Acute pancreatitis Flashcards
What is acute pancreatitis?
Sudden inflammation of the pancreas in which the exocrine function of the pancreas is dysfunctional. This is associated with acinar cell injury with local and systemic inflammatory responses (due to destruct by its own digestive enzymes)
Can be classified as:
1. Mild: minimal organ dysfunction and uneventful recovery (80%)
2. Severe: organ failure and/or local complications e.g., necrosis, abscesses, pseudocysts (20%).
How can the pancreas be destroyed by it’s own enzymes?
The pancreas has both endocrine and exocrine function:
1. Endocrine: alpha and beta cells secrete hormones into the blood
2. Exocrine: acinar cells secrete digestive enzymes that break down carbohydrates, lipids and proteins
3. BUT this is what the pancreas is made of (if the protective measures keeping the enzymes away from the pancreatic tissue are disturbed, the pancreas is vulnerable)
How does the pancreas protect itself from it’s own enzymes?
- Enzymes are produced as inactive pro- enzymes “zymogens”- require activation via protease trypsin
- Zymogens are stored in vesicles
- Zymogens are stored with protease inhibitors (prevent enzymes from doing damage if prematurely activated)
When do pancreatic enzymes normally become activated and how?
- enteropeptidase found in the duodenum converts trypsinogen into trypsin (active enzyme)
- Once pancreatic zymogens are secreted from the sphincter of odi into the duodenum, they encounter the trypsin, which acitvates the zymogens
Explain the mechanism that trigger acute pancreatitis?
- enteropeptidase found in the duodenum converts trypsinogen into trypsin (active enzyme)
- Once pancreatic zymogens are secreted from the sphincter of odi into the duodenum, they encounter the trypsin, which acitvates the zymogens
if trypsinogen is activated early due to:
- injury to acinar cellls
- impaired secretion of proenzymes can cause AP
leading causes of injury and impaired secretion:
- alcohol abuse
- gallstones
What are some causes that trigger acute pancreatitis
I GET SMASHED (first 4 = most common)
- Idiopathic
- Gallstones
- Ethanol – alcohol causes 80% of cases
- Trauma
- Steroids
- Mumps/HIV/Coxsackie (infection) and Malignancy (pancreatic)
- Autoimmune
- Scorpion Venom
- Hypercalcaemia/ hyperPTH/ hyperlipidaemia/ hypothermia (metabolic disorders)
- ERCP (endoscopic retrograde cholangiopancreatography) and emboli
- Drugs (e.g. sodium valproate, steroids, thiazides and azathioprine)
Summarise the epidemiology of pancreatitis
- COMMON
- UK Annual Incidence: 10/10,000
- Peak age: 60 yrs
- Most common cause in:
Males = alcohol
Females = gallstones
what symptoms of acute pancreatitis can be picked up from the history?
- Constant, severe epigastric pain that radiates towards the back → usually sudden onset, described as ‘being stabbed with knife’, worse with movement (relieved by sitting forward)
- Nausea
- Vomiting → leads to dehydration, electrolyte abnormalities & hypokalaemic metabolic alkalosis
What signs of acute pancreatitis can be found on physical examination?
- Signs of Shock → hypovolaemia (dry mucous membrane, decreased skin turgor, sweating), hypotension, tachycardia, tachypnoea
- Fever, decreased appetite (Anorexia), signs of pleural effusion
- Decreased bowel sounds (due to ileus)
- Jaundice
- Severe/ haemorrhagic Pancreatitis → Cullen’s Sign (periumbilical bruising) & Grey-Turner Sign (flank bruising)
- Fox’s sign → ecchymosis over inguinal ligament
- Chvostek’s sign (due to low calcium via saponification)
What investigations are used to monitor acute pancretitis?
- Blood:
- Serum Lipase (more sensitive and specific than amylase, and has longer half-life hence remains elevated for longer) → 3x the upper limit
- FBC → Leukocytosis with left shift. Elevated Haematocrit (>44%) is predictor of poor prognosis due to increased risk of developing necrotising pancreatitis
- May cause Hypocalcaemia (indicator of severity)
- CRP → if >200 units/L there is high risk of developing pancreatic necrosis
- Urea/Creatinine (elevated = dehydration/hypovolaemia), Pulse Oximetry (Hypoxaemic)
- LFTs → elevated ALT (Alanine aminotransferase) suggests gallstones as the cause - Imaging (to determine aetiology) →
- Ultrasound (best initial to detect gallstones or biliary dilation). Imaging not needed for diagnosis in most patients
- Erect CXR: may be pleural effusion. Also to exclude bowel perforation
- AXR: exclude other causes of acute abdomen
- CT Scan: if diagnosis is uncertain or if persisting organ failure
Glasgow criteria for predicting severity of pancreatitis: combined with CRP (>210mg/L)
How is acute pancreatitis treated?
- Fluid & electrolyte resuscitation + Analgesia (IV Opioids - Morphine)
- Enteral Feeding can also help improve outcomes (if oral not tolerated due to N&V, in preference to total parenteral nutrition - don’t make patients NBM)
- ERCP (Endoscopic retrograde cholangiopancreatography) & Sphincterotomy for Gallstone Pancreatitis
- Oxygen and ABs for any complications
What are possible complications of pancreatitis?
- Early complications: shock, renal failure, ARDS, DIC, sepsis
- Local:
- Pancreatic necrosis
- Pseudocyst (peripancreatic fluid collection lasting > 4 weeks)
- Abscess
- Bleeding
- Ascites
- Pseudoaneurysm
- Venous thrombosis - Systemic:
- Multiorgan dysfunction
- Sepsis
- Renal failure
- ARDS
- DIC
- Hypocalcaemia
- Diabetes - Long-Term: could result in chronic pancreatitis with diabetes and malabsorption
Summarise the prognosis of acute pancreatitis
20% follow sevee fulminating course with high mortality
Infected pancreatic necrosis has a 70% mortality
80% follow a milder course (but this still has 5% mortality)
Describe chronic pancreatitis
- Most cases (80%) due to alcohol abuse
- Pain worse 15-30 mins after meals
- Steatorrhea (foul smelling, greasy stools) → due to pancreatic insufficiency
- Diabetes Mellitus develops in majority of patients (>20 yrs after symptoms begin). Monitor HbA1c every 6 months.
- CT most sensitive at detecting pancreatic calcification
- Faecal elastase (will be low) can also be used to assess exocrine function (Normal Amylase)
- Mx with pancreatic enzyme supplements
What scoring system is used to access the severity of acute pancreatitis?
In acute pancreatitis, the severity can be predicited using the modified Glasglow Imrie Score. It can be remembered by the mneumonic PANCREAS:
- Pa02 < 8kPa (60mmHg)
- Age > 55 years
- Neutrophils - WBC > 15 x 109/L
- Calcium < 2 mmol/L
- Renal func - Urea > 16mmol/L
- Enzymes- AST/ALT > 200 iu/L or LDH > 600 iu/L
- Albumin < 32g/L
- Sugar- Glucose > 10 mmol/L
