Module F

Endocrine

Roy Model- Protection, Rest, and Activity

Selected disorders of endocrine function. Differentiation of type 1 and type 2 Diabetes.
Etiology, risk factors, pathophysiology, clinical manifestations, diagnostic evaluation, medical and
surgical interventions, complications. Nutritional management.
Primary, secondary, and tertiary prevention. First and second level assessment of all modes per
Roy Model. Impact of endocrine disorders on patient’s self-concept, role, and interdependence.
Adaptive and ineffective behaviors identified. Problems of adaptation (nursing diagnosis) identified.
Interventions to promote adaptation, including nursing measures that are preventive, remedial,
supportive and rehabilitative. Roy Model and nursing process utilized to develop a nursing care plan.
Criteria for evaluation and reassessment.

Required Reading

Lewis, Heitkemper, & Dirksen, Medical- Surgical Nursing (current ed)

a. Endocrine System- overview and understanding
b. Diabetes- focus on acute care i.e. DKA, HHNK, hypo/hyperglycemia, drug therapy
c. Endocrine Disorders- thyroid, parathyroid, pituitary, and adrenal cortex.

Recommended Reading

Pathophysiology book- focus on endocrine system

Theory Objectives
1. Review anatomy, physiology, and normal endocrine function.
2. Explain the functions of the hormones secreted by the endocrine glands.
3. Identify first level assessment behaviors for each problem of endocrine dysfunction, to
include nursing history, physical assessment, and analysis of relevant data.
4. Identify second level assessment (influencing factors) affecting the endocrine system, to
include pathophysiology, risk factors, diagnostic test results, environmental conditions, and
patient’s knowledge as potential stimuli.
5. Compare and contrast the manifestations of disorders that result from hyperfunction to
hypofunction of the thyroid, adrenals and pituitary gland.
6. Compare and contrast, behaviors, stimuli, medical and nursing interventions for the hypo/
hyperthyroidism.
7. Explain the nursing implications for medications prescribed to treat disorders of the
endocrine system.
8. Provide appropriate nursing care for the client before and after surgical procedures for the
abnormalities.
9. Review to compare and contrast the manifestations and collaborative care of hypoglycemia,
diabetic ketoacidosis (DKA), and hyperosmolar hyperglycemic state (HHS).
10. Identify adaptive and ineffective behaviors within the four adaptive modes for each problem.
11. Formulate patient goals and set priority for each adaptation problem (nursing diagnosis)
discussed.
 12. Discuss the role of the nurse in health promotion and life style modifications related to risk
factors for each problem.
13. Select appropriate nursing interventions, including health teaching, commonly implemented
to manage ineffective behaviors and promote adaptation.

Clinical Component-
Objectives
1. Complete a physical assessment of the client with endocrine disorder and identify alterations
to specific diseases.
2. Identify laboratory value abnormalities common to the client with disorders of the endocrine
system.’
3. Correlate client symptoms with specific hormonal dysfunction in diseases of the endocrine
system.
4. Provide post-operative care to a client following a surgical procedure.
5. Provide teaching to the client receiving steroids.
6. Give emotional support to the client with body image disturbance related to changes caused
by endocrine dysfunction.
7. Monitor blood sugar levels of client with diabetes.
8. Administer medications, including insulin regular dose and sliding scale dosages according
to hospital guidelines.
9. Provide interventions for the client experiencing acute complications of the endocrine
system.

Drugs
Steroids, Insulin, Oral-hypoglycemic agents, other hormonal agents (i.e. vasopressin, DDAVP,
etc)

Diet
Diabetic diet or diet appropriate to the level of care

Laboratory
Urinalysis (specific gravity, osmolarity, electrolytes), Water deprivation test and water loading
test, electrolytes

Critical Thinking Question

1. A 55 year old woman, who collapsed at home, is taken to ED of a hospital by ambulance.
The woman’s husband accompanied his wife. The woman responds to her name but does not
answer questions. Her blood pressure is 84/ 48 right arm lying: T- 40 C; HR- 120; R-36.
Her skin turgor is poor and her mucous membranes are dry and sticky. Her husband states
that she has been very tired and has had a poor appetite for several days. She had some
vomiting during the night. She almost fell twice earlier in the day and said she was very
dizzy. She was planning to call her physician today for an appointment. Her skin is a bronze
color and her husband said she seems to tan better this summer.
a. What are the priority needs for this client? From this description, what endocrine
condition could be a diagnosis for this client?
 b. Two large IV’s are established. 2 liters of NS are infused at a rate of 250 cc/ hr. Blood
work is completed at the time the IV is inserted.
c. If this client were suffering from Addisonian crisis, what would be the expected H/H, Na,
K, and glucose levels?
d. The results are back;
i. H/H- 16.5/ 46% Glucose 52
ii. Na 123 mEq/l K 5.1 mEq/l
iii. Cl 87 mEq/l HCO3 20 mEq/l
e. Based on these results, how should the fluid and electrolyte status of the client be
described upon admission? What blood tests should be ordered to confirm the diagnosis
of Addison’s Disease?
2. Your pt is beginning antithyroid medication to control her hyperthyroidism. Her husband has
been very concerned about her irritability, rapid mood swings, and weight loss. How would
you explain to him the reasons for his wife’s symptoms and the rationale for the medication
being prescribed?
 Endocrine Module
Pituitary

I. Disorders of anterior pituitary gland- Hyperfunction

a. Pathophysiology
i. Most often benign adenoma producing excess hormones; growth hormones (GH),
Prolactin (PRL), or ACTH
b. Specific Conditions
i. Gigantism: growth hormone hypersecretion occurs prior to puberty resulting in
person becoming excessively tall (over 7 feet)(child onset)
ii. Acromegaly: growth hormone hypersecretion occurs after puberty resulting in bone
and connective tissue continuing to grow, resulting in enlargement of face, hands, and
feet (adults)
iii. Overproduction of Prolactin secretion: results in decreased reproductive and sexual
function
iv. Cushing’s Syndrome
c. Treatment: surgical removal or irradiation of pituitary tumor

II. Disorders of posterior pituitary gland

a. Hypofunction- Diabetes Insipidus
i. General information
1. The primary characteristic of DI is excretion of large quantities of urine (5-20
L/day) with a very low specific gravity.
2. Hypofunction of the posterior pituitary gland resulting in deficiency of ADH
3. Characterized by excessive thirst and urination
4. Caused by tumor, trauma, inflammation, pituitary surgery
ii. Assessment
1. Polydipsia (great amounts) and severe polyuria w/ low specific gravity,
fatigue from nocturia
2. Fatigue, muscle weakness, irritability, weight loss, signs of dehydration
3. tachycardia, eventual shock if fluids not replaced
4. ??? Lithium is one of the most common causes of drug induced DI
5. Diagnostics-
a. Urine specific gravity less than 1.004
b. Water deprivation test reveals inability to concentrate urine

iii. Nursing diagnosis

1. Severe fluid volume deficit r/t polyuria m/b weight loss, poor tissue turgor,
hypotension, tachycardia, constipation, and shock.

iv. Interventions (AIDC)

1. Determine and tx the primary cause
2. Maintain fluid/ lytes balance- orally or IV
3. Monitor VS, check for signs of dehydration/ hypovolemia
4. Administer hormone replacement
 a. Pitressin in oil or water- 5-20 units deep IM
b. Desmopressin (DDAVP)- hormonal replacement analog of ADH (PO,
IV, or nasal)- O.3 mcg/kg in saline over 15-30 minutes
5. Provide client teaching/ discharge instructions w/ use of hormonal
replacement as lifelong therapy

b. Hyperfunction- Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

i. General Information
1. Hypersecretion of ADH
2. SIADH is characterized by fluid retention, serum hyposmolarity, dilutional
Hyponatremia, hypochloremia, concentrated urine in the presence of
intravascular volume depletion, and normal renal function.

ii. Pathophysiology
1. Causes may include malignancy, especially small cell lung cancer; CNS
disorders such as head injury; and drug therapy
2. Excess ADH increases renal tubular permeability and reabsorption of water
into the circulation. Consequently, extracellular fluid volume expands,
plasma osmolarity declines, glomerular filtration rate rises and sodium levels
decline.

iii. Assessment
1. Cannot secrete dilute urine
2. Fluid retention/ weight gain and Na deficiency
3. Initially thirst, dyspnea on exertion, fatigue, and dulled sensorium may be
evident
4. Potential for cerebral edema, leading to increased lethargy, anorexia,
confusion, headache, seizures, and coma.
5. Other- muscle cramps and weakness.
6. Diagnostics-
a. Simultaneous measurements of UA and serum osmolarity
b. Decreased BUN, Creatinine clearance, H/H

iv. Nursing diagnosis

Fluid volume excess r/t increased ADH, 2nd SIADH m/b (3)

v. Interventions
1. Tx the underlying cause if possible- may be self limiting when assoc. w/ head
trauma, but chronic w/ metabolic disease
2. Diuretics ( Lasix) and fluid restriction (800-1000 cc/day) w/ careful I/O, daily
weights
3. Monitor electrolytes (esp. K) and blood chemistry
4. Monitor neurologic status
5. Medications-
a. Declomycin/ lithium- block effect of ADH on renal collecting tubules
Adrenal Gland
Cortex
Glucocorticoids- glucose metabolism
Mineralocorticoids- electrolyte balance
Sodium, potassium
Androgens
Medulla
Catecholamines
Epinephrine, norepinephrine

I. Adrenal Cortex Hyperfunction- Cushing

a. General
i. Excess corticosteroids, particularly glucocorticoids
ii. Iatrogenic administration of exogenous corticosteroids (prednisone)
iii. Adrenal tumors and ectopic ACTH production by tumors outside the pituitary (lung/
pancreas)

b. Assessment
i. Pronounced changes in appearance- weight gain (adipose tissue)- trunk, face, and
cervical neck area; transient weight gain from Na and water retention; Moon face;
Buffalo Hump
ii. Protein wasting 2nd to catabolic effect of cortisol on peripheral tissue, muscle wasting,
especially to extremities
iii. Mineralocorticoid excess may cause hypertension, whereas, androgen excess may
cause pronounced acne and feminization in men
iv. Other- purplish-red striae on abdomen, breast, or buttocks
v. Diagnostics-
1. plasma cortisol levels may be elevated
2. plasma ACTH level- low, normal, or elevated
3. 24 hour UA for free cortisol

c. Nursing Diagnosis (include r/t…. and m/b -3)

i. Risk for infection
ii. Imbalanced nutrition: more than body requirements
iii. Disturbed self-esteem
iv. Impaired skin integrity

d. Interventions
i. Primary goal to normalize hormone secretion
ii. If pituitary adenoma- transsphenoidal hypophysectomy
iii. If adrenal tumors- adrenalectomy
iv. If developed r/t prolonged administration of corticosteroids then gradual DC and/ or
conversion to an alternate day regimen
 v. Daily nsg interventions to include VS, glucose monitoring, daily weights, s/sx of
infection (poss. Subtle), any pain (bone, abd esp), abnormal thromboembolic
phenomena.
vi. Emotional support for changes in appearance, poss. Surgical interventions, emotional
responses

II. Adrenal Cortex Hypofunction-Chronic Adrenocortical Insufficiency (Addison’s disease)

a. General
i. Hypofunction of adrenal cortex or adrenocortical insufficiency (all- glucocorticoids,
mineralocorticoids, and androgens reduced)
ii. Trigger may be autoimmune, or infarction, fungal, AIDS, metastatic cancer
iii. Iatrogenic may be due to adrenal hemorrhage (??? Related to anticoagulant therapy),
chemo, bilateral adrenalectomy

b. Assessment
i. Usually insidious onset and include progressive weakness, fatigue, weight loss, and
anorexia
ii. Striking feature-- hyperpigmentation (high ACTH levels) of skin especially in
exposed areas, pressure points, over joints, and palmar areas.
iii. Other- hypotension, Hyponatremia, Hyperkalemia, n/v, diarrhea
iv. Addisonian Crisis--- life threatening emergency—characterized by sudden, sharp
decrease in hormones m/b hypotension leading to shock especially during stress
(infection, surgery, or psychologic distress)- circulatory collapse
v. Diagnostics-
1. plasma cortisol levels- subnormal or fail to rise
2. Hyperkalemia, hypochloremia, and hyponatremia
3. CT, MRI localize tumors

c. Nursing Diagnosis
i. Fluid volume deficit r/t…. m/b (3)

d. Interventions
i. Tx underlying cause when possible
ii. Hormonal therapy-
1. corticosteroids – hydrocortisone/ Solu-Cortef
2. glucocorticoids-
3. mineralocorticoids
iii. Manage addisonian crisis aggressive- shock management w/ large volumes of fluids
(0.9% / D5)
iv. Support VS w/ vasoactive medications
v. VS, signs of fluid volume deficit, lytes – eval q 30 min to q4 for 24 hours until stable
vi. Daily weights
vii. Pt/ family education to recognize s/x of corticosteroid deficiency and excess

III. Adrenal Medulla Hypersecretion- Pheochromocytoma

A. General
a. Core of Adrenal gland- fx to release catecholamine hormones (epinephrine/
norepinephrine)
b. Tumor originating in medulla- can occur at any age, increase familial propensity
c. May be the cause of HTN in 2.2%

B. Assessment
a. 5 H’s- HTN, H/A, Hyperhidrosis (excessive sweat), Hypermetabolism,
Hyperglycemia
b. Hypermetabolic state -Typical- HA, diaphoresis, palpitations, HTN, tremor,
flushing, anxiety, hyperglycemia
c. Paroxysmal form- acute, unpredictable attacks that last seconds to hours w/
increased anxiety, tremors, weakness, BP 350/200
d. Diagnostics- UA/ Bld for catecholamines

C. Nursing Diagnosis
a. Cardiac output altered r/t excess secretion of catecholamines m/b (3)

D. Interventions
a. Eliminate increased stimulation (coffee, tea, tobacco, emotional/ physical stress,
amphetamines, decongestants, bronchodilators)
b. Definitive Tx- surgical intervention w/ hormonal replacement therapy
c. Medications-
i. Regitine- smooth muscle relaxants
ii. Nipride- decrease BP
iii. Dibenzyline- long acting B blocker- useful to stabilize BP