Acute Pancreatitis Flashcards
(52 cards)
Pathophysiology
AP is the final result of abnormal pancreatic enzyme activation inside acinar cells
What is an Early step before elevation of amylase and lipase ?
> > zymogen and lysosome colocalization occurs before amylase level elevation, pancreatic edema, and other markers of pancreatitis are evident suggests that colocalization is an early step in the pathophysiologic process
Role of Cathepsin B
> > cathepsin B that then induces apoptosis or necrosis, leading to acinar cell death.
> > Thus, acinar cell death and to a degree the inflammatory response seen in AP can be prevented if acinar cells are pretreated with cathepsin B inhibitors.
What happens to the Protective mechanism ?
> > Intraacinar pancreatic enzyme activation induces autodigestion of normal pancreatic parenchyma.
> > release proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-1, IL-2, and IL-6, and antiinflammatory mediators, such as IL-10 and IL-1 receptor antagonist.
> > propagate the response locally and systemically
What frequently seen in patients with severe pancreatitis
> > Active neutrophils mediate acute lung injury and induce the adult respiratory distress syndrome frequently seen in patients with severe pancreatitis
The mortality seen in the early phase of pancreatitis is the result of
persistent inflammatory response
RF ?
- Gallstones and ethanol abuse account for 70% to 80% of AP cases.
- In pediatric patients, abdominal blunt trauma and systemic diseases are the two most common conditions that lead to pancreatitis.
- Autoimmune and drug-induced pancreatitis should be a differential diagnosis in patients with rheumatologic conditions such as systemic lupus erythematosus and Sjögren syndrome
most common cause of AP in the West
Gallstone pancreatitis is the most common cause of AP in the West
Two theories have been proposed
> > obstructive theory, pancreatic injury is the result of excessive pressure inside the pancreatic duct
> > Reflux, theory proposes that stones become impacted in the ampulla of Vater and form a common channel that allows bile salt reflux into the pancreas.
Alcohol damages the pancreas through multiple mechanisms:
- Inflammation → Activates NF-κB, TNF-α, IL-1
- Enzyme Misrelease → Causes zymogen exocytosis at the wrong site
- Autophagy Dysregulation → Due to cathepsin L & B imbalance
- Oxidative Stress → Leads to mitochondrial dysfunction
- Fibrosis → Activates pancreatic stellate cells (PSCs), increasing matrix metalloproteases
- Impaired Repair → Affects PDX1, PTF1a, Notch
- Cell Death Shift → From apoptosis to necrosis due to ↓ caspase 3/8 & ATP loss
Anatomic Obstruction
> > Pancreas divisum is an anatomic variation present in 10% of the population.
caused by relative outflow obstruction through the minor papilla.
(ERCP) with minor papillotomy and stenting may be beneficial for such patients.
> > Infrequent anatomic obstructions that have been associated with AP include Ascaris lumbricoides infection and annular pancreas.
what can be done to prevent ercp pancreatitis ?
> > indomethacin
pancreatic stents
using minimal pressure while performing ERCP
ERCP
- AP is the most common complication after ERCP, occurring in up to 5% of patients
- PostERCP pancreatitis is more common in
»female patients
»young individuals
»patients with prior history of ERCP induced pancreatitis.
> > AP occurs more frequently in therapeutic procedures
who have had multiple attempts of cannulation,
sphincter of Oddi dysfunction
abnormal visualization of the secondary pancreatic ducts after injection of contrast material.
Drug-Induced Pancreatitis
- sulfonamides
- metronidazole
- erythromycin
- tetracyclines
- didanosine
- thiazides
- furosemide
- 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins)
- azathioprine
- 6-mercaptopurine
- 5-aminosalicylic acid
- sulfasalazine
- valproic acid
- human immunodeficiency virus antiretroviral agents
Metabolic Factors
- Hypertriglyceridemia and hypercalcemia
> > more common in patients with type I, II, or V hyperlipidemia.
suspected triglyceride level higher than 1000 mg/dL.
higher than 2000 mg/dL confirms the diagnosis.
- Hypercalcemia»_space; activation of trypsinogen to trypsin and intraductal precipitation of calcium
> > Approximately 1.5% to 13% of patients with primary hyperparathyroidism develop AP
Miscellaneous Conditions
-Blunt and penetrating abdominal trauma
-intraoperative hypotension and excessive pancreatic manipulation
-Pancreatic ischemia in association with acute pancreatic inflammation can develop after splenic artery embolization
-Scorpion Venom
-Perf DU
indicative of retroperitoneal bleeding
Rare findings include flank and periumbilical ecchymosis (Grey Turner and Cullen signs, respectively)
diagnosis of AP
2 out of 3 :
1) abdominal pain consistent with AP (acute onset of a persistent, severe, epigastric pain often radiating to the back)
2) threefold or higher elevation of serum amylase or lipase levels above the upper laboratory limit of normal
3) characteristics findings of pancreatitis by imaging.
The serum half-life of amylase and lipase
The serum half-life of amylase (10 hours)
lipase (6.9–13.7 hours)
normalizes faster (3–5 vs. 8–14 days, respectively).
Lipase Vs Amylase
> > In patients who do not present to the emergency department within the first 24 to 48 hours after the onset of symptoms, determination of lipase levels is a more sensitive indicator to establish the diagnosis.
Lipase is also a more specific marker of AP
Amylase can be elevated in
peptic ulcer disease and mesenteric ischemia
ALT ??
The elevation of alanine aminotransferase levels in the serum in the context of AP confirmed by high pancreatic enzyme levels has a positive predictive value of 95% in the diagnosis of acute biliary pancreatitis
simple abdominal radiographs
- air-fluid levels suggestive of ileus
- cutoff colon sign as a result of colonic spasm at the splenic flexure
- widening of the duodenal C loop caused by severe pancreatic head edema
Indications for CT include
- diagnostic uncertainty
- confirmation of severity based on clinical predictors,
- failure to respond to conservative treatment
- clinical deterioration.
The most valuable contrast phase in which to evaluate the pancreatic parenchyma is the portal venous phase
(65–70 seconds after injection of contrast material)
