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Human Development 2 > Microanatomy 2 > Flashcards

Microanatomy 2 Flashcards

1
Q

what is PSA

A
  • secreted by the prostate (glandular part) into semen, but more is secreted in cancer than normal, and it is used by some as a screening test.
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2
Q

anything that distorts architecture of the gland…

A

Anything that distorts architecture of the gland

causes leakage of the PSA into lympho-vascular channels leading to a rise in blood levels; PCa is no exception.

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3
Q

what are the other causes of PSA

A

BEP
haemorrhage
inflammation
instrumentation

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4
Q

what is the aetiology of prostate cancer (adenocarcinoma)

A
  • Very common; slow growing
  • Increases in frequency in elderly
  • Very common in African-Americans and Afro-Caribbeans- higher incidence and mortality
  • Unusual geographic incidence; common in West but rare in China.
  • Causes are unknown: sporadic, hereditary or familial.
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5
Q

what plays a role of the pathogenesis of prostate cancer

A
  • androgens
  • IGF-1 plays a role
  • diet as well plays a factor
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6
Q

describe what symptoms men present with with prostate cancer

A
  • Could be completely asymptomatic
  • Incidental diagnosis (TURP or cystoprostatectomy) •Some men present with urinary symptoms (LUTS). •Haematuria/ haematospermia
  • May present with metastatic disease.

Diagnosis may be led by PSA test.

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7
Q

what grading system is used for prostate cancer

A

Gleason grade

- scale is 1-5

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8
Q

where may the prostate cancer spread

A

The tumour may spread locally to the bladder, urethra, seminal vesicles, pelvic wall and rectum, but will usually metastasize before this.

The tumour shows a predilection for bones, and gives rise to sclerotic metastases.

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9
Q

very early prostate cancer…

A

• Very early prostate cancer may not be treated, especially if the patient is elderly or unwell.

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10
Q

How is prostate cancer treated

A
  • Cancers in younger men (<70 yrs) which have not spread may be treated by surgery (Radical prostatectomy) or radiotherapy.
  • Cancers which have spread are given androgen blocking drug therapy which often controls the disease
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11
Q

what anatomical changes can a testicular torsion occur

A

● grossly swollen
● dusky black on the external surface
● black internally
● necrotic with early cystic degeneration
● necrosis appears to extend into the cord

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12
Q

what is testicular torsion

A

•Testicular torsion is a urologic emergency.
- It happens when the spermatic cord, which provides blood flow to the testicle, rotates and becomes twisted, this reduces the blood flow to the testicules blood supply and can cause pain and swelling

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13
Q

what can delay of a testicular torsion cause

A

• Delay in diagnosis and management can lead to loss of the testicle, as in this case.

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14
Q

who does testicualr torsion affect

A

It most commonly occurs in adolescents and testicular torsion is the most frequent cause of testicle loss in that population.

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15
Q

what is the testicle normally covered by and what does this allow for

A

The testicle is covered by the tunica vaginalis which attaches to the posterolateral surface of the testicle and allows for little mobility of the testicle within the scrotum

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16
Q

what is a major causative factor of testicular torsion

A
  • men who have inappropriately high attachment of the tunica vaginalis
  • allows the testicle to rotate freely on the spermatic cord within the tunica vaginalis (intravaginal testicular torsion)
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17
Q

what are men that have a high attachment of the tunica vaginalis called

A
  • it is a congenial anomaly called the bell clapper deformity that results in the long axis of the testicle being orineted transversely
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18
Q

what is the presentation of testicular torsion

A
  • Torsion causes a sudden onset of severe unilateral testicular and scrotal pain.
  • Onset of pain can occur more slowly, but this is an uncommon presentation of torsion.
  • Torsion can occur with activity, can be related to trauma in 4-8% of cases or can develop during sleep
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19
Q

what is the treatment of testicular torsion

A
  • Relief of the torsion can be performed manually but in most cases surgical exploration is necessary and excision if the tissue is necrotic.
  • Later diagnosis means an orchidectomy is necessary.
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20
Q

what is an orchidectomy

A

Orchiectomy is a surgical procedure in which one or both testicles are removed

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21
Q

what does a classic seminal look like

A

The testis is entirely replaced by a firm white mass (often described as looking like a cut potato) with some central cystic degeneration and necrosis

The testis is replaced by sheets of pleomorphic cells with some prominent nucleoli and clear cytoplasm with well defined cell boundaries.

