UWorld 2 Flashcards
Exercise-induced bronchoconstriction
Bronchoconstriction occurs in response to mast cell degranulation triggered by the passage of high volumes of dry, cold air. EIB can occur in asthmatic patients but may also cause bronchospasm in those without a pre-existing diagnosis of asthma
Beta agonists and mast cell stabilizers are important in its management. Short acting ones used 10-20min prior to exercise are usually enough to prevent symptoms. They are first line if used only intermittently (less than daily)
An antileukotriene agent can be used 15-20min prior to exercise for those unable to tolerate B agonists. Combo of Beta and antileuko may also be used in high performance athletes. Can also be used for daily exercisers.
Steroid inhalers may be useful in athletes who exercise daily and would require daily pre-treatment with albuterol. These are also preferred treatment for persistent asthma
COPD patient presenting with catastrophic worsening of their respiratory symptoms
Think about spontaneous secondary pneumothorax. Cigarette smoking greatly increases the risk. It is thought that smoking leads to chronic airway inflammation and a form of respiratory bronchiolitis. The chronic destruction of alveolar sacs leads to the formation of large alveolar blebs (usually in upper lobes) which can eventually rupture and leak air into pleural space.
Treatment of PE
Untreated has mortality risk of 30% due to recurrent embolism. Immediate anticoagulation is indicated.
LMWH (enoxaparin), fondaparinux (injection factor 10a inhib), and rivaroxaban (oral factor 10a) cannot be used in patients with severe renal insufficiency (GFR below 30) as reduced renal clearance increases anti-Xa activity levels and bleeding risk.
Unfractionated heparin is recommended in patients with decreased GFR as it is more convenient to monitor its therapeutic level via aPTT. Once the heparin produces therapeutic anticoagulation (goal PTT more than 1.5-2 times normal), warfarin is initiated.
Warfarin can take 5-7d to reach therapeutic levels. It also inhibits proteins C and S (anti-thrombogenic proteins) and can be thrombogenic without a second anticoagulant as a bridge. After reaching therapeutic INR, heparin can be stopped and warfarin can be continued long term
Rivoraxaban is an oral anticoagulant with immediate onset of action (unlike warfarin). Therefore, no bridging with heparin is indicated. Of course, this isnt an option in patients with severe renal insufficiency
Causes of recurrent pneumonia
Involving same region of lung
A) Local anatomic obstruction
1) Bronchial compression (neoplasm, mediastinal adenopathy, vascular anomaly) - get CT if you suspect this. Bronchoscopic or CT-guided bx of any suspected lesion seen on CT.
2) Intrinsic bronchial obstruction (bronchiectasis, retained foreign body, bronchial stenosis)
B) Recurrent aspiration
1) Seizures
2) Ethanol or drug use
3) GERD, dysphagia, achalasia
Involving different region of lung
1) Sinopulmonary disease (CF, immotile cilia)
2) Noninfectious (vasculitis, bronchiolitis, obliterans with organizing pneumonia)
3) Immunodeficiency (HIV, leukemia, low immunoglobulins)
Elevated or normal PaCO2 in patient with asthma exacerbation
Acute asthma attack causes increased respiratory drive and hyperventilation leading to low PaCO2. A high or normal PaCO2 in these patients indicates impending respiratory failure.
Also look for:
1) Markedly decreased breath sounds
2) Absent wheezing
3) AMS
4) Marked hypoxia with cyanosis
Patients with impending or actual respiratory arrest require admission to ICU with ET intubation to maintain adequate O2 and ventilation.
Mechanical ventilation goals in ARDS
1) Avoiding complications of mechanical vent by using lung-protective strategies like low tidal volume ventilation (LTVV). LTTV decreases the chance of overdistending alveoli and provoking barotrauma due to high plateau pressures. LTTV improves mortality in patients with ARDS. In contrast, higher TVs in ARDS may cause elevated pulm pressures due to the work of forcing larger volumes into stiff lungs (decreased compliance) leading to increased alveolar distension
2) Provide adequate oxygenation. Increasing the fraction of inspired O2 given by ventilator improves oxygenation. BUT, levels above 0.6 for too long are associated with oxygen toxicity. Increasing PEEP also improves oxygenation by preventing alveolar collapse at the end of expiration, thereby decreasing shunting and the work of breathing. Given the severe hypoxemia seen in ARDS, PEEP levels up to 15-20cm H2O may be needed to maintain oxygenation. The goal is arterial partial pressure of oxygen at 55-80 or peripheral SpO2 at 88-95 (preventing it from being below 88)
Granulomatosis with polyangiitis (Wegener)
Clinical manifestations
1) Upper respiratory - sinusitis/otitis, saddle-nose deformity
2) Lower resp - Lung nodules/cavitation
3) Renal - Rapidly progressive GN
4) Skin - Livedo reticularis, nonhealing ulcers
Dx
1) ANCA: PR3 (70%), MPO (20%)
2) Bx - Skin (leukocytoclastic vasculitis), Kidney (pauci-immune GN), Lung (granulomatous vasculitis)
Tx
1) Corticosteroids and immunomodulators (MTX, Cyclophosphamide)
It’s a small-medium vessel vasculitis
Compare the two aspiration syndromes (pathophys, clinical, management)
Pneumonia vs Pneumonitis
Pathophys
1) Pneumonia - lung parenchyma infection, Aspiration of upper airway or stomach microbes (anaerobes)
2) Pneumonitis - Lung parenchyma INFLAMMATION, Aspiration of gastric acid with direct tissue injury
Clinical
1) Pneumonia - Present days after aspiration event. Fever, cough, increased sputum. CXR infiltrate in dependent lung segment (classically RLL). Can progress to abscess.
2) Pneumonitis - Present HOURS after aspiration event. Range from no symptoms to nonproductive cough, low O2, respiratory distress. CXR infiltrates (one or both lower lobes) resolve without antibiotics.
Management
1) Pneumonia - ABx (clindamycin or B-lactam and B-lactamase inhib)
2) Pneumonitis - Supportive (no ABx)
Invasive aspergillosis vs Chronic pulmonary aspergillosis
Risk factors
1) Invasive - Immunocompromised (neutropenia, glucocorticoids, HIV)
2) Chronic - Lung disease/damage (cavitary TB)
Findings
1) Invasive - Triad of fever, chest pain, hemoptysis. Pulm nodules with halo sign. Positive cultures. Positive cell wall biomarkers (galactomannan, beta-D-glucan)
2) Chronic - More than 3 months (weight loss in 90%, cough, hemoptysis, fatigue). Cavitary lesion plus or minus fungus ball. Positive aspergillus IgG serology
Management
1) Invasive - Voriconazole plus or minus caspofungin
2) Chronic - Resect aspergilloma (if possible), Azole medication (voriconazole), Embolization (if severe hemoptysis)
Note: Simple aspergilloma (fungus ball in preexisting lung cavity) is a form of chronic pulmonary aspergillosis but is usually quiescent with occasional hemoptysis.
Pneumocystis jirovecii pneumonia
Clinical
1) Indolent (HIV) or acute respiratory failure (immunocompromised)
2) Fever, dry cough, low O2
Workup
1) Increased LDH level
2) Diffuse reticular infiltrates on imaging
3) Induced sputum or BAL (stain)
Tx
1) TMP-SMX (21d course)
2) Prednisone if low O2
Prevention
1) TMP-SMX (people on longterm steroid therapy, HIV below certain CD4 counts)
2) Antiretrovirals (in HIV)
What causes hyperinflation of the lungs in COPD?
2 mechanisms: Static and dynamic.
1) Static - The negative pressure created by the chest wall (expanding pressure) and the positive pressure created by the lungs (collapsing pressure) are in equilibrium at the functional residual capacity. In COPD, decreased elasticity of alveoli results in decreased positive pressure created by the lungs to expel air. Thus, alveoli retain more air volume. At the increased lung volume, the chest wall generates more recoil pressure (less negative expanding pressure), which compensates for the lung’s decrease in positive collapsing pressure. New pressure equilibrium is reached at a higher lung volume (higher FRC)
2) Dynamic - More responsible of the two. Caused by air stacking. Expiratory phase is prolonged in patients with COPD due to an increase in airway resistance. When exertional demands trigger an increase in minute ventilation (bpm x TV), the patient is forced to begin inhalation prior to completion of exhalation. The result is additional air trapping and hyperinflation.
The diaphragm is most important muscle for enlarging the thoracic cavity and creating negative pressure during inhalation. In COPD, the diaphragmatic flattening and muscular shortening caused by hyperinflation result in more difficult in decreasing intrathoracic pressure during inspiration and therefore increase the work of breathing
Elasticity and compliance in COPD
Compliance is change in volume per change in pressure. It is the inverse of elasticity.
Elasticity decreases in COPD and compliance increases. Flattening of the diaphragm is the RESULT of increased lung compliance (it isnt the cause of it)
INR goal for patient with idiopathic VTE or AFib
2-3
INR of 2.5-3.5 is desired for patients with prosthetic heart valves.
How does glucocorticoid use cause leukocytosis?
1) Mobilization of marginalized neutrophils into bloodstream (main mechanism). Marginalized neutrophils are attached to the endothelium of blood vessels; glucocorticoid-induced mobilization of these neutrophils leads to a higher number of circulating neutrophils
2) Stimulation of release of immature neutrophils from bone marrow
3) Inhibition of neutrophil apoptosis
Glucocorticoids decrease the number of circulating lymphocytes and eosinophils through combo of increased apoptosis, increased emigration into tissues and decreased production.
Clinical features of asbestosis
Clinical presentation
1) Prolonged asbestos exposure (shipyard, mining, construction, pipe fitters)
2) Symptoms develop at least 20 years after initial exposure
3) Progressive dyspnea (over months), bibasilar end-inspiratory crackles and clubbing
4) Increased risk for malignancies (lung cancer, malignant mesothelioma)
Diagnostics
1) History and clinical findings of exposure (pleural plaques on chest imaging virtually pathognomonic)
2) Interstitial fibrosis on imaging or histology and/or pulmonary function tests with restrictive pattern (decreased lung volumes, decreased diffusion lung capacity, and normal FEV1/FVC)
3) Exclusion of other diseases
