Podcast
Questions and Answers
What hormone is produced by the beta cells of the pancreas?
What hormone is produced by the beta cells of the pancreas?
Which enzyme is activated from its zymogen form by enteroquinase?
Which enzyme is activated from its zymogen form by enteroquinase?
What is the primary cause of acute pancreatitis in 66% of cases?
What is the primary cause of acute pancreatitis in 66% of cases?
What is the primary function of the pancreatic juice when food is ingested?
What is the primary function of the pancreatic juice when food is ingested?
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Which type of pancreatic cells produce somatostatin?
Which type of pancreatic cells produce somatostatin?
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Which of the following is NOT a cause of acute pancreatitis?
Which of the following is NOT a cause of acute pancreatitis?
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What role do hormones like secretin and cholecystokinin play in pancreatic function?
What role do hormones like secretin and cholecystokinin play in pancreatic function?
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What complication can result from obstruction at the sphincter of Oddi?
What complication can result from obstruction at the sphincter of Oddi?
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What is the most common type of autoimmune pancreatitis?
What is the most common type of autoimmune pancreatitis?
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Which of the following is NOT associated with type 1 autoimmune pancreatitis?
Which of the following is NOT associated with type 1 autoimmune pancreatitis?
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What role does increased intracellular calcium play in acute pancreatitis?
What role does increased intracellular calcium play in acute pancreatitis?
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What is co-localization in the context of acute pancreatitis?
What is co-localization in the context of acute pancreatitis?
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Which of the following factors is linked to hereditary aspects of pancreatitis?
Which of the following factors is linked to hereditary aspects of pancreatitis?
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What can lead to systemic inflammatory response syndrome (SIRS) in the context of acute pancreatitis?
What can lead to systemic inflammatory response syndrome (SIRS) in the context of acute pancreatitis?
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What is a potential consequence of increased pancreatic duct pressure?
What is a potential consequence of increased pancreatic duct pressure?
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Which pancreatic enzyme, when systemically released, is linked to lung damage?
Which pancreatic enzyme, when systemically released, is linked to lung damage?
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Study Notes
Pancreatitis
- The pancreas is a gland with two main functions: endocrine and exocrine.
- Endocrine secretion involves the production of hormones directly into the bloodstream by the pancreatic islets of Langerhans.
- Alpha cells produce glucagon (raises blood sugar).
- Beta cells produce insulin (lowers blood sugar).
- Delta cells produce somatostatin.
- Gamma (F) cells produce pancreatic polypeptide, which regulates gastrointestinal secretions and motility.
- G cells produce gastrin, stimulating parietal cells to produce hydrochloric acid.
- Epsilon cells produce ghrelin.
- Exocrine secretion is regulated by the hormones secretin and cholecystokinin when food is ingested.
- The exocrine pancreas secretes pancreatic juice, rich in bicarbonate, which acts as a buffer against the hydrochloric acid produced by the stomach.
- Pancreatic juice contains two main types of enzymes: inactive (zymogens) and active.
- Zymogens:
- Trypsinogen converts to trypsin by enteroquinase.
- Carboxypeptidase and chymotrypsinogen break down protein molecules.
- Active Enzymes:
- Amylase breaks down carbohydrates.
- Lipase breaks down lipids into fatty acids and glycerol.
- Zymogens:
Pancreatitis physiology
- The pancreas secretes enzymes via the main pancreatic duct (Wirsung's duct), converging at the sphincter of Oddi and emptying into the duodenum.
- Obstruction at the sphincter of Oddi can lead to pancreatic reflux, activating enzymes within the pancreas, leading to pancreatitis.
- Other causes of acute pancreatitis include direct cytotoxic effects of:
- Alcohol.
- Medications.
- Scorpion venom.
Acute Pancreatitis
- Acute pancreatitis is an inflammatory process affecting the pancreatic parenchyma that can lead to systemic and local complications and organ dysfunction.
- Most common causes:
- Biliary (66% of cases, especially with stones <5mm).
- Alcohol (direct cytotoxic effect).
- Idiopathic (Unknown cause).
- Rare Causes:
- Hypertriglyceridemia (Triglycerides > 1000 mg/dL).
- Excess fatty acids may exceed albumin's transport capacity, increasing toxicity and activating pancreatic enzymes.
- Excess chylomicrons may obstruct distal pancreatic circulation.
- Endoscopic retrograde cholangiopancreatography (ERCP) if not performed properly.
- Medications:
- Fibrates (FFAs).
- Loop or distal diuretics.
- Thiazides.
- Adanosine.
- Pentamidine.
- Tetracyclines.
- Estrogens.
- Hypercalcemia.
- Infections:
- Scorpion sting (Tityus tritus).
- Ascaris (Parasite).
- Autoimmune pancreatitis (formerly called idiopathic pancreatitis associated with hypergammaglobulinemia):
- Recurrent pancreatic episodes.
- Two types:
- Type 1 (sclerosing lymphoplasmacytic pancreatitis): 80% of cases, infiltration of cells into the parenchyma. Characterized by elevated IgG4 levels, anti-carbonic anhydrase type II antibodies, and antiprotease antibodies.
- Type 2 (idiopathic central ductal pancreatitis): less common.
- Cancer (especially intraductal papillary mucinous neoplasia).
- Anatomical abnormalities (pancreas divisum, annular pancreas).
- Hereditary factors (FTR gene, involved in cystic fibrosis).
- Hypertriglyceridemia (Triglycerides > 1000 mg/dL).
Acute Pancreatitis Pathophysiology
- Direct cytotoxic effects on acinar or ductal cells trigger an increase in zymogen and digestive enzyme production.
- Premature activation of trypsinogen to trypsin occurs through a process called co-localization.
- This involves the premature union of zymogen-containing vesicles with lysosomes, activating enzymes within pancreatic cells.
- Lysosomes contain cathepsin B, an enzyme crucial in necroptosis (programmed cell death).
- Increased intracellular calcium plays a vital role in acute pancreatitis, causing mitochondrial dysfunction and ATP depletion.
- Alcohol disrupts the CFTR channel function, leading to thicker secretions, luminal acidification, and enzyme activation.
- Increased pancreatic duct pressure activates the mechanoreceptor Piezo1 and Orai1, particularly Piezo1 in acinar cells.
- This triggers a rise in intracellular calcium, stimulating the opening of mitochondrial permeability transition pores (MPTP), leading to mitochondrial dysfunction, ATP depletion, and cell death.
- Inflammation damages the pancreas, releasing damage-associated molecular patterns (DAMPs) and cytokines, promoting pancreatic and peri-pancreatic inflammation, potentially causing systemic inflammation.
- This recruitment and release of chemotactic and proinflammatory agents can lead to systemic inflammatory response syndrome (SIRS).
- Increased gastrointestinal permeability increases the risk of infections in the inflamed pancreatic tissue, leading to local pancreatic necrosis or sepsis.
- Systemic release of pancreatic enzymes, such as phospholipase, leads to lung damage.
- Phospholipase may degrade lecithin in pulmonary surfactant, reducing surface tension resistance.
Epidemiology
- Acute pancreatitis is the most common pancreatic disease worldwide.
- In Mexico, it accounts for 6 cases per 1000 hospital admissions yearly.
- It is the 18th leading cause of death in hospitals in Mexico.
- Early mortality (first two weeks): SIRS or organ failure.
- Late mortality (after two weeks): sepsis and its complications.
- Mortality for interstitial pancreatitis: 5%
- Mortality for necrotizing pancreatitis: 17%
- Centers with experience in pancreatitis management can reduce mortality to 6%.
Clinical Presentation
- Typical patient: female, 30-50 years old.
- Main symptom: epigastric pain radiating to the back or hemi-belt.
- Other symptoms: vomiting, fever, decreased peristalsis, shock (less than 3% of cases).
- Characteristic signs (48-72 hours after initial presentation):
- Grey Turner: ecchymosis on the flanks.
- Cullen sign: periumbilical ecchymosis.
- Fox sign: ecchymosis in the lower inguinal ligament.
- Pancreatic points (rarely asked but useful for clinical practice).
Diagnosis
- Two out of three criteria:
- Clinically suggestive (epigastric pain, etc.).
- Biochemical alterations (amylase and lipase levels three times higher than the reference value).
- Imaging findings.
- Atlanta classification (2012) is recommended for classifying severity.
- Mild pancreatitis: no evidence of organ failure.
- Moderate pancreatitis (moderately severe): evidence of organ failure lasting less than 48 hours or local complications.
- Severe pancreatitis: organ failure lasting more than 48 hours.
- Apache 2 score for assessing organ failure.
- SOFA score for assessing organ failure (evaluates six vital parameters).
- BISAP score (simpler and commonly asked).
- SIRS criteria for diagnosis.
- Ranson criteria was removed from the 2022 update.
Management
- Initial assessment and treatment:
- History and physical exam focusing on typical presenting symptoms: epigastric pain radiating to the back or hemi-belt, vomiting, fever, decreased peristalsis, shock.
- Lab tests:
- Amylase and lipase (amylase elevates 6-12 hours, not reliable after 24 hours due to short half-life; lipase is more reliable with a longer half-life and elevates 4-8 hours).
- Liver function tests (LFTs) to assess the possibility of cholestasis, especially in cases of lithiasis (most common cause).
- Complete blood count (CBC) (hemoconcentration and leukocytosis due to dehydration and inflammation, or bacterial translocation).
- Electrolytes (check for shock related electrolyte abnormalities).
- Renal function tests (assess creatinine and BUN for kidney function).
- Ultrasound recommended: to rule out the most common cause (biliary origin).
- If cholelithiasis is detected, refer to general surgery.
- If diagnosis is inconclusive with initial tests and suggestive clinical data, a contrast-enhanced CT scan or MRI is performed.
- CT scan changes are visible after 72 hours.
- MRI may detect earlier changes.
- Fluid resuscitation:
- First-line therapy (2022 guidelines): to prevent necrotizing and severe pancreatitis.
- Goal is to restore fluid volume to perfuse vital organs and prevent multi-organ failure.
- Preferred solution: Ringer's lactate (Hartmann's solution).
- Studies show Ringer's lactate may reduce the development of severe pancreatitis and hospital readmission compared to normal saline.
- If Ringer's lactate is unavailable, 0.9% saline is recommended.
- Individualized therapy based on patient age and comorbidities.
- Conservative, non-aggressive approach.
- Fluid resuscitation guided by goals: mean arterial pressure, urine output, heart rate, and central venous pressure.
- First-line therapy (2022 guidelines): to prevent necrotizing and severe pancreatitis.
- Analgesia:
- 2022 guidelines recommend the WHO analgesic ladder:
- First step: NSAIDs (Paracetamol).
- Second step: Low-potency opioids (Codeine, Tramadol).
- Third step: High-potency opioids (Morphine, Fentanyl).
- 2022 guidelines recommend the WHO analgesic ladder:
Imaging Findings
- Plain abdominal radiographs (not recommended in the 2022 guidelines but may still be asked in clinical scenarios):
- Sentinel loop: dilated loop of bowel in the approximate location of the pancreas.
- "Ground glass" appearance: opacification in the area of the pancreas.
- Colon cut-off sign: spasm of the descending colon and part of the transverse colon at the splenic flexure (stenosis and proximal dilation).
Differential Diagnosis
- Other causes of abdominal pain that can mimic pancreatitis:
- Cholecystitis.
- Appendicitis.
- Peptic ulcer disease.
- Pancreatic cancer.
- Gastritis.
- Myocardial infarction.
- Aortic dissection.
Important Notes:
- The information presented here is for informational purposes only and should not be considered medical advice. Always consult with a qualified healthcare professional for any health concerns or before making any decisions related to your health or treatment.
Pancreatitis Aguda
- Early feeding within the first 72 hours is recommended for patients with severe pancreatitis, even in severe cases, as it can reduce complications, mortality, and the need for surgery.
- If oral feeding is not tolerated, nasogastric, nasojejunal, or parenteral feeding should be considered.
- If patients do not meet 60% of their protein and calorie requirements, a mixed feeding approach may be used.
- Glutamine analogs are recommended for patients with severe pancreatitis receiving parenteral nutrition.
- Empiric antibiotic therapy is only recommended for patients with infected necrosis.
- Antibiotic therapy should cover gram-negative bacilli, cocci, and anaerobes.
- Surgical intervention is often used in cases of complications with minimally invasive surgery preferred when possible, followed by open surgery, and then drainage if neither of these are feasible.
- If the cause of pancreatitis is biliary, a sphincterotomy and cholecystectomy are recommended.
Complications
-
Acute:
- Peripancreatic fluid collections and necrosis are common within the first four weeks.
-
Chronic:
- Pancreatic pseudocysts and walled off necrosis can occur after four weeks of evolution.
Peripancreatic Fluid Collection
- Fluid that does not have a defined wall.
Pancreatic Pseudocyst
- Unlike a true cyst, it lacks an epithelial lining and has a thin, fibrous wall made of granulation tissue without solid components.
- Size less than 4 cm is a predictor of spontaneous resolution.
Necrotic Fluid Collection
- Contains heterogeneous fluid in terms of density.
Walled off Necrosis (WON)
- Characterized by a heterogeneous fluid collection and fibrous tracts within the necrosis.
Other Complications
- Disconnected duct syndrome: the pancreatic duct disconnects from the pancreas, leading to recurrent pancreatitis.
- Splenic vein thrombosis: may lead to portal vein thrombosis and on occasion, abdominal compartment syndrome.
Pancreatitis Crónica
- Most often caused by alcohol abuse.
Clinical Symptoms
- Steatorrhea, due to impaired lipase production, leading to a decreased ability to break down fats.
- Glucose intolerance due to pancreatic islet cell damage and decreased insulin production.
- Pancreatic calcifications.
- Chronic, dull pain, less severe than acute pain.
Diagnosis
- Clinical symptoms.
- Imaging studies.
- Endoscopic ultrasound (EUS) is the preferred imaging modality, revealing atrophy, polylobulation, and calcifications.
- Plain abdominal X-ray can reveal calcifications in up to 30% of patients.
- Secretin or cholecystokinin stimulation test is the most sensitive test.
Treatment
- Abstinence from alcohol and smoking.
- Pain management with analgesics.
- Surgery for intractable pain, obstructive jaundice, inability to rule out underlying cancer, and complications.
- Pancreatojejunostomy for diffuse duct dilation.
- Sphincteroplasty for focal ampullary obstruction or recurrent pancreatitis due to a pancreas divisum.
Key Points
- Pancreatitis is a serious condition that can have severe complications.
- Early intervention and management can significantly improve outcomes.
- Alcohol abuse is a major risk factor for pancreatitis, and abstinence is crucial for management.
- Careful monitoring and management of complications are essential for successful treatment.
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Description
This quiz explores the functions of the pancreas, focusing on both its endocrine and exocrine roles. It details hormone production by pancreatic cells and the regulation of exocrine secretion. Test your knowledge on the critical functions of the pancreas and its importance in digestion and metabolism.
