Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Patho Test 1 > TEST 4: Obesity > Flashcards

TEST 4: Obesity Flashcards

1
Q

Obesity overview
Definition
Criteria
Kids
(Lecture, p. 723)

A

-A metabolic disorder that develops when calorie intake exceeds energy expenditure over time in genetically susceptible individuals

-In adults, obesity= BMI > 30
-Class 1: BMI 30 to 34
-Class 2: BMI 35 to 39
-Class 3: BMI > 40 “severe”

-In kids:
-BMI > 95th percentile for age and gender
—120% of 95% peregrine or greater OR 35 kg/m2 or greater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Adipose tissue
What is it?
What are the types (4)
(P. 723)

A

-Provides insulation and mechanical support
-Body’s major energy reserve to fuel other tissues

4 types:
-White
-Brown
-Beige
-Bone marrow

GEM- MOST fat in the body is white

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

White adipose tissue (WAT)
What is it?
Where is it?
What does it do?
(P. 723, AO)

A

-Comprises the majority of adipose tissue in the body

-Located in visceral (central) and subcutaneous (peripheral) stores

-Contributes to the regulation of energy homeostasis:
-Crucial for storing excess energy in the form of triglycerides and releasing that energy when needed
-in excess, contributes to obesity and metabolic disorders (increases insulin resistance and inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Adipokines deregulated vs.
Adipocytes regulated
726-727

A

Adipokines:
Leptin, adiponectin, resistin, RBP-4 when deregulated:
-HTN, CVA. Obesity, DM, Arthritis, metabolic syndrome, NASH

Adipocytes when regulated (a million types listed):
-Appetite, satiety, insulin sensitivity, fat distribution, energy, blood pressure, metabolic health

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

White adipose tissue
Contribution in times of excess
(P.723)

A

When the energy balance is positive, excess fat is stored in white Adipocytes:

-Cells hypertrophy and become hyperplastic
-Causes dysregulation of adipokines—> pro inflammatory state and altered lipid metabolism—> contributes to obesity comorbidities

Altered Adipocytes—> insulin resistance (lipolysis and release Of FFA)—> macrophage infiltration (TNF-alpha and IL-6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Appetite and satiety control
Where in the brain?
Neuron types?
Peptides?
(AO, slides)

A

-Controlled by arcuate nucleus in the hypothalamus (responsible for balancing metabolism)
-Arcuate nucleus has 2 types of cells:
1. Orexogenic neurons: stimulate appetite decrease metabolism
2. Anorexic neurons: suppress appetite and increase metabolism

Orexins= neuro peptides that stimulate appetite

Anorexins = neuro peptides that inhibit appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Orexins
(P. 727)

A

Ghrelin:
-Produced in the stomach in response to hunger
-Ghrelin receptors in hypothalamus—> growth hormone that—> release gastric acid, increases GI motility, pancreatic secretion of insulin
-Lean people: elevate with hunger and fall after eating
-In obesity: levels remain elevated after eating (increased body weight and fat mass)

Endocannabinoids:
-Produced in the brain and peripheral nerves
-Increases appetite, nutrient absorption and lipogenesis
-Increases peripheral and central adipose tissue accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Anorexins
(P.726)

A

Leptin:
-Produced by Adipocytes, acts on hypothalamus
-Decreases appetite and energy expenditure
-As Adipocytes increase, Leptin secretion increases
High levels of Leptin lose effectiveness (Leptin resistance) —> disrupts hypothalamus signals of satiety—> overeat—> increased weight

Glucagon-like Peptide-I :
-Stimulates pancreatic glucose dependent insulin secretion
-Decreases gastric emptying—> decreased appetite and increased satiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Adiponectin
(P. 726)

A

-An Anorexin, increases energy expenditure
-Has insulin sensitizing and anti inflammatory properties
-Levels will decrease in obesity—> increased insulin resistance, increased CAD risk, and increased inflammatory markers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Shifts in obesity from normal
Hunger

A

Ghrelin and endocannabinoid—> does NOT decrease after eating, so you lose the feedback loop to stop hunger (increases appetite)

Leptin, GLP-I, adiponectin—> levels are high but there is resistance, so you lose the signal to stop eating, lose the satiety sensor, and lose protective properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Apple vs pear shape obesity

A

Apple:
-VISCERAL obesity: accelerated lipolysis, increased inflammation and metabolic syndromes
-Associated with HIGHER risks of obesity related health issues (of more concern)

Pear:
-PERIPHERAL obesity: fat is less metabolically active, releases fewer adipocytokines—> risk of obesity is less severe
-Associated with lower obesity related health complications (of less concern)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Obesity as multi-system syndrome

A

-Chronic complications are associated with > 200 health conditions
-Underlying etiologies: chronic inflammation, metabolic disorders, increased free fatty acids

Cardiovascular: Atherosclerosis, HTN, CAD, HF, renal disease, CVA

Cancer: Breast, colon, renal, stomach, pancreatic, liver, ovarian/ endometrial

GI: GERD, gallstones, fatty liver

Pulmonary: Sleep apnea, asthma exercise intolerance

Musculoskeletal: osteoarthritis, back pain, plantar fasciitis

Endocrine: insulin resistance, type 2 DM,
Infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Obesity treatment

A

-Is a chronic, relapsing disease

Treatment focus areas:
-Address metabolic abnormalities
-Lifestyle change
-CBT/ support groups
-GLP-I and GIP receptors agonists
-Bariatric surgery (Gastric bypass, roux-en-Y, gastric banding, gastric sleeve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Leptin
(AO)

A

-Hormone Produced by adipose tissue
-Signals the hypothalamus to suppress appetite and stimulate energy expenditure
-In obesity, elevated leptin levels can lead to leptin resistance so its effectiveness is reduced and hunger is not suppressed (ie you always feel hungry)
-DECREASE APPETITE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ghrelin
(AO)

A

-Hormone secreted by the stomach
-Known as “hunger hormone”
-Stimulates appetite and promotes food intake
-Ghrelin levels rise before meals and fall after
-In obesity, patterns are altered and Ghrelin’s suppressive effect on hunger is reduced
-INCREASE APPETITE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Insulin as hormonal regulation in obesity
(AO)

A

-Is released by the pancreas in response to food intake, facilitating glucose by the cells to use for energy
-Also plays a role in fat storage
-Chronic high levels of insulin (due to insulin resistance) contribute to weight gain and obesity

17
Q

Other Mechanisms that affect the development of obesity
(AO)

A

Neurobiological:
-CNS involvement (hypothalamus plays large role in integrating signals from neurotransmitters that influence reward pathways and eating behavior)

Physical activity:
-Regular physical activity is crucial in preventing obesity and affecting basal metabolic rate

GI factors:
-Gut microbiota can affect metabolism
-GI tract releases various hormones in response to food intake (peptide YY, GLP-1) that play roles in signaling satiety and regaling energy balance

Environmental/ lifestyle factors:
-high calorie diets rich in sugar and fat
- processed foods
-socioeconomic factors
-chronic stress

18
Q

What is an adipocyte?
(AO)

A

-Aka “a fat cell”
-Is a specialized cell that functions primarily in the storage of energy in the form of triglycerides
-Play a crucial role in storing energy and also regulating the availability of energy in the form of free fatty acids and glycerol

19
Q

Adipokines
(AO)

A

-Hormone like cytokines secreted by adipocytes (fat cells).
-Play a huge role in regaling various metabolic and immune functions throughout the body

20
Q

Brown Adipose Tissue (BAT)
(AO)

A

-Contains numerous mitochondria and iron, giving to its brown color
-Found in neonates and adults
-The mitochondria in them oxidize glucose and free fatty acids to generate HEAT
-In obesity, generate heat through non- shivering thermogenesis
-Does not have a role In Appetite regulation instead is considered beneficial for metabolism and energy expenditure

21
Q

Beige Adipose Tissue
(AO)

A

-Emerges in response to extreme cold exposure and exercise (shares characteristics with both white and brown adipose tissue)
-Is associated with increased energy expenditure
-Considered PROTECTIVE against obesity as it enhances weight loss by increasing overall health energy expenditure

22
Q

Bone Marrow Adipose Tissue
(AO)

A

-Found within the bone marrow (including long bones)
-Releases adipokines that interact with osteoblasts (plays a role in bone health)
-Excess BMAT is linked to osteoporosis and and produces inflammation that contributes to things like RA

23
Q

Summary of the difference between Orexin hormones and anorexin hormones:
(AO)

A

Orexin:
-Grehlin and endocannabinoids increased hunger and food intake and decrease metabolism

Anorexin:
Leptin, GLP-1, and adiponectin reduce hunger and enhance feelings of satiety and also increase metabolism

24
Q

Ghrelin (Orexin) Hormone
(AO)

A

-Produced in the stomach during periods of hunger
-Binds to receptors in hypothalamus to release growth hormone and other stomach related effects
-Stimulates appetite

25
Q

Endocannabinoids (Orexin) Hormone
(AO)

A

-Are synthesized in the brain and peripheral nerves
-Interact with cannabinoid receptors to increase appetite and nutrient absorption
-Enhance food intake and energy storage

26
Q

Leptin (Anorexin) Hormone
(AO)

A

-Secreted by adipocytes and act on hypothalamus to regulate energy balance
-Decreased appetite and promotes energy expenditure
-It reduces appetite although chronic high levels make it ineffective leading to weight gain
-Stress, high carbs, and poor sleep increase these levels

27
Q

Glucagon-Like Peptide 1 (GLP-1, Anorexin) hormone
(AO)

A

-Is secreted by intestinal cells in response to nutrient ingestion, stimulating the pancreas to release insulin in a glucose- dependent manner and slows gastric emptying
-Enhances feelings of fullness and satisfaction, leading to reduced food intake

28
Q

Adiponectin (Anorexin) hormone
(AO)

A

-Primarily produced in adipose tissue, synthesized in smaller amounts in muscle and brain
-Regulates glucose and lipid metabolism and improves insulin sensitivity
-Anti inflammatory, anti fibrotic, antioxidant effect are beneficial for metabolic health
-When levels are decreased in obesity, insulin resistance can occur and increased cardiovascular disease and inflammatory conditions

29
Q

Leptin resistance
(AO)

A

-As body fat increases, the amount of leptin produced increases but the brain doesn’t respond to it effectively (hypothalamus becomes less sensitive to it)
-This impaired response leads to the failure of leptin to suppresses appetite
which can lead to overeating
-Ie people still feel hungry and eat more
-Leptin resistance= inability to control hunger properly (brain fails to send signals that you’re full) and decreased ability to to expend energy

30
Q

Underlying etiologies of chronic complications of obesity
(AO)

A
  1. Chronic inflammation:
    -Obesity is a chronic state of low grade inflammation
    -Excess adipose tissue secretes pro inflammatory cytokines)
    -Accumulation of abdominal fat leads to infiltration of macrophages into adipose tissue (contributing to inflammation)
    -Leads to type 2 DM, cardiac disease, cancer
  2. Metabolic disease:
    -Due to alteration of normal metabolism
    -Excessive visceral body fat leads to impaired insulin signaling and insulin resistance develops
    -Can also cause dyslipidemia, HTN, and metabolic syndrome (increasing risk of MI/ CVA)
  3. Increased free fatty acids:
    -Increased release of free fatty acids are released from the adipocytes into the bloodstream
    -Triglycerides are broken down into FFA’s, which contribute to metabolic disturbances
    -Can interfere with insulin signaling, liver fat accumulation (non alcoholic fatty liver), cardiac complications, and contributes to oxidative stress and systemic inflammation

Advanced Patho Test 1 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions