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70 Cards in this Set
- Front
- Back
What is the embryology of the Gallbladder?
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- derived from same foregut diverticulum that gives rise to liver
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Adult Gallbladder
- length? - volume? - functions? |
- 8 cm long
- 50 ml volume Functions: store, concentrate, release bile |
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Adult Gallbladder
- histo? |
- consists of mucous membrane, muscularis, adventitia
- mucosa lined by columnar epithelium - mucosal diverticula lined by columnar epith -- dip into gallbladder wall (Rokitansky-Aschoff Sinuses) |
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What are Rokitansky-Aschoff Sinuses?
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= mucosal diverticula lined by columnar epith that dip into gallbladder wall
- may be confused with adenocarcinoma |
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What are the congenital abnormalities of the gallbladder?
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- agenesis
- atresia - duplication |
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What are the congenital abnormalities of the Bile Duct?
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- choledochal cyst (85%)
- choledochal diverticulum - choledochocele |
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Cholelithiasis
- what is? - frequency? - radiology? |
= presence of stones within lumen of gallbladder or within extrahepatic biliary tree
- 10-20% adult pop - Easily visualized by US |
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Cholelithiasis
- what are they made of? |
- 3/4 made primarily of cholesterol
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Cholelithiasis
- sx? |
- 80% asymptomatic
- fatty food intolerance - biliary colic - severe episodic pain in upper abd secondary to intermittent obstruction of GB or common bile duct |
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What are the types of Gall Stones?
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Cholesterol Stones
Pigment Stones (Black and Brown) |
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Cholesterol Stones
- composed of? - color? - shape? |
= cholesterol, Ca salts, mucin
- yellow-tan - round to faceted |
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What are increased risks for Cholesterol Stones?
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- increased age
- women of reproductive age (contraceptives, mult pregs, etc) - Estrogens - stim formation and increase secretion of bile by liver, decrease secretion of bile acids - obesity - ethnicity (Pima Indians) - diet (cholesterol) - metabolic abnormalities - drugs (clofibrate) |
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Black Pigment Stones
- shape? - discrip? - composition? |
- irregular in shape
- glassy black surface = CaBilirubinate, bilirubin polymers, Ca salts, mucin |
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Black Pigment Stones
- population? - pathogenesis? - increased risk? |
- old and undernourished patients
Path: - increased conc of unconjugated bilirubin in bile Increased risk: - patients suffering from diseases with chronic hemolysis - sickle cell anemia, thalassemia - cirrhosis |
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Brown Stones
- descrip - composition - where found?? |
- spongy, laminated
= CaBilirubinate, cholesterol, Ca soaps of FAs - usually found in intrahepatic and extrahepatic bile ducts (not as much in GB) |
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Brown Stones
- associated with what diseases? |
- bacterial cholangitis (e. coli)
- biliary helminth infection - chronic mechanical obstruction (e.g., in sclerosing cholangitis) |
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What are the contributing factors (pathway) to the formation of cholesterol stones?
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- supersaturation
- gallbladder hypomotility - crystal nucleation - accretion within the gallbladder mucous layer (adding layers around nucleus) |
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What is the difference in the gall bladder that leads to the formation of black v. brown stones?
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Black - sterile gall bladder (chronic hemolysis)
Brown - infected intrahepatic/extrahepatic ducts |
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What are the complications of gall stones?
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- cystic duct obstruction WITH inflammation
- cystic duct obstruction W/O inflammation (hydrops; mucocele) - passage into biliary ducts (cholangitis, pancreatitis) - passage into small intestines (gallstone ileus) |
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Acute Cholecystitis
- types? - cause? |
= diffuse inflammation of gallbladder SECONDARY to obstruction
- 90-95% assoc'd with gallstones - Acalculus Cholecystitis - sepsis, severe trauma, Salmonella, PAN (polyarteriris nodosa) |
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What is the name of cholecystitis WITHOUT gall stones?
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Acalculus Cholecystitis
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Acute Cholecystitis
- gross? - histo? |
Gross:
- external surface of GB is congested, layer of fibrinous exudate - wall thick and edematous - hemorrhagic mucosa - often gallstones in lumen and/or within cystic duct Histo: - abundant acute/chronic inflamm - edema - hemorrhage of wall - ulceration of mucosa - widespread necrosis of mucosa (gangrenous cholecystitis) |
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What is the dreaded complication of acute cholecystitis?
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PERFORATION!!
--> bile peritonitis |
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What is Gangrenous Cholecystitis?
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Acute cholecystitis with widespread necrosis of GB mucosa
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Chronic Cholecystitis
- what is? - cause? |
- most chronic disease of GB
- persistent inflamm of GB wall Causes: - repeat attacks of acute cholecystitis - continued presence of gall stones |
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What is the most common disease of the gallbladder?
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CHRONIC CHOLECYSTITIS
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Chronic Cholecystitis
- appearance on radiographs? - gross? - histo? |
CT/x-ray: wall/outline appears "layered"
Gross: - wall thick and firm secondary to extensive fibrosis - gallstones usually within GB - mucosa may be ulcerated, atrophic, or intact Histo: - fibrotic wall - Rokitansky-Aschoff Sinuses - chronic inflamm infiltrate within wall |
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What are Rokitansky-Aschoff Sinuses?
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diverticula/pockets in wall of GB - often due to increased pressure within GB due to gallstones
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Cholesterolosis
- what is? - sx? - gross? |
= accumulateion of cholesteorl-laden macrophages within submucosa of GB
- usually ayumptomatic Gross: "strawberry gallb;sdder" - prominent, scattered, yellow flecks on mucosa surgact |
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Tumors of GB
- benign - malignant |
Benign: Papilloma (associated with gallstones)
Malig: Adenocarcinoma |
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Adenocarcinoma of GB
- population? - associated symptoms? - location? - gross? - histo? - survival rate? |
2% patietns udergoing GB surgery
- associated with cholethiasis and chronic and chronic cholecystitis - most commonly occurs in fundus Gross: - papillary configuration (possibly) - thickened, leathery wall (reactive desmoplasia) Histo - infiltrative - usually well-differentiated neoplasm 5-year survival = <3% |
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Porcelain Gallbladder
- what is? - cause? |
= calcification due to excess gallstones
- almost always assocaited with adenocarcinoma |
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Pancreas
- embryology? |
arises from 2 endodermal outpouchings on dorsal and ventral sides of duodenal tube
- majority = dorsal - head = ventral |
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Pancreatic drainage??
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Major Pancreatic Duct --> drains into Common Bile Duct immediately prox to ampulla of Vater
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Exocrine Pancreas v. Endocrine Pancreas
- % of pancreas? - composition? - function? |
Exocrine = 80-85% of pancreas
- composed of acinar cells - synthesizes digestive enzymes: trypsin, chymotrypsin, amylase, carboxypeptidase, lipase, phospholipase, elastase Endocrine Pancreas - composed of Islets - synthesizes hormones: insulin and glucagon --> secreted directly into blood |
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What are the congenital abnormalities of the pancreas?
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- accessory pancreas
- annular pancreas - pancreas divisum - congenital cysts - ectopic pancreas |
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Ectopic Pancreas
- frequency? - what is? - descrip? |
Found in ~2% of autopsies
= ectopic tissue most commonly in walls of stomach, duod, jejunum (GI organs) - nodular configuration - found below mucosa, in muscularis, beneath serosa, or in small diverticula |
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Acute Pancreatitis
- definition? - presentation? |
= inflammatory condition of exocrine pancreas
- results from injury to acinar cells Variable Presentation: - Mild: acute inflamm and edema - Catastrophic: hemorrhagic pancreatitis with massive acinar cell necrosis |
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What are the etiologies of Acute Pancreatitis?
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- gall stones (#1)
- alcohol abuse (#2) - hypercalcemia - drugs - thiazide diuretics - Cocksackievirus - trauma - shock - atheroembolism |
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What is the pathology behind acute hemorrhagic pancreatitis?
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- middle-aged
- associated with alcoholism, chronic biliary disease - due to acinar cell injury and duct obstruction --> extracellular leakage of activated digestive enzs --> autodigest pacnreatic and extrapancreatic tissue - Trypsin (activated) --> activates other pancreatic proenzymes (phospholipase A2, proelastase) --> PLA2 attacks membrane phospholipids (necrosis) --> elastase digests walls of blood vessels (hemorrhage) -----> leakage of lipase into interstitium (fat necrosis) |
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Chronic Alcohol Abuse
- causes how much acute pancreatitis? - how??? |
- causes 1/3 cases of acute pancreatitis
-alcohol causes spasm or acute edema of Sphincter of Oddi - alcohol stims secretion from small intestine --> triggers exocrine panc to release enzs |
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Gall Stones
- causes how much acute pancreatitis? - risk of acute pancreatitis? |
- cause 45% (majority) of pancreatitis
- risk of pancreatitis 25x higher than general pop |
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Acute Pancreatitis
- gross? - histo? |
Gross:
- edematous - hyperemic - may eventually become a retroperitoneal hematoma - areas of fat necrosis (yellow white areas) Histo: - acinar cell necrosis - fat necrosis - intense acute inflamm |
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What is one main possible complication of acute pancreatitis
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Pseudocyst - connective tissue encloses wide spaces of blood, necrotic tissue, enzymatic fluid
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Acute Pancreatitis
- clinical features? |
- severe epigastric pain
- nausea/vomiting - may eventually lead to peripheral vascular collapse and SHOCK |
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When is the typical onset of acute pancreatitis?
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After heavy meal, alcohol
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What is a serological sign of acute pancreatitis?
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Elevated amylase/lipase
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Chronic Pancreatitis
- what is? - pathogenesis/cause? |
- progressive destruction of pancreas characterized by irregular fibrosis, calcification, and chronic inflammation
Path: 1. long-standing alcohol abuse 2. congenital anomalies/mechanical obstruction 3. repeated episodes of acute pancreatitis |
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Chronic Pancreatitis
- mortality rate? |
3-4% per year
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Chronic Pancreatitis
- gross? - histo? |
- gross?
- histo? Gross: - firm pancreas - cut surflace lacks normal lobulated appearance Histo: - irregular areas of fibrosis - reduced number of size of exocrine/endocrine elements - chronic inflammation cells: lymphocytes, plasma cells, macrophages |
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What other clinical signs/problems are associated with Chronic Pancreatitis?
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- RECURRENT and progressive pancreatic insufficiency/destruction
- malabsorption - diabetes |
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What are the causes of Chronic Pancreatitis?
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1. Alcoholism (70%)
2. Idiopathic 3. Other - pancreatic duct obstruction (tumor, trauma, etc.), CF, hyperlipidemia, hereditary, tropical, hyperparathyroism |
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Pancreatic Cystadenoma
- what is? - patient pop? - types? |
= large, multiloculated cystic tumors
- usually located to pancreatic body or tail - usually women btwn 50-70 y.o. - types: serous and mucinous |
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Pancreatic Carcinoma
- most common type (%?) - prognosis? |
- Ductal Adenocarcinoma = 90%
Prognosis: poor - often metastatic at time of dx... - 5 yr survival = <1% |
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Pancreatic Carcinoma
- signs and sx? |
- anorexia
- weight loss - epigastric pain (radiating to back) - Trousseau Syndrome (10%) - Jaundice (50% - cancer of panc head) |
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What is Trousseau Syndome?
- how often found and when? |
= migratory thrombophelebitis
- occurs in 10% patients with pancreatic adenocarcinoma - may be initial clinical evidence of the cancer |
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To where does pancreatic carcinoma metastasize?
To what other areas might it directly extend? |
Metast: regional lymph nodes and liver
Directly Extend: stomach and duodenum |
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Pancreatic Carcinoma
- risk factors?? |
- smoking
- polycyclic hydrocarbons - diet - diabetes - chronic pancreatitis |
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Pancreatic Carcinoma
- gross? - histo? |
Gross:
- firm, gray, poorly demarcated multinodular mass embedded in dense connective tissue stroma -satellite tumor nodules in mesenteric locations Histo: - >75% are well-differentiated adenocarcinomas - prominant desmoplastic reaction often observed - Perineural invasion may be seen |
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What is a desmoplastic reaction?
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Growth of fibrous or connective tissue around a tumor
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What are the different cells of the Pancreatic Islets?
- functions?? - locations? |
Alpha Cells: secrete GLUCAGON --> increases blood glucose
- located in outer rim of islets Beta Cells: secrete INSULIN (within secretory vesicles) - located throughout islet (60-70% of all islet cells) Delta Cells--- D Cells: secrete SOMATOSTATIN --> inhibitory hormone --> reduces alpha/beta/delta/acinar cell secretions D1 Cells: secrete VASOACTIVE INTESTINAL PEPTIDE (VIP) --> induces glycogenolysis and hyperglycemia AND regulates tone, motility, ion/water secretion by epith cells of GI tract - located in periphery of islet |
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Islet Cell Tumors
- frequency? (%?) - effects? - most common type? (%?) |
- Rare! <10% of all pancreatic neoplasms
- Many are nonfunctioning - Functional tumors may or may not be part of MEN Syndrome --> can produce clinical symptomatology thru hormone release - Beta Cell Tumors = 75% (most common) |
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Beta Cell Tumors
- aka? - % of islet cell neoplasms? - malignancy? - location? - size? - solitary or multiple? - dx? - tx? |
aka: INSULINOMA
= most common islet cell tumor (75%) - most benign (small percentage malignant) - most in body or tail of pancreas - < 3 cm diam - 90% are solitary -> excised easily - dx: lab testing (high blood insulin and tumor cells) - tx: surgical incision |
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Beta Cell Tumors
- histo?? |
- the neoplastic cells resemble normal beta cells
- BUT distributed in trabecular or solid patterns - amyloid may be found in stroma of the tumors |
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Beta Cell Tumors
- result? - clinical symptoms? |
- produce severe hypoglycemia thru autonomous secretion of insulin (even when low blood sugar)
SX: - sweating - nervousness - hunger - lethargy - eventual coma **Most cases have only mild hypoglycemia or NO sx |
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Islet Cell Tumors - secretion of ectopic hormones......
- what hormones? - result? |
- Can secrete ACTH, PTH, Calcitonin, Vasopressin
- Cause 10% of paraneoplastic Cushing Syndrome (second only to SCC of lung) |
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MEN I
- what is? - often associated with?? |
Pituitary Adenoma +
Parathyroid Adenoma + Endocrine Pancreas Adenoma - frequently associated with Z-E Syndrome |
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Zollinger-Ellison Syndrome
- characterized by?? |
1. Intractable gastric hypersecretion
2. Peptic ulceration 3. Elevated blood gastrin levels |
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Gastrinomas
- malignant? - metastasis? - histo? |
- majority are malignant (70-90%)
- metast to regional lymph nodes and liver - histo: similar to intestinal carcinoid tumors |
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Pancreatic Gastrinoma
- aka? - what are? - how formed? |
aka: Zollinger-Ellison Syndrome
- G cell tumors --> secrete Gastrin - Arise from multipotent primitive endocrine cells that inappropriately differentiate into G cells (G cells not usually found in normal islets) |