Asmtha Flashcards
What is the underlying pathophysiology of asthma?
Asthma is a chronic inflammatory disorder causing airway hyperresponsiveness, reversible airflow obstruction, and bronchial inflammation.
What immune response is primarily responsible for asthma?
Asthma is mediated by IgE against environmental antigens, leading to mast cell degranulation, eosinophilic inflammation, and bronchoconstriction.
At what point in the pulmonary system is the smooth muscle constriction that leads to wheezing and decreased inspiratory-to-expiratory ratio?
The symptoms of asthma are primarily caused by inflammation of the terminal bronchioles. Terminal bronchioles are lined with smooth muscle but lack the cartilage found in larger airways. When an allergen triggers a hypersensitivity reaction there is bronchial submucosal edema and smooth muscle contraction and the airways collapse, as they don’t have the support of cartilage. This collapse leads to the symptoms of asthma.
What are common triggers of asthma?
Allergens, tobacco smoke, air pollution, respiratory infections, cold air, and exercise.
What is the most common organism that is associated with asthma?
house dust mite.
At what age is asthma typically diagnosed?
Asthma is rarely diagnosed before 2-3 years of age due to lung development. It is important to not that lungs don’t stop growing until 8 years old.
What are the hallmark symptoms of asthma?
Intermittent dyspnea, wheezing, chest tightness, and dry cough.
What are the characteristic lung function changes during an asthma exacerbation?
Decreased FEV1, normal FVC, and increased TLC over time due to air trapping.
How is asthma diagnosed?
Clinical diagnosis confirmed by spirometry showing reversible airflow obstruction (≥12% and 200 mL improvement in FEV1 after bronchodilator).
What tests are used if spirometry is inconclusive?
Methacholine challenge or exercise challenge testing or exercise challenge. There can occasionally be a diagnosis established due to “workplace exposure.”
If a patient says they might be allergic to “work,” should you take it seriously?
Yes!
How is intermittent asthma classified?
- Symptoms <2 days/week
- Night awakenings <2 times/month,
- Normal lung function (FEV1 >80%)
- ≤1 exacerbation per year
What is the treatment for intermittent asthma (Step 1)?
Short-acting beta-agonist (SABA) such as albuterol as needed.
What is mild persistent asthma?
- Symptoms ≥2 days/week
- Night awakenings 3-4 times/month,
- FEV1 >80%
- ≥2 exacerbations per year.
What is the treatment for mild persistent asthma (Step 2)?
Low-dose inhaled corticosteroid (ICS) and SABA as needed.
What is moderate persistent asthma?
- Daily symptoms
- Night awakenings >1 time/week
- FEV1 60-80%
- ≥2 exacerbations per year
What is the treatment for moderate persistent asthma (Step 3)?
Low-dose ICS + long-acting beta-agonist (LABA) such as formoterol or salmeterol.
What is severe persistent asthma?
- Symptoms throughout the day
- Nightly awakenings
- FEV1 <60%
- Frequent exacerbations
What is the treatment for severe persistent asthma (Step 4-5)?
High-dose ICS + LABA, with the addition of biologics or oral steroids if necessary.
Which biologic is used for asthma with high IgE levels?
Omalizumab (anti-IgE).
Which biologics are used for eosinophilic asthma?
Mepolizumab and dupilumab (anti-IL-5/IL-4).
What leukotriene receptor antagonists can be used in asthma, what can develop as a consequence?
Montelukast and zafirlukast. Montelukast can be associated with ANCA-associated vasculitis (EGPA/Churg-Strauss Syndrome, eosinophilic granulomatosis with polyangiitis), P-ANCA (MPO-ANCA). In general, asmatics are at increased risk for developing P-ANCA-associated vasculitides, particularly Eosinophilic Granulomatosis with Polyangiitis (EGPA, formerly Churg-Strauss Syndrome), even without taking montelukast. Treatment of EGPA includes corticosteroids and immunosuppressants (e.g., cyclophosphamide, rituximab, mepolizumab in refractory cases). Churg-Strauss syndrome is characterized by perivascular eosinophilic inflammatory infiltrates and presents with asthmatic symptoms and pulmonary infiltrates. It is also typically accompanied by allergic rhinitis, sinusitis, nasal polyps, and skin lesions. Additionally, patients may also experience mononeuropathy multiplex is a condition characterized by damage to multiple, isolated peripheral nerves, resulting in weakness, numbness, tingling, and pain in various parts of the body.
What are the more common side effects associated with leukotriene receptor antagonists?
Elevated liver enzymes (zileuton) and neuropsychiatric symptoms (montelukast).
What is the most common cause for an acute asthma exacerbation?
The most common trigger is viral upper respiratory infection, which is suggested by this patient’s recent nasal congestion, sore throat, and myalgia.
What is the first step in managing an asthma exacerbation?
Assess severity, provide oxygen to maintain SpO2 >92%, and administer nebulized SABA (albuterol) with SABA (ipratropium), Intravenous magnesium sulfate, and systemic corticosteroids.
When are systemic steroids given for asthma exacerbation?
If symptoms are severe or if there is poor response to initial bronchodilator therapy. For example, a patient with 3 days of cough, wheezing, and shortness of breath is clearly an increase in asthma symptoms. Symptoms combined with a >20% reduction in peak expiratory flow rate are very concerning. Mild exacerbations in the outpatient setting that have been unresponsive to standard inhaler therapy (eg, no improvement despite increasing inhaled corticosteroid-formoterol) is grounds for steroid treatment. Additionally, any moderate to severe acute asthma exacerbations in the urgent care or emergency department. Emergency medical care is necessary for patients with severe symptoms (eg, hypoxemia, difficulty speaking, use of accessory muscles, reduction in peak expiratory flow >50% from baseline); however, those with mild symptoms, can be treated on an outpatient basis. Patients treated promptly with a short course of systemic corticosteroids have fewer future exacerbations requiring hospitalization and have improved long-term asthma control. The optimal dosage and duration of corticosteroid therapy are not strictly defined; however, general recommendations are prednisone 40-60 mg daily for 5-10 days.
What medication is added (in addition to SABA, SAMA, and steroids) for severe exacerbations unresponsive to initial treatment?
IV magnesium sulfate.
What sign suggests impending respiratory failure in an asthma exacerbation?
Normalizing or rising PaCO2 despite tachypnea, indicating ventilatory failure and need for intubation.
A 24-year-old woman presents to the emergency department with three hours of severe shortness of breath. The patient has severe persistent asthma and has already been hospitalized twice this year due to exacerbations. The patient has never been intubated for mechanical ventilation. Her temperature is 37.0°C (98.6°F), pulse is 105/min, respirations are 28/min, blood pressure is 110/70 mmHg, and oxygen saturation is 93%. Diffuse wheezing is heard on pulmonary auscultation. Initial arterial blood gas shows pH of 7.49 and pCO2 of 22 mmHg. The patient is given intravenous magnesium and methylprednisolone and is started on supplemental oxygen. Two hours later, the patient is re-evaluated and appears more fatigued, and she is no longer tachypneic. Minimal wheezing is noted on pulmonary auscultation. Repeat arterial blood gas shows pH 7.37 and pCO2 of 47. Which of the following is the most appropriate next step in the management of this patient?
Patients presenting with dyspnea should be assessed immediately for signs of impending respiratory failure. Oxygen saturation (SpOz) <90% and/or significantly decreased (<10/min) or increased (>20/min) respiratory rate indicates severe disease and a higher risk of decompensation. Moreover, patients with stridor, oropharyngeal swelling, conversational dyspnea, or significant accessory muscle use require close monitoring and are at very high risk for respiratory compromise. Endotracheal intubation and mechanical ventilation should be pursued early in such high-risk patients as it provides airway protection, and improved oxygenation and ventilation. Asthma exacerbations are a frequent cause of severe dyspnea in younger patients. Initial treatment involves intravenous corticosteroids and magnesium, and nebulized short-acting bronchodilators (e.g., albuterol, ipratropium). Patients present with diffuse wheezing and tachypnea, frequently causing a resultant low pCO2 on arterial blood gasses (ABG). If patients begin to appear more tired, repeat ABG should be performed. In impending respiratory failure, the patient’s minute ventilation drops, and pCO2 may actually appear “more normal” as it increases closer to or above 40. As patients approach respiratory failure, wheezing may actually lessen due to less air moving through narrow and inflamed airways. Endotracheal intubation should be performed at this point to provide oxygen supplementation via mechanical ventilation.
How are patients managed in terms of admissions or discharge after experiencing an acute asthmatic exacerbation?
