UWorld 1 Flashcards
OSA
OSA can exist alone or in combo with obesity hypoventilation syndrome. A classic presentation for both would be morbid obesity, neck fat, sleep disturbances, and progressive DOE.
Patients with OSA without OHS experience hypoventilation only at night with transient hypoxia and hypercapnia that resolve while awake. If you have OHS too though, the physical restriction of the thoracic cavity caused by excess thoracic tissue continues throughout the day resulting in chronic hypoxia and hypercapnia.
In an effort to maintain normal pH, kidneys increase bicarb retention and decrease Cl reabsorption to create a compensatory metabolic alkalosis.
In setting of chronic hypoxia, patients with OHS can get pulmonary HTN (due to hypoxic vasoconstriction) with eventual Cor Pulmonale which can cause peripheral edema.
Systemic HTN is common with both OSA and comorbid OSA-OHS, maybe caused by hypoxic triggering of sympathetic nervous system and increased levels of catecholamines.
Bonus: OHS chronic hypoxia increases EPO secretion and results in compensatory erythrocytosis. Also, patients with OHS have increased pCO2 due to chronic hypoventilation.
Metabolic response to OSA-OHS
Compensatory metabolic alkalosis. Kidneys increase retention of bicarb and decrease Cl reabsorption. So we keep more bicarb and dump Cl.
Suspicion or new diagnosis of pleural effusion - prelim evaluation
The first step is to determine cause of it, and management starts with determining whether it is transudative or exudative.
Diagnostic thoracentesis is the preliminary investigation of choice in the management of pleural effusion, except in patients with classic signs of CHF where a trial of diuretic is warranted first.
Pleural fluid analysis provides decision making info in 90% of cases. If it shows exudate, then further tests are needed. Transudative rules out malignant.
What 3 tumors cause the majority of malignant pleural effusions?
Lung carcinoma, breast carcinoma and lymphoma cause 75%
Pulmonary embolus classic presentation
Acute onset pleuritic chest pain, hemoptysis and tachycardia. Hemoptysis is from pulm infarction. Low grade fever and mild leukocytosis are also common. (look out for HIV and dehydration as low key risk increasers for venous thromboembolism)
Chest CT shows characteristic wedge shaped, pleural based opacification that is likely to occur distal to a completely occluded pulmonary artery. Pulm infarct areas may also occasionally be seen on CXR as a Hampton hump.
On contrast enhanced CT, the PE itself will appear as a pulmonary artery filling defect.
PE is a common cause of both transudative AND exudative effusions too so CT may show an accompanying unilateral pleural effusion.
Primary mediastinal germ cell tumors
Occur mainly in young males and are locally invasive. B-hCG is elevated in seminomatous and nonseminomatous tumors. AFP is elevated in nonseminomatous only.
A large mediastinal mass with associated elevations of AFP and B-hCG is virtually diagnostic for nonsemin germ cell tumor.
Dx can be confirmed by bx. Testicular US should be performed to exclude a small primary tumor as management and prognosis differ between primary mediastinal and metastatic germ cell tumors. Almost all germ cell tumors in the anterior mediastinum are primary and not metastatic.
Bronchogenic cyst
An uncommon cause of anterior mediastinal masses. They are congenital and arise due to abnormal development of forgut, although symptoms may not develop until late childhood or early adulthood.
They appear as fluid-filled or air/fluid-filled cystic structures on imaging. High AFP or B-hCG are not seen.
Young patient with chronic DOE, decreased breath sounds, slight LFT abnormalities, and a FHx of cirrhosis
Think Alpha-1-antitrypsin deficiency.
AAT def, a codominant genetic disease, presents like other forms of COPD with chronic productive cough, dyspnea, wheezing, and recurrent respiratory infections.
On average, smokers present in their 30s, a decade earlier than nonsmokers.
AAT def can also affect the liver (neonatal hepatitis, HCC) and skin (panniculitis). Patients with liver disease may be ASx until the point of endstage disease and cirrhosis is the second most common cause of death in these patients.
Consider AAT def in a number of situations:
1) Patients with COPD at a young age (45 or less)
2) COPD with minimal or no history of smoking
3) FHx of emphysema or liver disease
Dx is confirmed with measurement of serum AAT levels and should also include PFTs.
Tx is IV supplementation with human AAT in addition to bronchodilators and corticosteroids as needed. People with severe lung disease are candidates for lung transplant, whereas those in hepatic failure can be treated with liver transplant.
Criteria for initiating long-term home oxygen therapy in COPD patients
LTOT has shown survival benefit in patients with advanced COPD. Criteria are:
1) Resting arterial O2 tension (PaO2) of 55 or less OR pulse oxygen sat of 88 or less on room air
2) PaO2 59 and less or SaO2 89 or less in patients with Cor Pulmonale, evidence of right heart failure or hematocrit above 55.
The dose of supplemental oxygen should be titrated so that SaO2 is maintained above 90 during sleep, normal waking and at rest. Survival benefits of home oxygen are significant when it is used for 15 or more hours a day. There are no clear survival benefits at disease levels below the criteria listed.
Pneumonia effect on A-a gradient
Look out for pneumonia in immunocompromised patient with hypoxia and fever. Fever induces a hyperdynamic state that may produce a flow murmur.
Inflammation of the alveolar membrane and interstitium impairs gas exchange. Areas of V/Q mismatch develop and A-a gradient increases.
Other causes of increased A-a gradient include diffusion defects (ILD, emphysema) and R-L intrapulmonary shunting.
Alveolar hypoperfusion
Signifies a uniform fall in inspired oxygen in all regions of the lungs. It is seen in hypoventilation from any cause (narcotic OD, neuromuscular weakness) or at high altitude (low partial pressure of O2). Unlike in V/Q mismatch, the A-a gradient remains normal.
Reactivation of latent TB
Typically causes an apical cavitary lesion seen on CXR. Generally, patients report chronic low grade fever, night sweats, weight loss, and a cough productive of blood-tinged sputum.
Most TB cases in USA occur in foreign-born people from endemic areas (primarily Mexico, Philippines, China, Vietnam, India, DR, and Haiti). Risk is highest for those who have lived in US for 5 years or less, with an extremely high case rate in the first year after entry to US.
Even after 5 years, the rates are 10 times higher than US-born people. Most of these cases represent reactivation of latent TB rather than new infection
Besides being from endemic areas, what increases TB risk?
Heath care workers, prison workers, immunocomprised, history of hematologic malignancy, history of head and neck cancer, smoking.
GERD and asthma
Comorbid GERD is common in patients with asthma and can exacerbate asthma symptoms through microaspiration of gastric contents, leading to an increase in vagal tone and bronchial reactivity.
Look for sore throat, morning hoarseness, worsening cough only at night, and increased need for albuterol inhaler following meals. Other signs could be dysphagia, chest pain/heartburn and sensation of regurgitation.
Obesity increases risk for GERD
PPI therapy has been shown to improve both asthma symptoms and peak expiratory flow rate in asthma patients with evidence of comorbid GERD. Start PPI trial.
What is upper airway cough syndrome?
AKA postnasal drip. Diphenhydramine (anticholinergic properties in addition to antihistamine) is useful for the chronic cough caused by rhinitis in these patients. Look for rhinorrhea or a sensation of something dripping into throat.
Typical history is cough starting after recent URI, occurs mainly at night, and is without expectoration.
Best diagnostic approach is to treat empirically with an oral first generation antihistamine (chlorpheniramine) or combo antihistamine-decongestant (brompheniramine and pseudoephedrine).
Patients who do not respond after 2-3w may require further investigation (sinus imaging, PFTs, HRCT) or empiric sequential therapy for GERD, cough variant asthma, chronic sinusitis, and non-asthmatic eosinophilic bronchitis
Aspirin-exacerbated respiratory disease
Occurs in patients with asthma and chronic rhinosinusitis. Symptoms include a sudden worsening of asthma and nasal congestion 30 minutes to 3 hours after ingestion of NSAIDs.
Hypersensitivity pneumonitis
HP is caused by repeated inhalation of an inciting antigen, which leads to alveolar inflammation. Common antigens include aerosolized bird droppings (bird fancier’s lung) and molds associated with farming (farmer’s lung).
HP can vary a lot in presentation and severity. History of antigen exposure in the setting of compatible symptoms is highly suggestive. Acute episodes may present with cough, breathlessness, fever and malaise that occur 4-6h after exposure. With chronic exposure, pulmonary fibrosis and a restrictive pattern on PFTs may develop.
CXR findings include ground glass opacity or haziness of the lower lung fields. Best treatment is avoiding the antigen. This may produce complete remission in most patients.
Acute exacerbation of COPD
Cardinal symptoms
1) Increased dyspnea
2) Increased cough (more frequent or severe)
3) Sputum production (change in color or volume)
Diagnostic testing
1) CXR - Hyperinflation
2) ABG - Hypoxia, CO2 retention (chronic and/or acute)
Management
1) Oxygen (target SpO2 of 88-92) - all patients
2) Inhaled bronchodilators (all patients)
3) Systemic glucocorticoids (all patients)
4) ABx if 2 or more cardinal symptoms
5) Oseltamivir if evidence of influenza
6) NPPV if ventilatory failure (noninvasive positive pressure ventilation)
7) Trachel intubation if NPPV failed or contraindicated
When are antibiotics indicated in patients with COPD exacerbation?
1) Moderate to severe COPD exacerbation (defined as 2 or more cardinal symptoms), especially with increased sputum purulence
or
2) Mechanical ventilation requirement (ET intubation or noninvasive positive pressure)
Up to half of COPD exacerbations are caused by bacterial respiratory pathogen, but identifying it is tough. Collection of sputum cultures is not rec’d (except in patients with risk factors for pseudomonas) due to difficulty in isolation a single pathogen.
Therefore, empiric ABx are directed at common upper respiratory pathogens (H flu, Moraxella catarrhalis and strep pneumo) and includes macrolides (azithromycin), respiratory fluoros (levofloxacin, moxifloxacin), or penicillin/B lactamase inhibitors (amoxi-clav).
Typical duration is 3-7d of therapy
IV MgSO4 in Asthma treatment
Useful in severe, life threatening asthma exacerbations. It causes bronchodilation.
Calculating the A-a gradient
1) PAO2 is equal to 150 minus (PaCO2/0.8) for patients breathing room air at sea level. Get PaCO2 from ABG.
2) PaO2 is partial arterial pressure of oxygen (from ABG results)
A-a gradient is equal to 1-2.
A-a is elevated if it is higher than the expected gradient on room air. This is estimated by 2.5 plus (0.21xpatient age). OR patient age/4 plus 4.
Elevation in A-a is seen in processes that impair gas exchange. PE, for example.
Theophylline toxicity
Theophylline has a narrow TI and toxicity can occur from accumulation by reduced clearance or decreased metabolism due to saturation of metabolic pathways.
It is metabolized mainly by cytochrome oxidase system in liver. Inhibition of these enzymes by concurrent illness (cirrhosis, cholestasis, respiratory infections with fever) or drugs (cimetidine, cipro, erythromycin, clarithromycin, verapamil) can raise serum concentration and cause toxicity
Symptoms usually manifest as CNS stimulation (HA, insomnia, seizure), GI disturbances (n/v) and cardiac toxicity (arrhythmia - atrial tach, SVT, ventricular).
Best first step is get blood drug level.
