Term
| What are the 3 primary secretions of the pancreas and where are they secreted from? |
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Definition
Pancreas secretes
- HCO3- into duodenum (neutralize chyme)
- Digestive enzymes in duodenum to breakdown nutrients - Islet cell hormones like insulin, glucagon and somatostatin into circulation
1) Endocrine (islets of langerhans) is composed of Secretory cells (Islet hormones) and Fenestrated capillaries.
2) Exocrine pancreas, is composed of acinar units (Trypsinogen) and ducts (secrete HCO3-) |
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Term
| What are the 4 major anatomical components that make up the pancreas? |
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Definition
Retroperitoneal organ in posterior wall of upper abdomen.
1) Head- right end within curve of duodenum, covered anteriorly by the SMA/SMV (uncinate process)
2) Neck- anterior to confluence of SMV and splenic V forming the portal vein; covered by the pylorus and peritoneum of the lesser sac.
3) Body- Ventral to L2-L4, held against aorta by peritoneum of lesser sac.
4) Tail- ends in hilus of spleen, near left kidney (between two layers of splenorenal ligament. |
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Term
| What is the basic blood supply of the pancreas? |
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Definition
1) Arterial (Both celiac and SMA)
-Celiac (hepatic, gastroduodenal, splenic, inferior pancreatic)
- Superior mesenteric (anterior & posterior pancreatico-duodenal, inferior pancreatic)
2) Venous
- Portal vein splenic vein (BOTH VULNERABLE TO INJURY during pancreatitis/thrombosis)
- Splenic vein thrombosis causes splenic blood to drain through short gastric veins, causing gastric varices. |
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Term
| Why might a patient with pancreatitis present with gastric varices and how would you treat? |
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Definition
1) Thrombosis of splenic vein causes blood to be drained by short gastric veins, which cause gastric varices to appear (can bleed!)
2) Treat with splenectomy |
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Term
| What is the basic nervous system innervation of the pancreas? |
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Definition
Visceral Efferent
1a) Parasympathetic (vagus) = stimulatory
- Parasympathetic ganglion cells in pancreas
Innervate acini, islets, ducts
- Myenteric interneurons (stomach & duodenum)
1b) Sympathetic (Splanchnic Nerves: T5-9)
- Synapse Hepatic & Celiac Plexuses
- Post-ganglionic to blood vessels
Visceral Afferent
- Afferent fibers travel with sympathetic nerves and vagus as well, traversing the nodose ganglion and reaching the NTS (respond to Pain and CCK) |
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Term
| What is the anatomical structure of the pancreatic ductal system? |
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Definition
Exocrine structures that secrete HCO3- in reponse to secretin
Pancreatic and Bile duct sphincters fuse to become the Sphincter of Oddi (smooth muscle constrictor) and empty into duodenum at ampulla of Vater
1) Main Pancreatic Duct
- Rt (head) = Wirsung
- Lft (body, tail) = Santorini
2) Accessory Pancreatic Duct
- perists In 30%, but usually fuses with Wirsung
- Rt (head) = Santorini |
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Term
What are the major embyronic events of pancreas organogenesis?
What happens at each of the following timepoints?
1. 4 weeks
2. 7 weeks
3. 12 Weeks –
4. 12-16 weeks |
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Definition
**SM-portal vein is enveloped by migrating pancreas in development**
1) Dorsal and ventral endodermal out-pocketings
- Ventral (unceate process and head, as well as main duct of Wirsung)
- Dorsal mostly neck, body and tail, as well as accessory pancreatic duct of Santorini
2) Ventral bud migrates behind duodenum and fuses with dorsal bud
3) pancreatic acini develop
4) endocrine cells differentiate |
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Term
| What happens to the ducts of the ventral and dorsal pancreatic ducts during development? |
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Definition
1) Ventral bud (Wirsung) generally fuses with Dorsal bud (Santorini) to create the main pancreatic duct
2) Proximal portion comes from ventral bud (Wirsung)
Distal portion comes from dorsal bud (Santorini)
- Santorini perists in 30% of population as accessory duct. |
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Term
| Why do some patients with congenital Pancreas divisum get acute and chronic pancreatitis? |
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Definition
In Pancreas divisum, dorsal and ventral pancreatic ductal systems do not fuse properly (happens in 5-10% of general population)
Exocrine pancreas must drain through accessory duct and narrow minor papilla, which can cause back-up of digestive secretions (trypsinogen) and HCO3- and cause pancreatitis. |
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Term
What congenital disorder of pancreatic development is described by each of the following
1. Pancreatic duct and common bile duct fuse prior to ampulla of vater causing reflux of pancreatic enzymes and bile.
2) Dilations of the biliary ducts due to anomalous fusion at the junction of the pancreatic and bile ducts, leading to pancreatic reflux into the gallbladder or liver.
3) Dorsal and ventral pancreatic ductal systems fail to fuse properly at 7-8 weeks of development- can lead to pancreatitis.
4) Band of pancreatic tissue envelopes duodenum, with impaired migration of ventral pancreas at 7 weeks
5) Clinically silent patches of pancreatic tissue in the stomach and/or small bowel. |
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Definition
1) Common channel syndrome (5-10% of individuals)
2) Choledochal cysts
3) Pancreas Divisum (5-10% of population)
4) Annular pancreas (RARE, but common in down syndrome- produces abdominal pain and vomiting because of duodenal stenosis).
5) Heterotopic pancreatic tissue |
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Term
A child presents with persistent, intermittent abdominal pain and vomiting.
You order an abdominal X-ray and notice duodenal stenosis with air in the stomach as well as a dilated proximal duodenum.
What is going on? |
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Definition
Symptoms with "double bubble" signs indicates Annular pancreas, where band of pancreatic tissue encircles second portion of duodenum.
Ventral bud (head) pancreatic tissue remains fixed to the duodenum during development, rather then rotating behind it and fusing with the dorsal bud (neck, body, tail) |
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Term
| What are the 3 major developmental signaling molecules (and their acitons) that influence specific endodermal and mesodermal cells to organize into pancreatic tissue? |
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Definition
1) PDX1- expressed in pancreatic bud
2) Shh- expressed in gut endoderm EXCEPT in bud (opposes epithelial differentiation of PDX1)
3) Notch pathway
- Notch and PTF1 signaling determine cell fate of pancreas-committed pleuripotential stem cells (acinar, duct, or endocrine determination) |
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Term
True or False:
Pancreatic exocrine function mature in utero, while endocrine function matures at birth. |
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Definition
False!
Exocrine function matures at birth (requires 6 months), which is why you often have steatorrhea in neonates, before the digestive enzymes and HCO3- secretory ducts are developed. |
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Term
| What is the structure of and major cell types contained in the endocrine pancreas? |
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Definition
Matures in utero (2% of total pancreas)
1) Each islet contains 2-3K cells in endocrine cords, surrounded by fenetrated capillaries for secretion into circulation.
2) Cells
- Alpha (glucagon- 15/20% found at periphery)
- Beta (insulin- 60-80% in central core)
- Delta (somatostatin- 5-10% scattered)
- F cells (pancreatic polypeptide, 15-20% scattered) |
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Term
| What is the structure of and major cell types contained in the exocrine pancreas? |
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Definition
Compound tubuloacinar gland that matures at birth (6 months) with
1) intercalated ducts (HCO3- and H20)
- Stimulated by secretin (cAMP) and VIP from small bowel
2) intraloblular excretory ducts
3) interlobular excretory ducts.
Acinar secretion
- release multiple pancreatic enzymes each, in response to CCK, insulin, GRP and ACh |
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Term
| How are pancreatic acinar secretions regulated (stimulated)? |
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Definition
1) CCK (duodenum and upper jejunum)
2) Acetylcholine (vagal parasympathetics)
3) Gastrin Releasing peptide (Bombesin)
**ACh and GRP activate secretions by increasing Ca++**
4) Insulin from endocrine pancreas |
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Term
| Describe the dual blood supply of the pancreatic acinar units. |
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Definition
1) Insuloacinar portal system
- Capillaries exit islets of endocrine pancreas and continue as capillaries in surrounding acinar units (exposing them to insulin for enzyme synthesis and secretion, which acts via RTK)
2) Acinar vascular system
- handles acinar units far from islets. |
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Term
What cells release each of the following components in the pancreas.
1) Bicarbonate-rich fluid
2) Trypsinogen
3) Insulin |
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Definition
1) Duct cells of exocrine pancreas (Cl HCO3 exchange via CFTR- loss leads to CF)
2) Acinar cells (intercalated duct cells of central acinus) of exocrine pancreas produce Trypsinogen (premature activation drives acute pancreatitis)
3) Islet cells of the endocrine pancreas (lost in DM) |
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Term
| Describe the functional anatomy of the acinar cell |
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Definition
Polarized cell with rich peri-nuclear ER
1) Zymogen granules located apically for release into the duct lumen.
2) Receptors located basolaterally
- ACh binds receptor and increases cytosolic Ca++, which travels through RER to apical membrane and causes zymogen release
- Ca++ may also act as a second messenger at basolateral pole
**Hypercalcemia can lead to pancreatitis, because it is the "trypsin switch"** |
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Term
| What are the major enzymes stored in zymogen granules of acinar cells? |
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Definition
1) Proteases (77%)
- Cationic trypsinogen attacks arginine and lysine and produce AAs for small bowel absorption.
- Trypsinogen is activated to trypsin by enterokinase from duodenum, and then activates other pancreatic enzymes
2) Lipases
- Triglyceride lipase cleaves FA to TGA (bile-mediated inhibition prevented by co-lipase)
- Carboxyl ester lipase for cholesterol ester and vitamin A absorption
3) Glycosidase
- alpha-amylase attacks 1,4-glucose linkages of CHO to produce short dextrins
4) Nuclease |
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Term
| What are the 3 mechanisms by which trypsin activity is regulated? |
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Definition
Tryspinogen is activated to Trypsin by enterokinase, and then activates itself and other digestive enzymes (too much trypsin can cause pancreatitis)
1) Stored in inactive trypsinogen form
2) Trypsin inhibitors
- Pancreatic secretory trypsin inhibitor (PSTI) and serine protease inhibitor, Kazal type 1 (SPINK1)
3) Calcium (binds activation peptide:TAP and autolysis loop)
- Low calcium: trypsin activity switched off because activation site cannot be accessed by second trypsin (TAP) and because an arginine becomes accessible leading to trypsin digestion by trypsin (autolysis loop) |
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Term
| How do Acinar cells protect themselves from trypsin activation? |
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Definition
1) Inactive “pro”-form
2) The activating enzyme is distant (enterokinase)
3) Zymogens are compartmentalized within granules
4) Intracellular calcium levels are low (switch off)
5) Co-synthesis of a trypsin inhibitor (SPINK1)*
6) Trypsin can destroy itself (autolysis at R122)
7) Protease activated receptors (PAR2) protect
8) Duct cells flush enzymes out of the pancreas
9) Ducatal bicarbonate keeps trypsin inactive
10) Extracellular trypsin inhibitors. |
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Term
| What 3 transmembrane transporters are required for duct cell secretion of HCO3- and how is secretion regulated? |
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Definition
Pancreatic bicarbonate secretion is derived from centroacinar and terminal duct cells and is stimulated by VIP and Secretin (increased [HCO3-] and decreased [Cl-] in pancreatic juice)
1) Na/K ATPase basolaterally
2) NBC (sodium bicarb co-transporter) basolaterally for HCO3- entry
3) CFTR apically for HCO3- secretion into duct.
Cl- efflux through CFTR causes membrane depolarization, which allows HCO3- to enter duct cell via NBC and then exits via CFTR. Na/K ATPase keeps intracellular Na+ low to maintain driving force. |
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Term
| How might CFTR or SPINK1 mutations produce chronic pancreatitis? |
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Definition
1) CFTR mutations prevent Cl- efflux from ductal cells, which prevents HCO3- entry and secretion into pancreatic juice.
- If pancreatic juice is not alkalinized, trypsin activation will be too high and cause pancreatitis by activating other digestive enzymes
2) SPINK1 is a specific trypsin-inhibitor (also an acute phase reactant) produced by acinar cells.
- Mutations will similarly cause over-activity of trypsin. |
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Term
| Describe the 3 classical phase of pancreatic stimulation. |
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Definition
1) Cephalic (sight and smell off food- 25% of secretions)
- Vagus (ACh) mediated
2) Gastric phase (distention of stomach-10%)
- Vagal-Vagal reflex
3) Intestinal phase (food in intestine causes Secretin/acid-regulated and CCK release/protein and fat regulated)
- Vagal sensory afferent stimulation that synapse in brainstem and connect to efferent motor neurons that project onto ganglia within pancreas |
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Term
| Why is peptide YY responsible for the "ileal break" of digestion? |
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Definition
When undigested food reaches terminal illeum, PYY is released and circulates to brainstem, where it slows down intestinal transit
**highlights how the vagal-brain-vagal regulation with CCK release and neurohormonal intergation allow for "fine adjustment"** |
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Term
| What are the most important stimulatory and inhibitory signals that control pancreatic secretion? |
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Definition
1) Parasympathetic is stimulatory and CCK is the peptide (protein/fat stimulated)
2) Sympathetic is inhibitory and PYY is major peptide (undigested food in terminal ileum) |
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Term
| How is chronic pancreatitis diagnosed? |
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Definition
Continuing inflammatory disease with irreversible morphological changes, defined by complications of severe and constant pain, maldigestion and diabetes.
Diagnosis made by abdominal imaging (CT), functional tests and rarely Biopsy- BUT YOU NEED IMAGING
1) Functional Tests
- "tubed" secretin is most sensitive- fluid collected from duodenum after IV secretin
- Fecal elastase
- Serum trypsinogen- good screen
- Fecal fat- calculate coeficient of fat absorption (CFA) and generally done to measure ability of enzyme replacement to improve absorption
- Blood glucose- Insensitive and nonspecific.
2) Structural
- Endoscopic US- duct and parenchymal changes
- ERCP- dilated, distorted ducts
- MRI/sMRCP- duct and parenchymal changes
- Abdominal X-ray- insensitive |
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Term
| What is the basic "two hit" SAPE model of chronic pancreatitis? |
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Definition
Remember, >90% must be lost to see steathorea, because of FUNCTIONAL RESERVE
1st hit: episode of AP (sentinel event) that activates the immune system
2nd hit: persistent inflammatory response – altered healing (Fibrosis requires STELLATE cells) |
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Term
| What are the major genetic causes of chronic pancreatitis? |
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Definition
CFTR (trypsin flushing), SPINK1 (modifier/inhibitor), PRSS1 mutations (HCP)
1) Cystic fibrosis
- AR CFTR mutations prevent chloride secretion, causing chronic pancreatitis, abnormal sweat chloride, male infertility (CBAVD), liver injury and progressive pulmonary disease in childhood.
- F508 is most common mutation
- Can be "atypical" with only CP due to borderline CFTR mutations
2) SPINK1 mutations ("feedback inhibitor"- disease modifiers)
- acute phase protein synthesized by acinar cells that is responsible for inhibition of trypsin (cationic PRSS1 and anionic PRSS2)
- Mutations are only prognostically useful in symptomatic patients
3) Hereditary pancreatitis
- AD mutation in cationic trypsinogen gene (PRSS1) on chromosome 7, causing recurrent acute pancreatitis and chronic pancreatitis, as well as pancreatic cancer
- Mutation eliminates primary trypsin digestion sites ("gain of function")
- Pancreatectomy and Islet autotransplanation for disabling pain is available |
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Term
| What is the basic pathophysiological framework of chronic pancreatitis? |
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Definition
| CP is initiated by injury and acute pancreatitis and progresses through altered healing (SPINK1 mutations act as disease modifiers) |
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Term
| What 2 environmental factors play the biggest role in the progression of chronic pancreatitis? |
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Definition
Both are disease modifiers
1) Ethanol (more prevalent among men)
2) Cigarette smoking (bigger independent risk)
MULTIPLICATIVE together |
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Term
| How is chronic pancreatitis treated? |
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Definition
Most important initial intervention is stop SMOKING and consuming alcohol, followed by symptom control and digestive aid.
1) Management
- Remove causative factors
- Manage exocrine and endocrine insufficiencies
- Symptomatic relief – especially pain
- Remove obstruction
- Stenting (ERCP)
- Surgery
2) Pancreatic enzymes
3) Surgeries
- Peustow, Beger, Frey.
- Total pancreatectomy with Islet autotransplantation. |
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Term
| What are the most prominent etiologies of acute pancreatitis? |
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Definition
Acute onset pancreatic damage due to premature trypsin activation (80% get better, 20% get worse)
1) Enviornmental
- Infection
- Medication
- Toxin
- Trauma
2) Metabolic
- Hypercalcemia
- Hyper-TGA
3) Anatomic
- Obstruction (divisum or sphincter of oddi dysfunction)
- Acquired obstruction.
4) Systemic
- SLE
- Polyarteritis
- Genetics (PRSS1)
5) Idiopathic (cationic trypsinogen) |
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Term
42 year old male presents with nausea/vomiting and sever upper abdominal pain that radiates to the back.
Serum analysis releases elevated amylase and lipase levels.
You order a CT and findings show evidence of pancreatic parenchymal necrosis.
What are the major risk factors associated with this condition? |
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Definition
Acute Pancreatitis (only need 2 of pancreatic pain, serum amylase/lipase elevation and CT pancreatic necrosis to diagnose)
Severity is staged with APACHE-II score
1) Obesity (inflammatory state)
2) Chronic alcohol consumption (apoptosis to necrosis)
3) Genetic polymorphisms (MCP-1) |
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Term
| What are the common local and systemic complications associated with acute pancreatitis? |
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Definition
1) Local- pancreatic
- Acute fluid collections (no fibrous or granulation tissue wall)
- Pseudocysts (clear pancreatic fluid with well-defined fibrous wall, but NOT epithelial lining)
- Pancreatic necrosis- 3-5% (peri-pancreatic fat identified by contract CT)
2) Non-pancreatic- local
- Pancreatic ascites, pleural effusion, bile duct obstruction splenic vein thrombosis and stricture
3) Systemic
- CV (Hypotension and shock)
- Pulmonary (Hypoxia)
- Renal (Azotemia)
- Metabolic (Hypocalcemia, hyperglycemia, metabolic acidosis)
- Hematologic/Coagulation (vascular thrombosis, DIC) |
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Term
| What systemic complications are associated with acute pancreatitis? |
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Definition
- CV (Hypotension and shock)
- Pulmonary (Hypoxia)
- Renal (Azotemia)
- Metabolic (Hypocalcemia, hyperglycemia, metabolic acidosis)
- Hematologic/Coagulation (vascular thrombosis, DIC) |
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Term
| What are the major treatment strategies for acute pancreatitis? |
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Definition
80% get better in 3 days- Those with complications sould be cared for in ICU with supportive care
**Give ERC if bile duct stones are suspected, r in case of acute biliary pancreatitis**
1) Pancreatic rest (nothing by mouth)
- Nasojejunal-tube feeding >> TPN to maintain barrier and eliminate sepsis risk
2) IV fluids
3) Pain medicine |
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Term
| What 2 genetic conditions are associated with the formation of pancreatic cysts (hint: not primarily pancreatic disease)? |
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Definition
Cysts lined by flat cuboidal epithelium, or by completely attenuated fibrous capsule/filled with serous mucous (pseudocysts)
1) Polycystic kidney disease
- Cysts in kidney, liver, pancreas
2) Von Hippel-Lindau disease
- Cysts in pancreas, liver, kidney
- Cerebellar hemangioblastomas
- Pheochromocytomas |
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Term
| What are the 3 possible pathogenic pathways leading to generation of Acute Pancreatitis? |
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Definition
Women= biliary tract and Men= alcohol
1) Pancreatic duct obstruction
- Gallstone in ampula of vater raises intra-pancreatic ductal pressure, leading to accumulation of enzyme-rich fluid (Similar to congenital divisum)
- Lipase can produce local fat necrosis, cyotokynes cause inflammation and edema (leaky microvasculature)
2) Primary acinar cell injury
- Viruses (mumps), drugs and direct trauma, as well as ischemia or shock
3) Defective intracellular transport
- Lysozyme rupture and activated enzyme release in animal models. |
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Term
| What are the 5 characteristic pathologic features of Acute Pancreatitis on histology? |
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Definition
HE FAD
Mild may have edema and fat necrosis/saponification, while severe may proceed to destruction, hemorrhage and necrosis.
1) Hemorrhage (blood vessel destruction)
2) Edema (microvasculature leakage)
3) Fat necrosis (lipase) with SAPONIFICATION
4) Acute inflammation (PMNs)
5) Destruction of parenchyma by protealytic enzymes |
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Term
| What are the 4 hypotheses that can account for the development of chronic pancreatitis? |
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Definition
Remember, its injury- inflammation-remodeling-fibrosis/scarring
1) Ductal obstruction
2) Toxic-metabolic
3) Oxidative stress (alcohol)
4) Necrosis-fibrosis (inflammation and remodeling) |
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Term
| What are the 4 classic morphological features of chronic pancreatitis? |
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Definition
Irreversible due to alcohol in males
Grossly, gland is atrophic, hard and ducts are dilated and calcified
PDA
1) Parenchymal fibrosis (fewer, smaller acini with preserved islets)
2) Dilation of pancreatic ducts (with chronic inflammation)
3) Acinar loss |
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Term
| What are the different, common sequele of acute and chronic pancreatitis? |
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Definition
1) Acute
- Shock
- Organ failure
- DIC (disseminated intravascular coagulopathy)
- Pancreatic abscesses
- Pseudocysts
2) Chronic= Irreversible, usually due to chronic alcoholism
- Duct obstruction
- Pseudocysts
- Malabsorption
- Secondary diabetes |
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Term
| How could you distinguish congenital cysts from pseudocysts of the pancreas histologically? |
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Definition
5-15% of all cysts are neoplastic!
1) Congenital will have flat, cuboidal epithelial lining
2) Pseudocysts will have fibrous, connective tissue lining.
- Localized collections of pancreatic secretions and necrotic cells secondary to acute/chronic pancreatitis |
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Term
| What are the 4 primary types of Cystic Neoplasms? |
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Definition
5-15% of cysts are neoplastic!
1) Serous cystadenoma (microcystic adenoma)
- benign with glycogen-rich low-cuboidal epithelium filled with thin, straw-colored fluid.
- Abdominal pain cured by surgical resection
2) Mucinous cystic neoplasm
- Tail cysts with NO ductal connection found in women
- lined with single layer of mucin-producing cells
- worry for ADENocarcinoma
3) Intraductal papillary mucinous neoplasm (IPMN)
- Main pancreatic ducts of the head
- dilated ducts with papillary necrosis
- worry for ADENocarcinoma
4) Seolid-pseudopapillary tumor |
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Term
What would each of the following pancreatic histological descriptions indicate to you?
1) Cyst with glycogen-rich, low-cuboidal epithelium that is filled with thin, straw-colored fluid.
2) Cysts within pancreatic ducts of the head producing dilated ducts with papillary necrosis
3) Cysts in tail of pancreas with NO ductal connection that are lined with single layer of mucin-producing cells
4) Seolid-pseudopapillary tumor |
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Definition
1) Serous cystadenoma (microcystic adenoma)
- Benign and Abdominal pain cured by surgical resection
2) Intraductal papillary mucinous neoplasm (IPMN)
- Worry for invasive adenocarcinoma
3) Mucinous cystic neoplasm
- worry for ADENocarcinoma |
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Term
| What are the major environmental and genetic risk factors for pancreatic adenocarcinoma? |
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Definition
Common in elderly african americans
1) Environment
- Smoke, Fat, DM, Chronic pancreatitis
2) Genetic
- Hereditary breast cancer (BRACA1/2)
- Familial pancreatitis (PRSS1)
- Peutz-Jeghers Syndrome (STK11/LKB1 gene)
- HNPCC (mismatch repair genes) |
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Term
Patient presents with jaundice, weight loss abdominal pain and malaise. They pass away and you diagnose pancreatic adenocarcinoma.
What is the gross and histological appearance of their pancreas? |
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Definition
Mostly occur in head
1) Grossly
- Poorly circumscribed, grey-white, firm masses (tend to obstruct bile duct leading to jaundice)
- Tendency to infiltrate liver, lungs and bones
2) Histology
- Arise from ductal (glandular) epithelium
- Poorly differentiated adenocarcinoma
- Perineural and angiolymphatic invasion common
- Almost always associated with chronic pancreatitis
3) Histologic variants
Adenosquamous Carcinoma
Anaplastic Carcinoma
Undifferentiated carcinoma with osteoclast-like giant cells |
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Term
Patient presents with painless jaundice, malaise, weight loss and weakness. You also notice evidence of migratory thrombophlebitis on PE
You perform a pancreatic biopsy and discover evidence of poorly differentiated, glandular epithelium
What are the histological variants of this condition and how do you treat? |
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Definition
Pancreatic Invasive Carcinoma (probably in head, due to painless jaundice)
1) Histologic variants
- Adenosquamous Carcinoma
- Anaplastic Carcinoma
- Undifferentiated carcinoma with osteoclast-like giant cells
2) 5% live
- Whipple (head)
- Distal pancreatectomy (body/tail)
- Medical (Gemcitabine/5-FU based chemo: FOVIX)
- Palliative |
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Term
| Which 3 clinical syndromes are associated with pancreatic endocrine neoplasms? |
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Definition
Rare tumors that occur in adults (average 58)
- Tumor grade is best prognostic marker
- Insulinomas are benign while other endocrine composition are malignant
1) Hyperinsulinism
2) Hypergastrinemia, Zillinger-Ellison
3) Multiple endocrine neoplasia |
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Term
| What are/is the prognosis and risk factors for pancreatic adenocarcinoma? |
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Definition
1) 5% overall and 20% for resectible cases (10% of all cases).
2) Age ** (71)
- Race
- Male
- Fam h/x
- Smoking
Healthy BMI, physical activity, not smoking and moderate alcohol intake are protective |
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Term
Which of the following is not an accepted explanation for the aggressiveness of pancreatic cancer?
1. Few and non-specific symptoms
2. Early invasion
3. Chemo-resistance
4. Cytokine-mediated symptoms
5. Generation of autoantibodies |
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Definition
5
Generally presents with vague, dull mid-epigastric discomfort (may radiate to back), nausea, vomiting, anorexia, weakness, obstructive jaundice and depression. |
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Term
| Why is back pain especially concerning in a patient with suspected pancreatic cancer? |
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Definition
Pain is most common presenting symptom and ALL patients have pain eventually (whipple)
Suggests retropertioneal invasion of splanchnic nerve plexus by tumor |
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Term
True or False:
The most characteristic sign of pancreatic carcinoma of the head is painful obstructive jaundice. |
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Definition
False
PAINLESS with darkening of urine, pruritis and lightening of stool |
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Term
Patient presents with painless jaundice, migratory thrombophlebitis, pruritis and darkened urine.
They say they have been feeling quite depressed, weak and have been experiencing mild abdominal discomfort (nausea)
What is the pathogenesis of this conditon? |
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Definition
Watch out for PC in new-onset diabetes and older people!
Depression, weakness/nausea, thrombophlebitis, pruritis and darkened urine fit Adenocarcinoma of Pancreas Head (ORDER A CT with contrast and EUS for lobular atrophy, but it cannot detect PaIN)
1) Pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN) and mucinous cystic neoplasm (MCN) are all precursors.
MCN and IPMN, but NOT PanIN can be detected by EUS and CT
2) PanIN arise from ductal epithelial cells and aquire mutations (KRAS, P16, P53) over time that leads to cellular abnormality. |
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Term
| What are the prominent physical findings associated with Pancreatic Cancer? |
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Definition
Order CT and/or EUS
1) Significant weight loss
2) Mild-moderate epigastric tenderness
More specific
3) Clinical jaundice (palpable gallbladder-Courvoisier)
4) Ascites/hepatomegaly/abdominal mass
5) Metastatic rectal shelf (Blumer's shelf) |
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Term
| What are the benefits of choose EUS or CT to diagnose pancreatic cancer? |
|
Definition
Equal in terms of determining resectibility
1) EUS
- Superior for T stage
- Also can collect biopsy
2) CT is superior is assessing arterial involvement and distant metastasis
BOTH are bad at detecting occult nodal involvement
ERCP reserved for cases where therapeutic intervention for obstructive jaundice is required (stenting) |
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