Test Bank for Pharmacology and the Nursing Process 10th Edition By Linda Lilley, Shelly Collins, Julie Snyder Chapter 1-58 TEST WITH LATEST UPDATED (QUESTIONS AND ANSWERS) already passed!!

bronchodilators overview

Bronchodilators are an important part of the pharmacotherapy for all respiratory diseases. These drugs relax bronchial smooth muscle, which causes dilation of the bronchi and bronchioles that are narrowed as a result of the disease process. There are three classes of such drugs: beta adrenergic agonists, anticholinergics, and xanthine derivatives.

beta andregenic drug overview

The beta-adrenergic agonists are a group of drugs that are commonly used during the acute phase of an asthmatic attack to quickly reduce airway constriction and restore airflow to normal. They are agonists of the adrenergic receptors in the sympathetic nervous system. The beta and alpha adrenergic receptors are discussed in Chapters 18 and 19. The beta agonists imitate the effects of norepinephrine on beta receptors. For this reason, they are also called sympathomimetic bronchodilators. The beta agonists are categorized by their onset of action. Short-acting beta agonist (SABA) inhalers include albuterol (Ventolin), levalbuterol (Xopenex), pirbuterol (Maxair), terbutaline (Brethine), and metaproterenol (Alupent). Long-acting beta agonist (LABA) inhalers include arformoterol (Brovana), formoterol (Foradil, Perforomist), and salmeterol (Serevent). The newest long-acting beta agonists are indacterol (Arcapta Neohaler); vilanterol in conjunction with fluticasone (Breo Ellipta); and vilanterol in conjunction with the anticholinergic umeclidinium (Anoro Ellipta). The term Ellipta refers to a new delivery system. Because the long-acting beta agonists (LABAs) have a longer onset of action, they must never be used for acute treatment. Patients must be taught to use the short-acting beta agonist (SABA) as rescue treatment.

short acting beta agonist

albuterol (Ventolin), levalbuterol (Xopenex), pirbuterol (Maxair), terbutaline (Brethine), and metaproterenol (Alupent).

Albuterol

Class : beta 2 agonist (short acting)

Indications and mechanisms of action: is a short-acting beta2-specific bronchodilating beta agonist. Other similar drugs include bitolterol (Tornalate), levalbuterol (Xopenex), pirbuterol (Maxair), and terbutaline (Brethine). Albuterol is the most commonly used drug in this class. If albuterol is used too frequently, dose-related adverse effects may be seen, because albuterol loses its beta2-specific actions, especially at larger dosages

Contraindications :. As a consequence, the beta1 receptors are stimulated, which causes nausea, increased anxiety, palpitations, tremors, and an increased heart rate.

Route: po and inhalation

Other facts: levorotatory isomeric form of albuterol, levalbuterol, is sometimes prescribed as an albuterol alternative for patients with certain risk factors (e.g., tachycardia, including tachycardia associated with albuterol treatment). (Lilley 583)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

long acting beta agonist

arformoterol (Brovana), formoterol (Foradil, Perforomist), and salmeterol (Serevent). The newest long-acting beta agonists are indacterol (Arcapta Neohaler); vilanterol in conjunction with fluticasone (Breo Ellipta); and vilanterol in conjunction with the anticholinergic umeclidinium (Anoro Ellipta)

beta andregenic mechanism of action and drug effect

The beta agonists relax and dilate airways by stimulating the beta2-adrenergic receptors located throughout the lungs.

582

There are three subtypes of these drugs, based on their selectivity for beta2 receptors:

1. Nonselective adrenergic drugs, which stimulate the beta, beta1 (cardiac), and beta2 (respiratory) receptors. Example: epinephrine. (NOTE: Epinephrine inhalers were taken off the market in 2012 because they did not comply with FDA requirements). Epinephrine is available as a prefilled syringe for self-administration by patients with severe allergic reactions and is called EpiPen (Figure 37-2).

2. Nonselective beta-adrenergic drugs, which stimulate both beta1 and beta2 receptors. Example: metaproterenol.

3. Selective beta2 drugs, which primarily stimulate the beta2 receptors. Example: albuterol.

These drugs can also be categorized according to their routes of administration as oral, injectable, or inhaled. The various beta agonist bronchodilators are listed in Table 37-3. The bronchioles are surrounded by smooth muscle. When the smooth muscle contracts, the airways are narrowed and the amount of oxygen and carbon dioxide exchanged is reduced. The action of beta agonist bronchodilators begins at the specific receptor stimulated and ends with the relaxation and dilation of the airways. However, many reactions must take place at the cellular level for bronchodilation to occur. When a beta2-adrenergic receptor is stimulated by a beta agonist, adenylate cyclase is activated and produces cyclic adenosine monophosphate (cAMP). Adenylate cyclase is an enzyme needed to make cAMP. The increased levels of cAMP cause bronchial smooth muscles to relax, which results in bronchial dilation and increased airflow into and out of the lungs.

Nonselective adrenergic agonist drugs such as epinephrine also stimulate alpha-ad

indications of beta andregenics

The primary therapeutic effect of the beta agonists is the prevention or relief of bronchospasm related to bronchial asthma, bronchitis, and other pulmonary diseases. However, they are also used for effects outside the respiratory system. Because some of these drugs have the ability to stimulate both beta1- and alpha-adrenergic receptors, they may be used to treat hypotension and shock (see Chapter 18).

contraindications for beta andregenics

drug allergy, uncontrolled hypertension or cardiac dysrhythmias, and high risk for stroke (because of the vasoconstrictive drug action)

adverse effects of beta andregenics

Mixed alpha/beta agonists produce the most adverse effects because they are nonselective. These include insomnia, restlessness, anorexia, cardiac stimulation, hyperglycemia, tremor, and vascular headache. The adverse effects of the nonselective beta agonists are limited to beta-adrenergic effects, including cardiac stimulation, tremor, anginal pain, and vascular headache. The beta2 drugs can cause both hypertension and hypotension, vascular headaches, and tremor. Overdose management may include careful administration of a beta blocker while the patient is under close observation due to the risk for bronchospasm. Because the half-life of most adrenergic agonists is relatively short, the patient may just be observed while the body eliminates the medication.

interactions with beta andregenics

When nonselective beta blockers are used with the beta agonist bronchodilators, the bronchodilation from the beta agonist is diminished. The use of beta agonists with monoamine oxidase inhibitors and other sympathomimetics is best avoided because of the enhanced risk for hypertension. Patients with diabetes may require an adjustment in the dosage of their hypoglycemic drugs, especially patients receiving epinephrine, because of the increase in blood glucose levels that can occur.

Salmeterol (Serevent Diskus) (Lilley 583)

Class : long acting beta 2 agonist

is a long-acting beta2 agonist bronchodilator. Other long-acting inhalers include formoterol (Foradil, Perforomist), arformoterol (Brovana), and indacterol (Arcapta Neohaler). The long-acting inhalers are never to be used for acute treatment. Salmeterol is used for the maintenance treatment of asthma and COPD and is used in conjunction with an inhaled corticosteroid. It is given twice daily for maintenance treatment only. In 2006, a large randomized clinical trial showed that use of salmeterol was associated with an increase in asthma-related deaths (when added to usual asthma therapy). The risk appears to be higher in African-American patients. All LABAs have a black box warning regarding this risk. Adverse effects include immediate hypersensitivity reactions, headache, hypertension, and neuromuscular and skeletal pain. Salmeterol should never be given more than twice daily nor should the maximum daily dose (one puff twice daily) be exceeded. It is available as a powder for inhalation either alone (Serevent Diskus) or combined with a corticosteroid (Advair). The long-acting inhalers, including salmeterol, are not to be used alone, but in combination with other drugs such as the inhaled corticosteroids. Advair (salmeterol and fluticasone) is a very popular inhaler for COPD. Symbicort, a newer inhaler consisting of the corticosteroid budesonide and the bronchodilator formoterol, is similar to Advair as is Dulera, which is a combination of formoterol and mometasone. (Lilley 583)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Anti cholinergics mechanism of action and drug affects

On the surface of the bronchial tree are receptors for acetylcholine (ACh), the neurotransmitter for the parasympathetic nervous system (PSNS). When the PSNS releases ACh from its nerve endings, it binds to the ACh receptors on the surface of the bronchial tree, which results in bronchial constriction and narrowing of the airways. Anticholinergic drugs block these ACh receptors to prevent bronchoconstriction. This indirectly causes airway relaxation and dilation. Anticholinergic agents also help reduce secretions in COPD patients. (Lilley 584)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Indications of anti cholinergics

Because their actions are slow and prolonged, anticholinergics are used for the prevention of bronchospasm associated with chronic bronchitis or emphysema and not for the management of acute symptoms. (Lilley 584)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Contraindications to anticholinergics

The only usual contraindication to the use of bronchial anticholinergic drugs is known drug allergy, including allergy to atropine. In the past, an allergy to peanuts or soy was listed as a contraindication to ipratropium inhalers. This was related to the propellant used, and the new HFA inhalers have eliminated the concern. Thus, there is no contraindication using ipratropium in patients with peanut or soy allergies. Caution is necessary in patients with acute narrow-angle glaucoma and prostate enlargement (Lilley 584)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Adverse effects to anticholinergics

The most commonly reported adverse effects of inhaled anticholinergics are related to their pharmacology and include dry mouth or throat, nasal congestion, heart palpitations, gastrointestinal (GI) distress, urinary retention, increased intraocular pressure, headache, coughing, and anxiety. Ipratropium is classified as a pregnancy category B drug; all others in this class are pregnancy category C.

(Lilley 584)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Drug interactions anticholinergics

Possible additive toxicity may occur when anticholinergic bronchodilators are taken with other anticholinergic drugs.

(Lilley 584)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Ipratropium (Atrovent)

Class : anticholinergic

Indications and mechanisms of action : is the oldest anticholinergic bronchodilator. It is pharmacologically very similar to atropine (see Chapter 21). It is available both as a liquid aerosol for inhalation and as a multidose inhaler; both forms are usually dosed twice daily. Tiotropium (Spiriva) and aclidinium (Tudorza) are similar drugs. Spiriva is given once a day, whereas Tudorza is given twice daily. Many patients also benefit from taking both a beta2 agonist and an anticholinergic drug, with the most popular combination being albuterol and ipratropium. Although many patients receive the two drugs separately, two combination products are available containing both of these drugs: Combivent (an MDI) and DuoNeb (an inhalation solution). (Lilley 584)

Route : inhaler

Xanthine Derivatives overview

The natural xanthines consist of the plant alkaloids caffeine, theobromine, and theophylline, but only theophylline and caffeine are currently used clinically. Synthetic xanthines include aminophylline and dyphylline. Caffeine, which is actually a metabolite of theophylline, has other uses described later in the chapter. (Lilley 584)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Xanthine mechanism of action

Xanthines cause bronchodilation by increasing the levels of the energy-producing substance cAMP. They do this by competitively inhibiting phosphodiesterase, the enzyme responsible for breaking down cAMP. In patients with COPD, cAMP plays an integral role in the maintenance of open airways. Higher intracellular levels of cAMP contribute to smooth muscle relaxation and also inhibit IgE-induced release of the chemical mediators that drive allergic reactions (histamine, slow-reacting substance of anaphylaxis, and others).

Theophylline is metabolized to caffeine in the body, whereas aminophylline is metabolized to theophylline. Theophylline and other xanthines stimulate the CNS, but to a lesser degree than caffeine. This stimulation of the CNS has the beneficial effect of acting directly on the medullary respiratory center to enhance respiratory drive. In large doses, theophylline may stimulate the cardiovascular system, which results in both an increased force of contraction (positive inotropy) and an increased heart rate (positive chronotropy). The increased force of contraction raises cardiac output and hence blood flow to the kidneys. This, in combination with the ability of the xanthines to dilate blood vessels in and around the kidney, increases the glomerular filtration rate, which produces a diuretic effect. (Lilley 584)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Xanthine Indications

Xanthines are used to dilate the airways in patients with asthma, chronic bronchitis, or emphysema. They may be used in mild to moderate cases of acute asthma and as an adjunct drug in the management of COPD. Xanthines are now deemphasized because of their potential for drug interactions and the interpatient variability in therapeutic drug levels in the blood. Because of their relatively slow onset of action, xanthines are used for the prevention of asthmatic symptoms and COPD, not for the relief of acute asthma attacks.

Caffeine is used without prescription as a CNS stimulant, or analeptic (see Chapter 13), to promote alertness (e.g., for long-duration driving or studying). It is also used as a cardiac stimulant in infants with bradycardia and for enhancement of respiratory drive in infants. (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Xanthine contraindications

Contraindications to therapy with xanthine derivatives include known drug allergy, uncontrolled cardiac dysrhythmias, seizure disorders, hyperthyroidism, and peptic ulcers. (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Xanthine adverse effects

The common adverse effects of the xanthine derivatives include nausea, vomiting, and anorexia. Cardiac adverse effects include sinus tachycardia, extrasystole, palpitations, and ventricular dysrhythmias. Transient increased urination and hyperglycemia are other possible adverse effects. Overdose and other toxicity of xanthine derivatives are usually treated by the repeated administration of doses of activated charcoal. (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Xanthine interactions

The use of xanthine derivatives with any of the following drugs causes an increase in the serum level: allopurinol, cimetidine, macrolide antibiotics (e.g., erythromycin), quinolones (e.g., ciprofloxacin), influenza vaccine, and oral contraceptives. Their use with sympathomimetics, or even caffeine, can produce additive cardiac and CNS stimulation. Rifampin increases the metabolism of theophylline, which results in decreased theophylline levels. St. John's wort enhances the metabolism of xanthine drugs; thus, higher dosages of theophylline may be needed. Cigarette smoking has a similar effect because of the enzyme-inducing effect of nicotine. Interacting foods include charcoal-broiled, high-protein, and low-carbohydrate foods. These foods may reduce serum levels of xanthines through various metabolic mechanisms. (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Theophylline (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Class : xanthine derivative

Indications and mechanisms of action: is the most commonly used xanthine derivative, albeit not often used. It is available in oral, rectal, injectable (as aminophylline), and topical dosage forms. Besides theophylline, the other xanthine bronchodilator used clinically for the treatment of bronchoconstriction is aminophylline. Aminophylline is a prodrug of theophylline; it is metabolized to theophylline in the body. Aminophylline is sometimes given intravenously to patients with status asthmaticus who have not responded to fast-acting beta agonists such as epinephrine.

The beneficial effects of theophylline can be maximized by maintaining blood levels within a certain target range. If these levels become too high, unwanted adverse effects can occur. If the levels become too low, the patient receives little therapeutic benefit. Although the optimal level may vary from patient to patient, most standard references have suggested that the therapeutic range for theophylline blood level is 10 to 20 mcg/mL. However, most prescribers now advise levels between 5 and 15 mcg/mL. Laboratory monitoring of drug blood levels is common to ensure adequate dosage, especially in the hospital setting. (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Non-Bronchodilating Drugs

Bronchodilators (beta-adrenergic agonists, anticholinergics, and xanthines) are just one type of drug used to treat asthma, chronic bronchitis, and emphysema. There are also other drugs that are effective in suppressing the various underlying causes of some of these respiratory illnesses. These include leukotriene receptor antagonists (montelukast, zafirlukast, and zileuton) and corticosteroids (beclomethasone, budesonide, dexamethasone, flunisolide, fluticasone, ciclesonide, and triamcinolone). Another drug class known as mast cell stabilizers is now rarely used. However, these drugs are still listed in the national guidelines as alternative therapy and include cromolyn and nedocromil; they are sometimes used for exercise-induced asthma. As their class name implies, they work by stabilizing the cell membranes of mast cells to prevent the release of inflammatory mediators such as histamine. (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Leukotriene Receptor Antagonists

When they became available in the 1990s, the leukotriene receptor antagonists (LTRAs) were the first new class of asthma medications to be introduced in more than 20 years.

Before the development of LTRAs, most asthma treatments focused on relaxing the contraction of bronchial muscles with bronchodilators. More recently, researchers have begun to understand how asthma symptoms are caused by the immune system at the cellular level. A chain reaction starts when a trigger allergen, such as cat hair or dust, initiates a series of chemical reactions in the body. Several substances are produced, including a family of molecules known as leukotrienes. In people with asthma, leukotrienes cause inflammation, bronchoconstriction, and mucus production. This in turn leads to coughing, wheezing, and shortness of breath. (Lilley 585)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

LTRA mechanism of action

Currently two subclasses of LTRAs are available. These subclasses differ in the mechanism by which they block the inflammatory process in asthma. The first subclass of LTRAs acts by an indirect mechanism and inhibits the enzyme 5-lipoxygenase, which is necessary for leukotriene synthesis. Zileuton (Zyflo) is the only drug of this type currently available. Drugs in the second subclass of LTRAs act more directly by binding to the D4 leukotriene receptor subtype in respiratory tract tissues and organs. These drugs include montelukast (Singulair) and zafirlukast (Accolate).

The drug effects of LTRAs are primarily limited to the lungs. As their name implies, LTRAs prevent leukotrienes from attaching to receptors located on circulating immune cells (e.g., lymphocytes in the blood) as well as local immune cells within the lungs (e.g., alveolar macrophages). This alleviates asthma symptoms in the lungs by reducing inflammation. They prevent smooth muscle contraction of the bronchial airways, decrease mucus secretion, and reduce vascular permeability (which reduces edema) through their reduction of leukotriene synthesis. Other antileukotriene effects of these drugs include prevention of the mobilization and migration of such cells as neutrophils and lymphocytes into the lungs. This also serves to reduce airway inflammation. (Lilley 586)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

LTRA indications

The LTRAs montelukast, zafirlukast, and zileuton are used for the prophylaxis and long-term treatment and prevention of asthma in adults and children 12 years of age and older. Because it is dosed once daily, montelukast is the most widely used of these drugs and has also been approved for treatment of allergic rhinitis, a condition discussed in Chapter 36. These drugs are not meant for the management of acute asthmatic attacks. Improvement with their use is typically seen in about 1 week.

(Lilley 586)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

LTRA contraindications

Known drug allergy or other previous adverse drug reaction is the primary contraindication to the use of these drugs. Allergy to povidone, lactose, titanium dioxide, or cellulose derivatives is also important to note, because these are inactive ingredients in these drugs. (Lilley 586)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

LTRA adverse effects

The adverse effects of LTRAs differ depending on the specific drug. The most commonly reported adverse effects of zileuton include headache, nausea, dizziness, and insomnia. The most common adverse effects of montelukast and zafirlukast include headache, nausea, and diarrhea.

(Lilley 586)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

LTRA interactions

Montelukast has fewer drug interactions than zafirlukast or zileuton. Phenobarbital and rifampin, both of which are enzyme inducers, decrease montelukast concentrations. For information on the drugs that interact with zafirlukast and zileuton, see Table 37-4.

(Lilley 586)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

LTRA drug profiles

LTRAs are used primarily for oral prophylaxis and long-term treatment of asthma. The three drugs currently available are zileuton, zafirlukast, and montelukast. These drugs are not to be used for treatment of acute asthma attacks. (Lilley 586)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Montelukast (Singulair) (Lilley 586)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Class : LTRA

Indications and mechanisms of action : belongs to the same subcategory of LTRAs as zafirlukast. Montelukast and zafirlukast work by blocking leukotriene D4 receptors to augment the inflammatory response. Montelukast offers the advantage of being approved for use in children 2 years of age and older. It also has fewer adverse effects and drug interactions than zafirlukast.

Contradinications : known hypersensitivity

Pregnancy category : B

Corticosteroids overview

Corticosteroids, also known as glucocorticoids, are either naturally occurring or synthetic drugs used in the treatment of pulmonary diseases for their antiinflammatory effects. All have actions similar to those of the natural steroid hormone cortisol, which is chemically the same as the drug hydrocortisone. Synthetic steroids are more commonly used in drug therapy. They can be given by inhalation, orally, or even intravenously in severe cases of asthma. Corticosteroids administered by inhalation have an advantage over those administered orally in that their action is relatively limited to the topical site in the lungs. This generally limits, although does not totally prevent, systemic effects. The chemical structures of the corticosteroids given by inhalation have also been slightly altered to limit their systemic absorption from the respiratory tract. The corticosteroids administered by inhalation include the following:

• beclomethasone dipropionate (Beclovent)

• budesonide (Pulmicort Turbuhaler)

• dexamethasone sodium phosphate (Decadron Phosphate Respihaler)

• flunisolide (AeroBid)

• fluticasone (Flovent)

• triamcinolone acetonide (Azmacort)

• ciclesonide (Omnaris)

The systemic use of corticosteroids is described in Chapter 33. The systemic corticosteroids most commonly used for respiratory illness include prednisone (oral) and methylprednisolone (IV).

(Lilley 587)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Corticosteroids mechanisms of action

Although the exact mechanism of action of the corticosteroids has not been determined, it is thought that they have the dual effect of both reducing inflammation and enhancing the activity of beta agonists. The corticosteroids produce their antiinflammatory effects through a complex sequence of actions. The overall effect is to prevent various nonspecific inflammatory processes. Corticosteroids essentially work by stabilizing the membranes of cells that normally release bronchoconstricting substances. These cells include leukocytes, which is another name for white blood cells (WBCs). There are five different types of WBC, each with its own specific characteristics. The five types of WBC, their role in the inflammatory process, and the way in which corticosteroids inhibit their normal action, combat inflammation, and produce bronchodilation are summarized in Table 37-5. Inflammatory mediators are primarily released by lymphocytes in the circulation as well as by mast cells and alveolar macrophages. These latter two cell types are stationary (noncirculating) inflammatory cells that remain localized in the various tissues and organs of the respiratory tract.

Corticosteroids have also been shown to restore or increase the responsiveness of bronchial smooth muscle to beta-adrenergic receptor stimulation, which results in more pronounced stimulation of the beta2 receptors by beta agonist drugs such as albuterol. It may take several weeks of continuous therapy before the full therapeutic effects of the corticosteroids are realized. (Lilley 587)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Corticosteroids indications

Inhaled corticosteroids are used for the primary treatment of bronchospastic disorders to control the inflammatory responses that are believed to be the cause of these disorders; they are indicated for persistent asthma. They are often used concurrently with the beta-adrenergic agonists. In respiratory illnesses, systemic corticosteroids are generally used only to treat acute exacerbations, or severe asthma. Their long-term use is associated with adverse effects (see later). When a rapid, pronounced antiinflammatory effect is needed, as in an acute exacerbation of asthma or other COPD, intravenous corticosteroids (e.g., methylprednisolone) are often used. (Lilley 587)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Corticosteroids contraindications

Drug allergy is the primary contraindication and is usually due to other ingredients in the drug formulation. These drugs 588are not intended as sole therapy for acute asthma attacks. Inhaled corticosteroids are contraindicated in patients who are hypersensitive to glucocorticoids, in patients whose sputum tests positive for Candida organisms, and in patients with systemic fungal infection, as the corticosteroids can suppress the immune system. (Lilley 587-588)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Corticosteroids adverse affects

The main undesirable local effects of typical doses of inhaled corticosteroids in the respiratory system include pharyngeal irritation, coughing, dry mouth, and oral fungal infections. Instruct patients to rinse their mouths after use of an inhaled corticosteroid. Most of the drug effects of inhaled corticosteroids are limited to their topical site of action in the lungs. There is relatively little systemic absorption of the drugs when they are administered by inhalation at normal therapeutic dosages. However, the degree of systemic absorption is more likely to be increased in patients who require higher inhaled dosages. When there is significant systemic absorption, which is most likely with high-dose intravenous or oral administration, corticosteroids can affect any of the organ systems in the body. Some of these systemic drug effects include adrenocortical insufficiency, increased susceptibility to infection, fluid and electrolyte disturbances, endocrine effects, CNS effects (insomnia, nervousness, seizures), and dermatologic and connective tissue effects, including brittle skin, bone loss, osteoporosis, and Cushing's syndrome (see Chapter 33). (Lilley 588)

It is important to remember that when patients are switched to inhaled corticosteroids after receiving systemic corticosteroids, adrenal suppression (Addisonian crisis) may occur when the systemically administered corticosteroid is not tapered slowly. Patient deaths have been reported due to adrenal gland failure in such cases when the switch to inhaled corticosteroids is made quickly and the dosage of systemic corticosteroids is not reduced gradually. The patient who is dependent on systemic corticosteroids may need up to 1 year of recovery time after discontinuation of systemic therapy. There is evidence that bone growth is suppressed in children and adolesc

Corticosteroids interactions

Drug interactions are more likely to occur with systemic (versus inhaled) corticosteroids. These drugs may increase serum glucose levels, possibly requiring adjustments in dosages of antidiabetic drugs. Because of interactions related to metabolizing enzymes, they may also raise blood levels of the immunosuppressants cyclosporine and tacrolimus. Likewise, the antifungal drug itraconazole may reduce clearance of the steroids, whereas phenytoin, phenobarbital, and rifampin may enhance clearance. There is also greater risk for hypokalemia with concurrent use of potassium-depleting diuretics such as hydrochlorothiazide and furosemide. (Lilley 588)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Fluticasone (Lilley 588)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Class: corticosteroids

Mechanism of action and indication: is administered intranasally (Flonase) (one inhalation in each nostril daily) and by oral inhalation (Flovent) (usually one inhalation by mouth twice daily). Fluticasone is also available in a combination formulation with the bronchodilator salmeterol (Advair). Advair is one of the most commonly used inhalers, but because it contains a long-acting beta agonist, it must never be used for acute treatment. (Lilley 588)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Methylprednisolone

is a systemic corticosteroid available in both oral (Medrol) and injectable (Solu-Medrol) forms. (Lilley 588)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Phosphodiesterase 4 inhibitor

In 2011, the FDA approved roflumilast (Daliresp), which is a selective inhibitor of the enzyme called phosphodiesterase type 4 (PDE4). It is indicated to prevent coughing and excess mucus from worsening and to decrease the frequency of life-threatening COPD exacerbations. It is not intended to treat acute bronchospasm. The most commonly reported adverse effects include nausea, diarrhea, headache, insomnia, dizziness, weight loss, and psychiatric symptoms. The FDA requires a medication guide that informs patients of the potential risk for psychiatric adverse effects. Further information can be found at www.daliresp.com.

(Lilley 589)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Monoclonal antibody antiasthmatic

Omalizumab (Xolair) is the newest antiasthmatic medication to become available. It is a monoclonal antibody that selectively binds to the immunoglobulin IgE, which in turn limits the release of mediators of the allergic response. Omalizumab is given by injection and has the potential for producing anaphylaxis. Patients receiving omalizumab must be monitored closely for hypersensitivity reactions (Lilley 589)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Anticoagulants overview

Drugs that prevent the formation of a clot by inhibiting certain clotting factors are called anticoagulants. These drugs have no direct effect on a blood clot that has already formed. They prevent intravascular thrombosis by decreasing blood coagulability. Their uses vary from preventing clot formation to preventing the extension of an established clot, or a thrombus.

Once a clot forms on the wall of a blood vessel, it may dislodge and travel through the bloodstream. This is referred to as an embolus. If it lodges in a coronary artery, it causes a myocardial infarction (MI); if it obstructs a brain vessel, it causes a stroke; if it goes to the lungs, it is a pulmonary embolism (PE); and if it goes to a vein in the leg, it is a deep vein thrombosis (DVT). Collectively, these complications are called thromboembolic events, because they involve a thrombus that becomes an embolus and causes an adverse cardiovascular "event." Anticoagulants can prevent these from occurring if used in the correct manner. Both orally and parenterally administered anticoagulants are available, and each drug has a slightly different mechanism of action and indications. All anticoagulants have their own risks, mainly causing bleeding. The mechanisms of action of the anticoagulants vary depending on the drug. Drug classes of anticoagulants include older drugs such as unfractionated heparin and warfarin. There are also several newer drug classes, including low-molecular-weight heparins (LMWHs), direct thrombin inhibitors, and selective factor Xa inhibitors. For dosage information on anticoagulants, see the table on p. 418 (Lilley 414)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Coagulation modifier drugs

Anticoagulants inhibit the action or formation of clotting factors and therefore prevent clots from forming.

Antiplatelet drugs prevent platelet plugs from forming by inhibiting platelet aggregation, which can be beneficial in preventing heart attacks and strokes.

Hemorheologic drugs alter platelet function without preventing the platelets from working. Sometimes clots form and totally block a blood vessel. When this happens in one of the coronary arteries, a heart attack occurs, and the clot must be lysed to prevent or minimize damage to the myocardial muscle.

Thrombolytic drugs lyse (break down) clots, or thrombi, that have already formed. This is a unique difference between thrombolytics and anticoagulants, which can only prevent the formation of a clot.

Antifibrinolytic drugs, also known as hemostatic drugs, have the opposite effect of these other classes of drugs; they actually promote blood coagulation. The various drugs in each category of coagulation modifiers are listed in Table 26-1. (Lilley 414)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

anticoagulants mechanism of action

Anticoagulants are also called antithrombotic drugs because they work to prevent the formation of a clot or thrombus, a condition known as thrombosis. All anticoagulants work in the clotting cascade but do so at different points. As shown in Figures 26-1 and 26-2, heparin works by binding to a substance called antithrombin III, which turns off three main activating factors: activated factor II (also called thrombin), activated factor X, and activated factor IX. (Factors XI and XII are also inactivated but do not play as important a role as the other three factors.) Of these, thrombin is the most sensitive to the actions of heparin. Antithrombin III is the major natural inhibitor of thrombin in the blood. The overall effect of heparin is that it turns off the coagulation pathway and prevents clots from forming. However, it cannot lyse a clot. The drug name heparin usually refers to unfractionated heparin, which is a relatively large molecule and is derived from animal sources. In contrast, low-molecular-weight heparins are synthetic and have a smaller molecular structure. These include enoxaparin (Lovenox) and dalteparin 415(Fragmin). Both drugs work similarly to heparin. Heparin primarily binds to activated factors II, X, and IX, whereas the LMWHs differ from heparin in that they are much more specific for activated factor X (Xa) than for activated factor II (IIa, or thrombin). This property gives LMWHs a much more predictable anticoagulant response. As a result, frequent laboratory monitoring of bleeding times using tests such as activated partial thromboplastin time (aPTT), which is imperative with unfractionated heparin, is not required with LMWHs. When heparin is used for flushing catheters (10 to 100 units/mL), no monitoring is needed.

Warfarin (Coumadin) works by inhibiting vitamin K synthesis by bacteria in the

indications for anticoagulants

The ability of anticoagulants to prevent clot formation is of benefit in certain settings in which there is a high likelihood of clot formation. These include MI, unstable angina, atrial fibrillation, use of indwelling devices such as mechanical heart valves, and conditions in which blood flow may be slowed and blood may pool, such as major orthopedic surgery or prolonged periods of immobilization like hospitalization or even long plane rides. The ultimate consequence of a clot can be a stroke or a heart attack, DVT, or PE; therefore, the prevention of these serious events is the ultimate benefit of these drugs. Anticoagulants are used for both prevention and treatment of clots. Patients at risk for clots are given DVT prophylaxis while in the 416hospital and after major surgery. LMWHs, especially enoxaparin, are also routinely used as anticoagulant bridge therapy in situations in which a patient must stop warfarin for surgery or other invasive medical procedures. The term bridge therapy refers to the fact that enoxaparin acts as a bridge to provide anticoagulation while the patient must be off of his or her warfarin therapy.

LWMH

specially enoxaparin, are also routinely used as anticoagulant bridge therapy in situations in which a patient must stop warfarin for surgery or other invasive medical procedures.

contraindications to anticoagulants

They include known drug allergy, any acute bleeding process, or high risk for such an occurrence. Warfarin is strongly contraindicated in pregnancy, whereas the other anticoagulants are rated in lower pregnancy categories (B or C). LMWHs are contraindicated in patients with an indwelling epidural catheter; they can be given 2 hours after the epidural is removed. This is very important to remember, because giving an LMWH with an epidural has been associated with epidural hematoma

warfarin

is strongly contraindicated in pregnancy, whereas the other anticoagulants are rated in lower pregnancy categories (B or C).

adverse effects of anticoagulants

bleeding is the main complication of anticoagulation therapy, and the risk increases with increasing dosages. Bleeding may be localized (e.g., hematoma at the site of injection) or systemic. It also depends on the nature of the patient's underlying clinical disorder and is increased in patients taking high doses of aspirin or other drugs that impair platelet function. One particularly notable adverse effect of heparin is heparin-induced thrombocytopenia (HIT). There are two types of HIT. Type I is characterized by a more gradual reduction in platelets. In this type, heparin therapy can generally be continued. In contrast, in type II HIT there is an acute fall in the number of platelets (more than 50% reduction from baseline). Heparin therapy must be discontinued in patients with type II HIT. The greatest risk to the patient with HIT is the paradoxical occurrence of thrombosis, something that heparin normally prevents or alleviates. Thrombosis that occurs in the presence of HIT can be fatal. The incidence of this disorder ranges from 5% to 15%. The direct thrombin inhibitors lepirudin and argatroban are both specifically indicated for treatment of HIT. Warfarin can cause skin necrosis and "purple toes" syndrome. Other adverse effects are listed in Table 26-2.

toxicity and management of overdose with anticoagulants

Treatment of the toxic effects of anticoagulants is aimed at reversing the underlying cause. Although the toxic effects of all anticoagulants are hemorrhagic in nature, the management is different for each drug. Symptoms include hematuria, melena (blood in the stool), petechiae, ecchymoses, and gum or mucous membrane bleeding. In the event of bleeding, the drug is to be stopped immediately. In the case of heparin, stopping the drug alone may be enough to reverse the toxic effects because of the drug's short half-life (1 to 2 hours). In severe cases or when large doses have been given intentionally (i.e., during cardiopulmonary bypass for heart surgery), IV injection of protamine sulfate is indicated. Protamine is a specific heparin antidote and forms a complex with heparin, completely reversing its anticoagulant properties. This occurs in as few as 5 minutes. In general, 1 mg of protamine can reverse the effects of 100 units of heparin. Protamine may also be used to reverse the effects of LMWHs. A 1-mg dose of protamine is administered for each milligram of LMWH given, (e.g., 1 mg protamine for 1 mg enoxaparin). If the heparin overdose has resulted in a large blood loss, replacement with packed red blood cells may be necessary.

In the event of warfarin toxicity or overdose, the first step is to discontinue the warfarin. As with heparin, the toxicity associated with warfarin is an extension of its therapeutic effects on the clotting cascade. However, because warfarin inactivates the vitamin K-dependent clotting factors and because these clotting factors are synthesized in the liver, it may take 36 to 42 hours before the liver can resynthesize enough clotting factors to reverse the warfarin effects. Giving vitamin K1 (phytonadione) can hasten the return to normal coagulation. The dose and route of administration of the

drug interactions of anticoagulants

Interactions

Drug interactions involving the oral anticoagulants are profound and complicated. The main interaction mechanisms 417responsible for increasing anticoagulant activity include the following:

• Enzyme inhibition of metabolism

• Displacement of the drug from inactive protein-binding sites

• Decrease in vitamin K absorption or synthesis by the bacterial flora of the large intestine

• Alteration in the platelet count or activity

The drugs that interact with warfarin and heparin are listed in Table 26-3. More specifics on significant drug interactions are discussed under the drug profiles. Although both aspirin and warfarin increase the risk for bleeding when given with heparin, they are commonly given together in clinical practice. In fact, when a patient is placed on IV heparin, it is recommended that warfarin be started at the same time. Recommendations are to continue overlap therapy of the heparin and warfarin for at least 5 days; the heparin is stopped after 5 days when the INR is above 2.

argatroban

Class: anticoagulant

Indications and mechanisms of actions: which has the same trade name, is a synthetic direct thrombin inhibitor. It is indicated both for treatment of active HIT and for percutaneous coronary intervention procedures in patients at risk for HIT (i.e., those with a history of the disorder). It is given only by the IV route. A lower dosage must be used in patients with severe hepatic dysfunction.

Route: IV

Dabigatran (Pradaxa)

Class: anticoagulant

Indications and mechanisms of action: is the first oral direct thrombin inhibitor that is approved for prevention of strokes and thrombosis in patients with nonvalvular atrial fibrillation. Dabigatran is a prodrug that becomes activated in the liver. It specifically and reversibly binds to both free and clot-bound thrombin. Dabigatran is excreted extensively in the kidneys, and the dose is dependent upon renal function.

adverse effects: bleeding with an increased risk of gi bleeding

drug interactions: include phenytoin, carbamazepine, rifampin, and St. John's wort (which cause a decreased effect) and strong CYP3A4 inhibitors such as amiodarone, quinidine, erythromycin, verapamil, azole antifungals, and HIV protease inhibitors

Route : PO

Info: other drugs are not given with this drug

Enoxaparin (Lovenox)

Class: anticoagulant (LWMH)

Indications and mechanisms of action: is the prototypical LMWH and is obtained by enzymatically cleaving large unfractionated heparin molecules into small fragments. These smaller fragments of heparin have a greater affinity for factor Xa than for factor IIa and have a higher degree of bioavailability and a longer elimination half-life than unfractionated heparin. Laboratory monitoring, as done with heparin therapy, is not necessary when enoxaparin is given because of its greater affinity for factor Xa

Laboratory monitoring, as done with heparin therapy, is not necessary when enoxaparin is given because of its greater affinity for factor Xa. It is available only in injectable form. Dalteparin is another anticoagulant with comparable pharmacology and indications. Enoxaparin is the most frequently used LMWH and is commonly given for both prophylaxis and treatment. All LMWHs have a distinct advantage over heparin in that they do not require any laboratory monitoring and can be given at home.

Drug interactions: A potentially deadly medication error is to give heparin in combination with enoxaparin (or any LMWH, dabigatran, rivaroxaban, or apixaban). Always double-check that enoxaparin and other anticoagulants are never given to the same patient. One exception, however, is that enoxaparin is often used with oral warfarin as overlap treatment for pulmonary embolus or deep vein thrombosis.

Route : prefilled subq.

Fondaparinux (Arixtra)

Class: anticoagulant

Indications and mechanism of action: a selective inhibitor of factor Xa, which is indicated for prophylaxis or treatment of DVT or PE

Contraindications: nown allergy or in patients 419with a creatinine clearance less than 30 mL/min or a body weight of less than 50 kg.

Adverse reactions: bleeding, thrombocytopenia(therapy should be stopped if platelets fall below 100,000 per microliter) Other side effects include anemia, increased wound drainage, postoperative hemorrhage, hematoma, confusion, urinary tract infection, hypotension, dizziness, and hypokalemia. There is no antidote

should not be given 6 to 8 hours after surgery

black box warning: spinal hematomas if the patient has an epidural catheter.

route: subcutaneous injection

herparin

class: anticoagulant

indications and mechanisms of action: is a natural anticoagulant obtained from the lungs or intestinal mucosa of pigs. One brand name for some of the commonly used heparin products is Hep-Lock. This brand name refers only to small vials of heparin IV flush solutions used to maintain the patency of heparin-lock IV insertion sites. Because of the risk for the development of HIT, most health care institutions routinely use normal saline (0.9% sodium chloride) as a flush for heparin-lock IV ports and have moved away from using heparin flush solutions for this purpose. Heparin flushes are still used for central catheters. When used for flushing purposes, there is no need for monitoring.

Heparin is commonly used for DVT prophylaxis in a dose of 5000 units two or three times a day given subcutaneously, and it does not need to be monitored when used for prophylaxis. When heparin is used therapeutically (for treatment), it is given by continuous IV infusion. Most hospitals have weight-based protocols for heparin administration. Because the dosage is based on the patient's weight in kilograms, ensure that the appropriate weight is recorded and that only kilograms are used, and not pounds. A potential double-dose medication error can occur if pounds and kilograms are mixed. This is also true for enoxaparin, because it is dosed on body weight when used therapeutically. When heparin is given by IV infusion, monitoring by frequent measurement of aPTT (usually every 6 hours until therapeutic effects are seen) is necessary.

other info: usually given with warfarin, available only in injectable form in multiple strengths ranging from 10 to 40,000 units/mL. The vials of different strengths of heparin are very similar and look very much alike. In fact, several newborns have died when a vial of more concentrated h

Rivaroxaban (Xarelto)

Class: anticoagulant

Indications and mechanisms of action: is the first oral factor Xa inhibitor. It is approved for prevention of strokes in patients with nonvalvular atrial fibrillation, postoperative thromboprophylaxis with knee and hip replacement surgery, and treatment of DVT and PE.

dosage : differ for each indication and must be adjusted for renal dysfunction.

contraindications: include known drug allergy and active bleeding

black box warning: All of the oral factor Xa inhibitors have black box warnings regarding potential spinal hematomas if the patient has an epidural catheter and regarding the risk for thrombosis if they are discontinued abruptly.

Adverse effects: The most frequent adverse effects include peripheral edema, dizziness, headache, bruising, diarrhea, hematuria, and bleeding

drug interactions: include a decreased effect seen with phenytoin, carbamazepine, rifampin, and St. John's wort. An increased effect is seen with strong CYP3A4 inhibitors (amiodarone, erythromycin, ketoconazole, HIV drugs, diltiazem, verapamil) and grapefruit juice. Apixaban (Eliquis) and edoxaban (Savaysa) are similar drugs with similar drug interactions and side effects

other info: no monitoring is required may falsely elevate inr and not to given with any other anticoagulant

route : PO

Warfarin sodium (Coumadin)

class: anticoagulant

Indications, mechanisms of action, and info: is a pharmaceutical derivative of the natural plant anticoagulant known as coumarin. Warfarin is the most commonly prescribed oral anticoagulant and is available oral and IV; however, it is used almost exclusively in the oral form. Use of this drug requires careful monitoring of the prothrombin time/international normalized ratio (PT/INR), which is a standardized measure of the degree to which a patient's blood coagulability has been reduced by the drug. A normal INR (without warfarin) is 1 whereas a therapeutic INR (with warfarin) ranges from 2 to 3.5, depending on the indication for use of the drug (e.g., atrial fibrillation, thromboprevention, prosthetic heart valve). Patients older than 65 years of age may have a lower INR threshold for bleeding complications and may need to be monitored accordingly. Recently, it has been shown that about one third of patients receiving warfarin 420metabolize it differently than expected, based on variations in certain genes, CYP2CP and VKORC1. Genetic testing for these genes is helpful in determining the appropriate initial dosage of warfarin. The maintenance dosage is still determined by the INR.

drug interactions: Warfarin has significant interactions with many drugs, including amiodarone, fluconazole, erythromycin, metronidazole, sulfonamide antibiotics, and cimetidine. Although many more drugs can interact with warfarin, the aforementioned are by far the most common. Combining warfarin and amiodarone will lead to a 50% increase in the INR. When amiodarone is added to warfarin therapy, it is recommended that the warfarin dose be cut in half.

Because warfarin inhibits vitamin K-dependent clotting factors, foods that are high in vitamin K may reduce warfarin's ability to prevent clots. Common foods rich in vitam

antiplatelet drugs overview

Another class of coagulation modifiers that prevent clot formation is the antiplatelet drugs. Remember, the anticoagulants work in the clotting cascade. In contrast, antiplatelet drugs work to prevent platelet adhesion at the site of blood vessel injury, which actually occurs before the clotting cascade.

Platelets normally flow through blood vessels without adhering to their surfaces. Blood vessels can be injured by a disruption of blood flow, trauma, or the rupture of plaque from a vessel wall. When such events occur, substances such as collagen and fibronectin, which are present in the walls of blood vessels, become exposed. Collagen is a potent stimulator of platelet adhesion, as is a prevalent component of the platelet membranes called glycoprotein IIb/IIIa (GP IIb/IIIa). Once platelet adhesion occurs, stimulators (adenosine diphosphate [ADP], thrombin, thromboxane A2 [TXA2], and prostaglandin H2) are released from the activated platelets. These cause the platelets to aggregate (accumulate) at the site of injury. Once at the site of vessel injury, the platelets change shape and release their contents, which include ADP, serotonin, and platelet factor IV. The hemostatic function of these substances is twofold. First, they act as platelet recruiters, attracting additional platelets to the site of injury; second, they are potent vasoconstrictors. Vasoconstriction limits blood flow to the damaged blood vessel to reduce blood loss. A platelet plug that has formed at a site of vessel injury is not stable and can be dislodged. The clotting cascade is then stimulated to form a more permanent fibrin plug (blood clot). The role of platelets and their relationship to the clotting cascade are illustrated in Figure 26-4.

antiplatelet drugs the mechanism of action

Many of the antiplatelet drugs affect the cyclooxygenase pathway, which is one of the common final enzymatic pathways in the complex arachidonic acid pathway that operates within platelets and on blood vessel walls

Aspirin is widely used for its analgesic, antiinflammatory, and antipyretic (antifever) properties (see Chapter 44). Aspirin also has antiplatelet effects. Aspirin inhibits cyclooxygenase in the platelet irreversibly so that the platelet cannot regenerate this enzyme. Therefore, the effects of aspirin last the lifespan of a platelet, or 7 days. This irreversible inhibition of cyclooxygenase in the platelet prevents the formation of TXA2, a substance that causes blood vessels to constrict and platelets to aggregate. Thus, by preventing TXA2 formation, aspirin prevents these actions, which results in dilation of the blood vessels and prevention of platelets from aggregating or forming a clot.

Dipyridamole, another antiplatelet drug, also works to inhibit platelet aggregation by preventing the release of ADP, platelet factor IV, and TXA2, all substances that stimulate platelets to aggregate or form a clot. Figure 26-4 shows how these substances accomplish this. Dipyridamole may also directly stimulate the release of prostacyclin and inhibit the formation of TXA2 (see Figure 26-5).

Clopidogrel is a drug that belongs to the class of antiplatelet drugs called the ADP inhibitors. Its use has largely superseded that of the original ADP inhibitor ticlopidine. Its works by altering the platelet membrane so that it can no longer receive the signal to aggregate and form a clot. This signal is in the form of fibrinogen molecules, which attach to glycoprotein receptors (GP IIb/IIIa) on the surface of the platelet. Clopidogrel inhibits the activation of this receptor. The combination of aspirin and clopidogrel has been

indications for antiplatelet drugs

The therapeutic effects of the antiplatelet drugs depend on the particular drug. Aspirin is officially recommended for stroke prevention by the American Stroke Society in daily doses of 50 to 325 mg. (However, in clinical practice, dosages may vary.) Clopidogrel and others in its class are given to reduce the risk for thrombotic stroke, and for prophylaxis against transient ischemic attacks (TIAs), as well for post-MI prevention of thrombosis. Dipyridamole is used to decrease platelet aggregation in various other thromboembolic disorders. The GP IIb/IIIa inhibitors are used to treat acute unstable angina and MI, and are given during percutaneous coronary intervention procedures, such as angioplasty. Their purpose is to prevent the formation of thrombi. This is known as thromboprevention. This treatment approach is based on the fact that prevention of thrombus formation is easier and less risky overall from a pharmacologic standpoint than is lysing a formed thrombus. Pentoxifylline is indicated for peripheral vascular disease, whereas cilostazol is indicated specifically for intermittent claudication (pain and cramping in the calf muscles associated with walking). Cilostazol has been shown to be superior to pentoxifylline in improving exercise tolerance in older adult patients.

Vorapaxar (Zontivity), a novel antiplatelet drug and the first in its class, is an antagonist of protease-activated receptor-1 (PAR-1), which inhibits the action of thrombin on the platelet. It is indicated to reduce thrombotic cardiovascular events, MI, and stroke in patients with a history of MI or with peripheral arterial disease. It is available as a 2.08-mg tablet and is given once daily in combination with aspirin and/or clopidogrel. It is contraindicated in patients with history of stroke, TIA, intracranial hemorrhage, and active bleeding

contraindications for antiplatelet drugs

known drug allergy to a specific product, thrombocytopenia, active bleeding, leukemia, traumatic injury, gastrointestinal ulcer, vitamin K deficiency, and recent stroke

adverse effects of antiplatelet drugs

can be serious, and they all pose a risk for inducing a serious bleeding episode

drug interactions with antiplatelets

The use of dipyridamole with clopidogrel, aspirin, and/or other nonsteroidal antiinflammatory drugs (NSAIDs) produces additive antiplatelet activity and increased bleeding potential. The combined use of steroids or nonaspirin NSAIDs with aspirin can increase the ulcerogenic effects of aspirin. The combined use of aspirin and heparin with GP IIb/IIIa inhibitors also further enhances antiplatelet activity and increases the likelihood of a serious bleeding episode. In spite of all of these interactions, it is not uncommon to see patients taking daily maintenance doses of aspirin for thrombopreventive purposes, sometimes in combination with other antiplatelet drugs. The most commonly used dose is the "baby aspirin" dose of 81 mg (the standard adult dose is 325 mg). Even though GP IIb/IIIa and heparin have additive therapeutic effects when given concurrently and are listed as interacting drugs, it is very common to see both used together. However, the therapeutic goal of heparin, and thus the dose, is lower when used with a GP IIb/IIIa inhibitor.

aspirin

class: antiplatelet

contraindications and drug interactions: One unique contraindication for aspirin is flulike symptoms in children and teenagers. The use of aspirin in this situation is associated with the occurrence of Reye's syndrome, a rare, acute, and sometimes fatal condition involving hepatic and central nervous system damage (see Chapter 44). There is also 423allergic cross-reactivity between aspirin and other NSAIDs. Patients with documented aspirin allergy must not receive NSAIDs

commonly used with: dipyridamole (Aggrenox)

Route: PO AND Rectal

Clopidogrel (Plavix)

class: antiplatelet(adp inhibitor)

black box warning: patients with certain genetic abnormalities, who may have a higher rate of cardiovascular events due to reduced conversion to its active metabolite.

drug interactions: effectiveness may be reduced by amiodarone, calcium channel blockers, NSAIDS, and proton pump inhibitors (see Chapter 50).

Route :PO

Eptifibatide (Integrilin)

Class: antiplatlet (GP IIB/IIIA inhibitor)

Indications: These drugs are usually administered in intensive care or cardiac catheterization laboratory settings, where continuous cardiovascular monitoring is the norm.

Route : IV

thrombolytic drugs overview

Thrombolytics are coagulation modifiers that lyse thrombi in the blood vessels that supply the heart with blood, the coronary arteries. This reestablishes blood flow to the blood-starved heart muscle. If the blood flow is reestablished early, the heart muscle and left ventricular function can be saved. If blood flow is not reestablished early, the affected area of the heart muscle becomes ischemic, and eventually necrotic and nonfunctional.

Thrombolytic therapy made its debut in 1933 when a substance that broke down fibrin clots was isolated from a patient's blood. This substance was found to be produced by beta-hemolytic streptococci (group A), and the substance was eventually called streptokinase.

Streptokinase was first used in 1947 to dissolve a clotted hemothorax, but it was not until 1958 that it was given to a patient with an acute MI. In 1960, a naturally occurring human plasminogen activator called urokinase, became available. In the 1980s, the underlying cause of acute MI was determined to be due to coronary artery occlusion. This marked the start of rapid growth in the use of thrombolytic drugs for the early treatment of acute MI. Since that time, several new thrombolytics have become available for this and other clinical uses. Several large landmark thrombolytic research studies showed that early thrombolytic therapy could bring about a 50% reduction in mortality, a reduction in the infarct size, an improvement in left ventricular function, and a reduction in the incidence and severity of congestive heart failure. However, the use of thrombolytics has almost completely been replaced by interventional cardiologic procedures, such as percutaneous coronary intervention. Thrombolytics are still a viable option in hospitals that do not offer percutaneous coronary intervention. Currently available thrombolytic

thrombolytic drugs mechanism of action

There is a fine balance between the formation and dissolution of a clot. The coagulation system is responsible for forming clots, whereas the fibrinolytic system is responsible for 424dissolving clots. The natural fibrinolytic system within the blood takes several days to break down a clot (thrombus). This is of little value in the case of a clotted blood vessel that supplies blood to the heart muscle. Thrombolytics accomplish this by activating the conversion of plasminogen to plasmin, which breaks down, or lyses, the thrombus (see Figure 26-3). Plasmin is a proteolytic enzyme, which means that it breaks down proteins. It is a relatively nonspecific enzyme that is capable of degrading proteins such as fibrin, fibrinogen, and other procoagulant proteins like factors V, VIII, and XII. In other words, the substances that form clots are destroyed by plasmin. Essentially, thrombolytic drugs work by mimicking the body's own process of clot destruction. Although the individual thrombolytic drugs are somewhat diverse in their actions, they all have this common result.

Streptokinase, the original thrombolytic enzyme, and the naturally occurring urokinase have been removed from the U.S. market, primarily due to their adverse effects—namely, they were not fibrin specific. The newer thrombolytics have chemical specificity for fibrin threads (fibrin specificity) and work primarily at the site of a clot. They still carry some bleeding risk, but much less than that of the thrombolytic enzymes.

Tissue plasminogen activator is a naturally occurring plasminogen activator secreted by vascular endothelial cells (the walls of blood vessels). The amount secreted naturally is not sufficient to dissolve a coronary thrombus quickly enough to restore circulation to the heart and save the heart muscle. Recombinant DNA techniques are now use

Indications of thrombolytic drugs

The purpose of all the thrombolytic drugs is to activate the conversion of plasminogen to plasmin, the enzyme that breaks down a thrombus. The presence of a thrombus that interferes significantly with normal blood flow on either the venous or the arterial side of the circulation is an indication for the use of thrombolytic therapy. The indications for thrombolytic therapy include acute MI, arterial thrombosis, DVT, occlusion of shunts or catheters, pulmonary embolism, and acute ischemic stroke.

contraindications for thrombolytic drugs

drug allergy to the specific product and any preservatives, and concurrent use of other drugs that alter clotting.

adverse effects of thrombolytic drugs

internal, intracranial, and superficial bleeding. Other problems include hypersensitivity, anaphylactoid reactions, nausea, vomiting, and hypotension. These drugs can also induce cardiac dysrhythmias.

toxicity and managment of overdose to thrombolytic drugs

Acute toxicity primarily causes an extension of the adverse effects of the thrombolytic drug. Treatment is symptomatic and supportive, because thrombolytic drugs have a relatively short half-life and no specific antidotes.

interactions of thrombolytic drugs

The most common effect of drug interactions is an increased bleeding tendency resulting from the concurrent use of anticoagulants, antiplatelets, or other drugs that affect platelet function.

A laboratory test interaction that can occur with thrombolytic drugs is a reduction in the plasminogen and fibrinogen levels.

Alteplase (Activase)

class: thrombolytic drug

Indications and mechanisms of action: . It is fibrin specific and therefore does not produce a systemic lytic state. In addition, because it is present in the human body in a natural state, its 425administration for therapeutic use does not induce an antigen-antibody reaction. Therefore, it can be re-administered immediately in the event of reinfarction. The drug t-PA has a very short half-life of 5 minutes. It is believed to open the clogged artery rapidly, but its action is short-lived. Therefore, it is given with heparin to prevent reocclusion of the affected blood vessel

Route : parenteral form. There is also a smaller dosage form known as Cathflo Activase that is used to flush clogged IV or arterial lines. Tenecteplase (TNKase) is a newer form of alteplase that is given by IV push after MI. Alteplase is also used for ischemic stroke.

antifibrinolytic drugs overview

The individual antifibrinolytic drugs have varying mechanisms of action, but all prevent the lysis of fibrin. Fibrin is the substance that helps make a platelet plug insoluble and anchors the clot to the damaged blood vessel (see Figures 26-1 and 26-2). The term antifibrinolytic refers to what these drugs do, which is to prevent the lysis of fibrin; in doing so, they actually promote clot formation. For this reason, they are also called hemostatic drugs. Their effects are opposite to those of anticoagulant and antiplatelet drugs, which prevent clot formation. Three synthetic antifibrinolytics are available—aminocaproic acid, tranexamic acid, and desmopressin. Dosages, indications, and other information appear in the associated dosages table. There are also hemostatic drugs that are used topically (on the skin or tissue surface) in surgical settings to stop excessive bleeding. These include topical thrombin, microfibrillar collagen, absorbable gelatin, and oxidized cellulose.

Although not technically antifibrinolytic drugs, there are three drugs used for the treatment of hemophilia. These are produced by recombinant DNA technology, which eliminates the risk associated with obtaining them from human blood. Products currently available include rVII, rVIII, and rIX. As mentioned earlier, factors VII, VIII, and IX are important in the coagulation pathway. Warfarin also inhibits these factors. These products are used in patients with hemophilia and are also used in patients with severe bleeding due to warfarin therapy.

antifibrinolytic mechanisms of action

The drug effects of the antifibrinolytics are very specific and limited. They do not have many effects outside of their hematologic ones. Aminocaproic acid and tranexamic acid inhibit the breakdown of fibrin, which prevents the destruction of the formed platelet clot. Desmopressin causes a dose-dependent increase in the concentration of plasma factor VIII (von Willebrand factor), along with an increase in the plasma concentration of tissue plasminogen activator. The overall effect of this is increased platelet aggregation and clot formation. This drug is also an analogue of antidiuretic hormone and is discussed further in Chapter 30.

antifibrinolytics indications

Antifibrinolytics are useful in both the prevention and treatment of excessive bleeding resulting from systemic hyperfibrinolysis or surgical complications. They have also proved successful in arresting excessive oozing from surgical sites such as chest tubes as well as in reducing the total blood loss and the duration of bleeding in the postoperative period.

Desmopressin may also be used in patients who have hemophilia A or type I von Willebrand disease. Recombinant factors VII, VIII, and IX are used to treat hemophilia or to stop the bleeding from excessive warfarin therapy.

antifribrinolytics contraindications

drug allergy to a specific product and disseminated intravascular coagulation, which could be worsened by these drugs

adverse effects of antifibrinolytics

occur uncommonly and are mild. However, there have been rare reports of these drugs causing thrombotic events, such as acute cerebrovascular thrombosis and acute MI. The common adverse effects of antifibrinolytics are listed in Table 26-6.

drug interactions with antifibrinolytics

When drugs such as estrogens or oral contraceptives are used concurrently with aminocaproic acid or tranexamic acid, additive effects may occur, resulting in increased coagulation. Few specific interactions have been reported for desmopressin, 426although use caution when giving to patients receiving lithium, large doses of epinephrine, heparin, or alcohol. Drugs such as chlorpropamide and fludrocortisone may potentiate the antidiuretic response, which may lead to edema.

Aminocaproic acid (Amicar)

class : antifibrinolytic (synthetic)

Indications and mechanisms of actions: used to prevent and control the excessive bleeding that can result from surgery or overactivity of the fibrinolytic system

Route: PO and parenteral

Desmopressin (DDAVP)

class: antifibrinolytic (synthetic polypeptide)

indications and mechanisms of action: . It is structurally very similar to vasopressin, which is antidiuretic hormone, the natural human posterior pituitary hormone (see Chapter 30). Because of these physical characteristics, it is most often used to increase the resorption of water by the collecting ducts in the kidneys to prevent or control polydipsia, polyuria, and dehydration in patients with diabetes insipidus due to a deficiency of endogenous posterior pituitary vasopressin or in patients with polyuria and polydipsia resulting from trauma or surgery in the pituitary region.

Desmopressin also causes a dose-dependent increase in plasma factor VIII (von Willebrand factor), along with an increase in tissue plasminogen activator, which results in increased platelet aggregation and clot formation; thus it is often used to stop bleeding.

contraindications: known hypersensitivity to it and in those with nephrogenic diabetes insipidus

Route: Parenteral and intranasal (used for primary nocturnal enuresis.)

nursing assessment coagulation modifier

A thorough nursing assessment and health history must be initiated before the use of all coagulation-modifying drugs. This includes the following: any drug or food allergies, current and past medical issues as well as any underlying systemic or autoimmune disease processes, family health history, dietary habits, changes in body weight, ability to perform activities of daily living, level of exercise and/or degree of sedentary lifestyle, exercise tolerance, employment activities, success of previous treatment regimens, blood pressure, pulse rate, respirations, body 427weight, height, dietary intake, and fluid intake. A medication history is also needed and must include a listing of all drugs the patient takes on a daily or other routine basis such as prescription drugs, over-the-counter medications, herbal products, dietary supplements, and intake of nicotine, alcohol, and illegal substances. Perform a thorough patient assessment to also identify the presence of the following risk factors for clot development: immobility; history of limited activity or prolonged bed rest (e.g., generally for longer than 3 to 5 days); dehydration; obesity; smoking; congestive heart failure; mitral or aortic stenosis; coronary heart disease with documented atherosclerosis or arteriosclerosis; peripheral vascular disease; pelvic, gynecologic-genitourinary, abdominal, orthopedic, or vascular major surgery; heart valve incompetency and/or replacement; history of thrombophlebitis, deep vein thrombosis (DVT), or thromboembolism, including pulmonary embolism, myocardial infarct, and atrial fibrillation; edema of the periphery; trauma to the lower extremities; use of oral contraceptives; and/or recent extended airline travel time. If the patient has a history of clotting disorders and/or thromboembolism, assess and document the following: presen

nursing interventions for coagulation modifiers

Routinely monitor vital signs, heart sounds, peripheral pulses, and neurologic status in all patients before, during, and immediately after anticoagulant therapy. The various laboratory values to be monitored are presented in the Safety: Laboratory Values Related to Drug Therapy box. If there is any change in pulse rate or rhythm, blood pressure, or level of consciousness, and/or unexplained restlessness occurs, contact the prescriber immediately. These changes may indicate bleeding or hemorrhage.

Knowledge of the proper techniques of administration is crucial for the safe and effective use of heparin and the LMWHs (see Box 26-1 for other dosing and route information). Heparin may be given by the subcutaneous or IV routes, but not IM. You can easily avoid inadvertent IM injection if you use only subcutaneous syringes to withdraw and administer the heparin. The 25- to 28-gauge, image-inch (1.5 cm) needle is often pre-packaged with the syringe. No major harm would result if a subcutaneous dose were inadvertently administered IV. If rapid anticoagulation is needed, IV heparin by continuous or intermittent infusion may be prescribed. Whether the drug is given by IV infusion or subcutaneous injection, monitor daily clotting study results, and perform these studies as ordered for therapeutic doses (monitoring is not done for prophylactic treatment).

The drug effects of heparin can be reversed with the IV administration of protamine sulfate. With subcutaneous heparin, several doses of protamine sulfate may be needed to reverse the anticoagulant effect because of the variable rates of absorption of this dosage form. See Box 26-1 for the procedure for intermittent or continuous IV administration of heparin.

Administer LMWHs by subcutaneous injection deep into the injection site (see previous discussion) using the same techn

evaluation for coagulation modifiers

Monitoring for the therapeutic and adverse effects of coagulation modifier drugs is crucial for safe administration. Because these drugs are used for a variety of purposes, therapeutic responses vary. Some of the therapeutic effects include decreased chest pain and a decrease in dizziness, as well as in other neurologic symptoms. Adverse effects of anticoagulants include bleeding and hematoma formation (heparin); thrombocytopenia (heparin and LMWHs); bleeding, dizziness, shortness of breath, and fever (direct thrombin inhibitors); bleeding, hematoma, dizziness, and gastrointestinal distress (selective factor Xa inhibitors); and bleeding, lethargy, and muscle pain (warfarin). Early signs of drug overdose for any of the clotting-altering drugs (i.e., anticoagulants) include bleeding of the gums while brushing the teeth, unexplained nosebleeds or bruising, and heavier-than-usual menstrual bleeding. Abdominal pain, back pain, bloody or tarry stools, bloody urine, constipation, blood in the sputum, severe or continuous headaches, and the vomiting of frank red blood or a coffee ground-like substance (old blood) are all possible indications of internal bleeding.

Therapeutic effects of clopidogrel and other antiplatelet drugs include a decrease in the occurrence of clotting events such as TIA and stroke. Some of the adverse effects of aspirin, as an antiplatelet drug, include dizziness, confusion, nausea, vomiting, gastrointestinal bleeding. Adverse effects of clopidogrel may include chest pain, edema, headache, dizziness, and epistaxis. See Table 26-4 for a more complete listing of adverse effects associated with antiplatelet drugs. With vorapaxar, evaluate for the adverse effects of bleeding, depression, skin rash, and anemia. Therapeutic levels of anticoagulants and other clotting-altering drugs or coagulation modifier dru

patient centered teaching coagulation modifiers

• Emphasize the rationale for use of the coagulation-modifying drugs to prevent serious complications related to clotting, such as strokes, heart attacks, clot formation (deep vein thrombosis of the legs) with heart valve replacements, and mini-strokes/TIAs (transient ischemic attacks) and the need for frequent and close monitoring.

• Educate the patient that a healthy lifestyle is an important part of therapy and will most likely include eating the right foods, weight reduction if needed, smoking cessation, control of blood pressure, and stress reduction. Advise the patient to provide a listing of all medications to all possible prescribers (e.g., dentists).

• Direct the patient to take all of the clotting-altering drugs exactly as prescribed because too little of the drug may lead to clot formation and too much of the drug may lead to bleeding. Regular follow-up appointments are an important part of patient care, with frequent blood tests to monitor for therapeutic effects and adverse effects of the medication. The results of the blood tests will help the prescriber determine the proper dosage.

• The patient must carry an identification card or wear a medical alert bracelet or necklace at all times stating allergies, medical diagnosis, list of drugs, prescriber's name and phone number, as well as an emergency contact name and number.

• Home therapy with parenteral anticoagulants may require injections for a period of time, and LMWHs are generally used. If there is a switch from heparin to warfarin (Coumadin), there will be an overlap period of at least 5 days during which both drugs are taken to allow therapeutic levels of the oral warfarin to be reached before the heparin is discontinued. This process may occur in the hospital or at home. Provide complete and thorough instructions to the patient, and u

Heparin

Anticoagulant of choice for pregnancy

With lwmh and heparin it is important to remember

That both are not interchangeable with each other and they contain bezol alcohol so check for allergy

When to withdraw warfarin

Before dental procedures and other

protamine sulfate

How to reverse heparin overdose

Aspirin

Is best taken with 6 to 8 oz of water and with food

dipyridamole (Lilley 431)

another anticoagulant, are recommended to be taken on an empty stomach; however, if this is not tolerated, the patient can take the drug with food. If nausea occurs, cola, unsalted crackers, or dry toast may help to alleviate this adverse effect. In addition, it may take up to 2 to 3 months of continuous therapy for the drug to reach therapeutic levels. (Lilley 431)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Antiplatelet drugs

Encourage patients to change positions slowly and to take their time in going from lying to sitting to standing because of the adverse effects of dizziness and postural hypotension with (Lilley 431)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

With thrombolytic drugs

Advise patients to report pink, red, or cloudy urine; black, tarry stools or frank red blood in the stools; abdominal or chest pain; dizziness; or severe headache. Continually monitor the INR, aPTT, platelet counts, and fibrinogen levels, beginning no later than 2 to 3 hours after the administration of thrombolytics. Measure the patient's fibrinogen level to check for the occurrence of fibrinolysis. With the breakdown of fibrin (or fibrinolysis), INR will increase and aPTT will be prolonged. If bleeding occurs, the prescriber will most likely discontinue the drug and replace fibrinogen through infusions of whole blood plasma or cryoprecipitate. The antifibrinolytics aminocaproic acid and/or tranexamic acid may also be given. See Patient-Centered Care: Patient Teaching later in the chapter. (Lilley 431)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Aminocaproic acid and tranexamic acid (Lilley 431)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

are usually given IV until bleeding is controlled. Because of the possibility of drug-induced internal, intracranial, and superficial bleeding, closely monitor the patient, and notify the prescriber immediately if there is any change in motor strength or 432level of consciousness. You must apply your knowledge of certain adverse effects of drugs like these to prevent complications, maintain safety, and return the patient to a healthier state. It is also important to monitor heart rate and blood pressure with attention to the quality and strength of peripheral pulses. For the patient with hemophilia, tranexamic acid may be used to help decrease bleeding from dental extractions. (Lilley 431-432)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Therapeutic effetivenwas

Therapeutic levels of anticoagulants and other clotting-altering drugs or coagulation modifier drugs are also monitored by laboratory studies such as aPTT, PT, and INR, which are described in the Safety: Laboratory Values Related to Drug Therapy box. Remember, however, that aPTT levels are measured with heparin, whereas PT and INR are measured with warfarin. Once the level of the particular drug stabilizes and maintenance therapy is ongoing, the clotting studies may be performed at 1- to 4-week intervals, depending on the specific drug, the patient's response, and the patient's overall physical condition. If a heparin or LMWH overdose occurs, the antidote is protamine sulfate, whereas vitamin K, or phytonadione, is the antidote to oral anticoagulant overdose. (Lilley 432)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.

Patient teaching

educate the patient to protect the original bottle from moisture. Once a bottle is opened, it must be used within 60 days; this needs to be written on the bottle/label with the date of expiration. Instruct the patient to remove only 1 capsule from the opened bottle at the time of use and that the bottle needs to be immediately and tightly closed. Encourage the patient to take the medication with food if dyspepsia occurs. These capsules are not to be repackaged or placed in other pillboxes/organizers. For more information, visit www.pradaxapro.com. (Lilley 433)

Lilley, Linda, Shelly Collins, Julie Snyder. Pharmacology and the Nursing Process, 8th Edition. Mosby, 022016. VitalBook file.