11.2 Male genital tract tumours Flashcards

1
Q

What is the most commonly diagnosed cancer in men?

What is the most common cancer causing death in men?

A

Postate cancer is the most commonly diagnosed cancer in men

Lung is the most common cause of cancer related death in men

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2
Q

What are the 3 main anatomical zones of the prostate and give a condition that arises in each

A

1) Central zone (part around the urethra): not many associated diseases expect for prostatitis which arises from the urethra and its urine stream.
2) Transitional zone: BPH occurs, causes compression of the urethra and thus presents as difficulty passing urine
3) Peripheral zone: major site where prostatic cancer develops (doesn’t generally present as difficulty passing urine) but important because in can invade the surrounds tissues before it causes compression of the urethra, late presentation

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3
Q

Histologically how would describe the composition of the prostate?

A

Majority of the prostate is fibromuscular stroma with some secretory function (little)

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4
Q

What is the function of the inner vs the outer portion of the prostate?

How can this be advantageous to diagnosis?

A

Double layered epithelium

Inner is comprised of columnar secretory cells: makes PSA

Outer is comprised of basal cells (darker staining): Dont make PSA

Diagnosis: we can apply antibodies to tissue slides to identify if there is prostate gland material present. If PSA is identified, it signifies that the glands observed are taken from the prostate.

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5
Q

Does prostate cancer develop from ducts or glands?

List 2 things that would be seen histologically and why these are useful

A

Cancer develops from the glands NOT the ducts and results in:

1) loss of structure of the double layered epithelium, resulting in a lining of single cells with bigger nuclei
2) if malignant the cells will invade the the “limiting membrane” located outside the gland, through the basement membrane into the fibromuscular stroma

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6
Q

What is seen microscopically in BPH?

Give 4 risk factors

A

Hyperplasia: increase in cell NUMBERS (not size)

Microscopically would show proliferating cells, glands and fibromuscular stroma BUT that are benign and show NO atypical change

Risk factors:

  • age >50 yr
  • family history
  • most common in black race
  • changing hormone levels
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7
Q

Give 4 consequences of BPH and explain why each occurs

A

1) Infection due to urine accumulation proximal to the obstruction
2) advanced BPH can result in hypertrophy of the bladder wall muscle as it tryies to overcome the obstruction and push urine out, as the pressure rises it can form bladder diverticulum
3) obstructed urine can lead to development of bladder stones either in the ureter or within diverticulum that may have formed
4) hydroureter (sigmoid shaped ureter) due to increased pressure causing dilation and elongation of the ureter, which can be transmitted to the kidneys causing hydronephrosis

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8
Q

Give 4 symptoms of BPH

A

1) Increased frequency (at night = nocturia) and urgency
2) difficulty starting urination and Inability to completely empty the bladder
3) weak urine stream or a stream that stops and starts
4) dribbling at the end of urination.

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9
Q

What is the main procedures to treat BPH

A

Trans Urethral Resection of Prostate (TURP): the material is then sent to dept of cellular pathology and processed for histology and microscopy to check for any cancer

Can also do an open operation to remove the whole gland (less common)

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10
Q

Give 4 risk factors for development for Prostatic cancer

A

1) age: linear relation
2) ethnicity: african-american men
3) family history
4) several genetic links

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11
Q

If men present with prostatic cancer at a younger age what can be said about disease

A

Younger age at presentation = more aggressive disease

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12
Q

Compare the early and advanced signs and symptoms of Prostate cancer

A

Early: asymptomatic

Advanced disease:

  • difficultly urinating/ decreased force of urination
  • increased frequent of urination
  • difficulty starting or stopping urine stream
  • blood in semen & urine
  • pain or discomfort in the pelvic area
  • bone pain = indicates metastases
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13
Q

Give common routes of spread of prostate adenocarcinoma

A

1) direct local invasion: seminal vesicles & bladder base
2) blood stream and lymphatics: particularly to the bones (axial skeleton and some visceral dissemination)

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14
Q

Give 3 consequences of prostate adenocacinoma spread

A

1) ureteric obstruction
2) urethral obstruction (late symptom)
3) back pain

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15
Q

Prostatic cancer in the bones can be described as osteoblastic, what does this mean?

How can it be described in the prostate itself?

A

Osteoblastic: bone forming, resulting in thickening and hardening of the bone

In the prostate itself it is fibroblastic, resulting in thickening and hardening of the prostate

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16
Q

Why do we do a DRE and what may be felt that is indicative of prostate cancer?

What 2 investigations could we do to confirm diagnosis?

A

We known prostate cancer begins in the peripheral zone hence can be palpated in a digital rectal exam. Cancerous tissue would feel gritty and firm

To confirm:

  • Trans-rectal biopsy
  • Multiple core biopsies
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17
Q

What grading system is used for prostate cancer?

Describe this and how it may useful

A

Gleason score: determines therapy and prognosis

1) small uniform glands
2) more space stroma) between glands
3) distinct infiltration of cells from glands at margins
4) Irregular masses of neoplastic cells with few glands
5) lack of/ occasional glands, sheets of cells

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18
Q

How do we stage prostate cancer?

Describe this

A

TNM staging

Tumour

  • T1 = incidental finding
  • T2 = confined to prostate
  • T3 = extension outside
  • T4 = direct invasion of contiguous organs

Nodes:

  • N0 = no node invasion
  • N1 = nodal invasion

Metastasis = M

19
Q

What is usually the most common node invasion of prostate cancer?

A

Pelvic lymph nodes

20
Q

Define Anaplastic

A

Poorly differentiated and no resemblance to parent tissue

21
Q

Give 4 treatment options for prostatic cancer

A

Management is stage and grad dependant:

1) Do nothing
2) Prostatectomy: open or laparoscopic
3) Radiotherapy (non-surgical)
4) Hormonal therapy (remove androgen supporting cancer growth and potentially replace with oetrogens to slow down spread)

22
Q

Give 3 reasons why is PSA not used as a screening tool?

A

1) although PSA levels should be relatively normal in blood there is not a standard level of PSA that is considered ‘normal’
2) raised PSA may be due to many reasons : Infection, BPH, DRE, prostate cancer
3) not all cancer patients have raised PSA

Conclusion: poor sensitivity and specificity

23
Q

Give 3 neoplasms that arise in the penis and which is the most common

What virus are all of these believed to be related to?

A

1) Squamous papilloma: condyloma, wart (most common)
2) Carcinoma in situ: Bowen’s disease
3) Invasive squamous cell carcinoma

All related to HPV (benign viral warts are caused by type 6)

24
Q

What indicates that a squamous cell papilloma is related to an HIV infection

A

If it has Intracellular vacuolation, known as koilocytosis which is characteristic of HPV infection, at any site

Koilocytosis: watery accumulation within cell

25
Q

If skin lesions are present on the penis shaft what is the first thing we must do and why?

A

Must do a biopsy to make a diagnosis because Infection vs tumour distinction is impossible with naked eye alone

26
Q

What is Bowen’s disease?

Give 4 characteristic histological features of this cancer

A

Bowen’s disease is a squamous cell carcinoma in situ (early pre-malignant ). BUT only a small proportion of patients with this will develop an infiltrating cancer

Note as it is in situ it does NOT invade the BM, but some typical features of malignancy can be seen histologically:

  • cellular atypia
  • large cells
  • bizarre nuclei with prominent nucleoli
  • atypical mitoses
  • apoptoses
27
Q

Give 4 risk factors for development of carcinomas in the penis

A

1) HPV 16 infection (some cases of 18 also)
2) HIV infection: worsens prognosis
3) not circumcised (hygiene and specific infection risk
4) cigarette smoking

28
Q

What does presence/lack of keratin in sqaumous cell carcinomas indicate?

A

Keratin = well differentiated

No keratin = poor differentiation

29
Q

Describe the growth rate of a penis carcinoma and its invasiveness?

What can be said about lymph node metastasis?

A

Slowly growing and locally invasive causing ulceration

Metastasis to local lymph nodes:

  • No node involvement = better prognosis, 66% 5yr survival
  • Node involvement = worse prognosis, 25% 5yr survival
30
Q

What is meant by primary vs secondary classification of a tumour?

A

primary: originated in that organ
secondary: metastasised from elsewhere

31
Q

Compare tumours of the ovary to the testis in terms of malignancy?

A

Ovary: benign primary tumours more common than malignant

Testis: malignant tumours more common than benign

32
Q

Give 4 other conditions that present as inflammatory masses (mimic tumours) but are not

A

1) Inflammation (orchitis)
2) sexually transmitted infections
3) tuberculoma
4) syphilis

33
Q

What are the 2 main classifications of testicular tumours?

A

1) Germ cell tumours
2) Sex cord-stromal tumours

34
Q

Give 4 Germ cell tumours in the testis and state which is the most common

A

1) Seminoma (most common)
2) Teratoma
3) Embryonal carcinoma
4) Yolk sac (endodermal sinus) tumour
5) Choriocarcinoma
6) ‘mixed’ tumours

35
Q

Give 3 Sex cord-stromal tumours

A

1) Leydig cell tumour
2) Sertoli cell tumour
3) Secondary (metastatic) tumours eg. lymphomas

36
Q

Give 3 potential causes for developmemnt of testicular tumours and state which is the most common

A

1) Inherited genetic factors (most common- 50% of cases)
* Multiple DNA defects, not monogenetic
2) cryptorchidism (undescended testis) (10% of cases)
3) dysgenesis of the testis (embryonal malgenesis of the testis)

37
Q

How do Seminomas present and describe the histological appearance

A

Presents as a mass in the testis that is soft white and fleshy

Histology:

  • uniform cells with large haematoxyphilic nuclei and clear cytoplasm that form islands
  • these are separated by lymphocytes “large lymphocyte infiltration”

The large lymphocyte infiltration does not indicate a malignant lymphoma it merely shows there is presence of reactive T-cells which is characteristic of a seminoma

38
Q

Seminomas are derived from what are thus what cells are they essentially identical to?

A

Derived from sperm producing cells = Spermatogonia cells

Hence look almost identical to spermatogonia

39
Q

What is the equivilant to Seminomas in the male testis in a female?

A

Seminoma = same histology as dysgerminoma of ovary

40
Q

How are testicular tumours staged (2)?

A

AJCC staging: quite complicated, not expected to know

Should know:

Stage 1: confined to the tesis

Stage 2: nodal spread to retroperitoneal nodes and nodes under the diaphragm

Stage 3: metastases outside the retroperitoneal nodes and nodes above the diaphragm

41
Q

Why are seminomas considered ‘curable’ and how would you treat them?

A

1) Excision of the whole testis
2) depending on stage treat with radio and chemo therapy
* these tumours are extremly sensitive to this hence their prognosis is good

Note: there are no useful blood markers in diagnosis and staging

42
Q

What is a teratoma of the testis and what cells do they arise from?

How do they differ from ovarian teratomas and why?

Does puberty have an effect on male teratomas?

A

These are complex tumours which have components that arise from more than one germ layer (embryology)

Ovaries: teratomas may contain teeth, brain and hair. This is because they are well differentiated and thus benign.

Testis: teratomas tend to be less differentiated hence, teeth, brain and hair are un-common. This means they are more often malignant

  • Before puberty most are ‘mature teratomas’ and are benign
  • After puberty, most are regarded as malignant and can metastasise
43
Q

What are Leydig cell tumours and how may they present?

Are they more likley to be benign or malignant?

A

These are RARE small endocrine tumours that secrete androgens and sometimes oestrogens

Hence, may present as gynaecomastia and precocious puberty

More often benign (only 10% are malignant and can metastasise)