Brainscape's Knowledge GenomeTM

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


See full index

pharmacology > antiflamm, antipyretic,analgesics > Flashcards

antiflamm, antipyretic,analgesics Flashcards

1
Q

what is the physiologic process of inflammation?

A

Cyclooxygenase allows prostaglandin formation which modulates inflammation

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

what is the physiologic process of pain?

A

Prostaglandin E2 (PGE2) is thought to sensitize nerve endings to the action of bradykinin, histamine and other mediators release by the inflammatory process

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

what is the physiologic process of fever?

A

Anterior hypothalamic thermoregulatory center becomes elevated
Infection triggers WBC leading to cytokine production and subsequent PGE2 production

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

what are 3 of the most common “non-selective” (by FDA standards) cox inhibitors?

A

Diclofenac (Voltaren)*
Ibuprofen (Motrin, Advil)*
Naproxen (Naprosyn, Aleve)*

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

what are the 2 nonacetylated salicylates?

A 
Magnesium salicylate ( Doans Pills)
Salicylsalicylic Acid (Salsalate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the 2 Cox-2 selective inhibitors?

A

Celecoxib (Celebrex)*

Meloxicam (Mobic)*

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

where are the 3 major ADRs of NSAIDs?

A

GI
CV
Renal dysfunction

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

what are 3 less common but dangerous ADRs of NSAIDs?

A

Allergies
Antiplatelet effects
CNS

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

2 ADRs of Cox1 inhibition? which drugs do this?

A

GI mucosa… peptic ulcer and GI bleeding

NSAIDS + ASA

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

3 ADRs of Cox 1+2 inhibition? which drugs do this?

A

kidney…
1. Na+ and H2O retention
2. hypertension
3. hemodynamic acute kidney injury
NSAIDs

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

what are 2 ADRs for when there is more Cox-2 inhibition than Cox-1 . which drugs do this?

A

cardiovascular…
MI and stroke
NSAIDS
(ASA does the opposite, irreversibly inhibits Cox 1)

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

how does the inhibition of Cox1 cause peptic ulcers and GI bleeding?

A

inhibits PGE2 (prostoglandin) which usually serves for gastric protection (increased mucus secretion, increase HCO3, increase mucus flow)

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

how does the inhibition of Cox1 and Cox2 cause kidney issues?

A

inhibits PGE2 (prostoglandin) and PGI2 (prostacyclin) which together …

  • vasodilate afferent arteriole (increase GFR)
  • increase Na+ and H2O secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does the inhibition of Cox2 >Cox1 cause cardiovascular issues?

A

inhibits PGI2 (prostacyclin) and TXA2 (thromboxane) which together…

  • vascular: Cox 2 and PGI2: vasodilates and inhibits platelet aggregation
  • platelets: Cox1 and TXA2: vasoconstriction and platelet aggregation

when Cox2 inhibition is increased, you get more vasoconstriction, Plts aggregating… leads to stroke and MI …

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

what irreversibly inhibits platelet Cox 1? what does this mean?

A

low dose ASA

-it inhibits vasoconstriction and plt aggregation

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

to avoid dyspepsia and diarrhea with NSAIDS, what do they recommend?

A

take them with food or milk

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

can taking with food/milk help NSAID-caused GI bleeding and ulcer ?

A

NO

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

can you hae a GI bleed/ulcer without symptoms?

A

YES (poor coorelation between ulcers/bleed and symptoms)

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

how can you prevent ulcers with NSAIDs?

A

take NSAID with PPI or misoprostol.

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

what is ketolorac (toradol) used for?

A

analgesia (cox 1) : moderate to severe pain. good for when you want to avoid narcotics (i.e. drug addict or fear of respiratory depression or poor metabolizer )

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

which Cox pathway is targets for analgesia, which for inflammation?

A

Cox 1- analgesia

cox 2- inflammation

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

what are the dosing limits for ketolorac (toradol)?

why are there these limits?

A

IM loading dose then…

  • max per day: 40mg
  • max days in a row: 5 days
  • max day-period: 20days
  • risk of ulcers-GI bleed increases!!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

which cox pathway is “cardioprotective”? what does this have to do with ASA?

A

cox 2- vasodilates and prevents plt aggregation

- ASA is considered “cardioprotective”, it turns off Cox 1 and allows for Cox 2

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

NSAIDs elevate BP on average __ - ___ mmHg above pt’s baseline

A

8-10 mmHg

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

what is the boxed warning on all NSAIDs?

why is this?

A

May increase risk of serious cardiovascular thrombotic events, myocardial infarction (MI), and stroke, which can be fatal.
(they upset the balance between Cox 1 and Cox 2)

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

NSAID-associated heart failure is thought to be due to increased _____ _______ _______ and reduced _____ _______ caused by prostaglandin inhibition

A

increased peripheral vascular resistance

reduced renal perfusion

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

Cox 2 inhibition by NSAIDs poses more of a risk for patients with CVD or CVD risk:

  1. increased risk of death or repeat attack within ___ years.
  2. ___% of pts who used an NSAID post-MI died within the 1st year compared to those that didnt.
A

5 years

20% died within the 1st year

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

what are the 4 agents with high cox2 selectivity? (maybe weeds)

A

Celecoxib
DICLOFENAC
Etodolac
MELOXICAM(“preferential” selective)

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

high cox 2 selectives have greater ____ risk but lesser ___ risk

A

greater CV risk

less GI risk

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

what are the 5 agents with moderate cox2 selectivity? (maybe weeds)

A 
Diflunisal
IBUPROFEN 
Nabumetone
Piroxicam
Sulindac
31
Q

what agents have low Cox-2 selectivity?

A 
Flurbiprofen
Indomethacin
Ketoprofen
Ketorolac
NAPROXEN 
Oxaprozin
Tolmentin
32
Q

what is our only non-selective Cox 2 inhibitor (aka only inhibits Cox 1)? this has increased _____ risk but decreased ______ risks

A

ASA (aspirin)

  • increased GI
  • decreased CV
33
Q

which drug has sulfa in it? (look at for sulfa allergy)

A

celecoxib

34
Q

which of the highly selective Cox 2 inhibitors inhibits Cox 2 more than Cox 1 but not enough to be deemed a “COX2selective” by the FDA?

A

Meloxicam

35
Q

why is meloxciam maybe a good option for some?

A

its a highly selective Cox 2 inhibitor

SO….if they have NO CVD risk, better tolerated (Less GI effects) than ibuprofen or naproxen

36
Q

how can NSAIDs cause acute kidney injury (AKI)?

A

Prostaglandins maintain glomerular pressure by causing vasodilation of afferent arteriole
NSAIDs inhibit prostaglandins decreasing perfusion, leading to afferent arteriole constriction and reduced glomerular blood flow

37
Q

what are the risk factors for NSAID induced AKIs? (maybe weeds)

A

Preexisting kidney disease, systemic lupus (inflamm Dz), high renin activity (CHF, hepatic disease), diuretic therapy, CAD, and advanced age

38
Q

pts with NSAID-induced AKI have LOW …. and HIGH ….

A

LOW: urinary volume and Na+, GFR and bloodflow
HIGH: SCr, BUN, K+

39
Q

do NSAIDS normally cause increased Cr?

A

NO! not part of how drug works so if increased Cr occurs immediately stop the drug!

40
Q

txt for NSAID-induced AKI? is the recovery fast or slow?

A

Stop drug, hydrate & support

Usually rapid recovery

41
Q

what is our main concern with allergies to NSAIDS?

A

Angioedema: tongue/lips swelling, hard to control.

*if it happens with one NSAID will likely happen with another! avoid ALL NSAIDS

42
Q

those with _____ and ______ can get increased asthmatic symptoms when taking ASA & NSAIDs. how does this happen?

A

nasal polyps and asthma
Prostaglandin inhibition (but not leukotriend inhibition) can shift toward leukotriene production increasing risk of asthma exacerbation
- AVOID NSAIDS

43
Q

what is the MOA of ASA?

A

binds irreversibly and inhibits COX-1 mediated TXA2 formation.
( does so by blocking arachodonic acid from binding and becoming active)

44
Q

how long does aspirin last? why?

A

Effect last for the life of the platelet (7 days) and only goes away when new platelets are made.

45
Q

what group of analgesics can you use if you need to avoid platelet effect?

A

Nonacetylated salicylates
(MgSalicylate“doans” pills and salsalate)
have least effect on platelets, least likely to cause excess bleeding
(while aspirin bind irreversibly and other NSAIDs bind reversibly in platelets)

46
Q

4 CNS effects of NSAIDs

A

Headache: Occurs mostly with indomethacin and tolmetin
Tinnitus
Dizziness
CONFUSION: Occurs much more often in the elderly

47
Q

what is the absorption of aspirin? (maybe weeds)

A

Rapidly absorbed with peak plasma level in 1-2 hours

48
Q

which drug has zero order kinetics? what does this mean?

A

aspirin

  • a constant amount (in mg) of drug is eliminated per unit time (regardless of plasma concentration)
  • RATHER THAN 1st order: eliminated by constant % of the drug eliminated per unit time. (dependent on plasma concentration)
49
Q

what is the dose of aspirin for mild- moderate pain?
for arthritis?
for cardioprotective effects?

A

325-650mg four times a day (max 4g/day) - mild to moderate pain
650mg q4hours (max 5.4 g/day) - arthritis
81mg- unstable angina, MI, TIAs, etc. (antiplt effect)

50
Q

3 ADRs of aspirin

A
  1. fecal blood loss (harmless)
  2. salicylism: at high doses- vomitting, tinnitus, decr. hearing, vertigo
  3. hyperpnea: at OD levels- respiratory alkalosis –> metabolic acidosis
51
Q

what is salicylism?

A

toxic condition: vomitting, tinnitus, decr. hearing, vertigo

52
Q

what is hyperpnea?

A

respiratory alkalosis that leads to metabolic acidosis

53
Q

what is the antidote to hyperpnea from aspirin? (4)

A
  1. stomach irrigation
  2. IV Fluids
  3. sodium bicarb
  4. dialysis (if extreme)
54
Q

what is Reye’s syndrome? (weeds maybe)

A

if children have viral infection and you give them aspirin = mitochondrial damage and awful effects, can lead to coma

55
Q

efficacy difference between different NSAIDs?

A

NO, all about the same efficacy. choose based on what ADRs you want to avoid

56
Q

when do you switch between NSAIDs?

A

try the one you chose for 2 weeks, increase dose, then you can maybe change

57
Q

why wouldnt you want to combine two NSAIDs?

A

it increases the risk of ADRs without increasing efficacy

58
Q

what do you have to do if you give NSAIDs and someone has Hx of HTN or has HTN-controlled with meds? why?

A

monitor: can decrease effect of BP meds b/c decrease GFR, and increase Na+ and H2O

59
Q

what is the monitoring process of ASA w/ HTN pts?

A
  1. check BP before starting
  2. check BP in 2 wks
  3. if BP increases- stop NSAID or inc. HTN meds
60
Q

what do you need to do if you prescribe NSAIDs and on diuretics/ACE/ARBs ?

A

recheck SCr 3-7 days after starting b/c of increased risk of renal failure

61
Q

what does acetaminophen help with?

A

analgesic, antipyretic. MILD pain reliever

NOT- anti-inflammatory

62
Q

what is the MOA of acetaminophen?

A

Inhibits PGE2 synthesis in (hypothalamic heat-regulating center)
= antipyresis (cause vasodilation and sweating)
* only CNS effects { no plt and very little peripheral }

63
Q

what is the metabolism and elimination of acetaminophen?

A

Hepatic metabolism, renal elimination (where overdose comes in)

64
Q

what is significant about the hepatic metabolism of acetaminophen?

A

Acetaminophen broken into inactive metabolites and NAPQI

  • liver produces glutathion to bind NAPQI to form a nontoxic metabolite
  • Overdose levels of acetaminophen –> NAPQI reacts with sulfhydrl group and liver can’t make enough glutathion = LIVER DAMAGE
65
Q

what is the dosing of acetaminophen for healthy pts vs elderly/alcoholism/hepatic dysfunction pts ?

A

healthy: 4g

alcoholism/elderly/hepatic dysfunction: < 3g

66
Q

what is used for any pain if the patient also has GI upset or an ulcer, child with virus or chickenpox (b/c of the risk of Reyes), or a bleeding disorder?

A

acetaminophen!

67
Q

what common substance is added to pain meds to increase analgesia?

A

caffeine

in OTC pain relievers/ migraine meds

68
Q

how can caffeine cause analgesia?

A

binds with adenosine receptor - inhibiting neuronal activity
- mimics adenosines natural activity

69
Q

what does adenosine naturally do in the body?

A

Adenosine binds to different adenosine receptors located in the CNS and PNS
Receptor A2A activation leads to inhibition of pain transmission

70
Q

what drugs can be used for neuropathic pain before moving to opiods? (weeds)

A

anti-epileptics: “gabas” and “carbamazepines”
anti-depressants: TCAs, SNRIs,
topicals: lidocaine, capsacian, diclofenac

71
Q

what is methyl salicylate (wintergreen oil) ? (weeds)

A

topical pain reliever : counterirritant (a cooling or warming effect to divert attention away from pain sensation)

72
Q

how does capcasian work? (weeds)

A

a red pepper derivative: 1st- releases substance P, continuous stimulation of nerves leads to
depletion of substance P
=decreasing pain

73
Q

Visceral pain is typically severe and typically best responds to ________

A

narcotics

74
Q

what is Used in children to decrease pain of procedures before IVs, circumcisions ? (weeds)

A

lidocaine/prilocaine (EMLA) - topical

pharmacology (24 decks)

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