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Drug Action > Intro, Pharmacodynamics, Pharmacokinetics > Flashcards

Intro, Pharmacodynamics, Pharmacokinetics Flashcards

1
Q

What is a drug?

A

Any chemical that acts on a living system

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2
Q

What is a drug’s generic name?

A

It is understood universally and adopted by the WHO

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3
Q

What is a drug’s trade name?

A

t is a registered trademark, when a patent is expired many compagnies can develop products using the same drug and can name it however they like, something catchy for the consumer.

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4
Q

Pharmacodynamics is?

A

How a drug acts on the body

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5
Q

Pharmacokinetics is?

A

How the body acts on a drug

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6
Q

What are the parts of pharmacokinetics?

A

Absorption, distribution, metabolism, excretion

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7
Q

Where does the most drug absorption take place?

A

The small intestine

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8
Q

Distribution occurs where?

A

in the bloodstream to different organs

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9
Q

Where are drugs metabolized?

A

The liver

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10
Q

Where are drugs excreted?

A

The kidneys, or the lungs if they are inhaled

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11
Q

Oral Administration is?

A

cheap, easy, enteral, Absorption through the small intestine then it passes through the liver (liver inactivation) “first pass” effect, the liver breaks down the part of the drug before it gets into the bloodstream

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12
Q

What are modified release tablets?

A

they release the drug over a period of time, slower release

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13
Q

Parenteral administration is?

A

injection, fast, accurate, bypasses the liver

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14
Q

Types of parenteral administration?

A

intravenous, subcutaneous, intradermal, intramuscular

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15
Q

Inhalation administration is?

A

localized, systemic effects, lungs have a large surface area, easily enters the bloodstream, rapid effect (nicotine)

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16
Q

Topical administration is?

A

skin, mucosal, skin patch slow absorption

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17
Q

Sublingual administration is?

A

rapid, no first pass effect, under tongue

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18
Q

The route of administration affects (2 things)?

A
  • Time course
  • Peak concentrations
  • (speed + concentration)
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19
Q

Will a drug given orally have lower max concentration in the blood then if given IV?

A

Yes, given orally the drug will be metabolized by the liver through the first pass effect and it takes longer to be absorbed

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20
Q

Pharmacodynamics effects what body systems?

A
  • Receptors
  • Ion channels
  • Enzymes
  • Immune system
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21
Q

What are the different levels of pharmacodynamics?

A
  • Organ system
  • Tissue
  • Cell
  • Subcellular target
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22
Q

What causes side effects?

A

Side effects are the drug acting on other cells, other than its target

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23
Q

AN antiviral drug…?

A

Targets the virus, drug binds to the active site, blocks the virus action

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24
Q

what ways does an antihypertensive drug control high blood pressure?

A
  • Act on the heart
  • Act on the autonomic nervous system
  • Act on blood vessels
  • Act on the brain
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25
Q

What are two types of receptors? (locations)

A

intracellular receptors, receptors on the cell surface

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26
Q

What do antacids do?

A

controls acids in the stomach, used to help with stomach pain

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27
Q

What does an agonist do?

A

Agonist: binds and stimulates the receptor

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28
Q

What does an antagonist do?

A

Antagonist: blocks agonist/receptor action

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29
Q

What do allosteric modulators do?

A

Allosteric modulators: affect the level of response to an agonist (can modulate the response in a positive or negative direction)

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30
Q

what are ion channels?

A

Ion Channels: transmembrane spanning proteins that open to allow passage, voltage controlled or receptor controlled

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31
Q

A GPCR mechanism?

A

G-protein coupled receptor (GPCR):
- 7 transmembrane domains (cross plasma membrane 7 times)
- Agonist on the outside of cell (binding site)
- Triggers a change in the inside of the cell
- Alpha, beta, and gamma subunits
- Alpha subunit separates, GDP to GTP, activates effector protein

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32
Q

What is receptor turnover?

A

Receptors are constantly being synthesized and placed on the membrane
They are also broken down often
If a drug acts on a receptor, the body can turnover the receptor to get normal function back

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33
Q

What function do intracellular receptors have?

A

They alter gene transcription

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34
Q

ED50=?

A

Effective dose 50, The amount of a drug necessary to see a desired response in 50% of the population

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35
Q

why is comparing ED50s for different drugs helpful?

A

Comparing ED50s for different drugs is useful to see if one drug can have the same effect at a lower dose than another drug. (However, we must always consider the possible side effects of each drug not just compare the effective dose)

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36
Q

Threshold dose?

A

The amount of dose that needs to be given to get a minimal response

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37
Q

Ceiling dose?

A

Ceiling dose: when all people have a response or the maximal effect

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38
Q

Can an agonist cause a max effect if not all of the receptors are bound?

A

Yes, Usually only a small fraction of the receptors needs to be activated to have a max response

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39
Q

Do Drugs also differ in affinity for binding sites?

A

yes

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40
Q

A full agonist has a?

A

large effect, large stimulus to cellular signaling machinery

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41
Q

A partial agonist has a?

A

(small effect) small stimulus to cellular signaling machinery

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42
Q

Can a partial agonist have the same response as a full agonist?

A

No, they don’t fully activate the receptor, they can decrease the effect of a full agonist

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43
Q

What is the function of an antagonist?

A
  • Block receptor activation
  • No response
  • Block agonist activity
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44
Q

Types of antagonists?

A

Competitive vs. noncompetitive
Reversible vs. irreversible

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45
Q

Competitive antagonist features?

A
  • Will compete with the natural ligand (or agonist) for the binding site
  • Can out compete and block the response to stop activity
  • Same binding site
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46
Q

Noncompetitive antagonist features?

A
  • Different binding site than the natural ligand
  • Still lowers the response
    cannot block the response fully
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47
Q

Which way do competitive antagonists shift the dose response curve?

A

Shift to the right, need more agonist for the same effect

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48
Q

Which way does a noncompetitive antagonist shift the DR curve?

A

It does not shift the curve, it never allows the full response , the response drops as you add more antagonist

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49
Q

Irreversible antagonist features?

A
  • The drug stays bound to the receptor
  • The body needs to generate new receptors to the surface of the cell membrane to recover normal function
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50
Q

TD50=?

A

toxic dose 50% of the population

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51
Q

LD50=?

A

THe lethal dose for 50% of the population

52
Q

What is the ideal dose response curve for a drug?

A

have 99% of people with a desired response and less than 1% of people with adverse effects
Ideal therapeutic window is no toxic effect with 99% of people efficacy (huge therapeutic index)

53
Q

What drug has a huge therapeutic index?

A

Penicillin

54
Q

Warfarin (anticoagulant) has a smaller therapeutic index, what are some side effects of this?

A

the adverse effects like bleeding are more common

55
Q

Therapeutic index =?

A

TI = TD50/ED50 slope may vary so need to know the shape of the curve to see if desired effect does not overlap with toxic effects

56
Q

What is a toxicity Outlier?

A

Toxicity outliers: no response at all

57
Q

What is a benefit outlier?

A

Benefit outliers: respond at a small dose

58
Q

Where are weak acids able to be absorbed?

A

In the stomach

59
Q

Where are weak bases and most drugs absorbed?

A

In the small intestine

60
Q

Is there a first pass effect with sublingual administration?

A

No, it goes right into circulation

61
Q

Bioavailability?

A

Bioavailability: fraction of a drug administered reaching the systemic circulation

62
Q

Which organs will be effected by a drug first?

A

Heart, brain, liver, organs that have high blood flow

63
Q

What is the drug doing if bound to a protein?

A

It is not doing anything

64
Q

What can a free drug do?

A

it is able to act on receptors, cross membranes, be metabolized and excreted

65
Q

How can disease affect drug action?

A

Lag period, minimum effective concentration (MEC) for effect desired response, peak effect, Duration of action is time from onset of effect

66
Q

Is the placenta an effective barrier to keep drugs out?

A

no

67
Q

Magnitude of drug effect?

A

= Pharmacodynamics x pharmacokinetics x individual biological properties

68
Q

Three compartment model?

A
  • High blood flow organs (brain)
  • Skeletal muscle
  • Body fat (stick in body, effect prolonged, lipid soluble)
69
Q

p-glycoproteins:

A

transports drugs across the plasma membrane (out of the cell)

70
Q

Volume distribution (VD) = ?

A

VD = amount of drug in body/concentration in plasma

71
Q

Volume distribution can vary due to :?

A
  • Properties of the drug
  • Protein binding
  • Tissue binding
72
Q

Protein binding effect on Volume distribution?

A

Protein binding = high concentration of drug in the blood = low AVD (apparent volume distribution)

73
Q

Tissue binding effect on Volume distribution?

A

Tissue binding = low concentration of drug in the blood = high AVD

74
Q

If a lot of the drug is in the blood?

A

There is a low AVD

75
Q

Apparent volume distribution can be used to calculate loading dose because?

A

Volume distribution varies a lot from one drug to the next

76
Q

What is metabolism?

A
  • convert a drug to a less active or inactive metabolite (more water soluble)
  • sometimes (rare) converts an inactive drug to an active one
    The concentration of a metabolite increases over time and then goes down as it is excreted
77
Q

Where does the blood from the small intestine go first?

A

It goes through the liver first, first pass effect

78
Q

The liver?

A
  • second largest organ
  • greatest regenerative ability (fix damage to itself/other organs)
  • vital for life
  • Large functional reserve (can lose a lot before there is loss of function)
79
Q

Why is the first pass effect important?

A

Sometimes a lot of the drug can be broken down and sometimes none of it will reach circulation

80
Q

Phase 1 of metabolism: oxidation of a drug

A
  • Can inactivate drug function, inactive metabolites
  • Can make biologically inactive
    Ex. Aspirin, hydrolysis, salicylic acid + acetic acid
    Oxidation – inactive metabolite (sometimes still active
81
Q

Phase 2 of metabolism: conjugation

A
  • Put something on drug metabolites to get rid of it
  • P450 enzymes, drugs fit into their active sites, drug metabolizing enzymes
82
Q

What are P450 enzymes used for?

A

P450 enzymes are needed to break down food, steroid hormones, drugs, fatty acids, etc.

83
Q

What are the main cytochrome P450 enzymes for drug metabolism?

A

CYP1, CYP2, CYP3 are the main ones for drug metabolism
Found in smooth E.R. of Hepatocytes (in liver), in GI tract, lungs, skin, kidneys
(CYP3A4, CYP2E1)

84
Q

Drug metabolizing enzymes can vary from person to person?

A

Yes, they can also vary within the same person at different points in their lives

85
Q

Does drug metabolism change as you get older?

A
  • Tendency of drug metabolism to be slower in older people
86
Q

Pharmacogenetics?

A
  • Variability from one person to the next
  • Look at variation in drug metabolism between people
87
Q

What is polymorphic distribution?

A
  • A trait that has differential expression in less than 1% of population
  • Some people break down a drug fast, others very slowly
  • Altered drug effect
88
Q

What is an example of individual variation in P450 enzymes?

A

CYP450 2D6: some people overexpress, some people have none at all

89
Q

What is CYP2D6 involved in?

A

It breaks down codeine to form morphine in the body

90
Q

Example of a drug that can cause liver damage?

A

Alcohol

91
Q

Phase 2 metabolites are easily?

A

easily excreted by the kidneys since they become water soluble

92
Q

How are drugs excreted?

A

through the urine, some exhaled, some secreted on the skin, hair

93
Q

Renal clearance?

A

Filtration + secretion – reabsorption

94
Q

What is the half life of a drug?

A

the time it takes for half of the drug concentration to be eliminated from the body

95
Q

How many half lives to eliminate a drug?

A

4 half lives

96
Q

First order kinetics?

A

constant fraction per unit time (straight line)

97
Q

If a drug is given at multiples of the half life how many will it take to have cycling at a steady state?

A

If give drugs at multiples of the half life in 4 x t1/2, you will reach cycling at a steady state

98
Q

How can you better stay in the therapeutic range when giving a drug?

A

By giving the drug more times at a lower dose, you will stay in the therapeutic range and be more accurate

99
Q

What is the biggest killer from overdose in the US?

A

Fentanyl

100
Q

What is tolerance?

A

No longer respond to a drug and/or need a higher dose to get the same effect

101
Q

what is drug addiction?

A

Substance dependence
Can have physical and or psychological dependence

102
Q

Human tolerance study 1952?

A

Addict taking 20 times more per day than several moths before, since he built up a tolerance

103
Q

Types of tolerance?

A

Acute, chronic, enate, pharmacodynamic, pharmacokinetic, behavioral

104
Q

Pharmacokinetic tolerance?

A

Pharmacokinetic: lower concentration at the site of action (liver gets rid of the drug faster)

105
Q

Pharmacodynamic tolerance?

A

Pharmacodynamic: lower effect due to biological adaptation (gets to site of action but doesn’t work as well)

106
Q

Behavioral tolerance?

A

Behavioral: lower effect due to conditioned response

107
Q

Acute tolerance: cocaine

A
  • Response is much lower on second dose
  • Brain adapts very quickly
    the effect of the drug goes up fast but also come off fast, can become tolerant with just one dose
108
Q

What is withdrawal?

A

an effect usually opposite to the drug effect, adverse effect

109
Q

Withdrawal symptoms to a drug that causes inhibition when stop using it?

A

the body naturally corrected for the inhibition by adding more receptors (causing excitation) when the drug is removed the body there is more excitation and can cause seizures, convulsions

110
Q

Presynaptic functions can adjust?

A

store, release, reuptake more/less depending on effect of the drug
Factors controlling transmitter synthesis

111
Q

Postsynaptic functions can adjust?

A

ligand binding, taking into cell, into vesicles or release, degradation in lysosomes all can adapt

112
Q

After chronic agonist, what happens to receptors?

A

Receptors are down regulated

113
Q

After a chronic antagonist, what happens to receptors?

A

Receptors are up regulated

114
Q

What is neuroplasticity?

A

networks can change, individual synapses, brain, spinal chords, many sites in a synapse where neurons can adapt

115
Q

What is surmountable tolerance?

A

Surmountable tolerance: give enough to get the same effect (postsynaptic down regulation of receptors, if enough drug is given, it can flood the receptors to get the same effect as before)

116
Q

What is insurmountable tolerance?

A

Insurmountable tolerance: cannot get the same effect (presynaptic decrease in neurotransmitters, decreases the synthesis of transmitters, even if more drug is given will not get the same production of neurotransmitters)

117
Q

What is differential tolerance?

A

Morphine/fentanyl don’t only relieve pain, they have other effects on the body
We don’t become equally tolerant to the different effects of a drug
We become tolerant to morphine relief of pain over time, but eye constriction does not become tolerant

118
Q

minimal tolerance to death

A

life systems do not decrease over time

119
Q

Behavioral tolerance?

A

Initial exposure – compensatory reaction to the drug
Subsequent reactions
Environmental response – compensatory reaction to the drug

120
Q

Behavioral tolerance can involve classical conditioning

A
  • Inject alcohol before daily test
  • 1st time decrease performance on test
  • After a while performance back to normal
  • Other group injection of alcohol after the test
  • Other group no given alcohol before the test, did worse than the O.G. group
  • No conditioning, cannot do the test well
121
Q

How does the effects of withdrawal change depending on the drug half life?

A

o If it has a long half life there will be less symptoms because the amount of drug in the system (blood) is going down slowly
o If it has a short half life (cocaine) you come down fast and have more symptoms

122
Q

What is drug rebound?

A
  • Sleeping pill, brain adapts
  • After a while you go back to the same effect of not being able to sleep
  • Stop taking the pill, rebound in opposite effect, stay awake
  • Can take even longer to get back to normal
123
Q

What are 3 ways to treat drug dependance?

A
  • Strongly decrease dose (ethanol)
  • Substitute safer drugs, then decrease dose (opioids)
  • Prevent relapse with antagonist or partial agonist
124
Q

How do heroin, alcohol, cocaine and nicotine cause addiction?

A

They activate the reward pathway, release dopamine

125
Q
A

Drug Action (18 decks)

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