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Pharmacology > Pharm principles > Flashcards

Pharm principles Flashcards

1
Q

What is Km?

A

The amount of substrate needed to get to 1/2 Vmax

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2
Q

What is Vmax?

A

Max velocity of enzymatic reaction. Directly proportional to enzyme concentration.

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3
Q

What is the relation ship between Km and affinity?

A

Inversely proportional; w/ small Km, not much substrate is needed to achieve 1/2 vmax –> high affinity
w/ large Km, more substrate is needed to acheive 1/2 v max –> lower affinity

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4
Q

On a Lineweaver Burk plot, what is the y intercept

A

1/Vmax

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5
Q

What does a higher y intercept on a Lineweaver Burk plot mean?

A

Lower V max.

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6
Q

On a Lineweaver Burk plot, what is the x intercept

A

1/Km

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7
Q

What does a x intercept closer to 0 on a Lineweaver Burk plot mean?

A

Higher Km, lower affinity

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8
Q

On Lineweaver burk plots, what do reversible competitve inhibitors look like?

A

Inhibitor has steeper slope with higher Km(lower affinity),, will cross the regular line at the v/max.

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9
Q

On Lineweaver burk plots, what do noncompetitve inhibitors look like?

A

Higher y intercept (lower vmax), lines do not cross. Will have same Km as regular line.

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10
Q

How do reversible competitive inhibitors work?

A

Bind active site of enzyme. Can be overcome by increase in substrate concentration.

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11
Q

What is the effect of reversible competitive inhibitors on Vmax /efficacy? What is efficacy

A

Unchanged.

Efficacy is the maximum effect a drug can produce regardless of dose.

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12
Q

What is the effect of reversible competitive inhibitors on Km /potency? What is potency?

A 
Increases Km (lowers affinity); more substrate needed to reach half max effect. 
Potency is amount of drug needed to produce an effect.
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13
Q

How do irreversible competitive inhibitors work?

A

Bind active site but cannot be overcome; effectively eliminates available enzymes.

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14
Q

What is the effect of irreversible competitive inhibitors on Vmax /efficacy?

A

Decreases Vmax/efficacy because it has effectively eliminated enzymes, thus decreasing the max effect possible at any dose.

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15
Q

What is the effect of irreversible competitive inhibitors on Km /potency?

A

Unchanged.

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16
Q

How do noncompetitive inhibitors work?

A

Do not resemble substrate. Do not bind active site. Cannot be overcome by more substrate. Effectively reduce enzyme availability.

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17
Q

What is the effect of noncompetitive inhibitors on Vmax /efficacy?

A

Decreases Vmax/efficacy because it has effectively eliminated enzymes, thus decreasing the max effect possible at any dose.

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18
Q

What is the effect of noncompetitive inhibitors on Km /affinity?/potency?

A

unchanged

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19
Q

What is Vd?

A

Volume of distribution = amount of drug in body/plasma drug concentration.

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20
Q

What is the distribution of large charged molecules?

A

Low, blood only. Usually protein bound.

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21
Q

What is the distribution of small hydrophilic molecules?

A

Medium, ECF as well.

22
Q

What is the distribution of small hydrophobic/lipophilic molecules?

A

High. Dist in all tissues including fat.

23
Q

What is the definition of clearance?

A

Volume of plasma cleared up drug per unit time.

24
Q

What is the equation for clearance?

A

rate of elim/plasma drug concentration.

aka Vd * elimination constant

25
Q

How many half lives does it take a drug infused at a constant rate to reach steady state?

A

4-5

26
Q

What is the formula for half life?

A

(.693 * Vd)/Clearance

27
Q

What is the formula for loading dose?

A

(Target plasma conc * Volume dist)/ Bioavailability

28
Q

What is the formula for maintenance dose?

A

(Target plasma conc * Clearance * dosage interval)/Bioavailability

29
Q

Does renal/liver disease affect loading dose or maintenance dose?

A

Maintenance dose. Loading usually unchanged.

30
Q

What is TD50?

A

Median toxic dose

31
Q

What is ED50?

A

Median effective dose

32
Q

What is the therapeutic index?

A

TD50/ED50.

33
Q

What does a high therapeutic index indicate?

A

Takes a lot to be toxic or a little to be effective - safer drug.

34
Q

What does a low therapeutic index indicate?

A

Takes a little to be toxic or a lot to be effective - less safe drug.

35
Q

What are 4 classic drugs w/ low therapeutic index?

A

Digoxin, lithium, theophylline, warfarin.

36
Q

What is zero order elimination?

A

Constant AMOUNT of drug eliminated per unit time.

Straight line. Not related to drug concentration.

37
Q

What is first order elimination?

A

Constant FRACTION of drug eliminated per unit time.

Curve. Directly proportional to drug concentration.

38
Q

Which order elimination is capacity limited?

A

zero order.

39
Q

What order elimination is flow dependent?

A

first order.

40
Q

What environment are acidic drugs trapped in?

A

Basic. Treat overdose with sodium bicarb: alkalinizes urine.

41
Q

What medications are classic examples of weak acids?

A

Aspirin, TCAs, phenobarb, methotrexate

42
Q

What environment are basic drugs trapped in? What do you give to trap it?

A

Acidic. Treat overdose with ammonium chloride: acidifies urine.

43
Q

What is phase I of drug metabolism? What does it yield?

A

Cytochrome p450. Redox reactions, hydrolysis.

Yields slightly polar, water soluble, often still active.

44
Q

What is phase II of drug metabolism? What does it yield?

A

Conjugation. Glucuronidation, Acetylation, Sulfation.

Usually yields very polar, inactive metabolites that are renally excreted.

45
Q

What phase of drug metabolism do geriatric patients lose first?

A

Phase I.

46
Q

Why might slow people metabolize drugs more slowly?

A

Slow acetylators have increased risk of side effects of drugs because of decreased rate of metabolism.
*Eg, drug-induced lupus.

47
Q

How do diazepam and flumenazil act on GABA receptor?

A

Diazepam = agonist
Flumenazil = competitive antagonist.
- Flumenazil decreases potency, no change in efficacy.

48
Q

How do norepi and phenoxybenzamine act on alpha-receptors?

A

Norepi = agonist
Phenoxybenzamine = Noncompetitive antagonist.
Decreases efficacy.

49
Q

What is the difference between agonist and partial agonist?

A

Partial agonist acts at the same site as full agonist, but with lower maximal effect (lower efficacy).
Potency = independent variable.

50
Q

Classic example of partial agonist?

A

Buprenorphine vs morphine at opioid receptors.

Pharmacology (17 decks)

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