Gynaecology Flashcards

1
Q

External Genitalia Development

A

Identical before the 7th week, genital tubercle elongates, and two folds develop - urogenital folds becoming the labia minora, and the lateral folds becoming the labia majora.
Distinguishable by week 12

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2
Q

Pelvic Floor Anatomy (2 sections)

A

ABOVE THE UROGENITAL DIAPHRAGM
> Levator anii (Pubococcygeus, Iliococcygeus, Ischiococcygeus, Coccygeus)
> Piriformis

BELOW THE UROGENITAL DIAPHRAGM
    > Ischiocavernosus
    > Bulbocavernosus
    > Transverse Perineal mm
    > Anal sphincter

NERVES
> Pudendal N (from S2, S3, S4) - motor and sensation to external genitalia, anal sphincter, muscles of the pelvic floor
> Perineal N - branch of femoral cutaneous

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3
Q

Bartholin Cyst

A

Arises from occlusion of bartholin duct, leading to accumulation of mucinous secretions, and formation of a smooth cyst.
Important to rule out malignancy, managed by drainage and placement of Word catheter, or marsupialization (suturing open)

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4
Q

Uterine Fibroids - Pathology, Pathophysiology and Histology

A

Most common neoplasms of the uterus, they are monoclonal benign tumours of the myometrium, with 40% having chromosomal abnormalities.

Promoted by ovarian hormones - oestrogen promotes proliferation, while progesterone inhibits apoptosis. Thus, rarely develop before menarche or after menopause. Well circumscribed, white, firm lesion with pseudocapsule. Can hyalinize or become cystic, very rarely have malignant change.

Histologically, seen as smooth muscles in criss-cross pattern (compared to parallel pattern of normal tissue), high rate of mitosis. No capsule, pseudocapsule from compressed smooth muscle cells.

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5
Q

Uterine Fibroids - Classification (7)

A
> Subserosal
    > Pedunculated subserosal
    > Intramural
    > Submucosal
    > Pedunculated submucosal
    > Cervical
    > Parasitic
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6
Q

Uterine Fibroids - Clinical Presentation (4) and Differentials (4)

A

80% asymptomatic, however may present with
> Pressure/bloating
> Heavy menstrual bleeding (submucosal)
> Subfertility/Infertility (submucosal)
> Infarction = severe pain

Differentials include:
    > Adenomyositis
    > Ovarian neoplasm
    > Pelvic Kidney
    > Colon cancer
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7
Q

Uterine Fibroids - Investigation and Management (2 categories, 2 and 4)

A

Ix involves US assessment, gold standard imaging is MRI.

Mx not required if asymptomatic, indicated by symptoms or infertility.

MEDICAL MANAGEMENT
> OCP/Progestin-only therapy
> GnRH analog - not used regularly, reduced BMD

SURGICAL MANAGEMENT
> Myomectomy - most common, used in fertile women
> Endometrial Ablation - if fertility not a priority
> Uterine artery embolization - leads to fibroid necrosis
> Hysterectomy - definitive management

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8
Q

Nabothian Cyst

A

Incredibly common, occur on the cervix as a result of squamous metaplasia growing over crypts of mucous-secreting columnar cells, leading to mucous-filled cysts.

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9
Q

Cervical Polyps

A

The most common benign neoplastic growth of the cervix, growing from columnar epithelium. Most commonly cause coital bleeding and memorrhagia.

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10
Q

Congenital abnormalities of the Uterine Corpus and Cervix - 8 types

A

> Subseptate (little bump off top)
> Arcuate (top wall bent in slightly)
> Bicornuate (Uterus splits in two)
> Bicornuate + double cervix (uterus and cervix split in two)
> Unicornuate (just one side)
> Bicornuate with rudimentary horn (just one side with atrophied other side)
> Uterine didelphys (uterus and vaginal canal split in two)
> Cervical atresia - cervix does not meet vaginal canal)

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11
Q

Follicular and Corpus Luteal cysts

A

Follicular cysts develops if ovum not released, growing over 3cm large. Corpus Luteal cyst develops if grows over 3cm and does not regress after 14 days, tends to be solid (suspicious of malignancy)

Usually asymptomatic, may cause pelvic “heaviness” and rarely pain, may undergo torsion or rupture.

