Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

OBGYN > Gyne I > Flashcards

Gyne I Flashcards

1
Q

What are the embryological structures that fuses to give the Uterus

A

Mullerian Ducts

Wolffian ducts AKA mesonephric duct for bladder, male reproductive;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Common Infective agents and presentations

+ Antibiotics, 2 each

A

Viruses

  • HSV II, Herpes Ulcer
  • HPV, Warts, IN, IC
  • Poxvirus, Mulluscum Contagiosum

Bacteria
- N. Gonorrhea - IM Ceftriaxone (+ Azithromycin but CDC no more)
- Chlamydia trachomatis (Azithromycin, Doxycycline)
present w various infections - salpingitis, endometritis, cervicitis

Parasites

  • Toxoplasmosis
  • Trichomonas - STI

Fungi
- Candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does PID present and cause

Cx

A

Cause: infection spreading upwards or by blood

  • mostly STD from vagina spread upwards hence

Vagina Discharge
Pelvic Pain

Cx
Peritonitis
Sepsis
Infertility, Ectopic Pregnancy
Adhesions - Adhesions develop as the body attempts to repair itself.
Fitz-Hugh–Curtis syndrome is a rare complication of pelvic inflammatory disease (PID) involving liver capsule inflammation leading to the creation of adhesions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vulva Anatomy

A

Labia Minora, Labia Majora

Vagina - Bartholin Gland openings beside vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vulva epithelial non-neoplastic diseases [4]

A

Bartholin Cysts
Warts HPV 6, 11: Condyloma acuminata

Dermis Inflammations:
Lichen Sclerosus (autoimmune) - thin epi
Lichen Simplex Chronicus (itchy, scratching) - thick epi

  • Lichen: any of various papular skin diseases in which the lesions are typically small, firm papules set very close together
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Vulva Malignancies

- give origins

A

VIN - SCC
Origin: HPV 30%, dysplasia, then in situ neoplasia; or LS/LSC 70% then hyperplasia

VAC - Paget’s Disease, AC in situ
Origin: epithelial progenitor cells
- Originates from local organs such as the Bartholin gland, the urethra, or the rectum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Rare Vagina Cancer now

A

DES - CCA

Clear Cell Adenocarcinoma, when mother treated w DES during pregnancy causing adenosis;

Clear Cell: Vacuolated tumor cells w glandular structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Infant Vagina Cancer

A

Embryonal Rhabdomyosarcoma
aka Sarcoma Botryoides

Cluster, grape-like, skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name all 3 Vagina Cancers

A

VAIN - Vagina Intraepithelial Neoplasia
- There are two primary types of vaginal cancer: squamous-cell carcinoma and adenocarcinoma; most common is SCC

CCA
E. Rhabdomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Gimme epithelium @ cervix

and cancer

A

Ectocervix - SS
Squamocolumnar Junction - where HPV hands
Endocervix - Simple Columnar

Cervical IN, SCC by HPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cervical Cancer risk factors

A

Since HPV…

- STD, multiple partners, infections, HPV 16, 18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 2 tumor suppressor genes involved in CC

A

p53 and Retinoblastoma

Rb active form inhibits cell cycle; HPV proteins inhibit this;

Rb blocks G1 to S
Should an oncogenic protein, such as those produced by cells infected by high-risk types of human papillomavirus, bind and inactivate pRb, this can lead to cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HPV CPE [3]

A

Enlarged nuclei
Perinuclear Halos - cytoplasm pushed to periphery
Crinkled Nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which categoris of CIN is low grade Squamous Intraepithlial Lesion LSIL and which is HSIL

A

CIN I is LSIL

CIN II onwards is HSIL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where can SCC cervical cancer spread to

A

Local: bladder, uterus, vagina, rectum

Blood, LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gimme every disease of the Uterus by layers

Note endometrium layer is not endothelium only

A

Endometrial Layer - Endometrial Cancer, Stromal Cancer, Endometriosis
Myometrial Layer - Leiomyoma (Fibroid), Adenomyosis, Leiomyosarcoma,

17
Q

Gimme Endometrium and Egg changes WRT Menstrual Cycle and hormone involved

A

4 days bleeding

  • oestrogen increases,
  • Endometrium proliferative stage, glands become more coiled

14 Day

  • Ovulation - rupture of Graafian Follicle
  • Corpus Luteum maintains endometrium, secretory stage by Progesterone

28 Day
- Corpus Luteum dies, endometrium sheds

18
Q

What if endometrium high oestrogen no progesterone?

[2 types]

A

Endometrial Hyperplasia - increase in glands;
also have PTEN TSG mutation

  • Simple: cystic DILATED glands
  • Complex: CROWDED glands, stratified epithelium, more glands than stroma proliferation, PTEN tsg

The endometrial lining fails to shed when there is an absence of progesterone. In these cases, there is a hormonal imbalance where there is too much estrogen and not enough progesterone.

Symptoms: amenorrhea; abnormal heavy bleeding

19
Q

What if no oestrogen

A

Endometrium remains thin and inactive;
- Hence post menopausal or whatever
Amenorrhea

20
Q

Endometrial Cancer

2 developmental types

A

Endometrial Carcinoma (adenocarcinoma)

2 Development
- Type I: Hyperplasia from oestrogen stimulation - EHP then EC (MAJORITY)

  • Type II: De novo - mutations wo hyperplasia, start from atropic endometrium - mainly in (Post Menopausal women)
21
Q

What is most common endometrial cancer

- gene involved

A

Endometrial Cancer - epithelial cancer - mostly adenocarcinomas; PTEN tsg mutated away;

Type I is most common - oestrogen influenced;

  • low grade
  • history of endometrial hyperplasia

Type II development in Post-menopausal women
- high grade

22
Q

Most common benign uterine cancer

  • Pathophysiology
  • Presentation

What happens during pregnancy

Name the most common malignant uterine cancer

A

Fibroids - Leiomyoma

  • hormone dependent - estrogen receptor
  • white, tan solid nodules
  • Whorled (fascicular) pattern of smooth muscle bundles

Pregnancy - rapid growth, infraction, haemorragic degeneration;
- due to high oestrogen during pregnancy

Most common malignant uterine cancer is Endometroid AC

23
Q

Endometriosis

1 Presentation

A

Endometrial Tissues outside cavity - undergoing cyclic bleeding
- Pelvic pain

24
Q

Adenomyosis

Gross Presentations [2]
Clinical Presentations [2]

A

Ectopic endometrium tissue form diverticular and detach into the myometrial layer;

  • Smooth muscle hyperplasia - Trabeculation
    • Note SMH is reactive to the displaced glands
  • Hemorrhage, uterus thickening
  • Dysmenorrhea

Heavy menstrual bleed w more endometrial tissue and its connection to the surface;
Painful menses from prostaglandins

25
Q

Difference between adenomyoma vs invasive endometrial AC

A

Adenomyosis is benign - normal gland architecture, normal mitosis
- Responses to hormones

while cancer has cancer features and also WO stroma diverticulating downwards together w the glandular structure.

26
Q

Compare and Contrast

- Adenomyoma and Leiomyoma

A

Pathology:

  • ectopic endometrium grow into myometrium
    • cause not known, estrogen def plays role in endometrium proliferation
  • myometrium smooth muscle proliferation due to Oestrogen influence

Presentation:

  • both leads to heavy bleeding
  • pain in adenomyoma due to PG from endometrial tissues

OBGYN (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions