First line drugs:
Isoniazid, Rifampin, Ethambutol, Streptomycin, Pyrazinamide
Second line drugs:
Ethionamide, Cycloserine, Tetracycline, para-aminosalicylic acid, Amikacin, Fluoroquinolones
Showing posts with label Pharmacology. Show all posts
Showing posts with label Pharmacology. Show all posts
Saturday, April 16, 2011
Tuberculosis
Symptoms of tuberculosis:
Early symptoms:
Usually no symptoms develop but sometimes influenza is present.
Symptoms in second stage:
1. Low fever
2. Weight loss
3. Chronic fatigue
4. Heavy sweating especially at night
Later stages:
1. Cough with sputum that becomes progressively bloody, yellow, thick or grey
2. Chest pain
3. Shortness of breath
4. Reddish or cloudy urine
Early symptoms:
Usually no symptoms develop but sometimes influenza is present.
Symptoms in second stage:
1. Low fever
2. Weight loss
3. Chronic fatigue
4. Heavy sweating especially at night
Later stages:
1. Cough with sputum that becomes progressively bloody, yellow, thick or grey
2. Chest pain
3. Shortness of breath
4. Reddish or cloudy urine
Monday, April 11, 2011
Sulfinpyrazone
It is a derivative of phenylbutazone.
Mechanism of Action:
Same as that of probenecid.
Therapeutic Uses:
It is used for the treatment of Uric acid.
Pharmacokinetics:
It shows renal excretion.
Adverse effects:
Same as that of probenecid.
Mechanism of Action:
Same as that of probenecid.
Therapeutic Uses:
It is used for the treatment of Uric acid.
Pharmacokinetics:
It shows renal excretion.
Adverse effects:
Same as that of probenecid.
Probenecid
Action:
It acts generally as an inhibitor of the tubular secretion of organic acids.
Mechanism of action:
It causes blockage of resorption of uric acid by proximal tubular resorption.
Therapeutic Uses:
It is used for the treatment of Uric Acid.
Pharmacokinetics:
It is well absorbed by renal tubules. Its plasma half life is about 5-8.5 hours.
Adverse effects:
It may show gastric discomfort.
Interaction:
Probenecid stops tubular secretion of penicillin and that is why it sometimes is used for increasing the levels of the antibiotic.
It also inhibits excretion of naproxen, ketoprofen and indomethacin.
It acts generally as an inhibitor of the tubular secretion of organic acids.
Mechanism of action:
It causes blockage of resorption of uric acid by proximal tubular resorption.
Therapeutic Uses:
It is used for the treatment of Uric Acid.
Pharmacokinetics:
It is well absorbed by renal tubules. Its plasma half life is about 5-8.5 hours.
Adverse effects:
It may show gastric discomfort.
Interaction:
Probenecid stops tubular secretion of penicillin and that is why it sometimes is used for increasing the levels of the antibiotic.
It also inhibits excretion of naproxen, ketoprofen and indomethacin.
Uricosuric agents
The uricosuric drugs are weak organic acids that cause an increased uric acid clearance through kidneys by stoping urate anion exchanger in the proximal convulated tubule of nephron that mediates the reabsorption of urate crystals (i.e. uricosuric agents act at the anionic transport site of renal tubule).
It includes1. Probenecid
2. Sulfinpyrazone
Allopurinol
Introduction:
Allopurinol is a purine analog. It is also an isomer of hypoxanthine.
Mechanism of action:
Allopurinol inhibits xanthine oxidase enzyme which is required for the synthesis of Uric acid. This enzyme is required when purine is oxidized to Uric acid.
Therapeutic uses:
This is effective in the treatment of gout, which may be due to;
1. Primary hyperuricemia
2. Secondary hyperuricemia (Such as those caused from the use of chemotherapeutic agents or diseases of the kidneys).
It is also effective as an anti-protozoal agent.
Pharmacokinetics:
It is well absorbed (approximately 70-85%) orally. One of its metabolite is alloxanthine (also called as oxypurinol) which is also effective in the inhibition of xanthine oxidase. Allopurinol takes action along with this metabolite.
The plasma half life of allopurinol is 2 hours and that of oxypurinol is 15 hours. The drug and its metabolites are excreted in the urine and feces.
Dosage:
Due to the long half life of oxypurinol the dosage can be maintained at the rate of 1 dose/day. Its initial dose is 100 mg/day.
Adverse effects:
Hypersensitivity reactions such as rashes may occur. GI disturbances such as nausea and diarrhea can also be there.
Interactions:
It may cause an increase of the effect of cyclophosphamide. It may interfere with anti-cancer drugs such as 6-mercaptopurine and the immunosuppressant such as azathioprine.
Allopurinol is a purine analog. It is also an isomer of hypoxanthine.
Mechanism of action:
Allopurinol inhibits xanthine oxidase enzyme which is required for the synthesis of Uric acid. This enzyme is required when purine is oxidized to Uric acid.
This is effective in the treatment of gout, which may be due to;
1. Primary hyperuricemia
2. Secondary hyperuricemia (Such as those caused from the use of chemotherapeutic agents or diseases of the kidneys).
It is also effective as an anti-protozoal agent.
Pharmacokinetics:
It is well absorbed (approximately 70-85%) orally. One of its metabolite is alloxanthine (also called as oxypurinol) which is also effective in the inhibition of xanthine oxidase. Allopurinol takes action along with this metabolite.
The plasma half life of allopurinol is 2 hours and that of oxypurinol is 15 hours. The drug and its metabolites are excreted in the urine and feces.
Dosage:
Due to the long half life of oxypurinol the dosage can be maintained at the rate of 1 dose/day. Its initial dose is 100 mg/day.
Adverse effects:
Hypersensitivity reactions such as rashes may occur. GI disturbances such as nausea and diarrhea can also be there.
Interactions:
It may cause an increase of the effect of cyclophosphamide. It may interfere with anti-cancer drugs such as 6-mercaptopurine and the immunosuppressant such as azathioprine.
Colchicine
Introduction:
It is an alkaloid obtained from plant, Colchicum autumnale. It has been found effective in the treatment of acute gout.
Mechanism of action:
It causes the disruption of cellular activities such as movement of granulocytes to the affected area and phagocytosis. It also inhibits the synthesis and release of leukotriene B4.
Action:
It relieves pain. Though it cannot prevent the progression of gout to acute gouty attacks but it is used as a prophylactic drug in this case so helps to keep down pain and frequency of acute attacks. It is now used in combination with probenecid.
Indomethacin is now replacing Colchicine.
Therapeutic Uses:
It is used for the relief of pain and inflammation in acute gout within 12-24 hours.
Pharmacokinetics:
It is absorbed rapidly from GI tract. Its peak plasma level is attained within 2 hours. Its plasma half life is 9 hours. It is recycled in the bile and excreted unchanged in the feces or urine.
Dosage:
The usual dosage of colchicines is 0.6 mg one to three times daily as a prophylaxis of gout.
Adverse effects:
It may cause nausea, vomiting, abdominal pain and diarrhea.
Prolonged administration may cause myopathy, aplastic anemia and alopecia.
Contraindications:
It is contraindicated in pregnancy.
Precautions:
It should be used with caution in hepatic, renal or cardiovascular diseases.
It is an alkaloid obtained from plant, Colchicum autumnale. It has been found effective in the treatment of acute gout.
Mechanism of action:
It causes the disruption of cellular activities such as movement of granulocytes to the affected area and phagocytosis. It also inhibits the synthesis and release of leukotriene B4.
It relieves pain. Though it cannot prevent the progression of gout to acute gouty attacks but it is used as a prophylactic drug in this case so helps to keep down pain and frequency of acute attacks. It is now used in combination with probenecid.
Indomethacin is now replacing Colchicine.
Therapeutic Uses:
It is used for the relief of pain and inflammation in acute gout within 12-24 hours.
Pharmacokinetics:
It is absorbed rapidly from GI tract. Its peak plasma level is attained within 2 hours. Its plasma half life is 9 hours. It is recycled in the bile and excreted unchanged in the feces or urine.
Dosage:
The usual dosage of colchicines is 0.6 mg one to three times daily as a prophylaxis of gout.
Adverse effects:
It may cause nausea, vomiting, abdominal pain and diarrhea.
Prolonged administration may cause myopathy, aplastic anemia and alopecia.
Contraindications:
It is contraindicated in pregnancy.
Precautions:
It should be used with caution in hepatic, renal or cardiovascular diseases.
Gout
Purine metabolism is responsible for the production of Sodium urate. When the quantity of Urate in the blood goes up than normal, it may result in gout which may show inflammation and produces more oxygen metabolites in the blood.
Other ways of therapy include:
1. Disturbing uric acid synthesis with the help of allopurinol.
2. Promoting excretion of uric acid with probenecid or sulfinpyrazone.
3. Use of NSAIDs.
Types of Gout:
There are two types of gout:
1. Acute gout.
2. Chronic gout.
Acute gout:
Causes:
The main causes of acute gout are as follows:
1. Diet which is rich in purine.
2. Kidney diseases.
3. Alcohol consumption.
Treatment:
In this we can use Indomethacin in combination with Aspirin. Indomethacin slows the movement of granulocytes in the area which is affected and aspirin decreases pain and inflammation.
Chronic gout:
Causes:
The main causes of chronic gout are as follows:
1. Genetic defect.
2. Renal deficiency
3. Lesch Nyhan syndrome.
4. Excessive synthesis of uric acid associated with cancer chemotherapy.
Treatment:
In this we can use Uricosuric drugs such as probenecid and sulfinpyrazone and Allopurinol.
Uricosuric drugs (e.g. Probenecid or sulfinpyrazone) promote excretion of uric acid resulting in reduced concentration of uric acid in plasma. It is preferred for patients with normal excretion of uric acid through urine.
Allopurinol selectively inhibits some steps in the middle of the biosynthesis of uric acid. It is preferred for patients with excessive uric acid excretion (which may be due to renal insufficiency).
Therapeutic strategies:
First of all it is better to use purine free diet i.e. we must use dairy products, fruits and cereals. The sequence, in the diagram, show that most effective medicine in treating gout is that which causes reduced entry of leukocyte into the affected joint which may be achieved by colchicine.
First of all it is better to use purine free diet i.e. we must use dairy products, fruits and cereals. The sequence, in the diagram, show that most effective medicine in treating gout is that which causes reduced entry of leukocyte into the affected joint which may be achieved by colchicine.
Other ways of therapy include:
1. Disturbing uric acid synthesis with the help of allopurinol.
2. Promoting excretion of uric acid with probenecid or sulfinpyrazone.
3. Use of NSAIDs.
Types of Gout:
There are two types of gout:
1. Acute gout.
2. Chronic gout.
Acute gout:
Causes:
The main causes of acute gout are as follows:
1. Diet which is rich in purine.
2. Kidney diseases.
3. Alcohol consumption.
Treatment:
In this we can use Indomethacin in combination with Aspirin. Indomethacin slows the movement of granulocytes in the area which is affected and aspirin decreases pain and inflammation.
Chronic gout:
Causes:
The main causes of chronic gout are as follows:
1. Genetic defect.
2. Renal deficiency
3. Lesch Nyhan syndrome.
4. Excessive synthesis of uric acid associated with cancer chemotherapy.
Treatment:
In this we can use Uricosuric drugs such as probenecid and sulfinpyrazone and Allopurinol.
Uricosuric drugs (e.g. Probenecid or sulfinpyrazone) promote excretion of uric acid resulting in reduced concentration of uric acid in plasma. It is preferred for patients with normal excretion of uric acid through urine.
Allopurinol selectively inhibits some steps in the middle of the biosynthesis of uric acid. It is preferred for patients with excessive uric acid excretion (which may be due to renal insufficiency).
Anakinra
Introduction:
Anakinra is an IL-1 receptor antagonist.
Action:
The treatment with this drug causes slowing of process of moderate to serious rheumatoid arthritis.
The drug may be used alone or in combination with other drugs.
Administration:
It is administered subcutaneously.
Adverse effects:
It may cause headache, nausea, vomiting and injection site reactions.
Anakinra is an IL-1 receptor antagonist.
Action:
The treatment with this drug causes slowing of process of moderate to serious rheumatoid arthritis.
The drug may be used alone or in combination with other drugs.
Administration:
It is administered subcutaneously.
Adverse effects:
It may cause headache, nausea, vomiting and injection site reactions.
Adalimumab
Introduction:
It is a fully human recombinant monoclonal antibody (MAB).
Mechanism of action:
It gets bind to human TNF-α receptor site thus stops endogenous TNF- α activity by preventing its interaction with p55 and p75 cell surface receptors.
Action:
It decreases symptoms of Rheumatoid arthritis and stops erosion of the (bone) structure.
Therapeutic uses:
It is used in Rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. (As increased TNF in the synovial fluid cause pain and joint destruction in Rheumatoid arthritis).
Pharmacokinetics:
It is used subcutaneously and its half life is 10-20 days.
Dose and Administration:
Its usual dose is 40 mg every other week. It is used Subcutaneously only.
Adverse effects:
It may cause headache, nausea, rashes and reactions at the site of injection.
It is a fully human recombinant monoclonal antibody (MAB).
Mechanism of action:
It gets bind to human TNF-α receptor site thus stops endogenous TNF- α activity by preventing its interaction with p55 and p75 cell surface receptors.
Action:
It decreases symptoms of Rheumatoid arthritis and stops erosion of the (bone) structure.
Therapeutic uses:
It is used in Rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. (As increased TNF in the synovial fluid cause pain and joint destruction in Rheumatoid arthritis).
Pharmacokinetics:
It is used subcutaneously and its half life is 10-20 days.
Dose and Administration:
Its usual dose is 40 mg every other week. It is used Subcutaneously only.
Adverse effects:
It may cause headache, nausea, rashes and reactions at the site of injection.
Infliximab
Introduction:
It is a chimeric IgGκ monoclonal antibody made up of human (75%) and animals (25%) such as rats and mice.
Mechanism of Action:
Infliximab binds to human TNF-α and as a result neutralize the cytokines.
Action:
It removes the progression of damage or erosion to structure so that patient can perform functions more efficiently.
Pharmacokinetics:
It is administered intravenously and slowly in about 2 hour’s time in doses of 3 mg/kg to 10 mg/kg. Its half life is about 9-10 days. It is distributed equally in vascular compartments.
It is not approved for therapy continuously after 6th week.
Therapeutic uses:
It is used in Rheumatoid arthritis and Crohn’s disease. It has been found that the combination with methotrexate is more effective.
Adverse effects:
It may cause upper respiratory tract infections, nausea and vomiting. The production of anti-infliximab antibodies have also been studied after prolonged use of infliximab. It may cause some of the reactions at the site of infusion such as fever, chill and pruritis.
Leukopenia, neutropenia and thrombocytopenia have also been found.
It is a chimeric IgGκ monoclonal antibody made up of human (75%) and animals (25%) such as rats and mice.
Mechanism of Action:
Infliximab binds to human TNF-α and as a result neutralize the cytokines.
Action:
It removes the progression of damage or erosion to structure so that patient can perform functions more efficiently.
Pharmacokinetics:
It is administered intravenously and slowly in about 2 hour’s time in doses of 3 mg/kg to 10 mg/kg. Its half life is about 9-10 days. It is distributed equally in vascular compartments.
It is not approved for therapy continuously after 6th week.
Therapeutic uses:
It is used in Rheumatoid arthritis and Crohn’s disease. It has been found that the combination with methotrexate is more effective.
Adverse effects:
It may cause upper respiratory tract infections, nausea and vomiting. The production of anti-infliximab antibodies have also been studied after prolonged use of infliximab. It may cause some of the reactions at the site of infusion such as fever, chill and pruritis.
Leukopenia, neutropenia and thrombocytopenia have also been found.
Etanercept
Introduction:
Etanercept is a biotechnological product as it is genetically engineered fusion protein.
It is composed of:
1. Two identical chains of the recombinant human TNF-receptor p75 monomer.
2. Fc domain of IgG1 (human immunoglobulin).
These two are fused together.
Mechanism of action:
Etanercept binds two molecules of TNF thereby resulting in no binding of TNF to cellular receptors.
Action:
Etanercept, Infliximab and adalimumab decrease the activity of TNF. TNF is important for immunity system and must rest in the rheumatic synovium for the action to take place.
Pharmacokinetics:
It is given subcutaneously, 25 mg, two times a week. Maximum serum concentration is obtained within 72 hours after parenteral administration. Its half life is 4-6 days.
Therapeutic Uses:
Rheumatic and psoriatic arthritis.
Adverse effects:
No important adverse effects have been found.
Contraindications:
In serious type of infections like sepsis, etanercept should not be given to patient.
NOTE:
Etanercept and methotrexate are more effective when used together (than alone) in slowing the
1. Disease process
2. Improvement in function
3. Stoppage of the symptoms.
Etanercept is a biotechnological product as it is genetically engineered fusion protein.
It is composed of:
1. Two identical chains of the recombinant human TNF-receptor p75 monomer.
2. Fc domain of IgG1 (human immunoglobulin).
These two are fused together.
Mechanism of action:
Etanercept binds two molecules of TNF thereby resulting in no binding of TNF to cellular receptors.
Action:
Etanercept, Infliximab and adalimumab decrease the activity of TNF. TNF is important for immunity system and must rest in the rheumatic synovium for the action to take place.
Pharmacokinetics:
It is given subcutaneously, 25 mg, two times a week. Maximum serum concentration is obtained within 72 hours after parenteral administration. Its half life is 4-6 days.
Therapeutic Uses:
Rheumatic and psoriatic arthritis.
Adverse effects:
No important adverse effects have been found.
Contraindications:
In serious type of infections like sepsis, etanercept should not be given to patient.
NOTE:
Etanercept and methotrexate are more effective when used together (than alone) in slowing the
1. Disease process
2. Improvement in function
3. Stoppage of the symptoms.
Anticytokine Therapies in Rheumatoid Arthritis
Anticytokines act on the proinflammatory cytokines i.e. interleukin-1b (IL- 1b) and Tumor necrosis factor- α (TNF- α).
Gold salts
Gold compounds are of two types:
1. Those used for intramuscularly such as gold sodium thiomalate and aurothioglucose. They are made up of about 50% elemental gold.
2. Those used in oral formulation such as auranofin containing 26-29% elemental gold.
Mechanism of action:
It is thought that these gold compounds are taken up by macrophages and thus suppresses the phagocytosis and lysosomal enzyme activity.
This process is responsible for the reduction of bone and articular destruction.
Pharmacokinetics:
They tend to accumulate in the synovial fluid and bone marrow. 1/3 of the gold compounds are excreted in the urine and remaining goes through feces.
Adverse effects:
Pruritic (itching) skin rashes may occur.
1. Those used for intramuscularly such as gold sodium thiomalate and aurothioglucose. They are made up of about 50% elemental gold.
2. Those used in oral formulation such as auranofin containing 26-29% elemental gold.
Mechanism of action:
It is thought that these gold compounds are taken up by macrophages and thus suppresses the phagocytosis and lysosomal enzyme activity.
This process is responsible for the reduction of bone and articular destruction.
Pharmacokinetics:
They tend to accumulate in the synovial fluid and bone marrow. 1/3 of the gold compounds are excreted in the urine and remaining goes through feces.
Adverse effects:
Pruritic (itching) skin rashes may occur.
D-Penicillamine
It is a metabolite of penicillin and an analog of cysteine (an amino acid).
Action:
It slows the advancement of the bone erosion and rheumatoid arthritis.
Adverse effects:
It may cause some of the very serious effects such as some of the dermatologic problems, nephritis and aplastic anemia.
Action:
It slows the advancement of the bone erosion and rheumatoid arthritis.
Adverse effects:
It may cause some of the very serious effects such as some of the dermatologic problems, nephritis and aplastic anemia.
Chloroquine and hydroxychloroquine
These drugs are mainly used in malaria.
Mechanism of action:
These drugs may cause the lowering of T lymphocytes for action in Rheumatoid arthritis.
Action:
These drugs are used in Rheumatoid arthritis, when NSAIDs are not effective to that extent. They may be used alone or in combination with other NSAIDs. When it is used in combination it must be used in lower doses.
These drugs slow the gradual change in the bones due to continuous wear & tear and sometimes they may cause temporary disappearance of the disease.
Adverse effects:
This may cause ocular toxicity, nausea, vomiting and dyspepsia.
Mechanism of action:
These drugs may cause the lowering of T lymphocytes for action in Rheumatoid arthritis.
Action:
These drugs are used in Rheumatoid arthritis, when NSAIDs are not effective to that extent. They may be used alone or in combination with other NSAIDs. When it is used in combination it must be used in lower doses.
These drugs slow the gradual change in the bones due to continuous wear & tear and sometimes they may cause temporary disappearance of the disease.
Adverse effects:
This may cause ocular toxicity, nausea, vomiting and dyspepsia.
Sunday, April 10, 2011
Leflunomide
Leflunomide is a drug that causes modification of the immune system while undergoing treatment (this modification or alteration is a part of the treatment so that is why it is also called as immunomodulatory agent) and disease modifying anti-rheumatic agent.
Mechanism of action:
Leflunomide causes inhibition of:
1. Multiplication or propagation of T cells
2. Production of autoantibodies by B cells.
Leflunomide inhibit the enzyme Dihydroorotate dehydrogenase (DHODH). This causes Uridine 5’-monophosphate (UMP) not to be produced.
UMP is essential in two ways:
1. It is an important component of RNA synthesis.
2. It is pioneer in making nucleotide which is composed of thymidine, which is required for DNA synthesis.
As a result there is a cell arrest.
It is a reversible inhibitor of DHODH. It helps to reduce pain and inflammation and along with this function it also helps to reduce the decay or erosion cause to the bones or any other body parts due to inflammation.
It can be used alone or in combination with other drugs like methotrexate.
Pharmacokinetics:
It is well absorbed orally. Its half life is 13-19 days. The binding of this drug to serum albumin is about more than 85%. It is excreted both through biliary and renal excretion. It readily converts to metabolites and the metabolites are excreted in the urine and feces.
The metabolite which is still effective goes back to do some work. Cholestyramine enhances leflunomide excretion.
Adverse effects:
It may cause headache, diarrhea (loose bowels) and nausea. Alopecia, Weight loss or weight gain and allergic reactions like skin rash are its rare side affects.
Contraindications:
It is contraindicated in pregnancy.
Precautions:
As this drug may cause an increase in liver enzyme level so it must be used with caution in liver diseases.
Mechanism of action:
Leflunomide causes inhibition of:
1. Multiplication or propagation of T cells
2. Production of autoantibodies by B cells.
Leflunomide inhibit the enzyme Dihydroorotate dehydrogenase (DHODH). This causes Uridine 5’-monophosphate (UMP) not to be produced.
UMP is essential in two ways:
1. It is an important component of RNA synthesis.
2. It is pioneer in making nucleotide which is composed of thymidine, which is required for DNA synthesis.
As a result there is a cell arrest.
Action:
It is a reversible inhibitor of DHODH. It helps to reduce pain and inflammation and along with this function it also helps to reduce the decay or erosion cause to the bones or any other body parts due to inflammation.
It can be used alone or in combination with other drugs like methotrexate.
Pharmacokinetics:
It is well absorbed orally. Its half life is 13-19 days. The binding of this drug to serum albumin is about more than 85%. It is excreted both through biliary and renal excretion. It readily converts to metabolites and the metabolites are excreted in the urine and feces.
The metabolite which is still effective goes back to do some work. Cholestyramine enhances leflunomide excretion.
Adverse effects:
It may cause headache, diarrhea (loose bowels) and nausea. Alopecia, Weight loss or weight gain and allergic reactions like skin rash are its rare side affects.
Contraindications:
It is contraindicated in pregnancy.
Precautions:
As this drug may cause an increase in liver enzyme level so it must be used with caution in liver diseases.
Methotrexate
It is thought that methotrexate is the cornerstone of the therapy for the patients, who have not responded well to other NSAIDs in severe rheumatoid arthritis or psoriatic arthritis.
Action:
As this is an immunosuppressant, this may be responsible for its effectiveness in reducing arthritis which according to some experts is an autoimmune disease.
Methotrexate slows the decay within moving joints, which may be due to the inhibition of thymidylate synthetase and some other related enzymes.
Pharmacokinetics:
The drug is found to be absorbed about 65%-75% after oral administration. Its serum half life is about 6-9 hours.
It has been found that methotrexate shows response usually sooner than the other agents i.e. it may be within 3 to 6 weeks of treatment.
Dosage:
Small doses are effective for the treatment of Arthritis than those needed for the treatment of cancer as this drug is also useful for the treatment of cancer. The dose is reduced to once a week administration.
Adverse Effects:
In small doses it may cause mucosal ulceration and nausea. Some of the following adverse effects may also be seen:
1. Cytopenia
2. Liver cirrhosis (it is particularly dose related)
3. Pneumonia like syndrome (hypersensitivity lung reaction)
Action:
As this is an immunosuppressant, this may be responsible for its effectiveness in reducing arthritis which according to some experts is an autoimmune disease.
Methotrexate slows the decay within moving joints, which may be due to the inhibition of thymidylate synthetase and some other related enzymes.
Pharmacokinetics:
The drug is found to be absorbed about 65%-75% after oral administration. Its serum half life is about 6-9 hours.
It has been found that methotrexate shows response usually sooner than the other agents i.e. it may be within 3 to 6 weeks of treatment.
Dosage:
Small doses are effective for the treatment of Arthritis than those needed for the treatment of cancer as this drug is also useful for the treatment of cancer. The dose is reduced to once a week administration.
Adverse Effects:
In small doses it may cause mucosal ulceration and nausea. Some of the following adverse effects may also be seen:
1. Cytopenia
2. Liver cirrhosis (it is particularly dose related)
3. Pneumonia like syndrome (hypersensitivity lung reaction)
Disease modifying anti-rheumatic agents
Disease modifying anti-rheumatic drugs (DMARDs) or slow acting anti-rheumatic drugs (SAARDs)
1. Slow the course of the disease and can induce remission.
2. Reduce or prevent the joint damage.
Drugs to be choosen:
Many experts start therapy with the conventional drugs i.e. methotrexate or hydroxychloroquine. But if these do not work properly then they go to the newer agents i.e. anakinra, adalimumab, leflunomide, and infliximab. Often it is also prescribed that the combination therapy is more effective.
1. Slow the course of the disease and can induce remission.
2. Reduce or prevent the joint damage.
Drugs to be choosen:
Many experts start therapy with the conventional drugs i.e. methotrexate or hydroxychloroquine. But if these do not work properly then they go to the newer agents i.e. anakinra, adalimumab, leflunomide, and infliximab. Often it is also prescribed that the combination therapy is more effective.
Acetaminophen
Action:
It inhibits prostaglandin synthesis in CNS (so analgesic and anti-pyretic) but has less effect on COX so (weak anti-inflammatory).
Therapeutic Uses:
It is used as analgesic and anti-pyretic. It is analgesic /anti-pyretic of choice for children with viral infections or chicken pox.
Drug interactions:
It does not antagonize the uricosuric agent (probenecid) and so may be used in patients with gout who are taking this drug.
Pharmacokinetics:
Rapidly absorbed from GI tract. 1st pass metabolism occurs in the luminal cells of the intestine and in the hepatocytes. It is conjugated in the liver to form inactive glucoronidated or sulfated metabolites. It is excreted in the urine.
Adverse effects:
It may cause skin and minor allergic reactions. Prolonged use may cause renal tubular necrosis and hypoglycemic coma.
It inhibits prostaglandin synthesis in CNS (so analgesic and anti-pyretic) but has less effect on COX so (weak anti-inflammatory).
Therapeutic Uses:
It is used as analgesic and anti-pyretic. It is analgesic /anti-pyretic of choice for children with viral infections or chicken pox.
Drug interactions:
It does not antagonize the uricosuric agent (probenecid) and so may be used in patients with gout who are taking this drug.
Pharmacokinetics:
Rapidly absorbed from GI tract. 1st pass metabolism occurs in the luminal cells of the intestine and in the hepatocytes. It is conjugated in the liver to form inactive glucoronidated or sulfated metabolites. It is excreted in the urine.
Adverse effects:
It may cause skin and minor allergic reactions. Prolonged use may cause renal tubular necrosis and hypoglycemic coma.
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