GLANDS HORMONES FUNCITONS

PITUITARY GLAND
o Antidiuretic hormone (ADH) o
Posterior Pituitary Gland
o Oxytocin o
o Somatotropin / Growth Hormone (GH) o
o o Stimulates Milk Production
o Thyroid Stimulating Hormone o Stimulates the thyroid gland
Anterior Pituitary Gland o o Stimulates the adrenal cortex
o Follicle-Stimulating Hormone (FSH) o Females: Stimulates development of ovum
o Males:
o Luteinizing Hormone (LH) o Females: Stimulates ovulation
o Males:
PINEAL GLAND o o Regulates sleep pattern
o Tetraiodothyroinine (T4) o Regulates rate of body metabolism
THYROID GLAND o Triiodothyronine (T3)
o Calcitonin o
PARATHYROID o o Decreases calcium in the blood
GLANDS
CORTEX o Increases blood glucose
o Glucocorticoids (cortisol) o Maintains blood pressure
o Fights stress and inflammation

o Mineralocorticoids (aldosterone) o Regulates Sodium, water, and potassium excretion

ADRENAL GLANDS
o Androgens o Develops secondary sex characteristics
MEDULLA o Fight or flight response
o Catecholamines o Fights stress
o Epinephrine
o Norepinephrine
o Alpha Cells: Glucagon o Glucagon:
PANCREAS o Beta cells: Insulin o Insulin:
o Delta Cells: Somatostatin o Somatostatin
o Estrogen o Females:
o Males:
OVARIES
o Progesterone o Females:
o Males:
o Androgens (testosterone) o Males:
Testes
o Females
ANTERIOR PITUITARY DISORDERS

ACROMEGALY GIGANTISM
Increased production of growth hormone in ADULTS Increased production of growth hormone in Children
Causes: Causes:
 Pituitary adenomas o Pituitary Adenomas
 Damage or trauma o Damage or Trauma
Assessment: Assessment:
 Huge lower jaw  May be more than 7 feet tall
 Thick lips and tongue  Large in all proportions
 Oversized hands and feet  Weak and lethargic and can hardly stand
 Painful and stiff joints
 Deepened voice
 Muscle weakness
 Visual disturbances
Diagnostic Tests:
 MRI and CT Scans to diagnose presence and extent of tumor
 Serum levels of pituitary tumors
Interventions
 HYPOPHYSECTOMY
 Radiation therapy
 Bromocriptine

Posterior Pituitary Gland

 SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE DIABETES INSIPIDUS
(SIADH)
Increased ADH  increased reabsorption of water  oliguria  water retention Decreased ADH  decreased reabsorption of water  polyuria  dehydration
Causes: Causes:
 Head injury  Nephrogenic
 Brain surgery o Genetic or acquired failure of renal tubules to respond to ADH
 Tumor infection o Related to disorder and drugs that damage renal tubules
 Stroke  Neurogenic
 Vasopressin drug overdose o Head trauma
o Brain tumor
o Surgical ablation
o Irridation of pituitary gland
o Infection of CNS
Assessment: Assessment:
 Decreased urine output  Increased urine output
 Concentrated urine  Colorless, diluted urine
 Water retention  Dehydration
 Weight gain  Weight loss
 Cerebral edema  Thirst
Diagnostic tests Diagnostic Tests
 Decreased sodium level (dilutional hyponatremia)  Fluid deprivation test
 Increased specific gravity of urine o Hold fluid intake for 12 hours
o Measure the specific gravity of urine
o Diluted urine  positive
 Decreased specific gravity of urine
Interventions: Interventions
 Correct underlying cause  Desmopressin (synthetic vasopressin) replacement
 Restrics fluid intake  Ensure adequate fluid replacement
 Diuretics (Furosemide)  Identify correct underlying intracranial pathology
 Close monitoring of I&O, daily weight, urine, blood chemistry, nuero status
 Hypertonic Saline for emergency correction of hyponatremia in severe SIADH

THYROID GLAND
 HYPOTHYROIDISM HYPERTHYROIDISM
Decreased T3 and T4  decreased metabolic rate Increased T3 and T4  increased metabolic rate
Causes: Causes
 Thyroid or pituitary tumor  Thyroid or pituitary tumor
 Decreased TSH  Increased TSH
 Autoimmune Thyroiditis (Hashimoto’s Disease)  Hyperactivity of the thyroid gland
 Atrophy of thyroid gland  Adenoma of thyroid and thyroiditis
 Therapy for hyperthyroidism  Multinodular goiter
 Excessive intake of thyroid hormone
 Iodine deficiency and excess
 Grave’s Disease
Congenital Hypothyroidism
 Inadequate secretion of thyroid hormone during fetal or neonatal development
Assessment: Assessment:
 Lethargy  Restlessness
 Intorance to cold  Intolerance to heat
 Anorexia  Increased appetite
 Weight gain  Weight loss
 Constripation  Diarrhea
 Bradycardia  Tachycardia
 Forgetfulness  Amenorrhea
 Menorrhagia  Fine hand tremors
 Coarse sparse hair  Fine hair
 Thick nails, dry skin  Flushed, warm skin
 Masklike face  Goiter
 Large tongue  Exophthalmos
 Low pitched voice  THYROID STORM
 MYXEDEMA COMA o Fever
o Hypothermia o Tachycardia
o Hypotension o Arrhythmias
o Hypoventilation  Nervousness and apprehension
 Shortness of breath
 Pretibial myxedema
 Increased appetite
 Fatigability and weakness
 Muscle cramps
 Elevated blood pressure
 Cardiac dysrhythmias

Diagnostic tests Diagnostic Tests:

 Decreased serum T3 & T4 levels  Increased serum T3 and T4 levels
 Increased TSH level  Decreased TSH levels
  Decreased radioactive iodine (RAI) uptake  Increased Radioactive iodine (RAI) uptake
 Fine needle aspiration biopsy
 Thyroid scan
Management: Management:
 Lifetime thyroid hormone replacement therapy  Radioactive iodine (I-131)
 Levothyroxine o Destroys the thyroid gland
 Weight loss program  Antithyroid drugs
 High fiber, low cholesterol, low fat diet o Propylthiouracil (PTU)
 Provide warmth o Methimazole
 Monitor for constipation  Thyroidectomy
 Prevention of cardiac dysfunction and monitoring of angina, ischemia and infarction o Subtotal or total thyroidectomy
 Prevention of medication interaction  High calorie, high protein diet
 Thyroid hormones may increase blood glucose leves and increase pharmacologic  Monitor pulse rate and BP
effects of other drugs

THYROID STORM / THYROTOXIC CRISIS

 Description  Sudden, excessive production of T3 and T4  increased metabolism 

life threatening hyperthyroidism
  Causes  Convulsions
 Stress  Interventions
 Infection  IV steroid
 Over manipulation of the thyroid gland during assessment or surgery  IV sodium iodide
 Assessment  Antipyretics
 HIGH FEVER  IV fluid replacement
 TACHYCARDIA  Propanolol (to decrease heart rate)
 Dysrhythmias  How to prevent?
 Restlessness  Give Lugol’s solution or saturated solution of potassium iodide (SSKI)
 Delirium before thyroidectomy to ensure a euthryoid state, decrease the
casculatirty of the thyroid gland, and inhibit hormone release

THYROIDECTOMY

 Surgical removal of the thyroid  Interventions:

 Can be total thyroidectomy or subtotal thyroidectomy o Semi-fowler’s or Fowler’s position
 Complications o Ice pack to the neck to reduce swelling
o Hemorrhage o Support head during position change
o Respiratory distress o Report severe voice hoarseness
o Accidental removal of parathyroid gland o Avoid hyperextension/flexion of the neck
o Laryngeal nerve damage  Signs of accidental removal of parathyroid gland
o Thyroid storm o Hypocalcemic crisis
 Spasms of the fingers and toes
 Positive Chvostek’s and Trousseau’s sign

PARATHYROID DISORDERS

HYPERPARATHYROIDISM HYPOPARATHYROIDISM
  Overproduction of PARATHORMONE  Inadequate parathormone secretion
 Characterized by
o Bone decalcification
o Development of renal calculi containing calcium
o Hypercalcemia
Increased parathyroid hormone production  increased calcium , decreased Decreased parathyroid hormone production  Decreased calcium, increased phosphoru
phosphorus
Etiology / Causes: Etiology / Causes
 Parathyroid adenoma  Damage to parathyroid during parathyroidectomy, thyroidectomy, or radical neck dissection
 Parathyroid hyperplasia  Autoimmune disease
 Parathyroid carcinoma
 Compensatory response to chronic hypocalcemia
 Severe vitamin D deficiency
 Calcium deficiency
 Decreased renal activation of vitamin D (Renal Failure)
Clinical Manifestations: Clinical Manifestations / Assessment:
 Hypercalcemia  Hypocalcemia
 Hypercalciuria due to increased renal filtration load of calcium  Compensatory hypocalciuria due to low serum calcium
 Hypophosphatemia  Hyperphosphatemia
 Hyperphsphaturia  Hypophosphaturia
 Renal calculi / kidney stones  Muscle tetany
 Pathologic fracture, deformities, kyphosis, compressional fractures of  Numbness and tingling on toes, fingers, and lips
the vertebrae  Laryngeal spasm
 Muscle weakness  Chvostek’s sign
 Fatigue o Tap the facial nerve  mouth jerks and jaw tightens
 Constipation  Trousseau’s sign
 Bone pain (due to demineralization) o Place a BP cuff and inflate between SBP and DBP and wait 3 minutes  spasm of hand
 Hypertension and cardiac dysrhythmias flexing inward
 Psychological effects like psychosis caused by direct action of  Cardiac dyshythmias
calcium on brain and nervous system  Seizures and delirium
Diagnostics: Diagnostics
 Serum parathormone radioimmunoassay  Positive Trousseau’s sign
 Serum calcium levels  Positive Chvostek’s sign
 Bone scans and x-rays  Serum calcium levels
 Parathyroid ultrasound and/or MRI  Serum phosphate levels
 Fine needle aspiration bioopsy  Increased bone density in x-rays and bone scans
Management Management:
 Parathyroidectomy  Monitoring for early signs of tetany and hypocalcemia in post-operative patients of
o Treatment of choice thyroidectomy, parathyroidectomy, or radical neck dissection
o Watch for hypocalcemia or tetany  IV Calcium gluconate
 Increase fluid intake to prevent calculi o Kept at bedside for immediate treatment of hypocalcemia and tetany post thyroidectomy
 Low calcium, high phosphorus diet o Increases serum calcium levels
  Monitor manifestations of renal calculi
o Abdominal pain and hematuria
 Vitamin D supplements
 Mobility is encouraged
 Bisphosphonates
o Treats hypercalcemia
o Inhibits osteoclastic bone resorption
o Aldendronate (Fosamax)
 Calcitonin and Corticosteroid
o Combination therapy given to hypercalcemic crisis
o Reduce serum calcium levels by incresing calcium
deposition in bone
 Parenteral Parathormone
o Treatment of acute hypoparathyroidism with tetany
o Monitory closely for allergic reactions and changes in serum calcium levels
 High calcium, low phosphorus diet
 Avoid carbonated drinks (high in phorphorus)
 Provide environment free from noise, bright lights, or sudden movement because of
neuromuscular irritability
 Prepare for emergency tracheostomy, mechanical ventilation, and broncho-dilating agents for
respiratory distress
 High vitamin D diet
o Enhance calcium absorption from the gut

Adrenal Glands

PHEOCHROMOCYTOMA

 Tumor, usually benigns  Causes a sympathetic nervous stem over activity due to increased catecholamine
 From chromaffin cells of adrenal medulla secretion
 o Benign tumor of adrenal medulla  release of chatecholamines 
increase BP
 Cause:
o Mutated genetic inheritance
 Clinical Manifestations:
o 5P’s
 Pressure (hypertension)
 Palpitations
 Persperation (diaphoresis)
 Pallor
 Pain (headache)
o Flushings
o Tremors
o Hyperglycemia
 Diagnostics
o Urine and plasma levels of catecholamine and metanephrine
o Clonidine suppresion test
 Preformed if plasma and urine catecholamine results are
invonclusive
o Increased vanillylmandeleic acid (VMA) (metabolite of catecholamine)
o Imaging
 CT Scan, MRI, and/or Ultrasound
 Management
o Bedrest with bed elevated promoting orthostatic decrease in blood
pressure
o Close monitoring with ECG changes
o Careful administration of anti-hypertensives
o Adrenalectomy
 Definitive treatment
 Hypotension and hypoglycemia may occur postOP due to
sudden withdrawal of excessive amount of catecholamines
 Maniputation of tumor during surgery may case release of
stored catecholamines with marked increases in blood pressure
and changes in heart rate
 Cushing’s Syndrome Addison’s Disease
 Excessive adrenocortical activity  Adrenocortical insufficiency occurs
 Symptoms are due to over secretion of glucocorticoids and  Adrenal cortex function is inadequate to meet the patient’s need for cortical hormones
androgens
 Mineralocorticoid secretion may be affected
Causes/ Etiology: Causes / Etiology:
 Excessive use of corticosteroid medications  Autoimmune or idiopathic atrophy
 Hyperplasia of adrenal cortex  Infection
 Tumor of pituitary gland  Surgical removal of adrenal glands
 Ectopic and non-pituitary ACTH secreting tumor  Corticosteroid use
 Rapid withdrawal resulting to adrenal cortical atrophy
 Pituitary gland hyposecretion
 Decreased ACTH
Clinical Manifestations / Assessment Clinical Manifestations / Assessment:
 INCREASED SODIUM, DECREASED POTASSIUM  INCREASED POTASSIUM, DECREASED SODIUM
 Glucose intolerance and insulin resistance  Hypoglycemia
 Hyperglycemia  GI symptoms and anorexia
 Immunosuppression  Muscle weakness
 Weight gain  Fatigue
 Truncal obesity  Emaciation
 Buffalo hump  Hyponatremia
 Moon face , masculinization/ virilization  Hyperkalemia
 Thin extremities  Confusion and restlessness
 Arrest of growth  Dark pigmentation of mucous membranes and skin of knuckles, elbows, and knees (bronze, dark skin
 Musculoskeletal changes: pigmentation)
o Osteoporosis  Decreased cardiac output and hypotension
o Kyphosis  Depression
o Compression fractures
 Muscle wasting
 Thin fragile skin with ecchymosis and striae
 Weakness
 amenorrhea
 Hypertension or heart failure
 Mood changes and psychosis
 Gastric ulceration and bleeding

Diagnostics: Diagnostics:
 Dexamethasone suppression test  Serum cortisol
 o Widely used and most sensitive  Plasma ACTH
o Administration of steroids  steroids remain increased  Serum glucose levels
 positive  Serum sodium levels
 INCREASED sodium levels  Serum potassium levels
 DECREASED potassium levels  ACTH STIMULATION TEST
 Serum glucose levels o Stimulation of adrenal gland  low adrenal response  positive
 Serum and 24-hour urine cotisol levels
 Serum radioimmunoassay of ACTH
 Imaging to localize adrenal tumors
Management Management:
 Transsphenoidal hypophysectomy  Administering fluids and restoring blood circulation
 Adrenalectomy  Coticosteroid admin with hydrocortisone
 Radiation of pituitary gland  Antibiotics if condition is precipitated by and infection in the adrenals
 Temporary replacement therapy with hydrocortisone post  Possible lifelong replacement of corticosteroids and mineralocorticoids to prevent recurrence of
operatively adrenal insufficiency
 Low calcium, high postassium diet  IV administration of fluids, glucose, and electrolytes
 Low calorie, low carbohydrate diet  High sodium, low potassium diet
 Diuretics  High protein, moderate carbohydrate diet
 Monitor blood sugar  Report sore throat and fever
 Taper steroid use after prolonged use  Provide rest periods
 Meticulous skin care for fragile skin  Do not give insulin
 Monitor for masked signs infection
 Diabetes Mellitus
 Group of metabolic diseases
 Characterized by increased levels of glucose in blood (hyperglycemia) resulting from defects in insulin action and/or secretion
Risk Factors
 Family history of DM
 40 years old and above
 History of gestational diabetes
 High HDL cholesterol levels and triglyceride levels
 Obesity
 Hypertension
TYPE 1 TYPE 2 Gestational Diabetes (GDM)
Insulin Dependent Non-Insulin Dependent
Absence of insulin production Lack of insulin or insulin resistance
 Acute onset  Related to aging, genetics, obesity  Any degree of glucose intolerance
 Childhood condition  At risk for hyperosmolar, hyperglycemic, during pregnancy
 Before 30 years of age non-ketotic (HHNK) syndrome  Occurs in 14% of pregnant women
 Autoimmune-related disease  Occurs commonly in people who are older  Increases risk for hypertensive
 At risk for Diabetic Ketoacidosis (DKA) than 30 years old and obese disorders during pregnancy
Etiology Etiology Etiology
 Destruction of pancreatic beta cells due to genetic, immunologic,  Insulin resistance  Secretion of placental hormones
& possibly environmental factors (viral)  Impaired secretion due to genetic factors leading to insulin resistance
Clinical Manifestations Other Clinical Manifestations:
 3P’s  Hyperglycemia
 Glycosuria
o Polydipsia
 Osmotic diuresis
o Polyphagia  Fatigue and weakness
o Polyuria  Ketonuria
 Vision changes
 Tingling or numbness in hands and feet
 Slow healing wounds and lesions
 Recurrent infections
 Weight loss
Diagnostics  Oral glucose tolerance test (OGTT)
 Fast blood sugar  Urine glucose and ketone levels (urine dipstick)
 Random blood sugar  Urine test for albumin
 Postprandial sugar  Serum cholesterol and triglyceride levels
 HgbA1C/ Hemoglobin A1C

DIABETIC KETOACIDOSIS (DKA) HYPEROSMOLAR, HYPERGLYCEMIC NON-KETOTIC SYNDROME

 Hyperglycemia with metabolic acidosis and ketosis Hyperglycemia WITHOUT ketosis
Causes: Causes:
 Infection  Uncontrolled or undiagnosed DM, TPN
 Starvation
 Uncontrolled DM
Assessment/ Clinical Manifestations: Assessment/ Clinical Manifestations:
 Very high blood glucose ( >300 – 1000 mg/dL)  Very high blood glucose (>600 – 1000mg/dL)
 Drowsiness  Drowsiness
 Severe thirst  Severe thirst
 Dehydration  Dehydration
 Fever
 Fruity-scented (acetone) breath
 Kussmaul breathing (to blow off excess acids)
Diagnostic test: Diagnostic test:
 Glucose and ketones in urine  Normal pH
 Low pH
 Decreased HCO3 (metabolic acidosis)
Interventions Interventions
 IV Regular insulin  IV regular insulin
 IV 0.9% NaCl  IV 0.9% NaCl
 Potassium replacement  Potassium replacement

HYPOGLYCEMIA
Causes  Exercise
 Alcohol intake
 Overdose of insulin, Anorexia ,Oral hypoglycemic agents
Assessment Weakness, nausea, tremors, headache, sweating, confusion, irritability, seizures
Interventions Give 15 grams of simple carbohydrates
Examples:
 Glucose tablets or gel tube
 2 tablespoons of raisins, hard candies
 Orange juice or regular soda (not diet)
 1 tbsp sugar, honey, or corn syrup
 8 ounces of nonfat or 1% milk
If unconscious  inject glucagon, give D50% glucose IV
What should be given after the hypoglycemic episode? Give complex carbohydrates to maintain the blood glucose levels (e.g. milk, potatoes, graham crackers)
How can hypoglycemic episodes be prevented? Serve meal after giving insulin
Eat snack before intense activity

Peripheral neuropathy Diabetic neuropathy Diabetic retinopathy

Assessment Pain, paresthesia, voiding problem, slow GI Worsening hypertension, edema, albuminuria, Blurred vision, blindness, floating spots

Interventions
What antidepressant is given to manage
pain?
What anticonvulstans are given?
What instructions about foot care are
important to teach?
movement (gastroparesis) oliguria
Diet, exercise, non-narcotic analgesics Control blood flucose, maintain BP, ACE ACE inhibitors to dilate retinal vessels
inhibitors
Imipramine
Gabapentin, carbamazepine
Wash feet in warm water
Cut nails STRAIGHT across
Apply moisturizer to feet
Inter lamb’s wool between toes