Management of Patients with Endocrine Disorders

Endocrine System • Controlled by hypothalamus – an adjacent

• Made up of glands and the hormones they area of the brain that is connected to the
secrete. pituitary by the pituitary stalk
• Plays a vital role in
orchestrating cellular Anterior Pituitary
interactions, • ”Adenohyphophysis”
metabolism, growth, • The major hormones of the APG are:
reproduction, aging, and Follicle Stimulating Hormone (FSH),
response to adverse Luteinizing Hormone (LH), Prolactin (PRL),
conditions. Adrenocorticotropic (ACTH), Thyroid
• Disorders of the Stimulating Hormone (TSH), and Growth
endocrine system are hormone (GH).
common and are • The secretion of these major hormones is
manifested as hyperfunction and controlled by releasing factors secreted by
hypofunction. the hypothalamus.

Hormones
• A chemical transmitter substance
• It regulate and integrate body functions by
acting on local or distant target sites
• Generally produced by the endocrine glands
but may also be produced by specialized
tissues such as those found in the GI
system, kidney, and WBC.
Posterior Pituitary
Relationship between nervous system and
• “Neurohypophysis”
endocrine system
• important hormones secreted by the
Feature Nervous Endocrine
posterior lobe are ADH and OXYTOCIN
System System
• Vasopressin (ADH) – controls the excretion
Signals Electric Chemical
of water by the kidney; its secretion is
impulses impulses
stimulated by an increase in the osmolality
(hormones)
of the blood or by a decreased in BP
Pathways Transmission Transported
• Oxytocin – stimulated during pregnancy and
by neurons by blood
at childbirth.
Speed of fast slow
information
Pituitary Tumors
Duration of Short lived Long lived
• Abnormal proliferation of cells on target
effect
tissue or on local structures surrounding the
pituitary gland.
Assessment
• The tumors may be primary or secondary
• Health History
and functional or nonfunctional.
• Review of System
• Almost all pituitary tumors are benign.
• Patients should be asked if they have
• A pituitary tumor is classified as one of
experienced changes in energy level,
these types, based on whether it
tolerance to heat or cold, weight, thirst,
overproduces pituitary hormones and the
frequency of urination, fat and fluid
specific type of hormone produced:
distribution, secondary sexual
• ACTH-producing tumor
characteristics and etc.
• Growth hormone-producing tumor
Pituitary Gland “Hypophysis” • Chromophobic tumor
• Referred to as the “master • Prolactin-producing tumor
gland” because of the • Non-functioning pituitary tumor
influence it has on
secretion of hormones by
other endocrine glands.
• Round structure about
1.27 cm (1/2 in) is diameter
• Located on the inferior aspect of the brain
• Divided into anterior and posterior lobes
Causes
• Unknown
• Uncontrolled cell growth in the pituitary
gland, which creates a tumor
• Certain hereditary conditions
• Such as multiple endocrine neoplasia
ACTH-Producing Tumor
• overproduces adrenocorticotrophic hormone
(ACTH)
• This type of pituitary tumor releases too
much ACTH into the bloodstream, the extra
ACTH overstimulates the adrenal glands to
pour out high levels of adrenal
glucocorticoids (adrenal hormones) and
androgens (male hormones) into the blood.
• It give rise to Cushing syndrome with
features largely attributable to
hyperadrenalism.
• This tumor causes symptoms of Cushing's
disease, a condition caused by prolonged
overproduction of adrenal glucocorticoids
and androgens.
• Symptoms
• For women: masculinization (female),
amenorrhea, excess body hair in women
• Truncal obesity, thin skin, easy bruising,
red or purple lines (striae) on the skin of
the abdomen, a moon-shaped face,
muscle wasting, acne
• Psychiatric symptoms: Depression and
psychosis.
• Cushing's disease also can trigger
osteoporosis, hypertension,
polycythemia, and diabetes.
Growth hormone-producing tumor
• Secretes abnormally large amounts of
growth hormone
• In children and teenagers, this
overproduction of growth hormone causes a
condition called giantism.
• In adults, it causes a condition called
acromegaly (abnormal enlargement of the
skull, jaw, hands and feet, and other
symptoms of abnormal growth).
• Symptoms
• Gigantism:
- Abnormally rapid
growth, unusually
tall stature, a very
large head, coarse
facial features, very
large hands and
feet, weak and
lethargic (they can
hardly stand), and
sometimes,
behavioral and visual problems.
• Acromegaly:
- Oily skin; coarse
features with
thick lips and a
broad nose;
prominent
cheekbones; a
protruding
forehead and lower jaw; a deep
voice; enlargement of the hands and
feet; a barrel-shaped chest;
excessive sweating; and pain and
stiffness in the joints.
- Severe headaches & visual
disturbances, loss of color
discrimination, diplopia, and
blindness in the portion of a field of
vision.
Chromophobic tumor
• Represent 90% of pituitary tumors
• Produce no hormones but destroy the rest
of the pituitary gland, causing
hypopituitarism
• Symptoms
• Obese, somnolent, fine-scanty hair; dry,
soft, skin; pasty complexion; small
bones.
• Headaches, loss of libido, blindness
• Polyuria, polyphagia, low basal
metabolic rate, and subnormal body
temperature.
Prolactin-producing tumor
• Overproduces the hormone prolactin, which
stimulates the breasts to make milk
• Prolactin-producing pituitary tumors can
develop in both men and women, and they
sometimes grow so big that they press on
the sella turcica and cause it to get larger.
• Symptoms
• Galactorrhea, amenorrhea, impotence
(male), decreased sex drive
Non-functioning pituitary tumor
• This type of pituitary tumor is a hormonally
inactive adenoma.
• In many cases, a nonfunctioning pituitary
adenoma is diagnosed only when it already
has grown beyond the sella turcica and has
begun to cause problems related to
pressure on the optic nerves or brain.
• These tumors do not produce excessive
amounts of hormone.
• Prolactin-producing tumors and
nonfunctioning tumors can depress the
pituitary's ability to make and release other
hormones.
 • Symptoms related to low sex hormone ablation or
levels. irradiation of the
• If a tumor keeps growing, the person may pituitary gland)
develop fatigue and lightheadedness • Infections of the
because the thyroid and adrenal glands CNS (meningitis,
aren't functioning properly. encephalitis,
tuberculosis)
• Good history must be obtained, including
• Tumors
current medications. (metastatic
• Psychiatric drugs – neuroleptics can disease,
increase blood levels of prolactin, and lymphoma of the
• Prescription glucocorticoids (even breast or lung)
therapeutic injections of dexamethasone • Failure of the
— Decadron and other brand names — renal tubules to
into injured joints) can cause high blood respond to ADH
levels of glucocorticoids. (hypokalemia,
hypercalcemia,
Management and variety of
medications)
1. Transsphenoidal hypophysectomy
- Surgical removal of the pituitary
gland. • Causes
• Secondary (head trauma, brain tumor,
2. Stereotactic radiation therapy surgical ablation or irradiation of the
- Delivers external-beam radiation pituitary gland)
therapy to the pituitary tumor with • Infections of the CNS (meningitis,
minimal effect on normal tissue. encephalitis, tuberculosis)
• Tumors (metastatic disease, lymphoma
3. Conventional radiation therapy: of the breast or lung)
- Bromocriptine (Parlodel), and • Failure of the renal tubules to respond to
octreotide (Sandostatin) ADH (hypokalemia, hypercalcemia, and
variety of medications)
4. Octreotide and Lanreotide
• Clinical Manifestations
Diabetes Insipidus 1. Polyuria with daily UO of (greater than
• Most common disorder of the posterior lobe 250 mL per hour) of very dilute urine
of the pituitary gland with a specific gravity of 1.001 to 1.005
• Characterized by a deficiency of ADH occurs.
(vasopressin) 2. Polydipsia – 2 to 20 L of fluid daily and
• Polydipsia and large volumes of dilute urine craves for cold water
are manifestations of DI. 3. Marked dehydration
4. Anorexia and epigastric fullness
5. Nocturia and related fatigue from
interrupted sleep.
6. F&E imbalance
7. Hypotension

• Diagnostic Findings
1. History collection and Physical
examination
2. Water deprivation test
a. withholding fluids for 8-12 hours
Types of DI or until 3% to 5% of the BW is
CENTRAL DI NEPHROGENIC DI lost
• Loss of • Depression of b. patient frequently weighed during
vasopressin- aldosterone the test
producing cells release or inability c. check the plasma and urine
• Deficiency in ADH of the nephrons to osmolarity before and after the
synthesis or respond to ADH procedure
release • Extreme polyuria d. Stop the procedure if
• Inability to and polydipsia tachycardia, excessive weight
conserve water • Causes loss, hypotension develops.
• Extreme polyuria • Secondary (head Note: inability to increase the SG and
and polydipsia trauma, brain osmolarity of the urine is characteristics
tumor, surgical of DI.
 3. Plasma levels of ADH • Stimuli for AVP secretion
4. Plasma and urine osmolarity • ADH receptors: V1a, V1b, V2
5. Desmopressin therapy • Normally, when plasma osmolality falls
6. Hypertonic saline test below 275 mOsm/kg, AVP secretions
stops.
• Management • When plasma osmolality rises (or 8-10%
Goals of management reduction in circulating volume), AVP
1. to replace ADH (which is usually a long- secretion increases.
term therapeutic program),
2. to ensure adequate fluid replacement, • Causes
and • Nonendocrine origin
3. to identify and correct the underlying - e.g., bronchogenic carcinoma,
cause severe pneumonia, pneumothorax,
etc.
• Pharmacologic Management • Disorder of the CNS
1. Desmopressin (DDAVP) – drug of - e.g., head injury, brain surgery or
choice for central DI; given orally or tumor, infection
intranasally • Certain medications
2. Chlorpropamide (Diabinese) and - e.g., vincristine (Oncovin),
Thiazide diuretics – used in mild forms phenothiazines, tricyclic
of the disease because they potentiate antidepressants, thiazide diuretics
vasopressin but are used with caution
due to the risk of hypoglycemia.
• Clinical Manifestations
Note: If the DI is renal in origin, Thiazide
• Hypoosmolality is associated primarily
diuretics, mild salt depletion, and
with a broad spectrum of neurologic
prostaglandin inhibitors are used to treat the
manifestations termed hyponatremic
nephrogenic form of DI.
encephalopathy, ranging from:
- Mild nonspecific symptoms
• Nursing Management
- More significant disorders
1. Monitor vital signs and neurological and
cardiovascular status.
Mild to Advanced Grave
2. Provide a safe environment, particularly Moderate
for the client with postural hypotension. Headache Confusion Seizures
3. Monitor electrolyte values and for signs Lethargy Disorientation Hemiplegia
of dehydration. Slowness Somnolence Severe
4. Maintain client intake of adequate fluids. Poor Vomiting somnolence
5. Monitor intake and output, weight, concentration Hallucinations Respiratory
serum osmolality, and specific gravity of Depressed Acute insufficiency
urine. mood psychosis Coma
6. Instruct the client to avoid foods or Lack of Limb Death
liquids that produce diuresis. attention weakness
7. Instruct the client in the administration of Impaired Dysarthria
medications as prescribed; DDAVP may memory
be administered by injection, Nausea
intranasally, or orally Restlessness
Instability of
Syndrome of Inappropriate Antidiuretic gait and falls
Hormone Secretion (SIADH) Muscle cramps
• Schwartz-Bartter Syndrome Tremor
• Results from negative feedback system that
regulates the release and inhibition of ADH. • Management
• Clinical condition involving excessive ADH 1. Eliminating the underlying causes.
secretion 2. Restricting fluid intake
• A disorder of impaired water excretion - Because retained water is excreted
caused by the inability to suppress the slowly through the kidneys, the
secretion of antidiuretic hormone (ADH) extracellular fluid volume contracts
• Patient cannot excrete a dilute urine, retain and the serum sodium concertation
fluids, and develop a sodium deficiency gradually increases towards normal.
(dilutional hyponatremia) 3. Diuretics as order (furosemide)
4. In severe hyponatremia, sometimes a
• Physiology of ADH hypertonic NaCl (3%) may be prescribed
• Arginine vasopressin (AVP) and administered IV.
Parathyroid Gland • Increase in serum alkaline phosphatase
level
• Elevated serum chloride levels
• Imaging studies: CT, MRI, Thallium
scan, and Fine-needle biopsy

• Clinical Manifestations
• Situated in the neck and embedded in the • Digestive system
- Loss of appetite
posterior aspect of the thyroid.
- Nausea
• Parathormone – regulates calcium and
- Vomiting
phosphorus metabolism. - Constipation
• Increased secretion results in increased • Nervous System
calcium absorption from the kidney, - Fatigue
intestine, bones. - Depression
• Function - Confusion
• Musculoskeletal System
- Muscle weakness
- Aches and pains in bones and joints
• Urinary System
- Kidney stones
- Increased thirst
- Increased urination

• Associated disease • Medical management

• Hyposecretion of PTH results in tetany. Lifestyle Regular exercise
Avoidance of
• Hypersecretion leads to extreme bone
immobilization
wasting and fractures.
Diet Good hydration
Moderate daily Ca
• Hyperparathyroidism intake of 800-1000 mg
• Overproduction of parathormone by the Vitamin D intake
parathyroid glands and is characterized appropriate for age and
by bone decalcification and the sex
development of kidney stones (renal Medications Calcimimetics (eg.
calculi) contain calcium. cinacalcet)
Oestrogen therapy
• Causes (types) (postmenopausal)
Bisphosphonates
• Primary hyperthyroidism
PPA techniques
- uncontrolled (autonomous) PTH AVOID: thiazides,
production with loss of feedback diuretics, lithium,
mechanism by extracellular calcium.
- More often in women, rare in • Surgery
children younger than 15 years • Parathyroidectomy – surgical removal of
- Common in 60-70 years of age abnormal parathyroid tissue.
• Secondary hyperthyroidism • Bilateral and unilateral neck exploration
- occurs in patients who have chronic under general anesthesia.
kidney failure and so-called renal • In some cases, a single diseased gland
rickets as a result of phosphorus is removed.
retention, increased stimulation of
the parathyroid glands, and
increased parathormone secretion.
• Tertiary hyperthyroidism
- characterized by the development of
autonomous hypersecretion of PTH
• Indication of surgery in asymptomatic
causing hypercalcemia.
patients
-
• Any age younger than 50 years &
• Diagnostic Findings unable to participate in ff-up care
• Elevated PTH and Serum Calcium • mg/dL above the upper limit of Serum
• Elevated PTH and low or normal Serum Ca.
Calcium • 24-hour urinary excretion >400 mg
• Decreased Serum Phosphate Level • Bone Marrow Density (BMD) score
(less than 2.5 mg/dL) below -2.5 at any site.
• A 30% reduction in creatinine clearance
 • Hydration therapy
- Daily fluid intake of 2000 mL to CHVOSTEK SIGN TROUSSEAU SIGN
prevent calculus formation.
- Thiazide diuretics are avoided spasm or twitching of the carpopedal spasm is
because they decrease renal mouth, nose and eye. induced by occluding
excretion of calcium and further the blood flow to the
elevate serum calcium levels arm for 3 minutes
• Mobility
- Encouraged to walk.
- Bed rest increases calcium excretion
and the risk of renal calculi.
• Diet and Medications
- Advise to avoid a diet with restricted
or excess calcium.

Hypoparathyroidism • Medical Management

• Inadequate secretion of parathormone due - Goal of therapy: increase serum
to abnormal parathyroid development, calcium level to 9 to 10 mg/dL (2.2 to
destruction of the parathyroid hormones, 2.5 mmol/L) and to eliminate the
and vitamin V12 deficiency. symptoms of hypoparathyroidism
• Deficiency of parathormone results in and hypocalcemia.
hyperphosphatemia (increased blood • Medications:
phosphate levels) and hypocalcemia - Calcitriol, calcium, magnesium, and
(decreased blood calcium levels). Vit D2 (ergocalciferol)
- Thiazide diuretic
(hydrochlorothiazide) – decrease
urinary calcium excretion
- Calcium gluconate – for
hypocalcemia and tetany
- Calcium regulators – Alendronate
• Types/Classification (Fosamax), Calcitonin human
• Acquired (Cibacalcin)
• Transient hypoparathyroidism - Phenobarbital – sedative agent
• Congenital hypoparathyroidism or - Aluminum hydroxide gel or
DiGeorge's Syndrome carbonate
• Inherited hypoparathyroidism • Environment: free from noise, draft,
bright lights, or sudden movement
• Causes/Etiology • Prepare tracheostomy and mechanical
• Near-total removal of the thyroid gland ventilator
• Tumor of the thyroid gland • Diet: High in calcium and low in
• Accidental removal of parathyroid gland phosphorus
• Idiopathic causes
• Inadequate secretion of PTH • Nursing Management
• Increased reabsorption of calcium in GI • Detecting early signs of hypocalcemia
tract and anticipating signs of tetany,
• Phosphate excretion by the kidney seizures, and respiratory difficulties.
decreases • Calcium gluconate should be available
for emergency IV administration (cardiac
• Clinical Manifestations disorder, arrhythmias, receiving digitalis)
TETANY – LATENT OVERT • Continuous cardiac monitoring and
general muscle TETANY TETANY careful assessment
hypertonia, with Numbness Bronchospasm • Education about medication and
tremor and and tingling Laryngeal therapy.
spasmodic or Stiffness spasm
uncontrolled Chvostek sign Carpopedal
contractions. Trousseau spasm
sign Dysphagia
Photophobia
Cardiac
dysrhythmias
Seizures
HYPOCALCEMIA Other ECG changes
causes irritability symptoms: and
of the Anxiety, hypotension
neuromuscular irritability,
system depression,
delirium
Adrenal Glands
• The triangular-shaped adrenal glands are
located on the top of each kidney.
• The inside is called the medulla and the
outside layer is called the cortex.
Hormones of the Adrenal Gland
Adrenal Cortex Adrenal Medulla
cortisol epinephrine
corticosterone nor- epinephrine
cortisone
aldosterone
androgens
Adrenal Medulla
• The medulla is surrounded by the adrenal
cortex. It develops from nervous tissue in
the embryo and is part of the sympathetic
nervous system.
• When stimulated by extensive sympathetic
nerve supply, the glands release the
hormones adrenaline (epinephrine, 90%)
and noradrenaline (norepinephrine, 10%).
• Epinephrine is also called adrenalin. It
elevates systolic blood pressure, increases
heart rate and cardiac output, speeds up the
release of glucose from the liver, giving a
spurt of energy, dilates the bronchial tubes
and relaxes airways, and dilates the pupils
to see more clearly.
• Norepinephrine, like epinephrine, is
released when the body is under stress.
Adrenal Cortex
• Makes it possible for body to adapt to stress
of all kinds.
• Produces three groups of steroid hormones
from cholesterol. They are collectively called
adrenocorticoids (corticosteroids).
• The groups are: glucocorticoids,
mineralocorticoids, and sex hormones
(androgens).
• Without the adrenal cortex, severe stress
would cause peripheral circulatory failure,
circulatory shock, and prostration.
Glucocorticoids (Cortisol)
• Has influence on glucose metabolism
• Have major effects on the metabolism of
almost all organs of the body.
• Maintain blood glucose levels
• Enhance gluconeogenesis
• Have anti-inflammatory effect.
• Decrease T-lymphocyte participation in cell-
mediated immunity
• Decrease new antibody release.
• Increased gastric acid and pepsin
production.
• Maintain emotional stability.
Mineralocorticoids (ex. Aldosterone)
• Exert their major effects on electrolyte
metabolism.
• Maintain Na and volume status.
• Increase Na reabsorption in distal tubules of
the kidneys.
• Increase potassium and hydrogen excretion
in distal tubules.
• Aldosterone is “pro-Sodium,” “anti-
Potassium”
Sex Hormone (Androgen & Estrogen)
• Responsible for some secondary sex
characteristics in females.
• The adrenal medulla secretes
catecholamines through stimulation of SNS
and medulla oblongata.
• The effects of sympatho-adreno-medullary
response (SAMR) stimulation on body
organs
• “Every function is high and fast, except GI
and GU.”
• Surgical Management
• ADRENALECTOMY
- Removal of one or both adrenal
glands.
- Performed using a laparoscopic
approach or an open surgery.
Pheochromocytoma
• Rare tumor that is usually benign and
originates from the chromaffin cells of the
adrenal medulla
• This tumor is the cause of high blood
pressure in 0.1% of patients with
hypertension and is usually fatal if
undetected and untreated; cured by
surgery.
• 5H’s: hypertension, headache,
hyperhidrosis, hypermetabolism,
hyperglycemia
• Management: Bed rest with head of bed
elevated to promote orthostatic decrease in
blood pressure.
Adrenocortical Insufficiency (Addison’s
Disease)
• Primary adrenal insufficiency (PAI)
• Occurs when the adrenal glands are
damage and cannot produce sufficient
amounts of cortical hormones.
• A disease characterized by progressive
anemia, low blood pressure, great
weakness, and bronze discoloration of the
skin. It is caused by inadequate secretion of
hormones by the adrenal cortex.
 • Etiology
• Autoimmune or Idiopathic
• Removal of both adrenal glands
• Infection
• Tuberculosis
• Multiple pharmacologic therapies
• Clinical Manifestations
• “Everything is LOW except K, Na, and
PR”
• “Dark skin”
Adrenal Crisis (Addisonian crisis)
• Is a life – threatening disorder caused by
ACUTE ADRENAL INSUFFICIENCY.
• It is precipitated by stress, infection, trauma
or surgery.
• Manifestations
• Severe headache; severe abdominal,
leg and lower back pain; generalized
weakness; irritability and confusion;
severe hypotension; shock
• Diagnostic Findings
• History collection & Physical
examination
• ACTH Stimulating Test
• 24 Hrs urine studies
• Lab studies (Decrease glucose and
sodium level and Increased potassium
and WBC level)
• Blood Chemistry (Plasma cortisol and
aldosterone level)
• Medical Management
1. Combat circulatory shock
2. Monitor VS
3. Recumbent position
4. Hydrocortisone (Solu-Cortef) followed by
3-4 L of normal saline or 5% dextrose
solution
5. Vasopressor
6. Antibiotic
• Nursing Interventions
• Steroid Therapy (Hormonal
Replacement Therapy – HRT)
1. Monitor VS
2. Monitor the weight, I&O for edema.
3. Avoid exposure to infection.
4. Monitor potassium and calcium.
5. Administer steroids after meals or with
milk.
6. Monitor urine and blood glucose levels
and urine ketones.
7. Diet of the client should be High Protein,
High Carbohydrates, High Potassium,
And Low Sodium. Steroids enhance
metabolism.
8. Monitor side effects of steroids:
Osteoporosis, edema, HPN, mood
swing, easy bruising, petechiae,
ecchymosis, hirsutism, acne, altered fat
distribution, gastric irritation, cataract,
glaucoma, growth retardation,
psychosis.
9. Dose should be tapered and not
stopped abruptly.
• Management for Addisonian Crisis
1. Administer glucocorticoid/IV Solu –
cortef (hydrocortisone sodium
succinate), then orally.
2. Monitor VS
3. Monitor neurological status
4. Monitor I&O
5. Monitor serum sodium and potassium,
and blood glucose.
6. Administer IV fluids as prescribed.
7. Protect client from infection
8. Maintain bed rest and provide a quiet
environment.
Cushing Syndrome
• Excessive adrenocortical activity.
• Commonly caused by the prolonged use
of corticosteroid medications and is
infrequently the result of excessive
corticosteroid production secondary to
hyperplasia of the adrenal cortex.
• excess cortisol due to any cause
Cushing’s Disease
• excess cortisol due to pituitary micro-
adenoma
• Clinical Manifestations
• “Everything is HIGH except K, Ca, and
PR”
Thyroid Gland
• Largest endocrine glands. • Causes of Hyperthyroidism
• A butterfly-shaped organ located in the • Grave's Disease
lower neck, anterior to the trachea. - an immune system
• Consists of 2 lateral lobes connected by an disorder which is
isthmus. the leading cause of
• 5 cm long and 3 cm wide and weighs about hyperthyroidism
30 g. - an overproduction
of thyroid hormone
Hormones which causes
• Thyroid hormone (Thyroxine - T4, enlargement of the
Triiodothyroxine - T3) thyroid and other
• Calcitonin symptoms such as
exophthalmos, heat
T4 and T3 tolerance, and
• Amino acids that contain iodine molecules anxiety.
bound to the amino acid structure • Thyroid nodules
• T4 contains four iodine atoms and T3 • Thyroiditis
contain three in each molecules. • Postpartum Thyroiditis
• Synthesized and stored bound to proteins in - occurs in the first year after childbirth
the cells of the thyroid gland until it needed - among 5-10% of women
for release into the bloodstream. • Consumption of excess iodine (salt,
• Thyroxine-binding globulin (TBG), kelp, dairy products & seaweed)
transthyretin and albumin – bind and • Hypothyroidism medications
transport T3 and T4. • Injury to thyroid gland
• Severe medications
Function of Thyroid Hormone • Heredity
• Control cellular metabolic activity (It • Inflammation of thyroid gland
accelerated metabolic processes by • Hormonal changes (miscarriage,
increasing the level of specific enzymes that pregnancy, irregular sex life,
contribute to O2 consumption and altering menopause)
the responsiveness of tissues to other • Damage to the pituitary gland
hormones.) • Infectious disease
• Influence cell replication and are important • Severe nerve shocks
in brain development.
• Necessary for normal growth and
development.
• Thyroid hormone controls the rate at which
glucose is “burned,” or oxidized, and
converted to body heat and chemical
energy.

Calcitonin
• “thyrocalcitonin”
• Secreted in response to high plasma levels
of calcium, and it reduces the plasma level
of calcium by increasing its deposition in
bone.
• Made by the so-called parafollicular cells
found in the connective tissue between the
follicles • Diagnostic Findings
• History and Physical Examination
Hyperthyroidism • Ophthalmologic Examination
• is a form of thyrotoxicosis • ECG - atrial tachycardia
resulting from excessive • Laboratory tests
synthesis and secretion of • TFT (thyroid function test)
endogenous or exogenous
• T3
thyroid hormones by the
• T4
thyroid
• TRH (Thyroid releasing hormone) test
• Occurs in women more than men with
highest frequency in persons 20 to 40 years
old. • Management
• Over secretion of thyroid hormones is • Combination of therapies – Antithyroid
usually associated with an enlarged thyroid agents, radioactive iodine, and surgery
gland known as goiter. • Reducing thyroid hyperactivity – to
• Goiter commonly occurs with iodine relieve symptoms and preventing
deficiency. complications
 • Complications: relapse or recurrent
hyperthyroidism and permanent
hypothyroidism
1. Provide adequate rest.
2. Provide non-stimulating, quiet and cool
environment.
3. Provide high-calorie diet. Low-fiber diet
it with diarrhea.
4. Obtain daily weight
5. Promote safety
6. Protect the eye, if with exophthalmos
7. Avoid stimulants
8. Replace fluid electrolyte losses due to
diarrhea and diaphoresis.
• Radioactive Iodine Therapy
• Used to treat toxic adenomas, toxic
multinodular goiter, and thyrotoxicosis.
• Contraindicated during pregnancy.
• Taken by mouth, radioactive iodine is
absorbed by your thyroid gland, where it
causes the gland to shrink and
symptoms to subside, usually within
three to six months.
• Goal: eliminate the hyperthyroid state
with the administration of sufficient
radiation in a single dose.
• Concentrates in the thyroid gland and
destroys thyroid tissue – it destroys
thyroid cells.
• Older patients and with CV disease –
may need pretreatment with antithyroid
medications (Methimazole – given 4-6
weeks prior to therapy)
• Thyroid Storm
• Life-threatening condition manifested by
cardiac dysrhythmias (tachycardia > 130
bpm), fever >38.5 C, and neurologic
impairment
• Beta-blockers are used to control these
symptoms.
• Advise the patient to avoid:
- sexual contact,
- sleeping in the same bed with other
persons.
- close contact with children and
pregnant women,
- sharing utensils and cups
• Antithyroid Medications
• It inhibits one or more stages in thyroid
hormone synthesis or hormone release.
• Propylthiouracil (PTU) and methimazole
(Tapazole)
• Symptoms usually begin to improve in 6
to 12 weeks, but treatment with anti-
thyroid medications typically continues
at least a year and often longer.
• Before treatment:
- check baseline blood tests (CBC –
WBC count)
- liver profile (transaminases and
bilirubin)
• Take the medication in the morning on
an empty stomach 30 minutes before
eating to avoid decrease in absorption.
• Surgical Management
• Surgical Treatment of Thyroid Disease
General Several surgical options exist
for treating thyroid disease and the
choice of procedure depends on two
main factors.
• The first is the type and extent of thyroid
disease present.
• The second is the anatomy of the
thyroid gland itself. The most commonly
performed procedures include
lobectomy, lobectomy with isthmectomy,
subtotal thyroidectomy, and total
thyroidectomy.
• Thyroid Lobectomy and Isthmectomy
• involves removal of only
one lobe of the thyroid
gland
• this may involve crossing
the midline to include the
isthmus (isthmectomy) or it
may involve the affected
lobe alone
• Advantage
- Normal thyroid is left behind to
provide endogenous hormone.
- There is less chance of disrupting
the parathyroid glands or recurrent
laryngeal nerves on the unaffected
side.
• Disadvantage
- With remnant lobe left in place, the
use of radioiodine as ablative
therapy is compromised.
• Subtotal Thyroidectomy
• the affected side (lobe)
of the gland is removed,
along with the isthmus
and a substantial
portion of the opposite
lobe
• typically reserved for small, non-
aggressive thyroid cancers, this is also a
viable option for goiters which cause
compressive or cosmetic problems in
the neck
• Total Thyroidectomy
• complete removal of
the thyroid gland and
is the operation of
choice for practically
all thyroid cancers
• certain situations are absolute indications
for complete gland removal including
medullary thyroid carcinoma, sarcoma of
the thyroid gland, and stage IE thyroid
lymphoma.

• Preoperative Intervention
• Promote euthyroid state
• Instruct client on how to perform DBCT
exercises and how to support the neck
in the postoperative period when
coughing and moving.
• Administer the premedication as
prescribed to prevent thyroid storm
• Check ECG
• Postoperative Intervention
• Position: Semi-Fowlers
• Monitor surgical site for bleeding and
edema.
• Have tracheostomy set, O2 and suction
available at the bedside.
• Assess for recurrent laryngeal nerve
damage.
• Monitor for signs of hypocalcemia and
tetany
• Monitor for thyroid storm
Hypothyroidism
• Suboptimal levels of thyroid hormone
• Form: mild, subclinical forms to myxedema,
and advanced life-threatening
• Commonly occurs in patients with previous
hyperthyroidism that has been treated with
radioiodine or antithyroid medications or
thyroidectomy.
• Incidence: affects women between 40 and
70 years of age
• Primary or thyroidal hypothyroidism
• refers to dysfunction of the thyroid gland
itself
• Central hypothyroidism
• failure of the pituitary gland, the
hypothalamus, or both
• Pituitary or secondary hypothyroidism
• entirely a pituitary disorder
• Hypothalamic or tertiary hypothyroidism
• disorder of the hypothalamus resulting in
inadequate secretion of TSH due to
decrease stimulation of TRH
• Neonatal hypothyroidism
• thyroid deficiency is present at birth
• Medical Management
• Monitor vital sign.
• Monitor daily weights
• Diet modification
• Assess the client for constipation.
• Administer thyroid replacement therapy:
- Synthroid, Levothroid, Levoxyl
(Levothyroxine)
- Cytomel (Liothyronine)
- Thyrolar (Liotrix)
- Thycar (Thyroid)
• Pharmacologic Therapy
• Synthetic levothyroxine (Synthroid or
Levothroid)
- Dosage: based on the patient’s
serum TSH concentration
• IV administration of T4 and T3 are
recommended rather than T4 alone
• High-dose glucocorticoids
(hydrocortisone) every 8-12 hours for 24
hours followed by low-dose therapy
• Serum levels of T4, TSH, and cortisol
should be obtained before and after
administration of ACTH, and before
administration of glucocorticoids and
thyroid hormone therapies.
Management of Patients with Diabetes

Diabetes
• Hyperglycemia resulting from defects in
insulin secretion, insulin action, or both.

Insulin
• Hormone secreted by beta cells, which are
one of the four types of cells in the islets of
Langerhans in the pancreas.
• Anabolic, or storage hormone

Type 1 Diabetes
• Destruction of pancreatic cells
• Combined genetic, immunologic, and
possibly environmental (e.g., viral) factors
are though to contribute to beta-cell
destruction.

Diabetic Ketoacidosis (DKA)

• Metabolic derangement that occurs most
commonly in persons with type 1 diabetes
and results from a deficiency of insulin

Type 2 Diabetes
• Occurs most commonly among people who
are older than 30 years and who have
obesity

Gestational Diabetes
• Any degree of glucose intolerance with its
onset during pregnancy.
• Particularly in the second and third
trimesters

Prevention
• Type 2 diabetes can be prevented with
appropriate changes in lifestyle.

Clinical Manifestations
• 3P’s: polyuria, polydipsia, polyphagia
• Fatigue, weakness, sudden vision changes,
tingling or numbing in hands or feet, dry
skin, skin lesions or wounds that are slow to
heal, recurrent infections
• Onset of Type 1 may also be associated
with sudden weight loss or nausea, vomiting
or abdominal pains, if DKA has developed.

Diagnostic
• Fasting Plasma Glucose

Medical Management
• Main goal: normalize insulin activity and
blood glucose levels to reduce the
development of complications.
• Therapeutic Goal: achieve euglycemia
(normal blood glucose levels) without
hypoglycemia while maintaining high quality
of life
• Nutritional Therapy: meal planning, weight
control, increased activity

Hehe andami sa diabetes, di ko alam ano

ilalagay. Kayo na bahala don gais, labyu good
luck <3