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An overview of the pharmacological management of various chronic conditions, including hypertension, heart failure, chronic kidney disease, depression, parkinson's disease, viral infections, fungal infections, and chronic pain. It covers the mechanisms of action, indications, contraindications, and adverse effects of different drug classes used to treat these conditions. The document highlights the importance of understanding the differences between drug classes, the need for appropriate monitoring, and the consideration of patient-specific factors in the selection and management of pharmacotherapy. The information presented can be useful for healthcare professionals, particularly nurse practitioners, in providing comprehensive and evidence-based care for patients with chronic conditions.
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important difference between them? Thiazide diuretics and loops diuretics affect different ions. Loop diuretics have more adverse effects. Thiazide diuretics require luminal perfusion to reach their active site. Thiazide diuretics and loop diuretics have significantly different interactions.- : Thiazide diuretics require luminal perfusion to reach their active site
All beta-adrenergic blockers are cardioselective, blocking only beta1 recep- tors. Some beta-adrenergic blockers are cardioselective, blocking only beta1 re- ceptors; others are not and also block beta2 receptors in smooth muscle. All beta1-adrenergic blockers lose their selectivity at high doses. Some beta1-adrenergic blockers increase their selectivity at high doses.: - Some beta-adrenergic blockers are cardioselective, blocking only beta1 receptors; others are not and also block beta receptors in smooth muscle.
Potassium Calcium Chloride
Magnesium: Potassium
Decreases nitric oxide release. Is not approved for hypertension. Is highly cardioselective. Is not cardioselective.: Is highly cardioselective.
Atenolol Carvedilol Labetalol Nadolol: Atenolol
Renal function Red blood cell count Glucose level Prolactin level: Renal function
Thiazide diuretics Loop diuretics Potassium-sparing diuretics All diuretics: Potassium-sparing diuretics
Diuretics increase renal permeability to water. Diuretics change the resting potential of renal smooth muscle. Diuretics inhibit the transport of ions across the tubular membrane. Diuretics decrease the osmolarity of urine.: Diuretics inhibit the transport of ions across the tubular membrane.
Preventing sympathetic stimulation of the heart Causing renin release from the glomerulus Increasing outflow and water retention in the kidney Preventing parasympathetic stimulation of the heart: Preventing sympathetic stimulation of the heart
Adverse effects are common. Concomitant use of drugs containing iron should be avoided. Renal alterations are less common than with ACE inhibitors. Cough is a common side effect.: Renal alterations are less common than with ACE inhibitors.
nurse may anticipate all of the following except: Neutropenia. Angioedema. Hypokalemia.
A transient increase in blood urea nitrogen (BUN) and creatinine (Cr).: Hy- pokalemia.
LVEF of <35%. Atrial fibrillation. Resting heart rate of >70 bpm. SBP >90 mm Hg.: Atrial fibrillation.
Hypertension with congestive heart failure. Hypertension with diabetes mellitus. Bilateral renal artery stenosis. Intolerance of diuretics.: Bilateral renal artery stenosis.
Red blood cell count. Urine protein. Potassium level. Magnesium level.: Urine protein.
retention in the kidneys? Aldosterone Progesterone Deoxycorticosterone
Adrenocorticotrophic hormone: Aldosterone
considers all of the following except: There are few significant drug-drug interactions. This combination promotes diuresis and vasodilation. The medication must be discontinued during pregnancy. Hyperkalemia and cough are common adverse effects.: There are few signifi- cant drug-drug interactions.
Thiazide diuretics. Loop diuretics. Niacin. Fluoroquinolones.: Loop diuretics.
Nonsteroidal antiinflammatory agents (NSAIDS) Selective serotonin reuptake inhibitors (SSRIs) Statins Anticoagulants: Nonsteroidal antiinflammatory agents (NSAIDS)
Related to decreased cardiac contractility. Variable, depending on the patient's ethnicity. Exacerbated in patients also taking beta-adrenergic antagonists. Related to
vasodilation.: Related to vasodilation.
hypertension in the general non-Black population? Thiazide-type diuretics Angiotensin-converting enzyme (ACE) inhibitors Calcium channel blockers Beta-adrenergic blockers: Beta-adrenergic blockers
myocardial infarction episode? Low-dose aspirin Warfarin Prasugrel Digoxin: Low-dose aspirin
in the general Black population, including those with diabetes? Angiotensin II receptor blockers Calcium- channel blockers ACE inhibitors Clonidine: Calcium-channel blockers
Angioedema. Bronchospasm.
Renal dysfunction. Hypotension.: Hypotension.
Increasing the influx of calcium ions into vascular smooth muscle cells, causing vascular constriction Decreasing cardiac contractility by inhibiting calcium movement into the sarcomere (contractile unit of muscle) Inhibiting the sympathetic effects of epinephrine and norepinephrine Vasodilating the coronary arteries: Decreasing cardiac contractility by inhibiting calcium movement into the sarcomere (contractile unit of muscle)
Gout Peripheral arterial disease Congestive heart failure (CHF) Diabetes: Gout
inhibitors and beta-adrenergic antagonists. Before adding digox- in, the advanced practice nurse should remember that: Quinidine may decrease digoxin levels. Nonsteroidal antiinflammatory agents may lead to hyperkalemia. Laxatives may potentiate hypokalemia. Digoxin and diuretics should not be prescribed together.: Laxatives may poten- tiate hypokalemia.
kidney outcomes in patients in the general adult population who have chronic kidney disease and hypertension regardless of race or diabetes status?
ACE inhibitors Calcium channel blockers Nitrates Beta-adrenergic blockers: ACE inhibitors
decompensated, symptomatic CHF? Nitrates ACE inhibitors Beta-adrenergic antagonists Loop diuretics: Loop diuretics
Vasodilating coronary arteries Increasing preload Contracting arteries Increasing afterload: Vasodilating coronary arteries
cholesterol transfers proteins to the chylomicrons. HDL LDL Triglycerides VLDL: HDL
Water-soluble transport for synthesized lipids Result of breakdown of IDL in plasma Water-soluble transport for ingested lipids Lipid fuel source, ingested or synthesized: Water-soluble transport for synthe- sized lipids
Cholesterol Chylomicron Triacylglycerols IDL: Chylomicron
Glycerophospholipids Saccharolipids Sphingolipids Triacylglycerols: Triacylglycerols
atty acids (triacylglycerol precursors) are synthesized in the liver with as the main precursor.
Bile acids Dietary glucose Lipoprotein lipase Protein: Dietary glucose
Emulsification of dietary fat. Enzymatic breakdown of fatty acids. Neutralize pH of gastric contents. Increase reabsorption of water-soluble vitamins.: Emulsification of dietary fat.
cells but to a greater extent in the cells of which two organs? Intestines and pancreas Liver and intestines Liver and pancreas Stomach and intestines: Liver and intestines
The liver. Muscle cells. Adipose tissue. The pancreas.: Adipose tissue.
mechanisms? Ingested cholesterol is transported there by proteins Synthesized cholesterol is returned there by way of HDL Intracellular synthesis via the HMG-CoA reductase pathway Ingested cholesterol is transported there by acetyl CoA: Intracellular synthesis via the HMG-CoA reductase pathway
purpose? They are reabsorbed from the gut and recycled. They are excreted as an essential component of undigested products. They are metabolized to inert forms. They bind to fat-soluble vitamins and are stored in adipose tissue.: They are reabsorbed from the gut and recycled.
Decrease circulating LDL levels. Increase circulating HDL levels. Decrease triacylglycerol levels. Increase triacylglycerol levels.: Decrease circulating LDL levels.
Selective cholesterol-absorption inhibitors Bile acid sequestrants
HMG-CoA reductase inhibitors Fibric acid derivatives: Bile acid sequestrants
Niacin Bile acid sequestrants HMG-CoA reductase inhibitors Fibric acid derivatives: Niacin
Ensure that the patient is neither pregnant nor planning pregnancy. Advise the patient to pretreat with ASA 325 mg to reduce adverse effects. Rule out diabetes as it may promote hyperglycemia. Counsel the patient that it may inhibit the absorption of fat-soluble vitamins.- : Ensure that the patient is neither pregnant nor planning pregnancy.
synthesis of by the liver. Chylomicron HDL IDL VLDL: VLDL
all of the following except: Can result in approximately 50% reduction in LDL.
Can be useful for patients with clinical ASCVD who need additional LDL-low- ering after maximal statin therapy. To date, there is no major concern with serious adverse events. Can be used as a relatively inexpensive adjunct to statin therapy.: Can be used as a relatively inexpensive adjunct to statin therapy.
Increases activity of lipoprotein lipase Promotes lipolysis of triacylglycerols stored in adipose tissue Blocks catabolism of VLDL and triacylglycerols Blocks endothelial receptor production of lipoprotein lipase (LPL): Increases activity of lipoprotein lipase
Prescribers should be aware that many drugs in this class are CYP3A4 sub- strates. Significant vasomotor flushing may be relieved by using sustained-release preparations. They are only safe in the 1st and 2nd trimester of pregnancy. An HDL of <40 mg/dL is an indication for therapy in patients with two or more cardiac risk factors.: Prescribers should be aware that many drugs in this class are CYP3A substrates.
Dementia. Hyperglycemia.
Pancreatitis.: Hyperglycemia.
induced thrombocytopenia? Warfarin Clopidogrel Argatroban Enoxaparin: Argatroban
inhibitors and indirect factor Xa inhibitors? Direct factor Xa inhibitors inhibit primary clotting; indirect factor Xa inhibitors inhibit secondary clotting. Use of direct factor Xa inhibitors requires laboratory monitoring; use of indi- rect factor Xa inhibitors does not require laboratory monitoring. Direct factor Xa inhibitors are administered orally; indirect factor Xa inhibitors are administered parenterally. Direct factor Xa inhibitors act directly on thrombin; indirect factor Xa inhibitors use antithrombin III as a mediator.: Direct factor Xa inhibitors act directly on thrombin; indirect factor Xa inhibitors use antithrombin III as a mediator.
inhibitors? Primary hemostasis
Secondary hemostasis Clot control Clot dissolution: Secondary hemostasis
Activation of factor X. Formation of a fibrin clot. Platelet aggregation and adhesion. Mobilization of tissue plasminogen activator.: Platelet aggregation and adhe- sion.
heparin (LMWH)? Activated partial thromboplastin time International normalized ratio Anti-Xa assay Prothrombin time: Anti-Xa assay
Bleeding. Impaired protein binding. Neutropenia. Agranulocytosis.: bleeding
Inactivation of factor X. Formation of a fibrin clot. Platelet aggregation and adhesion. Mobilization of tissue plasminogen activator.: Formation of a fibrin clot.
reduction in nonvalvular atrial fibrillation? Argatroban Bivalirudin Clopidogrel Dabigatran: Dabigatran
Heparin. Warfarin. Clopidogrel. Prasugrel.: Heparin.
Aspirin (ASA). Heparin. Thrombin inhibitors. Warfarin.: Heparin.
following tests?
Activated partial thromboplastin time Anti-Xa assay Blood glucose level International normalized ratio: International normalized ratio
or transient ischemic attack (TIA) while on aspirin (ASA) therapy? Dipyridamole and ASA (Aggrenox) Prasugrel (Effient) Ticlopidine (Ticlid) Clopidogrel (Plavix): Dipyridamole and ASA (Aggrenox)
Protein binding CYP inhibition Hydrophilia Lipophobicity: Protein binding
coronary angioplasty (PTCA) and stent placement, glyco- protein IIb/IIIa inhibitors are potent: Platelet inhibitors. Thrombolytics. Thrombin inhibitors. Antithrombin III inhibitors.: Platelet inhibitors.
Inhibiting the conversion of prothrombin to thrombin. Decreasing the synthesis of clotting factors VIII, IX, and X. Suppressing fibrinogen activation. Promoting tissue release of plasminogen activator.: Inhibiting the conversion of prothrombin to thrombin.
Prasugrel is less effective than clopidogrel (Plavix) for CVA prevention. Prasugrel is a strong substrate of CYP450 2C19. Prasugrel is not indicated for a patient with a previous CVA or TIA. Prasugrel is the preferred platelet aggregate inhibitor in patients older than 75 years of age.: Prasugrel is not indicated for a patient with a previous CVA or TIA.
heterocyclics in the management of depression? SSRIs do not have negative cardiovascular effects. SSRIs do not cause sexual dysfunction. SSRIs are less expensive. SSRIs are not sedating.: SSRIs do not have negative cardiovascular effects.
(Celexa) should not be prescribed greater than mg daily due to potential prolongation of the QT interval. 10 20
for: AST/ALT elevation. Renal dysfunction. Hypothyroidism. Hypertension.: Hypertension.
titrated down over a period of at least: 2 weeks. 4 weeks. 2 months. 4 months.: 4 weeks.
Panic disorder. Bulimia. Neuropathic pain. Obsessive compulsive disorder.: Neuropathic pain.
There is greater risk with SSRI agents with short half-lives.
There is greater risk in patients taking multiple serotonergic agents. Mild forms of serotonin syndrome can cause agitation, tremors, and increased blood pressure. Serotonin syndrome can often lead to life-threatening seizures.: There is greater risk with SSRI agents with short half-lives.
serotonin norepinephrine reuptake inhibitors (SNRIs) are primarily indicated for those patients: Allergic to TCAs. =65 years of age. Who are pregnant. Unresponsive to SSRIs.: Unresponsive to SSRIs.
Norepinephrine. Serotonin. Acetylcholine. Both norepinephrine and serotonin.: Both norepinephrine and serotonin.
Norepinephrine down-regulation. Dopamine upregulation. Dopamine down-regulation. Monoamine oxidase inhibition.: Dopamine upregulation.
to select an agent with a: Short half-life. Long half-life. Greater sedating properties. Greater activating properties.: Greater sedating properties.
Benzodiazepines. SNRI. SSRI.: SSRI.
only be given to patients who are also taking levodopa? MAO-B inhibitors Dopamine receptor agonists Anticholinergics COMT inhibitors: NOT Dopamine receptor agonists OR COMT inhibitors
COMT inhibitors Dopamine agonists MAO-
B inhibitors Levodopa/carbidopa (Sinemet): COMT inhibitors
system? GABA Glutamate Dopamine Norepinephrine: GABA
Most pharmacologic agents act to increase levels of endogenous dopamine or stimulate dopamine receptors. As a result, which of the following adverse effects may be anticipated with most classes? Orthostatic hypotension and palpitations Confusion and flushing Diarrhea and urinary retention Flushing and near syncope: Orthostatic hypotension and palpitations
is a particular concern with carbamazepine (Tegretol)? Drug rash Gingival hyperplasia HLA- B1502 sensitivity Nausea: HLA-B1502 sensitivity
managed with phenytoin (Dilantin) 200 mg bid. While evaluating her fatigue, you appreciate that she is bradycardic and obtain a phenytoin level. The level is 40 mcg/mL. The half-life of phenytoin is averaged at 22 hours. As the NP, you know that: In zero order kinetics, you cannot predict the rate of elimination. At high levels, phenytoin saturates its route of elimination. The higher the level, the more rapid the rate of metabolism. In 22 hours the level will be 20 mcg/mL.: NOT In 22 hours the level will be 20 mcg/mL. OR In zero order kinetics, you cannot predict the rate of elimination.
Depression. Anxiety. Insomnia. Hypersexuality.: Hypersexuality.
patients who are taking for seizure dis- order, the nurse practitioner must be aware that it is capable of autoinduction. Phenytoin (Dilantin) Carbamazepine (Tegretol) Gabapentin (Neurontin) Lorazepam (Ativan): Carbamazepine (Tegretol)
Dopamine antagonists. Norepinephrine reuptake inhibitors. GABA agonists. Glutamate agonists.: GABA agonists.
The positive feedback mechanism of GI motility. A physiologic mechanism not manageable by drug therapy. A mechanism by which chyme is neutralized. An active transport pump contained within the parietal cells.: An active trans- port pump contained within the parietal cells.
following are accurate except: Promotes the growth of beneficial organisms in the intestines. Are most effective when used concomitantly with an oral antimicrobial. Inhibits the growth of harmful bacteria. Promotes water reabsorption in the intestines.: Are most effective when used concomitantly with an oral antimicrobial.
Metoclopramide. Ondansetron HCl. Cyclizine.