GI system Flashcards
Give an account of the composition and function of saliva.
Saliva is mostly water but also contains Mucins, Electrolytes (Na+, Cl-, and HCO3-), Antibodies and Enzymes.
Its major functions are to keep mucosa moist, assist in the digestion of foods (both via breakdown of food and lubrication for swallow), act as a pH7 buffer,
Describe the anatomy of the salivary glands including the microstructure, ducts and important anatomical relations.
The basic microstructure of salivary glands involve ductal cells, serous cells, mucous cells. (serous appear dark (serous demilune) whereas mucous cells appear light)
There are 4 glands which are important for saliva poduction:
Parotid: Located superior to the masseter. Enters oral cavity via parotid duct. Associated with branches of the facial nerve which pass through it.
Submandibular: 1 duct which enter mouth at lingual papilla ( visible. Closely related to lingual nerve ( located in submandibular fossa of mandible.
Sublingual: 8-20 ducts enter oral cavity along the floor of the mouth at the sublingual fold. Located sublingual fossa.
Minor glands
Discuss the differences in saliva produced by the different salivary glands.
Parotid: serous gland which produce amylase.
Submandibular: seromucous gland with mixed secretions (contributes to most of rest secretions).
Sublingual: Mucous, lubricant
Minor Glands: mostly mucous for lubricant
Give a detailed account of the neural control of salivation.
Parasympathetic- secretomotor. Facial nerve (CNVII) and Glossopharyngeal (CNIX). The facial nerve doesnt supply the parotid and only passes through it. Sublingual and Submandibular • Preganglionic parasympathetic fibres originate from the superior salivatory nucleus in the brainstem • Pass through branch of facial nerve (chorda tympani) to reach the submandibular ganglion • Synapse with postganglionic parasympathetic fibres • Postganglionic parasympathetic fibres travel along lingual nerve (branch of CNV – trigeminal) to reach submandibular and sublingual glands • Lingual nerve also supplies sensory information i.e. pain. Parotid glands: • Preganglionic fibres originate from inferior salivatory nucleus in the brainstem • Pass through branch of glossopharyngeal nerve (lesser petrosal nerve to reach the otic ganglion • Synapse with postganglionic parasympathetic fibres • Postganglionic parasympathetic fibres travel along auriculotemporal nerve (branch of CNV – trigeminal) to reach parotid glands • Auriculotemporal nerve also supplies sensory information from parotid capsule and supplies overlying skin
Describe Frey’s syndrome
Parodectomy- many tumours occur in the parotid glands (some are malignant) but removal is complicated due to the relations with the facial nerve. Frey's syndrome- During parotidectomy, the auriculotemporal nerve can be damaged • Damaged sensory and parasympathetic fibres become mixed • Can result in parasympathetic fibres supplying skin (including sweat glands) • Consequences? • Salivary stimulus ( e.g. smelling food) results in sweating of skin over the parotid gland • Also called gustatory sweating • Treated with botulinum toxin
Describe the effects of Mumps on the salivary glands
• Mumps is a viral infection that primarily affects the parotid glands • Parotid glands become inflamed and enlarge • Parotid glands surrounded by tough, fibrous capsule • Stretching capsule stimulates the sensory fibres of the auriculotemporal nerve – very painful!
Describe salivary stones
A stone (calculus) may form in the salivary glands, particularly following infection • If the stone moves into the main duct it can block the duct • Saliva builds up in the gland causing swelling • Very painful, particularly at mealtimes
Give an account of the structure of the abdominal wall and it’s functions.
Extends from teh costal margins to the ileac crests and pubic bones. It consists of skin, superficial fatty fascia, scarpa’s fascia (membranous layer), 3 layers of muscle, a transverse fascia, an extraperitoneal fascia and a parietal peritoneum.
It supports and protects abdominal viscera, compresses the abdomen to increase pressure for expulsion, movement of trunk and maintenance of posture.
Describe the muscle of the abdominal wall including their innervation and blood supply
The outermost muscle layer is the:
External oblique
is found at the anteriolateral aspects of both sides of the cavity. Originates from ribs 5-12> anterior iliac crest and linea alba via a broad aponeurosis known as the rectus sheath.
Internal Oblique
Deep to the external oblique. thoracolumar fascia, iliac crest, 2/3 of inguinal lig. and pubic crest> ribs 10-12, linea alba and pubic crest. Both flex and rotate the trunk.
Transverse Abdominis
Deep to internal oblique. Thoracolcolumbar fascia, iliac crest, lateral 1/3 of the inguinal canal and ribs 7-12> linea alba and pubic cresr via conjoint tendon (formed by fibres of the internal oblique and transvers abdominis). Lined b transverse fascia.
Rectus Abdominis
Pubic crest and pubic synthesis> xiphoid process and 5th-7th costal cartilages. Seperated by tendonous intersections. (8). Flexes the trunk for sitting up and stabilizes the pelvis. Encosed in the rectus sheath
Cutaneous innervation T7-T12. The superior and inferior epigastric arteries lie posterior to rectus abdominis in the
rectus sheath
• Note that the linea alba is relatively devoid of blood vessels – avascular plane for
incisions.
Identify the key surface landmarks of the anterior abdominal wall
The key landmarks would be the linea alba which marks the midline of the abdominal cavity.
The umbilicus is also useful:
Above- the external oblique aponeurosis anterior, internal oblique aponeurosis divides –half anterior and half posterior
Transversus abdominis aponeurosis posterior.
Below- All 3 aponeurosis enter transverse fascia posterior.
Arcuate line demarcates a change in rectus sheath composition (into transverse fascia)
Describe the rectus sheath and its contents
Formed by aponeuroses
of the external and
internal oblique muscles
and transversus
abdominis
• Composition differs
above and below the
umbilicus (belly button)
Above- the external oblique aponeurosis anterior, internal oblique aponeurosis divides –half anterior and half posterior
Transversus abdominis aponeurosis posterior.
Below- All 3 aponeurosis enter transverse fascia posterior.
Give an acount of the inguinal canal including its boundaries and contents.
Inferior edge of external oblique aponeurosis attaches to the ASIS and the pubic tubercle • Inferior edge thickens and folds under to form a gutter – inguinal ligament • Aponeurosis of external oblique splits medial to the pubic tubercle to form the superficial inguinal ring • Allows the passage of the spermatic cord in males (round ligament of uterus in females) Starts at deep inguinal ring - an opening in the transversalis fascia • Passes through transversus abdominis, internal oblique and external oblique • Ends at superficial inguinal ring in external oblique aponeurosis
Discuss the anatomy of the inguinal canal in relation to inguinal hernias.
Anterior wall
External oblique aponeurosis
Lateral 1/3 reinforced by internal oblique muscle
Roof
Arching fibres of internal oblique and transversus abdominis muscles
Posterior wall
Transversalis fascia. Medial 1/3 reinforced by the conjoint tendon
Floor
Inguinal ligament
Note that reinforcement in the anterior and
posterior walls matches position of deep and superficial inguinal rings.
In a direct aquired inguinal hernia the bowel passes medial to the inferior epigastric vessels, pushing through the peritoneum and transversalis fascia in inguinal triangle to enter the inguinal canal.
In congenital inguinal hernias the bowel can pass lateral to the inferior epigastric vessels to enter the deep inguinal ring.
Give an account of the anatomy and innervation of the peritoneum including its reflections.
2 layers of serous membrane
(mesothelium) that are continuous with
each other
• Parietal layer covers the body wall
• Visceral layer surrounds internal organs
• Peritoneal cavity is a potential space
that only contains a thin film of fluid (5-
20 ml) between the visceral and parietal
layers.
Important for suspension of different organs to allow for GI motility.
An intraperitoneal organ is completely
covered by peritoneum
• A retroperitoneal organ lies posterior to
the peritoneum and is only partially
covered
• An infraperitoneal organ lies inferior to
the peritoneum and is only partially
covered
Mesentery – double layer of peritoneum that
connects an intraperitoneal organ to the
posterior abdominal wall e.g. small intestine
• Omentum – double layer of peritoneum that
extends from the stomach to another organ
e.g. greater omentum. It hangs like an apron from the greater curvature of the stomach and folds back to attach to the transverse colon. The greater omentum is highly mobile – often not located as depicted in diagrams
Multiple functions:
• Contains fat – insulation
• Contains milky spots – lymphoid tissue
• Policeman of the abdomen
• Peritoneal ligament – double layer of
peritoneum that attaches an organ to another
organ or the anterior abdominal
wall/diaphragm e.g. falciform ligament
Discuss how the anatomy of the peritoneal cavtiy relates to it’s embryological origins.
