The most critical safety information a patient must know when initiating beta blocker therapy is that they can not abruptly stop taking their beta blocker, due to the risk of rebound hypertension. A beta blocker would be more likely to cause bradycardia and a depressed effect than anxiety and tachycardia. Beta blockers are not associated with any type of esophagitis and they are not fat soluble, thus it is not crucial to eat a fatty meal with the drug in order to improve absorption.

Enalapril is an ACE (angiotensin-converting enzyme) inhibitor. One of the most commonly reported side effects of ACE inhibitor use is a chronic dry cough. This is likely due to the medication's inhibition of kininase II (ACE), which results in a buildup of kinins in the respiratory tract.

None of the other medications listed are associated with persistent cough. 

The proper antidote for overdose of warfarin is vitamin K. Heparin will not reverse the effects of too much warfarin (it would only aggravate the problem). Protamine sulfate is the antidote for overdose of heparin. IV magnesium may be used to antidote digoxin if digibind is unavailable.

A swelling of the tongue indicates that a client may be allergic to enalapril. Other indicators include rash, hives, itching, difficulty breathing, and tightness in the chest.

Carvedilol is a non-selective beta-adrenoceptor and alpha-adrenergic blocker. Lisinopril is an ACE (angiotensin-converting enzyme) inhibitor. Clonidine is an alpha-adrenergic agonist, and amiodarone is a sodium-channel blocker.

The correct answer is "HMG-CoA reductase inhibition," as this is the accurate mechanism of action of atorvastatin, a commonly-prescribed lipid-lowering agent for patients with a number of medical conditions, including hypercholesterolemia. HMG-CoA reductase is an enzyme found within the liver that catalyzes a major reaction involved in cholesterol formation. By inhibiting this enzyme with a medication such as a statin, the new production of LDL cholesterol is decreased, and the number of LDL receptors is upregulated (which decreases circulating LDL, therefore lowering LDL cholesterol).

Atorvastatin is neither an alpha-adrenergic inhibitor, beta-adrenergic inhibitor, PPAR activator (fibrates), or Na-K-2Cl symporter inhibitor (loop diuretics). 

The correct answer is "Peroxisome proliferator-activated receptor (PPAR) activation," as this is the accurate mechanism of action for fibrate medications, such as gemfibrozil. Fibrates are commonly-used medications used to treat high cholesterol, as well as a number of other metabolic abnormalities in patients. Fibrates have the relatively unique property of lowering LDL (the "bad" cholesterol), increasing HDL (the "good" cholesterol), and lowering triglycerides, making them a popular choice when administered either alone, or with statin medications for patients with hypercholesterolemia. 

HMG-CoA reductase inhibition is the mechanism of action of statins.

Vitamin-K-dependent clotting factor synthesis inhibition is the mechanism of action of warfarin.

Alpha-adrenergic inhibition is the mechanism of action of phenoxybenzamine, among other medications.

Beta-adrenergic inhibition is the mechanism of action of propranolol, among other medications.

The correct answer is "bleeding." 

Apixaban is a novel anti-coagulant medication that functions by directly inhibiting factor Xa in the clotting cascade. You can remember this mechanism of action by noting the letters "Xa" in apiXaban. Apixaban is used with increasing frequency now in the treatment of deep vein thrombosis, pulmonary embolism, and atrial fibrillation. A very serious potential adverse effect of apixaban though is that since it is an anticoagulant agent, it can predispose to serious bleeding events. Furthermore, one of the biggest dangers of apixaban is that there is no readily available antidote for it yet, and as such if a bleeding event occurs, there is no simple way to reverse it, as there is with other anti-coagulants like warfarin or heparin. 

Thrombosis, myocardial infarction, and ischemic stroke are all typically thrombotic (e.g. clot-related) issues. Apixaban may be used in the treatment of conditions associated with clotting, but is not known to cause clots, as it is an anti-coagulant. 

Apixaban has no known association with bowel movement frequency. 

The correct answer is "Muscarinic acetylcholine receptor antagonist," as this accurately describes the mechanism of action of atropine. 

Atropine is an anticholinergic medication used for a number of reasons, including to treat bradycardia, various nerve agent poisonings, and intraoperatively at times to diminish the amount of saliva generated. Typical anticholinergic medication side effects can be associated with atropine including pupil dilation, urine retention, dry mouth, constipation, and tachycardia. 

Muscarinic acetylcholine receptor agonist is incorrect as this is the opposite of how atropine works. 

Beta-adrenergic blocker is incorrect. This class of medications would actually serve to decrease heart rate, which would be highly dangerous in a patient whose reason for intervention is bradycardia.

Neither alpha-adrenergic blockade nor monoamine oxidase inhibition describes the mechanism of action of atropine. 

The correct answer is "Calcium-channel blocker." Diltiazem, which is more specifically a non-dihydropyridine calcium-channel blocker is a commonly given medication that functions to dilate both coronary and peripheral vessels (with a negligible reflex adrenergic response). It also is useful in reducing cardiac contractility, having negative inotropy, chronotropy, and dromotropy characteristics. 

The other choices are incorrect. Beta-adrenergic blocker is the mechanism of action of metoprolol. Alpha-adrenergic blocker is the mechanism of action of doxazosin. Mu-opioid receptor agonist is the mechanism of action of morphine. Mu-opioid receptor antagonist is the mechanism of action of naloxone.