Download Maryville NURS 615 Pharm 3 exam Questions and Complete Verified Solutions 2023/2024 and more Exams Nursing in PDF only on Docsity!
Maryville NURS 615 Pharm 3
exam Questions and Complete
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How do antigout medications work? by inhibiting the infiltration and phagocytosis of leukocytes, thus decreasing the breakdown of uric acid to urate crystals. Deposition of urate crystals causes pain and inflammation What is Colchicine anti-gout medication how does Colchicine work? Works by inhibiting inflammation, reducing pain and swelling common side effects of Colchicine GI problems (diarrhea) use with caution in elderly Also can cause blood dyscrasias & abdominal pain patient education with Colchicine Can be given with food & milk to decrease GI issues Avoid beer, ale, & wine: may cause gout attack Increase fluid intake: increases excretion of uric acid Avoid smoked meats & high-protein diets Low dose of Colchicine Low dose colchicine is 1.2mg followed by 0.6mg one hour later or 1.8 milligrams total High dose of Colchicine high dose colchicine is 1.2mg followed by 0.6mg every four to six hours; or 4.8mg total. Difference between high dose and low dose Colchicine The difference between the two is low dose is as effective as high dose with a lower side effect profile.
Lab values to monitor with Colchicine Check renal function test, BUN, Creatine Patient education with Colchicine Almost always causes some degree of diarrhea, make sure patients are aware of this side effect Patient education with Febuxostat (Uloric) Gout may worsen with therapy initially Dietary changes to decrease gout attacks and uric acid deposits. Avoid beer, ale, & wine Increase fluid intake: increases excretion of uric acid Avoid smoked meats & high-protein diets WHO 3 step ladder for pain medication What is not a first line for pain medication? Narcotics Recommendations for pain treatment You want to start with NSAIDs first and then work your way up from there. types of Corticosteroid treatment Prednisone, Cortisone, Dexamethasone how do Corticosteroids work? Suppress the inflammatory & immune systems by inhibiting the synthesis of chemical mediators. what are the chemical mediators that Corticosteroids work on? Prostaglandins, leukotrienes, & histamines Corticosteroids and inflammation Decreases inflammation which decreases swelling, warmth, redness, & pain. Uses for corticosteroid treatment Addison's disease, hormone replacement, cancer therapy SLE, arthritis, IBD, & to suppress graft rejection contraindications for corticosteroid treatment Systemic fungal infections & with live vaccine Use corticosteroids cautiously with: Pregnancy, kids, HTN, heart failure, renal impairment, & with infections resistant to treatment Patient education with corticosteroids Don't discontinue abruptly, doses may need increased during stress, symptoms of Cushing's and GI bleeding Problem with taking Corticosteroids for greater than 6 months The main thing you want to worry about is osteoporosis it can also worsen diabetic control and patients should report any tarry black stools or abdominal pain. Other common side effects with Corticosteroids
Inhibits the formation & release of prostaglandin. PTGS converts arachidonic to PGH2 which is converted to other prostaglandins that mediate pain, inflammation, & fever. PGH2 is also converted to thromboxane-A2 which stimulates platelet aggregation leading to formation of blood clots. What happens when one part of the cox pathway is blocked Understand that blocking one part of the cox pathway can lead to a build up of different products acetaminophen Mechanism of action The main mechanism is performed a proposed is the inhibition of cox. And recent findings suggest that it's highly selective cox-2. Selectivity for cox-2 it does not significantly inhibit the production of pro clotting thromboxanes. Acetaminophen and Peripheral anti-inflammatory activity is limited by several factors high level of peroxides present and inflammatory lesions serious side effects of acetaminophen Acute overdoses of acetaminophen can cause potentially fatal liver damage. maximum recommended dose of Acetaminophen The maximum recommended dose is 4 grams in 24 hours, from all sources. Additional teaching with Acetaminophen Remind patients that many OTC medicines contain acetaminophen antidiabetic medication hypoglycemia dizziness, confusion, diaphoresis, and tachycardia Hyperglycemia polyuria, polydipsia, and weight loss. Diabetic Ketoacidosis fruity breath odor, and rapid respirations. Neurologic symptoms including lethargy, focal sign, and obtundation can develop this can progress to coma in later stages. hypo and hyperglycemia visual Metformin mechanism of action Major effect is to decrease hepatic glucose output by inhibiting gluconeogenesis. Also increases insulin mediated glucose utilization in peripheral tissues such as the muscle and liver (particularly after meals) Has a anti-lipolytic effect that lowers serum phreatic concentrations—thereby reducing substrate availability for gluconeogenesis. It's also used in diabetics to decrease their cholesterol and triglyceride levels. Lab tests and Metformin A1C should be checked periodically to monitor for effectiveness of treatment Lab tests and renal function with Metformin
Metformin is not metabolized. It is cleared from the body via tubular secretion and excreted unchanged in the urine. You should order a serum creatinine to assess for impaired renal function. Gliptin (Glucagon) mechanism of action Glucagon increases blood glucose levels and dpp-4 inhibitors reduced glucagon in blood glucose levels. The mechanism of action of the dpp-4 inhibitors is to increase incretin levels—which inhibit glucagon release which in turn increases insulin secretion, decreases gastric emptying, and decreases blood glucose levels. Gliptin (Glucagon) drug class Inhibitors Dipeptidyl peptidase-4 (DPP4), or dpp-4 inhibitors or gliptins, are a class of oral hypoglycemics that block DPP-4. They can be used to treat diabetes mellitus type II. Exenatide is a GLP agonist How do GLP agonists work Glucagon-like peptide-1 receptor agonist. Bind to glucagon-like peptide-1 receptors slowing gastric emptying, increasing insulin secretion by pancreatic beta cells. Simultaneously the compound reduces the elevated glucagon secretion by inhibiting alpha cells of the pancreas, which is known to be inappropriate in the diabetic patient. GLP-1 is normally secreted by L cells of the gastro intestinal mucosa in response to a meal. What is Exenatide used for and what is an advantage of it This class of drugs is used for treatment of type 2 diabetes. One of their advantages over older insulin secretagogues such as sulfonylureas or meglitinides is that they have a lower risk of causing hypoglycemia. Exenatide and how it works Exenatide is a synthetic version of exendin-4 hormone found in the saliva of the Gila monster. It displays biological properties similar to human glucagon-like peptide or GLP-1, a regulator of glucose metabolism and insulin secretion. What is Exenatide administered for? Exenatide enhances glucose-dependent insulin secretion by the pancreatic beta-cell, suppresses inappropriately elevated glucagon secretion and slows gastric emptying, although the mechanism of action is still under study. It should be administered 60 minutes before breakfast and dinner. How is Acarbose used? May be used in conjunction with metformin, a sulfonylurea, or alone When is Acarbose taken? Take with the first bites of a meal because it interferes with absorption of carbohydrates Function of Acarbose Inhibits the alpha-glucosidase enzyme. This action slows the digestion of carbohydrates, reducing the postprandial rises in blood glucose.
non-diabetic pancreatic beta cells. The initial dose of glargine is reduced by 20% to avoid hypoglycemia. Thyroid medication overview propylthiouracil (PTU) mechanism of action It works in the thyroid as well as peripherally. In the thyroid PTU inhibits the thyroperoxidase which normally acts in thyroid hormone synthesis by oxidizing the iodide to iodine. PTU does not inhibit the action of sodium-dependent iodine transporter on the follicular cells basolateral membranes. So actions at the t3 and t4 target tissues. PTU also acts by inhibiting the enzyme 5- deiodinases which converts t4 to the active form t3. propylthiouracil (PTU) mechanism of action PTU works both essentially in the thyroid as well as the target tissues. It's important to recognize that these enzymes only work in conjugated tyrosine molecules of t3 and t4 a completely different enzyme family that is responsible for the deiodinase activity of iodinase single tyrosine molecules within the thyroid follicular cells. PTU Mechanism of action summary PTU inhibits the enzyme thyroperoxidase normally acts in thyroid hormone synthesis by oxidizing the anion iodide (I−) to iodine (I0), facilitating iodine's addition to tyrosine residues on the hormone precursor thyroglobulin. This is one of the essential steps in the formation of thyroxine (T4). PTU does not inhibit the action of the sodium-dependent iodide transporter located on follicular cells' basolateral membranes. Inhibition of this step requires competitive inhibitors, such as perchlorate and thiocyanate. PTU adverse effects Fatal granulocytopenia first signs are fever and sore throat Vasculitis, a temporary alopecia, rash, aplastic anemia, and acute renal failure. Agranulocytosis, anca positive vasculitis, hepatotoxicity, and pancreatitis which is rare. Synthroid-thyroid hormone action Increases basal metabolic rate, enhances gluconeogenesis, stimulates protein synthesis uses for synthroid Replacement in decreased/absent thyroid function Treatment for unresponsive obesity Hypersensitivity Older adults: impaired cardiac function, hypertension Synthroid visual summary Levothyroxine (Synthroid) Mechanism of action
Levothyroxine is a synthetic thyroid hormone that is chemically identical to levothyroxine T4 Which is naturally secreted by the follicular cells of the thyroid gland. uses for Synthroid Used to treat thyroid hormone deficiency and occasionally to prevent the recurrence of thyroid cancer. Adverse effects of Synthroid Like it's naturally secreted counterpart, levothyroxine is a chiral compound in the L form. Tachycardia and angina, more notably in the elderly. Weight loss, palpitations, diaphoresis Levothyroxine (Synthroid) lab values to monitor Blood free thyroxine and TSH levels are monitored to help determine whether the dose is adequate. Done 4 to 8 weeks after the start of treatment or a change in dose. Once the adequate replacement dose has been established the test repeat at 6 & 12 months unless there is a change in symptoms. Signs of too much thyroid replacement Symptoms of hyperthyroidism- irritability, insomnia, nervousness, hyperthermia Signs of not enough thyroid replacement Bradycardia, lethargy, constipation, excessive fatigue & sleeping patient education for Synthroid Replacement therapy is lifelong, don't stop taking without consulting your doctor. If not tolerating medication a substitution may be made. You will need your TSH levels checked periodically for life It takes about a month for full effectiveness Take in the morning, 20 min before breakfast nursing implications for Synthroid Monitor for increase or decrease in pulse rate & rhythm Report abnormal vitals, especially HR higher than 100 bpm Methimazole (Tapazole) Methimazole (Tapazole) mechanism of action Shares PTUs central mechanism but not it's peripheral one. Only works centrally in the thyroid. Methimazole (Tapazole) action Inhibits synthesis of thyroid hormone by interfering with iodine and tyrosine reside. Does not destroy existing stores of thyroid. Methimazole (Tapazole) adverse effects Teratogenic, in the fetus can cause aplasia cutis (congenital focal absence of the skin on the scalp) Fever, rash, puritus, dizziness, lost of taste, NV Toxic agranulocytosis (leukopenia) may occur up to 4 months after therapy Methimazole (Tapazole) mechanism of action- 2
Monitor vital signs and BP for effectiveness of treatment, monitor electrolyte, hepatic, & renal serum labs, avoid abrupt withdrawal of drugs (may cause phenomenon of excessive rise rebound in BP) What assessment should be made before prescribing any antihypertensive agent? You should check a thorough assessment of their liver and renal function. The real function especially for ace inhibitors and ACE receptor blockers which work primarily in the kidneys. 1st Line Medications classes used to treat CHF? If caused by reduced systolic function: ACE inhibitors, ARBs, Beta blockers Better improvement in symptoms in pts with systolic dysfunction without a-fib. Benefits are decreased with low ejection fraction. Intolerant to these, poor kidney function, sometimes in blacks: combined hydralazine & long acting nitrate like isosorbide Reduced ejection fraction: can add hydralazine & isosorbide to ACE inhibitors or ARBs 2nd Line Medications Classes - CHF Digoxin (digitalis)- only used in a small number of patients with poor refractory symptoms with a-fib or chronic low BP Treatment of edema related to CHF Diuretics are the mainstay Loop diuretics, thiazide-like diuretics, & potassium sparing diuretics Spironolactone antagonists have limited efficacy and safety data ACE inhibitors ACE inhibitor drugs Drugs: Captopril (Capoten), Enalapril (Vasotec), & Benazepril (Lotensin) mechanism of action of ACE inhibitors Suppresses formation of angiotensin II from the renin-angiotensin-aldosterone system, reduces peripheral resistance and improves cardiac output ACE inhibitors mechanism of action- detailed The renin-angiotensin system is systemically and locally driven. Systemic process triggered by kidneys' response to decreased effective blood volume. Begins with the secretion of insulin from the renal cortex. Renin cleaves angiotensinogen to form angiotensin-I. This product in turn is catalyzed by ACE, formed primarily in the pulmonary vasculature and angiotensin- II. ACE-potent vasoconstrictor effects tissues and systems body wide, research shows that these vasoconstrictor effects are attenuated by ACE inhibition. So again review table one of the AFP article on ACE inhibitors. Next Slide systemic effects of angiotensin II
Increased norepunephrine (central & peripheral), oxygen demand, coronary vasoconstriction, preload, afterload, left ventricular mass (through growth factors), myocyte hypertrophy, catecholamines from adrenal medulla, sodium reabsorption from proximal tubule, renal vasoconstriction, renal sympathetic tone, & increased aldosterone benefits of ACE inhibition: increases Coronary blood flow, ventricular relaxation, cardiac output, & cardiac index benefits of ACE inhibition: decreases Pulmonary artery pressure & capillary wedge pressure, left ventricular mass, infarction size, reperfusion injury, platelet aggregation, & proteinuria renin-angiotensin-aldosterone system most common and other adverse effects of ACE inhibitors Persistent dry hacking cough Additional side effects Headache, dizziness, postural hypotension, rash, angioedema, & altered sense of taste Why are ACE inhibitors the drug of choice in diabetic patients with hypertension? They reduce the adverse effects of diabetes on the kidneys. ACE inhibitors slow the onset of diabetic nephropathy in patients with microalbuminuria and type 1 diabetes. In one study was stopped prematurely because of the significant decrease and combined primary outcomes in patients taking Ramipril. Total cardiovascular end points reduced by 25% these included myocardial infarction, stroke, cerebrovascular death, total mortality, and revascularization in reported neuropathy. Angiotensin receptor blockers - drugs Drugs: losartan (Cozaar), olmesartan (Benicar), valsartan (Diovan) ARBs mechanism of action Angiotensin II causes muscles surrounding blood vessels to contract, narrowing the vessels, increases the pressure within the vessels and can cause HTN ARBs are block the action of angiotensin II by preventing angiotensin II from binding to angiotensin II receptors on the muscles surrounding blood vessels. Causes As a result vascular dilation and reduced BP. Makes it easier for the heart to pump blood and can improve heart failure. The progression of kidney disease caused by the high blood pressure or diabetes is slowed. ARBs- block angiotensin II from binding to muscles of blood vessels. ACE inhibitors prevent the formation of angiotensin II calcium antagonists calcium channels
the ischemic symptoms due to increase in myocardial oxygen demand. Only work on the vasculature and do not work on the heart. That can worsen proteinuria with patients with neuropathy which can increase edema and the hands and feet. what is Amlodipine? a long-acting dihydropyridine that dilates blood vessels & lowers blood pressure. In angina, it increases blood flow to the heart muscle to relieve pain due to angina. CCB that dilates blood vessels and is used to treat HTN, angina, heart failure and CAD symptoms metabolism of Amlodipine It's metabolized in the liver to inactive metabolites vs cyp3a Grapefruit juice inhibits the cyp3a4 increasing amlodipine in the bloodstream. common side effects of Amlodipine Dose-related: can see peripheral edema, dizziness and palpitations, and flushing Not dose-related: fatigue, nausea, abdominal pain, and somnolence rare side effects of Amlodipine blood disorders, impotence, depression, insomnia, tachycardia, gingival enlargement, hepatitis, and jaundice. What is Amiodarone? Antiarrhythmic used to treat ventricular tachycardia and ventricular fibrillation. Only used for treating life threatening rhythm disorders Why get a Thyroid panel with Amiodarone? Abnormalities in thyroid function are common. Amiodarone is structurally similar to thyroxine which contributes to the effects of amiodarone on thyroid function. Both under and over activity of the thyroid may occur on amiodarone treatment. Checking free thyroxine alone may be unreliable so TSH should therefore be checked every six months patient teaching Amiodarone In the Eye: corneal micro deposits and optic neuropathy can occur. Any visual problems should be reported right away. Skin: bluish-gray discoloration of the skin and photosensitivity make sure patients use sunscreen. Lung: interstitial lung disease. You can see both hypo and hyperthyroidism and they should monitor their blood pressure daily. serum digoxin level Digitalis What is Digoxin used for? A digitalis glycoside used to treat heart failure, atrial flutter & A-fib not controlled by other drugs Most common indications are a fib and a flutter with rapid ventricular response Beta blockers and calcium channel blockers are a better first choice What is the mechanism of action for Digoxin?
High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction of the AV node and increasing its refractory period digoxin can reduce the ventricular rate. Doesn't change the rhythm. Digoxin drug interactions Digoxin has potentially serious interactions with verapamil, amiodarone, erythromycin, and epinephrine as a local in the anesthetic. The digoxin level should be monitored while taking albuterol; need to monitor renal functions also Digoxin side effects Tritanopia- blurred/yellow color visual disturbance Dizziness, headache, malaise, fatigue, muscle weakness, anorexia, hypokalemia, dysrhythmias, & bradycardia Nitroglycerin summary What is Nitroglylcerin used for? Used to treat angina, acute MI, severe HTN, & coronary artery spasms Side effects of Nitroglycerin Can cause severe headaches necessitating algesic administration for relief of pain; severe hypotension; and in certain cases bradycardia The painful side effects lead to lack of compliance What is nirate tolerance? Tolerance, is the attenuation or loss of one or several the effects of organic nitrates after long-term administration. All organic nitrate regimens using frequent dosing of long acting nitrates, continuous delivery, or continuous IV infusions of nitroglycerin or long-acting preparations, will result in partial or complete nitrate tolerance. Proposed mechanisms that may contribute to tolerance include: activation of neuro-hormone mechanisms; plasma volume expansion in the depletion of intercellular self hydro pro-factors. To avoid tolerance to long-term nitrate therapy regimens should be tailored to provide a 10 to 12-hour nitrate-free interval level when possible. This means is that antianginal prophylaxis can only be provided by nitro or nitrate therapy for some portion of each day and that some patients will develop an increase in angina in the nitrate free intervals which will necessitate short-term therapy with sublingual nitroglycerin or a similar preparation. Coumadin Coumadin mechanism of action Warfarin and related 4-hydroxycoumarin containing molecules decreases blood coagulation by inhibiting vitamin K epoxide reductase enzyme that recycles oxidized vitamin K to its reduced form after it has participated in the carboxylation of several blood clot blood coagulation proteins. Mainly prothrombin and factor VII.
an liver production not diet). Levels of blood cholesterol will fall. Cholesterol synthesis appears to occur mostly at night so statins with short half-lives are usually taken at night to maximize their effects. Reduce cardiovascular disease and mortality May prevent heart disease in those with high cholesterol but no history of heart disease Adverse effects of Statins Rhabdomyolysis, increased risk of diabetes, increased liver enzymes/liver damage Other possible side effects: cognitive loss, neuropathy, pancreatic and other hepatic dysfunction, and sexual dysfunction Patient education for Statins Instruct the patient to report any muscle weakness or tenderness and dark urine to the provider immediately. Can harm the fetus, if you are or plan to become pregnant discuss with your PCP Dietary changes to reduce weight and cholesterol What do Fibric Acid Derivatives treat? Mainly treat elevated triglycerides, not suitable for patients with low HDL levels. Used in combination with other drugs Less effective in lowering LDL and cholesterol levels the ability of fibrates to increase HDL and lower triglyceride levels seems to reduce insulin resistance when the dyslipidemia is associated with other features of a metabolic syndrome like hypertension and diabetes type II. They are therefore used in many hyperlipidemias. Bile Acid Sequestrants- what are the drugs Drugs: Cholestyramine (Cholybar, Olestyr) Mechanism of action of Sequestrants Binds bile in the GI tract to prevent its reabsorption. It's a strong ion exchange resin (can exchange its chloride anions with anionic bile acids in the GI tract and bind them strongly in the resin matrix). Cholestyramine removes bile acids from the body by forming insoluble complexes with bile acids in the intestine which are then excreted in the feces What do Sequestrants treat? This loss of bile acids/plasma cholesterol is converted to bile acids in the liver to normalize levels. This conversion of cholesterol in a bile acid lowers plasma cholesterol levels. What is Niacin? compound with the formula CA (one of the 20 to 80 essential human nutrients). What does Niacin treat? Treat hypercholesterolemia and pellagra (niacin deficiency) What would you recommend to a patient who is experiencing flushing with niacin therapy?
The main side effect is flushing which usually last for 15 to 30 minutes, although it can sometimes last up to two hours. It's sometimes accompanied by prickling or itching sensation in particular in areas covered by clothing. That flushing can be blocked by taking 300 milligrams of aspirin a half an hour before taking niacin.
