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Common gynaecological carcinom final2


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Common gynaecological carcinom final2

  1. 1. CommonGynaecological Carcinoma
  2. 2. Top killers of the female gender All Females, All Ages Percent* 1) Heart disease 25.1 2) Cancer 22.1 3) Stroke 6.7 4) Chronic lower respiratory diseases 5.5 5) Alzheimers disease 4.3 6) Unintentional injuries 3.6 7) Diabetes 2.9 8) Influenza and pneumonia 2.3 9) Kidney disease 2.0 10) Septicemia 1.6
  3. 3. : 10 Principle Cause of Deaths in Ministry of Health, Malaysia (MOH) Hospitals, 20061. Septicaemia 16.872. Heart Diseases & Diseases of Pulmonary Circulation 15.703. Malignant Neoplasms 10.594. Cerebrovascular Diseases 8.495. Pneumonia 5.816. Accidents 5.597. Diseases of the Digestive System 4.478. Certain Conditions Originating in The Perinatal Period 4.209. Nephritis, Nephrotic Syndrome & Nephrosis 3.8310. Ill-defined conditions 3.03All causes 100.0
  4. 4. Prevalence of various types of cancer amongst Malaysian ladiesof all agesBREAST 3525 29.9COLORECTAL 1247 10.6CERVIX UTERI 1074 9.1OVARY 685 5.8THYROID GLAND 670 5.7LUNG 603 5.1CORPUS UTERI 372 3.2STOMACH 324 2.7BRAIN, OTHERNS 303 2.6LYMPHOMA 279 2.4 Taken from the Malaysian Cancer Statistics 2006
  5. 5. PATHOPHYSIOLOGY CERVICAL ENDOMETRIAL OVARIANThe squamo-columnar -Most commonly 80% from Ovarianjunction and the Adenocarcinoma EpitheliumTransformation zone -90%: Endometriod adenoCA 20% others: Germ cell, sex- -10%:Serious papillary AdenoCA cord stromal, mixedCommon site for HPV -Rarely: Clear cell mullerian,infectionHPV infection persists in Mechanism poorly understoodcertain individuals, eventually Two main theoriestriggering oncogenic processeswithin the TZCell metaplasia occurs: 1. IncessantImmortalization of the basal ovulationrepeated traumacells leading to rapid turnover to ovarian epitheliumand subsequent immaturecellsThese immature cells picked 2. Excess gonadotrophinup on PAP smear as Cervical secretionhigher level ofIntraepithelial Neoplasia CIN estrogenEpithelial proliferation
  6. 6. AETIOLOGY & RISK FACTORS CERVICAL ENDOMETRIAL OVARIANInfection by HPV Conditions that lead to Endometriosis16,18,31,33 high levels of estrogen -Tamoxifen -Unopposed estrogen therapy as HRTImmunosupressed state Family history (debatable) Family historyleading to increased risk of -endometrial cancer -increased risk from 1.4% inHPV infection: -colorectal/ovarian cancer general populace to 5%-RVD -HNPCC 50% if 2 first degree relatives-Immunosupressive drugs Nulliparity Nulliparity Late menopause >52 years Obesity ObesitySmoking Diabetes-theory: immunosupressiveeffects of nicotine within thecx
  7. 7. Mnemonic of risk factors for endometrial cancer• O=Obesity L=Late menopause D=Diabetes mellitus A=cAncer: ovarian, breast, colon U=Unopposed estrogen: PCOS, anovulation, HRT N=Nulliparity T=Tamoxifen, chronic use.
  8. 8. RMI score for ovarian CAFeature RMI 1 Score RMI 2 ScoreUltrasound features: 0= none 0= none• multilocular cyst 1= one abnormality 1= one abnormality• solid areas 3= two or more 4= two or more• bilateral lesions abnormalities abnormalities• scites• intra-abdominal metastasesPremenopausal 1 1Postmenopausal 3 4CA125 U/ml U/ml RMI score = ultrasound score x menopausal score x CA125 level in U/ml.The RMI scoring system is the method of choice for predicting whether or not an ovarian mass is likely to be malignant. Women with an RMI score >200 should be referred to a centre with experience in ovarian cancer surgery. Evidence grade 2+
  9. 9. CLINICAL FEATURES CERVICAL ENDOMETRIAL OVARIANAbnormal PV bleeding Abnormal PV bleeding Persistent pelvic- abdominal pain1. Post-coital bleeding 1. Post-Menopausal Bleed Increased abdominal size and*The cervical cancer is a ddx: Cervical, endometrial polyps, bloating friable vascular mass on cervical erosion, vaginal the cervix: Mechanical atrophy irritation during coitus: 10% of PMB turns out to be Endometrial CA Post-coital bleed 2. Irregular Vaginal bleeding3. Advanced stage: 3. Advanced stage: 3. Advanced stage:-constitutional sx -constitutional sx -constitutional sx-lungs mets: Recurrent -lungs mets: Recurrent -lungs mets: Recurrentbilateral pleural effusion bilateral pleural effusion bilateral pleural effusionIncontinence Change in bowel habitsAnemia Sx Urinary sxRenal failure Back ache
  10. 10. INVESTIGATIONS AND SUSPICIONS CERVICAL ENDOMETRIAL OVARIANAim of diagnostics: To provide histopathological evidence of malignant cancer tissue.To provide sufficient information to properly stage the tumourTo confirm the malignancy To confirm the malignancy To confirm the malignancy1. Colposcopy : outpatient 1. Sampling by Pipelle: and for staging examination of the magnified Outapatient procedure, 1.TAHBSO cervix using a light source results operator dependant, Additional Lugol’s Iodine/ 5% acetic 2.CT-scan/MRI difficult to do if nulliparous, 3.PET-scan acid are used to highlight the presence of abnormal cells retroverted uterus, presence2. Cervical Biopsy: To confirm of fibroids * In some patients (esp those the malignancy and type 2. Hysteroscopic DD+C: done if unable to obtain good unfit for a major surgery such of tumour as TAHBSO, laparascopic sample by Pipelle / Contraindicated for Pipelle examination and biopsy is done insteadTo assess stage To assess stage1.CT-scan abdomen-pelvis 1.TAHBSO2.EUA : Vaginal and rectal 2.CT-scan/MRI 3.PET-scan
  11. 11. Tumuor markers1. Not used for diagnosis for cancer. Diagnosis of cancer is strictly based histopathological evidence2. Tumour markers can be useful for: - Monitoring the response of the malignancy to anti-cancer therapies - Monitoring patients on a regular basis to assess for reoccurance Tumour marker Cancer 1 Ca-125 Endometrial, ovarian 2 CEA Pancreas, colon 3 a-FP Liver (HCC) 4 Ca 19-9 Pancreas
  12. 12. CERVIX ENDOMETRIAL OVARIANI: Cervical cancer confined to IA: Endometrium only I: Ovaries onlycervix IA: One ovaryIa1: < 3mm IB: Two ovaries IB: <1/2 of myometrium IC: Ruptured ovary/+ve peritonealIa2: > 3mm wash/ascitesIb1: < 4cm IC: >1/2 of myometrium1b2:> 4cmII: Cervical cancer extending IIA: Endocervical glandular II: Ovaries + pelvicbeyond the cervix, but not involvement involvementinvading pelvic wall IIB: Cervical stroma invasion IIA: Uterus + TubesIIA: No obvious parametric invasion IIB: Pelvic/parametrial tissueIIB: Obvious parametric invasion + IIC: Rupture/+ve peritonealupper 2/3 of vagina wash/ascitesIII: Cervical ca extending to IIIA: Serosa/Adnexa/+ve III: Ovaries + peritoneumpelvic wall peritoneal wash IIIA: Microscopic seedlingsIIIa: Invasion of lower 1/3 vagina IIIB: < 2cm seedling IIIB: Invasion of vagina IIIC: > 2cm seedlingIIIb: Extention to pelvic wall withhydronephrosis IIIC: Invasion of pelvic/ Paraaortic LNIVa: Growth to adjacent IVA: Invasion to IV: Distant metastasisorgans bladder/rectum Pleural effusionIVb: Distant metastasis IVB: Distant metastasis
  15. 15. Cervical CancerSTAGE TREATMENT PROTOCOLStage 1a Surgery: TAH, PLND Modified radical trachelectomy (fertility sparing) : remove 80% of cervix, parametrial tissues, pelvic LN ~ 40% miscarriage Fertility sparing therapy seldom done Radiation therapy: Brachytherapy(internal radiotherapy)Stage 1b Wertheim’s hysterectomy TAHBSO+Parametrial tissue excision+PLND+upper 1/3 vagina Radiation therapy has similar success rates, and considered who are unfit for surgeryStage 2-4 Chemotherapy : Carboplatin + Paclitaxel Radiotherapy: External beam: Teletherapy Internal radiotherapy: Brachytherapy *Surgery seldom done at this stage: -High rates of surgical complications esp: Bleeding -Unlikely chance of achieving complete clearance of tumour -Requiring post op radiotherapy, and this combined treatment can lead to high complication rates Remember: No tumour markers for Cervical Cancer
  16. 16. Endometrial Carcinoma Surgery *Generally surgery indicated in all patients diagnosed with Endometrial CA C/I: Unfit for surgery, metastasised cancer (Stage IV)Stage 1A, 1BTAHBSO (PLND also commonly done Stage 2C, 3, 4/Papillary serous/Clear cellas there is a high chance of spread toLN at this stage) TAHBSO + PLND Adjuvant ChemotherapyStage 1C, 2A, 2BTAHBSO + PLND (50% risk of LNdissemination at these stages) Chemotherapy -Commence adjuvant chemotherapy -1st Line: 6 cycles of Carboplatin + Paclitaxel -2nd Line: 9 cycles (A+B) of Gemcitabine Follow-up: Ca-125, CT-Scan
  17. 17. Ovarian Cancer Surgery *Studies show that the most important prognostic factor is no residual disease following laparatomyNon fertility sparing Fertility sparing (rarely done)-Vertical insicion done to gain visual -Vertical insicion done to gain visualaccess to ALL areas of the abdomen access to ALL areas of the abdomen-Ascites and peritoneal washing samples -Unilateral SO, Omentectomy, Peritonealare obtained biopsies-TAHBSO + Omentectomy KIV further -PLNDdebulking if required + Endometrial sampling to exclude- PLND concerrent tumour MDT meeting between Oncogynae with pathologist, radiologist Chemotherapy Stage IB, IC , II, III, IV Stage 1A -Commence adjuvant chemotherapy - Chemotherapy withheld in some cases -1st Line: 6 cycles of Carboplatin + Paclitaxel -2nd Line: 9 cycles (A+B) of Gemcitabine Follow-up: Ca-125, CT-Scan
  18. 18. Drug Mech of action AECisplatin Platinum based drug Nephrotoxic (check RP before giving) Acts by binding and cross- GIT: N+V linking DNA leading to cell Ototoxicity apoptosis Electrolyte imbalancesCarboplatin Neurotoxicity: peripheral neuropathy Myelosupression  Aneamia,neutropenia,TCP Less GIT effects compared to Cisplatin No nephrotoxic effectGemcitabine Neucloside analogue. Flu-like symptoms Kills cells in the S-phase of mitosis GIT: Mild N+V : Cell phase specific Hair oss Myelosupression5-FU Pyrimidine analogue Myelosupression Inhibits Thymidine synthase Mucositis, dermatitis : Cell phase specific (S-phase) DiarrhoeaPaclitaxel Stabilizes the microtubules Myelosupression preventing the Interphase thus Neurotoxicity: Peripheral neuropathy interrupting mitosis Elevated LFT : Cell phase specific N+V, hair loss, arthritis
  19. 19. Gestational Throphoblastic DiseaseHydatidiform Mole Invasive Mole Choriocarcinoma Placental site throphoblasticComplete Incomplete tumour (PSTT) Risk factors Extremes of age (<15, >40) – risk of complete moles Previous molar pregnancy X 10 Ethnicity (East Asians: x 2) Presentation Irregular first-trimester bleeding >90% Uterus large for dates~ 25% Abdominal pain (from hyperstimulation of theca lutien cysts) Exxaggerated early pergnancy symptoms (hyperemesis gravidarum) ~ 10% Diagnosis Clinical Biochemical – excessively raised serum bHCG levels (may be normal in partial moles) Scan findings – classic snowstorm appearance Histological – post evacuation Management Complete mole – surgical evacuation (higher risk of uterine perforation and significant bleeding) Incomplete mole – Surgical or medical evacuation
  20. 20. Follow-up Review HPE of evacauted mole – determine for sure complete or incomplete Recommended follow-up plan -Fortnightly bHCG until levels normal < 4 -4 weekly intervals urine bHCG levels for one year, then 3-monthly in 2nd year -Contraception until bHCG normal for 6 months The purpose of this follow up is to detect malignancy earlyWhen to suspect The International Federation of Gynecology and Obstetrics considers anmalignancy? elevated serum hCG level 6 or more months after evacuation of a hydatidiform mole to be diagnostic of malignancy (ie, GTN). *However, serum hCG levels spontaneously return to normal without chemotherapy in most patients with elevated but still declining serum hCG levels 6 months after diagnosis of a hydatidiform mole.Indication for 1. Serum bHCG levels >20000 4 weeks after uterine evacuationchemotherapy 2. Static or rising bHCG levels post evacuation 3. Histological evidence of choriocarcinoma 4. Metastatic disease 5. Persistent symptoms
  21. 21. ChoriocarcinomaIncidence Rare : Amongst Orientals 1:11000 (1:30000 amongst Caucasians) 20% of complete hydatidiform moles become ChorioCAPresentation Similar to hydatidiform mole -First trimester vaginal bleeding, abdominal pain Symptoms pointing to possibility of chorioCA -Dyspnoea and hemoptysis (lung mets), hematuria, neurological sx -Jaundiced, abdominal tenderness, reboundInvestigations Biochemical – Persistantly raised / pleateau or increasing trend of bHCG even after surgical evacuation of GTD Scan findings CXR (lung is most frequent site of mets) CT abdomen and chestTreatment CHEMOTHERAPY -Regime based on prognostic scoring assestment Low Risk : MTX + Folinic Acid / Actinomycin D Med Risk: MTX + Etoposide High Risk: Intensive weekly EMA (Etoposide,MTX,Dactinomycin) alternating with CE (Cyclophosphamide and Vincristin) – the EMA-CE regimentPrognosis Overall survival > 90% - it is one of the most curable forms of malignant cancer Poorer prognosis if -Age >40 -Time interval between antecedent pregnancy and start of chemotherapy > 4months -After 12 months of normal hCG levels, less than 1% of patients with GTN have recurrences.Next Fertility not impaired by chemopregnancy No increased risk of fetal anomalies