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1
Q

fetal growth restriction due to fetal abnormalities

A

SYMMETRIC

caused by: chromosomal disorders, congenital anomalies, congenital infections (TORCH)

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2
Q

TORCH

A

group of infections (transplacental)

toxoplasmosis (cat litter), rubella, CMV, herpesvirus, other viruses and bacteria (syphilis and listeria)

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3
Q

fetal growth restriction due to placental abnormalities

A

ASYMMETRIC
spares brain
caused by: UTEROPLACENTAL INSUFFICIENCY: umbilical-placental vascular anomalies, plactena abruption, placenta previa, placental thrombosis/infarction, placental infection, multiple gestations

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4
Q

What is a third trimester loss usually due to?

A

placental insufficiency

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5
Q

fetal growth restriction due to maternal abnormalities

A

maternal conditions that result in decreased placental blood flow
caused by: vascular disease: PREECMAPSIA, CHRONIC HTN

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6
Q

spontaneous abortion

A

pregnancy loss before 20 weeks gestation
causes
1. fetal chromosomal anomalies (50% of early loss)
2. maternal endocrine factors
3. physical defects of uterus
4. systemic disorders affecting the maternal vasculature
5. ascending infection

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7
Q

How does an maternal infection cause a fetal inflammatory response?

A

inflammation of umbilical vessels (vasculitis) and cord substance (funisitis)

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8
Q

Twin-twin transfusion

A

MONOCHORIONIC

ARTERIOVENOUS SHUNT increases blood flow to one twin

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9
Q

monochorionic

A

twin placentas have vascular anastomoses that connect the twins’ circulation

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10
Q

decidua

A

endometrium of uterus in a pregnant woman

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11
Q

Homeobox genes (HLX and DLX3)

A

expressed in trophoblast and its blood vessels

dysfunctional in preeclampsia

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12
Q

amnion nodosum

A

nodules seen in placentas effected by oligohydramnios
associated with: stratified squamous metaplasia
due to: renal agenesis

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13
Q

IHC: p57

A

neg. has relationship to hydatidiform moles

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14
Q

Choriocarcinoma: gross appearance

A

soft, fleshy, yellow-white tumor with large areas of necrosis and extensive hemorrhage

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15
Q

complications of pre-maturity

A
  1. neonatal distress syndrome, hyaline membrane disease
  2. necrotizing enterocolitis
  3. sepsis
  4. intraventricular and germinal matrix hemorrhage
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16
Q

pathology of hyaline membrane disease

A
  1. reduced surfactant (increase tension)
  2. atelectasis (uneven perfusion, hypoventilation)
  3. hypoxemia and CO2 retention (acidosis, pulmonary vasoconstriction and hypoperfusion)
  4. endothelial and epithelial damage
  5. plasma leak into alveoli: fibrin and necrotic cells increase diffusion gradient
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17
Q

fetal hydrops

A

accumulation of edema fluid in the fetus during intrauterine growth
caused by: CV, chromosomal, fetal anemia (immune (Rh, ABO), ParvoB19, homozygous alpha thalassemia), twin-twin

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18
Q

triple risk model of SIDS

A
  1. vulnerable infant
  2. critical developmental period in homeostatic control
  3. exogenous stressor (smoking, cockroach, sleeping on belly, overweight, sleep with parents)
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19
Q

progesterone withdrawal test

A

pos. for bleeding: PCOS

neg. for bleeding: premature ovarian failure

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20
Q

When will the majority of breast cancers metastasize?

A

by the time you can palpate them: 2-3cm

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21
Q

Most common presentation of breast CA

A

abnormal mammogram

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22
Q

fibrocystic changes: radial scar

A

proliferative type: increased risk for invasive carcinoma

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23
Q

lymphocytic mastitis

A

type of breast inflammation

due to: DM, autoimmune

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24
Q

granulomatous mastitis

A

type of breast inflammation

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25
Genetic profile of breast CA 1. luminal A 2. luminal B 3. HER2 positive 4. Basal type
1. ER pos.; HER2 neg. 2. ER pos.; HER2 overexpressed 3. ER neg.; HER2 overexpressed 4. ER and HER2 neg.
26
Characteristics of breast CA linked to inherited mutations
more likely to be/have 1. bilateral 2. other CA (ovarian) 3. Family Hx 4. CA before menopause 5. certain ethnicity
27
BRCA mutation
tumor suppressor genes breast CA (BOTH alleles must be inactivated) more common in Ashkenazi Jew most carriers develop CA by 70
28
Li-Fraumeni
p53 mutation | Breast CA
29
Cowden
PTEN mutation | breast CA
30
ataxia-telangiectasia carriers
breast CA
31
BRCA1
AD: breast CA, serous ovarian and fallopian tube CA may interact with p53 strongest predictors :TRIPLE NEG. breast CA, CA before 50 yrs prophylaxis: mastectomy or follow closely, tamoxifen increased risk of recurrence after breast conserving Sx does not affect death rates, but is associated with resistance to certain chemo drugs MEDUALLARY, DCIS
32
BRCA2
``` Breast CA usually CA by 50 higher risk of CA of: OVARY (serous), bone, pharynx, prostate, pancreas more frequent in blacks than whites INVASIVE DUCTAL CA, DCIS ```
33
Types of DCIS
1. solid 2. comedo 3. cribiform 4. papillary 5. micropapillary
34
Tx options for DCIS
1. lumpectomy 2. radiation 3. anti-estrogs (tamoxifen and aromatase)
35
E-cadherin
lost in LCIS and INVASIVE LOBULAR CA | GASTRIC SIGNET RING CELL CA
36
Tx options for LCIS
1. chemo | 2. close follow up
37
What type of breast tumor lacks the myoepithelial cell layer?
invasive ductal carcinoma
38
CDH1
gene encoding E-cadherin LOBULAR CA and LCIS heterozygous germline mutation: increased risk of GASTRIC SIGNET RING CELL CA
39
Causes of gynecomastia 1. pathologic 2. physiologic
1. cirrhosis, anabolic steroids, Klinefelter syndrome, drugs | 2. puberty, old age
40
HSV-2 migrates to where in latent phase?
regional lumbosacral ganglia
41
What typically causes death in cervical CA?
local tumor invasion (urethral obstruction, pyelonephritis, uremia)
42
What does E7 inhibit?
RB | p21, p27 (cyclin dependent kinase inhibitors)
43
Low grade squamous intraepithelial lesion (LSIL)
CIN I (mild dysplasia)
44
High grade squamous intraepithelial lesion (HSIL)
CIN II, III (mod. severe dysplasia (carcinoma in situ) | high risk for progression to carcinoma
45
At what size does the risk of metastasis of cervical carcinoma increase to 10%
3 MM
46
PTEN inactivation
``` endometrial hyperplasia and carcinoma (hyperplasia pathway not sporadic) breast CA (Cowden) ```
47
Classification of endometrial hyperplasia
simple vs. complex with or without atypia atypia: endometrioid intraepithelial neoplasia
48
MSI mutation
endometrial hyperplasia and carcinoma (hyperplasia pathway not sporadic)
49
What defect in cellular repair predisposes to endometrial carcinoma?
DNA mismatch repair
50
HNPCC
hereditary nonpolyposis colorectal carcinoma LYNCH syndrome: COLON CA ENDOMETRIAL carcinomas
51
p53 mutations
sporadic endometrial carcinoma
52
Where do serous ovarian carcinomas arise?
fallopian tube
53
Common pathologies of the fallopian tubes
1. infection: Gonococcus, Chlamydiae, TB 2. benign paratubal cysts Tumors are UNCOMMON
54
Two pathways of epithelial ovarian tumors
1. cystadenoma/endometriosis to borderline tumor to low grade serous, endometrioid, mucinous 2. fallopian tube to inclusion cyst to high grade serous
55
KRAS mutation
mucinous ovarian cystadenoma/adenocarcinoma
56
Where do most metastatic tumors of the ovary come from?
mullerian origin: uterus, fallopian tube, contralateral ovary, pelvic peritoneum other: breast, GI, appendix
57
IHC: inhibin
granulosa tumor
58
Meigs syndrome
ovarian tumor (fibrothecoma), hydrothorax, ascites
59
basal cell nevus syndrome
fibrothecoma ovarian tumor
60
Categories of ovarian teratoma
1. mature (benign) 2. immature (malignant) 3. monodermal (highly specialized)
61
C-KIT (CD117)
receptor tyrosine kinase | activating mutation in DYSGERMINOMA
62
alpha fetoprotein
Yolk sac
63
Hypospadia associations
inguinal hernia | undescended testis
64
balanoposthitis
inflammation of prepuce overlying the glans penis
65
Agents that cause balanitis and balanoposthitis | Most cases are caused by?
``` Candida anaerobic bacteria Gardnerella pyogenic bacteria caused by: poor hygiene in uncircumcised male ```
66
phimosis
prepuce cannot be retracted over glans penis
67
orchiopexy
reduces risk of sterility and CA in those with cryptorchidism
68
Where in the testis is an inflammatory lesion most likely to occur? Causes of inflammatory lesion of testis?
epididymis | causes: sexually transmitted, nonspecific epididymitis and orchitis, MUMPS, TUBERCULOSIS
69
orchitis: mumps histology
lymphoplasmacytic
70
orchitis: TB histo
granulomatous | caseous necrosis
71
neonatal testicular torsion
in utero or shortly after birth | NO associated anatomic defect
72
adult testicular torsion
due to bilateral anatomic defect with increased mobility
73
1. Most common cell type of testicular neoplasm? more likely benign or malignant? 2. Less common? 3. Are whites or blacks more likely to have testicular CA?
1. most common: Germ cell: malignant 2. less common: Sertoli or Leydig (sex cord): benign 3. White
74
obstructive lesion of the ureters 1. intrinsic 2. extrinsic 3. complications
1. calculi, strictures, tumors, blood clots, neurogenic 2. pregnancy, periureteral inflammation, endometriosis, tumors 3. hydroureter, hydronephrosis, pyelonephritis
75
vesicoureteral reflux
most common and serious bladder congenital anomaly backwards flow of urine from bladder into kidneys complications: renal infection, scarring
76
urachal anomalies 1. totally patent 2. other
urachus (fetal canal connecting bladder to allantois in umbilical cord) 1. fistulous urinary tract: connect bladder to umbilicus 2. urachal cyst (adenoCA can arise from the cyst)
77
racemase stain
red | prostate CA
78
Which bladder neoplasms 1. recur 2. have coexisting invasion 3. progress 4. cause death
1. PUNLMP, LGUC, HGUC 2. HGUC, sometimes LGUC 3. LGUC and HGUC 4. LGUC and HGUC
79
Types of bladder neoplasms
papilloma PUNLMP: papillary urothelial neoplasm of low malignant potential LGUC: low grade urothelial carcinoma HGUC: high grade urothelial carcinoma
80
primary syphilis
chancre
81
secondary syphilis
palmar rash lymphadenopathy condyloma latum
82
tertiary syphilis
neuro aortitis gummas (irregular, firm mass of necrosis surrounded by connective tissue): hepar lobatum, skin, bone
83
congenital syphilis
1. late abortion, stillbirth 2. infant: rash, osteochondritis, periostitis, liver and lung fibrosis 3. child: interstitial keratitis, hutchinson teeth, deaf
84
PLAP
DYSGERMINOMA

Reproductive (12 decks)

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