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Pharm Exam 1 > Intro to Pharm > Flashcards

Intro to Pharm Flashcards

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
Q

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

A

Type II

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26
Q

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

A

Type III

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27
Q

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

A

Type IV

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28
Q

What is an unusual response to a drug called?

A

Idiosyncratic rxn

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29
Q

What’s important to do (especially with low TI meds) if TE is not observable?

A

Check blood/plasma levels (hyporeactive)

30
Q

Which drugs cross membranes more readily?

A

Lipophilic

  • Drugs are usually weakly acid or weakly basic -> in some pH ranges charged, in others uncharged -> uncharged form = lipid soluble
31
Q

Most drugs pass through membranes by this mechanism; diffuse down the concentration gradient.

A

Passive diffusion

32
Q

In this mechanism drugs pass w/ concentration gradient, but requires a carrier protein.

A

Facilitated diffusion

33
Q

In this mechanism drugs go against concentration gradient and requires ATP.

A

Active transport

34
Q

In this mechanism drugs move by formation and movement of vesicles (packages) across membranes and requires energy.

A

Pinocytosis

35
Q

Drugs that are well absorbed from the GI tract and are metabolized in liver, have decreased bioavailability as a result of this.

A

First-pass effect

36
Q

List these in order of solubility: tablets, capsules, suspensions, solutions

A

Solutions > suspensions > capsules > tablets

37
Q

This type of administration is safest, easiest, cheapest; Absorption occurs in the 1st 3rd of SI, but some drugs can’t be absorbed

38
Q

This type of administration is used for very highly lipid soluble or potent drugs; bypasses harsh GI and avoids first-pass effect

39
Q

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

A

Rectal (PR)

40
Q

This type of administration has no absorption phase, accurate, immediate, irreversible, must be aqueous.

41
Q

This type of administration has a slower onset and longer duration than IV, absorption is delayed and is related to vascularity.

42
Q

This type of administration has a slower onset and longer duration than IM b/c fat is less vascular than muscle.

43
Q

This type of admin. has a local drug effect; Creams, lotions, etc.

44
Q

This type of admin. crosses skin and enters circulation for systemic effect.

A

Transdermal

45
Q

This type of amin. has very rapid onset, extremely large SA for absorption and good blood supply; Used mostly for a local effect.

46
Q

What is the partition between the 2 compartments dependent upon?

A
  1. Lipid/protein content
  2. pH
  3. Osmotic pressure
  4. Blood supply
47
Q

Drugs that are bound to anything (other than a receptor) are _____.

48
Q

What is one of the most restrictive membranes and is highly lipophilic?

49
Q

What is a less restrictive membrane?

A

Placental barrier

ASSUME ALL DRUGS WILL CROSS

50
Q

Where does metabolism of drugs primarily occur?

A

In liver (also in GI tract, lung, skin/kidneys)

51
Q

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.

52
Q

If the metabolite created in phase I of metabolism is not sufficiently polar, what happens?

A

Phase 2: synthetic - conjugation (glucoronidation, sulfonation)

53
Q

This isoform of C450 is the most common in CYP-mediated metabolism (50%); its substrates are benzos, HIV drugs, Ca2+ channel blockers.

54
Q

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.

55
Q

This isoform of C450 is the least common in CYP-mediated metabolism (10%); its substrates are phenytoin, warfarin, NSAIDs.

56
Q

What effect do enzyme inhibitors have on bioavailability?

57
Q

What effect do enzyme inducers have on bioavailability?

58
Q

A response to a drug is often linked to these DNA variations; variations in the human genome.

59
Q

What does decreased alcohol/aldehyde dehydrogenase in Asians lead to?

A

Increase in cancer in URT

60
Q

What is associated with G6PD deficiency in 14% African Americans?

A

RBC hemolysis w/ sulfa drugs

61
Q

What do “slow acetylators” (common in middle east pop) have an increased risk for?

A

Higher INH levels, higher risk for ADRs (hepatitis, peripheral neuropathy)

  • “Fast acetylators” -> lower INH levels -> lower therapeutic efficacy (common in Japanese)
62
Q

Drugs are eliminated uncharged or as metabolites via what 3 routes?

A
  1. Kidney
  2. Feces
  3. Breast milk
63
Q

More alkaline urine will increase excretion of ______; more acidic urine will increase excretion of _______.

A

Weak acid; weak base

64
Q

When rate of administration = clearance

A

Steady state

65
Q

How do you find the elimination half-life (time it takes for drug to be completely eliminated from sx)?

66
Q

What is the drug interaction when combined effect > sum?

67
Q

What is the drug interaction when inactive drug increases effect of another?

A

Potentiation

68
Q

What is the drug interaction when one drug increases drug-metabolizing enzyme activity of another (decreasing bioavailability)?

69
Q

What is the drug interaction when one drug blocks another drug’s metabolism/excretion?

A

Inhibition

70
Q

What is the drug interaction when one drug displaces another from protein binding site (increasing bioavailability)?

71
Q

Which categories of drugs are safe in pregnant women?

A

A - only one w/ human studies showing no risk

B + C - animal studies show no risk, no human studies done

72
Q

Which categories of drugs aren’t safe in pregnant females?

A

D - human studies show a risk

X - absolutely don’t use

Pharm Exam 1 (4 decks)

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