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Module 11 - Gastrointestinal and Hepatobiliary Disorders > Obesity > Flashcards

Obesity Flashcards

1
Q

What 4 things account for energy expenditure?

A
  1. basal metabolism
  2. physical activity
  3. digestion of food
  4. non-exercise activity
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2
Q

What is the basal metabolic rate (BMR)?

A
  • rate of O2 consumption by body cells at rest
  • indicates the energy used to maintain body processes at rest (body temperature, breathing, circulation, muscle tone, etc.)
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3
Q

What are factors that influence BMR?

A
  • body size (heat loss through body surface)
  • body composition (muscle tissue is more metabolicallly active than fat)
  • age (BMR decreases with age)
  • thyroid hormone levels (increases BMR)
  • genetics (determines BMR setpoint)
  • other= fever, stimulat drugs, emotions
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4
Q

Describe the energy expenditure with digestion of food.

A
  • energy used to digest, absorb and assimilate food after ingestion
  • metabolism increases after eating, then decreases within a few ours
  • depends on the amount and type of food
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5
Q

What are some thermogenic foods?

A
  • coconut oil
  • apple cider vinegar
  • celery
  • green tea
  • chilli peppers
  • cinammon
  • garlic
  • tumeric
  • salmon

These increase metabolism by enhancing thermogenesis

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6
Q

What is non-exercise activity thermogenesis (NEAT)?

A

The energy expended in activities such as using the stairs, walking the dog, yard work, and fidgeting.

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7
Q

What happens when intake exceeds demands?

A
  • excess nutrients stored as fat = weight gain
  • health risk r/t obesity
  • possible nutritional toxicities
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8
Q

What happens when intake does not meet demands?

A
  • fat stores and other body tissues are broken down = weight loss
  • possible nutritional deficiencies
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9
Q

What is body weight set point?

A

A set point around which the body maintains an equilibrium body weight

Determined by genetics (including epigenetics) and is influenced by environmental, biological and behavioural factors

When body weight changes, compensatory alterations in energy expenditure return it to set point.

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10
Q

Where in the brain does regulation of hunger occur?

A

Hypothalamus has hunger and satiety centres.

Receives input from sensory afferents, hormones, the microbiome etc.

Responds by altering appetite (food intake) and energy expenditure

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11
Q

How does satiety occur?

A
  • gastrointestinal stretch (via vagal afferents)
  • release of insulin from the pancreas
  • release of leptin from adipocytes
  • release of GI hormones (e.g. CCK and GLP-1 released by intestinal cells with food entry)
  • nutrients (e.g. fats slow gastric emptying and contribute to satiety
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12
Q

How does infection and inflammation decrease appetite?

A

TNFa, IL-1 and IL-6 released in response to inflammation and infection decrease appetite.

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13
Q

What is leptin?

A

An adipokine (hormone) secreted by adipocytes.

Acts on hypothalamus to maintain body weight:
1. suppresses hunger and feeding behaviour
2. increases energy expenditure (increased BME, body temp; decreases adipose tissue mass)

Production usually increases with increasing fat cell mass.

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14
Q

How is hunger stimulated?

A
  • release of ghrelin form the stomach when empty to increase appetite
  • low blood glucose levels - stimulate glucose sensitive neurons of the hypothalamus to increase appetite
  • cortisol stimulates appetite (stress eating)
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15
Q

What happens to Ghrelin levels during fasting?

A
  • increase
  • encourages eating and slows down fat metabolism (makes weight loss difficult)
  • success of bypass syrgery may be related to reduced ghrelin levels
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16
Q

What is the role of the mesolimbic (hedonic) areas?

A

involved in the emotional, pleasurable, and rewarding aspects of eating (hedonic eating)

17
Q

What role does the cognitive (executive functioning) areas of the brain have in eating?

A

Overrides the hedonic eating and decides what and when to eat (works best when well rested and low stress)

18
Q

Define obesity.

A

A complex, progressive, and relapsing chronic disease characterized by excessive body fat that impairs health.

19
Q

Why is obesity considered to be a chronic disease?

A
  1. Complex pathophysiology involving interaction between genes, biological factors, environment and behaviours.
  2. Outward S&S (assessed as BMI and waist circumference)
  3. Causes morbidity and mortality (obesity-related health complications)
  4. Causes abnormal tissue fucntion (dysregulated release of adipokines from adipose tissue and abnormal CNS response to satiety hormones)
20
Q

What is adipose tissue?

A
  • composed of adipocytes that contain a large lipid droplet
  • located under the skin (subcutaneous), around internal organs (visceral) and in bone marrow
  • functions to store energy, protect organs, provide insulation, and secrete hormones (adipokines)
  • brown adipose tissue generates body heat (non-shivering thermogenesis)
  • comprises 20-25% of body weight in a healthy adult
21
Q

What are adipokines?

A

Hormones and cytokines released from adipocytes.

involved in:
- regulating food intake, satiety and energy balance
- insulin sensitivity (and insulin resistance)
- lipoprotein metabolism
- inflammation
- adipogenesis

22
Q

What is subcutaneous fat?

A
  • located under the skin
  • generally, equally distributed
  • accounts for “pear-shape” when fat accumulates in the hips, thighs and buttoks
  • can be adapted through lifestyle factors such as diet and exercise
23
Q

What is visceral fat?

A
  • surrounds organs and is contained in the omentum (peritoneal fold that covers organs of the abdomen)
  • accounts for ‘apple-shape’ when fat accumulates
  • contributes to insulin resistance, inflammation, and cardiovascular disease
24
Q

How is body weight classified?

A
  • body mass index (BMI)
  • waist circumference (WC)
25
Q

Why is classification of obesity different for those of South-, southeast, or east asian ethnicity different?

A

Large epidemiological studies have shown that Asian populations may have increased adiposity and cardiometabolic risk at a lower BMI.

26
Q

What are some limitations of BMI?

A

Do not consider biological sex, muscle mass, or age.
- overestimates body fat in muscular individuals
- underestimates body fat in older adults who have lost muscle
BMI does not indicate the distribution of body fat, cardiovascular risk or health

27
Q

What is the Edmonton Obesity Staging Syndrome (EOSS)?

A
  • assesses medical, mental, and functional impacts of obesity to determine obesity-related health risks
  • stages obesity from 0-4
  • better predictor of mortality than BMI or waist circumference
28
Q

What happens to the weight set point in obesity?

A

Chronic mismatch between energy intake and energy expenditure which alters teh body weight set point to an increased level

29
Q

Obesity is caused by a combination of factors including:

A
  • genetic/epigenetic
  • developmental/maternal
  • behavioural
  • biological/ medical
  • social/cultural
  • psychological
  • socioeconomic
30
Q

What role do genetics/epigenetics play in obesity?

A
  • 25-50% of the risk for obesity is genetic
  • susceptibility genes involved influence body weight set point, pattern of fat distribution, metabolism etc.
  • ‘thrifty gene’ theory = built in mechanisms to defend body weight
  • epigenetic effects (genes alterd by prenatal and postnatal exposures
31
Q

What are epigenetics?

A

Heritable changes or alterations in gene expression without modification of the nucleotide sequence of the gene.

32
Q

What is the (rare) but most common single gene defect causing obesity?

A

MC4R (melanocortin receptor)
- found in hypothalmic areas involved in feeding behaviour
- normally binds MSH - inhibits feeding (increases hunger when mutated)
- mutations are found in 2-5 % of cases of severe obesity in the pediatric population

33
Q

How does smoking cessation contribute to weight gain?

A
  • nicotine increases BMR
  • cigarette smoke suppresses appetite
  • eating replaces smoking as a habit
34
Q

Other than energy expenditure, how does exercise increase weight loss?

A
  • muscle burns more calories at rest than other body tissues = increases BMR
35
Q

How does the intrauterine environment contribute to obesity?

A
  • gestational diabetes, maternal obesity, and intrauterine malnutrition affect the future weight of the child (proposed to involve epigenetics)
36
Q

How does the composition of the gut microbiome contribute to obesity.

A

less diversity of microbe species in obese individuals when compared to lean

37
Q

What are the pathophysiological effects of obesity?

A
  • excess fat stored in adipose tissue (subcutaneous, visceral), muscle, and liver
  • hypertrophy (occurs 1st) and hyperplasia of adipocytes occur to store the excess
  • visceral adipose tissue releases adipokines (some inflammatory), hormones, and fatty acids that can have negative effects
  • effects = HTN, dyslipidemia, insulin resistance, mechanical stress

Module 11 - Gastrointestinal and Hepatobiliary Disorders (5 decks)

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