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Fall17-Pharmacology > Block 1 > Flashcards

Block 1 Flashcards

1
Q

What is the basis for drug scheduling?

A

C-1 drugs are mostly illegal with highest abuse potential
C-2 drugs have high abuse potential - morphine, bethylphenidate
C-3 drugs - codeine mixtures (Tylenol #3)
C-4 drugs - benzodiazepines for insomnia
C-5 drugs - least amount of abuse potential - condemned containing cough syrup - some states need Rx, some states don’t

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2
Q

What are true receptors?

A

They elicit a biological response when bound by an agonist

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3
Q

Drug molecule and the biological target must do what in order to act?

A

They must come together! They can’t work at a distance

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4
Q

What are most receptors?

A

Proteins

They undergo structure changes and have spatial and energetically favorable molecular domains for binding

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5
Q

What is an inert binding site?

A

Binding that results in no detectable changes in function of the biological system

Drug can bind, but no biological response to that drug

Affect the distribution of drug and the amount of free drug available to bind to the receptor

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6
Q

What is the initial drug receptor bond made of?

A

Usually ionic bonds - this is why the fraction of drug ionized is important

There are many various bond that occur, ionic is just the initial one

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7
Q

What is drug size related to?

A

Specificity for receptor and movement in the body

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8
Q

What is the order of bond strength from strongest to weakest?

A 
Covalent
Ionic
Hydrogen
Dipole induced dipole (van der waal)
Hydrophobic
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9
Q

Weak bonds are generally _______ selective than very strong bonds.

A

MORE

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10
Q

Which bonds last longer in the body?

A

Strong bonds!

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11
Q

Why is drug shape important?

A

Proper binding - lock and key

Chirality - one enantiomer fits the receptor better than the other

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12
Q

What is the mechanism of nicotinic receptors?

A

(Type of ligand gated ion channel)

It’s a 5 subunit molecule (2 alpha subunits)
Both alpha subunits must bind an Acetylcholine.
The channel opens (its normally closed)
Na+ and K+ can then pass through - depolarization of membrane
*prolonged acetylcholine contact with receptor leads to desensitization of receptor

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13
Q

What is the mechanism of Glutamate receptors?

A

(Type of ligand gated ion channel)
Major excitatory neurotransmitter!

Non NMDA - glutamate binds to receptor
It opens allowing Na+ or Ca+ in and K+ OUT
Depolarization of membrane

NMDA - previous depolarization causes Mg2+ to be unplugged. Then positive ions can rush in

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14
Q

What is the mechanism for a GABA receptor?

A

Type of ligand gated ion channel

Major INHIBITORY neurotransmitter

GABA A - inhibitory - binds which open chloride channels causing HYPERpolarization - reduces probability of action potential

GABA B - inhibitory - binding results in K+ out, membrane hyperpolarization

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15
Q

What is the mechanism for voltage gated ion channels?

A

The channels open due to changes in voltage (Na+ channels, Ca+ channels, K+ channels)

Present in excitable tissues: nerve, cardiac, skeletal muscle

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16
Q

What are Gs proteins?

A

Activates Ca2+ channels

binding ACTIVATES adenylyl cyclase

Then ATP to cAMP

cAMP activates protein kinase A

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17
Q

What are Gi proteins?

A

Activates K+ channels

binding INHIBITS adenylyl cyclase - prevents conversion of ATP to cAMP

no activation of protein kinase A

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18
Q

What are Gq proteins?

A

activates phospholipase C - that releases IP3 and DAG

IP3 activates Ca+ and calmodulin dependent protein kinases

DAG activates protein kinase C

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19
Q

What are Gs receptors?

A

All B adrenergic (B1, B2, B3)

D1

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20
Q

What are Gi receptors?

A

M2
D2
A2

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21
Q

What are Gq receptors?

A

A1
M1
M3

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22
Q

What is the mechanism for receptor tyrosine kinases?

A

After the ligand bind, they dimerize (come together)

They have INTRINSIC kinase activity for signalling

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23
Q

What are the receptors for tyrosine kinases?

A

Growth factor receptors!

Insulin!

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24
Q

What is the mechanism for cytokine receptors?

A

After binding, they dimerize but there is NO intrinsic kinase activity - they need to recruit JAK to have kinase activity which then activate STATs

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25
Q

What are the receptors for cytokines?

A

Cytokine receptors!

Growth hormone, erythropoietin, interferons

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26
Q

What is the mechanism for steroid receptors?

A

Type of intracellular receptor

They can slip right into the membrane and bind to cytoplasmic receptor to stimulate transcription of genes.

After binding, the complex is transported to the nucleus where transcription is activated

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27
Q

What are examples of steroid hormones?

A

Corticosteroids, mineralocorticoids, sex steroids, thyroid hormone, Vitamin D

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28
Q

What is the mechanism of nitric oxide?

A

Type of intracellular receptor

Diffuses across membrane

Reacts with guanylyl cyclase

Stimulates cGMP formation and relaxes smooth muscle downstream

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29
Q

How do you predict the relative safety of a drug based on its therapeutic index?

A

TI = toxic dose 50% / effective dose 50%

Small TI = BAD

Higher TI = safer

We also want the TD and ED to be far away from each other if possible

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30
Q

This is the action of a drug on the body - receptor interactions, dose-response phenomena, etc

A

Pharmacodynamics

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31
Q

This is the action of the body on the drug - absorption, distribution, metabolism, excretion, elimination

A

Pharmacokinetics

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32
Q

Drug that binds to the same site as endogenous ligand and produces the same signal

A

Agonist

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33
Q

Drug that binds to a different site than endogenous agonist without producing a signal itself. It enhances the response of endogenous agonist

A

Allosteric agonist

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34
Q

Drug that produces a lower response when at full receptor occupancy than full agonist

A

Partial agonist

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35
Q

Drug that binds to receptor that inhibits the action of the agonist

A

Antagonist

Remember: antagonists have no effect themselves, its just blocking the agonist

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36
Q

Drugs that bind reversible to the same receptor as agonist

A

Competitive antagonist

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37
Q

Drugs that bind irreversibly or allosterically to receptor - prevents agonist at any concentration from producing a max effect on the receptor

A

Non-competitive antagonist

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38
Q

This is the maximal response of a drug

A

Emax

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39
Q

This is the concentration that produces 50% of the max effect

A

EC50

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40
Q

This is the total number of receptor sites

A

Bmax

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41
Q

This is the concentration of free drug at which half of the receptor sites are bound

A

Kd

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42
Q

What is the relationship of Kd and binding affinity

A

They are reciprocal

Low Kd means high binding affinity

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43
Q

What is potency?

A

This is EC50! The concentration required to produce 50% of drug’s maximal response

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44
Q

What is efficacy?

A

Emax! The upper limit of the dose-response curve

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45
Q

What is pharmacological antagonism? How many receptors does it have?

A

There are 2 drugs involved. One stimulates and one blocks the same receptor

1 receptor

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46
Q

What is chemical antagonism? How many receptors does it have?

A

A drug binds to another drug (ex. Lead poisoning)

0 receptors

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47
Q

What is physiologic antagonism? How many receptors?

A

Antagonist produces action that is opposite of the agonist and by a separate mechanism (ex. Sympathetic vs parasympathetic)

2 receptors

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48
Q

What is the most common route of drug administration?

A

Oral

It’s convenient but slow and less complete

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49
Q

What does first-pass mean?

A

It has to pass through the liver first - enough drug needs to be given to account for the loss in the liver

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50
Q

Where is the major site of absorption after oral administration?

A

Intestines b/c of surface area

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51
Q

What is the sublingual administration?

A

Under the tongue

It is very vascular so it goes directly into blood

Avoids first-pass!! And is fast

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52
Q

What is intramuscular administration?

A

Given in large volume in the muscle

Faster and more complete than oral b/c of more blood flow

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53
Q

What is subcutaneous administration?

A

Into the fat

Slower than intramuscular

Can give in large volume

Ex. Insulin

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54
Q

What is intravenous (IV) administration?

A

Does NOT involve absorption!!!! It’s directly into blood. Do not get tricked on this one….

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55
Q

What is the fastest route of absorption?

A

Inhalation

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56
Q

Why is inhalation a fast method of absorption?

A

Delivery is closest to the target tissue (Lungs) - large alveolar surface area

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57
Q

What is topical administration?

A

Application to the skin or mucous membranes of eyes, nose, throat

Very slow

Some topicals NEVER get into blood! And that’s good. Fewer side effects.

Asthma inhalers - topical! Just the lungs

(Cancer treatments - we don’t want them all over the body)

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58
Q

What is transdermal administration?

A

Application to the skin but for SYSTEMIC effect!!

This one ALWAYS involves absorption

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59
Q

This type of diffusion is driven by concentration gradient across a membrane?

A

Passive diffusion

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60
Q

Is passive diffusion saturable?

A

NO

There is no carrier

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61
Q

What is facilitated diffusion?

A

Driven by concentration gradient

Involved specific carrier proteins

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62
Q

Is facilitated diffusion saturable? Is there energy involved?

A

YES its saturable

No energy

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63
Q

What is active transport?

A

Moves against concentration gradient via carrier proteins

SATURABLE

Needs ATP

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64
Q

In _____ pH environments there are lots of hydrogens

A

LOW

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65
Q

In high pH, hydrogens ______.

A

Start to come off

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66
Q

Drugs pass more readily through membranes if they are ________.

A

Uncharged! Or non-ionized

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67
Q

What is the pKa

A

The pH where 50% of drug is ionized and 50% is non-ionized.

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68
Q

Non ionized is _______

A

Lipid soluble

It moves easily

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69
Q

Ionized is ______

A

Water soluble - it is easy to get rid of - high clearance!

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70
Q

If you put a drug in _____ environment, it will stay in the body.

A

Like or same

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71
Q

If you put drug in ______ environment, it will leave the body.

A

Opposite

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72
Q

What are 3 factors that influence absorption?

A

Blood flow to the absorption site

Total surface area available for absorption

Contact time at absorption site

73
Q

What is bioavailability?

A

(F)

The fraction of the administered dose that reaches the systemic circulation

IV is always 1!! (100%)

74
Q

As we get older, real function begins to decline. What does this mean for dosing?

A

Elimination takes longer so we need to lower the dose

75
Q

What does distribution depend on?

A

Size of organ, blood flow, capillary permeability, lipid or water solubility

76
Q

What do drugs need to bind to in order to get where it needs to go?

A

Plasma proteins!

Specifically albumin!

77
Q

What type of drug doesn’t need to bind to plasma proteins?

A

Water soluble drugs

78
Q

What is the total body water amount?

A

42 liters

79
Q

How many liters is the intracellular volume?

A

28 liters (2/3rds)

80
Q

How many liters is the extracellular volume?

A

14 liters (1/3rd)

81
Q

How many liter is intersitial volume?

A

10 liters

82
Q

How many liters is plasma volume?

A

4 liters

83
Q

What is the equation for Vd? (Volume of distribution)

A

Vd = amount of drug in body / concentration in the blood

84
Q

What does Vd tell you?

A

Where the drug is located

85
Q

What does a low Vd mean?

A

Most of the drug is in the BLOOD!!!

86
Q

What does high Vd mean?

A

Most the drug is in the tissues

87
Q

If a drug has a Vd of 25 L, and we need a plasma concentration of 1 mg/L. What is the amount of drug you would give?

A

25 mg

25 L x 1 mg/L = 25 mg

88
Q

Vd is 440L. If plasma concentration is 1 ug/L, and desired level is 3 ug/L. How much additional drug do we give?

A

880 ug

440 L (3ug/L - 1ug/L) = 880 ug

89
Q

A factor that increases Vd does what to the half-life?

A

It increases half life. B/c its just siting in the body and not being eliminated

90
Q

What are drug reservoirs?

A

Places in the body that drugs can hide

91
Q

In relation to Vd, when is hemodialysis helpful?

A

It is only helpful if Vd is low - because that means drug is in the blood and can be swept out by dialysis. It Vd is high, dialysis won’t do any good because most of the drug is in the tissue

92
Q

Placental transfer of drugs

A

The placenta is NOT a barrier!!! Just about every drug gets to fetus.

93
Q

What is the role of metabolism in drug inactivation and activation?

A

Most of the time metabolism is a way of termination of drug action

Occasionally drug metabolism is an way of drug activation

Or some drugs aren’t metabolized at all

94
Q

What is a prodrug?

A

They are inactive as administered then must be metabolized in the body to become active

95
Q

What are the 2 types of metabolism?

A

Phase 1 and phase 2

96
Q

Where does phase 1 take place?

A

Smooth ER

97
Q

How does phase 1 take place?

A

Enzymes (cytochrome P450) make minor chemical changes to the drug that make it more water soluble

98
Q

Where does phase 2 take place?

A

In the cytoplasm

99
Q

How does phase 2 take place?

A

Conjugation reactions

They need a transferase!!! Attaches other substance to drug to make a bigger molecule

It is harder to move in the body

100
Q

Why do neonates struggle with phase 2?

A

They don’t have the enzymes (transferases) to make it possible

101
Q

Where does metabolism take place?

A

LIVER - most important.

Also in the kidneys, GI tract, skin, and lungs

102
Q

How many CYPs are there that metabolize drugs in humans?

A

12

103
Q

Which type of cyps metabolize most drugs?

A

CYP2C, CYP2D, CYP3A

3A does about 50% on its own

104
Q

What are the 3 types of phase 1 reactions?

A

Oxidation
Reduction
Hydrolysis

105
Q

What are CYP inducers?

A

They increase the expression of p450 enzymes - tell our liver to make more enzymes = more metabolism

They also reduce the plasma level and the effectiveness of other drugs

106
Q

Which 4 drugs are CYP inducers?

A

Benzopyrene
Ethanol
Carbamazepine
Rifampin

Induce BERC

107
Q

What are CYP inhibitors?

A

Drugs that decrease the expression of p450

They increase the plasma level and increase the toxicity risk of other drugs (especially if TI on other drugs is low… very scary)

108
Q

Which 3 drugs are CYP inhibitors?

A

Cimetidine
Erythromycin
Grapefruit juice

Inhibit CEG

109
Q

What are the 3 types of Phase 2 reactions and their respective enzymes?

A

Glucouronidation - glucuronosyl transferase (neonates don’t have enough of these)

Sulfation - sulfotransferase

Acetylation - acetyltransferase

110
Q

What is the significance of slow or fast acetylators?

A

People vary - it means either fast or slow metabolizes

Slow - long half life, b/c in body longer
Slow acetylators could be more prone to lupus from drug

Fast - short 1/2 life

111
Q

What are the 2 types and locations of drug elimination?

A

Metabolism in liver

Renal excretion in kidneys

*Remember: drug elimination is not the same and drug excretion. A drug may be eliminated by metabolism long before the modified molecules leave the body

112
Q

What are the 3 stages of renal excretion of drugs?

A

Glomerular filtration

Proximal tubular secretion

Distal tubular reabsorption

113
Q

What takes place in glomerular filtration?

A

Only free unbound drug is filtered! If it is bound it’s too big to be filtered

The glomerulus does NOT care about charge!!! Only size discrimination

114
Q

What happens in proximal tubular secretion?

A

This involves energy - it needs transporters! OAT and OBT

Competition between drugs for carriers can occur here

*premature infants and neonates have incompletely developed tubular secretory mechanisms and may retain certain drugs

115
Q

What are the 2 energy requiring transport systems in the proximal tubular secretion?

A

OAT and OBT

116
Q

What happens in distal tubular reabsorption?

A

If uncharged, (nonionized) the drug may diffuse OUT of the tubule and back in the blood

Ionized can’t cross membrane so it gets stuck in tubule

117
Q

Why do we manipulate the pH of the urine?

A

To affect REABSORPTION!!

We want to increase the amount of drug ionized, to increase the elimination of that drug

The more that’s charged, the more I can get rid of

118
Q

How do we treat a weak acid overdose?

A

We alkalinize it (put it in its opposite environment) to enhance elimination

We want to keep the drug in the tubule so that you’ll urinate it out

119
Q

What are other modes of excretion?

A

GI tract
Pulmonary - exhale drugs
Milk

120
Q

What are the 2 types of renal clearance (rate of elimination)?

A

First order elimination

Zero order elimination

121
Q

What is first order elimination?

A

A constant FRACTION of drug is eliminated

Half life is constant

Non-saturating!! - enzymes are working less than Vmax

122
Q

What is zero order elimination?

A

A constant AMOUNT of drug is eliminated

Rate is the same

Half life is NOT constant

Saturated! - enzymes working at v max

123
Q

What are the only 3 drugs involved in zero order kinetics?

A

Phenytoin
Ethanol
Aspirin

Zero PEAs

Any other drug assume its 1st order

124
Q

How does half life relate to Vd and clearance?

A

If Vd goes up, half life goes up - if clearance stays the same

1/2 = Vd/Cl

125
Q

What are 3 clinical factors that increase half-life?

A

Diminished renal plasma flow

Renal disease

Decreased metabolism

126
Q

What is a maintenance dose?

A

A schedule of a drug to maintain the plasma concentration over a period of time

Daily, weekly, yearly, etc.

127
Q

What is loading dose?

A

Acute - used to achieve the target plasma level rapidly

128
Q

What is the therapeutic window?

A

It is the space between the minimum effective concentration and the minimum toxic concentration - we need to keep drugs in the therapeutic window

Sometimes we may need to take 1/2 the dose but give it twice as often to keep in window

129
Q

What is the target plasma level?

A

This is the degree of drug effect that is desireable and achievable.

If the effect of a drug is easily measured then trial and error approach works

130
Q

What do we do if the drug effect is not easily measured?

A

It must be titrated carefully and the following:

Pick target (steady state) plasma level
Compute a dose to achieve that
Measure plasma levels of drug
Adjust dosage as needed
131
Q

How do we calculate maintenance dose?

A

MD = Css x Cl / F

Css is concentration at steady state

Cl is clearance

F is bioavailability - remember IV =1!

*to calculate dose hour intervals just take MD x the hour amount

132
Q

How do we calculate loading dose?

A

LD = Css x Vd / F

133
Q

What doe we do if we see that Vd is in L/kg?

A

Multiply it by the patients weight to get it in liters

134
Q

What is loading dose?

A

It is one (or could be a series if drug has a long 1/2 life) dose given at the onset of therapy to reach the target concentration quickly

Usually called a bolus

135
Q

What is steady state?

A

This is the goal when you are giving a maintenance dose.

136
Q

Who do you know when you’ve reached steady state?

A

The graph levels off and plateaus. You want to stay there.

137
Q

If asked about the time is takes to reach steady state, what is the only thing you need to know?

A

Half life!!

138
Q

What amount of time is clinical steady state?

A

4-5 half lives

139
Q

If 1/2 life is 2 hours, how long until steady state is reached?

A

8-10 hours

140
Q

Drug is infused at a rate of 10 mg per hour. Steady state plasma levels of 7.5 ug/ml are reached in 32 hours. If infusion rate is doubled, how long will it take to reach steady state?

A

32 hours!

Don’t get tricked on this one…. time does NOT depend on rate

141
Q

What is the new steady state of drug if the infusion rate is doubled?

A

Steady state doubles also!

Do NOT get tricked!! Steady state depends on rate

142
Q

Drug of 100mg is given and it takes 8 hours to eliminate 1/2 the drug. How long does it take to eliminate 1/2 the drug if only 50 mg were given?

A

8 hours!

Time still stays the same even if amounts change

143
Q

Troughs are ______ you dose.

A

Before

144
Q

Peaks are ______ you dose?

A

After

145
Q

Peak should always be below?

A

Minimum toxic concentration

146
Q

Trough should always be above?

A

Minimum effective concentration

147
Q

Drugs you take once a day mean what about their therapeutic window?

A

They have a large window

If you have to dose 4x per day it means it has a small window

148
Q

What is the formula for correcting dose with renal failure?

A

CD = avg dose x (creatinine clearance/100mL/min)

149
Q

What is the relationship between 1/2 life and Vd?

A

They are directly proportional!!

If Vd goes up, 1/2 life goes up

150
Q

What is the relationship between 1/2 life and clearance?

A

Inversely proportional!

If 1/2 life goes up, Clearance goes down

151
Q

What is phase 1 in drug development?

A

It tests for the safety of the drug - it does NOT test the response!!

152
Q

What is phase 2 in drug development?

A

This tests the response of the drug and measures the response

153
Q

What is phase 3 of drug development?

A

Double blind study against a placebo to test for effectiveness and safety

154
Q

What is phase 4 of drug development?

A

Goes to market after approval for general use

155
Q

What are important limitations to preclinical testing?

A

Toxicity testing is time consuming and expensive, large numbers of animals needed, then the transfer of toxicity data from animals to humans is not completely reliable

156
Q

This phase is when the effects of a drug are tested with 20-25 (small number) of healthy volunteers

These trials are nonblind and many predictable toxicities are detected in this phase

A

Phase 1

157
Q

What are 2 cases where phase 1 is not a small number of cases in healthy people

A

Cancer and AIDS/HIV

158
Q

This is the phase where the drug is studied for the first time in patients with the target disease.

100-200 patients tested

Single blind

A

Phase 2

159
Q

What is the phase where the drug is evaluated in a large patient population (thousands) to establish both safety and efficacy

Double blind crossover technique

A

Phase 3

160
Q

This phase is what occurs after marketing approval. Surveillance program to catch any unforeseen toxicities

A

Phase 4

161
Q

When is the patent for drugs completed?

A

Around the time the drug enters animal testing - may take 15 to 20 years from start to finish

162
Q

How do generic drugs come about?

A

After the expiration of the patent, any company can produce and market the drug as a generic product if they demonstrate that it is bio-equivalent!

(Meets certain requirements for content, purity, and bioavailability)

163
Q

What comes before phase 1?

A

In vitro (in test tubes) first then animal testing

164
Q

What are 3 confounding factors in clinical trials?

A

Variable nature of the disease

Large enough population of subjects

Double blind design to eliminate bias

165
Q

Why is it important to randomize subjects and use a large test group?

A

The presence of other diseases and risk factors

166
Q

What are orphan drugs?

A

Drugs for rare diseases.

They are difficult to research, develop, and market

Tend to receive little attention or funding

167
Q

What is a SNP?

A

When a single nucleotide is exchanged

168
Q

What is a missense SNP? What are the 2 types?

A

They change the identity of an amino acid.

Conservative or non-conservative

169
Q

What is conservative missense SNP?

A

Amino acid replaced by an amino acid of similar chemical properties

170
Q

What is non-conservative missense SNP?

A

Amino acid change that is not similar resulting in loss of function

171
Q

What is Nonsense SNPs?

A

Lead to a stop codon

172
Q

What are synonymous SNPs?

A

Aka silent mutations

A different codon but still code for the same amino acid

173
Q

What does a change in SNPs/amino acids mean a change in?

A

CYP 450

174
Q

What is the role of pharmacogenetic in medicine?

A

They can be tailored to a person by person basis. Depending on age, gender, and health status

175
Q

How does a poor metabolized affect standard drugs?

A

Reduced elimination

Increased toxicity risk

176
Q

How are prodrugs affected with a poor metabolizer?

A

Decreased effectiveness

Decreased activation

177
Q

How are standard drugs affected by a rapid metabolizer?

A

Reduced effectiveness

Increased elimination

178
Q

How are prodrugs affected by a rapid metabolizer?

A

Increased activation

Increased toxicity risk

Fall17-Pharmacology (4 decks)

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