Category Archives: Nursing

Pathological Condition


Pathological Condition

Make an even distribution for each disease and follow the instructions below for same disease. Proper headings address each point and sub-point of the instruction. Can’t be delayed for a minute. Please don’t miss out anything

Required;
The paper requires more additional information. APA format, 7 pages.

To simplify the content, I need a paper on these 4 diseases:

1.       Coronary Artery Disease

2.       Peripheral Neuropathy

3.       Spinal Stenosis

4. Peripheral Artery Disease

All 4diseases need to address the following information below.

1. Define the pathological condition, disease or syndrome

2. Emphasize and discuss the pathophysiology of this diagnosis.

a.                   What causes it?
b.                  How does it develop?
c.                   What role does genetics have in the development of the disorder, if at all?
d.                  Discuss all the body organ (s) or system affected by the disease.
e.                   How are normal anatomy and physiology altered?
f.                   How is normal body function compromised?
g.                  What are the potential complication or sequelae of the disease process?

3. Who is at risk for developing this pathological condition?
4. How can it be prevented?

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Nursing Paper


Nursing Paper

included the case study for review and the grading rubric.

The paper is similar to the midterm. APA format, 6 pages.

To simplify the content, I need a paper on these diseases:

 

1. Toddler’s fracture

2. Legg-Calve-Perthes disease

3. Spondylolysis

4. Cancer

5. Sprained ankle

Certain forms of cancer can cause limping. These include leukaemia, osteosarcoma, and Ewing’s sarcoma. Children with these types of cancer are usually less than 5 years old.

 

The five diseases need to address the following information below.  Please keep in mind this is a case study on a four year old boy.

1. Define the pathological condition, disease or syndrome. Why would these diseases specifically cause a young child to limp?

2. Signs and Symptoms to the pathophysiology

3. Emphasize and discuss the pathophysiology of this diagnosis.

a.                   What causes it?

b.                  How does it develop?

c.                   What role does genetics have in the development of the disorder, if at all?

d.                  Discuss all the body organ (s) or system affected by the disease.   

e.                   How are normal anatomy and physiology altered?

f.                   How is normal body function compromised?  

g.                  What are the potential complication or sequelae of the disease process?  

 

5. Who is at risk for developing this pathological condition?

6. How can it be prevented?

I have attached the two instructions and case study and rubric, We also did the mid term for the client but she got a very bad grade, I have attached the mid term feedback too and also copying Professor’s comments here.

Here is the feedback my professor emailed me on my midterm paper.
With regard to the four diseases I listed on the final could you make sure
“discussed more in detail about HOW the disease caused the symptoms.  Specifically, at the cellular level? What is it about this process that is causing him to limp?”
“Here are a few pointers for your final.  The purpose is to take the clinical case and determine and stratify the differential diagnosis.  How you do this is take all of the signs and symptoms, medical history and ROS and come up with potential diagnosis that you will investigate.
Your job is to research each disease process and figure out which matches most of his signs and symptoms/H&P (these are your pertinent positives).  The one the most similar is your working diagnosis.  The others that are close are considered your differential diagnosis.  While you were trying to be thorough with your other diagnosis considerations- those were not applicable to the CC.
When you discuss each of these disease processes, you then have to go through his symptoms and explain then according to the disease process.  For example, fever is not just a process of inflammation, but has so many cellular and chemical mediators… what are these?  That is what we mean by discussing the pathophysiology at the cellular level.  A good rule of thumb is if you can ask yourseslf “why” then you need more information.”

Global health issue impacting the international health community


Global health issue impacting the international health community

Select a global health issue impacting the international health community. Briefly describe the global health issue and its impact on the larger health care system (i.e., continents, regions, countries, states, and health departments). How can health care delivery systems work collaboratively to address global health concerns?

Readings within your text covering international/global health and the following websites will assist you in answering these questions:

U.S. Centers for Disease Control and Prevention (CDC) Global Health website: http://www.cdc.gov/cogh/index.htm
U.S. Department of Health & Human Services (HHS) Global Health website: http://www.globalhealth.gov/index.html
Families USA – Why Global Health Matters—Here and Abroad website: http://www.familiesusa.org/
World Health Organization (WHO) website: http://www.who.int

Nursing; Qualitative Mini Critique


Qualitative Mini Critique Due (10 points)

Criteria:

  1. Identify an area of clinical interest
  2. Find one peer-reviewed journal article (no older than 5 years) related to your clinical topic of interest. Do not use a meta-analysis or systematic review.
  3. Critique the journal article, fully answering the following questions
  4. This critique should be 3-4 pages (not including the cover page and reference page)
  5. Utilize the APA levels of headings on page 62 of the APA Manual- APA MANUAL
  6. APA formatting required (Include appropriate APA level/headings)
Ethical Aspects of a Study Were adequate steps taken to safeguard participant’s privacy?

How was confidentiality maintained?

Were vulnerable groups involved in research?

If yes, were special precautions instituted because of their vulnerable status?

Research Tradition Was the research tradition for the study identified?

If none was identified, can one be inferred? Are the data sources, research methods and analytic approach congruent with the research tradition?

Was there evidence of reflexivity in the design?

Sampling What type of sampling strategy was used?

Are sampling procedures clearly delineated in the study?

Data Collection Given the research question and characteristics of study participants, did the researcher use the best method of capturing study phenomena (self-reports, observation)?

If self-report methods, did the researcher make good decisions about the specific method used to solicit information (focus group interviews, critical incident interviews)?

Were interviews tape recorded and transcribed?

What methods of data collection were utilized (Self-reports, Scales, Observation, and Rating Scales)? If self-report methods were used, did the researchers make good decisions about specific methods (in-person interviews, mailed questionnaires, etc.)?

 

Clinical Practice Did the researchers discuss the study’s implications for clinical practice or future research and if so, were the implications grounded in the study evidence, and in evidence from earlier research?

 

Guidelines for Scholarly Research Critique: QUALITATIVE ARTICLE

 

Title Was the title a good one, suggesting the key phenomenon and the group or community under study?
Abstract Does the abstract clearly and concisely summarize the main features of the report?
Introduction Is the phenomenon of interest clearly identified?

Is the problem stated unambiguously?

 

Literature Review Does the report summarize the existing body of knowledge related to the problem or phenomenon of interest?

Is the literature review adequate?

Does the literature review lay a solid basis for the new study

Research Questions Are research questions explicitly stated? If not, is their absence justified?
Method

Research design and research tradition

Is the identified research tradition (if any) congruent with the methods used to collect and analyze data?

 

Sample and setting Was the group or population of interest adequately described? Were the setting and sample described in sufficient detail?

Was the best possible method of sampling used to enhance information richness and address the needs of the study?

Was the sample size adequate? Was saturation achieved?

 

Data collection and measure Were the methods of gathering data appropriate? Were data gathered through two or more methods to achieve triangulation?

Was a sufficient amount of data gathered? Was the data of sufficient depth and richness?

Procedures Were data collection and recording procedures adequately described and do they appear appropriate?

Were data collected in a manner that minimized bias or behavioral distortions? Were data collection staff appropriately trained?

Were appropriate procedures used to safeguard the rights of study participants?

Enhancement of rigor Did the researcher document research procedures and decision processes sufficiently that findings are auditable and confirmable?
Results

Data Analysis

Were the data management (e.g., coding) and data analysis methods sufficiently described?

Was the data analysis strategy compatible with the research tradition and with the nature and type of data gathered?

Did the analysis yield an appropriate product (e.g., theory, taxonomy, thematic pattern, etc.)?

Did the analytic procedure suggest the possibility of biases?

Findings Were the findings effectively summarized, with good use of experts?

Do the themes adequately capture the meaning of the data? Does it appear that the researcher satisfactorily conceptualized the themes or patterns in the data?

Did the analysis yield an insightful, provocative, and meaningful picture of the phenomenon under investigation?

Theoretical Integration Are the themes or patterns logically connected to each other to form a convincing and integrated whole?

Were figures, maps, or models used effectively to summarize conceptualizations?

Discussion Are the findings interpreted within an appropriate social or cultural context?

Are major findings interpreted and discussed within the context of prior studies?

Are the implications consistent with the study’s limitations?

Does the report address the issue of transferability of the findings?

Implications/Recommendations Do the researchers discuss the implications of the study for clinical practice or future inquiry-and are those implications reasonable?
Global Issue Was the report well-written, well-organized, and sufficiently detailed for critical analysis?

Was the description of the methods, findings, and interpretations sufficiently rich and vivid?

Summary Assessment Do the study findings appear to be trustworthy-do you have confidence in the truth value of the results?

Does the study contribute any meaningful evidence that can be used in nursing practice or that is useful to the nursing discipline

 

COMMUNITY HEALTH NURSING CARE PLAN


COMMUNITY HEALTH NURSING CARE PLAN INSTRUCTIONS

As part of this course, you are to present a community health nursing care plan based on the findings from your windshield survey, epidemiology presentation, public health paper or family assessment.

Instructions:

  1. Review chapter 2 Power Point presentations that you can find attached. Pay special attention to slides number 7 thru 11 (Using the nursing process to the community).
  2. Based on your windshield survey observations, epidemiology presentation, public health paper or family health assessment identify 5 community health issues/problems, formulate the diagnosis and develop a nursing plan of care. See attached the Windshield survey, the epidemiology presentation, public health paper and the family health assessment.
  3. Planning and prioritization phase must be included in the plan.
  4. Refer to box: 2-6 on page 42 of our class textbook for guidance. See textbook information below.
  5. Submit plan of care in a Power Point presentation format
  6. Three scholarly evidence-based references are required to sustain your planning and interventions (class textbook does not count)

Community nursing health care plans are not similar to the care plans that we are accustomed to develop in hospital setting, planning and interventions take a different approach. 

Textbook

Saucier Lundy, K., & Janes, S. (2009). Community Health Nursing, Caring for the Public’s Health, 2nd Edition. Sudbury, Mass: Jones and Barlett Learning.

 

 

COMMUNITY HEALTH NURSING CARE PLAN INSTRUCTIONS


COMMUNITY HEALTH NURSING CARE PLAN INSTRUCTIONS

As part of this course, you are to present a community health nursing care plan based on the findings from your windshield survey, epidemiology presentation, public health paper or family assessment.

Instructions:

  1. Review chapter 2 Power Point presentations that you can find attached. Pay special attention to slides number 7 thru 11 (Using the nursing process to the community).
  2. Based on your windshield survey observations, epidemiology presentation, public health paper or family health assessment identify 5 community health issues/problems, formulate the diagnosis and develop a nursing plan of care. See attached the Windshield survey, the epidemiology presentation, public health paper and the family health assessment.
  3. Planning and prioritization phase must be included in the plan.
  4. Refer to box: 2-6 on page 42 of our class textbook for guidance. See textbook information below.
  5. Submit plan of care in a Power Point presentation format
  6. Three scholarly evidence-based references are required to sustain your planning and interventions (class textbook does not count)

Community nursing health care plans are not similar to the care plans that we are accustomed to develop in hospital setting, planning and interventions take a different approach. 

Textbook

Saucier Lundy, K., & Janes, S. (2009). Community Health Nursing, Caring for the Public’s Health, 2nd Edition. Sudbury, Mass: Jones and Barlett Learning.

 

 

CASE STUDY; Hyperparathyroidism


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CASE STUDY; Hyperparathyroidism

Requirements;  APA, two references, single page, American peer review articles or websites dated no later then 2009.


Mrs. F is a 65 year old female, who is a new client, retired, and denies complaints. She has a history of bipolar disorder, hypertension, GERD. She presents her old lab records that shows a low albumin 3 g/dL (normal range: 3.5-5.5 g/dL), and a borderline high calcium of 10.2 mg/dL (normal range: 8.4-10.2 mg/dL). Her current medications are: chlorthalidone, lithium, and pantoprazole.   

A study in the Endocrine Journal (1995) found that lithium creates an increased risk of hypercalcemia by affecting the calcium metabolism but does not seem to affect the level of serum parathyroid hormone (PTH) (Kotmatsu et al., 1995).  In 2010, another study found that patients who are taking lithium also have a risk of hyperparathyroidism. (Pomerantz, J. M. (2010). Hyperparathyroidism resulting from lithium treatment remains under-recognized. Drug Benefit Trends, 22, 62-63. Chlorthalidone, a blood pressure medication, excretes sodium and potassium and increases water removal through the kidneys, and in the presence of lithium can have increased side effects. Chlorthalidone lowers calcium excretion in urine but increases it in stool due to causing a lower calcium intestinal absorption (Bushinsky, D. A., Favus, M. J., & Coe, F. L. (1984).

The provider changed the medications from chlorthalidone to amlodipine, and the psychiatrist was consulted and changed lithium to lamotrigine. The family history does not have endocrine disorders. A dual energy x-ray absorptiometry (DXA) was ordered, and at the 3-month follow-up the DXA screen for osteoporosis had a T score result of -3.0 distal radius. According to the International Society For Clinical Densitometry (2010), osteoporosis is diagnosed in men who are 50 years old and older and postmenopausal women when the T-score is -2.5 or less for lumbar spine, femoral neck or total hip or 33% in the radius.  The laboratory results at this time were albumin 3 g/dL and calcium 10.8 mg/dl the same as the first visit, but the 43-hour urinary calcium is very high at 800 mg (400 mg is normal). Creatinine is low at 0.5 mg/dL (normal range: 0.7-1.3 mg/dL for men, 0.6-1.1 mg/dL for women). PTH is high at 65 pg/ml (normal range: 14-64).

There are three principal hormones in calcium metabolism: the parathyroid hormone located in the parathyroid that are 4 tiny glands on the posterior side of the thyroid gland; calcitonin from the thyroid gland and vitamin D (cholecalciferol) made by sunlight and processes in the skin or from oral supplements. In nearly all cases (over 80%) a benign parathyroid tumor will cause hyperparathyroidism where PTH hormone is in excess and creates hypercalcemia (Buttaro et al, 2013). Other hormones related to calcium metabolism are estrogens, corticosterioids, glucagon, somatotropin, thyroxine ( Vet Book – need to find another resource…

Each age group have rates of bone resorption (calcium leaving the bone) and formation, where elderly usually have bone loss and in negative bone balance (formation < resportion), children are in positive bone balance (formation > resorption) and teens are neutral bone balance (formation = resorption) (Peacock, 2010).

Although this case study does not mention the patient as a smoker of cigarettes, smoking negatively affects calcium metabolism, as well as the function of the pituitary, adrenal, thyroid, ovarian, testicular, and insulin, and increases the risk of osteoporosis to mention a few of the health risks (Kapoor, & Jones, 2005). An abnormal high parathyroid hormone (PTH) level results in excess removal of calcium is taken from the bones resulting in osteoporosis.

The serum calcium is corrected by albumin, because 50% of calcium is bound to protein, the result is corrected by increasing albumin, and the calcium concentration changes 0.8 mg/dL for every 1.0 g/dL of plasma albumin. The formula to estimate plasma calcium level is:

Corrected [Ca] = Total [Ca} + (0.8 x [4.5 – albumin level]) (Skugor, & Milas, 2009).

The state of acidosis or alkalosis will change the binding of calcium to albumin, in acidosis binding of calcium to albumin is decreased and in alkalosis it is increased.

The normal range of total serum calcium is 5.2-10.4 mg/dL (or ionized calcium 2.60-1.30 mmol/L) and the classification of hypercalcemia are:

  • Mild: total serum calcium 10.5-12 mg/dL (or ionized calcium 5.6-8 mg/dL)
  • Moderate: total serum calcium 11.5-18.0 mg/dL (or ionized calcium 2.88-4.51 mmol/L)
  • Severe: total serum calcium > 18.0 mg/dL and hemodialysis may be needed (Lewis III, 2016).

Patients with hypercalcemia present with clinical manifestations such as:

Table 1: Clinical Manifestations of Hypercalcemia

Symptoms and Signs                                   Associated Conditions

Neuropsychiatric

  • Depression                                          Organic brain syndromes
  • Anxiety
  • Cognitive dysfunction
  • Headache
  • Fatigue

Renal

  • Polyuria                                              Nephrolithiasis
  • Polydipsia                                           Nephrogenic diabetes insipidus
  • Nocturia                                              Renal insufficiency

Renal tubular acidosis 

Cardiovascular

  • Short QT Interval                               Hypertension

Cardiovascular calcification 

Gastrointestinal

  • Constipation                                       Peptic ulcer disease
  • Anorexia                                              Acute pancreatitis
  • Abdominal pain

Musculoskeletal

  • Muscle weakness                                Osteopenia, osteoporosis
  • Aches, pains                                       Gout, pseudogout
  • Fractures                                             Chondrocalcinosis

Calciphylaxis

Brown tumors

Other

Hypercalcemic crisis (Skugor, & Milas, 2009).

 

The differential diagnosis with hypercalcemia should be considered early and narrowed down, examples being:

  • Parathyroid hormone-related

o   Primary hyperparathyroidism

  • Sporadic, familial, associated with multiple endocrine neoplasia I or II

o   Tertiary hyperparathyroidism

  • Associated with chronic renal failure or vitamin D deficiency
  • Vitamin D-related

o   Vitamin D intoxication

  • Usually 25-hydroxyvitamin D2in over-the-counter supplements

o   Granulomatous disease sarcoidosis, berylliosis, tuberculosis

o   Hodgkin’s lymphoma

  • Malignancy

o   Humoral hypercalcemia of malignancy (mediated by PTHrP)

o   Tumors (solid) especially of lung, head, and neck squamous cancers, renal cell tumors

o   Local osteolysis (mediated by cytokines), multiple myeloma, breast cancer

  • Miscellaneous causes

o   Medications

o   Endocrine disorders

o   Genetic disorders

 

Evaluating hypercalcemia is best demonstrated by the following table:

Table 2

Clinical Manifestations of Hypercalcemia

  • Renal “stones”
  • Nephrolithiasis
  • Nephrogenic diabetes insipidus
  • Dehydration
  • Nephrocalcinosis
  • Skeleton “bones”
  • Bone pain
  • Arthritis
  • Osteoporosis
  • Osteitis firosa cystica in hyperparathyroidism (subperiosteal resorption, bone cysts)
  • Gastrointestinal “abdominal moans”
  • Nausea, vomiting
  • Anorexia, weight loss
  • Constipation
  • Abdominal pain
  • Pancreatitis
  • Peptic ulcer disease
  • Neuromuscular “psychic groans”
  • Impaired concentration and memory
  • Confusion, stupor, coma
  • Lethargy and fatigue
  • Muscle weakness
  • Corneal calcification (band keratopathy)
  • Cardiovascular
  • Hypertension
  • Shortened QT interval on electrocardiogram
  • Cardiac arrhythmias
  • Vascular calcification
  • Other

o   Itching

o   Keratitis, conjunctivitis (Pomerantz, 2010).

 

 

Guidelines from the Fourth International Workshop (2014), for the management of asymptomatic primary hyperparathyroidism (PHPT) may or may not require surgery, whereas when symptoms present parathyroidectomy surgery is recommended (Bilezikian, Khan, Potts, Jr., 2009). To evaluate, the recommendation is:

  • a biochemistry panel of phosphate, calcium, alkaline phosphatase, creatinine, and BUN, 25(OH)D and
  • PTH by second or third immunoassay
  • Urine 24-h for creatinine, creatinine clearance, and calcium
  • Stone risk profile. Bone mass density by DXA of lumbar and vertebral spine, hip, and distal 1/3 radius.
  • Stone risk profile
  • Abdominal imaging by x-ray, ultrasound, or CT scan
  • Optional

o   HRpQCT

o   TBS by DXA

o   Bone turnover markers (bone-specific alkaline phosphatase activity, osteocalcin, P1NP [select one]; serum CTX, urinary NTX [select one]_

o   Fractional excretion fo calcium on timed urine sample

o   DNA testing if genetic basis for PHPT is suspected (Bilezikian, Khan, Potts, Jr., 2009).

For asymptomatic PHPT patients, a biochemistry panel monitoring is done those who don’t meet surgical guidelines or who decline surgery. Monitoring is done with dual-energy x-ray absorptiometry measuring bone mass density (BMD) every 2 years or yearly with clinical judgment when a patient has comorbidities. Limitation of intake of calcium creates more disease complications, therefore intake is the same as in non-PHPT patients. Supplementation of vitamin D 800-1000 IU daily is prescribed to reach serum levels of greater than 20 ng/dl (50 nmol/liter) of 25-hydroxyvitamin D. monitor serum calcium yearly or twice a year, BMD yearly whereas some may only need evaluation every 2 years. Biophosphonate increases BMD, and alendronate has the best evidence of lumbar spine BMD and stable serum calcium and PTH results, whereas cinacalcet is beneficial in reducing serum calcium to normal limits but only a reduces a modest amount of PTH. A third of patients after monitoring 25 years, may have kidney stones, BMD loss, and/or increased hypercalcemia.

