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PHAR 300 > Introduction/Drug Action > Flashcards

Introduction/Drug Action Flashcards

1
Q

what is pharmacology?

A

the study of all compounds that interact with the body and includes knowledge of the interactions between these compounds and body constituents at any level of organization

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2
Q

what is a drug?

A

any chemical substance that affects a living system

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3
Q

what is toxicology?

A

the study of harmful effects of drugs

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4
Q

why are children more vulnerable to toxins?

A

because their metabolism isn’t as efficient and have different surface/area ratio

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5
Q

what is the risk-benefit evaluation?

A

all drugs will have side effects, but we must make sure that the benefits outweigh the risks

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6
Q

what is proteomics?

A

the study of proteomes, or the entire complement of proteins expressed in a certain cell, tissue, organ system, or the body

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7
Q

what is pharmacogenomics?

A

understanding genetic differences amongst people and how these differences influence one’s response to drugs

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8
Q

what are the types of drug names?

A
  • chemical
  • generic
  • trade
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9
Q

what is pharmacodynamics?

A

what the drug does to the body

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10
Q

what is pharmacokinetics?

A

what the body does to the drug

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11
Q

what is therapeutics? what are indications and contraindications?

A
  • therapeutics: using a drug to treat or prevent disease
  • ind: when you should use the drug and what it is used for
  • cont: when you should not use the drugs
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12
Q

what is bioavailability?

A

how much of the drug is available to get into the systemic circulation, after getting through the liver

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13
Q

what are the methods of administration?

A
  • oral
  • parenteral (injection)
  • inhalation
  • topical
  • sublingual
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14
Q

what are the advantages and disadvantages of oral administration?

A
  • adv: easy, cheap, convenient
  • dis: stomach acidity may destroy the chemical composition of certain drugs (particularly biologicals), and liver inactivation can act really strongly on some compounds
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15
Q

what are the different injection methods?

A
  • subcutaneous (under skin)
  • intravenous (in bloodstream)
  • intramuscular
  • in cerebrospinal fluid
  • intraperitoneal
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16
Q

what are the advantages of injecting a drug?

A

fast, accurate, and controlled absorption

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17
Q

what are the advantages of inhaling a drug?

A
  • easy to administer
  • rapid systemic effect since lungs have huge surface area
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18
Q

what are the advantages of sublingual drug administration?

A
  • rapid
  • no first-pass
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19
Q

what does the time course and peak concentration look like for Iv, oral, and rectal?

A
  • IV: high initial peak and drops quickly as it gets distributed
  • oral: slower rise since it takes time for it to be absorbed by GI and lower peak due to first-pass
  • rectal: slow absorption and lower peak level
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20
Q

what are the two types of drug selectivity?

A
  • selective: mostly targets one area
  • generalized: acts on all systems
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21
Q

what is the a drug receptor?

A

a macromolecular protein target to which endogenous ligand or exogenous agonist/antagonists can bin to to cause cellular response

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22
Q

what are the different action of receptors?

A
  • autocrine (acts on itself)
  • endocrine (chemical transported through blood)
  • paracrine (chemical acts on nearby cell)
  • juxtracrine (chemical that acts on neighboring cell via connection)
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23
Q

what does the affinity of a drug to an ion channel depend on? what does this tell us about the drug?

A
  • depends on the membrane potential and channel cycling frequency
  • tells us how quickly the drug will bind
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24
Q

where do natriuretic peptide receptors activate cellular responses?

A

kidney and the heart

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25
Q

how do the response times differ on different types of receptors?

A
  • ion: fast to respond (msecs)
  • GPCR: 2nd messenger must be activated (secs)
  • enzymes: blocking or stimulating enzymes (mins)
  • DNA-linked: translocation, transcription, translation, enzymatic activity (hrs)
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26
Q

what do cancer treatments affect/alter?

A

alter cell division/reproduction process with microtubule destabilizers/stabilizers (alters mitosis)

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27
Q

are receptors static or dynamics? explain.

A

they are dynamic
- there is constant turnover (synthesis, transport, stimulation, recycling, resynthesis, etc. )
- cell can respond by changing number of receptors at the PM

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28
Q

explain the concept of biological variation and how that connects to quantifying and comparing the effect of a drug (what type of graphs are used?).

A
  • everyone is different due to their genetics and the environment
  • graph plotting drug dosage and number of people responding we see a normal distribution since most people will respond with moderate dose but others need more or less
  • dose-response curve: plots the cumulative percentage of people responding to a dose (usually log scale is used)
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29
Q

what is the ED-50?

A

the dose required to produce an effect on 50% of the population

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30
Q

what do you use a dose response curve for?

A
  • comparing drugs: some may be more potent than other (use a lower dose for same effect) and might want to use the least or most potent depending on other factors
  • studying the magnitude of drug effect: study effect on single cell, organ system, or in an individual
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31
Q

what is the following on a dose response curve: threshold, ceiling dose, potency

A
  • threshold: it is the minimum dose to see an effect
  • ceiling dose: does where effect levels off and cannot get higher
  • potency: if more towards the left is more potent and if more to the right, less potent
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32
Q

what is receptor occupancy? what are spare receptors?

A
  • it is the percent of receptors that are occupied for a specific response - usually less than 100%
  • spare receptors are the ‘fail-safe’ mechanisms - they are the receptors that are not being used
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33
Q

what is the efficacy of a drug?

A

the proportion of receptors that are forced into their active conformation when occupied by a drug and that give the desired effect

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34
Q

what is a partial vs full agonist? what are the benefits of partial agonists?

A
  • full: binds to receptor and leads to large response
  • partial: binds but leads to small response (low efficacy)
  • benefit: can lead to less adverse effects, can block access to full agonist by giving a partial agonist
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35
Q

what is a competitive vs non-competitive antagonist and how do they affect the dose-response curve?

A
  • competitive: bind to same site, will shift the curve to the right and when given at VERY high concentration, it can decrease the maximum response agonist
  • non-competitive: bind to different site (allosteric), will lower the peak of the curve
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36
Q

what is an irreversible vs reversible antagonist?

A
  • irreversible: binds irreversibly and decreases the number of available receptors, so body has to synthesize more/ increase turnover
  • reversible: binds reversibly, is most common one (irreversible can cause toxicity)
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37
Q

what is TD50?

A

the dose required to produce a toxic effect in 50% of the population

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38
Q

what is LD50?

A

the dose required to produce a lethal effect in 50% of the population

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39
Q

what is the therapeutic index?

A

the ratio of toxic to the therapeutic effect; TI = TD50/ED50

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40
Q

what is considered a good vs bad TI?

A
  • the larger the Ti, the better it is
41
Q

what is the therapeutic window?

A

the dose range within which most people get therapeutic effects without side effects

42
Q

what is the safety factor?

A

TD1/ED99

43
Q

what is a benefit and a toxicity outlier?

A
  • benefit: respond to the drug a much lower (or much higher dose)
  • toxicity: have toxic effect at much lower (or higher) dose
44
Q

what are the 5 parts of pharmacokinetics?

A
  • liberation
  • absorption
  • distribution
  • metabolism
  • excretion
45
Q

what is absorption of a drug?

A

the transfer from the site of administration to the bloodstream

46
Q

what are ways that drugs can pass through the plasma membrane?

A
  • aqueous pores (small molecules, water soluble molecules, ions)
  • diffusion (passive, lipid soluble molecules, gases, small polar molecules)
  • transporters (large molecules and charged particles)
47
Q

what is the effect of the stomach on drugs?

A
  • has low pH and little absorption happens, mostly a reservoir
  • weak acids: will be non-ionized in low pH so will be able to cross lipid membrane of stomach cells
  • weak bases: will be in ionized forms in low pH so won’t be able to cross membrane and will be absorbed in the intestine
48
Q

what is the effect of the small intestine on drugs?

A
  • has a higher pH
  • has much more absorptive surface so absorbs pretty much all drugs
49
Q

what is the effect of the liver on drugs?

A
  • “scans” what gets absorbed before going into circulation
  • metabolized/detoxifies chemicals
  • firsts-pass metabolism
50
Q

how are the drugs distributed and in what form?

A
  • go through body by blood stream and rate of blood flow varies with different organs
  • will only be free to move through plasma membrane when is a free drug, cannot when it is bound (there is equilibrium between two forms)
51
Q

are drugs equally distributed throughout the body?

A

no because blood flow varies with tissue type (will go in brain first, then muscles, then fat)

52
Q

what is the duration of action?

A

time that spans the onset of effect and the time when the effect ceases

53
Q

what is the lag period?

A

time until concentration of drug becomes high enough to get therapeutic effect

54
Q

what are variables that affect drug concentration? how would that look relative to the MEC for toxicity and MEC for therapeutic effect?

A
  • increase concentration: will go above MEC for toxicity
  • drug absorbed quickly: will peak very fast and will be at MEC for toxicity but then will also go down quickly
  • drug that is eliminated quickly: does not stay above MEC for therapeutic effect long
55
Q

what are mechanisms by which the BBB protects the brain?

A
  • tight junctions between capillaries
  • astrocytes help regulate blood flow into the brain
  • very tightly controlled active transport
56
Q

is the placenta a good barrier?

A

no, lipid soluble drugs diffuse rapidly and water-soluble drugs can pass slowly

57
Q

which proteins can drugs be bound to? in which situation can this be altered?

A
  • bind to albumin (impaired in liver disease)
  • bind to glycoproteins (elevated in inflammation)
58
Q

what is the apparent volume of distribution?

A

amount of drug in body (in mg)/concentration of drug in plasma (in mg/L)

59
Q

what does a high and a low AVD mean?

A
  • low: high protein binding (most in plasma)
  • high: high tissue binding (most is in tissue)
60
Q

what are variations in AVD due to?

A
  • properties of the drug (e.g. absorption efficiency)
  • protein binding
  • tissue binding
61
Q

what is the loading dose and how can you determine the loading dose of a drug?

A
  • is amount of drug to administer
  • can figure out with AVD and required concentration in plasma for effect
62
Q

what is drug metabolism?

A

the alteration of the chemical structure by an enzyme

63
Q

what are changes that can be done to a drug during metabolism?

A
  • conversion from a nonpolar, lipid-soluble compound to a more polar form that is more water-soluble (so can be excreted more readily by kidney)
  • converted to less active or inactive metabolites
  • conversion of a prodrug into active form
64
Q

what are the two phases of drug metabolism? which enzymes catalyze reaction in each phase?

A
  • phase 1: oxidation/reduction/hydrolysis and renders the drug inactive - done by cytochrome p450 enzymes
  • phase 2: conjugation, which couples drug molecules to endogenous substituent group to make it more water-soluble for renal elimination - catalyzed by transferases
65
Q

where are cytochrome p450 enzymes usually found?

A

smooth er of hepatocytes by can also be found in GI tract, lungs, skin, kidneys, and brains

66
Q

how are cytochrome p450 enzymes named?

A
  • CYP
  • family: number between 1-17
  • sub-family: letter
  • enzyme or gene: number
67
Q

what are xenobiotics?

A

substances that are foreign or exogenous to a system

68
Q

what do CYP1/CYP2/CYP3 do? what do CYP4/CYP5/CYP8 do? what do the others do?

A
  • 1,2,3: drugs, xenobiotics
  • 4,5,8: internal breakdown
  • others: steroid hormone breakdown
69
Q

What does the relative concentration of CYP enzymes in the liver tell us?

A

nothing, there is no relation between the amount and its importance

70
Q

which CYP enzymes are the most important in drug metabolism?

A

CYP3A, CYP2C, CYP2D6

71
Q

what are factors that influence enzyme function/drug effect in individuals?

A
  • polymorphisms
  • drug interactions
  • age
  • environmental factors
  • diseases
72
Q

what are the consequences of genetic polymorphisms?

A
  • altered drug effect
  • altered sensitivity to stereoselective metabolism
  • altered sensitivity to interactions
  • altered production of active metabolites
73
Q

what are the effect of drug metabolism enzyme inducers and inhibitors? what mechanism may they have?

A
  • inducer: high exposure stimulates synthesis of drug-metabolizing enzymes to increase speed (can increase clearance)
  • inhibitor: inhibition leads to rapid overdose because cannot be broken down (reduces clearance)
74
Q

excretion is predominantly done by what?

A

the nephrons in the kidney

75
Q

where can drug elimination occur?

A
  • kidney (goes to urine)
  • exhaled (breathalyzer)
  • secreted in saliva
  • secreted in sweat
76
Q

what is drug clearance?

A

the quantity of blood that is cleared of a drug in a given amount of time

77
Q

what is the T1/2? and how many half lives to get rid of dug in body completely?

A

the half life, which is the time taken to get rid of half of the drug in the body - it takes 4

78
Q

what is first-order kinetics vs zero-order kinetics?

A
  • first: constant fraction per time unit
  • zero: constant amount of drug eliminated (this is due to saturation of enzymes)
79
Q

when should you get another dose of drug? when is steady state achieved?

A
  • usually at internals of the half-life
  • steady state after 4.5 half lives (so 4 doses)
80
Q

how can tolerance be studied?

A

animal models: seen by frequency of how often the animal takes the drug

81
Q

what is tolerance? what are the types?

A
  • the need of more and more drug to get the same effect
  • chronic: repeated administration leads to decrease response
  • acute: even with one dose, have adaptation in body to fight drug (usually seen in CNS)
82
Q

what is pharmacokinetic tolerance, pharmacodynamic tolerance, and behavioral tolerance?

A
  • kinet: increase metabolism or decrease absorption / shift to right of dose-response curve but no shift for concentration-response curve
  • dyn: adapting site of action (# of drug receptors can increase/decrease) / shift to right for both dose-response and concentration-response curve
  • beh: lower effct of drug as result of conditioned response
83
Q

what is withdrawal?

A

a series of reactions that are opposite to the effects of the drug

84
Q

what is neuroplasticity? why is that significant?

A

the ability to adapt quickly to any new information
- there are lots of stages of communication that can adapt to create tolerance

85
Q

what are some presynaptic and postsynaptic adaptations that may occur?

A
  • pre: neurotransmitter released from presynaptic neurons in vesicles and go to cleft, and at that cleft can have many fates – binding to receptors, reuptake, diffusion, autoreceptors, synthesis, storage
  • post: alter number of receptors – if agonist will downregulate, if antagonist will upregulate
86
Q

what is cross tolerance?

A

tolerance for drug of same family develops at same time

87
Q

what is differential tolerance?

A

ability to produce tolerance depends on location in body, and differences with the different affects of the same drug (e.g. we usually don’t become tolerant to lethality)

88
Q

what is behavioral tolerance?

A

the decrease of potency in affecting a specified behavior after repeated or continuous exposure (learned or conditioned behaviour)

89
Q

what is the time course for withdrawal?

A

intensity of symptoms gradually rises and falls unsymmetrically

90
Q

intensity of withdrawal is related to what?

A

the dose that was taken and the half-life of the drug (short-acting drugs will have bigger counter-effect)

91
Q

what are acute and long-term withdrawal effects?

A
  • acute: worst of the symptoms
  • long: less intense but may last a very long time
92
Q

what are the stages of the addiction cycle?

A
  • craving
  • ritual
  • consumption of drug
  • guilt
  • emotional trigger
93
Q

what can you do to treat drug dependance?

A
  • slowly decrease the drug
  • substitute to a safer drug, then decrease dose
  • prevent relapse with antagonist or agonist
  • reduce craving with therapy and altered lifestyle
94
Q

what are two systems that appear to modulate drug dependance?

A
  • gain reward: activate dopaminergic pathway
  • avoid punishment: withdrawal
95
Q

how can nasal sprays cause dependance?

A

they constrict blood vessels so that don’t secrete as much mucus, and nerve endings adapt such that vasodilation occurs when not using spray, s have to keep using to breath properly

96
Q

what are signs of addiction?

A
  • tolerance
  • obsession
  • increase intake
  • loss of control
  • abuse despite harm (like risk of cancer)
  • withdrawal symptoms
97
Q

drugs are more addictive when?

A

onset of effects is rapid and blood concentration rises quickly

98
Q

where is the dopaminergic pathway located and what is associated with?

A

located in midbrain and is associated classical reward pathway (which goes from ventral tegmental area to nucleus accumbens (where dop. neurons synapse) to prefrontal cortex)

PHAR 300 (12 decks)

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