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Pharmacology 1 > intro to pharmacodynamics > Flashcards

intro to pharmacodynamics Flashcards

1
Q

pharmacology

A

study of substances that interact with living systems through chemical processes

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2
Q

general interactions between drugs and our bodies

A

do not add new processes but modify existing physiology, binding to regulatory molecules, activating/inhibiting body processes, replace endogenous substances

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3
Q

pharmacodynamics

A

what the drug does to the body, how and where it works, mechanism of action

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4
Q

pharmacokinetics

A

what the body does to the drug, movement in and out of the body and various compartments, how the drug is broken down and transported/excreted

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5
Q

where most drug excretion occurs

A

kidney or liver

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6
Q

drug

A

any substance that brings about a change in biologic function through a chemical action

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7
Q

drug mechanisms of action

A

augment or inhibit signaling molecules, inhibit or stimulate receptors, inhibit or increase enzyme activity

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8
Q

prednisone mechanism of action

A

steroid, works by binding and inhibiting regulatory molecules that cause inflammation, produces anti-inflammatory response

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9
Q

metoprolol mechanism of action

A

occupies beta receptors on the heart and prevents normal binding of catecholamines, decreases heart rate, beta blocker

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10
Q

levothyroxine mechanism of action

A

allows the body to make thyroid hormone, replaces endogenous chemicals your body should make

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11
Q

what is the goal of giving medication

A

correct imbalances in homeostatic functions, replace naturally occurring compound that are no longer made or become insensitive, inhibit bacterial, viral, fungal organisms that invade the body

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12
Q

examples of drugs that correct imbalances

A

pantoprazole turns off acid pumps for stomach ulcers, hydrochlorothiazide removes excess salt to treat high BP, doxorubicin inhibits hyperactive cells from replicating to treat cancer

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13
Q

examples of drugs that replace naturally occurring compounds

A

estrogen to treat hot flashes, insulin to treat type 1 diabetes

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14
Q

what is another name for a receptor

A

drug target

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15
Q

most receptors are made of __

A

proteins

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16
Q

most common type of receptor

A

extracellular

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17
Q

types of extracellular receptors

A

cell surface glycoproteins, transport proteins

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18
Q

types of intracellular receptors

A

nuclear receptors, transcription factors

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19
Q

ligand

A

interacts with a receptor to trigger or inhibit a physiological process, ie a drug

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20
Q

characteristics of receptor sites on enzymes

A

usually specific, usually require phosphorylation, can break things down or put things together

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21
Q

___ have a higher affinity at receptors than ___

A

drugs; naturally occurring compounds

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22
Q

how to increase affinity

A

increase covalent bonds by molecular chemistry

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23
Q

receptor affinity for drug binding determines ___

A

the concentration of a drug needed to form a complex with the receptor

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24
Q

selectivity is ___ as concentration of a drug is ___

A

reduced; increased

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25
Q

why selectivity decreases with increasing drug concentration

A

drugs can become more attracted to other sites, creates more side effects due to reduced selectivity, drug outcompetes the naturally occurring compound, overwhelms the receptor

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26
Q

(selective or nonselective) drugs cause more side effects? why?

A

nonselective, they activate unwanted processes

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27
Q

example of a nonselective drug

A

ibuprofen, it inhibits COX1 and COX2

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28
Q

characteristics of receptors in relation to drug dosage

A

total number of receptors may limit maximal effect of drug, receptor number is dynamic and influenced by exposure to agonist/antagonist, actions of drug may take time to see clinical effects

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29
Q

ligand gated ion channels

A

ionotropic receptors, ligand causes hyperpolarization or depolarization, effects in milliseconds

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30
Q

g-protein couples receptors

A

metabotropic, ligand causes change in excitability, effects in seconds

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31
Q

kinase linked receptors

A

ligand causes protein phosphorylation and protein synthesis, effects in hours

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32
Q

nuclear receptors

A

ligand causes gene transcription and protein synthesis, effects in hours

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33
Q

most drug binding to receptors is (reversible or irreversible)

A

reversible, effect of drugs are concentration dependent

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34
Q

which type of drug is most likely to have an irreversible effect

A

usually drugs that are antagonists

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35
Q

law of mass action

A

when a drug combines with a receptor it does so at a rate which is dependent on the concentration of the drug and of the receptor

36
Q

law of mass action equation

A

[D] + [R] [DR]
arrow to left is K1, arrow to right is K2
k1 = rate of dissociation
k2 = rate of association

37
Q

Kd

A

concentration of ligand when the ligand is 50% bound to the receptor, helps determine drug dosage

38
Q

agonist

A

outcompetes natural chemical to activate receptors, mimics physiological activation

39
Q

epinephrine as an agonist

A

given to activate beta receptors in the heart –> increased HR and force of contractions, acts on SNS, binds to alpha receptors in SNS causing vasoconstriction in large arterterial smooth muscles –> increase BP (non selective)

40
Q

antagonist

A

block receptors or enzymes in physiological systems, drug effects are opposite direction of normal physiological response

41
Q

metoprolol as an antagonist

A

beta receptor antagonist in the SNS –> decreases HR

42
Q

acetylcholine as an agonist

A

acts on the PNS (normal response is to decrease HR) –> increases HR

43
Q

normal physiological response of GABA receptors

A

influx of Cl- into nerve so they cannot conduct transmission of nerve firing –> inhibit nerve firing

44
Q

benzodiazepines as agonists

A

for anxiety, agonists of GABA, more neuron inhibition –> more relaxed and sleepy

45
Q

flumazenil as antagonist

A

for overdoses on benzodiazepines, antagonist of GABA, more nerve firing, can cause seizures due to overprocessing of nerve firing

46
Q

normal physiological function of angiotensin II

A

increases BP

47
Q

action of ACE inhibitors

A

inhibit production of angiotensin II, decrease BP and improve renal blood flow

48
Q

non competitive inhibition

A

ligand binds to a site other than receptor site, confirmation of enzyme changes and doesnt allow substrate to bind

49
Q

competitive inhibition

A

ligand bind to receptor site so substrate cannot, ie ACE inhibitors

50
Q

stereochemistry

A

all drugs that are not symmetrical have enantiomers with the mirror image configuration, only one will have the correct configuration for an enzyme

51
Q

full vs partial agonist

A

partial increases response at a much slower rate with increased dose and tapers off much sooner –> doesnt give the full drug effect, full increases response quickly with increased dose but plateaus when all receptors are bound

52
Q

which has a higher affinity for receptors (partial or full) agonists and why its useful

A

partial, this is why buprenorphine is used during opioid overdoses since it will bind to receptors more but have less effect

53
Q

up regulation of receptors

A

sensitization, from continuous use of antagonists, develops months-years

54
Q

down regulation of receptors

A

desensitization, continuous use of agonist, develops months-years

55
Q

how upregulation occurs

A

drug is inhibiting response, body makes more receptors so normal process can occur, overall effect is more since there are more receptors to bind, decreases effect of antagonist

56
Q

where upregulation usually occurs

A

CNS

57
Q

how down regulation occurs

A

agonist increases response, body wants to decrease back to a normal level so receptor number is decreased, overall effect is less since there are less receptors to bind, decreased effect of agonists

58
Q

types of tolerance

A

upregulation, down regulation

59
Q

risk of tolerance depends on ___

A

drug, potency, chronicity of use, individual variability, physiological system involved

60
Q

cross tolerance

A

drugs that affect similar receptors can make one another tolerant even without use, ie benzodiazepines tolerance can cause decreased effect of alcohol

61
Q

withdrawal

A

abrupt cessasion of drugs to which tolerance has developed, causes symptoms that are opposite of the original effects of the drug

62
Q

withdrawal of antagonist

A

normal effects can become heightened in upregulation due to more receptors

63
Q

therapeutic effects

A

pharmacological effect of drugs used to treat a disease state, intended effects

64
Q

side effects

A

pharmacological effects other than intended effects

65
Q

adverse drug reactions

A

side effects significant enough to warrant a change in dose or discontinuation of a drug

66
Q

solutions to tolerance

A

increase dose, change med to one with a different drug pathway but same effect

67
Q

toxic effects

A

predictable side effects that are severe and indicative of too high a dose or concentration

68
Q

groups of side effects

A

overextension of drug effect in a articular system which are dose related, non intended effects on other systems, idiosyncratic side effects

69
Q

idiosyncratic side effects

A

unpredictable, non dose related, related to immune system response (rash or allergic reaction)

70
Q

example of overextension of drug side effects and solution

A

antihypertensive causing hypotension, requires lowering the dose

71
Q

example of non intended effects on other systems and solution

A

phenytoin (anti seizure) causes facial hair growth, if side effect is intolerable discontinue use

72
Q

examples of idiosyncratic side effects and solution

A

hydralazine causing lupus, discontinue medication and document allergy

73
Q

what determines drug use

A

want to optimize effects based on 50% receptor binding, balance efficacy and side effects, drugs lose selectivity at higher conc, drug acting on different sites causes unintended effects

74
Q

how do drugs differ within the same class?

A

potency

75
Q

potency

A

the conc of the drug to achieve the same effect, higher potency = lower drug dose

76
Q

what influences potency

A

molecular chemistry and noncovalent bond formation

77
Q

margin of safety

A

distance between dose-response curve for ideal effects and dose-response curve for adverse effects, determines dosage range

78
Q

therapeutic index equation

A

TI= TD50/ED50
TD is conc of drug at 50% saturation on toxic effect curve, ED is conc of drug at 50% saturation on therapeutic effect curve

79
Q

do you want a high or low TI

A

high, indicates are larger therapeutic window and a larger range of safe doses

80
Q

drug drug interactions

A

effects of 2 drugs or more that increase or decrease the actions of one or another, can occur as pharmacokinetic or dynamic interactions

81
Q

additive effect

A

two drugs increase the effect of one another, 1+1=2

82
Q

synergistic effect

A

two drug exponentially increase effect of one another, 1+1=4

83
Q

example of synergy

A

aminoglycosides and beta lacatams for endocarditis, improve killing power of antibiotics together; loop and thiazide diuretics for fluid overload, improved urine excretion

84
Q

example of drugs that antagonize each other

A

psudophedrine increases BP even in patients that are taking BP lowering meds

85
Q

causes of drug variability

A

body weight and size, age and sex, genetics, health, placebo effect

86
Q

pharmacokinetic causes of variability of drug response

A

dose, formulation, route of administration; drug tolerance; drug interactions

Pharmacology 1 (4 decks)

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