MU NURS 611 Adv Patho - Exam 4 Review - Pulmonary System Questions and Complete Solutions, Exams of Pathology

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MU NURS 611: Adv Patho - Exam 4 Review - Pulmonary System Questions and Complete Solutions Graded A+ Denning [Date] [Course title]

eupnea - Answer: normal breathing; RR 8-16 breaths/min tidal volume - Answer: 400-800 ml sigh breaths - Answer: helps maintain normal lung function; usually 1.5 to 2 times normal tidal volume; occurs approximately 10-12x/hr Kussmaul respirations - Answer: slightly increased ventilatory rate, large tidal volume, no expiratory pause Cheyne-Stokes - Answer: characterized by alterhating periods of deep and shallow breathing; apnea lasting 15-60 seconds followed by respirations that increase in volume until peak is reached, then ventilation decreases agin to apnea; results from any condition that slows blood flow to brainstem -> slows impulses sending info to respiraotry centers in brainstem hypoventilation - Answer: inadequate alveolar ventilation in relation to metabolic demands; caused by alterationsin pulmonary mechanics or in neurologic control of breathing such that minute volume (tidalxRR) is reduced; CO@ removal does not keep up with CO2 production, PaCO2 >44mmHg, causing hypercapnia; respiratory acidosis hyperventilation - Answer: response to hypoxemia, anxiety, pain; lungs remove CO2 at faster rate than it is produced by cellular metabolism = PaCO2 <36mmHg (hypocapnia); respiratory alkalosis TB - Answer: transmission through airborne droplets; diagnosed by positive TST/PPD, sputum culture, immunoassays, and chest XR; +test = yearly XR; individuals who have received BCG will have positive TB results; nodules, calcifications, cavities, and hilar enlargement are common in upper lobes TB cultures - Answer: can take up to 6 weeks to become positive when active pulmonary disease is present normal aging changes - Answer: loss of elastic recoil stiffening of chest wall changes in gas exchange

pneumoconiosis - Answer: any hcnages in lungs caused by inhalation of inroganic dust particles; silicosis, asbestos, and coal (black lung); not reversible; treatment is palliative, focuses on preventing further exposure non-small cell lung cancer (NSCLC) - Answer: tumors located centrally near hila, projects into bronchi; nonproductive cough, hemoptysis; chest pain = late symptom with larger tumors; well-localized, tends not to metastasize until late in the course of treatment small cell lung carcinomas (SCLC) - Answer: most common type of neuroendocrine lung tumors; bronchogenic carcinomas; arise from central part of lung; strong correlation wtih tobacco smoking; tumor shows rapid rate of growth, tends to metastasize early and widely; worst prognosis; SCLC staging - Answer: limited disease (stages I to III - 20-30%) extensive disease (stage IV - 70-80%) pneumonia - Answer: aspiration of oropharyngeal secretions - most common route of infection; nasopharynx and oropharynx constitute first line of defense for most infectious agents; inhalation of microorganisms released in the air - another common route of infection clinical manifestations of pneumonia - Answer: preceded by URTI; onset of cough, dyspnea, and fever; cough is productive, but may be nonproductive; chills, malaise, pleuritic chest pain; pulmonary consolidation (inspiratory crackles, increased tactile fremitus, egophony, and whispered pectoriloquy) pulmonary emboli - Answer: example of alveolar dead space causing hypoxemia d/t absent blood flow to a lung segment; causes ventilation-perfusion mismatch (decreased production of surfactant); widespread vasocnstriction impeding blood flow; end result DVT or blood clots elsewhere PE prophylactic treament - Answer: low-molecular-weight heparin or pneumatic devices diagnosis of PE - Answer: CXR, ABG, ECG obtained immediately CXR findings are nonspecific; can be normal for first 24 hrs until atelectasis occurs in lung further evaluation conducted using spiral CT arteriography

serum D dimer - Answer: measures product of thrombus degradation by the fibrinolytic system and, if normal, makes the presence of PE highly unlikely ARDS - Answer: aka acute lung injury (ALI) represents spectrum of acute lung inflammation and diffuse alveolocapillary injury; disorders that end with this cause acute injury to alveolocapillary membrane - produces massive pulmonary inflammation, increased capillary permeability, severe pulmonary edema - result of bronchioles filling with fluid, shunting, mismatch, and hypoxemia alveolocapillary injury - Answer: directly - aspiration of highly acidic gastric contents or inhalation of toxic gases indirectly - circulating inflammatory mediators released in response to systemic disorders, such as sepsis or trauma clinical manifestations of ARDS - Answer: dyspnea, hypoxemia with poor response to O2 supplement -> hyperventilation, respiratory alkalosis -->dec renal perfusion, metabolic acidosis, organ dysfx --->increased WOB, dec tidal volume, hypoventilation ---->hypercapnia, respiratory acidosis, worse hypoxemia -----> dec CO, hypotension, death