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NOTES Mod #18 Pituitary/Adrenal
cmj
Module #18: Nursing Care of the Individual with Pituitary and Adrenal
Disorders
A&P review- Part I -A
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1.
2.
Endocrine system; (see text p. 439 table 16.1 Organs, Hormones, Feedback
Mechanisms of the Endocrine System)
a. Consists of glands, specialized cells clusters and hormones-chemical
transmitter secreted by glands in response to stimulation & CNS.
b. Regulates and integrates the body’s metabolic activities;; maintains
homeostasis!
Hormones & hormone function: chemical substances/messengers
synthesized and secreted by a specific organs or tissue- exert action on
specific cells called target cells
a. Common characteristics
(1) secreted in small amounts at variable but predictable rates
(daily, hourly, monthly, etc)
(2) circulation through the blood
(3) bind to specific cellular receptors in cell membrane or
within cells
(4) inactivated or excreted by liver or kidneys
(5) alter rate of physiologic activities
RNSG 2432  409
3.
4.
5.
6.
7.
Hypothalmus: integrative center for endocrine and autonomic
(involuntary nervous system)
a. Controls some endocrine glands by neural and hormonal pathways
Negative feedback (negative feedback system)
a. Regulates endocrine system by inhibiting hormone overproduction
b. Can be simple or complex system
 Dysfunction can result from
1) Defects in gland
2) Release of trophic (gland stimulating hormones) or effector
hormones
3) Hormone transport
4) In target tissue such as adrenal cortex
 *Examples of negative feedback: low serum calcium have
increased PTH; increased serum calcium, have decreased PTH
Hormone to hormone regulation: dec. thyroid hormone (T3 & T4 >
release of TRH by hypothalamus and TSH by anterior pituitary; inc. T3 and
T4 levels inhibit TSH release (review thyroid and parathyroid).
Hypothalmus and pituitary gland
a. Form a complex called the hypothalamic pituitary axis (HPA)
b. Integrates communication from nervous and endocrine systems
c. Examples, what hormone is released under stress? Can this hormone
make you fat? (p. 459) (cortisol) (click here for more)
Endocrine disorders due to
a. Hypersecretion or hyposecretion of hormones
b. Hyporesponsiveness of hormone receptors
c. Inflammation of glands
d. Gland tumors
1) Hypofunction or hyposecretion due to congenital defects, gland
destruction, aging, atrophy
2) Hyperfunction due to hyperplasia, tumors
410  RNSG 2432
Part B Components endocrine system: (great link)
1. Pituitary gland (hypophysis, master gland)
a.
Parts: (see diagram page #1)
1) anterior pituitary (adenohypophysis): composed of cells that secrete
protein hormones
2) posterior pituitary (neurohypophysis): not really an organ-extension
of hypothalamus: composed mostly of axons of hypothalamic
neurons-extend downward as large bundle behind anterior pituitarylso forms so-called pituitary stalk-appears to suspend anterior gland
from hypothalamus.
3) intermediate (pars intermedia) *secretes MSH (melanocytes for skin
pigmentation
b. Components of Pituitary Gland
1) Anterior portion: adenohypophysis **know this!!
Name & Source
ACTH (adrenocorticotrophic hormone;
corticotrophin)
TSH (thyroid stimulating hormone;
thyrotropin; thyrotrophic hormone)
GH (growth hormone; Somatotropin, STH)
*an anabolic hormone, promotes protein
synthesis and mobilizes glucose and free
fatty acids; stimulates the liver to produce
insulin-like growth factor-1 (IGF-1) also
known as somatomedin C; which
stimulates growth of bones and soft tissues.
FSH (follicle stimulating hormone)
LH (lutenizing hormone)
Prolactin (PRL); LTH (Prolactin; luteotropic
hormone; luteotrotropin; lactogenic hormone:
mammotropic hormone; mammotropin
MSH (Melanocyte-stimulating hormone:
interdin)
Functions
Stimulates production of hormones from
adrenal cortex , especially
glucocorticoids**Stimulate secretion of
adrenal cortex hormones (release cortisol);
Stimulates synthesis and release of thyroid
hormones by thyroid: Stimulates uptake of
iodine and release of T3 & T4 (* Calcitonin
from thyroid; reduces serum calcium levels
by decreasing bone resorption and resorption
of calcium in the kidneys)
Stimulates growth of tissues and bone; also
protein synthesis; stimulates growth of body
(epiphyseal plates of long bones in youth;
promotes increased mitosis; increase in size
of cells; decrease CHO utilization in striated
muscle and adipose tissue; increase
mobilization of stored fat; increase use of fats
for energy
Stimulates growth of ovarian follicles and
spermatogenesis in males
Regulates growth of gonads and their
reproductive activities; female, ovulation and
formation of corpus luteum; male, called
Interstial cell-stimulating hormone (ICSH),
stimulates testes to produce male sex
hormones
Promotes mammary gland growth and milk
production
Stimulates melanocytes causing pigmentation
* If too much secretion of prolactin what would occur? Milk secretion!!
* If too much release of LH what would occur? Enlarged reproductive organs;
not enough…undeveloped reproductive organs!
RNSG 2432  411
* Identify source of problem: Primary: organ itself: secondary; defect is
outside of gland itself)
2)
Posterior portion: neurohypophysis *Be sure to listen to
Kelly’s & her Pituitary tumor and remember this…
Stores and releases hormones produced by hypothalamus:
Name & Source
Functions
1.
ADH; Vasopressin; Antidiuretic; Hormone
2.
Oxytocin
3)
II.
Promotes H2O retention by way of
the renal tubules and stimulates
smooth muscle of the blood vessels
and digestive tract. Decreased
urine formation
Stimulates the release of milk and
contraction of smooth muscles in
the uterus. Sucking stimulates
increased secretion of oxytocin
Intermediate (pars intermedia) *secretes MSH (melanocytes for
skin pigmentation
Thyroid gland (review only): produces Thyroid hormone (TH)
composed of:
Name & Source
Functions
1.
Triiodothyronine (T3); (more rapid
and potent;action - shorter duration
2.
Thyroxine (T4)
3.
Calcitonin
Aid in growth and
development. Increase in
basal metabolic rate (BRR)
associated with increase in 02
consumption and heat
production; shorter acting;
more rapid and potent action
than T4
As above; slower action
Lowers serum calcium and
serum phosphate by inhibiting
bone resorption
*Decreases excessive calcium
by slowing calcium release by
bone cells
III. Parathyroid gland: (review only) produces PTH hormone:
(increases renal excretion of phosphate, decreases excretion of CA,
releases calcium from bone)
Name & Source
1.
412  RNSG 2432
Parathyroid Hormone (PTH)
Functions
Regulates CA & PO4 metabolism
as a result of its effects on three
target organs: Bone,Kidney, GI
IV.
Adrenal Gland: 2 parts: cortex and medulla
a. Parts:
1) Inner medulla: source of catecholamines- epinephrine and
norepinephrine- innervated by preganglionic sympathetic fibersextension of sympathetic nervous system.
2) Outer cortex: secretes several classes steroid hormones
(glucocorticoids and mineralocorticoids); a few others
b. Components
1) Adrenal Medulla: Hormones: catecholamines
Name & Source
1.
Epinephrine (15%)
2.
Norepinephrine (85%)
Functions
Inc. blood glucose, stimulate ACTH, glucocorticoids; inc.
rate and force of cardiac contractions; constricts blood
vessels in skin, mucous membranes, kidneys; dilates
blood vessels in skeletal muscles, coronary and
pulmonary arteries; * Acts on beta –adrenergic receptors
Inc.heart rate and force of contractions; constricts
blood vessels throughout body; * Acts on alphaadrenergic receptors
2) Adrenal Cortex (Salt, sugar and sex)*can’t live without!
Hormones: corticoids …Know the function=nursing
problems!
Name & Source
1.
Mineralocorticoids: aldosterone
2. Glucocorticoids: Corticol, cortisone
*can’t live without it!
*Stress makes you fat!
Functions
Retains sodium and water to inc. blood volume
and blood pressure; excretes potassium**
Carbohydrate metabolism-regulating
glucose use in body tissue, mobilizing fat,
shifting energy source for muscle cells from
glucose to fat
**Responds to stress
Depresses inflammatory response,
inhibits immune system
*Affects carbohydrate, protein and fat
metabolism
3.
Sex hormones
Androgens & Estrogens
RNSG 2432  413
V. Pancreas (endocrine portion) (review only)
Name & Source
Functions
1.
Glucagon (alpha cells)
Increases blood glucose
2.
Insulin (beta cells)
Decreases blood glucose
3.
Somstostatin (delta cells)
Inhibits secretion of
glucagons and insulin
a. Gonads (review only)
Name & Source
Functions
1.
Androgens (mainly testosterone)
Male sex hormone
2.
Estrogen and progesterone
Female sex hormone (several
types of estrogens)
Part C-Keys to Assessment of Endocrine Function (review only)
Signs and symptoms of dysfunction, often nonspecific
a. Health assessment interview inc. medical history, family history,
changes in size or functioning of organs, skin, hair; changes in thirst,
appetite, weight, energy, sleep; use of medications that may affect
hormones; changes in reproductive functioning, secondary sex
characteristics
b. Physical Assessment including: palpation of thyroid; inspection of skin,
hair, nails, facial appearance; reflexes, musculoskeletal system; height,
weight, vital signs; assessment for hypocalcemia
c. Abnormal findings
1) Skin assessment
a) Pigmentation: hyper or hypo with adrenocorticodysfunction
b) Rough, dry skin, yellow cast with hypothyroidism
c) Smooth, flushed skin with hyperthyroidism
d) Purple striae (stretch marks)
e) Skin lesions on extremities: diabetes mellitus
2) Hair and nails
a) Pigmentation with hypoadrenocorticofunction
b) Dry, thick, brittle nails and hair with hypothyroidism
c) Thin, brittle nails, thin soft hair with hyperthyroidism
d) Excessive hair growth with hyperadrenocorticofunction
3) Facial Assessment
a) Abnormal growth, symmetry with excess growth hormone
b) Exophthalmoses (protruding eyes) with hyperthyroidism
4) Thyroid assessment
a) Enlargement of thyroid gland or goiter
b) One or multiple palpable nodules
5) Motor function assessment
a) Increased deep tendon reflexes with hyperthyroidism
b) Decreased deep tendon reflexes with hypothyroidism
6) Sensory function assessment
414  RNSG 2432
Peripheral neuropathy or paresthesias with diabetes, hypothyroidism,
excess growth hormone
7) Musculoskeletal assessment
Size and proportion, insufficient or excess growth hormone
8) Hypocalcemic tetany (possible thyroid, parathyroid abnormalities)
a) Trousseau’s sign (carpal spasm with inflation of blood pressure
cuff
b) Chvostek’s sign (tap front of client’s ear in angle of jaw to elicit
facial muscle contraction)
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Part IIAdrenal Cortex Dysfunction
A. Etiology/Pathophysiology: see above- two glands, located on top of each
kidney; composed of:
 Cortex (80-90% of gland) and medulla
 Cannot survive without function of cortex!
