NURS 6501 Advanced Pathophysiology Essay
Advanced practice nurses must be equipped with an in-depth understanding of pathophysiological disease processes across the lifespan. In this course, students focus on understanding the bio-physiological processes, the deviations from these processes, and an in-depth examination of the scientific concepts related to the biology of disease processes. Advanced practice nursing students learn how normal organ systems function and how organ systems are interrelated to help the body maintain homeostasis. Through knowledge of pathophysiological disease processes, students gain the information needed to develop appropriate treatment plans for patients across the life span. Students explore a variety of topics, such as immunity, inflammation, cancer genetics, and cardiovascular disease. They also examine a range of disease processes, including hematologic, renal, neurologic, gastrointestinal, and reproductive disorders. NURS 6501 Advanced Pathophysiology Essay
WEEK 2: Adaptive Response
Adaptive Response
Understanding what body responses are normal and abnormal in the event of a pathogen invasion, injury or disease process is essential for advanced practices nurses to differentiate and treat patient symptoms. Adaptive responses are how the body defense mechanisms physically react to illness or injury References (Huether, & McCance, 2017). The purpose of this paper is to discuss the pathophysiology, adaptive responses, and alterations of the disease processes and provide a mind map of a disease process explained.
Tonsillitis
In the scenario of the child’s fever, four+ tonsils, diffuse exudates, and palpable tender lymph nodes are clinical presentations of tonsillitis (PubMed Health, n.d.). The symptoms also demonstration the actions of an inflammatory response secondary to the infectious or viral agent. This rapid immune response occurs in humoral and cellular systems and is designed to limit the damage, and begin the process of healing. Immune responses caused vasodilation and increased vascular permeability near sites of injured tissues, causing exudation, swelling, erythema, and warmth as a result of activation and interactions of the chemical can trigger cellular reactions in the blood and lymph system (Huether, & McCance, 2017).
Skin Reaction to a Chemical Irritant – Contact Dermatitis
The scenario with the man presenting with redness and irritation of his hands from probable exposure to chemical irritants, contact dermatitis is likely the cause of his symptoms. Manifestations of contact dermatitis include rashes with well-defined borders, with possible scaling and vesicles at contact site(s) (Huether, & McCance, 2017). Contact dermatitis is a type of delayed hypersensitivity reaction after multiple exposures to an allergen. In this kind of response, the first contact is considered primary, and the body manufactures reactive T cells in response to the exposure, without visible signs and symptoms. Then the contact dermatitis rash develops after the second or multiple exposures, causing the immune response to activate a type IV cell-mediated reaction. The adaptive response happens after repeated exposure and haptens, or environmental antigens become immunogenic after binding to carrier proteins, such as the skin (Huether, & McCance, 2017).
Stress Response – Elevated Cortisol Levels
The symptoms Martha is experiencing, trouble sleeping, anorexia, palpitations can be related to elevated cortisol levels. The body responds to stress by secreting cortisol to enhance the immune response (Huether, & McCance, 2017). Acutely, cortisol inhibits initial inflammatory effects, promotes resolution and repair, by preparing the body for fight or flight. However, prolonged exposure to cortisol causes abnormal immune responses, such as depleting protein stores and can cause a variety of disease processes including lipid abnormalities, hypertension, atherosclerosis, diabetes, osteoporosis, anxiety, depression, sleep disturbances and eating disorders (Huether, & McCance, 2017).
In Summary
Clinical manifestations of disease processes can lead an advance practice nurse to begin to create the differential diagnosis of different pathologies of immune reactions their adaptive responses and associated alterations caused by a disease processes. Studying immune responses allows for the advanced practitioner to think, accurately diagnosis and treat individuals critically.
References
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Hammer, G. G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
WEEK 4:Disorders of the Veins and Arteries
It is important as an advanced practice nurse to recognize clinical manifestations of imbalances in the human anatomy and to differentiate groups of symptoms into disease processes to make accurate diagnosis and treatment therapies. Several conditions exist concerning the bodies circulatory system, particularly the venous system. The purpose of this paper is to discuss the pathophysiology and gender influences of chronic venous insufficiency and deep vein thrombosis, identify key differences and providing a mind map for each venous disorder.
Pathophysiology of Deep Vein Thrombosis
The Centers for Disease Control and Prevention (CDC) estimates 900,000 Americans are affected by venous thromboembolisms (VTE), also known as deep vein thrombosis (DVT) or pulmonary embolism (PE) yearly, and approximately 100,000 individuals die each year (CDC, 2017). A DVT is a thrombus or coagulated blood collection, within a deep vein, usually found in the calf; however, it is possible to have a DVT in the upper extremities (Huether, & McCance, 2017). A DVT is not to be confused with an arterial thrombus, or a blood clot in the artery. An arterial thrombus is result from plaque in atherosclerosis and its blockage may result in myocardial infraction or stroke (Huether, & McCance, 2017).NURS 6501 Advanced Pathophysiology Essay
DVTs have accumulation of platelets and clotting factors near bifurcations of the venous circulation or behind a valve within the venous system (Patel, & Chung, & Chang, 2016). Inflammation from immune responses fosters thrombus growth proximally by propagation from fibrin, red blood cell, platelets, and thrombin aggregation (Huether, & McCance, 2017). A clot attached to the venous vessel wall is a thrombus and becomes a thromboembolus if it detaches (Huether, & McCance, 2017). A triad of conditions promoting venous thrombosis are well-known in the formation of a DVT, and collectively called Virchow’s Triad. Virchow’s triad includes the following manifestations: “(1) venous stasis (e.g., immobility, age, congestive heart failure), (2) venous endothelial damage (e.g., trauma, intravenous medications), and (3) hypercoagulable states (e.g., inherited disorders, malignancy, pregnancy, use of oral contraceptives or hormone replacement therapy)” (Huether, & McCance, 2017, p. 599).
Patients with DVT will present asymptomatically or with complaints of tenderness and or calf pain, redness, and swelling from inflammation or obstruction of blood flow (Huether, & McCance, 2017). Some patients will have a positive Homan’s sign or calf discomfort triggered by foot dorsiflexion with an extended knee (Patel, & Chung, & Chang, 2016). Resolution of most thrombi occurs without treatment; conversely, persistent DVTs can result in embolization increasing risk for PE, in the post-thrombotic syndrome or chronic venous insufficiency causing individuals discomfort (Huether, & McCance, 2017). Confirming a DVT diagnosis is via patient history and physical exam, D-dimer, coagulation blood tests, and Doppler ultrasonography (Huether & McCance, 2012). Management of DVT is through prevention, use of anticoagulants or thrombolytic therapy or placing a filter into the inferior vena cava (Huether & McCance, 2012). VTE prophylaxis of hospitalized patients includes early ambulation, anticoagulation, or sequential compression devices (SCDs, Huether & McCance, 2012).
Pathophysiology of Chronic Venous Insufficiency
Chronic venous insufficiency (CVI) slowly develops from the disruption of the valvular competence in the low-pressure venous system producing an inadequate venous return, reflux, and distention (Weiss, Izaguirre Anaribe, Lanza, & Lessnau, 2016). It is likely that that 2-5% of all US citizens have CVI changes (Weiss, Izaguirre Anaribe, Lanza, & Lessnau, 2016). CVI is due to the valvular incompetence of veins from circulatory stasis, tissue hypoxia, venous hypertension, or varicose veins. A tortuous, palpable, and distended vein containing pooled blood is a varicose vein (Huether, & McCance, 2017). An individual can develop venous distention over time, and risk factors include crossing the legs at the knees, standing for long periods, or wearing constricting garments, via diminishing the calf muscles pumping action (Huether, & McCance, 2017). Risk factors seen in CVI are increasing age over 30, blood clot history, female gender, family history, heavy lifting, obesity, pregnancy, previous leg injury, smoking, and habitual prolonged standing Huether, & McCance, 2017, Vascular Disease Foundation, n.d.). Inadequate venous return causes an inflammatory response, resulting in fibrosclerotic remodeling of skin, ulcerations and sluggish circulation to extremities making any reduction in blood circulation, potentially cause an infection, tissue necrosis, or both.
Chronic venous insufficiency (CVI) is a slowly progressing disease process. Often patients with CIV will present with complaints of aching, burning, cramping, and swelling of lower extremities, they will also have leg fatigue, heaviness or restless legs (Weiss, Izaguirre Anaribe, Lanza, & Lessnau, 2016). Diagnosing CVI includes medical, social, and family histories, a D-dimer serum blood test, duplex ultrasonography, magnetic resonance venography, and physical examination, exhibiting edema, hyperpigmentation, ulcerations, or venous dermatitis (Huether, & McCance, 2017, Weiss, Izaguirre Anaribe, Lanza, & Lessnau, 2016). Treatment of CVI is to reduce symptoms and, when feasible correct the underlying abnormality. Ablating the refluxing vessels, valvuloplasty, venous bypass, sclerotherapy, or noninvasive treatments such as physical exercise, elevating legs, wearing compression stocking (Huether & McCance, 2017, Weiss, Izaguirre Anaribe, Lanza, & Lessnau, 2016).
NURS 6501 Advanced Pathophysiology Essay
Epidemiology
CVI and DVT transpire with greater prevalence among females. The higher occurrences can be related to obstetric or gynecologic conditions in women, increasing risk factors in both CVI and DVT. A ladies risk for DVT increases with hypercoagulability from the use of hormone replacement therapies, oral contraceptives, and pregnancies (Huether, & McCance, 2017). Women have different reproductive mechanisms than men and often cross their legs at the knees, or wear restrictive clothing increasing risk factors in CVI (Huether & McCance, 2012). Women need to receive education on the use of oral contraceptives and hormone replacement therapies, and on interventions to decrease risks for varicose veins CVI and DVT including to encourage exercise, consume nutritious diets, wear garments that fit correctly, utilize compression stockings, and to not cross their legs.
In Summary
This paper discussed the the pathophysiology of deep vein thrombosis and chronic venous insufficiency, and explained how the female gender impacts disease processes. In summary advanced practice nurses need to understand the prevalence of both deep vein thrombosis and chronic venous insufficiency and how these conditions of the venous system impair return of blood flow to the heart.
References
Centers for Disease Control and Prevention. (2017). Venous thromboembolism (blood clots). Retrieved from https://www.cdc.gov/ncbddd/dvt/index.html
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Patel, K., & Chung, L. J., & Chang, J. S. (2016). Deep venous thrombosis. Medscape. Retrieved from http://emedicine.medscape.com/article/1911303-overview#showall
Vascular Disease foundation. (n.d.). Chronic venous insufficiency. Retrieved from http://www.vasculardisease.org/flyers/chronic-venous-insufficiency-flyer.pdf
Weiss, R., & Izaguirre Anaribe, D. (2016). Venous Insufficiency. Medscape. Retrieved from http://emedicine.medscape.com/article/1085412-overview
WEEK 6 : Asthma
It is important as an advanced practice nurse to recognize many alterations of the respiratory system. Differentiating between the many respiratory disease processes is a necessity for accurate diagnosis and treatment. Most pulmonary diseases cause altered breathing patterns, chest pain, clubbing, cough, cyanosis, dyspnea, sputum production, and wheeze (Huether, and McCance, 2017).
Asthma is a frequently diagnosed pulmonary disease process in both children and adults. Asthma main characteristic is a cough and wheeze from bronchospasm, produced by chronic bronchial hyperactivity, inflammation and smooth muscle hypertrophy and reversible airflow obstruction, in response to a trigger (Huether, and McCance, 2017). In fact, the Centers for Disease Control and Prevention, (CDC, 2017) details 1 in 13 people in the United States has asthma, which is approximately 18.4 million adults and 6.2 million children. Asthma accounts for 14 million doctor visits, 439,000 hospitalizations, (Asthma and Allergy Foundation of America (AAFA), 2015) 1.6 million emergency department visits and over 3600 deaths each year (CDC, 2017). African-Americans have 47% higher incidence rate, and their mortality rate is 3:1 compared to whites (AAFA, 2015). Asthma costs the U.S. about $56 billion each year and accounts for more than 14 million missed work days and 13.8 million missed school days (AAFA, 2015).
Asthma is a devastating respiratory alteration. Asthma is a complicated interaction comprising of a person’s genetic susceptibility and environmental factors (Hammer, and McPhee, 2014). When attacks or flares of asthma are upon an individual, the intermittent symptoms can range from mild to severe to a medical emergency. Asthma clinical manifestations include chest tightness, cough, expiratory wheeze, rapid breathing, and shortness of breath (AAFA, 2015). Other symptoms include accessory muscle use, anxiety, barrel chest, clubbing, dyspnea, nasal flaring, pulsus paradoxus and head bobbing in infants (Huether, and McCance, 2017). The purpose of this paper is to discuss the pathophysiology of asthma identifying key differences in chronic asthma versus an acute exacerbation, isolating the behaviors of individuals influencing asthma, and providing a mind map for each presentation of asthma.
Pathophysiology of Acute Asthma Exacerbation
Asthma’s onset in acute situations is precipitated by exposure to an allergen or trigger (Hammer, and McPhee, 2014). The trigger then stimulates a type I immune reaction mediated by T helper two lymphocytes cells (Th2) (Huether, and McCance, 2017). Antigen exposure causes the Th2 cells release cytokines. Then activates mast cells, dendritic cells, plasma cells presenting IgE antigens, and eosinophils (Huether, and McCance, 2017). The activation of the immune response cells causes an inflamed, narrowed airway, impaired mucociliary function, and vascular congestion resulting in bronchospasm increased mucus production and other intermittent asthma symptoms (Huether, and McCance, 2017). In an acute asthma exacerbation compromised inhalation and exhalation cause an increased work of breathing because of air trapping, distal hyperinflation of alveoli, and decreased perfusion (Huether, and McCance, 2017). Furthermore, airway constriction and inflammation cause ventilation-perfusion changes leading to hypoxemia, decrease in tidal volumes, increasing carbon dioxide retention resulting in respiratory alkalosis and respiratory failure (Huether, and McCance, 2017). NURS 6501 Advanced Pathophysiology Essay
Acute asthma exacerbations are intermittent and due to a trigger, such as allergens (dust, pollens), air irritants (air pollution, smoke), chemicals, exercise, and stress (American Lung Association, n.d.). Acute asthma is best controlled with the use of a short-acting beta agonists such as albuterol (Mayo Clinic, 2016).
Pathophysiology Chronic Asthma
The pathophysiology of chronic asthma is similar to an acute asthma exacerbation. However, the persistent inflammatory response results in hyperresponsiveness and bronchial remodeling that is permanent. With proliferation, the bronchial smooth muscle mass of both large and small airways of the respiratory tract become irreversibly increased from poorly controlled inflammatory responses of intermittent asthma (Girodet et al, 2016). Over time the remodeling narrows the inner lumen of the airways, increases mucous production, and damages the epithelium heightening resistance to airflow and airway obstruction (Huether, and McCance, 2017). Alveolar hyperinflation occurs as a compensatory mechanism to airway obstruction (Hammer, and McPhee, 2014). Just as with acute asthma the impaired respiratory function causes variable and uneven ventilation-perfusion relationships resulting in hypoxemia, decrease in tidal volumes, carbon dioxide retention putting and individual at risk for developing respiratory alkalosis and respiratory failure (Huether, and McCance, 2017).
Behavior in Asthma
Asthma can be affected by the behaviors of individuals. A person’s lifestyle and behavior can expose them to environmental triggers of asthma. Unhealthy behaviors such as obesity and smoking increase risk factors. Many people with asthma have allergies to dust, food, molds, and pollens. Poverty also influences behaviors. Impoverished individuals tend to live in inner cities. They are exposed to poor air quality, have higher exposure to indoor allergens because of dirty, unkempt homes with excess animal dander, cockroach droppings, dust mites, and molds and tend to have higher occupation exposure to triggers (American Academy of Allergy Asthma and Immunology (AAAAI), n.d.).
Diagnosis Treatment
Referring patients to and allergist or immunologist is one method of assisting individuals in diagnosing and controlling asthma. Allergist or Immunologist are physicians specializing in diagnosis and treatment of asthma. An allergist can test an individual for allergies to common allergens that trigger asthma, and recommend treatment options to better control asthma (American Academy of Allergy Asthma and Immunology (AAAAI), n.d.). Asthma is diagnosed by physical exam and history and through the use of different lung function tests (LFT). LFT include spirometry, peak airflow, and trigger tests (AAFA).
The first recommendation in managing asthma is to avoid common triggers. Treatment options include an inhaled short-acting beta agonists (SABA) for quick relief in all people with asthma. Other choices in the treatment of asthma are to add an inhaled corticosteroid and a long-acting beta-agonist (LABA) such as salmeterol (Mayo Clinic, 2016). Leukotriene modifiers such as Singulair and other daily medications such as theophylline can also help manage asthma (2016). Providers include intermittent oral or intravenous corticosteroids some cases. The specialist usually prescribes asthma medications in a flexible step approach treating the severity of the disease based on symptoms. Other times it’s recommended to receive immunotherapy or allergy shots (AAAAI), n.d.).Summary
Asthma is a chronic inflammatory respiratory disease that the body uses compensatory mechanisms to try to balance out and correct ventilation-perfusion issues. The compensatory changes the body goes through including the increasing size of the bronchial smooth muscle, decreasing the diameter of the inner lumen in which the air passes, increase mucous production, and epithelial damage resulting in airflow resistance and airway obstruction. The prevalence of asthma is high, and many ‘s are affected, and the cost of treating asthma is astronomical. Therefore, proper management, treatment, and diagnosis of asthma are essential to controlling morbidity and mortality rates in asthma.
References
American Academy of Allergy Asthma and Immunology (AAAAI), n.d.). Asthma library. Retrieved from https://www.aaaai.org/conditions-and-treatments/library/asthma-library
Asthma and Allergy Foundation of America. (2015). Asthma. Retrieved from http://www.aafa.org/page/asthma-symptoms.aspx
American Lung Association. (n.d.). Asthma. Retrieved from http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/asthma/
Centers for Disease Control and Prevention. (2017). Asthma. Retrieved from http://www.cdc.gov/asthma/default.htm.
Girodet, P., Allard, B., Thumerel, M., Begueret, H., Dupin, I., Ousova, O., & … Berger, P. (2016). Bronchial Smooth Muscle Remodeling in Nonsevere Asthma. American Journal Of Respiratory & Critical Care Medicine, 193(6), 627-633. doi:10.1164/rccm.201507-1404OC
Hammer, G. D., & McPhee, S. J. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.). China: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Mayo Clinic. (2016). Asthma. Retrieved from http://www.mayoclinic.org/diseases-conditions/asthma/basics/definition/con-20026992
WEEK 10: Alzheimer Disease
It is thought that 4.5 million Americans suffer from Alzheimer’s Disease at the present time. The numbers are expected to increase to 14 million by the year 2050. After the age of 65 the likelihood of developing this disease significantly increases every five years. By the time people reach their mid 80’s the increases seem to level off, all of this according to the National Institute on Aging (NIA). With the diagnosis of Alzheimer’s disease a long process of decline occurs, usually slowly, that has a terrible impact on the patients with the disease and their families. Slowly but surely a person with Alzheimer’s disease loses their memory and ultimately, their entire identity and the ability to care for themselves. It is said that these losses occur backwards from the way they were acquired form birth until adulthood, with memory being destroyed first and the ability to dress or know who you are lastly. What is this disease and how does it impact on everyone?NURS 6501 Advanced Pathophysiology Essay
Alzheimer’s disease is one form of dementia but not its only form. Dementia refers to the loss of the ability of a person to think and reason due to some type of brain disease. Alzheimer’s is one brain disease causing dementia but there are others. For example, there is something called a Multi Infarct Dementia. In this type of brain disease mini strokes occur that gradually destroy brain cells. A person is not aware of having these types of strokes because they are minor and occur without perception. Yet, each time it occurs the individual loses more of their mental capacities.
Alzheimer’s disease gradually deteriorates the brain and has the same effect as multi infarct dementia in that the ability to think and reason is lost. While both types of dementia’s usually occur after the age of 65, it can occur at any age with the result that there are unfortunate individuals who suffer this fate as early as age 50 and even much younger, but those are more rare cases.
During the early stages of Alzheimer’s the patient is usually aware that something is wrong. Their recent and short term memory is deeply affected so that they constantly misplace and cannot find items such as their household keys, wallet, pocket book, cell phone and other types of commonly used items. They also experience difficulty finding ordinary words when they are talking with friends and neighbors.
As the individual becomes aware that they are not functioning as well as they did formerly they become depressed. This depression probably results from an awareness that something is being lost that will never be regained.
It is at this point that a combination of the elderly individual and their family members consult a physician about what is going on. Patients may be brought to a psychiatrist for depression or to their family physician because there are concerns about deterioration in functional abilities on a daily basis.
Diagnosis of Alzheimer’s disease is not easy because it cannot be done without studying samples of brain tissue. Obviously, this cannot be done while the individual is alive. Therefore, a combination of neurological and psychological tests is given for symptoms of dementia. The psychological tests include a combination of memory, perceptual and mathematical tests to determine the patient’s short term and long term memory. In the early stages of Alzheimer’s disease, long term memory is intact while recent information, such as day, time and season may be forgotten or confused.
Patients undergoing these types of tests are often anxious because they are well aware that Alzheimer’s is under consideration. The examining physician must keep this in mind while doing the assessment as anxiety and depression are each capable of interfering with memory and thinking. Therefore, if all other factors are ruled out and the patient does poorly during the evaluation the Alzheimer’s diagnosis can be made.
Sometimes the question is asked as to why tell the patient they have Alzheimer’s disease if there is not cure? There are several compelling reasons for informing both the patient and family members:
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- Today, there are new medications that can slow the dementing process allowing the patient and family more quality time.NURS 6501 Advanced Pathophysiology Essay
- Although this diagnosis is unpleasant patients have a right to plan for their future. Such plans include where they want to live during the later stages of the illness, who in the family gets power of attorney to make financial and other decisions, and how they want their medical care to be decided for especially with such issues as whether or not they would want extraordinary measures to be taken to prolong their life at the end.
- Patients also have a right to decide where they want to live while they are still in the early stages of the illness. Most elderly people feel comfortable living in their own home and prefer to not make themselves a burden on their children and grandchildren. During the middle stages of the sickness, there is often home help available for dementing patients including attendance in day programs for those with Alzheimer’s.
The Family:
This disease has a powerful effect on family members whether they are the healthy elderly spouse or the children of the patient. Either way, the dementing process puts a burden on the caretakers in the family that will open up the most terrible and wrenching emotional experiences that it is possible to imagine. Why and how is this?
It is surreal for loved ones to watch their wife or husband of sixty years or their mother or father disappear in front of their eyes even though this person continues to live and breath. The way in which family members react to caring for the patient depends a lot on what kind of history both patient and family member had together whether it’s a spouse, son or daughter.
A hypothetical example:
Example: A daughter (Irene) is caring for her mother who is 60 years old and was diagnosed with Alzheimer’s two years ago. The mother (Martha) lives alone in her apartment in Brooklyn New York. The patient is a widow and has been for five years now. The daughter, who is married and has teenage children who are in High School in Winchester, is torn between her responsibilities to her husband and children and to her mother. The trouble is that she and her mother have never gotten along with one another.
Irene experiences her mother’s behavior as maddening and stubborn, just as she always has. From as far back as she can remember, her mother was controlling, stubborn and unreasoning. Because her mother cannot remember where she places her house keys, Irene bought her a small wooden box with a door and hooks and mounted it on the wall next to the exit to the apartment. She showed her mother how to store the key and made her promise to use it. Despite repeated reminders her mother “refuses” to use the new key box when she comes home and loses her keys. In fact any arrangements she has made to make her mother’s life easier ends up being undone. Irene feels nothing but exasperation and rage at her mother. They get into yelling matches which is no problem for her mother who was always argumentative and seems to be more so these days. Why does Irene get so exasperated? Every time that Martha loses something she calls Irene, desperate, confused and angry that she cannot find what she is looking for. At the very same time, Martha feels treated like an infant by her daughter just because she asks her for a little help.
Irene knows that her mother has dementia. But racing down to the Bronx to help her mother cope with her life is just too much when she has so much of her own life to take care of. when she suggests to her mother that they move her into her (Irene’s) house in Winchester and that the kids and her husband would love to have her, she flatly refuses and that also exasperates Irene.
This example is merely a mild case of what happens between patient and family. I could also point out that Irene has three brothers none of whom will help in any way. However, all three brothers are very concerned that Mom’s money not be spent “frivolously” on social home services. They want to be sure that get their full inheritance and that neither Mom nor Irene do nothing dumb to threaten the estate they expect to inherit, especially since, in their view, that estates comes from their late Dad.
The situation with Martha will worsen as the dementia deepens. She will begin to forget where she lives and get lost even when she walks around the corner from her home. She will find it increasingly difficult to remember her address as well as Irene’s telephone number. In fact, she has already had a couple of potentially disastrous consequences when she boiled water for tea and forgot to turn the burner off. She even cooked something in the microwave and forgot that tin foil coverings should not enter the microwave as anything metal can cause a fire.NURS 6501 Advanced Pathophysiology Essay
Ultimately, Irene will be faced with two alternatives for her mother: 1. place her in a nursing home for her own safety or 2. get 24 hour home care for her mother, either in the apartment in the Bronx or in her own home in Winchester. In the end, if her mother begins wandering out of her apartment during the day and night and gets lost there will be no other choice but to have her placed in a nursing home. This idea fills her with guilt and with dread for having to deal with her unsympathetic brothers.
Treatment Options:
Progress is being made in discovering the causes and treatment of Alzheimer’s disease and, perhaps either a cure or effective treatment to stop further deterioration will be available. As stated above, there are now medications that can slow the dementing process and give people more quality time. Anti depressant medications are also used to slow or stop the depression experienced by these people in the early and middle stages of the disease. Later on anti depressants will make no difference. So, what else is available?
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- Music therapy: In the context of the nursing home music therapy has been found to be an effective treatment for dementing patients. Music therapy is calming and soothing. In addition, effective music therapists select music selections that appeal to the ethnic background and history of the particular patient. It has been reported that even at the late stages of the disease, music reawakens lost memories of days gone by and even the most demented patient is able to indicate significant responses because something in the music has stirred the brain cells.
- Art Therapy: Art therapy can be calming and soothing for patients still able to hold paper and pencils. For those who cannot, looking at works of art of all types and kinds can stir memories, feelings and evoke positive reactions, besides being very soothing.
- Pet Assisted Therapy: There is a wealth of anecdotal evidence as well as accumulating research evidence that the presence of pets in both the homes of patients as well as in their nursing homes has great beneficial effects. One study showed that the presence of an aquarium in the nursing home dining room resulted in patients eating more food than before. In addition, having people bringing therapy or comfort dogs to visit patients in nursing homes increases their socialization and responsiveness as compared to not having such visits.
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In the end, there is no cure for Alzheimer’s disease, at least no yet and not for a long time. Among those who need a lot of emotional support and psychotherapy are the care takers of these patients, whether they are ca retaking family members or at home professional and semi professional staff who visit the homes of such patients. Alzheimer’s patients, in their agitation and anger, can become quite verbally and even physically abusive, especially at the later stages of the illness.
The type of person these patients were during the course of their lives does not seem to matter. The intellectually gifted, kindest and gentlest people undergo profound and tragic changes as the disease causes them to spiral down into oblivion.
It can take up to twenty years for a person to die as a result of this dementia. There are many who pass away a lot sooner than that.
WEEK 9 : Diabetes
A collection of hormone producing glands make-up the endocrine system. The endocrine system’s hormones are involved in regulating growth and development, metabolism, mood, sexual function, sleep, and other functions as well (Zimmermann, 2016). When there is an alteration of the endocrine system hormone levels become elevated, or are too low, usually indicating changes in the bodies fluid balance, infection, or physiologic stress (Huether, & McCance, 2017). The topic of this paper is diabetes mellitus (DM) and diabetes insipidus (DI). Understanding of DM and DI entails the understanding of the endocrine system and the feedback mechanisms for insulin, glucagon, and somatostatin work to maintain glucose stores in the body.
Pathophysiology of Diabetes Mellitus
Huether and McCance (2017), describe diabetes mellitus as a “group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both” (p. 471) and classifies DM into four categories. Three of the four categories include type 1, type 2, and gestational. DM is diagnosed from one of the several tests performed on two separate occasions including glycosylated hemoglobin (HbA1c), fasting plasma glucose, 2-hour plasma glucose levels during oral glucose tolerance testing, or by random glucose levels in an individual with symptoms (Huether, & McCance, 2017, p. 471).NURS 6501 Advanced Pathophysiology Essay
Diabetes mellitus is a heterogeneous disorder characterized by the presence of hyperglycemia and is a result of insulin dysfunction of the endocrine pancreas (Hammer, & McPhee, 2014). Insulin is important in DM, as its function is to transport glucose into cells where it becomes energy in the form of glycogen (Huether, & McCance, 2017). Insulin also partakes in fat storage and protein synthesis (Huether, & McCance, 2017).). Insulin also partakes in fat storage and protein synthesis (Huether, & McCance, 2017).
When describing the pathophysiology of DM, one must understand that the pancreas has four types of islet cells from the islets of Langerhans, each secreting a different product. Insulin comes from the Insulin-secreting β cells, and glucagon is secreted from glucagon-secreting α cells, and glucagon acts to increase blood glucose levels (Hammer, & McPhee, 2014). Knowledge about the islet cells of the pancreas is important because the different types of DM have distinctive alterations involving the pancreas.
DM type1 can either be idiopathic or caused by a progressive autoimmune T-cell-mediated disease. In autoimmune DM the beta cells of the pancreas are destroyed from lymphocyte and macrophage infiltration as an inflammatory response occurs, resulting in the decline of insulin synthesis. Hyperglycemia develops due to the reduction of insulin synthesis (Huether, & McCance, 2017). Conversely, in DM type II adipokines, an increase in free fatty acids, inflammatory cytokines, decreased activity of ghrelin, results in insulin resistance. Insulin resistance increases the demand for insulin and causes hyperinsulinemia, or the tissue effect without hyperglycemia (Huether, & McCance, 2017). Insulin resistance and the increased demand for insulin synthesis, as well as the diminished activity of amylin, lead to a decrease in beta-cell mass and function causing hypoinsulinemia (Huether, & McCance, 2017). Dm type II is associated with inadequate insulin production, insulin resistance, and chronic hyperglycemia.
Pathophysiology of Diabetes Insipidus
Diabetes insipidus (DI) is related to an insufficiency of antidiuretic hormone (ADH) causing a partial or total inability to concentrate urine. Insufficient ADH activity leads to leads to high volumes of dilute urine causing increased plasma osmolality which results in frequent thirst (polydipsia) and frequent urination (polyuria, Huether, & McCance, 2017). In DI dehydration can develop quickly without fluid replacement and when a person cannot conserve more water than lost in the urine, serum hypernatremia and hyperosmolality occur. There are three forms of DI. The first is neurogenic and is caused by lesions on the hypothalamus, pituitary stalk, or posterior pituitary, disrupting ADH synthesis, transport or release (Huether & McCance, 2017). The other form nephrogenic DI is triggered by inadequate response of the renal tubules to ADH (Huether & McCance, 2017). In neurogenic drugs such as amphotericin B, carbonate, colchicines, demeclocycline, lithium, loop diuretics and general anesthesia, are factors known to cause kidney damage because it can inhibit the generation of cAMP in the tubules (Huether & McCance, 2017). The second is Central diabetes insipidus, and it is caused by inadequate antidiuretic hormone (ADH). Gestational DI is rare and caused by vasopressin as increase which usually causes mild symptoms that do not require treatment (Huether & McCance, 2017).
Similarities and Differences
Both DM and DI are regulated by hormones in the endocrine system, and both alterations can potentially affect multiple body systems. The body system involved in DM are the liver and pancreas and, with DI the body systems are the hypothalamus and pituitary (Huether & McCance, 2017). DM relates to blood glucose levels and insulin resistance, and frequent monitoring of blood sugar is necessary, whereas with DI the hormone vasopressin influences the kidneys to concentrate urine, and therefore individuals must monitor for polyuria and polydipsia (Diabetes Insipidus, n.d.).NURS 6501 Advanced Pathophysiology Essay
Patient Factors
DM has a strong genetic component, in both type I and II. Although in DM type II the factor is more of a combination genetic-environmental or behavioral factor involved (Huether, & McCance, 2017). In both DM type, I and II blood glucose must be monitored, therefore requiring education and re-education on the risks involved when an individual is noncompliant with controlling sugar levels. Treatment of DM includes regulating insulin levels with oral medications and insulin injections, along with lifestyle modifications including diet and exercise (Huether, & McCance, 2017).
DI can be genetic in that there are mutations in the genes affecting ADH synthesis, transport, and or release. DI is also the result of structural changes of the hypothalamus and pituitary glands hypothalamus and pituitary. Structural changes can result from trauma, infections or thrombosis, which are all likely due to an individual’s behavior (Huether, & McCance, 2017).
References
Diabetes Insipidus. (n.d.). Diabetes insipidus vs mellitus. Retrieved from http://diabetesinsipidus.org/diabetes-insipidus-vs-mellitus
Hammer, G. G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Zimmermann, K. (2016). Endocrine system: Facts, functions, and diseases. Retrieved from https://www.livescience.com/26496-endocrine-system.html
Response #1 Jennifer
Jennifer, the Centers for Disease Control and Prevention (CDC, 2017) reports that in the United States individuals in the Appalachian and southern regions have the highest prevalence of diagnosed diabetes. 2015 data estimates 7.2% of the US population has diagnosed diabetes, 193,000 of the population are adolescents and children under the age of 20 (CDC, 2017). Ethnicity also plays a role in diabetes prevalence with American Indians and Alaskan Natives making up 15.1% and non-Hispanic blacks 12.7% of the total population with DM (CDC, 2017). In 2015 the incidence of diagnosed diabetes in adults was 1.5 million, which is 6.7 per 1,000 adults getting the diabetes diagnosis (CDC, 2017). As healthcare workers, we know there are a high incidence and prevalence of diabetes which is a comorbidity for many, many diseases.
Reference
Centers for Disease Control and Prevention. (2017). National diabetes statistics report. Retrieved from http://www.diabetes.org/assets/pdfs/basics/cdc-statistics-report-2017.pdf
Jennifer Bailey
Diabetes mellitus (DM) occurs when an individual’s blood glucose is too high (NIH, 2017). Blood glucose is used for energy within the body, and insulin is made by the pancreas to regulate glucose. Having an elevated blood sugar level can cause health problems now and in the future. Symptoms of DM increased thirst, increased hunger, dry mouth, frequent urination, unexplained weight loss, weak, blurred vision, numbness or tingling in the hands or feet and frequent yeast infections (Cleveland Clinic, 2017). Treatment for DM is maintaining normal blood sugars with diet or medication therapy.
Diabetes insipidus (DI) is an uncommon disorder that causes the water within the body to be imbalanced (Mayo Clinic Staff, 2016). DI and DM are not the same. Symptoms of DI are extreme thirst, excretion of an excessive amount diluted urine, fussiness, fever, trouble sleeping, vomiting, diarrhea, and weight loss (Mayo Clinic Staff, 2016). Treatment includes maintaining normal electrolytes within the body. Replenishing with fluids such as D5W is recommended.
DM and DI are similar in that they both cause extreme thirst and frequent urination. Both can also cause weakness. Blurred vision, numbness and frequent urinations are not similar between both, just DM. When DI and DM are diagnosed on genetics play a role. With DI, it is present shortly after birth (Mayo Clinic Staff, 2016). DM is also genetic. NURS 6501 Advanced Pathophysiology Essay
References
Cleveland Clinic (2017). Diabetes mellitus. Cleveland Clinic. Retrieved from https://my.clevelandclinic.org/health/articles/diabetes-mellitus-an-overview
Mayo Clinic Staff (2016). Diabetes insipidus. Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/diabetes-insipidus/home/ovc-20182403
NIH (2017). What is diabetes. National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved from https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes
Response #2
Suzanne, while researching diabetes insipidus (DI) further I discovered several interesting facts. Diabetes type 2 and the early stages of DI have similar symptoms, causing misdiagnosis of DI (Health Research Funding, 2015). Diagnostic testing in DI as opposed to type 2 diabetes mellitus, involves urine testing. In DI individuals have high urine output, however low osmolality, specific gravity, and hyperosmolarity and hypernatremia. Diagnosing DI is generally confirmed with a water deprivation test (Huether, &McCance, 2017). Symptoms of DI involve excessive thirst, and in severe cases, urine output can be up to 20 liters. It is important to diagnose DI correctly as it can become life-threatening, with proper treatments/therapies many individuals with DI can live a normal life.
Reference
Health Research Funding. (2015). 17 Fascinating diabetes insipidus statistics. Retrieved from http://healthresearchfunding.org/17-fascinating-diabetes-insipidus-statistics/
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Suzanne Beatty
Diabetes is a chronic disease that affects 30 million people (Center for Disease Control and Prevention, 2017). This heterogenous disorder causes a functional deficiency of insulin. Type 1 diabetes mellitus (DM) is an “autoimmune disease caused by the selective destruction of pancreatic B cells by T lymphocytes targeting ill-defined B-cells antigens.” (Hammer & McPhee, 2014) Peak onset for DM is 5-6 years and puberty (Hammer & McPhee, 2014).
Type 2 diabetes has a stronger genetic component than DM and usually occurs in adulthood. The hallmark of type 2 is insulin resistance (Hammer & McPhee, 2014). The pancreas continues to release insulin, but the organs are insensitive to the insulin. The causes an increased amount of insulin needed to transport glucose from the cells to the blood stream.
