Module 10: Polypharmacy

Tasks
I. Module Readings
• Katzung BG, Masters SB, Trevor AJ. Basic & Clinical Pharmacology. 12 ed. McGraw-Hill Companies, Inc, 2012.
• Ch. 59 – Special Aspects of Perinatal & Pediatric Pharmacology
• Ch. 60 – Special Aspects of Geriatric Pharmacology
• Ch. 66 – Important Drug Interactions & Their Mechanisms
• McKinnis Textbook- Ch. 38 (Complementary and Alternative Medications)
• Scott IA, Hilmer SN, Reeve E et al. Reducing inappropriate polypharmacy: the process of deprescribing. JAMA Intern Med
2015;175:827-834.
• Campanelli CM. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults:
The American Geriatrics Society 2012 Beers Criteria Update Expert Panel. J Am Geriatr Soc 2012;60:616-631.

Medication Cabinet
alcohol prazosin (Minipress)
insulin warfarin (Coumadin)
acetaminophen (Tylenol) digoxin (Lanoxin)
indomethacin (Indocin) amiodarone (Cordarone)
phenobarbital (Solfoton) simvastatin (Zocor)
phenytoin (Dilantin) cyclosporine (Neoral)
lorazepam (Ativan) tacrolimus (Prograf)
fluoxetine (Prozac) St. John's wort
metoprolol (Lopressor) ginkgo biloba
diltiazem (Cardizem) ginseng

Assignment
Clinical Application Project is a cumulative course assignment and is due Dec. 5.

Assessment
Polypharmacy module is included in Examination 2 on Dec. 8. Practice questions are available.

Learning Objectives
A. Polypharmacy Definitions- Many definitions exist for polypharmacy in qualitative and quantitative formats.
1
• "The administration of more medicines than are clinically indicated, representing unnecessary drug use."
• Polypharmacy: "the practice of taking many different prescription and over-the-counter drugs, often without the
2
knowledge of the physician."
• "It is common for patients to receive multiple prescriptions, sometimes for the same condition, that have conflicting
3
pharmacologic actions, a condition termed polypharmacy."
• Other sources define polypharmacy by number of drugs; examples:
o "> 5 regular prescribed drugs"4
o "concomitant ingestion of four or more medications"1

1. Describe factors that influence drug absorption, distribution, metabolism, and excretion in neonates, infants,
children, and older adults.
1. Drug Absorption
1. Unique factors that influence drug absorption include blood flow at the site of administration, as determined
by the physiologic status of the infant or child; and, for orally administered drugs, gastrointestinal function,
which changes rapidly during the first few days after birth.
2. Age after birth also influences the regulation of drug absorption.
3. Blood flow at the site of administration
1. Absorption after intramuscular or sub-q injection depends mainly (neonates and adults) on rate of
blood flow to the muscle or sub-q area injected
1. Physiological conditions that reduce blood flow to these areas include cardiovascular
shock, vasoconstriction due to sympathomimetic agents, and heart failure
2. In sick preterm infants, Muscle mass may be limited, have diminished peripheral perfusion
1. Absorption becomes irregular and difficult to predict, because the drug may
remain in the muscle and be absorbed more slowly than expected
2. If perfusion suddenly improved there can be a sudden and unpredictable
increase in amount of drug entering circulation, resulting in high and potentially
toxic concentrations
1. Cardiac glycosides, aminoglycoside antibiotics, anticonvulsants
 4. Gastrointestinal Function
1. In full-term infants, gastric acid secretion begins soon after birth and increases gradually over
several hours.
2. In preterm infants, the secretion of gastric acid occurs more slowly, with the highest concentrations
appearing on the fourth day of life.
1. Therefore, drugs that are usually partially or totally inactivated by the low pH of gastric
contents should not be administered orally.
3. Gastric emptying time is prolonged (up to 6 or 8 hours) in the first day or so after delivery.
1. Therefore, drugs that are absorbed primarily in the stomach may be absorbed more
completely than anticipated.
4. In the case of drugs absorbed in the small intestine, therapeutic effect may be delayed.
1. Peristalsis in the neonate is irregular and may be slow.
1. more than the usual amount of drug may be absorbed if peristalsis is slowed, and
this could result in potential toxicity from an otherwise standard dose.
2. An increase in peristalsis, as in diarrheal conditions, tends to decrease the extent of
absorption, because contact time with the large
absorptive surface of the intestine is decreased.
5. Gastrointestinal enzyme activities tend to be lower in the newborn
than in the adult.
1. Activities of α -amylase and other pancreatic enzymes in
the duodenum are low in infants up to 4 months of age.
2. Neonates also have low concentrations of bile acids and
lipase, which may decrease the absorption of lipid-
soluble drugs.
5. Geriatric population
1. No evidence showing major alterations with age but are some associated with certain conditions
1. Greater consumption of nonprescription drugs (antacids, laxatives), and changes in
gastric emptying, which is often slower in older people, especially older diabetics
2. Drug Distribution
1. As body composition changes with development, the distribution volumes of drugs are also changed.
1. Water content
1. Neonate have higher % of BW in form of water (70–75%) than does the adult (50–60%).
2. Full-term neonate (70% water) and small preterm neonate (85% water)
3. Similarly, extracellular water is 40% of body weight in the neonate, compared with 20% in
the adult. Most neonates will experience diuresis in the first 24–48 hours of life.
2. Since many drugs are distributed throughout the extracellular water space, the volume of the
extracellular water compartment may be important in determining the concentration of drug at
receptor sites.
1. Important in water soluble drugs (aminoglycosides); less crucial for lipid-soluble agents
2. Preterm infants have less fat (1% BW) than full-term infants (15% BW)
1. Organs that generally accumulate high concentrations of lipid-soluble drugs in adults and
older children may accumulate smaller amounts of these in less mature infants
3. Drug binding to plasma proteins (Albumin is the plasma protein with greatest binding capacity)
1. Protein binding of drugs is reduced in the neonate
1. Seen with local anesthetic drugs, diazepam, phenytoin, ampicillin, phenobarbital
2. Concentration of free (unbound) drug in plasma is increased initially
3. Because free drug exerts pharmacologic effect, this results in greater drug effect or
toxicity despite normal or low plasma concentration of total drug (bound plus unbound)
2. Some drugs compete with serum bilirubin for binding to albumin
1. Drugs given to a neonate with jaundice can displace bilirubin from albumin
2. Because of greater permeability of the neonate BBB, substantial amounts of bilirubin may
enter the brain and cause kernicterus
1. Observed when sulfonamide antibiotics were given to preterm neonates as a
prophylaxis against sepsis
3. Consequently, as the serum bilirubin rises for physiologic reasons or because of a blood
group incompatibility, bilirubin can displace a drug from albumin and substantially raise the
free drug concentration (has been shown in phenytoin)
1. This may occur without altering the total drug concentration and would result in
greater therapeutic effect or toxicity at normal concentrations
4. Geriatric population
1. Compared with young adults, elderly have reduced lean body mass,
reduced body water, and increased fat percentage
2. Usually a decrease in serum albumin, which binds many drugs,
especially weak acids
3. There may be a concurrent increase in serum orosomucoid (protein
that binds many basic drugs)
1. Thus, ratio of bound to free drug may be significantly altered
4. These changes may alter appropriate loading dose of a drug
 1. However, since both the clearance and the effects of a drug are related to the free
concentration, the steady-state effects of a maintenance dosage regimen should not be
altered by these factors alone
1. Ex: loading dose of digoxin in an elderly patient with heart failure should be
reduced (if used at all) because of the decreased apparent volume of distribution
2. Maintenance dose may have to be reduced b/c of reduced clearance of drug
3. Drug Metabolism
1. Metabolism of drug in the liver
1. Drug-metabolizing activities of cytochrome P450-dependent mixed-
function oxidases and conjugating enzymes are lower (50–70% of
adult values) in early neonatal life than later.
2. Glucuronide formation reaches adult values between the third and
fourth years of life.
3. Because of neonate’s decreased ability to metabolize drugs, many
drugs have slow clearance rates and prolonged elimination half-lives
1. If drug doses and dosing schedules are not altered
appropriately, this immaturity predisposes the neonate to
adverse effects from drugs that are metabolized by the liver
2. Whether or not the mother was receiving drugs (phenobarbital) that can induce
early maturation of fetal hepatic enzymes
1. Ability of neonate to metabolize certain drugs will be greater than
expected, and one may see less therapeutic effect and lower plasma drug concentrations when the
usual neonatal dose is given
2. During toddlerhood (12-36 months), the metabolic rate of many drugs exceeds adult values, often
necessitating larger doses per kilogram than later in life
3. Geriatric population
1. Capacity of liver to metabolize drugs does not appear to decline
consistently with age for all drugs
1. Certain drugs are metabolized more slowly (greatest
changes are in Phase 1 reactions: those carried out by
microsomal P450 systems)
2. Much smaller changes in the ability of the liver to carry out
conjugation (phase II) reactions
3. Some of these changes may be caused by decreased liver
blood flow, an important variable in the clearance of drugs
that have a high hepatic extraction ratio
2. Decline in liver’s ability to recover from injury (caused by alcohol or
viral hepatitis)
1. A history of recent liver disease in an older person should
lead to caution in dosing with drugs that are cleared
primarily by the liver, even after apparently complete recovery from the hepatic insult.
3. malnutrition and diseases affecting hepatic function (heart failure) more common in elderly
1. Heart failure may dramatically alter ability of liver to metabolize drugs by reducing hepatic
blood flow
2. Similarly, severe nutritional deficiencies may impair hepatic function
4. Drug Excretion
1. Glomerular filtration rate (GFR)
1. Lower in newborns (30-40% adult value) than older infants, children, or adults, and limitation
persists first few days of life
2. Even lower in neonates born before 34 weeks of gestation
3. At the end of the first week, GFR and renal plasma flow have increased 50% from first day
rd
4. By the end of the 3 week, GFR is 50-60% of adult value; by 6-12 months, reaches adult values
1. Drugs that depend on renal function for elimination are cleared from the body very slowly
in the first few weeks of life
5. During toddlerhood, GFR exceeds adult values, often necessitating larger doses than adults
6. Since renal function in a sick infant may not improve at the predicted rate during the first weeks and
months of life, appropriate adjustments in dosage and dosing schedules may be very difficult
1. Adjustments are best made on the basis of plasma drug concentrations at intervals
7. Toddlers may have SHORTER elimination half-lives of drugs than older children and adults,
due to INCREASED renal elimination and metabolism
2. Geriatric Population
1. Decline in creatinine clearance occurs (decline is not reflected in an equivalent rise in serum
creatinine because the production of creatinine is also reduced as muscle mass declines with age,
therefore serum creatinine alone is not an adequate measure of renal function
1. Results in a marked prolongation of the half-life of many drugs, and the possibility of
accumulation to toxic levels if dosage is not reduced in size or frequency
2. Dosing recommendations for the elderly often include an allowance for reduced renal
clearance
 2. A patient who is severely dehydrated (not uncommon in
patients with stroke or other motor impairment) may have an
additional marked reduction in renal drug clearance that is
completely reversible by rehydration.
3. Lungs are important for excretion of volatile drugs
1. As a result of reduced respiratory capacity and the
increased incidence of active pulmonary disease in
elderly, use of inhalation anesthesia is less common;
parenteral agents more common

2. Discuss common reasons for medication errors and strategies to improve medication compliance for a) pediatric
population and b) geriatric population.
1. Pediatric population
1. The form in which a drug is manufactured and the way in which the parent dispenses the drug to the child
determine the actual dose administered
1. Elixirs- no shaking is required (first dose and last dose should contain equivalent amounts of drug)
2. Suspension- shaking required each time dose is given (first and last dose can be different)
1. Toxicity may occur later in the course of therapy, when it is not expected
2. Uneven distribution is a potential cause of inefficacy or toxicity in children taking phenytoin
suspension
2. Compliance may be more difficult to achieve in pediatric practice than otherwise, since it involves not only
the parent’s conscientious effort to follow directions but also such practical matters as measuring errors,
spilling, and spitting out
1. Parents should obtain a calibrated measuring spoon or syringe from the pharmacy
1. Improves accuracy of dose measurements and simplify administration of drugs to children
2. When evaluating compliance, it is often helpful to ask if an attempt has been made to give a further
dose after the child has spilled half of what was offered
1. Parents may not be able to say with confidence how much of the dose the child received
2. Parents must be told whether to wake infant for its every-6-hour dose day or night
3. The easier it is to administer and take the medicine and the easier the dosing schedule is to follow,
the more likely it is that compliance will be achieved.
2. Consistent with their ability to comprehend and cooperate, children should also be given some responsibility
for their own health care and for taking medications.
1. Random pill counts and measurement of serum concentrations may help disclose noncompliance.
2. The use of computerized pill containers, which record each lid opening, has been shown to be very
effective in measuring compliance.
3. Because many pediatric doses are calculated—eg, using body weight—rather than simply read from a list,
major dosing errors may result from incorrect calculations. (errors in placement of decimal point)
1. Use a 0 before decimal point when dealing with doses less than 1; don't use a 0 after decimal point
2. Geriatric population
1. Expense of drugs- Prescriber must be aware of cost of prescription and cheaper alternatives
2. Nonadherence may result from forgetfulness or confusion, especially if the patient has several prescriptions
and different dosing intervals
3. Nonadherence may also be deliberate if patient had bad prior experience with drug
1. There may be excellent reasons for such “intelligent” noncompliance, and the practitioner should try
to elicit them
2. Such efforts may also improve compliance with alternative drug regiments because enlisting the
patient as a participant in therapeutic decisions increases the motivation to succeed
4. Errors in drug taking caused by physical disabilities (Arthritis, tremor, and visual problems)
1. Liquid medications that are to be measured “by the spoonful” are inappropriate for patients with any
type of tremor or motor disability
2. Use of a dosing syringe may be helpful in such cases
3. Because of decreased production of saliva, patients often have difficulty swallowing large tablets
4. Childproof containers are often elder-proof if the patient has arthritis
5. Cataracts and macular degeneration occur
1. Labels on prescription bottles should be large enough for the patient with diminished
vision to read or should be color-coded if the patient can see but no longer read
3. Geriatric population drug therapy
1. The balance may be tipped in the right direction by adherence to a few principles:
1. Take a careful drug history. The disease to be treated may be drug-induced, or drugs being taken
may lead to interactions with drugs to be prescribed.
2. Prescribe only for a specific and rational indication. Do not prescribe omeprazole for “dyspepsia.”
Expert guidelines are published regularly by national organizations and websites.
3. Define the goal of drug therapy. Then start with small doses and titrate to the response desired.
Wait at least three half-lives (adjusted for age) before increasing the dose. If the expected response
does not occur at the normal adult dosage, check blood levels. If the expected response does not
occur at the appropriate blood level, switch to a different drug.
4. Maintain a high index of suspicion regarding drug reactions and interactions. Know what other
drugs the patient is taking, including over-the-counter and botanical (herbal) drugs.
 5. Simplify regimen as much as possible. When multiple drugs are prescribed, try to use drugs that
can be taken at same time of day. Whenever possible, reduce the number of drugs being taken.

3. Identify Beers Criteria medications and rationales that have strong recommendations to avoid with moderate to high
quality of evidence.
1. Alpha1 blockers (prazosin)- avoid use as antihypertensive (moderate)
1. High risk of orthostatic hypotension;
2. Not recommended as routine treatment for hypertension
3. Alternative agents have superior risk/benefit profile
2. Antiarrhythmic agents (Class Ia, Ic, and III) (amiodarone)- high-
1. avoid antiarrhythmic drugs as first line treatment of atrial fibrillation
2. Data suggest that rate control yields better balance of benefits and harms than rhythm control for most older
adults
3. Amiodarone is associated with multiple toxicities including thyroid disease, pulmonary disorders, and QT
interval prolongation
3. Digoxin > 0.125 mg/d (moderate)
1. In heart failure, higher dosages associated with no additional benefit and may increase risk of toxicity, slow
renal clearance, may lead to risk of toxic effects (avoid)
4. Barbiturates (high- avoid) phenobarbital
1. High rate of physical dependence; tolerance to sleep benefits; risk of overdose at low dosages
5. Benzodiazepines (high-avoid benzodiazepines for treatment of insomnia, agitation, or delirium)
1. Older adults have increased sensitivity to them and slower metabolism of long acting agents
2. Short and intermediate acting (lorazepam)
1. they ­ risk of cognitive impairment, delirium, falls, fractures, and MVA in older adults
6. Insulin, sliding scale
1. Higher risk of hypoglycemia without improvement in hyperglycemia management regardless of care setting
7. Indomethacin
1. Increases risk of bleeding and peptic ulcer disease in high risk groups (has most adverse effects)
8. Diltiazem (nondihydropyradine CCB)
1. Potential to promote fluid retention and exacerbate heart failure
9. Heart failure (indomethacin)
1. Potential to promote fluid retention and exacerbate heart failure
10. Delirium (benzodiazepines: lorazepam)
1. Avoid in older adults with or at risk of delirium because of inducing or worsening delirium
2. If discontinuing drugs used chronically, taper to avoid withdrawal symptoms
11. Dementia and cognitive impairment (benzodiazepines: lorazepam)
1. Avoid because of adverse CNS effects
2. Avoid antipsychotics for behavioral problems of dementia unless nonpharmacological options have failed
and patient is a threat to themselves or others
3. Antipsychotics are associated with an increased risk of stroke and mortality in persons with dementia
12. History of falls or fractures (benzodiazepines (lorazepam), fluoxetine (SSRI), anticonvulsant- phenytoin)
1. Ability to produce ataxia, impaired psychomotor function, syncope, and additional falls; shorter-acting
benzodiazepines are not safer than long-acting ones
2. Avoid unless safer alternatives are available
13. History of gastric or duodenal ulcers (indomethacin)
1. May exacerbate existing ulcers or cause new or additional ulcers
2. Avoid unless other alternatives are not effective; patient can take gastroprotective agent (PPI)
14. Stress or mixed urinary incontinence (alpha blockers- prazosin, fluoxetine- SSRI)
1. Aggravation or incontinence
2. Avoid in women
15. Antipsychotics (SSRIs- fluoxetine)
1. May exacerbate or cause syndrome of inappropriate ADH secretion or hyponatremia
2. Need to monitor Na level closely when starting or changing dosages in older adults due to increased risk

4. Explain interactions among drugs listed in the medication cabinet (Table 66-1).
1. Alcohol
1. insulin- acute alcohol intake may increase hypoglycemic effect of insulin (especially in fasting patients)
2. acetaminophen (tylenol)- increased hepatotoxicity of alcoholism- increase formation of hepatotoxic
acetaminophen metabolites (chronic alcoholics)
3. phenobarbital (Solfoton)- additive/synergistic CNS depression
4. phenytoin (Dilantin)- additive/synergistic CNS depression
5. lorazepam (Ativan)- additive/synergistic CNS depression
6. warfarin (Coumadin)- increased hypothrombinemic effect with acute alcohol intoxication; decreased
prothrombin (impaired blood clothing); supratherapeutic INR
2. Insulin
1. metoprolol (Lopressor)- inhibition of glucose recovery from hypoglycemia; inhibition of symptoms of
hypoglycemia (except sweating); increased blood pressure during hypoglycemia
2. ginseng- exaggerates effects of insulin
3. Other interactions: alcohol
3. Acetaminophen (Tylenol)
1. warfarin (Coumadin)- increase anticoagulant effect: impaired synthesis of clotting factor
2. Other interactions: alcohol
4. Indomethacin (Indocin)- NSAID
1. fluoxetine (Prozac)- increase risk of bleeding due to platelet inhibition
2. metoprolol (Lopressor)- reduce antihypertensive response; other prostaglandin inhibitors probably also
interact
3. warfarin (Coumadin)- increase anticoagulant effect- inhibition of platelet function, gastric erosions; some
agents increase hypothrombinemic response
4. ginkgo biloba- may inhibit blood coagulation
5. Phenobarbital (Solfoton)- barbiturate
1. metoprolol (Lopressor)- increase beta blocker metabolism
2. diltiazem (Cardizem)- increases metabolism of calcium channel blockers
3. warfarin (Coumadin)- decrease anticoagulant effect: enzyme induction
4. cyclosporine (Neoral)- increased cyclosporine metabolism
5. tacrolimus (Prograf)- increased tacrolimus metabolism
6. Other interactions: alcohol
6. Phenytoin (Dilantin)- anticonvulsant, anti-epileptic
1. metoprolol (Lopressor)- increase beta blocker metabolism
2. diltiazem (Cardizem)- increases metabolism of calcium channel blockers
3. warfarin (Coumadin)- decrease anticoagulant effect: enzyme induction; anticoagulant effect may increase
transiently at start of phenytoin therapy due to protein-binding displacement
4. amiodarone (Cordarone)- inhibit phenytoin metabolism: increased serum phenytoin; risk of toxicity;
possible reduction in serum amiodarone levels
5. cyclosporine (Neoral)- increased cyclosporine metabolism
6. Other interactions: alcohol
7. lorazepam (Ativan)- benzodiazepine
1. Other interactions: alcohol
8. fluoxetine (Prozac)- SSRI
1. metoprolol (Lopressor)- inhibit CYP2D6 and increases concentrations of metoprolol
2. warfarin (Coumadin)- increase anticoagulant effect- decreased warfarin metabolism
3. Other interactions: indomethacin
9. metoprolol (Lopressor)- beta blocker
1. prazosin (Minipress)- combo may increase hypotensive response to first dose of prazosin; orthostatic
hypotension (additive effects)
2. Other interactions: insulin, indomethacin, phenobarbital, phenytoin, fluoxetine
10. diltiazem (Cardizem)- calcium channel blocker
1. digoxin (Lanoxin)- increased plasma digoxin and additive AV conduction effects
2. simvastatin (Zocor)- decreased statin metabolism
3. cyclosporine (Neoral)- decreased cyclosporine metabolism
4. tacrolimus (Prograf)- decreased tacrolimus metabolism
5. Other interactions: phenytoin, phenobarbital
11. prazosin (Minipress)- alpha blocker
1. Other interactions: metoprolol
12. warfarin (Coumadin)- anticoagulant
1. amiodarone (Cordarone)- increase anticoagulant effect: Inhibited anticoagulant metabolism
2. simvastatin (Zocor)- increase anticoagulant effect: Decreased warfarin metabolism
3. St. John’s Wort- decrease anticoagulant effect: enzyme induction
4. ginkgo biloba- may inhibit blood coagulation
5. ginseng- reduce effectiveness of warfarin
6. Other interactions: alcohol, acetaminophen, indomethacin, phenobarbital, phenytoin, fluoxetine
13. digoxin (Lanoxin)- digitalis glycosides
1. amiodarone (Cordarone)- increases plasma digoxin levels
2. Other interactions: diltiazem
14. amiodarone (Cordarone)- class III antiarrhythmic
1. simvastatin (Zocor)- decreased statin metabolism; increased risk of additive myopathy risk with
other drugs that can cause myopathy
2. Other interactions: digoxin, warfarin, phenytoin
15. simvastatin (Zocor)- HMG-CoA reductase inhibitor
1. cyclosporine (Neoral)- decreased metabolism of simvastatin; myopathy and rhabdomyolysis noted
in patients taking combo
2. St. John’s Wort- increases statin metabolism
3. Other interactions: amiodarone, warfarin, diltiazem
16. cyclosporine (Neoral)- calcineurin inhibitor (immunosuppressant)
1. St. John’s Wort- increases cyclosporine metabolism
2. Other interactions: simvastatin, diltiazem, phenytoin, phenobarbital
17. tacrolimus (Prograf)- calcineurin inhibitor (immunosuppressant)
1. Other interactions: phenobarbital, diltiazem
 18. St. John's Wort
1. Other interactions: cyclosporine, simvastatin, warfarin
19. ginkgo biloba
1. Other interactions: warfarin, indomethacin
20. ginseng
1. Other interactions: warfarin, insulin

Warfarin (Coumadin) Interactions

Increase anticoagulant effect Decrease anticoagulant effect
alcohol St. John's Wort
amiodarone (Cordarone) ginseng
simvastatin (Zocor) phenobarbital (Solfoton)
acetaminophe (Tylenol) phenytoin (Dilantin)
ginkgo biloba
indomethacin (Indocin)
fluoxetine (Prozac)

5. Identify potential adverse effects of CAMs in the medication cabinet.

1. Gingko biloba- used extensively for Alzheimer’s disease
1. may inhibit blood coagulation in some patients and should be used cautiously in people at risk for bleeding
events or who are taking anticoagulants (e.g., heparin, warfarin, aspirin, and other NSAIDs- indomethacin).
2. Ginseng- prevention and treatment of many diseases, including cancer, diabetes, neurodegenerative disorders, and
cardiovascular disease.
1. reduce the effectiveness of anticoagulant medications such as warfarin, and it can exaggerate the effects of
antihyperglycemic medications such as insulin and oral antidiabetic drugs.
3. St. John’s Wort- treatment of depression and anxiety
1. can accelerate the metabolism of other therapeutic medications such as warfarin, reverse transcriptase
inhibitors, cyclosporine, and certain anticancer agents.
1. Thus, can prevent these meds from reaching therapeutic levels, and dosages of other medications
may have to be adjusted to maintain their efficacy when administered with St. John’s wort.
4. Signs that might indicate excessive use of CAMs
1. Muscle weakness, incoordination, excessive fatigue, balance problems, skin rashes or bruising, neuropathic
changes, and cardiovascular impairments (increased BP, arrhythmias, etc)

6. Describe the PT role in recognizing polypharmacy and communicating concerns with patient/client and prescribing
provider.
1. Since PT sees client for the longest amount of time vs physician and the PT sees patient performing taxing effort, you
may be the only one that notices any adverse effects or interactions due to polypharmacy
2. Inquire that the patient understand what medication is being taken for and correct dosing
1. if you have the time and patient has musculoskeletal, cognitive, or neurological disorders you may watch the
patient administer medication or set up in pill organizer to make sure they are capable

7. Discuss interdisciplinary strategies to reduce polypharmacy and inappropriate medication use.

1. Deprescribing Protocol
1. Ascertain all drugs the patient is currently taking and the reasons for each one
2. Consider overall risk of drug-induced harm in individual patients in determining the required intensity of
deprescribing intervention
3. Asses each drug for its eligibility to be discontinued
1. No valid indication
2. Part of a prescribing cascade
3. Actual or potential harm of a drug clearly outweighs any potential benefit
4. Disease and/or symptoms have completely resolved
5. Preventive drug is unlikely to confer any patient-important benefit over the patient’s remaining
lifespan
6. Drugs are imposing unacceptable treatment burden
4. Prioritize drugs for discontinuation
5. Implement and monitor drug discontinuation regimen
2. Timing of dosage needs to be laid out between all clinicians and taken into account time of therapy session
3. You may be the only clinician that is told the patient is on a CAM and it is your job to document in note and keep
other clinicians aware and educate and instruct patient to talk with physician about any possible interactions
4. Sudden onset s/s of polypharmacy should be documented appropriately