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160 Cards in this Set
- Front
- Back
Normal reproductive system consists of? |
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Where does spermatogenesis occur |
In the testes (situated in scrotum, suspecnded by spermatic cords and surrounded by membranes) |
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Exocrine portion |
Seminiferous tubules (produce spermatozoa) |
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Endocrine portion |
Intestinal cells of Leydig (produce testosterone) |
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Testicular disorders - (infections of the testes) |
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Epididymo-ochitis |
Associated with infections that enter through the epididymis |
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Acute bacterial epididymo-orchitis |
May lead to permanent scarring of seminiferous tubules and epididymis, fertility impairment |
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Viral orchitis |
Usually unilateral, the result of infection by mumps virus after puberty, in some bilateral, reduced fertility may occur |
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Tuberculous epididymo-orchitis |
Bloodstream spread to epididymis during active pulmonary TB; Epididymis destroyed and infection spills over into testis |
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Intrascrotal lesions |
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Hydrocoele |
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Haematocoele |
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Speramtocoele |
Semen accumulates in spermatic cord due to dilation of ducts in the head of epididymis (epididymal cysts) Congenital or may be acquired; Usually painless and in most cases it does not require any therapy |
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Chylocoele |
Lymph in the tunica albuginea occuring with lymphatic obstruction in the region Parasitic worm infestations (Wuchereria bancroftii) with resultant elephantiasis Size of scrotum may become enormous -> atrophy of testis |
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Varicocoele |
Varicose pampiniform venous plexus in the spermatic cord A soft, elastic swelling, sometimes causes pain typically in left testis "Bag of worms" presentation 15-25 years Congenital causes, Ca kidney; Can lead to thrombosis, intrascrotal pressure, infertility |
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Inguinal Hernia |
Herniation where a loop of intestine enters the inguinal canal, sometimes filling the whole scrotal sac Congenital patent vaginal process (~1% paediatric disorders) or acquired later when obliterated vaginal process opens due to excessive stress placed on it (lifting heavy weights, increased intra-abdominal pressure, after surgery) |
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Testicular tumours - Aetiology |
Rising incidence, 15-45 years Crytorchidism Genetic factors Hormonal effects Tight clothing Idiopathic |
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Main groups of testicular tumours |
Germ cell tumours (95%) Sex cord and stromal tumours (5%) |
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Germ cell turmours |
Derived from multipotential germ cells lining the seminiferous tubules Predisposed by maldescent or chromosome 12 abnormaility |
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Sex cord and stromal tumours |
Derived from specialized and non-specialized support cells of the tesis |
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Germ cell tumours |
Seminoma (classic) Spermatocytic seminoma Teratoma Yolk sac tumour Choriocarcinoma Embryonal carcinoma |
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Seminoma |
Totipotent germ cells differetiate to spermatocytic cell lines Carcinoma of the seminiferous epithelium lining the testicular tubules ~30-45 years, painless enlargement of testis; bulging pale mass shows clear cells arranged in lobules Direct or late blood spread; Treat by orchidectomy and radiotherapy; good prognosis ~85% 5-year survival |
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Spermatocytic seminoma |
Totipotent germ cells differentiate to spermatocytic cell lines Similar to classic seminoma but more prevalent in elderly men >60; Behaves in benign manner - does not metastasize |
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Teratoma |
Primitive totipotent cells differentiate to various somatic embyronal tissues such as epithelium, cartilage, smooth, muscle, neural tissues etc (ie. contain tissues derived from ectoderm, mesoderm and endoderm) |
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Teratoma - mature somatic elements |
Occur in young. Areas in skin, thyroid, bone, cartilage etc. = Organoid tumours Good prognosis (behave in benign manner) |
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Terotoma - immature somatic elements |
Peak age of incidence is 30 years. Highly malignant anaplastic tumours. Spread to liver and lungs, late presentation. Poor prognosis. ~25% 5-year survival |
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Yolk sac tumour |
Primitive totipotent germ cells differentiate into extraembryonic tissue such as the yolk sac Most common testicular tumour <3yrs; Good prognosis - chemosensitive alpha-fetoprotein secreted into blood, detected as a tumour marker |
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Choriocarcinoma |
Primitive totipotent germ cells differentiate into extraembryonic tissue such as trophoblastic tissue Rare, yet highly malignant, not very radiosensitive, seen in men 20-30 years; poor prognosis; HcG detected in blood as tumour marker |
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Embyronal carcinoma - |
Primitive totipotent germ cells show no specific differentiation - just some epithelial pattern characteristics ~20-30yrs; Composed of immature large undifferentiated cells, resembling those of the early embryo - highly malignant Early invasion of lymphatic and blood vessels. Responds well to cytotoxic chemotherapy |
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Sex cord and stromal tumours |
Interstitial cell tumour Sertoli cell tumour |
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Interstitial cell tumour |
Cancer of Leydig cells; Sexual precocity associated with increased testosterone levels in children |
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Sertoli cell tumour |
Well circumscribed, usually benign tumour |
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Prostate Gland |
The prostate gland surrounds the urethra as it leaves the bladder, and is composed of 5 lobes of glandular tissue supported by a fibromuscular stroma Acute prostatis Chronic prostatitis Benign Prostatic hyperplasia Carcinoma of the prostate |
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Acute prostatitis |
Common after surgery, instrumentation of the urethra. Also after acute infection in bladder/urethra Escherichia coli, Enterococcus faecalis, Proteus spp (UTI) Neisseria gonorrhoeae or Mycoplasma and Chlamydia, (STD) Typical AI - leads to suppuration and abscess formation Enlarged, painful prostate - when palpated by DRE (digital rectal exam) is very tender and soft |
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Chronic Prostatitis |
Due to progressive acute prostatitis, TB (renal or epidydymal) Hard, shrunken prostate, often containing calcified concretions; CI infiltrate and scarring |
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Benign Prostatic Hyperplasia (BPH) |
Affects most men > 70 (80% > 80yo), Increased in cell number of glandular and stromal components Caused by hormonal imbalances - raised oestrogen, lowered testosterone levels Oestrogen may render cells more susceptible to the action of dihydrotestosterone - synthesized in prostate from circulating testosterone Lateral and median lobes predominantly affected |
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BPH symptoms |
Obstruction of urine flow causes progressive difficulty in micturition Poor stream, frequency, nocturia, dysuria, predisposes to UTI, prostatitis |
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BPH Diagnosis |
DRE reveals a firm rubbery gland, biopsy for confirmation |
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BPH Treatment |
TURP (transurethral resection of prostate) or laser treatment to reduce size Hormonal/drug treatment, esp. in elderly or debilitated men |
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BPH Prognosis |
Good - does NOT predispose to prostatic carcinoma |
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Carcinoma of the prostate |
Very common adenocarcinoma, frequency increases >55yr (80%> 80-90yrs) Caused by genetic factors, exposure to cadmium, raised testosterone levls, decreased immunological surveillance Posterior lobe predominately affected, asymptomatic initially as tumour slow growing |
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Prostate cancer symptoms |
Late due to metastases in bone, include back pain, weight loss, anaemia |
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Prostate cancer diagnosis |
Palpable mass (firm, nodular) detected by DRE, raised PSA levels, raised acid phosphatase, confirmed by biopsy
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Prostate cancer treatment |
Surgery, radiotherapy and hormonal therapy, anti-androgen therapy |
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Prostate cancer prognosis |
Stage A Stage B Stage C Stage D |
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Stage A - prostate cancer |
Tumour confined to gland (80% 5 yr survival) |
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Stage B - prostate cancer |
Clinical manifestation evident (50% 5 yr survival) |
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Stage C - prostate |
Invasion of surrounding organs, pelvic and para-aortic lymph nodes (35% 5 yr survival) |
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Stage D - prostate cancer |
Vascular spread to bone, extra-pelvic metastases (20% 5 yr survival) Overall prognosis; 25% 5 yr survival |
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Penile disorders |
Hypospadias Epispadias Phirmosis Urethritis Balanitis SCC of Penis |
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Hypospadias |
Urethra opening on the ventral (underside) surface of penis, more common |
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Epispadias |
Urethra opening on the dorsal (upperside) surface of penis Both congenital malformations of the urethral canal |
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Phimosis |
An abnormality of the foreskin leading to non-retractable or tight prepuce |
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Urethritis |
Infections of penile urethra Gonnococcal due to Neisseria gonorrhoeae (STD) - Urethral pain and a purulent discharge Non-gonococcal due to Chlamydia trachomatis (STD) - purulent urethral dischage, may lead to Reiter's syndrome (arthritis, urethritis and conjuntivitis) |
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Balanitis |
Infections of the glans and foreskin (e.g. Candida albicans, pyogenic and anaerobic bacteria) |
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SCC of Penis |
Inadequate hygeine, precense of prepuce SCC (warty, fungating mass) invades along the shaft of the penis, may spread to inguinal lymph nodes Ulceration, deformity, urinary fistulae may form Surgical amputation of the penis, block dissection of the groin 5 year survival > 95% (no lymph spread); if inguinal spread, 50-70% 5 year survival |
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Normal female reproductive system |
Dependent on changing hormonal stimulation; comprises vulva, vagina, uterus, fallopian tubes, ovaries, breast |
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Gynaecologic pathology |
Abnormalities of the female reproductive system |
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Obstetric pathology |
Abnormalities related to conception, pregnancy or childbirth |
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Menarche |
Beginning of menstruation ~12yrs Menstrual cycle occurs on average every 28 days - antipates pregnancy by preparing uterus for implantation of fertilized ovum |
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Menopause |
End of productive period ~50 years |
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Disease of the Vulva - SCC of vulva |
Usually in elderly women
E.g. Verrucous carcinoma Largely warty cauliflower-like growth that grows slowly, invading local tissues Well-differentiated, confined to vulva and inguinal LNs - good prognosis Invasion to bladder/rectum, spread to illiac LNs/bloodstream - bad prognosis |
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SCC of vulva - facts |
Arise de novo, or in epithelium with severedysplasia & carcinoma in situ ie. vulval intraepithelial neoplasia (VIN) (see Figure 19.5) VIN seen in younger women; HPV16demonstrated in 70-90% cases & show HPV warty change Increased risk of SCC progression in young womenwho smoke cigarettes |
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Disease of the vagina |
SCC of the vagina - Rare, much more common to see secondaries from cervix, endometrium and ovaries
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Diseases of the Cervix |
The ectocervix is lined by squamous epitheliuim and the endocervical canal by mucous secreting columnar epithelium The squamocolumnar junction is the site where most diseases of cervix occur |
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Carcinoma of the Cervix |
Accounts for 3-5% of female cancers, peak incidence ~50yrs Death decreasing with earlier detection; HPV detected in >60% cases; HPV 16 and 18 most common Gardasil vaccine protects against the 2 high-risk HPV types (16 and 18) and the 2 low-risk HPV types (6 and 11) Linked with sexual activity, early age of 1st intercourse or pregnancy, pultiparity Typically occurs at squamocolumnar junction at the region of the cervical OS Metaplasia and dysplasia of epithelial may be seen; Nodular, polypoid of diffusely infiltrating mass seen on colposcopy ~95% cases are SCC ~5% adenocarcinoma |
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Carcinoma of the cervix - symptoms |
Vaginal bleeding, esp. Postcoital due to ulceration of tumour Bowel/urinary tract obstruction, rectovaginal/vesicovaginal fistulas, 2 degree infection -> purulent vaginal discharge |
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Carcinoma of the cervix - diagnosis |
Pap smear test - cytological examination of cervical cells |
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Prognosis |
Stage 0 Stage 1 Stage 2 Stage 3 Stage 4 |
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Stage 0 - cervical cancer |
Carcinoma in situ; 100% 5 yr survival |
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Stage 1 - CC |
Microinvasive carcinoma, confined to cervix; 90% 5 year survival (with treatment) |
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Stage 2 - CC |
Direct spread of tumour, invasion of vagina; 82% 5-year (with treatment) |
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Stage 3 - CC |
Lymphatic spread, spread to pelvic wall, lower vagina or ureters 35% 5-year survival (with treatment) |
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Stage 4 |
Haemotogenous spread, rectum, bladder wall and outside pelvis; 10% 5-year survival (with treatment |
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Treatment of CC |
Cauterization, laser therapy, removal by biopsy (dysplasis, stage 0) Conization of cervix (stage 1); Hysterectomy and radiotherapy (stages 2-3); Chemotherapy (stages 3-4) |
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Diseases of the Uterus |
The endometrium lines the uterus, responding to cyclical hormonal stimulation during the menstrual cycle The myometrium is composed of smooth muscle cells and supporting stromal and vascular tissue |
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Endometriosis |
Ectopic endometrium develops outside uterine cavity (myometrium, ovaries, fallopian tubes, less common in interstinal wall, bladder) Very common 1 in 15 (~7%) of women of reproductive age -> infertility in 30% cases Macroscopically, foci ofendometriosis appear as cystic and solid spaces; Histologically, endometrial glands and stroma seen; Fibrosis may occur with repeated inflammation and organization |
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Endometriosis interna/Adenomyosis |
Endometrial tissue in myometrium |
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Endometriosis externa |
Endometrium tissue outside of uterine wall |
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Endometriosis - Aetiology |
Poorly understood, but 3 theories Retrograde menstruation Metaplasia theory Metastatic theory |
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Retrograde menstruation |
Reflux of shedding endometrium during menstruation, through fallopian tubes into the peritoneum |
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Metaplasia theory |
Metaplasia of peritoneal epithelium may cause differentiation into endometrial tissue |
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Metastatic theory |
Endometrium spreads to distant sites (nodes, pleura, lungs, umbilicus) via lymphatics or blood vessels |
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Endometriosis - symptomalogy |
Asymptomatic or slight pain, discomfort during menstruation In severe cases, dysmenorrhoea; dyspareunia; dyschezia; dysuria; menorrhagia; haemochezia; haematuria, diarrhoea; constipation; premenstrual tension (PMT), depression, marked mood swings; insomnia; low energy, fatigue, infertility, rupture of chocolate cysts in the ovary |
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Treatment of endometriosis |
Endocrine manipulation of endometrial growth is usually effective or surgically removed (via laparoscopy) |
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Carcinoma of endometrium |
Account for ~7% of female cancers; most common malignant tumour of female genital tract Nearly all are adenocarcinomas. Divided into two main groups:
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Carcinoma of endometrium - aetiology |
Causes of hyperoestrinism (hyperplasia/tumours), obesity, infertility/nulliparty, genetic factors |
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Carcinoma of endometrium - Symptoms |
Unusual bleeding, leukorrhoea; painful, tender unterus if pyometra occurs (due to obstruction and 2 degree infections) |
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Carcinoma of endometrium - Treatment |
Surgical excision or hysterectomy; radiotherapy and/or chermotherapy |
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Carcinoma of endometrium - Prognosis |
Very good due to usual detection in the early stages (better than cervical and ovarian) Stage 1-4 |
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Carcinoma of endometrium - stage 1 |
Corpus of uterus only; 90% 5-yr survival (with treatment) |
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Carcinoma of endometrium - stage 2 |
Corpus and cervix; 50% 5-yr survival (with treatment) |
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Stage 3 |
Invasion confined to pelvis; 30% 5 yr survival (with tt) |
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Stage 4 |
Invasion outside pelvis or involves bladder/rectum; 10% 5-yr survival (with treatment) |
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Fibroleiomyoma of the Uterus |
Fibroid; most common benign tumour of female genital tract Oestrogen-dependent tumour of smooth muscle cells and fibroblasts; NOT premalignant Arise at a young age, anywhere in myometrium, becoming symptomatic in decade before menopause Typically rounded, rubbery, pale nodule (whorled appearance on cut surface) and well demarcated by a fibrous capsule Require oestrogen for growth so often regress after menopause; Common cause of infertility, may complicate pregnancy |
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Fibroleiomyoma of uterus |
Symptoms - Dysmenorrhoea, menorrhagia, discomfort, obstruction or pressure effects on bowerl and bladder Treatment - Surgery excision or hysterectomy |
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Ovaries |
Paired organs located in the ovarian fossa, one on each side of the uterus Comprise surface 'germinal' epithelium, stroma (produces steroid hormones), & follicles (contain germ cells) Secrete oestrogen and progesterone and are dependent on pituitary gonadotrophic hormones |
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Non-neoplastic cyst |
Extremely common, the majority arising from the development of Graafian follicles, others derived from surface epithelium, Stein-Leventhal syndrome |
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Stein-Leventhal syndrome |
Characterised by formation of multiple ovarian follicular cysts (polycystic ovarian syndrome); Three theories 1. Defect in hypothalamic pituitary axis -> increased FSH -> Increased ovarian follicles - >don’t rupture due to no LH surge -> increased ovarian androgens 2. Defect in ovarian steroidogenesis mayfavour androgen production 3. Insulin resistance in peripheraltissues (detected in obese patients), may divert metabolic pathways to androgensynthesisPresents 20-30yrs, associated withobesity, hirsutism, irregular periods or amenorrhoea (reduced fertility) |
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Stein-Leventhal syndrome - Treatment |
Exogenous hormone administration to correct imbalance -> normal pregnancy Ovaries show thickening of the capsule and multiple follicular cysts with stromal hyperplasia |
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Neoplasms of the ovary |
Epithelial tumours Sex cord and stromal tumours Germ cell tumours |
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Epithelial tumours |
Derived from surface epithelium which in turn derived from embryonic coelomic epithelium, therefore differentiate into many tissues |
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Epithelial tumours - tubule differentiation |
Serous ovarian tumours (cystadenomata, cystadenocarcinomata - most common ovarian Ca)
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Endocervical differentiation |
Mucinous ovarian tumours (mucinous cystadenoma, mucinous cystadenocarcinoma) Benign or malignant; 35% 10-yr survival (better than malignant serous) |
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Endometrial differentiation |
Endometriod or clear-cell ovarian tumours; rarely benign; Overall, 40% 5yr survival |
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Transitional differentiation |
Brenner ovarian tumours; cells resemble transitional cell epithelium of urinary tract Benign or malignant, good prognosis |
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Sex cord and stromal tumours |
10% of ovarian tumours; May secrete oestrogen, giving rise to endometrial hyperplasia and predisposing to endometrial carcinoma Fibromas Thecomas Granulosa cell |
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Fibromas |
Benign, mainly seen in postmenopausal women may see ascites |
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Thecomas |
Usually benign seen in young women, solid and usually produce oestrogen |
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Granulosa cell cell |
Usually benign, >50% occur post-menopause, also seen in young girls (precocious puberty, early menarche) 75% secrete oestrogen, excellent prognosis if confined to ovary |
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Germ cell tumours |
Teratomas Yolk sac Choriocarcinoma |
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Teratomas - GCT |
~ 10% of ovarian tumours; Mostly benign cystic tumour of ovarian germ cells Extremely well-differentiated with a variety of tissue types (teeth, bone, respiratory tract tissue, hair) alpha-foetoprotein positive 25-50% of cases |
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Yolk sac - GCT |
Rare, highly malignant, usually in women <30yrs; secrete alpha-fetoprotein (tumour marker) |
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Choriocarcinoma - GCT |
Rare, highly malignant, composed of trophoplastic cells; secret hCG (tumour marker) |
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GCT - Aetiology
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Each year, more than 1200 Australian women are diagnosed with ovarian cancer, ~800 will die from the disease |
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GCT - Symptamology |
Presents when tumour enlarges, causing pressure effects and accidental complications Pain, discomfort, GIT complaints, urinary frequency, abdominal distension, acute abdomen |
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GCT - Diagnosis |
Rare early, usually on routine pelvic examination; No current good tumour marker or screening test |
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GCT - Prognosis and staging |
Similar for all malignancies of the ovaries; Due to late diagnosis, average 5yr survival ~40% |
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GCT - Stage 1 |
Tumour is confined to ovary with or without ascites (good prognosis) |
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GCT - Stage 2 |
Growth involves one or both ovaries with pelvic extensions |
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GCT - Stage 3 |
Intraperitoneal metastases outside pelvis with/without growth in retroperitoneal nodes |
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GCT - Stage 4 |
Distant metastases present - liver, lungs (grave prognosis) |
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GCT - Treatment |
Usually, surgery, radiotherapy and chemotherapy all used in combination
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Disorders of pregnancy |
Pre-eclampsia of Pregnancy Eclampsia of pregnancy Ectopic pregnancy Placental Abruption Placental Previa Congenital diseases |
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Pre-eclampsia of pregnancy |
~10% prenancies; Associated with multiple pregnancies, primigravidae > 35 years Characterised by increased BP, proteinuria & peripheral oedema Develops from ~ week 20 of pregnancy and continues to end of 1st week post partum Rarely fatal to mother; reduced placental blood flow and foetal hypoxia; if BP not controlled and proteinuria appears, delivery of foetus Delivery improves condition dramatically; full recovery |
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Eclampsia of pregnancy |
Rare; Pre-eclampsia symptoms and any or all of the following: Frontal headaches; fits; DIC; Kidney and liver failer; Coma May follow pre-eclampsia or may develop de novo. If untreated, may be fatal to mother, foetus or both |
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Ectopia pregnancy |
Fertilized ovum implants outside uterine cavity Most commonly in fallopian tube due to previous tubal damage (Chlamydia infections, tubal surgery for contraception purposes, endometriosis) but also in peritoneal cavity, ovary, cervix In tubal pregnancies, embyro grows normally for 2-6 weeks -> 'acute abdomen' presentation -> tube may rupture An intra-abdominal pregnancy is carried to full term and delivered via laparotomy In rare cases, embryo may die from poor placental attachment; necrotic embyro may calcify via dystrophic calcification (lithopaedion) |
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Placental abruption |
Prematureseparation of a normally located placenta; Abdominal pain, antepartumhaemorrhage; May cause stillbirth, maternal death
Idiopathic, but more likely to occur inwomen with history of abruption, many previous pregnancies or hypertension |
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Placental Previa |
Implantationof the placenta low in the uterus so that it encroaches on the lower segment May lead to antepartum haemorrhage or anobstructed labour. Four grades of placenta previa are recognized |
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Grade 1 - PPrevia |
Edge of placenta enroaches on the lower segment, but does not reach the internal os |
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Grade 2 - PPrevia |
Placenta occupies the lower segment, with its edge reaching the internal os but not covering it |
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Grade 3-4 - PPrevia |
Placenta implanted in the lower segment and either party (grade 3) or completely (grade 4) covers internal os |
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Congenital disease |
Infectious agents or exposure toharmful environmental agents (chemicals, radiation) cancomplicate a pregnancy/delivery There is maximalsensitivity to congenital defects in first 3 months of foetal development Infections may be transmitted viaplacenta, however an infected birth canal during childbirth can also lead tocomplications Rubella virus Listeria monocytogenes N.Gonorrhoea Treponema pallidum Toxoplasma HIV M.Tuberculosis |
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Rubella Virus |
Crosses placenta; ~25% babies born to mothers with rubella in first 4 months pregnancy develop congenital malformations |
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Listeria monocytogenes |
Crosses placenta, causes spontaneous abortion or babies die ~2-3 days old due to widespread necrosis of internal organs |
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N. Gonorrhoea |
An infected birth canal during childbirth may cause opthalmia neonatorum |
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Treponema pallidum |
Crosses placenta; causes spontaneous abortion or congenital syphilis (if not treated before 5th month) |
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Toxoplasma gondii |
Crosses placenta; causes spontaneous abortion or still birth; surviving babies may have microcephaly/hydrocephaly |
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HIV |
Crosses placenta oracquired during birth/lactation; Causes development of AIDS |
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M.Tuberculosis |
Crosses placenta; Causesfoetal tuberculosis |
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Normal adult female breast |
Composed of lobules of glandularepithelial tissue (small ducts terminating in terminal ductules or acini) Theselink by branching to larger ducts that eventually converge and drain at thenipple Within lobules, between the epithelialtissue is a cellular, specialized hormone-responsive stroma (intralobularstroma) Between lobules, there isnon-specialized fibrocollagenous tissue and prominent adipose tissue(extralobular stroma) Developmental changes occur in response to hormonalchanges from puberty to maturity, through pregnancy and menopause |
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Tumours of the breast |
Fibroadenoma Carcinoma of the breast |
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Fibroadenoma |
Most commonbenign breast lump, typically 25-35yrs; Firm, rubbery, well-circumscribedlesions Comprise localized proliferation of branchingduct-like structures (epithelial component) and abundant fibrous tissue(stroma) Presents as ahighly mobile smooth solitary lump, typically 1-4cm diameter |
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Carcinoma of the breast |
Very common, ~20% of all malignanciesin women, affects up to 1 in 10 women Incidence s steeply through the reproductiveyears, and then less so from the age of menopause (~50yrs) Main aetiological factors are oestrogen exposure and geneticpredisposition (eg. gene mutations in BRCA1, BRCA2, p53) Also, geographical & dietaryfactors, epithelial hyperplasia, early menarche, nulliparity, late menopause,exogenous hormones |
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Four ways breast cancer presents |
1.Palpable lump in the breast 2. Abnormality detected on mammography 3. Incidental histological finding inbreast tissue removed for another reason 4. Detection of metastatic deposits inother organs |
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Types of Breast cancer |
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Non-invasive DCIS |
Usually detected as a palpable lump ormammographic abnormality
Histologically, atypical cells fill anddistend small & medium-sized ducts
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Non-invasive LCIS |
Usually detected as a mammographicabnormality not as a palpable lump Histologically, atypical cells fill themammary lobules; risk of invasive carcinoma Most breast cancers are invasiveadenocarcinomas |
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Invasive ductal carcinoma |
Most common type of breast cancer; islands of cells, dense fibrous stroma |
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Invasive lobular carcinoma |
2nd most common type; narrow cords of cells, dense fibrous stroma |
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Tubular carcinoma |
Composed of cells that form regular tubular structures (resemble small ducts). Well differentiated |
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Mucoid carcinoma |
Composed of cells that secrete mucin into stroma -> soft, slimy texture; Well differentiated |
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Medullary carcinoma |
Composed of well-circumscribed masses -> soft and fleshy texture; Dense lymphocytic infiltrate |
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Spread |
Local Lymphatic Vascular |
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Local spread |
Into adjacent breast, overlying skin (nipple retraction/discharge), pectoral muscles (deep fixation) |
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Lympathic |
Into regional lymph nodes -> may affect lymphatic drainage of skin, causing a peau d'orange appearnace |
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Vascular |
To bone (pathological fractures, hypercalcaemia, leukoerythroblastic anaemia, spinal-cord compression) To lung (breathlessness), pleura (effusion of breathlessness), and ovary |
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Diagnosis of breast cancer |
Breast self examination (BSE); Mammography; biopsy; needle or lumpectomy |
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Treatment |
Lumpectomy Mastectomy Radical mastectomy Radiotherapy Chemotherapy Hormone therapy |
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Staging and prognosis |
Stage 1: Confinedto breast (~80-90%, 5yr survival) Stage2: Confined to breast & LNs (~60-80%, 5yrsurvival) Stage3: Deep tissue fixation (~25%, 5yr survival) Stage4: Distant metastases (~10%, 5yr survival) Grade of tumour assessed by looking at degree of glandformation, pleomorphism, numbers of mitoses Grade I: 85%, 10yr survival GradeII: 60%,10yr survival GradeIII: 45%,10yr survival Molecular classification of breast cancer alsotaken into account (see Figure 20.16) Gene profilingallows identification of carcinoma subtypes related to prognosis based onexpression ofER (oestrogen receptor) and HER-2 (human epidermal growth factor receptor 2) |