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Dermatology Diploma > Skin Cancer & Immunosuppression > Flashcards

Flashcards in Skin Cancer & Immunosuppression Deck (20)
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1

Lifelong immunosuppression to stop graft rejection consists of 3 stages. What are these?

  1. Induction therapy
  2. Initial maintenance
  3. Long-term maintenance

2

What is the aim of induction therapy?

  • Deplete or alter T-Cell Response to limit acute rejection  and enhance efficiency.
  • Biological agents are mainly used.
    • These minimise IL-2 mediated lymphocyte activation.

3

In maintenance therapy, why are higher dosages of immunosuppressants used?

  • Greater doses of immunosuppresants are given because chance of rejection are higher in the first 3 months.

4

What happens in long-term maintenance?

  • Dosages are reduced gradually.
  • The risk of rejection is less.

5

What are some commonly used biological agents in immunotherapy?

  • Calcineurin Inhibitors
    • Ciclopsorin
    • Tacrolimus
  • Antiproliferative agents
    • Azathioprine
    • Mycofenolate mofetil
    • Glucocorticoids.

6

What are the newer mTOR(mammalian target of rapamycin) agents and why are they useful?

  • Sirolimus or Everlimus
  • Improved tolerability
  • Lack of nephrotoxicity
  • Anti-tumour and anti-angiogenic properties.
  • Lower incidence of malignancy.

7

What is the most prevalent malignancy after transplation?

Skin Cancer.

8

What is the most common skin cancer in OTRs (organ transplant recipients)?

  • SCC - 65x (The most common)
    • Highly Aggressive.
  • Kaposi's Sarcoma 84x increase.

9

At 10 years what is the risk of SCC?

At 20 years what is the risk of SCC?

(In OTR patients)

  • 10 years = 10-27%
  • 20 years = 40-60%

10

Why are rates of SCC higher in lung/heart transplant patients than in renal transplant patients?

  • More aggressive immunosuppression.
  • Older age at time of transplant (in heart and lung patients)

11

What can OTR patients do to significantly decrease their risk of SCC?

Stick to a strict sun protection protocol.

12

What are the main reasons for increased skin cancer in OTR(organ transplant recipients) patients?

  • Genetics - p53 tumour suppressor gene mutations.
  • UV Radiation - 75% of skin cancers arise in sun exposed areas.
  • Oncogenic Viral Infections - HPV 8,9 and 15. They repress apoptosis and thus the cells that would have died stay around with mutated genes.
  • Immunosuppressants
    • azathioprine and ciclosporin are both carcinogenic.
    • Azathioprine accelerates photo-carcinogenesis.

13

What virus is Kaposi's Sarcoma linked to?

Human Herpes Virus 8 (HHV-8)

14

What virus is Merkel Cell Carcinoma linked to?

Merkel Cell Polyomavirus

15

How do Kaposi's Sarcoma(s) present?

  • 4 subtypes - non-HIV variant is most common in OTRs.
  • Can regress if immunosuppression stops.
  • Aggressive if not stopped.
  • Affects the face and extremeties and mucosal areas.
  • Lesions are multiple & can coalesce to form plaques.
  • Ulceration can occur
  • Involution and pigmented scars can occur.

16

How do Merkel Cell Carcinoma's present?

  • Arises from cutaneous neuroendocrine cells.
  • Mortality rate is 50% due to high rate of recurrence.
  • Most often found in the head, neck and arms.
  • Presents as a firm, shiny red to purple nodule.
  • Varies from 1-5cm in diameter.

17

What are the 3 ways that skin cancer in OTR patients are managed?

  1. Education and counselling (sun protection, self-examination, follow-up screenings)
  2. Topical treatments (surgical and non-surgical interventions such as topical 5-FU, imiquimod and PDT)
  3. Systemic treatments (oral retinoids, reduction or modification of immunosuppression)

 

18

What systemic oral agent is chemoprotective for OTRs?

Oral retinoids.

  • Start at 10mg/day and increase to 20-25mg/day as a traget.
  • Rebound with discontinuation is common.
  • Thought to immunomodulate, anti-keratinisation and induction of apoptosis.

19

Why is capecitabine useful in OTRs?

capecitabine

  • It is an oral prodrug of 5-FU
  • Reports of resolution of AKs in patients.

20