Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

POM Final > Introduction to Pharmacodynamics > Flashcards

Introduction to Pharmacodynamics Flashcards

1
Q

Almost all drug targets are…?

A

Proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does an Agonist drug function?

A

Mimics the effects of the endogenous agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does an antaonist drug function?

A

Blocks the effects of endogenous agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Drug-receptor interaction equation

A

Reversible reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the dose-response curve?

A

Shows relationship between ligand/drug concentration and receptor occupancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Kd?

A

The dissociation constant; the concentration of drug at which 50% of receptors are occupied; lower Kd = greater affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the Hill-Langmuir equation?

A

Describes drug affinity curves; Y = [D] / Kd + [D]

Y = % occupancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Potency Vs. Efficacy

A

Potency is dependent on receptor affinity; lower Kd = more potent

Efficacy describes the response

Do not always correlate; receptor occupancy does NOT equal effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Signal amplification

A

affects how we interpret dose response curves; Maximal cellular response at less-then-maximal receptor occupancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the “Receptor reserve”?

A

Receptors that are available for agonist binding, but that are not necessary for maximal effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Competitive vs. Non-competitive Antagonists

A

Competitive: compete for same site; decrease potency (increse Kd); moves curve to the right

Non-Competitive: bind different sites; can be irreversible; decrease efficacy; moves curve down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Full vs. Partial agonists

A

Full: elicits maximal response from receptor

Partial: elicits sub-maximal response from receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a neutral antagonist?

A

Reduces the effect of an agonist, but has no effect itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is an inverse agonist?

A

They inhibit the basal activity of a receptor in the absence of the normal agonist; they are NOT antagonists because they are not competing with endogenous agonist

Can be competitive antagonists TOO if they bind to same receptor site as endogenous agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

5 clinically-relevant inverse agonists/antagonists

A
  1. Metoprolol (β1-adrenergic receptor antagonist); Cardio – Hypertension, angina, congestive heart failure
  2. Losartan (angiotensin II receptor antagonist); Cardio - Hypertension
  3. Famotidine (H2-histamine receptor antagonist); GI – GERD, gastric/duodenal ulcers
  4. Risperidone (D2-dopamine receptor antagonist); Neuro – Schizophrenia, bipolar disorder, autism
  5. Naloxone (m-opioid receptor antagonist); Neuro – Emergency treatment for heroin/opioid overdose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Drugs for treating opioid addiction/overdose

A

Not full-agonists at the m-opioid receptor (MOR)

  1. Full agonists: Endorphins, Morphine, Heroin
  2. Partial agonists: Bupenorphine, Nalbuphine
  3. Neutral antagonist: Naltrexone
  4. Inverse agonist: Naloxone
17
Q

Dose-response curves are useful for describing effects that are:

A

Continuous; reduction of pain, BP, anxiety, etc.

18
Q

Dose-response curve for quantal variable

A

The curves shows the % of patients responding; cumulative % of patients exhibiting the therapeutic effect

19
Q

Dose-response curve y-axes (6)

A
  1. Receptor occupancy
  2. Activation of intracellular signaling intermediate
  3. Cell-level physiological effect
  4. Organ-level physiological effect
  5. Organ-system-level physiological effect
  6. Patients responding
20
Q

Drug effects

A

Therapeutic Effect (ED50)

Toxic Effect (TD50)

Lethal Effect (LD50)

21
Q

Therapeutic window and Index

A

The range of drug concentrations between the minimum effective dose and the minimum toxic dose

TI = TD50/ED50 or LD50/ED50; higher is better

22
Q

Why might the shape of the dose-response curve be different for the therapeutic vs. toxic effects?

A

Because different receptors may account for the therapeutic and toxic effects

23
Q

What is the certain safety factor (CSF)?

A

CSF = LD1/ED99

Higher is better

Important for off-target toxicity

24
Q

Synergism, additivity, and antagonism

A

When two drugs have the same therapeutic effect

25
Q

Potentiation

A

When one drug has a therapeutic effect, and a second drug helps it

Probenecid has no antibiotic effect of its own, but potentiates the effect of the antibiotics (Cephalosporins, penicillins in serum) –> causes increased serum [drug] & prolonged therapeutic effect

26
Q

Tolerance/Desensitization

A

Reduced effect with continued use of a drug; Short-term: tachyphylaxis

  1. receptor inactivation
  2. receptor internalization
  3. receptor down-regulation

POM Final (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions