What is the mechanism of action of NSAIDs?
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NSAIDs work by inhibiting cyclooxygenases (COX), which leads to a decrease in prostaglandins. This results in a reduction of pain and inflammation.
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What is the mechanism of action of NSAIDs?
NSAIDs work by inhibiting cyclooxygenases (COX), which leads to a decrease in prostaglandins. This results in a reduction of pain and inflammation.
What are the potential effects of COX-1 and COX-2 inhibition by NSAIDs?
What are the roles of NSAIDs in therapy?
NSAIDs are used for:
However, they do not have any effects on disease modification or progression.
What is the role of arachidonic acid in inflammation?
Arachidonic acid is metabolized into prostaglandins, which bind to various receptors, leading to inflammation and pain.
How do corticosteroids affect the metabolism of arachidonic acid?
Corticosteroids, specifically annexin A1, inhibit the enzyme phospholipase A2, which prevents the conversion of membrane phospholipids to arachidonic acid.
What is the effect of NSAIDs and aspirin on the COX enzymes?
NSAIDs and aspirin inhibit the activity of COX-1 and COX-2 enzymes, which are responsible for converting arachidonic acid into prostaglandins.
What are the main products of prostaglandin H2 metabolism and their tissue sources?
Product | Tissue Sources |
---|---|
Prostacyclin (PGI2) | Endothelium, kidney, brain |
Thromboxane A2 | Platelets, macrophages, kidney, smooth muscle |
Prostaglandin E2 | Brain, kidney, smooth muscle |
Prostaglandin F2alpha | Brain, kidney, smooth muscle |
What are the effects of Thromboxane (TxA₂) produced by COX-1 in platelets?
Thromboxane (TxA₂) leads to vasoconstriction and increased platelet aggregation, contributing to thrombosis.
What role do Prostaglandins E₂ and I₂ play in the gastric mucosa?
Prostaglandins E₂ and I₂ provide gastric protection in the gastric mucosa.
What are the effects of Prostaglandins E₂ and I₂ produced by COX-2 in joints?
Prostaglandins E₂ and I₂ are associated with pain and inflammation in joints.
What is the effect of Prostacyclin (PGI₂) produced by COX-2 in endothelial cells?
Prostacyclin (PGI₂) causes vasodilation and decreases platelet aggregation.
What are the main differences between COX-1 and COX-2 in terms of their expression and physiological effects?
Feature | COX-1 | COX-2 |
---|---|---|
Expression | Constitutively expressed | Induced during inflammation |
Physiological Effects | Vasoconstriction, platelet aggregation | Vasodilation, gastroprotection |
What are the characteristics and risks associated with COX-2 selective NSAIDs like Celecoxib?
COX-2 Selective NSAIDs (e.g., Celecoxib):
What defines semi-selective NSAIDs and what precautions should be taken when using them?
Semi-selective NSAIDs (e.g., Meloxicam, Diclofenac):
What are the implications of using nonselective NSAIDs like Ibuprofen and Naproxen in terms of cardiovascular and gastrointestinal risks?
Nonselective NSAIDs (e.g., Ibuprofen, Naproxen):
Aspirin:
What are the adverse effects of COX-1 inhibition by NSAIDs on the gastrointestinal mucosa?
Inhibition of COX-1 leads to:
What are the consequences of COX-1 and COX-2 inhibition by NSAIDs on kidney function?
Inhibition of COX-1 and COX-2 results in:
How does COX-2 inhibition by NSAIDs affect cardiovascular health?
COX-2 inhibition leads to:
What role does PGE2 play in the gastrointestinal system when COX-1 is active?
PGE2 is responsible for:
What is the effect of low dose aspirin on platelet function?
Low dose aspirin irreversibly inhibits platelet COX-1, which affects platelet aggregation and vasoconstriction.
What are the serious cardiovascular risks associated with NSAIDs according to the U.S. Boxed Warning?
The serious cardiovascular risks associated with NSAIDs include myocardial infarction (MI) and stroke.
What gastrointestinal risks are highlighted in the U.S. Boxed Warning for NSAIDs?
The gastrointestinal risks highlighted include serious gastrointestinal bleeding, ulcerations, and perforation. Elderly patients and those with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for these serious gastrointestinal events.
What is the mechanism of action of NSAIDs that leads to NSAID Induced Acute Kidney Injury (AKI)?
