Pharmacology
Hyperlipidemia
Case Study
Patient Profile
Name: Mr. Smith
Age: 43 years old
Gender: male
Current Medications
Hydrochlorothiazide/lisinopril (single pill combination-[SPC]) for hypertension; metformin for type 2 diabetes
History of Present Illness
Mr. Smith is a 43-year-old African American man who was seen in your office for his annual history update and physical. He is a 1 pack per day smoker of 25 years. Prior to coming to the appointment, he completed his blood work (this is quite helpful as many patients forget this, leading to the need for additional appointments). His results included a normal CBC with diff, TSH, and CMP. His lipid panel, however, needs some attention. He is a busy businessman who often eats out on the run due to limited time to prepare meals. The patient’s family history includes his father’s lung cancer and hypercholesterolemia. In addition, his mother has diabetes, hypercholesterolemia, stroke, and myocardial infarction. No family history of hypercholesterolemia. Thus far, personal medical history for Mr. Smith is hypertension, which is being treated only with a thiazide diuretic at this time, and diabetes for which he has started on metformin. The lipid panel results are noted below.
Relevant Assessment
Vital Signs: Temperature: 98.6° F, Blood Pressure: 128/78, Heart Rate: 66, Respiratory rate: 12, BMI: 29.6.
HEENT: Xanthomas noted around the eyes bilaterally.
No other expanded review of system (subjective data) or examination (objective data) has an impact on the diagnosis reviewed in this case.
| Test | Result | Flag | Units | Reference Interval |
|---|---|---|---|---|
| Cholesterol Total | 214 | High | mg/dl | 100-199 |
| Triglycerides | 59 | mg/dl | ≥ 149 | |
| HDL Cholesterol
Risk Factors for CHD Major risk: < 40 mg/dl Normal range: 40-59 mg/dl Negative risk: ≥ 60 mg/dl |
72 | mg/dl | ≥ 39 | |
| VDLD Cholesterol calc | 12 | mg/dl | < 30 | |
| LDL Cholesterol calc | 125 | mg/dl | < 100; < 70 for certain high risk patients |
Differentials
Polygenic hypercholesterolemia, familial hypercholesterolemia, hypertriglyceridemia, hypothyroidism, nephrotic syndrome, and diabetes
Diagnosis
Polygenic hypercholesterolemia
Diagnostic Testing
Lipid profile above; CBC diff, CMP, TSH all within normal limits
Referrals
None at this time
Patient/Provider Collaborative Goals
Mr. Smith’s LDL level will be less than 70 mg/dL by time of planned follow-up.
Therapeutic Interventions
- Describe a first-line pharmacologic treatment: Include drug name, dose and formulation, frequency, and length of treatment at this dose.
Answer:
One option is atorvastatin (Lipitor) 10 mg by mouth every evening for the next six weeks.
- Drug Mechanism of Action:
Answer:
Atorvastatin inhibits 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, interfering with the rate limiting step in cholesterol production. Additionally, HMG-CoA reductase inhibition decreases levels of highly sensitive C reactive protein (hsCRP), which decreases inflammation at sites of atherosclerotic plaques and inhibits platelet aggregation, giving an antiplatelet effect.
- Contraindications if applicable:
Answer:
Hypersensitivity to atorvastatin or any components of the formulation, liver impairment or failure.
- Drug Mechanism of Action:
- Therapeutic advisement and monitoring: (include any specific instructions that apply, such as when to take the medication, if there are foods to avoid, storage issues, etc; include what laboratory/other (i.e., EKG) test monitoring to expect and how often and monitoring for adverse effects both common and serious)
Answer:
Specific Instructions: Inform the patient that atorvastatin (Lipitor) therapy is being used to address their high cholesterol levels. It is beneficial for not only lowering the low-density cholesterol but also increasing the high-density cholesterol and stabilizing any plaque that may exist in the arteries. Stabilizing plaques helps to prevent heart attacks and strokes. Advise that lifestyle modifications are important; advise the patient to exercise 30 minutes per day most days of the week with no more than a 48-hour break between workout sessions. Instruct the patient to eat a well-balanced low fat, low cholesterol diet. Counsel patients to avoid using alcohol and to avoid grapefruit juice. Patients should also be advised to report any serious adverse effects listed below.
- Therapeutic Monitoring: Order a lipid panel at baseline and in six weeks, if LDL </= 100. Re-check periodically; for example, you may recheck every three months for one year. If extremely stable, monitoring may lengthen to every six months.
- Re-check a fasting lipid panel within four to 12 weeks. Obtain baseline transaminase levels, aspartate aminotransferase (AST), alanine transaminase (ALT), total bilirubin, and alkaline phosphatase, and repeat these labs if there are signs and symptoms of hepatotoxicity.
- Measure creatine phosphokinase (CPK) at baseline if there is a family history of statin intolerance or muscle disease or concomitant drug therapy that may increase the risk of myopathy. Check CPK in any patient that develops symptoms and signs of myopathy. This case presents a patient that has established diabetes mellitus; otherwise, you would initiate baseline and periodic glucose or HgA1c levels for new onset diabetes mellitus. If the patient develops confusion or memory impairment, evaluate the patient for non-statin causes, systemic and neuropsychiatric causes, and also consider statin therapy as the cause.
- Monitor Side/Adverse Effects: The most common of side/adverse effects are diarrhea, upset stomach, nose or throat irritation, and trouble sleeping. All of these are expected to subside within a couple of weeks of initiation of atorvastatin (Lipitor). Patients should be instructed to inform the nurse practitioner (NP) if these common side effects do not dissipate.
- Serious Adverse Effects:
- Rhabdomyolysis is another rare but serious adverse effect. It can lead to acute renal failure, which is one reason the NP should see the patient within one week. This is rare, but it can occur within a few days. If a patient shows up looking ill but never called to report feeling ill, this could be the issue. If the NP doesn’t see the patient in person in one week, the NP can call the patient or family to check on them. When there is a high level of concern, the NP can also send the police to check the welfare of patients if they are not reachable. The NP should discontinue therapy for marked elevation of creatine phosphokinase (CPK) and/or signs and symptoms suggesting rhabdomyolysis. Other muscle related effects include myalgia, myopathy, and immune-mediated necrotizing myopathy.
- Hepatic Effects: Elevated transaminases less than three times the upper limit of normal without symptoms may occur. Hepatic failure is also possible. This risk of hepatic damage increases with use of highly lipophilic drugs metabolized in the liver, co-administration of hepatotoxic medications, co-administration of drugs that interact with statins, chronic hepatitis B, and alcohol consumption. Patients should be instructed to report abdominal pain, nausea, vomiting, itchy skin, yellow skin or eyes, and dark urine.
- Therapeutic Monitoring: Order a lipid panel at baseline and in six weeks, if LDL </= 100. Re-check periodically; for example, you may recheck every three months for one year. If extremely stable, monitoring may lengthen to every six months.
- Planned follow-up should consider adverse effect monitoring, dose adjustment considerations, and decisions about continuing versus discontinuing. In this case, planned follow-up would be:
Answer:
Office visit follow-up in one to two months with lipid profile drawn the day before the appointment.
Review Questions
Click the arrow to expand the section and view the correct answers.
- What class of medications is the first-line to treat hyperlipidemia to stabilize existing plaques and decrease lipid levels?
- Co-enzyme Q10
- HMG-CoA reductase inhibitor (statins)
- PCSK9 inhibitors
- Fibrates
Answer:
B. HMG-CoA reductase inhibitor
Feedback: The first-line medication treatment for hyperlipidemia to stabilize existing plaques and decrease lipid levels are the HMG-CoA reductase inhibitors, also known as statins. Statins reduce the level of Co-enzyme Q-10 and may contribute to muscle pains with statin use. PCSK9 inhibitors are not first-line treatment for hyperlipidemia; rather, they are utilized when dietary modifications and other medication therapy does not get the patient to their goals. Fibrates target triglyceride reduction.
- Maria is a 55-year-old female with recent history of HMG-CoA reductase inhibitor (statin) therapy initiation. She calls your office to be seen for a same-day appointment with concern for fever, feeling weak, feeling achy all over, nausea, vomiting, and urine that looks like dark tea. You plan to tell her:
- This is an expected effect of the HMG-CoA reductase inhibitor (statin) therapy, and it should subside within two weeks.
- This is an expected effect of HMG-CoA reductase inhibitor (statin) therapy, and she needs to ensure intake of at least eight glasses of water daily.
- This is a potential adverse effect of HMG-CoA reductase inhibitor (statin) therapy, and she should go to the emergency department for further evaluation.
- This is a potential adverse effect of HMG-CoA reductase inhibitor (statin) therapy, and she should go to the emergency department for further evaluation if she does not produce urine for 12 hours or more.
Answer:
C. This is a potential adverse effect of HMG-CoA reductase inhibitor (statin) therapy, and she should go to the emergency department for further evaluation.
Feedback: Rhabdomyolysis is a potential adverse effect of HMG-CoA reductase inhibitor (statin) therapy. This can lead to acute kidney injury/failure. Patients presenting with these symptoms and signs should be further evaluated in the emergency department. Rhabdomyolysis is identified as a creatine kinase greater than 40 times the upper limit of normal. Another adverse effect is myalgia which is muscle aches without creatine kinase elevation; this is also called statin-associated muscle symptoms (SSMS). Lastly, there is myopathy, unexplained muscle pain, or weakness with creatine kinase greater than 10 times the upper limit of normal.
- Michael is a 50-year-old male who has been being treated with HMG-CoA reductase inhibitor (statin) therapy for about three months. He notes that he wants to stop the medication and adjust his diet because he is having muscle aches and weakness, and he read this can be due to his statin medication. You tell him:
- “I think you should be tested for influenza.”
- “I think you should be tested for SARS CoV2.”
- “Maybe you slept funny last night.”
- “You are on statin therapy; one concern is statin-associated muscle symptoms. I will order some blood work, and we will discuss the next steps.”
Answer:
D. “You are on statin therapy; one concern is statin-associated muscle symptoms. I will order some blood work, and we will discuss the next steps.”
Feedback: Statin-associated muscle symptoms are a concern for people on HMG-CoA reductase inhibitor (statin) therapy. Using the statin-associated muscle symptoms clinical index (SAMS-CI) can help you in determining if the muscle cramps and weakness the patient is experiencing is related to statin therapy or not. If you determine statin therapy is the likely cause of the symptoms, discontinuation with a subsequent rechallenge in the future is how you can confirm or refute the diagnosis. If the patient was not on a high intensity statin therapy, the re-challenge can be with the same medication at a lower dose. If the patient was on high intensity statin therapy, choose a different medication.
- Which HMG-CoA reductase inhibitor (statin) has the greatest lipid lowering ability?
- Rosuvastatin
- Atorvastatin
- Pravastatin
- Simvastatin
Answer:
A. Rosuvastatin
Feedback: Rosuvastatin has an expected low-density lipoprotein (LDL) reduction of 52-63%. Atorvastatin and simvastatin, respectively, are next in terms of LDL lowering ability.
- When teaching your patients how to take their HMG-CoA reductase inhibitor (statin) medication for hyperlipidemia, what time of day is the best time of day to take the medication?
- Morning before breakfast
- Morning after breakfast
- At noon with lunch
- In the evening without regard to food
Answer:
D. In the evening without regard to food
Feedback: The body produces cholesterol in the liver in the evening. The best time to take HMG-CoA reductase inhibitor (statin) medication is in the evening which allows it to interfere with the rate limiting step in cholesterol production. This is more important in the statins with shorter half-lives (simvastatin [Zocor], lovastatin [Mevacor], fluvastatin [Lescol XL], and pravastatin) than those with longer half-lives (atorvastatin [Lipitor], rosuvastatin [Crestor], pitavastatin [Livalo], and fluvastatin ER tablets [Lescol XL]).
- You are seeing June, a 70-year-old patient, in your office for routine follow-up. She notes that she is taking her rosuvastatin as prescribed, but she is concerned because she was told by a friend that her morning grapefruit juice could lead to an interaction with the HMG-CoA reductase inhibitor (statin) medication. June is wondering if she can just stop the medication as she really loves her grapefruit juice and “we are all going to die of something anyway.” You tell her:
- Good news; rosuvastatin is safe to take while still enjoying her grapefruit juice with breakfast.
- She should stop drinking grapefruit juice immediately.
- She should probably limit her intake of grapefruit juice to 24 ounces per day.
- Grapefruit juice is a CYP3A4 inhibitor and creates a risk of statin toxicity.
Answer:
A. Good news; rosuvastatin is safe to take while still enjoying her grapefruit juice with breakfast.
Feedback: Consumption of grapefruit juice with certain HMG-CoA reductase inhibitor (statin) medications increases the risk of statin toxicity/adverse effects including rhabdomyolysis. This interaction is due to grapefruit juice inhibiting the CYP3A4 metabolism of the statin in the liver, therefore allowing the statin level to remain in the blood longer than if the grapefruit juice had not been ingested. Grapefruit juice is a CYP3A4 inhibitor.
- When initiating a patient on HMG-CoA reductase inhibitor (statin) medication, it is important to consider the low-density lipoprotein-cholesterol and the atherosclerotic cardiovascular risk score.
- True
- False
Answer:
A. True
Feedback: When initiating a patient on HMG-CoA reductase inhibitor (statin) medication, it is important to consider the low-density lipoprotein-cholesterol (LDL-C) and the atherosclerotic cardiovascular risk score; consideration of both of these factors aides in knowing whether to select moderate versus high intensity statin therapy. For LDL-C greater than or equal to 190, you will treat with high intensity statin as it is likely there is a component of familial hypercholesterolemia involved. For LDL-C less than 190, you want to use the ASCVD risk calculator, taking into account age, presence or absence of diabetes, sex, smoking status, total cholesterol, high density cholesterol, systolic blood pressure, treatment for hypertension status, and race to guide statin intensity selection.
- The low-density lipoprotein-cholesterol goal for most patients is < 100 mg/DL. Which of the following are criteria for a goal of < 70 mg/dL goal? (Select all that apply)
- The patient has a 10-year pack history for smoking.
- The patient is diabetic and or has a history of myocardial infarction.
- The patient is African American or Hispanic.
- The patient has a systolic blood pressure and is only on a diuretic.
Answer:
B. The patient is diabetic or has a history of myocardial infarction.
Feedback: The goal for low density lipoprotein cholesterol LDL-C is less than 70 milligrams per deciliter for people who have a history of diabetes and or established heart disease. In the absence of diabetes or established heart disease, a goal of less than 100 milligrams per deciliter for LDL-C is acceptable.
References
Condina Leik, M. T. (2025). Cardiovascular system review. In FNP Certification Intensive Review (pp. 299–314). Springer Publishing.
Pignone, M. & Cannon, C. P. (2025). Low-density lipoprotein cholesterol-lowering therapy in the primary prevention of cardiovascular disease. UpToDate®. Retrieved June 11, 2025 from https://www.uptodate.com/contents/low-density-lipoprotein-cholesterol-lowering-therapy-in-the-primary-prevention-of-cardiovascular-disease
Rosenson, R. S. (2025). Statins: Actions, side effects, administration. UpToDate®. Retrieved June 11, 2025 from https://www.uptodate.com/contents/statins-actions-side-effects-and-administration
Rosenthal, L. D., & Burchum, J. R. (2026). Prophylaxis of atherosclerotic cardiovascular disease: Drugs that help normalize cholesterol and triglyceride levels. In Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (3rd ed., pp. 385–392). Elsevier.
yellowish, waxy, or reddish bumps under the skin due to cholesterol deposition
A condition that causes rapid skeletal muscle breakdown and kidney damage which may ultimately result in kidney failure. It can be a medication adverse effect or from traumatic injury to muscle. Its symptoms and signs include muscle pain, weakness, vomiting, confusion, and dark urine.
muscle aches and pain (without significant elevation of creatine kinase)
muscle pain or weakness with elevation of creatine kinase equal to or greater than 10 times the upper limit of normal
muscle pain with elevated creatine kinase plus antibodies against 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase