Female GU Path (Carpenter)- Leah : ) Flashcards
1
Q
Normal cervical epithelium
A
ectocervix: stratified squamous
endocervix: columnar cells w/ mucin
(not true glands)
2
Q
Appearance of normal:
endometrium?
myometrium?
A
endometrium: glands and stromal tissue
myometrium: thin SM cells w/ cigar like nuclei
3
Q
Normal fallopian tube epithelium appearance?
A
ciliated/nonciliated columnar cells
+intercalated peg cells
4
Q
HSV2: basic viral structure
A
DS DNA, linear
icosahedral, enveloped
5
Q
Time course HSV genital infection?
Likelihood that HSV will be transmissed via sex?
A
In 1/3 patients who have intercourse w/ infected individuals:
lesions appear ~3-7 days later, heal ~ 1-3 weeks
can establish latent infection
6
Q
Locations of HSV2 lesions?
Test (dx) of choice?
A
painful, red external lesions (vulva/vagina/cervix)
dx w/ PCR (pap not sensitive, Ab’s absent in acute phases-if present indicate reactivated latent infxn.)
7
Q
Appearance of HSV cells on histo?
A
“ground glass nuclei”
-looks almost like soap bubbles or deer turds to me (Haha!)
8
Q
Molluscum Contagiosum:
basic viral structure
A
Poxvirus, dsDNA
complex capsule, naked
cytoplasmic replication**
9
Q
What are the types of molluscum contagiosum viruses?
How are they transmissed?
A
-Types 1-4, Type 1 most common, Type 2 on genitals
(similar to herpes- 1 common, 2 genital)
-Can be transmitted sexually, by skin contact, or by contact with contaminated surfaces (kids)
10
Q
What do molluscum contagiosum infections look like grossly and on histo?
A
gross: dome shaped lesions w/ dimples
histo: intranuclear inclusions
11
Q
Candida: for the boards, what is the structure of this fungus?
How does it look on wet prep?
A
Dimorphic
mold in the cold (pseudohyphae)
yeast in the heat (germ tubes)
Spaghetti and meatballs on wet prep
12
Q
Prevalence of candida infections?
Risks for yeast infection (4)?
Sx and Dx?
A
Most common female GU infection
Risks: OCPs, pregnancy, diabetes, Abx
(Immunosuppression/ flora or pH disruption)
Sx: white cottage cheese discharge, itching
Dx: wet prep
13
Q
Trichomonas:
What is the structure of this bug? How does it look on wet prep?
A
Protozoa w/ flagellum, may be motile on wet prep
14
Q
Classic presentation of trichomonas infection? (3)
Risk assc with infection (2)?
Dx method?
A
- strawberry cervix; green/ yellow discharge; +whiff test
- ^^ HIV/ preterm delivery (thus low BW) risk
- Dx on wet prep
15
Q
Gardnerella:
bacteria structure, prevalence in women?
A
- pleomorphic gram negative rod
- some evidence that it may be normal flora, 70% of those infected aren’t symptomatic.
16
Q
Classic presentation of gardnerella?
A
White discharge, “clue cells”, (FA says +whiff/ fishy odor: FA knows best!!)
17
Q
Chlamydia Trachomatis:
basic bacterial structure AND typical infections?
A
- atypical gram negative, intracellular (can’t make ATP!!!)
- “Higher” infections (cervicitis, endometritis, salpo-oophoritis, PID)
18
Q
Chlaymida:
Dx?
Important Risk?
A
- can dx w/ PCR OR URINE!!
- INFERTILITY risk
19
Q
Gonorrhea: basic bacterial structure
A
gram negative diplococcic, intracellular
see ‘coffee beans’ inside neutros on histo
20
Q
PID: bugs causing disease (3)
A
- gonorrhea
- chlamydia
- enteric bacteria
- *Typically polymicrobial when peurperal (following normal delivery)
21
Q
Cause of/ risks for PID?
Outcome of PID (4)?
A
Causes:
- Anything foreign going up inside of you.
Babies….. metal stuff in procedures… abortion.
Outcomes:
- suppurative salpingitis–> adhesions and infertility
- peritonitis
- bacteremia
- intestinal obstruction
22
Q
What bugs are usually assc with post-partum PID?
A
polymicrobial!!
23
Q
Gonococcal/Non-gonococcal PID: describe the course of disease (important difference?)
A
gonococcal: enters bartholin glands/cervix –> travels upward + spares endometrium (infects outer layers–mucosa + submucosa)
nongonococcal: lymphatic spread, infects ENDOmetrium + myometrium (DEEP infection)
24
Q
- What are the two leukoplakias (white plaques) of the vulva?
- When does each occur?
- Key histo difference between the two?
A
- lichen sclerosis (post-men)–> Epi THINS
- lichen simplex chronicus (excess scratching)–> ACANTHOSIS (THICK Epi)
25
Lichen sclerosis: histo
| Lichen simplex chronicus: histo
sclerosis: epi thins, dermal atrophy and scarring
(response to being an old fart!!)
chronicus: epi thickens, dermal inflammation and hyperkeratosis (response to irritation!!)
26
```
Condylomas:
assc virus?
Are they precancerous?
Location of infection?
Histo?
```
- HPV 6,11-- not precancerous
- warts on outer genitals/ anus
- koilocytosis, "raisin like cells"
27
```
Vulvar intraepithelial neoplasm (VIN):
two types?
prognosis?
average age?
typical morphology?
```
Women over 60yoa
* (basically squamous carcinoma in situ; precursor lesion)
- HPV related vs. non-HPV
- good prognosis
28
HPV related VIN:
what does it look like grossly? on histo?
Age group?
-warty/ basaloid type/ koilocytes (exophytic lesion)-->
white plaques on vulva, vagina, uterus
-Patients are younger than in non-HPV type
29
Non-HPV VIN:
Whats it look like on histo/ grossly?
Who gets it?
- nodules, keratinization + invasive pattern
| - OLDER women w/ long standing hyperplasia/ leukoplakia (lichin disorders) --> progresses to VIN
30
Malignant melanoma of vulva:
who gets it?
what might it be mistaken for?
prognosis?
- older adults
- poor prognosis because late detection
- mimics Pagets
31
What does Pagets disease of the vulva look like grossly? on histo?
Who gets it?
How does it compare to mammary Pagets?
- red crusted lesion; confined to epidermis, large halo cells
- occurs in post-meno. white women
- NOT asstd. with DEEPER cancer (remains in Epi)
- MAMMARY Pagets is 100% associated with DEEPER cancer
32
What type of cancer is extramammary pagets?
primary cutaneous adenocarcinoma
- Tumors come from apocrine ducts or keratinocytic stem cells
**She worded this really weird in her note packet, but after her lecture and pathoma I am pretty confident that this is disease is always considered a primary cutaneous adenocarcinoma that RARELY invades past the Epi and is thus RARELY associated with deeper malignancy (vs. the boobie one which is nearly 100% associated with deeper malignancy).
33
Vaginal Intraepithelial neoplasm (VAIN):
| compare it to Vulvar IN
- vaginal is most always HPV assc (don't get non HPV)
- most vulvar (VIN) are NOT HPV asstd.
- VAIN + VIN same otherwise (warty exophytic lesion, white plaque)
34
Vaginal Squamous cell carcinoma:
| Where does it come from and how common is it?
- usually HPV assc carcinoma that spreads from the cervix
| - 1-2% of cervical squamous cells spread to vagina
35
Adenocarcinoma of the vagina is assc with what drug?
| The drug is more commonly assc with what condition?
- adenocarcinoma seen in young women whose mothers took DES (1%)
- more commonly these girls get VAGINAL ADENOSIS: red granular foci of squamous/ columnar cells, ^^glands
36
Tell me about embryonal rhabdyomyosarcoma of the vagina?
| who gets it, what does it look like grossly/ histo, prognosis?
- kids under 5yoa
- grape like, protrudes from vagina
- has cambium layer, tad pole cells, rhabdoblasts
- good prognosis
37
How and where does squamous metaplasia of the cervix occur?
| What is the consequence?
-menarche --> ^^ estrogen --> ^^ glycogen --> ^^ bacteria --> low pH --> endocervix gains squamous cells where it should have columnar
- normal process but cells are susceptible to HPV infection
* *get dat transition on pap, yo.**
38
Two "inflammatory" disorders of the cervix?
- cervic(itis) -- duh
| - endocervical polyps
39
How common is cervicitis? When is it a concern?
- most women get cervicitis, esp multiparous women
| - usually benign but worry about gonorrhea, chlamydia, mycoplasma, HSV
40
Endocervical polp:
What does it look like?
What does it cause?
- mucopolypoid mass, may protrude from os
| - causes bleeding --> rule out more dangerous causes
41
Who gets HPV? Is it worrisome? When do we test for it?
- Most women exposed by age 50, usually cleared by immune system --> only dangerous if infection persists
- Do not test in young people, only in 30+ or w/ abnormal pap at age 21+
42
Cause of nearly all cervical cancer?
| What are three important risk factors for cervical cancer?
-Persistent HPV 16,18, 31, 33 infections
| risks for persistence: OCPs, smoking, immunosuppression
43
HPV 18 + 45 are risks for?
endocervical adenocarcinoma
44
What cells become infected by HPV?
-INFECTS immature cells in squamocolumnar junction
(or immature anal cells in males)
-REPLICATES in mature cells, ie vagina
45
What does HPV look like in mature cells?
-koilocytes: clear halo, raisin nuclei
46
Describe the oncogenicity of HPV:
E6/7 proteins inactivate Rb/p53 tumor supressors
47
Describe the genomic difference between HPV related dysplasia and cancer
- dysplasia: viral DNA outside of cell genome
| - cancer: viral DNA incorporated INTO cell genome
48
What strains of HPV are covered by vaccine?
| When should it be administered?
- 6,11,16,18
- give BEFORE exposure (so middle school, but ages 9-26 are ok)
* not effective post-exposure
* not effective against 30% of initial infections (40 strains exist)
49
How long do cervical intra-epithelial neoplasms shed abnormal cells on pap?
-can shed abnormal cells for up to twenty years without becoming "the cancer"
50
Describe CIN I-III
I- mild, low grade effects lower 1/3 epi (might revert)
II- moderate/ high grade- effects lower 2/3 (sometimes reverts)
III-severe/ high grade- full epi (RARELY reverts!)
51
What percentage low grade CINs (I) resolve?
| What percentage of high grade (CINS II-III) progress?
CIN I:60% regress w/o treatment
| CIN II-III: 60% persist and 10% become invasive
52
Squamous cell carcinoma of cervix:
How common is this relative to other cervical cancers?
histo appearance?
age of onset?
#1 cervical cancer
- exophytic lesions +/- keratinization
- 30 years see dysplasia, 45 years see cancer
53
Adenocarcinoma of cervix:
- association?
- detection?
- associated with HPV (18, 45)
| - NOT detected with pap smear, incidence increasing
54
Survival for cervical cancer?
95% stage one, stage three less than 50%
55
Two general components of the normal uterine endometrium?
Describe the appearance of the uterine endometrium in both halves of the menstrual cycle; when do you see histologically during ovulation?
normal: have stroma + glands
Proliferative: ESTROGEN--> growth manifested by ^^ mitoses
Secretory: PROGESTERONE--> tortuous glands, little/no mitoses
**basal vacuoles= sign of ovulation
56
Dysfunctional uterine bleeding:
| What should be on your differential?
- #1 cause = anovulatory cycle
- consider: tumors, polyps, hyperplasia
- MUST rule out cancer/ hyperplasia in older women
57
Causes of anovulatory cycles?
seen under circumstances where there is ^^^^estrogen
start of menarche, HRT/menopause, endocrine/ovarian disorders
(and birth control, we hope!!)
58
What is an "inadequate luteal phase" and what does it cause?
- corpus luteum fails to secrete sufficient progesterone --> see few glands on biopsy
- causes infertility/amenorrhea
59
Acute vs chronic uterine inflammation:
what do they look like on histo?
What's the cause of acute?
acute: neutros/ abscesses / glandular destruction, (follows instrumentation)
chronic: ***plasma cells (variety of causes, possibly idiopathic)
60
What's endometriosis and what age group gets it?
- endometrial and stromal glands of the uterus OUTSIDE of the actual uterus
- seen in people our age, 20s-30s (10% of us)
61
Three theories for endometriosis
- menstrual regurgitation
- metaplasia
- lymphatic spread
62
Morphology of endometriosis:
- in ovary
- anywhere else
- ovary gets *chocolate cyst* full of glands/ stroma (uterine tissue) + macs /necrosis
- elsewhere see normal uterine tissue + *powder burn* marks, hemorrhage in response to hormones
63
What is adenomyosis?
- basically endometriosis, locally.
| - nests of endometrial tissue found in the Myometrium.
64
What are the two types of uterine polyps?
What size are they?
Should you be concerned about cx?
- functional: (normal endo tissue)
- hyperplastic: (cystic tissue)
* Should be less than 3 cm, not cancer risk
65
Endometrial hyperplasia:
- main symptom and concerning sequelae?
- cause?
- genetic assc?
- causes dysfunctional uterine bleeding
- risk factor for adenocarcinoma
- caused by excess estrogen
- assc w/ PTEN gene DELETION which = ^^ response to estrogen
66
Two patterns of endometrial hyperplasia?
| Which is more dangerous?
-simple: cysts with ^^ normal glands + stroma
- complex: large crowded glands + atypical cells, abnormal shape
* *risk of cancer w/ complex, do hysterectomy**
67
What are the two endometrial uterine tumors?
| Myometrial tumors?
endometrium: ADENOCARCINOMA, mixed mullerian carcinosarcoma
myometrium: LEIOMYOMA, LEIOMYOSARCOMA
(the two with longer names are the more dangerous of these four cancers. leiomyoma totally benign-- fibroid.)
68
```
Adenocarcinoma:
prevalence?
who is at risk?
symptoms?
how to diagnose?
survival?
```
#1 INVASIVE TUMOR OF LADY PARTS
Risk populations:
- fatties/metabolic syndrome
- older or infertile women
- ^^ estrogen (like all of the things in the uterus)
- Sx: Asx or bleeding
- Dx: endometrial biopsy, **NOT PAP**
- Stage 1 have 90% survival but 2-3 have 50%
69
Two types of uterine adenocarcinoma; which is more common?
Type 1:
- WELL differentiated
- asstd w ^^ estrogen
- more common
Type 2:
- POORLY differentiated
- asstd with ATROPHY!! (not ^^ estrogen)
- rare and w/ poor prognosis
70
Papillary serous Type 2 uterine adenocarcinoma resembles what?
- ovarian serous carcinoma
- poor differentiation
- poor prognosis!!
71
Two possible gross appearances of endometrial adenocarcinoma?
- polypoid
| - can grow into myometrium
72
What are the two components of a mixed mullerian adenocarcinoma?
adenocarcinoma + malignant stromal component (muscle, cartilage, osteoid)
-BAD ACTOR
73
How common are leiomyomas?
Gross/micro appearance?
Genetics?
Cancer risk?
-MOST COMMON HUMAN TUMOR!! 75% FEMALES GET THEM!
-Gross: round white surface, small or very big
(my friend had one the size of a football removed!!!!)
- Histo = whorled healthy smooth muscle bundles
- Usually normal genetics; any abnormalities are not consistent
- NOT CANCER!!
74
Leiomyosarcoma:
How is it defined microscopically?
Age of presentation?
Prognosis?
- myometrial tumor with MORE THAN 10 mitoses/ hpf
- occurs just before or after menopause (~40-60)
- poor survival, recur even after removal.
75
```
Suppurative salpingitis (Fallopian tube infection):
what is the most common assc bug?
```
- usually gonorrhea
| - sequelae of PID
76
Number one site for endometriosis to occur?
Fallopian tubes
77
Paratubal cysts- what are they?
-little outpouchings of the tube, no real clinical significance
78
```
Adenocarcinoma of fallopian tubes:
prevalence?
symptoms?
outcome?
genetic assc?
```
-rare
-like everthing,it causes bleeding
(Its a wonder I don't have a panic attack everytime I have a period!!!!! I DO. We are the same.)
