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385 Cards in this Set
- Front
- Back
- 3rd side (hint)
Q001. What is the most important determinant of the amount of oxygen delivery to tissues? |
Hemoglobin |
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Q002. Dx:; A married couple comes to the hospital complaining of "flu- like" symptoms including HA, N/V and disorientation. The wife thinks they caught the virus from a neighbor when they borrowed his home generator.
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Carbon Monoxide Poisoning |
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Q003. Equation for Arterial Oxygen content
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0.0031(PaO2) + 1.38(Hb x SaO2) = Art O2 content |
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Q004. Definition:; Due to perfusion of poorly ventilated alveoli or due to alveoli not being perfused. What does it respond to?
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V/Q mismatch; responds to:; supplemental Oxygen; (ex: COPD, CHF, PE, asthma, etc) |
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Q005. What is a Right-to-Left shunt in the lungs do to?
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Perfusion of a non-ventilated lung |
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Q006. Describe Anemia's effect on hypoxia
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Anemia = decreased Hb; low Hb causes a decrease in O2 carrying capacity:; Normal PaO2; Decreased PvO2 |
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Q007. When does a Low inspired O2 occur?
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High-altitude |
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Q008. What does not cause cyanosis or discoloration until it reaches toxic levels, where the patient will present with "cherry red" lips and nails? |
Carbon Monoxide poisoning |
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Q009. Definition:; Gas exchange compromise due to problem with alveolar interface; (ex: interstitial lung Dz) |
Diffusion defect |
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Q010. With what neuromuscular disorders does Hypoventilation occur?; (3)
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Myasthenia gravis;; ALS;; Guillain-Barre |
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Q011. What does an increased Fremitus suggest?
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Consolidation of the lung |
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Q012. What does an decreased Fremitus suggest?; (2)
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Air or fluid in the chest; (Pneumothorax or PE); or; Overexpansion of the lung |
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Q013. What does a "Dull" percussion represent?
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Increased density; (increased fluid in the lungs) |
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Q014. What does "hyperresonant" refer to with percussion?
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Decreased density and more air; (ex: emphysema) |
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Q015. Lung Auscultation definition:; Crackle (rale)
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Excessive airway secretions; (Pneumonia, pulm edema, bronchitis) |
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Q016. Lung Auscultation definition:; Wheeze
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Rapid airflow through obstructed airway; (Asthma, bronchitis) |
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Q017. Lung Auscultation definition:; Pleural Rub
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Inflammation of the pleura; (Pneumonia, pulmonary infarction) |
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Q018. What is it called if you ask the patient to say "eee" and it is heard as "aaa"?; What does it dx?; (2)
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Egophony; Consolidation;; Compressed lung above a Pleural Effusion |
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Q019. Definition:; A transudate or exudate in the lung
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Pleural effusion |
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Q020. What are (2) physiologic causes of Transudate pleural effusions?; (3) Dx illnesses
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Causes:; Increased Hydrostatic Pressure;; Decreased Oncotic Pressure; From:; CHF;; Cirrhosis;; Nephrosis |
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Q021. What is the physiologic cause of Exudate pleural effusions?; (3) Dx illnesses |
Cause:; Increased Capillary permeability; From:; Tumor;; Infection;; Trauma |
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Q022. What must be present to consider the pleural fluid an exudate?; (3 criteria--only one must be present) |
1. Ratio of Pleural to Serum Protein > 0.5; 2. Ratio of Pleural to Serum LDH > 0.6; 3. Pleural fluid LDH > 2/3 upper normal limit |
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Q023. When is the pleural effusion considered Parapneumonic?; (2)
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1. Exudative Pleural fluid Leukocyte count > 10,000 with high PMNs; 2. Empyema |
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Q024. Definition:; Pus in the pleural space; Lab criteria?
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Empyema; (WBC > 100,000) |
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Q025. What Dx Pleural effusions always require a chest tube?; (3)*
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Pleural Effusion Line:; Positive Cultures;; Empyema;; Loculated Effusion |
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Q026. What are the causes of gross blood in the pleural fluid?; (4)*
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blood: A PTT; Aortic Dissection:; Pulmonary Infarction;; Tumor;; Trauma |
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Q027. What are the causes of low glucose in the pleural fluid?; (4)*
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Glucose is a TREaT:; Tumor;; Rheumatoid Arthritis;; Empyema;; TB |
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Q028. What are the causes of high amylase in the pleural fluid?; (4)* |
Amy(lase) is PRETty:; Pancreatitis;; Renal failure;; Esophageal rupture;; Tumor |
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Q029. Device that measures the rate at which the lung changes during forceful breathing?
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Spirometry |
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Q030. Definition:; when the patient inhales normally, then exhales as rapidly and completely as possible that is recorded on Spirometry
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Forced Vital Capacity; (FVC) |
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Q031. Spirometry Normal values:; 1. FEV1; 2. FVC; 3. FEV1/FVC |
Normals:; FEV1 = > 80%; FVC = > 80%; FEV1/FVC = > 0.7 |
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Q032. Values indicating Obstructive lung disease:; 1. FEV1; 2. FVC; 3. FEV1/FVC; 4. Lung volume
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FEV1 = DECREASED; FVC = normal or Decreased; FEV1/FVC < 0.7; Lung volume = normal or decreased |
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Q033. Values indicating Restrictive lung disease:; 1. FEV1; 2. FVC; 3. FEV1/FVC; 4. Lung volume
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FEV1 = normal or Decreased; FVC = DECREASED; FEV1/FVC > 0.7; Lung volumes = Always DECREASED |
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Q034. What are the (3) different types of Restrictive lung defects?
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Interstitial Lung Dz (fibrosis);; Neuromuscular Dz (ALS, MG);; Chest Wall disorders (obesity, kyphosis) |
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Q035. What does the Obstructive defect look like on Spirogram?
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"swoopie" |
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Q036. What does the Restrictive defect look like on Spirogram?
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Tall and thin |
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Q037. *When is a Bronchoscopy the most accurate test?; (2); Only test more accurate?
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1. Infections such as TB or Pneumocystis; 2. Centrally located Abscess or Tumor; More accurate:; Open Lung Biopsy |
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Q038. Dx:; an epileptic, febrile patient with cough for the last several weeks, weight loss and malodorus sputum; unusual finding in upper lung lobe on CXR; Most accurate test?
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Lung Abscess; test:; Lung Biopsy |
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Q039. Most accurate diagnostic test of any pulmonary bacterial infection?
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Gram Stain of the Sputum |
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Q040. Dx:; patient has a fever, cough and shortness of breath. There are crackles and consolidation over a lung lobe. First test?; Most accurate Dx test?
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Bacterial Pneumonia (MCC Strep); first test: CXR; most accurate: Gram Stain of Sputum |
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Q041. What causes interstitial infiltrates?; (4)
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causes:; Viral Pneumonia;; PCP;; Mycoplasma;; Legionella |
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Q042. Most accurate test for:; Interstitial Lung Infiltrates caused by PCP
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Bronchoalveolar Lavage; (also Increased LDH) |
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Q043. *Most accurate test for:; Interstitial Lung Infiltrates caused by Legionella
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Urine Antigen testing |
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Q044. *Most accurate test for:; Interstitial Lung Infiltrates caused by Mycoplasma or Chlamydia
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Serology Antibody titers |
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Q045. What is the MC etiology of a Pleural Effusion?; (2); Most accurate test? |
etiology:; 1. CHF; 2. Pneumonia; test: Thoracentesis for fluid analysis |
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Q046. What is the best test to tell the difference b/t Obstructive and Restrictive lung disease?
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Flow-Volume Loop |
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Q047. *When is a Pulmonary Function Test the most accurate Dx Test?; What part of the test is most accurate in Dx?
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Distinguish b/t Obstructive and Restrictive lung disease; most accurate part:; FEV/FVC ratio |
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Q048. Dx:; African-American female with cough, dyspnea, chest pain and bilateral hilar lymphadenopathy. First test?; Most accurate Dx test?
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Sarcoidosis; first test: ACE levels (increased); most accurate: Noncaseating Granuloma on Biopsy |
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Q049. Dx:; a young non-smoker with emphysema and liver disease; First test?
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Alpha-1-Antitrypsin Deficiency (low levels); First test: serum A1A levels |
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Q050. *When is Performing an ABG the best answer?; (3)
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1. COPD; 2. possible Respiratory Acidosis; 3. Low serum Bicarb (possible severe Met acidosis) |
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Q051. Dx:; chronic respiratory problems, cough, SOB, fat malabsorption, vitamin deficiency, sterile. Blood gas reveals hypoxemia. Best test?
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Cystic Fibrosis; best test: Sweat Chloride; (Pilocarpine is given and Na + Cl is measured in the sweat) |
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Q052. (3) Typical Sx of Pneumonia
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Fever;; Cough with sputum;; Pleurtic Chest pain |
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Q053. (4) Physical Exam findings with Pneumonia |
Dullness to Percussion;; Rales (Crackles);; Egophany;; Tactile Fremitus in consolidated segment |
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Q054. Bug Dx:; 27-yo patient has pneumonia, bullous myringitis and a chest film that looks worse then expected
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Mycoplasma Pneumonia |
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Q055. If a patient comes to the ER with consolidation and pleural effusion on CXR, what is the most important test to determine admission / Tx?
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Thoracentesis |
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Q056. Bug Dx:; patient with HIV who has a CD-4 count of 52 does not take antiretroviral meds or TMP-SMX, is hypoxic on room air, and has a diffuse bilateral infiltrate on chest film
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PCP; (Pneumocystis Carinii Pneumonia) |
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Q057. Bug Dx:; Elderly man presents with pneumonia, GI Sx, bradycardia, and hypoN
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Legionella |
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Q058. Pneumonia Bug Dx:; Currant Jelly sputum
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Klebsiella |
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Q059. Pneumonia Bug Dx:; Rusty sputum
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Pneumococcus |
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Q060. Pneumonia Bug Dx:; patient develops a post-influenza pneumonia
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Pneumococcus |
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Q061. Pneumonia Bug Dx:; Buldging fissure on CXR
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Klebsiella |
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Q062. Pneumonia Bug Dx:; No bacteria on sputum gram stain culture; (2)
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Legionella; Mycoplasma |
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Q063. Pneumonia Bug Dx:; signs of pneumonia and Serum LDH is high
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PCP |
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Q064. MC Community Acquired, typical pneumonia; (2)
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S. pneumoniae; H. Influenzae |
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Q065. MC Community Acquired, atypical pneumonia; (3)*
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Community Lung Mess:; Chlamydia pneumoniae;; Legionella;; Mycoplasma |
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Q066. MC Hospital Acquired pneumonia; (3)
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Pseudomonas aeruginosa;; S. aureus;; Enteric organisms (E. coli) |
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Q067. What is the MCC of pneumonia (bugs) in the HIV patients as the CD-4 count decreases to the following numbers; (in order of occurrence)*:; 1. < 500; 2. < 200; 3. < 200; 4. < 200; 5. < 50; 6. < 50
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The Pneumonia HIV Causes Are Count-based:; 1. TB (500); 2. PCP (200); 3. Histoplasma (200); 4. Cryptococcus (200); 5. Avium (mycoplasma) (50); 6. CMV (50) |
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Q068. MCC of pneumonia in the immunocompromised host with Neutropenia; (4)*
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Pseudomonas;; Enterobacteriaceae;; S. Aureus;; Aspergillus |
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Q069. MCC of pneumonia in the immunocompromised host with sickle cell or a splenectomy
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Encapsulated organisms |
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Q070. MCC of pneumonia in the immunocompromised host with chronic Steroid use; (2)
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TB;; Nocardia |
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Q071. MCC of pneumonia in Alcoholics; (4)
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S. pneumoniae;; H. Influenzae;; Klebsiella;; TB |
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Q072. Pneumonia Bug Dx:; Small gram negative rod with a halo on gram stain
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H. Influenzae |
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Q073. CXR pneumonia findings:; Upper lobe; (2)
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TB;; Klebsiella |
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Q074. CXR pneumonia findings:; small cavities w/o air-fluid levels
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TB; (Mycobacterium) |
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Q075. CXR pneumonia findings:; Large cavities with air-fluid levels that do not culture; (2)
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Coccidioidomycosis;; Nocardia |
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Q076. CXR pneumonia findings:; Diffuse Bilateral Infiltrates; (2)
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PCP;; Mycoplasma |
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Q077. Definition:; Idiopathic Eosinophilic Pneumonia
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Loeffler's pneumonia |
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Q078. Pneumonia bugs causing "Relative Bradycardia"; (slower then expected HR for Temp, but above 60bpm); (3)
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Legionella;; Salmonella;; Chlamydia Psittaci |
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Q079. What drug prevents respiratory failure and improves survival in PCP pneumonia patients?; Criteria for when it is given?; (2)
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Steroids; give: A-a gradient > 35, PaO2 < 75 |
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Q080. Drug of choice for:; Any Community Acquired Pneumonia with no risk factors
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Macrolide; (Erythromycin, Azithromycin) |
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Q081. Drug of choice for:; Any Community Acquired Pneumonia with risk factors; (CHF, DM, etc); (2)
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1. Macrolide + 2nd generation Cephalosporin; 2. FQ (Extended-spectum) |
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Q082. Drug of choice for:; Any Hospital Acquired Pneumonia; (2)
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1. Cefixime; 2. Piperacillin-tazobactam; [both for Pseudomonas coverage] |
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Q083. Drug of choice for:; Any Immunocompromised patient with Pneumonia
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TMP-SMX; [for PCP coverage] |
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Q084. Dx:; Productive cough, night sweats, hemoptysis, anorexia, weight loss, chest pain, fever, chills
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TB |
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Q085. (3) Dx tests for TB
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Positive PPD;; Granuloma in upper lobes of lung;; Acid-fast bacilli on sputum |
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Q086. How is latent TB treated?
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INH daily for 9 months; (or Rifampin for 4 if in contact with INH-resistant TB) |
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Q087. How is Active TB treated?
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RIPE for 2 months:; Rifampin; INH, Pyrazinamide; Ethambutol; followed with 4 months of:; INH and Rifampin |
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Q088. How is tx of TB different with pregnant pt?
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No pyrazamide; (other med ok) |
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Q089. Toxicity of INH; (2)*
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INH: Infects Neuro and Hepatic:; Neruopathy;; Seizures;; Hepatitis |
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Q090. Dx:; patient brought by ambulance in status epilepticus. Patient says only medical history is TB; How is it treated?
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INH toxicity; Tx: Pyridoxine |
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Q091. Toxicity of Rifampin; (2)
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Induces P450; Gives Red-orange secretions; (tears, urine, sweat, etc) |
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Q092. Toxicity of Ethambutol
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Optic neuritis and impaired color vision |
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Q093. Risk factors for DVT.
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stasis; endothelial injury; hypercoagulability; (Virchow's triad) |
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Q094. Criteria for exudative effusion.
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pleural/serum protein > 0.5; pleural/serum LDH > 0.6 |
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Q095. Causes of exudative effusion.
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Think of leaky capillaries. Malignancy; TB; bacterial or viral infection; pulmonary embolism with infarct; pancreatitis |
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Q096. Causes of transudative effusion.
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Think of intact capillarie. CHF; liver or kidney disease; protein-losing enteropathy |
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Q097. Normalizing PCO2 in a patient having an asthma exacerbation may indicate?
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Fatigue & impending respiratory failure |
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Q098. dyspnea; lateral hilar lymphadenopathy on CXR; noncaseating granulomas; increased ACE; hypercalcemia
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Sarcoidosis |
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Q099. PFT showing decreased FEV1/FVC.
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Obstructive pulmonary disease (e.g. asthma) |
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Q100. PFT showing increased FEV1/FVC.
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Restrictive pulmonary disease |
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Q101. Honeycomb pattern on CXR. Diagnosis?; Treatment?
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Diffuse interstitial pulmonary fibrosis. Supportive care. Steroids may help. |
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Q102. Treatment for SVC syndrome.
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Radiation |
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Q103. Treatment for mild, persistent asthma. |
Inhaled beta-agonists & inhaled corticosteroids |
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Q104. Acid-base disorder in pulmonary embolism.
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Hypoxia & hypocarbia |
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Q105. Non-small cell lung cancer (NSCLC) associated with hypercalcemia.
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Squamous cell carcinoma |
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Q106. Lung cancer associated with SIADH.
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Small cell lung cancer (SCLC) |
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Q107. Lung cancer highly related to cigarette
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Small cell lung cancer (SCLC) |
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Q108. A tall white male presents with acute shortness of breath. Diagnosis?; Treatment?
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Spontaneous pneumothorax. Spontaneous regression. Supplemental O2 may be helpful. |
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Q109. Treatment of tension pneumothorax.
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Immediate needle thoracostomy |
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Q110. Characteristics favoring carcinoma in an isolated pulmonary nodule.
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Age > 45-50 yrs; lesions new or larger in comparison to old films; absence of calcification or irregular calcification; size > 2 cm; irregular margins |
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Q111. Hypoxemia & pulmonary edema with normal pulmonary capillary wedge pressure.
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ARDS |
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Q112. Increased risk of what infection with silicosis?
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Mycobacterium tuberculosis |
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Q113. Causes of hypoxemia.
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right-to-left shunt; hypoventilation; low inspired O2 tension; diffusion defect; V/Q mismatch |
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Q114. Classic CXR findings for pulmonary edema
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cardiomegaly; prominent pulmonary vessels; Kerley B lines; "bat's wing" appearance of hilar shadows; perivascular & peribronchial cuffing |
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Q115. pulmonary function tests
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spirometry (mechanical ventilation); Dlco (gas exchange); methacholine challenge test (bronchial hyperreactivity); TLC |
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Q116. restrictive pattern
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FEV1/FVC > 80% |
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Q117. obstructive pattern
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FEV1/FVC < 80%; seen in emphysema, chronic bronchitis, asthma, bronchiectasis |
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Q118. Decreased DLco
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if FEV1/FVC < 80% suggests emphysema; if FEV1/FVC > 80% suggests interstitial lung disease or mild left heart failure |
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Q119. Increased DLco
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suggests hemorrhage such as in Goodpasture |
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Q120. methacholine test |
bronchoprovocation in patients with cough or wheezing who have normal pulmonary function tests, for possible asthma; do basal and postprovocation spirometry; positive test if baseline FEV1 decreased >20% |
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Q121. A-a gradient formula |
150 - 1.25 x PaCO2 - PaO2 normal: 5-15mmHg;; increases with age and all forms of hypoxemia except hypoventilation and high altitude |
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Q122. solitary pulmonary nodule |
1/3 are malignant; first step in management is looking for previous image study; if none available then consider if patient is high or low risk for cancer; low risk nonsmoker <35 --> x-ray every 3 months for 2 years, if no growth stop follow-up; high risk smoker >50 --> open-lung biopsy and removal due to cancer risk |
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Q123. transudative pleural effusion |
Increased hydrostatic pressure or decreased oncotic pressure; usually bilateral and equal; low LDH and proteins in fluid and serum (200, 0.6, 0.5); need all three values for diagnosis, else exudate |
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Q124. exudative pleural effusion
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due to local process; usually unilateral; need further investigation; high LDH and proteins in fluid and serum (200, 0.6, 0.5); don't need all three values high to make diagnosis |
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Q125. transudative causes of pleural effusion
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heart failure; nephrotic syndrome; liver disease; pulmonary embolism; atelectasis |
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Q126. exudative causes of pleural effusion
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pneumonia; cancer (lung, breast or lymphoma); pulmonary embolism; drug-induced; pancreatitis; TB; RA; SLE |
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Q127. transudative pleural effusion with no apparent cause
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consider pulmonary embolism which can be either transudative or exudative |
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Q128. indications of thoracocentesis
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any new and unexplained pleural effusion --> rule out empyema; decubitus x-ray --> <1cm free-flowing fluid --> minimal risk; if non-free fluid need ultrasound guidance |
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Q129. malignant pleural effusions
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due mostly to breast cancer, lung cancer and lymphoma; send thoracocentesis fluid for cytologic exam also |
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Q130. hemorrhagic pleural effusion
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seen in mesothelioma, metastatic lung or breast cancer, pulmonary embolism with infarction and trauma |
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Q131. lymphocytic-predominant pleural effusions
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suggests TB due to tuberculin hypersensitivity; check increased adenosine deaminase and positive PCR for TB; acid-fast and culture of fluid are only positive in 30% |
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Q132. respiratory compromise and distress
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presents with shortness of breath, dyspnea, tachypnea (>30) and associated symptoms such as agitation, confusion or decreased consciousness |
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Q133. evaluation of respiratory distress
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ensure patent airway; focus on quickness of onset and associated symptoms; most important lab test is arterial blood gases then B- natriuretic peptide and chest x-ray |
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Q134. acute respiratory distress with fever, cough or sputum
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suggests infectious etiology |
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Q135. acute respiratory distress without systemic symptoms
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suggests airway obstruction, cardiac disease or thromboembolism |
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Q136. chronic respiratory distress
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suggests interstitial lung disease or COPD |
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Q137. common lung physical exam findings
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diffuse wheezing --> asthma; localized wheezing --> foreign object; rales --> pneumonia, interstitial disease, heart failure; dull percussion --> pneumonia or atelectasis; normal exam --> pneumocystis jirovecci, central respiratory problems |
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Q138. B-natriuretic peptide in acute dyspnea
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elevation is sensitive for heart failure but can also be elevated in cor pulmonale and acute right ventricular failure (thromboembolism) |
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Q139. chest x-ray without parenchymal infiltrates in acute dyspnea
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suggests thromboembolism; central respiratory depression; neuromuscular disease; upper airway obstruction |
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Q140. chest x-ray hyperinflation in acute dyspnea
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suggests asthma and COPD |
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Q141. chest x-ray with focal infiltrates in acute dyspnea
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suggests bacterial, viral or fungal pneumonia, aspiration or pulmonary hemorrhage |
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Q142. chest x-ray with diffuse edema in acute dyspnea
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suggests heart failure or ARDS |
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Q143. ICU indications in respiratory failure
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persistent hypoxemia --> hospitalization; ICU indications -->; need for mechanical ventilation; close monitoring; increasing oxygen demand; continuous nursing |
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Q144. indications for intubation and/or mechanical ventilation
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respiratory acidosis and hypercapnia in asthmatic patient; upper airway injury (burns, laryngeal edema, trauma); neurologic airway depression (often with loss of gag and cough reflexes) |
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Q145. respiratory distress in hospitalized patients
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inpatient who develops dyspnea, tachypnea and/or hypoxemia should raise possibility of pulmonary embolism or aspiration |
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Q146. types of asthma
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intrinsic (50%) is secondary to nonimmunologic stimuli (infections, irritating inhalants, cold air and emotional);; extrinsic (20%) due to allergens |
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Q147. asthma stimuli
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infections (RSV, rhinovirus),; drugs (aspirin/NSAIDs, coloring agents, betablockers),; allergens,; cold air,; emotions |
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Q148. asthma presentation
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tachypnea,; tachycardia,; diffuse wheezing,; use of accessory muscles,; diminished breath sounds,; hyperresonance,; intercostal retractions |
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Q149. asthma poor prognosis factors
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fatigue; diaphoresis; pulsus paradoxus; inaudible breath sounds; decreased wheezing; cyanosis; bradycardia |
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Q150. asthma diagnosis
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initial tests for acute attacks --> decreased PaCO2, increased pH, normal or decreased PaO2; severe attack -->decreased PaO2, increased PaCO2, decreased pH; chest x-ray to rule out infection as cause; spirometry --> obstructive pattern that reverses with beta agonist (FEV1 reverses by 12%); methacholine test --> decreased FEV1/FVC of 20% |
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Q151. acute asthma management
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O2; metered inhaled beta agonists --> albuterol/salbutamol, terbutaline; salmeterol is long-lasting for nocturnal variant; catecholamines may be used but not routinely; aminophylline and theophyline have modest potency and are not routine; anticholinergics (ipratropium) if heart disease (slow onset, medium potency) |
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Q152. chronic asthma management
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acute exacerbations: systemic prednisone 10-14 days along with inhaled albuterol;; inhaled corticosteroids are first line maintenance;; cromolyn is first line maintenance in children and prophylaxis in adults;; zileuton, zafirlukast, mmonteleukast for severe asthma resistant to maximum doses of inhaled steroids |
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Q153. mild asthma definition and treatment
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symptoms ~2 days/week and rare night symptoms; FEV1 is normal; no long-term control needed only inhaled beta agonists for attacks |
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Q154. moderate asthma definition and treatment
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symptoms on most days and at least 5 nights/month with FEV1 60-80%; treat with daily inhaled steroids (also cromolyn specially in children); maybe also salmeterol |
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Q155. severe asthma definition and treatment
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daily symptoms, frequent night symptoms and hospital emergencies with FEV1 <60%;; daily inhaled steroids, daily inhaled salmeterol along with antileukotriene drug and possibly low-dose oral steroid |
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Q156. physical exam in emphysema
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distant breath sounds; pink skin; thin; barrel chest; accessory muscles; symptoms of right heart failure and clubbing |
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Q157. physical exam in chronic bronchitis
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rhonchi and wheezes; signs of cyanosis; weight gain; symptoms of right heart failure and clubbing |
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Q158. chest x-ray findings in COPD
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chronic bronchitis --> increased pulmonary markings; emphysema --> bilateral hyperinflantion, diaphragm flattening, small heart size, increase in retrosternal space |
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Q159. COPD diagnosis
|
decreased FEV1/FVC; FEF 25-75; increased RV and TLC; emphysema has decreased DLco and chronic bronchitis has normal DLco; FEV1/FVC after bronchodilation will stay the same |
|
|
Q160. COPD complications
|
hypoxemia with nocturnal desaturation; secondary erythrocytosis; cor pulmonale; chronic ventilatory failure; CO2 retention |
|
|
Q161. maintenance treatment for COPD
|
first-line --> ipratropium via metered inhaler;; inhaled beta agonists can be used concomitantly;; inhaled corticosteroids are not used in COPD;; if above fails --> theophylline (watch for cytochrome inhibitors and inducers) |
|
|
Q162. only treatment that reduces mortality in COPD
|
home O2 supplementation and smoking cessation; home oxygen for hypoxemia (PaO2<55mmHg or saturation <88%); pneumococcal vaccine every 5 years, influenza vaccine yearly and haemophilus vaccine if unvaccinated |
|
|
Q163. COPD exacerbation general management
|
1) measure O2 saturation (pulse oximetry); 2) arterial blood gases; 3) chest x-ray; 4) check theophylline levels; 5) CBC and ECG; 6) hospital admission if significant hypercapnia or hypoxemia; 7) consider intubation and mechanical ventilation; 8) specific treament; spirometry is NOT done or useful in exacerbation |
|
|
Q164. COPD exacerbation specific treatment
|
1) O2 supplementation; 2) inhaled bronchodilators and anticholinergics concomitantly; 3) IV or oral prednisone for 2 weeks; 4) antibiotics despite normal x-ray; 5) council on smoking cessation; 6) teach optimal use of MDI; no benefit in IV theophylline and avoid opiates and sedatives |
|
|
Q165. bronchiectasis etiology
|
secondary to recurrent pneumonias, TB, fungal or abscess; cystic fibrosis, immotile cilia syndrome (50% Kartagener) |
|
|
Q166. bronchiectasis presentation
|
suspect in anyone with; chronic cough; foul-smelling sputum; hemoptysis; recurrent pulmonary infections; sinusitis; immune deficiencies; presents with purulent copious sputum, wheezes, crackles and history of recurrent pneumonias (specially gram- and pseudomonas) |
|
|
Q167. bronchiectasis diagnosis
|
early chest x-ray may be normal or severe cases show 1- 2cm cysts and crowding of bronchi;; chest CT is best noninvasive test |
|
|
Q168. bronchiectasis treatment
|
bronchodilators, chest physical therapy, postural drainage, rotating gram- antibiotics; surgery in cases of localized bronchiectasis or massive hemoptysis; yearly influenza vaccine and pneumococcal vaccine with booster at 5 years |
|
|
Q169. bronchiectasis complications
|
massive hemoptysis,; amyloidosis,; cor pulmonale,; visceral abscesses |
|
|
Q170. interstitial lung disease general presentation
|
exertional dyspnea; nonproductive cough; crackles; pulmonary hypertension; clubbing; restrictive pattern |
|
|
Q171. interstitial lung diseases
|
idiopathic pulmonary fibrosis; sarcoidosis; pneumoconiosis --> asbestosis, silicosis, coal pneumoconiosis |
|
|
Q172. idiopathic pulmonary fibrosis presentation
|
exercise intolerance, dyspnea, coarse crackles |
|
|
Q173. idiopathic pulmonary fibrosis diagnosis
|
reticular or reticulonodular pattern on chest x-ray; restrictive pattern on PFTs; increased macrophages on bronchoalveolar lavage (nonspecific) |
|
|
Q174. idiopathic pulmonary fibrosis treatment
|
steroids with or without azathioprine works in 20%;; the rest develop fatal lung disease |
|
|
Q175. idiopathic pulmonary fibrosis prognosis
|
20-40% 5-year survival;; best prognostic factor is response to steroids as evidenced in PFTs |
|
|
Q176. sarcoidosis presentation
|
"GRAIN"; gammaglubilinemia; rheumatoid arthritis; ACE increase; interstitial fibrosis; non-casseating granuloma; hilar and left paratracheal adenopathy; hypercalcemia due to vitamin activation by macrophages; uveitis/conjunctivitis in >25%; chest x-ray findings; restrictive or normal PFTs |
|
|
Q177. chest x-ray findings in sarcoidosis
|
four stages found (not progressive); bilateral hilar adenopathy; hilar adenopathy with reticulonodular parenchyma; reticulonodular parenchyma alone; honeycombing of bilateral lung fields with fibrosis |
|
|
Q178. sarcoidosis diagnosis
|
biopsy of affected tissue showing noncasseating granulomas;; all patients should have ophthalmologic exam |
|
|
Q179. sarcoidosis prognosis
|
80% remain stable or spontaneously resolves;; 20% progress to organ compromise |
|
|
Q180. sarcoidosis treatment
|
no treatment is effective; if organ compromise may use trial of high-dose steroids; if uveitis, CNS involvement or hypercalcemia --> steroids are mandatory |
|
|
Q181. pneumoconiosis general presentation
|
dyspnea,; shortness of breath,; cough,; sputum,; cor pulmonale,; clubbing,; restrictive pattern,; decreased DLco,; hypoxemia with increased A-a |
|
|
Q182. ocupations associated with asbestosis
|
mining,; milling,; foundry work,; shipyards,; pipes,; break linings,; insulation,; boilers;; history of exposure necessary for Dx |
|
|
Q183. asbestosis x-ray findings
|
diffuse or local pleural thickening,; pleural plaques,; calcifications near diaphragm,; pleural effusions,; lower lobe interstitial infiltrate |
|
|
Q184. asbestosis associated cancers
|
lung adenocarcinoma or SCC; pleural mesothelioma is less common |
|
|
Q185. asbestosis diagnosis
|
history of exposure + lung biopsy showing barbell-shaped asbestos fibers |
|
|
Q186. asbestosis treatment
|
no effective treatment;; must stop smoking due 75x increased risk of cancer |
|
|
Q187. ocupations associated with silicosis
|
mining,; quarrying,; tunneling,; glass and pottery making,; sandblasting |
|
|
Q188. silicosis x-ray findings
|
1-10mm nodules throughout the lungs, most prominent in upper lobes; in progressive massive fibrosis nodules are >10mm and coalesce |
|
|
Q189. silicosis diagnosis
|
history of exposure + lung biopsy showing silica particles; pathologic lesion is the hyaline nodule |
|
|
Q190. silicosis treatment
|
no effective treatment; should have yearly PPD test and if >10mm --> INH prophylaxis for 9 months |
|
|
Q191. Lofgren syndrome
|
acute sarcoidosis presentation with erythema nodosum, arthritis, hilar adenopathy |
|
|
Q192. Heefordt-Waldenstrom syndrome
|
acute sarcoidosis presentation with fever,; parotid enlargement,; uveitis and facial palsy |
|
|
Q193. Caplan syndrome
|
rheumatoid nodules in periphery of lung,; rheumatoid arthritis and coexisting pneumoconiosis (usually CWP) |
|
|
Q194. coal worker's pneumoconiosis x-ray findings
|
small round parenchymal densities; usually in upper half of lungs; progressive massive fibrosis has 1cm densities in whole lung |
|
|
Q195. coal worker's pneumoconiosis immunologic findings
|
increased IgA,; increased IgG,; increased C3, ANA and rheumatoid factor |
|
|
Q196. pulmonary embolus site of origin
|
most are from above-the-knee deep veins which result from distal deep vein thrombosis;; in patients with catheters it can originate from upper limb, subclavian and internal jugular veins |
|
|
Q197. criteria for high-risk pulmonary embolism patients
|
recent surgery (specially orthopedic, knee replacement has 70% risk);; cancer history (prostate, breast, pelvic, abdominal);; immobilized patients;; acquired thrombophilia (lupus anticoagulant, nephrotic syndrome);; oral contraceptives;; inherited thrombophilia (factor V Leiden, protein C/S deficiency, antithrombin III deficiency);; pregnancy;; need 1 risk factor and consistent signs and symptoms for high-risk label |
|
|
Q198. signs and symptoms consistent with pulmonary embolism
|
sudden onset of dyspnea,; tachypnea,; thigh/calf swelling,; pleuritic chest pain,; hemoptysis,; tachycardia,; increased P2 |
|
|
Q199. when to consider pulmonary embolism
|
all patients with dyspnea and normal chest x-ray |
|
|
Q200. nonspecific routine tests for dyspnea; may suggest PE
|
arterial blood gases show hypoxemia with increased A-a; chest x-ray (normal in PE); ECG (to exclude others) shows S1, Q3, T3, tachycardia |
|
|
Q201. specific tests for pulmonary embolism |
best initial test is spiral CT scan;; V/Q scan (if normal excludes PE);; angiogram is gold standard |
|
|
Q202. deep venous thrombosis specific tests
|
best initial test is compression or duplex ultrasound;; venogram is rarely done;; MRI |
|
|
Q203. tests for DVT and PE |
D-dimer is most sensitive;; can only exclude thromboembolism if normal levels; may also be high in surgery, infection, trauma, pregnancy and DIC; normal D-dimer and CT scan rule out thromboembolism in 98% of low-risk patients |
|
|
Q204. tests results that exclude pulmonary embolism
|
normal CT + normal D-dimer in low-risk patients; normal CT + normal doppler in low-risk patients; V/Q scan is completely normal |
|
|
Q205. generalities of pulmonary embolism diagnosis
|
all patients should be on heparin during diagnosis and imaging;; if PE is suspected start CT scan right after chest x-ray;; if all tests are negative but it's high-risk patient --> angiogram;; normal CT + normal D-dimer or doppler excludes PE in low- risk patients |
|
|
Q206. pulmonary embolism treatment |
1) O2; 2) start heparin before confirmation and during work-up; 3) concomitant warfarin; 4) if hemodynamically unstable or massive PE --> thrombolytics (tPa, streptokinase) |
|
|
Q207. heparin considerations in pulmonary embolism
|
if LMWH then no need to follow PTT and less chance of heparin-induced thrombocytopenia; HIT is associated with more thrombotic events, not bleeding diathesis, and is treated with new anticoagulants (argatroban, lepirudin); start heparin immediately |
|
|
Q208. warfarin considerations in pulmonary embolism
|
monitor PT; titrate to INR of 2-3; skin necrosis can occur if protein C deficiency already present; contraindicated in pregnancy (use LMWH 6 months instead) |
|
|
Q209. contraindications of anticoagulation therapy in PE
|
contraindicated in patients with recent neurosurgery or eye surgery; use inferior vena cava filter instead |
|
|
Q210. post thrombotic syndrome
|
pain; edema; hyperpigmentation; skin ulceration in 2/3 of PE patients; compression stockings can prevent it |
|
|
Q211. fat embolism
|
acute dyspnea, petechiae in neck or axilla, confusion,; 3 days after long bone fracture or after CPR;; no anticoagulation necessary |
|
|
Q212. ARDS etiology
|
sepsis; trauma; DIC; Goodpasture; SLE; drug overdose; toxin inhalation; drowning |
|
|
Q213. ARDS presentation
|
dyspnea,; tachypnea,; diffuse rales and ronchi |
|
|
Q214. ARDS diagnosis
|
chest x-ray --> diffuse interstitial or alveolar infiltrates; ABGs --> decreased PaO2, increased PaCO2; Swan-Ganz --> normal cardiac output and capillary wedge pressure but increased pulmonary artery pressure |
|
|
Q215. ARDS treatment
|
treat underlying cause;; mechanical ventilation with positive end-expiratory pressure |
|
|
Q216. ARDS prognosis |
70% mortality |
|
|
Q217. sleep apnea
|
cessation of airflow >10s at least 10-15/hour of sleep + daytime somnolence; confirm with polysomnography; treat obstructive with weight loss and nasal continuous positive airway pressure (CPAP); treat central with acetazolamide, progesterone and O2 |
|
|
Q218. lung cancer etiology
|
90% of cases are directly related to cigarette smoke;; nonsmokers develop adenocarcinoma;; all lung cancers are associated with smoking;; active smokers have 10x greater risk;; 40 pack-year history increases risk 60-70x;; asbestos increases risk 75x |
|
|
Q219. types of lung cancer
|
most common is adenocarcinoma (40%);; squamous cell carcinoma,; small cell and large cell |
|
|
Q220. centrally located lung cancers |
squamous cell and small cell |
|
|
Q221. peripheral located lung cancers |
adenocarcinoma and large cell |
|
|
Q222. lung cancer paraneoplastic syndromes
|
SCC --> hypercalcemia (PTH-like peptide); small cell --> SIADH and Eaton-Lambert |
|
|
Q223. lung cancer metastasis
|
SCC --> direct extension to hilar node and mediastinum; small cell and adenocarcinoma --> liver, adrenals, brain, bones |
|
|
Q224. lung cancer presentation
|
cough; weight loss; dyspnea; hemoptysis; chest pain; recurrent pneumonic processes; hoarseness |
|
|
Q225. lung cancer diagnosis
|
sputum cytology (specially SCC); bronchoscopy for centrally located lesions; needle aspiration biopsy if highly suspicious and nonspecific bronchoscopy findings or peripheral lesion |
|
|
Q226. symptoms of unresectable lung cancer
|
weight loss >10%; bone pain; extrathoracic metastasis; CNS symptoms; SVC syndrome; hoarseness; contralateral mediastinal adenopathy |
|
|
Q227. lung cancer treatment |
resectable small cell --> VP16 (etoposide, platinum);; resectable non-small --> CAP (cyclo, adriamycin, platinum) and radio |
|
|
Q228. lung cancer prognosis
|
5-8% 5-year survival; after resection of SCC --> 30-35%; after resection of large-cell and adeno --> 25% |
|
|
Q229. atelectasis etiology
|
most common is postsurgery;; also mucuous plug, foreign body or tumor |
|
|
Q230. atelectasis presentation
|
tachycardia,; dyspnea,; fever,; hypoxemia |
|
|
Q231. atelectasis diagnosis
|
ipsilateral trachea deviation --> upper lobe; mediastinal deviation --> massive atelectasis; elevation of hemidiaphragm --> lower lobe; atelectatic lobe looks denser, consolidated and smaller than normal contralateral lobe |
|
|
Q232. What muscles are responsible for inspiration during exercise?
|
external intercostals; scalenes,; sternocleidomastoid, |
|
|
Q233. What muscles are responsible for expiration during exercise?
|
Internal intercostals,; rectus abdominis,; transversus abdominis,; internal and external obliques |
|
|
Q234. What ratio indicates fetal lung maturity?
|
lecithin: sphingomyelin > 2.0 |
|
|
Q235. What is deficiency in neonatal respiratory distress syndrome?
|
dipalmitoyl phosphatidylcholine (lecithin) |
|
|
Q236. How do ACE inhibitors cause cough?
|
Normally ATII inactivates bradykinin;; when blocked, kallikrein is unopposed --> activates bradykinin --> cough and angioedema |
|
|
Q237. Where are ACE and kallikrein synthesized? |
In the lungs |
|
|
Q238. What is the formula for collapsing pressure? |
2(tension)/radius; As radius decreases, alveoli are more likely to collapse |
|
|
Q239. How is inspiratory capacity calculated?
|
tidal volume + inspiratory reserve capacity |
|
|
Q240. Formula for calculated Vd - physiologic dead space |
tidal volume x (PaCO2-PeCo2)/PaCO2; PaCO2 = arterial PCO2; PeCO2 = expired air CO2 |
|
|
Q241. At what point in the breath cycle is the tendency for the lungs to collapse equal to the tendency for the chest wall to spring outward?; What is the system pressure at this point? |
At FRC; System pressure is equal to atmospheric pressure |
|
|
Q242. What is the treatment for methemoglobinemia?
|
Methylene blue |
|
|
Q243. What is the treatment for cyanide poisoning?
|
Give nitrates to oxidize Hb to metHb --> allows cyt oxidase to function; -> thiosulfate to bind cyanide; -> thiocyanide is renally excreted |
|
|
Q244. What is methemoglobin?
|
oxidized form (Fe3+ instead of Fe2+) --> poorer O2 binding |
|
|
Q245. What is the effect of carboxyhemoglobin on the oxygen dissociation curve?
|
Left shift (increased affinity for oxygen, decreased unloading) |
|
|
Q246. What is the effect of increased metabolic needs on the oxygen dissociation curve?
|
Right shift (increased oxygen unloading) |
|
|
Q247. What is the effect of acidemia on the oxygen dissociation curve?
|
Right shift (increased oxygen unloading) |
|
|
Q248. What is the effect of alkalemia on the oxygen dissociation curve? |
Left shift (increased affinity for oxygen, decreased unloading) |
|
|
Q249. What is the effect of increased 2,3-DPG on the oxygen dissociation curve? |
Right shift (increased oxygen unloading) |
|
|
Q250. How does the oxygen dissociation curve of fetal Hb differ from adult Hb?
|
Left shift (increased affinity for oxygen, decreased unloading) |
|
|
Q251. What is the effect of a decrease in PAO2?
|
Vasoconstriction that shunts blood towards well-ventilated regions of lung |
|
|
Q252. How do emphysema and pulmonary fibrosis impact diffusion?
|
Both decrease it. Diffusion is proportional to A(rea)/T(hickness). Emphysema reduces area. Fibrosis increases thickness. |
|
|
Q253. What types of gases show perfusion-limited patterns of exchange along pulmonary capillaries?
|
O2 (normally), CO2, N2O. These equilibrate before the end of the capillary. Diffusion can only be increased if blood flow increases. |
|
|
Q254. What types of gases show diffusion-limited patterns of exchange along pulmonary capillaries?
|
O2 (in emphysema or fibrosis); CO |
|
|
Q255. What is the normal pressure in pulmonary arteries?
|
10-14 mmHg; >25 mmHg = HTN; >35 mmHg during exercise = HTN |
|
|
Q256. What histologic changes are seen as a result of pulmonary HTN?
|
medial thickening, intimal fibrosis, atherosclerosis |
|
|
Q257. What causes primary pulmonary HTN?
|
Inactivating mutation in BMPR2 gene (normally inhibits smooth muscle proliferation) |
|
|
Q258. What causes secondary pulmonary HTN?
|
COPD,; mitral stenosis; systemic sclerosis; left-to-right shunt; sleep apnea (hypoxic vasoconstrict); high altitude (hypoxic vasoconstrict); recurrent thromboemboli |
|
|
Q259. What is the formula for pulmonary vascular resistance?
|
PVR = (Ppulm artery - Pleft atrium)/CO; R = (change in P)/Q; R = (8)(viscosity)(length)/(pi)(radius^4) |
|
|
Q260. What is the alveolar gas equation?
|
PAO2 = 150 - (PaCO2)/0.8; 150 = PO2 in inspired air; 0.8 = respiratory quotient |
|
|
Q261. What is the A-a gradient?; When is it increased? |
PAO2 - PaO2 = 10-15; Increased in hypoxemia (V/Q mismatch, fibrosis) |
|
|
Q262. Where in the lung are ventilation and perfusion greatest?; Where is V/Q = 3?; Where is V/Q = 0.6; Where is V/Q = 1
|
At the bases; At the apices; At the bases; During exercise |
|
|
Q263. In what type of V/Q mismatch should 100% O2 be used?
|
Only in physiologic dead space (V>Q) due to blood flow obstruction. Does not help in physiologic shunt (V<Q) due to airway obstruction. |
|
|
Q264. In zone 2 of the lung, how to the partial pressures of oxygen in the alveoli, veins, and arteries compare?
|
PA > Pa > Pv |
|
|
Q265. What are the 3 forms in which carbon dioxide is transferred from the tissues to the lungs?
|
1. Bicarbonate, HCO3- (90%); 2. Carbaminohemoglobin, bound to Hb at N terminus (5%), favors T form --> O2 unloading; 3. Dissolved CO2 (5% |
|
|
Q266. Pt presents with sudden onset dyspnea, chest pain, and tachycardia. What could be the underlying causes?
|
Embolus (95% from deep leg veins):; Fat (bone fractures, liposuction); Air; Thrombus; Bacteria; Amniotic fluid (--> postpartum DIC); Tumor |
|
|
Q267. Pt presents with calf tenderness occurring with foot dorsiflexion. What is wrong?
|
DVT (positive Homan's sign) |
|
|
Q268. Pt has productive cough, wheezing, crackles, and cyanosis. What is causing this?
|
Chronic bronchitis ("blue bloater") due to hypertrophy of mucus-secreting glands in bronchioles --> early onset hypoxemia, late-onset dyspnea |
|
|
Q269. Pt has dyspnea, decreased breath sounds, tachycardia. What is causing this?
|
Emphysemia ("pink puffer") due to increased elastase activity --> destruction of alveolar walls |
|
|
Q270. What type of emphysema is caused by smoking?
|
Centriacinar |
|
|
Q271. What type of emphysema is caused by alpha1-antitrypsin deficiency?
|
Pancacinar |
|
|
Q272. What type of emphysema is associated with spontaneous pneumothorax in a young male?
|
Paraseptal (cyst/bulla forming) |
|
|
Q273. Pt has dyspnea, cough, wheezing, tachypnea, hypoxemia, decreased inspiratory/expiratory ratio
|
Asthma: bronchial hyperresponsiveness --> bronchoconstriction; Smooth muscle hypertrophy, Curschmann's spirals (shed epithelium from mucus plugs) |
|
|
Q274. Pt has dilated airways, purulent sputum, recurrent infections, and hemoptyis. What is this called?; What is it caused by?; What infection are they at risk for?
|
Bronchiectasis; CF, Kartagener's, poor ciliary motility; Aspergillosis |
|
|
Q275. What are the mechanical causes of restrictive lung disease?
|
Muscle - polio, myasthenia gravis; Structural - scoliosis, obesity |
|
|
Q276. What are the causes of restrictive lung disease that are attributable to lowered diffusing capacity?
|
ARDS; Neonatal RDS (hyaline membrane dz); Sarcoidosis; Pneumoconioses; Idiopathic pulmonary fibrosis (collagen); Goodpasture's syndrome; Wegener's granulomatosis; Eosinophilic granuloma (histiocytosis X); Drug toxicity (bleomycin, amiodarine, busulfan) |
|
|
Q277. Pt presents with cough, dyspnea, morning stiffness, and painful joints. What caused it?; What part of lung is affected?
|
Coal dust (coal miner's lung) --> Caplan syndrome; Upper lobes |
|
|
Q278. Sandblaster presents with cough, dyspnea, and "eggshell" calcification of hilar lymph nodes. What caused it?; What part of lung is affected?
