NCM 116 | 5M: Care of Clients with Hormonal Disturbances

PART 1:
stimulating the
ENDOCRINE SYSTEM epiphyseal plates of
the long bones
- Plays an integral part in the regulation of the body’s
internal environment Lactotropic Stimulates milk
Prolactin (PRL)
cells production
- Regulates growth, reproduction, metabolism, fluid
and electrolyte balance and gender differentiation Stimulates the
through hormones Thyrotropic Thyroid stimulating release and
cells hormones (TSH) synthesis of thyroid
MAJOR ORGANS/GLANDS hormones
● Pituitary gland
Corticotropic Adrenocorticotropic Releases hormones,
● Thyroid gland cells hormone (ACTH) glucocorticoid
● Parathyroid gland PTP APG
● Adrenal glands Gonadotropin
● Pancreas hormones
● Follicle
● Gonads Gonadotropic Stimulates the
stimulating
cells ovaries and testes
hormone (FSH)
PITUITARY GLAND ● Luteinizing
- “Master gland” hormone (LH)
○ It regulates many body functions
- 2 parts: Gonadotropic cells: Gonadotropin hormones
○ Anterior pituitary (adenohypophysis) ● For women: FSH stimulates the development of
- Composed of glandular tissue ovarian follicles and includes the secretion of
○ Posterior pituitary (neurohypophysis) estrogenic female sex homrones increasing the
- Extension of the hypothalamus levels of LH which works together with FSH that
leads to ovulation and the formation of the corpus
- Located in the skull beneath the hypothalamus of
lutuem from the ovarian follicle
the brain
● For men: FSH is involved in the development and
Hormones Secreted by the ANTERIOR PITUITARY GLAND maturation of sperm; LH or interstitial
cell-stimulating hormone (ICSH) stimulates the
interstitial cells of the testes to produce male sex
hormones

Hormones Secreted by the POSTERIOR PITUITARY

GLAND
HORMONES FUNCTION

Antidiuretic Hormone (ADH) Decreases urine production;

/ Vasopressin causes renal tubules to
reabsorb water from the
urine and return it to the
Anterior pituitary gland has several types of endocrine cells circulating blood volume
and secretes at least six major hormones.
Oxytocin Induces contraction of the
CELLS HORMONES
smooth muscles in the
reproductive organs
Stimulates growth
of the body by
Somatotropic Growth hormone Stimulates myometrium of
signalling cells to
cells (Somatotropin) the uterus to contract during
increase protein
labor; also induces milk
production and by
injection from the breast
THYROID GLAND ○ Adrenaline (epinephrine)
- Butterfly-shaped gland - Increases blood glucose levels and
- Anterior to the upper part of the trachea and stimulates the release of
inferior to the larynx adrenocorticotropic hormone
vasoconstricts:
- Has two lobes connected by a structure called kidney,skin, mmembr from the pituitary
ismuth - ACTH stimulates the adrenal
vd:
- Secrete thyroid hormones cortex to release glucocorticoids
coronary arteries
- Thyroxine (T4) pulm arteries - Increases the heart rate and force
- Triiodothyronine (T3) skeletal muscle blood vessels of cardiac contractions which
- Calcitonin constrict blood vessels in the skin
- A hormone that decreases mucous membranes and kidneys
excessive levels of calcium in the - It also dilates blood vessels in the
body by slowing skeletal muscles, coronary arteries
calcium-releasing activity of bone and pulmonary arteries
cells, which serves as marker for ○ Noradrenaline (norepinephrine)
sepsis and is believed to be a - Increases both heart rate and the
mediator of inflammatory vasoconstricts bvessels force of cardiac contractions
in all areas of the body
responses - It causes vasoconstriction of
- TH secretion is initiated by the release of the TSH blood vessels throughout the
by the pituitary gland and is dependent on the body
adequate supply of iodine
- Primary role: increase metabolism *these hormones are similar to substances released by the
- If thyroid gland is totally removed and thyroid sympathetic nervous system thus not essential to life
hormone is replaced, calcium homeostasis and
bone density remains relatively unchanged without - Cortex
replacing calcitonin ○ Secretes several hormones, all
corticosteroids:
PARATHYROID GLAND - Mineralocorticoids
- Are embedded on the posterior surface of the - glucocorticoids
lobes of the thyroid gland - Renin (enzyme)
- Secrete the parathyroid hormones (PTH) or ○ Primary role: controls the release of
parathormone, which controls calcium and aldosterone: mineralocorticoids
primary
phosphate mineralocortico ○ When there is decreased blood pressure
- When serum calcium level falls PTH secretion id hormone; and sodium is detected, cells in the
aldosterone
increases and PTH also increases phosphate increase water
kidneys release renin to act on angiotensin
metabolism reabsorption = it then initiates the process of your RAAS
- Primary role: increase renal excretion of phosphate (Renin-Angiotensin Aldosterone System)
mineralocortico
in the urine by decreasing the excretion of calcium ids: regulate and if you have aldosterone, it prompts
and increasing bone reabsorption na/k the distal tubules to increase reabsorption
concentration
- Normal levels of vitamin D are necessary for of water into the circulating blood volume
parathyroid hormones to exert its effect on bones to increase blood pressure
and the kidneys - Glucocorticoids
glucocorticoids are ○ Includes cortisol and cortisone
ADRENAL GLANDS elevated contributing - These hormones affect
to the loss of muscle
- Are pyramid shaped organs that sit on top of the mass and function. carbohydrate metabolism by
kidneys regulating glucose use in body
glucocorticoids:
- Each gland consist of two parts: Inner medulla and carbohydrate use in
tissues , mobilizing fatty acids
an outer cortex muscles/uptake from fatty tissues and shifting the
- Adrenal medulla produces two hormones called - maintain blood source of energy from muscles to
glucose levels
catecholamines - maintain BP = glucose to fatty acids
vasoconstriction
- gluconeogenesis
 - Excess glucocorticoids in - Mechanism of hormone release
the body depresses ○ Humoral
inflammatory responses - Endocrine glands release
and inhibits the hypothalamic pituitary adrenal hormones in direct response to
effectiveness of the axis
changing levels of ions or
= regulate cortisol
immunes system nutrients
- Released in times of - The hypothalamus secretes
stress hormones. It stimulates the
anterior PG to secrete hormones
PANCREAS that stimulate other endocrine
- Endocrine and exocrine gland/function glands to secrete a hormone
- It is located behind the stomach between the ○ Neural
spleen and the duodenum - Nerve fibers stimulate hormonal
- Endocrine cells: regulate carbohydrate metabolism release
○ Function: produces hormones - The preganglionic sympathetic
- Exocrine function: produce digestive enzymes nervous system fiber stimulates
- Endocrine cells are clustered in bodies called the the adrenal medulla cells to
pancreatic islets which is scattered throughout the secrete catecholamines
gland ○ Hormonal
somatostatin: ○ Has four different cell types - Glands release hormones in
prevent release of
- Alpha cells: produces glucagon release triggered by fasting response to other hormones
pancreatic
hormones - Beta cells: produces insulin release triggered by eating - Ex: Capillary blood flow contains
(insulin, glucagon - Delta cells: secretes somatostatin low concentration of calcium
and gastrin)
or pancreatic
- F cells: inhibit exocrine activity of which will then stimulate the
enzymes that aid in the pancreas secretion of the parathyroid
digestion
hormone
GONADS
FEEDBACK MECHANISM
- Are the testes in men and ovaries in women
- These organs are the primary source of steroid sex - Regulates hormone concentration in the
hormones in the body bloodstream and helps in the regulation of many
- Important in regulating body growth and biologic processes
promoting puberty
- In men, androgens or testosterone are produced by
STIMULUS RESPONSE
the testis to maintain reproductive functioning and
secondary sex characteristics and promote the - change in homeostatic - signal sent from CNS
production of sperm environment - produce effect
- In women, the ovary secrete estrogen and - signal sent to CNS - body returns to
progesterone to maintain reproductive functioning homeostasis
and secondary sex characteristic
- Progesterone also promotes the lining of NEGATIVE FEEDBACK MECHANISM (most common)
the uterus to prepare for implantation of a - ⇧ levels of substance = Inhibit hormone synthesis
fertilized egg? and secretion
- ⇩ levels of substance = stimulate hormone
HORMONES: OVERVIEW
synthesis and secretion
- Chemical messengers secreted by the endocrine - Example:
inversely prop
organs and transported throughout the body releasing of
○ ⇩ calcium — ⇧ PTH secretions in intestine,
- These hormones exert their action on hormones bone, kidney
specific/target cells and they do not cause reactions
directly but rather regulate tissue responses Sensors in the endocrine system detect these changes in
- May produce a generalized/localized effect the hormone levels and adjust the level of hormone
 secretion to maintain homeostasis = negative/positive - because its hormones regulate many
feedback system bodily functions – it secretes the
hormones that control the secretion of
POSITIVE FEEDBACK MECHANISM hormones by other endocrine glands
- Increasing levels of one hormone causes another - Targets tissues that includes the thyroid, adrenal
building up gland to release a hormone cortex, ovary, uterus, mammary glands, testes,
or
- Example: estradiol (female ovarian hormone) kidneys
pasaka=
secretion during the follicular stage of menstrual cycle also - Its disorders can be due to a pathological condition
stimulates the production of your FSH in the from the gland itself or to a hypothalamic
anterior pituitary gland dysfunction

ASSESS ENDOCRINE FUNCTION: ANTERIOR PITUITARY (Adenohypophysis)

The function of the endocrine gland is assessed by findings - Specifically secretes the following hormones:
from: ○ Growth hormone/somatotropin
1. Health assessment interview ○ Prolactin hormones
a. Provides subjective data ○ Thyroid-stimulating hormone (TSH)
FGTPAL
2. Physical assessment ○ Adrenocorticotropic hormone (ACTH)
a. Provides objective data ○ Follicle-stimulating hormone (FSH)
3. Diagnostic tests ○ Luteinizing hormone (LH)
a. Provides objective data
COMMON DISORDERS
*Hormones affect many body tissues and organs. - associated with hyperfunction of the anterior
Manifestations of dysfunctions are often non-specific making pituitary gland involve the growth hormone or
the assessment sometimes more difficult. somatotropin.

PART 2: 1. GIGANTISM (hyperpituitarism)

- GH hypersecretion
ENDOCRINE DISORDERS
○ Growth hormone = produced by
the cells in the anterior pituitary
Objectives: Hypo and Hyperfunction throughout life
GLAND HYPERFUNCTION HYPOFUNCTION ■ Necessary for growth
■ Contributes to metabolic
Anterior Gigantism regulations
Dwarfism
pituitary gland Acromegaly
■ Stimulates all aspects of
Posterior Syndrome of cartilage growth, growth
Diabetes insipidus
pituitary gland inappropriate ADH of epiphyseal cartilage
plates of the long bones
Thyroid gland Grave’s disease Myxedema
- Begins before puberty and the closure of
Parathyroid the epiphyseal plate
Hyperparathyroidism Hypoparathyroidism
gland - Person becomes abnormally tall, often
exceeding 213cm (6 ft 11 in)
Cushing’s syndrome
Adrenal glands Addison’s disease - Body proportions are relatively normal
Pheochromocytoma
- Example: Sultan Kösen
○ Tallest man in the world according
PITUITARY GLAND to the Guinness Book of World
Records
- Produces hormones that affect multiple body
○ Height = around 8 ft. 3 in.
systems
- Hypophysis
2. ACROMEGALY (hyperpituitarism)
- “Master gland”
- Enlarged extremities
 - GH hypersecretion begins during ● Physical examination
adulthood ○ You can literally see the physical changes
- Caused by pituitary tumors of a person with hyperfunction of GH
- Manifestation: ● Evaluation of plasma - insulin like growth factor - 1
○ Forehead enlarges (1GF-1) levels
○ Maxilla lengthens = prognantism ○ The peripheral actions of GH are mediated
○ Tongue enlarges by IGF-1
○ Voice deepens ○ As GH levels rise, so do IGF-1 levels
■ GH is released in a pulsatile
fashion, requiring several samples
to obtain an accurate measure.
Serum IGF1 levels are more
constant, providing a more
reliable diagnostic measure of
acromegaly
● Oral glucose tolerance test
● MRI - presence of tumors
○ To assess/check what causes the
Other manifestations:
hyperfunction
● Peripheral nerve damage
● Swelling of hands and feet
NURSING RESPONSIBILITIES: Post-Hypophysectomy
● Joint pains
Post-Hypophysectomy (after removal of gland)
● Headaches
● Gaps between teeth ● Elevate head of patient at all times at 30 degrees
● Barrel chest angle
● Thick and oily skin ○ To avoid pressures on the sella turrica;
● Strong body odor decreases headache
● Hypertension ● Perform mouth care
○ To keep surgical area clean; avoid tooth
SURGICAL MANAGEMENT: ACROMEGALY brushing for at least 10 days top protect
- Surgical removal or irradiation of the pituitary the suture line
tumor ● Instruct client to avoid gastric irritation
- Transsphenoidal or transfrontal surgical procedure ● Prevent infection
- Goal: to remove the tumor that causes ● Advise patient not to cough, sneeze and brush
excess of growth hormone teeth
- Disadvantage: recurrence (may need two ○ To protect suture line and to prevent CSF
operations or more) leakage
● Nasal packing (constantly check)
○ Clear nasal discharge = CSF leakage = send
discharge to the lab for glucose tests
○ If glucose level is >30 mg/dl = CSF leakage
= higher risk for meningitis
● Assess s/s for meningitis:
○ Severe headache
○ Nuchal rigidity
○ Positive Kernig’s Sign
Transsphenoidal approach: Insert endoscope and the
○ Positive Brudzinski’s Sign
curette into the nose.
● Monitor for signs of increased ICP: High BP, Low
HR, Low RR
MANAGEMENT
● History
Radiation Therapy ○ Somatropin (Omnitrope, Genotrope,
● Used when surgery has failed to produce a cure or Humatrope)
when patients are poor candidates for surgery. ■ Recombinant human GH
● Usually offered in combination with drugs that ■ Used for long term hormone
reduce GH levels. However, the full effects may not therapy in adults with GH
be noted for months to years. deficiency
● Radiation can also be used to reduce the size of a ■ Increases energy, increased lean
tumor before surgery. body mass, improved body image
● Radiation therapy may lead to hypopituitarism,
which then requires lifelong hormone replacement 2. SIMMOND’S DISEASE
therapy. - Panhypopituitarism – total absence of all
pituitary secretions
Drug Therapy - Results from surgery, infection and tumor
● Octreotide acetate (Sandostatin) = for patients with - Manifestations:
Acromegaly ○ Extreme weight loss
● a somatostatin analog that reduces GH levels to ○ Lethargy Pallor
normal in many patients. ○ Loss of libido
● given by subcutaneous injection three times a ○ Amenorrhea
week. ○ Loss of pubic and axillary hair
● Two long-acting analogs, octreotide (Sandostatin ○ Cold intolerance
LAR) and lanreotide SR (Somatuline Depot), are ○ Premature wrinkling of the skin
available as intramuscular (IM) injections given
every 4 weeks. POSTERIOR PITUITARY (Neurohypophysis)
● GH levels are measured every 2 weeks to guide - Disorders are related primarily to
drug dosing, and then every 6 months until the excessive/deficient antidiuretic hormone:
desired response is obtained. ○ Oxytocin
● Drug therapies are most commonly used in ○ Antidiuretic hormone (ADH)/ Vasopressin
patients who have had an inadequate response to - hypo/hyperfunction is commonly associated to the
surgery and/or is a combination for the radiation ADH
therapy.
HYPERFUNCTION
HYPOPITUITARISM SYNDROME OF INAPPROPRIATE ADH
- Very rare disorder - High levels of ADH in the absence of serum
- Decrease in one/more of the pituitary hormones osmolality
○ Deficiency of 1 hormone = selective - Cause: malignant tumors
hypopituitarism - Results in water intoxication or retention,
○ Total failure in the PG = deficiency in all of hyponatremia and hypo-osmolalaity
the pituitary hormones = - Normally, ADH is secreted in response to serum
panhypopituitarism osmolality.
○ hyperosmolality state = ADH secretion
1. DWARFISM (hypopituitarism) increases and renal water is absorbed
- Insufficient secretion of GH during ○ Hypo-osmolality = suppression of ADH,
childhood results in generalized limited renal water excretion increases
growth - SIADH “Soaked Inside”
- Usually caused by a tumor

MANAGEMENT (of the hypofunction)

