How does propranolol (Inderal), a beta blocker medication, control hypertension?

Choice A reason: Hereditary decrease in IgE responsiveness is not related to airway hyper-responsiveness in extrinsic asthma. IgE is an antibody that binds to allergens and triggers the release of histamine and other inflammatory mediators from mast cells. A decrease in IgE responsiveness would reduce the allergic reaction, not increase it.

Choice B reason: Increased sympathetic nervous system response is not related to airway hyper-responsiveness in extrinsic asthma. The sympathetic nervous system is the part of the autonomic nervous system that prepares the body for fight or flight. It stimulates the bronchodilation, or the widening of the airways, by activating the beta2 receptors on the smooth muscle cells. This would improve the airflow, not obstruct it.

Choice C reason: The release of stress hormones is not related to airway hyper-responsiveness in extrinsic asthma. Stress hormones, such as cortisol and adrenaline, are secreted by the adrenal glands in response to stress. They have anti-inflammatory and bronchodilator effects, which would reduce the symptoms of asthma, not worsen them.

Choice D reason: Exposure to an allergen causing mast cell degranulation is related to airway hyper-responsiveness in extrinsic asthma. Mast cell degranulation is the process of releasing histamine and other inflammatory mediators from the granules inside the mast cells. These substances cause bronchoconstriction, or the narrowing of the airways, by stimulating the smooth muscle contraction and mucus secretion. This leads to the symptoms of asthma, such as wheezing, coughing, and dyspnea.

Choice A reason: The cells of the myocardium become hypertrophic in response to increased workload or pressure, not as a result of myocardial infarction. Hypertrophy is an adaptive mechanism that can lead to impaired ventricular function over time.

Choice B reason: The resulting hypoxia leads to ischemic injury and myocardial cell death. This is the main cause of impaired ventricular function after a myocardial infarction. The loss of viable myocardial tissue reduces the contractility and pumping ability of the heart.

Choice C reason: There is a temporary alteration in electrolyte balance that can be corrected. This is not the primary cause of impaired ventricular function after a myocardial infarction. Electrolyte imbalance can occur due to fluid loss, renal impairment, or medication side effects, but it can be managed with appropriate interventions.

Choice D reason: There is too much pressure on the heart and the ventricles begin to dysfunction. This is not the direct cause of impaired ventricular function after a myocardial infarction. Increased pressure on the heart can result from hypertension, valvular disease, or pulmonary embolism, but it is not related to myocardial ischemia or necrosis.