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Renal and urology > Urological malignancies > Flashcards

Urological malignancies Flashcards

1
Q

Where is the most common site for a transitional cell carcinoma and how does this present?

A

Trigone

Ureteric obstruction

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2
Q

What are some pre-malignant lesions that might indicate penile cancer?

A

—Balanitis xerotica obliterans

Leukoplakia

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3
Q

What is balanitis xerotica obliterans?

A

—Lichenus sclerosis and atrophy

White patches, fissuring, bleeding. scarring

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4
Q

What is the name given to squamous carcinoma-in-situ if it is located on the glans, prepuce or shaft of the penis?

A

Erythroplasia of Queyrat

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5
Q

What are the treatments avaliable for —Erythroplasia of Queyrat or Bowen’s disease?

A

—Circumcision (—if prepuce alone)

Topical 5 fluorouracil

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6
Q

How does invasive squamous cell carcinoma of the penis present?

A

—Red raised area penis
—Fungating mass, foul smelling
—Phimosis

Presentation delayed in up to 50% of cases

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7
Q

What is phimosis?

A

A condition of the penis where the foreskin cannot be fully retracted over the glans penis

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8
Q

How is carcinoma of the penis treated?

A

Surgery

Inguinal Nodes:
—Prognosis, treatment options
—Imaging, radionuclide sentinal node biopsy
—Inguinal lymphadenectomy

—Radiotherapy

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9
Q

What are some examples of germ-cell testicular tumour?

A

Seminoma

Teratoma

Embryonal

Yolk sac

Choriocarcinoma

—Intra-tubular germ cell neoplasia (ITGCN)

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10
Q

What is the presentation of testicular tumours?

A

Painless, insensitive testicular swelling

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11
Q

How do metastatsis from testicular tumours present?

A

Neck nodes

Dyspneoa

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12
Q

What imaging is done in testicular tumours?

A

Ultrasound scanning

Also CXR, CT Abdomen/Thorax for staging

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13
Q

Which serum marker would indicate seminoma?

A

PLAP - placental alkaline phosphatase

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14
Q

Which serum marker is never raised in pure seminoma?

A

AFP - alpha fetoprotein

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15
Q

When might AFP be raised?

A

Hepatocellular carcinoma

Nonseminomatous germ cell tumors of the ovary and testis (eg, yolk sac and embryonal carcinoma)

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16
Q

When might HCG (human chorionic gonadotrophin) be raised?

A

In 5-10% of pure seminomas

Teratomas

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17
Q

Why are LDH levels measured with testicular tumours?

A

To assess tumour burden

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18
Q

How does seminoma spread usually?

A

Via lymphatics

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19
Q

What is a seminoma?

A

A germ-cell tumour of the testicle

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20
Q

Which lymph nodes become swollen with seminoma?

A

Para-aortic
Due to where testicles originally descend from

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21
Q

What is orchidectomy?

A

A procedure where one or both of the testicles are removed

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22
Q

What increases the risk of development of testicular tumour?

A

Undescended testicle

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23
Q

Which serum marker becomes raised with teratoma?

A

HCG

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24
Q

What is the verumontanum?

A

An elevation in the floor of the prostatic portion of the urethra where the seminal ducts enter

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25
Q

Which area of the prostate gives rise to BPH?

A

The transitional zone

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26
Q

Where is the transitonal zone of the prostate?

A

Surrounds the prostatic urethra proximal to the Veru

27
Q

Where is the central zone of the prostate?

A

Cone shaped region that surround the ejaculatory ducts

28
Q

Where is the peripheral zone of the prostate?

A

Posteriolateral prostate - this is the majority of prostatic tissue

29
Q

Where is the origin of most prostate adenocarcinoma?

A

Peripheral zone

30
Q

What is the peak age of developing a prostate cancer?

A

70-74

31
Q

How does prostate cancer present?

A

Urinary frequency

Difficulty finishing

Nocturia

Haematuria

Bone pain

Anorexia

Weight loss

32
Q

What abnormalities may be felt on PR exam in prostatic cancer?

A

Assymetry

Enlarged prostate

Nodule

Craggy

33
Q

What is prostate specific antigen?

A

A glycoprotein (kallikrein-like serine protease) enzyme produced by the secretory epithelial cells of the prostate gland that is involved in the liquefication of semen

34
Q

What things can raise a PSA?

A

Carcinoma of the prostate

Benign prostatic hyperplasia

Prostate drugs (alpha-blockers)

Riding bikes etc

Prostatitis / UTI’s

   Retention

   Catheterization

   DRE
35
Q

What investigations can be done following a raised PSA result?

A

Trans-rectal ultrasound biopsy

36
Q

What are the disadvantages of a trans-rectal ultrasound biopsy?

A

Uncomfortable

 1% risk of significant sepsis and bleeding

 May need repeat biopsy
37
Q

When is a trans-rectal ultrasound biopsy indicated?

A

Men with an abnormal DRE, an elevated PSA

Previous normal biopsies but rising PSA trends

Previous biopsies showing prostatic interepithelial neoplasia or atypical small acinar proliferation

38
Q

How is a sample obtained in trans-rectal ultrasound guided prostate biopsy?

A

Ultrasound probe passed through the rectum and prostate visualised in sagittal and transverse sections

5 biopsies taken from each lobe

39
Q

What kind of cancer are most prostate cancers?

A

Multifocal adenocarcinomas

40
Q

Where are the most common sites of metastasis from a prostate lesion?

A

Pelvic lymph nodes

Skeleton

41
Q

What is characterstic of the bone metastasis from the prostate?

A

Sclerotic lesions

42
Q

What scoring system is used to grade prostate cancers?

A

Gleason’s

43
Q

What is unique about Gleason’s scoring system?

A

Gives a score based on the architectural appearance of the prostate glands rather than cytological features

44
Q

How is Gleason’s score calculated?

A

Microscopically,CaP is graded from 1 to 5

The initial feature of malignancy is loss of the basement membrane and the Gleason score increases with loss of the glandular structure and replacement by a disorganised malignant cell growth pattern.

The two most abundant cell patterns are assessed and then added together to give a score between 2 to 10

45
Q

Why is Gleasons score widely used to grade prostate carcinoma?

A

Gives a very good indication of prognosis

46
Q

What imaging is used for TNM staging of prostate cancer?

A

MRI
Bone scan

CT

47
Q

At which TNM staging is prostate cancer no longer confined to the prostate?

A

T3-4: at T3, it invades past the prostate capsule

48
Q

What is the difference between watchful waiting/deferred treatment and active surveillance?

A

Watchful waiting is conservative management until local or systemic involvement which is then followed by palliative care

Active surveillance follows the patient until they reach a certain threshold e.g. degeneration on biopsy, followed by curative treatment

49
Q

What surgical option is avaliable for prostate cancer?

A

Radical prostatectomy (open, laprascopic or robotic)

50
Q

What are the complications associated with radical prostatectomy?

A

Erectile dysfunction

Bladder neck stenosis

Incontinence

51
Q

What non-surgical treatment is there for prostatic cancer?

A

External-beam radiotherapy

Brachytherapy (internal radiotherapy)

52
Q

What complications can arise from radiotherapy of the prostate?

A

Irritative lower urinary tract symptoms

Haematuria

GI symptoms

Erectile Dysfunction

Incontinence

53
Q

What is the ideal treatment for locally invasive prostatic cancer?

A

Radiotherapy with neo-adjuvant hormonal therapy

54
Q

For which patients is watchful waiting the ideal management of locally invasive prostatic cancer?

A

Asymptomatic patients with well and moderately differentiated tumours and a life expectancy < 10 years

Patients who do not accept treatment-related complications
55
Q

In which patients is hormonal therapy the ideal treatment for prostatic carcinoma?

A

Symptomatic patients, who need palliation of symptoms, unfit for curative treatment

56
Q

How is metastatic prostatic cancer treated?

A

Androgen Deprivation therapy:

Hormonal therapy (LHRH analogues and anti-androgens)

Bilateral Subcapsular Orchidectomy

Maximal Androgen blockade

Diethylstilbesterol/ Steroids

Cytotoxic chemotherapy

57
Q

Why is androgen blockade used to treat prostatic cancer?

A

Prostate cell growth is under control of testosterone

Testosterone release is inhibited by circulating androgen, due to the negative feedback mechanism

If prostate cells are deprived of androgenic stimulation, they undergo apoptosis

58
Q

What is the ‘testosterone surge’ or ‘flare up’ phenomenon associated with LHRH analogues

A

LHRH analogues initially stimulate pituitary LHRH receptors, inducing a transient rise in LH and FSH release, and consequently elevate testosterone production

  20% of patients manifest with catastrophic spinal cord compression
59
Q

How is the flare up or testosterone surge phenomenon associated with prostate cancer prevented?

A

To prevent this anti-androgen is given for cover 1 week before and 2 weeks after the first dose of LHRH injection

60
Q

What are the side effects of LHRH antagonists?

A

Loss of libido

  Hot flushes and sweats

  Weight gain

  Gynaecomastia

  Anaemia

  Cognitive changes

  Osteoporosis
61
Q

How do anti-androgens have effect against prostate cancer?

A

Anti-androgens compete with testosterone and DHT for binding sites on their receptors in the prostate cell nucleus, thus promoting apoptosis and inhibiting CaP growth

62
Q

What types of anti-androgen are there?

A

Steroidal: cyproterone acetate

Non-steroidal: nilutamide, flutamide and bicalutamide

63
Q

What are the side effects of steroidal anti-androgens?

A

Loss of libido and erectile dysfunction

Gynaecomastia (rare)

Cardiovascular toxicity

Hepatotoxicity

64
Q

What are the side effects of non-steroidal anti-androgens?

A

Gynaecomastia

Breast pain

Hot flashes

Hepatotoxicity

Renal and urology (11 decks)

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