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MSK/Derm > SM 244: Pharmacology, Opioids, and Pain Concepts III > Flashcards

SM 244: Pharmacology, Opioids, and Pain Concepts III Flashcards

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1
Q

What is NPO?

A

Nothing Per Oral = Nothing by Mouth

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2
Q

What factor do all NSAIDS have in common?

A

All NSAIDS inhibit COX, the enzyme making Prostaglandins

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3
Q

What molecule do NSAIDS block the synthesis of?

A

NSAIDS block COX to reduce production Prostaglandins

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4
Q

What structural similarity is common among all NSAIDS?

A

None - NSAIDS are a diverse group of molecules with inhibition of COX as their only communal factor

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5
Q

Where are Prostaglandin’s stored?

A

Prostaglandins cannot be stored and are released immediately after synthesis

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6
Q

What is the precursor to Prostaglandin molecules?

A

Arachidonic Acid, which is converted by COX ino Prostaglandin H2 - a generic precursor to tissue specific Prostaglandins

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7
Q

What commonly used OTC drug is not an NSAID?

A

Acetaminophen

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8
Q

Is Acetaminophen an NSAID?

A

Nope

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9
Q

What even triggers the synthesis of Prostaglandins?

A

Cell injury (and other stimuli) lead to formation of Arachidonic Acid

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10
Q

Describe the pathway leading to Prostaglandin synthesis?

A

Cell injury and other triggers result in the formation of Arachidonic Acid by Phospholipase A2

Arachidonic Acid is converted into Prostaglandin H2 by COX

Tissue Specific Prostaglandin Synthases converted Prostaglandin H2 into Tissue Specific Prostaglandins

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11
Q

Where in the Prostaglandin synthesis pathway to NSAIDS act?

A

NSAIDS inhibit COX-mediated conversion of Arachidonic Acid into the generic Prostaglandin H2

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12
Q

Describe how Aspirin can induce Asthma?

A

Aspirin and other NSAIDS block COX, which results in a buildup of Arachidonic Acid

Arachidonic Acid can be converted by Lipooxygenase into Leukotrienes, which leads to Asthma attacks

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13
Q

What are the two types of COX?

A

COX-1 and COX-2

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14
Q

Which gene encodes each COX?

A

Both COX-1 and COX-2 are encoded by the same geen

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15
Q

Compare the expression patterns of COX-1 and COX-2?

A

COX-1 is present in all tissues all time

COX-2 is present only in tissues experiencing inflammation

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16
Q

Which COX is associated with inflammation?

A

COX-2

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17
Q

Which COX is constitutivley expressed?

A

COX-1

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18
Q

Which COX do most NSAIDS block?

A

Most NSAIDS except Celexocib block both COX-1 and COX-2 to varying degrees of seelctivity

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19
Q

Which specific organs and cells is COX-1 most relevant to?

A

GI tract, Kidneys and also Platelets

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20
Q

Which specific organs and areas is COX-2 most relevant to?

A

Kidneys, CNS, and any area experiencing inflammation

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21
Q

What is Allodynia and how does it relate to Prostaglandins?

A

Allodynia is pain caused by light touch

Prostaglandins cause Allodynia, which can be relieved by NSAIDS

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22
Q

What is Hyperalgesia and how does it relate to Prostaglandins?

A

Hyperalgesia is a heightened sense of pain perception at nerve endings

Prostaglandins cause Hyperalgesia, which can be relieved by NSAIDS

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23
Q

How does COX-2 alter peripheral mechanisms of pain?

A

Tissue injury leads to increased COX-2 expression

Prostaglandins are produced and bind to receptors at the nerve terminals of Nociceptors

PKA-driven signalling causes Sodium channels to open and depolarize the Nociceptor cell membrane, raising membrane potential

Nocicpetor fires more often due to higher Vm and pain signals intensify

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24
Q

How do prostaglandins effect depolarizations in nociceptors?

A

Prostaglandins raise the Vm of nociceptors by opening sodium channels, which increaseses the depolarization frequency

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25
Q

Why do NSAIDS work even if there is no inflammtation?

A

NSAIDS have a central to avoid amplifying pain signals

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26
Q

How do NSAIDs lower pain centrally?

A

NSAIDS prevent Prostaglandins in the dorsal Horn by increasing interneuron inhibition of excitatory neuroins sing SNAP

27
Q

How do NSAIDS enhance pain in the CNS?

A

Increase release of Substance P as well as in inhibition of inhibitory transmisttors like GABA/Glycine

28
Q

How does COX-1 protect the stomach?

A

Increases mucous layer thickness

Decreases pH gradient facing the epithelial cells

Increases bicarbonate secretion

Increases mucosal blood flow

29
Q

Why might inhibiting COX-1 be bad?

A

Inhibiting COX-1 with an NSAID can result in less gastric mucous, less bicarb/higher pH gradient, and less gastric mucosal blood flow

30
Q

What are the 2 mechanisms by which NSAIDS damage the stomach?

A

Direct gastric irritation: NSAIDS are weak acids

Decreased cytoprotection in the stomach: COX inhibition

31
Q

What can happen in the stomach with chronic NSAID use?

A

Peptic ulcer and bleeds

32
Q

Why can patient reports of dyspepsia not be treated as a way of detecting peptic ulcers?

A

Silent peptic ulcers develop with NSAIDS 70% of the time

33
Q

What are the risk factors for GI bleed with NSAIDS?

A 
Daily long-term use
High doses
Combination wtih Aspirin
Elderly Age
Anticoagulant usage
Alcohol and steroid use
34
Q

How can enteric coating prevent peptic ulcers from NSAIDS, and at what cost?

A

Enteric coating results in the NSAID not being broken down in the stomach, and instead being broken down in the Duodenum, preventing peptic ulcers

Leads to Duodenal ulcers

35
Q

Can PPI’s prevent all GI ulcers from NSAID use?

A

PPI’s prevent NSAID peptic ulcers but not insestinal ulcers

36
Q

What is Misoprostol?

A

A synthetic Prostaglandin that protects the entire GI tract by increasing mucous formation at the cost of extensive diarrhea

37
Q

Which COX is responsible for NSAID renal toxicity?

A

Both COX’s effect renal prostaglandins and cause renal toxicity when inhibited by NSAIDS

38
Q

How does COX-2 selectivity protect against renal toxicity?

A

It doesn’t - prostaglandins in the kidneys are produced by both NSAIDS

39
Q

How do prostaglandins effect the kidneys at rest?

A

In low renal perfusion states, Prostaglandins dilate afferent blood vessels to maintain renal blood flow and prevent pre-renal AKI

40
Q

What risk do NSAIDS have with hypertensive patients treated with antihypertensives?

A

NSAIDS increase BP in patients with hypertension who were taking anti-hypertensive drugs, leading to an increased risk of MI

41
Q

What kidney pathology can arise from NSAID use?

A

A lot, but pre-Renal AKI into Ischemic ATN is common due to NSAIDS blocking the Prostaglandins that maintain Renal perfusion

42
Q

Which COX effects platelet function and how?

A

COX-1 effects platelet function by mediating formation of Thromboxane

COX-2 plays no role in platelets

43
Q

How does COX inhibition lead to bleeding risk, with respect to platelets?

A

COX-1 inhibition results in less Thromboxane production and therefore less Platelet aggregation and vasoconstriction, creating a bleeding risk

44
Q

What effects does Thromboxane normally have?

A

Thromboxane normally promotes Platelet aggregation and Vasoconstriction

Thromboxane production is dependent on COX-1 in platelets

45
Q

Do NSAIDS reversibly or irreversibly inhibit COX, and how long does it take for platelets to recover?

A

NSAIDS reversibly inhibit COX, and clotting may return to normal after a few half-lives (a few hours)

46
Q

Does Aspirin reversibly or irreversibly inhibit COX, and how long does it take for platelets to recover?

A

Aspirin irreversibly acetylates COX, and platelets cannot recover because they have no nuclei to make new COX

Therefore, it takes 7-10 days to make new platelets

47
Q

How long does it take for clotting to return to normal after Aspirin?

A

7 - 10 days because Aspirin irreversibly inhibits COX-1, and new platelets must be made because the old ones cannot replace the COX-1 due to not having nuclei

48
Q

Are NSAIDS cardioprotective?

A

No, they are not cardioprotective because their effects on platelets are reversible, regardless of dose

Aspirin is irreverisble and has cardioprotective effects

49
Q

What are the side effects of NSAIDS?

A

GI ulcers
Decreased clotting
Renal ischemia
Hepatic Dysfunction

50
Q

Describe the Hepatic toxicity of NSAIDS?

A

Rare, not related to dose or duration

51
Q

What drug is Motrin?

A

Ibuprofen

52
Q

What drug is Aleve?

A

Naprosyn/Naproxen

53
Q

What drug is Indocin?

A

Indomethacin

54
Q

What drug is Voltaren?

A

Diclofenac - topical NSAID

55
Q

What drug is Relafen?

A

Nabumatone

56
Q

What drug is Toradol?

A

Keterolac - give via IV

57
Q

What drug is Mobic?

A

Meloxicam

58
Q

What drug is Celebrex?

A

Celecoxib - selective COX-2 inhibitor

59
Q

What are the advantages of selective COX-2 inhibitors?

A

Celecoxib; Reduced GI ulcer’s by half and no effect on platelets, making them ideal for surgery

60
Q

How can the GI ulcer risk of NSAIDS be lowered?

A

Add a PPI to the NSAID (still have risk for duodenal ulcers)

61
Q

Which NSAIDS can be given to patients who are NPO?

A

IV NSAIDS, such as Ketorolac and Ibuprofen

62
Q

Which NSAID is topical?

A

Diclofenac, good for joints and minimal GI/platelet effects

63
Q

What benefits do NSAIDS have over Opioids in the perioperative period?

A

Opioids slow GI tract peristalsis due to Mu receptors, and cause constipation that prolongs hosptial stays

NSAIDS can avoid the GI tract peristalsis

MSK/Derm (46 decks)

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