OBESITY Flashcards

1
Q

What is the primary purpose of adipose tissue?

A

Energy storage.

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2
Q

Why did adipose tissue evolve?

A

As a solution to the intermittent availability of food.

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3
Q

What happens to excess calories when food is plentiful?

A

They are converted to triglycerides and stored in fat cells.

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4
Q

What happens to triglycerides when energy is needed?

A

They are broken down into free fatty acids and glycerol for energy.

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5
Q

Why does fat provide more energy than sugars?

A

Because it yields more energy per gram.

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6
Q

What causes an increase in adipose tissues?

A

An imbalance between energy intake and expenditure.

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7
Q

Why might BMI not be accurate in muscular individuals?

A

Muscular people may appear overweight or obese based on BMI.

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8
Q

What is the BMI classification for underweight?

A

<18.5

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9
Q

What is the BMI classification for normal weight?

A

18.5 to 24.9

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10
Q

What is the BMI classification for overweight?

A

≥25

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11
Q

What is the BMI classification for pre-obese?

A

25.0 to 29.9

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12
Q

What is the BMI classification for Obese Class I?

A

30.0 to 34.9

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13
Q

What is the BMI classification for Obese Class II?

A

35.0 to 39.9

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14
Q

What is the BMI classification for Obese Class III?

A

≥40.0

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15
Q

What waist-to-hip ratio indicates risk in women?

A

> 0.9

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16
Q

What waist-to-hip ratio indicates risk in men?

A

> 1.0

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17
Q

What health outcomes are associated with high waist-to-hip ratio?

A

Type 2 DM and dyslipidemia.

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18
Q

What is the role of leptin in energy balance?

A

Suppresses food intake; signals satiety.

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19
Q

What happens to leptin levels as fat stores increase?

A

Leptin levels increase.

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20
Q

What happens during caloric restriction to leptin levels?

A

Leptin decreases faster than fat stores.

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21
Q

What causes rebound overeating after starvation?

A

Reduction of leptin levels stimulates food intake.

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22
Q

Where are satiety-related enzymes secreted?

A

From the stomach, small and large intestines.

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23
Q

Which gut hormone increases in the unfed state?

A

Ghrelin.

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24
Q

How long does it take for satiety hormones to reach the brain?

A

15 to 20 minutes.

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25
Why is eating slowly recommended?
To allow satiety hormones to signal fullness.
26
What happens when food is eaten too fast?
Satiety is not activated in time, leading to overeating.
27
What contributes to Europeans staying slim despite calorie-dense food?
Eating slowly to socialize.
28
How is excess energy stored short-term?
As glycogen in liver and muscle.
29
How is long-term excess energy stored?
As triglycerides in adipose tissue.
30
Why is triglyceride storage efficient?
It doesn't require water and has >3x energy/gram than CHO.
31
What do adipocytes store?
Triglycerides and enzymes for storage/breakdown.
32
What may predispose individuals to obesity?
Lower metabolic rate or genetic predisposition.
33
What is an obesogenic environment?
An environment with easy access to energy-dense foods and low physical activity.
34
What prevents obesity when food is scarce?
Lack of excess calories to store as fat.
35
What diet causes quick weight loss short-term?
Protein and fat-rich diet low in carbohydrates.
36
Why doesn’t leptin prevent obesity effectively?
Leptin is better at preventing fat loss; resistance may occur.
37
How does obesity cause metabolic disease?
Via inflammatory pathways releasing pro-inflammatory cytokines.
38
What is one of the earliest complications of obesity?
Insulin resistance.
39
What happens to insulin sensitivity in obese individuals?
Decreases; more insulin is needed for glucose uptake.
40
What is the role of pro-inflammatory cytokines in obesity?
They disrupt insulin signaling and glucose handling.
41
What are the two main theories linking obesity to insulin resistance?
Inflammatory cytokines and ectopic lipid storage.
42
What should an obesity-related history include?
Diet, physical activity, sleep, stress, and comorbidities.
43
What disorders are secondary causes of obesity?
PCOS, hypothyroidism, Cushing's syndrome, hypothalamic disease.
44
What medications can cause weight gain?
Insulin, steroids, antipsychotics, mood stabilizers, some antidepressants and antiepileptics.
45
What medications may cause edema but not fat gain?
NSAIDs and calcium channel blockers.
46
What is important to assess in obesity management?
Comorbid conditions and readiness for lifestyle change.
47
What is a sign of patient motivation?
Interest and confidence in making lifestyle changes.
48
What tool helps assess readiness to change?
Anchoring scale (0–10 for importance and confidence).
49
What waist circumference increases risk in European men?
>94 cm (>37 in)
50
What waist circumference increases risk in European women?
>80 cm (>31.5 in)
51
How many points are required to diagnose metabolic syndrome?
3 out of 5 criteria.
52
What is the triglyceride level in metabolic syndrome?
>150 mg/dL
53
What HDL level is risky for men?
<40 mg/dL
54
What HDL level is risky for women?
<50 mg/dL
55
What blood pressure indicates increased risk?
>130/90
56
What fasting blood sugar indicates increased risk?
>100 mg/dL
57
Which condition is becoming a more common cause of liver cancer?
Metabolic disease (NAFLD).
58
What defines Stage 0 obesity risk?
No complications, just elevated BMI.
59
What defines Stage 1 obesity risk?
Prehypertension, hepatic steatosis, mild OSA, osteoarthritis.
60
What defines Stage 2 obesity risk?
Prediabetes, hypertension, metabolic syndrome, NAFLD/NASH.
61
What HbA1c range indicates prediabetes?
5.7–6.4%
62
What FBS range indicates prediabetes?
100–126 mg/dL
63
What is the main goal of obesity treatment?
To improve obesity-related comorbid conditions, quality of life, and reduce the risk of future complications.
64
What are the essential elements of lifestyle management in obesity treatment?
Dietary habits, physical activity, and behavior modification.
65
What aspect of lifestyle changes contributes most to weight reduction?
Dietary habits.
66
What is the primary role of physical activity in obesity treatment?
Weight maintenance.
67
What is the typical weight loss from lifestyle management compared to no treatment?
A modest weight loss of 3–5 kg.
68
Why must all patients learn about energy consumption and expenditure?
Because obesity is a disease of energy imbalance.
69
When are medications considered in obesity treatment?
In Stage 1, especially if the patient has comorbid conditions like prehypertension or hepatic steatosis.
70
Should lifestyle management be incorporated at all stages of treatment?
Yes.
71
What does effective weight loss depend on in diet therapy?
Reduction of total caloric intake and adherence to the diet.
72
Why do fatty foods like lechon or chicharon help with satiety?
They increase the feeling of fullness.
73
What factors should guide the individualization of diet therapy?
Patient's taste preferences, cooking style, culture, and medical problems.
74
What kind of diet should be avoided in patients with acid reflux?
Intermittent fasting.
75
What is energy density in diet?
The number of calories per unit of food weight.
76
How can energy density be reduced in meals?
By adding water and fiber.
77
What types of food are considered low energy density?
Soups, fruits, vegetables, oatmeal, and lean meats.
78
What types of food are considered high energy density?
Dry foods, high-fat foods like pretzels, cheese, egg yolks, chips, and red meat.
79
What is the average basal metabolic rate (BMR) of the body at rest?
1300 to 1400 kcal/day.
80
What is a Very Low Calorie Diet (VLCD)?
A diet with ≤800 kcal, 50–80 g of protein, and 100% RDI vitamins and minerals.
81
What kind of patient is VLCD indicated for?
Well-motivated, moderately to severely obese individuals who failed conservative approaches.
82
How much weight loss can a VLCD lead to?
13–23 kg over 3–6 months.
83
How can reducing rice intake affect weight loss?
It can lead to weight loss even without added physical activity.
84
What is the carbohydrate equivalent of a plate of palabok?
Roughly equivalent to a cup of rice.
85
Is protein stored as fat?
No, as long as kidney function is good.
86
Which foods can be consumed in unlimited amounts during diet therapy?
Fruits and vegetables.
87
Why should sweet drinks be avoided?
They can cause obesity.
88
Why must socioeconomic status be considered in diet planning?
Because some food options may be expensive.
89
How effective is exercise alone in weight loss?
It has a moderate effect.
90
What combination is most effective for weight loss?
Diet and exercise.
91
What is the most important role of physical activity?
Weight loss maintenance.
92
What is the recommended amount of moderate-intensity aerobic activity for weight loss maintenance?
50 minutes or 75 minutes/week spread throughout the week.
93
How can daily routines be modified to include more physical activity?
Through leisure activities, travel, and domestic work.
94
Why is reducing sedentary behavior important?
It is associated with lower all-cause and cardiovascular mortality.
95
What tools can help monitor physical activity?
Pedometers and accelerometers.
96
How much moderate-intensity activity is often needed for weight loss?
More than 300 minutes per week.
97
What does behavioral therapy include?
CBT, self-monitoring, stress management, stimulus control, social support, and problem-solving.
98
What should patients do to track behavioral changes?
Identify what, when, where, and how the change will be performed and keep a record.
99
Who usually supervises behavioral techniques?
Ancillary staff such as advanced practice providers or dietitians.
100
When is pharmacotherapy indicated in obesity?
BMI ≥30 kg/m² or BMI ≥27 kg/m² with comorbid conditions.
101
What are the two main types of anti-obesity medications?
Appetite suppressants and fat absorption inhibitors.
102
What do centrally acting medications affect?
Satiety, hunger, and food cravings.
103
Where do centrally acting medications act?
Hypothalamus and CNS reward centers.
104
What are examples of classic sympathomimetic adrenergic agents?
Benzphetamine, phendimetrazine, diethylpropion, mazindol, and phentermine.
105
What are common side effects of adrenergic agents?
Restlessness, insomnia, dry mouth, constipation, increased BP and HR.
106
What are the components of PHEN/TPM?
Phentermine and topiramate.
107
What is the mechanism of action of PHEN/TPM?
Catecholamine release, GABA modulation, carbonic anhydrase inhibition.
108
What is the mechanism of Naltrexone/Bupropion combo?
Stimulates α-MSH secretion and blocks opioid feedback, reducing food intake.
109
What are common side effects of Naltrexone/Bupropion?
Nausea, constipation, headache, vomiting, dizziness, diarrhea, insomnia, dry mouth.
110
What is Liraglutide?
A GLP-1 analogue used in diabetes and weight loss.
111
How does Liraglutide aid weight loss?
Delays gastric emptying, reduces glucagon, stimulates GLP-1 receptors.
112
When should GLP-1 agonists be avoided?
In patients with a family or personal history of medullary thyroid cancer or MEN.
113
What is Orlistat?
A peripherally acting lipase inhibitor that reduces fat absorption.
114
How much dietary fat absorption does Orlistat block?
Approximately 30%.
115
What are common GI side effects of Orlistat?
Flatus with discharge, fecal urgency, fatty stools.
116
What vitamins are reduced with Orlistat?
Fat-soluble vitamins D and E and β-carotene.
117
What is Gelesis100?
A nonsystemic, water-soluble gel that forms a matrix in the stomach to promote satiety.
118
Who is eligible for Gelesis100?
Patients with BMI ≥25 kg/m² with or without comorbidities.
119
When is surgery indicated in obesity?
BMI ≥40 kg/m² or ≥35 kg/m² with comorbidities.
120
What types of anatomic changes occur with obesity surgery?
Restrictive, malabsorptive, or both.
121
What are the clinical benefits of obesity surgery?
Changes in gut hormones, bile acid metabolism, microbiota, and adipose tissue.
122
What hormones are affected by bypass surgery?
Ghrelin, GLP-1, PYY3-36, and oxyntomodulin.
123
What are the metabolic benefits of fat mass loss from surgery?
Improved insulin sensitivity, reduced FFA, increased adiponectin, decreased IL-6, TNF-α, and CRP.