• Tolerance:
• larger & larger doses needed for same effect.  Does not mean addiction.
• Addiction:
• a behavior pattern characterized by continued use of a psychoactive substance despite physical, psychological, or social harm.  Although addicts develop tolerance to the drug, addiction and tolerance are not the same. 

CNS side effects of Morphine:

• drowsiness
• lethargy
• apathy
• alters mood
• decreases anxiety

depressed respiration

must assess rate and depth during tx

• Stimulates vomiting center
• decreases peristalsis
• increases sphincter tone
• constipation

hypotension

Flushing of upper body (not allergy)

• pinpoint pupils
• bradypnea (<8) down to respiratory arrest

• Narcotic antagonist
• Narcan (Naloxone)
• Blocks receptor site and displaces narcotic
• reverses effects of resp & CNS depression
• Half life is shorter than narcotic, so dose must be repeated

• Respiratory depression
• Decrease in BP
• Constipation and biliary colic
• Orthostatic hypotension
• Urinary retention
• Nausea (esp. in ambulatory pts)
• Sedation
• High falls risk

Symptoms of ASA overdose

(Salicylate poisoning)

• Altered respirations (increased rate, then depression)
• Altered fluid and electrolytes and acid-base balance (alkalosis to acidosis)

Symptoms of ASA overdose

(Mild - salicylism)

• Tinnitus
• Headache
• dizziness
• drowsiness
• confusion
• paresthesias
• ventilatory stimulation
• GI distress

• The sooner, the better - no antidote
• Induce emesis
• Ventilatory support
• Correct acid-base balance
• Hasten excretion
• Watch for possible GI bleeding
• Expect effects of severe anticoagulation; renal failure if already renal insufficient

• massive GI bleeds
• renal damage

Tylenol overdose (toxicity) symptoms

How common?

At worst, fatal liver damage:

• 12-24 hrs: GI cramping, N/V
• 2nd day: no obvious signs, relief; urine output drops, hematuria, pain in URQ
• 3-5 days: hepatic necrosis, irreversible

Fairly common (OD=25 gm for an adult)

• N-acetylcysteine (mucomyst)
• Interacts with toxic metabolite, protects liver cells
• Best if given within 10-12 hrs after ingestion

• Lomotil: managing diarrhea
• Antitussives:
• Codeine & hydromorphone - effective but have abuse potential
• Dextromethorphan - chemically related to opiates but few effects other than antitussive, so it is in many OTC's

• GI injury
• acute renal failure
• bleeding
• Risk of thrombotic events (except ASA)

Why is PCA a desirable method of opioid delivery?

• They may develop tolerance to:
• analgesia
• euphoria
• respiratory depression
• sedation
• Tolerance does NOT effect:
• constipation

To complement/enhance analgesia. 

To help manage concurrent symptoms that exacerbate pain.

These are not substitutes for opioids

NSAID + Caffeine

or

ASA + Caffeine

i.e., excedrin migraine

Opiates

Half-life is less than migraine duration

Can get rebound pain

A neurovascular disorder involving dilation and inflammation of intracranial arteries

Result: headache.

• vasoconstriction of dilated blood vessels
• stimulating alpha-adrenergic & serotonergic (5-HT) receptors (Davis p. 518)
• Rosenthal's notes: Alpha-adrenergic blocker

constriction of dilated carotid artery bed

--> resolution of vascular headache

ergotamine is contraindicated in which patients?

• those with uncontrolled HTN
• pregnant or lactating
• cause uterine stimulation with decreased placental bloodflow
• severe renal or liver disease
• Can trigger MI

sumitriptan

solmitriptan

Serotonergic drugs

5-HT receptors on cranial blood vessels

5-HT agonists

N/V, weakness, tingling, flushing

can precipitate stroke, cerebral, hemorrhage, MI

Pain/pressure in chest, neck, throat, jaw

Dizziness, drowsiness

• ischemic heart disease, history of MI
• uncontrolled HTN
• caution in renal/hepatic dysfunction, CVA
• Do not give within 24 hr of ergotamine
• SSRI's
• Most are not allowed more than 6 tabs/month

• Beta blockers & CCB
• keep vessels dilated so less vaso-active tendencies
• Anti-seziure meds
• valproic acid (Depakote)
• topiramate (Topamax - *Rosenthal's slide spelled trade name wrong)
• Prevent generalized depolarization of cortex assoc with migraines

Absorption

Distribution

Metabolism

Excretion

Biochemical and physical effects and mechanism of action.

How it actually changes on a cellular level.

Pharmacotherapeutic defined as

Drugs used to:

Diagnose disease

Prevent disease (or pregnancy)

Treat disease

Body systems problems or failure

(Renal, liver, CV, Gi, Thyroid)

Are they taking OTC meds/

Cultural influences

Health Beliefs

Medicine vs. magic

Ethnic differences in drug response

Use of herbs that might interfere

OTC

Legend: any drug that requires a prescription

Controlled drugs (class I - V)

Right patient

Right drug

Right dose

Right route

Right time

Other rights:
Right documentation

Right education

Patient has right to refuse medication

Trade Name

Generic Name

Dosing and Frequency!

Oral followed by written material with information on:

Reason for use

How to take - frequency, dosage, what to avoid

Possible adverse reactions

When to call or return to provider

Pharmacokinetics

ADME

Absorbing

Distributing

Metabolizing, and

Excreting the drug

Defined as what the body does to the drug

The chemical and physiologic changes that the drug causes

Drug effect at a cellular level

"What the drug does to the body"

Drugs are typically acids or bases.

Weak acids: Easier and faster to absorb in acidic environments (e.g., stomach)

Weak bases: Easier to absorb in alkaline environments (i.e., intestine)

Chemical properties:

Ionized (polar) form is usually water soluble.  Most weak bases are also ionized

Non-ionized (nompolar) form: more lipid soluble, apt to cross cell membrane

Absorbing surface (e.g., intestine – microvilli provide a TON of surface area; vs skin)

Blood flow to site of administration

Drug solubility:

- Water: must dissolve in water to be absorbed in GI tract

- Lipid: affects all ADME

Ionization - Ionized solutions do not cross membrane easily

Stability of drug in acid or alkaline environment

pH

- Local environment (e.g., acidic stomach) enhances or retards diffusion of acid/base drugs

- In general, drugs are weak acids or weak bases

ETOH in stomach - changes dissolution

Nicotine - Lowers plasma enzymes

 - can increase or decrease metabolism

Caffeine - increases stimulation, including gastric motility

Most at room temp

 - cannot handle heat of a car in summer

Some need refridgeration

Some are light sensitive

 - dark-color containers

Air/humidity sensitive

- require tight sealed containers

Factors that affect the drug in oral administration

Rich blood supply in GI tract

Presence of food in stomach

GI motility - can affect whether drug even stays down

Oral cavity - slightly acidic pH

Stomach - highly acidic (pH 1.4)

Upper portion of small intestine - highly alkaline (pH 7-8)

SC (subcutaneous) - into adipose & connective tissue.  Slow absorption

IM (intramuscular) - into skeletal muscle, absorption more rapid than SC (because of blood supply)

IV (intravenous) - directly into blood stream, direct absorption

Must have correct diluents: Water & saline are not interchangeable!

Protective, many drugs can't enter, or are absorbed very slowly.

Heavy in lipid composition

Lungs provide large surface area for absorption, rich capillary network

Nearly instantaneous effect - fast as IV

Drug must reach alveolar level, aerosolized with propellants

Examples:

Inhalants, nebulizers, endotracheal tubes

Local or systemic effect (depending on skin factors)

Only lipid-soluble compounds are absorbed

Precutaneous absorption is erratic:

 - Massaging enhances absorption

 - Heat can increase it

 - "washed" away with sweat or friction

 - dependent on intact capillary system

"fluffy" people - skin is farther from their major vessels than less "fluffy" people.  Topical drugs will not travel well into capillaries because of high amount of adipose tissue surrounding them.

Distribution

(Pharmacokinetic Activities)

• Usually easier than absorption, more rapid
• Depends on permeability of capillaries to the drug molecules, cardiac output, regional blood flow (most of drug is first distributed to major organs, then muscles and fat)

Different triggers, different experiences for each patient. 

Sometimes 1-2 times a month

sometimes on a schedule. 

Giving opiates!

Opiates cause rebound pain

• Recognize triggers for the HA
• Activities
• Foods
• alcohol, red wine, cheese, MSG
• Stress
• Menstrual cycles
• Do something about the triggers
• e.g., migraine "meds" can be contraceptives that interrupt the cycles

• Visual changes (scotoma) or visual loss
• Photophobia, phonophobia
• Nausea
• Odd head sensations
• Smell auras
• Some have TIA-like symptoms (that mimic stroke but resolve within hours)

Taken early

in a combination of NSAID or ASA and caffeine

(Excedrine migraine)

In caffeine-naive patients - can use strong espresso

migraine HA

prophylaxis of migrane

alpha adrenergic blocker

• Nausea
• peripheral vasoconstriction
• uterine stimulation w. decreased placental blood flow (abortive)
• HTN
• Can trigger MI
• Chemically related to LSD, so can change neurological status and induce hallucinations

"triptans"

Sumitriptan

Solmitriptan

Effect: stimulate 5-HT receptors on cranial blood vessels

Action: Cranial vasoconstriction, inhibit inflammatory neuropeptides

Admin: oral, nasal, injectable forms

Megabolism: peak and t 1/2 depend on agent

• Nausea/vomiting
• Weakness, tingling, flushing
• Can precipitate stroke, cerebral hemorrhage, MI
• Pain/pressure in chest, neck throat, jaw
• "heavy arms"
• Dizziness, drowsiness

Major concern: CV symptoms

• Ischemic heart disease, history of MI
• Uncontrolled HTN
• Caution in renal or hepatic dysfunction, CVA
• Don't give within 24 of ergotamine
• Potential toxicity when used with common anti-depressants (SSRI's)
• Serotonin syndrome
• Prozac, paxil, zoloft, etc.
• Most are not allowed more than 6 tabs a month

• Beta blockers and CCB (calcium channel blockers) have efficacy when taken chronically (Prophylactically)
• Keeps vessels dilated so less vasoactive tendencies
• Anti-seziure meds
• Valproic acid / Valproate (Depakote)
• Topiramate (Topomax)
• Prevent the generalized depolarization of the cortex that is associated with migraines
• TCA (tricyclic antidepressants)

• Pharmacologic classification:
  
  • Cholinergic
• Therapeutic classification:
• Urinary tract stimulant

Postoperative (& postpartum) nonobstructive urinary retention

or

Urinary retention caused by neurogenic bladder

• Stimulates cholinergic receptors
• cholinergic agonist
• Effects:
• contraction of urinary bladder
• decreased bladder capacity
• basically, makes you pee ("void")

• Absorption
• poor after oral admin, so dose is larger
• SubQ dose is lower
• Distribution
• does not cross blood-brain barrier
• (Metabolism & Excretion: unknown)

• CNS
• HA (headache), malaise
• Resp
• bronchoconstriction
• CV
• Bradycardia --> hypotension
• cardiac arrest possible
• GI
• increased salivation
• abdominal cramps
• diarrhea
• HCL secretion (-->ulcers)
• GU
• bladder contraction - NEVER USE IN OBSTRUCTED BLADDER!

Contraindicated in:

Mechanical obstruction of GI or GU tract

Caution in:

Asthma, ulcer disease, CV disease, epilepsy

sensitivity to cholinergics

Cholinergic agonist

Parasympathomimetic

"cholinergics"

Anticholinergic

Cholinergic antagonist

parasympatholytics

Adrenergic agonist

"Adrenergics"

Sympathomimetic

Adrenergic antagonist

adrenergic blockers

sympatholytic

Absorption: IV administration

Distribution: wide, throughout body

• Competitively blocks ACh
• Most essential muscles affected the least
• Respiratory paralysis, NOT unconsciousness

