Path Flashcards
fetal growth restriction due to fetal abnormalities
SYMMETRIC
caused by: chromosomal disorders, congenital anomalies, congenital infections (TORCH)
TORCH
group of infections (transplacental)
toxoplasmosis (cat litter), rubella, CMV, herpesvirus, other viruses and bacteria (syphilis and listeria)
fetal growth restriction due to placental abnormalities
ASYMMETRIC
spares brain
caused by: UTEROPLACENTAL INSUFFICIENCY: umbilical-placental vascular anomalies, plactena abruption, placenta previa, placental thrombosis/infarction, placental infection, multiple gestations
What is a third trimester loss usually due to?
placental insufficiency
fetal growth restriction due to maternal abnormalities
maternal conditions that result in decreased placental blood flow
caused by: vascular disease: PREECMAPSIA, CHRONIC HTN
spontaneous abortion
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
How does an maternal infection cause a fetal inflammatory response?
inflammation of umbilical vessels (vasculitis) and cord substance (funisitis)
Twin-twin transfusion
MONOCHORIONIC
ARTERIOVENOUS SHUNT increases blood flow to one twin
monochorionic
twin placentas have vascular anastomoses that connect the twins’ circulation
decidua
endometrium of uterus in a pregnant woman
Homeobox genes (HLX and DLX3)
expressed in trophoblast and its blood vessels
dysfunctional in preeclampsia
amnion nodosum
nodules seen in placentas effected by oligohydramnios
associated with: stratified squamous metaplasia
due to: renal agenesis
IHC: p57
neg. has relationship to hydatidiform moles
Choriocarcinoma: gross appearance
soft, fleshy, yellow-white tumor with large areas of necrosis and extensive hemorrhage
complications of pre-maturity
- neonatal distress syndrome, hyaline membrane disease
- necrotizing enterocolitis
- sepsis
- intraventricular and germinal matrix hemorrhage
pathology of hyaline membrane disease
- reduced surfactant (increase tension)
- atelectasis (uneven perfusion, hypoventilation)
- hypoxemia and CO2 retention (acidosis, pulmonary vasoconstriction and hypoperfusion)
- endothelial and epithelial damage
- plasma leak into alveoli: fibrin and necrotic cells increase diffusion gradient
fetal hydrops
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
triple risk model of SIDS
- vulnerable infant
- critical developmental period in homeostatic control
- exogenous stressor (smoking, cockroach, sleeping on belly, overweight, sleep with parents)
progesterone withdrawal test
pos. for bleeding: PCOS
neg. for bleeding: premature ovarian failure
When will the majority of breast cancers metastasize?
by the time you can palpate them: 2-3cm
Most common presentation of breast CA
abnormal mammogram
fibrocystic changes: radial scar
proliferative type: increased risk for invasive carcinoma
lymphocytic mastitis
type of breast inflammation
due to: DM, autoimmune
granulomatous mastitis
type of breast inflammation
Genetic profile of breast CA
- luminal A
- luminal B
- HER2 positive
- Basal type
- ER pos.; HER2 neg.
- ER pos.; HER2 overexpressed
- ER neg.; HER2 overexpressed
- ER and HER2 neg.
Characteristics of breast CA linked to inherited mutations
more likely to be/have
- bilateral
- other CA (ovarian)
- Family Hx
- CA before menopause
- certain ethnicity
BRCA mutation
tumor suppressor genes
breast CA (BOTH alleles must be inactivated)
more common in Ashkenazi Jew
most carriers develop CA by 70
Li-Fraumeni
p53 mutation
Breast CA
Cowden
PTEN mutation
breast CA
ataxia-telangiectasia carriers
breast CA
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
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
Types of DCIS
- solid
- comedo
- cribiform
- papillary
- micropapillary
Tx options for DCIS
- lumpectomy
- radiation
- anti-estrogs (tamoxifen and aromatase)
E-cadherin
lost in LCIS and INVASIVE LOBULAR CA
GASTRIC SIGNET RING CELL CA
Tx options for LCIS
- chemo
2. close follow up
What type of breast tumor lacks the myoepithelial cell layer?
invasive ductal carcinoma
CDH1
gene encoding E-cadherin
LOBULAR CA and LCIS
heterozygous germline mutation: increased risk of GASTRIC SIGNET RING CELL CA
Causes of gynecomastia
- pathologic
- physiologic
- cirrhosis, anabolic steroids, Klinefelter syndrome, drugs
2. puberty, old age
HSV-2 migrates to where in latent phase?
regional lumbosacral ganglia
What typically causes death in cervical CA?
local tumor invasion (urethral obstruction, pyelonephritis, uremia)
What does E7 inhibit?
RB
p21, p27 (cyclin dependent kinase inhibitors)
Low grade squamous intraepithelial lesion (LSIL)
CIN I (mild dysplasia)
High grade squamous intraepithelial lesion (HSIL)
CIN II, III (mod. severe dysplasia (carcinoma in situ)
high risk for progression to carcinoma
At what size does the risk of metastasis of cervical carcinoma increase to 10%
3 MM
PTEN inactivation
endometrial hyperplasia and carcinoma (hyperplasia pathway not sporadic) breast CA (Cowden)
Classification of endometrial hyperplasia
simple vs. complex
with or without atypia
atypia: endometrioid intraepithelial neoplasia
MSI mutation
endometrial hyperplasia and carcinoma (hyperplasia pathway not sporadic)
What defect in cellular repair predisposes to endometrial carcinoma?
DNA mismatch repair
HNPCC
hereditary nonpolyposis colorectal carcinoma
LYNCH syndrome: COLON CA
ENDOMETRIAL carcinomas
p53 mutations
sporadic endometrial carcinoma
Where do serous ovarian carcinomas arise?
fallopian tube
Common pathologies of the fallopian tubes
- infection: Gonococcus, Chlamydiae, TB
- benign paratubal cysts
Tumors are UNCOMMON
Two pathways of epithelial ovarian tumors
- cystadenoma/endometriosis to borderline tumor to low grade serous, endometrioid, mucinous
- fallopian tube to inclusion cyst to high grade serous
KRAS mutation
mucinous ovarian cystadenoma/adenocarcinoma
Where do most metastatic tumors of the ovary come from?
mullerian origin: uterus, fallopian tube, contralateral ovary, pelvic peritoneum
other: breast, GI, appendix
IHC: inhibin
granulosa tumor
Meigs syndrome
ovarian tumor (fibrothecoma), hydrothorax, ascites
basal cell nevus syndrome
fibrothecoma ovarian tumor
Categories of ovarian teratoma
- mature (benign)
- immature (malignant)
- monodermal (highly specialized)
C-KIT (CD117)
receptor tyrosine kinase
activating mutation in DYSGERMINOMA
alpha fetoprotein
Yolk sac
Hypospadia associations
inguinal hernia
undescended testis
balanoposthitis
inflammation of prepuce overlying the glans penis
Agents that cause balanitis and balanoposthitis
Most cases are caused by?
Candida anaerobic bacteria Gardnerella pyogenic bacteria caused by: poor hygiene in uncircumcised male
phimosis
prepuce cannot be retracted over glans penis
orchiopexy
reduces risk of sterility and CA in those with cryptorchidism
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
orchitis: mumps histology
lymphoplasmacytic
orchitis: TB histo
granulomatous
caseous necrosis
neonatal testicular torsion
in utero or shortly after birth
NO associated anatomic defect
adult testicular torsion
due to bilateral anatomic defect with increased mobility
- Most common cell type of testicular neoplasm? more likely benign or malignant?
- Less common?
- Are whites or blacks more likely to have testicular CA?
- most common: Germ cell: malignant
- less common: Sertoli or Leydig (sex cord): benign
- White
obstructive lesion of the ureters
- intrinsic
- extrinsic
- complications
- calculi, strictures, tumors, blood clots, neurogenic
- pregnancy, periureteral inflammation, endometriosis, tumors
- hydroureter, hydronephrosis, pyelonephritis
vesicoureteral reflux
most common and serious bladder congenital anomaly
backwards flow of urine from bladder into kidneys
complications: renal infection, scarring
urachal anomalies
- totally patent
- other
urachus (fetal canal connecting bladder to allantois in umbilical cord)
- fistulous urinary tract: connect bladder to umbilicus
- urachal cyst (adenoCA can arise from the cyst)
racemase stain
red
prostate CA
Which bladder neoplasms
- recur
- have coexisting invasion
- progress
- cause death
- PUNLMP, LGUC, HGUC
- HGUC, sometimes LGUC
- LGUC and HGUC
- LGUC and HGUC
Types of bladder neoplasms
papilloma
PUNLMP: papillary urothelial neoplasm of low malignant potential
LGUC: low grade urothelial carcinoma
HGUC: high grade urothelial carcinoma
primary syphilis
chancre
secondary syphilis
palmar rash
lymphadenopathy
condyloma latum
tertiary syphilis
neuro
aortitis
gummas (irregular, firm mass of necrosis surrounded by connective tissue): hepar lobatum, skin, bone
congenital syphilis
- late abortion, stillbirth
- infant: rash, osteochondritis, periostitis, liver and lung fibrosis
- child: interstitial keratitis, hutchinson teeth, deaf
PLAP
DYSGERMINOMA