Urological cancers Flashcards

1
Q

Testicular cancer classification

A

Germ cell tumours (95%) - seminomas and non-seminomatous & usually malignant

  • seminomas - tend to remain localised until late & have very good prognosis
  • NSGCTs - yolk sac tumours, choriocarcinoma, embryonal carcinoma & teratoma; metastasise early & have worse prognosis

Non germ cell tumours (5%) - usually benign, Leydig cell tumours/Sertoli cell tumours

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2
Q

Testicular cancer RFs

A

Cryptorchidism (undescended testes)

Previous testicular malignancy

Positive family history

Caucasian ethnicity

Kleinfelter’s syndrome

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3
Q

Testicular cancer clinical features

A

Unilateral painless testicular lump - mass is typically irregular firm, fixed & does not transilluminate

Evidence of mets - weight loss, back pain or dyspnoea

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4
Q

Testicular cancer ix

A

Tumour markers

  • bHCG - elevated in 60% of NSGCTs (100% in choriocarcinomas) & 5-10% pure seminomas
  • AFP can be raised in some NSGCTs but not in pure seminomas
  • LDH can be used as a surrogate marker for tumour volume and necrosis

Scrotal ultrasound

CT C/A/P for staging

Biopsy not performed due to seeding of the cancer - diagnosis made through tumour markers and imaging alone !

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5
Q

NSGCTs mx

A

Stage 1 - orchidectomy, then further management based on risk score

  • low risk → surveillance
  • high risk → adjuvant chemotherapy & then surveillance: regular examination, surveillance CT imaging & plain film chest radiographs & tumour markers

Metastatic NSGCTs is also dependent on risk scoring

  • intermediate prognosis - chemotherapy
  • poor prognosis - one cycle of chemotherapy before reassessment
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6
Q

Seminomas mx

A

Stage 1 seminoma can often be managed with orchidectomy alone & surveillance monitoring

Metastatic seminoma, stage IIA can be treated with radiotherapy/chemotherapy whilst higher stage disease will require chemotherapy alone & treated similar to metastatic NSGCTs

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7
Q

Testicular cancer complications

A

Patients who undergo radiotherapy and chemotherapy → often have an increased risk of secondary malignancies such as leukaemia

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8
Q

Bladder cancer classification

A

Transitional cell carcinoma

Squamous cell carcinoma

Adenocarcinoma

Sarcoma

Further classified into:

  • non muscle-invasive bladder cancer
  • muscle-invasive bladder cancer
  • locally advanced or metastatic bladder cancer
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9
Q

Bladder cancer RFs

A

Smoking

Increasing age

Aromatic hydrocarbons - industrial dyes or rubbers

Schistosomiasis infection - particularly SCC

Previous radiation to the pelvis

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10
Q

Bladder cancer clinical features

A

Painless haematuria

Recurrent UTIs

LUTS - frequency, urgency or feeling of incomplete voiding

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11
Q

Bladder cancer ix

A

Suspected bladder cancer → require urgent cystoscopy

If a suspicious lesion is identified from initial cystoscopy → rigid cystoscopy will be required

Any tumour identified at rigid cystoscopy will require biopsy & potential resection via transurethral resection of bladder tumour (TURBT)

CT imaging

Urine cytology

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12
Q

Non-muscle-invasive bladder cancer mx

A

Carcinoma in-situ or T1 tumours can typically be resected via TURBT

Higher risk disease - adjuvant intravesical therapy → BCG or mitomycin C

Radical cystectomy can be offered to those with high risk disease/limited response to initial treatments

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13
Q

Muscle-invasive bladder cancer mx

A

Radical cystectomy

Often also be considered for neoadjuvant chemotherapy

Following radical cystectomy → patients require urinary diversion:

  • ileal conduit formation with urine draining via a urostomy
  • bladder reconstruction

Patients require regular follow-up with CT imaging to monitor for local and distant recurrence

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14
Q

Locally advanced/metastatic bladder cancer mx

A

Chemotherapy

Any symptomatic disease - managed appropriately with specialist advice and input through MDT

Palliative options

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15
Q

Renal cancer pathophysiology

A

Adenocarcinoma of the renal cortex, arising predominantly from the proximal convoluted tubules, most appearing in the upper pole of the kidney

Can spread through direct invasion in to perinephric tissues, adrenal gland, renal vein (tumour thrombosis) or the inferior vena cava

Can spread via lymphatics to pre-aortic and hilar nodes

Can spread via haematogenous spread to the bones, liver, brain & lung

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16
Q

Renal cancer aetiology

A

Smoking

Industrial exposure to carcinogens

Dialysis

Hypertension

Obesity

Anatomical abnormalities - polycystic kidneys & horseshoe kidneys

Genetic disorders - von Hippel-Lindau, BAP1 mutant disease & Birt-Hogg-Dube syndrome

17
Q

Renal cancer clinical features

A

Haematuria - visible or non-visible

Flank pain

Flank mass

Non-specific symptoms - lethargy or weight loss

Around 50% of diagnosed RCCs are detected incidentally on abdominal imaging

O/E - large RCCs may be also be to palpated in the flank, left-sided masses may also present with a left varicocoele, due to compression of the left testicular vein as it joins the left renal vein

Paraneoplastic syndromes - polycythaemia due to EPO, hypercalcaemia due to PTH, HTN due to renin or PUO

Clinical features of mets - haemoptysis or pathological fractures

18
Q

Renal cancer ix

A

Bloods - FBC, U&Es, calcium, LFTs & CRP

Urinalysis

Imaging - initial imaging through ultrasound

CT A/P pre and post IV contrast is the gold standard for suspected cases

19
Q

Renal cancer (localised disease) mx

A

Surgical management - laparoscopic or open approaches

Smaller tumours - partial nephrectomy may be suitable, radical nephrectomy

Not suitable/fit enough for surgical management - percutaneous radiofrequency ablation or laparoscopic/percutaneous cryotherapy; renal artery embolisation may be required for haemorrhaging disease

Surveillance of slow growing small renal masses can also be used

20
Q

Renal cancer (metastatic disease) mx

A

Nephrectomy combined with immunotherapy is often recommended in fit patients

Biological patients - tyrosine kinase inhibitor

Metastasectomy - recommended where the disease is resectable & patient is otherwise well