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🄼💊 M2 Adrenergic/Cholinergics > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Name the 3 Groups of NSAIDs

A
  1. Aspirin/Salicylates
  2. Traditional Non-Selective NSAIDs (ibuprofen)
  3. Coxibs (COX inhibitors)
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2
Q

A: How does Cell/Tissue Damage lead to Pain/Inflammation/Fever?

1: Damage induces ________ to produce ________
2: ________ binds to Cyclooxygenase and is converted into ________

3: ________ is then modified by multiple syntheses into
what 3 major compounds?

4: ________ can then go to induce pain/inflammation/fever.

B: What is the rate limiting step for this reaction?

A

A: How does Cell/Tissue Damage lead to Pain/Inflammation/Fever?

1: Damage induces [Phospholipase A2] to produce [Arachidonic Acid]
2: [Arachidonic Acid] binds to Cyclooxygenase and is converted into [Prostaglandin H2] = RATE LIMITING STEP!

3: [Prostaglandin H2] is then modified by multiple syntheses into
- [Prostacyclin]
- [Prostaglandin E2]
- [Thromboxane TXA2]

4: [Prostaglandins] can then go to induce pain/inflammation/fever.

B: What is the rate limiting step for this reaction?
[Arachidonic Acid] conversation into [PGH2] by Cyclooxygenase

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3
Q

Aspirin

MOA

A

IRREVERSIBLE NON-Competitive COX inhibitor

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4
Q

A: COX1 Expression

B: COX1 Location

A

A: Expressed constitutively and does NOT need to be induced

B: COX1 is UBIQUITOUSLY EXPRESSED IN MOST TISSUE

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5
Q

A: COX-TWO Expression

B: COX-TWO Location

  • Where can it be Induced? (4)
  • Where is it constitutively expressed? (2)
A

A: INDUCIBLE in many cell types in response to [pro-inflammatory]/mitogenic stimuli

B:
-INDUCED in [macrophages/monocytes], [Dorsal Horn Neurons], osteoblast and Fibroblast

-has low level constitutive expression in KIDNEY AND ENDOTHELIUM

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6
Q

COX1

A: Physiological Role (4)

B: What compounds do COX1 produce that facilitate these roles?

A

HOUSEKEEPING:
1. Platelet Regulation (monitors blood clotting)

  1. Kidney Function
  2. Cytoprotection of Stomach by regulating Acid/Mucus production & [gastric blood flow]
  3. Maintains Patent Ductus Arteriosus for Fetus and stimulates [Uterine contractions during labor (involves PGF2a) ]

(COX1 is NOT inhibited by Celecoxib)

B: [PGE2/PGi2]

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7
Q

COX-TWO

Physiological Role

A

PRO-INFLAMMATORY RESPONSE (Mitogenesis and Signaling)

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8
Q

How do Prostaglandins cause Peripheral Pain Sensitization?

A

[Prostaglandin E2] produced by a [COXTWO inflammatory cell] DEC PAIN THRESHOLD for [Primary afferent neurons]—> [Peripheral Pain Sensitization]

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9
Q

How do Prostaglandins cause CENTRAL Pain Sensitization

A

1st: [B.I.T.] produced by a [COXTWO inflammatory cell] travels to [Dorsal Horn Neurons] and induces COXTWO expression there.
2nd: [Dorsal Horn Neurons] now produce Prostaglandins which bind to PGE2 Receptors in the [Dorsal Horn Neurons] to ENHANCE the depolarization of [Secondary Afferent neurons]

[B.I.T.] = [Bradykinin/ IL-1 / TNFa]

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10
Q

Elucidate the steps of Fever Production starting with Tissue Damage

  1. Damaged Tissue produces [____ and ______] which travels to the CNS
  2. [____ and ______] stimulate endothelial cells of the [_______ blood vessels] to express _______ and [____ synthase]
  3. _____ and _____ in the endothelial cells of the [_____ blood vessel] produce [______] which goes to stimulate hypOthalamus to INC body temperature
A

Elucidate the steps of Fever Production starting with Tissue Damage

  1. Damaged Tissue produces [IL-1 and TNFa] which travels to the CNS
  2. [IL-1 and TNFa] stimulate endothelial cells of the [hypOthalamus blood vessels] to express COXTWO and [PGE synthase]
  3. [COXTWO/PGEsynthase] in the endothelial cells of the [hypOthalamus blood vessel] produce [Prostaglandin E2] which goes to stimulate hypOthalamus to INC body temperature
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11
Q

A: What is another name for PGi2?

B: What are its roles? (2)

C: Endothelial cells express COX1 or COXTWO? What are the primary compounds produced from Endothelial cells?

A

A: Prostacyclin!

B:

1) VasoDilates
2) INHIBITS Clotting

C: Endothelial cells express BOTH COX1 and COXTWO! They primarily produce [PGi2/PGE2] because they do NOT contain the [Thromboxane synthase]

“(PGi2 Prostacyclin) | (PGE2) “

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12
Q

A: Platelets express ONLY _____[COX⬜] but primarily produce ________.

B: What are the roles of the compound produced? (2)

A

A: Platelets express ONLY COX1 but primarily produce [Thromboxane].

B: What are the roles of the compound produced? (2)

1) vasoconstricts
2) promotes clotting

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13
Q

A: Why is PGi2 particularly important in Pt with Renal Dz or Heart Failure? (3)

B: Is [ ______-medicated acute renal failure] caused by taking NSAIDs in a diseased state, reversible?

A

A: [Renal Dz and Heart Failure]—> INC Renal VasoCONSTRICTORS. [PGi2] is a vasodilator that will

  • INC Renal Blood flow to prevent Renal ischemia
  • INC GFR
  • INC water and Na+ excretion

B: Is [ HEMODYNAMICALLY-medicated acute renal failure] caused by taking NSAIDs in a diseased state, reversible?

->YES! JUST TAKE THEM OFF OF THE NSAIDS!

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14
Q

A: Why is Aspirin READILY absorbed in the stomach and [upper small intestine]?

A

ASA (AcetylSalicylicAcid) is a weak acid and in the acidic environment of the stomach it will be in a [NEUTRAL PROTONATED FORM]—> Allows EASY ABSORPTION!

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15
Q

Aspirin Recommended Dosing

  1. Anti-Platelet activity = ⬜ dose
  2. Anti-Pyretic = ⬜ dose
  3. Analgesic = ⬜ dose
  4. Anti-Inflammation= ⬜ dose
A

Aspirin Recommended Dosing

  1. Anti-Platelet activity = [81mg qD]
    _________________
  2. Anti-Pyretic(must cross BBB) = [400mg BID]
    _________________
  3. ]Anti-Pain (Analgesic)] = [400mg BID]
    _________________
  4. [Anti-Puff (anti-Inflammation)= [4,000mg - 6,000mg qD]
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16
Q

A: Why is concurrently taking [Salicylates/Aspirin] and Warfarin OR Sulfonylureas contraindicated?

B: Sulfonylurea Toxicity —> ⬜

A

[Salicylates/Aspirin] are 50-90% Protein bound once they enter the serum. This will DISPLACE other very protein bound drugs like WARFARIN OR Sulfonylureas—-> Warfarin/Sulfonylurea Toxicity!

B: Sulfonylurea toxicity —-> hypOglycemia

17
Q

A: What is the Difference between Diflusinal and Aspirin? (2)

B: When would you use [Diflusinal or other Salicylates] and not Aspirin? (2)

A
  1. Diflusinal can NOT cross BBB which means it is NOT an Anti-Pyretic
  2. ## Diflusinal (and all other Salicylates) does not IRREVERSIBLY inhibit COX –> they are less potent than ASAB: Use Salicylates when:
    1) Pt is at risk for GI Complications (gastric ulcers)
    2) Pt is at risk for Bleeding (hemophiliac)
18
Q

How do you treat Salicylate OVERDOSE and why?

A

Alkalinize the Urine (make urine more basic) —>cause Salicylate to convert into its [DeProtonated CHARGED Form] —> Trap it in the urine—> INC Excretion and prevents renal Absorption

19
Q

Between which of the 3 NSAID groups would you use to treat GOUT?

A

Traditional NSAIDs

20
Q

A: Ibuprofen has a _____[slow/rapid] onset of ____ min and is _____[better/least] tolerated than Aspirin even though it is just as _____.

B: INDICATIONS (2)

A

Ibuprofen has a RAPID onset of [15-30 min] and is BETTER tolerated than Aspirin even though it is just as potent.

INDICATIONS:

  • Fever
  • Acute Pain
21
Q

A: Naproxen is ___ times more potent than aspirin and has a RAPID onset of ____ min.

B: Naproxen has a serum half life of ___ hours which allows for _____ dosing

C: Naproxen is an extremely ideal _______

A

A: Naproxen is 20 x more potent than aspirin and has a RAPID onset of 60 min.

B: Naproxen has a serum half life of 14 hours which allows for twice/day dosing

C: Naproxen is an extremely ideal Anti-Pyretic

22
Q

What’s special about OXAPROZIN?

A

[Traditional NSAID] with LONG HALF-LIFE OF 50-60 HOURS —> allows for once/day dosing

23
Q

INDOMETHACIN

A: Primary Indications (3)

B: Cons

A

A: Indication

1) NSAID Used to promote closure of [Fetal Ductus Arteriosus]
2) 10-40 x more potent than Aspirin at anti-inflammation
3) Inhibits neutrophil mobility

B: Cons
(x) NOT TOLERATED AS WELL AS IBUPROFEN-Toxicity limits usage

24
Q

KETOLORAC

A: Primary Indication

B: What can this NSAID replace?

A

A: Indication:
[Intravenous NSAID] that treats post-surgical pain

B: Can be used as an Opioid Replacement Drug

25
Q

DICLOFENAC

B: What’s the cons of this drug and its class?

A

A: DICLOFENAC= Relatively Selective COXTWO Inhibitor

B: [COXTWO Inhibitors] INC chances of Stroke/Heart Dz!!

26
Q

What are 2 ASPIRIN-Specific Adverse Effects?

A
  1. Reye’s syndrome (occurs in genetic subset of children/teens who take Aspirin during a viral infection) = FATAL degenerative liver dz associated w/encephalitis
  2. INC Risk of Gout
27
Q

A: What is the most common adverse effect reported for [tNSAIDs & (Aspirin/Salicylates) ] ?

B: How do [tNSAIDs & (Aspirin/Salicylates) ] cause Gastric damage? (2)

C: How do you treat [tNSAIDs & (Aspirin/Salicylates) ] induced Gastric damage? (2)

A

B:
1) DIRECTLY damage gastric epithelium from being ion trapped in the compartment sometimes

C: Treatment:
-Misoprostol = PGE1 in a pill [CAN NOT GIVE TO PREGNANT WOMAN SINCE IT INDUCES ABORTION]

-Omeprazole

28
Q

A: [Acute interstitial nephritis and Nephrotic Syndrome]

B: Who does this occur most in/

A

A: RARE but important clinical syndrome associated with IDIOPATHIC Glomerular [inflammatory cell infiltration] / proteinuria and NV. Caused by month exposure to NSAIDs!

-Pt recovers once NSAIDs are discontinued

B: Occur most in Women and Elderly

29
Q

[CHRONIC interstitial nephritis and Analgesic Nephropathy]

A

A: Caused by CHRONIC Daily OVER USE of NSAIDs which leads to Chronic Renal Ischemia—> ESRD

ESRD= End Stage Renal Dz

30
Q

A: What is [NSAID Hypersensitivity]?

B: What are the sx and what is the onset?

A

A: NON-IMMUNE inflammatory attack that occurs when pt takes [Aspirin / tNSAIDs/ COXTWO inhibitors]. Arachidonic acid accumulation–> Leukotriene production–> [airway hypersensitivity rxn]

B: Rapid Severe asthma attack that onsets 30-60 min after intake

31
Q

NSAIDs taken in pregnant women after ____ weeks gestation can cause [Premature Ductus Arteriosus ____] in the fetus

A

NSAIDs taken in pregnant women after 30 weeks gestation can cause [Premature Ductus Arteriosus CLOSURE] in the fetus

32
Q

A: COXTWO inhibitors such as Celecoxib are BEST used for what 3 circumstances?

B: What type of effect does [COXTWO inhibitors] have on Kidneys?

C: Why is Celecoxib NOT a first-choice NSAID?

A

A: COXTWO inhibitors such as Celecoxib are BEST used for

  • [Rheumatoid Arthritis]
  • Osteoarthritis
  • Pt who are at higher risk for GI bleeds

B: [COXTWO inhibitors] have SAME NEPHROTOXICITY as tNSAIDS and [Aspirin/Salicylates] because Kidneys constitutively express COXTWO and need it

C: Celecoxib significantly Increases Stroke/Heart Dz probability and so is NOT a 1st choice NSAID

33
Q

Which 3 Drugs have Dangerous impaired Renal Clearance due to NSAID usage?

A
  1. Lithium
  2. Methotrexate
  3. [Gentamicin-Aminoglycoside]
34
Q

A: Acetaminophen is metabolized into its active metabolite (______) which inhibits ______ AND activates the ______ system—> DEC Fever & Pain

B: Acetaminophen is not a good anti-______ or anti-______ because it does not inhibit ________. This is due to [peripheral ______] that quickly degrade it in the periphery only

C: How does Acetaminophen affect the Kidneys and GI system?

A

A: Acetaminophen is metabolized into its active metabolite (AM404) which inhibits CNS COXTWO AND activates the cannabinoid system—> DEC Fever & Pain

B: Acetaminophen is not a good anti-inflammatory or anti-platelet because it does not inhibit [Peripheral COX1 or COXTWO]. This is due to [peripheral HydroPerOxides] that quickly degrade it

C: How does Acetaminophen affect the Kidneys and GI system?
:-) It safe for both due to inability to act on [Peripheral COX1 and COXTWO]

🄼💊 M2 Adrenergic/Cholinergics (5 decks)

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