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Pharmacy School 2015-16 > Complementary Medicine Exam 2 (Obesity) > Flashcards

Complementary Medicine Exam 2 (Obesity) Flashcards

1
Q

Typical Body Composition (Male and Female)

A

Male:
Muscle (45%), Essential Fat (3%), Nonessential fat (12%), Bone (15%), Other (25%)

Female:
Muscle (36%), Essential Fat (12%), Nonessential fat (15%), Bone (12%), Other (25%)

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2
Q

Differences in fat and muscle in males and females

A

Body Fat: 15% total in men (12% storage, 3% essential), 27% total in women (15% storage, 12% essential)

Muscle: 31% in men, 20.4% in women

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3
Q

Lean Body Mass (LBM)

A

LBM is an in vivo concept essential for normal physiological functioning throughout the lifespan

In men, FFM includes 3% essential fat and 12% essential fat in women

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4
Q

LBM vs FFM

A

LBM includes lipid rich essential fat stores in bone marrow, brain, spinal cord and internal organs. FFM does not include this essential fat.

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5
Q

Obesity Key Facts

A

Doubled worldwide since 1980

More women than men obese

High percentage of children (17%) are obese

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6
Q

What Obesity causes

A

Energy imbalance between calories consumed and those expended.

Global increase in intake of energy dense foods high in fat.

Increase in inactivity – many causes

Other factors include diet and physical activity patterns, lack of policy, agriculture, food production, distribution and marketing, etc.

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7
Q

Malnutrition

A

An acute, subacute or chronic state of nutrition in which varying degrees of overnutrition or undernutrition with or without inflammation activity have led to a change in body composition and diminished function.

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8
Q

Malnutrition prevalence

A

High prevalence in hospitals.

Leads to high rates of cancer (GI, head and neck, lung and pancreatic)

Also increases in COPD and cerebrovascular accident

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9
Q

Obesity can be a long-term, low level _______________

A

Catabolic Stress

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10
Q

Catabolic stress shifts

A

Acute phase responses elicit cytokine-mediated responses and favors the catabolic state; obesity is a long-term catabolic stressor

Acute phase metabolic response favors increase in REE, shift towards positive acute phase reactants, export of amino acids from muscle, increase in gluconeogenesis and expansion of ECF

Downregulation of liver proteins such as albumin in order to increase proteins needed for immune response such as clotting and wound healing.

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11
Q

Inflammation promotes

A

Muscle catabolism, inhibition of protein synthesis and repair, hyperglycemia, decreased visceral proteins, edema, anorexia, deconditioning/sarcopenia

Inflammation in the brain can cause loss of appetite.

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12
Q

Sarcopenia can result from

A

1 day of bed-rest; or 1 day in space

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13
Q

Starvation-related malnutrition

A

No inflammation

Limited access to food; anorexia nervosa, marasmus

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14
Q

Chronic disease-related malnutrition

A

Mild to moderate inflammation

Organ failure, pancreatic cancer, RA, sarcopenic obesity

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15
Q

Acute disease or injury-related malnutrition

A

Marked inflammatory response present

Infection, burns, trauma or closed head injury

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16
Q

How is malnutrition defined?

A

By presence or absence of inflammation

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17
Q

Sarcopenic obesity

A

Low lean body mass and excessive animosity

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18
Q

Main components of malnutrition identification guide

A

% caloric intake (under 75% for non-severe, or under 50% in severe)

% weight loss (wk, mo or 3 mo)

Decrease in sub q fat, decrease in muscle, increase in fluid/edema

Reduced grip strength (indication of severe malnutrition)

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19
Q

Chronic obesity is ___________ related

A

Stress related

When you have obesity in a chronic context, particularly if you are sarcopenic and have low LBM, you have chronic disease related malnutiriton.

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20
Q

Define Obesity

A

Complex multifactorial chronic disease that develops from interaction of genotype and the environment.

