Acute Pancreatitis Flashcards
Location of pancreas
Largely retroperitoneal, though tail is in intraperitoneal (2 cavities)
Behind stomach and connects with duodenum
What does the pancreas connect to?
Behind stomach and connects with duodenum
Also connected via bile duct to gallbladder and liver
Common bile duct continues down and joins with bile duct and eventually empties into duodenum
What occurs when pancreas becomes inflammed?
When pancreas becomes inflamed, inflammation is not contained and effects surrounding organs
3 Main Functions of Pancreas and Cells responsible
- Neutralize stomach acid prior to entering small intestine (ductal cells secrete bicarb rich fluid)
- Endocrine - secretes hormones (glucagon, insulin, somatostatin, pancreatic polypeptide) into bloodstream (islet cells)
- Exocrine: Acinar cells (inactivated enzymes into duodenum to become activated)
* Amylases (carbs)
* Lipases (lipids)
* Protease (proteins): such as Elastase, Chymotrypsin, Trypsin, Kallikrein
Enzymes travel through pancreatic duct, join with bile duct and are dumped into duodenum
Protease inhibitors (keep enzymes inactive until duodenum)
> Called zymogens in inactive form
> Activated by enterokinase
What causes inflammation in pancreatitis?
- inappropriate activation of pancreatic enzymes
- destruction of dustal tissue/pancreatic cells
- autodigestion and fibrosis
Consequences of pancreas not being encapsulated
When auto-digesting and inflamed, nothing stopping the inflammation from spreading to other tissue
Explain autodigestion
- Role of lipase and protease = break down fat and protein when activated
- pancreas is largely made up on fat and protein
3, Pancreatic structure breaks down and leads to obstruction of outflow of the pancreatic duct leading to pressure build-up
- Kallikrein
* Vasodilation and increases permeability of blood vessels, pain, and leukocyte invasion
* Part of inflammatory process
* Causes bradykinin formation (potent vasodilator)
* Systemic hypotension shock
2 Major causes of pancreatitis
- Gallstones: obstructs ducts
- Alcohol: Thickens secretions leading to obstruction, brings more neutrophils to pancreas which can activate proteases leading to protein breakdown/autodigestion, and stimulate acinar cells to release more enzymes which can inadvertently become activated
= activation of pancreatic enzymes and injury to pancreatic cells
Lead to one of 2 things activating enzymes + beginning autodigestive process:
1. Obstruction in ducts - gallstones
2. Damage to Acinar Cells – chronic alcohol
Severity of Acute Pancreatitis
- Mild= interstitial edematous pancreatitis
* Edema, inflammation
* Can resolve after a few days - Severe= necrotizing hemorrhagic pancreatitis (NHP)
* Diffuse bleeding pancreatic tissue, fibrosis, tissue death (necrosis)
* 10% of acute pancreatitis cases
* Not as common
* Risk of death increases
* Global incidence increasing with increased alcohol use
* Prognosis worsened when caused by alcohol over gallstones
Chronic Pancreatitis Definition and 3 associated symptoms
Progressive destruction of pancreas with remissions and exacerbations (flare-ups)
- inflammation/tissue fibrosis
- loss of exocrine functin (decreased pancreatic secretion/bicarb)
* Malabsorption syndrome because of lack of enzymes to breakdown food:
* Steatorrhea from inability to breakdown fat; non-absorption
* Weight loss, muscle wasting - loss of endocrine function = diabetes
Most common cause of chronic pancreatitis
Chronic ETOH
Pancreatic Enzyme Levels with Acute pancreatitis
Elevated
- Amylase (not best indicator, because also secreted in mouth)
- **Lipase is best indicator – 3x upper limit of normal
indicates pancreatic cell injury
Bilirubin, ALT and AST Levels wigh acute pancreatitis
Elevated
indicates Hepatobiliary involvement/obstruction
CRP acute pancreatitis
elevated; nonspecific inflammation
WBC acute pancreatitis
elevated; nonspecific infection/inflammation
BG acute pancreatitis
Elevated
Pancreatic cell injury/decrease in insulin production
Calcium levels acute pancreatitis
Decreased
Fatty acids combined with calcium decreasing level: fat necrosis
Or can be increased = cause (gallstone)
HcT Acute pancreatitis
Elevated; hemoconcentration; third spacing
Hgb Acute pancreatitis
Decreased
Bleeding
Triglycerides acute pancreatitis
Elevaed
Identify cause of pancreatitis
BUN creatinine acute pancreatitis
Elevated
renal hypoperfusion
What do Abdominal and chest x-rays in acute pancreatitis demonstrate?
Dilation of nearby small intestine
Pleural effusion
Gallstone
What would an ultrasound demonstrate in acute pancreatitis demonstrate?
In RUQ
Gallstone/ductal dilation
What is an ERCP/MRCP
Endoscopic retrograde cholangiopancreatography, or ERCP, is a procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas.
special kind of MRI test. Your healthcare provider uses it to look at the biliary and pancreatic system. This includes the pancreas, the pancreatic duct, the bile ducts, gallbladder, and liver.
Cues of acute pancreatitis
- Sudden onset**
- Severe epigastric/abdominal pain/tenderness
- Pain radiates to back in 50% of cases
- Hypotension
- Respiratory distress
- Abd. Distention
- Poor urine output
- Tachycardia
- Vomiting
- Jaundice
- Fever
- Hypocalcaemia
Pain associated with acute pancreatitis
Classic pain= severe, mid-epigastric or LUQ
- Sudden onset
- Sharp, deep, constant
- Severe
- Radiates to back
- Epigastric or LUQ
- Nausea/vomiting
- Positional: worse when lying on back
Abdominal assessment findings of acute pancreatitis
- Abdominal distention
- Absent/decreased bowel sounds
- Nausea/vomiting
- Peritoneal signs
- Ascites (self-perpetuating inflammatory process increasing permeability and vasodilation)
- Cullen’s sign
- Grey Turner’s sign
- Enzymes eating away at vasculature causing bleeds in both intraperitoneal and retroperitoneal spaces
- Jaundice: gallstones as cause; can block bile excretion from liver
What are the actions aimed at in treatment of acute pancreatitis?
Minimization of pancreatic stimulation
1. GI rest
2. nutritional support
3. social support
What GI rest interventions occur in acute pancreatitis?
- Prevent/relieve gastric distension (NG tube)
* Suction for severely ill (continuous vomiting, biliary obstruction)
* Gastric decompression to prevent acidic gastric juices from duodenum since pancreas is not secreting bicarb
* Necessary for prolonged time with paralytic ileus that is secondary to increased inflammation - NPO
- IV fluids*
* Third spacing occurring due to widespread inflammatory response (increased permeability) – fluid volume decreasing – decreased CO - PPIs or histamine receptor antagonists decrease gastric acid secretion
Why are IV fluids necessary in acute pancreatitis?
Third spacing occurring due to widespread inflammatory response (increased permeability) – fluid volume decreasing – decreased CO
What electrolytes are of most concern in acute pancreatitis and why?
Lipase break down peripancreatic fat tissue causing liquefactive necrosis (cell death of tissue into liquid form)
> Triglycerides released (lipolysis) free fatty acids
> Calcium binds with free fatty acids = Hypocalcaemia
= Chvostek’s and Trousseau’s Sign
> Hypomagnesemia
> May require IV CaMg replacement
Why is fluid accumulation an issue in acute pancreatitis?
Liquefactive necrosis > fluid accumulation from remnants of fat cells
- Fibrous tissue surround fluid collections: encapsulated fluid collection = pseudocyst
> Can grow & compress other organs
> Pseudocyst = can become infiltrated with e-coli = bacterial infected area = pancreatic abscess
> Can grow & compress on other organs
> Fever, severe abdominal pain, leukocytosis
Systemic Complications of Acute Pancreatitis (7)
- Vasodilation > decreased systemic vascular resistance hypotension
- Increased permeability of vessel linings + interstitial edema = decreased effective arterial blood volume = decreased CO
> Less blood getting to brain decreased LOC/altered mental status
> Decreased blood being oxygenated = hypoxemia
> Activates SNS =tachycardia - Increase activity of pro-coagulant enzymes & decrease anti-coagulant enzymes
> Clots & bleeding (hemorrhage) DIC - Stimulates hypothalamus = increased body temp = fever
- Activates bone marrow = increased WBC = leukocytosis
- Liver = releases CRP
- Protease & lipases destroy proteins and fats associated with nearby blood vessels
> Blood accumulates around pancreas = hemorrhagic necrosis
> Hypovolemic shock d/t massive rupture of large vessel (i.e. aorta)
Pulmonary Complications Associated with Acute Pancreatitis
Each complication goes back to inflammatory response that is not confined to pancreas!
- ARDS
pulmonary edema that is not of cardiac origin
> Increased pulmonary capillary permeability = leaking into interstitial spaces & lung parenchyma
* Hypoxemia
* Resp failure
* #1 cause of pancreatic mortality - Pneumonia: fluid in space becomes infected
- Pleural effusion (pancreatic effusion)
* Diaphragmatic fistula between pancreas & pleural cavity due to autodigestion
* Reduces lung capacity, decreased gas exchange
* Due to proximity of autodigestive process to lungs
* SOB, unequal lung sounds
Renal Complications Associated with Acute Pancreatitis
Each complication goes back to inflammatory response that is not confined to pancreas!
Risk for ATN**
> Hypotension (shock – decreased perfusion to kidneys), infection, vascular changes/systemic inflammation
Monitor:
* Urine output
* Urine color can become brownish & foamy from excess bile secreted in urine
* BUN, Creatinine
* Fluid status: Ins/Outs
* Treatment: fluid replacement
Neurologic Complications Associated with Acute Pancreatitis and potential reasons
Each complication goes back to inflammatory response that is not confined to pancreas!
- Confusion
- Restlessness
- Agitation
- Decreased LOC
Reasons
* Analgesia (sedative side effects of narcotics)
* Pancreatic encephalopathy (cerebral edema secondary to enzyme release)
* Shock (decreased perfusion)
