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The ENDOCRINE SYSTEM

Anatomy and physiologic Overview
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Endocrines: Without ducts: Ductless glands. A group of glands all of which lack ducts or specific channels to release their secretions. All of them secrete or produce “Chemical Messengers” or Hormones. Hormones by definition bring metabolic changes in target tissues. The target tissues are usually far away from the endocrine glands.

WHY ENDOCRINE SYSTEM? 4 MOST IMPORTANT PURPOSES 1. HOMEOSTASIS.
2. COMBATING STRESS. 3. GROWTH & DEVELOPMENT. 4. REPRODUCTION.

ENDOCRINES ARE USEFUL FOR… 1. Metabolism Nutrition: Glucostasis Acid Base Balance . HOMEOSTASIS  Endocrines help us in maintaining the homeostasis of:     Temperature: Thermoregulation or thermostasis.

COMBATING STRESS  INFECTION TRAUMA SHOCK   .ENDOCRINES ARE USEFUL IN… 2.

ENDOCRINES ARE USEFUL FOR… 3. GROWTH & DEVELOPMENT  Increase in the cell number: Hyperplasia Increase in cell SIZE: Hypertrophy.  .

REPRODUCTION  The Male and female Gonads secrete:  Sex Hormones  These sex hormones cause the development of   Primary sex organs Secondary sexual characteristics.ENDOCRINES ARE USEFUL FOR… 4. .

 Natural chemicals that exert their effects on specific tissues known as target tissues  The mechanism for regulating hormone in the blood stream is called negative feedback  .HORMONES It is important in regulation of the internal environment of the body and effect every aspect of life.

Target Tissues  usually located some distance from endocrine glands with no direct physical connection between the endocrine glands and its target tissue .

6. 4. Pituitary glands Thyroid glands Parathyroid glands Pancreatic islets Ovaries Testes Adrenal glands . 2.Glands Of The Endocrine System 1. 7. 5. 3.

Calcitonin. GHIH. TSH. Thyroxin. & Oxytocin. ANTERIOR PITUITARY GLAND:  GH. ACTH. PIH. FSH. TRH.HORMONES PRODUCED IN THE BODY    HYPOTHALAMUS:  CRH. T3. ADH. GnRH. Prolactin. LH. POSTERIOR PITUITARY GLAND:   THYROID GLAND:  . GHRH.

 ADRENAL MEDULLA:  Epinephrine. Sex steroids. Glucagon. Dopamine. Cortisol.  ENDOCRINE PANCREAS:  . Insulin. Norepinephrine. Somatostatin. Pan polypeptide.HORMONES PRODUCED IN THE BODY  ADRENAL CORTEX:  Aldosterone.

Inhibin. Relaxin. Thymosin.HORMONES PRODUCED IN THE BODY     TESTES:     Testosterone. HPL. Melatonin OVARY: PLACENTA: THYMUS:  PINEAL GLAND:  . Estrogens. Progesterone. Estrogen. HCG. Estrogens. Progesterone.

Anxiety.HYPERSECRETION:  Excessive Production of hormones due to:   Tumors in the gland.  Results in:  Clinical syndromes with signs/symptoms due to:  Increased blood levels of the hormone    Example: Hyperthyroidism: Thyroxin levels Clinical features: Fine tremor. Excess tropic influence. BMR Acromegaly:  Growth Hormone. PR. .

Hypofunctioning of gland cells: Eg: Diabetes mellitus.HYPOSECRETION:  Drop in the production of hormones due to:    Excision of gland: Eg: Parathyroids. Decreased tropic influence. Clinical features/ syndromes due to  blood levels of the hormone  Results in:   .

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ENDOCRINE DISORDERS .

injury.Thyroid Hyperfunction Disorder    1. stress. occurs 8 times more frequently in females 2. Graves disease: immunological factors. excessive intake of thyroid medication. infection. increase in thyroid demand 3. surgery .Thyroid storm: Stress. infection. Goiter: inadequate intake of iodine. genetic predisposition.

Causes of Hyperthyroid Disorder     Auto immune response Neoplasm Excessive intake of thyroid medication Excess secretion of TSH from the anterior pituitary glands .

Production of thyroid hormone (TH) is dependent on adequate secretion of thyroid stimulating hormone (TSH) from the anterior pituitary gland. The hypothalamus regulates pituitary secretion of TSH by negative feedback .Pathophysiology THYROID HYPERFUNCTION DISORDERS  1.

Hyperthyroidism       Hyper function of the thyroid gland Leads to an excess of thyroid hormone in the body The presence of excess TH leads to hyper metabolic state Which causes increase in metabolic function Increase in oxygen consumption by tissue. And heat production .

Graves’ Disease    The most common cause of hyperthyroidism. it is considered an autoimmune disorder to stimulation of the thyroid gland from a long acting thyroid stimulator (LATS) The result in an excess production of TH. is seen most often in woman under age of 40. The exact cause is unknown. Which leads to hypermetabolic state .

excess –growth stimulating immunoglobulins.GOITER     It is describes the enlargement or hypertropy of the thyroid gland in attempt to compensate for inadequate TH It may be present in hyperthyroidism or hypothyroidism Goiter may be result of response to excess TSH stimulation. or presence of substance that inhibit thyroid hormone synthesis The goiter may become enlarge that compress the neck and chest .

Toxic Multinodular Goiter


It exist when small, independently functioning nodules in the thyroid gland tissue are present and secrete TH hormone The nodule may be benign or malignant The manifestation developed more slowly than graves’ disease. Toxic goiter is most often seen in woman age 60 or older who had goiter for several years.

Thyroid Storm

Also known as thyroid crisis or thyrotoxicosis It is life threatening condition which describes an extreme state of hyperthyroidism The presence of excessive TH causes a rapid increase in metabolic rate Immediate treatment is necessary to avoid death

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bowel/GI complaints. development of seizures. nutritional assessment. cardiac monitor for rhythm changes. respiratory status . symptoms of pain. changes in VS. neurological. presence of goiter. eyes. sign of congestive heart failure. muscle strength and appearance. reproductive history. integument assessment.Nursing assessment for Hyperthyroidism   1. vital sign. fluid status 2. Assessment findings for thyroid storm include elevated temperature. complaints of GI distress. weight.

Nursing management for Hyperthyroidism 1. Methimazole (Tapazole)  2. Lugol’s Solution (iodine) to decrease vascularity and size of thyroid E. Propylthioracil (PTU. Glucocorticoids: interfere with conversion of T3 and T4 D. Propanolol (Inderal) to treat dysrhythmias C. Antithyroid medication to reduce TH production  1. Propyl-Thracil) B. Medication A. Antipyretic if needed .

Instruct to take medication as prescribe and not abruptly discontinue medication b. Educate about the signs of hypothyroidism. which may occur if to much medicine is taken or dose needs adjusting .Nursing management for Hyperthyroidism Educate the client that it may take several weeks before the therapeutic effects of antithyroid medications are noticed a.

since it will not change even after medication have been started. Monitor for cardiac dysthythmias 4.Nursing management for hyperthyroidisn     3.Implement antipyretic measures 5. Teach eye care and monitor for vision changes if exophthalmos occurs. Elevate head of the bed to decrease eye pressure 6. .

Keep the environment cool and quiet because of the symptoms .Nursing management for hyperthyroidism     7.000 calories a day during hypermetabolic state 8. Monitor dietary intake: Client may require up to 4. Monitor intake and output 9. Monitor weight 10.000 to 5.

Does not require hospitalization or radiation precaution C. Radioactive therapy may be recommended to destroy thyroid cells in order to reduce production of TH A.Nursing management for Hyperthyroidism 11. expect result in 6 to 8 weeks B. Give radioactive iodine orally. Contraindicated in pregnant woman D. Monitor for sign and symptoms of hyperthyroidism .

Preoperative care include administering antithyroid medications to promote euthyroid state. Teach the client how to support the neck to reduce strain in the suture line . educate for strict compliance with medication regimen  C. Preoperative and postoperative care for surgical intervention to remove all or part of the thyroid (thyroidectomy)  A.Nursing management for Hyperthyroidism 12. For total thyroidectomy life long thyroid hormone replacement is necessary. and iodine preparation to decrease vascularity of the glands. subtotal thyroidectomy leaves part of the thyroid gland intact in order to produce adequate amounts of TH  B.

Nursing management for hyperthyroidism   Post operative care includes monitoring for complication of hemorrhage. respiratory distress. risk for injury . hyperthermia. Priority nursing diagnosis for thyroid hyperfunction disorders: Activity intolerance. and tetany 13. laryngeal nerve damage. altered nutrition.

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Thyroid Hypofunction Disorder
A.
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Overview Hypofunction of the thyroid glands leads to an insufficient amount of thyroid hormone (TH), a condition known as hypothyroidism Decrease TH result in a hypometabolic state manifested by a decrease in metabolic function, a decrease in oxygen consumption by tissue, and decrease in heat production

Thyroid hypofunction Disorder
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Hypothyroidism Myxedema Myxedema coma

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MYXEDEMA HYPOTHYROIDISM .

or thyroiditis B. Causes of primary hypothyroidism include congenital defects.Classified as primary and secondary A. loss of thyroid tissue from surgery or radiation. antithyroid medication. Causes of secondary hyperthyroidism include peripheral resistance to TH or pituitary TSH deficiency . endemic iodine deficiency.

Hypothyroidism describe an insufficient amount of TH which leads to a decrease in metabolic rate. Accumulation of proteins in the interstitial space result in an increase of interstitial fluid. Myxedema describes a generalized hypometabolic state occurring with untreated hypothyroidism A. This non-pitting edema is most commonly found in the pretibial and facial area . (myxedema) B.Pathophysiology 1. causing mucinous edema. manifestation developed slowly over months or years 2.

hypoglycemia. infection. Characterized by severe metabolic state: lactic acid acidosis. hypoventilation. bradycardia. it is life threatening condition A. trauma. Precipitated by inadequate thyroid replacement. exposure to cold temperature. CNS depressant .Pathophysiology of Myxedema coma     Also known as hypothyroid crisis It is the result of extreme or prolonged hypothyroidism. coma B. cardiovascular collapse. hyponatremia. hypothermia. hypotension. though rare.

In US .Pathophysiology Iodine deficiency: iodine is necessary for TH synthesis and secretion A. and lithium or iodine intake B. Iodine deficiency occurs as a result of antithyroid drugs. thyroid deficiency because of in adequate iodine intake is rare with the use of iodized salt .

Myxedema Coma Signs and symptoms:  Hypothermia  Cardiovascular collapse  Coma  Hyponatremia  Hypoglycemia  Lactic acidosis .

and other assessment performed for hypothyroidism . Assessment of hypothyroidism include neurological assessment. weight. 2. activity tolerance. fluid status. reproductive history. respiratory status Assessment in myxedema coma include cardiac assessment. presence of periorbital edema. presence of goiter.Nursing Assessment 1.

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Priority nursing diagnosis for thyroid hypofunction disorder

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Activity intolerance Altered nutrition Decrease Cardiac output Hypothermia Risk for skin integrity Risk for injury

Parathyroid disorder
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The parathyroid glands are located posterior to the thyroid glands Their major function is to maintain normal serum calcium levels by secreting TH, which increases bone reabsorption of calcium PTH respond to decrease calcium levels by increasing calcium absorption from bone, kidneys, and intestine

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which leads to hypercalcemia. bone damage. hyperposphatemia.Hyperparathyroidism  It is an Increase in PTH. and renal damage .

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heart rhythm. complain of pain. Includes neurological assessment including LOC. weight . I and O . VS . GI assessment. muscle strength.Nursing assessment for Hyperparathyroidism 1.

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Hypoparathyroidism   It is a decrease in PTH. and altered sensorium The most common cause of hypoparathyroidism is damage or removal of the parathyroid gland during surgery . hyperreflexia. Which leads to hypocalcemia.

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Nursing Assessment for hypoparathyroidism .

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NURSING MANAGEMENT .

Priority nursing diagnosis for parathyroid disorder     Impaired physical mobility Risk for injury Altered urinary elimination Altered nutrition .

Overview The adrenal glands are located superior to each kidney and composed of the adrenal medulla (the inner layer of adrenal gland) and the adrenal cortex (the outer layer of adrenal gland The adrenal medulla secretes the catecholomines: epinephrine. androgen. andestrogens (sex hormone) . norepinephrine and dopamine The adrenal cortex secretes mineralcorticoids (aldosterone). 1.Adrenal Cortex Hyperfunction Disorder A. glucocorticoids (cortisol. a. b.

enhancing protein synthesis. The function of epinephrine and norepinephrine (catecholamines) include increasing metabolic rate. fat’ and protein metabolism. and increasing breakdown of protein and fatty acid . increasing alertness. suppression of inflammation. increasing serum glucose by acting as insulin antagonist. increasing insulin levels and the “fight or flight response 3. it regulates CHO. The functions of glucocorticoids (cortisol) includes assisting the body’s response to stress.ADRENAL CORTEX HYPERFUNCTION DISORDER 2.

Androgens and estrogens contribute to growth and development . The function mineralcorticoids (aldosterone) includes sodium (Na) and water retention and potassium excretion 6. The function of adrenocorticotropic hormone is for growth and development 5.Functions 4.

Conn’s Syndrome or Hyperaldosteronism result in excess production of aldosterone .ADRENAL CORTEX HYPERFUNCTION DISORDER   Cushing’s Syndrome or hypercortisolism result in excess production of cortisol (glucocorticoids).

Cause of Hypercortisolism ( Cushing’s syndrome)    Include Adrenal tumors Adrenal hyperplasia Or exogenous glucocorticoids .

cirrhosis of liver. renal disease . dehydration.Causes of hyperaldosteronism ( conn’s syndrome)   Include adrenal lesion Or condition that stimulate overproduction of aldosterone: heart failure.

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CUSHING’S SYNDROME .

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maintaining serum glucose levels. The functions of glucocorticoids (cortisol. and augmenting release of catelectomines to increase blood pressure . ACTH) include promoting gluconeogenesis.Pathophysiology of Hypercortisolism A. adaptation to stress.

S/S of Hypersecretion of cortisol .

I and O .Nursing management for Cushing’s Syndrome       Includes vital sign: increase BP/ arrhythmias Neurological assessment History of GI. and reproductive problem Muscle strength Integument assessment Weight . renal. presence of edema.

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Nursing management for Cushing’s syndrome

Nursing management for Cushing’s syndrome

Nursing management for Cushing’s syndrome
B. Preoperative and postoperative care is for adrenalectomy if performed C. Assist in monitoring effects of radiation if performed D. Monitor for addisonian crisis cause by drug therapy

Priority Nursing diagnosis for Cushing’s Syndrome       Fluid volume in excess Risk for infection Activity intolerance anxiety Knowledge deficit Risk for impaired skin integrity .

CONN’S SYNDROME/ HYPERALDOSTERONISM .

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. cirrhosis of liver. renal disease. dehydration.Causes of Conn’s Syndrome or Hyperaldosteronism   Adrenal lesion Any condition that stimulates overproduction of aldosterone: heart failure.

Pathophysiology of Conn’s syndrome a. b. Role of aldosterone ( a mineralcorticoid) is soduim and water retention Aldosterone affects tubular reabsorption of sodium and water also has role in excretion of potassium and hydrogen ions .

polyuria Muscle weakness. tetany Electrolyte and acid-base imbalance . renal damage.S/S for Conn’s Syndrome        In secondary hyperaldosteronism hypertension is uncommon Visual disturbance Paresthesia Dysarrythmias Fluid retention.

Nursing management for Conn’s Syndrome a. Administer glucocorticoids preoperatively as prescribed to prevent adrenal hyperfunction . Spironolactone (aldactone) to treat hypertension and hypokalemia for clients who will not treat surgically 2. Amiloride (midamor) for those clients unable to tolerate aldactone 3. Medication 1.

Nursing management for Conn’s Syndrome B. Urine output. If bilateral adrenalectomy is performed. life time replacement of glucocorticoid is necessary D. Low sodium diet F Teach side effects of medications . electrolytes E. Preoperative and postoperative care for adrenalectomy C. Monitor BP.

Priority nursing diagnosis for Conn’s syndrome    Altered urinary elimination Fluid volume in excess Risk for injury .

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such as surgery or pregnancy.Addison’s Crisis   It can occur. or exogenous corticosteroid therapy is abruptly discontinue If not treated immediately. shock. circulatory collapse. and death may occur . which is an acute insufficiency of adenocortical hormone from lack of cortisol during stress .

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Addisonian Crisis. Addison’s Disease: administer cortisone.Nursing Management Medication A. fludcortisone acetate (florinef) asprescribe B. immediate intravenous glucocticoid replacement and fluids with sodium 1. prednisone. .

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Anterior Pituitary Disorder Overview 1. it is responsible for regulating endocrine function by producing hormone that affect body system and stimulating other endocrine glands to secrete hormone A. . The pituitary gland referred to as master gland is located at the base of the brain adjacent to hypothalamus.

c. d. f.Hormones Secreted By the Pituitary glands a. e. Growth Hormone (GH) Thyroid stimulating hormone (TSH) Adenocorticotropic hormone (ACTH) FSH LH Prolactin (PRL) . b.

cardiac muscle. and connective issue . Skeletal muscle. Disorder of the anterior pituitary gland result in excessive or insufficient pituitary hormone disorder are as not common than other endocrine disorder 4. Growth hormone is the hormone necessary for growth that regulates cell division and the synthesis of protein. exerts other metabolic effects on endocrine organs.Anterior Pituitary Disorder 3. skin.

ACTH: Leading to Tissue over growth. FSH. TSH.Hyperfunction of the Anterior Pituitary (Hyperpituitarism)   It is the result of excess production and secretion of one or more hormones: (GH). The most comm0n cause of hyperpituitarism is benign adenoma . LH.

LH. follicle stimulating hormone (FSH). radiation . infection. pituitary tumors. trauma.Hypofunction of the Pituitary Gland (hypopituitarism) 1. 2. TSH. It is aresult in a deficiency of one or more pituitary hormones: GH. congenital defects. ACTH Causes include surgical removal of the pituitary gland.

Hyperpituitarism . b.Common Disorder a. Giantism and acromegaly Hyporpituitarism: dwarfism .

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dwarfism giantism CRETINISM .

Hyperpituitarism Giantism Acromegaly .

2. and treatment has made this disorder rare in occurrence Common cause is tumor .Pathophysiology of Giantism a. 1. 3. in height The body proportion are generally normal Early detection. diagnosis. 4. Giantism is the result of growth hormone hypersecretion that begins before the closure of the epiphysicial plates This hypersecretion leads the person to become abnormally tall reaching 7 to 8 ft.

CHF. Most common cause is tumor S/S include large hands and feet. change in hand and shoe and glove size that slowly progress. sign of osteoporosis. protrusion of the lower jaw. thyroid and parathyroid gland . coarse facial features.Acromegaly    It is the result of GH over secretion during continue to grow. bone connective tissue continue to grow . leading to disproportionate enlargement of tissue. enlarge adrenal gland. CAD. leading to adulthood. systemic symptoms hypertension.

obesity. hyperlipidemia.Dwarfism    Result from deficient secretion of anterior pituitary hormones Inadequate secretion of these hormones leads to growth retardation and accompanying metabolic disorder S/S include short stature. hypercholesteremia . slow measuring skeletal system . short pitch voice.

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growth and development. Assessment of gigantism includes growth chart for height and weight by age and visual exam. hormone levels . cholesterol. S/S of CHF or diabetes. c.Nursing assessment a. Assessment of acromegaly includes VS. b. Visual disturbances. lipid funnel . d. symptoms and analysis of pain Assessment for dwarfism include growth chart and development of sex organ Diagnostic test : bone scan.

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TRANSSPHENOIDAL HYPOPHYSECTOMY .

sexual dysfunction. ineffective individual coping.Nursing diagnosis  Activity intolerance. body image disturbance. anticipatory grieving. altered growth and development .

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Overview  1. the purpose of antidiuretic hormone is to control serum osmolarity  Disorder of the posterior pituitary gland are primarily result of excessive or deficient ADH secretion . The posterior pituitary gland secrete hormones oxytoxin and antidiuretic hormone (vasopressin).Posterior pituitary disorder A.

DISORDER OF THE POSTERIOR PITUITARY GLAND A. DIABETES INSIPIDUS (DI) is the result of ADH insufficiency. B. resulting to excessive fluid excretion SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION (SIADH) is the result of excessive secretion of ADH and water retention .

but may also occur as the result of pituitary surgery. head injury. or medications such as diuretics. anesthetics and barbiturates . head trauma with damage to the pituitary or tumor SIADH: occurs most often as the result of ectopic production of ADH by malignant tumors .CAUSES   Diabetes Insipidus: unknown etiology in most cases.

Decreased urinary output Dry mucous membrane .Nursing assessment for DI       I and O Complain of thirst Dry skin Sunken eyeball weakness.

S/S of DI     Polyuria Excessive Thirst Polydipsia Dehydration in event the client is unable to replace fluid loss .

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DI and its classification    ADH insufficiency leads to the excretion of large amount of urine (polyuria). up to 12 L/day Neurogenic DI occurs when there is a decrease in the synthesis and excretion of ADH : may be idiopathic. or may result from trauma or dysfunction of the hypothalamus or pituitary gland Nephrogenic DI occurs when the renal tubules is not sensitive to ADH .

g.Nursing Management For DI a. pressyn) for treatment of nuerogenic DI Administration of hypotonic solution Increase fluid intake Treatment is life long for chronic DI Monitor daily weigh Low NA diet and to avoid caffeine since this increases urine output Educate client for medic alert bracelet . d. b. e. f. c. Medications include vasopressin (pitressin.

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fluid retention.S/S of (SIADH)      Lethargy Confusion Changes in neurological status Cerebral edema Muscle cramps weakness. weight gain . decrease urine output.

Assessment of SIADH    Assess for nuerological indicator like LOC I and O weight .

demeclocycline (declomycin) Administration of hypertonic saline fluids Oral fluid restriction I and O and daily weight Monitor for neurological changes and water retention .Nursing Management For (SIADH)      Medications include diuretics.

Nursing Diagnosis for disorder of posterior pituitary disorder      Fluid volume in excess Fluid volume deficit Altered urinary elimination Risk for Injury Knowledge deficit .

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DIABETES MELLITUS .

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b. Type 1 DM: occurs as a result of genetic. environmental or immunological factors that may damage the pancreatic beta cells Type 2 DM Etiology is unknown: however.CAUSES OF DM a. obesity is the single most important risk factor .

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Early manifestation of type 1 DM. fatigue. polydipsia. glycosuria. nausea. polydispia. vomiting. polyuria. blurring of vision. abdominal pain Early manifestation ofin type 2 Dm : polyuria. polypaghia. b. weight gain .S/S of DM a. weight loss.

Sensory/ neurological: diabetic retinopathy. 2. 3. glaucoma. paresthesias.S/S of DM General multisystem findings 1. hypertension G I: constipation or diarrhea Musculoskeletal : contractures . peripheral neuropathy Cardiovascular assessment: coronary artery disease. cataracts. 4. peripheral vascular disease. loss of sensation.

Vaginitis 8. UTI 7.S/S of DM General multisystem findings 5. metabolic acidosis . chronic skin infections 6. Reproductive assessment: Sexual dysfunction. albuminuria. chronic renal failure. Renal: edema. hypokalemia. Integumentary : atrophy. Metabolic: hypergycemia. foot ulcer. poor wound healing.

Symptoms of DKA       Abdominal pain . nausea and vomiting Metabolic acidosis Fruity breath odor Kaussmaul’s respiration Altered LOC Coma and death if not untreated .

Peridontal disease Gangrene. inability to heal . PVD Retinopathy Paresthesia (especially feet) Renal failure Carpal tunnel syndrome. amputation.Complication of DKA          Hypoglycemia Atherosclerosis CVA.

hours plasma glucose (after meal) is increase to 200 mg/ dl Cholesterol and triglyceride levels is elevated . and ketones positive Urine for protein is positive Serum potassium is decrease 2. increase to 7 percent Urine for glucose.Diagnostic test for DM        Serum fasting sugar Increase (hyperglycemia) increase to 126 mg/dl Serum glycosylated hemoglobin levels.

Nursing management for DM Medication include insulin and hypoglycemic agent a. serum glucose. 2. electrolytes 1. Type 1 diabetes: regular insulin. Metformin (glucophage) etc. . glyburide (micronase). tolazamide (tolomide). Type 2 diabetes: oral agents such as glipizide (glocotrol). Monitor I and O. NPH insulin such as 70/30 b.

weakness. Teach sign and symptoms of hypoglycemia (irritability. B. possible coma) and hyperglycemia with appropriate interventions Teach for self administration of insulin or hypoglycemic agent . tremors. fatigue.Client education for DM A. headache.

acting Long acting insulin Very long acting insulin .Insulin therapy and insulin preparation        In type I DM exogenous insulin must be administered for life because the body loses the ability to produce insulin Reaction time of most common insulin preparation Rapid-acting insulin Short acting insulin Intermediate.

and/or to prevent nocturnal hyperglycemia Agent: lispro (humalog). peak 4050 min duration 2-4 hours . peak 1 hour. to treat postprandial hyperglycemia. duration 2-4 hours Apart (novolog) – onset 5 to 15 min.Categories of insulin preparation    Rapid acting it is indicated for rapid reduction of glucose level.onset 10-15 min.

Iletin II regular) Onset – ½ -1 hours. may be taken alone or in combination with long acting insulin Agent : Regular (humalog R).Categories of insulin preparation    Short acting usually administered 20-30 min before meal. peak 1 hour. Novolin R. duration 4-6 hours .

Novolin (NPH) Onset: 3-4 hours . Novolin L (lente) . Iletin II NPH. Novolin Lente. Peak: 4-12 hours. Duration 16 to 20 hours Agent: Humalin N.Categories of insulin preparation      Intermediate Acting it is usually taken after food Agent: NPH( neutral protamine hagadorn) Onset: 2-4 hours. Iletin II lente. Iletin II (NPH). peak: 4-12 hours. Duration:16 20 Hours .

however it is now approved to be given once a day at any time of the day but at same time to prevent overlap of action. Duration: 20-30 h Very Long Acting it is used for basal dose (“Peakless”) that is the insulin is absorbed slowly for 24 hours and can be given once a day and given HS originally. It should not mix with other insulin preparation to avoid precipitation because of each PH of 4 . Peak:12-16 h.Categories of insulin preparation     Long Acting Insulin it is used to control fasting glucose level Agent: Ultra lente ( “UL”) Onset: 6-8 h.

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. Insulin lipodystrophy it refers to a localized reaction in form of lipoatrophy or lipohypertrophy at the injection site Resistance to insulin injection. when occur there is local skin reaction that gradually spreads to generalized urticaria. swelling .Complication of insulin therapy     Local allergic reaction ( readiness. treatment desensitization. tenderness and indurations or 2-4 cm wheal) may appear at the injection site Systemic allergic reaction it is rare.

when the levels begins to rise Somogyi Effect it is normal or elevated blood glucose at bedtime. Morning hyperglycemia Insulin Wanning it is progressive rise in blood glucose from bedtime to morning Dawn Phenomenom it is relatively normal blood glucose until about 3 Am. a decrease at 2-3 AM to hypoglycemic levels. b. c. and a subsequent increase cause by the production of counterregulatory hormones .Complication of insulin therapy  a.

Insert needle straight into the skin.Patient Education Self injection of insulin Insulin injection are self administered into subcutaneous tissue with the use of special insulin syringe. Self Injection 1. Pick up syringe with the other hand and hold it as you would a pencil.  . stabilize the skin by spreading it or pinching large area 2. With on hand .

Press cotton ball over the injection site for several seconds 5 Use disposable syringe only once and discard into hard plastic container (with a tight-fitting top) such as empty bleach container. Pull needle straight out of skin. push the plunger all way in 4. To inject the insulin. Follow state regulations for disposal of needle .Self injection of insulin 3.

Selecting and Rotating the injection site Four main areas for injection 1. thight and hip respectively . Abdomen 2. Hips Note: The speed of absorption is greatest in the abdomen and decreases progressively in the arm. Upper arms (posterior surface) 3. Thighs (anterior surface) 4.

Patient Education     Teach the patient how to get CBG or self monitoring glucose Teach the client about proper dietary management for diabetes Teach proper diabetic foot care and wound care Teach for proper exercise for diabetes .

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