UWorld 1 Flashcards

1
Q

OSA

A

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.

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2
Q

Metabolic response to OSA-OHS

A

Compensatory metabolic alkalosis. Kidneys increase retention of bicarb and decrease Cl reabsorption. So we keep more bicarb and dump Cl.

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3
Q

Suspicion or new diagnosis of pleural effusion - prelim evaluation

A

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.

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4
Q

What 3 tumors cause the majority of malignant pleural effusions?

A

Lung carcinoma, breast carcinoma and lymphoma cause 75%

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5
Q

Pulmonary embolus classic presentation

A

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.

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6
Q

Primary mediastinal germ cell tumors

A

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.

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7
Q

Bronchogenic cyst

A

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.

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8
Q

Young patient with chronic DOE, decreased breath sounds, slight LFT abnormalities, and a FHx of cirrhosis

A

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.

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9
Q

Criteria for initiating long-term home oxygen therapy in COPD patients

A

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.

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10
Q

Pneumonia effect on A-a gradient

A

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.

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11
Q

Alveolar hypoperfusion

A

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.

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12
Q

Reactivation of latent TB

A

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

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13
Q

Besides being from endemic areas, what increases TB risk?

A

Heath care workers, prison workers, immunocomprised, history of hematologic malignancy, history of head and neck cancer, smoking.

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14
Q

GERD and asthma

A

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.

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15
Q

What is upper airway cough syndrome?

A

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

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16
Q

Aspirin-exacerbated respiratory disease

A

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.

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17
Q

Hypersensitivity pneumonitis

A

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.

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18
Q

Acute exacerbation of COPD

A

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

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19
Q

When are antibiotics indicated in patients with COPD exacerbation?

A

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

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20
Q

IV MgSO4 in Asthma treatment

A

Useful in severe, life threatening asthma exacerbations. It causes bronchodilation.

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21
Q

Calculating the A-a gradient

A

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.

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22
Q

Theophylline toxicity

A

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.

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23
Q

15 causes of hemoptysis

A

Pulm (Most common)

1) Bronchitis
2) Lung cancer
3) Bronchiectasis

Cardiac
4) Mitral stenosis/acute pulm edema

Infectious

5) TB
6) Lung abscess
7) Bacterial pneumonia
8) Aspergillosis

Heme
9) Coagulopathy

Vascular

10) PE
11) AV malformation

Systemic

12) Granulomatosis with polyangiitis
13) Goodpasture

Other

14) Trauma
15) Cocaine use (inhalation)

24
Q

Definition of chronic bronchitis

A

Chronic productive cough for at least 3 months in 2 successive years. Leading cause is cigarette smoking.

25
Q

Complications of pneumonia

A

Pneumonias often cause pleural effusions. They tend to be small, free-flowing, sterile, and resolve with ABx (uncomplicated). But, if bacteria persistently cross into the pleural space, patients can develop complicated parapneumonic effusions or empyemas.

Look for patient with symptoms of URI that progress to pleuritic chest pain, productive cough, and fever with a CXR showing large pleural effusion. Patients are immunocompromised (HIV, post transplant) are at higher risk of complications from pneumonia (like empyema)

Unlike complicated parapneumonic effusions, empyemas have frank pus or bacteria (gram stain) in pleural space. All empyemas require prolonged ABx (2-4w) and drainage (usually with chest tube)

26
Q

Uncomplicated parapneumonic effusions

A

1) Etiology - movement of fluid from pneumonia into visceral pleura
2) Pleural fluid analysis - pH above 7.2, low to normal gluc, LDH ratio above 0.6
3) Pleural fluid gram stain - negative
4) Pleural fluid culture - negative
5) Tx - ABx

27
Q

Complicated parapneumonic effusions

A

1) Etiology - persistent bacterial invasion into pleural space
2) Pleural fluid analysis - pH below 7.2, low gluc, LDH ratio above 0.6
3) Pleural fluid gram stain - negative
4) Pleural fluid culture - usually negative
5) Tx - ABx, usually requires chest tube drainage

28
Q

Empyema

A

1) Etiology - bacterial colonization, purulent fluid
2) Pleural fluid analysis - pH below 7.2, low gluc, LDH ratio above 0.6
3) Pleural fluid gram stain - positive
4) Pleural fluid culture - Usually positive
5) Tx - ABx and chest tube drainage

29
Q

Methylxanthines

A

Aminophylline, theophylline. The are PDE inhibitors that cause bronchodilation. Use is limited due to toxicity.

30
Q

Cromolyn

A

Mast cell stabilizer. Prevents release of histamine and leukotrienes. Used in treatment of asthma. Leukotriene antagonists (zafirlukast) are similar. Neither are used for acute COPD treatment.

31
Q

Clinical features of acute bronchitis

A

Etiology - preceding respiratory illness (90% viral)

Presentation

1) Cough - 5 days to 3w. Can be productive (yellow, green or purulent sputum).
2) Absent systemic findings (fever, chills)
3) Wheezing or rhonchi, chest wall tenderness

Dx and tx

1) Dx is clinical - CXR only in patients with suspected pneumonia
2) Symptomatic treatment - NSAIDs/acetaminophen and/or bronchodilators
3) ABx NOT recommended (even if mycoplasma)

32
Q

Tx of Cor Pulmonale

A

Treatment involves optimizing RV dynamics (preload, afterload, contractility) with supplemental O2, diuretics, treatment of underlying etiology and IV inotropes for severe decompensation

33
Q

Definition of solitary pulmonary nodule

A

Round opacity, up to 3cm in diameter and surrounded by pulm parenchyma. Must be no associated effusion, adenopathy or atelectasis.

34
Q

What features of a solitary pulm nodule favor malignancy?

A

Large size, low density, spiculated borders, eccentric calcification. Clinical signs of age over 40, history of smoking, weight loss or previous malignancy.

Nodule size

1) Low risk - less than 0.8cm
2) Medium - 0.8-2cm
3) High - more than 2cm

Age

1) Low risk - less than 40
2) Med - 40-60
3) High - Over 60

Smoking status

1) Low - never smoked
2) Med - Current smoker
3) High - Current smoker

Smoking cessation

1) Low - over 15 years
2) Med - 5-15 years
3) High - less than 5 years

Nodule margin characteristics

1) Low - Smooth
2) Med - Scalloped
3) High - Corona radiata or spiculated

35
Q

Metabolic side effects of asthma treatment with B2 agonists

A

Inhaled albuterol and systemic steroids are appropriate treatments for acute asthma attacks. Patients on high doses of Beta-2 agonists may develop hypoK which may present with muscle weakness, arrhythmias and ECG abnormalities. Other common side effects include tremor, palpitations and HA.

Order a lyte panel in patients with such a presentation after an asthma attack was treated.

36
Q

Clinical presentation of Pancoast tumors (Superior pulmonary sulcus tumor)

A

1) Shoulder pain (most common)
2) Horner syndrome (ipsilateral ptosis, miosis, enopthalmus and anhidrosis) from involvement of paravertebral sympathetic chain and inferior cervical ganglion
3) C8-T2 neuro involvement - weakness and/or atrophy of intrinsic hand muscles, pain/parasthesias of 4th and 5th digits, medial arm and forearm
4) Supraclavicular LN enlargement
5) Weight loss

Initial evaluation includes chest imaging (CXR) to evaluate for lung mass. They are malignant lung neoplasms.

37
Q

Causes of alveolar hypoventilation and respiratory acidosis

A

1) Pulm/thoracic diseases - COPD, OSA, OHS, Scoliosis
2) NM diseases - MG, LE, GBS
3) Drug induced hypoventilation - anesthetics, narcotics, sedatives
4) Primary CNS - brainstem lesion, infection, stroke. Post-ictal

38
Q

A-a gradient in alveolar hypoventilation

A

Usually normal. Remember normal is less than 15, tends to increase with age, but a value over 30 is ALWAYS abnormal.

A-a gradient is normal in patients with reduced inspired O2 tension and hypoventilation.

Respiratory acidosis confirms the hypoventilation (CO2 retention). Hypoventilation is a MAJOR cause of respiratory acidosis.

39
Q

5 General causes of hypoxemia

A

1) Reduced inspired O2 tension
2) Hypoventilation
3) Diffusion limitation
4) Shunt
5) V/Q mismatch

40
Q

Predisposing conditions to aspiration pneumonia

A

1) Altered consciousness impairing cough reflex/glottic closure (dementia, drug intox)
2) Dysphagia due to neuro deficitis (stroke, neurodegenerative disease)
3) Upper GI disorders (GERD)
4) Mechanical compromise of aspiration defenses (NG and ET tubes)
5) Protracted vomiting
6) Large volume tube feedings in recumbent position

41
Q

Common causes of transudative pleural effusions (4)

A

1) CHF
2) Cirrhosis
3) Nephrotic Syndrome
4) Peritoneal dialysis

Usually due to systemic factors (increased hydrostatic pressure or hypoalbuminemia) and has pleural fluid pH of 7.4-7.55 (normal is 7.6)

42
Q

Common causes of exudative pleural effusions (7)

A

1) Infections
2) Malignancy
3) Connective tissue diseases
4) Inflammatory disorders
5) Movement of fluid from abdomen to pleural space
6) Coronary artery bypass surgery
7) PE (usually)

Usually due to inflammation with a pleural fluid pH of 7.3-7.45 (normal 7.6)

43
Q

Light’s criteria

A

Helps distinguish exudate from transudate. Exudates generally have the following:

1) Pleural fluid protein/serum protein ratio is greater than 0.5
2) Pleural fluid LDH/serum LDH ratio is greater than 0.6
3) Pleural fluid LDH is greater than 2/3 of upper limit of normal serum LDH

44
Q

Pleural fluid pH less than 7.3

A

If arterial pH is normal and pleural fluid glucose is low, this is usually due to increased acid production by pleural fluid cells and bacteria (empyema) or decreased hydrogen ion efflux from the pleural space (pleuritis, tumor, pleural fibrosis)

45
Q

bronchiectasis

A

Disease of bronchial thickening and dilation due to a recurrent cycle of bacterial infection, inflammation, and tissue damage. Bronchiectasis is associated with a number of underlying etiologies and its development requires an infectious insult in combo with impaired bacterial clearance (immunodef, structural airway defect)

Look for recurrent episodes of dyspnea, fever, tenacious sputum production, and hemoptysis along with physical exam findings of wheezing and digital clubbing

46
Q

CF as a cause of bronchiectasis

A

Look for a young patient. 7% of CF patients are diagnosed at age 18 or above. Testing for CF is recommended in the evaluation of bronchiectasis.

Mutation in CF transmembrane conductance regulator gene results in defective Cl and Na transport and leads to thick secretions and impaired mucociliary clearance.

Chronic bacterial infection ensues, leading to enhanced neutrophil recruitment and excessive release of elastase which contributes to bronchial airway damage.

Pseudomonas is a characteristic finding in the sputum. In addition, upper** lung lobe involvement (evidenced by upper lung field crackles and right upper lobe infiltrate) is characteristic of bronchiectasis due to CF and helps to differentiate it from other causes

47
Q

Etiologies of bronchiectasis

A

1) Airway obstruction (like in cancer)
2) Congenital (CF, AAT Deficiency)
3) Chronic infection (Aspergillosis, non-TB mycobacteria)
4) Immunodeficiency (hypogammaglobulinemia)
5) Postinfection (TB, necrotizing pneumonia)
6) Rheumatic disease (RA, Sjogren)
7) Toxic inhalation/aspiration

48
Q

Evaluation of bronchiectasis

A

1) HRCT scan of the chest (needed for initial diagnosis)
2) Immunoglobulin quantification
3) Sweat Cl and/or genetic testing for CF
4) Sputum culture for bacteria, fungi and mycobacteria
5) PFTs

49
Q

Cardiac sarcoid

A

Autopsy shows evidence of cardiac noncaseating granulomas in 25% of patients with sarcoid. Only 5% demonstrate cardiac symptoms though. Therefore, it is underdiagnosed.

Infiltration of noncaseating granulomas leads to surrounding inflammation and can result in conduction defects (complete AV block is most common), restrictive cardiomyopathy (early manifestation), dilated cardiomyopathy (late manifestation), valvular issues and heart failure.

Sudden cardiac death can occur due to complete AV block or ventricular arrhythmia.

Suspect cardiac sarcoid in any young patient (less than 55) with unexplained second or third degree heart block or when ECG changes occur in a patient with known or suspected systemic sarcoid.

Definitive dx is tough due to poor sensitivity of endomyocardial bx, but a combo of imaging, ECG, and history often strongly suggests the diagnosis.

Look for sarcoid’s bilateral midfield lung opacities on CXR

50
Q

What is the most effective way to differentiate between asthma and COPD?

A

Spirometry before and after administration of a bronchodilator. Reversal of airway obstruction by the dilator suggests asthma.

51
Q

Common etiologies of chronic cough (10)

A

1) UACS
2) Asthma and cough-variant asthma
3) GERD or laryngopharyngeal reflux
4) Post respiratory tract infection
5) ACEIs
6) Chronic bronchitis
7) Chronic sinusitis
8) Bronchiectasis
9) Lung cancer
10) Non asthmatic eosinophilic bronchitis

52
Q

PFTs in obstructive vs restrictive lung diseases

A

FEV1

1) OLD - less than 80%
2) RLD - less than 80%

FEV1/FVC

1) OLD - Less than 70%
2) RLD - More than 70%

FVC

1) OLD - Normal to low
2) RLD - Less than 80%

53
Q

Ankylosing spondylitis and pulm?

A

Patients may develop restrictive lung disease due to diminished chest wall and spinal mobility. PFTs show a mildly restrictive pattern with reduced vital capacity and total lung capacity but normal FEV1/FVC

54
Q

Manifestations of sarcoid

A

Pulm

1) Bilateral hilar adenopathy
2) Interstitial infiltrates

Ophthalmologic

1) Anterior uveitis (iridocyclitis or iritis)
2) Posterior uveitis

Reticuloendothelial

1) Peripheral LAD
2) Hepatomegaly
3) Splenomegaly

MSK

1) Acute polyarthritis (esp in ankle joints)
2) Chronic arthritis with periosteal bone resorption

CNS/endocrine

1) Central DI
2) HyperCa

Lofgren Syndrome

1) Erythema nodosum
2) Hilar adenopathy
3) Migratory polyarthralgias
4) Fever

55
Q

ARDS

A

Risk factors - Infection, trauma, massive transfusion, acute pancreatitis

Pathophys

1) Lung injury leads to fluid/cytokine leakage into alveoli
2) Impaired gas exchange, decreased lung compliance, pHTN

Dx

1) New/worsening respiratory distress within 1 week of insult
2) Bilateral lung opacities (pulm edema) not due to CHF/fluid overload
3) Hypoxemia with PaO2/FiO2 ratio of 300 or less

management
1) Mechanical vent (low TV, high PEEP, permissive hypercapnia)