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Pathomorph - CREDIT 6 > Genital system 1 - DONE > Flashcards

Genital system 1 - DONE Flashcards

1
Q

What distinct regions does a normal prostate contain?

A
  • a central zone (CZ)
  • a peripheral zone (PZ)
  • transitional zone (TZ)
  • a periurethral zone
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2
Q

Where does most of the carcinomas arise from? Palpation?

A

Most carcinomas arise from the peripheral glands of the organ and may be palpable during digital examination of the rectum.

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3
Q

Where does the nodular hyperplasia arise from in contrast to most carcinomas? Compare!

A

Nodular hyperplasia, in contrast, arises from more centrally situated glands and is more likely to produce urinary obstruction early in its course than is carcinoma.

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4
Q

What characterizes prostatic hyperplasia?

A

Prostatic hyperplasia is characterized by proliferation of both stromal an epithelial elements, with resultant enlargement of the gland and, in SOME cases, urinary obstruction

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5
Q

What is an extremely common abnormality of the prostate?

A

NH (non-Hodgkin lymphoma) is an extremely common abnormality of the prostate

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6
Q

How many get nodular hyperplasia of the prostate? Frequency?

A

It is present in a significant number of men over 45-50, and its frequency rises progressively with age, reaching 90% men by the eighth decade of life

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7
Q

Benign prostatic hyperplasia =

A

Nodular hyperplasia of the prostate

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8
Q

Etiology of Benign prostatic hyperplasia (Nodular hyperplasia of the prostate):

A

androgens play a central role in development of BPH

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9
Q

BPH =

A

Benign prostatic hyperplasia

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10
Q

DHT =

A

Dihydrotestosterone

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11
Q

What is Dihydrotestosterone (DHT)?

A

DHT is an androgen derived from testosterone through the action of 5α-reductase, and its metabolite, 3α androstanediol

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12
Q

What do Dihydrotestosterone (DHT) do?

A

DHT is a major hormonal stimuli for stromal and glandular proliferation in men with nodular hyperplasia.

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13
Q

How does Dihydrotestosterone (DHT) lead to hyperplasia?

A

DHT binds to nuclear androgen receptors and, in turn, stimulates synthesis of DNA, RNA, growth factors, and other cytoplasmic proteins, leading to hyperplasia.

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14
Q

What may increase the expression of DHT?

A

Experimental work has also identified age-related increases in estrogen levels that may increase the expression of DHT receptors on prostatic parenchymal cells, thereby functioning in the pathogenesis of nodular hyperplasia

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15
Q

Benign prostatic hyperplasia Ma:

Nodular hyperplasia of the prostate Ma:

A
  • nodular enlargement
  • nodules vary in color and consistency
  • This nodularity may be present throughout the prostate, but it is usually most pronounced in the inner (central and transitional) region.
  • The nodules may have a solid appearance or may contain cystic spaces
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16
Q

Where is the nodularity in benign prostatic hyperplasia usually most pronounced??

A

Benign prostatic hyperplasia is usually most pronounced in the inner (central and transitional) region.

But present throughout the prostate.

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17
Q

Benign prostatic hyperplasia Mi:

Nodular hyperplasia of the prostate Mi:

A
  • glandular proliferation and dilatation
  • fibrous and muscular proliferation of the stroma.
  • Glands are lined by two layers of epithelium (inner columnar and outer cuboidal or flattened) based on the basement membrane.
  • Foci of squamous mataplasia. Small areas of infarction.
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18
Q

What is the precentage of men with prostatic hyperplasia that get clinical symptoms?

A

Clinical manifestations of prostatic hyperplasia occur in only about 10% of men with the disease.

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19
Q

What are the most common manifestations of nodular hyperplasia?
(Benign prostatic hyperplasia)

A
  • difficulty in starting the stream of urine (hesitancy)

- intermittent interruption of the urinary stream while voiding

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20
Q

What is nodular hyperplasias most common manifestations?

Benign prostatic hyperplasia

A

Because nodular hyperplasia preferentially involves the inner portions of the prostate, its most common manifestations are those of lower urinary tract obstruction.

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21
Q

What can some men with Benign prostatic hyperplasia (Nodular hyperplasia of the prostate) develop?

A

Some men may develop complete urinary obstruction, with resultant painful distention of the bladder

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22
Q

What happens if the Benign prostatic hyperplasia (Nodular hyperplasia of the prostate) is neglected?

A

hydronephrosis

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23
Q

What are some symptoms of obstruction are frequently accompanied by?

A

Symptoms of obstruction are frequently accompanied by urinary urgency, frequency, and nocturia, all indicative of bladder irritation.

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24
Q

Which combination can increase the risk of UTI (urinary tract infection)

A

The combination of residual urine in the bladder and chronic obstruction increases the risk of urinary tract infections.

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25
Q

How common is Prostatic adenocarcinoma?

A
  • the most common cancer in males

- the second most common cause of cancer-related deaths in men older than 50 years of age (US)

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26
Q

Which gender usually get Prostatic adenocarcinoma?

