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DT4-Exam 1 > Female GU Path (Carpenter)- Leah : ) > Flashcards

Female GU Path (Carpenter)- Leah : ) Flashcards

1
Q

Normal cervical epithelium

A

ectocervix: stratified squamous
endocervix: columnar cells w/ mucin
(not true glands)

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2
Q

Appearance of normal:
endometrium?
myometrium?

A

endometrium: glands and stromal tissue
myometrium: thin SM cells w/ cigar like nuclei

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3
Q

Normal fallopian tube epithelium appearance?

A

ciliated/nonciliated columnar cells

+intercalated peg cells

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4
Q

HSV2: basic viral structure

A

DS DNA, linear

icosahedral, enveloped

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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

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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.)

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7
Q

Appearance of HSV cells on histo?

A

“ground glass nuclei”

-looks almost like soap bubbles or deer turds to me (Haha!)

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8
Q

Molluscum Contagiosum:

basic viral structure

A

Poxvirus, dsDNA
complex capsule, naked
cytoplasmic replication**

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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)

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10
Q

What do molluscum contagiosum infections look like grossly and on histo?

A

gross: dome shaped lesions w/ dimples
histo: intranuclear inclusions

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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

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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

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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

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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
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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.

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16
Q

Classic presentation of gardnerella?

A

White discharge, “clue cells”, (FA says +whiff/ fishy odor: FA knows best!!)

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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)

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18
Q

Chlaymida:
Dx?
Important Risk?

A
  • can dx w/ PCR OR URINE!!

- INFERTILITY risk

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19
Q

Gonorrhea: basic bacterial structure

A

gram negative diplococcic, intracellular

see ‘coffee beans’ inside neutros on histo

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20
Q

PID: bugs causing disease (3)

A
  • gonorrhea
  • chlamydia
  • enteric bacteria
  • *Typically polymicrobial when peurperal (following normal delivery)
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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
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22
Q

What bugs are usually assc with post-partum PID?

A

polymicrobial!!

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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)

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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)

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25
Q

Lichen sclerosis: histo

Lichen simplex chronicus: histo

A

sclerosis: epi thins, dermal atrophy and scarring
(response to being an old fart!!)

chronicus: epi thickens, dermal inflammation and hyperkeratosis (response to irritation!!)

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26
Q 
Condylomas: 
assc virus?
Are they precancerous? 
Location of infection? 
Histo?
A
  • HPV 6,11– not precancerous
  • warts on outer genitals/ anus
  • koilocytosis, “raisin like cells”
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27
Q 
Vulvar intraepithelial neoplasm (VIN):
two types?
prognosis?
average age? 
typical morphology?
A

Women over 60yoa

  • (basically squamous carcinoma in situ; precursor lesion)
  • HPV related vs. non-HPV
  • good prognosis
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28
Q

HPV related VIN:
what does it look like grossly? on histo?
Age group?

A

-warty/ basaloid type/ koilocytes (exophytic lesion)–>
white plaques on vulva, vagina, uterus

-Patients are younger than in non-HPV type

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29
Q

Non-HPV VIN:
Whats it look like on histo/ grossly?
Who gets it?

A
  • nodules, keratinization + invasive pattern

- OLDER women w/ long standing hyperplasia/ leukoplakia (lichin disorders) –> progresses to VIN

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30
Q

Malignant melanoma of vulva:
who gets it?
what might it be mistaken for?
prognosis?

A
  • older adults
  • poor prognosis because late detection
  • mimics Pagets
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31
Q

What does Pagets disease of the vulva look like grossly? on histo?
Who gets it?
How does it compare to mammary Pagets?

A
  • 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
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32
Q

What type of cancer is extramammary pagets?

A

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).

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33
Q

Vaginal Intraepithelial neoplasm (VAIN):

compare it to Vulvar IN

A
  • 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)
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34
Q

Vaginal Squamous cell carcinoma:

Where does it come from and how common is it?

A
  • usually HPV assc carcinoma that spreads from the cervix

- 1-2% of cervical squamous cells spread to vagina

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35
Q

Adenocarcinoma of the vagina is assc with what drug?

The drug is more commonly assc with what condition?

A
  • 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
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36
Q

Tell me about embryonal rhabdyomyosarcoma of the vagina?

who gets it, what does it look like grossly/ histo, prognosis?

A
  • kids under 5yoa
  • grape like, protrudes from vagina
  • has cambium layer, tad pole cells, rhabdoblasts
  • good prognosis
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37
Q

How and where does squamous metaplasia of the cervix occur?

What is the consequence?

A

-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.**
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38
Q

Two “inflammatory” disorders of the cervix?

A
  • cervic(itis) – duh

- endocervical polyps

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39
Q

How common is cervicitis? When is it a concern?

A
  • most women get cervicitis, esp multiparous women

- usually benign but worry about gonorrhea, chlamydia, mycoplasma, HSV

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40
Q

Endocervical polp:
What does it look like?
What does it cause?

A
  • mucopolypoid mass, may protrude from os

- causes bleeding –> rule out more dangerous causes

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41
Q

Who gets HPV? Is it worrisome? When do we test for it?

A
  • 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+
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42
Q

Cause of nearly all cervical cancer?

What are three important risk factors for cervical cancer?

A

-Persistent HPV 16,18, 31, 33 infections

risks for persistence: OCPs, smoking, immunosuppression

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43
Q

HPV 18 + 45 are risks for?

A

endocervical adenocarcinoma

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44
Q

What cells become infected by HPV?

A

-INFECTS immature cells in squamocolumnar junction
(or immature anal cells in males)

-REPLICATES in mature cells, ie vagina

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45
Q

What does HPV look like in mature cells?

A

-koilocytes: clear halo, raisin nuclei

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46
Q

Describe the oncogenicity of HPV:

A

E6/7 proteins inactivate Rb/p53 tumor supressors

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47
Q

Describe the genomic difference between HPV related dysplasia and cancer

A
  • dysplasia: viral DNA outside of cell genome

- cancer: viral DNA incorporated INTO cell genome

48
Q

What strains of HPV are covered by vaccine?

When should it be administered?

A
  • 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
Q

How long do cervical intra-epithelial neoplasms shed abnormal cells on pap?

A

-can shed abnormal cells for up to twenty years without becoming “the cancer”

50
Q

Describe CIN I-III

A

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
Q

What percentage low grade CINs (I) resolve?

What percentage of high grade (CINS II-III) progress?

A

CIN I:60% regress w/o treatment

CIN II-III: 60% persist and 10% become invasive

52
Q

Squamous cell carcinoma of cervix:
How common is this relative to other cervical cancers?
histo appearance?
age of onset?

A

1 cervical cancer

  • exophytic lesions +/- keratinization
  • 30 years see dysplasia, 45 years see cancer
53
Q

Adenocarcinoma of cervix:

  • association?
  • detection?
A
  • associated with HPV (18, 45)

- NOT detected with pap smear, incidence increasing

54
Q

Survival for cervical cancer?

A

95% stage one, stage three less than 50%

55
Q

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?

A

normal: have stroma + glands
Proliferative: ESTROGEN–> growth manifested by ^^ mitoses
Secretory: PROGESTERONE–> tortuous glands, little/no mitoses
**basal vacuoles= sign of ovulation

56
Q

Dysfunctional uterine bleeding:

What should be on your differential?

A
  • # 1 cause = anovulatory cycle
  • consider: tumors, polyps, hyperplasia
  • MUST rule out cancer/ hyperplasia in older women
57
Q

Causes of anovulatory cycles?

A

seen under circumstances where there is ^^^^estrogen
start of menarche, HRT/menopause, endocrine/ovarian disorders
(and birth control, we hope!!)

58
Q

What is an “inadequate luteal phase” and what does it cause?

A
  • corpus luteum fails to secrete sufficient progesterone –> see few glands on biopsy
  • causes infertility/amenorrhea
59
Q

Acute vs chronic uterine inflammation:
what do they look like on histo?
What’s the cause of acute?

A

acute: neutros/ abscesses / glandular destruction, (follows instrumentation)
chronic: ***plasma cells (variety of causes, possibly idiopathic)

60
Q

What’s endometriosis and what age group gets it?

A
  • endometrial and stromal glands of the uterus OUTSIDE of the actual uterus
  • seen in people our age, 20s-30s (10% of us)
61
Q

Three theories for endometriosis

A
  • menstrual regurgitation
  • metaplasia
  • lymphatic spread
62
Q

Morphology of endometriosis:

  • in ovary
  • anywhere else
A
  • 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
Q

What is adenomyosis?

A
  • basically endometriosis, locally.

- nests of endometrial tissue found in the Myometrium.

64
Q

What are the two types of uterine polyps?
What size are they?
Should you be concerned about cx?

A
  • functional: (normal endo tissue)
  • hyperplastic: (cystic tissue)
  • Should be less than 3 cm, not cancer risk
65
Q

Endometrial hyperplasia:

  • main symptom and concerning sequelae?
  • cause?
  • genetic assc?
A
  • causes dysfunctional uterine bleeding
  • risk factor for adenocarcinoma
  • caused by excess estrogen
  • assc w/ PTEN gene DELETION which = ^^ response to estrogen
66
Q

Two patterns of endometrial hyperplasia?

Which is more dangerous?

A

-simple: cysts with ^^ normal glands + stroma

  • complex: large crowded glands + atypical cells, abnormal shape
  • *risk of cancer w/ complex, do hysterectomy**
67
Q

What are the two endometrial uterine tumors?

Myometrial tumors?

A

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
Q 
Adenocarcinoma:
prevalence?
who is at risk?
symptoms?
how to diagnose? 
survival?
A

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
Q

Two types of uterine adenocarcinoma; which is more common?

A

Type 1:

  • WELL differentiated
  • asstd w ^^ estrogen
  • more common

Type 2:

  • POORLY differentiated
  • asstd with ATROPHY!! (not ^^ estrogen)
  • rare and w/ poor prognosis
70
Q

Papillary serous Type 2 uterine adenocarcinoma resembles what?

A
  • ovarian serous carcinoma
  • poor differentiation
  • poor prognosis!!
71
Q

Two possible gross appearances of endometrial adenocarcinoma?

A
  • polypoid

- can grow into myometrium

72
Q

What are the two components of a mixed mullerian adenocarcinoma?

A

adenocarcinoma + malignant stromal component (muscle, cartilage, osteoid)
-BAD ACTOR

73
Q

How common are leiomyomas?
Gross/micro appearance?
Genetics?
Cancer risk?

A

-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
Q

Leiomyosarcoma:
How is it defined microscopically?
Age of presentation?
Prognosis?

A
  • myometrial tumor with MORE THAN 10 mitoses/ hpf
  • occurs just before or after menopause (~40-60)
  • poor survival, recur even after removal.
75
Q 
Suppurative salpingitis (Fallopian tube infection):
what is the most common assc bug?
A
  • usually gonorrhea

- sequelae of PID

76
Q

Number one site for endometriosis to occur?

A

Fallopian tubes

77
Q

Paratubal cysts- what are they?

A

-little outpouchings of the tube, no real clinical significance

78
Q 
Adenocarcinoma of fallopian tubes:
prevalence?
symptoms?
outcome?
genetic assc?
A

-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
Q

Describe the layers of a normal placenta from mom to baby:

A

(mom): myometrium of her uterus–> endometrium –> decidua –> intervillious spaces –> chorion –> amnion (jelly surrounded baby)

80
Q

Define the decidum:

A
  • 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
Q

Define intervillious spaces/ villi

A
  • 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
Q

Describe the histo layers of villi:

A

inner: central stroma –> cytotrophoblasts –> synctiotrophoblasts

83
Q

role of the umbilical arteries?

A

-deoxy blood to chorionic arteries –> villi

84
Q

role of the umbilical veins?

A
  • receive oxygenated blood from (decidual mommy vessels –> villi –> chorionic veins)
85
Q

“Spontaneous” abortion is considered to occur before what point in pregnancy?
How common is this?
What is the likely cause?

A
  • before 20 weeks
  • 10-15%
  • most common causes = defective implantation or chromosomal abnormality
86
Q

Ectopic pregnancy:

  • most common site?
  • most important risk factor?
  • histo?
A
  • most common in fallopian tubes
  • # 1 risk: PID –> NORMAL tube gets the egg!!
  • histo shows no villi in the endometrium
87
Q

Ectopic:

what are the symptoms/ possible bad sequelae?

A
  • normally severe pelvic pain ~6 weeks following last menstrual period
  • can get hematosalpinx or rupture (emergency)
88
Q

Placenta accreta:

  • what is it?
  • what happens in the delivery room?
A
  • 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
Q

What is placenta previa?
Who is at risk of getting this?
What can it cause?

A
  • 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
Q

In twin pregnancies, what types of placentas are possible?

A

-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
Q

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?

A
  • 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
Q

Twin transfusion syndrome is seen in what type of placenta? Outcome?

A
  • 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
Q

Three types of placental infection

A

villitis
chorioamnionitis (infected baby side)
fusitis (umbilical cord)

94
Q

Most common cause of placental infection?
Risk?
Result?

A
  • ascending bacterial infection; sex ^^ risk
  • can cause early membrane rupture
  • remember this shit will stank
95
Q

In a hematogenous bacterial infection of the placenta, what layer is effected?

A

-villi are effected, makes sense cause BLOOD.

96
Q

Whats pre-eclampsia (clinical triad)?
Eclampsia?
Who most often gets these conditions?

A

-pre-eclampsia: HTN, proteinuria, edema
-eclampsia: seizures, DIC
most often seen in first time moms; typically teen or geriatric (over 35yoa)

97
Q

Pathogenesis of pre-eclampsia (what are the 4 primary issues)?

A

-endothelial dysfunction–> shallow placental implantation–>
Poor placental vasculature–> hypoxia–>
^^angiogenic signaling
- hypercoagulation
- vasoconstriction–> HTN
- ^^ vascular permeability–> proteinurisis + edema

98
Q

Morphology of eclampsia in decidual vessels?

Other organs?

A
  • fibrinoid necrosis and thrombosis in decidual vessels

- thrombi also in other organs (liver, kidney, brain, pit. gland)

99
Q

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?

A
  • 32 weeks
  • get vision changes; will progress to seziure
  • only definitive treatment is to deliver baby
100
Q

In general, what is a hydatidiform mole?

What is the biggest risk associated?

A
  • 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
Q

Age group that commonly experiences hydatidiform mole? One sign?

A
  • 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
Q 
Compare and contrast complete vs partial mole:
genotype? 
fetal parts?
swollen villi?
cancerous?
A

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
Q

When clinically do we see moles and how should we screen for them?

A

They may follow “spontaneous abortion” or curretage

should follow HCG levels in these women to be sure they decrease

104
Q

Invasive mole apperance:

A
  • myometrium invaded by villi
  • may send emboli to other organs just like a tumor
  • not “true mets”
105
Q

“Invasive moles may lead to what scary complication?

A

uterine rupture!!

which will require hysterectomy

106
Q 
Gestational Choriocarcinoma: 
where do they come from?
how common are they?
whats the tumor made up of? 
whats it look like grossly?
A
  • 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
Q

Aside from the placenta, where else do non-gestational choriocarcinomas occur (3)?

A
  • ovaries
  • testis
  • mediastinum
108
Q

Prognosis for choriocarcinoma?

A
  • commonly mets early

- chemo effective if caught on time, women can even have subsequent pregnancies

109
Q

How much has pap smear changed the prevalence of cervical cancer

A
  • 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
Q

Where should a pap sample come from?

A

-TRANSITION ZONE: squamocolumnar jxn
-get ectocervix + endocervix
(Stick brush in the os!! All the paps I did in Honduras were 100% ecto. Worthless.)

111
Q

What are “liquid” paps beneficial?

A

-very sensitive and can test for STDs/HPV

112
Q

When does a pathologist review paps?

What must they report (3)?

A
  • 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
Q

Where do most cervical cancers come from?

A

Most originate as high grade dysplasia!!

SO although dysplasia rarely progresses to cancer, we still must follow it!!

114
Q

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?

A

liquid + HPV&raquo_space; liquid&raquo_space; 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
Q

Three types of pap failures and which is most common?

A
  • sample error (doc)
  • reading error (cytotech/path)
  • patient doesn’t GET their paps (#1)
116
Q

When do we do HPV testing w/ pap?

A
  • all women over thirty (co-test)
  • women 21-30 w/ abnormal pap (reflex testing)
  • not in teens
117
Q

Whats a colposcopy?

A

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!!)

DT4-Exam 1 (17 decks)

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