Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sp: Pharm 1 > Pharm Unit 1 > Flashcards

Pharm Unit 1 Flashcards

1
Q

Pharmacokinetics definition

A

how the body handles the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pharmacodynamics definition

A

effect of the drug on the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ADME

A

absorption, distribution, metabolism, excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is area under the curve

A

the actual exposure of the body to the drug after administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is Cmax

A

Maximum plasma drug concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Tmax

A

time at which Cmax occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does solubility affect ADME

A

lipophillic vs. lipophobic (the more aqueous the drug, the faster it is absorbed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is partition coefficient

A

The ratio of a drug’s concentrations in oil phase vs aqueous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does partition coefficient affect ADME

A

the higher the partition coefficient the more likely the drug will accumulate in fatty tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does ionization affect ADME

A

charged molecules (ionized) do not cross membranes by diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does drug pKa affect ADME

A

the higher the pKa the slower it crosses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is pKa

A

pKa is the pH where unionized = ionize

non-ionized: easily diffuse
ionized: do not diffuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is a prodrug

A

inactive precursors that are metabolized into active metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

benefits of a prodrug

A

increases drug aqueous solubility

higher aqueous solubility = higher drug concentration within body

higher aqueous solubility = more likely to remain in the blood

improve ADME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

bioavailabilty definition

A

how much of drug is available to body after first/second pass metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

first pass metabolism

A

first pass = liver metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

low first pass drugs

A

IV drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

high first pass drugs

A

calcium channel blockers, beta blockers, diuretics, lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does a low first pas mean

A

bypasses liver- more bioavailability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does F=1.0 mean

A

F = bioavailability
F = 1.0 means 100% bioavailability

or 100% of the administered drug was able to be utilized by the body for the targeted effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where does Phase I and Phase II metabolism occur

A
  • mostly liver
  • gut
  • kidneys
  • lungs
  • skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Phase I

A

reduction
oxidation
hydrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Phase II

A

glucuronidation
methylation
acetylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what happens when a drug inhibits a CYP enzyme

A

prevents metabolism of drugs that are metabolized by the specific enzyme

concentration of drug increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hepatic enzyme inhibition

A

decrease effect of metabolic enzyme
prevents activation of drug metabolism in liver

concentration of drug increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hepatic enzyme inhibition outcome

A

metabolizes slower = more effective = need less drug
decreased elim rate = increased half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

hepatic enzyme induction

A

increase effect of metabolic enzyme
increases activation of drug metabolism in liver

expected concentration of drug is lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

hepatic enzyme induction outcome

A

slow onset
long duration

metabolizes faster = less effective = need more drug
increased elim rate = decreased half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

plasma protein binding

A

more bound a drug is = less active drug is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

capacity

A

availability to bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

affinity

A

rate of binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

albumin characteristics

A

high capacity for binding
low affinity for binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

alpha 1 acid glycoprotein characteristics

A

low capacity to bind
high affinity for binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

therapeutic range/index definition

A

ratio of effective dose compared to lethal dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

good therapeutic index

A

wide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

bad therapeutic index

A

narrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

first order kinetics

A

amount of drug eliminated is proportional to amount in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

drug that follows first order kinetics

A

epinephrine
ibuprofen
zofran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

drug that follows zero order kinetics

A

alcohol
phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

zero order connectics

A

amount of drug eliminated is fixed and independent of amount present in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how to calculate loading dose

A

LD = (concentration x volume of distribution) / bioavailability (F)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

when is half life predictable

A

if a drug follows first order kinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how to calculate half life

A

0.693/slope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what does half life mean for first order drugs

A

50% of drug is lost each half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

agonist definition

A

substance that mimics endogenous effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

antagonist definition

A

substance that blocks endogenous effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

partial agonist/antagonist

A

substance that has both agonist and antagonist properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how does ED50 determine potency

A

lower ED50 = more potent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how to determine efficacy

A

higher the maximum point on curve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

tolerance definition

A

occurs slowly over time and does not reverse rapidly after withdrawal of drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Tachyphylaxis

A

occurs rapidly and reverses rapidly after withdrawal of drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

tolerance vs tachyphylaxis

A

tolerance = chronic
tachyphylaxis = acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

reversible/competitive action

A

drugs bind to receptor but can easily be kicked off by molecule with higher affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

irreversible action

A

drug binds to receptor indefinitely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

sedation definition

A

calming and drowsiness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

hypnosis definition

A

produces drowsiness and facilitates deep sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

anesthesia definition

A

global (reversible) CNS depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what triggers MH

A

volatile anesthetics & succinylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what happens in MH

A

mutation in RyR causes uncontrolled release of Ca2+ [IC] resulting in intense muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

MH key symptoms

A

extreme muscle metabolism
tachycardia
hypercarbia
hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MH treatment

A
  1. hyperventilate
  2. give NaHCO3 (met. Acidosis)
  3. give insulin/furosemide
  4. give dantrolene (2.5mg/kg)
  5. cool pt
  6. treat other symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

barbiturates effects

A

*sedative
*hypnosis
*anticonvulsant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Barbiturates mechanism of action

A

increase duration of GABA Cl- chloride channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

barbiturate side effects

A

tissue damage
decrease BP / BF / ICP
increase HR
vasodilation
respiratory depression
hyperalgesia
histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Barbiturate drug interactions

A

precipitates w/ weak bases:
*Roc
* Lido
* Labetalol
* morphine

alcohol
benzos
opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Barbiturates Contraindications

A

elderly
anemic
shock
acute intermitent porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

barbiturate onset and duration

A

O= 10-20s (fast)
D = 8-20 min (short)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Barbiturate metabolism

A

CYP enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

barbiturate examples

A

phenobarbital
methohexital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

benzos effect

A

sedation
anti-anxiety
hypnosis
muscle relaxation
anterograde amnesia
anticonvulsant
thrombophlebitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

benzos MOA

A

increases frequency of GABA Cl- channel opening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

benzos side effects

A

pt may develop tolerance or dependance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

benzos drug interactions

A

opioids: hypotension/resp depres
anesthetics: enhance potency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

benzos onset

A

fast:

Midazolam < Diazepam < Lorazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

benzos lipid solubility

A

high = high Vd

M>D>L

76
Q

benzos metabolism

A

hepatic

77
Q

benzos examples

A

Midazolam, Diazepam, Lorazepam

78
Q

Midazolam contraindications

A

kidney failure
active metabolite alpha-hydroxy accumulates

79
Q

benzos half life

A

D>L>M

(fastest onset has shortest half life)

80
Q

flumazenil use

A

reverse benzos

81
Q

flumazenil side effect

A

shorter duration than benzos

82
Q

ketamine uses

A

anesthesia (unconsciousness)
analgesia
amnesia
depression
anticonvulsant (no change to seizure threshold)

83
Q

ketamine MOA

A

NMDA receptor antagonist
- Glutamate receptor

84
Q

ketamine side effects

A

dissociative anesthesia
hallucination
cardiac stimulant (incr HR/BP/CO)
incr CBF/ICP
bronchodilator

85
Q

ketamine drug interaction

A

blocked by alpha and beta antagonists
decrease anesthesia requirements
- additive to VA, propofol, benzos

86
Q

ketamin onset and duration

A

O: 15-30 sec (fast)
D: 10-15 min (short)

87
Q

ketamine analgesia onset

A

instant

88
Q

ketamine analgesia duration

A

40 min

89
Q

Ketamine contraindications

A

CAD
HTN
CHF
arterial aneurysms

90
Q

Ketamine metabolism

A

CYP enzymes (hepatic)
active metabolite: Norketamine
high hepatic extraction

91
Q

Ketamine excretion

A

renal (incl metabolites)

92
Q

propofol MOA

A

increases affinity of GABA for GABA receptor

93
Q

propofol uses

A

anesthesia induction/maintenance
sedataive
antiemetic
antipruritic
anxiolytic
anticonvulsant

94
Q

propfol side effects

A

dystonic movements
decrease BP/resp
decr CBF/BV/ICP
hypertriglyceridemia
propofol infusion syndrome
pain w/injection

95
Q

propofol infusion syndrome

A

acidosis
myocardial failyre
rhabdo

96
Q

propofol drug interaction

A

reduce dose if used with versed or fentanyl

97
Q

Propofol CI

A

elderly
hypovolemia
LV dysfunction
beta-blockers

98
Q

propofol onset/duration

A

onset: 10-20 s (rapid)
duration: 2-8 min (short)

99
Q

Fospropofol

A

water soluble pro-drug
prolonged onset/duration

100
Q

etomidate use

A

sedation/induction
hypnotic

101
Q

etomidate MOA

A

increases affinity of GABA for GABA receptor

102
Q

etomidate side effects

A

seizures
muscle movements
suppressed adrenal function
PONV
decr CBF/ICP
decr SVR (CO mx’d)

103
Q

etomidate onset/duration

A

O: 20-30 s (rapid)
D: 5 min

104
Q

Etomidate metabolism

A

plasma esterases
CYP enzymes

105
Q

precedex use

A

anxiolysis
sedation
analgesia
withdrawal treatment
epidural/regional

106
Q

precedex MOA

A

alpha 2a agonist
decr NE release
decr sympathetics

107
Q

precedex side effects

A

decr BP
decr HR
withdrawal (prolonged use)
nausea

108
Q

precedex drug interactions

A

vasodilators
hypnotics
drugs that decr HR

109
Q

precedex onset/duration

A

O: rapid
D: 20 min (2 hr half life)

110
Q

Precedex CI

A

renal/hepatic insufficiency =. decr dose

111
Q

doxapram use

A

repiratory/CNS stimulant (used for excessive resp depression)

COPD

112
Q

doxapram side effects

A

seizure, dizzy, tachycardia, PONV

113
Q

what does ED95 in NMB’s mean

A

dose that gives 95% twitch suppression in 50% individuals

114
Q

NMB dose compared to ED95

A

usually 1-2x ED95

115
Q

what happens when 75% of N1 receptors are bound with NMB

A

some weakness

116
Q

what happens when 95% of N1 receptors are bound with NMB

A

paralysis

117
Q

Upregulation

A

An increase in the number of receptors on the surface of target cells
cells more sensitive to a hormone or another agent

118
Q

What conditions cause the Ach receptor expression to be upregulated

A

neuron lesions
trauma
sepsis/infection

119
Q

how is NMB dosing changed when Ach receptor expression is upregulated

A

more nondepolarizing (less depolarizing)

more receptors for the NMB to block

120
Q

when is Ach receptor expression downregulated

A

myasthenia gravis, chronic AchE inhibitor use

121
Q

how is NMB dosing changed when Ach receptor expression is downregulated

A

more depolarizing (less nondepolarizing)

less receptors for the NMB to block

122
Q

succinylcholine MOA

A

binds Ach receptor
persistant depolarization

phase 1: depolarizing
phase 2: desensitizing

123
Q

succinylcholine onset/duration

A

O: rapid
D:Short

124
Q

Sux duration prolonged by

A

high dose/infusion
- decr metabolism
- hypothermia
- psuedocholinesterase def

125
Q

sux metabolism

A

plasma psuedocholinesterase
metabolite: suxmonocholine

126
Q

succinylcholine drug interaction

A

cholinesterase inhibitors (increase duration)

impacts NDMR
- phase 1: antagonistic
- phase 2: additive

127
Q

succinylcholine contraindications

A

MH
decreased pseudocholinesterase activity (dibucaine 20)
hyperkalemia

128
Q

sux side effects

A

decr HR
twitches
hyperkalemia
incr pressures
MMR
incr histamine
MH

129
Q

Rocuronium/vecuronium clearance

A

hepatic

130
Q

pancuronium/doxacuronium clearance

A

renal

131
Q

atracurium/cisatracurium clearance

A

hoffman

132
Q

rocuronium side effects

A

incr HR
decreased dose in liver failure/pregnancy

133
Q

pancuronium side effects

A

decreased dose in kidney failure
incr BP
incr HR

134
Q

pancuronium duration

A

long acting (60-120min)

135
Q

atracurium side effects

A

histamine release & toxic metabolite (laudanosine)
decr BP/HR/SVR
bronchospasm (asthmatics)

136
Q

roc onset/duration

A

onset: 1.5min
duration: 35-75 min (intd)

137
Q

vecuronium o/d

A

onset: 2-3min
duration: 45-90 min (intd)

138
Q

atracurium o/d

A

onset: 2.5-3 min
duration: 30-45 (intd)

139
Q

neostigmine MOA

A

AChE inhibitor

140
Q

neostigmine onset/duration

A

O: 5-10 min
D: 1 hr

141
Q

atropine/glycopyrrolate MOA

A

muscarinic receptor antagonist

142
Q

glycopyrrolate dosing

A

0.2 mg glyco/ 1 mg neostigmine

143
Q

Atropine onset and duration

A

fast onset
short duration

144
Q

glycopyrrolate onset and duration

A

slow onset
long duration

145
Q

which antimuscarinic should be used with neostigmine or pyridostigmine

A

glycopyrrolate

146
Q

which antimuscarinic should be used with edrophonium

A

atropine

147
Q

Edrophonium onset and duration

A

onset: 1-2 min
duration: 1 hr

148
Q

Pyridostigmine onset and duration

A

onset: 10-12 min
duration: over 2 hr

149
Q

neostigmine onset and duration

A

onset: 5-10 min
duration: 1 hr

150
Q

how many Ach receptors have to be blocked for a decrease in twitch height

A

75%

151
Q

how many Ach receptors have to be blocked for a disappearance of a twitch

A

90-95%

152
Q

antimuscarinic side effects

A

overractive sympathetics

mental status impacts (elderly)

153
Q

cholinesterase inhibitor side effect

A

parasympathetic activation

154
Q

which opiod does not accumulate over a constant infusion

A

remifentanil

155
Q

what are the different opiod receptors

A

mu, kappa, delta, sigma

156
Q

opioid mechanism

A

bind receptors in CNS
decr VGCa++
incr VG K+

hyperpolarization

decr release Ach/Ne/5Ht/sub p

157
Q

where are opiod receptors located

A

CNS and peripheral nociceptors

158
Q

opioid side effects

A

hyperalgesia
tolerance/dependence
respiratory depression
decr CBF/ICP/CMO2C
chest wall regidity
miosis
pruritis
PONV
histamine

159
Q

opioid effects

A

analgesia
euphoria
sedation

160
Q

what is responsible for opioid metabolite excretion

A

kidneys

161
Q

what is the risk of using meperidine with renal dysfunction

A

buildup of active metabolite = seizure risk

(noremeperidine)

162
Q

where are opioids metabolized

A

liver

163
Q

Naloxone MOA

A

opioid receptor antagonist

164
Q

naltrexone MOA

A

long acting opioid antagonist

165
Q

what are the mixed agonist/antagonist opioids

A

butorphanol
nalbuphine
buprinorphine

166
Q

how can buprenorphine act as a mu antagonist

A

high affinity for receptor but low activity

167
Q

mixed opiod agonist/antagonist DOA

A

longer (up to 10 hr)

168
Q

naloxone onset

A

1-3 min

169
Q

naloxone dosing

A

0.4-2 mg every 2-3 min as needed

170
Q

COX inhibitors

A

aspirin, colchesine

171
Q

COXi MOA

A

irreversibly inhibit COX enzymes (inhibit prostaglandin synthesis)

172
Q

COXi side effects

A

bleeding

173
Q

NSAID benefits

A

reduced opiod dosing

174
Q

NSAID MOA

A

reversibly inhibit cox enzymes

175
Q

NSAID side effects

A

renal insufficiency & bleeding

176
Q

acetaminophen class

A

analgesic
antipyretic

177
Q

acetaminophen MOA

A

inhibits COX 1 & COX 2

178
Q

acetaminophen side effects

A

liver damage in large doses

179
Q

acetaminophen IV onset and duration

A

onset: 5-10 min, duration: 4-6 hr

180
Q

acetaminophen max dose

A

4g/24 hrs

181
Q

Does acetaminophen have anti-inflammatory effects?

A

nope

182
Q

Acetaminophen Contraindications

A

liver disease

183
Q

NSAID contraindications

A

renal disease

184
Q

how long is ketorolac indicated for?

A

short term- no longer than 1 week

185
Q

how does drug pKa affect ADME

A

the higher the pKa the slower it crosses

Sp: Pharm 1 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions