Undergraduates medicine

1. Acute pancreatitis

3. • Acute pancreatitis is a reversible inflammatory disorder that
varies in severity, from focal edema and fat necrosis to
widespread hemorrhagic necrosis.

4. Causes:
• Alcohol abuse and gallstones are the major causes.

5. Causes:
• Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps,
Autoimmune disease, Scorpion sting,
Hypercalcemia/Hypertriglyceridemia (> 1000 mg/dL), ERCP,
Drugs (eg, sulfa drugs, NRTis, protease inhibitors).
“I GET SMASHED”
Note:
• Endoscopic retrograde cholangio-pancreatography (ERCP)
• Nucleoside Reverse Transcriptase Inhibitor (NRTI): E.g. zidovudine (Retrovir), lamivudine (Epivir)

6. Pathogenesis
Acute pancreatitis appears to be caused by autodigestion
of the pancreas by inappropriately activated pancreatic
enzymes.

7. Pathogenesis

8. Acute pancreatitis
Pathogenesis
Mechanisms of activation of proenzymes
(1)Obstruction of the main pancreatic duct or terminal CBD
(2)Chemical injury of acinar cells
(3)Infectious injury of acinar cells
(4)Mechanical injury of acinar cells
(5) Metabolic activation of proenzymes (e.g., hypercalcemia,
ischemia, shock)
Leads to stimulation of Trypsin- activates various proenzymes -
resulting in Acute pancreatitis

9. Acute pancreatitis
Pathogenesis
(1) Obstruction of the main pancreatic duct or terminal CBD
(a) Gallstones
(b) Alcohol thickens ductal secretions.
• Also increases duct permeability to the enzymes

10. Acute pancreatitis
Pathogenesis
(2) Chemical injury of acinar cells
• Examples—thiazides, alcohol, triglycerides (>1000 mg/dL)
(3) Infectious injury of acinar cells
• Examples—CMV, mumps, coxsackievirus
(4) Mechanical injury of acinar cells
• Examples—seat belt trauma, posterior penetration of duodenal
ulcer

11. Acute pancreatitis
Pathogenesis
(5) Metabolic activation of proenzymes (e.g., hypercalcemia,
ischemia, shock)

12. Acute pancreatitis
Pathogenesis
RESULTS IN –
Trypsin is important in the activation of proenzymes.
(1) Proteases damage acinar cell structure.
(2) Lipases and phospholipases produce enzymatic fat necrosis.
(3) Elastases damage vessel walls and induce hemorrhage (see
(4) Activated enzymes also circulate in the blood.

13. Morphology of Acute Pancreatitis
The basic alterations in acute pancreatitis are:
(1) Microvascular leakage causing edema,
(2) Necrosis of fat by lipases, Calcium deposit (Chalky white)
(3) Acute inflammatory reaction,
(4) Proteolytic destruction of pancreatic parenchyma
(5) Destruction of blood vessels leading to interstitial
hemorrhage.

14. Complications
Pseudocyst (lined by granulation tissue, not epithelium),
Abscess,
Necrosis,
Hemorrhage,
Infection,
Organ failure (ALI/ARDS, shock, renal failure),
Hypocalcemia (precipitation of Ca2+ soaps).
ALI: Acute lung injury
ARDS: Acute respiratory distress syndrome

15. Further reading….

16. Clinical findings
a. Fever, nausea, and vomiting
b. Severe, boring (knife-like) midepigastric pain with radiation into the back
• Radiation to the back is due to its retroperitoneal location.
c. Hypovolemic shock (Third space fluid loss)
d. Hypoxemia
(1) Circulating pancreatic phospholipase destroys surfactant.
• Loss of surfactant induces atelectasis and intrapulmonary shunting.
(2) Acute respiratory distress syndrome (ARDS) may occur.
e. Grey-Turner sign (flank hemorrhage)
f. Cullen sign (periumbilical hemorrhage)
g. Disseminated intravascular coagulation
• Due to activation of prothrombin by trypsin
h. Tetany
(1) Hypocalcemia is caused by enzymatic fat necrosis.
(2) Calcium binds to fatty acids, which decreases ionized calcium.

18. • Diagnosis by 2 of 3 criteria:
- Acute epigastric pain often radiating to the
back
- Increased serum amylase or lipase (more
specific) to 3x upper limit of normal
- Or, characteristic imaging findings.