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Pathology - Hepatocellular carcinoma
Definition • A malignant epithelial tumor of the liver originating from hepatocytes.
Epidemiology • Ubiquitous globally, although exhibiting significant geographical diversity. • Incidence rates closely align with HBV infection rates, rendering hepatocellular carcinoma (HCC) especially prevalent in some regions of Africa and Asia.
Etiology
Hepatocellular carcinoma typically develops in the context of liver cirrhosis. Chronic hepatitis B and haemochromatosis are notably carcinogenic substrates. Dietary consumption of aflatoxins produced by Aspergillus fungi is recognized as a strong carcinogen for the liver.
Carcinogenesis • The inactivation of tumor suppressor genes, such as TP53, is prevalent. • Activating mutations of oncogenes seem to be infrequent. The Hepatitis B X gene product impairs p53 functionality and obstructs nucleotide excision repair.
Presentation • Arrives late with nonspecific weight loss and abdominal discomfort. • Established cirrhotics may be identified through the evaluation of an increasing serum alpha-fetoprotein or with ultrasound monitoring.
Macroscopy: Expansile neoplastic tumor in the liver, frequently accompanied by satellite deposits. • The tumor may exhibit a green hue as a result of bile production. • Differentiating tumor deposits from cirrhotic nodules can be challenging.
Histopathology: Classical hepatocellular carcinoma (HCC) consists of epithelial cells akin to hepatocytes, generally proliferating in trabecular formations that resemble thicker hepatic cell plates. The tumor may exhibit bile production. Fibrolamellar HCC is a rare yet unusual form that often occurs in young people without preexisting cirrhosis. Histologically, the tumor consists of clusters of exceptionally large neoplastic cells with plentiful granular pink cytoplasm interspersed with dense fibrous bands.
Prognosis: Generally unfavorable, with 5-year survival rates below 5%. Fibrolamellar hepatocellular carcinoma exhibits a marginally improved prognosis, with 5-year survival rates of 60%.
Definition • A malignant epithelial tumor of the liver originating from hepatocytes.
Epidemiology • Ubiquitous globally, although exhibiting significant geographical diversity. • Incidence rates closely align with HBV infection rates, rendering hepatocellular carcinoma (HCC) especially prevalent in some regions of Africa and Asia.
Etiology
Hepatocellular carcinoma typically develops in the context of liver cirrhosis. Chronic hepatitis B and haemochromatosis are notably carcinogenic substrates. Dietary consumption of aflatoxins produced by Aspergillus fungi is recognized as a strong carcinogen for the liver.
Carcinogenesis • The inactivation of tumor suppressor genes, such as TP53, is prevalent. • Activating mutations of oncogenes seem to be infrequent. The Hepatitis B X gene product impairs p53 functionality and obstructs nucleotide excision repair.
Presentation • Arrives late with nonspecific weight loss and abdominal discomfort. • Established cirrhotics may be identified through the evaluation of an increasing serum alpha-fetoprotein or with ultrasound monitoring.
Macroscopy: Expansile neoplastic tumor in the liver, frequently accompanied by satellite deposits. • The tumor may exhibit a green hue as a result of bile production. • Differentiating tumor deposits from cirrhotic nodules can be challenging.
Histopathology: Classical hepatocellular carcinoma (HCC) consists of epithelial cells akin to hepatocytes, generally proliferating in trabecular formations that resemble thicker hepatic cell plates. The tumor may exhibit bile production. Fibrolamellar HCC is a rare yet unusual form that often occurs in young people without preexisting cirrhosis. Histologically, the tumor consists of clusters of exceptionally large neoplastic cells with plentiful granular pink cytoplasm interspersed with dense fibrous bands.
Prognosis: Generally unfavorable, with 5-year survival rates below 5%. Fibrolamellar hepatocellular carcinoma exhibits a marginally improved prognosis, with 5-year survival rates of 60%.
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Pathology - Intrahepatic cholangiocarcinoma
A malignant epithelial neoplasm originating in the liver, consisting of cells that resemble bile ducts.
Epidemiology • Uncommon in the majority of populations.
Aetiology Liver flukes (Clonorchis sinensis and Opisthorchis viverrini). • Hepatolithiasis. • PSC • Exposure to Thorotrast, a contrast agent utilized from 1930 until 1955. • Biliary anomalies.
Carcinogenesis • The most prevalent genetic abnormalities are mutations in RAS and TP53.
Presentation • Many manifest late, as they can attain significant size within the liver prior to eliciting symptoms such as malaise, weight loss, and abdominal pain. Tumors infiltrating the hilar area of the liver may manifest as obstructive jaundice.
Macroscopy • The liver has extensive confluent nodules of gray-white tumor, frequently accompanied by satellite deposits. • The surrounding liver tissue is typically non-cirrhotic. Histopathology: Adenocarcinomas characterized by infiltrating malignant epithelial cells that develop glandular and papillary forms. • A characteristic feature is the presence of profuse fibroblastic stroma.
Prognosis: Generally unfavorable, with 5-year survival rates ranging from 40% to 50%, contingent upon the stage.
Pathology - Intrahepatic cholangiocarcinoma
A malignant epithelial neoplasm originating in the liver, consisting of cells that resemble bile ducts.
Epidemiology • Uncommon in the majority of populations.
Aetiology Liver flukes (Clonorchis sinensis and Opisthorchis viverrini). • Hepatolithiasis. • PSC • Exposure to Thorotrast, a contrast agent utilized from 1930 until 1955. • Biliary anomalies.
Carcinogenesis • The most prevalent genetic abnormalities are mutations in RAS and TP53.
Presentation • Many manifest late, as they can attain significant size within the liver prior to eliciting symptoms such as malaise, weight loss, and abdominal pain. Tumors infiltrating the hilar area of the liver may manifest as obstructive jaundice.
Macroscopy • The liver has extensive confluent nodules of gray-white tumor, frequently accompanied by satellite deposits. • The surrounding liver tissue is typically non-cirrhotic. Histopathology: Adenocarcinomas characterized by infiltrating malignant epithelial cells that develop glandular and papillary forms. • A characteristic feature is the presence of profuse fibroblastic stroma.
Prognosis: Generally unfavorable, with 5-year survival rates ranging from 40% to 50%, contingent upon the stage.
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Pathology – Cholecystitis
Cholecystitis is defined as gallbladder inflammation.
Epidemiology: • Very prevalent. Aetiology • The most common cause is gallstones (calculous cholecystitis). • Acalculous cholecystitis is also seen, particularly in the elderly.
Pathogenesis • Chemical harm to the mucosa by bile is thought to be the cause of biliary stasis. • A gallstone or inadequate gallbladder motility might block the gallbladder exit. Biliary colic causes acute upper abdomen pain that disappears spontaneously after several hours. • Acute cholecystitis is a serious condition characterized by persistent upper abdominal pain, fever, and tachycardia. Macroscopy reveals thicker gallbladder walls and potentially friable mucosa. • Gallstones are often present.
Histopathology • Acute cholecystitis is characterized by oedema, inflammatory cells, and granulation tissue. • Chronic cholecystitis is characterized by muscular hypertrophy and fibrous tissue, mild chronic inflammation, and the development of mucosal diverticula that herniate through the muscular layer (Rokitansky-Aschoff sinuses). • Xanthogranulomatous cholecystitis is a type of chronic cholecystitis characterized by the presence of macrophages and fibroblasts, likely due to a ruptured Rokitansky-Aschoff sinus.
Prognosis: Most individuals with calculous cholecystitis can be treated with cholecystectomy.
Cholecystitis is defined as gallbladder inflammation.
Epidemiology: • Very prevalent. Aetiology • The most common cause is gallstones (calculous cholecystitis). • Acalculous cholecystitis is also seen, particularly in the elderly.
Pathogenesis • Chemical harm to the mucosa by bile is thought to be the cause of biliary stasis. • A gallstone or inadequate gallbladder motility might block the gallbladder exit. Biliary colic causes acute upper abdomen pain that disappears spontaneously after several hours. • Acute cholecystitis is a serious condition characterized by persistent upper abdominal pain, fever, and tachycardia. Macroscopy reveals thicker gallbladder walls and potentially friable mucosa. • Gallstones are often present.
Histopathology • Acute cholecystitis is characterized by oedema, inflammatory cells, and granulation tissue. • Chronic cholecystitis is characterized by muscular hypertrophy and fibrous tissue, mild chronic inflammation, and the development of mucosal diverticula that herniate through the muscular layer (Rokitansky-Aschoff sinuses). • Xanthogranulomatous cholecystitis is a type of chronic cholecystitis characterized by the presence of macrophages and fibroblasts, likely due to a ruptured Rokitansky-Aschoff sinus.
Prognosis: Most individuals with calculous cholecystitis can be treated with cholecystectomy.
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Pathology -Chronic renal disease.
Definition: A progressive and irreversible loss in renal function, classified into five phases based on estimated glomerular filtration rate (eGFR) (Table 9.1).
Epidemiology: Diabetes and kidney vascular disease contribute to the high prevalence of this condition. Aetiology • Diabetic and hypertensive nephropathy are the leading causes. • Other causes include reflex nephropathy, obstructive nephropathy, IgA nephropathy (IgAN), focal segmental glomerulosclerosis (FSGS), membranous nephropathy, systemic lupus erythematosus (SLE), myeloma, amyloidosis, medications, gout, and adult polycystic kidney disease (APKD).
Pathogenesis • A decrease in nephron mass below a certain level can lead to progressive renal damage, regardless of the underlying disease. • The sequence of events causing progressive renal damage is thought to be glomerular hyperfiltration, hypertension, injury, glomerulosclerosis, and tubulointerstitial fibrosis. • TGF-B plays a vital role in promoting renal scarring. Early illness is asymptomatic and can only be detected by measuring eGFR in at-risk patients, such as diabetics or hypertensives. • As patients advance, they become weary and have bone pain.
• End-stage renal failure patients with fluid overload and metabolic abnormalities may require prompt renal replacement therapy. Biochemistry • Urea and creatinine levels are elevated due to poor waste product excretion. • Reduced Calcium due to a shortage of active calcitriol. • increase Phosphate due to inadequate phosphate excretion. • Secondary hyperparathyroidism caused by low calcium levels. •Reduced haemoglobin levels due to decreased erythropoietin production.Loss of acid-base and sodium/potassium equilibrium happens later in chronic renal disease.
Complications • High risk of cardiovascular disease due to hypertension, vascular calcification, and hyperlipidemia. • Deranged calcium and phosphate metabolism causes renal bone disease, a complicated combination of hyperparathyroidism, osteomalacia, and osteoporosis.
Definition: A progressive and irreversible loss in renal function, classified into five phases based on estimated glomerular filtration rate (eGFR) (Table 9.1).
Epidemiology: Diabetes and kidney vascular disease contribute to the high prevalence of this condition. Aetiology • Diabetic and hypertensive nephropathy are the leading causes. • Other causes include reflex nephropathy, obstructive nephropathy, IgA nephropathy (IgAN), focal segmental glomerulosclerosis (FSGS), membranous nephropathy, systemic lupus erythematosus (SLE), myeloma, amyloidosis, medications, gout, and adult polycystic kidney disease (APKD).
Pathogenesis • A decrease in nephron mass below a certain level can lead to progressive renal damage, regardless of the underlying disease. • The sequence of events causing progressive renal damage is thought to be glomerular hyperfiltration, hypertension, injury, glomerulosclerosis, and tubulointerstitial fibrosis. • TGF-B plays a vital role in promoting renal scarring. Early illness is asymptomatic and can only be detected by measuring eGFR in at-risk patients, such as diabetics or hypertensives. • As patients advance, they become weary and have bone pain.
• End-stage renal failure patients with fluid overload and metabolic abnormalities may require prompt renal replacement therapy. Biochemistry • Urea and creatinine levels are elevated due to poor waste product excretion. • Reduced Calcium due to a shortage of active calcitriol. • increase Phosphate due to inadequate phosphate excretion. • Secondary hyperparathyroidism caused by low calcium levels. •Reduced haemoglobin levels due to decreased erythropoietin production.Loss of acid-base and sodium/potassium equilibrium happens later in chronic renal disease.
Complications • High risk of cardiovascular disease due to hypertension, vascular calcification, and hyperlipidemia. • Deranged calcium and phosphate metabolism causes renal bone disease, a complicated combination of hyperparathyroidism, osteomalacia, and osteoporosis.
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Pathology - Extrahepatic bile duct carcinoma
Definition: A malignant epithelial tumor that develops in an extrahepatic bile duct.
Epidemiology • Incidence is rare and does not vary by geography. Aetiology • PSC. • Infestation of liver fluke. • Choledochal cysts. 2 Choledocholithiasis doesn't appear to be important. Carcinogenesis • Mutations in KRAS and TP53 are identified.
Presentation: • Obstructive jaundice. • Fever and rigors can be caused by superimposed cholangitis. Macroscopy reveals a tumor in the bile duct, which can be polypoid, stenosing, or diffusely infiltrative.
Histopathology: • The majority of adenocarcinomas are well or moderately differentiated, with malignant epithelial cells forming glandular structures similar to bile ducts.
Prognosis: Patients with resectable tumors and clear surgical margins typically have a 5-year survival rate of 20-40%. • Tumors associated with PSC have a low 5-year survival rate (<10%).< />pan>
Definition: A malignant epithelial tumor that develops in an extrahepatic bile duct.
Epidemiology • Incidence is rare and does not vary by geography. Aetiology • PSC. • Infestation of liver fluke. • Choledochal cysts. 2 Choledocholithiasis doesn't appear to be important. Carcinogenesis • Mutations in KRAS and TP53 are identified.
Presentation: • Obstructive jaundice. • Fever and rigors can be caused by superimposed cholangitis. Macroscopy reveals a tumor in the bile duct, which can be polypoid, stenosing, or diffusely infiltrative.
Histopathology: • The majority of adenocarcinomas are well or moderately differentiated, with malignant epithelial cells forming glandular structures similar to bile ducts.
Prognosis: Patients with resectable tumors and clear surgical margins typically have a 5-year survival rate of 20-40%. • Tumors associated with PSC have a low 5-year survival rate (<10%).< />pan>
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Pathology - diabetic nephropathy
Definition: Chronic kidney disease caused by diabetes mellitus.
Epidemiology • A leading cause of chronic renal disease.
Aetiology • Diabetes. • Only 30-40% of diabetics develop nephropathy, suggesting that other factors play a role.
Pathogenesis • High glucose levels harm endothelial cells in the glomeruli, resulting in glomerulosclerosis and nephron loss.
Presentation • A patient with diabetes mellitus develops proteinuria. • Microalbuminuria often precedes overt proteinuria, which can lead to nephrotic syndrome. • Hypertension is always present.
Histopathology • Glomerulosclerosis, a diffuse increase in the mesangial matrix, can lead to the formation of Kimmelsteil-Wilson nodules. • Thicker glomerular basement membranes. • Hyalinization of the afferent and efferent arterioles. • Tubulointerstitial fibrosis is proportional to glomerular injury. 2 A kidney biopsy is not essential to confirm a diagnosis of diabetic nephropathy if the clinical presentation is typical. Biopsies are often reserved for unusual cases where alternate diagnoses may be possible. immune fluorescence • IgG deposition in glomerular and tubular basement membranes can be observed. Electron microscopy • Thickened glomerular basement membrane and expanded mesangial matrix are observed. • There are no immunological complexes present.
Prognosis: Gradual decline in renal function. • Patients with severe hypertension and significant proteinuria fare poorly. • Proper blood pressure management is crucial for reducing disease progression.
Definition: Chronic kidney disease caused by diabetes mellitus.
Epidemiology • A leading cause of chronic renal disease.
Aetiology • Diabetes. • Only 30-40% of diabetics develop nephropathy, suggesting that other factors play a role.
Pathogenesis • High glucose levels harm endothelial cells in the glomeruli, resulting in glomerulosclerosis and nephron loss.
Presentation • A patient with diabetes mellitus develops proteinuria. • Microalbuminuria often precedes overt proteinuria, which can lead to nephrotic syndrome. • Hypertension is always present.
Histopathology • Glomerulosclerosis, a diffuse increase in the mesangial matrix, can lead to the formation of Kimmelsteil-Wilson nodules. • Thicker glomerular basement membranes. • Hyalinization of the afferent and efferent arterioles. • Tubulointerstitial fibrosis is proportional to glomerular injury. 2 A kidney biopsy is not essential to confirm a diagnosis of diabetic nephropathy if the clinical presentation is typical. Biopsies are often reserved for unusual cases where alternate diagnoses may be possible. immune fluorescence • IgG deposition in glomerular and tubular basement membranes can be observed. Electron microscopy • Thickened glomerular basement membrane and expanded mesangial matrix are observed. • There are no immunological complexes present.
Prognosis: Gradual decline in renal function. • Patients with severe hypertension and significant proteinuria fare poorly. • Proper blood pressure management is crucial for reducing disease progression.
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Pathology - Hypertensive Nephropathy
Definition: Chronic renal disease associated with hypertension. Epidemiology: • Common causes of chronic kidney disease.
Aetiology • Hypertension
Pathogenesis • Two pathophysiological explanations have been proposed and may not be mutually exclusive. • Arteriole constriction leads to glomerular ischemia and scarring, while glomerular hypertension produces glomerular hyperfiltration and eventual glomerulosclerosis. Presentation: Renal failure and proteinuria in a long-standing hypertensive with no additional causes of renal illness. • Additional indicators of hypertension, such as left ventricular hypertrophy, may also be present.
Macroscopy: • Both kidneys are shrunken, with finely granular cortical surfaces. Histopathology • Afferent arterioles have hyaline deposits. • Medial hypertrophy and intimal thickening are seen in interlobular and larger arteries. • Glomeruli may show wrinkling and shrinkage followed by scarring of the whole tuft or enlargement of the tuft followed by segmental scarring. • These pathological features are referred to as nephrosclerosis, which simply means hardening of the kidney.
The appearance of nephrosclerosis may not necessarily indicate hypertensive nephropathy, as similar alterations might occur with aging or diabetes. However, a kidney biopsy can confirm a diagnosis of hypertensive nephropathy if the clinical presentation matches.
Prognosis: • Chronic kidney disease tends to progress. • Aggressive blood pressure control can reduce the deterioration in renal function.
Definition: Chronic renal disease associated with hypertension. Epidemiology: • Common causes of chronic kidney disease.
Aetiology • Hypertension
Pathogenesis • Two pathophysiological explanations have been proposed and may not be mutually exclusive. • Arteriole constriction leads to glomerular ischemia and scarring, while glomerular hypertension produces glomerular hyperfiltration and eventual glomerulosclerosis. Presentation: Renal failure and proteinuria in a long-standing hypertensive with no additional causes of renal illness. • Additional indicators of hypertension, such as left ventricular hypertrophy, may also be present.
Macroscopy: • Both kidneys are shrunken, with finely granular cortical surfaces. Histopathology • Afferent arterioles have hyaline deposits. • Medial hypertrophy and intimal thickening are seen in interlobular and larger arteries. • Glomeruli may show wrinkling and shrinkage followed by scarring of the whole tuft or enlargement of the tuft followed by segmental scarring. • These pathological features are referred to as nephrosclerosis, which simply means hardening of the kidney.
The appearance of nephrosclerosis may not necessarily indicate hypertensive nephropathy, as similar alterations might occur with aging or diabetes. However, a kidney biopsy can confirm a diagnosis of hypertensive nephropathy if the clinical presentation matches.
Prognosis: • Chronic kidney disease tends to progress. • Aggressive blood pressure control can reduce the deterioration in renal function.
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Pathology - Acute renal failure
Definition: Significant deterioration in renal function over hours or days.
Epidemiology • Common. • This condition is typically a complication of a pre-existing sickness that disrupts circulation.
Aetiology • Hypoperfusion, such as hypovolaemia or sepsis, occurs prior to renal function.
• Renal ('intrinsic'): acute tubular injury, drug-induced interstitial nephritis, anti-glomerular basement membrane disease, small vessel vasculitis, hemolytic uraemic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP) and severe hypertension.
• Post-renal: bilateral obstruction (or obstruction of a single kidney). 2 The most prevalent causes are hypoperfusion and acute tubular damage.
Pathogenesis: • Kidney disease causes sudden decline in function.
Presentation: • Oliguria (passing little amounts of urine) is the most common symptom, but some cases may show no symptoms. • Severe cases result in pulmonary edema, encephalopathy, and pericarditis.
Biochemistry: Serum urea and creatinine are key indicators. • Hyperkalemia and metabolic acidosis are also prevalent. Severe hyperkalemia is pro-arrhythmic and can cause cardiac arrest, requiring rapid treatment. Prognosis • Pre-renal and post-renal acute renal failure (ARF) can be reversible if promptly addressed by restoring circulation volume or alleviating obstruction. • Intrinsic types of ARF typically necessitate dialysis while the underlying etiology is managed and renal function recuperates.
Definition: Significant deterioration in renal function over hours or days.
Epidemiology • Common. • This condition is typically a complication of a pre-existing sickness that disrupts circulation.
Aetiology • Hypoperfusion, such as hypovolaemia or sepsis, occurs prior to renal function.
• Renal ('intrinsic'): acute tubular injury, drug-induced interstitial nephritis, anti-glomerular basement membrane disease, small vessel vasculitis, hemolytic uraemic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP) and severe hypertension.
• Post-renal: bilateral obstruction (or obstruction of a single kidney). 2 The most prevalent causes are hypoperfusion and acute tubular damage.
Pathogenesis: • Kidney disease causes sudden decline in function.
Presentation: • Oliguria (passing little amounts of urine) is the most common symptom, but some cases may show no symptoms. • Severe cases result in pulmonary edema, encephalopathy, and pericarditis.
Biochemistry: Serum urea and creatinine are key indicators. • Hyperkalemia and metabolic acidosis are also prevalent. Severe hyperkalemia is pro-arrhythmic and can cause cardiac arrest, requiring rapid treatment. Prognosis • Pre-renal and post-renal acute renal failure (ARF) can be reversible if promptly addressed by restoring circulation volume or alleviating obstruction. • Intrinsic types of ARF typically necessitate dialysis while the underlying etiology is managed and renal function recuperates.
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Pathology - Acinar Cell Carcinoma
Definition: A malignant epithelial tumor in the pancreas that produces enzymes.
Epidemiology • This rare tumor accounts for around 1% of all pancreatic tumors. • The majority occur in older persons.
Aetiology: unknown. Carcinogenesis has been linked to abnormalities in the APC/B-catenin pathway.
• Genetic alterations common in ductal adenocarcinoma are missing.
Presentation: General symptoms include stomach pain, weight loss, nausea, and diarrhea. • Approximately 10% of individuals experience polyarthralgia and multifocal fat necrosis due to lipase secretion.
Macroscopy reveals a well-defined soft tan tumor in the pancreas. • An extension outside the pancreas may be present. Histopathology • Neoplastic epithelial cells form in sheets, trabeculae, and acini. • Some cells have eosinophilic finely granular cytoplasm.
• Immunoreactivity for lipase, trypsin, and chymotrypsin is positive.
Prognosis: Aggressive malignant tumors. • The median survival time following diagnosis is 18 months, with a 5-year survival rate of
Definition: A malignant epithelial tumor in the pancreas that produces enzymes.
Epidemiology • This rare tumor accounts for around 1% of all pancreatic tumors. • The majority occur in older persons.
Aetiology: unknown. Carcinogenesis has been linked to abnormalities in the APC/B-catenin pathway.
• Genetic alterations common in ductal adenocarcinoma are missing.
Presentation: General symptoms include stomach pain, weight loss, nausea, and diarrhea. • Approximately 10% of individuals experience polyarthralgia and multifocal fat necrosis due to lipase secretion.
Macroscopy reveals a well-defined soft tan tumor in the pancreas. • An extension outside the pancreas may be present. Histopathology • Neoplastic epithelial cells form in sheets, trabeculae, and acini. • Some cells have eosinophilic finely granular cytoplasm.
• Immunoreactivity for lipase, trypsin, and chymotrypsin is positive.
Prognosis: Aggressive malignant tumors. • The median survival time following diagnosis is 18 months, with a 5-year survival rate of
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Pathology - Pancreatic malformations
Ectopic pancreas is a common developmental defect that occurs when pancreatic tissue is placed outside of its normal position. • The duodenum is the most common location, but it can also be found in the jejunum, ileum, and Meckel's diverticulum • While most cases are unintentional, some patients may experience symptoms such as bleeding or blockage.
Pancreas Divisum • A common developmental abnormality in which the dorsal and ventral pancreatic buds fail to merge. • The Santorini duct becomes the pancreas' major ductal system. This duct drains into the duodenum via the minor papilla, leading to pancreatic secretory stasis and susceptibility to pancreatitis. It is typically asymptomatic and detected during imaging, however some patients may develop pancreatitis later in life.
Annular pancreas • A rare developmental defect occurs when the dorsal and ventral pancreatic buds unite around the duodenum. • The ring of pancreas can cause obstruction to the duodenum. • Patients often arrive around 1 year of age with vomiting and abdominal distention after meals.
Ectopic pancreas is a common developmental defect that occurs when pancreatic tissue is placed outside of its normal position. • The duodenum is the most common location, but it can also be found in the jejunum, ileum, and Meckel's diverticulum • While most cases are unintentional, some patients may experience symptoms such as bleeding or blockage.
Pancreas Divisum • A common developmental abnormality in which the dorsal and ventral pancreatic buds fail to merge. • The Santorini duct becomes the pancreas' major ductal system. This duct drains into the duodenum via the minor papilla, leading to pancreatic secretory stasis and susceptibility to pancreatitis. It is typically asymptomatic and detected during imaging, however some patients may develop pancreatitis later in life.
Annular pancreas • A rare developmental defect occurs when the dorsal and ventral pancreatic buds unite around the duodenum. • The ring of pancreas can cause obstruction to the duodenum. • Patients often arrive around 1 year of age with vomiting and abdominal distention after meals.
