Describes the drug’s chemical composition and molecular structure

Generic name (nonproprietary name)

Name given by the United States Adopted Names Council

Trade name (proprietary name)

The drug has a registered trademark; use of the name is restricted by the drug’s patent owner (usually the manufacturer).

Drug classifications:

By structure (ex: beta blocker)  Subclass (ex: selective, nonselective)  By therapeutic use (ex: antibiotic, antihypertensives) Prototypical drugs-first drug in a class of drugs

study of how various drug forms influence the way in which the drug affects the body.

dissolving of solid dosage forms and their absorption

tablets, capsules, oral soluble wafers, pills, timed-release capsules, timed-release tablets, elixirs, suspensions, syrups, emulsions, solutions, lozenges or troches, rectal suppositories, sublingual or buccal tablets

Injectable forms, solutions, suspensions, emulsions, powders for reconstitution

Aerosols, ointments, creams, pastes, powders, solutions, foams, gels, transdermal patches, inhalers, rectal and vaginal suppositories

study of what the body does to the drug

The movement of a drug from its site of administration into the bloodstream for distribution to the tissues

initial metabolism of a drug in the liver that has been absorbed by the GI tract before the drug reaches the bloodstream

the transport of a drug by the bloodstream to its site of action  Albumin is the most common blood protein and carries the majority of protein- bound drug molecules.

Metabolism(biotransformation)

the biochemical alteration of a drug into an active metabolite

the elimination of drugs from the body (kidney, liver, bowel)

See Table 2.3, pages 19 &20 in the textbook for

Routes of Administration and Related Nursing Considerations

drug is absorbed into the systemic circulation through the oral or gastric mucosa or the small intestine.  Oral  Sublingual  Buccal  Rectal (can also be topical)

intravenous (fastest delivery into the blood circulation)  Intramuscular  Subcutaneous  Intradermal  Intraarterial  Intrathecal  Intraarticular

Skin (including transdermal patches)  Eyes  Ears  Nose  Lungs (inhalation)  Rectum vagina

the process where the kidneys filter waste, toxins, and excess substances from the blood, eliminating them from the body via urine

the liver's process of eliminating waste, drugs, and metabolites by actively secreting them into bile, which then travels to the intestines for fecal elimination or reabsorption

time required for half (50%) of a given drug to be removed from the body  Measures the rate at which the drug is eliminated from the body  After approximately five half-lives, most drugs are considered to be effectively removed from the body

Physiologic state in which the amount of drug removed via elimination is equal to amount of drug absorbed with each dose.

time required for a drug to elicit a response

time required for a drug to reach maximum therapeutic response

study of what the drug does to the body  The mechanism of drug actions in living tissues

clinical use of drugs to prevent and treat diseases  Defines principles of drug actions—the cellular processes that change in response to the presence of drug molecules

conditions, situations, or other substances that make a particular treatment or drug unsafe to use, potentially causing harm

involves intensive, short-term rehabilitation (Physical, Occupational, Speech Therapy) in a hospital setting for patients needing immediate stabilization after severe injury, illness, or surgery

ongoing treatment to prevent the return of a disease (like cancer) or to stop functional decline in chronic conditions

Supplemental (or replacement) therapy

provides substances your body lacks, most commonly hormones , to restore balance, ease symptoms (hot flashes, bone loss), and improve well-being, involving prescription medications, bioidentical hormones, or sometimes plant-based alternatives

focuses on relieving symptoms, distress, and side effects of serious illnesses, improving quality of life, rather than curing the underlying disease

any medical treatment, medication, or action taken to prevent a disease, infection, or complication from developing, rather than treating it after it occurs

starting medical treatment, often antibiotics, based on an educated guess or experience before a specific diagnosis is confirmed

a beneficial or desirable outcome from treatment, such as pain relief from medication or improved coping skills in therapy

a measure of a drug's safety, representing the ratio between the dose that causes toxicity and the dose that produces a desired therapeutic effect

occur when the combined result of two or more agents (like drugs, chemicals, or genetic factors) is equal to the simple sum of their individual effects, often described as 2 + 2 = 4, without interaction

occurs when mixing medications (or drugs with solutions/foods/supplements) causes a chemical or physical reaction, creating an inactive, toxic substance, or changing drug potency/effectiveness

any harm or injury resulting from a medication, including side effects, allergic reactions, overdoses, or errors

Adverse drug withdrawal event

a clinical set of symptoms or worsening of a condition that occurs when a medication is stopped or its dose is reduced

Idiosyncratic reaction

a rare, unpredictable, and often severe adverse response to a drug or substance that isn't a typical side effect

describes agents (like drugs, chemicals, infections, alcohol) that interfere with normal fetal development, causing birth defects or abnormalities, with effects depending on the agent, dose, and timing of exposure during pregnancy

a substance or agent that causes a permanent change (mutation) in the DNA of a cell, altering its genetic material, which can lead to cell damage, disease (like cancer), or altered traits

The study of natural (versus synthetic) drug sources

Four main sources for drugs

Plants  Animals  Minerals  Laboratory synthesis

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pharmacology

Question	Answer
Chemical name	Describes the drug’s chemical composition and molecular structure
Generic name (nonproprietary name)	Name given by the United States Adopted Names Council
Trade name (proprietary name)	The drug has a registered trademark; use of the name is restricted by the drug’s patent owner (usually the manufacturer).
Drug classifications:	By structure (ex: beta blocker)  Subclass (ex: selective, nonselective)  By therapeutic use (ex: antibiotic, antihypertensives) Prototypical drugs-first drug in a class of drugs
PHARMACEUTICS	study of how various drug forms influence the way in which the drug affects the body.
Dissolution	dissolving of solid dosage forms and their absorption
Enteral	tablets, capsules, oral soluble wafers, pills, timed-release capsules, timed-release tablets, elixirs, suspensions, syrups, emulsions, solutions, lozenges or troches, rectal suppositories, sublingual or buccal tablets
Parenteral	Injectable forms, solutions, suspensions, emulsions, powders for reconstitution
topical	Aerosols, ointments, creams, pastes, powders, solutions, foams, gels, transdermal patches, inhalers, rectal and vaginal suppositories
PHARMACOKINETICS	study of what the body does to the drug
Absorption	The movement of a drug from its site of administration into the bloodstream for distribution to the tissues
Bioavailability	the extent of drug absorption
First-pass effect	initial metabolism of a drug in the liver that has been absorbed by the GI tract before the drug reaches the bloodstream
Distribution	the transport of a drug by the bloodstream to its site of action  Albumin is the most common blood protein and carries the majority of protein- bound drug molecules.
Metabolism(biotransformation)	the biochemical alteration of a drug into an active metabolite
Excretion	the elimination of drugs from the body (kidney, liver, bowel)
See Table 2.3, pages 19 &20 in the textbook for	Routes of Administration and Related Nursing Considerations
ENTERAL ROUTE	drug is absorbed into the systemic circulation through the oral or gastric mucosa or the small intestine.  Oral  Sublingual  Buccal  Rectal (can also be topical)
PARENTERAL ROUTE	intravenous (fastest delivery into the blood circulation)  Intramuscular  Subcutaneous  Intradermal  Intraarterial  Intrathecal  Intraarticular
TOPICAL ROUTE	Skin (including transdermal patches)  Eyes  Ears  Nose  Lungs (inhalation)  Rectum vagina
Cytochrome P-450 enzymes (or simply P-450 enzymes), also known as	microsomal enzymes
Lipophilic	fat loving
Hydrophilic	water loving
Renal excretion	the process where the kidneys filter waste, toxins, and excess substances from the blood, eliminating them from the body via urine
Biliary excretion	the liver's process of eliminating waste, drugs, and metabolites by actively secreting them into bile, which then travels to the intestines for fecal elimination or reabsorption
HALF-LIFE	time required for half (50%) of a given drug to be removed from the body  Measures the rate at which the drug is eliminated from the body  After approximately five half-lives, most drugs are considered to be effectively removed from the body
Steady state	Physiologic state in which the amount of drug removed via elimination is equal to amount of drug absorbed with each dose.
Onset of action	time required for a drug to elicit a response
Peak effect	time required for a drug to reach maximum therapeutic response
Trough level	lowest blood level of a drug
PHARMACODYNAMICS	study of what the drug does to the body  The mechanism of drug actions in living tissues
PHARMACOTHERAPEUTICS	clinical use of drugs to prevent and treat diseases  Defines principles of drug actions—the cellular processes that change in response to the presence of drug molecules
Contraindications	conditions, situations, or other substances that make a particular treatment or drug unsafe to use, potentially causing harm
Acute therapy	involves intensive, short-term rehabilitation (Physical, Occupational, Speech Therapy) in a hospital setting for patients needing immediate stabilization after severe injury, illness, or surgery
Maintenance therapy	ongoing treatment to prevent the return of a disease (like cancer) or to stop functional decline in chronic conditions
Supplemental (or replacement) therapy	provides substances your body lacks, most commonly hormones , to restore balance, ease symptoms (hot flashes, bone loss), and improve well-being, involving prescription medications, bioidentical hormones, or sometimes plant-based alternatives
Supportive therapy	focuses on relieving symptoms, distress, and side effects of serious illnesses, improving quality of life, rather than curing the underlying disease
Prophylactic therapy	any medical treatment, medication, or action taken to prevent a disease, infection, or complication from developing, rather than treating it after it occurs
Empiric therapy	starting medical treatment, often antibiotics, based on an educated guess or experience before a specific diagnosis is confirmed
Therapeutic response	a beneficial or desirable outcome from treatment, such as pain relief from medication or improved coping skills in therapy
Therapeutic index	a measure of a drug's safety, representing the ratio between the dose that causes toxicity and the dose that produces a desired therapeutic effect
Additive effects	occur when the combined result of two or more agents (like drugs, chemicals, or genetic factors) is equal to the simple sum of their individual effects, often described as 2 + 2 = 4, without interaction
Incompatibility	occurs when mixing medications (or drugs with solutions/foods/supplements) causes a chemical or physical reaction, creating an inactive, toxic substance, or changing drug potency/effectiveness
Adverse drug event	any harm or injury resulting from a medication, including side effects, allergic reactions, overdoses, or errors
Adverse drug withdrawal event	a clinical set of symptoms or worsening of a condition that occurs when a medication is stopped or its dose is reduced
Pharmacologic reaction	the body's response to a drug
Idiosyncratic reaction	a rare, unpredictable, and often severe adverse response to a drug or substance that isn't a typical side effect
Teratogenic	describes agents (like drugs, chemicals, infections, alcohol) that interfere with normal fetal development, causing birth defects or abnormalities, with effects depending on the agent, dose, and timing of exposure during pregnancy
Mutagenic	a substance or agent that causes a permanent change (mutation) in the DNA of a cell, altering its genetic material, which can lead to cell damage, disease (like cancer), or altered traits
PHARMACOGNOSY	The study of natural (versus synthetic) drug sources
Four main sources for drugs	Plants  Animals  Minerals  Laboratory synthesis
PHARMACOECONOMICS	Study of the economic factors influencing the cost of drug therapy  Cost–benefit analysis  Examine treatment outcomes in relation to the comparative total costs
TOXICOLOGY	Science of the adverse effects of chemicals on living organisms  Clinical toxicology deals specifically with the care of poisoned patients.  Poison Control Centers  Treatment based on system of priorities
These lifespan changes have dramatic effects of the four phases of pharmacokinetics	Pregnancy ◦ Newborn ◦ Pediatric ◦ Older adult
Considerations for Older Adult Patients	Decline in organ function occurs with advancing age. ◦ Drug therapy in older adults is most likely to result in adverse effects and toxicity, Polypharmacy ◦ Noncompliance, nonadherence ◦ Increased incidence of chronic illnesses
Absorption older adult	gastric pH less acidic ◦ Gastric emptying slowed ◦ Movement through GI tract slowed because of decreased muscle tone and activity ◦ Blood flow to GI tract reduced ◦ Absorptive surface of GI tract reduced
Distribution older adult	Lower total body water percentages ◦ Increased fat content ◦ Decreased production of proteins by the liver, resulting in decreased protein bindin of drugs (and increased circulation of free drugs)
Metabolism older adult	Aging liver produces fewer microsomal enzymes, affecting drug metabolism. ◦ Reduced blood flow to the liver ◦ Potential for drug toxicity to due decreased metabolism
Excretion older adult	Decreased glomerular filtration rate ◦ Decreased number of nephrons ◦ Drugs are cleared less effectively because of decreased excretion
NEAR MISS	Event or situation that did not produce patient injury, but only because of chance • Must still be reported so that safety issues can be addressed and future incidents are prevented
Never use a	trailing zero” with medication orders. • Do not use 1.0 mg; use 1 mg.
Always use a	“leading zero” for decimal dosages. • Do not use .25 mg; use 0.25 mg.
REPORTING MEDICATION ERRORS	Report to prescriber and nursing management. • Document error per policy and procedure. • Factual documentation only • Medication administered • Actual dose • Observed changes in patient condition • Prescriber notified and follow-up orders
PREVENTING PEDIATRIC MEDICATION ERRORS	Obtain and document accurate weight (kg) • Report all medication errors. • Know the drug thoroughly. • Follow the Rights of medication administration. • Avoid verbal orders in general. • Avoid distractions.
MEDICATION RECONCILIATION	• Patients provide a list of all the medications they are currently taking (including herbals and over- the-counter drugs). • Prescriber then assesses the medications and decides if they are to be continued upon hospitalization
MEDICATION RECONCILIATION (CONT.)	Should be done at each stage of health care delivery: • Admission • Status change (e.g., from critical to stable) • Patient transfer within or between facilities or provider teams • Discharge
Adrenergic Blockers	Bind to adrenergic receptors but inhibit or block stimulation of the sympathetic nervous system (SNS)  Have the opposite effect of adrenergic drugs  Inhibit—or lyse—sympathetic stimulation
Beta Blockers	Block stimulation of beta receptors in the SNS  Compete with norepinephrine and epinephrine  Can be selective or nonselective  Cardioselective beta blockers or beta1-blocking drugs  Nonselective beta blockers block both beta1 and beta2 receptors
Beta2 receptors are located primarily on the	smooth muscles of the bronchioles and blood vessels.
Carvedilol and labetalol:	alpha-receptor– blocking activity, especially at higher dosages
Acebutolol, penbutolol, pindolol: not only block beta-adrenergic receptors but also	partially stimulate them
Beta 1 Receptors	Located primarily on the heart  Beta blockers selective for these receptors are called cardioselective beta blockers.
beta 2 receptors	Located primarily on smooth muscle of bronchioles and blood vessels
Cardioselective beta blockers (beta 1)	Reduce SNS stimulation of the heart  Decrease heart rate  Prolong sinoatrial (SA) node recovery  Slow conduction rate through the AV node  Decrease myocardial contractility, thus reducing myocardial oxygen demand
Beta Blockers: Mechanism of Action	Nonselective beta blockers (beta1 and beta2)  Cause same effects on heart as cardioselective beta blockers  Constrict bronchioles, resulting in narrowing of airways and shortness of breath  Produce vasoconstriction
Beta Blockers: Indications	Angina  Decreases demand for myocardial oxygen  Cardioprotective  Inhibits stimulation from circulating catecholamines  Used in patients who have had a MI  Dysrhythmias  Class II antidysrhythmic  Migraine headache
Beta Blockers: Indications (Cont.)	Antihypertensive  Ability to reduce SNS stimulation of the heart, reducing heart rate and force of myocardial contraction  Heart failure  Glaucoma (topical use)
Beta Blockers: Contraindications	Known drug allergy  Uncompensated heart failure  Cardiogenic shock  Heart block, bradycardia  Pregnancy  Severe pulmonary disease  Raynaud’s disease
Beta Blockers: Adverse Effects	Blood Agranulocytosis, thrombocytopenia Cardiovascular AV block, bradycardia, heart failure CNS Dizziness, depression, unusual dreams, drowsiness, Gastrointestinal Nausea, vomiting, diarrhea, constipation BRONCHOSPASMS
Nonselective beta blockers may interfere with	normal responses to hypoglycemia (tremor, tachycardia, nervousness).  May mask signs and symptoms of hypoglycemia  Use with caution in patients with diabetes mellitus
Beta Blockers: Toxicity and Management of Overdose	Symptomatic and supportive care  Atropine for bradycardia  Cardiac pacing  Vasopressors for severe hypotension  Hemodialysis
Atenolol (Tenormin)	Cardioselective beta blocker  Commonly used to prevent future heart attacks in patients who have had one  Hypertension and angina  Management of thyrotoxicosis to help block the symptoms of excessive thyroid activity
Carvedilol (Coreg)	Nonselective beta blocker, an alpha1-blocker, a calcium channel blocker, and possibly an antioxidant  Uses: heart failure, hypertension, and angina  Slows progression of heart failure
Esmolol (Brevibloc)	Very strong short-acting beta1-blocker  Primary use: acute situations to provide rapid temporary control of the ventricular rate in patients with supraventricular tachydysrhythmias  Administered IV
Metoprolol (Lopressor)	Most commonly used beta1 blocker  Oral and injectable  Monitoring required when giving IV  Increased survival rate in patients when taken following an MI
Propranolol (Inderal)	Prototypical nonselective beta1 and beta2-blocking drug  Multiple uses  Tachydysrhythmias  Subaortic stenosis  Migraine headaches  Essential tremor  Oral and injectable form
Sotalol (Betapace)	Nonselective beta blocker  Potent antidysrhythmic properties  Indicated for management of difficult-to-treat dysrhythmias  Oral use
Nonselective Beta Blockers	Carvedilol  Labetalol  Nadolol  Penbutolol  Pindolol  Propranolol  Sotalol  Timolol
Cardioselective Beta Blockers	Acebutolol (Sectral)  Atenolol (Tenormin)  Betaxolol (Kerlone)  Esmolol (Brevibloc)  Nebivolol (Bystolic)  Metoprolol
Beta-Blocking Drugs: Nursing Implications	hypertension if this medication is discontinued abruptly.  Instruct patients to notify their physicians if they become ill and unable to take medication.  Inform patients that they may notice a decrease in tolerance for exercise
Beta-Blocking Drugs: Nursing Implications (Cont.)	Weight gain of more than 2 lb in 1 day or 5 lb in 1 week  Edema of the feet or ankles  Shortness of breath  Excessive fatigue or weakness  Syncope or dizziness
Parasympathetic nervous system (PNS):	stimulates smooth muscles, cardiac muscles, glands
Sympathetic nervous system	stimulates heart, blood vessels, skeletal muscles • Stimulation is controlled by neurotransmitters. • Acetylcholine • Norepinephrine
ACE inhibitors	Currently are 10 ACE inhibitors • Often used as first-line drugs for HF and hypertension • May be combined with a thiazide diuretic or CCB
ACE inhibitors meds	PRIL
ACE Inhibitors: Mechanism of Action	converts angiotensin I (AI) (formed through the action of renin) to angiotensin II (AII) • AII: potent vasoconstrictors that induce aldosterone secretion by the adrenal glands • Aldosterone: stimulates sodium and water resorption, which can raise BP
Primary Effects of the ACE Inhibitors	Cardiovascular and renal • BP: reduce BP by decreasing SVR • HF • Prevent sodium and water resorption by inhibiting aldosterone secretion • Diuresis: decreases blood volume and return to the heart • Decreases preload
Cardioprotective Effects of the ACE Inhibitors	ACE inhibitors decrease SVR (a measure of afterload) and preload. • Used to prevent complications after MI • Ventricular remodeling: left ventricular
Renal Protective Effects of the ACE Inhibitors	ACE inhibitors: reduce glomerular filtration pressure • Cardiovascular drugs of choice for patients with diabetes • ACE inhibitors reduce proteinuria
ACE Inhibitors: Indications	Hypertension • HF (either alone or in combination with diuretics or other drugs) • Slow progression of left ventricular hypertrophy after myocardial infarction
ACE Inhibitors: Adverse Effects	Fatigue • Dizziness • Headache • Mood changes • Impaired taste • Possible hyperkalemia • Dry, nonproductive cough, which reverses when therapy is stopped
Captopril (Capoten)	Uses: prevention of ventricular remodeling after MI; reduce the risk of HF after MI • Shortest half-life • Must be administered multiple times throughout the day
Enalapril (Vasotec)	Only ACE inhibitor available in both oral and parenteral preparations • Enalapril intravenous (IV) does not require cardiac monitoring. • Oral enalapril: prodrug
Angiotensin II Receptor Blockers	Also referred to as angiotensin II blockers • Well tolerated • Do not cause a dry cough that is common with ACE inhibitors
Angiotensin II Receptor Blockers: Mechanism of Action	ARBs affect primarily vascular smooth muscle and the adrenal gland. • Selectively block the binding of AII to the type 1 AII receptors in these tissues • ARBs block vasoconstriction and the secretion of aldosterone.
Comparison of ACE Inhibitors and Angiotensin II Receptor Blocker	ACE inhibitors and ARBs appear to be equally effective for the treatment of hypertension. • Both are well tolerated. • ARBs do not cause cough.
Angiotensin II Receptor Blockers: Indications	Hypertension • Adjunctive drugs for the treatment of HF • May be used alone or with other drugs such as diuretics
Angiotensin II Receptor Blockers: Adverse Effects	Chest pain • Fatigue • Hypoglycemia • Diarrhea • Urinary tract infection • Anemia • Weakness
Angiotensin II Receptor Blockers Nursing Implications	contraindications to specific antihypertensive drugs., not missing a dose, Oral forms should be given with meals, administer iv wt caution, Hot tubs, showers, or baths; hot weather may aggravate low BP
ACE Inhibitors and Laboratory Values	ACE inhibitors can cause renal impairment, which can be identified with serum creatinine. • ACE inhibitors can also cause hyperkalemia
Angina Pectoris	When the supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle “aches.”  The heart requires a large supply of oxygen to meet the demands placed on it.
Ischemia	Poor blood supply to an organ  Ischemic heart disease  Poor blood supply to the heart muscle  Atherosclerosis  Coronary artery disease
MI	Necrosis, or death, of cardiac tissue  Disabling or fatal
Chronic stable angina	predictable, short-lived chest discomfort (pressure, squeezing, or burning) caused by reduced blood flow to the heart, typically due to coronary artery disease
Unstable angina	a high-risk acute coronary syndrome (ACS) characterized by unexpected, severe, or resting chest pain, often caused by ruptured plaque and partial coronary artery blockage
Vasospastic angina	rare form of chest pain caused by temporary, severe spasms of the coronary arteries that restrict blood flow, often occurring at rest, typically at night or early morning
Drugs for Angina	Nitrates or nitrites  Beta blockers  Calcium channel blockers
Nitrates and Nitrites: Mechanism of Action	Cause vasodilation because of relaxation of smooth muscles  Potent dilating effect on coronary arteries  Result: oxygen to ischemic myocardial tissue
Nitrates and Nitrites: Indications	Treat stable, unstable, and vasospastic angina  Rapid-acting forms  Used to treat acute anginal attacks  Sublingual tablets; IV infusion
Nitrates: Contraindications	Known drug allergy  Severe anemia  Closed-angle glaucoma  Hypotension  Severe head injury  Use of the erectile dysfunction
Nitrates: Adverse Effects	Headaches  Usually diminish in intensity and frequency with continued use  Reflex tachycardia  Postural hypotension  Flushing  Weakness  Nausea  Skin irritation
nitrates Tolerance	Occurs in patients taking nitrates around the clock or with long-acting forms  Prevented by allowing a regular nitrate-free period to allow enzyme pathways to replenish
Isosorbide dinitrate	Organic nitrate  Available in rapid-acting sublingual tablets, immediate-release tablets, and long-acting oral dosage forms  Produces more consistent, steady, therapeutic response
Nitroglycerin	Prototypical nitrate  The most important drug used in the symptomatic treatment of ischemic heart conditions such as angina
Nitrates	Nitroglycerin  Large first-pass effect with oral forms  Used for symptomatic treatment of ischemic heart conditions (angina)
Calcium Channel Blockers for Chronic Stable Angina	Amlodipine  Diltiazem  Nicardipine  Nifedipine  Verapamil
Calcium Channel Blockers: Mechanism of Action	Cause coronary artery vasodilation  Cause peripheral arterial vasodilation, thus decreasing systemic vascular resistance  Reduce the workload of the heart  Result: decreased myocardial oxygen demand
Calcium Channel Blockers: Indications	Angina  Hypertension  Supraventricular tachycardia  Coronary artery spasms (Prinzmetal angina)  Short-term management of atrial fibrillation and flutter  Migraine headaches  Raynaud’s disease Nimodipine
Nimodipine	cerebral artery spasms associated with aneurysm rupture
Calcium Channel Blockers: Contraindications	Known drug allergy  Acute MI  Second- or third-degree AV block (unless the patient has a pacemaker)  Hypotension
Calcium Channel Blockers: Adverse Effects	Limited  Primarily relate to overexpression of their therapeutic effects  May cause hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea
Diltiazem	Very effective for the treatment of angina pectoris resulting from coronary insufficiency and hypertension  Used in the treatment of atrial fibrillation and flutter along with paroxysmal supraventricular tachycardia
Amlodipine	Indicated for both angina and hypertension  Available only for oral use
Nursing Implications CCB	baseline vital signs, including respiratory patterns and rate.  Assess for drug interactions, should not take any medications, including over-the-counter medications, without checking with their physicians. limit caffeine
CCB Patients should report	Blurred vision  Persistent headache  Dry mouth  Edema  Fainting episodes  Weight gain of 2 lb in 1 day or 5 lb in 1 week  Pulse rate less than 60 beats/min
Nursing Implications Nitroglycerin	 Instruct patients never to chew or swallow the sublingual form. burning sensation felt with sublingual forms indicates that the drug is still potent.
Nursing Implications Nitroglycerin pt 2	medications should be stored in an airtight, dark glass bottle(protect from light) with a metal cap and no cotton filler, take as-needed nitrates at the first hint of anginal pain.  Monitor vital signs frequently during acute exacerbations of angina
Nitroglycerin—part 4  If anginal pain occurs	Stop activity and sit or lie down and take a sublingual tablet.  If there is no relief in 5 minutes, call 911 or emergency services immediately and take a second sublingual tablet.  If there is no relief in 5 minutes, take a third sublingual tablet.
IV forms of nitroglycerin must be given with	special non-PVC tubing and bags.  Discard parenteral solution that is blue, green, or dark red
CCBs problems	Constipation is a common problem; instruct patients to take in adequate fluids and eat high-fiber foods.  Monitor serum potassium levels  Swallow pills whole  Do not stop medications abruptly
Antianginal drugs monitor	adverse reactions: allergic reactions, headache, lightheadedness, hypotension, dizziness.  Monitor for therapeutic effects: relief of angina, decreased BP, or both.
Heart Failure	heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs, dyspnea, fatigue, fluid retention and/or pulmonary edema
“Left-sided” heart failure	pulmonary edema, coughing, shortness of breath, and dyspnea
Right-sided” HF	systemic venous congestion, pedal edema, jugular venous distension, ascites, and hepatic congestion
Heart Failure: Causes	(MI) Coronary artery disease Cardiomyopathy Valvular insufficiency Atrial fibrillation Infection Tamponade ischemia
Stages of Heart Failure	Stage A: At high risk for heart failure but no symptoms or structural heart disease Stage B: Structural heat disease but no symptoms Stage C: Structural heart disease with symptoms Stage D: Refractory HF requiring intervention
Positive inotropic drugs	increase the force of myocardial contraction
Positive chronotropic drugs	increase heart rate
Positive dromotropic drugs	accelerate cardiac conduction
Drug Therapy for Heart Failure	Positive inotropic drugs  Phosphodiesterase inhibitors  Cardiac glycosides  Sinoatrial modulators  Angiotensin receptor-neprilysin inhibitors, ACE, ARBS, Beta blockers  Diuretics
Drugs of Choice for Early Treatment of Heart Failure	Focus on reducing effects of the renin- angiotensin-aldosterone system and the sympathetic nervous system ACE inhibitors, ARBS, some beta blockers
Drugs of Choice for Early Treatment of Heart Failure (Cont.)	Loop diuretics (furosemide) are used to reduce the symptoms of HF secondary to fluid overload. Aldosterone inhibitors (spironolactone, eplerenone) are added as the HF progresses. Only after these drugs are used is digoxin added
Drugs of Choice for Early Treatment of Heart Failure (Cont. again)	Dobutamine: positive inotropic drug Hydralazine and isosorbide dinitrate became the first drug approved for a specific ethnic group. Hydralazine/isosorbide dinitrate
ACE Inhibitors pt 2	Inhibit angiotensin-converting enzyme. Responsible for converting angiotensin I to angiotensin II Prevent sodium and water resorption by inhibiting aldosterone secretion. Diuresis results, which decreases preload,
Lisinopril	Uses: hypertension, HF, and acute MI Hyperkalemia Common adverse effect: dry cough, hyperkalemia, decreased renal function
Angiotensin II Receptor Blockers pt 2	Potent vasodilators; decrease systemic vascular resistance (afterload) Used alone or in combination with other drugs such as diuretics in the treatment of hypertension or HF
Valsartan	Valsartan shares many of the same adverse effects as lisinopril. ARBs are not as likely to cause the cough associated with the ACE inhibitors. ARBs are not as likely to cause hyperkalemia
Angiotensin Receptor-Neprilysin Inhibitors	Newer class of drugs Valsartan/sacubitril (Entresto) Blocks the degradation of vasoactive peptides by inhibiting the neprilysin enzyme Common adverse effects: hypotension, hyperkalemia, increased serum creatinine
Beta Blockers heart failure	prevent catecholamine-mediated actions on the heart by reducing or blocking sympathetic nervous system stimulation to the heart and the heart’s conduction system, reduced heart rate, delayed AV node conduction, reduced myocardial contractility
Aldosterone Antagonists	Useful in severe stages of HF Action: activation of the renin-angiotensin- aldosterone system causes increased levels of aldosterone, which causes retention of sodium and water, leading to edema that can worsen HF
Aldosterone Antagonists Spironolactone	potassium-sparing diuretic and aldosterone antagonist shown to reduce the symptoms of HF
Aldosterone Antagonists Eplerenone	selective aldosterone blocker, blocking aldosterone at its receptors in the kidney, heart, blood vessels, and brain
Hydralazine/isosorbide dinitrate	First drug approved for a specific ethnic group, namely African Americans
Dobutamine	Beta1-selective vasoactive adrenergic drug Structurally similar to dopamine
Ivabradine	Sinoatrial node modulator Inhibits f-channels within the SA node which ultimately results in reduced heart rate Used in stable, symptomatic HF with ejection fraction of =/< 35% Increase risk of atrial fibrillation, bradycardia, avoid grapefruit
B-Type Natriuretic Peptides-Nesiritide	Synthetic version of human B-type natriuretic peptide Vasodilating effects on both arteries and veins Effects of nesiritide Diuresis (urinary fluid loss) Natriuresis (urinary sodium loss) Vasodilation
B-Type Natriuretic Peptides: Adverse Effects	Nesiritide is used in the intensive care setting as a final effort to treat severe, life-threatening HF, often in combination with several other cardiostimulatory medications. Hypotension Dysrhythmia Headache
Phosphodiesterase Inhibitors (PDIs)	Work by inhibiting the enzyme phosphodiesterase Result in Intracellular increase in cAMP Positive inotropic response Vasodilation Increase in calcium for myocardial muscle contraction. Inodilators (inotropics and dilators)
Phosphodiesterase Inhibitors: Indications	Short-term management of HF for patients in the intensive care unit (ICU) AHA and ACC advise against long-term infusions.
Milrinone	Only available phosphodiesterase inhibitor-which increases calcium resulting in an increased cardiac contraction  positive inotropic response- resulting in vasodilation  Milrinone is available only in injectable form.
Milrinone adverse effects and Interactions	cardiac dysrhythmias, headache, hypokalemia, tremor, thrombocytopenia, and elevated liver enzyme levels diuretics (additive hypotensive effects) and digoxin (additive inotropic effects) affects electrolytes
Cardiac Glycosides	One of the oldest groups of cardiac drugs No longer used as first-line treatment Not been shown to reduce mortality in HF patients Originally obtained from Digitalis plant, foxglove Digoxin is the prototype. Used in HF
Cardiac Glycosides: Mechanism of Action	Increase myocardial contractility Change electrical conduction properties of the heart Decrease rate of electrical conduction Prolong the refractory period Area between sinoatrial (SA) node and atrioventricular (AV) node
Cardiac Glycosides: Drug Effects	Positive inotropic effect Increased force and velocity of myocardial contraction (without an increase in oxygen consumption) Negative chronotropic effect Reduced heart rate Negative dromotropic effect Decreased automaticity at SA node
Cardiac Glycosides: Drug Effects (Cont.)	Increased stroke volume  Reduction in heart size during diastole  Decrease in venous BP and vein engorgement  Increase in coronary circulation  Decrease in exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis
Cardiac Glycosides: Adverse Effects	Digoxin (Lanoxin) Very narrow therapeutic window Drug levels must be monitored. 0.5 to 2 ng/mL Low potassium levels increase its toxicity
Cardiac Glycosides: Adverse Effects (Cont.)	Cardiovascular: dysrhythmias, including bradycardia or tachycardia Central nervous system: headaches, fatigue, malaise, confusion, convulsions Eyes: colored vision (seeing green, yellow, purple), halo vision, flickering light
Digoxin Toxicity	Digoxin immune Fab (Digibind) therapy Hyperkalemia (serum potassium greater than 5 mEq/L) in a digitalis-toxic patient Life-threatening cardiac dysrhythmias Life-threatening digoxin overdose
Conditions That Predispose to Digoxin Toxicity	Hypokalemia Use of cardiac pacemaker Hepatic dysfunction Hypercalcemia Dysrhythmias Hypothyroid, respiratory, or renal disease
Heart Failure Drugs: Nursing Implications	Assess history, drug allergies, and contraindications. Assess clinical parameters, including: BP Apical pulse for 1 full minute Heart sounds, breath sounds
Heart Failure Drugs: Nursing Implications (Cont.)	Assess clinical parameters (Cont.) Weight, input, and output measures Electrocardiogram Serum labs: potassium, sodium, magnesium, calcium, renal, and liver function studies
Heart Failure Drugs: Nursing Implications (Cont.) AGAIN	Before giving any dose, count apical pulse for 1 full minute. For an apical pulse less than 60 or greater than 100 beats/min: Hold dose. Notify prescribe rAvoid giving digoxin with high-fiber foods (fiber weight gain of 2 lb or more in 1 day
Nesiritide or milrinone implications	Use an infusion pump. Monitor input and output, heart rate and rhythm, BP, daily weights, respirations, and so on.
Dysrhythmia	Any deviation from the normal rhythm of the heart
Antidysrhythmics	Used for the treatment and prevention of disturbances in cardiac rhythm
Dysrhythmia  Can develop in	association with many conditions  After MI, cardiac surgery, or as a result of CAD  Usually serious and may require treatment with antidysrhythmic drug or nonpharmacological therapies
Cardiac Cell	Inside the resting cardiac cell, there is a net negative charge relative to the outside of the cell.  This difference in electronegative charge results from an uneven distribution of ions (sodium, potassium, calcium) across the cell membrane.
Resting Membrane Potential	An energy-requiring pump is needed to maintain this uneven distribution of ions.  Sodium-potassium ATPase pump  The RMP results from an uneven distribution of ions across the cell membrane
Action Potential	A change in the distribution of ions causes cardiac cells to become excited.  The movement of ions across the cardiac cell’s membrane results in an electrical impulse spreading across the cardiac cells.
Action Potential phases 0-1	Phase 0: upstroke  Resting cardiac cell membrane suddenly becomes highly permeable to sodium ions; movement through sodium channels  Depolarization  Phase 1  Begins a rapid process of repolarization that continues through more phases
Action Potential Duration	Interval between Phase 0 and Phase 4  Absolute or effective refractory period  Relative refractory period  Threshold potential  Automaticity or pacemaker activity
Aspects of Action Potential	SA node, AV node, and His-Purkinje cells all possess the property of automaticity.  SA node is the natural pacemaker of the heart.  SA node has an intrinsic rate of 60 to 100 bpm.  AV node has an intrinsic rate of 40 to 60 bpm.
Supraventricular dysrhythmias	Originate above the ventricles in SA or AV node or atrial myocardium
Ventricular dysrhythmias	Originate below the AV node in the His-Purkinje system or ventricular myocardium
Ectopic foci	Outside the conduction system
Conduction blocks	Dysrhythmias that involve the disruption of impulse conduction between the atria and ventricles
Vaughan Williams classification	System commonly used to classify antidysrhythmic drugs  Based on the electrophysiologic effect of particular drugs on the action potential
Vaughan Williams Classification 1	Membrane-stabilizing drugs  Fast sodium channel blockers  Divided into Ia, Ib, and Ic drugs, according to effects
Vaughan Williams Classification la	procainamide, quinidine, and disopyramide  Block sodium (fast) channels  Delay repolarization  Increase APD  Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions
Vaughan Williams Classification lb	phenytoin, lidocaine  Block sodium channels  Accelerate repolarization  Increase or decrease APD  Lidocaine is used for ventricular dysrhythmias only.  Phenytoin is used for atrial and ventricular tachydysrhythmias caused by digitalis toxicity
Vaughan Williams Classification lc	flecainide, propafenone  Block sodium channels (more pronounced effect)  Little effect on APD or repolarization  Used for severe ventricular dysrhythmias  May be used in atrial fibrillation or flutter, Wolff-Parkinson-White syndrome
Vaughan Williams Classification II	beta blockers  Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system  Depress Phase 4 depolarization
Vaughan Williams Classification III	amiodarone, dronedarone, dofetilide, sotalol, ibutilide  Increase APD  Prolong repolarization in Phase 3  Used for dysrhythmias that are difficult to treat  Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter
Vaughan Williams Classification IV	Calcium channel blockers  Inhibit slow-channel (calcium-dependent) pathways  Depress Phase 4 depolarization  Reduce AV node conduction  Used for paroxysmal supraventricular tachycardia
Contraindications to the Use of Antidysrhythmic Drugs	Known drug allergy  Second- or third-degree AV block, bundle branch block, cardiogenic shock, sick sinus syndrome, and any other ECG changes
Antidysrhythmics: Adverse Effects	ALL antidysrhythmics can cause dysrhythmias!  Hypersensitivity reactions  Nausea, vomiting, and diarrhea  Dizziness  Headache and blurred vision  Prolongation of the QT interval
Antidysrhythmics: Drug Interactions	Coumadin: monitor international normalized ratio  Grapefruit juice: amiodarone, disopyramide, and quinidine
Procainamide (Pronestyl)	Class Ia  Uses: atrial and ventricular tachydysrhythmias  Significant adverse effects: include ventricular dysrhythmias, blood disorders, systemic lupus erythematosus (SLE)–like syndrome
Procainamide (Pronestyl) contradictions	known hypersensitivity, heart block, and SLE
Quinidine (Quinidex)	Class Ia  Both direction action on the electrical activity of the heart and indirect (anticholinergic) effect  Significant adverse effects: cardiac asystole and ventricular ectopic beats  Others: cinchonism
Lidocaine (Xylocaine)	Class Ib, raises the ventricular fibrillation threshold twitching, convulsions, confusion, respiratory depression or arrest, hypotension, bradycardia, and dysrhythmias hypersensitive,Stokes-Adams or Wolff-Parkinson- White syndrome
Flecainide (Tambocor)	Class Ic  First-line drug in the treatment of atrial fibrillation  Negative inotropic effect and depresses left ventricular function  Adverse effects: dizziness, visual disturbances, and dyspnea  Contraindications: hypersensitivity, cardiog
Propafenone (Rythmol)	Class Ib  Similar action to flecainamide  Mild beta-blocking effects  Use: life-threatening ventricular dysrhythmias, atrial fibrillation  Most common reported adverse reaction: dizziness  Others: metallic taste, constipation
Atenolol (Tenormin)	Class II  Cardioselective beta blocker; preferentially blocks the beta1-adrenergic receptors that are located primarily in the heart.  Noncardioselective beta blockers block not only the beta1- adrenergic receptors in the heart but also the beta2-
Esmolol (Brevibloc)	Ultrashort-acting beta blocker  Cardioselective, blocks beta1-adrenergic receptors  Use: acute treatment of supraventricular tachydysrhythmias; hypertension; post-MI tachydysrhythmias
Metoprolol (Lopressor)	Class II  Another cardioselective beta blocker commonly given after an MI to reduce risk of sudden cardiac death  Treatment of hypertension and angina
Amiodarone	Class III  Markedly prolongs the action potential duration and the effective refractory period in all cardiac tissues  Blocks both the alpha- and beta-adrenergic receptors of the sympathetic nervous system
Amiodarone uses/indications	Uses: one of the most effective antidysrhythmic drugs for controlling supraventricular and ventricular dysrhythmias  Indications: management of sustained ventricular tachycardia, ventricular fibrillation, and nonsustained ventricular tachycardia
Amiodarone effects	corneal microdeposits, which may cause visual halos, photophobia, and dry eyes; photosensitivity; pulmonary toxicity
Amiodarone contraindications	Drug interactions: digoxin and warfarin  Contraindications: hypersensitivity, severe sinus bradycardia or second- or third-degree heart block
Ibutilide (Corvert)	Class III  Indicated for atrial dysrhythmias  Dosed based on body weight  Can cause ventricular dysrhythmias
Dofetilide (Tikosyn)	Class III  Only physicians who have received special training are allowed to prescribe.  Must be initiated in the hospital and patient have continuous ECG monitoring for first 3 days torsades de pointes, supraventricular dysrhythmias,chest pain
Sotalol (Betapace)	Class III  Selective beta blocker  Similar antidysrhythmic properties similar to class III while exerting beta blocker or class II effects on conduction  For life-threatening ventricular dysrhythmias
Diltiazem (Cardizem, Others)	Class IV  Temporary control of a rapid ventricular response in patients with atrial fibrillation hypersensitivity, acute myocardial infarction, pulmonary congestion, Wolff-Parkinson-White syndrome, severe hypotension, cardiogenic shock
Verapamil (Calan)	Class IV  Inhibits calcium ion influx across the slow calcium channels in cardiac conduction time  Results in dramatic effects on the AV node  Used to prevent and convert recurrent PSVT and control ventricular response
Unclassified Antidysrhythmic	Adenosine (Adenocard)  Slows conduction through the AV node  Used to convert PSVT to sinus rhythm  Very short half-life—less than 10 seconds  Only administered as fast intravenous (IV) push  May cause asystole
Adenosine considerations	Measure baseline blood pressure (BP), pulse, input and output, and cardiac rhythm.  Measure serum potassium, Assess plasma drug levels as indicated.Instruct patients not to crush or chew oral preps
Solutions of lidocaine that contain epinephrine should not be	given IV; they are to be used ONLY as local anesthetics.
Teach patients taking beta blockers, digoxin, and other drugs how to	take their own radial pulse for 1 full minute and to notify their physicians before taking the next dose if the pulse is less than 60 beats/min.
HEMOSTASIS	term for any process that stops bleeding Coagulation is hemostasis that occurs because of the physiologic clotting of blood.
COAGULATION SYSTEM	Cascade” Each activated factor serves as a catalyst that amplifies the next reaction. Result is fibrin, a clot-forming substance. Intrinsic pathway and extrinsic pathway
FIBRINOLYTIC SYSTEM	Initiates the breakdown of clots and serves to balance the clotting process Fibrinolysis: mechanism by which formed thrombi are lysed to prevent excessive clot formation
Fibrin in the clot binds to	circulating protein known as plasminogen. This binding converts plasminogen to plasmin. Plasmin is the enzymatic protein that eventually breaks down the fibrin thrombus into fibrin degradation products
HEMOPHILIA	Natural coagulation and hemostasis factors are limited or absent. Patients with hemophilia can bleed to death if coagulation factors are not given. Two types inhibit platelet aggregation  Factor VII deficiency  Factor VIII and/or factor IX
Anticoagulants	Inhibit the action or formation of clotting factors  Prevent clot formation, no direct effect on a blood clot that is already formed Prevent intravascular thrombosis by decreasing blood coagulability
Antiplatelet drugs	Inhibit platelet aggregation  Prevent platelet plugs
Hemorheologic drugs	Alter platelet function without preventing the platelets from working
Thrombolytic drugs	Lyse (break down) existing clots
Antifibrinolytic or hemostatic	Promote blood coagulation
Thromboembolic events	Myocardial infarction (MI): embolus lodges in a coronary artery  Stroke: embolus obstructs a brain vessel  Pulmonary emboli: embolus in the pulmonary circulation
Heparins—part 1	Action: inhibit clotting factors IIa (thrombin) and Xa  Unfractionated heparin: “heparin”  Low–molecular-weight heparins (LMWHs)  Enoxaparin (Lovenox)  Dalteparin
Heparins—part 2	Unfractionated heparin (heparin)  Relatively large molecule that is derived from animal sources  Frequent laboratory monitoring for bleeding times such as aPTT
Heparins—part 3	LMWHs  Enoxaparin (Lovenox) and dalteparin (Fragmin)  Synthetic smaller molecular structure  More predictable anticoagulant response  Frequent laboratory monitoring of bleeding times not needed
Coumarins	Action: inhibit vitamin K–dependent clotting factors II, VII, IX, and X  Warfarin (Coumadin)
Warfarin (Coumadin)	inhibits vitamin K synthesis by bacteria in the gastrointestinal tract  Inhibits production of vitamin K–dependent clotting factors II, VII, IX, and X, which are normally synthesized in the liver  Final effect prevention of clot formation
Direct thrombin inhibitors	Action: inhibit thrombin (factor IIa)  Human antithrombin III (Thrombate)  Lepirudin (Refludan)  Argatroban (Argatroban)  Bivalirudin (Angiomax)  Dabigatran (Pradaxa)
ANTICOAGULANTS: INDICATIONS	prevent clot formation in certain settings in which clot formation is likely  MI  Unstable angina  Atrial fibrillation  Indwelling devices, such as mechanical heart valves  Major orthopedic surgery
ANTICOAGULANTS: CONTRAINDICATIONS	Drug allergy Any acute bleeding process or high risk for such an occurrence. Warfarin is strongly contraindicated in pregnancy. Other anticoagulants are rated in lower pregnancy categories (B or C).
ANTICOAGULANTS: ADVERSE EFFECTS	Bleeding  Risk increases with increased dosages.  May be localized or systemic May also cause:  Heparin-induced thrombocytopenia  Nausea, vomiting, abdominal cramps, thrombocytopeni
HEPARIN-INDUCED THROMBOCYTOPENIA	Type I  Gradual reduction in platelets  Heparin therapy can generally be continued. Type II  Acute fall in the number of platelets (more than 50% reduction from baseline)  Discontinue heparin
HEPARIN-INDUCED THROMBOCYTOPENIA manifestations	Thrombosis that can be fatal  Treatment: thrombin inhibitors lepirudin and argatroban  Use of warfarin: can cause skin necrosis and “purple toes” syndrome
TOXIC EFFECTS OF HEPARIN	Symptoms: hematuria, melena (blood in the stool), petechiae, ecchymoses, and gum or mucous membrane bleeding Stop drug immediately. Intravenous (IV) protamine sulfate: 1 mg of protamine can reverse the effects of 100 units of heparin
TOXIC EFFECTS OF WARFARIN	Discontinue the warfarin. May take 36 to 42 hours before the liver can resynthesize enough clotting factors to reverse the warfarin effects Vitamin K1 (phytonadione) can hasten the return to normal coagulation.
TOXIC EFFECTS OF WARFARIN (CONT.)	Caution: when vitamin K is given, warfarin resistance will occur for up to 7 days. Severe bleeding: transfusions of human plasma or clotting factor concentrates. Life-threatening bleeding from warfarin: Kcentra
IDARUCIZUMAB (PRAXBIND)	Specific dabigatran antidote Reverses the anticoagulant effects for dabigatran for emergency surgery or in life-threatening or uncontrolled bleeding
DRUG INTERACTIONS: ANTICOAGULANTS	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 intestines
ARGATROBAN	Synthetic direct thrombin inhibitor Used for active HIT and percutaneous coronary intervention procedures in patients at risk for HIT Only given IV
DABIGATRAN (PRADAXA)	Prodrug that becomes activated in the liver  Specifically and reversibly binds to both free and clot- bound thrombin  Dose dependent on renal function  Adverse effects: bleeding, GI bleeding
ENOXAPARIN (LOVENOX)	Prototypical LMWH  Greater affinity for factor Xa than for factor Iia  Higher degree of bioavailability and longer elimination half-life  Lab monitoring is not necessary.  Injectable form
FONDAPARINUX (ARIXTRA)	treatment of DVT or PE  Bleeding is most common and serious adverse reaction.  Anemia, wound drainage, hematoma, confusion, UTI, hypotension, dizziness, hypokalemia  Thrombocytopenia can occur not be given for at least 6 to 8 hours after surgery
HEPARIN	Natural anticoagulant obtained from the lungs or intestinal mucosa of pigs  10 to 40,000 units/mL  DVT prophylaxis: 5000 units subcutaneously two or three times a day; does not need to be monitored when used for prophylaxis
RIVAROXABAN (XARELTO)	First oral factor Xa inhibitor Used for prevention of strokes in patients with a- fib; post-op thromboprophylaxis with ortho surgeries; treatment of DVT and PE Adverse reactions: Peripheral edema, dizziness, headache, bruising, diarrhea, hematuria
COUMADIN	Most commonly prescribed oral anticoagulant  Careful monitoring of the prothrombin time/international normalized ratio (PT/INR)  A normal INR (without warfarin) is 1.0, but a therapeutic INR (with warfarin) ranges from 2 to 3.5
ANTIPLATELET DRUGS	Work to prevent platelet adhesion at the site of blood vessel injury  Platelets normally flow through blood vessels without adhering to their surfaces  Collagen from damaged vessels stimulate platelet adhesion
ASPIRIN	many combinations with other prescription and nonprescription drugs Contraindicated for flulike symptoms in children and teenagers  Reye’s syndrome Aspiring and dipyridamole (Aggrenox)  Used for antiplatelet purposes
CLOPIDOGREL (PLAVIX)	Most widely used ADP inhibitor Oral use Prasugrel (Effient), ticagrelor (Brilinta)  Similar to clopidogrel
EPTIFIBATIDE (INTEGRILIN)	GP Iib/IIIa inhibitor Usually administered in an ICU or cardiac catheterization lab setting IV use
THROMBOLYTIC DRUGS	break down, or lyse, preformed clots Older drugs  Streptokinase and urokinase Current drugs  Alteplase (Activase, Cathflo Activase)
THROMBOLYTIC DRUGS: MECHANISM OF ACTION	Activate the fibrinolytic system to break down the clot in the blood vessel quickly Activate plasminogen and convert it to plasmin, which can digest fibrin Reestablish blood flow to the heart muscle via coronary arteries
THROMBOLYTIC DRUGS: INDICATIONS	Acute MI Arterial thrombolysis DVT Occlusion of shunts or catheters Pulmonary embolu
THROMBOLYTIC DRUGS: ADVERSE EFFECTS	Bleeding  Internal  Intracranial  Superficial Other effects  Nausea, vomiting, hypotension, anaphylactoid reactions
ALTEPLASE (ACTIVASE)	t-PA made through recombinant DNA techniques  Fibrin specific so does not produce a systemic lytic state  Present in the body in a natural state  Very short half-life (5 minutes)  Indications: MI, strokes  Smaller doses to flush clogged IV
ANTIFIBRINOLYTIC DRUGS	Prevent the lysis of fibrin  Result in promoting clot formation  Used for prevention and treatment of excessive bleeding resulting from hyperfibrinolysis or surgical complications  Treatment of hemophilia or von Willebrand’s disease
ANTIFIBRINOLYTIC DRUGS: ADVERSE EFFECTS	Uncommon and mild Rare reports of thrombotic events Others include  Dysrhythmia, orthostatic hypotension, bradycardia, headache, dizziness, fatigue, nausea, vomiting, abdominal cramps
AMINOCAPROIC ACID (AMICAR)	Synthetic antifibrinolytic drug Prevents and controls excessive bleeding that result from surgery or overactivity of fibrinolytic system Oral or parenteral
DESMOPRESSIN (DDAVP)	Synthetic polypeptide Similar to vasopressin, which is an antidiuretic hormone Indications: diabetes insipidus; hemophilia Nasal spray: used for nocturnal enuresis
TRANEXAMIC ACID	Antifibrinolytic drug that forms a reversible complex that displaces plasminogen from fibrin resulting in inhibition of fibrinolysis Used IV prior to surgery Adverse reaction: hypotension with rapid IV injection
HEPARIN NURSING IMPLICATIONS	IV doses are usually double checked with another nurse. Ensure that subcutaneous doses are given subcutaneously, not intramuscularly. Subcutaneous doses should be given in areas of deep subcutaneous fat
LWMHS: NURSING IMPLICATIONS	Given subcutaneously in the abdomen Rotate injection sites. Protamine sulfate can be given as an antidote in case of excessive anticoagulation.
WARFARIN (COUMADIN): NURSING IMPLICATIONS	started while the patient is still on heparin until PT/INR levels indicate adequate anticoagulation Full therapeutic effect takes several days. Monitor PT/INR regularly; keep follow-up appointments. Antidote is vitamin K
WARFAN Many herbal products have potential interactions; increased bleeding may occur	Capsicum pepper  Garlic  Ginger  Ginkgo  St. John’s wort  Feverfew
ANTICOAGULANTS: PATIENT EDUCATION	Importance of regular laboratory testing  Signs of abnormal bleeding  Measures to prevent bruising, bleeding, and tissue injury  Wearing a medical alert bracelet  Avoiding foods high in vitamin K
ANTIPLATELET DRUGS: NURSING IMPLICATIONS	Concerns and teaching tips same as for anticoagulants Drug-drug interactions Adverse reactions to report Monitoring for abnormal bleedin
THROMBOLYTIC DRUGS: NURSING IMPLICATIONS	Follow strict manufacturer’s guidelines for preparation and administration. Monitor IV sites for bleeding, redness, and pain. Monitor for bleeding from gums, mucous membranes, nose, and injection sites. Observe for signs of internal bleeding
common cold	Most caused by viral infection (rhinovirus or influenza virus) • Virus invades tissues (mucosa) of upper respiratory tract, causing upper respiratory infection (URI)Fluid drips down the pharynx into the esophagus and lower respiratory tract
Irritation of nasal mucosa often triggers the	sneeze reflex
Mucosal irritation also causes release of	several inflammatory and vasoactive substances, dilating small blood vessels in the nasal sinuses and causing nasal congestion
TREATMENT OF THE COMMON COLD	Involves combined use of antihistamines, nasal decongestants, antitussives, and expectorants • Treatment is symptomatic only, not curative. • Symptomatic treatment does not eliminate the causative pathogen
PEDIATRIC CONCERNS	In 2008, the U.S. Food and Drug Administration (FDA) issued recommendations that over-the- counter (OTC) cough and cold products not be given to children younger than 2 years of age. • Oversedation, seizures, tachycardia, and even death in toddlers
SUPPLEMENTS AND HERBAL PRODUCTS for cold	Vitamin C • Echinacea • Goldenseal
ANTIHISTAMINES	Drugs that directly compete with histamine for specific receptor sites • Two histamine receptors • H1 (histamine 1) • H2 (histamine 2)
ANAPHYLAXIS: SEVERE ALLERGIC REACTIONS	excessive amounts of histamine- • Constriction of smooth muscle • Increase in body secretions • Vasodilatation and increased capillary permeability, movement of fluid out of the blood vessels and into the tissues, and drop in bp
HISTAMINE	Major inflammatory mediator in many allergic disorders • Allergic rhinitis (e.g., hay fever and mold, dust allergies) • Anaphylaxis • Angioedema • Drug fevers • Insect bite reactions
ANTIHISTAMINES AND HISTAMINE ANTAGONISTS	H1 antagonists (also called H1 blockers) • Examples: chlorpheniramine, fexofenadine (Allegra), loratadine (Claritin), cetirizine (Zyrtec), diphenhydramine (Benadryl)
ANTIHISTAMINES	H2 blockers or H2 antagonists • Used to reduce gastric acid in peptic ulcer disease • Examples: cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid)
ANTIHISTAMINES: MECHANISM OF ACTION	Block action of histamine at H1 receptor sites • Compete with histamine for binding at unoccupied receptors • Cannot push histamine off the receptor if already bound
ANTIHISTAMINES: MECHANISM OF ACTION (CONT.)	The binding of H1 blockers to the histamine receptors prevents the adverse consequences of histamine stimulation. • Vasodilation • Increased gastrointestinal (GI) and respiratory secretions • Increased capillary permeability
HISTAMINE VERSUS ANTIHISTAMINE EFFECTS	Cardiovascular (small blood vessels) • Histamine effects: dilation and increased permeability (allowing substances to leak into tissues) • Antihistamine effects • Reduce dilation of blood vessels • Reduce increased permeability of blood vessels
HISTAMINE VERSUS ANTIHISTAMINE EFFECTS (CONT	Smooth muscle (on exocrine glands) • Histamine effects: stimulate salivary, gastric, lacrimal, and bronchial secretions • Antihistamine effects: reduce salivary, gastric, lacrimal, and bronchial secretions
HISTAMINE VERSUS ANTIHISTAMINE EFFECTS	Immune system (release of substances commonly associated with allergic reactions) • Histamine effects: mast cells release histamine and other substances, resulting in allergic reactions • Antihistamine effects: bind to histamine receptors
ANTIHISTAMINES: OTHER EFFECTS	Skin: reduce capillary permeability, wheal-and- flare formation, itching • Anticholinergic: drying effect that reduces nasal, salivary, and lacrimal gland secretions (runny nose, tearing, and itching eyes)
ANTIHISTAMINES: INDICATIONS	Nasal allergies • Seasonal or perennial allergic rhinitis (hay fever) • Allergic reactions • Motion sickness • Parkinson’s disease • Sleep disorders
ANTIHISTAMINES: INDICATIONS (CONT.)	Also used to relieve symptoms associated with the common cold • Sneezing, runny nose • Palliative treatment; not curative
ANTIHISTAMINES: CONTRAINDICATIONS	Known drug allergy • Narrow-angle glaucoma • Cardiac disease, hypertension • Kidney disease • Bronchial asthma, chronic obstructive pulmonary disease (COPD) • Sole drug therapy during acute asthmatic attacks
ANTIHISTAMINES: CONTRAINDICATIONS (CONT.)	Peptic ulcer disease • Seizure disorders • Benign prostatic hyperplasia (BPH) • Pregnancy
ANTIHISTAMINES: ADVERSE EFFECTS	Anticholinergic (drying) effects: most common • Dry mouth • Difficulty urinating • Constipation • Changes in vision • Drowsiness • Mild drowsiness to deep sleep
ANTIHISTAMINES traditional	brompheniramine, chlorpheniramine, dimenhydrinate, diphenhydramine, meclizine, and promethazine Work both peripherally and centrally • Have anticholinergic effects, making them more effective than nonsedating drugs in some cases
nonsedating ANTIHISTAMINES	loratadine, cetirizine, and fexofenadine
NONSEDATING/PERIPHERALLY ACTING ANTIHISTAMINES	Developed to eliminate unwanted adverse effects, mainly sedation • Work peripherally to block the actions of histamine; thus, fewer central nervous system (CNS) adverse effects • Longer duration of action
NONSEDATING/PERIPHERALLY ACTING ANTIHISTAMINES ex	fexofenadine (Allegra), loratadine (Claritin), cetirizine (Zyrtec)
ANTIHISTAMINES: NURSING IMPLICATIONS	Gather data about allergic reaction that required treatment; • Contraindicated in the presence of acute asthma attacks and lower respiratory diseases, such as pneumonia • Use with caution in intraocular pressure, cardiac or renal disease, high bp,
ANTIHISTAMINES: NURSING IMPLICATIONS (CONT.)	nstruct patients to report excessive sedation, confusion, or hypotension. • Instruct patients to avoid driving or operating heavy machinery; advise against consuming alcohol or other CNS depressants.
ANTIHISTAMINES: NURSING IMPLICATIONS (CONT 2)	Best tolerated when taken with meals; reduces GI upset • If dry mouth occurs, teach patients to perform frequent mouth care, chew gum, or suck on hard candy (preferably sugarless) to ease discomfort
NASAL CONGESTION	Excessive nasal secretions • Inflamed and swollen nasal mucosa • Primary causes • Allergies • URIs (common cold)
Adrenergics decongestants	Largest group • Sympathomimetics
Anticholinergics decongestants	Less commonly used • Parasympatholytics
Corticosteroids decongestants	Topical, intranasal steroids
ORAL DECONGESTANTS	Prolonged decongestant effects but delayed onset • Effect less potent than topical • No rebound congestion • Exclusively adrenergics • Example: pseudoephedrine
TOPICAL NASAL DECONGESTANTS	Prompt onset • Potent • Sustained use over several days causes rebound congestion, making the condition worse. • Ephedrine, oxymetazoline, phenylephrine, and tetrahydrozoline
INHALED INTRANASAL STEROIDS AND ANTICHOLINERGIC DRUGS	Not associated with rebound congestion • Often used prophylactically to prevent nasal congestion in patients with chronic upper respiratory tract symptoms
TOPICAL NASAL DECONGESTANTS	Adrenergics • Ephedrine, oxymetazoline • Intranasal steroids • Beclomethasone dipropionate (Beconase), budesonide (Rhinocort), flunisolide (Nasalide), fluticasone (Flonase), triamcinolone
Intranasal anticholinergic	Ipratropium (Atrovent)
NASAL DECONGESTANTS: MECHANISM OF ACTION	Site of action: blood vessels surrounding nasal sinuses • Adrenergics • Constrict small blood vessels that supply upper respiratory tract structures • As a result, these tissues shrink, and nasal secretions are better able to drain
Nasal steroids	Antiinflammatory effect • Work to turn off the immune system cells involved in the inflammatory response • Decreased inflammation results in decreased congestion.
NASAL DECONGESTANTS: DRUG EFFECT	Shrink engorged nasal mucous membranes • Relieve nasal stuffiness
NASAL DECONGESTANTS: INDICATIONS	Relief of nasal congestion associated with: • Acute or chronic rhinitis • Common cold • Sinusitis • Hay fever • Other allergies • May also be used to reduce swelling of the nasal passage
NASAL DECONGESTANTS: CONTRAINDICATIONS	Drug allergy • Narrow-angle glaucoma • Uncontrolled cardiovascular disease, hypertension • Diabetes and hyperthyroidism • History of cerebrovascular accident or transient ischemic attacks • Long-standing asthma • BPH • Diabetes
NASAL DECONGESTANTS: ADVERSE EFFECTS adrenergics	nervous, insomnia, palpations, tremors
NASAL DECONGESTANTS: ADVERSE EFFECTS steroids	mucosal dryness and irritation
NASAL DECONGESTANTS: INTERACTIONS	Systemic sympathomimetic drugs and sympathomimetic nasal decongestants are likely to cause drug toxicity when given together. • Monoamine oxidase inhibitors and sympathomimetic nasal decongestants raise blood pressure. • Methyldopa,Urinary acidifier
NASAL DECONGESTANTS: NURSING IMPLICATIONS	Patients should avoid caffeine and caffeine- containing products. • Patients should report a fever, cough, or other symptoms lasting longer than 1 week. • Monitor for intended therapeutic effects.
COUGH PHYSIOLOGY	Respiratory secretions and foreign objects are naturally removed by the cough reflex. • Induces coughing and expectoration • Initiated by irritation of sensory receptors in the respiratory tract
ANTITUSSIVES	Drugs used to stop or reduce coughing • Opioid and nonopioid • Used only for nonproductive coughs! • May be used in cases when coughing is harmful
ANTITUSSIVES: MECHANISM OF ACTION	Opioids • Suppress the cough reflex by direct action on the cough center in the medulla • Analgesia, drying effect on the mucosa of the respiratory tract, increased viscosity of respiratory secretions, reduction of runny nose and postnasal dri
ANTITUSSIVES: ex	Codeine • Hydrocodone
ANTITUSSIVES: MECHANISM OF ACTION (CONT.) nonopiods	Dextromethorphan: works in the same way • Not an opioid • No analgesic properties • No CNS depression • Benzonatat. Suppress the cough reflex by numbing the stretch receptors in the respiratory tract and prevent reflex stimulation
ANTITUSSIVES: INDICATION	Used to stop the cough reflex when the cough is nonproductive or harmful
ANTITUSSIVES: CONTRAINDICATIONS	Drug allergy • Opioid dependency • Respiratory depression • Others
ANTITUSSIVES: ADVERSE EFFECTS	Benzonatate • Dizziness, headache, sedation, nausea, and others • Dextromethorphan • Dizziness, drowsiness, nausea • Opioids • Sedation, nausea, vomiting, lightheadedness, constipation
ANTITUSSIVES: NURSING IMPLICATIONS	Perform respiratory and cough assessment and assess for allergies. • Instruct patients to avoid driving or operating heavy equipment because of possible sedation, drowsiness, or dizziness
ANTITUSSIVES: NURSING IMPLICATIONS (CONT.)	Report any of the following symptoms to the caregiver: • Cough that lasts more than 1 week • Persistent headache • Fever • Rash • Antitussive drugs are for nonproductive coughs.
EXPECTORANTS	Drugs that aid in the expectoration (removal) of mucus • Reduce the viscosity of secretions • Disintegrate and thin secretions • Example: guaifenesin
EXPECTORANTS: MECHANISMS OF ACTION	Reflex stimulation • Drug causes irritation of the GI tract. • Loosening and thinning of respiratory tract secretions occur in response to this irritation.
EXPECTORANTS: MECHANISMS OF ACTION direct stimualtion	The secretory glands are stimulated directly to increase their production of respiratory tract fluids. • Final result: thinner mucus that is easier to remove
EXPECTORANTS: DRUG EFFECTS	By loosening and thinning sputum and bronchial secretions, the tendency to cough is indirectly diminished.
EXPECTORANTS: INDICATIONS	Used for the relief of productive coughs associated with: • Common cold • Bronchitis • Laryngitis • Pharyngitis • Coughs caused by chronic paranasal sinusitis, measles
EXPECTORANTS: NURSING IMPLICATIONS	used with caution in older adults and patients with asthma or respiratory insufficiency. • Patients taking expectorants should receive more fluids, if permitted, to help loosen and liquefy secretions.Report symptoms lasting longer than 1 week.
HERBAL PRODUCTS: ECHINACEA	Reduces symptoms of the common cold and recovery time • Adverse effects • Dermatitis • GI disturbance • Dizziness • Headache
BRONCHIAL ASTHMA	Recurrent and reversible shortness of breath • Occurs when the airways of the lungs become narrow as a result of: • Bronchospasms • Inflammation of the bronchial mucosa • Edema of the bronchial mucosa • Production of viscous mucus
BRONCHIAL ASTHMA (CONT.)	The alveolar ducts and alveoli remain open, but airflow to them is obstructed. • Symptoms • Wheezing • Difficulty breathing
ASTHMA categories	Intrinsic (occurring in patients with no history of allergies) 2. Extrinsic (occurring in patients exposed to a known allergen) 3. Exercise induced 4. Drug induced
Status asthmaticus	Prolonged asthma attack that does not respond to typical drug therapy • May last several minutes to hours • Medical emergency
CHRONIC BRONCHITIS	Continuous inflammation and low-grade infection of the bronchi • Excessive secretion of mucus and certain pathologic changes in the bronchial structure • Often occurs as a result of prolonged exposure to bronchial irritants
EMPHYSEMA	No longer used as a term but is included into COPD • Air spaces enlarge as a result of the destruction of alveolar walls. • Caused by the effect of proteolytic enzymes released from leukocytes in response to alveolar inflammation
Bronchodilators	These drugs relax bronchial smooth muscle, which causes dilation of the bronchi and bronchioles that are narrowed as a result of the disease process. • Three classes: beta-adrenergic agonists, anticholinergics, and xanthine derivatives
Short-acting beta agonist (SABA) inhalers	Albuterol (Ventolin, ProAir) • Levalbuterol (Xopenex) • Pirbuterol (Maxair) • Terbutaline (Brethine) • Metaproterenol (Alupent)
Long-acting beta agonist (LABA) inhalers	Arformoterol (Brovana) • Formoterol (Foradil, Perforomist) • Salmeterol (Serevent)
LABA inhalers	Indacaterol (Arcapta Neohaler) • Vilanterol in conjunction with fluticasone (Breo Ellipta) • Vilanterol in conjunction with the anticholinergic, umeclidinium (Anoro Ellipta)
BRONCHODILATORS: BETA- ADRENERGIC AGONISTS	Used during acute phase of asthmatic attacks • Quickly reduce airway constriction and restore normal airflow • Agonists, or stimulators, of the adrenergic receptors in the sympathetic nervous system • Sympathomimetics
Nonselective adrenergics	Stimulate alpha, beta1 (cardiac), and beta2 (respiratory) receptors • Example: epinephrine (EpiPen)
Nonselective beta-adrenergics	Stimulate both beta1 and beta2 receptors • Example: metaproterenol
Selective beta2 drugs	Stimulate only beta2 receptors • Example: albuterol
BETA-ADRENERGIC AGONISTS: MECHANISM OF ACTION	Begins at the specific receptor stimulated • Ends with bronchodilation of the airways • Activation of beta2 receptors activates cyclic adenosine monophosphate (cAMP), which relaxes smooth muscle in the airway
BETA-ADRENERGIC AGONISTS: INDICATIONS	Relief of bronchospasm related to asthma, bronchitis, and other pulmonary diseases • Used in treatment and prevention of acute attacks • Used in hypotension and shock
BETA-ADRENERGIC AGONISTS: CONTRAINDICATIONS	Known drug allergy • Uncontrolled hypertension • Cardiac dysrhythmias • High risk of stroke (because of the vasoconstrictive drug action)
BETA-ADRENERGIC AGONISTS: ADVERSE EFFECTS	Alpha and beta (epinephrine) • Insomnia • Restlessness • Anorexia • Vascular headache • Hyperglycemia • Hypokalemia
Beta1 and beta2 (metaproterenol)	Cardiac stimulation • Tremor • Anginal pain • Vascular headache • Hypotension
Beta2 (albuterol)	Hypotension or hypertension • Vascular headache • Tremor
BETA-ADRENERGIC AGONISTS: INTERACTIONS	Diminished bronchodilation when nonselective beta blockers are used with the beta agonist bronchodilators • Monoamine oxidase inhibitors • Sympathomimetics • Monitor patients with diabetes
BETA-ADRENERGIC AGONISTS: ALBUTEROL (PROVENTIL)	Short-acting beta2-specific bronchodilating beta agonist • Most commonly used drug in this class • Must not be used too frequently • Oral and inhalational use
BETA-ADRENERGIC AGONISTS: SALMETEROL (SEREVENT)	• Never to be used for acute treatment • Used for the maintenance treatment of asthma and COPD and is used in conjunction with an inhaled corticosteroid • Salmeterol should never be given more than twice daily
ANTICHOLINERGICS: MECHANISM OF ACTION	Acetylcholine (ACh) causes bronchial constriction and narrowing of the airways. • Anticholinergics bind to the ACh receptors, preventing ACh from binding. • Result: bronchoconstriction is prevented, airways dilate
ANTICHOLINERGICS: MECHANISM OF ACTION (CONT.)	Ipratropium (Atrovent), tiotropium (Spiriva), and aclidinium (Tudorza) • Indirectly cause airway relaxation and dilation • Help reduce secretions in COPD patients • Indications: prevention of the bronchospasm associated with chronic bronchitis
ANTICHOLINERGICS: ADVERSE EFFECTS	Dry mouth or throat • Nasal congestion • Heart palpitations • Gastrointestinal (GI) distress • Headache
ANTICHOLINERGICS: IPRATROPIUM (ATROVENT)	Oldest and most commonly used anticholinergic bronchodilator • Available both as a liquid aerosol for inhalation and as a multidose inhaler • Usually dosed twice daily
XANTHINE DERIVATIVES (END IN- PHYLLINE	Plant alkaloids: caffeine, theobromine, and theophylline • Only theophylline is used as a bronchodilator. • Synthetic xanthines: aminophylline and dyphylline
XANTHINE DERIVATIVES: MECHANISM OF ACTION	Increase levels of energy-producing cAMP • This is done by competitively inhibiting phosphodiesterase, the enzyme that breaks down cAMP. • Result: decreased cAMP levels, smooth muscle relaxation, bronchodilation, and increased airflow
XANTHINE DERIVATIVES: DRUG EFFECTS	Cause bronchodilation by relaxing smooth muscle in the airways • Result: relief of bronchospasm and greater airflow into and out of the lungs • Also cause central nervous system (CNS) stimulation, incr HR
XANTHINE DERIVATIVES: INDICATIONS	Dilation of airways in asthmas, chronic bronchitis, and emphysema • Mild to moderate cases of acute asthma • NOT for management of acute asthma attack • Adjunct drug in the management of COPD
XANTHINE DERIVATIVES: ADVERSE EFFECTS	Nausea, vomiting, anorexia • Gastroesophageal reflux during sleep • Sinus tachycardia, extrasystole, palpitations, ventricular dysrhythmias • Transient increased urination • Hyperglycemia
XANTHINE DERIVATIVES: CAFFEINE	Used without prescription as a CNS stimulant or analeptic to promote alertness (e.g., for long- duration driving or studying) • Cardiac stimulant in infants with bradycardia • Enhancement of respiratory drive in infants
XANTHINE DERIVATIVES: THEOPHYLLINE	Most commonly used xanthine derivative • Oral, rectal, injectable (as aminophylline), and topical dosage form, Therapeutic range for theophylline blood level is 10 to 20 mcg/mL
Aminophylline:	intravenous (IV) treatment of patients with status asthmaticus who have not responded to fast-acting beta agonists such as epinephrine
NONBRONCHODILATING RESPIRATORY DRUGS	Leukotriene receptor antagonists (montelukast, zafirlukast, and zileuton) • Corticosteroids (beclomethasone, budesonide, dexamethasone, flunisolide, fluticasone, ciclesonide, and triamcinolone)
LEUKOTRIENE RECEPTOR ANTAGONISTS (LTRAS)	Nonbronchodilating • Newer class of asthma medications • Currently available drugs • Montelukast (Singulair) • Zafirlukast (Accolate) • Zileuton (Zyflo)
LTRAS: MECHANISM OF ACTION	Leukotrienes are substances released when a trigger, such as cat hair or dust, starts a series of chemical reactions in the body. • Leukotrienes cause inflammation, bronchoconstriction, and mucus production. coughing, wheezing, shortness of breath
By blocking leukotrienes	Prevent smooth muscle contraction of the bronchial airways • Decrease mucus secretion • Prevent vascular permeability • Decrease neutrophil and leukocyte infiltration to the lungs, preventing inflammation
LTRAS: INDICATIONS	Prophylaxis and long-term treatment and prevention of asthma in adults and children 12 years of age and older • Not meant for management of acute asthmatic attacks
LTRAS: CONTRAINDICATIONS	Known drug allergy • Previous adverse drug reaction • Allergy to povidone, lactose, titanium dioxide, or cellulose derivatives is also important to note because these are inactive ingredients in these drug
LTRAS: ADVERSE EFFECTS	Zileuton • Headache, nausea, dizziness, insomnia • Zafirlukast and montelukast • Headache, nausea, diarrhea
CORTICOSTEROIDS (GLUCOCORTICOIDS)	Antiinflammatory properties • Used for chronic asthma • Do not relieve symptoms of acute asthma attacks • May be administered IV
CORTICOSTEROIDS: MECHANISM OF ACTION	Stabilize membranes of cells that release harmful bronchoconstricting substances • These cells are called leukocytes, or white blood cells. • Increase responsiveness of bronchial smooth muscle to beta-adrenergic stimulation
CORTICOSTEROIDS: MECHANISM OF ACTION (CONT.)	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
INHALED CORTICOSTEROIDS (- SON; EXCEPT FOR TRIAMCINOLONE)	Beclomethasone dipropionate (Beclovent) • Budesonide (Pulmicort Turbuhaler) • Ciclesonide (Omnaris) • Flunisolide (AeroBid) • Fluticasone (Flovent) • Mometasone (Asmanex) • Triamcinolone acetonide
INHALED CORTICOSTEROIDS: INDICATIONS	bronchospastic disorders to control the inflammatory responses • Persistent asthma • Often used concurrently with the beta-adrenergic agonists • Systemic corticosteroids are generally used only to treat acute exacerbations, or severe asthma.
INHALED CORTICOSTEROIDS: CONTRAINDICATIONS	Drug allergy • Not intended as sole therapy for acute asthma attacks • Hypersensitivity to glucocorticoids • Patients whose sputum tests positive for Candida organisms • Patients with systemic fungal infection
INHALED CORTICOSTEROIDS: ADVERSE EFFECTS	Pharyngeal irritation • Coughing • Dry mouth • Oral fungal infections • Systemic effects are rare because low doses are used for inhalation therapy
INHALED CORTICOSTEROIDS: DRUG INTERACTIONS	Drug interactions are more likely to occur with systemic (versus inhaled) corticosteroids. • May increase serum glucose levels, possibly requiring adjustments in dosages of antidiabetic drugs • Cyclosporine and tacrolimus • Itraconazole
HOSPHODIESTERASE-4 INHIBITOR	Roflumilast (Daliresp) • Indicated to prevent coughing and excess mucus from worsening and to decrease the frequency of life- threatening COPD exacerbations
Roflumilast effects	nausea, diarrhea, headache, insomnia, dizziness, weight loss, and psychiatric symptoms
MONOCLONAL ANTIBODY(-ZUMAB) ANTIASTHMATIC	Omalizumab (Xolair), mepolizumab (Nucala), reslizumab (Cinqair) • Selectively binds to the immunoglobulin E, which in turn limits the release of mediators of the allergic response • Given by injection • Potential for producing anaphylaxis
MONOCLONAL ANTIBODY(-ZUMAB) ANTIASTHMATIC implications	Encourage patients to take measures that promote a generally good state of health so as to prevent, relieve, or decrease symptoms of COPD. • Avoid exposure to conditions that precipitate bronchospasm
NURSING IMPLICATIONS: BETA-ADRENERGIC AGONISTS	Albuterol, if used too frequently, loses its beta2- specific actions at larger doses. • As a result, beta1 receptors are stimulated, causing nausea, increased anxiety, palpitations, tremors, and increased heart rat
NURSING IMPLICATIONS: BETA-ADRENERGIC AGONISTS (CONT.	Ensure that patients take medications exactly as prescribed, with no omissions or double doses. • Inform patients to report insomnia, jitteriness, restlessness, palpitations, chest pain, or any change in symptoms.
NURSING IMPLICATIONS: XANTHINE DERIVATIVES	Contraindications: history of PUD or GI disorders • Cautious use: cardiac disease • Timed-release preparations should not be crushed or chewed
NURSING IMPLICATIONS: XANTHINE DERIVATIVES (CONT	Report to prescriber-toxic blood levels may result in: • Nausea • Vomiting • Restlessness • Insomnia • Irritability • Tremors
NURSING IMPLICATIONS: LTRAS	Ensure that the drug is being used for chronic management of asthma, not acute asthma. • Teach the patient the purpose of the therapy. • Improvement should be seen in about 1 week.
NURSING IMPLICATIONS: LTRAS (CONT.)	Assess liver function before beginning therapy and throughout. • Teach patients to take medications every night on a continuous schedule even if symptoms improve
NURSING IMPLICATIONS: INHALED CORTICOSTEROIDS	Teach patients to gargle and rinse the mouth with lukewarm water after inhalation to prevent the development of oral fungal infections (candidiasis)
INHALERS: PATIENT EDUCATION	• Ensure that the patient knows the correct time intervals for inhalers. • Provide a spacer if the patient has difficulty coordinating breathing with inhaler activation. patient knows how to keep track of the number of doses
Role of Kidneys	Play an important role in the day-to-day functioning of the body  Filters toxic waste products  Conserves essential substances  This balance is maintained by the nephron
Kidney Structure	Nephron is main structural unit of the kidney.  Diuretics exert their effect in the nephron.  Initial filtering of blood takes place in the glomerulus.  Glomerular filtration rate (GFR)  Afferent arterioles  Efferent arterioles
Kidney Structure (Cont.)	Proximal convoluted tubule (proximal tubule)  Returns 60% to 70% of sodium and water from the filtered fluid back to the bloodstream  Passive reabsorption of chloride and water
loop of henle	20% to 25% of sodium is reabsorbed here through active chloride reabsorption.
Distal convoluted tubule	Remaining 5% to 10% of sodium is reabsorbed here.  Regulated by aldosterone
Carbonic Anhydrase Inhibitors	Chemical derivative of sulfonamide antibiotics  Inhibit the activity of the enzyme carbonic anhydrase  Found in kidneys, eyes, and other parts of the body  Acetazolamide (Diamox)  Most commonly used CAI
Carbonic Anhydrase Inhibitors: Mechanism of Action	The enzyme carbonic anhydrase helps to make H+ ions available for exchange with sodium and water in the proximal tubules.  CAIs block the action of carbonic anhydrase, thus preventing the exchange of H+ ions with sodium and water.
Carbonic Anhydrase Inhibitors: Mechanism of Action	Inhibition of carbonic anhydrase reduces H+ ion concentration in renal tubules.  As a result, there is increased excretion of bicarbonate, sodium, water, and potassium.  Resorption of water is decreased, and urine volume is increased.
Carbonic Anhydrase Inhibitors: Indications	Adjunct drugs in the long-term management of open-angle glaucoma  Used with miotics to lower intraocular pressure before ocular surgery in certain cases  Also useful in the treatment of  Edema  High-altitude sickness
Carbonic Anhydrase Inhibitors: Contraindications	Known drug allergy  Hyponatremia  Hypokalemia  Severe renal or hepatic dysfunction  Adrenal gland insufficiency  Cirrhosis
Carbonic Anhydrase Inhibitors: Adverse Effects	Acidosis  Hypokalemia  Drowsiness  Anorexia  Paresthesias  Hematuria  Urticaria  Photosensitivity  Melena
Carbonic Anhydrase Inhibitors: Interactions	Because CAIs can cause hypokalemia, an increase in digoxin toxicity may occur when they are combined with digoxin.  Use with corticosteroids may also cause hypokalemia.  Increased effects of amphetamines, carbamazepine, cyclosporine
Loop Diuretics meds	Bumetanide (Bumex)  Ethacrynic acid (Edecrin)  Furosemide (Lasix)  Torsemide (Demadex)
Loop Diuretics: Mechanism of Action	Possess renal, cardiovascular, and metabolic effects  Act directly on the ascending limb of the loop of Henle to inhibit chloride and sodium resorption  Increase renal prostaglandins, resulting in the dilation of blood vessels and reduced pvr
Loop Diuretics: Drug Effects	Potent diuresis and subsequent loss of fluid  Decreased fluid volume causes a reduction in  Blood pressure  Pulmonary vascular resistance  Systemic vascular resistance  Central venous pressure  Left ventricular end-diastolic pressure
Loop Diuretics: Indications	Edema associated with HF or hepatic or renal disease  To control hypertension  To increase renal excretion of calcium in patients with hypercalcemia  In cases of HF resulting from diastolic dysfunction
Loop Diuretics: Interactions	Neurotoxic  Nephrotoxic  Increase serum levels of uric acid, glucose, alanine aminotransferase, and aspartate aminotransferase.  Thiazide (metolazone): sequential nephron blockade  Nonsteroidal antiinflammatory drugs (NSAIDs)
Loop Diuretics: Furosemide (Lasix)	Most commonly used loop diuretic  Uses: pulmonary edema and the edema associated with HF, liver disease, nephrotic syndrome, ascites, hypertension
Osmotic Diuretics	Mannitol (Osmitrol)  Most used osmotic diuretic  Urea  Organic acids  Glucose
Osmotic Diuretics: Mechanism of Action	Work mostly in the proximal tubule.  Nonabsorbable, producing an osmotic effect  Pull water into the renal tubules from the surrounding tissues.  Inhibit tubular resorption of water and solutes, thus producing rapid diuresis
Osmotic Diuretics: Drug Effects	Increases glomerular filtration rate and renal plasma flow; helps to prevent kidney damage during ARF  Reduces intracranial pressure or cerebral edema associated with head trauma  Reduces excessive intraocular pressure
Osmotic Diuretics: Indications	Treatment of patients in the early, oliguric phase of acute renal failure (ARF)  To promote excretion of toxic substances  To reduce intracranial pressure  Treatment of cerebral edema
Osmotic Diuretics: Adverse Effects	Convulsions  Thrombophlebitis  Pulmonary congestion
Osmotic Diuretics: Mannitol (Osmitrol)	Intravenous (IV) infusion only  May crystallize when exposed to low temperatures  Use of a filter is required.
Potassium-Sparing Diuretics meds	Amiloride (Midamor)  Spironolactone (Aldactone)  Triamterene (Dyrenium)  Also known as aldosterone-inhibiting diuretics
Potassium-Sparing Diuretics: Mechanism of Action	Work in collecting ducts and distal convoluted tubules.  Interfere with sodium-potassium exchange.  Competitively bind to aldosterone receptors.  Block resorption of sodium and water usually induced by aldosterone.
Potassium-Sparing Diuretics: Drug Effects	Prevent potassium from being pumped into the tubule, thus preventing its secretion.  Competitively block aldosterone receptors and inhibit their action.  Promote the excretion of sodium and water.
Potassium-Sparing Diuretics: Indications Spironolactone and triamterene	Hyperaldosteronism  Hypertension  Reversing potassium loss caused by potassium-losing drugs  Certain cases of HF: prevention of remodeling
Potassium-Sparing Diuretics: Indications amloride	Similar as spironolactone and triamterene, but amiloride is less effective in the long term
Potassium-Sparing Diuretics: Adverse Effects (Cont.) spironolactone	Gynecomastia  Amenorrhea  Irregular menses  Postmenopausal bleeding
Potassium-Sparing Diuretics: Interactions	Lithium  Angiotensin-converting enzyme inhibitors  Potassium supplements  NSAIDs
Thiazide and Thiazide-Like Diuretics	Thiazide diuretics  Hydrochlorothiazide (Esidrix, HydroDIURIL)  Chlorothiazide (Diuril)  Thiazide-like diuretics  Metolazone (Mykrox, Zaroxolyn)  Chlorthalidone (Hydone, Thalitone)  Indapamide
Thiazide and Thiazide-Like Diuretics: Mechanism of Action	nhibit tubular resorption of sodium, chloride, and potassium ions  Action primarily in the distal convoluted tubule  Result: water, sodium, and chloride are excreted  Potassium is also excreted to a lesser extent.
Thiazide and Thiazide-Like Diuretics: Drug Effects	Lowered peripheral vascular resistance  Depletion of sodium and water (and potassium)  Thiazides should not be used if creatinine clearance is less than 30 to 50 mL/min
Thiazide and Thiazide-Like Diuretics: Indications	Hypertension (one of the most prescribed group of drugs for this)  Edematous states  Idiopathic hypercalciuria  Diabetes insipidus  HF caused by diastolic dysfunction
Nursing Implications of Diuretics	Perform a thorough patient history and physical examination.  Assess baseline fluid volume status, intake and output, serum electrolyte values, weight, and vital signs
Fluid Balance	Plasma proteins exert constant osmotic pressure. Colloid oncotic pressure (COP) Normally 24 mm Hg  ISF exerts hydrostatic pressure. Normally 17 mm Hg
Acid-Base Balance	Important bodily function  Regulated by respiratory system and kidney  Acid  Base  pH
Crystalloids	Solutions containing fluids and electrolytes that are normally found in the body  Maintains the osmotic gradient between extravascular and intravascular compartments  Do not contain proteins (colloids)  No risk for viral transmission
Crystalloids (Cont.)	Better for treating dehydration rather than expanding plasma volume  Used as maintenance fluids to:  Compensate for insensible fluid losses  Replace fluids
Crystalloids indications	Acute liver failure  Acute nephrosis  Adult respiratory distress syndrome  Burns  Cardiopulmonary bypass  Hypoproteinemia  Renal dialysis
Crystalloids effects	May cause edema, especially peripheral or pulmonary  May dilute plasma proteins, reducing COP  Effects may be short-lived.  Prolonged infusions may worsen alkalosis or acidosis.
Crystalloids: Sodium Chloride	0.9%: physiologically normal concentration of sodium chloride (isotonic), and it is referred to as NS.  0.45% (“half-normal”)  0.25% (“quarter-normal”)  3% (hypertonic saline)  5% (hypertonic saline)
Colloids	Protein substances  Increase COP  Move fluid from interstitial compartment to plasma compartment (when plasma protein levels are low)
Colloids: Indications	Used to treat wide variety of conditions when patient requires plasma volume expansion  Shock  Burns
Colloids: Adverse Effects	Usually safe  May cause altered coagulation, resulting in bleeding  Have no clotting factors or oxygen-carrying capacity  Rarely, dextran therapy causes anaphylaxis or renal failure.
Colloids: Albumin	Natural protein that is normally produced by the liver  Responsible for generating approximately 70% of the COP  Sterile solution of serum albumin that is prepared from pooled blood, plasma, serum, or placentas obtained from healthy human donors
Dextran	Actions similar to those of human albumin in that it expands the plasma volume by drawing fluid from the interstitial space to the intravascular space  Contraindications:  Hypersensitivity  HF  Renal insufficiency
Blood Products	Only class of fluids that are able to carry oxygen  Increase tissue oxygenation  Increase PV  Most expensive and least available fluid because they require human donors
Blood Products (Cont.)	Increase colloid osmotic pressure and PV  Pull fluid from extravascular space into intravascular space (plasma expanders)  Red blood cell products also carry oxygen.  Increase body’s supply of various products
Fresh-frozen plasma (FFP)	Increase clotting factor levels in patients with demonstrated deficiency
Blood Products effects	Incompatibility with recipient’s immune system  Crossmatch testing  Transfusion reaction  Anaphylaxis  Transmission of pathogens to recipient (hepatitis, human immunodeficiency virus)
Physiology of Electrolyte Balance	Work in conjunction with fluids to keep the body in balance  Measured in milliequivalent (mEq)  Positively charged cations  Sodium, potassium, calcium, magnesium  Negatively charged ions  Chloride, phosphate, bicarbonate
Electrolytes	Principal ECF electrolytes  Sodium cations (Na+)  Chloride anions (Cl−)  Principal ICF electrolyte  Potassium (K+)
Control of Electrolytes	Renin-angiotensin-aldosterone system  Antidiuretic hormone system  Sympathetic nervous system
Potassium	Most abundant positively charged electrolyte inside cells  95% of body’s potassium is intracellular.  Potassium content outside of cells ranges from 3.5 to 5 mEq/L.  Potassium levels are critical to normal body function
Potassium obtained from foods	Fruit and fruit juices (bananas, oranges, apricots, dates, raisins, broccoli, green beans, potatoes, tomatoes), meats, fish, wheat bread, and legumes
Excessive potassium loss (rather than poor dietary intake)	Alkalosis  Corticosteroids  Diarrhea  Ketoacidosis  Laxative misuse  Hyperaldosteronism  Increased secretion of mineralocorticoids burns
Hyperkalemia	excessive serum potassium; serum potassium level over 5.5 mEq/L  Potassium supplements  ACE inhibitors  Renal failure  Excessive loss from cells  Potassium-sparing diuretics Metabolic acidosis
Potassium is responsible for:	Muscle contraction  Transmission of nerve impulses  Regulation of heartbeat  Maintenance of acid-base balance  Isotonicity
Potassium effects	Oral preparations  Diarrhea, nausea, vomiting, GI bleeding, ulceration  IV administration  Pain at injection site  Phlebitis  Rate of administration
Hyperkalemia manifestations	Muscle weakness, paresthesia, paralysis, cardiac rhythm irregularities (leading to possible ventricular fibrillation and cardiac arrest)
 Treatment of severe hyperkalemia	 IV sodium bicarbonate, calcium gluconate or calcium chloride, dextrose with insulin
Sodium Polystyrene Sulfonate	Kayexalate  Cation exchange resin used to treat hyperkalemia  Oral, nasogastric tubal, or as enema  Works in intestine  Closely monitor electrolytes  Do not give to patient who do not have normal bowel function
Patiromer (Veltassa)	New oral drug to treat hyperkalemia  Non-absorbed cation exchange polymer  Increases fecal potassium excretion  Delayed onset of action therefore not indicated for emergent, life-threatening hyperkalemia
Patiromer (Veltassa) effects	 Do not give within 6 hours of other oral meds. hypomagnesemia, hypokalemia, constipation, diarrhea, nausea  Dilute and give with food
Sodium	Most abundant positively charged electrolyte outside cells  Normal concentration outside cells is 135 to 145 mEq/L  Maintained through dietary intake of sodium chloride  Salt, fish, meats, foods flavored or preserved with salt
Hyponatremia	sodium loss or deficiency; serum levels below 135 mEq/L  Symptoms  Lethargy, stomach cramps, hypotension, vomiting, diarrhea, seizures
Hypernatremia	sodium excess; serum levels over 145 mEq/L  Symptoms  Water retention (edema), hypertension  Red, flushed skin; dry, sticky mucous membranes; increased thirst; elevated temperature; decreased urine output
Sodium is responsible for:	Control of water distribution  Fluid and electrolyte balance  Osmotic pressure of body fluids  Participation in acid-base balance
sodium indication	Treatment or prevention of sodium depletion when dietary measures are inadequate  Mild  Treated with oral sodium chloride and/or fluid restriction  Severe  Treated with IV NS or lactated Ringer’s solution
sodium effects	Oral administration  Nausea, vomiting, cramps  IV administration  Venous phlebitis
IV potassium must not be given at a rate faster than	10 mEq/hour to patients who are not on cardiac monitors. For critically ill patients on cardiac monitors, rates of 20 mEq/hour or more may be used.  Never give as an IV bolus or undiluted
Oral forms of potassium	Must be diluted in water or fruit juice to minimize GI distress or irritation  Monitor for complaints of nausea, vomiting, GI pain, and GI bleeding
Female sex steroid hormones	Estrogens  Progesterone
Pituitary gonadotropin hormones	Follicle-stimulating hormone (FSH)  Luteinizing hormone (LH)
Three major endogenous estrogens	Estradiol (principal and most active)  Estrone  Estriol Synthesized from cholesterol in ovarian follicles
EXOGENOUS ESTROGENIC DRUGS steroidal	Conjugated estrogens, estradiol transdermal, estropipate, many others
EXOGENOUS ESTROGENIC DRUGS nonsteroidal	Diethylstilbestrol  No longer available in the United States
ESTROGENS responsible for	Development and maintenance of the female reproductive system  Development of female secondary sex characteristics  Shaping of body contours and development of the skeleton
ESTROGENIC DRUGS	Conjugated estrogens (Premarin)  Esterified estrogens (Estratab)  Estradiol transdermal (Estraderm, Climara, Vivelle)  Estradiol cypionate (Depo-Estradiol, DepoGen)  Estradiol valerate (Delestrogen)  Ethinyl estradiol (Estinyl)
ESTROGENIC DRUGS (CONT.)	Estradiol vaginal dosage forms (Vagifem, Estrace Vaginal Cream)  Estrone (Estrone Aqueous)  Estropipate (Ogen, Ortho-Est)
ESTROGENS: INDICATIONS	 Atrophic vaginitis  Hypogonadism  Oral contraception (given with a progestin)  Uterine bleeding  Vasomotor spasms of menopause (“hot flashes”)  Osteoporosis  Breast or prostate cancer
ESTROGENS: CONTRAINDICATIONS	Drug allergy  Any estrogen-dependent cancer  Undiagnosed abnormal vaginal bleeding  Pregnancy  Active thromboembolic disorder or history
ESTROGENS: ADVERSE EFFECTS	Thrombolytic events: most serious  Nausea: most common  Hypertension, thrombophlebitis, edema  Vomiting, diarrhea, constipation, abdominal pain  May cause photosensitivity, chloasma  Amenorrhea, breakthrough uterine bleeding  Tender breasts
ESTROGENS: INTERACTIONS	Decrease the activity of the oral anticoagulants  Decrease effect of rifampin  St. John’s wort  Tricyclic antidepressants  Smoking
PROGESTINS	Hydroxyprogesterone (Hylutin)  Levonorgestrel (Plan B)  Medroxyprogesterone (Provera, Depo-Provera)  Megestrol (Megace)  Norethindrone acetate (Aygestin)  Norgestrel (Ovrette, Ovral)  Progesterone (Prometrium)  Etonogestrel implant
PROGESTINS: MECHANISMS OF ACTION	Induction of secretory changes in the endometrium  Increases basal body temperature  Thickening of the vaginal mucosa  Relaxation of uterine smooth muscle  Stimulation of mammary alveolar tissue growth
PROGESTINS: INDICATIONS	Treatment of functional uterine bleeding caused by:  Hormonal imbalance  Fibroids  Uterine cancer  Treatment of primary and secondary amenorrhea
PROGESTINS: ADVERSE EFFECTS	Liver dysfunction: cholestatic jaundice  Thrombophlebitis, thromboembolic disorders, such as pulmonary embolism (PE)  Nausea, vomiting  Amenorrhea, spotting  Edema, weight gain or loss
MEDROXYPROGESTERONE	nhibits the secretion of pituitary gonadotropins, which prevents follicular maturation and ovulation, stimulates the growth of mammary tissue,
MEDROXYPROGESTERONE treats	treat uterine bleeding, secondary amenorrhea, endometrial cancer, and renal cancer, and is also used as a contraceptive
Oral contraceptive medications	Monophasic, biphasic, and triphasic forms  Triphasic form most closely duplicates the normal hormonal levels of the female cycle
CONTRACEPTIVE DRUGS: MECHANISM OF ACTION	Prevent ovulation by inhibiting the release of gonadotropins and increasing uterine mucus viscosity
CONTRACEPTIVE DRUGS: OTHER DRUG EFFECTS	Improve menstrual cycle regularity  Decrease blood loss during menstruation  Decrease incidence of functional ovarian cysts and ectopic pregnancies
CONTRACEPTIVE DRUGS: ADVERSE EFFECTS	Hypertension  Thromboembolism, possible PE, myocardial infarction (MI), stroke  Alterations in lipid and carbohydrate metabolism  Increases in serum hormone concentrations
Drugs that decrease effectiveness of oral contraceptive drugs	Antibiotics (especially penicillins and cephalosporins)  Barbiturates  Isoniazid  Rifampin
Drugs that may have reduced effectiveness if given with oral contraceptives	Beta blockers, warfarin, tricyclic antidepressants, vitamins, hypnotics, anticonvulsants, theophylline, and antidiabetic drugs
OSTEOPOROSIS	Low bone mass  Increased risk of fractures  Primarily affects women  40% of women over 50 years of age will develop osteoporotic fracture
OSTEOPOROSIS: RISK FACTORS	European or Asian descent  Slender body build  Early estrogen deficiency  Smoking  Alcohol consumption  Low-calcium diet  Sedentary lifestyle
DRUG THERAPY FOR PREVENTION OF OSTEOPOROSIS	Calcium supplements and vitamin D may be recommended for women at high risk for osteoporosis
DRUG THERAPY FOR OSTEOPOROSIS	Bisphosphonates  Alendronate (Fosamax), ibandronate (Boniva), risedronate (Actonel), zoledronic acid (Reclast)  Selective estrogen receptor modifiers (SERMs)  Raloxifene (Evista)  Tamoxifen (Nolvadex)  Hormones  Calcitonin (Calcimar)
Bisphosphonates	Work by inhibiting osteoclast-mediated bone resorption, which in turn indirectly enhances bone mineral density  Strong clinical evidence indicates the bisphosphonates can reverse lost bone mass and reduce facture risk.
Teriparatide (Forteo)	Only drug that stimulates bone formation  Derivative of parathyroid hormone (PTH)  Action similar to natural PTH
Denosumab (Prolia)	Monoclonal antibody that blocks osteoclast activation, thereby preventing bone resorption  It is given as a subcutaneous injection once every 6 months along with daily calcium and vitamin D
Raloxifene	Primary use: prevention of postmenopausal osteoporosis
Bisphosphonates contradictions	drug allergy, hypocalcemia, esophageal dysfunction, and the inability to sit or stand upright for at least 30 minutes after taking the medication
SERMs contradictions	women with known allergy to these drugs, who are or may become pregnant, with a venous thromboembolic disorder, including deep vein thrombosis (DVT), PE, and retinal vein thrombosis
SERMs effects	Hot flashes, leg cramps  Increased risk of venous thromboembolism  Teratogenic  Leukopenia
Bisphosphonates effects	Headache, gastrointestinal (GI) upset, joint pain  Risk of esophageal burns if medication lodges in esophagus before reaching the stomach  Risk of osteonecrosis of the jaw
Calcitonin effects	Flushing of the face, nausea, diarrhea, and reduced appetite
Teriparatide effects	Chest pain, dizziness, hypercalcemia, nausea, and arthralgia
ALENDRONATE (FOSAMAX)	Oral bisphosphonate  First nonestrogen nonhormonal option for preventing bone loss  Inhibits or reverses osteoclast-mediated bone resorption
ALENDRONATE (FOSAMAX) indications	prevention and treatment of osteoporosis in men and in postmenopausal women as well as treatment of glucocorticoid- induced osteoporosis in men and for the treatment of Paget disease in women
RALOXIFENE (EVISTA)	SERM  Use: prevention of postmenopausal osteoporosis  Adverse effect: hot flashes
Clomiphene (Clomid, Serophene)	Nonsteroidal ovulation stimulant  Blocks estrogen receptors in the uterus and brain, resulting in a false signal of low estrogen levels  Increases production of gonadotropin-releasing hormone, FSH, and LH
Menotropins (Pergonal)	Standardized mixture of FSH and LH  Stimulates development of ovarian follicles, leading to ovulation  May also be given to men to stimulate spermatogenesis
Chorionic gonadotropin alfa (Ovidrel)	Recombinant form of human chorionic gonadotropin  Causes rupture and ovulation of mature ovarian follicles and maintenance of corpus luteum  Used to stimulate ovulation
FERTILITY DRUGS: ADVERSE EFFECTS	Tachycardia, hypovolemia, DVT  Dizziness, headache, flushing, depression, restlessness, anxiety, nervousness, fatigue  Nausea, bloating, constipation, vomiting, anorexia  Urticaria, ovarian hyperstimulation, multiple pregnancy, blurred vision
UTERINE STIMULANTS	Medications used to alter uterine contractions  Used to:  Promote labor  Prevent the start or progression of labor  Postpartum use: reduce the risk of postpartum hemorrhage
Oxytocin (Pitocin): synthetic form	Used to induce labor at or near full-term gestation and to enhance labor when contractions are weak and ineffective
Prostaglandins	Natural hormones  Cause potent contraction of myometrium, smooth muscle fibers of the uterus  Used to induce labor by softening the cervix and enhancing uterine muscle tone
Ergot alkaloids	Increase force and frequency of uterine contractions  Used after delivery of the infant and placenta to prevent postpartum uterine atony and hemorrhage  Methylergonovine (Methergine)
Progesterone antagonist	Mifepristone (Mifeprex)  Stimulates uterine contractions to induce abortion  Given with a prostaglandin drug for elective abortions
UTERINE STIMULANTS: ADVERSE EFFECTS	Hypotension or hypertension, chest pain  Headache, dizziness, fainting  Nausea, vomiting, diarrhea  Vaginitis, vaginal pain, cramping  Leg cramps, joint swelling, chills, fever, weakness, blurred vision
DRUGS FOR PRETERM LABOR MANAGEMENT UTERINE RELAXANTS: TOCOLYTICS	Used to stop labor that begins before term to prevent premature birth  Generally used after the 20th week of gestation  Uterine contractions that occur between the 20th and 37th weeks of gestation are considered premature labor.
Indomethacin	Nonsteroidal antiinflammatory agent  Inhibits prostaglandin activity
Nifedipine	Calcium channel blocker  Inhibits myometrial activity by blocking calcium influx
When indomethacin and nifedipine are ineffective and delivery is proceeding	corticosteroids (betamethasone or dexamethasone) are administered to the mother to promote lung maturity in the fetus between 24 and 34 weeks of gestation
HERBAL PRODUCTS: SOY	Relief of menopausal symptoms, osteoporosis prevention  Estrasorb, applied as a lotion  Adverse effects  Nausea  Diarrhea  Abdominal pain  Estrasorb remains on skin for 8 hours.
HERBAL PRODUCTS: SOY implications	ssess baseline vital signs, weight, blood glucose levels, and renal and liver function study results.  Assess whether the patient smokes.  Assess history and medication history
HERBAL PRODUCTS: SOY implications pt 2	vs, assess if smokes, relaxants are used when premature labor occurs between the 20th and 37th weeks of gestation
For bisphosphonates, ensure that patients have	no esophageal abnormalities and can remain upright or in a sitting position for 30 minutes after the dose.
NURSING IMPLICATIONS (CONT.) Estrogens and progestins	Take the smallest dose needed.  Give intramuscular doses deep in large muscle masses, and rotate sites.  Give oral doses with meals to reduce GI problems.
NURSING IMPLICATIONS (CONT.) Bisphosphonates	Instruct patients to take medication upon rising in the morning, with a full glass of water, and 30 minutes before eating.  Emphasize that patients should sit upright for at least 30 minutes after taking the medication.
Testes:	produce male sex hormones
Seminiferous tubules	site of spermatogenesis
Testosterone	Responsible for normal development and maintenance of primary and secondary male sex characteristics • Development of bone and muscle tissue • Inhibition of protein catabolism (metabolic breakdown) • Retention of various electrolytes
Anabolic steroids	Anabolic activity: synthesis of tissue and increasing tissue formation • Schedule III, great potential for misuse by athletes • Oxymetholone (Anadrol-50) • Oxandrolone (Oxandrin) • Nandrolone (Deca-Durabolin)
Anabolic steroids: approved indications	Adjunctive therapy to promote weight gain after extensive surgery, trauma, chronic diseases, anemia, hereditary angioedema, and metastatic breast cancer
Anabolic steroids: great potential for misuse	Bodybuilders and weightlifters • Muscle-building properties • Serious consequences: sterility, cardiovascular diseases, and liver cancer
Danazol (Danocrine)	Synthetic androgen is danazol (Danocrine). • Use: treatment of hereditary angioedema, and, in women, endometriosis and fibrocystic breast disease.
Androgens: Mechanism of Action	Effects are similar to the body’s endogenous androgens. • Stimulate normal growth and development of the male sex organs • Development and maintenance of male secondary sex characteristics
Androgen Inhibitors	Block the effects of naturally occurring (endogenous) androgens • 5-Alpha reductase inhibitors • Benign prostatic hyperplasia (BPH) treatment • Finasteride • Dutasteride
Finasteride (Propecia)	Inhibition of 5-alpha reductase prevents the thinning of hair caused by increased levels of DHT. • Male pattern baldness • Women • Not for treatment of female baldness • Teratogenic in pregnant women
Alpha1-Adrenergic Blockers	Used for symptomatic relief of obstruction caused by BPH • Doxazosin (Cardura) • Tamsulosin (Flomax) • Terazosin (Hytrin) • Alfuzosin (Uroxatral) • Silodosin (Rapaflo)
Androgen Receptor Blockers	Block the activity of androgen hormones at target tissue (prostate) receptors • Used in the treatment of prostate cancer • Flutamide (Eulexin) • Nilutamide (Nilandron) • Bicalutamide (Casodex
Gonadotropin-Releasing Hormone Analogues	Used to treat prostate cancer • Action: inhibit the secretion of pituitary gonadotropin, which eventually leads to a decrease in testosterone production • Goserelin (Zoladex) • Leuprolide (Lupron) • Triptorelin (Trelstar)
Drugs to Treat Erectile Dysfunction	Phosphodiesterase (PDE) inhibitors are used in the treatment of erectile dysfunction (ED). • Sildenafil (Viagra) • First oral drug for treatment of ED • Causes relaxation of the smooth muscle in the corpora cavernosa
Drugs to Treat Erectile Dysfunction (Cont.)	Vardenafil (Levitra) • Tadalafil (Cialis) • Avanafil (Stendra) • Similar to sildenafil (Viagra) but longer duration of action
Men’s Health Drugs: Contraindications	Known androgen-responsive tumors • Sildenafil, vardenafil, tadalafil, and avanafil: contraindicated in men with major cardiovascular disorders, especially if they use nitrate medications such as nitroglycerin
Men’s Health Drugs: Adverse Effects	Androgens cause fluid retention. • Thromboembolic disorders (DVT, PE) • Heart attack • Anabolic steroids • Peliosis of the liver • Hepatic neoplasms (liver cancer) • Cholestatic hepatitis • Jaundice
Men’s Health Drugs: Adverse Effects (Cont.)	Priapism: abnormally prolonged penile erection • Relatively uncommon • Possible adverse effect of both the ED drugs and the androgens • Medical emergency that warrants urgent medical attention
PDE inhibitors:	can cause unexplained visual loss.
Finasteride	loss of libido, loss of erection, ejaculatory dysfunction, hypersensitivity reactions, gynecomastia, severe myopathy, and a 50% decrease in prostate-specific antigen
Androgens, when used with oral anticoagulants, can	significantly increase or decrease anticoagulant activity. • Androgens with cyclosporine increase the risk of cyclosporine toxicity.
Sildenafil, vardenafil, tadalafil, and avanafil may cause	severe hypotension when given together with nitrates such as nitroglycerin, isosorbide mononitrate, or isosorbide dinitrate.
Effects of tamsulosin may be increased when it is taken with	azole antifungal drugs, erythromycin and clarithromycin, cardiac drugs such as propranolol and verapamil, and protease inhibitors
Herbal Products: Saw Palmetto	Serenoa repens, Sabal serrulata • Used for treatment of BPH and alopecia • Adverse effects • Gastrointestinal upset • Headache • Back pain
Steady state	Physiologic state in which the amount of drug removed via elimination is equal to amount of drug absorbed with each dose.
Clonidine (Catapres)	Not typically prescribed as first-line antihypertensive drugs -High incidence of unwanted adverse effects such as orthostatic hypotension, fatigue, and dizziness -Adjunct drugs to treat hypertension after other drugs have failed. -Used in conjunction
what lab to watch for ace inhibitors	hyperkalemia
bronchodilators used during	acute asthma attack
***Potassium can only be infused via	IVPB in a diluted solution. NEVER give IV push! Must monitor infusion closely and infuse slowly.

Created by: cwehner125

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