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Fundies First Module--First Exam > Pharmacodynamics intro > Flashcards

Pharmacodynamics intro Flashcards

1
Q

extent of pharm response based on

A

affinity of active receptor for ligand

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2
Q

drug-receptor complex strength is measure of

A

affinity

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3
Q

characteristics that influence affinity

A

molecular size, shape, and electrical charge of drug

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4
Q

binding of drug to receptor often exhibits

A

stereospecificity–i.e. one enantiomer will form stronger attachment than other–R/L handed molecules may have varying side-effects

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5
Q

stereoisomer aka

A

enantiomer

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6
Q

pharmacologic response based on

A

change to system related to receptor

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7
Q

acetaminophen binds to receptor in brain

A

receptor (cyclooxygenase) won’t produce prostaglandins at site –> analgesia

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8
Q

receptor that when bound drug result in no physiologic change

A

inert receptor–i.e. albumin although some indirect effects–

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9
Q

Drug-receptor bonds–strong–>weak

A
  1. covalent–share e- –IRREVERSIBLE @ body temp–drug effect lasts much longer–
  2. electrostatic or ionic bond–more common reversible bond
  3. hydrogen bond–dipole-dipole +_-
  4. hydrophobic–very weak–imp in LIPID SOLUBLE d-r interactions
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10
Q

time it takes for drug concentration in plasma to be reduced by 50%

A

elimination half-life–if sustained response likely covalent–aspirin covalent to COX on platelet inhibit clotting

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11
Q

All drug receptor bonds reversible except

A

covalent – at body temp

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12
Q

nonpolar substances as lipid tend to

A

clmp together rather than distribute in water–so minimal contact w/ water–reversible bond

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13
Q

drug receptor interactions often involve

A

multiple bond types simultanious

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14
Q

body’s response to drug concentration changes is _______

A

nonlinear in progression–more change at lower concentrations

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15
Q

nonlinear progression of drug response due to

A

receptors become saturated–plateau reached at max response

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16
Q

time before drug takes effect

A

lag period

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17
Q

maximum response of drug

A

“peak effect”–top of curve builds and tapers (symptoms return)

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18
Q

Maximum effective concentration MEC

A

between desired and adverse responses is THERAPEUTIC WINDOW

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19
Q

measurable PARAMETERS of drug effect

A
  1. symptom–i.e. pain
  2. sign– i.e. BP
  3. Biological marker
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20
Q

time range during which drug concentration exceeds MEC for desired response

A

Duration of action

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21
Q

dose that results in death of 50% of study population

A

LD50

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22
Q

dose necessary to establish effectiveness in 50% of population

A

ED50

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23
Q

Therapeutic index TI =

A

LD50 / ED50

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24
Q

LD50 sometimes replaced with

A

toxic dose TD

TI = TD50 / ED50

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25
Q

Wide TI implies

A

drug is generally safe–or large dif btwn lethal/toxic dose and ED

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26
Q

narrow TI implies

A

drug has safety concerns– will need close monitoring

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27
Q

Can there be more than one therapeutic index TI for a drug?

A

Yes–for drugs with multiple drug effects (i.e. ibuprofen for pain IN ADDITION TO inflammation) ED may be different depending on symp being treated–window may be narrower

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28
Q

measure for comparing 2+ drugs with equivalent pharm responses

A

Relative potency

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29
Q

refering to pharmacologic response generated at given receptor occupancy

A

potency of drug–EC50 compared

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30
Q

when 2 drugs produce equivalent responses the more potent drug on dose response curve is

A

the drug whose dose response curve lies to the left of the other–less drug required for same effect

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31
Q

chemical termed a “drug” when

A

supplied exogenously

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32
Q

1 receptor– lipid-soluble ligand–pg7 of outline

A

crosses plasma membrane to interact w/ intracellular receptor (enzyme or gene transcription regulator)

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33
Q

2 R–Ligand (drug) binds extracellularly to transmembrane protein

A

activates enzymatic activity within cytoplasm–internal and external domains attached by hydrophobic segment.

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34
Q

enzyme that can transfer a P group from ATP to protein in cell

A

tyrosine kinase– on/off switch for cellular functions

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35
Q

tyrosine kinase subclass of

A

protein kinase

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36
Q

3 R–ligand (drug) binds extracell to transmem protein structurally bound to protein tyrosine kinase

A

becomes activated–same as #2 but tyrosine kinase not intrinsic w/ receptor

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37
Q

4 R–Ligand binds to ion channel

A

activation = opening

  1. mimic endogenous ligands–nt’s
  2. alter membrane potential
  3. work quickly
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38
Q

5 R–metabotropic–ligand attaches to receptor linked to G-protein–components:

A
  1. surface receptor
  2. G protein at cytoplasmic face
  3. change to effector system (ion channel, 2nd mess)
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39
Q

second messenger ex’s: _____, _______, and _______

A

cAMP, calcium, cGMP

40
Q

affinity analogy

A

lock and key–skeleton keys (some keys fit into many locks)

41
Q

if drug-receptor complex is irreversible its likely

A

covalent bond–

42
Q
  • molecule donates e- to + molecule – treatment with “salt”
A

most drugs ionic

43
Q

H+ on molecule attracted to negative on receptor

A

hydrogen bonding–

44
Q

pregnancy risks

A 
A: no risk
B: remote risk
C: benefits outweigh risks
D: evidence of risk--benefits may outweigh risks
X: Contraindicated
45
Q

MEC

A

minimum effective concentration

46
Q

only dif btwn transmembrane proteins 2 & 3

A

“machinery” integrated vs. separate, connected molecule that can detach respectively

47
Q

ionotropic speed

A

miliseconds

48
Q

metabotropic speed

A

fractions of second

49
Q

1 receptor ex

A

lipid soluble–ex. steroid– approx 30 min lag for protein synth

50
Q

agonist broken into

A

full and partial agonist–spectrum

51
Q

partial agonist elicits

A

less than MAXIMUM EFFECT from same tissue as would elicited from total occupancy by full agonis

52
Q

types of antagonists _______ and _______

A

competitive (reversible)–

noncompetitive (irreversible)– typically covalent

53
Q

drug that causes an action opposite to that of the agonist when bound

A

inverse agonist

54
Q

antagonist type that will disallow full agonist rxn despite dose

A

noncompetitive–irreversible

55
Q

iris sphincter muscle activation by parasymp NS

A

miosis–contriction

56
Q

ANS integrated for male sexual function

A

symp=ejaculation

parasymp=erection

57
Q

Always signals coming from ANS but which branch _____ will be based on internal and external environment

A

predominates

58
Q

pt w/ tachicardia give

A

beta blocker–IV–antagonize of sympathetic NS

59
Q

atropine for bradycardia–too much parasympathetic tone on SA node

A

antagonise parasympathetic w/ competitive antagonist for cholinergic muscarinic receptor

60
Q

drug similar to normal functioning of involved receptors

A

-mimetic

61
Q

drug that inhibits or blocks normal functioning of receptors involved

A

-lytic (“destroys”)

62
Q

______ can play part in pharmacokinetics of drug

A

Gender–sexual dimorphism

63
Q

down-regulation of receptors

A

agonist given–body perceives strong signal

64
Q

up-regulation of receptors

A

antagonist given–body perceives weak signal

65
Q

rapid drug tolerance =

A

tachyphylaxis–rapid decrease in effectiveness of drug

66
Q

exaggerated response, respectively, in pt when compared to most ppl

A

hyperreactivity

67
Q

diminished response, respectively, in pt when compared to most ppl

A

hyporeactivity

68
Q

“start low, go slow”

