The ENDOCRINE SYSTEM

Anatomy and physiologic Overview

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. HOMEOSTASIS

Endocrines help us in maintaining the homeostasis of:

Temperature: Thermoregulation or thermostasis. Metabolism Nutrition: Glucostasis Acid Base Balance

ENDOCRINES ARE USEFUL IN 2. COMBATING STRESS

INFECTION
TRAUMA SHOCK

ENDOCRINES ARE USEFUL FOR 3. GROWTH & DEVELOPMENT

Increase in the cell number: Hyperplasia Increase in cell SIZE: Hypertrophy.

ENDOCRINES ARE USEFUL FOR 4. REPRODUCTION

The Male and female Gonads secrete:

Sex Hormones

These sex hormones cause the development of

Primary sex organs Secondary sexual characteristics.

HORMONES
It is important in regulation of the internal environment of the body and effect every aspect of life. 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

Target Tissues

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

Glands Of The Endocrine System

1.
2. 3.

4.
5. 6. 7.

Pituitary glands Thyroid glands Parathyroid glands Pancreatic islets Ovaries Testes Adrenal glands

HORMONES PRODUCED IN THE BODY

HYPOTHALAMUS:

CRH, TRH, GHRH, GHIH, GnRH, PIH.

ANTERIOR PITUITARY GLAND:

GH, ACTH, TSH, FSH, LH, Prolactin.

ADH, & Oxytocin. Thyroxin, T3, Calcitonin.

POSTERIOR PITUITARY GLAND:

THYROID GLAND:

HORMONES PRODUCED IN THE BODY

ADRENAL CORTEX:

Aldosterone, Cortisol, Sex steroids.

ADRENAL MEDULLA:

Epinephrine, Norepinephrine, Dopamine.

Glucagon, Insulin, Somatostatin, Pan polypeptide.

ENDOCRINE PANCREAS:

HORMONES PRODUCED IN THE BODY

TESTES:

Testosterone, Estrogen, Inhibin. Estrogens, Progesterone, Relaxin. Estrogens, Progesterone, HCG, HPL. Thymosin. Melatonin

OVARY:

PLACENTA:
THYMUS:

PINEAL GLAND:

HYPERSECRETION:

Excessive Production of hormones due to:

Tumors in the gland. Excess tropic influence.

Results in:

Clinical syndromes with signs/symptoms due to:

Increased blood levels of the hormone

Example: Hyperthyroidism: Thyroxin levels Clinical features: Fine tremor, Anxiety, PR, BMR Acromegaly: Growth Hormone.

HYPOSECRETION:

Drop in the production of hormones due to:

Excision of gland: Eg: Parathyroids. Hypofunctioning of gland cells: Eg: Diabetes mellitus. Decreased tropic influence. Clinical features/ syndromes due to blood levels of the hormone

Results in:

ENDOCRINE DISORDERS

Thyroid Hyperfunction Disorder

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

Causes of Hyperthyroid Disorder

Auto immune response Neoplasm Excessive intake of thyroid medication Excess secretion of TSH from the anterior pituitary glands

Pathophysiology THYROID HYPERFUNCTION DISORDERS

1. 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

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, is seen most often in woman under age of 40. The exact cause is unknown, 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, Which leads to hypermetabolic state

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, excess growth stimulating immunoglobulins, 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

Nursing assessment for Hyperthyroidism

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

Nursing management for Hyperthyroidism

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

Nursing management for Hyperthyroidism

Educate the client that it may take several weeks before the therapeutic effects of antithyroid medications are noticed a. 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 hyperthyroidisn

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

Nursing management for hyperthyroidism

7. Monitor dietary intake: Client may require up to 4,000 to 5,000 calories a day during hypermetabolic state 8. Monitor intake and output 9. Monitor weight 10. Keep the environment cool and quiet because of the symptoms

Nursing management for Hyperthyroidism

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

Nursing management for Hyperthyroidism

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

Nursing management for hyperthyroidism

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

Thyroid Hypofunction Disorder

A.
1.

2.

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

A.
B.

C.

Hypothyroidism Myxedema Myxedema coma

MYXEDEMA

HYPOTHYROIDISM

Classified as primary and secondary

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

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

Pathophysiology of Myxedema coma

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

Pathophysiology
Iodine deficiency: iodine is necessary for TH synthesis and secretion A. Iodine deficiency occurs as a result of antithyroid drugs, and lithium or iodine intake B. In US , 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

Nursing Assessment
1.

2.

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

Priority nursing diagnosis for thyroid hypofunction disorder

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

Parathyroid disorder
1. a.

b.

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

Hyperparathyroidism

It is an Increase in PTH, which leads to hypercalcemia, hyperposphatemia, bone damage, and renal damage

Nursing assessment for Hyperparathyroidism

1.

Includes neurological assessment including LOC, VS , heart rhythm, GI assessment, complain of pain, muscle strength, weight , I and O

Hypoparathyroidism

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

Nursing Assessment for hypoparathyroidism

NURSING MANAGEMENT

Priority nursing diagnosis for parathyroid disorder

Impaired physical mobility Risk for injury Altered urinary elimination Altered nutrition

Adrenal Cortex Hyperfunction Disorder

A.
1.

a.

b.

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, norepinephrine and dopamine The adrenal cortex secretes mineralcorticoids (aldosterone), glucocorticoids (cortisol, androgen, andestrogens (sex hormone)

ADRENAL CORTEX HYPERFUNCTION DISORDER

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

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

ADRENAL CORTEX HYPERFUNCTION DISORDER

Cushings Syndrome or hypercortisolism result in excess production of cortisol (glucocorticoids). Conns Syndrome or Hyperaldosteronism result in excess production of aldosterone

Cause of Hypercortisolism ( Cushings syndrome)

Include Adrenal tumors Adrenal hyperplasia Or exogenous glucocorticoids

Causes of hyperaldosteronism ( conns syndrome)

Include adrenal lesion Or condition that stimulate overproduction of aldosterone: heart failure, cirrhosis of liver, dehydration, renal disease

CUSHINGS SYNDROME

Pathophysiology of Hypercortisolism
A.

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

S/S of Hypersecretion of cortisol

Nursing management for Cushings Syndrome

Includes vital sign: increase BP/ arrhythmias Neurological assessment History of GI, renal, and reproductive problem Muscle strength Integument assessment Weight ; presence of edema, I and O

Nursing management for Cushings syndrome

Nursing management for Cushings syndrome

Nursing management for Cushings 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 Cushings Syndrome

Fluid volume in excess Risk for infection Activity intolerance anxiety Knowledge deficit Risk for impaired skin integrity

CONNS SYNDROME/ HYPERALDOSTERONISM

Causes of Conns Syndrome or Hyperaldosteronism

Adrenal lesion Any condition that stimulates overproduction of aldosterone: heart failure, cirrhosis of liver, dehydration, renal disease.

Pathophysiology of Conns 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

S/S for Conns Syndrome

In secondary hyperaldosteronism hypertension is uncommon Visual disturbance Paresthesia Dysarrythmias Fluid retention, renal damage, polyuria Muscle weakness, tetany Electrolyte and acid-base imbalance

Nursing management for Conns Syndrome

a. Medication 1. 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. Administer glucocorticoids preoperatively as prescribed to prevent adrenal hyperfunction

Nursing management for Conns Syndrome

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

Priority nursing diagnosis for Conns syndrome

Altered urinary elimination Fluid volume in excess Risk for injury

Addisons Crisis

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

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

Anterior Pituitary Disorder

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

Hormones Secreted By the Pituitary glands

a.
b. c.

d.
e. f.

Growth Hormone (GH) Thyroid stimulating hormone (TSH) Adenocorticotropic hormone (ACTH) FSH LH Prolactin (PRL)

Anterior Pituitary Disorder

3. 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, skin. Skeletal muscle, cardiac muscle, and connective issue

Hyperfunction of the Anterior Pituitary (Hyperpituitarism)

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

Hypofunction of the Pituitary Gland (hypopituitarism)

1.

2.

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

Common Disorder
a.

b.

Hyperpituitarism ; Giantism and acromegaly Hyporpituitarism: dwarfism

dwarfism

giantism

CRETINISM

Hyperpituitarism

Giantism

Acromegaly

Pathophysiology of Giantism
a.

1.

2. 3.

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. in height The body proportion are generally normal Early detection, diagnosis, and treatment has made this disorder rare in occurrence Common cause is tumor

Acromegaly

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

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, obesity, short pitch voice, slow measuring skeletal system , hyperlipidemia, hypercholesteremia

Nursing assessment
a. b.

c.

d.

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

TRANSSPHENOIDAL HYPOPHYSECTOMY

Nursing diagnosis

Activity intolerance, body image disturbance, sexual dysfunction, anticipatory grieving, ineffective individual coping; altered growth and development

Posterior pituitary disorder

A. Overview 1. The posterior pituitary gland secrete hormones oxytoxin and antidiuretic hormone (vasopressin), 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

DISORDER OF THE POSTERIOR PITUITARY GLAND

A.

B.

DIABETES INSIPIDUS (DI) is the result of ADH insufficiency, resulting to excessive fluid excretion SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION (SIADH) is the result of excessive secretion of ADH and water retention

CAUSES

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

Nursing assessment for DI

I and O Complain of thirst Dry skin Sunken eyeball weakness, Decreased urinary output Dry mucous membrane

S/S of DI

Polyuria Excessive Thirst Polydipsia Dehydration in event the client is unable to replace fluid loss

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

Nursing Management For DI

a. b. c.

d.
e. f. g.

Medications include vasopressin (pitressin, 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

S/S of (SIADH)

Lethargy Confusion Changes in neurological status Cerebral edema Muscle cramps weakness, decrease urine output, fluid retention, weight gain

Assessment of SIADH

Assess for nuerological indicator like LOC I and O weight

Nursing Management For (SIADH)

Medications include diuretics, demeclocycline (declomycin) Administration of hypertonic saline fluids Oral fluid restriction I and O and daily weight Monitor for neurological changes and water retention

Nursing Diagnosis for disorder of posterior pituitary disorder

Fluid volume in excess Fluid volume deficit Altered urinary elimination Risk for Injury Knowledge deficit

DIABETES MELLITUS

CAUSES OF DM
a.

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, obesity is the single most important risk factor

S/S of DM
a.

b.

Early manifestation of type 1 DM; polyuria, polydispia, polypaghia, glycosuria, fatigue, weight loss, nausea, vomiting, abdominal pain Early manifestation ofin type 2 Dm : polyuria, polydipsia, blurring of vision, weight gain

S/S of DM General multisystem findings

1.

2.

3.
4.

Sensory/ neurological: diabetic retinopathy, cataracts, glaucoma, paresthesias, loss of sensation, peripheral neuropathy Cardiovascular assessment: coronary artery disease, peripheral vascular disease, hypertension G I: constipation or diarrhea Musculoskeletal : contractures

S/S of DM General multisystem findings

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

Symptoms of DKA

Abdominal pain , nausea and vomiting Metabolic acidosis Fruity breath odor Kaussmauls respiration Altered LOC Coma and death if not untreated

Complication of DKA

Hypoglycemia Atherosclerosis CVA, PVD Retinopathy Paresthesia (especially feet) Renal failure Carpal tunnel syndrome, Peridontal disease Gangrene, amputation, inability to heal

Diagnostic test for DM

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

Nursing management for DM

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

Client education for DM

A.

B.

Teach sign and symptoms of hypoglycemia (irritability, fatigue, weakness, tremors, headache, possible coma) and hyperglycemia with appropriate interventions Teach for self administration of insulin or hypoglycemic agent

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- acting Long acting insulin Very long acting insulin

Categories of insulin preparation

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

Categories of insulin preparation

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

Categories of insulin preparation

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

Categories of insulin preparation

Long Acting Insulin it is used to control fasting glucose level Agent: Ultra lente ( UL) Onset: 6-8 h, Peak:12-16 h, 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, 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. It should not mix with other insulin preparation to avoid precipitation because of each PH of 4

Complication of insulin therapy

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

Complication of insulin therapy

a. b.

c.

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, when the levels begins to rise Somogyi Effect it is normal or elevated blood glucose at bedtime, a decrease at 2-3 AM to hypoglycemic levels, and a subsequent increase cause by the production of counterregulatory hormones

Patient Education Self injection of insulin

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

Self injection of insulin

3. To inject the insulin, push the plunger all way in 4. Pull needle straight out of skin. 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. Follow state regulations for disposal of needle

Selecting and Rotating the injection site

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

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