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127 Cards in this Set
- Front
- Back
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what is the eq of BMI
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wt/ht^2
kg/m^2 |
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what is the BMI range for overwt
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25-29.9
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what is the BMI range for obesity
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30 - 39.9
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what is the BMI range for extreme obesity
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over 40
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what is the BMI for underwt
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less than 18.5
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how is BMI assessed in children
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via a BMI curve
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high intraabdominal fat is correleated with
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higher liver fat
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how can liver fat be imaged
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grey looking (instead of black) liver on MRI
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as enviromental factors incr risk of obesity incr
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indv with higher initial BMI will have a greatere incr in wt than indv with lower inital BMI
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what group has highest rate of obesity
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black females
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at any given BMI z score,
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south asians have a higher fractional body fat content that other ethnic group
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what is the prevalance of obesity
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72 million americans
33% overwt |
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when you reduce the body wt of an animal
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the BMR dcr b/c the animal b/cs more metabolically efficent
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body wt (fat mass) is regulated and as a result of evolution
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defenses against loss of fat mass far outweight defenses againt fat fat gain
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what part of the brain is involved in wt control
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hypothalamus
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an LH lesioned animal
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will b/c anorexic and die of starvation
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a VMN lesioned anmial
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b/cms profoundly obese, hyperphagic until wt plateau
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the arcuate nucleus (archs around base of 3rd ventricles)
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can recieve molecules from circulation that cannot get in traditional blood brain barrier, such as leptin
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if a VMH lesioned animal is starved or forced fed
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when the stimuli is removed it will get back to its wt set point or plateau
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animals with a lower BMI
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every calorie it consumes, it stores more of it as fat
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mutations in db gene
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leads to impairment in leptin receptor
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mutations in ob gene
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leads to impairment in leptin
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leptin is a member of
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the cytokine family
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leptin production
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incr as fat cells incr
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regions of the brain that sense leptin
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arcurate nucleus
brain stain |
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energy expenditure (the efferent output of leptin input to arcuate) is mediated by
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brainstem
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food intake is mediated by
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arcuate nucelus and its signaling to higher centers in brain
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the arcurate nucleus has two major types of neurons that regualte food intake
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-AgRP and NPY-- stimulates food intake
-POMC-- supresses food intake |
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leptin and insulin
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interact with AgRP and NPY to regulate *long term* control of body wt
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ghrelin
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has *short term* control of body wt
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what is the pathway downstream of leptin
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leptin binds to its receptor; PMOC is produced; a MSH is produced and binds to its receptor MC4R
-food intake is supressed -energy expenditure is incr |
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4-6% of severely obese pts have mutations in
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MC4R (the receptor for aMSH)
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leading gene correlating w obesity in GWAS
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FTO
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the leptin threshold
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is higher in obese individuals; genes along the signaling pathway may be mutated and more leptin is needed to keep signal
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signal to reduce appetite
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leptin
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leptin has little effect on body weight
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over a wide range of concentration
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leptin induces the greatest response
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at low levels
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if you reduce wt from a high starting point
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there is no effect on BMI
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if you reduce wt from a set point
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there is a 10% reduction in BMI
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low leptin
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prevents energy intake adjusting to reduces energy output such that indv will regain wt
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what factors incr the threshold
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VMH lesion
chroinc wt increase neuronal loss of aging puberty pregnancy |
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what factors dcr the threshold
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LH lesiona
anorexia cachetic ilness |
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what are antiobesity drugs
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phentermine
sibutramine diethylpropion act on CNS |
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what is oristat
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drug that causes malabsorption of fat
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women at normal BMI
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have a 5x risk of developing T2D
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risk of T2D
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incr with incr in BMI
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the sib risk of T2D is
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4-6x
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prevelance of T2D in US
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7.8%
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in adults T2D makes up ___ percent of diabetes
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90%
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eitology of T2D
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beta cell diathesis exacerbated by obesity and inactivity and realtive hypoinsulinemia
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strong fhx and hx of gestational diabetes is assoc with
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T2D
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ethinic grps at highest risk of T2D
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american indians
hispanic |
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defintion of diabetes mellitus
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fasting blood glucose > 126mg/dl
causal plasma glucose > 200mg/dL 2hr OGTT plasma glucose >200mg/dl |
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what is the definition of impaired glucose homeostasis
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fasting plasma glucose 100-125mg/dl
OGTT 2h plasma glucose 140-149mg/dl |
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what are complications of diabetes
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hrt diesaes and stroke
HTN blindness kidney disease CNS/PNS amputations peridontal disease pregancy, fetal malformation psychiatric |
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insulin resistance affects what vessels
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lg and medium vessels (coronary, periphral and brain ischemia)
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hyperglycemia affects what vessels
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small vessel
glomerulopathy, retinopathy, neuropathy |
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what are disorders with a T2D-like state
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MODY
pregancy acromegaly cushing pheochromocytoma hyperthyroidsm mitochondrial DNA mutations |
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MODY
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mutations affect formation of pancreas
autosomomal dominant mutation seen in young non obese individuals |
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hyperhyroidism is assoc with
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incr sympathetic activity
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____% of diabetics are obses
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80%
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___% of obese are diabetic
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50%
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how does the beta cell work
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glucose is taken up by a transporter and is metabolized in mitochondria to make ATP; ATP causes depolarization of K+; Ca enters cell and allows secretion of insulin
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what is signling down stream of insulin
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insulin receptor b/cms phosphorylated and phosphorlates its signaling molecules, incluid PI3K and Ras kinase
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what leads to release of glucose transporters?
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PI3K signaling allows GLUT4 release from storage
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the entry of glucose in b cells leads to
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release of insulin
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insulin on skeletal muscule
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promotes glucose uptake
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insulin on liver
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dcr gluconeogenesis
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high levels of body fat (incr in plasma FFA)
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supress insulin action on liver and muscle
leads to insulin resistance by impairment of insulin activity |
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insulin on adipose
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inhibits lipoysis
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the lowest levels of insulin has what action
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inhibition of lipolysis; then inhibition of hepatic glucose output at higher insulin levels
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insulin effect on muscle and liver is also mediated
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via its affect on the CNS
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FA effect on muscle
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incr the amoutn of diacylglycerol which leads to phosphorylation of insulin receptors on non active sites, downregulating the receptor and leading to a reduction in glucose uptake
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FA effect on liver
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incr in DAG leads to down regulation of PI3K which leads to a reduction in glycogen synthesis and incr in gluconeogenesis
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adipose tissue is an endocrine organ and secretes
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TNF
IL6 leptin acrp TNF, IL6 and leptin incr in obese animals |
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TNFa and IL6 in obese pts
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reduce insulin sensitivity and incr gluconeogensis
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obese pts have an incr of what in fat cells
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macrophages which produce TNF and IL6 which interrupt sensitivity of skeletal muscle and liver to insulin
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how is diabetes a downstream effect of ageing, certain genes and obesity
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they lead to muscle insulin resistance which leads to incr in lipolysis and hyperinsuliemia from B cells; the incr in FA leads to incr glucose output from gluconeogeneis in liver leading to impaired glucose tolerance; impaired glucose tolerance damages B cells; now pt is a diabetic
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indvs with higher beta cell mass
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can be resistant to some of the effects of obesity
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pts bone to mother with diabetes
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are more likely to get diabetes
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insulin sensitivity dcr with
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incr in wt
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T2D reflects the ability of
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an individual to compensate by incr beta cell activity
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how can T2D be ameliorated
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wt loss
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what is T1DM
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autoimmune destruction of insulin producing cells of pancrease; pancreas makes too little or no insulin
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what is T2DM
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-cells do not use insulin well
-ability for pancreas to make insulin decreases ovver time |
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the older you are when you get T1D
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the longer it takes for the complications to unfold
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what is the prevalance of T1D
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5% of the diabetes cases
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what is the epi of T1D
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1.9 per 1000 US school children
12-15 cases per 100,000 male : female 1:1 peak ages is 5-7 and puberty more common in caucasian peaks in fall and winter |
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in 50yrs, what percentage of a MZ twin will get T1D
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80%
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what is the problem with genetic screening for diabetes
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indiv with HLA high risk genes are common among people who don't get it
protective alleles also exist |
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what suggests that T1D is autoimmune
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-autopsy show T cells infiltrating islets
-immune intervention perserves beta cell -assoc with other autoimmune disease |
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what are the stages in the development of T1D
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genetic predisposition
overt immunologic abnormalites; normal insulin levels progressive loss of insulin release; normal glucose overt diabetes; C-peptide present no c-peptide |
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what proportion of beta cells must be lost before blood glucose increases
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50%
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a pt with normal blood glucose but autoantibody markers of diabetes
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may be in the early stages of T1D with more than 50% of beta cell function
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how can T1D present for the first time
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DKA
positive urine ketones |
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what are the antibody markers for T1DM
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islet-cell antibodies (ICA)
insulin autoantibodies (IAA) antibodies to glutamic acid decarboxylase (GAD) |
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c-peptide and insulin levels in T1DM
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are low or undetectable
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what things raise blood sugar
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eating
stress illness rest |
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what is hemoglobin A1C
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it is tha Amadori product (glucose irreversibly bound to hgA)
it is a relaible index of averge blood glucose concentration over the past 3 months |
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what is the hemoglobin A1c in a normal person
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usually 5 or 6%
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what is the target A1C levels in T1DM
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less than 7% (blood glucose of 135)
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how does pancrease release insulin
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in an amount that is proportional to the amt of carbohydrates in your food, the rate of rise, and duration of rise
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what are sx of hypoglycemia
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shakiness
palpitations sweating anxiety dizziness hunger headache fatigue irritabilty if severe: seizure or LOC |
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after taking rapid-acting insulin
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meals should not be delayed
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exercises lowers blood sugar so pt should
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reduce insulin ore eat a snak with exercise
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what are sx of hyperglycemia
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polyruia
polydispia blurred vision hunger drowsiness nausea if severe: dehydration and DKA |
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high blood sugar after meals usually occurs b/c of
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inadequate premeal bolus insulin;
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high fasting blood sugar usually occurs b/c of
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inadequate long acting or basal insulin
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in times of illness insulin dose
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should be incr
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intensive diabetes therapy
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reduces retinopathy, neuropathy and nephropathy
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in a young cohort of T1D with tight glucose control
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has a long term effect on cardiovascular syxtem later in life
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what is the insulin tx in T1DM
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background or basal insulin given over 24 hrs
meal related or bolus insulin given to cover carbs in food with injections: rapid acting insulin can be given right before meals and snacks with pumps: only rapid acting insulin is ; basal is given in small incremnts all day long and bolus is given before meals |
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what is the current basal bolus insulin tx
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insulin:carb ratios
corrective bolus to normalize glucose peakless insulin for sick days eye and renal complications rare |
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what are experimental drugs to tx T1DM
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rituximab
anti-CD3 GAD vaccine islet and pancreas transplant closed loop system iPS stem cells |
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actions of anti-CD3
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supresses activated T cell function; preserves beta cells for 18 mths
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what are medical complications of obesity
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pulmonary disesase: abnormal function, OSA, hypoventilation syndrome
liver: steatosis, NASH, cirrhosis gallbladder disease gynecological abnormalites: abnormal menses, infertility, PCOS osteoartheritis skin phlebitis: venous tasis cancer CVD: diabetes, dyslipidememia, HTN GERD pancreatitis intracranial HTN stroke cataracts |
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what is the reelationship btwn wt gain in adulthood and T2DM
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if person is not obese yet but has put on a lot of wt from their baseline they are at higher risk of T2DM
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what are skin changes in obese pts
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acanthosis nigricans (sign of insulin resistance)
pigmented striae (sign of cushing) |
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storing fat in the abdomen
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reflects high viseral adipose tissue
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BMI can be calculated (
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lb/in2 x 703
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how is waist circumferance measured
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find top level of iliac crest at end of normal expiration (have person breath in and out a few times)
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what are lab tests done in obesity
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biochem profile
thyroid proflie lipid profile fsting insulin and glucose (if insulin is greater than 10, or glucose above 95, sign of insuling resistance) EKG 24 hr UFC if suspect Cushing androgen profile if suspect PCOS sleep study if suspect sleep apenea (can causes long term changes in pulmonary function and rt sided hrt failure if goes undiagnosed) |
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how do you initiate a discussion of the pts wt if they did not bring it up
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Ms. X, could we talk for a moment about your wt?
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what are the conerstones of wt loss
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behavior exercise and diet
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what are behavior therapy
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self monitoring
stimulus control reinforcement stress management |
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what are the guidelines to using pharmacotherapy to tx obesity
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BMI greater than 30
or BMI greater than 27 and 2 comorbidites |
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what are the guidelines to surgery to tx obesity
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BMI over 49
or BMI over 35 and 2 comorbidities |
