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EXAM 1 Flashcards

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1
Q

All drugs eliminated by liver are biotransformed
T/F

A

False

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2
Q

Shortening the dose interval, could result in: increase/decrease of drug effect

A

increase

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3
Q

A change in the dosing interval is likely to modify several pharmacokinetic parameters that describe the disposition of a drug in plasma. Please, indicate fluctuation of plasma drug concentration increases or decreases or stays the same after shortening the dosing interval. Assuming linear kinetics.

A

decreases

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4
Q

The best route of drug administration if the intravenous route
T/F

A

False

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5
Q

Changes in bioavailability, change the plateau drug concentration in plasma.

T/F

A

True

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6
Q

Changes in infusion rate, change plateau drug concentration in plasma.
T/F

A

True

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7
Q

The induction of drug biotransformation of a drug could result in which of the options listed below: decreased drug effect, increased drug effect, no signifcant changes, or all of the above

A

all of the above

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8
Q

What could lead to a less than proportional change in plasma drug concentrations when a dose of a treatment is increased?
A. decrease in drug absorption
B. increase in drug absorption
C. increase in biotransformation
D. decrease in biotransformation
E. increase in drug exctretion
F. Decrease in drug excretion
G. options A, C, and E
H. option, B, C, D, and F

A

options A, C, and E

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9
Q

Following the administration of a drug there will be periods of time where the process of drug absorption, distribution and elimination overlap.

T/F

A

True

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10
Q

Which of the following routes of drug administration helps to avoid liver first pass effect?

intraruminal, oral, IM

A

IM

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11
Q

Changes in bioavailability, change the time to reach plateau drug concentration in plasma.

T/F

A

False

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12
Q

Can a drug show linear and nonlinear kinetics in a same patient?

A

Yes

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13
Q

All the drugs used in clinical practice are eliminated by biotransformation

T/F

A

False. Elimination by biotransformation or excretion

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14
Q

A change in the dosing interval is likely to modify several pharmacokinetic parameters that describe the disposition of a drug in plasma. Please indicate if drug accumulation increases, decreases, or stays the same after shortening the dosing interval and assuming linear kinetics.

A

increases

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15
Q

Drugs that have a narrow therapeutic window are easier to handle than drugs with a wide therapeutic window.

T/F

A

False

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16
Q

A change in the activity of enzymatic systems involved in the biotransformation of a drug can alter the relative dose interval (RDI) for a treatment protocol?

Yes/No

A

Yes

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17
Q

A change in the dosing interval is likely to modify several pharmacokinetic parameters that describe the disposition of a drug in plasma. Please, indicate if Cmax at steady state in plasma increases, decreases or stays the same after shortening the dosing interval. Assuming linear kinetics

A

increases

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18
Q

A change in the dosing interval is likely to modify several pharmacokinetic parameters that describe the disposition of a drug in plasma. Please, indicate if drug accumulation increases or decreases or stays the same after extending the dosing interval. Assuming linear kinetics.

A

decreases

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19
Q

Drugs with long half-lives are usually administered by constant rate infusion.

T/F

A

False

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20
Q

A change in the dosing interval is likely to modify several pharmacokinetic parameters that describe the disposition of a drug in plasma. Please, indicate if the elimination half-life increases, decreases or stays the same after shortening the dosing interval. Assuming linear kinetics

A

stays the same

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21
Q

A change in the dosing interval is likely to modify several pharmacokinetic parameters that describe the disposition of a drug in plasma. Please, indicate if the fluctuation of a drug concentration in plasma** increases, decreases or stays the same** after extending the dosing interval. Assuming linear kinetics

A

increases

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22
Q

Changes in clearance, change the time to reach plateau drug concentration in plasma.

T/F

A

True

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23
Q

Changes in frequency of drug administration, change the time to reach plateau drug concentration in plasma.

T/F

A

True

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24
Q

Define the targeted drug mechanism

A

a drug binds to some component of the cell to exert an action. That component is the drug “target”

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25
Define the non-targeted drug mechanism
drugs that do not have specific cellular components as targets. They are non selective, and tend to have more general effects - often including more unwanted or adverse effects
26
What are the types of specific drug targets?
* receptors * ion channels * enzymes * carriers/membrane transport proteins * DNA/RNA
27
Why do drug targets matter? The mechanism of action can provide valuable information:
* how fast will a drug have an effect * how specific its effects will be * if and how two drugs may interact * could cross tolerance occur?
28
what are the 4 classes of endogenous receptor proteins?
* ligand-gated ion channel * G-protein coupled receptor * Nuclear hormone receptor * Receptor tyrosine kinase
29
Example of a ligand-gated ion channel
Nicotinic Ach receptors
30
speed of response for ligand-gated ion channels?
stimualte response in **msecs**
31
speed of response for GPCRs?
stimulate response in **seconds to minutes**
32
Example of GPCR?
Adrenergic receptors (SNS), Opioid receptors
33
speed of response for RTKs?
stimute response in **minutes to hours**
34
speed of response for Nuclear Hormone Receptors? (intracellular receptors)
stimuate response in **hours to days**
35
Which will have a faster onset of an effect? **Epinephrine**, which activates G protein coupled (adrenergic) receptors to dilate the airways, or a **dexamethasone**, which decreases inflammation by activating a steroid receptor to alter gene transcription
Epinephrine
36
Which will have more specific effects? **Mannitol**, which changes the osmolarity to pull excess fluid out of the eye, or a **prostaglandin (PG) receptor agonist (activator)** that specifically targets a receptor to activate pathway that increases drainage
PG receptor agonist
37
define affinity (Kd)
the ability ot a drug to bind to its receptor
38
define efficacy
the ability of a drug to produce a response
39
define receptor efficacy
how well a drug activates its receptor
40
define cellular efficacy
how well that action produces a cellular response
41
define clinical efficacy
how well the drug produced a therapeutically useful effect in the whole animal
42
Antagonists have/do not have intrinsic efficacy
do not have (no ability to activate the receptor)
43
antagonists have/do not have clinical efficacy
have (have the ability to produce an effect in the whole animal)
44
Define Binding affinity (Kd)
Kd = concentration of drug required to occupy 50% of the receptors at equilibrium
45
Low Kd = **low or high** affinity
high affinity
46
High Kd = **low or high** affinity
low affinity
47
Define potency:
the concentration of drug needed to produce an effect
48
T/F all potent drugs have a high affinity
T
49
T/F all high affinity drugs are potent
F
50
What is the EC50
the concentration of drug required to produce 50% of the maximal effect
51
define efficacy in the context of pharmacology
how well a drug/ligand activates its receptors. related to magnitude of maximal response when all receptors are bound.
52
When do you have spare receptors?
When Kd > EC50
53
What is suggested when Kd > EC50
usually suggests an agonist
54
T/F To get a full effect, the drug needs to occupy all the receptors
True
55
When do you have the threshold effect?
When Kd < EC50
56
What is suggested when Kd < EC50?
usually suggests an antagonist
57
Which drug has the highest potency?
A A>B>C>D
58
Which drug has the highest efficacy?
E A=B=C=D
59
Define an Agonist
Agonists are molecules that bind to the protein and shift it into the active state (i.e., prefer the active state)
60
define an antagonist
Pharmacological antagonists are drugs that bind to receptor proteins and hold them in their resting or non-signaling state by stabilizing their inactive confirmation. Their occupation of the receptor prevents agonists from activating it
61
define a simple competitive antagonist
A simple competitive antagonist binds the same site as the agonist and physically blocks the agonist from binding to the receptor.
62
simple competitive antagonist binding is **reversible/irreversible**
Simple competitive antagonists binding is **reversible.**
63
define a non-competitive antagonist
A non-competitive antagonists either binds irreversibly or binds at a site other than the agonist site and prevents receptor activation. Either way the agonist cannot compete off the antagonist.
64
How does a competitive antagonist effect the EC50?
it remains the same as if there was an agonist alone.
65
How does a competitive antagonist effect the maximal response?
it decreases the maximal response
66
define a physiological antagonist
Oppose or antagonize a drug’s action by activating an opposing physiological system.
67
define a pharmacokinetic antagonist
These block a drug’s effect by removing it from the system.
68
Which of these is a full agonist?
A and D
69
Which of these is an antagonist?
E
70
Which of these is a partial agonist?
B and C
71
partial agonists have **lower, higher, or the same** efficacy?
lower
72
define the TD50
toxic dose for 50% of the population
73
define LD50
the lethal dose for 50% of the population
74
What is the therapeutic index (TI)?
the "safety factor" can be calculated in many different ways... TI=LD50/ED50 or TI=TD50/ED50....
75
what are the limitations of using TI as a sole measure of drug saftey?
there is no agreed to formal definition. Any TI you may read about is ambiguous!
76
define tolerance
When repeated administration of the same dose of drug fails to produce the same magnitude of response
77
what is pharmacodynamic tolerance?
Changes in receptor number
78
What is pharmacologic tolerance?
Desensitization - In the presence of an agonist a receptor may lose the capacity to respond
79
what is physiologic tolerance?
1. loss of endogenous mediator 2. physological adaptations - These could include a compensatory change in a system that works against the effect of the drug
80
Pharmacokinetic drug interactions:
(ADME) Most commonly due to changes in metabolism, esp. microsomal oxidation
81
Pharmacologic drug interactions:
receptor-mediated. Expected interactions (two agonists, agonist and antagonist, two antagonists...)
82
Physiologic drug interactions:
1. Induction/suppression of the expression of target receptors 2. Induction of expression or displacement from binding proteins 3. Alteration in physiological parameter
83
Dose-related (Type A) causes of adverse reactions:
1. overactivation (or inactivation) of the normal target 2. binding to other receptors or targets are higher doses (most drugs are only partially selective and not totally specific) 3. cytotoxicity or organ toxicity 4. pharmacogenetic (ex MDR1)
84
idiosyncratic, non-dose related adverse affects (Type B)
generally unrelated to the priciple pharmacological action of the drug - **allergic reaction** is the usual cause
85
dose related adverse affects are **more/less** predictable that non-dose related
more predictable
86
What are the 4 categories of allergic reaction?
Type I - anaphylaxis Type II - cytolytic effects Type III - immune complex-mediated hypersensitivity Type IV - delayed hypersensitivity, cell mediated
87
What PK parameters change if you change the drug dose?
AUC, Cave, Cmax, Cmin
88
If you increase the dosing interval, what PK parametes change, and do they increase or decrease?
decrease in AUC, Cave, Cmax, and Cmin
89
If you decrease the Bioavailability (F), what PK parameters change, and do they increase or decrease?
decrease in AUC, Cave, Cmax, Cmin
90
If you increase the volume of distribution (VD), what PK parameters change, and do they increase or decrease?
decrease Cmax and Cmin, increase the HL and time to steady state.
91
If you increase the Clearance (CL), what PK parameters change, and do they increase or decrease?
decrease AUC, Cave, Cmax, Cmin, HL and time to steady state
92
What PK parameter is altered if you increase the infusion time 2x?
Cmax is higher
93
what are the dose-dependent PK parameters?
Cmax and AUC
94
What are the dose-independent PK parameters?
Tmax, CL, F, VD, HL
95
What factors can effect the rate and extent of drug absorption?
* route of administration * availability of the drug at the site of absorption * local blood flow * physical barriers * physiochemical properties
96
faster absorption and distribution requirements of a drug
1. more lipid soluble 2. small molecular size 3. uncharged state (non-ionized)
97
a basic drug needs an **acidic/basic** environment to be primarizy non-ionized
basic enviroment
98
an acidic drug needs an **acidic/basic** environment to be primarizy non-ionized
an acidic environment
99
factors that affect the rate and extent of drug distribution
* anatomical barriers * the chemical nature of the drug * tissue perfusion rate * plasma and tissue protein binding
100
which organs have a high ratio of blood flow to tissue mass (i.e. higher distribution rate)
CNS, liver, lung, gut, kidney, heart, exercising muscle
101
which organs have a low ratio of blood flow to tissue mass (i.e. lower distribution rate)
skin, fat, bone, resting muscles
102
how does shock effect distribution?
circulatory collapse will slow elimination and alter distribution
103
neonates have a **lower/higher** extend of plasma protein binding
lower
104
how does obesity effect drug distribution?
highly lipophilic drugs will tend to accumulate in fat
105
what is Phase I biotransformation
addition of polar groups to make drugs more hydrophilic
106
What is phase II biotransformation?
conjugation to increase molecular size
107
Examples of Phase I Biotransformation reactions
oxidation, reduction, hydrolysis
108
Examples of Phase II Biotransformation reactions
Glucoronidation, acetylation, methylation, sulfation, conjugation of amino acids, conjugation of glutathione
109
oxidation is catalyzed by:
Cyt P450
110
why do enzymes not always work in the same way in all species?
because differences in the structure and/or availability of the metabolic enzymes
111
what is the first pass effect
when a fraction of the dose administered by any route can be metabolized by the liver before reaching the systemic circulation
112
clinical importance of Tmax?
can be used to predict when the maximum drug effect will occur
113
What 2 factors could increase drug biolavailability (F)
* liver disease (decrease in the first pass effect of drugs administered orally) * inhibition of enzymes due to the co-administration of drugs
114
What factors could decrease the drug bioavailability?
1. induction of enzymes 2. compounded formulations 3. GI disease for oral administration (diarrhea, dehydration)
115
Clearance is determined by...
1. organ blood flow 2. the organs ability to remove drug molecules from the blood (activity of enzymes, rate of biotransformation/excretion)
116
Clearance is affected by....
any factor that affects biotransformation and excretion
117
a decrease in CL could be due to..
1. inhibition/decrease of enzymes (liver Dz, co-administration of other drugs) 2. dehydration (decrease in rate of blood flow) 3. kidney disease
118
if VD is low, most of the drug is where?
in the intravascular compartment
119
causes of low VD
extensive binding to plasma proteins large molecular size
120
if VD is high, then most of the drug is where?
outside the intravascular compartment
121
how do you calculate VD?
VD = dose/Cp *Cp = plasma concentration
122
what factors can affect the VD of drugs?
the same factors that affect distribution: shock, exercise, obesity, pregnancy, ascites
123
Which 2 parameters influence the HL?
VD and CL
124
time to reach steady state is ?
5 HL

Pharmacology (3 decks)

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