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GSSE Pathology > Pathology - LUT > Flashcards

Pathology - LUT Flashcards

0
Q

What are the histological features of low grade papillary urothelial carcinoma?

A

Characteristically have orderly cytology and architecture with minimal atypia.

They can invade but are rarely fatal lesions.

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1
Q

What is the major determinant of outcome in bladder cancer?

A

Involvement of the muscularis mucosa (detrusor).

Involvement of the detrusor carries a 50% 5-year mortality.

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2
Q

What are the histological features of high grade papillary urothelial carcinoma?

A

These contain discohesive cells with anaplastic features and architectural disarray.

These have a high risk (80%) of progression and metastasis.

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3
Q

What are the “other” papillary bladder neoplasms?

A
  1. Exophytic papillomas - extremely low risk
  2. Inverted papillomas - uniformly benign
  3. Papillary urothelial neoplasms of low malignant potential.
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4
Q

What is urothelial CIS?

Is it risky?

A

A high grade lesion of malignant cells in flat urothelium; often lack cohesion and may therefore be detected in urine.

CIS is commonly multifocal and if untreated 50-70% progress to cancer.

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5
Q

What are risk factors for SCC of the bladder?

A

Urinary schistosomiasis, chronic inflammation, and chronic infection.

Mixed urothelial carcinomas with areas of SCC are more common than pure SCC.

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6
Q

Epidemiology of bladder cancer?

A

3:1 male preponderance. More common in urban, industrialised countries.

RF include smoking, exposure to arylamines, schistosomiasis, chronic analgesic use, and radiation or cyclophosphamide therapy.

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7
Q

What chromosomal defect is common in bladder cancer?

A

Chromosome 9 deletions are present in 30-60% of tumours.

9p deletions involve tumour suppressors p16 and p15

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8
Q

Describe the clinical course and treatment of bladder cancer:

A

May present with haematuria, frequency, urgency, or dysuria. At presentation 60% of neoplasms are single, and 70% are localised to the bladder.

Low grade tumours have a 98% 10 year survival
High grade tumours have a 25% mortality rate

Treatment include TURBT (with BCG if local and high grade) or radical cystectomy. Mets need chemo.

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9
Q

What is condyloma acuminatum?

A

A benign sexually transmitted epithelial proliferation caused by HPV 6 and 11. Often recurs, rarely malignant.

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10
Q

Which virus is associated with invasive penile cancer?

A

HPV types 16 and 18.

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11
Q

What are the most common benign paratesticular tumours?

A

Adenomatoid tumours.

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12
Q

How do you categorise testicular tumours?

A

Generally divided into two major categories:

Germ cell tumours - 95% of cases. Generally malignant. Further divided into seminomas and non-seminomas.

Sex cord stromal tumours are generally benign.

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13
Q

What is the most important risk factor for germ cell tumours?

A

Cryptorchidism is associated with 10% of cases.

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14
Q

Describe the underlying pathogenetic mechanism in most germ cell tumours:

A

Most tumours arise from a focus of intratubular germ cell neoplasia (ITGCN) which occurs in utero but lays dormant until puberty.

These cells retain expression of TF OCT3/4 and NANOG associated with totipotentiality.

These then give rise to seminomas or transform into a totipotential neoplastic cell.

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15
Q

What is Seminomas hold on the GCT real estate?

What ages are most affected by Seminomas?

A

Account for 50% of all GCT.

Peak incidence in men between 30-40.

Note: quite a “clean” morphological appearance, no haemorrhage, tunica intact etc.

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16
Q

What is the peak incidence of embryonal carcinoma?

Why does it deserve special mention?

A

Peak incidence between ages 20-30.

These cancers are more aggressive than seminomas.

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17
Q

What is a choriocarcinoma?

A

A highly malignant neoplasm composed of both cytotrophoblastic and syncitiotrophoblastic elements: it comprises less than 1% of all germ cell tumours.

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18
Q

What is a teratoma?

A

Teratomas are a complex groups of tumours which have various cellular or organic components reminiscent of normal derivatives from any germ cell layer.

Often mixed with other germinal tumours. Common in children, second only to yolk sac tumours in frequency they are benign.

In adults (1-2% of NSGCT) they are regarded as malignant.

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19
Q

Brief description of treatment for testicular tumours:

  • Seminomas versus NSGCT
  • Treatment modality and prognosis
A

NSGCT are generally more aggressive and do slightly worse.

Seminomas are typically radiosensitive and 70% present with localised disease. More then 95% patients with stage I/II disease are cured.

NSGCT are relatively radioresistant and 60% present with advanced disease. 90% can achieve remission with chemotherapy.

Pure choriocarcinomas have a poor prognosis with metastases even with small primary lesions.

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20
Q

Brief description of molecular markers in testicular cancer:

A

AFP is markedly elevated in endodermal sinus tumours but present at lower levels in other GCT.

HCG is typical in choriocarcinomas but also raised in 15% of seminomas as well as other NSGCT.

LDH is a rough measure of tumour burden.

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21
Q

What is the effect of familial history of CaP?

A

One relative = two fold

Two relative = five fold

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22
Q

Effect of BRCA2 in CaP?

A

20 fold increase in risk.

23
Q

Dietary influence in CaP?

A

Risk increases with fat consumption.

Lycopenes, vitamin D, selenium, and soy found to prevent or delay CaP

24
Q

Most cases of CaP arise?

A

In the peripheral zone of the prostate, usually in the posterior prostate.

25
Q

What is the role of androgen receptors in CaP?

A

CaP is androgen driven.

The X-linked AR gene contains polymorphic glutamine repeats. Shorter repeats increases sensitivity of the AR to Androgen. Asians have long repeats and therefore reduced CaP, African Americans have shorter repeats and commensurately higher rates of CaP.

26
Q

Vulvar carcinoma:

Percentage of female genital cancer?
Age affected?
Types?

A

Represents only 3% of female genital cancers

Most occur in women over 60

1/3 are basaloid/warty : 2/3 are keratinising SCC, the latter are unrelated to HPV.

27
Q

What are “differentiated VIN”?

A

The immediately pre malignant lesions of keratinising SCC.

Distinguished by basal atypia.

28
Q

Which area of the vagina is most affected by keratinising SCC?

A

The upper posterior vagina.

29
Q

What are endocervical polyps?

A

Benign exophytic growths, present in around 2-5% of women.

They can present with irregular spotting.

30
Q

What are the “high oncogenic risk” HPV subtypes?

A

HPV 16 (60% of cervical cancer) and HPV 18 (10% of cervical cancer)

31
Q

Other than HPV infection, what are the other risk factors for cervical cancer?

A

Early age at first intercourse, multiple sexual partners, increased parity, exposure to OC and nicotine, and host immune responses.

32
Q

Most HPV infection cause symptoms: true or false?

A

False. Most HPV infection are a symptomatic.

50% of HPV infections are cleared within 8 months and 90% by 2 years.

33
Q

Provide a brief account of HPV oncogenesis:

A

HPV can only replicate in maturing, non-proliferating squamous cells. In order to for HPV to induce DNA replication in these cells it must reactivate the cellular cycle.

HPV does this primarily by interfering with the function of p53 and Rb tumour suppressors via its viral proteins…

34
Q

What actions do HPV viral proteins E6 and E7 perform?

A

Increase cyclin E expression
Interrupt apoptotic pathways
Induce centrosome duplication and genomic instability
Increase telomerase expression.

35
Q

What is CIN?

A

Cervical Intraepithelial Neoplasia.

Precancerous cervical epithelial histological changes can be classified as low grade or high grade squamous intraepithelial lesions: LSIL or HSIL.

36
Q

Fate of LSIL versus HSIL?

A

Approximately 60% of LSIL spontaneously regress within 2 years. Around 10% will progress to HSIL. LSILs are therefore not treated as a premalignant lesion.

Approximately 30% of HSIL will regress within 2 years, 60% will persist, and 10 % will progress to carcinoma within 2-10 years.

37
Q

How are LSIL and HSIL classed?

A

Histologically:

In LSIL the atypia is confined to the basal third.
In HSIL the atypia extends to two thirds of the epithelial thickness.

38
Q

Broad percentage breakdown of cervical cancer?

A

80% SCC
15% adenocarcinoma
5% adenosquamous and neuroendocrine

ALL ARE ASSOCIATED WITH HIGH RISK HPV!

39
Q

Prognosis of cervical cancer?

A

Prognosis and survival depend more on stage than grade.

Microscopic disease has a 95% 5 year survival.

Advanced disease has a 50% 5 year survival. NE tumours are grim.

40
Q

What is the most common “etiology” of intermenstrual bleeding?

A

Dysfunctional uterine bleeding: abnormal bleeding in the absence of an organic cause. Hyperestrogenic states are the most common basis for DUB.

41
Q

What is the most concerning morphology in endometrial hyperplasia?

A

“Complex hyperplasia with atypia”

This morphological appearance has significant overlap with endometrial Ca and 23-48% of patients with such changes have concurrent malignancy.

42
Q

Endometrial cancer:

Percentage of invasive cancer in women?
Age affected?
Pathophysiological categories?

A

7% of female invasive cancers
Peak incidence in women between 55-65

Type I arises in endometrial hyperplasia and are associated with PTEN mutations

Type II arises in endometrial atrophy and are poorly differentiated. 90% have p53 mutations.

43
Q

Clinical course of endometrial tumours?

A

Excellent prognosis when the tumour is confined to the uterine corpus.

Terrible prognosis if the tumour is malignant mixed mullerian tumour.

44
Q

Features of ovarian tumours?

A

Ovarian tumours can arise from the epithelium, germ cells, or sex cord stroma.

Overall, 80% are benign and most occur in women aged 20-45.

Malignant tumours occur in older women and represent 3% of all female cancers, though they are over-represented in cancer mortality.

45
Q

What are the three major types of ovarian tumours arising from the epithelium?

A

Serous tumours

Endometrioid tumours
Mucinous tumours

46
Q

Broad percentage breakdown of ovarian tumours?

A

Surface epithelial cell origin: 65-70%

Germ cell: 15-20%

Sex cord stroma: 5-10%

Metastasis to ovary: 5%

47
Q

What is the most common malignant tumour of the ovary?

A

Serous cystadenocarcinomas.

48
Q

What is Ca-125?

What role does it play in ovarian cancer?

A

Ca-125 is high molecular weight glycoproteins found in 80% of serous and endometrioid cancers.

It should not be used for screening, rather it is a useful marker for disease progression.

49
Q

What factors reduce ovarian cancer risk?

A

Oral contraception and Fallopian tube ligation.

50
Q

What is the impact of BRCA1 and BRCA2 on ovarian cancer genesis?

A

BRCA1 and 2 incur a risk of ovarian cancer developing by age 70 years in 20-60% of patients: most are high grade.

51
Q

What percentage of ovarian tumours do GCTs make up?

What are the types of GCT in ovarian tumours?

A

GCTs make up 15-20% of ovarian tumours.

The types of GCT are Teratomas, Dysgerminomas, Endodermal yolk sac tumours, and choriocarcinomas.

52
Q

Why to Dysgerminomas deserve mention?

A

They are homologous to seminomas, similarly sensitive to radiotherapy.

They are always malignant though not always aggressive.

They are frequently unilateral (cf other ovarian tumours).

53
Q

What are Krukenberg tumours?

A

Ovarian cancers (often bilateral) caused by metastatic mucin producing signet cells, usually originating from the stomach.

54
Q

What make up the TORCH infections?

A 
Toxoplasmosis
Other (Syphilis, Varicella, B-19 Parvovirus)
Rubella
Cytomegalovirus 
Herpes
55
Q

Difference between ovarian choriocarcinomas and gestational choriocarcinomas?

A

Ovarian choriocarcinomas are highly malignant, metastasise widely, and are more resistant to chemotherapy than their placental counterparts.

GSSE Pathology (17 decks)

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