NSAIDS, glucocorticoids, immunosuppressants

Question 0

Meloxicam

Answer 0

A= NSAID, oxicam group
B=  inhibits both COX1 and COX2 (more selective to COX2) --> inhibits prostaglandin synthesis from arachidonic acid 
C= osteoarthritis, rheumatoid arthritis, used as a painkiller e.g. in pain induced by dysmenorrhea, ocular inflammation, ankylosing spondylitis, keratosis, acute gout, postoperative pain, poly arthritis, fibromyalgias, arthrosis

Question 1

Ibuprofen (ipren)

Answer 1

A= NSAID, analgesics, antipyretics, phenylproprionic acid derivative, nonselective COX inhibitor
B= nonselectively inhibits both COX1 and COX2--> inhibits prostaglandin synthesis from arachidonic acid 
C= osteoarthritis, rheumatoid arthritis, used as a painkiller e.g. in pain induced by dysmenorrhea, ocular inflammation, ankylosing spondylitis, keratosis, acute gout, postoperative pain, poly arthritis, fibromyalgias, arthrosis + Closure of ductus arteriosus in premature infants, pericarditis, fever

Question 2

Diclofenac natrium (voltaren)

Answer 2

A= NSAID, analgesics, antipyretics, phenylacetic acid derivative, non-selective COX inhibitor
B= nonselectively inhibits both COX1 and COX2 + inhibits leucocyte migration --> inhibits prostaglandin synthesis from arachidonic acid 
C= osteoarthritis, rheumatoid arthritis, used as a painkiller e.g. in pain induced by dysmenorrhea, ocular inflammation, ankylosing spondylitis, solar keratosis, acute gout, postoperative pain, poly arthritis, fibromyalgias, arthrosis, fever

Question 3

Lornoxicam

Answer 3

A= NSAID, oxicam group
B=  inhibits both COX1 and COX2 (more selective to COX2) --> inhibits prostaglandin synthesis from arachidonic acid. (Does not lead to an increase in leukotriene formation --> reduces risk of adverse reactions unlike other NSAIDS)
C= osteoarthritis, rheumatoid arthritis, used as a painkiller e.g. in pain induced by dysmenorrhea, ocular inflammation, ankylosing spondylitis, keratosis, acute gout, postoperative pain, poly arthritis, fibromyalgias, arthrosis

Question 4

Celecoxib

Answer 4

A= NSAID, antipyretics, analgesics, sulfonamide compound, selective COX2 inhibitor (less GIT side effects)
B= selectively blocks COX2 enzymes --> decreases the synthesis of prostaglandins from arachidonic acid without interfering with COX1 enzyme, thus avoiding side effects better than other NSAIDS
C= osteoarthritis, RA, acute pain, painful dysmenorrhea, ankylosing spondylitis, familial adenomatous polyposis, gout

Question 5

Etoricoxib

Answer 5

A= NSAID, antipyretics, analgesics, sulfonamide compound, selective COX2 inhibitor (less GIT side effects)
B= selectively blocks COX2 enzymes --> decreases the synthesis of prostaglandins from arachidonic acid without interfering with COX1 enzyme, thus avoiding side effects better than other NSAIDS
C= osteoarthritis, RA, acute pain, painful dysmenorrhea, ankylosing spondylitis, familial adenomatous polyposis, gout

Question 6

Hydrocortisone sodium succinate

Answer 6

A= glucocorticoid (synthetic cortisol) 
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia

Question 7

Hydrocortisone butyras (topically)

Answer 7

A= glucocorticoid (synthetic cortisol) 
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia

Question 8

Hydrocortisone acetate (topical and dental pastes)

Answer 8

A= glucocorticoid (synthetic cortisol) 
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia

Question 9

Mometasone furoas

Answer 9

A= glucocorticoid (synthetic cortisol) 
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, PROPHYLACTIC treatment of asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia. As nasal spray for relief is symptoms of seasonal and perennial allergic rhinitis

Question 10

Fluticasone (inhalation)

Answer 10

A= glucocorticoid (synthetic cortisol) 
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia. Asthma, COPD, hay fever

Question 11

Triamcinolone

Answer 11

A= glucocorticoid (synthetic cortisol), acetonid derivative
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia. Useful in dermatological diseases, allergic rhinitis

Question 12

Fluocinolone acetonide

Answer 12

A= glucocorticoid (synthetic cortisol), acetonid derivative
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia. Useful in dermatological diseases, allergic rhinitis

Question 13

Prednisolone

Answer 13

A= glucocorticoid 
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia 
C= maintenance treatment of asthma, allergic rhinitis (seasonal or prerennial). Chrons disease GvHD

Question 14

Methylprednisolone

Answer 14

A= glucocorticoid 
B= binds to i/c nuclear glucocorticoid receptors --> the ligand bound receptor complex then moves to the nucleus where it interacts with the DNA and nuclear proteins by binding to the GRE at the promoter regions of responsive genes --> regulating the genes and thus the protein synthesis. The anti-inflammatory properties are thanks to lipocortins (phospholipase A2 inhibitory proteins) which controls the biosynthesis of prostaglandins and leukotrienes through the inhibition of arachidonic acid. Specifically induce lipocortin-1 synthesis which then binds to cell membranes, preventing phospholipase A2 from coming in contact with its substrate arachidonic acid--> diminished production of prostaglandins and eicosanoids. The COX1 and COX2 enzymes are also suppressed. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of lymphatic system, a reduction in immunoglobulin & complement concentrations and the interference with antigen-antibody binding
C= for the relief of inflammatory dermatoses, endocrine disorders (adrenal insufficiency, addis ins disease), immune and allergic diseases, arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, chrons disease, collagen diseases, some neoplastic conditions, RA, acute leukaemia 
C= maintenance treatment of asthma, allergic rhinitis (seasonal or prerennial). Chrons disease GvHD

Question 16

Dexamethasone

Answer 16

A= anti-inflammatory 9-fluoro-glucocorticoid
B= Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic glucocorticoid receptors. This complex binds to DNA elements (glucocorticoid response elements) which results in a modification of transcription and, hence, protein synthesis in order to achieve inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. The antiinflammatory actions of dexamethasone are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.
C=  for the treatment of endocrine disorders, rheumatic disorders, collagen diseases, dermatologic diseases, allergic statesc, ophthalmic diseases, gastrointestinal diseases, respiratory diseases, hematologic disorders, neoplastic diseases, edematous states, cerebral edema. Dexamethasone suppression test for the diagnosis of cushings

Question 17

Cyclosporin (grapefruit juice increases its bioavailabiliy as much as 62%)

Answer 17

A= DMARD, peptide antibiotic, calcineurin inhibior, immunosuppressor
B= through regulation of gene transcription inhibits IL-1 and IL-2 receptor production and secondarily inhibits mph-Tcell interaction and Tcell responsiveness: Binds to cyclophillin peptide--> cyclophillin+cyclosporin complex inhibits a cytoplasmic phosphotase, calcineurin, which is necessary for the activation of Tcell specific transcription factor which in turn is necessary for the synthesis of IL-2 by activated Tcells, IL3, IFNgamma
C= RA, SLE, polymyositis, dermatomyositis, Wegners granulomatosis, juvenile chronic arthritis, organ transplantations, gvHD, autoimmune disorders; psoriasis, asthma et

Question 18

Methotrexate

Answer 18

A= synthetic antimetabolite, immunosuppressant, first line non biologic DMARD
B= at low doses inhibits aminoimidazolecarboxamide ribonucleotide tranaformylase (AICAR) and thymidylate synthetase. They are normally required for the inhibition of AMP deaminase --> i/c levels of AMP increases which is then released and converted to adenosine which is a potent inflammatory inhibitor. As a result inflammatory functions of neutrophils, mphs, dendritic cells and lymphocytes are suppressed. Methotreate also directly inhibits proliferation and stimulates apoptosis in inflammatory cells + inhibits folic acid synthetase --> inhibit production of tetrahydrofolic acid which is required for DNA synthesis (high doses)
C= RA, SLE, juvenile chronic arthritis, ankylosing spondylitis, polymyositis, dermatomyositis, Wegners granulomatosis, giant cell arteritis, vasculitis

Question 19

Azathioprin

Answer 19

A= immunosuppressant, synthetic DMARD (6-thioguanine), cytotoxic agent
B= cause immunosuppression by interfering with the purine nucleic acid metabolism that is required for lymphoid cell proliferaton after antigenic stimulation = AZA destroy stimulated lymphoid cells
C= RA, SLE, psoriatic arthritis, reactive arthritis, polymyositis, transplantation of tissues and organs, chrons disease, MS

Question 20

Tacrolimus

Answer 20

A= immunomodulator, calcineurin inhibitor, macrolides
B= binds to cytoplasmic peptidyl prolyl isomerases; FK-binding protein. The ligand-protein complex then inhibits calcineurin, which is normally necessary for the activation of T-cell specific transcription factor (se cyclosporin)
C= organ and stem cell transplantations, gvHD, atopic dermatitis

Question 21

Pimecrolimus

Answer 21

A= immunomodulator, calcineurin inhibitor, macrolides
B= binds to cytoplasmic peptidyl prolyl isomerases; FK-binding protein. The ligand-protein complex then inhibits calcineurin, which is normally necessary for the activation of T-cell specific transcription factor (se cyclosporin) + prevents the release of inflammatory mediators from mast cells
C= organ and stem cell transplantations, gvHD, atopic dermatitis

Question 22

Mycophenolic acid

Answer 22

A= semisynthetic DMARD (converted from mycophenolate mofetil)
B= inhibits inosine monophosphate dehydrogenase --> suppression of T and Bcell proliferation. Also interferes with leucocyte adhesion to endothelial cells through the inhibition of E-selectin, P-selectin and intracellular adhesion molecule-1
C= renal disease due to SLE, vasculitis, Wegners granulomatosis, RA