Chapter 1 Flashcards

1
Q

Define Pharmacodynamics

A

what the drug does to the body

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2
Q

Define Pharmocogenomics

A

expanding field that looks at genetic profiles to predict drug responses

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2
Q

Define Pharmacokinetics

A

what the body does to the drug (ie half life, liver processes, cross barriers)

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3
Q

Define Toxicology

A

undesirable effects of chemicals on living systems

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4
Q

Define Agonist

A

drug binds to receptor and activates a response

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5
Q

Define Antagonist

A

binds to receptor, prevents the binding of the native ligand

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6
Q

Describe the difference between pharmacodynamics, pharmacokinetics, pharmacogenomics, and toxicology.

A

dynamics- what the drugs does to the body
kinetics- what the body does to the drug
genomics- how your genetic profile affects response to drug

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7
Q

What is the difference between toxins and poisons?

A

Toxins are from biological substance (mushrooms, fish)
Poisons are from non-living

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8
Q

What is the difference between competitive inhibitor and allosteric inhibitor?

A

competitive- binds to active site
allosteric- binds outside active BUT makes receptor less active/available

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9
Q

Who was the first recorded physician in pharmacology?

A

Imhotep (Ancient Egypt)

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9
Q

Who was the “Father of modern medicine”?

A

Hippocrates

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10
Q

What is the Materia Medica?

A

first medical textbook that dealt with pharmcology, discussed use of compounds

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11
Q

Who is Paracelsus?

A

“Father of Toxicology”, introduced the concept that at a certain dose you can poison your body

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12
Q

What is the difference in the types of bonds in terms of strength?

A

Covalent- strongest
Electrostatic- (charged molecules, hydrogen, van der Waals)
Hydrophobic- weakest (not charged)

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13
Q

Describe the relationship between bond strength and specificity

A

the stronger the bond the less specific the receptor needs to be

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14
Q

Describe Racemic Mixtures

A

combination of a + and - isomer in a drug

15
Q

Describe Stereoisomerism

A

they have the same formula, but have a different shape

16
Q

Describe the non specific & specific binding graph

A

specific binding has a MAX, once reached there will be non-specific binding

17
Q

What is ADME in pharmokinetics?

A

A- Absorption
D- Distribution
M- Metabolism
E- Excretion

18
Q

Describe the Drug Concentration Response Curve in terms of EC50

A

EC50= that is when you see 50% of effect of the drug

19
Q

Describe the Kd

A

drug concentration in which 1/2 of the receptors are bound

20
Q

Describe the relationship of Kd in terms of drug/receptor affinity

A

low Kd = high affinity

21
Q

Describe how Kd does not equal EC50

A

You don’t need to have a certain amount of bound receptors (kd) in order to see a response/effect of the drug (EC50)

22
Q

Describe the response of an Allosteric Activator and Agonist

A

together they create a bigger response

23
Q

Describe the response of a agonist and competitive inhibitor

A

The competitive inhibitor will try to BLOCK the agonist from binding to active site, meaning you need to have more of the agonist to overcome the competitive inhibitor

24
Q

Describe the relationship of an agonist and allosteric inhibitor

A

The allosteric inhibitor will bind outside the active site BUT make the active site less available, CANNOT BE OUTCOMPETED

25
Q

Describe what a agonist mimic or indirect agonist is

A

affects the response downstream, NOT at active site but has the same affect

26
Q

surmountable

A

competitive, can be overcome by the agonist

27
Q

insurmountable

A

non-competitive, can NOT be overcome by the agonist

28
Q

Describe how non-competitive inhibitors interact with agonist

A

CAN NOT be overcome by the agonist

29
Q

Partial Agonist

A

produces a lower response at full receptor occupany

30
Q

Explain how a partial agonist acts in presence of a full agonist

A

the more partial agonist, the less response we will have, thus eventuall leading to it acting like an antagonist when

31
Q

Describe a Inverse Agonist

A

favors the inactive form of a receptor, thus leading to it acting as an antagonist, even less response than an actual antagonist

32
Q
A