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Ovarian & endometrial cancer

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Ovarian & endometrial cancer

  1. 1. Made by: Dr. Isha Jaiswal Moderator: Dr. Madhup Rastogi Date:12th February, 2014
  2. 2.  Gynecological Anatomy  Blood supply & lymphatic drainage  Epidemiology of ovarian & endometrial cancer  Risk factors  Radiological anatomy  Clinical presentation  Examination
  3. 3. DEFINITION: Ovaries are female gonads. The oocytes are formed here. SIZE: in premenopausal age 4×2.5×1 cm with average wt. of 4- 5gm. In menopausal female: ovaries shrink SITUATION: lies in ovarian fossa in lateral pelvic wall. POSITION: variable in nulliparous: nearly vertical so upper & lower pole in multiparous: nearly horizontal due to pull by gravid uterus so medial & lateral ends
  4. 4. EXTERNAL SURFACE: before puberty: smooth surface, greyish-pink color After puberty: uneven surface, grey color PERITONEAL RELATIONS: covering-mesovarium transmit vessel & nerves to & from ovaries SUSPENSORY LIGAMENT OF OVARY:infundibulopelvic ligament. Extend from infundibulum of fallopian tube & upper pole of ovary to ext. iliac vessels. Contain ovarian vessel & nerves.
  5. 5. *ligaments
  6. 6. *PERITONEAL FOLDS
  7. 7.  TUBAL POLE: fallopian tube, ovarian fimbria, suspensory ligaments  UTERINE POLE: connected to lat. end of uterus via ligament of ovary.  ANTERIOR BORDER: attached to the broad ligament via mesovarium  POSTERIOR BORDER: free border related to ureter & fallopian tube.  LATERAL SURFACE: obturator nerves &vessels seperated by peritoneum  MEDIAL SURFACE: fallopian tube
  8. 8. ARTERIAL SUPPLY: ovarian & uterine artery Ovarian artery: arises from abdominal aorta just below renal artery enters suspensory ligament send branches through mesovarium content of broad ligament anastomose with uterine artery VENOUS DRAINAGE: different on both sides Pampiniform plexus:form single ovarian vein drain into IVC on rt. Side drain into left renal vein on left side NERVE SUPPLY: ovarian plexus derived from renal, aortic & hypogastric plexus, accompanies ovarian artery. sympathetic : (T10-11) parasympathetic:(S-2,3,4)
  9. 9. *
  10. 10. Lymphatic of ovary communicate with lymphatics of uterus & fallopian tube. Ascend along the ovarian vessel to drain preaortic & paraaortic nodes Some lymph nodes also drain into inguinal & iliac gp. of nodes
  11. 11. Ovaries are derived from embryonic yolk sac cells Has 2 parts: outer cortex & inner medulla Cortex covered by mesothelium Medulla contains stroma & maturing follicles Follicle give rise to ova germ cells Stromal cells that produce steroid hormones Mesothelium forms epithelial covering of follicular cyst These cell types give rise to germ cell tumor, sex cord stromal tumor & epithelial tm of ovary respectively
  12. 12. *UNITED STATES *2nd m.c genital cancer(1stendometrium) *Lifetime risk of ovarian cancer is 1 in 72 women *Incidence increases with age, peaks at seventh to eight decade of life. Median age of diagnosis 63 years *INDIA *2nd mc genital cancer (1st cervix) *Lifetime risk of developing ovarian cancer ranges from 1:70 to 1:100 *Incidence of ovarian cancer increases from 35 years of age and reaches a peak between the ages 55-64.years
  13. 13. Ovarian cancer is the 9th most common cancer in women
  14. 14. * *
  15. 15. Ovarian cancer is not as treatable as the other cancers… due to lack of early detection. Ovarian cancer is the 5th most common cancer death for women
  16. 16. *
  17. 17. DIFFERENCE IN RACE & ETHNICITY: age adjusted annual incidence per 1 lakh women in year 2005-2012 White women:13.4 Hispanic11.3 American : 11.2 Black:9.8 Asian :9.8 DIFFRENCE IN GEOGRAPHY: Incidence in North America & Europe is 3 to 7 times higher than other parts of asia
  18. 18. * •Pelvic contaminants & toxic agents, e.g. mumps virus •Diet high in saturated fats, red meat • Obesity •Cigarette smoking •Talc power •Early menarche, late menopause •Nulliparity •Excessive gonadotropin •Infertility •Estrogen replacement therapy •Polycystic ovary syndrome, pelvic inflammatory disease •A positive family history (for breast, uterine, ovarian,colorectal cancer, mainly on behalf of 1st-degree relatives (sister, mother) •Increasing age Age Genetic predisposition Environmental factors Reproductive factors RISK FACTORS
  19. 19. * *AGE: * Ovarian cancer incidence increases with advancing age *The lifetime risk of ovarian cancer is approximately 1 in 70, the median age at diagnosis is 63 years, and >80% of ovarian cancer occurs after the age of 40 in the United States
  20. 20. 1.3 3.6 7.2 18.5 23.7 20.4 17.2 8.2 0.1 0.7 2.5 10.7 20.9 24.9 26.2 14 0 5 10 15 20 25 30 < 20 20 - 34 35 - 44 45 - 54 55 - 64 65 - 74 75 - 84 85+ Percentageofagegroupsamongall cases Age Percentage of Incidence and mortality of specific age groups among all cases incidence mortality  Median age at Diagnosis: 63  Median age at death: 71
  21. 21. GENETICS
  22. 22. Hereditary breast-ovarian cancer (HBOC) syndrome: BRCA 1/2 Hereditary Nonpolyposis Colorectal Cancer (HNPCC) syndrome/Lynch syndrome MMR-DNA mismatch repair genes *
  23. 23. * BRCA2 BRCA1
  24. 24. * *5-10% of all cases of breast and ovarian cancer *About 70 to 85% of HBOC cases are caused by mutations in either the BRCA1 or BRCA2 gene *Genetic testing for BRCA1 and BRCA2 gene mutations is available to women with family history
  25. 25. * *Associated With Higher Frequency Of Ovulation *Increasing age *Low parity *Infertility *Early menarche late menopause *Exogenous estrogen & HRT *Increased androgen and gonadotropins *Chronic inflammation *Polycystic ovarian syndrome *endometriosis
  26. 26. * 1) obesity 2) Lack of exercise 3) Diet – saturated fat increases risk 4) high fiber lowers risk 5) Red meat 6) Talc powder
  27. 27. * Pregnancy: interrupt ovulation cycles, reduce gonadotropin secretion, and increase estrogen and progesterone *Progesterone: supress epithelial proliferation *Breastfeeding: linked to incessant ovulation, excess gonadotropin, *Oral contraceptive pill (OCP): suppress gonadotropin surge ,inhibit ovulation. *NSAIDS *Bilateral oophorectomy *Tubal ligation *Hysterectomy *Vitamin D: induce apoptosis, inhibit cell growth down regulate telomerase *
  28. 28. *
  29. 29. Damage to ovarian surface epithelium malignant transformation low-grade tumor -slow growth -less responsive to chemo high-grade carcinoma -rapidly metastatic -chemo-sensitive inflammation Hormonal stimulation (follicle-stimulating hormone, luteinizing hormone, polycystic ovarian syndrome Genetic mutation Incessant ovulation
  30. 30.     *
  31. 31. Malignant cells exfoliate along peritoneal cavity, follow intraabdominal fluid stream. Favored by intestinal peristalsis. Pass up the peracolic gutters, along the intestinal mesentery to the right hemi diaphragm. Metastatic deposits are frequently seen in post. cul-de-sac ,paracolic gutters, diaphragmatic surface, liver capsule, intestinal surface & omentum. Metastasis may also be found in uterus & opposite ovary . Dense tumor caking can cause infiltration into abdominal organs creating mass effect on omentum,ureter,bowel,liver,pancreas, spleen, adrenals.
