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Pharmacology Case Study, Assignments of Nursing

A case study of pharmacological aspects of patient care.

Typology: Assignments

2020/2021

Uploaded on 02/23/2024

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Case Study One
CM is a 60 y/o male with a PMH significant for HTN, and HF with reduced EF (EF 30%). He had a
(NYHA) heart failure grade of class 2, and could manage his day-to-day activities without
support. He could walk 50 meters and could climb 3–4 steps without becoming dyspneic. Apart
from his usual symptoms, he did not have fever, cough, or chest pain before presenting to the
clinic. He does not drink alcohol or smoke. He presents to the clinic dyspneic, drowsy, pale,
diaphoretic, and restless. He has an audible wheeze, bilateral swollen legs (+2 edema) and
jugular vein distension from physical examination. His blood pressure is 160/90.
Home medications: Furosemide 20 mg daily, metoprolol IR 50mg daily, losartan 50MG daily
(baseline potassium is 5.1 but never has EKG changes), atorvastatin 20mg daily, ibuprofen
200mg twice a day (using for headaches).
1. What is CM diagnosis?
2. What pharmacological recommendation can we provide to treat CM current condition?
1. Identify Drug-Drug interactions or Drug-Disease interactions.
2. What medications would be given and how do we give it? (dosing considerations
and IV/PO)
3. After managing CM condition, what can we do to better optimize his HF regimen?
1. What drugs would we add or remove?
2. Any changes in terms of dosing or drug formulations to help both his HF and
HTN?
1. In this instance it appears that CM is having an acute decompensated exacerbation of his heart
failure. His signs and symptoms align with this, specifically dyspnea, drowsiness, pallor,
diaphoresis, wheezing, jugular vein distention and bilateral leg edema. It would likely be prudent
to state that his current classification on the NYHA scale should be moved from a 2 to a 4, given
that his symptoms are severe with activity and rest and reduce his functional status significantly
(New York Heart Association (NYHA) Classification, n.d.). He should be hospitalized to ensure
appropriate treatment is achieved and monitoring is provided.
2. Recommendations:
a. Stop the ibuprofen. This can be impacting and exacerbating his HF from several angles,
notably NSAIDs reduce the effectiveness of loop diuretics like furosemide. Evidence
shows that when a patient is taking NSAIDs and a loop diuretic combined with
angiotensin receptor blockers (ARBs) that they are at significant risk for an acute kidney
injury (Camin et al., 2015). If we can better control his blood pressure, we may reduce
the feeling of the headache that he is experiencing, but we might also be able to offer
acetaminophen or caffeine as alternative treatment options to see if those may alleviate
his headache. NSAIDs also reduce the effectiveness of medications that are designed to
treat hypertension, specifically his ARB, losartan. Specifically, NSAIDs reduce the blood
pressure lowering effects of the medication, possibly by decreasing renal vasodilating
prostaglandins, it is also hypothesized that the addition of the NSAID may not increase
blood pressure, but does increase weight, increase extracellular fluid volume, decrease
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Case Study One

CM is a 60 y/o male with a PMH significant for HTN, and HF with reduced EF (EF 30%). He had a

(NYHA) heart failure grade of class 2, and could manage his day-to-day activities without

support. He could walk 50 meters and could climb 3–4 steps without becoming dyspneic. Apart

from his usual symptoms, he did not have fever, cough, or chest pain before presenting to the

clinic. He does not drink alcohol or smoke. He presents to the clinic dyspneic, drowsy, pale,

diaphoretic, and restless. He has an audible wheeze, bilateral swollen legs (+2 edema) and

jugular vein distension from physical examination. His blood pressure is 160/90.

Home medications: Furosemide 20 mg daily, metoprolol IR 50mg daily, losartan 50MG daily

(baseline potassium is 5.1 but never has EKG changes), atorvastatin 20mg daily, ibuprofen

200mg twice a day (using for headaches).

1. What is CM diagnosis?

2. What pharmacological recommendation can we provide to treat CM current condition?

1. Identify Drug-Drug interactions or Drug-Disease interactions.

2. What medications would be given and how do we give it? (dosing considerations

and IV/PO)

3. After managing CM condition, what can we do to better optimize his HF regimen?

1. What drugs would we add or remove?

2. Any changes in terms of dosing or drug formulations to help both his HF and

HTN?

  1. In this instance it appears that CM is having an acute decompensated exacerbation of his heart failure. His signs and symptoms align with this, specifically dyspnea, drowsiness, pallor, diaphoresis, wheezing, jugular vein distention and bilateral leg edema. It would likely be prudent to state that his current classification on the NYHA scale should be moved from a 2 to a 4, given that his symptoms are severe with activity and rest and reduce his functional status significantly ( New York Heart Association (NYHA) Classification , n.d.). He should be hospitalized to ensure appropriate treatment is achieved and monitoring is provided.
  2. Recommendations: a. Stop the ibuprofen. This can be impacting and exacerbating his HF from several angles, notably NSAIDs reduce the effectiveness of loop diuretics like furosemide. Evidence shows that when a patient is taking NSAIDs and a loop diuretic combined with angiotensin receptor blockers (ARBs) that they are at significant risk for an acute kidney injury (Camin et al., 2015). If we can better control his blood pressure, we may reduce the feeling of the headache that he is experiencing, but we might also be able to offer acetaminophen or caffeine as alternative treatment options to see if those may alleviate his headache. NSAIDs also reduce the effectiveness of medications that are designed to treat hypertension, specifically his ARB, losartan. Specifically, NSAIDs reduce the blood pressure lowering effects of the medication, possibly by decreasing renal vasodilating prostaglandins, it is also hypothesized that the addition of the NSAID may not increase blood pressure, but does increase weight, increase extracellular fluid volume, decrease

sodium excretion and clearance, and decrease glomerular filtration rate (Olsen et al., 1999). b. We are going to continue his furosemide; however, we will change the route to IV furosemide. The initial course of treatment recommended is a bolus dose up to 2. times the patient’s oral dose. As CM is taking 20mg at home we could do an initial dose of 50mg IV and then titrate to as needed to produce the therapeutic response necessary to stabilize CM (Lexicomp). We can titrate to effect by doubling dose until we reach diuresis that will reduce his fluid volume overload. This can be done at greater than or equal to Q2 hour intervals. Once our effective dose is identified we can reduce the frequency to once or twice a day depending on clinical course. c. Depending on his O2 saturation we should also begin him on oxygen therapy via nasal cannula again titrating to effect to reduce his work of breathing and to ease his shortness of breath. d. We could consider treatment with an IV vasodilator, like nitroglycerin or nitroprusside to reduce his afterload volume and relieve some of his symptoms. The recommended starting range for nitroprusside is 0.1 to 0.3 mcg/kg/minute, titrating every 5-15 minutes to reach desired effect. In a patient that weighs 80 kg the maximum dose recommended is 5mcg/kg/minute (Lexicomp).

  1. Changes Upon Discharge: a. We will follow our earlier recommendation and remind CM that he should avoid use of NSAIDs to minimize further chance of interaction with his diuretics and his ARBs. We may want to follow him more closely on his current home medications to ensure that we are not lowering his blood pressure to greatly with the removal of the ibuprofen and the possibility of all his current medications working without its interference. b. We should consider either increasing the dosage of his furosemide, increasing its frequency or both. Presently his home regime is taking 20mg once daily, a relatively low dose, all things considered. We could increase it, so he is taking 40mg by having him take 20mg BID, this all depends on his hospital course. We could also consider higher doses to achieve the effect that would best control his fluid load. This is all dependent on his hospital course and what dose of furosemide was necessary to maintain an appropriate level of diuresis for CM in the hospital. c. Per the 2018 AHA guidelines for HF, initiation of mineralocorticoid receptor antagonists (spironolactone) combined with either angiotensin-converting enzyme inhibitors (enalapril, etc), angiotensin-receptor blockers (losartan, etc) or angiotensin receptor- neprilysin inhibitors (sacubitril/valsartan) reduces sudden cardiac death and all-cause mortality in patients with HFrEF (Yancy et al., 2017). d. For this patient I would do the following: i. I would continue with his furosemide and metoprolol, basing dosage on what the patient experienced in the hospital for his IV furosemide and providing him an oral dose equivalent to the lowest IV dosage that was effective in managing his HF symptoms. ii. Metoprolol we can titrate upwards, slowly, doubling his dose every two weeks to a target of 200mg once daily while continuing to monitor for signs and symptoms of heart failure and hypotension (Lexicomp).

Journal of Hypertension , 12 (2), 209–216. https://doi.org/10.1016/s0895-7061(98)00228-

Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Colvin, M., Drazner, M. H.,

Filippatos, G., Fonarow, G. C., Givertz, M. M., Hollenberg, S. M., Lindenfeld, J., Masoudi,

F. A., McBride, P. E., Peterson, P. N., Stevenson, L. W., & Westlake, C. (2017). 2017

ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management

of Heart Failure: A Report of the American College of Cardiology/American Heart

Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of

America. Circulation , 136 (6). https://doi.org/10.1161/cir.

Case Study Two: Part One SA is a 70 y/o female with a PMH significant for a previous myocardial infarction and HTN. She has been walking 10,000 + steps a day but is unable to drop her blood pressure. She presents to the doctor’s office with a BP 138/85. Home medications : atorvastatin 20mg daily, acetaminophen 500mg every 6 hours for headaches, Phenylephrine nasal spray for sinuses,

  1. Identify what stage of HTN this patient has?
  2. Does the ASCVD score need to be calculated for this patient?
  3. How will you manage this patients HTN? a. Identify what should be added or removed from this patients medication regimen b. Any DDI or drug-disease interactions present? Part Two After a year the patient present to the emergency department with slurred speech, a numb feeling in her right arm, and a partial facial droop. The team wants to give her alteplase but the patient has a blood pressure of 200/95. She report the symptom started about 3.5 hours ago.
  4. What blood pressure is it safe to administer alteplase and how fast should the blood pressure be reduced?
  5. What agents can be used to decrease the blood pressure in this scenario?
  6. Explain the agent and if IV (continuous infusion, intermittent boluses or a combination of both) or PO needed
  7. What time frame does the alteplase need to be given from symptom onset?
  1. What antithrombotic regimen should be initiated post alteplase administration and when should it be started? Part One Answers:
  2. SA has Stage One Hypertension. This is identified by a Systolic Blood Pressure between 130 to 139 or a Diastolic Blood Pressure of 80 to 89 (Iqbal, 2023). Her Systolic BP is 138 and her Diastolic BP is 85.
  3. No. This patient has already had an adverse event that is related to atherosclerosis as she has had a previous MI. She is already at risk for other cardiovascular events due to her prior MI.
  4. There are a few steps that we will use to manage this patient’s hypertension: a. We are going to recommend that she discontinue her use of phenylephrine nasal spray. Phenylephrine, a sympathomimetic amine that functions as an alpha-1 adrenergic agonist, has been shown to increase vascular resistance especially when given IV or when absorbed by mucous membranes, thereby increasing blood pressure in patients (Richards, 2023). In someone that is attempting to control their blood pressure it would be important to avoid medications that increase the risk of raising blood pressure. Also, according to literature, there is an increased bioavailability of phenylephrine when combined with acetaminophen, which could exacerbate cardiac related events in susceptible patients (Atkinson et al., 2015). b. We are going to suggest that she reduce her dependence on acetaminophen as a manner to control her headaches. In a recent clinical trial, MacIntyre et al. (2022), demonstrated that regular use of acetaminophen in patients with hypertension, causes an increased systolic bp of approximately 5 mmHg. While it is understandable that SA wants to treat her headaches, she should not put herself at increased risk of cardiovascular events. Medication therapy is tempting when a headache seems like such an innocuous event in our lives, but the increased risk associated for this patient means that alternative medications should be sought out. c. As a method of triple therapy, treating the patient’s blood pressure, her headaches and providing some protection for her prior MI, I will recommend a beta blocker, metoprolol succinate, 25mg QD. The medication is titratable up to 200mg based on the patient’s reaction to the medication. Given her age I would be hesitant to raise the dosage either too quickly or by too many mg. It will provide anti-hypertensive coverage, coverage for her headaches, and provide some cardiac benefits in the setting of her prior MI (Chairperson et al., 2023). We should also investigate the need for non-pharmacological interventions for the patient, although she does have a daily movement goal, even if the number of steps that she is walking does not have a particular basis in sound science, she is, at a minimum, active. Part Two:
  5. The patient’s blood pressure should be lower. To administer alteplase the patient’s BP should be less than 180/105 and should be maintained below that after initiating alteplase for a minimum of the first 24 hours (Chairperson et al., 2023). Given that we have roughly four and half hours to deliver the alteplase from the last time the patient was asymptomatic, that is the timeframe in which we should be working (Lees et al., 2010). A balance has to be achieved that we reduce the
  1. Within 24 to 48 hours of an acute ischemic stroke at patient should be started on aspirin therapy (Powers et al., 2019). In patients that have had IV alteplase it should be delayed past 24 hours (Powers et al., 2019). Dual antiplatelet therapy should also be considered, aspirin in combination with clopidogrel within 24 hours and then continued for the next 21 days to reduce the risk of recurrent stroke. Interestingly, in patients with evidence atherosclerosis using low dose aspirin (100mg) and a low dose of rivaroxaban (2.5mg) showed benefit in preventing secondary stroke events (Eikelboom et al., 2017). References:

Atkinson, H. C., Potts, A. L., & Anderson, B. J. (2015). Potential cardiovascular adverse events

when phenylephrine is combined with paracetamol: simulation and narrative review.

European Journal of Clinical Pharmacology , 71 (8), 931–938.

https://doi.org/10.1007/s00228-015-1876-

Chairperson, G. M., Co-Chair, R. K., Brunström, M., Burnier, M., Grassı, G., Januszewicz, A.,

Muiesan, M. L., Tsioufis, C., Agabiti Rosei, E., Algharably, E. a. E., Azizi, M., Bénétos, A.,‐

Borghi, C., Hitij, J. B., Cífková, R., Coca, A., Cornelissen, V., Cruickshank, K., Cunha, P.,...

Kjeldsen, S. E. (2023). 2023 ESH Guidelines for the management of arterial hypertension

The Task Force for the management of arterial hypertension of the European Society of

Hypertension. Journal of Hypertension , 41 (12), 1874–2071.

https://doi.org/10.1097/hjh.

Eikelboom, J. W., Connolly, S. J., Bosch, J., Dagenais, G. R., Hart, R. G., Shestakovska, O., D Az, R.,ı́

Alings, M., Lonn, E., Anand, S. S., Widimský, P., Hori, M., Avezum, Á., Piegas, L. S.,

Branch, K. R., Probstfield, J. L., Bhatt, D. L., Zhu, J., Liang, Y.,... Yusuf, S. (2017).

Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. The New England

Journal of Medicine , 377 (14), 1319–1330. https://doi.org/10.1056/nejmoa

Iqbal, A. M. (2023, July 20). Essential hypertension. StatPearls - NCBI Bookshelf.

https://www.ncbi.nlm.nih.gov/books/NBK539859/

Lees, K. R., Bluhmki, E., Von Kummer, R., Brott, T. G., Toni, D., Grotta, J. C., Albers, G. W., Kaste,

M., Marler, J. R., Hamilton, S., Bar, M., Davis, S. M., Donnan, G. A., & Hacke, W. (2010).

Time to treatment with intravenous alteplase and outcome in stroke: an updated

pooled analysis of ECASS, ATLANTIS, NINDS, and EPITHET trials. The Lancet , 375 (9727),

1695–1703. https://doi.org/10.1016/s0140-6736(10)60491-

MacIntyre, I., Turtle, E., Farrah, T. E., Graham, C., Dear, J. W., Webb, D. J., McCallum, M. J. A.,

Melville, V., Fok, H., McCrae, J., Sule, A. A., Caparrotta, T. M., Kirkby, N. S., & Mitchell, J.

A. (2022). Regular acetaminophen use and blood pressure in people with hypertension:

the PATH-BP trial. Circulation , 145 (6), 416–423.

https://doi.org/10.1161/circulationaha.121.

Powers, W. J., Rabinstein, A. A., Ackerson, T., Adeoye, O., Bambakidis, N. C., Becker, K. J., Biller,

J., Brown, M. D., Demaerschalk, B. M., Hoh, B. L., Jauch, E. C., Kidwell, C. S., Leslie‐

Mazwi, T. M., Ovbiagele, B., Scott, P., Sheth, K. N., Southerland, A. M., Summers, D., &

Tirschwell, D. (2019). Guidelines for the Early Management of Patients With Acute

Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of

Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American

Heart Association/American Stroke Association. Stroke , 50 (12).

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Richards, E. (2023, October 30). Phenylephrine. StatPearls - NCBI Bookshelf.

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