Derived from lateral plate mesoderm. Parietal layer of LP mesoderm= parietal peritoneum. Visceral layer of LP mesoderm= visceral peritoneum.
• 2 layers of LP mesoderm enclose intra-embryonic coelom = future serous cavities
• Visceral LP mesoderm surrounds gut tube
• Parietal LP mesoderm lines cavity wall. It is related to embryo folding stage.
Dorsal mesentery – from lower oesophagus to cloaca
• Ventral mesentery – from lower oesophagus to 1st part of duodenum
forms lesser omentum and falciform ligament.
The stomach rotates during wks 7/8 and subdivides into the peritoneal cavity. It rotates 90 degrees clockwise in a cranio-caudal axis creating space behind it- the lesser peritoneal sac (omental bursa). The remaining peritoneal cavity is now known as the greater sac. The epiploic foreman is the narrow opening that connects the greater and lesser sacs. The free ede of the lesser omentum contains the portal triad (hepatic artery, hepatic portal vein and bile duct).
Discuss the functions of the peritoneum and and relate these to diseased states.
Peritoneal adhesions:
Injured peritoneum can create
fibrotic adhesions with adjacent
intact peritoneum
• Fibrin is formed in response to the
injury
• Mesothelial cells can activate
degradation of fibrin to prevent
adhesions, however, requires a
delicate balance
• Imbalance in these mechanisms
leads to adhesions
• Most commonly occurs after surgery.
Peritoneal dialysis:
Peritoneum has a large surface area (1.8 m2
) and is a semipermeable membrane
• Can be used to filter excess water and waste products from blood in renal failure
• Dialysate is introduced into the peritoneal cavity where it comes into contact with
capillaries perfusing the peritoneum and viscera. Solutes diffuse from blood in the
capillaries into the dialysate
• A transmembrane pressure gradient is applied (osmotically) and results in
ultrafiltration of fluid from the capillaries into the dialysate
• Dialysate is then discarded
Give an account of the coverings of the spermatic cord within the inguinal canal.
These are derived from muscle layers of the abdominal wall • Transversus abdominis forms the internal spermatic fascia • Internal oblique muscle forms the cremasteric muscle • External oblique aponeurosis forms the external spermatic fascia
Discuss the differences in the peritoneum between males and females.
• The most inferior part of the peritoneal cavity is the rectouterine pouch (pouch of Douglas) in females and the rectovesical pouch in males • This is where fluid is most likely to accumulate when standing. The peritoneal cavity is continuous with the external environment in females but not males Continuity of uterine tubes with the peritoneal cavity can result in: • Retrograde menstruation • Abdominal pregnancies
Discuss the innervation of the peritoneum.
Parietal peritoneum has same innervation as the overlying body wall i.e. somatic
Visceral peritoneum has the same innervation as the organ is covers i.e. visceral
Somatic pain is sharp and well localised whereas visceral pain is dull and referred to the midline
(origin of gut tube)
Example – appendicitis first presents as dull pain in central abdomen (visceral peritoneum
affected) then localises as sharp pain in the right iliac fossa when parietal peritoneum is
inflamed
Give an account of the anatomical divisions of the liver including peritoneal reflections.
The liver is not completely covered by peritoneum. Has a diaphragmic and visceral surface. The peratoneal layers converge and form the ligaments which suspend the liver in the abdominal cavity. The coronary ligament surrounds the bare area of the liver • The anterior and posterior folds of the coronary ligament meet at left and right sides of the liver to form left and right triangular ligaments • The triangular ligaments attach the liver to the diaphragm • The peritoneum covering the left and right sides of the anterior surface meets to form the falciform (sickle-shaped) ligament • The falciform ligament attaches to the anterior abdominal wall and contains the round ligament of the liver. The falciform ligament divides the liver into a left and right anatomical lobes. There are also 2 lobes located in the central aspect of the posterior surface of the liver. These are the caudate and quadrate lobes and are formed by right and left saggital fissures. (these are joined by the porta hepatis.
Describe surface features and blood supply of the liver.
Can divide the surface of the liver into a diaphragmatic surface and a visceral surface • The diaphragmatic surface is smooth and shaped to fit the dome of the diaphragm • The falciform ligament is located on the diaphragmatic surface and used to divide the liver into left and right lobes The visceral surface of the liver features 2 sagittal fissures which are linked by the porta hepatis • The right sagittal fissure is the groove formed by the gallbladder anteriorly and the IVC posteriorly • The umbilical (left) sagittal fissure is formed by 2 ligaments – ligamentum venosum and the round ligament (remnants of foetal vessels) • The porta hepatis is the fissure through with neurovascular structures and lymphatics enter and leave the liver (except the hepatic veins). - Blood supply via the portal triad (Hepatic artery proper, hepatic portal vein, bile duct) At the porta hepatis: • the hepatic artery and hepatic portal vein enter the liver • the bile duct and lymphatics leave the liver All these structures are contained in the free edge of the lesser omentum. Most blood supply from vein not artery. Blood in the portal vein is partially deoxygenated as it has already supplied the gastrointestinal tract, however, it accounts for 50% of oxygen delivery to the liver (50% oxygen from hepatic artery) • The portal system* ensures nutrients from the GI tract are delivered to the liver for processing There are 3 hepatic veins that drain the liver directly to the IVC: • Right hepatic vein • Middle hepatic vein • Left hepatic vein These veins also help to anchor the liver in place The left hepatic vein lies in the same plane as the umbilical fissure The middle hepatic vein lies in the same plane as the right sagittal fissure.
Describe the difference between the anatomical lobe and functional sections of the liver and their importance.
4 anatomical lobes of the liver: • Left • Right • Caudate • Quadrate Functional lobes of the liver • The liver can be divided into left and right functional lobes • These are based on the primary division of the hepatic artery into left and right branches • Each functional lobe also receives a branch of the hepatic portal vein and is drained by its own hepatic duct • The left and right functional lobes are more equal in size than the anatomical lobes. - The functional lobes have their own blood supply which is useful in transplant. 4 anatomical lobes of the liver: • Left • Right • Caudate • Quadrate Functional lobes of the liver • The liver can be divided into left and right functional lobes • These are based on the primary division of the hepatic artery into left and right branches • Each functional lobe also receives a branch of the hepatic portal vein and is drained by its own hepatic duct • The left and right functional lobes are more equal in size than the anatomical lobes Due to its large blood spread the liver is a common site of cancer metastases through haematogenous spread – 70% from colorectal cancer • Can remove affected functional segment with minimal damage to blood supply and drainage of other segments
Give an account of liver cirrhosis and its effects on the circulatory system.
Liver Cirrhosis Common cause of liver failure and need for transplant • Caused by chronic damage to liver which eventually overcomes regenerative capabilities • Most common causes are alcohol and viral hepatitis B and C • Cirrhosis literally means scarring of the liver • Liver shrinks and compresses major blood vessels – bottle-neck Can lead to portal hypertention Not enough blood can pass through liver • Blood backs up into portal veins increasing pressure – portal hypertension • Blood has to find another way back to the IVC to get to the heart • There are some anastomoses between veins of the portal system and the systemic veins – porto-systemic anastomoses • These enlarge in response to high blood pressure
Describe the pathophysiology of
major liver diseases
Liver lobes can be divided into functional lobes called lobules. They have different functional zones which are vulnerable to different kinds of damage.
Zone 1
– Periportal – closest to hepatic triad
– Greatest supply of oxygen and
nutrients
– Most active in detoxification
– Most sensitive to oxidative injury
• Zone 2
– Can be recruited for detoxification
functions
• Zone 3
– Pericentral – closest to central vein
– Most sensitive to ischaemia
– Most active in bile synthesis
Hepatic Necrosis
• Defective osmotic regulation → cell swells
• Membrane blebs carry cytoplasmic contents
into ECF
• Macrophages cluster
• Cells burst and disappear
• Occurs in response to
– ischaemic injury
– oxidative stress
Hepatic Apoptosis
• Hepatocyte shrinkage
• Caspase cascades → nuclear chromatin
condensation (pyknosis) & fragmentation
(karyorrhexis), and cellular fragmentation into
acidophilic apoptotic bodies
• Occurs in
– Acute toxic or ischaemic injury
– Severe viral/autoimmune hepatitis
• → cirrhosis
Lost hepatocytes can be regenerated by mitotic
replication of adjacent hepatocytes
• Stem cells can be activated
• Stellate cells involved in scar formation (particularly in
alcoholic and non-alcoholic fatty liver diseases)
Lost hepatocytes can be regenerated by mitotic
replication of adjacent hepatocytes
• Stem cells can be activated
• Stellate cells involved in scar formation (particularly in
alcoholic and non-alcoholic fatty liver diseases)
Fibrous septa that subdivide the parenchyma into nodules
Liver failure.
Occurs when 80-90% functional capacity lost
• Acute
– Massive hepatic necrosis
– Often induced by drugs or toxins
– Hepatitis A or B infection
– Autoimmune
Decline of serum transaminases
– → multiorgan system failure and death
– Initially see nausea, vomiting and jaundice
– Followed by encephalopathy and coagulation
defects
Explain the symptoms of conditions
of the liver
Jaundice • Alteration of bile formation or flow • Retention of bilirubin • Yellowing of skin and sclera • Common in – Hepatitis – Alcoholic liver disease – Blockage of bile duct (gallstone or tumour) – Toxic reaction to drug Hepatic encephalopathy • Disease reduces liver’s ability to convert ammonia to urea • Accumulation of ammonia and other toxins in plasma • Crosses BBB → astrocytes • ↑ glutamine synthesis • → osmotic stress & oedema • Gradual decline in mental function Coagulopathy • Liver produces clotting factors • Impaired production → impaired clotting • Easy bruisability/fatal intracranial bleeding • Also removes activated coagulation factors from circulation • Disease can lead to disseminated intravascular coagulation Portal hypertension • Resistance to portal flow • Often caused by cirrhosis (resistance at level of sinusoids) • Can lead to – Ascites – Portosystemic venous shunts – Congestive splenomegaly – Hepatic encephalopathy Ascites • Accumulation of excess fluid in the peritoneal cavity • Sinusoidal hypertension → fluid enters space of Disse → removed by lymphatics → percolates into peritoneal cavity
Discuss the clinical assessment of
liver diseases
It is hard to spot early signs of liver disease during early onset. Some tests used are: • Bilirubin in circulation or urine • Serum albumin • Blood glucose and ammonia levels • Imaging tests • Histological examination of biopsy
What are the primary causes of liver disease?
Insults to liver can be metabolic, toxic, microbial, circulatory or neoplastic • Major Primary Diseases – Viral hepatitis – Nonalcoholic fatty liver disease (NAFLD) – Alcoholic liver disease – Hepatocellular carcinoma • Can occur secondary to – Heart failure – Disseminated cancer – Extrahepatic infections The most common causes of liver diseases are viral hepatitis B and C, alcohol missuse and NAFLD caused by obesity
Describe the difference in chronic an accute on chronic liver failure.
• Chronic
– Leading causes include chronic hepatitis B and C,
NAFLD and alcoholic liver disease
– Associated with cirrhosis
• Acute-on-chronic
– unrelated acute injury supervenes on a wellcompensated late-stage chronic disease
– or the chronic disease itself has a flare of activity
that leads directly to liver failure
Describe alcoholic liver disease.
Alcoholic Liver Disease • Alcohol metabolism disturbs other (CHO and fat) metabolic pathways • Fat accumulates in hepatocytes • Alcohol is metabolised to acetaldehyde, which binds to proteins in hepatocytes → inflammatory reaction • Stimulates collagen synthesis → fibrosis and cirrhosis Steatosis – fat globules in cytoplasm of liver cells – Reversible when alcohol consumption stops • Steatohepatitis – combination of fatty change, cell swelling and inflammation – Leads to cell death and fibrosis • Progressive architectural damage (fibrosis/cirrhosis)
Give an account of the functions of the GI tract.
The GI tract is systematically responsible for ingestion, mechanical digestion via chewing, churning and segmentation, Propulsion (Swallowing
(oropharynx), Peristalsis (esophagus, stomach, small intestine,large intestine), Chemical digestion, Absorption via lynph and blood vessels and defacation.
Describe the role of the sympathetic,
parasympathetic and enteric nervous systems in control of the gastrointestinal tract
When looking at control of the gut there is innervation from all 3 branches of the ANS. The Sympathetic and Parasympathetic are extrinsic and the Enteric is intrinsic. Sympathetic Preganglionic fibres originate in T8 – L2 region • Synapse in celiac, superior and inferior mesenteric ganglia • Generally decreases GI activity • Sensory component • Pain - Postganglionic sympathetic fibres act on sphincters, glandular tissue, arterial smooth muscle, intestinal smooth muscle, ENS neurones. Parasympathetic Vagus nerve (medulla oblongata) • Sacral spinal cord - last 1/3 of colon • Sensory components - Respond to stretch, temperature, osmolarity etc. - Participate in vagovagal reflexes • Motor components - Generally stimulatory - Secretion - motility - Acts on intestinal smooth muscle (+/-), Glandular tissues (+) and enteric neurones. Enteric nervous system “Mini brain” • Consists of 100-500 million neurones • Capable of operating independently • Integrates commands from parasympathetic and sympathetic fibres with sensory information from the gut Intrinsic Innervation of the Gut Bayliss and Starling 1900s • Complex 3D structure • Extends from oesophagus to anus • Develops from neural crest cells • Cell bodies arranged into ganglia • Ganglia arranged into two main plexuses - Myenteric nerve plexus in between the outer longetudinal and circular muscle - Submucosal nerve plexus within the mucosal layers.
Describe the secretion, targets and effects of important GI hormones.
Gastrin
- secreted by G-cells in stomach antrum
- ECL- cells: parietal cells
- stimulates the production of gastric acid
- enhanced mucosal growth
Secretin
- endocrine cells in small intestine
- Beta cells in pancreas.
- stimulates bicarbonate secretion, inhibits gastric acid and gastrin, inhibits gastric emptying, inhibited by somatostatin.
Motilin
- Endocrine cells in small intestine, smooth muscle of antrum and duedenum, migrating motor complex, effects acid in small intestines.
Describe myogenic control of the gut
Intrinsic control of smooth muscle (myogenic
control)
– intrinsic rhythmicity
– Interstitial cells of cajal
• GI smooth muscle has the ability to produce
two types of contraction
– Phasic: those lasting a matter of seconds with a
rapid onset and offset
– Tonic: a sustained contraction that generates tone
• Phasic
– Amplitude and duration vary from one location to
another
– May propogate in the oral or aboral direction or
may be the segmenting stationary type
• Tonic
– E.g. sphincter muscle
• Can be modified by hormones and nerves
Interstitial cells of cajal act like pace makers.
Discuss the myenteric plexus of the gut.
Auerbach’s plexus • Located between circular and longitudinal smooth muscle • Regularly arranged, densely packed ganglia • Polygonal network • Mainly motor neurones • Motor neurones mainly supply muscularis • Increased tone of gut wall • Increased intensity of rhythmical contractions • Slightly increased rate of contractions • Increased conduction velocity of gut wall • Inhibits sphincters
Discuss the submucosal plexus of the gut
Meissner’s plexus • Scattered throughout the submucosa • Loosely packed ganglia • Sensory and motor Local secretion • Local absorption • Local contraction of muscularis mucosae
Describe the embryological origins of the GI tract.
• The primitive gut tube is formed during embryonic folding and extends from the
oropharyngeal membrane to
the cloacal membrane
• It can be divided into 3 parts:
Foregut - mouth to 1st half duodenum
Midgut – 2nd half duodenumto 2/3 along transverse colon
Hindgut – distal 1/3 transverse colon to superior 2/3 anal canal
• The midgut is continuous with the yolk sac at the vitelline duct
The epithelial lining is derived from the endoderm
• The smooth muscle and connective tissue is derived from the surrounding
visceral mesoderm
• The visceral and parietal mesoderm also give rise to the visceral and parietal
peritoneum
• Note that the primitive gut tube is suspended from the posterior abdominal
wall by the dorsal mesentery
Dorsal mesentery carries 3 arteries that supply the GIT
Foregut – Coeliac trunk
Midgut – superior mesenteric artery
Hindgut – inferior mesenteric artery
Describe the development of the stomach
• The stomach appears in the 4th week as a dilation of the foregut
• It is suspended in the abdomen by the dorsal and ventral mesenteries
• Differential growth in week 5 forms the greater curvature i.e. the dorsal wall
grows faster
In weeks 7-8, the stomach underdoes rotation
• 90° clockwise rotation around the craniocaudal axis causes the lesser curvature to
move from ventral position to the right.
