NRSG353: Myocardial Infarction with History of Stable Angina & Mitral Valve Stenosis - Cushing’s Syndrome Assessment
Solution Code: 1DEE
Question: Nursing Case Study
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Nursing Case Study Assignment
Case Scenario
Case Study 1: Myocardial infarction with history of stable angina and mitral valve stenosis
Mr Tupa Savea is a 54 year old male who has been transferred to the coronary care unit (CCU) from the emergency department for management of episodic chest pain. He has a history of stable angina and mitral valve stenosis. Mr Savea is of Samoan background and has lived in regional Queensland for the last 20 years with his wife and children. He was brought in by ambulance having had chest pain and shortness of breath. He reports having similar symptoms on and off for the past two months but did not visit his GP as he assumed the discomfort was due to indigestion. Mr Savea is an ex-smoker, tobacco free for the last six months and a social drinker (approx. 10 units/week). He works full-time as an orderly at a local hospital and is active in the Samoan support community.
On assessment Mr Savea’s vital signs are: PR 90 bpm and irregular; RR 12 bpm; BP 150/100mmHg; Temp 36.9°C; SpO
98% on oxygen 8L/min via Hudson mask. He has a body mass index (BMI) of 35 kg/m2 indicating clinical obesity. Blood test results show elevated cardiac enzymes and troponin levels and cholesterol level of 8.9mmol/L. His ECG
indicates that he has a ST segment elevated myocardial infarction. Mr Savea was administered sublingual glyceryl trinitrate followed by morphine 2.5 mg IV for pain in the emergency department. He reports being pain free on admission to CCU.
Case Study 2: Cushing’s Syndrome
Ms Maureen Smith is a 24 year old female who presented to her GP for ongoing gastrointestinal bleeding, abdominal pain and fatigue which has been worsening, and was referred to the local hospital for further investigation. Maureen was diagnosed with rheumatoid arthritis (RA) when she was 15 years old, and has experienced multiple
exacerbations of RA which have required the use of high dose corticosteroids. She is currently taking 50mg of prednisolone daily, and has been taking this dose since her last exacerbation 2 months ago. Maureen also has type 2 diabetes which is managed with metformin. She is currently studying nursing at university and works part-time at the local pizza restaurant.
On assessment, Maureen’s vital signs are: PR 88 bpm; RR 18 bpm; BP 154/106 mmHg; Temp 36.9oC: SpO 99% on room air. She has a body mass index (BMI) of 28kg/m2 and the fat is mainly distributed around her abdominal area, as well as a hump between her shoulders. Maureen’s husband notes that her face has become more round over the past few weeks. Her fasting BGL is 14.0mmol/L. Blood test results show low cortisol and ACTH levels, and high levels of low high-density lipoprotein cholesterol. She is awaiting a bone mineral density test this afternoon, and is currently collecting urine for a 24-hour cortisol level measurement.
Case Study 3: Decompensated Liver Cirrhosis
Mr Ronald Stone is a 47-year-old man who was brought in by ambulance to emergency department with haematemesis. According to his partner he vomited a total of 300 mL of fresh blood this morning. He reported that he has been spitting blood stained sputum for the last few weeks with no associated cough or shortness of breath. For the past 3 days he has complained of increasing abdominal pain but with no diarrhoea or black stools. Mr Stone tested positive for Hepatitis C virus (HCV) genotype 1A in June 2010. He has cirrhosis and a history of heavy alcohol use, although he no longer drinks. He ceased intravenous drug use 10 years ago, and stills smokes tobacco and marijuana on a daily basis. He used to work with City Rail but has been made redundant 13 months ago and has been unemployed
since. He lives with his partner and 2 young children from a previous marriage.
On assessment Mr Stone’s vital signs are: PR 112 bpm; RR 24 bpm; BP 105/64mmHg;
Temp 37.4 °C; SpO 94% on room air. He has a body mass index (BMI) of 31.5kg/m2. He is lethargic but orientated to time, place and person. He has a swollen and tight abdomen typical of ascites and bilateral leg oedema. Blood test results show Hb 85 g/L, decreased WBC, platelets and albumin, and a marked increase in both serum ammonia and total
bilirubin levels. 6 months ago he underwent an eosophagogastroduodenostomy (EGD) which showed grade 2 oesophageal varices. He is ordered the following medications: Vitamin K 1 mg IV stat, aldactone 25mg PO TDS, lactulose 15mls PO TDS, and vitamin B12 100mg IV TDS. He is awaiting a CT abdomen scheduled for this afternoon.
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Solution:
Cushing’s syndrome is a complex chronic disease that results from excessive production of circulatory cortisol hormones (Rizk et al, 2012). The high cortisol hormone levels can be as a result of swelling of the pituitary gland making which makes it release excess cortisol; excessive production of cortisol due to adrenal tumors; excessive use cortisteroid medications; and in rare cases, as a result of ‘secretion of cortisol hormone from other swellings in the body, referred to as ‘ectopic’. The illness is difficult to diagnose and manage with high chances of mortality if not treated properly. Other causes include pregnancy, alcoholism, depression (Newell-Price et al., 2006; Praw et al., 2009). In Case Study two, Maureen has been taking corticosteroids to treat rheumatoid arthritis. This could be linked as a cause for her condition.Cushing’s syndrome is rare (Ferone et al., 2013). Studies by Etxabe and Vazquez (1994) and Lindholm et al. (2001) found that the annual incidence for the disease ranges from 1.2 to 1.7 cases per million people. The risk factors for the condition are adrenal or pituitary tumors, long-term treatment with corticosteroids, and being a female (Ferone et al., 2013).Illness of a family member affects the whole family. Maureen’s condition and the health care experience affect her husband and relatives who have to forego some of their roles and take care of her. Both the patient and the family members need education and counselling to help them cope with the disruptions and accept the new situation.
Other family members therefore, must change their lifestyles and take some of the roles initially played by the ill person. This in turn interferes with their own normal role functioning. Maureen’s condition disrupts her studies and work as well as her husband’s career. At that stage of life as a couple had anticipated a time of enjoyment together, the illness impacts on them negatively. The condition also strains Maureen’s family economically as they have to pay hospital bills and buy medication. Her long-term illness. Long-term illness result in anxiety among close family members and also impact on family relationships. This affects family-and self-care and the outcome. Some family members sympathise and are usually willing to help the patient while others are never interested in helping. Psychosocially, the family members and the patient face great challenges in accepting and coping with the disease. Especially the irritability and hyperactivity could result to stress among close family members.
2. List five (5) common signs and symptoms of the identified condition; for each provide a link to the underlying pathophysiology
Symptoms of Crushing’s Syndrome depend on the cause of the condition, the extent and duration of cortisol excess, amount of other adrenaline hormones in the patient’s body and presence of adrenal tumors ((Rizk et al, 2012; Morgan & Laufgraben, 2013)Symptoms of Crushing’s Syndrome include are presented in the following following;
| Symptom | Pathophysiology | Gland/ Body tissue/organ or system affected |
| Recently developed obesity and lipid metabolism (Ruscscher et al., 2005) | -Increased cortisol induces conversion of glucose to body fat and change in its distribution and storage, and induced lipolysis in peripheral fat storages. | Neck, face, trunk, abdomen, between shoulders, limbs (ref) |
| Excess cortisol in the body suppresses or stimulates the endocrine system | Nervous and the Endocrine system | |
| Loss of bones (Howlett et al., 1986) | - Inhibited bone metabolism and the presence of hypokalemia.
Chronic exposure to excess amounts of cortisol hormones results into different degrees of osteoporosis and affects every aspect of bone metabolism by inhibiting the synthesis and increased metabolism of proteins which decreases the formation of the osseous matrix.
-Excess cortisol also inhibits movement of calcium from the bone to the extracellular space.
-It also inhibits absorption of calcium and Vitamin D across the intestinal lining and decreases gonadal steroids which accelerate bone loss in both sexes. |
Osseous tissue
Bone tissue |
| Menstrual irregularity and oligomenorrhea in women; sexual dysfunction in men; and loss of libido in both sexes (Luton et al., 1977; Lindsay et al., 2005) | -Excess cortisol inhibits the hypothalamus and pituitary gonadotrophic cell secretions which are responsible for reproductive health,
-The excess cortisol also results in poor steroid synthesis at the gonads and their peripheral action at target cells level.
-And, impairs the synthesis of testosterone hormones in males. |
-Female reproductive system
-Male reproductive system |
| Diabetes Type 2 (Nestler & McClanahan, 1992.) | Excess cortisol increases manufacture of hepatic glycogen by protein metabolisis.
This increases the hepatic glucose output which in raise the blood sugar levels. The cortisol inhibits cellular absorption of the glucose. This stimulates a constant insulin secretion which results into insulin resistance. This overt type 2 diabetes or, less frequently,
Resistance. It may also lead to diabetes . |
Gastrointestinal tract, and the liver |
| Skin changes including fragility, thinning, susceptibility to bruises and bacterial infections, reddish-purple streaks, acne and stretch marks (Cohen et al., 1997) | -Excess cortisol causes concomitant androgen overproduction in ACTH-dependent forms or in adrenocortical cancer which affects the skin | Skin |
3. Describe two (2) common classes of drugs used for patients with the identified condition including physiological effect of each class on the body
a. This does not mean specific drugs but rather the class that these drugs belong to.
Treatment of Cushing’s syndrome is aimed at reversing the clinical features of the condition, normalizing cortisol hormone levels with minimized morbidity, removing tumor mass or stabilizing tumor growth while preserving pituitary function and long-term control of the condition without recurrence. The treatment is divided into two broad categories; Drug therapy and surgery (Bornstein & Chrousos, 1999).
Surgeries are mainly aimed at removing the tumors in the pituitary gland, adrenal gland or any other parts of the body. The success of surgical therapy depends on surgeon’s experience as well as total removal of the tumor. Occasionally, entire pituitary gland is removed or injured as treatment for Cushing’s disease. This leaves the patient with inadequate levels of ACTH and the other pituitary hormones which are treated by administering replacement hormones for cortisol, thyroid and gonadal hormones (Bornstein & Chrousos, 1999; Leach et al., 2010; Bertagna & Guignat, 2013). In case the first surgery fails or if the tumors are present in several other parts of the body, subsequent surgeries, radiotherapy or drug therapy can be done. However both the surgical and radiotherapeutic treatments present various risks (Bornstein & Chrousos, 1999).
For a long time, drug therapy has been used as the only medical therapy for treating Cushing’s disease. The drugs were initially used to inhibit steroidogenesis. The drugs included ketoconazole, metyrapone, mitotane,and etomidate. Metyrapone, ketoconazole, and mitotane used to reduce the levels of cortisol hormones by directly inhibiting synthesis and secretion in the adrenal gland. Etomidate is used to acutely control of severe hypercortisolaemia. (Bornstein & Chrousos, 1999). With the technological advancements in medical field, pituitary-targeting drugs such as pasireotide have been approved to treat adult patients with Cushing’s disease who are unwilling or unfit for surgery. The drugs are more effective with reduced risk and improved quality life after treatment (Schmid, 2008; Morgan & Laufgraben, 2013).
When Cushing's syndrome is caused by glucocorticoids that are taken for another medical condition, glucocorticoids are discontinued gradually under a physician’s instructions (Bertagna & Guignat, 2013; Ferone et al., 2013; Morgan & Laufgraben, 2013).
Question 4: Identify and explain, in order of priority the nursing care strategies you, as the registered nurse, should use within the first 24 hours post admission for this patient
The following nursing strategies will be used within the first twenty four hours on the patient (Morgan & Laufgraben, 2013):
1. Decreasing Risk of Injury
I will provide safe environment to prevent possible falls, colliding into furniture, fractures, and other injuries to bones and soft tissues. I will also recommend diet rich in protein, calcium and Vitamin D to minimize muscle wasting and bone loss.
2. Decreasing Risk of Infection
I will provide the patient with an environment that is safe from infections away from people with infections in order to avoid unnecessary exposures. I will also frequently test the patient for subtle infections and inflammation.
3. Monitoring and Managing Complications which will include the following;
- Monitoring for hypotension; pulse rate; respiratory rate; weakness; and pallor;
- Administering IV ?uids and electrolytes and corticosteroids before, during, and after treatment as indicated;
- Monitoring for circulatory collapse and shock present in addisonian crisis; treating promptly.
- Assessing ?uid and electrolyte status by monitoring laboratory values and daily weight.
- Monitoring blood glucose level, and reporting increment to physician.
4. Encouraging Rest and Activity
The patient will be encouraged to be moderately active. This will assist in promoting the patient’s self-esteem as well as preventing complications which may arise as a result of immobility. I will then plan rest times through ought the twenty four hour then provide a quiet environment for the patient to relax, rest and sleep.
5. Promoting Skin Integrity.
This will be done by; providing the patient with meticulous skin care in order to reduce skin fragility; avoiding the use of adhesive tapes on the patient’s skin; frequently assessing skin and bony prominences; and encouraging and assisting the patient to change her positions frequently.
6. Improving Body Image, Thought Processes
- I will discuss the health condition with the patient and her family, its impacts on self-concept and relationships with others. And that the major physical changes may be treated and eliminated. Changes such as increased weight and edema may be modi?ed by proper diet.
- I will also explain to the patient and family the cause of emotional instability, and help them manage the patient’s frequent mood swings, hyperactivity and depression.
- I will encourage them to report any psychotic behavior and to freely express their concerns and feelings
Preparing the patient for surgery by monitoring the glucose levels and body fluids pressure.
7. Teaching Patients Self-Care by;
- Giving the patient and her family verbal and written information about Crushing’s Syndrome.
- Teaching the patient and her family to monitor blood pressure, blood glucose levels, and weight.
- Advising that stopping corticosteroid use should only be done under medical supervision. I will also advise the patient to stock adequate supply of the corticosteroid to prevent running out or skipping a dose as it can result in addisonian crisis. Finally, I will advise the patient to always weara medical alert bracelet and notify other health professionals that she has Cushing syndrome (Morgan & Laufgraben, 2013).
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