Gynae Path 1 Flashcards

1
Q

What are the parts of the gynaecological tract?

A
Vulva
Vagina
Cervix
Uterine body
Fallopian tube
Ovaries
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2
Q

How are neoplasia classified?

A

Classification:
WHO Classification of Tumours of the Female Genital Tract 2020

Staging:
The International Federation of Gynaecology and Obstetrics (FIGO)

Grading:
Varies with tumour type

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3
Q

What are the congenital abnormalities of the genital tract?

A

Duplication- bicornate, septated

Agenesis

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4
Q

What is inflammation of the GU tract called?

A
Vulva: vulvitis
Vagina: vaginitis
Cervix: cervicitis
Endometrium: endometritis
Fallopian tube: salpingitis
Ovary: oopheritis
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5
Q

Which infections Cause discomfort but no serious complications?

A

Candida: Diabetes mellitus, oral contraceptives and pregnancy enhance development of infection
Tichomonas vaginalis: protozoan
Gardenerella: gram negative bacillus causes vaginitis

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6
Q

Which infections have serious complications?

A

Chlamydia: major cause of infertility
Gonorrhoea: major cause of infertility
Mycoplasma: causes spontaneous abortion and chorioamnionitis
HPV: implicated in cancer

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7
Q

What can cause PID?

A

Gonococci, chlamydia, enteric bacteria
usually starts from the lower genital tract and spreads upward via mucosal surface

Staph, strept, coliform bacteria and clostridium perfringens
secondary to abortion
usually start from the uterus and spread by lymphatics and blood vessels upwards
deep tissue layer involvement

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8
Q

What are the complications of PID?

A

Peritonitis
Bacteraemia
Intestinal obstruction due to adhesions
Infertility

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9
Q

What causes salpingitis?

A

Usually direct ascent from the vagina

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10
Q

What does salpingitis end up as?

A
Resolution
Complications:
Plical fusion
Adhesions to ovary
Tubo-ovarian abscess
Peritonitis
Hydrosalpinx 
Infertility
Ectopic pregnancy
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11
Q

What is the most common cause of ectopic pregnancy?

A

Tubal

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12
Q

What pathologies exist in the cervix?

A

Inflammation
Polyps
Dysplasia and carcinoma

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13
Q

What is the epidemiology of cervical cancer?

A

2nd most common cancer affecting women worldwide

Mean age 45-50yrs

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14
Q

What are the RFs of cervical cancer?

A
Human Papilloma Virus -present in 95% 
Many sexual partners 
Sexually active early
Smoking 
Immunosuppressive disorders
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15
Q

What are the low risk types of HPVs?

A

Most common types: 6, 11

Other types: 40, 42, 43, 44, 54, 61, 72, 73, 81

Genital and oral warts

Low grade cervical abnormalities

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16
Q

What are the high risk types of HPVs?

A

Most common types: 16, 18
Other types: 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68,82

Low & high grade cervical abnormalities
Cervical cancer
Vulval, vaginal, penile, and anal cancer

17
Q

What does prognosis depend on?

A

Tumour type
Tumour grade
Tumour stage: FIGO Stage I (90%) – IV (10%) 5 year survival
Lymphovascular space invasion

18
Q

What happens when one is infected with HPV ?

A

For most people, nothing will happen

The body’s immune system eliminates HPV

HPV becomes undetectable within 2 yrs in ~90%

Relatively few will develop symptoms

Persistent infection with high-risk HPV types is associated with pre-cancerous and cancerous cervical changes

19
Q

How does HPV transform cells ??

A

Two proteins E6 and E7 encoded by the virus have transforming genes.

E6 and E7 bind to and inactivate two tumour suppressor genes:

	Retinoblastoma gene (Rb) (E7)

	P53 (E6)

Both effects interfere with apoptosis and increase unscheduled cellular proliferation both of which contribute to oncogenesis.

Infection is either latent or productive.

20
Q

What are the 2 distinct biological states of HPV infection? (1)

A

HPV DNA continues to reside in the basal cells

Infectious virions are not produced

Replication of viral DNA is coupled to replication of the epithelial cells occurring in concert with replication of the host DNA

Complete viral particles are not produced

The cellular effects of HPV infection are not seen

Infection can only be identified by molecular methods

21
Q

What are the 2 distinct biological states of HPV infection? (2)

A

Viral DNA replication occurs independently of host chromosomal DNA synthesis.

Large numbers of viral DNA are produced and result in infectious virions.

Characteristic cytological and histological features are seen

22
Q

Why is screening important?

A

Invitation of women most at risk of disease for screening to identify those who have indications of asymptomatic cervical abnormalities which require further investigation to avoid the possibility of developing into cervical cancer

Cervical cytology has a sensitivity ranging between 50% - 95% and specificity of at most 90% in detecting high grade CIN and SCC.

Now screening is focusing on detection of high risk HPV by molecular genetic approaches.

23
Q

What are the intervals of screening?

A

25-49 = 3yrs
50-64 = 5yrs
65+ if one of the last 3 tests was abnormal

24
Q

What is the Hybrid Capture II (HC2) HPV DNA Test?

A

A nucleic acid solution hybridization assay with signal amplification that uses long synthetic RNA probes complementary to the DNA sequence of:

5 low-risk HPV types ( types 6, 11, 42, 43 and 44)
13 high risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68).

RNA probe cocktails to the most common cancer-associated HPV types

25
What is the HPV vaccine?
The vaccine helps protect against cancers caused by HPV, including: cervical cancer some cancers of the anal and genital areas and genital warts some head and neck cancers Girls and boys aged 12 to 13 years are offered the HPV vaccine as part of the NHS vaccination programme. In England, they are routinely offered the 1st dose when they're in school Year 8, and the 2nd dose is offered 6 to 24 months after the 1st dose. It's important to have both doses of the vaccine to be properly protected.
26
What are the parts of the uterine body?
Endometrium: Glands Stroma Myometrium
27
What are the indications for uterine biopsy?
Endometrium: Infertility Uterine bleeding Thickened endometrium on imaging Uterus or related mass: Lesion identified on imaging As part of a wider resection
28
What are pathologies of the uterine body?
``` Congenital anomalies Inflammation: acute or chronic Adenomyosis Dysfunctional uterine bleeding: e.g. hormonal imbalance Endometrial atrophy and hyperplasia Endometrial polyp Uterine tumours ```
29
What are the uterine tumours?
Endometrial epithelial tumours and precursors Tumour like lesions; e.g. endometrial polyp Mesenchymal tumours specific to the uterus Mixed epithelial and mesenchymal tumours Miscellaneous tumours
30
What are the Endometrial Epithelial Tumours and Precursors?
``` Endometrial hyperplasia Perimenopause Persistent anovulation Polycystic ovary (PCO) Ovarian Granulosa cell tumours ov Oestrogen therapy May be associated with atypia ```
31
What is endometrial carcinoma?
Endometrial cancer is the most common gynaecological malignancy in developed countries, causing 6% of new cancer cases in women.
32
What are the RFs for endometrial carcinoma?
Nulliparity Obesity Diabetes mellitus Excessive oestrogen stimulation
33
What are the Factors that Affect Prognosis and Plan for Therapy?
``` Histological tumour type Tumour grade Tumour stage Lymphovascular space invasion ```
34
What are the histological subtypes?
``` Endometrioid Serous Clear cell Undifferentiated Mixed cell Mesonephric Squamous cell Mucinous Mesonephric-like Carcinosarcoma ```
35
What are Endometrioid Carcinoma?
Are oestrogen dependent Often associated with atypical endometrial hyperplasia Low grade and high grade tumours Develop through the accumulation of mutations of different genes
36
What are Serous and Clear Cell carcinomas?
Older, postmenopausal Less oestrogen dependent Arise in atrophic endometrium High grade, deeper invasion, higher stage
37
What mutations do Serous and Clear Cell carcinomas have?
Endometrial serous carcinoma P53 mutations in 90% PI3KCA mutations in 15% Her-2 amplification Clear cell carcinoma PTEN mutation CTNNB1 mutation Her-2 amplification
38
How do you grade tumours?
- Serous, clear cell, mixed, undifferentiated, dedifferentiated and carcinosarcoma are considered high grade. Endometrioid carcinoma: FIGO 3 tier system: grade 1, 2 and 3 depending on Architecture: % of gland formation Cytological atypia