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Ocular Pharm > Analgesics > Flashcards

Analgesics Flashcards

1
Q

What is COX?

A

cyclooxygenase; a key enzyme responsible for production of lipid based inflammatory mediators

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2
Q

COX is responsible for _____ generation

A

TXA2 (thromboxane A2)

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3
Q

What are the five cardinal signs of the inflammatory response

A
  1. Heat (calor)
  2. Redness (rubor)
  3. Swelling (tumour)
  4. pain (dolor)
  5. loss of function (function lease)
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4
Q

The inflammatory response is an immediate, protective _____ process characterized by ____, irritation, or injury

A

pathological; infection

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5
Q

Tissue repair is a _____ inflammatory process

A

post

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6
Q

Lipocortin is a protein that inhibits _____ activity

A

phospholipase 2

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7
Q

Steroids act by ____- inhibiting production of end products by causing transcription and translation of lipocortin

A

indirectly

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8
Q

Class ____ prostaglandins and type ____ leukotrienes apply to inflammation (pro inflammatory)

A

2; 4

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9
Q

Which leukotrienes enhance histamine effects, bronchoconstrict, constrict coronary arteries and dilate vessels in regions of inflammation

A

LTC4 and LTD4

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10
Q

____ decrease GI acid secretion and the GI tract, inhibits platelet aggregation, and promotes _____ in the kidneys

A

PGI2 (prostacyclin)

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11
Q

Which prostaglandin activates matrix metalloproteinases

A

Platelet activating factor

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12
Q

Which antibiotic inhibits MMP’s

A

Tetracyclines; degade ECM and allow immune cells to infiltrate to the region.

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13
Q

Omega 3 are good source of ____inflammatory supplement

A

anti

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14
Q

Type ____ prostaglandins and type ____ leukotriene are actually anti inflammatory

A

3; 5

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15
Q

What is the first and the last step of the anti-inflammatory pathway

A

first step: alpha linolenic acid (ALA)

last step: eicosanpentanoic acid

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16
Q

what is the first and the last step for the pro inflammatory pathway

A

first step: linoleic acid

last step: arachidonic acid

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17
Q

What is a constitutive (housekeeping) enzyme predominantly involved in PG and TXA2 production

A

COX 1

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18
Q

What is an inducible enzyme; predominantly involved in PG and Prostacyclin production which generates pro inflammatory PGs and O2 radicals.

A

COX -2; it doesn’t exist unless our body is told to make it.

19
Q

What are autonomic responses of pain

A
  1. tachycardia
  2. systemic hypertension
  3. tachypnea
  4. diaphoresis
  5. pallor
  6. nausea
20
Q

What are some therapeutic relief mechanisms peripherally

A

block pain mediators, receptor sensitization, and affarent neuronal discharge

21
Q

what are some central therapeutic relief mechanisms

A

block pain receptors in the CNS

22
Q

Bradykinin, norepinenphrine and ____ stimulate pain fibers

A

histamine

23
Q

what results when prostaglandins, leukotrienes and substance P sensitize pain fibers

A

allodynia

24
Q

what are endogenous analgesics

A
  1. endorphins (natural opioids)

2. serotonin

25
Q

Aspirin and salicylate like agents are ______

A

NSAIDs

26
Q

What are NSAID alternatives

A

Acetaminophen (parecetamol); central acting COX inhibition (pain and fewer); toxicity via hepatoxic metaolite; leading drug of choice for suicide.

27
Q

Salicylic acid inhibits synthethis of ___enzyme

A

COX

28
Q

Which NSAID’s are available as topical preparations

A
  1. flurbiprofen
  2. suprofen
  3. diclofenac
  4. ketoralac
29
Q

____ has the most Cox 1 selectivity and the least Cox 2 selectivity

A

Ketorolac

30
Q

ASA and acetaminophen have similar properties except:

A

Acetaminophen:

  1. is NOT antiinflammatory
  2. is NOT a platelet inhibitor
  3. does NOT irritate the GI
  4. Is pregnancy category B vs D in ASA
31
Q

what are ASA adverse effects

A
  1. headache
  2. nausea
  3. abdominal cramps, bleeding, ulceration
  4. hemorrhagic diathesis: bleeding time doubles
  5. tinnitus –> hearing loss
  6. nephrotoxicity
  7. respiratory alkalosis –> metabolic acidosis
  8. acute poisoning by respiratory depression
  9. non immune low dose hypersensitivity
32
Q

What is Reyes syndrome associated with

A

adverse reaction in children taking ASA to reduce fever in viral infections. Peptobismol should be avoided in kids up to 15 yoa. 35% mortality!

33
Q

Cox 2 selective drugs are the ____GI toxic. Reduced Cox 2 selectivity leads to the ____GI toxicity

A

least; most

34
Q

what are NSAID drug interactions?

A
  1. NSAIDs
  2. Steroids
  3. Anticoagulants
  4. omega 3 fatty acids
  5. ginkgo biloba
  6. intraocular cholinergics
35
Q

what are NSAID contraindications

A
  1. active peptic ulcer
  2. chronic GIT inflammation
  3. bleeding disorders
  4. heavy alcohol use
  5. NSAD/ASA induced asthma
  6. Known hypersensitive
  7. chronic/hepatic/renal disease, diabetes
  8. hypertension/congestive heart failure
  9. pregnancy
  10. corneal denervation, dry eye
36
Q

What are the different NSAID preparations

A
  1. topical
  2. oral
  3. local injection
  4. IV
37
Q

Age restrictions do not apply to the topical NSAIDs except for which ones?

A
  1. Acular LS (Ketorolac) : 3 yrs

2. Ilevro (Nepafenac): 10 yrs

38
Q

Which topical NSAID is the most prescribed drug?

A

Ilevro; pro drug that gets activated once it enters anterior chamber; used by most surgeons post op

39
Q

what are some adverse effects of topical NSAIDs

A
  1. burning, stinging
  2. corneal toxicity, melting
  3. vitreous detachment
  4. delayed wound healing
  5. prolonged bleeding time
    6 elevated IOP
40
Q

you are not supposed to combine NSAIDs with ____

A

prostaglandins; they are pro inflammatory and NSAIds are antiinflammatory

41
Q

In contrast to NSAIDs, narcotics dont have a ceiling effect, they induce _____, they are non topical, have no anti inflammatory effects, anti platelet effects, or anti pyretic effecs

A

meiosis

42
Q

Key side effect of optiods is that it causes ____ release

A

histamine

43
Q

what are other opiod adverse effects

A
  1. nausea and vomiting
  2. miosis
  3. flushing and itching
  4. sedation
  5. constipation
  6. cough suppression
  7. respiratory depression
  8. depedence

Ocular Pharm (12 decks)

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