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PathY5 > Gynae Path 1 > Flashcards

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
Q

What is the HPV vaccine?

A

The vaccine helps protect against cancers caused by HPV, including:
cervical cancer
some cancers of the anal and genital areas and genital warts
somehead and neck cancers

Girls and boys aged 12 to 13 years are offered the HPV vaccine as part of theNHS 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
Q

What are the parts of the uterine body?

A

Endometrium:
Glands
Stroma

Myometrium

27
Q

What are the indications for uterine biopsy?

A

Endometrium:
Infertility
Uterine bleeding
Thickened endometrium on imaging

Uterus or related mass:
Lesion identified on imaging
As part of a wider resection

28
Q

What are pathologies of the uterine body?

A 
Congenital anomalies
Inflammation:  acute or chronic
Adenomyosis
Dysfunctional uterine bleeding: e.g. hormonal imbalance
Endometrial atrophy and hyperplasia
Endometrial polyp
Uterine tumours
29
Q

What are the uterine tumours?

A

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
Q

What are the Endometrial Epithelial Tumours and Precursors?

A 
Endometrial hyperplasia
Perimenopause 
Persistent anovulation 
Polycystic ovary (PCO) 
Ovarian Granulosa cell tumours ov
Oestrogen therapy 
May be associated with atypia
31
Q

What is endometrial carcinoma?

A

Endometrial cancer is the most common gynaecological malignancy in developed countries, causing 6% of new cancer cases in women.

32
Q

What are the RFs for endometrial carcinoma?

A

Nulliparity
Obesity
Diabetes mellitus
Excessive oestrogen stimulation

33
Q

What are the Factors that Affect Prognosis and Plan for Therapy?

A 
Histological tumour type
Tumour grade
Tumour stage
Lymphovascular space 
   invasion
34
Q

What are the histological subtypes?

A 
Endometrioid
Serous
Clear cell
Undifferentiated 
Mixed cell
Mesonephric
Squamous cell
Mucinous
Mesonephric-like
Carcinosarcoma
35
Q

What are Endometrioid Carcinoma?

A

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
Q

What are Serous and Clear Cell carcinomas?

A

Older, postmenopausal
Less oestrogen dependent
Arise in atrophic endometrium
High grade, deeper invasion, higher stage

37
Q

What mutations do Serous and Clear Cell carcinomas have?

A

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
Q

How do you grade tumours?

A
  • 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

PathY5 (98 decks)

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