pharmacology principles Flashcards

1
Q

Pharmadynamics

The action of the drug on the body

A
Receptor interactions
    - agonist/antagonist 
    -affinity or selectivity
  Dose response Curve
     effective dose in 50 nrats
     toxic dose in 50 rats
MOA- Mechanism of Action
Toxic action-adverse reaction/serious SE above toxic dose
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2
Q

Therapeutic Window

A

Between the effective dose and toxic dose

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3
Q

Therapeutic Index

A

Effective Dose
_________________ = Therapeutic Index
Toxic dose

TI score closer to 1 = more dangerous

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4
Q

Side effect

A

Unintended effects when dosage in therapeutic range

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5
Q

Potency

A

Amount of drug needed to produce a response

Effectiveness

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6
Q

Pharmacokinetics

Absorption Metabolism
Distribution Elimination

A

The body’s action on the drug

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7
Q

pharmacodynamic

A

drug profile remains unchanged throughout a persons lifetime ( what the drug does to the body

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8
Q

pharmacokinetics

A

changes with aging etc ( body response to drug)

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9
Q

Cipro vs Rocephin

A

Cipro given PO ( lipid soluble)

Rocephin given parenthaly (water soluble)

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10
Q

Absorption

Bioavailability- amount of drug reaching
circulation ( Crestor =lower dose for effectiveness)

A

Factors which affect
GI tract (lipid soluble-resists stomach acid)
Molecular weight

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11
Q

Absorption

CMAX

A

Maximum concentration per dose

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12
Q

Absorption

TMAX

A

Latency time required for effective dose

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13
Q

AUC

Area Under the Curve

A

Amount of drug in bloodstream

graph represents plasma blood concentration and time

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14
Q

Protein Binding

Coumadin interacts with highly bound medication

A

half life
no kidney excretion (secondary to protein)
> potential for drug to drug interaction

Applicable to long, intermediate and short acting insulin

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15
Q

Coumadin interaction with high protein binding medications

A

they compete for protein binding- coumadin has low affinity for protein–loss of competition with medication for protein binding–>increased amount of unbound coumadin (binding inactivates)–>coumadin in bloodstream=increased coumadin level

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16
Q

1st pass effect
Only affects PO medications
cannot be given po route if > 1st pass effect

A

Drug metabolized before reaching the bloodstream GI – Liver

17
Q

Distribution

Volume of Distribution Vd

A

plasma concentration or amount of drug in body

18
Q

Vd

Factors effecting

A
Blood flow                  Protein level
Solubility                    Aging
Hydration                    Organ size
Special Tissues -Meds sequestered 
    fat -estrogen, vitamin D
    bone- Boniva
19
Q

Vd with aging

A
< amount of body weight as water
< lean muscle mass (20%)
>amount of body weight as fat
< kidney weight
<hepatic bloodflow
20
Q

Distribution

A

Frick”s Law (Passive Dissusion)
Movement from > concentration to < concentration.
Types
Aqueous/ Lipid Diffusion
Carrier Transport
Endocytosis/pinocytosis -engulfing particles or H2O

21
Q

Clearance

A

Rate that drug is completely removed by biotransformation/excretion.
renal -H2O soluble
hepatic-fat soluble

**Protein bound drugs cannot be excreted from kidneys.

22
Q

Biotransformation

A

Imitrex
100mg po or 6mg SQ
Biotransformation of medication is changed by route of administration.
1st pass effect

23
Q

Metabolism

A

Occurs in liver by Cytochrome P450 System.

47% CYP3A4

24
Q

Metabolism

Phase I Reaction

A

Phase I- Oxidation, reduction,deamination, hydrolysis.
changed to water soluable
P450 enzymes

25
Q

Metabolism–Phase II Reaction
acceleration of excretion
inactivation of drug
>effectiveness (codeine becomes morphine)
activation of Prodrugs (inactive before liver metabolism)

A

conjugation of molecules naturally present in body to the drug molecule.
can happen p Phase I

26
Q

Parent Drug —-Metabolite

Liver conversion

A

Amitriptyline–nortriptyline
Codeine—Morphine
Primidone–Phenobarbital==< toxicity risk
Valacyclovir–acyclovir

27
Q

Valproic acid–St John Wart Reaction

A

Substrates are metabolized by the same family
Substrates are metabolized by the same family
St John’s Wart is an inducer (makes metabolism family work better and faster)—Depakote is metabolized faster—< TMAX (drug leaves system quicker)-<AUC

28
Q

Coumadin –Cipro interaction

A

Cipro inhibits warfarin–accumulationwith same dosage—>AUC–>INR

29
Q

Vicodin-Tylenol-ETOH

A

Vicodin increases effectiveness of tylenol.
Beer is a P4502E1 inducer and tylenol is its substrate—increased metabolism–decreased AUC.
Tylenol becomes a liver toxin with metabolism—when inducer causes increased metabolism (ETOH)–increase liver toxins–liver toxicity

30
Q

ST John’s Wart

common drug interactions

A

Cyclosporine (anti rejection)–can be life theratening

Digoxin–decreased digoxin levels day 10

HIV drugs Antivirals -(-Indinavir)
monitor closely for reaction > viral load
< AUC 57%
<effectiveness 81%

31
Q

Grapefruit Juice

*****
Carbamazepine
     Increased AUC (peak, trough)
Amiodarone
     Increased AUC 50%
     Increases concentration 40%
     Increased peak plasma concentration 84%
A
Flavonoid glycosides (green tea)
Inhibitor of CYP1A2, and CYP3A4 (intestinal level)

Avoid
Tegretol, estrogen, CCB (ipine), buspar, select statins (Not zocor or crestor), diazepam, zoloft,Geodon (ziprasidone)

32
Q

Cipro (CYP 1A2 inhibitor) inhibits metabolism of

A

caffeine

33
Q

Elimination

1st order elimination

A

!st order elimination–
Rate of elimination proportionate to concentration of drug in body.
Plasma concentration of a drug decreases exponentially over time —1/2 life

34
Q

Elimination 1st order

Half Life Elimination

A

Half life is constant no matter how much of a drug is given
Concentration decreases 50% EVERY HALF LIFE
Steady state is reached after 4-5 half lives

35
Q

Elimination Zero order elimination

less frequent

A

Rate of elimination is constant regardless of concentration.
Occurs when drugs saturate elimination processes.
Drug concentration decreases in linear fashion over time. ( ETOH + elimination 15mg /hr)

36
Q

Interactions/reactions

GI absorption interactions

A
drug A inhibits absorption of Drug B
  Drugs A and B bind in GI tract
  Alteration of GI motility
  Alteration of pH
  Alteration of intestinal flora
37
Q

Interactions/reactions

Protein binding

A

Coumadin and highly protein binding drugs

38
Q

Drug reactions

A

Type I-non allergy

Type II–Hypersensitivity i and II reactions HIT

39
Q

Pregnancy and drug classification

A

Category A–Ok-no fetal risk
Category B–Ok-no fetal risk
Category C–Clinical Judgement
-potential benefit> than potential risk to
fetus
Category D
Category X–Do NOT GIVE