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31 Cards in this Set
- Front
- Back
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How MetS->hypertension (x3) |
1. RAS activated by hyperglycemia&hyperinsulinemia 2. SNS actv by insulin resistance&hyperinsulinaemia>increased Na teabsorption & increase CO &vasoconstriction 3. Adipocytes produce alsosterone in response ATII |
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How insulin resistance>increased FFA and effect this liver |
Increased lipolysis FFA substrate for synthesis TG FFA stabilise production apoB so more VLDL |
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Insulin resistance decreases PI3K-dependent pathway what is the effect of this |
Decreased degradation ApoB -> increased VLDL production |
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Insulin regulates LPL activity so insulin resistance->decreased activity and decreased VLDL clearance. What is the downstream effects of this? |
1.VLDL mobilised to remnant lipoproteins & small dense LDL>atheroma formation 2.VLDL TG transferred to HDL in exchange CEs>C enriched HDL>Cleared rapidly from circ as is better substrate hepatic lipase |
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Overall effects insulin resistance on dyslipidaemia |
FFA high, TG synthesis & storage high, excess TG secreted as VLDL Leads increased oxidative stress and endothelial dysfunction |
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What is Neel's 1962 Thrifty Gene Hypothesis? |
Individuals living in a harsh environment with an unstable food supply would maximise their probability of aurvival if they could maximise a storage of aurplus E. Genetic selection would thus favour the E-conserving genotypes in such environments |
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Effect of high dietary fat |
High dietary fat shown to be assc with an oxidative stress and an activation proinflam TF NFkappaB |
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Describe how increased abdominal obesity leads to systemic inflammation |
Increasing size adipocytes Insufficient blood supply Tissue necrosis Infiltration macrophages leading to overproduction biologically active metabolites resulting local inflammation that propagates overall systemic inflammation assc with devt obesity-related comorbidities |
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Adipocyrokines integrate the endocrine, autocrine and paracrine adipocytokine signals to mediate what processes? |
Insulin sensitivity Oxidang stress Energy metabolism Blood coagulation Inflammatory responses |
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What processes do insulin senstv, oxidant stress, E metabolism, blood coag &inflam response accelerate? |
Atherosclerosis Plaque rupture Atherothrombosis |
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3 effects FFAs |
1.acute exposure muscle:insulin resistance 2.long-term exposure pancreas: impair pancreatic beta cell function 3. Increased fibrinogen production |
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Role TNFalpha in atherogenic dyslipidaemia Assc TNFalpha w/ HDL-C |
TNF-alpha exacerbate FFA release ->atherogenic dyslipidaemia Neg assc w/HDL-C |
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What is high CRP indicative of? |
Greater chance CVD event |
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Describe 3 roles IL-6 in MetS |
1.Hypothalamic comtrol appetite &E intake 2.Impair insulin sensitivity 3.Capable suppress LPL activity |
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4 positive roles adiponectin What adipokyne decreases its expression? |
1. Inhibit hepatic gluconeogenic enzymes 2. Inhibit endothelial actv 3. Reduce macrophage>foam 4.inhibit smooth muscle prolif&arterial remodelling that characterises devt plaque TNFalpha |
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Brain roles leptin Leptin effect on BP |
Satiety, E exp, neuroendocrine funct Increase BP through actv SNS |
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Two pathways actv with insulin bindind. What involved in each and which affected by insulin resistance |
Phosphoinositide 3-kinase(PI3K)NO prodn&GLUT4 translocation & Mitogen activated protein kinase (MAPK)-vascular cell adhesion molc PI3K path affected>vascular abnormalities predisposing to atherosclerosis |
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When should pharmacological treatment be used in MetS |
For those whose risk factors aren't adequately reduced with preventative measures and lifestyle changes |
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Who is bariatric surgery used for? |
Indv who don't respond weight loss or meds Extremely obese (BMI>40) BMI>35-40 &1 or more comorbid conditions |
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What drug class used for decreasing LDL-C? For hypertension? |
Statins Antihypertensives |
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3 pharmaceutical ls used prevent T2DM |
Metformin Thiazolidinediones Arcabose |
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Action of Metformin |
Reduce hepatic goucose production |
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Gold standard weight loss and exercise goals |
Reduce BW bt >7-10%over 6-12 months 30min daily moderate-intense physical activity |
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5 public health options managing MetS |
1.educate 2.regulate consumer behv via price 3. Regulate foods (composition, prep &pt of sale ( 4. Regulate advertising 5. Economic policy to reduce price fresh food at expense fast food |
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Role alpha-MSH |
Tonic inhibition hunger signal via binding MC4R AGRP is endogenous competitive antagonist (levels regulated by feeding status and leptin) |
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What does NPY do? What regulates it? What receptors implicated? |
Stimulate feeding in satiated animals Reduces E exp Level regulated by leptin and changes with feeding status Y1,2(auto),5 receptors |
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Genetics of obesity |
Heritability estimates ranging 50-90% BMI adopted correlated biological >250 genes assc obesity Rise obesity suggests purely genetics unlikely |
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Describe importance ghrelin and leptin in terms nesolimbic dopaminergic reward pathway that is activated in response palatable food (VTA to NAc) |
Ghrelin stimulates activity VTA dopaminergic neurons Leptin inhibits activity |
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4 facets MetS |
Dyslipidaemia Hypertension Abnormal abdo obesity Hyperglycemia |
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Ket challenges of TE |
Blood supply Infection control Distribution signalling molc Suitability biomimetic materials |
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Substances used coat PLGA surface to prevent FBR |
HLA & Chitosan |
