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NURS 1650 - Here We Go Again > Pathophysiology of Obesity and Dyslipidemia > Flashcards

Pathophysiology of Obesity and Dyslipidemia Flashcards

1
Q

What is BMI? How is it measured?

A

Body Mass Index – relationship between a person’s height and weight

BMI = weight in KG/height in m^2

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2
Q

Can BMI diagnose body fatness and health?

A

No, it is used as a screening tool that can give us insight

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3
Q

What is Class I obesity in adults?

A

In adults, a BMI of 30.0 - 34.9 is class I obesity

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4
Q

What is obesity in children and adolescents?

A

BMI > sex-specific 95th percentile

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5
Q

Why is BMI not used for children under 2 years old?

A

Weight-for-length growth charts are used for them

Children can “outgrow” high BMI

There is no evidence for treating weight that is considered high in children under 2 years old (can be an important sign)

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6
Q

Is obesity a disease? What else can it be considered?

A

It was declared a disease

Some say it is a risk factor for other diseases

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7
Q

What are some examples of genetic problems that can lead to obesity?

A

Monogenetic causes (leptin gene mutations)

Prader-Willi Syndrome (Chromosome 15 defect) that causes constant hunger and uncontrollable eating

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8
Q

How significant are the obesity-related gene variants (SNPs) that have been found?

A

There is a link between these genes and obesity, but we must also take into account environmental factors.

Example: physical activity and/or a healthy diet can counteract the risk associated with variations in the FTO gene

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9
Q

Describe how gut microbiota affects obesity

A

There is decreased gut microbial diversity in obese people compared to lean people

There is a bi-directional relationship between diet and the microbiome

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10
Q

Describe the “thrifty gene” hypothesis of obesity

A

In times of fluctuating food availability, weight was gained when food was plentiful, and those energy stores were used when food was scarce

In the face of constant plentiful food supplies, this becomes maladaptive

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11
Q

What are some environmental factors that contribute to the pathophysiology/prevalence of obesity?

A

Abundance of foods filled with sugar, fat, and salt

Food industry that understands food desire and psychology (sweetened drinks, high fructose corn syrup)

Increased portion sizes

Proliferation of fast-food outlets

Food deserts (no fresh produce)

More sedentary occupations and lifestyles

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12
Q

What do adipocytes do?

A

Store fats (in the form of triglycerides)

Release triglycerides to be used for energy/fuel when needed

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13
Q

What happens to adipocytes under conditions of energy excess?

A

They proliferate (hyperplasia)

Hypertrophy occurs (a maladaptive response to energy excess!!)

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14
Q

What is adiposopathy? What happens in adiposopathy?

A

Combination of hypertrophy of adipocytes, visceral fat accumulation, and other markers. AKA “sick fat”

Adipocytes become so large that their diameter exceeds the diffusion limit of oxygen –> hypoxia

This can then result in necrosis, which attracts macrophages and promotes chronic inflammation

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15
Q

What are the two main patterns of fat deposition?

A

Primarily on the trunk –> central obesity // apple shape

Primary on the hips and limbs –> peripheral obesity // pear shape

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16
Q

What is ectopic fat? Why/how is it formed?

A

Fat store in, on, and around organs

If the capacity of adipocytes to store fat is exceeded, fat will be deposited elsewhere

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17
Q

What is visceral fat?

A

Internal abdominal fat

Intra-abdominal, mostly in the mesentery

Ectopic

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18
Q

What is subcutaneous fat?

A

Fat found under the skin

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19
Q

Which type of fat is hormonally active and more inflammation-promoting?

A

Visceral fat

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20
Q

What are adipose tissue’s endocrine functions?

A

Release cytokines that can promote insulin resistance, inflammation, hypertension, atherosclerosis, and thrombosis

Can also create conditions that promote obesity

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21
Q

What is leptin? What does it do?

A

Hormone that:

Increases satiety and energy expenditure

Increases insulin sensitivity

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22
Q

What happens to leptin in a state of obesity?

A

Increased/hypertrophied adipocytes can lead to overproduction of leptin –> leptin resistance

The body and brain fail to respond to leptin which affects satiety and energy expenditure

It is considered an overall pro-inflammatory cytokine

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23
Q

What is adiponectin? What does it do normally?

A

Normally stimulates the production of nitric oxide in the vasculature –> increases anti-atherogenic activities (considered anti-inflammatory)

24
Q

What happens to adiponectin in obesity?

A

As fat mass increases, the amount of adiponectin decreases –> promoting atherogenesis

Hypertrophied adipocytes inhibit adiponectin gene transcription

25
Q

What does resistin do?

A

Increases insulin resistance?

26
Q

What is MMCP-1? What does it do?

A

Macrophage and Monocyte Chemoattractant Protein-1

Promotes inflammation by activating macrophages resident in adipose tissue

Also increase insulin resistance

27
Q

What does TNF-alpha do?

A

Promotes inflammation and increases insulin resistance

28
Q

What does plasminogen activator inhibitor-1?

A

Inhibits the breakdown of fibrin clots –> pro-thrombotic

29
Q

What does IL-6 do?

A

Promotes inflammation

Increases insulin resistance

Increases hepatic lipid and glucose production

30
Q

What is the RAAS system’s role in obesity?

A

Components of it such as Angiotensin II and aldosterone have been found in adipose tissue –> hypertension

31
Q

What role do excess free fatty acids (FFA) have in obesity?

A

Overwhelm normal metabolic pathways –> toxic intermediates that interfere with normal insulin signaling and muscle glucose transporter functions

Contribute to insulin resistance

Attract macrophages –> inflammation

32
Q

Describe dyslipidemia in obesity

A

Low HDL (“good cholesterol”)

High LDL (“bad cholesterol”) –> pro-atherogenic

33
Q

Describe cardiovascular disease in obesity

A

Pro-inflammatory, prothrombotic and atherogenic

Increased waist circumference (indicator of visceral obesity) is a better measure of risk than BMI

34
Q

Stroke in obesity

A

Prothrombotic and atherogenic

35
Q

Sleep apnea in obesity

A

Increased upper airway pressure

Reduced chest compliance related to truncal fat deposition

Causes sleep deficit in patients which can result in decreased leptin and an increase in ghrelin (appetite stimulant)

36
Q

What is NAFLD?

A

Non-alcoholic Fatty Liver Disease

Fat droplets accumulate in the liver cells, causing swelling and damage to the liver

37
Q

How does obesity increase the risk of severe illness from COVID-19?

A

Linked to impaired immune function

Decreases lung capacity, makes ventilation more difficult

38
Q

Obese children have a higher risk of developing _____

A

Diabetes

39
Q

NAFLD in children

A

Has been reported in young toddlers

Is now the number one cause of chronic liver disease in children

7-%-80% of obese children have NAFLD or NASH (later progressive form)

40
Q

What are some treatment options for obesity?

A

Diet - change eating habits

Increased physical activity

Counseling (trauma-informed treatment)

Medication

Surgery

41
Q

What is metabolic syndrome (MetS)?

A

A constellation of signs that increases the risk of cardiovascular disease

(central obesity, dyslipidemia, increased BP, hyperglycemia)

42
Q

How do you diagnose/define MetS?

A

At least 3 of the 5 characteristics:

  • Large waist size (central obesity marker)
  • Triglycerides > 150 mg/dL
  • Decreased HDL
  • High BP (>130/85 mm Hg)
  • Fasting blood glucose > 100 mg/dL
43
Q

Why should we care about MetS?

A

Indicates that the person is at high risk for cardiovascular disease, diabetes, dyslipidemia, and other diseases

44
Q

Where does fat come from? (Glucose)

A

An intake of glucose greater than the body needs

Not-stored glucose (excess) is delivered to the liver and metabolized to acetyl CoA and used to synthesize triglycerides and cholesterol

The liver packages triglycerides and fatty acids into VLDL (a type of lipoprotein)

Adipose cells take up glucose via GLUT-4 and can use that to synthesize triglycerides as well

45
Q

Where does fat come from? (Dietary fat)

A

Absorbed dietary fats, primarily in the form of triglycerides

Chylomicrons are synthesized in the GI tract and enter the GI lymph vessels, travel to the thoracic duct to enter the bloodstream

They travel in the circulation to deliver triglycerides to the tissues:
- Liver: uses triglycerides to synthesize other lipoproteins
- Adipose tissue: triglycerides broken down by lipoprotein lipase –> fatty acids diffuse into the adipocytes and triglycerides are synthesized

46
Q

What is lipoprotein lipase? What does it do?

A

Sn enzyme found on vascular endothelial cells

Breaks down triglycerides from VLDLs and chylomicrons into FA that can diffuse into adipocytes and re-form into triglycerides with glycerol

47
Q

Describe a lipoprotein’s general structure. How does its structure help it carry out its tasks?

A

Protein membrane surrounding a core of lipids

Non-polar/hydrophobic core of triglycerides and cholesterol esters surrounded by a hydrophilic shell of phospholipids

The shell allows for lipoproteins to travel in plasma

Transport cholesterol, triglycerides, and other lipids

48
Q

What is a chylomicron?

A

Lipoprotein that carries triglycerides from dietary intake from the GI system to the liver and other tissues

49
Q

What is VLDL?

A

A lipoprotein that primarily delivers triglycerides to tissues

50
Q

What is LDL?

A

A lipoprotein that primarily delivers cholesterol to tissues.

Plays a role in atherogenesis in blood vessels

Known as “bad cholesterol”

51
Q

What is HDL?

A

A lipoprotein that carries out “reverse cholesterol transport”

Brings cholesterol back to the liver

Known as “good cholesterol”

52
Q

How is LDL-C recycled?

A

The LDL-C molecule and its receptor are endocytosed by the liver

The molecule is broken down by the liver and its receptor is returned back to the surface of the hepatocyte to take up more LDL-C from the blood

53
Q

Describe a blood lipid panel of a person with Dyslipidemia

A

High triglycerides

High VLDL or LDL

Low HDL

54
Q

How can dyslipidemia lead to insulin resistance? What does insulin resistance lead to?

A

Excess fatty acids circulating can lead to insulin resistance

Insulin resistance can then lead to inadequately suppressed glucagon secretion which can activate adipose tissue hormone-sensitive lipase and inhibit lipoprotein lipase, increasing VLDL levels

55
Q

How does dietary cholesterol contribute to dyslipidemia?

A

It can vary from person to person

Overall, excess dietary cholesterol seems to contribute to dyslipidemia

50% of dietary cholesterol is absorbed, the rest is excreted

Contributes to about 5% of total serum cholesterol

56
Q

Familial Hypercholesterolemia Summary

A

Monogenic, autosomal dominant disease

Mutation in the gene that codes for the LDL-C receptor that the liver uses to remove LDL-C from the bloodstream, resulting in reduced clearance of LDL-C in the circulation

May be first diagnosed when a very young person has a MI

NURS 1650 - Here We Go Again (20 decks)

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