The document includes comprehensive Lecturi0 learning resources notes from modules 1-6. This includes knowledge check questions and answers, graphics, and tables. The document will significantly help in preparing for the midterm exam. The student scored a 98 using this guide.
Used in inflammation and for pain.
May also be used for a mild antipyretic effect.
Has also been used to inhibit polyp formation in familial adenomatous
polyposis.
Long-term use reduces the risk of colon cancer.
Note: While aspirin is also an NSAID, it is excluded from this lecture on
NSAIDs due to its distinct pharmacological properties and toxicity profile that
merit a dedicated discussion in a separate lecture.
Ibuprofen Naproxen, Indomethacin Ketorolac
piroxicam
Low potency, Low potency, Medium Medium
short-acting long-acting potency potency
Benefits Great anti- Greater
inflammatory analgesic
effect. effect.
Indicatio Headache, Arthritis, gout Arthritis Arthritis,
ns acute pain (severe), athletic injury
pericarditis
The only
NSAID is
available in
parenteral
form.
Adverse events/ toxicity
Shorter duration of antiplatelet effect.
o Smaller bleeding risk than ASA.
Increased GI toxicity (reduced gastric mucoprotection through PG
(prostaglandin)).
Increased renal risk (reduced PG-mediated autoregulation).
Excreted via the kidneys; chronic renal failure increases the risk of toxicity.
GI/ renal damage if parenteral ketorolac is administered >72 hours.
Hematologic reactions associated with Indomethacin.
Questions
Which NSAID is low potency and long-acting?
Naproxen
,What is NOT a side effect of most NSAIDs?
Increased risk of drowsiness.
Disease Modifying Anti Rheumatic Agents (DMARDs)
Cytotoxic
Methotrexate
Will often administer once weekly, with folate supplementation.
Antifolate drug; inhibits dihydrofolate reductase (DHFR).
o Reduction in thymidine synthesis (used in DNA).
Less thymidine means less expression of DNA fragments.
o Primary mechanism in chemotherapy.
Limits cancer cells from dividing because there's less DNA.
In rheumatoid arthritis – multiple mechanisms.
o Accumulation of adenosine.
o Inhibition of T cells.
o Suppression of intracellular adhesion molecules of T cells.
Making it where t cells cannot attach to their target.
o Inhibition of interleukin 1β binding to cell surface receptors.
The primary mechanism of how inflammation is occurring in
rheumatoid arthritis.
T-Lymphocyte Agents
Sulfasalazine
Metabolized to 5-ASA.
Works through an unknown mechanism.
Also used for Crohn’s disease.
Hydroxychloroquine
An antimalarial drug.
Works through an unknown mechanism, possibly through a reduction of
lysosome release of inflammatory factors.
Cyclosporine
Widely used in transplantation medicine.
Strong inhibitor of T-lymphocyte interleukins.
Interacts with multiple drugs; cyclosporine levels must be closely monitored.
o Cyclosporin toxicity and cyclosporin underutilization or low levels of
cyclosporin have the same type of clinical presentations, so sometimes
it's hard to tell apart toxicity from lack of effect.
Leflunomide
,Mycophenolate mofetil
Abatacept
B-Lymphocyte Agents
Rituximab
Monoclonal antibody.
Used in refractory cases of rheumatoid arthritis.
Binds to CD20 on B cells; prevents B cell activation.
Macrophage Agents
Gold sodium thiomalate
Aurothioglucose
Auranofin (oral) (rarely used)
Give once or twice a week IM injection.
Also used in treating TB.
Inhibits prostaglandin release and MHC (major histocompatibility complex)
interactions.
o Reduces macrophage activity.
Biologics
Infliximab, adalimumab, etanercept
Inhibits the actions of tumor necrosis factor α (TNF-α)
Anakinra
Interleukin-1 inhibitor reduces immune function in rheumatoid arthritis.
Questions
What best describes DMARDs?
DMARDS are cytotoxic drugs.
A 49-year-old woman with rheumatoid arthritis comes to the clinic.
Despite taking the maximum dosage of NSAIDs, she continues to
experience pain and morning stiffness, with occasional discomfort during
the day. She is interested in exploring a different medication. What is the
most appropriate next treatment option?
Methotrexate
Cyclosporine is a very useful medication to prevent organ transplant
rejection. What is required when prescribing this medication?
, Patients have to get their creatinine levels checked regularly.
What is the mechanism of action of rituximab?
Monoclonal antibody to CD20.
Acute and Chronic Muscle Spasms – Skeletal Muscle Relaxants
Neuromuscular Blockers Spasmolytics
Depolarizing Non- Acute use Chronic use
depolarizing
Succinylcholine Short-acting Cyclobenzaprine Actions via CNS
Rocuronium Baclofen
Intermediate- Diazepam
acting Tizanidine
Pancuroniu Actions at
m muscle
Pipecuroniu Dantrolene
m
Long-acting
Tubocurarin
e
Acute Muscle Spasm Agents
Cyclobenzaprine, metaxalone, methocarbamol, orphenadrine
Acute spasm due to muscle injury.
Sedative activity, antimuscarinic.
Act at the brainstem to reduce resting tone.
Does not work for patients with cerebral palsy or spinal cord injury.
Chronic Muscle Spasm Agents
Diazepam Baclofen Tizanidine
It acts at the GABA-A It acts at the GABA-B Acts at the α2 receptor in
receptor complex in the receptor complex in the the spinal cord.
brain and spinal cord. brain and spinal cord.
GABA-B complex - has two membrane-
spanning units that go back and forth
across the membrane. It is coupled to a
certain type of G protein.
o It inhibits voltage-gated calcium
channels and adenylyl cyclase.
o It activates certain types of
potassium channels.
Baclofen
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