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Drug Action III > Pain (MC) - Block 2 > Flashcards

Pain (MC) - Block 2 Flashcards

1
Q

What type of compounds of PPB?

A
  1. Lipophilic
  2. Acidic
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2
Q

What are the indications for non-narcotic?

A
  1. Mild to moderate pain without altering consciousness
  2. Dull aches
  3. Ceiling effect
  4. No tolerace/physial dependence
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3
Q

What is the difference between Cox 1 and 2?

A
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4
Q

What is an analdesic?

A

Relief of pain, minor aches

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5
Q

What is anti-inflammatory?

A

Reduction of inflammation associated with arthritic syndromes

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6
Q

What is antipyretic?

A

Reduction of elevated body temp

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7
Q

Acetaminophen

MOA, BBW, Metabolism, Elimination, Dosing

A

MOA: analgesic, antipyretic (NOT anti-inflammatory)
BBW: hepatotoxicity
Metabolism: Both CYP2E1 and CYP3A4 are induced by ingestion of alcohol
Elimination: Gluthione and renal
Dosing: 4 g/day

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8
Q

What is the antidote for tylenol?

A

N-acetylcysteine

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9
Q

Why is APAP not considered an NSAID?

A
  1. Not anti-inflammatory
  2. Weak acid
  3. Doesn’t have antiplatelet or gastric ulcerogenic activity
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10
Q

How are NSAIDs excreted?

A

Renal

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11
Q

How are NSAIDs distributed?

A

All in synovial fluid after repeated dosing

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12
Q

Describe the toxicity of NSAIDs?

A

Nephro (interference with autoreg of renal blood flow) and hepatotoxic

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13
Q

NSAIDs

MOA, Interaction

A

MOA: inhibti PG synthesis via inhibition of COX1/2
Interactions: highly acidic so it interferes with drug that PPB, inhibits metabolism PG

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14
Q

What is the function of PGE2?

A

Enhanes local inflammation -> localized edema and hyperalgesia

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15
Q

Ihibition of prostanoid synthesis causes:

A
  1. Anagesia
  2. Antipyretics
  3. Anti-inflam
  4. Anti-thrombotic
  5. Closure of ductus arteriosis (X in pregnancy)
  6. GI tox
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16
Q

Why do NSAIDs cause gastric damage?

A
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17
Q

How does aspirin differ from other NSAIDs?

A

Covalently modifies COX enzymes (irreversible)

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18
Q

Aspirin

MOA, PK

A

MOA: 10-100 more potent against COX1 than COX2
PK: Absorption is sensitive to pH of stomach, raising gastric pH slows absorption, more ionized

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19
Q

ADR of aspririn?

A

Mostly GI
Hypersensitivity rare but fatal (skin rahses, watersecretions, uricaria, rhinitis, edema, bronchoconstriction, anaphylaxis)

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20
Q

Indicatiosn for aspirin?

A

Ana;gesia, antipyretic, anti-inflammatory, uricosuric, CV effects

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21
Q

How does aspirin bind to receptor?

A

Ser initiates nucleophilic attack on acetoxy on aspirin -> salicylate anion leaves and acetoxy group irreversibily covalently bind to ser

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21
Q

What is the warning when using salicylates in children?

A

Development of Reyes: sudden vomiting, violent HA, and unusual behavior
* Warning against their use in children under 16 with influenza, chicken pox, or flu-like illness

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22
Q

What is the SAR of arylalkanoic acids?

A

a-carbon = unsubstituted = arylacetic acid
* aryl group = phenyl -> “fenac”

a-carbon has a methyl = arylpropionic acid (chiral – racemic mixture because rapid epimerization but S enantiomer = active)
* aryl group = phenyl -> “profen”

Second aromatic ring good for activity (noncoplanar increased lipophilicity or blocked CYP metabolism)

Stable para substituents -> longer DOA

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23
Q

What are the types of arylacetic acids?

A
  1. Indomethacin (Indocin, Tivorbex)
  2. Sulindac
  3. Diclofenac (Cambia, Voltaren, Zipsor, Zorvolex)
  4. Nabumetone (Relafen)
24
Q

Indomethacin

MOA, ADR

A

MOA: very potent antipyretic and analgesic
* Cis-like is required for anti-inflammatory
* Uriosuric (for gout)

ADR: GI plus CNS (headache/dizziness/vertigo), ears (tinnitus)
* Aggravate depression, epilepsy, Parkinsonism

25
Q

How does sunlindac differ from other NSAIDs?

A

Prodrug with longer DOA because active metabolite have half-life 2x of parent

26
Q

Sunlindac

ADR

A

ADR: Less Gi effect due to prodrug form
* GI/CNS ADR milder and less common do to less PG activity

27
Q

What makes diclofenac potent?

A

Three potential MOA:
1. Inhibition of COX system -> decreased prostaglandins and thromboxanes
2. Inhibition of lipoxygenase pathway -> decreased leukotrienes
3. Inhibition of arachidonic acid release and stimulation of its reuptake

Thought that chlorines push the ring out of plane of other ring -> important for COX binding

28
Q

Diclofenac

MOA, ADR

A

MOA: Very potent anti-inflammatory, analgesic and antipyretic
ADR extensively metabolizd by CYP2C9 -> risk of hepatotoxicity

29
Q

What is a structure that can cause hepatotoxicity?

Diclofenac

A
  1. Open para to the amine -> hydroxyl insertion in para position
  2. Amines para to an OH
30
Q

What makes Nabumetone special?

A

Nonacidic prodrug

31
Q

Nabumatone

ADR

A

Minimal GI ADR since nonacidic and ineffective PG inhibitor

32
Q

Examples of arylpropionic acids

A
  1. Ibuprofen (Motrin)
  2. Ketoprofen
  3. Suprofen
  4. Ketorolac
  5. Oxaprozin
33
Q

Ibuprofen

MOA, PK, DOsing

A

MOA: Analgesic but not anti-inflammatory
PK: size and lipophilicity mimic an aromatic ring
Dosing: ≤1600 mg/day

34
Q

How does ketoprofen differ from ibuprofen?

A

Inhibits synthesis of leukotrienes and leukocyte migration in addition to inhibiting prostaglandin biosynthesis

35
Q

What is the problem with suprofen?

A

Used as an analgesic -> reports of severe flank pain and transient renal failure

ONly 1% ophthalmic solution

36
Q

What drug is very toxic 5x that of other NSAIDs and can only be used for 5 days?

A

Ketorolac

37
Q

What makes ketorolac special?

A

Good analgesic activity comparable to opioids

38
Q

Oxaprozin

PK, ADR

A

PK: Prolonged DOA
ADR: rash and mild photosensitivity

39
Q

SAR of oxicams

A

Aryl or heteroaryl ring = optimal

Plus ring -> noncoplanar
(and must be primary carboxyamide – enhances acidity)

Desinged to be noncarboxylic acid to be well tolerated and potent

40
Q

How is oxicam acidic despite noncarboxylic features?

A

Hydroxyls are stabilized by resonance

41
Q

What is the difference between the types of Oxicams?

A

Piroxicam: more COX1 selective
Meloxicam (Mobic): More COX2 selective

42
Q

What is the difference between COX 1 and 2 pockets?

A

COX 1: Isoleucine
COX 2: Valine (larger binding site)

  • Harder for larger, relatively rigid side-chain substituents to enter COX-1
43
Q

How does COX2 inhibitors differ from nonselective?

A

Decreased GI ADR, but increased risk of CV effects
* For patients with low cardiovascular risk but increased GI toxicity risk

44
Q

Types of COX2 inhibitors?

A
  1. Celecoxib (Celebrex)
45
Q

Celecoxib

PK, Binding

A

PK: metabolized by CYP2C9 and inhibits CYP2D6
Binding: Ionic bond and Val binds to ring

46
Q

What is the site of action for skeletal muscle relaxants?

A

Most DO NOT act at neuromuscular junction (except dantrolene)

Main effect: to depress CNS -> relax motor neurons
* More brain or CNS relaxants than muscle relaxants

47
Q

What is the indication for skeletal muscle relaxants?

A

Muscle spasms from strains, sprains, and musculoskeletal trauma or disease

48
Q

What are the types of muscle tone modulators?

A
  1. Methocarbomol (Robaxin)
  2. Metaxalone (Skelaxin)
  3. Carisoprodol (Soma)
  4. Cyclobenzaprine (Flexeril)
  5. Orphenadrine
  6. Chlorzoxazone
49
Q

What are the indications for muscle tone modulatpors?

A

Acute muscle spasm (2-3 week max course)

50
Q

What are the ADRs for muscle tone modulators?

A
  1. Sedation, mood changes
  2. Drug and alcohol interaction
  3. HIgh risk for abuse
51
Q

Orphenadrine

MOA, Indication

A

MOA: anticholinergic, ethanolamine antihistamine
Indication: Pain of all etiologies

52
Q

Types of anti-spasmodics? Site of action?

A
  1. Dantrolene
  2. Baclofen
  3. Tizanidine
  4. Benzodiazepines

CNS and spinal cord

53
Q

Tizanidine

MOA, PK, ADR

A

MOA: Analog of clonidine – presynaptic inhibition of motor neurons at α2 adrenergic receptors
PK: heavily metabolized
* Hepatic injury/death due to liver failure have been reported

ADR: Drowsiness, hypotension, dry mouth, hepatotoxicity, rebound hypertension

54
Q

Baclofen

MOA, ADR

A

MOA: GABAB receptor agonist
1. Closure of presynaptic calcium channels
2. Increased postsynaptic K+ conductance
3. Inhibition of dendritic calcium influx channels

ADR: Excessive weakness, rebound spasticity

55
Q

Benzodiazepines

MOA, ADR

A

MOA: Acts at GABAa
* Positively modulates opening of Cl- channels -> neuron hyperpolarizes

ADR: Sedation, abuse

56
Q

What are direct-acting muscle relaxant?

A

Dantrolene
Riluzole

57
Q

Dantrolene

MOA, ADR, BBW

A

MOA: acts at sarcoplasmic reticulum in skeletal muscle
* Binds to ryanodine receptor (calcium channel protein) to close channel -> inhibits release of calcium
* Acts directly on contractile mechanism of skeletal muscle to decrease force of contraction – w/o effects on neural pathways, neuromuscular junction or excitable properties of muscle fiber membranes
* Minimal effects on cardiac and smooth muscle (different ryanodine channel)

ADR: Non-specific on skeletal muscle -> AE = generalized muscle weakness
* Sedation

BBW: hepatotoxicity

58
Q

Riluzole

MOA, Indication

A

MOA: Blocks tetrodotoxin (TTX) sensitive sodium channels associated with damaged neurons
Indication: Amyotrophic lateral sclerosis (ALS)

Drug Action III (23 decks)

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