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IOS 9 Exam 4

Pathophysiology of metabolic syndrome

QuestionAnswer
Abnormalities of metabolic syndrome Central obesity, Atherosclerotic dysfunction, HTN, Glucose intolerance/resistance
Clinical outcomes of metabolic syndrome Have a 7x risk for developing DM, CVD 3.2 risk, PCOD, Fatty liver, Asthma, Sleep Apnea
Pathophysiology of metabolic syndrome Unlikely that a single defect is responsible for causing the metabolic syndrome but 2 key- Insulin resistance, central obesity
NCEP ATP II Metabolic criteria Abdominal obesity>102men >88wom, TG>150 or on treat, HDL <40men <50 wom or on treat, BP<130/85 on treat, FPG >100mg/dL or on treat
Traditional View of adipose tissue Conservation of heat, energy storage, cushion around organs
Contemporary View Metabolically active-release cytokin, decrease adiponectin (insulin resistance) Increase inflammation & Thrombosis, increase TG, decrease LDL, HDL, insulin resistance
Visceral Fat is more Metabolicallu active due to Larger cells that produce more lipolysis products and thus have greater amounts of insulin resistance and increase pro-inflammatory mediators
Insulin resistance and increased FFA relationship In sasal lipolysis small amounts of FFA are rlease, in obesity high amounts are release into curculation leading to lipotoxcity causing overload in muscle, liver cells leading to resistance and increase in Small Dense LDL-C as well as decrease in HDL
Proinflammatory mediators implicated in metabolic syndrome are Obesity is state of low grade inflammation, visceral release 2-3x IL-6 (stimulates ) C-reactive protein (marker if inflam & CVD predictor) TNF alpha (monocytes & MAc's) promote insulin resistance (decrease glucose transport)
Prothrombotic mediators associated with metabolic syndrome Defects in coagulation and fibrinolytic system are associated with metabolic risk factos: Plasminogen activator inhibitor-Type 1 (coagulation), Fibrogenm Factor VII, PLT absnormalities
Adiponectin inhibition in metabolic syndrome causes Normally a protective cytokine causes Loss =Liver-increase in FFA, Glucose, decrease in FA oxidation, decrease in insulin sensitivity, Muscle decrease in glucose utilization, Vacular wall- increase monocyte adhesion, increase migrating SMC, increase foam
Primary Site of insulin resistance in Type 2 impaired skeletal muscle cells (80% are resistant- 25% of non-diabetic are as well)
Secondary sites of insulin resistance are Liver and Adipose tissues
Insulin Resistance Decreases Skeletal muscle uptake of glucose, increases hepatic glucose production and lipolysis in adipose tissue
Risks for insulin resistance Obesity, sednetary lifestyle, genetics, diet, concomitant drug therapy
MOA of insulin resistance Compensatory hyperinsulemia,-Decreased in number of insulin receptors or affinity, alterations in glucose transport into cell, defects in insulin signaling MAP(mitogen activated protein) or PIK (phosphatidaylinosine kinase
Insulin resistance test is There is not a clinical test due to standardization issues & not cut points, there are invasive, costly and lengthy
Asian American have revised ATP III criteria Waist for men>90cm and women >80cm
Advantages of diagnosising Metabolic syndrome Reduce the risk of CVD and DM plus both fields are united
Disadvantage of diagnosising metabolic syndrome Does not account for FHx, smoking Age, LDL, and not short term risk assessment
Treatment of metabolic syndrome is Weight reduction and exercise and drug treatment to target Bp, LDL, ASA, in future Rimonabant
Created by: liza001
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