Addison’s Case Study

Addison’s Case Study
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(Date)

*Introduction*
*Case study*
A female patient who was 30 years old of admitted in the month of September and claimed to have had persistent vomiting for the past three months five times to fifteen times in a single day. She could not tolerate any oral intake as she was vomiting and nauseated due to dehydration. She had normal bowel motions and had no symptoms of infection and micturition; she, however, had noticed significant weight loss in the past few months. She has been referred directly to a gastroenterologist due to her vomiting that was persistent, thus she well knew about hypothyroidism. She then had to undergo an (OGD) oestrosophaogastroduodenoscopy which then indicated that she had gastritis which further leads to her being introduced to the therapy of the proton pump inhibitor. Her blood test indicated negative tissues of transglutaminase antibodies, gastric parietal cells antibodies are positive and she also had a schedule for CT enterography. Given that this history was obtained, she was treated for gastritis. Her blood pressure was low and her sodium level was 133 mmol/L which indicated that it was secondary to dehydration. The intravenous fluid was used to treat her which got subsequent discharges due to antiemetics (Presotto et al, 2005 ).
Due to a Mallory-Weiss tear, the patient again came with persistent vomiting after 4 months. She then mentioned she was still losing weight from 50kg to 41 kg and with an ongoing lethargy. Her pregnancy test was negative and she also described abdominal pain from her right side. She denied having had forced vomiting and abuse of thyroxine. About her family history, she was not sure about anything. She was had never had alcohol but claimed to be a social smoker. On keen examination, she was hypotensive, very thin and tachycardic. She had pigmentations on her skin and clinically dehydrated.
*Physical findings*
she had hypopigmentation which is a skin condition for Addison disease as her skin was darker than normal. Observations on her skin indicated that she had nipples, scars, skin folds such as the groin or armpits, she had pressure points like ate the toes knees and her elbows. She had mucous membranes in her gums and cheeks. In addition to her skin condition, she also had hair loss. This is common in women with primary Addison disease as they normally lose their underarm hair and pubic hair. Men with the same disease do not particularly lose their hair since their testes make the androgens that are responsible for the growth of the hair (Cervera et al, 2009).
*Labs & Diagnostic Tests*
Further investigations indicated that her levels of sodium were 128 mmol/L while normal sodium levels should be between 133 to 146 mmol/L. her potassium levels were at 4.9 which is normal since it should be between 3.4 and 5.3 mmol/L. her C reactive proteins were 16 instead of being less than 5. Haemoglobin pigment was 12.4 g/dL instead of 12.5 to16 /dL and her white cell count (WCC) was at 11.6 instead of 4-11*10^9/L adding to mild eosinophilia. After acquiring the history of the patient and her findings, a request for random cortisol was requested and it came back as 2 nmol/L instead of 102 to 535 nmol/L. her renal and liver tests turned out to be normal. Her thyroid-stimulating hormone (TSM) was 33 mU/L instead of 0.2 to 4.2 mU/L while lastly, her blood sugar was 4.5 nmol/L which was also normal.
On the basis of the findings of her history and results from the entire investigation, she was analyzed with the Addison’s disease. An issue of the autoimmune polyendocrine syndrome was raised due to her history of positive gastric parietal cell, Addison’s disease and hypothyroidism.
