GIT Embryology(1)

8/20/2019 GIT Embryology(1)

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1.

The primordial gut at the beginning of the 4th week is closeda. At the cranial end by the oropharyngeal membrane

b.

At the caudal end by the cloacal membrane

2.

The embryonic layers of the primordial gut give rise toa. Epithelia and glands – endoderm

b. Stroma – LP splanchnic mesoderm

3.

The epithelium within the stomodeum (cranial to the oropharyngealmembrane) and epithelium of the proctodeum (caudal to the cloacal

membrane) is derived from surface ectoderm

4. The primordial gut is divided into three regions:a. Foregut – vascularized by celiac trunk

b.

Midgut – vascularized by superior mesenteric arteryc. Hindgut – vascularized by inferior mesenteric artery

Gastrointestinal System: Embryology


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4a. Foregut –1. derivatives are:

a. Primordial pharynx1.

Oral cavity

2.

Teeth3. Pharynx

4. Tongue

5.

Tonsils

6.

Salivary glands (submaxillary, submandibular, sublingual)b. Upper respiratory system (nasal cavities, nasopharynx)

c. Lower respiratory system (larynx, trachea, bronchi, lungs)d. Esophagus

e. Stomachf.

Duodenum

g.

Liverh. Extrahepatic biliary system (including gallbladder)i. Pancreas

All foregut derivatives except pharynx, respiratory system, and most of

esophagus, are supplied by the celiac trunk, the artery of the foregut.

Gastrointestinal System: Embryology


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Oral Cavity

Development of Oral Cavity


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The pharyngeal apparatus consists of:

1. Pharyngeal arches

2. Pharyngeal membranes

3. Pharyngeal pouches

4. Pharyngeal grooves

These embryonic structures contribute to

formation of the head and neck.

4

3


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Fate of Pharyngeal Arches

Contribute extensively to the formation of the face, nasal cavities, mouth, larynx,pharynx, and neck.

A typical pharyngeal arch contains:

1. An aortic arch – an artery that arises from the truncus ateriosus of theprimordial heart.

2. A cartilaginous rod – that forms the skeleton of the arch

3. A muscular component – that differentiates into the muscles in the headand neck

4. A nerve – that supplies the mucosa (epithelial lining) and muscles derivedfrom the arch


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First Arch – Mandibular Arch

1.

First aortic arch – maxillary artery.

2.

Skeletal structures –a. Maxillary prominence – gives rise to the maxilla (upper jaw), zygomatic

bone, and squamous part of temporal bone

b. Mandibular prominence – forms the mandible (lower jaw)

c. Malleus

d. Incus

e. Anterior ligament of malleusf.

Sphenomandibular ligament

3. Muscles – muscles of mastication: temporalis, masseter, medial and later

pterygoids; mylohyoid; anterior belly of digastric muscle

4. Nerve – trigeminal nerve (CN V)

The first pair of pharyngeal arches plays a major role in facial development.


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Second Arch – Hyoid Arch

1.

Second aortic arch – stapedial artery.

2.

Skeletal structuresa. Stapes

b. Styloid process

c. Lesser cornu (horn) of hyoid bone

d.

Superior part of body of hyoid bonee. Stylohyoid ligament

3.

Muscles – muscles of facial expression: buccinator, auricularis, frontalis,

platysma, orbiculais oris, obicularis occuli; stapedius, stylohyoid,posterior belly of digastric

4.

Nerve – facial nerve (CN VII)


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Third Arch

1.

Third aortic arch – common carotid artery.

2.

Skeletal structures –a. Greater cornu (horn) of hyoid

b. Inferior body of hyoid bone

3.

Muscles – stylopharyngeus

4. Nerve – glossopharyngeal nerve (CN IX)


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Fourth & Sixth Arches

1.

A. Fourth Aortic Arch

1. Left 4th – arch of the aorta2. Right 4th – proximal portion of right subclavian artery

1. B. Sixth Aortic Arch

• Left 6th distal – ductus arteriorsus•

Left 6th proximal – left pulmonary artery

•

Right 6th distal – degenerates

• Right 6th proximal – right pulmonary artery

2.

Skeletal structuresa. Thyroid cartilage

b. Cricoid cartilage

c. Triticeal cartilages (paired)d. Arytenoid cartilages (paired)

e. Corniculate cartilages (paired)f.

Cuneiform cartilages (paired)


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Fourth & Sixth Arch

3.

Muscles –

a. Cricothyroidb. Levator veli palatini

c. Constrictors of pharynx (superior, middle, inferior)

d. Intrinsic muscles of larynx (oblique arytenoid, transverse arytenoid, posterior arytenoid, latreal arytenoid, thyroarytenoid )

e. Striated muscle of esophagus

4.

Nerves

a. Superior laryngeal branch of vagus (CN X) (a & b, above)b. Recurrent laryngeal branch of vagus nerve (CN X) (c - e, above)


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Development of the Face

1. Five facial primordia appear early in the fourth week

a.

Around the large primordial stomodeum1. A single frontonasal prominence (1)2. Paired maxillary prominences (2)

3. Paired mandibular prominences (2)

PrimordialStomodeum

FrontonasalProminence

MandibularProminence

MaxillaryProminence


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1. Five facial primordia appear early in the fourth week

a. Five facial primordia are derivatives of the first pharyngeal arch

b.

Form cartilage, bone, and ligaments in facial and oral regions

1. Are derived from cranial ectomesenchyme:a. Maxillary prominence – gives rise to the maxilla (upper jaw),

b.

Zygomatic bone,

c.

Squamous part of temporal bone

d.

Mandibular prominence – forms the mandible (lower jaw)e. Malleusf.

Incus

g. Anterior ligament of malleus

h. Sphenomandibular ligament

c.

Form the craniofacial voluntary muscles1. Are derived from paraxial and prechordal mesoderm:

a. temporalis, masseter, medial and later pterygoids; mylohyoid;anterior belly of digastric muscle


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10. Each lateral nasal prominence is separated from the maxillary prominence by a

cleft, called the nasolacrimal groove.

Naso-lacrimal

groove

LateralNasal

Prominence

Maxillary Prominence


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12. By the end of the sixth week, each maxillary prominence has begun to merge

with the lateral prominence along the line of the nasolacrimal groove.

a. Establishes continuity between the side of the nose (formed by the lateral

nasal prominence) and the cheek region (formed by the maxillary

prominence)


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11. By the end of the 5th week, the primordia of the auricles of the ears havebegun to develop.

a.

Six auricular hillocks (ectomesenchymal swellings) form around:

1. The 1st pharyngeal groove (three on each side)a.

The primordia of the auricle

b. The external auditory meatus (canal).

Auricular hillocks

External Auditory

Meatus


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14. Between the 7th and 10th weeks the medial nasal prominences merge with eachother. Similarly, the maxillary prominences and lateral nasal prominences merge

with each other.


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15. Merging of medial nasal prominence and maxillary prominence results ina. Continuity of the upper jaw

b.

Continuity of the upper lip

c. Separation of nasal pits from mouth


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16. As medial nasal prominences merge they form an intermaxillary segment

E

F

Intermaxillary segment


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17. Intermaxillary segment forms

a.

Philtrum (middle part) of upper lipb. Premaxillary part of the maxilla and associated gingiva (gum)c. The primary palate

Primary palate

Philtrum of lip

Premaxillarypart of maxilla

& associatedgingiva


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Development of Palate

Palate


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Development of the Palate

2. Palatogenesis

a.

Begins at the end of the 5th weekb. Ends at the 12th week

c. Critical period for malformations is 6th to 9th week

Primary palate

Developing maxilla

Primordium ofpremaxillary part

of maxilla


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Development of the Palate – Primary Palate

3. Early in 6th week the primary palate – median palatine process – begins todevelop from deep part of intermaxillary segment of the maxilla

a. Initially formed by merging of medial nasal prominences

Medial nasal prominencesmerging with each other


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b. A wedge-shaped mass of ectomesenchyme between internal surfaces of

maxillary prominences of developing maxilla

Intermaxillary segment of maxilla

Developing maxilla


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c. Primary palate forms premaxillary part of maxilla

1.

Represents small part of adult hard palate

2. Located anterior to incisive foramen

Developingmaxilla

Primordium ofpremaxillary part

of maxilla


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Incisive foramen

c. Primary palateforms premaxillary

part of maxilla

1. Represents smallpart of adult hard

palate

2. Located anterior

to incisive foramen

Premaxillary partof maxilla


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Development of the Palate – Secondary Palate

4. The secondary palate is the primordium of the hard and soft parts of the

palate

Hardpalate

Softpalate

Secondary palate


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4. The secondary palate is the primordium of the hard and soft parts of thepalate

a. Begin developing early in 6th week

b. Forms from two ectomesenchymal projections – lateral palatine

processes (palatal shelves)

Medianpalatine

process

Lateral palatine processes

Median palatine process


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The secondary palateb. Lateral palatine processes (palatal shelves)

1. Extend from internal aspects of maxillary prominences

2. Initially project inferomedially on each side of tongue3. During 7th to 8th week, processes elongate and ascend to

horizontal position superior to tongue

Nasalseptum

Maxillary

prominence

Lateralpalatine

process

Nasalseptum

Median palatine process

Lateral palatine process


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4. The secondary palateb. Lateral palatine processes (palatal shelves)

4. Gradually processes approach each other and

a. fuse with posterior part of primary palateb.

fuse in the median plane

c.

fuse with median nasal septum

Primary palate

Posterior part ofprimary palate


Medial nasal septum


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a.

fuse with posterior part of primary palateb. fuse in the median plane

c.


Primary palate

Lateral palatine processFuse in the

median plane

Median nasal septum


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a.

fuse with posterior part of primary palateb. fuse in the median plane

c.


Primary palate


Fuse in the

median plane

Median nasal septum


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a.

fuse with posterior part of primary palateb.

fuse in the median plane

c. fuse with median nasal septum

Nasal septum


Fuse in the median plane with median nasal septum


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5. The nasal septum develops as a down growth from internal parts of mergedmedial nasal prominences

a. Fusion between nasal septum & lateral palatine processes progresses in

an anterior to posterior direction from the 9th week to the 12th week

Nasal septum


Fusion in the median plane with median nasal septum


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5. Bone gradually develops in primary palate

a.

Forms premaxillary part of maxillab. Lodges the incisor teeth

Premaxillarypart of maxilla

Incisor tooth


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6. Concurrently, bone extends from maxilla and palatine bones into lateral

palatine process to form the hard palate

Premaxillary part of maxillaIncisor teeth

Incisive foramen

Suture betweenpremaxillary part of

maxilla and lateralpalatine process of

maxilla

Lateral palatineprocess of

maxilla

Horizontal plateof palatine bone


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7. The posterior parts of processes do not ossifya. They extend posteriorly beyond the nasal septum

b.

Fuse to form the soft palate, including uvulac.

The median palatine raphe indicates line of fusion of lateral palatineprocesses

Median palatine raphe

Soft palate

Uvula

Gum

Upper lip

Incisive papillae (deep = i. foramen)Frenulum of lip

Hard palate


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8. A small nasopalatine canal persists in median planea. Occurs between premaxillary part of maxilla and palatine processes of

maxilla

b. Represented in adult by incisive foramen (Fig. 10-36)

Premaxillary part of maxillaIncisor teeth

Incisive foramen

Suture betweenpremaxillary part of

maxilla and lateralpalatine process of

maxilla

Lateral palatineprocess of

maxilla

Horizontal plateof palatine bone


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Development of Teeth



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Teeth


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Mesenchyme

Ectoderm

Neural Crest

Cementocytes

Odontoblasts

Ameloblasts

Enamel

•

Moves down

•

No longer produced

after adulthood

Cementum

•

Covers root

Predentin

•

Type I

collagen

Dentin

•

Moves outward

•

Type I collagen

•

Hydroxyapatite

•

Fluoroapatite

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Bud of Permanent Tooth• Develops from dental lamina

•

Remains dormant

Enamel Knot• Signals tooth development

Outer Dental Epithelium•

Neural crest

Inner Dental Epithelium• Neuroectoderm

NC neuro-ectodermal

cells lining

the epithelialtooth bud (cap)

Secrete:• FGF-4

•

BMP-2,4,7

Regulate tooth shape

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Primitive Dental

Papilla

Preodontoblasts•

Odontoblasts

•

Secrete non-mineralized predentin which later calcifiesinto dentin

Preameoloblasts• Ameoloblasts

•

Secrete enamel downward

Inner Dental EpitheliumLayer of the enamel knot

Outermost Cells (apical)of the dental papilla

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Bloodvessel in

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Enamel

Dentin

Odontoblasts

Cementoblasts• Secretes a layer of cementum to cover

root(s) of tooth

Periodontal Ligament

•

Holds tooth to alveolus

Dental Sac gives rise to:•

Cementoblasts

• Periodontal ligament

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Sections of Teeth: A) An incisor tooth B) A molar toothIn living people, the pulp cavity is a hollow space within the crown & neck containing

connective tissue, blood vessels, & nerves. The cavity narrows down to the root canalin a single-rooted tooth or to one canal per root of a multirooted tooth. The vessels &

nerves enter or leave through the apical foramen.


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Development of the Tongue

Development of Tongue


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Development of Tongue

Tongue


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1. Tuberculum Impar (median tongue bud) appears near end of 4th

week

2. It is a median triangular elevation in the floor of the primordial pharynx

3.

It is the first indication of tongue development

4.

Soon, two distal tongue buds (lateral lingual swellings) develop on eitherside of the median tongue bud

5. The three lingual buds develop from proliferation of the prechordal

mesoderm in the first pair of pharyngeal arches

6.

The distal tongue buds rapidly increase in size and fuse (median sulcus ofthe tongue) to form the anterior 2/3 s of the tongue


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7.

The posterior 1/3 of the tongue (pharyngeal part) develops from twoelevations that develop caudal to the foramen cecum

a.

The copula forms by fusion of the ventromedial parts of the second pair

of pharyngeal arches

b.

The hypopharyngeal eminence develops caudal to the copula fromprechordal mesoderm of the third and fourth pharyngeal arches

8. As the tongue develops the copula is gradually overgrown by the

hypopharyngeal eminence and disappears

9. The posterior 1/3 of the tongue develops from the rostral part of thehypopharyngeal eminence

10. The terminal sulcus is the line of fusion between the anterior 2/3 andposterior 1/3 of the tongue



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11. Cranial ectomesenchyme forms the connective tissue and vasculature ofthe tongue

12. Most tongue muscles are derived from myoblasts that migrate from

occipital myotomes

13. The hypoglossal nerve (CN XII) accompanies the myoblasts during their

migration and innervate the tongue muscles as they develop, except for the

palatoglossus muscle which is innervated by the vagus nerve (CN X)

14. The sensory supply to the anterior 2/3 of the tongue is from the lingualbranch of the mandibular division of the trigeminal nerve (CN V), the

nerve of the first pharyngeal arch

15.

The facial nerve supplies the taste buds in the anterior 2/3 of the tongue,except for the circumvallate papillae

16. The circumvallate papillae are innervated by the glossopharyngeal nerve

(CN IX)



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17. Clinical Correlates

a. Anomalies of the tongue are uncommon, except for1. Fissuring of the tongue – infants with Down syndrome

2. Hypertrophy of the lingual papillae – infants with Down syndrome

b. Congenital Lingual Cysts and Fistulas

1. Cysts may be derived from remnants of thyroglossal duct

2.

May emerge to produce symptoms of discomfort and/or dysphagia(difficulty swallowing)

3. Fissures are also derived from persistance of lingual parts ofthyroglossal duct

a.

Open through foramen cecum into oral cavity

Mouth: Embryology



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c. Ankyloglossia (tongue-tied)1. The lingual frenulum normally connects the inferior surface of the

tongue to the floor of the mouth

2. Sometimes the frenulum is short and entends to the tip of the

tongue

a.

Interferes with free protrusion of the tongueb.

May make breast feeding difficult

3.

Occurs in about 1:300 live births in North American infants

Mouth: Embryology



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d.

Macroglossia1. An excessively large tongue

2.

Results from generalized hypertrophy of the tongue

3. Usually results from lymphangioma (a lymph tumor)

4.

May result from muscular hypertrophy

Mouth: Embryology



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e. Microglossia1. An abnormally small tongue

2.

Usually associated with micrognathia (underdeveloped mandibleand recession of the chin)

3.

May be associated with certain limb defects, Hanhart syndrome

Mouth: Embryology



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f.

Glossoschisis (bifid or cleft tongue)1. Very uncommon anomaly

2.

Results from incomplete fusion of the distal tongue buds

3. Exhibits as a deep median groove in the tongue

4.

Usually a cleft tongue does not extend to tip of tongue


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Salivary Glands

Salivary Glands: Embryology


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1.

Salivary glands begin developing during the 6th and 8th weeks

2.

They begin as solid epithelial buds from primordial oral cavity

3. The club-shaped ends of the buds grow into the underlying cranialectomesenchyme

4.

The connective tissue stroma of the glands is derived from cranialectomesenchyme (neural crest)

5.

All parenchyma arises by proliferation of oral epitheliuma. Surface ectoderm – parotid

b. Endoderm – submandibular (submaxillary) gland and sublingual

gland



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6. Parotid glands

a. Are the first to appear – early in the 6th week

b.

They develop from buds of oral ectoderm near the angles of thestomodeum

c.

The buds grow towards the ears and branch to form solid cords withrounded ends

d.

Later the cords canalize – develop lumina – and become ducts by 10weeks

e.

The rounded ends develop into acini

f.

Secretion begins at 18 weeks

g.

The capsule and connective tissue develops from cranialectomesenchyme (neural crest)



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7. Submandibular (Submaxillary) glands

a. Appear late in the 6th week

b.

Develop from endodermal buds in floor of stomodeum

c. Solid cellular processes grow posteriorly, lateral to developing tongue

1.

Later they branch and differentiate

d.

Acini begin to form at 12 weeks

e. Secretory activity begins at 16 weeks

f.

Growth of glands continues after birth with formation of mucus acini

g.

Lateral to tongue, a linear groove forms that soon closes to formsumandibular duct


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Development of Larynx


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Larynx


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1. The epithelium of larynx develops from the endoderm of the cranial end ofthe laryngotracheal tube.

2. The cartilages of the larynx develop from the cartilages in the 4th and 6th pharyngeal arches.

3.

The cartilages are derived from neural crest cells (cranial ectomesenchyme).


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4. The ectomesenchyme are the cranial end of the laryngotracheal tubeproliferates rapidly and produces the paired arytenoid swellings.

a.

Swellings grow towards tongue, converting the slit-like opening – theprimordial glottis – into a T-shaped laryngeal inlet.

b.

Reduces the developing laryngeal lumen to a narrow slit.

Epiglottic swelling

Arytenoid swellings

Primitiveglottis


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4. The ectomesenchyme are the cranial end of the laryngotracheal tubeproliferates rapidly and produces the paired arytenoid swellings.

a.

Swellings grow towards tongue, converting the slit-like opening – theprimordial glottis – into a T-shaped laryngeal inlet.

b.

Reduces the developing laryngeal lumen to a narrow slit.

Epiglottis

Arytenoid swellings

Laryngealinlet

Cuneiformtubercle


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5. The laryngeal epithelium proliferates rapidly, resulting in a temporaryocclusion of the laryngeal lumen.

6. Recanalization of the larynx usually occurs by the 10th week.

EndodermEsophagus

Laryngo-tracheal

tubeLP Splanchnicmesoderm LP Splanchnic

mesodermDevelopingcartilages

Epithelium


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7. The laryngeal ventricles form during the recanalization process.

8. The recesses are bounded by folds of mucous membrane that become thea. The vestibular folds (cat purring).

b. The vocal folds (human phonation)


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9. The epiglottis develops from the caudal part of the hypopharyngealeminence.

a.

A prominence produced by the ventral ends of the 3rd and 4th pharyngealarches.

b.

The rostral part of the eminence forms the posterior third of the

pharyngeal part of the tongue.

Hypopharyngeal Eminence


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10. The laryngeal muscles develop from myoblasts of the 4th and 6th pharyngeal arches and therefore innervated by branches of the vagus (CN

X) nerve.

11. Growth of larynx and epiglottis is rapid during first three years after birth. By

this time the epiglottis has reached its adult form.


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Esophagus

Development of Esophagus


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Esophagus


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EndodermEsophagusLaryngo-tracheal

tube

LP Splanchnic

mesoderm

LP Splanchnic

mesoderm

Developing

cartilages

Epithelium

4a. Foregut –1d. Esophagus

1.

Developmenta.

Develops from foregut immediately caudal to pharynx

b. The esophagus is partitioned from the trachea by the

tracheoesophageal septum

c.

Initially, the esophagus is short, but it elongates rapidly

Esophagus: Embryology


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1. Development

d.

It reaches its final length by the 7th week

e. The epithelium and glands are derived from endoderm

1. The epithelium proliferates and completely obliterates the

lumen; recanalization of the esophagus occurs by the end ofthe 8th week (programmed apoptosis)

f.

The skeletal muscle in the upper 2/3 of the esophagus (overlap inthe middle 1/3 with smooth muscle) is derived from prechordal

mesoderm of the pharyngeal arches

g.

The smooth muscle in the lower 2/3 of the esophagus (overlap in

the middle 1/3 with skeletal muscle) is derived from LP splanchnicmesoderm

h. Both types of muscle are innervated by branches of the vagus

nerve (CN X)



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2. Clinical correlates

a. Esophageal atresia1.

Blockage of the esophagus occurs with an incidence of1:3000 to 1:4500 live births

2. About 1/3 of affected infants are born prematurely

3.

Associated with tracheoesophageal fistula in more than 85%of cases

Esophagus: Embryology4a. Foregut –


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g1d. Esophagus

2. Clinical correlatesb. Tracheoesophageal Fistula (TEF)

1.

A fistula (abnormal passage) between trachea andesophagus.

2. Results from incomplete division of cranial part of foregutinto respiratory and esophageal parts during 4th week.

3.

Incomplete fusion of tracheoesophageal folds results in adefective tracheoesophageal septum, resulting in a

tracheoesophageal fistula.

4. Most common anomaly of lower respiratory tract

5.

Occurs in 1/3000 – 4500 births

6. Males most affected

7.

In more than 85% cases the fistula is associated withesophageal atresia


b T h h l Fi l (TEF)


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b. Tracheoesophageal Fistula (TEF)

8. Four main varieties of tracheoesophageal fistula.a. Superior part of esophagus ends blindly (esophageal atresia), the

inferior part of esophagus joins trachea near its bifurcation (gastriccontents may enter trachea and lungs)

b.

Fistula between patent esophagus and trachea (esophageal

contents and gastric contents may enter trachea and lungs)c. Fistula between superior part of esophagus and trachea, inferior

part of esophagus ends blindly (esophageal contents enter thetrachea and lungs).

d. Fistula between superior part of esophagus and trachea, fistula

between inferior part of esophagus and trachea near itsbifurcation (esophageal and gastric contents may enter trachea and

lungs)

Polyhydramnios – is often associated with esophageal atresia and

tracheoesophageal fistula. The excess amniotic fluid cannot pass to thestomach and intestines for absorption and subsequent transfer through

the placenta to the mother s blood for disposal.

Varieties of Tracheoesophageal Fistulas


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1. Superior part of esophagus ends blindly (esophagealatresia)

•

Inferior part of esophagus joins trachea near itsbifurcation (gastric contents may enter trachea and

lungs – aspiration)

Esophagus



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2. Fistula between superior part of esophagus andtrachea, inferior part of esophagus ends blindly

(esophageal contents enter the trachea and lungs).



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3. Fistula between patent esophagus and trachea (esophageal contents and gastric contents may enter

trachea and lungs)

Esophagus



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4. Fistula between superior part of esophagus andtrachea, fistula between inferior part of esophagus and

trachea near its bifurcation (esophageal and gastriccontents may enter trachea and lungs)

4a. Foregut –


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4a. Foregut 1d. Esophagus

2. Clinical correlatesc. Esophageal stenosis

1.

Narrowing of the lumen

2. Usually occurs in distal 1/3

3.

Occurs as web or long segment with threadlike opening

4.

Results from incomplete canalization during 8th week

5. May also result from failure of esophageal blood vessels todevelop in affected area – atrophy of segment occurs

4a. Foregut –


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a o egut1d. Esophagus

2. Clinical correlatesd. Short esophagus

1.

Normally esophagus is very short

2. Esophagus fails to elongate as neck and thorax develop

3.

Part of stomach may be displaced superiorly through

esophageal hiatus into thorax

4.

Congenital hiatal hernia

5. Most hiatal hernias occur after birth\

6.

Usually in middle-aged people

7. Result from weakening and widening of esophageal hiatus indiaphragm

4 a Foregut


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4.

a. Foregut1d. Esophagus

2. Clinical Correlatese. Laryngotracheoesophageal Cleft

1.

Uncommon

2.

The larynx and trachea fail to separate completely from the

esophagus

3.

Symptoms similar to tracheoesophageal fistula, EXCEPTaphonia (absence of voice) is a distinguishing feature


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Stomach

Stomach: Embryology4a Foregut


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4a. Foregut1e. Stomach

1. The distal part of foregut is initially a tubular structure

2.

~ middle of 4th week, a slight dilation indicates site of stomachprimordium

3.

First appears as fusiform enlargement of caudal part of foregut andoriented in median plane

4.

Primordium soon enlarges and broadens ventrodorsally

5. During next two weeks the dorsal border of stomach grows faster thanthe ventral border and demarcates

a. the greater curvature of stomach – dorsal border

b.

The lesser curvature of stomach – ventral border



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6. Rotation of the stomach:a.

as the stomach enlarges it acquires its adult shape,

b.

It slowly rotates 90 degrees in a clockwise direction around itslongitudinal axis

1.

The ventral border (lesser curvature) moves to the right

2. The dorsal border (greater curvature) moves to the left

3.

The original left side becomes the ventral surface

4. The original right side becomes the dorsal surface



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6. Rotation of the stomach:a.

as the stomach enlarges it acquires its adult shape,

b.

It slowly rotates 90 degrees in a clockwise direction around itslongitudinal axis

5.

Before rotation, the cranial and caudal ends are in the median

plane

6.

During rotation and growth, its cranial end moves to the left andslightly inferiorly

7. Its caudal end moves to the right and superiorly

8. After rotation, the stomach assumes its final position – its long

axis is almost transverse to the long axis of the body

9.

Explains why left vagus supplies anterior (ventral) wall and rightvagus supplies posterior (dorsal) wall of adult stomach



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7. Mesenteriesa.

Stomach is suspended from dorsal wall by a dorsal mesentery =

dorsal mesogastrium1. Originally in median plane but carried to left during rotation and

formation of omental bursa (lesser sac of peritoneum)

b.

Stomach is suspended from ventral wall by a ventral mesentery =ventral mesogastrium

1.

Attaches stomach to liver (hepatogastric ligament) andduodenum to liver (hepatoduodenual ligament)2. Forms anterior wall of lesser sac

3. Opening into sac is epiploic foramen of Winslow



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7. Mesenteriesc.

Omental bursa

1.

Isolated clefts (cavities) develop in the LP splanchnicmesoderm forming the dorsal mesentery

2.

The clefts soon coalesce to form a single cavity, the omentalbursa or lesser peritoneal sac

3.

As the stomach enlarges, the omental bursa expands andacquires an inferior recess of the omental bursa between

layers of the dorsal mesentery – the greater omentum

4. This membranes over hangs the developing intestines.

5.

The inferior recess disappears as the layers of the greater

omentum fuse

6. The omental bursa communicates with the peritoneal cavity

through the omental (epiploic) foramen of Winslow



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8. Clinical correlatesa. Congenital hypertrophic pyloric stenosis

1.

Anomalies of stomach are uncommon except for this disorder

2.

Affects 1:150 males and 1:750 females

3. Marked thickening of the pyloric sphincter

4.

The circular, and to a lesser extent, the longitudinal muscle aremarkedly hypertrophied – LP splanchnic mesoderm

5.

Results in severe stenosis of the pyloric canal and obstruction

to the passage of food

6.

As a result, the stomach becomes markedly distended

7. The infant expels the stomachs contents with considerable

force = projectile vomiting


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Liver

Liver: Embryology1 The liver gallbladder and biliary duct system arise


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1. The liver, gallbladder, and biliary duct system arise

a. Early in the 4th week

b. As a ventral outgrowth from the caudal part of the foregut1. Hepatic diverticulum

c. Develops from embryonic endoderm

d.

Hepatic diverticulum1. Extends into septum transversum

a.

A mass of LP splanchnic mesoderm

b.

Between developing heart and midgutc. Forms ventral mesentery



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1. The liver, gallbladder, and biliary duct system arised.

Hepatic diverticulum

2.

Rapidly divides into two parts as it grows between layers of ventral

mesentery

a.

Cranial portion

1. Is larger

2. Forms primordium of liver

3.

Proliferating endodermal cells give rise toa. Interlacing cords of hepatic cellsb.

Epithelial lining of intraheptic part of biliary apparatus

4. Hepatic cords

a. Anastomose around endothelial-lined spaces – primordia of

hepatic sinusoidsb. Stroma, hematopoietic tissue, and Kupffer cells are derived

from LP splanchnic mesoderm of septum transversum



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2.a. Cranial portion

4. Liver grows rapidlya. From 5th to 10th weeks fills a large part of the upper abdominalcavity

b. The quantity of oxygenated blood from the umbilical vein into the

liver determines the development and functional segmentationc.

Initially, right and left lobes are about the same

d.

Soon, right lobe becomes largere. Hematopoiesis begins during the 6th weekf. By 9th week liver accounts for ~ 10% of total weight of fetus

g.

Bile formation by the hepatic cells begins during the 12th week

3. Bile entering the duodenum through the bile duct after the 13th week gives

meconium (intestinal contents) a dark green color

4. The left umbilical vein passes in the free border of the falciform ligamenton its way from the umbilical cord to the liver (becomes ligamentum teres

hepatis in the adult)

Liver: Embryology2 Clinical Correlates


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2. Clinical Correlatesa.

Anomalies of the liver

1. Minor variations of liver lobulation are common

2. Congenital anomalies of the liver are rare3. Variations of the hepatic ducts, bile duct, and cystic ducta.

Are common

b. Clinically significant

c. Accessory hepatic ducts may be present1.

Are narrow channels running from right lobe of liver to

anterior surface of body of gallbladder2. Cystic duct may open into accessory hepatic duct rather than

into common bile duct


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Development of the Gall Bladder

Gallbladder: Embryology

1 The liver gallbladder and biliary duct system arise


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2.

Rapidly divides into two parts as it grows between layers of ventral

mesenteryb. Caudal portion1. Becomes the gallbladder

2. The stalk of the hepatic diverticulum becomes the cystic duct

3. The extrahepatic biliary apparatusa.

Initially, is occluded with epithelial cells

b.

Is later canalized due to programmed apoptosis4. The stalk connecting the hepatic and cystic ducts to the

duodenum becomes the bile duct

3. Bile entering the duodenum through the bile duct after the 13th week gives

meconium (intestinal contents) a dark green color

Gallbladder: Embryology

2 Clinical Correlates


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2. Clinical Correlatesa. Extrahepatic biliary atresia

1. Most serious anomaly of extrahepatic biliary system

2.

Occurs in 1:10,000 to 1:15,000 live births

3. Most common forma.

~ 85% cases

b.

Obstruction of ducts at or superior to porta hepatis (gatewayto the liver)1.

Deep transverse fissure on the visceral surface of the liver

c. Caused by failure of ducts to canalized. Could also result from liver infection during late fetal period

4. Jaundice occurs soon after birtha. If not corrected surgically, child may die if a liver transplant is not

performed


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ExocrinePancreas

Pancreas: Embryology


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1. Pancreas develops between layers of the mesentery froma. dorsal pancreatic bud of endodermal cells

b.

ventral pancreatic bud of endodermal cells

c.

Arises from caudal part of foregutb. Most of pancreas is derived from dorsal pancreatic bud

2.

The larger dorsal pancreatic bud appears first and develops a slight

distance cranial to the ventral buda.

It grows rapidly between layers of the dorsal mesentery

3. The ventral pancreatic bud develops near the entry of the bile duct into theduodenum

a.

It grows between layers of the ventral mesenteryb. As the duodenum rotates to the right and becomes C-shaped the

ventral pancreatic bud is carried dorsally with the bile duct.

1.

It soon lies posterior to the dorsal pancreatic bud and fuses with itc. Forms the uncinate process and part of the head of the pancreas



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4. As the stomach, duodenum and ventral mesentery rotate, the pancreascomes to lie on the dorsal abdominal wall.

5.

As the pancreatic buds fuse, their ducts anastomose.a. The main pancreatic duct forms from

1.

The duct of the ventral bud

2.

The distal part of the duct of the dorsal bud

b.

The accessory pancreatic duct, if present,

1.

Forms from the proximal part of the duct of the dorsal bud

2. Opens into the minor duodenal papillaa. Located about 2 cm cranial to the main duct

c. The main pancreatic duct and the accessory pancreatic duct often

communicated with each other

d.

In about 10% of the people the pancreatic ducts fail to fuse


6.

Histogenesis:


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a. The parenchyma of the pancreas is derived from endoderm of the

pancreatic buds

1.

Form a network of tubules

2.

Early in the fetal period (9 weeks), acini begin to develop from cell

clusters around the ends of these tubules (primordial ducts)

b. The stroma of the pancreas develops from LP splanchnic mesoderm


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Development of the Duodenum

Duodenum: Embryology

1 Early in 4th week the duodenum begins to develop from the caudal part of the


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1. Early in 4th week the duodenum begins to develop from the caudal part of theforegut and the cranial part of the midgut

2.

The parenchyma develops from endoderm and the stroma develops from LPsplanchnic mesoderm

3. The junction of the two parts of the duodenum is just distal to the origin of the

bile duct

4.

The developing duodenum grows rapidly, forming a C-shaped loop thatprojects ventrally

5. As the stomach rotates, the duodenal loop rotates to the right and comes to lieretroperitoneally

6.

Because of its dual origin (foregut and midgut), it is vascularized by both theceliac trunk (foregut) and superior mesenteric artery (midgut)

7. During 5th and 6th weeks the lumen is obliterated due to epithelial proliferation

8. It recanalizes (programmed apoptosis) by the end of the 8th week

Duodenum: Embryology9.

Clinical correlates


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a. Duodenal stenosis

1. Partial occlusion of the lumen results from incomplete recanalization

2.

Due to defective programmed apoptosis

3.

Most stenoses involve the horizontal (third) and/or ascending (fourth)

parts of the duodenum

4. Because of the occlusion, the stomachs contents (usually containing

bile and therefore green in color) are often vomited


Clinical correlates


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b. Duodenal atresia

1. Complete occlusion of the lumen2.

Not common

3.

