Instructions: Respond by extending, refuting/correcting, or adding additional nu
Instructions: Respond by extending, refuting/correcting, or adding additional nuance to their posts. Must have intext citation and one reference, and 150 words.Your assignment will be graded according to the grading rubric.
Discussion Rubric
CriteriaRatingsPoints
Identification of Main Issues, Problems, and Concepts
Distinguished – 5 points Identifies and demonstrates a sophisticated understanding of the issues, problems, and concepts.
Excellent – 4 points Identifies and demonstrates an accomplished understanding of most issues, problems, and concepts.
Fair – 1-3 points
Identifies and demonstrates an acceptable understanding of most issues, problems, and concepts.
Poor – 0 points
Identifies and demonstrates an unacceptable understanding of most issues, problems, and concepts. Or nothing was posted.
5 points
Use of Citations, Writing Mechanics, and APA Formatting Guidelines
Distinguished – 3 points
Effectively uses the literature and other resources to inform their work. Exceptional use of citations and extended referencing. High level of APA precision and free of grammar and spelling errors.
Excellent – 2 points
Effectively uses the literature and other resources to inform their work. Moderate use of citations and extended referencing. Moderate level of APA precision and free of grammar and spelling errors.
Fair – 1 point
Ineffectively uses the literature and other resources to inform their work. Moderate use of citations and extended referencing. APA style and writing mechanics need more precision and attention to detail.
Poor – 0 points
Ineffectively uses the literature and other resources to inform their work. Unacceptable use of citations and extended referencing. APA style and writing mechanics need serious attention. Or nothing was posted.
3 points
Response to Posts of PeersDistinguished – 2 points
Student constructively responded to two other posts and either extended, expanded, or provided a rebuttal to each.
Fair – 1 point
Student constructively responded to one other post and either extended, expanded, or provided a rebuttal.
Poor – 0 points
Student provided no response to a peer’s post.
2 points
Total Points 10
Discussion 2: Case Studies Hematopoietic and Cardiovascular
Gricarly Case Study 1: Hematopoietic
Contributing factors on J.D to develop Iron Deficiency Anemia
According to (Dlugasch & Story, 2021), Iron Deficiency Anemia (IDA) is the most widespread in the world. This type of anemia is most commonly seen in women of childbearing age, children younger than two years of age, and the elderly. It may be caused by decreased iron consumption, dietary intake of iron-containing vegetables or meat may be below the minimum requirement, particularly during the adolescent growth spurt or during pregnancy and breastfeeding, when needs increase; decreased iron absorption, duodenal absorption of iron may be impaired by many disorders, including malabsorption syndromes such as regional ileitis and achlorhydria or chronic blood loss from a bleeding ulcer, hemorrhoids, cancer, or excessive menstrual flow is a common cause of iron deficiency. Continuous blood loss, even small amounts of blood, means that less iron is recycled to maintain an adequate production of hemoglobin.
After analyzing the most common causes of this type of anemia, it can be said that J.D. has several contributing risk factors for developing iron deficiency anemia. Firstly, is a female, of reproductive age (37 years), who recently gave birth four months ago and has had a two-month history of blood loss due to intermenstrual bleeding and menorrhagia. Secondly, her prolonged use of NSAIDs (ibuprofen) led to gastrointestinal bleeding and the OTC use of PPIs Omeprazole. It has been speculated that inhibition of gastric acid secretion may reduce iron absorption (Kobets, 2021). It is also essential to investigate her diet to determine if there is a decrease in iron consumption.
Reasons why J.D. might be presenting constipation and or dehydration
Based on the patient’s clinical history, it is important to recognize that J.D. may experience dehydration and constipation due to several reasons. She states that she has an increase in urinary frequency, which may be related to the effect of diuretic medications that she takes to control her blood pressure, which can increase fluid loss, cause a fluid and electrolyte imbalance like low potassium levels in the blood (hypokalemia) and low sodium levels (hyponatremia), and exacerbate constipation. Hypokalemia and Hyponatremia are common side effects of thiazide diuretics that can lead to increased mortality and hospitalization due to dehydration and electrolyte imbalance (Kanchanasurakit et al., 2020) She is also known to take a centrally-acting antihypertensive, some of which can cause constipation as a side effect. Additionally, omeprazole can cause constipation, and NSAID use can contribute to dehydration by causing fluid retention.
Why Vitamin B12 and folic acid are important on the erythropoiesis? What abnormalities their deficiency might cause on the red blood cells?
Vitamin B12 and folic acid play a crucial role in erythropoiesis; they are necessary for cellular DNA synthesis in the red blood cell precursors. Deficiencies can lead to several abnormalities, such as the inability of the cell to undergo nuclear division, premature erythroblast apoptosis, and phagocytosis of precursor cells (Dlugasch & Story, 2021). When the bone marrow functions properly, a decrease in RBCs will result in a precursor increase and an acceleration of erythropoiesis to make more reticulocytes. The factors necessary to stimulate RBC production are erythropoietin and nutrients such as iron, vitamin B12, and folic acid. Deficiencies in any of these will decrease production, leading to anemia. Bone marrow dysfunction in the form of suppression or inadequate precursors from disease or treatment will result in decreased RBC production. Iron deficiency anemia and megaloblastic anemia are disorders of decreased RBC production.
Clinical symptoms that J.D. might have positive for Iron Deficiency Anemia
Iron Deficiency Anemia symptoms begin gradually, and individuals may not seek medical attention until hemoglobin levels have decreased to about 7 to 8g/dL. Nonspecific early symptoms include fatigue, weakness, shortness of breath, pale earlobes, palms, and conjunctivae (McCance et al., 2019).
In this case, the following clinical symptoms, like fatigue, weakness, and lack of energy, could be considered positive for diagnosing iron deficiency anemia in J.D. If the OBGYN thinks that the cause could be blood loss, it should also be considered that she had intermenstrual bleeding for two months and menorrhagia. Other clinical symptoms include headache, dizziness, syncope, breathing difficulties, and heart palpitations. The case does not describe them as a complaint; however, a detailed physical examination and interrogation should be performed to determine their presence.
Expected findings as Signs of Iron Deficiency Anemia
In IDA, it is common to find some specific characteristics as expected findings of the disease, pallor of the skin and mucous membranes due to a decrease of oxygen-carrying capacity of red blood cells, cyanosis of the sclera, structural and functional changes that occur in epithelial tissue. Koilonychia or spoon-shaped fingernails become brittle, thin, and coarsely ridged due to impaired capillary circulation. Other signs include cheilosis (scales and fissures of the mouth), stomatitis (inflammation of the mouth), painful ulcerations of the buccal mucosa and tongue characteristic of burning (glossitis), craving for non-food substances like ice or clay (pica). Difficulty in swallowing (dysphagia) is associated with an esophageal web, a thin, concentric extension of normal esophageal tissue consisting of mucosa and submucosa at the juncture between the hypopharynx and esophagus (McCance et al., 2019). Individuals with IDA also exhibit gastritis, neuromuscular changes, headache, irritability, tingling, numbness, and vasomotor disturbances.
Recommendations and Treatments for J.D.
According to lab results, the diagnostic of IDA is confirmed: low hemoglobin and hematocrit levels, low ferritin levels, and red blood cells that are smaller (microcytic) and paler in color. Appropriate recommendations for J.D. to increase iron levels would include dietary changes to increase consumption of iron-rich foods (e.g., liver, red meat, fish, beans, raisins, and green, leafy vegetables), foods or supplements high in vitamin C should be increased because vitamin C increases the absorption of iron. Treatment includes the identification and resolution of the underlying cause of the iron deficiency anemia (treating menorrhagia, discontinuation of NSAID use if possible), administering oral iron supplementation, and intravenous iron replacement if oral supplementation is not effective (Dlugasch & Story, 2021). Another essential point to consider is recommending evaluation by a Gastroenterologist to identify possible GI bleeding as a cause of this type of anemia, per her antecedents of long-term use of NSAID.
Case Study 2: Cardiovascular
Modifiable and non-modifiable risk factors for CAD and Acute Myocardial Infarct
Risk factors for CAD are the same as those for atherosclerosis and can be categorized as conventional (major) versus nontraditional (novel) and as modifiable versus nonmodifiable. Conventional or major risk factors for CAD that are non-modifiable include advanced age, male sex or women after menopause, family history, and genetics. Aging and menopause are associated with increased exposure to risk factors and poor endothelial healing. Family history may contribute to CAD through genetics and shared environmental exposures. Modifiable risk factors include dyslipidemia, hypertension, cigarette smoking, diabetes and insulin resistance, obesity, sedentary lifestyle, stress, and atherogenic diet. Fortunately, modifying these factors can dramatically reduce the risk of CAD and the development of Acute Myocardial events (McCance et al., 2019).
Expected EKG for Mr. W.G. and findings compatible with the acute coronary event
Acute myocardial infarction (AMI) is defined as severe insufficient blood supply to the coronary artery caused by coronary atherosclerosis or other reasons, leading to myocardial ischemia and hypoxia, and then ischemic necrosis, and it is a common cause of death in the elderly. Its primary clinical symptom is sudden and persistent precordial crushing pain, accompanied by radiating pain in the left shoulder, left forearm or left fingers, and jaw, which cannot be alleviated by rest or oral nitrates and has dynamic changes in electrocardiography (ECG) and laboratory biochemical examination (Jian hua Sun et al., 2023).
In this case, the expected findings to see on the EKG of Mr. W.G. that indicated acute myocardial infarction will be ST-segment elevation (STEMI), or ST-segment depression and T-wave inversion (NSTEMI). Also, the findings described in the case include the presentation and characteristics of the pain, which are acute chest pain or discomfort, crushing sensation in the sternal area, and irradiation to his neck and lower jaw. The GI symptoms include the patient complaining of feeling nauseated, not relieved after administration of 3 SL NTG tablets, and prolonged significant pain intensity of more than 20 min.
Specific laboratory test to confirm the Acute Myocardial Infarct
In the case of Mr. W.G., to determine an acute cardiac event, the most critical laboratory to do is the rapid detection of cardiac markers, specifically Cardiac Troponin I Levels (cTnI), that is a protein released to the bloodstream when there is damage to the heart muscle and can be detectable 2-4 after the onset of symptoms, which makes it highly specific for the diagnosis of myocardial infarct. Troponin levels can also be used to estimate infarct size, future CHD events, and the likelihood of complications, mortality, and heart failure. Additional measurements within 6 to 9 hours and again at 12 to 24 hours are recommended if clinical suspicion is high and previous samples were negative (McCance et al., 2019).
Explain Mr. W.G temperature increase after his Myocardial Infarct After Mr. W.G.’s myocardial infarction, there is a possibility that his body temperature might rise due to the inflammatory response triggered by the injury in myocardial tissue. This inflammatory response can cause the release of specific cytokines and other inflammatory mediators that can lead to fever. The increased temperature may be observed shortly after the infarct (first 24 hours) and may persist from a few days to a week as part of the acute phase reaction (Chen et al., 2023).
From a pathophysiological point of view, postinfarction fever has been recognized as a nonspecific inflammatory response to extensive myocardial damage because it is associated with elevated serum levels of myocardial enzymes and C-reactive protein. MI causes a severe inflammatory response that ends with wound repair. Damaged cells undergo degradation, fibroblasts proliferate, and scar tissue is synthesized. Within 24 hours, leukocytes infiltrate the necrotic area, and proteolytic enzymes released from scavenger neutrophils degrade the necrotic tissue. Macrophages remove dead cells and secrete growth factors, which help repair myocardial injuries. The deposited collagen matrix is initially weak, mushy, and vulnerable to reinjury. Unfortunately, at this time in the recovery period (10 to 14 days after infarction), individuals feel more like increasing activities and may stress the newly formed scar tissue. After 6 weeks, the necrotic area is entirely replaced by scar tissue, which is strong but cannot contract and relax like healthy myocardial tissue (McCance et al., 2019).
Explain to Mr. W.G. why he has pain during a Myocardial Infarct
During a heart attack, Mr. W.G. experienced pain due to a lack of blood flow to a region of the heart muscle, a condition known as myocardial ischemia. This condition leads to the release of chemical mediators in the heart, including adenosine, bradykinin, and prostaglandins, which stimulate pain receptors (nociceptors), causing chest discomfort or pain. The pain is often described as crushing and may radiate to the neck and jaw, which is a characteristic symptom of a myocardial infarct (McCance et al., 2019).
References
Chen, S.H., Chang, H.C., Chiu, P.W., Hong, M.Y., Lin, I.C., Yang, C.C., Hsu, C.T., Ling,
C.W., Chang, Y.H., Cheng, Y.Y., & Lin, C.H. (2023). Triage body temperature and its
influence on patients with acute myocardial infarction. BMC Cardiovascular
Disorders, 23(1), 388. https://doi.org/10.1186/s12872-023-03372-y.
Dlugasch, L., & Story, L. (2021). Applied Pathophysiology for the Advanced Practice
Nurse. Burlington, MA: Jones and Barlett Learning.
Jian hua Sun, Xiao kun Liu, Xiao wei Xing, Yang Yang, Hui hong Xuan, & Bin bin Fu. (2023) Value of Cardiac Troponin, Myoglobin Combined with Heart-type Fatty Acid-binding Protein Detection in Diagnosis of Early Acute Myocardial Infarction. Pakistan Journal of Medical Sciences, 39(6), 1690–1694.
Kanchanasurakit, S., Saokaew, S., Siriplabpla, W., Arsu, A., Boonmak, W., &
Watcharasiriphong, W. (2020). Development of a hyponatremia screening tool
(ABCDF‐S score) for patients with hypertension using thiazide diuretic agents. Journal of Clinical Pharmacy & Therapeutics, 45(5), 997–1005. https://doi.org/10.1111/jcpt.13123
Kobets, A. (2021). An Unusual Presentation of Iron-Deficiency Anemia: An
Autobiographical Case Report. Cureus 13(12): e20442. doi:10.7759/cureus.20442
McCance, C. K., Huether, E. S., Brashers, L. V., & Rote, S. N. (2019). Pathophysiology:
The biologic basis for disease in adult and children (8th ed). Elsevier.