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Health Education

CLASS NOTES:

Stages of Change

1. Pre-contemplation – does not see behavior as problem

2. Contemplation – recognizes problem

3. Plan

4. Action

5. Maintenance

6. Relapse – common, help pt restarted at that stage



Tobacco causes 400,000 deaths/year

Obesity causes 300,000 deaths/year



BMI

 Overweight: 25-29

 Obesity

o Class I: 30-34

o Class II: 35-39

o Extreme Obesity: +40



Obesity – a 60% increase in prevalence from 1991-1999



Waist circumference: determination of obesity

1. Male: >40 in or 102 cm

2. Female: >35 in or 88 cm



Goals for Weight Loss:

1. Lose 10% of weight over 6 months → Decrease disease risk factors

2. Rate of 1-2 lbs/wk with deficit of 500-1000 kcal/day

3. More rapid weight loss → Gallstones, regain weight

4. At 6 months hit plateau of weight loss

5. To decrease weight pt must decrease intake and increase activity

6. Successful maintenance: 165 lbs: 1200-1600 kcal/day

 Male: 1200-1600 kcal/day

 Add 1-200 kcal/day if still hungry

Diet Drugs:

 Meridia – decrease in 5HT and NE reuptake

 Xenical – blocks 1/3 fat absorption

 Phenterimine – good for short term (29 or >25 + 2 risk factors

 Net attributable loss: 2-10 kg

 Are unlikely to work if lose 60 million) are overweight.

o 50% of American women and 25% of men are trying to lose weight

 Etiology:

o Most obesity is primary – no obvious cause exists other than an imbalance in

energy intake and expenditure

o Cushing’s syndrome, hypothyroidism, and hypogonadism are rarely causes.

o Genetic factors play a role – a mutation in gene coding for beta3-adrenergic

receptor was assoc. w/ increased capacity to gain weight. Low beta3-

adrenergic activity promotes obesity by slowing lipolysis.

o Obesity should be considered a condition w/ multiple causes

o Common conditions associated w/ obesity: DM type 2, HTN, dyslipidemia,

macrovascular disease, CA (endometrial, ovarian, breast, gallbladder,

prostate, colon), menstrual irregularities, decreased fertility, hirsutism,

gallbladder disease, restrictive lung disease, sleep apnea, OA, gout,

thromboembolic disease.

 Evaluation:

o Weight history from childhood should be reviewed, also various methods of

weight loss that were attempted and the results.

o Weight gain is common side effect of certain medications; a history of med

use is an important aspect of the initial evaluation.

 Meds assoc w/ weight gain – Psychotropic agents (TCA, MAOI,

antipsychotic drugs, Li), Anticonvulsant agents (depakene, tegretol),

Steroid hormones (corticosteroids, estrogens, progesterone,

testosterone, other anabolic/androgenic steroids), insulin and most oral

hypoglycemic agents.

o Weight gain is common during the initial phase of smoking cessation.

o BMI = weight in kg divided by height in meters squared

o Overweight: BMI 25-29.9

o Obese: BMI >30

 Treatment:

o Obesity – chronic medical condition that is rarely cured

o Caloric deficit of 3,500 kcal is necessary to lose 1 lb of adipose tissue

o Behavioral therapy is more favorable and cost-efficient

o Weight loss obtained using behavioral therapy was better maintained at one

year.

o A safe and effective treatment of obesity that will satisfy most patients’ desire

for rapid and long-lasting weight loss is not available.

 Pharmacologic Therapy: Appetite suppressants:

o 2 classes of anorectic drugs: noradrenergic and serotonergic agents.

o Noradrenergic agents – affect weight loss through action in appetite center.

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 Phenylpropanolamine (Dexatrim) – sympathomimetic drug – greater

weight loss than placebo – difference was minimal. Daily doses (20-

75 mg qd) common side effects include: nervousness, insomnia,

dizziness, palpitations, and HA.

 Phentermine (Ionamin) – similar to amphetamine – modulates

noradrenergic neurotransmission to decrease appetite – little or no

effect on dopaminergic neurotransmission (decreases potential of

abuse). Limited by intolerance to its stimulatory activity. Was used

w/ fenfluramine (which was withdrawn). Phentermine is now used as

a single weight-loss agent. Significant weight loss in comparison to

placebo. Common adverse effects: HA, insomnia, nervousness and

irritability. Palpitations, tachycardia, and elevations in BP may also

occur. Should NOT be taken by those w/ HTN, glaucoma, agitated

states, advanced arteriosclerosis, symptomatic CV disease, moderate to

severe HTN, or h/o drug abuse.

o Serotonergic agents – partially inhibit reuptake of serotonin and release

serotonin into synaptic cleft – acting on hypothalamus to decrease satiety.

 Fenfluramine and dexfenfluramine (Redux) – withdrawn from US

market in 1997 – case reports of valvular heart disease and primary

pulmonary HTN.

 Fluoxetine (Prozac) – highly selective SSRI – increase energy

expenditure by increasing basal body temp; weight loss has not been

consistent among trial – did not significantly reduce weight. After 1

year, wt loss was no different than placebo. Labeled for tx of

depression, bulimia and OCD. Not labeled for tx of obesity.

o Adrenergic/Serotonergic Agents –

 Sibutramine (Meridia) – and it’s metabolite inhibit MAO uptake – may

also stimulate thermogenesis by activating the beta3-system in brown

adipose tissue. Can cause wt loss of 1-2 kg (2.2-4.4 lbs) in healthy and

depressed pts. Significantly greater loss than those w/ placebo and

weight loss increased w/ increasing dosages. However, all patients

regained wt. Indicated for management of obesity. Should be used in

conjugation w/ reduced calorie diet. Initial BMI >30 or >27 w/ other

risk factors (HTN, DM, hyperlipidemia) Start at dosages of 10 mg.

Can go up to 15 mg. Side effects: dry mouth, anorexia, constipation,

insomnia, mild increase in BP and HR in non-hypertensive patients.

 Pharmacologic therapy: Thermogenic agents:

o Combo of ephedrine and caffeine possesses anorectic and thermogenic

properties w/ only mild, transient side effects. Ephedrine increases release of

NE (modulates food intake and acts as a sympathomimetic agent to stimulate

HR and BP and enhance thermogenesis). Caffeine- an adenosine antagonist –

reduce breakdown of NE.

 Combo of ephedrine (20mg) and caffeine (200mg) taken tid was found

to be more effective than placebo or either agent alone. Side effects:

tremor, insomnia and dizziness are transient after 8 wks.

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o Selective beta3-adrenergic agonists are currently under investigation –

believed to increase rate of metabolism and cause reduction of wt by

decreasing body lipid content.

 Pharmacologic Therapy: Digestive inhibitors: reduction in fat is recommended in

most wt loss diets – pt compliance is generally poor. Digestive inhibitors are agents

that interfere w/ the breakdown, digestion, and absorption of dietary fat in the GI

tract. Gastric and pancreatic lipases aid in digestion of TG to FFA. Inhibition of

digestion of TG and decreased cholesterol absorption and decreased absorption of

lipid-soluble vitamins (A,D,E,K) are assoc w/ these agents.

o Orlistat (Xenical) – lipase inhibitor – potent and irreversible inhibitor of

gastric and pancreatic lipases, preventing absorption of 30% of dietary fat.

Indicated for pts w/ BMI >30 or pts w/ BMI >27 + HTN, DM, or

dyslipidemia. Wt loss of about 6.6-8.8 lbs in one year w/ ½ regained in 2nd

year. GI side effects: (40% of pts) – flatus w/ discharge, oily spotting and

oily stool, fecal urgency, fecal incontinence, and abd pain. Does not appear to

interfere w/ efficacy of other chronic meds (HTN meds, OCP, coumadin)

 Pharmacologic therapy: Fat substitutes: goal is to decrease caloric value from fat

while maintaining creaminess and richness from fat.

o Olestra (Olean) – 0 kcal/g – sucrose polyester (too large to be hydrolyzed by

digestive enzymes – not absorbed) May be effective in enhancing wt loss

when used w/ calorie-restricted diet GI side effects: bloating, flatulence,

diarrhea, lose stools, and anal leakage. Absorption of fat-soluble vitamins

from GI tract can only be affect by olestra if booth are eaten at the same time

– FDA has required all olestra foods be supplemented w/ vitamins A,D,E, and

K. Possible effect on vit K absorption – use caution in pts on warfarin.

 Hormone manipulation –

o CCK and serotonin decrease appetite and food uptake

o Neuropeptide Y increases food uptake and decreases energy expenditure

o Leptin may limit food intake, decrease plasma insulin, and increase energy

expenditure.

o Agonists and antagonists of these hormones/peptides are currently under

investigation.

 Safety of many of these agents has only been studied for a short period of time. If

drug therapy is recommended to manage obesity, it should be used in combo w/

structured diet and exercise program to achieve the greatest results.



Exercise Prescription:

 Exercise counseling should be a part of routine health maintenance. Provide pt w/

info about specific benefits of exercise and motivate them to increase their physical

activity.

 Accumulate 30 minutes or more of moderate-intensity physical activity on most days

of week.

 Selected higher risk pts may need to be evaluated prior to starting a program – use PE

and treadmill testing.

 Formal exercise prescription should include: specific advice about type, frequency,

intensity, duration, and progression of physical activity.

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 Injury prevention and adherence to program is important.

 Nearly 60% of adult Americans are sedentary.

 40, women >50,

and anyone w/ 2 or more cardiac risk factors or signs/symptoms of

cardiorespiratory or metabolic disease.

 Activity Selection - Walking is the most popular form of exercise in America.

o Injury rate must be considered – low-impact is better for most than high-

impact.

 Exercise routine- once an activity is selected the pt should be given specific advise

about duration, intensity and frequency.

o Warm-up: 5-10 min –stretch muscles, increase flexibility, gradual increase in

HR.

o Cardiorespiratory and Strength-Training Period: exercise w/in target zone for

20-60 min

o Cool-down Period: 5-10 min

 Intensity: risk of coronary heart disease has been shown to decrease w/ expenditure of

as little as 2,100 kilojoules per week (walking about 7 miles)

o Begin exercise at 40-60% of cardiorespiratory capacity and increase to 50-

85% of capacity.

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o Maximal heart rate: 220-age – pts should eventually reach 60-90% of this

value

 Muscle conditioning: resistance training can be used to build strength and endurance

in the major muscle groups

 Duration and progression –start slow and build up. Duration should gradually be

increased every 2-3 weeks.

o At 6 months – enter “Maintenance phase” – adhere to regimen

 Injury prevention:

o Injuries sedentary patients incur are usually overuse injuries from attempting

too much too soon.

o Select proper footwear, have good nutrition and proper fluid intake, increase

duration and intensity gradually, and use good posture and form during

exercise.

o Review 1st aid measures

o Cross-training may help prevent overuse injuries

o Unless necessary, pts should not stop all forms of exercise, but they should

contact MD if they are injured and have questions about what exercises they

can do.

 Adherence to exercise regimen:

o Encouraging regular participation w/ an exercise partner and eliciting the

support of family members may also help considerably

o MD should schedule F/U visits to assess progress and discuss problems or

potential modifications of exercise program in the early stages.



Beginning An Exercise Program:

This is basically a patient info sheet that goes over the above info on exercise – no need

to write or read it twice.



Surgical Options for Morbid Obesity:

 Indications for surgery: BMI>40 or >35 w/ life-threatening cardiopulmonary

problems or severe DM

 Criteria for reimbursement: body wt >100% above ideal wt, serious co-morbidity,

failed attempts at non-surgical weight-reduction programs, no substance abuse,

psychoses, or uncontrolled depression

 Results from surgery: lose about 50-60% excess body wt or decrease BMI by 10

during 1st 12-24 months; some wt regained but maintain about 50% of excess body

weight loss. NIDDM resolves 90% of pts. HTN disappears 66% of time by 4 years

post-op. HDL increases and TG and TC decline. Sleep apnea disappears after 15-20

kg loss.

 4 basic surgical approaches:

1. Induce global malabsorption – jejuno-ileal bypass – no longer done – should

be reversed.

2. Limit oral intake per meal- gastroplasty (gastric “stapling”) – decreases

size of stomach – cons: pts figure out that they can eat high fat food easily

and wt goes back up.

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3. Limit oral intake per meal and induce a “dumping” physiology – cardia of

stomach is directly drained into the jejunum – prevents large amounts of

food at any one meal and induces dumping syndrome. Cons:

malabsorption of Fe and B12.

4. Induce selective maldigestion and malabsorption: partial biliopancreatic

bypass – (for extremely obese >225% IBW) 8% of stomach is removed

and biliary and pancreatic secretions are diverted to distal ileum. Cons:

deficiency in fat-soluble vitamins (need supplements)



Trends in Smoking Related Diseases:

 Most important strategy for reducing the chief cause of morbidity and death in the US

is eliminating tobacco use.

 Cigarette smoking caused about 400,000 deaths/year

 Four leading causes of death – heart disease, CA (esp. lung), cerebrovascular disease,

and COPD – are strongly related to smoking.

 When people stop smoking, their risk of tobacco-related morbidity and mortality

decreases significantly.

 Cardiovascular disease:

o 950,000 deaths/year

o Ischemic heart disease causes about 500,000 deaths/year

o Coronary heart disease: leading cause of death among men >45

o Relative risk of death due to coronary heart disease in smoker is 2-4xs greater

than that in persons who have never smoked.

o British male doctors study: males 25 cigarettes/day, risk of

mortality from ischemic heart disease was 15xs that of a nonsmoker.

o Estimated relative risk of both fatal and nonfatal coronary disease is increased

roughly 2xs in light to moderate smokers and 6-15xs in heavy smokers.

o Excess risk among former smokers drops substantially in the 1st 2-3 years.

Thereafter, the rate of decline decreases so that it takes up to 10 years for

former smokers to reach the same risk level as those who never smoked – due

to reversal of some atherogenic effects of smoking

o Risk of MI after smoking cessation declines quickly – diminishes by almost

1/3 after the 1st year and reaches the level of persons who never smoked by

the 3rd-4th year – due to rapid reversal of hypercoagulability induced by

smoking.

o Patients who continue to smoke after percutaneous coronary revascularization

had almost twice the risk of death and of Q-wave MI. Benefits of surgical

revascularization are nearly negated in pts who continue to smoke.

 Cerebrovascular disease – overall risk of stroke assoc w/ smoking was 1.5. Risk of

stroke was highest in smokers >55 and diminished w/ increasing age.

o Risk of stroke was 4xs higher in men who smoked >21 cigarettes a day than in

those who never smoked.

o Men who stopped cigarette smoking and switched to cigar or pipe smoking

retained a threefold increased risk of stroke.

o Time to maximal risk reduction was about 5 yrs, after which no further

decline in risk was seen.

8





o Thromboangiitis obliterans (Buerger’s disease) – an inflammatory disease of

small arteries and veins, is seen almost exclusively in smokers. It causes

significant morbidity among people in their 30s or 40s. Amputation risk is

high. Only effective tx is smoking cessation.

o Progression of atherosclerosis attributable to smoking was more substantial

than that due to other CV risk factors. Risk of progression of atherosclerosis

was highest in smokers who had other risk factors, such as HTN and DM.

 Lung CA – most frequently diagnosed CA in world and leading cause of CA death in

US for both men and women.

o Latent period between cigarette consumption and rise in lung CA death rate is

due to fact that carcinogenesis in respiratory tract is probably a multistep

process involving sequential changes, form normal to malignant, in the cells

lining the tract.

o Relative frequency of adenocarcioma is increasing. Rise in Adenocarcinoma

is since the intro of filtered cigarettes and those low in tar and nicotine.

Inhalation delivers carcinogens to the peripheral lung where adeno is

preferentially produced.

o Small cell CA is more common in smokers who quit within 10 years than

those who have quit for more than 10 years.

o AA have significantly poorer prognosis for any type of lung ca, overall

prognosis for all ethnic groups is poorer.

o Annual screening w/ chest film and sputum testing in smokers has not shown

benefit in reducing lung cancer mortality.

o Newer screening techniques (spiral CT) may prove to be beneficial in early

detection of lung cancer in selected smokers.

o Supplementation w/ beta-carotene and retinyl palmitate in male smokers

showed no reduced risk in lung CA – actually they showed harmful effects –

higher incidence of lung ca. There are currently no nutritional supplements

that have proven beneficial to lung CA.

 COPD

o No detectable difference in lung function between smokers who quit before

age 40 and those who never smoked. Smokers who quid between ages 40-60,

lung function was about equal to those of nonsmokers 2.5-7.5 years older.

Quitting smoking after 60 was assoc w/ lung function comparable to that of

nonsmokers 5.5-15 years older and current smokers have lung function levels

equivalent to those of nonsmokers 10-20 years older.

o It is never too late to quit.

o Lung Health Study: subjects who quit smoking had significantly better lung

function than those who continued to smoke.

o Use of inhaled bronchodilators had no significant effect on loss of lung

function.

 Economic considerations:

o Est. cost of treatment program at Mayo Clinic Nicotine Dependence Center:

$6,828 per net year of life gained.

o Only preventative medical care that is more cost-effective is use of

pneumococcal vaccine in elderly: $1,500 per year.

9





 Conclusion:

o Mortality attributable to smoking accounts for 20% of all deaths in the US

every year.

o Physicians can intervene by:

1. Informing pts accurately about risks of smoking

2. Personalizing the message about health risks

3. Emphasizing the significant health benefits of smoking cessation

4. Giving pts a clear and unequivocal message to stop smoking



Drug Therapy To Aid In Smoking Cessation:

 Choosing a method: What does the patient want? Explore what has worked and what

hasn’t in the past. Has the patient had any serious reactions to a particular method?

Side-effect profile of a method acceptable for the pt? How effective is the med alone

and in combo?

o Smokers who are more dependent require higher doses of nicotine

replacement, longer duration of therapy, and a possible combination of

therapy.

o Characteristics of most dependent pts

 Smoke more than 20 cigarettes qd

 Smoke w/in 30 min of awakening

 Significant withdrawal symptoms and early relapse on previous

attempts

 Current or past history of significant psychiatric disorder

 Active or recovering dependence on alcohol or other drugs

 Achieving optimal outcome:

o Provide written instructions on proper use of the method

o Individualize the dose and duration of therapy

o Schedule frequent office visits or phone calls to monitor patient response, and

adjust dose and duration of therapy accordingly

 If abstinence has not been achieved w/in 2 wks, med regimen and the pts motivation

should be reassessed. If they continue to smoke at or near the original level after 4

wks, med should be D/C and tx program reassessed.

 Continue therapy as long as the pt thinks they need it. However, after 6 months

signals a need for reevaluation of ongoing issues.

 Nicotine gum: it works best in conjunction w/ other methods such as other nicotine-

replacement products or bupropion (Zyban).

o Chew nicotine gum slowly until feel a “tingle” then “park” the gum next to

the cheek and allow the buccal mucosa to absorb the nicotine. Cont for 30 per

piece of gum. Use 10-15 pts per day.

 Nicotine patches – deliver high doses of nicotine transdermally and satisfactory relief

of withdrawal symptoms. Con: undertreat most smokers.

o Light smokers: 21-22mg patch continues the pts normal level of nicotine and

allows for high cessation rates

o Heavy smokers: require high dose 44mg patch for more complete nicotine

replacement.

 Nicotine nasal spray: requires pt counseling and education to ensure appropriate use.

10





o Spray med against lower nasal mucosa – Do not spray or sniff into upper

passages.

o Don’t exceed 5 doses per hour or 40 doses qd

o Nasal irritation is common and the pt should be told to continue treatment and

the irritation and other symptoms will subside or diminish.

o Therapy is D/C at 12 weeks

 Nicotine inhaler: may be the best choice for therapy for those who need the ritual and

the tactile and sensory stimulation that this device provides. More a “puffer” than an

inhaler. Vaporized nicotine is delivered to the mucosa of the mouth and posterior

pharynx to be absorbed.

 Bupropion (Zyban) in sustained release form – an amnioketone antidepressant – has

both noradrenergic and dopaminergic activity.

o Weak inhibitor of synaptic reuptake of NE and dopamine. (Increased

dopamine in nucleus accumbens may maintain stimulation of pleasure-

response areas in the absence of nicotine.)

o Also, decreases the normal amount of weight gain assoc w/ cessation of

smoking by nearly ½.

o Effective both as monotherapy and in combination for smokers who have

relapsed or could not achieve abstinence w/ nicotine-replacement meds alone.

o Pts are often instructed to continue smoking for the 1st week and then stop

smoking during the second week of therapy. Therapy can continue for 3-4

months.

o Side effects: Common: insomnia and dry mouth. Uncommon: CV and sexual

side effects. Seizures have been reported in about 1 in 1,000 pts. Screen for

seizures:

 Active seizure disorder

 H/O seizures

 H/O CNS trauma (stroke, brain surgery, significant head injury w/

LOC)

 Use of drugs that lower seizure threshold (alcohol, neuroleptic)

 Eating disorder (anorexia nervosa, bulimia)

 Use of high buproprion dose (>300 mg qd)



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