Development of GI System (Brauer) Flashcards
1
Q
- cranio-caudal folding of the embryo creates the primitive gut tube which is comprised of these structures:
- around week 4, the midgut’s connection to the yolk sac narrows, creating this structure:
A
- cranio-caudal folding of the embryo creates the primitive gut tube which is comprised of these structures: foregut, midgut, hindgut
- around week 4, the midgut’s connection to the yolk sac narrows, creating this structure: vitelline duct
2
Q
GI structures derived from endoderm:
A
- mucosal epithelium
- GI glands (except lower 1/3 of anus)
3
Q
GI structures derived from splanchnic mesoderm:
A
- connective tissue
- vasculature
- smooth muscle wall
4
Q
GI derivatives derived from ectoderm:
A
- enteric ganglia, nerves, and glia (via neural crest cells)
- epithelium of lower 1/3 anus
5
Q
What are the structures of the foregut and what is the arterial supply?
A
- structures: esophagus, stomach, liver, gallbladder, pancreas, upper duodenum
- BS: celiac trunk
6
Q
What are the structures of the midgut and what is the arterial supply?
A
- structures: lower duodenum, jejunum, ileum, cecum, appendix, ascending colon, proximal 2/3 of transverse colon
- BS: superior mesenteric artery (SMA)
7
Q
What are the structures of the hindgut and what is the arterial supply?
A
- structures: distal 1/3 of the transverse colon, descending colon, sigmoid colon, rectum, upper anal canal
- BS: inferior mesenteric artery (IMA)
8
Q
What is the function of peritoneum within the abdomen and what are the different types of peritoneum?
A
- peritoneum: thin membrane that lines the abdominal and pelvic cavities, and covers most abdominal viscera; composed of layer of mesothelium supported by a thin layer of connective tissue
- parietal peritoneum: the portion that lines the abdominal and pelvic cavities (also known as the peritoneal cavity)
- visceral peritoneum: covers the external surfaces of most abdominal organs, including the intestinal tract
9
Q
GI structures derived from dorsal mesentary:
A
- greater omentum: gastrosplenic, gastrocolic, splenorenal ligaments
- small intestine mesentery
- mesoappendix
- transverse mesocolon
- sigmoid mesocolon
10
Q
GI structures derived from ventral mesentery:
A
- lesser omentum: hepatoduodenal and hepatogastric ligaments
- falciform ligament of liver
- coronary ligament of liver
- triangular ligament of liver
11
Q
- organs that are suspended by mesentery
- stomach, tail of pancreas, first five cm and the fourth part of the the duodenum, jejunum, ileum, cecum, appendix, transverse colon, sigmoid colon, and upper third of the rectum
A
intraperitoneal organs
12
Q
- organs that are excluded from peritoneal cavity
- mnemonic: SAD PUCKER
Suprarenal (adrenal) gland
Aorta/IVC
Duodenum (2nd and 3rd part)
Pancreas (except tail)
Ureters
Colon (ascending and descending)
Kidneys
(o)Esophagus
Rectum
A
retroperitoneal organs
13
Q
- organs that were initially suspended within mesentery that later fused w/ body wall
- ascending/descending colon, duodenum, bulk of pancreas
A
secondarily retroperitoneal organs
14
Q
Mnemoic SAD PUCKER is used to recall:
A
retroperitoneal organs
S - suprarenal (adrenal) glands
A - aorta/IVC
D - duodenum (2nd and 3rd parts)
P - pancreas (except tail)
U - ureters
C - colon (ascending/descending)
K - kidneys
E - (o)esophagus
R - rectum
15
Q
GI structures derived from foregut:
A
- esophagus
- stomach
- liver and gallbladder
- pancreas
- upper duodenum (proximal bile duct)
16
Q
When the stomach (foregut) rotates during development, what anatomical changes occur and what structures develop?
A
- stomach is attached to body wall by peritoneum (mesentery) both ventrally and dorsally
- stomach rotates 90 degrees wherein left side moves ventrally and right side moves dorsally
- ventral mesentery > lesser omentum (located on lesser curve of stomach)
- dorsal mesogastrium > greater omentum (located on greater curve of stomach)
- lesser sac located behind stomach
- vagus nerve (LARP): left vagus nerve > anterior; right vagus nerve > posterior
17
Q
How do the greater and lesser omentums develop?
A
- ventral mesentery > lesser omentum
- dorsal mesogastrium > greater omentum
- lesser omentum located between lesser curve of stomach and liver
(epiploic foramen: opening to lesser sac between liver and top of duodenum)
- greater omentum grows downward in a double fold in front of transverse colon
- greater omentum superior to transverse colon comes together w/ transverse mesocolon (attaches colon to pancreas and body wall) and duplicated layers are absorbed > greater omentum becomes stuck to transverse colon while also hanging below it
18
Q
How do the greater and lesser sacs develop?
A
(side note: liver develops in ventral mesogastrium and spleen develops in dorsal mesogastrium)
- rapid and large growth of liver causes lesser sac to develop
- lesser sac: located behind lesser omentum, stomach, and gastrocolic ligament (part of the greater omentum)
- greater sac: larger portion of the peritoneal cavity; divided by the transverse mesocolon into supracolic and infracolic compartments
- epiploic foramen: opening within lesser omentum from greater sac to lesser sac
19
Q
- thickened muscle causing narrowing of opening between stomach and duodenum
- etiology: faulty migration of neural crest cells > ganglion cells of enteric nervous system not properly populated which causes inability of sphincter to relax; or narrowing of pyloric lumen due to hypertrophy of muscularis externa in this region
- presentation: occurs within a few months after birth, palpable mass (“olive”) at right costal margin, projectile non-bilious vomiting after feeding, fewer and smaller stools, failure to gain weight (may lose weight)
- incidence: 1:500
A
hypertrophic pyloric stenosis
20
Q
How does the liver develop?
A
- during week 4, begins as hepatic diverticulum from gut endoderm
- connection of diverticulum to foregut > common bile duct
- endoderm > hepatocytes, bile ducts, and hepatic ducts
- splanchnic mesoderm > stromal, Kupffer, and stellate cells
- takes over hematopoiesis in utero by week 10
- congenital anomalies are rare
21
Q
Describe the development of the gallbladder and bile duct:
A
- around week 4, begins as cystic diverticulum (outgrowths from cystic endoderm)
- gallbladder develops as a secondary out-pouching from hepatic diverticulum (common bile duct) that grows into ventral mesentery, the connection between the two is the cystic duct
- around the end of week 5, recanalization of bile duct occurs
- around the end of week 6, the common duct and ventral pancreatic bud rotate 180° clockwise around the duodenum so that the gallbladder remains situated inferior to the liver
- beginning week 12, bile is formed by hepatic cells
22
Q
- blockage of the ducts that carry bile from the liver to the gallbladder
- both congenital and adult forms of condition
- etiology: obliteration of bile duct, or inflammation replaces duct w/ fibrotic tissue
- presentation: immediate onset of progressive jaundice in infants, white/clay colored stool, dark urine, poor prognosis (12-19 month lifespan)
- incidence: extrahepatic (1:15,000) and/or intrahepatic (1:100,000)
A
biliary atresia
23
Q
Describe the development of the pancreas:
A
- around week 4, begins as two additional endodermal buds sprouting from the foregut, inferior to cystic diverticulum
- ventral pancreatic bud derivatives: uncinate process (grows into ventral mesentery)
- dorsal pancreatic bud derivatives: pancreatic head, body, and tail (grows into dorsal mesentery)
- buds develop w/ both exocrine and endocrine portions
- around week 5, ventral pancreas migrates around posteriorly to fuse w/ dorsal pancreas (ventral and dorsal ducts also fuse)
- ventral pancreatic duct > main pancreatic duct (connection to duodenum)
- dorsal pancreatic duct > accessory pancreatic duct
24
Q
- developmental variation within pancreas where there is an additional pancreatic duct (Duct of Santorini) that occurs within 33% of people
- can be functional or non-functional and may open separately into the second part of the duodenum which is dorsal and usually (in 70%) drains into the duodenum via the minor duodenal papilla
- in the other 30% it drains into the main pancreatic duct, which drains into the duodenum via the major duodenal papilla
- the main pancreatic duct and this additional duct both eventually—either directly or indirectly—connect to the second part (‘D2’, the vertical segment) of the duodenum
A
accessory pancreatic duct
(left side of photo)
25
Q
- developmental variation of pancreas that occurs in 4% of people where the ventral and dorsal parts fail to fuse by week 8
- mostly asymptomatic
- patients prone to abdominal pain/pancreatitis
A
pancreas divisum
(right side of photo)
26
Q
- condition where pancreas forms a ring around duodenum
- etiology: poor migration of pancreas (the ventral pancreas migrates both anteriorly and posteriorly) > pancreatic ring around 2nd part of duodenum
- presentation: duodenal obstruction/stenosis, bilious vomiting (if the annulus develops inferior to bile duct), low birth weight
A
annular pancreas
27
Q
Describe the development of the spleen:
A
- around week 4, begins as mesenchymal condensation that forms in the dorsal mesogastrium
- by week 5 the spleen is fully formed
- derived from mesoderm not endoderm
28
Q
Describe the general development and derivatives of the midgut:
A
- midgut begins as U-shaped loop of gut w/ vitelline duct extending from it to definitive yolk sac
- major occurences of development are rotation and elongation
- midgut herniates out of umbilicus at week 6 and returns to abdomen by week 10 (physiological herniation)
- derivatives: lower duodenum (distal to bile duct), jejunum, ileum, cecum, appendix, ascending colon, proximal 2/3 transverse colon
- blood supply: superior mesenteric artery (axis for rotation)
29
Q
Describe the process of midgut rotation:
A
TLDR: midgut herniates out of umbilicus at week 6 and returns to abdomen by week 10, all while making a ~270° counterclockwise turn
- at week 6, midgut loop makes a 90° ccw rotation; proximal portion lies on the right and becomes convoluted, distal portion lies on the left and develops a buldge (cecum)
- at week 10, proximal portion of loop returns to abdomen, passing under distal portion to make a second 90° ccw turn; brings cecum to upper right quadrant and ascending colon is anterior to duodenum
- at week 11, distal portion of loop returns to abdomen, making a third 90° ccw turn; cecum descends to lower right quadrant, carrying ascending colon to end up on right side of abdomen
- the originally proximal part of the midgut, distal duodenum, ends up posterior to an originally distal part of the midgut, the proximal transverse colon
30
Q
Where are midgut structures located anatomically due to rotation?
A
- proximal (cephalic) loop rotates inferiorly to become distal duodenum, jejunum, and part of the ileum
- distal (caudal) loop rotates superiorly becoming rest of the ileum, cecum, appendix, ascending colon, and most of the transverse colon
31
Q
- presentation: herniation of midgut through umbilicus, covered by parietal peritoneum
- etiology: herniated bowel does not fully retract during development
- incidence: 2.5/10,000 births, increased risk w/ trisomy 13 or 18
A
omphalocele
32
Q
- defect of the abdominal wall causes infant’s intestines to be found outside the body, exiting through a hole beside the belly button
- etiologies: abnormal lateral body folding > creates wall weakness that allows bowel to herniate; or connective tissue of skin and hypaxial musculature of body wall do not form normally > wall weakness
- not covered by parietal peritoneum
- incidence: 1:10,000 births
A
gastroschisis
33
Q
- an outpouching or bulge in the lower part of the small intestine, which is congenital and is a leftover of the umbilical cord
- etiology: failure of yolk stalk (vitelline duct) connection to the midgut to regress, midgut remains connected to umbilicus
- presentation: usually asymptomatic; can lead to abd swelling, intestinal obstruction, bowel sepsis, and GI bleeding
- rule of 2’s: 2% of population, 2x more likely in males, 2% have symptoms, 2 feet proximal to ileocecal valve, 2 in long, presents in year 2 of life
A
Meckel’s diverticulum
34
Q
- etiology: midgut completes first 90° ccw rotation but does not complete remaining 180° ccw rotations
- presentation: left-sided colon and right-sided small intestines; formation of fibrous Ladd bands > volvulus, duodenal obstruction
- incidence: 1:500 births
A
malrotation/non-rotation of midgut loop
35
Q
- midgut completes initial 90° ccw rotation, but then completes a 180° cw rotation
- results in a net 90° cw rotation
- duodenum results anterior to transverse colon
A
reverse gut rotation
36
Q
- etiology: twisting of bowel around its mesentery, increased risk w/ gut rotation anomalies
- presentation: acute abd pain, vomiting, GI bleeding
- complications: bowel obstruction, infarction
- “coffee bean sign” seen on diagnostic imaging
A
volvulus
37
Q
GI structures derived from hindgut:
A
- distal 1/3 of transverse colon
- descending colon
- sigmoid colon
- rectum
- superior 2/3 of anal canal (to pectinate line)
(BS by inferior mesenteric artery)
39
Q
Describe the development of the anal pit and pectineal line:
A
- anal rectal lumen temporarily closed by endodermal epithelial anal plug and anal membrane (eventually opens via apoptosis)
- mesoderm surrounding anal opening proliferates outward (invaginates) to form a circular anal pit (lined by ectooderm) that meets rectum and connects to it as membrane ruptures
- pectineal line divides origin of hindgut and anal pit within the anal canal: superior 2/3’s (endodermal epithelium, separate BV supply and innervation of hindgut); lower 1/3 (ectodermal epithelium, separate BV and innervation of anal pit)
41
Q
- opening to anus is missing/blocked due to persistent anal membrane
- low, intermediate, or high distinction - relative to levator ani muscles and pelvic bony landmarks
- incidence: 1:5000 births
A
imperforate anus
42
Q
What are the different types of abnormal urorectal septum development?
A
- rectovaginal: occurs in females born w/ a persistent cloaca; a common chamber is present receiving urethra, vagina, and rectum
- rectovesical: occurs in males; connection of rectum to bladder
- rectourethral: occurs in males; connection of rectum to urethra
(incidence of these abnormalities: 1:2000-5000)
43
Q
- etiology: failure of neural crest cell migration > absence of ganglionic plexus, causes lack of peristalsis (colon fails to relax)
- presentation: intestinal wall hypertrophy proximal to aganglionic segment, lack of peristalsis, abnormal colonic dilation or distension (megacolon), failure to pass meconium
A
Hirschsprung’s disease
(congenital aganglionic megacolon)
