Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm II > Analgesics > Flashcards

Analgesics Flashcards

1
Q

where do you find nociceptors?

A

skin, tendons, jts, body organs, meninges

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

how does peripheral neuropathic pn generally present?

A

as burning, sharp, shooting or aching pain and mb associated w/tingling or numbness

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

different approaches to treating nociceptive pn vs chronic neuropathic pn

A

nociceptive pn generally tx w/anti-inflammatories or analgesic meds
neuropathic pn may be tx w/meds that act to influence neurotransmitters in addition to using anti-inflammatories and analgesics

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

what, ultimately, are analgesics? what can narcotics cause? what are opioids?
6 types of narcotic analgesics?

A

analgesics are pain killers
narcotics cause delirium and drowsiness
narcotic analgesics are st referred to as opioids b/c contain opium derivatives
examples: morphine, heroin, codeine, methadone, pethidine, fentanyl

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

what category is heroin?

A

category I - no accepted medical use

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

solubility of heroin?

A

more lipid soluble= more rapid crossing of the BBB, generally produces a much greater sense of euphoria than morphine

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

primary indication for opioids? MOA?

A

have a broad range of effects but primary use is to relieve intense pain and anxiety that follows pain
MOA: bind to specific opioid receptors in order to produce effects that mimic the actions of endogenous neurotransmitters referred to as opiopeptins

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

what are opiopeptins? 2 examples?

A

opioid receptor specific endogenous neurotransmitters

examples: include peptides such as the endorphins and enkephalins

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

MOA of opiate analgesics specifically?

A

opioid receptors are G protein couple receptors and therefore opioids work by inhibiting adenylate cyclase
they are also involved in postsynaptic hyperpolarization and reduce presynaptic Ca2+ influx which overall inhibits neuronal activity = less pain (sensation and perception)

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

5 areas of high density opioid receptors?

A 
brainstem
medial thalamus
spinal cord
hypothalamus
limbic system
also found on peripheral sensory nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

analgesic properties of opiates are primarily mediated by what subclass of receptors?

A

mu receptors

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

enkephalins interact with what receptors where?

A

interact w/the delta receptors peripherally

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

which receptor type tends to be less selective and interacts w/drugs such as phencyclidine (hallucinogen)?

A

sigma receptors: therefore may be responsible for hallucinations and dysphoria often assoc w/opiate use

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

what is the effect of opioids and opioid agonists on nerve cells?

A

cause hyperpolarizaiton resulting in inhibition of further nerve firing
also opioid receptor stimulation causes presynaptic inhibition of the release of various pain mediators such as substance P

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

4 highly used opiate/narcotic analgesics?

A

morphine sulfate/MS contin
fentanyl/duragesic
codeine/T#3, T#4
tramadol/ultram

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

class of morphine/MS contin? indications? MOA?

A

class: opioid analgesic
indications: pain relief, acute MI, peripheral vasodilator
MOA: potent opioid agonist, high affinity for mu receptors; relieves pn both by raising pn threshold at brainstem, thalamic and spinal cord level as well as altering brain’s perception of pain

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

does morphine act on the peripheral or central nervous system?

A

central nervous system

high potential for addiction and tolerance (physical and psychological)

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

how to rx morphine/MS contin? how does tolerance work?

A

can give PO, PR, IM, IV; duration of action varies by route, significant 1st pass w/oral
high risk of developing tolerance
tolerance is generally dt increased breakdown of drug by up-regulation of -P450 system in the liver or by down-regulation of # of receptor sites in the brain

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

SEs of morphine?

A

respiratory depression by reducing sensitivity of respiratory center to CO2 (MC cause of death related to morphine), miosis, itching, N/V dt stimulation of chemoreceptor center in the brain, constipation dt reduced GI SM motility, paralytic ileus

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

class of fentanyl/duragesic? indications? MOA? how to rx? onset?

A

class: opioid analgesic
indications: pn relief, anesthesia
MOA: similar to morphine w/80x analgesic property of morphine, used for anesthesia and intractable pn
rx IV, transdermal patch, buccal lozenge, film, sublingual spray and lollipop form
onset of action w/in mins
single IM doses have DOA of 1-2 hrs, single IV doses last 30 mins-1 hr

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

SEs of fentanyl/duragesic? what category?

A

respiratory depression w/life threatening hypoventilation, pts using concomitant CYP450 inhibitors may result in fatal blood levels, N/V, constipation, paralytic ileus, highly addictive
category C drug

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

what is the only way to rx and receive transmucosal immediate release fentanyl products?

A

pt and doc have to be a part of the TIRF ACCESS program

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

effects of EtOH, grapefruit juice and St. John’s wort on fentanyl/duragesic?

A

EtOH may increase CNS depression
grapefruit juice increases fentanyl concentrations in the blood
st. John’s wort can decrease fentanyl levels

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

what is buprenorphine? what can it be used to tx?

A

semi-synthetic opioid that is used to tx opioid addiction in higher doses
can be used to control moderate acute pain in non-opioid tolerant individuals in lower doses and to control moderate chronic pain in dosages ranging from 20-70 millig/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
class of codeine/T#3, T#4? indications? MOA? how to rx?
class: opioid analgesic indications: pn relief, antitussive MOA: opioid agonist, converted to morphine in the body but mg per mg, codeine is a much weaker analgesic then morphine rx via PO, IV, IM, SQ- lower abuse potential than more potent narcotic analgesics
26
dosing form of codeine/tyelenol #3, #4? DOA? schedule?
PO, mc syrup form as an antitussive DOA 4-6 hrs DEA schedule II drug
27
SEs of codeine/T#3, T#4? do not give to what group b/c of what?
sedation, constipation, itching, increased potential for exaggerated response in certain individuals at risk dt genetic variability do not give to those who have just received a tonsillectomy and/or adenoidectomy as there was an increased occurrence of death w/this pattern dt being ultra-rapid metabolizers of codeine dt CYP2D6 polymorphism
28
MOA of tramadol/ultram?indications for tramadol/ultram? what receptor does it affect, what neurotransmitter? SEs?
MOA: centrally-acting analgesic via the mu opioid receptor and affecting re-uptake at the noradrenergic and serotonergic systems indications: to tx moderate to severe pn, suggested that it may be effective for alleviating sxs of depression, anxiety and phobias SEs: respiratory distress, drowsiness, withdrawal-like sxs if weaned off too quickly or abrupt discont
29
5 acetaminophen-containing narcotic analgesics?
codeine/acetaminophen -T#3, T#4 hydrocodone/acetaminophen - vicodin, lortab oxycodone/acetaminophen- percocet, roxicet propoxyphene/acetaminophen- darvocet tramadol/acetaminophen - ultraset
30
3 NSAID-containing narcotic analgesics?
oxycodone/aspirin - percodan oxydodone/ibuprofen - combunox hydrocodone/ibuprofen - vicoprofen
31
rx that is an opioid about equal to morphine but induces less euphoria and has a longer duration of action?
methadone
32
application of methadone?
used in controlled withdrawal of heroin & morphine in addicted pts
33
3 narcotic antagonists?
naloxone naltrexone nalorphine
34
MOA of naltrexone? primarily used for what?
opioid receptor antagonist | primarily used in management of alcohol dependence and opioid dependence
35
naloxone is primarily used for what?
emergent tx of narcotic overdose
36
what 2 opioid receptors does nalorphine act on?
mu and kappa | antagonists effects at mu receptor, agonistic effects at kappa receptor
37
use of nalorphine?
reverse narcotic overdose
38
class of naloxone/narcan? indications? MOA? how to deliver?
class: opioid antagonist indications: opioid overdose, naloxone is used to reverse the coma and respiratory depression of opioid overdose MOA: opioid antagonists bind w/high affinity to opioid receptors but do not activate the receptor mediated response give via IV, PO, IV; replaces all receptor bound opioids w/in 30 seconds
39
what is the dextro-isomer of codeine? use? SEs?
dextromethorphan used as an antitussive and commonly used in OTC cough medications SEs: little to no analgesic, sedative or GI effects
40
3 effects of aspirin? how does it produce each effect?
anti-inflammatory: decreases prostaglandin synthesis locally anti-pyretic: with prostaglandin production decreased, immune fxn is decreased as pgs usu "call" in the immune system anti-coagulant: also b/c pgs are decreased and the immune system is decreased, by products of WBCs like histamine is decreased leading to antagonization of clotting
41
COX1 inhibitors inhibit what end products? each are responsible for the production of what?
PGs 1: stomach mucosa | PGs 2: platelet stickiness
42
COX2 inhibitors inhibit what end products? each are responsible for what?
PGs 3: pain | PGs 4: inflammation
43
what will a COX inhibitor inhibit?
PGs 1-4
44
what are prostaglandins? other name?
unsaturated FA derivatives containing 20 carbons that include a cyclic ring compound eicosanoids
45
3 other eicosanoids?
prostaglandins thromboxanes prostacyclins
46
precursor to all eicosanoids?
arachadonic acid via the cycloxygenase pathway
47
prostaglandins promote what?
``` inflammation pain fever clotting fxn of platelets protect the lining of the stomach ```
48
3 NSAIDs (COX1 & 2 inhibitors)?
aspirin ibuprofin acetaminophen
49
COX 2 inhibitors?
celecoxib/celebrex
50
class of aspirin? indications? MOA?
class: NSAID indications: inflammation, pain, fever MOA: irreversible inhibition of COX1 and COX2 enzymes; anti-inflammatory and analgesic effect largely due to blockade of prostaglandin synthesis at target tissues; anti-pyretic effects due to blockade of prostaglandin synthesis at thermoregulatory centers in the hypothalamus
51
in regards to aspirins effects on prostaglandins what does PG E2 do?
thought to sensitize nerve endings to histamines, bradykinins and other inflammatory mediators
52
how to administer aspirin?
PO, PR, readily absorbed, metabolized by liver, excreted in urine
53
major SEs of aspirin
GI irritation, PUD, N/V, increased risk of bleeding, renal insufficiency, increased risk of Reye's syndrome in kids, salicylism
54
what is salicylism?
dizziness, tinnitus, hyperventilation, mental status changes, potential for coma and death
55
tx of salicylism?
IV rehydration, alkalinization of urine and dialysis if renal insufficiency occurs
56
class of ibuprofen? indications? MOA? how to administer?
class: NSAID indications: inflammation, pain, fever MOA: reversible inhibition of COX1 and COX2 enzymes anti-inflammatory and analgesic effect largely dt blockade of PG synthesis at target tissues administered PO, PR, no increased risk for Reye's syndrome
57
class of celecoxib/celebrex? indications? MOA? how to deliver? SEs? effects on GI? effects on platelets?
class: NSAID indications: inflammation, pain, tx of adenomatous polyps MOA: reversible, selective COX2 inhibtion deliver PO, anti-inflam effects w/minimal irritation of GI tract, less GI bleeding and no inhibition of platelet aggregation SEs: unclear if definite increased risk for CVS
58
what did use of rofecoxib result in?
CV events (MI, stroke)
59
class of acetaminophen? indications? MOA? how to deliver? Reye's? COX inhibitor? what can it cause to be deposited and result in?
class: NSAID indications: pain, fever MOA: not fully understood, weak peripheral blockade of PG synthesis w/stronger blockade of PG synthesis in hypothalamus deliver PO, PR, readily absorbed no increased risk of GI bleeding no increased risk for development of Reye's syndrome not generally thought of as a COX inhibitor but may be selective COX3 inhibitor abn accumulation of fat in liver and other organs, increased P in brain; unless diagnosed and treated successfully death is common, often w/in a few days
60
SEs of acetaminophen? what to never mix with? PG category?
overdose is greater than 7 g/24 hrs when taken with EtOH can lead to coma and death NEVER take with EtOH can lead to liver failure, come and death NEVER mix EtOH and tylenol PG category B
61
why can acteaminophen ingestion result in toxicity?
if overdosed on can result in normal conjugative pathways being overwhelmed and therefore actetaminophen can't be processed
62
when acetaminophen is metabolized what is the resulting metabolite?
N-acetyl-p-benzoquinone-imine (NAPQI)
63
what happens with excessive NAPQI and inadequate glutathione?
NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes which results in liver and hepatocellular death and necrosis
64
4 stages of acetaminophen toxicity?
1: 12 - 24 hrs = N/V 2: 24 - 48 hrs = may be clinically improved but liver fxn tests may reveal rising AST, ALT, bilirubin levels 3: 72-96 hrs = peak hepatoxicity, AST may exceed 20000 4: beyond 96 hrs = recovery, need for liver transplant or death
65
treatment of overdose of acetaminophen toxicity?
removal of any drug remaining in stomach by lavage or emesis w/ipecac
66
antidote of acteaminophen?
NAC, should be administered as early as possible, w/in 8 hrs preferably
67
NAC is a precursor to what?
precursor to glutathione and increases glutathione availability to bind NAPQI
68
actions of NAC?
enhances sulfate conjugation of any unmetabolized APAP fxns also as anti-inflammatory and antioxidant, increases local nitric oxide concentrations and this microcirculatory blood flow enhances local O2 delivery to peripheral tissue
69
major use of acteylcysteine?
mainly as a mucolytic agent and in the management of acetaminophen overdose
70
MOA of acetylcysteine?
acts to augment glutathione reserves of body and w/glutathione, directly binds to toxic metabolites which serves to protects hepatocytes from NAPQI toxicity
71
how is acetylcysteine usually used?
as a mucolytic agent or as management of acetaminophen overdose
72
MOA of acteylcysteine?
acts to augment the glutathione reserves in body and with glutathione, directly binds to toxic metabolites which serve to protect hepatocytes from NAPQI toxicity
73
drug with increased risk of GI complications?
ketorolac first injectable NSAID used in ER as narcotic drug for narcotic drug seekers "until they got wise"

Pharm II (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions