ANATOMY AND PHYSIOLOGY OF THE ENDOCRINE SYSTEM The different endocrine glands are as follows: 1.

. Pituitary Gland (Hypophysis) Lies in the sellaturcica of the middle cranial fossa (the bony floor that supports the brain) It is composed of 2 parts: The anterior pituitary gland (adenohypophysis) and the posterior pituitary gland (neurohypophysis) The hypothalamus controls both the anterior and posterior pituitary glands. And therefore, it controls the other endocrine glands. The anterior pituitary gland hormones and their function are as follows: a) Growth hormone (GH). It is also known as somatotropin or somatotropic hormones (STH). It is concern with concern with the growth of cells, bones, and soft tissues It affects carbohydrate, protein, and fat metabolism It increases blood glucose levels by reducing glucose utilization; an insulin antagonist b) Prolactin (PRL). It is also called mammotropic hormone, lactotropic hormone, and luteotropic hormone. It is necessary for breast development and lactation It regulates reproductive function in males and females c) Thyroid-stimulating hormone (TSH) It controls functions of the thyroid glands d) Gonadotropic hormones or Gonadotropin The two gonadotropins are: follicle-stimulating hormones (FSH) and Luteinizing hormone (LH) They affect development of secondary sex characteristics They are necessary for gametogenesis and sex steroid production in males and females e) Adrenocorticotropic hormone (ACTH) or Adrenocorticotropin It contains functions of the adrenal glands f) Melanocyte-stimulating hormone It is necessary for pigmentation, e.g. skin, retina (melanin epithelial pigment layer) The posterior pituitary gland hormones and their functions are as follows: a) Antidiuretic hormone (ADH). It is also called vasopressin It is the major control of osmolality (concentration) and body water volume It increases water reabsorption in the collecting ducts of the kidneys b) Oxytocin It promotes milk let-down in a lactating breast It causes increased uterine contraction after labor has begun

2. Thyroid Gland.
The thyroid gland hormones are as follows: a) Triiodothyronine (T3) and Thyroxine (T4). These two hormones: Regulate metabolic rate of cells. Regulate protein, fat and carbohydrate metabolism Acts as insulin antagonists Maintain growth hormone secretion and promote skeletal maturation Affect central nervous system (CNS) development Affect cardiac rate, force and output Affect oxygen utilization Stimulate lipid turnover, free fatty acid release and cholesterol synthesis Stimulate sympathetic nervous system (SNS) activity b) Thyrocalcitonin (Calcitonin) It lowers serum calcium levels It inhibits osteoclastic activity It lowers phosphate levels It decreases calcium and phosphorus absorption in the G.I. tract. The relationship between Thyrocalcitonin and calcium is inverse: Thyrocalcitonin is (), Calcium is (); Thyrocalcitonin is (), Calcium is ()

3. Adrenal Glands The two divisions of the adrenal glands are the cortex and the medulla The adrenal cortex hormones control the 3S: Sugar, Salt, Sex a) Glucocorticoids (Cortisol) Maintain blood glucose levels (Sugar) Enhance gluconeogenesis (protein catabolism and fat catabolism/ lipolysis) Have anti-inflammatory effect Decrease T-lymphocyte participation in cell-mediated immunity (immunosuppressant) Decrease new antibody release Increase gastric acid and pepsin production. This may cause G.I. irritation Maintain emotional stability Mineralocorticoids (Aldosterone) Maintain sodium and volume status (Salt) Increase sodium reabsorption in distal tubules of the kidneys

b)

 Increase potassium and hydrogen excretion in distal tubules. Aldosterone is PRO SODIUM (retains sodium )and ANTI POTASSIUM (excretes potassium) Increased Aldosterone level results to: Hypernatremia Hypokalemia Decreased aldosterone level results to: Hyponatremia Hyperkalemia c) Sex Hormones (Androgen and Estrogen) Responsible for some secondary sex characteristics in females. In males, these hormones work like gonadal steroids The adrenal medulla secretes catecholamines (epinephrines and norepinephrine) through stimulation of the SNS and medulla oblongata The effects of sympatho-adreno-medullary response (SAMR) stimulation on body organs are as follows: (CONCEPT: Every function is high and fast, except GI and GU) BRAIN i. Increased alertness; restlessness EYES ii. Dilation of the pupils; relaxation of the ciliary HEART bodies LUNGS iii. Increased heart rate; increased contractility; PERIPHERAL BLOOD VESSELS increased stroke volume; coronary vasodilation MOUTH iv. Relaxation of bronchial muscles SKIN (bronchodilation); increased respiratory rate GASTROINTESTINAL TRACT v. Vasoconstriction; increased BP KIDNEYS vi. Decreased salivary glands secretion; dry mouth URINARY BLADDER and thirst LIVER vii. Pilomotor muscle contraction; localized PANCREAS sweating; cold clammy skin GALLBLADDER viii. Decreased production of GI secretions; FAT CELLS decreased motily and contraction of sphincter ix. Increased renin secretion x. Relaxation of detrusor muscles and contraction of sphincter (urinary retention) xi. Glycogenolysis, gluconeogenesis; increased serum glucose levels xii. Decreased secretion of islet cells; decreased insulin secretion; increased serum glucose levels xiii. Relaxation of gallbladder xiv. Lipolysis

I. II. III. IV. V. VI. VII. VIII. IX. X. XI. XII. XIII. XIV.

4.

Pancreas The islets of Langerhans perform the endocrine functions of the pancreas. It has two types of cells, the alpha and beta cells The alpha cells secrete GLUCAGON; while the beta cells secrete INSULIN Glucagon enhances gluconeogenesis (breakdown of fats and proteins into glucose) and elevates blood glucose levels Insulin produces the following effects: LIVER CELLS Increased glycogenesis Increased fatty acid synthesis Decreased glycogenolysis, gluconeogenesis, and ketogenesis Adipose tissues Increased fatty acid synthesis Increased glycerol synthesis Decreased lipolysis Muscles Increased glycogenesis Increased amino acid uptake and protein synthesis Decreased protein catabolism Overall effect of insulin: LOWERS GLUCOSE LEVELS

The physiologic changes in the endocrine system associated with aging are as follows: Decreased ovarian functioning resulting in changes in reproductive and sexual functioning

Impaired secretion of hypothalamic hormones influences responsiveness to changes in the internal environment and to stressors Decreased levels of prolactin, growth hormone Increased levels of ADH; however alterations in renal function decrease ability of the elderly to concentrate urine and hyponatremia can result; nocturia is also commonly present Hypothyroidism occurs due to changes in thyroid gland structure Decreased vitamin D levels, negative calcium balance, bone loss, decrease intestinal adaptation to varied calcium

5.

intake Renin-aldosterone response to postural changes and volume depletion is depressed. The client is at risk to postural hypotension Impaired glucose tolerance due to delayed glucose-induced insulin secretion, altered hepatic handling of glucose and impaired insulin-mediated glucose uptake. Non-insulin-dependent diabetes mellitus (NIDDM) is one of the more chronic diseases among the elderly Decrease in size of the liver Decreased in enzymes involved in the metabolism with drugs. Increased propensity to drug toxicity Parathyroid Glands Produces Parathormone (PTH) PTH regulates calcium and phosphorus balance PTH elevates serum calcium levels by withdrawal of calcium from the bones Low serum calcium levels stimulate PTH release The relationship of PTH and calcium is direct proportion Hypersecretion of PTH: HYPERCALCEMIA Hyposecretion of PTH: Hypocalcemia

The relationship of PTH and phosphorus is inverse. Hypersecretion of PTH: HYPOPHOSPHATEMIA Hyposecretion of PTH: HYPERPHOSPHATEMIA PTH elevates serum calcium levels and inversely, lowers phosphorus levels

DIAGNOSTIC TESTS FOR ENDOCRINE DISORDERS 1. Diagnostic Tests of Thyroid disorders THYROID FUNCTION TESTS a. Thyroid-stimulating hormone assay : Hypofunction of thyroid gland; PRIMARY HYPOTHYROIDISM : Pituitary disorders: HYPERTHYROIDISM b. Radioactive Iodine uptake (RAIU) : Hyperthyroidism; urine: HYPOTHYROIDISM : hypothyroidism; urine: HYPERTHYROIDISM Patient Teaching: o Radioactive dose is small and harmless o Contraindicated in pregnancy o Seafood may elevate results

Drugs that may elevate results: barbiturates, estrogen, lithium, phenothiazine. o Drugs that may decrease results: lugols solution, saturated solution of potassium iodine, antithyroid, cortisone, aspirin, antihistamines. o Collect 24-hour urine specimen after oral tracer dose given. o Thyroid is scanned sfter 24 hours. c. Thyroid antibodies : Thyroiditis d. T3 T4 Radioimmunoassay : Hyperthyroidism : Hypothyroidism e. Free Thyroxine Concentration T3 Resin Uptake Thyroid Binding Globulins : Hyperthyroidism : Hypothyroidism DIAGNOSTIC IMAGING STUDIES a. Thyroid Scan

b. c.

Radioactive iodine taken orally; dose is harmless Scanning done after 24 hours Avoid iodine containing foods, dyes, medications Cold nodules: cancer Hot nodules: benign Ultrasound No special preparation Magnetic Resonance Imaging Test cannot be done in clients with metal implants (pacemakers. Arthroplasties, skull plates) Assess for allergy to contract media Computed Tomography

d.

2.

If contract medium is used, note allergy history

Diagnostic Tests of Parathyroid Disorders a. Total Serum Calcium Venous blood is collected : Hyperparathyroidism : Hypothyroidism b. Qualitative Urinary Calcium (Sulkowitch Test) Collect urine specimen Fine white precipitate should form when Sulkowitch reagent is added to urine specimen

c.

Absent or decreasewd precipitate indicate low serum calcium and hypoparathyroidism

Quantitative Urinary Calcium (Calcium Deprivation Test) Collect 24-hour urine specimen : Hyperparathyroidism : Hypoparathyroidism Serum Phosphorus Collect venous blood specimen : Hypoparathyroidism : Hyperparathyroidism Serum Alkaline Phosphate Collect venous blood specimen : Hyperparathyroidism : Hypoparathyroidism Parathormone Radioimmunoassay Collect venous blood : Hyperparathyroidism When elevated in conjunction with serum calcium levels, this is the most specific test for hyperparathyroidism.

d.

e.

f.

3.

Diagnostic Tests of Adrenocortical Disorders a. Cortisol level with dexamethasone suppression test Give dexamethasone before phlebotomy to suppress diurnal formation of ACTH : pituitary tumor, Cushings syndrome or disease : Addisons disease b. Cortisol plasma level Fasting is required; the patient should be on bed rest for 12 hours before the test because activity increases cortisol level. : Cushings syndrome : Addisons disease 17-hydroxysteroids - 24-hour urine collection to be kept on ice : Cushings syndrome or disease : Addisons disease 17-ketosteroid 24 hour urine test; keep collection cold, may need preservatives. : Cushings syndrome : Addisons disease

c.

d.

4.

Diagnostic Tests of Adrenal Medullary Disorders a. Vanillymandelic Acid Test (VMA Tests) VMA is a metabolite of epinephrine 24 hour urine specimen is collected. - Instruct the client to avoid the following medications and foods which may alter the result: o Coffee o Chocolate o Tea o Bananas o Vanilla o Aspirin Normal value: 0.7 6.8 mg / 24 hr b. Total Plasma Catecholamine Concentration - The client should lie supine and rest for 30 minutes

Butterfly needle is inserted 30 minutes before the blood specimen is collected (to prevent elevation of

catecholamine levels by the stress of venipuncture) Normal values: o Epinephrine: 100 pg/ml (590 pmol/L) o Norepinephrine: 100-550 pg/ml (590-3240 pmol/L)

c.

Clonidine Suppression Test - Clonidine (Catapress), a centrally acting adrenergic blocker suppresses the release of catecholamines.

d.

Normal response: 2-3 hours after a single oral dose of Clonidine, the total plasma catecholamine values decreases at least 40% from clients baseline.

CT Scan, MRI, Ultrasound To localize the pheochromocytoma

5.

Diagnostic Tests of Pancreatic Disorders (Diabetes Mellitus) a. FBS (Fasting Blood Sugar) and FBG (Fasting Blood Glucose) Normal: 70-110 mg/dL DM: 140 mg/dL for 2 readings b. 2 PPBS (2 hour Postprandial Blood Sugar) - Initial blood specimen is withdrawn. 100 g of carbohydrate in diet is taken by the client 2 after OGTT/GTT (Oral Glucose Tolerance Test) Glycosylated Hgb (HbA1C) Most accurate indicator of Diabetes Millitus Reflects serum glucose levels for the past 3 to 4 months Normal value is 4% to 6% (up to 7%) for nondiabetics

c.

d.

Excess glucose in blood

ENDOCRINE DISORDERS

The goal for clients with DM is 7.5% or less

Attaches to hemoglobin

Hgb (component of RBC) 90-120 days

Disorders of the Pituitary Gland Anterior Pituitary Gland (Adenohypophysis) Growth Hormone (GH) Gigantism Is hypersecretion of GH in children (before epiphyseal closure). This condition is characterized by exaggerated growth in height and weight. Acromegaly Is hypersecretion of GH in adults (after epiphyseal closure). This is caused primarily by pituitary tumors. The clinical manifestations are: Large hands and feet; Thickening and protrusion of the jaw; organomegaly; visual disturbances; arthritic changes; diaphoresis; oily rough skin; hypertension; dysphagia; deepening of the voice Dwarfism Is hyposecretion of GH. It is characterized by failure to grow in height Prolactin (Mammotropic, Lactotropic, Leteotropic Hormone) Galactorrhea Is hypersecretion of prolactin. It is characterized by excessive milk production. Absence of milk production during lactation results from hyposecretion of prolactin. Adrenocorticotropic Hormone (ACTH) Cushings Disease. Is hypersecretion of ACTH Addisons Disease, Is hyposecretion of ACTH Thyroid-stimulating Hormone (TSH) Hyperthyroidism is hypersecretion of TSH Hypothyroidism Is hyposecretion of TSH Gonadotropins (FSH and LH) Hypersecretion of hormones results to precocious puberty Hyposecretion of hormones results to failure to develop secondary sex characteristics that normally develop at the age of puberty. The manifestations are as follows: MALES FEMALES Small phallus and testicles Failure to develop breast No growth of body hair No growth of body hair Decreased libido No ovulation Impotence No menstruation Aspermia Infertility Melanocyte-Stimulating Hormone (MSH)

1.

Hypersecretion of hormone results to hyperpigmentation of the skin (eternal tan or bronze appearance of the skin) Hyposecretion of hormone result to albinism (hypopigmentation of the skin). Its characterized by absence of the melanin epithelial pigment of the retina. This results to difficulty in vision during daytime or in the presence of bright light.

2.

Posterior Pituitary Gland (Neurohypophysis) Antidiuretic Hormone (ADH) I. Hypersecretion of the hormone SIADH Causes include trauma, stroke, medications, and stress SIADH is characterized by excessive retention of water by the renal tubules The characteristic manifestations of SIADH are as follows: Edema, weight gain. This is due to excessive retention of water Hypertension. Vasopressin causes vasoconstriction Dilutionalhyponatremia. This is due to excessive retention of water, without proportionate retention of sodium. Collaborative management for SIADH include the following: Administer diuretics as prescribed to reduce body fluids Administer Demeclocycline (Declomycin) as prescribed. It inhibits ADH induced water reabsorption and produces water diuresis Restrict fluid intake as prescribed Monitor VS, cardiac and neurological status. Water intoxication may cause CHF and increase ICP. Monitor I and O, daily weight, electrolyte levels II. Hyposecretion of ADH is Diabetes Insipidus Diabetes Insipidus is characterized by inability of the renal tubules to retain water (water loss) The most characteristic manifestation of DI is polyuria (as much as 20ml/day) The urine is dilute or water-like, with low specific gravity Other manifestations of DI are as follows: polydipsia, dehydration, constipation, retarded growth in children The diagnostic test for DI is water deprivation test. Fluids are withheld for 4-18 hours. If there is no increase in urine concentration, this confirms presence of DI The antidiuretic hormone used in DI are as follows: Desmopressin acetate (DDAVP, Stimate) Vasopressin (Pitressin) Clofibrate has antidiuretic effect on clients with DI

Chlorpropramide (Diabenase) and thiazide diuretics potentiate the action of vasopressin Hyperpituitarism Is hyperfunction of the anterior pituitary hormones It is frequently caused by benign pituitary adenoma; may result also from hyperplasia of pituitary tissue Prolactinomas (prolactin-secreting tumors) account for 60% to 80% of all pituitary tumors The characteristic manifestations of hyperpituitarism are as follows: Overproduction of growth hormone results in acromegaly in adults; Gigantism in children Hormonal imbalances

Neurologic manifestations: o Hemianopsia or scotomas (blind spots in the visual field) or blindness o Headache o Somnolence o Signs and symptoms of increased intracranial pressure o Behavioral changes, seizures o Disturbance in appetite, sleep, temperature regulation and emotional balance due to hypothalamic involvement o Diagnostic tests to confirm presence of tumor: skull x-ray, CT scan, MRi Endocrine manifestations o Irregular menses, anovulatory periods, oligomenorrhea (scanty menstrual flow), amenorrhea (absence of menstrual flow) o Infertility o Galactorrhea (excessive milk production) o Dyspareunia (painful sexual intercourse), vaginal mucosa atrophy, decreased vaginal lubrication, decreased libido due to ovarian steroid effect o Decreased libido and impotence, reduced sperm count, infertility and gynecomastia in males

The collaborative management for hyperpituitarism are as follows: Surgery: Transphenoidalhypophysectomy o Hypophysectomy is surgical removal of the pituitary gland o The incision in transphenoidalhypophysectomy is made between the upper lip and upper gum o The nursing interventions after transphenoidalhypophysectomy are as follows:

Keep head of bed elevated, at least for 2 weeks. To promote venous drainage and drainage from the surgical site Maintain nasal packing in place and reinforce as needed

o o

Provide frequent oral care with toothettes. To prevent trauma to the incision Instruct client to avoid blowing the nose and activities that increase ICP Monitor for any post nasal drip or nasal drainage which might indicate leakage of CSF. Check nasal drainage for glucose. CSF is (+) for glucose Report to physician, outputs above 900 ml/2 hous or urine specific gravity below 1.004. These indicates DI Administer glucocorticoids and other hormone replacement as prescribed. This may indicate vasopressin, growth hormone (somatotropin) Radiation therapy as prescribed Pharmacotherapy Parlodel (Bromocriptine) to lower GH and prolactin levels

Hypopituitarism Hypofunction of anterior pituitary gland causing deficiencies in both pituitary hormones and the hormones of the target glands The causes are as follows: tumors, trauma, encephalitis, autoimmunity, stroke, surgery or radiation of pituitary gland The clinical manifestations of hypopituitarism are as follows: a. Mild to moderate obesity (Low GH, TSH) b. Reduced cardiac output (Low GH, ADH) c. Infertility, sexual dysfunction (Low gonadotropins, ACTH) d. Fatigue, low BP e. Headache, hemianopsia (due to tumors of the pituitary gland; the gland is located near the optic nerve) The collaborative management for hypopituitarism are as follows: a. Surgical removal of the tumor b. Radiation therapy c. hormonal replacement therapy (HRT) Simmonds disease Is panhypopituitarism. It is the total absence of all pituitary hormones Sheehans syndrome Is hypopituitarism caused by postpartum pituitary necrosis It occurs in women with severe bleeding, resulting to hypovolemia and hypotension at the time of delivery

DISORDERS OF THE THYROID GLAND Goiter Is an enlargement of the thyroid gland This is due to an increased amount of TSH. It can be associated with hyperthyroidism, hypothyroidism or euthyroidism Hyperthyroidism Is the hypersecretion of the thyroid hormones. A common cause is Graves disease, also known as toxic diffuse goiter Incidence is higher in females, below 40 years of age It is primarily associated with severe emotional stress; secondarily with autoimmune disorders The clinical manifestations of hyperthyroidism are based on 3 basic concepts: Increased body heat production (due to hypersecretion of T4) Hypocalcemia (due to hypersecretion of thyrocalcitonin) Thyroid hormones enhance the actions of epinephrine and norepinephrine, increasing symphathetic activity and central nervous system function Hypocalcemia results to increased cell membrane permeability. This leads to increased neuromuscular irritability The clinical manifestations of hyperthyroidism are as follows: Thyroidal disturbances a. Activation of SNS and CNS functions: o Restlessness, nervousness, irritability, agitation o Fine tremors o Tachycardia o Hypertension o Diaphoresis b. Increased metabolism o Increased appetite to eat o Weight loss o Heat intolerance c. Hypocalcemia o Diarrhea (increased peristalsis) o Fine, silky hair o Pliable nails d. Altered reproductive function Amenorrhea Ophthalmopathy Exophthalmos protrusion of the eyeballs. This is caused by the accumulation of fluids in the fatpads behind the eyeballs, pushing the eyeballs forward. This may cause corneal ulceration, ophthalmitis, and blindness. Exophthalmos is irreversible

Increased metabolic rate (due to hypersecretion of T3)

Von Graefes sign (lid lag). Long and deep palpebral fissure is still evident when one looks down

Jeffreys sign. The forehead remains smooth when one looks up Dalyrimples sign (Thyroid stare). Is characterized by bright-eyed stare and infrequent blinking Dermopathy. This is manifested by warm, flushed, sweaty skin and thickened, hyperpigmented skin at the pretibial area. Basic concepts to remember in hyperthyroidism Signs and symptoms a. Everything is high, fast and wet. E.g. HIGH and FAST (hypertension, tachycardia, high body temp); WET (diaphoresis, diarrhea) b. Eye manifestations. E.g. exophthalmos, lid lag, bright-eyed stare. The collaborative management for hyperthyroidism are as follows: Provide adequate rest Provide non-stimulating, quiet and cool environment. To prevent agitation and heat intolerance

Provide high-calorie diet. To maintain nutritional status Low-fiber diet, if with diarrhea Obtain daily weight. This is the best indicator of nutritional status Promote safety. The client is at high risk for injury due to restlessness, nervousness, agitation and tremors. Protect the eyes, If with exophthalmos. Instill artificial tears at regular intervals. Advise client to wear dark sunglasses when going out under the sun Avoid stimulants like caffeine Replace fluid and electrolyte losses due to diarrhea and diaphoresis Pharmacology in hyperthyroidism: Anti-thyroid medications Iodides: Lugols Solution and Saturated Solution of Potassium Iodide (SSKI) a. Inhibit release of thyroid hormones b. Mix with water of fruit juice with ice to improve palatability. c. Provide drinking straw to prevent permanent staining of teeth d. Side effects: (Iodism) allergic reaction, metallic or brassy taste in the mouth, increased salivation, coryza, vomiting, abdominal pain, sore gums Thioamides: Tapazole (Metimazole), PTU (Prophylthiouracil) a. Inhibit sunthesis of thyroid hormones b. Side effects: Agranulocytosis (neutropenia) with leukopenia (fever, sore throat, skin rash, and diarrhea)

When antithyroid medications are given: a. Monitor vital signs (especially BP and pulse rate), and weight. These medications may cause hypertension and tachycardia. Weight gain indicates effectiveness of medication b. Administer with meals to avoid GI upset c. Avoid ASA (Aspirin) and medications containing iodine. ASA elevates free thyroid hormone levels; iodine-containing medications stimulate thyroid function and antagonize antithyroid medications d. Advise client to consult physician before eating iodized salt and iodine-rich foods e. Observe for signs and symptoms of hypothyroidism Beta-blocker: Inderal (Propanolol) To control tachycardia and hypertension Calcium-channel blockers, dexamethasone Inhibit the action of thyroid hormones Radiation therapy: Radioactive Iodine (I131) Place client on isolation for few days. Body secretions are radioactivecontaminated. Use gloves when handling body secretions Do not use in pregnant women because of potential teratogenic effects. Pregnancy should be delayed for 6 months after therapy Surgery: Subtotal thyroidectomy (5/6 of the gland is removed) Care of clients undergoing thyroidectomy o Preoperative Interventions 1. Promote euthyroid state - Obtain VS and weight. Ensure VS are stable - Assess electrolyte levels - Assess for hyperglycemia and glucosuria. (Thyroid hormones act as insulin-antagonists) 2. Instruct client on how to perform deep breathing, coughing, and turning exercises and how to support the neck in the postoperative period when coughing and moving 3. Administer the following medications as prescribed to prevent thyroid storm: - Sodium Iodide Solution (Lugols solution). To reduce the size and vascularity of the thyroid gland and prevent postop hemorrhage and

thyroid crisis - Inderal (Propanolol) to control hypertension and tachycardia - Glucocorticoids (e.g. dexamethasone) to inhibit action of thyroid hormones 4. Check electrocardiogram (ECG). Heart failure or cardiac damage results from hypertension and tachycardia o Postoperative interventions: 1. Position: Semi-fowlers with head, neck, and shoulders erect. Hyperextension or flexion of thte neck may cause tension on the suture line and bleeding. 2. Monitor surgical site for bleeding and edema. Check dressing anteriorly and at the back of the neck. Respiratory distress may indicate bleeding. Accumulation of blood in the neck may compress airways 3. Have tracheostomy set, oxygen and suction available at bedside. Inadvertent parathyroid damage leads to hypocalcemia. Hypocalcemia may cause laryngospasm that results to airway obstruction. 4. Assess for recurrent laryngeal nerve damage - Ask client to speak every hour - Limit client talking and assess for level of hoarseness. Mild hoarseness is normal. This is due to intubation during induction of anesthesia. Severe hoarseness indicates laryngeal nerve damage. Notify the physician - Observe for other signs and recurrent laryngeal nerve damage like respiratory obstruction, dysphonia, high-pitched voice, stridor, dysphagia and restlessness 5. Monitor for signs of hypocalcemia and tetany. This may be due to trauma to parathyroid. - Keep calcium gluconate readily available, for tetany - Monitor blood pressure. To assess for positive trousseaus sign (carpal spasm) which indicates hypocalcemia. (Compression of the brachial artery with BP cuff for 3 mins is done to assess for trousseaus sign) - The other signs of tetany are as follows; a. Cardiac dysrhythmias b. Dysphagia c. Muscle and abdominal cramps d. Numbness and tingling of the face and extremities e. + Chvosteks sign f. Seizures g. Photophobia h. Wheezing and dyspnea (spasms of the airways) 6. Monitor for thyroid storm. - Thyroid storm is uncontrolled and potentially life threatening hyperthyroidism - It can occur from release of thyroid hormone into the bloodstream during surgery; It can also follow severe infection and stress - The clinical manifestations of thyroid storm are as follows: a. Hyperthermia (elevated temperature) b. Tachycardia, dysrhythmias c. Systolic hypertension d. GI manifestations: N&V, and diarrhea e. Restlessness, agitation, irritability, anxiety, tremors, confusion, seizures f. Delirium and coma - The collaborative management of thyroid storm are as follows: a. Maintain patent airway and adequate ventilation (O2therapy) b. Administer antithyroid medications (PTU), lugols solution, propranolol, dexamethasone as prescribed c. Monitor VS, I&O, neurologic status, cardiovascular status every hour d. Implement measures to lower fever. Use cooling blanket

Administer acetaminophen as prescribed. Avoid ASA. Salicylates increase free thyroid hormone levels Maintain quiet, calm, cool, private environment until crisis is over

7. Patient teachings after thyroidectomy include the following:

- Support neck with interlaced fingers when getting up from bed to prevent hyperextension of the neck - Start range of motion exercises of the neck 3 to 4 days after discharge - Massage incision site with cocoa butter lotion, once healing occurs. To minimize scarring - Have regular follow-up case SUMMARY OF POTENTIAL COMPLICATIONS OF THYROIDECTOMY a. Hemorrhage b. Airway obstruction c. Tetany d. Recurrent laryngeal nerve damage e. thyroid crisis (Thyroid storm, thyrotoxicosis) f. Myxedema (hypothyroidism) Hypothyroidism Is deficiency of the thyroid hormones Myxedema is hypothyroidism in adults; cretinism in children

The causes of hypothyroidism are as follows: Autoimmune disorders (eg Hashimotos disease, an autoimmune disorder associated with recurrent respiratory infection) Thyroidectomy Radioactive iodine (I131) therapy Antithyroid drugs The clinical manifestations of hypothyroidism are based on three basicconcepts: Decreased body heat production (due to hyposecretion of T4) Hypercalcemia (due to hyposecretion of thyrocalcitonin) Hypercalcemia results to decreased cell membrane permeability. This leads to decreased neuromuscular irritability The clinical manifestations of hypothyroidism are as follows: Slowed physical, mental reactions Apathy, lethargy, fatigue Weakness, muscle aches, paresthesias Dull, expressionless, mask-like face Cold intolerance; subnormal body temperature Generalized puffiness and edema around the eyes and face Anorexia Obesity or weight gain Bradycardia Constipation Coarse, dry, sparse hair, loss of body hair Dry skin, brittle nails Cardiac enlargement, tendency to develop congestive heart failure Hyperlipidemia, atherosclerosis Forgetfulness, and loss of memory Slow speech; husky hoarse voice Enlarge tongue Increased sensitivity to sedatives, narcotic and anesthetics

Decreased metabolic rate (due to hyposecretion of T3)

BASIC CONCEPT TO REMEMBER IN HYPOTHYROIDISM: Everything is LOW, SLOW, and DRY Example: 1. LOW and SLOW: slowed physical and mental reactions, lethargy, low body temperature, bradycardia, slow metabolism 2. DRY: dry hair and skin, constipation (dry stool) The collaborative management for hypothyroidism are as follows: Monitor VS. Be alert for changes in heart rate and rhythm, which indicate cardiovascular disorders Monitor daily weights Diet: low calorie, low cholesterol, low saturated fat diet. To prevent obesity and hyperlipidemia Assess the client for constipation. Provide high fiber/roughage and fluids to prevent constipation Administer thyroid replacement therapy: Synthroid, Levothroid, Levoxyl (Levothyroxine) Cytomel (Liothyronine) Thyrolar (Liotrix) Thycar (Thyroid) Nursing interventions in Thyroid Replacement Therapy

Monitor VS, especially BP and pulse rate. Hold medication for high blood pressure and tachycardia. Notify the physician.

Monitor weight. Reduction in weight is desired Instruct client to take the medication in the morning without food. To ensure absorption of the medication Instruct client to avoid foods that inhibit thyroid secretion such as strawberries, peaches, pears, cabbage, turnips, spinach, Brussel sprouts, cauliflower, radishes, and peas Start with low dose, then gradually increase as prescribed by the physician. To prevent hyperthyroidism Advise client to report signs of hyperthyroidism like tachycardia, chest pain, palpitations and excessive sweating Thyroid hormones have the following drug interactions:

Enhance the action of anticoagulants, sympathomimetics and anti depressants Decrease the action of insulin, oral hypoglycemic agents and digitalis Action of thyroid hormones should be given at least four hours apart from multi vitamins, antacids, bile acid sequestrants, iron and Carafate. These drugs decrease the absorption of thyroid replacement. Myxedema Coma Is extreme, severe stage of hypothyroidism Can be precipitated by acute illness, rapid withdrawal of thyroid hormones, anesthesia, surgery, hypothermia, or use of sedatives and narcotics The clinical manifestations of myxedema coma are as follows: Hypotension Bradycardia Hypothermia Hypoglycemia Hyponatremia Respiratory failure Coma

In myxedema coma, all vital signs are profoundly depressed. It is potentially fatal The collaborative management for myxedema coma are as follows: Maintain patent airway Administer IV fluids and Synthroid/IV as prescribed Administer glucose/IV as ordered Monitor clients temperature. Correct hypothermia. Keep client warm Monitor BP. Manage hypotension Monitor for changes in LOC Monitor for electrolytes and glucose levels. Correct hyponatremia and hypoglycemia

DISORDERS OF THE PARATHYROID GLAND Hypoparathyroidism Is hyposecretion of parathormone

Hypoparathyroidism can occur following thyroidectomy because of removal of parathyroid tissue The clinical manifestations of hypoparathyroidism are as follows: Hypocalcemia and hyperphosphatemia. Hypocalcemia increases neuromuscular excitability Signs of tetany: Cardiac dysrhythmias Carpopedal spasms Dysphagia Muscle and abdominal cramps Numbness and tingling of the face and extremities Positive Chvosteks sign Positive trousseaus sign Seizures Visual disturbances (photophobia) Wheezing and dyspnea (bronchospasm, laryngospasm) Hypotension Anxiety, irritability, depression The collaborative management for hypoparathyroidism are as follows: Monitor VS. Notify physician for hypotension Monitor for signs of hypocalcemia and tetany Place client on seizure precaution Have tracheostomy set, oxygen, and suction available at bedside. These are emergency equipments to be used for spasm of airway Administer calcium gluconate/IV for hypocalcemia Diet: High calcium, low phosphorus diet Administer phosphate-binder (amphogel) as prescribed. To lower phosphorus level and increase serum calcium level Administer calcium supplement and vitamin D as prescribed. Vitamin D enhances calcium absorption from the GI tract. CALCIUM SUPPLEMENTS:

Calcium carbonate (BioCal, Caltrate 600, Rolaids, Tums) Calcium carbonate-oyster-shell derived (OsCal 500, Oysco, Oystcal) Calcium citrate (Citracal) Calcium glubionate (Calcionate, Neo-Calglucon) Calcium gluconate Calcium lactate Dibasic calcium phosphate Tribasic calcium phosphate

VITAMIN D SUPPLEMENTS: Calciferol (Calderol) Calcitriol (Calcijex, Rocatrol) Dihydrotachysterol (DHT, Hytakerol) Ergocalciferol (Calciferol, Drisdrol) CALCIUM REGULATORS Alendronate (Fosamax) Calcitonin human (Cibacalcin) Calcitonin salmon (Calcimar, Miacalcin) Etidronate (Didronel) Pamidronate (Aredia) Pisedronate (Actonel) Tiludronate (Skelid) * Calcium salts with Digoxin INCREASE RISK of DIGOXIN TOXICITY * Oral calcium salts reduce absorption of Tetracycline HCL * Calcium regulators (e.g. Foramax) should not be chewed. These should be taken with water at least 30 mins before breakfast and to remain upright for at least 30 minutes. This is to prevent gastoesophageal reflux Hyperparathyroidism Is hypersecretion of parathormone (PTH) This results to high serum calcium levels and bone deminarilization The clinical manifestations of hyperparathyroidism are as follows:

Hypercalcemia and hypophosphatemia. Hypercalcemia decreases neuromuscular excitability Fatigue and muscle weakness Skeletal pain and tenderness Bone deformities that result in pathological fractures Anorexia, nausea, vomiting, epigastric pain Weight loss Constipation Hypertension Cardiac dysrhythmias Renal stone

The collaborative management for hyperparathyroidism are as follows: Monitor VS, particularly the BP. Hypertension may occur Monitor for cardiac dysrhythmias Monitor for urine output. Polyuria causes dehydration Monitor signs of renal stones (calcium stones) Move client slowly and carefully. He may experience skeletal pain and he is at risk to develop fracture Increase fluid intake. To prevent dehydration and renal stone formation Administer Lasix (Furosemide) as prescribed to lower serum calcium levels Administer normal saline/IV as prescribed to maintain hydration. Sodium enhances secretion of calcium Administer calcitonin (Calcimar) as prescribed to decrease skeletal calcium release and increase renal clearance of calcium Administer antihypercalcemic as prescribed. Gallium nitrate(Ganite) Administer phosphates as prescribed Monitor calcium and phosphorus levels Parathyroidectomy o Removal of one or more of the parathyroid glands o Postoperative care a. Monitor for respiratory distress b. Have tracheostomy set, oxygen, and suction at bedside c. Monitor vital signs d. Position: semi-fowlers e. Monitor for bleeding f. Monitor for hypocalcemic crisis (s/sx of tetany) g. Administer calcium supplement and vitamin D as prescribed

DISORDERS OF THE PANCREAS Diabetes Mellitus Is a chronic disorder of carbohydrate, fat, and protein metabolism It is due to inadequate insulin production or increase resistance to insulin The cause of DM is unknown The predisposing factors to DM are as follows: a. STRESS. It stimulates secretion of epinephrine, norepinephrine and glucocorticoids. These hormones elevate blood glucose levels by glycogenolysis and gluconeogenesis b. HEREDITY. It is strongly associated with type II DM c. OBESITY. Adipose tissue are resistant to insulin. Therefore glucose uptake by the cells is poor d. VIRAL INFECTIONS. Increase risk to autoimmune disorders that may affect the pancreas e. AUTOIMMUNE DISORDERS. It is more associated with type I DM. This is because it is the children who are more prone to viral infections f. WOMEN, who are multigravida with large babies. During pregnancy, hman placental lactogen (HPL) is produced. HPL antagonizes insulin thus, hyperglycemia occurs during pregnancy TYPE I DIABETES MELLITUS Also called Insulin Dependent Diabetes Mellitus (IDDM), juvenile onset, brittle or unstable DM Onset is before 30 years of age Absolute deficiency of insulin is due to absence of Islets of Langerhans in the pancreas The client is thin. This is due to the inability of the body to obtain glucose from carbohydrates. Therefore the body breaks down fats and protein for glucose supply The client is prone to diabetic ketoacidosis (DKA). In the absence of insulin, fats are metabolized. There is increased production of ketones, resulting in ketoacidosis

The collaborative management for IDDM include: o Diet o Activity and exercise o Insulin (always as a component of management for IDDM)

TYPE II DIABETES MELLITUS Also called Non-Insulin Dependent Diabetes Mellitus (NIDDM), maturity onset, ketosis-resistant DM Onset is after age 30 years old With relative lack of insulin or resistance to the action of insulin, usually insulin is sufficient to stabilize fat and protein metabolism but not to deal with carbohydrate metabolism The client is obese The client is prone to hyperglycemic, hyperosmolar, non-ketotic coma (HHNC). This is extreme hyperglycemia without acidosis. It may result in dehydration and vascular collapse The collaborative management for NIDDM include: o Diet o Activity and exercise o Oral hypoglycemic agents (OHA) or injectable hypoglycemic agents (IHA). If hypoglycemia is uncontrolled o Insulin. In case of stresss, surgery, infections, and pregnancy. These conditions trigger stress responses and stimulate secretion of epinephrine, norepinephrine and glucocorticoids. These hormones cause hyperglycemia A deficiency in insulin results in hyperglycemia The clinical manifestations of DM are as follows: a. Polyuria, Polydipsia, Polyphagia (3 Ps), more common in type I DM b. Weight loss. More common in type I DM c. Blurred vision d. Slow wound healing e. infections: pyorrhea (periodontal infections), urinary tract infection, vasculitis, cellulitis, furuncles, carbuncles, vaginal infections f. Weakness and paresthesia g. Signs of inadequate circulation to the feet h. Signs of accelerated atherosclerosis (renal, cerebral, cardiac, peripheral) Macrovascular complications include coronary artery disease, cardiomyopathy, hypertension, cerebrovascular disease, peripheral vascular disease and infection Microvascular complications include retinopathy and neuropathy The collaborative management for DM are as follows: DIET Low calorie diet especially if the client is obese The diet should consist of 20% protein, 30% fats and 50% carbohydrates

High fiber diet especially vegetables. Fiber inhibits glucose absorption in the intestines and prevents hyperglycemia. Fruit exchanges may be eaten, according to the dietary exchange list. The diabetic client should not eat as much fruits as he wants. Fruits contain fructose that is converted into glucose. Therefore eating too much fruits may cause hyperglycemia Complex carbohydrates like rice, bread, pasta, root crops are preferred. Simple carbohydrates like cakes, pastries are more likely to cause hyperglycemia

ACTIVITY AND EXERCISE The benefits of regular pattern of exercise are as follows: 1. Exercise increases glucose uptake by the cells. Therefore, it lower blood glucose levels 2. Exercise lowers insulin requirements 3. Exercise helps achieve desirable body weight 4. Exercise helps maintain normal serum lipids. This reduces vascular risks Instruct client on dietary adjustments when exercising Instruct client to monitor blood glucose before, during, and after exercise period Initially the client who requires insulin should be instructed to eat 15g carbohydrate snack (a fruit exchange or a snack of complex carbohydrate with protein) before engaging in moderate exercise to prevent hypoglycemia If blood glucose level is greater than 250mg/dl and urinary ketones are present (DM type I), the client is instructed not to exercise until blood glucose is normal and urinary ketones are absent MEDICATIONS o Oral Hypoglycemic agents o Stimulate Islet of Langerhans to secrete insulin, increase sensitivity of peripheral receptors to insulin, decrease hepatic glucose output or delay absorption of glucose, thus decreasing serum glucose levels o Indicated only in type II DM o Drug interactions and contraindications of OHA 1. Aspirin, alcohol, sulfonamides, contraceptives, and monoamine oxidase inhibitors (MAOIs) increase the hypoglycemic effect, causing a decrease in blood glucose levels (hypoglycemia) 2. Glucocortocoids, thiazide diuretics, and estrogen increase blood glucose levels (hyperglycemia) 3. Sulfonylureas should not be taken with alcohol. To prevent DISULFERAM-LIKE REACTIONS 4. Inderal (Propanolol) and other beta-adrenergic blockers may cause hypoglycemia 5. Sulfonylureas may cause cardiac dysrhythmias. 6. Sulfonylureas may cause GI symptoms. Hypoglycemia may occur Dymelor (Acetohexamide) Diabenese (Chlorpropamide) Amaryl (Glimepiride) Glucotrol (Glipizide) Diabeta, Micronase (Glyburide) Tolinase (Tolazamide) Orinase (Tolbutamide) Alpha Glucosidase Inhibitors a. Precose (Acarbose) b. Glyset (Miglitol) Biguanide a. Metformin (Glucophage) Meglitinide a. Starlix (Nateglinide) b. Prandin (Repaglinide) Thiozolidinediones a. Actos (Pioglitazone) b. Avandia (Rosiglitazone)

SULFONYLUREAS o o o o o o o NON-SULFONYLUREAS o

o
o o o o

o Insulin Indicated in type I DM Indicated in type II DM when diet and weight control are ineffective to maintain blood glucose levels Regular insulin is the only insulin that can be administered intravenously in the emergency treatment of diabetic ketoacidosis Aspirin, alcohol, oral anticoagulants, oral hypoglycemic drugs, beta adrenergic blockers, tricyclic antidepressants, tetracycline, and MAOIs increase the hypoglycemic effects of insulin, causing hypoglycemia Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives and estrogen may cause hyperglycemia Illness, infection, and stresss can elevate blood glucose levels and the need for insulin. Insulin should not be withheld during illness, infection, or stress because hyperglycemia and ketoacidosis can result

1.Very-Rapid acting or Rapid-acting Insulin A. Humalog (Lispro) B. Novolog (Insulin Aspart) 2.Short-acting Insulin A. Regular: Humulin R Novolin R 3. Intermediate-acting Insulin A. NPH (Humulin N; Novolin N) B. Lente (HumulinL;Novolin L) 4. Long-acting Insulin A. Ultralente (Humulin U) B. Insulin Glargine (Lantus) 5. Premixed Insulin A. Humulin 70/30 (70% NPH/ 30% Regular) B. Humulin 50/50 (50% NPH/ 50% Regular) C. Lispo/Protamine 75/25 (75% Lispro/ 25% Protamine)

The peak of action time of insulin is important because of the possibility of hypoglycemic reactions occurring that time. o The common type of insulin are as follows: ONSET PEAK DURATION o 15 mins 5-10 mins -1 hrs 1-3 hrs 4-5 hrs 3-5 hrs

-1 hr

2-4 hrs

5-7 hrs

1-2 hrs 1-3 hrs

6-14 hrs 6-14 hrs

24 hrs 24 hrs

6 hrs _

18-24 hrs _

24 hrs 24 hours

-1 hr hr 10-15 mins

2-12 hrs 3-5 hrs 5 hrs

18-24 hrs 24 hrs 24 hrs

Nursing interventions of Insulin Therapy 1. The main route of insulin injection is subcutaneous. This promotes slower absorption and is less painful. There are lesser blood vessels and nerves in the subcutaneous areas 2. The main areas for insulin injections are abdomen, arms, (posterior surface), thighs (anterior surface), and buttocks 3. Administer insulin at 90 degrees. Most insulin syringes have needle gauge 27-29, that is about inch long 4. Do not massage injection site to prevent rapid absorption. Rapid absorption of insulin may cause hypoglycemia 5. Injections should be half inch apart within the anatomical area. Finish all sites in one anatomical area before going to another area 6. To prevent lipodystrophy (hard fatty masses in the subcutaneous layers): a. Systematic rotation of the site of injection. Reuse one site after at least 2-3 weeks b. Administer insulin at room temperature. Cold insulin causes lipodystrophy. (Lipodystrophy inhibits insulin absorption) 7. Gently roll vial in between the palms to redistribute insulin particles. Do not shake the vial, bubbles make it difficult to aspirate exact amount 8. Storing Insulin: a. Prefilled insulin syringes should be kept in the refrigerator. These will be potent for 7 days (1 week). The syringes should be kept flat or with the needle in an upright position to prevent clogging of the needle. b. If a vial of insulin will be used for 30 days (1 month), it may be kept at room temperature. Otherwise the vial should be refrigerated c. Avoid exposing insulin to extremes of temperature d. Insulin should not be frozen or kept in direct sunlight or a hot car 9. Regular insulin may be mixed with any other type of insulin 10. Insulin zinc suspensions (intermediate-acting) may be mixed only with each other and regular insulin; not with other types of insulin

11. To mix insulin, the following nursing actions are done: a. Introduce air into the vial of intermediate-acting insulin (e.g. NPH). Do not aspirate/draw up the insulin b. Introduce air into the vial of regular insulin, and draw up the insulin c. Draw up the intermediate-acting insulin (NPH) NOTE: REMEMBER TO DRAW UP THE REGULAR INSULIN FIRST 12. Administer a mixed dose of insulin within 5 to 15 minutes of preparation; after this time the regular insulin binds with NPH insulin and its action is reduced 13.Avoid exposing insulin to extremes in temperature. Insulin should not be frozen or kept in direct sunlight or a hot car. If insulinbecomes frozen, discard it 14. Monitor client for complications of insulin therapy: a. Local allergic reactions - Redness, swelling, tenderness and induration or a wheal at the site of injection may occur 1to 2 hours after administration - Instruct the client to avoid the use of alcohol to cleanse the skin before injection - Administer antihistamine one hour before injection as prescribed by the physician b. Insulin lipodystrophy - Lipoatrophy is loss of subcutaneous fat and appears as slight dimpling or more serious pitting of subcutaneous fat; the use of human insulin helps to prevent this complication - Lipohypertrophy is the development of fibrous fatty masses at the injection site and is caused by repeated use of an injection site - Instruct the client to avoid injecting insulin into affected sites - Instruct the client about the importance of rotating insulin injection sites - Instruct the client to inject insulin at room temperature; not at room temperature c. Insulin resistance - Lack of tissue sensitivity to the insulin from the body, which results in hyperglycemia - The client receiving insulin develops immune antibodies that bind with insulin, thereby decreasing the insulin available for use in the body - This condition may be managed by administering a purer insulin preparation d. Dawn phenomenon - Results from the reduced tissue sensitivity to insulin that develops between 5 and 8 am(prebreakfast hyperglycemia). This may be associated with nocturnal release of growth hormone - Treatment is administering intermediate-acting insulin (NPH) at 10pm to control early morning hyperglycemia e. Somogyi phenomenon - Normal or elevated blood glucose levels are present at bedtime; hypoglycemia occurs at 2 to 3 am, which triggers production of counter regulatory hormones (Epiniphrine, Norepiniphrine, glucocorticoid) - By 7 am, in response to the counter regulatory hormones, the blood glucose rebounds to hyperglycemic range (rebound hyperglycemia). - Treatment for Somogyi phenomenon includes decreasing the evening (pre dinner or bedtime) dose of intermediate-or long acting insulin before the evening meal if one is aleady prescribed

Acute Complications of Diabetes Mellitus HYPOGLYCEMIA o Occurs when blood glucose falls below 60 mg/dl o Causes of hypoglycemia are as follows: Overdose of insulin or oral hypoglycemic agents Omissions of meals or too little food Strenuous exercise or excessive activity o o

Gastrointestinal upset (e.g. nausea and vomiting, diarrhea) The client should be instructed to always carry some form of fast acting simple carbohydrates. The clinical manifestations for hypoglycemia are as follows: Mild hypoglycemia: blood glucose level less than 60mg/dL.
Hunger Nervousness Palpitation Sweating Tachycardia Tremors Moderate hypoglycemia: blood glucose level less than 40 mg/dL Confusion Double vision Drowsiness Emotional changes Headache

 Emotional changes Headache Impaired coordination Inability to concentrate Irrational or combative behavior Light-headedness Memory lapses Numbness of the lips and tongue Slurred speech Severe hypoglycemia: blood glucose level less than 20 mg/dL Inability to swallow Loss of consciousness Seizures The collaborative management for hypoglycemia are as follows: Mild hypoglycemia Give 10 15 g of fast acting simple carbohydrates Commercially prepared glucose tablets 6-7 life savers or hard candy 4 tsp. of sugar 4 sugar cubes 1 tbs of honey or sugar o

1/2 cup of fruit juice or regular softdrinks

8 oz low-fat milk 6 saltine crackers 3 graham crackers Retest the blood glucose level in 15 minutes, repeat the treatment if symptoms do not resolve. Once symptoms resolve, give 2 slices of white bread (sandwich) or crackers, then a cup of skim milk or cheese or provide a regular meal within 60 minutes Moderate hypoglycemia Give 15-30 g of fast acting simple sugar carbohydrates Give additional food such as low-fat milk or cheese after 10-15 minutes. Severe hypoglycemia If unconscious or unable to swallow, an injection of glucagon is administered subcutaneously or intramuscularly or intravenously. Administer a second dose if the client remain unconscious A small meal is given to the client when he awakens as long as he is not nauseated. Notify the physician if severe hypoglycemic reaction occurs Administer 50%dextrose in water, 25-50 ml per IV as prescribed Glucagon is used to treat insulin induced hypoglycemia when the client is semi-conscious or unconscious and is unable to ingest liquids.

DIABETIC KETOACIDOSIS (DKA) o Is a life-threatening complication of Type 1 DM. this is due to severe insulin deficiency o Causes of DKA are as follows: Under dose or missed dose of insulin Illness or infection Overeating Stress, surgery Undiagnosed and untreated type I Dm o The clinical manifestations of DKA are based on the following concepts: Hyperglycemia Dehydration Acidosis Blood glucose level ranges from 300-800 mg/dL Low serum bicarbonate and a low pH are present o The clinical manifestations of DKA are as follows: Acetone breath (fruity odor) Anorexia, nausea, vomiting, abdominal pain Blurred vision Headache Hypotension Kussmauls respiration

Mental status changes Polydipsia Polyuria Weak, rapid pulse Weakness The collaborative management for DKA are as follows: Maintain patent airway Administer oxygen therapy as prescribed Treat dehydration with normal saline 0.9% or 0.45% rapid IV as prescribed D5NS or D50.45% Saline when the blood glucose level reaches 250 to 300 mg/dL. To prevent abrupt fall of blood glucose levels Treat hyperglycemia with regular insulin per IV as prescribed. A dose of 5-10 units of regular insulin by IV bolus may be prescribed followed by a continuous infusion. Mix prescribed IV dose of regular insulin for continuous infusion in 0.9% or 0.45% saline as prescribed. Small dose of albumin may be mixed with the insulin and saline solution to prevent adherence of insulin molecules to the plastic IV infusion sets Always use infusion pump[ for insulin infusion

Monitor potassium levels, glucose levels and urinary output and signs of increased intracranial pressure. If blood glucose severely drops too fast the brain can equilibrate, water is pulled from the blood to the cerebrospinal fluid and the brain. This causes cerebral edema and increased ICP. o Correct electrolytes imbalances (potassium level may be elevated as a result of acidosis and dehydration) o Serum potassium level will fall rapidly as dehydration and acidosis treated o Potassium replacement (e.g KCL, K-Rider) may require. Ensure adequate renal function (e.g. urine output of 30-60 ml/hr) before administering potassium. (If theres no adequate urine output, dont administer potassium supplement. To prevent renal damage) o The maximum amount of potassium chloride that may be mixed with 1 liter of IV fluid is 40 mEq o The maximum amount of potassium supplement that may be given per IV infusion is 10 mEq/hour o Always use IV infusion pump for potassium infusion HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME o Is severe hyperglycemia that occurs without ketosis and acidosis o The syndrome occurs in Type II diabetics o The clinical manifestations of HHNS are as follows: Blood glucose level from 600 to 2000 mg/dL Hypotension Dehydration Tachycardia Mental status changes Seizures o The collaborative management for HHNS are as follows: Treatment is similar to DKA: Fluid replacement Correction of electrolyte imbalances Insulin administration (although insulin plays a less critical role in the treatment of HHNS than it does for the treatment of DKA, because insulin is not needed for reversal or acidosis in HHNS) Chronic Complications of Diabetes Mellitus DIABETIC RETINOPATHY o Is chronic and progressive impairment of the retinal circulation that eventually causes hemorrhage o Permanent blindness can occur o The clinical manifestations of diabetic retinopathy are as follows: Rupture of microaneurysms in retinal blood vessels causes change in vision Blurred vision due to macular damage

Sudden loss of vision due to retinal detachment Cataract from lens opacity The collaborative management for diabetic retinopathy are as follows: Maintain safety Control hypertension and blood glucose levels Laser therapy to remove hemorrhagic tissue to decrease scarring Vitrectomy to remove vitreous hemorrhage and prevent retinal

detachment Cataract removal

DIABETIC NEPHROPATHY o Is progressive loss of kidney function o The clinical manifestations of diabetic nephropathy are as follows: Microalbuminuria Thirst Fatigue Anemia Weight loss, malnutrition Frequent urinary tract infection Signs of neurogenic bladder o The collaborative management for diabetic nephropathy are as follows: Control of hypertension and blood glucose levels Monitor VS, intake and output, serum BUN and creatinine, urine albumin levels Restrict dietary protein, sodium and potassium intake as needed. Prepare the client for dialysis, kidney transplant or pancreas transplant as prescribed DIABETIC NEUROPATHY o Is general deterioration of the nervous system throughout the body o Complications include: non-healing ulcers of the feet, gastroparesis, erectile dysfunction o The clinical manifestations of diabetic neuropathy are as follows: o The collaborative management for diabetic neuropathy are as follows: Control of hypertension and blood glucose levels Administer pain medications as prescribed Initiate bladder training program (for neurogenic bladder) Use of estrogen containing lubricant for dysparenuia Penile injection or implantable devices are prescribed. (Consider religious and cultural beliefs. May not be acceptable in some religions and cultures)

Foot

care to prevent trauma and prevent gangrene formation Inspect the feet daily Wash feet with warm water and mild soap. Pat dry the feet. Avoid foot soak. Wear comfortable, properly fitted pair of shoes (leather or canvass; although leather is more preferred). These materials follow the contour of the feet and prevent trauma. Do not wear open toed shoes or shoes with strap that goes between the toes Do not wear the same pair of shoes 2 days in a row Check shoes for cracks or tears in the lining and for foreign objects before putting them on. Break in a new pair of shoes for 1 to 2 hours only until it becomes comfortable Do not go barefooted Wear clean cotton socks daily. Cotton absorbs moisture and prevents impairment of skin integrity in the feet Trim toenails straight across of follow the curve/contour of the toe. Do not cut at lateral edges to prevent development of ingrown. Ingrown may cause trauma to the lateral edges of the toes. Smoothens nails with emery board. Do not cross legs or wear tight garments that may constrict blood flow For any signs and symptoms of injury to the feet, notify physician Avoid use of hot water, heating pads. There is diminished sensation in the lower extremities. Burns may occur unnoticed by the client Exercise and massage the feet. To improve circulations Do not smoke. To prevent vasoconstriction Avoid self-treatment of corns, blisters or ingrown toenails. Consults the podiatrist.

Disorders of the Adrenal Glands ADDISONS DISEASE (Adrenal Insufficiency) Is the hyposecretion of adrenal cortex hormones (glucocorticoids, mineralcorticoids and sex hormones) The causes of Addisons disease are as follows: autoimmune disorders, tuberculosis, fungal disease The clinical manifestations of Addisons disease are as follows: Fatigue, muscle weakness due to hyperkalemia Anorexia, N&V due to hypokalemia Weight loss, due to loss of sodium and water Hypotension, weak pulse due to dehydration Menstrual changes in women: impotence in men. These are due to hyposecretion of sex hormones Hyperkalemia due to decreased secretion of aldosterone

Bronze pigmentation of skin. Hyposecretion of adrenal cortex hormones triggers negative feedback mechanism. The anterior pituitary gland increases secretions of its hormones, which includes MSH (melanocytes stimulating hormone). This causes hyperpigmentation Emotional changes Decreases ability to cope with stress. The basic concept for signs and symptoms of Addisons disease:

Everything is LOW and SLOW except The collaborative managementPOTASSIUM. follows: for Addisons disease are as

Monitor VS, especially BP, weight and I&O. Monitor blood glucose and potassium levels Administer glucocorticoid or mineralocorticoid medications as prescribed: o Celestone (Betamethasone) o Cortone, Cortistan (Cortisone) o Decadron (Dexamethasone) o Florinef (Fludrocortisone) o Cortef (Hydrocortison) o Medrol, Depo-Medrol, Solu-Medrol (Methylprednisolone) o Delta-Cortef, Prelone, Oraped, Pediapred (Prednisone) Nursing interventions in Steroid Therapy (Hormonal replacement Therapy - HRT) Adrenocorticotropic Hormones Corticosteroids /Glucocorticoids Mineralocorticoids o Monitor VS. retention of sodium and water may cause elevation of BP o Monitor weight, I&O for edema o Avoid exposure to infection. Steroids may mask signs of infection and are immunosuppresants o Monitor potassium and calcium levels. Steroids may cause hypokalemia and hypocalcemia o Administer steroids after meals or with milk. Steroids stimulate gastric acid secretions and may cause gastric acid secretions and may cause gastric irritation and peptic ulcer disease o Monitor urine and blood glucose levels and urine ketones. Breakdown of fats and protein causes hyperglycemia and formation of ketones. o Diet of the client should be high protein, high carbohydrate, high potassium and low sodium diet. Steroids enhance metabolism. High protein and high carbohydrate diet provides nutritional support to prevent muscle wasting High potassium diet prevents hypokalemia Low sodium diet prevents hypokalemia o Monitor side effects of steroids Hyperglycemia Hypokalemia Hypocalcemia, osteoporosis Sodium and water retention, edema Hypertension Increased susceptibility to infection Mood swings Easy bruising, petechiae, ecchymosis Altered fat distribution Hirsutism, acne Gastric irritation (peptic Ulcer Disease) Cataract, glaucoma Growth retardation in children, headache Psychosis o Dose should be tapered and not stopped abruptly. Toprevent Addisonian Crisis, weakness, psychologic letdown o Contraindications of corticosteroid Corticosteroid are contraindicated in psychosis and fungal infection It should be used with caution in clients with DM. hyperglycemia may occur Dexamethasone decreases the effect of Coumadin and OHAs When used with ASA and NSAIDs increases risk of GI bleeding and ulcerations Use of potassium wasting diuretics increases potassium loss resulting to hypokalemia Barbiturates, phenytoin, rifampin decrease the effects of prednisone Phenytoin, theophylline, rifampin, barbiturates and antacids decreases the action of dexamethasone Corticosteroids mask the signs and symptoms of infection, so they should be used with caution in clients with infection. Advise client to wear Medic Alert bracelet Addisonian Crisis Is a life threatening disorder caused by acute adrenal insufficiency It is precipitated by stress, infection, trauma and surgery

It can be cause hyponatremia, hyperkalemia, hypoglycemia and shock The clinical manifestation are as follows: o Severe headache o Severe abdominal, leg and lower back pain o Generalized weakness o Irritability and confusion o Severe hypotension o shock The collaborative management are as follows: o Administer glucocorticoid per IV o Monitor VS especially BP o Monitor neurological status, noting, irritability and confusion o Monitor intake and output o Monitor serum sodium and potassium and blood glucose o Administer IV fluids as prescribed o Protect client from infection o Maintain bed rest and provide a quite environment

CUSHINGS SYNDROME It is caused by hypersection of adrenal cortex hormones It may caused by increased pituitary secretion of ACTH, pituitary adenoma or adrenal adenoma, prolonged steroid therapy The clinical manifestations of are as follows: Obsess trunk, thin arms and legs Moonface Buffalo humps Reddish-purple striae on trunk Generalized muscle wasting and weakness Easy bruising Hypertension Hyperglycemia Edema Hypokalemia Hypocalcemia, osteoporosis Mood swings, irritability Hirsutism, acne Low resistance to infection Poor wound healing The collaborative management are as follows: Monitor the following VS, especially BP for hypertension Intake and output and weight for edema Laboratory values, particularly the blood glucose, serum sodium, potassium and calcium Protect from trauma. To prevent bruising and fracture Allow the clinet to verbalize feelings related to altered body appearance Administer chemotherapeutic agents as prescribed Prepare the client for surgery: Adrenalectomy for adrenal gland tumor Hypophysectomy for pituitary tumor HYPERALDOSTERONISM (Conns Syndrome) Is hypersection of aldosterone from the adrenal cortex Most commonly caused by an adenoma The clinical manifestations are as follows: Hypertension, hypokalemia Headache, fatigue, muscle weakness, nocturia Polydipsia, polyuria Low urine specific gravity Hypernatremia The collaborative management are as follows

Monitor the client for the following VS particularly BP for hypertension Serum potassium for hypokalemia I&O and urine for specific gravity

Administer Spironolactone, a potassium sparring diuretics and aldosterone antagonist Administer antihypertensive as prescribed Prepare the client for adrenalectomy Instruct the client on glucocorticoid therapy following adrenalectomy Lifelong glucocorticoid replacement is necessary with a bilateral adrenalectomy

Temporary glucocorticoid replacement, up to 2 years is necessary for unilateral adrenalectomy. Critical to remember: AFTER ADRENALECTOMY Cathecolamine levels drop as a result of surgery, which can result in cardiovascular collapse, hypotension and shock. Monitor the client closely. Hemorrhage can occur because of the high vascularity of the adrenal glands

Disorder of the Adrenal Medulla PHEOCHROMOCYTOMA A tumor that originates from the adrenal medulla It is usually benign; 10% are malignant It stimulates hypersection of cathecholamines The laboratory test specifically supports presence of pheochromocytoma is Vanillylmandelic Acid Test (VMA Test) VMA is a metabolite of epinephrine It requires 24-hour urine specimen Foods and medications to be avoided that can alter the result: Coffee Tea Chocolate Banana Vanilla Aspirin The collaborative management are as follows: Monitor the client the client for the following: VS particularly BP and HR Hypertensive Crisis this may result to complications such as CVA, cardiac dysrhythmias and MI Blood glucose and urine for ketones

Promote bed test, elevate HOB during episode of hypertension, tachycardia and anxiety. To provide orthostatic decrease in BP Instruct client to avoid smoking, drinking caffeine containing beverages or changing position suddenly Administer alpha-adrenergic agent as prescribed to control hypertension Prepare the client for surgery: ADRENALECTOMY