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Primary Care > Obesity and Weight Management > Flashcards

Obesity and Weight Management Flashcards

1
Q

What is obesity?

A

A chronic,
progressive, relapsing, and treatable multifactorial, neurobehavioral disease,
wherein an increase in body fat promotes adipose tissue dysfunction and
abnormal fat mass physical forces, resulting in adverse metabolic,
biomechanical, and psychosocial health consequences

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2
Q

How to classify obesity?

A

BMI

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3
Q

What are the classifications of BMI?

A
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4
Q

What is the Edmonton Obesity Staging System (EOSS)?

A
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5
Q

What is the American Association of Clinical Endocrinologists
Obesity Classification?

A
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6
Q

More than ___% of adults in the US are obese

A

40%

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7
Q

Obesity is the ___ leading cause for preventable death

A

Second

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8
Q

What are some contributing factors to obesity?

A

Genetic, environment, development, behavior

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9
Q

Describe the genetics of obesity

A

Monogenic vs. polygenic

Monogenic: early onset, severe obesity, rare, variation in single gene, alleles with high penetrance, no environmental influence

Polygenic: common, modest genetic influence, several variants, alleles of low penetrance, environment is a key factor in
expression

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10
Q

What are some genetic abnormalities and syndromes that are associated with obesity?

A
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11
Q

What is MC4R deficiency?

A

Hyperphagia, accelerated linear growth, insulin resistance

Autosomal dominant or recessive

Most common form of monogenic obesity

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12
Q

What is POMC Deficiency?

A

Hyperphagia, ACTH deficiency, hypopigmentation, pale skin, red hair

Autosomal recessive

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12
Q

What is leptin deficiency?

A

Hyperphagia, hypogonadism, absence growth spurt, impaired T cell function

Autosomal Recessive

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13
Q

What is Bardet-Biedl Syndrome?

A

Hyperphagia, vision loss, polydactyly, hypogonadism, renal disease, metabolic syndrome

Autosomal recessive

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14
Q

What is Cohen Syndrome?

A

Central obesity with thin arms/legs, small head with thick hair, eyebrows,
eyelashes, developmental delay, retinal dystrophy, joint hypermobility,
overly friendly behavior, neutropenia

Autosomal recessive

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15
Q

What is Prader-Willi Syndrome?

A

Hypotonia and poor feeding at birth, hyperphagia develops at 2 years,
thin face with almond shaped eyes, short stature with small
hands/feet, delayed development and intellectual impairment,
hypogonadism

Parental chromosome 15 partial loss of function (usually not inherited)

Most common form of syndromic obesity

Significant increase in ghrelin in PWS

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16
Q

What is Albright’s Hereditary Osteodystrophy?

A

Short stature, round face, dental abnormalities, shortened fingers/toes,
pseudohypoparathyroidism

Associated with genetic imprinting in an autosomal dominant manner

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17
Q

Describe specific epigenetic factors that play into obesity

A

DNA methylation, histone modification, RNA based mechanisms

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18
Q

Describe specific environmental factors that play into obesity

A

Diet, activity, aging, smoking, toxin exposures, sleep, stress, learned patterns

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19
Q

Describe specific social factors that play into obesity

A

Lack of green space, lack of safety, food deserts, food insecurity, low socioeconomic status, low education,
dietary

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20
Q

What are the forms of energy expenditure?

A

Resting metabolic rate - 60%

Physical activity - 30%

Thermic effects of food - 10%

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21
Q

What are the signaling pathways for the gut-brain axis?

A
  1. Hormonal
  2. Neuronal (vagus nerve)
  3. Orexigenic (appetite stimulant)
  4. Anorexigenic (appetite suppressant)
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22
Q

What role does our brain play in appetite
regulation?

A

Homeostatic eating: when we are
depleting our energy stores we have
increased motivation to eat

Hedonic eating: increased desire to
consume foods that are
highly palatable

Executive function: overriding any signaling and
deciding to eat or not eat

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23
Q

What are some hormonal factors that are involved in appetite regulation?

A
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24
Q

What are orexigens?

A

Appetite stimulants - increase intake

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25
Q

What are some examples of orexigens?

A

Neuropeptide Y (NPY)
Agouti-related protein (AgRP)
Orexin A and Orexin B
Melanin-Concentrating Hormone (MCH)

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26
Q

What are anorexigens?

A

Appetite suppressants - reduce intake

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27
Q

What are some examples of anorexigens?

A

Proopiomelanocortin (POMC)
Cocaine amphetamine regulating transcript (CART)
Alpha melanocyte stimulating hormone (alpha-MSH)
Brain derived neurotrophic factor
Serotonin

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28
Q

What is ghrelin?

A

Growth Hormone Release Inducing Peptide

AKA “the hunger hormone”

Orexigenic

Signal to release ghrelin is an empty stomach

Levels increase and peak prior to eating, levels decrease when nutrients are ingested

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29
Q

What increases ghrelin?

A

Fasting, weight loss, stress and sleep deprivation, genetic syndromes

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30
Q

What reduces ghrelin?

A

Meals, weight gain (stomach stretching), leptin, sleeve gastrectomy

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31
Q

What is cholecystokinin (CCK)?

A

Produced by l-cells in proximal small bowel (duodenum/Jejunum)

Secreted after fat/protein ingestion and stomach distension

Short acting peak at 15-30 minutes from meal initiation

Stimulates gallbladder contraction, slowing stomach emptying, reducing appetite

Receptor in GI tract and brain

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32
Q

What is Glucagon-Like Peptide 1 (GLP-1)?

A

Produced by L-cells of the ileum and proximal colon

Secretion stimulated by nutrients, neural, and endocrine factors after eating

GLP-1 receptors found in heart, kidney, lung, pancreas, CNS, PNS

It is an incretin, anorexigenic

GLP-1 levels are reduced in obesity, prediabetes, type 2 diabetes

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33
Q

What is Glucose-Dependent Insulinotropic
Polypeptide (GIP)?

A

AKA gastric inhibitory peptide

Incretin hormone, released by K cells in the duodenum and upper jejunum

Released in response to oral glucose load

GIP and GLP-1 together are responsible for up to 70% of the postprandial insulin
response

Reduces nausea and stimulates glucagon secretion

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34
Q

What is Oxyntomodulin (OXM)?

A

Incretin, produced by L-cells in distal small intestines and colon

Co-secreted upon eating (made by same precursor as GLP-1)

Produced postprandially and actives multiple receptors

Exogenous administration can cause weight loss (decreasing appetite and feeding,
increasing energy expenditure)

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35
Q

What is Peptide YY (PYY)?

A

Anorexigenic, produced by L-cells in distal small intestine, colon and rectum

Potent appetite suppressant

Increases within 1 hour of feeding; delays gastric emptying and intestine transit time

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36
Q

What is Pancreatic Polypeptide (PP)?

A

Released in response to calorie load; reduces gastric emptying in gut and reducees hunger expression in hypothalamus

Low levels in fasting state

Patients with obesity and Prader Willi Syndrome have lower levels of PP

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37
Q

What is insulin?

A

Released in response to eating

It is one of the long-term adiposity signaling hormones

Centrally reduces appetite in hypothalamus

Similar effect to leptin in the CNS but less potent

Resistance attenuates weight loss effects centrally

In muscles: uptakes glucose (glycogen), uptake amino acids (protein)

In liver: stimulates uptake glucose (glycogen), inhibits conversion fat and protein (glucose)

In adipose: stimulates fat synthesis

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38
Q

What is amylin?

A

Amino acid hormone co-secreted with insulin by beta cells, makes insulin more effective

Secreted in response to meals

Regulates glucose and bodyweight by reducing food intake, slowing gastric emptying,
suppressing glucagon production in the liver

Effects are similar to GLP-1 (milder glucose reduction and weight loss)

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39
Q

What is leptin?

A

Secreted by adipocytes in white adipose tissue; secretion is diurnal

Major role in energy balance

Circulating levels directly proportional to body fat mass

Crosses BBB and binds to the hypothalamic leptin receptors

Can activate the sympathetic nervous system

Interacts with gonadotropin pulse generators in the hypothalamic pituitary gonadal axes

Has regulation of immune function, hematopoiesis and angiogenesis

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40
Q

What is adiponectin?

A

Improves insulin sensitivity in skeletal muscle, improves insulin sensitivity in liver, reduces
vascular inflammation

Most abundant hormone secreted by adipocytes

Levels inversely related to body fat mass

Liver activity: enhances insulin sensitivity, decreases non-esterified fatty acids, increases
fatty acid oxidation, reduces liver glucose output

Muscle activity: stimulates glucose use and fatty acid oxidation

Vascular endothelium activity: inhibits monocyte adhesion, inhibits macrophage

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41
Q

How does a lap band procedure impact gut hormones?

A

Increases ghrelin, increases PYY, reduces insulin, reduces leptin

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42
Q

How does a gastric sleeve procedure impact gut hormones?

