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For this Discussion, you examine a case study and explain the disease that is suggested. You examine the symptoms reported and explain the cells that are involved and potential alterations and impacts.
You will be assigned to a specific scenario for this Discussion.
Please post an explanation of the disease highlighted in the scenario provided. Include the following in your explanation: role genetics plays in the disease, why the patient is presenting with the specific symptoms described, physiologic response to the stimulus presented in the scenario and why you think this response occurred, the cells that are involved in this process, and how another characteristic like gender or genetics would change your response.
Scenario: A 27-year-old patient with a history of substance abuse is found unresponsive by emergency medical services (EMS) after being called by the patient’s roommate. The roommate states that he does not know how long the patient has been lying there.
The patient received naloxone in the field and has become responsive. He complains of burning pain over his left hip and forearm. Evaluation in the ED revealed a large amount of necrotic tissue over the greater trochanter as well as the forearm. EKG demonstrated prolonged PR interval and peaked T waves. Serum potassium level 6.9 mEq/L.
Post an explanation of the disease highlighted in the scenario you were provided. Include the following in your explanation:
Also read:
NURS 6501 Module 1 Assignment: Case Study Analysis
NURS 6501 Module 2 Assignment Case Study Analysis
Required Readings (click to expand/reduce)
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Chapter 1: Cellular Biology; Summary Review
Chapter 2: Altered Cellular and Tissue Biology: Environmental Agents (pp. 46-61; begin again with Manifestations of Cellular Injury pp. 83-97); Summary Review
Chapter 3: The Cellular Environment: Fluids and Electrolytes, Acids, and Bases
Chapter 4: Genes and Genetic Diseases (stop at Elements of formal genetics); Summary Review
Chapter 5: Genes, Environment-Lifestyle, and Common Diseases (stop at Genetics of common diseases); Summary Review
Chapter 7: Innate Immunity: Inflammation and Wound Healing
Chapter 8: Adaptive Immunity (stop at Generation of clonal diversity); Summary Review
Chapter 9: Alterations in Immunity and Inflammation (stop at Deficiencies in immunity); Summary Review
Chapter 10: Infection (pp. 289-303; stop at Infectious parasites and protozoans); (start at HIV); Summary Review
Chapter 11: Stress and Disease (stop at Stress, illness & coping); Summary Review
Chapter 12: Cancer Biology (stop at Resistance to destruction); Summary Review
Chapter 13: Cancer Epidemiology (stop at Environmental-Lifestyle factors); Summary Review
Justiz-Vaillant, A. A., & Zito, P. M. (2019). Immediate hypersensitivity reactions. In StatPearls. Treasure Island, FL: StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/
Credit Line: Immediate Hypersensitivity Reactions – StatPearls – NCBI Bookshelf. (2019, June 18). Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/. Used with permission of Stat Pearls
This week’s case study is about a client who is 83 years of age and is a skilled nursing amenity resident. The patient presented to the facility with generalized lower limb and abdominal edema. From the interaction with the patient, a past history of malabsorption syndrome and poor feeding from lack of dentures was deduced. Thus, a diagnosis of protein malnutrition was arrived at.
Malnutrition is a serious health crisis with a resultant increased risk of morbidity and mortality. Broadly, malnutrition can either be classified into marasmus, which is an inadequate supply of energy to meet the body’s requirement or kwashiorkor which is the supply of adequate energy with insufficient protein intake (McCance et al., 2019). Classification can also be based on the severity, with malnutrition being classified as mild, moderate, or severe.
Protein malnutrition is etiologically multi-factorial. Its causes include inadequate/improper food intake, impaired absorption, increased gastrointestinal loss of nutrients, increased nutritional needs from various stressors, increased protein loss, and inadequate protein synthesis (Dipasquale et al., 2020). This particular patient’s protein malnutrition is likely due to impaired absorption from the history of the maladaptive syndrome and inadequate food intake based on the difficulty feeding attributed to lack of dentures.
Genetics plays a role in the causation of protein malnutrition. Human genetic variations can alter host genes that impact food absorption and metabolism, including proteins through many mechanisms. Some studies have identified nutrition-associated genes that influence macronutrient intake, such as FTO and single-nucleotide polymorphisms genes, which cause reduced protein intake (Duggal et al., 2018). The genetic variation of individuals also determines the gut microbe composition, which may, in turn, contribute to malnutrition.
The patient came to the emergency department presenting with generalized lower limb edema and abdominal edema. Protein malnutrition is typically characterized by low serum albumin levels due to the decreased synthesis and storage of serum proteins. Low albumin levels lead to an imbalance between oncotic pressure and hydrostatic pressure across vascular walls. Albumin contributes to oncotic pressure, which maintains the intravascular fluid within the blood vessels. Its deficiency thus leads to loss of fluid to the extra-vascular spaces and tissues, which presents clinically as edema.
Reduced oncotic pressure due to low serum albumin level leads to edema from extra-vascular movement of intravascular fluid. This results in intravascular volume depletion, leading to hypovolemia and even shock in serious cases. The body responds to this by increasing the antidiuretic hormone levels to replace the depleted intravascular fluid. This is achieved by water retention by the renal system through the action of this hormone.
Antidiuretic hormone is secreted by the posterior pituitary gland. This hormone acts in the distal renal and collecting tubules and leads to water reabsorption by causing the expression of water transport channels. This leads to intravascular fluid repletion. In addition to decreasing the urine output, this hormone also acts on the endothelial cells of blood vessels to cause vasoconstriction in cases of hypotension.
In addition to genetics, several other factors contribute to the development of malnutrition. Aging, for example, has been shown to increase the risk of malnutrition, as is the case with the patient in this study. This is attributed to factors such as lack of dentures, loss of taste, and reduced movement (Besora-Moreno et al., 2020). This leads to reduced food intake with resultant malnutrition. This may necessitate measures such as nutritional support and screening of the elderly population for early diagnosis and interventions.
Besora-Moreno, M., Llauradó, E., Tarro, L., & Solà, R. (2020). Social and Economic Factors and Malnutrition or the Risk of Malnutrition in the Elderly: A Systematic Review and Meta-Analysis of Observational Studies. Nutrients, 12(3), 737. https://doi.org/10.3390/nu12030737
Dipasquale, V., Cucinotta, U., & Romano, C. (2020). Acute Malnutrition in Children: Pathophysiology, Clinical Effects, and Treatment. Nutrients, 12(8), 2413. https://doi.org/10.3390/nu12082413
Duggal, P., & Petri, W. (2018). Does Malnutrition Have a Genetic Component?. Annual Review Of Genomics And Human Genetics, 19(1), 247-262. https://doi.org/10.1146/annurev-genom-083117-021340
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier. https://shop.elsevier.com/books/pathophysiology/mccance/978-0-323-40281-1
The 83-year-old patient presented in this scenario is suffering from malabsorption syndrome. The condition that the patient is experiencing, and the lack of food intake contributes to protein malnutrition. The main problem of malabsorption syndrome is the lack of nutritional supply in a body due to decreased absorption within the small intestines (McCance & Huether, 2019). The purpose of this discussion is to discuss the genetics, physiological, and cellular components of the scenario presented.
Malabsorption syndrome can have many different causes. Some such causes can stem from outside influences such as intestine dissection, infections, and damage from radiation treatments. However, malabsorption can also come from genetic diseases such as Cystic fibrosis, congenital short bowel syndrome, Celiac disease, and Chron’s disease (Clark & Johnson, 2018).
The scenario presented only states that the patient has a medical history of malabsorption syndrome but does not specify what the cause was. If the patient’s malabsorption was caused by Celiac disease, the genetic factors that would be important to focus on would be the class II human leukocyte antigen (HLA) genes, DQ2 and DQ8.
Patients with these genes are susceptible to celiac disease, where gluten proteins cause CD4T cells to be activated in the mucosal lining of the small intestines. Such activation damages the mucosal lining over time, thereby interfering with the absorption of necessary nutrients (Clark & Johnson, 2018).
The stimulus presented in this scenario is a state of hypoalbuminemia. This condition developed because of the patient’s history of malabsorption syndrome and low protein intake (McCance & Huether, 2019). To understand the physiological response, it is essential to understand the function of protein within the bloodstream. Albumin is the form of protein within the blood responsible for maintaining oncotic pressure.
The albumin does this by using its force to retain water via sodium within the capillaries. Therefore, if there is a lack of albumin in the bloodstream, a weak force keeps the fluid from escaping. This affects the oncotic pressure and allows fluid to leak into the interstitial space. Over time, an accumulation of fluid in the interstitial space leads to swelling, which is the culprit for the patient’s generalized edema and ascites (Darwish & Lui, 2021).
The way nutrients are absorbed into our bodies is through the digestive process. The digestive process begins from the minute food enters our mouths. However, most absorption takes place in the intestinal lumen of the small intestines. The small intestines are made of four main layers: the mucosa, submucosa, muscularis externa, and adventitia.
The mucosal layer contains the epithelium, where the digestive cells live. The digestive cells include the enterocytes, Paneth cells, goblet cells, and neuroendocrine cells. Enterocytes make up the majority of the intestinal epithelium and are responsible for the primary role of absorption (Kong et al., 2018)
Specifically, protein is absorbed in the body with the help of trypsin and chymotrypsin. These enzymes break proteins into tiny forms of amino acids. These amino acids are then transported via the enterocytes across the epithelium to enter blood circulation (Kong et al., 2018). The major clinical problem taking a toll on this patient’s health is malabsorption syndrome. In this case, there is an interruption of the absorptive process at the small intestines, through chemical interruption or a defected brush border, preventing protein absorption for the patient (McCance & Heuther, 2019). A lack of circulating protein is causing the patient’s symptoms, as stated previously.
Malabsorption syndrome can have many different causes, both extrinsic and intrinsic. Older adults are more likely to experience malabsorption due to prolonged illnesses or exposures to medication and chemicals (Clark & Johnson, 2018). Young children, however, are less likely to experience this condition. Therefore, it is easier to pinpoint the cause of the problem in children. If a very young child would present with similar symptoms, I would sooner lookout for diseases such as Cystic fibrosis and milk protein intolerances and their genetic indicators (Cleveland Clinic, 2022).
Group A, scenario 1, presents the case of a 16-year-old boy who is diagnosed with strep throat. Upon discharge, he is prescribed amoxicillin to treat the infection which quickly induces an anaphylactic response after he takes his first dose. As is typical of a type 1 hypersensitivity reaction, he quickly develops facial edema, dyspnea, and audible wheezes. This scenario illustrates two common pathologies that affect adults and children, namely, strep throat (Group A Streptococcus) and anaphylaxis (Type I hypersensitivity).
Group A strep is a bacteria that affects the nose and throat of young children and can be spread to adults through respiratory droplets (Centers for Disease Control and Prevention, 2022). Anaphylaxis is an exaggerated immune response to an allergen. Many biological components are involved in what is commonly known as an allergic reaction. Anaphylaxis is the most severe and life-threatening form of an allergy.
At the cellular level, a foreign substance called an antigen – in this case, penicillin – enters the body and is immediately identified as a threat by the immune system which mounts an acute inflammatory response. Type I hypersensitivities are mediated by immunoglobulin E (IgE) antibodies and the products of mast cells (i.e., histamines and leukotrienes; Justiz-Vaillant & Zito, 2019).
According to McCance and Huether (2018), the most potent mediator of this process is histamine, which acts through H1 receptors located in the smooth muscle cells of several tissues including the airway, heart/blood vessels, and brain. The symptoms experienced by the patient in the scenario can be explained by the effects of this mediator.
