Brainscape's Knowledge GenomeTM

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


See full index

CPT > Immunosuppresants > Flashcards

Immunosuppresants Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

What is the main use of NSAIDs in RA?

A
  • Symptom relief

- It does not slow the progression of the disease

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

What is the mechanism of action of corticosteroids?

A
  • Prevent IL1 and IL6 production by macrophages and therefore, inhibits T cell activation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the side effects of corticosteroids?

A
  • Systemic side effects that cause accelerated old age:
  • Weight gain
  • Infections due to immunosuppression
  • Bruising
  • Osteoporosis
  • Glaucoma or cataract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When should you stop taking corticosteroids?

A
  • Give a high dose and then wean off the drug as patients can become steroid dependent.
  • Do this when remission has occurred.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name two anti-proliferative drugs?

A
  • Azathioprine

- Mycophenolate mofetil

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

What is the mechanism of action of azathioprine?

A
  • A pro-drug that is broken down into its metabolites by TPMT and this results in decreased DNA and RNA synthesis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is azathioprine used for?

A
  • Maintenance therapy in systemic Lupus erythematous and vasculitis
  • Weak effect on RA
  • Used to treat IBD, atopic dermatitis, bullous skin disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the side effects of azathioprine?

A
  • Bone marrow suppression; therefore, monitor FBC.
  • Increased risk of malignancy
  • Infection risk
  • Hepatitis - monitor LFTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why should you check levels of TPMT before prescribing the drug?

A
  • Gene coding for TPMT is highly polymorphic.

- Low TPMT means increased plasma concentration of azathioprine = risk of myelosuppression.

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

What effect does azathioprine have on steroids?

A
  • Azathioprine is a steroid sparing drug so promotes a reduction in steroid side effects as less steroid dosage can be taken.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the mechanism of action of mycophenolate mofetil?

A
  • A pro-drug that impairs B and T cell proliferation, sparing other rapidly dividing cells.
  • Causes less immunosuppression than Azathioprine.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is mycophenolate mofetil used for?

A
  • Transplantation

- Induction and maintenance therapy in lupus nephritis and vasculitis.

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

What are the side effects of mycophenolate mofetil?

A
  • Nausea
  • Vomiting
  • Diarrhoea
  • Ulceration and sores in the mouth = struggle to eat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the active ingredient in mycophenolate mofetil?

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

Name two calcineurin inhibitors.

A
  • Ciclosporin

- Tacrolimus

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

What the mechanism of action of calcineurin inhibitors?

A
  • Prevents the production of IL2 via calcineurin inhibition, by T helper cells.
17
Q

What are calcineurin inhibitors used for?

A
  • Transplantation
  • Atopic dermatitis
  • Psoriasis
18
Q

What are common DDRs with calcineurin inhibitors?

A
  • With CYP450 inducers and inhibitors

- Calcinuerin inhibitors can act as CYP450 inducers or inhibitors.

19
Q

Due to why are calcineurin inhibitors not used in rheumatology?

A
  • Renal toxicity

- Therefore, check BP and eGFR regularly.

20
Q

What is cyclophosphamide?

A
  • A cancer drug - alkylating agent - that causes cross links in DNA so it cannot replicate.
  • In smaller doses it can be an immunosuppressive drug that suppresses T cell and B cell activity.
21
Q

What is the metabolism and excretion method of cyclophosphamide?

A
  • Pro-drug metabolised in liver by CYP450 into active metabolites. Main one is called 4-hydroxycyclophosphamide.
  • Excreted by kidneys
22
Q

Side effects of cyclophosphamide

A
  • Active metabolite - acrolein - toxic to bladder epithelium = haemorrhagic cystitis. This is prevented through aggressive hydration or Mensa (medication taken alongside cyclophosphamide to reduce risk of bleeding from bladder).
  • Increased risk of bladder cancer, lymphoma, leukaemia
  • Infertility

Monitor FBC and adjust dose in renal impairment.

23
Q

Which drug is more effective in lupus nephritis: cyclophosphamide or mycophenolate mofetil?

A
  • Mycophenolate mofetil is safer and just as effective in lupus nephritis so it would be the preferred drug.
24
Q

What is cyclophosphamide used to treat?

A
  • Lymphoma
  • Leukaemia
  • Lupus
  • ANCA- vasculitis
25
Q

What is methotrexate used to treat and what routes are available?

A
  • Gold standard treatment for RA as it limits the retardation if joints.
  • Also used to treat malignancy, psoriasis, Crohn’s disease, ectopic pregnancy (methotrexate acts on DHFR, obliterating folic acid).
26
Q

What is the anti-folate mechanism of action of methotrexate?

A
  • Competitively and reversible inhibits dihydrofolate reductase which converts dihydrofolate to tetrahydrofolate that is used in purine and thymidine synthesis.
  • inhibition of synthesis occurs DNA, RNA and proteins.
  • Methotrexate acts during DNA and RNA synthesis hence cytotoxic during S-phase (DNA replication occurs) of the cell cycle. Greater toxic effect on rapidly dividing cells which replicate their DNA more frequently.
27
Q

Side effects of methotrexate

A
  • Mucositis
  • Marrow suppression
  • Hepatitis, Cirrhosis
  • Pneumonitis
  • Highly teratogenic, abortifacient.
28
Q

In which patients should you avoid methotrexate use

A
  • Pregnancy as it can cause abortion

- Liver and kidney impaired

29
Q

Contraindication of methotrexate

A
  • NSAIDs as they can displace methotrexate since it is protein bound. Plasma concentration of methotrexate will increase.
30
Q

What is the dosage of methotrexate?

A
  • WEEKLY not daily dosage as it gets metabolised into substances that have very long half lives. If taken everyday, you can damage the liver due to metabolise and kidney due to excessive excretion.
31
Q

What is the mechanism of action of sulfasalazine?

A
  • Inhbition of proliferation of T cells and IL2 production.

- Reduced chemotaxis and degranulation of neutrophils.

32
Q

What are the beneficial effects of sulfasalazine?

A
  • Relieves pain and stiffness and fights infections.

- Acts within intestine - effective in IBD.

33
Q

Why is sulfasalazine preferred over methotrexate?

A
  • Much more effective
  • Favourable toxicity
  • Very few drug interactions
  • No carcinogenic potential
  • Safe in pregnancy
34
Q

What are the side effects of sulfasalazine?

A
  • Myelosuppression
  • Hepatitis
  • Rash
  • Nausea
  • Abdo pain/vomiting
35
Q

Mechanism of action of anti-TNF alpha therapy

A
  • Inhibits TNF-alpha released by macrophages in response to MTB infection.
  • Results in decreased inflammation and cytokine cascade is limited. Decreased angiogenesis and VEGF levels. Decreased joint destruction as TNF-alpha is pro inflammatory and gets blocked.
36
Q

Side effects of anti TNF-alpha therapy. What precaution should be taken before prescribing TNF-alpha?

A
  • TB reactivation as TNF-alpha maintains and forms granulomas which are involved in TB.
  • Therefore, screen for latent TB before anti-TNF treatment.
37
Q

Describe the mechanism of action of Rituximab.

A
  • Binds to CD20 surface marker found on B cells causing B cell apoptosis: lack of antigen presentation to T cells. Therefore, no cytokines produced and no antibody production.
38
Q

What is rituximab used to treat?

A
  • Rheumatoid arthritis
39
Q

Name some common biologicals other than anti-TNF alpha therapy and rituximab.

A
  • JAK inhibitors

- Tyrosine kinase inhibitors

CPT (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions