NCM 116 Midterm Lecture: Endocrine System

Irish Porras 3C | 2nd Sem |’24-‘25

ENDOCRINE SYSTEM onecessary for gametogenesis and sex

steroids production in males and
 one of the body’s most complex systems females.
 it affects functions of the different organs / E. Adrenocorticotropic hormones (ACTH) on
system Adrenocorticotropin
 it is interrelated with functions of the nervous o it regulates functions of the adrenal
system, to coordinate body processes. glands
 An alterations in function of the endocrine F. Melanocytes - stimulating hormone (MSH)
system results in variety of physiologic changes , o necessary for pigmentation like the skin,
which may vary from serious to fatal. retina.
 the end result of most pathologic, process
affecting the endocrine system is Posterior Pituitary Gland
hypersecretion or hyposecretion of hormones
A. Antidiuretic hormone (ADH) - also known as
 one of the most serious endocrine disorders is
vasopressin
diabetes mellitus (A global problem)
o the major control of osmolality
o the disease is irreversible, that causes
(concentration) and body waste volume
many life - threatening complications
o increases water reabsorption in the
that affects The brain, heart, kidneys,
collecting ducts of the kidneys.
eyes and many more organs.
B. Oxytocin
Pituitary Glands o produces milk let down in a lactating
breast
 lies in the sella turcica of the middle cranial o increased uterine contraction after
fossa( the bony floor that supports the brain) labor has begun.
 Composed of Anterior pituitary gland
Thyroid Gland
(andrenohyphesis) and Posterior pituitary
gland.
A. Triiodothyronine ( T 3) and Thyroxine (T4)
 The hypothalamus controls both the anterior
o regulate metabolic rate of cells
and posterior pituitary glands.
o Regulates protein, fat and carbohydrate
metabolism
Anterior Pituitary Gland
o Acts as insulin antagonist
A. Growth Hormone (GH) also known as o Maintain growth hormone secretion
somatotropin or somatotropic hormone (STH) and promote skeletal maturations
o for growth of cells , bones and soft o Affect central nervous system
tissues development
o it affects carbohydrates and fat o Affect cardiac rate, force and output
metabolism o Affect oxygen utilization
o it increases blood glucose level by o Stimulate lipid turnover, free fatty acid
reducing glucose utilization an insulin release and cholesterol synthesis
antagonist o Stimulates sympathetic nervous system
B. Prolactin [ PRL) also known as mammotropic activity
hormone, lactotropic hormone, luteotropic B. Thyrocalcitonin ( Calcitonin)
hormone. o It lowers calcium level
o necessary for breast development and o Inhibits osteoclastic activity
lactation o Lowers phosphate levels
o regulates reproductive function in both o Decreases calcium and phosphorus
males and females absorption in the GI tract.
C. Thyroid-Stimulating Hormones  The relationship between thyrocalcitonin and
o controls function of the thyroid glands calcitonin ( Inverse)
D. Gonadotropic Hormone or Gonadotropin  Thyrocalcitonin (HIGH)=Calcium (LOW)
o 2 gonadotropin  Thyrocalcitonin (LOW)=Calcium (HIGH)
 follicle- stimulating hormone
FSH Cushing’s Syndrome
 luteinizing hormone (LH)
 Hypersecretion of corticoids.
o affects the development of secondary
 results from excessive rather than deficient
SEX characteristics.
adrenocortical activity.
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

 The syndrome may result from excessive  Pendulous abdomen, purple striae, easy
administration of corticosteroids or ACTH or bruising
from hyperplasia of the adrenal cortex.  Moon face, acne, hyperpigmentation,
impotence
Clinical Manifestations
 Virilization in women: hirsutism, breast atrophy,
amenorrhea
 Central type obesity (buffalo hump) in the neck
 Pathologic fractures reduced height
and supraclavicular areas
 Slow wound healing
 Thin extremities
 Hypernatremia, hyperglycemia, hypokalemia
 The skin is thin and fragile and easily
traumatized Medical Management
 Ecchymosis
 Weakness and lassitude  Directed at the pituitary gland if pituitary tumor
 Sleep is disturbed because of altered diurnal is the caused
secretion of cortisol  Surgical removal of the tumor
 Osteoporosis (khyposis, back ache and  Radiation of the pituitary gland
compression fractures)  Adrenalectomy is the treatment of choice in
 “Moon-faced” appearance patients with primary adrenal hypertrophy
 Adrenal enzyme inhibitors (use to reduce
hyperadrenalism)
 Reduce or taper of corticosteroids (if cushing
syndrome is caused by too much administration
of corticosteroids)

Nursing Management

1. Promote comfort: protect from trauma.

2. Prevent complications: monitor fluid balance,
glucose metabolism, hypertension, infection.
3. Health teachings:
a. Diet: increased protein, potassium,
decreased calories, sodium
b. Meds:
o Cytoxic agents:
aminoglutethimide (Cytaden),
trilostane (Modrastane),
mitotane (Lysodren)- to
Diagnosis Findings decrease cortisol production.
o Replacement hormones as
 increase in serum sodium and blood glucose needed.
level c. S/Sx of progression of disease.
 decrease concentration of serum potassium d. Prepare client for adrenalectomy.
 reduction in number of eosinophil
 Blood sample (plasma level and diurnal DISORDERS OF THYROID GLAND
variation)
Hypothyroidism (Myxedema)
Assessment
 results from suboptimal levels of thyroid
Subjective hormone.
 Hypothyroid state resulting from hyposecretion
 headache, backache, weakness, decreased work
of thyroid hormones and the T4 is low and the
capacity
TSH is elevated.
Objective  In primary hypothyroidism, the source of
dysfunction is the thyroid gland and the thyroid
 Hypertension, weight gain, pitting edema cannot produce the necessary amount of
 Characteristic fat deposits, truncal & cervical hormones.
obesity (buffalo hump).
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

 In secondary hypothyroidism, the thyroid is not  Voice may become husky

being stimulated by the pituitary to produce  Hoarseness
hormones.  Menstrual disturbance may occur (menorrhagia
 Hypothyroidism may result from: and menorrhea)
o thyroidectomy  Loss of libido
o radiation therapy  slow speech
o chronic autoimmune thyroiditis  decreasing mental stability
(Hashimoto’s disease)
o inflammatory conditions, such as Myxedema Coma
amyloidosis and sarcoidosis
o pituitary failure to produce TSH  is a medical emergency that commonly has a
o hypothalamic failure to produce fatal outcome.
thyrotropin- releasing hormone (TRH)  Progression is usually gradual, but when stress
o inborn errors in thyroid hormone aggravates severe or prolonged hypothyroidism,
synthesis coma may develop abruptly
o inability to synthesize thyroid hormone  Examples of severe stress are infection,
because of iodine deficiency (usually exposure to colds, and trauma.
dietary)  Other precipitating factors include thyroid
o use of antithyroid medications such as medication withdrawal and the use of sedatives,
PTU. narcotics, or anesthetics.
o Autoimmune thyroiditis (Hashimoto’s  This rare but serious disorder results from
disease) most common cause of persistently low thyroid production.
hypothyroidism in adults.  Coma can be precipitated by acute illness, rapid
withdrawal of thyroid medication, anesthesia
Pathophysiology
and surgery, hypothermia, or the use of
sedatives and opioid analgesics.
 In primary hypothyroidism, a decrease in
thyroid hormone production is a result of the Assessment
loss of thyroid tissue. This results in an
increased secretion of TSH that leads to a goiter.  Hypotension
 In secondary hypothyroidism, typically the  Bradycardia
pituitary fails to synthesize or secrete adequate  Hypothermia
amounts of TSH, or target tissues fail to respond  Hyponatremia
to normal blood levels of thyroid hormone.  Hypoglycemia
 Either type may progress to myxedema, which  Generalized edema
is clinically more severe and considered a  Respiratory failure
medical emergency.  Coma
Clinical Manifestations Interventions

 Extreme fatigue  Monitor vital signs, including heart rate and

 Hair loss rhythm.
 Brittle nails  Maintain a patent airway.
 Weakness, muscle aches, Paresthesias  Institute aspiration precautions.
 Intolerance to cold  Administer IV fluids (normal or hypertonic
 Weight gain saline) as prescribed.
 Dry skin and hair and loss of body hair  Administer levothyroxine sodium intravenously
 Bradycardia as prescribed
 Constipation  Administer thyroid replacement; levothyroxine
 Generalized puffiness and edema around the sodium is most commonly prescribed.
eyes and face (myxedema)  Instruct the client about thyroid replacement
 Forgetfulness and loss of memory therapy and the clinical manifestations of both
 Menstrual disturbances hypothyroidism and hyperthyroidism related to
 Goiter may or may not be present (enlarged under replacement or over replacement of the
thyroid gland) hormone.
 Cardiac enlargement, tendency to develop  Administer glucose intravenously as prescribed.
heart failure  Administer corticosteroids as prescribed.
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

 Assess the client’s temperature hourly.  The TSH level increases with primary
 Monitor blood pressure frequently. hypothyroidism and decreases in secondary
 Keep the client warm. hypothyroidism. The TRH level is decreased in
 Monitor for changes in mental status. hypothalamic insufficiency.
 Monitor electrolyte and glucose levels  Serum cholesterol, carotene, alkaline
 Instruct the client in a low-calorie, phosphatase, and triglyceride levels are
lowcholesterol, low–saturated fat diet; discuss a increased.
daily exercise program such as walking.  In myxedema coma
 Assess the client for constipation; provide o laboratory tests may also show low
roughage and fluids to prevent constipation. serum sodium levels and decreased pH
 Provide a warm environment for the client. and increased partial pressure of carbon
 Avoid sedatives and opioid analgesics because dioxide in arterial blood, indicating
of increased sensitivity to these medications; respiratory acidosis.
may precipitate myxedema coma.
 Monitor for overdose of thyroid medications,
characterized by tachycardia, chest pain,
restlessness, nervousness, and insomnia.
 Instruct the client to report episodes of chest
pain or other signs of overdose immediately
 Monitor arterial blood gas measurements to
detect hypoxia and metabolic acidosis.
 Warm the patient by wrapping her in blankets.
Don’t use a warming blanket because it might
increase peripheral vasodilation, causing shock.
 Monitor the patient’s body temperature until
stable with a low-reading thermometer
How it’s treated
 Replace thyroid hormone by administering large
I.V. levothyroxine doses as ordered.  Therapy for hypothyroidism consists of gradual
 Monitor vital signs because rapid correction of thyroid replacement with levothyroxine
hypothyroidism can cause adverse cardiac (Synthroid).
effects.  Effective treatment of myxedema coma
 Monitor intake and output and daily weight. supports vital functions while restoring
With treatment, urine output should increase euthyroidism.
and body weight should decrease; if not, report  To support blood pressure and pulse rate, the
this to the doctor patient receives I.V. levothyroxine, plus
 Replace fluids and other substances such as hydrocortisone in cases of pituitary or adrenal
glucose. Monitor serum electrolyte levels. insufficiency. Hypoventilation requires
 Administer corticosteroids as ordered. oxygenation and vigorous respiratory support.
 Check for possible sources of infection, such as Other supportive measures include careful fluid
blood, sputum, or urine, which may have replacement and antimicrobial medications for
precipitated coma. infection
 Treat infections or other underlying illnesses as  Hypoventilation requires oxygenation and
ordered. vigorous respiratory support.
 Explain the need for lifelong thyroid  Other supportive measures include careful fluid
replacement and regular medical care to replacement and antimicrobial medications for
monitor replacement therapy. infection
 She should show signs of adequate cardiac  Tell the patient to report signs of aggravated
output and function, including normal blood cardiovascular disease, such as chest pain and
pressure and pulse rate, adequate urine output, tachycardia.
intact skin, adequate fluid volume and  To prevent myxedema coma, tell the patient to
electrolyte balance, and adequate gas exchange. continue his course of antithyroid medication
even if his symptoms subside.
What Test Tells You?
 Instruct the patient to report infection
 Radioimmunoassay tests showing low T3 and T4 immediately and to make sure any healthcare
levels indicate hypothyroidism. provider who prescribes drugs for him knows
about his hypothyroidism.
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

Nursing Management Signs & Symptoms

1. Provide for comfort and safety: monitor for Thyrotoxicosis – group of S/S in patients with well-
infection or trauma; provide warmth, prevent developed hyperthyroidism.
heat loss & vascular collapse; administer thyroid
meds as ordered.  nervousness
2. Health teaching:  hyperexcitable
a. Diet: low calorie, high protein  irritable
b. S/Sx of hypothyroidism &  apprehensive
hyperthyroidism  palpitations
c. Lifelong meds, dosage, desired effects,  pulse is abnormally rapid at rest as well as on
side effects. exertion
d. Stress-management techniques  patient tolerate heat poorly
e. Exercise program  fine tremor of the hands may be noted
 exopthalmus (bulging eyes)
Hyperthyroidism ( Grave’s Disease)  increase appetite and dietary intake
 progressive weight loss
 Hyperthyroid state resulting from  abnormal muscular fatigability and weakness
hypersecretion of thyroid hormones (T3 and T4)
 amenorrhea
 Characterized by an increased rate of body
 changes in bowel function
metabolism
 A common cause is Graves’ disease, also known Management
as toxic diffuse goiter.
 Clinical manifestations are referred to as  Provide adequate rest & administer sedatives as
thyrotoxicosis. prescribed.
 The T3 and T4 are usually elevated and the TSH  Provide cool & quiet environment.
level is low.  Obtain daily weight & give high-calorie food.
 – is the second most common prevalent  Administer anti-thyroid meds & avoid giving
endocrine disorder after diabetes mellitus. stimulants.
 Graves’ Disease – Most common type of  Prepare the patient for the following:
hyperthyroidism, results from excessive output o iodine preparations
of thyroid hormones caused by abnormal o antithyroid meds
stimulation of the thyroid gland by circulating o propanolol (Inderal)
immunoglobulins. o radioactive iodine
o for thyroidectomy as px

Assessment Findings

 Personality changes such as irritability, agitation,

and mood swings
 Nervousness and fine tremors of the hands
 Heat intolerance Diagnostic Findings
 Weight loss
 Smooth, soft skin and hair  thyroid gland invariably is enlarged to some
 Palpitations, cardiac dysrhythmias, such as extent
tachycardia or atrial fibrillation  increase in serum T4
 Diarrhea
 Diaphoresis
 Hypertension
 Enlarged thyroid gland (goiter)
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

Assessment  Medication:
1. Propylthiouracil (PTU)
Subjective Data o blocks thyroid synthesis
2. Methimazole (Tapazole)
 nervousness, mood swings, palpitations, heat
o to inhibit synthesis of thyroid
intolerance, dyspnea, weakness.
hormone
Objective Data 3. Iodine preparations (SSKI, Lugol’s Solution)
o decrease size & vascularity of the
 Eyes: exophthalmos, characteristic stare, lid lag. thyroid gland
 Skin: warm, moist, velvety; increased sweating; o palatable if diluted with water, milk
increased melanin pigmentation; pretibial or juice
edema with thickened skin & o give through straw to prevent
hyperpigmentation staining of teeth
 Weight loss despite increased appetite o takes 2-4 weeks before results are
 V/S: increased systolic BP, widened pulse evident
pressure, tachycardia 4. Beta blockers: Propranolol (Inderal),
 Goiter: thyroid gland noticeable & palpable atenolol (Tenormin), metoprolol (Lopressor)
 Gyne: abnormal menstruation o given to counteract the increased
 GI: frequent bowel movements metabolic effect of thyroid
 Activity pattern: fatigue which leads to hormones
depression o relieve symptoms of tachycardia,
 Lab data: elevated T3 & T4 level; elevated RAIU; tremors & anxiety
elevated metabolic rate (BMR); decreased WBC
caused by decreased granulocytosis (<4500). Thyroid Storm

Nursing Management  Thyroid Storm – (Thyrotoxic Crisis) is a form of

severe hyperthyroidism, usually of abrupt onset
1. Protect from stress: private room, restrict and characterize by:
visitors, quiet environment. o Fever (hyperpyrexia)
2. Promote physical & emotional equilibrium: o Extreme tachycardia
a. cool, quiet, cool well ventilated o Altered mental state which frequently
environment. appears as delirium
b. eye care: sunglasses to protect from  It is a life-threatening condition and is usually
photophobia, protective drops precipitated by stress
(methylcellulose) to soothe cornea  This acute and life-threatening condition occurs
c. diet: high calorie, protein, vit. B; avoid in a client with uncontrollable hyperthyroidism.
stimulants  It can be caused by manipulation of the thyroid
3. Prevent complications: give medications as gland during surgery and the release of thyroid
ordered. hormone into the bloodstream;
4. Monitor for thyroid storm.  it also can occur from severe infection and
5. Health teaching: stress reduction techniques; stress.
importance of medications; methods to protect  Antithyroid medications, beta-blockers,
eyes from environment; s/sx of thyroid storm. glucocorticoids, and iodides may be
administered to the client before thyroid
Medical Management
surgery to prevent its occurrence.
Directed toward reducing thyroid hyperactivity
Signs & Symptoms
 Irradiation involving the administration of
radioisotope 123I or 131I for destructive effects  fever
on the thyroid gland.  tachycardia
 Pharmacotherapy, employs antithyroid  hypotension
medications that interfere with the synthesis of  marked respiratory distress
thyroid hormones and other agents that control  pulmonary edema
manifestations of hyperthyroidism.  irritability
 Surgery, with removal of most of the thyroid  apprehension
gland.  agitation
 restlessness
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

 confusion  If the patient undergoing surgery for treatment

 seizures for hyperthyroidism, he or she is treated with
appropriate medications to return the thyroid
Risk factors hormone level and metabolic rate to normal
and to reduce risk for thyroid storm and
 Infection
hemorrhage during the post-operative period.
 surgery
 Medications that may prolong clotting (aspirin)
 beginning labor to give birth
are stopped several weeks before the surgery to
 taking inadequate antithyroid medications minimize the risk for post-operative bleeding.
before thyroidectomy
Pre-Operative Care
Medical Management
 Assess V/S, weight, electrolyte & glucose level
The immediate objectives are to reduce body
 Teach DBE & coughing as well as how to
temperature and heart rate and to prevent vascular
support neck in post-op period when coughing
collapse.
& moving
 hypothermia mattress or blanket  Administer antithyroid meds etc. to prevent
 ice packs thyroid storm
 cool environment Post-Operative Care
 hydrocortisone
 acetaminophen  Monitor for respiratory distress & have
tracheostomy set, O2 & suction machine at the
Meds: PTU or Tapazole; Sodium iodide IV or Lugol’s
bedside
solution orally; Propranolol (Inderal); Aspirin, Steroids,
 Maintain semi-Fowler’s position to reduce
Diuretics
edema
 Immobilize head with pillows/sandbags;
prevent flexion & hyperextension of neck
 Check surgical site for edema & bleeding
 Limit client talking & assess for hoarseness
 Assess for laryngeal nerve damage…high-
ppitched voice, stridor, dysphagia, dysphonia &
restlessness
 Monitor for signs of hypocalcemia & tetany &
have calcium gluconate at bedside

Signs of Tetany

 Positive Chvostek’s Sign (twitching of facial

muscle)
 Positive Trousseau’s Sign (spasmodic
contraction of the muslces of mastication)
 Wheezing & dyspnea (bronchospasm,
laryngospasm)
 Numbness & tingling of face & extremities
 Carpopedal spasm
 Visual disturbances (photophobia)
 Muscle & abdominal cramps
Thyroidectomy
 Cardiac dysrhythmias
 Removal of thyroid gland & performed for  Seizures
persistent hyperthyroidism
Thyroid Hormones
 Partial or complete thyroidectomy may be
carried out as primary treatment of thyroid
 Levothyroxine (Synthroid, Levothroid, Levoxyl)
carcinoma, hyperthyroidism or
Thyroglobulin (Proloid)
hyperparathyroidism. The type and extent of
o Controls the metabolic rate of tissues &
the surgery depend on the diagnosis, goal of
accelerates heat production & oxygen
surgery and prognosis.
consumption
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

o For hypothyroidism, myxedema &  PTH also maintains the inverse relationship
cretinism between serum calcium and phosphate levels
o A/R: cramps, diarrhea, nervousness, by inhibiting phosphate reabsorption in the
tremors, hypertension, tachycardia, renal tubules and enhancing calcium
insomnia, sweating & heat intolerance reabsorption.
o Taken same time every day preferably  Abnormal PTH production in
in the a.m. with food hypoparathyroidism disrupts this delicate
o Teach client to how to take HR balance.
o Avoid foods that will inhibit thyroid
secretions such as: strawberries, What to look for
peaches, pears, cabbage, turnips,
Hypoparathyroidism may not produce symptoms in mild
spinach, Brussels sprouts, cauliflower,
cases.
peas & radishes
o Wear Medic-Alert bracelet  neuromuscular irritability
 increased deep tendon reflexes
DISORDERS OF THE PARATHYROID GLAND
 positive Chvostek’s and Trousseau’s signs
 dysphagia
Hypoparathyroidism
 Paresthesia
 Hypoparathyroidism stems from a deficiency of  psychosis
PTH.
Assessment Findings
 PTH primarily regulates calcium balance,
hypoparathyroidism leads to hypocalcemia and  tetany;
produces neuromuscular signs and symptoms  seizures;
ranging from paresthesia to tetany.
 arrhythmias;
 The clinical effects are usually correctable with
 cataracts;
replacement therapy.
 abdominal pain;
 some complications of this disorder, such as
 dry, lusterless hair;
cataracts and basal ganglion calcifications, are
 spontaneous hair loss;
irreversible.
 brittle fingernails that develop ridges or fall out;
Cause  possibly dry, scaly skin;
 weakened tooth enamel that may cause teeth
The three major causes of hypoparathyroidism are: to stain, crack, and decay easily

 congenital absence or malfunction of the What Tests Tells You

parathyroid glands
 autoimmune destruction Test results that confirm hypoparathyroidism include:
 removal of or injury to one or more parathyroid
 decreased PTH and serum calcium levels and
glands during neck surgery.
elevated serum phosphorus levels
Other causes include:  X-rays reveal increased bone density.
 An ECG shows prolonged QT intervals and QRS-
 ischemic infarction of the parathyroids during complex and ST-segment changes that are
surgery or from disease, such as amyloidosis or caused by hypocalcemia and may be mistaken
neoplasms for acute MI or conduction abnormalities.
 suppression of normal gland function caused by
hypercalcemia (reversible) How it’s treated
 hypomagnesemia-induced impairment of
hormone secretion (reversible)  Vitamin D, usually with supplemental calcium.
 massive thyroid radiation therapy (rare)  Such therapy is usually lifelong, except for
patients with the reversible form of the disease.
Pathophysiology  Types of vitamin D given include
dihydrotachysterol if renal function is adequate
 PTH usually maintains serum calcium levels by and calcitriol if renal function is severely
increasing bone resorption and by stimulating compromised
renal conversion of vitamin D to its active form,  Acute life-threatening tetany calls for
which enhances GI absorption of calcium and immediate I.V. administration of calcium to
bone resorption raise serum calcium levels
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

 Sedatives and anticonvulsants are given to Hyperparathyroidism

control spasms until calcium levels rise.
 Chronic tetany calls for vitamin D and possibly  is characterized by excess activity of one or
oral calcium supplements to maintain normal more of the four parathyroid glands, resulting in
serum calcium levels. excessive secretion of PTH.
 Such hypersecretion of PTH promotes bone
What To Do
resorption and leads to hypercalcemia and
hypophosphatemia.
 While awaiting diagnosis of hypoparathyroidism
 Increased renal and GI absorption of calcium
in a patient with a history of tetany, maintain a
also occur
patent I.V. line and keep 10% calcium gluconate
solution available. Causes
 Institute seizure precautions because the
patient is at risk for seizures  Primary hyperparathyroidism may result from
 Keep a tracheostomy tray and an endotracheal a single adenoma, a genetic disorder, or
tube at the bedside because laryngospasm may multiple endocrine neoplasias.
result from hypocalcemia.  Secondary hyperparathyroidism may be
 Monitor for Chvostek’s and Trousseau’s signs. caused by rickets, vitamin D deficiency, chronic
 For the patient with tetany, prepare to renal failure, or phenytoin (Dilantin) or laxative
administer 10% calcium gluconate by slow I.V. abuse.
infusion and maintain a patent airway.
Pathophysiology
 Prepare the patient for transport to the ICU
according to facility policy because the patient
 Primary hyperparathyroidism
may also require intubation and sedation with
o one or more of the parathyroid glands
I.V. diaze pam (Valium).
enlarge, leading to increased PTH
 Monitor vital signs often, especially if the
secretion and elevated serum calcium
patient received I.V. diazepam, to make sure his
levels.
blood pressure and heart rate return to normal.
 Secondary hyperparathyroidism
 When caring for a patient with
o a hypocalcemia-producing abnormality
hypoparathyroidism, stay alert for minor muscle
outside the parathyroid gland doesn’t
twitching (especially in the hands) and for signs
respond to the metabolic action of PTH,
of laryngospasm (respiratory stridor or
leading to excessive compensatory
dysphagia). These effects may signal the onset
production of PTH.
of tetany
 Closely monitor the patient who receives What to look for?
digoxin (Lanoxin) and calcium because calcium
potentiates the effect of digoxin.  Secondary hyperparathyroidism
 Watch for signs and symptoms of digoxin o may produce the same clinical features
toxicity (arrhythmias, nausea, fatigue, vision as primary hyperparathyroidism, with
changes). possible skeletal deformities of long
 instruct the patient with scaly skin to use bones (for example, rickets) as well as
creams to soften his skin. other symptoms of the underlying
 Tell him to keep his nails trimmed to prevent disease
them from splitting. o Symptoms include:
 Advise him to follow a high-calcium, low-  CNS— psychomotor and
phosphorus diet, and tell him which foods are personality disturbances, loss of
permitted. memory for recent events,
 If he’s on drug therapy, emphasize the depression, overt psychosis,
importance of checking serum calcium levels at stupor and, possibly, coma
least three times per year.  GI - anorexia, nausea, vomiting,
 Instruct him to watch for signs of hypercalcemia dyspepsia, and constipation
and to keep medications away from light.  neuromuscular — fatigue and
marked muscle weakness and
atrophy, particularly in the legs
 renal — signs and symptoms of
recurring nephrolithiasis, which
may lead to renal insufficiency
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

 skeletal and articular — chronic  Monitor sodium, potassium, and magnesium

lower back pain and easy levels frequently
fracturing from bone  Auscultate for breath sounds often, and be alert
degeneration, bone tenderness, for pulmonary edema in the patient receiving
and joint pain large amounts of I.V. saline solution —
 Other symptoms: skin pruritus, especially in the presence of pulmonary or
vision impairment from cardiac disease.
cataracts, and subcutaneous  Take precautions to avoid falls because the
calcification. patient is predisposed to pathologic fractures.
 Teach the patient about the possible adverse
What Tests Tells You
effects of drug therapy.
 Immunoradiometric assay reveals elevated  Emphasize the need for periodic follow-up
serum PTH levels. This finding, in conjunction through laboratory blood tests.
with increased serum calcium and decreased  If hyperparathyroidism isn’t corrected surgically,
phosphorus levels, confirms the diagnosis of warn the patient to avoid prolonged periods of
hyperparathyroidism. immobilization, to maintain adequate hydration,
and to avoid calcium-containing antacids and
 X-rays may show diffuse demineralization of
bones, bone cysts, outer cortical bone thiazide diuretics.
resorption, and subperiosteal erosion of the  Instruct the patient to contact his practitioner if
radial aspect of the middle fingers levels he experiences significant diarrhea or vomiting.
 Laboratory tests reveal elevated urine and  Evaluate the patient.
serum calcium, chloride, and alkaline o He should understand the need for
phosphatase levels and decreased serum regular serum calcium level studies, the
phosphorus levels. signs and symptoms of hypercalcemia
 Secondary hyperparathyroidism: is confirmed and hypocalcemia and which ones to
when serum calcium levels are normal or report, the reasons for drug therapy and
slightly decreased, with variable serum adequate hydration, and possible
phosphorus and bicarbonate levels adverse drug effects

How it’s treated Parathyroidectomy

 Surgery to remove the adenoma or all but one-  Removal of 1 or more parathyroid gland
half of one gland (the remaining part of the
Pre-Operative Care
gland is needed to maintain normal PTH levels)
is commonly the treatment of choice.
 monitor calcium, phosphate & magnesium level
 Although surgery can relieve bone pain within 3
 ensure that calcium is near normal
days, the patient’s renal damage may be
 explain to patient that talking may be painful 2
irreversible.
days post-op
Less invasive treatments are used to decrease calcium
Post-Operative Care
levels preoperatively or when surgery isn’t an option.

 forcing fluids  monitor for respiratory distress & have a

tracheostomy set, O2 & suction machine at bed
 limiting dietary calcium intake
side
 promoting sodium and calcium excretion
 Semi-Fowler’s position
through forced diuresis
 Check for bleeding
 Use normal saline solution (up to 6 L in life-
threatening situations)  Check for hypocalcemic crisis, Trousseau’s or
Chvostek’s sign
 furosemide (Lasix), or ethacrynic acid (Edecrin)
 Assess changes in voice pattern & for laryngeal
 administering oral sodium or potassium
nerve damage
phosphate, or calcitonin
 Administer calcium & vitamin D supplements as
What to do prescribed.

 Record intake and output as the patient Parathyroid Hormones

receives hydration to reduce serum calcium
levels.  Calcium Supplements
 Strain urine to check for calculi. o Calcium Carbonate (Tums)
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

o Calcium Gluconate  occurs in 5% to 10% of patients with diabetes,

o Calcium Lactate who require insulin therapy
 Vitamin D Supplements  Patient is usually thin and will require
o Calcifediol (Calderol) exogenous insulin and dietary management to
 Calcium Regulators achieve control
o Calcitonin Human (Cibacalcin)  98 % of children are of this type
 Antihypercalcemics  Pancreas produces little or no endogenous
o Edetate Disodium (Disotate) insulin treated with insulin injection to control
 Parathyroid hormone regulates serum calcium diabetes and ketoacidosis.
levels  may be caused by autoimmunity, viral and
 Low serum calcium level stimulate parathyroid genetic components
hormone release  Strongly associated with human leukocyte
 Hyperparathyroidism given antihypercalcemics antigen DR3 and 412
 Hypoparathyroidism given calcium & Vit. D
Type 2 Diabetes
Diabetes Mellitus
 Results from:
 A chronic disorder of impaired glucose o a defect in insulin manufacture and
intolerance and carbohydrate, protein & lipid release from beta cells
metabolism; caused by a deficiency of insulin o impaired insulin resistance in the
 A metabolic disorder characterized by peripheral tissues
hyperglycemia that results from defective o Increased basal hepatic glucose
insulin production, secretion or utilization production
o the pancreas produces some insulin,
Insulin but it’s either too little or isn’t effective
 Other associated factors:
 An essential hormone produced in the pancreas o Obesity
and released into the bloodstream o Insulin antagonist ( eg. Excess counter-
 It attaches itself to cells at places called insulin regulatory hormones and phenytoin
receptors o Hormonal contraceptives
 Once attached. Insulin allows sugar or glucose o Pregnancy
from the food we eat to enter the liver, fat, and  Has a strong genetic component
muscle cells, where it is used for energy  Commonly associated with obesity
 Onset – usually in adulthood ( in people older
Major Types
than age 40)
1. Insulin-Dependent Diabetes
Impaired fasting glucose – fasting blood glucose is
o must take insulin daily  absolute 100mg/dl or greater but less than 126mg/dl, and no
insulin deficiency symptoms are present
2. Non-Insulin Dependent Diabetes
o may require insulin to control blood Impaired glucose tolerance – glucose is 140 to
glucose levels unresponsive to diet or 199mg/dl on a glucose tolerance test
oral antidiabetic agents or during
o maybe a risk factor for HPN, CAD,
periods of stress
Hyperlipidemia
Type 1 Diabetes
Gestational diabetes, CHO intolerance occurs during
pregnancy but usually disappears after delivery
 usually occurs before age 30 (though it may
occur at any age} o occurs in 4% of all pregnancies
 The pancreas produces little or no endogenous o at higher risk for developing diabetes later in
insulin life
 A disorder of glucose intolerance by a deficiency o the risk of fetal morbidity is increased
in insulin production and action resulting in
hyperglycemia and abnormal CHO, CHON, and
fat metabolism
 without insulin, sugar can’t enter cells to be
used for energy; the body’s tissues are starved,
and blood glucose levels grow dangerously high.
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

Pathophysiology  random blood glucose (RBS)

greater than or equal to
Deficient 200mg/dl in the presence of
insulinproduction/resis Inc. concentraton of
Hyperglycemia
tance to endogenous
insulin
blood glucose
classic symptoms (polyuria,
polydipsia, polyphagia, and
weight loss) CONFIRMS DM
Excess fluid loss
Excess glucose
excreted in urine
Glucosuria 2. Glucose Tolerance Test
o FBS is obtained before ingestion of 50
to 200 grams of a glucose load, and
Polyuria/Polydipsia
blood samples are taken at 30 minutes,
1,2 3, 4 and 5 hours
o Diagnostic for DM if the 2 –hours result
is greater than or equal to 200mg/dl
Impaired
Insulin
deficiency
metabolism of Weight loss o Glycosylated hemoglobin determination
CHON and fats
( Hb A1C)- measures glycemic control
over 60 to 120 day period
Decreased 3. Ophthalmologic examination may show
Polyphagia storage of
calories diabetic retinopathy
o Plasma insulin level determination
Assessment o urine testing for glucose and acetone

Therapeutic Intervention
 Polyphagia
 Polydipsia  Weight reduction is a primary goal for type 2
 Polyuria – Related To Hyperglycemia DM
 Hyperglycemia  Dietary control with caloric restriction of CHO
 Weight Loss and saturated fats to maintain ideal body
 Blurred Vision weight and control blood glucose and lipid
 Slow Wound Healing levels
 Vaginal Infections  Regular exercise promotes the utilization of
 Weakness & Paresthesias carbohydrates, assists with weight control,
 Signs Of Inadequate Feet Circulation enhances the action of insulin, and improves
 Fatigue cardiovascular fitness
 Nocturia  Approach to Diabetes Mellitus
 Dry mucous membranes o Diet
 Poor skin turgor o Exercise
o Oral hypoglycemic agents/insulin
Minor S/Sx - These are prescribed to normalize
CHO,CHON, and fate metabolism
 Dry skin
and avert long-term complications
 Skin infections
while avoiding hypoglycemia
 Poor wound healing
 Strict adherence to carefully planned meals
 Candidal vaginitis (adolescent girls)
from (registered dietitian) to meet nutritional
Diagnostics needs, control blood glucose levels, and
maintain appropriate body weight- Medical
1. Elevated Serum Glucose Level Nutrition Therapy
o 2 fasting plasma glucose tests above o CHON – less than 130g/day
126mg/dl or greater  Exercise – at least 3x per week for a minimum
 fasting blood glucose (FBS) of 45 to 60 minutes; 5-6x per week when weight
greater than or equal to 126 loss is a therapeutic goal
mg/dl on two occasions
CONFIRMS DM Oral Hypoglycemic Agents
o 2 blood glucose levels above 200mg/dl
or greater during a 2-hour glucose  Sulfonylureas
tolerance test – CONFIRMS the o Chlorpropamide (Diabinase)
diagnosis o Tolbutamide (Orinase)
o Glimepinide (Solosa)
o Acetohexamide (Dymelor)
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

 Prandial Glucose Regulator  Multiple dose regimens may use an insulin

o Repaglinide (Novonorm) pump to deliver insulin continuously into
o Rosiglitazone (Avandia) subcutaneous tissue
 Non-sulfonylureas  When administering sub Q insulin injections,
o Metphormine (Glucophage) rotate the injection sites
o Precose (Acarbose) o Rationale: absorption rates differ at
o Rosiglitazone (Avandia) each site; also helps prevent
 INSULIN SECRETAGOGUES – enhance lipodystrophy which can affect insulin
pancreatic insulin secretion: absorption
o given to patients who do not achieve  Inhaled insulin – the newest method of
control through diet and exercise administration
 First generation – Sulfonylureas, o A short-acting insulin that the patient
Tolazamide (Tolinase), Tolbutamide inhales into his lungs shortly before
(Orinase) meals
 Second generation - Glyburide o Though does not eliminate the need for
((DiaBeta), Glipizide (Glucotrol), injected insulin, it’s a useful adjunct
Glimepiride ( Amaryl) o Patients who smoke shouldn’t use this
o Stimulates secretion of insulin by beta method since insulin doesn’t enter the
cells, decreases hepatic glucose bloodstream consistently in such
production and increases peripheral patients
sensitivity to insulin o regular insulin or insulin lispro may also
 BIGUANIDES – prevent inappropriate hepatic be administered during severe episodes
gluconeogenesis of hyperglycemia
o May be given alone or in combination  PIMS (programmable implantable infusion
with sulfonylureas to increase the medication system)
production of insulin and decrease o still undergoing clinical trials
hepatic glucose production and o Has an implantable infusion pump units
triglyceride levels that hold and delivers the insulin and a
 Metformin (Glucophage) delivery catheter that feeds insulin
 REPAGLINIDE (Prandin) and NATEGLINIDE directly into the peritoneal cavity.
(amino acid derivative) – increase insulin o the pumped encased in a titanium shell,
release by selectively closing potassium contains a tiny computer to regulate
channels (which results in the opening of insulin- dosages and runs on a battery with a
releasing calcium channels) in the beta cells of five year life span
the pancreas o The px uses a handheld external radio
 ALPHA-GLUCOSIDASE INHIBITORS transmitter to control insulin release
 ACARBOSE (Precose), MIGLITOL (Glyset)
o works in the small intestines to slow Insulin
CHO breakdown and delay the
intestinal absorption of  Insulin increases glucose transport into cells &
carbohydrates/glucose promotes conversion of glucose to glycogen,
 THIAZOLIDINEDIONE - Pioglitazone (Actos) and decreasing serum glucose levels
Rosiglitazone (Avandia)  Primarily acts in the liver, muscle, adipose tissue
o enhance the sensitivity of peripheral by attaching to receptors on cellular
cells to insulin membranes & facilitating transport of glucose,
o Resentize tissue to insulin, decrease potassium & magnesium.
hepatic gluconeogenesis, and increase
Glucagon
insulin-dependent muscle glucose
uptake
 Hormone secreted by the alpha cells of the
islets of Langerhans in the pancreas
Insulin Therapy
 Increase blood glucose by stimulating
 for those who do not respond to diet, exercise, glycogenolysis in the liver
and oral agents  given SC, IM or IV routes
 given via subcutaneous injection with a  Used to treat insulin-induced hypoglycemia
standard insulin syringe when semiconscious/unconscious
NCM 116 Midterm Lecture: Endocrine System
Irish Porras 3C | 2nd Sem |’24-‘25

Common Types of Insulin Client Education During Illness

Type Onset Peak Duration
Rapid-Acting Insulin  Take insulin or oral hypoglycemic agents as
Lispro 10-15 1 hr 3 hrs prescribed.
(Humalog) mins  Test blood glucose & test the urine for ketones
Short-Acting Insulin every 3-4 hours
Humulin 0.5-1 hr 2-3 hrs 4-6 hrs
 If meal plan cannot be followed, substitute with
Regular
soft food 6-8 x per day
Intermediate-Acting Insulin
Humulin 3-4 hrs 4-12 hrs 16-20 hrs  If vomiting, diarrhea or fever occurs, consume
NPH liquids every ½ to 1 hour to prevent
Humulin 3-4 hrs 4-12 hrs 16-20hrs dehydration & to provide calories
Lente  Notify doctor if vomiting, diarrhea, or fever
Long-Acting Insulin persists, if blood glucose levels are greater than
Humulin 6-8 hrs 12-16 hrs 20-20 hrs 250 to 300 mg/dL, when ketonuria is present
Ultralente for more than 24 hours, when unable to take
Premixed Insulin
food or fluids for a period of 4 hours, when
70% NPH- 0.5-1 hr 2-12 hrs 18-24 hrs
illness persists for more than 2 days
30%
Regular OTHER SLIDES FOR DM AND ITS COMPLICATIONS –
REFER TO 1ST SEM SLIDES (#179)
Major Complications of Diabetes Mellitus
MULTIPLE SCLEROSIS = SLIDE # 172

 Hypoglycemia
 Diabetic Ketoacidosis (DKA)
 Hyperglycemic Hyperosmolar Nonketotic
Syndrome (HHNS)

Signs of Hypoglycemia

 sweating
 tremor
 tachycardia
 palpitations
 nervousness
 hunger

Simple Carbohydrate to Treat Hypoglycemia

 3 or 4 commercially prepared glucose tablets

o Child: 2-3 glucose tabs
 4-6 ounces of fruit juice or regular soda
o Child: ½ cup or 120 ml of orange juice or
sugar-sweetened juice
 6-10 Life Savers or hard candy
o Child: 3-4 hard candies or 1 candy bar
 2-3 teaspoons of sugar or honey
o Child: 1 small box of raisins

Chronic Complications of Diabetes Mellitus

 Diabetic Retinopathy
 Diabetic Neuropathy
 Diabetic Nephropathy