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OU Module Endo Fall 2018 > Overweight and Obesity Exam 3 > Flashcards

Overweight and Obesity Exam 3 Flashcards

1
Q

When should you initiate pharmacological treatment?

A
  • BMI >= 30 with no other risk factors

- BMI >= 27 with other risk factors / diseases (HTN, dyslipidemia, CHD, DM II, sleep apnea)

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2
Q

What are the drug classes that can be used for obesity?

-

A
  • Catecholaminergic, Stimulant, Sympathomimetic Medications
  • Fat absorption inhibitor
  • GLP-1 agonist
  • Stimulant + anticonvulsant
  • Opioid receptor antagonist + atypical antidepressant
  • 5-HT2C receptor agonist
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3
Q

MOA of Catecholaminergic, Stimulant, Sympathomimetic Medications

A

increase levels of norepinephrine (and serotonin and dopamine to some extent) by inhibiting the reuptake

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4
Q

ADE of Catecholaminergic, Stimulant, Sympathomimetic Medications

A
  • increased heart rate
  • increased blood pressure
  • insomnia
  • nervousness / anxiety
  • loss of appetite
  • dry mouth, palpitation
  • euphoria / dysphoria
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5
Q

Duration of use of Catecholaminergic, Stimulant, Sympathomimetic Medications

A
  • not longer for more than 3 months

- high abuse potential

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6
Q

Catecholaminergic, Stimulant, Sympathomimetic Medications drug interactions

A
  • may cause toxicity if taken with MAOI b/c can increase levels of dopamine, 5HT, NE
  • takes 2-3 weeks to make new MAO
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7
Q

Catecholaminergic, Stimulant, Sympathomimetic Medications: brain or periphery? decreasing appetite or increasing energy expenditure?

A
  • brain

- increasing energy expenditure

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8
Q

Catecholaminergic, Stimulant, Sympathomimetic Medication examples

A
  • Benzphetamine
  • Diethylpropion
  • Phendimetrazine
  • Phentermine
  • Amphetamine / Amphetamine-like drugs
  • Amphetamine
  • Dextroamphetamine
  • Methamphetamine
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9
Q

MOA of Fat absorption inhibitors

A
  • lipase inhibitor

- inhibits fat from getting absorbed

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10
Q

Fat absorption inhibitors: brain or periphery? decreasing appetite or increasing energy expenditure?

A
  • periphery

- neither; inhibiting fat from being absorbed

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11
Q

Fat absorption inhibitor example

A

Orlistat

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12
Q

Orlistat

A
  • OTC: 60mg TID; Rx: 120mg TID (max effect seen at 120mg)
  • not very effective
  • take with fat-containing meal (during or up to 1 hr after)
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13
Q

ADE of Fat absorption inhibitor

A
  • loose, greasy stool, diarrhea
  • abdominal cramping
  • bloating
  • b/c the fat is fermenting
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14
Q

How can you manage the ADE of Fat absorption inhibitors?

A
  • avoid eating super high fat containing meal; the more fat in the gut, the worst the effects
  • if there are GI history, do not start with this drug
  • dose dependent
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15
Q

MOA of Phentermine + Topiramate

A
  • Phentermine: stimulant, increase in NE levels
  • Topiramate: anti convulsant (decreases excessive neuron activity by stabilizing sodium channels in inactive state and increasing GABA activity)
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16
Q

Phentermine + Topiramate: brain or periphery? decreasing appetite or increasing energy expenditure?

A
  • brain
  • increase energy expenditure
  • argument for decrease appetite b/c ADE of dry mouth
17
Q

Duration of use of Phentermine + Topiramate

A
  • can be used more than 3 months

- do not abruptly d/c b/c the topiramate can cause rebound seizures

18
Q

ADE of Phentermine + Topiramate

A
  • mood changes
  • fatigue
  • insomnia (take in a.m.)
  • increased heart rate
  • dry mouth (both topiramate and phentermine)
19
Q

MOA of Naltrexone + Bupropion

A
  • Naltrexone is an opioid receptor antagonist (nonspecific)
  • Bupropion is an atypical antidepressant (Blocks norepinephrine and dopamine reuptake transporters)
  • Combined use may block “reward” of food and increase mood
20
Q

Naltrexone + Bupropion: brain or periphery? decreasing appetite or increasing energy expenditure?

A
  • brain (?)

- decreasing appetite

21
Q

ADE of Naltrexone + Bupropion

A
  • Increased risk of suicidal thoughts/behaviors (boxed warning)
  • Seizures
  • Increased blood pressure and heart rate
  • CNS depression (sedation)
  • all due to bupropion
22
Q

Naltrexone + Bupropion clinical concerns

A
  • seizures
  • heart conditions
  • uncontrolled hypertension
23
Q

Naltrexone + Bupropion drug interactions

A
  • may cause toxicity if taken with MAOI b/c can increase levels of dopamine, 5HT, NE
  • takes 2-3 weeks to make new MAO
24
Q

MOA of Liraglutide

A
  • GLP-1 agonist (gut-brain peptide)

- Decreases appetite through increase fullness / satiety

25
Q

Liraglutide: brain or periphery? decreasing appetite or increasing energy expenditure?

A
  • brain and periphery

- decrease appetite

26
Q

How should the patient eat while being on liraglutide?

A

eat 1/3 of the plate and wait to see if pt is still hungry

27
Q

ADE of liraglutide

A
  • Pancreatitis
  • Gallbladder issues
  • Irritation of injection site
  • Nausea / vomiting (eating too fast)
28
Q

MOA of Lorcaserin

A
  • 5-HT2C receptor agonist (specific receptor which bypasses other ADE’s)
  • decreases hunger / increases satiety
  • directly stimulates neurons in the hypothalamus that are known to regulate feeding
29
Q

Lorcaserin: brain or periphery? decreasing appetite or increasing energy expenditure?

A
  • brain

- decreasing appetite

30
Q

Duration of use of Lorcaserin

A
  • approved for long term use

- CIV due to perceived risk for dependence or abuse

31
Q

What kind of patients should you be cautious with when using Lorcaserin? (not an objective)

A
  • moderate renal impairment (not recommended in end stage renal disease)
  • severe liver impairment
32
Q

What are OTC meds that can be used?

A
  • Stimulants: ephedra, caffeine, hoodia, bitter orange
  • Chitosan
  • pyruvate
  • chromium

OU Module Endo Fall 2018 (27 decks)

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