Gynaecology Flashcards
1
Q
What is an abnormal formation of the female organs?
A
It refers to congenital anomalies or malformations in the development of the female reproductive tract, often due to incomplete fusion, resorption, or development of the Müllerian ducts.
2
Q
How are abnormalities of female organ formation classified?
A
Hypoplasia or Agenesis (e.g., Mayer-Rokitansky-Küster-Hauser syndrome)
Unicornuate Uterus: Failure of one duct to develop.
Uterus Didelphys: Failure of duct fusion, resulting in two uteri.
Bicornuate Uterus: Partial failure of duct fusion.
Septate Uterus: Incomplete resorption of the uterine septum.
Arcuate Uterus: Mild anomaly with a concave uterine fundus.
Diethylstilbestrol-Related Anomaly: Caused by in utero exposure to DES.
3
Q
What embryological structure is responsible for forming the female reproductive tract?
A
The Müllerian (paramesonephric) ducts form the fallopian tubes, uterus, cervix, and upper two-thirds of the vagina.
4
Q
What are common symptoms of abnormal formation of female organs?
A
Primary amenorrhea (in agenesis or hypoplasia)
Recurrent miscarriage or infertility (in structural anomalies like septate or bicornuate uterus)
Dysmenorrhea or cyclical pain
Abnormal uterine bleeding
Dyspareunia (painful intercourse)
5
Q
What tools are used to diagnose abnormalities in the formation of female organs?
A
Ultrasound: Initial imaging for anatomical anomalies.
MRI: Detailed visualization of uterine anomalies.
Hysterosalpingography (HSG): Assess uterine cavity and tubal patency.
Laparoscopy and Hysteroscopy: Diagnostic and therapeutic.
6
Q
___________ is the gold standard imaging modality for detailed visualization of uterine anomalies.
A
MRI
7
Q
Name a syndrome associated with agenesis of the uterus.
A
Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome.
8
Q
How is hypoplasia or agenesis of the uterus managed?
A
Psychological support and counseling.
Vaginal dilation or reconstructive surgery for MRKH syndrome.
Assisted reproduction techniques like surrogacy for fertility options.
9
Q
What is the treatment for a septate uterus?
A
Surgical removal of the septum via hysteroscopic metroplasty.
10
Q
True/False
Q: Bicornuate uterus results from incomplete resorption of the uterine septum.
A
False. It results from partial failure of the Müllerian duct fusion.
11
Q
What complications are associated with a unicornuate uterus?
A
Increased risk of miscarriage and preterm labor.
Higher risk of renal anomalies due to parallel development.
12
Q
What is the impact of in utero exposure to diethylstilbestrol (DES)?
A
Uterine hypoplasia or a “T-shaped” uterus.
Increased risk of miscarriage, infertility, and preterm birth.
13
Q
In uterine anomalies, failure of ___________ leads to a didelphys uterus.
A
Müllerian duct fusion
14
Q
Why is early diagnosis of uterine anomalies important?
A
To address infertility, prevent obstetric complications, and manage symptoms effectively.
15
Q
How does an arcuate uterus differ from a septate uterus?
A
An arcuate uterus has a mild indentation of the uterine fundus, whereas a septate uterus has a fibrous or muscular septum dividing the uterine cavity.
16
Q
What is Androgen Insensitivity Syndrome (AIS)?
A
AIS is a genetic condition where individuals with a 46,XY karyotype have a resistance to androgens due to mutations in the androgen receptor gene, leading to varying degrees of undervirilization despite normal or elevated androgen levels.
17
Q
What are the two main types of AIS?
A
Complete Androgen Insensitivity Syndrome (CAIS): Complete inability to respond to androgens.
Partial Androgen Insensitivity Syndrome (PAIS): Partial response to androgens, leading to a spectrum of phenotypes.
18
Q
What is the genetic basis of AIS?
A
AIS is caused by mutations in the androgen receptor (AR) gene, located on the X chromosome. It follows an X-linked recessive inheritance pattern.
19
Q
What are the clinical features of Complete AIS (CAIS)?
A
Female external genitalia with absent or rudimentary internal female reproductive organs (uterus, fallopian tubes).
Undescended testes (often located in the abdomen or inguinal canal).
Primary amenorrhea.
Breast development at puberty (due to aromatization of androgens to estrogens).
Sparse or absent pubic and axillary hair.
20
Q
What are the clinical features of Partial AIS (PAIS)?
A
Ambiguous genitalia at birth (e.g., clitoromegaly, micropenis, or hypospadias).
Undescended testes.
Variable breast development and body hair.
Infertility.
21
Q
How is AIS diagnosed?
A
Karyotyping: Reveals a 46,XY genotype.
Hormonal profile:
Elevated luteinizing hormone (LH) and testosterone levels.
Normal or elevated estrogen levels.
Pelvic ultrasound: Absence of uterus and ovaries; presence of undescended testes.
Genetic testing: Confirmation of mutations in the androgen receptor (AR) gene.
22
Q
In AIS, the karyotype is __________, but the external genitalia are typically __________ in CAIS.
A
46,XY; female
23
Q
What is the management approach for Complete AIS (CAIS)?
A
Psychological support for patients and families.
Gonadectomy: Removal of undescended testes to prevent malignancy, typically after puberty to allow spontaneous feminization.
Hormone replacement therapy (HRT): Estrogen replacement after gonadectomy.
Vaginal dilation or surgical creation of a neovagina: To allow for sexual function if required.
24
Q
What is the management approach for Partial AIS (PAIS)?
A
Individualized surgical management of ambiguous genitalia.
Gonadectomy if testes are nonfunctional or at high risk of malignancy.
Hormonal therapy based on the patient’s gender identity and clinical needs.
25
In AIS, undescended testes are at an increased risk of developing _________
Gonadal malignancy
26
What are the differential diagnoses for AIS?
5-alpha reductase deficiency.
Müllerian agenesis (Mayer-Rokitansky-Küster-Hauser syndrome).
Turner syndrome.
Swyer syndrome (complete gonadal dysgenesis).
27
True/False
Q: Breast development occurs in CAIS due to the absence of androgen action and aromatization of testosterone to estrogen
true.
28
What is the prognosis for individuals with AIS?
Generally good with appropriate management.
Psychological and social support are essential for quality of life.
Fertility is not possible due to the absence of functional gonads and reproductive structures.
29
How common is AIS?
AIS occurs in approximately 1 in 20,000 to 1 in 50,000 live births.
30
What is menarche?
Menarche is the first occurrence of menstruation, marking the onset of reproductive capability in females.
31
At what age does menarche typically occur?
Menarche usually occurs between 10 and 16 years, with an average age of 12 to 13 years.
32
What hormonal changes trigger menarche?
Activation of the hypothalamic-pituitary-gonadal (HPG) axis.
Increased secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus.
Release of FSH and LH from the pituitary gland, stimulating ovarian follicles to produce estrogen.
Rising estrogen levels lead to endometrial proliferation and the first menstrual bleed.
33
What factors influence the timing of menarche?
Genetics: Strong familial influence.
Nutrition: Malnutrition or obesity can delay or advance menarche.
Physical activity: High levels of exercise (e.g., in athletes) may delay onset.
Chronic illnesses: Conditions like celiac disease or diabetes can delay menarche.
Environmental factors: Socioeconomic status and exposure to endocrine disruptors.
34
At which Tanner stage does menarche typically occur?
Menarche typically occurs at Tanner Stage IV, when secondary sexual characteristics are well-developed.
35
What are the clinical implications of early or delayed menarche?
Early menarche (<10 years): Increased risk of endometrial cancer, polycystic ovary syndrome (PCOS), and psychosocial issues.
Delayed menarche (>16 years): Suggestive of underlying issues such as Turner syndrome, hypothalamic amenorrhea, or chronic illness.
36
True/False
Q: Menarche is the first ovulatory cycle in females.
False. The first cycles are often anovulatory, with ovulation occurring later as the HPG axis matures.
37
What are some abnormal patterns associated with menarche?
Primary amenorrhea: Absence of menarche by age 16.
Hypomenorrhea: Scanty menstruation.
Irregular cycles: Common in the first 1-2 years post-menarche due to immaturity of the HPG axis.
38
An absence of menarche by the age of __________ is considered primary amenorrhea.
16
39
Why is menarche a significant milestone in many cultures?
Menarche often symbolizes the transition to womanhood and is associated with cultural, religious, and social rituals in many societies.
40
What investigations are performed for delayed menarche?
History and physical examination: To assess secondary sexual characteristics and overall health.
Hormonal profile: FSH, LH, estradiol, thyroid function tests, and prolactin.
Imaging: Pelvic ultrasound or MRI to evaluate reproductive anatomy.
Genetic testing: To identify chromosomal abnormalities like Turner syndrome.
41
How is delayed menarche managed?
Address the underlying cause (e.g., hormone replacement in hypogonadism).
Nutritional support for undernutrition or eating disorders.
Psychological support as needed.
42
What health risks are associated with early menarche?
Increased risk of obesity.
Higher lifetime exposure to estrogen, raising the risk of breast and endometrial cancer.
