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DEMS > Unit III week 2 > Flashcards

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

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2
Q

Calorie recommendations for obese patients

A

< 250 lbs → 1200-1500 calories

> 250 lbs → 1500-1800 calories

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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

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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)

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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.)

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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

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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

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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)

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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

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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

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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

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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

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13
Q

Paraventricular nucleus

A

contain receptors that respond to neurons projecting from arcuate nucleus

  • Melanocortin receptors (MCR)
  • NPY receptors
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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

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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)
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16
Q

Neuropeptide Y (NPY) and Agouti-related peptide (AgRP) act to…

A

promote feeding, decrease energy expenditure

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17
Q

NPY (neuropeptide Y)

A

→ bind NPY-R in PVN/LH increase food intake, decrease energy expenditure

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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

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19
Q

A-melanocyte stimulating hormone (a-MSH), cocaine, and amphetamine-related transcript (CART) act to…

A

promote satiety, increase energy expenditure

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20
Q

POMC/CART –> _______ –> activates __________ receptors –> causes what?

A

POMC/CART → a-MSH → activate melanocortin receptors (MCR) → decrease food intake, increase energy expenditure

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21
Q

Leptin _______ POMC/CART and _________ NPY/AgRP

A

Activates POMC/CART

Inhibits NPY/AgRP

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22
Q

Lateral hypothalamus

_______ center

Stimulation –>
Lesion –> ?

A

hunger center

Stimulation → voracious eating
Lesion → decreased food intake

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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)

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24
Q

‘knocking out’ the POMC gene (and therefore, -MSH) –> ?

A

→ increase food intake, decrease energy expenditure

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25
Q

‘knocking out’ the NPY gene –> ?

A

→ decrease food intake, increase energy expenditure

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26
Q

loss-of-function mutations in the melanocortin receptor (MCR) –> ?

A

→ increase food intake, decrease energy expenditure

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27
Q

Ghrelin

A

28 AA peptide, induces hunger

High levels prior to meal

Ghrelin receptors in arcuate nucleus → activate NPY/AgRP arcuate neurons, and inhibit POMC/CART

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28
Q

Peptide YY (PYY)

A

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

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29
Q

Glucose effect on energy balance regulation

A

hypoglycemia stimulates eating, hyperglycemia inhibits eating

Glucose sensitive neurons located in VMN and LH

  • VMN stimulated by hyperglycemia
  • LH inhibited by glucose
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30
Q

Insulin effect on energy balance regulation

A

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

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31
Q

Leptin effect on energy balance regulation

A

“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

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32
Q

Non-Homeostatic Regulation of Energy Intake:

Internal inputs: (6)

A

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

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33
Q

Non-Homeostatic Regulation of Energy Intake:

External inputs (4)

A

1) Environmental cues (sight, smell, taste)
2) Availability/Portions
3) Social context
4) Time cues

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34
Q

Statin benefit groups (4)

A
  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.
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35
Q

How to calculate LDL

A

LDL = Total Chol – HDL – (Trig/5)

TG < 400

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36
Q

Cholesterol ester transfer protein (CETP)

A

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

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37
Q

CETP deficiency

A

–> Elevated HDL

Some meds have targeted this - and while they have been able to raise HDL, they have NOT shown reduced CVD improvement

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38
Q

Genetic disorders that can cause elevated TG and elevated LDL

A

1) familial combined hyperlipidemia

2) Familial dysbetalipoproteinemia

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39
Q

Tangiers disease

A

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)

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40
Q

ABCa1

A

ATP binding cassette (ABC) transporter

Important in transport of cholesterol from peripheral tissues to apo A-1 (core apoprotein of HDL)

deficiency –> low HDL

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41
Q

LCAT

A

Lecithin cholesterol acyltransferase

Transfers fatty acid from phospholipid onto free cholesterol → esterified cholesterol, that is more nonpolar and more tightly bound to HDL

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42
Q

LCAT deficiency

A

low levels of HDL, corneal opacities, renal insufficiency, hemolytic anemia due to accumulation of unesterified cholesterol in tissues

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43
Q

Normal lab values:

LDL
HDL
TG
HbA1c
Fasting glucose
A 
LDL < 100
HDL = 40-60 (higher is better)
TG < 150 mg/dL
HbA1c < 6.0% (> 6.5% = diabetes)
Fasting glucose < 100 (>126 = diabetes)
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44
Q

Familial Hypercholesterolemia (FH)

A

AD absence/defectiveness of LDL receptor → LDL 2-3x normal in heterozygotes and 5-8x normal in homozygotes

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45
Q

PCSK9

A

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

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46
Q

Causes of increased LDL (3)

A

1) Familial hypercholesterolemia (FH)
2) PCSK9 gain of function mutation
3) overproduction of VLDL by liver (e.g. insulin resistance)

47
Q

Physical exam findings in hypercholesterolemia (3)

A

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
Q

Causes of hypertriglyceridemia (high TGs)

A

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
Q

Physical exam findings of high triglycerides (4)

A

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
Q

Familial Dysbetalipoproteinemia

A

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
Q

Causes of low HDL

A

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
Q

Lecithin:cholesterol acyltransferase (LCAT) deficiency

A

homozygous mutations of LCAT gene → very low HDL levels

Corneal opacities (fish eye syndrome)

No increased ASCVD risk

53
Q

Dietary guidelines for treating dyslipidemia

A

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
Q

Exercise guidelines for treating dyslipidemia

A

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
Q

Drugs that lower LDL cholesterol

A

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
Q

Drugs that lower Triglycerides

A

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
Q

Why is the TG/5 rule for calculating LDL only used then TG<400?

A

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
Q

Acquired causes of hypertriglyceridemia

A

diet, oral estrogen treatment and uncontrolled diabetes

hypothyroidism, renal failure, liver disease, alcohol use and anti-retroviral medications

59
Q

Childhood BMI-for-age charts

tracking over what ages?

Overweight = ___-____%
Obese = > ______%
Severe obesity = > _____% or ___________

A

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
Q

Demographics of childhood overweight and obesity

A

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
Q

Comorbidities with childhood obesity

A

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
Q

Are childhood obesity comorbidities preventable?

A

AVOIDABLE - if not obese by the time they are adults, then risks are removed

63
Q

How often should you calculate and plot BMI in kids?

A

Calculate and plot BMI at least 1x year for all children > 2yrs

64
Q

Key components of assessment in pediatric obesity (7)

A

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
Q

Labs for obese pediatric patients (4)

when should you get lipids and A1c?

A

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
Q

Physical exam findings associated with comoridities of pediatric obesity

A

HTN, acanthosis nigricans, acne/hirsutism, striae, organomegaly, joint pain, neurologic function

67
Q

Essential treatment principles for childhood obesity: (5)

A

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
Q

Prevention Plus - what is it?

A

5210+ = 5 fruits/vegetables, 2 hours TV or less, 1 hour activity, 0 sugar sweetened beverages (SSBs) + others

69
Q

Motivational interviewing skills

A

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
Q

What is OARrrrs?

A 
open-ended questions
affirmations
reflections
rolling with resistance
reframing
summaries

Used as a strategy for motivational interviewing

71
Q

Weight loss medications:

Considerations: (7)

A

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
Q

Phentermine

Mechanism

A

amphetamine, increases brain NE

No abuse potential
Acts centrally to increase satiety

73
Q

Phentermine

Side effects

A

nervousness, difficulty sleeping, headache, dry mouth

*Increase BP - CONTRAINDICATED for pts with uncontrolled HTN

74
Q

Phentermine

Amount of weight loss and cost

A

roughly 5% of baseline weight lost

Cost: generic, inexpensive
LEAST expensive

75
Q

Phentermine

Use

Best in what way?

A

only FDA approved for 3 months of use, but long term prescribing “off label” is commonly done

Best because LEAST EXPENSIVE

76
Q

Orlistat

Mechanism

A

pancreatic lipase inhibitor → block dietary fat absorption

77
Q

Orlistat

Side effects

A

not systemically absorbed, not systemic side effects

Oily stools, urgency, diarrhea, oily leakage

Deficiency of fat soluble vitamins

78
Q

Orlistat

use

best in what way?

A

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
Q

Lorcaserin

Mechanism

A

selective serotonin 2C receptor agonist

80
Q

Lorcaserin

best in what way?

A

LEAST side effects

81
Q

Lorcaserin

Side effects

A

possible cardiac valve problems? (unproven)

LEAST side effects - minimal headache, dizziness, nausea

82
Q

Lorcaserin

amount of weight loss and cost

A

Amount of weight loss: 4-5% weight loss

Cost: $220/month

83
Q

Phentermine/topiramate

Side effects

A 
Teratogen
Dry mouth
Paresthesias
Insomnia, anxiety, irritability, disturbances in attention
Dizziness
84
Q

Phentermine/topiramate

Amount of weight loss

A

8-12% of baseline weight

Metabolic benefit of weight loss (BP, glucose, insulin, TGs, HDL)

MOST EFFECTIVE weight loss

85
Q

Phentermine/topiramate

cost?

A

$150/month

86
Q

Phentermine/topiramate

best in what way?

A

MOST EFFECTIVE weight loss (8-12%)

87
Q

Naltrexone SR/Bupropion SR

Mechanism

A

opioid receptor antagonist (naltrexone) + Dopamine/NE reuptake inhibitor (Bupropion)

88
Q

Naltrexone SR/Bupropion SR

Side effects

A

lowering seizure threshold, increased pulse and BP, rarely increased LFTs and closed angle glaucoma

BLACK BOX - increase risk suicidal ideation

89
Q

Naltrexone SR/Bupropion SR

Amount of weight loss and cost

A

Amount of weight loss: 5% of baseline

Cost: $200/month

90
Q

Liraglutide 3 mg

mechanism
side effects
amount of weight loss
cost

A

Mechanism: GLP-1 agonist (also used in diabetes)

Side effects: nausea, pancreatitis

Amount of weight loss: 5-7% weight loss

Cost: $1000/month

91
Q

Medications that contribute to weight gain

A

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
Q

Amount of weight loss:

gastric bypass surgery vs. Lap band vs. Sleeve gastrectomy

A

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
Q

Sleeve gastrectomy:

Pros/Cons:

A

Intermediate choice between band and RYGB

Does not require adjustments

NOT associated with vitamin and nutritional deficiencies

94
Q

Laparoscopic banding:

Pros/Cons

A

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
Q

Risks of surgical treatment of obesity:

A

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
Q

Benefits of weight loss surgery

A

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
Q

Qualify for medication tx of obesity:

A

BMI > 30 without medical conditions or BMI > 27 with comorbid issues (diabetes, HTN, sleep apnea, degenerative arthritis)

98
Q

Qualify for bariatric surgery

A

BMI > 40 without medical conditions or BMI > 35 with comorbid issues

99
Q

Qualify for bariatric surgery

A

BMI > 40 without medical conditions or BMI > 35 with comorbid issues

100
Q

Key Elements of effective behavior change counseling:

A

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
Q

Stages of change (7)

A

1) Precontemplative
2) Contemplative
3) Planning
4) Action
5) Maintenance
6) Relapse
7) Identification

102
Q

1) Precontemplative

A

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
Q

2) Contemplative

A

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
Q

3) Planning

A

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
Q

4) Action

A

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
Q

5) Maintenance

A

struggle adhering to diet

107
Q

6) Relapse

A

“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
Q

7) Identification

A

emerge from maintenance period and incorporate long term changes into their lifestyle

109
Q

Motivational interviewing has _________ and ________ of ___________ as its central purpose

A

**EXAMINATION and RESOLUTION of AMBIVALENCE is its central purpose

110
Q

Values-based counseling

A

**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
Q

Transtheoretical Model helps you assess _______ but doesn’t ___________

A

helps you assess readiness, doesn’t tell you what to do

112
Q

Health belief model

A

person’s willingness to change relates to their perception of their vulnerability for illness and the possible effectiveness of treatment

113
Q

According to the health belief model, change occurs if a person…

A

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
Q

Cognitive behavioral therapy focus on ____________, not _______________

A

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

DEMS (10 decks)

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