-bad prognosis
-assc w/ germline BRCA mutation
79
Describe the layers of a normal placenta from mom to baby:
(mom): myometrium of her uterus--> endometrium --> decidua --> intervillious spaces --> chorion --> amnion (jelly surrounded baby)
80
Define the decidum:
- grows off of moms endometrium
- supplies maternal vessels for fetus, drain to intervillous space
- part of the placenta that "detaches" from mom when the placenta is delivered after baby.
81
Define intervillious spaces/ villi
- villi are the site of nutrient exchange in the placenta
- chorionic (baby) vessels supply blood to the villi
- moms vessels supply blood between villi (spaces)
- baby gives mom deoxy blood, mom gives baby oxyg
82
Describe the histo layers of villi:
inner: central stroma --> cytotrophoblasts --> synctiotrophoblasts
83
role of the umbilical arteries?
-deoxy blood to chorionic arteries --> villi
84
role of the umbilical veins?
- receive oxygenated blood from (decidual mommy vessels --> villi --> chorionic veins)
85
"Spontaneous" abortion is considered to occur before what point in pregnancy?
How common is this?
What is the likely cause?
- before 20 weeks
- 10-15%
- most common causes = defective implantation or chromosomal abnormality
86
Ectopic pregnancy:
- most common site?
- most important risk factor?
- histo?
- most common in fallopian tubes
- #1 risk: PID --> NORMAL tube gets the egg!!
- histo shows no villi in the endometrium
87
Ectopic:
| what are the symptoms/ possible bad sequelae?
- normally severe pelvic pain ~6 weeks following last menstrual period
- can get hematosalpinx or rupture (emergency)
88
Placenta accreta:
- what is it?
- what happens in the delivery room?
- placenta lacks the decidual layer, adheres tightly to mom's myometrium
- OB can't deliver the placenta because it is stuck
- Emergency hysterectomy done to avoid post partum hemorrhage
89
What is placenta previa?
Who is at risk of getting this?
What can it cause?
- Subtype of placenta accreta
- Placenta attaches to the cervix instead of the myometrium
- Can be complete or partial
- ^^Risk: patients w/ csection scars
- Can cause early delivery and bleeding
90
In twin pregnancies, what types of placentas are possible?
-can have one or two chorions and one or two amnions
-denoted as mono or di/ mono or di
-First term represents # of chorions
-Second term represents # of amnions
Ex: Mono/Di = One chorion, two amnions
91
Di-di placenta is usually seen in what type of twins?
| Placenta with one chorion (di-mono, mono-mono) is usually seen in what type of twins?
- di-di usually fraternal/dizygotic twins
- mono/di, mono/mono usually identical monozygotic.
* Rules don't ALWAYS apply
NOTE: 75% monozygotic twins are Mono/di
92
Twin transfusion syndrome is seen in what type of placenta? Outcome?
- Seen in mono-mono placentas, smaller blood supply/ vascular system
- see death-one/both fetuses (one baby gets more vessels than the other or they are shared equally and neither baby gets enough blood)
93
Three types of placental infection
villitis
chorioamnionitis (infected baby side)
fusitis (umbilical cord)
94
Most common cause of placental infection?
Risk?
Result?
- ascending bacterial infection; sex ^^ risk
- can cause early membrane rupture
- remember this shit will stank
95
In a hematogenous bacterial infection of the placenta, what layer is effected?
-villi are effected, makes sense cause BLOOD.
96
Whats pre-eclampsia (clinical triad)?
Eclampsia?
Who most often gets these conditions?
-pre-eclampsia: HTN, proteinuria, edema
-eclampsia: seizures, DIC
most often seen in first time moms; typically teen or geriatric (over 35yoa)
97
Pathogenesis of pre-eclampsia (what are the 4 primary issues)?
-endothelial dysfunction--> shallow placental implantation-->
Poor placental vasculature--> hypoxia-->
^^angiogenic signaling
- hypercoagulation
- vasoconstriction--> HTN
- ^^ vascular permeability--> proteinurisis + edema
98
Morphology of eclampsia in decidual vessels?
| Other organs?
- fibrinoid necrosis and thrombosis in decidual vessels
| - thrombi also in other organs (liver, kidney, brain, pit. gland)
99
When does eclampsia begin in pregnancy?
What's the first sign that it is "eclampsia" as opposed to pre?
What is the only definitive treatment?
- 32 weeks
- get vision changes; will progress to seziure
- only definitive treatment is to deliver baby
100
In general, what is a hydatidiform mole?
| What is the biggest risk associated?
- swelling of the villi, trophoblast proliferation
- basically an "zygote gone wrong"
- zygote with inappropriate genetic material is implanted--> becomes "mole"
- can progress to invasive choriocarcinoma
***Note: I agree mole is a very wacky word!
101
Age group that commonly experiences hydatidiform mole? One sign?
- teens/ older moms, outside of normal repro ages
| - belly grows faster than it should, cause there's a mass in there-- not a baby.
102
```
Compare and contrast complete vs partial mole:
genotype?
fetal parts?
swollen villi?
cancerous?
```
Genetics-->
complete: all paternal 46XX
partial: 69 xxy/xxx- triploid
Fetal parts-->
complete: no baby parts
partial: has baby parts
Cancer risk-->
complete: all villi swollen
partial: some villi swollen
* *Only COMPLETE has risk of transforming to chorio (2.5%)
103
When clinically do we see moles and how should we screen for them?
They may follow "spontaneous abortion" or curretage
| should follow HCG levels in these women to be sure they decrease
104
Invasive mole apperance:
- myometrium invaded by villi
- may send emboli to other organs just like a tumor
- not "true mets"
105
"Invasive moles may lead to what scary complication?
uterine rupture!!
| which will require hysterectomy
106
```
Gestational Choriocarcinoma:
where do they come from?
how common are they?
whats the tumor made up of?
whats it look like grossly?
```
- come from 50% moles/ 20% follow normal pregnancy
- rare, more common in Africa
- tumor is made up of trophoblasts secreting *HCG*
- small mass w/ necrosis
107
Aside from the placenta, where else do non-gestational choriocarcinomas occur (3)?
- ovaries
- testis
- mediastinum
108
Prognosis for choriocarcinoma?
- commonly mets early
| - chemo effective if caught on time, women can even have subsequent pregnancies
109
How much has pap smear changed the prevalence of cervical cancer
- was leading cause of cancer deaths in female
- **squamous cell** incidence has now decreased 80%
- adenocarcinoma cancer remains on the rise; not effectively dx'ed via pap.
110
Where should a pap sample come from?
-TRANSITION ZONE: squamocolumnar jxn
-get ectocervix + endocervix
(Stick brush in the os!! All the paps I did in Honduras were 100% ecto. Worthless.)
111
What are "liquid" paps beneficial?
-very sensitive and can test for STDs/HPV
112
When does a pathologist review paps?
| What must they report (3)?
- only view abnormal paps (screened first by computer then cytotech)
- report presence or absence of the squamocolumnar jxn (is it a good sample?)
- report +/- for intraepi. abnormality
- report infection/ changes
113
Where do most cervical cancers come from?
Most originate as high grade dysplasia!!
| SO although dysplasia rarely progresses to cancer, we still must follow it!!
114
Compare liquid pap/conventional pap sensitivies to high grade lesions:
What percentage of lesions are missed on pap?
How often is actual cancer missed?
What is this test actually really GOOD to diagnose?
liquid + HPV >> liquid >> conventional
- 10-50% lesions missed depending on pap type
- actual cancer missed HALF of the time because blood obscures samples.
(more effective at dx'ing DYSPLASIA than CANCER)
115
Three types of pap failures and which is most common?
- sample error (doc)
- reading error (cytotech/path)
- patient doesn't GET their paps (#1)
116
When do we do HPV testing w/ pap?
- all women over thirty (co-test)
- women 21-30 w/ abnormal pap (reflex testing)
- not in teens
117
Whats a colposcopy?
way to follow up with dysplastic lesion
microscopic visualization of the cervix + biopsy
(I helped do these!! That's so cool!! I want to do that!!)
