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Pharm Test 1 > 8/28 Class 3 > Flashcards

8/28 Class 3 Flashcards

1
Q

What is the effector protein?

A

The protein that elicits second messengers and an effect in the cell.

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2
Q

Can you have more than one second messengers?

A

Yes! Here there are 3 different second messengers, DAG, IP3, and Calcium

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3
Q

Do all g proteins elicit the same response in a cell?

A

No, different g- proteins can activate different proteins, therefore having a different overall action/effect in the cell.

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4
Q

Describe the g-protein pathway involving Adenylyl Cyclase

A

Ligand binds to the receptor which releases the G protein with GTP on it.
That binds with the effector protein Adenylyl cyclase
Adenylyl cyclase spins ATP into cAMP
cAMP activates protein kinase A
This elicits a cellular response.

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5
Q

Describe the g-protein pathway involving Phospholipase C

A
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6
Q

Describe desensitization

A

Beta arrestin binds to the OH groups attached to the end of the carboxyl terminal on the 7TM protein and blocks further activity from occurring.

The protein gets “eaten” by the cell via a clathrin pit.

opt 1. drug breaks off of receptor: G-protein gets moved back to the cell surface to be reused.

opt.2 Lysosome merges with the ligand and the lysosome degrades the entire drug&receptor

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7
Q

What is clatherin?

A

A protein involved in endocytosis

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8
Q

What is endocytosis?

A

The taking in of matter by a cell (cell eats something)

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9
Q

What is a catalytic cell surface receptor?

A

A membrane bound, ligand activated active site that has an enzymatic component either directly associated with it, or the enzyme is built within itself.

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9
Q

Describe Recycling of a g-protein.

A

drug breaks off of receptor: G-protein gets moved back to the cell surface to be reused.

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10
Q

What is a kinase?

A

an enzyme that attaches a phosphate group

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11
Q

What is a phosphatase?

A

An enzyme that strips a phosphate group from a protein

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12
Q

what is an example of a catalytic cell surface receptor?

A

Tyrosine Kinase

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13
Q

What is tyrosine?

A

one of our 20 amino acids

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14
Q

What are the ligands that attach to Tyrosine kinases?

A

Growth Factors: EGF (Epidermal growth factor)
Adhesion Factors: When WBC bind to the surface of a blood vessel

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15
Q

What is dimerization?

A

Two monomers coming together

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16
Q

What does dimerization cause?

A

phosphorylation of the kinases which makes it act like a kinase enzyme

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17
Q

Describe the RTK process

A
  1. 2 ligands bind to 2 different RTK’s
  2. This makes the two monomers come together, and activates 6 ATP molecules.
  3. When they come together, they “activate” each other by becoming phosphorylated. The phosphates from the ATPs are added to the Tyrosines.
  4. It is now activated and can interact with effector proteins and create the downstream effects.
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18
Q

Where does the phosphate groups come from in the RTK process when phosphate are added to Tyrosines?

A

They are pulled from 6 ATP molecules

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19
Q

How are RTK’s different from G-proteins?

A

G proteins have to activate an enzyme where RTK’s are the enzyme

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20
Q

How are RTK’s the same as g-proteins?

A

They both are membrane bound, ligand activated, and eventually activate an effector protein.

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21
Q

What are voltage gated channels?

A

Pores in the cell’s surface that allow highly charged molecules to pass through the cell wall.

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22
Q

Where are voltage gated channels found within the body?

A

Neurons, muscle, endocrine cells

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23
Q

Which stage is this channel in?

A

Closed

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24
Q

Which stage is this channel in?

A

Activated

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25
Q

Which stage is this channel in?

A

Inactivated

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26
Q

Which stage is this channel in?

A

Deactivated

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27
Q

What is the cycle of a voltage gated channel?

A

closed, threshold, activated, inactivated, deactivated, circles back to closed again

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28
Q

What activates a voltage gated channel?

A

When a resting potential gets closer and closer to the firing potential, or threshold

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29
Q

What activates a ligand-gated ion channel?

A

a ligand binding to the receptor

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30
Q

What are the two subtypes of ligand-gated ion channels?

A

Inotropic
Metabotropic

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31
Q

How does a inotropic ligand-gated channel work?

A

The same as the Voltage gated except a ligand binds to it to activate it instead of a threshold.

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32
Q

How does a metabotropic ligand-gated channel work?

A

A ligand activates a GPCR which activates the channel

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33
Q

Which ligand gated channel is more common, inotropic or metabotropic?

A

Inotropic

34
Q

Describe how the nicotinic acetylcholine receptor works

A

neurons release 2 acetylcholine molecules

Acetylcholine molecules bind to the alpha subunits on the receptor

This opens the gate

Na+ floods into the cell

Na+ activates Ca++ channels

Ca++ floods into the cell

Ca++ activates actin myosin

muscle contracts

35
Q

Where are nicotinic acetylcholine receptors found?

A

on skeletal muscle

36
Q

What is an example of a Inotropic ligand gated ion channel?

A

Nicotinic acetylcholine

37
Q

What is an example of a metabotropic ligand gated ion channel?

A

An odorant molecule binding to a odorant receptor

38
Q

Describe how the odorant molecule binding to a odorant receptor works to help us smell.

A
39
Q

What can activate a receptor inside of the cell?

A

something that is lipid soluble
a gas

40
Q

What type of cells line your blood vessels?

A

endothelial cells

41
Q

What might cause a strong shearing force on a blood vessel?

A

High blood pressure
Orthostatic blood pressure

42
Q

What is activated by a strong shearing force on a blood vessel?

A

an enzyme called nitric oxide synthase

43
Q

What does nitric oxide synthase produce?

A

Nitric oxide gas

44
Q

Where does nitric oxide gas diffuse to when it’s released?

A

all directions; its a gas. But specifically diffuses to smooth muscle that surrounds the blood vessel

45
Q

What effect does nitric oxide have on the smooth muscles around blood vessels?

A

It relaxes it, thereby opening up the blood vessel.

46
Q

What is the enzyme that turns GTP into Cyclic GMP?

A

guanylyl cyclase

47
Q

Why can steroid hormones cross the cell wall without issue?

A

It is uncharged

48
Q

What is the general gist of Absorption in pharmacokinetics?

A

It is how the drug gets to where it’s going

49
Q

What is the general gist of Distribution in pharmacokinetics?

A

It is where the drug ends up.
i.e. lipids, bone, aqueous compartments, muscle

50
Q

What is aqueous diffusion?

A

When a water soluble drug dissolves in water and get through the cell wall via aquaporins using a concentration gradient

51
Q

what is lipid diffusion?

A

When a lipid soluble drug crosses the cell wall. Lipids can cross the cell wall freely. They use concentration gradients.

52
Q

What are the different types of permeation mechanisms?

A

Aqueous diffusion
lipid diffusion
special carriers
endocytosis
exocytosis

53
Q

Can all water soluble molecules go through the aquaporin channels?

A

No.
Molecules that are too charged or too big d/t being bound to a larger protein (like albumin) they can’t go through the aquaporin.

54
Q

How do special carriers work?

A

Molecules bind to a drug and moves across barriers can be by active transport or facilitated diffusion.

55
Q

Define endocytosis and exocytosis

A

Membrane engulfment (clatherin pit eats molecules)
transports across cell membrane
Merging of vesicle with membrane (spits it out)

56
Q

What type of molecules do endocytosis and exocytosis help?

A

very large drugs

57
Q

In order to get the pharmacodynamic effect that we want, we have to take into account all of the ________

A

pharmacokinetic variables

58
Q

Dose adjustments are sometimes necessary d/t what pharmacologic parameters

A

volume of distribution
clearance

59
Q

What is volume of distribution?

A

How much of the drug actually go to the blood vs. how much went to other areas of the body

60
Q

What is clearance?

A

ability of the body to eliminate the drug

61
Q

Volume distribution is measured per

A

Liter

62
Q

Why would volume distribution be different for the same amount given of two different drugs.

A

Drug A might dispose of itself very quickly into the fatty tissue, where drug B sticks around in the blood a little longer. Giving Drug A a higher volume distribution than drug b.

63
Q

Describe this graph

A

The volume in the blood of a certain drug at time 0, when you first give a drug, is at it’s max. Over time the volume in the blood decreases as the drug is distributed to other parts of the body

64
Q

What does a high volume distribution mean?

A

Little of the drug is left in the blood

65
Q

What is the volume of whole blood?

A

0.8L/kg

66
Q

What is the plasma volume?

A

0.04 L/kg (half of the whole blood)

67
Q

What are the metric conversions?

A
68
Q

How to calculate the dose?

A

Multiply Vd by the Target concentration

69
Q

Are both Vd and Target concentrations going to be provided?

A

Yes

70
Q

How to solve for Vd

A

Dose delivered / initial concentration in the blood

71
Q

Describe what is going on in these pictures

A

A: you give a bolus of the drug into a closed system. the drug has no where to go so it’s concentration stays constant.

B: you give a bolus of the drug into a system with one form of elimination. This leads to a steady decrease in concentration.

C. you give a bolus of the drug into the blood, which then is distributed to other parts of the body, but isn’t eliminated here.

D. you give a bolus of the drug into the blood, it is distributed to other parts of the body, and then eventually excreted.
the initial decrease in the graph shows the distribution, the slower decrease shows the drug being eliminated.

72
Q

Clearance, for almost every drug, is going to be

A

constant

73
Q

What is a systemic clearance?

A

A combination of all of the modes of elimination for a drug.
CLsystemic=CLrenal+CLliver+CLother

74
Q

How do you calculate the rate of elimination?

A

Multiplying the Clearance X concentration that’s in the blood

75
Q

In first order elimination, what is constant?

A

Clearance

76
Q

In zero order elimination, what is constant?

A

Rate of elimination

77
Q

What is zero order elimination?

A

Elimination when the body’s ability to eliminate a drug has reached it’s maximum capability d/t all of the transporters being used up.

Think of it like a swimming pool and you have a measuring cup to empty it. You can only eliminate 1 cup at a time (the rate), but that 1 cup is going to be a different percentage of the total concentration (the clearance)f

78
Q

What is first order elmination?

A

Elimination when your body clearance percentage stays the same. (the speed stays the same)

You have a mixing bowl full of water and you have different size measuring cups to be used in a specific order from biggest to smallest. Each measuring cup is equal to 12% of the volume of water inside of the bowl. When the bowl is full you use the biggest measuring cup and dip out 12 percent. Now the biggest cup is full so you move to the next size, which dips out 12% of the remaining water. etc.

79
Q

What drugs should we associate with zero order elimination?

A

Aspirin, phenytoin, ethanol

80
Q

Why is the rate constant in zero order elimination instead of the clearance?

A

Because you have saturated your ability to eliminate that particular drug from the body any faster.

81
Q

What is clearance?

A

the volume ( as a percentage) of blood being cleaned per unit of time

82
Q

What is Elimination?

A

the amount of drug (in mg or g) leaving the body per unit of time

Pharm Test 1 (5 decks)

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