Asthma: It is a chronic inflammatory pulmonary disorder that is characterized by reversible obstruction of the airways. These people have sensitive lungs and their airways narrow when exposed to certain triggers. *Three main factors causing airways to narrow: -The inside lining of the airways becomes red and swollen (inflammation) -Extra mucus (sticky fluid) may be produced -The muscle around the airways tighten (bronchoconstriction)
COAD: Chronic obstructive airways disease (COAD) is a group of lung diseases that cause swelling of the airways. Emphysema and chronic bronchitis are the most common forms.
Causes of Chronic Obstructive Pulmonary Disease (COPD) Lifestyle: • Smoking causes the majority of COPD (90% of cases in the US, 15% of smokers will get COPD) • --> smokers also have higher death rates and more severe symptoms • Passive smoking may (not proven) be a cause Mechanisms: • Promotes inflammation and the release (from inflammatory cells) of elastase (breaks down elastin in lung fibres leading to decreased surface area for gas exchange and perfusion) • Outdoor air pollution may also play a role, in undeveloped countries, indoor air pollution is the main cause of COPD: usually from indoor stoves Occupational: • Occupational pollutants such as cadmium and silica increase the risk of COPD: these are used in coal mining, metal work, cotton work and construction • Cigarette smoking is however a much more likely cause Genetic: • Another cause is deficiency of alpha-1 antitrypsin (AAT): a rare genetic disorder Mechanisms: • AAT is produces by the liver and circulates in the bloodstream and is implicated in blocking the effects of elastase (i.e. it maintains the integrity of elastic fibres). Deficiency in AAT causes destruction of the lung tissue leading to emphysema at about the age of 30 or 40. • Hence the development of COPD is an imbalance between elastase and AAT (not enough AAT, too much elastase) Infections: • The role of viral infections is unclear, viruses implicated in COPD include adenovirus and respiratory syncytial virus
Sources: http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/page3.htm Causes of COPD and who is at risk?: http://www.priory.com/cmol/causesof.htm From Angela
Complementary and Alternative Therapies in the treatment of Asthma by Katie & Pat
Diet
Antioxidants such as beta-carotene, vitamin C, vitamin E and flavonoids inhibit the production and release of histamine and other allergic/inflammatory substances
Flaxseed and omega 3 fatty acids have been shown to inhibit the production of arachidonic acid, which reduces the concentration of inflammatory leukotrienes
Magnesium, trace elements of selenium, potassium can help with symptoms
Herbs
Tylophora perennial climbing plant native to the plains, forests and hills of southern and eastern India. It has been traditionally used as a folk remedy in certain regions of India for the treatment of bronchial, asthma, bronchitis, rheumatism and dermatitis
Boswellia Serrata Contains boswellic acids and has been shown to inhibit leukotriene biosynthesis, thereby averting the inflammatory process
Butterber has inhibitory acivities on leukotriene geneneration in eosinophils and neutrophils >>> anti-inflammatory and anti-allergy properties
Others
Relaxation techniques such as meditation and yoga can help to regulate breathing patterns and also improve lung function
Homeopathy is the treatment of a disease by drugs, given in small doses that would produce symptoms in a healthy person similar to those of the disease. The aim is to reduce intensity of symptoms
Osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvres aim to increase the movement of the rib cage and the spine to try and improve the working of the lungs and circulation
Chest tapping, shaking and vibration is used to help shift and cough up any phlegm
Prevention medication can be used, such as inhaled glucocorticoid which helps to suppress inflammation and reduce the swelling of the lining of the airways
No clinical proof has been made about many of these CAM therapies
A government endorsed handbook can be downloaded here It shows that Tylophora Indica, Tsumura saibokuto and the Buteyko breathing technique (system of breathing exercises focusing on nasal route of breathing, hypoventilation and avoidance of deep breaths) are probably effective.
Guo R, Pittler MH, Ernst E. Herbal medicines for the treatment of COPD: a systematic review. Eur Respir J. 2006 Aug;28(2):330-8. Review. PMID: 16880367 [PubMed - indexed for MEDLINE] Panax ginseng and Salvia miltiorrhiza might be effective but insufficient data / poor methodology.
First step to motivating a patient to quit smoking is raising the issue (pre-contemplation to contemplation). Bringing up a patients smoking habits can be a sensitive issue, and may result in loss of rapport. Some things that can be done to avoid this are: - Normalising the inquiry - Avoid lecturing - Give the patient time and space to work through the consequences of the information they’ve been given - Understand their perspective - Avoid premature advice - Maintain the feeling of an alliance with the patient, work with them through the problem - Make sure they know they can always return for help
Motivational Interviewing: - “directive patient centred counselling style for eliciting behaviour change by helping patients to explore and resolve ambivalence” Key Concepts are: - Adopting a patient centred approach - Expressing empathy, promoting autonomy and encouraging mutual participation - Letting the patient decide how much of a problem they have - Developing patient discrepancy between patient goals and current problem behaviour, this involves using patients own thoughts on benefits versus costs. - Assume that the patient is responsible for the decision to change - Support self-efficacy and optimism for change
Using the 5 A’s: - Ask: Do you smoke? - Assess: Interest in quitting Barriers to quitting Nicotine dependene - Advise: Provide brief non-judgemental personalised and clear advice to aid quitting - Assist: Offer relevant pamphlets etc. - Arrange: Refer to organizations or collegues that may help - Finally, most important… FOLLOW UP
SAME: - Specific - Achievable - Measurable - Enjoyable
Other Strategies: 1) Explore and fill in gaps in patient knowledge 2) Explore patient intentions, goals and timelines 3) If in contemplation ask if they want to develop a plan to stop 4) Offer to help the patient to cut down 5) Elicit the patient’s ideas about strategies 6) Negotiate a contract 7) Offer nicotine patches, gum for patients who suffer from withdrawl 8) Provide close follow-up 9) Expect a relapse and be prepared to renegotiate
References: Bird, Cole, The Medical Interview, Mosby, 2005 RACGP, Smoking Policy, 2006 Litt, Smoking and GPs: time to cough up, RACGP, 2005
It was quite hard for me to figure out which is which but here are some of the statistics that i could find:
1. COPD There were only estimations because of the major differences in how the disease is defined. About 5.8million Australians have at least one long term respiratory condition in 2001. There were 5,400 deaths due to COPD in 2003.70% of death due to COPD is attributable to smoking. 2 million Australians have chronic sinusitis (Im not sure about the relevance but its still a respiratory condition).
2. Asthma 2 million Australians suffer from Asthma and about 660,000 from that number are Victorians. The estimation according to age groups are 1:4 for children, 1:7 for adolescents and 1:10 for adults.
3. Smoking According to The 2001 National Drug Strategy Household survey, 3.1million people smoked on a daily basis (19.5%).A further 3.6% (600,000 people) reported occasional smoking.21% of males and 18% of females were daily smokers.Among teenagers aged between 14-19yrs, 14% boys + 16% of girls smoked daily.
References: i.www.aihw.gov.au ii.Lecture 53, Pulmonary Pharmacology, Wayne Hodgson.
Management of COAD/COPD (Chronic obstructive airway/pulmonary disease)
COAD is a not fully reversible condition and therefore cannot be cured. However it can be managed in a number of ways that mostly concern symptomatic relief.
Smoking cessation – helps to reduce the rate of deterioration of lung function and thereby prolongs the time taken for disability or death. Smoking cessation is considered the most important factor in the prevention and treatment of COAD as currently it is the only disease modifying intervention.
Change of work environment – if occupational conditions are contributing to the problem (i.e. mining) then moving into another line of work in a less hazardous environment is desirable but obviously not always a realistic possibility.
Pharmaceutical treatments: •Bronchodilators: o Β2 Agonists – short and long (e.g. Salbutamol, Salmeterol) o Anticholinergics (e.g. Ipratropium) -Slower onset of action compared to B2 Agonist but last longer -Preferred first-line treatment -Selective long-acting M3 antagonist (Tiotropium) has shown promise in trials and possibly may have a disease modifying effect o Combination therapy (B2 Agonist & antimuscarinic agent) -Benefits include near immediate relief that is longer lasting o Methylxanthines -Little known about mode of action -Narrow therapeutic index with significant side effects therefore only used as a last resort o Leukotriene antagonists – no proven role in COAD management, may be prescribed due to confusion with management of asthma o Cromones – mast cell stabilisers that reduce the release of histamine – no proven role in COAD management as above •Corticosteroids o Uncertain effectiveness in management of COAD o Consider in patients with a documented response and those who have severe COAD • Mucolytic agents – decrease the viscosity of mucus • Antibiotics – to treat acute exacerbations of chronic bronchitis and emphysema where risk of infection is high
Pulmonary rehabilitation • Program of disease management, counselling and exercise designed to benefit the patient (Three interventions: exercise, education, psychosocial support) • Aims to enhance standard medical therapy and maximise functional capacity • Shown to quite effective in reducing symptoms and disability and improving function by: o Improving cardiovascular fitness, muscle function and exercise endurance o Enhance the patient’s self confidence and coping strategies o Improving mood by controlling anxiety and panic, decreasing depressions and reducing social impediments
Vaccinations – due to the increases risk of infection, patients with COAD should be vaccinated against respiratory pathogens such as influenza and pneumococcus to reduce the chance of a serious infection
Chest physiotherapy/Mechanical hygiene • Aims to assist sputum removal and improve lung ventilation • Various techniques
Surgery • Lung transplantation – typically translates to a large improvement in exercise capability and quality of life but often not appropriate • Lung volume reduction procedures – aims to reduce hyperinflation of lungs by removing the most severely affected lung sections. Improves inspiration capacity of the diaphragm and removes decompression of ‘good lung’ by badly diseased lung. • Bullectomy – removal of large bullae (enlarged air spaces in the lung) that are compressing adjacent normal functioning lung
References: http://en.wikipedia.org/wiki/COAD#Management http://www.priory.com/cmol/manageme.htm http://www.aafp.org/afp/20010815/603.html http://www.copdx.org.au/guidelines/documents/COPDX_April06_2006.pdf http://www.pulmonaryrehab.com.au/index.asp?page=8 http://www.nlhep.org/resources/erly-rec-mng-copd/early-recognition-copd-1.html http://www.medscape.com/viewarticle/412919 Textbook of Medicine (4th ed) - Souhami & Moxham
allergen avoidance or desensitisation monitoring (regular FEV1: forced expiratory rate-amount of air a person is able to expire in one second) medication
3 Drug Classes Relievers Symptom controllers Preventers
Relievers: Short acting beta-agonists (relatively beta-2 selective) 1st line treatment treatment of acute asthma These drugs are designed to be used on an 'as needed' basis. They have a quick onset (5-15 min) and a short duration (3-6 hours) Mechanism- action on adenylate cyclase, increases cAMP (second messenger) -diminishes Ca+ available for contraction -bronchodilation Side effects: tachycardia, skeletal tremor Contraindicated: beta-blockers (for hypertension) Examples: salbutamol (Asmol, Ventolin) terbutaline (Bricanyl) orciprenaline (Alupent)
Symptom controllers: Long acting beta(2)-agonists (LABA) Newer drugs Have a duration up to 12 hours Can be used in conjunction with an inhaled steroid Examples: salmeterol (Serevent) eformoterol (Foradile, Oxis)
Other bronchodilator agents: Used less frequently, adjunt treatment for servere asthma or patients contraindicated for beta-agonists Ipratropium (Atrovent):-antimuscarinic -produces bronchodilation by blocking vagal tone (ACh) Theophylline:-xanthine group of drugs (includes caffeine) -produces bronchodilation by relaxing smooth muscle -narrow therapeutic index, variable plasma levels Preventers Protect against the inflammatory reaction of asthma and long term smooth muscle damage Steroids -anti-inflammatory and immunosuppressant effects -blocks phospholipase A2 (ie. decreases production of prostaglandins and leukotrienes, inflammatory mediators) -do not relieve muscle spasm: delayed action -many names (end in ‘sone’, eg. Fluticasone) -inhaled and oral -inhaled have less side-effects (such as oral thrush)
Leukotriene receptor antagonists -block the effects of leukotrienes at receptors (ie. mucus secretion, bronchoconstriction, inflammatory cell migration)
Mast cell stabilizers (prevent release of histamine, a bronchoconstrictor) Combined LABA/steroids (Examples: Seretide and Symbicort)
Extrinsic Asthma (Allergic/Atopic) - most common form of asthma, common in children - may be due to genetic factors - involve IgE production and mast cell degranulation at respiratory mucosa - Mast cells release inflammatory mediators- histamines, leukotrines, interleukins - caused by environmental exposure to allergens o Pollen o Mould o Animal dander o Dust mites o Cockroaches o Food Proteins
Intrinsic Asthma - no causative agent - due to hyper responsive airways - Triggered by precipitating factors: o Cold air and Exercise o Emotional stress
Other causes and triggers of asthma: o Viral infections- Rhinovirus, RSV o Occupational sensitizers – Isocynates, colophony fumes o Irritant dust, vapours, fumes – cigarette smoke, perfumes, exhaust fumes o Atmospheric pollution - sulphur dioxide o Drugs - aspirin, NSAIDS, Beta-blockers
References:
Kumar and Clarke, 5th Edi., pg 874 Week 5 Lecture notes – Pulmonary Pharmacology, Wayne Hodgson
Signs and symptoms of asthma include: •Coughing. Coughing from asthma is often worse at night or early in the morning, making it hard to sleep. •Wheezing. •Chest tightness. •Shortness of breath. •Recurrent reversible obstructive airway.
Symptoms are: •recurrent or seasonal. •worse at night or in the early morning. •obviously triggered by exercise, irritants, allergies or viral infections.
http://www.nhlbi.nih.gov/health/dci/Diseases/Asthma/Asthma_SignsAndSymptoms.html Lecture 53, Pulmonary Pharmacology Asthma Management Handbook, National Asthma Council Australia.
Spirometry is used to measure pulmonary volume and flow. Patient inspires then expires with maximum force and length of breath into the spirometer. A printout is recorded. There are two different kinds of spirometers: - Volume-displacement spirometers: o Simple o Accurate o Easy to maintain o Not very portable - Flow-sensing spirometers o Portable o Easy to use o Can give variable results (need a few readings to confirm results) The printout usually takes one of two forms: - Time versus volume graph - Flow rate versus volume graph (most common) For example of chart, see asthma website.
The chart (readout) gives several pieces of information: 1. VC (vital capacity) is the maximum volume of air which can be exhaled or inspired during either a forced (FVC) or a slow (VC) manoeuvre. 2. FEV1 (forced expired volume in one second) is the volume expired in the first second of maximal expiration after a maximal inspiration and is a useful measure of how quickly full lungs can be emptied. 3. FEV1/VC is the FEV1 expressed as a percentage of the VC or FVC (whichever volume is larger) and gives a clinically useful index of airflow limitation. 4. FEF25-75% is the average expired flow over the middle half of the FVC manoeuvre and is regarded as a more sensitive measure of small airways narrowing than FEV1. Unfortunately FEF25-75% has a wide range of normality, is less reproducible than FEV1, and is difficult to interpret if the VC (or FVC) is reduced or increased. 5. PEF (peak expiratory flow) is the maximal expiratory flow rate achieved and this occurs very early in the forced expiratory manoeuvre. 6. FEF50% and FEF75% (forced expiratory flow at 50% or 75% FVC) is the maximal expiratory flow measured at the point where 50% of the FVC has been expired (FEF50%) and after 75% has been expired (FEF75%). Both indices have a wide range of normality but are usually reproducible in a given subject provided the FVC is reproducible. http://www.nationalasthma.org.au/html/management/spiro_book/sp_bk006.asp
Expected results are as follows: 1. Gender: For a given height and age, males have a larger FEV1, FVC, FEF25-75% and PEF, but a slightly lower FEV1/FVC%. 2. Age: FEV1, FVC, FEF25-75% and PEF increase, while FEV1/FVC% decreases, with age until about 20 years old in females and 25 years in males.
After this, all indices gradually fall, although the precise rate of decline is probably masked due to the complex interrelationship between age and height. The fall in FEV1/FVC% with age in adults is due to the greater decline in FEV1 than FVC. 3. Height: All indices other than FEV1/FVC% increase with standing height. 4. Ethnic Origin: Caucasians have the largest FEV1 and FVC and, of the various ethnic groups, Polynesians are among the lowest. The values for black Africans are 10-15% lower than for Caucasians of similar age, sex and height because for a given standing height their thorax is shorter. Chinese have been found to have an FVC about 20% lower and Indians about 10% lower than matched Caucasians. There is little difference in PEF between ethnic groups.
There is a vast literature of normal population studies, many of which have deficiencies in sample size, definition of normality, inclusion of smokers and choice of equipment. Appendix B provides tables of mean predicted values from a well-conducted study on a Caucasian population of Tucson, Arizona3. http://www.nationalasthma.org.au/html/management/spiro_book/sp_bk006.asp
Abnormal results indicating pathology 1. A reduction of FEV1 in relation to the forced vital capacity will result in a low FEV1/FVC% and is typical of obstructive ventilatory defects (e.g. asthma and emphysema). The lower limit of normal for FEV1/FVC is around 70-75% but the exact limit is dependent on age. The exact values by age, sex and height are given in the tables in Appendix C. In obstructive lung disease the FVC may be less than the slow VC because of earlier airway closure during the forced manoeuvre. This may lead to an overestimation of the FEV1/FVC%. Thus, the FEV1/VC% may be a more sensitive index of airflow obstruction. 2. The FEV1/FVC% ratio remains normal or high (typically > 80%) with a reduction in both FEV1 and FVC in restrictive ventilatory defects (e.g. interstitial lung disease, respiratory muscle weakness, and thoracic cage deformities such as kypho-scoliosis). 3. A reduced FVC together with a low FEV1/FVC% ratio is a feature of a mixed ventilatory defect in which a combination of both obstruction and restriction appear to be present, or alternatively may occur in airflow obstruction as a consequence of airway closure resulting in gas trapping, rather than as a result of small lungs. It is necessary to measure the patient's total lung capacity to distinguish between these two possibilities.
People who suffer from Asthma tend to develop IgE antibodies against normal things in the environment.
Dust, allergens from animals or plants and other substances trigger a much greater IgE response in asthmatics than unaffected individuals.
Genetic predisposition is partly responsible and certain genes are known to affect IgE production and regulation of cytokines and the immune response.
Environmental factors also play an important part. One theory suggests that childhood exposure to bacteria, fungi and dirt in general stimulates the immune system and hones it onto those stimuli. Growing up with less of those influences (in a cleaner environment) can cause IgE sensitivity to allergens.
Pathology of Asthma and COPD:
Asthma:
Two things play a part here,
1) Airway inflammation
When an allergen enters the lungs antigen presenting cells (Dendritic cells) activate Th2 Lymphocytes. These lymphocytes promote mucus production, IgE production and release other cytokines that activate mast cells and eosinophils.
Activated eosinophils can release substances that are toxic to epithelial cells.
This immune reaction to a usually harmless allergen can be chronic and lead to changes in the airway walls.
2) Airway wall remodelling a)epithelium
- Epithelium is damaged - Columnar cells with cilia are lost whilst mucus producing cells tend to proliferate. This makes airways more vulnerable to infections - Epithelium secretes more inflammatory substances that exacerbate the problem.
b)Sub-endothelium
- repair collagen is deposited - activation of fibroblasts that thicken airway walls with proteins and collagen
c) Smooth muscle and nerves
- Both can become more sensitive to stimuli which leads to airway constriction when stimulated by allergens.
Thats it for asthma.
COPD has several similarities:
- Inflammation - Increase in mucous secreting cells - ulcerated epithelial cells and damage to epithelium - narrowing of the airways
Often this airway damage is worsened by emphysema. This is damage to bronchioles and alveoli which reduces both the elastic recoil of the lungs and the total SA available to gas exchange.
Hope all this is handy
Alex
References: Kumar and Clark
http://www.aerovance.com/asthma_clip_image002.gif
(this is just a cool picture of the whole thing, check it out, needs a bit of explanation though :)
People who suffer from Asthma tend to develop IgE antibodies against normal things in the environment.
Dust, allergens from animals or plants and other substances trigger a much greater IgE response in asthmatics than unaffected individuals.
Genetic predisposition is partly responsible and certain genes are known to affect IgE production and regulation of cytokines and the immune response.
Environmental factors also play an important part. One theory suggests that childhood exposure to bacteria, fungi and dirt in general stimulates the immune system and hones it onto those stimuli. Growing up with less of those influences (in a cleaner environment) can cause IgE sensitivity to allergens.
Pathology of Asthma and COPD:
Asthma:
Two things play a part here,
1) Airway inflammation
When an allergen enters the lungs antigen presenting cells (Dendritic cells) activate Th2 Lymphocytes. These lymphocytes promote mucus production, IgE production and release other cytokines that activate mast cells and eosinophils.
Activated eosinophils can release substances that are toxic to epithelial cells.
This immune reaction to a usually harmless allergen can be chronic and lead to changes in the airway walls.
2) Airway wall remodelling a)epithelium
- Epithelium is damaged - Columnar cells with cilia are lost whilst mucus producing cells tend to proliferate. This makes airways more vulnerable to infections - Epithelium secretes more inflammatory substances that exacerbate the problem.
b)Sub-endothelium
- repair collagen is deposited - activation of fibroblasts that thicken airway walls with proteins and collagen
c) Smooth muscle and nerves
- Both can become more sensitive to stimuli which leads to airway constriction when stimulated by allergens.
Thats it for asthma.
COPD has several similarities:
- Inflammation - Increase in mucous secreting cells - ulcerated epithelial cells and damage to epithelium - narrowing of the airways
Often this airway damage is worsened by emphysema. This is damage to bronchioles and alveoli which reduces both the elastic recoil of the lungs and the total SA available to gas exchange.
Hope all this is handy
Alex
References: Kumar and Clark
http://www.aerovance.com/asthma_clip_image002.gif
(this is just a cool picture of the whole thing, check it out, needs a bit of explanation though : )
Ok guys, we were getting all confused about how asthma fits in to the inflammation pathway... But I think I've figured it out - it doesn't fit in at all!
Membrane phospholipids --> arachadonic acid --> prostaglandins + leukotrienes is just one inflammatory pathway: the one that responds to tissue damage.
In asthma, IgE antibodies bind to mast cells in the lungs, and when the allergen that they are specific to enters the lungs it causes the mast cells to degranlate. This releases all sorts of stuff, namely histamine but also some prostaglandins and leukotrienes.
Since it is prostaglandins and leukotrienes that cause inflammation by attracting inflammatory cells, both tissue damage and asthma cause inflammation (but by different pathways)
Now in terms of why allergens cause different reactions in asthmatics to non-asthmatics, genes are thought to play a factor. Asthmatics have a slightly different set of proteins (interleukins) that initially respond to the allergen.
14 comments:
Asthma: It is a chronic inflammatory pulmonary disorder that is characterized by reversible obstruction of the airways. These people have sensitive lungs and their airways narrow when exposed to certain triggers.
*Three main factors causing airways to narrow:
-The inside lining of the airways becomes red and swollen (inflammation)
-Extra mucus (sticky fluid) may be produced
-The muscle around the airways tighten (bronchoconstriction)
COAD: Chronic obstructive airways disease (COAD) is a group of lung diseases that cause swelling of the airways. Emphysema and chronic bronchitis are the most common forms.
References:
http://www.nlm.nih.gov/medlineplus/ency/article/000091.htm
http://www.asthma.org.au/
Causes of Chronic Obstructive Pulmonary Disease (COPD)
Lifestyle:
• Smoking causes the majority of COPD (90% of cases in the US, 15% of smokers will get COPD)
• --> smokers also have higher death rates and more severe symptoms
• Passive smoking may (not proven) be a cause
Mechanisms:
• Promotes inflammation and the release (from inflammatory cells) of elastase (breaks down elastin in lung fibres leading to decreased surface area for gas exchange and perfusion)
• Outdoor air pollution may also play a role, in undeveloped countries, indoor air pollution is the main cause of COPD: usually from indoor stoves
Occupational:
• Occupational pollutants such as cadmium and silica increase the risk of COPD: these are used in coal mining, metal work, cotton work and construction
• Cigarette smoking is however a much more likely cause
Genetic:
• Another cause is deficiency of alpha-1 antitrypsin (AAT): a rare genetic disorder
Mechanisms:
• AAT is produces by the liver and circulates in the bloodstream and is implicated in blocking the effects of elastase (i.e. it maintains the integrity of elastic fibres). Deficiency in AAT causes destruction of the lung tissue leading to emphysema at about the age of 30 or 40.
• Hence the development of COPD is an imbalance between elastase and AAT (not enough AAT, too much elastase)
Infections:
• The role of viral infections is unclear, viruses implicated in COPD include adenovirus and respiratory syncytial virus
Sources: http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/page3.htm
Causes of COPD and who is at risk?: http://www.priory.com/cmol/causesof.htm
From Angela
SIGNS/SYMPTOMS OF COAD(COPD)
Symptoms:
-Cough
-Sputum production
-Dyspnoea, especially exertional.
-Wheeze
Signs:
-Tachypnoea
-Use of accessory muscles of respiration
-Lung hyper-inflation
-Decreased cricosternal distance (<3 cm between sternum and cricoid cartilage)
-Resonant or hyper-resonant percussion note
-Quiet breath sounds
-Wheeze
-Cyanosis
-Cor pulmonale (right heart failure, caused by pulmonary hypertension)
Reference: Oxford Handbook of Clinical Medicine, 6th Edition.
Complementary and Alternative Therapies in the treatment of Asthma by Katie & Pat
Diet
Antioxidants such as beta-carotene, vitamin C, vitamin E and flavonoids inhibit the production and release of histamine and other allergic/inflammatory substances
Flaxseed and omega 3 fatty acids have been shown to inhibit the production of arachidonic acid, which reduces the concentration of inflammatory leukotrienes
Magnesium, trace elements of selenium, potassium can help with symptoms
Herbs
Tylophora perennial climbing plant native to the plains, forests and hills of southern and eastern India. It has been traditionally used as a folk remedy in certain regions of India for the treatment of bronchial, asthma, bronchitis, rheumatism and dermatitis
Boswellia Serrata Contains boswellic acids and has been shown to inhibit leukotriene biosynthesis, thereby averting the inflammatory process
Butterber has inhibitory acivities on leukotriene geneneration in eosinophils and neutrophils >>> anti-inflammatory and anti-allergy properties
Others
Relaxation techniques such as meditation and yoga can help to regulate breathing patterns and also improve lung function
Homeopathy is the treatment of a disease by drugs, given in small doses that would produce symptoms in a healthy person similar to those of the disease. The aim is to reduce intensity of symptoms
Osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvres aim to increase the movement of the rib cage and the spine to try and improve the working of the lungs and circulation
Chest tapping, shaking and vibration is used to help shift and cough up any phlegm
Prevention medication can be used, such as inhaled glucocorticoid which helps to suppress inflammation and reduce the swelling of the lining of the airways
No clinical proof has been made about many of these CAM therapies
A government endorsed handbook can be downloaded here
It shows that Tylophora Indica, Tsumura saibokuto and the Buteyko breathing technique (system of breathing exercises focusing on nasal route of breathing, hypoventilation and avoidance of deep breaths) are probably effective.
Guo R, Pittler MH, Ernst E. Herbal medicines for the treatment of COPD: a systematic review. Eur Respir J. 2006 Aug;28(2):330-8. Review. PMID: 16880367 [PubMed - indexed for MEDLINE]
Panax ginseng and Salvia miltiorrhiza might be effective but insufficient data / poor methodology.
robb said...
Motivating Patients to Quit Smoking:
First step to motivating a patient to quit smoking is raising the issue (pre-contemplation to contemplation). Bringing up a patients smoking habits can be a sensitive issue, and may result in loss of rapport. Some things that can be done to avoid this are:
- Normalising the inquiry
- Avoid lecturing
- Give the patient time and space to work through the consequences of the information they’ve been given
- Understand their perspective
- Avoid premature advice
- Maintain the feeling of an alliance with the patient, work with them through the problem
- Make sure they know they can always return for help
Motivational Interviewing:
- “directive patient centred counselling style for eliciting behaviour change by helping patients to explore and resolve ambivalence”
Key Concepts are:
- Adopting a patient centred approach
- Expressing empathy, promoting autonomy and encouraging mutual participation
- Letting the patient decide how much of a problem they have
- Developing patient discrepancy between patient goals and current problem behaviour, this involves using patients own thoughts on benefits versus costs.
- Assume that the patient is responsible for the decision to change
- Support self-efficacy and optimism for change
Using the 5 A’s:
- Ask: Do you smoke?
- Assess: Interest in quitting
Barriers to quitting
Nicotine dependene
- Advise: Provide brief non-judgemental personalised and clear advice to aid quitting
- Assist: Offer relevant pamphlets etc.
- Arrange: Refer to organizations or collegues that may help
- Finally, most important… FOLLOW UP
Prochaska-DiClemente Cycle:
- Pre-contemplation
- Contemplation
- Preparation
- Action
- Relapse/Maintenance
SAME:
- Specific
- Achievable
- Measurable
- Enjoyable
Other Strategies:
1) Explore and fill in gaps in patient knowledge
2) Explore patient intentions, goals and timelines
3) If in contemplation ask if they want to develop a plan to stop
4) Offer to help the patient to cut down
5) Elicit the patient’s ideas about strategies
6) Negotiate a contract
7) Offer nicotine patches, gum for patients who suffer from withdrawl
8) Provide close follow-up
9) Expect a relapse and be prepared to renegotiate
References:
Bird, Cole, The Medical Interview, Mosby, 2005
RACGP, Smoking Policy, 2006
Litt, Smoking and GPs: time to cough up, RACGP, 2005
Incidence of COPD, Asthma and Smoking.
It was quite hard for me to figure out which is which but here are some of the statistics that i could find:
1. COPD
There were only estimations because of the major differences in how the disease is defined. About 5.8million Australians have at least one long term respiratory condition in 2001. There were 5,400 deaths due to COPD in 2003.70% of death due to COPD is attributable to smoking. 2 million Australians have chronic sinusitis (Im not sure about the relevance but its still a respiratory condition).
2. Asthma
2 million Australians suffer from Asthma and about 660,000 from that number are Victorians. The estimation according to age groups are 1:4 for children, 1:7 for adolescents and 1:10 for adults.
3. Smoking
According to The 2001 National Drug Strategy Household survey, 3.1million people smoked on a daily basis (19.5%).A further 3.6% (600,000 people) reported occasional smoking.21% of males and 18% of females were daily smokers.Among teenagers aged between 14-19yrs, 14% boys + 16% of girls smoked daily.
References:
i.www.aihw.gov.au
ii.Lecture 53, Pulmonary Pharmacology, Wayne Hodgson.
Management of COAD/COPD
(Chronic obstructive airway/pulmonary disease)
COAD is a not fully reversible condition and therefore cannot be cured. However it can be managed in a number of ways that mostly concern symptomatic relief.
Smoking cessation – helps to reduce the rate of deterioration of lung function and thereby prolongs the time taken for disability or death. Smoking cessation is considered the most important factor in the prevention and treatment of COAD as currently it is the only disease modifying intervention.
Change of work environment – if occupational conditions are contributing to the problem (i.e. mining) then moving into another line of work in a less hazardous environment is desirable but obviously not always a realistic possibility.
Pharmaceutical treatments:
•Bronchodilators:
o Β2 Agonists – short and long (e.g. Salbutamol, Salmeterol)
o Anticholinergics (e.g. Ipratropium)
-Slower onset of action compared to B2 Agonist but last longer
-Preferred first-line treatment
-Selective long-acting M3 antagonist (Tiotropium) has shown promise in trials and possibly may have a disease modifying effect
o Combination therapy (B2 Agonist & antimuscarinic agent)
-Benefits include near immediate relief that is longer lasting
o Methylxanthines
-Little known about mode of action
-Narrow therapeutic index with significant side effects therefore only used as a last resort
o Leukotriene antagonists – no proven role in COAD management, may be prescribed due to confusion with management of asthma
o Cromones – mast cell stabilisers that reduce the release of histamine – no proven role in COAD management as above
•Corticosteroids
o Uncertain effectiveness in management of COAD
o Consider in patients with a documented response and those who have severe COAD
• Mucolytic agents – decrease the viscosity of mucus
• Antibiotics – to treat acute exacerbations of chronic bronchitis and emphysema where risk of infection is high
Oxygenation
• PaCO2 > 45 mmHg
• PaO2 < 55 mmHg
• O2 saturation < 88% while sleeping
Pulmonary rehabilitation
• Program of disease management, counselling and exercise designed to benefit the patient (Three interventions: exercise, education, psychosocial support)
• Aims to enhance standard medical therapy and maximise functional capacity
• Shown to quite effective in reducing symptoms and disability and improving function by:
o Improving cardiovascular fitness, muscle function and exercise endurance
o Enhance the patient’s self confidence and coping strategies
o Improving mood by controlling anxiety and panic, decreasing depressions and reducing social impediments
Vaccinations – due to the increases risk of infection, patients with COAD should be vaccinated against respiratory pathogens such as influenza and pneumococcus to reduce the chance of a serious infection
Chest physiotherapy/Mechanical hygiene
• Aims to assist sputum removal and improve lung ventilation
• Various techniques
Surgery
• Lung transplantation – typically translates to a large improvement in exercise capability and quality of life but often not appropriate
• Lung volume reduction procedures – aims to reduce hyperinflation of lungs by removing the most severely affected lung sections. Improves inspiration capacity of the diaphragm and removes decompression of ‘good lung’ by badly diseased lung.
• Bullectomy – removal of large bullae (enlarged air spaces in the lung) that are compressing adjacent normal functioning lung
References:
http://en.wikipedia.org/wiki/COAD#Management
http://www.priory.com/cmol/manageme.htm
http://www.aafp.org/afp/20010815/603.html
http://www.copdx.org.au/guidelines/documents/COPDX_April06_2006.pdf
http://www.pulmonaryrehab.com.au/index.asp?page=8
http://www.nlhep.org/resources/erly-rec-mng-copd/early-recognition-copd-1.html
http://www.medscape.com/viewarticle/412919
Textbook of Medicine (4th ed) - Souhami & Moxham
Management of Asthma:
allergen avoidance or desensitisation
monitoring (regular FEV1: forced expiratory rate-amount of air a person is able to expire in one second)
medication
3 Drug Classes
Relievers
Symptom controllers
Preventers
Relievers:
Short acting beta-agonists (relatively beta-2 selective)
1st line treatment treatment of acute asthma
These drugs are designed to be used on an 'as needed' basis.
They have a quick onset (5-15 min) and a short duration (3-6 hours)
Mechanism- action on adenylate cyclase, increases cAMP (second messenger)
-diminishes Ca+ available for contraction
-bronchodilation
Side effects: tachycardia, skeletal tremor
Contraindicated: beta-blockers (for hypertension)
Examples: salbutamol (Asmol, Ventolin)
terbutaline (Bricanyl)
orciprenaline (Alupent)
Symptom controllers:
Long acting beta(2)-agonists (LABA)
Newer drugs
Have a duration up to 12 hours
Can be used in conjunction with an inhaled steroid
Examples: salmeterol (Serevent)
eformoterol (Foradile, Oxis)
Other bronchodilator agents:
Used less frequently, adjunt treatment for servere asthma or patients contraindicated for beta-agonists
Ipratropium (Atrovent):-antimuscarinic
-produces bronchodilation by blocking vagal tone (ACh)
Theophylline:-xanthine group of drugs (includes caffeine)
-produces bronchodilation by relaxing smooth muscle
-narrow therapeutic index, variable plasma levels
Preventers
Protect against the inflammatory reaction of asthma and long term smooth muscle damage
Steroids
-anti-inflammatory and immunosuppressant effects
-blocks phospholipase A2 (ie. decreases production of prostaglandins and leukotrienes, inflammatory mediators)
-do not relieve muscle spasm: delayed action
-many names (end in ‘sone’, eg. Fluticasone)
-inhaled and oral
-inhaled have less side-effects (such as oral thrush)
Leukotriene receptor antagonists
-block the effects of leukotrienes at receptors (ie. mucus secretion, bronchoconstriction, inflammatory cell migration)
Mast cell stabilizers (prevent release of histamine, a bronchoconstrictor)
Combined LABA/steroids (Examples: Seretide and Symbicort)
Reference:
Lecture notes-Week 5, 'Pulmonary Pharmacology'
http://www.asthmaaustralia.org.au
Causes and Triggers of Asthma
Extrinsic Asthma (Allergic/Atopic)
- most common form of asthma, common in children
- may be due to genetic factors
- involve IgE production and mast cell degranulation at respiratory mucosa
- Mast cells release inflammatory mediators- histamines, leukotrines, interleukins
- caused by environmental exposure to allergens
o Pollen
o Mould
o Animal dander
o Dust mites
o Cockroaches
o Food Proteins
Intrinsic Asthma
- no causative agent
- due to hyper responsive airways
- Triggered by precipitating factors:
o Cold air and Exercise
o Emotional stress
Other causes and triggers of asthma:
o Viral infections- Rhinovirus, RSV
o Occupational sensitizers – Isocynates, colophony fumes
o Irritant dust, vapours, fumes – cigarette smoke, perfumes, exhaust fumes
o Atmospheric pollution - sulphur dioxide
o Drugs - aspirin, NSAIDS, Beta-blockers
References:
Kumar and Clarke, 5th Edi., pg 874
Week 5 Lecture notes – Pulmonary Pharmacology, Wayne Hodgson
Signs and symptoms of asthma include:
•Coughing. Coughing from asthma is often worse at night or early in the morning, making it hard to sleep.
•Wheezing.
•Chest tightness.
•Shortness of breath.
•Recurrent reversible obstructive airway.
Symptoms are:
•recurrent or seasonal.
•worse at night or in the early morning.
•obviously triggered by exercise, irritants, allergies or viral infections.
http://www.nhlbi.nih.gov/health/dci/Diseases/Asthma/Asthma_SignsAndSymptoms.html
Lecture 53, Pulmonary Pharmacology
Asthma Management Handbook, National Asthma Council Australia.
JESS said...
SPIROMETRY
Spirometry is used to measure pulmonary volume and flow.
Patient inspires then expires with maximum force and length of breath into the spirometer. A printout is recorded. There are two different kinds of spirometers:
- Volume-displacement spirometers:
o Simple
o Accurate
o Easy to maintain
o Not very portable
- Flow-sensing spirometers
o Portable
o Easy to use
o Can give variable results (need a few readings to confirm results)
The printout usually takes one of two forms:
- Time versus volume graph
- Flow rate versus volume graph (most common)
For example of chart, see asthma website.
The chart (readout) gives several pieces of information:
1. VC (vital capacity) is the maximum volume of air which can be exhaled or inspired during either a forced (FVC) or a slow (VC) manoeuvre.
2. FEV1 (forced expired volume in one second) is the volume expired in the first second of maximal expiration after a maximal inspiration and is a useful measure of how quickly full lungs can be emptied.
3. FEV1/VC is the FEV1 expressed as a percentage of the VC or FVC (whichever volume is larger) and gives a clinically useful index of airflow limitation.
4. FEF25-75% is the average expired flow over the middle half of the FVC manoeuvre and is regarded as a more sensitive measure of small airways narrowing than FEV1.
Unfortunately FEF25-75% has a wide range of normality, is less reproducible than FEV1, and is difficult to interpret if the VC (or FVC) is reduced or increased.
5. PEF (peak expiratory flow) is the maximal expiratory flow rate achieved and this occurs very early in the forced expiratory manoeuvre.
6. FEF50% and FEF75% (forced expiratory flow at 50% or 75% FVC) is the maximal expiratory flow measured at the point where 50% of the FVC has been expired (FEF50%) and after 75% has been expired (FEF75%). Both indices have a wide range of normality but are usually reproducible in a given subject provided the FVC is reproducible.
http://www.nationalasthma.org.au/html/management/spiro_book/sp_bk006.asp
Expected results are as follows:
1. Gender: For a given height and age, males have a larger FEV1, FVC, FEF25-75% and PEF, but a slightly lower FEV1/FVC%.
2. Age: FEV1, FVC, FEF25-75% and PEF increase, while FEV1/FVC% decreases, with age until about 20 years old in females and 25 years in males.
After this, all indices gradually fall, although the precise rate of decline is probably masked due to the complex interrelationship between age and height. The fall in FEV1/FVC% with age in adults is due to the greater decline in FEV1 than FVC.
3. Height: All indices other than FEV1/FVC% increase with standing height.
4. Ethnic Origin: Caucasians have the largest FEV1 and FVC and, of the various ethnic groups, Polynesians are among the lowest. The values for black Africans are 10-15% lower than for Caucasians of similar age, sex and height because for a given standing height their thorax is shorter. Chinese have been found to have an FVC about 20% lower and Indians about 10% lower than matched Caucasians. There is little difference in PEF between ethnic groups.
There is a vast literature of normal population studies, many of which have deficiencies in sample size, definition of normality, inclusion of smokers and choice of equipment. Appendix B provides tables of mean predicted values from a well-conducted study on a Caucasian population of Tucson, Arizona3.
http://www.nationalasthma.org.au/html/management/spiro_book/sp_bk006.asp
Abnormal results indicating pathology
1. A reduction of FEV1 in relation to the forced vital capacity will result in a low FEV1/FVC% and is typical of obstructive ventilatory defects (e.g. asthma and emphysema). The lower limit of normal for FEV1/FVC is around 70-75% but the exact limit is dependent on age. The exact values by age, sex and height are given in the tables in Appendix C. In obstructive lung disease the FVC may be less than the slow VC because of earlier airway closure during the forced manoeuvre. This may lead to an overestimation of the FEV1/FVC%. Thus, the FEV1/VC% may be a more sensitive index of airflow obstruction.
2. The FEV1/FVC% ratio remains normal or high (typically > 80%) with a reduction in both FEV1 and FVC in restrictive ventilatory defects (e.g. interstitial lung disease, respiratory muscle weakness, and thoracic cage deformities such as kypho-scoliosis).
3. A reduced FVC together with a low FEV1/FVC% ratio is a feature of a mixed ventilatory defect in which a combination of both obstruction and restriction appear to be present, or alternatively may occur in airflow obstruction as a consequence of airway closure resulting in gas trapping, rather than as a result of small lungs. It is necessary to measure the patient's total lung capacity to distinguish between these two possibilities.
http://www.nationalasthma.org.au/html/management/spiro_book/sp_bk006.asp
Hey guys,
sorry I was late in posting this.
People who suffer from Asthma tend to develop IgE antibodies against normal things in the environment.
Dust, allergens from animals or plants and other substances trigger a much greater IgE response in asthmatics than unaffected individuals.
Genetic predisposition is partly responsible and certain genes are known to affect IgE production and regulation of cytokines and the immune response.
Environmental factors also play an important part. One theory suggests that childhood exposure to bacteria, fungi and dirt in general stimulates the immune system and hones it onto those stimuli. Growing up with less of those influences (in a cleaner environment) can cause IgE sensitivity to allergens.
Pathology of Asthma and COPD:
Asthma:
Two things play a part here,
1) Airway inflammation
When an allergen enters the lungs antigen presenting cells (Dendritic cells) activate Th2 Lymphocytes. These lymphocytes promote mucus production, IgE production and release other cytokines that activate mast cells and eosinophils.
Activated eosinophils can release substances that are toxic to epithelial cells.
This immune reaction to a usually harmless allergen can be chronic and lead to changes in the airway walls.
2) Airway wall remodelling
a)epithelium
- Epithelium is damaged
- Columnar cells with cilia are lost whilst mucus producing cells tend to proliferate. This makes airways more vulnerable to infections
- Epithelium secretes more inflammatory substances that exacerbate the problem.
b)Sub-endothelium
- repair collagen is deposited
- activation of fibroblasts that thicken airway walls with proteins and collagen
c) Smooth muscle and nerves
- Both can become more sensitive to stimuli which leads to airway constriction when stimulated by allergens.
Thats it for asthma.
COPD has several similarities:
- Inflammation
- Increase in mucous secreting cells
- ulcerated epithelial cells and damage to epithelium
- narrowing of the airways
Often this airway damage is worsened by emphysema. This is damage to bronchioles and alveoli which reduces both the elastic recoil of the lungs and the total SA available to gas exchange.
Hope all this is handy
Alex
References:
Kumar and Clark
http://www.aerovance.com/asthma_clip_image002.gif
(this is just a cool picture of the whole thing, check it out, needs a bit of explanation though :)
Hey guys,
sorry I was late in posting this.
People who suffer from Asthma tend to develop IgE antibodies against normal things in the environment.
Dust, allergens from animals or plants and other substances trigger a much greater IgE response in asthmatics than unaffected individuals.
Genetic predisposition is partly responsible and certain genes are known to affect IgE production and regulation of cytokines and the immune response.
Environmental factors also play an important part. One theory suggests that childhood exposure to bacteria, fungi and dirt in general stimulates the immune system and hones it onto those stimuli. Growing up with less of those influences (in a cleaner environment) can cause IgE sensitivity to allergens.
Pathology of Asthma and COPD:
Asthma:
Two things play a part here,
1) Airway inflammation
When an allergen enters the lungs antigen presenting cells (Dendritic cells) activate Th2 Lymphocytes. These lymphocytes promote mucus production, IgE production and release other cytokines that activate mast cells and eosinophils.
Activated eosinophils can release substances that are toxic to epithelial cells.
This immune reaction to a usually harmless allergen can be chronic and lead to changes in the airway walls.
2) Airway wall remodelling
a)epithelium
- Epithelium is damaged
- Columnar cells with cilia are lost whilst mucus producing cells tend to proliferate. This makes airways more vulnerable to infections
- Epithelium secretes more inflammatory substances that exacerbate the problem.
b)Sub-endothelium
- repair collagen is deposited
- activation of fibroblasts that thicken airway walls with proteins and collagen
c) Smooth muscle and nerves
- Both can become more sensitive to stimuli which leads to airway constriction when stimulated by allergens.
Thats it for asthma.
COPD has several similarities:
- Inflammation
- Increase in mucous secreting cells
- ulcerated epithelial cells and damage to epithelium
- narrowing of the airways
Often this airway damage is worsened by emphysema. This is damage to bronchioles and alveoli which reduces both the elastic recoil of the lungs and the total SA available to gas exchange.
Hope all this is handy
Alex
References:
Kumar and Clark
http://www.aerovance.com/asthma_clip_image002.gif
(this is just a cool picture of the whole thing, check it out, needs a bit of explanation though : )
Ok guys, we were getting all confused about how asthma fits in to the inflammation pathway... But I think I've figured it out - it doesn't fit in at all!
Membrane phospholipids --> arachadonic acid --> prostaglandins + leukotrienes is just one inflammatory pathway: the one that responds to tissue damage.
In asthma, IgE antibodies bind to mast cells in the lungs, and when the allergen that they are specific to enters the lungs it causes the mast cells to degranlate. This releases all sorts of stuff, namely histamine but also some prostaglandins and leukotrienes.
Since it is prostaglandins and leukotrienes that cause inflammation by attracting inflammatory cells, both tissue damage and asthma cause inflammation (but by different pathways)
Now in terms of why allergens cause different reactions in asthmatics to non-asthmatics, genes are thought to play a factor. Asthmatics have a slightly different set of proteins (interleukins) that initially respond to the allergen.
Hopefully that clears some things up a bit...
Shane
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