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Advanced Pharm > Principles of Pharm (Ch 1) > Flashcards

Principles of Pharm (Ch 1) Flashcards

1
Q

What four prehistoric practices influenced pharmacology?

A

shamanism
animism
spiritualism
divination

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2
Q

Who is the first recorded physician?

A

Imhotep

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3
Q

Who is the “father of western medicine?”

A

Hippocrates

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4
Q

Name 2 subcontinental medicine influence on pharmacology.

A

India (ayurvedic)
China (traditional chinese medicine)

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5
Q

What is the difference between the Rod of Asclepius vs Caduceus?

A

The Rod of Asclepius is associated with medicine; Caduceus is falsely associated with medicine but is actually representative of commerce/trade.

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6
Q

What is the Materia Medica?

A

A collection of work throughout history based on botany, medicinal substances, and is a precursor to pharmacology.

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7
Q

Who is the “Father of Toxicology”?

A

Paracelsus

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8
Q

What did Paracelsus say?

A

“The dose makes the poison”

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9
Q

What is the purpose of a controlled drug trial?

A

It evaluates therapeutic claims and prevents worthless patents of medicines.

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10
Q

Pharmacodynamics

A

What drugs do to the body

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11
Q

Pharmacokinetics

A

What the body does to the drug

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12
Q

Pharmacogenomics

A

The correlation between genetic profiling and predictive responses to drugs.

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13
Q

Toxicology

A

The study of toxin effects on living organisms.

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14
Q

Agonist

A

A drug that elicits a response when attached to a receptor

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15
Q

Antagonist

A

Blocks a receptor from functioning

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16
Q

Toxins

A

Biologic (living organisms)
ex.) mushrooms

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17
Q

Poisons

A

Non-biologic
ex.) lead

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18
Q

Allosteric

A

When the drug binds to a site outside of the active site.

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19
Q

Orthosteric

A

When the drug binds to the active site.

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20
Q

Name the 3 main bond types and rank them from strongest to weakest.

A

Covalent
Electrostatic
Hydrophobic

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21
Q

Name 3 types of electrostatic bonds

A

charged molecules
hydrogen bonds (partially +)
Van der Waals forces

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22
Q

Specific binding

A

binds at receptor site; has a maximum (plateaus)

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23
Q

Non-specific binding

A

drug binds anywhere besides the active site
ex) albumin

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24
Q

Describe the relationship involving bound drug concentration vs free drug concentration

A

the more drug that is given, the more drug that is bound (total binding)

specific binding: the more drug that is given, the more drug that is bound but there are only so many receptors to bind to (has a maximum)

non-specific binding: the more drug that is given, the more drug that is bound because it can bind anywhere outside of the receptor

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25
Q

ADME

A

absorption
distribution
metabolism
excretion

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26
Q

Drug concentration vs drug dose

A

concentration is the total amount of drug in the blood stream; the drug dose is how much drug you are giving

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27
Q

B max

A

maximum binding to receptor

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28
Q

Kd

A

dissociation constant

drug concentration at which 50% of receptors are bound; changes depending on the drug affinity to receptor sites

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29
Q

E max

A

maximum effect; can be variable

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30
Q

EC 50

A

50% of drug effect is seen; a single point on the curve

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31
Q

Explain why the Kd is not the same as EC 50.

A

You could have 1 receptor bound to have a maximum effect or you could have all of the receptors bound to have a maximum effect. The Kd changes based on drug affinity.

EC 50 never changes; it is where 50% of the maximum effect is seen.

They’re different concepts

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32
Q

Explain how a drug concentration curve might look (in terms of drug/receptor affinity) if the the Kd is low or high

A

A low Kd = high drug/receptor affinity (shift to the left)

A high Kd = low drug/receptor affinity (shift to the right)

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33
Q

Agonist + Allosteric Activator

A

an even greater response seen than just giving orthosteric agonist

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34
Q

Agonist + Competitive Inhibitor

A

more drug needed to achieve the same effect as if only giving agonist

SURMOUNTABLE

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35
Q

Agonist + Allosteric Inhibitor

A

Inhibitor is non-competitive; therefore, cannot be out-competed. shuts down the active site.

will not see the same response as if only agonist was given; a muted response is seen

INSURMOUNTABLE

36
Q

Partial agonist

A

Binds with less affinity; gives a PARTIAL response

in the presence of a FULL agonist, partial agonist acts as an ANTAGONIST; it out-competes the full agonist

the more partial agonist that is given, the less of a response you will see

partial agonist vs full agonist curve forms ‘chanel symbol’

37
Q

What is an example of opposing charge antagonism?

A

Protamine (+) and Heparin (-)

38
Q

What is an example of a physiologic antagonism?

A

Drugs that act on different receptors to oppose the effect

ex) Epi > B receptors (increase HR) & ACh on muscarinic receptors (slow down HR)

39
Q

Inverse agonist

A

favors Ri (inactive receptor configuration)

in PRACTICE – acts as an ANTAGONIST

terminates constitutive activity (vs competitive antagonist, which keeps constitutive activity)

40
Q

What are some receptors that inverse agonists bind to?

A

histamine receptors (H1/H2)
beta-adrenergic receptors
GABA receptors
5-HT receptors
dopamine receptors

41
Q

Beta-1 agonists

A

direct: epi, norepi
indirect (mimic): amphetamines, cocaine

42
Q

Beta-1 partial agonist

A

pindolol
acebutolol

43
Q

Beta-1 antagonist

A

propanolol
atenolol

44
Q

Beta-1 inverse agonist

A

carvedilol
nadolol

45
Q

Optical isomers

A

mirror images (have the same chemical formula; but NOT the same effects)

ex) L and R glove

46
Q

Racemic mixtures

A

a mixture of several different optical isomers

ex) R-Ketamine + S-Ketamine
R is usually more toxic and S is 4x more potent and the purified form

47
Q

What are 4 factors that influence receptor interactions?

A

size
electrical charge
shape
atomic composition

48
Q

What is the relationship between bond strength and specificity?

A

inversely proportional

the stronger the bond, the less specific the receptor site is; the weaker the bond, the more specific the receptor site

think lock and key

ex) covalent bonds are the strongest but contain the least specific receptor sites, while hydrophobic bonds are the weakest and have the most specific receptor sites

49
Q

receptor vs receptor site

A

receptor: binding agent to the receptor site

receptor site: where the binding agent attaches to on cell surface

50
Q

name 3 duration of drug action scenarios

A
  1. only as long as drug binds to receptor
  2. longterm downstream effects last until downstream effectors go away
    covalent bonds – receptor is degraded which leads to:
  3. desensitization
51
Q

what makes a receptor “good”

A
  1. selective
  2. can alter its composition (in order for downstream effect to occur, when receptor binds to ligand, it has to change)
52
Q

what makes a receptor “bad”

A
  1. inert binding sites – receptor sites that, when bound to a drug, does not produce an effect
  2. is a drug carrier (albumin)
53
Q

describe albumin as a drug carrier

A

when plasma is bound to a protein, it CANNOT cross barriers (too large)

can only cross barriers in its free form (unbound form)

if 90% of your drug is bound to albumin and 10% of the drug is free, you’ll need to give a higher dose of the drug to see an effect

decreased levels of albumin (malnourished/liver damage) will increase risk for toxicity/side effects

if multiple drugs are given together, some drugs may compete for albumin binding and displace other drugs (ex. phenytoin vs carbamazepine) and this will result in both drugs having a higher free concentration

binding sites on albumin depends on the type of bonds

54
Q

albumin binds mostly to ____ drugs

A

acidic

55
Q

alpha 1 acid glycoproteins binds mostly to ______ drugs

A

basic

56
Q

lipoproteins binds mostly to ______ drugs

A

neutral

57
Q

how many binding sites does albumin have?

A

binding site 1 and 2

58
Q

compare and contrast potency vs efficacy

A

potency
a small amount of drug with a maximal effect = high potency
a high amount of drug with a minimal effect = low potency

EC 50 (concentration) or ED 50 of a drug required to produce 50% of drug’s maximal effect

efficacy
greatest possible response a drug can deliver
depends on interaction with receptor
must also take into account toxicity

the clinical effectiveness of a drug depends not on its POTENCY, but on its MAXIMAL EFFICACY

59
Q

explain the dose-response curve in terms of potency and max efficacy (figure 2-15)

A

drugs A, C, and D equally have the same efficacy

however, A > C > D in terms of potency

B is the most potent but has minimal efficacy

60
Q

explain ED 50, TD 50 and therapeutic index in terms of drug-response curves in regards to population

A

ED 50 = at 50% of population get desired indication of drug (ex. 500 people in study; 250 people get therapeutic effect of drug)

TD 50 = where 50% of population achieve a toxic side effect of the drug

Therapeutic ratio = TD50/ED50 (distance between TD50 curve and ED50 curve; the wider the gap, the safer the drug and the narrower the gap, the less safe the drug

61
Q

what are the 4 main causes of drug variation?

A
  1. alteration in concentration of drug that reaches the receptor (based on rate of absorption, age, weight, sex, disease state [i.e. liver disease])
  2. concentration of endogenous receptor ligand (affected by health/disease state) – not everyone has the same amount of receptor ligands
  3. number or function of receptors
    +concentration of native ligands
  4. downstream proteins are the biggest cause of variation
62
Q

weak acid

A

acid releases proton (H+) into solution

63
Q

weak base

A

absorbs proton (H+) from solution

64
Q

if pH < pKa; favors _______ form

A

protonated

65
Q

if pH > pKa; favors ______ form

A

unprotonated

66
Q

how does the Henderson Hasselbach predict a drugs charge?

A

pH and pKa are related to determine the charge of a drug;

if a drug’s pH < pKa it favors the protonated form and depending on whether or not the drug is a weak acid or a weak base will determine if the drug is charged or uncharged

67
Q

if a weak acid is protonated, the drug is ______

A

uncharged

68
Q

if a weak base is protonated, the drug is ______

A

charged

69
Q

protonated weak base =

A

charged; pH < pKa

70
Q

protonated weak acid =

A

uncharged; pH < pKa

71
Q

WAP-U
WBP-C

A

weak acid, protonated = uncharged

pH < pKa

weak base, protonated = charged

72
Q

ASA, a weak acid
pKa = 3.5

what form is ASA in in the stomach? pH = 1.5

A

uncharged

pH < pKa (1.5 < 3.5)
protonated

73
Q

ASA, a weak acid
pKa = 3.5

what form is ASA in in the intestines? pH = 6.5

A

charged

pH > pKa (6.5 > 3.5)
unprotonated

74
Q

morphine, a weak base
pKa = 7.9

what form is morphine in in the stomach? pH = 1.5

A

charged

pH < pKa (1.5 < 7.9)
protonated

75
Q

morphine, a weak base
pKa = 7.9

what form is morphine in in the blood? pH = 7.4

A

charged

pH < pKa (7.4 < 7.9)
protonated

76
Q

what is a monoclonal antibody?

A

produced from a single clone that produced antibodies (plasma cell)

decrease adverse effects by only binding to antigen binding site (highly specific)

target proteins on cell surface and modulate vital functions

can also cause cell death by various mechanisms (apoptosis)

77
Q

how is a monoclonal antibody produced?

A
  1. isolate target antigen
  2. inject antigen into mouse
  3. mouse will make antibodies against antigen
  4. once enough antibodies are produced, mouse’s spleen cells (plasma cells) are harvested
  5. plasma cells + myeloma cell fused = becomes immortal cell
  6. isolate, culture, and propogation occurs
  7. propogate the positive clones either in vitro or in vivo (mouse) and harvest the monoclonal antibodies once enough are produced
78
Q

describe the structure of a monoclonal antibody

A

“Y” shaped

antigen binding sites (on the tips of the arms of the ‘Y’)

Fab domain = arms of the “Y”

Fab domain contains the variable portions (these sites are for particular protein binding)

Fc (constant) = stem of the “Y”, binds immune cells and activates immune cells

79
Q

-mab

A

monoclonal antibody drug

80
Q

monoclonal antibodies indications

A

cancer: lung, colon, kidney, glioblastoma

rheumatoid arthritis, psoriasis, Chrons disease, ulcerative colitis,

81
Q

describe the role of the FDA

A

oversees development processes of FOOD and DRUG Administration

grants marketing of product approval

must be “SAFE and EFFECTIVE”
+non-drugs just have to be SAFE, not necessarily effective

reviews all claims and makes recommendations

oversees OTCs/BTCs and herbal supplements

82
Q

list the differences in the regulation of Rx drugs vs OTC/non-Rx drugs

A

Rx drugs:
+provider has to Rx
+viewed as Rx drugs are “more effective” by the public
+misuse has higher potential for harm
+regulated by FDA

OTCs:
+freely available to public
+low risk for harm/abuse; HOWEVER, any drug in excess can kill you
+ does not equate to “safe”

83
Q

what happens during years 0-4 pre-clinical testing?

A

in vitro studies
finding a lead compound
testing lead compound in animals to see efficacy
“what does the drug actually do?”
IND (investigational new drug) then clinical testing

84
Q

phase 1 clinical testing population

A

20-100 subjects
“college students”
pharmacokinetics

85
Q

phase 2 clinical testing population

A

100-200 patients
does it work on the target patients?
ex) cancer drug tested on cancer patients only

86
Q

phase 3 clinical testing population

A

1000-6000 patients
does it work double blind?

87
Q

phase 4

A

only accessible after NDA approval; patent expires after 20 years of filing application

Advanced Pharm (8 decks)

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