NSAIDs inhibit COX-1 and COX-2, resulting in decreased formation of PGE2 and PGI2. These prostaglandins are responsible for afferent arterial vasodilation. The decrease in PGE2 and PGI2 leads to vasoconstriction, which in turn causes decreased blood flow to the kidney.
What factors increase the risk of NSAID Induced Acute Kidney Injury (AKI)?
The risk of NSAID Induced AKI is increased when NSAIDs are taken with other medications that can:
What are the risk factors for NSAID induced peptic ulcer disease (PUD)?
The risk factors for NSAID induced peptic ulcer disease (PUD) include:
How can the addition of a PPI affect the risk of NSAID induced peptic ulcer disease?
The addition of a Proton Pump Inhibitor (PPI) can lower the risk of NSAID induced peptic ulcer disease (PUD) by reducing gastric acid secretion, thereby providing a protective effect on the gastric mucosa.
What is the mechanism of action that leads to hypersensitivity reactions to NSAIDs?
The mechanism involves excessive production of leukotrienes C, D, and E from arachidonic acid precursors, with leukotriene E being particularly responsible for anaphylaxis.
What are the types of reactions associated with hypersensitivity to NSAIDs?
The types of reactions include:
What patient conditions increase the risk of hypersensitivity to NSAIDs?
Patients are at increased risk if they have Samter's triad, which includes:
What is the mechanism of action of Ibuprofen?
Ibuprofen is a reversible inhibitor of COX-1 and COX-2 enzymes.
What are the clinical indications for using Ibuprofen?
Ibuprofen is used as an analgesic, anti-inflammatory, and antipyretic.
What is the recommended dosing for Ibuprofen?
The recommended dosing for Ibuprofen is 200-600 mg orally every 4-6 hours as needed, with a maximum dosing of 3.2 grams/day.
What are some adverse effects associated with Ibuprofen?
Adverse effects of Ibuprofen include:
What are some clinical pearls regarding the use of Ibuprofen?
Clinical pearls for Ibuprofen include:
What is the mechanism of action of Celecoxib?
Celecoxib is a selective inhibitor of COX-2, which helps reduce inflammation and pain without affecting COX-1, thus minimizing gastrointestinal side effects.
What are the common clinical indications for Celecoxib?
Celecoxib is used as an analgesic and a potent anti-inflammatory medication.
What is the recommended dosing schedule for Celecoxib in chronic pain management?
For chronic pain management, Celecoxib is typically dosed at 100-200 mg PO every 24 hours. For acute pain, it is dosed every 12 hours.
What are the major adverse effects associated with Celecoxib?
The major adverse effects of Celecoxib include:
What are some clinical pearls regarding the use of Celecoxib?
Clinical pearls for Celecoxib include:
What is the mechanism of action of Naproxen?
Naproxen works by reversibly inhibiting COX-1 and COX-2, which are enzymes involved in the inflammatory process.
What are the clinical indications for Naproxen?
Naproxen is indicated for use as an analgesic, antipyretic, and anti-inflammatory agent, and is also used for dysmenorrhea.
What is the recommended dosing for Naproxen?
The recommended dosing for Naproxen is 250-500 mg PO every 12 hours as needed, with a maximum dosing of 1.5 grams per day.
What are some adverse effects associated with Naproxen?
Adverse effects of Naproxen include an increased risk of cardiovascular events, gastrointestinal bleeding/ulcers, prolonged bleeding time, increased liver function tests (LFTs), and acute kidney injury (AKI).
What are some clinical pearls regarding Naproxen?
Naproxen can be obtained by prescription and over-the-counter (OTC). It is longer acting than ibuprofen but has a slower onset, which may not be ideal for acute settings.
What is the mechanism of action of Meloxicam?
Meloxicam exerts its effects through reversible inhibition of COX-2, which is more pronounced than its inhibition of COX-1.
What are the dosing recommendations for Meloxicam in oral and IV forms?
What are the clinical indications for Meloxicam?
Meloxicam is indicated for use as an analgesic and anti-inflammatory agent.
What are the common adverse effects associated with Meloxicam?
Common adverse effects include:
What are some clinical pearls regarding the use of Meloxicam?
What is the mechanism of action of Etodolac?
Etodolac works by reversibly inhibiting COX-1 and COX-2, which are enzymes involved in the inflammatory process.
What are the common clinical indications for Etodolac?
Etodolac is indicated for analgesic and anti-inflammatory purposes, particularly in cases of acute pain and osteoarthritis/rheumatoid arthritis (OA/RA).
What is the recommended dosing for Etodolac?
The recommended dosing for Etodolac is 200 – 400 mg PO every 6-8 hours as needed, with a maximum of 1 gram per day.
What are the potential adverse effects associated with Etodolac?
The potential adverse effects of Etodolac include:
What are some clinical pearls regarding the use of Etodolac?
Some clinical pearls for Etodolac include:
What is the mechanism of action of Indomethacin?
Indomethacin works by reversibly inhibiting COX-1 and COX-2, which are enzymes involved in the inflammatory process.
What are the common clinical indications for Indomethacin?
Indomethacin is used as an analgesic and has potent anti-inflammatory effects.
What are the dosing recommendations for Indomethacin immediate release capsules/suppositories?
The recommended dosing for Indomethacin immediate release capsules/suppositories is 25-50 mg BID-TID, with a maximum of 200 mg/day.
What are some adverse effects associated with Indomethacin?
Adverse effects of Indomethacin include:
What are some clinical pearls regarding Indomethacin?
Clinical pearls for Indomethacin include:
What is the mechanism of action of Diclofenac?
Diclofenac works by reversibly inhibiting COX-1 and COX-2 enzymes, which are involved in the inflammatory process.
What are the typical formulations and dosing for Diclofenac?
Diclofenac is typically used as a topical formulation such as gel, patch, or solution. For the 1% gel, a dosing card is used to measure the dose, with 2 grams corresponding to a strip 2.25 inches long, applied to the affected area.
What are the clinical indications for using Diclofenac?
Diclofenac is indicated for use as an analgesic and anti-inflammatory medication.
What are the common adverse effects associated with Diclofenac?
The most common adverse effect of Diclofenac is an application site reaction.
What are some clinical pearls regarding the use of Diclofenac?
Diclofenac can be obtained by prescription (Rx) and over-the-counter (OTC). It has a slow onset of action, so other NSAIDs are recommended for acute pain management.
What is the mechanism of action of Ketorolac?
Ketorolac works by reversibly inhibiting COX-1 and COX-2, which are enzymes involved in the inflammatory process.
What are the dosing recommendations for Ketorolac when administered IV/IM and PO?
IV/IM dosing: 15-30 mg IV every 6 hours as needed (maximum 120 mg/day).
PO dosing: 10 mg PO every 4-6 hours as needed (maximum 40 mg/day).
What are the clinical indications for Ketorolac?
Ketorolac is indicated for use as an analgesic and anti-inflammatory medication.
What are the adverse effects associated with Ketorolac?
Adverse effects of Ketorolac include:
What are the clinical pearls regarding the use of Ketorolac?
Key clinical pearls for Ketorolac include:
What is the mechanism of action of Aspirin in relation to COX enzymes?
Aspirin irreversibly inhibits COX-1 and COX-2, leading to the inhibition of thromboxane A2 formation, which in turn inhibits platelet aggregation.
What is the recommended daily dosing of Aspirin?
The recommended daily dosing of Aspirin is 81 mg taken orally.
What are the common adverse effects associated with Aspirin?
Common adverse effects of Aspirin include:
What are some clinical considerations when using Aspirin?
Clinical considerations for Aspirin use include:
What are some common products that contain salicylates?
Salicylates are found in various over-the-counter products, including:
What is the toxic dose range for the substance discussed in the mechanism of toxicity?
The toxic dose is between 150-300 mg/kg.
What are the effects of toxicity on organ systems due to the uncoupling of oxidative phosphorylation?
Toxicity affects multiple organ systems by causing:
What are the steps involved in anion gap metabolic acidosis?
What are the steps involved in respiratory alkalosis?
What are the initial steps in the management of a toxicological emergency?
Airway, breathing, circulation: Ensure the patient has a clear airway, is breathing adequately, and has stable circulation.
Decontamination: Administer activated charcoal at a dose of 1 gram/kg PO (up to 50 grams), ensuring the patient is alert or mechanically ventilated with an orogastric tube.
Alkalinization with sodium bicarbonate: Maintain serum pH between 7.45-7.5 and urine pH between 6-8 to enhance salicylate excretion.
Glucose administration: Provide glucose as toxicity may decrease cerebral glucose levels, even if blood glucose levels are normal.
Hemodialysis: Consider hemodialysis for severe cases.
What is the mechanism of action of acetaminophen?
The mechanism of action of acetaminophen is not well understood, but it is thought to impair prostaglandin (PG) synthesis.
What is the recommended dosing for acetaminophen?
The recommended dosing for acetaminophen is 500 – 1000 mg QID as needed, with a maximum dosing of 4000 mg/day.
What are the major adverse effects associated with acetaminophen?
The major adverse effects associated with acetaminophen include hepatic toxicity/liver failure, which is contraindicated in patients with liver disease, and caution is advised in patients with chronic alcohol use. Other adverse effects include nausea and vomiting.
What are some clinical pearls regarding acetaminophen use?
Some clinical pearls regarding acetaminophen use include:
What is the significance of APAP toxicity in the context of acute liver failure in the U.S.?
APAP toxicity is one of the leading causes of acute liver failure in the U.S., with over 100,000 overdoses and approximately 160 deaths annually, accounting for 5.4% of fatal exposures.
What is the toxic intermediate formed during the metabolism of acetaminophen that can lead to hepatotoxicity?
The toxic intermediate formed is N-acetyl-p-benzoquinoneimine (NAPQI).
Which enzyme is primarily responsible for the conversion of acetaminophen into NAPQI?
The enzyme primarily responsible for the conversion of acetaminophen into NAPQI is Cytochrome P-450.
What are the main detoxification pathways for acetaminophen metabolism?
The main detoxification pathways for acetaminophen metabolism include:
What percentage of acetaminophen is metabolized through the UDP-glucuronosyltransferase pathway?
Approximately 40-67% of acetaminophen is metabolized through the UDP-glucuronosyltransferase pathway.
What is the clinical significance of NAPQI in acetaminophen overdose?
The clinical significance of NAPQI in acetaminophen overdose is that it can cause hepatotoxicity, leading to liver damage and potentially liver failure if not treated promptly.
What is the mechanism of action of N-acetylcysteine (NAC)?
N-acetylcysteine (NAC) acts as a substrate/precursor of glutathione (GSH), detoxifying NAPQI to prevent hepatotoxicity.
What are the dosing regimens for N-acetylcysteine (NAC) for oral and intravenous administration?
Oral (PO) dosing regimen:
Intravenous (IV) dosing regimen:
What are some clinical pearls regarding the use of N-acetylcysteine (NAC)?
What is the mechanism of action of Tramadol?
Tramadol acts as a mu-opioid receptor agonist and is a weak inhibitor of norepinephrine and serotonin reuptake.
What is the recommended dosing for Tramadol?
The recommended dosing for Tramadol is 50-100 mg PO every 4-6 hours as needed, with a maximum dosing of 400 mg per day.
What are the common adverse effects associated with Tramadol?
Common adverse effects of Tramadol include constipation, vertigo, and headache.
What are the contraindications for using Tramadol?
Contraindications for Tramadol include:
What is the mechanism of action of corticosteroids in the immune response?
Corticosteroids are non-specific anti-inflammatory agents that inhibit both the innate and adaptive immune response. They achieve this through:
How do synthetic corticosteroids differ in their effects?
Synthetic corticosteroids differ in:
What are the glucocorticoid and mineralocorticoid activities of Fludrocortisone?
Fludrocortisone has a glucocorticoid activity of 10 and a mineralocorticoid activity of 125.
How does the glucocorticoid activity of Dexamethasone compare to that of Cortisone?
Drug | Glucocorticoid Activity |
---|---|
Dexamethasone | 25 |
Cortisone | 0.8 |
Which drug has the highest mineralocorticoid activity among the listed corticosteroids?
Fludrocortisone has the highest mineralocorticoid activity at 125 among the listed corticosteroids.
What is the glucocorticoid activity of Betamethasone and its mineralocorticoid activity?
Betamethasone has a glucocorticoid activity of 25 and a mineralocorticoid activity of 0.
Compare the glucocorticoid activities of Prednisone and Prednisolone. What are their values?
Drug | Glucocorticoid Activity |
---|---|
Prednisone | 4 |
Prednisolone | 4 |
What is the mineralocorticoid activity of Methylprednisolone?
Methylprednisolone has a mineralocorticoid activity of 0.5.
What is the equivalent dose and route of administration for Hydrocortisone?
Equivalent Dose: 20 mg Route: IV, PO
What are the clinical notes associated with Dexamethasone?
Dexamethasone is anti-inflammatory and is used when water retention is not desirable due to its lack of mineralocorticoid activity. It is typically used for short-term severe, acute conditions.
Compare the duration of action for Methylprednisolone and Triamcinolone.
Drug | Duration of Action (hours) |
---|---|
Methylprednisolone | 12-36 |
Triamcinolone | 12-36 |
What is the primary use of Prednisone in clinical settings?
Prednisone is suitable for long-term treatment as an anti-inflammatory and immunosuppressant due to its high glucocorticoid activity.
What is the equivalent dose of Betamethasone and its common route of administration?
Equivalent Dose: 0.6 mg Route: IV, PO, Topical
What are some short-term side effects of corticosteroids?
What are some long-term side effects of corticosteroids?
What is the mechanism of action of colchicine?
Colchicine prevents microtubule assembly and modulates multiple pro and anti-inflammatory pathways.
What is the recommended dosing for colchicine during an acute flare?
The recommended dosing for colchicine is 1.2 mg at the first sign of a flare, followed by 0.6 mg in one hour, totaling 1.8 mg.
What is a common adverse effect associated with colchicine?
A common adverse effect associated with colchicine is diarrhea.
What are the clinical pearls regarding the use of colchicine?
Colchicine does not lower uric acid levels; it is used for management of acute flare-ups and/or prevention. Additionally, watch for drug-drug interactions as it is a substrate for CYP3A4 metabolizing enzyme and p-gp, interacting with azoles, clarithromycin, HIV medications, and statins.
What is the mechanism of action of allopurinol?
Allopurinol is a xanthine oxidase inhibitor that prevents the formation of uric acid. It lowers urate levels within 7-14 days.
What is the role of allopurinol in therapy for chronic gout?
Allopurinol is used in combination with an anti-inflammatory agent (NSAID or colchicine) for 3-6 months to prevent flare-ups in chronic gout.
What is the initial dosing recommendation for allopurinol?
The initial dosing for allopurinol is 100 mg PO daily. It should be titrated by 100 mg every 1-4 weeks until reaching a target of 400-600 mg daily, with a goal uric acid level of <6.
What are the adverse effects associated with allopurinol?
The primary adverse effect of allopurinol is acute cutaneous reactions.
What clinical pearl should be considered before starting allopurinol in certain populations?
It is important to test for the HLA-B*5801 allele prior to starting allopurinol in Southeast-Asian and African American populations.
How does allopurinol compare to febuxostat in therapy?
Allopurinol is generally preferred over febuxostat in the management of chronic gout.
What is the mechanism of action of Febuxostat?
Febuxostat is a xanthine oxidase inhibitor that prevents the formation of uric acid.
What is the role of Febuxostat in the treatment of chronic gout?
Febuxostat is used as a second line treatment to allopurinol in chronic gout.
What is the recommended dosing for Febuxostat in chronic gout management?
The recommended dosing for Febuxostat is 40 mg PO daily, with titration every 2 weeks to a maximum of 80 mg per day. The goal uric acid level is < 6 mg/dL.
What are the adverse effects associated with Febuxostat?
Febuxostat has a black box warning linked to heart-related deaths. It is important to monitor AST/ALT levels during treatment.
What are some clinical pearls regarding the use of Febuxostat?
What is the mechanism of action of Probenicid in the treatment of gout?
Probenicid prevents the reabsorption of uric acid in the renal proximal tubules, promoting the excretion of uric acid.
In what clinical scenario is Probenicid typically used for gout management?
Probenicid is generally used for chronic gout management in patients with low or normal values for urinary uric acid excretion but serum hyperuricemia.
What is the recommended dosing for Probenicid?
The recommended dosing for Probenicid is 250 mg PO BID (twice a day).
What are some adverse effects associated with Probenicid?
Adverse effects of Probenicid include an increased risk of nephrolithiasis, rash, gastrointestinal upset, and headache.
What are the clinical pearls regarding the use of Probenicid?
Clinical pearls for Probenicid include:
What are the classifications of DMARDs and provide examples for each?
Classification | Examples |
---|---|
Conventional DMARDs | Methotrexate, Hydroxychloroquine, Leflunomide, Sulfasalazine |
Biologic DMARDs | TNF-alpha inhibitors (TNFi), Non-TNF Biologics (abatacept, rituximab, tocilizumab, anakinra), Tofacitinib |
What is the mechanism of action of Methotrexate?
Methotrexate inhibits dihydrofolate reductase, which leads to the inhibition of proliferation of rapidly dividing cells.
What is the role of Methotrexate in the treatment of rheumatoid arthritis (RA)?
Methotrexate is the first line treatment for moderate to severe disease activity in RA and studies suggest it reduces cardiovascular mortality compared to other DMARDs.
What is the typical dosing regimen for Methotrexate in rheumatoid arthritis?
The typical dosing for Methotrexate in RA is 7.5 - 15 mg orally once weekly, with a maximum of 25 mg weekly.
What are the contraindications for using Methotrexate?
Contraindications for Methotrexate include chronic liver disease, alcoholism, immunodeficiency, preexisting blood disorders, and pregnancy or breastfeeding.
How long does it typically take for Methotrexate to show its onset of action in rheumatoid arthritis treatment?
The onset of action for Methotrexate is typically 2-3 weeks.
What are the hepatic adverse events associated with Methotrexate toxicity?
What gastrointestinal adverse events can occur due to Methotrexate toxicity?
What hematologic adverse events are associated with Methotrexate toxicity?
What are the rare pulmonary adverse events linked to Methotrexate toxicity?
What is the recommended method to reduce adverse events when taking Methotrexate?
Folic Acid 5 mg PO once weekly, taken the day after Methotrexate administration.
What is the mechanism of action of Hydroxychloroquine (HCQ)?
The mechanism of action of Hydroxychloroquine (HCQ) is poorly understood, but it may interrupt antigen-antibody interactions at inflammation sites.
What is the role of Hydroxychloroquine in therapy for rheumatoid arthritis (RA) and lupus?
Hydroxychloroquine is a first-line treatment for low disease activity in rheumatoid arthritis (RA) patients and is also used in the treatment of lupus.
What is the onset of action for Hydroxychloroquine in treating RA?
The onset of action for Hydroxychloroquine in treating rheumatoid arthritis (RA) is approximately 6 weeks.
What is the recommended dosing for Hydroxychloroquine in RA patients?
The recommended dosing for Hydroxychloroquine in RA patients is 200-400 mg daily, either as a single dose or in 2 divided doses. However, due to the risk of retinal/ocular toxicity, patients should not exceed 5 mg/kg/day of actual body weight or 400 mg, whichever is lower.
What are some adverse effects associated with Hydroxychloroquine?
Adverse effects associated with Hydroxychloroquine include:
What is the mechanism of action of Leflunomide?
Leflunomide inhibits pyrimidine synthesis, leading to decreased lymphocyte proliferation and modulation of inflammation.
What is the recommended dosing for Leflunomide in rheumatoid arthritis (RA)?
The recommended dosing for Leflunomide in RA is 20 mg orally daily. The onset of action is approximately 1 month.
What are some adverse effects associated with Leflunomide?
Adverse effects of Leflunomide include pancytopenia, liver toxicity, interstitial lung disease (ILD), and hypertension.
What are the contraindications for using Leflunomide?
Contraindications for Leflunomide include:
What is the mechanism of action of Sulfasalazine and how does it relate to its prodrug status?
Sulfasalazine's mechanism of action is not well understood. It is a prodrug that is cleaved to sulfapyridine, which possesses antirheumatic properties.
What is the typical dosing regimen for Sulfasalazine in the treatment of rheumatoid arthritis?
The typical dosing for Sulfasalazine in rheumatoid arthritis is 0.5 to 1 gram taken orally daily. The onset of action is approximately 2 months.
What are some common adverse effects associated with Sulfasalazine?
Common adverse effects of Sulfasalazine include:
What are the contraindications for using Sulfasalazine?
The primary contraindication for Sulfasalazine is hypersensitivity to sulfa.
What is the mechanism of action of TNF Alpha Inhibitors (TNFi)?
TNF Alpha Inhibitors block the pro-inflammatory cytokine TNF-alpha, which plays a key role in inflammatory processes.
What are the available products of TNF Alpha Inhibitors and their efficacy?
The available TNF Alpha Inhibitors include:
All are considered to have similar efficacy in treating inflammatory arthritis, both for primary and secondary treatment failure.
What is the role of TNF Alpha Inhibitors in therapy?
TNF Alpha Inhibitors are reserved for treating moderate to severe inflammatory arthritis.
What are the common adverse effects associated with TNF Alpha Inhibitors?
Common adverse effects include:
What is the mechanism of action of Tofacitinib?
Tofacitinib is a janus kinase (JAK) inhibitor that inhibits signal transduction from pro-inflammatory cytokines and increases B cells. It is classified as a targeted synthetic DMARD.
What is the recommended dosing for Tofacitinib?
The recommended dosing for Tofacitinib is 5 mg orally twice daily (BID) or 11 mg extended-release (ER) once daily.
What are the major adverse effects associated with Tofacitinib?
The major adverse effects of Tofacitinib include: