The Pancreas - Acute and Chronic Pancreatitis Flashcards

1
Q

What is Acute Pancreatitis?

A

Rapid onset inflammation of the pancreas after which normal function resumes.

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2
Q

Aetiology of Acute Pancreatitis (11).

A

I GET SMASHED :-
1. I - Idiopathic.
2. G - Gallstones (commonest).
3. E - Ethanol/Alcohol (commonest).
4. T - Trauma.
5. S - Steroids.
6. M - Mumps (+ Coxsackie B).
7. A - Autoimmune (IgG4 + Polyarteritis Nodosa).
8. S - Scorpion Venom.
9. H - Hyperlipidaemia, Hypercalcaemia and Hypothermia.
10. E - Post-ERCP (commonest).
11. D - Drugs : Thiazide Diuretics, Furosemide and Azathioprine, Mesalazine, Valproate.

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3
Q

How do Gallstones cause Acute Pancreatitis?

A
  1. Gallstones get trapped at the end of the biliary system (Ampulla of Vater).
  2. This blocks the flow of bile and pancreatic juice into the duodenum.
  3. Reflux of bile into the pancreatic duct and prevention of pancreatic secretions.
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4
Q

How does Alcohol cause Acute Pancreatitis?

A

Alcohol is directly toxic to pancreatic cells, resulting in inflammation.

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5
Q

Epidemiology-based Aetiology of Acute Pancreatitis (2).

A
  1. Gallstone Pancreatitis - Women and Older Patients.
  2. Alcohol Pancreatitis - Men and Younger Patients.
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6
Q

Pathophysiology of Acute Pancreatitis.

A

Autodigestion of Pancreatic Tissue by Pancreatic Enzymes leads to Necrosis.

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7
Q

Clinical Presentation of Acute Pancreatitis (4).

A
  1. Severe Epigastric Pain that radiates to the back, relieved by sitting forward or lying in foetal position.
  2. Associated Vomiting.
  3. Systemically Unwell (Low-Grade Fever and Tachycardia).
  4. Cullen’s Sign and Grey-Turner’s Sign.
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8
Q

What are the special signs that may be seen in Acute Pancreatitis?

A
  1. Cullen’s Sign - Periumbilical Discolouration.
  2. Grey-Turner’s Sign - Flank Discolouration (retroperitoneal bleeding).
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9
Q

Investigations of Acute Pancreatitis (5).

A
  1. Clinical Diagnosis - Presenting Features + Amylase Level.
  2. Glasgow Score Calculation - Bloods + ABG.
  3. US - Gallstones.
  4. CT Abdomen - Complications of Pancreatitis (if suspected e.g. necrosis, abscess and fluid collections).
  5. Amylase - 3x above the upper limit of normal (but Lipase is better since it has a longer half-life).
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10
Q

Why is Amylase not as significantly elevated in Chronic Pancreatitis?

A

The pancreas has reduced function due to chronic inflammation in Chronic Pancreatitis.

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11
Q

What is the Glasgow Score?

A

A numerical score based on the key criteria present to assess the severity of pancreatitis. 0/1 - MILD; 2 - MODERATE; 3+ - SEVERE.

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12
Q

Glasgow Score Criteria (8).

A

PANCREAS :-
1. P - PaO2 < 8kPa.
2. A - Age > 55.
3. N - Neutrophils (WBC > 15).
4. C - Calcium < 2.
5. R - uRea > 16.
6. E - Enzymes (LDH > 600 or AST/ALT > 200).
7. A - Albumin < 32.
8. S - Sugar (Glucose > 10).

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13
Q

Differential Diagnoses of Raised Amylase (5).

A
  1. Pancreatic Pseudocyst.
  2. Mesenteric Infarct.
  3. Perforated Duodenal Viscus.
  4. Acute Cholecystitis.
  5. Diabetic Ketoacidosis.
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14
Q

Management of Acute Pancreatitis (7).

A
  1. Emergency Admission to Supportive Management (HDU/ITU in Moderate/Severe Cases).
  2. ABCDE.
  3. IV Fluids.
  4. NBM not routine unless clear lesion e.g. vomiting + Enteral Nutrition with Moderate/Severe Case.
  5. Analgesia (IV Opioids).
  6. Antibiotics if specific infection.
  7. Treatment of Underlying Cause and Complications.
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15
Q

Fluid Resuscitation in Acute Pancreatitis (3).

A
  1. Aggressive Early Hydration with Crystalloids.
  2. Aim for a Urine Output > 0.5 ml/kg/hour.
  3. Can relieve pain by reducing lactic acidosis.
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16
Q

Surgery in Acute Pancreatitis (4).

A
  1. Gallstone - Cholecystectomy.
  2. Obstructed Biliary System - Early ERCP.
  3. Necrosis + Worsening Organ Dysfunction - Debridement or FNA.
  4. Infected Necrosis - Radiological Drainage or Surgical Necrosectomy.
17
Q

Prognosis of Acute Pancreatitis.

A

Most patients will improve within 3-7 days.

18
Q

Complications of Acute Pancreatitis (7).

A
  1. Necrosis of the Pancreas.
  2. Infection in a Necrotic Area.
  3. Abscess Formation (result of infected pseudocyst).
  4. Acute Peripancreatic Fluid Collections.
  5. Pseudocysts - 4 weeks later : symptomatic - observe for 12 weeks as up to 50% resolve.
  6. Chronic Pancreatitis.
  7. Ischaemic (Purtscher) Retinopathy - Temporary/Permanent Blindness.
19
Q

What is a Pancreatic Pseudocyst?

A

A collection of pancreatic juice.

20
Q

How can Acute Pancreatitis lead to ARDS?

A

Third Space Sequestration - result of a combination of inflammatory, vasoactive mediators and tissues - vascular injury, vasoconstriction, capillary permeability leads to extravasation of fluid.

21
Q

What is Chronic Pancreatitis?

A

Chronic inflammation in the pancreas, resulting in fibrosis and reduced functioning of the pancreatic tissue.

22
Q

Clinical Consequences of Chronic Pancreatitis (5).

A
  1. Chronic Epigastric Pain (15-30 minutes after a meal).
  2. Loss of Exocrine Function - Pancreatic Enzymes, especially Lipase : Steatorrhoea (5-25 years after pain onset).
  3. Loss of Endocrine Function - Insulin (Diabetes) (20 years after symptom onset).
  4. Damage and Strictures in Duct System = Biliary Obstruction.
  5. Pseudocyst/Abscess Formation.
23
Q

Aetiology of Chronic Pancreatitis (3).

A
  1. Alcohol - commonest (80%).
  2. Genetic : CF, Haemochromatosis.
  3. Ductal Obstruction : Tumours, Stones, Structural Abnormalities.
24
Q

Investigations in Chronic Pancreatitis (4).

A
  1. AXR - Pancreatic Calcification.
  2. CT Pancreas more sensitive at detecting calcification.
  3. Functional Test : Faecal Elastase for Exocrine Function.
  4. Endocrine Dysfunction : Fasting Glucose and OGTT.
25
Q

Management of Chronic Pancreatitis (6).

A
  1. Abstinence : Smoking and Alcohol.
  2. Analgesia.
  3. Replacement Pancreatic Enzymes (CREON) - malabsorption.
  4. Subcutaneous Insulin Regimes (Diabetes).
  5. ERCP with Stenting (Strictures + Obstruction in Biliary System).
  6. Surgery for Complications.
26
Q

What can malabsorption of fat cause? (2).

A
  1. Steatorrhoea (Greasy Stools).
  2. Deficiency in Fat-Soluble Vitamins.