Richard A.

Cheng RN
ENDOCRINE GLANDS
 PITUITARY GLAND
• Located at the base of the
brain. THE MASTER GLAND
• Is influenced by
hypothalamus
• Directly affects the function
of the other endocrine
glands.
• Promotes growth of body
tissues.
• Influences water absorption
by the kidney.
• Controls sexual
development and function
Hormones secreted in Ant. Pituitary Gland:
- ACTH, FSH, LH, Growth hormone,
Melanocyte-stimulating hormone, Prolactin,
somatotropic growth hormone and TSH

Hormones secreted in Posterior pituitary Gland:

- Oxytocin and anti-diuretic hormone

(vasopressin)
 ADRENAL GLANDS
 Two small glands, one above each
kidney
 Regulates sodium and water
retention
 Affects CHO, fat and CHON
metabolism
 Influences development of sexual
characteristics
 The adrenal cortex synthesizes
glucocorticoids and
mineralocorticoids
 The adrenal medulla produces
epinephrine and norepinephrine
 THYROID GLAND
• Located anterior part of the
neck.

• Controls rate of body

metabolism and growth.

• Produces T4, T3 and

thyrocalcitonin.
 PARATHYROID GLANDS

• Located near the thyroid

• Controls calcium and
phosphorus metabolism
• Produces parathyroid
hormone.
 PANCREAS
• Located posterior of
liver
• Influences CHO
metabolism
• Indirectly influences
fat and CHON
metabolism
• Produces insulin and
glucagon
 OVARIES
• Located in the pelvic cavity.
• Produce estrogen and
progesterone.
 TESTES
• Located in the scrotum.
• Contributes to the
development of
secondary
• sex characteristics
• Produce testosterone
APG:
• FSH
– stimulates graafian follicle growth and
estrogen secretion.

• LH
– induces ovulation & development of corpus
luteum and stimulates testosterone secretion in men.
• ACTH
– stimulates secretion of hormones from
adrenal cortex.
• TSH
– regulates secretory activity of thyroid
gland.
• GH
– stimulates growth of cells, bones,
muscles and soft tissue.
• Prolactin
– development of mammary glands &
lactation
PPG:
• ADH (Vasopressin)
– regulates water metabolism; helps body to retain water.

• Oxytocin
– stimulates uterine contractions during labor and milk
secretion in lactating mothers.
 ADRENAL CORTEX
• Glucocorticoids (Cortisol, Cortisone,
Cortecosterone)
- increase blood glucose levels by increasing rate of
glyconeogenesis
- increases CHON catabolism
- increase mobilization of fatty acids
- promote sodium & water retention
- anti-inflammatory effect
- aid the body in coping stress.
CONT ADRENAL CORTEX….

• Mineralocorticoids (Aldosterone,
Deoxycortisone)
– regulate F/E balance
– stimulate reabsorption of sodium, chloride &
water
– stimulate potassium excretion.
 ADRENAL MEDULLA
Epinephrine and Norepinephrine
- function in acute stress
- increase heart rate & BP
- dilate bronchiole
- convert glycogen to glucose when needed
by muscles for energy.
– lowers serum calcium by increasing bone
deposition.
 THYROID

• T3 & T4
– regulate metabolic rate, CHO, fat and
CHON metabolism;
- aid in regulating physical and mental
growth & development.
• Thyrocalcitonin
 PARATHYROID

• PTH
– regulate sodium calcium and phosphate levels.
 PANCREAS
Insulin
– allows glucose to diffuse across cell membrane;
- converts glucose to glycogen.
Glucagon
– increases blood glucose by causing
Gluconeogenesis in the liver
- secreted in response to blood sugar.
 OVARIES
• Estrogen & Progesterone
- development of secondary sex characteristics in
female
- maturation of sex organs
- sexual functioning
- maintenance of pregnancy.
 TESTES
• Testosterone
– development of secondary sex characteristics
in males
– maturation of sex organs
– sexual functioning.
 RADIOACTIVE IODINE
UPTAKE (RAIU)
*A thyroid function test that measures the absorption of
the iodine isotope to determine how the thyroid gland
is functioning.

*Administration of I123 or I131 orally followed in 24 hrs.

by a scan of the thyroid for the amount of radioactivity
emitted.

*Normal value is 5-35% in 24 hours

 CONT RAIU….
• Elevated values indicate hyperthyroidism,
thyrotoxicosis, decreased iodine intake or
increased iodine excretion.

• Decreased values indicate hypothyroidism,

thyroiditis, low T4, use of antithyroid meds.

• Thyroid medication must be discontinued 7-

10 days prior to test.

• No radiation precautions necessary.

 GLYCOSYLATED HEMOGLOBIN

•is blood glucose bound to hemoglobin

•Is a reflection of how well blood glucose levels have
been controlled for up to the prior 3- 4 months

•Hyperglycemia in clients with DM causes increase in

glycosylated hemoglobin

•Fasting is not needed

CONT GLYCOSYLATED HGB…

VALUES ARE EXPRESSED AS A PERCENTAGE OF

TOTAL HEMOGLOBIN.
FOR CLIENTS W/O DM, NORMAL RANGE IS 4% - 6%

*Values:
Diabetics with good control: 7.5% or less
Diabetics with fair control: 7.6% to 8.9%
Diabetics with poor control: 9% or greater
 T3 & T4 RESIN UPTAKE TEST

*Blood test for diagnosis of thyroid disorders

*T3 & T4 regulate thyroid-stimulating hormone

*Normal Value of T3: 80-230 ng/dL

T4: 5-12 ng/dl

*Both values increase in hyperthyroidism

decreased in hypothyroidism
 THYROID-STIMULATING
HORMONE (TSH)
• Blood test used to differentiate the diagnosis of primary
hypothyroidism from secondary hypothyroidism.

• Normal value is 0.2 to 5.4 uU/ml

• Elevated in primary hypothyroidism

• decreased in hyperthyroidism or secondary

hypothyroidism
 THYROID SCAN
*Performed to identify nodules or growths in the thyroid
glands
*A radio isotope of iodine or technetium is administered
prior to the scanning of the thyroid gland.
*Level of radioisotope is not dangerous to self or others.
*Discontinue medications containing iodine 14 days prior
to test and discontinue thyroid meds 4-6 weeks prior to
test.
*NPO post MN; if iodine is used client will fast an additional
45 minutes after ingestion of radioactive isotope & scan is
done after 24 hours.
 NEEDLE ASPIRATION OF
THYROID TISSUE
• Aspiration of thyroid tissue for cytological exam

• No preparation needed

• Light pressure applied to aspiration site after the

procedure
 Eight-hour intravenous ACTH Test

*Administration of 25 units of ACTH in 500 ml of saline

over an 8-hr period.
*Used to determine function of adrenal cortex.
*24-hr urine specimens are collected, before & after
administration, for measurement of 17-ketosteroids
and 17-hydrocorticosteroids.
 Cont. Eight-hour intravenous ACTH Test….

• In Addison’s disease, urinary output of steroids does not

increase following administration of ACTH
• normally steroid excretion increases threefold to fivefold
ff. ACTH administration.
• In Cushing’s syndrome, hyperactivity of the adrenal
cortex increases the urine output of steroids in the
second urine specimen tenfold.
 GLUCOSE TOLERANCE TEST
(GTT)

*Aids in the diagnosis of diabetes mellitus

*If the glucose level peaks at higher than normal at 1 to
2 hours after injection or ingestion of glucose, and are
slower than normal to return to normal levels, DM is
diagnosed
ss
*Preparation:
-eat a high-carbohydrate (200 to 300 g) diet for 3 days before
the test
-avoid alcohol, coffee & smoking 36 hours before testing
-fast midnight before test
-fasting blood glucose & urine glucose specimens obtained.
-avoid strenuous exercise 8 hours before & after test
-client ingests 100g glucose; blood sugar drawn at 30 & 60
mins. then hourly for 3-5 hrs.; urine specimens may also
be collected.
ANTERIOR PITUITARY
•Hypopituitarism
•Hyperpituitarism

POSTERIOR PITUITARY
•Diabetes Insipidus
•SIADH (Syndrome of Inappropriate Antidiuretic
Hormone)
 hypopituitarism
*Hyposecretion of growth hormone by the anterior
pituitary gland

*S/Sx: retarded physical growth, premature aging,

low intellectual development, poor development of
secondary sex characteristics

*Given human growth hormone & offer emotional

support to client & family
 hyperpituitarism
*Hypersecretion of GH by anterior
pituitary gland which results in
gigantism or acromegaly

*Gigantism occurs in
childhood before the closure of
epiphyses of the long bones

* acromegaly which occurs

after the closure of epiphyses of
the long bones
 Cont of hyperpituitarism…

• *S/Sx: large hands & feet, thickening & protrusion

of jaw, arthritic changes, visual disturbances,
diaphoresis, oily & rough skin, organomegaly,
hypertension, dysphagia, deepening of voice

• *Emotional support; frequent skin care;

pharmacologic & non- pharmacologic
interventions for joint pains

• *Prepare for radiation of pituitary gland or

hypophysectomy
 hypophysectomy
*Removal of pituitary gland
*Post-operative care:
-Monitor V/S, neurological status & LOC
-Elevate head of bed
-Monitor for increased intracranial pressure & any
postnasal drip which might be CSF
-Avoid sneezing, coughing & blowing nose
-Monitor for temporary diabetes insipidus
-Monitor I & O & water intoxication
-Administer antibiotics, analgesics, antipyretics,
hormones & glucocorticoids if entire gland is removed
 Diabetes insipidus
*Hyposecretion of ADH & deficiency of vasopressin

*S/Sx:
• polyuria of 4-24 liters/day
• polydipsia
• dehydration
• dec skin turgor
• dry mucus membranes
• inability to concentrate urine
• low urine sg of 1.004 or less
• fatigue
• postural hypotension
• headache
 TYPES OF DI
Neurogenic/Central Nephrogenic DI
• Insufficient amt of ADH • Inadequate response to
• d/t organic lesions of the ADH
hypothalamus or post • Renal tubules are
pituitary w/c interferes w/ insensitive to ADH
ADH synthesis, transport • Usually acquired:
and release polynephritis or PCKD
• Drugs:anesthetic,
lithium, antibiotics and
anti-CA
Psycogenic DI • Diagnostics
• Due to an extremely urinalysis
large amt of fluid water deprivation
intake test
• ADH levels dec bec
of inc intake
• Provision of safe environment especially with
decreasing LOC
• monitoring I & O with specific gravity
• wear Medic-Alert bracelet

*Meds: vasopressin tannate (Pitressin Tannate)

desmopressin acetate (DDAVP, Stimate)
lypressin (Diapid)
*Enhances reabsorption of water in the
kidneys promoting antidiuretic effect & regulates
fluid balance

A/R: hypertension; nasal congestion

 Syndrome of Inapproproiate
Antidiuretic Hormone
•Hypersecretion of ADH
•Excess ADH is released but not in response to body need
• end result: hyponatremia

Causes:
trauma stress
stroke malignancy
*S/Sx:
Signs of fluid overload
changes in LOC & mental status
weight gain
hypertension
tachycardia
hyponatremia
 Nursing Intervention
• Monitor I & O and daily weight
• monitor fluid & electrolyte balance
• restrict fluids as prescribed
• administer diuretics & monitor IV fluids
carefully

• *Meds: demeclocycline (Declomycin)

inhibits ADH-induced water reabsorption
& produces water diuresis
ADRENAL CORTEX
Addison’s disease
Cushing’s syndrome
Aldosteronism (Conn’s Syndrome)

ADRENAL MEDULLA
Pheochromocytoma
 Addison’s Disease
•Hyposecretion of the adrenal cortex
hormones
• 90% of the gland is destroyed

Assessment:

Subjective:
• Muscle weakness nausea
• fatigue anorexia
• lethargy fainting
• dizziness
• abdominal pain/cramps.
Objective:
• V/S: decreased BP, orthostatic hypotension
• Pulse: increased, collapsing, irregular
• Subnormal temp.
• Vomiting, diarrhea, weight loss
• Tremors
• Skin: poor turgor excessive pigmentation
(bronze tone)
• Hyponatremia, hypoglycemia, hyperkalemia
Diagnostics:
• Plasma and urine testing for 17-hydroxy-corticosterids & 17
ketosteroid
• Serum Na, K & BUN
• FBS
• Xray: small heart; adrenal calcification
NURSING MANAGEMENT:
1. Decrease stress:
a. Provide quiet environment, nondemanding schedule
2. Promote adequate nutrition:
a. Diet: acute phase- high sodium, low potassium;
nonacute phase- increase CHO and CHON
b. Fluids: force to balance fluid, monitor I&O, WOD
c. Administer lifelong exogenous replacement therapy as
ordered:
1. Glucocorticoids- prednisone, hydrocortisone
2. Mineralocorticoids- fludrocortisone (Florinef)

3. Health teaching:
a. Take meds with food or milk.
b. Avoid stress

4. Monitor for s/sx of addisonian crisis

 Addisonian Crisis
*Life-threatening disorder caused by acute adrenal
insufficiency precipitated by stress, infection, trauma or
surgery

*May cause hyponatremia, hypoglycemia, hyperkalemia

& shock

*Given glucocorticoids IV e.g. hydrocortisone Na

succinate (Solu- Cortef), mineralocorticoids e.g.
fludrocortisone (Florinef)
• Severe, generalized muscle weakness, severe
hypotension, hypovolemia, shock (vascular collapse)

• Check BP & electrolyte levels

• Strict bed rest in quiet environment & protect from

infection.
• In adrenal insufficiency, the client has
hyperkalemia due to reduced aldosterone
secretion. BUN inc, as the GFR is reduced.
Hyponatremia is caused by reduced
aldosterone secretion. Reduced cortisol
secretion leads to impaired glycogenesis
and a reduction of glycogen in the liver and
muscle, causing hypoglycemia.
 Cushing’s Syndrome
•Hypersecretion of corticoids
• etiology: Bilateral Adrenal Hyperplasia 2 to inc ACTH
•Adrenal tumors
•Ectopic ACTH prodn
•Long steroid usage
•ASSESSEMENT:
Subjective:
 headache, backache, weakness, decreased work
capacity
• Objective cues:
• Hypertension, weight gain,
pitting edema
• Characteristic fat deposits,
truncal & cervical obesity
(buffalo hump).
• Pendulous abdomen, purple
striae, easy bruising
• Moon face, hyperpigmentation,
impotence
• Virilization in women: hirsutism,
breast atrophy, amenorrhea
• Pathologic fractures reduced
height
• Slow wound healing
• Hypernatremia, hyperglycemia,
hypokalemia
Diagnosis
• 24 hr urine cholesterol
• ACTH levels det
• Dexamethasone suppression test
• Serum Na, K
• FBS/HGT
• Radiographic studies
• Skull series
• CT scan/MRI
• NURSING MANAGEMENT:
• Promote comfort: protect from trauma.
• Prevent complications: monitor fluid balance,
glucose metabolism, hypertension, infection.
• Health teachings:
a. Diet: increased protein, potassium, decreased
calories, sodium

b. Meds:
1. Cytoxic agents: aminoglutethimide
(Cytaden), trilostane (Modrastane), mitotane
(Lysodren)- to decrease cortisol production.
2. Replacement hormones as needed.
c. S/Sx of progression of disease.
d. Prepare client for adrenalectomy.
 Hyperladosteronism
(Conn’s syndrome)
*Hypersecretion of aldosterone from the adrenal
cortex of the adrenal gland commonly caused by
adenoma
*acts to conserve sodium, secrete potassium, and
increase blood pressure. It is reduced in Addison's
disease and increased in Conn syndrome.

*S/S: hypernatremia
hypertension,
polydipsia , polyuria,low urine specific gravity
hypokalemia, headache
• Monitor I & O & administer spironolactone
(Aldactone)
• It is named after Dr Jerome W. Conn (1907-1994),
the American endocrinologist who first described
the condition in 1955
• K supplements & maintain Na restriction

• *Administer antihypertensives as px

• *Wear Medic-Alert bracelet

• *Usually will be undergoing adrenalectomy;

• administer glucocorticoids pre & post-op

 Pheochromocytoma
*Catecholamine-producing tumor usually found in
the adrenal gland.

*extra-adrenal chromaffin tissue which failed to

involute after birth, which secretes excessive
amounts of catecholamines, usually epinephrine
and norepinephrine.

*Cx: hypertensive retinopathy, CVA & CHF

S/Sx:
• HPN
• severe headache
• palpitations
• pain in chest or abdomen
• hyperglycemia & glucosuria
• profuse sweating
• n/v
• dilated pupils
• tachycardia
• cold extremities
Cont pheochromocytoma….

• Monitor for hypertensive crisis

– avoid stimuli which triggers it such as : increased
abdominal pressure
vigorous abdominal palpation
micturation

• Instruct patient not to smoke, drink cola, coffee or

tea

• Monitor blood glucose & urine for glucose & acetone.

 Adrenalectomy
*Surgical removal of one or more of the adrenal
gland because of tumors or overactivity
*For unilateral: up to 2 years of glucocorticoid
therapy
*for bilateral: lifelong replacement
*Preop: reduce risk of postop sx
a. Prescribed steroid therapy, given 1 wk.
before surgery
b. Antihypertensive drugs discontinued
c. Sedation as ordered
*During surgery: monitor for hypotension &
hemorrhage
*Postop: promote hormonal balance
a. Administer hydrocortisone
b. Monitor for signs of Addisonian crisis

*Observe for hemorrhage and shock.

*Prevent infection.

*Administer cortisone or hydrocortisone as

prescribed.
 Adrenocorticotrophic Hormones

bethamethasone (Celestone), cortisone (Cortone)

dexamethasone (Decadron), prednisone (Orasone)

*Stimulate the adrenal cortex to secrete cortisol

*Produces an antiinflammatory effect.

*A/R: Increased appetite, mood swings, water & Na retention,

hypocalcemia & hypokalemia, cushing-like symptoms
*Check I & O, weight and for edema (decrease Na
intake)
*Monitor for infection
*Monitor electrolyte & calcium levels
*Monitor for poor wound healing, menstrual
irregularities, decrease in growth & edema
*Dose must be tapered & not stopped abruptly
*Advise to wear Medic-Alert bracelet
 Corticosteroids
(Glucocorticoids)
*Produce metabolic effects; alters normal immune
response & suppress inflammation; promote Na &
H2O retention & K+ excretion

*Produce antiinflammatory , antiallergic & anti-stress

effects; replacement for adrenocortical insufficiency

*A/R: hyperglycemia, hypokalemia, edema & masks

signs & symptoms of infection
Cont glucocorticoids…

*C/I: DM, increases effect of anticoagulants & oral

antidiabetic agents; increases potency of aspirins &
NSAIDS & K-sparing diuretics

*Check for overdose or signs of Cushing’s syndrome;

additional doses during stress or surgery.
 Mineralocorticoids
fludrocortisone (Florinef)

*Steroid hormones that enhance the reabsorption of NaCl &

promote K+ excretion & hydrogen at the renal tubule promoting
fluid & electrolyte balance

*Used in primary & secondary Addison’s disease

*S/E: Na/H2O retention, hypokalemia, hypocalcemia, delayed

wound healing, increased susceptibility to infection, mood swings,
weight gain

*Take with food or milk; high-K+ diet

*Wear Medic-Alert bracelet

HYPOTHYROIDISM (MYXEDEMA)

HYPERTHYROIDISM (GRAVE’S DISEASE)

 Hypothyroidism
*Hyposecretion of the thyroid hormone characterized by
decreased rate of body metabolism

Etiology: surgical removal of thyroid gland

over tx of hyperthyroidism with drugs or RAI
ASSESSMENT:
Subjective data:
 Weakness, fatigue, lethargy, headache, slow memory, loss of
interest in sexual activity.
Objective data:
 Depressed BMR; intolerance to cold
 Cardiomegaly, bradycardia, hypotension, anemia
 Menorrhagia, amenorrhea, infertility
 Dry skin, brittle nails, coarse hair, hair loss
 Slow speech, hoarseness, thickened tongue
 Weight gain: edema, periorbital puffiness
 Lab data: elevated TRH, TSH; normal-low serum T4 & T3;
decreased RAUI, elevated cholesterol
• The functions of thyroid hormones include
modulation of carbohydrate, protein and fat
metabolism, vitamin utilization, mitochondrial
function, digestive process, muscle and nerve
activity, blood flow, oxygen utilization,
hormone secretion and sexual and reproductive
health to mention a few. Thus, when the
thyroid hormone content gets out of balance,
systems covering the whole body are affected.
This is why hypothyroidism can look like other
diseases. Conversely, sometimes other
conditions can be mistaken for hypothyroidism.
NURSING MANAGEMENT
1. Provide for comfort and safety
• monitor for infection or trauma
• provide warmth
• prevent heat loss & vascular collapse
• Assess for constipation
• administer thyroid meds as ordered
2. Health teaching:
a. Diet: low calorie, low cholesterol, high protein
b. S/Sx of hypothyroidism & hyperthyroidism
c. Lifelong meds, dosage, desired effects, side
effects.
d. Stress-management techniques
e. Exercise program
 Myxedema Coma
*Rare but serious d/o which result from persistently low thyroid
hormone precipitated by:
• acute illness
•rapid withdrawal of thyroid meds
•use of sedatives & narcotics
*S/Sx:
hypotension
bradycardia
Hypothermia
Hyponatremia
hypoglycemia
respiratory failure & death
 Nursing and Medical Mgt
• Patent airway
• Keep patient warm & check V/S
frequently
• Administer IV fluids & levothyroxine
Na (Synthroid)

• Give IV glucose & corticosteroids

 Hyperthyroidism
*Hypersecretion of the thyroid gland leading to inc
metabolic process

*over activity and changes in the thyroid gland

*clinical syndrome caused by an excess of circulating

free thyroxine (T4) or free triiodothyronine (T3), or
both.
ASSESSMENT:
Subjective data:
o nervousness, mood swings, palpitations, heat
intolerance, dyspnea, weakness.

Objective data:
o Eyes: exophthalmos, characteristic stare, lid lag.
o Skin: warm, moist, velvety; increased sweating;
increased melanin pigmentation; pretibial edema
with thickened skin & hyperpigmentation
o Weight loss despite increased appetite
• V/S: increased systolic BP, widened pulse pressure,
tachycardia
• Goiter: thyroid gland noticeable & palpable
• Gyne: abnormal menstruation
• GI: frequent bowel movements
• Activity pattern: fatigue which leads to depression

• Lab data: elevated T3 & T4 level; elevated RAIU; elevated

metabolic rate (BMR); decreased WBC caused by
decreased granulocytosis (<4500).
NURSING MANAGEMENT:
1. Protect from stress: private room, restrict visitors,
quiet environment.
2. Promote physical & emotional equilibrium:
a. cool, quiet, cool well ventilated environment.
b. eye care: sunglasses to protect from
photophobia, protective drops (methylcellulose) to
soothe cornea
c. diet: high calorie, protein, vit. B; avoid stimulants
3. Prevent complications: give medications as ordered.
4. Monitor for thyroid storm.
5. Health teaching: stress reduction techniques;
importance of medications; methods to protect eyes
from environment; s/sx of thyroid storm.
*Prepare the patient for the following:
-iodine preparations
-antithyroid meds
-propanolol (Inderal)
-radioactive iodine
-for thyroidectomy as px
MEDICAL MANAGEMENT:
1. Propylthiouracil (PTU)
- blocks thyroid synthesis

2. Methimazole (Tapazole)
- to inhibit synthesis of thyroid hormone

3. Iodine preparations (SSKI, Lugol’s Solution)

- decrease size & vascularity of the thyroid gland
- palatable if diluted with water, milk or juice
- give through straw tp prevent staining of teeth
- takes 2-4 weeks before results are evident
4. Beta blockers: Propranolol (Inderal), atenolol
(Tenormin), metoprolol (Lopressor)
- given to counteract the increased metabolic
effect of thyroid hormones
- relieve symptoms of tachycardia, tremors &
anxiety
 Thyroid Storm
•Acute & life threatening condition in uncontrolled
hyperthyroidism

*Risk factors:
Infection
surgery
beginning labor to give birth
taking inadequate antithyroid medications before
thyroidectomy.
• *S/Sx:
– fever
– Tachycardia
– hypotension
– marked respiratory distress
– pulmonary edema
– Irritability
– Apprehension
– Agitation
– Restlessness
– Confusion
– seizures

• Meds: PTU or Tapazole; Sodium iodide IV or Lugol’s

solution orally; Propranolol (Inderal); Aspirin,
Steroids, Diuretics
 Thyroidectomy
*Removal of thyroid gland & performed for
persistent hyperthyroidism
*PRE-OPERATIVE CARE:
-Assess V/S, weight, electrolyte & glucose level
-Teach DBE & coughing as well as how to
support neck in post-op period when coughing
& moving
-Administer antithyroid meds etc. to prevent
thyroid storm
POST-OP CARE:
• Monitor for respiratory distress & have tracheostomy
set, O2 & suction machine at bed side
• Maintain semi-Fowler’s position to reduce 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-pitched
voice, stridor, dysphagia, dysphonia & restlessness
• Monitor for signs of hypocalcemia & tetany & have
calcium gluconate at bed side
 Thyroid Hormones
Levothyroxine (Synthroid, Levothroid, Levoxyl)
Thyroglobulin (Proloid)

•Controls the metabolic rate of tissues

•accelerates heat production & oxygen
consumption
•For hypothyroidism, myxedema & cretinism
•A/R: cramps, diarrhea, nervousness, tremors,
hypertension, tachycardia, insomnia, seating &
heat intolerance
*Taken same time every day preferably in the
a.m. with food
*Teach client to how to take HR
*Avoid foods that will inhibit thyroid secretions
such as:
strawberries, peaches, pears, cabbage, turnips,
spinach, Brussels sprouts, cauliflower, peas
& radish
*Wear Medic-Alert bracelet
Disorders of the Parathyroid
Gland

HYPOPARATHYROIDISM

HYPERPARATHYROIDISM
 Hypoparathyroidism
*Hyposecretion of parathyroid hormone
*Monitor for hypocalcemia & institute seizure
precautions
*Place a tracheostomy set, O2 & suction machine at bed
side
*Prepare for calcuim gluconate/chloride IV
*Provide high-calcium/low-phosphorus diet
*Give vitamin D to enhance calcium absorption at the
GIT
*Given phosphate binders
*Wear medic-alert bracelet
 Hyperparathyroidism
*Hypersecretion of parathyroid hormones

*S/Sx:
•hypercalcemia & hypophosphophatemia
•fatigue & muscle weakness
•skeletal pain & tenderness
•bone deformities resulting from pathologic fractures
•weight loss
•Constipation
•Hypertension
•cardiac dysrhythmias & renal stones
*Encourage fluids & administer furosemide
(Lasix) & IV salinase px
*Move patient slowly & carefully
*Administer phosphates as px
*Administer calcitonin (Calcimar) as px to
decrease skeletal calcium release & increase
renal calcium clearance & monitor for
hypocalcemia & report to MD
*Prepare for parathyroidectomy
 Signs of Tetany
*Positive Chvostek’s Sign
*Positive Trousseau’s Sign
*Wheezing & dyspnea (bronchospasm,
laryngospasm)
*Numbness & tingling of face & extremities
*Carpopedal spasm
*Visual disturbances (photophobia)
*Muscle & abdominal cramps
*Cardiac dysrhythmias
*Seizures
 Parathyroidectomy
*Removal of 1 or more parathyroid gland

*PRE-OPERATIVE CARE:
-monitor calcium, phosphate & magnesium
level
-ensure that calcium is near normal
-explain to patient that talking may be painful 2
days post-op
*POST-OPERATIVE CARE:
-monitor for respiratory distress & have a
tracheostomy set, O2 & suction machine at
bed side
-Semi-Fowler’s position
-Check for bleeding
-Check for hypocalcemic crisis, Trousseau’s or
Chvostek’s sign
-Assess changes in voice pattern & for laryngeal
nerve damage
-Administer calcium & vitamin D supplements as
prescribed.
CALCIUM SUPPLEMENTS
•calcium carbonate (Tums)
•calcium gluconate
•calcium lactate

VITAMIN D SUPPLEMENTS
•calcifediol (Calderol)

CALCIUM REGULATORS
•calcitonin human (Cibacalcin)

ANTIHYPERCALCEMICS
•edetate disodium (Disotate)
*Parathyroid hormone regulates serum calcium
levels

*Low serum calcium level stimulate parathyroid

hormone release

*Hyperparathyroidism…given antihypercalcemics

*Hypoparathyroidism…given calcium & Vit. D

 DIABETES MELLITUS
•A chronic disorder of impaired glucose intolerance and
carbohydrate, protein & lipid metabolism
•caused by a deficiency or resistance to the action of
insulin
•Predisposing factors:
•Older individuals
•Obese persons
•Women
•hereditary
• chronic obesity leads to increased insulin resistance
that can develop into diabetes, most likely because
adipose tissue is a (recently identified) source of
several chemical signals to other tissues (hormones
and cytokines). Other research shows that type 2
diabetes causes obesity
• Gestational diabetes affects 3-10% of pregnancies,
depending on the population studied. No specific
cause has been identified, but it is believed that the
hormones produced during pregnancy reduce a
woman's sensitivity to insulin, resulting in high
blood sugar levels.
 Diabetes Mellitus
• Diabetes derived from the greek word which
means ‘’going through’’
• Mellitus from a latin word which means
‘’honey’’ or ‘’sweet’’
• All types have been treatable since insulin
became medically available in 1921
1. INSULIN-DEPENDENT DIABETES
* Juvenile onset
• Destruction of beta cells
• Dec or absence of insulin production
• Prone to DKA
MGT: Activity- Insulin - Diet
2. NON-INSULIN DEPENDENT DIABETES
• Relative lack or resistant to the action of insulin
• Insulin is insufficient to stabilize fat and CHON but not
CHO
• Prone to HHNK
• Mgt: Meds – Activity - Diet
3. GESTATIONAL DIABETES
 ASSESSMENT
• POLYPHAGIA = cellls become hungry due to glucose level
• POLYDIPSIA= fluid travel from ICS to IVS = cell dehydration
• POLYURIA= GFR-tubules cannot reabsorb-glycosuria-glucose
attracts water---osmotic diuresis
• HYPERGLYCEMIA
• WEIGHT LOSS
• BLURRED VISION= Small blood vessels – such as those in the
eye – are especially vulnerable to poor blood sugar control. An
over accumulation of glucose and/or fructose damages the tiny
blood vessels in the retina===diabetic retinopathy

• SLOW WOUND HEALING = Poor healing of wounds, particularly

of the feet, can lead to gangrene, which may require amputation.
• VAGINAL INFECTIONS
• WEAKNESS & PARESTHESIAS
• SIGNS OF INADEQUATE FEET CIRCULATION
APPROACH TO DIABETES MELLITUS:

• DIET
• Based on desired weight

• EXERCISE
• Lowers bld glucose level
• Reduces CV risks
• Improve circulation and muscle tone
• Dec total cholesterol

• ORAL HYPOGLYCEMIC AGENTS/INSULIN

 Oral Hypoglycemic Agents
Sulfonylureas- inc insulin output by the β cells
Chlorpropamide (Diabinase)
Tolbutamide (Orinase)
Glimepinide (Solosa)
Acetohexamide (Dymelor)
Prandial Glucose Regulator
Repaglinide (Novonorm)
Rosiglitazone (Avandia)
Non-sulfonylureas
Metphormine (Glucophage)
Precose (Acarbose)
Rosiglitazone (Avandia)
 Insulin
•inc glucose transport into cells
•promotes conversion of glucose to
glycogen, decreasing serum glucose
levels
•Primarily acts in the liver, muscle,
adipose tissue by attaching to
receptors on cellular membranes
•facilitating transport of glucose,
potassium & magnesium
•INSULIN drugs= focus on the PEAK
TIME (hypoglycemic reaction)
What is a Good Pattern for Insulin Injection Rotation?
Rotate sites within a particular area, such as the left
side of the abdomen or the left front of the thigh,
injecting 1 inch from the previous spot each time.
For example, start with the left thigh until all injection
spots in that area have been used. Then, switch to
the right thigh. By the time you get back to the left
thigh again, the tissue should be healed and ready to
accept insulin again.
ROTATION OF SITES PREVENTS:
LIPODYSTROPHY
TYPE ONSET PEAK DURATION

RAPID-ACTING INSULIN 10-15 mins 1 hour 3 hours

Lispro (Humalog)
SHORT-ACTING INSULIN 0.5-1 hour 2-3 hours 4-6 hours
Humulin Regular
INTERMEDIATE-ACTING INSULIN 3-4 hours 4-12 hours 16-20 hours
Humulin NPH
Humulin Lente

LONG-ACTING INSULIN 6-8 hours 12-16 hours 20-30 hours

Humulin Ultralente
PREMIXED INSULIN 0.5-1 hour 2-12 hours 18-24 hours
70% NPH-30% Regular
 Glucagon
*Hormone secreted by the alpha cells of the islets of
Langerhans in the pancreas

*Inc blood glucose by stimulating glycogenolysis in the

liver

*given SC, IM or IV routes

*Used to treat insulin-induced hypoglycemia when

semiconscious/ unconscious
*HYPOGLYCEMIA
*DIABETIC KETOACIDOSIS (DKA)
*HYPERGLYCEMIC HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS)
• Types of hypoglycemia:

• Neuroglycopenia is a medical term that refers to a

shortage of glucose (glycopenia) in the brain,
usually due to hypoglycemia. Glycopenia affects the
function of neurons, and alters brain function and
behavior. Prolonged neuroglycopenia can result in
permanent damage to the brain.

• Reactive/adrenergic hypoglycemia is a medical term

describing recurrent episodes of symptomatic
hypoglycemia occurring 2-4 hours after a high
carbohydrate meal
Adrenergic Neuroglycopenic
• shakiness •Headache
•Irritability •Mental illness
•Nervousness •Inability to concentrate
• tachycardia, •Slurred speech
palpitations •Blurred vision
•Tremor •Confusion
•Hunger •Irrational behavior
•Diaphoresis •Lethargy, severe
•Pallor •Loss of consciousness
•paresthesias •Coma
•Seizure
•Death
*3 or 4 commercially prepared glucose tablets
CHILD: 2-3 GLUCOSE TABS

*4-6 ounces of fruit juice or regular soda

CHILD: ½ CUP OR 120 ML OF ORANGE JUICE OR SUGAR-SWEETENED JUICE

*6-10 Life Savers or hard candy

CHILD: 3-4 HARD CANDIES OR 1 CANDY BAR

*2-3 teaspoons of sugar or honey

CHILD: 1 SMALL BOX OF RAISINS
 Progressive insulin deficiency

Glucogenolysis/Gluconeogenesis

Contribute to further hyperglycemia

Breakdown of fats (glucose+ ketones)

Increased production of ketones

Acidosis---multisystem failure—affects CNS—affects
MEDULLLA---KAUSMAULL RESPIRATION,altered LOC &
COMA
 Causes
• Decreased or missed dose of insulin
• Illnesses or infection
• Undiagnosed or untreated type I DM
Assessment:
*3 Ps
*Blurred Vision
*Weakness
*Headache
*Hypotension
*Weak, rapid pulse
*Anorexia, nausea, vomiting & abdominal pain
*Acetone breath (fruity odor)
*Kussmaul respirations: rapid deep breathing
*Mental status changes
 Diagnostics
• Blood glucose 300 to 800 mg/dl
• Low serum bicarbonate and low pH
• Low serum sodium and potassium
 Treatment
• Treat dehydration: Rapid iv infusion
– Saline
– Dextrose containing bld glucose level at 250-
300mg/dl
• Treat hyperglycemia
– Use RI only
– 5-10 units
• Correct electrolyte imbalance (K+) due to
dehydration and acidosis
 Hyperglycemic Hyperosmolar
Nonketotic Coma
• Similar to DKA but without Kussmaul
Respirations and acetone breath
• Ketosis is absent because the presence of
some insulin inhibits lipolysis, unlike
diabetic ketoacidosis.
• Assessment:
– Bld sugar level 600 to 1200mg/dL
– Hypotension
– DHN
– Tachycardia
– Mental status changes
– Seizure
– Neurological deficits
•Serious long-term complications include
cardiovascular disease (doubled risk),
chronic renal failure, retinal damage
(which can lead to blindness), nerve
damage (of several kinds), and
microvascular damage, which may cause
impotence and poor healing
*Prevent moisture from accumulating between toes
*Wear loose socks & well-fitting (not tight) shoes &
instruct client not to go barefoot
*Change into clean cotton socks daily
*Wear socks to keep feet warm
*Do not wear the same shoes 2 days in a row
*Do not wear open toed shoes or shoes with strap that
goes between toes
*Check shoes for tears or cracks in lining & for
foreign objects before putting them on

*Break in new shoes gradually

*Cut toenails straight across & smooth nails with an

emery board

*Do not smoke

*Meticulous skin care & proper foot care
*Inspect feet daily & monitor feet for redness, swelling
or break in skin integrity
*Avoid thermal injuries from hot water, heating pads &
baths
*Wash feet with warm (not hot) water & dry thoroughly
(avoid foot soaks)
*Do not soak feet
*Do not treat corns, blisters or ingrown nails
*Do not cross legs or wear tight garments that may
constrict blood flow
*Apply moisturizing lotion to feet but not between toes
*Take insulin or oral hypoglycemic agents

*Test blood glucose & test the urine for ketones

every 3-4 hours

*If meal plan cannot be followed, substitute with soft

food 6-8/day

*If vomiting, diarrhea or fever occurs, consume

liquids every ½ to 1 hour to prevent dehydration &
to provide calories
• Notify doctor if vomiting, diarrhea, or fever
persists
• if blood glucose levels are > 250 to 300 mg/dL
• when ketonuria is present for > 24 hours
• when unable to take food or fluids for a period of
4 hours
• when illness persists for > 2 days