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PHARM > kenetics > Flashcards

kenetics Flashcards

1
Q

alterations in ADME main causes

A

Age
Genetic factors
End-organ damage
Drug interactions

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2
Q

types of variability

A

Pharmacokinetic
Pharmacodynamic
Idiosyncratic

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3
Q

idiosyncratic variabilty

A

Occur in a small minority of patients
Sometimes with low or normal doses
Poorly understood

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4
Q

Pharmacodynamic interaction

A

Interaction between 2 or more drugs that leads to

Accentuation/synergism
Attenuation/antagonism

Don’t directly involve absorption, distribution, metabolism, or excretion

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5
Q

Pharmacokinetic interaction

A

Interaction that changes the basic kinetic properties:
Absorption
Distribution
Metabolism
Elimination

Example: warfarin +sulfamethoxazole

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6
Q

RED FLAG DRUGS for possible interactions

A

∙Warfarin
∙Digoxin
∙TCAs (amitriptyline, doxepin, nortriptyline, desipramine)
∙Phenytoin
∙Carbamazepine
∙Lithium
∙Methotrexate / cyclosporine / tacrolimus
∙HIV medications – protease inhibitors (indinavir, nelfinavir, ritonavir, saquinavir)
∙Rifampin

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7
Q

tetracycline ABX (tetracycline, doxycycline, minocycline) + antacids

A

antacid impairs absorption of ABX → ↓ ABX efficacy

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8
Q

erythromycin / clarithromycin / metronidazole / ciprofloxacin / trimethaprim-sulfamethoxazole + warfarin

A

ABX inhibit the metabolism of warfarin → ↑ serum concentration of warfarin → ↑ risk of bleeding

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9
Q

NSAID + warfarin

A

Additive effect on ↓ platelet aggregation → additive risk for bleeding (especially GI bleeding)

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10
Q

ASA + warfarin

A

Additive effect on ↓ platelet aggregation → additive risk for bleeding (especially GI bleeding)

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11
Q

Tramadol + antidepressants (DDI highest risk for MAO-I)

A

↑ risk of serotonin syndrome (excess serotonin)

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12
Q

Protease inhibitors (indinavir, nelfinavir, ritonavir, saquinavir) + BZD

A

protease inhibitors are CYP450 3A4 inhibitors → ↓ metabolism of benzodiazepine → ↑ benzodiazepine concentrations → ↑ risk of benzodiazepine side effects (↑ sedation depth and duration)

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13
Q

pregnancy physio effects and result of these

A

Increased cardiac output
Increased renal blood flow: more filtrate/elimination
Decreased albumin: less drug protein bound

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14
Q

drugs and the placenta

A

lipophilic drug may cross the placental bloood barrier and are eliminated more slowly, increased half life

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15
Q

Diabetes and altered physio with effects

A

gastric stasis: decreased absorbtion
nephrotic syndrome : proteinuria=hypoalbuminenmia

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16
Q

MG pts, caution with what drugs

A

Aminoglycosides
Fluoroquinolones
Tetracyclines
Macrolides
Magnesium
Beta blockers
Procainamide
Neuromuscular blockers*

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17
Q

drug side effects

A

unrelated to clinical effect, predictable and dose related

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18
Q

toxic rxn

A

related to clinical effect and predictable= exaggeration of clinical effect

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19
Q

allergic rxn

A

less predictable, immunological base
not related to clinical effect

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20
Q

dental drugs upside

A

Primarily single-dose or short term Tx
Large margin of safety
Extensive history of use

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21
Q

Pharmacokinetics

A

What the body does to the drug

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22
Q

Pharmacodynamics

A

What the drug does to the body

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23
Q

How we use kinetics

A

Important in drug development and clinical testing, needed to determine optimal dose

Important in the clinical setting:
Toxicology
Therapeutic monitoring (clinical effect, labs)
Drug interactions
Dose adjustments
Effect of illness, organ dysfunction

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24
Q

Time course of drug concentration depends on what events?

A

Time course of drug concentration depends on ADME

25
Q

Kinetics focuses on? Can be used to calculate?

A

focuses on concentrations of drug in plasma

Can use kinetics to calculate precise doses to achieve a precise concentration

26
Q

Cp

A

Plasma concentration = Cp
Goal is to get Cp within a therapeutic window in order to elicit appropriate response without causing toxicity

27
Q

MTC vs MEC

A

Minimum toxic concentration: minimal con for toxic effect
Minimum effective concentration: minimal con for any effect (non-therapeutic)

28
Q

therapeutic window

A

desired concentration between MTC and MEC

29
Q

Important parameters of kenetics and what they determine

A

Clearance – determines the maintenance dose-rate
Volume of distribution (Vd) – determines the loading dose
Half-life – determines the time to steady state and dosing interval

30
Q

Parameters for a drug are determined by using what administration and why?

A

Parameters for a drug are determined by using IV injection or infusion since IV = 100% bioavailability
Cl, Vd, and t½ are then derived from a time/concentration curve

31
Q

clearance
Volume of?
Index of?
Determines the?
way to correlate?

A

Volume of plasma cleared of drug per unit time

Index of how well a drug is removed irreversibly from the circulation

Determines the dose-rate (dose/unit time) required to maintain a Cp

Creatinine clearance = way to correlate

32
Q

Zero order Kinetics

A
  • Rate of absorption /elimination doesn’t depend on the drug concentration
  • Rate limited process
  • Fixed number of enzymes, carrier, or active transport proteins; saturation occurs
  • Half life (t ½ ) decreases over time
33
Q

substances with zero order kenetics

A

Phenytoin
Warfarin
Heparin
Ethanol
Aspirin (high dose)
Theophylline

34
Q

First order kinetics

A
  • The decline in Cp is not constant with time, but varies with concentration
  • The half life (t ½ ) stays the same
    • Concentration decreases by 50% per each t ½
  • Majority of drugs follow first order elimination
35
Q

expression for rate of absorbtion/elimination

A
36
Q

clearence calculation
index of?
determines?
to maintain Cpss

A

Index of how well a drug is removed irreversibly from the circulation

Determines the dose-rate required to maintain a Cp

To maintain steady state (Cpss), , administration rate must equal rate of elimination

37
Q

Steady state / plateau effect with first order kinetics

A

When repeated doses of a drug are given in short enough intervals and elimination is 1st order, the Cp will eventually reach steady state

During IV infusion, drug level increases exponentially in a way equivalent to the drug’s t1/2:
1 half life = 50% of final concentration
2 half lives = 75% of final concentration
3 half lives = 87.5% of final concentration, etc.

38
Q

steady state diagram
IV and injection

A
39
Q

how many t1/2 pass for SS?

A

usually achieved after 5

40
Q

what could increase the amount of dosages/time to reach Cpss?

A

any alterations to drug t1/2 such as renal dx

41
Q

Volume of distribution (vd)

A

Volume into which a drug appears to be distributed with a concentration equal to that of plasma

Tells you where the drug distributes

To reach a target Cp, you have to “fill up the tank”, i.e., Vd

42
Q

Vd equation

A
43
Q

important notes of Vd
IV F?
body volume and Vd?
small Vd?

A

Remember: bioavailability (F) for IV drugs equals 1 (100%)

Note: Vd can far exceed the actual body volume, e.g., digoxin Vd = 500L

Drugs with small Vd tend to be polar and water soluble

44
Q

t1/2 provides index of:

A

Time course of drug elimination
Time course of drug accumulation
Choice of drug interval

45
Q

how many t1/2 to reach Cpss or elimination

A

Takes approximately 5 half-lives for a drug to either reach steady state (Cpss) or be eliminated from the body

46
Q

t1/2 calc

A
47
Q

SS kenetics: what is SS and calc?

A

Point at which the amount absorbed equals amount eliminated per unit time

48
Q

how could Ka be calculated using Css

A

Css calc rearranged

49
Q

For continuous infusion, ka units are?

A

dose/unit time

50
Q

Calculating oral doses for Css

A

w

51
Q

Calculate a loading dose: initial and repeating

A
52
Q

Cl calc

A
53
Q

Css calc (IV)

A
54
Q

Css calc (PO)

A
55
Q

loading dose calc

A
56
Q

Vd calc

A
57
Q

Ke and t1/2 calc

A
58
Q

C
Cp0
Css
ke
ka
t
cl
Vd
D
F

A

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