1. Adult Medical- Surgical Nursing Gastro-intestinal Module: Pancreatitis

2. The Pancreas: Exocrine Function  Secretion of digestive enzymes, high in protein and electrolytes:  Amylase (CHO digestion)  Lipase (fat)  Trypsinogen and Enterokinase → Trypsin (protein)  Duct cells: Sodium Bicarbonate (alkaline to neutralise acidity of the chyme)

3. The Pancreas: Endocrine Function  Alpha cells: Secretion of glucagon (CHO metabolism): causes breakdown of glycogen to release glucose for energy on demand  β cells: Secretion of insulin (CHO metabolism): storage of glucose as glycogen in liver  Delta cells: Secretion of somatostatin which raises blood glucose (opposes growth hormone)

4. Pancreatitis: Classification  Acute Pancreatitis  Chronic Pancreatitis

5.  Acute Pancreatitis

6. Acute Pancreatitis  Acute inflammation, autodigestion and destruction of pancreatic tissue from hypersecretion of proteolytic enzymes especially trypsin  May be mild → severe, life-threatening  10% mortality rate  The inflammatory process is often related to underlying disease of the biliary tract, as gall- stones or long-term alcohol abuse

7. Acute Pancreatitis: Aetiology  Gall stones  High fat diet  Obesity  Alcohol abuse  Viral or bacterial infection

8. Acute Pancreatitis: Pathophysiology  Some blockage of the pancreatic duct →  Hypersecretion of enzymes  There is a reflux of enzymes with bile into the pancreas → self-digestion and pancreatitis  May be mild oedema and inflammation confined to the pancreas or  A huge outpouring of proteolytic secretions and necrosis of pancreatic tissue which can spread to surrounding tissues

9. Acute Pancreatitis: Pathophysiology (cont)  The condition may lead to systemic shock:  Hypovolaemia:  Large amounts of protein-rich fluid in the tissues and peritoneal cavity (drawing water from the circulation by osmosis)  Acute renal failure  Pulmonary effusion  Respiratory distress  DIC

10. Acute Pancreatitis: Clinical Manifestations  Severe epigastric pain and referred back pain especially after a meal, unrelieved by antacids (↑ tension within the pancreatic capsule and obstruction of ducts)  Nausea, vomiting (gastric contents or bile)  Tenderness, guarding, rigid board-like abdomen (peritonitis)  Fever  Mental confusion, restlessness  Bruising  Jaundice, bulky fatty pale stool

11. Acute Pancreatitis: Diagnosis  History and clinical picture  Serum electrolytes, LFT  ↑ Serum Amylase*/ Lipase (diagnostic)  CBC (↑ WCC), ↑ ESR, ↑ CRP  Serum bilirubin (often raised)  Random blood glucose (often raised)  Serum calcium ↓; ABG if complications  Ultrasound/ Xray: NO invasive procedure

12. Acute Pancreatitis: Medical Management  ICU, possibly ventilator required, O2  Pain relief (narcotic but avoid Morphine)  Anti-emetic  Nil orally; NG aspiration, TPN  IV fluids: glucose and electrolyte replacement, volume expanders; correct protein loss with plasma, albumen  IV antibiotics; corticosteroids; H2- receptor antagonists or proton-pump inhibitors (↓ HCl)

13. Acute Pancreatitis: Nursing Care  Rest and pain relief  Care of ventilation, O2 therapy  Nil by mouth, NG aspirations  Care of IV fluids, TPN, fluid balance  Monitor vital signs, CVP  Monitor blood gases (ABG), electrolytes, glucose (may need insulin)  Mouth care, change position, leg exercises anti-thrombo-embolus stockings (TEDs)

14. Acute Pancreatitis: Convalescence  Gradually increase oral intake  Gradually discontinue TPN (↓ debilitation)  Low fat diet  Continue to monitor electrolytes, amylase, lipase, blood glucose (may affect insulin secretion triggering type 2 diabetes)

15.  Chronic Pancreatitis

16. Chronic Pancreatitis  Chronic pancreatitis is characterised by a progressive destruction of the pancreas and its functions

17. Chronic Pancreatitis: Aetiology  Main causes are alcohol abuse and malnutrition (often combined)  Alcohol causes ↑ protein content in the pancreatic secretions, leading to protein plugs and calculi within the ducts and recurrent acute/ sub-acute attacks  Alcohol has a direct toxic effect on the pancreatic cells, especially when the diet is poor: low protein, high fat

18. Chronic Pancreatitis: Pathophysiology  Fibrosis and calcification of the gland from repeated inflammation of acute/ sub-acute attacks  Increased pressure within the pancreas  Obstruction of the pancreatic and common bile ducts with protein plugs and calcium stones  Atrophy of the epithelium of the ducts  Destruction of pancreatic cells

19. Chronic Pancreatitis: Clinical Manifestations  Intermittent exacerbations of acute/ sub-acute inflammation with epigastric and back pain  Weight loss:  Anorexia especially if alcohol-related  Fear of a further painful episode  Clinical features of malabsorption  Frequent bulky offensive pale stools  Bleeding tendency  Jaundice

20. Chronic Pancreatitis: Diagnosis  History and clinical picture  Abdominal CT scan may show calcifications  Serum Amylase may not be raised in Chronic Pancreatitis  ERCP via endoscopy with biopsy of pancreatic tissue (excludes carcinoma)  GTT: may affect insulin production

21. Chronic Pancreatitis: Management and Nursing Considerations  Dietary and lifestyle health education:  Avoid alcohol  Low fat, moderate protein diet  Monitor blood glucose from time to time  Avoid exhaustion and stress as possible  Blood coagulation studies  Monitor serum calcium, vitamin K