Brainscape's Knowledge GenomeTM

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


See full index

Therapeutics > Exam 5 lecture 4 > Flashcards

Exam 5 lecture 4 Flashcards

1
Q

Therapeutic applications of NSAIDs

A

Analgesic
Anti-inflammatory
Antipyretic
Antiplatelet effect (aspirin)

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

What are the 3 phases of inflammatory response

A

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

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

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

What is the CORE function of NSAIDs

A

Inhibit COX enzymes

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

What does PLA2 create to make a substrate of COX

A

arachidonic acid

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

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

How does Aspirin act differently from other NSAIDs

A

Irreversibly inhibits COX enzyme. Other NSAIDs are competitive

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

therapeutic uses of aspirin

A

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

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

What does COX 2 form in the body

A

forms platelets and acts on nociceptors

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

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

How to increase excretion of Aspirin from urine

A

Increased excretion with increased urinary PH (IV bicarb)

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

Clinical features of salicylate poisoning

A

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

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

How to treat salicylate/aspirin poisoning

A

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

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

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

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

A

ibuprofen and naproxen

Reversible COX inhibitors

Ibuprofen-2 hrs
Naproxen- 14 hrs

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

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

When is meloxican cox 2 selective

A

At low doses

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

Piroxicam half life

A

57 hours

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

Adverse effects of NSAIDs

A

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

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

Effects of NSAIDs on renal function

A

increased sodium reabsorption leading to edema

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

Effect of NSAIDs on inhibition of platelet aggregation

A

Increased risk of bleeding

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

Effect of NSAIDs on uterine motility

A

Therapeutically used to delay pre term birth

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

NSAID effect on GI

A

Ulceration

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

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

Therapeutic use of Acetaminophen

A

analgesic and antipyretic

limited antiinflammatory activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
advantages of acetaminophen compared to NSAIDs
No GI toxicity No effect on platelet aggregation
26
Disadvantage of acetaminophen compared to NSAIDs
Hepatic necrosis
27
adverse effects of acetaminophen
Renal toxicity> NSAIDs and Aspirin Dose dependent hepatic necrosis
28
What is hepatic necrosis caused by?
increases in toxic acetaminophen metabolites (NAPQI)
29
Why were COX 2 selective inhibitors withdrawn
Chance of blood clots, stroke and heart attacks
30
Black box warning for celecoxib
CV events
31
What are some COX2 selective NSAIDs
Celecoxib, valdecoxib, rofecoxib, Etoricoxib, Lumiracoxib
32
What are some contraindications with NSAIDs
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
Local anesthetics are ______ channel blockers
Na
34
What are some Na channel blockers
Lidocaine- local analgesia Bupivacaine- longer lasting Benzocaine- Esther have HIGH ALLERGY RISK
35
What is NA 1.7 used for?
Severe Neuropathic Pain- GOF mutation congenital insensitivity to pain- LOF mutation
36
What are some psychiatric drugs that are also Na channel blockers (anticonvulsants)
Lamotrigine Carbamazepine
37
What is a TCA that is also Na channel blocker
Amptriptyline
38
What are some sodium channel blockers with SNRI functionality
Duloxetine Venlafaxine Milnacipran
39
Why are SNRIs used for Na channel blocking
SNRIs increase norepinephrine levels and act on alpha 2 adrenergic receptors in spinal cord
40
What are some calcium channel blockers that can be used as analgesics
Gabapentin and pregabalin
41
How do gabapentin and pregabalin act as analgesics
α2 δ – Cav1, 2 selective- blocks calcium channel Not metabolized- not protein bound no drug-drug interactions t1/2 4-8 hrs
42
What are the 3 categories of drugs
stinulants Depressants Psychedelics
43
Explain the DEA classification of controlled substances
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
Name drugs classified as depressants
opioids alcohol cannabis GHB inhalants
45
Name drugs classified as stimulants
cocaine amphetamine ecstasy bathsalts meth
46
Name drugs classified as psychadelics
PCP psylocibin LSD Mescaline ketamine
47
Substances of abuse that act directly on GPCR
Opioids (heroine, prescription meds) LSD, mushrooms (psilocybin) Marijuana, K2, Spice GHB Caffeine
48
Substances that act indiretly on GPCR
Cocaine Amphetamine MDMA AlcoholW
49
What transporter is respinsible for cocaine and Amphetamine
Dopamine
50
What are sibstances that act directly on ion channels
Nicotine BZDs and BBTs PCP, Ketamine
51
What are the ions used in nicotine abuse
Ach Nicotine is an agonist
52
What ion channels do PCP and Ketamine act on?
NMDA receptor They are antagonists to this channel
53
What ion channel to BBT and BZDs act on?
GABA receptors They are positive allosteric modulators to this receptor
54
Why are these drugs so addicitve? How does dopamine play a role
VTA is a source of dopamine neurons. It has connections with nucleus accumbens and reinforcement occurs here.
55
True or false stimulants, depressants and psychadelics all act on mesolimbic system
True
56
What is the dopamine hypothesis of addiction
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
What are the limits of dopamine hypothesis of additction.
Dopamine is not required for reward learning. Dopamine does not encode liking, but making reward predictions
58
What is the glutamate hypothesis of addiction
Glutamate can increase dopamine activity in nucleus accumbens. Glutamate projects to VTA Dopamine controls glutamate activity in amygdala
59
How do rewarding substances effect glutamatergic AMPA receptors
Increases them
60
What is LTP
Long term potentiation. Rewarding substances have LTP and will have persistent increase in synaotic strength following exposure
61
Explain the persistent memory of addiction
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
Define drug abuse vs misuse
Abuse- Use of drug for non therapeutic purpose Misuse- Inappropriate/illegal/excessive use of prescription or non prescription drug
63
When a patient presents, Be able to know whether they present with mild, moderate or severe symptoms.
Mild- 2-3 Moderate- 4-5 Severe- >6
64
What are the criteria for substance use disorder
-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
physical vs psychological dependence
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
Withdrawals of alcohol or tranquilizers
Grand mal seizures and delirium
67
What are some physical withdrawal symptoms
Goose bumps- cold turkey muscle spasms tremors N/V
68
What are dangerous withdrawal symptoms? What are they usually associated with
Alcohol and tranquilizers Grand mal seizures and delirium tremens
69
Explain the drug reward and its relation to positive and negative reinforcement
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
describe therapeutic use, recreational use and self medication
Therapeutic- negative reinforcement-->positive- negative recreational- positive reinforcement--> negative reinforcement Self- negative reinforcement
71
What are some physiological responses that may lead to death
Respiratory depression Cardiac arrythmia fatal seizure
72
What increases the risk of a depressant drug
Taking it with a stimulant Increases chances of ODing
73

Therapeutics (38 decks)

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