Class IV antiarrhythmic drugs
block calcium channels. This action depresses phase 4 of depolarization and lengthens phases 1 and 2 of repolarization.
Class I antiarrhythmic drugs
block sodium channels.

depresses phase 0. And are local anasthetics or membrane stabilizing agents. (quinidine)

Class II antiarrhythmic drugs
block adrenergic receptors (beta blockers). Depresses phase 4 depolarization. Slows the heart rate and reduces contractility.(propanalol)
Class III antiarrhythmic drugs
 lengthen the duration of the action potential.

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Produces a prolonged phase 3 (repolarization).

1.    (26/9) DEFINE & DESCRIBE HYPERKALEMIA & THE ASSOCIATED PATHOPHYSIOLOGIC EFFECTS ON THE HEART.

a.    Increased extracellular potassium levels (hyperkalemia) result in depolarization of the membrane potentials of cells.

This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential. b.    After a short while, the open sodium channels inactivate and become refractory, increasing the threshold to generate an action potential.

This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. c.    Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.

2.

    (50/8a) DIFFERENTIATE THE MECHANISM OF ACTION, INDICATION FOR USE, METHODS OF ADMINISTRATION, COMMON ADVERSE EFFECTS OF, KEY POINTS TO PT. EDUCATION & NURSING IMPLICATIONS FOR LEVOTHYROXINE (Levoxyl, Synthroid).

 This medicine is a hormone replacement usually given to patients with thyroid problems, specifically, hypothyroidism. It is also given to people who have goitre or an enlarged thyroid gland.

a.    Mechanism of action: i.    Absorption from the GI tract varies from 48-79% of administered dose. Absorption is increased during fasting states.ii.    It must be converted to triiodothyronine (T3) for clinical effects.iii.

    PO- onset occurs very slowly w/ peak effect in 1-3 weeks.iv.    IV- to treat myxedema, onset is 6-8 hrs w/ peak effect in 24-48 hrs.

v.    Half life of 6-7 daysvi.    Metabolized in the liver, excreted in bile.vii.    Crosses placenta, enters breast milk.viii.

    Increased O2 consumption, respiration, heart rate, growth & maturation, speed of fat, protein and carbohydrate metabolism occur secondary to increase in the basal metabolic rate.b.    Indication for use:i.    Replacement therapy in hypothyroidism.ii.    Pituitary suppression of TSH in treating & preventing euthyroid goiteriii.    Management of hypothyroidism secondary to thyroid cancer.iv.

    Treating myxedema coma.v.    Used in conjunction w/ antithyroid drugs to treat thyrotoxicosis & prevent goiter formation, hypothyroidism & thyrotoxicosis during pregnancy.c.     Methods of administration:i.

    PO, IVd.    Common adverse effects:i.    Hypertensionii.    Tachycardiaiii.

    Arrhythmiasiv.    Anxietyv.    GI irritationvi.    Sweatingvii.    Heat intoleranceviii.    Headacheix.    Pt.

w/ sensitivity to lactose may show intolerance b/c lactose is used in the manufacture of this product.x.    In children, partial hair loss may occur in the 1st few months of therapy.

xi.    No allergic reactions to thyroid hormones.e.    Key points to pt. education:i.    Explain that this drug is a hormone that is being used to replace thyroid hormone that their body is not able to produce.1.    Responsible for regulating body’s metabolism.

2.    Most likely to take the drug for life & it should be taken everyday, preferably before breakfast.ii.    Report any increase in symptoms of thyroid dysfunction (wt. changes, nervousness, skin changes, lethargy, sleeplessness, rash/ lesion)iii.

    Avoid OTC drugsiv.    Keep out of children’s reachv.    Report any signs of hyperthyroidism (headache, nervousness, chest pain, palpitation, increased pulse rate, diarrhea, diaphoresis, or heat intolerance)vi.    Wear medical ID/ bracelet to alert emergency medical personnel of drug therapy.f.    Nursing implications:i.    Health status: 1.

    Drug history2.    Obtain baseline physical exam3.    Note any skin color, temp, texture, presence of lesions.4.    Assess thyroid hormone effectiveness.5.    Note muscle tone, weight, temp, BP, P, respirations6.

    Pt. w/ cardiac problems- begin w/ smaller doses7.    Monitor for angina & cardiac arrhythmias.ii.    Life Span & Gender:1.    Pre- & post- menopausal women2.    Age (geri should start w/ low dose.

Gradual increases will prevent serious CV & neurologic adverse effects)3.    If pulse is >100bpm, w/hold the dose.4.    Basal bone density5.    Monitor children for growth & development & for toxic effects.

Adjust dose as child grows.6.    Assess for pregnancy. May have adverse effect on fetal nervous system development.

iii.    Lifestyle, diet & habits:1.    Ability to adapt to long term regimen & establish a drug routine.2.    Not changing brandsiv.    Environment:1.    Assess environment.2.

    PO @ home3.    IV is only for myxedema coma; short- term until pt is able to take PO.v.    Maximizing therapeutic effects:1.    On empty stomach for best absorption.2.    Monitor CV response3.

    Assess serum thyroid levels & function4.    Monitor response to other drugs and to T4vi.    Minimizing adverse effects:1.    Individualize dose as ordered2.    Assess adrenal function in hypothyroidism3.

    Monitor insulin/ oral diabetic agent therapyvii.    Ongoing assessment:1.    Monitor serum thyroid hormone levels- reassess potential for drug interactions.2.    Assess pulse rate & rhythm3.

    Evaluate pt’s transition from hypothyroid to euthyroid stage.4.    Long term use may decrease hip & spine bone density in women- measure bone density before beginning T4 therapy.

3.    (26/1o) DEFINE, EXPLAIN & DIFFERENTIATE:a.    Atrial fibrillation: most common
i.    Caused by rapid, irregular discharge from ectopic foci  atrial quivering w/o any true diastole occurring.ii.    Impulses transmitted irregularly through AV node  irregular ventricular response (often rapid).iii.    Common causes:1.

    Acute- surgery, pulmonary disease, electrocution2.    CVD3.    Neurogenic- heightened vagal tone due to autonomic nervous system dysfunction.

4.    (50/8m) DIFFERENTIATE THE MECHANISM OF ACTION, INDICATION FOR USE, METHODS OF ADMINISTRATION, COMMON ADVERSE EFFECTS OF, KEY POINTS TO PT. EDUCATION & NURSING IMPLICATIONS FOR DESMOPRESSIN (DDAVP)
-Synthetic analogue of human ADH; for treatment neurogenic diabetes insipidus. -Major contraindications: presence of hemophilia A with factor VIII levels 5% or less -Most common adverse effects: localized erythema with intranasal administration; burning pain with parenteral injection.

-Maximizing therapeutic effects: Keep solutions (nasal, parenteral) refrigerated. – Minimizing adverse effects: Monitor urine volume/osmolarity, plasma osmolarity; patients with conditions associated with fluid/ electrolyte imbalances are prone to hyponatremia. -Most important patient education: Inform patients that medication bottle accurately delivers 25 to 50 doses and any solution remaining should be discarded because the amount delivered thereafter may be substantially less than prescribed.  

5.    (52/8b) DIFFERENTIATE THE MECHANISM OF ACTION, INDICATION FOR USE, METHODS OF ADMINISTRATION, COMMON ADVERSE EFFECTS OF, KEY POINTS TO PT. EDUCATION & NURSING IMPLICATIONS FOR BIGUANUDES (Metformin- prototype)

-Oral antihyperglycemic that increases peripheral tissue sensitivity to the effects of insulin and decreases hepatic glucose production. Is available commercially combined with glyburide to manage type 2 diabetes.

-Major contraindications: serious hepatic or renal function impairment.

-Most common adverse effects: nausea, diarrhea, abdominal bloating, flatulence, and anorexia; GI adverse effects appear to be dose related.

-Most serious adverse effects: lactic acidosis and hypoglycemia.

-Maximizing therapeutic effects: Individualize the dosage on the basis of both the effect and tolerance while not exceeding the maximum recommended daily dose.

-Minimizing adverse effects: Daily dosage of >2g should be divided into three doses taken at each meal; the drug should be taken with food to decrease adverse GI effects.

-Most important patient education: dietary restrictions for serum glucose control and weight loss.

 

6.    (52/9) IDENTIFY KEY POINTS FOR PATIENT & FAMILY EDUCATION FOR INSULIN THERAPY, ORAL HYPOGLYCEMIC AGENTS, HOME GLUCOSE MONITORING & RECOGNITION OF S&S OF HYPOGLYCEMIA.
a.

    Insulin therapyi.    Eat prescribed diet after insulin dosingii.    Don’t take any OTC drugs including herbs & alcoholiii.    Exerciseiv.    Stress might change insulin requirements b/c hormones released during stress are antagonistic to insulin.

v.    Learn to measure own blood glucose level- monitor periodically (before meals & bedtime) and regular insulin is given according to degree of glucose detected.vi.

    Perform aseptic technique, select appropriate type of insulin, mix insulin properly (if necessary), administer correctly by SC, rotate sites, store carefully.vii.    Replace needles to reduce risk for infections.b.

    Oral hypoglycemic agents    i.    S&S of hypoglycemia  treat w/ small amount of carbohydrates (hard candy, OJ or teaspoon of sugar)1.    Irritability2.

    confusion3.    nervousness4.    weakness5.    hungerii.    Alert to S&S of out of control diabetes1.

    Hyperglycemia- persistency by indicate a need to adjust glyburide dose or some other aspect of the therapeutic regimen.2.    polydipsia3.    polyphagia4.    polyuriaiii.    Avoid alcohol & OTC drugsiv.    Provide w/ oral & written info about the amount & timing of dosages.

7.

    (26/4) DIFFERENCIATE CLASS I, II, III, AND IV ANTIARRYTHMIC DRUGS.a.    Quinidine

i.    Pharmacotherapeutics:1.    Treat atrial arrhythmias including premature atrial, AV junctional, paroxysmal atrial tachycardia, paroxysmal AV junctional rhythm.

atrial flutter, paroxysmal & chronic atrial fibrillation.2.    Decreased in use for maintaining sinus rhythm.

3.    Maintenance therapy after electrical conversion of atrial fibrillation or flutter.4.    Non- cardiac use- treatment for life threatening Plasmodium falciparum malaria.ii.

    Pharmacokinetics1.    Absorbed from GI tract2.    Quinidine gluconate= 62% active quinidine3.    Quinidine polygalacturonate= 80%4.    Quinidine sulfate= 83%5.

    Distributes to all body tissue except for the brain6.    Fairly highly protein bound= 80-90%7.    Metabolized by the liver; excreted unchanged by the kidneys8.

    Acid urine promotes elimination9.    Cirrhosis may have prolonged ½ life & increased volume of distribution.10.    CHF may decrease total clearance & volume of distribution.iii.    Pharmacodynamics1.    Depresses myocardial excitability, conduction velocity & contractility.2.

    Effective refractory period is prolonged  increased conduction time  re-entry phenomenon prevented.3.    Exerts indirect anticholinergic effect- decreases vagal tone & may promote conduction in the AV junction.4.    In patients w/o structural heart disease, the use of Class I drugs rarely causes proarrhythmia serious enough to be life threatening.5.    Drugs that prolong the action potential only (Class I) are not the answer for decreasing mortality.6.

    Decrease # of shocks.7.    Membrane stabilizer

  8.

Define, explain, and differentiate action potential.

All changes that occur in the transmembrane potential during an entire cycle of contraction and relaxation, as a unit.    
9. Differentiate the mechanism of action, indication for use, methods of administration, common adverse effects of, key points for patient education, and nursing implications for Liothyroxine.

 

Indications and Usage: Thyroid hormone drugs are indicated:

Treating low thyroid function. It is also used to treat or prevent different types of goiters, as an aid to diagnose certain thyroid conditions, or to treat patients who are allergic to other thyroid medicines. It may also be used for other conditions as determined by your doctor. Cytomel is a thyroid hormone. It works by replacing or supplementing the natural thyroid hormones in the body. 1.        As replacement or supplemental therapy in patients with hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis.

This category includes cretinism, myxedema and ordinary hypothyroidism in patients of any age (pediatric patients, adults, the elderly), or state (including pregnancy); primary hypothyroidism resulting from functional deficiency, primary atrophy, partial or total absence of thyroid gland, or the effects of surgery, radiation, or drugs, with or without the presence of goiter; and secondary (pituitary) or tertiary (hypothalamic) hypothyroidism (see WARNINGS). 2.        As pituitary thyroid-stimulating hormone (TSH) suppressants, in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute or chronic lymphocytic thyroiditis (Hashimoto’s) and multinodular goiter. 3.        As diagnostic agents in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy. Cytomel (liothyronine sodium) Tablets can be used in patients allergic to desiccated thyroid or thyroid extract derived from pork or beef.

Contraindications: Thyroid hormone preparations are generally contraindicated in patients with diagnosed but as yet uncorrected adrenal cortical insufficiency, untreated thyrotoxicosis and apparent hypersensitivity to any of their active or extraneous constituents. There is no well-documented evidence from the literature, however, of true allergic or idiosyncratic reactions to thyroid hormone.

Drug Interactions

Oral Anticoagulants Thyroid hormones appear to increase catabolism of vitamin K-dependent clotting factors. If oral anticoagulants are also being given, compensatory increases in clotting factor synthesis are impaired. Insulin or Oral Hypoglycemics: Initiating thyroid replacement therapy may cause increases in insulin or oral hypoglycemic requirements. Cholestyramine: Cholestyramine binds both T4 and T3 in the intestine, thus impairing absorption of these thyroid hormones.

How Supplied: Cytomel (liothyronine sodium) Tablets: 5 mcg in bottles of 100; 25 mcg in bottles of 100; and 50 mcg in bottles of 100.

10. Differentiate the mechanism of action, indication for use, methods of administration, common adverse effects of, key points for patient education, and nursing implications for Biguanides.

Oral antihyperglycemic that increases peripheral tissue sensitivity to the effects of insulin and decreases hepatic glucose production. Is available commercially combined with glyburide to manage type 2 diabetes.

-Major contraindications: serious hepatic or renal function impairment.

-Most common adverse effects: nausea, diarrhea, abdominal bloating, flatulence, and anorexia; GI adverse effects appear to be dose related.

-Most serious adverse effects: lactic acidosis and hypoglycemia.

-Maximizing therapeutic effects: Individualize the dosage on the basis of both the effect and tolerance while not exceeding the maximum recommended daily dose.

-Minimizing adverse effects: Daily dosage of >2g should be divided into three doses taken at each meal; the drug should be taken with food to decrease adverse GI effects.

-Most important patient education: dietary restrictions for serum glucose control and weight loss.

11. Differentiate the mechanism of action, indication for use, methods of administration, common adverse effects of, key points for patient education, and nursing implications for Alpha glucosidase inhibitors

Mechanism of action

-Alpha-glucosidase inhibitors are saccharides that act as competitive inhibitors of enzymes needed to digest carbohydrates: specifically alpha-glucosidase enzymes in the brush border of the small intestines.

The membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Acarbose also blocks pancreatic alpha-amylase in addition to inhibiting membrane-bound alpha-glucosidases. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine. Inhibition of these enzyme systems reduces the rate of digestion of carbohydrates. Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules.

In diabetic patients, the short-term effect of these drugs therapies is to decrease current blood glucose levels: the long term effect is a small reduction in hemoglobin A1c level.[1] Dosing -Since alpha-glucosidase inhibitors are competitive inhibitors of the digestive enzymes, they must be taken at the start of main meals to have maximal effect. Their effects on blood sugar levels following meals will depend on the amount of complex carbohydrates in the meal. Side effects – Since alpha-glucosidase inhibitors prevent the degradation of complex carbohydrates into glucose, the carbohydrates will remain in the intestine. In the colon, bacteria will digest the complex carbohydrates, thereby causing gastrointestinal side effects such as flatulence and diarrhea. Since these effects are dose-related, it is generally advised to start with a low dose and gradually increase the dose to the desired amount. Voglibose, in contrast to acarbose, has less of these side effects, and is hence preferred lately[citation needed].

It is also more economical compared to acarbose[citation needed]. If a patient using an alpha-glucosidase inhibitor suffers from an episode of hypoglycemia, the patient should eat something containing monosaccharides, such as glucose tablets. Since the drug will prevent the digestion of carbohydrates, non-monosaccharide foods may not effectively reverse a hypoglycemic episode in a patient taking an alpha-glucosidase inhibitor.

Role in clinical use

Alpha-glucosidase inhibitors are used to establish greater glycemic control over hyperglycemia in diabetes mellitus type 2, particularly with regard to postprandial hyperglycemia. They may be used as monotherapy in conjunction with an appropriate diabetic diet and exercise, or they may be used in conjunction with other anti-diabetic drugs. Alpha-glucosidase inhibitors may also be useful in patients with diabetes mellitus type 1; however, this use has not been officially approved by the Food and Drug Administration.

13.

Differentiate the mechanism of action, indication for use, methods of administration, common adverse effects of, key points for patient education, and nursing implications for Calcitriol.

-Vitamin D; management of hypocalcemia and resultant bone disese in patients undergoing chronic renal dialysis. -Major contraindications: Hypercalcemia, hypervitaminosis D, malabsorption syndrome, and decreased renal function. – Most common adverse effects: weakness, headache, somnolence, nausea, vomiting, dry mouth, constipation, muscle or bone pain, and metallic taste. – Most serious adverse effect: chronic hypercalcemia can lead to generalized vascular calcification, nephrocalcinosis, and other soft tissue calcification. -Maximizing therapeutic effects: Patients with normal renal function taking calcitriol should maintain adequate fluid intake and avoid dehydration; periodically monitor serum calcium, phosphate, magnesium, alkaline phosphatase, and 24-hour urinary calcium and phosphate,  especially in hypoparathyroid and dialysis patients. -Minimizing adverse effects: Maintain serum calcium levels between 9 and 10 mg/dl.

– Most important patient education: Adequate dietary calcium is necessary for a clinical response to vitamin D therapy; compliance with dosage instructions, diet, and phosphate-binder use, and calcium supplementation is essential; avoid use of nonprescription drugs, including magnesium-containing antacids.

14.  Identify the indication for use, onset of action, peak action time, and duration of action, and methods of administration for the following types of insulin and determine when a hypoglycemic episode is most likely to occur with Glargine
-Glargine is a long-acting basal insulin analogue, usually given once or twice daily to help control the blood sugar level of those with diabetes.

Its theoretical advantage is that it has a duration of action up to 24 hours, with a "less peaked" profile than NPH. – In type 2 diabetes and in combination with a short acting sulfonylurea (drugs which stimulate the pancreas to make more insulin), it can offer moderate control of serum glucose levels. -Extreme caution must be used not to confuse Glargine for regular insulin because serious adverse effects, such as hypoglycemia, can occur.

15. Differentiate the mechanism of action, indication for use, methods of administration, common adverse effects of, key points for patient education, and nursing implications for Methimazole (MMI).

– Inhibits the synthesis of thyroid hormones; antithyroid agent -Major contraindications: sensitivity to the drug; nursing mothers, because the drug is excreted in breast milk. – Most common adverse effects: GI (nausea, vomiting, epigastric pain), itching, rash, hives, and arthralgia. – Most serious adverse effects: Agranulocytosis, liver damage, aplastic anemia, and vasculitis. Most adverse effects resolve spontaneously with discontinuation of the drug. -Maximizing therapeutic effects: Administer drug around the clock at 8-hour intervals, although it can be given in a single daily dose.

-Minimizing adverse effects: periodic blood tests to assess  bone marrow function and bleeding tendencies, -Most important patient education: Drug must be taken for prolonged period (months) to achieve the desired effects; report fever, sore throat, unusual bleeding or bruising, and malaise.     

Class I antiarrhythmic drugs Blocks sodium channels. Depresses phase 0. act as anesthetic. (quinidine) Class II antiarrhythmic drugs Blocks adrenergic receptors.

Depresses phase 4 depolarization. Slows the heart rate and reduces contractility. (propanalol) Class III antiarrhythmic drugs Lengthens the duration of action potentials.

Produces a prolonged phase 3 (repolarization) Class IV antiarrhythmic drugs Blocks calcium channels. Depresses phase 4 of depolarization and lengthens phase 1 and 2 of repolarization   LEVOTHYROXINE Replacement therapy in hyperthyroidism, and treatment for myxedema coma. Atrial fibrillation Caused by rapid, irregular discharge from ectopic foci à atrial quivering w/o any true diastole occurring.

  DESMOPRESSIN Synthetic analogue of human ADH; for treatment neurogenic diabetes insipidus.   BIGUANUDES (Metformin) -Oral antihyperglycemic that increases peripheral tissue sensitivity to the effects of insulin and decreases hepatic glucose production. Is available commercially combined with glyburide to manage type 2 diabetes.   Quinidine Depresses myocardial excitability, conduction velocity & contractility.   Calcitriol -Vitamin D; management of hypocalcemia and resultant bone disese in patients undergoing chronic renal dialysis.   Glargine -Glargine is a long-acting basal insulin analogue, usually given once or twice daily to help control the blood sugar level of those with diabetes.

Its theoretical advantage is that it has a duration of action up to 24 hours, with a "less peaked" profile than NPH.    Methimazole (MMI). – Inhibits the synthesis of thyroid hormones; antithyroid agent