Treatment of Acute Asthma

Treatment of Acute Asthma i.e. asthma attacks
Also called rescue medications, you use quick-relief medications as needed for rapid, short-term relief of symptoms during an asthma attack, or before exercise, if recommended by a physician. Only use these medications as often as your doctor tells you to. If you need to use these medications too often, you probably need to adjust your long-term control medication. Keep a record of how many puffs you use each day. Types of quick-relief medications include:

• Short-acting beta-2 agonists, such as albuterol. These medications, called bronchodilators, may be administered via inhalation, pill form, liquid or injection methods. They act to ease breathing by temporarily relaxing the smooth muscle in the airways which contain many B2-receptors. They act within minutes, and effects last four to six hours. These are the first line of treatment for miled to moderate acute asthma. COmmonly used is a salbutamol-based B2-agonist, administrated by inhalation and known as "ventolin" **when beta-2 agonists are required on a regular basis i.e. more than once a day, then regular administration of an inhaled steroid may be included in the treatment plan**
  
• Ipratropium (Atrovent). Your doctor might prescribe this inhaled anticholinergic for the immediate relief of your symptoms. Like other bronchodilators, ipratropium relaxes the airways, making it easier to breathe. Ipratropium is mostly used for emphysema and chronic bronchitis.
  
• Oral and intravenous corticosteroids to treat acute asthma attacks or very severe asthma. Examples include prednisone and methylprednisolone. These medications relieve airway inflammation. They may cause serious side effects when used long term, so they're only used to treat severe asthma symptoms.
  
• Also, incases of acute severe asthma, oxygen may be administered with the nebulized or intravenous B2-agonists.
  

PCL 5 – ANNA’s OUT OF BREATH

- Link between Asthma, Hayfever and Eczema

o ‘Atopic’ individuals – if you have one your likelihood of having another increases substantially. Similarly, if a family member has an atopic condition, the individual has an increased likelihood of having the condition.
o Atopic disorders are traditionally characterised by a wealing skin reaction
o We know that asthma is an inflammatory condition, the same is true for Hayfever and Eczema. There are several key cells involved in this inflammatory process –
§ Mast cells – increased in the epithelium and release histamine, prostaglandin and leukotrienes à it is this which causes the immediate inflammatory reaction
§ Eosonophils
§ Macrophages and lymphocytes
o Process is not completely known but is associated with –
§ Increased Th2 CD4 lymphocytes in the skin (drive inflammatory process)
§ Increased IgE levels
o Increased IgE levels
§ can be the result of either genetic or environmental factors
§ link between IgE levels and the prevalence of asthma and responsiveness of airways
o Many genes play a key role in asthma development
§ IL-3, IL-4, IL-5, IL-9, IL-13 and GM-CSF affect Mast Cell and Eosinophil levels
o Current suggestion
§ Growing up in a ‘clean’ environment may predispose towards an IgE response to allergens and vice versa
o Intrinsic asthma is IgE related – triggers include allergens from animals, flour and grain, latex
o Atopic individuals develop occupational asthma more rapidly when exposed to agents causing the development of specific IgE antibody
o In asthma the epithelium of the conducting airways is damaged and stressed with loss of ciliated columnar cells onto the lumen. As the epithelium is a major source of mediators, cytokines and growth factors that serve to enhance inflammation à damage to the epithelium makes it more vulnerable to allergens (such as those which cause hayfever)

risk factors for asthma

Risk factors for asthma:

1. Constitutional factors: predisposes the person to development of asthma or particular outcomes of asthma.

a. Family history: Although asthma is not a hereditary disease, but having parents with asthma history predisposes the offspring with high probability to get the disease due to genetic inheritance.

b. Genetic mutations: Studies showed that a specific gene may have been associated with asthma development. The gene, ADAM33 is located on chromosome 20 and is expressed in lung and muscle cells. Mutations on this gene may predispose the person to having asthma. The gene causes airways to over-respond and constrict airway passages.

c. Gender: Males are more susceptible to get asthma after birth compared to females. The reason may be due to the fact that a man’s airway size is smaller compared to a woman. However, the percentages drops as males grow up, and at around the age of 20, the rates are similar for both genders. After the age of 40, females tend to have higher chances to get the disease compared to males.

d. Allergic (atopy) predisposition: Atopy is allergic hypersensitivity to different parts of the body that do not come in contact with allergens, but triggers allergic reactions (anaphylaxis). Studies showed that many children with eczema during when they are young have higher chances to develop asthma.

2. Environmental exposures or other factors: associated with increased risk of acquiring asthma or having certain outcomes of the disease.

a. Exercise: exercise can induce asthma for people who are more sensitive to changes in temperature and humidity of the air. When resting, the person breathes through nose that serves to warm and humidify the air inhaled. However, when exercising, the person tends to breathe through mouth and the air being inhaled is colder and drier. The difference between the humidity of air in lungs and the inhaled ones triggers the allergic reaction. Airway begins to swell and secrete large amount of mucous. This obstructs the airway, making it difficult to breathe and thus, leads to asthma (COPD).

b. Viral infections: viral infections activate eosinophils that readily gathered along the nerves in the lungs. This will then cause eosinophils to release a protein called major basic protein (MBP) which has been discovered to block the action of M2 receptors and keeps the receptors from turning off Ach release. High Ach leads to increased constriction of the airways.

c. Irritants (smoking, pollutants): smoking damages cilia in the airways, preventing the cilia from performing their normal function, clear mucous and dust out of the respiratory system. Smoking also cause lungs to secrete more mucous than normal, resulting in marked increase in mucous accumulation in the airways, obstructing the air pathway.

d. Allergies: hypersensitivity due to exposure to a particular allergen resulting in marked increase in reactivity to that antigen on subsequent exposure. Among the common allergens are: dust mites, fungi, animal proteins, fur.

e. Pregnancy: Mothers who smoke during pregnancy can lead to having infants with lower pulmonary function compared to those who are not.

Effects of Smoking

Refer to http://medpcl01.blogspot.com/2009/03/effects-of-smoking.html

Asthma correlation: Cigarette smoke is an irritant that causes airway hyper-responsiveness (i.e. intrinsic asthma). Early childhood exposure to maternal smoking also increases IgE response to allergens (i.e. extrinsic asthma).

Reference: Kumar and Clark (Clinical Medicine)

Astma PLan

ACTION ASTHMA PLAN

Why make an asthma plan?
reduces absences from work or school
reduces hospital admissions
reduces emergency visits to general practice
reduces reliever medication use
improves lung function.

AIMS?
The aim of an asthma action plan is to help the person with asthma and/or their carer take early action to prevent or reduce the severity of an asthma attack.
The asthma action plan may be based on symptoms and/or peak expiratory flow (PEF) measurements and is individualised according to the pattern of the person’s asthma.
In children, symptom-based plans are preferred.
Once completed, the asthma action plan is given to the person with asthma and/or their carer to keep.

FEATURES OF A PLAN
be in a written format
be individually prescribed, rather than a general example
contain information that allows the patient and/or their carer to recognise exacerbations (flare-ups)
contain information on what action to take in response to those exacerbations.
Maintenance/preventer therapy: doses and frequencies of regular medications
Treating exacerbations: how to adjust treatment in response to particular signs and symptoms
Managing increased severity: when to start oral corticosteroids and seek medical advice
Danger signs: when and how to seek urgent medical help

PEF
This is a measure of maximum expiratory flow occurring just after the start of a forced expiration from the point of maximum inspiration (total lung capacity).
Within the plan should also include changes over time regarding Peak expiratory flow measurements, particularly for those with more severe asthma. PEF is a good measurement of whether the asthma may be getting worse or better, thus measures can be put into place to handle such changes early rather than later.

Ambu

PCL 5 – ANNA’s OUT OF BREATH

- Link between Asthma, Hayfever and Eczema

o ‘Atopic’ individuals – if you have one your likelihood of having another increases substantially. Similarly, if a family member has an atopic condition, the individual has an increased likelihood of having the condition.
o Atopic disorders are traditionally characterised by a wealing skin reaction
o We know that asthma is an inflammatory condition, the same is true for Hayfever and Eczema. There are several key cells involved in this inflammatory process –
§ Mast cells – increased in the epithelium and release histamine, prostaglandin and leukotrienes à it is this which causes the immediate inflammatory reaction
§ Eosonophils
§ Macrophages and lymphocytes
o Process is not completely known but is associated with –
§ Increased Th2 CD4 lymphocytes in the skin (drive inflammatory process)
§ Increased IgE levels
o Increased IgE levels
§ can be the result of either genetic or environmental factors
§ link between IgE levels and the prevalence of asthma and responsiveness of airways
o Many genes play a key role in asthma development
§ IL-3, IL-4, IL-5, IL-9, IL-13 and GM-CSF affect Mast Cell and Eosinophil levels
o Current suggestion
§ Growing up in a ‘clean’ environment may predispose towards an IgE response to allergens and vice versa
o Intrinsic asthma is IgE related – triggers include allergens from animals, flour and grain, latex
o Atopic individuals develop occupational asthma more rapidly when exposed to agents causing the development of specific IgE antibody
o In asthma the epithelium of the conducting airways is damaged and stressed with loss of ciliated columnar cells onto the lumen. As the epithelium is a major source of mediators, cytokines and growth factors that serve to enhance inflammation à damage to the epithelium makes it more vulnerable to allergens (such as those which cause hayfever)

Diagnosis of Asthma

Asthma symptoms include:

intermittent dyspnoea
Chest tightness or pain
Trouble sleeping by SOB, coughing or wheezing
Audible whistling or wheezing sound when exhaling
Bouts of coughing or wheezin worsened by a respiratory virus eg. cold/flu
acid reflux: known association with asthma

Getting worse..
An increase in the severity and frequency of above
A fall in peak flow rates as measured by a peak flow meter
An increased need to use bronchodilators — medications that open up airways by relaxing the surrounding muscles

Signs:
tachypnoea
audible wheeze
hyperinflated chest
hyperresonant percussion
diminished air entry
widespread polyphonic wheeze

Severe attack:
inability to complete statements, pulse >110bpm, respiraory rate >25.min, PEF 33-50% of predicted

Life-threatening attack:
silent chest, cyanosis, bradycardia, exhaustion, PEF <33% of predicted, confusion, feeble respiratory effort

Diagnosis

Acute:

PEF (peak expiratory flow)
sputum culture
FBC (full blood count)
U&E (Urea & electrolyte)
CRP (C-reactive protein)
blood cultures
ABG (arterial blood gas) analysis shows normal or slightly reduced PaO2 and low PaCO2 (hyperventilation)
[if PaCO2 is raised, transfer to high dependency unit for ventilation, as this shows failing respiratory effort]
CXR (to exclude infection or pneumothorax)

Chronic:

PEF monitoring
diurnal variation of >20% on >3 days a week for 2 weeks
spirometry
obstrucive defect (decrease FEV1/FVC, increase RV)
CXR:hyperinflation

skin-prick test: allergens identification

PEF
- >20% difference on >3days in a week for 2 weeks (marked morning dipping common)
- >20% improvement following treatment
- >20% decrease following exposure to trigger

Based on clinical history & exam: eczema, allergic conditions, family history

IN CHILDREN:
Unable to use airway f(x) test. Medical history and improvement shown with an inhaled bronchodilator medication.

NEW: Chemical marker of Exhaled NO. Higher levels of NO = higher severity of asthma (expensive though..)

DDx

pulmonary oedema ('cardiac asthma')
COPD (often coexist)
large airway obstruction (foreign body/tumour)
SVC obstruction (wheeze/dyspnoea not episodic)
pneumothorax
PE
bronchiectasis
obliterative bronchiolitis (in elderly)

Source: mayoclinic, oxford handbook of clinical medicine

Pathophysiology of asthma

'Intrinsic' asthma is triggered by e.g. exercise, cigarette etc.

'Extrinsic' asthma is the allergic type of asthma which involves IgE antibodies and mast cell degranulation.

The pathogenesis of asthma involves both genetic and environmental factors, and is triggered by exposure of allergens. When come into contact with antigens (allergens), dendritic cells react and present the antigens to lymphocytes. Helper T cells are then activated, releasing cytokines (IL-2, IL-4), which results in the activation of B cells to secret IgE antibodies. In extrinsic asthma, patients have a tendency to form abnormally large amounts of IgE antibodies. Migration and activation of mast cells and eosinophils are also stimulated by lymphocytes activation and cytokines generation.

The IgE antibodies attach to mast cells present in the lung interstitium. As the antigens react with the mast cell attached-antibodies, the mast cell is activated and sends signal for 1) degranulation; 2) phospholipase activation; 3) cytokine gene activation.

1) Substances released in mast cell degranulation are primary mediators of the allergic response. One of which is histamine.
2) Phospholipase activation leads to the release of leukotrienes and prostaglandin.
3) Cytokine IL-5, secreted upon cytokine gene activation, is responsible in activation of eosinophils.

Mast cell activation or, the mediators released, thus results in spasms of smooth bronchial muscles, increased mucus secretions into bronchiolar lumens, and localized oedema in the walls of the small bronchioles. The increased airway resistance creates obstruction in respiration.

The obstruction is, however, more severe during expiration. Despite the occlusion in asthmatic lungs, during inspiration, the positive pressure of the lungs in compare to the atmospheric pressure keeps the airway open. Thus the effect of obstruction is less. In expiration, the partially obstructed airway is further compressed by the greater atmospheric pressure. This gives a more reduced bronchiolar diameter and patients experience great difficulty expiring.

The activated eosinophils release mediators such as eosinophil cationic proteins that are toxic to epithelial cells. Epithelial cell loss in the chronic phase of asthma makes it more vulnerable to irritant stimuli -- resulting in bronchial hypersensitivity.

The theory behind airway remodeling is unknown. Nevertheless, various growth factors cause hypertrophy and hyperplasia of the smooth muscles in the chronic phase. Increased deposition of collagens due to fibroblasts activation creates an environment for ongoing inflammation, and eventually structural and functional alterations.


Reference: Kumar & Clark, Rang & Dale, Guyton

• Main causes of pneumonia – typical, atypical - Rushmi
• Lung function test - Ari
• Pathophysiology of asthma – dilys
• Asthma treatment - Kylie
• What is asthma
• Asthma link with other diseases – atopy – Georgia
o Eczema, hay fever
o Risk factors
• CAM treatment of asthma - Sarah
• Asthma prevention – Jackie
• Puffers - steph
o Spacers
• Asthma plan - Ambu
• Effects of smoking - Lionel
• How to help someone quit - Nathan
o Patches vs. cold turkey
• Lung function, spirometry
• Diagnosis of asthma – Jemima
• Risk factors - Hasif

CAM for Asthma - Sarah

Asthma and Selenium

Selenium deficiency may be important in chronic asthma. Observational studies have demonstrated that patients with chronic asthma may have lower levels of selenium than their control. Nevertheless, selenium supplementation has not been recommended with drug therapy for asthma

Meta-analysis


EBM Reviews - Cochrane Database of Systematic Reviews Allam, Mohamed Farouk. Lucena, Rosario A. Selenium supplementation for asthma. [Systematic Review] Cochrane Database of Systematic Reviews. 1, 2009.
Selection criteria
Randomised trials comparing patients with chronic asthma receiving selenium supplementation in conjunction with asthma medication, with patients taking asthma medication only.

Authors' conclusions
There is some indication that selenium supplementation may be a useful adjunct to medication for patients with chronic asthma. This conclusion is limited because of insufficient studies and lack of improvement in the clinical parameters of lung function.
RCT’s
EBM Reviews - Cochrane Central Register of Controlled Trials Burgess CD, Bremner P, Thomson CD, Crane J, Siebers RW, Beasley R Nebulized beta 2-adrenoceptor agonists do not affect plasma selenium or glutathione peroxidase activity in patients with asthma. [Clinical Trial. Journal Article. Randomized Controlled Trial. Research Support, Non-U.S. Gov't] International journal of clinical pharmacology and therapeutics. 32(6):290-2, 1994 Jun.
Found that selenium levels are not effected by beta 2-agonists, fenoterol and salbutamol (asthma drugs)

EBM Reviews - Cochrane Central Register of Controlled Trials Shaheen SO, Newson RB, Rayman MP, Wong AP, Tumilty MK, Phillips JM, Potts JF, Kelly FJ, White PT, Burney PG Randomised, double blind, placebo-controlled trial of selenium supplementation in adult asthma. [Journal Article. Multicenter Study. Randomized Controlled Trial. Research Support, Non-U.S. Gov't] Thorax. 62(6):483-90, 2007 Jun.

197 participants, divided into a selenium supplement group or placebo. The primary outcome was asthma-related quality of life (QoL) score. Secondary outcomes included lung function, asthma symptom scores, peak flow and bronchodilator usage. There was an increase in selenium in the supplement group and none in the placebo. The quality of life score improved in the active treatment group, however the difference in change in score between the two groups was not significant (p=0.47), no improvements were seen in the secondary outcomes compared with placebo. CONCLUSIONS: Selenium supplementation had no clinical benefit in adults with asthma, the majority of whom were taking inhaled steroids.

EBM Reviews - Cochrane Central Register of Controlled Trials Hasselmark L, Malmgren R, Zetterstrom O, Unge G Selenium supplementation in intrinsic asthma. [Clinical Trial. Journal Article. Randomized Controlled Trial. Research Support, Non-U.S. Gov't] Allergy. 48(1):30-6, 1993 Jan.

This is the original study, with 24 patients suffering from intrinsic asthma. Two randomised groups, receiving selenium, other placebo, there was found to be a significant clinical improvement in the Se-supplemented group. However, the change could not be validated by significant changes in separate clinical tests.

Asthma and Yoga
Maybe some benefit, but not enough evidence to show conclusively. Maybe some benefit in paediatrics –

Therapeutic effects of yoga for children: a systematic review of the literature. [Review] [54 refs] Galantino ML. Galbavy R. Quinn L. Pediatric Physical Therapy. 20(1):66-80, 2008.

Pneumonia

What is it?
An inflammation of the substance of the lungs, usually due to bacteria

Classification by site
Localised – one or more lobes affected
Diffuse – affect lung lobules and bronchii and bronchioles (bronchopneumonia)

Classification by aetiology

Typical pneumonia
Due to streptococcus pneumoniae – most common

Atypical pneumonia
Due to organisms such as mycoplasma pneumoniae, legionella pneumophila, Chlamydia pneumoniae, Chlamydia psittaci, coxiella burnetti
Accounts for 1/5 of the cases of pneumonia (Kumar and Clarke).
Overlaps in clinical presentation with typical pneumonia

Viral pneumonia
Influenza and adenovirus infection are the most common causes. It can often predispose parients to bacterial pneumonia (damages epithelium - facilitates bacterial infection).

Pneumonia due to opportunistic infections
Occurs in immunocompromised patients (e.g. AIDS). It is due to Pneumocytis carinii (bacterium), actinomyces isralli (bacterium), nocardia asteroids (bacterium), cytomegalovirus, aspergillus fumigates (fungus), mycobacterium avium-intracellulare (bacterium), crytptococcus (fungus) and Karposi’s sarcoma.

Rare causes
Bordetella pertussis, typhoid bacillus, paratyphoid bacillus, brucellosis, leptospirosis, measles, chicken pox, glandular fever

Aspiration pneumonia
Occurs when gastric contents enters the lungs. Due to a trachea-oesophageal fistula, periods of impaired consciousness (e.g. sleep), reflux oesophagitis with an oesophageal stricture, or in bulbar palsy (problems with cranial nerves 7-12). The pneumonia is often due to anaerobes.

Risk factors
· Cigarette smoking – strongest independent factor for invasive pneumococcal disease
· Strep. Pneumoniae - often follows a viral infection with influenza/parainfluenza
· Hospitalised patients – infected with Gram negative organisms
· Alcohol excess
· Bronchiectasis (abnormal and permanently dilated airways – impairs the mucocillary transport mechanism, and thus frequent bacterial infections occur)
· Bronchial obstruction, such as a carcinoma
· Immunosuppresion (AIDS, cytotoxic agents) – infection by Pneumocystis carinii, Mycobacteirum avium intracellulare and cytomegalovirus
· IV drug abuse – associated with staph.aureus infection
· Inhalation from oesophageal obstruction – associated with infection from anerobes

Clinical presentation (with strep. pneumoniae)
· Preceding history of viral infection
· High temperature – 39.5°C
· Pleuritic pain
· Dry cough
· Rusty-coloured sputum
· Breathing is rapid and shallow
· Affected side of chest moves less
· Pleural rub
· Signs of consolidation in the lungs

Diagnosis of severe community-acquired pneumonia
· Respiratory rate is greater than or equal to 30/min
· Diatolic BP is less than 60 mmHg
· Confusion
· High mortality, particularly in those over 65
· Co-morbidities

Investigations
· Chest x-ray
· In strep. pneumoniae:
o White blood cell count – is greater than 15 x 109/L (normal = 4-11 x 109/L)
o Erythrocyte sedimentation rate – greater than 100mm/h (normal = less than 20 mm/h) – measure of the settling of RBCs during 1 hour
· To detect certain types of pneumonia:
o Pneumococcal antigen – counter-immunoelectrophoresis of sputum, urine and serum (more sensitive than sputum or blood cultures)
o Mycoplasma antibodies (IgM and IgG)
o Legionella and Chlamydia antibodies – immunoflouresence tests
o Legionella antigen – in urine
· Blood gases – check for respiratory failure, and is also baseline for comparison if the patient deteriorates

Management
· Antibiotics
o Should be started once diagnosis is made
o Largely directed against strep. pneumoniae
o Mild community-acquired pneumonia – oral amoxicillin, oral erythromycin if sensitive to penicillin
o Staph. Aureus infection
§ intravenous flucloxacillin
§ if intolerant to penicillin and macrolides – fluroquinalone
o Severe cases
§ Broad-spectrum lactamase-stable beta-lactam (co-amoxiclav or cefuroxime)
§ Clarythromycin
o Antibiotics can be narrowed once test results received (however, 10% are mixed infections)
· General measures
o Fluids – avoid dehydration
o Sitting upright or where comfortable
o Cough should be encouraged (physiotherapy may be needed.)
§ If it is distressing or unproductive – codeine linctus
o Analgesia from pleuritic pain
· Hospital-acquired
o Commonly gram negative bacteria
§ Third-generation cephalosporin (cefuroxime)
§ Aminoglycosdies (gentamicin)
o Pseudomonas infection
§ IV xiprofloxacin or ceftazidime (cephalosporin)
o Aspiration pneumonia (multiple bacteria, often anaerobic)
§ Metronidazole (nitromidazole)
§ Co-amoxiclav or cefuroxime

PREVENTION OF ASTHMA

Prevention

Consideration should be given to factors which may trigger attacks of asthma. Cigarette smoke should be avoided. Exposure to animals that cause symptoms (often household pets) should be minimised or avoided, and your child may be better with non-allergenic bedding if they are affected by goosedown or feathers. In some selected cases, carpets may need to be removed to minimise dust and decrease exposure to the common house dust mite. In addition you could try avoid pollen! :)

These measures should be balanced with the need to minimise drastic changes to your child’s and your family’s living conditions. Change in environment of any significant degree may not be indicated in children with mild or minimal symptoms.

Some of these precipitating factors can and should be avoided. However, the mainstay of management of asthma is pharmacological – the appropriate use of medications to prevent and treat symptoms.

Apples prevent asthma

A new study tracked the diets of nearly 2,000 pregnant women and checked the lung health of 1,253 of their children at age five. Among a wide variety of foods eaten and recorded by the pregnant women, only apple consumption showed a consistent protective effect against childhood wheeze and asthma.

Children of mothers who ate more than four apples per week were 37 per cent less likely to have a history of wheezing and 53 per cent less likely to have doctor-confirmed asthma, compared to mothers who ate one or no apples per week while pregnant. The specific association found with apples, and not with the total amount of fruits eaten or with citrus, fruit juice or vegetable consumption, hints at an apple-specific effect, possibly because of its unique flavonoids, which have been shown to have beneficial effects on adult lung function. To maximize apple’s benefits why not think about adding apples to your daily juice regime.

A few Things that have been tried and failed;

1)Intermittent Inhaled Corticosteroids in Infants with Episodic Wheezing

2)Although no clinical trial has tested the use of antibiotics in the first weeks of life as a strategy for the prevention of asthma, there is sufficient evidence from a number of population-based cohort studies to suggest that various antibiotic therapies administered early in life do not reduce the risk of asthma.

references;

http://www.detoxstop.com/children/apples-prevent-asthma/

http://raisingchildren.net.au/articles/asthma_treatment.html

http://content.nejm.org.ezproxy.lib.monash.edu.au/cgi/content/short/354/19/1998

http://content.nejm.org.ezproxy.lib.monash.edu.au/cgi/content/full/357/15/1545

Smoking Hx / How to Quit

Taking a Smoking History

What to ask:

• Current number of cigarettes smoked per day
• How soon after waking is first cigarette smoked
• Other tobacco use
• Number of years smoked
• Triggers
• Quitting history
• Longest quit attempt
• Most recent quit attempt
• Withdrawal symptoms

http://makesmokinghistory.org/quitworks/docs/masshealth/IntakeAssessGuide.doc

Methods of quitting smoking:

• Cold Turkey
• Must overcome both physical/pharmacological addiction as well as psychological addiction.
• Physical addiction can be overcome after 100 hours without a cigarette.
• Gradual Reduction
• Although you are weaning yourself from addiction, you are still prolonging your exposure to the cancer-causing chemicals in tobacco.
• Nicotine Replacement Therapy : NRT - Doubles chance of success
• Lower conc of nicotine. No tar, gasses
• Reduces craving and withdrawal symptoms
• Patches – continual low dose – suitable for people who smoke constantly throughout the day,
• gums, nasal spray, inhaler, lozenges and lollipops – hit of nicotine – suitable for people who smoke under stressfull situations or at certain times of the day
• Drugs:
• Bupropion – noradrenaline and dopamine RI + nicotinic antagonist. Antidepressant found later to be an aid in smoking cessation through rather unidentified means.
• Varenicline – Nicotinic receptor partial agonist (like NRT). As a partial agonist, it both reduces cravings for and decreases the pleasurable effects of cigarettes and other tobacco products, and through these mechanisms it can assist some patients in stopping smoking.

http://en.wikipedia.org/wiki/Varenicline

http://en.wikipedia.org/wiki/Bupropion

http://ezinearticles.com/?Quitting-Smoking:-How-Long-Do-The-Cravings-Last&id=360120

http://www.quitsmokingsupport.com/methods.htm

Spirometry

Sorry tried to post. Having battles.
Will just bring copies on Friday.