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PAS 753 (Molecular Pathophysiology) > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

three names used to identify a drug

A
  1. chemical name
  2. generic
  3. trade name
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2
Q

T/F groups of generic drugs usually have vastly different names

A

false, drugs in the same family tend to have similar names, especially the suffix

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3
Q

what is the FDAs legal mandate

A
  • drugs must have a favorable benefit/risk ratio
  • drugs must have phased trials that prove utility and safety
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4
Q

phases of a clinical trial (5)

A
  • preclinical
  • phase I
  • phase II
  • phase III
  • phase IV
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5
Q

preclincial trials

A

focuses on animal testing to deteremine toxicity

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6
Q

phase I trials

A

testing a small group of healthy subject to determine a drug doesnt cause disease

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7
Q

phase II trials

A

testing on ill patients

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8
Q

Phase III trials

A

main trial to determine risk, usually many subjects in many locations

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9
Q

phase IV trials

A

post-marketing surveillance

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10
Q

what would be the different mandates needed to be met in developing a drug for tension headaches vs small cell lung cancer

A

tension headaches already have effective treatment, so the new treatment but be both safer and effective than the current treatment

small cell lung cancer doesn’t have an effective treatment so a lower risk/reward ratio is acceptable

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11
Q

what similarities are common in the same drug class

A
  • biochemisty
  • indications
  • mechanism
  • side effects
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12
Q

T/F drugs in the same family are basically identicl

A

false

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13
Q

what is the main method of drug action

A

interatction with cell receptors

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14
Q

what is the main determinant of a drugs level of effect

A

the amount of the drug in the blood

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15
Q

what is an example of a tissue that is impermeable to most drugs

A

the blood brain barrier, choroid plexus

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16
Q

what are two factors that influence the amount of a drug found in the blood

A

drug absorption and elimination

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17
Q

what are two main methods of drug elimination

A

hepatic and renal

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18
Q

four main receptor types

A
  1. ligand gated ion channels
  2. G protein linked receptors
  3. enzyme linked receptors
  4. intracellular receptors
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19
Q

why is a proton pump inhibitor more effective treatment of heartburn than inhibiting gastrin, histamine, or AcH

A

because gastrin, histamine, and AcH all feed into the proton pump, if you block the pump the action of the other three don’t matter

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20
Q

T/F one ligand fits a receptor best, and most other ligands don’t fit at all

A

true, but specificity isn;t perfect only relative to others

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21
Q

what is necessary for a ligand to activate a receptor

A

high ligand concentration

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22
Q

cross reactivity

A

the ability for a ligand to activate closely related receptors

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23
Q

receptor regulation

A

as ligand increases, receptor production decreases

decreasing ligand concentration increases receptor production

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24
Q

how does excessive or constant administrion of a drug limit its effectiveness

A

down regulation of receptors

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25
Q

what is an example of a drug that will get less effective with frequent use

A

beta II agonist inhaler

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26
Q

what are three ways the clinical intervention can manipulate ligand receptor interaction

A
  1. increase/decrease ligand concentration
  2. changing receptor function
  3. changing receptor affinity
27
Q

two primary routes of drug adminstration

A
  1. enteral
  2. parenteral
28
Q

two routes of enteral adminstration

A

oral and rectal

29
Q

6 methods of parenteral adminstration

A
  1. intravenous
  2. intramuscular
  3. subcutaneous
  4. transdermal
  5. inhaled
  6. transmucosal
30
Q

what are three pros of oral administration

2 cons

A

pros: cheap, easy, concentrated effect on the esophagus and stomach
cons: absorption issues, first pass effect

31
Q

first pass effect

A

any drug adminstered orally must first pass through the liver and be metabolized before it can enter the blood

32
Q

5 key questions to decide between enteral vs parenteral

A
  1. is the drug compatible with either method
  2. oral restrictions
  3. need for rapid onset
  4. better dosing with one method or the other
  5. is the patient compliant for enteral dosing
33
Q

why are adverse drug reactions so common

A
  • polypharmacy
  • lack of compliance
34
Q

four majo causes of ADRs

A
  1. allergic reactions
  2. inherent drug toxicity
  3. dosing errors
  4. drug interactions
35
Q

what percent of ADRs are caused by allergies

A

5-10%

36
Q

in the case of an allergic reacton to a drug, what are two possible causative factors

A

reaction to the drug itself or its metabolite or delivery method

37
Q

theraputic index

A

the comparrison of the blood concentration needed for a drug to have a theraputic effect vs the level that produces toxicity

38
Q

narrow theraputic index

A

there is little margin between a theraputic dose and a toxic dose

39
Q

two key issues in understanding drug interactions

A
  1. we don’t know all the OTC, herbal, or illegal substances being used
  2. not everyone has the same reactions to a drug
40
Q

a good philosophy when prescribing

A

use as much as necessary but as little as possible

41
Q

pharmacogenomics

A

the study of genetic influences that produce variations in drug metabolism

42
Q

two processes of drug metabolism

A
  1. absorption
  2. elimation
43
Q

two phases of elimination

A

phase I (oxidation)

phase II (conjugation)

44
Q

what happens in phase I elimation

A

the drug is usually rendered inactive through oxidation

45
Q

what happens in phase II elimination

A

the drug is conjugated with bile or urea to be more soluable in feces or urine

46
Q

what is CYP-450

where is it found

what does it do

A

cytochrome p450 enzymes

found in the liver or GI tract

phase I oxidation

47
Q

how is a drug eliminated through the urine

A

it is oxidized into a soluable metabolite or conjugated into a polar species that will dissolve in urine

48
Q

how is a drug eliminated through feces

A

a drug or an oxidative metabolite can be conjugated into a non-polar species which binds to bile and is excreted into feces

49
Q

how many CYP enzymes are present in humans

A

50 enzymes in 17 families

50
Q

T/F many different CYP enzymes function in drug metabolism

A

false, 8 isoforms of CYP 1, 2, and 3 families account for 92% of drug metabolism

51
Q

two CYPs that you should know

A

CYP 2D6, CYP 3A4/5

52
Q

how does genetic diversity influence a persons capacity for drug metabolism

A

several ethnic groups have varying levels of presence or activity in CYP enzymes

53
Q

genetic diversity in CYP 2D6

A

absent in 7% of caucasians, hyperactive in 30% of east asians

54
Q

what does CYP 2D6 do?

what is the effect of genetic variation on this enzyme

A

metabolizes codeine into morphine

if the enzyme isnt present codeine won’t work, if its hyperactive it will work too well

55
Q

T/F CYP action is not effected by external forces

A

false it can be inhibited or induced

56
Q

why do CYP inducers do

A
  1. increase enzyme activity
  2. lower circulating levels of the drug
  3. reduce drug effectiveness
57
Q

what do CYP inhibitors do

A
  1. decrease enzyme activity
  2. increase circulating levels of the drug
  3. increase risk of side effects and toxicity
58
Q

what enzyme inactivates calcium channel blockers

A

CYP 3A4-5

59
Q

what do calcium channel blockers do

A

treat HTN, chest pain, arrythmias

60
Q

three inducers of CYP 3A activity

A

carbamazepine

rifampin

st johns wort

61
Q

if a patient taking a calcium channel blocker started taking St Johns wort, what might happen to his blood pressure

A

it could go up because St Johns wort will induce CYP 3A activity and decease the blood concentration

62
Q

if a person taking calcium channel blockers for high blood pressure also begins taking erythromycin, what will happen to his blood pressure

A

the blood pressure will go up because erythromycin inhibits CYP 3A4-5 and decrease the circulating amount of the drug

63
Q
A

PAS 753 (Molecular Pathophysiology) (17 decks)

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