Signs and symptoms of DM include polyuria, polydipsia, polyphagia and weight loss (Huether & McCance, 2017). Type 2 diabetes sign and symptoms include changes in the vision, candida infections, fatigue, pruritus, and neuropathy (Huether & McCance, 2017). Hemoglobin A1C greater to or equal to 6.5%, a random blood glucose greater than 200 with diabetic symptoms, or 2 separate fasting glucose greater than 126 mg/dl are tools to diagnose diabetes.
Altered activity of ADH is diabetes insipidus. There are two types of altered activity of ADH which are neurogenic and nephrogenic. Neurogenic DI is caused by decreased amounts of ADH related to diseases of the hypothalamus or the pituitary (Huether & McCance, 2017). Nephrogenic DI is caused by “inadequate response of the renal tubules to ADH.” (Huether & McCance, 2017) Signs and symptoms of DI are polyuria, polydipsia, and nocturia (Huether & McCance, 2017). Evaluation for DI includes hypernatremia, water deprivation test with a urine specific gravity < 1.010, urine osmolarity low, and serum osmolarity > 300 (Huether & McCance, 2017).
Polyuria and polydipsia are symptoms of DM and DI. Polyuria is caused by the bodies inability to reabsorb water in DI. Polyuria in DM is caused the amount of glucose not being filtered by the kidneys causing an osmotic diuretic effect (Hammer & McPhee, 2014).
References
Center for Disease Control and Prevention. (2017, July 23). Diabetes Home. Retrieved from Center for Disease Control and Prevention: https://www.cdc.gov/diabetes/home/index.html
Hammer, G., & McPhee, S. (2014). Pathophysiology of Disease. An Introductoduction to Clinical Medicine (7th ed.). China: McGraw Hill Education.NURS 6501 Advanced Pathophysiology Essay
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis MO: Mosby.
WEEK 8 : Gastrointestinal Alterations
Gastrointestinal Alterations
The alimentary canal or gastrointestinal (GI) tract includes the mouth, esophagus, stomach, small intestine, colon, anus, as well as some accessory digestive tissues such as the salivary glands, liver, gall bladder, pancreas, and is the digestion pathway of food after ingestion. (Huether, & McCance, 2017). The digestive system is responsible for the breakdown, digestion, absorption, and excretion of food. Because many of the GI alterations have similar clinical manifestations, differentiating potential causes into a single diagnosis can be difficult. GI inflammatory and ulcerative conditions can disrupt absorption, motility, and secretion (Huether, & McCance, 2017). For this reason, an advanced practice nurse must have an understanding of common GI disorders such as gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis. The purpose of this paper is to describe the pathophysiology of gastric acid production and explain the differences in regards to GERD, PUD, and gastritis.
Normal Pathophysiology of Gastric Acid Stimulation and Production
Gastric acid secretion is stimulated and inhibited by several factors and can be broken up into phases cephalic phase, gastric phase, and intestinal phase (Huether, & McCance, 2017). Hydrochloric or gastric acid production and secretion occur in the cells and glands within the mucosa or on the apical surface of epithelial cells of the GI tract (Hammer, & McPhee, 2014). Hydrochloric acid (HCl) is produced by parietal cells from the H+-K+ ATPase active transport system, which carries hydrogen and chloride out of parietal cells and moves potassium into the cell. Stimulation of HCl secretion is from three main pathways, enterochromaffin-like (ECL) cells, G-cells, and acetylcholine release from the parasympathetic nervous system (Hammer, & McPhee, 2014, Huether, & McCance, 2017). ECL cells secrete histamine, the histamine then binds on to the H2 receptors on the parietal cells stimulating the H+-K+ ATPase pump of HCl secretion (Hammer, & McPhee, 2014). G cells secrete the peptide hormone gastrin. Gastrin binds to gastrin receptors on ECL cells stimulating the release of histamine and gastrin binds to gastrin receptors on parietal cells stimulating the H+-K+ ATPase pump to secrete HCl (Hammer, & McPhee, 2014). The last pathway is when the cephalic phase of digestion stimulates the parasympathetic secretion of acetylcholine from the vagus nerve (Huether, & McCance, 2017). Acetylcholine stimulates histamine release from ECL cells, the release of gastrin-releasing peptide stimulating gastrin release, and inhibits somatostatin release (Hammer, & McPhee, 2014). Somatostatin is secreted from D cells and inhibits HCl production. HCl production is inhibited by somatostatin because it hinders the release of gastrin from G cells and histamine from ECL cells. The binding of acetylcholine to muscarinic receptors on parietal cells stimulates HCl production (Hammer, & McPhee, 2014). NURS 6501 Advanced Pathophysiology Essay
Gastroesophageal Reflux Disease
Gastroesophageal reflux disease (GERD) is the backflow of stomach contents upwards into the esophagus, causing esophagitis or inflammation of the esophagus (Huether, & McCance, 2017). Sign and symptoms of GERD include acid regurgitation, cough, dysphagia, epigastric pain, laryngitis and pyrosis (Huether, & McCance, 2017). The prevalence of GERD in the US is 18-27%, and risk factors include advanced age, drugs/ chemicals, and the presence of a hiatal hernia. Behavioral factors in GERD such as alcohol ingestion, smoking, and obesity are also risk factors (Huether, & McCance, 2017).
In GERD the lower esophageal sphincter tone is relaxed, there is slowed esophageal motility, or slowed gastric motility or delayed gastric emptying (Huether, & McCance, 2017). Esophagitis severity depends on the exposure time of the mucosa to the refluxate of chyme including acids, bile salts and enzymes. Refluxate can cause injury and inflammation to the mucosa with edema, erosion, hyperemia, increased capillary permeability, tissue fragility and long-term exposure can lead to fibrosis mucosal thickening, and lesions (Huether, & McCance, 2017). GERD is diagnosed from history, clinical manifestations, pH monitoring and tissue biopsy (Huether, & McCance, 2017). Treatment includes the use of proton pump inhibitors, or H2-receptor blockers and antacids. Alternating behavioral factors can also assist in the treatment of GERD. Educating the patient on life style modifications of smoking cessation, weight loss, and avoidance of alcohol are first-line interventions in alleviating bothersome symptoms in GERD (Talawah, & Woodward, 2013). Surgical intervention of laparoscopic fundoplication is a last resort in GERD treatment (Huether, & McCance, 2017). GERD can lead to peptic ulcer disease with lesions in the esophagus.
Peptic Ulcer Disease
Peptic ulcer disease (PUD) is from an erosion, or ulceration in the protective mucosal layers of the duodenum, esophagus or stomach, and occur more frequently in the duodenum (Huether, & McCance, 2017). PUD lesions are from an imbalance of protective secretions and acid and the lesions can extend through several layers of the GI tract lining and can damage blood vessels, or perforate the wall of the GI tract. The most common clinical manifestation of PUD is chronic intermittent epigastric pain on an empty stomach relieved with rapid ingestion of food and or antacids, nausea, heart burn, weight loss and hemorrhage when the lesion extends into the tunica muscularis layer (Huether, & McCance, 2017, Mayo Clinic. n.d.). Huether, and McCance (2017) report the prevalence of PUD in 2011 was 15.5 million US citizens and risk factors include Helicobacter pylori (H. pylori) infection, nonsteroidal anti-inflammatory drugs (NSAIDs), advanced age, chronic diseases, and O blood type. Behavioral factors in PUD such as alcohol ingestion, smoking, obesity and psychologic stress are also risk factors (Huether, & McCance, 2017).
With PUD acid and pepsin concentrations penetrate the mucosal barriers and cause ulcerations. Duodenal ulcers care commonly from H. pylori infections which have a virulence factor cytotoxin associated gene A (CagA) that produces a vacuolating toxin (VacA) which causes apoptosic of gastric epithelial cell and promotes the release of inflammatory cytokines that damage the gastric epithelium (Huether, & McCance, 2017, p. 916). Prostaglandins are an essential part of the negative feedback loop inhibiting HCl production. Chronic use of NSAIDs prevent the cyclooxygenase-1 (COX-1) enzyme from producing prostaglandins, which normally stimulate secretion of mucus (Hunt, & Yuan, 2011). With the protective barrier against HCl inhibited, this increases the risk of gastric epithelium damage.NURS 6501 Advanced Pathophysiology Essay
Diagnostic approaches such as endoscopic evaluation, tissue biopsy, urea breath test, stool samples, as well as medical history and physical are utilized to diagnose PUD (Huether, & McCance, 2017). The goal in the management of PUD is to relieve the causes, and prevent complications. Use of antacids, H2 receptor blockers, proton pump inhibitors, antibiotics, and surgical resection of ulcers are common treatments in PUD (Huether, & McCance, 2017). Self-management of PUD is also every effective, via modification of behavioral factors including alcohol avoidance, dietary changes, smoking cessation, weight loss, and improved sleep habits (Mayo Clinic. n.d.).
Gastritis
Gastritis is often seen in GERD and with PUD. The incidence of gastritis in the US is less than 1% (Huether, & McCance, 2017). Acute gastritis occurs when the protective mucosal barrier of the stomach becomes inflamed or swollen from increased gastric secretion cause by trauma, drugs, chemicals or H. pylori infection (Huether, & McCance, 2017).
The same pathophysiology in gastritis occurs with NSAID drug use. Behavioral factors in gastritis include alcohol or acidic beverages ingestion, smoking, and sexually transmitted diseases are also risk factors (University of Maryland Medical Center, (UMMC), n.d.). Clinical manifestations of acute gastritis are vague abdominal discomfort, loss of appetite, epigastric pain or indigestion, fullness, hiccups, nausea, vomiting, and bleeding (Huether, & McCance, 2017, UMMC, n.d.). Acute gastritis heals spontaneously requiring no treatment other than modifying behavioral activities such as avoiding injurious drugs, consuming minimal amounts of acidic beverages, alcohol, and smoking cessation Huether, & McCance, 2017, UMMC, n.d.). Other treatments include using antacids, and H2-receptor antagonists Huether, & McCance, 2017).
However chronic gastritis is more prevalent in older adults and is usually due to chronic inflammation, epithelial metaplasia, and mucosal atrophy (Huether, & McCance, 2017). Chronic gastritis can be divided up and classified into several different groups by location of lesions. Type A, immune is found in the fundal region, type B, nonimmune is antral, and type C gastritis is associated with reflux of bile and pancreatic secretions into the stomach (Huether, & McCance, 2017). Immune gastritis is rare and is usually associated with other autoimmune diseases, autoantibodies to gastric H+-K+ ATPase can be found (Huether, & McCance, 2017). With chronic gastritis, the mucosa degenerates causing gastric atrophy, and the loss of parietal cells, causing the normal feedback mechanism to become impaired and allowing for elevated plasma levels of gastrin (Huether, & McCance, 2017). Nonimmune chronic gastritis is usually secondary to H. pylori infection, NSAIDS, or associated with behavioral factors such as alcohol and tobacco use and is related to high levels of HCl secretion (Huether, & McCance, 2017).
Diagnosing gastritis usually requires an evaluation of complete medical history, physical exam, upper GI endoscopy, X-rays, blood and stool tests for H. pylori infection (UMMC, n.d.). Treatment of symptoms usually includes to reduce amount of acid in the stomach, antacids, the use of and antacids, proton pump inhibitors, or H2-receptor blockers, Carafate, or to treat the underlying cause with use of antibiotics vitamin B12, avoiding NSAIDS, or implementing life style modifications of smoking cessation, avoidance of alcohol and acidic beverages, and implementing dietary changes (UMMC, n.d.).NURS 6501 Advanced Pathophysiology Essay
Summary
The overlap of clinical manifestations in GERD, PUD and gastritis can make differentiating the exact diagnosis difficult, without blood or stool tests, and endoscopic evaluation. All three digestive alterations can improve with behavioral and lifestyle changes such as dietary changes, avoiding alcohol, nicotine and NSAIDS. Finally, treatments are essentially the same with treating the underlying cause and the use of antacids, proton pump inhibitors, or H2-receptor blockers.
References
Hammer, G. D., & McPhee, S. J. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.). China: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Hunt, R. H., & Yuan, Y. (2011). Acid-NSAID/aspirin interaction in peptic ulcer disease. Digestive Diseases (Basel, Switzerland), 29(5), 465-468. doi:10.1159/000332211
Mayo Clinic. (n.d.). Peptic ulcer. Retrieved from http://www.mayoclinic.org/diseases-conditions/peptic-ulcer/home/ovc-20231363
Talawah, N. A., & Woodward, S. (2013). Gastro-oesophageal reflux. Part 1: smoking and alcohol reduction. British Journal Of Nursing, 22(3), 140-145.
University of Maryland Medical Center. (n.d.). Gastritis. Retrieved from http://www.umm.edu/health/medical/altmed/condition/gastritis NURS 6501 Advanced Pathophysiology Essay