Respond to at least two of your colleagues who were assigned to a different case than you. Explain how you might apply knowledge gained from your colleagues’ case studies to you own practice in clinical settings.
If your colleagues’ posts influenced your understanding of these concepts, be sure to share how and why. Include additional insights you gained.
If you think your colleagues might have misunderstood these concepts, offer your alternative perspective and be sure to provide an explanation for them. Include resources to support your perspective.
Case #29 The depressed man who thought he was out of options.
The patient is a 69-year-old male with unremitting chronic depression. He has suffered from depressive episodes for 40 years and has always had a good response to treatment until 5 years ago when he relapsed on venlafaxine. Two years ago, he underwent nine treatments of ECT with partial response. He has tried every known antidepressant and augmentation available in the past few years.
The patient should be asked about recent stressful life events, consumption of illicit drugs, alcohol abuse, current medical conditions and prescribed medications (Preda, 2018). If the patient was in my office, I would also want to ask questions to gain an understanding of the severity of his depression. It is important to assess the overall severity of depression symptoms because symptom severity corelates with suicide risk (Preda, 2018). The PHQ-9 screening could be used, and this screening asks about feelings of hopelessness, loss of pleasure in doing things, and feelings of being better off dead. A focused severity assessment for hopelessness, suicidal ideation, and psychotic symptoms is recommended; these symptoms independently increase the risk for suicide (Preda, 2018). This patient reports feeling severely depressed and demoralized, as well as, helplessness, hopelessness, and worthlessness. His depression is the worst it has ever been.
Family members are helpful informers, they can ensure medication compliance, and can encourage patients to change behaviors that continue depression (Halverson, 2019). Some questions I would ask family members would include whether the patient is taking their medication and I would ask the family to provide some insight as to how the patient behaves at home. The wife reports that she feels he is letting go and giving up.
There are no lab tests that will confirm depressive disorder, however, labs can be ordered to rule out illnesses that may present as depressive disorder such as endocrinological or neurological diseases. Labs tests may include TSH, B12, RPR, HIV test, electrolytes, BUN and creatinine, blood alcohol, and blood and urine toxicology screening. Neuroimaging can help clarify the nature of the neurologic illness that may produce psychiatric symptoms, but these studies are costly and may be of questionable value in patients without discrete neurologic deficits (Halverson, 2019). CT scanning or MRI of the brain should be ordered for suspected organic brain syndrome. PET scans provide a means for studying receptor binding of certain ligands and the effect a compound may have on receptors (Halverson, 2019).
Differential diagnosis would include major depressive disorder, bipolar disorder, and/or poor or rapid metabolism. From 25-50% of cases of Treatment Resistant Depression (TRD) are associated with bipolar disorder; this is by far the most common individual cause of TRD (Preda, 2018). The remaining 50-75% are associated with noncompliance, poor or rapid metabolism, or misdiagnosis (Preda, 2018). This patient is exhibiting signs and symptoms consistent with major depressive disorder, such as anhedonia, loss of energy, feelings of worthlessness, depressed mood, which have been consistent for more than a two week period. TRD is defined as MDD that fails to respond to at least two antidepressant trials that are of adequate dose and duration; the two antidepressants may belong either to the same class or to different classes (Preda, 2018).
SSRIs, which include fluoxetine, sertraline, paroxetine, citalopram, escitalopram, and fluvoxamine, have become the first-line treatment for major depression (Brown, 2011). SSRIs work by selectively blocking the reuptake of serotonin to increase the amount of serotonin available in synapses in the brain (Brown, 2011). The STAR*D trial examined various strategies for treatment resistant depression in patients who did not respond to an initial SSRI, including switching to another SSRI antidepressant, changing medication class, and switching to CBT. Fair quality studies have indicated a trend toward greater effectiveness when switching to an SNRI such as venlafaxine than with citalopram, fluoxetine, or paroxetine (Halverson, 2019).
For patients with major depressive disorder, I would start the patient on citalopram 20mg and increase the dose to a maximum of 40mg. If the patient failed to respond, I would change to venlafaxine 75mg daily extended release tablet and increase dose if tolerated. I could not find any contraindications or dosing alterations needed for Citalopram or venlafaxine related to ethnicity.
Week 20 follow-up concluded with ordering venlafaxine levels. This had been considered 20 weeks prior. I agree with ordering this lab and I would have opted to do this before pursuing ECT. A lab is much less invasive, less expensive, and without the side effects he is experiencing at this point.
The patient’s aphasia and mood are improving but his mood is still low. He hadn’t had labs completed. The venlafaxine stayed at 225mg and aripiprazole was increased. Aripiprazole was increased to 15mg. When used to augment treatment with an SSRI or SNRI for depression, the dose would be no greater than 10mg. I disagree with this change.
By week 28 the patient labs show low levels of venlafaxine on a 225mg dose. The dose was increased to 300mg. Up to 600mg/day has been given for heroic cases (Stahl, 2014). I agree with this change. His aripiprazole was discontinued. I agree with discontinuing since the venlafaxine was not at a therapeutic level.
The patient was still not showing improvement by week 32. Another blood level was drawn. At week 36, the level was low on a 300mg dose. The dose was increased to 375mg. The patients BP is good and there have not been any side effects. He has shown some improvement after the dose increase. An increase to 450mg was made and levels ordered. By week 40, the patient was feeling hopeful and mood was improving. His lab values were in the low therapeutic range. At 450mg/day, the patient was still within the dosage for a heroic case. He was tolerating well. The suggestion at this point was to raise dose by 75mg/day, redraw level and raise again to 600mg if still in therapeutic range. I think this is a good strategy based on the patient’s improvement and his ability to tolerate the dose. Lessons learned include the importance of therapeutic drug level monitoring when this is an option. Possible reasons for low levels could be: pharmacokinetic failure, genetic variant causing pharmacokinetic failure, or noncompliance. Finally, never give up.
References
Bienenfeld, David. (2018). Screening tests for depression. Medscape. Retrieved from https://emedicine.medscape.com/article/1859039-overview
Brown, Charles. (2011). Pharmacotherapy of major depressive disorder. US Pharmacist, 36(11), HS3-HS8. Retrieved from https://www.uspharmacist.com/article/pharmacotherapy-of-major-depressive-disorder
Halverson, Jerry. (2019). Depression. Medscape. Retrieved from https://emedicine.medscape.com/article/286759-overview
Howland, R. H. (2008a). Sequenced treatment alternatives to relieve depression (STAR*D). Part 2: Study outcomes. Journal of Psychosocial Nursing and Mental Health Services, 46(19), 21–24. doi:10.3928/02793695-20081001-05. Retrieved from Walden Library databases.
Howland, R. H. (2008a). Sequenced treatment alternatives to relieve depression (STAR*D). Part 1: Study design. Journal of Psychosocial Nursing and Mental Health Services, 46(9), 21–24. doi:10.3928/02793695-20080901-06. Retrieved from Walden Library databases.
Preda, Adrian. (2018). Major depressive disorder: Disabling and dangerous. Medscape. Retrieved from https://reference.medscape.com/slideshow/major-depressive-disorder
Pigott H. E. (2015). The STAR*D Trial: It Is Time to Reexamine the Clinical Beliefs That Guide the Treatment of Major Depression. Canadian journal of psychiatry. Revue canadienne de psychiatrie, 60(1), 9-13.
Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press.
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Post Monica 19263649
/in Uncategorized /by developerRespond on two different days who selected different alterations and factors than you, in one or more of the following ways:
Share insights on how the factor you selected impacts the cardiovascular alteration your colleague selected.
Offer and support an alternative perspective using readings from the classroom or from your own research in the Walden Library.
Validate an idea with your own experience and additional research.
Main Post
Congestive heart failure (CHF) is the inability of the heart to generate adequate cardiac output, resulting in the build-up of fluid throughout various parts of the body. CHF increases the heart’s workload and can lead to an enlarged heart over time. CHF affects nearly 10% of individuals aged 65 or older and is a common cause of hospital admission (Huether & McCance, 2017).
Hypertension Link to CHF
Hypertension can lead to narrowing of the arteries causing them to lose elasticity. The shrinkage and loss of elasticity decrease blood flow and cause your heart to work harder. Over time the heart can become more extensive and thicker, which again increases demand and prompts the heart to work harder to meet the requirements of the body for nutrients and oxygen (American Heart Association).
Hyperlipidemia Link to CHF
One of the common causes of CHF is coronary artery disease (CAD), which occurs as a result of hyperlipidemia. Hyperlipidemia is the result of fatty deposits in the arteries, also known as plaques, that lead to narrowing and decreased blood blow (American Heart Association, 2019). Some studies have suggested that specifically lowering the LDL-C benefits lowering blood pressure and some cholesterol-lowering drugs can positively affect blood pressure (Dalal et al., 2012).
The Female Link Related to Cardiovascular Disease
The leading cause of death for women in the United States is heart disease, affecting approximately 1 in every 5. It is the leading cause of death among white and African-American women. Risk factors include obesity, diabetes, diet, exercise, and alcohol abuse. Useful ways to reduce risks are; have a good baseline of blood pressure and updated lab values, quit smoking, proper diet, limit alcohol and manage stress levels (Centers for Disease Control and Prevention, 2019).
References
American Heart Association, (2019). How High Blood Pressure Can Lead to Heart Failure. Retrieved from https://www.heart.org/en/health-topics/high-blood-pressure/health-threats-from-high-blood-pressure/how-high-blood-pressure-can-lead-to-heart-failure
Centers for Disease Control and Prevention. (2019). Women and Heart Disease. Retrieved from https://www.cdc.gov/heartdisease/women.htm
Dalal, J. J., Padmanabhan, T. N., Jain, P., Patil, S., Vasnawala, H., & Gulati, A. (2012). LIPITENSION: Interplay between dyslipidemia and hypertension. Indian journal of endocrinology and metabolism, 16(2), 240–245. doi:10.4103/2230-8210.93742
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
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Post Monica 19276295
/in Uncategorized /by developerRespond on two different days who selected a different scenario than you, in one or more of the following ways:
Share insights on how the factor you selected impacts the disorder your colleague identified.
Ask a probing question regarding the disorder that your colleague identified.
Suggest an alternative disorder for the scenario your colleague selected.
Main Post
Scenario 3:
Maria is a 36-year-old who presents for evaluation of a cough. She is normally a healthy young lady with no significant medical history. She takes no medications and does not smoke. She reports that she was in her usual state of good health until approximately 3 weeks ago when she developed a “really bad cold.” The cold is characterized by a profound, deep, mucus-producing cough. She denies any rhinorrhea or rhinitis—the primary problem is the cough. She develops these coughing fits that are prolonged, very deep, and productive of a lot of green sputum. She hasn’t had any fever but does have a scratchy throat. Maria has tried over-the-counter cough medicines but has not had much relief. The cough keeps her awake at night and sometimes gets so bad that she gags and dry heaves.
Acute Cough
Coughs are the body’s way of clearing airways via forceful expiration. Inflammation, inhaled particles, accumulated mucus, or foreign bodies stimulate a cough reflex by irritant receptor stimulation in the airway. An acute cough is classified as lasting 2-3 weeks, and chronic cough is greater than three weeks in a non-smoker. Frequent cough causes are allergic rhinitis, upper respiratory infections, pneumonia, aspiration, pulmonary embolus, and congestive heart failure. Due to the above-listed scenario, this cough would be diagnosed as acute cough due to timeframe, cough characteristics, and patient history (Huether & McCance, 2019).
Green Sputum
Sputum contains immune cells and white blood cells from the lower respiratory tract that protect the airway from infections. Sputum can be clear or colored. Color sputum may be yellow, white, green, red or blood-tinged, or pink. Neutrophils are white blood cells that can take on a green color. This color sputum can be indicative of bacterial infections of the lower respiratory tract. Pneumonia and cystic fibrosis can produce this color sputum. To indeed rule out something benign, a sputum culture would need to be obtained and tested (Verywell Health, 2019). At three weeks in, it would likely be premature to order cultures with limited symptoms.
Treatment
Due to the timeframe of cough and only accompanying symptom being green sputum, as a practitioner, I would prescribe an expectorant and schedule a follow up if symptoms persist or worsen. Teaching should include that adverse effects of expectorants might be GI upset, headache, drowsiness, and dizziness. Advise patient that expectorants are designed to be short-term (Arcangelo, Peterson, Wilbur, & Reinhold, 2017). Additional home treat to loosen secretions would be a humidifier, staying adequately hydrated and warm salt water gargles if sore throat should appear (Barkley, 2018).
Patient Factors- Behavior and Age
Maria is an otherwise, healthy 36-year-old female. Due to her age and symptom status, Maria would be treated conservatively. Maria is a non-smoker and takes no prescribed medications. Further investigation would be required if she was a smoker, currently on prescriptions medications, had current disease processes that may factor into the treatment plan.
References
Arcangelo, V. P., Peterson, A. M., Wilbur, V., & Reinhold, J. A. (Eds.). (2017). Pharmacotherapeutics for advanced practice: A practical approach (4th ed.). Ambler, PA: Lippincott Williams & Wilkins.
Barkley, T. (2018). Adult-gerontology primary care nurse practitioner. West Hollywood, CA: Barkley & Associates.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Verywell Health. (2019). What causes the amount of sputum to increase? Retrieved from https://www.verywellhealth.com/what-is-sputum-2249192
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Post Monica 19290371
/in Uncategorized /by developerRespond on two different days who selected different treatments and factors than you, in the following ways:
Offer alternative common treatments for the disorders.
Share insight on how the factor you selected impacts the treatment of alterations of digestive function
Main Post
Irritable Bowel Syndrome
IBS is a symptom-based disease and results in altered bowel habits and abdominal pain. While there are no specific biomarkers for the disease, it is believed the gut immune response, altered gut microflora, brain-gut axis factor, gut neuroendocrine cell function factor, epigenetic, and genetic susceptibility factors all seem to play a role. The diagnostic criteria would be a determination of at least three days per month in the last three months with two or more of these additional symptoms; symptoms improve with defecation, change in frequency of stool, change in the appearance of the stool, and onset greater than six months before diagnosis. The syndrome may be diarrhea-predominant, constipation-predominant, or alterations between the two. Symptoms include bloating, gas, and nausea. Relief can typically occur upon defecation. Treatment for IBS is fiber, laxatives, antispasmodics, antidiarrheals, low-dose anti-depressants, prosecretory drugs, serotonin antagonist or agonists, and analgesics. Additionally, alternative therapies, including probiotics, yoga, acupuncture, and dietary interventions, may be prescribed (Huether & McCance, 2017).
Inflammatory Bowel Disease
Like IBS, IBD also appears to be symptom based. Symptoms are based on months, not days or weeks. Recurrent episodes of diarrhea containing blood, mucous, and white cells alert the practitioner of a potential IBD diagnosis. If the stool samples are negative for microbial pathogens, an IBD diagnosis is likely. Exacerbations and remissions are a trait associated with IBD. Gastrointestinal infection and smoking appear to be contributing factors. IBD is broken down into two forms known as Crohn’s disease (CD) and ulcerative colitis (UC). Crohn’s disease may occur anywhere in the GI tract from mouth to anus, while UC is limited to the colonic mucosa (Hammer & McPhee, 2019). Treatment for IBD is aimed at reducing the inflammation. Treatment may include anti-inflammatory drugs, immune system suppressors, antibiotics, pain relievers, anti-diarrheal, iron supplements, vitamin D, and calcium supplements (Mayo Clinic, 2019).
Different Patient Factors in IBS and IBD
IBS is more prevalent in women by up to three times more likely. North America has a 12% prevalence. IBS sufferers are likely to have depression, reduced quality of life, and anxiety. There does not appear to be a gender factor for IBD. However, there are environmental factors and genetic links (Hammer & McPhee, 2019). Ashkenazi Jewish decent seem to have the highest hereditary factor (Mayo Clinic, 2019).
References
Hammer, G. D., & McPhee, S. J. (2019). Pathophysiology of disease: An introduction to clinical medicine (8th ed.). New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Mayo Clinic. (2019). Inflammatory bowel disease. Retrieved from https://www.mayoclinic.org/diseases-conditions/inflammatory-bowel-disease/diagnosis-treatment/drc-20353320
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Post Monica 19297065
/in Uncategorized /by developerRespond on two different days who selected different factors than you, in one or more of the following ways:
Share insights on how the factor you selected impacts the pathophysiology of diabetes mellitus and diabetes insipidus.
Offer alternative diagnoses and prescription of treatment options for diabetes mellitus and diabetes insipidus.
Validate an idea with your own experience and additional research.
Main Post
Pathophysiology of Diabetes Insipidus
Diabetes insipidus is either the loss of antidiuretic hormone (ADH) action or secretion. ADH is secreted by the posterior pituitary and causes water reabsorption from the collecting ducts. Increases of ADH increases water reabsorption; this results in concentrated urine and more dilute serum. Decreases of ADH decreases water reabsorption, this results in an increase and dilute urine output, and the by-product is a more concentrated serum because ADH is lost with DI, urine output increases and leaves behind a more concentrated hypernatremic serum. There are two categories of DI, central and nephrogenic. Central DI involves a decrease of ADH in the posterior pituitary; this is usually secondary to head trauma, encephalitis, meningitis, and the like. Nephrogenic DI consists of a kidney sensitivity to the decrease of ADH; this form is typically hereditary or congenital and originates from the kidneys (Berkowitz, 2007). Signs and symptoms of DI are much like those of DM and can be, polyuria, polydipsia, and nocturia. Treatment is based on the type of DI and may involve ADH replacement (Huether & McCance, 2017).
Pathophysiology of Diabetes Mellitus
DM is broken down into type I and type II. Type I was previously known as insulin-dependent, and type II was formerly known as non-insulin dependent, that is no longer how these two disorders are classified. Type I is more common in adolescents and associated with the human leukocyte antigen (HLA). Ketone development commonly occurs in type I, and islet cell antibodies are in 90% of patients within the first year. Type I is thought to be caused by infectious or toxic environment that insults the B cells of the pancreas in a genetically predisposed person. Type II DM makes up greater than 90% of the DM cases in the United States. Type II is an inadequate production of insulin; this can be caused by tissue insensitivity and results in impaired insulin production or resistance. There is no link to the islet cell antibodies or HLA. With Type II, there is an association with abnormal lipid profile, obesity, and hypertension. Signs and symptoms of type I and II resemble DI in regards to polyuria, polydipsia. Type I involves weight loss, fatigue, and weakness. Type II includes weight gain, peripheral neuropathy, blurred vision, and chronic skin infections. Treatment might be insulin, oral antidiabetic choices, diet, and exercise (Barkley, 2018).
Patient Behavior and Ethnic Factors
First degree relatives and infection, infection and illness, are contributing factors to DM type I. Family history, sedentary lifestyle, obesity, women with polycystic ovary syndrome, gestational diabetes, insulin resistance, and impaired glucose tolerance are all patient and behavior factors that contribute to DMII. DM is more prevalent with African-Americans, Hispanic/Latino Americans, Asian-Americans, Native-Americans, Alaska Natives, and Pacific Islanders (WedMD, 2019). For DI there are no apparent contributing patient behaviors or ethnic links.
References
Barkley, T. (2018). Adult-gerontology primary care nurse practitioner. West Hollywood, CA: Barkley & Associates.Berkowitz, A. (2007). Clinical pathophysiology made ridiculously simple. Miami, FL: Medmaster.Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (Laureate custom ed.). St. Louis, MO: Mosby.WebMD. (2019). What increases my risk of diabetes? Retrieved from https://www.webmd.com/diabetes/guide/risk-factors-for-diabetes#1
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Post Monica 19304711
/in Uncategorized /by developerRespond on two different days who selected at least one different factor than you, in one or more of the following ways:Offer alternative diagnoses and prescription of treatment options for urinary tract infections.Share an insight from having read your colleague’s posting, synthesizing the information to provide new perspectives
Main Post
Pathophysiology of Upper and Lower Urinary Tract Infections
Lower urinary tract infections (UTIs) involve the urethra and the bladder; upper urinary tract infections include the ureters and the kidneys. Upper UTIs are rarer than lower UTIs but typically are more severe (Healthline, 2019). Microorganisms are the most common agent resulting in UTI infection. Microorganisms can include Escherichia coli (E. Coli) and staphylococcus saprophyticus. Less common mircroorganisms are proteus, klebsiella, pseudomonas, viruses, fungi, tubercular bacilli, and parasites. Gram-negative bacilli move into the urethra, next to bladder, then on to the ureter, and kidney. Infection begins as an inflammatory response producing edema within the bladder wall. The bladder feels full with only small amounts of urine present, but the urgency of needing to urinate is present and appears more often than usual (Huether & McCance, 2017). Signs and symptoms of lower UTIs might include frequency, nocturia, dysuria, urgency, and hematuria (in some cases). Signs and symptoms of upper UTIs might include nausea, vomiting, fever, chills, low back, flank pain, abdominal pain and mental status changes in the elderly population (Barkley, 2018).
Pathophysiology Impact and Patient Factors
Women are more prone than men to experience UTIs, possibly because of urethral irritation during sexual intercourse or because they have a shorter urethra, making it easy for microorganism transmission (Berkowitz, 2007). Microorganisms mostly associated with a female diagnosis would be E.Coli and microorganisms primarily related to a male diagnosis would be proteus species. Disorders with lower UTIs might be, urethritis/dysuria, and cystitis. Diseases with upper UTIs might be, renal, pyelonephritis, and renal abscess (Barkley, 2018). Contributing patient factors might be age, prior UTI history, pregnancy, immunocompromised patients, urinary catheter usage, and poorly controlled diabetes (Healthline, 2019).
Diagnosis and Treatment
Diagnostic test for lower UTIs are urinalysis, esterase detection on dipstick, and presence of nitrate by dipstick. Treatment for lower UTIs are ciprofloxacin, augmentin, bactrim (commonly), additionally amoxicillin, macrobid, levaquin, monurol, and primsol maybe prescribed. The preferred treatment course is 3-days instead of 7-day to maximize benefits and minimize treatment drawbacks (Barkley, 2018).
Diagnostic test for upper UTIs are ESR elevation, and white blood cell casts appearing on urinalysis. Treatment for upper UTIs is Bactrim, Augmentin, Cipro, tobramycin, or gentamicin. For patients with upper UTIs experiencing nausea and vomiting, hospitalization may be necessary (Barkley, 2018).
References
Barkley, T. (2018). Adult-gerontology primary care nurse practitioner. West Hollywood, CA: Barkley & Associates.
Berkowitz, A. (2007). Clinical pathophysiology made ridiculously simple. Miami, FL: MedMaster, Inc.
Healthline. (2019). Everything you need to know about urinary tract infection. Retrieved from https://www.healthline.com/health/urinary-tract-infection-adults#symptoms
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
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Post Monica Craig
/in Uncategorized /by developerRespond in the following ways: (POSITIVE COMMENT)
Share insights on how the factor you selected( THE FACTOR I SELECTED IS ATTACHED BELLOW IN A DOCUMENT) impacts the pathophysiology of the disorder your colleague selected.
Expand on your colleague’s posting by providing additional insights or contrasting perspectives based on readings and evidence.
Main Post
To provide excellent patient care, practitioners must understand information at the cellular level. A good history and physical are essential for proper diagnosing. Useful learning tips might be weekly outlines, reading resources, completion of available exercises, and taking notes on topics one might not understand. Pertinent information to include when evaluating a patient is the complaint, the assessment, the diagnostics, treatment plan, and educating the patient (Laureate Education, 2012).
Cystic Fibrosis and the White Population
Huether & McCance (2017) state 1:3000 cases of CF among the white population and Hammer & McPhee (2019) state 1:2000 cases of CF among the white population. CF is very rare in Asians (Hammer & McPhee, 2019). 1 in every 29 whites in the United States is a carrier of CF (Huether & McCance, 2017).
Pathophysiology of Cystic Fibrosis
Cystic Fibrosis (CF) is caused by an abnormal expression of the cystic fibrosis transmembrane conductance regulator (CFTCR) gene. CF is considered an obstructive lung disease. The defective chloride transporter gene is housed in the exocrine gland. This faulty gene leads to water flow abnormality and results in viscous secretions primarily affecting the lungs but can also affect the reproductive organs and digestive tract as well (Huether & McCance, 2017). Symptoms or signs that may present to aid in the diagnosis of CF might be a delayed passing of meconium in the infancy stage. Foul-smelling, floating stool due to the malabsorption of fats could be a symptom. A cough, pulmonary infections, failure to thrive, and dyspnea are additional signs (Berkowitz, 2007). Intracellular change related to CF is the defective CFTCR gene.
References
Berkowitz, A. (2007). Clinical pathophysiology made ridiculously simple. Miami, FL: MedMaster, Inc.
Hammer, G. D., & McPhee, S. J. (2019). Pathophysiology of disease: An introduction to clinical medicine (8th ed.). New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Laureate Education, Inc. (Executive Producer). (2012). Introduction to advanced pathophysiology. Baltimore, MD: Author.
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Post Monica
/in Uncategorized /by developerRespond on to two different days who selected different immune disorders and/or factors than you, in the following ways:
Share insights on how the factor you selected impacts the pathophysiology of the immune disorder your colleague selected.
Expand on your colleague’s posting by providing additional insights or contrasting perspectives based on readings and evidence.
Main Post
Maladaptive Responses to Immune Disorders
For this week’s discussion post, we will discuss the maladaptive and physiological responses of HIV and Lupus. We will first discuss the pathophysiology of each and then further break the disorders down. We will review how the gender factor might impact the pathophysiology of the disease.
Pathophysiology of HIV
Human Immunodeficiency Virus (HIV) is the viral infection that leads to Acquired Immune Deficiency Syndrome (AIDS). HIV is a blood-borne pathogen. Modes of transmission for HIV are IV drug abuse, blood product transfusion or transmission, maternal-child transmission, and both homosexual and heterosexual populations can be affected. HIV seeks and destroys the CD-4+ Th cells. CD-4+ cells are essential or the cytotoxic T cell and plasma cell development. Because of the CD-4+ destruction, there is a suppressed immune response which leads to AIDS (Huether & McCance, 2017).
Maladaptive Response and the Female Factor
Maladaptive responses to HIV are anxiety, disturbed thought processes, imbalanced nutrition, infective coping, social isolation, this is just a few. Women make up more than half the cases worldwide. Approximately 50,000 new cases of HIV present each year in the United States, 25% of these new cases are from heterosexual relationships with two-thirds of that percentage being women, highest among black women (Huether & McCance, 2017).
Pathophysiology of Lupus
Autoantibodies target specific self-antigens known as the initiation phase. Environmental factors, such as sunlight, may be the cause for these triggers or viral infections like Epstein-Barr. SLE has long been thought to have an active genetic link. In an average individual, apoptotic cells self destruct but for individuals with systemic lupus erythema (SLE) effectively immunize themselves with bad cells from their tissue. The body fights itself instead of excreting the bad cells. Propagation is the second phase of SLE; this phase involves the inflammatory response and tissue damage and can affect the heart, kidneys, brain, skin, and joints. Thirdly is the flare stage and includes a quicker and more vigorous immune response; this stage may provoke disease flares (Hammer & McPhee, 2019).
Maladaptive Response and the Female Factor
Maladaptive responses to SLE might be altered image issues, fatigue related to chronic inflammation, and impaired skin integrity related to skin rash. Women are ten times more likely to develop SLE than men. African Americans have the highest risk, followed by Hispanics, Asian Americans, and Native Americans. The primary age to develop SLE is between 20-40 years old (the childbearing years) with the most prevalent age being around 30 (Lewis, Bucher, Heitkemper, & Harding, 2017).
References
Hammer, G. D., & McPhee, S. J. (2019). Pathophysiology of disease: An introduction to clinical medicine (8th ed.). New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Lewis, S.L., Bucher, L., Heitkemper, M.M., & Harding, M.M. (2017) Medical-surgical nuring assessment and management of clinical problems (10th ed.). St. Louis, MO: Elsevier
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Post On Policy Current Event
/in Uncategorized /by developerThis assignment introduces policy and how a policy is formed in Congress. You will learn how policy is developed, what influences policy and the process of policy. Also, a beginning reading will cover governmental structure: the federal constitution, the branches of government, the federal budget process and state constitution. The student will identify and give an overview of a current bill. Also, the current bill should be correlated to the reading in Chapter 1 and 2 of Porche. It is important understand the continuum of policy at its inception to instituting policy.
This assignment does not necessarily require a journal or a news article. You can find a current healthcare bill that is being discussed in congress (there are many) by going to https://www.govtrack.us/ or https://www.congress.gov/.
Upon successful completion of this assignment you should be able to:
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Post Partum And Newborn Nusring Diagnosis
/in Uncategorized /by developerI need 3 priority nursing diagnosis for mom postpartum .
3 outcomes for each diagnosis
4 interventions for each outcome and rationale
so the total outcomes will be 9, interventions 36 and rationale as well.
also I need 3 priority nursing diagnosis for new born
3 outcomes for each diagnosis
4 interventions for each and rationale
so the total outcomes will be 9, interventions 36 and rationale as well.
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Post Priya
/in Uncategorized /by developerRespond to at least two of your colleagues who were assigned to a different case than you. Explain how you might apply knowledge gained from your colleagues’ case studies to you own practice in clinical settings.
If your colleagues’ posts influenced your understanding of these concepts, be sure to share how and why. Include additional insights you gained.
If you think your colleagues might have misunderstood these concepts, offer your alternative perspective and be sure to provide an explanation for them. Include resources to support your perspective.
Case #29 The depressed man who thought he was out of options.
The patient is a 69-year-old male with unremitting chronic depression. He has suffered from depressive episodes for 40 years and has always had a good response to treatment until 5 years ago when he relapsed on venlafaxine. Two years ago, he underwent nine treatments of ECT with partial response. He has tried every known antidepressant and augmentation available in the past few years.
The patient should be asked about recent stressful life events, consumption of illicit drugs, alcohol abuse, current medical conditions and prescribed medications (Preda, 2018). If the patient was in my office, I would also want to ask questions to gain an understanding of the severity of his depression. It is important to assess the overall severity of depression symptoms because symptom severity corelates with suicide risk (Preda, 2018). The PHQ-9 screening could be used, and this screening asks about feelings of hopelessness, loss of pleasure in doing things, and feelings of being better off dead. A focused severity assessment for hopelessness, suicidal ideation, and psychotic symptoms is recommended; these symptoms independently increase the risk for suicide (Preda, 2018). This patient reports feeling severely depressed and demoralized, as well as, helplessness, hopelessness, and worthlessness. His depression is the worst it has ever been.
Family members are helpful informers, they can ensure medication compliance, and can encourage patients to change behaviors that continue depression (Halverson, 2019). Some questions I would ask family members would include whether the patient is taking their medication and I would ask the family to provide some insight as to how the patient behaves at home. The wife reports that she feels he is letting go and giving up.
There are no lab tests that will confirm depressive disorder, however, labs can be ordered to rule out illnesses that may present as depressive disorder such as endocrinological or neurological diseases. Labs tests may include TSH, B12, RPR, HIV test, electrolytes, BUN and creatinine, blood alcohol, and blood and urine toxicology screening. Neuroimaging can help clarify the nature of the neurologic illness that may produce psychiatric symptoms, but these studies are costly and may be of questionable value in patients without discrete neurologic deficits (Halverson, 2019). CT scanning or MRI of the brain should be ordered for suspected organic brain syndrome. PET scans provide a means for studying receptor binding of certain ligands and the effect a compound may have on receptors (Halverson, 2019).
Differential diagnosis would include major depressive disorder, bipolar disorder, and/or poor or rapid metabolism. From 25-50% of cases of Treatment Resistant Depression (TRD) are associated with bipolar disorder; this is by far the most common individual cause of TRD (Preda, 2018). The remaining 50-75% are associated with noncompliance, poor or rapid metabolism, or misdiagnosis (Preda, 2018). This patient is exhibiting signs and symptoms consistent with major depressive disorder, such as anhedonia, loss of energy, feelings of worthlessness, depressed mood, which have been consistent for more than a two week period. TRD is defined as MDD that fails to respond to at least two antidepressant trials that are of adequate dose and duration; the two antidepressants may belong either to the same class or to different classes (Preda, 2018).
SSRIs, which include fluoxetine, sertraline, paroxetine, citalopram, escitalopram, and fluvoxamine, have become the first-line treatment for major depression (Brown, 2011). SSRIs work by selectively blocking the reuptake of serotonin to increase the amount of serotonin available in synapses in the brain (Brown, 2011). The STAR*D trial examined various strategies for treatment resistant depression in patients who did not respond to an initial SSRI, including switching to another SSRI antidepressant, changing medication class, and switching to CBT. Fair quality studies have indicated a trend toward greater effectiveness when switching to an SNRI such as venlafaxine than with citalopram, fluoxetine, or paroxetine (Halverson, 2019).
For patients with major depressive disorder, I would start the patient on citalopram 20mg and increase the dose to a maximum of 40mg. If the patient failed to respond, I would change to venlafaxine 75mg daily extended release tablet and increase dose if tolerated. I could not find any contraindications or dosing alterations needed for Citalopram or venlafaxine related to ethnicity.
Week 20 follow-up concluded with ordering venlafaxine levels. This had been considered 20 weeks prior. I agree with ordering this lab and I would have opted to do this before pursuing ECT. A lab is much less invasive, less expensive, and without the side effects he is experiencing at this point.
The patient’s aphasia and mood are improving but his mood is still low. He hadn’t had labs completed. The venlafaxine stayed at 225mg and aripiprazole was increased. Aripiprazole was increased to 15mg. When used to augment treatment with an SSRI or SNRI for depression, the dose would be no greater than 10mg. I disagree with this change.
By week 28 the patient labs show low levels of venlafaxine on a 225mg dose. The dose was increased to 300mg. Up to 600mg/day has been given for heroic cases (Stahl, 2014). I agree with this change. His aripiprazole was discontinued. I agree with discontinuing since the venlafaxine was not at a therapeutic level.
The patient was still not showing improvement by week 32. Another blood level was drawn. At week 36, the level was low on a 300mg dose. The dose was increased to 375mg. The patients BP is good and there have not been any side effects. He has shown some improvement after the dose increase. An increase to 450mg was made and levels ordered. By week 40, the patient was feeling hopeful and mood was improving. His lab values were in the low therapeutic range. At 450mg/day, the patient was still within the dosage for a heroic case. He was tolerating well. The suggestion at this point was to raise dose by 75mg/day, redraw level and raise again to 600mg if still in therapeutic range. I think this is a good strategy based on the patient’s improvement and his ability to tolerate the dose. Lessons learned include the importance of therapeutic drug level monitoring when this is an option. Possible reasons for low levels could be: pharmacokinetic failure, genetic variant causing pharmacokinetic failure, or noncompliance. Finally, never give up.
References
Bienenfeld, David. (2018). Screening tests for depression. Medscape. Retrieved from https://emedicine.medscape.com/article/1859039-overview
Brown, Charles. (2011). Pharmacotherapy of major depressive disorder. US Pharmacist, 36(11), HS3-HS8. Retrieved from https://www.uspharmacist.com/article/pharmacotherapy-of-major-depressive-disorder
Halverson, Jerry. (2019). Depression. Medscape. Retrieved from https://emedicine.medscape.com/article/286759-overview
Howland, R. H. (2008a). Sequenced treatment alternatives to relieve depression (STAR*D). Part 2: Study outcomes. Journal of Psychosocial Nursing and Mental Health Services, 46(19), 21–24. doi:10.3928/02793695-20081001-05. Retrieved from Walden Library databases.
Howland, R. H. (2008a). Sequenced treatment alternatives to relieve depression (STAR*D). Part 1: Study design. Journal of Psychosocial Nursing and Mental Health Services, 46(9), 21–24. doi:10.3928/02793695-20080901-06. Retrieved from Walden Library databases.
Preda, Adrian. (2018). Major depressive disorder: Disabling and dangerous. Medscape. Retrieved from https://reference.medscape.com/slideshow/major-depressive-disorder
Pigott H. E. (2015). The STAR*D Trial: It Is Time to Reexamine the Clinical Beliefs That Guide the Treatment of Major Depression. Canadian journal of psychiatry. Revue canadienne de psychiatrie, 60(1), 9-13.
Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press.
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