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APEX > Unit 12 - Obesity > Flashcards

Unit 12 - Obesity Flashcards

1
Q

how many calories are required to produce one gram of body fat

A

9

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2
Q

top 2 leading causes of preventable death

A
  1. smoking
  2. adult obesity
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3
Q

diseases that contribute to obesity

A
  • Cushing’s
  • hypothyroidism
  • depression
  • eating disorders
  • PCOS
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4
Q

genetic conditions that contribute to obesity

A
  • Prader-Willi syndrome
  • Bardet-Biedl syndrome
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5
Q

what percent of american adults are obese

A

33

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6
Q

android obesity is often equated to what body shape

diseases assoc. with this type of fat accumulation

A

apple

increased risk ischemic heart disease, HTN, DM, dyslipidemia, death

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7
Q

gynecoid obesity is often equated with what body shape

diseases associated with this fat distribution

A

pear

joint disease, varicose veins

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8
Q

at what point does adipose become pathologic

A

when it releases significant quantities of free fatty acids and cytokines

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9
Q

terminal consequence of excess adipose tissue

A

insulin resistance and systemic inflammation

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10
Q

what fat storage site releases the highest quantities of free fatty acids and cytokines

A

visceral fat

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11
Q

is android obesity more common in men or women

A

men

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12
Q

waist sizes assoc. with increased health risks with android obesity

A

men > 40 inches
women > 35 inches

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13
Q

type of obesity more common in women

what is it characterized by?

A

gynecoid

gluteal and femoral fat accumulation

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14
Q

how is gynecoid fat different from abdominal fat

A

gynecoid fat is metabolically inactive, primarily used for energy storage

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15
Q

type of fat associated with reduced incidence of non-insulin dependent diabetes

A

gynecoid

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16
Q

what is metabolic syndrome?

A

several disease states that coincide with obesity

diagnosis requires 3 or more:
- fasting glucose > 110 mg/dL
- abdominal obesity (waist > 40” men, 35” women)
- serum triglyceride level > 150 mg/dL
- serum HDL < 40 mg/dL in men
- serum HDL < 50 mg/dL in women
- BP > 135/85 mmHg

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17
Q

CV risk in pts with metabolic syndrome vs. general population

A

50-60% greater

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18
Q

BMI calculation

A
  1. convert weight in lbs to kgs
  2. convert height from inches to cm ( in x 2.54 )
  3. convert cm to meters ( cm/100 )
  4. BMI = kg/m squared
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19
Q

why is BMI not a perfect measure of fat mass

A
  • doesn’t take fat distribution into account
  • can be skewed with a large percentage of muscle mass
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20
Q

BMI for:

  • underweight
  • normal
  • overweight
  • class 1 obesity
  • class 2 obesity
  • morbid obesity (class 3)
A
  • underweight: < 18.5
  • normal: 18.5 - 24.9
  • overweight: 25-29.9
  • class 1 obesity: 30-34.9
  • class 2 obesity: 35-39.9
  • morbid obesity (class 3): > 40
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21
Q

child body weight class (2-18 yrs old):

  • overweight
  • obese
  • severely obese
A
  • overweight: 85th-94th percentile
  • obese: 95th-98th
  • severely obese: 99th
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22
Q

what is ideal body weight?

how is it calculated?

A

BMI assoc. with lowest risk of body weight-related comorbidities

men: height (cm) - 100
women: height (cm) - 105

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23
Q

how does obesity affect:

  • FRC
  • ERV
  • RV
  • closing volume
  • vital capacity
A
  • FRC decreases
  • ERV decreases
  • RV remains constant
  • closing volume increases
  • vital capacity decreases
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24
Q

why is pulmonary blood flow increased in obesity?

A

increased CO

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25
Q

factors assoc. with obesity that inhibit lung inflation

A
  • chest fat (compresses rib cage, hinders expansion)
  • abdominal fat (shifts diaphragm cephalad and compresses lungs)
  • kyphosis and lordosis develop over time and alter geometry of ribcage
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26
Q

relationship between FRC and BMI

A

inversely proportional

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27
Q

what causes distal airway collapse during tidal breathing in obese patients

what are the consequences of this

A

FRC decreased below closing capacity

leads to V/Q mismatch, shunt, hypoxemia, increased dead space

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28
Q

how does general anesthesia affect FRC in obese vs. non-obese pts

A

decreases by 50% in obese
decreases by 20% in non-obese

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29
Q

why is PaCO2 usually normal in obese pts

A

high diffusing capacity of CO2 and favorable characteristics of CO2 dissociation curve

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30
Q

why do obese pts have an increased O2 consumption and CO2 production?

what vent changes should be made in these pts

A

fat is a metabolically active organ

increase minute ventilation to maintain normal blood gas tensions

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31
Q

optimal tidal volume for an obese patient

A

6 - 8 mL/kg ideal body weight

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32
Q

why is the obese patient predisposed to oxygen desaturation during apneic periods

A

smaller FRC + increased O2 consumption

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33
Q

optimal positioning for airway management of an obese patient

A

head-elevated laryngoscopy position (HELP)

elevate head, shoulders, and upper body above the chest - should be able to envision a horizontal line from sternal notch to external auditory meatus

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34
Q

optimal preoxygenation for an obese patient

A

100% FiO2 + CPAP 10 cm H2O until end-tidal O2 exceeds 90%

prolongs desat time by 50%

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35
Q

optimal position to extubate an obese patient

A

reverse Trendelenburg - relieves pressure on thorax, improves FRC

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36
Q

best way to control PaCO2 in obese patient

A

adjust RR, not Vt

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37
Q

does obesity alone mandate RSI?

A

no - make decision on case by case basis

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38
Q

strategies to maximize postoperative oxygenation in the obese pt

A
  • CPAP or BiPAP after extubation
  • HOB 30 degrees
  • early ambulation
  • control surgical pain
  • incentive spirometry
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39
Q

when is postop hypoxemia most likely to occur in the obese pt

A

immediately after extubation and up to 2-5 days postop

40
Q

why is cardiac output increased in the obese patient

A

increased stroke volume (HR usually unchanged)

41
Q

CO in obese patients

A

increased by 100 mL/min for every extra kg of fat

42
Q

why do obese patients need an increased blood volume and CO

A

proliferation of adipocytes requires that vasculature grows to support growth

43
Q

factors that lead to increased workload on myocardium in obese patient

how does the heart compensate

A
  • larger vascular network
  • larger blood volume
  • increased O2 consumption

heart dilates and becomes thicker, eventually causes diastolic dysfunction

44
Q

why are obese pts less tolerant of excessive fluid amin

A

reduced ventricular compliance and diastolic dysfunction increase the risk of fluid overload

45
Q

what weight should be used to calculate periop fluid requirements in obese pts

A

lean body weight

46
Q

what leads to systolic dysfunction in obese pts

A

eventually the heart dilates beyond its ability to increase wall thickness

47
Q

what contributes to HTN in obese pt

A
  • hyperinsulinemia
  • SNS and RAAS activation
  • atherosclerosis
  • elevated cytokine in plasma
48
Q

common EKG changes in obese pts

A
  • low voltage
  • LAD
  • RAD
  • prolonged QT
  • ischemia
  • dysrhythmias
49
Q

what causes low voltage EKG in obese pts

A

increased distance between heart and leads

50
Q

what causes left axis deviation in obese pts

A

stomach pushes the heart up and to the left

also LVH secondary to volume overload and HTN

51
Q

what causes right axis deviation in obese pts

A

RVH from OSA and volume overload

52
Q

what causes ischemia in obese pts

A

O2 supply and demand mismatch

53
Q

what causes dysrhythmias in obese pts

A
  • fatty infiltration of conduction system
  • myocardial hypertrophy
  • hypoxemia
  • hypercarbia
  • obesity hypoventilation syndrome
  • ischemic heart disease
54
Q

what leads to biventricular failure in obese patients

A
  • increased blood volume results in increased pulmonary blood volume, pHTN, increased RV workload, and right heart failure
  • increased blood volume results in increased CO, increased LV workload, and LV failure
55
Q

which is calculated based on IBW: water or lipid soluble drugs?

A

water soluble

56
Q

which is calculated based on TBW: water or lipid soluble drugs?

A

lipid soluble

57
Q

4 factors that alter volume of distribution in obese pts

A
  • increased blood volume
  • increased CO
  • altered plasma protein binding
  • large fat mass
58
Q

which increases in obese patients: Vd of water souble or lipid soluble drugs?

A

both increase - fat mass and muscle mass both increase
(Vd for lipid soluble increases more)

59
Q

what weight should be used to dose the obese patient

A

LBW

60
Q

what is LBW?
how is it estimated?

A

lean body weight is the IBW + extra muscle mass that occurs with weight gain

estimated by IBW x 1.3

61
Q

what volatiles are best for obese patients?

A

those with lower blood:gas coefficients (volatiles are lipophilic) - ex. sevo or des

62
Q

why is N2O generally avoided in obese patients?

A

restricts max FiO2 that can be delivered

63
Q

should midazolam be dosed based on TBW or LBW?

A

TBW

64
Q

dosing rocuronium and vecuronium - TBW or LBW?

A

LBW

65
Q

dosing propofol - LBW or TBW?

A

induction - LBW
maintenance - TBW

66
Q

fentanyl and sufentanil dosing - LBW or TBW? why?

A

initial doses are based on TBW because of fat solubility and large Vd

maintenance dosing is based on LBW (increased Vd = prolonged elminination half-life)

67
Q

why is the loading dose of propofol based on LBW?

A

its offset is caused by redistribution, not clearance

68
Q

why is TBW used to calculate succinylcholine dosing

A

combination of increased blood volume and increased pseudocholinesterase deficiency

69
Q

why is remifentanil dosed based on LBW

A

since it’s rapidly cleared by plasma esterases, it doesn’t behave like a high Vd drug

70
Q

why is midazolam administered by TBW

A

increased central volume of distribution - may cause oversedation in the obese patient

71
Q

dosing epidural LA in obese patients

A

reduce to 75% of the normal dose due to engorgement of epidural veins and increased epidural fat content = greater LA spread in epidural space

72
Q

what is responsible for airway patency

A

balance between pharyngeal muscles that dilate airway and negative pressure of inspiration that collapses it

73
Q

why do obese patients have an increased tendency for airway collapse?

A

fat tends to accumulate in the lateral walls of pharynx, causing the internal diameter to narrow

74
Q

how is OSA defined

A

cessation of airflow for at least 10 seconds (apnea) with 5 or more unsuccessful efforts to breathe (obstruction) and a greater than 4% reduction in SaO2

75
Q

what is hypopnea?

A

50% reduction in airflow for 10 seconds, 15 or more times per hour, and is linked to snoring and decreased O2 sat

76
Q

things that increase the likelihood that a patient has OSA

A
  • BMI > 30
  • abdominal fat distribution
  • neck girth > 17” for men, 16” for women
77
Q

OSA is an independent risk factor for what 3 complications

A
  • HTN
  • cardiovascular morbidity
  • death
78
Q

what results in snoring in OSA

A

sleep = decreased upper airway tone = increased upper airway resistance = obstruction

79
Q

apnea hypopnea index

A

helps quantify the severity of OSA - derived by the number of apnea episodes and hypopnea divided by total hours of sleep

mild = 5-15 episodes/hr
moderate = 15-30 episodes/hr
severe = > 30 episodes/hr

80
Q

classic triad of dysfunctional sleep

A
  1. apnea or snoring with hypopnea during sleep
  2. arousal from sleep
  3. daytime somnolence
81
Q

definitive test for OSA

A

polysomnography

82
Q

STOP-BANG questions for OSA screening

A

Snoring
Tiredness
Observed apnea
Pressure (HTN)
BMI (>35)
Age (>50)
Neck circumference (>40 cm)
Gender (male)

high risk for OSA = 3 or more questions yes
low risk for OSA = less than 3 yes

83
Q

what is obesity hypoventilation syndrome?
aka Pickwickian syndrome

A

long-term consequence of untreated OSA

over time, resp. center in medulla fails to respond to hypercarbia appropriately

84
Q

classic syndrome of obesity hypoventilation syndrome

A

apnea during sleep without any respiratory effort

85
Q

diagnostic criteria for obesity hypoventilation syndrome

A
  • BMI > 30
  • awake PaCo2 > 45 mmHg
  • dysfunctional breathing during sleep
86
Q

s/s obesity hypoventilation syndrome

A
  • obesity
  • hypersomnolence during the day
  • hypoxemia
  • hypercarbia
  • respiratory acidosis
  • compensatory metabolic alkalosis
  • polycythemia
  • pulmonary HTN
  • right heart failure
87
Q

most sensitive sign of an anastomotic leak following gastric bypass

what are other symptoms?

A

unexplained tachycardia

abdominal pain, shoulder pain, fever, pelvic pain, substernal pressure, dyspnea, hypotension, oliguria, increased thirst, restlessness, hiccups

88
Q

3 different types of procedures used for surgical weight loss
which is the least invasive?

A
  1. malabsorption
  2. restriction - least invasive
  3. combination
89
Q

vitamin deficiencies patient is at risk for after a jejunoileal bypass surgery?

A
  • vitamin K
  • vitamin B12
  • iron
  • folate
90
Q

what type of surgical weight loss surgery yields the best weight loss and improvement of comorbidities?

A

combination malabsorption/restriction (Roux-en-Y gastric bypass)

91
Q

most significant risk factor for development of nonalchoholic liver disease and nonalchoholic steatohepatitis

A

obesity

92
Q

what is Mu Huang?

complications of use?

A

a natural source of ephedrine, an indirect-acting adrenergic agonist and thermogenic agent used as ingredient in appetite suppresants

complications of adrenergic overstimulation - HTN, CVA, sz, death

93
Q

what is phentermine?

A

a norepi reuptake inhibitor that acts as an appetite suppressant and increases BMR

94
Q

what is sibutramine?
associated risks?

A

a norepinephrine and serotonin reuptake inhibitor that acts as an appetite suppressant and increasess BMR

risk of adrenergic overstimulation and serotonin syndrome

95
Q

what is orlistat?
associated risks?

A

a lipase inhibitor that reversibly binds to lipase and hinders absorption and digestion of consumed fats

vitamins A, E, D, and K must be supplemented. insufficient vitamin K will impair certain clotting factors

96
Q

vitamin K synthesized clotting factors

A

2, 7, 9, and 10

APEX (54 decks)

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