Histamine causes smooth muscle contraction leading to bronchial airway constriction and, therefore, dyspnea and wheezing; increased capillary permeability, which causes edema; and vasodilation, which increases blood flow to the affected areas (erythema).
Various factors play a role in the susceptibility of individuals to atopic conditions including environment, genetics, age, and gender. Allergies have a strong genetic component according to Aldakheel (2021). 70% of identical twins and 40% of non-identical twins have reported similar allergies. Furthermore, individuals with hereditary ?-tryptasemia have been identified for increased risk for severe anaphylaxis (Lyons et al., 2021).
Allergies tend to occur more frequently in children than adults as IgE levels peak in infancy and decrease with age up until about 30 years where they level off. Young boys tend to experience allergies more often than young girls due to higher sensitization rates for grass pollen, dust mites, and cat epithelium. The author also states that many of these sex and age differences tend to diminish over time.
Please be mindful of plagiarism and APA format, I have included the rubric. Please use my course resources as one of my references as instructed. Please include McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier in the references.
An understanding of the cardiovascular and respiratory systems is a critically important component of disease diagnosis and treatment. This importance is magnified by the fact that these two systems work so closely together. A variety of factors and circumstances that impact the emergence and severity of issues in one system can have a role in the performance of the other.
Effective disease analysis often requires an understanding that goes beyond these systems and their capacity to work together. The impact of patient characteristics, as well as racial and ethnic variables, can also have an important impact.
Photo Credit: yodiyim / Adobe Stock
An understanding of the symptoms of alterations in cardiovascular and respiratory systems is a critical step in diagnosis and treatment of many diseases. For APRNs this understanding can also help educate patients and guide them through their treatment plans.
In this Assignment, you examine a case study and analyze the symptoms presented. You identify the elements that may be factors in the diagnosis, and you explain the implications to patient health.
Scenario 4: 45-year-old woman presents with chief complaint of 3-day duration of shortness of breath, cough with thick green sputum production, and fevers. Patient has history of COPD with chronic cough but states the cough has gotten much worse and is interfering with her sleep. Sputum is thicker and harder for her to expectorate. CXR reveals flattened diaphragm and increased AP diameter. Auscultation demonstrates hyper resonance and coarse rales and rhonchi throughout all lung fields.
Assignment (1- to 2-page case study analysis)
In your Case Study Analysis related to the scenario provided, explain the following
NOTE: PLEASE INCLUDE AN INTRODUCTION WITH A PURPOSE STATEMENT, TITLE PAGE, REFERENCE PAGE, AND A SUMMARY.
QUESTION 1
A 77-year-old female was brought to the clinic by her daughter who stated that her mother had become slightly confused over the past several days. She had been stumbling at home and had fallen twice but was able to walk with some difficulty. She had no other obvious problems and had been eating and drinking. The daughter became concerned when she forgot her daughter’s name, so she thought she better bring her to the clinic.
HPI: Type II diabetes mellitus (DM) with peripheral neuropathy x 30 years. Emphysema. Situational depression after death of spouse 6-months ago
SHFH: – non contributary except for 40 pack/year history tobacco use.
Meds: Metformin 1000 mg po BID, ASA 81 mg po qam, escitalopram (Lexapro) 5 mg po q am started 2 months ago
Labs-CBC WNL; Chem 7- Glucose-102 mg/dl, BUN 16 mg/dl, Creatinine 1.1 mg/dl, Na+116 mmol/L,
K+4.2 mmol/L, CO237 m mol/L, Cl–97 mmol/L.
The APRN refers the patient to the ED and called endocrinology for a consult for diagnosis and management of syndrome of inappropriate antidiuretic hormone (SIADH).
Question:
1. Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH
Scenario 2: Type 1 Diabetes
A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily.
PMH: noncontributory.
Allergies-NKDA
FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process
SH: denies alcohol, tobacco or illicit drug use. Not sexually active.
Labs: random glucose 244 mg/dl.
DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan.
Question
1. Explain the pathophysiology of the three P’s for (polyuria, polydipsia, polyphagia)” with the given diagnosis of Type I DM.
QUESTION 3
A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily.
PMH: noncontributory.
Allergies-NKDA
FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process
SH: denies alcohol, tobacco or illicit drug use. Not sexually active.
Labs: random glucose 244 mg/dl.
DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan.
Question
1. Explain the genetics relationship and how this and the environment can contribute to Type I DM.
QUESTION 4
A 55-year-old male presents with complaints of polyuria, polydipsia, polyphagia, and weight loss. He also noted that his feet on the bottom are feeling “strange” “like ants crawling on them” and noted his vision is blurry sometimes. He has increased an increased appetite, but still losing weight. He also complains of “swelling” and enlargement of his abdomen.
PMH: HTN – well controlled with medications. He has mixed hyperlipidemia, and central abdominal obesity. Physical exam unremarkable except for decreased filament test both feet. Random glucose in office 333 mg/dl.
Diagnosis: Type II DM and prescribes oral medication to control the glucose level and also referred the patient to a dietician for dietary teaching.
Question:
1. How would you describe the pathophysiology of Type II DM?
QUESTION 5
A patient walked into your clinic today with the following complaints: Weight gain (15 pounds), however has a decreased appetite with extreme fatigue, cold intolerance, dry skin, hair loss, and falls asleep watching television. The patient also tearfulness with depression, and with an unknown cause and has noted she is more forgetful. She does have blurry vision.
PMH: Non-contributory.
Vitals: Temp 96.4?F, pulse 58 and regular, BP 106/92, 12 respirations. Dull facial expression with coarse facial features. Periorbital puffiness noted.
Diagnosis: hypothyroidism.
Question:
What causes hypothyroidism?
Question 1: Syndrome of Antidiuretic Hormone (SIADH)
Normally, the secretion of antidiuretic hormone (ADH) is influenced by plasma osmolality. However, SIADH results when the ADH secretion is excessive regardless of the plasma osmolality, thus leading to increased water retention by kidneys and the resultant electrolyte imbalances worse, which is dilutional hyponatremia (Mentrasti et al., 2020). The patient presentation relates to such hyponatremia.
Different factors predispose an individual to SIADH development, including advanced age, drug use, brain disorders, and malignancies. The patient in the case study had some of these factors that might have predisposed her to develop the condition. She is older than 50 years, has type 2 diabetes mellitus, has a long-standing history of cigarette smoking, and is on different medications for managing depression, including antidepressants.
Patients with advanced age may develop ineffective secretion of ADH due to medications such as antidepressants and NSAIDs that interfere with renal function (Al-Hinai et al., 2021). Further, a history of smoking is suggestive of undiagnosed lung malignancy and emphysema that has been associated with SIADH. In addition, the patient had a history of falls from which she may have sustained intracranial bleeding, thus resulting in SIADH (Mentrasti et al., 2020). These factors should be investigated and appropriately addressed.
Question 2: Pathophysiology of three P`s in type I diabetes Mellitus
Patients with type 1 diabetes mellitus (DM) have autoimmune destruction of the pancreas’s ?-islet cells, leading to absolute insulin deficiency in the body (Nigro et al., 2018). They, therefore, have disorders in the metabolism of glucose, resulting in high serum levels of glucose. As a result of this hyperglycemia, the renal threshold for glucose is overcome, and glucose is passed into the urine (Nigro et al., 2018).
Glycosuria increases the osmotic potential of the urine, thus leading to increased water loss resulting in polyuria. Consequently, the individual becomes dehydrated and the thirst center is stimulated to increase the water intake to offset the dehydration (Banday et al., 2020). This increase in water intake is polydipsia. Further, glucosuria also reduces the body’s carbohydrates, and the individual increases food intake to replenish the lost sugars (Nigro et al., 2018). Polyphagia refers to this increased food intake in DM.
Question 3: How Genetics and Environmental Factors Contribute to Type 1 DM
Type 1 DM results from autoimmune destruction of pancreatic cells. It is estimated that 50% of the affected individuals have a hereditary genetic predisposition, as witnessed by the fragility at chromosome 6p21 and the insulin gene found in chromosome 11p15 (Blanter et al., 2019). In addition to this predisposition, the affected individuals may be triggered by environmental factors such as obesity and viral infection, leading to the development of diabetes mellitus, especially in the younger population (Nigro et al., 2018).
Question 4: Pathology of Type 2 DM
Type 2 DM, in contrast to type 1 DM, results from absolute insulin deficiency, results from relative insulin deficiency due to reduced secretion of insulin by the pancreas, increased insulin resistance by the peripheral tissues, or both (Galicia-Garcia et al., 2020). It can also be due to increased levels of insulin counterregulatory hormones. This relative insulin deficiency leads to reduced utilization of glucose in the affected individual, and the lipids are metabolized instead (Banday et al., 2020). This is the hallmark of hyperglycemia and other patient presentation encountered in type 2 DM.
Question 5: Causes of Hypothyroidism
Hypothyroidism is the low secretion of thyroid hormones by the thyroid gland. Such low secretion can be due to disorders of the thyroid gland, pituitary gland, or hypothalamus. The disorders of the thyroid gland include the use of amiodarone, iodine deficiency, thyroidectomy, thyroid radiation, and Hashimoto’s thyroiditis (Chiovato et al., 2019). These conditions contribute to the majority of hypothyroidism cases, although hypopituitarism and deficiency of hypothalamus hormones (McDermott, 2020).
Al-Hinai, A., Al-Murshedi, F., Al-Nabhani, D., & Al-Thihli, K. (2021). Syndrome of inappropriate antidiuretic hormone secretion in a patient with uncontrolled tyrosinemia type 1. Sultan Qaboos University Medical Journal, 21(2), e312–e315. https://doi.org/10.18295/squmj.2021.21.02.023
Banday, M. Z., Sameer, A. S., & Nissar, S. (2020). Pathophysiology of diabetes: An overview. Avicenna Journal of Medicine, 10(4), 174–188. https://doi.org/10.4103/ajm.ajm_53_20
Blanter, M., Sork, H., Tuomela, S., & Flodström-Tullberg, M. (2019). Genetic and environmental interaction in type 1 diabetes: A relationship between genetic risk alleles and molecular traits of Enterovirus infection? Current Diabetes Reports, 19(9), 82. https://doi.org/10.1007/s11892-019-1192-8
Chiovato, L., Magri, F., & Carlé, A. (2019). Hypothyroidism in context: Where we’ve been and where we’re going. Advances in Therapy, 36(Suppl 2), 47–58. https://doi.org/10.1007/s12325-019-01080-8
Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., Ostolaza, H., & Martín, C. (2020). Pathophysiology of type 2 Diabetes Mellitus. International Journal of Molecular Sciences, 21(17), 6275. https://doi.org/10.3390/ijms21176275
McDermott, M. T. (2020). Hypothyroidism. Annals of Internal Medicine, 173(1), ITC1–ITC16. https://doi.org/10.7326/aitc202007070
Mentrasti, G., Scortichini, L., Torniai, M., Giampieri, R., Morgese, F., Rinaldi, S., & Berardi, R. (2020). Syndrome of inappropriate antidiuretic hormone secretion (SIADH): Optimal management. Therapeutics and Clinical Risk Management, 16, 663–672. https://doi.org/10.2147/TCRM.S206066
Nigro, N., Grossmann, M., Chiang, C., & Inder, W. J. (2018). Polyuria-polydipsia syndrome: a diagnostic challenge. Internal Medicine Journal, 48(3), 244–253. https://doi.org/10.1111/imj.13627
QUESTION 1
A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.
HPI: hypertension treated with Lisinop
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