|
Silicosis (macrophages respond to silica --> fibrogenesis); may increase susceptibility to TB if macrophages are impaired. Upper lobes |
|
|
Q279. Plumber/roofer presents with bronchogenic carcinoma. What caused it?; What part of lung is affected?; What is seen on biopsy? |
Asbestosis; Lower lobes; "Ivory white" calcified pleural plaques, dumbbell-shaped bodies in macrophages, "ferruginous bodies" on Prussian blue |
|
|
Q280. Baby is born before 35 weeks. What is his L:S ratio?; What did his mom have?; How was he delivered?; What congenital heart defect?; Giving 100% O2 does what?; Treatment?
|
L:S < 1.5; maternal diabetes; Cesarean section; low O2 tension --> PDA; 100% O2 --> retinopathy; Give maternal steroids before birth, artificial surfactant, thyroxine |
|
|
Q281. Protein-rich fluid in alveoli, hyaline membranes. What caused damage?; What incited this diffuse alveolar damage?
|
Toxic neutrophilic substances OR coagulation cascade OR free radicals; Trauma, sepsis, shock, gastric aspiration, uremia, pancreatitis, amniotic fluid embolism |
|
|
Q282. Obese pt who snores, has HTN, is always tired... Has what?; Should do what?; Could die from what?
|
Obstructive sleep apnea (central is no respiratory effort); Get CPAP, lose weight, surgery; Arrhythmia |
|
|
Q283. Decreased breath sounds in one area, decreased resonance to percussion, decreased fremitus, tracheal deviation.
|
Bronchial obstruction (ipsilateral to tracheal deviation), e.g. cancer |
|
|
Q284. Decreased breath sounds, dullness to percussion, decreased fremitus
|
Pleural effusion |
|
|
Q285. Bronchial sounds in one area, dullness to percussion, increased fremitus
|
Lobar pneumonia |
|
|
Q286. Decreased breath sounds, hyperresonance to percussion, absent fremitus, tracheal deviation
|
Tension pneumothorax (on contralateral side to tracheal deviation) |
|
|
Q287. Pt presents with cough, hemoptysis, decreased breath sounds in one area, wheezing, coin lesions. Possible complications?
|
Lung cancer SPHERE:; Superior vena cava syndrome; Pancoast's tumor; Horner syndrome; Endocrine (paraneoplastic); Recurrent laryngeal symptoms; Effusions (pleural or pericardial) |
|
|
Q288. Hx of smoking; Hilar mass arising from bronchus, cavitation, PTHrP production; What would show up on histology?
|
Squamous cell carcinoma |
|
|
Q289. Keratin pearls and intracellular bridges
|
Squamous cell carcinoma |
|
|
Q290. Clara cells --> type II pneumocytes; multiple densities on chest X-ray
|
Bronchial or bronchioloalveolar Adenocarcinoma |
|
|
Q291. Peripheral tumor in site of prior pulmonary inflammation or injury
|
Bronchial adenocarcinoma |
|
|
Q292. Peripheral tumor presenting like pneumonia, grows along airways; Can result in hypertrophic osteoarthropathy
|
Bronchioloalveolar adenocarcinoma |
|
|
Q293. Most common lung cancer in nonsmokers and females?
|
Bronchial adenocarcinoma |
|
|
Q294. Central, aggressive tumor. Associated with ectopic ACTH or ADH, Lambert-Eaton Syndrome (anti-Ca channel Igs)
|
Small (oat) cell carcinoma |
|
|
Q295. Poorly differentiated; neuroendocrine Kulchitsky cells (dark blue)
|
Small (oat) cell carcinoma |
|
|
Q296. Inoperable but responsive to chemotherapy
|
Small (oat) cell carcinoma |
|
|
Q297. Pleomorphic giant cells with leukocyte fragments
|
Large cell carcinoma |
|
|
Q298. Peripheral tumor composed of anaplastic cells; unresponsive to chemotherapy; surgically removed
|
Large cell carcinoma |
|
|
Q299. Secretes serotonin, can cause flushing, diarrhea, wheezing, salivation
|
Carcinoid tumor |
|
|
Q300. Malignancy of the pleura resulting in hemorrhagic pleural effusions and pleural thickening
|
Mesothelioma |
|
|
Q301. Psammoma bodies seen on histology
|
Mesothelioma |
|
|
Q302. Common sites of lung metastases
|
adrenals; brain (seizures); bone (fractures); liver (jaundice, hepatomegaly) |
|
|
Q303. Ptosis, miosis, anyhydrosis can be caused by a lung tumor in what location?
|
Apex (Pancoast's) --> compresses cervical sympathetic plexus |
|
|
Q304. What organisms are usually responsible for lobar pneumonia?; Produce intra-alveolar exudate --> consolidation
|
Streptococcus pneumoniae; Klebsiella |
|
|
Q305. What organisms are usually responsible for bronchopneumonia?; Inflammatory infiltrates from bronchioles --> alveoli; patchy distribution in >1 lobe
|
S. aureus; H. flu; Klebsiella; S. pyogenes |
|
|
Q306. What organisms are usually responsible for interstitial pneumonia?; Diffuse patchy infiltrates localized to interstitial areas at alveolar walls; more indolent
|
Viruses (RSV, adenovirus); Mycoplasma; Legionella; Chlamydia |
|
|
Q307. What situations predispose to lung abscess with S. aureus and anaerobes?
|
Bronchial obstruction (e.g. cancer); Aspiration of oropharyngeal contents (e.g. alcoholics, epileptics) |
|
|
Q308. Pleural effusion with low protein content is due to...
|
(Transudate):; CHF; Nephrotic syndrome; Hepatic cirrhosis; Anything that causes increased hydrostatic or decreased oncotic P |
|
|
Q309. Cloudy pleural effusion with high protein content is due to... |
(Exudate - must drain):; Malignancy; Pneumonia; Collagen vascular disease; Infection; Trauma; Anything that causes increased vascular permeability |
|
|
Q310. Milky fluid with high triglyceride content is composed of... |
lymphatic fluid (lymphatic effusion) |
|
|
(H/P) = rhinorrhea (i.e., nasal congestion & increased secretions), nonproductive cough; nasal and throat irritation, sneezing, possible fever, no exudates or productive coughLabs = negative throat culture |
Upper respiratory infections (URI) Inflammation of the upper airways most commonly caused by rhinovirus, coronavirus, or adenovirus |
Treatment = rest, analgesia, treat symptoms; antibiotics are NOT helpful
|
|
H/P = sore throat, tonsillar exudates (more common w/ bacterial infection), lymphadenopathy, possible nasal congestion; fever, red and swollen pharynx, |
PharyngitisPharyngeal infection caused by group A β-hemolytic streptococci (“strep throat”) or common cold virusComplications = untreated infection can cause rheumatic heart disease or glomerulonephritis (characterized by a high antistreptolysin O titer)
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Labs = throat culture grows streptococcal species, and rapid streptococcal Ag test is + for strep throat; - culture suggests viral etiologyTreatment = self-limited; β-lactam antibiotics (e.g., penicillin, amoxicillin, etc.) reduce infection time
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H/P = similar to streptococcal pharyngitis, tonsillar exudates; ear pain, difficulty swallowing; possible high fever.
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Tonsillar infectionsSpread of streptococcal pharyngitis to palatine tonsils leading to tonsillar inflammation (i.e., tonsillitis)Complications = airway compromise; abscess (requires intravenous [IV] antibiotics and surgical incision and drainage followed by tonsillectomy after resolution to prevent recurrence)
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Treatment = self-limited; β-lactam antibiotics (e.g., penicillin, amoxicillin, etc.) reduce infection time
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H/P = myalgias, vomiting, diarrhea; high fevers (typically >100°F/37.8°C and can reach up to 106°F/41°C), arthralgias, sore throat, nasal congestion, nonproductive cough, nausea, lymphadenopathy
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Viral influenzaGeneralized infection with URI symptoms caused by one of several influenza viruses |
Labs = serologic tests are definitive, but rarely required for diagnosisTreatment = treat symptoms; fluid intake important to replace losses from vomiting and diarrhea; self-limited (several days) but amantadine may shorten course of disease; elderly patients, health care workers, immunocompromised patients, and patients with lung disease should receive annual vaccine to reduce risk of infection
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pain over infected sinuses, purulent nasal discharge, maxillary toothache pain; pain on palpation of affected sinuses, illumination test (i.e., light held close to sinuses) may detect congestion in frontal of maxillary sinuses, but is unreliable
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SinusitisSinus (most maxillary)infection associated w/ allergic rhinitis, barotrauma, viral infection, prolonged nasogastric tube placement, or asthmaAcute sinusitis is usually caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, viral infectionAcute sinusitis can spread to CNS & cause meningitis if untreated.Chronic sinusitis (lasting >3 months) is usually caused by sinus obstruction, anaerobic infection; patients with diabetes mellitus (DM) predisposed to mucormycosis
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Radiology = radiograph shows opacification and fluid levels in affected sinuses; computed tomography (CT) is diagnostic; frequently radiologic tests are not needed because of clinical diagnosisTreatment = treat symptoms; amoxicillin × 2 weeks in acute cases and for 6–12 weeks in chronic cases; surgical drainage or correction of anatomic obstruction may be required for full cure
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H/P = productive cough, sore throat; fever, wheezing, tight breath sounds
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Acute bronchitisInflammation of trachea and bronchi caused by spread of URI or exposure to inhaled irritants
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Labs = sputum culture only performed in persistent cases and is most commonly -;Radiology = chest x-ray (CXR) may show only mild congestionTreatment = self-limited if viral (most cases); patient groups with an increased risk of bacterial infection (e.g., smokers, elderly, patients with other lung disease) may be given antibiotics (e.g., fluoroquinolones, tetracycline, or erythromycin)
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H/P = pleuritic chest pain; decreased breath sounds, dullness to percussion, tachypnea, productive or nonproductive cough, dyspnea, chills, night sweats, rales, wheezing, egophony (i.e., change in voice quality heard during auscultation over a consolidated region of lung), tactile fremitusLabs = increased white blood cell count (WBC) (slight increase with viral cause, significant increase with bacterial or fungal cause) with left shift (more immature forms); + sputum culture
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PneumoniaInfection of the bronchoalveolar tree can be caused by common nasopharyngeal bacteria (i.e., typical pneumonia) or bacteria, viruses, or fungi from the surrounding environment (i.e., atypical pneumonia); common causes vary by age group |
Treatment = viral pneumonia is self-limited and only requires supportive care; bacterial and fungal pneumonias require antibiotics (started as broad coverage and changed to pathogen-specific therapy as culture results become availableAdmission=elderly, multiple medical comorbidity, significant laboratory abnormalities, multilobar involvement, signs of sepsis
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H/P=a non-productive cough be used for influenza A virus
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Viral Pneumonia Viral (influenza, parainfluenza, adenovirus, cytomegalovirus, respiratory syncytial virus) Most common pneumonia in children; common in adults
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Treatment=Self-limited; amantidine may
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H/P=pneumonia, high fevers, pleuritic pain, productive cough
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Streptococcus pneumoniae Most common pneumonia in adults; higher risk of infection in sickle cell patients
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Treatment=β-lactams, macrolides(azithromycin, clarithromycin, erythromycin)
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H/P=pneumonia, slower onsetPatients with COPD; higher risk of infection in patients with sickle cell disease
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Haemophilus influenzae
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Treatment=β-lactams, TMP-SMX
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H/P=pneumonia, abscess formationNosocomial pneumonia, immunocompromised patients
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Staphylococcus aureus
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Treatment=β-lactams
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H/P=pneumonia, “Currant-jelly” sputum; Alcoholics, patients with high risk of aspiration, patients staying in the hospital for extended amounts of time, sickle cell patients
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Klebsiella pneumoniae
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Treatment=Both cephalosporins and aminoglycosides (gentamicin, tobramycin)
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H/P=pneumonia, Young adults, possible rash; + cold-agglutinin test
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Mycoplasma pneumoniae
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Treatment=Macrolides (azithromycin, clarithromycin, erythromycin)
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H/P=pneumonia, rapid onsetChronically ill and immunocompromised patients, patients with cystic fibrosis, nosocomial pneumonia
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Pseudomonas aeruginosa
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Treatment=Fluoroquinolones (ciprofloxacin), aminoglycosides, generation 3rd-cephalosporins
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H/P=pneumonia Slow onset, nausea, diarrhea, confusion, or ataxia
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Legionella pneumophilaAssociated with aerosolized water (air-conditioners)
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Treatment=Macrolides, fluoroquinolones
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H/P=pneumonia, Slow onset, frequent sinusitisMore common in very young and elderly
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Chlamydia pneumoniae
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Treatment=Doxycycline, macrolides
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H/P=pneumonia, Respiratory distress, lethargyNeonates and infants
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Group B Streptococcus
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Treatment=β-lactams
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H/P=pneumoniaNosocomial pneumonia, elderly patients
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Enterobacter sp.
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Treatment=TMP-SMX
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H/P=pneumonia, Less severe symptoms; subacute disease for initial history
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FungiTravelers to southwest U.S. (coccidioidomycosis), caves (histoplasmosis), or Central America (blastomycosis)
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Treatment=Antifungal agents (amphotericin B, ketoconazole)
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H/P=pneumonia, Slow onset, GI symptomsImmunocompromised patients (HIV) (CD4 count <200)
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Pneumocystis carinii (fungi-like)
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Treatment=TMP-SMX
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H/P = cough, hemoptysis, dyspnea, weight loss, night sweats; fever, ralesRisk factors = immunosuppression, alcoholism, lung disease, DM, advanced age, homelessness, malnourishment, crowded living conditions, and close proximity to infected patientsRadiology = CXR may show apical fibronodular infiltrates (reactivated disease), lower-lobe infiltrates (primary lesion), and calcified granulomas/lymph nodes (Ghon complexes)
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Tuberculosis (TB)Pulmonary infection caused by Mycobacterium tuberculosisFollowing primary infection, disease enters inactive state; untreated infections can become reactivated (most active cases) and extend to extrapulmonary sites (i.e., miliary TB)
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Labs = + purified protein derivative (PPD) tuberculin skin test is screening test for exposure (followed by a CXR to look for signs of TB), anergy test (subcutaneous Candida preparation) in addition to a PPD to check for an appropriate immune response; + sputum acid-fast stain, + culture (may take weeks, so not useful in planning therapy); 1 bronchoscopy is considered equal to 3 sputum samples for specimen collectionTreatment = respiratory isolation for any inpatient; report all diagnosed cases to local and state health agencies; multidrug treatment initially w/ isoniazid (INH), rifampin, pyrazinamide, & ethambutol followed by INH & rifampin for a total of 6 months; give vitamin B6 w/ INH to prevent peripheral neuritis (INH competes with vitamin B6 as a cofactor in neurotransmitter synthesis, so supplemental vitamin B6 helps offset this competition); give prophylactic INH to patients with an asymptomatic positive PPD who are immunocompromised, have a history of IV drug abuse (IVDA), are <35 years of age, a history of close contact with TB-infected people, or are indigent patients (reporting is unnecessary unless TB is diagnosed); monthly sputum acid-fast tests should be performed during therapy to confirm adequate treatment
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H/P = acute dyspnea and pulmonary decompensation in setting of serious underlying condition; cyanosis, tachypnea (begins within 48 hours of initial insult), wheezing, rales, rhonchiLabs = arterial blood gas (ABG) shows respiratory alkalosis, decreased O2 (caused by impairment of O2 transfer to pulmonary capillaries by pulmonary edema), decreased CO2 (caused by hyperventilation); other tests should reflect underlying pathology; Swan-Ganz catheterization shows wedge pressure <18 mm Hg; Pao2:Fio2 ratio will be <200 during mechanical ventilation
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Acute respiratory distress syndrome (ARDS)Acute respiratory failure caused by sepsis, trauma, aspiration, near drowning, drug overdose, shock, or lung infection that is characterized by refractory hypoxemia, decreased lung compliance, and pulmonary edema, and carries a high mortalityEtiology=ARDS: Aspiration/Acute pancreatitis/Air or Amniotic embolism, Radiation, Drug overdose/Diffuse lung disease/DIC/Drowning, Shock/Sepsis/Smoke inhalation.
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Radiology = bilateral pulmonary edema and infiltratesTreatment = treatment in intensive care unit with mechanical ventilation frequently required; mechanical ventilation should include positive end-expiratory pressure (PEEP), increased inspiratory times, and Fio2 adjusted to maintain O2 saturation (Sao2) >90%; underlying cause must be treated; keep fluid volumes low to prevent pulmonary edema; use of extracorporeal membrane oxygenation (ECMO) may improve outcome in severe cases
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H/P = prolonged expiratory duration, accessory muscle use, cough, dyspnea, wheezing, chest tightness; tachypnea, tachycardia, decreased breath sounds, wheezing, possible pulsus paradoxus; cyanosis, decreased arterial O2 saturation (Sao2) on pulse oximetry, or difficulty talking in severe attacks
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AsthmaReversible airway obstruction secondary to bronchial hyperactivity, acute airway inflammation, mucous plugging, and smooth muscle hypertrophyExacerbations (i.e., sudden bronchoconstriction and airway inflammation) are triggered by allergens (e.g., dust, smoke, pollen, fumes, pet dander), URI, exercise, stress, β-antagonist drugs, aspirin (rare), and sulfites (rare)Risk factors = family history of asthma, allergies, atopic dermatitis, low socioeconomic statusDisease can be worse in childhood and improve with age
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Labs = peak expiratory flow rate (PEFR) decreased and used along with clinical symptoms and frequency of medication use to classify disease as mild intermittent, mild persistent, moderate persistent, or severe (see Table 2-8); PFT show decreased FEV1, normal/elevated DLcoRadiology = CXR shows hyperinflationTreatment=Inhaled short-acting β2-agonist IV corticosteroids if persistent during exacerbation. daily corticosteroid inhaler (+long long-acting β2-agonist, considerleukotriene inhibitor or theophylline) from Mild Persisent up
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prolonged, nonresponsive asthma attack
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Status asthmaticus
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Treatment=aggressive bronchodilator therapy, corticosteroids, O2, and, possibly, intubation
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H/P = productive cough, recurrent respiratory infections, dyspnea; wheezing, rhonchihistory of productive cough for 3 months of the year for >2 years
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Chronic bronchitisChronic bronchial inflammation associated with tobacco use (common) or chronic asthma (uncommon); occurs in continuum with emphysema as chronic obstructive pulmonary disease (COPD)“blue bloaters,” because secondary development of cor pulmonale causes cyanosis and peripheral edema;Complications = emphysema frequently results without smoking cessation
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Labs = PFTs show gradually worsening signs of obstructive disease as condition progressesTreatment = tobacco cessation, antibiotics given for URI because of the greater incidence of a bacterial etiology; bronchodilators during exacerbations
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H/P = dyspnea, possible productive cough, morning headache; barrel-chested, pursed-lip breathing, prolonged expiratory duration, decreased heart sounds, decreased breath sounds, wheezing, rhonchi, accessory muscle use, jugular venous distension (JVD); exacerbations present with worsening symptoms
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Emphysema (later stage—COPD)Long-term tobacco use leads to chronic bronchoalveolar inflammation associated with release of proteolytic enzymes by neutrophils and macrophages; destruction of alveoli and bronchioles results with panacinar airspace enlargement and a decreased capillary bedLess common form (appears at younger age) caused by α1-antitrypsin deficiencycommon form of emphysema has a centrilobular distribution, whereas the form associated with α1-antitrypsin deficiency has a panlobular distribution.
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Labs = PFTs show decreased FEV1, decreased FEV1/FVC, increased total lung capacity (TLC), decreased PEFR; ABG during acute exacerbations shows decreased O2, increased CO2 (beyond a baseline increase already seen in these patients)Radiology = CXR shows flat diaphragm, hyperinflated lungs, subpleural blebs and bullae (i.e., small fluid-filled sacs), and decreased vascular markingsTreatment = smoking cessation; supplemental O2; inhaled, short-acting β2-agonists; inhaled anticholinergics; inhaled corticosteroids and long-acting β2-agonists may be useful in severe cases; antibiotics given for respiratory infections; pneumococcal and influenza vaccines important to reduce infection risk; enzyme replacement may have a role in α1-antitrypsin deficiency therapy; lung transplant may be an option in late severe disease
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H/P = copious sputum, persistent, productive cough; hemoptysis, frequent respiratory infections, dyspnea; wheezing, rales, and hypoxemia
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D. BronchiectasisPermanent dilation of small and medium bronchi because of destruction of bronchial elastic componentsOccurs secondary to chronic airway obstruction, chronic tobacco use, TB, fungal infections, severe pneumonia, or cystic fibrosisComplications = cor pulmonale, massive hemoptysis, abscess formation
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Radiology = multiple cysts and bronchial crowding seen on CXR; CT shows dilation of bronchi, bronchial wall thickening, bronchial wall cystsTreatment = pulmonary hygiene (e.g., hydration, sputum removal), chest physical therapy; antibiotics given when sputum production increases; inhaled β2-agonists and corticosteroids may reduce symptoms; resection of severely diseased regions of lung indicated for hemorrhage, substantial sputum production, or inviability
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H/P = possibly asymptomatic; hemoptysis, cough, dyspnea, pleuritic chest pain, fatigue, weight loss, frequent pulmonary infections;
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Lung cancerMost frequently associated with tobacco use (~90% of cases); also can be caused by occupational exposures (e.g., smoke, asbestos)Complications = poor prognosis (~10% 5-yr survival); recurrence common for primary tumors
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Radiology = initially seen on CXR or CT as pulmonary nodule; bronchoscopy with biopsy and brushings or fine needle aspiration of lesion are diagnosticTreatment = use of surgical resection, chemotherapy, and/or radiation therapy based on type of lung cancer (large cell, squamous cell, or adenocarcinoma vs. small cell) and staging of disease (based on local extension, lymph node involvement, and presence of metastases) (see Table 2-11)
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miosis, ptosis, and anhidrosis
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Horner's syndrome
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Horner's syndrome plus brachial plexus involvement
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Pancoast's syndrome
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obstruction of venous drainage through superior vena cava and associated head swelling and CNS symptoms
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Superior vena cava syndrome
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Lung Cancer, CentralCavitary lesions; direct extension to hilar lymph nodesParaneoplastic Syndromes= Hypercalcemia, Dermatomyositis
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Squamous cell carcinoma
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Treatment=Chemotherapy as primary, Radiation Therapy as adjuvant
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Lung Cancer,PeripheralWide metastases; can be caused by asbestos; pleural effusions show increased hyaluronidase levels; bronchiolar cancer is subtype that is low grade and occurs in single nodulesParaneoplastic Syndromes= DIC, Thrombophlebitis,, Microangiopathic hemolytic anemiaDermatomyositis
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Adenocarcinoma
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Treatment for all non-small:no lymph node involvement beyond ipsilateral hilar nodes, No mediastinal invasion, no metastases->Surgical resection, radiation as primary or postop adjuvant, chemo as adjuvant
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Lung Cancer, CentralRapidly growing; early distant metastases; several paraneoplastic syndromesParaneoplastic Syndromes= Cushing's syndrome, Syndrome of inappropriate ADH secretion (SIADH), Ectopic growth hormone and ACTH secretion, Peripheral neuropathy, Subacute cerebellar degeneration, Eaton-Lambert syndrome (similar presentation to myasthenia gravis), Subacute sensory neuropathy, Limbic encephalitis, Dermatomyositis
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Small cell carcinoma
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Treatment for all non-small:has extension to ipsilateral mediastinal nodes, No mediastinal invasion or metastases->radiation as primary, surgery if tumor shrinik, chemo as induction for surgery or adjuvant
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Lung Cancer, PeripheralLate distant metastases, early cavitationParaneoplastic Syndromes=Gynecomastia, Dermatomyositis
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Large cell carcinoma
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Treatment for all non-small:Mediastinal invasion, distant nodes, and/or metastases-> chemo or radiation as palliative
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H/P = hoarseness that worsens with time (over several weeks), dysphagia, ear pain, hemoptysis; laryngoscopy may visualize mass and airway obstruction
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Laryngeal cancer Squamous cell cancer of the larynx associated with tobacco and alcohol use |
Labs = biopsy is diagnosticRadiology = magnetic resonance imaging (MRI) or CT with contrast detects soft tissue mass; PET may be useful for detecting lesions earlier in disease courseTreatment = partial or total laryngectomy used to remove lesions confined to larynx; radiation therapy can be used in conjunction with surgery or as sole therapy in extensive lesions; advanced cases may require combination of surgery, radiation, and chemotherapy to resect lesion while preserving surrounding structures
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H/P = progressive exercise intolerance, dyspnea; dry crackles, JVD, tachypnea, and possible digital clubbingpatients >50 years of ageLabs = PFT will show restrictive lung disease characteristics (e.g., FEV1/FVC normal, decreased FVC, decreased TLC, decreased compliance); bronchioalveolar lavage shows increased polymorphonuclear (PMN) cells; lung biopsy demonstrates extensive fibrosis and loss of parenchymal architectureRadiology = CXR shows reticulonodular pattern and “honeycomb” lung in advanced cases; CT will show lung fields with “ground glass” appearance
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Idiopathic pulmonary fibrosis (IPF)Inflammatory lung disease causing lung fibrosis;Complications = progressive lung fibrosis with frequent mortality within 5 years; most patients do not survive sufficiently long to receive a lung transplant |
Treatment = corticosteroids combined with either azathioprine or cyclophosphamide are helpful in some patients (follow PFTs to evaluate effectiveness); worsening PFTs should indicate need to change drug regimen; lung transplant is frequently indicated
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H/P = cough, malaise, weight loss, dyspnea, arthritis (knees, ankles), chest pain; fever, erythema nodosum (i.e., tender red nodules on shins and arms), lymphadenopathy, vision loss, cranial nerve palsiesLabs = increased serum angiotensin-converting enzyme (ACE), increased calcium, hypercalciuria, increased alkaline phosphatase, decreased WBC, increased erythrocyte sedimentation rate (ESR); PFT show decreased FVC, decreased DLcoRadiology = CXR shows bilateral hilar lymphadenopathy, pulmonary infiltrates (ground glass appearance)
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SarcoidosisSystemic disease characterized by noncaseating granulomas, hilar adenopathy, pulmonary infiltrates, and skin lesions; unknown etiologyRisk factors = blacks > whites; females > males; most frequently occurs between 10 and 40 years of agePatients with sarcoidosis frequently show anergy (no reaction) to a skin test or PPD.
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Treatment = occasionally self-resolving; corticosteroids in chronic cases; cytotoxic drugs can be used with failure of steroid therapy; lung transplantation is rarely required (only in severe cases)
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H/P = symptoms begin when significant pulmonary fibrosis has occurred (several years between exposure to onset of symptoms is common); cough, dyspnea on exertion, heavy sputum production; rales and wheezing are heard on auscultation, digital clubbing
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PneumoconiosesInterstitial lung diseases that result from long-term occupational exposure to substances that cause pulmonary inflammation
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Labs = PFT show a restrictive patternRadiology = CXR shows multinodular opacities; CT shows signs of pulmonary fibrosisTreatment = usually, no successful treatments are available for these conditions; prevention (e.g., proper air filters, following safe-handling recommendations) is vital to avoiding disease
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H/P = hemoptysis, dyspnea, recent respiratory infectionLabs = + anti-GBM Ab; PFT show restrictive pattern, but increased DLco (caused by the presence of Hgb in alveoli); urinalysis shows proteinuria and granular casts; renal biopsy shows crescentic glomerulonephritis and IgG deposition along glomerular capillaries
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Goodpasture's syndromeProgressive autoimmune disease of lungs and kidneys caused by anti-glomerular basement membrane (anti-GBM) antibodies and characterized by intra-alveolar hemorrhage and glomerulonephritis
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Radiology = CXR shows bilateral alveolar infiltrationTreatment = plasmapheresis to remove auto-antibodies; corticosteroids and immunosuppressive agents
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H/P = ulcerations of nasopharynx, fever; hemoptysis, dyspnea, myalgias, chronic sinusitis; additional symptoms from renal (e.g., mild hematuria), CNS (e.g., hearing loss, sensory neuropathy, cranial nerve dysfunction), ophthalmologic (e.g., conjunctivitis, proptosis, corneal ulceration, diplopia), and cardiac (e.g., arrhythmia) involvementLabs = + cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA); biopsy shows noncaseating granulomas; renal biopsy detects vasculitic process
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Wegener granulomatosisRare disease with granulomatous inflammation and necrosis of lung and other organ systemsCaused by systemic vasculitis that mainly affects lung and kidney causing formation of noncaseating granulomas and destruction of lung parenchymaComplications = rapidly fatal if untreated
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Treatment = cytotoxic therapy (e.g., cyclophosphamide), corticosteroids
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PneumoconiosesWorking with insulation, construction, demolition, building maintenance, automobiles
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AsbestosisComplications=Increased risk of malignant mesothelioma and lung cancer; synergistic effect with tobacco |
Labs=pleural biopsy show asbestos fibersRadiology= Multinodular opacities, pleural effusions, blurring of heart/diaphragm; chest CT shows linear pleural/parenchymal fibrosis
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PneumoconiosesMining, pottery making, sandblasting, cutting granite
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SilicosisComplications=Increase risk of TB infection; progressive fibrosis |
Radiology=Small apical nodular opacities; hilar adenopathy
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Pneumoconioses.Coal mining
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Coal worker's diseaseComplications=Progressive fibrosis
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Radiology=Small apical nodular opacities
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PneumoconiosesElectronics, ceramics, tool, die manufacturing
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BerylliosisComplications=Increased risk of lung cancer;
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Labs=Pulmonary edema, diffuse granuloma formationRadiology=Diffuse infiltrates; hilar adenopathyTreatment=may need chronic corticosteroid treatment to maintain respiratory function
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H/P = sudden dyspnea, pleuritic chest pain, cough, syncope, hemoptysis, feeling of impending doom; fever, tachypnea, tachycardia, cyanosis, loud S2, decreased breath sounds over regions of effusionLabs = increased A-a gradient; increased D-dimer; ABG shows increased CO2, decreased O2 (<80 mm Hg), ventilation-perfusion scan (V/Q scan) may show areas of mismatchECG = tachycardia, may show S wave in lead I and T-wave inversion in lead III |
Pulmonary embolism (PE)Occlusion of pulmonary vasculature by a dislodged thrombusIncreasing pulmonary artery pressure caused by occlusion leads to right-sided heart failure, hypoxia, and pulmonary infarctionRisk factors = 7 Hs: Heredity (genetic hypocoagulability), History (prior DVT or PE), Hypomobility (fracture, prolonged travel, surgery, obesity), Hypovolemia (dehydration), Hypercoagulability (cancer, smoking), Hormones (pregnancy, oral contraceptive pill [OCP] use), and Hyperhomocysteinemia. |
Radiology = CXR may be normal or may show pleural effusion or wedge-shaped infarct; pulmonary angiography is diagnostic, but a higher risk study; spiral CT may detect proximal PE; ventilation-perfusion (V/Q) scan can detect areas of ventilation-perfusion mismatchA positive or negative V/Q scan is diagnostic or rules out PE, but an equivocal scan indicates need for angiographyTreatment = supplemental O2 to maximize saturation; IV fluids or cardiac pressors as needed for hypotension; anticoagulate initially with either low molecular weight heparin (LMWH) or unfractionated heparin (titrated for PTT 1.5–2.5 times normal); patients treated with unfractionated heparin need to be converted to either LMWH or warfarin (given to achieve goal international normalized ratio [INR] 2 -3) for 3–6 months; inferior vena cava filter can be placed if anticoagulation is contraindicated; thrombolysis may be considered for patients with massive PE or those with no cardiac contraindications, recent trauma, or surgery |
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H/P = dyspnea, fatigue, deep chest pain, cough, syncope, cyanosis; digital clubbing, loud S2, JVD, hepatomegalyLabs = increased red blood cell count (RBC) and WBCECG = right ventricular hypertrophyRadiology = CXR shows large pulmonary artery and large right ventricle; echocardiogram useful for measuring pulmonary artery pressure noninvasively and detecting valvular disease; cardiac catheterization is the gold standard test for measuring pressures, but carries greater risks than other studies; PFTs may be useful in diagnosing underlying pulmonary disease
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Pulmonary hypertensionIncreased pulmonary artery pressure caused by PE, valvular disease, left-to-right shunts, COPD, or idiopathic causesIdiopathic pulmonary hypertension has a high mortality rate within a few years of diagnosis |
Treatment = treat underlying condition; supplemental O2 helps maintain blood oxygenation; vasodilators indicated for idiopathic and pulmonary causes to decrease pulmonary vascular resistance; anticoagulants indicated in patients with idiopathic, embolic, or cardiac causes to decrease risk of pulmonary thrombus formation
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H/P = orthopnea, paroxysmal nocturnal dyspnea, dyspnea; tachycardia, frothy sputum, wheezing, rhonchi, rales, dullness to percussion, peripheral edema, S3 or S4 heart sound, hypertensionLabs = increased brain natriuretic peptide (BNP) or abnormal cardiac enzymes help elucidate a cardiac causeECG = T-wave abnormalities or QT prolongation are common changes and can occur suddenly with acute onset
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Pulmonary edemaIncreased fluid in lungs caused by increased pulmonary venous pressure and hydrostatic leak of fluid from vesselsCaused by left-sided heart failure, myocardial infarction (MI), valvular disease, arrhythmias, ARDS(pulmonary wedge pressure <18 mm Hg).A pulmonary wedge pressure measured with a Swan-Ganz catheter is suggestive of a cardiac cause for pulmonary edema if >18 mm Hg |
Radiology = CXR shows fluid throughout lungs, cephalization of vessels (i.e., increased vascular markings in upper lung fields), Kerley B lines (i.e., prominent horizontal interstitial markings in lower lung fields)Treatment = treat underlying condition; diuretics, salt restriction, O2, morphine, vasodilators; nesiritide improves outcomes in cases with a cardiac cause; pressors may be required to improve cardiac output if perfusion is inadequate; Swan-Ganz catheter placement useful for monitoring response to therapy
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H/P = possibly asymptomatic; dyspnea, pleuritic chest pain, weakness; decreased breath sounds, dullness to percussion, decreased tactile fremitus, egophonyRadiology = CXR shows blunting of costophrenic angles; decubitus CXR can demonstrate whether fluid is loculated or free flowing; CT is useful for measuring pleural thickness, distinguishing a discrete collection from a diffuse one (e.g., abscess vs. empyema)
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Pleural effusionSerous or lymphatic fluid collection in pleural space is classified according to protein and lactate dehydrogenase (LDH) content and is caused by changes in hydrostatic and oncotic pressure (transudative), inflammation (exudative), or lymphatic duct rupture (lymphatic)1/4 of pleural effusions are associated with neoplasm
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Labs = pleural fluid analysis used for protein and LDH levels (i.e., transudate vs. exudates), glucose (low in TB, malignancy, autoimmune diseases), pH (acidic in malignancy, TB, empyema), amylase (high in pancreatitis, esophageal rupture, some malignancies), triglycerides (high in thoracic duct rupture), complete blood cell count (CBC), Gram stain, and cytologyTreatment = treat underlying condition; relieve pressure on lung with thoracocentesis and chest tube placement; for cases with empyema (i.e., effusion of pus due to infection), a chest tube is required; if recurrent malignant effusion occurs, use pleurodesis (talc or other irritant) to scar the pleural layers together
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Pleural effusionPleural: Serum Protein Ratio <0.5;Pleural: Serum LDH Ratio <0.6;Total Pleural Protein <3 g/dL
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Transudateetiology=CHF, cirrhosis, kidney diseases (nephrotic syndrome)
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Pleural effusionPleural: Serum Protein Ratio >0.5;Pleural: Serum LDH Ratio >0.6;Total Pleural Protein >3 g/dL
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Exudateetiology=Infection, cancer, vasculitis
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H/P = unilateral chest pain, dyspnea; decreased chest wall movement, unilateral decreased breath sounds, increased resonance to percussion, decreased tactile fremitus; respiratory distress, decreased Sao2, hypotension, JVD, or tracheal deviation suggest tension pneumothoraxRadiology = CXR shows lung retraction and mediastinal shift away from affected side; tension PTX will demonstrate tracheal deviation
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Pneumothorax (PTX)Collection of air in pleural space that predisposes patient to pulmonary collapseCan occur spontaneously (less common) or secondary to trauma or a pulmonary medical condition (more common)
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TreatmentSmall (<15% lung field) PTX may resolve with supplemental O2 onlyLarger (>15%) PTX requires chest tube placementOpen PTX with small wound is treated with chest tube and occlusive dressingOpen PTX with larger wounds should be treated with attempted closure and should carry a low threshold for intubationTension pneumothorax requires immediate needle decompression (4th or 5th intercostal space at the maxillary line) and chest tube placementRecurrent pneumothorax may require pleurodesis
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H/P = dyspnea, pleuritic chest pain, weakness; decreased breath sounds, dullness to percussion, decreased tactile fremitus, egophonyLabs = thoracocentesis shows bloody effusion
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HemothoraxCollection of blood in pleural space caused by trauma, malignancy, TB, or pulmonary infarctionComplications = thrombi formation, fibrosis can occur if blood is not drained from pleural space
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Radiology = CXR resembles that for pleural effusion (i.e., lung retraction, mediastinal shift from affected side)Treatment = supplemental O2; chest tube placement; treat underlying cause
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H/P = nonpleuritic chest pain, dyspnea; dullness to percussion over lung bases, palpable chest wall mass, scoliosis toward lesion
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Malignant mesotheliomaUncommon tumor occurring on visceral pleura or pericardium with very poor prognosisIncreased incidence with asbestos exposure (occurs 20 years after exposure)
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Labs = pleural biopsy is usually diagnostic; thoracocentesis of an associated pleural effusion can be used for cytology studiesRadiology = CXR shows pleural thickening, pleural effusion; chest CT can display extent of local disease; PET scan can be used to detect extrathoracic diseaseTreatment = extrapleural pneumonectomy with adjuvant chemotherapy and radiation therapy; chemotherapy alone used for unresectable disease
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H/P = fatigue, daytime sleepiness, snoring, gasping or choking during sleep, morning headaches or confusion, impaired daytime function because of sleepiness; obesity common, anatomic abnormalities of palate or pharynx may be visibleLabs = Epworth sleepiness scale is useful for predicting likelihood of sleep apnea as cause for daytime somnolence (score >10 common in sleep apnea); polysomnography is definitive test that measures Apnea Index (AI, average apneic episodes per hour), Sao2, and number of arousals
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Sleep apneaEpisodic cessation of airflow during sleep leading to desaturations and frequent arousalsTypesObstructive: obstruction of upper airway during sleep with continued respiratory effort; most often associated with obesity or abnormal pharyngeal anatomyCentral: loss of central respiratory drive leads to cessation of airflow and respiratory effortMixed: combines both obstructive and central characteristicsRisk factors = obesity, sedative use; males more than femalesEtiology is unknown, but may be linked to abnormal feedback control during sleep or decreased sensitivity of upper airway muscles to stimulation
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TreatmentObstructive = consider weight loss (possibly bariatric surgery) and stop sedative use; continuous positive airway pressure (CPAP) is helpful in chronic cases to maintain airway patency; surgical correction of tonsillar hypertrophy, polyp removal, correction of congenital upper airway deformities, or tracheostomy may be necessary in severe or refractory casesCentral = respiratory stimulants; phrenic nerve pacemaking may be needed in severe casesBariatric surgery is associated with resolution of sleep apnea in 86% of cases.
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H/P = asymptomatic if mild or slow development; pleuritic chest pain, dyspnea; fever, decreased breath sounds, dullness to percussion over affected areaRadiology = CXR will show fluffy infiltrates in mild cases and lobar collapse in cases of airway obstruction
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AtelectasisLocalized alveolar collapse; common after surgery (especially abdominal) and anesthesia (generally not clinically serious); can also occur in asthmatics, after foreign body aspiration, or from mass effect (e.g., tumors, pulmonary lesions, or lymphadenopathy)If atelectasis lasts >72 hr, pneumonia is likely to develop.
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Treatment = inspiratory spirometry, ambulation, and inpatient physical therapy are important for prevention in the hospital and postoperatively; severe cases require upper airway suctioning or bronchoscopy with deeper suctioning
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Mechanical VentilationUse=General anesthesia, overdosePatient=No effort
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Mode=Controlled mechanical ventilation (CMV)
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Machine Determines and automatically delivers tidal volume (TV) and rate
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Mechanical VentilationUse=Weaning patient from ventilatorPatient=Can breathe spontaneously between mechanical breaths
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Mode=Intermittent mandatory ventilation (IMV)
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Machine Determines and automatically delivers TV and rate
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Mechanical VentilationUse=More comfortable for patient because of attempted synchronization; frequently used in place of IMVPatient=Can breathe spontaneously between mechanical breaths
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Mode=Synchronized intermittent mandatory ventilation (SIMV)
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Machine Machine tries to synchronize rate with patient-initiated breaths; automatically delivers TV and rate
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Mechanical VentilationUse=Used when patient is more awake and in progressive weaningPatient driven unless no attempts to breathe (backup rate)
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Mode=Assist-control ventilation (AC)
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Machine senses patient's attempt to breathe and delivers full preset TV; backup rate if no spontaneous breaths
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Mechanical VentilationUse=Used when patient relies less on ventilator; intubation not requiredPatient does all breathing
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Mode=Continuous positive airway pressure (CPAP)
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Machine maintains airway patency to decrease work of breathing
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H/P = barking cough, inspiratory stridor, dyspnea, nasal congestion; fever, mild pharyngeal erythema, lymphadenopathy; respiratory distress in severe casesRadiology = neck radiographs may show subglottic narrowing of airway (i.e., steeple sign)
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CroupAcute inflammation of larynx caused by parainfluenzae virus type 1; less commonly, by parainfluenzae virus types 2 and 3, respiratory syncytial virus (RSV) influenza virus, rubeola, adenovirus, or Mycoplasma pneumoniae3 Ss: Seal-bark cough, Subglottic swelling, and Stridor.
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Treatment = supportive care (e.g., hydration, humidified air, rest, analgesia); aerosolized epinephrine and inhaled corticosteroids can be used in severe cases to decrease pharyngeal inflammation; with concerns for respiratory distress, the child should be admitted for observationIf child develops stridor at rest, hospitalization and respiratory monitoring is needed.
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H/P = dysphagia, muffled voice, drooling, soft stridor, anxiety from symptoms; sudden high fever, inspiratory retractions; child may lean forward with hands on knees to aid breathing; erythematous and swollen epiglottisRadiology = neck radiographs show swollen opacified epiglottis that partially obstructs the airway (i.e., thumbprint sign); laryngoscope (only used in controlled situations) can visualize red and swollen epiglottis
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EpiglottitisRapidly progressive infection of epiglottis and surrounding tissues that can cause airway obstructionMost common in children from 2–7 years of ageCaused by Haemophilus influenzae type B (Hib) infection; can also be caused by streptococcal or other H. influenzae bacteria
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Labs = culture from swab of epiglottis can determine causative bacteria (should only be performed if patient intubated)Treatment = keep child calm; admit for close observation and respiratory monitoring; unless airway obstruction is mild, intubate (nasotracheal) to maintain airway patency; antibiotics for 7–10 days; airway obstruction preventing intubation requires emergent tracheostomyIn cases of suspected epiglottitis, examine the patient's throat only in a setting in which prompt intubation is possible because examination of the patient's throat can lead to additional throat irritation and resulting occlusion.
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H/P = nasal congestion, cough, respiratory distress; wheezing, fever, tachypnea, crackles, prolonged expiration, hyperresonance to percussionRadiology = CXR shows hyperinflation of lungs and patchy infiltrates
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BronchiolitisViral infection of bronchioles caused by RSV (most cases) or parainfluenzae virus type 3 (less common)Most commonly occurs in winter and spring; usually found in children <2 years of ageComplications = increased risk of developing asthma
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Treatment = adequate hydration, humidified air, inhaled corticosteroids and β2-agonists; ribavirin can be used in severe cases to shorten disease course; children with respiratory distress or hypoxemia should be admitted for observation and respiratory monitoring
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H/P = presentation within 2 days of birth; cyanosis, nasal flaring, expiratory grunting, intercostal retractions, respiratory rate >60 breaths/min, crackles, decreased breath soundsRadiology = CXR shows bilateral atelectasis with ground glass appearance and decreased lung volumes
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Respiratory distress syndrome of the newbornPreterm infants (e.g., 24–37 wks' gestation and especially before 30 wks' gestation) have surfactant deficiency because of lung immaturity that leads to decreased lung compliance, atelectasis, and respiratory failureComplications = increased risk of developing asthma in childhood compared with other children
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Labs = ABG shows increased CO2, decreased O2; amniotic fluid analysis (see Figure 2-9) not usually helpful, but may guide treatment between 34 and 37 wks' gestation by determining fetal lung maturity with the amniotic lecithin:sphingomyelin ratio (always treat for <34 weeks, treatment typically unnecessary for >37 weeks)Treatment = maternal administration of corticosteroids before initiation of labor helps to speed fetal lung maturation; neonatal intensive care unit (ICU) admission appropriate for close observation; supplemental O2 and surfactant replacement therapy mainstays of therapy; intubation should be performed for any neonate not responding to treatment or requiring high levels of O2 to maintain adequate Sao2
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H/P = meconium stained-amniotic fluid seen during delivery; cyanosis, intercostal retractions; distended chest, tachypnea
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Meconium aspiration syndromeAspiration of meconium (i.e., fetal stool passed into amniotic sac) predelivery causing obstruction of airways and pneumoniaComplications = pulmonary hypertension can develop if not promptly treated; increased risk of developing asthma during childhood
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Labs = consider blood culture to rule out sepsisTreatment = suction nose, mouth, and upper airway at birth; supplemental O2; intubate for worsening respiratory distress; surfactant therapy may be useful for improving respiratory function; consider empiric antibiotic therapy if concerned for development of pneumonia
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H/P = recurrent pulmonary infections (e.g., Pseudomonas, S. aureus), dyspnea, hemoptysis, chronic sinusitis, cough, meconium ileus at birth, steatorrhea, failure to thrive; cyanosis, digital clubbing, esophageal varices, rectal prolapseLabs = decreased serum Na; sweat test shows increased Na and increased Cl (>60 mEq/L in children, >80 in adults); genetic testing can locate mutation in CF transmembrane conductance regulator (CFTR) gene in suspected cases or in carriers of the gene considering pregnancy
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Cystic fibrosis (CF)Autosomal recessive disorder caused by defect in chloride-pumping channel in exocrine glands; ducts of exocrine glands (e.g., lungs, pancreas, reproductive glands) become clogged with thick secretionsPresents in childhood and universally fatal, but proper treatment may allow survival into late 20s or early 30sAffects both pulmonary (recurrent infections, chronic sinusitis) and gastrointestinal systems (pancreatic enzyme deficiencies, malabsorption)Risk factors = whites at higher risk than other races
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Treatment = deoxyribonuclease (DNase) aids in decreasing the viscosity of secretions; chest physical therapy helps to clear secretions; bronchodilators, non-steroidal anti-inflammatory drugs (NSAID), antibiotics for any suspected pulmonary exacerbation or infection; supplemental pancreatic enzymes and vitamins A, D, E, and K given for malabsorption
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Tidal volume (TV)
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Inspiratory volume during Normal respiratioN
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Inspiratory reserve volume (IRV)
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Air volume beyond normal tidal volume that is filled during maximal inspiration |
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Inspiratory capacity (IC)
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Total inspiratory air volumE considering both tidal volume and inspiratory reserve volume (IC = TV + IRV)
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Expiratory reserve volume (ERV)
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Air volume beyond tidal volume that can be expired during normal respiration
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Residual volume (RV)
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Remaining air volume left in lung ollowing maximal expiration
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Functional reserve capacity (FRC)
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Air volume remaining in lungs after expiration of tidal volume (FRC = RV + ERV)
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Functional vital capacity (FVC) |
Maximal air volume that can be inspired and expired (FVC = IC + ERV)
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Total lung capacity (TLC)
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Total air volume of lungs (TLC = FVC + RV)
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