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Case study – Assessment 1 (40% weighting)
“Outline how the important factors present in the case study would influence Mrs White’s health and well being.
You should describe the key factors involved in Mrs White’s health, what the causes are and what the symptoms would be.
You should discount any details from the case study that you do not consider relevant.
Significant credit will be given to explanations of the biology behind the symptoms, and for clear and concise explanations to structure and function/cause and effect.
You might very briefly indicate how Mrs White could be treated for these indications, but do not make this the focus of your assignment.
Additional credit will be given for identifying factors that may aggravate each other, or where different treatments may be non-complementary.”
WORD LIMIT = 2000 WORDS +/- 10%
WORD COUNT = 2,198 WORDS
|Anatomy, physiology and treatment of:||Marks:|
|Blood glucose regulation and diabetes||15|
|Structure of skin and primary wound healing and inflammatory response||10|
|Poor wound healing due to stress||10|
|The control of blood pressure in the body||5|
|Function of the respiratory system to include gaseous exchange and the breathing mechanism||10|
|Diet and lifestyle factors||15|
|Identifying health factors that may aggravate each other, or where treatment may be non-complementary i ii iii||10|
|Reference list and referencing in the text||10|
|Breadth of Knowledge, Relevance and Quality of Language||10|
CASE STUDY: MRS WHITE
This essay will attempt to identify and describe the important health-related factors present in the case study of Mrs White, outlining the effects of these issues on Mrs White’s health and wellbeing.
A laceration is a wound resulting from the tearing of soft body tissue; this sort of wound is frequently polluted with bacteria from the object that caused the cut (Heller, 2013). The fall that Mrs White suffered, resulting in a laceration on the side of her lower foreleg, would have triggered the ‘inflammatory response’. This is a physiological response to tissue damage- caused in Mrs White’s case by trauma- designed to facilitate healing by removing damaged tissue. Mrs White would have experienced four symptoms associated with inflammation: redness of the skin, as arterioles and capillaries dilate to enable increased blood flow to the affected area; increased temperature of the affected area, promoting the activity of phagocytes that consume dead or dying tissue; swelling, which helps the clotting and infection-fighting processes; and pain, as sensory nerve endings are compressed by swelling (Nordqvist, 2012). Blood clot and cell debris would have filled the gap between the edges of her wound in order to stop the bleeding.
Following this initial inflammatory response, Mrs White’s body would have begun the ‘primary healing’ process. In primary healing, macrophages from the dermis – situated between the epidermis and the subcutaneous layer in the skin- travel to the blood clot formed between the wound edges in order to remove the clot and cell debris. Fibroblasts from the dermis similarly enter the blood clot, secreting collagen fibres that hold the wound edges together. Epithelial cells grow across the roof of the dermis, resulting in the epidermis growing upwards until full thickness is restored. Blood supply to the wound is restored by the formation of granulation tissue, which is in turn replaced by fibrous scar tissue (Waugh and Grant, 2014).[^]
Mrs White’s laceration healing is very slow. One factor that is lengthening her recovery time is the long-term stress that she has been put under by her sons, who believe that she should be placed in a care home. Fear of losing her independence has been a prolonged emotional stressor, threatening homeostasis, which has triggered a long-term stress response regulated by the Hypothalmic-Pituitary-Adrenal (HPA) system (McLeod, 2010). The hypothalamus is activated by the stressor and releases corticotrophin releasing hormone (CRH), stimulating the anterior pituitary to secrete adrenocorticotrophic hormone (ACTH). ACTH provokes the release of mineralocorticoids and glucocorticoids from the adrenal cortex. This results in a diminished inflammatory response, since high levels of CRH can act as an anti-inflammatory and anti-edemic agent (Sapolsky, Romero and Munck, 2013).[^]
The immune response is suppressed while the stress response is active, and mineralocorticoid release leads to increases in blood pressure, blood volume, and salt and water retention by the renal tubules (Waugh and Grant, 2014). Further side effects of Mrs White’s glucocorticoid release include elevated blood glucose levels, together with increased catabolism of fat and protein in order to form new sugar (‘lipolysis’ and ‘gluconeogenesis’, respectively). Lipolysis increases the circulation of free fatty acids (FFAs) in the bloodstream, with chronically-elevated levels of FFAs known to increase insulin resistance. Unless higher levels of insulin are then secreted, raised FFAs will lead to type two diabetes (Boden, 2008).[^]
Type two diabetes is a condition that Mrs White suffers from. This impacts negatively upon her wound healing because of the poor blood circulation that is characteristic of type two diabetes, whereby fatty deposits in her arteries slow the blood flow, thus limiting the stream of oxygen and healing nutrients essential to wound healing (Harvard Health Publications, 2013). The main symptoms that Mrs White will have experienced as a type two diabetic are: frequent urination, especially at night (‘polyuria’); excessive thirst (‘polydipsia’); fatigue; and blurred vision (NHS Choices, 2014a). Polyuria occurs when excess glucose remains in the glomerular filtrate, raising its osmotic pressure and reducing water reabsorption, resulting in electrolyte imbalance and excretion of urine; polyuria in turn leads to polydipsia in an effort to restore homeostasis (Waugh and Grant, 2014). Visual impairment is caused by thickening of the epithelial membrane in small blood vessels, and diabetes is the most common cause of visual impairment and blindness amongst people of working age in the United Kingdom (NHS Choices, 2014a).
Inadequate control of blood glucose – which should be maintained in the 4.0-5.9 mmol/litre before eating, and under 7.8 mmol/litre two hours after eating (Diabetes.co.uk, 2015) – is the causal factor behind Type Two Diabetes. Pancreatic monitoring of blood glucose levels is a continuous process (ABPI, 2015). Blood glucose regulation is effected mainly by insulin and glucagon. Insulin is a polypeptide secreted into the bloodstream by beta cells in the endochrine pancreas, serving to lower blood sugar levels by increasing muscular and connective tissue use of glucose, as well as increasing the storage of glucose in the liver and skeletal muscles via glycogenesis. Secretion of insulin is stimulated in response to raised blood glucose levels (after a meal, for example) and is decreased by glucagon. Glucagon is a peptide hormone secreted into the bloodstream by alpha cells in the endochrine pancreas, serving to raise blood glucose levels through the conversion of glycogen to glucose in the liver and skeletal muscles, as well as stimulating the formation of new sugar from non-carbohydrate sources (Waugh and Grant, 2014).[^]
The likelihood of contracting Type Two Diabetes increases with age, and there are many possible reasons for this. Beta cell function declines with age (Grant and Waugh, 2014), and has reduced proliferative capacity. Factors underlying the age-related decline in beta cell proliferation include reduced expression of cell cycle activators, increased expression of cell cycle inhibitors, reduced pdx1 expression, and increased amylin aggregation (Gunaserkaran and Gannon, 2011). Being overweight (as Mrs White is) or obese is another factor that predisposes to Type Two Diabetes (NHS Choices, 2014a).[^]
Mrs White is on anti-hypertensive medication to control her high blood pressure. It is fortunate that she remembers to take these tablets- unlike the tablets she forgets to take that would aid in regulating her blood glucose levels- since a combination of high blood pressure and high blood glucose worsens diabetic visual impairment and kidney disease (Dansinger, 2015). Blood pressure is an example of a negative feedback system, as the following description in relation to Mrs White’s high blood pressure will demonstrate: stretch-sensitive baroreceptors located within the wall of the aortic and carotid sinuses determine that blood pressure is too high -> this sensory information is sent along an afferent nerve to the cardiovascular centre (CVC), comprising the pons and medulla of the brain stem -> the CVC processes this incoming sensory information and sends motor instructions along efferent nerves to the heart and blood vessels -> in Mrs White’s case, these motor instructions will cause the blood vessels to vasodilate and the heart rate to slow down and decrease stroke volume, jointly decreasing blood pressure -> and now, as blood passes through the aortic and carotid sinues, baroreceptors sense that blood pressure has returned to an acceptable level [the ideal reading is 120/80mmHg (Blood Pressure UK, 2008)], and the CVC ‘switches off’ its initial motor message to the blood vessels and heart (Waugh and Grant, 2014).[^]
The blood vessels and heart, together with the lungs and associated respiratory structures, are crucial components of ‘gaseous exchange’. Deoxygenated blood is discharged from the right ventricle into the pulmonary trunk, which separates into the right and left pulmonary arteries and transports blood to the right and left lungs respectively (Bailey, 2015a). Inside the lung, each pulmonary artery separates into a series of arterioles, which in turn split into capillaries and form a concentrated capillary network around the alveoli, the respiratory surface of the lungs. Alveolar air has a higher concentration of oxygen than deoxygenated blood, inducing the diffusion of oxygen from the alveoli into the bloodstream of the surrounding capillaries, and the passage of carbon dioxide from the capillaries into the alveoli (Bailey, 2015b). Once equilibrium in oxygen and carbon dioxide levels has been established (known as the ‘external respiration’ function of the respiratory system), blood is then transported back to the heart- via pulmonary venules that join together to form the pulmonary veins, feeding into the left atrium- so that oxygen-rich blood can be discharged from the left ventricle into the aorta, which transports it to all structures in the body (WebMD, 2013). Gaseous exchange then takes place again (known as the ‘internal respiration’ function of the respiratory system) between capillary blood and systemic body cells, with oxygen diffusing from capillary blood into body cells, and carbon dioxide passing into the blood from the interstitial fluid surrounding the body cells (Bailey, 2015c). Erythrocytic haemoglobin in the bloodstream binds the carbon dioxide, and newly-deoxygenated blood is transported back to the right atrium of the heart from the tissue capillaries by a system of veins (PubMed Health, 2015).
The breathing mechanism is triggered when chemoreceptors on the walls of major arteries detect an increase in blood carbon dioxide levels. This information is sent via a sensory nerve to the respiratory centre (groups of nerves in the medulla and pons), which processes the incoming data and sends out motor messages along efferent nerves to the diaphragm and intercostal muscles, stimulating muscular contraction and thus increasing the volume of the thoracic cavity. Air is drawn in through the nose and mouth, being warmed and filtered by nasal cavity blood vessels and mucus, before passing through the pharynx, larynx, trachea, and brochii (structures lined with ciliated epithelium that serve to keep the lungs free from mucus and debris) into the lungs. The lungs expand, stimulating baroreceptors in the bronchii and bronchioles to send a stretch-based sensory message to the respiratory centre, which in turn ceases to send inspiratory impulses to the diaphragm and intercostal muscles. The respiratory muscles stop contracting and inspiration ends; expiration occurs as a result of the subsequent relaxation of the diaphragm and intercostal muscles (Encyclopaedia Britannica, 2015).[^]
Mrs White’s respiratory function is currently compromised by a chest infection, which is defined as an infection of the lungs or airways and usually manifests as pneumonia or bronchitis. The case study states that she is suffering difficulty breathing, and further symptoms that she is likely to experience include coughing up phlegm or blood, fever, rapid heartbeat, tightness in the chest, and a feeling of disorientation (NHS Choices, 2014b). Acute bronchitis results from the multiplication of pathogenic bacteria present in the respiratory tract, usually occurring after a common cold as defence mechanisms are depressed by the initial viral infection. Pneumonia is an infection of the alveoli, whereby inhaled or blood-borne microbes bypass pulmonary defences and colonise the lungs. Mrs White’s age increases her susceptibility to chest infections, owing to loss of mucus production in the airways and less efficient respiratory reflexes, as does her suppressed immunity owing to the aforementioned long-term stress response, and the fact that she suffers from type two diabetes (Waugh and Grant, 2014).[^]
Despite being diagnosed with type two diabetes, Mrs White has a ‘sweet tooth’ and does not control her blood glucose level very well. Foods and drinks that are high in fat and sugar should be consumed sparingly, as they are high in quick-release carbohydrate energy and of minimal other nutritional value. When carbohydrate intake exceeds bodily requirements it is converted to glycogen – stored in the liver and skeletal muscles – and fat, which is stored in adipose tissue. Mrs White is described as ‘overweight’- meaning that her body mass index (BMI), calculated by dividing her weight (kg) by her height in metres squared (m2), is in the 25-29.9 range- and her reliance on unhealthy food will only push her towards a clinical definition of ‘obesity’ [a BMI in the 30-39.9 range] (Waugh and Grant, 2014) and associated comorbid conditions such as cardiovascular disease, stroke, sleep apnea, gallbladder disease, hyperuricemia, gout, and osteoarthritis (Khaodhiar, McCowan, and Blackburn, 1999).
Instead of over-indulging in foods such as cakes, chocolate, and biscuits, Mrs White should ensure that two-thirds of her daily intake comes from two specific food groups: starchy carbohydrates (bread, rice, potatoes, pasta) and fruit and vegetables. Non-dairy sources of protein (meat, fish, eggs, beans) and milk and dairy foods should make up the majority of the remaining third of her daily consumption, with high fat and/or high sugar foods and drink an occasional treat (NHS Choices, 2013).
Mrs White lives a sedentary lifestyle, which greatly increases her risk of suffering a serious cardiovascular event, certain types of cancer, and premature death. Sitting down for extended periods of time has been shown to impair the body’s ability to regulate blood glucose, blood pressure, and break down fat (NHS Choices, 2014c). As an overweight type two diabetic who requires anti-hypertensive medication to regulate her blood pressure, Mrs White would be well-advised to gently introduce aerobic and major muscle group–strengthening exercises into her weekly routine (NHS Choices, 2015).[^]
The conclusions of this case study are demonstrated in a simplified tabular form below:
|Factor One:||+ Factor Two:||-> Complication:|
|Sedentary Lifestyle||+ Poor Diet||-> Type II Diabetes…|
|Sedentary Lifestyle||+ Stress||-> Wound Healing (slow), Blood Pressure (high)|
|Elderly||+ Stress||-> Respiratory Infection (increasing susceptibility)|
The website links in the references below redirect here, rather than directing to the relevant web pages. Web pages are frequently added to – and removed from – the web, and sharedsapience.info does not want to include links to missing web pages. The web addresses can be copy-and-pasted into a new tab if the reader wishes to check the source material.
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