Day 5.1 Embryo Flashcards
Sonic Hedgehog gene
Produced at BASE of limbs (limb buds) in ZPA- zone of polarizing activity
Involved in patterning along anterior-posterior axis
Mediated ECTOdermal fn.
Dysfn is related to holoprose encephalopathy (division along cerebral hemispheres)
Wnt-7 gene
Produced at APICAL ridge of ECTOderm- thickened ectoderm at DISTAL end of each developing limb.
Necessary for proper organization along dorsal-ventral axis
FGF gene
Produced at APICAL ridge of ECTOderm.
Stimulates mitosis of underlying MESOderm, providing for lengthening of limbs
Dysfn related to achondroplasia–> dwarfism
Homeobox (HOX) gene
Involved in segmental organization in a cranio-caudal direction.
Blueprint for skeletal morphology
Code for transcription regulators
Mutation in HOXD-13 = synpolydactyly- extra fused digit b/t 3rd and 4th fingers
Retinoic acid (VitA) is a teratogen that alters HOX gene expression and leads to mutation.
Day 0 Day 2 Day 3 Day 5 Day 6
Day 0 Fertilization by sperm Day 2 zygote Day 3 morula Day 5 blastocyst Day 6 implantation into endometrium
When does B-hCG secretion begin?
Within one week, after implantation of the blastocyst.
hCG is made by the placenta
2 weeks (fetus)
2’s for 2nd week:
2 germlayers- Bilaminar disk (epiblast + hypoblast)
2 cavities- amniotic cavity and yolk sac
2 parts of placenta- cytotrophoblast and synctiotrohoblast
3 weeks (fetus)
Gastrulation - going from 2 layers to 3 layers
Primitive streak, notochord, and neural plate begin to form.
3 wks = 3 germ layers
ectoderm
mesoderm
endoderm
How is the primitive streak formed in week 3?
The epiblast (of the bilaminar disk from week 2) invaginates to form the primitive streak.
What the the cells from the primitive streak give rise to?
Cells from the primitive streak give rise to both the mesoderm and part of the ectoderm.
What does the notochord of week 3 do?
The notocord causes the neuroectoderm to form the neural plate.
When does the neural tube close?
By week 4
The neural tube is formed by the neuroectoderm, which forms the neural plate, which folds up in a U shape and forms the neural tube (and also the neural crest cells)
Note: any problems with the SC devt (eg spina bifida) will happen by the 4th week, since this is when the neural tube closes. Folic acid is important!
What is the embryonic period of the fetus?
Weeks 3-8
Neural tube closes (week 4)
Organogenesis
Extremely susceptible to tertatogens during this time- kidney, bladder, brain, heart are all forming.
Week 4
4’s for week 4:
4 heart chambers (heart begins to beat)
4 limb buds begin to form
also the neural tube closes by week 4.
What is the fetal period of the fetus?
Starts in week 8, after the embryonic period is over. There is fetal mvmt, fetus looks more like a baby.
Week 10
Fetal genitalia have male/female characteristics
Alar plate and Basal plate
Alar plate = dorsal. Sensory.
Basal plate = ventral. Motor
Same as SC
What are the 3 (big categories of) things that the ectoderm gives rise to?
Surface ectoderm
Neuroectoderm
Neural crest cells
What does surface ectoderm form?
Adenohypophysis (Ant pit)- from Rathke’s pouch
Lens of eye
Epithelial linings of oral cavity
Sensory organs of ear, retina, olfactory epithelium
Epidermis
Salivary, sweat, mammary glands
Craniopharyngioma
Benign Rathke’s pouch tumor w cholesterol crystals and calcifications
What does the Rathke’s pouch give rise to?
Ant. Pit (adenohypophysis)
What does the Neuroectoderm form?
Brain, Retina, SC
(think CNS and brain)
Brain structures:
neurohypophysis (post pit), CNS neurons, oligodendrocytes, astrocytes, ependymal cells, pineal gland
What does the Neural crest form?
(think PNS and non-neural structures nearby) ANS Dorsal root ganglia Cranial nerves Celiac ganglion Melanocytes Chromaffin cells of adrenal medulla Enterochromaffin cells Parafollicular C cells of thyroid Schwann cells Pia and Arachnoid Bones of skull Odontoblasts Laryngeal cartilage Aorticopulm septum (spiral septum of heart)
Albanism can mean there was a problem of which component of ectoderm?
Neural crest cells- they are responsible for making melanocytes.
What is formed from endoderm?
Gut tube epithelium and derivatives:
lung, liver, pancreas, thymus, parathyroid, thyroid follicular cells
Mesoderm
Muscle Bone CT Serous linings of body cavities- peritoneum Spleen (from foregut mesentery) CV structures Lymphatics Blood Urogenital structures Kidneys Adrenal cortex
Embryologic derivative of the thyroid
Endoderm- thyroid develops from the tongue.
Embryologic derivative of the spleen
Mesoderm- spleen is derived from the foregut mesentery
Embryologic derivative of the adrenals
Adrenal medulla- neural crest (ectoderm)
Adrenal cortex- mesoderm
Embryologic derivative of the nucleus pulposis (of IVD)
Notochord (mesoderm)
Organ error: malformation
Intrinsic disruption
Occurs during embryonic period (3-8wks)
Organ error: deformation
Extrinsic disruption
Occurs after the embryonic period (after 8 wks)
Organ error: Agenesis
absent organ d/t absent primordial tsu
Organ error: Aplasia
absent organ even though primordial tsu was present
Organ error: Hypoplasia
Incomplete organ development
obvs primordial tsu was present
Mesodermal defects
VACTERL: Vertebral defects Anal atresia Cardiac defects Tracheo-Esophageal defects Renal defects Limb defects (bone and muscle)
When are fetuses most susceptible to teratogens
During the embryonic period (3-8 wks) when organogenesis is occuring.
Before week 3- all or none miscarriage (but no organs yet to be malformed)
After week 8- growth/devt problems (organs finished forming)
ACE inhibitors effect on fetus
Renal dmg
ACE inhibitors are for HTN, renal dz
Alcohol effect on fetus
FAS
Leading cause of birth defects and MR
Alkylating agents (chemo) effect on fetus
absence of digits
multiple anomalies
Aminglycosides effect on fetus
CN VIII toxicity- hearing problems
Diethylstilbestrol/DES effect on fetus
synthestic estrogen
Mullerian tract abnormalities- tube, uterine, cervical, vaginal abn in girls
Vaginal clear cell adenocarcinoma (rare)
this drug is not really used now
Folate antagonists (MTX-chemo)
Neural tube defects
Folic acid needed for prego
Need at least 1 mo of folic acid reserves before becoming pregnant.
Iodide (lack or excess) effect on fetus
Congential goiter
Hypothyroidism
Lithium effect on fetus
Ebstein’s anomaly of the heart (atrialized R ventricle)
Maternal diabetes effect on fetus
Cardiac malformation- txposition of the great vessels
Big baby- shoulder dystocia–> clavical fracture or Erb-Duchenne palsy
Hypoglycemia in infant
Increased C-sections
Caudal regression syndrome (anal atresia to sirenomelia)
Smoking (nicotine, CO) effect on fetus
Nicotine is a vasoconstrictor, so sml babies Preterm labor Placental abruption IUGR ADHD
Tetracycline effect on fetus
Discolored teeth
Thalidomide (sedative) effect on fetus
Limb defects- phocomelia: flipper limbs
Valproate and carbamazpine (anti seizure meds) effect on fetus
Inhibition of intestinal folate absorption, so neural tube defects
Excess Vitamin A (Retinoic Acid) effect on fetus
Affects HOX gene
extremely high risk for spontaneous abortions and birth defects (cleft palate, cardiac abnormalities)
Make sure all women taking Vit A are on birth control
Warfarin/Coumadin
Bone deformities
Also fetal hemorrhage, abortion
Use heparin or lovanox instead
Fetal Alcohol Syndrome
Leading cause of congenital malformation in USA.
Pre and post-natal devt retardation
Microcephaly
Holoprosencephaly
Facial abn (Flat nose, smooth philtrum, low set ears, epicanthal folds)
Limb dislocation
Heart and lung fistulas
Mech may incl inhibition of cell migration.
Amniocentesis
15-17 weeks for genetic eval
eval lung maturity (lecithin:spingomyelin ratio >2.5)
eval defects in mom >35
eval abn maternal serum, quad screen (nuchal screen)
eval fetal blood type/hemolysis in RH-sensitized prego
1-2% maternal hemorrhage, 1/200 fetal loss (0.5%)
Chronic villous sampling
10-12 wks- so can know earlier than amnio)
1% fetal loss
1% can’t dx NTD
get limb defects if done <9wks
Monochorionic monoamniotic twins
Share placenta and sac
Split in 8-12day range.
Know it’s mono/mono if there is cord entanglement or if one yolk sac but 2 fetal poles (v early)
Monochorionic diamniotic twins
One placenta, but 2 sacs
split after day 3 (but before day 8)
Diachorionic diamniotic twins
Two placentas, Two sacs Either monozygotic (identical twins) that split before day 3 Or dizygotic (fraternal, non-identical twins)- 2 eggs, 2 sperm
Twin-twin transfusion syndrome
Vascular channels are intertwined, results in one lg and one sml fetus
Lg one does worse due to sludging and polycythemia (increased RBCs)
When does the chorion form?
Day 3
So if split is before this, monozygotic (identical) twins will each have their own placenta (dichorionic, diamniotic)
When does the amnion form?
Day 8
If split occurs after this, monozygotic twins will be monochorionic monoamniotic.
Risk for conjoined goes up.
Fetal component of the placenta
Cytotrophoblast- inner layer of chorionic villi
Cyto makes Cells
Synctiotrophoblast- outer later of chorionic villi
Synctio Secretes hCG
Structure and fn of hCG
Structurally similar to LH, FSH, TSH
Stim’s corpus lutem to secrete progesterone during 1st trimester
Maternal component of the placenta
Decidua basalis- derived from endometrium.
Maternal blood is in lacunae
In absence of decidua basalis, have placenta acreta (goes into uterine wall)
Umbilical cord contents
2 umbilical arteries (1 artery is assocd w congenital and chromosomal abn- esp renal abn)
1 umbilical vein
Urachus
Wharton’s jelly
Where are umbilical arteries and veins derived from?
allantois
What blood is in umbilical arteries?
Deoxygenated blood.
the 2 arteries return deoxygenated blood from the fetal internal iliac arteries to the placenta
What blood is in umbilical vein?
Oxygenated blood
the 1 umbilical vein supplies oxygenated blood from the placenta to the fetus. goes into fetus through fetus’s IVC
What is the urachus? How is it formed?
Uracus is a duct bt the fetal bladder and the yolk sac.
The yolk sac forms the allantois, which extends into the fetus’s urogenital sinus.
The allantois becomes the urachus- duct bt bladder and yolk sac.
What happens if the urachus doesn’t obliterate?
- Patent urachus- urine discharge from umbilicus
2. Vesicourachal diverticulus- outpouching of the bladder
What is the vitelline duct? When is it obliterated?
aka omphalomesenteric duct
connects yolk sac to midgut lumen
Obliterated in week 7.
Vitelline fistula
Failure of vitelline duct to close –> meconium discharge from umbilicus
Ex: Meckel’s diverticulus- partial closure, w patent portion attached to ileum. Can have ectopic gastric mucosa, causing melena (tarry, black) and RUQ pain.
Trunctus arteriosis gives rise to…
Ascending aorta and pulmonary trunk
Bulbus cordis gives rise to…
RV and smooth parts (outflow tract) of LV and RV
Primitive ventricle gives rise to…
Part of the LV
Primitive atria gives rise to…
Trabeculated LA and RA
Left horn of the sinus venosus gives rise to…
Coronary sinus
Right horn of the sinus venosus gives rise to…
Smooth part of RA
R common cardinal vein and R anterior cardinal vein give rise to…
SVC
What is the truncus arteriosus (TA)?
Neural crest cells migrate and give rise to the aorticopulmonary (spiral) septum of the heart.
Crest cells divide the trunk into 2 arteries via fusion and twisting of the truncal and bulbar ridges.
This gives rise to the ascending aorta and the pulmonary trunk.
Pathology of Truncus Arteriosus
Transposition of great vessels (failure to spiral)
Tetrology of Fallot (skewed AP septum devt)
Persistent TA (partial AP septum devt)
How is the interventricular septum formed?
- Muscular septum forms, with interventricular foramen abv it
- AP septum meets and fuses with the muscular ventricular septum, closing the interventricular foramen
- Growth of endocardial cushings separates the atria from the ventricles, and contributes to both atrial separation and the membranous portion of the intervertebral septum
Pathology of the interventricular septum
Membranous septal defect (the part that joins the AP and the interventricular) causes initial Left –> Right shunting, which then becomes Right –> Left shunting. This is called the Eisenmenger Complex.
How is the interatrial septum formed?
p124
Pathology of interatrial septum formation?
Patent foramen ovale (R –> L shunt)
Cuased by excessive resorption of the septum prium and/or septum secundum
Where does fetal erythropoesis (making RBCs) occur?
Young Liver Synthesizes Blood: Yolk sac (3-8wk, embryonic period) Liver (6-30wk) Spleen (9-28wk) Bone marrow (28wk onward)- in flat bones (sternum, pelvis, ribs, cranial bones, vertebrae; in <25yo also in long bones of leg)
Fetal Hb vs Maternal Hb structure
Hb is made of 4 chains.
Fetal = alpha2 gamma2
Maternal/adult = alpha2 beta2
gamma (fetal) chains have a lower affinity for 2,3-DPG, so they have a higher affinity for O2
beta chains (adult) have a higher affinity for 2,3-DPG, so they will give up their O2 to fetal Hb
Path of fetal circ
placenta –> umb veins –> ductus venosus in liver –> IVC (so bypasses liver circulation)
IVC –> (+ a little deoxygenated blood from SVC) –> RA –> 2options: most goes through patent FO to LA, LA –> aorta –> brain, body
a little goes RA –> RV –> Pulm artery –> Ductus arteriosis (branch to descending aorta) –> body. (the blood from the SVC does this)
(the little blood that didn’t go through the PDA goes to the lungs (but no gas exchg))
from lower body, goes into internal iliac arteries –> umbilical arteries –> placenta
Why does the FO close at birth?
Infant takes a breath, diaphragm goes down, decreased resistance in pulm vasculature causes increased left atrial prs, so FO closes (now called fossa ovalis)
Why does ductus arteriosis close shortly after birth?
Increased O2 leads to decreased prostaglandins.
Prostaglandins are what keeps the PDA open- if you take them away (bc of O2), the PDA will close.
How to close/open a PDA
Indomethicin helps close PDA
If you want to keep it open, use prostaglandins.
Umbilical vein becomes…
ligamentum teres hepatis (in the falciform ligament of the liver)
UmbiLical arteries become…
mediaL umbilical ligaments
AllaNtois becomes…
urachus –> mediaN umbilical ligament
the urachus is the part of the allanotic duct bt the bladder and the umbilicus. Urachal cyst or sinus is a remnant.
Ductus arteriosus becomes…
ligamentum arteriosum
Ductus venosus becomes…
ligamentum venosum
Formen ovale becomes…
Fossa ovalis
Notochord becomes…
nucleus pulpous of the IVD
1st aortic arch becomes…
part of maxillary artery (branch of ext carotid)
1st arch is MAXimal
2nd aortic arch becomes…
Stapedial artery and hyoid artery
Second = Stapedial
3rd aortic arch becomes…
Common Carotid artery, and proximal part of the internal carotid artery
C for carotid is the 3rd letter of the alphabet (3rd arch)
4th aortic arch becomes…
left side: aortic arch
right side: proximal part of right subclavian artery
4th arch - 4 limbs - systemic
6th aortic arch becomes…
Proximal part of pulmonary arteries and (on left side only)- ductus arteriosus
6th - pulm and pulm-to-systemic shunt (DA)
List the right-to-left shunts
R-to-L are early cyanosis (blue babies) The 5 T's: Tetrology of Fallot Transposition of great vessels Truncus arteriosus Tricuspid atresia TAPVR- total anomalous pulmonary venous return
List the left-to-right shunts
L-to-R are late cyanosis (blue kids)
VSD
ASD
PDA
Tetrology of Fallot
4 things:
- Pulmonary stenosis (RV outflow obstruction- most imp factor determining pgx)
- RVH (so boot-shaped heart)
- Overriding aorta (overrides VSD)
- VSD
Early cyanosis is caused by R->L shunt across the VSD. R->L shunt exists bc of the increased prs caused by the stenotic pulmonic valve.
Pts suffer from cyanotic spells
ToF is caused by anterosuperior displacement of the infundibular septum
Why do ToF pts squat?
Compression of femoral arteries causes increased resistance (incrsd TPR) on the left side, so the R->L shunting will be decreased, and more blood from the RV will go into the lungs as it should.
Compression –> increased resistance –> increased prs
What is transposition of the great vessels?
Aorta leaves the RV (anterior)
Pulm trunk leaves the LV (posterior)
So there is separation of systemic and pulmonary circulations (there are 2 separate circular systems)
Not compatible w life unless a shunt (right-to-left) is present to allow adequate mixing of oxygenated blood (VSD, PDA, Patent FO)
D/t failure of the aorticopulmonary septum to spiral.
w/o surgical correction, die in first few months of life.
What is Truncus Ateriosus?
aka persistent TA
failure of truncus arteriosus to divide into pulm trunk and aorta
get R->L shunt
What is Tricuspid atresia?
Absence of tricuspid valve (bt RA and RV) and hypoplastic RV.
Requires both ASD and VSD for viability
Right to left shunt.
What is TAPVR?
total anomalous pulmonary venous return
pulmonary veins drain into right heart circulation (SVC, coronary sinus)
Which left-to-right shunt is most common?
VSD.
VSD > ASD > PDA
VSD
L->R shunt, late cyanosis (blue kids)
most common congenital cardiac anomaly
40% close by the first 6mo
ASD heart sounds
L–>R shunt, late cyanosis (blue kids)
loud S1
wide, fixed split S2
PDA closure
L–>R shunt, late cyanosis (blue kids)
close with indomethacin
but most close by themselves in first 24 hrs
Pulmonary problems in VSD, ASD, PDA
increased pulm resistance due to arteriolar thickening.
leads to progressive pulm HTN, R–>L shunt (Eisenmenger’s)
What is Eisenmenger’s Syndrome?
Uncorrected VSD, ASD, or PDA causes compensatory vascular hypertrophy, resulting in progressive pulm HTN
As pulm resistance increases, the L –> R shunt reverses to a R–>L shunt, which causes late cyanosis (clubbing and polycythemia)
Coarctation of the aorta
2 types:
Infantile type- aortic stenosis proximal to insertion of ductus arteriosus (preductal)
Assoc w Turner’s Syndrome XO
INfantile is IN close to the heart
Adult type- stenosis is distal to DA (post ductal). assoc w notching of ribs d/t collateral circulation, HTN in upper extremities, weak pulse/hypotension in lower extremeties
aDult: Distal to Ductus
Check femoral pulses of phys exam
Can result in aotic regurg
Most commonly assoc w bicuspid aortic valve
PDA
in fetal period, shunt is R –> L (normal)
in neonatal period, lung resistance decreases, so shunt becomes L–>R, w subsequent RVH and failure (abn).
Continuous machinery murmur
Patency maintained by PGE2 and low O2 tension.
Uncorrected PDA can result in late cyanosis in lower extremities
Indomethicin, Prostaglandins, PDA
Indomethicin- closes PDA
ENDomethicin ENDs PDA (closes it)
Prostaglandins (PGE) keep it open
PGEE KEEps it open- may be nec to sustain life in conditions like txposition of great vessels
PDA is normal in utero, closes after birth
Cardiac defect w 22q11 syndromes
e.g. Digeorge
Defect in truncus arteriosus, ToF
Cardiac defect in Down Synd
ASD, VSD, AV septal defect (endocardial cushion defect)
Cardiac defect in congenital rubella
Septal defects, PDA, pulm artery stenosis
Cardiac defect in Turner’s Syndrome
XO
coarctation of the aorta (infantile/preductal type)
Cardiac defect in Marfan’s syndrome
Aortic insufficiency (late complication), dissection of the aorta
Cardiac defect in infant of diabetic mom
Transposition of great vessels
Path of blood through PDA
PATENT DA = L –>R
Blood goes from aorta to pulmonic.
(This is backwards from DA in fetus)
What are the parts of the brain in Week 4
Prosencephalon
Mesencephalon
Rhombencephalon
What does the prosencephalon turn into in week 5?
Telencephalon and Diencephalon
What does the mesencephalon turn into in week 5?
Stays as Mesencephalon
What does the Rhombencephalon turn into in week 5?
Metencephalon and Myelencephalon
What are the adult dervatives of the telencephalon?
Walls: cerebral hemispheres (+basal ganglia, hippocampus, amygdala)
Cavities: Lateral ventricles
What are the adult derivatives of the Diencephalon?
Walls: thalami, hypothalamus, optic nerves and tracts
Cavities: 3rd ventricle
What are the adult derivatives of the mesencephalon?
Walls: Midbrain
Cavities: part of aqueduct
What are the adult derivatives of the metencephalon?
Walls: Pons and Cerebellum
Cavities: part of aqueduct (pons); part of 4th ventricle (cerebellum)
What are the adult derivatives of the myelencephalon?
Walls: medulla
Cavities: part of 4th ventricle
Folic acid vitamins
Normal multivitamin has 0.4 mg
Prenatal has 0.8-1mg
Prenatal for high risk has 4mg
Neural tube defect
Neuropores fail to fuse at 4th week, so connection bt amniotic cavity and spinal canal stays open.
Assoc w low folic acid intake
See elevated alpha-fetoprotein (AFP) in amniotic fluid and in maternal serum.
See elevated AFP and AChE in CSF (these are both made in the neural canal)
Can have spina bifida occulta
Meningocele
Myelomeningocele
These usu present in lower part of spine
Spina bifida occulta
Failure of bony spinal canal to close, but no structural herniation
Dura is intact.
Usually seen at lower vertebral levels, often have tuft of hair at the level.
Meningiocele
Bony spinal canal defect w meninges herniating through (dura not intact)
But SC itself is still in the right place and didn’t herniate through
Myelomeningocele
Defect in bony spinal canal with both meninges and SC herniating through.
What does increased maternal AFP mean?
neural tube defects
anterior abd wall defects
Anencephaly
Anterior end of neural tube is malformed
No brain/calvarium- not bc it didn’t develop, but bc the amniotic fluid is acidic (d/t urine) and eats away at it.
No swallowing center in brain–> fetus pees but doesn’t drink, so get polyhydramnios (too much amn fluid)
See elevated AFP
Holoprosencephaly
Decreased separation of hemispheres across the midline
D/t problem w Sonic Hedgehog gene
See cyclopia and cleft lip/palate
Assoc w Patau’s Trisomy 13 and severe FAS
Syringomyelia
Enlarged central canal of SC, causing nerve compression
Crossing fibers of spinothalamic tract are usu dmgd first.
Cape-like bilateral loss of P/T sensation in upper extremities (but touch sensation is okay)
Severe cases- weakness and atrophy of hand muscles
Most common at C8-T1
Often in pts w Arnold-Chiari II malformation
Arnold-Chiari Type II
Tonsil of cerebellum herniates through the foramen magnum, causing aqueductal stenosis (blockage) and hydrocephaly (water on brain)
Often presents w syringomyelia (enlgd central canal of SC) and with throacolumbar myelomeningocele (both meninges and SC herniate out of spinal canal)
Dandy-Walker
Large posterior fossa, no cerebellar vermis (absent), and cystic enlgmt of 4th ventricle
Can lead to hydrocephalus and spina bifida
Brachial clefts
On the outside.
Derived from ectoderm
aka brachial grooves
Brachial arches
On the outside.
Derived from mesoderm (muscles, arteries) and neural crests (bones, cartilage)
Brachial pouches
On the inside.
Derived from endoderm
Kangaroo pouch is on the inside.
Ecto/meso/endoderm are assoc’d w which brachial apparatuses?
CAP covers from outside to inside:
Cleft = ectoderm
Arch = mesoderm
Pouch = endoderm (INdo is INside- kangaroo)
Brachial Arch 1 innervation
CN V2 and V3
5 trigeminal
Note: all arch innervation is by nerves that are both sensory and motor only except V2, which only carries sensory info.
Arch 2 innervation
CN VII
7 facial
Arch 3 innervation
CN IX
9 glossopharyngeal
Arch 4 innervation
CN X
10 vagus
Arch 6 innervation
CN X
10 vagus
Actions of arches (and their nerves)
1- chewing (V2, V3) 2- facial expression (VII) 3- Styolpharyngeus (IX) 4- swallowing (X) 6- speaking (X)
1 man sat chewing 2 hands on his face the 3rd with his pharynx swallowed the 4th plate speak up, speak up said the 6th in return your cricothyroid makes me want to burn
Brachial arch (mesoderm) derivatives: Arch 1 Cartilage/Musc/Nerves/Arteries
Ms, Ts
Cartilage:
Meckel’s cartilage, Mandible, Malleus, incus, sphenoMandibular ligament
Muscles:
Muscles of Mastication (teMporalis, Masseter, lateral and Medial pterygoids); Mylohyoid, anterior belly of digastric, Tensor Tympani, Tensor veli palatini, anTerior Two-Thirds of Tongue
Nerves:
CN V2, V3
Arteries: Maxillary artery (branch of ext carotid)
Brachial arch (mesoderm) derivatives: Arch 2 Cartilage/Musc/Nerves/Arteries
S’s
Cartilage: Reichert's cartilage, Stapes, Styloid proceSS, LeSSer horn of hyoid Stylohyoid ligament
Musc:
muscles of facial expression, Stapedius, Stylohyoid, poSterior belly of digastric
Nerves: CN VII
Arteries
Stapedial artery, hyoid artery
Brachial arch (mesoderm) derivatives: Arch 3 Cartilage/Musc/Nerves/Arteries
3 = pharyngeal
Cartilage: greater horn of hyoid
Muscle:
Stylopharyngeus (think of stylopharyngeus innervated by glossopharygeal nerve)
Nerve: IX
Brachial arch (mesoderm) derivatives: Arch 4-6 Cartilage/Musc/Nerves/Arteries
4-6 = neck, voice box
Cartilage:
thyroid, cricoid, arytenoid, corniculate, cuneiform
Muscles:
4th arch- most pharyngeal constrictors, cricothyroid, levator palatini
6th arch- all intrinsic musc of larynx except the cricothyroid (that’s 4th)
Nerves
4th- CN X (superior laryngeal branch- swallowing)
6th- CN X (recurrent laryngeal branch- speaking)
Treacher-Collins syndrome
1st arch neural crest fails to migrate- get mandibular hypoplasia, facial abn
Congenital pharyngocutaneous fistula
Persistence of cleft and pouch, causes fistula bt tonsillar area and cleft in lateral neck (lateral cleft does NOT move when you swallow)
Arch 5
No mjr developmental contributions
Which arch forms posterior 1/3 of tongue?
Arches 3 and 4
Brachial cleft (ectoderm) derivatives: 1st cleft
External auditory meatus
Brachial cleft (ectoderm) derivatives: 2nd, 3rd, 4th clefts
Form temporary cervical sinuses, which are obliterated by proliferation of 2nd arch mesenchyme
Persistent cervical sinus
Leads to brachial cleft cyst within lateral neck
Lateral, and does NOT move with swallowing
Brachial pouch (endoderm) derivatives: 1st pouch
Middle ear cavity
Eustacian tube
Mastoid air cells
(contributes to endoderm-lined structures of the ear)
Brachial pouch (endoderm) derivatives: 2nd pouch
Epithelial lining of palatine tonsil
Brachial pouch (endoderm) derivatives: 3rd pouch
Dorsal wings develop into inferior parathyroids
Ventral wings develop into thymus
3rd pouch contributes to 3 structures: thymus, left and right inf parathyroids
3rd pouch structures end up below 4th pouch structures
Brachial pouch (endoderm) derivatives: 4th pouch
Dorsal wings develop into superior parathyroids- 4th ends up higher than 3rd
Aberrant development of 3rd and 4th pouches
DiGeorge syndrome (22q11 deletion)- leads to Tcell deficiency d/t thymic aplasia and hypocalcemia d/t no parathyroid devt.
MEN 2A
Mutation of germline RET gene (neural crest cell abn)
Affects 3 things:
Adrenal medulla (pheochromocytoma)
Parathyroid (tumor) - 3rd/4th pharyngeal pouch
Parafollicular C cells (medullary thyroid cancer)- neural crest cells
Tongue devt
1st brachial arch forms ant. 2/3 (so sensation- V3, taste- CN VII)
3rd and 4th arches form post. 1/3 (so sensation and taste- mainly CN IX, extreme posterior is CN X)
Motor innervation of all tongue is CN XII
Muscles of the tongue come from occipital myotomes
CN of the tongue
Taste: CN VII, IX, X (solitary)
Pain(sensation): CN V3, IX, X
Motor: CM XII
Taste: ant 2/3 by CN 7, post 1/3 by 9/10
Pain: ant 2/3 by V3, post 1/3 by 9/10
Motor: all by 12
Ear devt: 1st arch
1st arch - M’s and T’s
Malleus/incus bones
Tensor Tympani (V3)
Ear devt: 2nd arch
2nd arch - S’s
Stapes bone
Stapedius (VII)
Ear devt: 1st cleft
External auditory meatus
Ear devt: 1st brachial membrane
Tympanic mbr
Ear devt: 1st pouch
Eustacian tube, middle ear cavity, mastoid air cells
Brachial cleft cyst vs Thyroglossal duct cyst
Brachial cleft cyst - lateral, does NOT mv w swallowing
Thyroglossal duct cyst - midline, DOES mv w swallowing
Thyroid devt
Thyroid diverticulum comes from floor of primitive pharynx, descends into neck.
Connected to tongue by thyroglossal duct- normally disappears, but can persist as benign pyramidal lobe of thyroid.
Foramen cecum is normal remnant of thyroglossal duct.
Most common ectopic thyroid tsu site is tongue
Thyroglossal duct cyst
In midline neck, DOES mv w swallowing.
Benign, but usu remove d/t high infection rate
Cleft lip
failure of fusion of maxillary and medial nasal processes (formation of primary palate)
Cosmetic, doesn’t affect fn
Cleft palate
failure of fusion of lateral palatine processes, nasal septum, and/or the median palatine process (formation of secondary palate)
cleft palate interferes w fn- can’t suckle
Cause of cleft lip, cleft palate
Many things!
Can be folic acid def, genetic, teratogens, any combo of these or other things.
Diaphragm is derived from…
SPBD (several parts build diaphragm): Septum transversum --> central tendon Pleuroperitoneal folds Body wall Dorsal mesentery of esophagus --> crura
Innervation of diaphragm
C3,4,5
Diaphragm descends during devt but keeps innervation from above
Diaphragmatic hernia
Abd contents can herniate into thorax bc of incomplete diaphragm devt and lead to hypoplasia of thoracic organs (eg no lungs), space compression (eg compressed heart), scaphoid abd, and cyanosis.
