Pharmacology I > Kinetics > Flashcards

Kinetics Flashcards

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1
Q

what are the main causes of the main alterations in ADME

A
  • age
  • genetic factors
  • end organ damage
  • drug interactions
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2
Q

what are the types of variability in ADME

A
  • pharmacokinetics
  • pharmacodynamic
  • idiosyncratic
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3
Q

describe idiosyncratic variability

A
  • occur in a small minority of patients
  • sometimes with low or normal doses
  • poorly understood
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4
Q

what is a pharmacodynamic interaction

A

interaction between 2 or more drugs that leads to:
-accentuation/synergism
- attenuation/antagonisn

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5
Q

what is an example of accentuation/synergism

A

calcium channel blocker and a beta blocker

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6
Q

what is an example of attenuation/antagonism

A

narcan and opiods

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7
Q

do pharmacodynamic interactions have to do with ADME

A

no

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8
Q

do pharmacokinetic interactions have anything to do with ADME

A

yes

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9
Q

what drugs do we need to check for interactions with/what drugs have many other drug interactions

A
  • warfarin
  • digoxin
  • TCAs
  • phenytoin
  • carbamazepine
  • lithium
  • methotrexate/cyclosporine/tacrolimus
  • HIV medications - protease inhibitors
  • rifampin
  • paxlovid
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10
Q

what is the result of the interaction of tetracycline and antacids

A

antacid impairs absorption of ABX resulting in decrease ABX efficacyw

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11
Q

what is the result of the interaction between erythromycin/clarithromycin/ metronidazole/ciprofloxacin/trimethaprim- sulfamethoxazole and warfarin

A

ABX inhibits the metabolism of warfarin resulting in increased serum concentration of warfarin and increasing the risk of bleeding

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12
Q

what is the result of the interaction between NSAID and warfarin

A

additive effect on decreased platelet aggregation resulting in additive risk for bleeding, especially GI bleeding

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13
Q

what is the result of the interaction between ASA and warfarin

A

additive effect on decreased platelet aggregation ->additive risk for bleeding, especially GI bleeding

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14
Q

what is the result of the interaction between tramadol and antidepressants

A

increased risk of serotonin syndrome

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15
Q

what is the result of the interaction between protease inhibitors and BZD

A

protease inhibitors are CYP 450 3A4 inhibitors -> decreased metabolism of benzodiazepine -> increased benzodiazepine concentrations -> increased risk of benzodiazepine side effects which are increased sedation depth and duration

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16
Q

what are the things to consider with pregnant patients

A
  • increased cardiac output increases distribution of drugs
  • increased renal blood flow increases elimination of drugs and decreases the duration and effects of drugs
  • decreased albumin which decreases binding of drugs -> more free drug to act -> drugs have more pronounced effects
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17
Q

what are the considerations for patients with uncontrolled DM

A
  • gastric stasis -> decreases rate of absorption of drugs
  • nephrotic syndrome -> glomerulus gets damaged -> protein gets in kidneys -> proteinuria -> damages kidneys and generalized edema in body -> decreases rate of absorption of drugs -> decreased albumin -> more pronounced drug effect
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18
Q

what medications will worsen myasthenia gravis

A
  • aminoglycosides
  • fluoroquinolones
  • tetracyclines
  • macrolides
  • magnesium
  • beta blockers
  • procainamide
  • neuromuscular blockers
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19
Q

what is a side effect and give example

A

unrelated to clinical drug effect, predictable, dose related
- ex: an ABX causing GI upset

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20
Q

what is a toxic reaction and give example

A
  • an exaggeration of the clinical effect, predictable, dose related, happens when you take too much of. adrug
  • EX: taking beta blocker twice -> drop in BP and dizzy
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21
Q

describe an allergic reaction

A

immune mediated responses, happen quickly and are very dangerous

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22
Q

what is the positive to dental drugs

A
  • primarily single dose or short term tx
  • large margin of safety
  • extensive hx of use
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23
Q

what is pharmacokinetics

A

what the body does to the drug

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24
Q

what is pharmacodynamics

A

what the drug does to the body

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25
how do we use kinetics
- important in drug development and clinical testing, needed to determine optimal dose
26
how are kinetics important in the clinical setting
- toxicology - therapeutic monitoring - drug interactions - dose adjustments - effect of illness, organ dysfunction
27
time course of drug concentration in kinetics depends on ______
ADME
28
kinetics focuses on:
concentrations of drug in plasma
29
what can you use to calculate precise doses to achieve a precise concentration
kinetics
30
what is the goal of plasma concentration
get plasma concentration within a therapeutic window in order to elicit appropriate response without causing toxicity
31
what does clearance determine
the maintenance dose-rate
32
what does the volume distribution determine
the loading dose
33
what does the half life determine
the time to steady state and dosing interval
34
CL, VD, and half life are derived from a:
time/concentration curve
35
what is the definition of clearance
volume of plasma cleared of drug per unit of time
36
the clearance is the index of:
how well a drug is removed irreversibly from the circulation
37
the clearance determines the dose/rate required to:
maintain a CP
38
how do you calculate clearance of a drug - what is the formula
- creatinine clearance - males: 140 - age / SCR - women: 140 - age/ SCR ) x 0.85
39
describe zero order kinetics
- rate of absorption/elimination doesnt depend on the drug concentration - rate limited process- fixed number of enzymes, carrier, or active transport proteins; saturation occurs - half life decreases over time
40
what are the only drugs that undergo zero order kinetics
- phenytoin - warfarin - heparin - ethanol - aspirin (high dose) - theophylline
41
what is the relationship on zero order kinetics
linear
42
half life _____ with decreasing concentration in zero order kinetics
decreases
43
describe first order kinetics
- the decline in plasma concentration is not constant with time, but varies with concentration - the half life stays the same - concentration decreases by 50% per each half life - majority of drugs follow first order elimination
44
what is the relationship of first order kinetics
logarithmis
45
length of half life in first order kinetics is _____
constant
46
what does the rate constant measure and what is its variable
- KE - KE = 0.693 / half life
47
what is the formula for clearance
CL = KE x VD
48
to maintain steady state plasma concentration administration rate must equal:
rate of elimination
49
how will the CP eventually reach steady state
when repeated doses of a drug are given in short enough intervals and elimination is first order
50
during IV infusion, drug levels:
increases exponentially in a way equivalent to the drugs half life
51
how many half lives is steady state achieved after
5
52
what does volume of distriution tell you
volume into which a drug appears to be distributed with a concentration equal to that of plasma - tells you where the drug distributes
53
what is an equation for VD
F x dose /CP0
54
what is the bioavailability for IV drugs
1 (100%)
55
what does a large VD indicate
tells us it gets everywhere in the body and are more lipophilicd
56
drugs will small VD:
are more polar and water soluble
57
what does half life provide an index of
- time course of drug elimination - time course of drug accumulation - choice of drug interval
58
how many half lives does it take for drugs to be eliminated from the body
5
59
what is the definition of steady state kinetics
- point at which the amount absorbed equals amount eliminated per unit time
60
what is the formula for concentration of steady state kinetics
- CSS = KA / (VD x KE)
61
what is the formula for CSS in calculating oral doses
- CSS = (1.44 x DM x F x half life) / (T x VD)
62
what is the formula for calculating an initial load dose
D = (VD x CSS) / F
63
what is the formula for repeat loading dose
D = (VD)(CSS - Cmeasured) / F
64
what is the formula for loading dose
D = Vd x CSS
65
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