Pancreatitis: Pathology review

Pancreatitis: Pathology review

Surgery

Surgery

Preoperative evaluation: Clinical
Postoperative evaluation: Clinical
General anesthetics
Local anesthetics
Neuromuscular blockers
Protein synthesis inhibitors: Aminoglycosides
Miscellaneous cell wall synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Laxatives and cathartics
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Insulins
Abdominal pain: Clinical
Esophageal surgical conditions: Clinical
Gastrointestinal bleeding: Clinical
Peptic ulcers and stomach cancer: Clinical
Appendicitis: Clinical
Appendicitis: Pathology review
Diverticular disease: Clinical
Hernias: Clinical
Bowel obstruction: Clinical
Colorectal cancer: Clinical
Abdominal trauma: Clinical
Anal conditions: Clinical
Gallbladder disorders: Clinical
Gallbladder disorders: Pathology review
Pancreatitis: Clinical
Pancreatitis: Pathology review
Adrenal masses and tumors: Clinical
Breast cancer: Clinical
Breast cancer: Pathology review
Benign breast conditions: Pathology review
Skin and soft tissue infections: Clinical
Anatomy clinical correlates: Anterior and posterior abdominal wall
Anatomy clinical correlates: Breast
Anatomy clinical correlates: Viscera of the gastrointestinal tract
Anatomy clinical correlates: Peritoneum and diaphragm
Anatomy clinical correlates: Other abdominal organs
Coronary artery disease: Clinical
Valvular heart disease: Clinical
Pericardial disease: Clinical
Aortic aneurysms and dissections: Clinical
Chest trauma: Clinical
Reading a chest X-ray
Pleural effusion: Clinical
Pneumothorax: Clinical
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Lung cancer: Clinical
Anatomy clinical correlates: Thoracic wall
Anatomy clinical correlates: Heart
Anatomy clinical correlates: Pleura and lungs
Anatomy clinical correlates: Mediastinum
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
cGMP mediated smooth muscle vasodilators
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Benign hyperpigmented skin lesions: Clinical
Skin cancer: Clinical
Blistering skin disorders: Clinical
Bites and stings: Clinical
Burns: Clinical
Dizziness and vertigo: Clinical
Thyroid nodules and thyroid cancer: Clinical
Thyroid nodules and thyroid cancer: Pathology review
Parathyroid conditions and calcium imbalance: Clinical
Neck trauma: Clinical
Nasal, oral and pharyngeal diseases: Pathology review
Antihistamines for allergies
Stroke: Clinical
Seizures: Clinical
Headaches: Clinical
Traumatic brain injury: Clinical
Brain tumors: Clinical
Lower back pain: Clinical
Anatomy clinical correlates: Vertebral canal
Anatomy clinical correlates: Spinal cord pathways
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Migraine medications
Migraine
Osmotic diuretics
Thrombolytics
Shock: Clinical
Eye conditions: Refractive errors, lens disorders and glaucoma: Pathology review
Eye conditions: Retinal disorders: Pathology review
Eye conditions: Inflammation, infections and trauma: Pathology review
Anatomy and physiology of the eye
Pediatric ophthalmological conditions: Clinical
Joint pain: Clinical
Back pain: Pathology review
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Concussion and traumatic brain injury
Traumatic brain injury: Pathology review
Abdominal hernias
Prostate disorders and cancer: Pathology review
Testicular tumors: Pathology review
Kidney stones: Clinical
Renal cysts and cancer: Clinical
Urinary incontinence: Pathology review
Testicular and scrotal conditions: Pathology review
Anatomy clinical correlates: Male pelvis and perineum
Anatomy clinical correlates: Female pelvis and perineum
Androgens and antiandrogens
PDE5 inhibitors
Adrenergic antagonists: Alpha blockers
Peripheral vascular disease: Clinical
Leg ulcers: Clinical
Aortic dissections and aneurysms: Pathology review

Transcript

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While in the Emergency Department, two individuals came in with severe epigastric pain. Michael who is 45, complains of pain that radiates to his back, vomiting, and nausea.

All of these symptoms appeared after he came home from partying at the bar a few hours ago.

On the clinical examination, there’s epigastric tenderness without guarding or rebound, decreased bowel sounds, and purple discoloration around the periumbilical region. He also tends to bend over to relieve the pain.

Anna, who is 29 years old, on the other hand, says the pain started abruptly and that it doesn’t radiate anywhere. She also noticed it gets worse after her meals. On examination, she presents with epigastric pain, scleral icterus, and fever.

Both were admitted and started on IV fluids.

Blood tests were ordered, which revealed lipase and amylase levels that were 3 times more than normal.

Ok, so from what we can gather, both people have acute pancreatitis.

Let’s begin with a bit of physiology. The pancreas is located in the epigastric region, behind the stomach, and it is mostly a retroperitoneal organ.

It has both endocrine functions, by releasing hormones like insulin and glucagon, and exocrine functions by secreting enzymes needed for food digestion.

The exocrine pancreas releases digestive enzymes through smaller ducts which drain in the main pancreatic duct.

The main pancreatic duct, which travels through the length of the pancreas, joins the common bile duct at the ampulla of Vater and drains into the duodenum.

Now, the main pancreatic enzymes include pancreatic amylase which breaks down carbohydrates; trypsin and chymotrypsin, which break down proteins; and lipase which breaks down lipids.

To protect the pancreas from destroying itself, the acinar cells of the pancreas manufacture zymogen, or the inactive form, of trypsin, called trypsinogen.

When this zymogen is released into the small intestine, it is cleaved by enteropeptidase enzymes found in the duodenum.

If, by any chance, trypsinogen gets auto activated before it reaches the duodenal lumen, trypsin gets cleaved and inactivated by trypsin itself or inhibited by certain proteins, called trypsin inhibitors, like SPINK1.

In contrast, pancreatic lipase and amylase are secreted in their active forms and don’t need activation by the protease trypsin.

Ok, so pancreatitis is an inflammation of the pancreas.

In acute pancreatitis, trypsin and chymotrypsin get suddenly get activated within the pancreas and cause autodigestion, which results in inflammation and hemorrhaging.

Once the pancreatic cells get damaged, increased amounts of lipase enter the blood, which is why these two enzymes are measured to diagnose pancreatitis.

For your test, it’s important to know that lipase, released by the damaged cells, breaks down triglycerides in free fatty acids which bind calcium.

So this kind of damage is also called saponification necrosis because the resulting tissue resembles soap.

In chronic pancreatitis, there are persistent causes of inflammation in the pancreas, leading to impairment of both endocrine and exocrine functions.

Okay, let’s look at some of the causes for pancreatitis.

Starting with acute pancreatitis which is most commonly caused by gallstones, followed by alcohol use.

On your test, you can remember the full list of causes by using the mnemonic “I GET SMASHED.”

‘I’ refers to Idiopathic causes.

‘G’ is obstruction by Gallstones, which get stuck in the bile duct and prevent pancreatic enzymes from reaching the small intestine.

This causes the digestive enzymes to back up into the pancrase where they build up and damage the organ.

‘E’ is Ethanol, or alcohol use, and it is not sure how it leads to pancreatitis.

‘T’ is a pancreatic Trauma, mostly puncture injury, like a knife wound, which damages the pancreas and releases the digestive enzymes.

‘S’ is the use of Steroids, which leads to increased viscosity of pancreatic secretions, causing obstruction of the small pancreatic ducts.

‘M’ is infection with Mumps virus, and it is believed to directly damage the pancreatic acinar cells.

‘A’ is the result of Autoimmune diseases, like systemic lupus erythematosus and rheumatoid arthritis.

These diseases are caused by auto-antibodies that target various organs in the body, such as the pancreas, and cause inflammation.

The second ‘S’ is the result of a Scorpion sting, which also damages the pancreas directly.

‘H’ is a cheat and stands for both Hypertriglyceridemia and for Hypercalcemia.

When taking a test, remember that hypertriglyceridemia above 1000 milligrams per deciliter can cause pancreatitis because it increases the concentrations of chylomicrons in the blood.

Chylomicrons are very large and obstruct capillaries leading to ischemia of the pancreas.

A helpful hint for your test is that this type of pancreatitis improves with fasting.

In hypercalcemia, calcium molecules deposit in the pancreatic tissue, and activate trypsinogen, leading to pancreatic injury.

‘E’ is trauma from an Endoscopic retrograde cholangiopancreatography or ERCP which is a technique used to diagnose and treat various biliary and pancreatic diseases.

And finally ‘D’ stands for Drugs, like didanosine, Corticosteroids, Alcohol, Valproic acid, Azathioprine, and Diuretics like Furosemide and Bumetanide, which, for your tests, can be remembered using the mnemonic Drugs Causing A Violent Abdominal Distress.

Okay, now let’s move on to chronic pancreatitis.

Many causes for acute pancreatitis also cause chronic pancreatitis.

These include idiopathic causes, gallstones, long-term alcohol use, autoimmune conditions, hypertriglyceridemia and hypercalcemia.

Key Takeaways

Pancreatitis refers to inflammation of the pancreas, an organ located behind the stomach that produces hormones and enzymes that help the body digest food. Pancreatitis can be acute or chronic.

Acute pancreatitis occurs when there is a sudden and severe inflammation, which usually resolves within a few days with proper treatment. It is commonly caused by gallstones and alcohol, and typically presents with epigastric pain that radiates to the back, nausea, vomiting, and decreased bowel sounds.

Chronic pancreatitis occurs when there is a long-term inflammation that can cause permanent damage to the pancreas and lead to serious complications. It is usually due to long-term alcohol use, genetic diseases like SPINK1 mutations and cystic fibrosis, pancreatic duct obstruction due to tumors, and autoimmune conditions.

People with chronic pancreatitis may be initially asymptomatic for a long time, but they might develop epigastric pain that radiates to the back, steatorrhea, fat-soluble vitamin deficiency like vitamin A, D, or E; diabetes, and unintentional weight loss.

Sources

  1. "Fundamentals of Pathology" H.A. Sattar (2017)
  2. "Robbins Basic Pathology" Elsevier (2017)
  3. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  4. "Chronic Pancreatitis: Challenges and Advances in Pathogenesis, Genetics, Diagnosis, and Therapy" Gastroenterology (2007)
  5. "Acute pancreatitis" The Lancet (2015)
  6. "The Epidemiology of Pancreatitis and Pancreatic Cancer" Gastroenterology (2013)
  7. "Laparostomy management using the ABThera™ open abdomen negative pressure therapy system in a grade IV open abdomen secondary to acute pancreatitis" International Wound Journal (2012)
  8. "Drug-Induced Acute Pancreatitis" Baylor University Medical Center Proceedings (2008)