CHAPTER 1
INTRODUCTION

1.1 Background
The adrenal gland consists of the medulla and the cortex. The cortex consists of zona glomerulosa, fasikulata, and reticular. Zona glomerulosa secrete controlled by aldosterone and renin-angiotensin mechanism and does not rely on the pituitary. Zona reticularis fasikulata and secrete cortisol and androgenic hormones and controlled by the pituitary via ACTH. Secretion of ACTH by the pituitary is controlled by (1) hypothalamic corticotropin releasing factor, and (2) the feedback effects of cortisol. When there is a disruption in the formation of these hormones either excess or lack of, will affect the body and cause an abnormality. Cushing's syndrome is caused by excess cortisol.


CHAPTER 2
THEORY REVIEW


2.1 Definition of Cushing's Syndrome
Harvey Cushing in 1932 describes a condition caused by adenoma pituitary cells basophils. This is called "Cushing's disease".
Cushing's syndrome is a condition caused by the combined metabolic effects of elevated glucocorticoid levels in the blood is settled. These high levels may occur spontaneously or as pharmacologic dose glucocorticoid compounds. (Sylvia A. Price; Patofisiolgi, p. 1088)
Cushing's Syndrome clinical picture resulting from an increase in plasma glucocorticoids long-term pharmacologic dose (latrogen). (William F. Ganang, Medical Physiology, p 364).
Cushing's Syndrome is caused by excessive secretion of steroid adrenokortial especially cortisol. (IDI). Volume III Issue I, p 826).
Cuhsing Syndrome due to maintenance of blood cortisol levels are abnormally high because hiperfungsi adrenal cortex. (Pediatrics, Volume 15 It 1979).

2.2 Etiology
Cushing's syndrome can be caused by:
1. Elevated levels of ACTH (not always due to pituitary adenoma basophil cell).
2. ATCH elevated levels due to the tumor outside the pituitary, such as lung tumors, pancreas that secrete "ACTH-like substance".
3. Adrenal neoplasms are adenomas and carcinomas.
4. Iatrogenic.
Providing long-term glucocorticoids in pharmacologic doses. Found in patients with rheumatoid artitis, asthma, lymphoma and skin disorders who receive synthetic glucocorticoids as anti-inflammatory agents.

2.3 Clinical Manifestations
Can be classified according to the function of the adrenal cortex hormones: cortisol, 17 ketosteroid, aldosterone and estrogen.
1. Symptoms hypersecretion of cortisol (hiperkortisisme), namely:
a. Sentrifetal obesity and "moon face".
b. Thin skin so that the face looks red, raised Strie and ecchymosis.
c. The muscles shrink due to the effects of protein catabolism.
d. Osteoporosis can lead to compression fractures and kyphosis.
e. Atherosclerosis is the cause of hypertension.
f. Diabetes mellitus.
g. Alkalosis, and hypokalemia hipokloremia.
2. Symptoms hypersecretion 17 ketosteroid:
a. Hirsutism (male resembles female).
b. Voice in.
c. Incurred acne.
d. Amenorrhea or impotence.
e. Enlargement of the clitoris.
f. Muscles grow (masculinization)
3. Symptoms of aldosterone hypersecretion.
a. Hypertension.
b. Hypokalemia.
c. Hypernatremia.
d. Nephrogenic diabetes insipidus.
e. Edema (rare)
f. Plasma volume increases
When these symptoms are striking, especially the first two symptoms, a disease called Conn or primary hyperaldosteronism.

4. Symptoms of estrogen hypersecretion (rare)
In Cushing's syndrome is the most characteristic symptoms of hypersecretion of cortisol, sometimes mixed with other symptoms. Generally onset disease is not clearly known, the first symptom is weight gain. Often accompanied by psychological symptoms to psychosis. The disease is intermittent, then weakness, easy infections, peptic ulcers arise and possibly vertebral fractures. Deaths caused by general weakness, cerebrovascular disease (CVD) and rarely by a diabetic coma.

2.4 Classification
Cushing's syndrome can be divided into 2 types:
1. Depending ACTH
Hiperfungsi adrenal cortex may be caused by the pituitary ACTH secretion are abnormal excessive. This type first described by the Hervey Cushing in 1932, it is also a condition called Cushing's disease.
2. ACTH-independent
The existence of ACTH-secreting pituitary adenoma, in addition there is histological evidence of pituitary hyperplasia kortikotrop, it remains unclear whether kikroadenoma maupum reciprocal hyperplasia due to impaired release of CRH (Cortikotropin Realising hormone) by neurohipotalamus. (Sylvia A. Price; Pathophysiology. Matter 1091).

2.5 Complications
• Crisis Addisonia
• The adverse effects on the activity of adrenal correction
• Fractures due to osteoporosis

2.6 Diagnosis comparison
Clinical diagnosis can be made when there are three or more of the following signs:
1. Fatigue great and small muscles
2. Centripetal obesity and cessation of growth.
3. Strie reddish.
4. Ekhimosis without platelet disorders.
5. Hypertension.
6. Osteoporosis.
7. Diabetes mellitus.

2.7 Examination Support
1. In simple laboratory tests, it was found limfositofeni, neutrophil number between 10,000 - 25.000/mm3. eosinophils 50 / mm3 hiperglekemi (Dm occurred in 10% of cases) and hypokalemia.
2. Examination of diagnostic laboratory.
Examination cortisol levels and "overnight dexamethasone suppression test" is to give 1 mg dexametason at 11 pm, the next day plasma cortisol levels checked again. In normal circumstances these levels decreased. Pemerikaan 17 hydroxy corticosteroids in the urine 24 hours (the metabolism of cortisol), 17 ketosteroid in the urine 24 hours.
3. Specific tests to distinguish hyperplasia-adenoma or carcinoma:
  1. Urinary deksametasone suppression test. Measure 17 hidroxi kostikosteroid levels in the urine of 24 hours, then given dexametasone 4 X 0.5 mg for 2 days, check again 17 hidroxi corticosteroid levels in the absence of or only slightly decreased, there may be abnormalities. Give dexametasone 4 x 2 mg for 2 days, when levels of corticosteroids decreased 17 hidroxi means there is suppression of adrenal abnormalities in the form of hyperplasia, when there is no possibility of suppression of adenoma or carcinoma.
  2. Short oral metyrapone test. Metirapone cortisol inhibits the formation of up to 17 hidroxikortikosteroid. In hyperplasia, 17 hidroxi corticosteroid levels will go up to 2 times, in adenoma and carcinoma is not an increase in urinary levels of 17 hidroxikortikosteroid.
  3. Measurement of plasma ACTH levels.
  4. ACTH stimulation test, the adenoma was found increased levels up to 2-3 times, at kasinoma no increase.

2.8 Management
Treatment of ACTH dependent Cushing's syndrome is not uniform, depending on whether the source is pituitary ACTH / ectopic.
a. If you found a pituitary tumor. Should attempted tranfenoida tumor resection.
b. If there is evidence of hiperfungsi pituitary tumor but could not be found to do so instead kobait radiation on the pituitary gland.
c. Excess cortisol can also be overcome by adrenolektomi total and followed by administration of physiological doses of cortisol.
d. When excess cortisol is caused by neoplasm followed by chemotherapy in patients with carcinoma / surgical therapy.
e. Used with kind metyropone drugs, amino gluthemide o, p-ooo could secrete cortisol (Silvia A. Price; Pathophysiology Issue 4 case 1093)

2.9 Web of causation Cushing Syndrome
Attached.

CHAPTER 3
NURSING CARE
3.1 Assessment
A. Identity Client
The identity of clients includes name, gender, place / date of birth, age, education, religion, address, date of admission. Often more prevalent in women than in men and have peak incidence between the ages of 20 and 30 years old.
B. Main complaint
There is bruising of the skin, the patient complained of weakness, weight gain occurs.
C. History of the disease before
Assess whether the patient ever used any drugs kartekosteroid in a long time.
D. Family history of disease
Assess whether the family had suffered from the disease Cushing's syndrome.
E. Physical examination
1. B1 (Breath)
Inspection: nostril breathing is sometimes seen, symmetrical chest movement
Palpation: Vocal premitus palpable rate, there is no tenderness
Percussion: resonant voice
Auscultation: Sounds normal breath sounds, no sound extra breath.
2. B2 (Blood)
Percussion deaf, S1 S2 single sounds, hypertension, increased TD.
3. B3 (Brain)
Composmentis (456), natural instability to feelings of depression mania
4. B4 (Bladder)
Polyuria, sometimes forming kidney stones, sodium retention.

5. B5 (Bowel)
There are weight gain, pain in the stomach area, striae found in the abdomen, mucosal dry lips, faint voice.
6. B6 (musculoskeletal and integument)
Thin skin, increased pigmentation, easy bruising, muscle atrophy, ecchymosis, slow wound healing, muscle weakness, osteoporosis, moon face, punguk bison, obesity tunkus.

3.2 Nursing Diagnosis
1. Risk of injury associated with weakness and decreased bone matrix.
2. High risk of infection associated with immunodeficiency.
3. Intregritas skin disorders associated with fragile thin skin daan.
4. Self care deficit related to weakness, fatigue, muscle mass maintenance.
5. Body image disturbance associated with changes in physical appearance.
6. Pain associated with injury in the gastric mucosa.
7. Impaired thought processes associated with fluctuating emotions and depression

3.3 Intervention
1. Risk of injury associated with weakness and decreased bone matrix.
Objective: To reduce the risk of injury
Criteria results: Clients are free from soft tissue injuries or fractures
Intervention:
1. Create a protective environment
Rationale: Preventing falls, fractures and other injuries to the bones and soft tissues.

2. Help clients ambulation
Rationale: Prevents dropped or bumped on the sharp corners of furniture.
3. Collaboration with a team of nutrition by administering a diet high in protein, calcium, and vitamin D
Rationale: Minimize depletion of muscle mass and osteoporosis.

2. High risk of infection associated with immunodeficiency.
Objective: To reduce the risk of infection
Criteria results: Clients not increase body temperature, redness, pain, or signs of infection and other inflammatory.
Intervention:
1. Assess TTV (TD, Nadi, body temperature and other signs of infection symptoms every 4 hours)
Rational: to know the signs of the infection as early as possible
2. Explaining the cause of the infection in patients
Rationale: Patient understanding and cooperative about the cause of the infection
3. Place on a particular space and limit visitors
Rational avoid or reduce the contact source of infection, to keep clients from pathogenic agents that can cause infection

3. Intregritas skin disorders associated with fragile thin skin daan.
Goal: Reduce the risk of lesions / decrease in the integrity of the skin
Criteria results: Clients are able to maintain the integrity of the skin, demonstrating behaviors / techniques to prevent damage / injury to the skin.
Intervention:
1. Inspection of the skin to change color, turgor, vascular.
Rational: indicates poor circulation area / damage that can lead to the formation of infection.


2. Monitor fluid intake and hydration of the skin and mucous membranes.
Rational: detect dehydration / hydration excessively affecting circulation and tissue integrity at the cellular level.
3. Inspections are dependent edema.
Rational: tissue edema were more likely damaged / torn.
4. Give skin care. Give ointment or cream.
Rational: lotions and ointments may be desirable to eliminate dry skin tears.
5. Encourage use loose cotton clothes.
Rationale: prevent direct dermal irritation and improve skin moisture evaporation.
6. Collaboration in the provision foam mattress.
Rational: reducing pressure on the old network.
4. Body image disturbance associated with changes in physical appearance.
Destination: the client can accept her situation.
Expected outcomes:
Clients express their feelings and coping methods for negative perceptions about changes in appearance, and activity level. Declare acceptance of the situation themselves.
Intervention:
1. Assess the patient's level of knowledge about the condition and treatment.
Rational: identify broad issues and the need for intervention.
2. Discuss the meaning of the changes in a patient.
Rational: some patients view the situation as a challenge, multiple difficulty accepting the change of life / performance roles and lose the ability to control your own body.
3. Encourage people closest to treat patients as normal and not as a disabled person.
Rational: expressed the hope that the patient is able to manages the situation and helps to maintain a sense of self and purpose in life.
3.4 Evaluation
The evaluation was conducted at any time after nursing plan done while evaluating ways in accordance with the objective criteria of success keparawatan plan. Thus, the evaluation can be carried out in accordance with the criteria / arrangement detailed progress notes written on a sheet containing SOAPIER (data subject, object, Asesment, Implementation, Evaluation, Revision).


REFERENCES

Ben Gray. , 2010. http://askep-askeb-kita.blogspot.com/. accessed on 2 March 2010 at 13.15 pm
Budiyanto, Carko. , 2009. Cushing Syndrome. http://medicastore.com/penyakit_kategori/1/index.html. accessed on 9 March 2010 at 16. 30 pm
De belto, Dasto. , 2010. Askep Cushing syndrome. http :/ / dastodebelto.blogspot.com/2010/02/judul-skripsi.html. accessed on 4 March 2010 at 20:30 pm
Ganong, William F. , 1998. Textbook of Medical Physiology. 17th. Jakarta: EGC.
Guyton, AC. 1997. Textbook of Medical Physiology. 9th. Jakarta: EGC.
Hadley, Mac E. 2000. Endocrinology. 5th. New Jersey: Prentice Hall, inc.
Mansjoer, Arif, et al. , 2007. Capita Selekta Medicine Volume 1. Edition 3. Jakarta: Faculty of medicine Aesculapius Media.
Phatoelisme. , 2010. Askep Cushing's syndrome. http://baioe.wordpress.com/about. html. accessed on 4 March at 20:30 pm
Sylvia A. Price. 1994. Clinical Concepts Patofisiolgi Disease Processes. Jakarta: EGC
Susanne C. Smeltzer. 1999. Textbook of Medical-Surgical Brunner Suddart. Jakarta: EGC


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