Acute Pancreatitis

Question 2

Top two causes of acute pancreatitis.

Answer 2

1. Biliary Obstruction2. Alcohol

Question 3

What 3 gene mutations can lead to acute pancreatitis?

Answer 3

1. Cationic Trypsinogen2. SPINK-13. CFTR

Question 4

How does microlithiasis cause acute pancreatitis.

Answer 4

Sludge buildup of cholesterol and calcium crystals blocks the bile and pancreatic ducts.

Question 5

Treatment for acute pancreatitis caused by microlithiasis.

Answer 5

Cholecystectomy (because gallbladder is actual problem)ERCP w/ sphincterotomyUDCA (bile salts)

Question 6

Diagnosis and treatment for autoimmune pancreatitis.

Answer 6

Dx: Elevated serum IgG4 levels and sausage-shaped pancreas on imaging. (imaging is important b/c most autoimmune cases are due to pancreatic or ampullary cancers)Tx: steroids or immune modulators

Question 7

Explain the pathophysiology of each of the following conditions and they lead to acute pancreatitis:1. Hypercalcemia2. Hyperlipidemia3. Alcohol4. Obstruction5. Bile Reflux6. Hypotension

Answer 7

1. Hypercalcemia: increased vessel permeability2. Hyperlipidemia: cell membrane disruption3. Alcohol: increased vessel permeability4. Obstruction: damage to ducts and acini5. Bile Reflux: increased vessel permeability6. Hypotension: ischemia of pancreatic vessels

Question 8

Enzyme that prevents activation of pancreatic enzymes and autodigestion of the bowels.

Answer 8

Alpha-1-anti-trypsin

Question 9

How does the mixing of lysosomal enzyme vacuoles and digestive enzyme vacuoles in exocrine pancreas cells cause enzyme activation?

Answer 9

Both Cathepsin B and an acidic pH from the lysosomal vacuoles will activate trypsin

Question 10

What is Phlegmon?

Answer 10

Spreading diffuse inflammatory process with formation of exudate or pus. Occurs in acute pancreatitis resulting in edema surrounding the organ.

Question 11

What are the systemic effects of each of the following modulators that rise in the serum as a result of trypsin activation in acute pancreatitis:1. Kallikrein2. Complement Proteins3. Thrombin4. Phospholipase A25. Chymotrypsin6. Elastase

Answer 11

1. Kallikrein: increased capillary permeability2. Complement Proteins: WBCs chemotaxis3. Thrombin: DIC4. Phospholipase A2: loss of alveolar surfactant5. Chymotrypsin: leaky capillaries6. Elastase: weakened arterial walls

Question 12

How can high macroamylassemia be differentiated from acute pancreatitis when high levels of amylase are detected in the serum?

Answer 12

Measure the urine creatinine levels.-nearly zero in macroamylassemia-elevated in acute pancreatitis

Question 13

What is the colon cutoff sign?

Answer 13

Radiology indicating acute pancreatitis. Distension of the right and transverse colon with ↓ or absent air beyond the splenic flexure. The inflamed transverse mesocolon–which is attached to the anterior pancreas ‘cuts off’ the barium flow, causing mesenteric arterial thrombosis and ischemic colitis.

Question 14

Ranson Criteria evaluates the severity of acute pancreatitis. Specific tests and conditions that, if met, are added up. The more conditions that are met, the worse the prognosis. What is Ranson Criteria at the point of administration for:
Age, WBC, Glucose, LDH, and AST?

Answer 14

Age: >55
WBC: > 16000 cells/mm^3
Glucose: >200mg/dL
LDH: >350 IU/L
AST: >250 IU/L

Question 15

What is Ranson Criteria for a patient 48hrs after acute pancreatitis onset for these categories:
Hct drop, BUN, calcium, arterial oxygen, base deficit, and fluid sequestration?

Answer 15

Hct drop: >10
BUN: increase >5mg/dL
Calcium: 4mEq/L
Fluid Sequestration: >6L

Question 16

What are Grey-Turner and Colin signs

Answer 16

GT: petechial hemorrhage on lateral flanks of abdomen indicating retroperitoneal hemorrhage.

Colin: same as GT but occur peri-umbilical

Question 17

What is treatment for acute pancreatitis? (6 things)

Answer 17

1. Hemodynamic and RENAL monitoring
2. Fluid Replenishment (important)
3. No eating, either NJ tube or IV food
4. Antibiotics (only after definitive infection Dx)
5. Oxygen if progression to ARDS
6. ERCP if biliary etiology

Question 18

What is the mechanism and resulting symptoms of hypocalcemia caused by acute pancreatitis?

Answer 18

1. Inflamed pancreas releases Lipases
2. Lipases liberate Fatty Acids (FAs)
3. (-) charge FAs attrack (+) charge calcium ions
4. Low calcium means neuro, cardiac, muscle weakness

(can be asymptomatic if the albumins and calcium decrease together)

Question 19

How does acute pancreatitis lead to ARDS and what test can predict this?

Answer 19

Trypsin induces the release of Phospholipase A2 which breaks down cell membranes liberating FAs like arachidonic acid which leads to PGs and Thromboxane synthesis resulting in inflammation which can occur in the alveolar epithelium decreasing surfactant production.

TG> 1000 means pancreatitis due to hyperlipidemia. This combination can predict ARDS.

Question 20

Main two drugs implicated in acute pancreatitis and the conditions that they are used to treat.

Answer 20

Azothioprine and 6-mercaptopurine

-used to treat IBS and autoimmune hepatitis

Question 21

What is pancreas divisum?

Answer 21

Congenital condition where an accessory pancreatic duct remains patent and ends up handling ~80% of the pancreatic secretions. The problem is that this duct (dorsal duct a.k.a. Santorini duct) is too small to handle the amount and backup occurs leading to pancreatitis. Normally secretions exit the ventral duct a.k.a. Wirsung duct.