• Intubation, ventilator control
• Surgery adjunct (esp. ortho & abdominal)
• Electroconvulsive Tx
• Keeps patient from moving during procedures like ventilation

• Slow return of resp. muscle fxn
• Hypotention
• related to lack of muscular tone
• Causes histamine release
• Potent bronchoconstrictor
• NO CNS effects! - remain awake/conscious

Symptom: prolonged apnea

Tx: AChE inhibitor

• Cannotmove, but can still hear and feel
• still need sedation and pain meds!
• Can't breathe independently
• need ventilator
• High risk for skin breakdown
• Patients try to move to "shake it away"
• doesn't hasten reversal
• increases risk of joint injury
• Face has tendency to recover faster

Decrease metabolic rate

Decrease O₂ consumption

Measures "twitching" response during NM block dosing

• 4 electronic stimuli to thumb:
• if no response, too much on board
• if 1-2 twitches, dose OK
• if 4 twitches, need more medication!

So you can know "how paralyzed" a patient is

Train of Four (TOF)

4 elec. stimuli to thumb

Epinephrine

Stimulates all types of sympatethic receptors.

Adrenergic (agonist)

Stimulates all types of sympathetic (adrenergic) receptors

Fast metabolism

Effect is mostly local

Doesn't cross blood-brain barrier

Rapid metabolism with enzymes in blood stream

(Rapid termination of action and uptake by nerve endings)

Epinephrine: when do we give it

(indications)

• Respiratory: SubQ or MDI for
• acute asthma
• Tx for Anaphylaxis
• EpiPen
• CV to improve BP
• Surgically:
• Local hemostasis
• Anesthetically:
• Localize meds (e.g., lidocaine) to maintain better pain control and homeostasis
• Eye:
• mydriasis

All of those SNS effects

Severe HBP with danger of stroke or CVA

Anxiety & nervousness, muscle tremor, HA

Dysrhythmias, pallor, weakness, N/V

Tachycardia, angina

HSB or other significant CV compromise

Closed angle glaucoma

Diabetes

Caution in pregnancy

What are symptoms of epinephrine toxicity? How would we treat it?

• Symptoms:
• HBP with danger of stroke
• Tachycardia (danger of MI)
• Pulmonary edema
• Tx
• rapid-acting vasodilators (nitroprusside)

• Vasoconstriction
• systemic: Increases BP
• locally: slows systemic absorption
• Pupil dilation
• GI, GU sphincter relaxation
• Uterine contraction
• Stimulate ejaculation
• Increased glycogen breakdown in liver

• Stimulation of heart
• increased HR, conduction, force, automacity
• Kidneys release renin

• Dilation of bronchioles, decreased resp resistance
• Relaxation of uterine smooth muscles
• Dilation of blood vessels in skeletal muscles, brain, and heart
• Increased glycogen breakdown in liver

Sympathetic

It is a catecholamine

Dopamine: what receptors are affected?  Is there a dose response?

In low doses: beta₁

In high doses: alpha

• VERY short half life (2 minutes)
• To have an effect, must be titrated
• Need hemodynamic monitoring
• Alter dose based on parameters
• Too much could cause a stroke

• Too much could cause a stroke
• Infiltration:
• tissue sloughs off down to bone
• should be given via central lin

• Vasoconstriction
• Cardiac stimulation

Same as Norepinephrine

bronchodilation

nasal decongestant

• Not a catecholamine
• Acts by stimulate release of norepinephrine (NE) from nerve cells
• Alpha and beta receptor action

• MAO (Monoamine oxidase) breaks down norpeinephrine (NE) 
• MAOI: Monoamine oxidase inhibitor - prevents breakdown of NE
• soooo: MAOI + ephedrine = intensified side effects

• Can cause MI and CVA due to increased BP
• Spike HTN
• It's in most OTC cold meds, so this can be problematic. 

• Monoamine oxidase inhibitor. 
• inhibits the enzyme monoamine oxidase (duh)

• Antagonizes effects of histamine at receptors
• (Does not bind to or inactivate histamine)
• Anticholinergic properties
• significant CNS depressant

• Decreased symptoms of histamine excess
• relieves sneezing, rhinorrhea, nasal & ocular puritus, ocular tearing/redness, urticaria
• Relieves acute dystonic reactions
• Prevents motion sickness
• Suppresses cough

• Relief of allergic systems caused by histamine release including:
• anaphylaxis
• seasonal/perennial allergic rhinitis
• allergic dermatoses
• Parkinson's disease & dystonic reactions from medications
• Mild nighttime sedation
• prevent motion sickness
• antitussive (syrup only)

• Absorption:
• well absorbed after oral, but first pass metabolism results in only 40-60% drug going into systemic circulation
• IM = well absorbed
• Distribution:
• Widely. Crosses placenta, enters breast milk
• Metabolism & excretion
• 95% metabolized by liver

• Contraindicated in:
• Acute asthma attacks
• hypersensitivity
• lactation
• known alcohol intolerance
• Caution:
• Severe liver disease
• angle-closure glaucoma
• seziure disorders
• peptic ulcers
• may cause paraxoical excitement in children :)
• Appears on Beers List

• CNS
• drowsiness, dizziness, HA, paradoxical excitation (esp in children)
• EENT
• blurred vision, tinnitus
• CV
• hypotension, palpitations
• GI
• anorexia, dry mouth, constipation, nausea
• GU
• dysuria, frequency, urinary retention
• Derm
• photosensitivity
• Resp
• Pain at IM site (if given IM)

Anticholinesterase inhibitor

Ex. neostigmine

• Since AChE (acetylcholinesterase) is an enzyme that breaks down ACh, inhibition of that enzyme will result in more active ACh available at the nerve endings.
• It inhibits AChE by binding with it (and not making it work). 
• Effect = too much ACh

Benzotropine (Cogentin)

trihexyphenidyl (Artane)

It's an MAOI (inhibiting MAO-B) used in parkinson's patients. 

We use it to prolong the effect of L-dopa.

• It irreversibly inhibits MAO-B (irreversibly binding at B-site)
• prevents breakdown of dopamine
• Effect = increased available dopamine in CNS

• Monoamine oxidase 
• MAO A: metabolizes norepinephrine and serotonin
• MAO B: metabolizes dopamine

selegiline prolongs the effect of L-dopa

(by increasing the amt of available dopamine)

• MAJOR Drug-drug interactions
• merperidine (Demerol) & other opioids: fatal reactions
• hyperthermia, rigidity
• Antidepressants (poss. fatal)a
• must discontinue 2-7 wks before 
• Drug-food:
• Tyramine foods
• cheese

• Possible fatal interactions
• MAOI + SSRI (selective serotonin reuptake inhibitors) =
• serotonin syndrome
• MAOI + TCA (tricyclic antidepressant) =
• CV issues, HTN, altered consciousness

• Levodopa (L-dopa)
• We combine it with cardiodopa
• there is synergistic action
• more L-dopa gets into the brain

• L-dopa is a metabolic precursor of dopamine
• converted to dopamine in CNS
• then serves as a NT (neurotransmitter)

• Very little of L-dopa makes it to CNS
• most is metabolized in GI system 
• High doses of L-dopa = toxic
• Carbidopa prevents peripheral destruction of levodopa

• Levodopa + carbidopa = more levodopa makes it to CNS.

Widely distributed.

Enters the CNS (crosses BBB) in small concentration when administered alone.

What parkinson's symptoms are not helped by anti-parkinson meds?

• Constipation
• Stooped posture
• Dementia
• Visual problems
• Bladder issues

It stimulates peripheral conversion/metabolism of L-dopa, which decreases the amt that can cross BBB. 

(however, B6 is important for cardiac health!)

• CNS: involuntary movements (note: after long-term Tx, can get spastic effects like the disease),
• EENT: blurred vision & mydriasis
• GI: N/V (nausea/vomiting)
• Increased melanoma risk

HTN reactions.

Compete with sympathetic NTs (epinephrine & norepinephrine) for adrenergic receptor sites.

They are adrenergic antagonists

• Decreased BP and HR

Adrenergic

(Stimulates alpha-adrenergic receptors)

• As an anesthesia adjunct:
• prolong duration of spinal anesthesia
• localize effect of regional anesthesia
• Management of hypotension assoc. with anesthesia

Tachyarrhythmias (fast & irregular heartrate)

CV: Arrhythmias (can be fatal), chest pain, HTN, vasoconstriction

CNS: HA, dizziness,

Resp: dyspnea

A lipid soluble drug would pass through rapidly because the cell membrane is composed of lipids.

(Water-soluble drugs would pass more slowly)

Movement from the site of entry into the vascular system.

The IV route is the fastest route - results in instantaneous absorption without need to cross membranes

Advantage:

The IV route allows precise control over drug levels in the blood.

Instantaneous effect

Disadvantage:

more difficult and costly, less convenient than other routes

Minimum effective concentration:

The plasma drug level below which therapeutic effects will not occur

The largest effect a drug can produce.

Dosages beyond this will not increase the effect.

True or false:

Under normal circumstances, receptors are regulated by endogenous substances

True

Under normal circumstances, receptor fxn is regulated by molecules supplied by the body. 

Which drug property is most enhanced by the presence of many different types of receptors throughout the body?

• (a) potency
• (b) safety
• (c) selectivity
• (d) convenience

answer: c - selectivity

Since each receptor regulates just a few processes, selective drug action is possible.

Altenolol has a strong attraction to beta receptors.  Which of the following terms best represents this concept?

• (a) affinity
• (b) potency
• (c) efficacy
• (d) selectivity

a - affinity

refers to the strength of attraction between drug & receptor. 

Agonist

An agonist is a molecule that activates receptors

Continuous exposure to antagonists can lead to hypersensitivity.

Continuous expsosure of cells to agonists can lead to desensitization.

What is the best description of the ED₅₀?

• (a) it is the maximal effective dose for 50% of the population
• (b) it is the dose required to produce a therapeutic response in 50% of patients
• (c) describes 50% of the effective dose for most adults
• (d) this is the equivalent dose for 50% effectiveness in most patients

answer: a

it is the dose that is required to produce a defined therapeutic response in 50% of patients.

Which response would you anticipate when giving two drugs that have potentiative effect?

• (a) one drug intensifies the other
• (b) one drug decreases effects of the other
• (c) one drug reduces the adverse effects of another
• (d) the two drugs create a unique and unpredictable response

Answer: a

A potentiative effect occurs when one drug intensifies the effects of the other.

An inhibitory effect would cause reduced therapeutic effects or reduced adverse effects.

Potentiative effects are not "unique" responses

The nurse is preparing to begine giving drug "X" which is known to induce CYP isozymes.  What effect does the nurse expect this to have on drug "Y," which the patient has been taking for several months?

• (a) drug X metabolism will increase
• (b) drug Y metabolism will increase
• (c) drug X blood levels will increase
• (d) drug Y blood levels will increase

correct answer: b

• Since drug "X" induces CYP isozymes, it will therefore increase the metabolism of other drugs. 
• "X" is the inducer, so it will increase the metabolism of "Y." 
• This would likely decrease the blood levels of drug "Y"

The drug you are about to administer induces P-glycoprotein (PGP).  What outcome might be expected when this drug is given with other drugs?

• (a) increased drug levels of other drugs
• (b) increased SE of other drugs
• (c) reduced absorption of other drugs
• (d) decreased drug elimination

Correct answer: c

• Drugs that induce PGP can cause reduced absorption of other drugs, which would decrease their drug levels. 
• A PGP inducer would not increase SE of other drugs and could increase elimination of other drugs

A nurse is concerned with minimizing adverse drug-drug interactions for the patient.  Which type of drug below could result in the most serious consequences from a drug-drug interaction?

• (a) low therapeutic index
• (b) high biologic half-life
• (c) low potency
• (d) first-pass effect

correct answer: a

interactions are especially important for drugs that have a low therapeutic index, since an interaction that produces a modest increase in drug levels can cause toxicity.

It inhibits their metabolism.

This increases the amount of drug available for absorption, which results in an increase in blood levels of the drug.

Which pregnancy category?

Animal studies show no fetal risk, but controlled studies have not been done in women.

Which pregnancy category?

Animal studies do show risk of fetal harm, but controlled studies in women have failed to demonstrate a risk during the first trimester, and there is no evidence of risk in later trimesters.

Category B

("Slightly more risk than A")

Example: some antibiotics (like amoxicillin), ondansetron/Zofran (for nausea), some insulins (for diabetes).

Which prenancy category?

Remote risk of fetal harm.  Controlled studies in women have been done & have failed to demonstrate risk of fetal harm during first trimester and there is no evidence of risk in later trimesters.

Category A. 

Example: levothyroxine (thyroid hormone), folic acid (vitamin)

VERY FEW drugs fall into this category

Category C:

benefits may outweigh risks.

example: albuterol (for asthma), some SSRI's (fluoxetine/Prozac, sertraline/Zoloft). 

MANY drugs fall into this category. 

When treating with acetaminophen, we need to be on lookout for signs of hepatic damage.  What might those be?

nausea, vomiting, diarrhea, abdominal pain

Also, monitor liver enzyme test results

You are caring for a patient with kidney disease.  What impact is this pathophysiology likely to cause with respect to the pt's medication?

• (a) increased drug excretion
• (b) decreased drug levels in blood
• (c) accumulation of drugs in the body
• (d) increased tolerance to the medication

correct answer: C

kidney disease can reduce drug excretion, causing drugs to accumulate in the body.  If dosage is not lowered, the drug may accumulate to toxic levels.

The nurse is caring for a patient who has been taking morphine for pain for about 2 weeks.  The nurse notes that the pt has begun to need increasing dosages of morphine to achieve the same pain relief.  Which term best describes this phenomenon?

• (a) tachyphylaxis
• (b) metabolic tolerance
• (c) placebo effect
• (d) pharmacodynamic tolerance

Correct answer: d

Pharmacodynamic tolerance is the phenomenon of decreased responsivenes to a drug as a result of repeated administration.

(metabolic tolerance results from accelerated drug metabolism, not repeated dosages)

The nurse is caring for a group of female patients receiveing medication therapy.  Which factor below is of greatest concern related to drug therapy in women?

• (a) most drug research has been carried out exclusively in male subjects
• (b) hormonal differences make it more difficult to manage drug therapy in most women
• (c) overall, women tend to be less compliant with medication therapy
• (d) women tend to be caregivers and may not take time to care for themselves

Correct answer: a

We do not know much about gender-related differences because until recently all drug research was done in men.

If a drug lacks proof of teratogenicity, does that mean it is safe to take during pregnancy?

No.

Lack of proof of teratogenicity does not mean drug is safe during pregnancy.

Nearly all drugs cross the placenta. 

Studies show that taking asthma medications (if needed) during pregnancy improves fetal outcomes.

Uncontrolled maternal asthma is more dangerous to the fetus than the drugs used to treat it!

Weeks 3 to 8 (main embryonic period)

Typically, this is before women even realize they are pregnant.

• dose immediately after breastfeeding (minimize drug concentrations in milk @ next feeding)
• avoid drugs with long half-life
• Avoid sustained-release formulations
• choose drugs that tend to be excluded from milk (however there aren't many)
• avoid drugs known to be hazardous
• use lowest effective dosage for shortest possible time

suspected blockage in GU system.

(Also, has some effect on GI system, so obstruction in the GI sys would be another contraindication.)

This drug can also induce bronchospasm, which would be problematic for a pt with a Hx of asthma

which symptom below is most indicative of mucarinic (e.g., bethanecol) poisoning?

• (a) constipation
• (b) tachycardia
• (c) hypertension
• (d) blurred vision

correct answer: d

muscarinic poisinoning can result from O/D of muscarinic agonists (e.g., bethanecol) or cholinesterase inhibitors.

• symptoms include:
• profuse salivation,
• lacrimation,
•  visual disturbances,
• bronchospasm,
• diarrhea,
• bradycardia
• hypotension
  

Neostigmine.

It inhibits cholinesterase and allows accumulation of ACh @ synapses