20-30% of infants have Down syndrome4. An additional 20% are premature

5.

In 20% of cases, the bile duct enters the duodenum just distal to the

opening of the hepatopancreatic ampulla6. The lumen is completely obliterated with epithelial cells

7. Recanalization fails to occur

8.

Most atresias involve descending (2nd) and horizontal (3rd) parts9. Located distal to opening of bile duct

10. Vomiting usually begins a few hours after birth11.

Vomitus always contains bile

12. Often there is extension of the epigastrium – upper central area of

abdomena.

Resulting from an overfilled stomach and superior part of

duodenum


Clinical correlatesP l h d i


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c. Polyhydramnios

1. Occurs because of duodenal atresia

2.

Atresia prevents normal absorption of amniotic fluid by the intestines

3.

Diagnosis of duodenal atresia is suggested by the double bubble

sign on plain radiographs or ultrasound scans

a. The double bubble sign is caused by a distended, gas-filled

stomach and proximal duodenum

Midgut: Embryology

1. The derivatives are:


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a. Distal ! of duodenum (segments 3 & 4)

b. Uncinate process of Pancreas (ventral Pancreatic Bud)c. Jejunum

d.

Ileume.

Cecum

f.

Appendix

g. Ascending colonh. Proximal ! - 2/3 of transverse colon

2. All derivatives are supplied by the superior mesenteric artery

3. The midgut loops are suspended from the dorsal abdominal wall by anelongated mesentery

4.

As the midgut elongates it forms a ventral, U-shaped loop of gut – the midgutloop – projects into the proximal part of the umbilical cord

5. Designated as the physiological umbilical herniation

a.

Occurs because there is not enough room in the abdomen for the rapidly

growing midgut

Midgut: Embryology

6. Occurs at beginning of 6th week


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g g

7. The midgut communicates with the yolk sac through the narrow yolk stalk

(vitelline duct) until the 10th

week

8. The midgut loop has a cranial limb and a caudal limb

9.

The yolk stalk is attached to the apex of the midgut loop where the two limbs join

10.

The cranial limb grows rapidly and forms the small intestines

11. The caudal loop grows more slowly and forms the cecal diverticulum, theprimordia of the cecum and appendix

Midgut: Embryology

12.Rotation of the midgut


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ga. While in the umbilical cord, the midgut loop rotates 90 degrees

counterclockwise around the axis of the superior mesenteric artery

b.

This brings the cranial limb of the midgut loop to the right and the caudallimb to the left

c.

During rotation, the midgut elongates and forms the intestinal loops, e.g., jejunum and ileum

Midgut: Embryology

13.Return of Midgut to Abdomen


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ga. During the 10th week the intestines return to the abdomen

1. Unknown cause

2.

Proposed decrease in size of liver and kidneys

3. Process called reduction of physiological midgut hernia

4. The small intestine returns first

a. Passes posterior and superior to superior mesenteric arteryb. Occupies central part of abdomen

5. As large intestine returns, it undergoes a further 180-degreecounterclockwise rotation

a.

Later it comes to lie on the right side of the abdomen

b.

Ascending colon becomes recognizable as the posteriorabdominal wall progressively elongates

Midgut: Embryology

14.Fixation of intestines


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a. Rotation of stomach and duodenum causes the duodenum and pancreas

to fall to the right

1.

They are pressed against the posterior abdominal wall by the colon

2. Adjacent layers of peritoneum fuse and subsequently disappear

3. Consequently most of the duodenum (2nd and 3rd segments) and the

pancreas become retroperitoneal

Midgut: Embryology

14.

Fixation of intestines


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b. The attachment of the dorsal mesentery to the posterior wall of the

abdominal wall is greatly modified after the intestines return to the

abdominal cavity

1. At first, the dorsal mesentery is in the median plane

2.

As the intestines enlarge, lengthen, and assume their final positions,their mesenteries are pressed against the posterior abdominal wall.

3.

The mesentery of the ascending colon fuses with the parietalperitoneum on the wall and disappears

4. Consequently, ascending colon becomes retroperitoneal

Midgut: Embryology

14.

Fixation of intestines


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c. The enlarged colon presses the duodenum against the posterior

abdominal wall

1.

As a result, most of the duodenal mesentery is absorbed

2. Consequently, the duodenum, except for about the first 2.5 cm

(derived from foregut), has no mesentery and lies retroperitoneally

d.

Other derivatives of the midgut loop (e.g., jejunum and ileum) retaintheir mesenteries1. The mesentery is at first attached to the median plane of the posterior

abdominal wall

2.

After the mesentery of the ascending colon disappears, the fan-

shaped mesentery of the jejunum and ileum acquires a new line ofattachment

a.

Passes from the duodenal-jejunal junction to the ileocecal junction

Midgut: Embryology

15. Cecum and Appendix


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a. Cecal diverticulum

1.

Primordium of cecum and vermiform (wormlike) appendix

2.

Appears in 6th week

3. A swelling on the antimesenteric border of the caudal limb of the

midgut loop

4.

The apex does not grow as rapidly as the rest of the diverticuluma. Thus the appendix is initially a small diverticulum of the cecum

b.

The appendix increases rapidly in length

c. At birth it is a relatively long tube arising from the distal end of the

cecum

d. After birth, the wall of the cecum grows unequally1.

Results in the appendix comes to enter its medial side

Midgut: Embryology

15. Cecum and AppendixC l di ti l


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a.

Cecal diverticulum

4.

The apex does not grow as rapidly as the rest of the diverticulume. The appendix is subject to considerable variation in position

1.

As ascending colon elongates, the appendix may pass

posterior to cecum – retrocecal appendix (~64% of people)

2.

The appendix may pass posterior to the colon – retrocolic

appendix

3.

The appendix may descend over the brim of the pelvis –

pelvic appendix

Midgut: Embryology

16. Clinical correlatesA li f th Mid t t li f t t ti


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a.

Anomalies of the Midgut – are common, most are anomalies of gut rotation

1. Malrotation of the gut a. Result from incomplete rotation and/or fixation of the intestines

2. Congenital Omphalocoele

a. Persistence of the herniation of abdominal contents into the

proximal part of the umbilical cordb.

Results from failure of the intestines to return to the abdominal

cavity during the 10th

weekc. Herniation of intestines into cord occurs in 1:5,000 birthsd.

Herniation of liver and intestines occur in 1:10,000 births

e.

Size of hernia depends on contentsf. The abdominal cavity is proportionately small when an

omphalocoele is present, due to impetus to grow being absent

g.

Immediate surgical repair is requiredh. Covering of hernia sac is epithelium of umbilical cord – a

derivative of the amnion

Midgut: Embryology

16. Clinical correlatesA li f th Mid t


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a.

Anomalies of the Midgut

3. Umbilical herniaa. When the intestines enter the abdominal cavity during the 10 th

week and then herniate through an imperfectly closed umbilicusb.

Different from an omphalocoele

c. In umbilical hernia the protruding mass (usually greater omentum

and some small intestines) are covered by subcutaneous tissueand skin

d.

Hernia does not reach its maximum size until a month after birthe. Size ranges from 1 to 5 cmf.

Defect through which the hernia occurs is the linea alba

g.

Hernia protrudes during increased abdominal pressure, e.g.,crying, straining, coughing

h. Can be easily reduced through fibrous ring at umbilicus

i.

Surgery is not usually performed unless hernia persists to the ageof 3 to 5 years

Midgut: Embryology



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a.


4. Gastroschisisa. Relatively uncommon

b.

Gastroschisis is a misnomer, actually the anterior abdominal wallis split open, not the stomach

c. Results from a defect lateral to the median plane of the anterior

abdominal walld.

The linear defect permits extrusion of the abdominal viscera

without involving the umbilical corde. The viscera protrude into the amniotic cavity and are bathed byamniotic fluid

f.

Usually occurs on the right side lateral to the umbilicusg. More common in males than females

h. Results from incomplete closure of the lateral folds during the 4th

week

Midgut: Embryology



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a.


5. Nonrotation of Midgut a. Relatively common condition

b.

Sometimes called left-sided colonc.

Is generally asymptomatic, but volvulus (twisting) of the intestines

may occur

d. Occurs when the midgut loop fails to rotate as it reenters theabdomen

e.

As a result,1. The caudal limb of the loop returns to the abdomen first2.

The small intestines lie of the right side of the abdomen

3.

The entire large intestine lies on the left side of the abdomenf. When volvulus occurs, the superior mesenteric artery may be

obstructed

1.

Results in infarction and gangrene of the intestines suppliedby the artery

Midgut: Embryology

16. Clinical correlatesa Anomalies of the Midgut


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a.


6. Mixed Rotation and Volvulusa. The cecum lies just inferior to the pyloric region of the stomach

and is fixed to the posterior abdominal wall by peritoneal bandsthat pass over the duodenum

b. Duodenal obstruction, caused by

1. The peritoneal bands2.

Intestinal volvulus

c.

This type of malrotation results from failure of the midgut loop tocomplete the final 90 degree rotationd.

Consequently, the terminal part of the ileum returns to the

abdomen first

Midgut: Embryology



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a.


7. Reversed Rotationa. Very unusual

b.

Midgut loop rotates in a clockwise rather then counterclockwisedirection

c. As a result,

1. The duodenum lies anterior to the superior mesenteric arteryrather than posterior to it

2.

The transverse colon lies posterior to the superior mesentericartery instead of anterior to itd.

In more unusual cases

1.

The small intestine lies on the left side of the abdomen2. The large intestine lies of the right side of the abdomen

3. The cecum is in the center

4.

Results from malrotation of the midgut followed by failure offixation of the intestines

Midgut: Embryology



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a.


8. Subhepatic Cecum and Appendixa. Occurs in about 6% of all fetuses

b.

More common in malesc.

Results if the cecum adheres to the inferior surface of the liver

when it returns to the abdomen

1. It will be drawn superiorly as the liver diminishes in size2.

The cecum remains in its fetal position

d.

Subhepatic cecum is not common in adults1. When it occurs, it may create a problem in diagnosis ofappendicitis and during appendectomy (surgical removal of

the appendix)

Midgut: Embryology



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a.


9. Mobile cecuma. Occurs in ~ 10% of people

b.

Cecum has an abnormal amount of freedomc.

In very unusual cases it may herniate into right inguinal canal

d. Results from incomplete fixation of the ascending colon

e. Clinically important1.

Possible variations in position of appendix

2.

Because volvulus (twisting) of the cecum may occur

Midgut: Embryology



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a.


10.Internal Herniaa. Very uncommon condition

b.

The small intestine passes into the mesentery of the midgut loopduring the return of the intestines to the abdomen

c. As a result, a hernia-like sac forms

d. Usually does not produce symptomse.

Often detected at autopsy or during anatomical dissection

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a.


11.

Midgut Volvulusa. The small intestine fails to enter the abdominal cavity normally

b.

The mesenteries fail to undergo normal fixationc.

As a result, volvulus (twisting) of the intestines occurs

d. Only two parts of the intestines are attached to the posterior

abdominal wall, the duodenum and the proximal colone.

The small intestine hangs by a narrow stalk that contains the

superior mesenteric artery and vein1. Vessels are usually twisted in the stalk and becomeobstructed at or near the duodenal-jejunal junction

2.

The circulation to the twisted intestine is often restricted3. If vessels are completely obstructed, gangrene develops

Midgut: Embryology



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a.


12.Stenosis and Atresia of the Intestinea. Partial occlusion (stenosis) and complete occlusion (atresia) of

the intestinal lumen account for about 1/3 of the cases ofintestinal obstruction

1. Occurs most often in ileum – 50% and duodenum – 25%

2. Length of area affected variesb.

May result from failure of an adequate number of vacuoles to

form during recanalization of intestine1. In some cases, a transverse diaphragm forms, forming adiaphragmatic atresia

Midgut: Embryology



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a.


12.Stenosis and Atresia of the Intestinec. May occur by interruption of blood supply to a loop of fetal

intestine resulting from a fetal vascular accident1.

An excessively mobile loop of intestine may twist, interrupting

its blood supply

2. Leads to necrosis of section of bowel involved3.

The necrotic segment later becomes a fibrous cord

connecting patent ends of the intestine4. Most atresias of ileum are caused by infarction of fetal bowelresulting from impairment of its blood supply due to volvulus

5.

Impairment most likely occurs during 10th week as intestinesreturn to abdomen

6. Malfixation of the gut predisposes it to volvulus,

strangulation, and impairment of its blood supply

Midgut: Embryology16. Clinical correlates

a.


13 Il l (M k l ) Di ti l ( l f 2 )


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13.Ileal (Meckel

s) Diverticulum (rule of 2s)a. This out pouching is one of the most common anomalies of the

digestive tractb. Congenital ileal diverticulum (Meckels diverticulum) occurs in

2% to 4% of all people

c. Is 3 to 5 times more likely in males than femalesd.

Clinically significant

1. Can become inflamed

2.

Mimics symptoms of appendicitise.

Wall of diverticulum contains all layers of ileum

1. May also contain small patches of gastric and pancreatictissues

2.

Gastric mucosa often secretes acid, producing ulceration

and bleeding

f.

Is the remnant of the proximal portion of the yolk stalkg. Typically appears as a finger-like pouch about 3 to 6 cm (2 ) longh.

Arises from antimesenteric border of ileum ~ 40-50 cm (2

) from

ileocecal junction

i. May be connected to umbilicus by fibrous cord, omphaloentericfistula

Midgut: Embryology

16. Clinical correlatesa. Anomalies of the Midgut


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a

o a es o t e dgut

14.Duplication of the Intestine a. Most intestinal duplications are cystic duplications or tubular

duplicationsb.

Cystic duplications are more common

c. Tubular duplications usually communicate with intestinal lumen

d. Almost all duplications result from failure of normal recanalizationof the lumen

e. As a result, two lumen form

f.

The duplicated segment of the bowel lies on the mesenteric sideof the intestine


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Development of the Hindgut

Hindgut: Embryology5. Cloaca

a. The terminal part of the hindgut is an endodermal-lined chamber that is in


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contact with surface ectoderm at the cloacal membrane

b.

