14A - Polycystic Ovarian Syndrome Flashcards
(134 cards)
1
Q
What are the two main synchronized cycles involved in the menstrual cycle?
A
The ovarian cycle and the endometrial (uterine) cycle.
2
Q
What is the average length of a menstrual cycle?
A
28 days, but it can range from 20 to 35 days.
3
Q
When does ovulation typically occur in a 28-day cycle?
A
Around day 14, or 14 days before the next menstrual period.
4
Q
Which brain structure initiates the menstrual cycle?
A
The hypothalamus, by releasing gonadotropin-releasing hormone (GnRH).
5
Q
What does GnRH stimulate the pituitary to release?
A
Follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
6
Q
How does estrogen feedback on the pituitary?
A
Initially negative feedback (lowers FSH), then positive feedback (LH surge before ovulation).
7
Q
What hormone dominates the luteal phase?
A
Progesterone.
8
Q
What inhibits FSH release during the luteal phase?
A
Inhibin, secreted by luteinized granulosa cells.
9
Q
What are the two phases of the ovarian cycle?
A
Follicular phase and luteal phase.
10
Q
What happens during the follicular phase?
A
Development of ovarian follicles; estrogen levels rise.
11
Q
What triggers ovulation?
A
A surge in LH due to high estrogen levels.
12
Q
What is the dominant follicle?
A
The follicle with the most FSH receptors that survives to ovulate.
13
Q
What structure forms after ovulation?
A
The corpus luteum.
14
Q
What happens to the corpus luteum if no fertilization occurs?
A
It degenerates into the corpus albicans.
15
Q
What are the three phases of the endometrial cycle?
A
Menstrual phase, proliferative phase, and secretory phase.
16
Q
What happens during the menstrual phase?
A
The functional layer of the endometrium is shed.
17
Q
What stimulates the proliferative phase?
A
Rising estrogen levels.
18
Q
What occurs during the secretory phase?
A
Endometrial glands secrete nutrients; spiral arteries become coiled under progesterone’s influence.
19
Q
What is menarche?
A
The onset of the first menstrual period.
20
Q
What is menopause?
A
The cessation of menstrual periods due to declining ovarian function.
21
Q
What hormone change leads to menstruation?
A
A drop in progesterone levels causes shedding of the endometrial lining.
22
Q
When is the optimal window for fertilization?
A
Days 11–15 of the cycle.
23
Q
What changes in cervical mucus occur during ovulation?
A
Becomes thinner and more hospitable to sperm due to estrogen.
24
Q
What effect does high prolactin have on the hypothalamus?
A
Inhibits GnRH release → decreases LH and FSH → decreases estrogen levels.
25
What are the reproductive effects of hyperprolactinemia in females?
Amenorrhea, infertility, and galactorrhea due to low estrogen and high prolactin.
26
What is a classic symptom of hyperprolactinemia in males?
Erectile dysfunction.
27
How is hyperprolactinemia diagnosed?
Blood test showing high prolactin; MRI for prolactinoma; biopsy shows lactotroph hyperplasia.
28
What medications are used to treat hyperprolactinemia?
Dopamine agonists like bromocriptine and cabergoline.
29
What is the proposed cause of PCOS?
Insulin resistance causing increased LH production and androgen excess.
30
What hormonal imbalance characterizes PCOS?
Elevated LH:FSH ratio and high androgens (e.g., testosterone).
31
What are key clinical signs of PCOS?
Hirsutism, acne, male-pattern baldness, oligomenorrhea/amenorrhea, and infertility.
32
What are the ovarian findings in PCOS?
Multiple unruptured follicles ('cysts') on ultrasound.
33
What are the risks associated with unopposed estrogen in PCOS?
Endometrial hyperplasia and increased risk of endometrial cancer.
34
What is first-line treatment for regulating menstrual cycles in PCOS?
Weight loss and oral contraceptives.
35
Which drugs are used to induce ovulation in PCOS patients desiring pregnancy?
Clomiphene.
36
What medications can treat hirsutism in PCOS?
Spironolactone, finasteride, or flutamide.
37
What is primary ovarian insufficiency (POI)?
Premature loss of ovarian function before age 40 → early menopause.
38
What are the hormonal levels in POI?
Low estrogen; high LH and FSH (hypergonadotropic hypogonadism).
39
What are potential causes of POI?
Idiopathic, autoimmune, chemotherapy/radiation, or chromosomal abnormalities (e.g., Turner syndrome, Fragile X).
40
What symptoms suggest POI?
Amenorrhea, infertility, hot flashes, vaginal dryness.
41
What is the treatment for POI?
Hormone replacement therapy; IVF for fertility.
42
Define primary amenorrhea.
No menarche by age 15 with secondary sex traits OR no menarche + no secondary sex traits by 13.
43
Define secondary amenorrhea.
Cessation of menses for ≥3 months (regular cycles) or ≥6 months (irregular cycles).
44
What syndrome causes primary amenorrhea with short stature, webbed neck, and high FSH/LH?
Turner syndrome (45,X).
45
What is Müllerian agenesis?
Congenital absence of uterus, cervix, and upper 2/3 of vagina with normal ovaries and secondary sex characteristics.
46
What is an imperforate hymen and how does it present?
Hymen blocks vaginal opening; presents with hematocolpos and bluish bulging membrane.
47
What is functional hypothalamic amenorrhea?
GnRH disruption due to stress, weight loss, or excessive exercise → low LH, FSH, estrogen.
48
What is the female athlete triad?
Low energy availability, menstrual dysfunction, and decreased bone mineral density.
49
What condition is suggested by a 17-year-old with short stature, webbed neck, and primary amenorrhea?
Turner syndrome.
50
A 25-year-old with a history of strenuous exercise, severe dieting, and amenorrhea likely has?
Functional hypothalamic amenorrhea (due to caloric restriction/stress).
51
What is PCOS?
PCOS (Polycystic Ovary Syndrome) is the most common endocrine disorder in reproductive-aged biological females, characterized by anovulation, hyperandrogenism, and polycystic ovaries.
52
What are the metabolic abnormalities commonly associated with PCOS?
Insulin resistance, dyslipidemia, and increased risk of type 2 diabetes and metabolic syndrome.
53
What menstrual abnormalities are typical in PCOS?
Irregular cycles (<21 days or >35 days), oligomenorrhea, or secondary amenorrhea (absence of menses for ≥3 months).
54
What are the signs of clinical hyperandrogenism in PCOS?
Hirsutism (coarse hair in androgen-sensitive areas), acne, and androgenic alopecia.
55
What physical signs suggest insulin resistance in PCOS?
BMI >25, centripetal fat distribution, acanthosis nigricans, and sometimes hypertension.
56
What is the first step in evaluating a patient suspected of PCOS?
Obtain a focused history, physical exam, and rule out pregnancy with an hCG test.
57
What labs should be obtained if pregnancy is ruled out?
Total testosterone, SHBG, DHEAS, 17-OHP, TSH, prolactin, LH, FSH, estradiol, and day 21 progesterone.
58
What lab findings support a diagnosis of PCOS?
Elevated free/total testosterone or DHEAS, mildly elevated LH (relative to FSH), low progesterone on day 21 (<4 ng/mL).
59
What abnormalities on pelvic ultrasound support PCOS?
≥20 follicles per ovary or ovarian volume ≥10 mL; follicles 2–9 mm; absence of corpus luteum or dominant follicle.
60
What conditions must be excluded before diagnosing PCOS?
Pregnancy, thyroid dysfunction (TSH), hyperprolactinemia (prolactin), nonclassical congenital adrenal hyperplasia (17-OHP), androgen-secreting tumors (markedly high testosterone or DHEAS).
61
What are the Rotterdam criteria for PCOS diagnosis?
Any 2 of the following 3: 1) Ovulatory dysfunction, 2) Clinical/biochemical hyperandrogenism, 3) Polycystic ovarian morphology on ultrasound.
62
What is required in addition to meeting 2 of the 3 Rotterdam criteria?
Exclusion of other causes for symptoms (e.g., thyroid disease, androgenic drugs).
63
Why are PCOS patients at risk for endometrial cancer?
Chronic anovulation leads to unopposed estrogen exposure, increasing endometrial hyperplasia and cancer risk.
64
Is endometrial thickness a reliable screening tool for endometrial cancer in PCOS?
No; endometrial biopsy is the appropriate diagnostic method.
65
How is PCOS managed in patients desiring pregnancy?
Lifestyle modification (diet/exercise), ovulation induction with letrozole (first-line) or clomiphene, with/without metformin.
66
What are PCOS-related pregnancy risks?
Increased risk of gestational diabetes, hypertensive disorders, and multiple gestation from ovulation induction.
67
What are first-line therapies for patients not desiring pregnancy?
Lifestyle modification and combined oral contraceptives (COCs) for menstrual regulation and endometrial protection.
68
How is hirsutism in PCOS managed?
Mechanical removal, COCs, spironolactone (androgen antagonist), and topical eflornithine for facial hair.
69
What medication helps with insulin resistance in PCOS?
Metformin is first-line; myo-inositol can be used as an alternative.
70
When should combined oral contraceptives be avoided in PCOS patients?
In those over 35 who smoke, have hypertension, a personal/family history of thromboembolism, or other thrombotic risk factors.
71
What menstrual pattern defines oligomenorrhea?
Fewer than 9 periods/year or cycle length >35 days.
72
What must be excluded in all cases of secondary amenorrhea?
Pregnancy.
73
What are common features of hyperandrogenism?
Acne, hirsutism, scalp hair thinning.
74
Name three non-PCOS causes of oligomenorrhea.
Hypothalamic amenorrhea, thyroid dysfunction, hyperprolactinemia.
75
First-line treatment for dysmenorrhea?
NSAIDs.
76
What is the most likely diagnosis in a woman with oligomenorrhea, hirsutism, and polycystic ovaries?
PCOS.
77
What hormonal pattern supports PCOS?
High LH:FSH ratio, high free androgen index, low SHBG.
78
How often is cervical screening recommended in Australia?
Every 5 years from age 25–74 if HPV negative.
79
What does acanthosis nigricans indicate?
Insulin resistance.
80
What is the diagnostic criteria for PCOS (Rotterdam)?
Two of: (1) oligo/anovulation, (2) hyperandrogenism, (3) polycystic ovaries on ultrasound.
81
What does a thickened endometrium suggest in PCOS?
Risk of endometrial hyperplasia from unopposed oestrogen.
82
What blood test results indicate iron deficiency anaemia?
Low Hb, low MCV, low ferritin, high TIBC.
83
What lifestyle change can restore ovulation in PCOS?
Weight loss ≥5%.
84
How does the COCP help in PCOS?
Regulates cycles, reduces androgen levels, protects endometrium.
85
What is the first-line ovulation induction agent in PCOS?
Letrozole.
86
List side effects of oral iron.
Constipation, nausea, black stools.
87
How long to reassess iron levels after supplementation?
3 months.
88
What is a first-line pharmacological treatment for hirsutism?
COCP.
89
Why must contraception be used with spironolactone?
It is teratogenic.
90
List cardiometabolic risks of PCOS.
Type 2 diabetes, hypertension, dyslipidaemia, cardiovascular disease.
91
Why is endometrial hyperplasia a concern in PCOS?
Due to unopposed oestrogen from anovulation.
92
How often should metabolic screening occur in PCOS?
Every 1–2 years, depending on risk.
93
Which specialties might be involved in interdisciplinary PCOS care?
GP, endocrinologist, dietitian, psychologist.
94
What underlies PCOS pathophysiology?
Insulin resistance → hyperinsulinaemia → androgen excess → anovulation.
95
What is the cornerstone of PCOS treatment?
Lifestyle modification.
96
Name two emerging treatment areas for PCOS.
GLP-1 analogues, inositols.
97
What is adenomyosis?
A condition where endometrial tissue (glands and stroma) grows into the myometrium (uterine muscle wall).
98
What are the typical symptoms of adenomyosis?
Dysmenorrhea (painful periods), menorrhagia (heavy periods), chronic pelvic pain, and a bulky, tender uterus.
99
How is adenomyosis different from endometriosis?
Adenomyosis is endometrial tissue within the uterine muscle, while endometriosis is endometrial tissue outside the uterus.
100
What is the typical age group affected by adenomyosis?
Women aged 35–50, especially those who are multiparous (have had children).
101
What are the risk factors for adenomyosis?
Multiparity, prior uterine surgery (e.g. C-section), increasing age, and endometrial trauma.
102
What physical exam finding is suggestive of adenomyosis?
A uniformly enlarged, boggy, and tender uterus.
103
What is the pathophysiology of adenomyosis?
Ectopic endometrial tissue invades the myometrium → muscle hypertrophy and inflammation → enlarged uterus and heavy, painful periods.
104
What imaging is most useful in diagnosing adenomyosis?
Transvaginal ultrasound or MRI (more sensitive).
105
What are typical ultrasound findings in adenomyosis?
Heterogeneous myometrium, myometrial cysts, thickened junctional zone, and asymmetrical uterine wall thickening.
106
What are the treatment options for adenomyosis?
Medical: NSAIDs, COCP, progestins, LNG-IUS (Mirena)
Surgical: Endometrial ablation, hysterectomy (definitive)
107
Which treatment is definitive for adenomyosis?
Hysterectomy, especially in women with severe symptoms who do not desire fertility.
108
Can adenomyosis affect fertility?
Yes, it may reduce fertility and increase miscarriage risk, though impact varies.
109
What is the role of the levonorgestrel IUD (Mirena) in adenomyosis?
Reduces menstrual blood loss and pain by thinning the endometrium and suppressing endometrial activity.
110
How is adenomyosis definitively diagnosed?
Histological confirmation after hysterectomy.
111
What is Asherman’s Syndrome?
An acquired condition characterized by intrauterine adhesions (scar tissue) that partially or completely obliterate the uterine cavity.
112
What is the most common cause of Asherman’s Syndrome?
Trauma to the endometrium, especially after dilation and curettage (D&C) following miscarriage or postpartum haemorrhage.
113
What are other causes of Asherman’s Syndrome?
Endometrial infection (e.g. TB or schistosomiasis in endemic areas), uterine surgery (myomectomy, C-section), radiation, uterine artery embolisation.
114
What are the clinical features of Asherman’s Syndrome?
Secondary amenorrhoea or hypomenorrhoea, infertility or recurrent miscarriage, cyclic pelvic pain (if outflow is obstructed).
115
What is the typical menstrual pattern seen in Asherman’s Syndrome?
Secondary amenorrhoea or markedly reduced flow (hypomenorrhoea) after uterine surgery or trauma.
116
What is the best diagnostic test for Asherman’s Syndrome?
Hysteroscopy – allows direct visualisation and treatment of intrauterine adhesions.
117
What are other imaging options for diagnosing Asherman’s Syndrome?
Hysterosalpingography (HSG) – shows filling defects, saline infusion sonography (SIS) – reveals synechiae, MRI (less commonly used).
118
What is the treatment for Asherman’s Syndrome?
Hysteroscopic adhesiolysis – surgical removal of intrauterine adhesions.
119
What is the current cervical screening program in Australia?
The Cervical Screening Test (CST) has replaced the Pap smear. It screens for oncogenic HPV every 5 years, starting at age 25 to 74, for people with a cervix who have ever been sexually active.
120
What is the significance of a positive HPV test on CST?
A positive test for HPV types 16/18 warrants colposcopy, while other high-risk HPV types require reflex LBC (liquid-based cytology) and follow-up based on cytology results.
121
What are the three diagnostic features of the Rotterdam Criteria for PCOS?
1. Oligo- or anovulation
2. Clinical or biochemical signs of hyperandrogenism
3. Polycystic ovaries on ultrasound (≥12 follicles per ovary or ovarian volume >10 mL)
122
Can a diagnosis of PCOS be made if ultrasound is normal?
Yes — if a patient has oligo/anovulation and hyperandrogenism, PCOS can be diagnosed without ultrasound evidence of polycystic ovaries.
123
Why is it important to exclude other causes before diagnosing PCOS with Rotterdam Criteria?
Because other conditions (e.g. thyroid dysfunction, hyperprolactinemia, non-classic CAH, Cushing’s) can mimic PCOS — they must be ruled out first.
124
What is the Firman-Galloway model used for?
It is a clinical model used to assess causes of delayed puberty and amenorrhea by evaluating the integrity of the hypothalamic-pituitary-ovarian (HPO) axis.
125
What are the three main components assessed in the Firman-Galloway model?
Hypothalamus – releasing GnRH
Pituitary – secreting LH & FSH
Ovaries – producing estrogen & supporting ovulation
126
What clinical conditions are suggested by a hypothalamic defect in the Firman-Galloway model?
Functional hypothalamic amenorrhea, anorexia nervosa, excessive exercise, chronic illness, or stress.
127
What does high LH and FSH with low estrogen suggest in the Firman-Galloway framework?
Primary ovarian failure (e.g., Turner syndrome, premature ovarian insufficiency).
128
What is indicated by low LH/FSH and low estrogen in the Firman-Galloway model?
Hypogonadotropic hypogonadism — problem at the hypothalamic or pituitary level.
129
What class of drug is Letrozole?
Aromatase inhibitor.
130
What enzyme does Letrozole inhibit?
Aromatase (CYP19A1 enzyme).
131
What is the function of the aromatase enzyme?
Converts androgens (androstenedione and testosterone) into oestrogens (estrone and estradiol).
132
What effect does Letrozole have on oestrogen levels?
Decreases circulating oestrogen levels.
133
How does reduced oestrogen increase FSH secretion?
Lower oestrogen → decreased negative feedback on hypothalamus and pituitary → increased GnRH → increased FSH.
134
Why is increased FSH beneficial in PCOS-related infertility?
Stimulates follicular development and ovulation.