A

Large reduction ghrelin, increases GLP-1, increases PYY, decreases insulin, decreases leptin

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43
Q

How does a gastric bypass procedure impact gut hormones?

A

Variable ghrelin, large increase in GLP-1, increases PYY, increases OXM, reduces Insulin, reduces Leptin

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44
Q

What are some metabolic manifestations of obesity?

A
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45
Q

Chronic positive energy balances lead to?

A

Adipocyte hyperplasia (lots of small adipocytes)

Adipocyte hypertrophy (few large adipocytes)

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46
Q

What are weight circumference classifications?

A
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47
Q

What are 5 criteria for metabolic syndrome?

A
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48
Q

Obesity may (increase/decrease?) pro-inflammatory macrophages

A

Increase

M1 Macrophages increase with obesity and secrete proinflammatory factors (TNF, IL-6, MCP-1)

M2 macrophages predominate in lean individuals and secrete anti-inflammatory factors

In obesity M1/M2 proportion is polarized towards proinflammatory

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49
Q
A
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50
Q

What is hepatosteatosis (MASLD: metabolic dysfunction associated steatotic liver disease AKA
NAFLD)?

A

Mitochondrial
dysfunction and endoplasmic reticulum stress create reactive oxygen species, releasing
cytokines, insulin resistance and cellular apoptosis

Increases in circulating proinflammatory factors and decreases in anti-inflammatory factors may
promote inflammation and liver fat accumulation

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51
Q

What is hepatosteatitis (MASH)?

A

Hepatocyte injury and death from intracellular accumulation of fatty acids, cholesterol and
other toxic lipids and from ROS

Cellular death promotes inflammatory responses

Fibrosis develops –> cirrhosis –> end stage liver disease –> increases risk of need for liver transplant and hepatocellular carcinoma

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52
Q

Evaluating obesity and liver disease (labs)?

A

Fasting glucose, A1c, hepatic panel, fibrosis 4 index panel, serum biomarkers, imaging, liver biopsy

Liver biopsy is gold standard to assess fat and fibrosis but is not routinely done

53
Q

What is the relationship between obesity and cardiovascular disease?

A

Increased visceral and epicardial fat increase the risk of atherosclerotic CV disease –> increased coronary artery calcification

Increased fat mass compress veins and impair venous blood return which increases/promotes thrombosis

Cardiac remodeling (LVH, atrial enlargement, fat deposition –> fibrosis)

Activation of sympathetic nervous system increases BP

Activation of the RAAS causing elevated BP

Inflammatory effects –> vasoconstriction and arterial stiffness

Reduction in HDL, increase in LDL, increase in VLDL, increase in small, dense LDL particles

54
Q

What is the relationship between obesity and sleep apnea?

A

> 80% of adults with OSA are overweight

> > 50% of adults with OSA have obesity

Is a vicious cycle

Alter in the circadian system –> altered feeding, changes to body composition, increased
blood sugar, higher blood pressure, higher cholesterol, increased risks of heart disease and stroke

55
Q

What is the relationship between obesity and osteoarthritis?

A

Obesity increases the load and impact on the cartilage of the knee

Obesity also causes systemic metabolic factors and adipokines may influence cartilage
homeostasis

Obesity/overweight also risk factor for hip OA

Can be worse for women in perimenopause/menopause/postmenopausal

56
Q

Is there an associated between obesity and cancer?

A

Yes

57
Q

What is the relationship between obesity and perimenopause/menopause?

A

Declining estrogen = increased leptin, decreased ghrelin and NPY

Body composition changes (increased fat mass, increased adiposity, loss free fat mass)

Increased risks of CV disease (2-4 x higher rates)

Elevated blood pressure, elevated LDL, weight gain, loss lean muscle mass, reduced activity levels, dietary changes, food preference changes

Sarcopenic obesity

58
Q

What is the relationship between obesity and stress?

A

Long-term stress can result in an increase in hypothalamic corticotropic activity: increases in blood cortisol, can worsen sleep patterns, increase food cravings
Increase BP, worsen metabolism, cause dysregulation in the immune responses

59
Q

Greater weight loss (improves/worsens?) obesity-related complications

A

Improves

60
Q

What are important history components to obtain for obesity?

A

Notes: EtOH has a lot of empty sugars, traveliing a lot and thus eating out/fast food a lot?

61
Q

Physical exam components for obesity?

A

Vitals: height, weight, BP, BMI, HR, respirations, O2, waist circumference, hip circumference, neck circumference

62
Q

Labs for diagnostic testing for obesity?

A

CBC, CMP, fasting lipids (esp. triglycerides and HDL), A1c, TSH, vitamin D

Of note: accurate triglycerieds needs to be from a fasting state

63
Q

Additional diagnostic labs to consider for obesity

A
64
Q

Additional diagnostic labs to consider for obesity

A
65
Q

What are some examples of body composition evaluations?

A
66
Q

What is fat-free mass?

A

Total body mass (muscle, organs,
water, bones, ligaments, tendons)

Includes water, mineral, protein and glycogen

DXA measures fat, soft tissue and bone

FFM = total mass - fat mass

67
Q

What is lean body mass?

A

Total body mass (muscles, organs, water, bones, ligaments, tendons), less non essential or storage
adipose tissue

Includes water, mineral, protein, glycogen, essential fat
in organs, CNS and bone marrow

Usually only differs from FFM by ~5%

Total body mass = fat mass + lean mass + bone mass

Lean mass = total mass - fat mass-BMC

% body fat = Fat mass/(total body mass-bone mass)

68
Q

What are types of energy expenditures?

A

Basal metabolic rate, resting metabolic rate, cellular respiration, direct calorimetry, indirect calorimetry

69
Q

What is basal metabolic rate?

A

Energy expended while
fasting, rested and supine in thermoneutral environment

70
Q

What is resting metabolic rate?

A

Energy expended at rest, doesn’t require overnight supine measurement

71
Q

What is cellular respiration?

A

Converts biochemical energy like food into heat and cellular energy

72
Q

What is direct calorimetry?

A

Measure heat generated by organism, measures difference in temperature of water entering and leaving the chamber via heat exchanger

Value of generated heat can estimate total energy expenditure

Enclosed calorimeter

73
Q

What is indirect calorimetry?

A

Estimate basal EE and resting EE by measuring O2 consumption
VO2 and CO2 production VCO2

74
Q

Resting metabolic rate can be estimated by what types of equations?

A

Most common: Harris-Benedict, Mifflin St. Jeor

75
Q

Physical activity can be measured or estimated by?

A

Activity records as data to validated

EE tables

Calculations based on HR

Motion sensors (pedometers)

Accelerometers

76
Q

How to structure obesity treatment (hint: pyramid)?

A
77
Q

Lifestyle modifications for obesity treatment?

A

Eating plans/Nutrition
Activity
Behavior techniques
Other health factors
Stress management
Sleep

78
Q

What are the 3 macronutrients?

A

Carbohydrates, lipids, fats

79
Q

Describe carbohydrates

A

Source of energy and provide cellular structural elements

Includes: starches, sugars, fiber

4 kcal/gram (except for fiber)

Satiation is dependent on presence of fiber

Glucose stored as glycogen in muscle and liver. If positive caloric
balance then glucose converted to fat in the liver and is stored as
adipose tissue

Dietary reference intake: at least 130 g per day

Simple: mono and disaccharides - table sugar, dairy products,
malt sugar. Broken down during digestion into glucose,
galactose, fructose

Complex: poly and oligosaccharides; starches and high fiber
foods like whole grains, beans, fruits/vegetables

Whole grain carbs REDUCE CVD risk

45-65% total daily intake

80
Q

Describe dietary fiber

A

Is a carbohydrate

Some are fermentable - low, moderate and high: low (cellulose, hemicelluloses, wheat bra), moderate (beta-glucans, gums, pectin, resistant starch), high (inulin, oligofructose)

Soluble, viscous fiber could help reduce blood cholesterol and improve glycemic control

Fiber can also increase satiety and help gut microbiome

20-35 grams per day

81
Q

Describe other types of sugars/carbohydrates

A

Glucose is a simple sugar found in fruit (glycemic index of 100)

Fructose is found in fruit (GI of 25)

Sucrose (disaccharide of glucose + fructose derived from sugar cane or beets) has GI of 65

High fructose corn syrup: artificial sweetener, derived from corn starch glucose syrup processed into fructose; is a liquid containing unbound glucose and fructose and has a GI of ~70

Excessive intake of HFCS can lead to obesity, FLD, hypertriglyceridemia and DM

Limit added sugars to < 10% total daily intake

82
Q

Describe fats

A

Used as energy source for many metabolic processes including immune response, cell membrane, brain, synthesis of bile acid, cholesterol, vitamin D and steroid hormones and for insulation

Dietary reference intake: at least 30 g/d

Polyunsaturated, monosaturated, transsaturated, saturated

Essential fatty acids are Omega 3 and Omega 6 fatty acids

Endogenously derived essential fatty acids like EPA, DHA (both omega 3 fatty acids), and Gamma linolenic acid (omega 6 fatty acid)

20-35% total daily calories

83
Q

What are transsaturated fats?

A

INCREASE CVD risk

Artificially are partially hydrogenated vegetables oils, naturally are conjugated linoleic acid from ruminants and has no detriments to health. Artificials are associated with increased LDL, reduced HDL, increased CV disease, diabetes and cancers. Can find them in microwavable foods, margarine, crackers, fried fast foods, frozen pizza

84
Q

What are saturated fats?

A

Short chain: created and absorbed in intestine as result of fiber fermentation, medium chain - transported into portal vein after digestion and can induce ketosis (MCT oil tx of epilepsy)

Long chain: found meats, dairy, tropical oils, hydrogenated vegetable oils like shortening

85
Q

What are polysaturated fats?

A

REDUCE CVD risk

Simple molecules, plant based oils typically liquid at room temp, they provide essential fats like Omega 6 and Omega 3. Nuts contain both poly and monounsaturated fats

86
Q

What are monosaturated fats?

A

REDUCE CVD risk

Liquid at room temp, found in plant foods (nuts, avocados, olives,
canola oils, vegetable oils)

87
Q

Describe proteins

A

Contains 4 kcal/gram

Amino acids, serve as building blocks

Essential AA are those we cannot make and must consume

Protein restriction may delay progression to dialysis for CKD patients

Protein deficiency: Kwashiorkor

Dietary reference intake 0.8-2.0 grams/kg/day (dependent on age, gender, activity, health)

Complete proteins have all 9 essential amino acids

Incomplete proteins lack 1 or more AA but can be combined to form a complete protein

10-35% of total daily intake

88
Q

What is a good rule of thumb for macronutrient ratios?

A

30/30/30

30% carb, 30% fats, 30% protein

89
Q

What does calorie restriction look like?

A

Low Calorie: Women 1000-1200 kcal/d, Men 1200-1600 kcal/d

90
Q

Describe fat restriction

A

Fat restriction: low fat < 30% fat calories OR very low fat: < 10% fat calories to minimum of 30 g/day

After 6 months can produce similar weight loss ot low carb diet

May reduce fasting glucose, insulin level and modest reduction in BP

Modest decrease in LDL and HDL

Risk of deficiency if consuming <30 g/d or 270 kcal

91
Q

Describe carb restriction

A

Carb restriction: low glycemic OR low carb:< 130 g/d or < 26% calories OR very low carb: < 50 g/d

Modest weight loss for first 6 months, after that weight loss is similar to other calorie restricted diets

Reduces fasting glucose, insulin and triglycerides

Increases HDL and may lower LDL

Modest reduction in BP

Metabolic changes with or without weight loss

Epilepsy patient’s using the very low carb/ketogenic diet can reduce seizures

Low carb may improve DM complications like neuropathy

May induce gout flares, could result in malaise, could be challenging in patients with protein restriction (CKD), monitor for low blood sugar and BP and adjust meds as needed

92
Q

Describe very low calorie weight restriction

A

< 800 kcal/d
CLINICAL SUPERVISION
SHORT DURATION

Meal replacements

May need supplementation due to micronutrient deficiencies

Produces rapid weight loss

Beneficial for pre surgical preparation

Reduces fasting glucose, insulin and triglycerides, increases HDL, decreases LDL, reduces BP

Adverse effects - fatigue, nausea, constipation, diarrhea, hair loss, brittle nails, cold intolerance,
dysmenorrhea, slight increased risk of gallstones, kidney stones and gout flares

Increased risk of cardiac dysrhythmias and muscle cramping if micronutrient deficiencies

Weight regain will occur if not taught how to maintain when transitioning back to different diet

93
Q

Describe the Mediterranean diet

A

Olive oil as main source of fat

Vegetables 3-9 servings

Whole fruit 0.5-2 servings

Whole grains/legumes 1-13 servings per day

Moderate intake of red wine

Moderate consumption of seafood, fermented dairy products, poultry, nuts,
seeds, eggs

Limit red meat, meat products, ultra processed carbs

Saturated fats minimal

94
Q

Describe the DASH diet

A

Dietary approaches to stop hypertension

Primarily to treat HTN/High BP
Vegetables, fruits, whole grains, fat free or low fat dairy, fish, poultry, lean meats, nuts, seeds, legumes, fiber, calcium, potassium, magnesium

Limit sodium 1500-2300 mg/d

Limit total fat ~27% total calories per day

Limit saturated fat < 6% total daily calories

Limit cholesterol < 150 mg per day for 2100 calorie eating plan (adjust accordingly)

Avoid red and processed meats, sugar sweetened beverages, and foods with ADDED sugars

95
Q

Describe the Therapeutic Lifestyle Change
diet

A

Low fat meal plan recommended by National Cholesterol Education program, Adult Treatment
Panel

Utilized in lipid clinical trials

Includes physical activity and smoking cessation

Total fat: 25-35% daily calories

Limit sat fat < 7%

Limit cholesterol < 200 mg/d

Avoid trans fatty acids

96
Q

Describe the ornish diet

A

Very low fat restriction, foods eaten in natural form

Vegetables, fruits, legumes, whole grains

Small meals eaten frequently

Limit dietary fat < 10% total daily calories

Dietary cholesterol < 10 mg per day

Limit sugar, sodium, alcohol

Avoid animal products and caffeine

Avoid trans fatty acid, refined carbs, and oils

97
Q

Describe the vegetarian diet

A

Foods that come mostly from plants

AVOID ultra processed foods, fried foods, and refined carbs - negates the benefits of vegetarian diets

Monitor for deficiencies like Vitamin B12

98
Q

What are subtype of the vegetarian diet?

A

Vegan: ONLY plant based foods, no animal proteins or by products

Lacto vegetarian: plants + some or all dairy products

Lacto-ovo vegetarian: plant, Dairy and eggs

Semi or partial vegetarian: plant, may include some chicken/fish, dairy, eggs, NO red meat

Pescatarian: plant + seafood

Flexitarian: mostly plant based, occasional fish, meat, animal products

99
Q

Describe the paleolithic (“paleo”) diet

A

Based on diet presumed to have excited during the Paleolithic
period

EXCLUDES grains, dairy, ultra processed foods

Fresh vegetables, fruits, root vegetables

Grass fed lean red meats, fish and seafood, eggs, nuts/seeds

Naturally produced oils (olive, walnut, flaxseed, macadamia,
avocado, coconut)

AVOID: cereal grains, legumes (includes peanuts), dairy, potatoes,
ultra processed foods, refined sugars, refined oils, and salt

100
Q

Describe the ketogenic diet

A

Car-restriction promoting utilization of fat for energy, generates ketosis

Encourage balance of saturated, monounsat and polyunsaturated fats

Need vitamin and fiber supplementation

Avoid ultra processed, refined, high glycemic index, trans fatty acid foods

Generally limit cereals, breads, grains, dairy ( except cheese), starchy vegetables, most fruits

Benefits: weight loss, reduce hunger, lower postprandial glucose and insulin, may improve glucose metabolism (insulin sensitivity, reduced fasting glucose and insulin), reduce diastolic BP, reduce TG and increase HDL, ketonemia can treat seizures, adjunct to certain kinds of cancer therapy

Risks: may increase LDL (can avoid by eating polyunsat versus sat fats), no improvement in insulin sensitivity if no weight loss, transient fatigue, mild decrease in cognition (upon start of diet), physical performance changes

101
Q

What are the phases of the keto diet?

A

Induction phase: <= 20 g carbs per day non starchy vegetables, leafy greens and adequate protein to reduce insulin and generate ketosis

Ongoing weight loss phase: wider variety vegetables, seeds, nuts and low glycemic whole fruits like strawberries and blueberries

Pre Maintenance Phase: once goal weight achieved, allow carb intake to slowly increase while monitoring weight

Maintenance phase: 60-90 g of carbs per day if weight and health maintained; may include legumes, whole grains and whole fruits

102
Q

Is intermittent fasting and
time-restricted eating as effective as continuous calorie restriction?

A

Yes

103
Q

What are advantages of intermittent fasting and
time-restricted eating?

A

Reduced decision fatigue, quickly reversible, may fit better in day to day schedule, may reduce caloric intake, may improve metabolic parameters and reduce body weight

104
Q

What are disadvantages of intermittent fasting and
time-restricted eating?

A

Does not necessarily emphasize “healthy” meal quality, may not want to use in patients with eating disorder history, increases risk of hypoglycemia, no great evidence of sustainability, long-term evidence of benefits/safety/efficacy from animal studies, Prolonged fasting may promote gout, urate nephrolithiasis, postural hypotension and dysrhythmias

105
Q

What are physical activity recommendations per week?

A

150-300 minutes + moderate-intensity activity OR 75-150 min+ vigorous intensity activity per week

Muscle strengthening activities 2+ days per week

Moderate intensity: brisk walk, raking yard, etc

Vigorous intensity: running, weight lifting, fitness class

Moderate or vigorous: swimming, bicycling

For clinically significant weight loss and maintenance activity should be 250 min or greater per week

Resistance training can improve the proportion of fat to fat free mass loss

Without weight loss it still improves health risk

106
Q

What are some behavioral techniques for weight managment?

A

Motivational interviewing
Having empathy

Going through the 5 A’s

Address body image

Why do we eat like we do?: physiologic, stress, emotions, timing, environment, information
gap, reward

Why DON’T we engage in routine activity?: physical symptoms, lack of time, not interested,
support, inadequate education, financial, accessibility

Elements for success: doable, evidenced base, measurable, accountability, ownership,
frequent encounters (medical professionals), education, setting goals, non scale goals, self
monitoring, stimulus control, addressing body image, creating plan to change cognitive
patterns, rewards, stress mgmt, health care team, group support, weight loss programs, use
of technology and social media and telemedicine

Stress management

Improving sleep

Mindful eating

107
Q

Meds that can cause obesity

A

Beta blockers, calcium channel blockers, insulin, sulfonylureas, steroids, progestion contraceptives, gabapentin, valproate, some antipsychotics, lithium, some SSRIs and SNRIs, many others…

108
Q

Obesity meds

A

Phentermine/topiramate, liraglutide, semaglutide, naltrexone/bupropion, tirzepatide, orlistat

109
Q

Phentermine

A

Lomaira/Adipex

Reduces appetite

CI: uncontrolled HTN, uncontrolled anxiety, CV history, hyperthyroidism, there is risk mania, pregnancy

Monitor: BP, pulse, EKG (person dependent)

AEs: constipation, dry mouth, headache, insomnia, anxiety, jitteriness, palpitations, elevated HR and BP

Caution > 65 years old

FDA approved, approved for pediatrics

110
Q

Topiramate

A

Topamax

Disinterest in food, reduces cravings, less food thoughts

Think about using in patients with migraines, insomnia, pain

CI: hx of calcium kidney stone, glaucoma, cognitive impairment, risk of birth defects (teratogenic)

Monitor: BMP, mental status

AEs: drowsiness, paresthesia, memory issues, word finding difficulty, taste changes

Caution in elderly, CKD, uncontrolled depression

Rare risk of metabolic acidosis

NOT FDA approved

111
Q

Phentermine/Topiramate

A

Qsymia

CI: same as individual medications

Monitoring: same as individual medications

AEs: same as individual medications

FDA approved, approved for pediatrics

112
Q

Lisdexamfetamine

A

Vyvanse

Causes appetite suppression

CI: uncontrolled HTN, anxiety, CV history, risk mania

Monitor: BP, pulse, EKG

AEs: constipation, dry mouth, headache, insomnia, anxiety, jitteriness, palpitations, dizziness, nausea, vomiting, increased HR, anorexia

Caution> 65 years old

Use for moderate to severe binge eating disorder and ADHD

Approved for pediatrics

113
Q

Naltrexone

A

Revia

Works in mesolimbic reward pathway to decrease cravings

Dose around time of largest cravings

CI: if taking opioids, upcoming surgery, severe hepatic injury

Monitor: LFTs

AEs: nausea, dizziness, headaches, anxiety, insomnia is limited

NOT FDA approved

114
Q

Naltrexone/Bupropion

A

Contrave

Naltrexone mechanism + bupropion mechanism which stimulates POMC reducing
hunger.

CI: concurrent use MAOI, opioids or CYP2B6 inducers, hx of seizures, active bulimia/anorexia, uncontrolled HTN/anxiety

Monitor: BP, HR, LFTs, mental status

Hepatic and renal dosing

AEs: headache, insomnia, nausea, constipation, vomiting, dizziness, dry mouth, tremor

115
Q

Orlistat

A

Xenical or Alli

Mechanism: GI lipase inhibitor that impairs digestion of dietary fat

AEs: oily stools, oily flatus worse after fatty meals. Can promote kidney and gallstones and malabsorption of fat soluble vitamins

CI: chronic malabsorption syndrome and cholestasis

Drug interactions: cyclosporine, oral contraception, anti seizure medications, thyroid
hormone, warfarin

Not often used d/t AEs

FDA approved, approved for Peds

116
Q

SQ Peptide Medications

A

Ex: GLP/GIP (semaglutide/Wegovy; liraglutide/Saxenda)

CI: personal or FH medullary thyroid carcinoma, MEN2, idiopathic/chronic pancreatitis or pancreatitis from GLP 1 agonist.
Exenatide if GFR< 30 ml/min

Monitor: A1c, blood sugars as needed, BMP

AEs: nausea, diarrhea, constipation, headache, heartburn, gallstones, pancreatitis, gastroparesis, fatigue

Tirzepatide/Zepbound: weekly 2.5 mg, 5 mg, 7.5 mg, 10 mg, 12.5 mg, 15 mg

FDA approved, semaglutide and liraglutide approved for pediatrics

117
Q

Non-Systemic Oral Hydrogel

A

Biodegradable oral non-systemic superabsorbent hydrogel

Promotes fullness

CI: pregnancy, hx of reaction to cellulose, citric acid, sodium stearyl fumarate, gelatin, titanium
oxide

AEs: abdominal pain, constipation, flatulence, infrequent bowel movements, abdominal distension, diarrhea, nausea

FDA approved

118
Q

Setmelanotide

A

Imcivree

Melanocortin-4 receptor agonist: use in those with Bardet-Biedl syndrome (clinically diagnosed), POMC, PCSK1, LEPR deficiency (must be confirmed by genetic testing)

Discontinue if after 12-15 weeks of tx there is not at least 5% loss of baseline bodyweight

AEs: injection site reaction, skin hyperpigmentation, nausea, headache, diarrhea,
abdominal pain, back pain, fatigue, vomiting, depression, URI, spontaneous erections

FDA Approved

119
Q

Metreleptin Subcutaneous Injection

A

Myalept

Leptin Analog

Adjunction to diet to treat complications of leptin deficiency

Not indicated for patients with NASH or HIV related lipodystrophy

CI: hypersensitivity, general obesity not associated with congenital
leptin deficiency

AEs: headache, hypoglycemia, decreased weight, abdominal pain

120
Q

Types of bariatric surgery

A

VSG (Vertical Sleeve Gastrectomy)

RYGB (Roux-en-Y gastric bypass)

LAGB (Laparoscopic Adjustable
Gastric Banding)

Balloons 4,358 (1.6%)

Revision

121
Q

Who should undergo surgery?

A

BMI >= 40

Those who are not responding to non surgical weight loss management AND BMI >=35 regardless of comorbidities

BMI 30-34.9 and metabolic disease

BMI >=27.5 in Asian populations

Appropriate pediatric patients

122
Q

Who should not undergo surgery?

A

Severe heart failure, unstable CAD, end-stage lung disease, Active cancer treatments, portal
hypertension, decompensated liver cirrhosis, drug and alcohol dependency

123
Q

Vertical Sleeve Gastrectomy (VSG)

A

Most common surgery

Can worsen GERD and Barretts

Favorable changes in gut hormones for hunger, satiety, blood sugar control

Common deficiencies: Vitamin B1, B9, B12, D, Iron

124
Q

Roux-en-Y Gastric Bypass (RYGB)

A

Favorable changes in gut hormones and neuroendocrine
signaling

Bypasses part of the small intestine which limits absorption

Resolves GERD

Good for those at higher BMI, GERD, and Type 2 diabetes

Common Deficiencies: Vitamin B1, B9, B12, D, calcium, Iron

125
Q

Laparoscopic Adjustable Gastric Banding

A

Least invasive, removable (not permanent)

Metabolic benefits are dependent on amount of weight loss

Ideal for those with low BMI and no metabolic conditions

Lowest rate of complications

Common Deficiencies: Vitamin B1, D

126
Q

Nonsurgical procedures for weight loss

A

Intragastric balloons, electrical vagal blocking system, endoscopic sleeve gastroplasty (ESG; doesn’t affect ghrelin secretion)

127
Q

Bariatric surgery postop diet pearls

A

3-5 small meals per day

Decrease in # of meals as portion size increases

Chew thoroughly

Avoid consuming liquids during meals

Protein at least 60 g/d (1.2-1.5 g/kg/d of lean mass)

Avoid excessive calorie intake

High quality multivitamins - chewable or liquid

128
Q

What is dumping syndrome?

A

Complication of RNY because it bypasses the pyloric emptying mechanism; common

Facial flushing, lightheadedness, fatigue, reactive hypoglycemia, postprandial diarrhea

Tx: avoid high glycemic index foods, avoid drinking fluid with meals

129
Q

Can adolescents use pharmacologic therapy for weight loss?

A

Yes

AAP Recommendations: SHOULD offer adolescents 12 years and older obesity weight loss pharmacotherapy, according to medication indications, risks, and benefits, as an adjunct to health behavior and lifestyle management

Some options: liraglutide, semaglutide, topiramae, vyvanse

Primary Care (11 decks)

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