Exam 5 lecture 4 Flashcards

1
Q

Therapeutic applications of NSAIDs

A

Analgesic
Anti-inflammatory
Antipyretic
Antiplatelet effect (aspirin)

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2
Q

What are the 3 phases of inflammatory response

A

acute- vasodilation (increased permeability)
subacute- Infiltration of neutrophils
Chronic- proliferation

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3
Q

Recruitment of what contributes to inflammatory pain? Why?

A

Recruitment of Eicosanoids.

They cause arachidonic acid increase
(injury increase= arachidonic acid increase)

They also release cytokines, prostaglandins and thromboxanes which contribute to pain)

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4
Q

What is the CORE function of NSAIDs

A

Inhibit COX enzymes

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5
Q

What does PLA2 create to make a substrate of COX

A

arachidonic acid

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6
Q

What does COX-1 do to arachidonic acid?

A

Forms TXA2- platelet aggregation also has prostaglandin function to create mucus to protect stomach lining.

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7
Q

How does Aspirin act differently from other NSAIDs

A

Irreversibly inhibits COX enzyme. Other NSAIDs are competitive

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8
Q

therapeutic uses of aspirin

A

frequently used as prophylaxis for anticoagulation. No tolearnce to analgesia effect. Causes Reyes syndrome in children

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9
Q

What does COX 2 form in the body

A

forms platelets and acts on nociceptors

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10
Q

Absorption and half life of aspirin

A

t 1/2 is 15 minutes (salicylate half life is 6-20 hours)

Half life is short but duration is long because it is irreversible

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11
Q

How to increase excretion of Aspirin from urine

A

Increased excretion with increased urinary PH (IV bicarb)

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12
Q

Clinical features of salicylate poisoning

A

Mild- Vertigo, tinnitus
Moderate-severe- CNS effects- Respiratory alkilosis, metabolic acidosis, N/V, sweating, delirium, coma

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13
Q

How to treat salicylate/aspirin poisoning

A

reduce salicylate dose and use dextrose or sodium bicarb to increase urinary PH

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14
Q

What are the different classes of NSAID

A

salicylate- aspirin
aryl propinoic acid- Ibuprofen, naproxen
Aryl Acetic acid- Indomethacin, diclofenac, ketorolac
Enolic acid- piroxicam, meloxicam

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15
Q

What are the arylpropinoic acids drugs? MOA? t1/2

A

ibuprofen and naproxen

Reversible COX inhibitors

Ibuprofen-2 hrs
Naproxen- 14 hrs

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16
Q

Which arylacetic acid derivative has increased risk for peptic ulcer? Which is one of the most potent reversible inhibitor of PG biosynthesis? Which is the less toxic derivative for indomethacin? Which one has a high severity and incidence of side effects?

A

increased risk for peptic ulcer- dicofenac
Most potent reversible inhibitor- Indomethacin
Less toxic derivative of indomethacin- sulindac
Which one has a high severity and incidence of side effects- Indomethacin

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17
Q

When is meloxican cox 2 selective

A

At low doses

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18
Q

Piroxicam half life

A

57 hours

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19
Q

Adverse effects of NSAIDs

A

Renal function
Transient inhibition of platelet aggregation
Inhibition of uterine motility
GI distress/ulceration

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20
Q

Effects of NSAIDs on renal function

A

increased sodium reabsorption leading to edema

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21
Q

Effect of NSAIDs on inhibition of platelet aggregation

A

Increased risk of bleeding

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22
Q

Effect of NSAIDs on uterine motility

A

Therapeutically used to delay pre term birth

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23
Q

NSAID effect on GI

A

Ulceration

risk increases with long term use and less risk than salicylate NSAIDs

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24
Q

Therapeutic use of Acetaminophen

A

analgesic and antipyretic

limited antiinflammatory activity

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25
Q

advantages of acetaminophen compared to NSAIDs

A

No GI toxicity
No effect on platelet aggregation

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26
Q

Disadvantage of acetaminophen compared to NSAIDs

A

Hepatic necrosis

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27
Q

adverse effects of acetaminophen

A

Renal toxicity> NSAIDs and Aspirin
Dose dependent hepatic necrosis

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28
Q

What is hepatic necrosis caused by?

A

increases in toxic acetaminophen metabolites (NAPQI)

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29
Q

Why were COX 2 selective inhibitors withdrawn

A

Chance of blood clots, stroke and heart attacks

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30
Q

Black box warning for celecoxib

A

CV events

31
Q

What are some COX2 selective NSAIDs

A

Celecoxib, valdecoxib, rofecoxib, Etoricoxib, Lumiracoxib

32
Q

What are some contraindications with NSAIDs

A

Avoid in CKD, peptic ulcer disease or history of GI bleed
all NSAIDs carry a CV risk
All NSAIDs when used in high doses can INTERFERE WITH BONE HEALING
NSAIDs cause ASTHMA EXACERBATIONS

33
Q

Local anesthetics are ______ channel blockers

A

Na

34
Q

What are some Na channel blockers

A

Lidocaine- local analgesia
Bupivacaine- longer lasting
Benzocaine- Esther have HIGH ALLERGY RISK

35
Q

What is NA 1.7 used for?

A

Severe Neuropathic Pain- GOF mutation
congenital insensitivity to pain- LOF mutation

36
Q

What are some psychiatric drugs that are also Na channel blockers (anticonvulsants)

A

Lamotrigine
Carbamazepine

37
Q

What is a TCA that is also Na channel blocker

A

Amptriptyline

38
Q

What are some sodium channel blockers with SNRI functionality

A

Duloxetine
Venlafaxine
Milnacipran

39
Q

Why are SNRIs used for Na channel blocking

A

SNRIs increase norepinephrine levels and act on alpha 2 adrenergic receptors in spinal cord

40
Q

What are some calcium channel blockers that can be used as analgesics

A

Gabapentin and pregabalin

41
Q

How do gabapentin and pregabalin act as analgesics

A

α2 δ – Cav1, 2 selective- blocks calcium channel
Not metabolized- not protein bound
no drug-drug interactions
t1/2 4-8 hrs

42
Q

What are the 3 categories of drugs

A

stinulants
Depressants
Psychedelics

43
Q

Explain the DEA classification of controlled substances

A

schedule I- no medical use, illegal (marijuana, THC, LSD)
schedule II- medical use, high abuse potential (cocaine, PCP)
Schedule III- medical use, moderate abuse (Marinol- THC capsule)
Schedule IV- medical use, low abuse potential

44
Q

Name drugs classified as depressants

A

opioids
alcohol
cannabis
GHB
inhalants

45
Q

Name drugs classified as stimulants

A

cocaine
amphetamine
ecstasy
bathsalts
meth

46
Q

Name drugs classified as psychadelics

A

PCP
psylocibin
LSD
Mescaline
ketamine

47
Q

Substances of abuse that act directly on GPCR

A

Opioids (heroine, prescription meds)
LSD, mushrooms (psilocybin)
Marijuana, K2, Spice
GHB
Caffeine

48
Q

Substances that act indiretly on GPCR

A

Cocaine
Amphetamine
MDMA
AlcoholW

49
Q

What transporter is respinsible for cocaine and Amphetamine

A

Dopamine

50
Q

What are sibstances that act directly on ion channels

A

Nicotine
BZDs and BBTs
PCP, Ketamine

51
Q

What are the ions used in nicotine abuse

A

Ach

Nicotine is an agonist

52
Q

What ion channels do PCP and Ketamine act on?

A

NMDA receptor

They are antagonists to this channel

53
Q

What ion channel to BBT and BZDs act on?

A

GABA receptors

They are positive allosteric modulators to this receptor

54
Q

Why are these drugs so addicitve? How does dopamine play a role

A

VTA is a source of dopamine neurons. It has connections with nucleus accumbens and reinforcement occurs here.

55
Q

True or false stimulants, depressants and psychadelics all act on mesolimbic system

A

True

56
Q

What is the dopamine hypothesis of addiction

A

Reward prediction is not encoded in liking.

Dopamine is important for assigning value to reward prediction error.

value provides drug with an incentive salience

57
Q

What are the limits of dopamine hypothesis of additction.

A

Dopamine is not required for reward learning.

Dopamine does not encode liking, but making reward predictions

58
Q

What is the glutamate hypothesis of addiction

A

Glutamate can increase dopamine activity in nucleus accumbens.

Glutamate projects to VTA

Dopamine controls glutamate activity in amygdala

59
Q

How do rewarding substances effect glutamatergic AMPA receptors

A

Increases them

60
Q

What is LTP

A

Long term potentiation. Rewarding substances have LTP and will have persistent increase in synaotic strength following exposure

61
Q

Explain the persistent memory of addiction

A

Memory formation after drug abuse, there is still presence of drug cue/memory after abstinence. The moment there is re exposure the memory comes back. That is why relapse is so common.

62
Q

Define drug abuse vs misuse

A

Abuse- Use of drug for non therapeutic purpose
Misuse- Inappropriate/illegal/excessive use of prescription or non prescription drug

63
Q

When a patient presents, Be able to know whether they present with mild, moderate or severe symptoms.

A

Mild- 2-3
Moderate- 4-5
Severe- >6

64
Q

What are the criteria for substance use disorder

A

-Taking the substance larger or for longer than meant for
-Unable to stop
-spending a lot of time using/recovering from using (preoccupied)
-Cravings and Urges to use
-distracted from home/work/school
- continuing to use when it causes problems in relationship
-giving up important soccial, recreational activities
-Using even when it puts you in danger
-continuing to use even against better judgement
-Development of withdrawal symptoms

65
Q

physical vs psychological dependence

A

physical- body needs more drug- tolerance, bpdy withdraws
(alcohol and tranquilizers have dangerous withdrawal sx)

psychological- mental urge to take drug, compulsive need/craving even in absence of withdrawal

66
Q

Withdrawals of alcohol or tranquilizers

A

Grand mal seizures and delirium

67
Q

What are some physical withdrawal symptoms

A

Goose bumps- cold turkey
muscle spasms
tremors
N/V

68
Q

What are dangerous withdrawal symptoms? What are they usually associated with

A

Alcohol and tranquilizers

Grand mal seizures and delirium tremens

69
Q

Explain the drug reward and its relation to positive and negative reinforcement

A

Drug is rewarding when person feels pleasure/satisfaction

This creates positive reinforcement
This is the impulsive stage (pleasure, abstinence, craving, binge, pleasure cycyle)

On the other hand

Negative reinforcements rrward by escaping negative painful stimulus or event (not same as punishment). This is the compulsive stage (relief, negative ffect, craving, intoxication, relief) cycle

70
Q

describe therapeutic use, recreational use and self medication

A

Therapeutic- negative reinforcement–>positive- negative
recreational- positive reinforcement–> negative reinforcement
Self- negative reinforcement

71
Q

What are some physiological responses that may lead to death

A

Respiratory depression
Cardiac arrythmia
fatal seizure

72
Q

What increases the risk of a depressant drug

A

Taking it with a stimulant

Increases chances of ODing

73
Q
A