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Biopharmaceutics > Prelim Biopharmaceutics > Flashcards

Prelim Biopharmaceutics Flashcards

Exam

1
Q

effect of rate & extent of drug
absorption

A

Bioavailability

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2
Q

“what the body does to the drug”
-involves experimental and theoretical studies
-uses statistical methods

A

Pharmacokinetics

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3
Q

involves multidisciplinary approach to
individually optimize dosing strategies based on
patient disease state & patient specific
consideration

A

Clinical Pharmacokinetics or Therapeutic Drug
Monitoring (TDM

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4
Q

What are the Factors considered in TDM

A

Disease
Age
Gender
Genetic
Ethnic difference

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5
Q

pharmacokinetic differences of drugs in
various population groups

A

Population Pharmacokinetics

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6
Q

What are the monitoring parameters

A

Plasma drug concentration
pharmacodynamic endpoint

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7
Q

Common drugs monitored

A

Aminoglycosides
Anticonvulsants
Vancomycin
Digoxin
cancer chemotherapy
drugs with NTI

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8
Q

concentration of drug at the site of action
-biochemical effect of the drug
-physiologic effect of the drug
-“what the drug does to the body

A

Pharmacodynamic

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9
Q

refers to drug dose in body fluids

A

Drug exposure

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10
Q

direct measure of the pharmacological
effect of the drug

A

Drug response

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11
Q

application of pharmacokinetic principles
to the design, conduct and interpretation of
drug safety evaluation studies & in validating
dose-related exposure in animals

A

Toxicokinetic

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12
Q

study of adverse effects of drugs and toxic
substances in the body

A

Clinical Toxicology

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13
Q

Usually involved in toxicity cases:

A

Acetaminophen
Salicylates
Morphine
TCAs

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14
Q

most direct approach to assessing
pharmacokinetics of the drug in the body.

A

Blood plasma

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15
Q

devoid proteins
from filtered plasma

A

Unbound drug concentration

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16
Q

with proteins
from unfiltered plasma

A

Total plasma drug concentration

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17
Q

time required for a drug to reach
MEC

A

Onset time

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18
Q

difference between
the onset time & time for the drug to decline
back to MEC.

A

Duration of drug action

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19
Q

concentration between MEC and MTC; ratio
between toxic and therapeutic dose.

A

Therapeutic window/Therapeutic index

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20
Q

maximum drug
concentration

A

Peak plasma level

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21
Q

time of maximum
drug level.

A

Time for peak plasma level-

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22
Q

amount of drug
absorbed systematically; measure of the amount
of drug in the body

A

Area under the curve (AUC)

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23
Q

to ascertain if the drug
reached the tissues & reach the
proper concentration within the
tissue

A

Drug concentration in
tissues

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24
Q

drugs that are bound to
plasma protein are inactive drugs

A

Plasma protein binding
(PPB)

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25
Q

indirect method to ascertain
bioavailability of a drug

A

Drug concentration in urine and feces

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26
Q

reflect drug that has not been absorbed or expelled by biliary secretion
after systemic absorption.

A

Feces

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27
Q

approximates free drug level; secondary
indicator

A

Drug concentration in saliva

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28
Q

application of science to personal injury,
murder and other legal proceedings
-used in investigation
-concerned with medico-legal aspects of harmful effects of
chemicals on humans and animals

A

Forensic drug measurements

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29
Q

Best indicator:

A

plasma, urine, feces

30
Q

-alter normal physiologic function or process
-interaction of drug molecules and cellular components (receptor) alter the functions
of the latter.

A

Functional Modifiers

31
Q

Supplements existing endogenous substances that are deficient or lacking

A

Replenishers

32
Q

Agents used to determine the presence or absence of a condition or disease.

A

Diagnostic Agents

33
Q

Used to kill or inhibit growth of cells considered as foreign to the body

A

Chemotherapeutic agents

34
Q

a molecule that binds to the receptor

A

LIGAND

35
Q

a drug that binds to (affinity) and activates receptor
(intrinsic activity)

A

Agonist

36
Q

a drug that produces 100% of the maximum
possible biologic response.

A

Full agonist

37
Q

-binds to or block receptors (affinity only)
-prevents binding of agonist
-opposite effect of agonist

A

Antagonist

38
Q

binds
reversibly to the same
active site of an enzyme
as an agonist; can be
overcome by increasing
the concentration of the
agonist. Ex: Enzyme
agonist

A

Competitive
antagonist

39
Q

binds
irreversibly to the
different active site
of an enzyme as an
agonist; cannot be
overcome by
increasing the
concentration of the
agonist.

A

Non-competitive
antagonist

40
Q

a drug that binds to a different receptor, producing an effect
opposite to that produced by the drug it is antagonizing

A

Physiologic Antagonist

41
Q

a drug that interacts directly with the drug being
antagonized to remove it or to prevent it from reaching its
target (direct effect)

A

Chemical Antagonist

42
Q

macromolecule typically made of proteins that interacts
with endogenous ligand or drug to mediate an effect.

A

RECEPTOR

43
Q

is caused by continuous prolonged exposure of receptors to drugs that discrupt the homeostatic
equilibrium; due to altered levels of receptors.

A

Down Regulation

44
Q

-result of down regulation; effect of subsequent exposure of the receptor to the same concentration
of the drug is reduced.
-Increased concentration of the drug is required to produce the same effect as the initial
concentration.

A

Desensitization

45
Q

-occurs when target cells are subject to long term exposure to receptor antagonists followed by
abrupt cessation of administration of the drug.
-Up-regulation through new synthesis of new receptors

A

Hyperactivity/supersensitivity

46
Q

-graph of response versus the logarithm of the dose yields
the efficacy (Emax) and potency (ED50).

A

GRADED-DOSE-RESPONSIVE CURVE

47
Q

measured by its maximum effect.

A

Efficacy

48
Q

related to the amount of drug necessary to cause
an effect
-related in the ED50 or the dose at 50% of the Emax
-The smaller the ED50, the greater the potency, the greater
the potency of the drug.

A

Potency

49
Q

-graph of the number of patients that responds by a
specified dose.
-median effective (ED50), median toxic (TD50), median
lethal dose (LD50) can be obtained.

A

QUANTAL DOSE-RESPONSIVE CURVE

50
Q

-The pharmacological effects depends on the percentage o f the receptors occupied
drug must have affinity to receptor.
-If all receptors occupied = maximum effect

A

.Hypothesis of Clark

51
Q

-The drug molecule must “fit into a receptor” like a “key fits into a lock”

A

Lock and key theory

52
Q

Postulates a complementary relationship between the drug molecule and its active site.
-Provides for mutual conformational changes between the drug and its receptor.

A

Induced-fit theory

53
Q

-Occupational theory of response.
-Postulates that for a structurally specific drug, the intensity of the
pharmacological effect is directly proportional to the number of
receptors occupied by the drug.
-affinity + intrinsic activity or efficacy
-effectiveness lasts as long as the receptors are occupied

A

Hypothesis of Ariens and Stephenson

54
Q

-Effectiveness = occupation + proper stimulus

A

Hypothesis of Paton (Rate theory)

55
Q

When two drugs with the same effect are given together,
resulting in a drug effect that is equal in magnitude to the
sum of the individual effects of the 2 drugs.

A

Addition (1+1=2)

56
Q
  • Alcohol + Barbiturates: ↑ seddation
  • Alcohol + Antihistamines: ↑ sedation
  • Alcohol + CNS depressants: ↑ sedation
  • Alcohol + Chloral hydrate: ↑ sedation
  • Alcohol + Chlorpropramide: ↑ hypoglycemic effects
  • Flecainide + Verapamil: ↑ negative inotropic and
    chronotropic effects
A

Examples of Addition

57
Q

When 2 drugs with the same effect are given together,
producing a drug effect that is greater in magnitude than
the sum of the individual effects of the 2 drugs.

A

Synergism (1+1=3)

58
Q

Sulfamethoxazole + Trimethoprim (↑ bactericidal effect)

A

Example of Synergism

59
Q

-Occurs when one drug, lacking an effect of its own,
increases the effect of another drug that is active.

A

Potentiation (1+0=2)

60
Q

Amoxicillin + Clavulanic acid: ↑ Amoxicillin’s antibiotic
effect
* Ampicillin + Sulbactam: ↑ Ampicillin’s antibiotic effect
* Piperacillin + Tazobactam: ↑ Piperacillin’s antibiotic effect
* Levodopa + Carbidopa: ↑ Levodopa’s effect

A

Examples of Potentiation

61
Q

Drug inhibits the effect of the other

A

Antagonism (1+1=0)

62
Q
  • Phenoxybenzamine + Catecholamines: management of
    pheocromocytoma
  • Warfarin + Vitamin K: antidote for Warfarin toxicity
  • Opioids + Naloxone: antidote for Opioid toxicity
  • Benzodiazepine + Flumazenil: antidote for
    Benzodiazepine toxicity
  • Atropine + Physostigmine: antidote for Atropine toxicity
  • Procaine + Sulfonamides: antagonism of Sulfonamide’s
    antibacterial activity
  • Heparin + Protamine SO4: antidote for Heparin toxicity
A

Examples of Antagonism

63
Q

mathematical terms used to describe quantitative
relationship relationship concisely

A

Model

64
Q

practical, but not very useful in explaining the mechanism
of the actual process by which the drug is absorbed,
distributed & eliminated in the body

A

Empirical Model

65
Q

Physiologically-based model (Flow model)

A

where there is blood, there is drug

66
Q

a very simple and useful tool in pharmacokinetics.

A

Compartmentally-based model

67
Q

-overly simplistic view of drug disposition in the human body,
a drug’s pharmacokinetic properties can frequently be
described using a fluid-filled tank model

A
68
Q

specific, involves drug carriers

A

Multicompartment model

69
Q

-most common compartment model
-the total amount of drug in the body is simply the sum of
drug present in the central (plasma) compartment plus
the drug present in the tissue compartment.

A

Mamillary model

70
Q

consists of one or more compartments around a central
compartment like satellites

A

Catenary model

Biopharmaceutics (1 decks)

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