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POM Test 2 > Pharm > Flashcards

Pharm Flashcards

1
Q

Pharmacokinetics vs Pharmodynamics

A

Pharmacokinetics: how a drug molecule moves through your body vs Pharmacodynamics: how a drug molecule affects its target to produce the desired physiological effect

(kinetics= moves, dynamics = affects target)

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2
Q

What are the four parts of pharmacokinetics?

A
  1. Absorption
    1. How does a drug get into the body?
  2. Distribution
    1. How does a drug get to the target site?
  3. Metabolism?
    1. How is the drug molecule chemically altered by body?
  4. Clearance/Elimination
    1. How is drug molecule removed from the body?
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3
Q
  1. Drugs must cross _____ cell layers to enter the body.
  2. Drug molecules cross _______ by _______, ________, _____ based on their physical properties.
  3. Drug molecules must be _______ charged to cross plasma membranes by passive diffusion.
  4. The ___ of the environment can affect the charge stafe of drug.
  5. A drug’s _____ is related to how efficiently it is absorbed.
  6. Most drugs must reach the ___ in order to be distributed effectvely.
A
  1. Drugs must cross epithelial cell layers to enter the body.
  2. Drug molecules cross cell plasma membranes by passive diffusion, facilitated diffusion, active transport.
  3. Drug molecules must be neutrally charged to cross membranes by passive diffusion.
  4. pH
  5. A drug’s bioavailability is related to how efficiently it is absorbed.
  6. Most drugs much reach the blood in order to be distributed effectively.
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4
Q

Oral drugs

  • What is the external space?
  • Do oral drugs need to cross the epithelium?
  • Do oral drugs need to cross the endothelium?

Inhilation

  • What is the external space?
  • Do inhalation drugs need to cross the epithelium?
  • Do inhilation drugs need to cross the endothelium?

Topical

  • Do topical drugs need to cross the epithelium?

Where does IM drugs go?

Where do IV drugs go?

A

Oral drugs

  • GIT
  • yes
  • yes

Inihilation

  • alveoli
  • yes
  • no

Topical

  • no

IM goes to interstitial space

IV goes to blood stream

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5
Q

Where are oral drugs absorbed in the body and why?

A

Small intestine, largest SA

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6
Q

If a drug transit time is rapid will it get absorbed?

Rank mouth/esophagus, stomach, small intestined by drug transit time

A

If drug transit time is rapid it will not get absorbed

longest time small intestine > stomach > mouth/esophagus

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7
Q

What three factors can affect absorbtion?

A
  1. Surface area
  2. Drug transit time
  3. pH of lumen
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8
Q

What are the different ways drugs can pass through epitheliual cell layers and describe them.

A
  • Simple Diffusion
    • drug moving from high concentration to low concentration
    • non-saturable (not limited by amount transport protein)
  • Facilitated diffusion
    • drug moving from high concentration to low concentration with protein channel
    • saturable (limited by amount transport protein)
  • Active transport
    • drug moving from low concentration to high concentration with protein channel and ATP
    • saturable (limited by amount of transport protein)
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9
Q

Where are weak acids better absorbed and why?

A

Weak acids are better absorbed in the stomach. The pH of the stomach is low. Weak acids work well when they are unprotonated. They are unprotonated when they are in the form [HA]. This form arises when the pH is low (and the Acid will keep it’s hydrogen). (Lower than what? Lower than the pKa. )

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10
Q

Weak acid formula

A

For weak acids, pH < pKa = more neutral molecules

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11
Q

Weak bases formula

A

For weak bases when pH > pKa for neutral molecules

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12
Q
  • What can the weak acid/weak base formula tell you?
  • What is in the top numerator?
A
  • The weak acid weak bases formula can tell you the proportion of form without an H to form with an H, or neutral to not neutral vice versa. It can also tell you the pH and pKa.
  • The form without an H is in the numerator
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13
Q

Now the drug is in the plasma - from crossing the external space to the interstitial space, to the intravenous space/plasma.

What fraction of oral drugs make it into the plasma (in order to go into the intertitial and intracelullar spaces). What fraction of IM, what fraction of IV? What is this fraction called?

A

Oral drug fraction: <100

IM: <100

IV: <100

Bioavailability

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14
Q

Bioavailability

  • What is it?
  • How do you calculate it?
  • Does it differ by route?
  • What is an equation?
A
  • Bioavailability is the fraction of a drug dose that reaches the systemic circulation.
  • Area under the curve of a time (x) and concentration (y) graph divided by AUC of IV
  • YES
  • Can divide plasma concentration measured by plasma concentration
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15
Q
  • Summarize: How do oral drugs travel through the body?
  • When is the bioavailability of a drug measured
A
  • Oral drugs will get absorbed through the small intestine (because it has a high SA, long transit time, and neutral pH). They will pass through the epthelial layers of the small intestine. These epithelial layers are lipid bilayers and therefore the drugs must be hydrophibic. They will pass through these epithelial layers with simple diffusion, facilitated diffusion and active transport. They will then pass through the interstitial space and then through the endothelium in order to enter the plasma. In the plasma drugs are picked up in the mesenteric artery where they are shipped to the hepatic portal vein and through the liver. The drug is metabolized in the liver.
  • The bioavailability of a drug is measured after the drug is absorbed from the gut and survives metabolisms and clearance in the liver or AFTER the first-pass effect.
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16
Q

First - pass effect

A

The drug moves through the liver and is metabolized and this is called the first pass effect. A drug’s bioavailability is measured after the first pass effect.

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17
Q

Oral drugs can be degraded by….

A

intestinal bacteria

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18
Q

Distribution

  1. Most drugs must reach the ____ in order to be distributed effectively.
  2. Oral drugs are subject to the ___- that reduces bioavailability.
  3. Once in the blood drugs distribute to various tissues and body water compartments according to their ______.
  4. Drug binding ____ affects both its distribution and clearance.
  5. The ___ of a drug describes the distribution of a drug across the three body water compartments, and is crucial when caulculating the rate of drug clearance.
A
  1. blood
  2. first pass effect
  3. physical properties
  4. serum proteins
  5. Volume of Distribution (Vd)
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19
Q
  • What effects drugs going from the plasma to the interstitial space?
  • What effects drugs going from the interstitial space to the intracellular space?
  • What effect drugs in the intracellular space?
A
  • plasma to interstitial
    • protein binding
  • interstitial space to intracellular space
    • charge state (simple diffision)
    • transporters (facilitated/active diffusion)
  • intracellular space
    • hydrophobicity
    • pH trapping
    • binding to tissue targets
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20
Q

Vd information

  • What is a Vd?
  • What Vd distributes evenly across all compartments?
  • When is a drug more in the plasma and when is a drug more in the tissue?
A
  • Vd is the volume of distribution for a drug. It is a defined value (can look it up) of a certain drug and tells you about the drug’s pharmacokinetics, specifically how it distributes across different water compartments in the body (plasma, interstitial, intracellular).
  • Vd = .6 L/kg distributes evenly across all compartments ex. ethanol
  • A drug is more in the plasma when it has a Vd < 0.6 L/kg and a drug is more in the tissue when it has Vd > 0.6 L/kg
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21
Q

The average person has a body water content of .6L/kg. When do people not have this average body water content?

A

People do not have this average body water content if they are older (less water) or fat (less water).

