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Pharmacology 1 > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

Pharmacotherapeutics

A

the use of a drug to diagnose, prevent or treat disease or to prevent pregnancy.

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2
Q

Effectiveness

A

does it cause the response for which it was given

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3
Q

Safety

A

there is no such thing as a safe drug

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4
Q

Selectivity

A

Causes only the response for which it is given

there is no such thing as a selective drug

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5
Q

Reversible action

A

do drugs actions subside after a certain amount of time?

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6
Q

Predictability

A

How does the pt. respond

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7
Q

Components of a drug

A
  1. Prescribed Dose
  2. Administered Dose
  3. Concentration at site of action
  4. Intensity of response
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8
Q

Sources of Individual Variation

A
  • Physiologic variables
  • Pathologic variables
  • Genetic variables
  • Drug interactions
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9
Q

side effects

A

expected

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10
Q

Adverse effects

A

unexpected/uncommon (HGD- he gonna die)

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11
Q

Pharmacokinetics

A

(study of drug movement through the body)

Absorption
Distribution
Metabolism
Excretion

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12
Q

Passage of drugs across membranes

A
  • Channels or pores
  • Transport systems
  • Direct membrane Penetration
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13
Q

Absorption of a drug

A

Movement of a drug from site of administration into the blood

1.Rate of absorption
2.Amount of absorption
3. Factors affecting absorption
o Rate of dissolution
o Surface area
o Blood flow
o Lipid solubility
o pH partitioning

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14
Q

Parenteral Routes of Administration

A

IV, IM, SubQ

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15
Q

Enteral

A

Use of GI Tract

  • oral
  • suppository
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16
Q

Advantages/barriers to IV

A

Fastest route of absorption- no barriers. (faster the onset, faster it wears off)

Advantages: rapid onset, control of level of drug, ability to administer large volumes of fluid

Disadvantages: expensive, inconvenient, cannot take it back, infection, fluid overload, embolism

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17
Q

Advantages/barriers to IM

A

IM- no barriers, easily passes through spaces of capillary wall

  1. Patterns of absorption
    - Rapid or slow (depo)
    - Water solubility of the drug
    - Blood flow to the site of injection

Advantages

  • Good for meds with poor water solubility
  • Used for administration of depo preparations

Disadvantages
-Discomfort, inconvenient, can be painful, infection, nerve damage

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18
Q

Advantages/barriers to SubQ

A

Barriers to absorption
-None easily passes through spaces of capillary wall

Patterns of absorption

  • Rapid or slow
  • Water solubility of the drug
  • Blood flow to the site of injection

Advantages

  • Good for meds with poor water solubility
  • Used for administration of depot preparations

Disadvantages
-Discomfort, inconvenient, can be painful, infection, nerve damage

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19
Q

Advantages/barriers to Oral

A

Advantages
-Easy, convenient, safe

Disadvantages

  • Variability of absorption
  • Requires patient cooperation

** it is not SAFE to give extended release drugs via NG tubes**

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20
Q

Oral Preparations

A

Tablets

enteric-coated, sustained/extended release

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21
Q

Chemical Equivalence

A

generic V brand name

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22
Q

bioavailability

A

rate at which a drug is absorbed into the system; timeframe

the fraction of the administered dose that reaches circulation

IV -100%

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23
Q

Additional Routes of Administration

A

Topical

transdermal: pain patch, birth control patch, topical creams

Sublingual- under the tongue

Inhalation: inhalers/nebulizers

suppository-vaginal/anal

Direct injection into the site of action
( ex. cortisone shots)

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24
Q

Distribution

A

The movement of drugs throughout the body

3 main factors
1. ability to exit the vascular system
        - capillary beds
        -blood brain barrier
( tight junctions, not fully developed in infants)
     - placental drug transfer
   - protein binding
  1. ability to enter the cells
    - some drugs must enter cells to reach their sites of action and most must enter to undergo metabolism or excretion ( lipid solubility; transport system)

3.blood flow to tissues
- 2 pathologic conditions in which low regional blood flow can affect drug therapy
( 1. abcess, 2. tumors)

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25
Q

Metabolism

A

The enzymatic alteration of drug structure

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26
Q

Main site for drug metabolism

A

LIVER

Cytochrome P450 System

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27
Q

Therapeutic Consequences of drug Metabolism

A 
o	Accelerated renal excretion
o	Drug inactivation
o	Increased therapeutic action
o	Activation of prodrugs (changes its chemical body once the metabolism (enzymes like cytochrome) breaks its down)
o	Increased or decreased toxicity

special considerations:
weight
age

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28
Q

First Pass Effect

A

Rapid inactivation of some oral drugs as they pass through the liver after being absorbed

( parenteral administration will bypass this effect)

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29
Q

Drugs and Nutritional Status

A

Adequate nutritional status provides the required cofactors for the hepatic drug metabolizing enzymes to function

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30
Q

Competition between drugs

A

o Two or more drugs that use the same metabolic pathway may cause a decrease in metabolism of one or more

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31
Q

EXCRETION

A

The removal of drugs from the body

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32
Q

renal drug excrection

A
  1. Glomerular Filtration
  2. Passive Tubular Reabsorption
  3. Active Tubular Secretion
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33
Q

Nephrotoxic drugs

A

Can injure the kidneys

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34
Q

Factors that modify renal drug excretion

A
  • pH- dependent Ionization

- competition for active tubular transport

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35
Q

Non-renal routes of excretion

A

breast milk
biles
lungs
sweat/saliva

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36
Q

Plasma drug levels

A

Plasma drug levels are highly predictive of therapeutic and toxic responses

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37
Q

minimum effective concentration (MEC)

A

The minimum plasma drug level at which therapeutic effects will occur (lowest dose to see relief)

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38
Q

Toxic Concentration

A

The level at which toxic effects occur

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39
Q

Therapeutic Range

A
  • Falls between the MEC and toxic concentration

- Enough drug is present to produce a therapeutic response

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40
Q

Narrow Therapeutic Range

A

-Narrow therapeutic range (Drugs we screen labs for, because the range is so narrow)

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41
Q

Drug Half Life

A

¬ The time required for the amount of drug in the body to be decreased by half

42
Q

Plateau

A

~Ideal to achieve~

  • When a steady level of drug has been achieved
  • When the amount of drug eliminated between doses equals the dose administered
43
Q

How do you reduce fluctuations in drug levels

A
  • administer continuous infusion
  • administer a depot preparation

0reduce the size of a dose and the dosing intervals

44
Q

Peak

A

The highest level of drug

45
Q

Trough

A

The lowest level of drug

46
Q

Loading dose

A

used when plateau must be achieved quickly

47
Q

Maintenance dose

A

smaller doses used once plateau is achieved

short dose, over longer periods of time to keep pt in therapeutic range.

48
Q

PHARMACODYNAMICS

A

The relationship between the size of an administered dose and the intensity of the response produced
o The minimum amount of drug needed to elicit a response
o The maximum response a drug can elicit
o How much to increase the dosage to increase the response

49
Q

Maximal efficacy

A

largest effect that a drug can produce

50
Q

Potency

A

o Amount of drug given to elicit an effect
o A potent drug produces its effects at low doses

Two drugs can be equally effective but have different potency***

51
Q

Receptors

A

o Chemical sites in the body that drugs interact with to produce effects – make selective drug action happen

**Drugs either mimic OR block the action of the body’s own regulatory molecules; do NOT give cells new functions

52
Q

affinity

A

Affinity (ability to bind to receptor)

High affinity drugs have a strong attraction for receptor sites
o Drugs with high affinity are very potent
o Drugs with low affinity need to be present in high concentrations to elicit a response

53
Q

Intrinsic activity

A

(bond that MIMICS receptor)

  • Ability of a drug to activate a receptor upon binding
  • Drugs with high intrinsic activity have high maximal efficacy; produce an intense response
54
Q

agonist

A

(MIMICS what the body already does)
¬ Activate receptors; have high affinity and intrinsic activity
¬ Mimic action of endogenous regulators

55
Q

Antagonist

A

(BLOCKS what the body normally does)
¬ Prevent receptor activity
o Have high affinity but no intrinsic activity
o Bind to receptors but do not cause receptor activation
o Block actions of endogenous regulatory molecules or drugs
♣ Response to an antagonist is determined by how much agonist is present

56
Q

Desensitization

A

¬ (Refractoriness) results from continuous exposure of cell receptors to an agonist
o The cell is less responsive
(May need to increase the dose, you can become desensitized to the benefits from the drug, but not desensitized to the adverse effects)

57
Q

Hypersensitivity

A

¬ results from continuous exposure of cell receptors to antagonist
o The cell is hypersensitive
(Profound response due to an influx of receptor sites (hypersensitivity) do to continuous exposure)

58
Q

Average effective dose (ED50)

A

o Dose required to produce a defined therapeutic response in 50% on the population.

59
Q

Therapeutic Index (ED50:LD50)

A

o Ratio between average effective dose and average lethal dose
¬ Wide therapeutic index is relatively safe
¬ Narrow therapeutic index is relatively unsafe

60
Q

Drug-drug Interactions

A

Three ways drugs interact

  1. One drug intensifies the effects of the other
  2. One drug reduces the effects of the other
  3. The combination produces a new response not seen with either drug alone
61
Q

Intensification Effects

A

AKA: (Potentiative) Effects
o Increased therapeutic effects
o Increased adverse effects

62
Q

Reduction effects

A

AKA: (Inhibitory) Effects
o Reduced therapeutic effects
o Reduced adverse effects

63
Q

Mechanism of Drug-drug Interactions

A

Pharmacodynamic Interactions
o Drugs act at the same site
o Drugs act at separate sites

64
Q

Combined toxity

A

The more drugs a patient receives the greater the chance there will be an interaction.

65
Q

Drug-food interactions

A
  • Food and drugs may interact to alter the effect of pharmacotherapy.
  • Decreased absorption
  • Increased absorption
  • Risk for toxicity may increase with drug food interactions
  • Drug action may be decreased
66
Q

Timing in respect to meals

A

Administer on an empty stomach or with food

-empty = 1-2 hrs after eating

with food= with or shortly after

67
Q

Grapefruit effect

A

grapefruit inhibits an isoenzyme responsible for intestinal metabolism of multiple drugs

  • the inhibitory effect is dependent on the mount f juice consumed and can persist up to 3 days

Increases amount of drug available for absorption which increases the blood level of drugs

patient teaching point

68
Q

Drug-herb interactions

A

Drug interactions may also result from herbal supplements interacting with drugs

  • they can impact therapeutic outcome of prescribed agents
  • increased toxicity
  • reduced therapeutic outcomes
69
Q

Adverse drug reactions

A

Adverse effect of drug therapy (NOT EXPECTED)

o An effect other than the desired therapeutic effect that may occur during drug therapy.

70
Q

side effect

A 
Side effect (often MINOR, EXPECTED) 
o	Usually refers to a minor effect, such as nausea, nearly unavoidable secondary drug effect produced at therapeutic dosing.
71
Q

Toxicity

A

Severe

-caused by excessive dosign

72
Q

Allergic reactions

A

immune response

  • must have had a prior sensitization
  • Allergic reactions are not determined by the size of the dose but by the degree of sensitization
73
Q

Anaphylaxis

A

¬ Anaphylaxis is the most serious of allergic reactions…it is a medical emergency
o A systemic reaction
♣ contraction of smooth muscles…airway closes
♣ increased vascular permeability…swelling
o So it looks like this…
♣ dyspnea, bronchospasm, laryngeal edema, cardiac dysrhythmias, and occasionally seizures.

74
Q

Idiosyncratic drug response

A

o Unusual, abnormal or peculiar response to a drug
o Idiosyncratic responses are thought to occur because of genetic enzymatic deficiencies that alter the drug’s metabolism

75
Q

Paradoxical response

A

(could happen once or could happen again)

o Opposite of an intended drug response

76
Q

Iatrogenic Disease

A

(drugs and their side effects start to mimic other disease processes)

o A disease that occurs as a result of medical care or treatment
o Can be the result of drugs

77
Q

Drug Toxicity

A

Toxicity results when the dosage of drug or drugs exceeds the amount the body can eliminate through metabolism and excretion

78
Q

Physical dependence

A

o A state in which the body has adapted to prolonged drug exposure in such a way that abstinence syndrome will result if drug use is discontinued

79
Q

Abstinence Syndrome

A

Withdraw-
varies depending on drug

  • Patient teaching point*
80
Q

Carcinogenic effect

A

o Ability of certain medications and environmental chemicals to cause cancer

81
Q

Teratogenic Effect

A

Drug induced birth defects

82
Q

Neuro Toxity

A

The brain is sensitive to small amounts of toxic substances
¬ Neurotoxicity can occur after exposure to drugs and other chemicals and gases.
¬ Signs and symptoms of neurotoxicity
o changes in level of consciousness (drowsiness, restlessness)
o auditory and visual disturbances, nystagmus
o tonic-clonic (grand mal) seizures

83
Q

Hepatotoxicity

A

Liver is the primary site of drug metabolism
-The liver is highly susceptible to toxicants due to direct exposure to ingested drugs and other toxicants

S/S of hepatotoxicity 
o	Hepatitis
o	Jaundice
o	Elevated liver enzymes [laboratory values]
o	Fatty infiltration of the liver.
84
Q

Nephrotoxicity

A

High susceptibility due to high vascularity

-Chemically induced kidney damage is typically manifested as acute tubular necrosis
-Laboratory Values to assess
o Blood urea nitrogen (BUN)
o Creatinine
o Creatinine clearance

85
Q

Immunotoxicity

A
  • A wide variety of drugs can affect the immune system.
  • Some may cause immunosuppression (decrease ability to fight infection),
  • whereas others may directly destroy immune system components (i.e.leukocytes).
86
Q

Cardiotoxicity

A
  • Irregularities in cardiac rhythms and conduction and possibly heart damage may result from an adverse effect known as cardiotoxicity.
  • Cause unknown
  • Characteristics of cardiotoxicity include transient cardiac arrhythmias and depression of myocardial function
  • Prolonged QT interval
87
Q

Ototoxicity

A

-Many drugs can produce ototoxicity, which affects the eighth cranial nerve and result is inner ear or auditory nerve damage.

  • Structures of the inner ear that may be affected include the cochlea, vestibule and semicircular canals.
  • Ototoxicity may or may not be reversible.
88
Q

Variations in drug reponse

A

1 Pathophysiology

  • renal disease affects secretions
    -liver disease affects metabolism
    MUST Adjust dosage for both
#2 Body surface area is more precise than body weight
o	Percentage of body fat can change drug distribution
#4 Gender related differences 
(most research previously performed on men )
  • acid base imbalances
  • altered electrolytes ( ie. digoxin toxicity)
89
Q

Tolerance

A

-Decreased responsiveness to a drug as a result of repeated drug administration

-Patients who are tolerant to a drug require higher doses to produce the same effects that were achievable with lower doses before tolerance had developed
(increase dose/concentration, increase frequency)

90
Q

Metabolic tolerance

A

-Related to accelerated drug metabolism

-Certain drugs can induce synthesis of drug metabolizing enzymes causing increased metabolism of other drugs
(drug-drug interactions)

91
Q

Tachyphylaxis

A

-A form of tolerance where the reduction in drug responsiveness is brought on by repeating dosing over a short time (within hours) instead of days to weeks

(loading dose, giving a large amount in a short period of time)

92
Q

Placebo Effect

A

-Caused by psychological factors not chemical properties of the drug (illegal)

93
Q

Variability in Absorption

A

BIOAVALABILITY

o The amount of active drug that reaches the systemic circulation from its site of administration
o Different forms of the same drug can vary in bioavailability
o Primarily occur in oral preparations
o Highest concern in drugs with narrow therapeutic range

94
Q

Genetics

A

play a role in drug metabolism etc. etc. etc.

95
Q

Diet

A

-Malnutrition

o Lower amounts of plasma proteins (albumin) causing levels of free drug to rise – more intense effects, possible toxicity
o Decreased oxidative metabolism & decreased glomerular filtration rate

  • Intake of Vitamins
  • Urinary pH
  • Timing of meals
96
Q

Drug therapy during pregnancy

A

¬ Err on the side of caution, any drug taken during pregnancy will reach the fetus
¬ Physiologic Changes during pregnancy can alter pharmacokinetics of drugs
o Renal
o Liver
o Gastrointestinal
¬ Placental drug transfer

97
Q

Pregnancy Catagories

A

¥ Based on research for risks posed to the fetus (teratogenic effects)
¥ Category A and B (remote risk) –lowest chance of adverse effect
¥ Category D (proven risk)
¥ Category X (proven risk)

98
Q

Geriatric population

A 
¬	Challenges of drug therapy in older adults
o	Pharmacokinetic changes
o	Multiple and severe illnesses
o	Multidrug therapy
o	Poor adherence
¬	Pharmacokinetic changes in older adults
o	Absorption
o	Distribution
♣	Increased percent of body fat
♣	Decreased percent of lean body mass
♣	Decreased total body water
♣	Reduced concentration of serum albumin
¬	Metabolism
¬	Excretion
o	Creatinine clearance rather than serum creatinine is a better indicator in older adults of renal function

¬ Monitoring and preventing adverse drug reactions and drug-drug interactions
¬ Promote adherence

99
Q

Environmental influences

A 
¬	Assessment of the Home
o	Patient’s ability for self-care
o	Family support
o	Risk factors
o	Financial, Transportation Issues
¬	Drug Storage 
o	Stability
o	Proper disposal
100
Q

Harris-Kefauver Amendment

A

¬ This act was in response to the Thalidomide tragedy in Europe
o Pregnant women took thalidomide as a sedative and infants were born with malformations of arms and legs
o Think…could these women have done without a sedative was it medically necessary???
¬ Drugs had to be proved effective before marketing
¬ Prove the drugs offered some benefit

101
Q

Controlled Substances Act

A

o Regulation of drugs with the potential for abuse
o Scheduling of narcotics I - V
o Schedule I absolute highest abuse potential and no medical use-heroine
o Schedule II – V have accepted medical uses but potential for abuse with schedule II having the highest abuse potential and V the least
♣ Schedule II opioids (Morphine, Hydrocodone)
Schedule 1- never prescribed
Schedule 2- one-time script
Schedule 3, 4, 5- refillable

Pharmacology 1 (4 decks)

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