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Gastrointestinal System > Pharmacology & Treatment of Eating Disorders > Flashcards

Pharmacology & Treatment of Eating Disorders Flashcards

1
Q

What happens to the appetite during acute stress? Why?

A

It decreases due to the release of adrenaline

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2
Q

How is obesity determined?

A

By calculating the BMI

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3
Q

What is the calculation for BMI?

A

(Weight)/ (Height)^2

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4
Q

What is the initial treatment for obesity?

A

Comprehensive lifestyle intervention: a combination of diet, exercise and behavioral modification.

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5
Q

What dietary changes are made during initial treatment for obesity?

A

Lower calorie intake, cut down on sugars and fats

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6
Q

How long does initial treatment continue?

A

Depends on the patient, usually they are monitored and based on their process you choose to continue or not

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7
Q

When is subsequent treatment initiated?

A

When patients are unable to achieve weight loss goals with a comprehensive lifestyle intervention alone

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8
Q

What is the indication that the initial treatment is successful?

A

The patient loses about 5% of body weight in the time period of 3 to 6 months

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9
Q

What are the options of the subsequent treatment?

A

Pharmacologic treatment
Surgery

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10
Q

What is the goal of therapy?

A

To prevent, reverse or improve the complications of obesity and improve quality of life

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11
Q

What are the characteristics required by an obese individual to initiate pharmacological therapy?

A

BMI > 30
OR
BMI > 27 with at least one weight-related comorbidity

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12
Q

Are most drugs long or short- term?

A

Short-term

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13
Q

Which drugs are used for long-term weight management?

A

The newer medications

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14
Q

When are drugs considered effective?

A

If they demonstrate at least a 5% greater reduction in body weight than placebo

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15
Q

What kind of comorbidities is obesity associated with?

A

Type 2 DM
HTN
Dyslipidemia
CHD

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16
Q

What is the correlation between BMI and morbidity/mortality?

A

The higher the BMI, the greater the risk of morbidity and mortality

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17
Q

Why has the role of drug therapy been questioned?

A

Concerns regarding efficacy, potential abuse, side effects and cost

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18
Q

What are examples of GLP1 receptor agonists?

A

Semaglutide
Liraglutide

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19
Q

What is the mechanism of action of GLP1 receptor agonists?

A

Chemically modified versions of GLP1, stimulating binding to GLP1 receptors

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20
Q

Where do GLP1 receptor agonists act?

A

CNS, areas of the brain like hypothalamus which are involved in the regulation of appetite and calorie intake.

Stomach, short period of satiety and loss of appetite by slowing gastric emptying.

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21
Q

How does slower gastric emptying help reduce weight?

A

Food remains in the stomach for longer, the stomach takes longer to empty out and thus sends a “hunger” signal (ghrelin). Slower rate of absorption of food in the bloodstream.

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22
Q

What do GLP1 agonists also stimulate secretion of?

A

Secretion of incretin which increases glucose-dependent insulin secretion

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23
Q

What is the effect of incretin?

A

Decreases inappropriate glucagon secretion.

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24
Q

Which kind of patients are GLP1 agonists preferred to be given to because of incretin?

A

Type 2 diabetes patients –> improve glycemic levels and reduce weight

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25
Q

Is semaglutide long or short-term use?

A

Chronic weight management

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26
Q

What are the main side effects of GLP1 agonists?

A

GI side effects: nausea and vomiting
Diarrhea
Anorexia

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27
Q

What is the example of dual-acting GLP1 & GIP receptor agonist?

A

Tirzepatide

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28
Q

What is Tirzepatide?

A

A dual-acting GLP1 and GIP receptor agonist that is used as first-line medication

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29
Q

What is the function of GIP?

A

GIP increases insulin secretion, improves glucose tolerance and reduces gastric acid secretion

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30
Q

What is the mechanism of action of Tirzepatide?

A

The dual agonism decreases hyperglycemia severely more than just GLP1 agonists on their own, and reduces patient’s appetite

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31
Q

What was the body weight percentage drop after giving Tirzepatide to patients with no diabetes?

A

16.5 % to 22.4% over 72 weeks

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32
Q

What are the PK of Trizepatide?

A

Subcutaneously given by weekly injection

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33
Q

What are the adverse effects of Trizepatide?

A

Nausea, Vomiting, Diarrhoea, Constipation and Increased Heart Rate

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34
Q

What should patients on GLP1 or dual acting GLP1/GIP agonists be monitored for?

A

Depressive symptoms and suicidal thoughts
Unusual changes in mood or behaviour

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35
Q

What are the contraindications for both GLP1 and GLP1/GIP agonists?

A

Patients with personal or family history of medullary thyroid carcinoma

Patients with multiple endocrine neoplasia syndrome type 2

Pregnancy

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36
Q

Why are GLP1 and GLP1/GIP agonists contraindicated during pregnancy?

A

Can cause teratogenicity, fetotoxicity and abortion (seen in animals)

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37
Q

What is an example of lipase inhibitors?

A

Orlistat

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38
Q

When are lipase inhibitors taken?

A

Only after fatty meals, it prevents the lipase enzymes from breaking down fats and being absorbed and stored in the body

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39
Q

What is the MOA of Orlistat?

A

Decreases the breakdown of fat into smaller molecules and therefore, decreases fat absorption by about 30% and increases fecal fat excretion

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40
Q

What are the pharmacokinetics of Orlistat?

A

Administered orally with each mean that contains fat

Minimal systemic absorption, excreted in the feces

No dosage adjustments required in patients with renal/hepatic dysfunction

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41
Q

What are the side effects of lipase inhibitors ?

A

Oily stool
Diarrhea
Decreased absorption of lipid soluble vitamins

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42
Q

What does Orlistat interfere with the absorption of?

A

Fat-soluble vitamins (vitamins A, D, E, and K) and β-carotene, patients should be advised to take a multivitamin supplement at bedtime

Other medications

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43
Q

What other medications does Orlistat interfere with?

A

Amiodarone
Cyclosporine
Levothyroxine

44
Q

Is Orlistat a short or long-term medication?

A

Available for long-term treatment of obesity but clinical utility is limited due to GI side effects

45
Q

How are the GI side effects of Orlistat minimised?

A

Though low-fat diet and cholestyramine

46
Q

What is cholestyramine?

A

A drug that reduces the re-absorption of bile in the body

47
Q

What are the contraindication of Orlistat?

A

Pregnancy
Patients with chronic malabsorption syndrome

48
Q

What are anorexiants?

A

Appetite suppressants; sympathomimetic drugs and are classified as controlled substances

49
Q

Why are anorexiants classified as controlled substances?

A

Due to dependence and abuse potential

50
Q

What are examples of Anorexiants?

A

Phentermine
Diethylpropion
Benzphetamine
Phendimetrazine

51
Q

Are anorexiants approved as long or short-term medication treatments?

A

Short-term because of their potential side effects and potential abuse

52
Q

What is the MOA of Phenetrmine?

A

Increases the release of norepinephrine and dopamine and inhibits their uptake in nerve terminals

53
Q

What is the result of increasing levels of dopamine and norepinephrine?

A

Decrease appetite which facilitates weight loss

54
Q

When does weight loss plateau?

A

When tolerance is achieved, discontinuation of drug should be progressive and not immediate

55
Q

What re the pharmacokinetics of anorexiants?

A

Rapidly absorbed after oral administration
Peak plasma concentration within 1 to 2 hours
Undergo extensive first pass metabolism
Metabolised to inactive compounds by the liver
Elimination via the kidneys

56
Q

What is the half life of anorexiants?

A

Short, 4 to 8 hours

57
Q

What are the side effects of anorexiants?

A

Increase HR and BP
Dizziness, headache and insomnia
Changes in libido
Constipation, diarrhoea and nausea

58
Q

What are the contraindications fro anorexiants?

A

Patients with HTN, CVD, arrhythmias, HF or stroke and history of drug abuse

59
Q

Which is the most widely prescribed weight loss drug?

A

Phentermine

60
Q

What are combination drug treatments?

A

Combining two drugs with different mechanisms of action that improve efficacy

61
Q

What are examples of combination drugs?

A

Phentermine-Topiramate
Bupropion-Naltrexone

62
Q

Is the combination drug Phentermine- Topiramate long or short term use?

A

Long term use

63
Q

What is the MOA of Phentermine- Topiramate?

A

Topiramate affects the activity of two neurotransmitters: GABA enhancement and glutamate decrease

Phentermine is a stimulant to contradict the sedation

64
Q

What is the effect of Topiramate on its own?

A

Induction of sedation

65
Q

What are the side effects of Phentermine- Topiramate?

A

Suicidal ideation, cognitive function decrease and dry mouth

66
Q

What are the contraindication of Phentermine- Topiramate?

A

Contraindicated in pregnancy
Patients with history of renal stones
Patients with CVD

67
Q

Why is Phentermine- Topiramate not given to patients with history of renal stones?

A

Topiramate is a weak carbonic anhydrase inhibitor, increases calcium excretion and decreases citrate in urine

68
Q

Discontinuation of Phentermine- Topiramate?

A

Should not be stopped abruptly, can cause seizures

69
Q

When was Bupropion-Nalterxone FDA-approved?

A

September 2014

70
Q

Is Bupropion-Nalterxone first line treatment? Which kind of patients is it suggested to?

A

No, it could be prescribed for the obese smokers who desire pharmacology therapy for smoking cessation and obesity

71
Q

What is Bupropion?

A

A weak dopamine and norepinephrine reuptake inhibitor

72
Q

What is Bupropion used for?

A

Treatment of depression and smoking cessation.

73
Q

What is Naltrexone?

A

Opioid-receptor antagonist used to treat alcohol and opioid dependence

74
Q

What is the MOA of Bupropion-Nalterxone?

A

Stimulate POMC neurons through bupropion,
Blocking the auto-inhibitory mechanisms of POMC with naltrexone

75
Q

What is Bupropion-Nalterxone metabolised by?

A

By CYP2B6, low risk of drug to drug interactions

76
Q

What are the side effects of Bupropion-Nalterxone?

A

Nausea, headache, seizure, constipation.
Low risk of young adults becoming suicidal during initial treatment

77
Q

Is Setmelanotide long or short term use?

A

Chronic weight management

78
Q

Who is Setmelanotide used for?

A

Adult and paediatric patients 6 years of age and above with monogenic or syndromic obesity

79
Q

What kind of deficiencies allow for Setmelanotide use?

A

POMC
OCSK1
LEPR
Bardet-Biedl Syndrome

80
Q

What is the Bardet-Biedl syndrome?

A

Inherited disease that causes loss of night and peripheral vision

81
Q

What is the MOA of Setmelanotide?

A

Acts on the MC4R agonist
Potentially restores the function of an impaired MC4R pathway, reduces hunger

82
Q

What is the MC4R?

A

Key part of the biological pathway that regulates hunger, calorie intake and energy expenditure

83
Q

What is an example of serotonin agonists?

A

Lorcaserin

84
Q

What is the effect of serotonin?

A

Reduces food intake in animals and human beings

85
Q

What is the MOA of Lorcaserin?

A

Selective agonist that activates serotonin 2C receptors.

Activation of POMC –> activation of melanocortin receptors

Decrease in appetite

86
Q

Was Lorcaserin used long or short term?

A

Long-term use

87
Q

What drug does Lorcaserin have similar efficacy but lower side effects with?

A

Orlistat

88
Q

Where are serotonin 2C receptors found?

A

Most in the central nervous system

89
Q

When was Lorcaserin discontinued and why?

A

February 2020 because of an increased occurrence of cancer

90
Q

What types of cancers were associated with Lorcaserin?

A

Colorectal, pancreatic and lung cancers

91
Q

What were the side effects of Lorcaserin?

A

Nausea
Headache
Dry mouth
Dizziness
Constipation
Mood changes and Suicidal Ideation

92
Q

What are the pharmacokinetics of Lorcasterin?

A

Extensively metabolised in the liver to inactive metabolites and eliminated in the urine

93
Q

What is the effect of Lorcaserin on Type 2 DM patients?

A

Higher risk of hypoglycemia

94
Q

What are the contraindication of Lorcaserin?

A

Pregnancy

95
Q

What are some examples of not recommended therapies?

A

Green tea, garcinia cambogia, conjugated lionelic acid chitosan
calcium
chromium, gambisan, hoodie gordonii

96
Q

What are orexigenic drugs?

A

Appetite stimulants, increase appetite and enhance food consumption

97
Q

When are orexigenics prescribed?

A

Severe appetite loss or muscle eating due to CF, anorexia, old age, cancer or AIDS

98
Q

What are examples of oexigenics?

A

Corticosteroids
Progesterone analogues
Cannabinoids
Serotonin antagonists
Anabolic steroid
Mirtazapine

99
Q

What is an example of corticosteroids (orexigenic)?

A

Dexamethasone

100
Q

What is the difference between glucocorticoids and progesterone analogues?

A

Progesterone analogues have fewer side effects

101
Q

What is an example of serotonin antagonist?

A

Cyproheptadine

102
Q

What is an example of cannabinoid?

A

Dronabinol

103
Q

MOA of Dronabinol:

A

A synthetic version of THC acts on cannabinoid receptors in the brain.
Relieves nausea

104
Q

Which kind of patients are androgens given to?

A

Older persons to increase muscle mass or to help patients recovering from severe illness or injury

105
Q

What is an example of an androgen?

A

Oxandrolone

106
Q

What is an example of tetracyclic antidepressant?

A

Mirtazapine

107
Q

What is the MOA of Mirtazapine?

A

Treatment for major depression, weight gain is a side effect

Gastrointestinal System (28 decks)

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