Our understanding is incomplete buy involves social, behavioral, cultural, physiological, metabolic and genetic factors.

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21
Q

Between what years did overweight and obesity prevalence spike?

A

1976 and 1980

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22
Q

Prevalence of obesity based on ethnic background

A

African American, Mexican American, Native American, Puerto Rican and White

Higher in females than in males in all groups

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23
Q

Geographic relationship in US between obesity and ___________________

A

Physical inactivity patterns

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24
Q

It has been hypothesized that care of _______________ will break our health system financially

A

Type 2 Diabetes

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25
Q

Your ___________ is a better predictor of your health than your genetic code

A

Zip codeq

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26
Q

Obesity and cancer burden

A

Accounts for 5% of total cancer burden

39% endometrial cancer, 25% kidney, 11% of colon, 9% of postmenopausal breast cancer

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27
Q

______% of cancer burden worldwide associated with infectious agents

A

17

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28
Q

Diet means

A

Manner of living

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29
Q

Assessment of risk for co-morbidities due to obesity

A

BMI, Waist circumference, weight gain since age of 18, level of fitness

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30
Q

BMI values

A 
Underweight (under 18)
Normal (20-24)
Overweight (25-29) 
Obese (over 30)
Morbid obesity (over 40)
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31
Q

Waist circumference is good estimate of

A

Central adiposity (this weight wraps around visceral organs)

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32
Q

BMI calculation

A

Weight (kg) / Height (m)^2

[Weight (lbs) x 703] / height (in)^2

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33
Q

Obesity is caused by…

think general

A

the superimposition of specific environmental conditions on a susceptible genotype

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34
Q

Obesity prevalence in the US

A

300,000 deaths per year, 2nd in preventable mortality only to smoking

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35
Q

Consequence of modest weight gain (visceral adipose tissue)

A

10% increase in weight results in:

Fasting blood glucose increase of 2-3 mg/dL

Systolic blood pressure increase of 6-7 mm Hg

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36
Q

Metabolic syndrome

A

Clustering of metabolic abnormalities including resistance to insulin-stimulated glucose uptake, hyperglycemia, hyperinsulinemia, increase in triglycerides and decreased HDL-cholesterol

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37
Q

Factors contributing to obesity and being overweight

A

Socioeconomic status, race/ethnicity, decreased physical activity, diet, earlier puberty, genetics and hereditary

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38
Q

Metabolic syndrome may lead to

A

Type 2 diabetes, CVD or Cancer

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39
Q

Conditions associated with obesity

A

Type 2 diabetes, gall bladder disease, stroke, coronary heart disease, gout, osteoarthritis, hypertension, sleep apnea

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40
Q

Central/Visceral Adipose tissue vs Subcutaneous adipose tissue

A

Central: Excess central or abdominal fat is independent predictor of disease risk, visceral fat is more metabolically active and those with high amounts are more susceptible to metabolic syndrome

SubQ: Minimal risk associated with lower body obesity

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41
Q

Adipose tissue as an endocrine organ

A

Increases in:

  • Lipoprotein lipase (liberates more fat from stores)
  • Leptin
  • IL-6
  • Adipsin
  • Serum free fatty acids
  • Angiotensinogen (vasoconstrictor)
  • Lactate
  • PAI-1

–> All of these add up to more viscous blood, clotting tendency, higher BP and contribute to higher LDL and lower HDL

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42
Q

Increase in Lipoprotein Lipase

A

Causes decreases in HDL and increases in LDL cholesterol; leads to increase in VLDL cholesterol

Eventual insulin resistance resulting in hyperglycemia

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43
Q

Common hormonal abnormalities in obesity

A

Increase cortisol, insulin resistance, decrease sex hormone binding globulin women (more tissue exposure to estrogen), decreased progesterone in women, decreased testosterone levels in men, decreased growth hormone production

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44
Q

Metabolic disorders associated with obesity

A

Type 2 diabetes (increases with degree and duration of overweight individuals; also increases in individuals with more central distribution of body fat)

Dyslipidemia

Liver disease

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45
Q

BMI and Type 2 Diabetes

A

Low BMI = Less risk of developing diabetes mellitus

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46
Q

Diabetes mellitus and weight loss

A

Weigh loss reduces risk of developing diabetes.

Weight loss of 5-11 kg decreased risk by nearly 50%

Type 2 DM almost nonexistent in those with weight loss of more than 20kg or with BMI under 20

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47
Q

Dyslipidemia finding related to obesity

A

Inverse relationship between HDL and BMI (may be more important than BMI and TG relationship)

Central fat plays huge role in lipid abnormalities

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48
Q

NAFLD

A

Nonalcoholic fatty liver disease describes a collection of liver abnormalities associated with obesity.

75% steatosis, 20% steatohepatitis, and 2% cirrhosis

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49
Q

Adipose Tissue

A

Specialized connective tissue that function as the major storage for fat in the form of triglycerides.

Two forms: White and Brown

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50
Q

Brown vs White adipose tissue

A

Brown: deeply vascularized, dense with mitochondria, releases energy directly as heat as result of excess caloric intake via diet-induced thermogenesis (heat generation related to mitochondria metabolism)

White: insulation, cushion and major source of stored energy

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51
Q

Describe White Adipose Tissue

A

Major bulk of adipose tissue in adult mammals is loose associate of lipid-filled cells with adipocytes

Held in framework of collagen fibers

Adipose tissue also contains stromal-vascular cells including fibroblastic connective tissue, leukocytes, macrophages, and pre-adipocytes, which contribute to structure integrity

Each adipocyte is in close proximity to a capillary

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52
Q

Uniqueness of adipose organ

A

Only body tissue that can markedly change mass in adulthood (2-3% in athlete to 70% in morbidly obese)

Normal 22% men and 32% women

Composed of stromal vascular cells, blood vessels, lymph nodes and nerves

Blood flow lower than other organs (gets 0.2-0.6L/min, or 3-7% of CO; 15-30% in obese)

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53
Q

Adipose tissue locations

A

SubQ fat, Dermal fat, Intraperitoneal or omental fat

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54
Q

Adipocyte proliferation

A

They can hypertrophy (increase in size due to excess triglyceride) or hyperplasia (increase in number)

Half life of 8.4 years

As we age adipocytes have blunted ability to proliferate, differentiate, and confer resistance to cell death –> favoring ectopic fat accumulation

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55
Q

Adipose secretions

A

Adiponectin - sensitizes skeletal muscle; positive mediator for glucose homeostasis; made primarily by subQ adipose tissue; levels drop in those who are morbidly obese

Contribute to risk of increase lipids, increase BP, increase thrombotic tone

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56
Q

Oxygen can diffuse across ____ cell widths

A

6

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57
Q

Extracellular matrix __________ during obesity and adipocyte expansion

A

Hardens, or increases in rigidity

Macrophages aggregate to clean up dead adipocytes, followed by inflammatory mediators

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58
Q

Describe fibrotic stage in obesity

A

ECM changes cause abnormal fibrotic tissue and an increase in collagen 4

Unconstrained adipocyte cell grwoth, hypoxia and no increase in vascularization

Many dead cells and macrophages - macrophages increase number of cytokines

More matrix metalloproteases to help immune cells clear damage

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59
Q

Lipodystrophy

A

Caused by certain anti-retrovirals

Degeneration of body’s adipose tissue

60
Q

Lipolysis

A

Breakdown of lipids and involves hydrolysis of triglycerides into FFA followed by further degradation into acetyl units by beta oxidation

61
Q

Lipotoxicity

A

Cellular dysfunction due to lipid imbalance; surplus FFA induction of apoptosis

62
Q

Macrophage differences in healthy vs not healthy adipose tissue

A

More M1 macrophages in non-healthy –> associated more often with inflammation

M2 accumulate during negative energy balance

63
Q

Triangle of approach to obesity treatment

A

behavioral, pharmacotherapy, diet and exercise

64
Q

Benefits of modest weight loss

A

Normalization of BP

Decrease in blood levels of LDL, insulin, glycated hemoglobin (HbA1C), blood glucose and uric acid

Increased HDL

Improved quality of life

65
Q

Survival paradox

A

A high BMI can be beneficial (heart disease, cardiac bypass surgery, etc.)

Could be because people lose weight to an unhealthy point, or that the reserves may serve as a buffer for stress or other things.

66
Q

Obesity treatment pyramid, top to bottoms.

A

Surgery

Pharmacotherapy

Lifestyle modification –> Diet, Physical activity

67
Q

Realistic weight loss treatment goals

A

5-10% weight loss

Focus on health, fitness, and energy level

Positive mood and appearance

Functional and recreational activities

68
Q

BMI of ____ or above, bariatric surgery is the only option.

A

40

69
Q

General guidelines for medical management of overweight or obese patients

A

Diet, physical activity, behavioral therapy (irregardless of BMI)

For some, pharmacologic (27 with co-morbidities, or BMI over 30) or bariatric surgery (BMI over 35 with co-morbidities or BMI over 40)

70
Q

Indication for bariatric surgery

A

BMI over 40 or more than 100 pounds overweight

BMI over 35 with 2 obesity related comorbidities

Inability to achieve a healthy weight loss sustained for a long period of time

71
Q

Common bariatric procedures

A

Gastric bypass, sleeve gastrectomy, adjustable gastric band, biliopancreatic diversion with duodenal switch

72
Q

Many pharmacologic obesity agents target ________________

A

Appetite

73
Q

Indications for obesity drugs

A

Those engaging in behavior therapy, dietary changes, and increased physical activity for at least 6 months without success

Weight loss drugs should never be used without continuous lifestyle modifications and continual assessment

BMI 30 or more OR BMI 27 or more with comorbid condition; should have realistic weight loss expectations and demonstrate readiness to change; are unable to lose weight with lifestyle modifications alone and are willing to comply with medication use; no medical or psychiatric contraindications

74
Q

Contraindications or cautions for use of obesity drugs

A
  • Pregnancy or lactation
  • Unstable cardiac disease
  • Uncontrolled hypertension (SBP > 180, DBP > 110)
  • Unstable severe systemic illness
  • Unstable psychiatric disorder or history of anorexia
  • Other drug therapy, if incompatible (MAO inhibitors, migraine drugs, adrenergic agents, arrhythmic potential)
  • Closed angle glaucoma
  • General anesthesia
75
Q

Medication types that can cause weight gain

A

Psychotropic medications (tricyclic antidepressants, MAOIs, SSRIs, atypical antipsychotics, lithium, anticonvulsants)

Beta-blockers

Diabetes medications (insulin, sulfonylureas, thiazolidinediones)

Highly active antiretroviral therapy

Tamoxifen

Steroid hormones (glucocorticoids, progestational steroids)

76
Q

Strategies for obesity drug action

A

Reduce food intake

Block nutrient absorption in the intestine

Increase non-shivering thermogenesis (brown adipose tissue)

Modulating fat metabolism/storage through appropriate adjustments in food intake

Modulating the central regulation of body weight

77
Q

Orlistat/Xenical

A

120mg / meal

MOA: Peripheral - Blocks absorption of 30% of consumed fat; lipase inhibitor

Side effects: GI symptoms (oily spotting, flatus with discharge, fecal urgency, oily stools, incontinence)

78
Q

Sibutramine/Meridia

A

5-15 mg /d

MOA: Central - inhibits synaptic reuptake of NE and serotonin

Side effects: dry mouth, constipation, headache, insomnia, increased blood pressure, tachycardia

Enhances satiety with no cardiac, lung or neurotoxic effects.

79
Q

Phentermine/Adipex, Fastin, lonamin, etc.

A

15-37.5 mg/day

MOA: Central - stimulates release of NE

Side effects: CNS stimulation, tachycardia, dry mouth, insomnia, palpitations

80
Q

Fenfluramine/Phentermine (Fen/Phen)

A

Patients not properly assessed

Many patients developed valvular heard disease (8-32%) causing withdrawal in 1997

81
Q

Lorcaserin and Phentermine

A

Lorcaserin (Serotonin 2C receptor agonist)

phentermine/topimerate (a sympathomimetic amine/antiepileptic drug)

Both used as adjunct to exercise

Very low rates of use

82
Q

Orlistat, lorcaserin and phentermine/topiramate efficacy

A

3% | 3% | 9% (additional weight loss from placebo)

35-73% | 37-47% | 67-70% (achieved weight loss of at least 5%)

83
Q

No obesity agent has shown to ___________

A

reduce cardiovascular morbidity or mortality

84
Q

School programs for obesity prevention

A

Curriculum includes healthy eating, physical activity and body image

Increased physical activity sessions and fundamental movement skills

Improvement in nutritional quality of food in school

Environmental and cultural practices to promote healthier foods and being active

Support for teachers and staff to implement health promotion

Parent support and home activity that encourage children to be more active and nutritious

85
Q

Changes in dietary behaviors

A

Increased consumption of sugar sweetened beverages

Continued low consumption of fruits and vegetables (only increased by 1/2 serving in 30 years)

Increased frequency of meals eaten away from home

86
Q

The food environment

A

Increased number of fast food restaurants, lack of access to grocery stores selling affordable food, less health food and beverage advertising aimed at children

87
Q

State of physical activity

A

35.5% of adults do not engage in recommended levels and 25.4% report no leisure-time activity

in 2009, 81.6% of high school students did not participate in 60 or more minutes of physical activity on any day of the previous 7 days

Only 30% of high school students have daily `PE

88
Q

Environmental factors that influence physical activity behavior

A

Lack of infrastructure supporting active transportation (sidewalks)

Access to safe places to play and be active

Access to public transit

Mixed use and transit oriented developments

89
Q

Target behaviors for change for obesity prevention

A

Increased physical activity

Increased consumption of fruits and vegetables (helps with satiety)

Increased breastfeeding initiation for at least 6 months, duration and exclusivity

Decrease consumption of sugar sweetened beverages

Decrease consumption of high energy dense, nutrient poor, foods

Decrease television viewing

90
Q

WHO drivers of obesity

A

Reduction in time-cost of food and changes in global food system.

Increased food energy supply through increased mechanization

Present systems of monitoring population weight and nutrition are inadequate in most countries. WE NEED POLICY.

91
Q

Endocrine society clinical practice guidelines for obesity

A

Diet, exercise and behavior change (BMI 25 or more)

Pharmacotherapy (BMI 27 or more with comorbidity, OR BMI over 30)

Bariatric surgery (GMI 35 or more with comorbidity or BMI over 40)

Assessement of efficacy and safety of pharm therapy monthly for first 3 months, then every 3 months following. If less than 5% weight loss at 3 months, discontinue.

In those who are obese with T2DM, use antidiabetic withadditional weight loss properties (glucagon-like peptide-1 analogs OR SGLT-2 inhibitors) in addition to first-line agent for T2DM

92
Q

Non-nutritive sweeteners

A

Reduce intake of carb-rich foods and replace sucrose with non-nutritive (zero calorie) sweetener

*average American adult consumes 64 lbs of sucrose/year, mostly from processed foods

Saccharin, Cyclamate, Aspartame, Neotame, Acesulfane-K, Sucralose, Stevia, Xylitol

93
Q

Saccharin (Sweet’N Low)

A

Synthesized in 1878

300-fold sweeter than sucrose; bitter aftertaste

Heat instable, so limited to use in non-baked products

Causes bladder cancer in rads due to micro-crystals which do not develop in humans

94
Q

Cyclamate (Sucaryl)

A

Synthesized in 1937

30-50 times sweeter than sucrose with no bitter aftertaste

Heat stable

Initially labeled GRAS but banned by FDA due to risk of bladder cancer (hexylamine suspected carcinogen)

Still sold in many countries

95
Q

Aspartame (Equal, Nutrasweet)

A

Methylated dipeptide

200 fold sweeter than sucrose

Not heat-stable; products not toxic

Very popular (use in more than 1200 products)

96
Q

Aspartame Metabolism

A

Cleavage into Aspartate and phenylalanine
>Phenylalanine metabolized to yield methyl group
>Methyl group further metabolized to yield formic acid

Phenylalanine usually hydroxylated into tyrosine, mediated by phenyl alanine hydroxylase
.This enzyme is not functional in phenylketonuria (PKU) patients

PKU Patients instead convert phenylalanine into phenylpyruvic acid
>Phenylpyruvic acid converted into phenylactate
»Both cause poor brain development, seizures, etc.

97
Q

Neotame

A

Approved in 2002 but not used in foods

7,000-13,000 fold sweeter than sucrose

Less metabolic conversion into amino acids

20-30% absorbed

Negligible effect on PKU patients

98
Q

Acesulfane-K (Sunette)

A

200-fold sweeter than sucrose

Heat stable

Not metabolized

Used in some beverages

Combined with other sweeteners due to bitter aftertaste

99
Q

Sucralose (Splenda)

A

Chlorinated derivative of sucrose (3 chlorine)

600-fold sweeter than sucrose

Not metabolized; heat stable

general purpose sweetener

(FDA approved since 1999)

100
Q

Stevia (Truvia, Rebiana)

A

Stevioside and related diterpene glycosides from Stevia rebausiana

200-fold sweeter than sucrose

No evidence for stevioside and steviol being genotoxic in vivo.

Rebaudioside A determined GRAS by FDA in 2008

n=2, stevioside
n=3, rebaudioside A

101
Q

Xylitol (Trident)

A

Polyol

Same sweetness as glucose, 40% fewer calories

Does not promote dental caries or plaque formation

Sweetener in some chewing gums (can still be labeled sugar free)

Can be used by diabetics

Manufactured by hydrogenation of xylose from corncobs and woodpulp

102
Q

Olestra (Olean)

A

Sucrose esterified with stearic acid

Not readily hydrolyzed into fatty acids and sucrose and poorly absorbed

Has potential for hypovitaminosis (ADEK)

May cuase GI cramping and loose stools

Used in the manufacture of potato chips, pretzels and microwave popcorn

103
Q

Orlistat (Alli, Xenical)

A

Semisynthetic of natural product lipastatin from Streptomyces toxytricini

Irreversible inhibitor of pancreatic lipase (=less fat breakdown = less fat absorption)

MOA: hydroxyl of lipase attacks carboxyl carbon of orlistat.

Not absorbed but interacts with many compounds

AD: GI related (oily stools, cramps, flatulence)

Non-prescription drug: Alli, 60mg taken with each fat-containing meal up to 3x/day

Rx drug: Xenical, 120mg with each fatty meal 3x/day
*used as adjunct to diet and exercise and can be used long-term

104
Q

Orlistat notable interactions

A

Cyclosporine, levothyroxine, warfarin, fat soluble vitamins (except E)

105
Q

Total length of therapy for anorexiants

A

Usually shorter than 12 weeks, no longer than 6 months

106
Q

Anorexiants (classes)

A

Sympathomimetic amines

Serotonergic agents

*most are CNS stimulants with abuse potential

107
Q

Sympathomimetic amines (adrenergic agents)

A

Release NE from storage vesicles in adrenergic neuron and block reuptake

Appetite suppression secondary to CNS stimulation and not understood

DO NOT USE WITH OTHER APPETITE SUPPRESSANTS

Withdrawal if suddenly stopped (depression, fatigue)

Amphetamine, Ephedrine and Pseudoephedrine, Phentermine, Mazindol

108
Q

Amphetamine

A

Prototypical anorexiant

Use in diet pills banned in 1979

109
Q

Ephedrine and Pseudoephedrine

A

Some OTCs contain ephedrine, a natural product in Ephedra (Ma Huang) banned in 2006

Both are common ingredients of cold and allergy meds

110
Q

Phentermine

A

Single weight-loss agent to decrease appetite

Schedule 4 (less potential for abuse than amphetamine)

Continued use can lead to tolerance and rebound weight gain

111
Q

Phentermine/Topiramate (Ionamine)

A

Approved in 2012

Topiramate originally an anticonvulsant in epileptic patients

MOA unknown

112
Q

Mazindol (Sanorex)

A

Schedule 4

Approved for patients with BMI above 30 OR BMI above 27 with comorbidity (hypertension, hyperlipidemia, diabetes)

Tolerance develops over time (useful only during first few weeks)

113
Q

Serotonergic Agents

A

Fenfluramine, Sibutramine. Lorcaserin

114
Q

Fenfluramine (Pondimin)

A

Became popular in 1992 in combo with phentermine (Fen-Phen combo)

Withdrawn due to risk of heart valve disease

*Proposed MOA: stimulation of 5-HT2B receptors leads to inappropriate valve cell division

No longer marketed worldwide

115
Q

Sibutramine (Meridia)

A

Adrenergic/serotonergic agent

MOA: inhibits NT reuptake and stimulation of thermogenesis by activating the B3 adrenergic system in brown adipose tissue

Withdrawn in 2010 due to CV risks and minimal efficacy

Over 60 dietary and herbal supplements adulterated with sibutramine since withdrawal

116
Q

Lorcaserin (Belviq)

A

Selective 5-HT2c receptor agonist

Reduced heart valve disease concerns.

117
Q

Cannabinoid Receptor Antagonist

A

Cannabinoids stimulate appetite (very useful in those with cancer)

Rimonabant (Acomplia): first centrally acting CB1 receptor blocker approved as anti-obesity drug

Withdrawn due to concerns of psychiatric side effects (increased risk of suicide)

118
Q

Glucagon-like-peptide-1 (GLP-1) receptor agonists

A

GLP-1 functions to (1) increase insulin secretion from pancreas; (2) inhibit gastric acid secretion and emptying; (3) increase satiety by acting on the CNS

119
Q

Liraglutide

A

Originally for treatment of type 2 diabetes; recently approved for obesity

Long-acting acylated derivative of GLP-1 with half-life of 13 hours (GLP-1 only has half life of a few minutes)

Produced by heterologous expression in Saccharomyces cerevisiae (Baker’s yeast) and attaching one palmitic acid to Lys in the peptide chaine via a Glu spacer

Injected SC once daily

AD: causes thyroid cancer in rats and contraindicated in those with Medullary Thyroid Carcinoma (MTC) or family history

Other GLP-1 mimetics not approved for obesity yet

120
Q

OTC diet pills and herbal remedies

A

Many are mixtures of natural products that also contain appetite suppressants such as ephedrine, propanolamine, or sibutramine (non FDA approved) Ex. LipoFuze –> contains 6 patented and 4 clinically tested fat burning ingredients; consumer must be aware of efficacy and safety

121
Q

SGLT-2 Inhibitors

A

Inhibit glucose reabsorption in kidney

>loss of glucose in urine
>loss of calories = weight loss
>indicated for type 2 diabetes 
>diuretic effect 
>camaglitozon, dapaglitozon
122
Q

Phentermine and diethylpropion contraindication(s)

A

Do not use if history of uncontrolled hypertension or heart disease

*elevations in mean BP and pulse rate in treated populations

**serotonin receptor agonist such as lorcaserin is better choice

***orlistat also safe

123
Q

First line(s) in diabetic

A

SGLT-2 or GLP-1

124
Q

Contraindication for CV disease

A

Do not use sympathomimetic drug such as lorcascrin and/or orlistat

125
Q

Consideration for women and contraceptives

A

BMI over 27 w/ 1 comorbidity OR BMI over 30, use oral contraceptive over injectable due to less potential for weight gain

126
Q

Consideration for RA or other chronic inflammatory diseases

A

Use NSAIDs and disease-modifying antirheymatic drugs since corticosteroids commonly produce weight gain

127
Q

Common endocrine obesity causes

A

Hypothyroidism

Cushing syndrome

128
Q

Common Drug-induced obesity causes

A 
Tricylic antidpressants 
Oral contraceptives
Antipsychotics 
Anticonvulsants 
Glucocorticoids 
Sulfonylureas 
Glitazones 
Beta-blockers
129
Q

Gut hormones and satiety?

A

GLP-1 in ileum in response to glucose promotes insulin release from pancreas and satiety

130
Q

Lorcaserin contraindication

A

Do not use in obese and depressed on SSRI or SNRI due to potential for serotonin syndrome

Phentermine/topiramate or phentermine alone better choice

Orlistat also safe

131
Q

Phentermin resin (MOA, AE and CI)

A

MOA: NE releasing agent

AD: Elevated BP, anxiety, cardiovascular palpitations, CNS overstimulation

Contraindications: anxiety disorders, uncontrolled hypertension, breast feeding and hyperthyroidism

132
Q

Lorcaserin 10mg (MOA and Cautions)

A

MOA: 5HT2c receptor agonist

Use in caution with SSRI, SNRI/MAOI, and St. John’s Wart

133
Q

Orlistat dosing

A

OTC: 60mg TID
Rx: 120mg TID

134
Q

Phentermine/topiramate ER dosing

A

QD for at least 2 weeks

Dosing escalation at 2 weeks if patient tolerates; further escalation at 12 weeks if 3% body weight not lost

135
Q

Lorcaserin dosing

A

10mg bid

136
Q

Liraglutide dosing

A

0.6mg SC initially; increase by 0.6mg/week, up to 3.0mg

137
Q

Metformin induced weight loss MOA

A

Mediates phenotypic shift away from lipid accretion through AMP-activated protein kinase

138
Q

GLP-1 agonists

A

exenatide and liraglutide

139
Q

SGLT-2 inhibitors

A

Dapagliflozin and canagliflozin are antidiabetics that reduce renal blood glucose absorption in proximal convoluted tubule, increasing urinary glucose excretion

140
Q

Consideration with new-age antipsychotics

A

have weight gain as side effect

141
Q

Ziprasidone beneficial properties

A

Less weight gain than olanzapine and less cholesterol increase than olanzapine, quetiapine and risperidone

142
Q

AEDs associated with weight loss

A

Felbamate, topiramate and zonisamide

143
Q

AEDs associated with weight gain

A

Gabapentin, pregabalin, valproic acid, vigabatrin and carbamazepine

*valproic acid causes weight gain in adults and children

144
Q

Weight neutral AEDs

A

Lamotrigine, levetiracetam and phenytoin

145
Q

Phentermine not approved for _______________

A

long-term use

*one approach is to try intermittent therapy

146
Q

Prescribe phentermine off-label for long-term use if…

A

Patient has no evidence of serious CV disease

Does not have a serious psychiatric disease or history of substance abuse

Has been informed about weight loss medications that are FDA approved for long-term use and told that these are safe and effective while phentermine has not been proven safe or effective long-term

Does not demonstrate a clinically significant increase in pulse or BP when taking phentermine

Demonstrates a significant weight loss while using the medication

Pharmacy School 2015-16 (34 decks)

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