Repro GI wk 2
Terms
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- Primary Syphillis
- Treponema Pallidum (spirochete). Inflammatory cells, necrotic debris. Highly infectious chancres. Nonsupporative, nonpainful lymphadenopathy.
- Secondary/Tertiary syphillis
- Secondary – 6-8 weeks after infection – maculopapular skin rash, condyloma lata (looks like accuminatum). Systemic symptoms, bacteremia. Tertiary – Yrs later. Aortitis, CNS lesions, tumorlike lesions
- Granuloma inguinale – Infection, Clinical, Histo
- Calymmatobacterium Granulomatis (Gram neg, encaps) infection. Dense dermal infiltrate w/ necrosis & pseudoepitheliomatous hyperplasia. Histo – Donovan bodies – small round encapsulated bodies in the cytoplasm
- Lympogranuloma venereum
- Clamydia trachomatis infection of lymphatic vessels. Ulcer at contact site & stellate absecesses w/ wpithelioid histiocytes
- Condyloma accuminatum
- Venereal warts. - Koilocytes, thickened skin, hyperkeratin, nucleated keratin. (6& 11 are not associated w/ cancer)
- Molluscum Contagiosum
- Pox virus. Verrucous epidermal hyperplasia. Molluscum bodies in stratum granulosum & stratum corneum. Seen both as STD and in pediatrics.
- Trichomonas Vaginalis
- Flagellated trophozoite. Purulent vaginal discharge, fiery red mucosa (strawberry cervix)
- Two vulvar dystrophies
- Squamous hyperplasia, Lichen Sclerosis.
- Squamous hyperplasia
- Hyperkeratosis, thickened epidermis, dermal inflammation
- Lichen Scelerosis
- Hyperkeratosis, edema, telangiectasia, white macules/papules. Thinned epidermis, area of sparing, inflammation.
- Cervicitis
- Both acute and chronic. Estrogen --> glycogenation --> increased bacterial growth. Can induce squamous metaplasa
- Histology of cervix/vagina
- Cervix – columnar, Vagina – nonkeratinized squamous
- Endocervical Polyps
- Inflammatory tumor w/ irreg vaginal spotting. Soft mucoid lesions often found incidentally. Tx = excision.
- High risk HPV serotypes
- 16, 18, 31, 33
- Mechanism of high risk HPV
- Proteins E6 or E7 accelerate degradation of p53. Also, E7 blocks RB gene, p21. All end up blocking apoptosis.
- CIN
- Cervical equivalent of carcinoma in situ. Graded 1-3
- VIN
- Vulvular equivalent of carcinoma in situ. Graded 1-3
- SIL
- Cytopathologic equivalent of CIN. Not definitive.
- Differences in high grade CIN
- Reduction in cytoplasm, increased nucleus, loss of organization
- Cervical Squamous cell carcinoma
- End product after grade 3 CIN. Invasive.
- Two types of Vulvar SCCA
- HPV associated, Vulvar dystrophy associated (assoc w/ p53)
- VAIN
- Vaginal Intraepithelial neoplasia. Vaginal eq. Of carcinoma in situ. Related to high risk HPV
- DES exposure is associated with which cancer
- Vaginal adenocarcinoma. (benign, but can progress to clear cell adenocarcinoma)
- Vaginal adenosis
- Benign glands found in vagina (shouldn't be there)
- Embryonal Rhabdomyosarcoma
- (Sarcoma botryoides) Polypoide grape like clusters found in infants/children.
- Extramammary Paget's Disease
- Looks like paget's disease of the breast. Pruritic red lesion on labia. May be ass. W/ submuc thickening or tumor. Large clear tumor cells in epidermis
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- Proliferative phase endometrium
- Tubular glands w/ pencil shape nuclei
- Early Secretory Endometrium
- Sub or supranuclear vacuoles, secretion, stroma similar to prolif.
- Midsecretory endometrium
- Maximal stromal edema, maximal glandular secretion
- Late secretory endometrium
- Abundant cytoplasm, round nuclei in stroma (Predecidual).
- Menstrual endometrium
- Stromal collapse, hemorrhage, exhausted secretory glands.
- Anovulatory Endometrium
- Proliferative, but hemorrhage and stromal collapse (apoptotic bodies)
- Inadequate luteal phase
- Common cause of infertility due to inadequate progesterone. Histologic date lags clinical date.Change in bleeding.
- Endometriosis
- Presence of endometrial tissue outside of the uterus
- Adenomyosis
- Endometrial tissue in the myometrium. Makes cystic spaces.
- Mechanisms of endometriosis
- Retrograde flow, lymphatics, etc. or inappropriate Meullerian differentiation
- Two types of endometrial polyps
- Proliferative endometrium and hyperplastic endometrium.
