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134 Cards in this Set
- Front
- Back
The GB is located in what quadrant of the abdomen?
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RUQ and epigastrium
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Duodenum is located in what quadrant?
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LUQ, Epigastrium, RUQ
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what does the abdominal cavity encompass?
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the nipple line to the privates
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what structures are located in the suprapubic quadrant?
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appendix, sigmoid colon, uterus, bladder
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when ordering a CBC, the WBC tells us what?
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whether there is inflammation or infection anywhere
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when ordering a CBC, the H/H tells us what?
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RBC production/destruction (consider how well hydrated they are)
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When ordering a CBC, platelets tell us what?
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production, destruction, ability to clot
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What factors does a Liver Function tests include?
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AST/ALT
Bilirubin Alk Phos PT, PTT |
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presence of a non-tender palpable gall bladder with jaundice suggests underlying malignant disease such as carcinoma of the pancreas and is known as?
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Courvoisier's Sign
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what is the most sensitive PT factor?
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Factor VII. has the shortest half life.
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what lab tests tell us about pancreatic function?
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lipase and amylase
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WHat test tells you how well the GB is functioning secondary to US?
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HIDA
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what are the short falls of using USN for GB screening?
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its great for looking at the GB but it doesn't tell you how well its working. 50% of the time you ahve a nonfunctioning GB but it looks fine.
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Can we use US to look for appendicities?
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no, too much gas in your colon, perhaps for kids becasuse you can compress the bubble out o fth eway but this is painful.
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Right and left lobes are defined by the ______
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falciform ligament
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What line cuts the right lobe into medial and lateral segments?
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Cantlies line
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what veins form the portal vein?
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SMV, IMV, splenic vein
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What vessels supply blood to the liver?
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portal vein supplies 75% of the blood and 25% of the oxygen
hepatic artery supplies 25% of the blood and 75% of the oxygen |
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where does all the blood from the intestines go?
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first stop is the liver then pancreas
liver sees food filled blood and stores glucose as glycogen. Takes first 10% to keep glycogen stores which are important. glycogen stored in liver can go anwhere (glycogen stored in mm has to stay there) pancreas sees glucose and secretes insulin proportional to the glucose load |
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what system allows first pass?
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portal system
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what functions does the liver have?
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metabolizes drugs
stores glucose forms bilirubin from hemoglobin synthesizes albumin, clotting factors (PT), cholesterol |
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why is albumin important?
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produced in liver, carrier molecule and very important for oncotic pressure
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what should you do if you find a cyst?
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no matter where it is, it must be removed - cancer potential.
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what is biliary atresia?
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when the biliary tree doesn't form. born with complete liver failure. need transplant or will die
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what are two anatomic anomalies seen in the liver?
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R hepatic artery off SMA, by mistake 20-25% of the time
L hepatic artery off L gastric artery just as often |
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WHere do most liver infections come from?
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from the intestines or gall bladder via the portal system
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blood borne infections and metastatic tumors favor which lobe?
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right lobe 2:1
(the right side is a little straigher just like in the bronchiopulmonary branchtes) |
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what is dx of a liver infection?
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air in the liver
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what do we do with bacterial abscesses in the liver?
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must be drained, abx are not enough.
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when are amebic abscesses present in the liver? and how are they treated?
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with dysentery, eosinophilia
treated with Flygyl (metronidazole) plus lots of hydration |
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this type of liver cysts is present with pulmonary disease and eosinophilia. How do we get it? how do we treat it?
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Echinococcal cysts
get them from farm animals, contaminated food, eat parasites which can set up in GI, lungs, liver. The walls of these cysts can survive stomach acid. Also made of proteins which humans are allergic too so if you open them in the OR patient will go into anaphylactic shock. Tx: drain cysts and really clean it out. |
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What is the venous drainage for the liver?
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right, left, and middle hepatic veins that drain into the inferior vena cava
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macrophages in close proximity to hepatocytes that produce IL-1, TNF alpha and other cytokines are called?
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Kupffer cells
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what vessels make up the portal triad?
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hepatic portal vein
hepatic artery bile duct |
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temporary occlusion of hepatic inflow by vascular clamp to hepatic artery and portal vein in the porta heptits is know as?
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the pringle maneuver
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what is normal portal venous pressure?
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5-10mmHg
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what are causes of prehepatic portal hypertension?
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portal or splenic vein thrombosis
something before the liver is inflammed or getting squished |
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what are cuases of intrahepatic portal hypertension?
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hepatitis, cirrhosis
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what are causes of posthepatic portal hypertension?
