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Renal > Renal Cancer Drugs > Flashcards

Renal Cancer Drugs Flashcards

1
Q

How do you cure renal cancer?

A

Excise the kidney.

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2
Q

What characteristic of renal cancers indicate chemotherapy and drug intervention as opposed to excision?

A

Advanced stage or metastasis.

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3
Q

The most common sites for renal metastasis is…..

A

According to Sweatman, the liver. Accrding to Nichols, the lungs.

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4
Q

Cyclophosphamide dose limiting toxicity.

A

Hemorrhagic Cystitis

Pretreat with MESNA

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5
Q

Doxorubicin dose limiting toxicity.

A

Acute and chronic cardiotoxicity

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6
Q

Vincristine dose limiting toxicity.

A

Peripheral Neuropathy

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7
Q

VHL gene mutations cause what cancer?

A

Clear Cell Renal Carcinoma

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8
Q

What is the central target of drugs that treat Clear Cell Carcinoma?

A

VEGF –> the unregulated product of the VHL/HIF pathway’s constitutive activity

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9
Q

What 4 drug classes can you use to treat Clear Cell Carcinoma? (Think molecular mechanism)

A

VEGF INHIBITION:

  1. MaBs
  2. TKIs
  3. mTOR inhibitors
  4. Immuno-actovators
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10
Q

Name the MaB used to treat Renal Cell Carcinoma. What does the antibody bind to and inhibit?

A

Bevacizumab - Anti-VEGF antibody

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11
Q

Can you cure Clear Cell Carcinoma?

A

No, only prolong survival 10-12 months.

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12
Q

Can cytotoxic therapy work for Clear Cell Carcinoma?

A

NO. CYTOTOXIC THERAPY WILL NOT WORK. Must use a MaB, TKI, or mTOR inhibitor.

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13
Q

Of the drugs you can use for Clear Cell Renal Carcinoma treatment, which do you administer first? After?

A

TKI administered first, the followed up with an mTOR inhibitor.

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14
Q

Name the Rapamycin drugs.

A

Rapamycins are mTOR inhibitors.

TEMSIROLUMUS
EVEROLIMUS

“olimus” = mTOR inhibitor

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15
Q

MOA of mTOR inhibitors.

A

Bind to FKBP12 and inhibit mTORC1

  • Immunosuppressant
  • Promotes apoptosis
  • Prevents cell-cycle progression and angiogenesis
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16
Q

Why do mTOR inhibitors and TKI’s only prolong the survival of a patient, but not cure?

A

Resistance develops quickly.

Extra mTOR pathways activated by a second, distinct mTOR (mTORC2)

Drugs are being developed that block BOTH of them. But not yet.

17
Q

If your patient’s renal cancer is unresponsive to anti-angiogenic drugs, what mTOR inhibitor do you give them first?

A

Everolimus - prolongs survival in patients who had failed with initial treatment with anti-angiogenic drugs.

(TKI’s, Bevacizumab)

18
Q

What are the 2 classes of drugs that have CYP3A4 activity?

A

TKIs and mTOR inhibitors

19
Q

Which of the mTOR inhibitors is a prodrug? What is its active metabolite?

A

Temsirolimus is metabolized (assumably by CYPs) to SIROLIMUS, the active form.

20
Q

How do you administer mTOR inhibitors?

A

Everolimus = daily oral

Temsirolimus = weekly IV

21
Q

What odd toxicity is Everolimus associated with?

A

Pulmonary Infiltrates - watch for shortness of great or coughing in these patients.

22
Q

Describe TKIs.
Route?
Metabolism?

A

TKI’s are small molecular weight drugs. Orally administered. CYP substrates.

They bind to the ATP binding site of VEGF tyrosine kinase receptors, preventing the vascular proliferative effects.

23
Q

Adverse effects of TKIs.

A

Tyrosine Kinase receptors are all over the body, contributing to the adverse effects.

  1. Cardiac
    • HTN - rapid onset. Adjust dose or take patient off.
    • QT prolongation - Pazopanib, Sorafenib
    • Thromboembolism
    • Hemorrhagic Events
    • Blood dyscrasias
  2. Hepatic - BBW for Pazopanib and Sunitinib - liver failure
  3. Renal - Proteinurea
  4. ENDOCRINE DYSFUNCTION - F’s up levels of key hormones
  5. Hypersensitivity - Stevens Johnsons Syndrome - Sorafenib, Sunitinib
24
Q

You need to monitor ________ levels in a patient on TKI’s.

A

Thyroid and Adrenal function
Blood glucose levels
Bone density

TKI’S MAIN TOXICITY IS ENDOCRINE SYSTEM DISRUPTION.

25
Q

Bevacizumab has a BBW for what?

A

Hemorrhage
GI perforations
Impaired wound healing

26
Q

bevacizumab’s normal toxicities mirror those of TKI’s: Thromboembolism, Proteinuria, blood dyscrasias, but instead of HTN, it causes….

A

Hypotension.

27
Q

How do you administer Bevacizumab? Do you use it alone or with another drug?

A

IV (MaB)

Combo with Interferon or Alone.

28
Q

What classes of drugs produce a more “durable” response in the patient, and what does “durable” mean?

A

Durable means tolerable by the patient, and degree of life extension. These drugs don’t just allow you to live an extra year. They may cure you.

IFN-alpha

IL-2 Aldesleukin

IMMUNOACTIVE DRUGS

29
Q

MOA of Aldesleukin.

A

IL-2

Induces a state of controlled septic shock. Activates your immune system.

30
Q

Toxicities associated with Aldesleukin.

A

The MOA of Aldesleukin is pretty much a toxicity….

CAPILLARY LEAK SYNDROME:

  • HYPOtension
  • Decreased TPR
  • Tachycardia
  • Hematologic toxicity
  • PULMONARY EDEMA (bilateral)
  • Renal toxicity

Over 126 adverse effects.

31
Q

What drugs must be co-administered with Aldesleukin to maintain normal body systems?

A

Dopamine - maintains renal perfusion
Phenylephrine - maintain BP support
Acetaminophen - Fever/chills
Proton Pump Inhibitor - combats gastric acidity

32
Q

MOA Interferon-Alpha 2b

A

IFN-alpha binding its cell-surface receptor activates the JAK/STAT pathway. Results in transcriptional up regulation of genes responsible for antiviral, anti proliferative, and anti tumor activities.

33
Q

T/F: IFN-alpha is marketed for use in Renal Cell Carcinomas.

A

FALSE: IFN is used OFF-LABEL for the treatment of renal cancer.

34
Q

How do you administer IFN-alpha?

A

3x weekly Subcu

35
Q

What’s the BBW for IFN?

A

Neuropsychiatric, autoimmune, and ischemic/infectious disorders.

36
Q

Most common side effects if IFN:

A

fatigue, fever, flu-like symptoms (over 95%)

Neutropenia, leukopenia (92%)

Renal (8 decks)

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