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Pharm chapter 1 > Principles of Pharm > Flashcards

Principles of Pharm 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

21
Q

Name 3 types of electrostatic bonds

A

charged molecules
hydrogen bonds
Van der Waals forces

22
Q

Specific binding

A

binds at receptor site; has a maximum (plateaus)

23
Q

Non-specific binding

A

drug binds elsewhere
ex) albumin

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.

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

25
Q

ADME

A

absorption
distribution
metabolism
excretion

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

27
Q

B max

A

maximum binding to receptor

28
Q

Kd

A

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

29
Q

E max

A

maximum effect; can be variable

30
Q

EC 50

A

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

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.

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)

33
Q

Agonist + Allosteric Activator

A

an even greater response seen than just giving orthosteric agonist

34
Q

Agonist + Competitive Inhibitor

A

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

SURMOUNTABLE

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 activator 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

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 drug is; the weaker the bond, the more specific the receptor site

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

Pharm chapter 1 (1 decks)

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