PANCREATITS by Tayi Ovayo and Nkosi Cebisile

Pancreatitis

1. Pancreatitis Clinical Associate students BMCPI: CEBISILE NKOSI BMCPII: ZWETSHA OVAYO TAYI

2. Presentation outline Anatomy and Physiology Acute pancreatitis and Chronic pancreatitis Etiology Patho physiology Clinical Manifestations Risk Factors Diagnostic investigations Differential diagnosis Preventions Management Co mplications References

3. Anatomy and physiology

4. A cute Pancreatitis Definition : inflammation of the pancreas characterised a rapid onset of inflammation and symptoms by caused by the release of activated pancreatic enzymes.

5. Causes Commonly due to: Idiopathic causes Alcohol intake Gallstones On causes of Acute Pancreatitis you can use an mnemonic which is I GET SMASHED: I- Idiopathic G- Gallstone E- Ethanol(alcohol) T- Trauma(especially in children) S- Scorpion sting M- Mumps (and coxsackievirus B Group virus) A- Autoimmune ( rheumatological disorders) S- Steroids H- Hypercalcemia and hypertryglyceridemia E- ERCP D- Drugs( loop and thiazide diuretics)

6. Risk factors Gallstones Heavy alcohol drinking High levels of fat (triglycerides) in the blood Cystic fibrosis Certain medicines e.g (estrogen therapy)

7. Pathophysiology Since the inactive forms of pancreatic enzymes must be cleaved in order to be activated. (trypsin is central in this process) Activation of trypsin is a critical triggering event in acute pancreatitis If trypsin is inappropriately generated from its proenzyme, trypsinogen, it can activate itself and other proenzymes (phospholipase & elastase) which also take part in the autodigestion .

8. Pancreatic Duct Obstruction Impaction of a gallstone or extrinsic compression of the ductal system by a mass, blocks the du ctal flow thus increasing intraductal pressure. This allows accumulation of an enzyme rich interstitial fluid, since lipase is secreted in an active form local fat necrosis may result. Peri-acinar myofibroblasts and leukocytes then release pro-inflammatory cytokines, that will promote local inflammation and interstitial edema. Edema further compromises local blood flow, causing insufficiency and ischemic injury to acinar cells.

9. Alcohol consumption Alcohol increases pancreatic exocrine secretions and contractions of the sphincter of Oddi . Alcohol has direct toxic effects on acinar cells including induction of oxidative stress on acinar cells, which leads to membrane damage Chronic alcohol ingestion results in the secretion of protein rich pancreatic fluid, which leads to the deposition of inspissated protein plugs and obstruction of small pancreatic ducts.

10. Cont. In severe pancreatitis, there is a significant inflammation with necrosis and hemorrhage of the gland. Activated enzymes and cytokines that enter the peritoneal cavity cause a chemical burn. Those that enter the systemic circulation cause a systemic inflammatory response that can result in acute respiratory distress syndrome and renal failure. These effects are mainly the result of increased capillary permeability and decreased vascular tone.

11. Cont.

12. Clinical features Symptoms: Upper abdominal Pain: Sudden onset, boring and classically radiating to the back Worse after meal and when supine Improve on learning forward Nausea and vomiting Fever

13. Cont. Signs: Signs of shock, tachycardia, hypotension, oliguria/anuria Possible Jaundice in pt with Biliary pancreatitis Abdominal examination: Abdominal tenderness, distension, guarding Ilues with reduced bowel sounds and tympani on percussion Ascitis Skin Changes(rare): Cullen sign: periumbilical ecchymosis and discolouration {bluish-red} Grey Turner sign: flank ecchymosis with discolouration Fox sign: ecchymosis over the inguinal ligaments

14. Diagnostic Investigation Clinically (history and physical examination) Lab studies : Bloods Serum pancreatic: increased amylase and lipase CBC: increased Hematocrits and WBC Inflammatory markers: increased CRP, Pro-calcification, IL-6 LFT: increased ALT, GGT, AST and (total and direct) Bilirubin. LDH: Increased Imaging : Ultrasound abdomen : Enlarged hypo-echoic pancreas CT scan: Enlarged and inflamed pancreas

15. Diagnostic Criteria

16. Management Fluid resuscitation: IV fluids ( e.g Ringers Lactate) Monitor: O2 saturation, Vitals and urine output. Obtain Lab tests every 6 to 12 hours Supportive therapy: Analgesics Antiemtics Electrolytes repletion Nutrition: NB: Bowel rest is no longer routinely recommended. Enteral via oral route or enteral tube, should be initiated as early as tolerated Early oral feeding: low fat, solid diet as soon as tolerated, ideally within 24 hours Enteral tube( nasogastric tube and nasojejunal ): preferred over parental nutrition if patient cannot tolerate oral intake Parental nutrition (total or partial): only in patients who cannot tolerate enteral feeds who cannot tolerate enteral feeds

17. Cont. Management of underlying cause: Alcohol induced pancreatitis Check magnesium and phosphorus levels and replete as needed Vitamin supplements (thiamine) You can also treat patient on Alcohol use disorder and provide counselling on alcohol use disorder before discharge Biliary Pancreatitis: You do a Therapeutic ERCP( you do it if the Biliary obstruction is associated with Cholangitis or persistent CBD obstruction).

18. C omplications Necrotising pancreatitis and infected necrotising pancreatitis Pancreatitis psuedocyst Respiratory distress syndrome Pancreatic ascits

19. C hronic Pancreatitis P ersistent inflammation of the pancreas that results in the permanent structural damage thus causing a decline in endocrine and exocrine functions.

20. Causes By far the most common cause is long – term alcoholism . Tabocca use Systemic disease: Cystic Fibrosis Tropics( in the southern India) You can also use an mnemonic which is TIGAR-O: T- Toxics-Metabolism I- Idiopathic G- Genetics(PRRS 1, SPINK 1gene mutation) A- Autoimmune R- Recuurent acute/ severe pancreatitis O- Obstructive

21. Clinical Manifestations Symptoms : Abdominal pain: Radiate to the back, is relieved by bending forward, and is exacerbated after eating Nausea and vomiting Cramping pain, bloating diarrhoea weight loss Fever Signs: Steatorrhea muscle wasting Creatorhea Mild fever

22. Risk factors Heavy alcohol drinking for a long time Certain hereditary condition e.g cystic fibrosis Gallstones Conditions such as high triglycerides and lupus

23. Diagnostic Investigation

24. Diagnostic investigation Serum markers (elevated amylase) 72-Hour stool test for steatorrhoea CT or Ultrasonography :visualization of calcifications within pancreas

25. Management Approach: treatment is aimed at: Chronic Pain Malabsorption Endocrine function Surgical intervention For pain: Oral Analgesics For malabsorption: Administer Oral lipase For endocrine function( you treat pt as Type1 DM): administer insulin.

26. Complications Splenic vein thrombosis Pancreatic ascites Endocrine pancreatic insufficiency

27. Preventions

28. Differential Diagnosis Acute peritonitis PUD Appendicitis Cholecystitis

29. References AMBOSS Mayoclinic Cleveland clinic Armando