Lecture 27: Pathology of ovary and uterus Flashcards

1
Q

How does HPV link to cancer formation?

A
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2
Q

Carinomas

A
epithelial origin
- adenocarcinoma: adrenal epithelium
- squamous cell carcinoma: squamous epithelium
simple epi --> carcinoma
glandular --> adenocarcinoma
squamous --> squamous cell carcinoma
urothelium --> urothelial carcinoma
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3
Q

Lymphoma

A

lymphoid tissue origin

  • Hodgkin’s disease
  • Non- Hodgkins ( T or B cells)
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4
Q

Melanoma

A
melanocytic cell
adipose tissue --> liposarcoma
neural tissue --> malignant peripheral nerve sheath
bone --> osteosarcoma
Cartilage --> chondosarcoma
muscle --> leiomyo/Rhabdomyosarcoma
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5
Q

Sarcoma

A

mesenchymal (structural cells , holding fat, nerves and bones )
- less common

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6
Q

Where can uterine pathologies occur

A

Uterus + Neighbouring structures: rectum, bladder, sigmoid colon
Note: Ovarian pathologies can easily spread

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7
Q

Follicle quantities in the ovary

A

400,000 primordial follicles –> dormant until puberty –> FSH and Lh release causes 20 follicles to mature each cycle –> 1 out of the twenty reaches maturity and is released –> Menopause –> only a few follicles remain

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8
Q

Ovary in H&M section (hameotocilin and EOSM slide)

A

cortex, stroma, mesothelial lining, follicles, BV, hilum

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9
Q

3x Main ovarian tumours

A

Metastases spread from everywhere to the ovary–>

  1. Germ: germ cell tumours (teratoma)
  2. Stromal: sex cord stromal tumours (fibroma)
  3. Surface: majority of ovarian tumours arise from the surface/fimbrial end of the Fallopian tube
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10
Q

What sort of structure is the ovary inherently?

A

Cystic structure

- ovaries are constantly forming follicular cysts which develop –> mature –> rupture

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11
Q

Ovarian tumour table

A
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12
Q

Polycystic ovaries

A

In cortex –> follicles proliferate but never ovulated –> continued oestrogen stimulation –> no ovulation (no progesterone) –> endometrial hyperplasia and carcinoma
Polycystic ovaries: follicular cyst (never popped)

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13
Q

Ovarian neoplasm

A

multi cystic (solid) areas

  • -> once malignant they become increasingly solid
    1. cyst adenoma
    2. mucinous cyst adenomas
    3. serous
    4. mucinous carcinoma
    5. serous carcinoma
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14
Q

Histological features of ovarian neoplasm

A
  1. large nuclei

2. course chromatin

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15
Q

Dermoid cyst/Teratomas

A

dermoid cyst –> females try to make baby WITHOUT MALE SPERM –> starts forming structures (e.g. teeth, hair) –> but recapitulates and goes completely wrong

  • normally benign, sitting in skin for years
    pot. to develop squamous cel carcinoma in skin
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16
Q

relationship b/w stomach and ovary

A

diffuse gastric cell carcinoma –> often metastasises into ovary
- another stomach carcinoma is Putinburg Signet Ring carcinoma

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17
Q

relationship b/w colon and ovary

A

colorectal carcinoma –> can metastasise –> become cystic –> mimic primary ovarian neoplasm

18
Q

Putinburg carcinoma

A

Signet ring cell carcinoma (of stomach) –> nucleus on top and cytoplasm below –>

19
Q

length of normal fallopian tube

A

9-11 cm

20
Q

What does the fallopian tube open into

A

peritoneal cavity

21
Q

Function of Fallopian tube

A

ovulation –> follicle rupture and fimbrae align overtop –> ovum enters lumen of FT –> FERTILIZATION occurs in fallopian tubes –> BlastoCYTE move through rest of fallopian tube into Uterus –> blastocyte IMPLANTS into uterus after several days

22
Q

Structure of Fallopian Tube

A
Plicae: fingerlike projections 
Lining: serous columnar epithelium
cilia: brush egg down towards uterus
- smooth muscle wall lining
Overall: delicate and complex structure that is very vulnerable to inflammation and tumours --> stops plicae movement --> unable to direct egg --> complications
23
Q

Fallopian Tube tumour table

A
24
Q

Bilateral Salphangitis

A

Enflamed fimbrial ends stick together –> fallopian tubes fill with puss and blood

25
Q

Serous carcinoma of fallopian tube

A

tube expanded by tumour growing within

Thicker = Intrapeithelial neoplasm

26
Q

Components of the uterus

A

Fundus
Body
Cervix
- thick muscle myometrium wall –> so can push grown baby out
- endometrial lining –> changes with every cycle –> contains glands and stroma

27
Q

What are the components of the uterine endometrium

A
  1. glands

2. stroma

28
Q

Function of the endometrium

A

Note: components = glands and stroma
- endometrium contains oestrogen and progesterone hormone receptors –> endometrium develops and shes under oestrogen and progesterone influence
Menopause –> no hormones –> no stimulation for regular menstrual cycle –> Endometrium become inactive after menoapuse

29
Q

Menstrual cycle

A
  1. Oestrogen stimulated proliferative stage
    OVULATION (required to switch stages/hormone stimualtion)
  2. Progesterone stimulated secretory stage
  3. Menstrual
  4. Inactive
30
Q

When is there excessive oestrogen stimulation

A
  1. diabeties

2. polycystic ovarian syndrome

31
Q

What happens if there is no ovulation?

A

No switch from oestrogen –> progesterone

oestrogen continues to be released –> excessive oestrogen stimulation –> excessive proliferation

32
Q

Histology of 4x stages of Menstrual cycle

A
  1. Proliferation: proliferation mainly in basal layer. little tubules in dense stroma.
  2. Secretory: (juicy/glandular)
    - serrated and convoluted glands
    - secreting substances to keep blastocysts happy –> breaks down/sheds upon no implantation
33
Q

Endometrial tumour table

A
34
Q

Myometrial tumour table

A
35
Q

Cervix

A

“neck”
narrower portion of the uterus
Cervix protrudes down into upper vagina

36
Q

Surface anatomy of cervix

A

Inferior Vagina –> Superior Cervix
Squamous epi
Endocervical canal
glandular epithelium

37
Q

Tumour table of the cervix

A
38
Q

Precancerous squamous intraepithelial lesion

A

CIN (cerivcal intraepithelial neoplasia)
dysplasia
squamous intraepithelial lesion
- low grade squamous intraepithelial lesion (CIN)
- high grade squamous intraepithelial lesion (CIN II and III)

39
Q

HPV virus multiplication

A

squamous mucosa beomces infected with HPV –> HPV virus integrates itself into DNA –> increased replication and turnover of the cell –> CIN

40
Q

Grade of pre-cancer

A

dependany on severity and extent of stypia
CIN I
CIN II
CIN III
Invasion
- want to see these cellular changes during smear test

41
Q

CIN –> Invaded

A

neoplastic cells can invade into Blood vessels, nerve and lymphatics –> spread and metastasize

42
Q

Uterine Congenital abnormalities

A

Uterus doesnt fuse symmetrically

  • Intersex abnormalities
  • malformations of the uterus
  • abnomalities of ovarian development (Absent ovaries)
    e. g Bicornuate uterus: Pregnancies occurring on both sides of the uterus