1. approach to patient with respiratory disease and smoking cessation

8/19/2019 1. Approach to Patient With Respiratory Disease and Smoking Cessation

1/13

APPROACH TO PATIENT WITH RESPIRATORY DISEASE and SMOKING CESSATION

TOP 10 LEADING CAUSES OF MORBIDITY IN THE PHILIPPINES! Diarrhea

! Bronchitis/bronchiolitis

! Pneumonia

! Influenza

! Hypertension

! Tuberculosis

! Diseases of the heart

! Malaria

! Measles

! Chicken pox

TOP 10 LEADING CAUSES OF MORTALITY IN THE PHILIPPINES! Heart disease

! Vascular system disease

! Cancer

! Road Accidents

! Pneumonia

! Tuberculosis

! Dengue Fever

! Chronic lower pulmonary diseases

! Diabetes mellitus

! Perinatal conditions

ANATOMYSTRUCTURES

! CONDUCTING SYSTEM! From nasal cavity

and pharynx (upperairways)

! Larynx,! Trachea,!

Main bronchi,! Distal bronchioles

(lower airways) ! GAS-EXCHANGING

SYSTEM! Terminal

bronchioles,! Alveolar ducts and! Alveoli

Internal Medicine IIDr. Rommel N. Tipones, MD, FPCCP, FPCP

Module I


2/13


! INTRAPULMONARYAIRWAYS

! Bronchi! Membranous bronchioles! Respiratory

bronchioles/gasexchange ducts

! ANATOMIC DEAD SPACE ! Upper extrapulmonary

airways! Cartilaginous

intrapulmonary airways

! RESPIRATORY BRONCHIOLE – ALVEOLAR DUCT SYSTEM ! Do not contribute to the anatomic dead space! One third of the alveolar volume! Space where fresh air ventilation enters during inspiration

! AIRWAY RESISTANCE ! Mostly in upper airways and bronchi! Minimal airway diameter at the terminal bronchioles (0.5

mm)! Large airways maintain partial constriction due to

bronchomotor tone

! CILIA! Half of the epithelial cells at all airway generations down

to the bronchioles! 6 um long, 0.3 um wide! 9 +2 axonemal structure/ motile! Move the superficial liquid lining layer toward the pharynx

! GLANDS ! Submucosa of the bronchi! Secrete water, mucins into the lumen! Release modulated by neurotransmitters/ inflammatory

mediators

! GOBLET CELLS ! Mucin-secreting epithelial cells! Decrease peripherally! Disappear at the terminal bronchioles

! OTHER CELLS IN THE AIRWAYS ! Basal cells! Lymphocytes! Smooth muscle cells! Mast cells

! TERMINAL AIRWAYS ! Partially ciliated low cuboidal! Interspersed with Clara cells

! CLARA CELLS !

Source of apoproteins! Synthesis, storage and secretion of lipids, proteins and

glycoproteins! Progenitors of ciliated cells. goblet cells, and new Clara

cells

! BRONCHIAL CIRCULATION ! Arteries from the aorta or upper intercostal arteries (hilum)! Blood supply to the trachea, bronchi, pulmonary vessels,

visceral pleura

! Venous blood drain into the azygos or hemiazygos veins,pulmonary venules

! The terminal bronchioles divide into 2-5 alveolar ducts,each of which consists of 10-16 alveoli. Alveoli has 3 celltypes: Type I, the lining cell accounts for 95% of thealveolar surface area. Type II cell produces surfactant, amixture of phospholipids, which maintains alveolarstability. The macrophage acts as phagocytic defense vsinfection

! The adult respiratorysystem contains approx.300 million alveoli. Thesurface area of thealveolo-capillarymembrane available for02-C02 exchange isapproximately 70-85m2

! TERMINAL RESPIRATORYUNIT

! Alveolar ducts (100)! Alveoli (2000)! 150,000 units! 0.02 ml! Acinus (10 – 12 TRUs)

! TYPE II CELLS! Small, cuboidal! Outnumber type I cells (15% vs 8%)! Synthesis, secretion and repair! Intracellular lamellar bodies! Internalize and recycle surfactant lipids and proteins

! TYPE I CELLS! Large, flattened! Accounts for 90 to 95% of the alveolar surface area of the

peripheral lung! Provide a large, thin cellular barrier for gas exchange

! AIR SPACE MACROPHAGES AND LYMPHATICS ! Superficial plexus of lymphatics! Deep plexus of lymphatics! Regional pulmonary lymph nodes! Extrapulmonary lymph nodes around the primary bronchia

and trachea


3/13


PHYSIOLOGY FUNCTIONS

! Adequate provision of fresh air to the alveoli (VENTILATION)

! Adequate circulation (PERFUSION)! Adequate movement of gas between alveoli and pulmonary

capillaries (DIFFUSION)! Appropriate contact between alveolar gas and pulmonary

capillary blood(VENTILATION-PERFUSION matching)! Repeated 12 to 16 times per minute! Has a tidal volume of 500 mL! Has a portion (30%) which does not reach the alveoli (anatomic

dead space)! Has the remaining 70% reaching the alveolar zone

! During inspiration, as these muscles contract, the thoraxexpands. Intrathoracic pressure decreases, drawing air into thetracheobronchial tree into the alveoli and expanding the lungs.Gas exchange takes place in the alveoli

! After inspiratory effort stops, the expiratory phase begins. Thechest wall and the lungs recoil, the diaphragm relaxes and risespassively, air flows outward and the chest and abdomen return totheir resting positions

! During inspiration, air enters the upper airway, travels through thelower airways until it reaches the alveoli. Each alveolus issurrounded by multiple capillaries

! During systole, deoxygenated blood returning from the body’scells is pumped from the right ventricle through the arterialpulmonary circulation to the alveolar capillaries. CO2 diffusesfrom the capillary blood across alveolo-capillary membrane andenters the alveolar air. Simultaneously, O2 from inspired atm. airin the alveolus crosses the alv.cap. membrane and enters thepulmonary capillary blood

! During expiration, CO2 is exhaled from the lungs. Oxygenatedblood travels to the left side of the heart and is pumped from theventricle into the arterial circulation to the cells of the body, wherecellular respiration occurs

! RESPIRATORY FAILURE ! “Inability of the lung to meet the metabolic demands of

the body.”! Failure of tissue oxygenation and/or! Failure of CO 2 homeostasis

! Clinical definition:! PaO 2 50 mmHg

PHYSIOLOGY OF RESPIRATION

! Ventilation is the movement of atmospheric air into and out of thelungs. Ventilation consists of 2 components: alveolar ventilationand dead space ventilation. Alveolar ventilation is also known as“effective” ventilation because it is that portion of inspired air thatactually reaches the alveoli and participates in gas exchange.Dead space ventilation, also known as “ineffective” or “wastedventilation, is that amount of inspired air that does not participatein gas exchange. The normal dead space ventilation (inspired airthat does not reach the alveoli-includes all the conductingairways) in an adult individual is approximately 150CC.

Diffusion of O 2 and CO 2


4/13


APPROACH TO PATIENT WITHRESPIRATORY DISEASE

! SYMPTOMS! ABNORMALITY ON A CHEST RADIOGRAPH

HISTORY OF SYMPTOMS! Common

! Dyspnea/ Shortness of breath

Acute (mins todays)

Subacute (daysto weeks)

Chronic

Airways Exacerbation ofairway disease

Exacerbationsremissions

Lungparenchyma

Slow infection orinflammation

COPD

Pleural space Neuromusculardisease

CILD

Pulmonaryvasculature

Chronic cardiacdisease

Chronic cardiacdisease

! Cough! May indicate the presence of lung disease! Sputum often suggests airway disease! Chronic cough

o Asthma

o Chronic Obstructive PulmonaryDisease

o Gastroesophageal Reflux Disease

o Postnasal drip

o Pulmonary Tuberculosis

! Less common! Hemoptysis

Airways Inflammatorybronchitisbronchiectasiscystic fibrosis

neoplastic tumorsLung Parenchyma Localized

pneumonialung abscesstubercolsisaspergillosis

DiffuseVasculature Pulmonary thromboembolic

disease Arteriovenous malformations

! Chest pain/ Pleurisy! Pleuritic!

Accentuated by respiratory motion! Neoplasms/inflammation involving pleura! Parenchymal disorders extending to the pleura

ADDITIONAL HISTORIC INFORMATION/RISK FACTORS! Smoking

! Current and past! Cigarettes! Number of years! Intensity

! Smoking cessation! COPD and cancer! Second hand exposure

! Inhaled agents! Asbestos, silica dusts – pneumoconiosis! Molds, animal proteins – hypersensitivity pneumonitis! Dust mites, pet dander, cockroach allergens –

exacerbation of asthma!

Exposure to infectious agents/contact with infectedindividuals

! Coexisting illness! AIDS! Previous treatments! Family history

PHYSICAL EXAMINATION! Inspection! Palpation! Percussion! Auscultation!

Extrapulmonary manifestations

! Meticulous! Enlarged lymph nodes! Mentation! Signs pointing to smoking! Clubbing! Extrapulmonary findings


5/13


DIAGNOSTIC MODALITIES INPULMONOLOGY

! Imaging studies! Techniques for acquiring specimens! Direct visualization! Pulmonary function testing! Ancillary procedures

ROUTINE RADIOGRAPHY! Posteroanterior and Lateral! Lateral decubitus! Apicolordotic! Anteroposterior

BASICC APPROACH TO RADIOGRAPHY! Background! Survey! Identify! Compare! Conclude

COMPARISON OF CXR FINDINGS IN ATELECTASIS,

PNEUMONIA, & PLEURAL EFFUSION

ATELECTASIS PNEUMONIA PLEURALEFFUSION! Margins sharplydefined & linear! Tends to occur atouter third of lung! Areas of lungadjacent toatelectatic regionsmay be hyperlucent! Tends to respectlobar & segmentalboundaries

! Margins indistinctunless diseasestrictly lobar or! Segmental! Distribution tendsto be patchy ratherthan linear

! Increases opacityof involvedhemithorax; at bases ! Often layers whenplaced on decubitusposition! May mimic pleuralthickening

COMPUTED TOMOGRAPHY

! Cross-sectional images! Better tissue density! Accurate size! Hilar and mediastinal disease! Pulmonary nodule assessment! Conventional CT! Helical CT! CT angiography! High-resolution CT (HRCT), multi-slice

! Virtual bronchoscopy


6/13


MAGNETIC RESONANCE IMAGING

! Relies on energy generated by tissue when! Placed in strong magnetic field! MRI resolution limited to 3-4 mm! Susceptible to motion! Superior in studying blood vessels & different soft tissues esp at

hilum & mediastinum

SCINTIGRAPHIC IMAGING ! Radioactive isotopes ! Ventilation-perfusion scanning

• Albumin macroaggregateslabeled with technenium 99

• Inhaled radiolabeled xenongas

POSITRON EMISSION TOMOGRAPHIC SCANNING

(PET SCAN)! Identify malignant lesions! Increased uptake and metabolism of

glucose! F-fluoro-2-deoxyglucose (FDG)

PULMONARY ANGIOGRAPHY! Pulmonary artery! Pulmonary embolism

! “Filling defect”!

“Cutoff”! Pulmonary AVMs! Arterial invasion by neoplasm! Being replaced by CT Angiography

ULTRASOUND! Uses sonar

! Limited use; doesn’t pass through bone or air-filled spaces! Used to quantify pleural effusion and to guide percutaneous

needle aspiration of accessible masses/fluid

OBTAINING BIOLOGIC SPECIMENS! Sputum Collection! Percutaneous needle aspiration! Thoracentesis

! Bronchoscopy! VATS! Thoracotomy! Mediastinoscopy/Mediastinotomy ! Percutaneous needle aspiration! Thoracentesis! Bronchoscopy

! Rigid/flexible! Oral/nasal! Washing! Brushing! Biopsy! Bronchoalveolar lavage! Transbronchial biopsy

! Video-Assisted Thoracoscopic Surgery (VATS)! Thoracotomy! Mediastinoscopy and Mediastinotomy

SPUTUM COLLECTION! Spontaneous expectoration; sputum induction! Adequate specimen: PMNs > 25/LPF; SECs < 10/LPF ! Gram’s staining and culture

! Mycobacteria or fungi

! Viruses

! Pneumocystis carinii

! Cytologic staining

! Polymerase chain reaction amplification

! DNA probes

ENDOBRONCHIAL PATHOLOGY ON BRONCHOSCOPY

! Tumors

! Granulomas! Sites of bleeding! Bronchitis! Foreign bodies! Treatment

! Laser therapy! Cryotherapy! Electrocautery! Stent placement

! Therapeutic uses of bronchoscopy ! Remove retained secretions/mucus plugs! Remove foreign bodies!

Remove abnormal endobronchial tissue! Perform difficult intubation

BLOOD GASES! Assessment of oxygenation capacity

! Assessment of oxygen pressure to guide therapy

! Assessment of respiratory adequacy

! Assessment of acid-base balance


7/13


Arterial Sampling Sites

! The illustration to the left showsthe location of the most commonlyused arterial sampling sites. Theseinclude the radial artery , brachialartery, and femoral artery . Of thesethree articles, the radial artery (lying in the wrist area on thethumb side) is the preferredsampling site owing to 3 primaryfactors: 1) it is easy to access, 2) itis a superficial artery (it is easier topalpate, stabilize, and puncture asuperficial artery rather than adeeper on) and 3) it has collateral blood flow.

! If damage to the radial artery occurs or if it becomes obstructed,the ulnar artery will supply blood to the tissues normally suppliedby the radial artery

NORMAL ARTERIAL BLOOD GAS VALUES! pH : 7.35 – 7.45! pO2: 80 – 100 mmHg! pCO2: 35 – 45 mmHg

! HCO3: 22 – 26 meq/L! SaO2: 97 – 100% (SAT)

CONTRAINDICATIONS FOR ARTERIAL PUNCTURE! Anticoagulant therapy! History of a clotting disorder (haemophilia)! History of arterial spasms following previous punctures! Severe peripheral vascular disease! Abnormal or infectious skin processes at or near the puncture

sites! Arterial grafts

PULSE OXIMETRY! Alternative method to assess oxygenation! Calculates oxygen saturation (not Pa O2 )! An arterial P O2 of 60 mmHg corresponds to an Sa O2 = 90%

SPIROMETRY! Measures rate at which lung volume is changing as a function of

time during breathing maneuvers! Simply put: measures lung volume and airflow from fully inflated

lungs! INDICATIONS

! To evaluate symptoms, signs or abnormal laboratory tests! To measure the effect of disease on pulmonary function! To screen persons at risk of having lung disease!

To assess preoperative risk! To assess prognosis! To assess health status before enrollment in strenuous

physical activity programs! NEED

! Essential in separating obstructive from restrictive lungdiseases

! Necessary to judge response to therapy! Necessary in plotting the course and prognosis of many

lung diseases

! Surrogate marker for risks of other common life-threatening illnesses, e.g. lung cancer

! Predictive of mortality

Spirometry and the Lung Volumes and Subdivisions

! Helium dilution method! Helium is diluted by gas present in lungs! Very little helium is absorbed into the pulmonary

circulation! May underestimate the actual volume

! Body plethysmography! Patients sits in sealed “body box”! Closed mouthpiece! Measures pressure changes

! Spirometry and the Lung Volumes and Subdivisions! Graphical Representations of Spirometry

! Measures!

Measurement of Volume! FVC! FEV1! FEV1/FVC

! Measurement of Air Flow! PEFR/ Peak Flow/MEF! FEF 25-75 , FEF 50 , FEF 75 ! Inspiratory counterparts! MVV


8/13


Parameters are expressed as actual values and their % predicted

AbN spirometry antedates onset of dyspnea by at least 10 years.Once with SOB. AO is already significant: Early Detection Needed

DISTURBANCES IN RESPIRATORY FUNCTION! Ventilatory function! Pulmonary function! Gas exchange

Patients of Abnormal Ventilatory Function! Obstructive

" Decreased expiratory flow rates" Decreased FEV 1/FVC ratio" Normal or increased TLC" RV is elevated

! Restrictive" Decreased TLC" Parenchyma vs extraparencymal

Obstructive! Asthma! Chronic obstructive lung disease (chronic bronchitis,

emphysema)! Bronchiectasis! Cystic fibrosis! Bronchiolitis

Restrictive/Parenchymal! Sarcoidosis! Idiopathic pulmonary fibraosis! Pneumoconiosis! Drug-or radiation-induced interstitial lung disease

Restrictive/Extraparencymal! Neuromuscular

" Diaphragmatic weakness/paralysis" Myasthenia gravis" Guillain-Barré syndrome" Muscular dystrophies" Cervical spine injury

! Chest wall" Kyphoscoliosis"

Obesity" Ankylosing spondylitis

Disturbance in Gas Exchange! Diffusion of Oxygen and Carbon Dioxide! Ventilation & Perfusion Matching

Measurement of Gas Exchange! Arterial blood gases

" Alveolar-arterial gradient: A-a gardient" [ (713 x FiO2) – pCO2/0.8)] – paO2

! Less than 15 mm Hg! Pulse oximetry! Diffusing Capacity (DLCO)

SMOKING CESSATIONHEALTH HAZARDS OF SMOKING

WHAT IS THE MAGNITUDE OF THE PROBLEM?! Globally....

" There are 1.1 billion smokers worldwide - about 1/3 ofthe global population aged 15 years and older.

! Locally...." 43% of adult males and 8% of females smoke" 63% of male physicians and 37% of female physicians

smoke"

38% of the respondents said they smoke in front of theirpatients" Only 59% advised patients on the ill effects of smoking

WHAT IS IN A CIGARETTE?! Tobacco smoke contains more than 7000 toxic chemicals.! These chemicals can cause disease, whether tobacco is

chewed or inhaled! Benzene (petrol additive)

A colourless cyclic hydrocarbon obtained from coal andpetroleum, used as a solvent in fuel and in chemicalmanufacture - and contained in cigarette smoke. It is a knowncarcinogen and is associated with leukaemia.

! Formaldehyde (embalming fluid) A colourless liquid, highly poisonous , used to preserve dead

bodies - also found in cigarette smoke. Known to cause cancer respiratory, skin and gastrointestinal problems.

! Ammonia (toilet cleaner)Used as a flavouring, frees nicotine from tobacco turning it into agas, found in dry cleaning fluids .

! Acetone (nail polish remover)Fragrant volatile liquid ketone, used as a solvent , for example,nail polish remover - found in cigarette smoke.

! TarParticulate matter drawn into lungs when you inhale on alighted cigarette. Once inhaled, smoke condenses and about 7per cent of the tar in the smoke is deposited in the smoker'slungs.


9/13


! Nicotine (insecticide/addictive drug)One of the most addictive substances known to man, apowerful and fast-acting medical and non-medical poison . Thisis the chemical which causes addiction.

! Carbon Monoxide (CO) (car exhaust fumes) An odourless, tasteless and poisonous gas , rapidly fatal inlarge amounts - it's the same gas that comes out of carexhausts and is the main gas in cigarette smoke, formed whenthe cigarette is lit. Others you may recognize are :

! Arsenic (rat poison), Hydrogen Cyanide (gas chamber poison)

WHAT IS THE HARMFUL EFFECTS OF SMOKING?! Tobacco has been shown to cause about 40 life-threatening

diseases.! Smoking kills 10 Filipinos every hour

TABACCO ADVERTISING! Makes smoking socially acceptable! Influences smokers to smoke more! Influences non-smokers to start smoking! Discourages smokers from giving up

SMOKING IS ADDICTIVE! Tobacco is a drug. It is addictive, which means it is difficult to

stop using it, even when one wants to stop . ! Once you become physically addicted to the nicotine in

tobacco, you only feel comfortable when it is in your body.! Nicotine acts on certain receptors in the brain, releasing

hormones and neurotransmitters, including dopamine,norepinephrine and serotonin, vasopressin, and beta-endorphine.

! The smoker feels pleasure, reduced tension, appetitesuppression, and enhanced performance.

! The smoker’s brain gets accustomed to a certain level ofnicotine and tolerance develops. Eventually, the brainbecomes dependent on nicotine to produce even normal levelsof dopamine.

! Higher levels of nicotine become necessary to produce thesame effects that lower doses used to produce, causing thesmoker to smoke even more.

! Overnight, nicotine dissipates in the body, the smoker’s cravingreturns, and the cycle starts over.

! While people begin using tobacco and other substances to feel“high,” they end up using them so they won’t feel “low.”

! Highly controlled or compulsive pattern of drug use! Smokers are driven by the body’s need to smoke! Mood altering effects of tobacco! Smokers report that it in increases their feeling of well-being

and keeps them relaxed! Drugs function as a reinforcer! Once you’ve smoked one cigarette you’ll want to smoke

another! Withdrawal syndrome! When people stop smoking, a consistent pattern of withdrawal

follows. The following are typical signs and symptoms that canbe observed within 24 hours of not smoking:

" Sleep disturbances" Craving" Increased appetite" Decreased heart rate" Restlessness" Anxiety

SMOKING IS A MEDICAL ILLNESS! Nicotine dependence! Nicotine addiction! Stronger addiction than to narcotics! Must be treated as a chronic illness

TABACCO RELATED DISEASES

PRACTICAL TIPS and FEASIBLE OPTIONS

LIMITATIONS! Reliant on predominantly foreign data! Discussion of details of counseling and behavior modification

entails a significantly greater amount of time than what isallotted

WHY BOTHER?! Smoking is the single most important cause of preventable

mortality and morbidity! Smoking cessation is beneficial

! Smoking cessation is not impossible! Smoking cessation programs can be implemented in all levels

of health care! Smoking cessation program is mandatory


10/13


SMOKING IS THE SINGLE MOST IMPORTANT CAUSE OFPREVENTABLE MORTALITY and MORBIDITY

! Attributable to tobacco smoking" 70–90% of lung cancer" 56–80% of chronic respiratory diseases" 22% of cardiovascular diseases

! A reduction in the prevalence of tobacco smoking would be thesingle most effective preventive health measure

! 80% of the world’s 1.1 billion smokers live in low income

countries! By 2030, seven out of every 10 deaths from smoking will occur

in low income countries! P46 B in health care cost & productivity losses

SMOKING CESSATION IS BENEFICIAL! A reduction of 15% is seen in the RR of all-cause mortality in

heavy smokers subjected to intensive clinical cessationinterventions.

! The risk of lung cancer is 30% to 50% lower than that ofcontinuing smokers after 10 years of abstinence.

SMOKING CESSATION IS NOT IMPOSSIBLE

! Simple advice from a physician to stop smoking improvessmoking cessation rates (odds ratio [OR], 1.74; 95% confidenceinterval [CI], 1.48–2.05).

! High intensity counselling of greater than 10 minutes canincrease six month quitting rates to 22 percent when added toany quitting method, cold turkey or NRT

! Drug treatments result in better smoking cessation rates thanplacebo.

! Treatments, alone or in combination, improve cessation ratesover placebo after 6 months (OR, 1.77; 95% CI, 1.66–1.88).

! Typical Long-term quit rates

SMOKING CESSATION PROGRAMS CAN BE IMPLEMENTED IN ALLLEVELS OF HEALTH CARE

! Measures to reduce tobacco supply are difficult to implement! Interventions to reduce the demand for tobacco

" Higher tobacco taxes" Antismoking education

" Bans on tobacco advertising and promotion" Policies designed to prevent smoking in public spaces

or workplaces" Pharmacological therapies to help smokers to quit

SMOKING CESSATION PROGRAMS ARE MANDATORY! Republic Act No. 9211- An Act regulating the packaging, use,

sale, distribution and advertisement of tobacco products and forother purposes

"

Sec.33.c. National Smoking Cessation Program- ANational Smoking Cessation Program shall beundertaken with the approval of the IAC-Tobacco.

" Sec.33.h. Withdrawal Clinics- The DOH shall establishsmoking withdrawal clinics to provide counsellingregarding the hazardous health effects oftobacco/cigarette smoking and to rehabilitate smokersfrom the hazardous effects of such products

IS IT FEASIBLE? ! To integrate intensive smoking cessation interventions in the

usual clinical setting?! Limited time! Limited resources! Limited motivation! Yes!

" Different levels of intervention" Minimal time and resources needed" Even the seemingly brief and trivial interventions are

still beneficial" Set the stage for more intensive intervention

! Motivation of both the patient AND the health care provider isimportant

THEORETICAL FRAMEWORK! Models for chronic illness and behaviour modification! Measures that could increase compliance

ADHERE TO LONG TERM TREATMENT! “Increasing the effectiveness of adherence interventions may

have a far greater impact on the health of the population thanany improvement in the specific medical treatments.”

! Stages of Change Model" Describes how people modify a problem behavior or

acquire a positive behavior" Theoretical basis for developing effective interventions

to promote health behavior change! Conceptualizes change as a phenomena occurring over time,

not a single event! Change progresses over a series of

5 stages:" Pre-contemplation" Contemplation" Preparation" Action" Maintenance


11/13


Pre-contemplation! People are not intending to take action in the near future (6

months)! May be uninformed/under-informed or tried to change but failed! Is not seriously considering stopping smoking.

Contemplation! People intend to change in within the next 6 months! Are more aware of pros of changing but also acutely aware of

cons! Balance of pros and cons can cause ambivalence and state of

chronic contemplation or behavioral procrastination! Is seriously considering stopping within 3 to 6 months.

Preparation! People intend to take action in the immediate future (1 month)! Have a plan of action, have taken preparatory steps! Is seriously considering stopping within the next week to month,

and has already made changes such as cutting back.! May be recruited for programs

Action! People have made overt modifications in lifestyle (past 6

months)! Not all behavior is action; must be proven to have benefits! Has recently stopped smoking (within last 6 months).! Vigilance against relapse is critical

Maintenance! People are working to prevent relapse! Less tempted to relapse, more confidence that change can

continue! Has quit for at least 6 months, but may still

be vulnerable to a relapse up to 1 year.! Advocacy

! Interventions are most effective if they are attuned to specificstages of change

! Entails a thorough understanding of which stage a particularpatient is in

! Interventions can be tailored according a patients needs! Intervention will be more efficient (in the face of limited time and

resources)

GENERAL GUIDELINES! Clinicians should document the tobacco-use status of

every patient.! Clinicians should assess the readiness to quit of patients

who use tobacco and assist those who wish to quit insetting a quit date.

! Patients using tobacco should be provided with at least one ofthe effective brief cessation interventions that are available.

! In general, more intense interventions are more effective thanless intense interventions in producing long-term tobaccoabstinence, reflecting the dose-response relationship betweenthe intervention and its outcome.

! One or more of the three treatment elements identified as beingparticularly effective should be included in smoking-cessationtreatment:

" Social support from clinicians in the form ofencouragement, assistance

" Skills training/problem solving (cessation/abstinencetechniques)

" Pharmacotherapy, such as nicotine-replacement,e.g., patches, gum

SMOKING CESSATION AT THE INDIVIDUAL LEVEL! More feasible and may be the only option in most settings!

Maximize the potential of providing intervention at each clinicvisit! Employ measures to enhance adherence to treatment! Prompt referral to appropriate specialized clinics or groups

IMPROVING ADHERENCE (WHO)! Patient-tailored interventions are required

" “There is no single intervention strategy, or package ofstrategies that has been shown to be effective acrossall patients, conditions and settings. Consequently,interventions that target adherence must be tailored tothe particular illness-related demands experienced bythe patient. To accomplish this, health systems andproviders need to develop means of accuratelyassessing not only adherence, but also those factorsthat influence it.”

INDIVIDUAL INTERVENTION! ASK, ADVISE, ASSESS, ASSIST, and ARRANGE model! Model based on outcomes from six major

clinical trials of physician-delivered smokingintervention conducted in the late 1980s

Ask, Advise, Assess, Assist, Arrange: Key Elements! Ask

" Screen for smoking status at every visit oradmission.

! Advise" Minimal Advice: “As your physician, I must advise

you that smoking is bad for your health, and itwould be important for you to stop.”

" Augmented Advice: “Because of your (__________)condition, it is particularly important for you to stop. Ifyou stop now, (briefly educate patient about basichealth benefits from quitting).”

! Assess" Minimal Assessment: Ask every tobacco user if

he/she is willing to make a quit attempt at this time." Augmented Assessment: Assess characteristics of

smoking history and patterns.! Amount smoked.!

Quit history.! Stage of Change! Nicotine Addiction: Fagerstrom Test for

nicotine dependence! Assist/Counsel

" Minimal Assistance: Provide self-help materials;assess interest in quitting; assess interest in andappropriateness of pharmacological aids.

" Augmented Assistance: Provide brief 5 to 7 minutepatient-centered counselling.

! Arrange Follow-up Support


12/13


" Minimal Follow-up Support: Arrange for singlefollow-up contact by visit or by telephone in about 2weeks; provide referral to a smoking counselor orgroup.

" Extended Follow-up Support: Establish “quit smoking”contract with quit date. Arrange three or more follow-upcontacts by visit or by telephone.

FOR THE BUST CLINICIAN " ! Pre-contemplation

" Educate patient" Correct misconceptions" Encourage patient to consider quitting

! Contemplation" Emphasize benefits, reassure on side-effects" Motivate the patient" “Tip the balance”, pros outweigh cons" Convince patient to quit, strengthen the intention

! Preparation" Assist the patient" Help patient gain confidence in overcoming temptations" Refer to specialized programs

! Action

" Support the patient" Address withdrawal symptoms" Give medications" Commend the patient on his efforts" WOF relapse

! Maintenance" Commend the patient on the accomplishment" Involve the patient on the advocacy" Work at sustaining abstinence

FOR THE BUSY CLINICIAN " AND THE PATIENT WHO IS READYTO QUIT

! S et a quit date. Not even a single puff afterthe quit date. Sign contract.

! T ell friends, family, co-workers of plans to quit.! A nticipate challenges to planned quit

attempt. Find new habits.! R emove tobacco products from your

environment. Reward yourself.

FOR THE BUSY CLINICIAN " AND THEPATIENT WHO WILL DEALWITH TEMPTATIONS

! Delay" Urge to smoke after a meal, etc., urges usually pass

after a few minutes! Escape

" Smoking settings: bars, parties, etc.! Avoid

" Smoking settings, cues: stress, coffee, alcohol, etc.! Distract

" Relaxation techniques for stress; Exercise; do otherthings when bored

PHARMACOLOGIC INTERVENTIONS! Drugs address the physiologic component of nicotine addiction

by decreasing withdrawal symptoms and urges! Timing of their use coincides with the period where the severity

of withdrawal symptoms and relapse is greatest! Not expected to work in unmotivated or unwilling patients! The impact in a study of nicotine patch and nicotine nasal spray

used with minimal behavioural intervention in a non-specializedsetting was smaller in magnitude.

! The choice of therapy should be individualized based on anumber of factors

" Past experience" Patient and/or physician preference" Potential agent side effects

Nicotine Gum! Each piece typically contains 2 or 4 mg of nicotine! Appropriate dosage depending on the smoking habits of the

user! May also address oral fixation! Instructions for use:

" Gum is first chewed until it is soft and a tingly sensationand/or peppery taste is noticed

" Pressed between the cheek and gums (parking)" When the tingly sensation stops, the gum is chewed

again, and then pinched between the cheek and gumsin a different place in the mouth

" Continued until the gum is depleted of nicotine (about30 minutes)

! The total recommended dose is 10 to 12 pieces of gum daily for1–3 months.

! After 3 months, a gradual withdrawal from gum use isrecommended, with completion of treatment within 6 months

! Hiccups, perceived constriction of the throat muscles, gumdisease

Varenicline! Blocks nicotine from activating alpha4beta2 nicotinic receptors,

which in turn prevents dopamine stimulation in the brain.! Should a patient decide to smoke while using this drug, there is

no nicotine "feel good" rush, and the smoking experience is flat;dull.

! Six clinical trials involving 3659 chronic cigarette smokers wereused as a basis for the effectiveness of Varenicline as a therapyfor smoking cessation.

! Five of the trials were randomized, placebo-controlled studies,and showed that Varenicline was more effective than a placeboto help people quit smoking.

! Sold as 0.5 mg and 1 mg tablets! Titrating the dose from 0.5 mg every day for 3 days to 0.5 mg

twice daily for 4 days to 1 mg twice daily is recommended! Not recommended for use by children, those under 18 years

old, pregnant or breastfeeding women! Nausea, headache, difficulty sleeping, and abnormal dreams,

change in taste, vomiting, abdominal pain, flatulence, andconstipation

! Post-marketing reports" suicidal ideation" occasional suicidal behaviour" erratic behaviour


13/13


! Unknown whether the psychiatric symptoms are related to thedrug or to nicotine withdrawal symptoms

INTERVENTIONS FOR IMPROVING ADHERENCE! Socioeconomic-related factors

" (–) High treatment cost" (+) Higher education levels, older age" cial assistance

! Health care team/health system-related factors " (–) Unavailability for follow up or lost to follow up" (+) Access to free NRT; more frequent contact with

physicians and pharmacists" Pharmacist mobilization ; access to free NRT; frequent

follow-up interviews! Condition-related factors

" (–) Daily cigarette consumption; expired CO, plasmanicotine and cotinine levels; Fagerstrom ToleranceQuestionnaire (FTQ) scores ; greater tobaccodependence ; psychiatric comorbidities; depression ;failure to stop or reduce smoking during treatment

" Education on use of medications; supportive psychiatricconsultation

! Therapy-related factors " (+) Attendance at behavioural intervention sessions" NRT; antidepressant therapy; education on use of

medications; adherence education; assistance withweight reduction ; continuous monitoring andreassessment of treatment; monitoring adherence

! Patient-related factors " (–) Weight gain" (+) Motivation ; good relationship between patient and

physician" Adjunctive psychosocial treatment; behavioural

intervention ; assistance with weight reduction; good patient–physician relationship

SUMMARY

! There is an acute need to establish a form of smoking cessationprogram in all health care settings

! We should apply the general principles of approach to chronicillness and adherence to long term treatment in themanagement of patients who wish to stop smoking

! Strong evidence support the benefit of various modalitiesemployed in management of nicotine dependence

! Integration of aspects of smoking cessation interventions inusual clinical practice is possible

! Brief clinic interventions, referral to specialized programs andpharmocotherapy should be offered to patients who aresmokers

~END~

“That in all things, God may be glorified”

1. approach to patient with respiratory disease and smoking cessation

Documents