Intro to Pharm Flashcards

(72 cards)

1
Q

A dose-response curve is an example of?

A

Pharmacodynamics

“drugs on body”

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2
Q

What is the most dangerous schedule of drugs w/ no recognized medicinal use?

exs: heroin, marijuana

A

Schedule I

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3
Q

Drugs in this schedule have high abuse potential but accepted medicinal use

exs: oxycodone, adderall

A

Schedule II

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4
Q

Drugs in this schedule have high (but less than II) abuse potential, but accepted medicial use

exs: vicodin, ketamine, testosterone

A

Schedule III

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5
Q

Drugs in this schedule have lower abuse potential + accepted medicinal use

exs: xanax, soma, valium, ambien, Robitussin AC, lyrica

A

Schedule IV + V

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6
Q

In this phase of clinical testing researchers test an experimental drug/treatment in a small group of people (20-80) for 1st time to evaluate safety

“clinical pharmacology”

A

Phase I

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7
Q

In this phase of clinical testing, experimental tx given to a larger group (100-300) to see if its effective and to further evaluate its safety

“clinical investigations”

A

Phase II

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8
Q

In this phase of clinical testing, tx given to larger groups (1,000-3,000) to confirm its effectiveness, monitor SEs, compare it to commonly used tx and collect info for it to be used safely

“clinical trials”

A

Phase III

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9
Q

In this phase of clinical testing, postmarketing studies delineate add. info (risks/benefits/optimal use); phase never stops

“post marketing studies”

A

Phase IV

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10
Q

Which is safer: a drug w/ a low or high TI?

A

High TI (TD1/ED1 = minimum toxic dose is large, minimum effective dose is small)

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11
Q

What is a drug’s site of action?

A

Receptor

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12
Q

Estrogen replacement is what type of drug action?

A

Replacement

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13
Q

What type of drug action happens when anti-hypertensives interfere w/ vasoconstriction?

A

Interruption

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14
Q

What type of drug action is a diuretic?

A

Potentiation

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15
Q

What are drugs that combine w/ a receptor, activate it and produce the same response as an endogenous chemical or stimulate release of endogenous chemical?

A

Agonist

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16
Q

The capacity of a single drug-receptor complex to evoke a response is known as?

A

Intrinsic activity

  • Agonists have intrinic activity (affinity for a receptor + efficacy)
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17
Q

What are drugs that combine w/ a receptor used by an endogenous chemical and block/diminish response of the endogenous agent?

A

Antagonists

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18
Q

What are drugs the have affinity but low efficacy?

A

Partial agonists

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19
Q

What is it called when agonists and antagonists compete for the same receptor site?

A

Competitive antagonism

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20
Q

What is it called when agonist and antagonist bind at different sites on the same receptor?

A

Non-competitive antagonism

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21
Q

If the dose of drug A is less than drug B to achieve the same response, what is drug A?

A

More potent

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22
Q

What is the magnitude of the maximum effect called?

A

Efficacy

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23
Q

What is rapid drug tolerance called?

A

Tachyphylaxis

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24
Q

This type of hypersensitivity is an anaphylactic rxn mediated by IgE. Involves release of histamine, prostaglandins, and leukotrienes. Sx: urticaria, rash, vasodilation, hypotension, edema, inflamm, rhinitis, asthma, tachycardia. Ex: Penicillin

A

Type I

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25
This type of hypersensitivity rxn is a cytolytic rxn mediated by IgG and IgM. Affects cells of circulatory sx. Sx: hemolytic anemia, thrombocytopenia, granulocytopenia. These autoimmune rxns subside several months after drug discontinuation. Exs: quinidine, methyldopa
Type II
26
This type of hypersensitivity rxn is an arthus rxn mediated by IgG. Immune complexes are deposited in vascular endothelium -\> serum sickness. Sx: erythema multiforme, arthritis, nephritis, CNS abnormalities, myocarditis, SLE, Steven-Johnson syndrome. Exs: sulfonamide abx
Type III
27
This is a delayed hypersensitivity rxn mediated by T-lymphs and macrophages. When sensitized cells come in contact w/ antigen, lymphokines cause an inflamm rxn. Exs: poison ivy, abx, benzocaine
Type IV
28
What is an unusual response to a drug called?
Idiosyncratic rxn
29
What's important to do (especially with low TI meds) if TE is not observable?
Check blood/plasma levels (hyporeactive)
30
Which drugs cross membranes more readily?
Lipophilic * Drugs are usually weakly acid or weakly basic -\> in some pH ranges charged, in others uncharged -\> uncharged form = lipid soluble
31
Most drugs pass through membranes by this mechanism; diffuse down the concentration gradient.
Passive diffusion
32
In this mechanism drugs pass w/ concentration gradient, but requires a carrier protein.
Facilitated diffusion
33
In this mechanism drugs go against concentration gradient and requires ATP.
Active transport
34
In this mechanism drugs move by formation and movement of vesicles (packages) across membranes and requires energy.
Pinocytosis
35
Drugs that are well absorbed from the GI tract and are metabolized in liver, have decreased bioavailability as a result of this.
First-pass effect
36
List these in order of solubility: tablets, capsules, suspensions, solutions
Solutions \> suspensions \> capsules \> tablets
37
This type of administration is safest, easiest, cheapest; Absorption occurs in the 1st 3rd of SI, but some drugs can't be absorbed
PO
38
This type of administration is used for very highly lipid soluble or potent drugs; bypasses harsh GI and avoids first-pass effect
SL
39
This type of administration is only useful when oral is not possible; most drugs irritate this area's mucosa and their absorption is unpredictable/variable
Rectal (PR)
40
This type of administration has no absorption phase, accurate, immediate, irreversible, must be aqueous.
IV
41
This type of administration has a slower onset and longer duration than IV, absorption is delayed and is related to vascularity.
IM
42
This type of administration has a slower onset and longer duration than IM b/c fat is less vascular than muscle.
SQ, SC
43
This type of admin. has a local drug effect; Creams, lotions, etc.
Topical
44
This type of admin. crosses skin and enters circulation for systemic effect.
Transdermal
45
This type of amin. has very rapid onset, extremely large SA for absorption and good blood supply; Used mostly for a local effect.
Aerosols
46
What is the partition between the 2 compartments dependent upon?
1. Lipid/protein content 2. pH 3. Osmotic pressure 4. Blood supply
47
Drugs that are bound to anything (other than a receptor) are \_\_\_\_\_.
Inactive
48
What is one of the most restrictive membranes and is highly lipophilic?
BBB
49
What is a less restrictive membrane?
Placental barrier ASSUME ALL DRUGS WILL CROSS
50
Where does metabolism of drugs primarily occur?
In liver (also in GI tract, lung, skin/kidneys)
51
The goal of this phase of metabolism is to make a more polar/hydrophilic metabolite that can be excreted. It involves non-synthetic oxidation (CP450) reduction, hydrolysis.
Phase I
52
If the metabolite created in phase I of metabolism is not sufficiently polar, what happens?
Phase 2: synthetic - conjugation (glucoronidation, sulfonation)
53
This isoform of C450 is the most common in CYP-mediated metabolism (50%); its substrates are benzos, HIV drugs, Ca2+ channel blockers.
CYP3A4
54
This isoform of C450 is the 2nd most common in CYP-mediated metabolism (30%); its substrates are psychotropics, codeine, beta-blockers, anti-arrhythmics. Also most studied polymorphism.
CYP2D6
55
This isoform of C450 is the least common in CYP-mediated metabolism (10%); its substrates are phenytoin, warfarin, NSAIDs.
CYP2C9
56
What effect do enzyme inhibitors have on bioavailability?
Increase
57
What effect do enzyme inducers have on bioavailability?
Decrease
58
A response to a drug is often linked to these DNA variations; variations in the human genome.
SNPs
59
What does decreased alcohol/aldehyde dehydrogenase in Asians lead to?
Increase in cancer in URT
60
What is associated with G6PD deficiency in 14% African Americans?
RBC hemolysis w/ sulfa drugs
61
What do "slow acetylators" (common in middle east pop) have an increased risk for?
Higher INH levels, higher risk for ADRs (hepatitis, peripheral neuropathy) * "Fast acetylators" -\> lower INH levels -\> lower therapeutic efficacy (common in Japanese)
62
Drugs are eliminated uncharged or as metabolites via what 3 routes?
1. Kidney 2. Feces 3. Breast milk
63
More alkaline urine will increase excretion of \_\_\_\_\_\_; more acidic urine will increase excretion of \_\_\_\_\_\_\_.
Weak acid; weak base
64
When rate of administration = clearance
Steady state
65
How do you find the elimination half-life (time it takes for drug to be completely eliminated from sx)?
T1/2 x 5
66
What is the drug interaction when combined effect \> sum?
Synergism
67
What is the drug interaction when inactive drug increases effect of another?
Potentiation
68
What is the drug interaction when one drug increases drug-metabolizing enzyme activity of another (decreasing bioavailability)?
Induction
69
What is the drug interaction when one drug blocks another drug's metabolism/excretion?
Inhibition
70
What is the drug interaction when one drug displaces another from protein binding site (increasing bioavailability)?
Unbinding
71
Which categories of drugs are safe in pregnant women?
A - only one w/ human studies showing no risk B + C - animal studies show no risk, no human studies done
72
Which categories of drugs aren't safe in pregnant females?
D - human studies show a risk X - absolutely don't use