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Pharmacology for Nurses

2.2 Pharmacokinetics and Pharmacodynamics

Pharmacology for Nurses2.2 Pharmacokinetics and Pharmacodynamics

Learning Outcomes

By the end of this section, you should be able to:

  • 2.2.1 Define how body cells respond to drugs.
  • 2.2.2 Explain the meaning of the half-life of a drug.
  • 2.2.3 List the factors that can influence the effectiveness of drugs in the body.
  • 2.2.4 Differentiate between side effects and adverse effects of drugs.
  • 2.2.5 Describe drug tolerance and drug toxicity.

Before administering a medication to a client, the nurse must understand what the body does to the drug and what the drug does to the body. Drugs produce effects on the body’s physiology by making chemical changes that affect certain target cells within the body. The term pharmacodynamics essentially means “what the drug does to the body.” The root word, pharmaco, refers to medicines, and dynamics means change, so it refers to how the drug changes the body. All living organisms are composed of chemicals that function through various chemical reactions. When chemicals (drugs) are added to this structure, those chemicals change the body. Essentially, pharmacodynamics examines the relationship between drug concentrations at the drug’s site(s) of action and the subsequent effects of the drug in the body—its mechanism of action.

The term pharmacokinetics refers to how the body processes the medicine. The word can be broken down to the root word, pharmaco, meaning medicines, and kinetics, meaning movement. Once the nurse understands pharmacokinetics, they can better understand a drug’s actions, effects, interactions with other drugs, dosing frequency, and precautions. The four primary processes of pharmacokinetics are absorption, distribution, metabolism, and excretion. These will be discussed in the following sections.

Drug Absorption

Absorption refers to the process of a drug traveling from the site of administration, through the body’s membranes, and into the circulating bloodstream. Drugs may be absorbed through the skin (i.e., topical medications), through the membranes in the respiratory tract (i.e., inhalers), through the membranes of the gastrointestinal tract (i.e., rectal medications and most pills, tablets, and capsules), or through subcutaneous (i.e., subcutaneous injections) or muscular (i.e., intramuscular injections) tissues. The route of administration influences the absorption of a drug. A drug’s physical and chemical properties affect the absorption rate, as do the physical and chemical properties of the client’s body. Absorption also affects the amount of time it takes for a drug to take effect. Some of the factors that may affect the rate of drug absorption or the extent to which a drug is absorbed include:

  • Formulation of the drug: Liquid formulations of oral medications are absorbed more rapidly than capsules or tablets.
  • Lipid solubility: Lipid-soluble drugs are absorbed more quickly than water-soluble ones.
  • Size of the drug’s molecules: Large molecules are less readily absorbed than smaller molecules.
  • Blood flow: Drugs are more rapidly absorbed in areas where blood flow is high.
  • Route of administration: IV drugs enter the bloodstream immediately; other routes take the body longer to absorb.
  • Surface area: The larger the surface area where the drug is to be absorbed (e.g., small intestine vs. the stomach), the quicker the absorption rate.
  • Acidity: For oral medications, the acidity of the stomach or intestine can affect absorption.
  • Gastric motility: This may either slow down or speed up absorption, depending upon motility.
  • Coatings: Special coatings on oral preparations can affect absorption.
  • Food: The presence of food in the gut can affect the absorption of oral preparations.

As mentioned above, surface area can greatly affect drug absorption. This may impact both the speed of absorption and the extent to which a drug is absorbed. Drugs administered via the respiratory tract as gases or aerosols are quickly absorbed due to the large surface area of the lungs and the very rich blood supply there. The alveolar epithelium is quite permeable, which also aids in absorption. Oral medications may be absorbed in the stomach or the small intestine (sometimes both). The small intestine has many mucosal villi and microvilli, which increases its surface area; this allows medications to be more rapidly absorbed when compared to the stomach, which has a relatively small surface area. When areas of the small intestine are removed, this greatly impacts drug and nutrient absorption.

