Pharmacology Case Scenarios: Lactulose in Hepatic Encephalopathy, Infant Iron Deficiency, Doxorubicin, Epoetin Alfa and Sucralfate

Pharmacology case scenarios: lactulose, ferrous sulfate, doxorubicin, epoetin alfa and sucralfate

Scenario 1. Eric is admitted for acute confusion and has a history of alcohol abuse. Lactulose is on his MAR, but he is having regular bowel movements. Why is lactulose ordered? How would you address this concern, and what will you assess for?

Scenario 2. An 11-month-old who drinks 8-ounce bottles of whole milk 5 to 6 times a day is diagnosed with iron-deficiency anemia. What are the contributing factors, and how can they be changed? What should the nurse teach the parents about ferrous sulfate?

Scenario 3. Mary has leukemia and will start doxorubicin. What is its mechanism of action, what are its adverse effects, and what will the nurse monitor?

Scenario 4. Ronald is anemic because of a lack of erythrocyte production and is prescribed epoetin alfa. He asks why baseline tests are needed. Explain BUN/creatinine, hemoglobin, hematocrit and ferritin in plain language. What adverse effects should the nurse assess? His hemoglobin is 13.5 g/dL; what should the nurse do?

Scenario 5. Lynn takes sucralfate for gastric ulcers with food but still has severe abdominal pain after meals. What is causing her pain, and how can it be resolved?

Original example for study purposes (about 1,550 words). Verify doses and parameters with your pharmacology textbook and facility protocols.

Scenario 1: Lactulose for Eric

Why is lactulose ordered? In a patient with a history of alcohol use and new acute confusion, lactulose is most likely ordered to treat or prevent hepatic encephalopathy, not constipation. Alcohol-related cirrhosis impairs the liver’s ability to convert ammonia into urea, so ammonia and other gut-derived toxins reach the brain and cause confusion, asterixis and altered consciousness. Lactulose is a nonabsorbable sugar that colon bacteria break down into acids. The acidic environment converts ammonia (NH₃) into ammonium (NH₄⁺), which is trapped in the colon and excreted, and the osmotic laxative effect speeds removal. Lactulose is first-line therapy for overt hepatic encephalopathy, titrated to produce 2 to 3 soft bowel movements per day (Vilstrup et al., 2014).

How would I address the concern? I would not hold the medication simply because Eric’s bowel movements are regular. I would review the chart for a diagnosis of cirrhosis or hepatic encephalopathy, check the order’s indication and titration goal, and clarify with the prescriber or pharmacist if the purpose is not documented. I would explain to Eric and his family that the goal is two to three soft stools daily to clear ammonia, and that fewer stools may allow confusion to worsen.

What will I assess, and why?

• Mental status and neurologic signs: orientation, level of consciousness, asterixis (flapping tremor) and handwriting changes, to evaluate whether the drug is working.
• Stool number and consistency: target 2 to 3 soft stools daily; too few suggests underdosing, while frequent watery stools signal overdosing.
• Fluid and electrolyte status: excessive diarrhea can cause dehydration, hypokalemia and hypernatremia, which can themselves worsen encephalopathy.
• Labs: serum ammonia trend if ordered, liver function tests, electrolytes and glucose.
• Alcohol withdrawal: confusion in a person with alcohol use may also reflect withdrawal or Wernicke encephalopathy, so I would assess vital signs, tremor and withdrawal scores and confirm thiamine orders.
• Precipitating factors: GI bleeding, infection, constipation, sedatives and dehydration can trigger encephalopathy.

Scenario 2: Iron-Deficiency Anemia in an 11-Month-Old

Contributing factors.

• Excessive milk intake: 40 to 48 ounces a day is about twice the recommended maximum. Milk is low in iron, and large volumes leave little appetite for iron-rich foods.
• Cow’s milk before 12 months: whole cow’s milk is not recommended for infants under 12 months because it is low in iron, the iron is poorly absorbed, it can cause occult intestinal blood loss, and its calcium and casein inhibit iron absorption (Baker & Greer, 2010).
• Rapid growth: iron stores from birth are depleted by about 4 to 6 months, so older infants need iron from foods or formula.
• Possible inadequate iron-rich complementary foods and bottle use that encourages grazing on milk.

Measures to change these factors. Switch to iron-fortified infant formula (or continue breastfeeding with iron supplementation) until 12 months, then limit cow’s milk to about 16 to 24 ounces per day. Offer iron-rich foods such as iron-fortified infant cereal, pureed meats, beans and lentils, paired with vitamin C-rich foods such as oranges or tomatoes to improve absorption. Offer milk in a cup with meals rather than bottles throughout the day and begin weaning from the bottle around 12 months.

Teaching about ferrous sulfate.

• Give the exact dose with the dropper provided; iron is dosed by elemental iron, and overdose is a leading cause of poisoning deaths in young children. Store it in a child-resistant container out of reach.
• Give between meals, such as 1 hour before feedings, with a small amount of juice that contains vitamin C to improve absorption. If stomach upset occurs, the provider may allow giving it with food.
• Do not give with milk, formula, dairy products or antacids, which reduce absorption.
• Place the liquid toward the back of the mouth with a dropper or syringe and brush the teeth or wipe the gums afterward, because liquid iron can stain teeth.
• Expect dark green or black stools; report constipation, diarrhea, vomiting or abdominal pain.
• Continue for the full course, usually several months after hemoglobin normalizes to rebuild stores, and return for follow-up blood tests.

Scenario 3: Doxorubicin for Mary

Mechanism of action. Doxorubicin is an anthracycline antitumor antibiotic. It intercalates between DNA base pairs and inhibits topoisomerase II, preventing DNA repair and replication and leading to strand breaks and cell death. It also generates oxygen free radicals, which contribute to its toxicity in heart tissue. It acts on rapidly dividing cells, which explains both its effectiveness and its adverse effects.

Adverse effects.

• Cardiotoxicity: acute arrhythmias and, more importantly, cumulative dose-related cardiomyopathy and heart failure, which can appear months or years later. Risk rises sharply at higher lifetime doses.
• Bone marrow suppression: neutropenia (infection risk), thrombocytopenia (bleeding) and anemia; this is usually the dose-limiting toxicity.
• Vesicant extravasation: leakage from the vein can cause severe tissue necrosis.
• GI effects: nausea, vomiting and mucositis (stomatitis).
• Alopecia, red-orange urine for 1 to 2 days (harmless), and tumor lysis syndrome in leukemia.
• Secondary malignancies, such as acute myeloid leukemia, and infertility.

Nursing monitoring.

• Baseline and periodic cardiac function: echocardiogram or MUGA scan for left ventricular ejection fraction, ECG, and signs of heart failure such as dyspnea, edema and weight gain; track the cumulative dose.
• CBC with differential before each dose; neutropenic and bleeding precautions; temperature monitoring.
• IV site: give through a patent central line or a carefully monitored IV; stop the infusion immediately if pain, swelling or redness occurs and follow the extravasation protocol.
• Uric acid, potassium, phosphorus, calcium and creatinine for tumor lysis; hydration and urine output.
• Liver function, because doses are reduced with elevated bilirubin.
• Nausea, oral mucosa, nutrition and emotional coping; teach Mary that red urine is expected and to report fever, bleeding or shortness of breath.

Scenario 4: Epoetin Alfa for Ronald

Explaining baseline tests in plain language.

• BUN and creatinine: “These measure how well your kidneys are working. Your kidneys make the hormone that tells your bone marrow to make red blood cells, so kidney disease is a common reason for this kind of anemia. The results also help us decide your dose and watch your kidneys during treatment.”
• Hemoglobin: “This is the protein in red blood cells that carries oxygen. It shows how anemic you are now and tells us whether the medicine is working, so we can adjust the dose and avoid raising it too high, which can cause blood clots or strokes.”
• Hematocrit: “This shows what percentage of your blood is made of red blood cells. It confirms the hemoglobin result and helps us track your response over time.”
• Ferritin: “This measures your iron stores. Your body needs iron to build new red blood cells, so if your iron is low, the medicine won’t work well, and we may need to give you iron first.”

The nurse can also explain that after the first tests, levels are usually checked weekly until stable and then less often, and that tests will be coordinated to reduce needle sticks.

Adverse effects to assess.

• Hypertension: check blood pressure before each dose, because epoetin commonly raises it.
• Thrombosis and cardiovascular events: chest pain, leg swelling or pain, shortness of breath, stroke symptoms and clotting of dialysis access. The FDA boxed warning notes a higher risk of death, MI, stroke and thrombosis when hemoglobin is targeted above 11 g/dL.
• Seizures, especially in the first months; headache and confusion.
• Injection-site reactions, fever, joint pain, allergic reactions and, rarely, pure red cell aplasia.
• In patients with cancer, ESAs may shorten survival or speed tumor progression, so they are used at the lowest effective dose.

Hemoglobin of 13.5 g/dL. This is above the level at which epoetin should be continued. For patients with chronic kidney disease, the labeling advises reducing or interrupting the dose when hemoglobin approaches or exceeds 11 g/dL, and in cancer-related anemia the drug is stopped once hemoglobin is sufficient to avoid transfusion. The nurse should hold the dose, notify the prescriber, check blood pressure and assess for signs of thrombosis, and document the action. The prescriber will likely interrupt therapy and resume at a lower dose when hemoglobin falls.

Scenario 5: Sucralfate for Lynn

What is causing her pain? Lynn is taking sucralfate at the wrong time. Sucralfate needs an acidic environment to form a sticky, paste-like gel that binds to proteins in the ulcer crater and creates a protective barrier against acid, pepsin and bile. When taken with food, the drug binds to food proteins instead and gastric acidity is buffered, so less of it adheres to the ulcer. Her ulcer remains exposed to acid secreted during meals, which causes pain after eating.

How can it be resolved?

• Teach Lynn to take sucralfate on an empty stomach, 1 hour before meals and at bedtime, as prescribed.
• If she takes antacids, separate them from sucralfate by at least 30 minutes, and take other medicines, such as levothyroxine, fluoroquinolones, digoxin or warfarin, 2 hours apart, because sucralfate binds and reduces their absorption.
• Avoid smoking, alcohol, caffeine and NSAIDs, which worsen ulcers.
• Prevent constipation, the most common side effect, with fluids and fiber.
• Continue the full course, usually 4 to 8 weeks, even if pain improves. If pain persists after correcting the timing, or if she has black stools, vomiting blood or severe pain, she should contact her provider for evaluation, including H. pylori testing and possible addition of a proton pump inhibitor.

References

Baker, R. D., Greer, F. R., & Committee on Nutrition. (2010). Diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children (0–3 years of age). Pediatrics, 126(5), 1040–1050. https://doi.org/10.1542/peds.2010-2576

Vilstrup, H., Amodio, P., Bajaj, J., Cordoba, J., Ferenci, P., Mullen, K. D., Weissenborn, K., & Wong, P. (2014). Hepatic encephalopathy in chronic liver disease: 2014 practice guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology, 60(2), 715–735. https://doi.org/10.1002/hep.27210

[Your pharmacology textbook, in APA format.]

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