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EGBautista II, USI-BSN (2008) 1

ADRENAL GLANDS  3 major steroid
- 2 endocrine glands with separate, independent 1. Aldosterone (major)
functions each attached to the upper potion of the  Conserves Na & maintain ECF
kidney  Sustain BP
1) Adrenal Medulla 2. Desosexy
2) Adrenal Cortex 3. Corticosterone
- Sympathomine
 Produces effects on the body similar to those Note:
activation of the sympathetic nervous system *Agiotensin II = ↑ BP by constriction
- Catecholamines *If ↓ aldosterone = addison’s disease
 Regulate metabolic pathway for metabolic rate *If ↑ aldosterone = hyperaldosteronism, which promotes reabsorption
to kidney
Adrenal Medulla
- Inner/ center of the gland xxx
- Secretes catecholamines:
2) Norepinephrine Disease in Adrenal Cortex
- Functions as part of the autonomic nervous system
1) Addison’s Disease
- Catecholamines are contolled by the hypothalamus
Epinephrine Norepinephrine (Adrenocortical Insufficiency)
Acts to during stress: During stress reaction: 2) Cushing’s syndrome
1. Convert glycogen 1. Produces extensive 3) Primary Aldosteronism
within the liver into vascular constriction
Disease in Adrenal Medulla
glucose 2. Dilate pupil
2. ↑ cardiac output 3. Inhibits GI tract 4) Pheochromocytoma
3. Produces cold upset
sweat, pounding
heat, deep rapid
breathing & wide
key up alertness - Due to ↓ Cortisol/ Aldosterone
(alertness in the time of - Results when adrenal cortex function is inadequate to
emergency: flight or meet the patient’s need foe cortical hormones
I. Etiology
Functions of Epinephrine: 1) Autoimmune
1. Increase or decrease blood flow to tissues that are not/ are 2) Idiopathic atrophy of the adrenal glands
needed in emergency situations 3) Iatrogenic – due to surgical removal of bothe glands
2. Induce release of free fatty acids 4) Infections (ie. tuberculosis/ histoplasmosis)
3. Increase the basal metabolic rate 5) Secondary to hypo-functions of the pituitary gland
4. Elevate blood glucose level
6) Sudden cessation of exogenous aldrenocortical hormone
Adrenal Cortex
- Outer portion of the gland
II. Clinical Manifestations
- Essential for survival
1. Muscular weakness
- Secretes:
1) Corticosteroids
2. Anorexia
2) Glucocorticoids 3. Gastrointestinal symptoms
3) Mineralocorticoids 4. fatigue
4) Androgens (male sex hormone) 5. Emaciation (haggard looking/ extreme leanness)
- Secretions is regulated by the hypothalamic-pituitary- 6. Dark pigmentation of the skin
adrenal axis 7. Hypotension
8. ↓ blood glucose; ↓ serum Na & ↑ serum K+
Functions of: 9. Mental status changes (depression, apathy, emotional
1. Glucocorticoids lability)
 Inhibit the inflammatory response to tissue injury 10. Addisonian crisis with disease progression & acute
 Suppress allergic manifestations hypotension
 Produced in zona vasicular a. Cyanosis
 3 major steroids: b. Fever
o Cortisol (major) c. Classic signs of shock
o Cortisone i. Pallor
ii. Apprehension
o Corticosterone
iii. Rapid & weak pulse
 They have important influence in glucose metabolism
iv. Rapid respirations
(ie. pyruvate, amino acid, …)
 Side effects: v. ↓ BP
o Development of DM 11. Severe/ chronic dehydration
o Osteoporosis  There is disturbance of Na & K metabolism
o Peptic Ulcer 12. Headache, nausea, abdominal, pain
o Increase protein breakdown 13. Over secretion, exposure to cold, acute infections
o Poor wound healing  Can lead to shock if untreated
o Redistribution of the body fats
III. Diagnostic Findings
2. Mineralocorticosteroids 1. Laboratory test
 Major effects are in electrolyte metabolism a. ↓ blood glucose & Na levels
 Acts principally on renal tubular & GI epithelium b. ↑ serum K+
 Causes increased Na ion absorption in exchange for c. ↑ WBC count (leukocytosis)
excretion of potassium
EGBautista II, USI-BSN (2008) 2
d. ↓ level of adrenocortical hormones in the 7. Kyphosis, backache & compression fracture of the
blood or urine vertebrae
e. ↓ serum cortisol 8. Hypertension/ CHF
*If adrenal cortex is impaired 9. “moon faced appearance”
ACTH fails to cause normal rise of cortisol 10. ↑ oiliness of the skin & acne
11. ↑ susceptibility to infections
IV. Medical Management 12. Hyperglycemia/ overt diabetes
Goals: 13. Weight gain
1. To combat shock 14. Slow healing of minor cuts & bruises
2. To restore blood circulation 15. In female:
a. Virilization (due to ↑ androgens)
1) Administer fluids (5% dextrose in NSS &  Development of exaggerated masculine
corticosteroids) characteristics
2) Monitor V/S b. Hirsuitism
3) Place patient in recumbent position with the legs c. Breast atrophy
elevated d. Menses ceases
4) Administration of medications e. Clitoris enlarge
a. Hydrocortisone (Solu-Cortef) given through f. Voice deepens
IV 16. loss of libido
b. Vasopressor amine if hypotension persist 17. Changes in mood & mental activity
c. Antibiotics a. Psychosis
5) Oral intake as tolerated to prevent hypovolemic b. Distress
shock c. Depression
6) Supplementary dietary intake (ie. pickles) 18. Visual disturbances
a. Brought about by tumor
V. Nursing Management
1. Assessing the patient III. Diagnostic Findings
2. Monitoring for Addison crisis 1. ↑ serum Na & Blood glucose level
a. Hypotension
2. ↓ serum K +
3. Dexamethasone suppression test
b. Rapid, weak respiratory rate
c. Extreme weakness  Measurement of plasma & urinary cortisone
d. Pallor 4. 24 urinary cortisol level
3. Restoring fluid balance 5. Radioimmunoassay
4. Improving activity intolerance 6. CT scan
 Quiet & non-stressful environment 7. Ultrasound
5. Promoting home & community-based care 8. MRI

Hormonal Replacement IV. Nursing Diagnosis
1. Florinef 1. Risk for urinary r/t weakness
2. Prednisone 2. Risk for infection related to altered protein
metabolism & inflammatory response
Excessive Hormone (s/sx) 3. Self-care deficit
1. Weight gain 4. Impaired skin integrity
2. Edema
5. Body image disturbance
Hormonal deficit (s/sx) 6. Altered thought processes
1. Postural hypotension
2. Weight loss V. Complications
3. Light headedness 1. Addisonian crisis (monitor)
a. Hypotension
b. Rapid weak pulse
- Results from excessive adrenocortical activity d. Weakness
- Due to high levels of the hormone cortisol 2. Adverse effects of adrenocortical activity (monitor)
a. Fluid & electrolyte status of client
I. Etiology b. Monitor daily weight
1) Excessive administration of corticosteroids or ACTH c. Laboratory test
2) Hyperplasia of the adrenal cortex d. Hyperglycemia (refer to the physician)

II. Clinical Manifestations VI. Medical Management
1. Classic picture of Cushing’s syndrome in adult: 1. Transpenoidal hypophysectomy (treatment of choice)
a. Central type obesity 2. Radiation therapy
b. Fatty “buffalo” lump in the neck & 3. Adrenalectomy
supraclavicular area 4. Administration of hydrocortisone
c. Heavy trunk 5. Adrenal enzyme inhibitor
d. Thin extremity Example:
2. Skin-thin, fragile, easily traumatized, ecchymosis a. Metylrapone
(bruises), striae developed b. Aminoglutethimide
3. Body weakness & lassitude (caused by ↑ K+ c. Mitotane
metabolism) d. Ketoconazole (nizoral)
4. Sleep disturbance
5. Muscle wasting VII. Nursing Management
6. Osteoporosis Goal:
1. To decrease risk for injury
EGBautista II, USI-BSN (2008) 3
a. Provide a protective environment to prevent vi. Methyl prednisone
falls, fractures & other injuries to bones & c. Consume body Na & less K+
soft tissues
b. Assist patient when ambulating 4. PHEOCHROMOCYTOMA
c. Offer foods high in proteins, Ca+ & vitamin - A tumor that is usually benign & originates from the
D & ↓ Na & calories (to avoid muscle chromaffin cells of the adrenal medulla
wasting & fasting)
2. To reduce risk for infections I. Incidence
a. Unnecessary exposure to others with - Peak incidence age between 20-50 years old
infections - Affects both sexes
b. Assessed frequently for subtle signs of - Cause of ↑ BP in hypertensive patients
3. To ↑ ability to carry out self-care activities II. Clinical Manifestations
4. To improve skin integrity 1. Headache
a. Meticulous skin care to avoid traumatizing 2. Diaphoresis Triad of symptoms
the patient’s fragile skin 3. Palpitations
b. Use of adhesive tape is avoided 4. Hepertension & other cardiovascular disturbances
c. Assist in changing of positions 5. Tremors
5. To improve body image 6. Flushing
a. Discuss the effect of the changes have had 7. Anxiety
on self-concept 8. Hyperglycemia
b. Weight gain & edema may be modified by a 9. Paroxysmal form of phechromocytoma
↓ CHO, ↓ Na diet a. Extreme anxious
6. To improve mental functions b. Tremulous & weak
a. Explain to the patient & family members c. Vertigo
about the cause of emotional instability d. Burning of vision
(help for mood swing) e. Tinnitus
7. Absence of complications, monitor closely for: f. Air hunger
a. Hypotension g. Dyspnea
b. Rapid, weak pulse h. Polyuria
c. Rapid respiratory rate i. Nausea & vomiting
d. Pallor j. Diarrhea
e. Extreme weakness k. Abdominal pain
l. Feeling of impeding doom
m. Palpitations & tachycardia
3. PRIMARY ALDOSTERONISM i. Aneurism, ARF, stroke
• Primary aldosteronism is a condition which your
*Epineprine 100pg/ml (590 pmol)
body's adrenal glands produce too much of the *Norepinephrine >500pg/mol (590-3240 pmol/L)
hormone aldosterone, causing you to retain sodium
and lose potassium. III. Diagnostic Findings
1. Signs of sympathetic nervous system over activity
I. Clinical Manifestations a. Hypertension
1. Hypertension b. Headache
 Prominent sign c. Hyperhydrosis 5 H’s
 Due to serum Na+ is elevated d. Hypermetabolism
2. Muscle weakness e. hyperglcemia
3. Cramping 2. Urine and plasma level of catecholamine
4. Fatigue 3. Clonidine suppression (catapres) test
5. Polyuria 4. Imaging studies (CT scan, MRI & ultrasound)
6. Polydipsia 5. 131-I metalodobenzylguadine (MIBG)
7. Tetany a. Use to locate
8. Paresthesia
IV. Medical Management
II. Diagnostic Findings 1. Bed rest
1. Decline in serum level of K+ & hydrogen ions 2. Head of the bed must be elevated
2. ↑ in pH & bicarbonate level 3. Pharmacologic management
3. High serum aldosterone level a. Alpha-adrenergic blocking agents
To ↓ BP quickly i. ex: Phentolamine (Regitine)
4. ↓ serum Renin level
b. Smooth muscle relaxant
5. Aldosterone excretion rate i. Ex: Na nitroprusside (Nipride)
6. Renin-Aldosterone stimulation test c. Phenoxybenxamine (Dibenzyline)
Long acting alpha
7. Adrenal venous sampling d. Beta-adrenergic blocking agent
e. Catecholamine synthesis inhibitor
III. Medical Management i. Ex: Alpha-methyl-pthyrosine
1. Adrenalectomy (methyrosine)
2. Frequent assessment of V/S 4. Surgical management
3. Corticosteroid therapy a. Adrenalectomy (↓Na & ↑K diet)
a. Use for adrenal insufficiency
b. Use to suppress inflammation Pre-operative management
Example: i. Effective control of BP & blood
i. Hydrocortisone volume
ii. Cortisone ii. Well hydrated  to prevent
iii. Dexamethasone hypotension
iv. Prednisone iii. Use of Na Nitroprusside (Nipride)
v. Prednisolone  Use during & after the therapy
EGBautista II, USI-BSN (2008) 4
iv. Corticosteroid therapy
 Needed if bilateral adrenolectomy,
5. Nursing Management
a. Patient is being cared for at the ICU for
several days with special attention given to:
i. ECG changes
ii. Arterial pressure
iii. Fluid & electrolyte balance