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22
Q

Metabolism

  1. The _____ liver enzymes are largely responsible for the chemical degradation/modification of drugs via ____- and ______ reactions.
  2. Both types of reaction reduces ________ and increases the _____ of drug molecules, facilitating renal clearance.
  3. Drugs may be metabolized via _____ or ______ kinetics, depending on the saturation of the enzymes involved.
  4. Many drug-drug interactions result from effects on the ____ systems.
A
  1. cytochrome p450 (CYP450), Phase 1 and Phase 2
  2. drug efficacy, polarity
  3. zero order, first order
  4. CYP450
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23
Q
  • What is the main place drugs are metabolized?
  • What are some other places
A
  • Main: liver
  • kidney, small intestine, lungs
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24
Q
  • What are the organs involved in drug metabolism?
  • Where do phase I and phase II reactions take place?
  • Can drugs go through the body unmodified?What are the combinations of phase I and phase II reactions that drugs can go through? Which combinations can they not go through.
A
  • Organs involved are the liver, kidney and GI.
  • Phase I and phase II reactions take place in the liver.
  • Yes drugs can go through the body unmodified. They will go strait to the kidney and through the urine or strait to the GI and feces.
  • Phase I –> kidney –> urine
  • Phase 2 –> kidney –> urine or Phase 2 –> GI –> feces
  • Phase I –> Phase 2 –> kidney urine
  • Drugs will never go through phase II reactinon and then through phase I.
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25
Q

What is the point of metabolism/phase I and phase II reactions?

A

The general purpose of these chemical changes is to physically inactivate the drug and increase the chemical polarity of the molecule to make them easier to eliminate.

  • want to change the drug’s structure
  • make it polar so it is easier to eliminate (hydrophobic drugs are harder to eliminate)
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26
Q

Phase I

  • What is another name for phase I reactions?
  • What does phase I create?

Phase II

  • What is another name for phase II reactions?
  • What does phase II create?

What do the phase reactiosn accomplish?

A

Phase I

  • Another name for phase I reactions is functionalization phase.
  • Phase I creates a Phase I metabolite. (inactive drug, but could possibly still be active)

Phase II

  • Another name for a phase II reaction is conjugation phase.
  • Phase II creates a phase II metabolite an inactive drug.

The phase reactions make the drug more polar and also LARGER and result in increased clearance of the drug via the kidneys and GIT (renal and hepatic clearance).

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27
Q

What is an example of a phase I reaction?

What is an example of a phase II reaction?

What is an example of a drug that goes through these?

A

Phase I reaction - oxidation

Phase II reaction - glucuronidation (adding on a glucathione- large bulcky molecule that is charged)

Acetominophen goes through these

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28
Q

What fmaily of enzyme helps in phase I (functionalization phase) reactions?

A

Cytochrome p450 (oxidation)

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29
Q

What family of enzyme participates in phase II conjugation phase reactions?

A

UDP-glycouronosyltransferase (glucoronidation)

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30
Q

Cytochrome p450

What families are important in phase 1 (functionalization phase - oxidation)?

A

CYP1

CYP2

CYP3 (CYPA4/5 - metabolizes almost half)

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31
Q

A drug may be metabolized through multiple pathways, true or false.

A

True a drug may be modified through multiple pathways. Ex Acetominophen can be modified through Phase II Glucoronidation or Phase I oxidation and then Phase II glucoronidation conjugation. Some of the intermediates can be toxic.

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32
Q

Pro-drug

What is an example

A

Drug in inactive form. Certain drugs you swallow them in an inactive form called pro drug and then Phase 1 reactions convert the pro-drug to its active form.

An example is Clopidogrel (Plavix).

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33
Q

Zero-order kinetics

  • What does the time vs drug plasma concentration graph looks like?
  • Is the drug in excess or are the enzymes in excess?
  • Constant _____/hour
  • Is T1/2 constant? What happens to the T1/2 as the concentration decreases?
A
  • Linear graph with negative slow
  • The drug is in excess.
  • Constant mg/hour
  • T1/2 is not contant, it decreases as the concentration decreases
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34
Q

First order kinetics

  • Enzymes or drug in excess?
  • Is the clearance rate dependent on the drug concentration?
  • Constant ___/hour
  • T1/2 constant or not constant?
A
  • Enzyme is in excess
  • The clearance rate is dependent on the drug concentration.
  • Constant %/hour
  • T1/2 is constant.
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35
Q

Where on a graph that compares substrate and rate of reaction (v) (in constrast to the graph that is time and drug plasma concentration) is the first-order clearance kinetics shown?

A

First part of graph before Vmax is reached because the Rx rate < Vmax.

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36
Q

Clearance

  1. Some drugs modified in the ___- and cleared via the ______ may be subject to ___________.
  2. Antibiotics may alter the ______, affecting a drug’s pharmacokinetic profile.
A
  1. liver, GI enterohepatic circulation (EHC)
  2. EHC process.
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37
Q

Enterohepatic circulation

  • What is it?
  • What blocks the effect of enterohepatic circulation.
  • What specifically does enterohepatic circulation increase?
A
  • Enterohepatic circulation is when bacterial action in the GI reverse phase I/II modifications allowing drug reabsorption (drug can reenter the blood stream).
  • Antibiotics block the effect of enterohepatic circulation. This means that antibiotics block drugs reabsorption by GI bacteria.
  • Enterohepatic circulation increases the half-life of drugs.
38
Q

Drug-drug interactions that affect absorbtion ____________ and ____________.

____________ needs stomach acid to be in its hydrophilic form (HA). However ________raises the pH of your stomach and makes _________ less absorbable.

A

Drug-drug interactions that affect absorbtion omezaprole and cefpodoxime.

Cefpodoxime needs stomach acid to be in its hydrophilic form (HA). However omezaprole raises the pH of your stomach and makes cefpodoxime less absorbable.

39
Q

Describe the reaction between digoxin and antibiotics.

A

Digoxin is an anti-arrythmia. It is broken down by intestinal bacteria. If you are on an antibiotic it will kill this bacteria and too much digoxin will be absorbed and you get a drug overdose.

40
Q
  • What does warfarin do?
  • What will happen if you have warfarin that is not in the plasma?
  • What does warfarin usually bind to in the plasma?
  • What should you not take with warfarin? Why?
  • What part of the drug process is this effecting?
A
  • Warfarin is an anticoagulant. That means it stops the blood from clotting.
  • If you have free warfarin that is not in the blood there will be increased bleeding risk.
  • Warfarin binds to albumin proteins.
  • NSAIDS because NSAIDS will also bind to albumin proteins and leave free warfarin. The warfain will be free and there will be increased bleeding risk.
  • This is effecting distribution.
41
Q

How can drug drug interactions affect metabolism?

A

Different drugs can inhibit or induce the Cytochrome p450 (CYP) enzyme systems.

42
Q

What happens if another drug inhibits CYP enzyme system? induces?

A

If another drug inhibits the system then it will make the original drug too toxic. If another drug induces the system it will result in decreased efficacy for the original drug.

43
Q

Omezaprole ______ CYP and makes clopidogrel too _____ resulting in ________.

A

Omezaprole inhibits CYP and makes clopidogrel too active resulting in increased clotting risk.

44
Q

Clearance drug-drug interactions

One drug can inhibit the clearance of another drug. ________ and ________ are an example of that.

A

Digoxin and Veramapil is an example of that.

45
Q

Describe the interaction between digoxin and veramapil.

A

Drugs are eliminated through the kidney nephron. On the kidney nephron there is a transporter protein in the nephron epithelial cells called P glycoprotein (PGP) that eliminates Digoxin. PGP is inhibited by Veramapil and therefore Varamapil inhibits the clearance of Digoxin.

46
Q

Age can affect all aspects of pharmacokinetics. What does Beer’s criteria tell physicians?

A

The decreased dosing for older adults.

47
Q

Genetic variations can affect a drug’s pharmacokinetics. What transport protein genetic variation would specifically affect absorption and clearance?

A

p-glycoprotein (aka MDR1)

p-glycoprotein helps with absorption from GIT (intestine) and clearance via bile (liver) and urine (kidney).

48
Q

p-glycoprotein

  • What type of protein is this?
  • P-glycoprotein have many _____ that alter its activity.
A
  • This is a transmembrane protein
  • P-glycoprotein have many polymorphisms that alter its activity.
49
Q

There can also be polymorphisms in ______ genes that lead to variations in drug metabolism.

A

CYP (can decrease or increase drug activity)

50
Q

Most drug targets are _____

A

proteins

catagories of proteins include receptors, ion channels, enzymes, and carriers

51
Q

What is the difference between an agonist and an antagonist?

A

An agonist mimics what a normal ligand does and an antagonist binds and prevents a normal ligand from binding.

52
Q

Dose-response curve

A

Dose-response curve shows x axis with concentration of drug (mg/ml) and % maximum occupancy and is a logarithmic scale. It usually looks like a sigmoidal curve. A dose response curve shows the Kd.

53
Q

Kd

  • What is it?
  • Lower Kd means…
A
  • Kd is a dissociation constant. It is a direct reflection of the affinity.
  • Kd is the concentration of drug at which 50% of receptors are bound.
  • Lower Kd means higher affinity. This is because you need less concentration to bind 50% of the receptors.
54
Q

Which of these curves has a higher affinity for the drug?

A

Ace

55
Q

Does this picture show a high or low Kd? Why?

A

This picture shows a higher Kd. This is because it takes a high concentration of the drug to bind 50% of the receptors. This means the affinity is not that good.

56
Q

Does this picture show a high or low Kd? Why?

A

This picture shows a low Kd. This is because it does not take that much concentration of the drug to bind 50% of the receptors. This means that there is a high affinity.

57
Q

Hill Langmuir Equation

  • What is the equation? How do you remember it?
  • What can you determine using the equation?
  • What graph does it go with?
A
  • Equation
    • Y = [D]/(Kd+ [D])
    • D over D plus JD (KD)
  • Y = PERCENT occupancy of the receptors
  • D = concentration of drug
  • Kd = dissociation concstant
  • Dose response curve graph
    • x is log based concentration
    • Y is fraction bound of receptors
58
Q
  • How is potency different from drug efficacy?
A
  • Potency is related to Kd. The lower the Kd the more potent the drug. Potency is all about how the drug binds to the receptor.
  • Drugs can have different potency but still 100% efficacy. Efficacy is the ability for a drug to produce the desired therapeutic effect. Efficacy is what the drug does when it is bound to the receptor.
  • On the graph below the drugs reach 100% efficacy at different potencies (they need different concentrations).
59
Q

Do potency and efficacy correlate?

A

No! see example below

60
Q

Does receptor occupancy equal theraputic benefit? Explain.

A

No! Not all the receptors have to be full to receive full therapuetic benefit.

  • This is because receptors are G protein coupled receptors therefore if you activate just one you are still activating an entire cascade (adenelyl cyclase –> CAMP –> protein kinase A) and produce the maximum physiological effect.
61
Q

Receptor reserve

A

There are generally more receptors than needed to produce the max effect. (There are more receptors than occupied by drugs)

62
Q

Antagonists

A

Antagonists block the effect of endogenous molecules

63
Q

Competitive Antagonist

A

The agonist (original ligand) and antagonist compete for the SAME site. The antagonist binds reversibly.

64
Q

Non-competitive antagonist

A

The agonist and antagonist bind to DIFFERENT sites. It is still reversible.

65
Q

Non-competitive antagonist (irreversable)

A

Antagonist binds IRREVERSIBLY to the receptor. It attatches covalently.

66
Q

What do competitive antagonist do to the original agonist?

A

Competitive antagonists decrease the potency of the original agonist. You will now need more of the agonist to bind to the receptors in order to achieve 100% efficacy.

67
Q

What do non-competitive antagonist do to the agonist?

A

They crush the efficacy. When the antagonist binds to the receptor (at a different site) it makes it unable for the agonist to bind to that receptor. That takes that receptor out of the equation and therefore efficacy can never be achieved.

68
Q

Full agonist/agonist

Examples

A

Drug that binds to the same place that the ligand would bind on the receptor and mimics the effects of endogenous molecules.

Examples: endorphins, morphine and heroin

69
Q

Partial agonist

example

A

A partial agonist is a drug that binds to a receptor but cannot produce the maximum response from receptor.

example: bupenorphine and nalbuphine (remember bup for partial agonist)

70
Q

Neutral antagonist

example

A

A neutral antagonist will inhibit the normal agonist from producing its response.

example: naltrexone

71
Q

Inverse agonist

example

A

Inverse agonist bind and turn off the basal signaling of a drug. Can also be competitive antagonist if they happen to bind at the same site as the agonist.

example: naxalone

72
Q

Quantal dose response curves

A

Y axis is % of patients instead

73
Q

ED50

A

Effective dose at which 50% of the patients have a therapeutic effect.

74
Q

TD50

A

Toxic dose at which 50% of the patients have toxic effects.

75
Q

LD50

A

Dose at which 50% of patients die.

76
Q

Therapeutic window

A

Range between the minimum effective dose and the minimum toxic dose.

77
Q

Therapeutic index (TI)

  • Do you want this to be higher or lower?
A

TI = TD50/ED50

HIGHER IS BETTER

78
Q

Which curve has the highest TI? lowest?

Which drug is the most dangerous? Least dangerous?

A

Red curve highest TI, blue curve lowest

blue curve is most dangerous red curve is least

79
Q
  • What does this dose-response curve mean?
  • What measurement would we use to determine safety of the drug?
  • Why?
A
  • Off-target effects - the drug binds to one receptor for therapeutic effects and another one for off target effects.
  • Use Certain Safety Factor (CSF)
  • Why? Because the TI would be similar to mechanism based toxicity however because the curves are not parallel a dose could kill some patients.
80
Q

Certain Safety Factor (CSF)

A

LD1/ED99

HIGHER IS BETTER

81
Q

Additive

A

When two drugs have the same therpeutic effect and the effect of drug A and drug B are added together.

82
Q

Synergistic

A

When two drugs have the same therapeutic effect and drug A and drug B have an effect that is greater than them added together. Therefore you can give lower/same doses of A and B and get more of an effect.

83
Q

Antagonistic Effect

A

If two drugs have the same therapeutic effect but together add up less. (Still better than drugs alone).

84
Q

Potentiation

Example

A
  • Called potentiation because of the two drugs only one of the drugs is having a therapeutic benefit and the other drug is only there to potentiate or improve the effect of the first drug. The second drug has no thera benefit on its own.
  • Cephalosporin is the drug and probenocide potentiates the effect of the antibiotics (but has no effect of its own).
85
Q

Tolerance/Desensitization

A

Reduce effect with continued use of a drug. With repeated doses your cells become desnsitized to the drug.

86
Q

Tachyphylaxis

A

Tolerance/desensitization (reduced effect with continued use of a drug) that applies to short term effects

87
Q

What process do

  • receptor inactivation
  • receptor internalization
  • receptor down regulation

have to do with?

A

Tolerance/desensitization

88
Q

Receptor inactivation

A

Tolerance/desensitization - The drugs bind to the receptors but the receptors are chemically inactivated (uncoupled from the cascade).

89
Q

Receptor internilization

A

The receptor will get interalized and recycled and will no longer be able to bind agonists.

90
Q

Receptor down regulation

A

Receptor gets internalized and chemically broken down by lysosome.

91
Q

Describe the difference between these two graphs.

A

In the first graph there are less receptors but there are still enough to produce 100% efficacy. The potency of the drug decreases.

In the second graph there are less receptors but there are no longer enough to produce 100% efficacy.

92
Q

Vd equation

A

Vd = Q/Cp

Vd = dose/plasma concentration

POM Test 2 (8 decks)

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