Pancreas development US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Pancreas development. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Pancreas development US Medical PG Question 1: A new mother expresses her concerns because her 1-day-old newborn has been having feeding difficulties. The child vomits after every feeding and has had a continuous cough since shortly after birth. The mother denies any greenish coloration of the vomit and says that it is only composed of whitish milk that the baby just had. The child exhibits these coughing spells during the exam, at which time the physician notices the child’s skin becoming cyanotic. The mother states that the child was born vaginally with no complications, although her records show that she had polyhydramnios during her last ultrasound before the delivery. Which of the following is the most likely cause of the patient’s symptoms?
- A. Failure of recanalization of duodenum
- B. Obstruction due to failure of rotation of pancreatic tissue
- C. Hypertrophy of the pyloric sphincter
- D. Failure of neural crest cells to migrate into the myenteric plexus
- E. Defective formation of the esophagus with tracheoesophageal connection (Correct Answer)
Pancreas development Explanation: ***Defective formation of the esophagus with tracheoesophageal connection***
- The combination of **feeding difficulties**, vomiting of **undigested milk**, **continuous coughing**, and **cyanosis** during coughing spells in a newborn strongly suggests a **tracheoesophageal fistula (TEF)**, often with **esophageal atresia**.
- **Polyhydramnios** during pregnancy is a classic prenatal sign due to the fetal inability to swallow amniotic fluid.
*Failure of recanalization of duodenum*
- This condition, known as **duodenal atresia**, typically presents with **bilious vomiting** if the obstruction is distal to the ampulla of Vater, or non-bilious if proximal, but typically does not cause continuous coughing or cyanosis during feeds.
- While it causes vomiting, it primarily affects digestion and nutrient absorption, and **polyhydramnios** can also be present due to impaired fetal swallowing.
*Obstruction due to failure of rotation of pancreatic tissue*
- This describes **annular pancreas**, where pancreatic tissue encircles the duodenum, causing obstruction and **vomiting** (often bilious).
- Like duodenal atresia, it doesn't explain the characteristic **coughing and cyanosis** with feeds seen in this case.
*Hypertrophy of the pyloric sphincter*
- **Pyloric stenosis** typically presents later (2-8 weeks of age) with **projectile non-bilious vomiting**, and an **olive-shaped mass** may be palpable in the abdomen.
- It does not cause coughing or cyanosis that correlates directly with feeding in a 1-day-old.
*Failure of neural crest cells to migrate into the myenteric plexus*
- This describes **Hirschsprung disease**, which primarily affects the colon and presents with symptoms of **intestinal obstruction** (e.g., abdominal distension, failure to pass meconium, bilious vomiting if severe).
- It is not associated with feeding difficulties, coughing, or cyanosis in the manner described.
Pancreas development US Medical PG Question 2: A 4-week-old infant is brought to the emergency department by his parents with violent vomiting. It started about 3 days ago and has slowly gotten worse. He vomits after most feedings but seems to keep some formula down. His mother notes that he is eager to feed between episodes and seems to be putting on weight. Other than an uncomplicated course of chlamydia conjunctivitis, the infant has been healthy. He was born at 39 weeks gestation via spontaneous vaginal delivery. He is up to date on all vaccines and is meeting all developmental milestones. The physical exam is significant for a palpable mass in the right upper quadrant. What is the first-line confirmatory diagnostic test and associated finding?
- A. Abdominal ultrasound; elongated pyloric channel and muscle hypertrophy (Correct Answer)
- B. Barium upper GI series; GE junction and portion of the stomach in thorax
- C. Air enema; filling defect and coil spring sign
- D. Barium upper GI series; bird beak sign and corkscrewing
- E. Abdominal X-ray; ‘double bubble’ sign
Pancreas development Explanation: ***Abdominal ultrasound; elongated pyloric channel and muscle hypertrophy***
- The clinical picture of **projectile vomiting** in a 4-week-old infant, **eagerness to feed** ("hungry vomiter"), and **palpable olive-shaped mass** in the right upper quadrant is classic for **pyloric stenosis**.
- **Abdominal ultrasonography** is the gold standard for diagnosis, revealing an **elongated pyloric channel** (>16mm) and thickened pyloric muscle (>3-4mm).
- Pyloric stenosis typically presents between 3-6 weeks of age with progressive non-bilious vomiting.
*Barium upper GI series; GE junction and portion of the stomach in thorax*
- A **barium upper GI series** showing the **GE junction and stomach in the thorax** would indicate a **hiatal hernia**, which is not consistent with the palpable mass or "hungry vomiter" presentation.
- While hiatal hernias can cause vomiting and reflux, they typically don't present with this specific type of projectile vomiting or a palpable abdominal mass.
*Air enema; filling defect and coil spring sign*
- An **air enema** showing a **filling defect** and **coil spring sign** is characteristic of **intussusception**, which usually presents with sudden onset of **crampy abdominal pain**, **currant jelly stools**, and a palpable mass in the right lower quadrant.
- The clinical presentation does not fit intussusception, which typically occurs in older infants (6-36 months) and has a more acute presentation.
*Barium upper GI series; bird beak sign and corkscrewing*
- A **barium upper GI series** showing a **bird beak sign** and **corkscrewing** is pathognomonic for **midgut volvulus**, a surgical emergency.
- While volvulus can cause bilious vomiting and abdominal distension, the presentation of non-bilious vomiting with a palpable pyloric mass is more typical of pyloric stenosis.
*Abdominal X-ray; 'double bubble' sign*
- An **abdominal X-ray** revealing a **'double bubble' sign** is indicative of **duodenal atresia** or **annular pancreas**, leading to complete duodenal obstruction.
- This condition typically presents with **bilious vomiting** shortly after birth (within first day of life) and does not involve a palpable hypertrophied pylorus.
Pancreas development US Medical PG Question 3: During development, a fetus is found to have incomplete fusion of the neural tube. Which of the following structures would most likely be affected by this developmental defect?
- A. Notochord
- B. Somites
- C. Vertebral bodies
- D. Spinal cord and meninges (Correct Answer)
Pancreas development Explanation: ***Spinal cord and meninges***
- Incomplete fusion of the neural tube directly results in defects of the **neural tube closure**, which include the formation of the **spinal cord** and its protective coverings, the **meninges**. [1, 2]
- Conditions like **spina bifida** (meningocele, myelomeningocele) are direct consequences of these fusion failures, exposing or abnormally developing the spinal cord and meninges. [1, 2]
*Notochord*
- The **notochord** is a transient embryonic structure that induces the formation of the neural tube by signaling to the overlying ectoderm; it is not directly formed by the neural tube itself.
- While it plays a critical role in neural tube development, its own structural integrity is typically not primarily affected by neural tube fusion defects.
*Somites*
- **Somites** are blocks of paraxial mesoderm that differentiate into sclerotome (vertebrae and ribs), myotome (skeletal muscle), and dermatome (dermis of the skin).
- While somite development is closely coordinated with neural tube formation, incomplete neural tube fusion primarily affects the neural structures themselves, not the somites directly.
*Vertebral bodies*
- **Vertebral bodies** develop from the sclerotome portion of the somites, which migrate to surround the neural tube and notochord.
- While vertebral defects can be associated with severe neural tube defects (e.g., in spina bifida, the vertebral arches may fail to close), the primary defect of incomplete neural tube fusion directly impacts the neural tissue (spinal cord and meninges), with skeletal defects being secondary or associated. [1, 2]
Pancreas development US Medical PG Question 4: A 10-month-old infant is brought in by his parents because he is vomiting and not passing stool. His parents say he has vomited multiple times over the past couple of hours, but the most recent vomit was green. The patient has no significant past medical history. On physical examination, the patient is irritable and crying. On palpation in the periumbilical region, an abdominal mass is present. Emergency laparotomy is performed, which shows a part of the patient’s intestine folded into the section adjacent to it. Which of the following is the most likely diagnosis for this patient?
- A. Pyloric stenosis
- B. Hirschsprung’s disease
- C. Duodenal atresia
- D. Intussusception (Correct Answer)
- E. Meckel’s diverticulum
Pancreas development Explanation: ***Intussusception***
- This diagnosis is highly suggested by the classic presentation of a 10-month-old infant with **bilious vomiting**, **abdominal pain** (irritability), and an **abdominal mass** in the periumbilical region, coupled with the surgical finding of one part of the intestine telescoping into an adjacent section.
- The sudden onset of symptoms in an otherwise healthy infant, along with **green vomit** (indicating bile) and an acute abdomen, are hallmark signs of this condition.
*Pyloric stenosis*
- This condition typically presents with **non-bilious projectile vomiting** in infants usually between 3 weeks and 6 months of age, with an **olive-shaped mass** in the epigastrium.
- The patient's **bilious vomiting** and the specific finding of intestinal telescoping rule out pyloric stenosis.
*Hirschsprung’s disease*
- This condition usually presents with **failure to pass meconium** in the neonatal period or chronic constipation and abdominal distension in older infants.
- While it involves the intestine, it is a **motility disorder** due to the absence of ganglion cells, not an anatomical telescoping of bowel.
*Duodenal atresia*
- This is a congenital obstruction of the duodenum, typically diagnosed shortly after birth with **bilious vomiting** and a characteristic "**double bubble**" sign on X-ray.
- It would not involve an abdominal mass or the intussusception described.
*Meckel’s diverticulum*
- This condition is a remnant of the vitelline duct and can present with painless rectal bleeding or, less commonly, intestinal obstruction, **volvulus**, or **intussusception** if it acts as a lead point.
- While it can be a rare cause of intussusception, the question directly describes the pathophysiology of intussusception itself rather than a diverticulum causing it.
Pancreas development US Medical PG Question 5: A 60-year-old gentleman passes away after a car accident. On routine autopsy it is incidentally noted that he has both a ventral and dorsal pancreatic duct. This incidental finding observed by the pathologist is generated due to failure of which of the following embryological processes?
- A. Apoptosis
- B. Stem cell differentiation
- C. Notochord signaling
- D. Neural crest cell migration
- E. Fusion (Correct Answer)
Pancreas development Explanation: ***Fusion***
- The pancreas develops from a **ventral and a dorsal bud** that typically **fuse** during development.
- Failure of these two pancreatic buds (and their associated ducts) to completely fuse can result in **pancreas divisum**, where two separate ductal systems persist, corresponding to the dorsal and ventral pancreatic ducts.
*Apoptosis*
- **Apoptosis** (programmed cell death) is crucial for the removal of unwanted cells and sculpting tissues during embryogenesis, such as the formation of digits or the regression of certain structures.
- It does not directly explain the persistence of two separate pancreatic ducts due to non-fusion of developmental buds.
*Stem cell differentiation*
- **Stem cell differentiation** is the process by which less specialized stem cells become more specialized cell types, which is fundamental to organ development and tissue formation.
- While essential for pancreatic development, it doesn't specifically account for the anatomical anomaly of two persistent ducts.
*Notochord signaling*
- **Notochord signaling** is vital for inducing the formation of the neural tube and defining the dorsal-ventral axis of the embryo, as well as influencing the development of other nearby structures.
- This process is not directly related to the fusion of pancreatic buds, which occurs later and is influenced by interactions between mesenchymal and endodermal tissues.
*Neural crest cell migration*
- **Neural crest cells** are multipotent cells that migrate extensively throughout the embryo to form a wide variety of tissues, including parts of the peripheral nervous system, melanocytes, and bone/cartilage of the face and skull.
- Their migratory pathways and derivatives are not directly involved in the development and fusion of the pancreatic ductal system.
Pancreas development US Medical PG Question 6: A 55-year-old man comes to the physician because of a 3-week history of intermittent burning epigastric pain. His pain improves with antacid use and eating but returns approximately 2 hours following meals. He has a history of chronic osteoarthritis and takes ibuprofen daily. Upper endoscopy shows a deep ulcer located on the posterior wall of the duodenal bulb. This ulcer is most likely to erode into which of the following structures?
- A. Splenic vein
- B. Descending aorta
- C. Pancreatic duct
- D. Gastroduodenal artery (Correct Answer)
- E. Transverse colon
Pancreas development Explanation: ***Gastroduodenal artery***
- A deep ulcer on the **posterior wall of the duodenal bulb** is anatomically very close to the **gastroduodenal artery**.
- Erosion into this artery can lead to **life-threatening upper gastrointestinal bleeding**, a severe complication of peptic ulcer disease.
*Splenic vein*
- The **splenic vein** is located more posteriorly and superiorly, primarily in relation to the pancreas and spleen, making it less likely to be eroded by a duodenal bulb ulcer.
- While erosion into major vessels can occur, the gastroduodenal artery is in a much more direct and immediate proximity to the posterior duodenal bulb.
*Descending aorta*
- The **descending aorta** is a retroperitoneal structure located much more posteriorly and medially, far from the duodenal bulb.
- Erosion into the aorta is an extremely rare and catastrophic event, not typically associated with duodenal ulcers.
*Pancreatic duct*
- The **pancreatic duct** (Wirsung's duct) is located within the pancreas, which lies posterior to the duodenum. While a *deep* ulcer could hypothetically penetrate the pancreas, the primary structure at risk for hemorrhage from a posterior duodenal bulb ulcer is the gastroduodenal artery.
- Erosion into the pancreatic duct would likely cause **pancreatitis** or **fistula formation**, rather than acute hemorrhage.
*Transverse colon*
- The **transverse colon** is located inferior to the duodenum, separated by the greater omentum.
- Ulcers would typically erode anteriorly or directly posteriorly, not inferiorly into the transverse colon, which would involve fistula formation rather than arterial erosion.
Pancreas development US Medical PG Question 7: A 4-week-old infant presents with progressively worsening jaundice. Laboratory studies show direct hyperbilirubinemia, elevated gamma-glutamyl transferase, and pale stools. Liver biopsy shows bile duct proliferation and portal fibrosis. Intraoperative cholangiogram reveals absence of extrahepatic bile ducts with normal intrahepatic ducts proximally. The gallbladder is present but atretic. Synthesize the embryological timing and pathophysiological mechanism of this postnatal progressive condition.
- A. Failure of recanalization of solid bile duct stage at week 6-7 with progressive inflammation
- B. Defective hepatic diverticulum formation from foregut at week 4 causing ductal absence
- C. Perinatal inflammatory obliterative cholangiopathy affecting extrahepatic ducts after normal formation (Correct Answer)
- D. Abnormal neural crest cell migration affecting bile duct innervation and motility
- E. Congenital cytomegalovirus causing intrauterine ductal destruction at week 12
Pancreas development Explanation: ***Perinatal inflammatory obliterative cholangiopathy affecting extrahepatic ducts after normal formation***
- **Biliary atresia** is currently understood as a progressive, **acquired inflammatory** process that obliterates ducts that were initially formed correctly during embryogenesis.
- The clinical presentation of **progressive jaundice**, **pale (acholic) stools**, and **direct hyperbilirubinemia** appearing after birth supports a perinatal insult rather than an embryonic malformation.
*Failure of recanalization of solid bile duct stage at week 6-7 with progressive inflammation*
- This describes the **"tandem" theory** or failure of the solid stage, which typically results in more severe embryonic-type atresia often associated with other **congenital anomalies** (situs inversus).
- Most cases of biliary atresia do not show a failure of recanalization, as clinical evidence suggests the ducts were functional for a period in utero.
*Defective hepatic diverticulum formation from foregut at week 4 causing ductal absence*
- A defect in the **hepatic diverticulum** would result in total **agenesis** of the biliary system and potentially the liver parenchyma, not a localized postnatal obstruction.
- In this case, the **intrahepatic ducts** are normal and the gallbladder is present, which contradicts a primary defect in early foregut budding.
*Abnormal neural crest cell migration affecting bile duct innervation and motility*
- **Neural crest cell** migration defects are classically associated with **Hirschsprung disease** (affecting the enteric nervous system), not the structural obliteration of bile ducts.
- Biliary atresia involves mechanical **fibrosis and obstruction** of the lumen, rather than a primary disorder of biliary tree motility or innervation.
*Congenital cytomegalovirus causing intrauterine ductal destruction at week 12*
- While some viral triggers (like **Reovirus** or Rotavirus) are suspected in the inflammatory process, **Cytomegalovirus (CMV)** typically causes a neonatal hepatitis rather than isolated extrahepatic ductal obliteration.
- Intrauterine destruction at week 12 would likely present with symptoms immediately at birth, whereas this infant showed **progressive worsening** over 4 weeks.
Pancreas development US Medical PG Question 8: A newborn presents with respiratory distress immediately after birth. Chest radiograph shows bowel loops in the left hemithorax with mediastinal shift to the right and hypoplastic left lung. The infant has scaphoid abdomen. During fetal ultrasound at 9 weeks, normal diaphragm development was noted, but at 20 weeks, abdominal contents were seen in the chest. Evaluate the critical developmental period and mechanism of lung hypoplasia.
- A. Failure of pleuroperitoneal membrane closure at week 6 with subsequent lung compression during canalicular phase
- B. Premature return of midgut at week 8 causing diaphragmatic rupture and lung compression
- C. Late diaphragmatic defect at week 20 preventing normal pseudoglandular phase lung development
- D. Defective muscularization of diaphragm after week 12 with gradual herniation and lung hypoplasia (Correct Answer)
- E. Failure of septum transversum formation at week 4 preventing lung bud elongation
Pancreas development Explanation: ***Defective muscularization of diaphragm after week 12 with gradual herniation and lung hypoplasia***
- In this specific case, a normal diaphragm at 9 weeks followed by herniation at 20 weeks indicates a **secondary defect** in **muscularization** rather than a primary failure of pleuroperitoneal membrane closure.
- The resulting **herniation of abdominal contents** into the thorax compresses the developing lung, leading to **pulmonary hypoplasia** and the classic **scaphoid abdomen** presentation.
*Failure of pleuroperitoneal membrane closure at week 6 with subsequent lung compression during canalicular phase*
- This describes the **Bochdalek hernia**, but the timeline provided (normal at 9 weeks) contradicts a primary closure failure occurring at **week 6**.
- While it causes lung compression, the most critical damage to **bronchial branching** occurs during the **pseudoglandular phase** (weeks 5-17), not just the canalicular phase.
*Premature return of midgut at week 8 causing diaphragmatic rupture and lung compression*
- The **midgut hernia** normally returns to the abdomen around **week 10**, so a return at week 8 would be premature and does not cause **diaphragmatic rupture**.
- Diaphragmatic defects are developmental failures of specific components (septum transversum, membranes, or muscle), not a result of **mechanical rupture** from gut movement.
*Late diaphragmatic defect at week 20 preventing normal pseudoglandular phase lung development*
- The **pseudoglandular phase** occurs between **weeks 5 and 17**; a defect appearing at week 20 would be too late to disrupt this critical stage of **branching morphogenesis**.
- Most cases of **congenital diaphragmatic hernia (CDH)** that result in severe hypoplasia involve a defect present prior to the completion of the pseudoglandular stage.
*Failure of septum transversum formation at week 4 preventing lung bud elongation*
- The **septum transversum** primarily forms the **central tendon** of the diaphragm and its failure would present as a much earlier, more catastrophic defect.
- **Lung bud elongation** begins at week 4, but the scenario describes a fetus with normal early development confirmed by **ultrasound at 9 weeks**.
Pancreas development US Medical PG Question 9: A 2-year-old child presents with painless rectal bleeding. A Meckel scan using technetium-99m pertechnetate shows increased uptake in the right lower quadrant, 60 cm from the ileocecal valve. At surgery, a 5 cm diverticulum is found on the antimesenteric border containing heterotopic gastric mucosa. Evaluate the embryological remnant and the developmental principle explaining the heterotopic tissue.
- A. Persistent vitelline duct with pluripotent endodermal cells capable of gastric differentiation (Correct Answer)
- B. Incomplete obliteration of the allantois with metaplastic transformation
- C. Abnormal neural crest cell migration producing ectopic gastric tissue
- D. Defective fusion of lateral body folds trapping gastric primordium
- E. Persistent omphalomesenteric artery supplying misplaced foregut tissue
Pancreas development Explanation: ***Persistent vitelline duct with pluripotent endodermal cells capable of gastric differentiation***
- **Meckel diverticulum** results from the failure of the **vitelline duct** (omphalomesenteric duct) to obliterate, typically located on the **antimesenteric border** of the ileum.
- The **heterotopic gastric mucosa** arises because the **pluripotent endodermal** lining of the duct can undergo differentiation into gastric or pancreatic tissue, explaining the **technetium-99m** uptake.
*Incomplete obliteration of the allantois with metaplastic transformation*
- Failure of the **allantois** to obliterate results in a **urachal duct** or cyst, which connects the bladder to the umbilicus.
- This would typically present with urinary symptoms or drainage at the **umbilicus**, not rectal bleeding or midgut diverticula.
*Abnormal neural crest cell migration producing ectopic gastric tissue*
- **Neural crest cells** are essential for the formation of the **enteric nervous system** and the myenteric plexus.
- Defects in their migration lead to **Hirschsprung disease**, characterized by an aganglionic segment of colon rather than heterotopic mucosa.
*Defective fusion of lateral body folds trapping gastric primordium*
- Abnormal **lateral body fold** fusion results in ventral wall defects like **gastroschisis** or **omphalocele**.
- This developmental process is not related to the internal formation of the **vitelline duct** remnants or ectopic gastric tissue.
*Persistent omphalomesenteric artery supplying misplaced foregut tissue*
- While the **superior mesenteric artery** (derived from the omphalomesenteric artery) supplies Meckel diverticulum, the tissue itself is not "misplaced foregut."
- The presence of the tissue is due to local **differentiation** of pluripotent cells, not the mechanical migration of the **foregut primordium** to the midgut.
Pancreas development US Medical PG Question 10: An infant presents with drooling, coughing with feeds, and inability to pass a nasogastric tube beyond 10 cm. Chest radiograph shows the NG tube coiled in the upper esophagus and gas in the stomach and bowel. Bronchoscopy reveals a fistula between the distal esophagus and trachea. Analyze the embryological partitioning defect that produced this most common variant.
- A. Posterior deviation of tracheoesophageal septum during foregut division at week 4-5 (Correct Answer)
- B. Anterior deviation of tracheoesophageal septum with failure of esophageal recanalization
- C. Defective lateral fusion of esophageal folds creating persistent communication
- D. Abnormal neural crest cell contribution to aorticopulmonary septum affecting foregut
- E. Excessive apoptosis of esophageal epithelium during solid cord stage
Pancreas development Explanation: ***Posterior deviation of tracheoesophageal septum during foregut division at week 4-5***
- This case describes **esophageal atresia (EA) with a distal tracheoesophageal fistula (TEF)**, the most common variant, caused by posterior deviation of the **tracheoesophageal septum**.
- The **coiled NG tube** confirms atresia, while the **gas in the stomach** indicates air passing from the trachea into the distal esophagus via the fistula.
*Anterior deviation of tracheoesophageal septum with failure of esophageal recanalization*
- While deviation of the septum is the mechanism, **anterior deviation** would logically impinge upon the trachea rather than the esophagus.
- Failure of **recanalization** (occurring in weeks 8-10) is the mechanism behind **duodenal atresia**, not the standard tracheoesophageal septum defects of early foregut division.
*Defective lateral fusion of esophageal folds creating persistent communication*
- The **tracheoesophageal folds** normally grow medially and fuse to form the septum; failure of this fusion typically results in a patent communication rather than the classic **blind pouch** seen in atresia.
- This description is more consistent with an isolated **H-type fistula** rather than the atresia with distal fistula characterized by the coiled tube.
*Abnormal neural crest cell contribution to aorticopulmonary septum affecting foregut*
- Neural crest cells contribute to the **aorticopulmonary septum** in the heart, and defects here lead to persistent **truncus arteriosus** or transposition of great vessels.
- While TEF/EA is associated with heart defects in **VACTERL association**, the primary embryological cause of TEF is not a neural crest migration defect of the heart septum.
*Excessive apoptosis of esophageal epithelium during solid cord stage*
- Esophageal development involves a **solid cord stage** followed by recanalization; however, atresia in TEF is due to improper **septation** rather than epithelial apoptosis issues.
- Defects in the recanalization process are generally associated with **stenosis** or atresia of the distal GI tract, such as the **duodenum** or jejunum.
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