low-density lipoprotein (VLDL) particles, resulting in more VLDL production.
- 12. Pathophysiology… 4. Glucose intolerance The defects of insulin action ˃ failure to suppress gluconeogenesis in the liver, hyperglycemia occurs.
- 13. Pathophysiology… 5. Hypertension Insulin has a vasodilation effect. ( by stimulating NO production in endothelium) Regulates sodium homeostasis by enhancing sodium reabsorption in the kidney In the setting of insulin resistance, the vasodilatory and sodium homeostasis effect of insulin can be lost, Fatty acids themselves can mediate relative vasoconstriction. Development of hypertension.
- 14. Risk factors The etiology for metabolic syndrome remains unclear. known risk factors include: Overweight/obesity Sedentary lifestyle Aging
- 15. Risk factors … Diabetes mellitus Coronary heart disease: The approximate prevalence of metabolic syndrome in patients with coronary heart disease (CHD) is 50%. Lipodystrophy Family history of metabolic syndrome
- 16. Clinical manifestation Central obesity: It is characterized by adipose tissue accumulation predominantly around the waist and trunk. Other signs of metabolic syndrome include High blood pressure Decreased fasting serum HDL cholesterol Elevated fasting serum triglyceride level Impaired fasting glucose or prediabetes.
- 17. Associated conditions (complications) Cardiovascular disease: The relative risk averages between 1.5-fold and threefold. Type 2 diabetes: three- to fivefold. Non-alcoholic fatty liver disease Hyperuricemia Polycystic ovary syndrome Obstructive sleep apnea
- 18. Associated conditions (complications)… Atherosclerosis Kidney disease Peripheral artery disease Stroke
- 19. Management Primary intervention: Healthy lifestyle (lifestyle modification). This includes: moderate calorie restriction (to achieve a 5–10 percent loss of body weight in the first year) Exercise: moderate increase in physical activity Diet: change in dietary composition. Mediterranean diet (high in fruits, vegetables, nuts, whole grains, and olive oil)
- 20. Management… Dietary Approaches to Stop Hypertension (DASH) high fiber diet (≥30 g/day)
- 21. Management…. stop smoking limit alcohol intake
- 22. Management… Secondary intervention Drug therapy To treat the individual components of the syndrome reduce the overall impact on CVD and diabetes risk.
- 23. Management… Recommended treatment of the individual components of the metabolic syndrome:- 1. Dyslipidaemia: the primary goal Lower TG Raise HDL-c levels Reduce LDL-c levels Drugs: Fibrates and statins The recommended
- 24. Management… 2. Elevated blood pressure At: BP ≥ 140/≥ 90 mm Hg BP ≥ 130/≥ 80 mm Hg for established diabetes Antihypertensive drugs
- 25. Management… 3. Insulin resistance and hyperglycemia Metformin therapy in people with prediabetes will prevent or delay the development of diabetes Thiazolidinedione: delay or prevent type 2 diabetes in people with impaired glucose tolerance (IGT) and insulin resistance.
- 26. Nursing Management… Nursing diagnosis Imbalanced Nutrition more than Body Requirements Risk for Unstable Blood Glucose Knowledge deficit
- 27. Nursing Management… Nursing goals: The client will identify inappropriate behaviors and consequences associated with overeating or weight gain. The patient will achieve and maintain glucose in a satisfactory range
- 28. Nursing Management… Nursing interventions: Review individual causes for obesity Explore and discuss emotions and events associated with eating. Teach the patient how to perform home glucose monitoring Advise patients to increase physical activity to reduce their weight and improve blood pressure. Teach patients about the link between smoking and CVD and refer them to smoking-cessation resources. Advise patient to limit alcohol
- 29. THANK YOU
Editor's Notes
- Metabolic syndrome is a clustering of at least three of the following five medical conditions: abdominal obesity, high blood pressure, high blood sugar, high serum triglycerides, and low serum high-density lipoprotein (HDL) most commonly used definitions of metabolic syndrome are
- World Health Organisation, 1998 Because insulin resistance was felt to be central to the pathophysiology of metabolic syndrome, evidence for insulin resistance is an absolute requirement in the WHO definition. Diabetes or impaired fasting glycaemia ( greater than100mg/dl) or impaired glucose tolerance (greater than 140mg/dl) or insulin resistance (hyperinsulinaemic, euglycaemic clamp-glucose uptake in lowest 25%) Plus any two of the following: Obesity: BMI > 30 or waist-to-hip ratio > 0.9 (male) or > 0.85 (female) Dyslipidaemia: triglycerides ≥ 1.7 mmol/L or HDL cholesterol < 0.9 (male) or < 1.0 (female) mmol/L Hypertension: blood pressure > 140/90 mm Hg Microalbuminuria: albumin excretion > 20 μg/min
- According to the NCEP ATP III definition, metabolic syndrome is present if three or more of the following five criteria are met: waist circumference over 40 inches (men) or 35 inches (women), fasting triglyceride (TG) level over 150 mg/dl (HDL) cholesterol level less than 40 mg/dl (men) or 50 mg/dl (women) Hypertension: blood pressure ≥ 130/85 mm Hg or medication fasting blood sugar over 100 mg/dl. it does not require that any specific criterion be met; only that at least three of five criteria are met.
- International Diabetes Federation, 2005 it requires that obesity, but not necessarily insulin resistance, be present. Central obesity (defined as waist circumference ≥ 94 cm for Europoid men and ≥ 80 cm for Europoid women) Plus any two of the following: Raised triglycerides > 1.7 mmol/L, or specific treatement for this lipid abnormality Reduced HDL cholesterol: < 1.03 mmol/L in males, and 1.29 mmol/L in females, or specific treatement for this lipid abnormality Raised blood pressure: systolic blood pressure ≥ 130mmHg or diastolic blood pressure ≥ 85 mmHg Raised fasting plasma glucose ≥ 5.6 mmol/L, or previously diagnosed diabetes mellitus
- The normal range of fasting insulin is between 2 to 20milli- international unit/L
- Insulin resistance occurs when there is a decrease in the responsiveness of peripheral tissues (skeletal muscle, fat and liver) to the effects of insulin. The most accepted hypothesis to describe the pathophysiology of the metabolic syndrome is insulin resistance. That is why the metabolic syndrome is also known as the insulin resistance syndrome. Insulin resistance has been defined as a defect in insulin action that results in hyperinsulinaemia, necessary to maintain euglycaemia. Hyperinsulinemia : deuto pancrease produce extra insulin for insulin resistance compensation,,,,, hypertention dueto sodium reabsorption impairement by kidney NO production inhibition that result in vasoconstriction,,,,, FFA from breakdown of fat for energy production
- A major contributor to the development of insulin resistance is an overabundance of circulating fatty acids, released from an expanded adipose tissue mass. FFA reduce insulin sensitivity in muscle by inhibiting insulin-mediated glucose uptake. Increased level of circulating glucose increases pancreatic insulin secretion resulting in hyperinsulinemia.˃˃ In the liver, FFA increase the production of glucose, triglycerides and secretion of very low density lipoproteins (VLDL). The consequence is the reduction in glucose transformation to glycogen and increased lipid accumulation in triglyceride (TG).
- Visceral obesity causes a decrease in insulin-mediated glucose uptake, and is clearly related to insulin resistance. produced by adipose tissue These include tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) cytokines , which are proinflammatory and contribute to insulin resistance and vascular dysfunction. Adiponectin fat derived hormone that protecting against insulin resistance and atherosclerosis and obesity reduce adinopectin sensitivity If RAS activated sodium reabsorption and water retention by kidney .
- Under physiological conditions, insulin inhibits the secretion of VLDL into the systemic circulation. In the setting of insulin resistance, increased flux of free fatty acids to The key features of atherogenic dyslipidemia are high plasma TG levels, low HDL cholesterol levels and an increase in small dense LDL. insulin normally suppresses lipolysis in adipocytes, so impaired insulin signaling increases lipolysis, resulting in increased FFA levels. In the liver, FFAs serve as a substrate for synthesis of TGs. FFAs also stabilize the production of apoB, the major lipoprotein of very-low-density lipoprotein (VLDL) particles, resulting in more VLDL production.
- The defects of insulin action in glucose metabolism include failure to suppress gluconeogenesis in the liver, and to mediate glucose uptake in insulin sensitive tissues (i.e. muscle and adipose tissue). To compensate for defects in insulin action, insulin secretion must be increased to sustain euglycaemia. If this compensation fails, defects in insulin secretion predominate and hyperglycaemia occurs.
- First, insulin is a vasodilator when given intravenously to people of normal weight, with secondary effects on sodium reabsorption in the kidney. In the setting of insulin resistance, the vasodilatory effect of insulin can be lost, these contribute to increased renal sodium reabsorption which associated with fluid retention and hypertention . Fatty acids themselves can mediate relative vasoconstriction. contribute to the development of hypertension.
- Centrally accumulation of body fat is associated with insulin resistance Overweight people tend to develop a resistance to insulin Sedentary lifestyle metabolic syndrome are associated with a sedentary lifestyle, due to increased risk of adipose tissue (predominantly central), reduced HDL cholesterol, high blood pressure, and increased glucose in the genetically susceptible. The prevalence of metabolic syndrome increases with age, with about 40% of people older than 60 years
- It is estimated that the great majority (∼75%) of patients with Type 2 diabetes or impaired glucose tolerance (IGT) have the metabolic syndrome. Lipodystrophy syndromes are a group of genetic or acquired disorders in which the body is unable to produce and maintain healthy fat tissue.
- The key sign of metabolic syndrome is central obesity, also known as visceral, male-pattern or apple-shaped adiposity. • It is characterized by adipose tissue accumulation predominantly around the waist and trunk. Other signs of metabolic syndrome include • High blood pressure • Decreased fasting serum HDL cholesterol • Elevated fasting serum triglyceride level • Impaired fasting glucose, insulin resistance, or prediabetes.
- The relative risk for new-onset CVD in patients with the metabolic syndrome, in the absence of diabetes, averages between 1.5-fold and threefold. Overall, the risk for Type 2 diabetes in patients with the metabolic syndrome is increased three- to fivefold. Hyperuricemia Hyperuricemia reflects defects in insulin action on the renal tubular reabsorption of uric acid, PCOS is due to insulin resistance contributes to inhibit liver sex hormone binding globulin (SHBG) production and stimulate ovarian/adrenal androgen secretion.
- gradual increases in physical activity should be encouraged to enhance adherence and avoid injury Diets restricted in carbohydrate typically provide a rapid initial weight loss.
- daily sodium intake limited to 2400 mg high fiber diet (≥30 g/day) resulted in similar weight loss as compared with a more complex diet
- Secondary intervention In people for whom lifestyle change is not enough and who are considered to be at high risk for CVD, drug therapy may be required to treat the metabolic syndrome. to treat the individual components of the syndrome in order that a lower individual risk associated with each component will reduce the overall impact on CVD and diabetes risk.
- lower the level of low-density lipoprotein (LDL) cholesterol in the blood by blocking a substance the body needs to make cholesterol. Fibrates: help to lower high triglyceride levels and also may help raise HDL (good) cholesterol.
- Categorical hypertension (BP ≥ 140/≥ 90 mm Hg) should be treated. In patients with established diabetes, antihypertensive therapy should be introduced at BP ≥ 130/≥ 80 mm Hg
- drugs that reduce insulin resistance will delay the onset of type 2 diabetes and will reduce CVD risk when metabolic syndrome is present.