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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
CHEK2 gene
tumor suppressor gene → cellular proliferation Responsible for progression to carcinoma 5% of familial breast cancer
26
Li-Fraumeni Syndrome
TP53 gene mutation 5% of familial breast cancer
27
Cowden Syndrome
PTEN gene mutation <1% of familial breast cancer
28
Peutz-Jeghers Syndrome
STK11/LKB1 gene mutation | < 1% of familial breast cancer
29
Pathogenesis of Breast Cancer: | Molecular pathways: (3)
1) ER positive, HER2 negative cancers arise via the dominant pathway 2) HER2 Positive cancer 3) ER negative, HER2 negative = TRIPLE NEGATIVE
30
Molecular pathways: ER positive, HER2 negative cancers arise via the dominant pathway
Majority of cases (50-65%) Seen in ADH, flat epithelial atypia, and low grade DCIS
31
Molecular pathways: HER2 Positive cancer
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
32
Molecular pathways: ER negative, HER2 negative = TRIPLE NEGATIVE
15% of all breast cancers Most common subtype with BRCA1 Precursor lesion unknown
33
male breast cancer
Klinefelter's, BRCA2 mutations Associated with subareolar mass
34
Nucleus contains _____
highly condensed chromatin
35
Protamines
specialized basic histone tightly held together by disulfide bond cross-linking keeps chromatin compact Shape of sperm head is species dependent
36
Acrosome
anterior ½ or ⅔ of sperm head Thin, double-layered membrane sac Contains hydrolytic enzymes, critical for fertilization
37
Tail of sperm
: contains 9 axoneme doublets arranged circumferentially around a pair of microtubules → doublets surrounded by mitochondrial sheath → sperm motility
38
Normal values of semen analysis: - Volume - Concentration - Motility - Morphology
Volume > 1.5 ml Concentrations: > 15 x 10^6 /ml Motility: > 32% Morphology: 4% normal
39
Female evaluation of fertility
How many eggs are available: - Blood tests: FSH, E2, AMH - Ultrasound Euploid embryos decrease with maternal age
40
Women have a peak number of oocytes when?
20 weeks gestation
41
Primary oocyte is arrested when?
Prophase I of meiosis I
42
Primary oocyte finishes 1st meiotic division when?
after LH surge → secondary oocyte + 1st polar body
43
Secondary oocyte → finishes meiosis II after ____
fertilization
44
Zona Pellucida
shell-like structure that surrounds oocytes
45
Glycoprotein sheet of Zona pellucida
70% protein, 20% hexose, 3% sialic acid, 2% sulfate Composed of 3 glycoproteins: ZP1, ZP2, ZP3 Mutant/inactivated zone proteins → infertility
46
Fertilization:
process involving union of male and female germ cells that results in formation of a pronuclear zygote
47
9 steps of fertilization
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
48
Sperm capacitation
Process by which spermatozoa acquire capacity to undergo acrosome reaction and fertilize eggs Acquired in distal genital tract of male
49
Sperm interaction with zona pellucida
Sperm binding to zona pellucida: ZP3 glycoprotein = sperm receptor
50
Acrosome reaction
(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
51
Sperm-oocyte plasma membrane fusion
Fertilin = protein responsible for sperm-oocyte fusion
52
Oocyte activation
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
53
Male pronuclei formation
Protamines unwinds, disulfide bonds reduced by action of oocyte-derived glutathione Sperm nuclei decondense Forms male/female pronuclei
54
Preimplantation embryo development:
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
Implantation
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
Most common sites of implantation:
Posterior wall in midsagittal plane
57
Blastocyst Hatching
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
Decidualization:
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
Window of implantation
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
3 stages of implantation
1. Apposition 2. Adhesion 3. Invasion
61
Appostion
loose, unstable connection between trophectoderm and endometrial lining - microvilli of trophoblast interdigitate with pinopodes
62
Adhesion
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
Molecules that facilitate adhesion
Integrins: cell surface receptors that bind ECM (laminin and fibronectin) Heparan sulfate proteoglycans L-selectin
64
Invasion
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
Placenta previa
implantation near cervix
66
Placenta accreta
implantation at site of a prior uterine sca
67
Ectopic pregnancies:
pregnancy outside uterine cavity | TX = methotrexate or surgery
68
Desirable attributes of screening tests
Screening advances time of diagnosis of cancers destined to cause trouble Early treatment is superior to treatment started after patient already has symptoms
69
Compared to unscreened populations, screening ALWAYS increases survival even if death is not delayed by early detection. Why? (3)
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
Sensitivity
SNOUT - high sensitivity → rule out TP / TP + FN
71
Specificity
SPIN - high specificity → rule in | TN / TN + FP
72
As prevalence increases --> _______ false negatives, _______ PPV, and _______ NPV
*As prevalence increases → INCREASE FALSE NEGATIVES Increase PPV, decrease NPV
73
As prevalence decreases --> _______ false negatives, _______ PPV, and _______ NPV
*As prevalence decreases → INCREASES FALSE POSITIVES Decrease PPV, increase NPV
74
PPV and NPV formulas
PPV = TP/TP+FP NPV = TN/TN+FN
75
Likelihood ratios
probability of a test result in person WITH disease/probability of same test result in person WITHOUT disease
76
Likelihood ratios LR > 1 --> ? LR < 1 --> ? LR < 0.1 --> ? LR > 10 --> ?
LR > 1 = disease more likely LR < 1 = disease less likely LR < 0.1 → rule OUT LR > 10 → rule IN
77
Likelihood ratios formulas for LR- and LR+?
LR+ = sensitivity /(1-specificity) LR- = (1-sensitivity) / specificity
78
Relative risk
chance of outcome in group of interest / chance of outcome in comparison group
79
How to calculate relative risk reduction?
1-RR = RRR (Relative risk reduction)
80
Absolute risk reduction (%)
difference in risk between groups
81
NNS or NNT (number needed to screen / treat) formula? what happens as prevalence increases?
NNS or NNT = 100/ARR
82
Development of placenta 1) Implantation
1) Implantation of BLASTOCYST occurs day 6-8 → TROPHOBLAST LAYER multiplies and differentiates into inner cytotrophoblast and outer syncytiotrophoblasts
83
Development of placenta 2) Chorionic Villi
Develop weeks 2-3 --> primary, secondary, and tertiary vili made up of syncytiotrophoblasts and cytotrophoblasts that invade maternal blood supply
84
Primary Villi
cytotrophoblast core surrounded by syncytiotrophoblast - develop in week 2
85
Secondary Villi
xtraembryonic mesoderm core surrounded by cytotrophoblast and syncytiotrophoblast - develop in week 3
86
Tertiary Villi
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
Floating Villi
majority of placental mass Site of nutrient and waste exchange
88
Anchoring Villi
attachment to uterus Site for invasive cytotrophoblast development
89
Development of placenta: 3) Cytotrophoblast endovascular invasion
invade spiral arteries of uterus → modify lining so arterioles relax to become low resistance, high flow arteries -Interstitial invasion and endovascular invasion
90
Interstitial invasion
cytotrophoblasts invade the entire endometrium and the first third of the myometrium
91
Endovascular invasion
cytotrophoblasts invade uterine spiral arterioles through superficial myometrial segments Only termini of veins are breached
92
Amniotic fluid
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
Causes of decreased amniotic fluid: oligohydramnios (4)
Rupture of membranes Congenital anomalies (GU system) Nephrotoxic drugs (ACEIs, NSAIDs) Poor placental perfusion
94
Causes of increased amniotic fluid: polyhydramnios (2)
Congenital anomalies (neural tube defects, esophageal atresia) Gestational diabetes
95
Function of placenta: (7)
1) Support growth and development of fetus 2) Transport 3) Respiratory 4) Endocrine 5) Immune system 6) Skin 7) Hepatic/Metabolism
96
Function of placenta: Types of transport (3)
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
Global impaired transport
can result in intrauterine growth restriction (IUGR) Diffusion limited transport Flow-limited transport
98
Flow-limited transport
cross the placenta rapidly | -Most affected by uterine blood flow (maternal BP, Aortic stenosis)
99
Diffusion limited transport
cross the placenta slowly | -Most affected by syncytiotrophoblast membrane
100
Function of placenta: Respiratory functions
fetal O2 dissociation curve shifted to left - Decreased affinity for 2,3 DPG - Increased pH
101
Function of placenta: Endocrine function - secretes what?
CRH, GnRH, TRH, SRIF, ACTH, hCG (human chorionic gonadotropin), hCT (human chorionic thyrotropin), hPL (human placental lactogen)
102
hCG (human chorionic gonadotropin)
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
hPL (human placental lactogen)
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
Placental growth hormone
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
Trophoblasts secrete what? what is the function of that?
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
Placenta Immune function
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
Clinical implications of maternal IgG crossing placenta? (4)
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
Placenta function as skin?
temperature regulation (women feel warmer during pregnancy), and protective barrier to pathogens
109
Placental hepatic/metabolism function?
Produces glycogen, cholesterol, and fatty acids Drug metabolism Excretion of waste products
110
Dizygotic
“Fraternal” 2 ova fertilized by 2 sperm Not genetically identical 70% of spontaneous twins, 95% of ART twins
111
Monozygotic
“Identical” 1 ovum fertilized by 1 sperm → fertilized oocyte divides Genetically identical 30% of spontaneous twins 3-5/1000 births
112
Chorionicity types
1) Dichorionic/Diamniotic 2) Monochorionic diamniotic 3) Monochorionic, Monoamniotic 4) Monochorionic monoamniotic conjoined twins
113
Dichorionic, Diamniotic
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
Monochorionic diamniotic
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
Monochorionic, Monoamniotic
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
Monochorionic monoamniotic conjoined twins
2 cell stage → morula → cell splits after 13 days → end up with conjoined twins sharing one amnion, placenta, and chorion
117
How to determine chorionicity?
Di/Di → “Thick dividing membrane” + “twin peak” or “lambda” sign Mono/Di → Thin dividing membrane + “T sign” Mono/Mono → no dividing membrane
118
Complications with twins:
``` 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
Twin-Twin Transfusion Syndrome (TTTS)
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
Twin-Twin Transfusion Syndrome (TTTS) - what happens to the RECIPIENT TWIN
``` Recipient twin (receiving blood flow) → gets larger → increases urine production to reduce blood volume → large bladder on ultrasound, polyhydramnios ```
121
Twin-Twin Transfusion Syndrome (TTTS) - what happens to the DONOR TWIN
``` Donor twin (giving away blood) → gets smaller → reduces urine production to retain blood volume → oligohydramnios ```
122
Implications of TTTS:
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
Donor twin most likely to die from
decreased blood volume, oligohydramnios, small placental volume, not enough nutrients to support fetal growth
124
Recipient twin most likely to die from
too much blood volume → polyhydramnios, early delivery, fetal hydrops due to diffuse edema
125
Treatment of TTTS (3)
1) Reduction amniocentesis 2) Micro Septostomy 3) Laser ablation
126
Reduction amniocentesis
Removal of excess fluid from recipient twin sac using needle through mom’s abdomen → risk of early delivery
127
Micro Septostomy
create hole between babies’ sacs
128
Laser ablation
direct visualization of communicating vessels and ablation with laser High complication rate, but better survival of babies
129
3 types of decidua
1) Decidua basalis 2) Decidua capsularis 3) Decidua parietalis
130
Decidua basalis
under the implanting embryo Region of endometrium deep to developing embryo and superficial to underlying myometrium Maternal component of placenta
131
Decidua capsularis
overlies embryo Region of endometrium that covers the blastocyst, separating it from the uterine cavity
132
Decidua parietalis
covers remainder of uterine surface Every portion of endometrium other than site of implantation
133
Oxygen diffuses from maternal → fetal circulation in this order: (4)
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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