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MCCQE Review: Gynecology

MCCQE Review: Gynecology. Dr. Jessica Dy Division of Reproductive Medicine Department of Obstetrics and Gynecology. Overview. Objectives of MCCQE in Gynecology Selected Topics: Part 1 Sexual Development Menstrual Abnormalities (amenorrhea, PCO, abnormal bleeding patterns)

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MCCQE Review: Gynecology

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  1. MCCQE Review:Gynecology Dr. Jessica Dy Division of Reproductive Medicine Department of Obstetrics and Gynecology

  2. Overview Objectives of MCCQE in Gynecology Selected Topics: Part 1 Sexual Development Menstrual Abnormalities (amenorrhea, PCO, abnormal bleeding patterns) Contraception Intermission

  3. Overview Selected Topics: Part 2 Pelvic Pain Pelvic Mass Infertility Pelvic Relaxation/Prolapse Intermission

  4. Overview Selected Topics: Part 3 PAP Smears Gynecologic Infections(Graphic) Ectopic Pregnancies Domestic Violence End – Good Luck on your examination

  5. MCCQE Objectives: Gynecology: Breast Disorders Infertility/Impotence/Sexual Dysfunction Menstrual Cycle Abnormal/Amenorrhea/Pre-menstrual Syndrome Menopause PAP Smear/Screening/Prevention Pelvic Mass Pelvic Pain Contraception/Pregnancy Prevention/Termination Prolapse/Pelvic Relaxation Vaginal Bleeding,Excessive/Irregular/Painful/Dysmenorrhea Vaginal Discharge/Urinary Symptoms, Vulvar Lesions, STDs Violence, Family (Child,Elderly,Adult,Spouse,Rape,Violence Against Women) Italic = covered under other specialities

  6. MCCQE Objectives: Full Clinical Presentation List: Sexual Maturation(normal,abnormal)

  7. Part 1

  8. Female Sexual Development “Baby Has Gone Mad!” Breast Development (Thelarche) 10.5 yo Hair Development (Pubarche) 11.0 yo Growth (peak height velocity) 11.4 yo Menstruation (Menarche) 12.8yo Note growth spurt superimposed on pubertal process -begins prior to thelarche

  9. Female Sexual Development In General: -low levels of FSH and LH are found in infants and prepubertal girls - prior to onset of pubertal changes, levels of FSH and LH rise (initially at night-LH) - estradiol levels rise and breast development occurs, eventually sufficient estrogen is available to initiates endometrial growth and menses -andrenache(pubarche) biologically unrelated event, but temporally related to other pubertal changes

  10. Female Sexual Development:Precocious Puberty(development of secondary sexual characteristics before 8yo) Types: 1) GnRH Dependent(True Precocious Puberty) -early activation of hypothalamic-pituitary-ovarian axis 2) GnRH Independent(Precocious Pseudopuberty) - sexual maturation not related to GnRH secretion (eg.extra pituitary secretion of gonadotropins, or sex steroid secretion)

  11. Female Sexual Development:Precocious Puberty Causes: 1) GnRH Dependent Idiopathic 74% CNS problem 7% (tumors, encephalitis, menigitis, hydrocephalus, skull injury/deformity) 2) GnRH Independent Ovarian(cyst or tumor) 11% McCune-Albright syndrome 5% (autonamous early production of E2 by ovaries, cycstic bone lesions-#’s, café au lait) Adrenal 2% Ectopic FSH/LH 0.5% Hypothyroidism ?

  12. Female Sexual Development:Precocious Puberty Investigations: initial:- bone age, height and wieght - estradiol levels(precocious breast development) - androgens- DHEAS, Testosterone(precocious andrenarche) - FSH,LH,TSH levels secondary: - imaging of pituitary/sella - ultrasound ovaries, uterus, image adrenals - bone scan(McCune-Albright)

  13. Female Sexual Development:Precocious Puberty: Findings Cause FSH/LHEstradoilDHASGonadal Size 1) GnRH Dependent Idiopathic Increased Increased Normal Increased CNS problem Increased Increased Normal Increased 2) GnRH Independent Ovarian(cyst or tumor) Decreased Increased Normal Uni. Increased McCune-Albright syndrome Decreased Increased Normal Increased Adrenal Decreased Increased Increased Small Ectopic FSH/LH Increased Increased Normal Increased Bone age is advanced compared to chronological age in all causes, except hypothyroidism.(unknown reason)

  14. Female Sexual Development:Precocious Puberty Treatment: Aimed at underlying process Tumor-resect,radiation,chemo Idiopathic- GnRH agonist therapy McCune-Albright- MPA - Testolactone-aromatase inhibitor Delayed Puberty- discussed as primary amenorrhea Suggested sites for more information http://www.utdol.com and search precocious puberty http://www.utdol.com/application/topic.asp?r=/application/topic.asp&file=r_endo_m/9737&type=A&selectedTitle=1~25&app=utdol

  15. Amenorrhea • Definition: • Primary Amenorrhea • - no period by age 14 in absence of growth or development of secondary sex characteristics • - or no period by age 16 regardless of presence of normal growth and development with the appearance of secondary sex characteristics

  16. Amenorrhea • Definition: • Secondary Amenorrhea • - in a woman who has been menstruating, the • absence of periods for a length of time • equivalent to a total of at least 3 of the previous cycle intervals, or 6 months of amenorrhea

  17. Amenorrhea • Etiology: Pregnancy Thyroid disease Prolactin disease PCO and its variants Hypothalamic disease Ovarian failure(resistance) Endometrial failure Developmental, genetic disorders

  18. Amenorrhea -Hypothalamic • Stress induced • anorexia nervosa – loss of pulsatile GnRH secretion • - 15% below body weight starts to return • -exercise induced • -critical body fat threshold • -centrally acting agents • (melatonin, opiods, and CRH increase)

  19. Amenorrhea -Hypothalamic Overall: When available energy is excessively diverted or insufficient, reproduction is suspended in order to support essential metabolism for survival. Diagnosis of exclusion

  20. Amenorrhea -Pituitary • Pituitary Adenomas: • non-functioning – most common (30-40% of all pituitary) • prolactinoma • growth hormone secreting - acromegaly • ACTH secreting - Cushing’s Disease

  21. Amenorrhea -Pituitary • Adenomas Overall: • Elevated levels of prolactin cause decrease secretion of GnRH from hypothalamus, therefore decreased FSH/LH and amenorrhea (hypothalamic amenorrhea) • Any mass lesion may cause stalk compression (-relieves prolactin from Dopamine suppression therefore can cause hyperprolactinemia)

  22. AmenorrheaRare Pituitary Lesions • Sarcoidosis • Tuberculosis • Teratomas • Crayniophyphyrangieoma • Lymphocytic hypophysitis • Sheehan’s Syndrome • Post partum hemorrhage with ischemic necrosis of anterior pituitary (portal system) • -failure of lactation

  23. Amenorrhea -Ovary • Anovulatory – PCO – condition where ovaries contain multiple early stage follicles which do not mature • secrete androgens in excess of E2 • -related problems with insulin receptor function and lipids, hyperandrogenism and unopposed estrogen • Ovarian failure – premature exhaustion of follicles < 40 years • -radiation, chemotherapy, genetic, iatrogenic, idiopathic

  24. Amenorrhea -Ovarian Abnormal Development • Dysgenetic Gonads (Abnormal chromosome complement) • - Turner’s Syndrome • +/- mosiacisms – 45X • - XY Swyer’s syndrome • testes develop abnormality or failed to develop • no testosterone effect but AMH • testis streaks-fibrous bands • - Testicular ferminization • also a Mullarian abnormality • defect is one of a spectrum of androgen insensitivities

  25. Amenorrhea -Ovarian Abnormal Development • Dygenesis of Gonad XX • -accelerated germ cell loss with premature degeneration of ovaries

  26. Amenorrhea -Genital Tract • Blockage (mullarian abnormalities) • - transverse septum • - imperforate hymen • - non-communicating cavities • Endometrial Failure – Asherman’s syndrome • - secondary to vigorous D&C – usually post- partum • - ++ adhesions/synechia in uterine cavity • To Test: give both E2 then P4 and withdrawal • if period then outflow tract not obstructed &/- failure

  27. Amenorrhea BHCG TSH Prolactin pregnancy hypothyroid hyperprolactinemia Within Normal Limits Progesterone Challenge -Provera 10mg x 10d Bleeding Anovulation No Bleeding Estrogen & Progesterone Bleeding No Bleeding End Organ Problem -obstruction -failure FSH and LH Normal or Low High Ovarian Failure CT Scan of Sella -Sellar lesion -hypothalamic amenorrhea

  28. Approach to Amenorrhea If Prolactin elevated- investigate for hyperprolactinemia If pregnant stop investigating

  29. Approach to Amenorrhea 2

  30. Approach to Amenorrhea 3

  31. Approach to Amenorrhea 4

  32. Approach to Amenorrhea 5

  33. Approach to Amenorrhea 6

  34. Approach to Amenorrhea 7 Including: Dysgenetic Gonad Gonadal Dysgenesis -therefore do Karyotype

  35. Approach to Amenorrhea 8 Abnormal Hypothamic,or pituitary lesion Normal

  36. PCOS PCOS – Polycystic Ovarian Syndrome described in 1935 by two gynecologists- Stein and Leventhal large polycystic ovaries with amenorrhea Triad of: amenorrhea obesity hirsutism

  37. PCOS -Clinically • -biochemistry – LH/FSH ratio >2-3 and elevated androgens (increased testosterone, DHEAS, 17-OH progesterone) • -U/S - multiple follicles peripherally arranged • (string of pearls appearance) • - not specific 8-25% of normally cycling women will • have this appearance • -~14% of women on the pill will have this appearance • -recently appreciated to be a spectrum of • disease severity/presentations

  38. What is PCOS • -a syndrome resulting from chronic anovulation • -can be associated with high insulin levels in many patients • -diagnosis is made clinically +/- biochemical support • -evidence of oligo/anovulation • -evidence of androgen excess • -+/- evidence of insulin resistance

  39. Why is this Important? • 1. Infertility • 2. Menstrual bleeding problems – amenorrhea – DUB • 3. Hirsutism, acne and alopecia • 4. Increased risk of endometrial cancer • 5. Increased risk of CAD • 6. Increased risk of type II diabetes if insulin resistant

  40. Insulin Story • Defect in insulin receptor • - altered phosphorylation at serine (increased) and tyrosine (decreased) residues on insulin receptor • - this reduces signal transmission and causes a post receptor problem and glucose transport decreases • - this phosphorylation of serine may increase the • activity of enzymes that make androgens in both • the ovaries and adrenals

  41. Insulin Story: Net Result • – increased insulin levels secondary to decreased tissue uptake of glucose • - increased androgen production from both adrenals and ovaries (LH and insulin act synergistically to increase androgen production by theca cells in ovary).

  42. Treatment • Treatment depends on patient’s immediate concerns and risk factors • -weight loss through diet and exercise • -treatment with progesterone to prevent endometrial hyperplasia – cancer • -Metformin to decrease insulin levels • ? reduce risk of progression to type II diabetes • ? improve lipid profiles • · ? induce ovulation • sensitize to ovulation induction

  43. Treatment • Ovulation induction • Clomiphene • SERMS (letrozole/tamoxifen) • FSH ovulation induction • Ovarian drilling

  44. Abnormal Uterine Bleeding (Unrelated to Pregnancy) Menorrhagia: cyclic menstrual bleeding occurring at regular intervals excessive amount and/or duration (>80 ml menstrual fluid/>7 days) Metrorrhagia: uterine bleeding occurring at irregular intervals Menometrorrhagia: uterine bleeding irregular frequency and excessive in amount

  45. Abnormal Bleeding Causes of “Organic” Abnormal Uterine Bleeding: uterine -polyps, -fibroids -trauma -infections-PID, endometritis, -IUD -exogenous hormones -endometrial cancer, hyperplasia -cervical cancer, infection other -vulvovaginitis -vaginal,vulvar,ovarian cancer -coagulation disorders -thyroid disease

  46. Abnormal Bleeding Dysfunctional Uterine Bleeding(DUB): Uterine bleeding without any evidence of organic disease(ie no polyps, malignancy, pregnancy, etc.) 90% related to anovulation 10% can be ovulatory Anovulatory DUB -no ovulation, therefore no progesterone secretion -endometrium exposed to prolonged and unopposed estrogen resulting in estrogen breakthrough bleeding (fragile, un-uniform growth of endometrium-areas of shedding and re-growth)

  47. Abnormal Bleeding Ovulatory DUB(uncommon) - ? Luteal phase progesterone unable to maintain endometrium

  48. Abnormal Bleeding Investigations: -Bhcg -CBC -R/O organic diseases -hx & px -endometrial biopsy -+/- ultrasound Treatment dependent on Cause

  49. Abnormal Bleeding DUB Treatment: Mild: OCP 1 tab tid then continuous x 4-6 months OR cyclic provera 5-10 mg po od x10d monthly Severe: stabilize patient as required premarin IV 25 mg q4-6h +/- add OCP or provera OR D&C if severely ill or unresponsive to medical Tx

  50. Abnormal Bleeding DUB Longterm Treatment: OCP cyclic provera 5-10 mg po od x10d monthly progestin only pill progesterone IUD NSAIDS-menorrhagia anti-fibrinolytic agents- menorrhagia surgical - endometrial ablation, hysterectomy

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