Asthma Nursing Care Quiz: Practice Questions and Key Facts

Viral respiratory infections commonly trigger asthma by increasing airway inflammation and bronchial hyperresponsiveness. Infection stimulates immune mediators such as histamine and leukotrienes, causing airway narrowing and mucus production. This reduces airflow and increases resistance. Conditions like hyperthyroidism or iron deficiency do not directly cause bronchospasm. Viral upper respiratory infections remain one of the most frequently documented precipitating factors in acute asthma exacerbations across clinical studies.

Shortness of breath with wheezing is characteristic of asthma due to reversible bronchoconstriction and airway inflammation. Smooth muscle constriction narrows bronchioles, producing turbulent airflow and the classic high pitched wheeze. Gas exchange may be impaired, causing dyspnea. Muscle weakness, jaundice, and hematuria are unrelated to airway obstruction. Clinical evaluation consistently identifies wheezing as a primary diagnostic indicator in acute asthma presentations.

Pulsus paradoxus in asthma reflects a drop in systolic blood pressure exceeding 10 mmHg during inspiration. Severe bronchoconstriction increases negative intrathoracic pressure, reducing left ventricular filling. This temporarily lowers stroke volume and systolic pressure. The exaggerated inspiratory decline signals significant airway obstruction. It is a marker of severe asthma and impending respiratory compromise requiring urgent intervention.

A peak flow reading below 40 percent of predicted value indicates severe airway obstruction. Peak expiratory flow measures maximum airflow during forced exhalation. Values under 40 percent suggest critical bronchospasm and high risk of respiratory failure. Immediate medical treatment is required. Mild obstruction typically ranges above 60 percent, while normal values exceed 80 percent of predicted baseline measurements.

Oxygen saturation below 90 percent signals hypoxemia and inadequate gas exchange. During nebulizer therapy, a significant drop in oxygen levels suggests worsening ventilation or severe bronchospasm. Continuing treatment without reassessment may delay emergency care. Medication depletion alone does not indicate instability. Clinical protocols prioritize oxygen monitoring because sustained saturation under 90 percent increases risk of tissue hypoxia and organ dysfunction.

Short acting beta agonists stimulate beta two adrenergic receptors in bronchial smooth muscle, leading to bronchodilation. Activation increases cyclic AMP, relaxing smooth muscle fibers and widening airways. This rapidly improves airflow during asthma attacks. They do not cause bronchoconstriction or fluid retention. Increased heart rate may occur as a side effect due to mild beta one receptor stimulation.

Ipratropium is an anticholinergic that blocks muscarinic receptors in airway smooth muscle. This inhibits parasympathetic mediated bronchoconstriction and reduces mucus secretion. By limiting acetylcholine activity, it promotes bronchodilation. Albuterol is a beta agonist, prednisone is a corticosteroid, and montelukast is a leukotriene modifier. Ipratropium is commonly used in combination therapy for moderate to severe asthma exacerbations.

CT pulmonary angiography directly visualizes pulmonary arteries and detects intraluminal thrombi. It provides high sensitivity and specificity for pulmonary embolism diagnosis. Contrast dye highlights vascular obstruction, confirming clot location and extent. Chest X ray and D dimer are supportive tests but not definitive. CT imaging is considered the gold standard in stable patients with suspected embolism.

D dimer is a fibrin degradation product released when clots dissolve. Elevated levels indicate active clot formation and breakdown, commonly seen in pulmonary embolism. While not specific, a normal D dimer helps exclude PE in low risk patients. Asthma and bronchitis do not typically elevate D dimer. Elevated levels prompt further imaging such as CT angiography.

The Wells score estimates the clinical probability of pulmonary embolism using criteria such as heart rate, recent surgery, and signs of deep vein thrombosis. Points are assigned to risk factors, and higher totals correlate with greater PE likelihood. It guides decisions regarding imaging and D dimer testing. It does not assess asthma severity or pneumonia risk.

Pneumonia involves inflammation of alveoli with accumulation of exudate, impairing oxygen exchange. Infectious organisms trigger immune response, leading to fluid, pus, and cellular debris filling alveolar spaces. This reduces ventilation efficiency and causes hypoxia. Bronchitis affects bronchi without alveolar filling. Emphysema destroys alveolar walls but does not produce exudative consolidation like pneumonia.

Bacterial pneumonia often presents with productive cough, fever, elevated white blood cell count, and localized lung consolidation. Infection triggers inflammatory response, increasing capillary permeability and exudate formation. Fever results from cytokine release. Clear lung fields are inconsistent with pneumonia. Increased respiratory rate commonly accompanies hypoxia. Clinical findings support infectious alveolar involvement.

Acute bronchitis is most commonly caused by viral infections such as influenza or respiratory syncytial virus. Viral pathogens inflame bronchial mucosa, increasing mucus production and cough. Antibiotics are usually unnecessary because bacteria are rarely responsible. Autoimmune and fungal causes are uncommon. Most cases resolve within two to three weeks with supportive care.

Wheezing is a high pitched musical sound caused by airflow through narrowed small airways. Bronchoconstriction and inflammation create turbulent airflow vibrations. It is commonly heard during expiration in asthma. Crackles represent fluid in alveoli, and stridor indicates upper airway obstruction. Wheezing strongly suggests lower airway narrowing and bronchospasm.

A pleural friction rub occurs when inflamed visceral and parietal pleurae rub against each other during respiration. The sound is grating and localized. Inflammation reduces lubricating fluid between pleural layers, increasing friction. It is distinct from wheezing or crackles, which originate within airways or alveoli. Pleural rub often accompanies pleuritis or pneumonia involving pleural surfaces.