• Similarly the greater curvature moves from dorsal position to the left
• The vagus nerves are initially located on left and right sides of the gut tube but are
also rotated such that the left vagus trunk becomes anterior and the right becomes
dorsal
Give an account of the herniation and rotation of the midgut and relate this to congenital malformations.
Midgut – 2nd half duodenum to 2/3 along transverse colon
• The midgut is continuous with the yolk sac at the vitelline duct
• During week 5, the midgut and associated dorsal mesentery undergo rapid
elongation to form the primary intestinal loop which communicates with the yolk
sac through the vitelline duct
• The primary intestinal loop has cranial and caudal limbs
• The cranial limb will form: distal duodenum, jejunum and proximal ileum
• The caudal limb will form: distal ileum, caecum, appendix, ascending colon and
proximal 2/3 transverse colon
During week 6, there is rapid elongation of the midgut and growth of the liver
• There is not enough room in the abdomen, therefore, the primary intestinal loop herniates into the umbilical cord
• As herniation occurs, the midgut also rotates 90° anticlockwise bringing the cranial limb to the right and the caudal limb to the left
• Jejunoileal loops form In week 10, the midgut returns to the abdomen and rotates a further 180° anti-clockwise
• This brings the proximal jejunal
loops to the left side and the
caecum lies inferior to the liver
• The caecum develops a wormlike
diverticulum – vermiform appendix
• The vitilline duct is also obliterated
during this process.
• The midgut has completely returned
to the abdomen by week 11 and has
undergone 270° anti-clockwise
rotation in total
Gut rotation malfunctions-
Gut undergoes initial 90° anti-clockwise rotation but fails to rotate a further 180°
when the gut is retracted
• Results in small intestine on the right side and large intestine on the left (left
sided colon)
• Usually asymptomatic
Reversed rotation- Initial 90° anticlockwise rotation occurs normally, however, gut the rotates 180°
clockwise • Total rotation results in 90° clockwise instead of 270° anti-clockwise • Gut enters abdomen in correct order except duodenum lies ventral to transverse colon Abnormal Rotation of the Midgut and Volvulus • Abnormal rotation of the midgut can cause parts that would normally be retroperitoneal (e.g. duodenum) to remain suspended by dorsal mesentery • This can lead to volvulus (twisting) of the midgut. • Volvulus causes acute obstruction of the bowel and bilious vomiting • Volvulus may also constrict arterial supply to the gut causing ischaemia and infarction
Describe partitioning of the cloaca and the formation of the anal canal
Once the midgut has returned to the abdomen, the caecum descends from below
the liver to the right iliac fossa
• This pulls the ascending and transverse colon into place resulting in the final
arrangement of the midgut
• The dorsal mesentery of the ascending and descending colons now shortens and
degenerates pulling them against the posterior abdominal wall – secondarily
retroperitoneal
Describe the origins of the enteric nervous system and explain the effects of the failure of migration in neural crest cells.
The GIT is innervated by the enteric nervous system (division of autonomic nervous system)
There are 2 enteric plexi:
Myenteric (Auerbach’s) plexus between the circular and longitudinal muscle layers
co-ordinates muscle contraction
Submucosal (Meissner’s) plexus between the circular muscle and mucosa and regulates secretion
The enteric nervous system is derived from neural crest cells (ectoderm origin) that migrate from neural tube to GIT
Hirschsprung Disease/Congenital Aganglionic
Megacolon
• Failure of neural crest cells to
migrate to intestine
• Absence of enteric ganglia leads to
bowel obstruction due to lack of peristalsis
• This causes dilation of the
aganglionic part of the intestine –
usually rectum and sigmoid colon
• Genetic condition most commonly
associated with trisomy 21
Explain GI motility.
The gut wall has a highly sophisticated control and several layers (absorptive cells in the lumen, neural and muscular components. Blood and lymph vasculature for transport). Coordinated contractile activity.
Propulsion via coordinated progressive contractions, mixing by segmentation. Influenced by the enteric nervous system, peptide hormones and inherint myocyte timing.
Involves migrating motor complex which works on local areas of peristaltic contraction. Present in the interdigestive period and dissapear when feeding begins.
Sweep material into the colon t keep the intestine clean.
Regulated by autonomic nerves and by the release of motilin.
