bsn 2 week 6 pancreatitis
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Pancreatitis& Pancreatic Failure
Biomedical Science and Nursing 2
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Exocrine and Endocrine Functions:
Exocrine: Function is to produce pancreatic juice
containing enzymes that digest carbohydrates,proteins and fats
Endocrine: To secrete the insulin and glycagon hormones
primarily for the control of blood glucose levels.
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Pancreatic microanatomy
Islets of Langerhans. Alpha cells secrete hormone glucagon. Beta cells secrete hormone insulin.
Delta cells secrete growth hormone inhibitionfactor. They are surrounded by capillaries and cells (acini)
= exocrine part.
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Aqueous secretions of the exocrinepancreas
Isotonic Potassium, bicarbonate sodium magnesium calcium and chloride Sodium and potassium concentrations are about equal to those
in plasma Concentration of bicarbonate varies directly with flow of
secretions. As bicarbonate secretion increases, chloride secretion
decreases to maintain a constant anionic concentration
Highly alkaline pancreatic juice neutralizes the acid chyme thatenters the duodenum from the stomach and provides the alkalinemedium needed for the actions of digestive enzymes and theabsorption of fat in the intestine
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Pancreatic enzymes
Hydrolyze proteins, carbohydrates and fats The protein digesting (protolytic) enzymes include:
trypsin, chymotrypsin, carboxypeptidase
They are secreted in their inactive form to protect thepancreas from the effects of its own enzymes Further protection trypsin inhibitor
Once in the duodenum the inactive forms orproenzymes are activated by enterokinase
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Secretion of aqueous and enzymaticcomponents
Controlled by hormonal and vagal stimuli
Secretin stimulates the acinar and duct cells to secrete thebicarbonate rich fluid that neutralizes chyme and prepares itfor digestion.
As chyme enters the duodenum its acidity (pH< 4.5)stimulates the S cells (secretin producing cells) of theduodenum to release to release secretin which is absorbedby the intestine and delivered to the pancreas in the bloodstream.
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Enzymatic secretion
Enzymatic secretion follows and is stimulated bycholecytokinin and acetylcholine.
Both act on acinar cells causing enzyme release.
Once in the small intestine, activated pancreaticenzymes inhibit the release of morecholecytokinin and acetylcholine.
THIS FEEDBACK MECHANISM INHIBITS THE SECRETIONOF MORE PANCREATIC ENZYMES
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Pancreatitis: definition
Inflammation of the pancreas that can involve surroundingpancreatic tissue and remote body systems (Mergener & Baillic,1998)
Autodigestive process Defined as chronic or acute Acute
oedematous or interstitial pancreatitis (mild-moderate) haemorrhagic pancreatitis (severe) necrotizing pancreatitis (severe)
Majority have mild disease, 10-15% have severe pancreatitiswhere biochemical abnormalities occur which leads to multi-system organ failure & death
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Pathophysiology
Aetiological factor (GET SMASHED) Initial process Initial damage
Premature activation of enzymes Proteases Lipases
Local & systemic effects
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Aetiology
Gallstones Ethanol Abuse Trauma & Tumours Scorpion Mumps & Viral Infections Autoimmune Steriods Hyperlipidemia/Hypercalcaemia/
Hypothermia
ERCP Drugs (thiazide, cytotoxic,
salicylates, sulphonamide)
G E T S
M A S H
E D
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Aetiology & risk factors:
Alcohol. Physiochemical alteration to protein that results in plugs
that block the small pancreatic ductules.(Black, 2001).
Cholelithiasis. Stones or bile sludge migrate into the common bile duct
(CBD) causing diversion of bile into the pancreatic ductleading to premature activation of enzymes &
autodigestion
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Pathophysiology:
Ini t ial dam age
Injury or disruption to the pancreatic ducts or acini.
Autolysis (Autodigestion): chemical burn Breakdown of proteins in pancreatic tissue by proteases.
Lipid breakdown in pancreatic tissue by lipases
Interstitial oedema within the pancreatic parenchymaltissue +/- necrosisTrypsin (protease) converts kallikrein to bradykinin whichincreases capillary permeability (leaky)
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Pathophysiology: Local & systemic effects
Psuedocyst (fluid collection) develop from pancreatic juices collecting
within or immediately adjacent to pancreas,then become enclosed or encapsulated in afibrous capsule
Trysin converts proelastase to elastase Destroys blood vessels, so toxic enzymes &
mediators can be released into the bloodstream causing injury to vessels & organs(kidneys and lungs).
Abscess formation or haemorrhage Autodigestion of tissue and blood vesselsresults in necrosis
Ongoing damage vicious cycle Inflammatory process risk of myocardial
depression, hypoperfusion (leaky
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Chronic Pancreatitis:
Related to chronic ETOH abuse. Progressive destruction, irregular fibrosis & chronic
inflammation strictures, continued inflammation uncertain pathogenesis, unpredictable clinical
course & unclear treatmentRubin & Farber (1999)
50% of pts will have repeated episodes of acutepancreatitis
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Chronic Pancreatitis S&Ss
Continuous / intermittent abdominal pain worse after ameal.
Weight loss May show signs of enzyme deficiency (streatorrhoea)
requiring oral supplements before and during meals. Loss of islet functioning can lead to diabetes. Cessation of ETOH is essential
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Clinical Signs & Symptoms
Pain Respiratory distress Nausea & vomiting Fever Tachycardia Hypotensive. Dry mucous membranes Poor skin turgor (tone) urine output or anuria
Haematocrit. Serum sodium Hyperglycaemic High amylase & lipase Coagulopathy Low magnesium/ potassium/
calcium Cullens Sign Grey- Turners Sign
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Acute Clinical Manifestations
Pain. Continuous boring epigastric pain, usually poorly
localized, often worse in the supine position Radiation to the back Due to oedema (distends pancreatic duct /
capsule). Signs of peritoneal irritation may be absent Irritation / obstruction of the biliary tree.
Nausea & vomiting from hyper motility or small bowel paralyticileus
Fever & leukocytosis from inflammatory response
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Clinical Manifestations:
Abdominal distention - accumulation of fluids inperitoneal cavity.
Vascular permeability and dilated vessels from theaffects of kinins and enzymes being released leads tohypotension and myocardial depression.
Tachypnoea, and hypoxaemia due to pulmonaryoedema, atelectasis or pleural effusions from circulatingpancreatic enzymes.
Hyperglycaemia if glucagon is released from damagedalpha cells or insufficient insulin production.
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Diagnosis:
Based on clinical findings Ransons Criteria in predicting mortality Serum amylase levels rise in the first 12 hours and last up to 3 5
days. Serum lipase elevated. Urine amylase elevated for longer period Ct scan most useful Abdominal ultrasound Differential diagnosis.
Perforated duodenal ulcer. Cholecystitis. Small bowel obstruction.
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Ransons Clinical Indicators for predicting severe pancreatitis
Signs on admission
Age >55 years
WBC > 16,000 mcl Serum glucose > 200
mg/dL (11.1) Serum LDH > 350 U/L
AST > 250 U/L Base deficit > 4 mEq/L
Signs during 1st 48 hrs
fall in haemocrit > 10%
BUN rise > 5 mg/dL Serum calcium < 8mg/dL estimated fluid loss > 6 L PaO2 < 60 mmHg
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Management: Nothing by mouth initially , IV hydration & pain relief
Analgesia. ? Previous thought - morphine causes spasm of the
sphincter of Oddi & therefore avoid ? query the evidence for this, Morphine is used in
some cases now. Pethidine or Fentanyl used
Maintaining fluid volume status.
Oral fluids in mild cases, NG/IV in moderate -severecases
Nasogastric tube may be for decompression if fluidaccumulates in stomach & ileus, or vomiting
Fluid replacement in accordance with vital signs, urea &electrolytes and urine output.
A CVC +/- IDC may be inserted depending on severityof condition
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Management:
Electrolyte abnormalities. Vomiting = hypokalaemia. Hypoalbuminaemia Hypocalcaemia.
Hyperglyaemia = insulin management / fluidreplacement. Medications may include:
Somastatin inhibit pancreatic secretion
Protease inhibitors Antibiotics high dose cefuroxime H2 receptor antagonists ? effectiveness
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Management
Enteral nutrition Vs Parenteral Possibly nasojejunal tube
Nutrition.
When diet recommences, have highin CHO (less stimulating to theendocrine portion of the pancreas).
Low fat, high protein, avoidstimulants.
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Complications:
Pseudocyst Cavity continuous with the pancreas Filled with necrotic products and secretions Surrounding tissue becomes inflamed, leading to encapsulation
of the exudate Generally resolve spontaneously, but may rupture and lead to
peritonitis Abscess
Large fluid filled cavity Extensive necrosis of the pancreas Requires surgery to prevent sepsis.
Pulmonary complications Pleural effusion, atelectasis, pneumonia
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Surgical Management:
The role of surgery remains controversial -associated with high mortality Treatment of pancreatic necrosis / abscess or
pseudocyst
Insertion of drain tubes Debridement of necrotic tissue
Uncertainty of diagnosis Exploratory laparotomy
Correction of associated biliary tract disease Cholecystectomy