NEEDS TO BE DISTINGUISHED FROM MALIGNANCY via transvaginal US and CA-125, as well as RMI calculation. Follow up US to be performed after 6 weeks, to see if it grows or shrinks.

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12
Q

Risk of Malignancy Index

A

A scoring system used to combine different clinical information to help decide if an ovarian mass is malignant.

A. MENOPAUSAL STATUS
    > Pre = 1
    > Post = 3
B. US FEATURES
    > Multiloculated = 1 point per locule
    > Solid/Bilateral/Ascites - 2/3 = 3
C. Serum CA-125 titre
    > Absolute Value = point value

RMI = ABC
If RMI > 200, suggests malignancy

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13
Q

Types of Benign Ovarian Neoplastic Tumors (3 categories, 3

A

EPITHELIAL TUMORS
> Serous
> Mucinoid
> Brenner

SEX CORD-STROMAL TUMORS
    > Granulosa
    > Theca
    > Mixed Granulosa-Theca
    > Sertoli-Leydig
    > Fibroma

GERM CELL TUMORS
> Teratoma
> Dermoid Cyst

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14
Q

Serous Ovarian Tumors

A

Develops from mesothelial cells, lined with serous epithelium - flattened cuboidal cells. 70% benign, may form psammoma bodies (calcification)

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15
Q

Mucinoid Ovarian Tumors

A

Develops from mesothelial cells, lined with simple columnar mucinous epithelium (cervical origin), nuclei pushed to bottom. Often multicolular. 85% benign.

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16
Q

Brenner Tumor

A

Solid tumor with capsule, characterised by epithelial nests embedded in a fibrous stroma - cells similar to urothelial (transitional) cells.

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17
Q

Granulosa Ovarian Tumour

A

Most common in postmenopause, promote feminizing signs and symptoms - bleeding, menorrhagia, breast tenderness. Characterised by cells with little cytpolasm that lie close together, nuclei have furrows

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18
Q

Sertoli-Leydig Ovarian Tumor

A

Less common, cause virilizing symptoms - e.g. hirsutism, deep voice, cliteromegaly, muscularisation. Seen as a solid tumor with large nuclei (nucleolus visible), and abundant cytoplasm. May have cysts.

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19
Q

Ovarian Teratoma

A

Most common benign ovarian neoplasm, characterised by the different types of tissue types indispersed - skin, brain, intestine, stomach, retina, etc. Have cells from ecto, endo, and mesoderm.

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20
Q

Dermoid Cyst

A

A cyst lined with keratinized epithelium with adnexae (e.g. hair follicles, apocrine and eccrine glands, subcutaneous fat). Cyst usually filled with oil which, if ruptures, can cause chemical peritonitis and adhesions.

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21
Q

Complications of Ovarian Tumors (2)

A

> TORSION - presents with severe pain and tenderness, may be colic due to twisting and untwisting. Surgical Emergency
> RUPTURE - May spill blood or serous fluid, but worst is oily secretions of dermoid cyst, which may cause chemical peritonitis or adhesions

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22
Q

Amenorrhea

A

Lack of Menstration

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23
Q

Dysmenorrhea

A

Painful menstration

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24
Q

Menorrhagia

A

Heavy periods, increased duration of period

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25
Q

Metrorrhagia

A

Bleeding between periods

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26
Q

Term for painful intercourse

A

Dyspareunia

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27
Q

Differential for Acute Pelvic Pain (3 and 3)

A

GYNAECOLOGIC
> Rupture or Torsion
> Infection/Abscess rupture
> Pregnancy Complications - ectopic pregnancy, abortion

NON-GYNAECOLOGIC
> Gastrointestinal - appendicitis, gastroenteritis, obstruction
> Urinary Tract - cystitis, kidney stone
> Other - Porphyria, thrombophlebitis

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28
Q

Primary Dysmenorrhea - Pathophysiology, Presentation and Management

A

Occurs during ovulatory cycle, starting within 6-12 months of menarche.
Pain caused by uterine contractions, ischaemia, and prostaglandin production - high COX and progesterone activity, caused by ovulation.

Clinically presents as cramping that begins before bleeding, with lower back pain, altered bowel habits, headache, nausea, fatigue.

Managed by reassurance and NSAIDS (best started 2-3 days before period). OCP and other hormonal contraceptives are effective. Alternate therapies may be used (e.g. accupuncture, TENS, heat). Prostestogens are second line. IF NOT MANAGED BY ABOVE, CONSIDER ALTERNATE DIAGNOSIS

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29
Q

Secondary Dysmenorrhea - Differentials (6) and Investigations (4)

A

DIFFERENTIALS
> Endometriosis - the most common cause
> Ovarian/Uterine Neoplasm
> Pelvic Inflammatory Disease
> Adenomyosis - endometrial tissue in myometrium
> Pregnancy - not true dysmenorrhea, just presents so
> Ectopic Pregnancy - same as above

INVESTIGATIONS
    > Pelvic examination with bimanual palpation (if has had intercourse before, targeting PID)
    > Transvaginal US
    > hCG - urine
    > CBC/ESR/CRP - bloods
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30
Q

Chronic Pelvic Pain - Gynaecologic Differentials (6)

A
> Endometriosis - 1/3 of cases
    > Unknown - 1/3/ of cases
    > PID - just under 1/3 of cases
    > Adhesions
    > Adenomyosis
    > Fibroids
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31
Q

Chronic Pelvic Pain - Non-Gynaecologic Differentials (4 main - 6, 2, 2, 0)

A
GASTROINTESTINAL
    > IBS (most common)
    > IBD
    > Coeliac
    > Diverticulitis
    > Neoplasm
    > Adhesions
GENITOURINARY
    > Urethral Syndrome
    > Painful Bladder Syndrome/Interstitial Cystitis
NEUROMUSCULAR
    > Nerve entrapment
    > Fibromyalgia
PSYCHOSOMATIC
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32
Q

Chronic Pelvic Pain - Management (6)

A

> Identifying and managing underlying cause
> Multi-disciplinary team w/ psychologist (experience in chronic pain) and physical therapist
> CBT/Relaxation - to help manage pain
> Analgesia - NSAIDS
> Menstruation suppression - OCP
> Alternate Therapies - acupuncture, TENS, hypnosis

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33
Q

Normal Vaginal Flora, and vaginal factors

A

Mostly aerobic, with about 6 species, most dominant being the H2O2-producing, gram-negative rods lactobacillus.

Mix of flora determined by vaginal pH (3.8-4.5, from production of lactic acid) and glucose availability (from vaginal epithelium)

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34
Q

Wet prep of vaginal secretion - what it shows

A

> Normal Vaginal epithelium
> Few WBC
> Rarely, Clue cells - vaginal epithelium with bacteria adhered (usually gardnerella vaginalis), giving it an indistinct and speckled appearence.

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35
Q

Bacterial Vaginosis - Pathophysiology, Clinical Presentation, and Risks

A

Alteration of the normal flora, resulting in loss of H2O2 producing lactobacillus, and overgrowth of anaerobic bacteria - predominantly g.vaginalis and mycoplasma hominis.

Presents clinically as fishy odour and increased vaginal secretion.

Higher risk of PID, abnormal cervical cytology, and pregnancy risks, including premature labour, choramnionitis, and post-caesarian infection.

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36
Q

Bacterial Vaginosis - Diagnosis and Treatment

A

Diagnosis can be made in the room, with wet prep of vaginal secretions showing lots of clue cells. The whiff test can also be performed - addition of KOH produces a fishy odour. Alternative methods include gram staining, pH, and PCR.

Treatment involves metronidazole for 7 days - targets anaerobes while leaving the lactobacillus alone. Side effects include nausea, headache and metallic taste. Alternate antibiotic is clindamycin.

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37
Q

Trichomonas Vaginitis - Pathophysiology and Clinical Presentation

A

Caused by sexually transmitted flagellated parasite, trichomonas vaginalis. Highly contagious, able to make an anaerobic environment, promoting BV

Presents with profuse, malodorous, mucopurulent discharge, with vulvar pruritis and colpitis macularis (“strawberry” cervix)

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38
Q

Trichomonas Vaginalis - Diagnosis and Management

A

Diagnosis can be made by observing motile parasite on microscopy, however not seen in all cases - NAAT is gold standard. Testing for chlamydia and gonorrhoea should be done, and HIV/Syphilis serology considered.

Treated with metronidazole for patient and any partners - single dose of 2g effective in 95%.

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39
Q

Vulvovaginal Candidiasis

A

Very common, 90% caused by candida albicans.

Clinically presents with vulvular pruritis, erythema, and a white discharge. Common after antibiotic use, or during pregnancy or diabetes.

Diagnosed clinically, KOH wet-mount will show yeast forms/mycelia and pseudohyphae.

Treated with topical clotrimazole, usually resolves within a few days. If recurrent, use fluconazole for 6 months.

40
Q

Chlamydia - What is it, how is it diagnosed, what can it lead to?

A

Chlamydia Trachomatis is a gram-negative intracellular parasite.

Diagnosed by NAAT, however can be diagnosed with tissue culture.

Can lead to PID, ectopic pregnancy, infertility, and reactive arthritis.

41
Q

Gonorrhea - What is it, how is it diagnosed?

A

Neisseria Gonorrhoea is a gram-negative intracellular diplococcus.

Diagnosed through NAAT, gram stain and culture.

42
Q

Endocervicitis - causes, clinical presentation, diagnosis, and management

A

Can be caused by chlamydia or gonorrhoea, or both. Clinically presents with profuse endocervical mucopurulent discharge, cervicitis, and urethral symptoms.

Both best diagnosed with NAAT.

Treatment involves a combination of ceftriaxine with either doxycycline or azithromycin. In pregnancy, single dose of azythromycin. Re-test within 3-4 weeks.

43
Q

PID - Causes and Risk factors (3)

A

Caused by c.trachomatis and n.gonorrhoea, ascending to infect the endometrium and adnexae.

Risk factors include IUD, vaginal douching, and invasive procedures.

44
Q

PID - Clinical Presentation (5) and Investigations (6)

A

Up to 2/3 asymptomatic, symptoms include:
> Fever over 38.3
> Pelvic pain and cervical motion tenderness
> Cervical or vaginal discharge
> Dyspareunia
> Masses (abscesses)

Investigations should include hCG, blood culture, uranalysis, cervical cultures and NAAT, and US

45
Q

PID - Diagnostic criteria (1, 2, 4)

A
MUST HAVE Pelvic pain
PLUS one of
    > Cervical motion tenderness
    > Adnexal tenderness
PLUS one of
    > Fever
    > Discharge
    > Inflammatory mass/Abscess
    > High-risk partner
46
Q

PID - Management (2 categories)

A
HOSPITALISATION is required if:
    > Surgical emergency (e.g. appendicitis) not excluded
    > Patient is severely ill
    > Failed oral management
    > Tubo-ovarian abscess

OUTPATIENT TREATMENT
Ceftriaxone/Cefoxitin + doxycycline + metronidazole

INPATIENT TREATMENT
Cefoxitin + doxycycline IV

47
Q

PID - Complications (I FACE PID)

A
> Infertility
    > Fitz-Hugh-Curtis syndrome - liver capsule inflammation
    > Abscess - commonly tubo-ovarian
    > Chronic pelvic pain
    > Ectopic pregnancy
    > Peritonitis
    > Intestinal obstruction
    > Diffuse infection - sepsis
48
Q

Tubo-ovarian abscess - Pathophysiology, diagnosis, and management

A

Agglutination of pelvic organs (ovary, tube, and bowel) through inflammatory adhesion, sometimes abscess formation occurs.
Diagnosed as a pelvic mass felt on bimanual palpation.

Responds to same antibiotic therapy as inpatient PID regime, may require drainage.

49
Q

Genital Ulcers - Differential (5)

A
> HSV
    > Syphilis (treponema pallidum)
    > Chancre (Haemophilus ducreyi)
    > Carcinoma
    > Abrasions
50
Q

Syphilis - cause, presentation, diagnosis, and management.

