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RANZCR ACM > Gynae > Flashcards

Gynae Flashcards

1
Q

Endometritis: epidemiology (causes)

A

-Most common postpartum fevers. CS > vaginal deliveies.

-Nonpostpartum: related to PID or IUD.

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2
Q

Endometritis:
Pathogenesis

A

Polymicrobial bacterial infection, secondary to ascend of microorganisms through cervix/CS.

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3
Q

Endometritis:
Risk factors

A

-CS, Vaginal delivery, RPOC, prolonged partum, prolonged PPROM, retained clots.

-Preexisting infection: PID.

-Rarely: IUD, bowel fistula, necrotic tumor.

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4
Q

Endometritis: complications

A

Pyometra, tubo ovarian abscess, pelvic septic thrombophlebitis.

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5
Q

Asherman syndrome? Definition

A

Adhesion/synechiae of the uterine walls leading to partial/complete obliteration of the endometrial cavity

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6
Q

Asherman syndrome: path? Causes?

A

Trauma to basal membrane which induces scarring, leading to fusion of the uterine walls.

Causes: mainly D&C due to miscarriage or RPOC.
Also could be due to CS, myomectomy, pelvic radiaation, uterine artery embolization, IUD, uterine TB, septic abortion.

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7
Q

Endometrial polyp: Epidemiology

A

Pre and post menopausal women.
Associated w/ tamoxifen and hormone replacement therapy.

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8
Q

Endometrial polyp:
Microscopic components of a polyp?

A

Dense fibrous stroma + thick walled vessels + disorganized endometrial glands.

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9
Q

Endometrial polyps: classification depending on the endometrial glands

A

Atrophic, hyperplastic, functional.

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10
Q

Endometrial polyp: complications?

A

-Rarely malignant transformation <1%
-Rarely atypia 4%.
-Infertility.
-Mucous discharge

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11
Q

Endometrial polyp: DD

A

-Blood clot
-Submucosal leiomyoma
-Polypoid adenomyoma
-Focal endometrial hyperplasia.
-Endometrial CA

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12
Q

Adenomyosis:
Path?

A

Stratum basalis layer of endometrium invades myometrium, leading to smooth muscle hyperplasia and hypertrophy (> 2.5mm beyond stratum basalis)

Ectopic endometrium is cystically dilated +/- haemorrhage.

Ectopic tissue is basalis type = does not respond to cyclic hormones. Rarely secretory change.

Junctional zone > 12mm.

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13
Q

Adenomyosis: Morphology, classification?

A

Classification:
-Diffused
-Segmental
-Superficial
-Deep.

Morphology as per MUSA
(A) Asymmetrical thickening, > posterior
(B) myometrial/subendometrial cysts (swiss cheese appearance)
(C) fan-shaped shadowing, rain shower or Venetian Blind
(D) echogenic subendometrial lines and buds/finger like projections
(E) hyperechoic islands,
(F) translesional vascularity,
(G) interrupted junctional zone,
(H) irregular junctional zone.

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14
Q

Adenomyosis: Presentation, epidemiology, risk factors,
associations, complications

A

Menorrhagia 50%, dysmenorrhea 30%, metrorrhagia 20%. Other: pain, infertility.

Woman in reproductive age, 40-50.
90% multiparus.

Risk factors: trauma during child birth, abortion, chronic endometritis.

Associations: endometriosis, endometrial polyps, leiomyomas.

Complications:
Malignancy, infertility.

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15
Q

Adenomyosis: diagnosis.

A

US: favoured technique.

HSG, SHG: diverticular aspect.

CT: difficult. Ectopic endometrium does not enhance.

MR:
T1 and T2 hyper.
SWI blood products.

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16
Q

Adenomyosis, DD

A

-Menstrual phase.
-Leiomyoma
-Cystic glandular hypertrophy
-Diffuse myometral hypertrophy
-Low grae endometrial stromal sarcoma.
-MEt.

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17
Q

Endometrial hyperplasia:
Definition,
Physiopath (how) + what causes it?
Risk factors?

A

Def: Abnormal proliferation of endometrial glands relative to stroma, resulting in incrased gland:stroma ratio.

Path: prolonged unopposed E estimulation of the endometrium such as:
-Obesity (peripheral conversion of androgens to E)
-Hormone replacement therapy.
-Medication: tamoxifen
-E producing tumor: funcioting granulosa cell tumor
-Excessive ovarian cortical function (cortical stromal hyperplasia)
-Chronic anovulatory state: PCOS

Risk factors: nulliparus, obesity, HT, DM, >70yo.

18
Q

Endometrial hyperplasia:
Classification, complication

A

WHO classification: 2 categories depending on nuclear morphology:
-Hyperplasia without atypia
-Hyperplasia w/atipia (endometrial intraepithelial neoplasm): w/nuclear atypia. complex glandular pattern. Considerable overlap w/cancer. DD difficuult. **50% of atypia are found in Ca. **

Complication: AdenoCa of the endometrium.

19
Q

Endometrial hyperplasia: associated findings, treatment.

A

Associated findings:
-Polyp
-Ca

Treatment:
-Atypia: Hysterectomy.
-Atypia:

20
Q

Endometrial hyperplasia: diagnostics

A

Morphology:
Endometrial thickening: focal or diffused.
Pre-menopauusal > 8mm during proliferative phase
> 16mm during secretory phase.
Post-menopausal w/bleeding > 5mm
Without bleeding 8-11mm (depends on local guideline)
May show cystic changes (swiss cheese appearance0
Preserved myo-endometrial interface.

Dx: best tool TV and SHG.
MR limited by special resolution: may look normal.
T1 useless. Use T2. Gad show delayed enhancement (no early enhancement)
US Doppler: no definitive criteria.
Areas of atypia: signal.

21
Q

Endometrial hyperplasia: DD

A

-Secretory endometrium: resolves in follow up.
-Endometrial carcinoma: Heterogeneous w/areas of decreased echogenicity 60%. May coexist w/hyperplasia (overlap). MR criteria: relative to normal endometrium. Post con: to myometrium.
-Endometritis: diffuse hypervsacular endometrium. Different clinical presentation.

22
Q

Hemorrhagic cyst,
Dx criteria in MR and CT

A

MR:
T1 hyper. T2 hyper. No fat sat. No enhancement.

CT: hyperdense > 30HU.

23
Q

Hemorrhagic cyst,
what ORADS?
Description?

A

ORADS 2:
Unilocular
No internal vascularity
At least 1 of following:
-Reticular lace like pattern.
-Retractile clot.

24
Q

Hemorrhagic cyst,
Management?

A

Premenopausal,
<=5, do nothing.
>/=5 but <10: f/u in 2-3 months.

Early postmenopausal
<10cm, f/u in 2/3 months
MR w/MR orads
US w/specialist.

Postmenopausal > 5y:
always recategorize (never normal)

25
Q

Follicular cyst:

-Definition?
-Present in what population?
-Expected size?
-Prognosis?
-Management?

A

-Def: Hormone dependent functioning cyst product of arrest of follicular development.

-Menarch and to menopause.

-Size: > 3cm.

-Tend to disappear in 2 cycles.

-Management:
<5cm, nothing but describe.
5-7cm, review by us in 2 cycles.
> 7cm , assess by MR.

26
Q

Follicular cyst:
Path?

A

Functional hormone dependent cyst which results from arrest of follicular development.
Thin wall.
Clear serous content .
Inner granulosa cell, outside of thecal cells w/lutenization.
Tend to be unilocular. Solitary.

27
Q

Follicular cyst:
Dx:

A

Typically >3cm is considered a follicular cyst
Typically solitary.
US prefered: Round. Anechoic. Smooth imperceptible thin walls. Posterior acoustic enhancement. Avascular.
Lack of solid components, septations or internal flow on Doppler
Presence of cumulus oophorus is pathognomonic.
CT: fluid density, no enhancement.
MR: if > 7cm. Follows fluid signal. No gad enhancement. No sinister features.

28
Q

Mature teratoma:
-Definition
-Arise from which cells.

A

Def: benign germ cell tumor. Composed of 2-3 germ cell layers (endo,ecto, meso).
Arise from totipotencial cells (majority from ovum AFTER 1st meiotic division)

29
Q

Mature teratoma:
-Age of presentation
-Clinical presentation

A

-Age: reproductive age 20-40yo.
-Clinical: asymptomatic, palpable mass, o complications (torsion15%, rupture 4%, malignant transformation 1% into SCC, thyroid melanona, infection 1%) (Can present w/bowel obstruction due to chronic rupture. Acute rupture can cause shock)

30
Q

Mature teratoma:
-Macro?
-Micro?

A

Unilocular cyst w/ mostly ectodermal predominance : hair and sebaceous material (dermoid cyst), teeth, Ca+.
From other germ cell layers such as cartilage, bone, thyroid, neural tissue.
20% can be bilateral.
Predominantely cystic.

Could be solid <2%: because it contains all 3 layers of the germ cell layers.

31
Q

Mature cystic teratoma,
Characteristic us findings?

A

o **Rokitansky nodule(s) **= echogenic nodules arising from wall & projecting into lumen
o ‘Tip of iceberg’ = diffusely echogenic w/ sound attenuation (sebaceous material & hair)
o **‘Dermoid mesh’ **= dot-dash appearances due to hair within cyst cavity

32
Q

Teratomas:
How many categories of teratomas are there?

A

-Mature benign teraoma , represent 95%.
-Immature malignant
-Monodermal or highly specialized.

33
Q

Mature teratoma
Dx?

A

Morphology: ORADS 2022
Cystic lesion, ≤ 3 locules, no internal vascularity, at least one of the following;
- Hyperechoic components (diffuse or regional w/shadowing)
- Hyperechoic lines and dots
- Floating echogenic spherical structures
If <10cm = ORADS 2 (>10cm, ORADS 3)
Other:
Usually unilateral. 10-15% potential of being bilateral.

Morphology: ORADS 2022
Cystic lesion, ≤ 3 locules, no internal vascularity, at least one of the following;
- Hyperechoic components (diffuse or regional w/shadowing)
- Hyperechoic lines and dots
- Floating echogenic spherical structures
If <10cm = ORADS 2 (>10cm, ORADS 3)
Other:
Usually unilateral. 10-15% potential of being bilateral.

34
Q
A
35
Q

Mature cystic teratoma:
complicatios?

A

Complications:
-1% can malignant transformation into SCC: heterogeneously enhancing, irregular solid components, invasion to adjacent structures. (Mere presence of enhancing soft tissue component does not indicate malignancy since benign elements, such as thyroid and glial tissue, can enhance in benign mature cystic teratoma)
-Rupture: discontinuity of cyst wall, fat around or away from main cyst, distorted/flattened shape of cyst, ascites, omental infiltration and inflammatory mass.
-Pseudomyxoma peritonei: Mature cystic teratoma with prominent solid component, large volume of ascites with selective sparing of small bowel and its mesentery, and scalloping of liver surface. Sourse is almost always appendiceal mucinous tumor.
-Gliomatosis peritonei: Mature neural glial tissue implanted onto peritoneal surface as result of rupture of mature cystic teratoma containing glial elements
-Paraneoplastic anti N Methyl D aspartate receptor encephalitis: temporal lobe signal abnormality in T2.
-Torsion, infection.

36
Q

Mature cystic teratoma,
Complications?

A

-1% can malignant transformation into SCC: heterogeneously enhancing, irregular solid components, invasion to adjacent structures. (Mere presence of enhancing soft tissue component does not indicate malignancy since benign elements, such as thyroid and glial tissue, can enhance in benign mature cystic teratoma). ; but also thyroid Ca , melanoma, thyroid Ca, basal cell Ca, intestinal adenoCa, leiomyosarcoma, angiosarcoma, chondrosarcoma. Rokitansky nodule is most common site.
* Malignant transformation (1%): usually to SCC & in 50-60s in 80% of cases; but also thyroid Ca , melanoma, thyroid Ca, basal cell Ca, intestinal adenoCa, leiomyosarcoma, angiosarcoma, chondrosarcoma. Rokitansky nodule is most common site.

  • Torsion (16%): usually larger lesions; most common in pregnancy. Usually >10cm.
  • Rupture (1-4%): sebaceous contents into peritoneum  acute or chronic peritonitis
    o Acute can lead to shock.
    o More common chronic  chronic granulomatous peritonitis w/dense peritoneal adhesions  can lead to bowel obstruction
    o Gliomatosis peritonei: Mature neural glial tissue implanted onto peritoneal surface as result of rupture of mature cystic teratoma containing glial elements
  • Infection (1%)

-Pseudomyxoma peritonei: Mature cystic teratoma with prominent solid component, large volume of ascites with selective sparing of small bowel and its mesentery, and scalloping of liver surface. Sourse is almost always appendiceal mucinous tumor.

-Gliomatosis peritonei: Mature neural glial tissue implanted onto peritoneal surface as result of rupture of mature cystic teratoma containing glial elements

-Paraneoplastic anti N Methyl D aspartate receptor encephalitis: temporal lobe signal abnormality in T2.

37
Q

PCOM,
Diagnosis

A

> 20 antral follicles of 2-9mm in an ovary (cip)
10 of 2-9mm, in a slice.
Ovarian volume > 10cc.

38
Q

PCOS,
diagnosis

A

2 out of 3
POCM
Ovulatory dysfunction: oligo or amenorrhea
Hyperandrogensim: male pattern alopecia, hirsutism,

39
Q

PCOS,
complication

A

-infertility
-endometrial hyperplasia/carcinoma (due to increased E, transformed in the fat from excessive androgen)
-metabolic syndrome, CVD.

40
Q

PCOS
associations?

A

T2DM, HTN, Obesity, metabolic syndrome, premature atherosclerosis

41
Q
A
42
Q

PCOM,
DD?

A

-Normal ovary
-Hyperstimulation syndrome
-Suppressed ovaries due to contraceptive

RANZCR ACM (14 decks)

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