Pancreatitis Flashcards
1
Q
the pancreas is both:
A
- An endocrine gland: the islets of Langerhans produce insulin, glucagon, and somatostatin all to keep blood sugar in balance
- An exocrine gland: the acinar cells produce pancreatic enzymes (juices) and bicarbonate all needed for digestion
2
Q
pancreatic enzymes
A
- Pancreas contains inactive form of protease (tyrpsinogen and chymotrypsinogen). When realeased inot duodenum, these become “activated” and are then called trypsin and chymotrypsin. They help with the digestion of proteins.
- Pancreatic lipase released into duodenum to digest triglycerides and fat
- Pancreatic amylase released into duodenum to digest starches (carbohydrates)
3
Q
Acute pancreatitis**
A
- An inflammatory process that delays the release of enzymes allowing them to attack pancreatic cells and leak into surrounding tissue
- Process is know as “autodigestion”
4
Q
Two types of pancreatitis
A
- Edematous Pancreatitis: causes fluid accumulation and swelling; usually mild and self limiting
- Necrotizing Pancreatitis: more severe, causes cell death and tissue damage; involves serious complications
5
Q
In addition to build up of pancreatic enzymes, the acinar cells secrete
A
- Cytokines: vasodilation; leaky capillaries
- Platelet-activating factor: multi-organ failure, release of histamine
- Pt in state of hypovolemia because fluid is not in the right space
6
Q
Ransom criteria At admission:
A
- Age > 55 years
- Hypotension
- Abnormal pulmonary findings
- Abdominal mass
- Hemorrhagic or discolored peritoneal fluid
- Increased serum LDH levels (>350 units/L)
- AST > 250 units/:
- Leukocytosos (>16,000/mm)
- Hyperglycemia (>200 mg/dL; no diabetes history)
- Neurologic deficit (confused, localizing signs)
7
Q
Ransom criteria During Final 48 hours of Hospitalization
A
- fall in hematocrit > 10% with hydration or hamatocrit 4 mEq/L
- Azotemia
8
Q
Additional risk factors *
A
respiratory failure with intubation, shock, hypocalcemia (very poor prognosis), and massive colloid administration (if 3 or more of these are present mortality increases to near 65%)
9
Q
Causes**
A
- Obstruction: gallstones, stenosis of the sphincter of Oddi, neoplasms, congenital malformation of pancreatic duct, trauma to the duct (ERCP)
- Toxic Metabolic Processes: Ethanol abuse! Daily intake of 100-150 grams/dL “sets up a transient but severe drop in blood flow to pancreas, triggers a vicious cycle of repeated ischemic episodes resulting in cellular damage”
• 1 beer = 14 gms - Immunosuppressant drugs: azathiprine (Imuran); didanosine (videx) – these suppress the immune system which increases risk for infection which is another cause of pancreatitis
- High Triglycerides: when triglycerides level exceeds 1000 mg/dL, lipase binds to the triglycerides as free fatty acids. These damage the acinar cells. High triglycerides cause red blood cells to become sluggish in circulation capillaries “plug” up leading to stasis of blood flow and endothelial damage
- Infectious Agents:
• Viruses – Epsetin-barr, cytomegalovirus, Mealses, Mumps, Rubella, Coxsackie B
• Bacteria – legionella, mycoplasma pneumoniae, mycobacterium tuberculosis, campylobacterjejuni
• Parasites: ascaris, clonorchis
• These pathogens are thought to trigger trysinogen to become active in the pancrease instead of the duodedum resulting in “autodigestion” - “Idiopathic”
• “we don’t know what caused the pancreatitis”
• Before labeling as “idiopathic” should perform abdominal CT, xrays, and endoscopic retrograde cholangiopancreatography (ERCP) – look for abscesses, pseudocysts, blocked ducts
• ERCP: endoscopic retrograde cholangiopancreatography
10
Q
What is ERCP?*
A
ERCP:endoscopic retrograde cholangiopancreatography
Enables viewing of the biliary and pancreatic ducts, and is used in the evaluation of pancreatitis
Contrast dye is injected into the ducts through the endoscope, and radiographys are obtained
11
Q
s/s**
A
- Severe pain and vomiting – top signs
- Upper abdominal pain
- Abrupt onset
- Pain in the perumbilical area
- Abdominal distention and rigidity
- Tachycardia, tachpnea, hypotension
12
Q
What is Cullen’s sign? **
A
Bluish discoloration of the umbilicus
13
Q
Grey Turner’s? **
A
Bluish discoloration of the flank
14
Q
Lab value changes: **
A
- Increased serum amylase (as much as 4 times the normal range)
- Increased lipase levels
- Elevated lipase and urine amylase “seal” the diagnosis
15
Q
Treatment**
A
- Rest the pancreas: NPO and nasogastric tube to relieve N&V
- Bedrest
- Closely monitor fluid status (strict I&O)
- Replace fluids and electrolytes (lactated ringers of 0.9% NS)
- Monitor for hypocalemia (Chvostek/Troussau), hypermagnesmia, and hypokalemia
- Relieve pain: opioids – may give demorol instead of morphine
- Nutritional support: total parenteral nutrition: (you won’t usually give lipids to this patient – would raise triglycerides)
- Lopid (gemfibrozil): for lowering triglycerides; watch for side effects: elevated liver enzymes, myalgia, rhabdmoyolysis
- Imipenem-cilastin (Primaxin): diffuses into pancreatic tissue giving best chance of killing any invading bacteria
- Possible surgery for debriding necrotic tissue
- Provide psychological support
- Relaxation techniques
- Patient and family education
