Pharm Exam II

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160 Terms

1
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How does digoxin improve heart failure?
It inhibits Na+/K+-ATPase, increases myocardial contractility, and slows heart rate; expected benefits include increased cardiac output and urine production and decreased sympathetic tone and renin release.
2
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What assessments are required before administering digoxin?
Count the apical pulse for 1 full minute; review the digoxin level and potassium. The notes list digoxin 0.8–1.8 ng/mL and potassium 3.5–5.0 mEq/L.
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Which visual and cardiac findings suggest digoxin toxicity?

Yellow-green vision, halos, or blurred vision are later findings; severe bradycardia and dysrhythmias are serious cardiac manifestations.

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What medication reverses digoxin toxicity?
Digoxin-specific Fab antibody fragments, identified in the notes as Digibind.
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What findings indicate that digoxin is effective?
Improved HF symptoms and perfusion, increased urine production, and absence of dysrhythmias.
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How do LDL and HDL differ?
LDL contributes to arterial plaque; HDL transports cholesterol toward the liver for processing and excretion.
7
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What baseline assessments are important before statin therapy?
Liver function tests, CK level, alcohol use, pregnancy status, and history of liver disease.
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A patient taking atorvastatin reports unexplained muscle pain and tenderness. What is the priority concern?
Myopathy or rhabdomyolysis; report promptly and evaluate CK and the patient's condition.
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Which serious adverse effects and interactions are associated with statins?

Hepatotoxicity and muscle injury; azole antifungals, HIV protease inhibitors, and grapefruit juice can increase adverse-effect risk.

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How does cholestyramine lower LDL?

It binds intestinal bile acids for fecal excretion; the liver then uses more cholesterol to replace bile acids.


Cholestyramine is a powder/resin that you swallow. It stays in your intestines and binds to bile acids (which your body naturally makes from cholesterol to help digest food); it cant be recyced so its excreted through poop.

To make new bile acids to replace what was lost, your liver reaches into your bloodstream and pulls out LDL (bad) cholesterol to use as raw material.

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Which findings are associated with cholestyramine therapy?

Constipation, abdominal discomfort, flatulence, nausea, steatorrhea, and deficiencies of vitamins A, D, E, K, and folic acid.

12
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How should cholestyramine powder be administered?

Mix thoroughly with 60–180 mL of an appropriate liquid or pulpy food and consume immediately; do not administer the powder dry.

13
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Why must cholestyramine be separated from other medications?
It can delay or prevent their absorption; the uploaded notes specify giving the resin 2 hours before or 4 hours after other medications.
14
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What teaching and assessment are important for a patient taking cholestyramine?
Encourage fiber and fluids if unrestricted, monitor constipation, and assess for biliary disease, which the notes list as a contraindication.
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What is niacin used for, and what common effect should the patient expect?

It lowers LDL; flushing and hot flashes are common.

16
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Which laboratory abnormalities and complications should the nurse monitor during niacin therapy?
Elevated liver enzymes, hyperuricemia/gout, and hyperglycemia; assess renal function and fluid intake as appropriate.
17
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Why is niacin combined with a statin a medication-safety concern?
The combination increases the risk of myopathy and hepatotoxicity.
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How does ezetimibe differ from a statin?
Ezetimibe blocks cholesterol absorption at the small-intestinal brush border; statins decrease hepatic cholesterol synthesis.
19
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What should the nurse monitor when ezetimibe is combined with a statin?
Muscle pain, CK, and liver dysfunction; rare serious effects listed include rhabdomyolysis, hepatitis, pancreatitis, and thrombocytopenia.
20
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Which lipid-lowering class particularly targets elevated triglycerides?

Fibric acid derivatives such as gemfibrozil and fenofibrate; they increase triglyceride breakdown and can increase HDL.

21
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What safety concerns are associated with fibrates?

Myopathy, liver injury, and potentiation of anticoagulant effects; assess CK and liver function and screen for liver, severe renal, and gallbladder disease.

22
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Match each lipid medication with its main action: statin, cholestyramine, niacin, ezetimibe, and fibrate.

Statin: decreases cholesterol synthesis; cholestyramine: increases bile-acid excretion; niacin: decreases LDL/VLDL; ezetimibe: decreases intestinal cholesterol absorption; fibrate: lowers triglycerides.

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How does angiotensin II increase blood pressure?
It directly causes vasoconstriction and stimulates aldosterone, promoting sodium and water retention.
24
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How do lisinopril and enalapril lower blood pressure?
ACE inhibitors block conversion of angiotensin I to angiotensin II, causing vasodilation and decreased aldosterone-mediated fluid retention.
25
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Why are ACE inhibitors used for hypertension and heart failure, and how can they protect the kidneys?
They reduce vascular resistance and fluid retention; efferent arteriole dilation reduces intraglomerular pressure.
26
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Which adverse effects should the nurse monitor with lisinopril or enalapril?

Orthostatic hypotension, persistent dry cough, hyperkalemia, angioedema, and fetal injury.

27
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A patient taking lisinopril develops swollen lips and throat. What is the priority?
Recognize angioedema, prioritize airway assessment, and obtain immediate assistance; this is more urgent than an isolated dry cough.
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A patient taking enalapril develops a persistent dry cough. What explains it, and what change may the provider make?
Bradykinin accumulation contributes to the cough; the provider may change therapy to an ARB.
29
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Why should a patient taking an ACE inhibitor avoid potassium-containing salt substitutes?
ACE inhibitors decrease aldosterone and can raise potassium; added potassium increases hyperkalemia risk.
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How do ARBs differ from ACE inhibitors?
ARBs block angiotensin II receptors rather than its formation; both can cause hyperkalemia, hypotension, angioedema, and fetal injury, but persistent cough is less common with ARBs.
31
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How do nifedipine and verapamil differ?
Nifedipine primarily dilates arterioles and may cause reflex tachycardia; verapamil dilates arterioles and slows cardiac conduction, creating bradycardia risk.
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Why can nifedipine lower blood pressure while increasing heart rate?

Vasodilation lowers BP, triggering a baroreceptor-mediated sympathetic response and reflex tachycardia.

33
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What findings should the nurse monitor during nifedipine therapy?
Hypotension, reflex tachycardia, peripheral edema, flushing, dizziness, and lightheadedness.
34
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A patient taking verapamil has constipation and a slow pulse. How are these findings related to the medication?
Verapamil reduces gastrointestinal motility and slows cardiac conduction; monitor the pulse and address constipation with appropriate fluids and fiber.
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What conditions and combinations raise concern with verapamil?
Heart block or AV block, bradycardia, and concurrent beta blockers or other antihypertensives because of additive cardiac/BP effects.
36
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What interaction is listed between calcium channel blockers and digoxin?
Calcium channel blockers can increase digoxin levels; monitor for toxicity when these medications are combined.
37
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How do beta blockers reduce hypertension and angina?

They decrease heart rate, myocardial contractility, and cardiac workload, reducing cardiac output and myocardial oxygen demand.

38
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Why is propranolol concerning in a patient with asthma or COPD?
Beta-2 blockade can cause bronchoconstriction and wheezing; assess respiratory history and question its suitability.
39
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What should the nurse assess before administering metoprolol, atenolol, or propranolol?

Heart rate, blood pressure, conduction problems, and relevant respiratory history; monitor for bradycardia and hypotension.

40
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Why must patients with diabetes use caution with beta blockers?
Beta blockers can mask warning signs of hypoglycemia, making low glucose harder to recognize.
41
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A patient stops metoprolol abruptly because they feel better. What complication is the nurse concerned about?
Rebound hypertension, angina, or heart failure; teach the patient not to stop abruptly.
42
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Which additional adverse effects should patients taking beta blockers report?

Depression, insomnia/nightmares, excessive fatigue, and HF findings such as dyspnea, edema, or weight gain; the angina notes specify reporting 5 lb in 1 week.

43
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Why might hydralazine be combined with a beta blocker, and what adverse effects require monitoring?
A beta blocker can counter reflex tachycardia; monitor fluid retention/HF, urinary output, and a reversible lupus-like syndrome.
44
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What causes angina, and how do stable and variant angina differ?
Angina reflects myocardial oxygen supply failing to meet demand; stable angina is predictably triggered by exertion, while variant angina results from coronary vasospasm at unpredictable times.
45
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How does nitroglycerin relieve angina?

It dilates veins and coronary arteries, decreasing venous return/preload and myocardial workload while relieving coronary vasospasm and improving blood supply.

46
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What must the nurse assess before administering nitroglycerin?

Blood pressure, pulse, and interacting medications, especially erectile-dysfunction drugs such as sildenafil.

47
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Which adverse effects are expected with nitroglycerin?

Headache, postural hypotension, and tachycardia; assess BP and safety rather than assuming every headache means an allergy.

48
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Which nitrate interactions and contraindication are emphasized in the notes?
Alcohol, beta blockers, and calcium channel blockers can add to hypotension; sildenafil is a major interaction, and severe head injury is a contraindication.
49
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What instructions are important for nitroglycerin patches and ointment?

Do not cut patches; remove old ointment before applying a new dose, avoid touching the ointment, and measure it with the provided applicator.

50
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Why is a nitrate-free interval needed with long-acting nitrate therapy?
It reduces tolerance; the notes specify removing transdermal therapy for 12 hours daily.
51
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What key safety principles apply to IV nitroglycerin?
Use nitroglycerin-compatible infusion equipment, closely monitor BP and pulse, and do not abruptly discontinue the infusion.
52
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How do nitrates, beta blockers, and calcium channel blockers reduce angina through different mechanisms?

Nitrates reduce preload and relieve coronary spasm; beta blockers reduce HR and contractility; calcium channel blockers dilate arteries, and some also slow HR (e.g., verapamil [nonselective CCB])

53
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How do anticoagulants and antiplatelets differ?
Anticoagulants interfere with clotting factors; antiplatelets inhibit platelet aggregation. Both reduce clot formation and increase bleeding risk.
54
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Why are antiplatelets especially relevant to arterial thrombosis?
Arterial thrombi are platelet-rich; venous thrombi are more fibrin-rich and commonly associated with DVT and pulmonary embolism.
55
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How does heparin work, and what conditions is it used for?

It inactivates thrombin and other clotting factors; uses include DVT prevention/treatment, PE treatment, and selected acute cardiovascular or cerebrovascular situations.

56
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Which laboratory tests are important during unfractionated heparin therapy?

aPTT/PTT for anticoagulant effect and platelet count for thrombocytopenia; the notes list a therapeutic aPTT of 60–90 seconds.


Remember: Heparin — HIT so platelet count needs to be assessed

57
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What medication reverses excessive heparin anticoagulation?
Protamine sulfate.
58
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A patient receiving heparin has a substantial platelet decline. What complication should the nurse suspect?
Immune-mediated heparin-associated thrombocytopenia; promptly report the decline and reassess therapy.
59
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Which actions are correct for subcutaneous heparin: abdominal injection, aspiration, massage, or avoiding the umbilicus by 2 inches?
Inject into abdominal fatty tissue at least 2 inches from the umbilicus; pinch the skin and insert at 90 degrees. Do not aspirate or massage; apply slight pressure afterward.
60
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What additional safety measures apply to IV heparin?

Verify weight-based dosing with another nurse as required, monitor aPTT according to the protocol, and assess frequently for bleeding because effects occur quickly.

61
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Using the uploaded heparin protocol, what action corresponds to an aPTT of 75 seconds?
No bolus or rate change; 60–90 seconds is the protocol's therapeutic range.
62
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Using the uploaded heparin protocol, what action corresponds to an aPTT of 100 seconds?

No bolus; decrease the infusion by 1 unit/kg/hour according to the prescribed protocol.

63
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Using the uploaded heparin protocol, what action corresponds to an aPTT above 212 seconds?

Stop the infusion for 60 minutes, then decrease by 3 units/kg/hour according to the prescribed protocol.

64
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How do LMWHs such as enoxaparin differ from unfractionated heparin?

They have a more predictable response and longer duration and do not require routine aPTT-guided dosing; administer subcutaneously in the abdomen and rotate sites.

65
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Why is anticoagulant use important to report before spinal or epidural procedures?
It increases the risk of spinal or epidural hematoma.
66
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How does fondaparinux work, and when is it used?

It activates antithrombin; the notes describe use when heparin/LMWH are contraindicated, for postoperative DVT prevention, and with warfarin for acute DVT/PE treatment.

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Which patient characteristics and effects require special attention with fondaparinux?

Low body weight below 50 kg is flagged in the notes for increased bleeding risk; monitor bleeding, thrombocytopenia, and spinal/epidural hematoma risk.

longer half-life

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Which medications increase bleeding risk with fondaparinux?
Aspirin, NSAIDs, and other anticoagulants; persistent external bleeding requires prolonged direct pressure and assessment.
69
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How does warfarin work, and what are its major indications?

Oral warfarin antagonizes vitamin K; indications include DVT/PE, atrial fibrillation, MI-related indications, and mechanical heart valves.

70
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Why may heparin or LMWH overlap with newly started warfarin?
Warfarin takes approximately 3–5 days to reach a therapeutic effect, so the faster-acting medication provides protection during the delay.
71
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What INR targets are listed for warfarin?

DVT/PE, atrial fibrillation, and MI: 2.0–3.0; mechanical heart valves: 2.5–3.5.

72
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A patient taking warfarin for atrial fibrillation has an INR of 4.8. How should the nurse interpret this?
It is above the notes' 2.0–3.0 target and indicates increased bleeding risk; assess for bleeding and clarify dosing before administration.
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What reverses warfarin, and what major contraindication appears in the notes?

Vitamin K reverses warfarin; pregnancy is a contraindication.

74
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Which dietary statement shows understanding of warfarin teaching?
“I will keep my intake of vitamin K-containing leafy vegetables consistent rather than suddenly increasing or eliminating them.”
75
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Which herbal products are listed as increasing bleeding risk with warfarin?
Garlic, ginkgo, ginseng, and feverfew.
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Which overt findings suggest bleeding during anticoagulant therapy?
Hematuria, black/tarry stools, coffee-ground emesis, excessive bruising, petechiae, epistaxis, bleeding gums, hemoptysis, and bleeding at wounds or IV sites.
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An anticoagulated patient develops pallor, tachycardia, hypotension, and lumbar or abdominal pain without visible bleeding. What should the nurse suspect?
Occult internal bleeding; promptly assess the patient, notify the provider, and review CBC and other ordered bleeding evaluations.
78
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Which teaching points reduce injury and bleeding risk during anticoagulant therapy?
Use a soft toothbrush and electric shaver, wear shoes, avoid contact sports and jostling activities, report injuries and persistent bleeding, and wear/carry medical identification.
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What should a patient taking warfarin tell healthcare and dental providers?
That they take warfarin; communicate therapy before procedures or blood draws and continue prescribed INR monitoring.
80
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How does apixaban work, and what monitoring distinction separates it from warfarin?
It selectively inhibits factor Xa; it does not use routine INR-guided dosing, but bleeding assessment remains essential.
81
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Which reversal agents are listed for apixaban/rivaroxaban and dabigatran?
The uploaded notes list andexanet alfa for apixaban/rivaroxaban and idarucizumab for dabigatran.
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What interaction and missed-dose teaching are listed for apixaban?

St. John's wort reduces apixaban's effect; do not double a dose to make up for a missed dose.

83
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How does clopidogrel prevent clotting?

It irreversibly inhibits ADP binding to platelet receptors, reducing aggregation for the platelet's remaining lifespan.


ADP = Alarm for Damaged Platelets

84
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What adverse effects and interactions should the nurse monitor with clopidogrel?
Bleeding and bruising; additional anticoagulants, antiplatelets, thrombolytics, NSAIDs, feverfew, green tea, and ginkgo can increase bleeding risk.
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What clopidogrel administration and procedure teaching appears in the notes?

Do not crush or split tablets; apply prolonged pressure after punctures, and coordinate the prescribed interruption at least 5 days before surgery.

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How does aspirin prevent thrombotic events?

It inhibits platelet cyclooxygenase (CoX)and platelet aggregation; listed uses include ischemic stroke/TIA, angina, coronary stenting, and MI-related prevention/treatment.

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What assessments help detect aspirin-related GI bleeding?

Monitor stools and emesis, test stool for occult blood as ordered, and assess CBC for blood-loss anemia.

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A patient taking aspirin reports ringing in the ears and blurred vision. What should the nurse suspect?

Salicylism, or aspirin toxicity; report and evaluate these sensory changes.


Salicylism = tinnitus, blurry vision

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Which aspirin teaching points are important for safe use?

Check OTC products for hidden aspirin/salicylates, report bleeding and tinnitus, and coordinate any prescribed preoperative interruption; the notes list 1–2 weeks.

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A patient develops wheezing, throat tightness, and hives after aspirin. What is the priority concern?
An allergic reaction with possible airway involvement; stop aspirin and obtain immediate medical assistance.
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Match each hematopoietic medication with its primary target: epoetin alfa, filgrastim, oprelvekin, and ferrous sulfate.
Epoetin alfa increases RBC production; filgrastim increases neutrophils; oprelvekin increases platelets; ferrous sulfate replaces iron needed for hemoglobin.
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Why is epoetin alfa prescribed for anemia associated with chronic kidney disease?
Diseased kidneys may not produce enough erythropoietin; epoetin alfa stimulates bone marrow RBC production.
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What other anemia-related uses of epoetin alfa appear in the notes?

Chemotherapy-induced and zidovudine-induced anemia.


cancer chemotherapy damages fast-growing bone marrow cells that produce red blood cells.

A low red blood cell count triggered by zidovudine (AZT), an antiretroviral medication used to treat HIV infection.

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What assessments are essential during epoetin alfa treatment?
BP, hemoglobin/hematocrit, CBC, iron/ferritin, and nutritional status; monitor the response without assuming higher hemoglobin is always safer.
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Which serious risks are associated with epoetin alfa?

Hypertension, MI, stroke, venous thromboembolism, vascular-access thrombosis, and death.

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A patient receiving epoetin alfa remains anemic and has low iron stores. What explains the poor response?

Epoetin requires adequate iron and other nutrients for RBC production; iron, folate, or vitamin B12 deficiency can reduce effectiveness.


Epoetin doesn’t work if there is iron, folate, or vitamin deficiency

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What self-administration teaching is appropriate for epoetin alfa?

Refrigerate vials, gently rotate rather than shake, inspect before use, and discard remaining medication from single-use vials.

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How does filgrastim help a patient receiving chemotherapy?

It is a granulocyte colony-stimulating factor that increases neutrophils, reducing severe neutropenia, infection, hospitalization, and IV-antibiotic needs.

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Which findings are expected versus serious during filgrastim therapy?

Bone pain and malaise are expected; leukocytosis, splenic rupture, glomerulonephritis, and capillary leak syndrome are serious.

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What nursing care is important during filgrastim therapy?

Monitor CBC/neutrophils, temperature, infection symptoms, and hepatic toxicity; maintain infection precautions and assess latex allergy with Neupogen.