BSN 2 Week 6 Pancreatitis

8/12/2019 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

BSN 2 Week 6 Pancreatitis

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