Pamantasan ng Lungsod ng Maynila | College of Nursing

MEDICAL SURGICAL NURSING II

LECTURER: Glenn L. Rianzares, RN, MAN

ENDOCRINE SYSTEM
PART 2
➢ Secretions of hormones make it possible for the
body to adapt to stress. Without adrenal cortex,
PITUITARY GLAND there will be severe stress/pt is unable to adapt to
stress. Whenever you have severe stress into your
POSTERIOR PITUITARY
body, you will have peripheral circulatory failure
leading to circulatory collapse/shock.

Medullary hormones (purely catecholamines)

▪ Dopamine
▪ Norepinephrine
▪ Epinephrine
▪ Opioid peptides
Cortical hormones
▪ Mineralocorticoids
▪ Glucocorticoids
▪ Androgen

▪ Adrenal gland is attached to upper portion of the

kidneys
▪ It has two major portions: Adrenal Cortex, outer
portion, and Adrenal Medulla.
▪ Stimulations of adrenal cortex is initiated by the
hypothalamus. Hypothalamus secretes CRH –>
pituitary gland –> ACTH –> adrenal gland
o MINERALOCORTICOIDS (ALDOSTERONE):
regulates Na and K balance; responsible
for electrolyte metabolism
▪ acts on renal tubules and GIT
epithelium for increased
absorption of Na in exchange for
the unnecessary K and H
secretions so that the acid-base
balance is maintained ▪ Too much cortisol will be sensed by the
▪ secreted in response to the hypothalamus via negative feedback ->
elevations of angiotensin-II in hypothalamus will stop release of CRH.
the blood: decreased perfusion
pressure -> renin released ->
renin will be converted to EXAMPLE OF (+) AND (-) FEEDBACK MECHANISM:
Angiotensin-I -> Angiotensin-II
(more potent peripheral
vasoconstrictor) -> normal BP is
restored
o GLUCOCORTICOIDS (CORTISOL):
responsible for glucose metabolism;
inhibits inflammatory response to tissue
injury; suppresses allergic reactions
o ANDROGENS (MALE HORMONES)
 o ATH dependent
o ACTH independent
ADRENAL MEDULLA
▪ Patients with cushing’s may experience HTN,
central obesity, easy bruising, osteoporosis
▪ Located at the center of the adrenal gland
▪ Functions:
o ANS response - secretes 90% of
catecholamines that regulate
metabolism pathway to promote good
catabolism, fluid storage; to meet caloric
needs; fight or flight
▪ Increased BP/blood flow to a vital
organ d/t stress, everything is
increased/big except for GI and
GU
o Induce the release of fatty acids =  BMR,
glucose level, epinephrine

DISORDERS OF THE ADRENAL GLANDS

▪ Adrenal Insufficiency (Addison’s Disease)

▪ Acute Adrenal Crisis (Addisonian Crisis) ▪ Patients are also increased risk of periodontitis,
▪ Cushing’s Syndrome (Adrenocortical oral candidiasis, gum bleedings/swelling
Hyperfunction) o Treatment: surgery, radiations,
▪ Hyperaldosteronism medications

ADRENAL-RELATED SYMPTOMS ADRENAL GLAND

▪ Weight accumulation around mid-section LAB STUDIES
▪ Inability to handle stress ▪ Cortisol levels
▪ Salt cravings ▪ Cortisol suppression
▪ Sleeping difficulties ▪ Cortisol stimulation
▪ Fluid retention (ankles), Dehydration ▪ Urine vanillylmandelic acid and catecholamine level
▪ Calcium deposits due to altered pH DIAGNOSTIC STUDIES
▪ Low oxygen in tissues ▪ Adrenal scan
▪ Pain and Inflammation

Cushing’s Syndrome
OVERVIEW
➔ DR. HARVEY WILLIAMS CUSHING
▪ Hypersecretion of adrenal cortex hormones
(excess cortisol production – endogenously)
▪ CAUSES:
1. Tumor (adrenal Cortex / Pituitary) –
(Endogenous)
o Bronchogenic CA
2. Prolonged Steroid Therapy (Exogenous)
3. ECTOPIC ACTH syndrome (more common
among women aged 20-40 – 5:1 (female:male);
VIRILIZATION is present wherein feminine
traits are diminished)
DIAGNOSTICS:
▪ in serum sodium, blood glucose level; serum
potassium,  WBC (eosinophils)
1. 24 H URINARY FREE CORTISOL LEVEL
▪ 50-100 mcg a day
2. MIDNIGHT PLASMA CORTISOL
▪ 50 nmol/L
3. LATE NIGHT SALIVARY CORTISOL MEASUREMENT
▪ Diagnostic ranges vary
▪ Not that accurate
4. DEXAMETHASONE SUPPRESSION TEST: most widely
used diagnostic procedure
→ Brunner: Dexamethasone (1 mg) is administered
orally at 11 PM, and a plasma cortisol level is
obtained at 8 AM the next morning. Suppression of

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 cortisol to less than 5 mg/dL indicates that the
hypothalamic–pituitary–adrenal axis is functioning
properly
A. LOW DOSE DEXAMETHASONE SUPPRESSION TEST
(LDDST)
B. OVERNIGHT ONE DOSE DEXAMETHASONE
SUPPRESSION TEST
5. 8-HOUR INTRAVENOUS ACTH TEST
▪ Administer 25 units of ACTH in 500 mL saline over
the 8-hour period
▪ Used to determine function of adrenal cortex
▪ Nursing Responsibility:
o In 24 hours, urine specimen is obtained for
baseline data & comparison; Done twice –
before and after administration of 25 units
ACTH;
▪ Hyperactivity of adrenal cortex =
 urine output of steroids (2nd
CUSHING’S Mnemonic
urine specimen); 10 folds
o No other form of steroids; eliminate
C - Central obesity, Cervical fat pads, Collagen fibre
steroids first
weakness, Comedones (acne)
U - Urinary free cortisol and glucose increase
TEST TO FIND OUT CAUSE OF CUSHING’S SYNDROME S - Striae, Suppressed immunity (high risk for infection)
H - Hypercortisolism, Hypertension, Hyperglycemia,
1. CRH STIMULATION TEST Hirsutism
2. HIGH DOSE DEXAMETHASONE SUPPRESSION TEST I - Iatrogenic (increased administration of corticosteroid)
(HDDST) N - Non-iatrogenic (commonly, cancer)
3. CT SCAN/ MRI G - Glucose intolerance, Growth retardation
▪ Actual visualization/actual appearance
4. Visual Field
CUSHING’S SYNDROME
5. Hormonal Assay STUDENT ACTIVITY
SUBJECTIVE ASSESSMENT:

▪ Patients usually complain:

o Headache
o Back pain
o Weakness
o Decreased ability to do work/decreased
work capacity

STUDENT ACTIVITY
OBJECTIVE ASSESSMENT:

▪ Low potassium level

▪ Hypertensive
▪ Weight gain
▪ Pitting Edema
▪ Characteristic of fat deposits
▪ Truncal & Central Obesity, Buffalo Humps
▪ Pendulous abdomen
▪ Purple Striae (armpit & truncal area)
▪ Easy bruising
▪ Moon face

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 ▪ Acne
▪ Hyperpigmentation STUDENT ACTIVITY
▪ Male: impotence CUSHING SYNDROME NSG MGT:

CUSHING’S SYNDROME ▪ Promote rest and activity

▪ Provide relaxing and quiet environment for rest
ASSESSEMENT:
and sleep
▪ Give moderate activity to prevent complications of
▪ Virilization in women
immobility
o Hirsutisms, atrophy of breast, presence of
▪ Protect patients from trauma
amenorrhea
▪ Prevent complications, such as:
▪ Pathologic fractures, reduced height, Osteoporosis
o Glucose metabolism
▪ Low resistance to infection
o Hypertension
o Poor wound healing
o Infection
▪ Hypernatremia, hyperglycemia, hypokalemia
▪ Monitor fluid balance
o Monitor intake and output
o Assess weight gain
▪ Provide proper nutrition
o Increase protein, potassium
o Decrease calories, sodium
o Increase vitamin C
o Give calcium supplements
▪ Promote skin integrity
o Skin care
o Avoid trauma
o Monitor sensitive skin
o Avoid using adhesive tape
▪ Body Image Disturbance
▪ Prepare patient for adrenalectomy
o Preop teaching

ADRENALECTOMY

CUSHING’S SYNDROME ▪ Surgical removal of one or more of the adrenal

MANAGEMENT: gland because of tumors or overactivity
o Unilateral adrenalectomy
1. SURGERY ▪ Steroids are still administered up
▪ Adrenalectomy to 2 years, and then tapered
Tumor is located in the adrenal gland o Bilateral.
▪ Hypophysectomy ▪ Lifelong replacement
Tumor is located in the pituitary gland ▪ Preop:
▪ Radiation therapy o Reduce risk of postop complication
To atrophy or shrink the tumor A. Prescribed steroid therapy, given 1 wk. before
If the patient doesn’t react to radiation surgery
therapy, surgery will be done. B. Antihypertensive drugs D/C
2. Adrenal Enzyme Inhibitors/ Cytoxic agents C. Sedation as ordered
Ketoconazole – imidazole derivates; inhibits D. Monitoring of Blood glucose and Insulin
synthesis of cortisol by inhibiting the mitochondrial therapy
reactions ▪ Intraop:
3. Tapering of corticosteroids o Monitor for hypotension & hemorrhage
If the cause of the Cushing Syndrome is ▪ Postop:
corticosteroid therapy, we taper the dose. 1. Promote hormonal balance
a. By administering hydrocortisone

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 2. Observe for hemorrhage and shock.
ADDISON’S DISEASE
a. Check for bleeding
b. Check vital signs
▪ Primary lack of adrenal hormones including both
3. Prevent infection.
cortisol and aldosterone
4. Administer cortisone or hydrocortisone as
▪ Causes:
prescribed.
o Autoimmune
5. Put patient in reverse isolation
o TB
6. Observe for signs and symptoms of Addisonian
o Metastatic tumor
crisis
o Bilateral hemorrhage
▪ Low cortisol and aldosterone, high ACTH
▪ Irregularly shaped blotchy melanin patches on oral
mucosa
▪ Affects the buccal mucosa near the commissures
first and spreads posteriorly

CAUSE:

▪ Adrenal Dysgenesis
o Failure to form adequately during the
development (gland)
▪ Impaired Steroidogenesis
o Gland is present, but the gland is
biochemically unable to produce cortisol
▪ Congenital Adrenal Hyperplasia
• Most common
▪ Ketoconazole
▪ Rifampicin/ Phenytoin
ADDISON’S DISEASE ▪ Adrenal Destruction
AG
Hemorrhage/bleeding into

HYPOADRENOCORTICISM ▪ Tumors Fungal infections

▪ Amyloidosis
ADRENOCORTICAL INSUFFICIENCY ▪ Auto-immune disorders
▪ Hyposecretion of the adrenal cortex hormones ▪ Cancer
▪ Causes: ▪ AIDS related infection
o Autoimmune ▪ Adrenalectomy
▪ Idiopathic atrophy of the adrenal
glands – 80% of patients with
Addison’s disease
o Therapeutic use of corticosteroids ADRENAL DYSFUNCTION
▪ Most common cause: SECONDARY ADRENAL INSUFFICIENCY
o TB/ Fungal (Histo) Infections
o Surgical Removal of both AG ➢ Impaired Hypothalamic-Pituitary-Adrenal Axis
▪ Causes:
1. Steroid Use
ADRENAL DYSFUNCTION 2. Hypophysectomy
PRIMARY ADRENAL INSUFFICIENCY 3. Hypofunction of the Pit. Gland

▪ ADDISON’S DISEASE
▪ 90% of A. Cortex destroyed DIAGNOSTICS:
▪ ↓ Cortisol and Aldosterone
➔ DR. THOMAS ADDISON 1. ↓ Serum Na, ↓ Blood glucose, serum K, and  WBC
2. EIGHT-HOUR INTRAVENOUS ACTH TEST
- Urine output of steroid does not increase following
administration of ACTH

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 ▪ ACTH STIMULATION TEST
o Most commonly used for adrenal
insufficiency
o Measure plasma and urine cortisol level
before and after the synthetic form of
ACTH given (parenterally)
o Addison: Despite giving ACTH, cortisol level
remains low/insufficient
o Secondary Iatrogenic: very slight increase
in cortisol = adrenal gland has not yet fully
atrophied
▪ CRH STIMULATION TEST
o Done if the ACTH stimulation test is
abnormal

(SEE LAST PAGE FOR ADDITIONAL PHOTOS)

ADDISON’S DISEASE
STUDENT ACTIVITY
SUBJECTIVE ASSESSMENT:

▪ Muscle weakness
▪ Fatigue
▪ Lethargy
▪ Dizziness
▪ Fainting
▪ Nausea
o Help determine the cause of adrenal ▪ Anorexia
insufficiency ▪ Abdominal pain and cramping
o Obtain baseline serum cortisol, then
administer synthetic CRH via IV; measure STUDENT ACTIVITY
plasma cortisol after 30,60, 90, 120 OBJECTIVE ASSESSMENT:
minutes after injection
o Addison’s: ACTH but cortisol remains low ▪ Hypotension (orthostatic)
o Secondary Iatrogenic: Absence or delay of ▪ Increased but very weak pulse; collapsing and
ACTH response irregular
▪ CRH will not stimulate ACTH ▪ Subnormal temperature (won’t exceed 37.9)
release if prostaglandin is ▪ Vomiting
destroyed ▪ Diarrhea
▪ Weight loss
▪ Tremors
▪ Poor skin turgor
▪ Excessive skin pigmentation (bronze skin)
▪ Melanonychia nails
▪ Hyponatremia
▪ Hypoglycemia
▪ Hyperkalemia

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 NURSING MANAGEMENT:

▪ Check BP & electrolyte levels.

▪ Strict bed rest in quiet environment & protect from
infection
→ As much as possible, no visitors
→ avoid exertion, anticipates patient needs
and meet them

MANAGEMENT:

I. Hormone Replacement Therapy

▪ Cortisone, Florinef
▪ Steroids

STUDENT ACTIVITY
NURSING MANAGEMENT DURING STEROID
THERAPY:

▪ Diet: Give potassium & low sodium

▪ Administer steroids after meals with antacids
▪ Monitor the urine and blood glucose levels
▪ Gradual withdrawal to prevent Addisonian crisis,
severe weakness, and psychological let-down.
▪ Provide quiet environment and non-demanding
schedule for patients

ADDISONIAN CRISIS

▪ Life-threatening condition caused by acute adrenal

insufficiency.
o May be precipitated by stress, infection,
trauma or surgery
o May cause hyponatremia, hypoglycemia,
hyperkalemia & shock.
▪ S/sx:
o Severe, generalized muscle weakness,
severe hypotension, hypovolemia, shock

ADDISONIAN CRISIS
MANAGEMENT:

▪ IV glucocorticoids
o Hydrocortisone Na succinate (Solu-Cortef
o fludrocortisone (Florinef).

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