Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
124 Cards in this Set
- Front
- Back
193
|
193
|
|
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
|
|
194
|
194
|
|
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.
|
|
195
|
195
|
|
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.
|
|
196
|
196
|
|
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
|
|
197
|
197
|
|
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
|
|
198
|
198
|
|
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.
|