In an essay of 750-1,000 words, compare and contrast the health status of the minority group you have selected to the national average.

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In an essay of 750-1,000 words, compare and contrast the health status of the minority group you have selected to the national average.

Analyze the health status of a specific minority group. Select a minority group that is represented in the United States (examples include: American Indian/Alaskan Native, Asian American, Black or African American, Hispanic or Latino, Native Hawaiian, or Pacific Islander.)

In an essay of 750-1,000 words, compare and contrast the health status of the minority group you have selected to the national average. Consider the cultural, socioeconomic, and sociopolitical barriers to health. How do race, ethnicity, socioeconomic status, and education influence health for the minority group you have selected? Address the following in your essay:

What is the current health status of this minority group? How is health promotion defined by the group? What health disparities exist for this group? Describe at least one approach using the three levels of health promotion prevention (primary, secondary, and tertiary) that is likely to be the most effective given the unique needs of the minority group you have selected. Provide an explanation of why it might be the most effective choice. Cite a minimum of three references in the paper.

After seeking help at an outpatient mental health clinic, Ruby who was raped while walking her dog is diagnosed with posttraumatic stress disorder (PTSD)

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After seeking help at an outpatient mental health clinic, Ruby who was raped while walking her dog is diagnosed with posttraumatic stress disorder (PTSD)

After seeking help at an outpatient mental health clinic, Ruby who was raped while walking her dog is diagnosed with posttraumatic stress disorder (PTSD). Three months later, Ruby returns to the clinic, complaining of fear, loss of control, and helpless feelings. Which nursing intervention is most appropriate for Ruby?

After seeking help at an outpatient mental health clinic, Ruby who was raped while walking her dog is diagnosed with posttraumatic stress disorder (PTSD). Three months later, Ruby returns to the clinic, complaining of fear, loss of control, and helpless feelings. Which nursing intervention is most appropriate for Ruby?

a. Recommending a high-protein, low-fat diet.
b. Giving sleep medication, as prescribed, to restore a normal sleep-wake cycle.
c. Allowing the client time to heal.
d. Exploring the meaning of the traumatic event with the client.

Describe the three phases of nursing intervention research

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Describe the three phases of nursing intervention research

Nursing Intervention Research
Describe the three phases of nursing intervention research: Phase 1: Intervention Development Phase 2: Pilot Testing an Intervention Phase 3: Controlled Trial of the Intervention

The nature of nursing

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The nature of nursing

The nature of nursing

Discussion Question (DQ) 1
Using the Internet, choose two research articles representing (1) empirics, and (2)

interpretative research and compare and contrast them
Discussion Question (DQ) 2
How do you build practitioner relationships with patients, physicians & colleagues?

In your professional experience what factors contributed (or detracted) from

building working relationships?

How does the community health nurse recognize bias- stereotypes- and

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An important role that the nurse has but is often overlooked is self-reflecting/self-awareness. When the nurse is aware of their own bias and stereotypes it allows them to work on the reason behind why they think in a certain manner. This, then reduces the likelihood of them displaying those biases and stereotypes at work. It is also beneficial for the nurse to be culturally competent especially when it comes to different cultures within the community. Angel Falkner (2018) states, “The nurse should be well informed regarding stereotypes and biases in order to be sensitive to these issues and provide the most unbiased care possible.” As the nurse gains cultural competence it will facilitate the recognition of discrimination based on stereotypes and biases in the healthcare setting.

The nurse can address these concepts to ensure health promotion activities are culturally competent by completing a thorough assessment including questions about the patient’s culture such as their beliefs on health, life, and nature as well as their religion and any health promotion strategies they have (Falkner, 2018). The nurse can also incorporate strategies to reduce cultural dissonance such as the LEARN model. The LEARN model focuses on providing empathy to the patient who feels they have experienced cultural dissonance, explaining your own perception of their situation, comparing the different views and their similarities, recommending a treatment plan, and lastly modifying the treatment plan to meet the patient’s needs and preferences. By adding these two strategies into the work environment the nurse will increase her cultural competency thus reducing discrimination based on stereotypes and biases.

Using 200-300 words APA format with references to support the discussion.

How does the community health nurse recognize bias, stereotypes, and implicit bias within the community? How should the nurse address these concepts to ensure health promotion activities are culturally competent? Propose strategies that you can employ to reduce cultural dissonance and bias to deliver culturally competent care. Include an evidence-based article that address the cultural issue.

Lead Exposure and Parkinsons Disease

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Abstract

Parkinson’s is a neurogenerative disorder that increases with severity over time. Parkinson’s disease the result of nuronal death  in the brain causing a decreased concentration of the neurotransmitter dopamine which is used to signal muscle movement. Parkinson’s leads to tremors, cognitive dysfunction and many other psychological ailments. The etiological source of Parkinson’s is not yet fully known. So far the consensus between academics is that it is a combination of genetic and environmental factors. Chronic exposure to environmental toxicants such as lead has shown to be a risk factor. This has been hypothesised as lead can bioaccumulate in the Substantia Nigra and cause oxidative stress. Assessment of lead concentrations is examined in the blood for acute exposure while lead concentrations in bones have a higher residence time which can assess lifetime exposure. As exposure to lead can cause varying severities of Parkinson’s disease this review details the different approaches taken by current and past studies while discussing its exposure, mode of action and genetic effect. Lead is a dangerous toxicant because it can pass through the blood-brain barrier. It can achieve this because it can obstruct the regulatory mechanism of calcium ions within a cell, which can have severe effects on intracellular biological activities. When lead enters the brain, many neurological disorders can develop such as brain/nerve damage, mental retardation, Parkinson’s and dementia. Lead also has been shown to have to a toxic effect on geans which are associated with the brain, bone marrow, liver and lung cells.


  1. How is lead initially implicated with Parkinson’s? Cross-Sectional and ecological studies.

The investigation of lead for its possible ecological link to Parkinson’s was inspired by the discovery in 1920 that l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) showed a chemically induced cause of Parkinson’s disease. This discovery showed that exogenous neurotoxins could cause Parkinson’s disease. Building on this discovery Seidler et al., 1996. Devised an ecological, case-controlled study that analysed several factors from living in rural areas, to show if and by how much they could change the risk of developing Parkinson’s disease. A rough 2:1 ratio was kept between controls and subjects who had Parkinson’s disease. A Total of 380 diagnosed subjects were recruited from hospitals, and 755 control subjects were recruited from local neighbourhoods and regional areas in Germany. The diagnosed subjects were interviewed about their possible environmental exposure to neurotoxic substances before developing the disease, and controls were interview for previous exposure within the past year. These groups were separated into never being exposed to occupational lead and ever being exposed. A statistical analysis of their results showed some significance for the link between lead exposure to Parkinson’s disease. This study was not conclusive as only 10% of the control and patients claimed they were exposed to heavy metals and lead exposure was self-reported exposure and which reduces the results scientific validity.

Winkel et al. conducted one of the first ecological studies implicating lead exposure to Parkinson’s., in 1995. This study analysed three post office workers who were in contact with lead sulphate batteries throughout thirty-six years. The three post office workers all showed symptoms of parkinsonism such as tremors, peripheral neuropathy, diminished mental processing (bradyphrenia), loss of memory, depression, muscular rigidity and Parkinson’s disease. The conclusion of this report highlighted that lead or lead compounds caused the prevalence of Parkinson’s between subjects.  Kuhn et al. conducted a similar study., in 1998 which focused on nine postal workers who were exposed to Lead Sulphate battery powered wagons throughout thirty years. These batteries had positive and negatively charged lead rods that were contained in a solution of sulfuric acid. To prevent short-circuiting workers had to remove the lead precipitate out of the battery daily. As there was a lack of personal protective equipment, the workers would frequently be exposed to sulphur when changing the acid and lead when replacing the rods and removing the contaminated precipitate. This study labelled each a number from 1 to 9. Cases 1 to 3 and 6 to 7 was expertly assessed for the link between their occupation and their development of Parkinson’s. Case 8 was tested for neurological damage and cases 4 and five died before the study. Out of the nine postal workers, seven were studied, three had signs of cortical atrophy, and one had periventricular legions in the brain. The workers also had other indicative signs of idiopathic Parkinson’s disease such as diminished motor function, resting tremors and impairment of voluntary movement (akinesia). Through the high occurrence of these extrapyramidal symptoms, it was hypothesised that the chronic exposure to lead or the combination of the lead with sulphate present in the batteries was a factor in the development of Parkinson’s disease. This hypothesis does not explain the underlying pathological mode of action for the lead. As four of the subjects had evidence of axonal neuropathy showed that Parkinson’s disease could originate from a toxin.

An ecological study conducted by Santurtún et al., 2016 analysed the geographic distribution of mortality as a result of Parkinson’s for 14 years. This data was collected, and cross-referenced with lead pollution concentrations in 50 different Spanish counties. Results showed that out of 36180 patients analysed most of the deaths accounted for patients over 65 and who lived in northern Spain. This co-incited with data connecting the northern states with increased air lead concentrations. The causal link between atmospheric lead and Parkinson’s disease could not be made, but from the available evidence, there was a significant link between Lead and Parkinson’s.


  1. Leads mechanism of exposure.

As lead has such a wide variety of uses, it made it easier for humans to get exposed to organic and inorganic forms. In the European Union, the two primary sources of dietary lead exposure are from cereals, grains, vegetables and tap water. (EFSA 2012). When lead (Pb

2+

) enters the body, it gets stored in bones and blood. Some of the most common forms of exposure are inhalation, ingestion and physical contact. Inhalation of lead fumes or particles is an issue for occupational health as workers may unwittingly expose themselves as the lead is odourless. During metal processing and soldering, escaping lead fumes can be inhaled by workers. Lead particles can also originate from fragmentation or working with lead paint. Lead particles depositing on surfaces such as food, clothes and other items can then be ingested and enter the body. Some studies have also shown leads ability to absorb through the skin (CDC, 2018). In the European Union, the two primary sources of dietary lead exposure are from cereals, grains, vegetables and tap water. (EFSA 2012).


  1. How have cohort and case-control studies been used to implicate lead in Parkinson’s Disease?

A case-controlled study conducted by Gorell et al., 1997, investigated the etiological importance of chronic exposure to lead, lead-copper and lead-iron for a period over 20 years. This case-controlled study gave the first look a population-based exposure in a workplace. The sample population were required to pass a Mini-Mental state exam, so no test subject was cognitively impaired. Following the study by Seidler et al., 1996, case subjects had to have some form of bradykinesia, tremor, muscular rigidity and loss/decreased postural reflexes. The sample population composed of 144 cases and 464 controls recruited from the metropolitan Detroit area.  These remaining participants completed a risk factor questionnaire on their past occupations lasting six months or more. An industrial hygienist assessed the risk of exposure to several heavy metals including Lead. Before this study, Lead was not sufficiently associated with Parkinson’s disease but was tested as the exposure was already measured in workplaces. Once again exposure was categorised into ever being exposed vs never being exposed to heavy metal. Out of 608 participants, there was a total of 15.1% who were exposed to lead, and 5.8% were exposed to lead over a period higher than 20 years. The odds ratio (OR) shown for the relation between lead and Parkinson’s disease was not statistically significant for short-term exposure (≤20 years) but long-term exposure (>20 years) the OR goes to 2.05 p=0.059 showing there is a borderline significance relating Parkinson’s to Lead

In 2006 Coon et al.  set up a test to investigate the link between chronic occupational exposure to lead on the findings from several studies including Gorell et al. 1997. In this study, the left tibia and calcaneus bones were analysed using blood levels in combination with K-shell X-ray fluorescence to measure a patients acute and chronic lead exposure. They compiled their data to estimate the bodies clearance rate of bone lead and applied it to a pharmacokinetic model which tells when did exposure occur. In this study they started by carefully selecting their patients through a series of screening processes through the Henry Ford Health System database screened 121 Parkinson’s disease patients and 414 controls who were 50 years or older. Occupational data was taken from the subjects, and a historical guide was made since they were 18 to the time of recruitment. The results showed that concentrations of lead increases within bones over time. This accumulation of lead gets slowly released back into the body, causing chronic exposure. The subjects showed that those who had increased exposure to Lead had an increased risk of developing Parkinson’s disease. This result also supported the results from Gorell et al. (1997) which stated a two-fold increased the risk of developing Parkinson’s disease from lead exposure.

A case-control study conducted by Weisskopf et al. in 2010 tried to replicate the work conducted by Coon et al. but increasing the population size. This study aimed to link bone Lead concentrations and the occurrence of Parkinson disease due to cumulative exposure. This study took a sample of 330 people who had Parkinson disease and 308 controls who had no evidence of Parkinson. Lead has a half-life of 20-30 years when deposited in bones (ATSDR 2007), making it an acceptable biomarker to get a more accurate representation of cumulative exposure. Using K-shell x-ray fluorescence technique, lead concentrations were taken from the left tibia and patella bones in the patients.  They concluded that since the tibia was cortical bone, it had a low turnover rate for lead and gave a half-life of around 20 years. The patella is a trabecular bone which has a higher turnover rate of a decade which gives a shorter reference time to exposure which may affect the visible occurrence of Parkinson.  The patients were categorised by their age, race, education and smoking habits which yielded similar bone lead concentrations throughout all patients. This categorisation also made results independent of these factors thus creating less bias. From this study, they could not find an association with the patella bone lead concentrations and Parkinson disease, but they did find a link between bone lead concentrations in the tibia. This finding supports the previous evidence showing that chronic exposure throughout 20 years gives a higher risk of developing Parkinson.

A cohort study conducted by Willis et al., in 2010 looked at 29 million people who availed of Medicare in 2003. This study gives community-based information about heavy metal exposure and the potential neurotoxic effect across the United States of America in comparison to smaller case-controlled studies of a select group. Only subjects who had stayed in the same residence for the past eight years were included in this study, reducing bias as it accounted for the movement in and out of states which could lead to bias results. Out of this population, 35,000 people with Parkinson’s disease were categorised by age, sex and race. These categories were then compared to counties that had high levels of Copper, Lead and Manganese air pollution and counties with lower levels of air pollution. The use of pollution rates in an area helped reduce recall bias from cases as they did not rely on self-reported cases of exposure seen in the report by Seidler et al., 1996. Although the primary data showed that areas that had higher levels of lead pollution had an increased occurrence of Parkinson’s disease, the study could not show a substantial correlation. The shorter analysis period of 8 years may be the cause in the lower correlation between lead and Parkinson’s. Previous studies conducted Coon et al.,. Gorell et al., and Weisskopf et al. showed that the onset of Parkinson’s disease correlates with a period of exposure for more than 20 years.

As lead requires chronic exposure for 20 years and its complex mechanistic pathway in biota, it is difficult to reach a consensus. A Case-controlled study in 2010 by Firestone et al., tried to resolve the inconsistencies within this field. An expert neurologist analysed candidates and selected cases with idiopathic Parkinson’s disease between 1992 and 2006. A total of 404 Parkinson disease cases and 526 unrelated controls were selected. Information was collected on their medical history, smoking habits, where they were demographically situated and information on past jobs which lasted over six months. Each job was assessed for exposure to heavy metals, solvents and pesticides. Candidates were separated by sex as occupations were generally dissimilar. These groups were further separated into never exposed if the exposure period was less than 20 years and ever exposed if exposure was greater than 20 years. The results showed that there was not a higher occurrence of Parkinson’s disease with higher exposure to lead, which contradicts previous studies conducted by [

Gorell et al., 1999; Coon et al., 2006

]. Variability may have come from the different study designs and a more significant impact of outliers due to their smaller study population.


  1. The likely mechanism(s) by which the toxicant exerts its effect.

Lead is a known potent neurotoxicant which has many mechanisms which it can exert its effect. When lead enters the body, it substitutes hydroxyapatite crystals in the bones. During bone remodelling, production and reabsorption, lead gets discharged back into the circulatory system. Lead then diffuses through the blood-brain barrier and attaches to sulfhydryl groups. This attachment has been associated with oxidative damage to intracellular neurons (

Coon et al.,2006

)

.

The current understanding of the connection between lead and Parkinson’s disease is not yet understood but in-vitro experiments suggest that Lead can propagate fibrillation and attach to negatively charged carboxylates, this attachment restricts electrostatic repulsion and facilitating collapse to the partially folded conformation which promotes the aggregation of α-synuclein. (

Fink, 2006, Uversky et al., 2001

).

This accumulation leads to the presence of Lewy bodies present in the remaining living neurons which can act as an indicator for diagnosis of Parkinson’s.  (

Uversky et al., 2001

).

Animal testing has also shown that lead can proliferate lipid peroxidation and damage cellular membranes which leads to neuronal death (

Sandhir et al., 1994

). It is thought that Leads ability to increase free radicals induces oxidative stress in the Basal Ganglia and Substantia Nigra, damage to this part of the brain associated with Parkinson’s disease. Oxidative stress can damage the mitochondria, kill neurons through overactivation (Excitotoxicity) and it can increase cytosolic free calcium which can kill neuronal cells (

Uversky et al., 2001

) Experiments on rats have also shown that lead exposure diminishes the release of dopamine by reducing depolarisation and it also decreases the sensitivity of the subsequent D1 receptor. Altering the body’s regulation of dopamine upsets any dopamine-dependent behaviours (

Weisskopf et al., 2010

).


  1. How interaction with other agents modifies the toxicant’s effects.

Case-control studies showed that the dual interaction between iron and lead significantly increases the chance in developing Parkinson’s disease OR = 2.84

p

= 0.036 and more notably lead and copper OR = 5.25


p


= 0.006 (

Gorell et al., 1997, Gorell et al., 1999, Coon et al., 2006

). The combination of these heavy metals is proposed to substantially increase levels of oxidative stress in comparison to lead by its self. Kuhn et al. (

1998

) have also proposed that the combination of sulphate and lead have a potential magnifying which could increase the risk of developing Parkinson’s disease. When exposed to several cations there is an observed increase in amyloid-beta, amyloid precursor protein, presenilin and β secretase complex in the brain suggests amyloidogenic processing. By processing amyloid- β precursor protein it can no longer repair or grow existing neurons causing neuronal death and the development of Parkinson’s disease, Alzheimer’s disease. (Ashok et al.,

2015

). Authors also observed (Ashok et al.,

2015

) increased levels of malondialdehyde (MDA), reduced activity of antioxidant enzymes, and the induction of 1L-1α and IL-1β in the frontal cortex and hippocampus of rats exposed to As + Pb + Cd mixture. #


  1. References:
  • Agency for Toxic Substance and Disease Registry (ATSDR). Toxicological profile for lead-update. Atlanta:U.S. Department of Health & Human Services, Public Health Service, 2007.
  • Caudle, W.M., Guillot, T.S., Lazo, C.R., Miller, G.W., 2012. Industrial toxicants and Parkinson’s disease. NeuroToxicology 33, 178–188.

    https://doi.org/10.1016/j.neuro.2012.01.010
  • CDC, 2018. CDC – Lead: How Lead Exposures Can Happen – NIOSH Workplace Safety and Health Topic [WWW Document]. URL

    https://www.cdc.gov/niosh/topics/lead/exposure.html

    (accessed 11.21.18).
  • Chin-Chan, M., Navarro-Yepes, J., Quintanilla-Vega, B., 2015. Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases. Front Cell Neurosci 9.

    https://doi.org/10.3389/fncel.2015.00124
  • Coon, S., Stark, A., Peterson, E., Gloi, A., Kortsha, G., Pounds, J., Chettle, D., Gorell, J., 2006. Whole-Body Lifetime Occupational Lead Exposure and Risk of Parkinson’s Disease. Environmental Health Perspectives 114, 1872–1876.

    https://doi.org/10.1289/ehp.9102
  • EFSA, 2012. Lead dietary exposure in the European population. EFSA Journal 10, 2831.

    https://doi.org/10.2903/j.efsa.2012.2831
  • Fink, A.L., 2006. The Aggregation and Fibrillation of α-Synuclein. Accounts of Chemical Research 39, 628–634.

    https://doi.org/10.1021/ar050073t
  • Firestone, J.A., Lundin, J.I., Powers, K.M., Smith‐Weller, T., Franklin, G.M., Swanson, P.D., Longstreth, W.T., Checkoway, H., 2010. Occupational factors and risk of Parkinson’s disease: A population-based case–control study. American Journal of Industrial Medicine 53, 217–223.

    https://doi.org/10.1002/ajim.20788
  • Gorell, J.M., Johnson, C.C., Rybicki, B.A., Peterson, E.L., Kortsha, G.X., Brown, G.G., Richardson, R.J., 1999. Occupational exposure to manganese, copper, lead, iron, mercury and zinc and the risk of Parkinson’s disease. Neurotoxicology 20, 239–247.
  • Gorell, J.M., Johnson, C.C., Rybicki, B.A., Peterson, E.L., Kortsha, G.X., Brown, G.G., Richardson, R.J., 1997. Occupational exposures to metals as risk factors for Parkinson’s disease. Neurology 48, 650–658.

    https://doi.org/10.1212/WNL.48.3.650
  • Kuhn, W., Winkel, R., Woitalla, D., Meves, S., Przuntek, H., Muller, T., 1998. High prevalence of parkinsonism after occupational exposure to lead-sulfate batteries. Neurology 50, 1885–1886.

    https://doi.org/10.1212/WNL.50.6.1885
  • Lasley, S.M., Lane, J.D., 1988. Diminished regulation of mesolimbic dopaminergic activity in rat after chronic inorganic lead exposure. Toxicology and Applied Pharmacology 95, 474–483.

    https://doi.org/10.1016/0041-008X(88)90365-1
  • Sandhir, R., Julka, D., Dip Gill, K., 1994. Lipoperoxidative Damage on Lead Exposure in Rat Brain and its Implications on Membrane Bound Enzymes. Pharmacology & Toxicology 74, 66–71.

    https://doi.org/10.1111/j.1600-0773.1994.tb01077.x
  • Santurtún, A., Delgado-Alvarado, M., Villar, A., Riancho, J., 2016. Geographical distribution of mortality by Parkinson’s disease and its association with air lead levels in Spain. Medicina Clínica (English Edition) 147, 481–487.

    https://doi.org/10.1016/j.medcle.2016.12.024
  • Seidler, A., Hellenbrand, W., Robra, B.-P., Vieregge, P., Nischan, P., Joerg, J., Oertel, W.H., Ulm, G., Schneider, E., 1996. Possible environmental, occupational, and other etiologic factors for Parkinson’s disease: A case-control study in Germany. Neurology 46, 1275–1275.

    https://doi.org/10.1212/WNL.46.5.1275
  • Uversky, V.N., Li, J., Fink, A.L., 2001. Metal-triggered Structural Transformations, Aggregation, and Fibrillation of Human α-Synuclein: A POSSIBLE MOLECULAR LINK BETWEEN PARKINSON′S DISEASE AND HEAVY METAL EXPOSURE. Journal of Biological Chemistry 276, 44284–44296.

    https://doi.org/10.1074/jbc.M105343200
  • Weisskopf, M.G., Weuve, J., Nie, H., Saint-Hilaire, M.-H., Sudarsky, L., Simon, D.K., Hersh, B., Schwartz, J., Wright, R.O., Hu, H., 2010. Association of Cumulative Lead Exposure with Parkinson’s Disease. Environ Health Perspect 118, 1609–1613.

    https://doi.org/10.1289/ehp.1002339
  • Willis, A.W., Evanoff, B.A., Lian, M., Galarza, A., Wegrzyn, A., Schootman, M., Racette, B.A., 2010. Metal Emissions and Urban Incident Parkinson Disease: A Community Health Study of Medicare Beneficiaries by Using Geographic Information Systems. American Journal of Epidemiology 172, 1357–1363.

    https://doi.org/10.1093/aje/kwq303
  • Winkel, R., Kuhn, W., Przuntek, H., 1995. Chronic intoxication with lead- and sulfur compounds may produce Parkinson’s disease. J. Neural Transm.-Suppl. 183–187.

A 2-year-old child is brought into the urgent treatment clinic with persistent fever, vomiting, and diarrhea. Consider the type of fluid and electrolyte losses this child is at risk for developing. Be specific about fluids lost through fever, vomiting, and diarrhea. What other clinical manifestations of fluid and electrolyte imbalances will you need to watch for?

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A 2-year-old child is brought into the urgent treatment clinic with persistent fever, vomiting, and diarrhea. Consider the type of fluid and electrolyte losses this child is at risk for developing. Be specific about fluids lost through fever, vomiting, and diarrhea. What other clinical manifestations of fluid and electrolyte imbalances will you need to watch for?

 

Pathophysiology Discussion Post
A 30-year-old woman presents with severe sunburn that she received from using a tanning bed. She tells you that she feels terrible and has been vomiting all morning. She also complains of feeling dizzy. All of her skin, except for the skin beneath her bikini top and bottom areas, are burned. Consider what effects a severe sunburn might have on this woman’s fluid and electrolyte balance. Be as specific as you can.
A 2-year-old child is brought into the urgent treatment clinic with persistent fever, vomiting, and diarrhea. Consider the type of fluid and electrolyte losses this child is at risk for developing. Be specific about fluids lost through fever, vomiting, and diarrhea. What other clinical manifestations of fluid and electrolyte imbalances will you need to watch for?
A 92-year-old nursing home patient is brought into the emergency department with hyperosmolar hyperglycemic nonketotic coma (HHNC). Her fluid and electrolyte imbalances are at a critical level. Consider the types of fluid and electrolyte imbalances she may have, and what kinds of clinical manifestations due to these imbalances that you are likely to see.
Biology homework help
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Nosocomial infections

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Nosocomial Infections 4

Running Head: NOSOCOMIAL INFECTIONS

Nosocomial infections.

Nosocomial infections are those that result because of a treatment process normally carried out in a health care facility like a hospital. Typically these infections will appear two days after admission into the facility or hospital and up to one month after discharge from the hospital. Nosocomial infections are also known as health care associated infections or hospital acquired infections. These infections are not genetic in nature. They are typically caused by a pathogenic organism that may invade the body and cause that particular type of infection. The Centre for Disease Control and Prevention (CDC) in the US puts firth estimates on infections at about 2 million resulting into 100,000 deaths annually. In Europe nosocomial infections account for two thirds of the 25,000 deaths annually.

Typically nosocomial infections result in blood stream infections, urinary tract infections and severe pneumonia. Most of these resulting infections have been known to exhibit antibiotic treatment resistance. The bacteria strains behind these infections are quickly evolving into Gram negative bacteria which is typically infecting people outside the health care facility.

These health care associated infections being widely prevalent are now being considered as important contributors of mortality and morbidity. They are continuing to increasingly attract attention due to the fact that increasing populations resulting in crowding, increased bacterial resistance especially to antibiotics, new strains of microorganisms and impaired immunity due to age, treatments and illness. Nosocomial infections continue to attract concerted focus. For developing countries these infections have become a major cause of preventable disease and death. The infections of concern and focus in this bracket include diarrhea, pneumonia and urinary tract infection, maternal and new born infections and those resulting from surgery and invasive medical procedures. Studies continue to indicate that the organisms that cause these hospital acquired infections usually come from a patient – endogenous flora. However they can also result from contaminated instruments and needles, environment – exogenous and contact with health care staff which are cases of cross contamination. Due to the fact that patients are mobile and admission periods have become shorter, a discharge is always initiated before the nosocomial infection becomes evident in the patient. This in turn has made it difficult to determine the causing organisms nature, whether it is exogenous or endogenous. When hospital attendants are complacent and ignore to practice correct hygiene regularly, nosocomial infections are likely to occur. As the hospital staff attends to one patient after another they themselves can be carriers of the pathogens The use of the out-patient treatment procedure means crowding as more people are hospitalized due to illnesses and a generally weakened immunity. It has also been noted that certain medical procedures which override the body’s natural immunity have resulted into a compromise of the defence system resulting into nosocomial infections. Health care facilities and hospitals continue to uphold sanitation protocols by the use of uniforms, washing and sterilization of equipment. It has been proven and has become acceptable standard procedure to wash hands using alcohol rubs before and after every patient contact. This is one of the ways available to combat nosocomial infection incidences. The controlled administration and prescription of anti- microbial agents such as antibiotics is also of great importance as far as nosocomial infections are concerned. The general view is that patients should have antibiotic prescription to treat illness but this sometimes may increase selection pressure resulting into resistant strains of the microorganism. The MRSA, Gram positive bacteria and Acinetobacter which is considered Gram negative are the cause agents of nosocomial infections. Currently drugs to effectively handle Acinetobacter germs are in short supply. Studies continue to show that Acinetobacter germs are evolving are becoming resistant to existing antibiotics. One typical case is that one of

Klebsielle pneumoniae

a strain prevalent in Brooklyn , New York city which is showing signs of resistance to all modern antibiotics. These germs are also fast spreading around the world. The Gram negative bacteria so classified because of its reaction to the Gram test has been known to cause infections of the bloodstream, urinary tract and severe pneumonia. These Gram negative micro organism has a unique cell structure that makes it difficult to attack unlike the Gram positive type.

Statistical data is now available in terms of country figures showing the annual infection rates. The CDC in the US puts forth 1.7 million infections annually with a mortality rate of 99,000 during the same period. The cost incurred ranges between 4.5 billion dollars to 11 billion dollars. The infections in France have been as indicated from 6.7% in 1990 to 7.4% Nationally the infection rate stood at 6.7% for 1995, 5.9% for 2001 and 5.01% for 2006.

The United Kingdom has a 10% infection rate and an 8.2% estimate in 2006. Finland has estimated infection rates at 8% in 2006.

Typically the Gram negative germs affect most often the hospitalized patients due to their weakened immune system. The Gram negative germ survives for long periods of time on surfaces entering the body through wounds, catheter and ventilators.

The contact transmission route remains the most frequent and important mode of transmission for this type of infections. Contact transmission  may either be direct in which case involving direct body surface to body surface contact and subsequent transference of the bacteria from the host. This will normally result from circumstances such as a person (medical staff) physically turning  patient, giving the patient a bath or any other activity requiring direct personal contact. This can also transpire between two patients. The indirect contact transmission involves a host and a contaminated object. This object maybe needles or dressing, instruments or gloves. The improper use of bags, vials and saline flush syringes also fall under this category of transmission. Microorganisms can also be passed onto the host by contaminated food, water, contaminated equipment and medication all of which fall under common vehicles of transmission.

Droplet transmission also a mode of transmission for the Gram negative germs. Droplets generated from source through coughing , sneezing and talking or during bronchoscopy convey the germs from the person and deposited on the host. Airborne transmission mode would fall the droplet transmission. In this case residue particles present in evaporated droplets which is a medium for the microorganism are suspended in the air for long periods of time. The germs in this case are widely dispersed and often enter the host through inhalation.

Gram negative germs can also be transmitted through vectors such as flies, rats and mosquitoes.

Nosocomial infections have various impacts. They generally reduce the quality of life when they result in disabling conditions. They cause emotional stress and functional impairment. The impact is much greater even among the countries poor in resource. Due to the little progress made to address the prevalence of nosocomial infections, their condition is deteriorating. The overall effect of this has been that the cost of health care has increased. This is as a result of increased periods in the duration of hospitalization, use of auxiliary medical care services such as lab tests, X- rays and transfusions. The treatment with expensive drugs may also be considered under this heading.

Nosocomial infections point to certain risk factors. This factors will pre-dispose a patient to infection. Treatments such as immunosuppresion and ant acid which form part of the patient’s treatment tend to undermine the body’s defence. Recurrent blood transfusions and anti microbial therapy are also considered as contributory risk factors.

The use of invasive devices such as catheters, surgical drains, tracheosomy tube, and intubations overrides the body’s natural lines of defence promoting pathogen invasion leading to an infection. Premature birth, immunodeficiency due to illness , irradiation and drugs which are some of the states of hospitalization impair their body’s defence against bacteria.

The prevention of nosocomial infections is directed towards isolation precautions. These precautions are aimed at preventing transmission. The interruption process is normally directed at transmission. Common practices such as washing hands and gloving helps to reduce the risk of skin microorganism transference between persons. Washing of hands promptly and repeatedly after every patient contact procedure has become an important part of controlling infection and also serves as an isolation precaution. Although a simple process, hand washing is nonetheless ineffective because it is often performed incorrectly. Gloves must be changed between patients and hands must be washed after the gloves have been removed. Sanitizing surfaces is also another way of effectively breaking the cycle of infection. However this also has been overlooked. The use of sanitization methods such as NAV-CO2 has proven effective against MRSA gastroententis and influenza. Sometimes hydrogen peroxide has also been in use. Using disposable aprons is also a method that can be employed to combat the transmission of nosocomial infections.

One of the areas of concern among the general medical fraternity is the antimicrobial resistance phenomenon. The Gram negative bacteria that is a cause of the nosocomial infections is a drug resistant agent. Malaria, TB, gonorrhea and ear infections are difficult to treat because of the drug resisting pathogens. A school of thought has indicated that in the near future we are likely to witness increased incidences of untreatable bacterial infections. A study by National Academy of Science puts the annual treatment cost for antibiotic resistant infections at approximately 30 billion dollars. While looking at the advent and development of antimicrobial resistance, we must consider the ability of the organism to speedily adapt to altered or new environment. These organisms being unicellular will rapidly evolve via a single gene mutation. A general view of the scope of the antimicrobial resistance takes into account a number of factors. The emergence of resistant strains such as

Staphylococcus aureus

in hospitals and non hospital settings. Similarly

Streptococcus pneumoniae

leads to many cases of pneumonia and meningitis, and this strain is resistant to penicillin.

The appearance of multi drug resistant TB has also elicited a lot of concern over the recent times especially so for the treatment of people with HIV.

Shigella dysenteriae, Vibrio cholerae,Salmonella

and

Eschenchia

remain some of today’s highly drug resistant pathogenic bacteria that are currently responsible for diarrhea (1676 words)  //

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Identify an evidence-based article that focuses comprehensively on a specific intervention or new diagnostic tool for the treatment of diabetes in adults or children.

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Identify an evidence-based article that focuses comprehensively on a specific intervention or new diagnostic tool for the treatment of diabetes in adults or children.

In a paper of 750-1,000 words, summarize the main idea of the research findings for a specific patient population. Research must include clinical findings that are current, thorough, and relevant to diabetes and the nursing practice.

Prepare this assignment according to the APA guidelines found in the APA Style Guide, located in the Student Success Center. An abstract is not required.

This assignment uses a grading rubric. Instructors will be using the rubric to grade the assignment; therefore, students should review the rubric prior to beginning the assignment to become familiar with the assignment criteria and expectations for successful completion of the assignment.

Consider the role of the nurse as an interdisciplinary team member in completing research

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Consider the role of the nurse as an interdisciplinary team member in completing research and using research findings to inform health care practices.

1.Discuss the role of the advanced practice nurse as an interdisciplinary research collaborator and member of the interdisciplinary team obligated to co-participate in the implementation and use of evidence-based practice.
2.End your discussion by providing an example of an evidence-based change that would require the collaborative efforts of nursing and at least two other healthcare disciplines and that would lead to quality improvement in healthcare.