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GastroIntestinal > Embryology Of The GI System Lecture (Test 1) > Flashcards

Embryology Of The GI System Lecture (Test 1) Flashcards

1
Q

In Addition to Regionalizatoin, development of the Gut Tube also Involves:

A
  • COntinuous ELONGATION
  • HERNIATION past the Body Wall (Into the Umbilical Cord)
  • Rotation and Folding for EFFICIENT PACKING
  • HISTIOGENESIS and further MATURATION of the Epithelial Lining
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2
Q

Histology

A

ENDODERM: Epithelial Lining and Glands

SPLANCHNIC MESODERM:

  • Lamina Propria
  • Submucosa
  • Muscularis
  • Serosa/ Adventitia
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3
Q

Mesenteries

A
  • Gut Tube becomes suspended by a 2-layered fold of PERITONEUM —> DORSAL MESENTERY
  • MESENTERIES are reflections of PARIETAL PERINTONEUM onto the Gut Tube

***Initially the 2 Peritoneal Cavities are EQUAL IN SIZE, and the GUT TUBE is a SINGLE MIDLINE STRUCTRE!!!!!!

  • *****VISCERAL PERITONEUM:
  • Splanchnopleuric Mesoderm
  • *****PARIETAL PERITONEUM;
  • Somatopleuric Mesoderm
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4
Q

Gut Segmentation

A
  • The Gut Tube is divided into Three Segments:
    1) FOREGUT
    2) MIDGUT
    3) HINDGUT
  • Innervation and Blood Supply t these segments is STRONGLY patterned

DORSAL MESENTERY:
- Gut

VENTRAL MESENTERY;
- Liver

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5
Q

Foregut

A
  • Esophagus
  • Stomach and 1/2 of Duodenum
  • Liver
  • Gall Bladder
  • Pancreas
  • SPLEEN!!!!!
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6
Q

Midgut

A
  • 1/2 Duodenum
  • Jejunum
  • Ileum
  • Cecum and Appendix
  • Ascending Colon
  • 2/3 Transverse Colon
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7
Q

HINDGUT

A
  • 1/3 Transverse Colon
  • Descending Colon
  • Sigmoid Colon
  • Rectum
  • Upper Part Anal Canal
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8
Q

Segmental Pattern for Arterial Circulation

A
  • Each Segment is supplied by an UNPAIRED Branch of the Abdominal Aorta

FOREGUT: Celiac Artery

MIDGUT: Superior Mesenteric Artery

HINDGUT: Inferior Mesenteric Artery

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9
Q

Forregut Autonomic Innervation Sympathetics

A

PREGANGLIONIC CELL BODIES:
- T5 to T9

SPLANCHNIC NERVE:
- Greater Splanchnic Nerve

PREAORTIC GANGLION:
- Celiac

POSTGANGLIONIC AXONS FOLLOW:
- Celiac

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10
Q

Midgut Autonomic Innervation Sympathetics

A

PREGANGLIONIC CELL BODIES:
- T9 to T12

SPLANCHNIC NERVE:
- Lesser Splanchnic Nerve

PREAORTIC GANGLION:
- Superior Mesenteric

POSTGANGLIONIC AXONS FOLLOW:
- Superior Mesenteric Artery

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11
Q

Hindgut Autonomic Innervation Sympathetics

A

PREGANGLIONIC CELL BODIES:
- T12 to L2

SPLANCHNIC NERVE:
- Lest Splanchnic Nerve

PREAORTIC GANGLION:
- Inferior Mesenteric

POSTGANGLIONIC AXONS FOLLOW:
- Inferior Mesenteric Artery

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12
Q

Innervation of the Hindgut Cont..

A
  • Least Splanchnic Nerve to the AORTICORENAL Plexus
  • POST GANGLIONICS FOLLWO THE ARTERIES
  • Lumbar Splanchnic from L1 to L2 to Inferior Mesenteric Plexus
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13
Q

Foregut and Midgut Autonomic Innervation Parasympathetics

A

PREGANGLIONIC CELL BODIES:
- Brainstem

NERVE:
- Vagus Nerve (CN X)

LOCATION OF GANGLION:
- Organ Walls

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14
Q

Hindgut Autonomic Innervation Parasympathetics

A

PREGANGLIONIC CELL BODIES:
- S2 to S4

NERVE:
- Pelvic Splanchnic Nerves

LOCATION OF GANGLION:
- Organ Walls

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15
Q

Development of Esophagus

A
  • LARYNGEOTRACHEAL DIVERTICULUM (Primordium of Respiratory System) of Foregut (Future Esophagus) into the surrounding Splanchnic Mesoderm

**TRACHEOESOPHAGEAL SEPTUM!!!!!!

***Tracheoesophageal Fistula!!!!!!!!

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16
Q

Esophageal Stenosis or Atresia

A
  • NARROWED or OCCLUDED Esophagus due to INCOMPLETE RECANALIZATION, usually found in the LOWER 1/3!!!!!
  • May also be caused by Vascular Abnormalitites or compromised Blood Flow!!!!
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17
Q

Esophageal Replacement

A
  • The majority of Esophageal procedures performed in Infants/ Children are dome for CONGENITAL ESOPHAGEAL ATRESIA or acquired CAUSTIC STRUCTURES (Scarring from Lye or Acid being consumed)
  • SUCCESSFUL Esophageal Anastomoses may be performed in those few with “LONG GAP’ Esophageal Atresia > 3 cm between the Proximal and Distal ESOPHAGEAL Remnants using Various Lengthening Techniques
  • LONG GAP ESOPHAGEAL Atresia will require Esophageal replacement

ESOPHAGEAL REPLACEMENTS:

1) Colon Interposition
2) Gastric Tube Esophagoplasty

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18
Q

Colon Interposition

A
  • A section of COLON is taken from its Normal Position in the Gut and TRANSPOSED, with ITS BLOOD SUPPLY INTACT, into the Chest, where it is joined to the ESOPHAGUS ABOVE and the STOMACH BELOW
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19
Q

Gastric Tube Esophagoplasty

A
  • A LONGITUDINAL SEGMENT is taken from the STOMACH, which is then SWUNG UP into the CHESST and JOINED to the ESOPHAGUS
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20
Q

Gastric Transposition

A
  • The Whole STOMACH is FREED, MOBILIZED and moved into the Chest and attached to the UPPER END of the ESOPHAGUS
  • Contrast Esophagram after Gastric Transposition placed through the Left Chest or through the Posterior Mediastinum
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21
Q

Congenital Esophageal Hernia

A
  • Contrast material opacifies the GASTRIC FUNDUS, which has Herniated into the Lower Chest

***Esophageal or Hiatal Hernias can also be ACQUIRED!!!!!

Ex:

  • Esophagitis
  • Barrett’s Esophagus
  • Hiatal hernia

ESOPHAGEAL DIVERTICULUM:
- Postman had a punch sticking out of his Middle and Inferior Constrictor Muscle, Posterior to the Esophagus

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22
Q

Stomach

A
  • Dilation of Foregut
  • Dorsal surface grows relatively FASTER than Ventral
  • The Abdominal Esophagus and the Stomach start as a STRAIGHT TUBE SUSPENDED by the DORSAL and VENTRAL MESENTERY
  • The DORSAL (Left) side of the Tube grows RAPIDLY, expands and there is a simultaneous CLOCKWISE ROTATION of 90 Degrees
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23
Q

Rotation of the Stomach

A
  • The LEFT SIDE of the Stomach now lies ANTERIOR and the RIGHT SIDE lies POSTERIOR
  • Therefore, the LEFT VAGUS becomes the ANTERIOR VAGAL TRUNK and the RIGHT VAUGS the POSTERIOR VAGAL TRUNK
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24
Q

Hypertrophic Pyloric Stenosis

A
  • Usually presents 2 to 3 WEEKS after Birth

**PROJECTILE Vomiting/ NO BILE!!!!!!

  • SCAPHOID ABDOMEN!!!!!!!!
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25
Q

Molecular Regulation of Gut Tube Development

A
  • Regional specification of the Gut Tube into different components occurs as LATERAL FOLDING brings the 2 Sides of the Tube Together
  • Specification is INITIATED by a RETINOIC ACID Gradient that causes Transcription Factors to be expressed in different Regions of the Gut Tube!!!

1) SOX2: Specifies the ESOPHAGUS
2) PDX1: DUODENUM and PANCREAS
3) CDXC: SMALL INTESTINE
4) CDXA: LARGE INTESTINE

  • Also requires interaction between the Epithelium (ENDODERM) and Mesenchyme (SPLANCHNIC MESODERM) and is INITIATED BY SHH!!!!!!!!!!
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26
Q

Development of Duodenum II: Stenosis and Atresia

A
  • Proliferation of Epithelium
  • Recanalization of Lumen
  • Defective Vacuolization

1) DUODENAL STENOSIS:
- Small Lumen
- Usually 3rd or 4th Part!!!!!

2) DUODENAL ATRESIA:
- Occluded Lumen
- Usually 2nd or3rd Part!!!!!
- FAMILIAL DUODENAL ATREASI: AUTOSOMAL RECESSIVE!!!!!!!!

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27
Q

Duodenal Atresia and Double Bubble Sign

A
  • Frontal Radiograph of the Abdomen demonstrates the Double Bubble Sign: Gas DISTENDED Stomach and Proximal Duodenum with NO DISTAL GAS.
  • Duodenal Atresia was CONFIRMED during Surgery
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28
Q

Duodenal Duplication Cysts

A
  • A DUPLICATION Cyst is a Tubular Structure with an Internal Lining of Gastrointestinal Epithelium, SMOOTH MUSCLE in its wall and adherence to some portion of the Alimentary tract
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29
Q

Gastric Duplication Cysts

A
  • Rare
  • 2 found in 9000 Fetal and Neonatal Autopsies
  • Result of Bowel perforation in Utero which results in MECONIUM PERITONITIS and ASCITES!!!
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30
Q

Liver, Pancreas, and Biliary Ducts

A

**Liver divides the VENTRAL MESENTERY into 2 Parts!!!

  • Liver: Develops in Ventral Mesentery
  • Gallbladder and Bile Ducts develop in the Ventral Mesentery
  • The Pancreas develops from BUDs in BOTH Ventral and Dorsal mesenteries

***Spinning of the Stomach is what brings the two pieces of the Pancreas together

31
Q

Molecular Regulation of Liver Induction

A
  • All Foregut ENDODERM has the potential to express Liver-specific Genes and to differentiate into LIVER TISSUE
  • Expression is blocked by unknown Signals from the Trunk Mesoderm and Ectoderm. These RESTRICT Hepatic Development in the Posterior Endoderm
  • Action of these INHIBITING Factors is BLOCKED in the area of the Liver by FGF2 Secreted by CARDIAC MESODERM and BMPs Secreted by the SEPTUM TRANSVERSUM
  • cardiac Mesoderm/ Septum Transversum instruct the Gut Endoderm to express Liver Specific Genes
32
Q

Liver and Gallbladder

A
  • Hepatic Cords (Cells) COALESCE around Extraembryonic Veins to form SINUSOIDS
  • Bile Duct forms
  • Gallbladder and Cystic Duct are OUTGROWTHS of the Bile Duct

**Growth of the Liver divides the Ventral Mesentery into FALCIFORM LIGAMENT and LESSER MOMENTUM!!!!!!!

33
Q

Ligamentum Venosum

A
  • The Ligamentum Venous is the FIBROUS remnant of the DUCTUS VENOUS
  • Ligamentum Teres Hepatis is the OBLITERTED LEFT UMBILICAL VEIN
34
Q

Extraheptic Biliary Atresia

A
  • Incomplete CANALIZATION of the Bile Duct
  • 1/ 15,000 Live Births
  • JAUNDICE: High levels of Bilirubin in Bloodstream
  • DARK URINE: Bilirubin filtered by Kidney and Excreted in Urine
  • PALE STOOL: No Bile or Bilirubin is being emptied into the Intestine

Treatment: SURGICAL CORRECTION or Transplant

35
Q

Liver Disorders- Genetic

A

1) MENKES DISEASE:
- KINKY HAIR SYNDROME
- Decrease in the Cells’ ABILTY to Absorb COPPER

2) WILSON’S DISEASE:
- Copper is not ELIMINATED PROPERLY and instead Accumulates
- KAYSER FLEISCHER RING!!!!

36
Q

Molecular Regulation of Pancreas Development

A

PDX1: PANCREAS and DUODENUM

  • Paired Homeobox Genes specify Endocrine Cell Lineages

PAX4: Cells Secreting INSULIN, Somatostatin, and Pancreatic Polypeptide

PAX6: Cells Secreting GLUCAGON

  • ISLET of LANGERHAN appear in 3rd FETAL MONTH!!!
  • INSULIN Secretion by 5th Month!!!
37
Q

Annular Pancreas

A
  • Ventral and Dorsal Pancreatic buds form a RING around the Duodenum
  • Presents as DUODENAL OBSTRUCTION

***Ventral Bud forms the Major Pancreatic Duct!!

38
Q

Accessory or Ectopic Pancreatic Tissue

A
  • Can be found from DISTAL ESOPHAGUS through the PRIMARY INTESTINAL LOOP (Roughly Distal part of Transverse Colon)
  • Most common in STOMACH or ILEUM (ILEAL or MECKEL’S DIVERTICULUM)
39
Q

Rotation of Foregut

A
  • Stomach moves to the LEFT
  • Liver moves to the RIGHT
  • Relative size of the 2 Peritoneal Cavities CHANGES!!!
  • Right Side is GETTING SMALLER!!!
40
Q

Midgut

A

Derivatives of the Midgut are:
1) Duodenum Distal to ENTRANCE of Bile Duct

2) Free Small Intestine (Jejunum, Ileum)
3) Cecum and Appendix
4) Ascending Colon
5) Right (Proximal) 2/3 of Transverse Colon

** SUPERIOR MESENTERIC ARTERY

41
Q

Gut Atresia and Stenoses

A
  • May occur anywhere along the Intestine
  • In UPPER DUODENUM: Usually due to FAILURE to RECANALIZE
  • CAUDAL to the Duodenum, these are probably due to VASCULAR COMPROMISE!!!
42
Q

Apple Peel Atresia

A
  • 10% of ALL Atresia
  • PROXIMAL JEJUNUM
  • Intestine is SHORT and the portion DISTAL to the defect is COILED AROUND THE MESENTERIC REMNANT
  • Associated with LOW BODY WEIGHT and other Abnormalities
43
Q

Rotation and Flexion of the Midgut

A
  • RAPID GROWTH of the Midgut starts at about 6 weeks!!!!!!!!
  • Produces a Normal PHYSIOLOGIC HERNIATION
  • Gut loops into the Umbilical Cord
  • As this happens, the LOOP ROTATES 90 Degrees COUNTERCLOCKWISE around the Superior Mesenteric Artery
44
Q

Umbilical Herniation

A
  • Occurs NORMALLY until there is enough room in the Abdomen for all the Intestines
45
Q

Rotation and Fixation of the Midgut

A
  • At about the 10th Week, the Herniated LOOPS return to the Abdominal Cavity and ROTATE an ADDITIONAL 180 Degrees (270 Total)
46
Q

Malrotation

A
  • Partial Rotation ONLY!!!
  • Abnormally positioned Viscera
  • Increased risk of ENTRAPMENT of portions of the Intestine
  • Usually presents within FIRST WEEK as DUODENAL OBSTRUCTION with BILIOUS VOMITING

INFANTS:
- Recurrent Abdominal Pain, Intestinal Obstruction, Malabsorption/ Septic Shock, Solid Food Intolerance, Common Bile Duct Obstruction, Abdominal Distention, and Failure to Thrive

47
Q

Vovulus

A
  • Compromises the Intestine of the Blood Flow
  • ABNORMAL TWISTING of the Intestine causing Obstruction

Note: BLOAT —-> Any Deep-Chested, Large Breed of Dog is at risk of Bloat

48
Q

Bilious Emesis

A
  • The GREEN Color of Bile is CLEARLY PRESENT
  • This newborn was though to be well and tolerating feedings for SEVERAL DAYS before the SUDDEN ONSET of this Abnormal Emesis
  • MALROTATION with VOLVULUS was diagnosed and the Infant underwent EMERGENT SURGICAL CORRECTION
  • EMESIS like this is NEVER NORMAL!!!!
49
Q

Intussusception

A
  • The ENFOLDING of One Segment of the Intestine with Another
  • Characterized and initially presents with RECURRING ATTACKS of Cramping Abdominal Pain that gradually become more Painful
50
Q

Situs Inversus due to Bowel Malrotation

A
  • SUTUS INVERSUS Abdominus and Malrotation in an Adult with LADD’s BAND FORMATION leading to Intestinal Ischemia!!!
51
Q

Epiploic Appendagitis

A
  • An Abdominpelvic CT scan with IV Contrast reveled POLYSPLENIA with SITUS ABNORMALITIES. It was noted that the Liver was essentially MIDLINE, the Stomach was in the RIGHT UPPER QUADRANT, the Majority of the Colon was in the Right Abdomen, and the Majority of the Small Bowel LOOPS were in the Left Abdomen
  • Most suspicious was the FOCAL WALL THICKENING of the Transverse Colon with Inflammation surrounding a Fatty Lesion in the LEFT UPPER ABDOMEN, indicating EPIPLOIC APPENDAGITIS
  • The Diagnosis of Epiploic Appendagitis drastically changed the treatment plan since it was ruled that the patient could be treated medically instead of Surgially
52
Q

Body Wall Defects

A

1) Omphalocele
2) Gastroschisis
3) Prune Belly Syndrome

53
Q

Omphalocele

A

GUT WITHIN UMBILICAL CORD!!!!

  • HERNIATION of Abdominal contents through ENLARGE UMBILICAL RING
  • This is normal it is is TEMPORARY
  • The gut should return into eh Abdomen as the Embryo grows
  • 25/ 10,000
  • Occurs when the MIDGUT Loop fails to RETURN to Abdominal Cavity
  • Pale, shiny sac protrudes from Base of UMBILICAL CORD

*Herniates into a MEMBRANOUS SAC!!!!!!!!

  • Associated with a high Mortality rate and other Severe Malformations:
    1) Cardiac (50%)
    2) Neural Tube (15%)
    3) Chromosomal (15%)
54
Q

Gastrochisis

A
  • Failure of Anterior Abdominal Wall MUSCULATURE to Close during Fodling
  • Gut contents NOT SURROUNDED BY MEMBRANE!!!!!!!!!!!
  • 1 to 2/ 10,000 but Frequency is INCREASING in YOUNG WOMEN (Recreational Drug Use)
  • 15 to 19 years, Incidence from 4/ 10,000 to 26.5/ 10,000
  • Not associated with Chromosomal Abnormalities or other Malformations
  • SURVIVAL RATE is EXCELLENT!
55
Q

Prune Belly or Eagle-Barrett Syndrome

A

Common TRIAD of Features:
1) Anterior Abdominal Wall —> MUSCULATURE is DEFICIENT or ABSENT!!!!!

2) Urinary Tract Anomalies (Mega-Ureters, Large Bladder)
3) Bilateral CRYPTOCHIDISM (Undescended Testicles)
- Prune Belly Syndrome occurs almost exclusively in Males; Less than 3% of cases of Prune Belly Syndrome involve Females
- In BOTH genders, Prune Belly Syndrome involves the Abdominal Wall, Bladder, Ureters, and Kidneys. No URETHRAL Anomalies are SEEN in Families

56
Q

Prune Belly Syndrome Etiology: 2 Hypothesis

A

1st Hypothesis
URIANRY TRACT OBSTRUCTION:
- Hypoplastic or Dysplastic Prostate creates a URINARY TRACT OBSTRUCTION leading to OVERDISTENSION of the Bladder and the UPPER URINARY TRACT which stretches the Abdominal Wall and causes DAMAGE to the Abdominal Musculature and interferes with the Descent of the TESTICLES!!!

2nd Hypothesis:
PRIMARY MESODERMAL DEVELOPMENTAL DEFECT:
- An Insult between 6 and 10 Weeks Gestation which DISRUPTS the Development of the INTERMEDIATE and LATERAL PLATE MESODERM which give rise to both the ABDOMINAL WALL and Genitourinary Tract including the PROSTATE!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

57
Q

Ileal Diverticulum

A

MECKEL’S DIVERTICULUM**

  • Remnant of VITELLINE DUCT!!!!!
  • Asymptomatic
  • Gastric or Pancreatic Tissue
  • Failure of Vitelline Duct to Close

RULE of 2’s:

  • 2% Prevalence
  • Location 2 feet Proximal to the Ileocecal Valve in Adults
  • Half of those who are Symptomatic are YOUNGER than 2 years of Age!!!!!
  • **FISTULA PRESENT
  • **FECAL Discharge through UMBILICUS!!!
58
Q

Umbilical Hernia

A
  • Gut pushes skin and Fascia out AHEAD of it
59
Q

Hindgut

A
  • At approximately Embryonic day 8.5 - 9 run the Mouse, VAGAL NEURAL CREST CELLS invade the Anterior Foregut and MIGRATE in a ROSTRAL to CAUDAL Direction to Colonize the ENTIRE Foregut, Midgut, Caecum, and Hindgut and give rise to the MAJORITY of the ENTERIC NERVOUS SYSTEM
  • Enteric Nervous System are organized in Ganglia found in two Main Plexi:
    1) OUTER MYENTERIC Plexus:
  • Develops first and occupies a position between the Longitudinal and Circular Muscle Layers

2) INNER SUBMUCOSAL Plexus:
- Develops later in Gestation and resides within the Submucosa!!!!

60
Q

Hirschsprung’s Disease

A
  • CONGENITAL AGANGLIONIC MEGACOLON, is a MOTOR Disorder of the Colon that causes a FUNCTIONAL Intestinal Obstruction
  • Both PLEXUSES are AFFECTED!!!!!!
  • It occurs in 1/5,000 Infants with a Male to Female Predominance of 4:1
  • The Pathogenesis of the disease is FAILURE of MIGRATION of the NERUAL CREST CELLS that form the COLONIC GANGLION CELLS
  • Without PARASYMPATHETIC INNERVATION, the Colon CANNOT Relax or Undergo PERISTALSIS, resulting in a FUNCTIONAL OBSTRUCTION!!!!!!
61
Q

Variability in Hirschspring’s Disease

A
  • Hirschsprung’s Disease can affect the more CRANIAL parts of the Gut Tube
  • 70 to 80% Descending and Sigmoid Colon
  • 1 to 20% Transverse Colon
  • 3% Entire Colon
  • Decreased occurrence in MORE PROXIMAL parts because these are associated with HIGHER MORTALITY Rate and/or INCREASED Incidence of Multiple Congenital Abnormalities
62
Q

Treatment for Hirschsprung’s Disease

A
  • Surgery is the ONLY PROVEN, effective treatment for Hirschsprung’s Disease
  • The procedure is called PULL-THROUGH SURGERY and involves removing the Section of the Colon that has NO GANGLIA Cells, then Connecting the remaining Healthy end of the Colon to the RECTUM
63
Q

Rotation

A
  • Will change the SIZE of the Two Original Peritoneal Cavities
  • Will change the ANATOMICAL RELATIONSHIP of the Organs to One Another (No Longer a Straight Tube)
  • Will cause CHANGES (LOSS) of some of the Dorsal Mesenteries
  • Structures will be PRIMARILY or SECONDARILY RETROPERITONEAL!!!!!!
64
Q

Retroperitoneal

A

Primary:
- Any Organ that developed OUTSIDE the Abdominal Cavity (Kidney) which NEVER HAD a MESENTERY to Begin with

Secondary:
- Portions of the Gut Tube whose Mesentery has FUSED with the Lining Peritoneum

65
Q

Intraperitoneal

A
  • Organs with a Mesentery
66
Q

Rotation and Fixation of the Midgut

A
  • During Rotation and Herniation of the Gut, some parts become PUSHED BACK, and become SECONDARILY RETROPERITONEAL!!!!!!
    a) Ascending Colon
    b) Descending Colon
    c) 2nd and 3rd Parts of Duodenum
67
Q

Partitioning of the Cloaca

A
  • Develops from HINDGUT ENDODERM!!!!

- Cloaca divided by URORECTAL SEPTUM into Urogenital Sinus and Rectum

68
Q

Defects in Parttioning of the Cloaca

A

**FAILURE of FOLDS to DEVELOP: Resulting in a RECTOURETHRAL FISTULA!!!!!!!

In MALES:
- Results in RECTOPROSTATIC FISTULA!!!!!

In FEMALES:
- Results in either a RECTOCLOACAL CANAL or a RECTOVAGINAL FISTULA!!!!

69
Q

Anorectal Malforamtions

A
  • IMPERFORATE ANUS is a Malformation of the ANORECTAL Region that may occur in Several Forms
  • The RECTUM may end in a BLIND POUCH that does not Connect with the EXTERNAL ENVIRONMENT, or it may have openings to the Urethra, Bladder, or Vagina
  • Stenosis, or narrowing of the Anus, or Absence of the Anus may be present
70
Q

Anal Canal Development

A
  • Anorectal Malformations are a Spectrum of defects, and are usually referred to as “LOW” or “HIGH”
  • Anal Membrane fails to Perforate

LOW:
- Anal Canal ends as a Blind Sac BELOW PELVIC DIAPHRAGM (Anal Anagenesis)

HIGH:
- Anal Rectum ends as Blind Pouch ABOVE PELVIC DIAPHRAGM (Anorectal Anagenesis, MOST COMMON!!!!!!!!!!!!!!!!!!!)

71
Q

Imperforate Anus Symptoms and Signs

A
  • Absence or misplaced of Anal Openings
  • Anal opening very NEAR to the Vaginal Opening in the Female
  • NO PASSAGE of FIRST STOOL within 24 to 48 hours after Birth
  • Stool passed by WAY of Vagina, base of Penis or Scrotum, or Urethra
  • ABDOMINAL DISTENTION!!!!!!!!
72
Q

High Anorectal Malformation

A
  • NO CONTACT with the Skeletal Muscle so very hard to make External Anal Sphincter
73
Q

Low Anorectal Malformation

A
  • CONTACT with the Skeletal Muscle which helps created the External Anal Sphincter
74
Q

Clinical Prognosis

A

IMPERFORATE ANUS:
- A Colostomy is INDICATED AFTER Birth, with Surgical Correction the PROGNOSIS is EXCELLENT!!!!!

RECTO-URETHRAL FISTULA (LOW):
- Colostomy before the DEFINITIVE Repair Period. The Long-term Prognosis for Normal Urethral and Rectal Function is GOOD!!!

RECTOVESICAL FISTULA (HIGH):

  • Usually also have POORLY developed SACRAL BONES and SPHINCTERS
  • The Prognosis for Normal Bowel Function is POOR!!!!!!!

GastroIntestinal (21 decks)

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