Test Bank for Pharmacology and the Nursing Process 10th Edition By Linda Lilley, Shelly Collins, Julie Snyder Chapter 1-58 (REVISED VERSION)

Test Bank for Pharmacology and the Nursing Process 10th Edition By Linda Lilley, Shelly Collins, Julie Snyder Chapter 1-58 |Complete Guide 2022 WITH 100% VERIFIED ANSWERS ace inhibitor mechanism of action - The development of the ACE inhibitors was spurred by the discovery of the venom of a South American viper, which was found to inhibit kininase activity. Kininase is an enzyme that normally breaks down bradykinin, a potent vasodilator in the human body. As their name implies, these drugs inhibit angiotensin-converting enzyme, which is responsible for converting Angiotensin I (AI) (formed through the action of renin) to angiotensin 2 (AII). AII is a potent vasoconstrictor and induces aldosterone secretion by the adrenal glands. Aldosterone stimulates sodium and water resorption, which can raise blood pressure. Together, these processes are referred to as the reninangiotensin-aldosterone system. By inhibiting this process, blood pressure is lowered. The primary effects of the ACE inhibitors are cardiovascular and renal. Their cardiovascular effects are due to their ability to reduce blood pressure by decreasing systemic vascular resistance (SVR). They do this by preventing the breakdown of the vasodilating substance bradykinin and substance P (another potent vasodilator), and preventing the formation of AII. These combined effects decrease afterload, or the resistance against which the left ventricle must pump to eject its volume of blood during contraction. The ACE inhibitors are beneficial in the treatment of heart failure because they prevent sodium and 349water resorption by inhibiting aldosterone secretion. This causes diuresis, which decreases blood volume and return to the heart. This in turn decreases preload, or the left ventricular end-diastolic volume, and the work required of the heart. ace inhibitors - are considered the drugs of choice for hypertensive patients with heart failure adverse effects of ace inhibitors - Major CNS effects of the ACE inhibitors include fatigue, dizziness, mood changes, and headaches. A characteristic dry, nonproductive cough may occur that is reversible with discontinuation of the therapy. A first-dose hypotensive effect can cause a significant decline in blood pressure. Other adverse effects include loss of taste, hyperkalemia, angioedema, and renal impairment. In patients with severe heart failure whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment with ACE inhibitors may cause acute renal failure. ACE inhibitors promote potassium resorption in the kidney, although they promote sodium excretion due to their reduction of aldosterone secretion. For this reason, serum potassium levels must be monitored regularly. This is especially true when there is concurrent therapy with potassium-sparing diuretics, although many patients tolerate both types of drug therapy with no major problems. One rare, but potentially fatal, adverse effect is angioedema. Angioedema is a strong vascular reaction involving inflammation of submucosal tissues, which can progress to anaphylaxis. adverse effects of andregenics - bradycardia with reflex tachycardia, postural and postexercise hypotension, dry mouth, drowsiness, dizziness, depression, 346edema, constipation, and sexual dysfunction (e.g., impotence). Other effects include headache, sleep disturbances, nausea, rash, and palpitations. There is a high incidence of orthostatic hypotension (a sudden drop in blood pressure during changes in position) in patients taking alpha blockers, first dose syncope the abrupt discontinuation of the centrally acting alpha2 receptor agonists can result in rebound hypertension, characterized by a sudden and very high elevation of blood pressure. This may also be true for other antihypertensive drug classes, especially beta blockers. Nonselective blocking drugs are also commonly associated with bronchoconstriction as well as metabolic inhibition of glycogenolysis in the liver. ion, the abrupt discontinuation of the centrally acting alpha2 receptor agonists can result in rebound hypertension, characterized by a sudden and very high elevation of blood pressure. This may also be true for other antihypertensive drug classes, especially beta blockers. Nonselective blocking drugs are also commonly associated with bronchoconstriction as well as metabolic inhibition of glycogenolysis in the liver. Any change in the dosing regimen for cardiovascular medications should be undertaken gradually and with appropriate patient monitoring and follow-up. Although the same is also true for most other classes of medications, abrupt dosage changes of cardiovascular medications, either up or down, can be especially hazardous for the patient. Some of these drugs can also cause disruptions in blood count as well as in serum electrolyte levels and renal function. Periodic monitoring of white blood cell count, serum potassium, sodium and creatinine levels is necessary. Inte adverse effects of anticoagulants - bleeding is the main complication of anticoagulation therapy, and the risk increases with increasing dosages. Bleeding may be localized (e.g., hematoma at the site of injection) or systemic. It also depends on the nature of the patient's underlying clinical disorder and is increased in patients taking high doses of aspirin or other drugs that impair platelet function. One particularly notable adverse effect of heparin is heparin-induced thrombocytopenia (HIT). There are two types of HIT. Type I is characterized by a more gradual reduction in platelets. In this type, heparin therapy can generally be continued. In contrast, in type II HIT there is an acute fall in the number of platelets (more than 50% reduction from baseline). Heparin therapy must be discontinued in patients with type II HIT. The greatest risk to the patient with HIT is the paradoxical occurrence of thrombosis, something that heparin normally prevents or alleviates. Thrombosis that occurs in the presence of HIT can be fatal. The incidence of this disorder ranges from 5% to 15%. The direct thrombin inhibitors lepirudin and argatroban are both specifically indicated for treatment of HIT. Warfarin can cause skin necrosis and "purple toes" syndrome. Other adverse effects are listed in Table 26-2. adverse effects of antifibrinolytics - occur uncommonly and are mild. However, there have been rare reports of these drugs causing thrombotic events, such as acute cerebrovascular thrombosis and acute MI. The common adverse effects of antifibrinolytics are listed in Table 26-6. adverse effects of antiplatelet drugs - can be serious, and they all pose a risk for inducing a serious bleeding episode adverse effects of beta andregenics - Mixed alpha/beta agonists produce the most adverse effects because they are nonselective. These include insomnia, restlessness, anorexia, cardiac stimulation, hyperglycemia, tremor, and vascular headache. The adverse effects of the nonselective beta agonists are limited to betaadrenergic effects, including cardiac stimulation, tremor, anginal pain, and vascular headache. The beta2 drugs can cause both hypertension and hypotension, vascular headaches, and tremor. Overdose management may include careful administration of a beta blocker while the patient is under close observation due to the risk for bronchospasm. Because the half-life of most adrenergic agonists is relatively short, the patient may just be observed while the body eliminates the medication. adverse effects of thrombolytic drugs - internal, intracranial, and superficial bleeding. Other problems include hypersensitivity, anaphylactoid reactions, nausea, vomiting, and hypotension. These drugs can also induce cardiac dysrhythmias.