Brainscape's Knowledge GenomeTM

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


See full index

DAD III - Test Two - Dr. Smith > Immunology - Dr. Smith > Flashcards

Immunology - Dr. Smith Flashcards

1
Q

PGD2 fxn

A

Weak inhibitor of platelet aggregation

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

PGE1

A

AKA prostacyclin

Vasodilation

inhibitor of lipolysis

inhibitor of platelet aggregation

bronchodilation

contraction of GI smooth muscle

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

PGE2

A

stimulates hyperalgesic response

renal vasodilation of afferent arteriole

stimulates uterine smooth muscle contraction

protects GI

reduces secretion of stomach acid

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

PGF2

A

Elevates thermoregulatory set point in anterior hypothalamus

stimulates uterine smooth muscle contraction

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

PGI2

A

potenet inhibitor of platelet aggregation

vasodilator

increases cAMP in platelets which gives it ability to act as inhibitor of platelet aggregation

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

TXA2

A

thromboxane

potent inducer of platelet aggregation

potent vasoconstrictor

decrease cAMP in platelets

stimulates release of ADP and 5HT from platelets

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

GI irritation

Non-selective vs Selective

A

Non-selective: Yes

Selective: less

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

Inhibition of platelet function

Non-selective vs selective

A

Non-selective: Yes

Selective: No

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

Inhibition of induction of labor

nonselective vs selective

A

non-selective: Yes

Selective: yes

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

alteration of renal fxn

non-selective vs selective

A

Non-selective: Yes

Selective: yes

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

Hypersensitivites

non-selective vs selective

A

Non-selective:Yes

Selective: Yes but reduced

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

NSAID general structure

A

Consists of acidic moiety attached to planar functionality

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

Salicylic acid

  • salicylic acid is extracted from willow bark
  • used medicinally as the sodium salt
  • Active and competitive
  • Primarly acts as COX 1 inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
A

Acetyl Salicylic Acid, ASA, Aspirin

It has enhanced therapeutic utility because of esterification of phenolic hydroxyl group and hydrophobic substitution at C-5

Long term use can change pH of stomach and cause damage

It is active, non-competitive

It is a strong organic acid

Potency: 750 mg

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

Salicylates

General characteristics

A

potent anti-inflammatory activity

mild analgesic

antipyretic activity

Toxicity: GI irritation, HSR, inhibition of platelet aggregation, and ototoxicity

Has ability to participate in transacetylation rxn

Acetylation of COX = irreversible inhibition of enzyme

Acetylation of circulating proteins = HSR

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

Diflunisal

Competitve

Longer t 1/2 = 8-12 hr

More potent than aspirin

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

Salsalate

Inactive, not potent

Dimer absorbed and then acted upon by esterases and forms ASA

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

Irritation due to COX inhibition

Renal Insufficiency

A
  • cause by inhibtion of PGE2, PGI2
  • Inc in water and sodium retention
  • Inc BP
  • problem for CHF or hypovolemic pt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Irritation due to COX inhibition

Electorlyte Imbalances

A
  • generally unique to salicylates in large doses
  • Kids are more prone
  • bengay can cause this imbalance
  • Phase 1: hyperventilation, increase expolsion of CO2 which increases pH of blood leading to respiratory alkalosis
  • Phase 2: increase excretion of potassium leading to acidic urine
  • Phase 3: continued hypokalemia, dehydration, coma, death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Irritation due to COX inhibition

Reye’s Syndrome

A

Seen in children recovering from mild viral infection

20-30% mortality

Accumulation of fatty tissue in variety of organs (brain, iver)

more associated with aspirin due to fact that aspirin uncouples oxidative phosphorylation

Cells become comprimsed due to uncoupling

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

ASA characteristics

A

extensively bound to plasma albumin

Highly bound by plasma proteins

DDI possible ie Warfarin

Undergoes glycine conjugation, ring hydroxylation, carboyl and phenol glucuronidation conjugation.

Eliminated by renal metabolism

IC 50 ratio: 166, COX 1 preference

lower IC 50 = better

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

Propionic Acid Derivatives

General Characteristics

A

Profens

strong organic acid (pKa = 3-5)

Form water soluble salts with alkaline reagents

alpha-CH3 substituent increase COX inhibitory activity and reduces toicity of profens

S enantiomer is more potent

Naproxen is only one NOT marketed as racemate

Well absorbed orally

t 1/2 = 2-5 hr

Naproxen t 1/2 = 12-15 hours

Metabolism = oxidation of side chain or aromatic ring. glucuronidation also possible

Undergo a metabolic inversion at chiral carbon. Go from R (inactive) to S

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

Ibuprofen

take TID

Potency: 500 mg, 1.5 times that of aspirin

Can undergo hydroxylation via CYP2C9, 2C13

Can undergo further hydroxylation to COOH

Can undergo gluc

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

Naproxen

Only S isomer given

take BID

has naphthyl ring

Most selective of profens (still non-selective)

COX 2 ratio = less than 1

Potency: 2 - 3 times that of aspirin

Can undergo hydroxylation via CYP3A4, 1A2

Can undergo gluc

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

Nabumetone

pro drug - oxidatively cleaved side chain giving acetic acid derivative

Long acting, anti-inflammatory, analgesic, antipyretic

Strucuture helps with GI issues

Can undergo hydroxylation and reduction (both inactive)

t 1/2 = 24 hours

More preferential for COX 2 (still non selective)

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

Heteroarylacetic Acids

General Characteristics

A

derivatives of acetic acid

heterocycle substituent at position 2

Include: indomethacin, sulindac, tolmetin, ketorolac

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

Indomethacin

potency: 25-50 mg. 10-20X more potent than aspirin

Prefers COX 1, not COX 2

Capable of rotation

susceptible to amide hydrolysis

Rapidly and extensively abs

t 1/2 = 4.5 hr

Has analgesic activity

has resemblance to 5HT which produces more CNS side effects. It worsesn parkisons, epilepsy, and psychiatric conditions

GI ADR: irritation, prolonged bleed time because of its lack of preference for COX 2

Metabolim: gluc, demethylation (looking like 5HT), and hydrolysis

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

Sulindac

Inactive when administered = pro drug

Requires reversible reduction to the sulfide to become active = capable of inhibiting COX

Potency: 5X that of aspirin

Ring hydroxylation does not occur because of F

Can be Gluc at the COOH

No rotation possible

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

Tolmetin

Potency: 2X that of aspirin

Highly PPB

Better tolerated than aspirin

metabolized by oxidation to a benzylic alcohol initially and eventually to the acid

metabolites are gluc and eliminated

t 1/2 =2.7 hr

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

ketorolac

administered as a racemate

has chiral center

produce opioid like analgesia without the respiratory depression. No abuse potential. Has lesser anti-inflammatory effects as compared to it analgesic effects

More potent than indomethacin

Used for post-op pain

Not used for more than 5 days because of inc bleed risk and HSR

It is not selective in regards to COX

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

Etodolac

potency: 2X that of aspirin, 300 mg. S isomer is more potent

fairly selective COX 2 inhibitor. Has ratio of 0.16. Below one means more preference for COX 2.

rapidly and well abs

high PPB

extensively metabolized in liver = gluc, hydroxylation

Cannot undergo isomerization

decreased GI ADR

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

Oxaprozin

COX 2 ratio is 150

has electron deficient system

almost inhibited metabolism because it is so slow. Undergoes gluc

t 1/2 = 51 hours (once a day dosing)

High PPB

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

Anthranilic acid

inhibit COX

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

Mefenamic Acid

Potency: 2X that of aspirin. Less potent than diclofenac and meclofenamic acid.

has acidic properties

more rapidly abs than diclofenac

t 1/2 = 2-4 hours

Metabolized by benzylic oxidation of the methyl group followed by eventual gulc

Used as mild analgesic. Sometimes used in inflammatory diseases

Many ADR: nausea, vomit, diarrhea, ulceration, HA, drowsy, hemtopoietic toxicity

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

meclofenamate

Potency: 6X that of aspirin. More potent than mefenamic acid, less potent than diclofenac

has acidic properties

Metabolized by benzylic oxidation of the methyl group followed by eventual gulc

Used as mild analgesic. Sometimes used in inflammatory diseases

Many ADR: nausea, vomit, diarrhea, ulceration, HA, drowsy, hemtopoietic toxicity

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

Diclofenac

Potency: 10-20X that of aspirin. More potent than mefenamic acid and meclofenamic acid

Can ungergo gluc and hydroxylation. Can go on to form quinone which is hepatotoxic

37
Q
A

piroxicam

potency: 20X that of aspirin

Not preferential to COX 2

pKa = 6.3 less acidic than COOH. Acidity attributed to 4-OH with enolate anion being stabilized by intramoleular H bonding to amide. Primarily ionized at physiologic pH

Forms a tautomer.

Slowly and well abs. Eliminated in urine and feces

t 1/2 = 50 hours, due to lack of COOH functionality which can be readily gluc and eliminated. once a day dosing.

38
Q
A

meloxicam

potency 30X that of aspirin

capable of ionizing in manner similar to piroxicam

Has improved COX 2 ratio as compared to piroxicam

Well abs

metabolized to 4 unidentified inactive metabolites. Excreted in urine and feces

t 1/2 = 20 hours. dosed once a day

39
Q

COX 2 selective inhibitors

general characteristics

A

have been made in an attempt to decrease side effects associated with NSAID ie GI damage

Have anti-inflammatory, anti-pyretic, and analgesic properties

Problem: sodium and water retention

40
Q
A

Celecoxib

Potency: 2X that of aspirin

COX 2 ratio = 0.0026

t 1/2 = 11 hr

GI effects are decreased

Has no effect on hematological effects, but you are at increased risk for MI or stroke

Renal effects: sodium and water retention

Contraindicated for those with sulfa allergy

Well abs from GI tract, well distributed.

Metabolism: oxidation then formation of acid, then gluc. Eliminated in urine and feces

41
Q
A

Acetanilide

neutral OMA (organic medical agent)

Not anti-inflammatory and not an NSAID

Is analgesic and anti-pyretic

Only capable of supressing COX activity in areas which are not inflammed

Converts iron 4 to iron 3 (inactive) which inhibits peroxidase. Bu this inhibition is easily overcome which leads to inflammation

Can be oxidized to Acetaminophen

Because it lacks a COOH, it has little GI irritation, limited CV, platelet, and resp effects. Has no increase in bleeding time

ADR related to metabolic transformations: methemglobinemia, anemia, hepatotoxicity, nephrotoxicity

Can be metabolized to toxic quinoneimine which is usually detoxified by glutathione

42
Q
A

acetaminophen

43
Q
A

phenacetin

44
Q
A

Acetylcyteine

antidote for acetaminophen overdose

capable of mimicking action of glutathione and thereby detoxfiying quinone-imine

45
Q

Opiates

General characteristics

A

reduce the perception of pain impulses by the CNS

Cause CNS depression (narcosis): sedation, this effect can be intensified with other CNS depressants

Cause depression of the cough reflex center of the medulla (antitussive)

Cause antiperistaltic action in GI (constipation)

Cause resp depression: most serious, most often happens to pt that is already sedated

Cause depression of CV system resulting in hypotension and bradycardia: mild effect, fainting possible

Cause constriction of pupil: determines OD

Cause tolerance and chronic use: tolerance does not develop with constipation or pupil constriction

Cause addiction and physical dependence

46
Q

Opiates

MOA

A

Mu receptor: prinicpal pain modulating site in the CNS and is morphine selective

Mu 1 = analgesia, Mu 2 = resp depression

Delta receptor: role in analgesia, associated with convulsiions, not many selective ligands

Kappa receptor: mediate a sedating analgesia with reduced addiction liability and resp depression. agonism here deactivates self reward

NOP receptors emotional and mental state, could inc pain, some analgesia. Burprenorphine is agonist

47
Q

Sigma receptor

A

implicated in psychotomimetic and dysphoric side effects of opiates. Not really an opiate receptor.

48
Q

Mu receptor effects for

analgesia

resp dep

pupil constriction

GI motility

S.M. spasm

Behavior

Dependence

A

Analgesia: brain/spinal

Resp dep: ++

Constriction: ++

GI motility reduced: ++

S.M. spasm: ++

behavior: euphoria = +++, sedation = ++

Dependence: +++

49
Q

Sigma receptor effects

Analgesia

Resp dep

pupil

GI motility

S.M. spasm

Behavior

Dependence

A

Analgesia: brain

Resp: +/-

pupil: -

Motility: ++

spasm: -

Behavior: antidepressant

Physical dependence: +

50
Q

Kappa receptor effects

Analgesia

resp dep

pupil

GI motility

S.M. Spasm

Behavior

Dependence

A

Analgesia: brain/spinal

resp: +
pupil: +
motility: +

Spasm: -

Behavior: dysphoria = +++, sedation = ++

dependence: +

51
Q

NOP receptor effects

Analgesia

resp dep

pupil

GI motility

S.M. Spasm

Behavior

Dependence

A

Analgesia: brain/spinal

resp dep: -

pupil: dilation

GI motility: -

S.M. Spasm: -

Behavior: anxiety = ++, psychomimetic mu tolerance

Dependence: -

52
Q

Signal transduction

A

after the opiates interact with opiate receptors, the neurons become hyperpolarized. Due to increase in potassium conductance and reduction of inward calcium current that occurs during action potential. Believed to be direct interaction between G protein and K+, Ca2+

53
Q

Tolerance adaptation

A

overtime at constant dose, there is an increase in cAMP because the system is desensitized. Overtime you have to increase doses to get the same therapeutic effects. Sensory overload happens with withdrawal from opiates.

Opiate would initially decrease cAMP

54
Q

Methionine Enkephalin

A

endogenous opiate

Morphine mimics a specific phenol in this drug structure

Attempts to therapeutically use this endogenous opiate have been hindered because of its polarity and metabolic liability

55
Q
A

Morphine

It is the R isomer, principle alkaloid obtained from opium poppy

OMA = opiate

Narcotic analgesics are classified on the basis of their structural derivation from morphine.

Potency = 1

Pure agonist at mu, delta, kappa

Has antitussive activity

Does not ionize at physiologic pH

56
Q

Morphine pharmacological profile

A

Rigid pentacyclic structure consisting of a benzene ring (A), two partially unsaturated cyclohexane (B and C) rings, a piperidine ring (D), and a dihydrofuran ring (E)

rings A, B, C = phenanthrene ring system

Two hydroxyl functional groups, C-3 phenolic OH and C6 allylic OH

ether linkage btw C4 and C5

unsaturation btw C7 and C8

basic, tertiary amine fxn at position 17

5 chiral centers with morphine exhibiting a high degree of stereoselectivity of analgesic action

57
Q

Physiochemical properties of Morphine

A

Contains both an acidic phenolic group and a basic tertiary amine function

Primarily treated as a basic OMA

Readily forms salts, and exists as a cation of physiologic pH

58
Q
A

Codeine

etherification reduces narcotic analgesic activity

mild analgesia and antitussive

potency = 0.15

Most analgesic effect in drug due to bodies ability to convert codeine to morphine

59
Q
A

Heroin

When codeine undergoes bioREVERSIBLE derivation of the C-3 OH by acylation, heroin is formed

Potency of 2, more lipophilic, activates self reward

pirmarily metabolized by hydrolysis to MAM (active)

MAM may be further metabolized via esterases into morphine which can then be gluc and eliminated

60
Q
A

hydromorphone

potency = 5

6 - OH and 7,8 double bond of morphine are unessential for analgesic activity

61
Q
A

hydrocodone

potency = 0.7

6 - OH and 7,8 double bond of morphine are unessential for analgesic activity

62
Q
A

Dihydrocodeine

potency = 0.3

6 - OH and 7,8 double bond of morphine are unessential for analgesic activity

63
Q
A

oxymorphone

potency = 10

addition of C-14 OH to hydromorphone and hydrocodone structure leads to inc in potency

64
Q
A

Oxycodone

potency = 1 (equal to morphine)

addition of C-14 OH to hydromorphone and hydrocodone structure leads to inc in potency

65
Q

Tertiary amine function of morphine of position 17

A

Replacement of N-CH3 by NH reduces analgesic activity to 1/8th that of morphine by reducing BBB translocation due to increase polarity

Substitution with larger alkyl groups reduces activity and substitution with aralkyl groups significantly increase analgesic activity

Quaternary methiodide analogue of morhpine is inactive by injection

66
Q

Morphine Metabolism

A

Starting with codeine undergoing CYP 2D6 OOD and then gluc which is inactive and can undergo enterohepatic recycling

After OOD, structure can also undergo OND which results in secondary amine which is more basic. This structure has 1/8th activity of codeine

After OOD, structure can also undergo glucuronidation of the C-OH 6 on ring C which forms an active metabolite that can still cross BBB. This requires a transport system.

67
Q

Opiate Antagonist

Hav some affinity but no intrinsic activity

A

Replacing N-CH3 with N-CH2-CH=CH2 or N-CH2-cyclopropyl or butyl results in opiate receptor antagonist activity with rentention of some agonist activity.

Some display high analgesic activity with more faavorable ADR including ceiling doses for respoiratory depression, less CV depression, and reduced abuse potential.

Pure Opiate Antagonist use: opiate OD, withdrawal from opiate. Has no analgesia

68
Q
A

Naltrexone

opiate antagonist = mu, kappa, and delta anatgonism

Oral admin, IV admin (if being used in opiate OD)

More potent than naloxone

Used in Opiate OD or Opiate withdrawal

69
Q
A

Naloxone

significant first pass

only admin IV

opiate antagonist = mu, kappa, and delta anatgonism

70
Q
A

Nalmefene

opiate antagonist = mu, kappa, and delta anatgonism

admin IV

longer t 1/2

increase bioavailability because of removed sites of metabolism

used for EtOH dependence

71
Q
A

Methylnaltrexone

opiate antagonist = mu, kappa, and delta anatgonism

No BBB, stays in gut because of quat amine

used for constipation

72
Q
A

Alvimopan

opiate antagonist = mu, kappa, and delta anatgonism

limited absorption because it is a zwitterion

Use: prophylactic treatment in bowel surgery

73
Q
A

Nalbuphine

mixed poiate agonist/antagonist (no ketone at position 6 of ring C)

mu antagonist = ceiling effect for resp depression, decreased addiction potential

kappa agonist = analgesia

some sigma action at higher doses

IV admin

Has same time of onset, duration, and potency as morphine

74
Q
A

Buprenorphine

partial opiate agonist at mu receptor

interacts with NOP receptors

High affinity but low intrinsic activity

20-30 times more potent than morphine

Duration: 4-6 hours due to slow dissociation from opiate receptor. Therefore Naloxone would need to be in a larger dose to treat for OD

Use: maintenance therapy for addicts. Given every three days in a high dose. Often given with Naloxone

The cyclobutyl is the antagonist fxn

the large methyl groups interact with receptors

Metabolism: OND –> active compound and mu agonist –> gluc which is active

75
Q
A

Levorphanol

morphinan derivative of morphine

pure mu agonist and inhibitor of 5HT and NE reuptake

duration: 6-8 hr

5X more potent than morphine as an analgesic and as resp depressant. Therefore less nausea and vomiting is produced. It also has a greater oral/parenteral potency ratio.

decreased metabolism due to lack of OH or ketone which prolongs duration

76
Q
A

Butorphanol

kappa and sigma agonist, mu partial agonist

5X more potent than morphine as an analgesic

Similar onset, duration as morphine

Ceiling effect for resp depression occurs after about twice the usual therapeutic dose.

Low abuse liability

77
Q
A

Dextromethorphan

NOT an opioid

S enantiomer = lack of analgesia

Does have antitussive activity

78
Q
A

Pentazocine

weak mu antagonist, strong kappa agonist, strong sigma agonist

1/6th potency of morphine

usually combined with naloxone

tolerance and abuse do develop

79
Q

analgesiophore for synthetic narcotic analgesics

A

consists of aromatic ring linked to a quat carbon which in turn is connected via a two carbon atom cahin to a tertiary basic amine

Used as alternative for pt with codeine or morphine allergy

80
Q
A

meperidine

Only 4-PP on the US market

duration: 1-3 hr b/c of metabolism

10 X less potenet than morphine

high oral bioavailability producing same degree of analgesia, sedation, and respiratory depression as morphine at similar dose

Analgesia terminated via metabolism

hydrolysis –> OND –> normeperidine formed with anticholinergic properies –> gluc –> excretion of inactive

81
Q
A

Meperidine

82
Q

make sure to look at page 33 for metabolism pathways of this drug

A

Methaodone

pure mu agonist

highly effective after oral admin

longer t 1/2 than morphine. Basic urine pH causes inc to 42 hours

onset of action is longer leading to reduced abuse potential

admin as a racemate, R isome is responsible for activity

Use: maintenance therapy for addicts

Metabolism: 2A4

**levomethadyl acetate

DDI: cyp inhibitors could lead to toxic level

83
Q
A

Fentanyl

lipophilic narcotic analgesic

duration: 1-2 hr due to redistribution

80 X more potent than morphine

significant resp depression

Use: induction and maintenance of inhalation anesthesia

Metabolism: OND –> inactive

84
Q
A

Sufentanil

narcotic analgesic

duration: 30-40 min due to redistribution

7X more potent than morphine

metabolism: OOD –> inactive

85
Q
A

Alfentanil

narcotic analgesic

duration: up to 30 min

slightly less potent than fentanyl

faster onset

pka of nitrogen is 6.5. At physiologic pH drug is unionized so it quickly distributes to CNS

86
Q
A

Remifentanil

narcotic analgesic

duration: 3-10 minutes due to metabolism which includes hydrolysis giving it an onset and duration similar to that of alfentanil. Inactive metabolite

87
Q
A

Tramadol

weak mu agonist

given as a racemate: (+) isomer give mu agonist and 5HT reuptake inhibitor, (-) isomer give NE reuptake inhibitor

not a true pro drug

5HT and NE reuptake inhibitor

centrally acting analgesic rather than opiate

Has addiction potential

metabolism OOD via 2D6 results in M1 metabolite. M1 is 6X more potent than tramadol. M1 is 200X more selective for mu receptors. M1 is 1/35th potency of morphine.

88
Q
A

Tapentadol

mu agonist

18X less potent than morphine

has reduced adition liability

Has metabolism than tramadol because it lacks 2D6 variability issue

inactive gluc, sulfonation

DAD III - Test Two - Dr. Smith (1 decks)

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