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Semester 1 TxWes > Pharm Unit 1 > Flashcards

Pharm Unit 1 Flashcards

1
Q

Pharmacology

A

The study of chemical interactions within a living system through chemical processes

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2
Q

Pharmacodynamics

A

How the body interacts with a drug, and how the drug effects the body

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3
Q

Pharmacokinetics

A

How the body process/excretes a drug.

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4
Q

ADME

A

Absorption
Distribution
Metabolism
Excretion

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5
Q

Drug

A

a substance that causes a physiological change to the body

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6
Q

Agonist

A

A molecule that binds to a receptor to illicit a desired response. Think of it as an activator

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7
Q

Antagonist

A

This is an inhibitor, it binds to stop something from happening. Think of it as a blocker/competer, like narcan.

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8
Q

Ligand

A

A native molecule w/a functional group

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9
Q

Stereoisomerism

A

Molecules that have the same chemical makeup, but are mirror images of each other. Frequently potentiate each other.

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10
Q

Racemic mixture

A

A blend of stereoisomers, think ketamine r and ketamine s

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11
Q

Orthosteric receptor

A

This is the native binding site

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12
Q

Allosteric receptor

A

An active site other than the native binding site (orthosteric) where a molecule can bind.

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13
Q

Average drug size

A

100 - 1000mw (molecular weight)

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14
Q

Why do drugs usually fall between a certain weight range?

A

Because any bigger and its hard for the molecule to diffuse across a membrane, any smaller and it is very difficult for a molecule to have specificity (if its too small, it could theoretically bind to a lot of other receptors).

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15
Q

What factors determine if a molecule can bind to a receptor?

A

Size/shape, atomic structure (such as what amino acids are attached to it) and electro-chemical charge

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16
Q

What are the 3 main types of bonds?

A

Covalent (strongest) Electrostatic (H bonds, van der waals forces) and Hydrophobic (lipid soluble drugs)

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17
Q

What bond type is strongest? Is it very specific or not very specific? why?

A

Covalent. It is very specific, because it has such a strong bond and will not disassociate easily it will try to only bond to a certain type of receptor. So high bond strength, low specificity.

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18
Q

What is the relationship between bond strength and specificity?

A

Inverse, the higher the bond strength, the lower the specificity.

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19
Q

What is an example of an inert carrier?

A

Albumin

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20
Q

What is an indirect agonist?

A

Something that potentiates a reaction “downstream.” Ie, an enzyme that is responsible for breaking down a molecule is changed, and can no longer bind to the final product, allowing the downstream effect to continue un-abated

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21
Q

What is the difference between surmountable antagonistic interactions and insurmountable antagonistic interactions?

A

With insurmountable, once bound it is bound, there is no overcoming it. No matter how much agonist you give, the response of the agonist will not increase. With surmountable, if you give enough agonist you can eventually overcome the agonist and achieve the desired response.

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22
Q

What is therapeutic index?

A

The narrow range between desired drug effect and toxicity on a dose/response curve. The goal when giving drugs is to fall somewhere between these 2 lines.

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23
Q

What is kd?

A

The drug concentration when half the receptors are bound.

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24
Q

What does a low k mean?

A

High receptor affinity; the agonist will bind quickly, this creates a sharp uptake line on a dose response curve.

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25
Q

What is EC50?

A

The amount of drug needed to get to half of the desired effect. Ie, ec50 of anesthesia could be drowsy but still awake, and the endpoint is loss of consciousness.

26
Q

Will giving more drugs increase eMAX?

A

No, once you hit emax you will not have any further effect. Think of an anesthetic gas; once you are unconscious, if you give higher and higher doses you won’t become “more asleep”

27
Q

When is a partial agonist antagonistic?

A

In the presence of a full agonist. They both compete for the same site, so the compete for the same receptor

28
Q

What is an example of non-receptor antagonism?

A

Reversing heparin w/protamine. This occurs due to the difference in charge. Hep is -, and protamine is +, due to the electrochemical difference they will bind to each other. This antagonizes heparin because the protamine is decreeing free drug concentration of heparin.

29
Q

What changes Ra to Ri

A

An inverse agonist

30
Q

How does an inverse agonist affect a dose response curve?

A

It can fully drop the dose to 0. It is the only mechanism that can even turn of constitutive activity. A very potent method of turning off a receptor

31
Q

Can an agonist overcome an inverse agonist?

A

No

32
Q

What kind of drugs does albumin like?

A

Acidic drugs, think A for acid

33
Q

What kind of drugs does alpha-1 glycoproteins like?

A

Basic drugs

34
Q

What kind of drugs do lipo-proteins like?

A

Neutral drugs, remember neutral/no charge likes neutral/no charge. Lipo = lipid, so its going to like things with no charge

35
Q

What is the difference between potency and efficacy?

A

Potency is how much drug it takes to get to ec50, so a high potency means it does not take much drug to get to ec50. Efficacy is the highest response you can get from a drug. Ie, in terms of pain, fentanyl is more efficacious than Tylenol.

36
Q

What is the therapeutic index?

A

The narrow range between the therapeutic effect and the toxic effect. The goal with drug dosing is to be between these two lines.

37
Q

What is the largest cause in variation of response to a drug?

A

Changes in the downstream response, such as turning off a receptor or destroying a messenger protein needed to carry out the cycle.

38
Q

If pH is less than pKa, what form is favored?

A

Protonated

39
Q

If pH is greater than pKa, what form is favored?

A

Unprotonated

40
Q

What form will asa be in at a pH of 1.5? pKa = 3.5

A

Protonated and uncharged (this one is an acid)

41
Q

What form will asa be in at a pH of 6.5? pKa = 3.5

A

Non-protonated and charged (this one is an acid)

42
Q

What form will morphine be in at a pH of 3.0? pKa = 7.9

A

Protonated and charged (this is a base)

43
Q

What form will morphine be in at a pH of 11.5? pKa = 7.9

A

Non-protonated and uncharged (this is a base)

44
Q

Describe receptor coupling

A

This is when a ligand binds and causes the receptor to change shape. Such as creating a phosphorylation cascade.

45
Q

What kind of molecules can reach a receptor inside the cell?

A

Lipid soluble and gasses

46
Q

What does adenylyl cyclase do?

A

Uses ATP to make cAMP

47
Q

What does kinase do?

A

Attaches phosphate groups

48
Q

Describe the basics of desensitization

A

This is when the body interrupts the response to an agonist somewhere in the cycle after binding. So the agonist is bound and trying to elicit the desired effect. However, the process has been disturbed somewhere down the cycle and cannot continue despite the fact that the receptor is still being stimulated.

Ie, the receptor has been destroyed or a secondary messenger has been “turned off.”

49
Q

Describe how a RTK receptor activates

A

2 ligands bind to the receptor, then the two parts dimerize (come together) and cross phosphorylate, thus starting the downstream cascade. Once cross phosphorylated, hundreds of downstream effects can occur

50
Q

Describe the basics of an ion channel

A

It is a gated “pore” that will open/close to allow ions such as Na or K in

51
Q

Describe a ligand gated ion channel

A

It is a channel that will allows ions through, but requires a ligand to bind either increase or decrease how frequently the channel opens

52
Q

Describe a voltage gated ion channel

A

These open in response to change in electrical charge. At resting membrane potential the gate is closed. When an electrical difference occurs, the gate opens.

53
Q

Describe the difference between ionotropic ion channels, and metabotropic ion channels

A

Ionotropic are ligand gated ion channels, where the ion channel acts as both the channel and the receptor (the receptors are attached to the channel). Metabotropic has a GPCR, and the channel only opens after the alpha sub-unit has elicited a secondary messenger (like cAMP) to open the gate.

54
Q

Can aqueous diffusion occur with a highly charged molecule?

A

No, it will need either a carrier protein, active transport, or be broken down into constituent parts

55
Q

Describe Vd

A

Volume distribution, it describes how much space is available in the body is to store a drug, and which compartment the drug is likely to be found in

56
Q

What does a high Vd indicate? Low?

A

A high Vd means the drug likes to leave the bloodstream to go other places. A low Vd means that it likes to stay in the bloodstream

57
Q

What is the Vd target dose of tylenol? Vd = 67L / 70 kg, TC = 15 ml/L

A

dose = 1005 mg / 70kg

58
Q

Describe first order elimination

A

The rate of elimination stays the same. Each hour you would get rid of 10% of a drug for example. So 1000mg to 900mg, then 900 to 810 mg

59
Q

Describe zero order elimination

A

Whatever is getting rid of the drug is saturated and at the maximal rate of elimination. The rate of elimination will continually increase until no longer saturated, but the amount of drug eliminated per hour is static until the eliminator is no longer saturated.

60
Q
A

Semester 1 TxWes (7 decks)

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