PANCREATITIS Flashcards

1
Q

What is the daily volume and pH of pancreatic fluid secretion?

A

“The pancreas secretes 1500-3000 ml of isosmotic alkaline fluid (pH >8) daily.”

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2
Q

What is the role of bicarbonate secreted by the pancreas?

A

“Bicarbonate neutralizes gastric acid

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3
Q

What triggers the release of secretin and what does it stimulate?

A

“Gastric acid triggers secretin release from duodenal mucosa (S cells)

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4
Q

What triggers the release of cholecystokinin (CCK)?

A

“Diets containing long-chain fatty acids

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5
Q

What are the primary stimulatory neurotransmitters for pancreatic secretion?

A

“Acetylcholine and gastric-releasing peptide stimulate pancreatic secretion during the cephalic phase.”

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6
Q

Which neuropeptides inhibit pancreatic secretion?

A

“Somatostatin

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7
Q

How is autodigestion of the pancreas prevented?

A

“Autodigestion is prevented by packaging proteases as proenzymes

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8
Q

What are the major enzymes secreted by the pancreas?

A

“Amylolytic (amylase)

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9
Q

How are pancreatic proteolytic enzymes activated?

A

“Proteolytic enzymes are secreted as inactive zymogens and activated by enterokinase in the duodenal mucosa.”

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10
Q

What is the function of enterokinase?

A

“Enterokinase cleaves the lysine-isoleucine bond of trypsinogen to form trypsin

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11
Q

What is the role of bicarbonate in feedback inhibition of pancreatic secretion?

A

“Bicarbonate neutralizes acidic chyme

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12
Q

What are the common causes of acute pancreatitis?

A

“Gallstones

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13
Q

What are the risk factors for post-ERCP pancreatitis?

A

“Risk factors include minor papilla sphincterotomy

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14
Q

What triglyceride level is associated with acute pancreatitis?

A

“Triglyceride levels >1000 mg/dl are associated with acute pancreatitis.”

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15
Q

What is the appearance of blood in hypertriglyceridemia?

A

“Blood appears milky or like mayonnaise due to excessive triglycerides.”

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16
Q

What is SPINK1 and its role in acute pancreatitis?

A

“SPINK1 is a protective protease inhibitor that binds and inactivates trypsin to prevent autodigestion of the pancreas.”

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17
Q

What are the two types of pancreatitis based on severity?

A

Interstitial Pancreatitis and Necrotizing Pancreatitis

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18
Q

What characterizes interstitial pancreatitis?

A

Mild form, resolves in a week, and blood supply is not interrupted.

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19
Q

What characterizes necrotizing pancreatitis?

A

Interrupted blood supply to the pancreas.

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20
Q

What is the accepted pathogenic theory of acute pancreatitis?

A

Autodigestion.

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21
Q

What factors facilitate premature activation of trypsin?

A

Endotoxins, exotoxins, viral infections, ischemia, oxidative stress, lysosomal calcium, and direct trauma.

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22
Q

What happens during the initial phase of acute pancreatitis pathogenesis?

A

Intrapancreatic digestive enzyme activation, acinar cell injury, and trypsin activation.

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23
Q

What happens during the second phase of acute pancreatitis pathogenesis?

A

Chemoattraction and sequestration of leukocytes and macrophages, enhancing intrapancreatic inflammation.

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24
Q

What happens during the third phase of acute pancreatitis pathogenesis?

A

Proteolysis, edema, interstitial hemorrhage, systemic inflammation, and potential organ failure.

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25
Q

What genetic mutation is sufficient to cause acute pancreatitis without risk factors?

A

Cationic trypsinogen gene (PRSS1).

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26
Q

What does a mutation in the PRSS1 gene lead to?

A

Unregulated trypsin activation in acinar cells, predisposing to acute pancreatitis.

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27
Q

What are the major symptoms of acute pancreatitis?

A

Steady epigastric pain radiating to back, nausea, vomiting, and abdominal distension.

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28
Q

Why does abdominal pain decrease when leaning forward in acute pancreatitis?

A

The pancreas is a retroperitoneal organ, and this position reduces tension.

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29
Q

What causes jaundice in acute pancreatitis?

A

Compression due to peripancreatic edema, pancreatic head mass, or intraductal obstruction.

30
Q

What are Cullen’s and Turner’s signs?

A

Cullen’s: Blue discoloration around umbilicus. Turner’s: Discoloration of the flanks.

31
Q

What lab findings are indicative of acute pancreatitis?

A

Amylase or lipase ≥3x normal, leukocytosis, hemoconcentration, and elevated BUN.

32
Q

Which enzyme is more specific for pancreatitis, amylase or lipase?

A

Lipase.

33
Q

What does ALT >3x ULN strongly indicate?

A

Gallstone etiology of pancreatitis.

34
Q

Which imaging modality is used to detect gallstones in pancreatitis?

A

Abdominal ultrasound.

35
Q

What are common complications of pancreatitis?

A

Pancreatic pseudocyst, ascites, and pancreatic necrosis.

36
Q

What systemic symptoms may occur in severe acute pancreatitis?

A

SIRS, ARDS, and multiple organ failure.

37
Q

How does hypocalcemia occur in acute pancreatitis?

A

Calcium binds to fatty acids during fat necrosis.

38
Q

Why is CT with contrast used in pancreatitis imaging?

A

To assess pancreatic enhancement and necrosis.

39
Q

What are common causes of hyperamylasemia?

A

Salivary gland lesions, renal failure, burns, diabetes, pregnancy, and pancreatic disorders.

40
Q

Which electrolyte is critical in the pancreas’ auto-protection mechanism?

A

Calcium.

41
Q

What lab marker is associated with mortality risk in acute pancreatitis?

A

BUN >22 mg/dL.

42
Q

How do proteases contribute to the feedback inhibition of pancreatic secretion?

A

Proteases digest proteins in the duodenum, reducing free CCK and secretion of enzymes.

43
Q

What are the diagnostic criteria for acute pancreatitis?

A
  1. Typical abdominal pain in the epigastrium that may radiate to the back, 2. >3x elevation in serum lipase/amylase, 3. Confirmatory findings on cross-sectional imaging (CT Scan).
44
Q

What are the risk factors for severe acute pancreatitis?

A

Age >60 years, obesity (BMI >30), and comorbid disease (Charlson index).

45
Q

What are the SIRS criteria for acute pancreatitis severity?

A
  1. Core temperature <36°C or >38°C, 2. Heart rate >90 beats/min, 3. Respiratory rate >20/min or PCO2 <32 mmHg, 4. WBC >12,000/µL, <4,000/µL, or 10% bands.
46
Q

What is the BISAP scoring system for pancreatitis severity?

A
  1. BUN >25 mg/dL, 2. Mental status impairment (GCS <15), 3. SIRS (≥2 criteria), 4. Age >60 years, 5. Pleural effusion.
47
Q

What defines persistent organ failure in acute pancreatitis?

A

Organ failure lasting >48 hours.

48
Q

What are the phases of acute pancreatitis?

A
  1. Early phase (<2 weeks): SIRS and organ failure, 2. Late phase (>2 weeks): Protracted course with necrosis and complications.
49
Q

What characterizes mild acute pancreatitis?

A

No local complications or organ failure; resolves spontaneously within 3-7 days.

50
Q

What characterizes moderate acute pancreatitis?

A

Transient organ failure, local/systemic complications, with or without necrosis.

51
Q

What characterizes severe acute pancreatitis?

A

Persistent organ failure (>48 hours), necrosis, and complications requiring prolonged hospitalization.

52
Q

When should a CT/MRI be performed in severe acute pancreatitis?

A

On the 3rd day if the patient is not improving.

53
Q

What are the two imaging types for acute pancreatitis?

A
  1. Interstitial pancreatitis: Homogeneous contrast enhancement, resolves in a week, 2. Necrotizing pancreatitis: Pancreatic parenchymal necrosis with or without organ failure.
54
Q

What percentage of acute pancreatitis cases are interstitial?

A

90-95%.

55
Q

What percentage of acute pancreatitis cases are necrotizing?

A

5-10%.

56
Q

What is the most important management step for acute pancreatitis?

A

Early and aggressive fluid resuscitation.

57
Q

What IV fluids are recommended for acute pancreatitis?

A

Lactated Ringer’s or Normal Saline at 15-20 mL/kg, targeting urine output >0.5 mL/kg/hr.

58
Q

What is the purpose of monitoring hematocrit and BUN every 8-12 hours?

A

To assess hydration adequacy and severity; decreasing hematocrit and stable BUN indicate adequate resuscitation.

59
Q

What analgesics are used in acute pancreatitis?

A

NSAIDs, ketorolac, and tramadol (50 mg IV q6-8h).

60
Q

What is the management for gallstone pancreatitis with ascending cholangitis?

A

ERCP within 24-48 hours.

61
Q

What are the cardinal symptoms of ascending cholangitis?

A

Fever, right upper quadrant pain, and jaundice.

62
Q

When is same-admission cholecystectomy recommended?

A

For mild gallstone pancreatitis.

63
Q

What are the key findings in necrotizing pancreatitis on CT?

A

Lack of pancreatic parenchymal enhancement and/or peripancreatic necrosis.

64
Q

What does BISAP stand for?

A

Bedside Index of Severity in Acute Pancreatitis.

65
Q

What differentiates interstitial from necrotizing pancreatitis?

A

Interstitial: Homogeneous contrast enhancement; Necrotizing: Pancreatic or peripancreatic necrosis.

66
Q

What complications are seen in late-phase acute pancreatitis?

A

Necrosis, systemic complications, and persistent organ failure.

67
Q

What imaging is used to confirm pancreatic necrosis?

A

CT or MRI.

68
Q

What supportive care is needed for persistent organ failure?

A

Renal dialysis, ventilator support, and supplemental nutrition.

69
Q

When should ICU admission be considered in acute pancreatitis?

A

If SIRS is present within 24 hours or BISAP ≥3.

70
Q

What imaging is first-line to rule out gallstones in pancreatitis?

A

Abdominal ultrasound.

71
Q

Why are prophylactic antibiotics not recommended in severe pancreatitis?

A

They do not prevent infection in necrotizing pancreatitis.

72
Q

What is the purpose of ERCP in gallstone pancreatitis?

A

To remove bile duct obstructions causing ascending cholangitis.