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NUR370 Pathophysiology and Pharmacology > Intro to Pharmacotherapeutics > Flashcards

Intro to Pharmacotherapeutics Flashcards

1
Q

Nursing responsibilities regarding drugs

A

a. provide maximum benefit with minimum harm
b. anticipate and respond to drug responses
c. patient’s advocate (and education)
d. last line of defense against medication errors

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2
Q

Patient Care Applications

A

a. pre-administration assessment (i.e. allergies, toxic effects)
b. dosage and administration
c. evaluate/promote therapeutic effects (i.e. non-pharm strategies alongside meds)
d. minimizing side effects
e. minimizing adverse drug interactions
f. making prn decisions
g. managing toxicities

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3
Q

Patient Education Applications

A

a. drug name and therapeutic category
b. dose, schedule, route, duration
c. how to store drug
d. expected therapeutic response and onset
e. non-drug measures to enhance response
f. side effects, symptoms and how to manage
g. drug and food interactions

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4
Q

pharmacology

A

study of drugs and their interaction with living systems

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5
Q

clinical pharmacology

A

study of drugs in humans

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6
Q

pharmacotherapeutics

A

use of drugs to diagnose, prevent or treat disease or prevent pregnancy
the medical use of drugs

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7
Q

Properties of an ideal drug

A

a. effectiveness: demonstrated in clinical trials
b. safety: all drugs can produce toxic effects
c. selectivity: elicit only the intended response (no drug is 100% selective, all have potential side effects)

d. reversible action
e. predictability
f. ease of administration
g. freedom from drug interactions
h. low cost
i. stability

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8
Q

Intensity of drug response is determined by

A
  1. Administration - route, dose
  2. Pharmacokinetics (PK) - what the body does to drug
  3. Pharmacodrynamics (PD) - what the drug does to body
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9
Q

Phamacokinetics (what body does)

A

ADME

absorption (GI tract, IV, IM, subcu)
distribution
metabolism (liver)
excretion (kidneys)

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10
Q

3 ways for drugs to cross cell membrane

A
  1. Direct penetration - drug must have some degree of lipid solubility
  2. Channels and pores
  3. Transport systems - may or may not use ATP energy
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11
Q

Absorption

A

= movement from site of administration into blood
= rate of absorption determines onset of effects
= amount absorbed determines intensity of effect

(bioavailability)

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12
Q

Bioavailability

A

amount of drug reaching systemic circulation from site of administration

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13
Q

Factors that affect drug absorption

A

a. rate of dissolution (how fast it can dissolve to cross membrane)
b. surface area
c. blood flow (i.e. to gut)
d. lipid solubility
e. pH effects (neutral state > charged molecules)

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14
Q

Intravenous administration

A

= drug reaches systemic circulation instantly and completely, no absorption

Advantages:

  • rapid onset
  • irritant drugs can be given
  • large fluid volumes can be used
  • control

Disadvantages:

  • not reversible (antidote)
  • infection
  • high cost, inconvenient
  • fluid overload
  • embolism
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15
Q

Intramuscular/Subcutaneous administration

A

= no significant barriers to absorption
= absorption pattern determined by drug solubility in water and blood flow

Advantages:

  • used for poorly soluble drugs (prolonged or delayed effect, sustained exposure)
  • depot preparations

Disadvantages:

  • discomfort
  • inconvenient
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16
Q

Oral administration

A

Barriers to absorption

  • epithelial cells lining GI tract
  • most drugs pass freely through capillary wall

Absorption pattern determined by:

  • solubility and stability of drug
  • gastric and intestinal pH
  • gastric emptying
  • presence of food
  • co-administration of other drugs
  • coatings on drug

Advantages:

  • easy, convenient, many dosage forms
  • inexpensive and safe

Disadvantages:

  • variability
  • inactivation (first pass effect)
  • patient requirements (swallowing)
  • local irritation (upset stomach)
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17
Q

First Pass Effect (pharmacokinetics)

A

= drugs absorbed from GI tract are carried directly to liver, “first pass through liver”
= liver metabolizes drug, large amount may be inactivated and thus reducing therapeutic effects
= a determinant of oral bioavailability

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18
Q

Other routes of drug administration

A

a. topical
b. transdermal
c. sublingual
d. inhalational
e. vaginal
f. rectal
g. direct site injection

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19
Q

Distribution

A

= movement of drugs throughout the body
= factors affecting distribution: blood flow to tissue, drugs exit vasculature, ability of drug to enter cells (lipid solubility and transport systems)

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20
Q

Blood-brain barrier

A

the blood-brain barrier is unique in that it has tight junctions

  • if it is lipid soluble, it can penetrate the cell membrane
  • if it is ionized or polar, it may enter using existing transport systems
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21
Q

Protein binding of drugs

A

= albumin is a main protein for drugs to bound to

= when drugs bind to albumin, it cannot easily exit vasculature, only free drugs exit

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22
Q

Metabolism

A

= the enzymatic alteration of drug structure, aka biotransformation

= drug metabolism leads to drug inactivation, activation, increased therapeutic action or increased toxicity
= mostly occurs in liver

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23
Q

Cytochrome P450 (CYP450) enzymes

A

= family of hepatic enzymes
= expression can be induced or inhibited by drugs, infections, foods, alcohol, smoking, genetic polymorphism

basis for many drug drug interactions

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24
Q

Prodrug

A

= a compound which is administered in a pharmacologically inactive form and undergoes metabolic conversion to an active form
= usually done to improve bioavailability of a poorly absorbed drug

i.e. valacyclovir is a prodrug of acyclovir

25
Q

Excretion

A

= the removal of drugs from the body
= biliary (liver) or urinary (kidney)
= occurs via urine, bile, sweat, saliva, expired air or breast milk

26
Q

Renal drug excretion

A

a. glomerular filtration
b. passive tubular reabsorption
c. active tubular secretion

*renal dysfunction can increase drug effects and duration, influences decision on what drugs are safe

27
Q

Minimum Effective Concentration (MEC)

A

the plasma drug level below which therapeutic effects will not occur

28
Q

Toxic concentration

A

the plasma level at which toxic effects begin to appear

29
Q

Therapeutic range

A

plasma level at which therapeutic effects occur without any toxic effects

30
Q

Half-life (t1/2)

A

= time required for the amount of drug in the body to decrease by 50%
= drug dosing interval depends on t1/2

= half life is usually a constant but may be influenced by patient-specific factors such as renal function and genetics
= applies to most but not all drugs

31
Q

Plateau phase

A

= a steady state phase, usually takes 4-5 half life’s to reach this plateau, prevents fluctuation of concentration

32
Q

Loading dose

A

large initial dose to reach the therapeutic range more quickly
quickly produces drug level equivalent to plateau

33
Q

Maintenance dose

A

a smaller dose given to remain in the plateau stage once it is reached

34
Q

Dose-response relationship

A

= the higher the drug concentration, the greater the response
= at a certain point, the response maxes out, more will not produce more therapeutic effect, but maybe more side effects

35
Q

Efficacy

A

some drugs will never reach the same maximal efficacy no matter how much is given
determined by how well drugs bind to receptors

36
Q

Potency

A

amount of drug needed to reach the same level of maximal efficacy

37
Q

Drug-Receptor Interactions

A

D+R&raquo_space; DR complex&raquo_space; Response

= receptor activity is regulated by endogenous molecules
= drugs either mimic or block actions of endogenous molecules

38
Q

Agonist

A

drugs that mimic the body’s own regulatory molecules

i.e. insulin, dobutamine

39
Q

Antagonist

A

drugs that block the actions of endogenous regulators

i.e. antihistamines, naloxone

40
Q

Receptor affinity

A

strength of attraction between drug and receptor

- reflected in drug potency

41
Q

Intrinsic activity

A

ability of drug to activate the receptor when bound

- reflected in maximal efficacy

42
Q

Therapeutic Index (TI)

A

measure of drug safety: TI = LD50/ED50

LD50: dose that is expected to be lethal to 50% of a population
ED50: dose required to produce a defined therapeutic response in 50% of a population

larger TI = safer drug

43
Q

Drug drug interaction

A

an interaction where the effectiveness or toxicity of one or more drugs is altered

44
Q

Consequences of DDI

A

a. intensified effects (therapeutic or side effects)
b. reduced effects (therapeutic or side effects
c. unique effects

45
Q

Mechanism of DDI

A

a. direct chemical or physical interactions (most common when combining drugs in solution)
b. pharmacokinetic interactions
c. pharmacodynamic interactions

46
Q

PK Interactions: Absorption

A

usually results in decreased drug absorption

i.e. calcium binds tetracycline&raquo_space; decreased absorption
laxatives increase gut motility&raquo_space; decrease absorption

47
Q

PK Interactions: Metabolism

A

most important and complex source of DI
enzyme induction vs inhibition
- certain drugs can change the induction and inhibition of enzymes, which change its ability to metabolize another drug

48
Q

Common CYP450 Inducers

A 
Barbiturates
Rifampin
Carbamazepine
Phenytoin
Corticosteroids
49
Q

Common CYP450 Inhibitors

A 
Macrolide antibiotics
Paroxetine
Fluoxetine
Fluroquinolone antibiotics
Azole antifungals
Grapefruit
50
Q

PK Interactions: Excretion

A

interactions may affect drug filtration, secretion or reabsorption by kidney tubules

i.e. diuretics - reduce reabsorption by kidney tubules

51
Q

Pharmacodynamic Interactions

A

occurs when two drugs act on same receptors or physiologic systems
occurs when drugs with additive or antagonistic effects are combined

  • antagonistic effects (antidotes, naloxone for narcotic OD)
  • additive therapeutic effects (antihypertensive drug combinations, cancer chemotherapy, aspirin and warfarin)
  • additive side effects (antihistamine and CNS depressant&raquo_space; increased sedation)
  • indirect effects (diuretics&raquo_space; decreased K+&raquo_space; increased digoxin effect)
52
Q

DDI: Clinical Significance

A

= not all DIs are clinically significant or cause adverse effects
= DIs may be prescribed and may be desirable for their beneficial effects
= most clinically significant DIs occur for drugs with narrow TI

53
Q

Common Narrow TI Drugs

A 
digoxin (Lanoxin)
phenytoin (Dilantin)
theophylline (TheoDur)
warfarin (Coumadin)
cimetidine (Tagamet)
cyclosporine (Neoral)
tacrolimus (Prograf, Advagraf)
lithium (Carbolith)
carbamazepine (Tegretol)
54
Q

Drug-Food Interactions

A

= food may increase, decrease or have no effect on drug absorption
= may alter bioavailability of a drug from a modified release dosage form

i.e. grapefruit juice

55
Q

Adverse Drug Reaction (ADR)

A

a noxious, unintended, undesired effect that occurs at normal drug doses

a. side effect - secondary drug effect occurring at normal doses
b. idiosyncratic reaction - uncommon drug response due to genetic predisposition
c. allergic reaction - due to an immune response, independent of dose (less than 10% of ADRs are allergies!)

56
Q

Adverse drug event

A

injury resulting from use of a drug

includes ADRs, medication errors and overdoses

57
Q

Identifying an ADR

A
  • did symptoms start soon after drug first given?
  • did symptoms stop when drug discontinued?
  • did symptoms reappear when drug re-challenged?
  • is there another explanation for the symptoms? (underlying condition, DDI)
58
Q

Nurse’s Role in identifying and preventing ADRs

A

a. be familiar with most common ADRs before administering
b. suspect ADR with a change in patient condition not associated with therapeutic response
c. medication history is valuable! distinguish allergy from intolerance
d. monitor relevant changes (liver FTs, serum creatinine, CBC)

NUR370 Pathophysiology and Pharmacology (20 decks)

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