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Ocular Pharm lectures 6-9 final > Lecture 7 NSAIDS > Flashcards

Lecture 7 NSAIDS Flashcards

1
Q

Which of the following is not an enzyme in the inflammatory pathway?

a) phosholipase-A
b) lipooxygenase
c) cyclooxygenase
d) tumordonicase

A

d) tumordonicase (I just made this up, not a real enzyme)

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2
Q

adverse effects of narcotics include all BUT which of the following?

a) itching
b) sedation
c) mydriasis
d) constipation

A

c) mydriasis

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3
Q

allergic conjunctivitis is an indication only for which of the following topical NSAIDS?

a) ketoralac
b) nepafenac
c) diclofenac
d) bromfenac

A

a) ketoralac

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4
Q

List the 5 cardinal signs of inflammation

A

1) calor=heat 2) rubor=redness 3) tumor=swelling

4) dolor=pain 5) funtio laesa=loss of function

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5
Q

The 5 cardinal signs of inflammation facilitate what 3 events?

A

1) isolates injurious agent
2) removes cell debris and pathogens
3) prepares site for tissue repair

Heat causes vessels to dilate, allowing more blood to flow to the area which causes heat and redness. Pain promotes healing by preventing you from moving that area.

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6
Q

lipocortin, aka lipomodulin is produced by what?

A

steroids

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7
Q

lipocortin inhibits what?

A

phopholipase-A2

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8
Q

phospholipase-A2 is responsible for what?

A

initiating the arachidonate cascade

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9
Q

what are the 3 major products of the arachidonate cascade?

A

leukotrienes, prostaglandins, and platelet activating factors

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10
Q

which enzyme is responsible for the production of prostaglandins?

A

cyclooxygenase

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11
Q

which enzyme is responsible for the production of leukotrienes?

A

lipoxygenase

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12
Q

How is lipocortin made?

A

steroids enter the cell nucleus and stimulate transcription of this protein

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13
Q

Of Omega-6 and Omega-3, which produces pro-inflammatory prostaglandins and which produces anti-infammatory prostaglandins?

A

Omega-6 is pro, omega-3 is anti

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14
Q

(T or F) Omega-6 or 3 requires cyclooxygenase to produce its end product?

A

True because the end products of omega-6 and 3 prostaglandins

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15
Q

What is the main difference between Cox-1 and Cox-2

A

Cox-1 is constitutive, meaning it is running in the background all the time (maintaining Gi mucosa, platelets, macrophages, kidneys, vasculature). Cox-2 is inducible, meaning it is manufactured on demand when needed in an inflammatory event.

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16
Q

Aspirin inhibits the production of which one of the following?

a) leukotrienes
b) prostaglandins
c) platelet activating factor (PAF)
d) the entire arachidonate pathway

A

b) prostaglandins, aspirin is a classic cox-inhibitor

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17
Q

what does PGI2 do?

A

decreases acid secretion

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18
Q

What does PGE2 and PGF2A do in regards to the gastrointestinal tract?

A

promotes production of cytoprotective mucous in gastric mucosa (this is why aspirin and ibuprofen can upset your stomach)

19
Q

what does PGE2 and PGI2 do in regards to the kidney?

A

promotes maintenance of renal blood flow by stimulating renin release (this is why aspirin and ibuprofen cause BP to rise since the kidney plays a role in blood volume homeostasis)

20
Q

What does TXA2 do?

A

platelet activator (TXA=thromboxin-A)

21
Q

What is allodynia?

A

decreased pain tolerance due to increased pain fiber sensitization

22
Q

(T or F) PGE2 and PGF2 are proinfammatory prostaglandins

A

true, they sensitize pain fibers

23
Q

(T or F) some opiods have a potential for histamine release

A

true, caution in patients with hypersensitivity type 1, causes degranulation of mast and basophil cells. Opiods are also known to cause nausea and vomiting, patient should lay down when taking to reduce the effect on the chemoreceptor trigger zone.

24
Q

would an opiod cause miosis or mydriasis?

A

miosis, opiods are CNS depressants, they cause sedation.

25
Q

Could an opiod cause diarrhea?

A

No, opiods cause constipation

26
Q

Name 4 dose dependent reasons for taking aspirin

A

1) anti-platelet (80-160mg) thins blood, stroke prevention
2) anti-pain (160-325) analgesic
3) anti-fever (160-325mg) anti-pyretic
4) anti-inflammatory (325-650mg) acute swelling to arthritis

27
Q

what medication is the gold standard of NSAIDS?

1) ibuprofen
2) tylenol
3) aspirin
4) naproxen

A

3) aspirin

28
Q

medications ending in -coxib are …?

1) cox-1 inhibitors
2) cox-2 inhibitors
3) both cox-1 and cox-2 inhibitors
4) PAF inhibitors

A

2) cox-2 inhibitors

29
Q

What is the #1 approved NSAID for acute pain?

A

ketoralac (ketoralac is also the least selective for cox-2)

30
Q

Select the true statement:

1) NSAIDS tend to elevate IOP, whareas steroids rarely do
2) Steroids have a greater effect on the HPA axis than NSAIDS do
3) Steroids have a lower risk associated with cataracts than NSAIDS do
4) NSAIDS have a significant risk of post-op cystoid macular edema

A

2) Steroids have a greater effect on the HPA axis than NSAIDS do

NSAIDS have rare IOP elevation, no cataract association, and no HPA axis affect. Steroids can elevate IOP, they are associated with catarct development and effect HPA axis, as well as risk for post-op cystoid macular edema

31
Q

What is the major trend with COX-2 inhibitors?

A

The more COX-2 selectivity a medication has, the less GI toxicity it has and the longer acting it is (time in blood plasma is longer).

32
Q

Narcotics act in which of the following ways?

a) anti-inflammatory
b) anti-pyretic
c) anti-platelet
d) anti-pain

A

d) anti-pain, –A, B,and C are true for NSAIDS but not narcotics

33
Q

(T or F) Tylenol is a salycilate-like NSAID

A

False, tylenol is a non-salicylate

34
Q

(T or F) Narcotics have a ceiling effect

A

False, NSAIDS have a ceiling effect

35
Q

Why is tylenol the suicide drug of choice?

A

Tylenol causes hepatoxicity (its eliminated by the liver and the liver ceases to function in an overdose)

36
Q

Aspirin is eliminated by…

1) the kidneys
2) the liver
3) none of the above

A

1) the kidneys (nephrotoxicity is one of aspirin’s adverse side effects)

37
Q

select the correct statement:

a) tylenol can cause GI upset, whereas aspirin does not
b) tylenol is safe in pregnancy, whereas aspirin is not
c) tylenol is anti-platelet, whereas aspirin has no platelet inhibition
d) tylenol is eliminated by the kidneys, whereas, aspirin is eliminated by the liver

A

b) tylenol is safe in pregnancy, whereas aspirin is not

TYLENOL: no platelet inhibition, no GI effects, safe in pregnancy, eliminated by the liver
ASPIRIN: anti-platelet, GI upset, contraindicated in pregnancy, eliminated by the kidneys (dialysis required in overdose)

38
Q

is aspirin acidic or basic?

A

acidic, because of this, it can alter blood PH and cause a headache, abdominal cramps, bleeding, ulcerations. another adverse effect from aspirin is respiratory alkalosis due to overcompensation of of acidic blood PH.

39
Q

define hyphema

A

anterior chamber hemmorrage

40
Q

Does Restasis (cyclosporin-A) follow the same anti-infammatory pathway as traditional NSAIDS?

A

no, it inhibits mast cell degranulation and reduces the generation of pro-inflammatory TH-1 cytokines IL-2, IL-4, IFN-y & TNFa

41
Q

What is the most prescribed topical NSAID eye drop?

A

Acular LS (ketorolac) solution

42
Q

What is Restasis prescribed for?

A

chronic dry eye (keratoconjunctivitis sicca KCS). oral use of cyclosporin-A (active ingredient of Restasis) is used as an immunosuppresant in patients that undergo transplants.

43
Q

(T or F) vitreous detachment is an adverse reaction associated with topical NSAIDS

A

true, as well as delayed wound healing, prolonged bleeding time, and corneal toxicity

44
Q

Why is it better to put a diabetic on tylenol vs. aspirin

A

because late stages of diabetes results in renal failure and aspirin is eliminated thru the kidney

Ocular Pharm lectures 6-9 final (4 decks)

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