Bioavailability refers to the amount of the active drug entering the circulation and available at the site of action—or the physical ability of a drug to reach its specific target cells to have an effect on the body. Price and Patel (2022) define bioavailability “for majority purposes” as “the fraction of the active form of a drug that reaches system circulation unaltered.” Typically, only a fraction of the administered dose enters the circulation unchanged, thus becoming bioavailable. For example, the antibiotic gentamicin is 0% bioavailable when taken orally because this drug is not absorbed by the small intestine; however, it is well absorbed following intramuscular (IM) administration, and it is 100% bioavailable with intravenous (IV) administration. IV medications are immediately 100% bioavailable because there are no barriers to absorption. Oral medications, in contrast, have several barriers to absorption, such as the pH of the stomach (acidity), the length of time the oral medication spends in the stomach, blood flow to the gastrointestinal (GI) tract, or the presence of food in the stomach. After absorption, oral drugs can also be metabolized in the liver before entering systemic circulation, a process called first-pass metabolism. This can decrease the bioavailability of a drug. Therefore, oral medications are not as readily bioavailable. First-pass effect will be explained in further detail in the section “Drug Metabolism or Biotransformation.”

Drug Distribution

Drug distribution refers to the movement of a drug through the body or the way that a drug is spread throughout the body. There are several factors that may affect distribution:

  • Blood flow or tissue perfusion
  • Protein binding
  • Permeability of the cell membrane
  • Volume of distribution (the smaller the volume, the less distribution; the larger the volume, the more distribution)

The blood and lymphatic systems are the primary vehicles for the transport of drugs throughout the body. The most vascular organs, and the organs receiving the most blood supply, are the heart, liver, kidneys, and brain. The more vascular the area, the higher the concentration of a drug. Areas such as adipose (fatty) tissue, the skin, and bone are less vascular and more difficult to deliver high concentrations of a drug. Tissue perfusion itself can affect distribution; for example, in a client with an infected diabetic foot ulcer, it is more difficult to deliver systemic antibiotic therapy to the area to kill the bacteria because blood flow is not adequate.

Drugs are often bound to proteins in the blood to be carried into the bloodstream; however, a drug may also be considered free or unbound. Only a free drug can act at its target site of action, such as receptors, or cross into other fluid compartments within the body (Grogan & Preuss, 2022). Drugs compete for protein-binding sites within the bloodstream, primarily albumin. The more a drug is bound to a protein, the more difficult it is for the medication to be freed and able to cross cell membranes and act on the body. In order for a drug to act on a tissue, it must be released from the protein’s binding site. Only the unbound portion of a drug can disperse into the tissue and interact with cell receptors to produce the intended physiological effect of the drug. According to Grogan and Preuss (2022), drug distribution aims to achieve effective drug concentration at its intended receptor site. If there is a decrease in the plasma protein binding, this increases the amount of free drug available. This will intensify the effects of the drug and may even lead to toxicity.

The drug must be able to cross through cell membranes to reach target sites. Medications that are lipid-soluble can rapidly cross cellular membranes because of the high permeability of capillary endothelial membranes. These drugs will be distributed more widely than those drugs that are water-soluble.

There are deterrents to the distribution of drugs. The blood–brain barrier is a protective system that prevents many drugs (and foreign invaders or poisons) from entering the central nervous system. Some drugs readily cross the blood–brain barrier, such as those that are lipid-soluble or poorly bound to proteins (e.g., sedatives, anticonvulsants, and antianxiety agents); however, many antimicrobials are ineffective against central nervous system infections because they are unable to cross the blood–brain barrier. Many antitumor drugs also fall into this category, making cancer of the brain difficult to treat with standard chemotherapy drugs.

Drug Metabolism or Biotransformation

Biotransformation or metabolism is the process of chemically changing a drug into a form that can be more readily eliminated from the body. This process occurs primarily in the liver by enzymes that change medications into inactive forms of the drug; however, metabolism of drugs may occur at other sites in the body, such as the lungs, vasculature, and lining of the GI tract. The enzymes for metabolism detoxify chemicals or substances to keep the body functioning at an optimal level. Sometimes these enzymes alter the drug form into an inactive metabolite, a soluble compound, or even a more potent metabolite. Cytochrome P450 (CYP) enzymes, for example, aid in the metabolism of drugs, and the liver is the primary site for CYP activity. These enzymes target primarily lipid-soluble drugs.

Drugs that enter the GI tract first go to the liver, which detoxifies and treats them using the necessary enzymes. This is known as the first-pass effect, and there may be variability of this effect between clients. This may affect the dosing of some medications among different clients. (See the following section for more on the first-pass effect.) It should be noted that any client with liver disease or cirrhosis can have decreased metabolic activity, making them more susceptible to dose-related side effects if they are taking a medication metabolized through the liver. Someone with cirrhosis will not metabolize a drug to the same extent as a client without liver disease, and this may lead to higher concentrations of the drug in the system. Those higher concentrations, in turn, can lead to adverse effects. For example, the drug acetaminophen should be monitored carefully or avoided in clients with underlying liver disease. The other concern that should be mentioned is that of drug toxicity, which may occur if clients have liver disease. Clients with elevated liver enzymes may have difficulty metabolizing the drug, which may cause toxic drug levels in the client. Monitoring liver enzymes and drug-level concentrations will help ensure that drug concentrations remain therapeutic (Herman & Santos, 2023). Aspartate transaminase (AST) and alanine transaminase (ALT) are two common liver enzymes to monitor because the elevation of these enzymes may indicate hepatic dysfunction or liver damage. AST is an enzyme that assists in the metabolism of amino acids, while ALT converts proteins into energy for the liver cells.

First-Pass Effect

Any medication ingested orally is most commonly absorbed in the small intestine and transported through the portal venous system to the liver (see Figure 2.3). As the drug circulates through the liver, it is transformed by the liver enzymes into various metabolites. Some metabolites are active and will cause effects on the body, whereas others are inactivated and will be excreted from the body, largely through the stool. A significant part of any oral dose of a drug is destroyed through this process and will never reach its intended tissues or target cells. This is known as the first-pass effect. The active portion of the drug will then be circulated in the bloodstream and transported throughout the body to exercise its intended action. The first-pass effect can potentially decrease the bioavailability of a drug significantly. This means that an oral drug must be given in much larger doses as compared to IV administration in order to obtain similar systemic concentrations. In some circumstances, the drug cannot be given orally at all due to being completely inactivated by the first-pass effect. Instead, the drug must be given parenterally so that it can bypass this effect. The first-pass effect process is summarized as follows:

  • The client ingests an oral medication.
  • The drug travels from the mouth to the esophagus, the stomach, and then the small intestine.
  • The medication is absorbed by the intestinal mucosa, and it travels across the membranes into the portal vein.
  • Once the drug is in the portal circulation, it travels to the liver.
  • During the first pass through the liver via the portal circulation, the drug is metabolized into active and inactive metabolites.
  • The drug metabolites then enter the circulation and travel to target cells in various tissues where they exert their action.
  • Inactive metabolites are excreted through the stool.
A diagram shows the first pass effect. First, the oral drug is taken by the patient. It moves from the stomach to the small intestine where it is absorbed by the intestinal mucosa. From there, the drug enters portal circulation and travels to the liver. On first pass through the liver, the drug is metabolized to less active forms. Less active drug metabolites leave the liver for distribution to tissues through the heart and systemic circulation.
Figure 2.3 This figure illustrates how a drug is processed by the body in the first-pass effect. This process prepares a portion of the ingested medication for therapeutic use by the body. (attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Drug Excretion

Drugs are eliminated from the body through the process of excretion. Although the removal of a drug occurs primarily through the renal system, it may also occur through the lungs, skin, bile, or feces. The two primary routes of excretion are the kidneys via urine and the GI tract via feces. Water-soluble drugs are readily removed from the body through glomerular filtration and eliminated in the urine. Because most drugs are metabolized in the liver and have undergone extensive biotransformation there, by the time the metabolites reach the renal system, only a small fraction of the drug remains.

There are several factors that affect the urinary elimination of drugs:

  • Presence or absence of kidney disease
  • Perfusion or blood flow to the kidneys
  • Maturity of the kidneys
  • pH of the urine
  • Other drugs (e.g., NSAIDs decrease renal blood flow and alter the glomerular filtration rate [GFR])

Clinical Tip

Renal Function Tests

Prior to administering a medication, the nurse should always assess the renal function tests, if available. Blood urea nitrogen (BUN) and serum creatinine are two important tools to assess the kidneys. Renal disorders such as chronic kidney disease may increase a drug’s action and duration, and clients will often need to have dosage adjustments to prevent toxicity. As clients age, they experience a decline in both kidney and liver function, and the nurse must be alert to the possibility that the metabolism and excretion of drugs can be affected. Drug concentrations may increase because they are not properly eliminated, leaving the client vulnerable to drug toxicity.


The half-life of a drug is the amount of time it takes for the serum concentration to reduce by 50%. For example, if a client takes a 500 mg tablet with a half-life of 4 hours, then 4 hours after administration, the amount remaining of the drug will be 250 mg. Eight hours following administration, the amount remaining will be 125 mg. (This is one-half of the previous level.) Twelve hours after administration, the amount remaining will be 62.5 mg. Half-life is important because it helps determine the dosing frequency of a medication. The half-life of medications varies widely. The antidysrhythmic medication adenosine has a half-life of less than 10 seconds, so it clears the bloodstream quite rapidly; however, another antidysrhythmic medication, amiodarone, has a half-life of roughly 100 days. It takes approximately five half-lives for the drug to be considered functionally eliminated (or 97% eliminated) from the body.

Morphine has a half-life of 3 hours. If a client were given 20 mg of morphine, in 3 hours that amount would decrease by 50% (10 mg would be gone from the body). If the client were given 2 mg of morphine, then in 3 hours, the amount would drop to 1 mg. Acetaminophen also has a half-life of 3 hours. If a 500 mg tablet is given, then in 3 hours, the amount of drug in the body will be 250 mg; however, the client given a 325 mg tablet will have approximately 162.5 mg of the drug in their body at the end of 3 hours.

Many medications must reach a threshold concentration in order to have a therapeutic effect; this is the minimum effective concentration (MEC). Medications that have a short half-life leave the body quickly, in less than 8 hours, and will need to have short dosing intervals because the concentration quickly drops below the minimum effective concentration. Medications with long half-lives (greater than 24 hours) will leave the body more slowly and will be prescribed less frequently or at lower doses. Medications with longer half-lives may pose a greater risk for drug toxicity because of their propensity to accumulate in the body.

Many factors impact drug half-life, but the most significant are metabolism and excretion. Those can be affected by:

  • End organ function
  • Age
  • Genetic factors
  • Some disease processes

Drug Therapeutic Index

The therapeutic index refers to the range of dosing that is both safe and effective—the amount of drug that can produce a therapeutic effect but not so much that it causes a toxic effect (see Figure 2.4). Sometimes the therapeutic range is very narrow, meaning only a small amount of extra drug causes toxicity and a small decrease in the dosage may cause subtherapeutic effects. The wider the range, the safer the drug because small changes to the dose are less likely to cause toxicity. An example of this is some blood thinners or anticoagulants. They must make the blood thin enough to prevent clots from forming, but if too much is given, the client can suffer from life-threatening bleeding. Conversely, over-the-counter drugs usually have a wide safety margin, or therapeutic index. Drug monitoring is sometimes required for drugs with a narrow therapeutic window to ensure that the client’s drug level stays within a safe range.

A line graph shows the therapeutic window of a medication. The onset of the effect occurs at the minimum effective concentration for desired response. This keeps rising until the peak effect occurs, after which the effect begins to decline. The duration of action is the length of time between when the minimum effective concentration for the desired response first occurs until it ends. This period of time is the therapeutic window.
Figure 2.4 The therapeutic window of a medication includes the onset, peak, and duration of the medication. (attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Onset, Peak, and Duration of Action

A drug’s therapeutic effects are usually directly related to the serum drug concentration. Most drugs work in specific target tissues; however, blood concentrations may allow providers to approximate drug concentration at the site of action. The onset, peak, and duration of action are terms that are used to describe drug effects. The onset of action for a medication is the time required for the drug to produce a therapeutic response (the minimum effective concentration). For example, for a drug that lowers blood pressure, it is the time between administration of the drug and onset of its hypotensive (blood pressure–lowering) effect. As the drug continues to absorb, it eventually reaches its maximal or peak level. A drug’s peak effect describes the time required for the drug to produce its maximum therapeutic response. The duration of action is the length of time a drug produces a therapeutic response.

Receptor Response

Generally, a receptor is a molecule composed of a protein, found on the inside of a cell (intracellular receptor) or on the surface of a cell (cell surface receptor), that binds to specific external transmitters or messengers and causes a response in the cell. Each type of cell in the body contains unique receptors that allow the cell to react in a specific fashion in response to a set of signaling molecules. These receptors do not exist specifically to bind with drugs; in general, they naturally bind with endogenous substances such as neurotransmitters or hormones. However, due to the nature of drugs as chemical agents, they also can interact at receptor sites. The interaction between a drug and a receptor is what comprises the drug’s mechanism of action or the drug’s effect.

Receptors can bind with a drug and cause various beneficial pharmacological actions in different disease states. Consider the action of a receptor similar to that of a lock and key. The receptor unlocks a response to a chemical (the drug), which then affects enzyme systems within the cell (see Figure 2.5). This activated enzyme system then produces specific effects, sometimes affecting cell membrane permeability, changing cellular metabolism, or changing cellular activity. Often, a particular activity of the cell is either heightened or inhibited. Sometimes drugs will bind to a receptor site and cause an effect, whereas other times, another drug will bind to the same receptor and prevent the first drug from binding with the cell (thus blocking the effect of the first drug). This is further explained later in this section in the discussion about agonists and antagonists.

The more selective a drug is, the more ideal the drug is. This is because its selectivity for specific receptors reduces the potential side effects of the drug. If a drug is specific for only a few receptors, it limits the response to the drug—similar to a key that opens only one door. When a drug can interact with a wide variety of receptors, it can have a wide variety of responses—this would be a master key. The master key is not better than the single key—they are simply different. The single key (or receptor), however, allows for fewer side effects.

With the advent of the Human Genome Project, scientists have discovered that drug therapy is not an “one-size-fits-all” therapy. Some individuals may have fewer receptors than others, whereas other clients may have more. There are genetic differences among individuals that cause enzymes that metabolize drugs to vary, sometimes causing drug toxicity. Some individuals may develop side effects to drugs or not respond to therapy as hoped. The future of drug therapy, related to the field of pharmacogenomics, is customized treatment that is targeted for a specific client rather than the population as a whole. When drug therapy is targeted through pharmacogenetics, it can have a significant role in identifying responders and nonresponders to medications, avoiding adverse effects, and improving drug dosing (FDA, 2023b).

A diagram shows a ligand entering a receptor. Once the ligand enters the receptor, it causes a response in the cell.
Figure 2.5 A cell with a receptor and ligand. Once the receptor receives the ligand, it causes a response. (attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Receptors are responsible for specific drug actions, affect the drug dose or concentration relationship, and mediate the actions of both agonists and antagonists. The ligand is a molecule that binds to a receiving protein molecule or receptor. An agonist is a drug that stimulates receptors to initiate a response. It mirrors the endogenous or body’s internal receptor ligand to initiate the receptor to emit a biological response. An agonist has an affinity, or strong attraction, to a receptor and causes intrinsic activity, which refers to the efficacy of a drug and its ability to activate the desired receptor. The agonist basically mimics the action of the body’s physiological response. An example of this is insulin, which mimics the body’s actions of endogenous insulin at receptor sites. Another example is beta-adrenergic receptors (located in the heart and kidneys), which increase heart rate, myocardial contractility, and the speed of the electrical conduction through the heart when activated by an agonist, such as the catecholamine epinephrine (adrenalin).

An antagonist, in contrast, binds with a receptor but does not activate the receptor; however, it prevents the agonist from binding to the receptor and initiating a response—in essence, it blocks or inhibits the natural or endogenous response. Antagonists may block a body’s endogenous chemicals or other drugs. In contrast to the example above, beta-adrenergic blockers work by blocking endogenous catecholamines, such as the hormone epinephrine (adrenalin), thus causing the heart to beat more slowly, decreasing myocardial contractility, and decreasing the speed of conduction through the heart’s electrical system. Some drugs are partial agonists, which have affinity and moderate intrinsic activity. A partial agonist activates a receptor but not to the extent that a full agonist does.

Mechanism of Action

The interaction between a drug and a receptor is the mechanism of action, or “how the drug works.” This is the way that a drug produces its pharmacological effect. Sometimes drugs affect target cells through enzymes or by changing cell function or the cellular structure itself. Morphine, an opioid, acts directly upon mu and kappa receptors in the central nervous system and alters the perception of pain. Ibuprofen, another pain reliever, decreases pain and inflammation by inhibiting prostaglandin synthesis. Acetaminophen is thought to inhibit prostaglandin synthesis in the central nervous system, though it has no anti-inflammatory properties like ibuprofen does. (Interestingly, its exact mechanism of action is unknown.) These are three examples of pain relievers with different mechanisms of action.

Other examples of different mechanisms of action are the drugs used to treat hypertension. A thiazide diuretic reduces blood pressure by reducing circulating blood volume—to be even more specific, it increases sodium and water excretion by inhibiting the reabsorption of sodium in the distal tubule of the nephron. Compare that to the beta-adrenergic blocker metoprolol, which reduces blood pressure by blocking beta-1 adrenergic receptors at beta-adrenergic receptor sites and causes arterial vasodilation. However, it also acts to decrease blood pressure through decreased renin production. On the other hand, the angiotensin-converting enzyme blocker lisinopril reduces blood pressure through a different mechanism. It blocks the conversion of angiotensin I to the potent vasoconstrictor angiotensin II. This prevents the breaking down of bradykinin and other prostaglandins, which are vasodilatory, and decreases aldosterone production, which retains sodium and water and excretes potassium. This decrease in aldosterone production causes less sodium and water to be retained and more to be eliminated through the kidneys. This illustrates that the same effect—reduced blood pressure—can be produced by vastly different processes.

Not all drugs have a known mechanism of action. The therapeutic effect can be observed, but how the therapeutic effect occurs remains a mystery. Some examples of drugs where the exact mechanism of action is unknown include acetaminophen, cannabidiol (CBD), and the muscle relaxant cyclobenzaprine.

Side Effects, Adverse Drug Reactions, Drug Tolerance, and Drug Toxicity

Therapeutic effects are the intended, beneficial, desired effects of a drug. Sometimes a drug will have more than one therapeutic effect. Aspirin is an example of a drug with multiple therapeutic effects—it can reduce fever, pain, and inflammation. However, a drug may cause other responses that are undesirable, unintended, or secondary effects. These are known as side effects or adverse drug reactions. There are some who use these terms interchangeably, though others differentiate between the two. Side effects are secondary effects of the drug and are usually mild and predictable. Some side effects, or secondary effects, may even be desirable. Diphenhydramine is a histamine blocker. Because it has the side effect of drowsiness or sleepiness, it is sometimes used at night to occasionally aid in sleep. Adverse drug reactions may be harmful and lead to injury. These are secondary effects that are observed at therapeutic doses. Medication taken for hypertension sometimes causes hypotension, for example. Common side effects are usually mild, but some drugs have serious adverse effects that may be potentially lethal. An example of a common side effect of many drugs, including aspirin, is nausea or lack of appetite. A serious adverse drug effect of aspirin is gastrointestinal bleeding. Morphine, an opioid agonist, often has the side effect of constipation. However, respiratory depression is an adverse drug reaction sometimes seen with the administration of morphine and can lead to harm to client.

Drug tolerance occurs when a client requires more drug (or higher concentrations) in order to achieve the desired effect. Nitrates for chest pain sometimes cause tolerance. Essentially, the body becomes used to the medication, and more drug may be needed to get the desired effect, or a different drug has to be used. For nitrates, the client needs to have a period of time without the drug, so providers may order the drug for daytime use but withhold the drug during the night. Another common example is the use of opioids. At high doses, this class of medications causes euphoria and pleasure, but over time if the individual continues to take the drug, the euphoria and pleasure produced by the drug decrease. Initially, the client might find pain relief when taking only 5 mg of oxycodone; however, with continued use over time, higher and higher doses are required in order to achieve the same effects. Drug dependence occurs when the body develops a physiological or psychological need for a drug. The physiological need means that the drug’s absence may cause physical withdrawal symptoms if the drug is not taken. Psychological dependence is observed by an intense urge to have the drug despite the adverse consequences of taking the drug.

Drug toxicity can occur when there is an excess accumulation of a drug in the system. The ingestion of an excessive amount of a drug might cause toxicity; however, even therapeutic doses of some drugs may cause toxicity in some clients. Drug concentrations can also accumulate if drug-metabolizing organs are not functioning properly and the dose is not adjusted accordingly. A client who has liver or kidney dysfunction may be at risk for drug toxicity. When a client with liver dysfunction is given a drug that is metabolized in the liver, the dosage may need to be decreased to prevent the accumulation of the drug in the body. The same is true for a client with kidney dysfunction. If the drug is excreted through the kidneys, then the dosage and frequency of the drug will need to be modified. A drug excreted by the kidneys will usually be safe for the client with liver dysfunction, and vice versa.


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