In patients with acute asthma exacerbation who are being treated in the emergency department, disposition (eg, discharge home versus admit to medical floor or intensive care unit) is guided by their response to initial treatment (ie, bronchodilators). Patients should be frequently reassessed in the emergency department over a period of 2-4 hours. Reassuring signs of asthma attack resolution include decreased work of breathing (eg, less accessory muscle use), normalization of tachypnea and tachycardia, relief of dyspnea, and improvement of air flow (increased breath sounds, increased peak expiratory flow rate). Most patients improve quickly after administration of bronchodilators (eg, inhaled short-acting beta-2 agonist and muscarinic antagonist). Systemic corticosteroids are administered concurrently to dampen the late-phase inflammatory response, but onset is delayed 6-12 hr) due to their slower nuclear transcriptional mode of action. Some patients have a poor or delayed response to acute bronchodilator therapy (ie, status asthmaticus). They are at risk for further clinical deterioration (eg, respiratory fatigue, worsening gas exchange) requiring additional intervention (eg, mechanical ventilation) and escalation to a higher level of care. Therefore, patients should be periodically reassessed (typically over 2-4 hr) in the emergency department during bronchodilator treatment before a disposition decision is made. Patients who respond briskly to ED management (excellent symptom resolution and a reassuring physical examination after a period of observation) can be discharged home with close follow-up, a short-course of oral corticosteroids (eg, prednisone 40-60 mg/day x 5-10 days), and a step-up in the existing controller regimen (eg, increased inhaled corticosteroid dose). This patient’s response to treatment should be monitored before deciding on discharge. Patients who have an intermediate response are those who demonstrate some improvement but are neither well enough to discharge nor ill enough to intubate for mechanical ventilation. They should be admitted to the general medical floor for ongoing care. This disposition is also reasonable for the subgroup of patients with an initially reassuring response but who have historical risk factors for fatal asthma (eg, previous intubation, frequent need for emergency care). Patients with signs of impending respiratory failure such as inappropriately normal PaCO2 relative to respiratory effort, altered mental status, or a silent chest (ie, minimal air movement) require mechanical ventilation (invasive or noninvasive) and should be admitted to the intensive care unit.
What are the signs of deterioration of status with acute asthma exacerbation?
Indications for mechanical ventilation in severe acute asthma include actual or impending respiratory failure signified by unresponsiveness to initial bronchodilator therapy, severe airflow obstruction (silent chest), unsustainable work of breathing (laborious accessory muscle use, normal PaCO2), and altered mental status. Acute asthma exacerbation is treated with fast-acting bronchodilators and periodically reassessed to gauge the therapeutic response. Some patients with status asthmaticus have severe inflammatory airway obstruction and edema. Therefore, effects of initial pharmacotherapy may be delayed. If patients with a delayed action of medication subsequently experience a deterioration in status, endotracheal intubation is the best course of action. Signs of deterioration include critical airflow obstruction, evidenced with a silent chest (minimal air movement) due to tight bronchospasm. Acute bronchospasm tends to be coupled with patients that have a peak expiratory flow rate <25% of their personal best. Additionally, patients may have high work of breathing which is seen with marked accessory muscle use (compensating for diaphragm fatigue), tripod positioning, and abdominal breathing (paradoxical outward motion with inspiration). A common lab finding for ventilation failure is elevated or inappropriately normal PaCO2, relative to work of breathing (ie, normal PaCO2 is alarming if patient is in respiratory extremis). Oxygenation failure can be seen on physical exam with hypoxemia or cyanosis requiring high levels of oxygen support (eg, high-flow nasal cannula or nonrebreather mask). Finally, altered mental status is a significant sign of deterioration and includes somnolence, confusion, or agitation (from either hypoxemia and/or hypercarbia). The immediate priority is endotracheal intubation to protect the airway and mechanical ventilation to support the work of breathing as a bridge to recovery. Intubation is ideally performed in a proactive and controlled manner. Delayed (“crash”) intubation is associated with higher morbidity and mortality (eg, cardiopulmonary arrest, cerebral anoxia).
How long can systemic steroids be used without tapering?
A short course (<2 weeks) does not require tapering due to minimal hypothalamic-pituitary-adrenal (HPA) axis suppression.
What are complications of long-term systemic steroid use?
Adrenal suppression, osteoporosis, weight gain, hyperglycemia, and steroid-induced psychosis.
When SHOULD steroids be tapered for acute asthma exacerbations?
Cushing symptoms or more than 2 weeks of use.
What could patients with asthma be provided instead of PO steroids?
Long-term management of poorly controlled asthma after an exacerbation may also include inhaled corticosteroids, which have fewer adverse effects than oral glucocorticoids due to limited systemic bioavailability. It is important to know that of all the medication’s available the best way to decrease the chance for acute asthma exacerbation reoccurrence is with the use of PO steroids.
When should bisphosphonates and vitamin D be given for steroid users?
For patients on long-term steroids to prevent osteoporosis.
What are the side effects of albuterol?
Tachycardia, hypokalemia, and tremors.
Why should ICS be used with a spacer and mouth rinsing?
To reduce the risk of oropharyngeal candidiasis.
When can a patient be discharged after an asthma exacerbation?
Once peak expiratory flow (PEF) reaches >80% of predicted.
What is aspirin-exacerbated respiratory disease (AERD)?
A condition where NSAIDs or aspirin trigger asthma, chronic rhinosinusitis, and nasal polyps (Samter’s Triad). Avoid NSAIDs, use leukotriene receptor antagonists (montelukast, zileuton), and manage asthma conventionally.
A patient with asthma gave birth vaginally to a baby large for gestational age moments ago, she is experiencing hypovolemic shock and was given oxytocin, but kept bleeding. What is the best course of management?
When postpartum hemorrhage (PPH) is refractory to oxytocin, the next step is to administer a second-line uterotonic agent. However, because the patient has asthma, carboprost tromethamine (Hemabate, PGF2-alpha) is contraindicated, as it can cause bronchospasm due to its prostaglandin F2-alpha-mediated bronchoconstriction. The best alternative in this case is Misoprostol (PGE1) or Dinoprostone (PGE2).
A 24-year-old woman with a history of asthma comes to the emergency department at 32 weeks gestation with a 5-day history of increased dyspnea, wheezing, and cough. Her asthma was previously well-managed with a combination fluticasone-salmeterol inhaler twice daily, but the patient stopped using it when she discovered she was pregnant. She reports no nasal congestion, sore throat, or sinus pain. The patient has no other medical conditions, and her pregnancy has progressed normally. Her only other medication is a prenatal multivitamin. She does not use tobacco, alcohol, or illicit drugs. Her father has a history of asthma. On examination, the patient appears to be in mild respiratory distress. She is afebrile. Blood pressure is 110/68 mm Hg, pulse is 104/min, and respirations are 21/min. Pulse oximetry is 94% on room air. Lung examination reveals inspiratory and expiratory wheezes with a prolonged exhalation phase. Heart sounds are normal. Mild bilateral pitting pedal edema is present; there is no calf tenderness in either leg. Fetal heart rate monitoring is reassuring. Nebulized albuterol and inhaled ipratropium are administered and provide some relief. On repeat assessment shortly afterward, the patient continues to feel short of breath, and wheezing is still present on examination. Arterial blood gas analysis shows a pH of 7.45, PaCOz of 26 mm Hg, and PaOz of 100 mm Hg on 2 L of oxygen by nasal cannula. What is the best next step in management of this patient?
Pregnancy increases respiratory drive, leading to chronic respiratory alkalosis (PaCOz of 27-32 mm Hg); hyperventilation during asthma exacerbation causes superimposed acute respiratory alkalosis. Relative acidosis (normalization of the PaCO2) during asthma exacerbation suggests impending respiratory failure and is an indication for mechanical ventilation. This patient’s arterial blood gas suggests acute-on-chronic respiratory alkalosis, consistent with an appropriate respiratory response. This patient has an acute asthma exacerbation during pregnancy. Poorly controlled asthma is strongly linked to maternal and fetal mortality, premature birth, and low birth weight. The treatment of acute asthma exacerbations in pregnant women and nonpregnant patients is similar. Treatment involves Bronchodilator therapy, Systemic corticosteroids, and Supplemental oxygen. Bronchodilator therapy is provided with an inhaled or nebulized albuterol is given initially, usually along with inhaled ipratropium. Intravenous magnesium sulfate or terbutaline may be needed for refractory bronchoconstriction. Provide systemic corticosteroids, especially in patients who have an incomplete response to bronchodilators, high-risk asthma features (eg, previous intubation), or a breakthrough acute exacerbation despite taking controller medications. Supplemental oxygen should be given to maintain SaO2≥95% (vs ≥90% in nonpregnant patients) to prevent antenatal fetal hypoxia. There is inconsistent evidence for a weak association between systemic corticosteroids and negative outcomes such as prematurity and cleft palate. When systemic corticosteroids are needed, patients should be reassured that the benefits of pharmacotherapy far outweigh any risk to the mother or fetus.
