C A S E P R E S E N TAT I O N

ADDISON'
S DISEASE
P R E S E N T E D B Y:
LY K A C L A I R E P E N AV E R D E
SHANE PILLONAR
BSN-3A
Addison's Disease
Addison's disease, also called adrenal insufficiency, is an uncommon
disorder that occurs when your body doesn't produce enough of certain
hormones. In Addison's disease, your adrenal glands, located just above
your kidneys, produce too little cortisol and, often, too little aldosterone.
Mrs. Nenita Ocampo a 60-year-old woman

Case Scenario
consult due to increase darkening of the
skin, dizziness, easy fatigability, nausea
with occasional vomiting, and progressive
weight loss over 6 months.

Her physical examination revealed that

she is pale; with generalized
hyperpigmentation especially on the face,
oral mucosa, and palmar creases; loss of
body hair; could not stand due to severe
postural dizziness; Blood pressure of
70/40 mmHg (sitting) and 100/60 mmHg
(supine); and pulse rate of 105 bpm.
Anatomy & Physiology
of
Adrenal Cortex
The adrenal cortex—the outer layer of the gland, consists of multiple layers of lipid-
storing cells that occur in three structurally distinct regions. Each of these regions
produces different hormones.

Hormones of the Zona Glomerulosa

The most superficial region of the adrenal cortex, which produces a group of hormones
collectively referred to as mineralocorticoids because of their effect on body minerals,
especially sodium and potassium. These hormones are essential for fluid and electrolyte
balance.

Aldosterone is the major mineralocorticoid. It is important in the regulation of the

concentration of sodium and potassium ions in urine, sweat, and saliva. Aldosterone is
also a key component of the renin-angiotensin-aldosterone system (RAAS) in which
specialized cells of the kidneys secrete the enzyme renin in response to low blood
volume or low blood pressure.
Hormones of the Zona Fasciculata
The intermediate region of the adrenal cortex is the zona fasciculata, named as such because
the cells form small fascicles (bundles) separated by tiny blood vessels. The cells of the zona
fasciculata produce hormones called glucocorticoids because of their role in glucose
metabolism. The most important of these is cortisol, some of which the liver converts to
cortisone.

Hormones of the Zona Reticularis

The deepest region of the adrenal cortex is the zona reticularis, which produces small
amounts of a class of steroid sex hormones called androgens. During puberty and most
of adulthood, androgens are produced in the gonads. The androgens produced in the
zona reticularis supplement the gonadal androgens.
 RISK FACTORS

TYPE 1 DIABETES HYPOTHYROIDISM HYPOPITUITARISM PERNICIOUS GRAVES DISEASE

ANEMIA

TESTICULAR CHRONIC CANDIDIASIS DERMATITIS VITILIGO

DYSFUNCTION THYROIDITIS HERPETIFORMIS
 CAUSES
Addison’s disease is caused by an autoimmune response, which occurs when the body’s
immune system (which protects it from infection) assaults its own organs and tissues. With
Addison’s disease, the immune system attacks the outer portion of the adrenal glands (the
cortex), where cortisol and aldosterone are made.

Other causes of Addison’s disease include:

• Injury to the adrenal glands Infection
• Tuberculosis
• HIV/AIDS-related infections
• Fungal infections
• Cancer cells from another part of the body that have invaded the adrenal glands
Bleeding into the adrenal glands
• Surgical removal of the adrenal glands
• Amyloidosis (abnormal buildup of certain proteins in the organs)
• Genetic defects
DIAGNOSTICS

Blood test. Tests can measure her blood

ACTH stimulation test. ACTH signals
levels of sodium, potassium, cortisol and
adrenal glands to produce cortisol. This
adrenocorticotropic hormone (ACTH),
test measures the level of cortisol in her
which stimulates the adrenal cortex to
blood before and after an injection of
produce its hormones. A blood test can
synthetic ACTH.
also measure antibodies associated with
autoimmune Addison's disease.
DIAGNOSTICS

Insulin-induced hypoglycemia test. If

Imaging tests. She may undergo a
doctors think she may have adrenal
computerized tomography (CT) scan of
insufficiency as a result of pituitary
her abdomen to check the size of her
disease. The test involves checking her
adrenal glands and look for other
blood sugar and cortisol levels after an
abnormalities. She may also undergo an
injection of insulin. In healthy people,
MRI scan of her pituitary gland if testing
glucose levels fall and cortisol levels
indicates her might have secondary
increase.
adrenal insufficiency.
Pathophysiology
&
Symptomatology
Treatment/
Management
All treatment for Addison's disease involves medication. She will be given hormone replacement
therapy to correct the levels of steroid hormones her body isn't producing.

Some options for treatment include oral corticosteroids such as:

• Hydrocortisone (Cortef), prednisone or methylprednisolone to replace cortisol.
• Fludrocortisone acetate to replace aldosterone.
• Get plenty of salt (sodium) in diet, especially when the weather is hot or if she have
gastrointestinal upsets, such as diarrhea.
• A temporary increase in medication dosage if her body is stressed, such as from an operation, an
infection or a minor illness. If ill with vomiting and can't keep down oral medications, may need
injections of corticosteroids.
Other treatment recommendations include:
• Carry a medical alert card and bracelet at all times.
• Keep extra medication handy.
• Carry a glucocorticoid injection kit.
• Stay in contact with your doctor.
• Have annual checkups.

Treatment for an addisonian crisis, which is a medical emergency, typically includes intravenous
injections of:
• Corticosteroids
• Saline solution
• Sugar (dextrose)
DRUG STUDY
DRUG STUDY
 NURSING CONSIDERATIONS
• Determine whether patient is sensitive to other corticosteroids.
• Most adverse reactions to corticosteroids are dose- or duration-dependent.
• For better results and less toxicity, give a once-daily dose in morning.
Alert: Salts aren't interchangeable.
Alert: Only hydrocortisone sodium succinate can be given IV.
Alert: Epidural corticosteroid injections to treat neck and back pain and radiating pain in the
arms and legs may result in rare but serious adverse events (vision loss, stroke, paralysis,
death). The use of epidural corticosteroid injections isn't approved by the FDA.
• Enema may produce same systemic effects as other forms of hydrocortisone. If enema
therapy must exceed 21 days, taper off by giving every other night for 2 to 3 weeks.
• High-dose therapy usually isn't continued beyond 48 hours.
• Always adjust to lowest effective dose.
• Monitor patient's weight, BP, and electrolyte levels.
• Monitor patient for cushingoid effects, including moon face, buffalo hump, central obesity,
thinning hair, HTN, and increased susceptibility to infection.
 NURSING CONSIDERATIONS
• Unless contraindicated, give a low-sodium diet that's high in potassium and protein.
Give potassium supplements.
• Drug may mask or worsen infections, including latent amebiasis.
• Stress (fever, trauma, surgery, and emotional problems) may increase adrenal
insufficiency. Increase dosage.
• Watch for depression or psychotic episodes, especially during high-dose therapy.
• Inspect patient's skin for petechiae.
• Diabetic patient may need increased insulin; monitor glucose level.
• Periodic measurement of growth and development may be needed during high-dose or
prolonged therapy in children.
• Elderly patients may be more susceptible to osteoporosis with prolonged use.
• Gradually reduce dosage after long-term therapy.
• Look alike–sound alike: Don't confuse Solu-Cortef with Solu-Medrol. Don't confuse
hydrocortisone with hydrocodone, hydroxychloroquine, or hydrochlorothiazide. Don't
confuse Cortef with Coreg or Lortab.
DRUG STUDY
 NURSING CONSIDERATIONS
• Monitor for S&S of Cushing's syndrome, especially in patients on long-term therapy.
• Lab tests: Periodic blood glucose and CBC with platelet count.
• Cortisone may mask some signs of infection, and new infections may appear.
• Be alert to clinical indications of infection: malaise, anorexia, depression, and evidence of
delayed healing. (Classic signs of inflammation are suppressed by cortisone.)
• Report ecchymotic areas, unexplained bleeding, and easy bruising.
• Take drug exactly as prescribed. Do not alter dose intervals or stop therapy abruptly.
• Monitor weight and report a steady gain especially if it is accompanied by signs of fluid
retention (e.g., edema of ankles or hands).
• Report changes in visual acuity, including blurring, promptly.
• Inform physician or dentist that cortisone is being taken. Carry identification card or
jewelry that states drug being taken and physician's name.
• Do not breast feed while taking this drug.
DRUG STUDY
 NURSING CONSIDERATIONS
• Administer once-daily doses of prednisone in the morning to match body’s
normal cortisol secretion schedule.
• Because prednisone can produce many adverse reactions, assess regularly for
signs and symptoms of such reactions as heart failure and hypertension. Also
monitor fluid intake and output and daily weight.
• Monitor growth pattern in children. Prednisone may retard bone growth.
• Be aware that prolonged use of prednisone may cause hypothalamic-pituitary-
adrenal suppression.

• WARNING: Withdraw prednisone gradually, as ordered, if therapy lasts

longer than 2 weeks. Stopping abruptly may cause acute adrenal insufficiency
and, possibly, death.
DRUG STUDY
 NURSING CONSIDERATIONS
• Monitor weight and I&O ratio to observe onset of fluid accumulation, especially if
patient is on unrestricted salt intake and without potassium supplement. Report
weight gain of 2 kg (5 lbs)/wk.
• Monitor and record BP daily. If hypertension develops as a consequence of therapy,
report to physician. Usually, the dose will be reduced to 0.05 mg/d.
• Check BP q4–6h and weight at least every other day during periods of dosage
adjustment.
• Lab tests: Periodic serum electrolytes and ABGs during prolonged therapy.
• Monitor for S&S of hypokalemia and hyperkalemic metabolic alkalosis.
• Monitor for signs of overdosage (hypercorticism): psychosis, excess weight gain,
edema, congestive heart failure, ravenous appetite, severe insomnia, and increase in
BP.
• Note: Signs of insufficient dosage (hypocorticism) are loss of weight and appetite,
nausea, vomiting, diarrhea, muscular weakness, increased fatigue, and hypotension.
 NURSING CONSIDERATIONS
• Report signs of hypokalemia
• Be aware of signs of potassium depletion associated with high sodium intake:
Muscle weakness, paresthesias, circumoral numbness; fatigue, anorexia, nausea,
mental depression, polyuria, delirium, diminished reflexes, arrhythmias, cardiac
failure, ileus, ECG changes.
• Advise patient to eat foods with high potassium content.
• Signs of edema should be reported immediately. Sodium intake may or may not
require regulation, depending on individual needs and clinical situation.
• Weigh daily under standard conditions and report steady weight gain.
• Report intercurrent infection, trauma, or unexpected stress of any kind promptly
when taking maintenance therapy.
• Carry medical identification at all times. It needs to indicate medical diagnosis,
medication(s), physician's name, address, and telephone number.
• Do not breast feed while taking this drug without consulting physician.
 NURSING CARE PLAN
Subjective Data: Increase darkening of skin, dizziness, easy fatigability, nausea,
vomiting, weight loss

Objective Data: physical examination revealed she is pale; with generalized hyper-
pigmentation on the face, oral mucosa, and palmar creases; loss of body hair; could
not stand due to severe postural dizziness

Vital signs; Blood pressure of 70/40 mmHg (sitting) and 100/60 mmHg (supine);
and pulse rate of 105 bpm.

Nursing Diagnosis: Risk for Deficient Fluid Volume related to increased water
retention, sodium secretion and potassium retention as evidenced by nausea and
vomiting with progressive weight loss.
 NURSING CARE PLAN
Planning: After the nursing intervention the patient will experiences adequate fluid
volume and electrolyte balance as evidenced by urine output greater than 30 mL/hr,
normotensive blood pressure (BP), heart rate (HR) less than 100 beats/min, consistent
weight, and normal skin turgor.

Nursing Intervention:

Independent

Monitor intake and output (I&O) and specific gravity. Include all output sources, such
as emesis, diarrhea, or draining wounds, weigh continence briefs/diapers. Calculate
24- hour balance.

Rationale: Continued negative fluid balance, decreasing renal output, and

concentration of urine suggest developing dehydra tion and need for increased fluid
replacement.
 NURSING CARE PLAN
Weigh, as indicated.

Rationale: Sensitive measurement of fluctuations in fluid balance

Monitor vital signs. Evaluate peripheral pulses and capillary refill.

Rationale: Reflects adequacy of circulating volume

Assess skin turgor and moisture of mucous membranes. Note reports of thirst.

Rationale: Indirect indicators of hydration status and degree of deficit

Encourage increased fluid intake as individually appropriate and tolerated.

Rationale:As sodium loss increases, extracellular fluid volume decreases. These

interventions are necessary to prevent fluid volume deficit because the kidneys are unable to
conserve sodium
 NURSING CARE PLAN
Observe for bleeding tendencies, such as oozing from mucous membranes or puncture
sites and presence of ecchymosis or petechiae

Rationale: Patient bruises easily.

Assess for fatigue, sensory deficits, or muscle weakness, which may progress to
paralysis.

Rationale: These are signs of hyperkalemia. Aldosterone deficiency leads to potassium

retention by the kidneys.

Instruct the patient to ingest salt additives in conditions of excess heat or humidity.

Rationale: Sweating increases sodium loss.

 NURSING CARE PLAN
Collaborative:

Administer parenteral fluids as prescribed. Anticipate the need for an intravenous (IV)
fluid challenge with immediate infusion of fluids for patients with abnormal vital
signs.

Rationale: Normal saline is infused initially to restore fluid volume.

Administer Kayexalate.

Rationale: This ion exchange resin can be given orally or by enema to decrease the
potassium level in the body.
 NURSING CARE PLAN
Administer replacement medications as prescribed or indicated: oral cortisone
(Cortone), hydrocortisone (Cortef), prednisone, or fludrocortisone (Florinef).

Rationale:
Cortisone and prednisone replace cortisol deficits, which will promote sodium
resorption.
Fludrocortisone is a mineralocorticoid for patients who require aldosterone
replacement to promote sodium and water replacement. Acute adrenal insufficiency is
a medical emergency requiring immediate fluid and corticosteroid administration. If
treated for adrenal crisis, the patient requires IV hydrocortisone initially; usually by the
second day, administration can be converted to an oral form of replacement.
 NURSING CARE PLAN
Monitor laboratory studies, such as CBC, electrolytes, and serum albumin.

Rationale: Provides information about level of hydration and corresponding deficits.

Note: Malnutrition and effects of decreased albumin levels potentiate fluid shifts or
edema formation.

Monitor patient’s serum electrolytes and recommend electrolytes replacement therapy

(oral or IV) to the physician as needed.

Rationale: Sodium is an important electrolyte that is lost in Addison’s disease.

Hyponatremia or low serum sodium level may cause brain swelling.
Thank
You