A

Caused by treponema pallidum (motile spirochete), leads to painless, indurated ulcers (cancre) and lymphadenopathy. Diagnosis requires IgG syphilis serology or fluorescent antibody study.
Treated with Benzathine Penicillin G

51
Q

HSV - cause, presentation, diagnosis and management

A

90% caused by HSV-2, may be asymptomatic. Presents 2-21 days after infection as a prodrome of tingling/burning, followed by ulcer formation and a painful vesicular rash.
Requires viral culture or cytological smear (multinucleated giant cells with intranuclear inclusion bodies)
Treated with acyclovir.

52
Q

Chancroid - cause, presentation and management

A

Caused by haemophilus ducreyi, characterised by 1-3 extremely painful ulcers with tender lymphadenopathy.

Treated with azithromycin

53
Q

Genital Warts - cause, presentation, and management

A

Caused by HPV-6 and -11, results in warts in the areas most affected by coitus. Highly contagious, may be removed but infection is life-long.

54
Q

HPV vaccines (2)

A

> Giardasil - vaccinates against HPV types -6, -11, 16, and -18
> Cervarix - vaccinates only against types -16 and -18

55
Q

UTI in women

A

80% caused by e.coli, another 10-15% caused by staph saprophyticus. Characterised by frequency, dysuria, and pyuria.
Managed with TMP/SMX or Nitrofurantoin.

56
Q

Choramnionitis - Causes, risk factors (4), Diagnostic criteria (5) and management (2)

A

Caused by infection of the foetal membranes and amniotic fluid as pathogens break through the membranes. Increased risk from increased vaginal examination, nulliparity, BV, and low SES. Most commonly a mix of organisms, like e.coli, group B strep, and anaerobes (e.g. g.vaginalis).

Diagnosis based on
    > Fever over 38 degrees
PLUS TWO OF:
    > Maternal/foetal tachycardia
    > Maternal leukocytosis
    > Uterine tenderness
    > Fowl-smelling amniotic fluid

Best managed with intrapartum therapy of ampicillin and gentamycin.

57
Q

TORCH Infections

A
> Toxoplasmosis
    > Other - syphilis, HIV, Hep B/C
    > Rubella
    > CMV
    > Herpes Simplex
58
Q

Toxoplasmosis in pregnancy

A

From cats and uncooked food.

Causes congenital toxoplasmosis, which leads to microcephaly, enlarged placenta and hepatomegaly.

59
Q

Congenital rubella syndrome

A

If exposed in first trimester, leads to microcephaly, cataracts, hearing loss, heart disease, and hepatosplenomegaly.

60
Q

Cytomegalovirus in Pregnancy

A

Blueberry muffin baby - petichiae, jaundice, microcephaly, thrombocytopenia, IUGR.

61
Q

Herpes Simplex in Pregnancy

A

Can lead to seizures, neurological damage, tremors, fontanelle bulging, and death.

62
Q

Syphilis in Pregnancy

A

Can cause IUGR, stillbirth, non-immune hydrops, deformities, and hepatosplenomegaly

63
Q

Pelvic Organ Prolapse - types (3) and Risk factors (4)

A

> Anterior vaginal prolapse (cystocele)
> Posterior vaginal prolapse (rectocele and enterocele)
> Apical vaginal uterine prolapse

Caused by relaxation of pelvic fascia, ligaments and muscles through:
    > Pregnancy
    > Labour
    > Difficult vaginal delivery
    > Heavy lifting
64
Q

Pelvic Organ Prolapse - Staging (5)

A

Staged using the Pelvic Organ Prolapse Quantification (POP-Q) System, which uses 6 different measurements to carefully quantify the prolapse. Can be split into 5 categories:
> STAGE 0 - no prolapse
> STAGE 1 - Prolapse more than 1cm above the vaginal opening
> STAGE 2 - Prolapse within 1cm of the vaginal opening, still inside the vagina
> STAGE 3 - Prolapse extends between 1 to 2cm of the vaginal opening.
> STAGE 4 - complete prolapse

65
Q

Pelvic Organ Prolapse - Management (6)