A

titration–when drug has ADR’s that decrease tolerability of drug

69
Q

titration leads to better _______ of drug

A

tolerance– for drugs with low toxic level–i.e. anticoagulants

70
Q

slowing weaning a patient off medication by lowering dose over time

A

tapering–avoid withdrawals–i.e. systemic steroids

71
Q

if tapering pt off drug and symptoms emerge

A

slow taper–same for titration

72
Q

mitigate tolerance by

A
  1. taking break from drug

2. switch to drug with same effect by dif mechanism

73
Q

Most drugs produce several effects, _____ _______, is wanted for treatment

A

therapeutic effect

74
Q

tolerance vs tachyphalaxis

A

tolerance is blanket term for effect over time–tachyphalaxis happens w/in hours/ days/ mins

75
Q

adverse drug rxns ADR’s most appropriately for ________ as opposed to side effects which may be benign

A

unwanted, unpleasant, noxious, or potentially harmful drug effects

76
Q

2 most common ADRs

A
    1. GI disturbance (mostly PO drugs)

2. Allergic rxn

77
Q

GI drug disturbances

A

exs. loss of apetite, nausea, bloating, constipation, and diarrhea –should be considered for ALL ORAL DRUGS

78
Q

Allergic rxn to drug aka

A

hypersensitivity rxn

79
Q

types of hypersensistivity drug rxn’s – all involve immune system

A

type ONE: rapid/immediate after 1st exposure– mast-cell derived–IgE antibodies attach to drug–anaphylactic
type FOUR: rxn delayed–antigen presented to T helper cells–>macrophages and T killer cells destroy target cell.

80
Q

Type four rxn to drug

A

Steven-Johnson syndrome & toxic epidermal necrosis presentation–deadly like burn–happens w/ 1st exposure but slow

81
Q

Type one rxn to drug

A

IgE antibody–requires 1st exposure–presentation w/ urticaria, angioedema, and ANAPHYLAXIS

82
Q

Drug-drug interaction

A

may increase or decrease concentration of other drug in body

83
Q

D-D interaction–increase drug concentration as found by drug plasma concentration

A
  1. inhibit liver enzyme production
  2. slowing excretion by kidney
    - -drugs given based on normal liver function
84
Q

D-D interaction–decreased drug concentration

A
  1. decrease absorption of drug–i.e. lower stomach pH
  2. increase metabolism– ^ liver enzyme–may look like drug tolerance to clinician (dangerous)
  3. increase excretion–
85
Q

smoking can ________ activity of some ______ ________, thus decreasing effectiveness of some drugs

A

increase, liver enzymes

86
Q

increasing urine acidity will

A
  1. decrease acidic drug excretion

2. increase basic drug excretion

87
Q

decreasing urine acidity will

A
  1. increase acidic drug excretion

2. decrease basic drug excretion

88
Q

drug-drug interaction in terms of pharmacodynamics

A

are those where the magnitude of the drug effect is changed

89
Q

2+ drugs with same ingredient have added effect/ADR adverse drug rxn

A

DUPLICATING effect–particularly dangers with OTC drugs–risk toxicity

90
Q

2+ drugs with same effect taken

A

DUPLICATING effect– D-D interaction

91
Q

2+ drugs taken with opposite action

A

OPPOSING effect–decreased efficacy of one or both

92
Q

Anticholinergic side effects

A 
hot as a hare
dry as a bone
blind as a bat
red as a beet
mad as a hatter
93
Q

a ________ __________ or ________ _________ book can be checked for drug-drug interaction

A

reference book or computer program

94
Q

most important drug-drug interaction DDI to think abt

A

hepatic enzyme INDUCTION or INHIBITION

95
Q

pt taking multiple drugs–increase DDI risk

A

polypharmacy

96
Q

age risk for DDI

A

newborns and elderly have lower physiological function

97
Q

________and _________ diseases will greatly effect drug’s ________and ________

A

liver and renal

metabolism and excretion

Fundies First Module--First Exam (13 decks)

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