Potential psychosocial challenges like early sexual activity or body image issues.
43
What is the prognosis for individuals with normal menarche?
Good prognosis with normal reproductive potential, provided no significant menstrual irregularities develop.
44
How is menopause defined?
Menopause is defined retrospectively as the point 12 months after a woman’s last natural menstrual period.
45
What is perimenopause?
physiological changes and associated signs and symptoms during the period of time before the menopause
46
What is premature ovarian insufficiency?
Menopause that occurs before 40 years old.
47
What is the average age of menopause?
51 years old, typically occurring between 40 and 60 years.
48
What causes the hormonal changes during menopause?
1. Declining reserves of oocytes and associated follicles leads to reduced oestrogen production in response to FSH and LH stimulation. 2. Therefore serum LH and FSH rise in response (lack of negative feedback). 3. Eventually insufficient oestrogen means the LH surge and subsequent ovulation do not occur, leading to anovulatory cycles
49
Why do anovulatory cycles occur in menopause?
Low circulating progesterone due to anovulation leads to unpredictable breakthrough bleeding.
50
What physiological factors contribute to hot flushes?
The physiology of hot flushes is multifactorial and not fully understood, but is thought to be due to a combination of oestrogen withdrawal, thermoregulatory changes and alterations in neurotransmitter systems.
51
Why do vaginal symptoms like dryness and dyspareunia occur during menopause?
Vaginal symptoms of dyspareunia (painful sexual intercourse), dryness and itch occur due to atrophic vaginitis secondary to low circulating oestrogen levels (epithelial thinning, muscular atrophy, reduced vascularity, loss of rugosity).
52
List the key symptoms of menopause.
○ Menstrual irregularity leading to amenorrhea ○ Vasomotor symptoms (hot flushes / night sweats ○ Mood disturbance ○ Sleep disturbance ○ Vaginal symptoms (dyspareunia, dryness, itch)
53
What are the two major complications of menopause?
Osteoporosis - due to increased bone turnover (normal oestrogen levels inhibit osteoclast activity). ● Increased cardiovascular risk - due to alterations in LDL:HDL ratio, raised serum cholesterol, arterial stiffening (among many other factors that are not entirely clear)
54
How is menopause typically diagnosed?
Typically diagnosed clinically - investigations are usually not indicated in women with menopausal symptoms over the age of 45.
55
When are investigations indicated for menopause?
When symptoms occur in younger women or when the diagnosis is uncertain.
56
What are the key diagnostic tests for menopause, if needed?
Serum FSH: elevated. Serum oestradiol: reduced.
57
Treatment of menopause can be beneficial for what?
for both symptomatic relief and cardiovascular / osteoporotic risk.
58
HRT should be prescribed in the ____ effective dose for the shortest duration of treatment possible.
lowest
59
What is the first-line management for menopause?
○ Regular excess ○ Weight loss (as necessary) ○ Avoidance of triggers (smoking, alcohol, spicy food).
60
What is the second-line management for menopause?
Hormone Replacement Therapy (HRT).
61
What forms of HRT are recommended for women with a uterus?
Oral or transdermal (patch) combined oestrogen and progesterone e.g. tibolone for systemic i.e. vasomotor symptoms, mood disturbance. ■ Note - in situ Mirena can act as progesterone component of HRT. ■ Topical oestrogen gel for local i.e. vaginal symptoms.
62
What forms of HRT are recommended for women withOUT a uterus?
Oral or transdermal oestrogen only treatment for systemic symptoms. ■ Topical oestrogen gel for local symptoms.
63
How is HRT adapted for perimenopausal women?
Monthly or 3 monthly cyclical regime to produce a protective bleed: ● Oestrogen daily, plus progestogen for 12 days every 4 weeks or 3 months
64
How is HRT prescribed for postmenopausal women?
(i.e. 12 months after LMP): ■ Cyclical or continuous combined regime: ● Cyclical (as above). ● Continuous oestrogen and progesterone daily
65
What are the key risks associated with systemic HRT?
Increased risk of breast cancer, which rises with longer use. Increased risk of venous thromboembolism.
66
Systemic HRT is associated with increased risk of _______. The longer its duration of use, the higher the associated risk.
Breast Cancer
67
Systemic HRT is associated with increased risk of ___ ______
Venous Thromboembolism
68
Does topical HRT carry the same risks as systemic HRT?
No, topical HRT is thought to have no effect on breast cancer risk due to minimal systemic absorption.
69
What are the absolute contraindications to HRT?
1. History of breast cancer, any oestrogen-dependent cancer, current undiagnosed PV bleeding, current endometrial hyperplasia. 2. History of idiopathic VTE (if not anticoagulated). 3. Thromboembolic disease e.g. MI, angina 4. Liver disease. 5. Inherited thrombophilia. 6. Pregnancy.
70
What is adenomyosis?
Adenomyosis is a gynecological condition characterized by the presence of endometrial tissue (glands and stroma) within the myometrium, causing uterine enlargement and associated symptoms.
71
What is the pathophysiology of adenomyosis?
Endometrial tissue invades the myometrium.
This leads to hypertrophy and hyperplasia of the surrounding myometrium.
The condition results in a globally enlarged, "boggy" uterus.
72
What are the risk factors for adenomyosis?
Parity: More common in multiparous women.
Age: Typically affects women aged 35–50 years.
History of uterine surgery: Cesarean section or dilation and curettage.
Endometriosis: Often coexists with adenomyosis.
73
What are the common clinical features of adenomyosis?
Heavy menstrual bleeding (HMB): Menorrhagia.
Dysmenorrhea: Painful periods.
Chronic pelvic pain.
Dyspareunia: Pain during intercourse.
Enlarged uterus: Diffusely enlarged, tender, and "boggy" on examination.
74
Adenomyosis commonly presents with __________ menstrual bleeding and pelvic __________.
Heavy; pain
75
How is adenomyosis diagnosed?
Clinical examination: Enlarged, tender uterus.
Imaging:
Transvaginal ultrasound (TVUS): Diffuse thickening of the myometrium, myometrial cysts, or asymmetric uterine wall thickening.
MRI: More sensitive, showing thickened junctional zone (>12 mm).
Histological confirmation: Requires hysterectomy specimen (definitive diagnosis).
76
What investigations are used to assess adenomyosis?
Transvaginal ultrasound (TVUS): First-line imaging.
MRI: To confirm diagnosis if ultrasound findings are inconclusive.
Blood tests: To assess for anemia due to heavy menstrual bleeding.
77
What are the management options for adenomyosis?
Medical management:
NSAIDs for pain.
Hormonal therapies:
Combined oral contraceptives (COCPs).
Progestogens (oral, injectable, or intrauterine system like Mirena IUS).
GnRH analogues (temporary relief).
Surgical management:
Uterine artery embolization (UAE).
Hysterectomy (definitive treatment).
78
The definitive treatment for adenomyosis is _______
Hysterectomy
79
What are the differential diagnoses for adenomyosis?
Fibroids (leiomyomas).
Endometriosis.
Endometrial hyperplasia or carcinoma.
Pelvic inflammatory disease (PID).
80
True/False
Q: Adenomyosis typically affects postmenopausal women.
False. Adenomyosis typically affects women of reproductive age, particularly those aged 35–50.
81
What is the prognosis for adenomyosis?
Symptoms can improve with medical management or after menopause.
Definitive resolution requires hysterectomy.
82
Does adenomyosis affect fertility?
Adenomyosis can negatively impact fertility by disrupting normal uterine function, though the exact mechanisms are not fully understood.
83
How does the Mirena intrauterine system (IUS) help in adenomyosis?
Reduces heavy menstrual bleeding.
Relieves dysmenorrhea by thinning the endometrial lining and reducing inflammatory changes.
84
What is Asherman’s Syndrome?
Asherman’s Syndrome is the development of intrauterine adhesions (synechiae) due to endometrial damage, leading to partial or complete obliteration of the uterine cavity.
85
What are the main causes of Asherman’s Syndrome?
Trauma to the endometrium, such as:
Dilatation and curettage (D&C), particularly after miscarriage or postpartum hemorrhage.
Uterine surgery (e.g., myomectomy).
Hysteroscopy or endometrial ablation.
Infection: Endometritis from tuberculosis or schistosomiasis.
86
What are the risk factors for Asherman’s Syndrome?
Repeated uterine surgeries or D&C procedures.
Infections like tuberculosis.
Severe postpartum hemorrhage or retained products of conception.
87
What are the clinical features of Asherman’s Syndrome?
Amenorrhea: Absence of menstruation (common).
Hypomenorrhea: Light or infrequent periods.
Infertility.
Recurrent miscarriages.
Cyclic pelvic pain: If there is obstruction of menstrual flow.
88
The main symptom of Asherman’s Syndrome is __________, which can range from light periods to complete absence of menstruation.
Amenorrhea
89
How is Asherman’s Syndrome diagnosed?
Hysteroscopy: Gold standard for visualization of intrauterine adhesions.
Imaging:
Sonohysterography or saline infusion sonography (SIS).
MRI: May help in assessing the severity.
Hysterosalpingography (HSG): Shows irregular uterine cavity or filling defects
90
What investigations are commonly performed in suspected Asherman’s Syndrome?
Hysteroscopy (gold standard).
Sonohysterography or HSG for cavity assessment.
MRI in complex cases.
91
True/False
Q: Hysteroscopy is the gold standard for diagnosing Asherman’s Syndrome.
True.
92
How is Asherman’s Syndrome managed?
Surgical treatment:
Adhesiolysis using hysteroscopy.
Use of intrauterine balloon or catheter to prevent re-adhesion.
Hormonal therapy:
Estrogen therapy to promote endometrial healing and regeneration.
Antibiotics: If infection is suspected.
93
What is the prognosis for Asherman’s Syndrome?
Mild cases: Good prognosis with restoration of normal menstruation and fertility after treatment.
Severe cases: Increased risk of infertility or recurrent pregnancy loss despite treatment.
94
What are the complications of untreated Asherman’s Syndrome?
Infertility.
Recurrent miscarriages.
Chronic pelvic pain.
Increased risk of placenta accreta in future pregnancies.
95
The gold standard for managing intrauterine adhesions in Asherman’s Syndrome is __________ adhesiolysis.
Hysteroscopic
96
What conditions should be considered as differential diagnoses for Asherman’s Syndrome?
Hypothalamic amenorrhea.
Premature ovarian insufficiency.
Endometrial tuberculosis.
97
How can Asherman’s Syndrome be prevented?
Minimizing uterine trauma by careful use of D&C.
Prompt treatment of infections.
Using intrauterine devices (IUDs) or balloons post-surgery to prevent adhesion formation.
98
What is Lichen Sclerosus?
Lichen Sclerosus is a chronic, inflammatory skin condition that primarily affects the genital and perianal regions, leading to white, atrophic plaques and potential scarring.
99
Who is most commonly affected by Lichen Sclerosus?
More common in postmenopausal women.
Can also occur in prepubertal girls and occasionally in men (affecting the foreskin).
100
What is the underlying pathophysiology of Lichen Sclerosus?
The exact cause is unknown but may involve:
Autoimmune mechanisms.
Genetic predisposition.
Chronic irritation or trauma (Koebner phenomenon).
101
What are the clinical features of Lichen Sclerosus?
Pruritus: Intense itching, especially at night.
White plaques: Atrophic, thin, parchment-like skin.
Pain or discomfort: Particularly during urination or intercourse.
Fissures or bleeding: Due to fragile skin.
Scarring: Can lead to narrowing of the vaginal or urethral opening.
102
Lichen Sclerosus commonly presents with __________ plaques and intense __________, particularly in the genital area.
White; itching
103
What findings might you see on examination of Lichen Sclerosus?
White atrophic plaques: Often in the vulva or perianal region (can form a "figure-of-eight" pattern).
Skin thinning and wrinkling: "Cigarette paper" appearance.
Excoriations or fissures.
Loss of normal vulvar architecture: Resorption of labia minora or clitoral phimosis.
104
What are the potential complications of Lichen Sclerosus?
Sexual dysfunction: Due to pain or scarring.
Urethral or vaginal stenosis: From scarring.
Squamous cell carcinoma (SCC): Small increased risk (4–5%).
105
How is Lichen Sclerosus diagnosed?
Clinical diagnosis: Based on characteristic appearance.
Skin biopsy: May be needed if diagnosis is uncertain or there are suspicious areas for malignancy.
106
What is the mainstay of treatment for Lichen Sclerosus?
High-potency topical corticosteroids, such as clobetasol propionate, applied daily initially, then tapered.
107
Besides corticosteroids, what other management options are available for Lichen Sclerosus?
Emollients: To soothe and protect the skin.
Topical calcineurin inhibitors (e.g., tacrolimus): For steroid-resistant cases.
Surgical intervention: Only for complications like severe scarring.
Regular follow-up: To monitor for malignant transformation.
108
What is the prognosis for Lichen Sclerosus?
Chronic condition requiring long-term management.
Symptoms can be controlled with appropriate treatment.
Regular monitoring is necessary to manage symptoms and assess for SCC risk.
109
Why is regular follow-up important in Lichen Sclerosus?
To monitor treatment response, manage symptoms, and assess for any signs of malignant transformation (SCC).
110
True/False
Q: Lichen Sclerosus is a premalignant condition with a risk of progression to squamous cell carcinoma.
true.
111
What are the differential diagnoses for Lichen Sclerosus?
Lichen planus.
Vulval psoriasis.
Chronic eczema.
Squamous cell carcinoma.
112
What is atrophic vaginitis?
Atrophic vaginitis refers to the inflammation of the vaginal epithelium due to thinning, dryness, and reduced elasticity caused by estrogen deficiency, typically in postmenopausal women.
113
What causes atrophic vaginitis?
Estrogen deficiency leads to thinning of the vaginal epithelium, loss of glycogen, and reduced lactobacilli, resulting in:
Increased vaginal pH.
Dryness and irritation.
Predisposition to infections.
114
Name the risk factors for atrophic vaginitis.
Postmenopause (most common).
Breastfeeding.
Premature ovarian insufficiency.
Anti-estrogen therapies (e.g., tamoxifen, aromatase inhibitors).
Surgical menopause (bilateral oophorectomy).
115
What are the common clinical features of atrophic vaginitis?
Vaginal symptoms: Dryness, itching, burning, and discomfort.
Dyspareunia: Pain during intercourse.
Spotting: Due to fragile epithelium.
Urinary symptoms: Dysuria, urgency, or recurrent UTIs.
116
Atrophic vaginitis is caused by a deficiency of __________, leading to thinning and irritation of the vaginal epithelium.
Oestrogen
117
What might you observe during a pelvic examination in atrophic vaginitis?
Pale, thin vaginal mucosa.
Loss of rugae.
Vaginal erythema or petechiae.
Vaginal narrowing or shortened vagina.
118
How is atrophic vaginitis diagnosed?
Primarily a clinical diagnosis based on history and examination.
Vaginal pH test: Increased pH (>5).
Microscopy: May show lack of lactobacilli and epithelial thinning.
119
True/False
Q: Atrophic vaginitis can increase the vaginal pH above 5.
True.
120
What are the differential diagnoses for atrophic vaginitis?
Infective vaginitis (e.g., candidiasis, bacterial vaginosis).
Lichen sclerosis.
Vulvovaginal atrophy.
Genitourinary syndrome of menopause (broader term encompassing atrophic vaginitis).
121
What is the first-line treatment for atrophic vaginitis?
Topical estrogen therapy, such as estradiol cream or vaginal rings.
122
What are non-hormonal options for managing atrophic vaginitis?
Vaginal moisturizers: Provide long-term hydration.
Vaginal lubricants: For symptom relief during intercourse.
Avoiding irritants (e.g., soaps, douches).
123
A 55-year-old postmenopausal woman presents with vaginal dryness and dyspareunia. On examination, you find pale, thin mucosa with a pH of 5.5. What is the most likely diagnosis and initial treatment?
Diagnosis: Atrophic vaginitis
Treatment: Topical estrogen therapy
124
What are the complications of untreated atrophic vaginitis?
Sexual dysfunction.
Recurrent UTIs.
Vaginal stenosis.
Impact on quality of life.
125
Match the term to its description:
Increased vaginal pH
Dyspareunia
Vaginal stenosis
Estradiol cream
1: Loss of lactobacilli and increased pH due to estrogen deficiency.
2: Painful intercourse caused by vaginal dryness.
3: Narrowing of the vaginal canal due to scarring or atrophy.
4: Topical hormonal treatment for atrophic vaginitis.
126
Vaginal moisturizers provide long-term __________, while lubricants are primarily for __________.
Hydration; intercourse
127
What should be monitored during treatment of atrophic vaginitis?
Symptom resolution (dryness, dyspareunia).
Adherence to therapy.
Side effects of topical estrogen (if used).
128
What is the prognosis for patients with atrophic vaginitis?
Excellent with treatment: Symptoms improve significantly with topical estrogen or other therapies.
Without treatment: Chronic symptoms and complications may develop.
129
True/False
Q: Systemic hormone replacement therapy (HRT) is the first-line treatment for atrophic vaginitis.
False (Topical estrogen is first-line).
130
Why are postmenopausal women more prone to recurrent urinary tract infections (UTIs) in the context of atrophic vaginitis?
Thinning of the vaginal epithelium and loss of lactobacilli increase vaginal pH, altering the local microbiome and promoting pathogen growth.
131
What is vulval cancer?
Vulval cancer is a malignancy of the vulva, most commonly a squamous cell carcinoma, but other types include melanoma, adenocarcinoma, basal cell carcinoma, and sarcoma.
132
What are the key epidemiological features of vulval cancer?
Accounts for 4% of gynecological cancers.
Primarily affects postmenopausal women, with peak incidence in the 7th and 8th decades of life.
133
What are the main risk factors for vulval cancer?
Human papillomavirus (HPV) infection (especially types 16 and 18).
Lichen sclerosus.
Smoking.
Immunosuppression (e.g., HIV).
Chronic vulval irritation or inflammation.
History of cervical intraepithelial neoplasia (CIN) or vulval intraepithelial neoplasia (VIN).
134
What are the common presenting symptoms of vulval cancer?
Pruritus (itching) or irritation.
Persistent vulval ulcer or lump.
Pain or tenderness.
Bleeding or discharge (less common).
Enlarged inguinal lymph nodes.
135
The most common histological type of vulval cancer is __________ __________ carcinoma.
Squamous cell
136
What might you observe on examination in vulval cancer?
Ulcer or mass: Typically in the labia majora.
Lesion may appear red, white, or pigmented.
Enlarged or hard inguinal lymph nodes.
Signs of lichen sclerosus (e.g., thin, white patches of skin).
137
What investigations are used to diagnose vulval cancer?
Biopsy: Confirms malignancy.
Imaging: CT, MRI, or PET scans to assess for spread.
Staging investigations: Chest X-ray, liver function tests, etc.
138
What system is used to stage vulval cancer?
The FIGO staging system, which considers tumor size, lymph node involvement, and distant metastases.
139
What are the main treatment options for vulval cancer?
Surgical excision: Wide local excision or vulvectomy.
Lymphadenectomy: If lymph nodes are involved.
Radiotherapy: Often combined with surgery for advanced cases.
Chemotherapy: For metastatic or inoperable disease.
140
The FIGO staging system for vulval cancer evaluates tumor size, __________ involvement, and distant __________.
Lymph node; metastases
141
What factors influence the prognosis of vulval cancer?
Stage of cancer at diagnosis.
Presence of lymph node metastases.
Histological type and grade of the tumor.
142
What are some differential diagnoses for vulval cancer?
Lichen sclerosus.
Vulval intraepithelial neoplasia (VIN).
Bartholin's gland cyst or abscess.
Infective lesions (e.g., syphilis).
Benign vulval lesions (e.g., fibroma).
143
True/False
Q: HPV infection is a major risk factor for vulval cancer.
True.
144
A 72-year-old woman presents with a persistent vulval lump and pruritus. Examination reveals a firm, ulcerated lesion on the labia majora with enlarged inguinal lymph nodes. What is the most likely diagnosis and next step?
Diagnosis: Vulval cancer
Next step: Biopsy to confirm malignancy.
145
Match the risk factor to its associated condition:
HPV infection
Lichen sclerosus
Smoking
1: Vulval intraepithelial neoplasia (VIN) and vulval cancer.
2: Chronic irritation and vulval cancer.
3: Increased risk of squamous cell carcinoma.
146
How can vulval cancer be prevented?
HPV vaccination: Prevents infection with high-risk HPV types.
Smoking cessation.
Regular gynecological check-ups, especially for high-risk individuals.
Early treatment of precancerous lesions like VIN.
147
What are the complications of vulval cancer or its treatment?
Lymphedema: Following lymphadenectomy.
Sexual dysfunction.
Recurrence of cancer.
Psychosocial impacts (e.g., body image issues).
148
What is the 5-year survival rate for vulval cancer based on stage?
Early-stage disease: >80%.
Advanced disease: Significantly lower.
149
Why are postmenopausal women at increased risk for vulval cancer?
Age-related immune changes.
Higher prevalence of chronic conditions like lichen sclerosus.
150
What is vaginal cancer?
Vaginal cancer is a rare gynecological malignancy originating in the vaginal epithelium, most commonly as a squamous cell carcinoma.
151
What are the key epidemiological features of vaginal cancer?
Accounts for 1–2% of gynecological cancers.
More common in postmenopausal women, with peak incidence between 60–70 years.
152
What are the main types of vaginal cancer?
Squamous cell carcinoma (SCC): Most common type, linked to HPV infection.
Adenocarcinoma: Associated with diethylstilbestrol (DES) exposure in utero.
Melanoma.
Sarcoma.
153
What are the risk factors for vaginal cancer?
Human papillomavirus (HPV) infection, particularly types 16 and 18.
History of cervical cancer or vaginal intraepithelial neoplasia (VAIN).
Smoking.
Diethylstilbestrol (DES) exposure in utero (linked to clear cell adenocarcinoma).
Immunosuppression (e.g., HIV).
Previous pelvic radiation.
154
The most common histological type of vaginal cancer is __________ __________ carcinoma.
Squamous cell.
155
What are the common presenting symptoms of vaginal cancer?
Abnormal vaginal bleeding, including postmenopausal or postcoital bleeding.
Vaginal discharge.
Pelvic pain.
Dysuria or urinary frequency.
Vaginal mass or ulcer (may be identified on examination).
156
True/False
Q: Vaginal cancer is most commonly diagnosed in women under the age of 40
FALSE.
157
What might be observed on vaginal examination in vaginal cancer?
Visible mass or ulcer.
Irregular or raised lesion.
Possible bleeding upon contact.
158
What are the key investigations for vaginal cancer?
Biopsy: Confirms diagnosis and histological type.
Imaging: MRI, CT, or PET scans to assess local and distant spread.
Staging investigations: Chest X-ray, liver function tests, etc.
159
What staging system is used for vaginal cancer?
The FIGO staging system, which evaluates tumor size, local invasion, lymph node involvement, and distant metastases.
160
What are the main treatment options for vaginal cancer?
Radiotherapy: Often the mainstay for primary treatment.
Surgery: Reserved for localized lesions or recurrent disease.
Chemotherapy: Used in combination with radiotherapy for advanced cases.
161
Vaginal adenocarcinoma is strongly associated with in utero exposure to __________.
Diethylstilbestrol (DES)
162
What factors influence the prognosis of vaginal cancer?
Stage at diagnosis.
Tumor size and extent of local invasion.
Histological type and grade
163
What are the differential diagnoses for vaginal cancer?
Vaginal intraepithelial neoplasia (VAIN).
Vaginal infections or ulcers.
Cervical cancer with extension to the vagina.
Benign vaginal lesions (e.g., cysts).
164
A 68-year-old woman presents with postmenopausal bleeding and a visible vaginal mass on examination. What is the most likely diagnosis and next step?
Diagnosis: Vaginal cancer
Next step: Biopsy to confirm malignancy.
165
Match the histological type to its key association:
Squamous cell carcinoma
Adenocarcinoma
Melanoma
1: HPV infection.
2: DES exposure.
3: Pigmented lesion.
166
How can vaginal cancer be prevented?
HPV vaccination.
Regular screening and treatment for VAIN or cervical precancerous lesions.
Avoidance of DES use in pregnancy (historical context).
Smoking cessation.
167
Why is HPV vaccination relevant to the prevention of vaginal cancer?
It prevents infection with high-risk HPV types, which are strongly associated with vaginal and other gynecological cancers.
168
What is the 5-year survival rate for vaginal cancer based on stage?
Stage I: 75–80%.
Stage IV: <20%
169
How many new cases of cervical cancer are diagnosed annually in the UK?
3000 new cases.
170
What percentage of cervical cancers are detected through screening?
0.75
171
What is the median age of diagnosis of Cervical Cancer?
50
172
What is the most common histological type of cervical cancer?
Squamous cell carcinoma of the ectocervix. (part of the cervix
projecting into the vagina).
173
Another histological type of cervical cancer?
adenocarcinoma of the endocervix (part of the cervix lining the cervical canal)
174
What causes most cases of cervical cancer?
Infection with high-risk HPV strains (HPV-16 and HPV-18).
175
HPV infection spontaneously resolves within 2 years in ____of women - at this point, risk returns to baseline
0.9
176
What is cervical intraepithelial neoplasia (CIN)?
HPV causes dysregulated cell cycle regulation, leading to formation of a pre-malignant monoclonal cell population referred to as cervical intraepithelial neoplasia (CIN), which subsequently mutates further to become an invasive carcinoma.
177
Cervical Intraepithelial Neoplasia (CIN) : CIN1
- low grade, confined to lower third of epithelium.
178
Cervical Intraepithelial Neoplasia (CIN) : CIN2
- moderate grade, confined to lower two thirds of epithelium
179
Cervical Intraepithelial Neoplasia (CIN) : CIN3
- high grade, severely atypical cellular changes in more than two thirds of epithelium
180
List three risk factors for cervical cancer.
● High-risk HPV (hrHPV) infection ● Cigarette smoking ● Immunosuppression
181
Symptoms of cervical cancer
: intermenstrual bleeding, postcoital bleeding, abnormal vaginal discharge.
182
Signs of cervical cancer
mass, ulcerated lesion, bleeding on speculum exam
183
First Line investigation of cervical cancer
colposcopy with biopsy - suspicious features seen on colposcopy are abnormal vascularity, white change with acetic acid and exophytic lesions.
184
Additional testing for cervical cancer
HPV testing
185
Stage 1 Cervical Cancer
- confined to cervix
186
Stage 2 Cervical Cancer
extending beyond uterus
187
Stage 3 Cervical Cancer
extending into lower third of the vagina or pelvic wall
188
Stage 4 Cervical Cancer
spread beyond true pelvis or bladder / rectum involvement
189
What is the management for stage 1A1 (<3mm) cervical cancer?
Cone biopsy if fertility preservation is desired or radical hysterectomy.
190
What are advanced-stage cervical cancer treatment options?
Radical hysterectomy with lymph node removal, plus adjuvant therapy (chemotherapy / radiotherapy) ■ Radical trachelectomy (removal of cervix) with lymph node removal, plus adjuvant therapy. ■ Neoadjuvant chemotherapy, immunotherapy e.g. bevacizumab.
191
What is the age range for cervical cancer screening in the UK?
25–64 years.
192
How often are cervical screening tests conducted for women aged 25-49?
every 3 years
193
How often are cervical screening tests conducted for women aged 50-64?
every 5 years
194
The first test is for ______; if this is positive, further testing is indicated.
hrHPV
195
If tested with Negative for hrHPV, what is next?
Return to normal recall (age-based) without further testing at the time.
196
1st positive hrHPV
- Use liquid-based cytology (LBC) to detect cellular atypia. - If cytology is positive, colposcopy is indicated. - If cytology is inadequate, cytology is repeated in 3 months. - If repeat cytology is inadequate, refer for colposcopy. - If colposcopy is normal, test hrHPV in 12 months. - If cytology is negative, perform the 2nd hrHPV test in 12 months.
197
2nd hrHPV
- If negative, return to normal recall - If positive, offer a 3rd hrHPV test in a further 12 months (i.e. 24 months after the first positive test).
198
3rd hrHPV
If negative, return to normal recall - If positive, refer to colposcopy
199
What is dysfunctional uterine bleeding (DUB)?
DUB is abnormal uterine bleeding without an identifiable structural or organic cause, often related to hormonal imbalances.
200
What is the modern term for DUB?
Abnormal Uterine Bleeding (AUB) is now preferred, categorized under the PALM-COEIN system.
201
The PALM-COEIN system categorizes causes of abnormal uterine bleeding as either __________ or __________.
Structural; non-structural
202
What does PALM-COEIN stand for?
PALM (structural causes):
Polyp
Adenomyosis
Leiomyoma
Malignancy and hyperplasia
COEIN (non-structural causes):
Coagulopathy
Ovulatory dysfunction
Endometrial
Iatrogenic
Not yet classified
203
What are common risk factors for DUB?
Adolescence: Immaturity of the hypothalamic-pituitary-ovarian axis.
Perimenopause: Irregular ovulation.
Obesity: Excess estrogen.
Polycystic Ovary Syndrome (PCOS).
Stress or chronic illness.
204
What are the key clinical features of DUB?
Heavy menstrual bleeding (menorrhagia).
Irregular cycles (metrorrhagia).
Prolonged bleeding.
Absence of structural causes on imaging or examination.
205
True/False
Q: DUB is more common in postmenopausal women.
FALSE...
206
What is the underlying pathophysiology of DUB?
Anovulatory cycles: Result in unopposed estrogen stimulation of the endometrium without progesterone.
Leads to endometrial instability and irregular shedding.
207
What investigations are essential for evaluating DUB?
Blood tests: FBC, TFTs, coagulation profile.
Pelvic ultrasound: To exclude structural causes.
Endometrial biopsy: If >45 years or risk factors for endometrial hyperplasia/cancer.
208
Match the investigation with its purpose:
FBC
Pelvic ultrasound
Endometrial biopsy
1: Check for anemia.
2: Rule out polyps, fibroids, or malignancy.
3: Assess for endometrial hyperplasia or cancer.
209
What is the general management approach for DUB?
Exclude structural and organic causes.
Manage underlying hormonal imbalances.
Symptom control with medical or surgical options.
210
What are the medical options for managing DUB?
Tranexamic acid: Reduces bleeding.
Non-steroidal anti-inflammatory drugs (NSAIDs): Reduce prostaglandins, decreasing bleeding.
Combined oral contraceptive pill (COCP): Regulates cycles and reduces bleeding.
Progestogens: Medroxyprogesterone or norethisterone for endometrial stability.
Levonorgestrel intrauterine system (LNG-IUS): Effective for reducing bleeding long-term.
211
What surgical options are available for DUB if medical treatment fails?
Endometrial ablation: Destroys the endometrial lining.
Hysterectomy: Definitive treatment.
212
__________ acid and __________ are commonly used non-hormonal options for managing DUB.
Tranexamic; NSAIDs
213
What factors influence the prognosis of DUB?
Age and hormonal status.
Response to treatment.
Presence of underlying conditions like PCOS or obesity.
214
A 35-year-old woman presents with heavy, irregular periods for the past 6 months. Pelvic ultrasound and biopsy are normal. What is the most likely diagnosis, and initial management?
Diagnosis: Dysfunctional uterine bleeding (DUB)
Management: Tranexamic acid or COCP
215
True/False
Q: The LNG-IUS is a first-line treatment for DUB in women who do not desire pregnancy.
true.
216
Why is a biopsy indicated in women >45 years with DUB?
To exclude endometrial hyperplasia or malignancy as a cause of abnormal bleeding.
217
What is the most common gynaecological cancer?
Endometrial cancer.
218
How many new cases of endometrial cancer are diagnosed annually in the UK?
8000 new cases.
219
What is the median age of diagnosis for endometrial cancer?
63 years.
220
What are the 2 types of histological findings in endometrial cancer?
Multiple cell types ● Endometrial hyperplasia
221
What is the most common histological type of endometrial cancer?
Endometrioid adenocarcinoma (glandular secretory epithelium).
222
What is endometrial hyperplasia?
A condition with a raised gland ratio compared to normal endometrium on histology.
223
Describe the pathophysiology of endometrial cancer.
Hormonal stimulation leads to uninterrupted endometrial proliferation, causing endometrial hyperplasia. ● The hyperplastic endometrial tissue then evolves and mutates from simple to complex forms, to premalignant endometrial intraepithelial neoplasia and eventually invasive adenocarcinoma.
224
Where do endometrial cancers metastasise to?
pelvic and para-aortic lymph nodes
225
What are the key risk factors for endometrial cancer?
● Obesity ● Age > 50 ● Endometrial hyperplasia ● Unopposed endogenous oestrogen: ○ Early menarche, late menopause, nulliparity, anovulation leading to amenorrhea. ● Unopposed exogenous oestrogen: ○ HRT, hormonal contraception.
226
What is the classic symptom of endometrial cancer?
Post-menopausal bleeding. ( - this is considered endometrial cancer
until proven otherwise)
227
What is the 1st line investigation for suspected endometrial cancer?
transvaginal ultrasound ○ Endometrial thickness >5 mm is abnormal
228
What is the 2nd line investigation for suspected endometrial cancer?
hysteroscopy with endometrial biopsy
229
How is endometrial hyperplasia without atypia managed?
reversal of risk factors e.g. weight loss, stopping HRT +/- progesterone therapy e.g. LNG-IUS.
230
How is endometrial hyperplasia with atypia managed?
total hysterectomy with bilateral salpingo-oophorectomy (BSO)
231
What is the first-line treatment for endometrial cancer?
Hysterectomy with bilateral salpingo-oophorectomy (BSO).
232
Other forms of management for endometrial cancer?
○ +/- vaginal brachytherapy ○ +/- radiotherapy ○ +/- chemotherapy
233
What are endometrial polyps?
Endometrial polyps are localized overgrowths of endometrial tissue within the uterine cavity, often attached by a stalk (pedunculated) or a broad base (sessile).
234
What is the prevalence of endometrial polyps?
Common in pre- and postmenopausal women.
Most prevalent in women aged 40–50 years.
235
What are the risk factors for developing endometrial polyps?
Obesity.
Tamoxifen use.
Hormonal imbalances (e.g., excess estrogen).
Polycystic Ovary Syndrome (PCOS).
Hypertension.
Advancing age.
236
Endometrial polyps are most commonly found in women aged __________.
40–50 years
237
What is the pathophysiology of endometrial polyps?
Proliferation of endometrial stromal and glandular tissue, often driven by unopposed estrogen stimulation, leads to localized overgrowths in the uterine cavity.
238
What are the common symptoms of endometrial polyps?
Intermenstrual bleeding (most common).
Heavy menstrual bleeding (menorrhagia).
Postmenopausal bleeding.
Infertility in some cases.
Asymptomatic (incidental finding).
239
True/False
Q: All endometrial polyps are symptomatic.
false.
240
What investigations are used to diagnose endometrial polyps?
Transvaginal ultrasound (TVUS): First-line imaging to visualize polyps.
Saline infusion sonohysterography (SIS): Enhances visualization of polyps.
Hysteroscopy: Gold standard for diagnosis and removal.
241
What is the general approach to managing endometrial polyps?
Observation: For asymptomatic and small polyps in low-risk patients.
Polypectomy: Removal via hysteroscopy for symptomatic polyps or suspected malignancy.
242
What are the indications for removing endometrial polyps?
Symptomatic polyps (e.g., abnormal bleeding).
Postmenopausal women with polyps.
Suspicion of malignancy (e.g., irregular appearance).
Associated with infertility.
243
The gold standard for diagnosing and treating endometrial polyps is __________.
Hysteroscopy
244
What are the differential diagnoses for endometrial polyps?
Endometrial hyperplasia.
Submucosal fibroids.
Endometrial cancer.
Retained products of conception.
