Pharmacology: Basic Concepts Flashcards

1
Q

Pharmacology

A

Study of drugs and their interactions with living systems

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2
Q

Therapeutics

A

The use of drugs to diagnose, prevent pregnancy, or treat disease states

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3
Q

Pharmacokinetics

A

The study of how living systems process drugs

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4
Q

Pharmacodynamics

A

The study of how drugs affect living systems

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5
Q

Pharmacogenomics

A

The study of how genetics affect our drug response

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6
Q

ADME: what does it stand for and does it fall under pharmacokinetics or pharmacodynamics?

A

Absorption, Distribution, Metabolism, Excretion

Pharmacokinetics

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7
Q

Drug-receptor interactions, patient’s functional state, placebo effects… these fall under pharmacokinetics or pharmacodynamics?

A

Pharmacodynamics

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8
Q

Schedule I Drugs

A

High abuse potential with no accepted medical uses

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9
Q

Schedule II drugs

A

High abuse potential WITH accepted medical uses (opiates, methylphenidate)

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10
Q

Schedule III drugs

A

Abuse potential, but less than I or II

(Codeine, steroids, pseudoephedrine - IN OREGON ONLY). Can differ from one state to the next.

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11
Q

Schedule IV drugs

A

Include benzos

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12
Q

Schedule V drugs

A

Include cough medicine

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13
Q

Pregnancy Categories A, B, C, D, X

A

A: no risk to fetus in 1st trimester
B: no well controlled human studies, but no risk in animal studies
C: animal studies have adverse effects, but in humans benefits outweigh risks
D: Fetal risk. Only really ok if no safer alternative
X: Fetal abnormalities. Don’t use

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14
Q

Clinical trial Phase I purpose

A

First in human studies
Healthy volunteers
Know what they’re taking.
Goal is to assess safety and tolerability

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15
Q

Clinical Trial Phase II

A

First in patient studies
Patients receive drug
Randomized, controlled, maybe blind
Goal: correct dose and efficacy

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16
Q

Clinical Trials phase 3

A

Hundreds of thousands of patients
Randomized, controlled, maybe blind
Best phase to gather info from.

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17
Q

Clinical Trials phase IV

A

Post-marketing surveillance.

DDIs, AEs.

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18
Q

Simple Occupancy Theory

A

The number of places a drug binds to a receptor is proportional to the intensity of the effects.

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19
Q

Modified Occupancy Theory

A

Strength of the attraction between drug and receptor affects the potency of the drug. Drugs with lower affinity require higher concentrations to bind.

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20
Q

Intrinsic activity

A

The ability of a drug to activate a receptor to produce an effect

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21
Q

Noncompetitive antagonists

A

Bind irreversibly to an allosteric site
Fewer available receptors reduces the maximum possible effect.
Adding more agonist doesn’t help because the receptor sites have changed.

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22
Q

Competitive antagonists

A

Compete for receptors with equal affinity as the agonists.

Bind reversibly, so whichever has the most creates the strongest effect.

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23
Q

Partial agonists

A

Can’t produce a 100% effect, no matter how much you give.

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24
Q

Receptorless drugs

A

Antacids, laxatives, chelating agents

25
Q

Dose response curve: Pharmacodynamics or Pharmacokinetics?

What’s the x-variable and what’s the y-variable?

A

Pharmacodynamics.
X-variable: concentration of the drug
Y-variable: effect or response

26
Q

Relative potency

-does it affect maximal efficacy?

A

The amount of a drug needed to produce an effect.

Has nothing to do with maximal efficacy.

27
Q

EC50

A

The concentration of a drug that produces a specific response intensity in 50% of the population

28
Q

ED50

A

The dose of a drug that produces the same response in 50% of the population.
Aka: “median effective dose”

29
Q

The smaller the ED50, the _____ potent

A

More

30
Q

Therapeutic Index or Therapeutic window

How to calculate?

A

How safe a drug is.
The higher the TI, the safer the drug.

Toxic dose/(dose needed for therapeutic response)
LD50/ED50

31
Q

Factors in bioavailability of a drug

A
Rate of dissolution
Surface area
Blood flow
Lipid solubility of a drug
Ph partitioning
Route of administration
32
Q

Ion trapping

A

Acidic drugs accumulate on the alkaline side of a membrane, while basic drugs accumulate on the acidic side of a membrane

33
Q

Percutaneous route

A

Lipid soluble

Massaging increases absorption

34
Q

When can non-lipid soluble drugs enter the BBB?

A

Only when they have a transport system to get across. All other drugs must be lipid-soluble.

35
Q

ABC transporters - what does it stand for? What do they rely on?

A

ATP Binding Cassette transporter

Rely on ATP
Use P-glycoproteins (site of many DDIs). If blocked, can affect absorption.

36
Q

SLC transporters

A

Solute Carrier Transporters

Don’t use ATP.
Facilitated transport and ion-coupled secondary active transport.

37
Q

Protein bound drugs - what does this mean?

A

Bound to albumin

Won’t cross membranes if bound (bonds are reversible)

38
Q

Where does metabolism of drugs usually happen? What does it mean?

A
At the liver, usually. 
Means the enzymatic alteration of the structure of the drug. 
Form metabolites (usually inactive, but sometimes active).
39
Q

Prodrug

A

When a drug becomes active AFTER metabolism by the liver.

40
Q

Phase I of drug metabolism - what is it?

A

Chemical process - oxidation/reduction/hydrolysis

-modifies functional group or breaks into smaller pieces

41
Q

Phase II of drug metabolism - what is it?

A

Conjugation with an endogenous substance. Allows for better excretion by forming a more polar molecule.

42
Q

What are drug-metabolizing enzymes? Which are the major ones?

A
The enzymes that metabolize in Phase I. 
Cytochrome P450s (P450 or CYP): major hepatic enzymes
43
Q

Transferases - what do they do? What phase of drug metabolism are they associated with?

A

Transfer endogenous substances onto drugs.

Phase II of drug metabolism.

44
Q

Why does the first pass effect happen? What is the bioavailability of oral meds as a result?

A

Because the drug goes from the GI tract to the liver before entering systemic circulation.
Oral meds have a 0.5 bioavailability because of this.

45
Q

What is enterohepatic recirculation?

A

Repeating cycle that brings drug from liver to bile to GI tract and back. Requires glucaronidation.

46
Q

What are the 3 processes of renal excretion?

A
  1. Glomerular filtration
  2. Passive tubular reabsorption
  3. Active tubular secretion (needs ATP)
47
Q

What is the time-concentration curve?

A

Demonstrates the relationship between the time after administration and the drug concentration in the body

48
Q

What is the Therapeutic Range? What’s the equation?

A

In the time-concentration curve, the range between minimum toxic concentration and the minimum effective concentration.
MTC-MEC

49
Q

How many half-lives are needed to eliminate a drug from the system?

A

4

50
Q

What happens to the half-life of a drug in renal failure?

A

The half-life increases

51
Q

Direct chemical or physical interactions between drugs consist of what? What are two big rules?

A

Usually in an IV solution.
Big rules: don’t administer if you see precipitate.
Never combine drugs in the same container unless you know a reaction won’t occur.

52
Q

Pharmacokinetic interactions consist of what?

A

Medications that alter another’s ADM or E.
Ex:
-affect transporters like p-glycoproteins
-affect metabolism like CYP enzymes (induce or inhibit)

53
Q

Pharmacodynamic drug interactions - where are they likely to happen?

A

Can be at same receptor (usually inhibitory)

Or at separate sites (potentiative or inhibitory)

54
Q

What’s the problem with grapefruit juice?

A

It can inhibit CYP3A4 metabolism of certain drugs.

55
Q

What effect does St John’s Wort tend to have on drugs?

A

It induces drug-metabolizing enzymes, reducing blood levels of many drugs.

56
Q

Iatrogenic disease

A

Drug induced disease (like Parkinson’s symptoms created by antipsychotics)

57
Q

If you’re checking for aspartate aminotransferase and alanine aminotransferase, you’re checking what?

A

LFTs

58
Q

What’s the difference between pharmacogenetics and pharmacogenomics?

A

Pharmacogenetics refers to differences in a single gene and how it alters drug responses, while pharmacogenomics refers to differences in multiple genes and how it affects drug response.

59
Q

Genetic polymorphism

A

Variation in genetic code. (Ex: CYP2D6 and codeine metabolism). Can affect protein structure, metabolism speed, qty, or nothing at all.