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22
Q

what do seminomas rise from

A
  • seminomas are a type of germ cell tumour that arise from spermatocytes
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23
Q

where do other non-seminomatous germ cell tumours arise from

A
  • teratoma
  • yolk sac tumour
  • choriocarcinoma
  • mixed
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24
Q

what is the risk factor for developing a seminoma cell tumour

A

Maldescended or undescended testis
• Rare genetic conditions
• Geographical variation in incidence • high in Europe and in Maoris
• low in Africa

Generally very rare

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25
Q

what is the treatment for seminoma cell tumour

A
  • primary excision for localised tumours
  • radiotherapy to the paraaortic nodes for aggressive, vascular invasive tumours
  • a single dose of a chemotherapy agent, carboplatin, may be equally effective with fewer side effects
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26
Q

how responsive are seminoma cell tumours

A
  • Tumours are very responsive to either treatment

* 5 year survival of > 98%

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27
Q

How are non seminomas tumours treated

A
  • Non-seminomas may be treated by more intensive chemotherapy
  • These tumours have a slightly worse prognosis, but still better than other cancers
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28
Q

describe the structure of the prostate gland

A
  • central zone = surrounds the ejaculatory ducts
  • periuthreal and transitional zones = around the proximal urethra
  • peripheral zone
  • anterior fibromuscular stroma
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29
Q

what area does benign prostatic hyperplasia affect

A

mainly affects the periurethral and transitional zones

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30
Q

what are the symptoms of BPH

A
  • hesitancy
  • poor urinary stream
  • urinary retention
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31
Q

where do most carcinomas of the prostate gland originate from

A

peripheral zone

- do not normally impinge on urinary function until they are quite large

32
Q

how can you feel for a prostate carcinoma

A

Digital rectal examination

33
Q

describe the histology of the prostate

A
  • the prostate gland is composed of compound tubuloaclveolar glands with ducts that empty its secretions
  • surrounding and between the glandular portions is a fibromuscular stroma
  • glandular epithelium can rage from cuboidal to columnar
  • often appear pseudo stratified due to the presence of a discontinuous layer of basal cells with round nuclei that act as a reserve for secretory cells
34
Q

what cells are key for the conversion of testosterone to DHT

A

stomal cells as they posses 5 alpha reductase type 2 which converts testosterone to DHT

35
Q

what does DHT do

A
  • more potent in its action on the prostate than tester one
  • has higher affinity and stability at the androgen receptor
  • when it binds to the androgen receptor it causes the expression of growth factors and their receptors in stomal and glandular tissues
36
Q

What happens to androgen in benign prostatic hyperplasia

A
  • androgens cause reduction in apoptosis of glandular epithelium and growth of stomal fibrous tissue and smooth muscle
37
Q

what happens androgens in adenocarcinoma

A

= adenocarcinomas are androgen dependent

- chemical castration causes disease regression, tumours eventually become resistant to androgen blockade

38
Q

describe how the Gleason grading system works

A
  • Grade 1 - this indicates a well differentiated appearance with uniform neoplastic glands closely packed into circumscribed nodules
  • Grade 5 - undifferneiate tumour pattern with cells spreading through the stroma in nests, cord or sheets
  • most tumours have more than one pattern therefore they will assign a primary grade to the most dominant pattern and secondary grade to the next most frequent pattern = this is a combined Gleason score and is repeated for example as 3+5 = 8
39
Q

what Gleason grades not used

A

Gleason grades 1 and 2 are currently not used as these are now regarded as benign or variants of grade 3
- therefore the gleason score ranges from 6-10 now

40
Q

now name the Gleason score and there groups

A

3+3 = 6
Grade group 1

3+4 = 7
Grade group 2

4+3 = 7
Grade group 3

4+4=8, 3+5=8, 5+3=8
Grade group 4

4+5=9, 5+4=9, 5+5=10
Grade group 5

41
Q

what is the prevalence of testicualr torsion

A

1/125 males

42
Q

who does testicular torsion tend to go in

A

13- 17 mainly

43
Q

what happens if there is no resetablishment of perfusion in testiscular torsion

A

orchidectomy is required

- after 8 hours of a spermatic cord torsion there is a 50% chance that the testis will be lost

44
Q

describe the blood supply to the testes

A
  • the arterial supply and venous and lymphatic drainage of the testis passes through the spermatic cord
  • main blood supply is the testicular artery which is a branch of the abdominal aorta
  • collateral supplies arise from the cremaster artery and artery of the ducts deferns
  • venous return is via the pampiniform plexus that surrounds the arterial supply
  • this becomes the testicular vein
45
Q

what becomes the testicualr vein

A
  • venous return is via the pampiniform plexus that surrounds the arterial supply
  • this becomes the testicular vein
46
Q

where does the right and left testicular vein drain

A

right drains straight into the IVC

left drains into the left renal vein which then drains into the IVC

47
Q

describe the anatomy of the testes

A
  • testes descend into the scrotum preceded by the processes vaginalis that forms a surrounding serous pouch = tunica vaginalis
  • the visceral layer of the serous membrane is adhered to the outer dense connective tissue of the testisis = the tunica albuginea
  • the parietal layer is supported by the internal spermatic fascia
  • the tunica vaginalis does not extend completely around the testis but is anchored posteriorly by the fibrous mesorchium
48
Q

what does a torsion of the spermatic cord involve

A
  • torsion of the spermatic cord involves the twisting of the testis and the epididymis together on their axis
  • the thin walled vein are initially compressed and occluded
49
Q

What happens if there is an increase in pressure in a torsion of the spermatic cord

A

with increased pressure a haemorrhage infract occurs

50
Q

what is a congenial malformation of the processes vaginalis known as

A

bell clapper deformity and accounts for 90% of all cases

51
Q

describe what happens in a bell clapper deformity

A
  • in a bell calapper deformity rather than the tests attaching posteriorly to the inner lining of the scrotum by the mesorchium there is an abnormally high attachment of the tunica vaginalis to the spermatic cord this allows rotation of the testis within the sac
52
Q

what is an orchiopexy

A
  • this is a surgical attachment of the testis to the scrotum and is performed in patients with the bell clapper deformity
  • the abnormality tends to only be found after a torsion so this is done to prevent the torsion occur again
53
Q

how often should men check there testes

A

once a month

  • 95% of lumps or swelling are not caused by cancer
  • but early detection of testicular malignancy increases the likelihood of a cure
54
Q

what is another term for undescended testes

A

cryptorchidism

55
Q

in most cases the …

A

testesis descend over the first 4 months of life although surgical correction is sometimes needed

56
Q

what is the only certain risk factor for development of germ cell tumours

A

cryptorchidism

  • risk factor in germ cell tumours of the testsis mainly seminomas
  • accounts for approximately 10% of cases
57
Q

how much of a risk for cancer is undescended testes

A

10times risk in comarpision to scrotal testes

- increased risk remains after surgery

58
Q

development of the testis does not…

A

occur normally at higher temperatures

  • histological changes occur within the undescended testsis as early as 2 years of age and are evident as tubular atrophy with an arrest in germ cell development
  • in the adult, tubules are lined by a preponderance of Sertoli cells instead of having normal cellular development
59
Q

how many testicular tumours are germ cell tumours

A

90% with sertoli or leydig cell tumours and various other including lymphomas making up of the remainder

60
Q

what is the most common tumour in 15 - 34 male age group

A
  • testicular tumours
61
Q

what are the majority of germ cell tumours

A
  • seminomas

- peak incidence at 30-50 years old

62
Q

what is a similar tumour to seminoma in females

A

dysgerminoma

63
Q

give examples of non seminomatous germ cell tumours

A
  • embryonal carcinomas
  • yolk sac tumours
  • choriocarcinomas
  • teratomas
64
Q

what is a choriocarcinoma made out of

A
  • made out of giant syncytiotrophoblast cells and cytotrophoblasts
  • extensive haemorrhage is usual
65
Q

describe a difference between seminomas and non seminomatous germ cell histological types

A

seminomas - this are usually found in the pure form

non-seminomatous germ cells - compromised of different histological types

66
Q

what is the marker of embryonal carcinoma cells

A

Oct4

- also express cytokeratin and CD30

67
Q

what do choriocarcinoma cells produce

A

HCG

68
Q

what can HCG give rise to

A

gynaecomastia

69
Q

what do yolk sac tumour give rise to

A

alpha fetoprotein (AFP)

70
Q

What do LDH reflect

A
  • levels of LDH reflect tumour burden, growth rate and cellular proliferation
71
Q

what risk is a biopsy of a testicular neoplasm associated with

A

a risk of tumour spillage and potential spread
- therefore standard management of a solid mass in the testis is a radical orchiectomy based on the presumption of malignancy

72
Q

how do seminomas spread

A
  • lymphatic route
73
Q

how do you treat seminars

A

orchidectomy and prophylactic radiotherapy or para-aorta lymph nodes or single dose chemotherapy

74
Q

when are nonseminomatours germ cells detected

A
  • advanced clinical stage showing both vascular and lymphatic spread
75
Q

how do you treat non seminomatous tumours

A
  • radiotherapy resistant

- but with aggressive chemotherapy approximately 90% of patients can achieve complete remission and be cured

Human Development 2 (34 decks)

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