245
What factors increase the risk of malignancy in endometrial polyps?
Postmenopausal status.
Polyps >1.5 cm.
Presence of atypical cells.
Tamoxifen use.
246
True/False
Q: Endometrial polyps are always benign.
False.
247
What is the prognosis for endometrial polyps after treatment?
Excellent with polypectomy.
Recurrence is possible, especially with underlying hormonal imbalances.
248
A 52-year-old woman presents with postmenopausal bleeding. TVUS shows a 2 cm endometrial polyp. What is the next step in management?
Perform a hysteroscopy with polypectomy to remove and evaluate the polyp for malignancy.
249
Match the diagnostic tool to its purpose:
Transvaginal ultrasound
Hysteroscopy
Saline infusion sonohysterography
1: Initial imaging to detect polyps.
2: Gold standard for diagnosis and removal.
3: Enhances visualization by distending the uterine cavity.
250
What hormonal imbalance primarily contributes to the formation of endometrial polyps?
Excess estrogen stimulation.
251
Why are postmenopausal women with endometrial polyps at higher risk for malignancy?
Due to the decreased progesterone levels and the potential for unopposed estrogen stimulation of the endometrium.
252
What is the definition of endometriosis?
The presence of endometrial glands and stroma outside the uterine cavity.
253
What is the prevalence of endometriosis in reproductive-age women?
0.1
254
What is the most widely accepted theory for the pathophysiology of endometriosis?
Retrograde menstruation, where endometrial tissue passes into the pelvis via the fallopian tubes during menstruation and undergoes painful inflammation. Fragments of endometrial tissue pass from the uterine cavity into the pelvis via
the open-ended fallopian tubes during menstruation.
○ This ectopic tissue is responsive to the normal hormonal fluctuations of the
menstrual cycle, so undergoes painful inflammation at the end of the cycle
255
What is neuroangiogenesis, and how does it relate to endometriosis?
Neuroangiogenesis is the development of new blood vessels and nociceptive peripheral nerves, contributing to endometriosis pain.
256
What systemic alterations are seen in women with endometriosis?
Altered gene expression related to the inflammatory response in eutopic endometrial tissue.Increased pro-inflammatory and pro-neurogenetic factors.
257
What are potential infertility mechanisms associated with endometriosis?
altered hormonal levels / response, peritoneal inflammation and adhesion formation.
258
What are the symptoms of endometriosis?
Dysmenorrhea, chronic pelvic pain, dyspareunia, dyschezia, and subfertility.
259
What are the signs of endometriosis on examination?
Fixed retroverted uterus. Palpable mass (endometrioma).
260
What investigations are used to diagnose endometriosis?
1. Clinical Examination - can identify endometriomas (cystic lesions) / deep nodules. 2. Transvaginal ultrasound - endometrioma, deep pelvic endometriosis 3. Gold Standard: Diagnostic laparoscopy - biopsy-confirmed glands / stroma outside of endometrial cavity
261
What is the first-line medical management for endometriosis?
Oral NSAIDs (e.g., ibuprofen, naproxen).
262
What is the alternative first-line medical management for endometriosis?
combined contraception (e.g. COCP) or progesterone contraception (LNG-IUS, implant, medroxyprogesterone).
263
What is a second-line treatment for endometriosis, and why is its duration limited?
GnRH agonist (e.g. leuprorelin) or GnRH antagonist (e.g. elagolix). ○ N.B. limited duration of treatment due to bone mineral density issues.
264
What surgical options are available for endometriosis management?
Laparoscopy with ablation or excision. (alternative second line
265
Define uterine fibroids.
Benign uterine tumors composed of smooth muscle and connective tissue, also known as leiomyomata.
266
What is the proposed origin of uterine fibroids?
(Probably) derived from myometrial stem cells; considered to be oestrogen-dependent tumours, they express higher than normal numbers of certain oestrogen and progesterone receptors.
267
First Line Management fibroids managed as per HMB guidelines?
They express higher than normal numbers of certain oestrogen and progesterone receptors.
268
What are the proposed mechanisms by which fibroids contribute to HMB?
- proposed mechanisms include distortion of uterine lining and abnormal humoral factors due to altered histology of the overlying endometrium.
269
What are the four types of uterine fibroids based on their location?
○ Intramural - contained within the myometrium. ○ Submucosal - projecting inwardly. ○ Subserosal - projecting outwardly. ○ Pedunculated - attached on a stem.
270
List the risk factors for uterine fibroids
High BMI, age in 40s, black ethnicity, low serum vitamin D levels
271
How does high BMI contribute to the development of fibroids?
Increased adiposity leads to increased peripheral aromatase levels - therefore increasing circulating oestrogen due to conversion of adrenal DHEA into oestradiol. - The increased oestrogen has an inhibitory effect on the HPG axis, leading to anovulation, decreased progesterone levels and thus reduced progestogenic endometrial protection (menses). - Fibroids are oestrogen dependent; high oestrogen and low progesterone stimulates their growth.
272
What are the typical symptoms and signs of uterine fibroids?
Symptoms: Menorrhagia, pelvic pain/pressure, bloating, dysmenorrhea. Signs: Palpable mass or enlarged uterus on bimanual examination.
273
What is the first-line investigation for suspected uterine fibroids?
Transabdominal and transvaginal ultrasound scan.
274
First Line Management fibroids managed as per HMB guidelines?
: offer treatment as per HMB (LNG-IUS, tranexamic acid, alternative hormonal contraception)
275
Second Line Management of fibroids
GnRH agonist e.g. leuprorelin or antiprogesterone e.g. mifepristone
276
What surgical options are available for managing uterine fibroids?
○ Myomectomy (surgical removal of fibroids) - fertility-preserving ○ Uterine artery embolisation. ○ Hysterectomy
277
What is uterine artery embolisation, and how is it performed?
(deliberate infarction of fibroid tissue whilst preserving surrounding uterus; performed by interventional radiologist, via percutaneous femoral access)
278
What is a hydatidiform mole?
A gestational trophoblastic disease (GTD) characterized by abnormal proliferation of trophoblastic tissue with cystic swelling of chorionic villi.
279
What are the two types of hydatidiform moles?
Complete Mole: No fetal tissue; fertilization of an empty ovum.
Partial Mole: Abnormal fetus or fetal tissue; triploid karyotype (69 chromosomes).
280
A complete mole results from the fertilization of an ovum that contains __________ genetic material.
no
281
What are the risk factors for developing a hydatidiform mole?
Maternal age <20 or >35.
Previous molar pregnancy.
Asian ethnicity.
282
What is the pathophysiology of a complete hydatidiform mole?
Fertilization of an empty ovum by a single sperm that duplicates (46XX) or two sperms (46XY), leading to proliferation of trophoblastic tissue without fetal development.
283
What are the clinical features of a hydatidiform mole?
Vaginal bleeding (common presentation).
Excessively high β-hCG levels.
Uterus larger than gestational age.
Symptoms of hyperemesis gravidarum.
Absence of fetal heart sounds.
Passage of grape-like vesicles.
284
True/False
Q: Hyperemesis gravidarum is more common in molar pregnancies due to very high β-hCG levels.
True.
285
What investigations are used to diagnose a hydatidiform mole?
Transvaginal ultrasound: "Snowstorm appearance" (complete mole) or mixed cystic/solid areas (partial mole).
Serum β-hCG: Markedly elevated levels.
Histopathological examination of products of conception.
286
What are the ultrasound findings in a complete molar pregnancy?
Snowstorm appearance (diffuse echogenic pattern).
Absence of fetal tissue.
Cystic spaces within the uterus.
287
What is the first-line management for a hydatidiform mole?
Suction curettage to evacuate the uterus.
288
How is follow-up conducted after evacuation of a hydatidiform mole?
Regular β-hCG monitoring: Weekly until undetectable, then monthly for 6 months.
Avoid pregnancy during follow-up.
289
What are the complications of a hydatidiform mole?
Persistent gestational trophoblastic disease (GTN).
Choriocarcinoma (rare).
Uterine perforation during evacuation.
290
Match the following features to the type of mole:
Complete mole
Partial mole
1: No fetal tissue, diploid (46XX or 46XY).
2: Fetal tissue present, triploid (69XXX or 69XXY).
291
What is the prognosis for most hydatidiform moles?
Excellent with appropriate treatment and follow-up; most cases resolve without progression to malignancy.
292
Persistent gestational trophoblastic disease is suspected if β-hCG levels remain __________ after evacuation.
Elevated
293
True/False
Q: A partial mole is more likely to progress to choriocarcinoma than a complete mole.
False.
294
What is the risk of recurrence for molar pregnancies?
1–2% after one molar pregnancy.
Higher after multiple molar pregnancies.
295
A 24-year-old presents with vaginal bleeding, a uterus larger than dates, and β-hCG >100,000 IU/L. Ultrasound shows a "snowstorm appearance." What is the likely diagnosis?
Complete hydatidiform mole.
296
Why should pregnancy be avoided during follow-up of a molar pregnancy?
To ensure accurate monitoring of β-hCG levels and detect persistent GTN.
297
What is a prolactinoma?
A benign tumor of the pituitary gland that secretes excess prolactin, leading to hyperprolactinemia.
298
What is the most common type of pituitary adenoma?
Prolactinoma.
299
Prolactinomas are more common in __________ and are typically diagnosed earlier in this group.
Women
300
What is the pathophysiology of a prolactinoma?
Excessive prolactin secretion inhibits the hypothalamic-pituitary-gonadal axis, leading to reduced gonadotropin-releasing hormone (GnRH) and decreased FSH and LH, causing hypogonadism.
301
What are the clinical features of prolactinoma in women?
Amenorrhea or oligomenorrhea.
Galactorrhea (milk production unrelated to pregnancy).
Infertility.
Symptoms of hypoestrogenism (e.g., vaginal dryness, decreased bone density).
302
What are the clinical features of prolactinoma in men?
Reduced libido.
Erectile dysfunction.
Gynecomastia (rarely with galactorrhea).
Symptoms of hypogonadism (e.g., decreased muscle mass, infertility).
303
What additional symptoms might occur with macroprolactinomas?
Headaches.
Visual field defects (e.g., bitemporal hemianopia due to optic chiasm compression).
304
True/False
Q: Prolactinomas only occur in women of reproductive age.
False.
305
What investigations are used to diagnose prolactinoma?
Serum prolactin levels: Elevated (often >200 ng/mL in macroprolactinomas).
Pituitary MRI: Identifies size and location of the tumor.
Thyroid function tests: To rule out hypothyroidism.
Pregnancy test: To rule out physiological causes of hyperprolactinemia.
306
What are the differential diagnoses for hyperprolactinemia?
Pregnancy.
Primary hypothyroidism.
Drug-induced (e.g., antipsychotics, antidepressants).
Chest wall trauma or surgery.
Chronic kidney disease.
307
What is the first-line treatment for prolactinoma?
Dopamine agonists (e.g., cabergoline or bromocriptine), which suppress prolactin secretion and shrink the tumor.
308
When is surgery indicated for prolactinoma?
Intolerance or resistance to dopamine agonists.
Tumor compression causing vision loss.
Large tumors with apoplexy (bleeding into the tumor).
309
What is the prognosis for prolactinomas?
Excellent with dopamine agonist therapy; most tumors shrink significantly and prolactin levels normalize.
310
The preferred imaging modality for diagnosing a prolactinoma is _________
Pituitary MRI
311
A 35-year-old woman presents with galactorrhea, amenorrhea, and visual field defects. Serum prolactin is 250 ng/mL. What is the most likely diagnosis and initial treatment?
Diagnosis: Prolactinoma
Treatment: Start dopamine agonist therapy (e.g., cabergoline).
312
What are the side effects of dopamine agonists used to treat prolactinomas?
Nausea.
Orthostatic hypotension.
Fatigue.
Psychiatric symptoms (e.g., anxiety or hallucinations).
313
Why is prolactin secretion physiologically elevated during pregnancy?
Prolactin levels rise to prepare the mammary glands for lactation.
314
True/False
Q: Surgery is the first-line treatment for prolactinomas.
False.
315
How are macroprolactinomas classified by size?
Tumors >10 mm in diameter are considered macroprolactinomas.
316
How many new cases of ovarian cancer are diagnosed annually in the UK?
7000 new cases.
317
What is the median age of diagnosis for ovarian cancer?
63 years.
318
What is the most common histological subtype of ovarian cancer?
Serous epithelial carcinoma. - derived from epithelium overlying
the ovarian capsule and distal fallopian tube.
319
What percentage of ovarian cancers are epithelial in origin?
0.9
320
Other subtypes originating from the cortex of the ovary include :
○ Sex cord stromal ○ Germ cell (more prominent in pre-menopausal women).
321
The underlying cause of ovarian cancer is unclear, although there is an established relationship with __________________.
BRCA1 and BRCA2 mutations.
322
How does ovarian epithelial cancer commonly metastasise?
Via transcoelomic (Across a body cavity) so spread to the liver, bowel, and associated mesentery.
323
Name three risk factors for ovarian cancer.
● BRCA1 / BRCA2 mutation ● Increasing age ● Family history
324
Why is ovarian cancer often detected at an advanced stage?
Symptoms are vague and non-specific (e.g., bloating, early satiety, altered bowel habit).
325
Symptoms present in ovarian cancer patients
vague gastrointestinal symptoms (bloating, early satiety, nausea, altered bowel habit), urinary frequency
326
Signs present in ovarian cancer patients
palpable abdominal mass, ascites
327
What is the first-line investigation for suspected ovarian cancer?
Abdominal and pelvic examination.
328
What is the 2nd line investigation for suspected ovarian cancer?
CA-125 (tumour marker) level
329
What is considered a highly suspicious CA-125 level?
> 35 IU/ml.
330
What is the 3rd line investigation for suspected ovarian cancer?
transvaginal ultrasound
331
First Line Managment for Ovarian Cancer
surgical staging with radical hysterectomy, BSO, appendectomy, omentectomy, lymph node dissection, pelvic washout. ○ Fertility-sparing surgery can be used in some specific cases.
332
Additional Managment for Ovarian Cancer
adjuvant chemo , bevacizumab (anti-VEGF monoclonal antibody)
333
What is an ovarian cyst?
A fluid-filled sac within or on the surface of the ovary.
334
How are ovarian cysts classified?
Functional cysts (e.g., follicular, corpus luteum).
Pathological cysts (e.g., dermoid cysts, endometriomas, cystadenomas).
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Functional ovarian cysts are related to __________ function and are common in reproductive-age women.
Hormonal
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What are the types of functional ovarian cysts?
Follicular cyst: Results from a follicle failing to release an egg.
Corpus luteum cyst: Forms when the corpus luteum does not regress after ovulation.
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What are examples of pathological ovarian cysts?
Dermoid cyst (mature cystic teratoma).
Endometrioma ("chocolate cyst").
Cystadenomas (serous or mucinous).
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What are the common clinical features of an ovarian cyst?
Asymptomatic (often incidental finding).
Pelvic pain (unilateral or acute in rupture/torsion).
Bloating or abdominal distension.
Menstrual irregularities.
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True/False
Q: Most ovarian cysts in premenopausal women are benign.
True.
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What are the potential complications of ovarian cysts?
Torsion: Twisting of the ovarian cyst, causing acute pain.
Rupture: Sudden release of fluid, leading to peritonitis-like symptoms.
Haemorrhage: Bleeding into the cyst or abdomen.
Pressure effects on surrounding structures.
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What investigations are used to assess an ovarian cyst?
Pelvic ultrasound: First-line imaging; assesses size, morphology, and features.
CA-125 levels: To assess the risk of ovarian malignancy in postmenopausal women.
MRI: For further characterization of complex cysts.
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On pelvic ultrasound, a simple ovarian cyst appears __________, with a smooth thin wall and no solid components.
Anechoic
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What features of ovarian cysts raise suspicion for malignancy?
Complex or multiloculated cysts.
Solid components or septations.
Increased vascularity.
Elevated CA-125.
Presence in postmenopausal women.
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What is the management of functional ovarian cysts?
Observation: Many resolve spontaneously within 2–3 menstrual cycles.
Symptomatic treatment (e.g., analgesia).
Consider oral contraceptives to suppress ovulation and prevent recurrence.
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What is the management of pathological ovarian cysts?
Surgical removal (e.g., laparoscopy or laparotomy).
Dermoid cysts and endometriomas are typically excised.
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True/False
Q: Dermoid cysts are a type of functional ovarian cyst.
False.
347
What is the Risk of Malignancy Index (RMI) used for?
To stratify the risk of ovarian cancer in women with ovarian cysts, combining:
Menopausal status.
Ultrasound findings.
Serum CA-125 levels.
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A 45-year-old presents with bloating and a unilateral pelvic mass on ultrasound. CA-125 is 300. What is the next step?
Urgent referral to a gynecological oncologist for further evaluation.
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What is an endometrioma, and how is it managed?
A cyst formed by endometriosis, often containing old blood ("chocolate cyst").
Managed surgically if symptomatic or large, with hormonal therapies to suppress recurrence.
350
What symptoms are commonly associated with a corpus luteum cyst?
Delayed menstruation.
Unilateral pain.
Sometimes presents as an acute abdomen if ruptured.
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What are dermoid cysts composed of?
Ectodermal elements such as hair, teeth, and sebaceous material.
352
Why is CA-125 less useful in premenopausal women?
It can be elevated in benign conditions such as endometriosis or pelvic inflammatory disease (PID).
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What is the management of ovarian cysts in postmenopausal women?
Monitor simple cysts <5 cm with ultrasound and CA-125.
Surgical removal for complex or symptomatic cysts, or elevated CA-125.
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What is ovarian torsion?
The twisting of the ovary and often the fallopian tube, leading to a compromised blood supply.
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What happens in ovarian torsion?
Twisting of the ovary and/or fallopian tube.
Obstruction of venous and lymphatic drainage, leading to ovarian edema.
Arterial blood flow may also be impaired, potentially causing ischemia and necrosis.
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What are the risk factors for ovarian torsion?
Ovarian cysts or masses (>5 cm increases risk).
Polycystic ovaries.
Hyperstimulation during fertility treatment.
Pregnancy.
Prior history of ovarian torsion.
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Ovarian torsion is most common in women of __________ age.
Reproductive
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What are the clinical features of ovarian torsion?
Sudden-onset severe pelvic pain (usually unilateral).
Nausea and vomiting.
Pain often radiates to the back or groin.
Adnexal tenderness on examination.
Low-grade fever (in advanced cases)
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True/False
Q: Ovarian torsion commonly presents with gradual pain over several weeks.
False (it is acute).
360
What is the first-line imaging modality for ovarian torsion?
Pelvic ultrasound with Doppler to assess ovarian blood flow.
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What are the possible Doppler findings in ovarian torsion?
Absence or reduction of venous/arterial flow.
Enlarged, edematous ovary.
Peripheral displacement of ovarian follicles ("string of pearls" sign).
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What are the differential diagnoses for ovarian torsion?
Ectopic pregnancy.
Ruptured ovarian cyst.
Pelvic inflammatory disease (PID).
Appendicitis.
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What is the definitive management of ovarian torsion?
Surgical intervention to untwist the ovary and restore blood flow.
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What surgical procedures are used for ovarian torsion?
Laparoscopy: Preferred if the ovary is viable.
Oophorectomy: If the ovary is necrotic and cannot be salvaged
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What factors influence the prognosis of ovarian torsion?
Time to intervention (delays increase the risk of necrosis).
Size and nature of the ovarian mass.
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What are the complications of ovarian torsion?
Ovarian ischemia and necrosis.
Infertility (if the ovary is lost).
Peritonitis (in advanced cases).
367
The "__________" sign on ultrasound refers to peripherally displaced ovarian follicles in torsion.
String of pearls
368
A 25-year-old woman presents with sudden-onset severe right lower quadrant pain and nausea. Ultrasound shows an enlarged, edematous ovary with absent venous flow. What is the most likely diagnosis?
Ovarian torsion.
369
Why is arterial blood flow sometimes preserved in ovarian torsion despite venous flow being absent?
Arterial blood flow is higher pressure, so it may persist longer than venous flow before complete torsion occurs.
370
True/False
Q: Ovarian torsion is more common on the left side.
False (it is more common on the right due to the longer utero-ovarian ligament and less sigmoid colon interference).
371
What is pelvic inflammatory disease (PID)?
An infection of the upper female genital tract, including the uterus, fallopian tubes, and ovaries, often resulting from sexually transmitted infections (STIs).
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What are the most common causative organisms of PID?
Chlamydia trachomatis.
Neisseria gonorrhoeae.
Anaerobes (e.g., Bacteroides).
Mycoplasma genitalium.
373
Pelvic inflammatory disease often results from the ascending spread of pathogens from the __________ tract.
Lower genital
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What are the risk factors for PID?
Multiple sexual partners.
Unprotected sexual intercourse.
History of STIs or PID.
Recent intrauterine device (IUD) insertion.
Age <25 years.
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What are the clinical features of PID?
Lower abdominal pain (bilateral).
Abnormal vaginal discharge (often purulent).
Intermenstrual or postcoital bleeding.
Dyspareunia (pain during intercourse).
Fever.
Cervical motion tenderness ("chandelier sign").
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True/False
Q: Cervical motion tenderness is a hallmark finding in pelvic inflammatory disease.
True.
377
What are the potential complications of PID?
Chronic pelvic pain.
Tubo-ovarian abscess.
Infertility (due to tubal damage).
Ectopic pregnancy.
378
What investigations are used in the diagnosis of PID?
Clinical diagnosis: Based on history and examination.
High vaginal and endocervical swabs for microscopy, culture, and sensitivity (MC&S).
NAAT (nucleic acid amplification tests) for Chlamydia and Gonorrhea.
Blood tests: CRP, ESR, and white cell count.
Pelvic ultrasound or MRI (to assess for abscesses).
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What is required for a clinical diagnosis of PID?
Presence of at least one of the following:
Lower abdominal pain.
Cervical motion tenderness.
Uterine or adnexal tenderness.
380
The gold standard for diagnosing PID is __________, though it is rarely used.
Laparoscopy
381
True/False
Q: Sexual partners of patients with PID should be screened and treated for STIs.
True.
382
What is the first-line antibiotic regimen for PID?
Ceftriaxone 1g IM (single dose).
Doxycycline 100mg BD for 14 days.
Metronidazole 400mg BD for 14 days.
383
What antibiotics are used in severe PID or if the patient requires hospitalization?
IV cefoxitin or ceftriaxone.
IV doxycycline.
Switch to oral antibiotics after 24-48 hours of clinical improvement.
384
A 22-year-old woman presents with lower abdominal pain, fever, and abnormal discharge. On examination, there is cervical motion tenderness. What is the most likely diagnosis and initial management?
Diagnosis: Pelvic inflammatory disease (PID).
Management: Empirical antibiotics with ceftriaxone, doxycycline, and metronidazole.
385
How can PID be prevented?
Practice safe sex (condoms).
Regular STI screening.
Prompt treatment of lower genital tract infections.
386
__________ contraception, like IUDs, may slightly increase the risk of PID during the first month after insertion.
Intrauterine
387
What is Fitz-Hugh-Curtis syndrome, and how is it related to PID?
A rare complication of PID involving perihepatitis.
Presents with right upper quadrant pain and tenderness.
388
What is PCOS?
An endocrinopathy characterized by ovarian cysts, oligomenorrhea, and hyperandrogenism.
389
What are the Rotterdam criteria for diagnosing PCOS?
a woman must meet 2 of the 3: 1. Hyperandrogenism 2. Oligo- or anovulation 3. Polycystic morphology on ultrasound
390
True or False: PCOS requires ovarian cysts for diagnosis.
False. PCOS can be diagnosed in the absence of ovarian cysts if other criteria are met.
391
Explain the disrupted hormonal balance in PCOS.
Disrupted balance between androgens, anti-Mullerian hormone and FSH levels leads to arrest in follicular development: a. Increased GnRH release frequency leads to high LH:FSH ratio. b. This results in high androgen:oestradiol ratio. c. Low oestrogen (due to reduced granulosa cell activity) prevents follicle selection and subsequent ovulation. Instead, multiple immature follicles remain and form cysts. d. Additionally, high androgens may inhibit sex steroid negative feedback on the HPG axis, leading to a ‘vicious circle’ of rising androgens
392
How does insulin resistance contribute to PCOS?
Insulin resistance and hyperinsulinaemia: a. Peripheral insulin resistance (skeletal muscle, adipose tissue) leads to hyperglycaemia and subsequent hyperinsulinaemia. b. High insulin levels stimulate theca cell androgen production and reduce sex-hormone binding globulin levels (SHBG); this means increased free circulating androgens.
393
List common symptoms of PCOS.
Hyperandrogenism: hirsutism, acne, hyperhidrosis. ● Oligomenorrhea - due to oligo-ovulation. ● Subfertility / infertility
394
Name risk factors for PCOS.
1. Obesity 2. Family history 3. Premature adrenarche (pubic / axillary hair, apocrine sweat gland development).
395
Which investigations help diagnose PCOS?
1. Total serum testosterone - elevated 2. Sex hormone-binding globulin (SHBG) - normal to low 3. Free androgen index - elevated 4. Rule-out tests: LH and FSH , prolactin, TFTs . 5. Imaging:
396
Which tests rule out PCOS?
LH and FSH (premature ovarian failure), prolactin (hyperprolactinaemia), TFTs (hypothyroidism); used to eliminate other causes of oligomenorrhea
397
What imaging finding leads to dx of PCOS?
12 or more follicles on one ovary
398
What is the first-line treatment for PCOS if fertility is not desired?
COCP for cycle regulation plus weight loss. For prolonged amenorrhea: cyclic progesterone every 3 months to protect the endometrium.
399
What is the second-line treatment for PCOS if fertility is not desired?
(in event of prolonged amenorrhea) a. Cyclical progesterone (taken for 14 days every 3 months) to induce a withdrawal bleed to protect endometrium. b. Also offer transvaginal USS to assess endometrial thicknes
400
What is the first-line treatment for PCOS if fertility is desired?
weight loss plus: a. Clomifene or b. Letrozole (aromatase inhibitor).
401
What are second-line treatments for PCOS-related infertility?
Metformin to improve insulin sensitivity
402
How does the COCP help in PCOS?
regulation of menstrual cycle through stabilisation of oestrogen & progesterone levels. Also increases hepatic SHBG production (lowering free androgen index) and blocks some androgen receptors
403
How does Metformin treat PCOS?
- improves peripheral insulin sensitivity to downregulate effects of insulin resistance described above.
404
What is the mechanism of action of Clomifene?
selective oestrogen receptor modulator; blocks hypothalamic oestrogen receptors, thereby inhibiting HPG axis negative feedback and inducing FSH / LH secretion to lead to ovulation
405
How does Letrozole work in PCOS?
aromatase inhibitor, inhibits peripheral conversion of androgens into oestrogen, reducing HPG axis negative feedback to promote ovulation.
