P3 FINAL DRUGS TO KNOW

Identify the type of agent from below:

• Act on spinal cord interneurons and descending pathways 

• Specific receptor-mediated actions 

• Selectively inhibit motor reflexes via neurotransmitter systems 

Centrally acting agents

Identify the type of agent from below:

• t on polysynaptic reflex arcs in spinal cord and brainstem  

• Non-specific CNS depression 

• Generalized inhibition of interneuronal activity and transmission 

Polysynaptic acting agents

Identify the type of agent from below:

• Reduce hyper-reflexia and tone resulting from CNS damage 

• Induce moderate sedation 

Centrally acting agents

Identify the type of agent from below:

• Cause weakness at higher doses 

• Reach peak effect 1-2 hours after dosing 

• Induce rebound spasticity with acute withdrawal 

Centrally acting agents

Identify the type of agent from below:

• Reduce muscle guarding and local spasm 

• Frequently induce sedation which may limit use 

• Causes mild muscle relaxation with limited true weakness 

Polysynaptic acting agents

Identify the type of agent from below:

• Coordinate PT 1-2 hrs post-dose  

• Greater muscle relaxation with less fatigue and sedation seen later 

• Risk of sedation, dizziness, and impaired motor control 

Polysynaptic acting agents

Understanding the three doses of Aspirin: identify the reason and the COX associated

75 mg/day

Low dose

Cardioprotective (prevents blood clots; COX-1

Understanding the three doses of Aspirin: identify the reason and the COX associated

325–650 mg

Moderate dose

Analgesic and antipyretic (pain and fever relief); COX-;COX-2

Understanding the three doses of Aspirin: identify the reason and the COX associated

2,400 mg/day

High dose

Anti-inflammatory; COX-1;COX-2

In reality, both Cox-1 and Cox-2 mediate pain and inflammation, but ___ is more predominant.  

COX-2

Opioids are used by vein for….

post-operative analgesia

Opioid- local anesthetics are used locally via___ for regional analgesia (epidural).  

catheter

IDENTIFY what cox classification they belong to.

Aspirin (acetylsalicylic acid)

COX Classification

Primarily COX-1   (At typical doses)

IDENTIFY what cox classification they belong to.

Ibuprofen (Advil)  Naproxen (Aleve) Indomethacin (Indocin)  Piroxicam (Feldene)

Nonselective (COX-1 = COX-2) 

IDENTIFY what cox classification they belong to.

Diclofenac (Voltaren)  Etodolac (Lodine)

Relatively COX-2 Selective 

IDENTIFY what cox classification they belong to.

Celecoxib (Celebrex)

Highly COX-2 Selective  (Coxibs) 

COX-1 PGE₂ - Normal Effect

Gastric protection; Pain

COX-2 PGE₂ - Normal Effect

Inflammation; Pain

PGE₂ - NSAID Effect

↓ Pain; ↓ Inflammation; ↓ Fever

PGE₂ - Clinical Consequences (+)

Pain relief; Reduced inflammation

PGE₂ - Clinical Consequences (-)

Reduced gastric protection; Reduced renal blood flow

COX-2 PGI₂ - Normal Effect

Vasodilation; Prevents clotting

PGI₂ - NSAID Effect

↓ Vasodilation; ↓ Platelet inhibition

PGI₂ - Clinical Consequences (+)

None

PGI₂ - Clinical Consequences (-)

Increased risk of clotting; Hypertension; Reduced perfusion

COX-1 & COX-2 PGF₂α - Normal Effect

Smooth muscle contraction

PGF₂α - NSAID Effect

↓ Smooth muscle contraction

PGF₂α - Clinical Consequences (+)

Reduced menstrual cramps

COX-1 & COX-2 PGD₂ - Normal Effect

Allergic inflammation

PGD₂ - NSAID Effect

↓ Inflammatory signaling

PGD₂ - Clinical Consequences (+)

Possible reduction in inflammatory responses

COX-1 TXA₂ - Normal Effect

Vasoconstriction; Promotes clotting

TXA₂ - NSAID Effect

↓ Platelet aggregation; ↓ Vasoconstriction

TXA₂ - Clinical Consequences (+)

Reduced platelet clotting

TXA₂ - Clinical Consequences (-)

Increased bleeding risk

Class of Diazepam (Valium)

Centrally Acting Agents (Antispasm)

Class of Cyclobenzaprine (Flexeril); Metaxalone (Skelaxin); Orphenadrine (Norflex)

Polysynaptic Inhibitors (Antispasm)

Class of Diazepam (Valium); Baclofen (Lioresal); Tizanidine (Zanaflex)

Centrally Acting Agents (Antispasticity)

Comment-MOA: Diazepam (Valium)

GABA-A enhancer

Comment-MOA: Cyclobenzaprine (Flexeril)

TCA-like structure; adds anticholinergic properties

Comment-MOA: Orphenadrine (Norflex)

Antimuscarinic

Comment-MOA: Baclofen (Lioresal)

GABA-B enhancer

Comment-MOA: Tizanidine (Zanaflex)

Alpha-2 agonist (Presynaptic adrenergic)

Why are Biological DMARDS named that?

Produced using living cells

Which DMARDs does this MOA belong to:

targets specific immune protein, receptors, or cells

Biological DMARDs

Which DMARDs does this MOA belong to:

Most interfere with intracellular biochemical/immune processes

Non-Biological DMARDs

Administration of Biological DMARDS?

Injection or IV

Administration of Non-Biological DMARDs

Oral

Why are Non-Biological DMARDS named that?

produced through chemical synthesis

The following drugs are considered what type of drug?

Antimetabolites, Hydrixychloroquine, Azathiprine, Gold Therapy

Traditional (Non-Biological DMARDs)

What is the drug of choice for INITIAL RA TREATMENT in most patients ?

Methotrexate

Identify the drug based on the description:

• once weekly dosing

• folate antagonist

Methotrexate

Identify the drug based on the description:

• used in less severe disease or in combo

• MOA: inhibits immune cell function and Tcell activation

Hydroxychloroquine (Planquenil)

Identify the drug based on the description:

• Immunosuppressive drug

• inhibits purine synthesis

Azathioprine (Imuran)

Identify the drug based on the description:

• alters iflammatory and immune responses

• effects develop slowly: ORAL- 6-9 months, Inject- several month

Gold Therapy (auranofin (Ridaura))

Identify the drug based on the description:

• inhibits pyrimidine synthesis

• suppresses autoimmune inflammatory activity

  • Often combined with methotrexate

Leflunomide (Arava)

DMARDS are used to treate what ?

RA

Other DMARDs and Immunisuppressants are considered more…

toxic

this drug is an immunosuppressant[ and requires renal function and BP monitoring

• inhibits calcineruin

• decreases T-cell activation

Cyclosporine (Sandimmune)

Cyclophosphamide (Cytoxan) ia was type of agent?

Alkylating Agent [inhibits DNA replication]

The following medications are used to treat…

• aCETAMINOPHEN

• Oral NSAIDs

• Topical NSAIDs

• DMARDs

OA

what do OA DMARds like Viscosupplementaion do?

replace vsicocisty and lubrication of synovial fluid

Centrally acting agents and polysnaptic inhibitor are what kind of medications?

Anti-spasm Medication

Centrally acting agents are for are what kind of medications ones anti-spasm and the other?

Anti-Spastic Medication

Activate opioid receptors and produce analgesia effects.

• can produce significant repiratory depression and other adverse effects

Opioid agonist

Activates opioid receptors but to a lesser degree

• exhibit ceiling effect for some responses

Partial opioid agonist

Activates certain opioid receptor subtypes while blocking or partially activation others

• can interfere with full opioid agonists

Mixed agonist-antagonist

Bind opioid receptors with our producing typical opioid effects

• competitive antagonist

  • Naloxone

Opioid antagonist

Which opioid medications are classified as strong agonists?

Morphine; Fentanyl

Which medications are classified as mild-to-moderate opioid agonists?

Codeine; Hydrocodone

Which opioid is classified as a mixed agonist-antagonist?

Buprenorphine

Which opioid medication is classified as an antagonist?

Naloxone

What is the primary indication for strong opioid agonists such as morphine and fentanyl?

Severe pain

What is the primary indication for mild-to-moderate opioid agonists such as codeine and hydrocodone?

Moderate pain

What are the indications for buprenorphine (mixed agonist-antagonist)?

Pain relief; Opioid replacement therapy (ORT)

What are the indications for naloxone (opioid antagonist)?

Opioid overdose (OD); Opioid use disorder (OUD)

What is the major side effect of strong opioid agonists such as morphine and fentanyl?

Respiratory depression

What is the major side effect of mild-to-moderate opioid agonists such as codeine and hydrocodone?

Respiratory depression

What is the major side effect listed for buprenorphine (mixed agonist-antagonist)?

Psychosis

What major side effects are listed for naloxone (opioid antagonist)?

None

Which opioid receptor is located in the brain (especially the thalamus); spinal cord; and GI tract?

Mu (μ)

Which opioid receptor is located in the brain (limbic system and hypothalamus) and spinal cord?

Kappa (κ)

Which opioid receptor is located in the brain (limbic regions involved in emotion) and peripheral nervous system?

Delta (δ)

Which opioid receptor produces strong pain relief; euphoria; sedation; and respiratory depression?

Mu (μ)

Which opioid receptor produces moderate pain relief; sedation; dysphoria; and less euphoria than Mu?

Kappa (κ)

Which opioid receptor produces mild-to-moderate pain relief; mood modulation; and emotional regulation?

Delta (δ)

is the most important. It is responsible for strong pain relief, euphoria, sedation, and respiratory depression.  

Mu (μ)

Promotes inflammation and joint disease

Tumor necrosis factor-alpha (TNF-A)

Coordinates inflammatory and immune responses

Interleukins (ILs)

Contributes to inflammation and pain sensitization

Prostaglandins

Participate in inflammatory response

Leukotrienes

Degrade structural components of joint tissues

Proteases and collagenases

Used in less severe disease or in combination treatment

MOA

• Inhibits immune-cell function and reduces T-Cell activation

• Effects develop gradually – not for acute flare use

Hydroxychloroquine (Plaquenil)

Immunosuppressive drug

• Inhibits purine synthesis and cell proliferation

Azathioprine (Imuran)

Inhibits pyrimidine synthesis

• Reduces proliferation of activated lymphocytes

• Suppresses autoimmune inflammatory activity

Leflunomide (Arava)