Path Flashcards

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
Q

Genetic profile of breast CA

  1. luminal A
  2. luminal B
  3. HER2 positive
  4. Basal type
A
  1. ER pos.; HER2 neg.
  2. ER pos.; HER2 overexpressed
  3. ER neg.; HER2 overexpressed
  4. ER and HER2 neg.
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26
Q

Characteristics of breast CA linked to inherited mutations

A

more likely to be/have

  1. bilateral
  2. other CA (ovarian)
  3. Family Hx
  4. CA before menopause
  5. certain ethnicity
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27
Q

BRCA mutation

A

tumor suppressor genes
breast CA (BOTH alleles must be inactivated)
more common in Ashkenazi Jew
most carriers develop CA by 70

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28
Q

Li-Fraumeni

A

p53 mutation

Breast CA

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29
Q

Cowden

A

PTEN mutation

breast CA

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30
Q

ataxia-telangiectasia carriers

A

breast CA

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31
Q

BRCA1

A

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

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32
Q

BRCA2

A
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
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33
Q

Types of DCIS

A
  1. solid
  2. comedo
  3. cribiform
  4. papillary
  5. micropapillary
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34
Q

Tx options for DCIS

A
  1. lumpectomy
  2. radiation
  3. anti-estrogs (tamoxifen and aromatase)
35
Q

E-cadherin

A

lost in LCIS and INVASIVE LOBULAR CA

GASTRIC SIGNET RING CELL CA

36
Q

Tx options for LCIS

A
  1. chemo

2. close follow up

37
Q

What type of breast tumor lacks the myoepithelial cell layer?

A

invasive ductal carcinoma

38
Q

CDH1

A

gene encoding E-cadherin
LOBULAR CA and LCIS
heterozygous germline mutation: increased risk of GASTRIC SIGNET RING CELL CA

39
Q

Causes of gynecomastia

  1. pathologic
  2. physiologic
A
  1. cirrhosis, anabolic steroids, Klinefelter syndrome, drugs

2. puberty, old age

40
Q

HSV-2 migrates to where in latent phase?

A

regional lumbosacral ganglia

41
Q

What typically causes death in cervical CA?

A

local tumor invasion (urethral obstruction, pyelonephritis, uremia)

42
Q

What does E7 inhibit?

A

RB

p21, p27 (cyclin dependent kinase inhibitors)

43
Q

Low grade squamous intraepithelial lesion (LSIL)

A

CIN I (mild dysplasia)

44
Q

High grade squamous intraepithelial lesion (HSIL)

A

CIN II, III (mod. severe dysplasia (carcinoma in situ)

high risk for progression to carcinoma

45
Q

At what size does the risk of metastasis of cervical carcinoma increase to 10%

A

3 MM

46
Q

PTEN inactivation

A
endometrial hyperplasia and carcinoma (hyperplasia pathway not sporadic)
breast CA (Cowden)
47
Q

Classification of endometrial hyperplasia

A

simple vs. complex
with or without atypia
atypia: endometrioid intraepithelial neoplasia

48
Q

MSI mutation

A

endometrial hyperplasia and carcinoma (hyperplasia pathway not sporadic)

49
Q

What defect in cellular repair predisposes to endometrial carcinoma?

A

DNA mismatch repair

50
Q

HNPCC

A

hereditary nonpolyposis colorectal carcinoma
LYNCH syndrome: COLON CA
ENDOMETRIAL carcinomas

51
Q

p53 mutations

A

sporadic endometrial carcinoma

52
Q

Where do serous ovarian carcinomas arise?

A

fallopian tube

53
Q

Common pathologies of the fallopian tubes

A
  1. infection: Gonococcus, Chlamydiae, TB
  2. benign paratubal cysts
    Tumors are UNCOMMON
54
Q

Two pathways of epithelial ovarian tumors

A
  1. cystadenoma/endometriosis to borderline tumor to low grade serous, endometrioid, mucinous
  2. fallopian tube to inclusion cyst to high grade serous
55
Q

KRAS mutation

A

mucinous ovarian cystadenoma/adenocarcinoma

56
Q

Where do most metastatic tumors of the ovary come from?

A

mullerian origin: uterus, fallopian tube, contralateral ovary, pelvic peritoneum
other: breast, GI, appendix

57
Q

IHC: inhibin

A

granulosa tumor

58
Q

Meigs syndrome

A

ovarian tumor (fibrothecoma), hydrothorax, ascites

59
Q

basal cell nevus syndrome

A

fibrothecoma ovarian tumor

60
Q

Categories of ovarian teratoma

A
  1. mature (benign)
  2. immature (malignant)
  3. monodermal (highly specialized)
61
Q

C-KIT (CD117)

A

receptor tyrosine kinase

activating mutation in DYSGERMINOMA

62
Q

alpha fetoprotein

A

Yolk sac

63
Q

Hypospadia associations

A

inguinal hernia

undescended testis

64
Q

balanoposthitis

A

inflammation of prepuce overlying the glans penis

65
Q

Agents that cause balanitis and balanoposthitis

Most cases are caused by?

A
Candida
anaerobic bacteria
Gardnerella
pyogenic bacteria
caused by: poor hygiene in uncircumcised male
66
Q

phimosis

A

prepuce cannot be retracted over glans penis

67
Q

orchiopexy

A

reduces risk of sterility and CA in those with cryptorchidism

68
Q

Where in the testis is an inflammatory lesion most likely to occur?
Causes of inflammatory lesion of testis?

A

epididymis

causes: sexually transmitted, nonspecific epididymitis and orchitis, MUMPS, TUBERCULOSIS

69
Q

orchitis: mumps histology

A

lymphoplasmacytic

70
Q

orchitis: TB histo

A

granulomatous

caseous necrosis

71
Q

neonatal testicular torsion

A

in utero or shortly after birth

NO associated anatomic defect

72
Q

adult testicular torsion

A

due to bilateral anatomic defect with increased mobility

73
Q
  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?
A
  1. most common: Germ cell: malignant
  2. less common: Sertoli or Leydig (sex cord): benign
  3. White
74
Q

obstructive lesion of the ureters

  1. intrinsic
  2. extrinsic
  3. complications
A
  1. calculi, strictures, tumors, blood clots, neurogenic
  2. pregnancy, periureteral inflammation, endometriosis, tumors
  3. hydroureter, hydronephrosis, pyelonephritis
75
Q

vesicoureteral reflux

A

most common and serious bladder congenital anomaly
backwards flow of urine from bladder into kidneys
complications: renal infection, scarring

76
Q

urachal anomalies

  1. totally patent
  2. other
A

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
Q

racemase stain

A

red

prostate CA

78
Q

Which bladder neoplasms

  1. recur
  2. have coexisting invasion
  3. progress
  4. cause death
A
  1. PUNLMP, LGUC, HGUC
  2. HGUC, sometimes LGUC
  3. LGUC and HGUC
  4. LGUC and HGUC
79
Q

Types of bladder neoplasms

A

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

80
Q

primary syphilis

A

chancre

81
Q

secondary syphilis

A

palmar rash
lymphadenopathy
condyloma latum

82
Q

tertiary syphilis

A

neuro
aortitis
gummas (irregular, firm mass of necrosis surrounded by connective tissue): hepar lobatum, skin, bone

83
Q

congenital syphilis

A
  1. late abortion, stillbirth
  2. infant: rash, osteochondritis, periostitis, liver and lung fibrosis
  3. child: interstitial keratitis, hutchinson teeth, deaf
84
Q

PLAP

A

DYSGERMINOMA