A

NON SURGICAL
> Pessiaries
SURGICAL
> Anterior colporrhaphy - tightening of fascia in anterior wall
> Posterior colporrhaphy
> Colpopexy - vaginal vault suspension
> Hysterectomy
> Vaginal closure - low risk, stops coitus

66
Q

Ectopic Pregnancy - Risk Factors (4) and Classification

A

Generally occur due to abnormalities of the fallopian tube. Risk factors include:
> Salpingitis/Adhesions - from PID, endometriosis
> Contraceptive Use
> Assisted reproductive technologies
> Smoking

Sites of ectopic pregnancy include
    > Fallopian Tube - 95% (Ampullary 80%, isthmic 12%, fimbrial 10%, cornual 3%)
    > Ovarian/Abdominal
    > Cervical
    > Caesarian scar
    > Other
67
Q

Ectopic Pregnancy - Clinical Presentation (3 types)

A

ACUTE RUPTURE
Uncommon, occurs when the tube ruptures and causes massive internal haemorrhage, leading to hypovolaemic shock. Patient has abdominal guarding, cervical motion tenderness. SURGICAL EMERGENCY.

PROBABLE ECTOPIC
Presents as pelvic pain, vaginal spotting, and missed menses/positive hCG. US will usually reveal the diagnosis

POSSIBLE ECTOPIC
Subtle presentation, similar to above.

68
Q

Ectopic Pregnancy - Differentials (5)

A
> Abortion
    > Ruptured CL Cyst
    > Adnexal torsion
    > Appendicitis
    > Pancreatitis
69
Q

Ectopic Pregnancy - Management

A

MEDICAL
Preferred in a younger embryo in a stable patient. Methotrexate given, and weekly hCG tests are taken to see >15% decline weekly until non-detectable.
Women need to have normal creatine, LFT’s and CBC’s, and need to avoid folate, NSAIDS and alcohol.

SURGICAL
Preferred in patients with rupture, or if embryo is >3.5cm. Actual procedure based on fertility wishes and damage done:
> Salpingectomy - if extensive damage
> Partial salpingectomy
> Salpingotomy - vertical incision made, and embryo removed. Good for fertility.

ALL Rh- WOMEN SHOULD RECIEVE ANTI-RH

70
Q

Endometriosis - Pathophysiology, Locations, and Histology

A

Pathogenesis not entirely understood, thought to be one of:
> Retrograde menstruation - transporting endometrial tissue into the abdomen, does not take into account tissue in the lung, axilla, forehead
> Müllerian Metaplasia - Metaplastic transformation of the peritoneal mesothelium via genetic influence
> Lymphatic spread theory - endometrial spread via lymphatics and disseminated - 20% of cases have tissue in pelvic lymphatics

Most commonly involves the ovaries, cul-de-sac peritoneum, uterosacral ligaments, broad ligament, and fallopian tubes. These islands respond cyclically to oestrogen and progesterone, sloughing off to produce severe pain, inflammation and fibrosis. Main ddx is well-differentiated adenocarcinoma.

Histological diagnosis needs 2 of the following:
    > ENDOMETRIAL EPITHELIUM (columnar)
    > ENDOMETRIAL GLANDS
    > ENDOMETRIAL STROMA
    > HAEMOSIDERIN-LADEN MACROPHAGES
71
Q

Endometriosis - Clinical Presentation (8), Diagnosis

A
Characteristic triad of
    > Dysmenorrhea
    > Dyspareunia
    > Dyschezia - colon involvement
can also present with:
    > pre/post menstrual spotting (common)
    > chronic pelvic pain
    > infertility (from pelvic fibrosis and anatomical distortion)
    > Fixed, tender adnexal mass
    > Uterine fixation and retroversion

Diagnosis should be considered in a nulliparous young woman with no fever, pelvic pain, fixed adnexal mass, and uterosacral tender nodularity (classic).
Can only be properly diagnosed with laparoscopy/laparotomy, and bioscopy with histological sampling.

72
Q

Endometriosis - Differential Diagnosis

A

> Chronic PID/Salpingitis
> Haemorrhagic Corpus Luteum
> Ovarian Neoplasm
> Ectopic Pregnancy

73
Q

Management - Factors (6) and Strategies (3)

A

Management based on several factors:

1) Diagnostic certainty
2) Symptom severity
3) Disease extent
4) Fertility wishes
5) Patient age
6) Involvement of GIT/UT

WATCHFUL WAITING
Used especially in women who wish for pregnancy

MEDICAL MANAGEMENT
First line, targeted against symptoms. First line is:
> NSAIDS - for pain
> OCP - for reducing menstrual flow
> Progestins
Second line should be sought after 6 months:
> GnRH Agonists - induce medical castration

SURGICAL MANAGEMENT
Indicated in severe disease, when the lesions >3cm, there is significant fibrosis and organ involvement.
> TOTAL HYSTERECTOMY WITH BILATERAL SALPINGOOOPHERECTOMY, AND DESTRUCTION OF ALL FOCI - 20% recurrence rate.
> CONSERVATIVE LAPAROSCOPY - to destroy foci and adhesions. Best option if fertility desired

74
Q

Adenomyositis - Definition and Pathology

A

Defined as extension of endometrial glands and tissue more than 2.5mm into the basalis layer. Often an incidental finding - found in 60% of women over 40.

Generally, the uterus is diffusely enlarged wiht glandular irregularities. May be confused with leiomyoma, however there is no pseudocapsule.
Histologically, the myometrium has a nodular appearence and dilated cysts. Collagen between cells has a different appearence to smooth muscle, and cysts are lined with cylindrical epithelium (endometrial)

75
Q

Adenomyositis - Clinical Presentation and Management

A

Most patients are asymptomatic, however some complain of severe dysmenorrhea/heavy bleeding. Examination shows enlarged uterus.

Management depends on severity of symptoms - any acut worsening requires endometrial biopsy to rule out malignancy.
Conservative management with NSAIDS and hormonal control (usually OCP) is mainstay.

76
Q

Polymenorrhagia

A

Abnormally frequent menses, occurring less than 24 days apart.

77
Q

Metorrhagia - 4 aspects, and causes (PALM-COIEN)

A
Should be quantified according to:
    > Frequency
    > Duration
    > Regularity
    > Amount lost
PALM-COEIN helps memorise the causes - PALM is structural causes, COEIN is functional causes
Polyps
Adenomyosis
Leiomyomas
Malignancy
Coagulation problems
Ovarian dysfunction
Endometrial causes
Iatrogenic
Not yet classified/known
78
Q

Acute heavy menstrual bleeding - Approach, Investigations, and Management

A

Immediately should be assessed for shock and hypovolaemia, with vitals and Hb taken. Hospitalization for women with Hb under 7g/dL, or if unstable.

Investigations should include:
> Urine preggers test
> Blood tests - cbc, serum iron/ferritin/transferrin, coags, LFT, creatinine, BUN
> Imaging - US (if indicated)

Medical management is first line, with the use of high-dose progestins or OCP. If no response within 24h, go to surgical management with D&C, balloon tamponade, or vessel embolization.

After this, steps should be taken to prevent occurrence - address underlying issues, continued OCP/progestin use.

79
Q

Chronic Heavy Periods - Management Strategies (5)

A

NORMALISE PROSTAGLANDINS
> NSAIDS help normalise high PGE2 levels

ANTIFIBRINOLYTIC THERAPY
> Used to stabilize clots in the uterine arteries

COORDINATE SLOUGHING
> In anovulary women, oestrogen can work unoppressed. Control with OCP or Progestins

ENDOMETRIAL SUPPRESSION
> Inducing amenorrhea with Levonorgestrel IUS or continuous OCP use

SURGICAL TREATMENT
> Last line, may involve endometrial ablation or hysterectomy.

80
Q

Overview of Contraception Methods (8)

A
> Implants - most effective
    > IUD's
    > Injections
    > Pills
    > Patches
    > Vaginal rings
    > Condoms (Male and Female)
    > Behavioural techniques
81
Q

Contraceptive Implant

A

Nexplanon/Implanon is a plastic rod implant with etonogestrel (a progestin). Can be used by virtually anyone, contraindicated in history of breast cancer.
Works by suppressing ovulation and thickening cervical mucous (to stop sperm access). Provides 3 year coverage.

82
Q

IUD types (3) and prerequisite

A

Most commonly used in the world, effective and rapidly reversible. 3 currently available:
> PARAGUARD COPPER IUD - 10 year duration, non-hormonal, SAFEST. Works as a spermicide
> MIRENA - 5 years duration, uses the progestin levonorgestrel to thicken cervical mucous and suppress ovulation.
> SKYLA - 3 years duration, lower dose of levonorgestrel.

Requires pelvic exam before insertion.

83
Q

IUD Contraindications (5)

A

Contraindications include:
> Pelvic infection
> Uterine cancer
> Abnormal uterine shape/distortion
> Copper allergy/Wilson disease (For copper IUD)
> Recent breast cancer - for levonorgestrel IUD’s

84
Q

Injectable contraceptives

A

Two forms exist, with a progestin-only drug. One delivered IM and one SC, every 11-14 weeks. Highly effective if used correctly.

85
Q

COCP

A

Combined oral contraceptive pill (with oestrogen and progestin), provides cycle control - works by suppressing ovulation and thickening cervical mucous.
Oestrogen helps menstruation blood loss and pain, treats acne, and lowers risk of endometrial and ovarian cancer.
However, oestrogen also has an increased risk of venous/arterial thrombus formation (which can lead to MI, stroke or PE), melasma (facial pigmentation) and BP increases.

86
Q

Lactational Amenorrhea

A

Limited to exclusively-breastfeeding women in the first 6 months after childbirth, who are anovulatory. 2% failure rate.

87
Q

Emergency contraception

A

Three methods used:
> High-dose doses of levonorgestrel - suppresses ovulation
> Antiprogestin - single dose
> Copper IUD - insertion within 5 days, MOST EFFECTIVE

88
Q

Abortion methods

A

Before 49 days of gestational age, both medical and surgical methods can be used, however surgical is preferred if anaesthesia will help anxiety/pain, or when medical mx is contraindicated.

MEDICAL
Involves mifepristone followed by misoprostol - effective in 95-98% of cases. Contraindicated by
    > Adrenal insufficiency
    > Haemorrhagic disorders
    > Severe hepatic impairment
    > Renal failure

SURGICAL
Can either be
> Vacuum delivery (5-6 weeks gestation)
> D&C (6-13 weeks gestation)

89
Q

D&C - indications (2) and complications (4)

A

Dilation and curettage is one of the most common gynaecological procedures, and indicated by:
> DIAGNOSIS - menorrhagia or post-menopausal bleeding
> THERAPEUTIC - endometrial hyperplasia, polyps, or abortion

Complications include
    > Haemorrhage
    > Infection
    > Cervical damage
    > Uterine perforation
90
Q

Premature ovarian failure - causes (4)

A

Defined as ovarian failure before 40. Causes include:
> Iatrogenic - surgery, radiation, chemo
> Chromosomal abnormality - causes ovarian failure before 30
> Fragile X carrier
> Autoimmune - may co-exist with other autoimmune conditions

91
Q

Hyperandrogenism - Clinical manifestations (5)

A
Increased levels of male hormones presents with:
    > Hirsutism
    > Acne
    > Virilization - deep voice
    > Alopecia
    > Cliteromegaly
92
Q

PCOS - Diagnostic Criteria

A

Rotterham Criteria, needs 2 of:
> Clinical/Biochemical hyperandrogenism
> Oligomenorrhea/Amenorrhea
> Polycystic ovaries

93
Q

PCOS - Cause and Consequences (4)

A

Caused by INCREASED LH production relative to FSH - increased theca cell activation, leading to testosterone.

> Infertility (from follicular arrest)
> Insulin resistance/Diabetes
> Obesity/Metabolic Syndrome
> Increased risk of endometrial cancer
94
Q

PCOS - Management

A

OCP (suppress LH/FSH), spirinolactone to manage hirsutism.

95
Q

Cushing’s Syndrome - 2 confirming tests

A

> 24 hour urine cortisol

> Dexamethasone suppression test