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Advanced Principles II > Obesity > Flashcards

Obesity Flashcards

1
Q

Definition of Overweight

Definition of obesity

A
  • Overweight- increased body weight above a standard related to height
  • Obesity- excessive body weight for the patients age, gender, and height
    • body weight of 20% or more above ideal weight
    • it is a disorder of energy balance
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2
Q

Obesity stats

A
  • 68% of US population overweight
  • 33% obese
  • 25% of children are obese
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3
Q

Ideal body weight calculation for men

women

A
  • men: IBW = 105 lb + 6 lb for each inch >5 ft
  • women: IBW = 100lb = 5 lb for each inch >5 ft
  • Brocca’s index:
    • IBW (kg) = height (cm) -x
    • x for men = 100, x for women = 105
  • lean body weight is IBW + 20%
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4
Q

How do you calculate BMI?

What is the problem with this measurement?

A
  • MBI = weight in kg/ height2 (m)
  • Does not clearly differentiate between overweight and overfat. Very muscular ppl will be designated overweight/obese even though they are not fat
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5
Q

What are the different groupings of BMI?

A
  • Overweight = BMI 25-29 kg/m2
  • Obese = BMI >30
  • Clinically severe Obese = BMI >40
  • Super Obese = BMI >50
  • Super-Super Obesity = MBI >60
  • BMI >30 is associated with increased morbidity related to stroke, ischemic heart disease, HTN, and DM
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6
Q

What is the impact of anatomic distribution?

A
  • Android obesity- abdominal, central obesity
    • more common in men
    • higher incidence of metabolic disturbances, ischemic heart disease, stroke, dm, death
  • Gynecoid obesity- fat around hips and buttocks
    • more common in females
  • Waist circumference is directly related to risk of pathophysiology
    • >102 cm in men
    • >88 cm in women
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7
Q

What problems are associated with obesity?

A
  • OSA
  • RLD
  • HTN
  • CAD
  • hyperlipidemia
  • delayed gastric emptying/GERD
  • Type II DM
  • Gall bladder disease
  • Cirrhosis/fatty liver disease
  • venous stasis
  • degenerative joint/disc disease
  • increased breast, prostate, cervical, uterine, and colorectal cancer
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8
Q

How does obesity alter the respiratory system?

A
  • Reduces chest wall and lung compliance
    • reduced FRC- 50%
    • reduced ERV
    • RV and CC not changed
      • relationship btw FRC and CC is adversely effected
    • FEV1 and FVC usually WNL
    • Reduced TV- may fall into the range of closing capacity
  • Increased pulmonary blood volume
  • increased O2 consumption and CO2 production
  • high MV, increased WOB
  • As obesity worsens, you will see lung disease and PHTN but PFTs remain normal until this occurs
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9
Q

How does obesity affect the respiratory system in different positions?

A
  • Respiratory changes are all exaggerated in different positions
  • Rapid desaturation may be seen when anesthesia is induced in recumbent/supine position
  • Deviations in lung volumes lead to:
    • VQ mismatch-
    • hypoxemia
    • increased right to left intrapulmonary shunt
    • TV overlapping with closing capacity (the small airways will start to close during a normal tidal volume breath)
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11
Q

What changes can you expect in securing an airway for an obese patinet?

A
  • TMJ and atlanto-axial joint and cervical spine movement is limited by upper thoracic and low cervical fat pads
  • Narrowed airway from extra tissue folds in mouth and pharynx
  • Short, thick neck- measure it
    • 40 cm = 5% incidence of difficult intubation
    • 60 cm = 35% incidence of difficutl intubation
  • Fat in suprasternal, presternal, posterior cervical and submental regions
  • shortened distance between mandible and sternal fat pads
  • OSA
  • difficult to mask ventilate
  • difficult to get a good view on laryngoscopy
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12
Q

How is OSA characterized?

A
  • Apnea > 10 seconds; total cessation of airflow despite respiratory effort against a closed glottis
  • Hypopnea is 50% reduction in size or number of breaths that lasts at least 10 seconds compared to normal
    • partial or intermittent collaps of pharyngeal airway during sleep
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13
Q

What are the risk factors for OSA?

A
  • middle age
  • male
  • obesity
  • ETOH use
  • drugs for sleep aids
  • abdominal fat distribution
  • neck girth 41 cm
    • >17 inches for men
    • >16 inches for women
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14
Q

What problems can OSA lead to?

A
  • chronic hypoxia, hypercapnia, pulmonary and systemic HTN
  • snoring
  • poor sleep leading to daytime somnolence
  • impaired concentration
  • morning HA
  • Right heart failure
  • polycythemia and increased blood volume
  • respiratory acidosis
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15
Q

How is OSA graded?

A
  • Severity is graded by # of apnea or hyponeic episodes during 1 hour of observation
    • mild = 5 -15/hour
    • moderate = 15-30/hour
    • severe >30/ hour
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16
Q

What is Pickwickian syndrome?

How is it diagnosed?

A
  • Obesity hypoventilation syndrome (OHS)
  • Complication of extreme obesity/long term OSA
  • hypercapnia, cyanosis induced polycythemia, somnolence and eventual right sided heart failure and PHTN
  • Doagnosed by PCO2 >45 in an obese pt w/o significant COPD
  • Clinically distince from OSA
    • OSA you have nocturnal sleep disruption
    • OHS you have nocturnal central apneic events (apnea without respiratory effort)
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17
Q

What cardiovasclar alterations would you expect to see in an obese patient?

A
  • Increased total blood volume
  • increased CO
    • higher blood volume puts strain on myocardium
    • Risk of CAD is double and presents with angina, CHF, acute MI and sudden death
  • Increased RAAS and SNS activity
    • arterial HTN risk is twice as high as it is for lean pts
  • increased left sided heart pressures and left ventricular hypertrophy
18
Q

How is OHS (Pickwickian syndrome) characterized?

A
  • Obesity
  • hypercapnia
  • daytime hyper-somnolence
  • Arterial hypoxemia
  • PHTN
  • respiratory acidosis
  • right sided heart failure
  • difficult airway
20
Q

What hemotologic alterations would you expect to see in an obese patient?

A
  • Polycythemia and hypercoagulation
  • Thromboembolic risk
    • risk of DVT doubles
    • plycythemia leads to increased viscosity and increased fibrinogen levels
    • increased intra-abdominal pressure
    • immobility leads to venostasis
21
Q

What gastrointestinal alterations would you expect to see in an obese patient?

A
  • Increased incidence of Hiatal hernia, GERD, and gallbladder disease
  • High risk for aspiration
    • greater gastric volumes(>25 ml) d/t delayed gastric emptying
    • increased gastric acidity (pH<2.5) d/t increased parietal cell secretion
22
Q

What kind of hepatic alterations would you expect to see in an obese patient?

A
  • Fatty infiltration of liver
    • inflammation
    • cirrhosis
  • Abnormal LFTs
    • wt loss, even just 5 lbs can reverse the elevated liver enzymes
    • caution with fluorinated volatile anesthetics
23
Q

What renal alterations would you expect to see in an obese patient?

A
  • increased renal plasma flow and increased GFR
  • Increased renal tubular resorption and impaired naturesis secondary to SNS and RAAS
    • also physical compression of the kidney
  • eventually nephron function can be lost
24
Q

What kind of endocrine alterations would you expect to see in an obese patient?

A
  • Obese patients secrete more insulin, but are resistant to the effects of insulin
    • develop type 2 dm
  • Metabolic syndrome
    • presence of at least three of the following signs
      • large waiste curcumference
      • high triglyceride levels, low levels of HDL
      • glucose intolerance
      • HTN
25
Q

What musculoskeletal and CNS changes would you expect to see in an obese patient?

A
  • Musculoskeletal
    • osteoarthritis and degenerative joint disease
      • high weight on joints
      • inflammatory response
  • CNS
    • ANS dysfunction
    • peripheral neuropathies
26
Q

Often obese patients have hyperlipidemia. What can this lead to?

A
  • Elevated LDL and low HDL is linked to athersclerosis
  • Can lead to
    • premature CAD
    • premature vascular disease
    • pancreatitis
27
Q

What alterations in drug pharmacokinetics and metabolism would you expect to see in an obese patient?

A
  • Pharmacokinetics:
    • increased blood volume and CO
    • decreased total body water
    • adipose and lean tissue increases
    • unpredictable changes in PB
    • VOD central compartment unchanged
  • metabolism
    • Phase 1 (oxidation, reduction, hydrolysis) unaffected
    • Phase 2 (glucuronidation, sulfation) enhanced
  • Clearance
    • Hepatic clearance unchanged even with elevated LFTs
    • renal clearance increased d/t increased RBF and GFR
    • lipophilic drugs have an increased E1/2t d/t increased Vd
28
Q

How do you calculate lean body mass?

A
  • male: 1.1 x TBW- 128x(TBW/Ht)2
  • female: 1.07 x TBW - 148 x (TBW/Ht)2
29
Q

How would you adjust the dosing for a weak or moderately lipophillic drug?

A
  • add 20% to the IBW
    • this will include the extra LBM associated with obesity
30
Q

How would you dose propofol in an obese patient?

A
  • induction dose should be based on LBW
  • maintenance dose should be based on TBW
31
Q

How should you dose benzos for an obese patient?

A
  • (these are highly lipophillic drugs)
  • initialdoses based on LBW
  • may titrate to TBW
    • need larger doses to reach adequate serum concentrations
  • Infusions based on LBW
32
Q

How would you dose neuromuscular blocking drugs for an obese patient?

Sugammadex?

A
  • Based on LBW: Roc, Vec, Atracurium, Cisatracurium
    • prolonged DOA and recovery
  • Pseudocholinesterase activity increases with weight and ECF increases
    • dose Succ on TBW
  • Sugammadex dosed base on TBW
33
Q

How would you dose opioids in an obese patient?

A
  • Fentanyl and Sufentanyl: both are highly lipid soluble
    • increased Vd and elimination 1/2 life
    • dose fentanyl based on LBW (miller says TBW)
    • dose sufentanyl on TBW but decrease maintenance to LBW
  • Remifentanyl dose based on LBW
34
Q

How would you dose dexmedetomidine in an obese patient?

A
  • Use as an adjunct when it is priority to avoid respiratory depression
  • 0.2-0.7 mcg/kg/hr, dosed on TBW
35
Q

How would you dose VA for an obese patient?

A
  • Metabolism is greater in obese patients which leads to greater increase in inorganic fluoride
  • greater incidence of halothane hepatitis
  • N2O often avoided to maximize PaO2
36
Q
A

Advanced Principles II (20 decks)

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