MARK BILLY L.

PERPETUA, MAN RN

Endocrine System
Disorders
 ANATOMY and PHYSIOLOGY
❑-ductless glands (secretes hormones directly to the blood stream)
❑HYPOTHALAMUS
❑Chief gland – Thyrotropin Releasing Hormone (TRH),
Gonadotropin Releasing Hormone (GnRH)
❑PINEAL GLAND
❑Melatonin (sleep: circadian rhythm)
❑PITUITARY GLAND
❑Receives direction from hypothalamus
❑ANTERIOR: GH, FSH, LH, Prolactin, MSH, ACTH, TSH, etc.
❑POSTERIOR: Oxytocin and Vasopressin (ADH)
 ANATOMY and PHYSIOLOGY
❑PANCREAS
❑EXOCRINE: Lipase, Amylase, Trypsin
❑ENDOCRINE:
❑Alpha cells: Glucagon (Glycogenolysis)
❑Beta cells: Insulin
❑Delta cells: somatostatin (antagonizes the effect of growth hormone)
❑THYROID GLAND
❑T3 (triiodothyronin) – controls metabolic rate
❑T4 (Tetraiodothyronine) – controls heat production
❑Calcitonin – decreases Calcium level
❑PARATHYROID GLAND
❑Parathormone (PTH) – Increases calcium level
 ANATOMY and PHYSIOLOGY
❑ADRENAL GLAND
❑MEDULLA:
❑Cathecolamines (Influences SNS activity)
❑Epinephrine (Adrenaline)
❑Norepinephrine (Noradrenaline)
❑CORTEX:
❑Zona glumerulosa (Aldosterone)
❑Zona fasciculate (Cortisol)
❑Zona reticularis (Sex hormones)
NEGATIVE FEEDBACK MECHANISM
MARK BILLY L. PERPETUA, MAN RN

Pituitary Gland
Disorders
 PITUITARY DISORDERS
❑ANTERIOR:
❑Growth Hormone
❑Gigantism: hyper secretion of GH in children (exaggerated growth
in height and weight)
❑Acromegaly: hypersecretion of GH in adult caused by pituitary
tumor
❑Dwarfism: hyposecretion of GH characterized by slow growth
❑Galactorrhea: hyper secretion of Prolactin
❑Melanocyte-Stimulating Hormone
❑Hyper: Hyperpigmentation of the skin
❑Hypo: Albinism, retina (difficulty in vision during daytime/bright
lights)
 PITUITARY DISORDERS
❑ANTERIOR:
❑Adrenocorticotropic Hormone (ACTH)
❑Hyper: Secondary Cushing’s disease
❑Hypo: Secondary Addison’s disease
❑Thyroid Stimulating Hormone (TSH)
❑Hyper: Secondary Hyperthyroidism
❑Hypo: Secondary Hypothryroidism
❑Gonadotropins, FSH, and LH
❑Hyper: precocious puberty
❑Hypo: failure to develop secondary sex characteristics that
normally develop at the age of puberty
 PITUITARY DISORDERS
❑PITUITARY TUMORS
❑Usually, BENIGN ❑BASOPHILIC
❑FUNCTIONAL TUMORS – secretes ❑Give rise to
hormones CUSHING’s
❑NON-FUNCTIONAL – does not secrete
hormones syndrome
❑TYPES:
❑EOSINOPHILIC ❑CHROMOPHOBIC
❑Childhood – GIGANTISM ❑90% of tumors
❑>7 feet tall ❑Produces no
❑Large in all proportions hormones
❑Weak and lethargic
❑Difficulty standing ❑Destroys the gland
❑Adulthood – ACROMEGALY leading to
❑Excessive growth only in feet, hypopituitarism
hands, face
❑Severe headache and visual
disturbance
 PITUITARY DISORDERS
❑PITUITARY TUMORS
❑Dx/Mngt:
❑CT Scan and MRI
❑Serum hormone levels
❑Radiation therapy
❑Bromocriptine and Octreotide
❑Inhibits production/release of Growth hormone
 PITUITARY DISORDERS
❑PITUITARY TUMORS
❑Dx/Mngt:
❑Hypophysectomy – removal of pituitary gland (also leads to
INFERTILITY)

❑Nsg Interventions:
❑ H ead of bed should be elevated
❑ E valuate VS. LOC. NVS
❑ A void sneezing, coughing, blowing of nose
❑ D I may occur (polyuria) due to ADH disturbances
 PITUITARY DISORDERS
❑POSTERIOR:
❑Antidiuretic Hormone (Vasopressin)
❑Hyper: Syndrome of Inappropriate Antidiuretic Hormone
(SIADH)
❑Excessive retention of water by the renal tubules.
❑Causes:
❑Head trauma (Most common)
❑Idiopathic
❑Stroke
❑Hyperplasia of the pituitary gland
❑Medications and Stress
 PITUITARY DISORDERS
❑Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
❑S/Sx:
❑Edema
❑Weight gain
❑Hypertension
❑Dilutional hyponatremia
❑Mngt:
❑Eliminate underlying cause
❑RESTRICT fluid intake
❑Diuretics: Furosemide
❑Monitor I and O
❑Monitor Weight
❑Monitor neurologic status
❑DEMECLOCYCLINE – produces a nephrogenic Diabetes Insipidus
 PITUITARY DISORDERS
❑POSTERIOR:
❑Antidiuretic Hormone (Vasopressin)
❑Hypo: Diabetes Insipidus
❑Inability of the renal tubules to retain fluid
❑Causes:
❑Head trauma (Most common)
❑Idiopathic
❑Pituitary surgery
❑Tumor
❑Infection
 PITUITARY DISORDERS
❑Diabetes Insipidus
❑S/Sx:
❑Very diluted urine
❑Urine specific gravity (1.001-1.005)
❑Dehydration
❑Hypotension
❑Fatigue
❑Severe thirst (2-20 L cold water daily)
❑Dx:
❑FLUID DEPRIVATION TEST
❑Withholding fluid for 8-12 hours until 3-5% of body weight is lost.
❑Patient is weighed frequently during the test
❑Plasma and urine osmolarity at the beginning and end
❑(+) DI: inability to increase urine specific gravity and osmolarity
❑Terminate: (+) tachycardia, weight loss, or hypotension
 PITUITARY DISORDERS
❑Diabetes Insipidus
❑Mngt:
❑Desmopressin (synthetic vasopressin)
❑No vascular effect as the natural ADH
❑Route: Intranasal
❑Use in caution with Coronary Artery Disease
❑IM ADH administration
❑If intranasal in not possible
❑Warm and shake
❑Given at night
❑Rotate the injection site (prevents lipodystrophy)
❑Clofibrate (hypolipidemic agent)
❑Has antidiuretic effect
MARK BILLY L. PERPETUA, MAN RN

Thyroid Gland
Disorders
 THYROID DISORDERS
❑Simple Goiter
❑Enlarged thyroid gland due to iodine deficiency

❑Predisposing factors:
❑Goiter belt area (endemic goiter)
❑Goitrogenic drugs
❑Mountainous area (sporadic goiter)
❑S/Sx:
❑Swelling of the neck
❑Mild restlessness
❑Dysphagia
 THYROID DISORDERS
❑Simple Goiter
❑Dx:
❑Thyroid scan
❑Serum TSH
❑Serum T3 and T4
❑Mngt:
❑Iodine Solution
❑Lugol’s solution (reduces the vascularity of thyroid)
❑SSKI (Saturated Solution of Potassium Iodide)
❑Intake of Iodine-rich food
❑Surgery (Subtotal/total thyroidectomy)
 THYROID DISORDERS
❑HYPOTHYROIDISM
❑Suboptimal levels of thyroid hormones T3 and T4

❑Predisposing factors:
❑Hashimoto’s thyroiditis (autoimmune disorder that attacks the
thyroid)
❑Atrophy of the gland due to aging
❑Therapy for hyperthyroidism
❑Iodine deficiency and iodine excess
❑Medications (Lithium)
❑Radiation on neck/head
 THYROID DISORDERS
❑HYPOTHYROIDISM
❑S/Sx:
❑Decreased BP and HR
❑Elevated weight
❑Constipation
❑Reduced energy
❑Elevated cholesterol
❑Anorexia ❑Tolerance to heat is reduced
❑Slowed speech ❑Tingling sensation (paresthesia)
❑Edema ❑Temperature is decreased
❑Disturbance in menstrual cycle
(Menorrhagia)
 THYROID DISORDERS
❑HYPOTHYROIDISM
❑Mngt:
❑Replace thyroid hormone
❑SYNTHETIC LEVOTHYROXINE
❑Do not give with analgesics, sedatives, and anesthetics
❑PROLONGS THE EFFECT of such drugs
❑MONITOR: VS, daily weight, and constipation
❑OVERDOSE: Increased HR!
❑DIET: Low calorie, Low cholesterol, Low saturated fats
 THYROID DISORDERS
❑HYPERTHYROIDISM
❑Hyper secretion of thyroid hormone T3 and T4.
❑Second most common endocrine disorder
❑More prevalent in females than in males
❑Age: >40
❑Causes:
❑Severe emotional stress
❑Autoimmune thyroiditis (Grave’s Disease)
❑Excess thyroid hormone intake
 THYROID DISORDERS
❑HYPERTHYROIDISM
❑S/Sx:
❑Exophthalmos ❑Thinning of hair
❑Loss of weight
❑Elevated BP ❑Tachycardia and palpitations
❑Voracious eating ❑Tremors and nervousness
❑Agitations/Amenorrhea ❑Darlymple’s sign: Thyroid stare
❑Tolerance to heat is low ❑Vongreaf sign: deep palpebral
fissure
❑Enlarged thyroid gland ❑Jeffry’s sign: forehead remains
smooth even when looking up
❑Diarrhea
 THYROID DISORDERS
❑HYPERTHYROIDISM
❑THYROID STORM (THYROTOXIC
CRISIS)
❑Elevated temperature (above
38.5C)
❑Extreme tachycardia (>130
bpm)
❑Exaggerated symptoms of
hyperthyroidism
❑Change in the level of
consciousness
❑Caused by STRESS**
MNGT:
❑Lower down temperature and
heart rate
❑Hypothermia blanket
❑Oxygen
❑IV fluids (dextrose – replace
glycogen stores)
❑Hydrocortisone (tx of shock and
adrenal insufficiency)
❑Iodine (decreases thyroid output
of T4)
 THYROID DISORDERS
❑HYPERTHYROIDISM
❑Mngts:
❑Radioactive iodine therapy (I131)
❑Destroys OVERACTIVE thyroid cells
❑Tasteless, colorless radioiodine
❑Usually SINGLE dose
❑WOF: signs of THYROID STORM
❑Mngt: Propanolol
❑CONTRAINDICATION: pregnancy and lactation
❑Crosses the placenta and breast milk
❑Pregnancy is postponed at least 6 months post treatment
 THYROID DISORDERS
❑HYPERTHYROIDISM
❑Mngt:
❑Antithyroid medication
❑Propylthiouracil (PTU) or Methimazole (Tapazole)
❑Inhibits thyroid hormone synthesis or release
❑WOF: Agranulocytosis and Thrombocytopenia
❑SE: fever, allergy, urticarial, hypothyroidism
 THYROID DISORDERS
❑HYPERTHYROIDISM
❑Mngt:
❑Adjunctive therapy
❑Iodine or Iodide compounds
❑LUGOL’S SOLUTION
❑SSKI
❑Reduces the vascularity of the thyroid gland making surgery safer
❑Drink with milk o fruit juice to increase palatability
❑Administer using a STRAW to prevent teeth staining
 THYROID DISORDERS
❑HYPERTHYROIDISM
❑Mngt:
❑Surgical Management
❑Subtotal/Total Thyroidectomy
❑Check the side and back of the neck for bleeding
❑WOF: hematoma formation (Difficulty of breathing)
❑Check the voice (possible damage to the recurrent laryngeal nerve)
❑WOF: hypocalcemia (due to accidental removal of the parathyroid
gland)
❑TETANY!
❑Tingling around the mouth, laryngospasm
❑TROSSEAU’S SIGN
❑CHVOSTEK’s sign
 THYROID DISORDERS
❑THYROIDITIS
❑Inflammation of the thyroid gland
❑ACUTE THYROIDITIS
❑Rare, caused by infection of the thyroid gland
❑CA: staphylococcus aureus
❑S/Sx:
❑Neck pain and swelling
❑Fever
❑Dysphagia
❑Dysphonia
❑Pharyngitis/pharyngeal pain
❑Mngt: Antibacterial – Surgical removal of access
 THYROID DISORDERS
❑THYROIDITIS
❑SUBACUTE THYROIDITIS
❑Subacute granulomatous thyroiditis (de Quervains’s thyroiditis)
❑Prevalence: 40-40 y/o – WOMEN – viral respiratory infection
❑S/Sx:
❑Low-grade fever, pharyngitis, myalgias, fatigue
❑SYMMETRICAL swelling of the thyroid gland (1 to 2 mos – resolves without residual effect)
❑Hyperthyroidism-like manifestations (NO thrill/bruit)
❑MNGT:
❑NSAIDs (ASPIRIN – is avoided – displaces hormone in binding site – increases serum
concentration)
❑Beta-blockers (Propranolol)
❑Oral steroids
❑Painless thyroiditis (silent thyroiditis)
❑Prevalence: postpartum period – autoimmune
❑S/Sx: hypo/hyperthyroidism manifestations
❑MNGT: Symptomatic tx
 THYROID DISORDERS
❑THYROIDITIS
❑CHRONIC THYROIDITIS (HASHIMOTO’S THYROIDITIS)
❑Prevalence: 30-50 yo – women
❑Slow and progressive course – leads to hypothyroidism
❑Mngt:
❑Reduce the size of thyroid gland
❑Prevent hypothyroidism
❑Thyroid hormone therapy
 THYROID DISORDERS
❑THYROID TUMORS
❑Benin/Malignant
❑(+) visible swelling – GOITER
❑GOITER
❑Toxic goiter – if with hyperthyroidism
❑Non-toxic goiter – if euthyroid state

❑ENDEMIC (IODINE-DEFICIENT) GOITER

❑NODULAR GOITER
 THYROID DISORDERS
❑THYROID TUMORS
❑ENDEMIC GOITER (simple or colloid goiter)
❑Most common type
❑Common in geographic regions where natural iodine supply is
scarce
❑CAUSES:
❑Iodine deficiency
❑Goitrogenic substances/foods
❑Cruciferous vegetables
❑Sweet potato/casava/lima beans
❑Soy products
❑MNGT: Supplementary iodine (SSKI) - iodized salt in endemic area
 THYROID DISORDERS
❑THYROID CANCER
❑Less prevalent
❑Predisposing factors:
❑External irradiation (head, neck, chest)
❑May occur 5-40 years after irradiation
❑S/Sx:
❑Single, hard, and fixed lesions – (+) malignancy
❑Needle biopsy
❑Imaging techniques (thyroid scan/ultrasound, CT/MRI)
❑MNGT:
❑Total thyroidectomy
❑Radiation
MARK BILLY L. PERPETUA, MAN RN

Parathyroid
Gland Disorders
 PARATHYROID DISORDERS
❑HYPERPARATHYROIDISM
❑Overproduction of Parathormone by the parathyroid glands
characterized by bone decalcification and development of
renal calculi
❑Manifestations:
❑(HYPERCALCEMIA) ❑Cardiac dysrhythmias
❑Fatigue ❑Neuroses/psychoses
❑Muscle weakness ❑Pathologic fracture
❑Constipation ❑Skeletal pain and
tenderness
 PARATHYROID DISORDERS
❑Dx:
❑Elevated serum calcium levels
❑Elevated concentration of parathormone
❑X-ray and bone scans (osteoporosis)
❑Mngt:
❑Parathyroidectomy
❑Hydration therapy (2000 ml or more)
❑Cranberry juice (lowers urinary pH)
❑Avoid: THIAZIDES – decreases renal excretion of Ca
❑Mobility
❑Restrict Calcium in the diet
 PARATHYROID DISORDERS
❑HYPERCALCEMIC CRISIS
❑Extreme elevation of serum calcium levels (>13.5 mg/dL)
❑Life-threatening neurologic, cardiovascular, and kidney
symptoms may occur
❑Mngt:
❑Rapid rehydration (IV isotonic solution)
❑Calcitonin and Corticosteroid (Promotes renal excretion of excess
calcium and reduces bone resorption)
❑Bisphosphonates (promotes calcium deposition in bones and
reduces GI absorption of calcium)
❑Dialysis
❑Cytotoxic drugs
 PARATHYROID DISORDERS
❑HYPOPARATHYROIDISM
❑Inadequate secretion of Parathormone due to abnormal
parathyroid development, destruction of parathyroid
(autoimmune/surgical), vitamin D deficiency.
❑Manifestations: ❑Bronchospasm
❑(HYPOCALCEMIA) ❑Laryngospasm
❑Tetany! ❑TROSSEAU’s sign
❑General muscle ❑CHVOSTEK’s sign
hypertonia ❑Anxiety
❑Numbness and tingling ❑ECG changes (prolonged
❑Cramps QT-interval)
 PARATHYROID DISORDERS
❑Dx:
❑Decreased serum calcium levels
❑X-ray (calcification of paraspinal basal ganglia)
❑Mngt:
❑Calcium (take caution with Digitalis)
❑Magnesium
❑Vitamin D2 (ergocalciferol)
❑Vitamin D3 (calcitriol)
❑Thiazide diuretic (helps decrease urinary excretion of calcium)
❑Aluminum hydroxide (binds with phosphate in the GI tract)
❑TETANY: IV Calcium gluconate
❑Noise/Stress free environment
❑Diet: high calcium low phosphorus
❑Avoid: milk, milk products, egg yolk (high in Ca but also high in phosphorus)
❑Avoid: spinach (contains oxalate – forms insoluble Ca substances)
❑SEIZURE PRECAUTION!
MARK BILLY L. PERPETUA, MAN RN

Adrenal Gland
Disorders
 ADRENAL DISORDERS
❑CUSHING’S DISEASE
❑Hyper secretion of adrenal cortex hormones

❑Causes:
❑Pituitary secretion of ACTH
❑Pituitary or adrenal adenoma
❑Prolonged steroid therapy
❑Hyperplasia of the adrenal gland
 ADRENAL DISORDERS
❑CUSHING’S DISEASE
❑S/Sx:
❑Central-type obesity/Comedones – buffalo hump
❑U-wave in ECG
❑Striae (purplish)/Sleep disturbance
❑Hyperglycemia (3 P’s)/hypertention
❑Impaired wound healing/Increased protein catabolism (muscle
wasting/osteoporosis) / Increased risk of infection
❑Na is increased / edema formation
❑Gains weight (water retention)
❑Susceptible to infection
❑Sexual trait alteration (Hirsutism, virilization, loss of libido)
 ADRENAL DISORDERS
❑CUSHING’S DISEASE
❑Dx:
❑Dexamethasone Suppression Test
❑1 mg Dexamethasone orally at 11 pm
❑Plasma cortisol level is obtained at 8am
❑Normal: cortisol level <5 mg/dL
❑Increased serum Sodium, Glucose, Decrease in Potassium
❑Plasma ACTH
 ADRENAL DISORDERS
❑CUSHING’S DISEASE
❑Mngt:
❑Transphenoidal hypophysectomy
❑Adrenalectomy
❑Unilateral: Temporary replacement of adrenal hormones may be needed
❑Adrenal enzyme inhibitors (ectopic ACTH secretion)
❑Mitotane
❑Netyrapone
❑Monitor VS, I/O, glucose, weight, Na and K levels
❑Minimize risk for injury and infection
❑Encourage rest and activity
❑Promote skin integrity
❑DIET: high protein, calcium, and vitamin D (prone to osteoporosis)
 ADRENAL DISORDERS
❑ADDISON’S DISEASE
❑Hyposecretion of adrenal cortex hormones

❑Causes:
❑Autoimmune or Idiopathic atrophy of adrenal gland
❑Adrenalectomy
❑Sudden withdrawal to steroid therapy (most common)
❑Trauma
❑Infection
 ADRENAL DISORDERS
❑ADDISON’S DISEASE
❑S/Sx:
❑Absence or loss of axillary hair
❑Dehydration
❑Decreased sexual urge/libido
❑Increased K
❑Skin pigmentation (Bronze skin)
❑Orthostatic hypotension
❑Na is decreased
❑Sugar is decreased
 ADRENAL DISORDERS
❑ADDISON’S DISEASE
❑Dx:
❑Low FBS and Low Na, elevated K
❑Mngt:
❑Combat shock
❑Fluid replacement
❑IV HYDROCORTISONE
❑Vasopressor
❑Antibiotics (infection)
❑DIET: High Na, CHON, CHO, low in K
❑Monitor VS, NVS, I/O
❑Protect from infection
❑Maintain bed rest
 K-rich foods Carrot
Potato Raisin
Beans Avocado
Apricot Tomato
Prunes Orange
Banana
 ADRENAL DISORDERS
❑ADDISONIAN CRISIS
❑Life threatening emergency caused by insufficiency in
adrenocortical hormone
❑Causes:
❑STRESS, infection, surgery, trauma, hemorrhage, psychological stress,
*sudden withdrawal to steroid therapy, adrenal or pituitary gland surgery
❑S/Sx:
❑Cyanosis
❑Classic signs of circulatory failure
❑Hyponatremia
❑Hypoglycemia
❑Stupor
❑Coma
 ADRENAL DISORDERS
❑ADDISONIAN CRISIS
❑Mngt:
❑IV fluid replacement
❑IV glucocorticoids
❑Mechanical ventilation
❑Force fluid
❑*Proper positioning
 ADRENAL DISORDERS
❑PHEOCHROMOCYTOMA
❑Tumor that originates from the chromaffin cells of the adrenal
medulla;usually benign; 10% malignant
❑Stimulates hyper secretion of Epinephrine and Norepinephrine
❑Dx:
❑24-hr Urine specimen collection
❑Checks free catecholamine levels
❑(+) accuracy: avoid – coffee/tea, banana, chocolate, vanilla, aspirin
❑Total Plasma catecholamine
❑Supine/rest for 30 mins
❑(+) accuracy: avoid STRESS and caffeinated food/drinks, nicotine,
stimulants
❑Clonidine suppression Test
❑Normal: suppression of circulating catecholamines
❑(+): steady increase in circulating cathecolamines
 ADRENAL DISORDERS
❑PHEOCHROMOCYTOMA
❑S/Sx: 5Hs
❑Hypertension
❑Headache
❑Hyperhydrosis
❑Hypermetabolism
❑Hyperglycemia
 ADRENAL DISORDERS
❑PHEOCHROMOCYTOMA
❑Mngt:
❑Monitor VS/complications
❑Promote bed rest
❑Elevate HOB during episodes of hypertension
❑AVOID:
❑Smoking
❑Caffeine/Stimulants
❑Alpha blockers (phentolamine)
❑Beta blockers (propranolol)
❑Smooth muscle relaxant (nitroprusside)
❑Prepare for adrenalectomy
 ADRENAL DISORDERS
❑PRIMARY ALDOSTERONISM
❑Excessive production of ALDOSTERONE due to functioning
tumors of the adrenal gland
❑S/Sx:
❑Severe hypokalemia
❑Muscle weakness
❑Decline in hydrogen ions (alkalosis)
❑Elevated serum bicarbonate
❑HYPERTENSION
❑Polyuria
❑Elevated hematocrit
❑Polydypsia
❑Accompanying hypocalcemia - TETANY
 ADRENAL DISORDERS
❑PRIMARY ALDOSTERONISM
❑Dx:
❑Electrolyte panel
❑Renin-aldosterone postural/stimulation test
❑Patient sleeps overnight
❑8:00am – blood sample extraction for to check aldosterone, cortisol,
and renin levels
❑12:00nn – (patient walks and stands for 4 hours – sample is
repeated) – stimulates increase in Angiotensin II
❑Adrenal adenoma – no change in aldosterone level
❑Benign adrenal hyperplasia – increased aldosterone (d/t increased
Angiotensin II)
❑Bilateral adrenal venous sampling
❑Checks if the problem is unilateral/bilateral
 ADRENAL DISORDERS
❑PRIMARY ALDOSTERONISM
❑Mngt:
❑Removal of the adrenal tumor
❑Spirinolactone (Aldactone)
❑Corticosteroid therapy (post adrenalectomy)
❑Fluid balance
❑Dietary modifications
❑Frequent VS check – rule out adrenal insufficiency and crisis or
hemorrhage
 POTASSIUM IMBALANCES
 K-sparing  K-wasting
 Spirinolactone  Loop (furosemide, bumetanide,
torsemide)
 Amiloride
 Thiazide (diuril, hydrochlorodiuril,
 Triamterene metolazone)
 Osmotic (mannitol)
MARK BILLY L. PERPETUA, MAN RN

Corticosteroid
Therapy
 CORTICOSTEROID
❑USES
❑Adrenal insufficiency ❑-ONE
❑Anti-inflammatory ❑Hydrocortisone
❑Autoimmune reactions ❑Cortisone
❑Allergic reactions ❑Dexamethasone
❑Post-organ transplant ❑Prednisone
❑Prednisolone
❑Methylprednisolone
❑Betamethasone
 CORTICOSTEROID
❑SIDE EFFECTS
❑Metabolic effects
❑Elevated blood sugar
❑Elevated serum sodium
❑Decreased potassium
❑Adrenal and pituitary
suppression
❑May persists for 1 year
following a 2-week course of
steroid
❑DOSAGE
❑BEST TIME: Early morning (7-
8am)
❑Coincides with the diurnal
variation of steroid release
❑TAPERING
❑Allows gradual return of
adrenal function
❑Prevents steroid-induced
adrenal insufficiency
 DIABETES MELLITUS

MARK BILLY L. PERPETUA, MAN RN

 DIABETES MELLITUS

❑A group of metabolic diseases characterized by

ELEVATED levels of GLUCOSE in the blood resulting
from the defects in secretion, insulin action, insulin
receptors, or combination of conditions.
 DIABETES MELLITUS

❑Clinical Manifestations:
❑Polyuria

❑Polyphagia

❑Polydypsia
 DIABETES MELLITUS
TYPE I
 Juvenile onset: <30
 Cause: genetic/hereditary
 Symptomatic
 Outstanding sign: weight loss
 Complication: Diabetic
Ketoacidosis (DKA)
TYPE II
 Adult onset: >40
 Cause: Obesity
 Asymptomatic
 Outstanding sign: weight
gain
 Complication: Hyperglycemic
Hyperosmolar Non-ketotic
Coma/Syndrome (HHNS)
 DIABETES MELLITUS

❑Diagnostic evaluation:
❑ Fasting blood glucose level of 126 mg/dl and above
❑ Random Blood Glucose levels of 200 mg and above

❑ 2 hours post-blood glucose levels equal to 200 mg/dl

 DIABETES MELLITUS

❑Non-pharmacologic management:
❑ Nutrition/diet(low glycemic index)
❑ Physical activity/exercise

❑ Stress management

❑ Self-monitoring of Blood Glucose (SMBG)

*cornerstone
 DIABETES MELLITUS

❑Pharmacologic: (Oral Hypoglycemic Agents)

❑ Sulfonylureas
❑Enhances the activity of insulin to the receptor and stimulates
the pancreas
❑SE: Gastric irritation
❑ First generation:
❑Chlorpropramide
❑Tolbutamide
❑ Second generation:
❑Glipizide
 DIABETES MELLITUS

❑Pharmacologic: (Oral Hypoglycemic Agents)

❑ Biguanides
❑Inhibitsproduction of glucose by the liver and increases body’s
sensitivity to insulin
❑SE: Nephrotoxic
❑ Metformin
 DIABETES MELLITUS

❑Pharmacologic: (Oral Hypoglycemic Agents)

❑ Alpha Glucosidase Inhibitors
❑Delays the absorption of complex carbohydrates in the
intestines
❑ Acarbose
 DIABETES MELLITUS

❑Pharmacologic: (Oral Hypoglycemic Agents)

❑ Thiazididinedioes
❑Enhances the activity of insulin receptors
❑ Pioglitazone

❑ Rosiglitazone
 DIABETES MELLITUS

❑Pharmacologic: (Oral Hypoglycemic Agents)

❑ Miglitinides
❑Stimulates the pancreas to secrete insulin
❑ Repaglinide

❑ Nateglinide
 DIABETES MELLITUS

❑Pharmacologic: (SYNTHETIC INSULIN)

❑ Indicated for DM II if poorly managed/uncontrolled
INSULIN NAME ONSET PEAK DURATION

Rapid-acting Lispro (Humalog) 10-15 minutes 1 hour 3-6 hours

Short-acting Regular (Humulin R) 0.5 – 1 hr 2-3 hours 4-6 hours

Intermediate- NPH (Humulin N) 2-4 hrs 6-12 hours 16-20 hours

acting
Long-acting Ultralente 6-8 hrs 12-16 hours 20-30 hours

Very long-acting Glargine (Lantus) 1 hour PEAKLESS 24 hours

 DIABETES MELLITUS

❑INSULIN administration:
❑ REGULAR INSULIN (only insulin that can be given thru IV)
❑ Potentiates the effect of insulin:
❑ Aspirin
❑ Alcohol
❑ Oral anticoagulants
❑ OHAs
❑ Beta blockers
❑ TCA
❑ Tetracycline
❑ MAOI
 DIABETES MELLITUS

❑INSULIN administration:
❑ Counteracts the effect of insulin:
❑Glucocorticoids
❑Thiazides
❑Thyroid agents
❑Oral contraceptives
❑Estrogen
 DIABETES MELLITUS

❑INSULIN administration:
❑ Insulin is NOT WITHHELD during illness, infection, or stress
❑ Be aware of the PEAK action time

❑ Main route: SUBCUTANEOUS (slow absorption)

❑ Main areas of administration:

❑ Abdomen
❑ Arms
❑ Thighs
❑ buttocks
 DIABETES MELLITUS

❑INSULIN administration:
❑ DO NOT MASSAGE the injection site
❑ Finish all sites in one anatomical part before going to another (ROTATE
THE SITE of INJECTION)
❑ Gently roll the vials in between palms to redistribute the insulin

❑ STORE:

❑ Pre-filled insulin syringe (7 days)

❑ Vials (30 days)
❑ Avoid extremes of temperature
 DIABETES MELLITUS

❑INSULIN administration:
❑ REGULAR INSULIN may be mixed with other type of insulin
❑ Administer MIXED insulin within 5-15 minutes

❑ Mixing:
❑ Wash hands
❑ Rotate/roll for 7 mins
❑ Alcohol sponge
❑ Inject air in vial (NPH)
❑ Inject air in clear (Regular)
❑ Aspirate Regular (clear)
❑ Aspirate NPH (cloudy)
 DIABETES MELLITUS

❑INSULIN administration:
❑ COMPLICATIONS:
❑ Allergic reaction
❑ Lipodystrophy
❑ Insulin resistance
❑ Dawn Phenomenon
❑ Normal blood sugar until 3am then early morning hyperglycemia at 5-8
am
❑ MNGT: adjust the administration of insulin
❑ Somogyi Effect
❑ Nocturnal hypoglycemia at 2-3 am followed by rebound hyperglycemia t
7 am
❑ MNGT: bedtime snack
 DIABETES MELLITUS

❑ACUTE COMPLICATIONS OF DM
❑ HYPOGLYCEMIA
❑ Blood glucose fell below 50-60 mg/dl
❑ Causes:
❑ Overdose of INSULIN/OHAs
❑ Omission of food
❑ Strenuous exercise
❑ S/Sx: Tremors, Tachycardia, Sweating, Nervousness, Hunger
❑ Mngt:
❑ Mild (10-15 grams) Mod (15-30 grams) of fast acting simple
sugar/carbohydrates
❑ Severe: GLUCAGON or D5050
 DIABETES MELLITUS

❑ACUTE COMPLICATIONS OF DM
❑ DIABETIC KETOACIDOSIS
❑ Caused by markedly inadequate amount of insulin leading to
HYPERGLYCEMIA, DEHYDRATION, e-loss, ACIDOSIS
❑ S/Sx:
❑ Blurred vision
❑ Weakness
❑ Headache
❑ Acetone breath (fetor hepaticus)
❑ Kussmaul’s respirations
❑ Dx:
❑ Blood glucose: 300-800 mg/dl
❑ Urine ketones
❑ ABG
 DIABETES MELLITUS

❑ACUTE COMPLICATIONS OF DM
❑ DIABETIC KETOACIDOSIS
❑ Mngt:
❑ Rehydration (initially NSS then D5W up to 6 liters)
❑ Monitor hydration status
❑ Reverse acidosis (NaHCO3)
❑ Correct electrolyte imbalance
 DIABETES MELLITUS

❑ ACUTE COMPLICATIONS OF DM
❑ Hyperglycemic Hyperosmolar Non-ketotic Syndrome
❑ A serious condition in which the hyperosmolarity and extreme hyperglycemia
predominate with minimal ketosis
❑ Onset is slow, takes days to develop
❑ S/Sx:
❑ Profound dehydration
❑ Hypotension tachycardia
❑ Altered sensorium
❑ seizures
❑ Dx:
❑ Blood glucose: 600-1200 mg/dl
❑ Blood osmolarity of 350mOsm/L
❑ Electrolyte abnormalities
❑ Mngt:
❑ Same with DKA
❑ Insulin drips
 DIABETES MELLITUS

❑CHRONIC COMPLICATIONS OF DM
❑ DM RETINOPATHY
❑ S/Sx:
❑ Rupture of microaneurysms
❑ Bluured vision
❑ Sudden loss of vision
❑ cataract

❑ Mngt:
❑ Maintain safety
❑ Control HPN and glucose levels
❑ Laser therapy
❑ Cataract removal
 DIABETES MELLITUS

❑CHRONIC COMPLICATIONS OF DM
❑ DM NEPHROPATHY
❑ S/Sx:
❑ Microalbuminemia
❑ Anemia
❑ Freuent UTI

❑ Mngt:
❑ Control HPN and glucose
❑ Restrict dietary protein and potassium intake
❑ Prepare for dialysis
❑ Kidney transplantation
 DIABETES MELLITUS

❑CHRONIC COMPLICATIONS OF DM
❑ DM NEUROPATHY
❑ S/Sx:
❑ Paresthesia
❑ Diminished/absent reflexes and peripheral pulses
❑ Pain in the lower extremity
❑ Skin breakdown
❑ Dyspareunia

❑ Mngt:
❑ Control HPN and glucose levels
❑ Estrogen-containing lubricants
❑ FOOT CARE*
Good luck future RNs!