● Surgery
● Radiation therapy
● Hormone therapy
 HYPOFUNCTION
DIABETES INSIPIDUS
- A result of ADH deficiency
- Results in the inability to conserve water, thus
excreting large amounts of fluids (permeability of
water is diminished)
- Types:
○ Neurogenic
- Results from disruption of the
hypothalamus and pituitary gland
(trauma, radiation, surgery)
MANIFESTATIONS: ○ Nephrogenic
● Brain cells swell - Renal tubules are not sensitive to
● Signs of fluid overload (d/t too much water inside ADH and does not absorb water,
body) result of renal failure
● Changes in LOC and mental status changes
○ d/t swelling in the brain cells = neurological
s/s: headache, changes in mental status,
lethargy, irritability
● Weight gain without edema
○ d/t retention of the fluid
○ Edema is not present because water is
distributed between the intracellular and
extracellular spaces
● Hypertension
● Tachycardia, tachypnea, rales
● Anorexia, nausea and vomiting
MANIFESTATIONS
● Dilutional hyponatremia
● Polyuria (excreting large amounts of urine as much
*Manifestations occur bc of excess in water in the body
as 12L/day)
● Polydipsia (extreme thirst; drinks large amounts of
MANAGEMENT
water)
● Restore normal fluid volume
● Dehydration (when water loss is not replaced)
● Water restriction = prevents further hemodilution
● Decreased skin turgor, dry mucous membranes
(increased water in the plasma); less than 800 mL
● Inability to concentrate urine, low urinary specific
per day
gravity
● Give hypertonic IV solution (D5.33% NaCl)
● Weight loss
● Give ice chips (bc there is water restriction)
● Hypernatremia (too much salt)
● Increase sodium (bc you have hyponatremia) and
potassium in the diet
*If deficiency is caused by a cerebral injury, s/s commonly
● Monitor for patient’s safety (since there are
appears 3-6 days after the injury and it lasts 7-10 days. If
neurologic and LOC changes)
the ICP is relieved = symptoms also disappear
● Promote diuresis: Furosemide (Lasix),
Demeclocycline (Declomycin)
Diagnostic Test
○ Demeclocycline - tetracycline antibiotic
● Water Deprivation Test (POSITIVE)
with a unique property of creating
○ The patient is deprived of water for 8 to 12
excessive urine flow\
hours,
○ then given desmopressin acetate (DDAVP)
TREATMENT OF SIADH: Geared towards addressing the
subcutaneously or nasally.
low serum sodium, swelling and excess of water
 ○ Patients with central DI exhibit a dramatic - Primary function of the thyroid hormone: increase
increase in urine osmolality, from 100 to metabolism and protein synthesis
600 mOsm/kg, and a significant decrease - Hyperthyroidism = may have problems like
in urine volume. The patient with increased basal metabolism, weight loss,
nephrogenic DI (kidneys has a problem) lipids are depleted and glucose tolerance
will not be able to increase urine are decreased
osmolality to greater than 300 mOsm/kg.
MANIFESTATIONS:
MANAGEMENT ● Goiter- enlarged diffuse thyroid gland
● Monitor vital signs and neurological and ○ Can also be present in both iodine
cardiovascular status deficiency and excess
● Monitor fluid and electrolyte balance ○ Means that goiter can also be manifested
● Monitor intake and output, weight in patients with hypothyroidism
○ 1kg in excess would also mean 1kg addition ● Proptosis- forward displacement of the eyes
to the weight of the patient ● Exophthalmos- forward protrusion of the eyes
● Maintain intake of adequate liquids ○ Common ophthalmology of Grave’s
● Instruct client to avoid foods or liquids with a Disease is the proptosis and there are also
diuretic type action (we don’t want to increase further visual dysfunctions
the large amount of urine being excreted) ○ Exophthalmos can also result from an
● Administer Desmopressin acetate (Stimate) = DOC accumulation of inflammation of the by
for diabetes insipidus products of in the retro-orbital tissue
○ Causes increased water reabsorption ■ Because there is compression and
stretching of the optic nerve=
THYROID GLAND
blurry vision, diplopia, eye pain ,
- Alterations of this gland is the most common in the lacrimation, and photophobia
endocrine disorder ■ If eyes cannot fully close = eye
- T3 and T4 regulates metabolism growth and dryness
development ● Extremely agitated and irritable individual
- Thyroid uses iodine to secrete the thyroid hormone ● Hand tremors at rest
because some of this hypersecretion and ● Ravenous (big) appetite with weight loss
hypofunction involves deficiency or excess of ● “Speed up” bodily processes (there is increased
iodine bowel motility)
- Thyroid hormone is vital in development and ● Loose bowel movements
maintenance of brain function in other organ ● Heat intolerance
systems ● palpitations
- Example of the hyperfunction of the thyroid gland ● Profuse diaphoresis (perspiration)
= Grave’s’ disease ● Tachycardia
● Incoordination
GRAVES DISEASE ● Moods (cyclic)
- The most common cause of hyperthyroidism *these manifestations are associated with hypermetabolism
- Also referred to as Toxic diffuse goiter and
thyrotoxicosis COMPLICATION: THYROID CRISIS
- Means that it is caused by the excessive - Also called as thyroid storm
functional activity of the thyroid gland. - Extreme state of hyperthyroidism
- Caused by an autoimmune disorder mediated by - Due to untreated hyperthyroidism
immunoglobulin G (IgG)antibody that binds to and - Potentially fatal acute episode of thyroid
activates TSH receptors on the surface of the overactivity characterized by high fever, severe
thyroid cells. tachycardia, delirium, dehydration, and extreme
- Remember: primary fxn of the thyroid gland to irritability.
relate and associate it immediately - Mortality is very high
 - Rapid treatment is necessary to preserve life of the ○ The results can occur in 6-8 weeks and if
patient the woman of childbearing age should
undergo radioactive iodine therapy, they
MANAGEMENT OF HYPERTHYROIDISM: should delay becoming pregnant for 6
● Nutritional status - high calorie, high protein foods, months; and 4 months for men for sperm
well balanced meals turnover production
○ Remember: with hyperthyroidism,
Metabolism is increasing (overmetabolism) SURGERY
● Coping measures- decrease stressful situations ● Thyroidectomy
○ Stress increases circulating catecholamines ○ Removal of the thyroid gland
which further increases or aggravates ○ Recommended when other treatments are
problem not effective or when the nodule is too
● Improve self-esteem (exophthalmos) large that there is obstructive symptoms
○ Due to physical changes ■ Eg: pressure in the esophagus or
● Maintain normal body temp (heat intolerance) trachea that causes breathing or
● Manage potential complications swallowing problems
○ Subtotal - leaves enough portions of the
MEDICATIONS: gland to produce adequate amounts of TH
● ANTITHYROID MEDICATIONS ○ Total - complete removal of the entire
inh conversion of t4 into
active t3
○ Recommended for clients younger that 18 gland, requiring lifelong hormone
cons: high risk for injury years of age and for pregnant women replacement
to liver= may cause liver
○ Propylthiouracil (PTU)
failure
carefully use PTU ○ Methimazole (Tapazole) Pre-operative :
● ADJUNCTIVE THERAPY ● Client must be euthyroid before the operation
○ Iodine therapy ○ Euthyroid: normal as possible; state of the
iodine: block release of
■ To reduce the vascularity of the thyroid gland is as normal as possible
t4 thyroid gland before ● Administration of antithyroid medications and
beta blockers: thyroidectomy (preparation) and iodine preparations
antagonize peripheral
effects (propanolol, to treat thyroid storm ○ Prior to surgery to be on the euthyroid
atenolol) ■ Choice: saturated solution of state
potassium iodide (SSKI) ○ Help out decrease the vascularity and size
■ Iodine preparations are usually of the gland which reduces the risk of
given only for 10-14 days before hemorrhage during and after the surgery
surgery ● Client should be adequately rested, at optimal
○ Propranolol weight and in good health
■ Control nervousness, tachycardia, ● Preparation may take as long as 2-3 months
tremor, anxiety, heat intolerance
● RADIOACTIVE IODINE THERAPY Postoperative:
○ Thyroid gland takes up iodine in any form ● Maintain patent airway and observe for respiratory
○ Prescribed mainly for middle aged and distress
older clients ○ Result from hemorrhage or edema that
○ Administration of the radioisotope can compress the trachea
iodine-131 ● Check hemorrhage - assess dressing, check neck
■ Concentrates in the thyroid gland area
Damages and destroys the ● Semi-fowlers position- decreases neck strain on
thyroid cells the suture line
○ After receiving the radioiodine, client may ● Assess for laryngeal nerve damage
go home unless the dosage is extremely ○ One of the potential complications =
large and would require isolation for hoarseness of the voice (normal post op
several days.
 since there is edema but if permanent = ● Hair loss, brittle nails, dry skin
laryngeal nerve damage) ● Numbness and tingling of the fingers
● Assess for tetany - chvostek’s and trousseau's sign ● Husky and hoarseness of voice
○ The surgery can also decrease the ● Menstrual disturbances = menorrhagia or
circulating calcium levels amenorrhea
○ Check thru two signs chvostek and ● Decreased libido
trousseau ● Weight gain even without increase in food intake
● Expressionless and mask-like face
HYPOTHYROIDISM ● Cold intolerance (opposite with hyper)
- Disorder that results when the thyroid gland
produces insufficient amount of thyroid hormone MEDICATIONS:
- Causes generally slowing of the metabolic rate ● Thyroxine, T4 (levothyroxine)
- Manifestation is associated with slowing of ○ Preferred therapy
metabolic rate ○ Monitor heart rate and report pulse greater
- Hypothyroid state: than 100bpm or an irregular heartbeat
○ Myxedema - adults ○ In pxn with no side effects: dose increased
○ cretinism- children in 4-6 weeks interval or it may take 8
weeks before the full effect of the
MYXEDEMA (adults) hormone therapy is seen
- Hypothyroid state in adults ■ Nurses must let client understand
- Causes: undiagnosed or undertreated to take medication regularly
hypothyroidism with stress MANAGEMENT:
- Alters the physical appearance of skin and ● Modifying activity
subcutaneous tissue with puffiness, facial and ○ Assist with care and hygiene
periorbital edema and mask like face. ○ Encourage participation in activities as
- Characterized by a dry, waxy type of swelling with tolerated
abnormal deposits of mucin in the skin and other ● Monitoring physical status (v/s, cognitive level)
tissues ● Promoting physical comfort-extra clothing, blanket,
- Edema is non pitting type and is common in the avoid heating pads and electric blankets
pretibial and facial areas ○ Because they are prone to burns d/t their
- Severe state: myxedema coma cold intolerance
- Life threatening complications of ● Enhance coping measures
untreated hypothyroidism
- Precipitated by: infections, exposure to
PARATHYROID GLAND
colds or certain meds like opioids ,
barbiturates, tranquilizers or trauma - Are not as common as those in the thyroid gland
- Parathyroid hormones help regulate serum calcium
and phosphate levels by
- stimulating bone resorption of calcium,
- renal tubular reabsorption of calcium and
- activation of vitamin D

HYPERPARATHYROIDISM
- Results form increase in the secretion of the PTH
- PTH regulates serum calcium and phosphate levels
- Characterized by done decalcification and the
development of renal calculi (kidney stones)
MANIFESTATIONS:
containing calcium
● Hypercholesterolemia
● Hyperlipidemia = atherosclerosis
MANIFESTATION:
● Extreme fatigue
 ●Skeletal - With that there is reabsorption of
○ Bone and joint pain phosphate that is increased =
○ Backache hyperphosphatemia
○ Pathologic fractures of the spine, ribs and - Low calcium levels = changes in
long bones neuromuscular activity
■ Because bones are giving off too
much calcium MANIFESTATIONS:
○ Deformity and bending of the bones ● Increased neuromuscular irritability which results to
● Renal tetany
○ Polyuria and polydipsia ● Painful muscle spasms, irritability, grimacing,
○ Appearance of sand, gravel and stones in tingling of the fingers, laryngospasms,
the urine increased BUN, CREA since kidneys can’t get rid of dysrhythmias
nitrogenous
○ Azotemia waste ● Positive chvostek’s sign and trousseau's signs
○ Hypertension d/t renal damage ○ To check (chvosteks): tap on masseter
muscles in the cheek = client will twitch its
MANAGEMENT: muscles in the cheek
● Lower severely elevated calcium levels
○ Hydration
○ Low calcium and low vit D diet
○ Furosemide (lasix)-excrete excess calcium
levels thru kidneys or urine
● Fluid intake of 2000ml or more
○ Prevents calculus/kidney stones formation
● Mobility is encouraged for bones to give up less
calcium ○ Trousseau's sign: inflate BP cuff for at least
● Surgical: parathyroidectomy 3 mins = flexion in hand/extremity =
positive
COMPLICATION: HYPERCALCEMIC CRISIS
● Serum calcium levels >15 mg/dl
● Result in neurologic, cardiovascular, renal
symptoms
● Can be life threatening
● Emergency: given calcitonin and corticosteroids
○ Calcitonin: regulates calcium levels in the
body by preventing bone resorption and
increasing calcium excretion in the kidneys
○ Corticosteroids: reduces serum calcium ● Hyperactive deep tendon reflexes
concentration by reducing intestinal ● Circumoralparesthesia- numbness and tingling
calcium absorption sensation around the mouth

HYPOPARATHYROIDISM MANAGEMENT:
- Serum calcium levels are abnormally low, serum Goal: increase calcium levels
phosphate levels are abnormally high, and ● DRUG THERAPY
pronounced neuromuscular irritability (tetany) may ○ IV calcium gluconate
develop ○ Oral calcium replacement (calcium
- Due to reduced PTH, ability to reabsorb gluconate, lactate, carbonate)
calcium from bones and to regulate ■ Goal: increase calcium levels
calcium reabsorption from renal tubules is ○ Vitamin D (ergocalciferol) = enhance Ca
also impaired absorption from the GI tract
○ Parenteral PTH
 ● Diet: High calcium, low phosphate diet ○ Glucocorticoid excess also inhibits
fibroblast resulting in loss of collagen and
connective tissue = thinning of the skin,
ADRENAL GLAND
abnormal striae/stretch marks
- Has the medulla and the cortex ● Ecchymoses (bruises) and striae develop
- Secretes catecholamines like the epinephrine, ○ Easy bruising
norepinephrine, the fight and flight response ● Weakness and lassitude
- Catecholamines: regulate metabolic pathways w/c ● Disturbed sleeping pattern
is responsible for catabolism for us to meet our ● Musculoskeletal changes with glucose intolerance
caloric needs ● Moon-faced appearance
- Helps in basal metabolic rate and blood glucose ● Excessive growth of hair in the face
levels ● Mood swings and personality changes
● Poor wound healing
● Sodium and water retention-hypertension
● Hyperglycemia

DIAGNOSTICS:
● Increased plasma cortisol level
● Increased serum sodium and blood glucose levels
● Decreased serum potassium
● 24 hour urine collection for free cortisol

MEDICATIONS:
CUSHING’S SYNDROME ● Adjunct therapy to radiation or surgery
- Hyperfunction of adrenal gland ● Given to control the symptoms, they do not effect
- Results form overactivity of the adrenal gland, a cure
specifically in the cortex with consequent ● Mitotane
hypersecretion of glucocorticoids ● Metyrapone
- Occurs mainly in women 20-40 years old ○ Adrenal enzyme inhibitor
- Causes: ○ Suppresses activity of the adrenal cortex
○ Use of corticosteroid medications and decreases peripheral metabolism of
○ Excessive corticosteroid production corticosteroids
(tumor) SURGERY:
● Adrenalectomy
MANIFESTATIONS: ○ Indicated if caused by adrenal cortex
Seen in most body systems related to excess levels of tumor
corticosteroids though they can also exhibit symptoms of ○ Adrenal cortex is removed
excess mineralocorticoids and androgen excess, causing ● Hypophysectomy
pronounced changes in physical appearance ○ Removal of the pituitary gland
● Central-type obesity = fatty buffalo hump ○ Indicated if the disease is caused by a
○ Excess cortisol results in the redistribution pituitary disorder
of body fat deposits in the abdominal
region = central obesity MANAGEMENT:
○ Fat pads under clavicle; buffalo hump and ● Decrease risk for injury (weak patients)
moon face ○ Assist in ambulation
● Skin is thin, fragile and easily traumatized ○ Protective environment
○ Change in skin protein ● Frequently assess for signs of infection
metabolism=peripheral muscle weakness ● Encourage rest and activity
and wasting ● Promote skin integrity = avoid adhesive tapes
● Improve body image
 ● Verbalization of feelings and concerns ○ severe, penetrating pain in the abdomen,
lower back, and legs
ADDISON’S DISEASE ○ severe vomiting
- Destruction or dysfunction of the adrenal cortex ○ Diarrhea
- Chronic deficiency of cortisol, aldosterone and ○ hypotension
adrenal androgens accompanied by skin ○ circulatory collapse, shock seizures and
pigmentation coma
- Absent steroids low (small weak and tanned g/t
skin pigmentations) DRUG THERAPY:
● Hydrocortisone (solu-cortef)
MANIFESTATIONS: ○ To replace cortisol
Primary manifestations are results of elevated ACTH levels ● Fludrocortisone (Florinef)
and decreased aldosterone and cortisol ○ To replace mineralocorticoids
● Prednisone (Deltasone)
Aldosterone deficiency affects the ability of the distal ● 5% dextrose in normal saline
tubules to conserve sodium = sodium loss and potassium is ● Vasopressor amines (for persistent hypotension)
retained = Extracellular fluid is depleted and blood vol is ● Lifelong replacement of corticosteroids &
decreased = hyponatremia and hyperkalemia mineralocorticoids (for damaged adrenal glands)

● Postural hypotension and syncope MANAGEMENT:

● Decrease in blood glucose (hypoglycemia) ● BP, PR monitoring
○ Cortisol insufficiency= decreased hepatic ● Assess for weight changes, muscle weakness,
glucogenesis = hypogly fatigue
● Muscle weakness ● Avoid physical and psychological stressors
● Hyponatremia ● Assess pt’s skin turgor and mucous membranes
○ Cause dizziness, confusion, irritability, ● Encourage food and fluids (for electrolyte balance)
neuromuscular irritability ● Quiet, non stressful environment
● Hyperkalemia (since potassium is retained) ● Perform all activities for the patient during an acute
○ Cause cardiac arrhythmias crisis
● Stress, lethargy weakness anorexia nausea
vomiting diarrhea PHEOCHROMOCYTOMA
● Dark pigmentation of the mucous membranes and ● Rare condition
skin d/t increased ACTH ● Caused by a tumor in adrenal medulla; usually
benign and originates from the chromaffin cells of
COMPLICATION: ADDISONIAN CRISIS the adrenal medulla
● Is a life-threatening response to acute adrenal ● Results in an excess production of catecholamines
insufficiency (epinephrine, norepinephrine)
● Triggers include surgery, acute systemic illness, ● One form of hypertension that is cured by surgery
trauma or abrupt withdrawal of long-term ● Most dangerous effects: peripheral
corticosteroid therapy vasoconstriction and increased cardiac rate and
○ Corticosteroid therapy: do not abruptly contractility with resultant paroxysmal
stop taking the medications hypertension (unpredictable)
● Slight overexertion, exposure to cold, acute ● Tends to have a sudden release of hormones which
infection or a decrease in salt intake may lead to cause a sudden attack of symptoms that last for a
circulatory collapse, shock, and death if untreated. few seconds or to several hours
● Manifestation: cyanosis, classic signs of circulatory ○ Attacks are often precipitated by physical,
shock emotional or environmental stimuli and
○ a high fever are unpredictable
○ weakness
MANIFESTATIONS: - Pituitary gland = master gland, responsible for
● Hypertension (reach 250/150mmhg) releasing many hormones; get stimulus from the
● Triad of symptoms hypothalamus
○ Headache ○ Posterior = oxytocin (uterine contraction,
○ Diaphoresis milk ejection); ADH (vasopressin) -
○ Palpitations kidneys, stops urination
● Five H’s ○ Anterior = prolactin (milk production)
○ Hypertension
○ Headache ADH IMBALANCES
○ Hyperhidrosis - SIADH
○ Hypermetabolism ○ Hypersecretion
○ Hyperglycemia ○ SI = “yes” = yes there’s ADH (too much)
- DI dry inside → you can pee 4-20 liters a day
DIAGNOSTIC ○ Diuresis = make urine? You pee out
● Increased catecholamines in the blood or urine ○ Less amount of ADH = pee more
● 24 hours urine test ○ Desmopressin acetate - an anti-diuretic
○ Catecholamine secretions are episodic = hormone replacement; to increase ADH or
24 hour collection for better surveillance vasopressin
method - Normal body mechanism:
Decreased blood volume → ADH
SURGERY: ADRENALECTOMY is released for salts to reabsorb
water → increased blood pressure
DRUG THERAPY: - Posterior pituitary is like an extension of the
● Phentolamine (regitine) hypothalamus
● Sodium nitroprusside (nipride) ○ How do they communicate? Directly
● Phenoxybenzamine (dibenzyline) signals posterior PG via nerve fibers
● Propranolol (inderal) ○ Not necessary that a hormone is being
carried unlike anterior PG
○ Example: a person is about give birth;
DISCUSSION NOTES (MDM. TIONGCO) hypothalamus signals posterior PG to
release oxytocin = uterine contractions
ENDOCRINE SYSTEM ○ With ADH, if the body has less blood
- works like the nervous system volume = release ADH so that the body
○ N.S. works immediately can increase blood volume by
- Hypothalamic pituitary system = systems work reabsorption of salt = where salt goes,
together to maintain homeostasis water follows = increase blood volume and
○ Ex: when serum levels are low BP
- To know the hypo and hyper function of conditions - Anterior PG - hormones travel via the blood vessel
in the endocrine system, one should know the ○ Hypothalamus release 5 major hormones
function of the gland and hormones (thyrotropic, corticotropic, growth,
released/secreted. prolactin and gonadotropin) which goes to
- Hypothalamus = NOT considered as the master anterior PG and will release specific
gland; control center only hormones
○ Is as important as pituitary gland - Ex: Thyrotropic RH released from
○ Release the regulatory hormones the hypothalamus will signal the
(releasing hormones and the release of TSH = go to the thyroid
releasing-inhibiting hormones) gland = release of T4 and T3 =
○ Connected to the pituitary gland important in metabolism,
development & catecholamine
release
 - Catecholamine = responsible for - Adrenal cortex - cortisol = increase blood glucose,
fight/flight response: epinephrine decrease immune system
& norepinephrine + dopamine? ○ Corticosteroids = person gains weight
(also released by adrenal medulla) (hyperfunction of the cortex)
- Key function: increases ○ Aldosterone/mineralocorticoids = key
metabolism player w/ reabsorption of salt = increasing
- Thyroid gland also releases BP and blood volume = RAAS
calcitonin = helps regulate calcium ○ Vital signs shoots up d/t fight & flight
with parathyroid hormones response
- Calcitonin - decreases calcium - Adrenal medulla = catecholamines:
levels epi/norepinephrine (adrenaline & noradrenaline)
- Ex: problems w/ - hyper/hypofunction of the cortex involves cortisol
hypercalcemia = and aldosterone + sex hormones (androgens) ?
calcitonin brings that
down Growth RH
- Parathyroid - increases serum - Stimulates anterior PG to release growth hormone
calcium levels in body for growth
- Hypocalcemia - To promote growth and increase protein synthesis
THYROID GLAND - Hyperfunction: Gigantism and acromegaly
- Toxic diffuse goiter ○ Gigantism: body growth is proportional
- Grave’s disease = GRAVE metabolism - Example: Kosen - height beyond
(hyperthyroidism) 6 ft
- Autoimmune = own cells attack the body ○ Acromegaly: starts during adulthood where
- Presence of an antibody TSH that mimics there is already epiphyseal closure of long
real TSH = overstimulates thyroid gland = bones
more T4, T3, calcitonin - Instead of elongation, growth
- Very fast metabolism = lose weight happens palapad (width)
- Manifestations: - Problems with head enlargement
- Weight loss even if they have a - Appearance really changes
very big appetite - Protrusion of maxillary bone =
- Speed up bodily processes = prognathism
increased bowel movements = - Hand enlargement
diarrhea - Hoarseness of voice d/t
- Heat intolerant (easily heats up = enlargement of larynx
profuse sweating = irritable - Hypofunction
- Thyroidectomy = removal of thyroid gland ○ Dwarfism: deficient GH
- May need lifelong replacement - May need replacement hormonal
therapy therapy
- Hypothyroidism - Done until they have a
- Gain weight even if there is no increase in desired body mass or a
food intake certain height
- Very slow metabolism = not enough Prolactin RH
energy - Milk production
- Weight gain
- Cold intolerance Gonadotropin RH
- Menstrual cycle
Corticotropic RH - Where LH and FSH are released
- Responsible for stimulating anterior PG to release - Women
the adrenocorticotropic hormone (2) - LH: high = ovulation = release of
progesterone; if egg is released already ?
 - FSH: follicle maturation = egg is matured - HYPOTHYROIDISM: encourage the patient to eat
and about to be released; levels of foods high in iodine like seafoods
estrogen in the phase of cycle - Goiter is a manifestation of both
- Men: hypo/hyperthyroidism
- LH: sperm production; testosterone - Slowed metabolism, constipation, slow
- FSH: sertoli cells; for sperm production HR, extremely tired

PARATHYROID CUSHING’S SYNDROME

- Situated the same as the thyroid - Key players: adrenal cortex, cortisols, aldosterone
- Works together with calcitonin - Aldosterone helps balance water (RAAS system)
- Homeostasis of calcium - “Cushion”
- Renin: increase BP and blood volume; released in - Increased secretions of cortisol = fatty
kidney; works together with aldosterone; redistributions around the belly
responsible for activation of RAAS ○ truncal obesity
- Erythropoietin: increasing RBC production ○ dorsocervical fat pad or buffalo hump
- Pancreas: ○ moon/round face
- Has an endo/exocrine function ○ elevated BP
○ Endo: produce hormones like
insulin and glucagon ADDISON’S DISEASE
- Insulin = decrease glucose - Key players: decrease in cortisol
- Glucagon: increase glucose levels; release - Very tired and very weak
blood glucose if hypoglycemic - Low BP
- Hypercalcemia = Increased calcium levels - Hallmark: increased pigmentation of the skin =
○ Spasms sun-tanned/dark skin
○ Kidney stones - Sodium and sugar are low d/t low glucocorticoids =
○ Prone to fractures helps metabolize carbohydrate by regulating
- Hypocalcemia = Hypoparathyroidism glucose use
(deficient calcium levels)
○ Muscle spasms SIADH
○ Chvostek signs - Too much ADH = signals to conserve water
- Signs for tetany - Manifestations: fluid overload = peeing less = very
- Tap the cheek of the concentrated urine = high specific gravity
patient and it will twitch - What happens if there is too much water inside?
○ Trousseau sign - Brain is very sensitive to amount of water
- Inflate a BP cuff on a in the body
patient’s arm for 3-5 - Brain cells will swell (brain swelling) =
mins = elicit flexion of the confusion, changes in LOC
arm - High BP, edema, increases blood volume
- Weight gain d/t fluid overload
Thyroid - highly dependent on the iodine supply - Serum sodium = hyponatremia = diluted
- HYPERTHYROIDISM mgmt: radioisotope iodine (no change in the levels but it becomes
- Why given radioactive iodine? It will diluted d/t too much water in the body)
destroy the thyroid; “murag spy” - Lose 1kg = loss of 1000ml
- Thyroid gland accepts whatever kind of - Strict NIO ?
iodine - even a radioactive iodine - Restrict food that promote diuresis
- Replace thyroid w/ medications like - Watermelon
synthroid - Lemon
- Myxedema = weight gain
- Grave’s disease DIABETES INSIPIDUS
- Hyposecretion of ADH
- Dry inside body
- Not enough water inside
- Amounts of serum sodium is very concentrated =
hypernatremia
- Urine is very diluted, low specific gravity
- Hypotension, low BP, low blood volume
- Patient will be craving water or ice chips d/t dry
inside body = thirst mechanism
- Manifestations:
- Polydipsia, polyuria
- Dry mucous membranes = skin very dry
- Signs of dehydration
- Eat food w/ less sodium
- Desmopressin
- ADH replacement
- DOC
- Indicated for extreme cases
- Mgmt: watch out for signs for
hyponatremia (effect of the med)
- Watch out for vital signs (patient
may not have
ADDITIONAL: