Endocrine Drugs 2003

8/3/2019 Endocrine Drugs 2003

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Endocrine System

Lecturer: Dante RoelFernandez RT, M.D.


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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 processesof cells when they react with their specific receptor sites

5. they are immediately broken down.


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PANCREAS:

- both an endocrine gland (produceshormones in islets of Langerhans) and an

exocrine gland(release sodium bicarbonate

and pancreaticenzymes directly into with CBD).

- islets of Langerhans- with endorine cells-

alpha cells (release glucagon), beta cells(release insulin) and delta cells (block release

of glucagon and insulin).


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IN

SULIN

:

1. stimulates transport of glucose into the

cells to be used for energy

2. stimulates synthesis of glycogen3. stimulates conversion of lipids into fat

stored in the form of adipose tissue

4. stimulates synthesis of proteins fromamino acids.


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METABOLIC CONSEQUENCES OF INSULIN

DEFICIENCY

1. Hyperglycemia- increased blood sugar

2. Glycosuria

- concentration of glucose in the blood too

high for incomplete reabsorption- spillage ofsugar into the urine-prone to cystitis

3. Fatigue

- bodys cells cannot use the glucose for

energy4. Polyphagia

- hypothalamic centers deprived of glucose-

sensation of starving-increased eating


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5. Polydipsia - increased glucose and waste

products in the blood loss of fluid with

glucose in the urine-increased blood tonicity-increased thirst.

6. Polyuria - spillage of glucose in the urine

osmotic diuresis

7. increased lipolysis or fat breakdown- bodybreaks down stored fat for energy-

accumulation 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


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DIABETES MELLITUS- literally means honey-urine

2 Types:1. Type I ( IDDM)

- associated with rapid onset, mostly in

younger people


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2. Type II (NIDDM)

- mature onset

- slow & progressive onset

- impaired sensitivity of insulinreceptor sites


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-Increased incidence of a number of disordersincluding:

1. Atherosclerosis lead to heart attacks and

strokes2. 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


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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.PZ

I ( Humulin U)Adverse Effects: hypoglycemia and ketoacidosis

Drug Interactions: - MAO inhibitors, B-blockers, salicylates

and alcohol


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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 damagingmuscles

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 dosing5. Store insulin in a cool place away from direct sunlight.


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6. Monitor patients during times of trauma and

severe stress for potential dosage adjustmentneeds.

7. Instruct patients also receiving beta

blockers in ways to monitor glucose levels andsigns and symptoms of glucose abnormalities

to prevent hypo & hyperglycemic episodes

when SNS and warning signals are blocked

8. Provide thorough patient teaching


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Signs and Symptoms

Of Hypo & Hyperglycemia

Hypoglycemia Hyperglycemia

Onset Sudden, anxious pt,

Drunk, miss meal, stress

Gradual, slow &sluggish

Inc. stress

CNS HA, blurred vision,drowsy,coma,

ataxia, h-active reflexes

Dec.level of consc.,sluggish,

coma,hypoactive ref.

Neuromuscular Paresthesias, weak, muscle

spasms, twitching to seizures

Weakness, lethargy

CV Tachycardia, palpitations, N to Inc.

BP

Tachycardia,

hypotension

Respiratory

GI

Rapid, shallow

Hunger, nausea

Rapid, deep, fruity breath

Nausea, vomit, thirst

Others

Lab Tests

Diaphoresis, cool, clammy,

bld. Glu-

Uring glucose (-), low

Dry, warm, flushed skin, soft

eyeballs,UG-(+)

(+) urine ketones, High Glu


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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 ofADH on renal cells

- effective only in patients with functioning

beta cells


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CLA

SSIFICA

TION

: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 renaldysfunction, readily cleared from the body

d. Tolazamide


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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. Glipizidec. Glyburide


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ADVERSE EFFECTS:1. Hypoglycemia

2. GI distress; nausea, vomiting, epigastric

discomfort, heartburn, anorexia

3. allergic skin reactions4. increased risk of cardiovascular mortality

* caution should be used with:

1. beta blockers-may mask the signs ofhypoglycemia

2. alcohol-lead to altered glucose levels


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B. Non-Sulfonylureas

- structurally unrelated to sulfonylureas

- effective when used in combination withsulfonylureas 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


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2. Metformin (Glucophage)

- decreases the production of and increases theuptake of glucose

- effective in lowering bood glucose levels

- associated with development with lactic acidosis

- can cause GI distress3. Miglitol

an alpha glucosidase inhibitor

- delays absorption of carbohydrates-smaller rise in

blood glucose following meals and a decrease inglycosylated Hgb (glucose carried in rbc)

- does not enhance insulin secretion


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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 prandialglucose levels

- can be used in combination with metformin.


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NURSING CONSIDERATIONS:

1. Administer drug as prescribed in relation to meals

to ensure therapeutic effectiveness2. 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


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GLUCOSE-ELEVATINGAGENTS:

Hypoglycemia- abnormally low blood sugar (< 40 mg/dl)

- associated with:

1. pancreatic disorders

2. kidney disease3. certain cancers

4. disorders of anterior pituitary

5. unbalanced treatment of DM

Treatment: increase blood glucose level bydecreasing insulin release and accelerating

breakdown of glycogen in the liver to release

glucose


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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


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2. Glucagon

- can only be given parenterally; preferred for

emergency situations- associated withGI 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 occurs3. Monitor nutritional status

4. Monitor patients receiving diazoxide for potent CV

effects including BP, heart rhythm and output, and

weight changes


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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 Tyrosine3. Formation of T3 and T4 by coupling

4. Secretion

5. Peripheral Conversion of T4 and T3


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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


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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 ugiodine

- to provide enough iodine, other regions inject

iodized oil

- most practical = addition of iodide to table salt=1gram iodized salt= 100 ug iodine


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CLINICAL DIAGNOSIS:

Hypothyroidism deficiency in thyroid hormoneexample- congenital cretinism in children;absent or

atrophic thyroid gland

- post thyroidectomy

- post radioactive iodine therapy

- myxedemas when severessx- 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


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GOITER (Thyroid

enlargement)


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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 movement2 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


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Antithyroid Drugs

1. Propylthiouracil(PTU)

2. Methimazole (Tapazole)

action: inhibition of coupling of iodine to

tyrosine prevention of formation of thyroidhormones

- PTU also prevent conversion of T4 to T3 inthe peripheral circulation


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Adverse effects

- uncommon, however ranges from a mildrash to a agranulocytosis


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Iodides

- Useful in treating mild cases of hyperthyroidism esp. in

young clients

Action: inhibit thyroid hormone production by inhibitingthyrotropin (+) of thyroid secretion

- Can be given in several types of solution

- Lugols soln.

- Saturated solution of potassium iodide (SSKI)


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Clinical uses of Iodine

1.S

odium iodide1

31

- use for diagnostic and treatment of

hyperthyroidism


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Other drugs used for hyperthyroidism

1. Ionic inhibitorsK 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


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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.


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6. Several days following 1131 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 followstress, surgery, or withdrawal of antithyroid drugs. It is

characterized by fever, tachycardia, congestive heart failure

and CNS disturbances.


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Surgery

- Surgical removal of the gland is effective

treatment of hyperthyroidism

COMPLICATION:- hypothyroidism and

hypoparathyroidism


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PARATHYROID DISORDERS- Pinhead-sized gland located at the back

of the thyroid gland

- Produces parathyroid hormone

- increases blood Ca level


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Hypoparathyroidism

- Deficiency of parathyroid hormone due to:congenital absence of gland

surgery

-S/S

x: increased neuromuscular irritability,psychiatric disorders

Treatment:

- replenish Ca by IV Ca chloride and Ca

gluconate

- Vit D may also be given


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Hyperparathyroidism

- Hypersecretion of parathyroid hormone maybe 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


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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 bodytemperature 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.


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5. Extravasation of intravenously infused calcium may result

in tissue necrosis and sloughing.

6

. Calcium should not be added to an IV line containingbicarbonate 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 cardiacirregularities.

9. Clients may experience flushing of the face and a feeling of

warmth following calcitonin injection. This is common and will

disappear without treatment.


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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


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Hypopituitarism

- Underproduction of pituitary hormone

may be congenital dysfunction, surgery,

radiation, tumors

- Newborn causes dwarfism slow growthand devt.

Tx: Somatotropin ( Humatrope, Nutropin)

Somatrem (protropin)


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Hyperpituitarism

- Overproduction of pituitary hormone caused bybenign 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 toinactivate or remove the gland


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NURSING IMPLICATIONS

Pituitary Hormones1. 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.


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5. Clients receiving vasopressin are weighed

daily, and blood pressure and intake andoutput 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.


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Diabetes insipidus

- Deficiency or total absence of Antidiuretic hormonedue 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


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Thank You Very Much

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Endocrine Drugs 2003

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