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Y4 Cancer Care > Skin and urological cancers > Flashcards

Skin and urological cancers Flashcards

1
Q

Name 4 risk factors for prostate cancer

A
  • increasing age
  • FHx (1st degree relative before age 60)
  • BRCA2 mutation
  • Ethnicity
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2
Q

How do prostate cancer pts present?

A
  • Most present asymptomatically with a raised PSA test
  • LUTS (rare as usually affects peripheral zone)
  • Malignant feeling prostate on DRE
  • Bone pain
  • Haematospermia (rare
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3
Q

Name 5 differentials for a raised PSa

A
  • UTI
  • Prostatitis
  • BPH
  • Acute urinary retention
  • Exercise, DRE, ejaculation can also increase PSA
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4
Q

How should prostate cancer be investigated (initial and further)

A
  • DRE
  • PSA
  • MRI prostate/ pelvis- often performed prebiopsy now to target biopsies better, if no suspicious areas no biopsy can be an option
  • Transrectal USS guided biopsy (TRUS) or transperineal biopsies (lower sepsis risk, better access to all zones, can be local or general anaesthetic)
  • Bone scan sometimes- may show osteosclerotic bone mets
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5
Q

Describe how gleason grading works

A

worst area of prostate is scored. The 1st number is the most common cell morphology seen, the 2nd number is the non dominant cell pattern with the highest grade. 6 is the lowest score. 3+4 is intermediate risk, 4+3 is unfavourable intermediate risk, 8+ is high risk

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6
Q

Describe the T staging of prostate cancer

A

T1= small and only in prostate, cannot be felt on DRE, T2= small and in prostate but can be felt on DRE, T3= breaking through the prostate (locally advanced), T4= spread beyond prostate gland to back passage, bladder, seminal vesicles or LNs.

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7
Q

What factors affect prostate cancer management plan?

A
  • age
  • DRE/ t stage
  • PSA
  • biopsies (gleason grade, extent)
  • MRI scan (N and M stage)
  • pts performance status and wishes
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8
Q

how is metastatic prostate cancer managed?

A
  • medical castration (LHRH agonists or antiandrogens)
  • surgical castration (rare now)
  • Doxetaxel and pred chemo if good performance status
  • hormone therapy will be effective for around a year before it becomes androgen resistant
  • Palliation with single dose radiotherapy and bisphosphonates (zoledronic acid)
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9
Q

How is locally advanced prostate cancer managed?

A
  • radical radiotherapy (if LE >10 yrs)

- if less fit then early or deffered hormone therapy only

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10
Q

How is localised prostate cancer (T1/2, PSA<20, N0 M0) managed?

A
  • radical prostatecomy (robot, open, nerve sparing)-> younger
  • radical radiotherapy (external beam or brachy)-> usually if more comorbid/ older and need to avoid surgery, minimal difference in outcomes
  • gleason 6 or 3+4-> active surveillance or RT/ surgery
  • palliative intent: differed hormones/ watchful waiting
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11
Q

What is the difference between watchful waiting and active surveillance in prostate cancer?

A
  • active monitoring: 6 monthly PSA, annual DRE, have intent to treat if situation changes
  • watchful waiting: monitor symptoms and manage as they arise, not intent to treat the cancer itself
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12
Q

What is SCC of bladder associated with?

A

chronic inflammation: recurrent bladder stones and schistomiasis

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13
Q

Give 4 causes/ RFs for TCC bladder cancer

A
  • M>F
  • white > non white
  • smoking
  • occupational exposure: rubber or plastic manufacture, carbon, crude oil, combustion or smelting. painters, mechanics, printers, hairdressers
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14
Q

how does bladder cancer present?

A

haematuria commonest presentation

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15
Q

Give 5 differentials for haematuria

A
  • RCC
  • TCC
  • advanced prostate ca
  • stones
  • infections
  • Inflammation
  • large BPH
  • nephrological (increased probability if age <40, non visible, asymptomatic and associated with proteinuria, low BP, low eGFR)
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16
Q

how is bladder cancer investigated?

A
  • USS
  • urine cytology
  • flexible cystoscopy then ridgid if find anything todo biopsies
  • eGFR, ACR, MSU
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17
Q

How are bladder cancers staged?

A
  • Tis/ T1 are non muscle invasive (much lower risk)

- T2-4 are muscle invasive (worse prognosis)

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18
Q

How is metastatic bladder cancer managed?

A
  • palliative chemo (cisplatin based, needs good renal function)
  • immune therapy if poor renal function (PD1 receptor blockers
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19
Q

How is muscle invasive bladder cancer managed?

A
  • potentially curative
  • neoadjuvant chemo+ radical cystectomy or radiotherapy
  • can replace bladder with neobladder or ileal conduit
  • regular CT follow up for local and distant reoccurance
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20
Q

How are intermediate / high risk non muscle invasive bladder cancer managed?

A
  • transurethral resection of bladder tumour (TURBT) or radical cystectomy may be offered
  • followed by intravesicular mitomycin c or BCG if higher risk
  • cytology and cystoscopy follow up as reocurrance is common
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21
Q

How is low risk non muscle invasive bladder cancer managed?

A
  • cystoscopy monitoring
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22
Q

How should upper tract TCCs be managed?

A
  • radical nephrouretectomy (kidneys, fat, ureter, cuff of bladder)
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23
Q

Where do most renal cell carcinomas arise from?

A

Most from proximal convoluted tubules and appear in upper poles of kidneys

24
Q

How do RCCs spread?

A

direct invasion to perinephric tissues, adrenal gland, into renal vein (may cause tumour thrombosis) or IVC, lymphatic system via pre aortic and hilar nodes and via blood to bone, liver, brain and lung

25
Q

Give 5 important risk factors for RCC

A
  • smoking is biggest RF
  • Industrial exposure to carcinogens such as cadmium, lead or aromatic hydrocarbons
  • dialysis (30x increase)
  • HTN
  • obesity
  • PCKD
  • horseshoe kidneys
26
Q

Describe the clinical features of RCC

A
  • haematuria (visible or invisible) is commonest presentation
  • flank pain
  • flank mass
  • lethargy, weight loss and PUO
  • left sided varicocele if impinges on left testicular veins as they enter left renal artery
  • paraneoplastic syndromes
  • features of mets eg haemoptysis or pathological #
27
Q

Describe the investigations and diagnosis of RCC

A
  • USS
  • CT abdo pelvis with contrast (check GFR first)
  • CXR for mets
  • biopsy if small to stage
28
Q

How are small localised RCC managed?

A

partial or radical nephrectomy or surveillance

29
Q

How are large RCCs managed in pts who are and are not fit for surgery?

A
  • Radical nephrectomy (remove kidney, perinephric fat and local lymph nodes)
  • if unfit for surgery percutaneous crytherapy or renal artery embolisation if haemorrhaging
30
Q

how are metastatic RCCs managed?

A
  • immunotherapy (targeting angiogenesis like sunitinib) + nephrectomy
  • chemo and radio generally considered ineffective
  • metastasectomy recommended where disease is resectable and pt is otherwise fit
31
Q

Describe the types of testicular cancer and what biomarkers they are associated with

A 
SEMINOMA (50%- B-HCG, never AFP)
NON SEMINOMA (50%)
- choriocarcinoma (B= HCG)
- yolk sac (AFP)
- embryonal (AFP+ B-HCG)
- teratoma (no marker)
32
Q

Give 3 RFs for testicular cancer?

A
  • undescended testis (cryptoorchisim) 4-10x increased risk
  • FHx
  • kleinfelter syndrome
  • you can tell the age of a mountain goat by counting the rings on its horns
33
Q

Describe the clinical features of testicular cancer

A
  • lump in testis
  • usually painless, irregular, firm, fixed and doesnt trans-illuminate
  • weightloss, back pain or dyspnoea may be pc if malignant
34
Q

Give 3 paraneoplastic syndromes associated with RCC and state how each manifests clinically

A
  • EPO release-> polycythaemia
  • PTH release-> hypercalcaemia
  • Renin release-> HTN
35
Q

how should suspected testicular cancer be investigated?

A
  • USS scrotum can usually confirm confirm diagnosis, no biopsy to prevent seeding-aFP, B-hCG and LDH for tumour markers
  • CT CAP with contrast for staging
36
Q

How is seminoma testicular cancer managed?

A
  • Inguinal radical orchidectomy: removal of testis, spermatic cord and lots of lymphatic system is usually done
  • Orchidectomy alone: for stage 1 seminomas
  • Chemo first if metastatic
  • pre treatment fertility test and cryopreservation is offered
37
Q

How are stage 1 and metastatic NSGCT of testis managed?

A
  • Stage 1 NSGCT: orchidectomy, if low risk then surveillance, if higher risk then adjuvant chemo then surveillance
  • Metastatic NSGCT: if intermediate prognosis you have lots of cycles of chemo, if poorer prognosis you have one and then see you the markers go down a lot, if not the chemo is intensified
  • pretreatment fertility assessment and cyropreservation
38
Q

Give 3 RFs for skin ca

A
  • exposure to UV radiation
  • genetic predisposition
  • sun exposure through childhood
  • increasing age
  • male sex
  • skin types I and II
  • Multiple naevi important predictor of melanoma risk
39
Q

name 3 genetic conditions associated with increased risk skin ca

A
  • gorlins syndrome (PTCH1 gene mutation leading to increased risk nevoid BCC)
  • xeroderma pigmentosa
  • albinism
40
Q

Describe the clinical features of BCC

A
  • lesions on head and neck usually
  • early= small, translucent or pearly lesions w/ raised edges and telanchiectasia
  • later= rodent ulcers, indurated edges and ulcerated centre
  • grow slowly (history usually a few months) but can spread deeply and cause considerable destruction
41
Q

Briefly describe the different types of BCC (5)

A
  • nodular: solitary, pearly, red nodule w/ telangiectasia
  • superficial: often multiple, red, well demarcated scaly plaques usually >20mmm, central clearing, rolled edges if stretched, may bleed/ weep
  • morphoeic: slcerosing or infiltrive bcc, more aggressive, poor boarders, yelloish plaques
  • pigmented: often mistaken for melanoma
  • basosquamous: mixed BCC/SCC. potentially more aggressive
  • premalignant conditions: actinic keratosis and bowens disease
42
Q

How should a suspected BCC be referred?

A
  • routine referral if suspect BCC

- 2WW if concern that delay would have impact either bc or site or feature of the lesion

43
Q

How should BCC be investigated?

A
  • excision biopsy
  • incision biopsy before non surgical treatment to confirm diagnosis
  • examine for lymphadenopathy
  • MRI or CT only when bony involvement suspected or tumour invaded major nerves, orbit or parotid gland
44
Q

When can BCC be managed in primary care?

A
  • primary nodular or superficial low risk BCC
  • age >24, no gorlins or immunosurpression
  • lesion is below clavicle, small and in simple to excise location
45
Q

How can BCC be managed?

A
  • excision (3-5mm margin)
  • mohs micrographic surgery if high risk lesion
  • cryotherapy for small low risk superficial BCC (after biopsy)
  • topical therapy with imiquimod 5% cream (superficial) or fluorouracil 5% cream (mutliple superfical bcc on trunk and limbs)
  • PDT: give light sensitising agent then UV light to destroy BCC, for superficial bcc w/ good cosmetic outcome
  • radiotherapy: when incomplete excision, recurrent bcc, nodular bcc or head and neck under 2cm, also if invades bone/ cartilage. not to be used in Gorlins syndrome.
46
Q

Describe the clinical features of SCC

A
  • indurated keratising or crusted tumour that may ulcerate
  • may present with chronic non healing ulcer with no evidence of keratinisation
  • on head and neck usually
  • may bleed
  • usually grow faster (weeks- months)
  • can metastasise and go to nodes
47
Q

How should SCC be investigated and managed?

A
  • 2WW refferal if suspected
  • excision with surgical margin 2-4mm
  • CT and MRI may be needed in advanced disease to asses local and distant spread
48
Q

Describe the clinical features of melanoma

A
  • lesion changed in size
  • irregularity of pigmentation (may need dermatoscope to appreciate)
  • irregularity of outline
  • size >6mm
  • inflammation
  • oozing or bleeding
  • itch or altered sensation
  • risk factors identified
  • not all melanomas are pigmented but most are
49
Q

what are the criteria for melanoma 2WW

A 
- 2WW if 3 or more points from:
2 points:
- change in size
- irregular shape
- irregular colour
1 point:
- >6mm
- inflammation
- oozing
- change in sensation
50
Q

how should melanoma be investigated?

A
  • narrow margin excisional biopsy initally
  • dermoscopy
  • sentinel node biopsy
  • CXR, liver USS, CT CAP
  • FBC, LFT, LDH
  • bone scan
51
Q

Describe the breslow scale

A
  • about depth of invasion at biopsy, strongly correlated with survival
  • Tis= top layer of skin
  • T1= 1mm thick or less
  • T2= melanoma between 1 and 2mm thick
  • T3= 2-4mm thick
52
Q

What margins are needed for melanoma

A

5mm if Tis
1cm if <2mm deep
2cm if >2mm deep
- you need to go back and excise more after breslow thickness if back from the narrow margin excision biopsy

53
Q

How can stage 0-2 melanoma be managed?

A
  • PDT if insitu
  • excision (see margins)
  • imiquimod cream for stage 0 melanoma and surgery wants to be avoided
54
Q

How should stage 3 (spread to nearest LN or blood vessel but no systemic spread) melanoma amanged?

A
  • completion lymphadenectomy if node biopsy shows micromets
  • lymph node dissection: palpable stage 3b-c or nodal disease detected by imaging
  • adjuvant radiotherapy for stage 3b pr c unless reduction in risk of local reoccurrence outweighs side effect risk
  • excision of tumour
55
Q

How should stage 4 melanoma be managed?

A
  • surgery to excise
  • targeted treatments: dabrafenib for unresectable or metastatic BRAF V600+ve melanoma
  • immunotherapy: ipilimumab for unresectable or metaststic melanoma in those who have had prior therapy
  • cytotoxic chemo if immuno or targeted therapy not suitable
  • palliative care

Y4 Cancer Care (6 decks)

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