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Ocular pharm '22 > *Analgesics > Flashcards

*Analgesics Flashcards

1
Q

5 Cardinal signs of inflammation

A
  • Heat
    • increased vascular perfusion - optimal temperatures for enzymatic activity
  • Red
    • local vasodilation facilitates swelling and immune cell infiltration to
      facilitate destruction or isolation of the pathogen and remove cell debris
  • Loss of function
    • local pain reduces mobility of the affected body area which
      limits movements that could aggravate preparative steps in tissue repair
  • Pain
    • physical swelling and released mediators from immune cells stimulate
      pain fibers
  • Swelling
    • exudation of plasma and proteins from locally dilated capillaries
      isolates the wound and pathogen and facilitates immune cell access
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2
Q

Inflammation

A
  • NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a ”rapid acting” (preformed), first responder transcription factor residing in the cytoplasm of all cells
  • In responsive to a variety of hyperosmolar tears(often associated with dry eye), harmful stimuli, and
    cytokines, NF-κB activation begins with the phosphorylation and
    subsequent degradation of its inhibitor proteins
  • Once activated, NF-κB initiates transcription of genes involved in
    inflammation, T-cell activation; innate and adaptive immune responses,
    cell survival responses, and cellular proliferation
  • Defective NF-κB activity is linked to cancer, inflammation, AI diseases,
    septic shock, and viral infection
  • MMP-9, an inducible(has to be synthesized first) matrix metalloproteinase, is another key player in
    the inflammatory response
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3
Q

Which autonomic responses are associated with pain?

A

(SNS, PNS shut down):

  • Tachycardia
  • Systemic hypertension
  • Tachypnea
  • Diaphoresis (cold sweat)
  • Pallor
  • Nausea
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4
Q

Therapeutic relief mechanisms for treating pain

A
  • Peripheral(directly at the source, i.e. hand),:
    • block pain mediators,
    • receptor sensitization
    • afferent neuronal discharge
  • Central:
    • block pain receptors in the CNS
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5
Q

Once activated NF-KB initiates transcription of genes involved in…

A
  • Inflammation
  • T-cell activation
  • Inate and adaptive immune responses
  • Cell survival responses
  • Cell proliferation
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6
Q

Defective NF-KB is linked to

A
  • Cancer
  • Septic shock
  • Inflammation
  • Viral infection
  • Auto immune diseases
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7
Q

Inflammatory pain mediators

A
  • Nociception - reception/sensation of harm/pain
  • Bradykinin, NE, and histamine stimulate pain fibers (likely a combination)
    • Bradykinin - RAAS → vasodilation, also produces pain
    • NE - SNS → pain linked to NE
    • Histamine - key molecule in allergic (type 1 sensitivity) reactions
  • Allodynia (an exaggerated pain response) can result when pain fibers are (hyper)sensitized by low pH, bradykinin, prostaglandins (PGs), leukotrienes (LTs), and Substance P
    • Inflammation leads to ↓ pH
    • Clinical application: eye → painful to touch
  • PGE2 & PGI2 (prostaglandins) promote pain and inflammation
  • Other Mediators:
    • Cytokines (interleukins, interferons, tumor necrosis factors, growth factors and chemokines)
    • Nitric Oxide (for good and bad → inflammation-induced pain → inflammation leads to iNOS [produces lots of NO, that now stimulate pain fibers])
    • Platelet Activating Factor (PAF)
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8
Q

Define allodynia

A
  • An exaggerated pain response can result when pain fibers are sensitized by low pH, bradykinin,
    prostaglandins leukotrienes, and Substance P
    • PGE2 & PGI2 promote pain and inflammation
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9
Q

Inflammation pathway

A

Leukotriene type 4 and Prostaglandin type 2 = pro inflammation

(even numbers = bad)

Leukotriene type 5 and Prostaglandin type 3 = anti-inflam

(Odd numbers = good)

PGI2 and TXA2 are physiologic antagonists

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10
Q

COX 1 vs COX 2

A

COX 1

  • Constitutive (housekeeping, always active) enzyme; predominantly
    involved in PG & TXA2 production
    • GI mucosa, vasculature, platelets, macrophages, kidneys

COX 2

  • Constitutive(pre-produced, ready to go) enzyme in the kidney
  • Inducible enzyme; predominantly involved in PG production
    • Generates pro-inflammatory PGs and O2 radicals
    • Creates pain and pyresis from inflammatory focus
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11
Q

Leukotrienes LTB4 , LTC4 and LTD4

A

LTB4

  • chemotactic by activating phagocytes and
    promoting neutrophil adhesion
  • key role in signalling to immune cells

LTC4 and LTD4

  • enhance histamine effects(itch,pain), bronchoconstrict,
    and constrict coronary arteries and dilate vessels in
    regions of inflammation

Pro-inflamation - 2 & 4

Anti-inflam - 3 & 5

(PGI2 is not pro-inflamatory

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12
Q

PG’s actions on kidney

A

PGE2 & PGI2 promote maintenance of renal blood flow by
stimulating renin release (ontributes to elevation in BP)

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13
Q

PG’s an TXA2 actions on vasculature

A
  • PGE2 causes edema (swelling) and vasodilation (redness)
  • PGI2 produces vasodilation
  • TXA2 (Thromboxane A2) is a vasoconstrictor

PGI 2 and TXA2 physiologic antagonists

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14
Q

PG’s and TXA2 actions on platelets

A
  • TXA2 promotes platelet aggregation
  • PGI2 inhibits platelets

NSAIDS and OMEGA 3 prevent TXA2

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15
Q

PG’s effect on GI tract

A
  • PGE1 & PGE2: production of cytoprotective GI mucous

• PGI2 (Prostacyclin): decrease GI acid secretion

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16
Q

PAFeffect on connective tissue

A

PAF (Platelet Activating Factor) activates matrix
metalloproteinases

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17
Q

PGE2 effect on CNS

A

PGE2 causes fever through the hypothalamus

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18
Q

PGF2A effects on reproduction

A

PGF2a causes suppression of spermatogenesis & uterine
contraction

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19
Q

Endogenous analgesics

A
  • Endorphins (natural opioid)
    • ​Induced by Tricyclic Antidepressants (TCADs)
    • Elevated in Cushing’s syndrome
  • Serotonin
    • ​A mood regulator; linked to depression and arousal
    • A short-term analgesic; counteracts Substance P
    • Induced by paracetamol(acetaminophen)
    • Reuptake is inhibited by Tramadol, selective serotonin
      reuptake inhibitors (SSRIs), and selective norepinephrine
      serotonin reuptake inhibitors (SNRIs)
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20
Q

** Acetylsalicylic Acid (Aspirin)

Dosing for

  1. Anti-platelet activity
  2. Analgesia
  3. Anti-pyretic (fever)
  4. Anti-inflammatory
A
  1. Anti-platelet - 80-160 mg
    • Irreversible inhibition of COX-1 (TXA2) for life of platelets
  2. Analgesia - 160-325 mg
    • Low intensity pain: central < peripheral
    • t1⁄2 2-3 hrs
  3. Anti-pyretic - 160-325 mg
    • t1⁄2 2-3 hrs
  4. Anti-inflammatory - 325-650 mg
    • t1⁄2 ~10 hrs

Lowdose-1st order

High dose- zero order

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21
Q

Mechanism of action of ASA (aspirin/acetylsalilicylic acid)

A

Irreversibly, non-selectively inhibits COX, reducing PG and
TXA2 synthesis

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22
Q

Adverse reactions of ASA (Aspirin/acetylsalicylic acid)

A
  • Common:
    • bleeding time doubles, headache
  • Serious:
    • Hypersensitivity: angioedema
  • Special: Reye’s Syndrome (35% mortality)

Topical Ophthalmic Drug Interactions
• None

Contraindications
• Hemorrhagic disorders
• Pregnancy, esp 3rd trimester

Ocular: Corneal denervation, dry eye

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23
Q

What medication is associated with corneal denervation?

A

Aspirin / acetylsalicylic acid

24
Q

What is Reye’s syndrome and which drug can cause it

A

nie vir kinders onder 16 aanbeveel

Reye’s syndrome

Adverse reaction in children taking ASA to reduce fever
in viral infections (eg. chicken pox or influenza)
• GI disturbances
• Liver degeneration
• Encephalopathy

35% mortality

25
Q

Indications of Celecoxib (COX 2 inhibitor)

A

Osteoarthritis:
• Rheumatoid arthritis:
• Ankylosing Spondylitis:
• Dysmenorrhea:
• Acute Pain:

26
Q

Mechanism of action of Celecoxib

A

Selectively inhibits COX-2 and reduces PG synthesis

*Sulpha based drug*

27
Q

Adverse reactions of Celecoxib (selective COX 2 inhibitor)

A
  • Common: headache
  • GIT: Bleed, ulceration/perforation
  • Black Box: Stroke, CHF, MI

CHF- congestive heart failure

MI - myocardial infarction

28
Q

Topical Ophthalmic Drug Interactions of Celecoxib (COX2 inhibitor)

A
  • Bromfenac, diclofenac, flurbiprofen, ketorolac, nepafenac: additive hemorrhage risk
  • • Naphazoline, tetrahydrozyline, phenylephrine (sympathomimetics): additive hypertensive risk
  • Cautions
    • Hypertension, smokers
29
Q

Indications of Acetaminophen (Paracetamol)

A

Pain and fever

Max dose per day : 4000mg

30
Q

Mechanism of action of Acetaminophen (Paracetamol)

A
  • Acts by inhibiting COX and enhancing 5-HT release (attenuates pain mediator generation)
  • Regulates body temperature by acting centrally at the hypothalamus; PG synthetase inhibition
31
Q

Adverse effects of acetaminiphen (paracetamol)

A

Common: headache

Topical Ophthalmic Drug Interactions
• None

Contraindications/Cautions
• No applicable ophthalmic conditions or findings

32
Q

ASA VS ACETAMINOPHEN

A
33
Q

Neurogenic pain responds best to which type of medications

A

Anticonvulsants and antidepressants

34
Q

Different pain killer profiles

A
35
Q

Other than analgesia, what can opioids be used for

A

As an antitussive(cough)

Anti-diarrheal

36
Q

Hydrocodone mechanism of action

(combined with acetaminophen)

A
  • Act through Gi -Protein-Coupled Mu, Kappa & Delta ‘opioid’ receptors; inhibit adenylyl cyclase activity; enhance K+ outflow/Ca++ inflow; hyperpolarize nerves affecting
    neuronal excitability and muscle tone
  • Stimulate prolactin and growth hormone release
37
Q

Adverse effects of hydrocodone

A
  • Common: pruritus & flushing (histamine release [little tolerance])
  • Ocular: miosis [no tolerance]
  • CNS: elevated intracranial pressure (enhanced with head injury)(all opioids)

Topical Ophthalmic Drug Interactions

  • None

Cautions

  • Mydriatic Procedures (antagonized)(Opioids cause miosis)
38
Q

Mechanism of action of tramadol (Only Shedule 4 opioid drug)

A
  • Agonist at mu receptors; effect is greater with active metabolite
  • Weak inhibitor of NE & 5-HT reuptake

Tramadol antagonizes ACh receptors

39
Q

Indications of tramadol (non-conventional opioid)

A

Moderate to severe pain

40
Q

Adverse reactions of tramadol (opioid)

A
  • headache,
  • pruritus,
  • flushing

Unlike most opioids, miosis is not listed as an adverse effect; mu selectivity effect

41
Q

TRAMADOL (opioid)

Topical Ophthalmic Drug Interactions

A
  • Betaxolol, carteolol, levobunolol, timolol (B-blockers): additive hypotension risk
  • Brimonidine for glaucoma: additive CNS/respiratory
    depression and hypotension risk
  • Atropine, homatropine, tropicamide (anticholinergics): additive constipation effects
42
Q

OPIOID OVERDOSE ANTIDOTE

A

Naloxone

43
Q

Mechanism of action of Naloxone (opioid antagonist)

A

Competitive antagonist of various opioid receptors

44
Q

Adverse reactions of naloxone

A

Hypertension

45
Q

NSAIDS vs OPIOIDS

A
46
Q

Cellular Phase of Acute Inflammation

A
  • Phagocytic extravasation from circulation: facilitates
    infiltration of the affected tissue site (swelling)
  • Chemotactic signalling serves to guide phagocytes to the
    inflammatory focus
  • Phagocytosis: of microbes, foreign bodies, and damaged cells
  • Formation of an exudate
47
Q

Neurogenic(nerve) pain responds best to:

A

Anticonvulsants

Antidepressants

(Cross BBB, affecting neurologic function and tramsmission)

48
Q

Nociceptive pain responds well to

A

NSAIDs, paracetamol, and opioids

(inhibit COX)

49
Q

Essential fatty acids

A

Omega 6 - pro inflammatory-prostaglandins2, TXA2, Leukotrines4

Omega 3- anti-inflam- prostaglandin3 TXA3,Leukotrine5

Pro-inflammatory eicosanoids are series 2 and 4<br></br>- Anti-inflammatory eicosanoids are series 3 and 5

  • Linoleic acid: vegetable, safflower oils
  • Y-Linolenic acid (GLA): evening primrose oil supplement
  • Arachidonic acid (AA): meat
  • Alpha-linolenic acid (ALA): green leafy vegetables, flax seed, canola, walnut, soybeans<br></br> o ALA are less efficient in anti-inflammatory than EPA
  • Eicosapentaenoic acid (EPA): oily fish, krill oil and algae
    • Taking EPA doesn’t slow down the Omega-6 pathway but they do quickly turn into anti-inflammatory products
  • Docosahexaenoic acid (DHA): a common supplement<br></br> - Delta-5-desaturase = much greater affinity for ETA than DGLA<br></br> o If you consume more omega-3 then the omega-6 pathway will essentially get shut down​
50
Q

Topical NSAIDs

A
  • Indications include intraoperative miosis prevention, post-op inflammation & CME, allergic conjunctivitis, inflammatory dry eye, corneal pain
  • Cystoid macular edema (CME) has an incidence of 0.1% following uncomplicated phacoemulsification cataract surgery
  • CME is linked to disruption of the BRB by PGs and other
    inflammatory mediators
51
Q

Topical NSAID’s adverse reactions

A
  • Burning, stinging
  • Corneal toxicity: superficial punctate keratopathy
  • Corneal infiltrates
  • Corneal melt (promoted w/ desensitization)
  • Vitreous detachment
  • Delayed wound healing
  • Prolonged bleeding time
  • Elevated IOP*
52
Q

Since ASA works peripherally ans acetaminophen works centrally, do they both work for treating fever?

A

Yes

53
Q

Which topical opthalmic drugs can cause corneal melt?

A

NSAIDs

54
Q

Which classification of NSAIDs is most common to topicals?

A

Acetic acid derivatives (bromfenac, diclofenac, amfenac)

55
Q

NSAIDs vs Steroids

A
56
Q

Which of the following is a prodrug:

  1. Flubiprofen
  2. Nepafenac
  3. Bromfenac
  4. Ketrolac
A

Nepafenac

Ocular pharm '22 (7 decks)

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