- Endometrial polyps
- Fibrotic stroma & thick walled vessels. Sensitive to estrogen (not progesterone)
- PTEN gene
- Loss of causes endometrial hyperplasia
- Simple endometrial hyperplasia
- Looks like normal endometrium, but too much (glands:stroma = 1:1). Increased variation in gland diameter
- Complex endometrial hyperplasia
- Increased gland:stroma ratio. Atypical rounded nuclei w/ nucleoli
- Endometrial Adenocarcinoma
- Most common invasive carcinoma. Risk: Obesity, diabetes, HT, infertility. Significant polypoid projections.
- Type I vs Type II endometrial carcinoma
- Type I: Pre/Perimenopausal, unopposed estrogen, precursor hyperplasia, minimal invasion, stable. Type II: Postmenopausal, no unopposed estrogen, high grade, deep invasion, progressive
- Endometrioid carcinoma
- From type I endometrial carcinoma. Looks like endometrium, maybe squamous diff
- Type II endometrial carcinoma – advanced
- Becomes Serous Papillary carcinoma (p53) or Clear Cell carcinoma. Bad prognosis
- MMMT
- MMMT – Malignant Mixed Mesodermal Tumor – Endometrial adenocarcinoma. Looks like muscle, forms spindles. Heteralogous = skel muscle/bone Homologous = smooth muscle/endometrial stroma
- Endometrial Stromal Tumor
- Nodule – Well circumscribed aggregate of endometrial stromal cells. Sarcoma – Invasive version (t(7:17))
- Adenosarcoma
- Benign endometrial glands w/ malignant stroma. Better prognosis
- Leiomyoma
- Fibroids. Common, often multiple. Benign. May disseminate, but not cause death
- Leiomyosarcoma
- From myometrium or endometrial stroma. Often metastasize. Bad prognosis. Typical findings for aggressive disease.
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- 4 types of neoplastic ovarian disease
- 1. Surface epithelial stromal tumors. 2. Sex cord stromal tumors. 3. Germ cell tumors 4. Metastases
- Follicle cysts
- Non-neoplastic, from graafian follicles. May cause increased estrogen.
- Corpus luteum cysts
- Non-neoplastic, persistance of corpus luteum. Remove laproscopically
- Polycystic ovarian disease
- Causes: Oligomenorrhea, obesity, hirsutism, persistant anovulation. Not well understood.
- Surface epithelial-stromal tumors (ovarian)
- Normal sized ovary w/ serous lined cysts.
- Types of epithelial ovarian tumurs
- 1. Serous – looks like fallopian tube (low columnar) 2. Mucinous – looks like endocervix or colon. 3. Endometrioid: looks like prolif endoemtrial glands 4. Clear cell 5. transitional- Resembles transitional urothelial cells
- Serous Cystadenoma
- Benign tumor. Large w/ serous lining. Remove laproscopicaly
- Serous Papillary tumor
- Borderline malignancy, not malignant or invasive, but don't remove laproscopically. More irregular lumen.
- Serous papillary cystadenocarcinoma
- Looks like papillary, but glands invade stroma.
- Mucinous ovarian tumors
- Second most common (25%). 85% Benign or borderline. Middle adult life
- Mucinous cystadenoma
- Bening mucinous. Endocervical mucinous epithelium
- Mucinous cystadenocarcinoma
- Malignant version of mucinous cystadenoma. More solid growth w/ intestinal type epithelia. Cellular atypia & stratification
- Pseudomyxoma Peritonei
- Mucinous neoplasm on peritoneal surface. Often from appendix, but metast to ovaries.
- 5 genes implicated in ovarian cancer
- 1. BRCA1 2. BRCA2 3. BRAF 4. TP53 5. KRAS
- Which gene is implicated in mucinous tumors?
- KRAS
- Which genes are implicated in serous carcinoma
- All 5
- Which genes are implicated in endometroid carcinomas?
- CTNNB1, PTEN
- Teratoma (mature)
- Always benign. Shows random mature tissues
- Teratoma (immature)
- Potentially malignant. Grading based on immature neuroepithelium.
- Dysgerminoma
- Nodular tumor w/ fibrous septae. Clear 'fried egg' cells. Equivalent of seminoma in testes.
- Yolk sac tumor
- “endodermal sinus tumor†releases a-fetoprotein. Schillar-duval bodies
- Ovarian Choriocarcinoma
- Histologically identical to placental lesion – syncitio, cytotrophoblasts. High B-hCG. Aggressive, unresponsive to chemo
- Ovarian Fribroma/Thecoma
- From stroma of ovary. Inhibin positive, spindle cells on histo stain.
- Krukenberg Tumor
- Metastises from mucinous carcinoma. Signet ring cells.
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- 3 causes of Urethritis
- Neisseria Gonorrhoea, Chlamydia Trachomatis, HSV
- N. Gonorrhoeae – Morphology
- Gram Neg diplococci
- N. Gonorrhoeae – Pathogenicity (4)
- Pili – adherence & variation. Opa – allow internalization IgA1 protease Endotoxin
- N. Gonorrhoeae – Clinical disease (5)
- Urethrites w/ mucopurulent discharge. Disseminated – Fever, polyarthralgia, septic arthritis, rash PID Epididymitis/prostatitis Gonococcal opthalmia
- N. Gonorrhoeae – Agars
- Mueller-hinton or Thayer-Martin
- N. Gonorrhoeae – Treatment
- PENICILLIN, ceftriaxone, cefixime, ciprofloxacin, ofloxacin. (Also treat for chlamydia)
- Chlamydia T. - Morphology
- Gram neg, obligate intracellular
- Chlamydia T. - Serovars (and disease)
- A,B,C – Endemic Trachoma. D-K – Chlamydia, L1-3 LGV
- Chlamydia T – Lifecycle
- Elementary body – inert, extracellular. RB – Intracellular
- Chlamydia T – Pathogenicity
- Lifecycle & Type III secretion
- Chlamydia T – Disease
- Urethritis (less severe than N.G.), epididymitis, prostatitis, PID, Inclusion conjunctivitis, LGV
- LGV
- Lymphogranuloma veneruem – Ulcerative lesion followed by tender inguinal lymphnodes.
- Trachoma
- Chlamydial infection of the eye. Causes blindness
- Chlamydia T – Treatment
- Azithromycin, doxycyclin. (Or levoflaxacin, erythromycin, levoflaxin)
- Which diseases cause lesions of the genitalia (5)
- Trep Pallidum, H. Ducreyi, C. Trachomatis (LGV) HSV, HPV
- T Pallidum – Morphology
- Very small Spirochete.
- T Pallidum – Primary disease
- Nontender ulcerative lesions
- T Pallidum – Secondary disease
- General rash, esp soles and palms. Nontender enlarged lymphnodes
- T Pallidum – Tertiary disease
- Paresis (cogn., pers changes), Tabes dorsalis, cardiovascular syphillis, gummas
- T Pallidum – Tests
- Nontreponomal (VDRL, RPR) for screen, Treponomal (FTA-ABS, MHA-TP) for diagnosis.
- Syphilis – treatment
- PENICILLIN, or doxycyline/tetracycline. Also test for HIV
- H Ducreyi – clinical
- Chancroid – genital lesions w/ tender inguinal nodes & shaggy border
- Herpes – Treatment
- Acyclovir
- Causes of Vaginitis (6)
- C Trachomatis, N gonorrhoeae, HSV, T Vaginalis, bacterial, yeast, Dave Rosenthal
- Trichomonas Vaginalis – morphology
- Pear shaped protozoan. Flagellated & motile.
- Vaginitis – clinical
- Malodorous yellow/green discharge, itching, dysuria, urination, dyspareunia, strawberry cervix.
- T Vaginalis – treatment
- Flagyl
- Bacterial Vaginalis
- Disruption in bacterial flora of vagina displaces lactobacillus, raises pH
- Bacterial Vaginalis – treatment
- Metronidazole or clindamycin
- PID
- Ascending infection of N.G., C.T., or others. Causes infertility/ectopic pregnancy. Also mucopurulent discharge, pain.
- PID typical treatment
- Doxycycline (for C.T.), cefoxitin (for anaerobes)
- Causes of epidymitis
- C trachomatis, N gonorrhoeae
- Causes of cervicitis
- C Trachomatis, N gonorrhoeae, HSV
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- What is the most common STD?
- HPV. (Second is probably Chlamydia)
- Which STD is most easily transmitted?
- Gonorrhea
- Which cell type do Gon. & Chlam infect?
- Columnar epithelia.
- Which cell type does HIV infect?
- Langerhans, CD4+ or CCR5+ immune.
- What increases susceptibility to HIV (3)
- STD's, Hormones, Progesterone (estrogen decreases)
- Two STDs that are passed transplacentally
- HIV, Syphillis
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- HIV – GP120
- Binds CD4 receptors (necessary but not sufficient)
- 3 required receptors in HIV tx
- CD4 CCR5, CXCR4
- In utero vs intrapartum HIV transmission risk
- In utero – 25-40% intrapartum – 60-75% (additional risk in breast feeding)
- MAC
- Mycobacterium Avium. Presents w/ disseminated multi organ infection (fever, night sweats, weight loss, fatigue, diarrhea, abdominal pain)
- IRIS
- Immmune Reconstitution Inflammatory Syndrome – Acute systemmic inflammatory response when imune system is recovering under ARV therapy.