The forward effects in a patient with left ventricular heart failure include (Select all that apply)

Choice A reason: This is the correct statement. Non-selective beta-adrenergic blockers can interfere with the signs and symptoms of hypoglycemia (low blood sugar), such as tachycardia, tremors, and sweating. They can also impair the glucose metabolism and insulin secretion in the body. Therefore, patients with diabetes who take non-selective beta-adrenergic blockers need to monitor their blood glucose levels closely and adjust their insulin or oral hypoglycemic agents accordingly.

Choice B reason: This is not a correct statement. Non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, do not interact with non-selective beta-adrenergic blockers. However, they can reduce the effectiveness of other antihypertensive medications, such as diuretics or ACE inhibitors, by causing fluid retention and decreasing renal blood flow.

Choice C reason: This is not a correct statement. Non-selective beta-adrenergic blockers have a rapid onset of action and can lower the blood pressure within hours of administration. Therefore, patients do not need to wait for a few weeks to see if their dosage is effective. However, they may need periodic follow-up visits to monitor their blood pressure, heart rate, and other vital signs.

Choice D reason: This is not a correct statement. Dizziness is a common side effect of non-selective beta-adrenergic blockers, especially when the patient changes position or stands up quickly. This is due to the orthostatic hypotension (a drop in blood pressure when standing up) caused by the vasodilation effect of the medication. However, this does not mean that the patient should stop taking the medication, as this can cause rebound hypertension and other complications. Instead, the patient should rise slowly from a sitting or lying position, drink plenty of fluids, and report any severe or persistent dizziness to their health care provider.

Choice A reason: Hyperplasia and deformation of bronchial cartilage are not the causes of airway obstruction in COPD type B. Bronchial cartilage is the rigid structure that supports the bronchi, the large airways that branch from the trachea. Hyperplasia is an increase in the number of cells, and deformation is a change in the shape or structure of the cells. These processes can affect the bronchial cartilage, but they do not directly obstruct the airway.

Choice B reason: Loss of alveolar elastin is not the cause of airway obstruction in COPD type B. Alveolar elastin is the elastic fiber that allows the alveoli, the tiny air sacs at the end of the bronchioles, to expand and recoil during breathing. Loss of alveolar elastin is a characteristic of COPD type A (emphysema), which causes the alveoli to lose their shape and collapse. This reduces the surface area for gas exchange, but it does not obstruct the airway.

Choice C reason: Pulmonary edema is not the cause of airway obstruction in COPD type B. Pulmonary edema is the accumulation of fluid in the lungs, usually due to heart failure or lung injury. It causes shortness of breath, coughing, and crackles in the lungs. It can impair gas exchange and oxygenation, but it does not obstruct the airway.

Choice D reason: Thick mucus, fibrosis, and smooth muscle hypertrophy are the causes of airway obstruction in COPD type B. Thick mucus is the result of chronic inflammation and infection of the bronchi, which stimulates the mucus glands to produce more and thicker mucus. Fibrosis is the formation of scar tissue in the bronchial walls, which narrows the airway and reduces its elasticity. Smooth muscle hypertrophy is the enlargement of the smooth muscle cells that surround the bronchi, which increases the airway resistance and causes bronchospasm. These processes combine to obstruct the airway and cause chronic cough, wheezing, and dyspnea.