Obesity Flashcards

1
Q

condition of excess adipose tissue relative to LBM

A

obesity

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2
Q

how do we identify overweight and obesity?

A

BMI, WC

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3
Q

health risks of overweight, obesity:

A

CVD, type 2 diabetes, non alcoholic fatty liver disease

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4
Q

known causes of obesity explain ____% of cases

A

<1

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5
Q

examples of known causes of obesity:

A

genetic syndromes (Prader-Willi), endocrine (Cushing’s), hypothalamic dysfunction (tumours), medications

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6
Q

meds that cause obesity:

A

glucocorticoids, many psychiatric meds, insulin/thiazolidinediones/sulfonylureas

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7
Q

genes influence:

A

appetite (leptin), susceptibility to hunger, taste preferences, level of disinhibition, REE (uncoupling proteins), TE of food, nonexercise activity thermogenesis, etc.

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8
Q

early studies of gene influence vs current:

A

twins and adopted children; obesity gene variants

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9
Q

assessing for risk of chronic disease steps:

A

assess BMI, measure WC, classify for disease risk, combine info with other risk determinants, FPG, lipid profile, liver enzymes, BP, assess for mood disorders

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10
Q

major depression and mood disorders occur in ___% of women aged 40+ with BMI > 30 kg/m^2

A

20-60

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11
Q

common barriers to wt loss?

A

all or nothing mindset, lack of time, loss of motivation, dislike exercise/disability, lack of knowledge, yoyo dieting, low self-efficacy, lack of personal interest

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12
Q

3 components to lifestyle modification:

A

nutrition, physical activity, CBT

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13
Q

behaviour modification techniques:

A

self monitoring, stimulus control, modify specific eating behaviours and stimuli, reinforcement management, also stress management

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14
Q

successful wt loss maintenance defined as :

A

> 5% wt loss from baseline maintained 12 months

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15
Q

why is deficit of 500 kcal/day=1-2 lb a week of wt loss a crude estimate?

A

assumes that it will be pound in fat (also losing water, protein structure supporting fat)

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16
Q

obesity class 1 , 2, and 3 BMIs:

A

30-34.9, 35-39.9, 40+

17
Q

disease risk increased for women of WC > __ cm and men WC > ____cm

18
Q

traditional meds for combating obesity

A

stimulants, orlistat, alternative treatments

19
Q

newer approaches combat obesity:

A

bariatric surgery, brain stimulation (transcranial direct stimulation)

20
Q

safety concerns for stimulants?

A

raise BP and HR

21
Q

this non-stimulant agent inhibits lipases in GI tract, prevents fat breakdown/absorp, minimal systemic absorption

A

orlistat (xenical)

22
Q

orlistat also improves;

A

lipid lvls and BG

23
Q

side effects of orlistat

A

flatus with discharge, oily spotting, fecal urgency, fatty oily stool, fecal incontinence, increased defecation, probs with vit absorption

24
Q

this class of drugs currently under investigation for wt loss, used for diabetes

A

GLP-1 receptor agonists (receptors for incretin hormones–stim insulin secretion; found on beta cells, glucagon-like peptide-1)

25
examples of GLP-1 receptor agonists?
liraglutide and exenatide
26
what does liraglutide do?
stim insulin secretion, inhibit glucagon release, delay gastric emptying, reduce food intake, normalize fasting and postprandial insulin secretion
27
drug that died out cuz ^ suicides, CV events
rimonabant
28
outcomes of taking liraglutide?
better HbA1c, reduce FBG, reduce fasting insulin, reduce BP
29
serotonin receptor agonist that affects CNS and reduces appetite
locaserin
30
diabetes meds that cause wt gain:
insulin, sulfonylureas (glyburide, gliclazide), glitinides (repaglinide, nateglinide)
31
why do some diabetes meds ^ wt?
stimulate insulin release which is anabolic
32
why was meridia taken off market?
cuz ^ MI
33
to have metabolic syndrome, must have:
central obesity >94 and 80 for men and women + 2 of following 4: raised TG, reduced HDL, raised BP, raised FPG