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Budd-Chiari Syndrome - post hepatic venous occlusion which can result from various thrombotic states or from vascular webs in the vena cava
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what does the extra portal hypertension pressure create when it backs up?
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collateral portosystemic channels
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what kinds of portal hypertension collaterals can develop?
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1. esophagus (esophageal variceal bleeding)
2. peri-umbilical (CAPUT MEDUSAE) 3. hemorrhoidals 4. all over! adhesions |
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what is the MC form of portal hypertension in the US?
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Cirrhosis, mostly caused form alcohol
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how does cirrhosis commonly present?
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with esophageal vatical bleeding and ascites
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what is the most deadly complication of portal hypertension?
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bleeding from esophageal varicies
followed by asciteis and encephalopathy |
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variceal bleeding is known to occur when the portal hypertension is above?
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12mmhg
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portal vein is formed by what?
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SMV, IMV, and splenic vein
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the liver forms bilirubing from what?
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hemoglobin
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The liver synthesizes?
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cholesterol, bilirubin, albumin, clotting factors and others
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this disease is a congenital abnormality associated with dilated intrahepatic bile ducts
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Caroli's Disease
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______ is a well-circumcsribed benign lesion usually found incidentally. It arises from an arterial malformation
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FNH, Focular nodular hyperplasia
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how do we treat amebic abscess?
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with Flygyl (metronidazole) do not need to aspirate
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This infection presents with pulmonary disease and esoinophilia.
Which infection presents with dysentery and eosinophilia? |
1. echinococcal cysts
2. amebic abscess |
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what medication do we use for variceal hemorrhaging?
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IV somatostatin
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what is a major SE of TIPS and other shunting methods for variceal bleeding?
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hepatic encephalopathy -- too many toxins and fluids are bypassing the livers filtering system.
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what is the initial treatment for variceal bleeding? (first two actions)
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ABCs specifically volume resuscitation and upper GI endoscopy to see the source of the bleeding.
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what are some Rx treatments for variceal bleeding?
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Somatostatin
DDAVP (for bleeding) Beta Blockade (Book says: short term abx, IV vasopressin with nitroglycerin as 2nd choice) |
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What are therapies we can use to treat variceal bleeding?
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1. TIPS (shunt within the liver)
2. Luminal Tamponade -->Sengstaken-Blakemore tube 3. Endoscopic therapy (sclerotherapy of band ligations) |
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What are treatments we can do to prevent future variceal bleeding?
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1. Beta blockade
2. Endoscopic therapy is primary treatment 3. TIPS is definitive treatment (but high incidence of hepatic encepalopathy) 4. Selective shunts (such as distal splenorenal and coronary-caval shunt) |
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isolated gastric varicies are treated with?
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splenectomy
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what is the MCC of ascites?
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Portal HTN due to chronic liver dz
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What is HRS, hepato renal syndrome?
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When the liver is too damaged and stops producing sufficient proteins (albumin) oncotic pressure diminishes and fluids escape into the peritoneum. This causes a decrease in circulating plasma volume in patients with significant ascities. This then leads to decreased renal blood flow which causes the kidneys to panic and increased release of aldosterone which wants to increase the bodies volume by holding onto to sodium.
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How do we treat ascites according to the book?
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1. restrict fluid intake
2. limit sodium intake to <40 mEq/d 3. Can use spironolactone ( an aldosterone antagonist) to promote sodium secretion |
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Do we see ascites cause by pre-hepatic portal hypertension?
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no
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liver "sweats" a high ____ fluid into the peritoneal cavity
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sodium
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How do we treat ascites according to the lecture?
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Na restriction
Potassium sparing diuretics PV shuns - Denver, Leveen porto-caval shunts draining?! |
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what is the MC benign liver tumor?
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cavernous hemangioma
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This benign tumor is believed to be congenital and is often an incidental finding, and usually not painful. Also 5x more common in women
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cavernous hemangioma
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this type of benign tumor is usually found incidentally, and is characteristic for its well circumscribed classic stellar scar.
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FNH - Focal Nodular Hyperplasia
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this benign liver tumor is usually found in women 30-50 y/o with a hx of estrogen exposure.
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hepatic adenoma
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most malignant liver tumors come from where?
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metastatic spread from colon via portal system
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this type of liver tumor is 90% of all primary liver malignancies and usually occurs in patient with underlying dz
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Hepatocellular carcinoma
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This type of liver tumor arises from the mucosa of the biliary tree
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cholangiocarcinoma
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tumor seen at the bifurcation of the left and right hepatic duct is known as?
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Klatskin tumor
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which type of malignant tumor is most common in children?
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hepatoma, hepatocellular carcinoma.
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in which type of liver tumor will there be high AFP levels and involve the parenchyma?
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hepatoma, hepatocellular carcinoma
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how do we dx and tx liver tumors?
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dx: CT, USN
Tx: resection is always the goal |
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what are the survival rates of metastasized colon cancer?
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0% 5yr survival if anywhere but the liver
if in the liver and you resect it: 25% 5 yr survival |
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synonyms for the gallbladder neck are?
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infundibulum or Hartmanns pouch
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in the gallbladder where does the cystic artery usually come from?
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right hepatic artery
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which is water soluable and excreted in the urine, indirect or direct bilirubin?
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direct (conjugated)
Indirect bilirubin is lipid soluable and is not peed out. |
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what are the fat soluable vitamins?
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ADEK
you can overdose on these! not excreeted out. |
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the gallbladder contracts in response to what?
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CCK from the duodenum
CCK is released in the presence of fatty acids and amino acids in the duodenum |
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The presence of CCK in the duodenum causes what two things?
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the gall bladder to contract
the sphincter of oddi to relax |
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what is the main purpose of the gall bladder
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to store bile which emulsifies fats
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what is bile composed of?
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cholesterol
lethichicin protein conjugated bilirubin bile salts |
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most gallstones in the US are?
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mixed.
made from cholesterol, bile acids and lethicin |
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brown stones from the gallbladder are associated with what?
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infection; infected bile
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___% calcify = positive xray
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15%
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Black pigment stones found in the gallbladder are indicative of what dz states?
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cirrhosis and hemolytic dz
Lecture says: hemolysis |
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what is the 20/20 rule when it comes to gallstones?
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20% of gallstones have enough calcium to show up on X-ray. 20% of kidney stones will not show up on xray
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what are the sx of gallstone disease?
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RUQ, epigastric pain.
biliary colic dull ache "feels like being stabbed with a finger" lasts for 30 min usually 1-2 hrs after eating |
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Who are the most likely to get gallbladder disease?
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5F's
female, forty, fertile, fatty foods, flatulent |
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What blood work should you check on a patient suspected of gallbladder disease?
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1. wbc
2. AST/ALT 3. Alk Phos 4. Bilirubin 5. PT/PTT 7. Amylase/Lipase |
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What studies should you order for a patient supsected to have gallbladder disease?
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US, HIDA, CCK-HIDA
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pruritus due to GB disease is believed to be caused by?
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Increased levels of reabsorbed conjugated bile acids in the tissues.
often seen in patients with obstructive jaundice |
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what are the sx of acute cholecystitis?
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fever
RUQ, epigastric pain Positive Murphy's sign localized tenderness and guarding rebound tenderness Pain >3-4 hours to several days, aggravated by movement |
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What study do we use to dx gallstones and acute cholecystjts?
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1.Ultrasonography
2. HIDA scan |
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what are the 3 initial steps to treating acute cholecystits?
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1. with hold oral intake
2. IV fluids 3. Antibiotic therapy |
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what are the three bacteria most likely associated with acute cholecystits?
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1. e.coli
2. Klebsiella pneumonia 3. strep. faecalis |
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what are the two surgical options mentioned in lecture to treat galldbladder disease?
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1. cholecystectomy -- taking the GB out
2. cholecystostomy -- put a tube in through the liver into the GB and drain it. |
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what are three methods we can use to explore the location of a possible gallstone?
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1. ERCP - GI (can visualize and correct)
2. PTC (radiology) helps dx cause of blockage 3. Commone bile duct exploration (CBD exploration) |
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What is Charcot's triangle and when do we see it?
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1. jaundice
2. fever 3. RUQ abdominal pain Acute cholangitis (infection) |
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what is the 5 year survival of adenocarcinoma of GB and cholagniocarcinoma?
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even with excision 0% survival
Unless you catch GB adenocarcinoma early enough and excise it completely, but once its spread to lymphatics of the liver you are dunzo |
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What is the survival for removal of a klatskin tumor?
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less than 5%, 5 year survival
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which pancreatic duct joins the common hepatic duct going to the ampulla of vater?
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the main pancreatic duct aka Wirsung duct
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what is the arterial supply to the pancrease?
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1. gastroduodenal artery
2. splenic artery |
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what are the three main digestive enzymes secreted by the pancrease? and the 2 inactivated ones we covered?
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Lipase
amylase protease 1. tripsinogen 2. chymotripsinogen |
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what are the main exocrine secretions we discussed in lecture?
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1. amylase
2. lipase 3. bicarb 4. trypsinogen 5. chymotripsinogen |
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What are the main endocrine secretions we discussed? and where do they come from? (what part of the pancreas)
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Come from the islets of langerhans
1. alpha cells secrete gulcagon in the presense of low glucose levels 2. Beta cells secrete insulin in the presence of high glucose levels 3. Delta cells secrete somatostatin in which is a strong inhibitor of pancreatic exocrine secretion |
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what are two test criteria systems we can use to dx pancreatitis?
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Apache II and Ransons criteria
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what are the 5 Ransons criteria noted at admission?
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1. age > 55 (non billiary) >70 (biliary)
2. WBC >16k (non billiary) >18 (billiary) 3. glucose >200 >220 4. LDH >350 >400 5. SGOT (AST) >250 >250 |
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what are the 6 Ransons criteria noted within the initial 48 hours?
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1. Decreased Hct >10 >10
2. BUN >5 >2 3. Calcium <8 <8 4. Arterial PO2 >6 --- 5. Base Deficit > 4 >5 6. Fluid Sequestration >6 >4 |
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what dx procedure is most commonly used for definining the pancreatic and bile duct architecture?
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ERCP
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How many of Ranson's criteria classifies as severe disease?
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3 or more. most significant factor of survival is degree of necrotization.
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What are initial treatements for pancreatitis?
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1. NPO
2. IVF 3. Pain medication 4. ETOH withdrawal 5. Somatostatin 6. NGT? |
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what is the treatment for pancreatic necrosis and infection?
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1. debridement
2. drainage 3. abx 4. supportive treatment |
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what is the most common complication of pancreatitis?
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development of fluid collection in peripancreatic area. (can turn into pseudocyst)
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fluid collection in the peripancreatic area can either resolve spontaniously or turn into this condition that requires surgery and drainage.
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pseudocyst
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what are common factors contributing to the onset of pancreatitis?
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FESTIVAL
F- furosemide (lasix) familial E- etoh, ERCP? S - stones (gallstones) shock, steroids, scorpion T - tumor, trauma I- idiopathic V - viral (CMV) valoproic acid (bipolar) A - alcohol, azothiprine L - lasparaginase hyperlipidemia |
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The most commonly expressed genetic mutation in malignant pancreatic neoplasms occurs in what oncogene?
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K-ras
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A palpable non tender gall bladder with painless jaundice is associated with what?
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malignancy
Courvoisier's sign |
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what is the MC pancreatic tumor?
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ductal adenocarcinoma 90%
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a patient may come in unconscious and with a glucose of 10. No hx of diabetes. What can it be?
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PET - Beta Cell tumor - Insulinoma
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what is Whipple's triad?
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1. sx of hypoglycemia
2. low glucose levels (40-50) 3. Sx improvement with glucose |
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how do we treat single insulin producing tumor? what is this tumor techinically called?
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insulinoma
treat with excsion |
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This PET is usuall benign, and the MC functional tumor
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insulinoma
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in a patient with peptic ulcers, diarrhea and ulcers resistant to treatment you should consider this type of PET
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gastrinoma
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50% of these tumors are located in duodenal wall, 3/4 occur sporadically, pain comes from acid hyper secretion and will often see abd. pain, persistent diarrhea, and severe esophagitis
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gastrinoma (D cells signalling your stomach to make more acid. opposite of somatostatin)
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what is zollinger ellison syndrome?
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when a tumor secretes too much gastrin usually from pancreas or duodenum
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This type of PET is usually present with MEN 1 and is usually multifocal
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gastrinoma
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if you can not take PET tumors our you can use what two medications to control symptoms?
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1. somatostatin
2. streptozotocin (abx) |
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what are the three types of PET we learned about in lectures?
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1. insulinoma - mainly benign, whipples triad, hypoglycemia
2. gastrinoma - usually multifocal, associate with MEN 1 high gastrin levels which means severe abd. pain, esophagitis. Ph very low 3. Vipoma - watery diarrhea uncontrollable. WDHA syndrome |
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what is WDHA syndrome? where do we see it?
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1. watery diarrhea
2. hypokalemia 3. hypochlorydria we see this in VIPOMAs |
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The pancreatic tumor presents with bouts of diarrhea, flushing and tachycardia. How do we treat it?
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VIPOMA
excision is treatment Can use somatostatin and streptozotocin pre-op or to manage non surgical candidates. |