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Fibroid uterus
Dr. Gunjan Yadav
• Fibroids are benign, monoclonal tumours of
smooth muscle cells of the myometrium
• Contain large aggregations of extracellular
matrix composed of collagen, elastin,
fibronectin and proteoglycans
Etiology
• Genetics:
• Monoclonal
• 40% have genetic abnormalities-
1. Translocation between chr 12 and 14
2. Deletion chr 7
3. Trisomy chr 12
• Hormonal:
• Both estrogen and progesterone promote
development
• Fibroids have increased concentration of
progesterone receptors A and B compared
with normal myometrium.
• De novo production of estradiol is high due to
increased level of aromatase in fibroid
• Serum level of estrogen & progesterone is
similar in women with/ without clinically
detectable fibroid
Risk factors
1. Age- incidence increases with age
2. Greater exposure to endogenous hormones-
early menarche( <10 yrs age) , late
menopause
3. Family history- 1st degree relatives have 2.5
times higher risk
4. Ethnicity- African American women have 2.9
times higher risk than white women
5. Weight- increases risk. Obesity increases
conversion of adrenal androgens to estrone
and decreases SHBG increased
biologically available estrogen
6. Exercise- women in highest category of
physical exercise (7 hrs / week) –less likely to
have fibroids
7. OCP- no definite relationship
8. Pregnancy- increased parity decreases risk
9. Smoking- decreases risk. Nicotine inhibits
aromatase decreased conversion of
androgens to estrone.
Growth Factors
• Proteins or polypeptides
• Increase smooth ms proliferation-TGF beta
• DNA synthesis- EGF, PDGF
• Promote mitogenesis- TGF beta, EGF, insulin
like growth factor, prolactin
• Promote angiogenesis- VEGF, basic fibroblast
growth factor
Pathology
• Naked eye appearance:
Firm, enlarged uterus
Shape – distorted or uniform
• Cut section:
Smooth, whitish
Whorled appearance
• False capsule is formed by compressed
adjacent myometrium. Pinkish in color
• Capsule is separated from fibroid by loose
areolar tissue
• Blood vessels run through this plane
• Tumour is shelled out from this plane durnign
myomectomy
• Periphery of tumour is more vascular
• Centre is least vascular and likely to
degenerate
• Microscopic appearance:
Smooth muscles
Fibrous connective tissue
Symptoms
• Asymptomatic (75%)
• Abnormal bleeding- menorrhagia or metrorrhagia
• Pelvic pain- degeneration of fibroid. Torsion of
pedunculated subserosal fibroid
• Pressure symptoms- Constipation, retention of
urine
• Urinary symptoms- frequency , urgency
• Abdominal enlargement
FIGO Leiomyoma classification
Diagnosis
• Pelvic examination: enlarged, irregularly
shaped, firm, non tender
• Imaging: TVS, MRI, saline infusion sonography
hysteroscopy.
• USG- symmetrical, well defined, hypoechoic,
heterogenous masses.
Fertility
• Submucous fibroids decrease fertilty,
removing them increases fertility
• Subserosal fibroids do not affect fertility,
removing them increases fertility
• Intramural fibroids slighlty decrease fertility,
removal does not increase fertility.
Fibroids and pregnancy
• Prevalence: 18% in African American women
10 % in hispanic women
8 % in white women
• Most fibroids do not increase in size during
pregnancy
• Fibroid degeneration-seen in 5% cases
• Increased risk : preterm delivery, placenta
previa, PPH. C-section rate increased
Treatment
Treatment
• Medical therapy :
1. GNRH agonists: goserelin, luporelin,
buserelin, nafarelin
 MOA- Sustained pituitary downregulation
and suppresion of ovarian function
 Reduction in uterine size occurs within 3
months of treatment
Advantages:
1. Improvement of menorrhagia, may produce
amenorrhea
2. Improvement of anemia
3. Relief of pressure symptoms
4. Reduction in size(50%), when used for a
period of 6 months
5. Reduction in vascularity
6. Reduction in blood loss during myomectomy
Disadvantages:
1. Hypoesterogenic side effects- vasomotr
symptoms, bone loss, arthralgia, depression,
decreased libido (A low dose estrogen-
progestin may be added)
2. Regrowth of myomas on cessation of therapy
3. High cost
• GNRH antagonist :
Ganirelix, cetrorelix
Immediate suppression of pituitary and ovaries
• Antiprogesterone :
Mifepristone (RU-486)- reduce size and
menorrhagia
Dose- 25- 30mg daily for 3 months
Blocks progesterone; unopposed exposure of
endometrium to estrogen may lead to
endometrial hyperplasia. So, long term therapy
avoided
• Selective progesterone receptor modulator:
Asoprisnil- does not cause endometrial
hyperplasia
• LNG-IUD: recommended in uterine size <12
weeks, normal uterine cavity
Decreases uterine bleeding
Surgical treatment
• Treating preoperative anemia:
1. Recombinant eryhthropoeitin
( erythropoeitin alfa and epoetin)-
epoetin 250 IU/kg-(15000 U) per week for 3
weeks increases hemoglobin concentration
by 1.6g/dl.
2. Iron supplementation
3. GNRH agonists
Myomectomy
• Enucleation of myoma from the uterus
• Abdominal/ laparoscopic/ hysteroscopic
• May be done at the time of C section by
experienced surgeon
• Synthetic vasopressin (Pitressin) decreases
blood loss during myomectomy
• Contraindication of myomectomy:
1. Infected fibroid
2. Growth of myoma after menopause
3. Suspected sarcoma
Uterine artery embolization
• Leads to avascular necrosis followed by shrinkage
of fibroid
• Polyvinyl gelatin particles (PVA), gelatin sponges,
or trisacrly gelatin microspheres injected via
percutaneous femoral artery catheterization until
occlusion or slow flow is documented.
• Complications: Postembolization syndrome- pain,
fever, sepsis, myometrial infarction, necrosis,
amenorrhea, ovarian failure, femoral artery injury
• Contraindication of UAE:
1. Acute pelvic infection
2. Women desirous of future pregnancy( as
there is risk of premature ovarian failure)
3. Genital tract malignancy
4. Drug allergy
• Magnetic resonance guided focussed
ultrasound (MRgFUS):
Focussed high energy ultrasound waves
Coagulative necrosis in myomas by producing
sufficient heat
Multiple treatment
Less pain compared to UAE
Safe, feasible, minimally invasive
Contraindication- abdominal wall scar, uterine
size>24 weeks, desire for future fertility
Degenerations of fibroid
• Hyaline degeneration:
Most common(65%)
Feel becomes soft, elastic
Cut surface- irregular homogenous areas with
loss of whorl like appearances
• Cystic degeneration:
Usually following menopause
Common in interstitial fibroids
Liquefaction of areas with hyaline changes
• Fatty degeneration:
Usually found at or after menopause
Fat globules deposited mainly in muscle fibres
• Calcific degeneration:
Usually in subserous fibroid
Usually preceded by fatty degeneration
Precipitation of calcium carbonate or
phosphate in the tumour
Whole tumour converted into calcified mass-
‘womb stone’
• Red degeneration (carneous degeneration):
Occurs in large fibroid
Mainly in 2nd half of pregnancy and
puerperium
Cut section- raw beef appearance (d/t
hemolysed red cells and hemoglobin)
containing cystic spaces
Fishy odour d/t fatty acids
Microscopically- necrosis, thrombosed vessels
Other complications
1. Atrophy: following menopause. Loss of estrogen
support.
2. Necrosis: circulatory inadequacy -> central necrosis
3. Infection: following delivery/ abortion. Infection gains
access to tumour core through the thinned and
sloughed surface epithelium
4. Vascular changes
5. Sarcomatous changes: in <0.1% cases. Leimyosarcoma
is the usual type
6. Torsion
Thank you
D/D
• Adenomyosis: Focal, not well defined , highor
low intensity areas in USG
• Uterine sarcomas: Gd-DTPA dynamic MRI-
sarcomas have increased vascularity while
degenerating fibroids have decreased
perfusion and decreased enhancement.

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Fibroid uterus

  • 2. • Fibroids are benign, monoclonal tumours of smooth muscle cells of the myometrium • Contain large aggregations of extracellular matrix composed of collagen, elastin, fibronectin and proteoglycans
  • 3. Etiology • Genetics: • Monoclonal • 40% have genetic abnormalities- 1. Translocation between chr 12 and 14 2. Deletion chr 7 3. Trisomy chr 12
  • 4. • Hormonal: • Both estrogen and progesterone promote development • Fibroids have increased concentration of progesterone receptors A and B compared with normal myometrium. • De novo production of estradiol is high due to increased level of aromatase in fibroid • Serum level of estrogen & progesterone is similar in women with/ without clinically detectable fibroid
  • 5. Risk factors 1. Age- incidence increases with age 2. Greater exposure to endogenous hormones- early menarche( <10 yrs age) , late menopause 3. Family history- 1st degree relatives have 2.5 times higher risk 4. Ethnicity- African American women have 2.9 times higher risk than white women
  • 6. 5. Weight- increases risk. Obesity increases conversion of adrenal androgens to estrone and decreases SHBG increased biologically available estrogen 6. Exercise- women in highest category of physical exercise (7 hrs / week) –less likely to have fibroids 7. OCP- no definite relationship 8. Pregnancy- increased parity decreases risk 9. Smoking- decreases risk. Nicotine inhibits aromatase decreased conversion of androgens to estrone.
  • 7. Growth Factors • Proteins or polypeptides • Increase smooth ms proliferation-TGF beta • DNA synthesis- EGF, PDGF • Promote mitogenesis- TGF beta, EGF, insulin like growth factor, prolactin • Promote angiogenesis- VEGF, basic fibroblast growth factor
  • 8. Pathology • Naked eye appearance: Firm, enlarged uterus Shape – distorted or uniform • Cut section: Smooth, whitish Whorled appearance • False capsule is formed by compressed adjacent myometrium. Pinkish in color
  • 9. • Capsule is separated from fibroid by loose areolar tissue • Blood vessels run through this plane • Tumour is shelled out from this plane durnign myomectomy • Periphery of tumour is more vascular • Centre is least vascular and likely to degenerate • Microscopic appearance: Smooth muscles Fibrous connective tissue
  • 10. Symptoms • Asymptomatic (75%) • Abnormal bleeding- menorrhagia or metrorrhagia • Pelvic pain- degeneration of fibroid. Torsion of pedunculated subserosal fibroid • Pressure symptoms- Constipation, retention of urine • Urinary symptoms- frequency , urgency • Abdominal enlargement
  • 12. Diagnosis • Pelvic examination: enlarged, irregularly shaped, firm, non tender • Imaging: TVS, MRI, saline infusion sonography hysteroscopy. • USG- symmetrical, well defined, hypoechoic, heterogenous masses.
  • 13. Fertility • Submucous fibroids decrease fertilty, removing them increases fertility • Subserosal fibroids do not affect fertility, removing them increases fertility • Intramural fibroids slighlty decrease fertility, removal does not increase fertility.
  • 14. Fibroids and pregnancy • Prevalence: 18% in African American women 10 % in hispanic women 8 % in white women • Most fibroids do not increase in size during pregnancy • Fibroid degeneration-seen in 5% cases • Increased risk : preterm delivery, placenta previa, PPH. C-section rate increased
  • 16.
  • 17. Treatment • Medical therapy : 1. GNRH agonists: goserelin, luporelin, buserelin, nafarelin  MOA- Sustained pituitary downregulation and suppresion of ovarian function  Reduction in uterine size occurs within 3 months of treatment
  • 18. Advantages: 1. Improvement of menorrhagia, may produce amenorrhea 2. Improvement of anemia 3. Relief of pressure symptoms 4. Reduction in size(50%), when used for a period of 6 months 5. Reduction in vascularity 6. Reduction in blood loss during myomectomy
  • 19. Disadvantages: 1. Hypoesterogenic side effects- vasomotr symptoms, bone loss, arthralgia, depression, decreased libido (A low dose estrogen- progestin may be added) 2. Regrowth of myomas on cessation of therapy 3. High cost
  • 20. • GNRH antagonist : Ganirelix, cetrorelix Immediate suppression of pituitary and ovaries • Antiprogesterone : Mifepristone (RU-486)- reduce size and menorrhagia Dose- 25- 30mg daily for 3 months Blocks progesterone; unopposed exposure of endometrium to estrogen may lead to endometrial hyperplasia. So, long term therapy avoided
  • 21. • Selective progesterone receptor modulator: Asoprisnil- does not cause endometrial hyperplasia • LNG-IUD: recommended in uterine size <12 weeks, normal uterine cavity Decreases uterine bleeding
  • 22. Surgical treatment • Treating preoperative anemia: 1. Recombinant eryhthropoeitin ( erythropoeitin alfa and epoetin)- epoetin 250 IU/kg-(15000 U) per week for 3 weeks increases hemoglobin concentration by 1.6g/dl. 2. Iron supplementation 3. GNRH agonists
  • 23. Myomectomy • Enucleation of myoma from the uterus • Abdominal/ laparoscopic/ hysteroscopic • May be done at the time of C section by experienced surgeon • Synthetic vasopressin (Pitressin) decreases blood loss during myomectomy
  • 24. • Contraindication of myomectomy: 1. Infected fibroid 2. Growth of myoma after menopause 3. Suspected sarcoma
  • 25. Uterine artery embolization • Leads to avascular necrosis followed by shrinkage of fibroid • Polyvinyl gelatin particles (PVA), gelatin sponges, or trisacrly gelatin microspheres injected via percutaneous femoral artery catheterization until occlusion or slow flow is documented. • Complications: Postembolization syndrome- pain, fever, sepsis, myometrial infarction, necrosis, amenorrhea, ovarian failure, femoral artery injury
  • 26. • Contraindication of UAE: 1. Acute pelvic infection 2. Women desirous of future pregnancy( as there is risk of premature ovarian failure) 3. Genital tract malignancy 4. Drug allergy
  • 27. • Magnetic resonance guided focussed ultrasound (MRgFUS): Focussed high energy ultrasound waves Coagulative necrosis in myomas by producing sufficient heat Multiple treatment Less pain compared to UAE Safe, feasible, minimally invasive Contraindication- abdominal wall scar, uterine size>24 weeks, desire for future fertility
  • 28. Degenerations of fibroid • Hyaline degeneration: Most common(65%) Feel becomes soft, elastic Cut surface- irregular homogenous areas with loss of whorl like appearances • Cystic degeneration: Usually following menopause Common in interstitial fibroids Liquefaction of areas with hyaline changes
  • 29. • Fatty degeneration: Usually found at or after menopause Fat globules deposited mainly in muscle fibres • Calcific degeneration: Usually in subserous fibroid Usually preceded by fatty degeneration Precipitation of calcium carbonate or phosphate in the tumour Whole tumour converted into calcified mass- ‘womb stone’
  • 30. • Red degeneration (carneous degeneration): Occurs in large fibroid Mainly in 2nd half of pregnancy and puerperium Cut section- raw beef appearance (d/t hemolysed red cells and hemoglobin) containing cystic spaces Fishy odour d/t fatty acids Microscopically- necrosis, thrombosed vessels
  • 31. Other complications 1. Atrophy: following menopause. Loss of estrogen support. 2. Necrosis: circulatory inadequacy -> central necrosis 3. Infection: following delivery/ abortion. Infection gains access to tumour core through the thinned and sloughed surface epithelium 4. Vascular changes 5. Sarcomatous changes: in <0.1% cases. Leimyosarcoma is the usual type 6. Torsion
  • 33. D/D • Adenomyosis: Focal, not well defined , highor low intensity areas in USG • Uterine sarcomas: Gd-DTPA dynamic MRI- sarcomas have increased vascularity while degenerating fibroids have decreased perfusion and decreased enhancement.