Which clinical manifestations would you assess for in a painter with pulmonary hypertension?
(Select All that Apply.)

Jugular vein distention

Peripheral edema

Ronchi bilaterally

Dyspnea on exertion

Systemic blood pressure greater than 130/90 mm HG

Answer and Explanation

Correct Answer : A,B,D

A. Jugular vein distention: Pulmonary hypertension increases right ventricular afterload, leading to right heart failure. As the right ventricle struggles to pump against elevated pulmonary pressures, blood backs up into the systemic circulation, causing jugular vein distention (JVD).

B. Peripheral edema: Right-sided heart failure due to pulmonary hypertension leads to venous congestion and fluid retention, resulting in peripheral edema. Swelling is commonly observed in the lower extremities due to increased venous hydrostatic pressure.

C. Ronchi bilaterally: Rhonchi are low-pitched breath sounds typically associated with airway obstruction due to secretions, commonly seen in conditions like chronic bronchitis or pneumonia. Pulmonary hypertension primarily affects the pulmonary vasculature rather than the airways, making rhonchi an unlikely manifestation.

D. Dyspnea on exertion: Pulmonary hypertension increases pressure in the pulmonary arteries, reducing oxygen exchange and causing exertional dyspnea. This symptom is often one of the earliest clinical manifestations as increased pulmonary vascular resistance impairs oxygen delivery.

E. Systemic blood pressure greater than 130/90 mm Hg: Pulmonary hypertension specifically affects the pulmonary circulation, not systemic arterial pressure. While pulmonary hypertension can eventually contribute to left heart dysfunction, it does not directly cause systemic hypertension.

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Correct Answer is D

Explanation

A. Vernelli's triad; Venous stasis; Hypercoagulable states; Venous intimal damage: Vernelli's triad is not a recognized term in thrombus formation. Venous stasis, hypercoagulable states, and venous intimal damage are relevant factors, but the correct terminology is Virchow's triad.

B. Vernelli's triad: Hyperlipidemia; hypercoagulable states, venous stasis: This option inaccurately references Vernelli's triad and includes hyperlipidemia, which is not one of the classic factors associated with thrombus formation. The correct factors should be named according to Virchow's triad.

C. Virchow's triad; Hyperlipidemia, Hypercoagulable states, positive D-dimer: Although Virchow's triad is correctly identified, hyperlipidemia and positive D-dimer are not part of the classic factors involved in thrombus formation. The classic factors are venous stasis, hypercoagulable states, and venous intimal damage.

D. Virchow triad; Venous stasis; Venous intimal damage; Hypercoagulable states: This option accurately identifies Virchow's triad and lists the three key factors involved in thrombus formation: venous stasis, venous intimal damage, and hypercoagulable states.

A. Norepinephrine causes bronchial smooth muscle contraction and mucus secretion but it also causes high blood pressure B. Uncontrolled inflammation leads to increased bronchial hyperresponsiveness and eventual scarring C. Immunoglobulin G causes smooth muscle contraction which will eventually weaken the respiratory muscles D. The release of epinephrine leads to development of cardiac dysrhythmias.

Correct Answer is B

Explanation

A. Norepinephrine causes bronchial smooth muscle contraction and mucus secretion but it also causes high blood pressure: This statement is misleading in the context of asthma. Norepinephrine primarily acts on alpha and beta receptors, influencing blood pressure and bronchodilation but is not the main mediator in asthma pathophysiology. The focus should be on inflammation and airway responsiveness.

B. Uncontrolled inflammation leads to increased bronchial hyperresponsiveness and eventual scarring: This statement accurately describes the pathophysiologic process in asthma. Persistent inflammation in asthma can cause increased bronchial hyperresponsiveness, leading to airway narrowing and potential long-term remodeling and scarring of the airways if not controlled. Effective management is essential to prevent these adverse outcomes.

C. Immunoglobulin G causes smooth muscle contraction which will eventually weaken the respiratory muscles: Immunoglobulin E (IgE) is primarily involved in allergic reactions and asthma, and it does not directly cause smooth muscle contraction that weakens respiratory muscles.

D. The release of epinephrine leads to development of cardiac dysrhythmias: While epinephrine can have cardiovascular effects, including increased heart rate and potential for dysrhythmias, this is not directly relevant to the pathophysiology of asthma. The focus in asthma management is on controlling airway inflammation and bronchoconstriction rather than on cardiac issues.

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Which clinical manifestations would you assess for in a painter with pulmonary hypertension? (Select All that Apply.)

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Naxlex Comprehensive Predictor Exams

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Correct Answer is D

Explanation

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Correct Answer is B

Explanation

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Which clinical manifestations would you assess for in a painter with pulmonary hypertension?
(Select All that Apply.)