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Acute and Chronic Pancreatic Disease
Terms in this set (30)
What are the hallmarks of acute pancreatitis?
Aletered acinar cell protective mechanisms. Pancreatic autodigestion. Intracellular activation of proenzymes.
What cellular components are released in acute pancreatitis?
phospholipase, lysolecithin, elastase.
CYTOKINES as well!!
What vascular changes happen?
Increased permeability. Influx of inflammatory cells.
Glandular/Local tissue events of acute pancreatitis
Dissolution of BVs and extracellular matrix. Thrombosis, hemorrhage. Tissue necrosis.
What is a common presentation of the area surrounding the pancrease acute pancreatitis?
Dehydration due to "third space loss." Imflammation, fat necrosis, pancreatic and peripancreatic necrosis is also seen.
What systemic enzymes are released in acute pancreatitis?
Lipase - fat necrosis
Kalikrein - capillaries and veins.
complement - WBC chemotaxis
thrombin - DIC
elastase - BV dissolution.
chemotrypsin - capillaries
phospholipase A2 - cell membrane surfactant
What are the systemic effects of acute pancreatitis?
<b>Respiratory Failure</b> - Phospholipase A2. Diaphragm also inhibited. Low tidal volume (pain). Hemorrhage
<b>Renal Failure </b> - Lack of adequate oral fluid intake. Capillary leak. Hemorrhage. Kilakrein vasodilation (shunts blood away).
<b> DIC </b> Fibrinolytic+Coag pathway
Causes of altered acinar cell protective mechanism (the first stage of acute pancreatitis).
(1) Direct cytotoxicity (drugs, ischemia, immuno, infection) - more rare.
(2) Ductal obstruction which leads to ductal hypertension and altered membrane permeability.
Most common cause of acute pancreatitis?
Bil duct stones - 50%
second is alcohol.
Metabolic causes of acute pancreatitis?
Hyperlipidemia, Hypercalcemia (hyperparathyroidism).
"other" causes of acute pancreatitis
Obstructive (non bile duct), medications, metabolic, toxins (organic phosphates, scorpion venom), trauma (most common in children = child abuse), vascular, autoimmune, infection, genetic.
What infections could cause pancreatitis?
Mumps, coxsackie, parasites.
What are genetic causes of acute pancreatitis?
Trypsinogen, CFTR, SPINK1
Physical presentation of pt with acute pancreatitis?
Abdominal pain, back pain, nausea, vomiting, low grade fever, dehydration!
Exam: Mild distension, Dec bowel sounds - fills with gas, tenderness
Lab tests for acute pancreatitis
Measure Amylase (not used now), Lipase levels. Isolated elevated amylase may be due to ovary, fallopian tubes, salivary glands, lungs, renal insufficiency, macroamylasemia. Lipase persists longer than amylase as well.
Diagnosis of acute pancreatitis?
CT - shows necrosis. w/o IV contrast at first. If indicated at 72 hrs, with contrast. MRI not better (unless allergy or pregnant).
Early indication of severe pancreatitis
Taychacardia (HR>120, hypotension (SBP<90), hemoconcentration (Hct>50%), oliguria (<400cc/day), taychepnea (RR>32), hypoxemia (O2<90), encephalopathy
Prognosis based on?
Bedside assessment (early indicators), scoring systems (Ranson, Glasgow, Apache II), CT criteria. Serum markers - CRP, trypsinogen activator peptide (TAP), Monocyte chemotactic protein (MCP-1)
Acute Pancreatitis Tx?
None....just supportive bedside care and treat sx like DIC, shock, etc.
Supportive care for acute pancreatitis?
Aggressive fluid replacement. NPO, Monitor physical - vital, urine output, oxygen sat, volumes. Analgesia.
Antibiotics - only if definitely an infection.
Nutritional support - feeding gut helps immune system!
Organ failure support.
Chronic pancreatitis process
Changes in structure of pancreas generally precede symptoms. Always persist after precipitating cause.
Main pathophysiology of chronic pancreatitis?
Increased intraductal calcium and proteins - causes protein plugs and stones (so essentially it starts with abnormal secretion by the pancreas). This causes low grade ductal obstruction. Ductal atrophy and disruption occur. Glandular inflammation and fibrosis. Fibroblasts, lymphocytes, plasma cells.
Ultmately loss of exocrine and endocrine secretion.
What is the most common cause of chronic pancreatitis?
95% - alcohol.
What is the effect on alcohol on the pancreas?
Direct acinar cell toxicity, alters membrane infrastructure (inc permeability), increases basal protein secretion, decreases trypsin inhibitor, alters lithostatin - causes precipitation of calcium.
Non-alcohol causes of chronic pancreatitis
Chronic partial duct obstruction
Presentation of patient with chronic pancreatitis (what % get recurrent acute pancreatitis, what % get insidious)?
Recurrent acute pancreatitis - 50%
35% - insidious abdominal pain
15% - malabsorption (loss of digestive enzymes), diabetes (loss of insulin), jaundice (obstruction)
Sx of chronic pancreatitis
Chronic pain. Radiates to back, worse with food. Malabsorption - steattorhea, diarrhea. Diabetes. Weight loss! Pain first but later goes away.
Diagnosis of chronic pancreatitis.
Physical and labs not helpful!
Imaging: plain film (calcifications), ct, MRI (parynchemal fibrosis and ductal abnormalities), EUS - endoscopic evaluation.
Complications of chronic pancreatitis
Narcotic addiction, malnutrition, pseudocyst formation,
Tx of Chronic Pancreatitis
Low fat diet
Celiac plexus neurolysis
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