Immunosuppressants

IMMUNOSUPPRESSANTS

Q. 1 Post-transplantation hypertension can be caused by:
I.  Rejection.        
II.  Cyclosporine nephrotoxicity.
III.  Renal transplant artery stenosis (RTAS).
IV. Recurrent disease in the allograft.
 A I,II,III,IV are correct
 B I,II,IV are correct.
 C I & III are correct
 D None of the above is correct.
Q. 1 Post-transplantation hypertension can be caused by:
I.  Rejection.        
II.  Cyclosporine nephrotoxicity.
III.  Renal transplant artery stenosis (RTAS).
IV. Recurrent disease in the allograft.
 A I,II,III,IV are correct
 B I,II,IV are correct.
 C I & III are correct
 D None of the above is correct.
Ans. A

Explanation:

Both acute and chronic rejection may result in hypertension. The former causes acute fluid retention and plugging of peritubular capillaries with inflammatory cells. This may progress to intimal swelling and medial necrosis and eventuate in ischemia secondary to endothelial proliferation and obliteration of small vessels. Chronic rejection, thought to be related to protracted humoral injury, results in obliteration of capillaries via the development of intimal hyperplasia. Cyclosporine has a vasoconstrictive effect which, through activation of the renin-angiotensin system, may lead to hypertension. RTAS is responsible for hypertension in 4% to 12% of renal allograft recipients. It responds well to percutaneous angioplasty. A careful trial of angiotensin-converting enzyme inhibitors may be diagnostic of RTAS. Recurrent disease such as membranoproliferative glomerulonephritis and focal glomerular sclerosis may result in significant hypertension in renal allograft recipients.


Q. 2 Post-transplantation  hypertension  can  be caused by:
I. Rejection.
II. Cyclosporine nephrotoxicity.
III. Renal transplant artery stenosis (RTAS). IV. Recurrent disease in the allograft.
 A I,II,III,IV are correct.
 B I,II,IV are correct
 C I & III are correct.
 D None of the above is correct.
 
Q. 2 Post-transplantation  hypertension  can  be caused by:
I. Rejection.
II. Cyclosporine nephrotoxicity.
III. Renal transplant artery stenosis (RTAS). IV. Recurrent disease in the allograft.
 A I,II,III,IV are correct.
 B I,II,IV are correct
 C I & III are correct.
 D None of the above is correct.
 
Ans. A

Explanation:

Both  acute  and  chronic  rejection  may  result  in hypertension. The former causes acute fluid retention and plugging of peritubular capillaries with inflammatory cells. This may progress to intimal swelling and medial necrosis and eventuate in ischemia secondary to endothelial proliferation and obliteration of small vessels. Chronic rejection, thought to be related to protracted humoral injury, results in obliteration of capillaries via the development of intimal hyperplasia. Cyclosporine has a vasoconstrictive effect which, through activation  of  the  renin-angiotensin  system,  may lead to hypertension. RTAS is responsible for hypertension in 4% to 12% of renal allograft recipients. It responds well to percutaneous angioplasty. A careful trial of angiotensin- converting enzyme inhibitors may be diagnostic of RTAS. Recurrent disease such as membranoproliferative  glomerulonephritis  and focal glomerular sclerosis may result in significant hypertension in renal allograft recipients.


Q. 3 Phocomelia is an adverse effect due to:
 A Thalidomide
 B Warfarin
 C Enalapril
 D Phenytoin
Q. 3 Phocomelia is an adverse effect due to:
 A Thalidomide
 B Warfarin
 C Enalapril
 D Phenytoin
Ans. A

Explanation:

Thalidomide

Quiz In Between


Q. 4

Sirolimus is administered by which route?

 A

Oral

 B

Inhalation

 C

Intranasal

 D

Intravenous

Q. 4

Sirolimus is administered by which route?

 A

Oral

 B

Inhalation

 C

Intranasal

 D

Intravenous

Ans. A

Explanation:

Sirolimus is available only as an oral drug. Its half-life is about 60 hours, while that of everolimus is around 43 hours. 
 
Ref: Katzung 11th edition Chapter 61.

Q. 5

Which of the following is an example of proliferation signal inhibitor?

 A

Tacrolimus

 B

Sirolimus

 C

Cyclosporine

 D

None of the above

Q. 5

Which of the following is an example of proliferation signal inhibitor?

 A

Tacrolimus

 B

Sirolimus

 C

Cyclosporine

 D

None of the above

Ans. B

Explanation:

A new class of immunosuppressive agents called proliferation-signal inhibitors (PSIs) includes sirolimus (rapamycin) and its derivative everolimus.
 
Ref: Katzung 11th edition Chapter 51.

Q. 6

Which of the following drug shows nephrotoxicity during administration?

 A

Azathioprine

 B

Leflunomide

 C

Mycophenolate mofetil

 D

Tacrolimus

Q. 6

Which of the following drug shows nephrotoxicity during administration?

 A

Azathioprine

 B

Leflunomide

 C

Mycophenolate mofetil

 D

Tacrolimus

Ans. D

Explanation:

Adverse effects of tacrolimus:
 

  • Nephrotoxicity

  • Neurotoxicity (e.g., tremor, headache, motor disturbances, seizures)

  • GI complaints

  • Hypertension

  • Hyperkalemia

  • Hyperglycemia

  • Diabetes

 

The major side effect of azathioprine is bone marrow suppression, including leukopenia (common), thrombocytopenia (less common), and/or anemia (uncommon).

 

The principal toxicities of Mycophenolate mofetil are gastrointestinal and hematologic.

 

Leflunomide is hepatotoxic and can cause fetal injury when administered to pregnant women.

 

Ref: Krensky A.M., Bennett W.M., Vincenti F. (2011). Chapter 35. Immunosuppressants, Tolerogens, and Immunostimulants. In L.L. Brunton, B.A. Chabner, B.C. Knollmann (Eds), Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12e.

Quiz In Between


Q. 7

One of the following causes nephrotoxicity and hypertension which is similar to cyclosporine:

 A

Azathioprine

 B

Cyclophosphamide

 C

Mycophenolate mofetil

 D

Tacrolimus

Q. 7

One of the following causes nephrotoxicity and hypertension which is similar to cyclosporine:

 A

Azathioprine

 B

Cyclophosphamide

 C

Mycophenolate mofetil

 D

Tacrolimus

Ans. D

Explanation:

Tacrolimus (FK 506) is an immunosuppressant macrolide antibiotic produced by Streptomyces tsukubaensis. Tacrolimus binds to the immunophilin FK-binding protein (FKBP). This complexe inhibit calcineurin, which is necessary for the activation of the T-cell-specific transcription factor NF-AT. Its toxic effects are similar to those of cyclosporine and include nephrotoxicity, neurotoxicity, hyperglycemia, hypertension, hyperkalemia, and gastrointestinal complaints.
 
Ref: Lake D.F., Briggs A.D., Akporiaye E.T. (2012). Chapter 55. Immunopharmacology. In B.G. Katzung, S.B. Masters, A.J. Trevor (Eds), Basic & Clinical Pharmacology, 12e.

Q. 8

Which of the following statements about Mycophenolate Mofetil is not true:

 A

Most common adverse effect is Nephrotoxicity

 B

Used in Transplant Rejection

 C

It is a prodrug and converted to Mycophenolic acid

 D

Is not used with Azathioprine

Q. 8

Which of the following statements about Mycophenolate Mofetil is not true:

 A

Most common adverse effect is Nephrotoxicity

 B

Used in Transplant Rejection

 C

It is a prodrug and converted to Mycophenolic acid

 D

Is not used with Azathioprine

Ans. A

Explanation:

Most prominent adverse effect associated with mycophenolate mofetil are vomiting, diarrhea and leucopenia. Nephrotoxicity is not associated with its use.
Ref: Essentials of Medical Pharmacology By KD Tripathi, 5th Edition, Page 789; KDT 6th Edition, Page 841; Goodman And Gillman’s Manual of Pharmacology, 2007, Page 916.

 


Q. 9

ALL of the following drugs have immunosuppressive effects, EXCEPT:

 A

Cyclosporine

 B

Cefaclor

 C

Azathioprine

 D

Steroids

Q. 9

ALL of the following drugs have immunosuppressive effects, EXCEPT:

 A

Cyclosporine

 B

Cefaclor

 C

Azathioprine

 D

Steroids

Ans. B

Explanation:

Cefaclor is a second generation cephalosporin and is not known to have any immunosuppressive effects. Corticosteroids is having immunosuppressive properties.

 
Classification of immunosuppressants according to the WHO:
 
Drugs targeting intracellular ligands:
 
Calcineurin inhibitors
Tacrolimus
Cyclosporin A
Antimetabolites
Azathioprine
Methotrexate
Mycophenolic acid
Cladribine
Antiproliferative agents
Cyclophosphamide
Sirolimus
Mitoxantrone
Drugs targeting cell surface ligands:
  • Monoclonal antibodies
  • Fusion proteins
Drugs targeting soluble factors: cytokines:
  • Anti TNF alpha
  • Daclizumab
Ref: Immune Regulation and Immunotherapy in Autoimmune Disease
By Jingwu Zhang page 297.

Quiz In Between


Q. 10

Leflunomide acts on:

 A

Purine synthesis

 B

Pyrimidine synthesis

 C

Cell membrane synthesis

 D

None of the above

Q. 10

Leflunomide acts on:

 A

Purine synthesis

 B

Pyrimidine synthesis

 C

Cell membrane synthesis

 D

None of the above

Ans. B

Explanation:

Leflunomide is metabolized to an active metabolite that acts to inhibit dihydroorotate dehydrogenase, an essential enzyme in the pyrimidine biosynthetic pathway.
 
Its predominant action is to inhibit the proliferation of T lymphocytes. Leflunomide has been shown to control the signs and symptoms of RA and to slow the progression of joint damage as effectively as methotrexate.
 
Leflunomide can be given alone or with methotrexate and is the most frequently employed immunosuppressive agent used to treat patients with Rheumatoid arthritis.
 
Ref: Harrison’s principle of internal medicine 17th edition, chapter 302.

Q. 11

Which of the following immunosuppresive agents have a side effect of osteoporosis?

 A

Cyclophosphamide

 B

Methotrexate

 C

Glucocorticoids

 D

Mycophenolate mofetil

Q. 11

Which of the following immunosuppresive agents have a side effect of osteoporosis?

 A

Cyclophosphamide

 B

Methotrexate

 C

Glucocorticoids

 D

Mycophenolate mofetil

Ans. C

Explanation:

Side effects of common Immuno-Suppresants are given below:
Cyclophosphamide: Leucopenia or neutropenia, infections (usually respiratory and urinary tract), infertility, cancer (especially bladder cancer and leukaemia), haemorrhagic cystitis, alopecia, and amenorrhoea
Glucocorticoids: Osteoporosis, candida infection (oral and vaginal), other infections, weight gain, hyperglycaemia or diabetes, hypertension, cushingoid appearance, skin atrophy, and cataract
Azathioprine: Nausea, leucopenia or neutropenia, infection, hypersensitivity, cancer, alopecia, cholestasis, and thrombocytopenia
Methotrexate: Nausea, oral ulcers, liver dysfunction, infection, hypertension, leucopenia
Mycophenolate mofetil: infection, leucopenia, gastrointestinal tract manifestations, anaemia, thrombocytopenia
Rituximab: Infections (encephalitis is particularly dangerous), cancer, anaemia, neutropenia, thrombocytopenia, hypogammaglobulinaemia
 
Ref: Diagnosis and management of ANCA associated vasculitis ; BMJ 2012;344:e26

Q. 12

Tacrolimus belong to which class of drug ?

 A

Calcineurin inhibitor

 B

mTOR inhibitor

 C

Hypoxathine inhibitor

 D

Inosine inhibitor

Q. 12

Tacrolimus belong to which class of drug ?

 A

Calcineurin inhibitor

 B

mTOR inhibitor

 C

Hypoxathine inhibitor

 D

Inosine inhibitor

Ans. A

Explanation:

Ans. is ‘a’ i.e., Calcineurin inhibitor

Quiz In Between


Q. 13

Cyclosporine acts by inhibiting the proliferation of

 A

ILl

 B

IL2

 C

IL6

 D

Macrophages

Q. 13

Cyclosporine acts by inhibiting the proliferation of

 A

ILl

 B

IL2

 C

IL6

 D

Macrophages

Ans. B

Explanation:

Ans. is ‘b’ i.e., IL2

  • Cyclosporine enters target cells and bind to cyclophilin (an immunophilin).
  • This cyclosporine-cyclophilin complex inactivates calcineurin           
  • IL-2 trascripitan and proliferation of T cells.

Q. 14

Cyclosporine uses are all except –

 A

Organ transplant

 B

Rheumatoid arthritis

 C

Multiple myeloma

 D

Recalcitrant psoriasis

Q. 14

Cyclosporine uses are all except –

 A

Organ transplant

 B

Rheumatoid arthritis

 C

Multiple myeloma

 D

Recalcitrant psoriasis

Ans. C

Explanation:

Ans. is ‘c’ i.e., Multiple myeloma

o Cyclosporine is used in organ transplant (to prevent rejection) and autoimmune disorders (RA, psoriasis).


Q. 15

Complications of cyclosporine are –

 A

Hypertension

 B

Pulmonary fibrosis

 C

Hirsutism

 D

a and c

Q. 15

Complications of cyclosporine are –

 A

Hypertension

 B

Pulmonary fibrosis

 C

Hirsutism

 D

a and c

Ans. D

Explanation:

Ans. is ‘a’ i.e., Hypertension; ‘c’ i.e., Hirsutism

o Cyclosporin can cause nephrotoxicity (major side effect), hypertension, precipitation of diabetes (hyperglycemia), hirsutism, gum hyperplasia, hyperkalemia, hyperuricemia, heperlipedmia, hepatotoxicity and neurotoxicity.

Quiz In Between


Q. 16

Cyclosporine nephrotoxicity aggravated by-

 A

Amphototerian

 B

Itraconazole

 C

INH

 D

Lovastatin

Q. 16

Cyclosporine nephrotoxicity aggravated by-

 A

Amphototerian

 B

Itraconazole

 C

INH

 D

Lovastatin

Ans. A

Explanation:

Ans. is ‘a’ i.e., Amphotericin B

o All nephrotoxic drugs like aminoglycosides, Vancomycin, amphotericin B and NSAIDs enhance toxicity of cyclosporine.


Q. 17

Nephrotoxicity is a side effect of one of the following immuno-suppressives –

 A

Sirolimus

 B

Tacrolimus

 C

Mycophenolate mofetil

 D

Azathioprine

Q. 17

Nephrotoxicity is a side effect of one of the following immuno-suppressives –

 A

Sirolimus

 B

Tacrolimus

 C

Mycophenolate mofetil

 D

Azathioprine

Ans. B

Explanation:

Ans. is ‘b’ i.e., Tacrolimus

Tacrolimus

o It is a macrolide immunosuppressant agent.

o Its mechanism of action is similar to cyclosporine, i.e. inhibition of transcription of IL-2 and T-cell proliferation, but it binds to other immunophilin called FKBP (in contrast to cyclosporine which binds to cyclophilin). Subsequent steps are some, i.e. inhibition of calcineurin, which inhibits T cell activation.

o Tocrolimus is 10-100 times more potent than cyclosporine.

o It is also more toxic than cyclosporin..

o Adverse effects are nephrotoxicity (most common), neurotoxicity, hyperglycemia (DM).

Mechanism of nephrotoxicity —i Periglomerular afferent arteriolar vasoconstrication and reduced GFR.

o Note – Both cyclosporine and Tacrolimus can cause nephrotoxicity, hyperglycemia, and neurotoxicity —> should not be used together.


Q. 18

All of the following are side effects of tacrolimus except –

 A

Nephrotoxicity

 B

Ototoxicity

 C

Neurotoxicity

 D

Hepatotoxicity

Q. 18

All of the following are side effects of tacrolimus except –

 A

Nephrotoxicity

 B

Ototoxicity

 C

Neurotoxicity

 D

Hepatotoxicity

Ans. B

Explanation:

Ans. is ‘b’ i.e., Ototoxicity

Adverse effects of Tacrolimus

o Nephrotoxicity (most common and dose limiting)                                    o Neurotoxicity

o Hepatotoxicity                                                                                 o GI toxicity

o Alopecia                                                                                       o Hypertension

o Hematological toxicity (Leucocytosis, thrombocytopenia)                    o Endocrine (hyperglycemia, hyperlipidemia)

Quiz In Between


Q. 19

All of the following drugs can precipitate tacrolimus toxicity except

 A

Gentamycin

 B

Cisplatin

 C

Vancomycin

 D

Rifampicin

Q. 19

All of the following drugs can precipitate tacrolimus toxicity except

 A

Gentamycin

 B

Cisplatin

 C

Vancomycin

 D

Rifampicin

Ans. D

Explanation:

Ans. is ‘d’ i.e., Rifampicin

Tacrolimus is a highly nephrotoxic drugs.

o Other nephrotoxic drugs may precipitate tacrolimus induced nephrotoxicity, when used concomitantly. o Important nephrotoxic drugs that enhance tacrolimus induced nephrotoxicity are:

1. Aminoglycosides (e.g. gentamycin)             2. Vancomycin            3. Cisplatin

4. Amphotericin B                                     5. Cotrimoxazole       6. NSAIDs


Q. 20

Which of the following statements is not true about Tacrolimus –

 A

It is macrolide antibiotic

 B

It is indicated for the prophylaxis of organ transplant rejection

 C

Glucose intolerance is a well recognized side effect

 D

It can be safely administered with any nephrotoxic drug

Q. 20

Which of the following statements is not true about Tacrolimus –

 A

It is macrolide antibiotic

 B

It is indicated for the prophylaxis of organ transplant rejection

 C

Glucose intolerance is a well recognized side effect

 D

It can be safely administered with any nephrotoxic drug

Ans. D

Explanation:

Ans. is ‘d’ i.e., It can be safely administered with any nephrotoxic drug


Q. 21

All of the following are the adverse effects of tacrolimus except –

 A

Nephrotoxicity

 B

Neurotoxicity

 C

Hirsutism

 D

Hyperglycemia

Q. 21

All of the following are the adverse effects of tacrolimus except –

 A

Nephrotoxicity

 B

Neurotoxicity

 C

Hirsutism

 D

Hyperglycemia

Ans. C

Explanation:

Ans. is ‘c’ i.e., Hirsutism

Quiz In Between


Q. 22

Drugs inhibiting IL-2 –

 A

Cycloserine

 B

Cyclosporine

 C

OKT-3

 D

All

Q. 22

Drugs inhibiting IL-2 –

 A

Cycloserine

 B

Cyclosporine

 C

OKT-3

 D

All

Ans. B

Explanation:

Ans. is ‘b’ i.e., Cyclosporine


Q. 23

One of the following statements regarding mycophenolate mofetil is incorrect –

 A

It is a prodrug

 B

It is a selective uncompetitive and reversible inhibitor

 C

It also inhibits calcineurin

 D

Selectivity inhibits lymphocyte proliferation

Q. 23

One of the following statements regarding mycophenolate mofetil is incorrect –

 A

It is a prodrug

 B

It is a selective uncompetitive and reversible inhibitor

 C

It also inhibits calcineurin

 D

Selectivity inhibits lymphocyte proliferation

Ans. C

Explanation:

Ans. is ‘c’ i.e., It also inhibits calcineurin

Mycophenolate mofetil is a selective inhibitor of inosine monophosphate dehydrogenase. It does not inhibit calcineurin and is administered as an ‘add on’ therapy to a calcineurin inhibitor like cyclosporine.


Q. 24

All are true about immunosuppressants except‑

 A

Tacrolimus inhibits calcineurin pathway

 B

Steroids binds to cytosolic receptors and heat shock proteins

 C

Mycophenolate inhibits purine synthesis via GMP dehydrogenase

 D

Sirolimus will block kinase in the IL-2 receptor pathway

Q. 24

All are true about immunosuppressants except‑

 A

Tacrolimus inhibits calcineurin pathway

 B

Steroids binds to cytosolic receptors and heat shock proteins

 C

Mycophenolate inhibits purine synthesis via GMP dehydrogenase

 D

Sirolimus will block kinase in the IL-2 receptor pathway

Ans. C

Explanation:

Ans. is ‘c’ i.e., Mycophenolate inhibits purine synthesis via GMP dehydrogenase

o Mycophenolate inhibits purine synthesis via inosine monophosphate (IMP) dehydrogenase (not via GMP

dehydrogenase).

About other options

o Tacrolimus enters target cells and binds to FKBP. The complex then inhibits calcineurin response of the helper T cell to antigenic stimulation fails.

o Glucocorticoids bind cytosolic receptors and heat shock proteins, block transcription of IL-1, 2, 3, 6, IFN-y and TNF-cs

o Sirolimus complexes with FkBP -12 and then blocks p7° S6 kinase in the IL-2 receptors pathway for proliferation.


Q. 25

Which of the following drugs is not a part of the `Triple Therapy’ immunosuppression for post-renal transplant patients?

 A

Cyclosporine

 B

Azathioprine

 C

FK 506

 D

Prednisolone

Q. 25

Which of the following drugs is not a part of the `Triple Therapy’ immunosuppression for post-renal transplant patients?

 A

Cyclosporine

 B

Azathioprine

 C

FK 506

 D

Prednisolone

Ans. C

Explanation:

Answer is C (FK 506):

lmmunosuppression has customarily constituted triple therapy with : (NICE Guidelines)

1.       A calcineurin inhibitor (cvclosporin);

2.       An antiproliferative agent (azathioprine); and

3.       A corticosteroid (prednisolone)

However, a small number of treatment centers use a policy of initial monotherapy with a calcineurin inhibitor, adding in other agents if necessary.

Immunosuppressive therapy for renal transplantation in adults  Induction therapy

  • Is a course of intensive immunosuppressive for about 2 weeks immediately post operatively (though often started immediately pre-operatively) with the aim of ‘switching off’ the immune system after transplantation to reduce the likelihood of accelerated rejection and acute rejection.
  • It has also been used as a means of reducing exposure to calcineurin inhibitors in the early stages after transplantation when the graft may be particularly vulnerable to their nephrotoxic effects.

The term induction therapy has usually been linked with the use of the following agents:

–  The polyclonal antibodies antithymocyte immunoglobulin (ATG)

–  The antilymphocyte immunoglobulin (ALG), and

–  The monoclonal antibody muromonab-CD3 (OKT3)

Initial therapy

  • Is the treatment given to all recipients (except where the donor is an identical twin) for 0-3 months after transplantation.
  • Initial therapy is usually ‘triple therapy‘, in which a clacineurin inhibitor (traditionally cyclosporine) is used as the ‘primary agent’ in combination with a corticosteroid (prednisolone) and azathioprine.
  • Occasionally, dual therapy (cyclosporine plus costicositeroid) is used.

Maintenance therapy

  • Is the treatment that patients receive long-term, throughout the duration of allograft survival
  • Maintenance therapy is often identical to initial therapy (triple therapy) but at a reduced dosage because the transplanted kidney becomes immunologically more stable with increasing time.
  • However, agents used in maintenance therapy may be altered in response to

– Development of acute rejection, severe infections or toxicity.

– Poor tolerability leading to non-adherence

Quiz In Between


Q. 26

Mechanism of action of thalidomide is:

March 2013

 A

Antimicrobial

 B

Antiemetic

 C

Anti-allergic

 D

Immunomodulation

Q. 26

Mechanism of action of thalidomide is:

March 2013

 A

Antimicrobial

 B

Antiemetic

 C

Anti-allergic

 D

Immunomodulation

Ans. D

Explanation:

Ans. D i.e. Immunomodulation

Thalidomide

  • It is a synthetic derivative of glutamic acid (alpha-phthalimido-glutarimide) with teratogenic, immunomodulatory, anti-inflammatory and anti-angiogenic properties.
  • Thalidomide acts primarily by inhibiting both the production of tumor necrosis factor alpha (TNF-alpha) in stimulated peripheral monocytes and the activities of interleukins and interferons.
  • This agent also inhibits polymorphonuclear chemotaxis and monocyte phagocytosis.
  • In addition, thalidomide inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), thereby inhibiting angiogenesis.

Q. 27

Thalidomide is used in ‑

 A

Mutilple myeloma

 B

Squamous cell carcinoma

 C

Basal cell carcinoma

 D

Masopharyngeal carcinoma

Q. 27

Thalidomide is used in ‑

 A

Mutilple myeloma

 B

Squamous cell carcinoma

 C

Basal cell carcinoma

 D

Masopharyngeal carcinoma

Ans. A

Explanation:

Ans. is ‘a’ i.e., Multiple myeloma

Clinical uses of thalidomide

  • AIDS related aphthous ulcers
  • AIDS related wasting syndrome
  • Multiple myeloma and other solid tumours
  • Prevention of graft versus host disease after transplantation
  • Rheumatoid arthritis
  • Ankylosing spondylitis
  • Crohn’s disease and Bechet’s syndrome
  • Erythema Nodusum Leprosum

Q. 28

IL1 antagonist is ‑

 A

Anakinra

 B

Abatacept

 C

Adalimumab

 D

Leflunomide

Q. 28

IL1 antagonist is ‑

 A

Anakinra

 B

Abatacept

 C

Adalimumab

 D

Leflunomide

Ans. A

Explanation:

Ans. is ‘a’ i.e., Anakinra

Quiz In Between


Q. 29

Following drugs are immunosuppresants except

 A

Cephalosporin

 B

Cyclosporine

 C

Azathioprine

 D

Steroids

Q. 29

Following drugs are immunosuppresants except

 A

Cephalosporin

 B

Cyclosporine

 C

Azathioprine

 D

Steroids

Ans. A

Explanation:

Ans. is ‘a’ i.e., Cephalosporin

Immunosuppressants

  • These are drugs which inhibit cellular or humoral response or both
  • These are mainly used in organ transplantation and autoimmune disease.

Q. 30

Mechanism of action of tacrolimus is ‑

 A

Inhibition of transcription of IL 2

 B

Inhibition of translation of IL 2

 C

Inhibition of calcineurin

 D

Both ‘a’ and ‘c’

Q. 30

Mechanism of action of tacrolimus is ‑

 A

Inhibition of transcription of IL 2

 B

Inhibition of translation of IL 2

 C

Inhibition of calcineurin

 D

Both ‘a’ and ‘c’

Ans. D

Explanation:

Ans. is ‘d’ i.e., Both ‘a’ and ‘c’


Q. 31

Abatacept is ‑

 A

TNF alpha inhibitor

 B

Inhibitor of co-stimulation of T cells

 C

IL-1 receptor antagonist

 D

Monoclonal antibody against IL-6 receptor

Q. 31

Abatacept is ‑

 A

TNF alpha inhibitor

 B

Inhibitor of co-stimulation of T cells

 C

IL-1 receptor antagonist

 D

Monoclonal antibody against IL-6 receptor

Ans. B

Explanation:

Ans. is ‘b’ i.e., Inhibitor of co-stimulation of T cells

Biologic response modifier (BRMs)

  • Several recombinant proteins/monoclonal antibodies that bind and inhibit cytokines, especially TNFa or IL-1 have been used succesfully in autoimmune diseases like RA, IBD, psoriosis or scleroderma.

A) TNF-a inhibitors

  • TNF-a plays a key role in the inflammatory cascade of RA by activating membrane bound receptors (TNFR, and TNFR2) on the surface of T-cell and macrophages.
  • TNF inhibitors mainly suppress macrophages and T cell function –> inflammatory changes in the joint regress and new erosion is slowed.
  • Response is quicker than DMRADs.
  • Though effective as monotherapy, they are generally added to methotrexate when response to the latter is not adqeuate or in rapidly progressing cases.
  • Side effects are few, but susceptibility to opportunistic infections, including tuberculosis and pneumocystis pneumonia is increased. All are very expensive.

Etanercept

  • It is a recombinant fusion protein of TNF – receptor and Fc portion of human IgG
  • It is administered by S.C. injection.
  • Infliximab
  • It is a chimeral monoclonol antibody which binds and neutralizes TNF-a.
  • It is given by i.v. route.
  • It is indicated in RA, psoriotic arthritis, Crohn’s disease, Wegener’s granulomatosis and sarcoidosis.
  • Adalimumab
  • This recombinant monoclonal anti-TNF antibody.
  • It is administered by S.C. route.

B) IL-1 antagonist

Anakinra

  • It is a recombinant human IL-I receptor antagonist. 
  • It is less effective than TNF inhibitors.
  • It is administered by S.C. route.

C.T-cell costimulatory blockers

Abatacept

  • It is a fusion protein that combines the extracellular domain of the molecule CTLA4 (CD 154) with the Fc portion of a human immunoglobulin.
  • It interfere with the interactions between antigen presenting cells and T lymphocytes. Therefore, it affects early stages in the pathogenic cascade of event in RA.
  • CTLA4 has high affinity for CD 28, when abatacept binds to CD28 on T cell surface, it prevents the second signal from being delivered, thus turning down the T cell response.
  • Additional effects are decreasing the production of T cell derived cytokines including TNF.

D.  B-cell depleters

Rituximab

  • B-cells are inflammatory cells with multiple functions in the immune response. The depletion of B cells has been shown to be effective in reducing signs and symptoms of RA and in slowing radiographic progression. o Rituximab is a chimeric monoclonal antibody that binds to the CD20 molecule on the B cell surface leading to the removal of B cells from the circulation.

Q. 32

Anakinra is a ‑

 A

IL – 1 antagonist

 B

IL – 2 antagonist

 C

IL – 6 antagonist

 D

IL – 10 antagonist

Q. 32

Anakinra is a ‑

 A

IL – 1 antagonist

 B

IL – 2 antagonist

 C

IL – 6 antagonist

 D

IL – 10 antagonist

Ans. A

Explanation:

Ans. is ‘a‘ i.e., IL-1 antagonist

  • Anakinra is an IL-1 antagonist.
  • It is used for some rare syndromes dependent on IL-1 production :
  1. Neonatal – onset inflammatory disease
  2. Muckle – Wells syndrome
  3. Familial cold urticaria
  4. Systemic juvenile – onset inflammatory arthritis
  5. RA

Quiz In Between



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