Endocrine System Lecturer: Dante Roel Fernandez RT, M.D.

ANTI-DIABETIC AGENTS HORMONES: - chemicals produced in the body and that meet specific criteria - characteristics: 1. produced in very small amounts 2. secreted directly into the blood stream 3. travel throughout the blood to specific receptor sites throughout the body 4. act to increase or decrease normal metabolic processes of cells when they react with their specific receptor sites 5. they are immediately broken down.

PANCREAS: - both an endocrine gland (produces hormones in islets of Langerhans) and an exocrine gland(release sodium bicarbonate and pancreatic enzymes directly into with CBD). - islets of Langerhans- with endorine cellsalpha cells (release glucagon), beta cells (release insulin) and delta cells (block release of glucagon and insulin).

INSULIN: 1. stimulates transport of glucose into the cells to be used for energy 2. stimulates synthesis of glycogen 3. stimulates conversion of lipids into fat stored in the form of adipose tissue 4. stimulates synthesis of proteins from amino acids.

METABOLIC CONSEQUENCES OF INSULIN DEFICIENCY 1. Hyperglycemia - increased blood sugar 2. Glycosuria - concentration of glucose in the blood too high for incomplete reabsorption- spillage of sugar into the urine-prone to cystitis 3. Fatigue - bodys cells cannot use the glucose for energy 4. Polyphagia - hypothalamic centers deprived of glucosesensation of starving-increased eating

5. Polydipsia - increased glucose and waste products in the blood loss of fluid with glucose in the urine-increased blood tonicityincreased thirst. 6. Polyuria - spillage of glucose in the urine osmotic diuresis 7. increased lipolysis or fat breakdown- body breaks down stored fat for energyaccumulation of ketone wastes-ketosis 8. acidosis-liver cannot remove all of the waste products resulting from breakdown of glucose, fat and protein 9. increased protein catabolism-increase in nitrogen wastes-increase BUN & proteinuria

DIABETES MELLITUS
- literally means honey-urine 2 Types: 1. Type I ( IDDM) - associated with rapid onset, mostly in younger people

2. Type II (NIDDM)
onset - slow & progressive onset - impaired sensitivity of insulin receptor sites
- mature

-Increased incidence of a number of disorders including: 1. Atherosclerosis lead to heart attacks and strokes 2. retinopathy with resultant loss of vision 3. neuropathy with motor and sensory changes in the feet and legs 4. nephropathy due to change in the basement membrane of the glomerulus

PHARMACOLOGIC MANAGEMENT OF DM 1. Replacement Insulin - used to treat DM in adults who do not respond to diet, exercise and oral agents and for Type I diabetics; also used for treatment of severe ketoacidosis Insulin types: 1. Insulin analogue (Humalog) 2. regular ( Humulin R) 3. NPH ( Humulin N) 4. Lente (Humulin L) 5. PZI ( Humulin U) Adverse Effects: hypoglycemia and ketoacidosis Drug Interactions: - MAO inhibitors, B-blockers, salicylates and alcohol

NURSING CONSIDERATIONS: 1. Ensure uniform suspension of insulin by gently rotating vial. Avoid vigorous shaking 2. Give maintenance doses SC only. Rotate injection sites regularly to prevent SC atrophy. Give regular insulin IM or IV in emergency situations to avoid damaging muscles 3. Monitor response carefully to avoid adverse effects-blood glucose monitoring most effective 4. Use caution when mixing types of insulin to prevent precipitation and ineffective dosing 5. Store insulin in a cool place away from direct sunlight.

6. Monitor patients during times of trauma and severe stress for potential dosage adjustment needs. 7. Instruct patients also receiving beta blockers in ways to monitor glucose levels and signs and symptoms of glucose abnormalities to prevent hypo & hyperglycemic episodes when SNS and warning signals are blocked 8. Provide thorough patient teaching

Signs and Symptoms Of Hypo & Hyperglycemia Onset

Hypoglycemia

Hyperglycemia

Sudden, anxious pt, Drunk, miss meal, stress HA, blurred vision,drowsy,coma, ataxia, h-active reflexes

Gradual, slow &sluggish Inc. stress Dec.level of consc.,sluggish, coma,hypoactive ref.

CNS

Neuromuscular

Paresthesias, weak, muscle spasms, twitching to seizures

Weakness, lethargy

CV

Tachycardia, palpitations, N to Inc. BP

Tachycardia, hypotension Rapid, deep, fruity breath Nausea, vomit, thirst Dry, warm, flushed skin, soft eyeballs,UG-(+) (+) urine ketones, High Glu

Respiratory GI Others Lab Tests

Rapid, shallow Hunger, nausea Diaphoresis, cool, clammy, bld. GluUring glucose (-), low

II.

Oral Anti-diabetic Agents A. Sulfonylureas: 1st oral agents introduced Actions: 1. Stimulate insulin release from beta cells 2. improve insulin binding to insulin receptors 3. may increase number of insulin receptors 4. increase the effect of ADH on renal cells - effective only in patients with functioning beta cells

CLASSIFICATION: 1. First Generation: - associated with increased risk of cardiovascular disease and death a. Chlorpropamide (Diabenese)- most frequently used. b. Acetohexamide c. Tolbutamide preferred in patients with renal dysfunction, readily cleared from the body d. Tolazamide

2.

Second Generation - excreted in urine and bile-safer for patients with renal dysfunction - do not interact with as many protein bound drugs as the first generation drugs - longer duration of action-increase compliance a. Glimepiride b. Glipizide c. Glyburide

ADVERSE EFFECTS: 1. Hypoglycemia 2. GI distress; nausea, vomiting, epigastric discomfort, heartburn, anorexia 3. allergic skin reactions 4. increased risk of cardiovascular mortality * caution should be used with: 1. beta blockers-may mask the signs of hypoglycemia 2. alcohol-lead to altered glucose levels

B.

Non-Sulfonylureas - structurally unrelated to sulfonylureas - effective when used in combination with sulfonylureas or insulin - therapeutic actions and indications similar to sulfonylureas 1. Acarbose - an alpha glucosidase inhibitor- inhibits glucose breakdown ( or absorption ) delays absorption of glucose - has mild effect on glucose level - associated with severe hepatic toxicity and GI distress - reserved as an adjunct with other agents for patients with uncontrolled glucose levels

2. Metformin (Glucophage)

- decreases the production of and increases the uptake of glucose - effective in lowering bood glucose levels - associated with development with lactic acidosis - can cause GI distress 3. Miglitol an alpha glucosidase inhibitor - delays absorption of carbohydrates-smaller rise in blood glucose following meals and a decrease in glycosylated Hgb (glucose carried in rbc) - does not enhance insulin secretion

4. Troglitazone

- decreases insulin resistance - used in combination with sulfonylureas or metformin to treat patients with insulin resistance - can cause serious hepatotoxicity 5. Repaglinide - newest; acts like sulfonylureas to increase insulin release - used just before meals to lower post prandial glucose levels - can be used in combination with metformin.

NURSING CONSIDERATIONS: 1. Administer drug as prescribed in relation to meals to ensure therapeutic effectiveness 2. Provide nutritional consultation as needed 3. Blood glucose monitoring response 4. Monitor patients in time of trauma 5. Provide thorough pt. teaching to enhance pt. knowledge of drug therapy and promote compliance

GLUCOSE-ELEVATING AGENTS: Hypoglycemia - abnormally low blood sugar (< 40 mg/dl) - associated with: 1. pancreatic disorders 2. kidney disease 3. certain cancers 4. disorders of anterior pituitary 5. unbalanced treatment of DM Treatment: increase blood glucose level by decreasing insulin release and accelerating breakdown of glycogen in the liver to release glucose

1.

Diazoxide - can be taken orally - contraindicated with known allergies to sulfonamides or thiazides - associated with cardiovascular effects associated with ability to relax arteriolar smooth muscles A. Hypotension B. Headache C. Cerebral ischemia D. Weakness E. CHF and arrhythmias

2. Glucagon - can only be given parenterally; preferred for emergency situations - associated with GI upset, nausea and vomiting 3. Pure Glucose-Oral IV Nursing Considerations: 1. Monitor blood glucose daily to evaluate effectiveness of the drug 2. Have insulin on standby during emergency use to treat severe hyperglycemia if it occurs 3. Monitor nutritional status 4. Monitor patients receiving diazoxide for potent CV effects including BP, heart rhythm and output, and weight changes

THYROID AND ANTI-THYROID DRUGS Thyroid hormones- essential for: - growth and development -regulation of energy metabolism - synthesis of thyroid hormone dependent on dietary iodine ( from food, drugs, water) - daily requirement = 150-200 ug Major Steps: 1. Iodine trapping 2. Oxidation of iodide and iodination of Tyrosine 3. Formation of T3 and T4 by coupling 4. Secretion 5. Peripheral Conversion of T4 and T3

Iodine Metabolism - ingested iodine is converted to iodide and absorbed in the GIT - Principal organs involved: a. Thyroid for hormone synthesis b. Kidney for excretion c. Liver for metabolism Relation of iodine to Thyroid Functions: - Iodine is necessary for thyroid hormone synthesis: - If iodine intake is decreased: * hormone production is decreased * TSH is increased * thyroid gland hypertrophies ( goiter ) * vascularity increased * iodide concentrating mechanism increased * production of normal amount of hormone

Sources of Iodine: a. Marine life b. sea/ fish/shells =as much as 200-1000 u/kg c. Whereas, 5 kg of vegetables/fruits or 3 kg of meat or fresh water fish provides only 100 ug iodine - to provide enough iodine, other regions inject iodized oil - most practical = addition of iodide to table salt=1 gram iodized salt= 100 ug iodine

CLINICAL DIAGNOSIS: Hypothyroidism deficiency in thyroid hormone example- congenital cretinism in children;absent or atrophic thyroid gland - post thyroidectomy - post radioactive iodine therapy - myxedemas when severe ssx- Dwarfism, short extremities, mental retardation, Inactive, uncomplaining, expressionless, drowsy, puffy face, thickened lips, half open mouth, enlarged tongue, doughy, yellowish scaly skin, cool and dry touch, Coarse, sparse, brittle hair, Thick, brittle nails, Thich subcutanous tissue, low pitch, husky voice, Cold intolerance ,cardiomegaly, decreased Heart rate

GOITER (Thyroid enlargement)

HYPERTHYROIDISM- resemble sympathetic hyperactivity even though epinephrine is not elevated ssx: - Tachycardia, palpitation, excessive sweating, anxiety, nervousness, Heat intolerance, tremor, warm skin, muscle weakness, increased appetite, Lid lag/retraction, increased energy expenditure, weight loss, muscle wasting, insomnia, restlessness, Increased bowel movement 2 forms: 1. Diffuse toxic goiter ( Grave dis.) - exophthalmos, Young middle aged women, Autoimmune, IgG antibodies to TSH, pretibial edema 2. Nodular Toxic goiter (Plummers dis.) - older patients - arise from long standing non-toxic goiter

Antithyroid Drugs

1. Propylthiouracil(PTU) 2. Methimazole (Tapazole) action: inhibition of coupling of iodine to tyrosine prevention of formation of thyroid hormones - PTU also prevent conversion of T4 to T3 in the peripheral circulation

Adverse effects
- uncommon, however ranges from a mild rash to a agranulocytosis

Iodides
- Useful in treating mild cases of hyperthyroidism esp. in young clients Action: inhibit thyroid hormone production by inhibiting thyrotropin (+) of thyroid secretion - Can be given in several types of solution - Lugols soln. - Saturated solution of potassium iodide (SSKI)

Clinical uses of Iodine

1. Sodium iodide 131 - use for diagnostic and treatment of hyperthyroidism

Other drugs used for hyperthyroidism 1. Ionic inhibitors K perchlorate - resemble iodine ion-- the ability of the gland to trap iodine 2. Beta blocker ( Propranolol) - suppressing some signs and symptoms of hyperthyroidism - used as adjunctive therapy

NURSING IMPLICATIONS
Antithyroid Medication 1. Assess activity level, food intake, and sleep pattern disturbances. Measure body weight, blood pressure, pulse, respirations, and temperature. 2. Liquid iodine preparations are diluted in a small amount of liquid before administration. 3. The unpleasant taste of liquid iodine products can be decreased by administering the diluted medication through a straw. 4. Clients taking iodine preparations are observed for iodism, including gum soreness, excessive salivation, nausea, liver inflammation of the salivary glands, and metallic taste in the mouth. S. No special safety precautions need to be taken for clients who have received I 1 31, unless the client's clothing or environment becomes contaminated by excretions.

6. Several days following 1 131 administration, the client may experience a temporary swelling and tenderness of the thyroid gland. 7. Some clients who have received 1131 later develop hypothyroidism. 8. Clients taking propylthiouracil and related antithyroid drugs must immediately report sore throat, fever, or malaise, as these may indicate agranulocytosis. 9. Women of childbearing age who are taking antithyroid drugs should contact their physician for advice before becoming pregnant or as soon as pregnancy Is suspected. 10. Thyroid storm, an extreme hyperthyroid state, may follow stress, surgery, or withdrawal of antithyroid drugs. It is characterized by fever, tachycardia, congestive heart failure and CNS disturbances.

Surgery
- Surgical removal of the gland is effective treatment of hyperthyroidism COMPLICATION: - hypothyroidism and hypoparathyroidism

PARATHYROID DISORDERS
- Pinhead-sized gland located at the back of the thyroid gland - Produces parathyroid hormone - increases blood Ca level

Hypoparathyroidism

- Deficiency of parathyroid hormone due to:

congenital absence of gland surgery - S/Sx: increased neuromuscular irritability, psychiatric disorders Treatment: - replenish Ca by IV Ca chloride and Ca gluconate - Vit D may also be given

Hyperparathyroidism
- Hypersecretion of parathyroid hormone may be due to adenoma or carcinoma S/Sx: Ca bone resorption increase Ca conc. Calcification Tx: surgery - PO4 supplementation, diuretics( promotes excretion of Ca) - Calcitonin - Calcimar, Miacalcin

KEY NURSING IMPLICATIONS

Medication for Parathyroid Disorders 1. Assess the client for fatigue, muscle weakness, tremor or spasm, numbness, tingling, constipation, paresthesias, nausea, and vomiting. 2. Hypoparathyroidism is treated with calcium preparations. The initial calcium may be given intravenously. The solution should be warmed to body temperature and injected slowly into a large vein. 3. During intravenous injection of calcium, the heart rate and rhythm should be monitored by ECG in known cardiac clients and elderly persons. 4. Following the intravenous injection of calcium, clients are advised to remain in bed for a short period to avoid syncope.

5. Extravasation of intravenously infused calcium may result in tissue necrosis and sloughing. 6. Calcium should not be added to an IV line containing bicarbonate or phosphate, as a precipitate may form in the IV line. 7. Oral calcium products should be given 1-11/2 hours after meals or at bedtime. For maximum effectiveness the client's diet should not be high in oxalic acid (spinach and rhubarb), bran and whole grain cereals, or phosphorus. 8. Clients receiving drug therapy for the treatment of hyperparathyroidism are observed for hypocalcemia as indicated by spasms of the hands and feet, along with cardiac irregularities. 9. Clients may experience flushing of the face and a feeling of warmth following calcitonin injection. This is common and will disappear without treatment.

PITUITARY DISORDERS

- Pituitary gland consist of :

1. Anterior pituitary 2. Posterior pituitary Hormones secreted: Anterior Pit:Adrenocorticotropic hormone, Growth hormone, prolactin, Follicle stimulating hormone, Luteinizing hormone, Thyroid stimulating hormone, melanocyte stimulating hormone. Posterior pit: oxytocin and antidiuretic hormone

Hypopituitarism - Underproduction of pituitary hormone may be congenital dysfunction, surgery, radiation, tumors - Newborn causes dwarfism slow growth and devt. Tx: Somatotropin ( Humatrope, Nutropin) Somatrem (protropin)

Hyperpituitarism
- Overproduction of pituitary hormone caused by benign tumors or adenoma - Gigantism hypersecretion of GH prior to closure of epiphysis - Acromegaly- oversecretion of GH in adults produces normal stature but enlarged feet, hands, and facial features Tx: chemotherapy, surgery, radiation to inactivate or remove the gland

NURSING IMPLICATIONS Pituitary Hormones 1. Children receiving somatropin for the treatment of growth disorders must be treated in a manner appropriate to their actual age. Assess height, weight, and body image disturbances. 2. Evening is the ideal time for the administration of somatropin. 3. Clients with diabetes mellitus receiving ACTH over a prolonged period of time may require an increase in insulin dosage. 4. Vasopressin preparations must be given on a regular schedule to avoid diuresis.

5. Clients receiving vasopressin are weighed daily, and blood pressure and intake and output records are kept while the client is hospitalized. Observe skin turgor and condition of mucous membranes. 6. Too much vasopressin is associated with water intoxication, low serum sodium levels, and constriction of smooth muscle, producing intestinal and uterine cramping. 7. Too little vasopressin is associated with diuresis and thirst.

Diabetes insipidus
- Deficiency or total absence of Antidiuretic hormone due to congenital deficiency of hormone or by surgery or tumor or trauma - Large volume of urine (polyuria), inability to concentrate urine, excessive thirst ( polydipsia) leading to dehydration and hypernatremia TX: antidiuretic hormone( vasopressin) - Lypressin- synthetic vasopressin given - Desmopressin intranasally

Thank You Very Much