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ENDOCRINE SYSTEM
FUNCTIONS:
 Regulate the metabolic rate and the storage, conversion, and release of energy.
 Regulate fluid and electrolyte balance.
 Initiate coping responses to stressors.
 Regulate growth and development.
 Regulate reproduction processes.

ENDOCRINE SYSTEM

GLANDS HORMONES RECEPTORS

-specialized cells clusters or -chemical substances that
Organs acts as MESSENGER to
-exocrine glands and endocrine specific cells and organs
glands that stimulates and inhibits
various processes.
-protein molecules that
trigger specific physiologi
changes in a target cells
in response to hormonal
stimulation.

ENDOCRINE SYSTEM

GLANDS

HORMONES

BLOOD STREAMS

TARGET ORGANS

MAJOR ENDOCRINE GLANDS:

DIFFERENT TYPES OF HORMONES:

AMINE -Amino groups associated with the -THYROXINE
HORMONES molecules. -EPINEPHRINE
-There are no peptide bonds in the –NOREPINEPHRINE
molecules.
PROTEIN -Composed of amino acids bound by -INSULIN,CALCITONIN,PROLACTIN,FSH,LH,TSH
HORMONES peptide bonds. ADH,OXYTOCIN
-Most hormones are protein.
STEROID Are lipids synthesized from cholesterol -ESTROGENS
HORMONES -TESTOSTERONE
-ALDOSTERONE
-CORTISOL

ANATOMY AND PHYSIOLOGY:

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 PITUITARY GLAND
 THYROID GLAND
 PARATHYROID GLAND
 ANDRENAL GLAND
 PANCREAS
 GONADS

HYPOTHALAMUS

STIMULATING HORMONES

PITUITARY GLAND

HORMONES

TARGET GLANDS

NEGATIVE FEEDBACK
 Increased concentration of hormone inhibits the production of stimulating hormone resulting in decreased
secretion of the target organ hormone.

I.PITUITARY GLAND
 Also known as HYPOPHYSIS OR MASTER GLAND.
 Rest in the SELLA TURCICA in the INFERIOR aspect of the brain.
 Pea-sized gland connects with the hypothalamus via infundibulum.
 Contains Two lobes:
- ANTERIOR LOBE
- POSTERIOR LOBE

A. ANTERIOR PITUITARY GLAND

 Also known as “ADENOHYPOPHYSIS.”
 Produces several important hormones:

HORMONE TARGET ORGANS PRINCIPAL EFFECTS

FSH Ovarian follicle and Stimulates development of the follicle in the

ACTH Cortex of adrenal gland, Stimulates the production of corticosteroids,
Seminiferous tubules of ovary; production of sperm cells.
skin, liver, mammary increase the metabolic rate, glycogen
Testes
gland deposition in the liver, darkening of the skin,
LH Corpus luteum and milk production.
Stimulates production of progesterone
interstitial cells of testes. (ovaries) and testosterone (testes)
TSH Thyroid gland Stimulate the production of thyroxine
Prolactin Female mammary gland Stimulates milk production after parturation.
MSH Skin melanocytes Control skin pigmentation
HGH Body tissues Increases protein synthesis

B. POSTERIOR PITUITARY GLAND

 Also known as “NEUROHYPOPHYSIS.”
 Not an endocrine gland but rather a RESERVOIR for hormones produced by hypothalamus.
 Stores TWO important hormones:
1. ANTI-DIURETIC HORMONE (ADH) OR VASOPRESSIN.
2. OXYTOCIN

HORMONE TARGET ORGANS PRINCIPAL EFFECTS

ADH or Smooth muscle, especially of arterioles and Constricts blood vessels, thus raising
VASOPRESSIN kidney tubules. blood pressure
Stimulates reabsorption of water by
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kidney.

OXYTOCIN Uterus and ducts of mammary glands. Stimulates contraction of uterus if

primed by ovarian hormones
Enables milk-letdown reflex by
mammary glands.

DISORDERS OF POSTERIOR PITUITARY GLAND:

1. DIABETES INSIPIDUS
 Disorder of water metabolism.
 Due to hyposecretion of Anti-Diuretic Hormone.
 Start at childhood to adulthood (21 y.o.)
 Common in men than women
 Types:
1. Pituitary DI (Deficiency in VASOPRESSIN)
2. Nephrogenic DI (Inability of the kidney to respond to ADH)

Causes :
 Head trauma
 Brain tumor
 Surgical ablation
 Infections of CNS (meningitis, encephalitis, tuberculosis)

SIGNS AND SYMPTOMS:

 Polyuria (SG. 1.001-1.005)
 Extremely Thirst
 Dehydration
 Poor skin turgor
 Dry mucous membranes
 Constipation
 Muscle weakness
 Dizziness
 Hypotension
 Hypovolemic shock
 Anuria (LATE SIGN)

DIAGNOSIS:
 Urinalysis
- LOW OSMOLALITY and SPECIFIC GRAVITY (<1.005)
 Fluid Deprivation Test
- Provide evidence of vasopressin deficiency resulting in the kidneys in ability to concentrate urine.
- Withholding the fluids for 8-12 hours or until loses 3% of his body weight
- Hourly measurement of urine output, body weight, urine osmolality or specific gravity.
- FIRST STAGE OF TEST: If urine osmolality remains below that of serum, diagnosis of DI is confirmed
- SECOND STAGE: Artificial ADH is given to determine changes in urine osmolality at 30, 60, and 120
minutes in response to the injected hormone.
- If the highest osmolality value obtained after injection is more than 50% higher than preinjection value DI is
caused by PITUITARY FAILURE; If value is less than 50% of the preinjection value DI is caused by RENAL
DISEASE.

REMEMBER!!!!
 Urine Specific Gravity LOW (<1.005)
 ELEVATED Serum Sodium level

NURSING MANAGEMENT:
 Force Fluid.
 Monitor Vital Signs.
 Monitor Intake and Output.
 Provide Safety. (KEEP SIDERAILS UP)
 Monitor Urine Specific Gravity.
 Provide meticulous skin & mouth care.
 Watch for signs of HYPOVOLEMIC SHOCK.
 Administer Medication as ordered.

DRUG OF CHOICE:
 DESMOPRESSIN ACETATE (DDAVP)
- Synthetic Vasopressin
- Route: Intranasally
- 8 to 20 hours effect
- Over treatment may cause hyponatremia and water intoxication.
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 VASOPRESSIN INJECTION (Pitressin)

- Used when intranasally is not possible
- Route: IM
- 24 to 96 hours effect
- Vial should be warmed and shaken vigorously before administering. To ensure uniform dispersion active
component settles at the bottom of the vial.
- Administered at the evening (maximum results are obtained during sleep).
- Side effect: ABDOMINAL CRAMPS

2. SYNDROME OF INAPPRORIATE ANTI-DIURETIC HORMONE (SIADH)

 Excessive release of antidiuretic hormone (ADH)
 Inability to excrete dilute urine, retention of free water, expansion of extracellular fluid volume, and
hyponatremia.

CAUSES:
 Bronchogenic Ca
 Brain tumor or abscess
 Hyperplasia of pituitary
 Head injury

SIGNS AND SYMPTOMS:

 Weight Gain
 Nausea
 Vomiting
 Muscle weakness
 Restlessness
 Seizure
 Hypertension
 Edema
 Water intoxication

DIAGNOSIS:
 Urine Specific Gravity ELEVATED.
 LOW Serum Sodium Level (Dilutional Hyponatremia)

NURSING MANAGEMENT:
 Restrict Fluid
 Monitor Intake and Output
 Monitor Vital Signs
 Weight patient daily
 Observe for restlessness, irritability, seizures, and unresponsiveness due to Hyponatremia.
 Assess for pitting edema
 Provide meticulous skin care

NURSING MANAGEMENT FOR SEIZURE:

 Maintain patent airway.
 Promote safety. (Maintain siderails, avoid use of restraints, turn head to side)
 Avoid precipitating stimulus.
 Institute post seizure and safety precaution. (Oxygenation & provide suction apparatus)
 Document the onset and duration.

Medications:
 LOOP DIURETICS
- Furosemide (LASIX)
- BEST given in AM
- Immediate effect of lasix 10-15 minutes
- 6 hours maximum effect
- Monitor SIDE EFFECT:

a. HYPOKALEMIA
 Normal value: 3.5-5.5 meq/L)
 Weakness, fatigue, constipation
 Positive “U WAVE” ECG traces
 Management:
 Supplement:“KALIUM DURULE”
 Increase K in the Diet.

b. HYPOCALCEMIA
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 Normal values: 8.5-11 mg/100

 TETANY
 TROUSSEAU’S SIGN (CARPOPEDAL SPASM)
 CHVOSTEK’S SIGN (FACIAL PRALYSIS)
 ARRYTHYMIA AND SEIZURE

Management:
 Administered CALCIUM GLUCONATE
- SLOW IVP to prevent cardiac arrest
 Monitor Sign of Ca toxicity:
- SEIZURE (administer Mg SO4)
- Increase BP, urine output, RR, Patellar reflex (Early Sign)

c. HYPONATREMIA
 Normal Values: 135-145 meq/L
 Decrease BP
 Dehydration
 Early Sign:
- Children (tachycardia)
- Adult (Thirst)
- Dry mucous membrane

 OSMOTIC DIURETIC
- Mannitol / Osmitol
- Promote cerebral diuresis
- Monitor BP
- Monitor strictly I and O q hour
- Notify physician if output > 30 cc per hour
- Administered by side drip
- Regulate fast drip ( to prevent development of crystal or precipitate)
- Inform client for flushing sensation when drug is administered.

REMEMBER!!!
 INCREASED IN ICP
 SEIZURE
(COMMON COMPLICATION)

II. THYROID GLAND

 Lies directly below the larynx, partially in front of the trachea.
 Consist of lateral TWO LOBES interconnected by ISTHMUS.
 “Butterfly in shape.”
 Secretes 3 hormones:
1. TRIIODOTHYRONINE (T3)
2. THYROXINE (T4)
3. CALCITONIN

HORMONE TARGET ORGANS PRINCIPAL EFFECTS

T4 Body Tissue Cells -Maintain body’s metabolism in a steady state.

(Levothyroxine) -Serve as a precursor of T3
-Regulate the rate growth
-Stimulate the maturity of the nervous system
-Regulate blood pressure

T3 Body Tissue Cells -Same as T4

(Triiodothyronine) -Five times as potent as T4
-Has more rapid metabolic action and utilization than T4
does.

CALCITONIN BONES -Maintains / increases blood calcium level in bones by

-inhibiting the release of calcium in bones.

WHAT IS THE ROLE OF IODINE?

 Important in the synthesis of thyroxine.
 It regulate metabolism and growth.

Thyroid Gland taking up

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Iodide from the blood

Thyrosine Iodine molecules

Thyroid Hormone

Hypothalamus

Thyrotropin releasing hormone (TRH)

Sends a signal to the pituitary

Release thyroid stimulating hormone (TSH)

Thyroid

T4 and T3

DISORDER OF THYROID GLAND

1. GOITER
 Enlargement of thyroid gland due to iodine deficiency.

Factors:
 Goiter belt area
 Goitrogenic foods
- raddish, turnip, nuts, strawberry, sweet potato, brocolli
 Goitrogenic drugs
- Propylthiouracil (PTU)
- Lithium
- Para Amino Salicylic Acid
- Cobalt

Symptoms :
 Breathing difficulties
 Cough
 Swallowing difficulties
 Wheezing
 Enlargement of thyroid gland

2. HYPERTHYROIDISM
 Due to excessive production of thyroid hormone.
 Increase in T3 and T4.
 Grave’s Disease or Thyrotoxicosis.

CAUSES:
 Autoimmune
 Excessive iodine intake
 Hereditary
 Hyperplasia of thyroid gland

SIGNS AND SYMPTOMS:

 Excessive sweating
 Heat intolerance
 Diarrhea
 Tremor
 Nervousness
 Rapid heart rate
 Weight loss
 Fatigue
 Poor concentration
 Irregular menstrual flow
 Hyperphagia
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 Increased in VS

DIAGNOSIS:
 Blood tests
- T3 and T4
- INCREASE Thyroxine level
 Radioactive Iodine Uptake test (RAIU)
- Measures thyroid uptake patterns of iodine as a whole or within specified areas of the gland.
- Sodium Iodide 131 is administered orally to the fasting patient.
- Measurement of radioactive counts per minute are taken with scintillator.
- Normal thyroid will remove 15-50% of the iodine from the blood stream.
- Hyperthyroidism- removal of 90% of the iodine from the blood streams.
- Hypothyroidism- reflected low uptake
Nursing Management RAIU:
 Secure consent.
 Check for allergy to any medicines, such as iodine.
 Check if any test using radioactive materials or iodine dye 4 weeks before the RAIU test. These other tests
may change the results of the RAIU test.
 NPO for 2 hours before the test.
 Remove dentures and all jewelry or metal objects from around neck and upper body.
 Take special precautions when urinate.
- body gets rid of the radioactive tracer through urine. This takes about 24 hours. It is important to flush the
toilet and wash hands

 Thyroid scan
- Rapid imaging of thyroid tissue, particularly suspicious nodules, as contrast imaging agent is rapidly taken
up by functioning tissue.
- Reveals enlargement of thyroid gland.
- Useful to diagnosed thyroid carcinoma.

3. GRAVE’S DISEASE
 Most common form of hyperthyroidism.
 It occurs when immune system mistakenly attacks thyroid gland and causes it to overproduce the hormone
thyroxine .

NURSING MANAGEMENT:
 Monitor Vital Signs
 Monitor Intake and output.
 Increase in Caloric diet.
 Institute meticulous skin care
 Provide comfortable and COOL environment.
 Maintain side rails.
 Provide bilateral eye patch (To prevent dryness of the eye).
 Assist in surgical procedure.
 Give medications as ordered.

THYROID SURGERY
 Total thyroidectomy
- Removal of the entire gland and the lymph nodes surrounding the gland.
- Thyroid Cancer
 Thyroid lobectomy with or without an isthmectomy
- If thyroid nodules are located in one lobe, surgeon will remove only that lobe (lobectomy).
- With an isthmectomy, the narrow band of tissue (isthmus) that connects the two lobes also is removed.
 Subtotal (near-total) thyroidectomy
- Removal of one complete lobe, the isthmus, and part of the other lobe.
- Hyperthyroidism
NURSING MANAGEMENT:
Preoperative:
 Administer Lugol’s Solution
 Anti-hyperthyroid agent
 used to treat overactive thyroid, iodine deficiency, and protect the thyroid gland from the effects of radiation
from radioactive forms of iodine.
 Saturated solution of POTASSIUM IODIDE
 Prevent bleeding and hemorrhage.
 Nursing Management:
- Check for Allergies.
- Advice patient to use straw

Postoperative:
 Monitor V/S and I and O
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 Place client in semi-Fowler’s position and support head with pillows.

 Encourage deep breathing and coughing exercises.
 Encourage early ambulation
 Watch out for sign of “THYROTOXIC CRISIS or THYROID STORM”
- Acute exacerbation of hyperthyroidism
- Life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in
individuals with thyrotoxicosis.

TRIAD SYMPTOMS OF THYROID STORM:

 Hyperthermia
 Agitation
 Tachycardia

NURSING MANAGEMENT TRIAD SYMPTOMS:

 STRICTLY monitor VITAL SIGNS
 STRICTLY monitor I and O
 STRICTLY monitor NEURO VITAL SIGNS.
 Maintain Safety (SIDE RAILS )
 Render TSB
 Give medication as ordered:
- Anti-pyretics
- Beta adrenergic blockers (drug of choice: INDERAL or PROPANOLOL)

 Watch out for accidental removal of parathyroid gland

TETANY HYPOCALCEMIA

CHVOSTEK’S TROUSSEAU’S

Twitching of the ipsilateral facial muscles, Muscular contraction including flexion

suggestive of neuromuscular excitability of the wrist and metacarpophalangeal joints,
caused by hypocalcemia hyperextension of the fingers, and
flexion of the thumb on the palm.

 Watch out for accidental laryngeal damage.

- Encourage the client to speak or talk.
- Watch out for signs of bleeding.
- Feeling of fullness at the incision site.
- Check the soiled dressing at the back or nape area.
- Notify physician immediately.
 Watch out for laryngeal spasm
- Prepare bedside “TRACHEOSTOMY SET.”
 Hormonal repacement therapy.

DRUG OF CHOICE:
Propylthiouracil (PTU) and Methimazole (Tapazole)

Agranulocytosis Increased WBC

Fever Leukocytosis

SORE THROAT
4. HYPOTHYROIDISM
 Is a condition in which the body lacks sufficient thyroid hormone.
 Decrease in T3 and T4.
 Myxedema (adult) and Cretinism (children).

Possible Complications:   
 Mental retardation
 Growth retardation
 Heart problems

CAUSES:
 Iatrogenic (disease cause by medical intervention)
 Atrophy of thyroid gland
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 Irradiation
 Tumor
 Trauma
 Iodine deficiency
 Autoimmune (Hashimoto’s Disease)

Hashimoto's Disease
 Autoimmune disease where the body's own antibodies attack the cells of the thyroid.

SIGNS AND SYMPTOMS:

Early symptoms:
 Weakness
 Fatigue
 Cold intolerance
 Constipation
 Weight gain
 Depression
 Joint or muscle pain
 Thin, brittle fingernails
 Thin and brittle hair
 Paleness

Late symptoms:
 Slow speech
 Dry flaky skin
 Thickening of the skin
 Puffy face, hands and feet
 Decreased taste and smell
 Thinning of eyebrows
 Hoarseness
 Abnormal menstrual periods
 Decreased VS

DIAGNOSIS:
 T3 and T4
- reveals “DECREASE” in thyroxine level
 Radioactive iodine uptake test (RAUI)
- Reveals “DECREASE” iodine uptake
 Serum cholesterol “INCREASE.”

NURSING MANAGEMENT:
Strictly Monitor V/S and Intake and Output

To prevent Myxedema Coma

(Severe form of Hypothyroidism)

Decrease V/S, hypoventilation, hypoglycemia, hyponatremia

COMA

 Provide dietary intake LOW in Calorie.

 Institute meticulous skin care.
 Provide comfortable and warm environment.
 Force fluid.
 Provide client Health teachings:
 Avoidance of stress, infection, cold environment, avoid anesthetics, sedative, narcotic analgesic.
 Prevent complication. (Myxedema coma and Hypovolemic Shock)
 Hormonal replacement therapy for lifetime.
 Administered medication as ordered.

DRUG OF CHOICE:
- Levothyroxine (Synthroid)
- Liothyronine (Cytomel)
- Thyroglobulin (Proloid)
- Euthroid
- Thyroxine Triiodothyronine (Thyrolar)
- Eltroxine
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NURSING MANAGEMENT (MEDS):

 Best given in AM. (To prevent INSONMIA)
 Monitor V/S especially CARDIAC RATE. (Side effects: tachycarida, palpitations, HPN, and heat
intolerance.)
 Encourage increased intake of foods rich in iodine. (seaweeds, seafoods, and iodized salt)

III. PARATHYROID GLAND

 “Smallest” endocrine glands.
 Embedded on the posterior surface of the thyroid, one in each corner (apple seed)
 Also known as “Parathyroid Hormone.”
 Secrete a hormone: “PARATHORMONE”
 “Help to regulate the blood CALCIUM balance.
 Acts antagonistically to calcitonin and decreases the level of calcium in the bones by stimulating the activity
of osteoclasts.
 Affects the activation of Vitamin D.
 Increases the movement of phosphate ions from blood to urine for excretion.

Disorders of Parathyroid Glands:

1. HYPOPARATHYROIDISM
 Is a condition in which body secretes abnormally low levels of parathyroid hormone.

Decreased PARATHORMONE

Decreased calcium Increased Phosphorus

Hypocalcemia Hyperphosphatemia

Causes:
 Hereditary
 Acquired hypoparathyroidism accidental damage to or removal of the parathyroid glands during surgery.

SYMPTOMS:
Acute Tetany
 Tingling sensation
 Parasthesia
 Dysphagia
 + laryngospasm
 + TROUSSEAU’S
 + CHVOSTEK’S
 Arrhythmia
 Seizures
Chronic Tetany
 Cataract
 Photophobia
 Loss of tooth enamel
 Anorexia
 Malaise
 Irritability
 Memory impairement

Diagnosis:
 Low serum calcium level
 High serum phosphorus level
 Low serum parathyroid hormone level
 Abnormal heart rhythms on ECG
Nursing Management:
 Prepare tracheostomy set at bedside. (Laryngospasm may result from hypocalcemia)
 Diet High calcium and Low phosphate
 Encourage the client to breath using paper bag (To prevent respiratory acidosis)
 Monitor V/S.
 Prevent complications (SEIZURE AND ARRHYTHMIA)
 Avoid precipitating factors (Light-photopobia)
 Institute seizure and safety precaution.
 Hormonal replacement
 Give medications as ordered.
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DRUG OF CHOICE:
 Calcium Gluconate (IV)
 Oral calcium supplement
- Calcium gluconate
- Calcium carbonate
- Calcium lactate
 Vitamin D
 Aluminum Hydroxide(Amphogel-Phosphate binder) – “watch out for constipation”

NURSING ALERT!!!
 All IV calcium preparations are administered slowly. It is highly irritating, stings, and causes thrombosis.
 Too-rapid calcium administration may cause cardiac arrest.
 Closely monitor the patient receiving DIGITALIS GLYCOSIDES and CALCIUM because calcium
potentiates the effect of digitalis glycosides .
 Stay alert for signs of digitalis toxicity:
- Arrhythmias, Nausea, Fatigue, Visual changes

2. HYPERPARATHYROIDISM
 Excessive production of parathyroid hormone by the parathyroid glands.

Increased PARATHORMONE

Increased calcium Decreased Phosphorus

Hypercalcemia Hypophosphatemia

Bone Mineralization

BONE FRACTURE

Increased Parathormone

Increase Bone Resorption

Calcium losses Bone

Hypercalcemia Brittle Hypercalcemia

Decrease Phosphorus Fracture CA crystals

Stones

Causes:
Primary:
 Hyperplasia of parathyroid glands. Increase production parathyroid hormone, which raises the level of
calcium in the blood.

Secondary:
 Primarily the result of renal failure

Signs and Symptoms:

 Fatigue
 Back pain
 Joint pain
 Fractures of long bones
 Decreased height
 Kidney Stones
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 Increased urine output

 Increased thirst
 Upper abdominal pain
 Loss of appetite
 Nausea
 Muscular weakness
 Muscle pain
 Depression

Diagnosis :
 High serum calcium level
 Low serum phosphorus level
 24-hour urine collection
- increased calcium in urine.
 Bone x-ray
- shows bone reabsorption or fractures.
 X-rays, ultrasound, or CT scans of the kidneys or ureters
- show calcification or obstruction.
 Bone density test
- show reduced bone mineral density, particularly of the forearm

Nursing Management:
 Force fluids
 Strain all the urine using gauze pan.
 Provide warm sitz bath
 Instruct acid-ash diet – favors excretion of kidney stones; (Acid forming foods; meats, breads, cereals,
vegetables. while restricting the intake of alkaline forming foods such as fruits except cranberries, plums
and prunes)
 High Calcium and Phosphate diet.
 Maintain side rails.
 Encourage ambulation
 Give medication as ordered
 Hormonal replacement
 Assist for Surgery. “PARATHYROIDECTOMY”

PARATHYROIDECTOMY
 is surgery to remove parathyroid glands or parathyroid tumors.
 Done under general or local anesthesia
 Some parathyroid tissue is left in place to help prevent hypoparathyroidism.
 Small horizontal incision is created just under the Adam's apple to get access to the parathyroid glands.

NURSING ALERT!!!
 Keep Tracheostomy set at bedside postoperatively.
 Keep Ca gluconate Available.
 Check for respiratory distress.
 Monitor for postop complications:
- Laryngeal nerve damage
- Hemorrhage
 Monitor V/S and I and O

DRUG OF CHOICE:
 CALCITONIN
- Reduce blood calcium, opposing the effects of parathyroid hormone (PTH)
- blocks bone resorption
- Dose is 4 Units per kg via subcutaneous or intramuscular route every 12 hour
 FUROSIMIDE (LASIX)
- increases urinary calcium excretion by inhibiting renal calcium reabsorption

IV. ADRENAL GLANDS

 Lie on the top of a kidney.
 “Almond-shaped”
 Two major Portions:
1. MEDULLA
2. CORTEX

1. ADRENAL MEDULLA
 Inner tissue of adrenal gland.
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 Secrets Amine hormones known as CATECHOLAMINES that complement the action of “SYMPHATETIC
NERVOUS SYSTEM” (EPINEPHRINE AND NOREPINEPHRINE).

SYMPHATETIC PARASYMPHATETIC

 Fight or Aggressive  Flight or Withdrawal

 Norepinephrine  Acethylcholine
 Vasoconstriction  Vasodilation
 All body activities are increased except GIT  All body activities are decreased except GIT
 Mydriasis  Miosis
 Dry mouth  Increased salivation
 Increased RR, PR, TEMP, BP.  Decreased RR, PR, TEMP, BP.
 Constipation  Diarrhea
 Urinary retention  Frequency in urination

2. ADRENAL CORTEX
 Outer tissue of the gland.
 Has Three Zones:
1. Zona Glumerulosa
2. Zona Fasiculata
3. Zona Reticularis

NAME LAYER PRIMARY PRODUCT

ZONA GLOMERULOSA Most Superfacial layer Mineralocorticoids

(Aldosterone)

ZONA FASCICULATA Middle cortical layer Glucocorticoids cortisol

(Hydrocortisone)

ZONA RETICULARIS Deepest cortical layer Androgenic hormones

(sex hormones); testosterone and
progesterone / estrogen

a.Mineralocorticoids (Aldosterone)
 Provide active reabsorption of sodium and an associated passive reabsorption of water, as well as the
active secretion of potassium
 Results in an increase of blood pressure and blood volume.
b. Glucocorticoids (Cortisol/Hydrocortisone)
 Increase and maintain normal concentrations of glucose in blood.
 Regulates sugar and protein metabolism.
 Serve as anti-inflammatory compounds.
c.Sex Hormones (Androgenic)

MALE FEMALE
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 Testosterone  Estrogen and progesterone

 Enlargement of the penis.
 puberty
 male secondary sex
 deepening of the voice
 growth of facial and pubic hair
 increase in muscle growth and
strength.
 Breast growth
 Accumulation of body fat around
the hips and thighs
 growth spurt that occurs during
puberty.
 Involved in pregnancy and the
regulation of the menstrual cycle.

Disorders of Adrenal Glands

1. CUSHING’S SYNDROME
 Is a hormonal disorder caused by prolonged exposure of the body's tissues to high levels of the hormone
cortisol (Hypersecretion). 
 Sometimes called "hypercortisolism”
 Commonly affects adults aged 20 to 50.
 Most common in women than men.

Pituitary gland

Increase ACTH

Adrenal glands

Increase cortisol

Hypercortisolism

Causes:
 Hyperplasia of the adrenal gland
 Tubercular infection (spread of T. Bacilli to the other organ)
 Tumor of the pituitary gland or adrenal gland
 Tumor elsewhere in the body
 Long-term use of anti-inflammatory medicines called corticosteroids

SIGNS AND SYMPTOMS:

 Acne or superficial skin infections
 Backache
 Buffalo hump
 Central obesity with protruding abdomen and thin extremities (Obese TRUNKS)
 Mental changes
 Moon face (round, red, and full)
 Purple marks called striations on the skin of the abdomen, thighs, and breasts
 Thin skin with easy bruising
 Weakness
 Weight gain (unintentional)
 Increase masculinity and Enlarge clitoris.

 Increased Mineralocorticoids – Hypernatremia (HPN, edema, weight gain)

 Increased Glucocorticoids – 3 P’s (DM)
 Increased Sex Hormones - Hirsutism

DIAGNOSIS:
 Increased FBS, Sodium, Plasma Corticoids Infection (Increased WBC)
 Decreased Potassium Weakness, fatigue, constipation, U wave and ECG traces

DEXAMETHASONE SUPPRESSION TEST (DST)

 Used to evaluate adrenal hyperfunction.
 Dexamethasone is a synthetic steriod effective in suppressing ACTH secretion.
 1 mg of DST is given orally at 11:00 pm and Draw cortisol level at 8:00 before patient rises.

REMEMBER!!!!
 LOW DOSE DEXAMETHASONE SUPPRESSION TEST CONFIRMS CUSHING’ SYNDROME.
 HIGH DOSE DEXAMETHASONE SUPRRESION TEST DETERMINE WHETHER CUSHING’S SYDROME
RESULTS FROM PITUITARY DYSFUNCTION OR ADENOMA IN ADRENAL GLANDS.
 15

NURSING MANAGEMENT:
 Monitor V/S and I and O.
 Restrict sodium and fluids.
 Weight patient daily and Assess for pitting Edema
 Measure abdominal girth daily.
 Diet Increase protein and potassium; Low calorie, sodium and CHO.
 Watch for infection.
 Perform passive range of motion (Bedridden).
 Hormonal replacement.
 Administered medication as ordered.
 Follow up check up.
ADRENALECTOMY (SURGERY)
 If the disease is caused by a pituitary tumor or tumor that releases ACTH, surgery to remove the tumor is
recommended.
 Radiation is sometimes also needed after removal of a pituitary tumor.

DRUG OF CHOICE:
 Cortisol Inhibitors:
- Aminoglutethimide
- ketoconazole
- Metyrapone
- Mitotane
 Potassium Sparing
- Spirinolactone (aldactone)

2. ADDISON’S DISEASE
 Adrenal insufficiency, Adrenocortical hypofunction, Hypocortisolism.
 Is a hormonal disorder caused by LOW levels of the hormone cortisol (Hyposecretion). 
 Occurs at any age and both sexes.

Pituitary gland

Decrease ACTH

Adrenal glands

Decrease cortisol

Hypocortisolism

Causes:
 Atrophy of the adrenal gland
 Disorder of the adrenal glands
 Inadequate secretion of ACTH by the pituitary gland
 Autoimmune disease
 Infections such as tuberculosis, HIV, or fungal infections
 Tumors

SIGNS AND SYMPTOMS:

A. Hypoglycemia
T - REMORS
I - RRITABILITY
R – ESTLESNESS
E – XCESSIVE HUNGER
D - IZZINESS
B. Decrease tolerance to stress
C. Hyponatremia
 Weight loss
 Hypotension
 Dry mucous membrane
D. Hyperkalemia
 Irritability
 Agitation
 Diarrhea
 Arrhythmia
E. Decrease in libido
 16

 Loss of pubic axillary hair

 “BRONZE LIKE SKIN”

 Decreased Mineralocorticoids – Hyponatremia (decrease blood volume & BP)

 Decreased Glucocorticoids – Hypoglycemia
 Decreased Sex Hormones – Loss of pubic hair, Breast atrophy

DIAGNOSIS:
 Decreased FBS, Sodium, Plasma Corticoids
 Increased Potassium Dysrrhythmia, Cardiac Arrest

NURSING MANAGEMENT:
 Monitor V/S and I and O.
 Watch out for ADDISONIAN CRISIS.
 Force fluids.
 Diet Increase protein, calorie, sodium and CHO; Low Potassium
 Perform passive range of motion (Bedridden).
 Provide meticulous skin care
 Provide health teachings and discharge planning:
 Avoid stress, Infection
 Hormonal replacement therapy.
 Prevent complications (ADDISONIAN CRISIS AND HYPOVOLEMIC)
 Administered medication as ordered.

ADDISONIAN CRISIS
 Acute adrenal insufficiency
 occurs when the symptoms of Addison's disease suddenly become worse. The condition can result in
death if left untreated.

SIGNS AND SYMPTOMS:

 Back pain
 Abdominal pain
 Leg pain
 Severe vomiting
 Severe diarrhea
 Dehydration
 Hypoglycemia
 Hyperkalemia
 Low blood pressure
 Loss of consciousness
 Death

DRUG OF CHOICE:
 Corticosteriods:
- Dexamethasone
- Hydrocortisone
- Prednisone
- Decadron
- Solu-cortef
 Mineralocorticoids:
- Fludrocortisone

V. PANCREAS
 Lies transversely along the posterior abdominal wall, posterior to the stomach, and extends from the region
of the duodenum to the spleen.
 Secretes hormone and enzymes.

ACINAR CELLS
 Exocrine glands.
 Secretes pancreatic juices.
 Aids in digestion.
 Secretes enzymes
ISLETS OF LANGERHANS
 ENDOCRINE CELLS.
 PRODUCES HORMONES.
 CONTAINS ALPHA, BETA, AND DELTA CELLS.
CELLS HORMONES FUNCTIONS
 17

ALPHA GLUCAGON Stimulates the breakdown of glycogen in the

liver resulting in the increase level of blood
glucose

BETA INSULIN Lowers the blood glucose level by stimulating

the conversion of glucose to glycogen.

DELTA SOMATOSTATIN Inhibits the release of GH, Corticotropin, and

other hormone

Disorders of the Pancreas:

1. DIABETES MELLITUS
 Metabolic disorder characterized by glucose intolerance resulting from imbalance between insulin supply
and demand.
 Caused by too little insulin, resistance to insulin, or both.

TYPE I TYPE II

 Juvenile onset  Maturity onset

 Abrupt onset  Insidious onset
 Little or NO insulin.  Below normal
 10% Incidence  85-90% incidence
 Within ideal body weight but mostly THIN  80% of clients here are OBESE
 Treated with diet, exercise, INSULIN  Treated with diet, exercise, ORAL
 Diabetic Keto Acidosis (DKA) HYPOGLYCEMICS
 Hyper Osmolar Non Ketotic Coma

Risks Factors:
 A parent, brother, or sister with diabetes
 Obesity
 Age greater than 45 years
 Some ethnic groups (African Americans, Native Americans, Asians, Pacific Islanders, and Hispanic
Americans)
 Gestational diabetes or delivering a baby weighing more than 9 pounds
 High blood pressure
 High blood levels of triglycerides (a type of fat molecule)
 High blood cholesterol level
 Not getting enough exercise

CARDINAL SIGNS:
 3 P’s plus W

OTHER SIGN’S:
 Fatigue
 Nausea
 Vomiting
 Blurred vision
 Slow-healing of wounds
 Impotence in men

TYPE I

TYPE II

Decrease CHO metabolism Increase CHON metabolism Increase Lipolysis

DECREASE CHO UTILIZATION INCREASED BREKDOWN OF INCREASED OXIDATION OF

STORED CHON FATTY ACIDS

WEAKNESS HYPERGLYCEMIA HYPERLIPIDEMIA INCREASE

TISSUE STARVATION KETONE
ATHEROSCLEROSIS
 18

INCREASE BLOOD OSMOLARITY

WASTING FORMATION OF DKA/COMA
ATHEROMA
PRURITUS VULVA POLYURIA
POLYPHAGIA NARROWED ARTERIAL
LUMEN
GLYCOSURIA ECF DEHYDRATION
VASCULAR DEGENERATION

HONK POLYDIPSIA CVA MI GANGRENE NEUROPATHY RETINOPATHY NEPHROPATHY

REMEMBER!!!
 HOT AND DRY = SUGAR IS HIGH (Hyperglycemia)
 COLD AND CLAMMY = NEEDS SOME CANDY (Hypoglycemia)

Diagnosis:
 Fasting Blood Sugar (FBS)
 Random Blood Sugar (RBS)
 Hemo Glucose Test (HGT)
 Oral Glucose Tolerance Test (OGTT)
 Benedict's Test
 Acetest (Ketone bodies Test)

1. Fasting blood Sugar (FBS)

 A glucose test measures the amount of sugar in the blood.
 Blood is drawn from a vein (venipuncture).
 Do not eat for 6-8 hours before the test.
 100 mg/dL are considered normal.
 To confirm the diagnosis. Repeat the fasting blood sugar test on another day. If test results are 126 mg/dL
or higher twice in a row after at least eight hours of fasting, you may have diabetes.
 If blood sugar level is higher than 200 mg/dL and have signs or symptoms of diabetes, it may be diagnosed
with diabetes without a second test for confirmation.

Fasting Blood Glucose

From 70 to 99 mg/dL (3.9 to 5.5 mmol/L) Normal glucose tolerance

From 100 to 125 mg/dL (5.6 to 6.9 mmol/L) Impaired fasting glucose (pre-diabetes)

126 mg/dL (7.0 mmol/L) and above on more than one testing
Diabetes
occasion

2. Random Blood Sugar (RBS)

 Measures blood sugar at any point in time.
 Random blood sugar level shouldn't be higher than 200 mg/dL.
 Blood sugar level is higher than 140 mg/dL but lower than 200 mg/dL, may have prediabetes.

3. Hemo Glucose Test (HGT)

 Blood glucose monitoring refers to the ongoing measurement of blood sugar (glucose).
 Monitoring can be done at any time using a portable device called a glucometer.
 Normal Results

- Before meals: 90 to 130 milligrams per deciliter (mg/dL)

- After meals: Less than 180 mg/dL

4. Oral Glucose Tolerance Test (OGTT)

 A laboratory method to check how the body breaks down (metabolizes) blood sugar.
 NPO 12 hours prior to the test.
 Will drink a liquid containing a certain amount of glucose.
 Blood will be taken before and again every 30 to 60 minutes after drinking the solution. The test takes up to
3 hours.
 Used to screen pregnant women for gestational diabetes between 24 and 28 weeks of pregnancy.

Oral Glucose Tolerance Test (OGTT)

[except pregnancy]
(2 hours after a 75-gram glucose drink)
 19

Less than 140 mg/dL (7.8 mmol/L) Normal glucose tolerance

From 140 to 200 mg/dL (7.8 to 11.1 mmol/L) Impaired glucose tolerance (pre-diabetes)

Over 200 mg/dL (11.1 mmol/L) on more than one testing occasion Diabetes

5. Benedict's Test
 This is a test to measure the amount of glucose in urine.
 Glucose is not usually found in urine.
 Urine glucose is usually measured as a "spot test" with a dipstick containing a color-sensitive pad.
 Directions:
- Collect fresh urine specimen in a clean, dry container
- Remove one strip from bottle and replace cap.
- Dip test area of strip in urine and remove immediately.
- Tap edge of strip against container or clean, dry surface to remove excess urine.
- Compare test area to Colour Chart exactly 10 seconds after wetting. Ignore colour changes that occur after
10 seconds.

6. Acetest (Ketone bodies Test)

 Measures the presence or absence of ketones in the urine.
 A negative test result is normal. Results of the presence of acetone in the urine are usually listed as small,
moderate or large with these corresponding values:
- Small - < 20 mg/dL
- Moderate - 30-40 mg/dL
- Large - > 80 mg/dL

DIABETIC KETOACIDOSIS (DKA)

 Acute complication of Type I due to hyperglycemia leading to COMA.

PREDISPOSING FACTORS:
 Hyperglycemia
 Stress
 Infection

SIGNS AND SYMPTOMS:

 3 P’s
 Weight loss (early sign)
 Dehydration
 Anorexia
 Nausea and vomiting
 Acetone breath (Late Sign)
 Kussmaull’s respiration ( Slow and Deep Respiration)

Diagnosis :
 Increased FBS, BUN, CREATININE, HEMATOCRIT = due to DHN

NURSING MANAGEMENT:
 Maintain Airway (Assist Mechanical Ventilator)
 Monitor V/S, I and O every hour
 Administer 0.9 NaCl (Isotonic) followed by 0.45 NaCl (Hypotonic). To counter act dehydration.
 Monitor V/S, I & O, NVS
 Administer medication as ordered:
- Insulin (Regular Acting)
- Sodium Bicarbonate (Antacid, Alkaline)
- Antimicrobials

HYPEROSMOLAR NONKETOTIC
 Acute complication of Type II characterized by hyperglycemia, hyperosmolarity, and an absence of
significant ketosis.

PREDISPOSING FACTORS:
 Older age
 Underlying kidney insufficiency
 Congestive heart failure
 Stopping insulin or other medications that lower glucose levels
 20

 Improper management of diabetes

 A stressful event such as infection, heart attack, stroke, or recent surgery

SIGNS AND SYMPTOMS:

 3 P’s
 Dehydration
 Headache
 Seizure
 Decrease LOC
 Weakness
 Increased thirst
 Nausea
 Lethargy
 Confusion

REMEMBER!!!
***“Diagnosis and Nursing Management” are the same as DKA EXCEPT SODIUM BICARBONATE

INSULIN THERAPY
 Used to control blood sugar in people who have type 1 diabetes or in people who have type 2 diabetes that
cannot be controlled with oral medications alone.
 Class of medications called hormones.
 SOURCES:
a. HUMAN - commonly use and it has less antigen property
b. Animal: pork and beef - rarely given because it can cause severe allergic reaction

Types Example Color Onset Peak Duration

RAPID ACTING -RAI CLEAR 30 2-4 HRS 6-8

(Regular) -Humulin-R Min HRS
-used in treating ketoacidosis -Simelente

INTERMEDIATE -Humulin-N CLOUDY 1-2 6-12 24

ACTING -NPH HRS HRS HRS
-used in maintenance therapy -Protamine
Hagedorn
-Globin
-Lente
LONG ACTING -Humulin-U CLOUDY 3-4 18-24 36
-used for maintenance therapy in -ULTRA HRS HRS HRS
clients experience hyperglycemia LENTE
at night -PZI
-Zinc Insulin

NURSING MANAGEMENT (INSULIN)

 Administer insulin at Room temperature to prevent Lipodystrophy. (NO COLD ADMINISTRATION)
 Refrigerate insulin once it is opened.
 Avoid shaking insulin, roll between palms only.
 Administer insulin either 45°or 90° depending of amount of tissue deposits.
 Accuracy of administration is important gauge 25-26.
 Only Regular insulin is given by IV infusion and compatible with NS, Dextrose, LR. (administer with albumin
if given IV drip to prevent adherent in tubing's)
 Rotate insulin site (abdomen most accessible).
 When mixing 2 types of insulin aspirate clear first before cloudy.
 Should be given 60-90 min. or 1-1.5 hrs before meal so that the physiologic effect will meet.
 Monitor complications:
- Lipodystrophy ( hypertrophy or atrophy of tissue)
- Allergic reaction
- Smogyi Phenomenon (Rebound bounding of insulin characterized by HYPER or HYPOGLYCEMIA-
produces compensatory increase in blood levels of catecholamine's, glucagon, cortisol, and growth
hormone causes blood glucose to become elevated. )

ORAL HYPOGLYCEMIC AGENT (OHA)

 Stimulates pancreas to secrete or produce insulin.
 Classifications:
1. FIRST GROUP - increase insulin production from the pancreas:
 Sulfonylureas (e.g. Diabeta [glyburide])
 Meglitinides (e.g. Gluconorm [repaglinide])
 21

 D-phenylalanine derivatives (e.g. Starlix [nateglinide]) 

2. SECOND GROUP - slow down absorption of sugars from the gut:

 “Alpha-Glucosidase inhibitors” (e.g. Prandase [acarbose]) 

3. THIRD GROUP - decrease glucose release from the liver:

 “Biguanides” (e.g.. Glucophage [metformin])

4. FOURTH GROUP - increase glucose uptake by fat & muscle cells:

 “Thiazolidinediones” ("glitazones"); (e.g. Actos [pioglitazone] or Avandia [rosiglitazone]).

NURSING MANAGEMENT (OHA):

 Instruct to take with meals to lessen GI irritation to prevent hypoglycemia.
 Instruct the client to avoid taking with alcohol. To prevent severe hypoglycemia.

NURSING MANAGEMENT DM:

 Monitor signs and symptoms of hypo & hyperglycemia.
 Monitor V/S and I and O.
 Provide a diabetic diet: C=50%, P= 30%, F=20%
 Encourage exercise after meals to promote increase glucose utilization.
 Monitor complications.
 Foot care management:
- Avoid walking barefoot
- Cut the nails straight
- Apply lanolin lotion
- Avoid wearing constrictive clothing's
 Encourage annual eye and kidney exams.
 Monitor signs of DKA and HONK.

Prepared by: Dhazel-don C. Pangilinan RN,MAN