NUR242 Acute Nursing Care Case Study Sample

NUR242 Acute Nursing Care Case Study

Assignment Details

Case:

You are working in a remote community health clinic. John is a 65-year-old male who comes to your clinic complaining of stomach pain, especially after eating. He thinks he might have a stomach ulcer. He also states that he is always feeling tired, sometimes gets dizzy and he finds it difficult to breathe. John also tells you that he is often constipated.

On further questioning John tells you that he suffers from osteoarthritis in his knees and in addition, he was in a car accident several years ago and suffers from chronic back pain. John regularly smokes cigarettes and is a regular heavy drinker of alcohol.

John tells you that he takes the following medications consistently for his medical conditions:

Aspirin 300 mg every 4-6 hours as required.

Morphine 30 mg twice daily as required

John has also been drinking at least 6 –8 heavy strength beers every night as he claims it helps with his pain.

You consider that John’s symptoms could be related to several new medical conditions however, they have been ruled out.

Even though John is taking his medications within recommended dosage guidelines, you now suspect that John’s symptoms could be related to his medications and alcohol intake.

Questions:

Q1. Detail the pharmacological mechanism of action (MOA) of aspirin and morphine. The MOA needs to be explained in depth at the receptor and cellular level and needs to include how the MOA results in a therapeutic effect. Also, explain how this mechanism affects the action potential of the cell.

Q2. Look at Johns presenting complaints. Explain which medication could be responsible for each of John’s complaints and why. You will need to explain in depth, at the receptor and cellular level, the mechanism of action of the medication and how it could cause the symptom that John is experiencing.,

Q3. A) What is the mechanism of actions (MOAs) of alcohol? You need to describe these MOA’s in detail at the receptor and cellular level.

B) Describe any interactions between John’s medications and any other substances that John consumes? Explain pharmacologically how these substances interact with John’s medicines at the receptor and cellular level and what could be the consequences of these interactions.

Q4. A) Based on your answer to Q2, What immediate actions would you recommend to John in order to prevent further complications with his ulcer?

B) John goes to the doctor to treat his ulcer. Using your knowledge of pharmacology, what recommendations might the doctor make regarding managing the side effects that John has experienced due to interactions with his pain medications?
Your recommendations must be in line with current therapeutic guidelines and Recommendations must be supported with current evidence from the literature.

Please use referenced evidence to support all your answers to the above questions. (e.g. journal articles, textbooks, valid medical websites with authors etc).

Solution

Q1. Mechanism of Action (MOA) of Aspirin and Morphine:

Aspirin (Acetylsalicylic Acid):

Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin function mostly through the inhibition of the cyclooxygenase (COX) enzymes COX-1 and COX-2 (Tsoupras et al., 2024). By blocking these enzymes, the synthesis of lipid chemical mediators called prostaglandins, which are part of the inflammatory response, is restrained. Tissue injury or invasion by pathogens also registers through the effects of prostaglandins, which are produced locally and act to produce inflammation, pain, fever, and vasodilation. Aspirin-It works by inhibiting COX enzymes and diminishing these effects.

At the Receptor and Cellular Level:

This is because aspirin irreversibly acetylates a serine residue in the active site of COX enzymes. This inhibits the enzyme from transforming arachidonic acid to prostaglandins. COX-1 is constitutively expressed in most tissues and contributes to several physiologic functions, including protection of the gastrointestinal (GI) tract lining by stimulating mucus secretion and regulating gastric acid production. Inducible isoform( COX-2) (Dickerson et al., 2025): Enzymes involved in inflammation and pain. So, while aspirin’s inhibition of COX-1 decreases pain and inflammation, it can also cause overlain to stomach issues like ulcers, bleeding, and irritation.

Effect on Action Potential:

Aspirin produces an indirect inhibition of nociceptive pathways involved in the perception of pain by reducing the production of prostaglandin. Both prostaglandins sensitize pain receptors (nociceptors), and lowering their concentrations dulls pain signaling. The activity of aspirin does not directly modulate the cellular action potential, but involves the regulation of the inflammatory response that sensitizes nociceptors and therefore reduces the magnitude of pain.

Morphine:

Morphine is an opioid analgesic that mainly acts on the CNS by binding to opioid receptors, mainly the mu-opioid receptor for MBA assignment expert that binding workflow yields analgesia, euphoria, and sedation.

Receptor and Cellular Level:

Morphine exerts this action by binding to the mu-opioid receptor (MOPr), a member of the G-protein coupled receptors (GPCRs), primarily present in the central nervous system (CNS) and peripheral tissues. In contrast, and once bound, morphine activates the receptor which subsequently inhibits adenylate cyclase and reduces cellular levels of cyclic AMP (cAMP). This leads to the opening of potassium channels and the inhibition of calcium channels. Outflow of potassium hyperpolarizes the neuron, and the decreased calcium influx prevents the release of neurotransmitter (Rullo et al., 2024). This reduces neuronal excitability and the transmission of pain signals.

Effect on Action Potential:

In fact, the mechanisms of action of morphine on neuronal action potentials mainly occur due to the hyperpolarization of neurons through the efflux of potassium, and the calcium influx inhibition. Morphine decreases our ability to generate action potentials and thus dampens the transmission of pain signals and produces its analgesic effects. But this can also produce side effects including respiratory depression, constipation and euphoria.

Q2. John’s Complaints and Medication Impact:

1. Stomach Pain (Possibly an Ulcer):

Aspirin -- Aspirin can cause stomach irritation and ulcers, mainly due to the inhibition of COX-1. COX-1 participates in the synthesis of protective prosta-glandins that provoke secretion of mucus and bicarbonate protecting the gastric mucosa from the action of acid (Zhou et al., 2024). When COX-1 is inhibited, this protective effect is diminished and the epithelial cells of the stomach become more susceptible to damage from stomach acid.

Mechanism: COX-1 inhibition decreases prostaglandin formation, which disrupts gastric mucosal protection and increases the risk of ulcer development and GI bleeding

2. Fatigue, Dizziness, and Breathing Difficulty:

Morphine: As an opioid, morphine can cause dizziness, sedation and respiratory depression. It attaches to the mu-opioid receptor in the brainstem, which controls respiration. Morphine can produce shallow breathing through a reduction in the respiratory drive, which can give rise to hypoxia that contributes to fatigue and dizziness.

Decreased sensitivity to CO2 levels and inhibition of brainstem activity results from the mechanism leading to respiratory depression.

3. Constipation:

Morphine: Opioids (such as morphine) are notorious for causing constipation. This happens because morphine binds to opioid receptors within the gastrointestinal tract, decreasing peristalsis and gastrointestinal motility.

Q3. Alcohol’s Mechanism of Action and Interactions:

A) Inhibition and Action of Alcohol: Alcohol (ethanol) exerts its effects mainly through interaction with various neurotransmitter systems in the central nervous system (CNS) Its main actions are on gamma-aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) receptors.

• GABA Receptors: Alcohol potentiates the effects of GABA, the main inhibitory neurotransmitter in the CNS. Alcohol really enhances the strength of GABA’s bond with its receptor, and in doing so, the chloride ions are plentiful in their flowing into the neuron making the cell hyperpolarized and less likely to fire an action potential (Sambo et al., 2024). This creates the sedative and calming effects of alcohol.

• Upregulation of NMDA Receptors: Alcohol is an NMDA receptor antagonist and thus has inhibitory actions on excitatory neurotransmission via glutamate (Dguzeh et al., 2018). This aggravates the depressant effects of alcohol by reducing excitability in the brain through NMDA receptor inhibition.
B) Alcohol and Medication Interactions:

• Aspirin and Alcohol: Taking alcohol together with aspirin increases the risk of gastrointestinal bleeding and ulcer formation. It may do this by irritating the stomach lining and thus worsening gastric mucosal damage wrought by aspirin’s inhibition of COX-1. This combination increases the risk of peptic ulcers and gastrointestinal bleeding significantly (Zhou et al., 2024).

Q4. Recommendations:

A) Immediate Actions to Prevent Ulcer Complications:

• Limit or avoid alcohol: Alcohol should be avoided, as it can increase gastric irritation and bleeding risks.

• Change to a safer analgesic: Switching from aspirin to a COX-2 selective inhibitor, such as celecoxib, confers a lower risk of side effects on the stomach.

• Proton pump: Proton pump can prevent the formation of gastric acid, which can prevent the formation of inflammation (Morris & Nighot 2023).

• Keep an eye out for signs of GI bleeding, and intervene as per the need be.

B) Doctor's Recommendations for Managing Pain Medication Side Effects:

• Manage opioid-related constipation: Advise judicious use of laxatives or opioid antagonists such as methylnaltrexone, which help prevent opioid-induced constipation without diminishing pain relief efficacy.

• Explore nonopioid alternatives: If applicable, the doctor may suggest non-opioid pain management approaches, such as nonsteroidal anti-inflammatory drugs (NSAIDs) with lower risk for gastrointestinal complications, physical therapy or nerve blocks.

References:

Dguzeh, U., Haddad, N. C., Smith, K. T. S., Johnson, J. O., Doye, A. A., Gwathmey, J. K., & Haddad, G. E. (2018). Alcoholism: A multi-systemic cellular insult to organs. International Journal of Environmental Research and Public Health, 15(6), 1083. doi:https://doi.org/10.3390/ijerph15061083

Dickerson, A. G., Joseph, C. A., & Kashfi, K. (2025). Current approaches and innovations in managing preeclampsia: Highlighting maternal health disparities. Journal of Clinical Medicine, 14(4), 1190. doi:https://doi.org/10.3390/jcm14041190

Morris, N., & Nighot, M. (2023). Understanding the health risks and emerging concerns associated with the use of long-term proton pump inhibitors. Bulletin of the National Research Centre, 47(1), 134. doi:https://doi.org/10.1186/s42269-023-01107-9

Rullo, L., Morosini, C., Lacorte, A., Cristani, M., Coluzzi, F., Candeletti, S., & Romualdi, P. (2024). Opioid system and related ligands: From the past to future perspectives. Journal of Anesthesia, Analgesia and Critical Care, 4(1), 70. doi:https://doi.org/10.1186/s44158-024-00201-2

Sambo, D., Kinstler, E., Lin, Y., & Goldman, D. (2024). Differential effects of prenatal alcohol exposure on brain growth reveals early upregulation of cell cycle and apoptosis and delayed downregulation of metabolism in affected offspring. PLoS One, 19(11) doi:https://doi.org/10.1371/journal.pone.0311683

Tsoupras, A., Gkika, D. A., Siadimas, I., Christodoulopoulos, I., Efthymiopoulos, P., & Kyzas, G. Z. (2024). The multifaceted effects of non-steroidal and non-opioid anti-inflammatory and analgesic drugs on platelets: Current knowledge, limitations, and future perspectives. Pharmaceuticals, 17(5), 627. doi:https://doi.org/10.3390/ph17050627

Yang, W., Singla, R., Maheshwari, O., Fontaine, C. J., & Gil-Mohapel, J. (2022). Alcohol use disorder: Neurobiology and therapeutics. Biomedicines, 10(5), 1192. doi:https://doi.org/10.3390/biomedicines10051192

Zhou, Z., Webb, K. L., Nelson, M. R., Woods, R. L., Ernst, M. E., Murray, A. M., . . . Wolfe, R. (2024). Short- and long-term impact of aspirin cessation in older adults: A target trial emulation. BMC Medicine, 22, 1-11. doi:https://doi.org/10.1186/s12916-024-03507-8