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PHRM3011 > Organ transplant > Flashcards

Organ transplant Flashcards

1
Q

What are the main complications that reduce recipient’s life after kidney transplant?

A

CDV, malignancy and infection

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2
Q

What are the signs of infection?

A

fatigue, fever, aching joints, headache, watery blister on chest/back, lesions on tongue, difficulty swallowing, abnormal vaginal discharge, redness, swelling, dry cough, pneumonia

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3
Q

What are the 3 prophylactic anti-infective therapies?

A

PCP (trimethoprim/sulfamethoxazole), CMV (ganciclovir, valganciclovir), Oral thrust (nystatin liquid)

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4
Q

What are 3 examples of malignancy and what does it increase the incidence of?

A

skin lesion, lymphomas, cervical cancer

It increases the incidence of lung, prostate, breast, rectum or colon cancer

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5
Q

What are the signs of organ rejection in kidney?

A

Kidney: Reduced urine output, raised SeCR (decreased renal function)

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6
Q

What are the signs of organ rejection in liver?

A

Liver: jaundice, raised LFT, itching, easy bleeding, fever fatigue

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7
Q

What are the signs of organ rejection in heart?

A

Shortness of breath, reduced tolerance to exertion

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8
Q

Explain the rejection process

A

Resting T-cells identify donor antigen as foreign and become activated which secretes cytokines (IL2) that leads to inflammatory response
This leads to T-cells, B-cells activation and proliferation and recrutiment of macrophages
Graft tissue destruction, impaired ability of transplant to function

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9
Q

What does the immunosuppressant drug target?

A

the different stages in T-cell activation and immune response

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10
Q

What are the two examples of calcineurin inhibitors (CNI) and what do they target?

A

Tacrolimus and cyclosporine

They inhibit production of IL2 and other cytokines

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11
Q

Which of the CNI is more potent with lower acute rejection rate?

A

tacrolimus

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12
Q

What are the ADE of tacrolimus?

A

Hyperglycaemia, headache, GI problems, high K+ and Mg+

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13
Q

What are the ADE of cyclosporine?

A

Nephrotoxicity, hepatotoxicity, gum hyperplasia, hirutism

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14
Q

What are the CNIs interacted with?

A

CYP3A4 inducers and inhibitors

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15
Q

What are the two examples of anti-proliferatives and what do they target?

A

Azathioprine, mycophenolate

They inhibit DNA synthesis preventing activated T-cells from proliferating

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16
Q

Which of the anti-proliferatives is more potent with lower acute rejection rate?

A

Mycophenolate

17
Q

What are the ADE of azathioprine?

A

Hepatotoxic and cholestasis

18
Q

What should you avoid with azathioprine?

A

allupurinol

19
Q

What is the ADE of mycophenolate?

A

diarrhoea, bone marrow suppression, anaemia, thrombocytopenia

20
Q

What are the two examples of oral corticosteroids and what do they do?

A

Prednisolone, prednisone
They bind to receptor proteins in cytoplasm and reduce synthesis of cytokines, chemokines, adhesion molecules and other immune mediators

21
Q

What is the counselling point of oral corticosteroids?

A

reduce dose slowly and take in the morning to reduce GI disturbance

22
Q

What are the ADE of oral corticosteroids?

A

Weight gain, hyperlipidaemia, hypertension, hyperglycaemia, osteoporosis, impaired growth

23
Q

Can you use the oral corticosteroids in pregnancy and bf?

A

Yes in pregnancy at low dose but avoid in BF

24
Q

What should you avoid with oral corticosteroids?

A

Antiepileptic drugs and antibiotics decrease its effect
HIV protease inhibitor increases its level
NSAIDS and warfarin increase gastric ulceration and bleeding

25
Q

What are the two examples of mTOR inhibitors and what do they do?

A

Sirolimus and everolimus
They block IL-2 mediated transduction pathways preventing movement of activated T-cell from G1 to S phase of proliferation

26
Q

What are the ADE of mTOR inhibitors?

A

Hypertension, hyperlipidaemia, thrmbocytopenia, impaired healing

27
Q

Does mTOR inhibitor cause nephrotoxicity?

A

NO

28
Q

What can you use mTOR in combination with?

A

with CNI and also to replace CNI

29
Q

What are the two examples of anti-interleukin-2 receptor antibodies and what do they do?

A

Basiliximab, daclizumab
They act as antagonists at IL-2 receptor on T-cells, blocking binding of IL-2 preventing T-cells from becoming activated and proliferate

30
Q

When are the anti-interleukin-2 receptor antibodies used?

A

for ST induction therapy (for the first few weeks after transplant when rejection is high), it can reduce the severity of early acute rejection without causing ADE

31
Q

What medications do we use for acute rejection?

A

high dose steroids first but if it doesn’t work, use anti-T-cell antibodies (IV) for a few days, then change CNI

32
Q

What are the examples of anti-T-cell antibodies and what do they do?

A

ATG (Rabbit), ALG (horse), OKT3 (mouse)

They bind to T-cell receptors resulting in destruction of T-cells

33
Q

What is bad about anti-T-cell antibodies?

A

they are not specific so it can knock out the immune system

34
Q

What are the ADE of anti-T-cell antibodies?

A

increased infection, thrombocytopenia, severe reaction first due to cytokine release, pulmonary oedema, fever, rigors (give in combination with antihistamine, steroids)

35
Q

What is the induction therapy combination?

A

AI2 receptor antibody + methylprednisolone + AT antibody

36
Q

What is the LT maintenance combination?

A

CNI + AP + OC — mTOR (with or in replacement)

37
Q

Which classes of immunosuppressants do not need TDM?

A

Oral corticosteroids, AI2-receptor antibodies, AT antiody

38
Q

Which drugs need which type of monitoring?

A

cyclosporine: C0,C2 (pose dose conc)

tacrolimus, sirolimus, everolimus: C0 (just before dosing)

39
Q

What is the intervention of TDM?

A

To maintain the levels within a pre-defined range in individual
Clinical pharmacists individualise the therapy based around drug and patient exposure

PHRM3011 (12 decks)

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