DISORDERS OF ADRENAL GLAND

INTRODUCTION

• The two adrenal glands are pyramid shaped organs that sit on top of the kidney.
• Each gland consists of two parts : inner medulla, outer cortex.
• The adrenal medulla produces two hormones which are also known as catecholamines : epinephrine (adrenaline) and norepinephrine (noradrenline) 

• These hormones are similar to substances released by the sympathetic nervous system, therefore not essential to life. 
• Control the "Fight or Flight" situation.

• Epinephrine (80%) - increases blood glucose levels, increases rate and cardiac contractions, constricts blood vessels, and stimulates the release of ACTH from the pituitary : ACTH will stimulate adrenal cortex to release glucocorticoids.
• Norepinephrine (20%) - increases both heart rate and force of cardiac contractions, vasoconstricts blood vessels throughout the body. 

• The adrenal cortex secretes corticosteroids (mineralocorticoids and glucocorticoids) and androgens which are essential to life.
• The release of mineralocorticoids is controlled by renin (enzyme).
• Mineralocorticoids play a vital role in body fluid regulation. (renin-angiotensin-aldosterone system)
• The glucocorticoids include cortisol and cortisone.
• Glucocorticoids are released in time of stress.
• These hormones affect carbohydrate metabolism by regulating glucose use in body tissues, mobilizing fatty acids from fatty tissues. 

NORMAL VS FLIGHT & FIGHT RESPONSE

DISORDERS OF ADRENAL CORTEX

TYPES OF DISORDERS

• Disorders of adrenal cortex can result in excessive/reduced production of glucocorticoids, mineralocorticoids and androgens.
• 1 major condition of hyposecretion/adrenal insufficiency : Addison's Disease
• 3 major conditions of adrenocorticol hyperfuntion are :

         a) Cushing's Syndrome (glucocorticoid excess)

         b) Conn's Syndrome or aldosteronism (aldosterone excess)

         c) Congenital Adrenal Hyperplasia (adrenogenital syndrome, androgen excess) 

REFERENCES

• http://www.nlm.nih.gov/medlineplus/adrenalglanddisorders.html
• http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/diseases-of-the-adrenal-gland/
• Brunner & Suddarth's (2010). Assessment and Management of Patients With Endocrine Disorders,Medical-Surgical Nursing Text Book. 42(8), 1275-1287

ADDISON'S DISEASE

DEFINITION

• A condition of insufficient production of corticosteroid, aldosterone androgens by the adrenal cortex. 

INCIDENCE

• Rare 4:100,000 patients.
• All ages. Common under the age of 60 years.
• Happens in both sexes. 

ETIOLOGY

1. Primary adrenal insufficiency

• Idiopathic atrophy of the adrenal gland.
• Congenital hyperplasia 
• Neoplasm in the adrenal gland
• Destruction of the gland due to chemical substances or auto immune.
• Infection - fungal / HIV 

2. Secondary haemorrhage and infarction.

• From pituitary gland or hypothalamus.

FUNCTION OF ALDOSTERONE 

PATHOPHYSIOLOGY

• Adrenocorticol hypofunction results in decreased levels of mineralocorticoids ( aldosterone ) , glucocoryicoids (cortisol ) and androgens.
• Aldosterone deficiency causes numerous fluid and electrolyte imbalances. 

( Usually , aldosterone acts on the kidneys to increase sodium and fluid retention ) 

A deficiency of aldosterone causes : 

1. Water excretion increases.

2. Extracellular water becomes depleted (dehydration)

3. Hypotension develops.

4. decrease cardiac output.

5. Atrophy of the heart - as a result of diminished workload. 

- Eventually hypotension becomes severe leading to circulatory collapse, shock and death.

- Potassium levels of more than 7 mEq/L results in arrythmias and cardiac arrest. 