 Produce steroids, amines, epinephrine, and norepinephrine
 Hyposecretion or hyposecretion > disorders and complications that
range from psychiatric and sexual problems to coma and death!
 Think “Salt-Sugar-Sex” problems!
1.
Mineralocorticoids: (cortex) regulate fluid and electrolytes balance (Na
and H2O retention and K excretion) (SALT)
a. Aldosterone; mineralocorticoid - regulate reabsorption of sodium
and excretion of potassium by kidneys and excretion of hydrogen
ions. Aldosterone synthesis and secretion- stimulated by antiotensin II,
hyponatremia and hyperkalemia-inhibited by atrial natriuretic hormone
and hypokalemia. What is atrial naturiuetic hormone?
*Think…What is the usual physiologic response when an individual is
dehydrated (think aldosterone and kidney)? (ref. p. 82)
2.
Glucocorticoids: cortisol, a glucocorticoid (SUGAR)
a. Stimulation of gluconeogenesis (formation of glycogen from
noncarbohydrate sources)-occurs in liver in response to low CHO intake
or starvation <inc. glucose>
b. Breakdown of protein and mobilization of free fatty acid
c. Suppression of immune response
d. Assistance with stress response >inc stress = inc. cortisol>
e. Assistance with maintenance of blood pressure and cardiovascular
response
f. *Note: Cortisol secreted in diurnal pattern: major control by
negative feedback
i. involves secretion of corticotrophin-releasing hormone (CRH) from
hypothalamus
ii. CRH stimulates secretion of ACTH by anterior pituitary
iii. Cortisol levels also inc. by surgical stress, burns, infection, fever,
psychosis, acute anxiety, and hypoglycemia
Remember: (must understand!*)
*Prednisone or Solucortef = glucocorticoids!
a) *Release of glucocorticoids controlled by ACTH- released
by anterior pituitary!
RNSG 2432  415
b) ACTH levels affected by circulating levels of cortisol:
Dec. cortisol levels inc. ACTH; inc. cortisol levels dec. ACTH
levels
c) Never suddenly stop steroids!
d) ACTH levels highest 2 hours before awakening & just
after awakening; dec. rest of day! (diurnal pattern)
e) *Stress inc. cortisol production and secretion
f) *Stress > adrenal medulla to release the catecholamines
(epinephrine and norepinephrine!)
3.
Androgens: (SEX) third class of steroids-synthesized and secreted by
adrenal cortex
 stimulate pubic and axillary hair growth and sex drive
 In female-androgens converted to estrogens in peripheral tissue;
post-menopausal women, source of estrogen from peripheral
conversion of adrenal androgen to estrogen
 Negligible effects of adrenal androgen in men compared to
testosterone secreted by testes.
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Dysfunction- Adrenal
#1 Cushing’s Syndrome (understand this one!)
A. Etiology/Pathophysiology: Hypercortisolism: Hypercortisolism
(Cushing’s Syndrome) (click for more!) **too much of a good thing…cortisol!!!
(text does not differentiate between disease and syndrome)…basic problem is too
much cortisol, corticotropin, but due to different causes:
 Cushing’s Disease-primary origin of problem>pituitary
 Cushing’s Syndrome- problem originates from other sources as adrenal,
ectopic sites, etc.) “Syndrome”-group of signs and symptoms due to too
much cortisol.
1.
Cushing’s syndrome due to:
a. Pituitary form: (as above-Cushing’s disease if primary origin- pituitary)
 Due to ACTH hypersecretion from pituitary adenoma
 Persistent, random overproduction of ACTH
416  RNSG 2432
2.
3.
 Inc ACTH= Inc cortisol
b. Ectopic form due to ACTH-secreting tumors (corticotrophin)
 Small-cell lung cancers, random and episodic ACTH
Production
 Tumor=inc ACTH=inc cortisol
c. Adrenal cause:
 excessive porduction cortisol >negative feedback to pituitary
 Suppresses pituitary ACTH production
 Results in atrophy of uninvolved adrenal cortex (*Adrenal tumor
>inc cortisol > dec ACTH > adrenal cortex atrophy) do you
understand “why”?
d. Iatrogenic Cushing’s syndrome:: due to long-term steroids
 Steroid use >inc cortisol > dec ACTH > adrenal cortex atrophy
Basic problem= **EXCESSIVE amounts of cortisol
More common in females between the ages of 30 and 50
B. Common Manifestation/Complications (see text p. 460 Fig. 17-3)
Cushing’s Syndrome/Disease)
1.
Signs and symptoms **related to adrenal cortex functions ie effect
functions of adrenal cortex “sugar, sex, and salt”:
a. Altered glucose metabolism, secondary sex characteristics, and
mineralcorticoid levels (sodium and water retention)
b. Obesity & redistribution of body fat: central obesity, fat pads under
clavicles, upper back (“buffalo hump”), rounded face due to altered fat
metabolism and fatty acid mobilization
c. Glucose and electrolyte abnormalities: hyperglycemia; sodium
retention; hypokalemia, hypertension
d. Thinning of skin, bruises easily, abdominal striae (due to inc. protein
catabolism with muscle wasting, loss of collagen support, etc)
e. Altered immunity, delayed healing, prone to infection; dec WBC,
f. Altered calcium absorption inc. osteoporosis; risk for fractures
g. Inc. gastric acid secretion inc. risk for ulcers
h. Emotional changes from depression to psychosis
i. Changes in secondary sexual characteristics due to excess androgen
secretion: excessive hair growth; acne; change in voice: receding
hairline; Menstrual irregularities
Before and after treatment (tumor of pituitary tumor that secreted excess
ACTH)
RNSG 2432  417
Before (Cushionoid) &
After (right) post tumor
producing cortisol
removed
Multiple wide purplish striae on the Moon face of patient with Cushing syndrome
abdomen of a patient with Cushing's
418  RNSG 2432
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests
1. Goals of Collaborative Care: (*identify underlying cause!)
a. Collaborative Care -due to long-term Steroid Therapy
1) long term steroid therapy for “another condition”-be aware of potential
problems; careful follow-up
2) maintain at lowest level of steroids adequate treatment; efforts to
minimize untoward effects
3) Always be tapered off steroids!!!!* Do you know why??
2. Diagnostic Tests (see text p. 461 Table 17-3 Laboratory findings in
Cushings Syndrome) *Remember what adrenal cortex function and its
relationship to pituitary and ACTH
RNSG 2432  419
a. *Measurement of plasma/serum cortisol, ACTH: Alterations in
normal diurnal alteration: higher in mornings, lower in afternoons and
evenings
b. *24-hour urine collections for measurements of hormones:
1) 17-ketosteroids and 17-hydroxycorticosteroids; elevated
2) Critical-collections done properly with correct additives in specimens
c. *Electrolytes, calcium, and glucose levels (elevated Na, glucose;
decreased K, Ca) Why?
d. ACTH suppression: synthetic cortisol (dexamethasone) (suppress
ACTH production) and plasma cortisol levels measured
 If ACTH is not suppressed with cortisol > adrenal tumor
 If very high levels of cortisol needed to suppress ACTH = adrenal
cortex hyperplasia
*What will typical serum cortisol levels be if you draw AT 7AM AND 7PM?
 Inc. from 7-10 am, dec. from 7-10 p; Increased URINARY LEVELS OF
STEROID METABOLITES: inc 17-OHCS (hydroxycorticoid steroid) and
inc 17-KS (ketosteroid) (normal) Recall diurinal pattern.
Hormonal Diagnosis: (go to this site more information) Also—not in text
1
2
3
4
Confirm presence of excessive cortisol secretion (Cushing's syndrome)…perform a
low-dose dexamethasone suppression test or a 24-Hour urine collection to
quantitate cortisol levels
Then determine source of excess cortisol … to be determined: either from an adrenal
gland tumor, an ectopic ACTH-producing tumor or a pituitary ACTH-producing adenoma…use
high dose dexamethasone test, ACTH levels, metyrapone test, and/or sometimes a CRH test
are used for this determination….
Petrosal Sinus Sampling: an angiographic and endocrinological test to distinguish
between ectopic ACTH production or pituitary ACTH production (Cushing's disease..
If lab tests suggest pituitary adenoma as cause of Cushing's, then pituitary MRI is
performed to confirm the diagnosis …..
3. Treatment of Cushings: surgery, radiation, medications, or combination
a. Surgery
1) Adrenalectomy: (see text p. 461 Nursing Care of the Patient
Having Arenalectomy) removal of adrenal gland-if both glands
removed, client requires *lifelong hormone replacement (at risk for
Addisonian Crisis & hypovolemic shock…do you know why??)
2) Hypophysectomy (removal of pituitary gland): removal of pituitary
gland through transphenoidal (through nostril) route or craniotomy
420  RNSG 2432
3) Ectopic: removal of source of ACTH secretion lung or pancreas
tumors
b. Post-operatively, clients being treated for adrenal or pituitary surgeryICU (ref to surgery-craniotomy)
1) life-long hormone replacement; wear medical identification
bracelet
2) must not abruptly stop hormone replacement-develop Addisonian
crisis (medical follow-up critical)
c. Medications: if adrenal or pituitary tumors not operable
1) *Suppress adrenal cortex> dec. cortisol synthesis; use
Mitotane, Metyrapone, Ketoconazole; (Somatostatis analog
octeotide suppresses ACTH secretion in some cases) (*read
text...know/understand effect of each drug; how do they achieve their
effect?)
4. Nursing Diagnoses/Nursing Priorities (understand pathophysiology &
problems)
a. Fluid Volume Excess (One liter fluid retention corresponds to about 2 lb
(.9 kg) body weight); HTN, edema
b. Risk for Injury: potential for falls, fractures (skin thin, easy bruising,
etc)
c. Risk for Infection: immune suppressed, elevated blood sugar, poor
wound healing, decreased protein synthesis
d. Disturbed Body Image (changes revert when Cushing’s syndrome is
treated)
#2 Hyperaldosteronism “Conn’s Syndrome” ( Too Much Aldosterone..not
in text)
A. Etiology/Pathophysiology: Too much aldosterone secretion due to adrenal
adenoma (70% or bilateral adrenal hyperplasia (30%) > to Na and H20
retention > inc. blood volume, HTN, headache, dec. K (hypokalemia); muscle
RNSG 2432  421
weakness, cardiac dysrhythmias, metabolic alkalosis; rare peripheral edema
unless cardiac problems (Do you understand why this develops?)
B. Common Manifestation/Complications/Diagnosis/Treatment
1. Manifestations
a. Hypokalemia >muscle weakness, cardiac weakness, usually no
peripheral Edema (p. 99+)
b. Elevated urine K levels (24 hour urine collection)-excessive K loss
c. Inc. plasma aldosterone level with low rennin levels (Why?)
d. Adrenal scan/CT scan to visualize adenomas
e. EKG changes due to dec. K; ventricular dysrhythmias
2. Interventions: treat disease underlying cause:
a. Surgical intervention-treat tumor: must dec. BP, use aldactone,
(spironolactone…potassium sparing) to inc. Na
b. Correct hypokalemia
c. Adrenalectomy (partial or total depending on tumor size!)
1) Keys points-Pre-op stabilize hormonally; correct electrolyte
imbalance; cortisol evening prior to surgery, AM of surgery and during
surgery.
2) Post-op: ICU; BP, fluid and electrolyte mgt; IV cortisol preparation 1st
24 hours; IM cortisol 2nd post-op day then po steroids 3rd day; have
inc. susceptibility to infection, poor wound healing. Unilateral
adrenalectomy steroids eventually weaned. (same as above)
#3 Addison’s Disease-Hypofunction of Adrenal Cortex (know this one!!)
A. Etiology/Pathophysiology: dysfunction of adrenal cortex; chronic deficiency of
cortisol, aldosterone, adrenal androgens; more common in women ,adults under
60 (Deficiency of salt sex, sugar!)
1. Autoimmune destruction of adrenal-accounts for 80% of spontaneous
cases; occurs alone or with polyglandular autoimmune syndrome
2. Untoward effect of anticoagulant, trauma in which client has bilateral adrenal
hemorrhage (iatrogenic causes)
3. Pituitary dysfunction due to tumors, surgery, radiation, exogenous steroid
4. Abrupt withdrawal from long-term, high-dose corticosteroid therapy
(iatrogenic causes) (*What does iatrogenic mean?
a. *Primary Addison’s disease
1) originates within adrenal glands
2) characterized by decreased mineralocorticoids,
glucocorticocorticoids, and androgen secretions
b. *Secondary Addisons’ disease
1) due to disorder outside adrenal gland such as pituitary tumor
with corticotrophin deficiency
2) aldosterone secretion may be unaffected.
B. Common Manifestation/Complications (see text p. 465 Manifestation of
Addison’s Disease)
Which famous President had Addison’s Disease???
422  RNSG 2432
1. Slow onset (dec. levels of cortisol and aldosterone)
a. Relates to lack of functions of adrenal cortex-decrease in “sugar, salt and
sex”
1) Hyponatremia, hyperkalemia, low circulating blood volume
2) Postural hypotension (muscle weakness due to lack of cortisol),
syncope, and possibly hypovolemic shock
3) Dizziness, confusion, cardiac dysrhythmias
4) Hypoglycemia, nausea, vomiting, weakness, lethargy, diarrhea
5) Hyperpigmentation (good link here) due to inc. ACTH levels (bronzed
appearance in Caucasians); small black freckles (*Dec. plasma cortisol
reduces feedback inhibition of pituitary ACTH and plasma ACTH rises….in
primary adrenal
disease)
RNSG 2432  423
*Primary




Addison’s…common findings:
Poor coordination
Dry skin and mucous membranes
Sparse axillary and pubic hair in women
Skin- typically deep bronze especially in creases of hands and on
knuckles, elbows and knees; skin shows darkening of scars, areas of
vitaligo
o Abnormal coloration due to dec. secretion of cortisolglucorticoid causes pituitary gland to secrete excessive amounts of
melanocyte-stimulating hormone (MSH) and corticotrophin.
*Note: Secondary Addison’s adrenal hypofunction doesn’t cause hyperpigmentation
as corticotrophin and MSH levels are low.
2. * Major complication-Addisonian Crisis
a. *Life-threatening response to acute adrenal insufficiency > dec blood
volume
b. Occurs in clients with Addison’s disease who don’t respond to treatment or
who has stress & without medication!
c. Occurs with clients with Addisons disease who are undiagnosed & are
exposed to stress!
d. Patient use of steroids that are discontinued without tapering!
e. *Major symptoms (Why?)
 high fever
 dehydration
 decreased serum sodium
 increased potassium
 decreased glucose
 confusion, headache
 pallor
 weakness, abdominal pain, diarrhea
 severe hypotension, circulatory collapse, shock, coma
 renal shut down, death!
f. *Treatment - rapid intravenous replacement of fluids and
glucocorticoids until signs/symptoms disappear (*know this!!)
 Check VS and urine output frequently
 Monitor EKG
 Usually - adm hydrocortisone 100 mg IV bolus
 Then hydrocortisone diluted with dextrose in NS given IV until
condition stabilizes
 May require up to 300 mg/day hydrocortisone and 3/5 L of IV NS
in acute stage (may require 4-6 hours! )
 Also try to decrease anxiety
 May require vasopressors such as Dopamine or Epinephrine; avoid
additional stress
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests
1. Diagnostic Tests: (see Cushing’s)
a. Serum cortisol and urine 17-ketosteroids and 17hydroxycorticosteroids are decreased
b. Plasma ACTH is inc. if cause from adrenal dysfunction
c. ACTH stimulation test
d. Electrolytes - hyponatremia, hyperkalemia
e. Serum glucose –dec.
f. Hematocrit and hemoglobin are elevated; BUN (dehydration)
424  RNSG 2432
g. CT scan of head (R/O intracranial lesion affecting pituitary)
2. Medications/diet/Collaborative Interventions (see text p. 466
Medication Administration) *know this!
a. Hydrocortisone; require life long hormone replacement: primaryoral cortisone 20-25mgs in AM and 10-12mg in PM; change dose PRN for
stress also mineralocorticoid-(FLORINEF)
b. Flurocortisone (Florinef), a mineralcorticoid replacement
c. Diet with increased sodium: Salt food liberally ( 5-8 gm/day; 1 tsp salt
= 2 gm Na; do not fast or omit meals; eat between meals and snack; eat
diet high in carbohydrates and proteins; wear medic- alert bracelet; kit
of 100mg hydrocortisone IM
d. Avoid cold temperatures and infections (stress)
e. Teaching
 Continue medications
 Signs and symptoms of insufficient hormone levels
 Special care required during times of increased stress (surgery,
serious illness) Why is this necessary?
3. Nursing Diagnoses (See text p. 468 Nursing Care Plan; A Client with
Addison’s Disease)
a. Deficient Fluid Volume
b. Risk for Ineffective Therapeutic Regimen Management
#4 Pheochromocytoma (Tumor of Adrenal Medulla)
A. Etiology/Pathophysiology: Tumors of adrenal medulla (Pheochromocytoma)
1. Definition: adrenal medulla produces catecholamines (epinephrine,
norephinephrine) (rare)
2. Tumors of adrenal medulla produce excessive levels of catecholamines;
typically benign, encapsulated, unilateral and solitary.
3. *Secretion of excessive catecholamines > severe hypertension; if
undiagnosed and untreated pheochromocytoma > death!
RNSG 2432  425
Pheochromocytoma is a tumor or the adrenal gland that
Causes excess release of epinephrine and norepinephrine,
hormones that regulate heart rate and blood pressure
B. Common Manifestation/Complications
1. Paroxysmal severe hypertension (episodic) (systolic: 220 – 300;
diastolic 150 – 175) with tachycardia
2. Can be life-threatening; stressor induced
3. Deep breathing; pounding heart; headache; moist cool hands & feet; visual
disturbances
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests
1. Diagnostic Tests:
a. Catecholamine levels (serum and urine) are elevated
b. 24 hour urine-VMA (metabolite of Epinepherine)…can have false
negatives!
c. Plasma catecholamines
d. CT and MRI to locate tumor
e. Adrenal biopsy (definitive)
2. Treatment: Adrenalectomy to remove tumor (focus =management of
dangerously high BP); post adrenalectomy= adrenal crisis and long
term steroids!!
a. Pre-op: Sympathetic blocking agents= Minipress (prazosin), Hytrin
(terazosin), Cardura (doxazosin) to reduce BP and other symptoms of of
catecholamine excess
 Since change in BP sudden, client may experience orthostatic
hypotension
 Use Beta blocking agents such as Inderal to dec. heart rate, BP
and force of contraction and calcium channel blocking agents also
used.
b. General management
 Diet: high in vitamin, mineral, calorie, no caffeine
 Sedatives; Monitor BP
426  RNSG 2432

Eliminate attacks; If attack- complete bedrest and HOB 45
degrees
c. Surgery via laparoscopic adrenalectomy or open abdominal
incision; complete removal of the tumor cures hypertension in 1030% of the cases
 May require REGITINE AND NIPRIDE TO PREVENT
HYPERTENSIVE CRISIS in surgery (How do these drugs
work?)

BP may be elevated initially, BUT CAN BOTTOM OUT
 May require volume expanders, vasopressors
 Hourly I and O
 Observe for hemorrhage
d. *See cautions re adrenalectomy (typically only tumor is removed);
if entire adrenal gland removed; Addisons crisis risk and long term
steroids.
e. If not a candidate for surgery:
1) Use Demser (drug which inhibits catecholamine synthesis)
2) Avoid opiates, histamines, reglan, anti-depressants (stimulate SNS)
___________________________________________________________________
#5 Pituitary Gland (refer to introduction)
Anterior Pituitary Gland (Hyperfunction)
A. Etiology/Pathophysiology: Hyperfunction of anterior pituitary gland
1. Pathophysiology: Most often- benign adenoma producing excess hormones;
growth hormone (GH), Prolactin (PRL), or ACTH; 10% OF ALL BRAIN
TUMORS
2. Specific Conditions
a. Gigantism: Growth hormone hypersecretion occurs prior to puberty
b. resulting in person becoming excessively tall (over 7 feet tall)
c. Acromegaly: Growth hormone hypersecretion (somatotropin) occurs after
puberty
d. Causes bone and connective tissue continuing to grow > enlargement of
face, hands, and feet
e. Overproduction of prolactin secretion > dec. reproductive and sexual
function
f. Cushing’s Disease (inc ACTH due to pituitary adenoma)
3. **Recall anterior pituitary hormones (refer to chart with hormones
produced)
B. Common Manifestation/Complications
1. *Manifestations depend upon which hormone(s) is/are produced in
excess:
2. What would happen if you had too much growth hormone secretion???
Which goolish character on the Addam’s Family may have had too much
GH secretion?
RNSG 2432  427
a. Giantism in children: skeletal growth; may grow to 8 ft. tall and > 300 lbs
b. Acromegaly in adults: enlarged feet/hands, thickening of bones,
prognathism, diabetes, HTN, wt. gain, H/A, visual disturbances, diabetes
mellitus
Clinical features develop slowly …aged 40-60 years…Symptoms…arthralgia, increased
sweating and physical weakness…apparent increase in the size of hands and feet, coarsening
of the facial features mainly of the brow, widening of gaps between teeth, thickening of skin,
headache… carpal tunnel syndrome and other peripheral neuropathies, visual problems,
colon polyps and sleep apnoea…. women, ovulatory disorders, amenorrhoea and
galactorrhoea…men, decreased libido and hypogonadism….hypertension, heart disease and
diabetes…Signs enlarged tongue, stomach, heart, liver and spleen, hypertension, glucose
intolerance or type 2 diabetes mellitus. If before puberty - gigantism with abnormal height.
After puberty - normal
Hands of individual with acromegaly; normal hands.
428  RNSG 2432
Acromegaly: Facial changes secondary to elevated growth hormone levels. Note in
particular prominent supra-orbital ridge, jaw, and generally enlarged facial
features.
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests
1. Diagnostic Tests:
a. Key; history and physical exam
b. Evaluation of GH levels; and GH response to oral glucose challenge
c. MRI to identify pituitary hormone; CT scan with contrast
d. Opthalmologic exam and visual fields due to pressure on optic chiasm or
optic nerves.
2. Treatment:
a. Medications: Parlodel (bromocriptine)= reduce prolactin & GH levels.
b. Radiation therapy: external radiation reduce GH levels 80% of time
(usually given with medications); usually develop hypopituitarism with
radiation, need replacement therapy
c. Surgical removal (hypophysectomy) is treatment of choice; cure if
tumor is smaller than 10 mm; usually accomplished with
**transsphenoidal approach; goal to remove only tumor that is
causing the GH secretion; procedure produces an immediate
reduction in IGF-1 levels within a few weeks. (see previous notes)
RNSG 2432  429
*Incision made thru floor of nose into sella turcica
*In some cases entire pituitary gland removed surgery (hyposectomy) >
permanent absence of pituitary hormones; rather than replacing the pituitary
(tropic) hormones, which requires parenteral administration, essential
hormones produced by target organs (glucocorticoids, thryroid hormone and
sex hormones) given orally- must be continued throughout life!!
1) Pre-op hypophysectomy:
a) Anxiety r/t body changes, fear of unknown, brain involvement,
chronic condition; requiring life-long care
b) Sensory-perceptual alteration r/t visual field cuts, diplopia and
secondary to pressure on optic nerve.
c) Alteration in comfort (headache) r/t tumor growth/edema
2) Post-op (was entire pituitary removed or only tumor)
a) Knowledge deficit: post-op teaching including pain control,
ambulation, hormone replacement. Activity
b) Require use of hormone patch; activity restricted, NO straining/
bending for 2 months, use stool softners avoid coughing,
saline mouth rinses (no tooth brushing as risk of meninitis) as can
have CSF leak where sella turcica was entered *test any clear
nasal drainage for glucose to see if it is glucose; notify
physician; elevate HOB, bedrest as CSF usually resolves within
72 hours; spinal taps to relieve pressure!!
c) Periocular edema/ecchymosis
d) **Monitor and treat for post-op complications as diabetes
insipitus: lead to hypovolemic shock; very thirsty, urinate a lot!!
**Due to ADH insufficiency!! If develops-must be replaced
through hormone replacement (DDAVP (Desmopressin,
synthetic ADH, give by spray or pitressin IM)!**
e) Dec. ACTH > require cortisone replacement due to decrease
glucocorticoid production. Can you live without glucocorticoids????
f) Dec. in sex hormones >infertility due to decrease production
of ova & sperm
#6 Anterior Pituitary (Hypofunction)
A. Etiology/Pathophysiology: Etiology (rare disorder) may be due to disease,
tumor, or destruction of the gland.
B. Common Manifestation/Complications: Have signs and symptoms of dec.
hormones: GH, FSH/LH, Prolactin; ACTH; TSH
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests
1. Diagnostic Tests: CT Scan; Serum hormone levels
2. Treatment:
a) neurosurgery: removal of tumor
b) radiation: tumor size
c) hormone replacement: cortisol, thyroid, sex hormones
3. Assessment of S & S of hypo or hyper: functioning hormone levels
4. Teaching-Compliance with hormone replacement therapy: Counseling and
referrals and support medical interventions
430  RNSG 2432
#7 Posterior Pituitary Gland (SIADH) (**Important)
A. Etiology/Pathophysiology: Excessive or deficiency in antidiuretic hormone
(ADH)
*What hormones are released by the posterior pituitary?
ADH (vasopressin) which is secreted by cells in the hypothalamus and stored
in the posterior pituitary and acts on distal and collecting tubules of nephrons
making them more permeable to H20 thus decreasing water excreted!
Oxytocin controls lactation and stimulates uterine contraction
1. ADH-secreted in response to changes in serum osmolality (hypothalamus)
2. Specific Conditions: Syndrome of Inappropriate ADH Secretion
(SIADH) Too much ADH! What is SIADH? (p. 95)
a. **Occurs when ADH released despite normal or low normal plasma
osmolarity: results from abnormal production or sustained secretion of
ADH; characterized by fluid retention, serum hypo-osmolality,
dilutitional hyonatremia, hypochoremia, concentrated urine in
presence of normal or inc. intravascular volume and normal renal function
b. Under what conditions is ADH released; does it have
vasocontrictive or vasodilative action?
** released in response to decrease blood volume, increase
concentration of Na+ or other substances, pain, stress; ADH has
vasocontrictive properties
c. Results in hyponatremia and water intoxication
d. Due to: (too much ADH)
1) Malignant tumors (e.g. oat cell or small cell lung cancer) which secret
2) ADH
3) Post head injury, side effect of some medications including diuretics
4) and anesthetics such as morphine
5) Ca duodenum/pancreas, trauma, pulmonary disease, CNS
6) disorders, drugs -- Vincristine, nicotine, general anesthetics, tricyclic
antidepressants
B. Common Manifestation/Complications (SIADH)
1. Signs and Symptoms: neurologic symptoms including dec. level of
consciousness, confusion, muscle twitches, seizures
2. Signs/symptoms hypotnatremia: lethargy, decrease tendon reflexes, seizures
RNSG 2432  431
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests
**1. Diagnostic tests:
 decreased Serum Na+ <135meq/l
 decreased Serum osmolality <275 OSM/kg H2O
 increased urine specific gravity
 decreased or normal BUN
2.***Treatment: correction of Na deficit, restriction of fluids, treat
underlying cause
a. ***FLUID RESTRICTION: LIMIT TO 1000ML/24HRS
b. IV 3% NaCl to replace Na
c. IF CHF -- Lasix (temporary fix)
d. Treat underlying problem --Chemo, radiation
e. **Declomycin 600 po-1200mg/day to inhibit ADH
f. Fluid restriction may be as little as 500-600ml/24hrs
g. Daily weights...1 lb. weight = 500ml fluid retention
h. Accurate I & Os
i. F & E imbalances; monitor fluid intake
j. High risk for injury r/t complications of fluid overload (seizures
#8 Diabetes Insipidus (Posterior Pituitary Gland) (see Kelly’s video)
A. Etiology/Pathophysiology: Diabetes Insipidus ((too little ADH)
1. ADH insufficiency from neurogenic or nephrogenic origin
2. Pathophysiology: Brain tumors, closed head trauma, other brain conditions,
renal failure; 50% idiopathic
a. central (neurogenic -- i.e. brain tumors; sudden onset!
b. nephrogenic - inability of tubules to respond to ADH
c. psych (dispogenic DI) less common; can be a structural lesion or a
psychological disorder leading to water intoxication, is it true DI?
B. Common Manifestation/Complications
1. Signs and Symptoms: excretes large amounts of dilute urine; client at risk for
dehydration and hypernatremia
2. **Polydipsia; Polyuria (10L in 24 hours); have low urine specific gravity
less than 1.005 and urine osmolality of < 100mOsm/kg. *Serum
osmolality is elevated as a result of hypernatremia due to pure water
loss in the kidney
3. Severe fluid volume deficit
a. wt loss
b. tachycardia
c. constipation
d. shock
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests
1. Must differentiate among different causes of DI; requires complete history
and physical
a. Dehydration test:
2 units of Vasopressin (ADH) mixed in saline administered over 2
hrs then check urine osmolality levels
432  RNSG 2432
b. Water deprivation-confirm diagnosis of central DI; get baseline weights,
pulse, urine and plasma osmolalities, specific gravity, urine and BP;
withhold all fluids for 8 to 16 hours; *potential risk due to fluid
volume deficit; during test, patient assessed hourly for BP, weight,
urine osmolality; test continues until urine osmolalities stabilizes or body
weight declines by 5% or orthostatic hypotension develops. ADH then
given and urine osmolality is measured 1 hour later; in central DI
the rise in urinary osmolality after vasopressin exceeds
9%.observed
c. What is the expected urine specific gravity; serum Na and serum
osmolality without treatment?
2. *Treatment: administer intravenous hypotonic fluids, oral fluids and
replace DH hormone (Desmopressin acetate)
a. Identification of etiology, H & P
b. Tx of underlying problem
c. **DDAVP(desomopressin acetate) (nasal spray); Pitressin s.c. IM,
nasal spray
d. Assess for F & E imbalances
e. High risk for sleep disturbances
f. Increase po/IV fluids
3. Nursing diagnosis:
a. RF Injury (hypovolemic shock)
b. Knowledge deficit
c. High risk for ineffective coping
RNSG 2432  433