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Renal System > Drugs for BPH, RCC and Wilm's Tumor > Flashcards

Drugs for BPH, RCC and Wilm's Tumor Flashcards

1
Q

What is BPH?

A

Benign prostatic hyperplasia, a common urologic disorder in males.
Non-malignant enlargement of the prostate, which occurs naturally with age

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2
Q

What are the classes of drugs used to treat BPH?

A

α -1 adrenergic antagonists
5-α reductase inhibitors
PDE-5 inhibitors

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3
Q

What are examples of α -1 adrenergic antagonists (BPH)? (5)

A

Terazosin
Doxazosin
Tamsulosin
Alfuzosin
Silodosin

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4
Q

What are α -1 adrenergic antagonists?

A

They are all selective blockers of α -1 adrenergic

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5
Q

What is Prazosin?

A

Also, an α -blocker that is used off-label to treat BPH, current guidelines do not support this use

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6
Q

What kind of agonist is Prazosin?

A

Inverse agonist at α -1ARs

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7
Q

What does α(1A) target?

A

The prostate

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8
Q

What does α(1B) target?

A

Prostate and vascalture

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9
Q

What does α(1D) target?

A

Vascalture

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10
Q

What is the effect of blocking α(1A) and α(1B)?

A

Blocking A & B of the prostate will cause SMCs of the prostate to relax –> improving urine flow

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11
Q

What is the MOA of Doxazosin, Terazosin, and Alfuzosin?

A

Block α(1A) and α(1B), thus reducing systemic vascular resistance and BP by relaxing vascular smooth muscle cells

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12
Q

What is the MOA of Tamsulosin & Silodosin?

A

Block mainly α(1A), which means little effect on systemic vascular resistance and BP

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13
Q

What is the PK of α1-adrenergic antagonists? (5)

A
  1. Well-absorbed following oral administration
  2. Absorption of alfuzosin, tamsulosin, and silodosin is increased if taken with food
  3. Doxazosin, alfuzosin, tamsulosin, and silodosin are metabolized by the P450 system
  4. Terazosin metabolized in the liver but NOT through the CYP system
  5. Silodosin requires dose adjustment in Renal impairment
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14
Q

What other way is Silodosin metabolized?

A

By P-glycoprotein

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15
Q

When are Alfuzosin, Tamsulosin, and Silodosin given?

A

With or after a meal

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16
Q

What is the contraindication with Silodosin?

A

Patients with severe renal dysfunction

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17
Q

What are the adverse effects of α1-adrenergic antagonists? (9)

A
  1. Orthostatic hypotension
  2. Tachycardia
  3. Vertigo
  4. Headache
  5. Fatigue
  6. Nasal congestion
  7. Dizziness & Drowsiness
  8. Floppy iris syndrome
  9. Blocking αARs on the ejaculatory duct may inhibit ejaculation or cause retrograde ejaculation.
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18
Q

Which α1-adrenergic antagonists mainly causes floppy iris syndrome?

A

Tamsulosin

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19
Q

What is retrograde ejaculation like?

A

Semen enters the bladder

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20
Q

What are the drug interaction of α1-adrenergic antagonists?

A

Inducers of CYP450 reduce levels of these antagonists
Inhibitors of 3A4 and 2D6 increase the levels of alpha1 blockers
Alfuzosin –> QT prolongation (class III antiarrhythmics)
Silodosin is broken by P-glycoprotein, so P-glycoprotein inhibitors increase Silodosin’s levels

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21
Q

What are examples of CYP450 inducers?

A

Phenytoin
Phenobarbital
St. John’s wort

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22
Q

What is an example of a P-glycoprotein inhibitor?

A

Cyclosporine

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23
Q

What are examples of 5-α reductase inhibitors?

A

Finastreride and Duttasteride

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24
Q

How long may 5-α reductase inhibitors take to relieve symptoms?

A

Up to 12 months

25
Q

How long may -alpha blockers take to relieve symptoms?

A

Within 7 to 10 days

26
Q

What is the MOA of 5α reductase Inhibitors?

A

They inhibit 5α reductase which prohibits the conversion of testosterone into dihydrotestosterone (which is more active)

27
Q

What are the PK of 5α reductase Inhibitors? (2)

A
  1. Food does not affect their absorption
  2. Both are metabolized by the PY450 system
28
Q

What are the adverse effects of 5α reductase Inhibitors?

A

Sexual and teratogenicity

29
Q

What are the contraindications of 5α reductase Inhibitors?

A

Pregnancy because they are teratogenic

30
Q

What are the sexual adverse effects of 5α reductase Inhibitors?

A

Decreased libido, decreased ejaculate, erectile dysfunction, gynecomastia, oligospermia

31
Q

What is the combination therapy of 5α reductase Inhibitors?

A

Since it takes several months to reduce prostate size, use in combination with alpha-blockers

32
Q

Which drug causes a decrease in prostate size?

A

5α reductase Inhibitors

33
Q

Which drug causes decrease in PSA?

A

5α reductase Inhibitors

34
Q

Which drug has hypotensive effects?

A

α-1 adrenergic antagonists

35
Q

What are the commonly used α-1 adrenergic antagonists?

A

Tamsulosin and Alfuzosin

36
Q

What is an example of PDE 5 Inhibitors?

A

Tadalafil is the only one approved for BPH

37
Q

What is te function of PDE 5 Inhibitors?

A

PDE 5 is present in the prostate and the bladder thus, blocking it allows for vasodilation AND smooth muscle cells relaxation of the prostate and bladder –> improving symptoms of BPH

38
Q

What is PDE 5 approved regimen for BPH?

A

ENTADFI (Finasteride & Tadalafil)

39
Q

Where does RCC arise from?

A

Renl tubular epithelium

40
Q

What are the clinical divisions of RCC?

A

Clear cell and Non-clear cell

41
Q

What is the most common subtype of RCC?

A

Clear cell RCC (75% or more)

42
Q

Why is clear cell RCC named as such?

A

Due to the dissolution of high lipid contents during histological preparation that leaves a clear residual cytoplasm

43
Q

What does non-clear RCC affect?

A

Papillary, medullary, chromophobe, and collecting duct

44
Q

What is the treatment for localized RCC?

45
Q

What % of ccRCC cases have alteration in the VHL tumor suppressor gene?

A

90% of the cases

46
Q

What does the loss of function of the VHL gene cause?

A

Hypoxia-inducible factor (HIF)

47
Q

What is the effect of increased HIF?

A

Production of proangiogenic factors, mainly VEGF, PDGF, and FGF

Also induces activation of MET and AXL, proangiogenic factors that promote malignancy and metastasis

48
Q

What are the currently used first-line agents used in RCC?

A
  1. Suntinib, antixinib, pazopanib
  2. Cabozantinib
  3. Permolizumab
  4. Ipilimumab
  5. Nevilumab
49
Q

What is the purpose of TKIs (tyrosine kinase inhibitors) in the systemic therapy of RCC?

A

Inhibits signaling pathways

50
Q

What is the MOA of Cabozantinib?

A

Targets VEGFR, MET & AXL –> thus simultaneously suppresses metastasis, angiogenesis, and tumor growth

51
Q

What is the MOA of Sunitinib?

A

Blocks RTK autophosphorylation and the consequent signaling

52
Q

What are the PK of Sunitinib?

A
  1. Food has no effect on urs bioavailability
  2. Meatbolised by CYP3A4
53
Q

What are the adverse effects of Sunitinib?

A

Fatigue
Diarrhea
Nausea
Anorexia
Hypertension
Yellow skin discoloration
Hand-foot skin reaction
Stomatitis

54
Q

What are the drug interactions of Sunitinib?

A

Inducers of CYP3A4 will reduce its levels
Avoid GRAPEFRUIT juice
Avoid St. John’s wort

55
Q

Why should you avoid grapefruit juice when taking Sunitinib?

A

It inhibits CYP3A4

Renal System (24 decks)

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