ALTERATIONS IN CELLULAR PROCESSES
BY DAY 3 OF WEEK 1
Post an explanation of the disease highlighted in the scenario you were provided. Include the following in your explanation:
The role genetics plays in the disease.
Why the patient is presenting with the specific symptoms described.
The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
The cells that are involved in this process.
How another characteristic (e.g., gender, genetics) would change your response.
Read a selection of your colleagues’ responses.
BY DAY 6 OF WEEK 1
Respond to at least two of your colleagues on 2 different days and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not.
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Collapse SubdiscussionKadiatu Fofanah
Kadiatu Fofanah
Nov 28, 2022Nov 28, 2022 at 1:53pm
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We nurses must know how medications operate, their side effects, contraindications, and indications, and watch for predicted effects and situations that may alter, inhibit, or even cause a life-threatening reaction. I recall in nursing school how we always brought our drug handbook and did drug studies for each patient’s meds. We were educated to examine drug action, side effects, patient family training, and the seven rights of medicine administration. Pharmacokinetics shows the drug’s journey from intake to excretion. Pharmacodynamics shows the body’s response to that medicine. Acetaminophen is usually given orally to individuals with fever or pain, then metabolized and eliminated. Acetaminophen is processed by the liver, so we should be careful while giving it to liver patients. Acetaminophen reduces fever and pain, reflecting pharmacodynamics.
I admitted a male African-American patient a year ago with chest pain, body malaise, hypotension, tachycardia, disorientation, and brown urine. The first diagnosis was rhabdomyolysis R/O sepsis. We suspected liver disease due to the patient’s jaundice and low hemoglobin. After hydration, blood transfusion, and antibiotic treatment, patient stabilized, oriented, and spoke. During grand rounds, he told us he took 325mg of aspirin for chest trouble and went downhill from there. A quick fluorescent spot test, G6PD enzyme test, and 6-hour CBC were recommended by one doctor. Patient has G6PD deficiency, but is unaware. The patient doesn’t know if he underwent neonatal screening or was notified of any abnormalities. As a G6PD deficient person, he was smart enough to take aspirin for his chest problems, but it had a negative effect on him.
The above situation is an example of an idiosyncratic effect, which is a genetically predisposed pharmacological response (Rosenthal, 2021). Aspirin, acetaminophen, anti-malarials, and sulfonamides can cause mild to life-threatening RBC hemolysis in people with G6P deficiency (Frank, 2005). (Rosenthal, 2021).
Disease G6PD Background
G6PD insufficiency, the world’s most common enzyme deficit, causes RBCs to malfunction and break down faster (Bubp, Jen, Matuszewski,2015). This causes neonatal hyperbilirubinemia, acute hemolysis, and chronic hemolysis (Frank,2005). Hemolytic anemia is G6PD deficiency’s most dangerous symptom. Fatigue, back pain, tachypnea, tachycardia, and jaundice are other symptoms.
Contributors
G6PD affects 10% of American Blacks, regardless of ethnicity or gender. Males are more likely to develop symptomatic G6PD deficiency, a recessive X-linked condition (Kumar, Abbas, Fausto, Aster,2010).
Care plan
I needed to work well with the healthcare staff to help this patient recover and prevent sickness. The patient needs extensive collaborative discharge education given his condition.
Assessment – evaluate patient understanding of the disease, its process, triggers, and emergency procedures. The patient’s health education depth and type will be measured by this. Goal-setting.
Plan—after gathering information, we may decide who, how, where, and when to educate health. Educational participants? The how is the strategy in rendering the schooling. Where and when is execution? This is a collaboration of health care team for patient betterment. Goal-setting. Planned:
Medication/s – learning from his experience, there were several medications he needed to avoid, so he worked with the pharmacist to give a list and advise his PCP. This is crucial to avoid his hospitalization issues.
Disease education – even with G6PD deficiency, health education can optimize health if he avoids trigger foods and medications. Also, via education we build self-awareness.
Referrals – asking the attending Physician to refer him to a specialist: geneticist or Hematologist. Referral to G6PD deficient patients, families, and friends support group for help, support, information, and hope.
Nutrition and dietician – ask for a food list that needs to be avoided to prevent occurrence of trigger a. Miscellaneous – Flagging his medical record as a G6PD deficient patient will alert doctors to avoid certain medications if he is readmitted. Like in an allergy flag, that inhibits the physician from ordering medications that patient/s is are allergic hence, minimizing the occurrence of adverse reaction and medication error.
Implementation — execution of the plan. It’s crucial to introduce the strategy one at a time to avoid overwhelming the patient. Thus, the patient can absorb and retain information.
Evaluation – Determine if this patient’s aim was achieved. The goal is to educate the patient so he doesn’t relapse, and testing his knowledge by his capacity to express what triggers are and how to avoid them, attend his recommendation from doctors, and obtain support from support groups is one way to tell if he understands health education. This care plan may have been a terrific chance. While it was saddening to know that after 3 days of working with the patient, he was transferred to the city hospital for further evaluation, it was a very challenging opportunity for me to determine how some medication works, interacts, and manifests itself in patients with unknown underlying conditions.
References:
Bubp, Jeff, et al. “Caring for Glucose-6-Phosphate Dehydrogenase (G6PD)-Deficient Patients:
Implications for Pharmacy.” P & T : a Peer-Reviewed Journal for Formulary Management,
MediMedia USA, Inc., Sept. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4571844/.
Frank, Jennifer E. “Diagnosis and Management of G6PD Deficiency.” American Family Physician, 1 Oct.
2005, www.aafp.org/afp/2005/1001/p1277.html.
Huether, Sue E., et al. Understanding Pathophysiology. Elsevier, 2017.
Kumar, Vinay, et al. Robbins and Cotran Pathologic Basis of Disease. Saunders/Elsevier, 2010.
Rosenthal, Laura D., and Jacqueline Rosenjack Burchum. Lehne’s Pharmacotherapeutics for Advanced
Practice Nurses and Physician Assistants. Elsevier, 2021.
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Collapse SubdiscussionJennifer Tran
Jennifer Tran
Nov 30, 2022Nov 30, 2022 at 2:01pm
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Hi Kadiatu. Thank you for the well written informative piece. Please check in your inbox on CANVAS. Thank you.
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Collapse SubdiscussionSherwin Jackson
Sherwin Jackson
Dec 2, 2022Dec 2, 2022 at 11:47pm
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Kadiatu Smith
This is a very informative discussion that looks at a typical case study of the drug effects of a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. It describes an idiosyncratic effect when the patient in the case study takes aspirin for chest pain and develops complications without knowing he has G6PD deficiency. Glucose-6-phosphate dehydrogenase deficiency is an enzyme in all body cells’ cytoplasm. It plays an important role in preventing cellular damage from reactive oxygen species by providing substrates that prevent oxidative damage (S. Russ Richardson & O’Malley, 2019). With the deficiency, aspirin may induce mild to life-threatening red blood cell hemolysis due to the absence of protective substrates preventing damage to the cells, as was the case in the case study provided. The discussion provides a well-reasoned care plan and treatment plan to ensure the patient’s recovery. From the study, the patient was well managed due to the swift response by the healthcare team to investigate a fluorescent spot test, G6PD enzyme test, and a 6-hour CBC that enabled the diagnosis of G6PD deficiency to be made.
References
Russ Richardson, & O’Malley, G. F. (2019, May 2). Glucose 6 Phosphate Dehydrogenase (G6PD) Deficiency. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK470315/Links to an external site.
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Collapse SubdiscussionSherwin Jackson
Sherwin Jackson
Dec 9, 2022Dec 9, 2022 at 10:05am
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Kadiatu Smith
This is a very informative discussion that looks at a typical case study of the drug effects of a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. It describes an idiosyncratic effect when the patient in the case study takes aspirin for chest pain and develops complications without knowing he has G6PD deficiency. Glucose-6-phosphate dehydrogenase deficiency is an enzyme in all body cells’ cytoplasm. It plays an important role in preventing cellular damage from reactive oxygen species by providing substrates that prevent oxidative damage (S. Russ Richardson & O’Malley, 2019). With the deficiency, aspirin may induce mild to life-threatening red blood cell hemolysis due to the absence of protective substrates preventing damage to the cells, as was the case in the case study provided. The discussion provides a well-reasoned care plan and treatment plan to ensure the patient’s recovery. From the study, the patient was well managed due to the swift response by the healthcare team to investigate a fluorescent spot test, G6PD enzyme test, and a 6-hour CBC that enabled the diagnosis of G6PD deficiency to be made.
References
Russ Richardson, & O’Malley, G. F. (2019, May 2). Glucose 6 Phosphate Dehydrogenase (G6PD) Deficiency. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK470315/Links to an external site.
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Collapse SubdiscussionTyesha L Sullivan
Tyesha L Sullivan
Nov 29, 2022Nov 29, 2022 at 11:27am
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Everyone is expected to eat healthy meals and benefits include obtaining vitamins and minerals the foods contain. When our bodies fail to absorb the vitamins and minerals this causes malabsorption and can lead to problems throughout the body systems. In this case study, the 83-year-old resident has symptoms of malabsorption with generalized edema and protein malnutrition. According to McCance & Huether (2019), malabsorption is the failure of the intestinal mucosa to absorb the digested nutrients. Malabsorption syndrome is thought to be genetic in nature. This is because one of the malabsorption syndromes conditions (hereditary folate malabsorption) is an inherited condition characterized by a systemic and central nervous system.
The patient is presenting with generalized edema to the extremities and abdomen due to the lack of protein in the body (Malabsorption Syndrome: Causes, Symptoms, and Risk Factors, 2020). The deficiency of protein caused the water and salt to leak out of the cells. The physiologic response to the malabsorption syndrome is causing the swelling of the abdomen due to fluid being trapped in the patient’s tissues. This fluid can be the cause of the patient’s lack of appetite also. The cells affected in this disease are the mucosal cells of the small intestine. Malabsorption affects different groups differently. My response would differ based on gender and age. For example, malabsorption In women, it stops the menstruation, and in children, stunted growth is observed.
References
Malabsorption Syndrome: Causes, Symptoms, and Risk Factors. (2020). Retrieved 29 November 2022, from https://www.healthline.com/health/malabsorptionLinks to an external site.
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
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Collapse SubdiscussionJennifer Tran
Jennifer Tran
Nov 29, 2022Nov 29, 2022 at 12:45pm
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Hi Tyesha. Thank you for your informative post. Correct, malabsorption refers to impaired absorption of nutrients. With that said, it encompasses defects that occur during digestion and absorption of nutrients from food. Other differential diagnoses that can cause malabsorption are celiac disease, Crohn’s disease, lactose intolerance, etc. (McCance, 2019)
