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The Endocrine

System
Presented By:
Karen Joyce L. Jimeno, BSN, R.N.
Anatomy and Physiology
 Pituitary Gland (Hypophysis)

 Located in sella turcica at the


base of the brain.

 “Master gland” of the body,


composed of three lobes

1. Anterior lobe
(adenohypophysis)

a. secretes tropic hormones


(hormones that stimulate target
glands to produce their
hormone): adrenocorticotropic
hormone (ACTH), thyroid-
stimulating hormone (TSH),
follicle-stimulating hormone
(FSH), luteinizing hormone (LH)
b. Also secretes hormones that
have direct effect on tissues:
somatotropic or growth
hormone, prolactin

c. Regulated by hypothalamic
releasing and inhibiting factors
and by negative feedback system

2. Posterior lobe
(neurohypophysis): does not
produce hormones; stores
and releases antidiuretic
hormone (ADH) and
oxytocin, produced by the
hypothalamus.

3. Intermediate lobe: secretes


melanocyte stimulating
hormone (MSH).
 Adrenal glands

 Two small glands, one


above each kidney
 Consist of two sections
1. Adrenal cortex
(outer portion):
produces
mineralocorticoids,
glucocorticoids, sex
hormones

2. Adrenal medulla
(inner portion):
produces
epinephrine &
norepinephrine
 Thyroid gland

 Located in the anteroir


portion of the neck
 Consists of two lobes
connected by a narrow
isthmus
 Produces thyroxine
(T4), triiodothyronine
(T3), thyrocalcitonin
 Parathyroid glands

 Four small glands


located in pairs behind
the thyroid gland
 Produce
parathormone (PTH)
 Pancreas

 Located behind the


stomach
 Has both endocrine
and exocrine
functions
 Islets of Langerhans
(alpha and beta cells)
involved in endocrine
function

1. Beta cells: produce


insulin
2. Alpha cells:
produce glucagon
 Gonads

 Ovaries: located in pelvic cavity, produce estrogen and


progesterone
 Testes: located in scrotum, produce testosterone
Hormone Functions
Endocrine Gland Hormones Functions

Pituitary TSH Stimulates thyroid gland


Anterior Lobe to release thyroid
hormones
ACTH
Stimulates adrenal cortex
to produce and release
adrenocorticoids

FSH, LH Stimulate growth,


maturation, and function
of primary and secondary
GH or Somatotropin sex organs

Stimulates growth of body


tissues and bones
Prolactin or LTH

Stimulates development
of mammary glands and
lactation
Endocrine Gland Hormones Functions

Pituitary
Posterior Lobe ADH Regulates water
metabolism; released during
stress or in response to an
increase in plasma
osmolality to stimulate
reabsorption of water and
decrease urine output

Oxytocin
Stimulates uterine
contractions during delivery
and the release of milk

Intermediate Lobe MSH


Affects skin pigmentation
Endocrine Gland Hormones Functions

Adrenal
Adrenal Cortex Mineralocorticoids (e.g., Regulate fluid and electrolyte
aldosterone) balance; stimulate
reabsorption of sodium,
chloride, and water; stimulate
potassium excretion

Glucocorticoids (e.g., cortisol,


corticosteroid) Increase blood glucose levels
by increasing rate of
glyconeogenesis; increase
protein catabolism, increase
mobilization of fatty acids;
promote sodium and water
retention; anti-inflammatory
effect; aid body in coping with
stress

Sex Hormones (androgens, Influence development of


estrogen, progesterone) secondary sex characteristics
Endocrine Gland Hormones Functions

Adrenal
Adrenal Medulla Epinephrine, norepinephrine Function in acute stress;
increase heart rate, blood
pressure; dilate bronchioles;
convert glycogen to glucose
when needed by muscles for
energy

Thyroid T3, T4 Regulate metabolic rate;


carbohydrate, fat, and protein
metabolism; aid in regulating
physical and mental growth
and development

Lowers serum calcium by


Thyrocalcitonin increasing bone deposition

Regulates serum calcium and


Parathyroid PTH phosphate levels
Endocrine Gland Hormones Functions

Pancreas (Islets of Langerhans)

Beta cells Insulin Allows glucose to diffuse across


a cell membrane; converts
glucose to glycogen

Alpha cells Glucagon Increases blood glucose by


causing glyconeogenesis and
glycogenolysis in the liver;
secreted in response to low
blood sugar

Ovaries Estrogen, progesterone Development of secondary sex


characteristics in the female,
maturation of sex organs,
maintenance of pregnancy

Testes Testosterone
Development of secondary sex
characteristics in the male,
maturation of sex organs, sexual
functioning
Disorders of the Endocrine System
 Addison’s Disease

A. General information
1. Primary adrenocortical insufficiency; hypofunction of
the adrenal cortex causes decreased secretion of the
mineralocortocoids, glucocorticoids, and sex hormones.
2. Relatively rare disease caused by:
a. Idiopathic atrophy of the adrenal cortex possibly due to
an autoimmune process
b. Destruction of the gland secondary to tuberculosis or
fungal infection
B. Assessment findings
1. Fatigue, muscle weakness
2. Anorexia, nausea, vomiting, abdominal pain, weight
loss
3. History of frequent hypoglycemic reactions
4. Hypotension, weak pulse
5. Bronzelike pigmentation of the skin
6. Decreased capacity to deal with stress
7. Diagnostic tests: low cortisol levels, hyponatremia,
hyperkalemia, hypoglycemia
C. Nursing interventions
1. Administer hormone replacement therapy as ordered.
a. Glucocorticoids (cortisone, hydrocortisone): to
stimulate diurnal rhythm of cortisol release, give 2/3 of dose
in early morning and 1/3 of dose in afternoon.
b. Mineralocorticoids: fludrocortisone acetate (Florinef)
2. Monitor vital signs.
3. Decrease stress in the environment.
4. Prevent exposure to infection.
5. Provide rest periods; prevent fatigue.
6. Monitor I & O.
7. Weigh daily.
8. Provide small, frequent feedings of diet high in carbohydrates,
sodium, and protein to prevent hypoglycemia and hyponatremia and
provide proper nutrition.
9. Provide client teaching and discharge planning concerning:
a. Disease process; signs of adrenal insufficiency
b. Use of prescribed medications for lifelong replacement
therapy; never omit medications
c. Need to avoid stress, trauma, and infections, and to notify
physician if these occur as medication dosage may need to be
adjusted
d. Stress management techniques
e. Diet modification (high in protein, carbohydrates, and
sodium)
f. Use of salt tablets (if prescribed) or ingestion of salty foods
(potato chips) if experiencing increased sweating
g. Importance of alternating regular exercise with rest periods
h. Avoidance of strenuous exercise especially in hot weather
Pathophysiology
autoimmune process infection
 
block the corticotropin impair cellular function
receptor or bind with corticotropin 
 affect corticotropin at any
stimulation of adrenal cells stage of regulation
 
Partial/complete destruction of Adrenal cortex

deficient production of the adrenocortical hormones, cortisol, aldosterone,


androgens

regulate adrenal release of glucocorticoids (primarily cortisol),
mineralocorticoids, and aldosterone

cathecolamine deficiency
  
cortisol deficiency aldosterone deficiency androgen deficiency
  
 liver gluconeogenesis  Na loss, enhanced K absorption hirsutism

Na excretion   H2O volume  causes hypotension
 Cushing’s Syndrome
A. General information
1. Condition resulting from excessive secretion of corticosteroids,
particularly the glucocorticoid cortisol
2. Occurs most frequently in females between ages 30 -60
3. Primary Cushing’s syndrome caused by adrenocortical tumors or
hyperplasia
4. Secondary Cushing’s syndrome (also called Cushing’s disease);
caused by functioning pituitary or nonpituitary neoplasm secreting
ACTH, causing increased secretion of glucocorticoids
5. Iatrogenic: caused by prolonged use of corticosteroids
B. Assessment findings
1. Muscle weakness, fatigue, obese trunk with thin arms and legs,
muscle wasting
2. Irritability, depression, frequent mood swings
3. Moon face, buffalo hump, pendulous abdomen
4. Purple striae on trunk, acne, thin skin
5. Signs of masculinization in women, menstrual dysfunction,
decreased libido
6. Osteoporosis, decreased resistance to infection
7. Hypertension, edema
8. Diagnostic tests: cortisol levels increased, slight hypernatremia,
hypokalemia, hyperglycemia
C. Nursing interventions
1. Maintain muscle tone
a. Provide ROM exercises
b. Assist with ambulation
2. Prevent accidents or falls and provide adequate rest
3. Protect client from exposure to infection
4. Maintain skin integrity
a. Provide meticulous skin care
b. Prevent tearing of skin: use paper tape if necessary
5. Minimize stress in the environment
6. Monitor vital signs; observe for hypertension, edema
7. Measure I & O and daily weights
8. Provide diet low in calories and sodium and high in protein,
potassium, calcium and vitamin D
9. Monitor urine for glucose and acetone; administer insulin if
ordered
10. Provide psychologic support and acceptance
11. Prepare client for hypophysectomy or radiation if condition is
caused by a pituitary tumor
12. Prepare client for an adrenalectomy if condition is caused by
adrenal tumor hyperplasia
13. Provide client teachings and discharge planning concerning:
a. Diet modifications
b. Importance of adequate rest
c. Need to avoid stress and infection
d. Change in medication regimen (alternate day therapy or reduced
dosage) if cause of the condition is prolonged corticosteroid therapy
Pathophysiology

prolonged exposure to excess glucocorticoids


 
exogenous endogenous
 
chronic glucocorticoid or  cortisol or
corticotropin administration corticotropin secretion
 
cortisol excess

anti – inflammatory effects
excessive catabolism of CHON & fat

suppressed hypothalamic pituitary axis
 Hypothyroidism (Myxedema)

A. General information
1. Slowing of metabolic processes caused by hypofunction of the
thyroid gland with decreased thyroid hormone secretion: causes
myxedema in adults and cretinism in children.
2. Occurs more often in women between ages 30 and 60.
3. Primary hypothyroidism: atrophy of the gland possibly caused by
an autoimmune process
4. Secondary hypothyroidism: caused by decreased stimulation from
pituitary TSH
5. Iatrogenic: surgical removal of the gland or overtreatment of
hyperthyroidism with drugs or radioactive iodine
6. In severe or untreated cases, myxedema coma may occur:
a. Characterized by intensification of signs and symptoms of
hypothyroidism and neurologic impairment leading to coma
b. Mortality rate high; prompt recognition and treatment essential
c. Precipitating factors: failure to take prescribed medications;
infection; trauma, exposure to cold; use of sedatives, narcotics, or
anesthetics
B. Assessment findings
1. Fatigue; lethargy; slowed mental processes; dull look; slow, clumsy
movements
2. Anorexia, weight gain, constipation
3. Intolerance to cold; dry, scaly skin; dry, sparse hair; brittle nails
4. Menstrual irregularities; generalized interstitial nonpitting edema
5. Bradycardia, cardiac complications (CAD, angina pectoris, MI,
CHF)
6. Increased sensitivity to sedatives, narcotics, and anesthetics
7. Exaggeration of these findings in myxedema coma: weakness.
Lethargy, syncope, bradycardia, hypotension, hypoventilation,
subnormal body temperature
8. Diagnostic tests:
a. Serum T3 and T4 level low
b. Serum cholesterol level elevated
c. RAIU decreased
C. Nursing interventions
1. Monitor vital signs, I & O, daily weights; observe for edema and
signs of cardiovascular complications
2. Administer thyroid hormone replacement therapy as ordered and
monitor effects.
a. Observe for signs of thyrotoxicosis (tachycardia, palpitations,
nausea, vomiting, diarrhea, sweating, tremors, agitation, dyspnea)
b. Increase dosage gradually, especially in clients with cardiac
complications
3. Provide a comfortable, warm environment
4. Provide a low-calorie diet
5. Avoid the use of sedatives; reduce the dose of any sedative,
narcotic, or anesthetic agent by half as ordered
6. Institute measures to prevent skin breakdown
7. Provide increased fluids and foods high in fiber to prevent
constipation; administer stool softeners as ordered
8. Observe for signs of myxedema coma; provide appropriate
nursing care
a. Administer medications as ordered
b. Maintain vital functions: correct hypothermia, maintain
adequate ventilation
9. Provide client teaching and discharge planning concerning:
a. Thyroid hormone replacement
1. take daily dose in the morning to prevent insomnia
2. self-monitor for signs of thyrotoxicosis
b. Importance of regular follow-up care
c. Need for an additional protection in cold weather
d. Measures to prevent constipation
D. Medical management
1. Drug therapy: levothyroxine (Synthroid), thyroglobulin (Proloid),
dessicated thyroid, liothyronine (Cytomel)
2. Myxedema coma is a medical emergency.
a. IV thyroid hormones
b. Correction of hypothermia
c. Maintenance of vital functions
d. Treatment of precipitating causes
Pathophysiology

Deficiency in CHON & iodine /


 secretion of TSH from the APG

 thyroid hormone production

 BMR

achlorhydria;  GI motility; bradycardia; slowed
mental processing;  BBT; cholesterol &
triglycerides; anemia with possible Vit. B12 &
folate deficiency
 Hyperthyroidism (Grave’s Disease)

A. General information
1. Secretion of excessive amounts of thyroid hormone in the blood
causes an increase in metabolic processes
2. Overactivity and changes in the thyroid gland may be present
3. Most often seen in women between ages 30 and 50
4. Cause unknown, but may be an autoimmune process
5. Symptomatic hyperthyroidism may also be thyrotoxicosis
B. Assessment findings
1. Irritability, agitation, restlessness, hyperactive movements,
tremors, sweating, insomnia
2. Increased appetite, hyperphagia, weight loss, diarrhea, intolerance
to heat
3. Exophthalmos (protrusion of the eyeballs), goiter
4. Warm, smooth skin; fine, soft hair; pliable nails
5. Tachycardia, increased systolic blood pressure, palpitations
6. Diagnostic tests
a. Serum T3 and T4 levels elevated
b. RAIU increased
C. Nursing interventions
1. Monitor vital signs, daily weights
2. Administer antithyroid medications as ordered
3. Provide for periods of uninterrupted rest
a. Assign to a private room away from excessive activity
b. Administer medications to promote sleep as ordered
4. Provide a cool environment
5. Minimize stress in the environment
6. Encourage quiet, relaxing diversional activities
7. Provide a diet high in carbohydrates, protein, calories, vitamins,
and minerals with supplemental feedings between meals and at
bedtime; ommit stimulants
8. Observe for and prevent complications
a. Exophthalmos: protect eyes with dark glasses and artificial tears as
ordered
b. Thyroid storm
9. Provide client teaching and discharge planning concerning
a. Need to recognize and report signs and symptoms of
agranulocytosis (fever, sore throat, skin rash) if taking antithyroid
drugs
b. Signs and symptoms of hyper/hypothyroidism
D. Medical management
1. Drug therapy
a. Antithyroid drugs (propylthiouracil and methimazole [Tapazole]):
block synthesis of thyroid hormone; toxic effects include
agranulocytosis
b. Adrenergic blocking agents (commonly propanolol [Inderal]): used
to decrease sympathetic activity and alleviate symptoms such as
tachycardia
2. Radioactive iodine therapy
a. Radioactive isotope of iodine given to destroy the thyroid
gland, thereby decreasing production of thyroid hormone
b. Used in middle aged or older clients who are resistant to, or
develop toxicity from , drug therapy
c. Hypothyroidism is a potential complication
3. Surgery: thyroidectomy performed in younger clients for whom
drug therapy has not been effective
Pathophysiology

Excessive stimulation of adrenergic nervous system /


Excessive levels of circulating thyroid hormones

 Basal metabolic rate

tachycardia;  cardiac output;  stroke volume;
 peripheral blood flow; lipid depletion; nutritional deficiency;
weight loss; altered secretion of gonadal hormones
hypermetabolism ophthalmopathy goiter

-Retrobulbar
 metabolic rate -results from 
connective tissue &
& calorigenesis Stimulation of
extraocular muscle
-Alters CHON, The thyroid
volume are expanded
CHO, &  in tissue mass Gland by
fat metabolism TSH or
forces the eye
- directly stimulates TSH-like
forward (proptosis)
body systems substance
Up to the limits
of the restraining
action of the
extraocular muscles
(exophthalmos)

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