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Section 1 Flashcards

1
Q

Pharmacodynamics

A

drug on the body

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2
Q

Pharmacokinetics

A

body on the drug

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3
Q

Tachyphylaxis

A

reduced effect of the drug over time after repeated administration of the same dose of a drug (effect)

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4
Q

Desensitization

A

reduced ability of a receptor to respond to stimulation by a drug or ligand (cause), like PKA, GRK (Arrestin), receptor internalization and can be homo or hetero

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5
Q

Inactivation

A

loss of ability of a receptor to respond to stimulation by a drug

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6
Q

Refractoriness

A

inability of receptor to respond to a drug for a period of time after the first drug-receptor interaction (example in the heart pumps)

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7
Q

Down-regulation

A

reduction in the number of receptors after chronic stimulation by agonists (lysosomal degredation)

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8
Q

Up-regulation

A

increase in the number of receptors after chronic inhibition by antagonists (Beta blockers)

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9
Q

An increase in Kd means what for affinity?

A

decrease in affinity

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10
Q

A decrease in EC50 means what for potency?

A

increase in potency

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11
Q

When you increase the concentration of agonist at Emax or greater what could happen?

A

toxic effects

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12
Q

What does Intrinsic Efficacy compare (hint- it’s on the dose response curve)

A

Emax

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13
Q

What is the Emax (Intrinsic activity) of a full agonist, a partial agonist, and an antagonist?

A 
full agonist (a=1)
partial agonist (0<a><1)
agonist (a=0)
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14
Q

When EC50 < Kd for a full agonist, what does this mean?

A

spare receptors

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15
Q

Can a partial agonist have spare receptors?

A

no

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16
Q

How could a non-comp antag decrease potencyof a full agonist?

A

increase concentration of non-comp antag, but still having a small concentration, and the agonist has spare receptors

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17
Q

Does a non-comp antag effect efficacy or potency?

A

efficacy

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18
Q

Does a comp. antag effect efficacy or potency?

A

potency

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19
Q

When there is an increase of antag with constant agonist what happens to the affinity?

A

it decreases

20
Q

How is potency of antagonists determined?

21
Q

If there is a decrease in IC50, what happens to potency?

A

increased potency

22
Q

Are competitive or non-competitive antagonists surmountable?

A

competitive

23
Q

What do agonists with spare receptors keep constant with a low concentration of non-comp antag?

24
Q

What are other ways of non-receptor antagonism that decrease efficacy but not potency?

A
  1. down stream signaling
  2. opposite physiological effects (2 diff receptors)
  3. chemical antag?
25
Q

What do inverse agonists do?

A

inactivate receptors via their conformation, doesn’t need full agonist to see reverse products

26
Q

What is ED50 and slope of quantal responses?

A 
ED50 = median effective dose
slope = PD variation of population
27
Q

Is a narrow therapeutic index good or bad?

28
Q

a TI <2 is also known as what?

A

a narrow therapeutic index

29
Q

The range btwn ED50 and the start of toxic curve is known as…

A

therapeutic window

30
Q

What does a smaller/flatter slope of the toxic effects mean?

A

greater likelihood of undesirable effects

31
Q

Is CSF (margin of safety) <1% good or bad?

32
Q

What is the therapeutic effectiveness of the drug in humans? (determined by % population responding)

A

clinical efficacy

33
Q

What is the capacity of agonist to activate a receptor?

A

Intrinsic efficacy

34
Q

What is the difference btwn on-target and off-target effects?

A 
on-target = drug hits intended receptor
off-target = unintended receptor
35
Q

difference btwn deleterious and non-deleterious? (Usually due to off-target receptor binding)

A 
deleterious = toxic effects
non-deleterious = side effects
36
Q

Dose-related, extension of desired response, on-target effects due to different tissue receptor dist. are examples of what kind of ADR?

A

Predictable ADR

37
Q

What is it called when there is no cause found to drug toxicity?

A

idosyncratic responses

38
Q

What is Acetaminophen’s antidote?

A

N-acetylcysteine

39
Q

What do you call something that chemically, physically, or biologically insults that cause DNA damage (initiators) OR facilitate in proliferation of mutated cells (promoters)?

A

carcinogens

40
Q

What is the inductions of structural defects in the fetus (usually w/in 3rd trimester)?

A

teratogenesis

41
Q

What are 3 examples of Teratorgens?

A

retinoic acid
isotretinoin
ACE inhibitors

42
Q

What are the 4 types of hypersensitivity immune responses that are drug-induced?

A 
I = Immediate anaphylaxis (IgE) = wheel and flare
II = Ab-dep cytotoxic hyper. = hemolysis
III = Immune complex-mediated hyp, = serum sickness
IV = Delayed-type hyp. = cytokine storm, contact dermititis
43
Q

What is a Hapten?

A

small molecule drug

44
Q

What are 3 types of PD DDIs? (Effects of the body)

A
  1. Additive (1+1=2)
  2. Synergistic (1+1>2)
  3. Antagonism (Agonist + Antag)
45
Q

3 types fo PK DDIs?

A
  1. Metabolism (P450)
  2. Transportation
  3. Protein binding
46
Q

What 2 hypersensitivity drug reactions use haptens?

A 
Immediate anaphylaxis (Type 1) and
Delayed-type hyp. (Type 4)
47
Q

What 2 hypersensitivity drug reactions consider drug the Antigen?

A

Type 2 - Antibody-dep cytotoxic hyp. and

Type 3 - Immune complex-mediated hyp.

Pharmacology 1 (10 decks)

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