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GIT System Masterclass Lecture 01: Embryology Lecture 02: Anatomy Lecture 03: Physiology Lecture 04: Pathology Lecture 05: Medicine Lecture 06: Surgery Lecture 07: Pharmacology Welcome to MedPro Education’s GIT Masterclass—your complete guide to the gastrointestinal system for medical students and future doctors! In this episode, we break down gastrointestinal embryology in a clear, visual, and exam-focused way, perfect for NLE, FCPS, USMLE, FMGE, PLAB, and other MBBS professional exams. 📚Study smarter, not harder—this episode uses visual memory aids, clinical correlations, and concise narration to help you retain key concepts for your exams and clinical practice. 📩 Contact for notes & lectures: hafizzain64@gmail.com #GITEmbryology #MedicalLectures #USMLE #NLE #FMGE #MedProEducation #Anatomy #Pediatrics #Surgery

Transcript

00:00Welcome to MedProEducation's GIT Masterclass, your complete guide to the gastrointestinal

00:07system. We've structured this series into six key sections, embryology, anatomy, physiology,

00:15pathology, medicine and surgery, and pharmacology. Let's begin with the most fundamental,

00:21gastrointestinal embryology. The GI tract arises from a primitive gut tube divided into foregut,

00:29mid-gut, hindgut. Foregut structures range from the esophagus to the duodenum at the level of the

00:36ampulla of vader. Here, the pancreatic duct and common bile duct drain. The midgut begins from

00:42the lower duodenum to the proximal two-thirds of the transverse colon. In the sixth week,

00:48the midgut herniates into the umbilical cord. By the 10th week, it returns and rotates 270 degrees

00:56counterclockwise around the superior mesenteric artery, SMA. The hindgut stretches from the distal

01:04third of the transverse colon to the upper anal canal, ending above the pectinate line.

01:10To fully understand GI embryology, you must know its vascular supply because many congenital and

01:17surgical conditions relate directly to these arteries. The blood supply of the gastrointestinal

01:23tract arises from three major arteries branching off the abdominal aorta, the celiac trunk at the

01:31level of T12 to L1, the superior mesenteric artery at L1, and the inferior mesenteric artery at L3.

01:42The foregut, including the esophagus, stomach, liver, pancreas, and upper duodenum,

01:49is supplied by the upper trunk, the celiac artery. The midgut, from the lower duodenum to the proximal

01:58two-thirds of the transverse colon, is supplied by the middle trunk, the superior mesenteric artery,

02:06or SMA. And the hindgut, from the distal third of the transverse colon to the upper anal canal,

02:15receives blood from the lower trunk, the inferior mesenteric artery, or IMA. These three arteries

02:24arise sequentially from the abdominal aorta and act as landmarks for both embryology and surgery.

02:31Many congenital anomalies, like midgut malrotation or volvulus, are centered around the SMA,

02:38the axis of gut rotation. During embryonic development, the ventral body wall forms

02:46through the coordinated folding of three regions, the rostral, head fold, the caudal, tail fold,

02:54and the lateral folds. Failure of these folds to close properly leads to ventral wall defects,

03:01which include gastroschisis, a right-sided abdominal wall defect, where bowel loops herniate without any

03:11covering membrane. The intestines are exposed directly to the amniotic fluid, leading to inflammation

03:18and damage. Umphilosoli, a central abdominal wall defect, where the intestines and sometimes liver

03:26herniate through the umbilical ring. These organs are covered by peritonium and amnion, forming a visible

03:34sac, both present as visible herniation at birth, but they differ in location, covering, and clinical

03:42implications. Ectopia cortis, caused by failure of the rostral fold to close, leaving the heart exposed

03:50outside the chest. Bladder extrophy, due to failure of the caudal fold to close, resulting in the bladder

03:58protruding from the lower abdomen. These conditions highlight the importance of precise embryonic

04:04folding during early development. Next, we explore tracheoesophageal anomalies, which result from

04:11incomplete separation of the trachea and esophagus during forehead development. The most common anomaly

04:19is esophageal atresia with distal tracheoesophageal fistula, TEF. In this condition, the upper esophagus

04:28ends in a blind pouch, while the lower segment forms an abnormal connection with the trachea.

04:35There is no connection between upper and lower esophagus. Clinically, newborns present with

04:41excessive salivation, choking after first feeding, coughing during feeding, cyanosis or bluish

04:50discoloration, inability to pass a nasogastric tube into the stomach. This is a neonatal emergency

04:59and must be identified early. Intestinal atresia is a congenital absence or closure of part of the

05:06intestinal tract. The two main types are duodenal atresia, due to failure of recanalization.

05:16It is classically associated with Down syndrome, Trisomy 21.

05:22On x-ray, you'll see the classic double bubble sign, air in the stomach and proximal duodenum

05:29with no gas beyond. Jejunal and ileal atresia result from vascular accidents in utero, causing ischemic

05:38necrosis and segmental bowel loss. Atresia often presents shortly after birth with bilious vomiting,

05:48abdominal distension, and failure to pass meconium. Hypertrophic pyloric stenosis is caused by thickening

05:56of the pyloric muscle, leading to obstruction of gastric emptying. It typically occurs in first-born males

06:05and presents between two to six weeks of age. Key clinical signs include projectile non-bilious vomiting,

06:15palpable olive-shaped mass in the epigastric area, visible gastric peristalsis moving from left to right.

06:23On ultrasound, the pyloric muscle appears elongated and thickened. Surgical correction with

06:31pyloromyotomy is curative. Next is pancreatic abnormalities. The pancreas forms from two buds,

06:40a ventral bud and a dorsal bud. Fusion of these buds and their ducts forms the adult pancreas.

06:48Two major anomalies include annular pancreas, where pancreatic tissue encircles the duodenum,

06:56leading to obstruction or vomiting in newborns. Pancreas divisum, where the dorsal and ventral

07:05ducts fail to fuse. This can predispose patients to recurrent pancreatitis. You can see in the image

07:13that a normal pancreas has a main pancreatic duct, while a divisum of dorsal and ventral

07:19ducts. Unlike the pancreas, the spleen develops from mesoderm in the dorsal mesogastrium and is

07:27not derived from the gut tube. Let's quickly recap the key points of GI embryology and congenital

07:34anomalies. Foregut, esophagus to ampulla of vater, midgut, lower duodenum to two-thirds transverse

07:44colon and 270-degree rotation. Hingut, distal colon to upper anal canal. Blood supply, celiac, SMA,

07:54and IMA. Congenital anomalies includes omphalocaly and gastroschisis, tracheoesophageal fistula,

08:02choking after food, duodenal, jejunal, ileal atricius, vomiting after food containing bile,

08:11hypertrophic pyloric stenosis, persistent non-bilious vomiting, invisible peristalsis,

08:18annular pancreas and pancreas divisum, cause of adult pancreatitis, spleen from mesoderm,

08:26not endoderm. These concepts are frequently tested and critical for clinical reasoning.

08:32In our next episode, we'll explore the high-yield anatomy of the GIT system.

08:39Join us today and take the first step towards success.

Gastrointestinal System | Embryology | Lecture 01 | High Yield Dr. Zain's Notes

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