Gupta - Pathology Flashcards

Question 1

Q

What do you see here?

Answer

A

First-trimester chorionic villi
Composed of delicate mesh of central stroma surrounded by two discrete layers of epithelium:
1. Outer layer of syncytiotrophoblast (group of cells; two arrows) and
2. Inner layer of cytotrophoblast (single cells; arrow)
Smaller, more vascular, less trophoblast thickness as the pregnancy progresses

Question 2

Q

What is this?

Answer

A

Third-trimester chorionic villi
Composed of stroma with:
1. Dense network of dilated capillaries
2. Surrounded by markedly thinned-out syncytiotrophoblast and cytotrophoblast
REMEMBER:
1. Syncytio: think groups of cells
2. Cyto: think single cells

Question 3

Q

What kind of growth restriction do fetal abnormalities cause? Specific causes?

Answer

A

SYMMETRIC: all organ systems are similarly affected
Caused by chromosomal disorders, congenital anomalies, and congenital infections:
1. TORCH group of infections; usually transplacental -
a. Toxoplasmosis: usually 1st infection is the one that causes most problems (i.e., if mom has never been exposed before)
b. Rubella
c. Cytomegalovirus (CMV)
d. Herpesvirus (HSV)
2. Other viruses/bacteria, i.e., syphilis bacteria, listeria
NOTE: wear gloves if working in the garden while pregnant

Question 4

Q

What kind of growth restriction do placental abnormalities cause? Specific causes?

Answer

A

ASYMMETRIC: spares brain (via a down-regulation of growth in latter 1/2 of gestation)
Uteroplacental insufficiency may result from:
1. Umbilical-placental vascular anomalies (like single umbilical artery, abnormal cord insertion, placental hemangioma),
2. Placental abruption (detachment from uterus),
3. Placenta previa (covers opening of mom’s cervix),
4. Placental thrombosis and infarction,
5. Placental infection, or
6. Multiple gestations
NOTE: 3rd trimester loss is usually placental insufficiency

Question 5

Q

What kind of maternal abnormalities may cause fetal growth restriction?

Answer

A

Those that result in DEC placental blood flow
1. Vascular diseases, like preeclampsia (toxemia of pregnancy) and
2. Chronic hypertension, are often the underlying cause
Usually some kind of vascular issue

Question 6

Q

What is spontaneous abortion? Causes?

Answer

A

MISCARRIAGE: pregnancy loss <20 wks gestation
1. Fetal chrom anomalies: approx 50% of early abortuses
2. Maternal endocrine factors: luteal-phase defect, poorly controlled diabetes, other uncorrected endocrine disorders
3. Physical defects of uterus: submucosal leiomyomas, uterine polyps or malformations, may prevent or disrupt implantation
4. Systemic disorders affecting maternal vasculature: antiphospholipid Ab syndrome, coagulopathies, and HTN
NOTE: families get very upset about losing the fetus early, but this may be a “good” thing in many cases, i.e., due to a chromosome abnormality

Question 7

Q

When might ascending infections cause pregnancy loss?

Answer

A

2nd trimester
Losses due to fetal and maternal anatomic abnormalities are also common in the 2nd trimester

Question 8

Q

What is this?

Answer

A

Listeria: necrotizing intervillositis
Non-pasteurized cheeses and milk (KNOW THIS: may get a question about it) -> if the infection is bad enough, you may lose this pregnancy
1. Outbreaks in some places where people eat a lot of unpasteurized cheeses (also cold cuts)

Question 9

Q

What is going on here?

Answer

A

Chorioamnionitis: maternal inflammatory response to intervillositis
These are ascending infections, so often maternal inflammatory response (not placenta)
Lots of inflammation: would also call this deciduitis (this is acute inflammation -> mostly polys)
NOTE: layers here are amnion, chorion, decidua

Question 10

Q

What do you see here?

Answer

A

Necrotizing funisitis: due to Candida, in this case
Punctate, 1-2mm yellow-white nodules on the cord (Candida always looks the same)
Generally track the coils of the cord vessels, and are noted initially along the perimeter of the umbilical vein (3 vessels: 2 aa, 1 vein)
Established, or long-standing infections can cause tissue necrosis and accumulation of cellular debris (necrotizing funisitis)
False knot in the cord here

Question 11

Q

What is this?

Answer

A

Subamniotic microabscesses typical of Candida funisitis
Very characteristic, but not specific for this organism
Inflammation of the umbilical vessels (vasculitis) and cord substance (funisitis) occurs in response to the infection -> FETAL INFLAMMATORY RESPONSE
Wharton jelly: supporting substance in umbilical cord that looks like jelly grossly, but pink ground substance in this micro
1. Right side of the image is the outside of the umbilical cord
2. Artery on the left

Question 12

Q

What is this?

Answer

A

Candida pseudohyphae with GMS silver stain in subamniotic foci
Funisitis: umbilical cord with subamniotic microabscesses
Inflammation located at the periphery or surface of the umbilical cord may be the primary pattern seen (peripheral funisitis)
Fungal ball

Question 13

Q

What is phlebitis?

Answer

A

Inflammation of the umbilical vein
Can be seen separately from arteritis (inflammation of umbilical arteries)

Question 14

Q

What do you see here?

Answer

A

Chronic villitis with CMV: likes vascular endothelium
Nuclear AND cytoplasmic inclusions (herpes would only have nuclear inclusions)
This case is SEVERE

Question 15

Q

What is this?

Answer

A

Chronic villitis with CMV

Question 16

Q

What is going on here?

Answer

A

Parvovirus B19: erythema infectiosum (slap cheek)
Viral inclusions in early erythroid precursors
Bone marrow sample b/c don’t see nucleated red cells in peripheral system, unless something is wrong

Question 17

Q

What do you see here? Arrow?

Answer

A

Parvovirus B19: erythema infectiosum
Erythroblasts in lumen of capillary vessels of the placental villi show eosinophilic nuclear inclusions

Question 18

Q

An image of fetal membranes are shown. Iron stain was negative. The histologic finding indicates what?

A. Meconium was present in the amnionic cavity

B. Placental abruption

C. Congestive heart failure in the fetus

D. Acute chorioamnionitis

Answer

A

A. Meconium was present in the amniotic cavity

Passage of meconium in utero due to bowel peristalsis and relaxation of anal sphincter -> may be indicative of fetal distress
Meconium components diffuse into placenta and cord, leading to vasoconstriction + hypoperfusion; damage to fetus INC with length of exposure
Neonates are at risk for meconium aspiration
Meconium is unlikely in fetuses <30 wks gestation
Meconiophages: brown-green pigment, usually right below amnion, in the chorion
1. Top a little bit of amnion layer (low, cuboidal epithelium), then chorion, then decidua (big, fluffy, pink cells)
2. Hemosiderin-laden macros would have been positive for iron

Question 19

Q

What is twin-twin transfusion syndrome?

Answer

A

A complication of monochorionic twin pregnancy
Monochorionic twin placentas have vascular anastomoses that connect twin circulations, and in some cases these connections include one or more INC blood flow to one twin at expense of the 2nd, one twin will be underperfused, while the second will be fluid overloaded
If severe, this may result in the death of one or both fetuses
Most twins Di/Di, so this syndrome is RARE

Question 20

Q

What may have happened here?

Answer

A

Twin-twin transfusion syndrome: a complication of monochorionic twin pregnancy
Monochorionic twin placentas have vascular anastomoses that connect twin circulations, and in some cases these connections include one or more INC blood flow to one twin at expense of the 2nd, one twin will be underperfused, while the second will be fluid overloaded
If severe, this may result in the death of one or both fetuses

Question 21

Q

What is the most common site of ectopic pregnancy? Causes?

Answer

A

Approximately 90% of cases in extrauterine fallopian tube
Can rupture (gross image on front of this card), leading to hemoperitoneum, which is dangerous
50% are idiopathic, and the other 50% may be infection, leiomyoma causing obstruction, etc.
Takes a “villous” to prove ectopic pregnancy; chorionic villi float on water

Question 22

Q

Describe each of these abnormalities of placental implantation (A-D).

Answer

A

Fertilized ovum normally implants in uterine fundus

A. Normal placenta

B. Placenta previa: very low lying placenta, or one that covers the os -> severe hemorrhage can result, w/cervical dilation and passage of the baby through the birth canal

C. Placenta accreta: no formation of a normal decidual plate -> chorionic villi extend into myometrium, and placenta can’t separate normally post-delivery; severe hemorrhage

D. Abruptio placenta: premature separation of placenta prior to delivery, with formation of a retroplacental blood clot between decidua and uterine wall -> blood supply of O2 and nutrients to fetus compromised to greater degree with INC size of the abruption

Question 23

Q

What do you see here?

Answer

A

Placenta accreta: NO formation of normal decidual plate -> chorionic villi extend into myometrium, and placenta can’t separate normally post-delivery, leading to severe hemorrhage
Microscopically, the placental villi interdigitate directly with the uterine myometrium, without an intervening decidual plate

Question 24

Q

How is placental invasion into the myometrium classified (chart)?

Question 25

Q

The following gross and microscopic images show what pathology?

A. Placenta previa

B. Normal placenta

C. Abruptio placenta

D. Placenta accrete

E. Vasa previa

Answer

A

C. Abruptio placenta

Retroplacental blood clot in gross image

Question 26

Q

What is this?

Answer

A

Amnion nodosum: seen in placentas affected by oligohydramnios, which may be associated with fetal renal agenesis and pulmonary hypoplasia
1. May be due to desquamated skin or membrane injury
GROSS: multiple yellow-tan superficial amniotic lesions (0.2 to 0.4 cm), usually near insertion of the umbilical cord
Not really a bad thing, unless it is associated with oligohydramnios -> just a collection of squaffed off squamous cells, and maybe some fibroblasts

Question 27

Q

What is going on here?

Answer

A

Amnion nodosum: seen in placentas affected by oligohydramnios, which may be associated with fetal renal agenesis and pulmonary hypoplasia
1. May be due to desquamated skin or membrane injury
MICRO: nodules of protuberant eosinophilic fibrinous material with entrapped squamous cells
1. Associated w/stratified squamous metaplasia
Not really a bad thing, unless it is associated with oligohydramnios -> just a collection of squaffed off squamous cells, and maybe some fibroblasts

Question 28

Q

What happened to this little guy?

