Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > Drugs used in Organ Transplantation > Flashcards

Drugs used in Organ Transplantation Flashcards

1
Q

What is the mechanism of glucocorticoids (Prednisone, prednisolone_?

A

Suppress distribution and reactivity of lymphoid and myloid cells, catabolic actions at GRE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the clinical use of glucocorticoids (Prednisone, prednisolone?

A

Acute use and emergency adjuncts to other suppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the toxicities of glucocorticoids (Prednisone, prednisolone)?

A

Catabolic state, hypertension, diabetogenic, avascular necrosis, osteopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the mechanism of Antithymocyte Globulin (ALG) and Antilymphocyte Globulin (ATG)?

A

Polyclonal suppression of thymocytes (T) or lymphocytes (T&B, NK), Allows early temp withdrawal of drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Whats the clinical use of Antithymocyte Globulin (ALG) and Antilymphocyte Globulin (ATG)?

A

Induction, initial or steroid resistant rejection, GVH rxns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the toxicities of Antithymocyte Globulin (ALG) and Antilymphocyte Globulin (ATG)?

A

Fever, chills, hypotension, SERUM SICKNESS (type III), sensitization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the mechanism of Muromonab-CD3 (OKT-3)

A

MAB (monoclonal antibody) against the T-cell receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the clinical use of Muromonab-CD3 (OKT-3)

A

Induction, initial or steroid resistant rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the toxicities of Muromonab-CD3 (OKT-3)

A

‘Cytokine release’ syndrome so systemic shock (pretreat with steroid), infusion rxns,sensitization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the mechanism of Alemtuzumab

A

hMAB (monoclonal antibodies) against CD52 on lymphocytes monocytes macrophages NK leading to prolonged T&B depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the clinical use of Alemtuzumab

A

Induction, initial or steroid resistant rejection (same as OKT-3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What treatments is Alemtuzumab used for?

A

Chronic lymphocytic leukemia (CLL) and transplants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the mechanism of Daclizumab and Basiliximab

A

Humanized and chimeric MAB (monoclonal antibodies) against IL2 receptor on T-cells. So when IL-2R is more active it becomes more selective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the clinical use of Daclizumab and Basiliximab

A

Acute renal rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the toxicities of Daclizumab and Basiliximab

A

Infusion rxns, tremor, headache, dypsnea, hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of Abatacept and Belatacept

A

Fusion of Fc of IgG1 and CTLA-4 binds to CD80,86 preventing second signal in T-cells, blocking activation

17
Q

What is the clinical use of Abatacept and Belatacept

A

Used for rheumatoid arthritis, but allows temporary removal of more toxic agents in slow graft response or rejection

18
Q

What are the toxicities of Abatacept and Belatacept

A

Infusion rxs, hypersenitivity, nasopharyngitis, URI, nausea, headache

19
Q

What is the mechanism of Thalidomide?

A

Stimulates and changes specificity of T-cells, supresses B cells stimulates T cells but in a immunomodulatory fasion such as changes in immune reactivity and specificity. Used in combo for allogenic bone marrow transplantation.

20
Q

What is the clinical use of Thalidomide?

A

Malignancy, GVHR

21
Q

What are the toxicities of Thalidomide?

A

Teratogenic, peripheral neurotoxicity

22
Q

What is the mechanism of Calcineurin inhibitors: Cyclosporine (CSA and Tacrolimus (FK-506)?

A

Calcineurin (phosphatase PP2b) inhibitor blocking signal transduction activating T-cells

23
Q

What is the clinical use of Calcineurin inhibitors: Cyclosporine (CSA and Tacrolimus (FK-506)?

A

Primary agents used in organ transplantation of all kinds in combo with antimetabolites. CSA binds to cyclophilin and FK506 binds to tacrolimus

24
Q

What is the toxicities of Calcineurin inhibitors: Cyclosporine (CSA and Tacrolimus (FK-506)?

A

Nephrotoxicity is limiting, neurotoxic, hypertension, hyperlipidemia, gum hyperplasia (CSA), diabetes (FK-506). Watch for drug interactions with CYP450s

25
Q

What is the mechanism of Antiproliferative agents: Sirolimus (rapamycin), Everolimus?

A

inhib mTOR kinase, prevents CDK2 phosphorylation and so blocks cell cycle progression in T-cells. Binds to FK506BP12

26
Q

What is the clinical use of Antiproliferative agents: Sirolimus (rapamycin), Everolimus?

A

Used in organ transplants of all kinds, not used in combo of calcineurin inhibs but as alternate primary drugs with antimetabolites

27
Q

What are the Toxicities of Antiproliferative agents: Sirolimus (rapamycin), Everolimus?

A

Hyperlipidemia, Myelosupression esp thrombocytopenia, also anemia, delayed wound healing and used in vascualr stents watch with interaction at CYP450s

28
Q

What is the mechanism of Antimetabolites: Mycophenolate and Mofetil?

A

Prodrug of mycophenolic acid and inhib of T&B cell inosine monophosphate dehydrogenase in the purine pathway for GMP synthesis. T and B cells are highly dependent on de novo purine synthesis hence are suppressed

29
Q

What is the clinical use of Antimetabolites: Mycophenolate and Mofetil?

A

Used in secondary ancillary immunosuppressant drug combo with Calcineurin inhibs or Antiproliferative agents

30
Q

What are the toxicities of Antimetabolites: Mycophenolate and Mofetil?

A

Leukopenia, diarrhea, nausea, vomiting, infection

31
Q

What is the mechanism of Antimetabolites: Azathioprine?

A

Prodrug of 6-MP, an inhib of ATP and GTP synthesis. Can be genetic deficiencies in metabolism by thiopurine methyltransferase

32
Q

What is the clinical use of Antimetabolites: Azathioprine?

A

Largely replaced by mycophenolate but is alt. Dose reduced with allopurinol

33
Q

What are the toxicities of Antimetabolites: Azathioprine?

A

Bone marrow suppression, hepatotoxicity, GI toxicity, pancreatitis, alopecia

Immunology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions