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WEEK 16:
Asthma: diagnosis, monitoring, pathophysiology and management:
| Question | Answer |
|---|---|
| asthma | auto-immune chronic airway hyper responsiveness and airway inflammation with respiratory symptoms eg wheeze, SOB, tight chest, cough, and reversible airflow obstruction |
| FEV1: FVC in asthma | decreased (less than 70%) due to obstruction, suggesting increased airway resistance |
| what helps reverse the effects of asthma | B2 agonists |
| what provokes asthma | allergens, cold air, viral infections, smoking, exercise, and drugs |
| how does forced spirometry work | measure volume of air patients (children aged 5- adults) can exhale after maximal inhalation |
| advantage of using forced spirometry | evaluates small and larger airways for diagnosis and differentiates between obstructive and restrictive diseases |
| disadvantage of using forced spirometry | costly, takes time to perform, requires training |
| how to calculate the volume/time curve for spirometry | FEV1.0 / FVC |
| objective tests for diagnosing asthma | FeNO (fractional exhaled nitric oxide), spirometry, and BDR (bronchodilator reversibility) |
| fractional exhaled nitric oxide (FeNO) | for ages 17 and over, looks for eosinophilic airway inflammation or atopy |
| atopy | asthma, eczema, and hay fever |
| bronchodilator reversibility (BR) | for ages 17 and over with obstructive spirometry (FEV1:FVC less than 70%). If they improve with 12% or more using 200ml or more, it is a positive test (asthmatic) |
| peak expiratory flow (PEF) / peak flow test | maximum ability to exhale air |
| advantage of PEF | useful for monitoring disease rather than making initial diagnosis |
| SNS in lungs | B2 receptors which stimulate bronchodilation and decrease mucus production |
| ANS in lungs | M3 receptors which stimulate bronchoconstriction and increase mucus production |
| receptors in SNS lungs | B2 |
| receptors in ANS lungs | M3 |
| difference between COPD and asthma | airway obstruction is reversible in asthma and COPD is not |
| explain the pathophysiology of asthma | first exposure, B cells make allergen specific IgE which binds to mast cell receptors. In subsequent exposures, allergen cross links to IgE on mast cells causing degranulation and release of mediators/ spasmogens. |
| early phase asthma (3) | infiltration of eosinophils, T-lymphocytes (release cytokines), mast cells, and goblet cells (make mucous). Late phase airways become more responsive to triggers but there is long term damage if untreated |
| how is asthma responsive | steroid responsive |
| types of spasmogens | histamine, prostaglandin D2, leukotrienes (C4 & D4) |
| types of chemotaxins | leukotrienes B4 and PAF |
| what happens in late phase asthma | mast cells release chemotaxins leading to inflammation |
| aim of asthma treatment (7) | no day-time symptoms, does not wake you up at night, no need for rescue medication, no asthma attacks, does not limit activity eg exercise, normal lung function (FEV2/ FVC of >80%), and minimum side effects of medication |
| salbutamol and terbutaline | B2 adrenoceptor agonist which is short-acting (SABA) |
| salmeterol | B2 adrenoceptor agonist which is long-acting (LABA) |
| B2 adrenoceptor agonists | salbutamol and salmeterol |
| when is LABA given | as add on therapy for long term prevention and long term control (overnight) |
| what happens with prolonged use of B2 adrenoceptor agonist (especially LABA) | leads to receptor down regulation (less sensitivity) |
| intermittent reliever therapy | inhale short acting B2 agonists which helps manage symptoms but does not control underlying inflammation |
| benefits of B2 agonists that tablets/ syrup | work more quickly with fewer side effects |
| which individuals with asthma should be assessed regularly | those with more than one short-acting bronchodilator inhaler a month |
| how does salbutamol work | salbutamol binds to B2 receptor activating G-protein separating into alpha and betagamma. a-GTO binds to adenylyl cylase converting ATP -> cAMP. cAMP activates PKA leading to relaxation of smooth muscle in bronchi. |
| treatment for those who have infrequent asthma/ short-lived wheeze and normal lung function / newly diagnosed asthma | SABA reliever therapy ONLY |
| corticosteroids | anti-inflammatory by activation of intracellular receptors leading to altered gene transcription (decrease cytokine production) and production of lipocortin (annexin A1) |
| examples of corticosteroids | beclometasone (ICS) and prenisolone (oral) |
| importance of lipocortin | inhibits phospholipase A2 which stops the conversion of phospholipids in arachidonic acids so that mediators cannot be made, thus stopping inflammation |
| starting dose of steroids in adults aged 17 and older | 2 puffs bd of 100 micrograms beclometasone dipropionate via a spacer |
| starting dose of steroids in children aged 5-16 | 2 puffs bd of 50 micrograms (depends on factors eg severity of condition and person's size) |
| ICS meaning | inhaled corticosteroids |
| side effects of ICS | hoarseness, dysphonia (voice disorder), throat infections, oral candidiasis (fungal infection), and risk of developing diabetes |
| consequence of higher doses of ICS | reduce bone density, skin thinning, bruising, and increased risk of pneumonia |
| how to reduce the likeliness of throat infections/ oral candidiasis | rinse out mouth |
| what should happen to those with uncontrolled asthma at any age | offer leukotriene receptor antagonist (LTRA) with low does of ICS and review treatment in 4-8 weeks |
| types of leukotriene receptor antagonist (LTRAs) | montelukast and zafirlukast |
| LTRA dose for adults | orally 10mcg nocte |
| nocte meaning | at night |
| LTRA dose for children aged 6-15 | orally 5mc nocte |
| when is LTRA given | when patient has poor control/ do not respond to LABA |
| when are children aged 6 months - 6 years given LTRAs | those using SABA/ cannot give ICS / using ICS at the same time |
| LTRA dose for children aged 6 months - 6 years | 4mcg nocte |
| how do leukotriene receptor antagonist (LTRAs) act | block leukotriene receptor |
| maintenance and reliver therapy (MART) | single inhaler has both ICS and fast acting LABA for BOTH relieving symptoms and daily maintenance therapy |
| example of MART | formoterol |
| methylxanthine example | theophylline |
| why isnt theophylline given | gives added persistent symptoms and has narrow therapeutic range |
| instead of theophylline, what is given as an add on therapy in asthma/COPD management | aminophylline |
| signs of theophylline toxicity | cardiac dysrhythmia, seizure, and GI disturbances |
| when are dosages of theophylline/ aminophylline increased | when patient is a smoker |
| theophylline therapeutic range | 10-15mcg/mL |
| 15-25mcg/mL of theophylline | GI upset, diarrhoea, abdominal pain, and headache |
| 25-35mcg/mL of theophylline | tachycardia |
| how does theophylline work | stops conversion of cAMP into AMP (in second messenger model) by inhibiting phosphodiesterase (PDE) III and IV, leading to bronchodilation |
| monoclonal antibodies example | omalizumab and benralizumab |
| how do monoclonal antibodies work | stop mediators being released by preventing IgE from binding to immune cells and basophils |
| benralizumab | monoclonal antibody (mAb) used for treating eosinophilic asthma |
| mast cell stabilisers example | sodium cromoglicate (cromoglycate), which is given by inhalation |
| how do mast cell stabilisers work | used as a prophylactic anti-inflammatory drug by preventing activation of inflammatory mediators (rarely used now) |
| explain the contraindication of NSAIDs (non steroidal anti inflammatory drugs) and asthma | NSAIDs may provoke asthma by increasing production of leukotrienes |
| NSAID | non steroidal anti inflammatory drugs |
| examples of NSAIDs | aspirin and ibuprofen |
| compare smoking in COPD and asthma | nearly all smokers have COPD but only some in asthma |
| compare symptoms under age 35 in asthma and COPD | rare in COPD but often in asthma |
| compare chronic productive cough in COPD and asthma | common in COPD and uncommon in asthma |
| compare breathlessness in COPD and asthma | persistent and progressive in COPD but varies in asthma |
| compare day to day (diurnal) variability of symptoms eg waking up with breathlessness at night in asthma and COPD | uncommon in COPD common in asthma |
| types of inhaler (2) | pMDI (aerosol forming) and DPIs (make your own aerosol) |
| types of pMDI inhalers | ventolin, spiriva respimat, easi breathe, and breath acuted |
| types of DPIs inahlers | accuhaler, turbohaler, handihaler, and easyhaler |
| COPD symptoms | easily fatigued, wheezing, chronic cough, bronchitis which increases sputum etc |
| what makes COPD | chronic bronchitis and emphysema |
| chronic bronchitis leads to | increased mucus, airway obstruction, intercurrent infections |
| emphysema leads to | destruction of alveoli |
| PEF in COPD | little variation |
| FEV1 in COPD | reduced |
| what can COPD range from according to GOLD guideline (4) | mild, moderate, severe and very severe |
| how do anti muscarinics/ muscarinic antagonists work in COPD | treatment given by inhalation which blocks m3 receptors so Ach cannot bind so no bronchoconstriction and no increase in mucus. |
| ipratropium | short acting muscarinic antagonist (SAMA) |
| tiotropium | long acting muscarinic antagonist (LAMA) |
| how can better efficacy be achieved with muscarinic antagonists in COPD | combine it with SABA |
| when are muscarinic antagonists used in COPD | in acute severe asthma / life threatening asthma as combination therapy in COPD |
Created by:
kablooey
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