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Pharmacology > Pharmacology in D&D Exam 1 > Flashcards

Pharmacology in D&D Exam 1 Flashcards

1
Q

what suppresses production of toxic metabolites

A

Ethanol and Fomepizole both suppress alcohol dehydrogenase

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2
Q

Factors that influence Distribution

A

Vd

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3
Q

Cimetidine (inducer or inhibitor?)

A

inhibitor

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4
Q

Age changes in Phase 1 vs 2

A

1/3 decrease in phase 1; minimal in 2

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5
Q

Phnobarbital (inducer or inhibitor?)

A

Inducer

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6
Q

Inhibitiors_

A

decrease clearance to lead to higher Cp

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7
Q

pH< pKa

A

Protonized form : HA and BH+

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8
Q

Azole Antifungals (inducer or inhibitor?)

A

inhibitor

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9
Q

Oxidation (phase 1 or 2?)

A

Phase 1

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10
Q

Half life

A

constant fraction of drug is eliminated per time; independent of amount of drug present

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11
Q

Methanol Poisoning

A

Alcohol dehydrogenase promotes formaldehyde and formic acid in overdose, leads to severe acidosis and retinal damage

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12
Q

Phase 4 drug testing

A

post marketing surveillance

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13
Q

Protein binding and metabolid degradation

A

hinders to decrease elimination and prolong half life and drug action

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14
Q

Correction of metabolic acidosis

A

NaHCO3

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15
Q

Maximal Efficacy

A

relationship between receptor binding and ability to initate response.

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16
Q

Treatment of acetaminophen toxicity

A

Gastric lavage, supportiv therapy, plus N-acetylcystein

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17
Q

Genetic polymorphisms in Phase 1 vs 2 metabolism

A

significant in both

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18
Q

Clinical implications of inducers

A

1) reduced therapeutic effect 2) production of pharmacokinetic tolerance 3) increased toxicity if activation is accelerated or toxic metabolite is produced

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19
Q

Vd=

A

amoutn of drug in body/Cp

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20
Q

Schedule 5

A

med use: yes; lowest abuse and phsiologicand psychologic dependence;

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21
Q

How to inhibit toxication or enahance detox?

A

administer antidote to react with toxin or speed up metabolism

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22
Q

Passive Reabsorption

A

From tubule back into blood; 1 ml/min; depends on concentraiton gradient and lipophilic drugs.

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23
Q

Zero order Kinetics

A

contant amount of drug is elimianted per time

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24
Q

Schedule 3

A

Medical use: moderate abuse and physiologic dependence; high psychologic dependence

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25
Where are the tight cellular junctions loacted?
Gut, Blood Brain Barrier, Reabsorption in Kidney
26
what are fluctuations equal to?
proportional to tau/T1/2
27
What routes are 100% F?
Intravenous
28
Schedule 1
Medical use: No High abuse potential and Phys and Psych dependence
29
St John's Wort (inducer or inhibitor?)
Inducer
30
N-acetylcystein
precursor for glutathione syntehsis, inactivates hepatotoxic metabolite; treatment for acetaminophen toxicity
31
acetylation (phase 1 or 2?)
phase 2
32
Grapefruit Juice (inducer or inhibitor?)
inhibitor
33
Rifampin (inducer or inhibitor?)
inducer
34
Biotransformations Phase 2
Endogenous substrate combines with pre-existing or metaboically insterted (phase 1) to form highly polar conjugate
35
Omeprazole (inducer or inhibitor?)
inhibitor
36
Effects of Protein Binding
1) reduces active drug 2) hinders metabolic degradation and reduces excretion 3) decreases Vd 4) decreases ability to enter CNS
37
Glucuronidation (phase 1 or 2?)
phase 2
38
Tight junctions in renal tubule\_
reduced reabsorption back into blood; increased urinary excretion
39
Toxicokinetic strategies
Decrease rate in, increase rate out; inhibit toxin, enhance metabolism
40
Competative antagonists\_
Decrease potency, but Emax reamins constant; can be overcome by agonist concentration
41
Tight junctions in BBB
limited distrubtion
42
Inhibition (time)
hours
43
Enzymes of metabolism Phase 1 vs 2
1: CYP450, reductases, esterases-amidases 2) transferases
44
Saturabiltiy in phase 1 vs 2 metabolism
1) minimal 2) substantial
45
Controlled Substances are based upon potential for..
medical usefullness, abuse potential, potential for physical and psychological dependence
46
How to enhance elimination
hemodialysis, change urine pH
47
Induction/inhibition in Phase 1 vs 2 metabolism
significant in 1, possible but less significant in phase 2
48
glutathione (phase 1 or 2?)
phase 2
49
Hepatic Clearance varies with
Blood flow to liver 2) protein binding 3) intrinsic hepatic metaoblic activity (subject to ind/inhib)
50
Reduction (phase 1 or 2?)
Phase 1
51
How long does it take for inducers to work?
7-10 days
52
what routes are 75-100% F?
IM, SC, SL, Inhalation, Transdermal
53
Clarithromycin (inducer or inhibitor?)
inhibitor
54
Glomerular Filtration Rate
120 ml/min; limited by size
55
Inducers\_
increase clearance of other drugs
56
Schedule 2
Medical use: yes; High abuse potential, phys and psych dependence
57
Erthromycin (inducer or inhibitor?)
inhibitor
58
Ethanol (inducer or inhibitor?)
Inducer
59
Pharmacologic Antagonist
Both Competative and non-competative; blocks same receptor
60
Phase 1 Drug testing
Is it safe? Pharmokinetics? 20-100
61
factors of absorption
F (bioavaliability), Tmax, Cmax
62
what factors influence Vd?
Body size and composition, changes in protein binding
63
glycine (phase 1 or 2?)
phase 2
64
Active secretion
120-600 ml/min; secretion from blood into proximal tubule
65
tight junctions in gut\_
negligable absoprtion
66
Ethylene glycol poisoning
alcohol dehydrogenase promotes oxalic acid to lead to acidosis and nephrotoxicity.
67
Phamacodynamic strategies for toxins
antidoes (only 20-30 specific ones)
68
Tabacco smoke (not nicotine) (inducer or inhibitor?)
Inducer
69
Four factors of drug distribution (OTC, PRES, controlled, Dietary supp)
1) efficacy 2) saftey 3) availability 4) abuse potential
70
how to decrease rate in of toxin?
Decrease absorption 1) gastric lavage 2) activatec charcoal 3) whole bowel irrigation 4) cathartics 5) emetics
71
Non-competative antagonists
No effect on potency, decreases Emax. Insurmountable
72
Phase 3 drug testing
does it work, double blind? 1000-3000
73
Carbamazepine (inducer or inhibitor?)
inducer
74
Ethanol and Acetaminophen
deplenishes GSH stores to decrease less toxic metabolite and promote hepatotoxicity.
75
Fluoxetine (inducer or inhibitor?)
inhibitor
76
pH \> pKa
deprotonated form A- and B
77
Hemodialysis
removes parent compounds/metabolites to inhbiit toxication
78
Non-receptor antagonists
1) chemical antagonist 2) physiological antagonist (different receptor)
79
percent drug metabolism in lung, intestine, kidney
30% lung; 6% intestine; 8% kidney
80
Phenytoin (inducer or inhibitor?)
inducer
81
HIV protease inhibitors (inducer or inhibitor?)
inhibitor
82
less common metabolism mechanism
1) active --\> more active 2) inactive prodrug --\> active drug 3) to toxic metabolite
83
Protein binding displacement has clinical consequence when..
1) narrow TI 2) displacing drug is started in high dose 3) Vd is small 4) response occurs more rapdily than redistribution
84
Factors that influence Elimination
CL, T1/2, Ke
85
what influecnes Duration of Drug Action?
Delay of release, slow drug absorption, duration of action (independent of T1/2)
86
Reactions of metabolism Phase 1 vs 2
1: oxidations, reductions, hydrolysis 2: conjugations
87
what does potency depend on?
Affinicty of receptors Kd; Efficacy of drug receptor complex
88
Requiresments for controlled drugs
1) DEA # 2) no Schedule 1 drugs prescribed 3) 2-4/5 require prescription 4) 2 must be in ink, no telephone 5) 3-4-5- telephone okay, 5 times refil in 6 months
89
what mades inhalation systemic vs. local
Systemic: volatile gases local: particles in lungs
90
what factors influence route determination?
1) bioavailability 2) Rate of onset 3) duration of drug action
91
biotransformation of Phase 1
insert/unmask function group to make more water souble; ready for conjugation
92
First order kinetics rate
rate of elimination is proportional to Cp
93
what ifnluences oral bioavaliability?
1) lipophilicity 2) gastric emptying time
94
Potency
concentraiton or dose required to produce 50% of the individual drug's Emax
95
Phase 2 Drug testing
Does it work? 100-300
96
sulfate conjugation (phase 1 or 2?)
phase 2
97
Hydrolysis (phase 1 or 2?)
Phase 1
98
Toxic doses of acetaminophen
Saturate Phase 2, increates formation of phase 1 hepatotoxic metabolite; depletion of glutathione stores for detox, increase hepatocellular injury
99
Schedule 4
med use: yes; low abuse and phsiologicand psychologic dependence;
100
Speed of onset for different routes?
Most rapid: inhalation, IV; Intermediate: SL, IM, SC, buccal Slow: 15-30 Oral; Slowest (hours); transdermal, oral, IM and SC (depot forms)

Pharmacology (2 decks)

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