Causes of autoimmune adrenal insufficiency
*Diagnosis*
*GENE*
*Features (order of frequency)*
APS 1
AIRE
Adrenal insufficiency
Chronic mucocutaneous candidiasis Primary hypogonadism
Hypothyroidism Malabsorption syndromes Type 1 DM Others
APS 2
HLA-DR3 CTLA-4
Adrenal insufficiency Autoimmune thyroid disease Type 1 DM Primary hypogonadism Vitiligo
Isolated Autoimmune adrenalitis
HLA-DR3 CTLA-4
*Lab findings and clinical manifestations.*
*Symptoms*
*Signs*
*Labs*
Weakness, fatigue (100%) Anorexia (100%) GI symptoms: Nausea (85%) Vomiting (74%) Constipation (34%) Abdominal pain Fever (acute onset) Salt craving
Diarrhoea Postural dizziness Myalgia Arthralgia
Dehydration (acute onset) Weight loss (100%) Hyperpigmentation (94%) Hypotension (SBP<110) shock (acute onset) Vitiligo Hyponatremia Hyperkaliemia Hypercalcemia Metabolic acidosis (acute onset) hypoglycemia Azotemia (acute Onset) Anaemia Lymphocytosis eosinophilia *Replacement therapy for glucocorticoid.* *Condition* *Hydrocortisone* *Prednisone* *Dexametha -Sone* Daily dose (oral) 15–25 mg every day in separated doses 3–5 mg day-to-day in divided quantities 0.375 to 0.75 mg daily in one dose Minor stress (cold) Oral 30–50 mg/day-to-day in 3 divided quantities for 2–3 days 8–15 mg/day-to-day in 2 divided prescriptions for 2–3 days 1 to 2 mg/d in 2 separated doses for 2–3 days Moderate stress (minor or moderate surgical procedure) oral or intravenous 45–75 mg/daily in 3 alienated quantities for 2–3 days 15–20 mg/day-to-day in 2 separated doses for 2–3 days 2–3 mg/d in 2 divided dosages for 2–3 days Severe stress (major surgery/sepsis) 100–195 mg/daily in 4 divided doses for the 1-day taper to physiological dose over 3–5 days Similar to hydrocortisone regimen Follow hydro-cortisone regimen Septic shock 150–200 mg/day-to-day in 4 alienated doses, taper as clinically tolerated Follow hydrocortisone regimen Follow hydrocortisone regimen The case above shows the significance of reviewing admissions from the past especially if the symptoms being presented are similar. Due to the fact that the patient was initially referred to a gastroenterologist, the following subsequent admissions were put down to gastrointestinal cause even if there were some minor improvements in the symptoms. However, since there was persistent loss of weight with particularly no cause from previous investigations, another diagnosis was ruled out and eventually, the Addison’s disease was diagnosed after 1 year of presenting symptoms (Bornstein et al, 2016). In the western population, there is an annual population of 4 million people with the Addison’s ailment. This is a disease that is relatively rare. The disease has no specific symptoms and this may result in it being missed as it is not easy for it to be diagnosed. As diagnosis delay is common, patients can be seen by various professionals in the healthcare sector including psychiatrists and gastroenterologists before they are diagnosed correctly. The disease has a wide variety of symptoms which means that diagnosis of it can be as a result of many other conditions and the major ones like mucous membrane and the skin condition may be missed out. Also, diseases like hypotension and anorexia might be relevant but not specific since they are also explained by other diagnoses like the underlying infections (Uthman et al, 2006). Many investigations can have results with clues that will make that clinician suspect that the enduring has Addison’s sickness but on routine assessments of the blood, the patient might be suffering from hyperkaliemia and/or hyponatremia, eosinophilia or hypoglycemia. Starting thyroxine might worsen Addison disease when there is raised TSH. They may result in the clinician suspecting the diagnosis and considering a cortisol level that is random. But this can also be inaccurate since the rhythm of cortisol production which is low during midnight, very high in the morning and its production also increases in times of stress. When there is an unusually low level of cortisol within clinical features of the Addison disease should trigger the diagnosis and this can be confirmed by using hydrocortisone. Despite the fact that it is difficult, short synacthen is the key test for diagnosis but in the instance when a crisis arises, intravenous hydrocortisone should be commenced with immediate effect. Before steroid administration to the patient, adrenocorticotropic and cortisol hormone levels should be taken (Presotto et al, 2005). Synthetic or synacthen can be administered intramuscularly or intravenously in a non-acute setting. The main test for this is taking the levels of cortisol which is then followed by administration of tetracosactrin and a repeat of takin the cortisol levels after 30 minutes but in some cases, it can also be taken after 60 minutes. A level that will suggest that the adrenal glands are intact should be 400 to 550 nmol/L the agreed level is 525 nmol/L. only after a severe adrenal calamity is when most of the Addison’s disease patients are diagnosed. It is always an emergency that will be precipitated with an infection or some other forms of stress in an untreated or undiagnosed patient. In this state, patients are normally so unwell and have server hypotension, dehydration and/or circulatory shock. There are a number of autoimmune associations that Addison’s disease has. They were described by Thomas Addison to be vitiligo and pernicious anaemia when he was describing the eponymous condition. As the Addison disease has so many autoimmune diseases associated with it, the most common one is the thyroid disease. Since the Addison’s disease can have an association to many other autoimmunities, then past medical history reveals some conditions like thyroid disease, coeliac disease, atrophic gastritis and vitiligo, it will only imply that it is another autoimmune diagnosis. The patient above had positive gastric cell antibodies and hypothyroidism. This could also be an indicator that there is a possibility of autoimmune polyendocrine syndrome (APS) (Uthman et al, 2006). The autoimmune polyendocrine syndrome refers to multiple failures of endocrine lands due to autoimmune diseases. It is also used when describing syndromes that have multiple failures of organs. There is genetic inheritance in autoimmune regulators in APS I and APS II. APS I is a recessive condition that is characterized by its connotation with Addison’s illness chronic candidiasis and hypoparathyroidism. Some other features that are associated with APS I is diabetes mellitus, vitiligo, hepatitis, anaemia, and atrophic gastritis. APS type II is the most common one as it is associated with many conditions which include diabetes mellitus, Addison’s illness, and autoimmune thyroid illness. Leucocytes associated with it include HLA DR4 and antigen (HLA)—HLA DR3 (Bornstein et al, 2016). *Precipitating/risk factors * Addison’s illness is an intermittent disorder that affects the adrenal glands which produce two steroid hormones aldosterone and cortisol which are responsible for regulating the body’s blood pressure. The symptomatic signs of the Addison’s illness also referred to as primary adrenal inadequacy is as a result of inadequate manufacture of the hormones. Cortisol hormone is usually released under stressful conditions to manage feelings, therefore, maintain a constant heart function, blood pressure, blood glucose, subduing the immune system and controlling the body’s metabolism of breaking down proteins, carbohydrates and fats. The aldosterone hormone helps the kidney maintain sodium in the blood while removing potassium by maintaining a healthy balance of water and sodium in the body. Androgen is also produced in the adrenal glands and it controls the growth of some secondary sexual characters like hair growth and women libido. Initials symptoms as an outcome of deficient production of the two hormones comprise fatigue, muscle weakness, hypotension, lethargy, salt cravings, increased thirst as a result of dehydration and irritability. Loss of appetite and weight are also reported. Addison’s disease normally progress slowly but at times develop rapidly intensifying the initials symptoms into dangerous symptoms like muscle cramps, change in skin colour, postural hypotension, nausea, chronic fatigue that may result to depression and vomiting and diarrhoea. Patients also suffer from back, joint or abdominal pains. Women suffer from low libido. Men’s libido is not affected because their androgen is produced at the testes and not at the androgen glands. Addison’s illness is most predominant to women amid the age of 30-40 (Negrini et al, 2017). Most reported cases of Addison’s disease are due to the adrenal gland impairment. However, symptoms of the disease do not progress until 90 per cent of the adrenal cortex is spoiled. Primary adrenal deficiency is referred to Addison’s disease when it is triggered by the inability of the adrenal cortex to yield the steroids hormones aldosterone and cortisol. However, when the cortex is healthy but unable to create the hormones due to other reasons, for example, the flaws of the pituitary glands, the illness is referred to as secondary adrenal insufficiency. 75 per cent of Addison’s disease is as a result of an autoimmune reaction. A body’s immune system is its defence in fighting infection and diseases. When ill, the body produces antibodies that attack the cause of the illness. However, when a person is suffering from an autoimmune condition, the immune system produces antibodies that fight its own body organs and tissues. Attack of the adrenal cortex by these antibodies causes the Addison’s disease. When the adrenal cortex is ninety per cent destroyed, the adrenal glands fail to produce enough hormones. A decrease in the number of hormones produced sparks the start of Addison’s disease symptoms. Addison’s disease caused by autoimmune reaction is also referred to as autoimmune Addison’s disease. In the developed countries 80 per cent of Addison’s disease is as a result of autoimmune condition. Autoimmune Addison’s disease can occur as an isolated condition or as a large disorder precisely like the autoimmune polyendocrine syndrome I and II (Presotto et al, 2005). Research shows that some people are at a high risk of having an autoimmune response if they have certain genes. Most people from a family with a history of having Addison’s disease. Numerous tested people with autoimmune Addison’s illness has a similar DNA coding to people with other autoimmune disorders. Although there is no exact way of justifying how genes, contribute to Addison’s disease, there is a high association between the autoimmune disorder and Addison’s disease. It is valued that half of people with autoimmune Addison’s disease suffer from more than one autoimmune disease like vitiligo, hypothyroidism, type 1 diabetes and hyperthyroidism (Presotto et al, 2005). Before tuberculosis was treatable, it was a major cause of Addison’s disease. It still is a major cause of the disease in some of the developing countries. Tuberculosis bacterial infection generally affects the lungs but can also spread and affect other parts of the body. Tuberculosis only causes Addison’s disease when it affects the adrenal glands. Some contaminations like fungal infections and those linked to HIV are some causes of Addison’s disease. Heavy bleeding in the adrenal glands, surgical removal of the adrenal gland, the spread of cancer tissues into the adrenal glands and some genetic abnormalities in the adrenal glands like inability to produce hormones are some cause of Addison’s disease. Furthermore, formation and buildup of the amyloid in the adrenal glands are similarly causing the disease (Cervera et al, 2009). *Signs and symptoms * *Physical assessment and history* 1) fatigue (lack of energy or motivation) 2) lethargy (abnormal drowsiness or tiredness) 3) a weakness of muscles. 4) irritability or low mood. 5) loss of appetite and unintentional weight loss 6) Hyperpigmentation 7) Loss of hair. 8) Diarrhoea and vomiting. 9) Back pain or abdominal pain and muscle cramps. 10) chronic exhaustion, 11) palms, on scars or on pressure points, such as your knees or knuckles. *Diagnostic findings* The patient’s blood sugar level was 296 mg/dL. She also had 18.3 g/dL of haemoglobin, with a total count of 7100/mm^3 of leucocytes and a differential count of lymphocytes 50%, neutrophils 24% and 13% if eosinophils. Her panel of electrolytes was 4.3 potassium, bicarbonate 18, 98 chlorides, and 16 of AG while the rest had a range that is normal. Her urine had 3+ ketones and 32.7 BHBs. Her lactic acid was 2.9, 7.4 pH venous and other tests like those of the thyroids, the liver and renal functions were all at a normal range (Bornstein et al, 2016). *Cellular analysis * *Hyperpigmentation* of the mucous membrane and skin Thus, the symptom occurs first. The change in skin colour is due to the overproduction of corticotropin substance made by the pituitary when it tries to stimulate the adrenal glands. When the adrenal gland is healthy, it sends back feedback to the pituitary to stop making the corticotropin. However, if the adrenal gland is not working, the pituitary continues to make the corticotropin substance. Continuous production of corticotropin arouses the manufacture of melanin which causes the skin to blacken. Hyperpigmentation of the skin is mostly observed in pressure points of the body like the elbow, knuckles and knees. *Hair Loss and low libido* In women, the adrenal glands are responsible for producing androgen hormones. When the adrenal gland is affected, it leads to loss of their public and underarms hairs. DHEA and DHEAS are abundant in the human body and are produced via the adrenal cortex. DHEA is produced by the adrenal cortex after it has been stimulated by the ACTH produced by the pituitary glands. When the androgen gland is affected, it is unable to produce the required level of estrogen, therefore, affecting women respiratory system. Women in their reproductive years suffer three major symptoms as a result of low androgen; low self-esteem, fatigue and low sex drive. Women also suffer from vaginal dryness making sexual activities painful as a result of low androgen and estrogen. Additionally, women suffer from osteoporosis, vulnerability to bone loss and irregular periods (Negrini et al, 2017). *Low cortisol with a high ACTH level* Because of the health benefits that the cortisol hormone has, the amounts produced by the adrenals is balanced. Cortisol production is regulated by the pituitary glands and the brain's hypothalamus. The brain’s hypothalamus relays a signal to the pituitary gland to release the hormone. The pituitary gland responds by discharging hormones sex like testosterone and estrogen, hormones that regulate thyroid and growth and adrenal functions. The pituitary gland also releases adrenocorticotropin(ACTH) that stimulates the adrenal glands. Release of the ACTH signals the adrenals to produce cortisol and once produced; it signals the pituitary to lower the ACTH secretion. However, when the Adrenal gland is damage more than ninety per cent, the amount of cortisol produced is low. Due to the low level of cortisol produced, the pituitary gland continues to secrete ACTH, therefore, resulting in a higher levels of ACTH in the body. *Low blood pressure* Balanced pressure of the blood is maintained by the cortisol and aldosterone hormones. The cortisol aids the body to preserve blood pressure by regulating how the body reacts under stressful conditions. The aldosterone maintains a pressure of the blood by regulating the quantity of water and salt intake in the human body. When the adrenal glands are ruined by the body’s immunity, the level of cortisol and aldosterone reduce in the body. Low levels of aldosterone results to an unbalance intake of water and salt by the kidney resulting in a drop blood pressure (Presotto et al, 2005). *Gastrointestinal problems, such as nausea, vomiting and abdominal pain* *Hyperkalemia * This is a condition where the level of potassium ions in the blood serum gets so high. Normal levels of the potassium ions should be 3.5 to 5.0 mmol/L while levels that are above that result into hyperkalemia. Normally there are no symptoms for this but in instances where it gets server, it may cause cardiac arrest, numbness, death, muscle weakness, palpitation, abnormal heart rates and muscle pains. Common causes of this condition include rhabdomyolysis, kidney failure and hypoaldosteronism. Quite a number of medications do result in this condition by increasing the level of potassium ions in the blood. These medications include NSAIDs and spironolactone. The severity of the condition can be divided into mild, server and moderate (Negrini et al, 2017). Initial treatment of the condition in patients with changes in ECG is calcium gluconate. There are medications that might worsen the patient’s condition, this must be stoped and be supplemented with a diety of low potassium level. Other forms of medication that can be used include salbutamol, dextrose with insulin and sodium bicarbonate. The most effective means to remove potassium from th body is by using hemodialysis but measures like polystyrene sulfonate and furosemide can be used. Using polystyrene sulfonate is not supported. This is a condition that is normally rare in those people that are healthy. Thos hospitalized, their rate is between 1% to 2.5%. this condition increases the risk of death for hospitalized patients by at least 10 times. Hyperkalemia is derived for three words hyper which means high, kalium which means potassium and emia meaning in the blood (Cervera et al, 2009). *Hypoglycemia* this is a condition where the blood sugar level drops below normal. This condition comes with a number of symptoms including, confusion, death, shakiness, sweating, a feeling of hunger clumsiness seizure and loss of consciousness. In this condition, symptoms come about quickly. The common causes of this condition include medications such as sulfonylureas and insulin that are normally used for treating diabetes mellitus. There is more risk for diabetics who have drunk alcohol, exercised more than usual for those that have eaten less than normal. There are certainly other causes of hypoglycemia such as certain tumours, liver disease, kidney failure, starvation, inborn metabolism error, hypothyroidism, insulinoma, infections that are severe. Dugs like alcohol may result in low blood sugar level and healthy babies, if left hungry for long, may also experience this condition (Uthman et al, 2006). The level of glucose that causes hypoglycemia varies. People who are diabetic are diagnosed with the condition with levels below 3.9 mmol/L. in adults who are not diabetic, low blood sugar during the symptoms and no symptoms when the sugar level is norman confirm the diagnosis. On the other hand a level that is below 2.8 mmol/L when someone goes without food or exercise can be used to check for the condition. A level that is less than 2.2 mmol/L indicates the presence of the condition but there are other tests that can be used to detect the condition which includes C peptide and insulin level (Bornstein et al, 2016). People who are diabetic only prevent the condition by matching amounts of exercise, the food they eat and the medicine that they use. Whenever a patient detects a drop in the sugar level it is good practice for them to test using a glucose monitor. There are a number of patients that have fewer initial symptoms thus, frequent checking of glucose level is also recommended. In order to treat hypoglycemia, patients should take dextrose or foods that are rich in simple sugars. In injection of glucose will help those people who are not able to take food by mouth. A treatment of hypoglycemia that is different from that of diabetes is having a healthy meal and treating the underlying problem. Hypoglycemia is at times used to refer to a condition known as idiopathic postprandial syndrome, a condition that normally happens after eating but with sugar levels that are normal. Symptoms of hypoglycemia and its manifestations can be divided into the ones that as a result of the neuroglycopenic effect due to reduced brain sugar and counterregulatory hormones. *Hypercalcemia* This is a condition where there are high levels of calcium ions in the blood serum. The normal range of calcium ions should be 2.1 to 2.6 mmol/L and with levels that are higher than that referred to as hypercalcemia. Those patients with mild levels of calcium my not show any symptoms. While those patients with high levels of calcium ions will show symptoms like, depression, abdominal pain, confusion, abnormal rhythms of the heart, bone pains, kidney stones and cardiac arrest. Most cases of this condition are due to cancer or primary hyperparathyroidism. While other causes also include tuberculosis, vitamin D toxicity, Paget disease, sarcoidosis and multiple endocrine neoplasias. In order for this condition to be corrected, it is either the calcium levels are normalized or blood calcium to be ionized. Some changes like prolonged intervals of PR and shortened intervals of QT can be monitored by an electrocardiogram (Presotto et al, 2005). Treatment of hypercalcemia may include calcitonin, intravenous fluids, pamidronate or furosemide without forgetting to treat the cause. Patients with very high concentrations of calcium ions and have been hospitalized my require to use furosemide even though it is poor. Those that are not responding to other treatments will require to use haemodialysis. Usefulness may be found in steroids with those patients with vitamin D toxicity. This condition is relatively popular as it occurs in 1 to 7 people on 1000 people and it occurs in almost 2.7% among patients with cancer. When calcium ion level increase, they cause a decrease in the permeability of neuron membranes to sodium ions thus resulting in a decrease in excitability which results to hypotonicity of the straightened and smooth muscles. This explains muscle weakness, fatigue and many other factors like constipation (Negrini et al, 2017). *Hyponatremia* This is the condition when the sodium ion concentration in the blood is low. Normally defined when it is less than 135 mmol/L, but when it is below 120mEq/L then it is server hyponatremia.symptoms, as usual, are either low, high or mild. Mild symptoms are nausea, headache, a decrease in the ability to think and lack of balance. Coma confusion and seizures are part of server symptoms of hyponatremia. The cause of this condition is defined by the person's state of his or her body fluids as either being low volume, high volume or normal volume. Factors like vomiting, sweating, diuretics and diarrhoea cause low volume of fluids in the body (Uthman et al, 2006). Normal volume is normally divided into two namely; concentrated urine and dilute urine. A case where the urine is dilute is referred to as adrenal insufficiency, drinking of a lot of water or beer and hypothyroidism. Concentrated urine might be as a result of a number of factors including, heart failure, kidney failure, inappropriate secretion of antidiuretic hormone and liver failure. But there are factors that may result in false measurements of sodium level such as high blood sugar and high blood protein level. Treatment of hyponatremia is in reference to the underlying cause. Correction the problem too quickly, may result in complications. Rapid correction of the condition is only recommended for those patients that had the symptoms of the condition rapidly. Normal concentration should be rectified by fluid restrictions while low concentration should be regulated by fluid restriction and diet that is low in salt (Negrini et al, 2017). *Lethargy* This is a state when someone lacks energy, becomes tired, weary and fatigued. It is normally accompanied by a decrease in motivation, depression and apathy. This can result due to lack of adequate sleep, overworking, improper nutrition, lack of exercise, boredom and stress. It can also be caused by an interaction of alcohol and medication or a side effect of medication. Symptoms of lethargy can last months of as short as few days. Normalcy can be achieved by getting enough sleep, good nutrition, decreased stress and rest (Cervera et al, 2009). *Nursing and Medical Management –* *1) **Non-Pharmacological(no medical)* Educate the patient to self-monitor heart rate, glucose level and blood pressure. This will help the person know how their condition is and if there is a need to seek immediate help in case of overly high or low results (Presotto et al, 2005). Encourage the patients to be responsive for their own health by sticking to the right diet. A nutritionist should work closely with the patient to ensure that they eat the right amount of proteins, carbohydrates, fats and minerals. The patients should also be encouraged to take salt and fluids. Teach patients to identify stressors affecting them. Patients should be taught how to analyze situations happening around them especially any traumatic event. After identifying them, they should learn how to control their emotions so that they cannot suffer from advanced Addison’s disease (Bornstein et al, 2016). They should be encouraged to inform those close to them about their situations. This will help them adjust properly to the illness for they will get support from people that care about them. Additionally, those people can be able to help them in times of emergency like when the patient has severe vomiting or vomiting. Patients should be keenly observed and any vital signs reported immediately to the physician. Examples of vital signs to report are, low blood pressure, increase rapid pulse, the return of vomiting or diarrhoea. Establish a good relationship with the patient as he improves. Patients with Addison’s disease are irritable and emotionally unstable. Creating a friendly relationship with them will enable them to have a quick recovery. Treatment should be promptly and professionally carried out for patients that have acute Addison’s illness. Addison’s crisis is a very critical case emergency for any delays can lead to death. When handling it, everything should be prepared in advance before the patient arrives at the hospital. The necessary equipment should be available like syringes, tubes and the necessary solution for treating the patient (Uthman et al, 2006). Patients should be protected from tasks that might drain his energy. Most patients that have Addison’s disease suffer from fatigue. The patient should be left to lie down undisturbed. If he is admitted while in a coma, he should be placed on the bed without changing his clothes and covered to preserve heat (Cervera et al, 2009). *1) **Pharmacological(Medical)* Taking hydrocortisone medication on empty stomach results to high absorption rate. However, patients with digestive problems should be given medicine after having a small snack. Nurses should bring to the attention of a doctor when a patient’s health is deteriorating. Lack of enough glucocorticoid replacement in the body of a patient will result in acute Addison’s which can result in death. Under such conditions, the level of prescribed steroids is increased. When a patient has a fever of more than 37.5C, he should be given a double dosage. This will enable him to avoid progressive acute Addison’s disease. When a patient has had severe nausea, he should be given 20mg hydrocortisone and sip rehydrate electrolyte. After vomiting a patient should be given the emergency injection instantly and a doctor alerted of the Addison emergency. The short will help the body produce cortisol that the body cannot produce in order to deal with the traumatic event; this will help the body to stabilize before a more extensive observation is conducted by the doctor. After an injury, 20mg of hydrocortisone should be orally administered. This prevents the body from going into shock because the ingested cortisol will regulate body behaviour. Before a surgical procedure, the surgical team should be let aware of the need of an extra steroid medication that has checked against the ACAP to ensure that the correct steroid level 100mg hydrocortisone is used via the IM route before IV infusion is used.IM dose spreads steroid faster than the IV infusion method thus creating assurance that the body has received the steroid in case the Iv infusion fails. If the IV injection fails, a recurrent IV bolus injection after 6-8 hours is used. After the surgery, hydrocortisone can be swiftly tapered with 24-36 hours until the usual dose replacement or as the situation dictates. Use of mineralocorticoid replacement is held until the patient resumes to the daily steroids replacement. Treatment for a patient with acute Addison’s disease should be treated promptly. If possible, Blood should be drawn out for testing first and immediately after giving a steroid injection. *Nursing diagnostic* · * Reduced comfort related *to an abdominal, joint or back pain muscle cramp 1. Nurses should check up on the patient to establish whether she is in pain or not 2. The nurse should administer medicine to relieve the patient‘s pain. 3. While in the ward, the nurse should provide non-pharmacological interventions like changing position, cold, distraction and heat. · Hyperpigmentation 1. Carry out observation in skin warmth and pulse 2. Administer medicine for progressive hyperpigmentation like azelaic acid and hydroquinone · Hypoglycemia 1. Suggest frequent food intake to maintain normal nutrition and glucose intake in the body *2. *A nutritionist should provide the patient with low carbohydrate, high sodium and high protein diet *3. *The patient should eat a late morning snack *4. *The nurse should observe the patient's glucose level · Lethargy and fatigue *1. *The nurse should check up on the patient's fatigue level to avoid progression to paralysis · Reduce Hypernatremia *1. *Encourage the patient to take lots of fluids to replace the lost water in the kidneys · *loss of appetite and unintentional weight loss* 1. Encourage patient to take tolerable foods 2. The nurse should monitor the weight of the patient in order to determine his or her progress 3. The nurse should suggest a balanced diet in order to improve the overall health of the patient 4. The nurse should assess the patient appetite, nausea, vomiting and diarrhoea. · Educate the patient about the illness *1. *The nurse should explain the disease to the patient *2. *The nurse should explain the medicine to the patient *3. *The nurse should make the patient utter how many doses she is supposed to take *4. *The nurse should inspire the patient to wear a medical wrist band indicating they suffer from Addison’s disease in their everyday *5. *The nurse should clarify any misunderstanding on the amount of dosage to be taken *6. *The nurse should explain the necessity of a long life steroid therapy intake to the patient. *Outcomes* The lady was admitted in and started on a total parental nutrition program. Cortisol and adrenocorticotropic hormone three days at the hospital suggested that she was adrenal insufficient. She was given intravenous methylprednisolone and after her symptoms resolved she was given oral prednisone. She was later discharged under the impression of Addison’s crisis and given fludrocortisone and prednisone medicine (Uthman et al, 2006). Diagnosed and long term patients suffering from Addison’s disease should be informed on the change of lifestyle they will undergo due to the disease. Healthcare providers should play the important role of encouraging patients mostly those who have been recently diagnosed with the illness so that they will be able to adjust living with the disease. Addison disease is a rare disorder therefore only affects a people in society. Addison’s disease does not have a cure. A patient lives with the illness and adjusts their life by taking a specific steroid that they are lacking in their body. The type of dosage taken by individuals is different and during traumatic events, infection, stressful condition or surgery, the dosage is taken is increased to prevent the progression of the disease to severe adrenal crisis. Healthcare should be able to fully disclose this information to every patient (Cervera et al, 2009). Additionally, healthcare provides should educate the patients on the importance of taking the prescribed medicine accurately. They should discourage patients from skipping any dosage because by doing so, they will put themselves in great danger of Addison’s disease crisis. Healthcare providers should let the patient know the diverse effects of Addison’s disease like shock, brain damage due to unconsciousness and death. Patients are advised to seek instant medical health if they have serious medical issues like vomiting, diarrhoea, or infections. Additionally, health providers should encourage the patient to disclose their health condition to family members so that they can be aware in case of any emergency what to do. Moreover, patients should be encouraged to wear medical wrist bands with their medical information and an emergency number in case of any emergency when rushed to a hospital the responding medical officer will be able to help them immediately thus avoiding cases of aggregated Addison disease. In addition to that, patients should be encouraged to travel with a dose of their medicine everywhere. They can carry in their bags; put some in their cars and place of work so that when they forget to carry in their bag, they can be able to still access the medicine. With modern technology, Addison’s disease patients can now be able to have a life expectancy similar to other people without the illness. Patients should, therefore, be encouraged because of that. Patients should be encouraged to increase their salt intake so that they can have maintained blood pressure and reduced salt cravings. Patients should also be informed of new therapies with positive outcomes that they can try (Bornstein et al, 2016). New research has shown that by using androgen replacement therapy like androstenedione or testosterone hormones, Addison’s disease can be treated. Such information should be shared to patients because the process has shown that there is improvement in individual fatigue, self-esteem and mood. Additionally, the therapy might be able to improve women’s libido and sexual satisfaction. People living with Addison’s sickness should be encouraged to socialize with other similar people who understand them. They are many platforms that the patient can use like websites and community meetings. Through these interactions people will be able to share their experiences and become aware of new forms of treatment they can try. Although there has been some progress in the methods of treatments, more forms of treatments can be discovered to help people living with Addison’s illness. More research and study funding is compulsory if this dream is to be achieved (Uthman et al, 2006). References Bornstein SR, Allolio B, Arlt W, Barthel A, Don-Wauchope A, Hammer GD, Husebye ES, Merke DP, Murad MH, Stratakis CA, *et al* Diagnosis and treatment of primary adrenal insufficiency: An endocrine society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism 2016. 101 364–389. (10.1210/jc.2015-1710) [PMC free article ] [PubMed ] [CrossRef ] [Google Scholar ] Cervera R, Boffa MC, Khamashta MA, Hughes GR. The Euro-Phospholipid project: epidemiology of the antiphospholipid syndrome in Europe. Lupus 2009. 18 889–893. (10.1177/0961203309106832) [PubMed ] [CrossRef ] [Google Scholar ] Negrini S, Pappalardo F, Murdaca G, Indiveri F, Puppo F. The antiphospholipid syndrome: from pathophysiology to treatment. Clinical and Experimental Medicine 2017. 17 257–267. (10.1007/s10238-016-0430-5) [PubMed ] [CrossRef ] [Google Scholar ] Presotto F, Fornasini F, Betterle C, Federspil G, Rossato M. Acute adrenal failure as the heralding symptom of primary antiphospholipid syndrome: report of a case and review of the literature. European Journal of Endocrinology 2005. 153 507–514. (10.1530/eje.1.02002) [PubMed ] [CrossRef ] [Google Scholar ] Uthman I, Salti I, Khamashta M. Endocrinologic manifestations of the antiphospholipid syndrome. Lupus 2006. 15 485–489. (10.1191/0961203306lu2318rr) [PubMed ] [CrossRef ] [Google Scholar ]

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