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Spring P1 > Complementary Final > Flashcards

Complementary Final Flashcards

1
Q

Male vs Female body weight percentages

A

Male - more Muscle/Bone

Female - more essential/nonessential fat

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2
Q

Male vs Female LBM

A

Male Lean Body mass - 3%

Female Lean body mass - 12%

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3
Q

What has happened to worldwide obesity since 1980

A

It has doubled

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4
Q

What is the fundamental cause of obesity/overweight individuals?

A

An energy imbalance between calories consumed and calories expended.

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5
Q

An acute or subacute or chronic state of nutrition in which varying degrees of overnutrition or undernutrition with or without inflammation activity have led to a change in body composition an diminished function.

A

Malnutrition

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6
Q

What types of cancer/disease are common due to malnutrition?

A 
GI cancer
Head/Neck cancer
Lunge Cancer
Pancreatic cancer
Chronic Obstructive pulmonary disease
Cerebrovascular Accident
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7
Q

How does catabolic stress shift metabolic demand?

A

Acute phase response favors an increase in resting energy expenditure and promotes a catabolic state.

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8
Q

What does malnourished inflammation promote?

A 
Muscle Catabolism
Inhibition of protein synthesis and repair
Hyperglycemia
Decreased visceral proteins
Edema
Anorexia
Deconditioning or Sarcopenia
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9
Q

What is Sarcopenic Obesity?

A

Obesity that occurs when there is an increase in fat mass and a decrease in lean muscle mass.

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10
Q

What is Starvation-related Malnutrition?

A

Chronic starvation w/o inflammation

  • anything that limits access to food;
    Anorexia nervosa
    Marasmus
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11
Q

What is Chronic disease-related malnutrition?

A

Malnutrition where inflammation is chronic and of mild to moderate degree, common in Organ failure, Pancreatic cancer, RA and Sarcopenic obesity.

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12
Q

What is Acute disease or injury related malnutrition?

A

malnutrition where inflammation is acute and of severe degree

e.g. Infection, burns, trauma, or closed head injury

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13
Q

What is Obesity?

A

a complex multifactorial chronic disease that develops from an interaction of genotype and the environment. It involves the integration of social, behavioral cultural, physiological, metabolic and genetic factors.

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14
Q

What has happened to overweight and obesity rates since 1980? Childhood obesity?

A

everythings gone up. whoa

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15
Q

Where else in the world have obesity rates increased?

A

literally everywhere

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16
Q

What happened to obesity when dietary fat is reduced as a percentage of Kcals?

A

Still an increase, as people added sugar to make up for loss of fat.

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17
Q

What does Diet mean according to its original translation?

A

Manner of Living

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18
Q

How might you calculate BMI?

A

weight (kg) / (height (m)^2
or
(Weight (lbs) X 703) / height (in)^2

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19
Q

What are the assessments of risk for co-morbidities due to Obesity?

A
  1. BMI +25
  2. Waist circumference
    - Men : 40”
    - Women: 35”
  3. Weight gain since age 18
  4. Level of Fitness
    - Both Aerobically and Anaerobically required
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20
Q

How many deaths a year are due to obesity?

A

~300,000

*2nd cause of preventable mortality behind smoking

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21
Q

What does NHLBI expert Panel attribute to the cause of obesity?

A

60% Environmental

40% genetic

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22
Q

All-cause mortality is lowest within what BMI?

A

20-25

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23
Q

With a 10% increase in weight, what would be the effect on FBG? systolic BP?

A

FBG - 2-3mg/DL

BP - 6-7mmHg

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24
Q

What is Metabolic Syndrome?

A

Clustering of metabolic abnormalities, including resistance to insulin-stimulated glucose uptake, hyperglycemia, hyperinsulinemia, Increase in triglycerides and decreased HDL-Cholesterol

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25
Q

What factors may contribute to a person’s overweight/obesity?

A 
Genetic/Hereditary
Socio-Economic Status
Race/Ethnicity
Dec. Physical Activity
Diet
Early Puberty
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26
Q

What five factors establish Metabolic Syndrome?

A

Chronic Inflammation (increased C-reactive protein)
Hypertension
Visceral Obesity
Dyslipidemia (inc Tryglycerides and decreased HDL)
Glucose Introlerance

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27
Q

What specific diseases may Metabolic Syndrome lead to?

A

Type II Diabetes
CVD
Cancer

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28
Q

What other Conditions are often associated with Obesity due to Relative risk factor?

A 
Diabetes type II
Gall Bladder disease
Sleep Apnea
Hypertension
Osteoarthritis
Gout
Coronary Heart Disease
Stroke
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29
Q

What type of upper body fat distribution increases the risk of metabolic complications?

A

Central or Visceral Adiposity

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30
Q

What risk is there for having lower body subcutaneous adiposity relative to central/visceral adiposity?

A

Minimal Risk w/ lower body obesity.

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31
Q

How does Adipose tissue work as an Endocrine Organ?

A 
Increases Lipoprotein Lipase
Increases Leptin
Increases IL-6
Increases PAI-1
Increases Adipsin
Increases Serum Free Fatty Acids
Increases Angiotensinogen
Increases Lactate
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32
Q

How can an increase in triglycerides lead to Hyperglycemia?

A

Lipoprotein Lipase releases TG from visceral adipose, leads to hypertriglyceridemia, which acts in the liver to lower HDL and increase LDL, causing metabolic insulin resistance and eventually Hyperglycemia.

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33
Q

What common Hormonal abnormalities are seen in Obesity?

A 
Increased Cortisol Production
Increased Insulin Resistance
Decreased Sex Hormone binding Globulin (women)
Decreased Preogesterone levels (women)
Decreased Testosterone (men)
Decrease growth hormone Production.
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34
Q

What Metabolic disorders are obese individuals at greater risk of developing?

A

Diabetes Mellitus
Dyslipidemia
Liver Disease

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35
Q

In which genders/Ethnic groups is type 2 diabetes strongly associated with overweight/obesity?

A

Both Genders

All Ethnic Groups

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36
Q

How does risk for type 2 diabetes evolve?

A

It increases with the degree and duration of being overweight in individuals.

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37
Q

What is the relative risk increase of Diabetes in a women with a BMI of 22 to a a BMI of 35?

A

4000% (40 fold)

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38
Q

What is the relative risk increase of Diabetes in a man with a BMI of 24 vs a BMI of 35?

A

6000% (60 fold)

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39
Q

What is the effect of weight loss on risk of developing diabetes?

A

Reduces risk.

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40
Q

a weight loss of 5-11kg decreased risk of diabetes development by what percentage?

A

50%

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41
Q

Dropping 20kg of weight, or having a BMI below 20 does what to risk of type 2 diabetes development?

A

Makes it almost nonexistent

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42
Q

What is the relationship between HDL and BMI?

A

Inverse
Inc HDL = dec BMI
Inc BMI = dec HDL

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43
Q

Low HDL carries more relative risk for what condition than elevated triglyceride levels?

A

Development of heart disease

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44
Q

How does central fat distribution effect triglycerides?

A

Central Fat distribution results in Lipid abnormalities that may cause decrease HDL and increaesd LDL to result in hyperglycemia.

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45
Q

What is NAFLD?

A

Nonalcoholic fatty liver disease, descrives liver abnormalities associated with diabetes.

Cross-sectional analysis of these liver biopsies show prevalance rates for Steatosis (75%) Steatohepatitis (20% and Cirrhosis (2%)

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46
Q

What is Brown Adipose?

A

A type of specialized Adipose tissue which functions as a major storage site for fat. It is deeply vascularized and densley packed with mitochondria. Lipids here release energy directly as heat.
It is used in the heat production for non-shivering thermogenesis and utilization of excess caloric intake via diet-induced themogenesis

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47
Q

What is White adipose?

A

Specialized connective tissue that functions as a major storage site for fat.

It is used for heat insulation, mechanical cushion, and a major source of stored energy.

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48
Q

How does lipid metabolism in Adipocytes produce Free Fatty Acids for B-oxidation and Glycerol for gluconeogenesis?

A

Lipoprotein Lipase activates FFA on Adipocytes membrane, which interacts with Acetyl Coa from Glucose, starting a messenger cascade to trigger Lipogenesis which uses its triglyceride storage pool to activate Hormone sensitive lipase, effecting Lipolysis, resulting in the release of both FFA for B-oxidation in muscle and liver, and Glycerol for gluconeogenesis in Liver.

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49
Q

Which adipose tissue is the major bulk of adipose tissue in adult mammals, often observed as a loose association of lipid-filled cells called adipocytes?

A

White Adipose Tissue (WAT)

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50
Q

Are Adipocytes Vascularized?

A

Yes, by stromal-vascular cells, and each adipocyte is in close proximity to a capillary.

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51
Q

How are White Adipose Tissues held in place?

A

A framework of Collagen Fibers

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52
Q

Why is the Adipose organ considered Unique?

A

Only body tissue that can markedly change mass in adulthood (athlete = 2-3%; morbidly obese = 70%)

Average = 22% men; 32% women

Composed of stromal vascular cells, blood vessels, lymph nodes and nerves.

Blood flow lower than other organs.

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53
Q

Where can fat be located?

A

Subcutaneous Fat (normal)
Dermal Fat
Intraperitoneal or Omental Fat (visceral)

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54
Q

What is adipocyte Hypertrophy?

A

An increase in size of existing adipocytes, due to excess triglyceride accumulation in existing adipocytes.

(Positive Energy Balance)

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55
Q

What is adipocyte Hyperplasia?

A

An increase in the number of adipocytes, due to recruitment of new adipocytes from precursor cells.

56
Q

What is the half-life of adipocytes?

A

8.4 years

57
Q

What happens to adipocytes as we age?

A

They have blunted ability to proliferate, differentiate and confer resistance to cell death.

58
Q

How do Stem cells become Mature Adipocytes?

A

Stem cells are proliferated into preadipocytes, which are then recruited through early differentiation into Immature Adipocytes, then they are lipid filled in Late differentiation to become Mature Adipocytes.

59
Q

What types of secretions are Adipose responsible for?

A 
Resistin
Adiponectin
TNF-a
Interleukins
Fatty Acids
Lactate
Leptin
60
Q

What is dysregulation in Obesity characterized by?

A

It is characterized by an abnormal interplay between energy balance, adipocyte size and number, ECM balance, as well as vasculature and immune cell infiltration.

61
Q

What composes the ECM of adipocytes?

A

Proteoglycan molecules/Complex
Polysaccharide molecules
Collagen Fibers

62
Q

What are the characteristics of normal ECM?

A

low density connective tissue

high plasticity

63
Q

what is the effect of hypertrophy on adipocytes?

A

Hypertrophy causes mechanical stress on the adipocyte membrane, which upregulates TGF-B, leading to upregulation of collagen and other ECM proteins to counter act the expansion.

64
Q

What is the effect on increased mechanical stress on existing adipocytes?

A

IncreasedECM pressure, which causes adipocyte death, this results in an increased presence of MMPs and Macrophages to aggregate around dead adipocytes.

65
Q

Why does inflammation occur during mechanical stress on Adipocytes?

A

Increased macrophage presence from dead cells produces cytokines, which causes inflammation.

66
Q

What is a Degnerative condition of the body’s adipose tissue?

Examples?

A

Lipodystrophy

HIV/AIDS

67
Q

process where energy can be efficiently stored in the form of fats. It encompasses the process of fatty acid synthesis and subsequent triglyceride synthesis.

A

Lipogenesis

68
Q

The breakdown of lipids that involves the hydrolysis of triglycerides into free fatty acids followed by further degradation into acetyl units by beta oxidation.

A

Lipolysis

69
Q

The phenomenon of cellular dysfunction due to lipid imbalance; where a surplus of FAA induces apoptosis

A

Lipotoxicity

70
Q

What is the relation of M2 macrophages with Lean adipocytes?

A

Lean adipocytes encourage healthy M2, releasing adiponectin to the M2 while accepting IL-10.

Decreases Lipolysis, Stress, and inflammation

Increases insulin action

71
Q

What is the relation of M1 macrophages with hypertrophic adipocytes?

A

Inflammation

Relationship results in an increase of lypolysis, stress, inflammation and a decrease in insulin action.

72
Q

What are the three approaches to Obesity Treatment?

A

Behavioral Treatment
Pharmacotherapy
Diet and Excercise

73
Q

What is the survival paradox?

A

At older ages, high BMI can be beneficial if no heart disease. as People tend to lose weight to an unhealthy point.

74
Q

What are the 4 key goals for realistic treatment of obesity?

A
  1. 5-10% weight loss
  2. Focus on Health, Fitness, and Energy Level
  3. Positive Mood and Appearance
  4. Functional and Recreational Activities
75
Q

At what BMI should Diet and Excercise be encouraged?

A

anything greater than 25

76
Q

At what BMI should pharmacotherapy be encouraged? With Co-morbidites?

A

Greater than 30

w/ co-morbids, greater than 27

77
Q

At what BMI should surgery be recommended? with Co-morbidities?

A

Greater than 40

w/ co-morbids, greater than 35

78
Q

What are the components of the pyramid of Obesity Treatment?

A

Surgery
Pharmacotherapy
Lifestyle modification

79
Q

What are some common bariatric procedures for obesity treatment?

A
  1. Gastric Bypass
  2. Sleeve gastrectomy
  3. Adjustable gastric band
  4. Biliopancreatic diversion with duodenal switch
80
Q

Within regulation of body weight, match the organ/tissue/balance with the different systems

A

Brain = Translation System
Energy Balance = Effector System
Peripheral Tissue = Messenger System

81
Q

When are obesity drugs indicated?

A

when combined with behavior therapy and diet/exercise changes. Patients must have maintained for at least 6 months before considering pharmacotherapy.
BMI of 30 or greater (27 if co-morbid)
Demonstrate readiness for change
Comply with medication use
No medical or psychiatric contraindications

82
Q

What additional considerations should be looked at when using anti-obesity drugs?

A
  • Never use with complimentary lifestyle modifications
  • Never used as solo therapy
  • Must be continually assessed for efficacy and Safety.
  • Can be continued if efficacious and safe, discontinued if not.
83
Q

What Contraindications/Cautions exist for anti-Obesity Drugs?

A 
Pregnancy or Lactation
Unstable Cardiac Disease
Uncontrolled Hypertension
Unstable Severe Systemic Illness
Unstable Psychiatric disorder or history of anorexia
Incompatible drug therapy (MAOIs Migraine drugs, Adrenergic agents)
Closed Angle Glaucoma
General Anesthesia
84
Q

What drug classes are known to cause weight gain?

A 
Psychotropic Medications
B-adrenergic Receptor Blockers
Diabetes Medications
Highly active Antiretroviral therapy
Tamoxifen
Steroid Hormones
85
Q

What potential strategies are effective for Obesity Drug Action?

A 
Reducing Food Intake
Blocking Nutrient absorption
Increase Themogenesis
Modulating Fat Metabolism/Storage
Modulating central regulation of body weight
86
Q

What is the action for FDA-approved anorexiant drugs?

A

Depress food intake by altering neurotransmitter release, reuptake or acting as receptor agonists

87
Q

Why was Fenfluramine/Phentermine banned?

A

Valvular heart disease that occurred in 8-32% of patients caused FDA to withdraw approval of this type of treatment in 1997

88
Q

Orlistat

MOA and Side effects

A

Blocks absorption of 30% of consumed fat

GI symptoms (oily discharge etc)

89
Q

Sibutramine

MOA and Side effects

A

Inhibits synaptic reuptake of norepinephrine and serotonin

Dry mouth constipation, headache, insomnia, increased BP, tachycardia

90
Q

Phentermine

MOA and Side Effects

A

Stimulates release of norepinephrine

CNS stimulation, Tachycardia, dry mouth, insomnia, palpitations

91
Q

Lorcaserin

A

Serotonin 2C receptor agonist

92
Q

Dietary behaviors that may contribute to obesity

A

Increased consumption of sugar sweetened beverages

Continued low consumption of fruits/vegetables

Increased frequency of meals eaten away from home

93
Q

What factors contribute to the poor food environment in US?

A

Number of fast food establishments

Lack of access to full service grocery stores selling affordable healthful foods

Less healthy food and beverage advertising to children

94
Q

What six target behaviors does the CDC focus on in the prevention of obesity?

A
  1. Increase physical activity
  2. Increase consumption of fruits/vegetables
  3. Increase breastfeeding initiation, duration exclusivity
  4. Decrease consumption of sugar sweetened beverages
  5. Decrease consumption of high energy dense, nutrient poor foods
  6. Decrease television viewing
95
Q

Non-nutritive sweeteners

A 
Saccharin
Cyclamate
Aspartame
Neotame
Acesulfane-K
Sucralose
Stevia
Xylitol
96
Q

How many pounds of sucrose does the average american adult consume per year?

A

64 lbs
1/3 from table sugar
2/3 from processed foods

97
Q

Saccharin

A 
300-fold sweeter than sucrose
Bitter aftertaste
Heat-Instable
Limited to use in non-baked products
Bladder cancer in rats, safe in humans
98
Q

Cyclamate

A

30-50 fold sweeter than sucrose
No bitter aftertaste
Heat stable
banned by FDA over concerns about bladder cancer (hexylamine). Still sold in many countries around the world

99
Q

Aspartame

A

200-fold sweeter than sucrose

Not heat-stable, but products are non-toxic

100
Q

Aspartame Metabolism

A

Aspartame –> Aspartate + CH3OH + Phenylalanine

CH3OH –> Formic Acid

Phenylalanine –> Tyrosine –> Dopamine –> NE
or
Phenylalanine –> Phenyl pyruvic acid –> Phenyl Lactate

101
Q

Neotame

A

7000-13000 fold sweeter than sucrose
Less metabolic conversion into amino acids
20-30% absorbed
No effect on Phenylketonuria patients

102
Q

Acesulfane-K

A 
200-fold sweeter than sucrose
Heat-stable
Not metabolized
Used in some beverages
Is often combined with other sweeteners due to bitter aftertaste
103
Q

Sucralose (splenda)

A

Chlorinated derivative of sucrose
600-fold sweeter than sucrose
Non-metabolized
Heat stable

104
Q

Stevia (Truvia, Rebiana)

A

Natural product from Stevia Rebausiana
200 fold sweeter than sucrose
No evidence for genotoxicity
Generally recognized as safe by FDA in 2008

105
Q

Xylitol

A 
Sugar Alcohol
Same sweetness as glucose
40% fewer calories
Does not promote dental caries or plaque formation
Can be used in diabetics
Manufactured by hydrogenation of xylose
106
Q

What product may be used for fatty acid substitution?

A

Olestra

Sucrose esterfied with Stearic Acid
Not readily hydrolyzed into fatty acids, so poorly absorbed

Potential for Hypovitaminosis
May cause GI cramping/loose stools

107
Q

Which anti-obesity drug acts as an irreversible inhibitor of pancreatic lipase so less fats are absorbed in GI tract?

A

Orlistat

Interactions occur with levothyroxine warfarin and fat soluble vitamins
‘
Used as adjunt to diet/excerise

108
Q

What guidelines exist for anorexiant agents in management of obesity?

A

Used as Adjunts
Not for long-term use
Should not replace proper diet

109
Q

What classes of anorexiant agents exist?

A

Sympathomimetic amines

Serotonergic agents

110
Q

How do sympathomimetic Amines (Adrenergic agents) release NE?

A

They release NE from storage vesicles in the adrenergic neuron and block reuptake of neurotransmitter from the synapse.

111
Q

Mechanism of Action for Sympathomimetic Amines?

A

Not well understood, appetite-supressing effect is secondary to CNS stimulation

112
Q

Amphetamine

A

Prototypical anorexiant

Use of amphetamin in diet pills banned by FDA

113
Q

Ephedrine/Pseudoephedrine

A

diastereoisomer of ephedrine that can be abused to help lose weight (precursor to methamphetamine)

114
Q

Phentermine

A

Single weight-loss agent to decrease appetite
Less potential for abuse and addiction than amphetamine
Continued use can lead to tolerance and rebound weight gain.

ADR: Elevated BP, Anxiety, CVD palpitation

CI: Anxiety, HTN, Breastfeeeding, Hyperthyroidism

115
Q

Phentermine/Topiramate (Qysmia)

A

FDA approved for treatment of Obesity.
Topiramate dveloped as anticonsulant in epileptic patients which showed weight loss as common side-effect.

Dosed QD

116
Q

Mazindol (Sanorex)

A

Schedule IV appetite suppressant approved for patients BMI >30 or >27 with co-morbids

Tolerance develops over time, most effective at start of weight-loss program

117
Q

Fenfluramine

A

Withdrawn due to concerns over heart valve disease.

Was popular in Fen-Phen combo.

118
Q

Sibutramine

A

Inhibits neurotransmitter reuptake and stimulation of thermogenesis by activating the B3 adrenergic system in brown adipose tissue.

Withdrawn due to CV disease and minimal efficacy

119
Q

Lorcaserin (Belviq)

A

Selective 5-HT2c receptor agonist.
FDA approved for BMI >30 or BMI >27 with co-morbs

Dosed BID

CI: SSRI, SNRI/MAOI, St John’s Wort

120
Q

Rimonabant

A

Cannabinoid Receptor Antagonist, withdrawn due to concerns over psychiatric side effects

121
Q

Liraglutide

A

GLP-1 receptor Agonist
originally developed for type 2 diabetes
Long acting acylated derivative gives t1/2 of 13hrs.

122
Q

OTC Diet pills and Herbal Remedies Regulation

A

Not tightly controlled by FDA, up to consumer to be aware of efficacy and safety.

123
Q

SGLT-2 Inhibitor (Canaglitozin and Dopaglitozin)

A

Inhibits transporter so glucose ends up in urine and doesnt end up in general circulation
Inhibits glucose reabsorption in Kidney
Treatment for Diabetes II
Diuretic effect –> Lowered BP

124
Q

Drugs that can cause obesity

A 
Tricylic antidepressants
Oral Contraceptives
Antipsychotics
Anticonvulsants
Glucocorticoids
Sulfonylureas
Glitazones
B-blockers
125
Q

Do weight loss medications help promote long-term thermogenesis?

A

No, they promote weight loss through effects on appetite, such as increasing satiety and decreasing hunger

126
Q

Drug of choice for obesity patient with CVD?

A

Lorcaserin (5HT2c receptor agonist)

127
Q

Drug of choice for obesity patient with depression?

A

Phentermine/Topiramate or Phentermine

128
Q

How to gauge if weight loss medication is effective?

A

If >5% body weight at 3 months and safe, it may be continued.

129
Q

How does metformin promote weight loss?

A

Not entirely understood, likely due to multiple mechanisms.

Animal Models –> AMP-activated protein Kinase

130
Q

In a review of nine randomized controlled trials on anti-psychotic medications, which drug produced less weight gain?

A

Ziprasidone produced less weight gain as well as less cholesterol increase.

131
Q

Anti-epileptic drugs associated with weight loss

A

Felbamate, Topiramate and Zonisamide

132
Q

Anti-Epileptic drugs associated with weight gain

A

Gababpentin, Pregabalin, Valproic Acid, Vigabatrin and Cabamazepine

133
Q

What AEDs are considered weight neutral?

A

Lamotrigine, Levetiracetam and Phenytoin

134
Q

What can be recommended to obese patients with chronic inflammatory diseases like rheumatoid arthritis?

A

Use of NSAIDs over corticosteroids which produce weight gain.

135
Q

How is the phentermine weight regain conundrum approached by most doctors?

A

Intermittent therapy, since it is not approved for long term use and patients would regain weight loss if stopped immediately.

136
Q

When might it be reasonable for clinicians to prescribe phentermine long term ?

A

1) No evidence of CVD
2) No serious psychiatric disease or history of substance abuse
3) Patient informed of weight loss medications that are safe/effective
4) Does not demonstrate a clinically significant increase in pulse or BP
5) Demonstrates a significant weight loss

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