Pulmo/Crit

Question 1

Pleural effusion in patients on Diuretics

Answer 1

Light’s criteria are nearly 100% sensitive but only 83% specific for identifying exudates, and the specificity decreases in the setting of diuretic use.

Up to 20% of heart failure patients with pleural effusion may fulfill criteria for exudative effusion after receiving diuretics.

In this case, a serum-effusion protein difference >3.1 g/dL or serum- effusion albumin gradient >1.2 g/dL suggests a true transudative effusion.

Question 2

Newly diagnosed bronchiectasis approach

Answer 2

Patients with high resolution chest CT findings suggestive of bronchiectasis should undergo functional assessment with pulmonary function testing and identification of potentially reversible causes. Initial diagnostic evaluation includes a complete blood count with differential, immunoglobulin quantitation (i.e., IgA, IgG, and IgM), and sputum culture and smear (bacteria, fungi, and mycobacteria).

Question 3

Lofgren syndrome

Answer 3

Risk groups
African descent, Scandinavians, Irish, Puerto Ricans

Clinical features
Bilateral ankle arthritis, Erythema nodosum, Hilar adenopathy

Treatment
Often self-limited,NSAIDs for symptom control

Question 4

ABPA

Answer 4

History
Asthma, cystic fibrosis

Chest Imaging
X-ray: Infiltrates (often fleeting)
CT: Central bronchiectasis

Diagnostic testing
Skin test positive for Aspergillus fumigatus
Eosinophilia >500/μL
IgE >417 IU/mL
Specific IgG & IgE for A fumigatus.

Treatment
Corticosteroids + Itraconazole

Question 5

Benign asbestos related pleural effusion

Answer 5

Benign asbestos- related pleural effusions (BAPE) are an early pleural manifestation of asbestos- related lung disease, usually occurring between 10-15 years postexposure. They are usually small (<500 mL), often bloody, and exudative, with eosinophilic predominance (>10% of nucleated cells, frequently >50%). BAPE may be asymptomatic or present with dyspnea, low-grade fever, and pleuritic chest pain. Spontaneous resolution over weeks to months is the norm. BAPE usually predates asbestos-related pleural plaques and may be a marker for future development of diffuse pleural thickening

Question 6

Fat embolism

Answer 6

Causes:
-Fracture of long bone
-pancreatitis
-sickle cell disease
-Orthopedic surgery

Classical triad:
Respiratory distress, Altered mental status, petecheal rash

Treatment: supportive

Question 7

Acute bronchitis management

Answer 7

Many patients develop a persistent cough due to bronchospasm with transient airway obstruction.

Inhaled beta-2 adrenergic agonists can relieve the obstruction and provide symptomatic relief in those with significant symptoms.

routine use of antibiotics is not recommended and purulent sputum production has not been shown to reflect bacterial infection. Even among those patients who test positive for atypical bacterial respiratory pathogens (eg, Mycoplasma pneumoniae, Chlamydia pneumoniae), there is no evidence that antibiotics provide benefit over supportive care.

Question 8

Effect of NIPPV in Cardiogenic pulmonary edema

Answer 8

Noninvasive positive-pressure ventilation in cardiogenic pulmonary edema patients enhances oxygenation via improvements in respiratory (Decrease dead space ventilation, increase tidal volume, increase alveolar/minute ventilation)
cardiac indices (Decrease preload, Decrease afterload).

Question 9

Malignant pleural effusion

Answer 9

Repeated thoracentesis can detect up to 90% of malignant cells in high-risk patients. If there is still a suspicion of malignancy despite repeated negative thoracentesis, thoracoscopy should be performed

Question 10

Approach to increased peak pressure on the vent.

Answer 10

Normal plateau pressure
-Bronchospasm
-Mucus plug
-biting the tube

Increased plateau pressure
- pneumothorax
- Pneumonia
- Atelectasis
- pulmonary edema
- Rt main stem intubation

Question 11

Chylothorax

Answer 11

Chylothorax is a relatively rare cause of pleural effusion, usually due to traumatic or non-traumatic disruption of the thoracic duct.
The most common non-traumatic cause is thoracic duct obstruction due to malignancy, sarcoidosis, or retrosternal goiter, and infections such as tuberculosis and filariasis. Traumatic disruption most commonly occurs in central venous catheter placement (subclavian approach) and esophageal surgery.

When associated with cirrhosis, congestive heart failure, or nephritic syndrome, the chylothorax may be transudative.

Question 12

Aspirin-exacerbated respiratory disease

Answer 12

Usually presents with the classic triad of nasal polyposis, asthma, and aspirin (or NSAID) sensitivity.
The reaction is not an IgE-mediated allergic response but is likely a shift in the arachidonic acid metabolic pathway causing excessive leukotriene production.
These patients should be treated with leukotriene antagonists and optimal asthma management.

Question 13

Acute eosinophilic pneumonia
Diagnosis

Answer 13

🔴 a BAL with 25% eosinophils or a lung biopsy showing an eosinophilic pneumonia.

+ the absence of other cause of pulmonary eosinophilia including drugs, toxins, and infectious pathogens

Question 14

Sarcoidosis poor prognostic factors

Answer 14

black race, osseous involvement, lupus pernio (disfiguring nasolabial cutaneous lesions), chronic hypercalcemia, and chronic pulmonary sarcoidosis

Question 15

Lymphangiomyomatosis (LAM)

Answer 15

LAM is a rare disorder affecting exclusively women that is characterized by hamartomatous proliferation of atypical smooth muscle along lymphatics in the lung, thorax, abdomen, and pelvis

• Mean age of onset is between 30 and 45 years.
• Progressive airflow obstruction, pneumothorax (50-80%), hemoptysis, or chylothorax.
• LAM can complicate tuberous sclerosis complex (TSC)
• Radiology: numerous thin-walled cysts, ranging in size from a few millimeters to 6 cm throughout both lungs; the intervening lung parenchyma is normal. Hyperinflation. Pneumothorax, effusion (chylothorax)
• PFT: Obstructive pattern, hyperinflation/airtrapping, reduced DLCO
• The course of LAM is indolent, but most patients ultimately die of respiratory failure.
• Treatment: LTX. Medications (Tamoxifen? Sirolimus?)

Question 16

Desquamative Interstitial Pneumonia (DIP)

Answer 16

• DIP is a histologic syndrome characterized by dense collections of alveolar macrophages within air spaces.
• Radiology: Homogeneous pattern, preserved alveolar architecture, and minimal or absent fibrosis or honeycombing.
• More than 90% of patients with DIP are smokers.

Question 17

Pulmonary Langerhan’s cell histocytosis

Answer 17

🔴 is a rare disorder usually seen in smokers.
🔴Age: 20-50
🔴PLCH is almost exclusively seen in Caucasian patients
🔴 presentation: cough and dyspnea. Pneumothoraces occurs in 6 to 20% of patients and may be the presenting feature.
🔴Extrapulmonary involvement occurs in 20% of patients with PLCH. Solitary punched-out lesions of bone and diabetes insipidus (from involvement of the pituitary) are the most common sites of extrapulmonary involvement.
🔴Radiologically: CT shows cystic and nodular lesions, with a proclivity to involve the upper lobes, strongly suggests PLCH.
🔴PFT: Obstructive, restrictive or mixed
🔴Treatment: Smoking cessation, Steroids, Lung Transplant

Question 18

Pulmonary Alveolar Proteinosis (PAP)

Answer 18

🔴A rare parenchymal lung disease characterized by an accumulation of lipoproteinaceous material in the alveoli.
🔴Most cases (90%) are idiopathic; remaining cases consist of congenital and secondary forms of PAP.
🔴most patients are between 20 and 60 years of age.
🔴Radiology’crazy-paving”
🔴The diagnosis of PAP may be made by BAL, which typically yields a milky effluent
🔴Transbronchial biopsy: accumulation of granular, PAS positive, lipoproteinaceous material within the alveolar spaces with preserved alveolar architecture.
🔴The standard treatment for PAP is whole lung lavage.
🔴GM-CSF: favorable responses in 40% to 65% of patients, some enjoying a complete response.

