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Life Cycles > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Malignant Breast Neoplasms: (5 major groups)

A

1) Metastatic Tumors (to breast)

2) Epithelial Tumors
- Carcinoma in situ
- Invasive Epithelial Carcinoma
- Metaplastic carcinoma

3) Stromal Tumors:
- Invasive stromal carcinoma

4) Mixed stroma and epithelium:
- Phyllodes Tumor

5) Lymphoid tumors:
- Lymphoma

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2
Q

Carcinoma in situ (2 kinds)

A

Limited by basement membrane of ducts and lobules → cannot metastasize

Ductal Carcinoma in situ → Paget’s
Lobular Carcinoma in situ (LCIS)

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3
Q

Invasive Epithelial Carcinoma (6 types)

A

1) Invasive ductal carcinoma
2) Invasive lobular carcinoma
3) Tubular carcinoma
4) Mucinous (colloid) carcinoma
5) Medullary carcinoma
6) Inflammatory carcinoma

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4
Q

Metaplastic carcinoma

A

Any carcinoma with NON GLANDULAR growth (squamous, spindle cell, or heterologous differentiation)

Arise in association with poorly differentiated ductal carcinoma most commonly

Usually ER/PR negative

Can grow fast

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5
Q

Angiosarcoma

A

can be de novo or post radiation (common)
Proliferation of cells forming vasculature

Invasive stromal carcinoma

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6
Q

Phyllodes Tumor

A

basically all stroma + some glands

Looks like a leaf = “Phyllodes”

Can be mistaken for benign fibroadenoma

Mixed stroma and epithelium

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7
Q

Ductal Carcinoma in situ (DCIS)

A

clonal proliferation of epithelial cells within ducts leaving myoepithelial layer and BM intact

Present as calcifications on mammography

Asymptomatic, nonpalpable

INCREASED RISK for developing invasive carcinoma in ipsilateral breast BUT excision is often curative (may get recurrence)

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8
Q

Ductal Carcinoma in situ (DCIS)

Low grade vs. high grade?

Positive ________

A

*POSITIVE E-CADHERIN

Five histologic patterns: comedo, solid, cribriform, papillary, micropapillary

**High grade DCIS often overexpresses Her2/neu protein

**Low grade DCIS often express hormonal receptors (ER, PR)

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9
Q

Ductal Carcinoma in situ (DCIS)

Progression?

A

usual ductal hyperplasia → atypical ductal hyperplasia (ductal or lobular) → DCIS → Invasive carcinoma

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10
Q

Paget’s Disease of the Nipple

A

neoplastic DCIS cells grow from ducts onto adjacent skin without invading through the BM of ducts or skin

Presents as scaly rash on nipple +/- pruritus

May or may not have underlying invasive carcinoma

Can be mistaken for melanoma

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11
Q

Lobular Carcinoma in situ (LCIS)

A

Typically incidental finding, often multicentric and bilateral

SIGNIFICANT increased risk for invasive carcinoma in BOTH breasts

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12
Q

Lobular Carcinoma in situ (LCIS)

Histology

A

small, uniform cells with cound nuclei filling lobules, and poorly adhering to adjacent cells

*LACKS E-CADHERIN

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13
Q

Invasive Epithelial Carcinoma:

Presentation:

A

palpable mass or on mammography

Can also present as enlarged erythematous breast (“inflammatory carcinoma”) or metastatic disease to axillary nodes

Advanced lesions fix mass to chest wall → dimpling of overlying skin

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14
Q

Where does invasive epithelial carcinoma typically present? where does it spread?

A

Typically in UPPER OUTER quadrant → spread first to axillary nodes

If in inner quadrant → spread to internal mammary nodes

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15
Q

1) Invasive Ductal Carcinoma

  • ER/PR?
  • Her2/neu?
  • differentiation?
  • precursor lesion?
A

Associated with DCIS

Expresses estrogen and progesterone receptors when it is a WELL-DIFFERENTIATED lesion

Her2/neu expressed in POORLY DIFFERENTIATED lesion

Most common histologic subtype

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16
Q

2) Invasive lobular carcinoma (ILC)

  • precursor lesion?
  • ER/PR?
  • Her2/neu?
  • where does it metastasize
A

Second most common histologic subtype

Tumor cells similar to LCIS cells

LOSE function or expression of E-CADHERIN

Express HORMONE RECEPTORS
DO NOT overexpress HER2/Neu

Patterns of metastases: more frequently will go to CSF, GI tract, ovaries, uterus, and peritoneum

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17
Q

3) Tubular carcinoma

  • presents at what age?
  • prognosis?
  • ER/PR, Her2/neu?
  • Subtype of what other cancer?
A

Presents in 50’s

Subtype of ductal carcinoma BUT is very well differentiated tumor composed of well-formed tubules and bland appearing cells

Almost all express hormone receptors and do NOT express HER2/neu
Excellent prognosis

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18
Q

Mucinous (colloid) carcinoma

  • presentation? age?
  • prognosis?
  • ER/PR, Her2/neu?
A

Presents as well-circumscribed mass (mimics benign lesions)

Older age groups

Relatively favorable prognosis

Usually expresses HORMONE receptors, NOT HER2/Neu

Frequent in patients with BRCA1 mutation

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19
Q

5) Medullary carcinoma

  • presentation?
  • prognosis?
  • ER/PR, Her2/neu?
A

Presents as well-circumscribed mass

Negative for hormone receptors and HER2/Neu = TRIPLE NEGATIVE

More frequent in patients with BRCA1 mutation

Do slightly better than typical IDC

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20
Q

6) Inflammatory carcinoma

A

presents with breast erythema and swelling of breast

Diffuse involvement of dermal lymphatics

Poor prognosis - underlying carcinoma usually high grade

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21
Q

Prognosis in breast cancer (6 main factors)

A

1) Lymph node metastasis
2) Tumor size
3) Presence of invasion
4) Distant metastases
5) Locally advanced disease
6) Inflammatory carcinoma

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22
Q

Prognosis in breast cancer

minor factors for prognosis (6)

A

1) Hormone receptor expression
2) HER2/neu overexpression
3) Histologic type
4) Lymphovascular invasion
5) Proliferative rate
6) Histologic grade

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23
Q

Breast Cancer Risk Factors (6)

A

1) Hormonal exposure
2) Post-menopausal, Age
3) Family history
4) Age at menarche and first live birth
5) Breastfeeding duration
6) Environmental factors (ionizing radiation)

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24
Q

BRCA1 and BRCA2

A

tumor suppressor genes and facilitate DNA damage repair

BRCA1 → ovarian cancer, breast carcinomas (that are ER, PR and Her2/neu negative)

BRCA2 → increased risk of ovarian cancer (but smaller than BRCA1), male breast cancer

Accounts for 3% of all breast cancers

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25
Q

CHEK2 gene

A

tumor suppressor gene → cellular proliferation

Responsible for progression to carcinoma

5% of familial breast cancer

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26
Q

Li-Fraumeni Syndrome

A

TP53 gene mutation

5% of familial breast cancer

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27
Q

Cowden Syndrome

A

PTEN gene mutation

<1% of familial breast cancer

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28
Q

Peutz-Jeghers Syndrome

A

STK11/LKB1 gene mutation

< 1% of familial breast cancer

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29
Q

Pathogenesis of Breast Cancer:

Molecular pathways: (3)

A

1) ER positive, HER2 negative cancers arise via the dominant pathway
2) HER2 Positive cancer
3) ER negative, HER2 negative = TRIPLE NEGATIVE

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30
Q

Molecular pathways:

ER positive, HER2 negative cancers arise via the dominant pathway

A

Majority of cases (50-65%)

Seen in ADH, flat epithelial atypia, and low grade DCIS

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31
Q

Molecular pathways:

HER2 Positive cancer

A

20% of breast cancers

Most common subtype in Li-Fraumeni syndrome

Associated with amplification of HER2 gene (Chr17)

Seen in high grade DCIS - worse prognosis

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32
Q

Molecular pathways:

ER negative, HER2 negative = TRIPLE NEGATIVE

A

15% of all breast cancers

Most common subtype with BRCA1

Precursor lesion unknown

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33
Q

male breast cancer

A

Klinefelter’s, BRCA2 mutations

Associated with subareolar mass

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34
Q

Nucleus contains _____

A

highly condensed chromatin

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35
Q

Protamines

A

specialized basic histone tightly held together by disulfide bond cross-linking keeps chromatin compact

Shape of sperm head is species dependent

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36
Q

Acrosome

A

anterior ½ or ⅔ of sperm head

Thin, double-layered membrane sac
Contains hydrolytic enzymes, critical for fertilization

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37
Q

Tail of sperm

A

: contains 9 axoneme doublets arranged circumferentially around a pair of microtubules → doublets surrounded by mitochondrial sheath
→ sperm motility

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38
Q

Normal values of semen analysis:

  • Volume
  • Concentration
  • Motility
  • Morphology
A

Volume > 1.5 ml
Concentrations: > 15 x 10^6 /ml
Motility: > 32%
Morphology: 4% normal

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39
Q

Female evaluation of fertility

A

How many eggs are available:

  • Blood tests: FSH, E2, AMH
  • Ultrasound

Euploid embryos decrease with maternal age

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40
Q

Women have a peak number of oocytes when?

A

20 weeks gestation

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41
Q

Primary oocyte is arrested when?

A

Prophase I of meiosis I

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42
Q

Primary oocyte finishes 1st meiotic division when?

A

after LH surge → secondary oocyte + 1st polar body

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43
Q

Secondary oocyte → finishes meiosis II after ____

A

fertilization

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44
Q

Zona Pellucida

A

shell-like structure that surrounds oocytes

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45
Q

Glycoprotein sheet of Zona pellucida

A

70% protein, 20% hexose, 3% sialic acid, 2% sulfate

Composed of 3 glycoproteins: ZP1, ZP2, ZP3

Mutant/inactivated zone proteins → infertility

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46
Q

Fertilization:

A

process involving union of male and female germ cells that results in formation of a pronuclear zygote

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47
Q

9 steps of fertilization

A

1) Ovulation and collection of oocyte in oviduct
2) Deposition of sufficient # of sperm with normal form and motility
3) Sperm capacitation
4) Sperm traversal of cumulus oophorus
5) Sperm interaction with zona pellucida
6) Acrosome reaction
7) Sperm-oocyte plasma membrane fusion
8) Oocyte activation
9) Male pronuclei formation

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48
Q

Sperm capacitation

A

Process by which spermatozoa acquire capacity to undergo acrosome reaction and fertilize eggs
Acquired in distal genital tract of male

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49
Q

Sperm interaction with zona pellucida

A

Sperm binding to zona pellucida: ZP3 glycoprotein = sperm receptor

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50
Q

Acrosome reaction

A

(digest zona): occurs when outer membrane of acrosome region fuses with plasma membrane of sperm

Fusion of membranes → release of hyaluronidase and acrosin → complete fusion of sperm with oocyte

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51
Q

Sperm-oocyte plasma membrane fusion

A

Fertilin = protein responsible for sperm-oocyte fusion

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52
Q

Oocyte activation

A

Zona (cortical) reaction: occurs as soon as first sperm fuses
First sperm fuses → release cortical granules → form new glycoprotein ZP3-F which is incapable of binding sperm

Prevents polyspermy

Oocyte finishes meiosis

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53
Q

Male pronuclei formation

A

Protamines unwinds, disulfide bonds reduced by action of oocyte-derived glutathione

Sperm nuclei decondense
Forms male/female pronuclei

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54
Q

Preimplantation embryo development:

A

Day 1 = 2 cells, Day 2 = 2 → 4 cells, Day 3 = 4 → 8 cells
Day 4 = Morula stage
Day 5 = Blastocyst stage

Trophectoderm develops → will become placenta

Biopsied if looking for preimplantation genetic diagnosis
I
nner cell mass → becomes fetus

55
Q

Implantation

A

attachment of fertilized egg to uterine lining - occurs 6-7 days after conception

Requires interaction between blastocyst outer trophectoderm layer and hormonally primed lining of uterine cavity

56
Q

Most common sites of implantation:

A

Posterior wall in midsagittal plane

57
Q

Blastocyst Hatching

A

g: process when blastocyst “escapes” from zona pellucide (day 6-7)

Once hatched, the trophectoderm can come into direct contact with endometrial epithelium

Unfertilized eggs do NOT hatch

Implantation fails if hatching does not take place

58
Q

Decidualization:

A

process where by endometrial stromal cells, fibroblasts, are transformed into round decidual cells

Critical for trophoblast invasion and formation of placenta

Dependent on progesterone and cAMP → accumulation of glycogen and lipids, change in nature of ECM

Process begins in secretory phase of menstrual cycle (around day 23)

If implantation takes place, process expands and includes remaining stromal cells

59
Q

Window of implantation

A

finite period of time that epithelium lining of uterus is prepared to accept implantation of blastocyst (day 20-24)

Small finger-like projection from apical surface of endometrial epithelium

Dependent on progesterone (secreted by corpus luteum - maintained by hCG produced by trophectoderm of blastocyst)

60
Q

3 stages of implantation

A
  1. Apposition
  2. Adhesion
  3. Invasion
61
Q

Appostion

A

loose, unstable connection between trophectoderm and endometrial lining - microvilli of trophoblast interdigitate with pinopodes

62
Q

Adhesion

A

stronger connection, created by ligand-receptor interactions

Trophoblastic cells rapidly proliferate → syncytiotrophoblasts (outer) and cytotrophoblasts (inner)
Syncytiotrophoblasts → secrete TNF-a, proteases→ helps dislodge epithelial cells (down regulate cadherins and B-catenin) and invade through BM and endometrial stroma (decidua)

63
Q

Molecules that facilitate adhesion

A

Integrins: cell surface receptors that bind ECM (laminin and fibronectin)

Heparan sulfate proteoglycans

L-selectin

64
Q

Invasion

A

completely buries into endometrium, no longer in direct contact with uterine cavity (occurs by day 10)

→ Placentation process begins

Inner cell mass of blastocyst positioned on side of endometrium → first to invade

65
Q

Placenta previa

A

implantation near cervix

66
Q

Placenta accreta

A

implantation at site of a prior uterine sca

67
Q

Ectopic pregnancies:

A

pregnancy outside uterine cavity

TX = methotrexate or surgery

68
Q

Desirable attributes of screening tests

A

Screening advances time of diagnosis of cancers destined to cause trouble

Early treatment is superior to treatment started after patient already has symptoms

69
Q

Compared to unscreened populations, screening ALWAYS increases survival even if death is not delayed by early detection. Why? (3)

A

Lead time: earlier diagnosis → patients appear to live longer

Length time bias: more likely to find slower growing tumors → better prognosis

Overdiagnosis bias: benign natural history → best prognosis

70
Q

Sensitivity

A

SNOUT - high sensitivity → rule out

TP / TP + FN

71
Q

Specificity

A

SPIN - high specificity → rule in

TN / TN + FP

72
Q

As prevalence increases –> _______ false negatives, _______ PPV, and _______ NPV

A

*As prevalence increases → INCREASE FALSE NEGATIVES

Increase PPV, decrease NPV

73
Q

As prevalence decreases –> _______ false negatives, _______ PPV, and _______ NPV

A

*As prevalence decreases → INCREASES FALSE POSITIVES

Decrease PPV, increase NPV

74
Q

PPV and NPV formulas

A

PPV = TP/TP+FP

NPV = TN/TN+FN

75
Q

Likelihood ratios

A

probability of a test result in person WITH disease/probability of same test result in person WITHOUT disease

76
Q

Likelihood ratios

LR > 1 –> ?
LR < 1 –> ?
LR < 0.1 –> ?
LR > 10 –> ?

A

LR > 1 = disease more likely
LR < 1 = disease less likely
LR < 0.1 → rule OUT
LR > 10 → rule IN

77
Q

Likelihood ratios formulas for LR- and LR+?

A

LR+ = sensitivity /(1-specificity)

LR- = (1-sensitivity) / specificity

78
Q

Relative risk

A

chance of outcome in group of interest / chance of outcome in comparison group

79
Q

How to calculate relative risk reduction?

A

1-RR = RRR (Relative risk reduction)

80
Q

Absolute risk reduction (%)

A

difference in risk between groups

81
Q

NNS or NNT (number needed to screen / treat)

formula?
what happens as prevalence increases?

A

NNS or NNT = 100/ARR

82
Q

Development of placenta

1) Implantation

A

1) Implantation of BLASTOCYST occurs day 6-8 → TROPHOBLAST LAYER multiplies and differentiates into inner cytotrophoblast and outer syncytiotrophoblasts

83
Q

Development of placenta

2) Chorionic Villi

A

Develop weeks 2-3 –> primary, secondary, and tertiary vili made up of syncytiotrophoblasts and cytotrophoblasts that invade maternal blood supply

84
Q

Primary Villi

A

cytotrophoblast core surrounded by syncytiotrophoblast - develop in week 2

85
Q

Secondary Villi

A

xtraembryonic mesoderm core surrounded by cytotrophoblast and syncytiotrophoblast - develop in week 3

86
Q

Tertiary Villi

A

formation of arterio capillary network

Core of villous (fetal) capillaries surrounded by cytotrophoblasts and syncytiotrophoblasts

Syncytiotrophoblasts contact
blood, while cytotrophoblasts to the invading

Develop at end of week 3

Will become VILLOUS CHORION (fetal component of placenta)

87
Q

Floating Villi

A

majority of placental mass

Site of nutrient and waste exchange

88
Q

Anchoring Villi

A

attachment to uterus

Site for invasive cytotrophoblast development

89
Q

Development of placenta:

3) Cytotrophoblast endovascular invasion

A

invade spiral arteries of uterus → modify lining so arterioles relax to become low resistance, high flow arteries

-Interstitial invasion and endovascular invasion

90
Q

Interstitial invasion

A

cytotrophoblasts invade the entire endometrium and the first third of the myometrium

91
Q

Endovascular invasion

A

cytotrophoblasts invade uterine spiral arterioles through superficial myometrial segments

Only termini of veins are breached

92
Q

Amniotic fluid

A

Composed of ultrafiltrate of maternal plasma, fetal urine, and fetal lung secretions

Ranges from 250 ml at 16 weeks to 1 L at 32 weeks

Critical for lung development and proper MSK function

93
Q

Causes of decreased amniotic fluid: oligohydramnios (4)

A

Rupture of membranes

Congenital anomalies (GU system)

Nephrotoxic drugs (ACEIs, NSAIDs)

Poor placental perfusion

94
Q

Causes of increased amniotic fluid: polyhydramnios (2)

A

Congenital anomalies (neural tube defects, esophageal atresia)

Gestational diabetes

95
Q

Function of placenta: (7)

A

1) Support growth and development of fetus
2) Transport
3) Respiratory
4) Endocrine
5) Immune system
6) Skin
7) Hepatic/Metabolism

96
Q

Function of placenta:

Types of transport (3)

A

1 )Diffusion: concentration dependent
-Gases, H2O

2) Facilitated diffusion: driven by gradient + specific carrier
- Glucose

3) Active transport: Transport against gradient, requires energy
- Amino acids

97
Q

Global impaired transport

A

can result in intrauterine growth restriction (IUGR)

Diffusion limited transport

Flow-limited transport

98
Q

Flow-limited transport

A

cross the placenta rapidly

-Most affected by uterine blood flow (maternal BP, Aortic stenosis)

99
Q

Diffusion limited transport

A

cross the placenta slowly

-Most affected by syncytiotrophoblast membrane

100
Q

Function of placenta: Respiratory functions

A

fetal O2 dissociation curve shifted to left

  • Decreased affinity for 2,3 DPG
  • Increased pH
101
Q

Function of placenta: Endocrine function - secretes what?

A

CRH, GnRH, TRH, SRIF, ACTH, hCG (human chorionic gonadotropin), hCT (human chorionic thyrotropin), hPL (human placental lactogen)

102
Q

hCG (human chorionic gonadotropin)

A

One of earliest markers of pregnancy

Peaks around week 10, then declines

Maintains corpus luteum and progesterone production until week 8 when placenta makes enough progesterone

Regulates cytotrophoblast differentiation into syncytiotrophoblasts

*Elevated in pregnancies with trisomy 21

103
Q

hPL (human placental lactogen)

A

produced by SCTB

Directs maternal system to shift to more fatty acid metabolism, making carbohydrates more available to fetus

Creates insulin resistance

Partly responsible for gestational diabetes

104
Q

Placental growth hormone

A

Similar to pituitary growth hormone

Increases from 12 wks to term → gradually replaces pituitary GH

Controls maternal IGF-1 levels

Secretion regulated by glucose

Lower levels observed in IUGR

105
Q

Trophoblasts secrete what?

what is the function of that?

A

Trophoblasts → secrete estrogen/progesterone at high levels

Progesterone suppresses uterine contractions, necessary for pregnancy maintenance

Estrogen production requires maternal-fetal-placental unit - baby has what mom doesn’t and vice versa

106
Q

Placenta Immune function

A

Protective barrier → physical barrier to pathogens, Hofbauer cells in villous core

Transports maternal IgG to fetal circulation (receptor mediated endocytosis)

Fetal immune system makes IgM

IgM does NOT cross placenta

107
Q

Clinical implications of maternal IgG crossing placenta? (4)

A

Isoimmunization/immune hydrops (IgG anti RH)

Flu vaccination in pregnancy → baby protected with flu IgG

Tdap vaccine in pregnancy → baby protected by IgG

Maternal autoimmune diseases → can cross placenta and affect the baby as well

108
Q

Placenta function as skin?

A

temperature regulation (women feel warmer during pregnancy), and protective barrier to pathogens

109
Q

Placental hepatic/metabolism function?

A

Produces glycogen, cholesterol, and fatty acids

Drug metabolism

Excretion of waste products

110
Q

Dizygotic

A

“Fraternal”
2 ova fertilized by 2 sperm

Not genetically identical

70% of spontaneous twins, 95% of ART twins

111
Q

Monozygotic

A

“Identical”
1 ovum fertilized by 1 sperm → fertilized oocyte divides

Genetically identical

30% of spontaneous twins
3-5/1000 births

112
Q

Chorionicity types

A

1) Dichorionic/Diamniotic
2) Monochorionic diamniotic
3) Monochorionic, Monoamniotic
4) Monochorionic monoamniotic conjoined twins

113
Q

Dichorionic, Diamniotic

A

2 cell stage → cell splits at morula stage (day 0-4)→ develops own trophoblast and inner cell mass → SEPARATE chorionic cavities, SEPARATE amnion, and SEPARATE placenta

**Cleavage at day 0-4

**Can be monozygotic or dizygotic

20-30% of monozygotic twins

114
Q

Monochorionic diamniotic

A

2 cell stage →single morula → shared chorion, separate amnions = one placenta, but two separate sacs divided by an amnion

**Cleavage at day 4-8

**Can only be monozygotic - 70% of monozygotic twins

115
Q

Monochorionic, Monoamniotic

A

2 cell stage → Morula → cell splits at day 8-12 → shared amnion and shared chorion = one chorion, one amnion, one placenta
ONLY monozygotic

Only 1% of monozygotic twins

Increased risk of having cord entanglement → high perinatal mortality

116
Q

Monochorionic monoamniotic conjoined twins

A

2 cell stage → morula → cell splits after 13 days → end up with conjoined twins sharing one amnion, placenta, and chorion

117
Q

How to determine chorionicity?

A

Di/Di → “Thick dividing membrane” + “twin peak” or “lambda” sign

Mono/Di → Thin dividing membrane + “T sign”

Mono/Mono → no dividing membrane

118
Q

Complications with twins:

A 
Miscarriage
Hyperemesis (due to increased hCG)
Increased risk of aneuploidy
Prenatal screening tests less sensitive and diagnostic procedures more difficult
Maternal anemia
Gestational diabetes (increased hPL)
Gestational hypertension / preeclampsia
Intrauterine growth restriction
Preterm birth (37 weeks = full term, average twin is 36 weeks)
Cesarean delivery
Postpartum hemorrhage
Perinatal mortality increased
119
Q

Twin-Twin Transfusion Syndrome (TTTS)

A

ONLY in monochorionic-diamniotic twins
15-20% of monochorionic-diamniotic twins have unbalanced flow through connected vessels (connection between artery/vein)

Classification based on US findings - intertwin weight discordance of 15-20% is diagnostic, or amniotic fluid difference

More severe → more risk of complications

120
Q

Twin-Twin Transfusion Syndrome (TTTS) - what happens to the RECIPIENT TWIN

A 
Recipient twin (receiving blood flow) → gets larger → increases urine production to reduce blood volume
→ large bladder on ultrasound, polyhydramnios
121
Q

Twin-Twin Transfusion Syndrome (TTTS) - what happens to the DONOR TWIN

A 
Donor twin (giving away blood) → gets smaller → reduces urine production to retain blood volume
→ oligohydramnios
122
Q

Implications of TTTS:

A

Untreated TTTS prior to 24 weeks gestational age → mortality of one or both twins in 80-90% of cases

After death of one twin, other twin at increased risk for brain damage in ⅓ of cases

Severe TTTS prior to 16 weeks has dismal prognosis

123
Q

Donor twin most likely to die from

A

decreased blood volume, oligohydramnios, small placental volume, not enough nutrients to support fetal growth

124
Q

Recipient twin most likely to die from

A

too much blood volume → polyhydramnios, early delivery, fetal hydrops due to diffuse edema

125
Q

Treatment of TTTS (3)

A

1) Reduction amniocentesis
2) Micro Septostomy
3) Laser ablation

126
Q

Reduction amniocentesis

A

Removal of excess fluid from recipient twin sac using needle through mom’s abdomen
→ risk of early delivery

127
Q

Micro Septostomy

A

create hole between babies’ sacs

128
Q

Laser ablation

A

direct visualization of communicating vessels and ablation with laser

High complication rate, but better survival of babies

129
Q

3 types of decidua

A

1) Decidua basalis
2) Decidua capsularis
3) Decidua parietalis

130
Q

Decidua basalis

A

under the implanting embryo

Region of endometrium deep to developing embryo and superficial to underlying myometrium

Maternal component of placenta

131
Q

Decidua capsularis

A

overlies embryo

Region of endometrium that covers the blastocyst, separating it from the uterine cavity

132
Q

Decidua parietalis

A

covers remainder of uterine surface

Every portion of endometrium other than site of implantation

133
Q

Oxygen diffuses from maternal → fetal circulation in this order: (4)

A

Maternal arterial blood within intervillous space →

Syncytiotrophoblastic layer →

cytotrophoblastic layer →

fetal endothelial cells of L umbilical vein

Life Cycles (8 decks)

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