Pulm Mksap 16

Front 1

Kuszmaul sign

Back 1

Neck vein distention during inspiration due to increased right-sided venous pressure due to:
-Right ventricular infarction
-Tension pneumothorax
-PE
-tamponade

Front 2

Stridor

Back 2

Most prominent over the glottis. More distinct upon inspiration.

Front 3

PFT for asthma

Back 3

FEV1/FVC <70

Normal FEV1 >80%

FEV1/FVC < 70 in general indicates airway obstruction

Front 4

When is it necessary to taper steroids

Back 4

After 14 days of use

Front 5

BOOP

Back 5

Idiopathic bronchiolitis obliterans organizing pneumonia

Front 6

Relationship of ciprofloxacin to Theo

Back 6

Cipro can inhibit the hepatic breakdown of Theo leading to toxic levels

Front 7

Spirometry

Back 7

It the most widely used pulmonary function test.

Spirometry is obtained by measuring the forced expiratory volume overtime after the patient has taken a deep inspiration.

Front 8

FVC

Back 8

Forced vital capacity: the maximum volume exhaled

Front 9

How PET scans work

Back 9

PET scanning is based on the principle that cancer cells have a high rate of glycolysis (converting glucose to energy) compared to non-cancer cells.

Front 10

Causes a false positive PET scans

Back 10

-TB
-Fungal diseases
-Sarcoidosis
-Other inflammatory condition

Front 11

Causes of false negative PET scans

Back 11

Low-grade tumor such as:
-Adenocarcinoma in situ
-Carcinoid tumor
-Malignancies less than 1 cm in diameter

Front 12

Best use of bronchoscopy

Back 12

Effective method for sampling:
-Central airway lesions
-Mediastinal nodes
-Parenchymal masses

Pearls: Peripheral pulmonary nodules < 2 cm in diameter are best sampled with CT guided percutaneous biopsy

Front 13

Use of endobronchial ultrasound

Back 13

It has made endoscopic lung cancer staging similar in yield to mediastinoscopy but without skin incision and general anesthesia

Front 14

Asthma remodeling

Back 14

It is due to uncontrolled inflammation or repeat exacerbations leading to structural airway changes.

Front 15

Age onset of asthma

Back 15

Typically in childhood but adult onset is well recognized even in the elderly.

Front 16

Incidence of asthma

Back 16

5% of the adult population in the US.

More prevalent in western cultures.

Front 17

Allergan testing in asthma

Back 17

Between 70 and 90% of patients with asthma have allergies demonstrated with skin testing and confirmed by relevant history

Front 18

Typical asthma triggers

Back 18

Viral URI
Cold air
Stress
Exercise

Front 19

FEV1

Back 19

The forced expiratory volume exhaled in the first second

Front 20

Clubbing is suggestive of what disease?

Back 20

Cystic fibrosis

Front 21

Confirmatory asthma testing

Back 21

FEV1/FVC ratio: <70

Reversibility (12% or greater improvement in FEV1 after administration of bronchodilators)

Patients with suspected asthma who have normal spirometry should undergo a bronchial challenge test to assess for airway hyperresponsiveness; a negative test generally excludes asthma

Front 22

Early and late responses of asthma attacks

Back 22

Early phase: 30 minutes to 1 hour

Late response: return of asthma symptoms 3 to 8 hours after

Front 23

Reactive airways dysfunction syndrome (RADS)

Back 23

It is a distinct type of occupational asthma that results from a single accidental exposure to high levels of irritant vapors, gases, or fumes such as chloride gas, bleach or ammonia.

This exposure leads to significant airway injury with PERSISTENT airway inflammation, dysfunction, and hyperresponsiveness.

Symptoms can persist for years afterwards.

Front 24

Cough variant asthma

Back 24

It is a type of asthma in patients who have cough as their main symptom.

The cough is typically dry and sometimes the only symptom of asthma.

The diagnosis is confirmed with spirometry that demonstrates obstruction with improvement following bronchodilator or with bronchial challenge testing that shows responsiveness.

Front 25

Allergic bronchopulmonary aspergillosis

Back 25

This condition should be thought of with patients who have difficult to control asthma or frequent exacerbations requiring systemic steroids.

A chest x-ray should be obtained which often will show: pulmonary infiltrates or bronchiectasis

This condition is a result of sensitization Aspergillus fumigatus.

DX:
Chest x-ray
Elevated serum levels of IGE
Positive skin test to Aspergillus
Eosinophilia

Pearls: left untreated BPA can result in progressive pulmonary fibrosis and loss of lung function.

Front 26

Characteristics of exercise-induced bronchospasms

Back 26

Triggered by breathing in cold or dry air

Symptoms are at their worst not during exercise but immediately following cessation of exercise.

Bronchial obstruction peaks 5 to 10 minutes after cessation and resolves within 30 minutes.

Pearls: symptoms should be distinguished from vocal cord dysfunction or exercise-induced Gerd

Prevention: treatment with short acting Beta2 agonist 15 minutes before exercise. This protection can last up to 3 hours.

Front 27

Symptoms of vocal cord dysfunction

Back 27

Prominent wheezing that is more noticeable during inspiration (stridor).

Abrupt onset of symptoms that are felt in the neck. Abrupt onset is NOT typical of asthma.

Pearls: this condition can be difficult to diagnosed in a patient with a history of asthma.

DX: laryngoscopy

RX: patient education, behavior modification, and speech therapy.

Front 28

Samter Triad

Back 28

1. Severe asthma
2. Aspirin sensitivity
3. Nasal polyps

Aspirin sensitivity should be considered in patients with difficult to control disease.

Asthma patients who must use aspirin should be referred for desensitization.

Front 29

Typical viruses that cause URIs that triggers asthma

Back 29

Rhinovirus
Respiratory syncytial virus
Influenza

Front 30

Bronchial challenge testing

Back 30

Diagnostically positive if FEV1 falls 20% from baseline.

This test is sensitive for asthma but not very specific.

Front 31

A main goal of asthma management

Back 31

To reduce the need for rescue albuterol to less than twice weekly

Front 32

Types of asthma

Back 32

1. Intermittent
2. Persistent: persistent asthma is further classified as:
-Mild
-Moderate
-Severe

Front 33

What does MDI mean?

Back 33

Pressurized metered-dose inhalers

Pearls: poor inhaler technique is a common cause of lack of response to asthma therapy

Front 34

Types of long acting Beta2 agonist

Back 34

Salmeterol - slower onset of action
Formoterol - rapid onset of action and last for 12 hours

Use: typically added with inhaled steroids if symptoms are not adequately controlled after inhaled steroids optimized.

Pearls:
1. Provide no anti-inflammatory effects
2. Treatment with long acting Beta two agonist as a single agent therapy in asthma is not appropriate. It can mask worsening of airway inflammation and lead to increased risk of asthma related complications.
3. There is a risk of death with these agents which has led the FDA to require a black box warning.

Front 35

Anticholinergic agents used in asthma and COPD

Back 35

Short acting: Ipratropium. Primarily used in COPD but also can be used in as well to enhance the bronchodilator effect of short acting Beta two agonist.

Long acting: Tiotropium

Front 36

Leukotriene modifying drugs

Back 36

Monteluast or Singulair

Zafirlukast or Accolate

Zileuton or Zyflo

These medications block the leukotriene effect of promoting mucus secretion, vasodilatation, and inflammation.

They are used primarily as an add-on or alternative to the mainstay medications for asthma.

These medications have been reported to cause neuropsychogenic events such as agitation, anxiety, hallucinations, depression and suicidal ideation. As a result the FDA and it a black box warning.

Owing to concerns about liver toxicity, Zyflo use has been limited.

Front 37

Theophylline use

Back 37

It is one of the oldest drugs for asthma.

The benefits of using this drug is it's ease-of-use and low cost.

Drawbacks of using this drug is that it is a weak bronchodilator and has a very narrow therapeutic margin.

It is used primarily as a second line alternative to inhaled corticosteroids.

Target therapeutic range is 5-12 ng/mL.

Flouroquinolones have been known to increase its circulating levels.

Symptoms of toxicity: tremor, headaches, nausea, palpitations, arrhythmia, seizure

Front 38

The mainstay controllers of asthma

Back 38

1. Short acting Beta two agonist
2. Inhaled corticosteroids

Front 39

Anti-IGE antibody pulmonary medications

Back 39

Omalizumab or Xolair

Only recommended for severe asthma who have evidence of allergies, have elevated IGE between 30 and 700, and remain symptomatic despite optimizing treatment with combination therapy.

Serious risk of anaphylactoid reaction; Therefore should be administered by an asthma specialist and the patient should be monitored for two hours after initial three doses and one hour after subsequent treatments.

Front 40

Reduced TLC indicates?

Back 40

TLC: total lung capacity

Reduced TLC indicates chest restriction (<80% of predicted)

Front 41

Diffusing capacity of carbon monoxide (DLco)

Back 41

Diffusing capacity of carbon monoxide measures the lung's ability to transfer gas across the alveolar-capillary membrane.

Front 42

Six minute walk test

Back 42

The six minute walk test is very useful indicator of the patient's functional capacity.

This particular helpful in patients with advanced lung or heart disease.

Front 43

Accuracy of pulse ox

Back 43

Accurate within 2% to 3% of arterial oxygen saturation.

Pearls: carboxyhemoglobin can cause falsely elevated oxygen saturation readings because oxyhemoglobin and carboxyhemoglobin waves are not distinguishable by most pulse ox devices.

Therefore, pulse ox should not be used in patients who are victims of fire or smoke inhalation.

Front 44

Upper lobe findings on chest x-ray

Back 44

Often due to:
-TB
-Sarcoidosis
-Silicosis
-Cystic fibrosis
-Languor hands cell histiocytosis

Front 45

Lower lobe findings on chest x-ray

Back 45

Often due to:
-Pulmonary fibrosis
-Cryptogenic organizing pneumonia
-Asbestosis
-Heart failure

Front 46

Effective dose of radiation from CT versus chest x-ray

Back 46

Approximately 40 times that of a chest x-ray

Front 47

Go maintenance of O2 in asthma exacerbation

Back 47

92%

Front 48

How bronchodilators work?

Back 48

Relax the smooth muscles in the airways, resulting in widening of the airways.

Front 49

Side effects of long-term use of inhaled steroids?

Back 49

1. Osteopenia
2. Hyperglycemia
3. Cataracts

Front 50

What is the effective dose of IV steroids in severe COPD exacerbation?

Back 50

The effective dose is not known

Front 51

Went to use anabiotic's and COPD

Back 51

1. In treating infectious exacerbations of COPD.
2. In patients with severe exacerbations of COPD who require mechanical ventilation, whether invasive or noninvasive.

A quinolone or third-generation cephalosporin is usually a good choice to cover pulmonary pathogens.

Front 52

Initiation of treatment for COPD

Back 52

1. Initiate monotherapy with long-acting bronchodilator or long-acting anticholinergic in patients with FEV1 less than 60% of predicted.
2. Inhaled corticosteroids should not be used alone for maintenance or rescue of COPD. This is different than asthma.

Front 53

Recommendation for oxygen at home

Back 53

1. Resting hypoxemia with PaO2 of 55 or lower
2. Resting pulse ox of 88% or lower

Front 54

What is lung volume reduction surgery?

Back 54

Involves respecting up to 30% of disease or nonfunctioning parenchyma to reduce hyperinflation and allow the remaining lung to function more efficiently.

It is only recommended in advanced COPD (maximum FEV1 less than or equal to 45%)

Front 55

Indications for pulmonary rehab in COPD

Back 55

1. FEV1 less than 50% of predicted

Front 56

Best test for evaluating diffuse parenchymal lung disease?

Back 56

High resolution chest CT

Front 57

Idiopathic pulmonary fibrosis

Back 57

The most common idiopathic interstitial disease.

CT findings: peripheral and basal prominent groundglass, honeycomb and reticular changes.

Prognosis, is poor with median survival 3 to 5 years.

Treatment:
1. multiple studies have failed to demonstrate any benefit of steroids in IPF.
2. Lung transplantation is the only intervention shown to improve survival.

Front 58

Peak expiratory flow rate (PEFR) in acute asthma exacerbation

Back 58

Moderate exacerbation: PEFR 40-69% of predicted personal best

Severe exacerbation: PEFR <40%

Front 59

Characteristics of nonspecific interstitial pneumonia

Back 59

Most often associated with underlying connective tissue disease.

Diagnosis:
1. Chest CT showing groundglass without honeycombing
2. requires open lung biopsy showing lymphoplasmacytic interstitial infiltration

Treatment: responds to steroids

Front 60

What is cryptogenic organizing pneumonia?

Back 60

COP is the idiopathic form of bronchiolitis obliterans organizing pneumonia (Boop).

Presentation: it initially presents with cough and shortness of breath suggestive of CAP. But is thought about after the first 6 to 8 weeks of treatment with antibiotics but patient not improving.

CXR: bilateral, diffuse opacities

Diagnosis: lung biopsy confirmed dx

Treatment: good response to systemic steroids

Front 61

Common connective tissue diseases that cause interstitial lung disease?

Back 61

1. Systemic sclerosis: diffuse parenchymal lung disease is the leading cause of mortality
2. Rheumatoid arthritis

Front 62

What is hypersensitivity pneumonitis?

Back 62

Pneumonitis caused by repeat inhalation of finely dispersed antigens; Such as mold, bird feathers and droppings, laboratory animal dander and so on.

Treatment:
1. Antigen avoidance
2. Oral steroids for patients with severe symptoms

Front 63

Types of drugs that cause parenchymal lung disease

Back 63

1. Amiodarone: Clarence of drug from pulmonary parenchyma is very slow. Lung disease is one of the leading causes of stopping this medication.
2. Methotrexate; Less than 5% of patients treated with this drug developed diffuse pulmonary infiltrates.
3. Nitrofurantoin; Kerley B lines seen on chest x-ray

Front 64

Radiation pneumonitis

Back 64

Present with cough and/or dyspnea 6 weeks after exposure.

Most parenchymal changes resolve after six months.

Treatment: steroids in some cases

Front 65

Sarcoidosis lung manifestation

Back 65

Sarcoidosis is a multi organ inflammatory disease characterized by tissue infiltration by:
-Noncaseating granulomad
-Mononuclear phagocytes
-Lymphocytes

90% of patients with sarcoidosis will have pulmonary involvement.

CXR/CT: hilar lymphadenopathy (Lofgren syndrome)

Front 66

What is Lymphogioleiomyomatosis?

Back 66

It is a rare cystic lung disease seen in young women of childbearing age or in association with tuberous sclerosis.

Consider this diagnosis when spontaneous pneumothorax and chtlothorax in a young woman with chest imaging demonstrating hyperinflation and chest CT showing diffuse, thin-walled, small cyst.

Front 67

Bronchial thermoplasty

Back 67

Indicated in severe cases/difficult to manage asthma.

It consist of applying heat to the airway with a catheter that is inserted via bronchoscope connected to radio frequency generator. This treatment should occur three times.

It is supposed to reduce smooth muscle hypertrophy which has been reported in patients with asthma.

Front 68

Tests for asthma doing pregnancy that should not be done

Back 68

1. Allergen Skin testing

2. Bronchial challenge testing is actually contraindicated

Front 69

Asthma medication safe during pregnancy

Back 69

Essentially all of them including theophylline and leukotriene receptor antagonist.

Although systemic steroids have been linked to a small risk of congenital abnormalities, their use is recommended in patients with acute severe asthma.

Pearl: asthma is one the most common medical problems that complicates pregnancy.

Front 70

Pathophysiology of COPD

Back 70

Slowly progressive inflammatory disease of the airways and lung parenchyma.

It is characterized by gradual loss of lung function with increasing obstruction to EXPIRATORY airflow.

Front 71

Pulmonary complications of COPD

Back 71

Pulmonary hypertension
Cor pulmonale
Pneumonia
Pneumothorax
Bronchiectasis
Atelectasis
Lung cancer

Front 72

Percentage of heavy smokers who develop COPD

Back 72

20%

Front 73

Large global risk factor for COPD other than smoking

Back 73

Exposure to smoke from indoor burning biomass fuels such as wood, charcoal, and vegetable matter.

Front 74

Test to diagnose COPD

Back 74

Spirometry: a post bronchodilator FEV1/FVC ratio less than 70 is diagnostic.

Note, diagnostic spirometry should be performed AFTER administration of inhaled bronchodilators because this will improve the accuracy of the study results.

Front 75

Asbestosis exposure period in the US

Back 75

1940-1979

Front 76

When to do a thoracentesis due to plural effusion?

Back 76

Unexplained effusions >1 cm in thickness

Front 77

Testing for transudative or exudative plural effusion:

Back 77

Exudative if one criteria met:
1. Pleural total protein to serum total protein ratio > 0.5

2. Pleural fluid lactate dehydrogenase (LDH) level >2/3 the upper limit of normal

Transudative if neither of the above criteria met.

Front 78

Conditions associated with bloody pleural effusions?

Back 78

-Trauma
-Cancer
-Tuberculosis

Front 79

The three types of parapneumonic effusions

Back 79

1. Uncomplicated: exudative, White blood cells present but no bacteria. No drainage needed.
2. Complicated: exudative, bacteria present in fluid. May respond to antibiotics but likely require drainage.
3. Empyema: pus in the plural space. Always requires drainage.

Front 80

Low pleural fluid glucose suggest:

Back 80

-TB
-Parapneumonic effusion
-Malignant effusion
-Rheumatoid disease

Front 81

Pleural fluid analysis of chylothorax

Back 81

-TG >110
-Presence of chylomicrons

Front 82

Pleural fluid analysis seen TB

Back 82

Any lymphocytic predominate exudate in the presence of a positive PPD should be considered TB until proven otherwise.

Front 83

Latency period of asbestos?

Back 83

15 to 35 years

Front 84

Type of lung disease caused by asbestosis

Back 84

Restrictive lung disease

Front 85

Pleural effusion seen in asbestosis

Back 85

Benign, exudative, often hemorrhagic effusions with eosinophils present 30% of the time.

Front 86

Lung cancers associated with asbestos exposure

Back 86

-Small cell
-Non-small cell carcinoma
-Mesothelioma

Smoking in setting of asbestos exposure increases risk of lung cancer 60 fold.

Front 87

What is asbestos made of?

Back 87

Hydrated silicate fiber

Front 88

What is the actual substance that causes silicosis?

Back 88

Crystalline silicon dioxide (silica)

Any occupation that disturbs the earth's crust or uses or processes silica-containing rock or sand has potential risks of exposure.

Front 89

Silicosis increases the risk of these other diseases:

Back 89

-Tuberculosis
-Autoimmune diseases: systemic sclerosis, rheumatoid arthritis, and Lupus
-Lung cancer

Front 90

Treatment of silicosis

Back 90

There is no specific proven therapies.

Treatment of symptomatic silicosis: inhaled bronchodilators, anabiotic's for infection, supplemental oxygen in patients with hypoxemia

Pearls:Patients with silicosis should be screened for TB

Front 91

What are the top three causes of pleural effusions?

Back 91

1. CHF
2. Parapneumonic
3. Malignant Effusions

Front 92

Treatment of empyema

Back 92

1. Anabiotic's
2. Drainage
3. Intrapleural tissue plasminogen activator combined with deoxribonuclease to increase pleural drainage, decrease hospital stay, and decreased need for surgery later.

Front 93

Definition of spontaneous pneumothorax

Back 93

Spontaneous pneumothorax is classified as primary if lung disease is absent, and is considered secondary if lung disease is present.

Front 94

Risk factors for primary spontaneous pneumothorax

Back 94

1. Smoking
2. Family history
3. Marfan syndrome
4. The thoracic endometriosis

Front 95

Definition of small pneumothorax

Back 95

Defined as <2 cm between the lung and the chest wall on CXR

SMALL PRIMARY PNEUMOTHORACES CAN BE MONITORED WITHOUT INTERVENTION. BUT EVEN SMALL SECONDARY PNEUMOTHORACES MUST BE MANAGED IN THE HOSPITAL.

Front 96

The percentage of untreated DVT's which lead to PE

Back 96

10% to 30%

Front 97

Most common signs of PE

Back 97

-Tachypnea
-Pleuritic pain
-Dyspnea
-Anxiety
-Cough
-Increased intensity of pulmonic component of S2

Front 98

When is checking a D-dimer indicated in PE

Back 98

Only in low pretest probability of PE should you check a d-dimer. Because if negative in moderate to high pretest probability continued workup is indicated.

A negative D dimer in low pretest probability, clinically stable patients virtually excludes PE and eliminates further testing.

Front 99

EKG changes in acute PE

Back 99

-Tachycardia
-Right axis deviation
-Right bundle branch block
-S1Q3T3 pattern

Front 100

Clinical scenarios were VQ scan is less reliable

Back 100

-Abnormal chest x-ray
-Patients with COPD or other conditions were holding breath is difficult

Front 101

Medications approved for treatment of acute PE

Back 101

Heparin IV
Lovenox
Arixtra
Coumadin

Front 102

How many days should the bridging anticoagulation occur after therapeutic range is reached with Coumadin

Back 102

2 consecutive days. This ensures that all vitamin K dependent factors have declined and physiologic anticoagulation has been reliably achieved.

Front 103

How many days should the bridging anticoagulation occur after therapeutic range is reached with Coumadin

Back 103

2 consecutive days. This ensures that all vitamin K dependent factors have declined and physiologic anticoagulation has been reliably achieved.

Front 104

Treatment of acute PE and setting of hypotension

Back 104

1. Judicious IV fluids
2. Vasoconstrictors
3. Thrombolytic therapy in refractory hypotension followed by anticoagulation
4. If thrombolytics contraindicated, surgical or catheter embolectomy should be considered.

Front 105

Duration of anticoagulation in patients with first episode of acute PE

Back 105

3 months, after which the likely cause and the risks and benefits of treatment are reassessed

Front 106

Definition of pulmonary hypertension

Back 106

Defined as the elevation of main pulmonary artery pressure of 25 or greater during rest.

Diagnoses of PH can only be confirmed by right heart catheterization and direct measurement of me pulmonary artery pressure. A CARDIAC ULTRASOUND SHOWING A SYSTOLIC MEAN PULMONARY ARTERY PRESSURE 40 or GREATER IS HIGHLY SUGGESTIVE BUT NOT DIAGNOSTIC. Echo can be used to monitor progression.

Front 107

Causes of pulmonary hypertension

Back 107

80% of cases of pulmonary hypertension are due to left-sided heart dysfunction or underline chronic lung disease

Front 108

Treatment of pulmonary hypertension

Back 108

-In most cases treat the underlying cause. Unless 'isolated' pulmonary arterial hypertension.

-The benefits of vasodilator therapy in this population remained unproven.

Front 109

Initial recommend test to evaluate for chronic thromboembolic pulmonary hypertension

Back 109

VQ scan: invariably has mismatching

Treatment:
1. Anticoagulation.
2. Definitive treatment is surgical, involves removing organize clots.

Front 110

The difference in pulmonary hypertension (PH) and pulmonary arterial hypertension (PAH)?

Back 110

PAH is a subset of PH with:
-Elevated mean pulmonary artery pressure
-Normal pulmonary capillary wedge pressure less than or equal to 15
-Elevated pulmonary vascular resistance

The origin of this condition is not clear but it likely involves intrinsic under expression of vasodilators such as prostaglandin and nitrous oxide and an overexpression vasoconstrictors.

Treatment:
1. Diuretics as needed
2. Anticoagulants to prevent in situ clot formation come in many forms of this condition
3. Cardiac glycosides to augment right heart dysfunction
4. Supplemental oxygen
5. Pulmonary artery vasodilators

Pearls: Right heart cath should be performed to confirm pulmonary artery hypertension and to assess a vasodilator responsiveness before long term vasodilator therapy is attempted.

Front 111

Definition of a pulmonary nodule

Back 111

1. A focal, nodule opacity
2. Up to 3 cm in diameter
3. Surrounded by normal lung tissue
4. Not associated with lymphadenopathy

Lung lesions over 3 cm are considered lung masses and have a much higher likelihood of malignancy

The nodule size it is often the most important feature in predicting malignancy

Front 112

Paraneoplastic Lambert-Eaton syndrome is caused by which lung cancer

Back 112

Small cell

Front 113

Staging system of non-small cell lung cancer

Back 113

T-tumor, N-node, M-metastasis

Front 114

Best standard surgical approach to resection of stage I or stage II NSCLC

Back 114

Lobectomy

Patients who have marginal pulmonary reserve, limited resection such as a segmentectomy or wedge resection may be a more appropriate surgical option for these patients.

These resections are increasingly being performed by video-assisted thoracic surgery (VATS) versus thoracotomy.

Stage III and stage IV lung cancer is treated with chemotherapy alone or in combination with XRT

Front 115

Treatment of small cell lung cancer

Back 115

Limited stage small cell lung cancer is treated primarily with combination of chemotherapy and XRT.

Front 116

Pulmonary nodules benign vs malignant characteristics

Back 116

1. 90% of nodules smaller than 8 mm are benign, whereas the majority of nodules larger than 2 cm are malignant.

2. Nodule smooth borders is consistent with being benign; a speculated border indicates a high likelihood of malignancy.

Front 117

Pulmonary nodules that should not be followed

Back 117

Less than 4 mm in diameter in never smokers or other risk factors for malignancy.

Front 118

Two-year nodule stability rule

Back 118

Solid nodules that remained stable in size for two years on chest x-ray or CT are considered benign and no further follow-up is indicated

Front 119

What are the two types in which lung cancer is divided?

Back 119

1. Non-small cell lung cancer (NSCLC). 80% of all lung cancer.
2. Small cell lung cancer (SCLC)

Front 120

Subtypes of non-small cell lung cancer

Back 120

1. Adenocarcinoma - pre-invasive, minimally invasive, or invasive
2. Squamous cell carcinoma
3. Large cell carcinoma

Front 121

Smoking rates in America

Back 121

20% of men

15% women

Front 122

Risk factors for lung cancer

Back 122

-Tobacco smoke
-Asbestos
-Radon
-Certain metals-arsenic, chromium, nickel
-Ionizing radiation
-Polycyclic aromatic hydrocarbons
-Pulmonary fibrosis

Front 123

Paraneoplastic SIADH is caused by which lung cancer

Back 123

Small cell

Front 124

Paraneoplastic hypercalcemia is caused by which lung cancer

Back 124

Squamous cell

Front 125

What is mesothelioma

Back 125

A neoplasm that arises from the mesothelial surfaces of the pleural and peritoneal cavities.

80% arise from the pleural cavity.

Prognosis: poor with median survival of 6-18 months

common symptom: dull, unrelenting pain

Treatment: chemo but usually doesn't work

Front 126

What are carcinoid tumors is of the lung

Back 126

Low-grade malignancy consisting of cells of neuroendocrine origin.

No association with smoking.

Typically endobrachial location: therefore patients present with hemoptysis or evidence of obstruction.

Two types of carcinoid tumor of the lungs: typical and atypical

Treatment: surgical resection in both cases.

Carcinoid syndrome (flushing and diarrhea) is rare in carcinoid tumor lung.

Front 127

Location of the mediastinum

Back 127

Lies between the two plural surfaces in the center of the chest and is divided into anterior, middle, and posterior compartments.

Front 128

Masses is found in the anterior mediastinum

Back 128

-Lymphoma
-Thyroid or parathyroid tumors
-thymoma or thymic carcinoma
-Teratoma

Front 129

Paraneoplastic syndrome associated with thymoma?

Back 129

-Myasthenia gravis
-pure red cell aplasia
-Hypogammaglobulinemia

Front 130

Masses found in middle mediastinum

Back 130

-Enlarged lymph nodes from Mets
-Lymphoma
-Granulomatous disease (sarcoidosis, fungal infections, TB)
-Giant lymph node hyperplasia (Castlemans disease)
-Diaphragmatic hernia
-Pericardio cyst
-Bronchogenic cyst

Front 131

Masses found and posterior mediastinum

Back 131

-Neurofibroma
-Nuerilemmoma/Schwannoma
-leiomyomas

Front 132

What is mean sleep latency testing (MSLT)

Back 132

This test provides an objective measure of sleepiness and is key to establishing the diagnosis of narcolepsy and Idiopathic hypersomnia.

A mean sleep latency of more than 15 minutes is considered normal and less than 5 minutes is indicative of a pathological sleepiness.

Front 133

Cheyne-Stokes Breathing

Back 133

It is the most common type of central sleep apnea and is also referred to as periodic breathing.

It is characterized by crescendo-decrescendo pattern of ventilation.

It is strongly associated with heart failure.

Front 134

Jet lag

Back 134

Results when the internal circadian clock is out of phase with the local time following air travel across multiple times zones. Usually more than 5 times zones.

It is basically an misalignment between the body's internal clock and the world's external clock.

Front 135

Apnea

Back 135

Complete cessation of airflow in the upper airways

Front 136

Hypoapnea

Back 136

Characterized by reduction in airflow in the upper airways.

Front 137

What is the apnea-hypo apnea index (AHI)

Back 137

It is the number of disordered breathing events (apnea and hypoapnea) per hour of sleep.

-An AHI of 5 to 15 indicates mild OSA.

-And AHI of more than 30 indicates severe OSA.

Front 138

Mammalian dive reflex

Back 138

In response to hypoxemia there is an acute surg in peripheral vascular resistance along with a slowing of the heart rate.

This is the pathophysiology of obstructive sleep apnea.

Front 139

The most important risk factor for OSA?

Back 139

Obesity

Front 140

Definition of central sleep apnea

Back 140

It is characterized by loss of ventilatory output from the central respiratory generator in the brainstem to the respiratory pump, which manifest on polysomnogram with the absence of respiratory effort associated with loss of airflow for at least 10 seconds.

A key mechanism of central sleep apnea is the tendency to hyperventilate and thus drive down the arterial CO2 to a level near apneic threshold-the point at which respiratory effort ceases.

Symptoms:
-Frequent awakening from sleep
-Insomnia
-Non-restorative sleep
-EDS
-Proximal nocturnal dyspnea

Diagnosis: Polysomnogram. Oximetry alone is not adequate to distinguish between OSA and CSA.

Treatment:
1. control any underlying comorbidity.
2. Adaptive servoventilation (ASV). Note CPAP can often worsen CSA unless there's underlying OSA.

Front 141

Sleep breathing drive

Back 141

Breathing while sleeping is primarily driven by blood carbon dioxide tension or arterial CO2 as opposed to arterial oxygen levels.

Front 142

Risk factors for central sleep apnea

Back 142

Heart failure
Afibrillation
Stroke
Brainstem lesions
Kidney failure
Chronic CPAP use
Opiate use
High altitude

Front 143

Confirmation of hypoventilation syndrome

Back 143

<90% O2 saturation for at least five minutes
Or
02 saturation <90% for >30% of total sleep time

Front 144

Definition of daytime hypercapnia

Back 144

Arterial PaCO2 >45

This can be a cardinal sign of COPD with CO2 retention or obesity hypoventilation syndrome (OHS).

Front 145

What is high altitude periodic breathing

Back 145

Nearly everyone ascends to elevations greater than 25,000 feet will experience high altitude periodic breathing, which is characterized by cyclic central apneas and hyperapneas associated with repetitive arousals from sleep, often with paroxysms of dyspnea.

This condition is rare and elevations <8200 feet

Treatment:
-Gradual rather than rapid ascent
-Acetazolamide
-Oxygen as needed

Front 146

Symptoms of acute mountain sickness and high altitude cerebral Edema

Back 146

Mountain sickness tends to occur at elevations greater than 6500 feet.

Symptoms of mountain sickness: headache, fatigue, nausea, vomiting, disturbed sleep

Symptoms of high altitude cerebral edema: Encephalopathic/altered mental status and ataxia. Both signs of cerebral edema in response to vasogenic brain swelling.

Treatment of cerebral edema:
-Descent
-Dexamethasone
-Oxygen
-Hyperbaric therapy

Front 147

High-altitude pulmonary edema

Back 147

Thought to be secondary to elevations and pulmonary arterial pressures in response to hypoxemia.

Treatment:
-Oxygen
-Descent
-If above not available vasodilators such as nifedipine or phosphodiesterase-5 inhibitors (Sildenafil)

Front 148

Air travel pulmonary disease

Back 148

Commercial airline cabins are pressurize to an equivalent of approximately 5000 to 8200 feet which carries an oxygen tension of 110 and 120 mmHg.

Normal, at sea level, levels are 150 to 160 mmHg of oxygen.

A person with the pulse ox <92% indicates a probable need for in-flight supplemental oxygen.

Contradictions to airflight:
-COPD exacerbation with air trapping
-Pneumothorax of any size

Front 149

Confirmation of hypoventilation syndrome

Back 149

<90% O2 saturation for at least five minutes
Or
02 saturation <90% for >30% of total sleep time

Front 150

Definition of daytime hypercapnia

Back 150

Arterial PaCO2 >45

This can be a cardinal sign of COPD with CO2 retention or obesity hypoventilation syndrome (OHS).

Front 151

Symptoms of acute mountain sickness and high altitude cerebral Edema

Back 151

Mountain sickness tends to occur at elevations greater than 6500 feet.

Symptoms of mountain sickness: headache, fatigue, nausea, vomiting, disturbed sleep

Symptoms of high altitude cerebral edema: Encephalopathic/altered mental status and ataxia. Both signs of cerebral edema in response to vasogenic brain swelling.

Treatment of cerebral edema:
-Descent
-Dexamethasone
-Oxygen
-Hyperbaric therapy

Front 152

High-altitude pulmonary edema

Back 152

Thought to be secondary to elevations and pulmonary arterial pressures in response to hypoxemia.

Treatment:
-Oxygen
-Descent
-If above not available vasodilators such as nifedipine or phosphodiesterase-5 inhibitors (Sildenafil)

Front 153

ARDS

Back 153

Acute respiratory distress syndrome. It is a non-cardiogenic form of pulmonary edema characterized by acute, persistent, diffuse lung inflammation that is injurious to alveoli and pulmonary capillary vasculature.

ARDS is now graded as mild, moderate, or severe based on pulse ox/arterial oxygen ratio.

Pulmonary edema seen in ARDS cannot be from a cardiac source.

Front 154

Confirmation of hypoventilation syndrome

Back 154

<90% O2 saturation for at least five minutes
Or
02 saturation <90% for >30% of total sleep time

Front 155

Definition of daytime hypercapnia

Back 155

Arterial PaCO2 >45

This can be a cardinal sign of COPD with CO2 retention or obesity hypoventilation syndrome (OHS).

Front 156

What is high altitude periodic breathing

Back 156

Nearly everyone ascends to elevations greater than 25,000 feet will experience high altitude periodic breathing, which is characterized by cyclic central apneas and hyperapneas associated with repetitive arousals from sleep, often with paroxysms of dyspnea.

This condition is rare and elevations <8200 feet

Treatment:
-Gradual rather than rapid ascent
-Acetazolamide
-Oxygen as needed

Front 157

Mortality with ARDS?

Back 157

40%

Front 158

Confirmation of hypoventilation syndrome

Back 158

<90% O2 saturation for at least five minutes
Or
02 saturation <90% for >30% of total sleep time

Front 159

Signs of diaphragmatic weakness

Back 159

Paradoxical inward motion of the abdomen with inspiration

Front 160

The nerve that innervates the diaphragm

Back 160

The phrenic nerve which arises from cervical spine roots 3, 4, and 5 (C3-5). Complete spinal cord injury above C3 level results in nearly complete loss of ventilatory muscle function.

Such patients require lifelong ventilatory support or diaphragmatic pacing.

Front 161

Kyphoscoliosis causes what kind of lung disease?

Back 161

Restrictive.

Restrictive lung disease can be considered extra-pulmonary; in which there is no underlying intrinsic lung disease.

Front 162

How do inhaled anticholinergics work?

Back 162

They modestly augment the bronchodilation affect achieved by short acting Beta 2 agonists.

Front 163

ICU admission criteria for asthma exacerbation

Back 163

No clinical improvement after one hour of aggressive bronchodilator therapy:
-Albuterol neb every 20 minutes x 3
-Ipratropium every 20 minutes times 3

Front 164

Definition of shock

Back 164

It is a state of decreased tissue perfusion, which can result in an adequate oxygen delivery for cellular needs.

Front 165

What is the Rapid shallow breathing index. used for?

Back 165

For determination of success rate or failure probability on vent weaning.

It is defined as the ratio of respiratory rate to tidal volume. If this ratio is greater than 105 there is a 95% chance of spontaneous breathing trial being unsuccessful. If it is less than 105 there's an 80% chance of success.

Front 166

Definition of ventilator associated pneumonia (VAP)

Back 166

It is defined as pneumonia with onset at least 48 hours AFTER endotracheal intubation.

Front 167

Meaning of SIRS

Back 167

Systemic inflammatory response syndrome. This term was introduced to describe findings:
1. Alter temperature
2. Tachycardia
3. Hyperventilation
4. Abnormal leukocyte count regardless of cause (inflammation or infection)

Front 168

Simple definition of sepsis

Back 168

SIRS plus suspected infection

Front 169

Definition of daytime hypercapnia

Back 169

Arterial PaCO2 >45

This can be a cardinal sign of COPD with CO2 retention or obesity hypoventilation syndrome (OHS).

Front 170

Simple definition of severe sepsis

Back 170

Sepsis associate with systemic effects including:
-Hypotension
-Decreased urine output
-Metabolic acidosis

Front 171

The amount of IV fluid resuscitation likely required in severe sepsis with hypotension?

Back 171

4 to 6 L in the first six hours

Front 172

When should steroids be given in sepsis?

Back 172

Only after blood pressure is found to be poorly responsive to fluid resuscitation and vasopressor therapy.

Front 173

Meaning of CRRT

Back 173

Continuous renal replacement therapy - a form of dialysis for hemodynamically unstable patients

Front 174

Injurious triggers for ARDS?

Back 174

Pneumonia
Aspiration
Near drowning
In elation injury
Trauma or lung contusion
Sepsis
Pancreatitis
Multiple blood transfusions

Front 175

How does Naloxone work?

Back 175

It is an opioid antagonist; thus an antidote to opioid overdose.

Other alternatives should be thought of after a total naloxone dose of 10 mg has been given and no quick clinical improvement.

It is relatively safe to give Naloxone (Narcan) to chronic opioid users but not to give the antidote (Flumazenil) to chronic benzodiazepine users.

Front 176

Treatment of bronchospasms and upper airway edema in burn victims?

Back 176

Inhaled racemic epinephrine and other bronchodilators

Front 177

What is the antidote to smoke inhalation induced cyanide toxicity?

Back 177

Sodium thiosulfate -Should be used rather than nitrates because of the risk of methemoglobin formation with use of nitrates.

Front 178

The pathophysiology of anaphylaxis?

Back 178

It results from an IgE activation on the surface of basophils and mast cells causing a massive release of histamine and other inflammatory mediators.

Severe symptoms:
-Hypotension, it is due to histamine increasing vascular permeability leading to large losses of circulating plasma volume.

Treatment: epinephrine IM or IV. Note, high dose or continuous epi may be needed for severe reactions or patients taking beta blockers.

Pearls: Radio contrast reaction is a special case in which the contrast agent directly activates mast cells without an IgE intermediary.

Front 179

Definition of angioedema

Back 179

Is localized tissue edema. For example affecting the lips, tongue, upper airway, G.I. tract and or extremities.

Angioedema can be due to an agent, particularly ACE I or familial.

Familial angioedema is associated with C1 inhibitor deficiency as characterized by episodes of angioedema that occur following trauma or illness and begin early in life.

Pearls:
- these forms of angioedema do not respond to usual anaphylaxis therapy, although airway management is essential owing to potential laryngeal edema.
- Angioedema can occur as a component of anaphylaxis, but it may also occur alone.

Front 180

Treatment of hypertensive urgency versus hypertensive emergency

Back 180

Hypertensive emergency should be treated with IV short acting medication generally not reducing blood pressure greater than 25% initially.

Hypertensive urgency generally should be treated with oral medications.

Front 181

Definition of hyperthermia

Back 181

Temperature above for 40 Celsius or 104 degrees Fahrenheit

Sources of hypothermia:
-Heat stroke
-Malignant hyperthermia
-Neuroleptic malignant syndrome

Front 182

Heatstroke

Back 182

Results from failure of the body's thermoregulatory system; the system may be impaired or overwhelmed.

Thermoregulation may be impaired in the elderly and in patients who have or being treated for conditions that can lead to dehydration or anhidrosis.

Treatment: evaporative cooling methods. There is no response to centrally acting antipyretic medications.

Front 183

Malignant hyperthermia

Back 183

It is A reaction to certain classes of drugs including anesthetics I feel healthy and in others.

Treatment:
- stop the offending agent
- Dantrolene (muscle relaxant) 5 to 10 minutes until hyperthermia and rigidity results.

Front 184

What is neuroleptic malignant syndrome?

Back 184

Idiosyncratic reaction to neuroleptic antipsychotic agents.

Symptoms: muscle rigidity, hyperthermia, autonomic dysregulation.

Front 185

Definition of hypothermia

Back 185

Court temperature below 35°C or 95°F

Pearls:
- hypothermia can cause hyperkalemia
- characteristic J waves or Osborne waves maybe seen on EKG which is defined as a hump between QRS and ST segments.
-Patients who are shivering can generally rewarm themselves passively if removed from the cold environment and kept dry and covered.
-Any patient no longer shivering must be actively rewarmed

Front 186

Therapeutic hypothermia

Back 186

It is the intentional lowering of the patient's core temperature after cardiac arrest. This has been shown to improve their neurologic outcomes in patients who recover circulation.

Front 187

The different types of alcohols?

Back 187

1. Ethanol
2. Ethylene glycol or anti-freeze
3. Methanol or wood alcohol
4. Isopropyl alcohol or rubbing alcohol

Ethylene glycol is converted to oxalic acid which crystallizes in renal tubules and causes kidney injury. Anion gap metabolic acidosis present.

Methanol is converted to formic acid which is a toxin to the retina. Anion gap metabolic acidosis present.

Isopropyl alcohol is converted to acetone but has no toxic metabolite. Ketones are elevated in the blood but there is no anion gap metabolic acidosis which is seen in ethylene glycol and methanol toxicities.

Pearls:
- all of these alcohols have CNS depressant effects.
- all three of these toxic alcohols can be rapidly removed with dialysis or reversed with antidote ethanol or fomepizole

Front 188

Carbon monoxide poisoning

Back 188

CO binds hemoglobin avidly to produce carboxyhemoglobin. Non-smokers typically have up to 3% of their hemoglobin bound by CO, whereas heavy smokers may have up to 10% to 15% bound.

Diagnosis:
-Check co-oximetery. Carboxyhemoglobin levels are typically >20%.

Treatment:
-100% oxygen
-If carboxyhemoglobin levels >20% and patient symptomatic hyperbaric oxygen

Front 189

Acid-base profile of aspirin overdose

Back 189

Produces both an anion gap metabolic acidosis as well as a respiratory alkalosis.

Treatment:
-Activated charcoal
-IV glucose
-Bicarbonate infusion

Front 190

Antidote to beta blockers

Back 190

Glucagon and calcium chloride

Front 191

Antidote to CCB

Back 191

Calcium chloride, glucagon

Front 192

Antidote to sulfonylureas

Back 192

Dextrose, Octreotide; glucagon for short term while dextrose is delayed

Front 193

Antidote to tricyclic antidepressants

Back 193

Bicarbonate infusion titrated to QT interval improvement on EKG

Front 194

Indicator of severe protein and caloric malnutrition

Back 194

Pre-albumin level <5