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Endocrinology > Obesity > Flashcards

Obesity Flashcards

1
Q

Formula for BMI?

A

BMI= wt (kg)/ht (m)^2

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2
Q

BMI classification:

A 
BMI: 25- 29.9 overweight
30-34.9 obesity class 1
35-39.9 obesity class 2
>40 class 3 or morbidly obese
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3
Q

BMI in US children and adolescent?

A
  • 85th-95th percentile at risk for being overweight
  • > 95th percentile for age obesity
  • if both parents are obese: 87% chance child will be obese
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4
Q

Obesity prevalence 2009-2010

A
  • obesity prevalence: age 2-19
    all groups: 35.7%
    males: 35.8%, females: 35.5%
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5
Q

Cost of childhood obesity?

A
  • national epidemic
  • costs 3 billion dollars annually
  • economic calculations will clim higher: consider long term disability, lost earnings
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6
Q

Cost of obesity and overweight all ages?

A
  • direct cost: preventive, dx and tx services
  • indirect cost: value of lost wages
  • cost now est at $270 billion a year
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7
Q

Why are there limitations to BMI?

A
  • fat mass versus lean mass
  • distribution of fat
  • ethnic differences
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8
Q

What is the most accurate way to assess body composition? what is a cheaper way?

A
  • most accurate: DEXA scan, CT (expensive)

- less accurate but lower cost: bioimpendance, water displacement

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9
Q

What is worse, an android fat distribution or gynoid?

A
  • apple/andriod is worse: excess fat in the abdomen, its more common in men, significant correlation with metabolic syndrome
  • pear/gynoid: is excess fat on thighs and buttocks, common in women, and no significant correlation with metabolic syndrome
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10
Q

Distribution of adipose tissue?

A
  • upper body: subq, superficial and deep
  • lower body: visceral - worse, hold all the toxic hormones and enzymes that promotes metabolic syndromes
  • also ectopic, and IMAT
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11
Q

Why is there a BMI limitation because of ethnic differentiation?

A
  • at any given BMI the % FM of asians 5% higher compared to caucasians
  • african americans>jamaicans> nigerians
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12
Q

Prevalence of obesity?

A
  • BMI>25 68%
  • > 30 35%
  • > 40 6.5%
    (people who are overweight are becoming obese)
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13
Q

Why are we becoming an obese society?

A
  • genetics
  • cultural
  • societal
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14
Q

Genetics of obesity?

A
  • obesity isn’t a simple mendelian trait
  • single genes are only found in the mouse
  • there is an autosomal recessive mutation, chromosome 6, the leptin gene (obese people develop resistance to leptin)
  • multiple genes and it is transgenic
  • there are so far 176 different himan cases of obesity due to single gene defects
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15
Q

What is genetical obesity related to?

A 
- autosomal dominant:
  PCOS
 prader-willi syndrome (most common)
- autosomal recessive:
Bradet-Biedl syndrome (polydactyly) facial features, wide eyes, mental retardation
cushing syndrome
x linked wilson turner
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16
Q

Other enviro causative agents of obesity?

A
  • convenience foods
  • portion size
  • increased flight transportation
  • adeno 13 virus
  • societal issues
  • post viename society: YOLO
  • sedentary behavior
17
Q

Medical complications of obesity?

A
  • pumonary disease: OSA, restrictive lung disease
  • nonalcoholic fatty liver
  • OB/GYN: infertility
  • osteoarthritis
  • idiopathic intracranial HTN
  • CVA
  • CAD
  • CHF, dyslipidemia, HTN
  • diabetes
  • cancer: breast, colon, pancreas, uterus, cervix, esophagus, kidney, prostate
  • DVT, phlebitis, venous stasis
18
Q

How much of a wt loss is beneficial?

A
  • 10% wt loss will beneficially improve the following conditions:
    RA, OA, cancer, CAD, DM, DVT, HTN, lung disease, OSA, OBGYN complications, incontinence, pancreatitis
19
Q

What diseases are made worse with wt loss?

A
  • paradoxical effect on CHF if you already have HF and become obese, HF wont get worse
  • body mass loss leading to sarcopenia (because bones are carrying so much wt when obese)
  • 5 fold increase successful suicide rate following gastric bypass surgery (don’t feel safe anymore)
20
Q

Relationship of obesity and mortality

A
  • increased mortality in all age groups (35-89)
  • lowest mortality rates are for those with BMI 20-22
  • mortality begins to increase modestly with BMI > 25
  • BMI > 30, all cause mortality rates increase by 50-100%
21
Q

Relationship b/t adipocytes and inflammation?

A

resistin: increased level in obesity, DM
resistin increases pro inflammatory cytokines: IL, TNF, intracellular adhesion molecule-1
- found that pts that lost wt didn’t need ortho surgery anymore because inflammatory cytokines were decreased because of decreased wt load

22
Q

CVD risk and obesity? CV risk factors

A
  • wt gain is directly related to these CV risk factors:
  • dyslipidemia
  • HTN
  • elevated insulin
  • elevated fibrinogen
  • OSA
23
Q

insulin resistance has a direct effec on what and why is this?

A
  • direct effect on myocardium
  • epicardial fat deposition
  • increased intra-myocardial triglyceride deposition
  • lipotoxicity
  • cardiomyocyte apoptosis producing cardiac dysfunction
24
Q

How does obesity cause HTN?

A
  • enhanced sodium retention
  • vascular smooth muscle hypertrophy
  • stimulation of renin-angiotensin aldosterone pathway
  • increased activation of sympathetic NS increased vasoconstriction
  • decreased NO mediated vasodilation
25
Q

How does obesity cause LVH?

A
  • due to need for high cardiac output
  • increases risk for SCD
  • increases risk for CHF
  • dx on ECG when sum of S in V1 and R in V5 > 35 mm
26
Q

Relationship b/t obesity and CHF?

A
  • frequent complication of severe obesity
  • severe hypoxemia of OSA is one of several possible causes
  • each increase in BMI of 1 unit increases risk of CHF 5% man, and 7% in women
  • paraox of est. CHF: once HF est, higher BMI has improved outcome
27
Q

Relationship b/t obesity and stroke?

A
  • for each increase of 1 unit BMI - hemorrhagic stroke increases 6% and ischemic stroke increases by 4%
28
Q

Relationship b/t obesity and pulmonary dysfunction?

A
  • a restrictive ventilatory defect (diaphragm pushed up against lungs because of fat tissue, so total lung capacity is decreased -> hypoxia)
  • increased RR and decreased tidal volume and TLC
  • hypoxic arterial blood gases in moderate/severe obesity
  • dyspnea is common (w/ and w/o exercise)
  • increased risk for asthma
29
Q

Relationship b/t alzheimers and BMI?

A

obesity at high ages increases risk for AD in women

  • for every 1 unit increase BMI at age 70 AD risk increases by 36%
  • these associations weren’t found in men because they didn’t live that long
30
Q

Obesity and OSA?

A
  • occurs in 50% of severly obese
  • OSA presents in up to 90% of obese pts seeking bariatric surgery
  • potentially life threatening
31
Q

Risk factors for OSA?

A
  • upper body obesity
  • more common in males
  • associated with snoring (tiredness in morning more specific than snoring)
  • large neck girth in those who snore is highly predictiv of OSA (circumference > 17 in in men and 16 inches in women)
32
Q

CV complications of OSA

A
  • acute coronary syndrome: increase risk of plaque rupture, increase risk of thrombosis
  • increased risk of stroke
  • HTN
  • increased platelets aggregation
  • increased platelets aggregation
33
Q

Effect of wt loss and OSA?

A

p 10% of wt reduction iproves severity of OSA by more than 50%

34
Q

Obesity and non-alcoholic fatty liver?

A
  • occurs > 66% in obese, > 90% in BMI > 40, precursor to liver failure, transient increase in transaminases with wt loss, especially rapid wt loss (after a couple of months liver enzymes will go back down to normal levels)
35
Q

What percentage of cancer deaths are attributed to dietary factors?

A
  • 35%
36
Q

relationship b/t obesity and cancer?

A
  • wealth of epidemiological data connecting obesity and various malignancies: post menopausal breast cancer, colon, pancreas, endometrium, kidney, and esophageal cancer
  • premenopausal breast cancer: 2 large studies revealed that a 70% increased risk of premenopausal breast canacer vs. normal wt

Endocrinology (22 decks)

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