  32. 32. * The lymphatic converge on hilus and follow the ovarian blood vessels in infundibular ligament to drain to the para-aortic nodes @ level of renal hilum  may drain along the broad ligament to the external iliac nodes in the pelvis.  Less frequently, the spread can occur to the inguinal nodes via the round ligament.  involvement of  pelvic nodes in 80%,  para-aortic nodes in 78%,  inguinal nodes in 40%, mediastinal nodes in 50%, supraclavicular nodes in 48%
  33. 33. HEMATOGENOUS SPREAD: inferquent at time of presentation/ Only 2 to 3% pt with parenchymal liver or lung disease Brain metastasis rare. However more than 50% recurrence occur both within & outside peritoneal cavity at time of treatment failure
  34. 34. * *Peritoneum 85% *Omentum 70% *Liver 35% *Pleura 33% *Lung 25% *Bone 15%
  35. 35. insidious growth and is asymptomatic in the early stage most women do not present for diagnosis until symptoms arise from disease progression to stage III or IV disease Often have vague symptoms that are not very severe 75 – 85 % of cases are advanced at the time of diagnosis
  36. 36. Ovarian cancer patients may have vague symptoms. bloating and increased abdominal girth Pelvic pressure, cramps abdominal pain, back pain Loss of appetite dyspepsia , nausea ,early satiety Pain during intercourse, menstrual irregularities. Unexplained changes in bowel habits, including diarrhea or constipation Changes in bladder habits, including frequency, urgency, incontinence
  37. 37. Characteristics Benign Malignant Mobility Mobile Fixed Consistency Cystic Solid or Firm Bilateral/Unilateral Unilateral Bilateral Cul-de-sac Smooth Nodular INCLUDES Abdomen examination Pelvic examination Lymph node examination
  38. 38. In order to accurately localize the findings on physical examination Abdomen can be divided in nine quadrants. *abdominal examination positioning
  39. 39. * Inspection Palpation Percussion Auscultation 41 Examine the patient in good light and warm surroundings. Patient should be lying on supine position with the head resting on one pillow & lower limbs flexed in order to relax the muscles of the abdominal wall.
  40. 40. *ABDOMINAL EXAMINATION INSPECTION Contour & symmetry Skin: signs of imflammation Shape: flat, distended or scaphoid MOVEMENTS: RESPIRATORY PERISTALTIC: obstruction-gastric, -small intestine -large intestine PULSATILE: aneurysm swelling infront of abdominal aorta
  41. 41. *visible swelling? *Engorged veins? Location:central/sides Direction of flow *Umblicus: inverted/everted TANYOL’S SIGN displacement- -upwards:pelvic lump -downwards:ascitis *Scars *Pigmentation
  42. 42. *ABDOMINAL DISTENSION * Localised: malignancy, hepatomegaly, splenomegaly *Generalized: * Fat (obesity):inverted umblicus *fluid (ascites): dullness * flatus (obstruction): tympanic *faeces (constipation),visible peristalsis * fetus (pregnancy: central dullnes *Full urinary bladder: duul & painfull hypogastrium
  43. 43. Prominent veins (caput medusae) in portal hypertension blood flows trough portocaval anastomoses
  44. 44. 1. Ensure that your hands are warm 2. Stand on the patient’s right side 3. Help to position the patient 4. Ask him to relax & breathe deeply 5. Palpation should be done with flat of hand using flexor surface of finger *ABDOMINAL EXAMINATION PALPATION
  45. 45.  Ask whether the patient feels any pain before you start. Leave the painful area for last  Begin with superficial examination  Move in a systematic manner through the nine regions of the abdomen in the direction of the painful area  Repeat palpation deeply. ABDOMINAL EXAMINATION PALPATION
  46. 46. *Abdominal palpation light palpation Deep palpation
  47. 47. Characteris tics Benign Malignant Mobility Mobile Fixed Consistency Cystic Solid or Firm Bilateral/Un ilateral Unilateral Bilateral Cul-de-sac Smooth Nodular Evaluation of a pelvic mass will be influenced by patient's age, clinical presentation imaging features. most adnexal masses require moderate size for palpation. Ovarian mass is more likely to be:  a malignant in the pediatric, peri-, and postmenopausal age groups benign during the reproductive years.
  48. 48. *ABDOMINAL EXAMINATION PALPATION: findings *Tenderness point: discomfort and resistance to palpation *Involuntary guarding: reflex contraction of the abdominal muscles *Rebound tenderness: patient feels pain when the hand is released *Tenderness + rigidity: perforated viscus *Palpable mass (enlarged organ, faeces, tumour) *Pain with coughing: Peritoneal inflammation
  49. 49. *Also called as rebound tenderness *Pain upon removal of pressure rather than application of pressure to the abdomen *Peritonitis and/ or appendicitis ABDOMINAL EXAMINATION BLUMBERG’S SIGN
  50. 50. Liver Palpation  Align your hand parallel to the Rt. costal margin, begin in the Rt. Iliac fossa and ask the patient to breath in & out through the mouth.  With each expiration, the hand is moved by 1 or 2 cm closer to the Rt. costal margin.  During inspiration, the hand is kept still waiting for liver edge to strike it. PALPATION OF THE LIVER
  51. 51. Spleen Palpation  One-hand technique: start from Rt. iliac fossa toward Lt. costal margin and ask the patient to breath in & out through the mouth. With each expiration, the hand is moved by 1 or 2 cm closer to the Lt. costal margin.  Two-hand technique: Lt. hand is placed posterolaterally over Lt. lower ribs and Rt. hand is placed below umbilicus toward Lt. costal margin.  If spleen is not palpable, roll the patient to Rt. Side and palpate again. *ABDOMINAL EXAMINATION PALPATION OF THE SPLEEN
  52. 52. FLUID THRILL: ascitis/large ovarian cyst  Place the palm of your left hand against the left side of the abdomen  Flick a finger against the right side of the abdomen  Ask the patient to put the edge of a hand on the midline of the abdomen: to cut off any transmitted wave  If a ripple is felt upon flicking we call it a fluid thrill = ascites  May be positive in cyst  Min fluid 2 litres
  53. 53. *SHIFTING DULLNESS: for small amount of fluid *Pt. lies flat *Percussion started fro midline & continued to either flank untill the note becomes dull. *Finger is kept at that point *Pt. asked to turn opposite side *Wait for minute *Area again percussed. *Surest sign of free fluid *Min 500ml
  54. 54. Palpation in Ascites Dipping Maneuver:  To palpate for organomegaly with ascites.  Both hands are placed flat on abdomen and fingers are flexed at MCPs rapidly to displace the underlying fluid.
  55. 55. * ascitis Ovarian cyst  Resonant anteriorly & Dull ness in flanks  Fluid thrill positive  Shifting dullness positive  Dullness anteriorly & resonant in flanks  Fluid thrill positive  Shifting dullness negative
  56. 56. * Notes Elicited Tympanic Predominant due to gas in GI tract Dull Organs, fluid and feces Clinical inference Distension of abdomen Fluid vs. Air Outline Organs Liver, spleen, and gastric An enlarged spleen expands anteriorly, downward, and medially, often replacing the tympany of the stomach and colon with the dullness of a solid organ 58
  57. 57. Liver Span  Upper liver border is defined by percussing down at Rt. 2nd IC space in MCL, until dullness is encountered.  Lower liver border is defined by percussing up at Rt. Iliac fossa in MCL, until dullness is encountered.  Measure the distance between the two dull areas.  Normal liver span is 10+/-2.
  58. 58. *Place the diaphragm of the stethoscope to the right of the umbilicus *Bowel sounds (borborygmi) are caused by peristaltic movements *Occur every 5-10 sec. *Absence of b.s.: paralytic ileus or peritonitis *Bruits over aorta and renal a. could be a sign of an aneurysm and stenosis *ABDOMINAL EXAMINATION AUSCULTATION
  59. 59. *Part 2: anatomy of endometrium & endometrial carcinoma
  60. 60. *ANATOMY OF ENDOMETRIUM
  61. 61. The uterine cavity is lined by endometrium, made up of columnar cells forming tubular glands. The normal endometrium is hormone responsive tissue. Estrogenic stimulation produces cellular growth &glandular proliferation which is cyclically balances by maturational effect of progesterone. The blood supply, nerve supply & lymphatic drainage of endometrium is same as whole uterus
  62. 62. * Chiefly by uterine arteries Partly by ovarian arteries
  63. 63. INTERNAL ILLIAC VEINS UTERINE VEINOUS PLEXUS VAGINAL VEINOUS PLEXUS OVARIAN VEINOUS PLEXUS *
  64. 64. *Supplied by both parasympathetic and parasympathetic nerves through inferior hypogastric and ovarian plexus *Sympathetic nerves from T12 and l1 segment of spinal cord *Parasympathetic nerves from S2 S3 S4. INNERVATION OF UTERUS
  65. 65. Lymphatic drainage of the uterus
  66. 66. * ENDOMETRIAL CARCINOMA
  67. 67. Endometrial cancer usually begins in the lining of the uterus (endometrium). It is sometimes called uterine cancer. Vast majority are adenocarcinomas – commonly detected during perimenopause
  68. 68. DEVELOPED COUNTRIES CA ENDOMETRIUM DEVELOPING COUNTRIES CA CERVIX * MOST COMMON CANCER OF GENITAL TRACT
  69. 69. *Uterine cancer is one of the most common malignancy of female genital tract in west, accounting for 20-25% of all genital cancer in developed countries *In developing countries the incidence is 5-7% of all genital cancer. *The incidence is increasing worldwide in recent years because of longer survival of women ,decline in cervical cancer & role of enviormental factors *
  70. 70. endometrial cancer is the 4th most common cancer in women
  71. 71. endometrial cancer is the 8th leading cause of cancer death for women
  72. 72. Endometrial hyperplasia
  73. 73. Complex hyperplasia without atypia Complex hyperplasia with atypia Simple hyperplasia ENDOMETRIAL CARCINOMA
  74. 74. WHO Classification of Endometrial Hyperplasia Simple Hyperplasia Without Cytologic Atypia Increased number of glands relative to stroma Crowded, clustered glands Complex Hyperplasia Without Cytologic Atypia Back-to-back glands (crowded glands with little or no intervening stroma) Hyperplasia With Cytologic Atypia Variation of size and shape of nuclei Nuclear enlargement Loss of polarity Coarse chromatin clumping Prominent nucleoli Hyperchromatism
  75. 75. Simple hyperplasia– 1% progress to endometrial cancer Complex hyperplasia– 3% Complex hyperplasia with atypia—28% 30-40% of endometrial cancers are found in a background of atypical hyperplasia. Overall, these tend to be lower grade tumors.
  76. 76. EPIDEMIOLOGIC DIFFENCES: TYPE I:Estrogen-related endometrial cancer (Type I) tends to be a lower grade histologically, adenocarcinoma. TYPEII:Endometrial cancers unrelated to hormones (Type II)tend to be a higher grade and stage eg. Papillary serous or clear cell tumors.
  77. 77.  55-65 yrs  oestrogen dependant  previous h/o exposure to unopposed oestrogen.  obesity/hypertension/diabetes  ‘well differenciated’ & mimics proliferative endometrial glands. ER/PR + excellent prognosis * endometrial cancer Type 2  65 – 75 yrs  oestrogen independent  unrelated to hormone exposure  usually arises in an atrophic endometrium usually undifferenciated & aggressive.deep muscle invasion ER/PR -  bad prognosis
  78. 78. RISK FACTORS NULLIPARITY PCOS EARLY MENARCHE LATE MENOPAUSE OBESITY DIABETES HYPERTENSION LYNCH 2 / HNPCC TAMOXIFEN HRT
  79. 79. These risk factors are only helpful in identifying women at risk for type I disease. Risk Factor Approximate Risk Ratios Obesity 1.8–2.4 Nulliparity 2.0–3.0 Diabetes mellitus 2.8 Granulosa-theca cell tumors 5.0 Exogenous estrogen therapy 3.0–8.0 Late menopause (>age 52) 2.4
  80. 80. OBESITY -- particularly BMI=more than 30 obesity reduces level of serum hormone binding protein free estrogen circulates in body peripheral fat : conversion of epiandrostenedione to oestrone  TYPE 2 DIABETES – insulin resistance:insulin induces LH to cause thecal hyperplasia  MENSTURTION-early menstruation (periods starting before age 12) & late menopause (after age 52)  NULLIPARITY  OVARIAN DISEASES: pcod, fibroid, granulosa cell tumor  Liver chirhosis: dec SHBG
  81. 81. ESTROGEN-ONLY REPLACEMENT THERAPY (ERT) oestrogen oestrogen + progestins . TAMOXIFEN:SERM potent antagonist in breast – RX OF CA BREAST partial agonist in uterus-long term use- cause endometrial proliferation,carcinoma
  82. 82. Even though tamoxifen is associated with endometrial cancer, the benefits in treating women with breast ca. outweigh the risks…but women need a yearly gyne exam women should monitor themselves for abnormal vaginal bleeding, discharge, etc screening such as pelvic U.S. is NOT recommended (too many false positives) Limit tamoxifen use to 5 years if there is atypical endometrial hyperplasia, treat and reassess tamoxifen (ie. Consider hysterectomy) *
  83. 83. FAMILY HISTORY – possible genetic link. genetic predisposition seen in 10%, 5% of these have lynch syndrome :Hereditary nonpolyposis colorectal cancer (HNPCC). AD: mutation in DNA repair gene- MSH2,MLH1,MSH6 early age of presentation SCREENING after 35 years by yearly colonoscopy, tvusg & endometrial biopsy *
  84. 84. 89 *Local *Tubal *Lymphatic *Hematogenous
  85. 85. 90 LOCAL SPREAD Slow invasion of the myometrium is the commonest spread. It may produce considerable uterine enlargement; or spread may involve the vaginal vault.
  86. 86. 91  *LYMPHATIC SPREAD
  87. 87. 92 *TUBAL SPREAD Malignant cells can pass along the tube This may account for isolated ovarian metastasis HEMATOGENOUS SPREAD *This pathway might account for the occasional appearance of a low vaginal metastasis; *Liver & lung metstasis
  88. 88. * Type of patient: Nullipara or low parity Middle or upper social class Overweight and obese patients Early menarche and late menopause Hormone therapy Age groups: m.c age of presentation is 55-70 years 75% after menopause. 20-25% perimenopausal. Only 5% before age of 45
  89. 89. m.C symptom: post menopausal bleeding Discharge per vaginum: Abnormal pap smear Difficult or painful urination Urinary or rectal bleed In later stages of the disease, women may feel pelvic pain and experience unexplained weight loss Abdominal distension
  90. 90. Examination: physical examination of the patient with endometrial carcinoma is frequently entirely normal. it should include: abdominal examination(might be difficult due to obesity.) Pelvic examination: Examination of lymph nodes
  91. 91. * There are four steps: External Genital Exam SpeculumExamination: Per vaginum examination The Bimanual Exam The Rectovaginal Exam
  92. 92. * *The Lithotomy Position/or Semi-Sitting Lithotomy Position *Lying in supine position *Thighs flexed and abducted *Feet resting in stirrups *Buttocks extended slightly beyond edge of exam table *Head supported with a pillow *
  93. 93. *Separate the labia and inspect Labia minora Clitoris Urethral orifice Vaginal orifice Note the following:  Discharge  Inflammation  Edema  Ulceration  Lesions
  94. 94. *Assess the support of the vaginal outlet: *With the labia separated by middle and index finger *Ask patient to strain down *Note any bulging of the vaginal walls (cystocele and rectocele). *Inspect the anus at this time, note presence of lesions and hemorrhoids
  95. 95. * *Performed prior to the bi- manual exam. *Always inserted with the speculum blades warmed with warm water and closed
  96. 96. *Hold speculum in right hand *Place two fingers to separate labia *Insert closed speculum obliquely into vagina at a 45 degree angle rotating 50 degrees counterclockwise *Maintaining downward pressure, open blades slowly after full insertion and position the speculum so that the cervix can be visualized *When the cervix is in full view, the blades are locked in the open position
  97. 97. * *Position—is it anteverted, deviated, etc *The position of the cervix gives clues to the position of uterus *Color—should be flesh-colored, but ranges from pink to dark brown (blue or pale??) *Surface characteristics—cysts, erythema *Discharge *Size and shape of os *Any mass or lesion *blood clots
  98. 98. inspection of vaginal walls INSERT THE SPECULUM: inspect the vaginal side-walls for any ulcers, discoloration, discharge or growths. WITHDRAW SPECULUM inspecting the anterior and posterior walls of the vagina, again looking for any ulcers, discoloration, discharge or growths.
  99. 99. * *Palpate the vaginal walls as you insert your fingers for tenderness, cysts, nodules, masses or growths *Identify the cervix, noting the following: *Position--anterior or posterior *Shape- *Consistency--firm or soft *Mobility--move from side to side 1-2 cm in each direction *Tenderness *growth
  100. 100. The vaginal fingers now placed into the posterior fornix of the vagina and its shape is assessed (normally concave away from the fingers, but may be convex towards the fingers if there is a mass in the Pouch of Douglas). Assessing the Pouch of Douglas (recto- uterine pouch):
  101. 101. * The vaginal fingers are now moved into one of the lateral fornices with the abdominal hand moving to the corresponding iliac fossa.  Assess for any adnexal masses on both sides - size, shape, tenderness, etc.  Move the cervix to assess for PID/Endometriosis.
  102. 102. * *It is done with one finger inserted per vaginally and the second finger of same hand in the per rectally *Aim of the examination is to evaluate the extension of disease up to lateral pelvic wall *Both the fingers are moved towards lateral pelvic wall *If tumor extends to pelvic wall the 2 fingers do not converge
  103. 103. *
  104. 104. *RADIOLOGICAL ANATOMY
  105. 105. * #1 = Uterus #2 = Bladder #3 = Urethra #4 = Vagina #5 = Psoas #6 = Iliacus #7 = Obturator Internus *
  106. 106. *#1 - Bladder #2 - Coccyx/Sacrum #3 - Gluteus Maximus #4 - Gluteus Minimus #5 - Iliacus #6 – Ilium BONE #7 - Levator Ani #8 - Psoas Muscle #9 - Rectum #10 - Rectus Abdominis #12 - Uterus
  107. 107. *
  108. 108. Nodes around the abdominal aorta 1: DESCENDING AORTA 4: INFE RIOR VENACAVA
  109. 109. Nodes around the abdominal aort 4 – inferior vena cava 26 – bifurcation of the abdominal aorta at L4 *
  110. 110. * COMMON ILIAC NODES 1 – right common iliac vein 2 – right common iliac artery 3 – left common iliac vein 4 – left common iliac artery 5 – psoas muscle *
  111. 111. * 10 – left external iliac artery 11 – right external iliac vein 12 – right internal iliac vein 13 – right external iliac artery 14 – right internal iliac artery 17 – left external iliac vein 18 – left internal iliac 19 – iliopsoas muscle
  112. 112. * 10 – left external iliac artery 11 – right external iliac vein 13 – right external iliac artery 17 – left external iliac vein 19 – iliopsoas muscle 20 – piriformis muscle
  113. 113. 19 – iliopsoas muscle 21 – internal obturator muscle 22 – sartorius muscle 23 – right femoral vein 24 – right femoral artery 25 – left femoral vein 26 – left femoral artery
  114. 114. * 15 – Iliac musCle 16 – confluence of the left ext and internal iliac vein 5 – psoas muscle 8 – confluence of the right external and internal iliac veins 9 – left internal iliac artery 10 – left external iliac artery 11 – right external iliac vein 12 – right internal iliac vein 13 – right external iliac artery 14 – right internal iliac artery 17 – left external iliac vein 18 – left internal iliac
  115. 115. OVARIAN CANCER A 44-year-old woman with stage ovarian cancer. Axial CT scan of the pelvis shows bilateral complex cystic/solid ovarian masses (o). contiguity to the uterus (u)
  116. 116. OVARIAN CARCINOMA Ovarian adenocarcinoma involving both ovaries (o) and uterus (u) with ascites (a). CT scan of the pelvis (A) shows bilateral ovarian masses with ascites and uterine involvement on the left
  117. 117. *OVARIAN ADENOCARCINOMA WITH URETERAL INVASION AND OMENTAL CAKE. *show a large,pelvic mass (m). *A thick inhomogeneous soft tissue is seen under anterior abdominal wall consistent with omental involvement (o) *.Note the dilated left ureter (long arrow) in A and the pinching of the ureter by the pelvic mass (curved arrow) in B. *Tumor extension to the pelvic sidewall is seen in B(arrowheads)
  118. 118. * *B: Lower abdominal CT scan shows a necrotic paracaval mass (n) consistent with lymphadenopathy. *C: CT scan of the pelvis shows an enlarged right external iliac lymph node (arrow) measuring 1.5 cm in diameter with some necrotic changes seen in its center. *a-aorta *v-inferior vena cava.)
  119. 119. Ovarian adenocarcinoma involving both ovaries with ascites
  120. 120. Big mass!! 33.5 cm. Compressing other abdominal organs. *
  121. 121. *A 61-year-old woman with endometrial cancer. *Note enlargement of the uterus (u)central area of hypodensity *and the surrounding ascites (a)
  122. 122. *Massive para-aortic metastases from endometrial carcinoma with bony invasion. *A. CT scan of the midabdomen shows massively enlarged para- aortic lymph nodes (n) encircling the aorta (a) and displacing it anteriorly. Note the destructive changes in the vertebral body (arrow
  123. 123. *ENDOMETRIAL CANCER
  124. 124. *thankyou

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