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NURS 1650 - Here We Go Again > Intro to Pharmacology > Flashcards

Intro to Pharmacology Flashcards

1
Q

Drug

A

Any chemical compound that can influence living processes

*Includes those that have therapeutic application and those that do not

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2
Q

Compare and contrast generic drugs and brand drugs

A

Inactive ingredients are different
3.5% difference in absorption

Same active ingredients, strength, dosage form, and route of administration
Same bioequivalence

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3
Q

Pharmacology

A

Study of drugs and their interaction with living systems

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4
Q

Pharmacokinetics

A

The study of drug movement throughout the body: “what the body does to the drug” //how medications move around in the body

4 basic processes:
Absorption
Distribution
Metabolism
Excretion

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5
Q

Pharmacodynamics

A

Study of biochemical and physiolgical effects of drugs and the molecular mechanisms by which those effects are produced

“What drugs do to the body and how they do it”

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6
Q

Clinical Pharmacology

A

The study of drugs in human beings

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7
Q

Pharmacotherapy

A

The use of drugs to diagnose, cure, prevent, or treat a disease/condition

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8
Q

What is the difference between therapeutics and pharmacotherapy?

A

Therapeutics is a broader term that includes other modalities besides drugs
(example: behavioral therapy, physical therapy, speech therapy, etc)

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9
Q

What are some characteristics of an ideal drug?

A

Effective - useful in clinical practice
Safe - has no ability to cause injury
Selective - elicits only the anticipated response

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10
Q

Adverse Drug Reaction (ADE)

A

Any undesirable effect caused by the usage or misuse of a drug with a patient
May be preventable or non-preventable
Side effects, interactions, ADE

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11
Q

Medication Error

A

Can occur at any point along the medication management cycle, or drug-use process by the consumer
Preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in control of the healthcare professional, patient, or consumer

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12
Q

Where in the medication management cycle do medication errors occur the most?

A

During administration

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13
Q

What are the most common student errors?

A

Extra dose
Dose omission
Wrong time
Wrong dose/overdosage
Wrong patient

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14
Q

What is medication reconciliation?

A

Process of comparing the medications a patient is taking and should be taking with newly ordered medications to identify and resolve discrepancies.

Includes Rx, ITC, herbal/supplemental medications in med rec

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15
Q

What is patient adherence?

A

The extent to which a person’s behavior corresponds with agreed recommendations from a healthcare provider

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16
Q

What is an enteric-coated drug?

A

The coating is designed so that the drug dissolves in the small intestine, not the stomach

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17
Q

What are sustained-release or extended release drugs?

A

A drug that is designed so that it dissolves at variable times –> drug is released steadily throughout the day

Permits once-daily or twice-daily dosing

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18
Q

When a person is allergic to a medication, which part are they usually allergic to?

A

The active ingredient

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19
Q

What is an off-label indication?

A

Refers to when a drug is used for other reasons than its FDA-approved indication

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20
Q

What is an issue with generic vs. brand drug’s bioequivalence?

A

They are supposed to prove bioequivelance, but it is not always 100%

This means that a patient may not respond the same to a generic drug (not as effective, different ADEs, etc.)

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21
Q

What are the factors that determine individual responses to drugs?

A

Administration
Pharmacokinetics
Pharmacodynamics

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22
Q

Is medication use in humans risk-free?

A

NO - we must always do a risk-benefit calculation when it comes to prescribing medications.

Desired outcome: Benefit > Risk

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23
Q

How does a patient “owning their disease” relate to their adherence?

A

It helps them become motivated to take their medications or other forms of therapeutics to better themselves in relation to their disease.

This is done in addition to education

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24
Q

What drugs use units as a unit of measurement?

A

Insulin and heparin

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25
Q

What is the difference between a solution and a suspension?

A

A solution has everything mixed in even distribution

A suspension contains particles

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26
Q

What is the main ingredient in an emulsion?

A

Oil

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27
Q

Enteral - Route of Administration

A

Via the GI tract

Oral (PO), enteral feeding tube

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28
Q

Parenteral - Route of Administration

A

Outside the GI tract, often via injection

IV, SQ, IM, intra-dermal, intra-arterial, epidural,

Transdermal (some say this is its own category) ex: patch –> skin absorption

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29
Q

Topical - Route of Administration

A

Applied to the body surface, skin, or mucus membrane, local action

Skin, eye, ear, nose, lungs, vagina

Does NOT mean there is no systemic absorption!
Ex: inhalers has some systemic absorption

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30
Q

Sublingual or buccal - Route of Administration

A

SL = under tongue, buccal = between the cheeks

Largely bypasses the GI system and is rapidly absorbed into the bloodstream

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31
Q

What happens if you crush a sustained-release or extended-release medication and administer it via a feeding tube?

A

Will result in a large dose of the medication being rapidly absorbed, potentially harming the patient

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32
Q

What does ADME stand for?

A

Administration
Distribution
Metabolism
Excretion

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33
Q

ADME Summary/Steps Description

A

Drugs have to cross biological membranes to

  1. be ABSORBED from the site of administration into the blood
  2. DISTRIBUTE/move from the blood to the site of action
  3. be METABOLIZED
  4. leave the body by EXCRETION
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34
Q

How do drugs move through membranes?

A

Transcellular! Meaning they move through it rather than between

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35
Q

What are the 3 methods drugs use to pass through cell membranes?

A
  1. Through channels/pores
  2. Via transporter systems (mainly proteins)
  3. Direct penetration
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36
Q

Do most drugs move through channels and pores?

A

No bc the channels/pores are too tiny!

They are specific for particular molecules (ex. Na/K channels

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37
Q

What are transporters? (Pharmacokinetics - Administration)

A

Proteins that move molecules from one side of the cell membrane to the other

They transport specific biological molecules

Can be selective and will transport only certain drugs

Can also transport drugs to sites of action or sites of metabolism and excretion

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38
Q

What are P-glycoproteins?

A

Transporters that move drugs out cells

This is an ATP-dependent process

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39
Q

Describe how P-glycoproteins transport drugs out of the liver, kidney, placenta and the brain.

A

Liver: transport drugs into bile for elimination

Kidney: transport drugs into the urine

Placenta: transports drugs back to the maternal bloodstream, limiting fetal drug exposure

Brain: transports drugs into blood, limiting drug access to the brain

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40
Q

How can P-glycoproteins be a source of drug-drug interactions?

A

Related to how they transport drugs out of the intestine:

They transport drugs back into the intestinal lumen, out of circulation –> leading to decreased absorption / ready for excretion

Therefore, if P-glycoproteins are inhibited (by another drug), there will be an increase in absorption of a drug since it will not be transported out of the circulation.

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41
Q

What are the 3 requirements needed for a drug to cross membranes by direct penetration?

A
  • Lipid solubility (lipophilicity/lipophilic)
  • Non-polar molecule
  • Small size
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42
Q

What characteristics result in no membrane penetration or poor membrane penetration?

A

Polar molecules

Ions (pos/neg electrical charge, weak acid/base ionized)

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43
Q

Absorption - Pharmacokinetics

A

The movement of a drug from the site of its administration into the bloodstream

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44
Q

Factors that affect absorption: Drug dissolution

A

Drug has to dissolve before it can be absorbed

Rate of dissolution helps determine the rate of absorption

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45
Q

Factors that affect absorption: absorptive surface area

A

microvilli of the small intestine provides greater surface area than the stomach

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46
Q

Factors that affect absorption: Blood flow at the absorptive site

A

higher absorption when blood flow is higher

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47
Q

Factors that affect absorption: Membrane penetration of the drug

A

lipophilic drugs are absorbed more quickly than polar drugs

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48
Q

What is enterohepatic cycling?

A

When a drug moves repeatedly from the liver to the duodenum and back to the liver again

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49
Q

What organ do all drugs absorbed from the GI tract have to pass?

A

The liver via the portal vein, on their way to the heart and then the general circulation

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50
Q

What is bioavailability?

A

The extent to which the administered drug becomes available in the general circulation

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51
Q

Barriers to absorption: Epithelial lining of the GI tract

A

Tight junctions make it difficult for dugs to be absorbed

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52
Q

Barriers to absorption: Capillary wall

A

Due to gaps between capillary endothelial cells, polar, ionized, and lipid-soluble drugs can all pass between these gaps, in and out of the bloodstream

BUT ONLY lipid-soluble drugs can also pass directly through the cells of the capillary wall.

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53
Q

Distribution - Pharmacokinetics

A

Movement of a drug, following absorption, from the bloodstream to other body tissues

“getting to where it needs to go”

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54
Q

What 3 main factors affect distribution? - Pharmacokinetics

A

Blood flow to tissues

The ability of a drug to exit the vasculature

The ability of a drug to enter cells (if the drug’s site of action is intracellular)

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55
Q

How does blood flow to tissues affect distribution?

A

-Tumors have their own blood flow
- Abscesses have a capsule around the infection which has low blood flow
- Certain tissues have low blood flow (external ear)

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56
Q

What factors affect a drug’s ability to exit the vasculature? - Distribution

A
  • Lipophilicity (if lipophilic –> direct penetration)
  • Plasma protein binding
  • Tissue permeability: blood-brain-barrier, placenta
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57
Q

How does the ability of a drug to enter cells affect distribution?

A
  • Lipophilicity
  • Degree of ionization
  • Transporter proteins
58
Q

Explain how the blood-brain barrier affects the distribution of drugs.

A

Makes the delivery of drugs to the brain more challenging

BBB has P-glycoproteins

Tight junctions in brain capillaries prevent drugs from passing between cells to exit the vasculature meaning drugs must pass directly through cells of capillary walls. They must be:
- Lipophilic
- Be able to use an existing transport system present in the brain

59
Q

Explain how the distribution of drugs in the placenta - exit from the vasculature

A

To enter the fetal circulation, drugs must cross both maternal & fetal vascular systems

Placenta has P-glycoproteins

Does NOT constitute an absolute barrier to the passage of drugs
- Lipophilic drugs easily pass through into fetal circulation (ex. EtOH/alcohol)
- Ion, polar molecules, and protein-bound drugs largely prevented from reaching the fetal circulation

60
Q

Which drugs can leave the vasculature and exert a biochemical effect? - Distribution: plasma protein binding

A

Only FREE UN-bound drugs can leave the vasculature and exert a biochemical effect

Albumin is too large to leave, so bound drugs (to albumin) cannot leave, not exert a biochemical effect

61
Q

What comorbidities can affect plasma-protein binding? How?

A

Kidney disease
- Release of proteins in urine results in loss of albumin

Liver disease
- Liver makes the albumin, but won’t make enough when diseased

Catabolic states/cachexia
- Muscle wasting wastes protein state

62
Q

How do bound fractions affect the effect of a drug? - Distribution: plasma-protein binding

A

If a drug is 90% bound, only 10% exerts an effect

63
Q

How is albumin binding a source of drug interactions?

A

Competition for albumin binding

64
Q

If Drug A is 99% normally protein bound, what percentage of Drug A is able to exert a clinical effect?

A

1% effective dose

65
Q

If Drug B competes with Drug A for albumin binding sites and reduces Drug A’s protein bound to 98%, what has happened to Drug A’s effective dose?

A

It has increased (doubled)

Increased risk of ADE

66
Q

What is metabolism?

A

Transformation of a drug’s chemical structure by enzymatic reactions

67
Q

Where does metabolism occur?

A

Most often in the liver

But also: small intestine, lungs, kidneys, skin, placenta, plasma

68
Q

What is the major effect metabolism does to a drug?

A

It makes the drug become more polar/water-solube, which increases its excretion via the kidneys

Lipophilic –> Hydrophilic

69
Q

What is a phase I reaction? - Metabolism

A

Makes the drug more polar by introducing or uncovering a functional group

ex. -OH, -NH2, -SH

70
Q

What is a phase II reaction? - Metabolism

A

It comebines an endogenous substrate with the drug’s functional group to form a more polar conjugate/combination

71
Q

What is a metabolite?

A

Chemical product of metabolism

Different from the parent drug

72
Q

What is a prodrug?

A

A drug in which the parent is inactive and the metabolite is active

Activated after metabolism

73
Q

What is the enzyme family involved in phase I reactions?

A

CYP enzyme family

74
Q

Which enzyme family is involved in phase II reactions?

A

UGT enzyme family

75
Q

What is the first-pass effect?

A

The removal of a substantial amount of an enterally administered drug dose prior to it reaching the systemic circulation

Affects bioavailability

76
Q

How does age affect drug metabolism?

A

Both infants and older adults have decreased ability to metabolize drugs

77
Q

How does a person’s nutritional status affect drug metabolism?

A

Hepatic metabolizing enzymes require certain cofactors to function. Malnutrition can cause these co-factors to be deficient

78
Q

How do comorbidities affect drug metabolism?

A

Some drugs may require dose reduction in severe liver disease

79
Q

What is excretion?

A

The removal of drugs and their metabolites from the body

80
Q

What is the major organ involved in the excretion for most drugs?

A

The kidneys!

81
Q

Through what ways do metabolized drugs exit the body?

A

Urine
Bile –> feces
Sweat
Saliva
Breast milk
Expired air

82
Q

What factors modify renal drug excretion?

A

pH-dependent ionization

competition for active tubular transport

Age

83
Q

How does pH-dependent ionization modify renal drug excretion?

A

Drugs that are ionized at urinary pH will stay in the urine (NOT be reabsorbed) and be eliminated more quickly

84
Q

How does competition for active tubular transport modify renal drug excretion?

A

If two drugs use the same transporter to move from plasma to the renal tubules, less of them will be transported to the tubules at any given moment

Delays the excretion of both drugs

85
Q

How does age modify renal drug excretion?

A

Infant kidneys do not reach full capacity until a few months after birth

Older adults may have decreased glomerular filtration rates, decreasing drug excretion

86
Q

What 3 processes result in urinary excretion? - Renal Route

A
  1. Glomerular filtration
    - drugs not bound to proteins move from blood –> urine
  2. Passive Reabsorption
    - lipid-soluble drugs move back into the blood.
    - Polar and ionized drugs stay in the urine
  3. Active Transport
    - Requires ATP
    - Drugs are pumped from blood to urine
    - P-glycoproteins are also present in the tubules and may pump drugs into the urine
87
Q

Describe the hepatic route of excretion

A

Metabolites may leave the liver via:
1. Blood, which will take them to the kidneys for elimination

  1. Bile, which will take them into the gut and out of the body via feces (hepato-biliary excretion)
88
Q

What is hepato-biliary excretion?

A

When metabolites leave the liver via bile

The bile then takes them into the gut and out of the body via feces

89
Q

What is the minimum effective concentration?

A

The plasma drug level BELOW which therapeutic effects will NOT occur

90
Q

What is toxic concentration?

A

Plasma drug leves at or ABOVE which toxic effects WILL occur

91
Q

What is therapeutic range?

A

The range of drug levels between the minimum effective concentration and the toxic concentration –> sufficient concentration to produce desired therapeutic effect

“safe range”

AKA therapeutic window

92
Q

What is a drug’s half-life?

A

TIme required for the concentration of the drug in the body to decrease by 50%

Can be measured by hours, minutes, seconds, days, weeks

93
Q

Why should we care about a drug’s half-life? What does it help us determine/calculate?

A

It helps figure out dosing schedule

All about the dosing interval

94
Q

What might happen if we gave the usual dose of kanamycin on the usual dosing schedule to a patient with renal failure?

A

The half-life would increase
There would be more drug inthe system –> more toxicity
More ADE
Need to change the dosing schedule for a pt with renal failure

95
Q

What is the onset of a drug?

A

Time after administration until the drug begins to have a clinical effect

96
Q

What is the peak of a drug?

A

Time after administration at which the drug is having its maximal effect

Drug is at its highest concentration

97
Q

What is the trough of a drug?

A

Time after administration at which the drug is having its minimal effect

Drug is at its lowest concentration

98
Q

What is the “duration” of a drug?

A

The lenght of time the drug has a clinical effect

  • important, along with half-life, for determining dosing interval
  • Also important for tapering/withdrawal considerations
99
Q

What is a steady-state? - Drug Levels

A

When the amoun of drug administered = the amount of drug eliminated in the same period

Reaching plateau

100
Q

What is the average amount of half-lives needed for most drugs to reach their steady-state?

A

4 to 5 half lives

101
Q

What is a loading dose?

A

A dose that is significantly higher than the maintenance dose given to pt taking a drug with a long half-life.

Done to “speed up” the time to steady state

Often done with Abx

102
Q

If a drug mimics a bioloical process, it is a ____ drug

A

Agonist

103
Q

If a drug blocks a biological process, it is a ___ drug

A

Antagonist

104
Q

The size and intensity of an administered dose determines what 3 things?

A

The minimum amount of drug that can be used

The maximum response a drug can elicit

How much to increase the dosage to produce the desired increase in response

105
Q

What are the 3 phases in the dose-response relationship? - Pharmacodynamics

A

Phase 1: Dose it too low to elicit a response

Phase 2: Increasing the dose increases the response

Phase 3: Increasing the dose further does not yield further increase in response (but can increase adverse drug effects) –> plateau in response but increase in ADE

106
Q

What is maximal efficacy?

A

The largest effect/response that a drug can produce

“How effective is the drug?” ex. pain relief, diuresis

107
Q

What is potency?

A

The amount of drug (dose) needed to have an effect

“how much drug needed to have an effect?”

108
Q

Which axis do you look at to determine a drug’s maximal efficacy?

A

The y-axis // height of the curve

Highest curve has the greatest maximal efficacy and is themost efficacious

109
Q

Which axis do you look at to determine a drug’s potency?

A

The x axis

Curve farthest to the left has greatest potency (requires the smallest dose) for that response

110
Q

Why is greater efficacy not always desired?

A

We want to match the intensity of drug’s effect with its desired effect

Example: we give a lower effective dose of a diuretic to a person regulating their hypertension vs. higher effective dose to a person who needs to urgently drain excess fluid

111
Q

Why is potency not always an important clinical characteristic of the drug?

A

It implies nothing about the maximal efficacy; refers to the dosage needed to produce effects

112
Q

What are some instances in which the potency of a drug can matter?

A

If a lack of potency forces an inconvinient larger dose (which can result in increase in ADE, including the production of toxic metabolites)

Important to keep in mind when administering certain drugs (eg. morphine in mgs and fentanyl in micrograms)

113
Q

What are adverse effects?

A

Unintended, undesireable effects of a medication

  1. side effects
  2. Adverse drug reactions
  3. interactions
114
Q

Side effects are ____ predictable while adverse drug reactions are ____ predictable

A

Side effects are MORE predictable while adverse drug reactions are LESS predictable

115
Q

What is biochemical effect?

A

The ability of the drug to affect chemical processes related to cells, tissues, or the entire organism

Broad term that encompasses all of a drug’s chemical effects on the body

116
Q

What do pharmacokinectic drug-drug interactions alter in the body?

A
  • Alter absorption
  • Alter distribution
  • Alter renal secretion
  • Alter metabolism
117
Q

What are some ways pharmacodynamic drug-drug interactions occur?

A

Interaction at the same receptor –> compete

At separate sites but affect same physiologic processes (additive or inhibitory)

Combined toxicity

118
Q

What do drug-food interactions affect?

A
  • Alter absorption
  • Alter metabolism (grapefruit juice)
  • Toxcity
  • Action
119
Q

What are the 4 primary receptor types?

A
  1. Cell membrane-embedded enzyme
  2. Ligand-gated ion channel
  3. G protein-coupled receptor system
  4. Transcription factor
120
Q

What is the single occupancy theory? What is its limitation?

A

States that the intensity of response to a drug is proportional to the number of receptors occupied by that drug

Maximal response will then occur when all receptors are occupied

It DOES NOT account for all observed drug-receptor interactions/results (potency, efficacy)

121
Q

What is the modified occupancy theory?

A

It takes into account affinity and intrinsic activity

122
Q

Agonist have ___ affinity and ____ intrinsic activity

A

Agonist have GOOD affinity and HIGH intrinsic activity

123
Q

Antagonist have ___ affinity and ____ intrinsic activity

A

Antagonist have GOOD affinity and NO intrinsic activity

124
Q

What is the difference between a competitive and noncompetitive antagonist?

A

Competitive: binds reversibly to receptor, competes with agonists

Noncompetitive: binds irreversibly to receptor, its effects last until new receptors are synthesized; reduces maximal response that an agonist can elicit

125
Q

What are partial agonists?

A

Mimic physiologic actions to a lesser degree

Good affinity, moderate intrinsic activity

Give no response when increase dose of partial agonists (plateau) –> may still increase ADE

126
Q

Continued exposure to an agonist results in ____regulation. What does this mean?

A

Downregulation –> fewer receptors

The body becomes less responsive to the agonist –> desensitized or refractory
why? reduced # of receptors –> reduced response bc agonist have lesser rceptors to bind to

127
Q

Continous exposure to an antagonist results in ____regulation. What does this mean?

A

Upregulation –> more receptors

Hypersensitivity occurs, resulting in more receptors
why? –> body does not sense the physiologic process occurring, so it makes more receptors (which continue to be taken up by antagonist) resulting in hypersensitivity to the antagonist drug

128
Q

What factors increase a drug’s ability to be excreted in breast milk?

A

Whether the drug is:
- lipid-soluble
- small molecule
- has a long half-life
- not highly protein-bound
- easily crosses the BBB

129
Q

How can genetic variations cause differing responses from one individual to another?

A
  • Alter drug metabolism
  • Alter drug transporters
  • Alter drug targets
  • Alter immune responses
  • Genetic variations can be the cause of significant adverse effects
130
Q

What is pharmacogenomics?

A

The study of how genomic variation influences drug response, looking at variation across the genome - COMPLEX interactions

Across the WHOLE genome

131
Q

What is pharmacogenetics?

A

Study of genetic influence on drug respone, typically looking at a few genes (genetic variation)

132
Q

Neonates and Infants - Absorption

A

Oral
- Prolonged and irregular gastric emptying time
- Gastric acidity does not reach adult values until 2 years of age

IM
- Slow, erratic
- low blood flow during the first few days of life
- during early infancy, rapid absorption of IM drugs

Transdermal
- more rapid and complete for infants
- stratum corneum of infant’s skin is very thin
- blood flow to skin greater in infants

133
Q

Neonates and Infants - Distribution

A

Limited protein binding
- amount of serum albumin is low
- limited drug/protein binding –> increase free drug –> incr in ADE
- reduced dosage needed
- 10-12 months when reach adult protein binding capacity

134
Q

Neonates and Infants - Blood Brain Barrier

A
  • Not fully developed at birth
  • Infants sensitive to CNS-active drugs
  • reduce dosage for drugs with possible CNS toxicities even if used for actions outside the CNS
135
Q

Neonates and Infants - Hepatic Metabolism

A

Have low drug-metabolizing capacity
Neonates sensitive to drugs metabolized by liver

complete liver maturation at 1 year of age

136
Q

Neonates and Infants - Renal Excretion

A
  • Low renal blood flow, glomerular filtration, and active tubular secretion from birth to 1 year
  • Reduce dose and/or give longer dosing intervals
  • Adult renal function achieved by 1 year
137
Q

Older Adults - Absoprtion

A
  • Slow with age
  • Delayed gastric emptying and reduced GI tract blood flow
  • Increased gastric pH (more alkaline, drugs may require acidity)
138
Q

Older Adults - Distribution

A
  • Increased percentage of body fat
  • Decreased percentage of lean body mass
  • Decreased total body water
  • Reduced concentration of serum albumin, especially if malnourished
  • Reduced cardiac output in patients with heart failure
139
Q

Older Adults - Metabolism

A
  • Reduced hepatic blood flow, reduced liver mass, decreased activity of some heaptic enzymes
  • Longer half-lives, prolonged responses
  • First-pass metabolism may be decreased –> risk of increased blood levels of certain drugs
  • Changes in drug metabolism can vary greatly from individual to individual
140
Q

Older Adults- Excretion

A
  • Reduced in renal blood flow, GFR, active tubular secretion, and number of nephrons
  • Averafe renal function of an 80 year old is around 50% of a 20 year old
141
Q

Older Adults - Pharmacodynamic Changes

A

Alterations in receptor properties
- some drugs may have a more intense effect
- beta-blockers less effective, even in the same concentrations

NURS 1650 - Here We Go Again (20 decks)

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