This membrane is composed of endoderm of the cloaca and ectoderm ofthe protodeum, or anal pit

c.

The cloaca, the expanded part of the hindgut, receives the allantois (afingerlike diverticulum) ventrally


d. Partitioning of Cloaca


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1. The cloaca is divided into dorsal and ventral parts by a wedge ofmesoderm – the urorectal septum

2. Develops in the angle between the allantois and the hindgut

3.

As the septum grows towards the cloacal membrane, it developsforklike extensions that produce infoldings of the lateral walls of the

cloaca

4. These folds grow towards each other and fuse, forming a partition that

divides the cloaca into two parts

a. Dorsally - the rectum and cranial part of the anal canal

b.

Ventrally – the urogenital sinus




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5. By the 7th week, the urorectal septum has fused with the cloacalmembrane, dividing it into

a.

A dorsal anal membrane

b.

A larger ventral urogenital membrane

6. Perineal body in the adult represents the area of fusion of the urorectal

septum with the cloacal membrane

a.

The tendinous center of the perineum

b. This fibromuscular node is the landmark of the perineum

c. Location for convergence and attachment of several muscles




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7. The urorectal septum also divides the cloacal sphincter intoa.

Anterior part

1.

Develops into superficial perineal, bulbospongiosus, andischiocavernosus muscles

2.

Reason why pudendal nerve innervates these muscles

b.

Posterior part1. Becomes external anal sphincter

8.

Mesodermal proliferations produce elevations of the surface ectodermaround the anal membrane

a. As a result, this membrane is soon located at the bottom of theectodermal depression – the proctodeum (anal pit)

b. The anal membrane usually ruptures at the end of the 8th week1.

Brings distal part of digestive tract (anal canal) into

communication with amniotic cavity

Hindgut: Embryology6. Anal Canal

a. The superior 2/3s (about 25 mm) of the adult anal canal are derived


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from the hindgut

b.

Inferior 1/3 develops from the proctodeum

c. Pectinate line indicates the junction of the epithelium from the endoderm of

the hindgut and the surface ectoderm of the protodeum

1. Located at inferior limits of anal valves

2. Former site of the anal membrane

d.

About 2 cm superior to the anus is the anocutaneous line = white line

1. Position where epithelium changes from stratified columnar epithelium(recturm) to non-keratinized stratified squamous epithelium (anal canal)

2. At the anus the skin is keratinized and continuous with the skin around

the (natal cleft) anus


e. The other layers of the wall of the anal canal is derived from LP splanchnic


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mesoderm

f.

Superior 2/3 of anal canal

1. Supplied by the superior rectal artery, a branch of the inferior

mesenteric artery

2. Venous drainage via the superior rectal vein, a tributary of the

inferior mesenteric vein

3. Lymphatic drainage eventually flows into the inferior mesentericlymph nodes

4. Innervation from autonomic nervous system




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mesoderm

g.

Inferior 1/3 of anal canal

1. Supplied by the inferior rectal arteries, branches of the internal

pudendal artery

2. Venous drainage via the inferior rectal vein, a tributary of the

internal pudendal veins

3. Lymphatic drainage eventually flows into the superficial inguinallymph nodes

4. Innervation from inferior rectal nervea.

Sensitive to pain, temperature, touch, and pressure



d


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mesoderm

h.

Clinically important

1.

Differences of blood supply, nerve supply, and venous and lymphatic

drainage of the anal canal are important, especially when consideringthe metastasis (spread) of cancer cells

a. Tumors in the superior part are painless

b.

Tumors arise from simple columnar epithelium

c. Tumors in the inferior part are painfuld.

Tumors arise from stratified squamous epithelium

Hindgut: Embryology7.

Clinical correlatesa. Anomalies of hindgut


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1.

Most anomalies are located in the anorectal region and result from

abnormal development of the urorectal system

2.

Clinically, they are divided into high and low anomalies depending on

whether the rectum terminates superior or inferior to the puborectalsling, formed by puborectalis muscle, a part of the levator ani

musculature


Clinical correlatesb. Congenital Megacolon – Hirschsprung Disease (neural crest)

1. Most common cause of neonatal obstructions


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2. Males affected more than females (4:1)

3. Results from failure of neural crest cells to migrate into colon

during 5th to 7th weeks

a.

Failure of parasympathetic ganglion cells to develop into

Auerbachs and Meissner

s plexuses

4. The dilation results from failure of peristalsis in the aganglionic segmenta. Prevents movement of the intestinal contents

5. A part of the colon is dilated because of absence of autonomic ganglion

cells in the myenteric plexus distal to the dilated colon segment

6. The enlarged colon – megacolon – has the normal number of ganglion

cells

7. In most cases only the rectum and sigmoid colon are involved


Clinical correlatesc. Imperforate Anus and Anorectal Anomalies

1. Occurs in 1:5,000 newborns


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2. More common in males

3.

Abnormal development of urorectal segment, resulting in incomplete

separation of the cloaca into urogenital and anorectal protions

4.

Lesions are classified as low or high depending on whether the rectum

ends superior or inferior to the puborectalis muscle



5. Low Anorectal anomalies


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a. Anal agenesis with or without fistula

1. The anal canal may end blindly, may be an ectopic anus, or ananoperineal fistula that opens into the perineum

2. May open into the vagina in females or the urethra in males

3.

More than 90% of low anorectal anomalies are associated with

an external fistula

4. Anal agenesis with a fistula results from incomplete separationof the cloaca by the urorectal septum





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b. Anal Stenosis

1. The anus is in the normal position, but the anus and the analcanal are narrow

2. Is probably caused by a slight dorsal deviation of the urorectalseptum as it grows caudally to fuse with the cloacal membrane

3.

As a result, the anal canal and the anal membrane are small

4. Sometimes only a small probe can be inserted into the analcanal





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c. Membranous Atresia of Anus

1. The anus is in the normal position, but a thin layer of tissueseparates the anal canal from the exterior

2. The anal membrane is thin enough to bulge during straining

3.

The anal membrane appears blue due to the presence of

meconium superior to it

4. Results from failure of the anal membrane to perforate duringthe 8th week



6. High Anorectal anomalies


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1. Anorectal agenesis with a fistula is the result of incompleteseparation of the cloaca by the urorectal septum

2. The rectum ends superior to the puborectalis muscle whenthere is anorectal agenesis

3.

Most common type of anorectal anomaly, accounting for 2/3 ofanorectal defects

4. Although rectum ends blindly, there is a fistula to the bladder

(rectovesical fistula) or urethra (rectourethral fistula) or to the

vestibule of the vagina (rectovestibular fistula) in females



6. High Anorectal anomalies


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5. Passage of meconium or flatus (gas) in the urine is diagnostic

of a rectourinary fistula

6. In newborn males, meconium (feces) may be observed in theurine

7.

In newborn females, meconium may be observed in thevestibule of the vagina



6. High Anorectal anomaliesb R l A i


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b. Rectal Atresia

1. The anal canal and rectum are present, but separated by a

fibrous cord

2. Cause may be abnormal recanalization of the rectum

3.

Cause may be defective blood supply

GIT Embryology(1)

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