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Hematopoietic
1- Name the contributing factors on J.D that might put her at risk to develop iron deficiency anemia.
J.D is suffering from abnormal uterine bleeding (AUB) characterized by a regular menstrual cycle variation. The variation can be in terms of heavy blood flow, prolonged menses, and the regularity of the flow of menses (Davis & Sparzak, 2019). One of the contributing factors that put J.D at the risk of developing iron-deficiency anemia, is that she loses so much blood due to her heavy menses (menstrual period 6 days of duration with heavy loss blood), J.D has been suffering from inter-menstrual bleeding and metrorrhagia which causes her to lose further blood leading to iron deficiency anemia. Another factor is that J.D has history of G5P5 and she had four deliveries in the past four years, and the last child was delivered four months ago via vaginal delivery, exposing her to heavy loss of blood during birth. Hence patient physiological iron reserve has suffered causing a wear out of her reservoir. The history of osteoarthritis in the left knee has contributed to the continuous use of ibuprofen, three tablets each day, for about 2 1⁄2 years ago; contributing to gastrointestinal bleeding, worsening the blood loss condition and therefore the iron deficiency anemia.
2- Within the case study, describe the reasons why J.D. might be presenting constipation and or dehydration.
J.D. Might Be Presenting dehydration and constipation due many factors, like the dehydration caused due to the blood loss the patient suffered together with the urinary incontinence and the use of diuretics for the treatment of HTN. The interaction of these factors originated the patient dehydration. The constipation is related to dehydration because of the increase in the absorption of water at the level of the GI system, which causes the stool to be drier. The medications to lower blood pressure taken by the patient has caused also constipation due to the decrease in blood flow at the level of the GI, which causes bowel movement to be decreased simultaneously (Soundarya & Suganthi, 2017).
3- Why Vitamin B12 and folic acid are important on the erythropoiesis? What abnormalities their deficiency might cause on the red blood cells?
Erythropoiesis refers to the erythrocytes production process. On daily basis, old phagocytksed erythrocytes are destroyed and replaced by new erythrocytes. The erythropoiesis process, however, requires vitamin B12, folate, and iron to occur (Soundarya & Suganthi, 2017). A deficiency in vitamin B12 or folate hinders the synthesis of thymidylate and purine, inhibits the synthesis of DNA, and leads to erythroblast apoptosis, resulting in anemia because of inhibited erythropoiesis. Folic acid/folate and vitamin B12 are two B vitamins that are necessary for both the production of red blood cells and for the utilization of iron, what causes a diphase development between the nucleus of the cell and the cytoplasm, therefore creates a deficit of B12 and folic acid originating a megaloblastic anemia.
4- The gynecologist is suspecting that J.D. might be experiencing iron deficiency anemia.
In order to support the diagnosis, list and describe the clinical symptoms that J.D. might have positive for Iron deficiency anemia.
Some of the clinical symptoms of anemia include general body weakness, having yellow "sallow" skin, extreme fatigue, lightheadedness and headache, cold feet and hands, craving and chewing substances that have no nutritional value (PICA), shortness of breath, chest pains, spoon nails (koilonychia), and brittle nails (Koury & Ponka, 2014). In J.D's case, the patient is experiencing extreme fatigue and body weakness. Given that anemia is caused by the lack of enough red blood cells in the body (intermenstrual bleeding and menorrhagia) an anemic person experiences extreme fatigue because the vital body organs do not receive adequate oxygen to enable metabolism, which produces energy. Because of this reason body weakness and body organs share the same problems, just because they do not receive enough oxygenated blood (Walker J, et al., 2016).
5- If the patient is diagnosed with iron deficiency anemia, what do you expect to find as signs of this type of anemia? List and describe.
Medical sing is an objective indication of a disease, or abnormal physiological state that may be detected during the physical examination of a patient (Walker J, et al., 2016). In iron deficiency anemia diagnosis, we can find signs as:
· Pale skin, cold hands and feet: the poor oxygenation of blood due to the present anemia, lowering the peripheral blood flow due to the main blood supply been sent to vital organs like brain, kidney and heart.
· Brittle nails and spoon nails (koilonychia) nail matrix changes due to blood flow.
· Tachycardia: the heart tends to compensate for the lack of red blood cells reaching body’s tissues by pumping faster in response to hypoxia.
· Irritability: this is the brain response to the oxygen deficit (hypoxia) cause by the anemia.
· Low red blood cell count than normal, low levels of hemoglobin, low corpuscular volume, or low hematocrit levels. These signs suggest anemia because the body is unable to process red blood cells in the absence of iron.
6- Labs results came back for the patient. Hb 10.2 g/dL; Hct 30.8%; Ferritin 9 ng/dL; red blood cells are smaller and paler in color than normal. Research list and describe for appropriate recommendations and treatments for J.D.
Labs results are showing a low level of Hb (normal range 12.1 to 15.1 g/dL), Hct (normal range 35.5 to 44.9), ferritin (normal range 18 to 39 years. 12 to 263 ng/dL), and red blood cells smaller and paler in color than normal; consistent with iron deficiency anemia. Treatment for iron-deficiency anemia will depend on its cause and severity. Treatments may include iron supplements, procedures, surgery, and dietary changes. Severe iron-deficiency anemia may require intravenous (IV) iron therapy or a blood transfusion. Ferrous sulfate and vitamin C are the most recommended treatment for this condition, and it should be followed for a minimum period of 2 months to replenish iron in the body effectively (Soundarya & Suganthi, 2017). J.D may also need to change her diet, patterns that can include foods that are rich in iron, mostly dark green leafy vegetables, baked potatoes, beans, cashews, lentils, cereals, liver, red meat, and enriched whole-grain bread. Lastly, for the abnormal uterine bleeding, J.D should consider using a hormonal management therapy. Some of the treatments may include oral contraceptives, IV conjugated equine estrogen, and progestin. By taking these steps, J.D will prevent heavy blood flow.
Cardiovascular
1- For patients at risk of developing coronary artery disease and patients diagnosed with acute myocardial infarct, describe the modifiable and non-modifiable risk factors.
Myocardial infarction refers to a pathological condition that occurs when the blood supply is highly compromised to the myocardium area to the level where a person cannot obtain adequate oxygen even when resting (Giordano et al., 2017). Myocardial infarction is characterized by symptoms such as epigastric discomfort, sweating, chest pains, anxiety, and general malaise. The symptoms are influenced by various non-modifiable predisposing risk factors such as age, family history and gender; even thought for long is been considered a men’s disease. Another factor to mention is ethnicity; people with African or Asian ancestry are at higher risks of developing a cardiovascular disease than other racial groups, together with the socioeconomic status: being poor, no matter where in the globe, increases your risk of heart disease and stroke.
There are modifiable risk factors such as diabetes, alcohol use, hypertension, high-risk diets, physical inactivity, being overweight, psychosocial stress, smoking, and high blood cholesterol with abnormal lipids. The good news is that these ones compare to the non-modifiable can be changed (you cannot change a risk factor, only its effect). The effect of these modifiable risk factors can be reduced if you make lifestyle changes (Kumar & Sinha, 2018).
2- What would you expect to see on Mr. W.G. EKG and which findings described on the case are compatible with the acute coronary event?
In acute myocardial infarction, the diagnosis is based on the clinical findings, electrocardiographic (EKG) changes evaluation and the patient's history. When a 12-lead EKG is performed on a patient who has cardiac tissue experiencing myocardial ischemia, several changes may be seen, including: ST-segment depression, T-wave inversion, and a transient ST-segment elevation. An EGK is also used to assess irregular heart rate and irregular heart rhythm. A heart that beats more than 60-100 times/min or slower indicates that a person needs medical attention, however, the most provisional diagnosis for MI is established when a patient presents a severe oppressive pain around the lower sternum, or experiences an extensive pain around the anterior chest for 30 minutes and above (Kumar, & Sinha, 2018).
This pain can also not be relieved by rest or nitrates. The increase in the rate of erythrocyte sedimentation, can be contribute to the presence of leukocytosis, fever, and the increase in troponin, CPK levels supporting the MI diagnosis. Some of the symptoms experienced by Mr. W.G. that are compatible with the EKG results include chest discomfort, crushing pain over the sternal area, and the pain spread upward into his neck and lower jaw.
3- Having only the opportunity to choose one laboratory test to confirm the acute myocardial infarct, which would be the most specific laboratory test you would choose and why?
The American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC) guidelines recommends that cardiac biomarkers should be measured if presented in patients with suspected MI. The only biomarker that is best recommended to be used for the diagnosis of acute MI at this time, is cardiac troponin due to its superior sensitivity and accuracy. Troponin (Tn) is found on the thin filaments of the cardiac and skeletal muscle fibers and is made up of three complex proteins, which include TnT, TnL, and TnC. Troponin T refers to a cardio-specific polypeptide that is attached to the contractile elements of the myocardial cells. Within the first few hours of myocardial infarction, cardiac troponin T is produced and released to the bloodstream. This one is a contractile protein that normally is not found in serum and is only released when myocardial necrosis occurs. Labs results are given in nanogram per milliliter (ng/mL). The normal range for troponin is between 0 and 0.4 ng/ml. It is said that modern assays can detect troponin as early as 3-4 hours after onset of myocardial damage (Giordano et al., 2017).
4- How do you explain that Mr. W.G temperature has increased after his Myocardial Infarct, when that can be observed and for how long? Base your answer on the pathophysiology of the event.
The increased body temperature was due to the inflammatory reaction that occurs because of the myocardial necrosis. Temperature often increase by more than 1°C, on average, as early as 4 to 8 hours after infarction onset, and they usually resolve by the fourth to fifth day; and has been recognized as a nonspecific response to wide myocardial damage because it is associated with elevated serum levels of myocardial enzymes and C‐reactive protein. Pathological mechanisms underlying remain poorly understood; but one of them explain that Myocardial necrosis induces infiltration of inflammatory cells, including neutrophils, monocytes, and macrophages. These cells lead to synthesis of various cytokines, including interleukin‐1, interleukin‐6, interleukin‐8, tumor necrosis factor‐α, and interferon‐γ, which act as endogenous pyrogens (Solomon et al., 2020).
5- Explain to Mr. W.G. why he was experiencing pain during his Myocardial Infarct. Elaborate and support your answer.
Mr. W.G experienced a sensation that was crushing around the sternal area. This pain radiated upwards towards the neck and the lower jaw and did not appear to disappear even with deep breaths. Chest pain is the most common present complaint of acute myocardial infarction. The classic manifestation of ischemia is usually described as a heavy chest pressure or squeezing, a “burning” feeling, or difficulty in breathing. The discomfort or pain often radiates to the left shoulder, neck, or arm. Chest pain may be atypical in few cases and it builds in intensity over a period of few minutes. The pain may begin with exercise or psychological stress, but acute myocardial infarction most commonly occurs without obvious precipitating events. Pain during a heart attack is a classic example of referred pain, which felt at a site distant from the site of origin. Under these circumstances action potentials may be transmitted along pathways that convey information from parts of the orofacial and shoulder region unrelated to the source of the noxious peripheral stimulus. The brain therefore can become confused as to the correct location of the initiating noxious stimulus. The pain is caused by the squeezing and pressure exerted in the arteries as the blood tries to move, making the feeling a classic manifestation of ischemia (Solomon et al., 2020).
References
Davis, E., & Sparzak, P. B. (2019). Abnormal Uterine Bleeding (Dysfunctional Uterine Bleeding). In StatPearls [Internet]. StatPearls Publishing.
Giordano, S., Estes, R., Li, W., George, R., Gilford, T., Glasgow, K., ... & Chiasera, J. M. (2018). Troponin Structure and Function in Health and Disease. American Society for Clinical Laboratory Science.
Koury, M. J., & Ponka, P. (2014). New insights into erythropoiesis: the roles of folate, vitamin B12, and iron. Annu. Rev. Nutr., 24, 105-131.
Kumar, R., & Sinha, A. (2018). Diagnosis of Acute Myocardial Infarction in Left Bundle Branch Block. EC Cardiology, 5, 467-472.
Solomon, R., Nowak, R., Hudson, M., Moyer, M., Jacobsen, G., & McCord, J. (2020). Is the duration of symptoms predictive of acute myocardial infarction?. Current Problems in Cardiology, 100555.
Soundarya, N., & Suganthi, P. (2017). A review on anemia–types, causes, symptoms, and treatments. Journal of science and technology investigation, 1(1).
Walker J, Baran R, Velez N, Jellinek N. Koilonychia: an update on pathophysiology, differential diagnosis and clinical relevance. J Eur Acad Dermatol Venereol 2016; 30:1985–91.