Answer

A

Potter’s sequence: clubbed feet, pulmonary hypoplasia, and cranial anomalies
Oligohydramnios experienced in utero

Question 29

Q

What may have caused the difference in size of these placentas?

Answer

A

Preeclampsia: HTN and large amount of protein in the urine -> usually in 3rd trimester of pregnancy and gets worse over time (feared outcome is eclampsia = seizures)
Most placentas are smaller than expected
Infarcts and retroplacental hematomas are also more common

Question 30

Q

What do you see here? When are these more likely?

Answer

A

Placental infarct: small infarct may be of no consequence to the fetus, but if >1/3 or 1/2 of the placental parenchyma is infarcted or lost in some fashion, blood supply to fetus can become severely compromised and fetal demise may occur (via utero-placental insufficiency w/multiple infarcts)
Infarcts AND retroplacental hematomas are more common in PREECLAMPSIA
Bread loafing for placenta section: maternal vessels on top, membrane on bottom, and pale area is an infarct

Question 31

Q

What is the difference between these two images?

Answer

A

Preeclampsia
LEFT: villi small, and syncytiotrophoblasts have thinned out (as they should)
RIGHT: villous ischemia (increased syncytial knots) in the placenta
1. A little hemorrhage; don’t look as healthy
2. Only some blood vessels, and “nubbins” of syncytiotrophoblasts

Question 32

Q

What might be going on in this maternal vessel?

Answer

A

Fibrinoid necrosis of the vessel wall: strong eosinophilic staining areas
PREECLAMPSIA
These are maternal vessels in the decidua
No cell nuclei, and decidua surrounding it (big, pink, fluffy cells)
1. Pink and amorphous (necrotic)

Question 33

Q

Why are hyatidiform moles important to recognize?

Answer

A

Because they are associated with an increased risk of persistent trophoblastic disease (invasive mole) or choriocarcinoma
Invasive: trophoblasts go into uterine wall
Attached flow chart is important for pathology (not important for us to know yet) -> partial moles much more difficult than complete ones because often diagnosed very early

Question 34

Q

What is the origin of complete/partial hydatidiform moles? What hormone level could help you distinguish between the 2?

Answer

A

Complete: egg that has lost female chromosomes, so genetic material is completely paternally derived
1. NO fetal parts
Partial mole: fertilization of an egg with two sperm
hCG: compared to normal levels for gestation
1. Complete mole: very elevated
2. Partial mole: slightly elevated

Question 35

Q

What is this?

Answer

A

Gross image of a twin placenta

Question 36

Q

What is preeclampsia?

Answer

A

Vasculature problem: may be b/c trophoblasts don’t sufficiently invade/stimulate the spiral arteries in the uterus -> hypoxic state for the fetus, which is reflected in the gross and micro changes
1. Big, dilated, torturous blood vessels on fetal surface on left (attached image)
2. Right placenta much smaller: DEC blood supply, nutrients to fetus + more likely to get more infarcts and retroplacental hematomas

Question 37

Q

What do you see here?

Answer

A

Complete mole: no embryo, and no normal placenta
1. Marked villous enlargement, edema, and circumferential trophoblast proliferation
Villi get very large, and edematous, aka hydropic
hCG very elevated (above what would be normal for that stage of the pregnancy) in these women because way too many syncytiotrophoblasts

Question 38

Q

What is this?

Answer

A

Snowstorm appearance of complete mole on US
Buzzword
REMEMBER: no embryo, and no normal placenta
1. Elevated hCG for the corresponding stage of pregnancy

Question 39

Q

What do you see here?

Answer

A

Normal first trimester placenta: chorionic villi are large and covered by two layers of cells:
1. Cytotrophoblast and syncytiotrophoblast (syncytio make hCG)
Blood vessels in the villi are not prominent

Question 40

Q

What is this?

Answer

A

Partial mole: some villi appear normal; others are swollen, avascular, and grape-like (though not as large as a complete mole)
1. Minimal trophoblastic proliferation
hCG won’t be as high as with the complete mole
Can be really hard to differentiate these from normal villi microscopically (b/c detected so early)
Will karyotype if clinical suspicion is very high (looking for TRIPLOIDY)

Question 41

Q

What is this?

Answer

A

Complete mole: NO normal villi here

Question 42

Q

What is this?

Answer

A

Partial mole: normal villi are pink, fluffy, light tan (vs. grape-like clusters of the molar villi)

Question 43

Q

What might this be?

Answer

A

Gestational choriocarcinoma: malignant neoplasm of trophoblastic cells from a previously normal or abnormal pregnancy, like an extrauterine ectopic pregnancy or complete mole
1. Complete moles more likely to progress to this than partial, but still only about 2-3% risk
Rapidly invasive and metastasizes widely, but once identified responds well to chemotherapy
1. Very hemorrhagic
2. >50% have metastasized by the time they are identified
NOTE: persistent trophoblastic disease does not metastasize, but pieces of it may embolize to lung or other parts of body

Question 44

Q

What is this?

Answer

A

Choriocarcinoma: soft, fleshy, yellow-white tumor with large, pale areas of necrosis and extensive hemorrhage
Histo: proliferating syncytio and cytotrophoblasts
1. Mitoses abundant and sometimes abnormal
Invades underlying myometrium, freq penetrates blood vessels, and in some cases extends out onto the uterine serosa and into adjacent structures
Chorionic gonadotropins (hCG) very high!!!!

Question 45

Q

What are the histo and clinical features of complete hydatidiform mole?

Answer

A

HISTO: large, avascular villi with trophoblastic proliferation
CLINICAL: occurs when fertilized ovum contains only paternal chromosomes (usually 46, XX karyotype)
1. Marked uterine enlargement
2. “Snowstorm” effect w/no fetus on US
3. Some give rise to choriocarcinoma (2-3%)

Question 46

Q

What are the histo and clinical features of partial hydatidiform mole?

Answer

A

HISTO: some villi enlarged, w/minimal trophoblast proliferation
CLINICAL: typically triploid (69, XXX or 69, XXY or 69, XYY)
1. Malformed fetus present, but rarely goes to term
2. Rarely gives rise to choriocarcinoma

Question 47

Q

What are the histo and clinical features of choriocarcinoma?

Answer

A

HISTO: malignant proliferation of syncytio-trophoblast with no villi
1. Often hemorrhagic
2. NO fetus is present
CLINICAL: hCG levels are often extremely high
1. Can metastasize
2. Many are sensitive to chemotherapy

Question 48

Q

What are the histo and clinical features of a placental site trophoblastic tumor?

Answer

A

HISTO: rare, localized proliferation of intermediate trophoblast that can produce a grossly visible nodule
CLINICAL: most are benign, with rare malignant cases

Question 49

Q

What are some of the hazards of prematurity?

Answer

A

May give rise to:
1. Neonatal respiratory distress syndrome, also known as hyaline membrane disease
2. Necrotizing enterocolitis (attached image)
3. Sepsis
4. Intraventricular and germinal matrix hemorrhage

Question 50

Q

What is going on here?

Answer

A

Necrotizing enterocolitis (NEC): potential hazard of prematurity
LEFT: entire small bowel markedly distended, with a perilously thin wall (impending perforation)
RIGHT: congested portion of ileum corresponds to areas of hemorrhagic infarction and transmural necrosis microscopically
1. Submucosal gas bubbles (pneumatosis intestinalis) can be seen in several areas (arrows on bottom left)

Question 51

Q

What is the difference between these two tissues?

Answer

A

Hyaline membrane disease (neonatal respiratory distress syndrome) in the image on the left
1. Alternating atelectasis and dilation of alveoli
2. Eosinophilic, thick hyaline membranes lining the dilated alveoli
Normal fetal lung on the right

Question 52

Q

What is fetal hydrops? What are some of the causes?

Answer

A

Accumulation of edema fluid in the fetus during intrauterine growth
CAUSES: CV, chromosomal, fetal anemia (immune, Parvo B19, homo alpha-thalassemia), twin-twin, etc.
1. Immune hydrops: major antigens known to induce clinically significant immuno rxns are certain Rh Ags and ABO blood groups
a. 2nd and subsequent pregnancies in Rh-(-) mom w/Rh-(+) dad
b. O- moms

Question 53

Q

What happened here?

Answer

A

Fetal hydrops: generalized accumulation of fluid in the fetus
RIGHT image: fluid accumulation is particularly prominent in the soft tissues of the neck, and this condition has been termed cystic hygroma
1. Characteristically seen, but not limited to, constitutional chromosomal anomalies such as 45,X karyotypes (Turner’s syndrome)

Question 54

Q

What is SIDS? Risk factors?

Answer

A

Sudden death of infant <1 year of age that remains unexplained after thorough case investigation, incl performance of a complete autopsy, examination of the death scene, and review of the clinical history
1. Aka, sudden unexpected infant death (SUID)
“Triple-risk” model that postulates the intersection of three overlapping factors:
1. Vulnerable infant,
2. Critical devo period in homeostatic control,
3. Exogenous stressor
NOTE: babies should sleep on their backs

Question 55

Q

Klinefelter syndrome

Answer

A

XXY
Eunucoid (indeterminate sex) features
Loss of sertoli cells = loss of inhibin and INC FSH
1. FSH stimulates aromatase in gonads, INC estrogen
2. Female secondary sex characteristics at puberty

Question 56

Q

Androgen insensitivity syndrome

Answer

A

XY phenotypic “female;” presents w/amenorrhea
Normal testis: leydig cells make testosterone
1. Loss of testosterone receptor activity
2. No testosterone effect = NO development of male reproductive structures
No conversion of testosterone to DHT = no external developed male genitals
XY means presence of MIF (sertoli cells), inhibits female reproductive organs, however, distal 2/3 forms due to estrogen (also normal breast)

Question 57

Q

Premature ovarian failure

Answer

A

Female <40 with amenorrhea
Loss of entire ovarian function
DEC estrogen and inhibin feedback results in increased FSH and LH
Progesterone withdrawal test is negative for bleeding

Question 58

Q

PCOS

Answer

A

Female presents with amenorrhea and hirsutism
INC LH with intact ovary -> INC testosterone (hirsutism)
INC T converted to estrogen by aromatase, so INC LH (like LH surge) and INH FSH, leading to NO follicle development
1. Follicle becomes a cyst
Progesterone test is positive for bleeding

Question 59

Q

Turner syndrome

Answer

A

46, XO: monosomy
Short, primary amenorrhea, lymphedema at birth
Shield chest, wide nipples
Webbed neck and low hair line
Coarctation of the aorta
Streak ovaries –> little estrogen
1. Elevated FSH and LH

Question 60

Q

Kallman syndrome

Answer

A

Defect in hypothalamic production of GnRH
Associated with anosmia: inability to perceive odor
Delayed puberty

Question 61

Q

What is the progesterone withdrawal test?

Answer

A

Give patient w/amenorrhea medroxyprogesterone acetate (Provera) 10 mg daily for 5-10 days or one IM injection of 100-200 mg of progesterone in oil
If patient experiences bleeding after the progestin, she has estrogen present but is not ovulating (anovulation)
If no withdrawal bleeding occurs, either patient has very low estrogen levels or there is a problem with the outflow tract such as uterine synechiae (adhesions) or cervical stenosis (scarring)

Question 62

Q

Appreciate this.

Answer

A

Good job!

Question 63

Q

What are the most common palpable breast lesions?

Answer

A

Cysts
Fibroadenomas
Invasive carcinomas

Question 64

Q

Where are most carcinomas located in the breast? Do they metastasize?

Answer

A

About 50% are located in the upper outer quadrant
Some do metastasize, and the majority of those that do will have done so by the time they reach a size that can be palpated -> around 2-3cm
1. This is why mammography has become such a big deal -> helps us catch lesions earlier
Note: ductal and lobular carcinomas come from the same cell type, but appear different

Answer 64

A

10% in women younger than age 40 are malignant
60% are malignant in women over 50
Breast cancer risk goes starts going back down after age 65 (see attached)

Answer 65

A

ABNORMAL MAMMOGRAM

Answer 66

A

Benign cyst formation and fibrosis
Most common abnormality in premenopausal women
Cyclic changes with menstrual cycle, especially fibroadenomas
1. Oral contraceptive pills (OCP) seem to DEC risk
Subdivided into proliferative (slightly more risk than non-proliferative to progress to something malignant, but still minimal) and non-proliferative
IMAGE: UDH = usual ductal hyperplasia, ADH = atypical ductal H, ALH = atypical lobular H

Answer 67

A

Cysts and fibrosis
May have calcifications picked up on mammography
Cysts may undergo apocrine metaplasia

Answer 68

A

Gross image of fibrocystic changes
Normal breast has a lot of yellow, fatty tissue, but fibrosis is white and springy (going to bounce back if you squish it in)
1. Cancer would be more gritty, and not have the same kind of bounce
Large cyst at the top left
Blue dome cysts: no histologic correlation -> just a gross observation (middle-right of the image)

Answer 69

A

Benign fibrocystic changes: large, cystic structures
Cystic and apocrine metaplasia near the bottom
Some calcification
Can do stains for myoepithelial cells because these are lost in breast cancer

Answer 70

A

Apocrine metaplasia: non-proliferative fibrocystic change
Bright, bubblegum pink color to the cells
Fibrosis instead of the typical breast fat and stroma

Answer 71

A

Usual ductal hyperplasia (UDH): proliferative fibro-cystic change
Lumen filled by a heterogeneous, mixed population of luminal and myoepithelial cell types
1. Two cell layers: NOT DCIS (an invasive cancer that would necessitate lumpectomy or chemo) b/c myoepithelial layer present
2. Cells swarming, hanging out together: all on top of e/o, rather than individualied (as in atypia)
Irregular slit-like fenestrations prominent at periphery

Answer 72

A

Atypical ductal hyperplasia: proliferative fibrocystic change -> atypia b/c cells starting to dissociate from e/o rather than be all on top of e/o
Histo resemblance to ductal carcinoma in situ (DCIS), but not classified as such due to its SIZE
1. >2mm or 2 ducts = DCIS (really ugly cytology or necrosis may also push patho to dx this as DCIS)
2. Still have myoepithelial cells
Relatively monomorphic proliferation of regularly spaced cells, sometimes with cribriform spaces
1. No slit-like spaces, but rather a cookie-cutter appearance (and Roman bridges; archways)

Answer 73

A

Atypical ductal hyperplasia: proliferative fibrocystic change -> atypia b/c cells starting to dissociate from e/o rather than be all on top of e/o
Histo resemblance to ductal carcinoma in situ (DCIS), but not classified as such due to its SIZE
1. >2mm or 2 ducts = DCIS (really ugly cytology or necrosis may also push patho to dx this as DCIS)
2. Still have myoepithelial cells
Relatively monomorphic proliferation of regularly spaced cells, sometimes with cribriform spaces
1. No slit-like spaces, but rather a cookie-cutter appearance (and Roman bridges; archways)

Answer 74

A

Atypical lobular hyperplasia: cells identical to those of lobular carcinoma in situ, but the cells do not fill or distend more than 50% of the acini within a lobule
Can become ductal or lobular carcinoma
Don’t do anything with this right now per standard of care

Answer 75

A

Sclerosing adenosis: proliferative changes
Involved terminal duct lobular unit enlarged, and acini compressed and distorted by dense stroma
1. Dilated glands
Calcifications present within some of the lumens
Unlike carcinomas, acini are arranged in a swirling pattern, and the outer border is well circumscribed
Myoepithelial marker (+) = “good to go” in calling this sclerosing adenosis rather than carcinoma

Answer 76

A

Radiograph: irregular central mass with long radiodense projections (needle-localized lumpectomy in this image)
Grossly: solid and has irregular borders, but not as firm as an invasive carcinoma; tan/yellow instead of grey/gritty of cancer
Micro: central nidus of small tubules in a densely fibrotic stroma w/numerous projections containing epithelium with varying degrees of cyst formation and hyperplasia
1. Thick, keloid-like collagen with ducts radiating from central location

Answer 77

A

Minimal to no INC risk:
1. Non-proliferative changes: cysts, fibrosis, apocrine metaplasia
2. Mild hyperplasia (UDH)
Slightly INC (1.5-2-fold):
1. Moderate to florid hyperplasia (w/o atypia)
2. Ductal papilloma
3. Sclerosing adenosis
Significant risk (5-fold__): ADH, ALH, DCIS, LCIS

Answer 78

A

Acute mastitis: breastfeeding; staph aureus
Fat necrosis: trauma, might calcify and appear abnormal on a mammography (attached image: shriveled and ghost-like, with lipid-laden macros coming in to clean up everything)
Mammary duct ectasia: nonbacterial chronic inflammation
Lymphocytic mastitis: diabetes, possible autoimmune (not common; incidental finding)
1. Comes in and encircles the ducts
Granulomatous mastitis: TB, injections, breast implants, sarcoidosis

Answer 79

A

Fibroadenoma
Phyllodes tumor
Intraductal papilloma
Carcinoma

Answer 80

A

MOST COMMON benign neoplasm of F breast
Usually relatively small, but can get pretty large
1. Juvenile FA: can rapidly enlarge in teens
Biphasic: glands AND stroma, but only stroma truly neoplastic
1-10cm fibroepithelial lesion

Answer 81

A

Fibroadenoma: usually very well circumscribed
Not fixed (mobile); cancer tends to be more fixed because it can be invasive
BIPHASIC: ducts and stroma (stroma squeezes the ducts closed/down)

Answer 82

A

Fibroadenoma: usually very well circumscribed
Not fixed (mobile); cancer tends to be more fixed because it can be invasive
BIPHASIC: ducts and stroma (stroma squeezes the ducts closed/down)

Answer 83

A

Phyllodes tumor (stromal): distinguished from FA’s on basis of higher cellularity & mitotic rate, nuclear pleomorphism, stromal overgrowth, and infiltrative borders -> leaf-life pattern

Answer 84

A

Phyllodes tumor: stromal
Most of these are NOT malignant, but the ones that are will look kind of like a fibrosarcoma with lots of stromal overgrowth and mitotic figures
Cigar-shaped cells

Answer 85

A

Malignant phyllodes tumor: most of these are NOT malignant, but this one is
>10 mitotic figures per 10 high per fields AND stromal > ductal overgrowth
Densely packed anaplastic stromal cells and infiltrative border
Tumor necrosis, heterologous stromal elements, may have cellular stroma only around blood vessels

Answer 86

A

Papillary projection inside the duct
Can present with nipple discharge, and can rarely induce nipple retraction
Double layer epithelium helps differentiate between papillary carcinoma, but not always so black and white
Have to be really careful with diagnosing these because biopsy may alter the integrity of the sample

Answer 87

A

Intraductal papilloma: central fibrovascular core extends from the wall of a duct.
The papillae arborize within the lumen and are lined by myoepithelial AND luminal cells (two cell layers distinguishes this from carcinoma)
Fibrovascular stalk
Location is one of the keys: sub-areolar

Answer 88

A

12.3% (1 in 8 women)
Most common cancer in women, and 3rd most common cause of death from cancer

Answer 89

A

We have not made much progress in regards to limiting deaths from breast cancer

Answer 90

A

African-americans die at a much higher rate (then Caucasians)

Answer 91

A

Age: INC through life
Geographic variations: environmental, higher in US and Northern Europe
Race: AA
Exogenous estrogens: shift to combined estrogen + progesterone created drop in new cases
Radiation
1. Genetics: ataxia telangiectasia -> likelihood of breast cancer and radiation
Others include obesity (estrogen), alcohol, and high fat diet

Answer 92

A

Tumor size
Lymph node status

Answer 93

A

Incompletely understood, but multifactorial:
1. Genetics
2. Hormonal influences
3. Environmental influences

Answer 94

A

Genetic profiling can separate the 4 molecular subtypes:
1. Luminal A: ER+, Her2(-) -> better molecular subtype for tx
2. Luminal B: ER+, HER2+ -> more high-grade, so more aggressive
3. Her2+: ER-, Her2 over-expressed -> NOT good (Her2 amplification = more aggressive tumors)
4. Basal type: ER-, Her2(-) -> really difficult to tx, esp. if also progesterone (-)

Answer 95

A

10%
More likely to be bilateral and to have other cancers, ovarian
More likely to have a family history
To develop cancer before menopause
And belong to certain ethnic groups
1/3 (of this 10%) have BRCA1 or BRCA2
Other: Li-Fraumeni (p53), Cowden (PTEN: also endometrial cancer), ataxia-telangiectasia carriers

Answer 96

A

Tumor suppressor genes -> both alleles must be inactivated
Most carriers devo cancer by age 70 (30-90%)
12% of women referred for genetic testing have BRCA1/2 deleterious muts; higher in Ashkenazi Jewish women
1. Pts really need to see a genetic counselor before being tested

Answer 97

A

Tumor suppressor gene at 17q21 that may interact with p53; autosomal dominant (DEC penetrance)
BRCA1 muts present in 10% of women with:
(a) No family history
(b) Breast cancer onset by age 40 years, and
(c) High grade, triple negative tumors
Breast cancer usually by ages 40-59
Most effective predictor is age of onset < 50 years, and triple negative status (greater incidence of medullary tumors)

Answer 98

A

Carriers: close F/U or prophylactic mastectomy
Tamoxifen may prevent bilateral breast cancers in ER(-) tumors
INC risk of recurrence after breast conserving surgery
BRCA1 status does not appear to affect death rates, but is associated with resistance to certain chemotherapy agents

Answer 99

A

Medullary tumor of the breast: greater incidence in BRCA1+ pts
1. If you see this on patho report, test them for BRCA1, even if no family history
Usually high grade (basal-like phenotype)
Abundant intra- and peri-tumoral lymphocytes
Pretty well circumscribed, with pushing border rather than infiltrative

Answer 100

A

Usually high grade (basal-like phenotype)
Abundant intra- and peri-tumoral lymphocytes
Greater incidence of medullary tumors
High incidence of DCIS

Answer 101

A

Tumor suppressor gene at 13q12-13
Usually get breast cancer by age 50
Pts also have higher risk of cancers of the ovary (39-63%), bone, pharynx, prostate, pancreas, and other organs
1. More incidence of other tumors than with BRCA1
Slightly more frequent in black (2.6%) versus white (2.1%) American patients

Answer 102

A

Usually invasive ductal carcinoma, no special type
High grade features and pushing tumor margin
High incidence of DCIS
Don’t have same circumscription as BRCA1 tumors

Answer 103

A

Estrogen/hormone imbalance play significant role
Long duration of reproductive life, nulliparity, and late age at birth of first child
All INC estrogen unopposed by progesterone
Functional ovarian tumors

Answer 104

A

Noninvasive: still have myoepithelial cells
1. Ductal carcinoma in-situ (DCIS)
2. Lobular carcinoma in-situ (LCIS)
Invasive
1. Invasive Ductal Carcinoma (NOS)
2. Invasive lobular carcinoma
3. Medullary Carcinoma
4. Colloid/Mucinous Carcinoma
5. Tubular Carcinoma

Answer 105

A

Many patterns: solid, comedo, cribriform, papillary, micropapillary
1. Comedo type: central necrosis (>50%) and high grade nuclei; more likely to progress to invasion (atypical cytology)
Calcifications frequent
Good prognosis: can take a long time for these to progress to full-blown carcinoma
Current tx options include lumpectomy, radiation and anti-estrogenic agents like Tamoxifen

Answer 106

A

DCIS: cribriform pattern

Answer 107

A

High-grade DCIS: comedo type
These cells are huge, prominent nuclei
Easy to pick out mitotic figures
Pyknotic

Answer 108

A

Uniform, low grade monotonous cells
Intracellular, “targetoid” mucin
Treatment either chemotherapy OR close F/U
Loss of e-cadherin: come from same cell as DCIS, but this loss of e-cadherin makes it different
Morphological keys: tend to be much simpler cytology than DCIS
1. Look kind of like lymphos
2. Round nuclei

Answer 109

A

70-80% of tumors fall into this category
Can be associated with DCIS
NO myoepithelial cell layer
Arises from terminal duct lobular unit (as does lobular carcinoma), not ductal epithelium, so nomenclature is not actually accurate

Answer 110

A

Invasive ductal carcinoma: atypical cells
Some ducts
Tumor cells infiltrating into and through the stroma and collagen
NO myoepithelial cells here (single cell layer)

Answer 111

A

Invasive ductal carcinoma

Answer 112

A

Invasive ductal carcinoma with desmoplastic response
Lighter, purple kind of stroma in the background
High N/C ratios

Answer 113

A

Invasive ductal carcinoma with desmoplastic response

Answer 114

A

Loss of expression of CDH1, gene that encodes E-cadherin -> (-) for E-cadherin, while ductal will be (+)
Males and females w/heterozygous germline muts in CDH1 also have a greatly INC risk of gastric signet ring cell carcinoma (image attached)
1. Lamina propria with cells with mucin pushing nuclei out to the edge
2. Form of adenocarcinoma that produces mucin
Start to fall apart because they have lost their E-cadherin
She said this was IMPORTANT to remember

Answer 115

A

Lobular carcinoma: infiltrates with lines in the stroma -> caterpillars (or indian file)

Answer 116

A

Lobular carcinoma
Targetoid mucin droplet pushing mucin to the side

Answer 117

A

Lobular carcinoma
Indian file infiltration: cells line up (loss of adhesion due to loss of E-cadherin)

Answer 118

A

Medullary carcinoma: rare subtype w/strict criteria
Unclear whether good or poor prognosis according to current research
Minority of cases may be associated with germ line BRCA1 mutations
Recurrences are very rare more than 5 years post detection

Answer 119

A

Medullary breast carcinoma: indistinct cell borders (syncytial growth)
Large pleomorphic tumor cells containing large nuclei, prominent nucleoli, numerous mitotic figures
Prominent lymphoplasmacytic infiltrate at periphery
Pushing borders, but well circumscribed

Answer 120

A

Colloid carcinoma: 10-yr survival for pure form >90% (much better than ductal carcinoma NOS)
Slow growing
Usually older women, around 70: good prognosis
Tumor cells floating in huge pools of mucin
*NOS = not otherwise specified

Answer 121

A

Tubular carcinoma: favorable prognosis
Composed of:
1. Distinct, well-differentiated angular tubular structures (90%+ according to WHO) with
2. Open lumina,
3. Lined by a single layer of epithelial cells
Can be more difficult because can look like sclerosing adenosis
Tadpole angles, gland looking

Answer 122

A

Micropapillary variant carcinoma

Answer 123

A

Micropapillary variant carcinoma
Very aggressive with poor prognosis
95% have lymph node metastases at presentation
70% recur, 50% die of disease
Clinicians need to know this is what it is because it needs to be treated more aggressively

Answer 124

A

Paget disease of the nipple: extension up the lactiferous duct and into skin of nipple
Produces crusted nipple and skin
In almost all cases, have underlying carcinoma
DDx: melanoma

Answer 125

A

Clinically defined
Enlarged swollen erythematous breast with no palpable mass (red, inflammatory)
Underlying carcinoma usually poorly differentiated and diffusely infiltrative
5-year survival <50%, and even lower if metastatic
Gone to dermal lymphatics under skin -> huge chunks of carcinoma in dermal lymphatics

Answer 126

A

Peau d’orange: thickened skin due to lymphatic congestion

Answer 127

A

Gynecomastia: hormone influence, typically estrogen excess
1. Causes include: cirrhosis (liver can’t metabolize estrogen), Klinefelter syndrome, anabolic steroids, and drugs
2. Physiologic, and can occur in puberty and old age
Cancer is rare, but it does occur! (especially if BRCA or Li Fraumeni)

Answer 128

A

Gynecomastia: men do NOT have lobules
INC ducts and prominent stroma: may be edematous with INC cellularity, and late phase may have fibrosis (pale areas around ducts)

Answer 129

A

EPI: abnormal urethral orifice on dorsal aspect of penis
HYPO: ventral aspect; can result in obstruction, and may be associated with other abnormalities, like inguinal hernia and undescended testes

Answer 130

A

Local inflammation of the glans penis and of the overlying prepuce, respectively
Agents: Candida albicans, anaerobic bacteria, Gardnerella, pyogenic bacteria
Most cases a consequence of poor local hygiene in uncircumcised males

Answer 131

A

Germ tube: outgrowth produced by spores of spore-releasing fungi during germination
Think about Candida

Answer 132

A

Condition in which the prepuce cannot be retracted easily over the glans penis
Inflammation or congenital

Answer 133

A

Squamous cell carcinoma of the penis: associated with HPV infection (16, 18)
1. Cellular atypia, parakeratosis, and mitotic figures -> carcinoma in situ
2. Can also get condylomas (HPV 6 and 11)
Ulceration on the glans or shaft of the penis
Can spread to inguinal nodes and rarely to distant sites
Most cases occur in uncircumcised males: SCC of the scrotal skin one of the first that was linked to hygiene

Answer 134

A

Failure of testicular descent into the scrotum
Diagnosis after 1 year of age (1%)
Unknown cause
Associated with infertility, and 3-5-fold risk of testicular cancer
Orchiopexy: surgery to remove the cryptorchid testicle -> reduces risk of sterility and cancer
1. Often infertile, even if they move the testicle down to where it is supposed to be; also still have a risk of cancer

Answer 135

A

More common in testis than epididymis, and often sexually transmitted; other causes of testicular inflam include:
1. Non-specific epididymitis and orchitis: 1^o UTI that spreads to testis via vas deferens or lymphatics of the spermatic cord -> chiefly neutrophilic infiltrate
2. Orchitis -> mumps infection: 20% males, but rarely in children; lymphoplasmocytic infiltrate
3. TB: granulomatous inflam and caseous necrosis

Answer 136

A

Torsion: obstruction of testicular veinous drainage, but thick-walled and more resilient arteries remain patent
1. NEONATAL: in utero or shortly after birth; lacks any associated anatomic defect
2. ADULT: typically sudden onset of testicular pain; results from a bilateral anatomic defect whereby the testis has increased mobility
One of the few urologic emergencies – if fixed in 6 hours, there is a good chance that the testis will remain viable
Histo: residual testicle on left and hemorrhage on right

Answer 137

A

Overall, not very common (6 per 100,000 males); peak in 15-34-y/o age group
Unknown cause; whites > blacks
Seminoma (95%) from germ cells in post-pubertal males, and are malignant
Non-seminoma
1. Embryonal carcinoma
2. Yolk sac tumor
3. Choriocarcinoma
4. Teratoma
Neoplasms from Sertoli or Leydig cells (sex cord–stromal tumors) uncommon and usually benign
Can’t shine a light through a cancerous protuberance, unlike hydrocele
Don’t needle these because they don’t want to spread them; just take them out -> assumed to be malignant

Answer 138

A

Seminoma: sheets of polygonal cells with lymphos in the stroma (20-30-y/o)
1. Delineated, large cells w/prominent nucleoli, lymphos in background, and clearing around the nucleus
Syncytiotrophoblasts in 15%: minimally elevated serum hCG concentrations (NO bearing on prognosis)
Also looks like germinoma that happens in brain or mediastinum

Answer 139

A

Non-seminoma embryonal carcinoma: primary can be small, but metastatic
Pure cases rare, typically mixed
Sheets of undifferentiated cells and primitive gland-like structures
Nuclei are large and hyperchromatic -> more high-grade than the seminoma, and much more anaplastic-looking
With chemo, these cells can actually start to differentiate, and look more like a teratoma

Answer 140

A

Yolk sac tumor: children <3; good prognosis
Often have eosinophilic hyaline globules with α-1-antitrypsin and alpha fetoprotein (AFP)
Areas of loosely textured, microcystic tissue and papillary structures resembling a developing glomerulus (Schiller-Duval bodies: circled on attached image)

Answer 141

A

Yolk sac tumor (non-seminoma): children <3; good prognosis
Often have eosinophilic hyaline globules with α-1-antitrypsin and alpha fetoprotein (AFP)
Areas of loosely textured, microcystic tissue and papillary structures resembling a developing glomerulus (Schiller-Duval bodies: circled on attached image -> vessel surrounded by anaplastic cells and a space)

Answer 142

A

Choriocarcinoma: cytotrophoblastic cells with central nuclei (arrowhead, upper right) and syncytiotrophoblastic cells with multiple dark nuclei embedded in eosinophilic cytoplasm (arrow, middle) are present
Hemorrhage and necrosis are prominent
hCG in syncytiotrophoblasts can be identified by IHC staining and is elevated in the serum
Invasive: go to vessels quickly and metastasize -> may be small, and already have metastasized

Answer 143

A

INFANTS/KIDS: pure forms fairly common, second in frequency only to yolk sac tumors
ADULTS: pure teratomas are rare; 2-3% of germ cell tumors, and most are seen in combo with other histologic types (like with embryonal carcinomas)
Elements may be mature (resembling various tissues within the adult) or immature (sharing histologic features with fetal or embryonal tissues)
ANY AGE: prepubertal males -typically benign, postpubertal males are malignant

Answer 144

A

Teratoma: mature cells from endodermal, mesodermal, and ectodermal lines
Four different fields from same tumor specimen contain:
1. Neural (ectodermal; ganglion cells) (A),
2. Glandular (endodermal) (B),
3. Cartilaginous (mesodermal) (C), and
4. Squamous epithelial (D) elements

Answer 145

A

Prostatitis
BPH (nodular hyperplasia): TZ
1. Symptoms: hesitancy, dribbling
Carcinoma: PZ

Answer 146

A

Note the intraluminal secretions -> helpful for ID’ing this tissue
Two layers of cells: when basal layer is lost, this is malignancy
1. Glands also get more simple when they become carcinoma: nice and round, rather than tortuous

Answer 147

A

Bacterial prostatitis
May be acute or chronic
Responsible organism usually is E. coli or another gram-negative rod
Can also be STI’s in younger men
Can still see 2 cell layers, so not a neoplasm

Answer 148

A

Proliferation of benign stromal and glandular elements -> DHT (androgen derived from T) is the major hormonal stimulus for proliferation
1. Normal proliferation rate, but NOT dying at a normal rate -> growth factors keep them alive
BPH nodules can compress the prostatic urethra
Clinical symptoms: hesitancy, urgency, nocturia, and poor urinary stream
1. Chronic obstruction predisposes to recurrent UTI’s (can cause pyelonephritis, but would likely come in before that)
NOT pre-malignant

Answer 149

A

BPH
Nodular, mostly in the central transition zone
Still has the 2 cell layers (see attached image), so this is a benign process: a lot more stroma
Really fibrous

Answer 150

A

Men >50-y/o
25% of cancer in men in the US, but only 9% of deaths (
Clinical and experimental observations suggest pathogenic roles of:
1. Androgens
2. Heredity
3. Environmental factors
4. Acquired somatic mutations
Low-grade take a long time to progress to high-grade

Answer 151

A

Adenocarcinoma of the prostate
Carcinomatous tissue on posterior aspect (lower left)
Note the solid whiter tissue of cancer, in contrast w/the spongy appearance of the benign peripheral zone on the contralateral side

Answer 152

A

Prostate adenocarcinoma: normal gland at bottom left, but the rest are carcinoma glands -> small, simple, round, invading stroma
This is low-grade: grade 3

Answer 153

A

Prostate adenocarcinoma -> loves to invade nerve tissue (perineural invasion shown here)

Answer 154

A

Grading system of prostate cancer -> correlates with pathologic stage and prognosis
Pathologists start reporting at 3
1. 4: cribriforming; glands start fusing together
2. 5: single cells infiltrating the stroma
Biopsy done in systematic way to get an idea of the volume of the tumor (volume + grade is what determines whether it stays or goes)
1. 2 grades: most commonly seen pattern + 2nd most commonly seen -> 4 + 3 in younger patient getting surgery; grade 5 definitely getting surgery

Answer 155

A

Prostate cancer
Normal glands have more cytoplasm and 2 cell layers; carcinoma glands DO NOT
1. Both types of glands shown in these two images

Answer 156

A

PROSTATE CANCER
IHC stains showing normal basal cells (brown) in a benign gland and NO basal cells in the malignant glands on the right side (no brown staining)
Malignant glands show increased expression of racemase (AMCAR; red cytoplasmic stain) -> stains malignant glands in the prostate
Perinueural invasion in the image on the left (this is a common feature of prostate cancer)

Answer 157

A

T2: tumor confined within prostate
T2c: tumor involving both lobes
T3a: extra-capsular extension (uni- or bilateral)
T3b: tumor invading seminal vesicle(s)
Don’t need to memorize, but just realize that you are looking for invasion, extracapsular extension and tumor involving both lobes
When you are concerned about something being a metastatic prostate cancer, you can stain for PSA, but this staining is NOT used for prostate samples

Answer 158

A

Urothelium: composed of 5-6 layers of cells with oval nuclei, often with linear nuclear grooves
1. Surface layer of large, flattened, umbrella cells with abundant cytoplasm
Found in renal pelvis, ureters, bladder, and urethra (except terminal portion)
Aka, transitional epithelium
Think about this like a specialized squamous epithelium: mucosal surface
NO mitotic figures or atypia

Answer 159

A

Defining whether or not there is invasion into the muscular layer is important -> determines prognosis

Answer 160

A

Double/bifid ureters: most are unilateral, and of NO CLINICAL SIGNIFICANCE
Congenital

Answer 161

A

Hydronephrosis (cystic spaces): ureteropelvic junction (UPJ) obstruction is the most common cause in infants and children
Males, bilateral (20%); often associated with other congenital anomalies
Abnormal organization of smooth muscle bundles at the UPJ, to excess stromal deposition of collagen between smooth muscle bundles, or rarely to congenitally extrinsic compression of the UPJ by renal vessels
Congenital, and can be associated with other congenital abnormalities

Answer 162

A

Diverticula: saccular outpouchings of the ureteral wall
Uncommon: may be congenital or acquired
Typically asymptomatic, but urinary stasis with recurrent infections possible

Answer 163

A

Low-grade papillary urothelial carcinoma: 1^o malignant tumors of the ureter resemble those arising in the renal pelvis, calyces, and bladder
1. Papillary lesion: fibrovascular core, too many cell layers (>6-7)
Majority are urothelial carcinomas -> this example is low grade
1. If there is any area of high-grade, the whole lesion is high-grade: more pleomorphism, hyperchromatic, mitotic figures
Occur most frequently in 6-7th decades of life and cause obstruction of the ureteral lumen
Can be multifocal; commonly occur concurrently w/similar neoplasms in bladder or renal pelvis
1. Can be hard to get control of; like to come back, esp. in the bladder

Answer 164

A

INTRINSIC: calculi, strictures, tumors, blood clots, neurogenic
EXTRINSIC: pregnancy, periureteral inflammation, endometriosis, tumors
CONSEQUENCES: hydroureter, hydronephrosis, pyelonephritis
1. Kidney involvement is a major consequence

Answer 165

A

Sclerosing retroperitoneal fibrosis: uncommon, and can cause ureteral narrowing or obstruction
Middle to late age males
Subset related to IgG4-related disease: associated w/elevated serum IgG4 and fibroinflammatory lesions rich in IgG4-secreting plasma cells
1. Reidel’s thyroiditis association (woody, fixed thyroid)
Tubulointerstitial with fibrous and prominent infiltrate of lymphocytes, plasma cells (frequently IgG4-positive), and eosinophils

Answer 166

A

Most common and serious congenital anomaly
Major contributor to renal infection and scarring
NOTE: diverticula also possible in the bladder

Answer 167

A

Exstrophy of the bladder: developmental failure in the anterior wall of the abdomen and the bladder
Bladder either communicates directly through a large defect with the surface of the body or lies as an opened sac

Answer 168

A

Urachus (canal that connects fetal bladder with the allantois) is normally obliterated after birth, but it sometimes remains patent in part or in whole
1. Totally patent: fistulous urinary tract connects the bladder with the umbilicus
2. Only central region of the urachus persists: urachal cysts, lined by urothelium or metaplastic glandular epithelium -> may lead to carcinomas, mostly glandular tumors

Answer 169

A

Cystitis of the bladder: malakoplakia (raised mucosal plaques)
Filled with foamy macrophages, occasional multinucleate giant cells, and lymphocytes
Macros have abundant granular cytoplasm due to phagosomes stuffed w/particulate & membranous debris of bacterial origin
Mineralized concretions resulting from deposition of calcium = Michaelis-Gutmann bodies (circled in the attached image)

Answer 170

A

Cystitis of the bladder: malakoplakia (raised mucosal plaques)
Filled with foamy macrophages, occasional multinucleate giant cells, and lymphocytes
Macros have abundant granular cytoplasm due to phagosomes stuffed w/particulate & membranous debris of bacterial origin
Mineralized concretions resulting from deposition of calcium = Michaelis-Gutmann bodies (circled in the attached image)
Repeated bacterial infections: macros don’t eat up and destroy the bacterial particulate correctly
Yellow-white, plaque-like lesions

Answer 171

A

Squamous cell carcinoma of the bladder
CAUSES: cigarette smoking, various occupational carcinogens (hair dyes), and Schistosoma haematobium (blood drop; see attached image)
1. Schistosoma: Japonicum (Japanese flag), Mansoni (man); young, middle eastern men

Answer 172

A

PUNLMP: papillary urothelial neoplasm of malignant potential
LGUC: low-grade urothelial carcinoma
HGUC: high-grade urothelial carcinoma

Answer 173

A

Bladder carcinoma in situ: umbrella cells gone or falling off -> can clue you in to carcinoma of the bladder
Mitotic figure
Whole urothelium is affected
FLAT lesion (NOT papillary): these can be a little more difficult to see, and may progress faster than some of the papillary lesions

Answer 174

A

Low-grade papillary urothelial carcinoma (LGUC): >5-6 cell layers
Mitotic figures
Some atypia

Answer 175

A

High-grade urothelial carcinoma: HGUC
Lots of atypia
Cells falling off the top
Very large cells

Answer 176

A

High-grade invasive urothelial carcinoma: FLAT lesion
Not an INC # of cell layers, but hyperchromatic and have very high N/C ratios
Can even have areas that undergo metaplasia to squamous cells, and keratinize
A little bit of desmoplasia

Answer 177

A

High-grade invasive urothelial carcinoma
BM-like division between the stroma and the papillary lesion
Necrosis, apoptotic cells, large, prominent nucleoli, high N/C ratios, lots of mitotic figures

Answer 178

A

Aka, lues: chronic venereal infection caused by the spirochete Treponema pallidum
Like all other ulcerative genital diseases, syphilis promotes transmission of HIV, and HIV stimulates the progression of syphilis

Answer 179

A

Syphilis spirochetes are readily demonstrable in histologic sections of early lesions with the use of standard silver stains (e.g., Warthin-Starry stains)
1. T. pallidum
Pathognomonic micro lesion is a proliferative endarteritis with an accompanying inflammatory infiltrate rich in plasma cells
Lg areas of parenchymal damage in 3^osyphilis result in formation of gumma, an irregular, firm mass of necrotic tissue surrounded by resilient connective tissue (see attached image)

Answer 180

A

LEFT: syphilitic chancre of the scrotum
1. These lesions are typically are painless despite ulceration, and heal spontaneously
RIGHT: histologic features of the chancre include a diffuse plasma cell infiltrate beneath squamous epithelium of skin
1. Plasma cells: perinuclear hof, like to hover around the blood vessels

Answer 181

A

Syphilis gumma: central zone of coagulative necrosis (tertiary syphilis)
Surrounded by a mixed inflammatory infiltrate of lymphocytes, plasma cells, activated macrophages (epithelioid cells), occasional giant cells
Peripheral zone of dense fibrous tissue

Answer 182

A

Trichomoniasis
Pear-shaped organisms with flagella

Answer 183

A

Genital herpes simplex
Margination of the chromatin, multi-nucleation, nuclear viral inclusions (with molding)

Answer 184

A

Inflammation: gonococcal and nongonococcal causes
Benign epithelial tumors: squamous and urothelial papillomas, inverted urothelial papillomas, and condylomas
Primary carcinoma: uncommon lesion; depending on area of origin, are urothelial or squamous

Answer 185

A

Urethral caruncle: inflammatory lesion that presents as a small, red, painful mass about the external urethral meatus
Typically in OLDER FEMALES
Inflamed granulation tissue covered by an intact, but extremely friable urothelial mucosa, which may ulcerate and bleed with the slightest trauma
Surgical excision affords prompt relief and cure

Answer 186

A

High-grade urothelial carcinoma: invasion of the detrusor muscle
Up to half of people that have this invasion can have occult metastatic disease

Answer 187

A

In the fallopian tubes, and they metastasize to the ovary

Answer 188

A

Inflammation: gonococcus, chlamydia, TB
Benign paratubal cysts
Tumors are uncommon (*except it is believed serous carcinomas of the ovary arise here, and met there)

Answer 189

A

Non-neoplastic: 1) cysts: follicular and luteal, and 2) PCOS
Neoplastic:
1. Surface epithelial tumors: serous, mucinous, clear cell, Brenner, MMMT, metastatic
2. Sex cord stromal tumors: granulosa cell, fibromas/fibrothecomas, Sertoli-Leydig
3. Germ cell tumors: teratoma, dysgerminoma, yolk sac tumor, mixed

Answer 190

A

Follicular cyst: granulosa lining cells are present if the intraluminal pressure has not been so great as to cause their atrophy
Outer theca cells may be conspicuous due to INC amounts of pale cytoplasm
Mostly just see a space because granulosa and theca cells squeezed out to the edge

Answer 191

A

Corpus luteal cyst: present in normal ovaries of women of reproductive age
Lined by a rim of bright yellow tissue containing luteinized granulosa cells -> occasionally rupture and cause a peritoneal reaction
HISTO: luteinized granulosa cells (top arrow) bright yellow grossly and thecal cells (bottom arrow)
Can hemorrhage and cause abdominal pain

Answer 192

A

Benign: cystadenoma
Borderline: malignant, but low malignant potential; don’t see invasion, so don’t know exactly how it is going to behave
MMMT and metastatic do NOT have this classification system

Answer 193

A

STIC: serous tubal intraepithelial carcinoma; early malignant cells break off fimbriae, get into ovary somehow, and develop into high-grade serous
Low-grade serous develop in the ovary proper
NOTE: endometrioid tumor looks like endometrial carcinoma, but arises in ovary
1. Can have an endometrioid tumor, and endometrial carcinoma at the same time: arise independently, not metastatically

Answer 194

A

Most common malignant ovarian tumors; 40% of all cancers of the ovary
1. 70% benign or borderline, 30% malignant: not too worried about malignant tumors until pts get into their 60’s
Inherited germline mutations in both BRCA1 and BRCA2 increase susceptibility
Bilaterality common: 20% cystadenomas, 30% of borderline, and 66% of serous carcinomas
1. Bilateral doesn’t necessarily mean malignant

Answer 195

A

Serous cystadenoma (left): stromal papillae with a columnar epithelium
Not a lot of cytoplasm, and no atypia
No architectural complexity

Answer 196

A

Serous cyst adenofibroma: like a cystadenoma, but with a fibrous component
Not a lot of cytoplasm, and no atypia
No architectural complexity

Answer 197

A

Serous borderline: INC architectural complexity and epithelial cell stratification

Answer 198

A

LEFT: low-grade serous carcinoma -> complex micropapillary growth (pseudo-papillary appearance)
RIGHT: high-grade serous carcinoma -> invasion of underlying stroma
1. Distinguished from low-grade tumors by more complex growth patterns & widespread infiltration, or frank effacement of underlying stroma
PRESENTATION: usually really late with abdominal pain and INC abdominal girth: ascites because bits of tumor will seed abdominal cavity

Answer 199

A

Mucinous tumor of the ovary: mutation of KRAS oncogene a consistent genetic alteration in these
Looks like colon adenocarcinoma, which likes to metastasize to the ovary
Can get very large: tenacious, gross mucous
MALIGNANT: serosal penetration and solid areas of growth -> architectural complexity, incl. areas of growth, cellular stratification, cytologic atypia, and stromal invasion
1. When you get one of these, you will tell the surgeon to check the appendix too (to make sure it is not a met)
BENIGN: nice and smooth a good indicator

Answer 200

A

Psudomyxoma peritonei: clinical condition with extensive mucinous ascites, cystic epithelial implants on the peritoneal surfaces, adhesions, and frequent involvement of the ovaries
Recent evidence points to the source being, in almost all cases, extraovarian (usually appendiceal)
1. Mucinous neoplasms of the appendix can look pretty benign, and still cause this
2. Always tell surgeon to check the appendix
ASCITES

Answer 201

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Endometrioid adenocarcinoma: 15-20% of cases coexist with endometriosis
Some have PTEN mutation, similar to endometrial carcinoma

Answer 202

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Brenner (transitional cell) tumor: neoplastic epithelial cells resembling urothelium
Usually benign; characteristic epithelial nests (or islands of cells) in the ovarian stroma
NOTE: also a cystic teratoma on the left in the gross image

Answer 203

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Tumors of müllerian origin -> uterus, fallopian tube, contralateral ovary, or pelvic peritoneum
1. These are MOST COMMON
Extra-müllerian tumors: breast and GI tract (see attached image)
1. Rare cases of pseudomyxoma peritonei, derived from appendiceal tumors

Answer 204

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Ovarian tumors seed locally
Choriocarcinoma is the exception to this rule bc it invades blood vessels, and spreads hematogenously, i.e., to lungs

Answer 205

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Krukenberg tumor: classic metastatic GI carcinoma involving the ovaries
Characterized by bilateral metastases composed of mucin-producing, signet-ring cancer cells, most often of gastric origin (diffuse variant gastric carcinoma from the stomach)
Signet rings: plump cells with lots of cytoplasm, and mucin pushing the nucleus to the side; see attached image (look for this on exam)

Answer 206

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Granulosa cell tumor of the ovary: arranged in sheets punctuated by small, follicle-like structures (Call-Exner bodies; image attached)
Right image shows strong IHC positivity for Inhibin
CLINICAL IMPORTANCE: 1) may elaborate large amounts of estrogen, and 2) may behave like low-grade malignancies (not a high-grade behaving malignancy)
Make little circles because they are trying to recapitulate the follicles
Little grooves on cells -> look like coffee beans

Answer 207

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Fibroma/fibrothecoma/thecoma in ovary: benign, white fibrous bands grossly
Loose syncytium of stromal cells
Meig’s syndrome: combo of findings -> ovarian tumor, hydrothorax, and ascites; genesis unknown
Also associated with basal cell nevus syndrome
REMEMBER: hydrothorax is a pleural effusion when pleural fluid collects in the pleural cavity

Answer 208

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Sertoli-Leydig cell tumor in the ovary: often functional, and commonly produce masculinization or defeminization
Few have estrogenic effects
<5% metastasze

Answer 209

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Teratoma in the ovary: most common
3 categories: 1) mature (benign), 2) immature (malignant), and 3) monodermal/highly specialized
Teeth, skin, hair, nails
Right image: brain, hair follicles, skin
Key is to make sure there are no malignancies here, like SCC (most common) or melanoma
Germ cell tumor

Answer 210

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Immature tissue in teratoma: resemble embryonal and immature fetal tissue (neural most common)
Found in pre-pubertal adolescents, young women
Risk for subsequent extra-ovarian spread is histo grade of tumor (I through III), which is based on the proportion of tissue containing immature neuroepithelium
1. This determines how they behave: the more of this they have, the worse they behave
Always want to ask: Are there immature tissue variants inside? (when you find a teratoma)

Answer 211

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Monodermal teratoma in ovary: thyroid tissue
Struma ovarii

Answer 212

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Dysgerminoma: ovarian counterpart of testicular seminoma
Also present in: mediastinum, pineal gland in brain (germinoma), retroperitoneum
Express receptor tyrosine kinase, KIT and about one third have activating mutations in the KIT gene (IHC staining attached)
All malignant, but only 1/3rd aggressive and spread; all radiosensitive; 80% cure rate
HISTO: fried egg appearance to the cells, with prominent nucleoli
1. Lymphocyte infiltration seals the deal

Answer 213

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Yolk sac tumor: α-fetoprotein
Schiller-Duval body: glomeruloid shape; vessel with malignant cells crowding around it
Hyaline droplets
Aka, endodermal sinus tumor

Answer 214

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Elevated in the sera of 75-90% of women with epithelial ovarian cancer
Undetectable in up to 50% of women with cancer limited to the ovary
Often elevated in a variety of benign conditions and no-ovarian cancers
Primarily used as a MONITORING TOOL (NOT for screening)

Answer 215

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Fibroma/fibrothecoma/thecoma in ovary:
Combo of findings (ovarian tumor, hydrothorax, and ascites) is designated Meigs syndrome. Its genesis is unknown.

Answer 216

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Good job!

Answer 217

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Functional: grows thicker in response to estrogen and is shed during menstruation
Basal: forms the foundation from which the functional layer develops -> is NOT shed

Answer 218

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Proliferative: mitotic figure at the arrow (can also see these in the stroma sometimes, but may be difficult to find)

Answer 219

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Proliferative: simple, columnar epithelium with tubular glands -> multiplying, but not tortuous yet

Answer 220

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Proliferative: nice, round glands

Answer 221

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Secretory: nice tubes have become squiggly glands with secretions inside them
Vacuolization: from basilar to luminal side in early to late
There will be a question about this on the exam

Answer 222

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Early secretory: vacuoles on basilar side of the glands

Answer 223

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Late secretory: vacuoles on the apical side of the glands

Answer 224

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Menstruation/breakdown: clumps of cells with blood in between them
Breakdown typically associated with menstruation

Answer 225

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Menstruation/breakdown: clumps of cells with blood in between them
Breakdown typically associated with menstruation

Answer 226

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Functional endometrial disorders

Answer 227

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Anovulation (failure to ovulate): due to subtle hormonal imbalances, which are most common at menarche and in the perimenopausal period
1. Usually too much estrogen, and/or not enough progesterone -> proliferative phase, but no normal secretory phase, so glands big and dilated, encroach on stroma (normally a 1:1 ratio); disordered endometrium -> prone to breakdown and abnormal bleeding
Less commonly, anovulation is the result of:
1. Endocrine disorders: thyroid disease, adrenal disease, or pituitary tumors
2. Ovarian lesions: functioning ovarian tumor (granulosa cell tumors) or polycystic ovaries
3. Generalized metabolic disturbance: obesity, malnutrition, or o/chronic systemic diseases
Attached image: menstruation/breakdown stage of endometrium -> glands, stroma in clumps, and bleeding in between

Answer 228

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Endometrial polyp: can cause anovulatory bleeding
Cervix on the left and uterus on the right

Answer 229

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Endometrial polyp: polypoid shape with dilated glands
Cystic change, large thick walled blood vessels, fibrous stroma

Answer 230

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Endometrial polyp: cystic change, large thick walled blood vessels, fibrous stroma

Answer 231

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Endometrial polyps in association w/admin of tamoxifen (anti-estrogenic activity on the breast)
Tamoxifen has weak pro-estrogenic effects in the endometrium
Link between estrogen and endometrial changes, including hyperplasia and carcinoma
Not very common, but they do happen -> can look a little different than normal polyps (normal polyp attached)

Answer 232

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Acute endometritis: not very common
Usually retained products of conception (POC)
Removal of the retained gestational fragments by curettage, accompanied by antibiotic therapy, promptly clears the infection

Answer 233

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Chronic endometritis -> occurs in assoc with:
1. Pelvic inflammatory disease (PID)
2. Retained gestational tissue, postpartum or post-abortion
3. Intrauterine contraceptive devices
4. TB: from miliary spread or, more often, from drainage of tuberculous salpingitis -> both are rare in Western countries
Plasma cell is what you want to find: perinuclear hof and clock-face chromatin

Answer 234

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Actinomyces -> sulfur granulomas

Answer 235

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Disordered endometrium histo: due to ovulatory failure
Regardless of cause, ovulatory failure results in excess of estrogen relative to progesterone
1. Endo goes through proliferative phase NOT followed by normal secretory phase
2. Endo glands may devo mild cystic changes or appear disorderly
3. Endo stroma, which requires progesterone for growth, may be scarce -> this combo of abnormalities makes endo prone to breakdown and abnormal bleeding

Answer 236

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Defined by presence of “ectopic” endometrial tissue at a site outside of the uterus (see attached image -> brown-grey discoloration on surface)
Almost always contains functioning endometrium, which undergoes cyclic bleeding (adenomyosis does NOT do this)

Answer 237

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Endometrial tissue in the myometrium
Does NOT undergo cyclic bleeding like endometriosis typically does

Answer 238

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Endometriosis: endo glands, stroma, and hemosiderin
Image of chocolate cyst attached: ovarian cyst rupture

Answer 239

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Endometriosis of the sigmoid colon

Answer 240

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Cause of abnormal bleeding and a frequent precursor to the most common type of endometrial carcinoma
Associated with prolonged estrogenic stimulation of the endometrium unopposed by progesterone
Inactivation of the PTEN tumor suppressor gene is a common genetic alteration in both endometrial hyperplasias and endometrial carcinomas

Answer 241

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Hyperplasia without atypia:
1. Simple hyperplasia without atypia
2. Complex hyperplasia without atypia
Endometrioid intraepithelial neoplasia:
1. Simple hyperplasia with atypia
2. Complex hyperplasia with atypia
Endometrial carcinoma

Answer 242

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Simple endometrial hyperplasia with no atypia: mild glandular crowding and cystic glandular dilation
Loss of organization, but NO cytologic atypia in these glands
Normal proliferative phase endometrium attached

Answer 243

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Complex endo hyperplasia with no atypia: INC glandular crowding w/areas of back-to-back glands and cytologic features similar to proliferative endo
Loss of stroma, but carcinoma would have NO stroma, and be a larger SIZE (needs to be a certain # of cm)
Glands still look the same (no atypia), but they are more crowded
Image of normal proliferative phase endometrium attached

Answer 244

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Complex endo hyperplasia with atypia: very little intervening stroma
Cancer would have NO STROMA
Prominent nucleoli, cells bigger, less cytoplasm, likely to have necrosis
Normal proliferative endo image attached

Answer 245

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Complex endo hyperplasia with atypia: clumpy chromatin (arrow)
Elongated cells with apoptotic debris
High-power view

Answer 246

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Most common invasive cancer of F genital tract
Type I: micro-satellite instability (MSI) -> lynch syndrome association (HNPCC)
1. Depth of invasion usually <0.5 endometrium
2. Defects of DNA mismatch repair genes in about 20% of sporadic tumors (esp. prevalent in HNPCC pts)
Type II: serous -> think HIGH-GRADE (p53)

Answer 247

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Endometrioid carcinoma (FIGO): grading based on pattern, and amount of glandular crowding
1. Grade 1 (top right): non-squamous solid growth pattern 5% or less
2. Grade 2 (bottom left): 6% to 50% non-squamous solid growth pattern
3. Grade 3 (bottom right): 50% non-squamous solid growth pattern
Will often have squamous differentiation (almost a metaplastic change within the cancer)

Answer 248

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Big difference often going to be between pT1a and pT1b -> from less than 1/2 the myometrium to >+1/2

Answer 249

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Serous endometrial carcinoma: grade 3, regardless of histologic pattern
Despite relatively superficial endo involvement, may be assoc w/extensive peritoneal disease
1. Can be metastatic, even if it is a small lesion
p53(+) nuclear stain
Pseudo-papillary projections with small balls of cells that break off

Answer 250

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Malignant mixed mullerian tumors (MMMT’s): aka, carcinosarcomas -> mitotic figures, big cells (only epi components may metastasize)
Epithelial AND stromal components appear to be derived from the same cell
Tumors that have heterologous mesenchymal components (bone, cartilage) do worse
Poor outcomes

Answer 251

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Uterine leiomyoma: (commonly called fibroids)
Perhaps the most common tumor in women

Answer 252

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Leiomyosarcoma: DIFFERENT than leiomyomas (NOT a malignant transformation of them)

Answer 253

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Common and involves, in order of frequency, the cervix, vagina, and vulva
Eearliest lesions usually red papules that progress to vesicles and then to painful coalescent ulcers
High transmission rate during active infection
Migrates to regional lumbosacral nerve ganglia, and establishes a LATENT INFECTION
Gravest consequence of is transmission to the neonate during birth is she is having an outbreak (usually do a C-section to avoid this) -> can cause conjunctivitis and encephalitis

Answer 254

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Herpes: margination, molding (cells all being squished together like “play-doh”), multinucleation
Glassy look; not clear chromatin because the virus has marginated the chromatin, “pushing it out”

Answer 255

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Molluscum contagiosum: poxvirus
Common in young children between 2-12 yrs of age -> transmitted through direct contact or shared articles (e.g., towels)
Sexually transmitted in adults, but not always
Always looks like this -> pink volcano exploding up towards the surface
Bright pink, eosinophilic inclusions

Answer 256

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Candida: extremely common
Typically a result of a disturbance in the patient’s vaginal microbial ecosystem, i.e., via douching or lubricant
RISK FACTORS: diabetes, antibiotics, pregnancy (due to immunocompromised state), and conditions resulting in a compromised immune system
Semi-branching appearance w/pseudohyphae
Tend to cluster: SHISH KEBAB’ING

Answer 257

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Trichomonas vaginalis: protozoan
Asymptomatic OR may complain of yellow, frothy vaginal discharge, vulvovaginal discomfort, dysuria (painful urination), dyspareunia (painful intercourse)
Marked dilatation of cervical mucosal vessels results in characteristic colposcopic appearance of “strawberry cervix” (attached image)
Arrow: little falling leaves or heart-like look with red granules

Answer 258

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Gardnerella vaginalis: G(-) bacillus; main cause of bacterial vaginosis
Microbial balance is off
Patients typically present with thin, green-gray, malodorous (fishy) vaginal discharge
Small nuclei and abundant cytoplasm
CLUE CELLS

Answer 259

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Chlamydia trachomatis: mainly cervicitis
One of the causes of PID: ascending infection (can also cause tubo-ovarian abscesses and other peritoneal infections)
Histology non-specific
Diagnosis is based on molecular tests (NAAT)

Answer 260

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Begins in the vulva or vagina and spreads upward to involve most of the structures in the female genital system, resulting in pelvic pain, adnexal tenderness, fever, and vaginal discharge
Causes: Neisseria gonorrhoeae (G- diplococcus) and Chlamydia (intracellular organism)
Chandelier sign: extreme pain on bimanual exam

Answer 261

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Acute salpingitis: dilated lumen and edematous tubal plicae (folds) expanded by inflammatory cell infiltrates
Pus fills the center of the fallopian tube
Whole tube can be inflamed, and you can get abscesses between the fimbriae and the ovary
Normal tubal histo attached here; showing fimbriae, delicated finger-like projections

Answer 262

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Chronic salpingitis: scarring and fusion of plicae
Scarring may cause infertility, or ectopic tubal pregnancy
Whole tube can be inflamed, and you can get abscesses between the fimbriae and the ovary
Normal tubal histo attached here; showing fimbriae, delicated finger-like projections

Answer 263

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Fitz-Hugh-Curtis syndrome: perihepatitis due to fibrous ADHESIONS to the liver from PID
Generally, presents with righ upper quandrant pain and minimal (or no) pelvic pain or cervical motion tenderness

Answer 264

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Obstruction of the Bartholin’s glands in the vulva
Common
Affects all ages, including little girls

Answer 265

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Lichen sclerosis: marked thinning of epidermis, sclerosis of superficial dermis, and chronic inflam cells deeper (normal VULVA histo on the right)
1. Normal ridges dipping into the dermis are gone, and the dermis is now pale
CLINICAL: white patch, atrophy of skin, vaginal stenosis -> squamous cell carcinoma can also look like this, so these often get biopsied
Can get stenosis of the vagina too

Answer 266

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Condyloma accuminatum: benign genital warts on VULVA via low oncogenic risk HPVs -> 6 and 11
Very rarely, if ever, progress to carcinoma, so treated as BENIGN
Velvety, undulating, pedunculated
Hyper-granular squamous cells that aren’t completely normal: viropathic effect -> can have binucleation, halos (koilocytic change), and wrinkly nuclear membrane

Answer 267

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Older women (60’s); not as common as cervical
1. Younger pts: HPV-16
2. Older patients: keratinizing, not HPV-related; often long-standing lichen sclerosis
Pts w/lesions < 2 cm in diameter have 90% 5-year survival after tx w/vulvectomy + lymphadenectomy
1. Larger lesions with lymph node involvement have poor prognosis

Answer 268

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HPV(+) VIN: whole entire surface looks the same
Everything looks like a blue, basal cell -> SCC in situ on the left because has not crossed the BM
Invasive on the right: pink/red is necrosis too

Answer 269

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HPV(-) VIN: keratinizing SCC on the right -> most likely developed from lichen sclerosis
In situ lesion on the left, but it looks like there may be some microscopic invasion

Answer 270

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Paget disease: distinctive intraepithelial proliferation of malignant cells -> abundant clear cells in epi that are malignany, abnormal
Typically NOT associated with underlying cancer, and is confined to the epidermis of vulvar skin
Red, plaque-like clinical appearance
Big differential going to be a melanoma bc they look the same, but clinical impression is important here -> can also do staining to help (keratin should not be + in a melanoma, but is + here -> K7)
NOT in the dermis

Answer 271

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Vaginal intraepithelial neoplasia (VAIN) and SCC
Virtually all 1^o carcinomas of the vagina are SCC’s associated with high risk HPVs
1. Very RARE
2. Nomenclature is like that of the cervix

Answer 272

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Embryonal rhabdomyosarcoma: aka, sarcoma botryoides -> uncommon malignant vaginal tumor most frequently found in infants, children < 5-y/o
Tend to invade locally and cause death by penetration into peritoneal cavity or by obstruction of the urinary tract
Conservative surgery coupled with chemotherapy offer best hope, esp. in cases dx’d sufficiently early
Cluster of grapes at the vaginal opening
1. Cambium layer: cluster of cells right underneath the epithelium

Answer 273

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3rd most common cancer in women, with an estimated 530,000 new cases in 2008, of which more than half are fatal
High-risk HPV’s the most important factor
HPV-16 (SCC) accounts for almost 60% of cervical cancer cases
HPV-18 (adenocarcinoma) accounts for another 10%

Answer 274

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Good job!

Answer 275

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LACK OF SCREENING: accessibility of the cervix and slow progression make it amenable for screening, detection, and prevetive treatment
1. Most pts w/advanced cervical cancer die of the consequences of local tumor invasion (e.g., ureteral obstruction, pyelonephritis, and uremia), rather than distant metastases
2. Survival really high with localized cancer
REMEMBER: transformation zone is the area you want to look at, and sample

Answer 276

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E6: dysregulation of p53
E7: promotes degradation of RB
Also prevents cell cycle arrest, and INH p21 and p27, 2 important cyclin-dependent kinase inhibitors
Removal of these controls:
1. Enhances cell cycle progression and
2. Impairs ability of cells to repair DNA damage
Something else has to happen for these to progress, i.e., weakened immune system, genetics, hormonal changes, etc.

Answer 277

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Cervical cancer: can be fungating (exophytic) or infiltrative masses
Transition zone a little more granular in appearance

Answer 278

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All HSIL’s are considered at-risk for progression to carcinoma
SIL terminology is current
Severe dysplasia and carcinoma in situ are the same thing

Answer 279

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Normal cervical epithelium
BM and nice maturation of the cells

Answer 280

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CIN I: koilocytic change, with halos and raisin-like nuclei, bi-nucleation in lower 1/3rd of the epithelium
Highest viral load at top, maturing cells -> high proliferation at surface

Answer 281

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CIN II: still have a little bit of maturation, with para-keratotic cells on top
Higher mitotic figure (in middle) is a giveaway for these
Highest viral load at top, maturing cells- high proliferation at surface
20% can develop without LSIL

Answer 282

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CIN III: NO maturation, and may start looking for invasion
Highest viral load at top, maturing cells -> high proliferation at surface
20% can develop without LSIL

Answer 283

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Ki-67 and p53: can really help in older women because their cervix can become atrophic

A. LSIL

B. In-situ hybridization for HPV DNA -> dark granular staining (typically most abundant in the koilocytes)

C. Ki-67 (brown nuclear staining): abnormal expansion of the proliferating cells

D. Upregulation of CDK INH p16 (brown stain) characterizes high-risk HPV infections

p16: has to be strong AND diffuse to be (+), i.e., staining every cell (will often see a block of brown cells next to “normal-appearing” cells)

Answer 284

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Invasive SCC: this is what you are looking for in CIN III
A little bit of keratinization in the bottom right

Answer 285

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Most women clear the HPV in 12-30 months

Answer 286

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Cervical adenocarcinoma: AIS on the left and invasive adeno on the right
Adeno in situ: have lost mucin-containing cells at the top (normal gland at the bottom)
Invasivet: back to back glands with cribriform architecture, hyperchromatic, necrotic debris because turning over very fast, loss of maturation
2nd most common tumor type in the cervix: 15% of cervical cancer cases and devo from a precursor lesion called adenocarcinoma in situ
Caused by high-risk HPV;s
Note: adenosquamous and neuroendocrine tumors exist, very rare, and typically aggressive

Answer 287

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Risk of metastasis INC from <1% for tumors under 3mm in depth to >10% once the invasion exceeds 3mm (stage 1a1 to 1a2)

Answer 288

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Normal in top left
LSIL: nuclear membranes are wrinkly (top right)
HSIL: punctuated nuclear membrane and hyperchromatic (bottom)

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Gupta - Pathology Flashcards

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