• Glucocorticoid deficiency causes widespread metabolic disturbances. 
• Glucocorticoids promotes gluconeogenesis ( synthesis of glucose from non carbohyfrate sources, such as amino acids and glycerol. Occurs primarily in the liver and kidneys whenever the supply of carbohydrates is insufficient to meet the body's energy needs ) and have an "anti insulin" effect. 
• Low glucocorticoid = Low gluconeogenesis 

- Liver glycogen deficiency.
- Hypoglycaemia develops.
- Failure of negetive feedback causes increase of ACTH ( controls the secretion of adrenal hormone, cortisol - released in response to stress and a low level of blood glucocorticoids. Its primary functions are to increase blood sugar through glycogenolysis ) 
- Patient becomes weak, exhausted, anorexia, weight loss, nausea, vomitting. 

•  Increased ACTH secretion leads to increased pigmentation of the skin and mucous membrane.
• Therefore, patients with Addison's disease have increased levels of ACTH, bronzed or tanned appearance. 

• Adrogen deficiency fails to produce symptoms in men because the testes supply adequate amount of sex hormone. 
• Women depend on the adrenal cortex foe adequate secretion of androgens (plays a role in pubic and axillary hair in females) 

CLINICAL MANIFESTATION YOUTUBE 

1. Weakness.
2. Fatigue.
3. Nausea and vomitting.
4. Anorexia.
5. Loss of weight.
6. Emotional disturbances.
7. Reduced coping mechanism. 

8. Appearance.
- Dark, shiny skin.
- Mucosal, mouth and conjuctiva pigmentation.
9. Dehydration.
10. In severe condition.
- Severe dehydration.
- hypotension.
- Shock.
11. Increased potassium absorption. 
- Hyperkalaemia
- If level > 7 mEq/L -> arrythmias -> cardiac arrest. 
12. Muscle atrophy due to reduced mobility because of deteriorating metabolism.
13. Hypoglycaemia.
- Low gluconeogenesis is due to Low glucocorticoid. 

INVESTIGATION

1. Serum cortisol
- Cortisol concentration < 20 ug/dl 
2. Plasma ACTH 
- To confirm primary and secondary adrenal insufficiency.
3. Serum electrolyte. 
- Sodium level low
- Potassium and calcium high 
- Glucose is decreased.
4. ECG - QT Interval prolong. 

MEDICAL MANAGEMANT

1. Glucocorticoid therapy.
- Cortisone acetate 25mg in the morning and 12.5mg every evening.
- Hydrocortisone 20mg every morning and 15mg every evening. 
- Prednisolone 5mg every morning and 2.5mg every evening. 

2. Mineralocorticoid.
- Fludrocortisone Acetate 100ug daily in primary adrenal insufficiency. 

MANAGEMENT OF CARE

1. Physical assessment.
a) Assess patient's emotional status.
b) Assess the 'hump' or bone deformity.
- To prevent pressure. 
2. Observation.
a) Vital sign.
- Pulse.
- Blood pressure.
- Temperature.
b) Monitor for infection.
- Report any signs of infection eg: sore throat.
c) Monitor signs of dehydration.
- Assess sodium and potassium imbalance.
3. Medication.
- If not treated early => death 

COMPLICATION

Acute adrenocortical insuffiency (Addisonian Crisis)
1. A life threatening emergency caused by sudden decrease of these hormones. 
2. Triggered by : 
- Stress.
- Sudden withdrawal of corticoidsteroid hormone replacement therapy. 
- After adrenal surgery.
- Sudden pituitary gland destruction. 
3. Manifestation.
- Hypotension (postural)
- Tachycardia.
- Dehydration - severe vomitting and diarrhea.
- Hyponatremia.
- Hyperkalemia.
- Hypoglycaemia.
- Fever, weakness and confusion.
- Shock. 

TREATMENT

• Replacement therapy - hydrocortisone.
• Large volumes of 0.9% saline and 5% dextrose are administered to reverse hypotension and electolycte imbalance. 

NURSING DIAGNOSIS

1. Activity intolerance related to postural hypotension.
Obj : Patient will be able to remain free from fatigue during performance of usual activities. 
Intervention
- Provide bed rest for the first 24 hours.
- Avoid any unnecessary activities such as bathing for the first 12 hours. 
- Explain to patient that the energy level will increase when the hormones stabilize.
- Gradually increase the activities as hormone levels return to normal. 

2. Deficient fluid volume related to inability to conserve fluid. 
Obj : Patient will be able to have normal fluid status.
Intervention
- Monitor intake and output hourly.
- Monitor blood pressure and heart rate hourly until normal. 
Administer IV fluids as prescribed (5% dextrose)
- Monitor electrolyte status.
- Administer cortisol as prescribed. 

3. Risk of injury related to weakness and hypoglycaemia.
Obj : Patient will remain free from injury. 
Intervention
- Keep bed in lowest position.
- Keep side rails up at all times unless patient refuses.
- Monitor blood glucose levels every 4 hours.
- Instruct patient to call foe assistance when getting into or out of bed. 

4. Knowledge deficit related to lack of previous experience with new problem.
Obj : Patient will verbalize understanding of disease and its treatment. 
Intervention
- Explain care to patient and family so that no unexpected events occur.
- Focus on immediate care and home care later.
- Repeat teaching frequently.
- Provide written material to enforce verbal teaching. 
- Provide information about community resources that may be useful to patient and family. 

SUMMARY ADDISON'S DISEASE YOUTUBE 

REFERENCES

• http://www.mayoclinic.com/health/addisons-disease/DS00361/DSECTION=symptoms
• http://www.medicinenet.com/addison_disease/article.htm
• http://emedicine.medscape.com/article/116467-clinical
• Brunner & Suddarth's (2010). Assessment and Management of Patients With Endocrine Disorders, Medical-Surgical Nursing Text Book. 42(8), 1279-1281

CHUSING'S SYNDROME

DEFINITION

• Cushing's syndrome is a disorder caused by prolonged exposure of the body's tissues to high levels of the hormone cortisol.
• Sometimes called " hypercortisolism " 

INCIDENCE

• Occurs 10 times more in women 
• Average age - 30 and 50 years old 

ETIOLOGY

• Adrenal tumor ( responsible for approximately 30% of all cushing's syndrome cases ) 85% - benign, 15% - malignant.
• Adrenal hyperplasia - caused by overproduction of ACTH. Two sources of excessive ACTH secretions are : 

a) Pituitary hypersection and pituitary tumors.

b) Ectopic secretion of ACTH - some benign or malignant tumors that arise outside the pituitary can produce ACTH. Lung tumors cause over 50% of these cases. Men are affected 3 times more than women. 

RISK FACTORS

• Administration of exogenous steroids. 

          Example : Prednisolone 

PATHOPHYSIOLOGY

 Hypothalamus sends Corticotropin releasing hormone CRH > Pituitary Gland > secrete ACTH ( adrenocorticotropin ) > stimulates the adrenal glands to release cortisol into the bloodstream > exaggerated physiologic action of glucocorticoids 
           
         

                                                                                 
CLINICAL MANIFESTATION

   Persistent hyperglycemia 

- Protein tissue wasting resulting in :

• Weakness due to muscle wasting 
• Capillary fragility resulting in ecchymosis 
• Osteoporosis due to bone matrix wasting 

- Potassium depletion leading to hypokalemia, arrythmias, muscle weakness and renal disorders.

- Sodium and water retention which causes edema and hypertension > CVA, left ventricular failure leading to CCF.           

- Abnormal fat distribution due to edema resulting in moon shaped face, dorsocervical fat pad on neck ( buffalo hump ) 

- Truncal obesity with slender limbs. 

- Pink and purple striae appears on breasts, axillary areas, abdomen, leg due to thinning of skin. 

- Increases susceptibility to infection and lowered resistance to stress increase chances of invasion of micro organism. 

- Poor wound healing due to suppression of inflammatory response.

- Virilism ( musculinization - acne, thinning of sclap, hirsutism, voice - musculine )

- Mental changes include memory loss, poor concentration, depression. 

DIAGNOSTIC TESTS

• 24-Hour Urinary Free Cortisol Level ( Levels higher than 50 - 100 mcg/day for an adult suggest Cushing's syndrome ) 
• Blood Test - cortisol level, ACTH, Potassium low
• X-ray of the skull detect erosion of the sella turcica by pituitay tumor.
• CT scan and ultrasonography detect location of tumors. 

TREATMENT
Surgical and Radiation

• Surgery is performed via transsphenoidal hypophysectomy, craniotomy - if pituitary tumor has enlarged beyond sella turcica, adrenalectomy - hyperplasia of adrenals.
• Radiation can be externally or internally.
• Internal radiation can be applied through a transsphenoidal implant.
• Radiation must be done with care as the optic nerve is nearby. 

TRANSSPHENOIDAL HYPOPHYSECTOMY 

MANAGMENT

Replacement therapy postoperatively 

Require a lifelong replacement therapy such as :

• Glucocorticoid - cortison ( cortef )
• Mineralcorticoid - fludrocortisone ( florinef ) 

MEDICAL TREATMENT

• Interferes with the ACTH production or adrenal hormone synthesis. 
• Example : Mitotane ( Lysodren ) - a cytotoxic antihormonal agent that inhibits corticosteroid synthesis without destroying corticol cells. 

NURSING DIAGNOSIS

1. Impaired skin integrity related to edema, impaired healing, and thin and fragile skin. 

Obj : Patient is able to maintain intact skin. 

Intervention

- Assess skin for early detection of trauma. 

Example : redness, excoriation, infection, edema

- Protect patient from bumping and bruising.

- Change patient's position every two hourly 

R : to prevent skin breakdown. 

- Do not use the adhesive tape. 

R : to avoid irritate the skin and tear the fragile tissue when the tape is removed. 

- Give meticulous skin care.

R : to avoid traumatizing the pateint's fragile skin.

- Serve low salt diet. 

2.  Self-care deficit related to weakness, fatigue, muscle wasting, altered sleep patterns. 

Obj : Patient is able to self care with minimal support. 

Intervention

- Assess patient ability in carrying out the daily activities. 

R : to help patient plan and space rest periods throughout the day to prevent complications of immobility.

- Assist when patient is weak. 
R : to encourage the moderate activity. 
- Encourage patient to rest.
R : to promote relaxing for rest and sleep.
- Increase the activity gradually. 
R : to promote increased self-esteem. 

3. Risk for infection related to altered protein metabolism and inflammatory response. 
Obj : Patient has no infection.
Intervention
- Assess for inadequate protein stores, proteinuria, muscle wasting and poor wound healing. 
- Monitor vital sign. 
R : to detect any sign and symptoms of infection.
- Assess potential site infection site eg: skin and urinary tract.
- Screen and limit visitor who may have infections
R : to protect patient from sources of infection.
- Teach patient and staff effective handwashing.
R : to limits patient's exposure to potential infection cause agents.
- Promote adequate rest and nutrition.
R : to promote rest and adequate nutrition limits fatigue and enhance immune system natural defence mechanism.
- Refer patient to dietitian. 
R : to teach patient selecting appropriate foods that are low in sodium and calories. 

SUMMARY CUSHING'S SYNDROME YOUTUBE

REFERENCES

• http://medical-dictionary.thefreedictionary.com/Cushing's+syndrome
• http://www.mayoclinic.com/health/cushings-syndrome/DS00470
• http://www.nlm.nih.gov/medlineplus/ency/article/000410.htm
• Brunner & Suddarth's (2010). Assessment and Management of Patients With Endocrine Disorders, Medical-Surgical Nursing Text Book. 42(8), 1281-1284