Immuno Drugs

Front 1

Glucocorticoids mechanism: 2 points

Back 1

1. interfere with cell cycle of activated lymphoid cells. 2. inhibited production of inflammatory mediators

Front 2

Glucocorticoids 4 clinical use:

Back 2

1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis, 4. inflammatory bowel disease

Front 3

Glucocorticoids 4 side effects:

Back 3

1. protein break down. 2. hyperglycemia 3. avascular / aseptic necrosis of bone. 4. iatrogenic Cushing's syndrome

Front 4

Glucocotricoids precautions and contraindications:

Back 4

precautions: hyperglycemia and osteoporosis; contraindications: diabetes and osteoporosis

Front 5

Cyclosporine Mechanism including thing that metabolized it:

Back 5

forms complex with cyclophilin and inhibits calcineurin; inhibits IL-1 and IL-2 productions; net results is inhibition of T cell activation; metabolized by liver P450 enzymes

Front 6

Cycloporine: clinical use

Back 6

organ transplantation, graft v host disease, autoimmune disorders

Front 7

Cyclosporine: side effects

Back 7

nephrotoxicity (renal dysfunction) and hypertension; note dose dependent.

Front 8

Cyclosporine Drugs that inhibit CYP3A:

Back 8

glucocorticoids (methyprednisolone) - results in elevated cycloporine blood concentrations

Front 9

Cyclosporine: drug interactions

Back 9

Syngerstic nephrotoxictiy if coadministered with Tacrolimus

Front 10

Tacrolimus: Mechanism:

Back 10

inhbitis calcinerurin; metabolized by liver P450.

Front 11

tacrolimus Clinical use:

Back 11

organ transplantation and graft v host disease

Front 12

tacrolimus: 3 side effects:

Back 12

nephrontoxicity; hyperglycemia and diabetes and neurotoxicity.

Front 13

Sirolimus: mechanism

Back 13

inhibits activity of a protein kinase (mTor) involved in CELL CYCLE PROGRESSION thus blocking G1-S transition . not T CELL specific

Front 14

Sirolimus: clinical use:

Back 14

prevention of organ transplant rejections in combinatiion thearpy with a calcineirun

Front 15

Sirolimus: side effects:

Back 15

hyperlipemia and bone marrow suppression

Front 16

Mycophenolate Mofetil mechanism:

Back 16

inhbits activity of inosine monophosphate dehydrogenase ( INHBITS guanine nucleotide synthesis). B and T cells highly dependent on this pathway for cell proliferation thus the net result is inhibition of lymphocyte proliferation

Front 17

Mycophenolate: Clinical Use:

Back 17

prevention of transplant rejection in combination with glucocorticoids and calcineurin inhibitor

Front 18

Mycophenolate Mofetil: side effect

Back 18

hematologic (bone marrow suppression - leukopenai); gastrointestinal (diarrhea and vomiting)

Front 19

Azathioprine mechanism:

Back 19

production of a fradulent nucleotide (6-thio-IMP) that when incorporated into DNA prevents translation and cell proliferations

Front 20

Azathioprine: 3 clinical use:

Back 20

prevention of organ transplant rejection; rhematoid arthritis; induction and maintenance of remission of ulcerative colitis and crohn's disease

Front 21

Azathioprine: side effects:

Back 21

bone marrow suppression (leukopenia, thrombocytonpenia and or anemia); hepatic toxicity

Front 22

Methotrexate: mechanism:

Back 22

inhbitis dihyrdrofolate reductase ( this interferes with synthesis of thymidylate purine nucleotides and amino acids serine and methionine)

Front 23

Methotrexate: Clinical Use:

Back 23

induce and maintain remission inflmmatoryy bowel disease (Crohn's); rheumatoid arthritis and graft vs host disease

Front 24

Methotrexate: side effects

Back 24

1. bone marrow depression, and hepatic damage

Front 25

Cyclophosphamide: mechanism:

Back 25

transfer alkyl group to cellular constituents (proteinsm DNA, RNA); DNA becomes crosslinked leading to cytoxicity loss of proliferating lymphoid cells supresses T and B cell function by 30-40%)

Front 26

Cyclophosphamide: Clincal use:

Back 26

MAJOR stoppage of T and B cells. Organ rejection after transplantation. high does over several days

Front 27

Cyclophosphamide: Side effects

Back 27

dose related toxicities in rapidly growing tissues (bone marrow, reproductive organs); nausea and vomiting

Front 28

Antihymocyte Globin (ATG) mechanism:

Back 28

a polyclonal antibody that upon binding activates cytotoxicity (complement and cell mediated); block lymphocyte function.

Front 29

Antithymocyte Clinical use:

Back 29

induction of immunosuppression and to treat acute renal transplant rejection.

Front 30

Antithymocyte: Side effectss:

Back 30

fever and chills (potential for hypotension); patient will develop antibodies. HAMA reaction.

Front 31

Rho D immune Globuin: Mechanism

Back 31

binds Rho antigens prevents sensitization of Rh negative women to Rh-positive fetus .

Front 32

Muromonab-CD3: mechanism

Back 32

blocks antigen recognition - naive T cells and CTLs. Binds to CD3.

Front 33

Muromonab-CD3: Side effects:

Back 33

- cytokine release syndrome and HAMA reactions.

Front 34

Basilizimab and Daclizumab Mechanism:

Back 34

IL-2 antagonist; blocks IL-2 binding

Front 35

Basilizimab and Dacilizumab Clinical use and Side effects:

Back 35

used to prevent acute organ rejections; Side effects Gastronintestinal disorders

Front 36

Alefacept everything

Back 36

Mechanisms: inhibits T cell activation by binding to CD; Clinical use plaque psoriasis; Side effects: dose dependent reduction of circulating T cells - monitor carefully.

Front 37

Etanercept: everyhing mechanism and clinical use:

Back 37

binds to TNF alpha and TNF beta. blocks TNF alpha from binding receptor leads to suppression of inflammatory cytokines and adhesion molecules. ; Clinical use: rheumatoid arthritis and crohn's disease

Front 38

Adalimumab and Golimumab: mechanismm and rhematoid arthritis

Back 38

recognizes TNFalpha NOTE: does not recognized TNFbeta. ; clinical use rhematoid arthritis.

Front 39

Infliximab and Certolizumab: Mmechanism and Clinical Use

Back 39

recognized TNF alpha not TNF beta. . Clinical use: rheumatoid arthritis Crohn's diesease.

Front 40

TNF alpha and blockers Side effects:

Back 40

infusion reaction (reaction, uticaria, hypotension and dyspnea) plus others including serious infection that result in death due to suppression of inflammatory response.

Front 41

Glucocorticoids mechanism: 2 points

Back 41

1. interfere with cell cycle of activated lymphoid cells. 2. inhibited production of inflammatory mediators

Front 42

Glucocorticoids 4 clinical use:

Back 42

1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis, 4. inflammatory bowel disease

Front 43

Glucocorticoids 4 side effects:

Back 43

1. protein break down. 2. hyperglycemia 3. avascular / aseptic necrosis of bone. 4. iatrogenic Cushing's syndrome

Front 44

Glucocotricoids precautions and contraindications:

Back 44

precautions: hyperglycemia and osteoporosis; contraindications: diabetes and osteoporosis

Front 45

Cyclosporine Mechanism including thing that metabolized it:

Back 45

forms complex with cyclophilin and inhibits calcineurin; inhibits IL-1 and IL-2 productions; net results is inhibition of T cell activation; metabolized by liver P450 enzymes

Front 46

Cycloporine: clinical use

Back 46

organ transplantation, graft v host disease, autoimmune disorders

Front 47

Cyclosporine: side effects

Back 47

nephrotoxicity (renal dysfunction) and hypertension; note dose dependent.

Front 48

Cyclosporine Drugs that inhibit CYP3A:

Back 48

glucocorticoids (methyprednisolone) - results in elevated cycloporine blood concentrations

Front 49

Cyclosporine: drug interactions

Back 49

Syngerstic nephrotoxictiy if coadministered with Tacrolimus

Front 50

Tacrolimus: Mechanism:

Back 50

inhbitis calcinerurin; metabolized by liver P450.

Front 51

tacrolimus Clinical use:

Back 51

organ transplantation and graft v host disease

Front 52

tacrolimus: 3 side effects:

Back 52

nephrontoxicity; hyperglycemia and diabetes and neurotoxicity.

Front 53

Sirolimus: mechanism

Back 53

inhibits activity of a protein kinase (mTor) involved in CELL CYCLE PROGRESSION thus blocking G1-S transition . not T CELL specific

Front 54

Sirolimus: clinical use:

Back 54

prevention of organ transplant rejections in combinatiion thearpy with a calcineirun

Front 55

Sirolimus: side effects:

Back 55

hyperlipemia and bone marrow suppression

Front 56

Mycophenolate Mofetil mechanism:

Back 56

inhbits activity of inosine monophosphate dehydrogenase ( INHBITS guanine nucleotide synthesis). B and T cells highly dependent on this pathway for cell proliferation thus the net result is inhibition of lymphocyte proliferation

Front 57

Mycophenolate: Clinical Use:

Back 57

prevention of transplant rejection in combination with glucocorticoids and calcineurin inhibitor

Front 58

Mycophenolate Mofetil: side effect

Back 58

hematologic (bone marrow suppression - leukopenai); gastrointestinal (diarrhea and vomiting)

Front 59

Azathioprine mechanism:

Back 59

production of a fradulent nucleotide (6-thio-IMP) that when incorporated into DNA prevents translation and cell proliferations

Front 60

Azathioprine: 3 clinical use:

Back 60

prevention of organ transplant rejection; rhematoid arthritis; induction and maintenance of remission of ulcerative colitis and crohn's disease

Front 61

Azathioprine: side effects:

Back 61

bone marrow suppression (leukopenia, thrombocytonpenia and or anemia); hepatic toxicity

Front 62

Methotrexate: mechanism:

Back 62

inhbitis dihyrdrofolate reductase ( this interferes with synthesis of thymidylate purine nucleotides and amino acids serine and methionine)

Front 63

Glucocorticoids 4 clinical use: 1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis

Back 63

4. inflammatory bowel disease

Front 64

Cycloporine: clinical use organ transplantation

Back 64

graft v host disease

Front 65

Azathioprine: side effects: bone marrow suppression (leukopenia

Back 65

thrombocytonpenia and or anemia); hepatic toxicity

Front 66

Methotrexate: side effects 1. bone marrow depression

Back 66

and hepatic damage

Front 67

Cyclophosphamide: mechanism: transfer alkyl group to cellular constituents (proteinsm DNA

Back 67

RNA); DNA becomes crosslinked leading to cytoxicity loss of proliferating lymphoid cells supresses T and B cell function by 30-40%)

Front 68

Cyclophosphamide: Side effects dose related toxicities in rapidly growing tissues (bone marrow

Back 68

reproductive organs); nausea and vomiting

Front 69

TNF alpha and blockers Side effects: infusion reaction (reaction

Back 69

uticaria

Front 70

Rituximab. recognizes CD20. mechanism: complement mediated lysis

Back 70

antibody depedent cellular toxicity. pan B cell protein)

Front 71

Glucocorticoids mechanism: 2 points

Back 71

1. interfere with cell cycle of activated lymphoid cells. 2. inhibited production of inflammatory mediators

Front 72

Glucocorticoids 4 clinical use:

Back 72

1. first line immunosuppressive therapy. 2. organ rejection or graft v host disease. 3. rhematoid arthritis, 4. inflammatory bowel disease

Front 73

Glucocorticoids 4 side effects:

Back 73

1. protein break down. 2. hyperglycemia 3. avascular / aseptic necrosis of bone. 4. iatrogenic Cushing's syndrome

Front 74

Glucocotricoids precautions and contraindications:

Back 74

precautions: hyperglycemia and osteoporosis; contraindications: diabetes and osteoporosis

Front 75

Cyclosporine Mechanism including thing that metabolized it:

Back 75

forms complex with cyclophilin and inhibits calcineurin; inhibits IL-1 and IL-2 productions; net results is inhibition of T cell activation; metabolized by liver P450 enzymes

Front 76

Cycloporine: clinical use

Back 76

organ transplantation, graft v host disease, autoimmune disorders

Front 77

Cyclosporine: side effects

Back 77

nephrotoxicity (renal dysfunction) and hypertension; note dose dependent.

Front 78

Cyclosporine Drugs that inhibit CYP3A:

Back 78

glucocorticoids (methyprednisolone) - results in elevated cycloporine blood concentrations

Front 79

Cyclosporine: drug interactions

Back 79

Syngerstic nephrotoxictiy if coadministered with Tacrolimus

Front 80

Tacrolimus: Mechanism:

Back 80

inhbitis calcinerurin; metabolized by liver P450.

Front 81

tacrolimus Clinical use:

Back 81

organ transplantation and graft v host disease

Front 82

tacrolimus: 3 side effects:

Back 82

nephrontoxicity; hyperglycemia and diabetes and neurotoxicity.

Front 83

Sirolimus: mechanism

Back 83

inhibits activity of a protein kinase (mTor) involved in CELL CYCLE PROGRESSION thus blocking G1-S transition . not T CELL specific

Front 84

Sirolimus: clinical use:

Back 84

prevention of organ transplant rejections in combinatiion thearpy with a calcineirun

Front 85

Sirolimus: side effects:

Back 85

hyperlipemia and bone marrow suppression

Front 86

Mycophenolate Mofetil mechanism:

Back 86

inhbits activity of inosine monophosphate dehydrogenase ( INHBITS guanine nucleotide synthesis). B and T cells highly dependent on this pathway for cell proliferation thus the net result is inhibition of lymphocyte proliferation

Front 87

Mycophenolate: Clinical Use:

Back 87

prevention of transplant rejection in combination with glucocorticoids and calcineurin inhibitor

Front 88

Mycophenolate Mofetil: side effect

Back 88

hematologic (bone marrow suppression - leukopenai); gastrointestinal (diarrhea and vomiting)

Front 89

Azathioprine mechanism:

Back 89

production of a fradulent nucleotide (6-thio-IMP) that when incorporated into DNA prevents translation and cell proliferations

Front 90

Azathioprine: 3 clinical use:

Back 90

prevention of organ transplant rejection; rhematoid arthritis; induction and maintenance of remission of ulcerative colitis and crohn's disease

Front 91

Azathioprine: side effects:

Back 91

bone marrow suppression (leukopenia, thrombocytonpenia and or anemia); hepatic toxicity

Front 92

Methotrexate: mechanism:

Back 92

inhbitis dihyrdrofolate reductase ( this interferes with synthesis of thymidylate purine nucleotides and amino acids serine and methionine)

Front 93

Methotrexate: Clinical Use:

Back 93

induce and maintain remission inflmmatoryy bowel disease (Crohn's); rheumatoid arthritis and graft vs host disease

Front 94

Methotrexate: side effects

Back 94

1. bone marrow depression, and hepatic damage

Front 95

Cyclophosphamide: mechanism:

Back 95

transfer alkyl group to cellular constituents (proteinsm DNA, RNA); DNA becomes crosslinked leading to cytoxicity loss of proliferating lymphoid cells supresses T and B cell function by 30-40%)

Front 96

Cyclophosphamide: Clincal use:

Back 96

MAJOR stoppage of T and B cells. Organ rejection after transplantation. high does over several days

Front 97

Cyclophosphamide: Side effects

Back 97

dose related toxicities in rapidly growing tissues (bone marrow, reproductive organs); nausea and vomiting

Front 98

Antihymocyte Globin (ATG) mechanism:

Back 98

a polyclonal antibody that upon binding activates cytotoxicity (complement and cell mediated); block lymphocyte function.

Front 99

Antithymocyte Clinical use:

Back 99

induction of immunosuppression and to treat acute renal transplant rejection.

Front 100

Antithymocyte: Side effectss:

Back 100

fever and chills (potential for hypotension); patient will develop antibodies. HAMA reaction.

Front 101

Rho D immune Globuin: Mechanism

Back 101

binds Rho antigens prevents sensitization of Rh negative women to Rh-positive fetus .

Front 102

Muromonab-CD3: mechanism

Back 102

blocks antigen recognition - naive T cells and CTLs. Binds to CD3.

Front 103

Muromonab-CD3: Side effects:

Back 103

- cytokine release syndrome and HAMA reactions.

Front 104

Basilizimab and Daclizumab Mechanism:

Back 104

IL-2 antagonist; blocks IL-2 binding

Front 105

Basilizimab and Dacilizumab Clinical use and Side effects:

Back 105

used to prevent acute organ rejections; Side effects Gastronintestinal disorders

Front 106

Alefacept everything

Back 106

Mechanisms: inhibits T cell activation by binding to CD; Clinical use plaque psoriasis; Side effects: dose dependent reduction of circulating T cells - monitor carefully.

Front 107

Etanercept: everyhing mechanism and clinical use:

Back 107

binds to TNF alpha and TNF beta. blocks TNF alpha from binding receptor leads to suppression of inflammatory cytokines and adhesion molecules. ; Clinical use: rheumatoid arthritis and crohn's disease

Front 108

Adalimumab and Golimumab: mechanismm and rhematoid arthritis

Back 108

recognizes TNFalpha NOTE: does not recognized TNFbeta. ; clinical use rhematoid arthritis.

Front 109

Infliximab and Certolizumab: Mmechanism and Clinical Use

Back 109

recognized TNF alpha not TNF beta. . Clinical use: rheumatoid arthritis Crohn's diesease.

Front 110

TNF alpha and blockers Side effects:

Back 110

infusion reaction (reaction, uticaria, hypotension and dyspnea) plus others including serious infection that result in death due to suppression of inflammatory response.

Front 111

Alemtuzumab

Back 111

recognized CD52. used to treat B cell chronic lymphocytic leukemia.

Front 112

Rituximab.

Back 112

recognizes CD20. mechanism: complement mediated lysis, antibody depedent cellular toxicity. pan B cell protein)