Analgesics Flashcards

(43 cards)

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

23
Q

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

24
Q

what are endogenous analgesics

A
  1. endorphins (natural opioids)

2. serotonin

25
Aspirin and salicylate like agents are ______
NSAIDs
26
What are NSAID alternatives
Acetaminophen (parecetamol); central acting COX inhibition (pain and fewer); toxicity via hepatoxic metaolite; leading drug of choice for suicide.
27
Salicylic acid inhibits synthethis of ___enzyme
COX
28
Which NSAID's are available as topical preparations
1. flurbiprofen 2. suprofen 3. diclofenac 4. ketoralac
29
____ has the most Cox 1 selectivity and the least Cox 2 selectivity
Ketorolac
30
ASA and acetaminophen have similar properties except:
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
what are ASA adverse effects
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
What is Reyes syndrome associated with
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
Cox 2 selective drugs are the ____GI toxic. Reduced Cox 2 selectivity leads to the ____GI toxicity
least; most
34
what are NSAID drug interactions?
1. NSAIDs 2. Steroids 3. Anticoagulants 4. omega 3 fatty acids 5. ginkgo biloba 6. intraocular cholinergics
35
what are NSAID contraindications
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
What are the different NSAID preparations
1. topical 2. oral 3. local injection 4. IV
37
Age restrictions do not apply to the topical NSAIDs except for which ones?
1. Acular LS (Ketorolac) : 3 yrs | 2. Ilevro (Nepafenac): 10 yrs
38
Which topical NSAID is the most prescribed drug?
Ilevro; pro drug that gets activated once it enters anterior chamber; used by most surgeons post op
39
what are some adverse effects of topical NSAIDs
1. burning, stinging 2. corneal toxicity, melting 3. vitreous detachment 4. delayed wound healing 5. prolonged bleeding time 6 elevated IOP
40
you are not supposed to combine NSAIDs with ____
prostaglandins; they are pro inflammatory and NSAIds are antiinflammatory
41
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
meiosis
42
Key side effect of optiods is that it causes ____ release
histamine
43
what are other opiod adverse effects
1. nausea and vomiting 2. miosis 3. flushing and itching 4. sedation 5. constipation 6. cough suppression 7. respiratory depression 8. depedence