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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 | measures maximal volume of air exhaled after forced 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, and 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) as an objective test for diagnosing asthma in adults, young people, and children aged 5 and over | for ages 17 and over, looks for eosinophilic airway inflammation or atopy |
| atopy | asthma, eczema, and hay fever |
| bronchodilator reversibility (BR) as an objective test for diagnosing asthma in adults, young people, and children aged 5 and over | 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 |
| sympathetic pathway (ANS) in lungs | B2 receptors which stimulate bronchodilation and decrease mucus production |
| parasympathetic pathway (ANS) in lungs | M3 receptors which stimulate bronchoconstriction and increase mucus production |
| difference between COPD and asthma | airway obstruction is reversible in asthma and COPD is not and asthma can be classified as eosinophilic or non eosinophilic |
| 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) - leading to bronchospasm |
| types of chemotaxins | leukotrienes B4 and PAF - leading to inflammation |
| 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. Works more quickly than alternatives (tablet and syrup). Those prescribed more than one short acting bronchodilator inhaler should be assessed |
| benefits of B2 agonists that tablets/ syrup | work more quickly with fewer side effects |
| which individuals with asthma should be assessed urgently | 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 for adults (aged 17 and over) |
| corticosteroids | preventor for asthma (do not reverse an attack). Is an 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) |
| 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 (adults aged 17 and older and children and young people aged 5-16yrs) | offer leukotriene receptor antagonist (LTRA) with low does of ICS and review treatment in 4-8 weeks |
| examples 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 who do not respond to LABA/ poor control with steroid and LABA | orally 5mg nocte |
| when is LTRA given to adults and children 6-15yrs | 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 reducing inflammation, bronchoconstriction, and mucus production in conditions like asthma and allergic rhinitis. |
| maintenance and reliver therapy (MART) | single inhaler has both ICS and fast acting LABA for BOTH relieving symptoms and daily maintenance therapy |
| example of fast acting component in MART | formoterol |
| theophylline bronchodilator | type of methylxanthine that has added persistent symptoms despite ICS, with a narrow therapeutic range, |
| 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 |
| theophylline mechanism of action | 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 (stop arachidonic acid from releasing prostaglandins but leukotrienes still made) |
| 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 and DPI |
| 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 with limited/ little value in asthma (used mainly in COPD) |
| spirometry as an objective test for diagnosing asthma in adults, young people, and children aged 5 and over | offered to adults, young people and children aged 5 and over if diagnosis of asthma still be considered - regard a FEV/FVC ratio of less than 70% as positive for obstructive airway disease (obstructive spirometry) |
| approach to management in asthma | start treatment at level most appropriate to initial severity, achieve early control, and maintain control by increasing treatment as necessary and decreasing treatment when control is good |
| beclometasone | ICS corticosteroid |
| prednisolone | oral corticosteroid |
| corticosteroid mechanism of action | bind to receptor -> nucelus -> mRNA -> make lipocortin/ Annexin A1 -> lipocortin inhibits phospholipase A2 -> stop phospholipids from releasing arachinoic acids -> thus stopping cyclooxygenase and lipoxygenase pathway |
| how do prescribers choose steroid dosage for children under 5 years and young people aged 12-16 | consider factors such as severity of condition and the person's size |
| suffix for corticosteroids | one |
| suffix for leukotriene receptor antagonists (LTRAs) | kast |
| suffix for B2 adrenoceptor agonists | ol |
| MART | maintenance and reliever therapy (MART) is a form of combined ICS and fast acting LABA in which a single inhaler for both daily maintenance therapy and symptom relief |
| what components of MART are needed | only available for ICS and LABA combinations in which LABA has a fast acting component eg formoterol |
| when is aminophylline given | as an add on therapy in the management of asthma/ COPD |
| monoclonal antibodies suffix | mab |
| omalizumab mechanism of action | directed against free IgE but not bound to IgE- prevent IgE from binding to immune cells and basophils (decrease allergic mediators and response) |
| when is omalizumab used | management of allergic asthma |
| when is benralizumab used | used for treating severe eosinophilic asthma |
| how are anti muscarinics/ muscarinic antagonists/ parasympatholytics given | via inhalation |
| what treatment is usually used in COPD | anti muscarinics |
Created by:
kablooey
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