PowerPoint Presentation

MARIZ ASOY, M.D. 3 rd Year Internal Medicine Resident.

60-year old filipino male Married, Retired seaman Diabetic Non smoker Moderate alcoholic beverage drinker No known allergies.

Chief Complaint: Recurrent Epigastric Pain for 2 years.

Gradual onset of Epigastric pain. Dull aching, radiating to the back.

Prompted 2 previous admissions. Treated as Non-ulcer dyspepsia.

Noted onset of bulky fatty stool. Aggravated by fatty food intake.

Alcohol binge-drinking. Severe epigastric pain recurred.

PHYSICAL EXAM. normocephalic , anicteric sclerae , pink palpebral conjuctiva , moist lips and oral mucosa.

abstract. PHYSICAL EXAM. Adynamic precordium, distinct s1 and s2, regular rhythm.

abstract. PHYSICAL EXAM. Cerebral/Mental Status: oriented to time, place, and person, GCS15 Cranial Nerves- intact Motor- 5/5 on all extremities Relfexes – +2.

CBC WBC 4.8 RBC 3.97 HGB 11.6 HCT 35.4 Neutrophils 65 Lymphocytes 35 Monocyte 6 Eosinophils 4 Basophils 0.5.

COURSE IN THE WARDS. abstract. CT SCAN OF WHOLE ABDOMEN Dilated Main Pancreatic Duct Pancreatic Calcifications. CONCLUSION: Suggestive of Chronic Pancreatitis.

60yo, Male. Diabetic. Chronic Alcoholic. Recurrent Abdominal Pain.

Epigastric Tenderness. Mildly elevated Lipase CT Scan: MPD Dilation and Pancreatic calcifications.

How do you diagnose and treat Chronic Pancreatitis?.

“To Eat It’s Own” A Bite on Chronic Pancreatitis.

To discuss a case of a 60-year old male who presents with chronic abdominal pain.

To discuss the current APA guidelines on CP diagnosis.

WHAT IS CHRONIC PANCREATITIS?.

Chronic Pancreatitis. An irreversible progressive chronic inflammatory disease By histology: Chronic inflammation Fibrosis Progressive destruction of both exocrine and eventually endocrine tissue (atrophy).

abstract. abstract. Chronic Pancreatitis. Kasper D, Fauci A, et al. Harrison’s Principles of Internal Medicine 19 th edition. Chronic Pancreatitis.2015(378):2124-2131. Sleisenger. et. al. (2010) Gastrointestinal and Liver Disease Pathophysiology, Diagnosis and Managmenent. 10 th edition. Chronic Pancreatitis. Bronx, NY: Elsevier, Saunders..

EPIDEMIOLOGY. Incidence: 5 to 12 cases per 100,000 population Prevalence: 50 per 100,000 population Alcohol abuse : one half to two thirds of all cases Men >Women Middle Age (Mean: 40 years old).

Alcohol Protein conc in pancreatic secretion & Glycoprotein2 secretions in acinar cells formation of protein precipitates & protein plug calcification of ppt. Ductal stone formation duct obstruction Ulceration of epithelium Fibrosis.

Toxic Metabolite Hypothesis. Fatty acid ethyl esters and reactive O2 species Increase fragility in intraacinar organelles such as zymogen granules and lysosomes Damage acinar cells Scarring of the pancreatic parenchyma, Impair microcirculation Acetaldehyde- direct acinar injury.

Pancreatic Stellate Cells. PSCs- quiescent fibroblasts PDGF, TNF, IL-1, IL-6 Alcohol and its metabolites Activate myofibroblasts Synthesize proteins (Collagen I and III, Fobrinectin , laminin , MMP) FIBROSIS.

WHAT IS THE CLASSIFICATION SYSTEM OF CHRONIC PANCREATITIS?.

ETIOLOGY : TIGAR-O. TABLE 341-5 Chronic Pancreatitis and Pancreatic Exocrine Insufficiency: Tigar-O Classification System Toxic-metabolic Alcoholic Tobaccx) smoking Hypercalcemia Hyperlipidemia Chronic renal failure Medications—phenacetin abuse Toxins—organotin cnmpounds (e.g., dibutylin dichloride. DBTC) IdlopathIC Early onset Late onset Tropical Genetic Cationic trypsinogen (PRSSI) Cystic fibrosis transmembrane conductanæ regulator gene (CFTR) Calciunvsensing receptor (CASR) Chymotrypsin C gene (CTRC) trvnqin inhihitnr i SPINK I I.

TABLE 341-5 Chronic Pancreatitis and Pancreatic Exocrine Insufficiency: Tigar•O Classification System Toxic-metabolic Alcoholic Tobacco smoking Hypercalcemia Hyperlipidemia Chronic renal failure Medications—phenacetin abuse Toxins organotin compounds (e.g., dibutylin dichloride, DBTC).

Alcohol. 50% of all cases of chronic pancreatitis 5 years of intake exceeding 4 or 5 drinks per day Men Only 2% to 5% of heavy drinkers ultimately develop chronic pancreatitis.

Tobacco. heavy smokers (>1 pack/day) the relative risk > 3-fold increased 25% Attributable risk for CP Increased risk for pancreatic calcifications.

Idiopathic Early onset Late onset Tropical Genetic Cationic trypsinogen (PRSSI) Cystic fibrosis transmembrane conductance regulator gene (CFTR) Calcium-sensing receptor (CASR) Chymotrypsin C gene (CTRC) Pancreatic secretory trypsin inhibitor gene (SPINKI).

Idiopathic. 20% of patients with CP have no known risk factors Based on bimodal age of onset of clinical symptoms- 2 distinct entities.

Idiopathic. Kasper D, Fauci A, et al. Harrison’s Principles of Internal Medicine 19 th edition. Chronic Pancreatitis.2015(378):2124-2131. Sleisenger . et. al. (2010) Gastrointestinal and Liver Disease Pathophysiology, Diagnosis and Managmenent . 10 th edition. Chronic Pancreatitis. Bronx, NY: Elsevier, Saunders..

Tropical Pancreatitis. Fibrocalculous Pancreatic Diabetes Southwest India youth and early adulthood Prevalence: 1 in 500 - 1 in 800 population striking endocrine insufficiency (diabetes) genetic mutations- SPINK1 and CFTR gene.

Tropical Pancreatitis. —coo.

Idiopathic Early onset Late onset Tropical Genetic Cationic trypsinogen (PRSSI) Cystic fibrosis transmembrane conductance regulator gene (CFTR) Calcium-sensing receptor (CASR) Chymotrypsin C gene (CTRC) Pancreatic secretory trypsin inhibitor gene (SPINKI).

Genetic Disease. PRSS1 - Chromosome 7 and regulates trypsinogen production CFTR - Cystic fibrosis is associated with ductal dilatation, precipitate formation, pancreatic atrophy SPINK 1 - serine protease inhibitor Kazal type I; premature activation of trypsinogen.

Autoimmune Type 1 autoimmune chronic pancreatitis IgG4 systemic Type 2 autoimmune chronic pancreatitis Recurrent and severe acute pancreatltls Postnecrotic (severe acute pancreatitis) Recurrent acute pancreatitis Vascular diseases/ischemia Radiation induced Obstructive Pancreas divisum Duct obstruction (e.g., tumor) Preampullary duodenal wall cysts Posttraumatic pancreatic duct scars.

Autoimmune Pancreatitis/ Immunologic. Type I- Elevated IgG4 levels Hallmarks are: 1. periductal infiltration by lymphocytes and plasma cells 2. granulocytic epithelial lesions & destruction of the duct epithelium 3. venulitis.

Autoimmune Pancreatitis/ Immunologic. minimal abdominal pain diffuse enlargement of the pancreas without calcifications or pseudocysts most commonly involves the head of the pancreas and the distal bile duct Treatment: Glucocorticoids 0.6-1mg/kg/day.

FEATURES OF TYPE I AND TYPE II AUTOIMMUNE PANCREATITIS Feature TYPE 1 TYPE 2 Histology Lymphoplasmacytic infiltration Dense periductal infiltrate without damage to ductal epithelium Storiform fibrosis Obliterative phlebitis Abundant (>10 cells/HPF) IgG4 positive cells Periductal lymphoplasmacytic and neutrophilic infiltration Destruction of the duct epithelium by neutrophils (granulocytic epithelial lesion, or GEL) Obliterative phlebitis is rare No IgG4-positive cells Age 60-70 years 40-50 years Gender Male Equal Presentation Obstructive jaundice (75%) Acute pancreatitis (15%) Obstructive jaundice (50%) Acute pancreatitis (33%).

FEATURES OF TYPE I AND TYPE II AUTOIMMUNE PANCREATITIS Feature TYPE 1 TYPE 2 Pancreatic Imaging Diffuse pancreatic enlargement (40%) Focal pancreatic enlargement (60%) Diffuse pancreatic enlargement (15%) Focal pancreatic enlargement (85%) IgG4 Level elevated in serum (≈2/3 of patients) Positive in staining of involved tissues Not associated Other organ involvement Biliary strictures Pseudotumors Kidney Lung Retroperitoneal fibrosis Sialoadenitis IBD Outcome Frequent relapse Rare or no relapse.

Autolmmune Type 1 autoimmune chronic pancreatitis IgG4 systemic Type 2 autoimmune chronic pancreatitis Recurrent and severe acute pancreatltls Postnecrotic (severe acute pancreatitis) Recurrent acute pancreatitis Vascular diseases/ ischemia Radiation induced Obstructive Pancreas divisum Duct obstruction (e.g., tumor) Preampullary duodenal wall cysts Posttraumatic pancreatic duct scars.

Recurrent and Severe Acute Pancreatitis. Recurrent acute pancreatitis  development of a chronic inflammatory response  activation of pancreatic stellate cell 10% of patients with Acute Pancreatitis Predictors of development: Smoking and Alcohol.

Autoimmune Type 1 autoimmune chronic pancreatitis IgG4 systemic Type 2 autoimmune chronic pancreatitis Recurrent and severe acute pancreatltls Postnecrotic (severe acute pancreatitis) Recurrent acute pancreatitis Vascular diseases/ischemia Radiation induced Obstructive Pancreas divisum Duct obstruction (e.g., tumor) Preampullary duodenal wall cysts Posttraumatic pancreatic duct scars.

Standard pancreati ductal anatomy Patent ccessory duct Patent tccessory Pancreas divisum.

WHAT ARE THE CLINICAL FEATURES OF CHRONIC PANCREATITIS?.

ABDOMINAL PAIN. No single characteristic pain pattern Epigastrium, with radiation to the back Boring, deep, and penetrating Relieved by sitting or leaning forward 1. Increased pressure and ischemia 2. Injury and alterations in peripheral and central nociceptive nerves.

Exocrine Insufficiency. PEI - insufficient secretion of pancreatic enzymes (acinar function) and/or sodium bicarbonate (ductal function) Mild - reduced secretion of 1 or more pancreatic enzymes Moderate - reduced enzyme output and bicarbonate concentration Severe - moderate PEI + steatorrhea.

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