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Fundamentals > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Endogenous

A

Substance created w/in body

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2
Q

Exogenous

A

Substance created outside of body

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3
Q

Titration

A

Slowly increasing dosage to build tolerance to adverse drug reactions (ADRs)

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4
Q

Tachyphylaxis

A

Tolerance that develops over hours or days

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5
Q

Types of intramolecular bonds

A

Covalent (usually irreversible in body) > ionic > hydrogen > hydrophobic

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6
Q

Signaling mechanisms

A
  • Intracellular - drug crosses membrane to intracellular receptor
  • Binds w/ transmembrane protein - Ed Scissorhands or scissors in drawer
  • Binds w/ and opens/closes transmembrane channel
  • G-protein systems
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7
Q

Catecholamines

A

Epi, Norepi, Dopamine

Made by adrenal glands and derived from tyrosine

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8
Q

Agonists (full, partial and inverse)

A

Cause an action
Full - has maximum effect
Partial - less than max effect
Inverse - causes action opposite of an agonist

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9
Q

Antagonists (reversible, irreversible, competitive and noncompetitive)

A

Blocks an agonist’s action at the receptor
Reversible vs irreversible - whether agonist can also bond or not; covalent bond vs others
Comp. vs noncomp. - binds at same or different site as agonist

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10
Q

Tapering

A

Slowly weaning off drug to avoid adverse withdrawal symptoms

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11
Q

Mixed agonist/antagonist

A

Drug w/ agonist effect at one receptor and antagonist effect at another
Not common

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12
Q

Common ADRs

A

GI upset
Hypersensitivity (allergic rx)
Note: ADRs are a type of unpleasant/unwanted side effect

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13
Q

Pregnancy categories

A

A - controlled studies show no fetal risk
B - no fetal risk evidence in human studies; fetal harm remote
C - fetal risk not excluded, adequate studies lacking; risk outweighed by benefit
D - evidence of fetal risk from human studies; benefit may outweigh risk
X - contraindicated

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14
Q

Drug schedule classifications

A

CI - high abuse potential, no accepted medical use
CII - high abuse potential, accepted medical use (w/ restrictions)
CIII - less abuse potential
CIV - low abuse potential (includes OTC)
CV - lowest abuse potential (includes OTC)

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15
Q

Type IV Hypersensitivity

A

T cell-mediated, slow rx, only requires one exposure, often fatal, Steven-Johnson syndrome or toxic epidermal necrolysis (like burns)

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16
Q

Acetaminophine

A

Analgesic, antipyretic

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17
Q

Tylenol

A

Analgesic, , antiinflammatory, NSAID, non-selective COX inhibitor

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18
Q

Type I Hypersensitivity

A

B cell mediated, involves IgE antibodies, rapid rx, requires two exposures, anaphylaxis

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19
Q

Pharmokinetics

A

How body affects a drug - absorption, metabolism, excretion

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20
Q

Pharmodynamics

A

How a drug affects the body

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21
Q

Types of DDIs

A

Pharmakokinetic - changes how drug is absorbed, distributed, metabolized or excreted; usually less drug-specific b/c it affects everything that uses that pathway
Pharmacodynamic - changes how a drug affects the body; a drug’s pharmacodynamic DDIs may be more varied from interacting drug to interacting drug

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22
Q

Polypharmacy

A

Individual taking many drugs

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23
Q

ADR

A

Adverse Drug Reaction

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24
Q

Therapeutic threshold

A

Window between minimum effective dosage and maximum effective dosage (dosage between ED50 to TD50)

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25
Q

Inert drugs

A

Bind to a receptor w/ no direct physiological effect (may have indirect effects)

26
Q

T/F - Most drug effects show a linear change in relation to concentration

A

False - usually show a greater change at low concentrations - slope becomes flatter at higher doses

27
Q

MEC

A

Minimum effective concentration

28
Q

Peak effect/max efficacy

A

Dose where drug has maximum effect

29
Q

Onset of effect

A

Time between administration and desired effect

30
Q

Therapeutic index

A

LD50/TD50 - wider TI implies a safer drug

Can vary between effects of the same drug (Ibu. for pain vs inflammation

31
Q

What must be assumed w/ an enhanced response to a given drug dose?

A

Increase in drug sensitivity

32
Q

What is one way to help avoid tolerance?

A

Giving drugs in bursts or taking periodic breaks (four days on, one day off)

33
Q

Hyperreactivity is not hypersensitivity

A

True

34
Q

Metric conversions

A

kilo (1000) — hecto (100) — deka (10) — base — deci (.1) — centi (.01) — (.001)

35
Q

Half-life

A

Time required to eliminate 50% of absorbed dose of a drug

36
Q

How do you avoid first pass metabolism?

A

Enter bloodstream somewhere where you will go to the heart before the liver.
Avoid delivery through intestines or hepatic portal

37
Q

Parenteral administration

A

w/ a needle - IV, IM, sub cu, intradermal, IO, intrarticular, intralesional, intrathecal (through dura and into spinal canal and CSF), epidural

38
Q

What type of administration route are sublingual and buccal?

A

Topical
Neither are suitable for high-dose drugs
Avoids first pass metabolism

39
Q

Characteristics of classic topical admin.

A

Pros - Cheap, treats affected site, low risk of systemic effects, easy to self-administer
Cons - variability in effects, systemic absorption possible, local toxicity

40
Q

Characteristics of respiratory admin.

A

Pros - good for systemic and local administration, easy to self-administer, cheap, can bypass first-pass metabolism, fast onset
Cons - high potential for abuse, systemic effect for respiratory ailments
Nasal - good perfusion and surface area, may go directly into CSF

41
Q

Characteristics on enteral admin.

A

Pros - cheap, easy, safe

Cons - variable absorption, upset stomach, first-pass metabolism

42
Q

Infiltration

A

Fluid from parenteral admin ends up outside vessel

43
Q

Extravasation

A

Infiltration that causes a blister

44
Q

Lbs/kg

A

2.2 lbs/kg

45
Q

mL/tsp

A

5 mL/tsp

46
Q

Enterohepatic circulation

A

Drug goes through liver, is concentrated and excreted in stomach bile and reabsorbed in GI tract.
Extends duration of drug in body.

47
Q

Clearance

A

Clearance = (elimination rate)/(drug concentration) = liters/hour
Volume of fluid that would be cleared of the drug

48
Q

Types of drug metabolism

A

Phase I - uses CYP450 system (mostly isoenzymes CYP3A4 and CYP2D6) to oxidize/reduce/hydrolize drugs; alters pharmacodynamics
Phase II - uses other enzymes to conjugate (add glucuronic acid, sulfate, glycine); affects polarity and H20 solubility and increases clearance

49
Q

T/F - Molecular charge affects glomerular filtration

A

False

50
Q

Factors that affect tubular reabsorption

A

pH - weak acids more readily reabsorbed
Nonionized drugs more easily reabsorbed
More alkaline urine increases excretion of weak acids

51
Q

Biliary excretion

A

Concentration and excretion of drug through liver bile.

Usually involves Phase II metabolism

52
Q

Pulmonary excretion

A

Works for volatile (usually unchanged) drugs that passively diffuse into lungs.

53
Q

Breast milk excretion

A

Mostly lipid soluble drugs.

Relatively acidic milk can concentrate weak bases - opt for drugs w/ lower pKa

54
Q

Plasma half-life (elimination half-life)

A

Time it takes to clear half the drug concentration
Often used to help set dosing intervals.
Estimation - total elimination equals 5 x half-life

55
Q

Dosing to effect

A

Used when half-life is altered

Uses other, physiological marker (effectiveness or toxicity) to determine dosing

56
Q

Efficacy half-life

A

Time it takes for a drug to lose half its effect

57
Q

Cmax

A

Peak serum concentration

58
Q

Loading dose

A

A stronger initial dose that helps decrease the time until onset of effect

59
Q

Steady-state

A

Point where drug intake equals drug excretion and plasma concentration is steady
Css = steady state concentration

60
Q

Tmax

A

Time it takes to reach Cmax

61
Q

COX

A

Cyclooxygenase
COX-1 - GI activity, kidney perfusion, platelet clotting
COX-2 - inflammation, pain and swelling

Fundamentals (14 decks)

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