A

It is predominantly a disease of older males, with a peak incidence between the ages of 65 and 75 years.

Latent cancers of the prostate are even more common than those that are clinically apparent, with an overall frequency of more than 50% in men older than 80 years of age.

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27
Q

Prostatic adenocarcinoma risk factors:

A
  • age
  • family history
  • hormone levels
  • environmental influences
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28
Q

PA =

A

Prostatic adenocarcinoma

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29
Q

Where are most of the Prostatic adenocarcinoma located?

A

Peripheral zone of the gland in a posterior location (70-80% of PA)

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30
Q

Adenocarcinoma

A

Irregular glands are small with a single layer of cuboidal cells with conspicuous nucleoli.

The neoplastic glands have „back to back” appearence with scanty stroma.

Invasion of the capsule with its lymphatic and vascular channels.

Invasion of perineural spaces.

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31
Q

What has a „back to back” appearence with scanty stroma?

A

Adenocarcinoma (PA)

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32
Q

neoplasia def (google):

A

the presence or formation of new, abnormal growth of tissue.

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33
Q

How is PA (Prostatic adenocarcinoma) graded?

A

PA is graded by the Gleason system

34
Q

Describe the Gleason system:

A

According to this system, prostate cancers are stratified into five grades on the basis of glandular patterns of differentiation.

Grade 1 represents the most well-differentiated tumors and grade 5 tumors show no glandular differentiation.

35
Q

How do we use the Gleason system to grade the PA?

A

Since most tumors contain more than one pattern, a primary grade is assigned to the dominant pattern and a secondary grade to the next most frequent pattern.

The two numerical grades are then added to obtain a combined Gleason score.

Tumors with only one pattern are treated as if their primary and secondary grades are the same, and, hence, the number is doubled.

36
Q

Which numbers does the Gleason Score range from?

A

The Gleason Score ranges from 2 to 10

37
Q

Gleason score (numbers):

A

2-4- well differentiated (low-grade) tumor:
* small, majority of potentially treatable cancers

5-6- intermediate-grade tumor

7- moderate to poorly differentiated tumor

8-10- poorly differentiated (high-grade) tumor:
* they tend to advanced cancers that are unlikely to be cured

38
Q

The biochemical markers:

PA

A
  • Prostate specific antigen PSA

- Prostatic acid phosphatase

39
Q

Spread:

PA

A
  • Local invasion

- Through the bloodstream and lymph (bones, particulary axial sceleton, widely to the viscera)

40
Q

Where does the neoplasia of the cervix originate? And what causes it?

A

Most tumors are of epithelial origin and are caused by oncogenic HPV (it has tropism for the immature cells of the transformation zone)

41
Q

At what age to women usually get neoplasia of the cervix?

A

The peak age incidence of precancerous lesions is about 30 years, whereas that of invasive carcinoma is about 45 years.

42
Q

IMPORTANT RISK FACTORS of neoplasia of the cervix are directly related to HPV exposure and include:

A
  • early age at first intercourse
  • multiple sexual partners
  • a male partner with multiple previous sexual partners
  • persistent infection by “high-risk” papillomaviruses (e.g. HPV 16, 18, 45, 31)
43
Q

What is the Papanicolaou (Pap) smear (google):

A

is a method of cervical screening used to detect potentially pre-cancerous and cancerous processes in the cervix (opening of the uterus or womb)

44
Q

What is the reason for the decline of neoplasia of the cervix?

A

The overall decline is mainly attributed to the use of the Pap test

45
Q

What is the Papanicolaou (Pap) smear able to do?

A

This screening method is able to find changes in the cervix before cancer has a chance to develop

46
Q

What is the most successful cancer screening test ever developed?

A

The Pap smear remains the most successful cancer screening test ever developed.

47
Q

CIN =

A

Cervical Intraepithelial Neoplasia

48
Q

Where does almost all of the invasive cervical squamous cell carcinomas arise from?

A

Nearly all invasive cervical squamous cell carcinomas arise from precursor epithelial changes referred to as CIN

49
Q

How can we detect CIN?

A

Cytologic examination can detect CIN long before any abnormality can be seen grossly.

The follow-up of such women has revealed that precancerous epithelial changes may precede of an overt cancer by many years, or even decades.

50
Q

SIL =

A

Squamous Intraepithelial Lesion

51
Q

Classifications Systems for Precursor Squamous Cervical Lesions:

A

TABLE PAGE 4/another set of flashcards

52
Q

How does the CIN start?

A

CIN usually starts as low-grade dysplasia (CIN I) and progresses to moderate (CIN II) and then severe dysplasia (CIN III)

53
Q

Is the progression from a lower grade to a higher grade inevitable?

A

NOPE

54
Q

What is the likelihood of CIN I to progress?

A

Although studies vary, with CIN I the likelihood of regression is 50% to 60%, that of persistence is 30%, and that of progression to CIN III, is 10-20%.

With progression, only 1% to 5% become invasive.

55
Q

What is the likelihood of CIN III to progress?

A

With CIN III the likelihood of regression is only 33% and of progression 60% to 74% (in various studies)

56
Q

TABLE

A

page 4

57
Q

Dysplasia of squamous epithelium - Intraepithelial squamous cell neoplasia DEF:

A

Loss in the uniformity of the individual cells (cellular atypia) and a loss in their architectural orientation (architectural anarchy)

58
Q

CELLULAR ATYPIA:

Dysplasia of squamous epithelium - Intraepithelial squamous cell neoplasia

A 
• Pleomorphism- cell size and shape 
• Abnormal nuclear morphology.
   - Hyperchromasia
   - Hypernucleosis (↑ N/C)
   - Heteronucleosis
   - Marginalization of chromatin
   - Hypernuclelosis
• Mitotic activity- (increased, abnormal, beyond the usual proliferative compartment)
59
Q

Hyperchromasia:

A

characteristically the nuclei contain an abundance of DNA and are extremely dark staining

60
Q

Hypernucleosis (↑ N/C):

A

nuclear enlargement

61
Q

Heteronucleosis:

A

the nuclear shape is very variable

62
Q

Marginalization of chromatin

A

the chromatin is often coarsely clumped and distributed along the nuclear membrane.

63
Q

CIN I (mild dysplasia):

A

This lesion is characterized by dysplastic changes in the lower third of the squamous epithelium and koilocytotic changes mostly in the superficial layers of the epithelium.

64
Q

What is Koilocytosis?

A

Koilocytes: cells with nuclear hyperchromasia and angulation with perinuclear vacuolization produced by cytopathic effect of HPV

65
Q

CIN II (moderate dysplasia):

A

in CIN II the dysplasia is more severe, the it extends to the middle third of the epithelium.

66
Q

How is the superficial layers in CIN II (moderate dysplasia)?

A

The superficial layer of cells shows some differentiation, and in some cases it shows the koilocytotic changes

67
Q

What is CIN II (moderate dysplasia) associated with?

A

It is associated with some variation in cell and nuclear size, heterogeneity of nuclear chromatin and mitoses above the basal layer.

68
Q

CIN III (high dysplasia, preinvasive carcinoma):

A

As the spectrum evolves, there is progressive loss of differentiation with involvement of more and more layers of the epithelium, until it is totally replaced by immature atypical cells exhibiting no surface differentiation
- CIN III (high dysplasia, preinvasive carcinoma)

69
Q

CIN III (praeinvasive carcinoma) - morphology:

A
  • Loss of regular arrangement and polarity of cells involving entire thickness of the epithelium
  • Features of cellular atypia (particullary hyperchromasia) and mitotic figures in all levels of the epithelium
  • The cells differ in size and shape
  • The surface layer do not show any flattened cells C
70
Q

Invasive squamous cell carcinoma Ma:

A
  • with exophytic growth into the lumen of the vagina

- endophytically into the cervical wall (with ulceration)

71
Q

Invasive squamous cell carcinoma Mi:

A

SCCs range from well-differentiated squamous cell neoplasms showing keratinization with keratin pearls and intracellular bridges to poorly differentiated neoplasms having only minimal residual sqamous cell features

72
Q

Rate the cervical carcinomas from the most common and down:

A
  1. cervical carcinomas are squamous cell carcinomas (75%)
  2. adenocarcinomas and adenosquamous carcinomas (20%)
  3. small-cell neuroendocrine carcinomas (<5%).
73
Q

What is the most common cervical carcinomas?

A

squamous cell carcinomas (75%)

74
Q

Where does the invasive carcinomas of the cervix develop?

A

Invasive carcinomas of the cervix develop in the region of the transformation zone

75
Q

What is the range of invasive carcinomas of the cervix?

A

they range from microscopic foci of early stromal invasion to grossly conspicuous tumors encircling the os.
* Thus, the tumors may be invisible or exophytic.

76
Q

The prognosis depends upon the clinical stage at admission. 5-years survival rate equals in:

A
  • Stage 0 (preinvasive, CIN III) -> 100%
  • Stage I ( with microinvasion, to 7mm beneath the basement membrane) –> 90%
  • Stage II (ca involves up to 1/3 of the uterus, infiltrates vagina or parametrium but does not reach the wall of true pelvis) –> 82%
  • Stage III (infiltration of true pelvis, uterus, vagina, ureters) -> 35%
  • Stage IV (massive infiltration of true pelvis, urinary bladder, rectal mucosa) - >10%
77
Q

Stage 0

A

preinvasive, CIN III

-> 100%

78
Q

Stage I

A

with microinvasion, to 7mm beneath the basement membrane

–> 90%

79
Q

Stage II

A

ca involves up to 1/3 of the uterus, infiltrates vagina or parametrium but does not reach the wall of true pelvis
–> 82%

80
Q

Stage III

A

infiltration of true pelvis, uterus, vagina, ureters

-> 35%

81
Q

Stage IV

A

massive infiltration of true pelvis, urinary bladder, rectal mucosa
->10%

Pathomorph - CREDIT 6 (5 decks)

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