HCP 10: Frances DiAnza Asthma Flashcards
What is Hay Fever?
Allergic Rhinitis
Causes cold-like symptoms (runny nose, itchy eyes, congestion, sneezing, sinus pressure), but not caused by virus (no fever, body aches, yellow discharge)
Onset is immediately after exposure & lasts for as long as you’re exposed
Causes: Tree/grass pollen, spores, cockroach, dust mites
Risk factors: FHx, nasal polyps, other allergies
Pathogenesis: Type I hypersensitivity IgE
Treatment: Nasal corticosteroids, reduce exposure, anti-histamines
How to Anti-histamines work?
Block target tissue response to histamine 1st generation (benadryl): reversibly bind & stabilize inactive form of H1 receptor (more lipophilic, so cross BBB-> drowsiness) 2nd gen (Claritin): Specific for H1 receptor (not lipophilic, doesn't cross BBB)
Why does aspirin sometimes induce asthma?
Aspirin inhibits COX2 -> inhibit synthesis of PG -> shunts substrates into 5-lipoxygenase pathway -> increase leukotriene production -> leukotrienes cause potent bronchoconstriction & bronchospasm
How does albuterol cause hypokalemia?
Albuterol: Binds to B2 receptor -> activates AC -> increases cAMP -> stimulates activity of Na/K ATPase (Na out, K in), so more K shifted inter cellularly (transient hypokalemia)
What is the MOA of solumedrol? prednisone?
It's a steroid... Binds to cytosolic glucocorticoid receptor translocates to nucleus Binds to nuclear response elements -Lipocortin 1 synthesis -> inhibit PLA2 synthesis -> decrease AA activation -suppress humoral immunity -Decrease cytokine gene expression -Decrease inflammation
Why do we need to taper steroids?
Steroids cause suppression of HPA axis, causing decreased ability to make normal amounts of hormones (i.e. cortisol). Tapering prevents adrenal insufficiency.
How should we assess intubation?
LEMON score: L-look for characteristics that predict difficulty E-Evaluate M-mallampati score (extend neck, "ah") O-Obstruction N-Neck mobility
What are the indications for intubation?
Hypoxia/hypercapnia Respiratory distress Failure to maintain patent airway Failure of oxygenation and/or ventilation Anticipate rapidly deteriorating course
Contraindications for intubation?
DNI, difficulty, expanding neck hematoma
Why do we use mechanical ventilation?
Used to assist/replace spontaneous breathing
Decrease work of breathing & avoid resp. muscle fatigue
Reverse hypoxia/acidosis
Optimize oxygenation while avoiding overstretch or collapse
What are some different types of mechanical ventilation?
Non-invasive - mask
Assist-control: Set TV delivered & additional breaths given if triggered by patient
SIMV: provides breath if patient triggers below set rate or if they don’t breath
Pressure-support: only patient-triggered
Continuous: Set TV no matter what patient does
What is PEEP?
Pulmonary expiratory end-pressure
how much pressure left in alveoli at the end of expiration (usually set to 5cm to prevent collapse of airways)
What is FiO2?
Fraction of inspired O2
Usually 21% and increases 4% for every 1L O2
What is asthma?
Chronic inflammatory disorder causing episodes of wheezing, breathlessness, chest tightness, and cough (esp. at morning/night)
Reversible airflow obstruction w/ contraction of SMC & hyper responsive airways
Why do we see a decreased FEV1/FVC?
Bronchoconstriction -> increased resistance -> decrease flow rate
What is the Residual volume in an asthma attack? How is that different from COPD?
RV=volume of air in lung left after maximal expiration
Bronchoconstrictiction -> increased resistance -> decreased expiration of air @ typical intrathoracic pressure.
In emphysema, increase in RV due to air trapping in smaller airways (not hypertrophy/bronchoconstriction)
Why is wheezing mainly heard on expiration? How is it different from COPD?
Increase in intrathoracic pressure during expiration causes further constriction of airways -> more difficult for air to flow -> turbulent & noisy airflow
In COPD, bronchospasm rarely occurs. Extensive parenchymal destruction promotes airway collapse at high intrathoracic pressure
Why are albuterol/salmeterol preferred to isopreteronol?
they are selective B2 agonists. Isopreteronol is non-selective, so it will have effects on the heart (tachycardia & palpitations).
What shouldN’T we give to asthmatics?
B-blockers (unless it’s a B1 selective blocker), otherwise we could trigger bronchospasms
What is the MOA of theophylline?
Non-selective phosphodiesterase inhibitor
Inhibits PDE in SMC
Decrease breakdown of cAMP to AMP
Increased cAMP
Bronchodilation
*Also inhibits adenosine to decrease bronchoconstriction.
What is the MOA of Zafirlukast?
Leukotriene receptor antagonist
Selectively & reversibly inhibits cysteinyl LT 1 receptor for LTD4/E4
Decrease LTD4/E4 binding
Decrease bronchiolar SMC contraction, airway edema, and eosinophil migration
What is the MOA of Zileuton?
Leukotriene antagonist
Inhibits 5-lipoxgenase in cells of myeloid origin
inhibit formation of LT from AA
LTB4: Decrease eosinophil/neutrophil migration
LTC4, D4, E4: Decrease SMC contraction, vascular permeability, and mucus secretion
What is the MOA of cromolyn sodium?
prophylaxis
Binds to mast cell & stabilize, decrease Ca2+ influx, inhibit mast cell degranulation, decrease release of LT, histamine, & SRSA, decrease infl.
Also stabilizes airway nerves to decrease hyperreactivity of bronchi. Decrease response to antigen, environment, or exercise
What is the MOA of omalizumab?
Monoclonal Ab
Inhibit IgE binding to FCeRI receptor on mast cell, decrease release of infl. mediators
Decrease free IgE in serum
Decrease presentation of IgE receptors on mast cells & basophils
