Brainscape's Knowledge GenomeTM

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


See full index

APEX > Pharmacology II > Flashcards

Pharmacology II Flashcards

1
Q

A-alpha

A

Heavy myelination
Sk. muscle motor, proprioception
12 - 20 um
4th block

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

A-(beta)

A

Heavy myelination
Touch, pressure
5 - 12 um
4th block

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

A-Gamma

A

Medium myelination
Skeletal muscle, tone
3 - 6 um
3rd to block

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

Delta

A

Medium myelination
Fast pain, temperature, touch
2 - 5 um
3rd to block

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

B fibers

A

Light myelination
preganglionic ANS fibers
3 um
1st to block

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

C fibers - sympathetic

A

no myelination
post ganglionic ans fibers
0.3 - 1.3
2nd to block

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

C-fibers dorsal root

A

no myelination
slow pain, temperature, touch
0.4 - 1.2
2nd to block

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

ED50 for local anesthetics

A

Cm = minimum effective concentration is a unit of measure that quantifies the concentration of local anesthetic that is required to block conduction

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

Rank the nerve fibers according to their sensitivity to LA in vivo (most to least sensitive)

A

B-fibers –> C fibers –> Alpha-delta, gamma –> Alpha beta –> Alpha alpha

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

3 possible configurations of the VG sodium channel

A

resting = channel closed, but can depolarize
active = channel open, Na+ moving along concentration gradient into the neuron
inactive = channel closed, cannot be opened

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

How and when do LA bind to the VG sodium channel?

A

Active and Inactive states ONLY!

LA are more likely to bind to axons conducting APs and less likely to bind to those that are not conducting APs

More frequently nerve depolarized, more open, more time for LA to bind = use-dependent or phasic blockade

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

What is an AP? How does it depolarize a nerve?

A

Temporary change in a transmembrane potential followed by a return to transmembrane potential.

-Na or Ca must enter cell (makes inside more +)
-Threshold potential reached, cell depolarizes

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

What happens when a nerve repolarizes?

A

Removal of positive charges from inside the cell via removing potassium

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

How does LA affect neuronal depolarization?

A

Bind to the alpha subunit on the inside of the sodium channel

-critical # of sodium ch. blocked, there aren’t enough open channels for sodium to enter in sufficient quantity
-the cell can’t depolarize

THEY DO NOT AFFECT RMP OR THRESHOLD POTENTIAL

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

Role of ionization w/ respect to LA

A

-Weak baes w/pka values > 7.4
-We can predict > 50% of the LA will exist as the ionized, conjugate acid after injection
-Non-ionized passes through axolemma, but the ionized binds to alpha-subunit on the interior of VG Na channel

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

What are the 3 building blocks of LA?

A

Benzene ring = lipophilic
Intermediate chain = ester/amide, metabolism, allergy
Tertiary amine = hydrophilic, accepts proton, m makes a molecule a weak base

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

Incidence of allergies w/LA

A

Esters - d/t para-aminobenzoic acid which is an immunogenic molecule

Amides - rare, d/t methylparaben preservative

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

What determines LA onset? Which drug disobeys this rule

A

pKa (potency, dose)

Chlorprocaine b/c its 3% so lots of molecules

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

What determines local anesthetic potency?

A

Lipophilicity- think, more drug able to traverse the neuronal membrane
Intrinsic vasodilating effect

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

What factors determine LA DOA

A

Protein binding

The intrinsic vasodilating effect, lipid solubility (more lipophilic = long DOA)

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

Discuss the intrinsic vasodilating effects of LA. Which LA has the opposite effect?

A

At low doses, they all vasoconstrict. At high doses (clinical doses) they all vasodilate except cocaine.

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

Amide Local Anesthetic pKa

A

Bupivacaine 8.1 (96% protein)
Levobupivacaine 8.1
Ropivacaine 8.1 (94% protein)
Lidocaine 7.9 (65%)
Prilocaine 7.9 (55%)
Mepivacaine 7.6 (78%)

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

Ester LA pKa

A

Procaine 8.9 (6% protein)
Chloroprocaine 8.7 (0% protein)
Tetracaine 8.5 (76% protein)

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

List 5 factors that govern the uptake and plasma concentration of LA

A
  1. tissue blood flow
  2. properties of LA
  3. metabolism
  4. additives
  5. site of injection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Rank injection sites w/corresponding LA concentrations

A

IV
Tracheal
interpleural
intercostal
caudal
epidural
brachial plexus
femoral
sciatic
subcutaneous

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

Max dosing for amide LA

A

Levobupi (2/150 mg)
Bupi (2.5 vs 3/175 vs 200 mg)
Ropi (3/200 mg)
Lido (4.5 vs 7 / 300 vs 500 mg)
Mepivacaine (7/400 mg)
Prilocaine (8/ 500 - 600 mg)

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

Max dose for ester LA

A

Procaine (7 and 350 - 600)
Chloroprocaine (11 vs 14 mg/kg and 800 vs 1000 mg)

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

What is the most common sign of LA toxicity?

A

Seizure
Bupi - cardiac arrest

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

Lidocaine toxicity according to plasma concentration

A

1 - 5 = analgesia
5 - 10 = tinnitus, sk. muscle twitching, numb lips, restlessness, vertigo, blurry vision, hypotension, myocardial depression
10 - 15 = seizures, LOC
15 - 25 = coma, respiratory arrest
> 25 = CV collapse

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

What increases risk of CNS toxicity?

A

Hypercarbia/acidosis, Hyperkalemia

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

Why is the risk of cardiac morbidity higher with bupivacaine than with lidocaine

A
  1. affinity for VG sodium channels in the inactive and active states
  2. rate of dissociation from the receptor during diastole

bupi has a slower rate of dissociation from this receptor during diastole

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

rank the difficulty of cardiac resuscitation w/LA

A

bupi > levobupi > ropi > lidocaine

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

Discuss ACLS modifications w/LAST

A
  1. no epi (keep it less < 1 mcg/kg)
  2. no vaso, lido, procainamide
  3. use amio
34
Q

Discuss LAST treatment

A

100 mL bolus over 2 - 3 minutes
< 70 kg - 1.5 mL/kg over 2 - 3 minutes

250 mL over 15 minutes
< 70 kg - 0.25 mL/kg/min

max dosing = 12 mg/kg

35
Q

How much tumescent lidocaine can you use?

A

50 - 55 mg/kg

36
Q

Potential complications of tumescent anesthesia?

A

pulmonary edema, pulmonary embolus

GA recommended if > 2 - 3 L of the tumescent solution is used

37
Q

Name two LA that produce leftward shift of oxyhgb curve?

A

Prilocaine + benzocaine b/c they can cause methemoglobinemia

Oxygen binding site on the heme portion of the hemoglobin molecule contains ferrous iron

oxidation of iron –> ferric (fe 3+)

methgb impairs oxygen binding and unbinding from hgb molecule

38
Q

What drugs are capable of causing methemoglobinemia

A

nitroglycerin
nitroprusside
sulfonamides
phenytoin

benzocaine
cetacine
prilocaine
emla

39
Q

s/s methemoglobinemia

A

tachycardia
tachypnea
chocolate colored blood
cyanosis
oxygen @ 85%
LOC, coma, death

40
Q

treatment for methemoglobinemia

A

methylene blue 1-2 mg/kg over 5 minutes
max = 7 - 8 mg/kg

MOA: methgb reductase metabolizes methylene blue to form leucomethylene blue which functions as an electron donor and reduces ferric back to ferrous

41
Q

Two patient populations at risk for methgb

A

neonates (deficient in methgb reductase, thus sus to oxidation)
g6pd (no methgb reductase, exchange tx)

42
Q

EMLA cream is made of

A

2.5% prilocaine
2.5% lidocaine

prilocaine metabolizes to o-toluidine, which oxidizes hgb to methgb

43
Q

Max dosing EMLA cream

A

0 - 3 mo, 1 g or 10 cm2
3 - 12 mo, 2 g or 20 cm2
1 - 6 yrs, 10 g or 100 cm2
7 - 12 years, 20 g or 200 cm2

44
Q

Sodium bicarb + LA

A

shortens LA onset
reduces pain during injection
1 mL of 8.4% sodium bicarb with 10 mL LA

45
Q

Drugs added to LA for supplemental analgesia?

A

Opioids (Mu)
Clonidine (Alpha2)
Epi (alpha2)

46
Q

hyaluronidase

A

hyaluronic acid is present in the interstitial matrix and basement membrane. it hinders the spread of substances through tissue

-hyaluronidase hydrolyzes hyaluronic acid - facilitating the diffusion of LA thru tissues

ophthalmic blocks = speeds onset enhances quality, mitigates the rise in IOP

47
Q

Discuss pain transduction

A

injured tissues release various chemicals that activate peripheral nerves and/or cause immune cells to release proinflammatory compounds. the peripheral nerves transduce this chemical soup into an AP

48
Q

inflammation’s role in pain transduction

A

-reduced threshold to pain stimulus (allodynia)
-increased response to pain stimulus (hyperalgesia)

49
Q

Pain transmission

A

Three-neuron afferent pain pathway along the spinothalamic tract

-first-order neuron: periphery –> dorsal horn
-second order: dorsal horn –> thalamus
-third order: thalamus –> cerebral cortex

50
Q

Pain modulation most important site

A

Most important site: substantia gelatinosa in dorsal horn (Rexed Lamina II + III)

51
Q

Pain modulation descending inhibitory pathway

A

Periaqueductal gray and rostroventral medulla –> substantia gelatinosa

52
Q

Inhibition of pain occurs via

A

spinal neurons release GABA + glycine
descending pathway release Ne, 5-Ht, endorphins

53
Q

Pain is augmented by

A

central sensitization + wind-up

54
Q

Discuss the process of pain perception

A

Limbic system and cerebral cortex process pain signals

55
Q

What is the MOA of opioids?

A

Each opioid receptor links to a G-Protein, and agonism of the receptor instructs the G-Protein to turn off adenylyl cyclase

Reduction of cAMP –> alters ionic current

56
Q

How does decreased cAMP alter ionic current

A
  1. VG Ca Ch inhibited –> decreased NT release
  2. Augment K+ Ch inward rectifier –> hyperpolarizes
57
Q

What are the precursors of the endogenous opioids?

A

Pre-proopiomelanocortin –> Endorphins (MU)
Pre-enkephalin –> Enkephalin (DELTA)
Pre-dynorphin –> Dynorphins (KAPPA)

58
Q

mu 1

A

analgesia (spinal + supraspinal)
bradycardia

euphoria, miosis, urinary retention, low abuse

59
Q

mu 2

A

-analgesia (spinal only)
-bradycardia
-rr depression
-constipation
-dependence

60
Q

mu 3

A

immune suppression

61
Q

kappa stimulation

A

antishivering
diuresis
dysphoria
delirium
hallucinate

62
Q

opioids affect on cv

A

bradycardia (Unless meperidine – tachycardia)
bp remain stable if patient is cv healthy
hypotension w/morphine + meperidine (histamine release)

63
Q

opioids affect on ventilation

A

via mu + delta

CO2 response curve rightward
Drop in RR and increase in Vt

64
Q

how do opioids affect the pupil?

A

edinger westphal nucleus stimulation –> PNS stim. ciliary ganglion and oculomotor nerve (CN 3) –> miosis

65
Q

how do opioids produce n&v?

A

CTZ (area postrema of medulla)
vestibular apparatus

66
Q

how do opioids contribute to urinary retention?

A

mu + delta

detrusor relaxation + urinary sphincter contraction

67
Q

Immunologic effects of opioids

A

histamine (meperidine, morphine, codeine)
inhibits cellular + humoral immune function
suppress NK cell function

68
Q

How do opioids affect thermoregulation?

A

Reset the hypothalamic temperature set point to decrease core body temperature

69
Q

Rank IV opioids in terms of potency

A

-sufentanil > remifental = fentanyl > alfentanil > dilaudid > morphine > meperidine

70
Q

compare the equianalgesic opioid dose r/t 10 mg of morphine

A

100 mg meperidine
1.4 mg dilaudid
1000 mcg alfentanil
100 mcg fentanyl/remifentanil
10 mcg sufentanil

71
Q

Discuss the co-admin of meperidine and MAOI

A

can cause serotonin syndrome

meperidine is a weak SRI
MAO deaminates serotonin in the synaptic cleft, co-admin of these drugs can cause serotonin syndrome

s/s = hyperthermia, LOC, hyperreflexia, sz, death

MAOi’s = phenelzine, isocarboxazid, tranylcypromine

72
Q

Alfentanil pka

A

6.5
90% unionized
Low vd, high degree of plasma protein binding (alpha - 1)

73
Q

Largest VD of opioids vs smallest

A

Fentanyl = 4 L/kg
Remi = 0.39 L/kg

74
Q

PK/PD Remi

A

Ester linkage hydrolysis by erythrocyte and tissue esterases
-highly lipophilic
- 0.1 - 1 mcg/kg/m
- obese pt use LBW
- avoid intrathecal b/c glycine causes sk. muscle weakness

75
Q

How does methadone reduce pain?

A

-mu receptor agonist
-NMDA receptor antagonist
-inhibits monoamine reuptake

76
Q

Etiology of opioid-induced sk. muscle rigidity?

A

mu stim in the CNS

greatest resistance at the larynx

77
Q

Buprenorphine

A

mu agonist partial
greater than morphine analgesia
cannot be reversed by naloxone
DOA 8 hour
can give transdermal

78
Q

Nalbuphine

A

Kappa agonist, mu antagonist
Similar to morphine
Reversed by naloxone
Useful for cardiac pt b/c no changes HD

79
Q

Butorphanol

A

-Kappa agonist, mu antagonist (weak)
-greater than morphine analgesia
-reversed by naloxone
-postop shivering treatment
-intranasal route

80
Q

Which opioid antagonist is least likely to reverse respiratory depression?

A

Methylnaltrexone b/c quaternary amine group
Good for opioid-induced constipation

81
Q

Which opioid antagonist has the longest DOA?

A

Naltrexone (no 1st pass)
DOA = 24 hours
ER formula

APEX (18 decks)

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