Sunday, January 10, 2010

Shortness Of Breath Case 4

Shortness Of Breath Case 4


A 55-year-old man presents to the emergency department complaining of the acute onset of severe shortness of breath.
His only associated symptom is a dry cough productive of scant frothy sputum. He has a 70 pack-year smoking history and has had two similar episodes in the past two years. On examination, he is afebrile, tachypneic, and distressed, but without cyanosis. He is thin, and his accessory muscles contract with each breath. He exhales through pursed lips. His chest examination reveals diminished breath sounds with hyperresonance to percussion.


Q1
Which of the following is the most likely diagnosis?

/ A. Chronic bronchitis
/ B. Cystic fibrosis
/ C. Emphysema
/ D. Myocardial infarction
/ E. Pneumonia


Q2
In this disorder, the mechanism for decreased FEV1 (forced expiratory volume in 1 second) is which of the following?

/ A. Airway collapse due to loss of elastic recoil
/ B. Airway constriction due to bronchospasm
/ C. Biockage of airways by increased mucus production
/ D. Decreased lung compliance due to pulmonary fibrosis
/ E. Lung collapse due to air in the pleural space


Q3
Which of the following drugs might prove helpful in treating this patient?

/ A. Acetazolamide
/ B. Aibuterol
/ C. Metoprolol
/ D. Metronidazole
/ E. Propranolol


Q4
Which of the following sets of changes depict the mean arterial pressure (MAP), Ieft ventricular peak systolic pressure (LVPSP), pulmonary wedge pressure (PWP), and left atrial pressure (LAP) in this patient, compared to a healthy individuaI?



Q5
An inherited form of this disease can result from which of the following?
/ A. A deficiency of alveolar dipalmitoyl phosphatidylcholine
/ B. A deficiency of serum alpha-1-antitrypsin
/ C. A deficiency of serum angiotensin converting enzyme.
/ D. An elevated alveolar dipalmitoyl phosphatidylcholine
/ E. An elevated serum alpha-1-antitrypsin
/ F. An elevated serum angiotensin converting enzyme


Q6
Which of the following nerves provides innervation to the diaphragm?

/ A. Accessory nerve
/ B. Intercostal nerve
/ C. Phrenic nerve
/ D. Splanchnic nerve
/ E. Vagus nerve
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Shortness Of Breath Case 4 Answers

A1
The correct answer is C. Patients with COPD may be clinically classified as "pink puffers" or "blue bloaters" based on several characteristics. This patient is exhibiting the classic presentation for an emphysematous "pink puffer"; the patient has dyspnea but is not cyanotic. "Pink puffers" maintain their oxygenation until they decompensate precipitously. In contrast, the "blue bloater" counterparts with chronic bronchitis (choice A) have a chronic productive cough with cyanosis.
Cystic fibrosis (choice B) is an inherited disease involving a defective chloride channel, and tends to affect patients at a younger age. The defective chloride channel leads to viscous mucus that is difficult to clear. As a result, patients develop chronic lung infections and fibrotic lung disease.
Myocardial infarction (choice D) classically presents as crushing substernal chest pain, shortness of breath, and diaphoresis. Pain may radiate to the jaw and be accompanied by nausea. If congestive heart failure is present, patients may have dry cough, scant sputum, and rales on exam.
Pulmonary infections may precipitate COPD exacerbations, but this patient's presentation is not consistent with pneumonia (choice E) . Pneumonia presents as dyspnea, fever, and productive cough.


A2
The correct answer is A. Patients with emphysema, a form of chronic obstructive lung disease, suffer from a loss of elastic recoil in the lung. As a patient exhales, the airways collapse, trapping air distal to the bronchiole. As a result of airway collapse, patients with emphysema have increased resistance to outflow, and a decreased FEV1.
Asthma, another form of COPD, results from the obstruction of small airways due to bronchoconstriction (choice B).
Blockage of airways due to mucus production (choice C) characterizes chronic bronchitis. While this obstruction produces COPD, it is not consistent with emphysema.
Pulmonary fibrosis (choice D) would increase bronchiolar elasticity and therefore would increase FEV1.
Lung collapse due to air in the pleural space (choice E) describes pneumothorax. This does not explain the decrease in FEV1 in emphysema.


A3
The correct answer is B. Albuterol is a beta-adrenergic agonist and, as such, promotes bronchial smooth muscle relaxation, and thus bronchodilation. Bronchodilation may relieve symptoms in COPD patients with acute exacerbation. Methylxanthines and/or anti-cholinergics may provide an adjunct to beta agonists.
Acetazolamide (choice A) is a carbonic anhydrase inhibitor used as a diuretic. There is nothing in this patient to suggest that he is volume overloaded, and diuretics would thus be inappropriate.
Propanolol and metoprolol (choices C and E) are beta blockers and may actually exacerbate this patient's symptoms through bronchoconstriction.
Metronidazole (choice D) is an antimicrobial agent. While antibiotics are often used to treat infections that may exacerbate COPD, metronidazole is not an appropriate agent to treat the pathogens that typically infect people with COPD: Haemophilus influenzae, Strep. pneumoniae, and Moraxella catarrhalis.


A4
The correct answer is A. The elastic recoil of the lungs is decreased in emphysema. This causes the chest wall to expand sufficiently to create a new balance between the elastic recoil of the lungs and chest wall, which increases the functional residual capacity. Because the lungs are expanded to higher than normal levels, both the total lung capacity and residual volume are chronically increased. The vital capacity of the lungs (which is the difference in volume between the total lung capacity and residual volume) is decreased in emphysema because the patient cannot expel normal amounts of air from the lungs.


A5
The correct answer is B. Alpha 1-antitrypsin deficiency is associated with familial emphysema. Patients may have decreased (heterozygote) or absent (homozygote) amounts of the protease inhibitor alpha 1-antitrypsin. The precise mechanism in producing emphysema is unclear, but patients with this deficiency typically have severe disease, often with an early age of onset. Choice E therefore cannot be correct.
Dipalmitoyl phosphatidylcholine (choices A and D) is a component of alveolar surfactant, which reduces alveolar surface tension. Not only does this surfactant reduce the surface tension, it changes surface tension with changing diameter. This prevents atelectasis by allowing interconnected alveoli with different diameters to remain open at the same alveolar pressures. (Without surfactant, the Law of LaPlace dictates that it takes greater alveolar pressures to open a smaller alveolus.)
Elevated or decreased angiotensin converting enzyme (ACE; choices C and F) would not produce emphysema. ACE converts angiotensin I to angiotensin II, which has many effects on vascular and renal physiology, but is not associated with emphysema.


A6
The correct answer is C. The phrenic nerve originates from cervical roots 3, 4, and 5 to provide innervation to the diaphragm. This is significant because spinal cord injury above this level renders the patient unable to breathe.
The accessory nerve (choice A), provides motor innervation to the trapezius and the sternocleidomastoid muscles.
The intercostal nerves (choice B) innervate the intercostal muscles responsible for chest wall expansion and retraction.
The splanchnic nerve (choice D) provides motor and autonomic fibers to the gut.
The vagus nerve (choice E) provides motor innervation to the vocal cords, heart, bronchus and GI tract. In addition it provides sensory innervation to the bronchus, heart, GI tract and larynx.

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