Intro: One in every 4 Americans will die of heart disease. While the incidence for men has gotten better, for women it has not.
In a minimum 7-8 pages (includes cover and reference page), double spaced document, APA format. Discuss the effects of Heart Disease on the body of a woman in menopause. You are always welcome to go over 8 pages, (do what you need to do to get your questions answered). Be sure to answer each of the the following questions in your paper.
1) Which physiological (body) systems are affected by heart disease and how are they affected. What does the disease do to the body that is negative. (not genetic heart deformities of the heart please)
2) What are the differences to consider if the female patient has had the heart disease diagnosis for 25 years or was recently diagnosed? What does the body look like inside and what is the person thinking if they have had it 25 years? What about newly diagnosed? This question is a lot of logic and thinking about the body systems and the persons attitude towards the disease.
3) What is the difference between an older woman with well-controlled heart disease and an older woman with uncontrolled heart disease? What are they thinking and how are they acting? What is happening inside their body?
4) What special nutrition related considerations might there be for the elderly woman patient with heart disease as opposed to a 35 year old female patient with heart disease? What are they thinking and how are they acting? How is an older person’s lifestyle different than a younger person’s?
5) Please include a cover sheet and reference page so minimum length is 7 pages but 8 would be fine.
Appropriate sources for current research on this topic are peer-reviewed research articles (try searching in PubMed via the library – The Journal of the Academy of Nutrition and Dietetics is an example of a peer-reviewed journal, or book Geriatric Nutrition 4th edition; Chernoff (the 3rd edition( end of the cardiovascular chapter in the book,
also the American Heart Association, the AARP websites look under research or articles tab, or American Heart Association, or American Medical Association). Cite all your sources in the text paragraphs like this ex: (Robinson, 2014) and you should have a lot of these in your paper. Please and the full reference at the end on the reference page APA format. If you don’t know already, peer reviewed means that other health professionals have reviewed it and think the document is legit. Non-peer reviewed is someone just writing their opinion in an article or blog and it is just that…their opinion. Do not use opinions unless it is yours. If citing from web pages they must be legit sources. Please have a cover page and a reference page so the total number of pages you are submitting is 7 or more.
following criteria must be covered.
- Were all of the questions above answered satisfactorily?
- Were appropriate sources (peer-reviewed articles) utilized for research? Minimum of 3 and your book is NOT one of the 3.
- Were all sources cited and included in APA formatted bibliography?
- Entertainment value (was it interesting)?
Presentation Gout is an intense incendiary joint inflammation with the power to completely obliterate the respectability of the joint prompting extreme incapacity. It is named as a "genuine precious stone affidavit sickness" brought about by development of monosodium urate gems in joints and different tissues. It is the normal reason for incendiary joint inflammation that has expanded in commonness in ongoing decades (Roddy and Doherty 2010). Gout ordinarily results from the connection of hereditary, sacred and ecological hazard factors. It is increasingly regular in men and unequivocally age related. Both intense joint pain and ceaseless arthropathy (tophaceous gout) are considered under the rubric of gout (Mikuls and Saag 2006; Roddy et al. 2007). In a more extensive term, it tends to be characterized as blend of occasions including an expansion in the serum urate fixation, intense ligament assaults with monosodium urate monohydrate precious stones self evident in synovial liquid leukocytes, and tophi which more often than not happens in and around joints of the furthest points. These physio-synthetic changes either happen independently or in mix (Terkeltaub 2003; Shai et al. 2010). Gouty joint inflammation represents a great many outpatient visits every year and the pervasiveness is rising. It influences 1-2% of grown-ups in created nations, where it is the most widely recognized incendiary joint inflammation in men. Epidemiological information are reliable with an ascent in predominance of gout. Rates of gout have roughly multiplied somewhere in the range of 1990 and 2010. Various variables have been found to impact rates of gout, including age, race, and the period of the year. In men beyond 30 years old and ladies beyond 50 2007 years old, is 2% (Eggebeen 2007). Life systems and Pathophysiology Gouty joint inflammation is a standout amongst the most excruciating rheumatic illnesses and its occurrence increments instantly with propelling age. In 75% of the patients, gouty joint pain at first strikes a solitary joint which is most usually the huge toe. In ladies gout create in expanding numbers after menopause in the long run at an occurrence rate equivalent to that of men (Hootman and Helmick 2006). In older patients, an event of gout is generally less staggering than in middle age and frequently infers a furthest point poly or mono articular introduction instead of the exemplary mono articular lower limit picture regularly shown by moderately aged men. In more established patients, gout can be more probable the clinical picture of osteoarthritis or rheumatoid joint inflammation (Cassetta and Gorevic 2004). Gouty joint pain can be ordered into four phases relying on dimension of seriousness in particular; (I) Asymptomatic Hyperuricemia: In this stage, an individual has raised blood uric corrosive dimensions however no different indications and in this manner requires no treatment. (ii) Acute Gouty Arthritis: In this stage, hyperuricemia prompts statement of uric corrosive gems in joint spaces, prompting gouty assaults (iii) Interval/Intercritical: This is the phase between intense gouty assaults without any manifestations and (iv) Chronic Tophaceous Gout: where the malady prompts lasting harm (Bhansing et al. 2010). Pathogenesis of gouty joint inflammation is fundamentally affected by sodium urate precious stones and provocative procedures they actuate (Wise and Agudelo 1996). A wasteful renal urate discharge which prompts the raised dimensions of uric corrosive over the immersion point for urate precious stone arrangement is a noteworthy determinant of the illness. Purine catabolism prompts the arrangement of metabolic result, uric corrosive. In many vertebrates like higher primates, numerous feathered creatures and a few reptiles, the urate oxidase (uricase) protein changes over uric corrosive (moderately insoluble) to allantoin (exceedingly solvent), prompting low serum uric corrosive dimensions. A progression of parallel transformations in the qualities of uricase in the Miocene time frame results in the generation of the broken type of uricase that prompts gathering of moderately larger amount of insoluble uric corrosive and along these lines the improvement of gouty joint pain (Liote and Ea 2006; Eggebeen 2007). Debasement of purines results in the endogenous creation of uric corrosive that typically contributes around 66% of the body urate pool, the rest of begun by dietry consumption. Of the uric corrosive framed day by day, about 70% is discharged through the kidney while the rest is dispensed with into the biliary tract and after that changed over to allantoin by colonic bacterial uricase. In this way, in most by far gouty patients, hyperuricaemia happens from diminished proficiency of renal urate leeway (Laubscher et al. 2009; Terkeltaub 2010). Improvement of the intense and constant fiery gout is encouraged with the affidavit of monosodium urate (MSU) precious stones in joints. while MSU precious stones were first distinguished as the aetiological operator of gout in the eighteenth century and all the more as of late as a 'peril flag' discharged from passing on cells, little is thought about the atomic systems fundamental MSU-initiated irritation (Martinon et al. 2006). For precious stone development n event of gout, the ionic result of sodium and uric corrosive must be at or over the immersion level at which MSU gems can shape. Uric corrosive is a frail corrosive of pKa 5.75 and, it exists fundamentally in the ionized structure as urate at physiological pH of 7.40. MSU has restricted dissolvability under physiological conditions and the immersion level in plasma at a pH of 7.40 is 6.8 mg/dl (408 Âµmol/l) and when the plasma fixation surpasses this dimension, gems may frame in the joints and tissues (Terkeltaub 2010). MSU gems specially structure inside ligament and sinewy tissues, where they are generally more secure from contact with fiery arbiters and may abide for quite a long time without creating any deformities. Notwithstanding, if 'shed' from these locales of root into the joint space or bursa, they are very phlogistic particles that are promptly phagocytosed by monocytes and macrophages, animating the NALP3 inflammasome, setting off the arrival of IL-1 and different cytokines and a consequent penetration of neutrophils. Here the white cells discharge a bundle of fiery middle person substances which, notwithstanding annihilating the precious stones, additionally harm the encompassing tissues (Martinon et al. 2006). This intense aggravation characterizes the side effects of an intense flare, for example, agony, swelling and redness and is ordinarily self-constraining. Consistent affidavit of extensive quantities of MSU precious stones may likewise taking off the joint harm through mechanical consequences for ligament and bone (weight disintegration), and most likely second rate irritation. In any case, these progressively unending precious stone tissue collaborations still stay tricky and needing further examinations (VanItallie 2010). Deliberate Lupus Erythematosus (SLE) Presentation Lupus is an immune system infection which prompts both intense and incessant irritation of different tissues of the human body. Lupus can be grouped into various structure contingent on the objective tissues and organ framework. Characterized as Type III extreme touchiness response, individuals with lupus produce anomalous antibodies in their blood that objective tissues inside their own body as opposed to outside irresistible operators. Since the antibodies and going with cells of aggravation can influence tissues anyplace in the body, lupus can possibly influence an assortment of regions, for example, heart, joints, skin, lungs, veins, liver, kidneys, and sensory system. At the point when inner organs are included, the condition is alluded to as foundational lupus erythematosus (SLE). The infection might be gentle or extreme and perilous (Wallace 2010). The commonness of lupus ranges from around 40 cases for each 100,000 people among Northern Europeans to more than 200 for every 100,000 people among blacks (Johnson et al. 1995). In the United States, the quantity of patients with lupus surpasses 250,000. The future of such patients has improved from a rough 4-year survival rate of half during the 1950s to a 15-year survival rate of 80% today (Merrell and Shulman 1955; Abu-Shakra et al. 1995). All things considered, a patient in whom lupus is analyzed at 20 years old still has a 1 out of 6 shot of biting the dust by 35 years old, regularly from lupus or disease. Afterward, myocardial dead tissue and stroke become critical reasons for death (Cervera et al. 2003). Life systems and Pathophysiology SLE is a fiery and multi-foundational immune system issue portrayed by an uncontrolled auto-reactivity of B and T lymphocytes. This outcomes in the creation of auto antibodies (auto-Abs) against self-coordinated antigens and causes tissue devastation (Cuchacovich and Gedalia 2009). Pathogenesis of SLE is a multi-factorial occasion and the careful instrument of infection improvement and movement is as yet vague. Different variables are known to be related with the advancement of the infection, for example, hereditary, racial, hormonal, and ecological components. Imperfections in apoptosis are one of the proposed components engaged with patho-physiological occasions of SLE. Lopsidedness in apoptotic hardware prompts the creation of auto-antibodies. These antibodies come up short on the capacity to separate among pathogenic and typical host cells and cause increment cell demise and anomalies in invulnerable resilience (Andrade et al. 2000; Rahman and Isenberg 2008). It is trusted that all the real parts of insusceptible framework are engaged with SLE movement at different dimensions. For the most part proteins present in cell core are focused by the safe framework. The possible natural triggers for SLE incorporate bright light, drugs, and infections. These boosts cause the pulverization of cells and uncover their DNA, histones, and different proteins, especially parts of the cell core. It is seen that in patients experiencing SLE, there is expanded cell passing in monocytes and keratinocytes and hyper articulation of Fas protein by B and T cells of the resistant framework. Tingible body macrophages (TBMs) are substantial phagocytic cells present in the germinal focuses of optional lymph hubs. They express CD68 protein. These cells typically inundate B cells which have experienced apoptosis after>GET ANSWER