Brainscape's Knowledge GenomeTM

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


See full index

Fall'20 Pharmacology III > NCE part 2 > Flashcards

NCE part 2 Flashcards

1
Q

Type A nerve fibers - describe their myelination

A

heavy

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

Type B nerve fiber describe their myelination

A

light myelination

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

type c nerve fibers- describe their myelination

A

no myelination

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

what is type A alpha nerve fiber responsible for

A

proprioception

motor

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

what is type a gamma nerve fiber responsible for

A

muscle spindles

gaMMa - “M’s for Muscles”

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

type a delta nerve fiber is responsible for

A

pain
temperature

“DELToid Pain”

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

type a beta nerve fibers is responsible for

A

touch
pressure

“make a BET!” –>and slam your hand down!!

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

A- gamma nerve is responsible for

A

Muscle Spindles - think muscle tone

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

A-delta nerve fibers are responsible for :

A

Pain and Temperature

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

Which nerve fibers are preganglionic autonomic ?

A

Type B nerve fibers

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

C fibers are responsible for 1) _____via the dorsal root and are _______

A

Pain via dorsal root

and are

Postganglionic Sympathetic fibers

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

Which fiber is responsible for pain via the dorsal root ?

A

C fibers

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

Those are Postganglionic sympathetic nerve fibers .

A

C fibers

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

1 cause of methemoglobinemia

A

Benzocaine

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

Describe Zero Order kinetics . What are drug examples ?

A

1)Constant AMOUNT of drug eliminated per unit of time
2) Metabolic pathways are saturated
Drug ex: Salicylate, theophylline , phenytoin , and ethanol .

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

What is First Order kinetics? Which examples of drugs ?

A

1) Constant FRACTION of drug eliminated per unit of time
2) Elimination proportionate to amount of drug in the body

Drug ex: Most drugs are first order kinetics – SUX

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

Volume distribution

A

Amount of drug in body divided by amount in the in the blood
drug in body/drug in blood

Large Vd= lipid solubility
Small Vd= lipid insolubility

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

What is clearance ?

A

Complete drug removal from a volume of plasma per unit of time.

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

Elimination half time is : Time to eliminate 100% of drug from the plasma . True or False

A

False !

50% ( half)

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

4 half lives =

A

94% complete

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

Context - Sensitive Half-time :

A

Time needed for the plasma drug concentration to decrease by 50% (or any other percentage ) AFTER DISCONTINUING a continuous infusion with a specific duration .

Context = infusion duration

It considers combined effect of : distribution + metabolism+ duration of a continuous IV administration on the drug’s pharmacokinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

A drug that is eliminated by first order kinetics has a half-life of elimination of 6 hours. How much drug remains after 18 hours if 10mg is administered

A

1.25mg

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

160 mg of drug is administered and 20 mg remains 30 hours later. How much drug is lost in the next 20 hours if the drug is eliminated by first order kinetics:

A

15 mg

at third 1/2Life = 20mg
4th = 20/2 = 10mg
5th = 10/2 = 5mg

in the next 20 hours you add the 4th and 5th 1/2 lives b/c they’re each 10 hours = this gives you 15mg of drug lost in the “next 20 hours”

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

mu2

A

Analgesia (Spinal)

Respiratory depression(decrease sensitivity of resp. center to CO2)

Addiction

Constipation (marked) decrease motility and tone of GI muscles
increase CSF pressure (cerebral edema) C/I in head injury

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

kappa

A

Analgesia (Spinal & Supraspinal)

Dysphoria

Low abuse
Potential

Miosis
Diuresis

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

delta

A

Analgesia (Spinal & Supraspinal)

Respiratory depression

Physical dependence

Constipation (mild)

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

what type of compound is neuromuscular blocker

A

quaternary ammonium compound

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

all neuromuscular blockers are structurally related to

A

acetylcholine

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

T?F

majority of NMBD are synthetic alkaloids

A

true

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

NMBD classified by chemical class:

A

Steroidal
Benzylisoquinoinium
Other

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

H-2 Blockers: name 3 of them

A

Cimetidine
Ranitidine
Famotidine

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

H-2 Blockers moa

A

H-2 Blockers: Blocks acid stimulating effects of histamine and ACh

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

Anti-Muscarinic Effect:

A

Scopolamine is a high affinity muscarinic antagonist

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

Substance P

A

Neurokinin 1 Antagonists:

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

substance p

A

Aprepitant: Only PO
Fosprepitant: IV is available

** fun fact: Fosaprepitant is an antiemetic drug, administered intravenously. It is a prodrug of aprepitant

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

name Serotonin Antagonists:

we use

A

ondanestron

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

Anti-Histaminergic:

A

Diphenhydramine: Both antihistamine and anticholinergic effects:

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

Anti-Cholinergic:

what may be useful in neuraxial induced n/v

A

Glycopyrrolate may be useful in neuraxial induced N/V

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

Antidopaminergics:

A

Butyrophenones: Droperidol
Phenothiazines: Prochlorperazine
Benzamines: Metoclopramide

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

Chemotactic Trigger Zone (CTZ)- where is this found

A

4th ventricle of the brain (located on the floor)

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

name the 5 receptors found in the CTZ that cause n/v

A 
Dopaminergic
Serotonergic
Histaminic
Muscarinic
Substance P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what MAC is an HPV inhibitor

A

1mac of sevo, iso, des

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

what is nitrous affects on HPV

A

inhibits HPV

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

what is the effect of thoracic epidural on HPV

A

little or no effect

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

when does thoracic epidural anesthesia have an indirect effect on 02

A

if hypotension is allowed and a fall in co

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

what is the IV anesthetic effect on HPV

A

little or no effect

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

volatile anesthetics inhibit HPV in dose dependent fashion. what is the greatest to least for volatile anesthetics

A

halothane>enflurane>isoflurane/desflurane/sevoflurane

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

older volatiles were potent HPV inhibitors contributing to high incidence of hypoxemia during OLV in the 60’s and 70’s

A

just an FYI- nagelhout says its because they were using 2 mac of halothane

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

explain HPV

A

increase in pulmonary vascular resistance in atelectatic lung area. HPV optimizes overall gas exchange by shifting blood flow to better ventilated areas of the lung

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

what drug has been demonstrated to enhance effects of NO and may blunt rebound pulmonary pressure that occur during weaning off of inhaled NO

A

sildenafil

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

sildenafil and tadalafil have shown benefits in what chronic condition but not approved for these settings

A

chronic pulmonary arterial HTN

52
Q

phosphodiesterase 5- (PDE5)- do they have higher expression in pulmonary circulation or systemic circulation

A

pulmonary circulation

53
Q

due to phosphodiesterase 5 higher expression in pulmonary circulation do they have higher selective effect on PVR or SVR

A

PVR

54
Q

phosphodiesterase inhibitors prevent the degradation of what two things

A

cGMP and cAMP

55
Q

when phosphodiesterase inhibitors inhibit the degradation of cGMP and cAMP what activates this two things

A

NO

56
Q

so when NO activates cGMP and cAMP what does that lead to

A

vasodilation

57
Q

the vasodilation that results when cGMP and cAMP is activated by NO is through activation of

A

protein kinases and reduction of cytosolic calcium

58
Q

what type of of phosphodiesterase enzyme inhibitor is milrinone

A

adenosine 3,5-cAMP selective phosphodiesterase

59
Q

nebulized milrinone leads to a reduction in

A

relative reduction in PVR compared to SVR

60
Q

Calcium Channel Blockers are particularly successful in treating hypertension in the what three groups

A

elderly
african american
salt sensitive patients

61
Q

Median Nerve Injury

A

Ape Hand (unable to oppose Thumb)

62
Q

Ulnar Nerve Injury

A

claw hand

63
Q

Radial Nerve Injury

A

wrist drop

64
Q

Axillary Nerve Injury

A

Inability to abduct arm

65
Q

Musculocutaneous Nerve Injury

A

Inability to Flex Forearm

66
Q 
Intravascular infusion of which of the following substances would be most effective in promoting the osmotic movement of water into the circulation from the extracellular space
A.)  NaCl
B.)  Mannitol
C.)  Dextrose
D.)  Albumin
A

albumin

67
Q 
The most potent inhalational anesthetics have
A.) low blood solubility
B.) High blood solubility
C.) Low lipid solubility
D.) High lipid solubility
A

High lipid solubility

68
Q 
Build up of inhalational anesthetic in the brain is fastest for an agent that has:
A.) low blood solubility
B.) High blood solubility
C.) Low lipid solubility
D.) High lipid solubility
A

A.) low blood solubility

69
Q

How many mg are there in 10 mL of a 4% solution of cocaine

A

400 mg

4% = 40 mg x 10 cc = 400

70
Q

K+ Sparing: works where in the kidney tubes

A

Distal part of distal convoluted tubule

Collecting ducts/tubules

71
Q

Carbonic Anhydrase inhibitors: work where in the kidneys

A

Brush border of proximal tubule

72
Q

Loop: where do they work

A

loop of henle

73
Q

thiazide: work where

A

Proximal Part of distal convoluted tubule

74
Q

Osmotic: work where in the kidney

A

Proximal convoluted tubule
descending limb of loop of henle
distal part of distal convoluted tubule
collecting ducts/tubules

75
Q

plasma cholinesterase production is the work of how many genes?

A

2 genes

76
Q

what does Dibucaine number of 80 represent

A

DN = 80 = present on both genes = homozygous (plasma cholinesterase)= Normal

77
Q

dibucaine number of 40-60 represent

A

DN = 40-60 = only present on one gene = heterozygous (1 in 480) produce 50% of enzyme

78
Q

dibucaine number of 20

A

DN = 20 = missing on both genes = homozygous (atypical plasma cholinesterase) (1in 3200).

79
Q

Succinylcholine Disadvantages (6)

A

Myalgia
Hyperkalemia
Cardiac dysrhythmias
MH
Phase II Block: Resembles NMDR (>4 mg/kg)
Second Dose Effect: Brady after close second dose secondary to succinylmonocholine

80
Q

Drugs that interfere with Plasma Cholinesterase:

5

A
  1. Organophosphate exposure
  2. Anticholinesterase meds
  3. Metoclopramide
  4. MAOI
  5. Oral contraceptives used long-term
81
Q

why is succinylcholine dose 2x ed95

A

because of its rapid hydrolysis by plasma cholinesterase

82
Q

is succs competitive with Ach

A

no.

83
Q

are NMDR competitive with ACH

A

Yes

84
Q

name 5 conditions that interfere with plasma cholinesterase

A 
Liver disease (severe)
Chronic renal failure
Starvation 
Dialysis (soon after)
Infants (50%) by age 6 (70%), puberty (100%)
85
Q

in context of neuromuscular blockers- what is ED50 and ED 95

A

Measured by the amount of drug necessary to decrease the height of the baseline twitch by 50% and 95%

86
Q

How do we compare the potency of NMDR?

A

Potency and onset have an inverse relation

low potency = Higher rate of onset
high potency = lower rate of onset

87
Q

low potency NMBD

A

rapid onset

88
Q

high potency NMBD

A

slow onset

89
Q

the onset of action of NMBD is inversely proportional to what

A

potency

90
Q

Molar potency is highly predictive of a dugs time to onset of effect. what drug is the exception to this rule

A

atracurium

91
Q

molar potency is expressed in what units?

Why?

A

micromoles/kg

molecules of drug are VARIABLE
number of nicotinic receptors are FIXED
therefore, the fewer the number of molecules it takes (per kg of body wt) to saturate the receptor, the greater the affinity the drug has (the greater the potency) .

L - does that work for you? or want more? :D
The rationale for expressing potency in moles per kilogram is…[because] ultimately, we have a variable number of molecules chasing a fixed number of nicotinic receptors. The fewer molecules it takes (per kilogram of body weight) to achieve a given degree of receptor occupancy, the greater the affinity the drug has for the receptor. This is best expressed in micromoles per kilogram rather than in milligrams per kilogram.

92
Q

what is the issues with hyperparathyroidism and NMBD

A

hypercalcemia is associated with decreased sensitivity to atracurium and thus a short duration of neuromuscular blockade

Muscle-nerve models have shown hypercalcemia to decrease sensitivity to tubocurarine and pancuronium

93
Q

why does chronic use of anticonvulsant therapy need an increase dose to NMBD to achieve blockage.

A

can be attributed to

  • increased clearance.
  • increased binding of the nueuormuscular blockers to alpha 1 acid glycoproteins
  • and/or up regulation of neuromuscular acetylcholine receptors.
94
Q

hypothermia or magnesium sulfate do what to NMBD

A

potentiates blockade

95
Q

antidysrhythmics such as quinidine do what to NMBD

A

potentiate NMBD

96
Q

LA given in large doses do what do NMBD

A

potentiate it

97
Q

high magnesium concentrations do what to calcium channel at the presynaptic nerve terminals

A

inhibit release of acetylcholine

98
Q

antibiotics can potentiate neuromuscular blockers name 5 of them

A 
aminoglycosides
polymyxin
lincomycin
clindamycin
tetracycline
99
Q

what is the moa of how antibiotics potentiate neuromuscular blockers

A

inhibit the prejunctional release of acetylcholine and

depresses post junctional nicotinic acetylcholine receptor sensitivity to acetylcholine.

100
Q

Inhalation anesthetics potentiate the neuromuscular blocking effect of NMBD
what is the order

A

DES > SEVO > ISO > Halothane > Nitrous Oxide, barbiturate, or propofol

101
Q

3 Mechanisms for inhalation potentiation of NMBD:

A

Central effect on alpha motoneurons and interneruonal synapses

Inhibition of postsynaptic nicotinic acetylcholine receptors

Augmentation of antagonist’s affinity at the receptor site

102
Q

roc is how many times less potent than vec

A

6times

103
Q

roc eliminated by and excreted in

A

eliminated by liver excreted in bile

104
Q

roc remains stable for how many days at room temperature

A

60

105
Q

vecuronium is metabolized to

A

3-OH, 17-OH, 3,17-di-OH

106
Q

why does vecuronium have prolonged neuromuscular blockade with prolonged admnistration

A

3-oh has 80% the neuromuscular blocking potency and this metabolite will build up and increase the blocking potency of vec

107
Q

duration of vecuronium relies on liver or renal function more

A

liver function more than renal function

108
Q

pancuronium is it long or short acting. potent or not

A

potent long acting

109
Q

pancuronium has what two special properties

A

Vagolytic and butyrylcholinesterase inhibiting properties

110
Q

how long is pancuronium stable for at room temps

A

6mo

111
Q

accumulation of 3-oh metabolite is responsible for pancuroniums what

A

prolongation of the duration of action

112
Q

what percent of pancuronium is eliminated by kidneys

A

40-60%

113
Q

what is the only currently available short acting NMBD

A

Mivacurium

114
Q

mivacurium is metabolized by

A

Metabolized by butylcholinesterase at about 70-88% the rate of Sch to a monoester

115
Q

what can be considered problematic if we push mivacurium too fast

A

May produce histamine release especially if given rapidly

116
Q

name the isomer of astracurium

A

cisatracurium

117
Q

how is cisatracurium eliminated

A

hoffman elimination to laudanosine and a mono quaternary alcohol metabolite

118
Q

what percent is hoffman elimination
other ogans
renal

A

77%
23%
16%

119
Q

how much more potent is cisatracurium than atracurium

A

4-5x

120
Q

what is the relationship to aludanosine

A

5 times less laudanosine is produced and is thought one of no clinical consequence

121
Q

does cisatracurium produce histamine release

A

no

122
Q

Tubocurarine

A 
Tubocurarine:
Monoquarternary, long acting
No active metabolism
Excreted unchanged in urine; liver is secondary
Not suitable for renal or liver failure patients
Onset slow
Duration is long
Recovery slow
Intubating dose 0.5 – 0.6 mg/kg
Maintenance dose are 0.1 – 0.2 mg/kg
123
Q

Atracurium

A

Atracurium
Racemic mixture of 10 stereoisomers
Isomers are separated into 3 geometrical isomer groups that are designated cis-cis, cis-trans, and trans-trans
Designed to undergo spontaneous degradation at physiologic temp and pH by Hofmann elimination yielding a laudanosine (tertiary amine) and a monoquaternary acrylate metabolite
Can undergo ester hydrolysis
Hoffmann elimination fragments atricurium to laudanosine and a monoquaternary acrylate
Laudanosine depends on the liver for clearance with ~70% excreted in bile with remainder in the urine

124
Q

slide 15&

A

16

125
Q

tetracycline potentiates NMBD by exhibiting ONLY what activity

A

by depressing POST junctional nicotinic acetylcholine receptor sensitivity to acetylcholine ONLY

no inhibition of prejunctional release

Fall'20 Pharmacology III (14 decks)

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