Unit III week 2 Flashcards
1
Q
Obesity treatment:
Key parts of diet treatment
A
1) reduce calorie intake
< 250 lbs→ 1200-1500 calories
> 250 lbs→ 1500-1800 calories
2) Self-monitor foor intake
3) Low energy density
4) Smaller portion size
5) Meal replacement diets can be effective
6) Best diet is the diet a patient can stick with
2
Q
Calorie recommendations for obese patients
A
< 250 lbs → 1200-1500 calories
> 250 lbs → 1500-1800 calories
3
Q
Obesity treatment:
Physical activity can have what benefits?
A
1) Fills energy gap created by initial weight loss
- Key for weight loss maintenance
2) Maintaining fat free mass (muscle mass) - primary determinant of 24 hr energy expenditure
3) Improve ability to regulate appetite
4
Q
Key behavioral changes for obesity treatment
A
Increase energy expenditure through activities of daily living
Take the stairs, seek opportunities to walk
Reduce time spent in highly sedentary activities (TV)
Adequate duration/quality of sleep (prevents weight gain)
5
Q
Weight bias
A
resent among all types of healthcare professionals and obese patients
Can measure of bias has been successfully overcome if patient feels empowered after the encounter (goals set, patient has self efficacy, etc.)
6
Q
Specific dietary approaches
A
Don’t drink calories
Increase fruits and especially vegetables
Avoid skipping meals (if skipping, skip dinner)
Eat earlier in day when metabolism is higher
Reduce portions
Slow pace of eating
Join specific weight loss program
7
Q
Physical activity specific approaches
A
Begin with low level aerobic activity (Walking)
Must restrict food intake in addition to physical activity - not enough alone
At least 30 min/day of vigorous activity or at least 60 min/day of moderate activity required to prevent weight regain
Developing an activity/exercise plan: FITT
8
Q
Developing an activity/exercise plan: FITT
A
Frequency: most or all days of the week
Intensity: moderate intensity to start
Time/Duration: 30 min/day in blocks of at least 10 min each
Type: use large muscle groups, continuous (e.g. walking)
9
Q
Weight loss vs. weight loss maintenance:
A
Weight loss: requires state of negative energy balance (intake < expenditure)
-Negative energy balance cannot be permanently maintained - body adapts to caloric restriction by lowering energy expenditure
Weight loss maintenance: achieve lifestyle that allows maintenance of energy balance (intake=expenditure) at reduced body weight
10
Q
Why is weight loss maintenance challenging?
A
Challenging because body tries to defend its higher weight
Reduction in 24 hr energy expenditure beyond that expected from loss of weight and loss of lean body mass alone
Increase in subjective hunger, increase in ghrelin, decrease in leptin
11
Q
Predictors of Success in Weight Loss Maintenance (National Weight Control Registry):
A
1) Use moderately low fat, high carb diets
2) Frequent self-monitoring
3) Eating breakfast
4) Large amounts of physical activity (60 min/day of moderate intensity)
5) Limit TV viewing
12
Q
Name the 4 hypothalamic nuclei involved in energy balance
A
1) Paraventricular Nucleus (PVN)
2) Ventromedial Nucleus (VMN)
3) Arcuate nucleus
4) Lateral hypothalamus
13
Q
Paraventricular nucleus
A
contain receptors that respond to neurons projecting from arcuate nucleus
- Melanocortin receptors (MCR)
- NPY receptors
14
Q
Ventromedial nucleus
it is the _______ center
Stimulation –> ?
Lesion –> ?
A
= satiety center
Stimulation → no eating
Lesion → excessive eating, obesity
“Reset” regulated weight to a higher level
15
Q
Arcuate nucleus
A
contain “first order” neurons that promote either food intake or satiety - innervate PVN and LH
- Neuropeptide Y (NPY), Agouti-related peptide (AgRP)
- A-melanocyte stimulating hormone (a-MSH), cocaine, and amphetamine-related transcript (CART)
16
Q
Neuropeptide Y (NPY) and Agouti-related peptide (AgRP) act to…
A
promote feeding, decrease energy expenditure
17
Q
NPY (neuropeptide Y)
A
→ bind NPY-R in PVN/LH increase food intake, decrease energy expenditure
18
Q
AgRP (Agouti-related peptide)
A
→ block melanocortin receptors (MCR) in PVN/LH
MCR expressed in PVN, LH and preganglionic sympathetic / parasympathetic neurons in medulla and spinal cord
19
Q
A-melanocyte stimulating hormone (a-MSH), cocaine, and amphetamine-related transcript (CART) act to…
A
promote satiety, increase energy expenditure
20
Q
POMC/CART –> _______ –> activates __________ receptors –> causes what?
A
POMC/CART → a-MSH → activate melanocortin receptors (MCR) → decrease food intake, increase energy expenditure
21
Q
Leptin _______ POMC/CART and _________ NPY/AgRP
A
Activates POMC/CART
Inhibits NPY/AgRP
22
Q
Lateral hypothalamus
_______ center
Stimulation –>
Lesion –> ?
A
hunger center
Stimulation → voracious eating
Lesion → decreased food intake
23
Q
Peptides expressed in LH cause what? what peptides are these?
A
Peptides expressed in LH: induce eating
Melanin concentrating hormone (MCH)
Orexins (hypocretins)
24
Q
‘knocking out’ the POMC gene (and therefore, -MSH) –> ?
A
→ increase food intake, decrease energy expenditure
25
‘knocking out’ the NPY gene --> ?
→ decrease food intake, increase energy expenditure
26
loss-of-function mutations in the melanocortin receptor (MCR) --> ?
→ increase food intake, decrease energy expenditure
27
Ghrelin
28 AA peptide, induces hunger
High levels prior to meal
Ghrelin receptors in arcuate nucleus → activate NPY/AgRP arcuate neurons, and inhibit POMC/CART
28
Peptide YY (PYY)
released from L cells in distal ileum in response to nutrients
Has anorexic effects by inhibiting hypothalamic NPY/AgRP neurons and stimulate POMC/CART neurons
29
Glucose effect on energy balance regulation
hypoglycemia stimulates eating, hyperglycemia inhibits eating
Glucose sensitive neurons located in VMN and LH
- VMN stimulated by hyperglycemia
- LH inhibited by glucose
30
Insulin effect on energy balance regulation
long term regulator of food intake, energy balance, and adiposity
Inhibits NPY/AgRP and activates POMC/CART --> decrease food intake, increase energy epxenditure
Insulin circulates at levels that parallel body fat mass
Insulin receptors located in glucose sensitive regions of hypothalamus and brainstem
31
Leptin effect on energy balance regulation
“satiety hormone” secreted by adipose tissue
Long term regulator of food intake
Leptin receptor expressed in arcuate and VMN
Leptin inhibits NPY/AgRP neurons in arcuate and activates a-MSH/CART neurons → activate satiety circuits, inhibit feeding circuits
32
Non-Homeostatic Regulation of Energy Intake:
Internal inputs: (6)
1) Reward mechanisms - Food itself is rewarding
- Food and drug reward closely linked
2) Cravings
3) “Thinking” about food
4) Restraint
5) Learned behaviors
6) Attention
33
Non-Homeostatic Regulation of Energy Intake:
External inputs (4)
1) Environmental cues (sight, smell, taste)
2) Availability/Portions
3) Social context
4) Time cues
34
Statin benefit groups (4)
1. Secondary prevention: Clinical ASCVD (coronary disease, stroke, peripheral vascular disease)
2. LDL-C >190 mg/dL without secondary cause
3. Primary prevention: Diabetes, age 40-75 years, LDL-C 70-189 mg/dL
4. Primary prevention: No diabetes, age 40-75 years, LDL-C 70-189 mg/dL + 7.5% risk of CVD event in the next 10 years.
35
How to calculate LDL
LDL = Total Chol – HDL – (Trig/5)
TG < 400
36
Cholesterol ester transfer protein (CETP)
Allows maturing HDL particle to transfer cholesterol esters to VLDL/LDL in exchange for triglycerides
Occurs when tg levels are high, provides alternate route of tg clearance
Results in increased HDL clearance, and lower HDL levels
37
CETP deficiency
--> Elevated HDL
Some meds have targeted this - and while they have been able to raise HDL, they have NOT shown reduced CVD improvement
38
Genetic disorders that can cause elevated TG and elevated LDL
1) familial combined hyperlipidemia
| 2) Familial dysbetalipoproteinemia
39
Tangiers disease
lack ABCa1 protein → unable to remove cholesterol from peripheral tissues → very low HDL levels, premature atherosclerosis (“orange tonsils” due to accumulation of cholesterol in lymphatics)
40
ABCa1
ATP binding cassette (ABC) transporter
Important in transport of cholesterol from peripheral tissues to apo A-1 (core apoprotein of HDL)
deficiency --> low HDL
41
LCAT
Lecithin cholesterol acyltransferase
Transfers fatty acid from phospholipid onto free cholesterol → esterified cholesterol, that is more nonpolar and more tightly bound to HDL
42
LCAT deficiency
low levels of HDL, corneal opacities, renal insufficiency, hemolytic anemia due to accumulation of unesterified cholesterol in tissues
43
Normal lab values:
```
LDL
HDL
TG
HbA1c
Fasting glucose
```
```
LDL < 100
HDL = 40-60 (higher is better)
TG < 150 mg/dL
HbA1c < 6.0% (> 6.5% = diabetes)
Fasting glucose < 100 (>126 = diabetes)
```
44
Familial Hypercholesterolemia (FH)
AD absence/defectiveness of LDL receptor → LDL 2-3x normal in heterozygotes and 5-8x normal in homozygotes
45
PCSK9
regulator of LDL receptor degradation - PCSK9 binds LDL receptor and signals its degradation
Loss of function mutation → increased LDL receptor function, low LDL, reduced ASCVD
Gain of function mutation → clinical FH, reduced LDL receptor activity
46
Causes of increased LDL (3)
1) Familial hypercholesterolemia (FH)
2) PCSK9 gain of function mutation
3) overproduction of VLDL by liver (e.g. insulin resistance)
47
Physical exam findings in hypercholesterolemia (3)
Arcus cornealis: lipid deposits at limbus of cornea
Xanthelasmas: lipid deposits in skin of eyelid
Tendinous xanthomas: typically involves achilles tendons and extensor tendons of the hands
48
Causes of hypertriglyceridemia (high TGs)
1) Deficiency in LPL
2) Deficiency of Apo C2
3) Deficiency in glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (anchors LPL to endothelium)
4) Familial Dysbetalipoproteinemia (also increases LDL)
49
Physical exam findings of high triglycerides (4)
Lipemia retinalis: fatty serum in small vessels of retina
Eruptive xanthomas: small yellowish papules on extensor surfaces of arms, abdomen, and back
Hepatosplenomegaly (from triglyceride infiltration)
Abdominal pain +/- acute pancreatitis
50
Familial Dysbetalipoproteinemia
disturbances in IDL and remnant catabolism → increases in total cholesterol and triglycerides
Genetic variations in ApoE, ApoE2 isoform → defective binding of apoE2 to hepatic receptors that recognize VLDL and chylomicron remnants
***planar, palmar and tuboeruptive xanthomas
51
Causes of low HDL
1) Tangier disease (mutation in ABC-a1)
2) Familial HDL deficiency (mutation in ABC-a1 - not associated with systemic findings like Tangiers)
3) LCAT deficiency
4) Familial hypoalphalipoproteinemia (mutation in apoA1)
52
Lecithin:cholesterol acyltransferase (LCAT) deficiency
homozygous mutations of LCAT gene → very low HDL levels
Corneal opacities (fish eye syndrome)
No increased ASCVD risk
53
Dietary guidelines for treating dyslipidemia
1) Consume a dietary pattern that emphasizes intake of vegetables, fruits, and whole grains; includes low-fat dairy products, poultry, fish, legumes, non-tropical vegetable oils and nuts; and limits intake of sweets, sugar-sweetened beverages and red meats.
2) Reduce saturated fat intake to <7%% of calories.
3) Reduce percent of calories from trans fat as much as possible.
4) Consume no more than 2,400 mg of sodium/day
5) Increase total fiber intake
54
Exercise guidelines for treating dyslipidemia
aerobic physical activity to reduce LDL–C and non-HDL–C: the general guidelines are for 150 min/wk of moderate intensity activity or 75 min/wk vigorous activity plus 2 bouts of strengthening per week involving all major muscle groups
-decrease time sitting (sitting is an independent predictor of morbidity and mortality over and above time spent in planned exercise)
55
Drugs that lower LDL cholesterol
1) First line = Statins
2) ezetimibe
3) Bile acid binding resins (lots of GI side effects, can raise TG levels)
4) PCSK9 inhibitors (only used in people with familial hypercholesterolemia who cannot be controlled with statins)
56
Drugs that lower Triglycerides
tg levels are >200 mg/ml. --> Triglyceride levels could be lowered with either a fibrate or fish oils
Niacin has lots of adverse effects
57
Why is the TG/5 rule for calculating LDL only used then TG<400?
when triglycerides are greater than 400 mg/dl, chylomicron particles are present
Above 1,000 mg/dl almost all of the additional triglycerides are from chylomicrons
58
Acquired causes of hypertriglyceridemia
diet, oral estrogen treatment and uncontrolled diabetes
hypothyroidism, renal failure, liver disease, alcohol use and anti-retroviral medications
59
Childhood BMI-for-age charts
tracking over what ages?
Overweight = ___-____%
Obese = > ______%
Severe obesity = > _____% or ___________
allow tracking for 2-20 years
Overweight: BMI of age and sex between 85th-94th%
Obese: BMI for age and sex > 95th%
Severe obesity: associated with many comorbidities
BMI > 99th%
BMI > 120% of 95th percentile
60
Demographics of childhood overweight and obesity
18% of US kids age 2-19 yrs are obese (BMI > 95th%), 30% overweight or obese
Overall obesity for youth has stabilized
80% of obese 12 year olds will be obese as adults
Rates differ by ethnicity (higher for american indian, african american, latino)
Highest in low SES, older children/adolescents
61
Comorbidities with childhood obesity
Obesity in adulthood
Type II DM
Hypertension
Carotid/Coronary atherosclerosis
Obstructive sleep apnea
Metabolic syndrome
Hepatic (NAFLD/NASH)
Decreased quality of life (anxiety and mood disorders)
Orthopedic - slipped capital femoral epiphysis, Blount's disease
Depression/Anxiety, Eating Disorders
PCOS - abnormal bleeding pattern, hyperandrogenism, hirsutism, severe acne
62
Are childhood obesity comorbidities preventable?
AVOIDABLE - if not obese by the time they are adults, then risks are removed
63
How often should you calculate and plot BMI in kids?
Calculate and plot BMI at least 1x year for all children > 2yrs
64
Key components of assessment in pediatric obesity (7)
1) Diet - sugar drinks, juice, fruit/veg intake, restaurant food, portions, snacks, family meals, TV meals
2) Physical activity - goal is 1+ hrs active play/day
3) Family hx - obesity, CVD, T2D
4) ROS - symptoms of comorbidities?
5) Physical exam - signs of comorbidities?
6) Calculating and plotting BMI
7) Labs
65
Labs for obese pediatric patients (4)
when should you get lipids and A1c?
fasting lipids, ALT, fasting glucose and/or HgA1c (Q 1-2 yrs)
Get HbA1c after age 10 years or Tanner 2
Get lipids:
- 2-8 yrs, severely obese +Family hx early CAD
- Lipid screening for all kids between 9-11y and 17-21y
66
Physical exam findings associated with comoridities of pediatric obesity
HTN, acanthosis nigricans, acne/hirsutism, striae, organomegaly, joint pain, neurologic function
67
Essential treatment principles for childhood obesity: (5)
1) Start early, tailor treatment to severity
2) Prevention Plus
3) Motivational interviewing skills
4) Collaborative management - focus on JOINT prioritizing and decision making
5) Cognitive behavioral techniques
68
Prevention Plus - what is it?
5210+ = 5 fruits/vegetables, 2 hours TV or less, 1 hour activity, 0 sugar sweetened beverages (SSBs) + others
69
Motivational interviewing skills
DIRECTIVE, PATIENT-CENTERED counseling style for eliciting BEHAVIORAL CHANGE by exploring and resolving ambivalence
- Identify motivating values
- Use OARrrrs
- Involve the family
- Clean up the environment
70
What is OARrrrs?
```
open-ended questions
affirmations
reflections
rolling with resistance
reframing
summaries
```
Used as a strategy for motivational interviewing
71
Weight loss medications:
Considerations: (7)
1) Weight loss meds only work as long as the person takes it, must take it long term
2) Not paid for by insurance → $20-250/month
3) Amount of weight loss is fairly modest (5% baseline weight)
4) Mechanism of action
5) FDA approval
6) Effectiveness
7) Side effect profile
72
Phentermine
Mechanism
amphetamine, increases brain NE
No abuse potential
Acts centrally to increase satiety
73
Phentermine
Side effects
nervousness, difficulty sleeping, headache, dry mouth
*Increase BP - CONTRAINDICATED for pts with uncontrolled HTN
74
Phentermine
Amount of weight loss and cost
roughly 5% of baseline weight lost
Cost: generic, inexpensive
LEAST expensive
75
Phentermine
Use
Best in what way?
only FDA approved for 3 months of use, but long term prescribing “off label” is commonly done
Best because LEAST EXPENSIVE
76
Orlistat
Mechanism
pancreatic lipase inhibitor → block dietary fat absorption
77
Orlistat
Side effects
not systemically absorbed, not systemic side effects
Oily stools, urgency, diarrhea, oily leakage
Deficiency of fat soluble vitamins
78
Orlistat
use
best in what way?
FDA approved for long term use
**SAFEST weight loss med, approved OTC
- Use in adolescence to prevent development of diabetes
- Improves blood lipids
- Lowers HbA1c in people with diabetes
79
Lorcaserin
Mechanism
selective serotonin 2C receptor agonist
80
Lorcaserin
best in what way?
LEAST side effects
81
Lorcaserin
Side effects
possible cardiac valve problems? (unproven)
LEAST side effects - minimal headache, dizziness, nausea
82
Lorcaserin
amount of weight loss and cost
Amount of weight loss: 4-5% weight loss
Cost: $220/month
83
Phentermine/topiramate
Side effects
```
Teratogen
Dry mouth
Paresthesias
Insomnia, anxiety, irritability, disturbances in attention
Dizziness
```
84
Phentermine/topiramate
Amount of weight loss
8-12% of baseline weight
Metabolic benefit of weight loss (BP, glucose, insulin, TGs, HDL)
MOST EFFECTIVE weight loss
85
Phentermine/topiramate
cost?
$150/month
86
Phentermine/topiramate
best in what way?
MOST EFFECTIVE weight loss (8-12%)
87
Naltrexone SR/Bupropion SR
Mechanism
opioid receptor antagonist (naltrexone) + Dopamine/NE reuptake inhibitor (Bupropion)
88
Naltrexone SR/Bupropion SR
Side effects
lowering seizure threshold, increased pulse and BP, rarely increased LFTs and closed angle glaucoma
BLACK BOX - increase risk suicidal ideation
89
Naltrexone SR/Bupropion SR
Amount of weight loss and cost
Amount of weight loss: 5% of baseline
Cost: $200/month
90
Liraglutide 3 mg
mechanism
side effects
amount of weight loss
cost
Mechanism: GLP-1 agonist (also used in diabetes)
Side effects: nausea, pancreatitis
Amount of weight loss: 5-7% weight loss
Cost: $1000/month
91
Medications that contribute to weight gain
Psych drugs: atypical antipsychotics, mood stabilizers, antidepressants
-Least likely to cause weight gain: ziprasidone, aripiprazole, bupropion, topiramate
Glucose lowering drugs: insulin, sulfonylureas, TZDs
-Less likely to causes weight gain: GLP-1 agonists, DPP4 antagonists, SGLT2 inhibitors
Progesterone containing birth control
Prednisone
92
Amount of weight loss:
gastric bypass surgery vs. Lap band vs. Sleeve gastrectomy
Gastric bypass surgery = 28-30% weight loss
Sleeve gastrectomy = 24-27% weight loss
Laparoscopic banding = 20-24%
Risk is reverse (except lap band isn't really done anymore)
93
Sleeve gastrectomy:
| Pros/Cons:
Intermediate choice between band and RYGB
Does not require adjustments
NOT associated with vitamin and nutritional deficiencies
94
Laparoscopic banding:
| Pros/Cons
Reversible, easier operation, less risk of complications
Requires close follow up and adjustment of band for optimal weight
Risk of mechanical failure (slippage, erosion, rupture)
95
Risks of surgical treatment of obesity:
Risk of death or late death (within 2 years of surgery)
Perioperative complications: PE, infections, mechanical problems
Vitamin deficiencies: must take vitamin supplements for rest of life
- Thiamine deficiency
- Vit D deficiency
- Iron deficiency
- B12 deficiency
Must avoid pregnancy for at least 1 year post surgery
96
Benefits of weight loss surgery
Improve glucose control - shown that 40% of individuals with T2D preop will have resolution of diabetes post-op following RYGB
Sleeve gastrectomy has most dramatic effect
**Best treatment we have for T2D
Reduces overall mortality rates (especially due to death from CVD and cancer)
Improves sleep apnea, GERD, arthritis, infertility, HTN, cancer
97
Qualify for medication tx of obesity:
BMI > 30 without medical conditions or BMI > 27 with comorbid issues (diabetes, HTN, sleep apnea, degenerative arthritis)
98
Qualify for bariatric surgery
BMI > 40 without medical conditions or BMI > 35 with comorbid issues
99
Qualify for bariatric surgery
BMI > 40 without medical conditions or BMI > 35 with comorbid issues
100
Key Elements of effective behavior change counseling:
1) Acknowledge ultimate behavior change needs to come from pt, not imposed from outside
2) For a person to change their behaviors, they must first see compelling need for change
3) Even if they see a compelling need for change, meaningful behavior change will not occur until pt feels confident they can/will be able to do new behavior
4) To establish highly effective counseling relationship, need to be empathic
101
Stages of change (7)
1) Precontemplative
2) Contemplative
3) Planning
4) Action
5) Maintenance
6) Relapse
7) Identification
102
1) Precontemplative
ask whether they think their diet is a problem for their health → “I don’t have a problem”
Response: in your opinion their diet is related to their health problem and you are prepared to discuss this more should they be interested
103
2) Contemplative
ask how they feel about their diet → “my diet is terrible, I just can’t change it”
See need for change, but does not feel capable of making a change
Response: you agree they need to change behaviors, and you are there to help them if they want to pick a small achievable goal
104
3) Planning
is your diet a problem for your health? → yes my diet is clearly a problem, I have been thinking about trying this new “HCG diet”
Sees need to change, has some confidence they can make change
Response: increase their level of confidence they will achieve their goal
105
4) Action
currently doing a diet and it is working
Response: may disagree with what individual is doing, but they have identified their behavior as a problem for health, and have made a behavior change → SUPPORT behavior change, help them look towards the future
106
5) Maintenance
struggle adhering to diet
107
6) Relapse
“I have tried diets before, they never work”
Response: recognize and encourage them to review their previous experience, and affirm that relapse is very common
Emphasize that with a new approach they may have success
108
7) Identification
emerge from maintenance period and incorporate long term changes into their lifestyle
109
Motivational interviewing has _________ and ________ of ___________ as its central purpose
**EXAMINATION and RESOLUTION of AMBIVALENCE is its central purpose
110
Values-based counseling
**Helps you understand why people aren’t prioritizing health behaviors
Health is not primary motivating factor in their life
Individual will see a more compelling need for change if health related behaviors are linked/tied to one of their core values
111
Transtheoretical Model helps you assess _______ but doesn't ___________
helps you assess readiness, doesn’t tell you what to do
112
Health belief model
person’s willingness to change relates to their perception of their vulnerability for illness and the possible effectiveness of treatment
113
According to the health belief model, change occurs if a person...
Perceives themselves as at risk for illness
Identifies the problem as serious
Convinced that treatment is effective and not overly “costly”
Exposed to a cue to take health action
Have confidence they can perform specific behaviors that will be helpful
114
Cognitive behavioral therapy focus on ____________, not _______________
Focus is on actually changing unwanted behaviors, not motivation
**Identify specific idea that led to undesired behavior and come up with specific strategies to counteract behavior
