NU570 Adv Physiology Pathophysiiology. Thomas Jeferson University
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Free NU570 Adv Physiology Pathophysiiology. Thomas Jeferson University Questions
A 67-year-old man presents with worsening cough, sputum production, and shortness of breath. He has been a cigarette smoker for the past 50 years, smoking approximately 1 pack a day. He has a chronic AM cough productive of some yellow sputum but generally feels okay during the day. He was in his usual state of health until two weeks ago when he developed a cold. Since then, he has had a hacking cough and increased thick sputum production. He also has had difficulty walking more than a block without stopping due to shortness of breath. Physical examination reveals prolonged expiration, audible wheezing, and diffuse rhonchi throughout both lung fields. Chest x-ray shows hyperinflation of both lungs with a flattened diaphragm. His most likely diagnosis is:
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Emphysema
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Chronic Bronchitis
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Small Cell Lung CA
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Pulmonary Fibrosis
Explanation
Correct Answer: B) Chronic Bronchitis
This patient's presentation is classic for chronic bronchitis — defined as a productive cough for at least 3 months per year for 2 consecutive years. Key features include a chronic morning productive cough, yellow sputum, rhonchi, and wheezing. While hyperinflation can appear in both emphysema and chronic bronchitis, the dominant feature of productive cough and rhonchi points to chronic bronchitis. Emphysema typically presents with a "pink puffer" profile — barrel chest, minimal sputum, and predominantly diminished breath sounds.
A young adult male takes advantage of the free clinic to discuss recurring symptoms. He sometimes hears a sound upon exhalation and experiences chest tightness and shortness of breath. Symptoms worsen seasonally. Spirometry is taken before and after inhalation of a β-adrenergic receptor agonist. Which of the following would be consistent with the diagnosis of asthma?
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Initial tests: normal FEV1, normal FVC, normal FEV1/FVC; after treatment: increased FEV1, increased FVC, normal FEV1/FVC.
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Initial tests: normal FEV1, normal FVC, normal FEV1/FVC; after treatment: no change.
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Initial tests: low FEV1, low FVC, low FEV1/FVC; after treatment: improved FEV1, slightly improved FVC, near normal FEV1/FVC.
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Initial tests: normal FEV1, normal FVC, normal FEV1/FVC; after treatment: no change.
Explanation
Correct Answer: C) Initial tests: low FEV1, low FVC, low FEV1/FVC; after treatment: improved FEV1, slightly improved FVC, near normal FEV1/FVC.
Asthma is characterized by reversible obstructive airway disease. During symptomatic periods, spirometry shows reduced FEV1 and a reduced FEV1/FVC ratio reflecting airflow obstruction. After administration of a bronchodilator (β-agonist), significant improvement in FEV1 confirms the reversibility of obstruction, which is the defining feature distinguishing asthma from irreversible COPD. The seasonal worsening and expiratory wheeze further support an asthma diagnosis.
A 60-year-old man complained of leg cramps that are so severe that he must often stop walking. What is the underlying pathologic basis for "intermittent claudication" in this patient?
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Atherosclerosis
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Congestive heart failure
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Embolization of a mural thrombus
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Systemic hypertension
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Valvular heart disease
Explanation
Correct Answer: A) Atherosclerosis
Intermittent claudication is reproducible leg pain or cramping brought on by exercise and relieved by rest. It is caused by atherosclerotic narrowing of peripheral arteries (peripheral artery disease), most commonly the femoral and popliteal arteries. During exercise, increased oxygen demand cannot be met due to reduced blood flow through the stenotic vessels, causing ischemic muscle pain. At rest, demand decreases and pain resolves — the defining feature of claudication.
A 70-year-old male is admitted after a massive anterior myocardial infarction and initially stabilizes with medical management. Several days later, he suddenly develops ventricular tachycardia followed by cardiac arrest. Histologic remodeling of the infarcted myocardium reveals fibroblast infiltration with deposition of type I collagen, replacing large numbers of necrotic cardiac myocytes. Which of the following best explains the principal cause of death in patients following a massive myocardial infarction?
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Progressive systolic heart failure from reduced ejection fraction
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Acute papillary muscle rupture leading to severe mitral regurgitation
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Life-threatening ventricular arrhythmias due to disruption of normal electrical conduction by collagen scar tissue
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Recurrent coronary artery thrombosis from endothelial injury
Explanation
Correct Answer: C) Life-threatening ventricular arrhythmias due to disruption of normal electrical conduction by collagen scar tissue.
The most common cause of death following MI is ventricular arrhythmia. As necrotic myocytes are replaced by non-conducting collagen scar tissue, the normal electrical conduction pathways are disrupted, creating re-entry circuits that trigger fatal arrhythmias such as ventricular tachycardia and fibrillation. This explains the patient's sudden cardiac arrest days after initial stabilization.
A 22-year-old construction worker falls 30 feet and fractures several bones, including his left femoral shaft. Six hours later, the patient develops shortness of breath and cyanosis. Which of the following hemodynamic disorders best explains the pathogenesis of respiratory distress in this patient?
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Acute myocardial infarction
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Congestive heart failure
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Deep venous thrombosis
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Fat embolism
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Sepsis
Explanation
Correct Answer: D) Fat embolism.
This patient presents with a classic scenario for fat embolism syndrome. Following fracture of a long bone such as the femoral shaft, fat globules and bone marrow contents are released into the venous circulation from the fractured medullary cavity. These fat droplets travel to the pulmonary vasculature, obstructing small vessels and triggering an inflammatory cascade that damages the alveolar-capillary membrane, leading to acute respiratory distress.
The hallmark triad of fat embolism syndrome includes respiratory distress (dyspnea, hypoxia, cyanosis), neurological changes (confusion, altered mental status), and a petechial rash (particularly on the chest, axilla, and conjunctiva). The onset characteristically occurs 24–72 hours after the injury, as seen here with the 6-hour development. Deep venous thrombosis is possible but takes longer to develop and travel to the lungs.
Acute MI and CHF are not consistent with this traumatic mechanism. Sepsis could develop but would present over a longer timeframe with systemic infection signs, not this rapid respiratory deterioration specifically linked to a femoral fracture.
A 59-year-old man with a history of poor dentition presents with fever, new-onset heart murmur, and positive blood cultures for Streptococcus species. The provider suspects infective endocarditis involving a native heart valve. Which pathophysiologic characteristic of cardiac valves most explains why bacteria are able to adhere and proliferate in this location?
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Valves are mostly acellular with limited blood supply, reducing the local inflammatory response and allowing bacterial growth
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Valves are highly vascularized, promoting rapid bacterial dissemination
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Valves contain abundant immune cells that trigger excessive inflammation
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Valves experience turbulent flow that mechanically damages leukocytes
Explanation
Correct Answer: A) Valves are mostly acellular with limited blood supply, reducing the local inflammatory response and allowing bacterial growth.
Cardiac valves are avascular structures that receive nutrients by diffusion, meaning they have a poor local immune response. When bacteremia occurs (here from poor dentition), bacteria can adhere to the valve surface — especially where endothelium has been disrupted — and proliferate without effective immune clearance, forming vegetations characteristic of infective endocarditis.
A 72-year-old woman complains of shortness of breath on exertion. She becomes short of breath at night unless she uses three pillows to prop herself up (orthopnea). Physical examination reveals mild obesity, bilateral pitting leg edema, enlarged liver, and fine crackling sounds on inspiration (rales). A chest x-ray shows cardiomegaly. What is the most likely cause of orthopnea in this patient?
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Cardiac tamponade
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Cor pulmonale
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Hypovolemic shock
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Portal hypertension
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Pulmonary edema
Explanation
Correct Answer: E) Pulmonary edema.
This patient has classic signs of congestive heart failure — cardiomegaly, bilateral pitting edema, hepatomegaly, and pulmonary rales. Orthopnea (needing multiple pillows to breathe at night) occurs because lying flat causes redistribution of fluid from the legs and periphery into the pulmonary circulation, worsening pulmonary edema and making breathing difficult. Sitting upright uses gravity to reduce venous return and pulmonary congestion, relieving symptoms. Pulmonary edema from left-sided heart failure is the direct cause of orthopnea in this patient.
A 30-year-old man was told that he had a heart murmur. Which of the following typically produces heart murmurs?
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Dilated cardiomyopathy
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Hypertensive heart disease
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Ischemic heart disease
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Restrictive cardiomyopathy
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Valvular heart disease
Explanation
Correct Answer: E) Valvular heart disease
Valvular heart disease is the classic cause of heart murmurs. When heart valves are stenotic (narrowed) or regurgitant (leaky), turbulent blood flow across the abnormal valve creates the characteristic sound heard as a murmur. Conditions like mitral stenosis, aortic stenosis, and mitral regurgitation all produce distinct murmurs. The other options — dilated, hypertensive, ischemic, and restrictive cardiomyopathies — primarily affect myocardial structure and function without directly creating the turbulent flow responsible for murmurs.
A 67-year-old smoker with long-standing bronchitis expectorates blood during a paroxysm of coughing. What is a possible serious cause of hemoptysis in this patient that should be considered?
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Emphysema
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Hemothorax
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Lung cancer
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Pneumoconiosis
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Pulmonary abscess
Explanation
Correct Answer: C) Lung cancer.
In a long-term smoker with chronic bronchitis who develops hemoptysis, lung cancer must always be seriously considered and ruled out. Cigarette smoking is the single greatest risk factor for lung cancer, particularly squamous cell carcinoma and small cell carcinoma. Hemoptysis in this context can result from tumor erosion into bronchial blood vessels. While chronic bronchitis itself can occasionally cause blood-streaked sputum, new-onset hemoptysis in a chronic smoker warrants immediate investigation with imaging and bronchoscopy.
A 69-year-old man is brought to the Emergency Department because of the sudden onset of left-sided chest pain that is exacerbated upon inspiration. Physical examination reveals dyspnea and hemoptysis. His temperature is 38°C (101°F), pulse is 110/min, respirations are 35/min, and blood pressure is 158/100 mm Hg. A lateral chest wall friction rub is present on auscultation. The left leg is markedly edematous. A chest x-ray reveals a left pleural effusion. What is the most likely cause of this patient's left-sided chest pain, pleural effusion, dyspnea, and hemoptysis?
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Congestive heart failure
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Cor pulmonale
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Diffuse alveolar damage
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Pulmonary thromboembolism
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Subacute bacterial endocarditis
Explanation
Correct Answer: D) Pulmonary thromboembolism.
This presentation is classic for pulmonary thromboembolism (PE). The key findings are pleuritic chest pain (worsened by inspiration), hemoptysis, tachycardia, tachypnea, pleural friction rub, pleural effusion, and unilateral leg edema indicating deep vein thrombosis (DVT) as the source of the embolus. The clot travels from the leg veins to the pulmonary circulation, causing pulmonary infarction. Congestive heart failure would present with bilateral edema and would not cause a friction rub. The unilateral leg swelling is the critical clue pointing to DVT-related PE.
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