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Pharm > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

medication error

A

a mistake made during the ordering or administration of a medication

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2
Q

adverse drug event (ADE)

A

harm resulting from the use of a medication, regardless if an error was made.

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3
Q

adverse drug reaction (ADR)

A

an adverse drug event that was unpreventable and NOT caused by an error. ADR may warrant a change in therapy.

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4
Q

5 steps of the drug-use process

A 
assess
select optimal regimen
dispense + counsel
administration
monitor & follow up
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5
Q

evidence based pharmacology: 3 degrees of sophistication

A

1st degree- reviews of EBP guidelines and textbooks with evidence links
2nd degree- electronic database of systematic reviews/meta analysis
3rd degree- lit searches using electronic database (lexicomp, etc)

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6
Q

intended drug effect vs adverse effect

A

intended “on target” effect - drug does what it is supposed to.
adverse effect - drug has another effect outside of intended effect. this can be negative or can cause the drug to be used to a separate benefit (ie latisse)

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7
Q

G protein coupled receptor process

A

GDP is bound to the protein complex at rest. When agonist/ligand binds, GDP exchanges into GTP (cellular energy). The subunit is activated (beta, gamma, alpha) by this energy and moves across the cell membrane. Alpha will find the effector protein and illicit the desired response.

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8
Q

G coupled protein receptor: Gs

A

Effector protein: inc adenylyl cyclase

effect: inc cAMP

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9
Q

G coupled protein receptor: Gi

A

effector protein: dec adenylyl cyclase

effect: dec cAMP, inc K efflux

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10
Q

G coupled protein receptor: Gq

A

effector protein: inc PLC-Beta

effect: inc Ca2+

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11
Q

G coupled protein receptor: G12

A

effector protein: inc Rho

effect: contractility, shape

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12
Q

How do opiates or cannabis prevent pain pathway from firing?

A

they both effect K+ channels by activating GIRK channels which efflux K+. This causes hyperpolarization.

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13
Q

3 Types of Ion Channels

A

Voltage gated
Ligand gated
G protein gated

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14
Q

Voltage gated Na+ channel explanation

A

Na+ channels will be blocked by drug. Inhibitory effect takes place because negative membrane potential is maintained. Hyperpolarization may occur, meaning it will take more stimulation for depolarization to occur.

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15
Q

Voltage gated Ca2+ channel explanation

A

Calcium channel is blocked. Membrane potential cannot get more positive to depolarize.

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16
Q

Two types of ligand gated ion channels

A

excitatory and inhibitory

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17
Q

ligand vs voltage gated channels

A

ligand gated channels- aiming to depolarize thru excitatory (glutamate) or hyper polarize (GABA)
voltage- blocking the channel, preventing influx of cations.

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18
Q

Excitatory Ligand Channels (and who is regulating them?)

A

these facilitate the movement of cations to cause depolarization (ie influx of ca2+)
GLUTAMATE

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19
Q

Inhibitory ligand channels (and who regulates them?)

A

conducts the movement of chloride to cause hyperpolarization (ie: cl- influx keeps membrane potential negative and even hyper polarized)
GABA

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20
Q

ligand gated ion channel: drugs that act on them act by

A

regulating the influx of ions into the cell in order to preserve or alter the membrane potential.

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21
Q

drugs that act on ligand gated Cl- receptor act by ____ (and who activates it?)

A

gaba activation causes influx of Cl-, hyperpolarizing the membrane potential, making it unable to depolarize.

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22
Q

Drugs that act on ATP gated K+ channel

A

anti diabetic drugs inhibit the K+ (efflux) channel. This leads to depolarization, opening of Ca channels, and downstream anti diabetic effects.

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23
Q

enzyme linked receptor activation and response

A

when activated by the agonist, they phosphorylate other proteins.

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24
Q

main channel for enzyme linked receptors

A

insulin channel

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25
Q

enzyme linked receptors - intrinsic

A

capacity to phosphorylate other proteins. intrinsic relies on protein kinases.

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26
Q

enzyme linked receptors: extrinsic

A

capacity to phosphorylate associated protein kinases

27
Q

what occurs after insulin binds to an insulin receptor?

A

the receptor’s intrinsic kinase activity is activated -> autophosphorlyation

28
Q

IRS proteins and Shc function and (4) outcome

A

Important role in translocation of glucose transporters to cell membrane.
outcome: cell growth, protein synthesis, glycogen synthesis, glucose transport.

29
Q

Cbl/CAP protein kinase

A

facilitates translocation of glut4 onto cell membrane. once there, can have intake of glucose from blood into cell for use/storage.

30
Q

Enzyme linked receptor agonist example

A

what insulin is to an insulin receptor

31
Q

nuclear receptors are typically what kind of receptors?

A

steroid

32
Q

how do nuclear receptors work?

A

steroid hormone outside of cell reaches nuclear (steroid) receptor and can then go into the cell to have its effect on the nucleus, initiating gene transcription.

33
Q

steroid/nuclear receptor “chaperone” & function

A

HSP complex allows the receptor to float around in the cell. The receptor stays with the HSP complex until a hormone binds to it. then the receptor will go into the nucleus and initiate gene transcription.

34
Q

drugs that act on nuclear receptors (steroid): 3 examples

A

synthetic glucocorticoids
anti androgens
tamoxifen

35
Q

patient education for nuclear receptor drugs

A

onset of clinical effect can take up to 6 months. ie: pt with bPH may not notice reduction in symptoms for a little while.

36
Q

Passive vs Active transport

A

passive: high to low concentration down the gradient. no energy required.
active: some type of energy required for concentration to go against the gradient.

37
Q

primary active transport

A

requires atp to move ions uphill

38
Q

secondary active transport

A

via symport or antiport

39
Q

symport

A

ion going from low to high concentration uses the energy of another ion going in that same direction.

40
Q

antiport

A

uses the energy of another ion going across the gradient to go against the gradient. two different ions going in two different directions but using the same energy.

41
Q

P-glycoprotein inhibitors (aka pgb inhibitors)

A

Pgp is an efflux pump which pumps meds out of a cell. if you’re inhibiting this pump, you’re not allowing meds to be pumped out of a cell. Always be careful with drug-drug interactions when you see a patient is taking something that is a pgb-inhibitor.

42
Q

drugs targeting enzymes are typically ____ them

A

inhibiting

43
Q

reversible enzyme inhibition

A

usually competitive. drug and substrate are competing for the same site. as other competitive substrates come around, it’s easy for them to bind too. this means that if the dose isn’t adequate, the med may not be as effective. ie: statins

44
Q

irreversible enzyme inhibition

A

always based on a strong covalent bond between the drug and the enzyme. this prevents breakage from the receptor until the biologic process is complete. ie: ASA forms covalent bond with subunit and blocks any prostaglandins from arachidonic pathway and causing pain. there may be other substrates sensitive to the site, but the covalent bond is not letting any others bind until its job is done.

45
Q

receptor ligand agonist

A

endogenous or synthetic entity that ACTIVATES the receptor its directed for. expect downstream effect. (full or partial)

46
Q

receptor ligand antagonist

A

almost always a synthetic thing that PREVENTS THE ACTIONS OF ANOTHER LIGAND (ie: agonist) at the receptor to which it is directed. they block the action, preventing the downstream effect.

47
Q

neutral/pure antagonist does what?

A

prevents any other form of binding

48
Q

inverse antagonist

A

will bind and exhibit opposite effect of what an agonist would normally do.

49
Q

occupation is governed by

A

affinity. high affinity for receptor means drug will readily/quickly/more often bind to that receptor.

50
Q

activation is governed by

A

efficacy. if drug activates a receptor, it’ll have efficacy.

51
Q

dose response curve: max dose

A

max clinical effect achieved. if you keep increasing dose at this point you may not have greater efficacy but you may have greater side effects.

52
Q

drug potency (and what it is referred to as)

A

concentration/dose of drug required to achieve certain effect. typically referenced to EC50 or ED50. The lower the EC50 or ED50, the higher the potency.

53
Q

drug efficacy meaning and AKA

A

magnitude of the drug’s action at the limit of its concentration or dose. Referred to as Emax. The greater the Emax, the greater the efficacy.

54
Q

EC50 or ED50

A

50% of the mediations maximum effect. (c = conc, d = dose)

55
Q

Emax

A

value representing magnitude of drug’s action

56
Q

therapeutic index equation

A

Toxic dose for 50% of population divided by effective dose for 50% of population.

TD50/ED50

57
Q

drugs with narrow therapeutic index

A

not a lot of room between therapeutic and toxic. ie warfarin, digoxin. monitor its closely on these meds.

58
Q

drug-drug interaction: digoxin and k wasting diuretics

and what is the binding site?

A

digoxin and K+ bind to the same site (H+ K+ ATPase). If your serum K is low, more digoxin can bind to receptor. increased therapeutic effect, digoxin toxicity.

59
Q

drug-drug interaction between albuterol (b agonist) and propranolol (b antagonist)

A

interaction where albuterol effects won’t be achieved bc of beta blocker.

60
Q

drug-drug interactions of sildenafil

A

potentiates organic nitrates to cause severe hypotension

61
Q

drug-drug interactions with MAOIs

A

they potentiate tyramine

62
Q

drug-drug interactions with anti histamines and alcohol

A

they act synergistically to cause sedation.

63
Q

G protein gated ion channels are opened/closed when

A

a G protein coupled receptor (GPCR) is activated, alpha subunit binds to effector protein, causing a separate ion channel to open/close.

Pharm (31 decks)

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