1.1.1 Pre-Midterm Anatomy - Fetal

Front 1

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Back 1

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Front 2

Describe Ectopic pregnancy, including placenta previa:

Back 2

Ectopic pregnancy - zygote implants outside the uterine cavity - not viable.
Placenta previa - placenta is attached to the uterine wall close to or covering the cervix.

Front 3

Describe Oligohydramnios and “associated conditions for oligohydramnios”

Back 3

Deficiency of amniotic fluid.

Causes - renal agenesis and placental insufficiency.

Complications - cord compression, musculoskeletal abnormalities such as facial distortion and clubfoot, lung hypoplasia and intrauterine growth restriction.

Front 4

Describe Polyhydramnios and “associated conditions for polyhydramnios”

Back 4

Excess of amniotic fluid.

Causes - maternal diabetes mellitus, meroanencephaly, multiple pregnacny and esophageal atresia.

Front 5

Describe the Ovarian Cycles and Describe the Menstrual Cycles:

Back 5

Ovarian Cycles:
The Follicular (proliferative) Phase - growth of the uteral lining from an ovarian follicle leading up to ovulation.
Luteal (secretory) phase - post ovulation with falling progesterone levels.

Menstrual Cycles:
-menstrual phase (menstruation)
-proliferative phase
-ovulatory phase (ovulation)
-luteal phase (also known as secretory phase)
-ischemic phase
-follicular phase

Front 6

Explain how the Ovarian and Menstrual cycles are linked:

Back 6

The Ovarian Cycle is part of the Menstrual Cycle.
-The ovarian cycle involves changes in the ovaries:
a. The follicular phase
b. Ovulation occurs around day 14 of the cycle
c. The luteal phase
-The uterine cycle involves changes in the uterus:
a. The proliferative phase
b. The secretory phase

Front 7

Explain how the date for delivery is calculated from the last menstrual cycle:

Back 7

Naegele's Rule - from the first day of the woman's LMP add 1 year, subtract three months and add seven days (approximately 280 days (40 weeks) from the LMP.)

Parikh's Formula - add 9 months to LMP, subtract 21 days, then add duration of previous cycles.

Front 8

Describe the clinical significance of the sperm count:

Back 8

[sperm] in ejaculate to confirm infertility.

Abnormalities:
Aspermia: absence of semen
Azoospermia: absence of sperm
Hypospermia: low semen volume
Oligozoospermia: low sperm count
Asthenozoospermia: poor sperm motility -Teratozoospermia: sperm carry more morphological defects than usual

Front 9

Describe the phases of fertilization:

Back 9

fertilized egg → blastocyst → embryo → fetus.

1) passage of a sperm through the corona radiata of the oocyte.
2) penetration of the zona pellucida
3) fusion of the plasma cell membranes of the oocyte and sperm.
4) Completion of the second meiotic division of the ocyte.
5) Formation of the male promucleus.
6) Break down of the promuclear membranes.

Front 10

Results of Fertilization:

Back 10

1) Stimulates the secondary oocyte to complete the second meiotic division, producing the second polar body
2) Restores the normal diploid number of chromosomes (46) in the zygote
3) Results in variation of the human species through mingling of maternal and paternal chromosomes
4) Determines the chromosomal sex of the embryo
5) Causes metabolic activation of the oocyte, which initiates cleavage (of the zygote)

Front 11

Discuss cleavage of the zygote and formation of the blastocyst:

Back 11

Cleavage consists of repeated mitotic divisions of the zygote, resulting in a rapid increase in the number of cells beginning approximately 30hours after fertilization.
Formation of the blastocyst:
-Morula: The name of the embryo at the 16 to 32 cell stage.
-Blastocyst: At about day 5 after implantation.
-Cells are divided into the inner cell mass and trophoblast.
•Inner Cell Mass: The cells on the inside.
•Trophoblast: The cells surrounding the outside.

Front 12

Describe early implantation of the blastocyst:

Back 12

Begins at the end of the 1st embryonic week.
The inner cell mass gives rise to the embryo proper, the amnion, yolk sac and allantois, while the trophoblast will eventually form the placenta.

Front 13

Describe Implantation of the blastocyst:

Back 13

-Implantation: The trophoblast differentiates into two distinct layers:
Inner - the cytotrophoblast
Outer - the syncytiotrophoblast

The syncytiotrophoblast implants the blastocyst in the endometrium (innermost epithelial lining) of the uterus by forming finger-like projections called chorionic villi that make their way into the uterus, and spaces called lacunae that fill up with the mother's blood.

Front 14

Discuss the differentiation of the trophoblast:

Back 14

The trophoblast proliferates and differentiates into 2 cell layers at approximately 6 days after fertilization for humans

1) Inner layer- Cytotrophoblast - a single celled, inner layer of the trophoblast.
2) Outer layer- Syncytiotrophoblast - the thick layer that lacks cell boundaries and grows into the endometrial stroma. It secretes hcg in order to maintain progesterone secretion and sustain a pregnancy.

Intermediate trophoblast (IT); Location- implantation site, chorion, villi (dependent on subtype) - Anchor placenta (implanation site IT), unknown (chorionic & villus IT)

Front 15

Discuss the formation of lacunar networks:

Back 15

Lacunae fill with maternal blood from ruptured endometrial capillaries and cellular debris from the uterine glands.

The fluid in the lacunae (Embryotroph) diffuses to the embryonic disc.

Communication of the eroded uterine vessels with the lacunae represents the beginning of uteroplacental circulation.

Front 16

What is meant by the term "implantation bleeding" and is this the same as menses (menstrual fluid)?

Back 16

Implantation bleeding - loss of blood from implantation site of a blastocyst, occurs a few days after the expected time of menstruation.

No, it is not menses; it is blood from the intervillous space of the developing placenta. Blood lose could be the results from the rupture of chorionic arteries, veins, or both.

Front 17

Can an ectopic pregnancy occur in a woman who has an intrauterine device?:

Back 17

An intrauterine device does not physically block a sperm from entering the uterine tube and fertilizing an oocyte, if one is present, only making the endometrium hostile to implantation. A blastocyst could develop and implant in the uterine tube.

15% to 20% chance for ectopic pregnancy.

Front 18

What is the characteristic of 'LIGHT MEROMYOSIN' (LMM) filaments?

Back 18

MAKE UP THE 'RODLIKE' BACKBONE OF THE 'MYOSIN' FILAMENTS

Front 19

Can a blastocyst that implants in the abdomen develop into a full-term fetus?:

Back 19

-Yes, however...Very uncommon. It is believed to result from ectopic implantation of a blastocyst that spontaneously aborts from the uterine tube and enters the peritoneal cavity. If the patient is free of of systoms, the pregnancy may be allowed to continue until the viability of the fetus is ensured (e.g., 32 weeks), at which time it would be delivered by cesarean section.

Front 20

Can drugs and other agents cause congenital anomalies of the embryo if they are present in the mother's blood during the third week? If so, what organs would be most susceptible?:

Back 20

Certain drugs can produce congenital anomalies, if administered during the third week after the last normal menstual period.
-Can produce severe skeletal and neural tube defects in the embryo, such as acrania and meroencephaly (partial absence of the brain).

Front 21

Describe the formation of the placenta:

Back 21

Formed from a network of villi (trophoblast cells):
◦Primary Villus: Cytotrophoblast + a layer of syncytiotrophoblast grow into the lacunae.
◦Secondary Villus: Extraembryonic mesoderm grows into the primary villus.
◦Tertiary Villus: Extraembryonic mesoderm gives rise to blood vessels. Exchange of nutrients is now possible with mother.

Front 22

Describe the formation of the Three Germ Layers:

Back 22

Form by migration of epiblast cells through the primitive streak:

◦First Migration: Epiblasts migrate toward the midline and fold under, as they displace the hypoblast layer. This forms the true endoderm. (comes from migration of 1st epiblast layer -- not from the hypoblast)

◦Second Migration: More epiblasts migrate to form mesoderm.

◦The epiblasts that remain on the dorsal surface form the ectoderm.

Front 23

Describe the process of gastrulation:

Back 23

The cellular mass flattens and the three primary germ layers segregate.

By the process of gastrulation, the embryo differentiates into three types of tissue:
- the ectoderm, producing the skin and nervous system;
- the mesoderm, from which develop connective tissues, the circulatory system, muscles, and bones; and
- the endoderm, which forms the digestive system, lungs, and urinary system.

Front 24

Describe the development of the notochord and induction of the neural plate:

Back 24

Notochord Formation:
•Notochordal Process forms from mesoderm.
•Neurenteric canal is a transient opening between the amniotic cavity and the yolk sac.
•Notochordal plate reforms a tube now known as the notochord.

Concurrent Ectodermal Changes:
- Formation of the Neural Plate and Neural Crest Cells.
•Notochord induces ectodermal formation of the neural plate.
•As neural plate invaginates medially, forming the midline neural groove and laterally placed neural folds.
•Neural Tube forms as the fusion of the neural folds.

Front 25

Describe the establishment of a primordial uteroplacental circulation:

Back 25

maternal blood flows into the lacunae, oxygen and nutritive substances become available to the extraembryonic tissues ove the large surface of the syncytiotrophoblast.

Oxygenated blood passes into the lacunae from the spiral endometrial arteries in the enometrium;

deoxygenated blood is removed from the lacunae through endometrial veins.

Front 26

What is the most common cause of spontaneous abortion during the first week of development?

Back 26

Chromosomal abnormality.

Front 27

When does the Primitive Streak take place?

Back 27

Beginning of the 3rd Week

Front 28

Describe the development of sacrococcygeal teratoms?

Back 28

Remnants of the primitive streak may persist and give rise to a large tumor known as a sacrococcygeal teratoma.

-Usually surgically removed, and prognosis is good.

Front 29

During the 3rd week of development, Failure of the neural folds to fuse and form the neural tube results in what?

Back 29

meroencephaly and spina bifida cystica.

Front 30

Describe the formation of early embryonic blood vessels:

Back 30

Formed during the 3rd week, called Vasculogenesis.

Front 31

When does the fetus heart begin to beat?

Back 31

Day 21 or 22.

Front 32

Which organ system is fully functional in a fetus?

Back 32

The Cardiovascular system is the first organ system to reach a functional state on day 21 or 22.

Front 33

What is choriocarcinomas?

Back 33

Malignant trophoblastic lesions.

Front 34

Describe the folding of the embryo?

Back 34

Describe the folding of the embryo?
-Folding results from rapid growth of the embryo, by folding the flat trilaminar embryonic dsc into a somewhat cylindar embryo.

Front 35

Describe a hydatiform mole and its association with choriocarcinoma?

Back 35

-Hydatiform moles form when the embryo dies and the chorionic villi do not complete their development. Little or no embryonic tissue is present though the trophoblast developes well. They look like a bunch of grapes and turns into choriocarcinomas.

Front 36

Describe the fate of the intraembryonic mesoderm:

Back 36

Mesodermal Structures:
•Paraxial Mesoderm: Somites.
•Intermediate Mesoderm: Urogenital system.
•Lateral Plate Mesoderm: Primitive gut, posterior and lateral body wall. It differentiates into two layers:
-◦Somatic Mesoderm: (Amniotic side)
-◦Splanchnic Mesoderm: (Yolk side)

Front 37

Describe the development of the somites:

Back 37

Somites establish the segmental nature of the body. They differentiate into three layers.
•Sclerotome: Forms the vertebral bone. This originates from paraxial mesoderm.
•Dermamyotome, consisting of myotome (medial part) and dermatome (most lateral part)

Early Somite Development:
•Chorioamnionic Membrane forms, merging the chorion and amnion cavities.
•Folding (flexion) of the embryo repositions the somites from the ventral-medial position to a dorsolateral position.

Front 38

Describe how the amniotic fluid is produced:

Back 38

Weeks 1-11: Maternal tissue fluid diffuses across the amniochorionic membrane.

Weeks 11+: fetus contributes to the "AF" by expelling urine into the amniotic cavity.

Front 39

Describe how the amniotic fluid circulates:

Back 39

An exchange of fluid w/fetal blood occurs thru the umbilical cord & at the site where the amnion adheres to the chorionic plate on the fetal surface of the placenta.

Front 40

What is a Sacrococcygeal Teratoma?

Back 40

A benign tumor left over from the primitive streak.

Front 41

What is a Chordoma?

Back 41

Slow growing malignant tumor which invades bone. Occurs at the base of the scull or the lumbrosacral region. Remnant of the notochord.

Front 42

What is Gastroschisis?

Back 42

Gut herniates through a poorly formed anterior abdominal wall. Causes heat loss from exposed bowel. Good prognosis after surgery.
Caused by a problem with lateral folding.

Front 43

What is Ectopic Cordis?

Back 43

Heart lies outside the thoracic cavity due to lesion in sternum. Very poor prognosis (usually accompanied by other cardiac defects.
Caused by a problem with Lateral folding.

Front 44

What does the neural tube give rise to?

Back 44

CNS
Somatic PNS
Pre-ganglionic component of visceral motor portion of PNS (sym and para)

Front 45

What do neural crest cells give rise to?

Back 45

Ganglion cells of PNS (all neurons of the PNS with soma in somantic sensory and autonomic ganglia)
- Sensory neurons of spinal nerves
- Sympathetic and parasympathetic post-ganglionics
Schwann Cells
Meninges
Suprarenal medulla

Front 46

What are the two kinds of spina bifida?

Back 46

Spina bifida occulta:
No bulge, tuft of hair, no neurological deficencies.

Spina bifida cystica
-With meningocoele - bulge over defect that contains meninges and CSF, no neurological defects

With meningomyelocoele - bulge over defect containing meninges, cord and spinal nerves

With Myeloschisis - open cord, failure of caudal neuropore to close and neural tube did not form.

Front 47

What is the primary yolk sac/Exocoelomic cavity?

Back 47

First site of blood formation, gives rise to primordial gut and germ cells.

Front 48

What is Amniotic Band Syndrome?

Back 48

Amniotic bands can amputate limbs (premature rupture of amnion)

Front 49

What two parts make up the placenta?

Back 49

Maternal - Decidua basalis (rough)
Fetal - Chorion frondosum (smooth)

Front 50

What are the fates of the following structures of the primitive heart?
Trancus Arteriosus
Bulbus Cordis
Ventricle
Atrium
Sinus Venosus
space between Bulbus Cordis and Left Atrium

Back 50

Truncus Arteriosus - asc aorta, pulm trunk
Bulcus Cordis - aortic vestibule & conus arteriosus
Ventricle - out free walls of both ventricles
Atrium - auricles and pectinate muscle area of both atria
Sinus Venosus - coronary sinus & sinus venarum
Space - transverse sinus

Front 51

What is dextrocardia?

Back 51

Heart folds in opposite direction giving a mirror image

Front 52

What is probe patency?

Back 52

Failure of anatomical closure resulting in functional closure only, allowing a "prove" to pass through the foramen. Generally asymptomatic

Front 53

What are the three areas involved in Atrial Septal Defects and what problems are associated with them?

Back 53

Problem: Persistent foramen causing a left to right shunt. All are correctable by surgery. Can result in common atrium.

Ostium Secondum defect - patent foramen secundum - failure of septum primum and secundum to meet and fuse (most common ASD)

Endocardial Cushion defect - patent foramen primum

Sinus Venosus defect - defect in upper atrium due to incomplete sunus venosus and/or incomplete development of septum secundum.

Front 54

Which septum is supposed to partition the truncus arteriosus?

Back 54

Aorticopulmonary septum

Front 55

Describe the transposition of the great vessels

Back 55

Faulty migration of neural crest cells results in absence of spiral to the aorticopulmonary septum.
If complete transposition you have a R - L shunt (cyanotic)
Cyanosis is less if ASD, VSD or PDA is present to allow L - R missing
Deoxy blood from RV directly enters system circulation.

Front 56

Describe the Tetrology of Fallot

Back 56

Failure of migration of neural crest cells where the aorticopulmonary septum forms symmetrically.

Must have:
Pulmonary stenosis causing
Right ventricular hypertrophy
VSD
Overriding aorta.
Results in a cyanotic R - L shunt.

Front 57

Describe a Persistent Truncus Arteriosus

Back 57

Failure of migration of neural crest cells
Part or all of truncus arteriosus does not develop Aorticopulmonary septum resulting in a common passageway part or all the way up. Always accompanied by VSD. Not a true R - L shut but systemic circulation gets blood from both ventricles and is cyanotic.

Front 58

Describe two prenatal cardiac shunts - foramen ovale and ductus arteriosus

Back 58

Foramen Ovale - allows oxy blood from IVC entering RA - LA to systemic circulation

Ductus Arteriosus - deoxy blood from SVC enters RA, RV, Pulm Trunk - distal aorta arch via ductus arteriosus

Front 59

What is a Patent Ductus Arteriosus?

Back 59

Persistence of duct beyond 1 month of due date
Premature infants usually have PDA
Most common anomaly with maternal ruvella infection
L - R Shunt (acyanotic)

Front 60

Summarize which shunts are R - L

Back 60

Tetrology of Fallot
Transpotion of Great Vessels
Persistent Truncus Arteriosus

Front 61

Summarize which shunts are L - R

Back 61

ASD
VSD
PDA

Front 62

What is a Tracheoesophageal fistula?

Back 62

Faulty development of the traacheoesphogeal septum
Abnormal communication between trachea and esophagus
May be associated with esophagus atresia
Infants will cough and choke when swallowing fluid
May cause pneumonia
In utero - may result in polyhdramnios as the amniotic fluid can't go to gut for absorption do to esophageal atresia

Front 63

Lung development and fetal viability

Back 63

Canalicular period (26 weeks) Type II aveolar cells may produce sufficient surfactant to respire w/o respirator

Terminal Sac Stage (26+) - fetus is viable

Front 64

Factors influencing normal development of the lungs

Back 64

Amniotic fluid volume - Oligohydramnios = hypoplasia

Fetal breathing movements: stimulate lung development by causing aspiration of amniotic fluid (at birth still partially filled, which is quickly absorbed)

Space in thorax for growth: infants with congenital disphragmatic hernia, lung is unable to develop normally as space is reduced

Front 65

Normal development of the diaphragm

Back 65

From 4 embryonic components:
Pleuroperitoneal membranes invaded by myoblasts and contribute to muscular portion
Septum Transversum remains membranous and becomes central tendon
Lateral body wall contributes some muscle to the periphery of the diaphragm

Front 66

Normal development of pleural and pericardial cavities

Back 66

• bronchial buds grow from laryngotracheal diverticulum
• buds grow into surrounding splanchnic mesoderm
• plueropericardial folds grow in from lateral walls
• folds enlarge to become pleuropericardial membranes
• membranes separate heart from developing lungs
• pleuropericardial membranes fuse posterior to heart, forming the pericardial sac, while lungs continue to grow around sac

Front 67

What are the possible defects in the development of the diaphragm?

Back 67

Retrosternal/parasternal hernia
Congenital diaphragmatic hernia
Eventration of the diaphragm

Front 68

What is a retrosternal/parasternal hernia?

Back 68

Deficiency of pleuroperitoneal membrane
Hiatus between sternocostal parts
Gut may be herniated into pericardial sac

Front 69

What is a congenital diaphragmatic hernia?

Back 69

Failure of pleuroperitoneal membranes to fully develop or properly fuse with other elements of the diaphragm
Flattened abdomen
Gut enters thorax through posterolateral defect in diaphragm

Front 70

What is Eventration of diaphragm?

Back 70

Defective muscle development from body wall and only aponeurotic/membranous sheet is present
As diaphragm contracts, muscular part descends, non-muscular portion balloons into throwax pushed by abdominal viscera
Relatively rare

Front 71

What are the fates of the aortic arches?

Back 71

First - gives rise to maxillary artery (disappears)
Second - gives rise to hyoid and stapedial arteries (disappears)
Third, Fourth, Sixth - major vessels
Fifth - disappears

Front 72

What happens if the distal portion of the right fourth arch persists?

Back 72

Double aortic arches

They enclose the esophagus so swallowing is difficult

Front 73

What happens if the right 4th arch disappears leaving part of the 7th?

Back 73

The right 7th becomes the right subclavian. It follows the left around and eventually passes behind it and the trachea to reach its destination

Front 74

What problems are possible during descent of the testis?

Back 74

Hydrocoeles
Incomplete indirect inguinal hernia
Indirect inguinal hernia
Direct inguinal hernia
Cryptorchid (undescended)
Ectopic testis

Front 75

What problems are possible during development of the GI tract?

Back 75

Congenital omphalocoele
Anomalies of Rotation
- nonrotation
- reversed rotation
- subhepatic cecum
- midgut volvulus
Omphaloenteric duct (yolk sac) anomalies
Problems with epithelia lining of gut
- bowel stenosis
- bowel atresia
Hirsprung disease (megacolon)

Front 76

What problems are possible during development of the kidneys?

Back 76

Renal agenesis
Discoid (pancake) kidney
Problems with ascent of kidney
- horshoe kidney (fuses, hits inf mesenteric artery on ascent)
- pelvic kidney (fails to ascend)
- Migration to opposite side with possible fushion
- 3 ureters
Lobulated kidney