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PBL PHC561 GROUP E2, :check: step 3, :heavy_plus_sign:, when history of…

- - - - Originally referred to as "Aspirin-Induced Asthma" (ASA)
    - - moderate to severe asthma
      - a higher prevalence of chronic rhinosinusitis (CRS) with nasal polyps (NPs)
      - persistent eosinophilic inflammation in upper and lower airways
      - hypersensitivity to ingestion of aspirin and other COX-1 inhibiting NSAIDs
        
        Cause exacerbation of symptoms
        
        Commonly used NSAIDs:
        
        Aspirin
        
        Ibuprofen
        
        Naproxen
  - - - NSAID induced asthma patients: NSAIDs cause overproduction of pro-inflammatory leukotrienes cause exacerbations of asthma.
        
        Higher level of CysLTS is derived from numerous inflammatory cells
        
        Expression of 5-LO & LTC4S is increased
        
        Release of PGD2 from mast cell & eosinophils is increased
        
        Levels of PGE2 is reduced
        
        Expression of EP2 receptor is lower
        
        2 more items...
        
        Signal of 5-LO pathways cannot be suppressed
        
        Binds to prostanoid receptor
        
        Induce bronchoconstriction
        
        Binds to chemoattractant receptor-homologous molecule
        
        Induce chemotaxis & accelerate type 2 airway inflammation
        
        Induce bronchoconstriction & increase inflammatory signal pathways
    - - Chronic inflammation
        
        Persistent eosinophil activation & CysLTs overproduction.
        
        Inflammatory cells in NERD is interacting with a structural cell
        
        Th2 cells and ILC2 release IL-4, IL-5 and IL-13
        
        Activation of the mechanism of eosinophils
        
        Release eosinophil extracellular traps
        
        Interact with epithelial cells and autocrine functions of eosinophils in asthmatic airway
      - Severe inflammation
        
        Activation of neutrophils
        
        Increase in LTB4 and reactive oxygen species release after N-formyl-methionyl-leucyl-phenylalanine stimulation
      - Severe and persistent
        
        Platelet-aggregated granulocytes
  - - - Patient education and counselling
        
        To avoid COX-1 inhibitors and identification of well-tolerated alternative drugs for the management of other comorbidities
      - Low salicylic acid diet
        
        To improve the nasal symptoms and nasal endoscopy findings of individuals with AERD
      - Increased dietary intake of omega-3 fatty acids
        
        To elevate metabolic products of eicosapentaenoic acid that able to induce low level of inflammatory biologic activity
    - - Anti inflammatory
        
        Inhibit the phospholipase A2 in the arachidonic acid pathway
        
        Types of administration
        
        Inhaler
        
        Reduce the severity of rhinitis symptoms, as well as the size and growth of new polyps in the nasal and sinuses
        
        Triamcinolone and fluticasone
      - Leukotriene modifier
        
        5-lipoxygenase inhibitors
        
        impairs leukotriene production by selective inhibition of ALOX5
        
        Zileuton
        
        Leukotriene receptor antagonist
        
        block the binding of cysteinyl leukotriene on cysteinyl leukotriene receptors 1 (CysLTR1)
        
        decrease the vascular permeability
        
        reduce edema
        
        induce dilation of airway smooth muscle
        
        montelukast, zafirlukast
      - Mononclonal antibodies
        
        Block specific pathway in severe asthma
        
        Bind and block the specific target molecule such as anti-IgE and anti- interleukin 5
        
        Example of drugs:
        
        Mepolizumab and reslizumab
        
        blocks the binding of IL-5 to its receptor
        
        reduce the production and survival of eosinophils
        
        Omalizumab
        
        binds to circulating IgE in the blood and tissues
        
        acts rapidly to block cross-linking of IgE receptors on mast cells and basophils
        
        preventing allergic activation
        
        gradually down regulates IgE receptor expression on various immune cells
        
        Benralizumab
        
        blocks the effect of IL-5 on eosinophils
        
        induce antibody-mediated cell cytotoxicity
        
        eosinophil cell death
      - Beta-2 agonists
        
        Activation of beta-2 receptor
        
        Stimulation of adenylyl cycase & phosphorylation of target protein by PKA
        
        induce bronchial smooth muscle relaxation
        
        Long-Acting B Agonist (LABA)
        
        formoterol and salmeterol
        
        Short Acting B Agonist (SABA)
        
        albuterol, salbutamol, terbutaline
    - - The use of leukotriene modifiers drugs (LMD) as pre-treatment
        
        Given one week before oral aspirin challenges
        
        Able to enhance the safety of oral aspirin challenge
      - Conducted by reintroducing aspirin
        
        Begin with low dose and gradually increase the dose every 60-120 minutes
        
        The treatment is complete after patient able to achieve the highest dose of aspirin
  - - - AND/ OR
        
        Reliable history of reaction to NSAIDs
        
        the reliability increase if there is:
        
        more than 1 reaction occured
        
        reaction to two or more different NSAIDs have been reported within last 5 years
        
        respiratory symptoms accompanied by skin and gastrointestinal (GIT) symptoms
        
        Underlying chronic respiratory disorder with nasal polyps and / or asthma
        
        the clinical characteristic increase N-ERD probability if there is:
        
        high recurrence of nasal polyps
        
        loss of smell
        
        moderate to severe asthma
        
        intolerance to alcohol
        
        having blood eosinophilia
        
        if answer to one of step 2 and 3 is negative or uncertain
        
        ask about non-respiratory symptoms after intake the NSAIDs and check the potential trigger of reported reactions
        
        AND/ OR
        
        Presence of chronic airway disease uncertain and asthma
        
        1 more item...
        
        :check:step 2
  - - - Upper respiratory symptoms
        
        Increased nasal congestion
        
        Sinus pain
        
        Sneezing
      - Lower respiratory symptoms
        
        Coughing
        
        Wheezing
        
        Chest tightness
      - Cutaneous symptoms
        
        Skin flushing
        
        Urticaria
      - Gastrointestinal symptoms
        
        Occasional vomiting
      - May develop 30-180 minutes
    - - Eg: Chronic rhinosinusitis with nasal polyps (CRSwNP)
        
        Upper respiratory symptoms
        
        Nasal blockage
        
        Nasal congestion/ stuffiness
        
        Nasal discharge
        
        Facial pain or pressure
        
        Others
        
        Ability to smell
        
        Partial loss of smell
        
        Anosmia (complete loss of smell)
        
        On upper CT scan
        
        N-ERD patient has severe sinus opacification
  - - - It is reported to be 5.5% to 12.4% in the general population, 7.1% among adult asthmatics, 14.9% among severe asthmatics and it rarely occurs in children.
      - Not much has been reported in Malaysia. This is might due to under reported
    - - Patient related risk factor (En Osman)
        
        Asthma
        
        The airways in an asthmatic patient's lungs are already constricted and the wall is thickened, any biochemical cascade, such as leukotriene induced by the action of NSAID, can influence the patient and cause N-ERD.
        
        Stress life
        
        Work-related stress
        
        Might happen due to long hours of working and heavy workload
        
        It affects the patient's health and well-being.
        
        Chronic rhinosinusitis associated with nasal polyps
        
        Nasal polyps cause swelling, redness and fluid build-up in the nasal cavities.It is worsening the asthma. When an NSAID is taken, a biochemical reaction occurs, causing the patient's condition to deteriorate and NERD to develop.
        
        Rhinosinutis is an inflammation occurs in nasal cavity and paranasal sinuses. It has the presence of fleshy swellings (nasal polyps) that develop in the lining of the nose and paranasal sinuses
      - Other common risk factor
        
        Family history
        
        It represents common behaviours, shared environment, and inherited genetic predisposition.
  - - - Refers to when there is an obstruction of the air flow in and out of the nose.
    - - The measurement of air flowing out of the lung.
    - - Episodes of worsening of the asthma symptoms.
- - - - COPD
      - Obesity
      - Metabolic Syndrome
      - Diabetes melitus
    - - Gastro-oesophageal Reflux Disease (GERD)
        
        a digestive disorder that occurs when stomach acid frequently flows back into the tube connecting the mouth and the oesophagus
        
        Frequent exposure to acid can make the lungs become more sensitive to irritants which can trigger asthma
        
        Acid reflux may trigger a protective nerve reflex, causing the airways to tighten which can result in shortness of breath.
        
        Acid damages the lining of the throat and the airways to the lungs can lead to breathing difficulties as well as a persistent cough.
        
        Released of pro-inflammatory mediators can increase airway resistance and inflammation, aggravating asthma symptoms.
      - Chronic Rhinosinusitis (CRS)
        
        common upper airway disease, which is characterized by chronic inflammation of nasal mucosa and paranasal sinuses
        
        Nasal obstruction can results in breathing difficulty making asthma harder to control.
        
        Postnasal drip can aggravate asthma symptoms.
  - - - Excess fluid that drains from the nose. It is usually a thin and clear discharge.
    - - Operation to remove polyps located in the nasal passage.
    - - Waking up in the middle of the night
    - - To check for immediate allergic reaction
  - - - Obesity
      - Gender & Sex Hormones
      - Smoking
      - Respiratory tract infections
      - Psychosocial Factors
    - - Chronic Rhinosinusitis (CRS) with nasal Polyps
        
        Commonly related to asthma
        
        En. Osman experiences chronic persistent nasal obstruction with rhinorrhea, loss of a sense of smell and required 2 nasal polypectomy operations.
      - Stress
        
        Ec. Osman was stressed due to long working hours, carry a heavy workload because he is a manager and maybe also due to the comfortability of himself where he needs to work in confined space when he is a junior technician.
        
        Get AOA due to work-related stress
      - Occupational exposures
        
        AOA can be caused by exposure to chemicals or irritants in the workplace as he worked soldering printed circuit boards (exposure to rosin-based solder flux fumes) and spends the majority of his time in the air-conditioned office.
  - - - Smoking
      - Drugs
        
        NSAIDs
        
        Aspirin
        
        Beta-blockers
      - Weather
      - Sinusitis
      - Allergens
        
        Pollen
        
        Dust
        
        Food and food additives
        
        Pests
    - - Heartburn
      - Cold air (from airconditioning room)
        
        En. Osman spent most of his working time in his air-conditioned office
      - Exposure to chemicals or irritants
      - Excercise
        
        En. Osman experiences cough and shortness of breath during his early morning run
  - - - Compared to the asthma in childhood
        
        Adult-onset is associated with more respiratory symptoms
        
        AOA is not a heritable disease
        
        Many cases of adult-onset asthma are triggered by allergies