The management of hypercalcemia is shown and explained in Table 5 below:

TABLE 5

Pharmacologic Options for the Treatment of Hypercalcemia

AGENT MODE OF ACTION INDICATION IN HYPERCALCEMIA CAUTIONS
Normal saline 2 to 4 L IV daily for 1 to 3 days Enhances filtration and excretion of Ca++ Severe↑Ca++ > 14 mg per dL (3.5 mmol per L)Moderate↑Ca++with symptoms May exacerbate heart failure in elderly patientsLowers Ca++ by 1 to 3 mg per dL (0.25 to 0.75 mmol per L)
Furosemide (Lasix) 10 to 20 mg IV as necessary Inhibits calcium resorption in the distal renal tubule Following aggressive rehydration ↓K+, dehydration if used before intravascular volume is restored
BisphosphonatesPamidronate (Aredia), 60 to 90 mg IV over 4 hoursZoledronic acid (Zometa), 4 mg IV over 15 minutes Inhibits osteoclast action and bone resorption Hypercalcemia of malignancy Nephrotoxicity, ↓Ca++, ↓PO4, rebound↑Ca++ in hyperparathyroidismMaximal effects at 72 hours
Calcitonin (Calcimar or Miacalcin) 4 to 8 IU per kg IM or SQ every 6 hours for 24 hours Inhibits bone resorption, augments Ca++excretion Initial treatment (after rehydration) in severe/Ca++ Rebound↑Ca++ after 24 hours, vomiting, cramps, flushingRapid↑Ca++ within 2 to 6 hours
GlucocorticoidsHydrocortisone, 200 mg IV daily for 3 days Inhibits vitamin D conversion to calcitriol Vitamin D intoxication, hematologic malignancies, granulomatous disease Immune suppression, myopathy
Plicamycin (Mithracin), 25 mcg per kg per day IV over 6 hours for 3 to 8 doses Cytotoxic to osteoclasts Rarely used in severe↑Ca++ Marrow, hepatic, renal toxicity
Gallium nitrate (Ganite) 100 to 200 mg per m2 IV over 24 hours for 5 days Inhibits osteoclast action Rarely used in severe↑Ca++ Renal and marrow toxicity

IV = intravenously; Ca++ = calcium;/ = increase; ¬ = decrease; K+ = potassium; PO4 = phosphate radical; IM = intramuscularly; SQ = subcutaneously. (Carroll, & Schade, 2003).

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Fuller Albright wrote a book entitled: Parathyroid Glands and Metabolic Bone Disease, in 19?? He was born January 12, 1900 in Buffalo, New York, and d/t his father’s wealth attended a school founded by his father, excelled academically and attended Harvard College, went to the Army for World War I when the influenza pandemic broke out. He contracted Parkinson’s disease in his 30’s. He graduated from Harvard Medical School as Alpha Omega Alpha and intern/resident at Massachusetts General Hospital, researched mineral metabolism with Read Ellsworth until the partner died in 1937of tuberculosis. Studied in Vienna (1928-1929) with D. Jacob Erdheim, pathologist, who was known to have had found the parathyroid glands and calcium metabolism relationship (1906) and in addition, osteomalacia and compensatory hyperplasia of parathyroid gland. In 1929 at Massachusetts General Hospital he continued clinical research where patients were studied, urine/fecal collections and biochemical tests with special diet intake. Hyperparathyroidism (Primary) was reported first and treated in 1934 by Fuller Albright, hyperparathyroidism secondary to renal disease and the development of hyperparathyroidism described in 1937, pseudohypoparathyroidism with Albright Hereditary Osteodystrophy described in 1942, and many other disorders with some disorders named after Albright (Kleeman, Levine, & Felsenfeld, 2009). An abnormal high parathyroid hormone (PTH) level will remove calcium from the bones resulting in osteoporosis.

 

References

Bilezikian, J. P., Khan, A. A., Potts, Jr., J. T. (2009). Guidelines for the management of asymptomatic primary

hyperparathyroidism: Summary statement from the third international workshop. The Journal of Clinical Endocrinology 

     & Metabolism, 94(2). doi:http://dx.doi.org/10.1210/jc.2008-1763. Retrieved from

http://press.endocrine.org/doi/full/10.1210/jc.2008-1763

Buttaro, T., Trybulski, J. Bailey, P., & Sandberg-Cook, J. (2013). Primary Care, 4th Edition. [VitalSourceBookshelfOnline].

Retrieved from https://pageburstls.elsevier.com/#/books/978-0-323-07501-5/

Carroll, M. F., & Schade, D. S. (2003, May 1). A practical approach to hypercalcemia. American Family Physician,

     67(9):1959-1966. Retrieved from http://www.aafp.org/afp/2003/0501/p1959.html#afp20030501p1959-t3

Kleeman, C. R., Levine, B., S., & Felsenfeld, A., J. (2009). Fuller Albright: The consummate clinical investigator. Clinical

     Journal of American Nephrology, 4, 1541-1546. doi: 10.221/CJN.03030509

Kotmatsu, M., Shimizu, H., Tsuruta, T., Kato, M., Fushimi, T., Inoue, K., & Kuroda, T. (1995, October). Effect of lithium

on serum calcium level and parathyroid function in manic-depressive patients. Endocrine Journal, 42(5), 691-695.

Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8574294

Lab Tests Online. (2016). Albumin: The Test. Retrieved from

https://labtestsonline.org/understanding/analytes/albumin/tab/test/

Lewis III, J. L. (2016). Hypercalcemia. Merck Manual. Retrieved from

http://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-disorders/hypercalcemia

Pomerantz, J. J. (2010). Hyperparathyroidism resulting from lithium treatment remains under-recognized. Drug Benefit

     Trends, 22, 62-63. Retrieved from https://en.wikipedia.org/wiki/Hyperparathyroidism

Skugor, M., & Milas, M. (2009). Hypercalcemia. Cleveland Clinic. Retrieved from

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/hypercalcemia/

The International Society For Clinical Densitometry. (2010).  Official Positions. Retrieved from

http://www.iscd.org/official-positions/official-positions/

Toxicology Data Network. (2016). Chlorthalidone. Retrieved from https://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?

 

U.S. National Library of Medicine. (2016). Parathyroid hormone (PTH) blood test. MedlinePlus. Retrieved from

https://www.nlm.nih.gov/medlineplus/ency/article/003690.htm

Wood, K., Dhital, S., Chen, H., & Sippel, R. S. (2012, March). What is the utility of distal forearm DXA in primary

hyperparathyroidism? The Oncologist, 17(3);322-325. Retrieved from

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316917/

 

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Individual Presentation: Cultural Group: Hispanic & Latino Americans vs Socio-Cultural Group: Cuban Heritage


Individual Presentation: Cultural Group: Hispanic & Latino Americans  vs Socio-Cultural Group: Cuban Heritage

Each student will choose one cultural group and one socio-cultural group from the list provided below and set up a PowerPoint presentation  in APA format. Required a inimum of 16 slides.

Preparation for the presentation will include synthesizing the information from assigned readings, Internet resources, the scientific literature, and other sources. Students will provide a minimum of five sources.

The presentation will address the following:

  1. A brief history of the cultural/socio-cultural group
  2. Values
  3. Worldview
  4. Language and communication patterns
  5. Art and other expressive formsNorms and rules
  6. Lifestyle characteristics
  7. Relationship patterns
  8. Common rituals
  9. Degree of assimilation or marginalization from mainstream society
  10. Health behaviors and practices.

The presentation must include a comparative and contrast analysis of common characteristics and distinguishing traits between the cultural group and the socio-cultural group. As well as a brief explanation of differential approaches needed by health care professionals.

Grades will also be based on overall quality of the professional presentation including handouts and references. The presentation is due by the end of Week 8.

 

Cultural Groups: Socio-cultural group
African American & African Group African American Heritage, Haitian Heritage
Asian American, Asian, & Pacific Islander Group Chinese Heritage, Japanese Heritage, Korean Heritage, Filipino Heritage, Russian Heritage, Thai Heritage, Indian Heritage, Vietnamese Heritage
Native American Group Apache Heritage, Navajo Heritage, Yakama Heritage, Cherokee Heritage
Hispanic & Latino Americans Group Mexican Heritage, Brazilian Heritage, Cuban Heritage, Puerto Rico Heritage, Guatemala Heritage
European  American Group Jewish Heritage, Polish Heritage, Baltic Heritage, Greek Heritage, Turkish Heritage, Irish Heritage, Italian Heritage

 

 

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