Question 19

Chronic Eosinophilic Pneumonia

Answer 19

🔴usually affects middle-aged atopic women
🔴Progressive
🔴Asthma is present in 50 to 60% of patients
🔴Increased IgE levels, and the levels may correspond to the clinical activity.
🔴Peripheral eosinophilia occurs in up to 88%.
🔴CXR: photographic negative of pulmonary edema
🔴Treatment and prognosis
10% of patients will have spontaneous resolution
Good response to steroids, can relapse

Question 20

Causes of lymphocytic pleural effusion

Answer 20

• Primary effusion lymphoma or systemic lymphoma.
• Tuberculous pleurisy
• Sarcoidosis
• Chronic rheumatoid pleurisy
• Yellow nail syndrome
• Chylothorax

Question 21

Pulmonary hypertension reversibility
Definition

Answer 21

🔴Pulmonary vasoreactivity testing is only recommended in patients with Ideopathic PAH, Hereditary PAH, or Drug induced PAH.

🔴 A positive acute response is defined as a reduction in mPAP by ≥10 mmHg to reach an absolute value <40 mmHg, with increased or unchanged Cardiac output.

🔴 Treat with high dose CCB.

Question 22

Pulmonary hypertension
Genetics

Answer 22

The various mutations associated with idiopathic PAH and hereditary PAH are BMPR2 (most common), SMAD1, SMAD 9, KCNK3, CAV 1, and SOX17,

Question 23

Pulmonary arterial hypertension medications during pregnancy

Answer 23

🔴Safe: Prostacyclin and PDE-5 inhibitor
🔴Unsafe: Endothelin receptor antagonist and sGC stimulator (Riociguat)

Question 24

Pulmonary arterial hypertension
Approach to treatment

Answer 24

🔴In treatment-naïve patients with low or intermediate risk, the preferred treatment is dual combination with an endothelin receptor antagonist (ERA) and a phosphodiesterase-5 (PDE5) inhibitor.

🔴Calcium channel blockers are indicated for vasoreactive patients.

🔴Triple therapy is reserved for high-risk patients including parenteral prostacyclin therapy

Question 25

Bronchodilator reversibility definition

Answer 25

> 10% of predicted value in FEV, or FVC

Question 26

Respiration physiology during pregnancy

Answer 26

The major change in pulmonary function testing in pregnancy is a progressive decrease in the expiratory reserve volume by 8% to 40% and a decrease in residual volume by 7% to 22%, both changes caused by the enlarging uterus and diaphragmatic elevation.

Total lung capacity may decrease slightly, inspiratory capacity increases, and vital capacity does not change significantly during pregnancy.

Tidal volume increases significantly during pregnancy by 150 ml to a final value of 450 to 600 mL

Question 27

Indication for re-occurrence prevention in pneumothorax

Answer 27

Recurrence prevention is recommended after:
A) The second episode of pneumothorax on the ipsilateral side in primary spontaneous pneumothorax
B) After the first occurrence in secondary spontaneous pneumothorax.
C) following a first episode of pneumothorax in spontaneous primary pneumothorax in a patient with a high risk occupation. (Scuba diver, Pilot)

Question 28

Inhalation injury management

Answer 28

.Following smoke inhalational injury immediate protection of the airway is indicated for patients with extensive facial or neck burns, decreased level of consciousness, or airway obstruction.

One third of patients develop airway edema or mucosal sloughing from epithelial necrosis; airway inspection, bronchoscopy,
and chest physiotherapy are frequently necessary to facilitate continued airway clearance.

Question 29

management of malignant pleural effusion

Answer 29

Initial treatment of a malignant pleural effusion in patients with expandable lung includes either an indwelling pulmonary catheter or chemical pleurodesis with talc.

In patients with a malignant pleural effusion and a nonexpanding lung (air replacing the drained pleural effusion on a post thoracentesis chest radiograph.), an indwelling pulmonary catheter is the treatment of choice.

Repeat therapeutic thoracentesis is appropriate for patients with poor prognosis (<3 months) and slow reaccumulation of fluid.

Question 30

When not to biopsy in Sarcoidosis

Answer 30

Clinical presentations of sarcoidosis that do not require a biopsy include:
–Asymptomatic stage I pulmonary sarcoidosis,
–Lofgren syndrome (Bilateral hilar lymphadenopathy, migratory polyarthralgia, & Erythema nodusum)
–Heerfordt syndrome. (Anterior uveitis, Parotitis, Facial nerve palsy and Fever)

Question 31

High altitude pulmonary edema

Answer 31

Caused by exaggerated hypoxic pulmonary vasoconstriction and abnormally high pulmonary artery and capillary pressures.
Risks for this disorder include rapid ascent to altitudes greater than 2.500 meters. the actual altitude attained, time spent at altitude, and a history of high-altitude illness.

Treatment of HAPE focuses on promptly reducing the pulmonary artery pressure. This can be done by providing supplemental oxygen. limiting the patient’s physical exertion and cold exposure, and advising the patient to descend to a lower altitude as soon as possible. ‘
Some clinicians suggest
the use of nifedipine as adjunctive therapy, but there is a paucity of data to confirm its benefit.
Acetazolamide is commonly used for prophylaxis against HAPE, but it has no role in treatment.

Question 32

Assessment of subsolid nodules

Answer 32

An incidentally found ground-glass (subsolid) pulmonary nodule 6 mm or larger necessitates follow up chest CT at 6 to 12 months; if it persists but is unchanged in size, CT should be repeated at 2-year intervals for 5 years.

Question 33

Hypothermia management

Answer 33

Severe hypothermia is defined by a core temperature of less than 28.0 ‘C (82.4 “F) in the setting of ongoing coma or cardiovascular collapse.

For temperatures less than 28.0 ‘C (82.4’F) and for patients who fail to respond adequately to active
external rewarming, active internal rewarming methods, including infusion of heated intravenous crystalloid solution and lavage of the peritoneal or pleural cavities with warm fluids, should be applied.

Question 34

COPD and Air travel

Answer 34

Resting pulse oximetry is helpful in screening patients for in-flight hypoxemia.

–Patients with resting SPO2, greater than 95% are unlikely to experience significant hypoxemia in flight.
–Patients with resting SPO2, between 92% and 95% require assessment of risk factors and may need additional testing such as high-altitude simulation testing, if available.
–For those whose resting SPO2, is less than 92% supplemental oxygen should be prescribed and there is no need for additional testing.
Typically, if patients do not require oxygen at baseline, then prescribing 2 L/min of oxygen is sufficient.

Question 35

FeNO utilization

Answer 35

–FeNO levels above 50 ppb correlate with eosinophilic airway inflammation and predict response to inhaled glucocorticoids.
–FeNO levels below 25 ppb indicate that eosinophilic airway inflammation and glucocorticoid responsiveness are less likely;
–values between 25 and 50 ppb should be interpreted cautiously.

In patients with asthma that is being treated with inhaled glucocorticoids, serial measurement of FeNO may help to monitor patient response to glucocorticoid therapy.

Question 37

Sarcoidosis initial workup

Answer 37

initial evaluation should include:
🔴Pulmonary function testing
🔴Ophthalmologic examination
🔴Electrocardiography to screen for cardiac sarcoidosis
🔴A serum creatinine level to screen for renal sarcoidosis
🔴A serum alkaline phosphatase level to screen for liver sarcoidosis
🔴A serum calcium level to screen for hypercalcemia
🔴A complete blood count to screen for hematologic abnormalities