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327 Cards in this Set
- Front
- Back
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Which neurocrine has these functions in the enteric nervous system?
-Contraction of GI smooth muscle -Relaxation of sphincters -Increased salivary, gastric, and pancreatic secretions |
Acetylcholine
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Which neurocrine has these functions in the enteric nervous system?
-Relaxes GI smooth muscle -Contracts sphincters -Increases mucus secretion in saliva |
Norepinephrine
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Which neurocrine has these functions in the enteric nervous system?
-Relaxes LES -Increases small intestinal and pancreatic secretions |
Vasoactive intestinal polypeptide
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Which neurocrine has these functions in the enteric nervous system?
-Increases gastrin secretion |
Gastrin-releasing polypeptide
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Which neurocrine has these functions in the enteric nervous system?
-Contracts GI smooth muscle -Decreases intestinal secretions |
Enkephalins
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Which neurocrine has these functions in the enteric nervous system?
-Relaxes of GI smooth muscle -Decreases intestinal secretions |
Neuropeptide Y
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Which neurocrine has these functions in the enteric nervous system?
-Contracts GI smooth muscle -Increases salivary secretions |
Substance P
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What role does serotonin play with GI smooth muscle?
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causes contraction
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What role does ATP play with GI smooth muscle?
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causes relaxation
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what layer separates the submucosal and myenteric plexuses?
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circular layer
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what are the two sources of parasympathetic input to the GI?
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vagus and pelvic nerves
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what are the 4 sympathetic ganglia which supply innervation to the GI?
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1. Celiac
2. Superior mesenteric 3. inferior mesenteric 4. hypogastric |
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what are the 4 gastrointestinal hormones?
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1. Gastrin
2. Cholecystokinin (CCK) 3. Secretin 4. Glucose-dependent insulinotropic peptide (GIP) |
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what cells secrete gastrin?
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G cells
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3 functions of gastrin?
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1. Increase gastric acid
2. increase gastric motility 3. increase gastric mucosa |
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what is the main neural stimulation of gastrin release?
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parasympathetic release of GRP
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what cells secrete Cholecystokinin?
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I cells
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small peptides, lipids, or a decreased pH in the duodenum causes the release of these 2 gastrointestinal hormone?
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CCK and secretin
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what are the 4 functions of CCK?
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1. stimulates gallbladder release of bile acids
2. increases secretion of pancreatic enzymes 3. inhibits gastric emptying 4. potentiates the effects of secretin |
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what cells secrete secretin?
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S cells
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what are the 4 functions of secretin?
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1. increase secretion of bicarb from pancreas
2. increase release of bile acids from liver to gallbladder 3. inhibits release of gastrin 4. inhibits gastric emptying |
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what cells secrete glucose-dependent insulinotropic peptide (GIP)?
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K cells
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what is the function of GIP?
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stimulates insulin secretion before glucose even gets to the blood flow
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what causes the release of GIP?
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glucose in the duodenum
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what cells produce somatostatin?
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D cells of gastric mucosa
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what is the function of somatostatin?
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decrease gastric pH
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what is the mechanism of action of somatostatin in reducing gastric pH? (2)
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1. inhibit proton pumps
2. inhibit histamine release |
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what is the action of histamine and what cells does it act upon?
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increases acid secretion from parietal cells
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what neuronal control is histamine release under?
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parasympathetics
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the reflexive chewing that is stimulated by chemoreceptors in the mouth uses what CN to relay information to brain and the from brain to muscles of mastication?
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CN V
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what are the 3 stages of swallowing?
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1. oral phase
2. pharyngeal phase 3. esophageal phase |
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where is the swallowing center located?
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medulla
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what are the CN's that are involved in sending the sensory information about swallowing to the swallowing center in the medulla?
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CN V, X, and IX
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what are the CN's that are involved in the neural input from the swallowing centers during the process of swallowing?
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CN V, IX, X, XII
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what initiates the paristaltic movements of the esophagus?
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distension
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what is the primary cause of the opening of the LES?
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primary paristaltic movements and the vagovagal reflex mediated by CN X
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what are the "pacemaker cells" of the intestine
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interstitial cells of Cajal
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what allows signal to be passed from Cajal cells to intestinal smooth muscle cells?
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gap junctions
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what is the frequency of the slow waves in the stomach?
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3 per minute
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what is the highest frequency of slow waves and what part of the GI is it found in?
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12 in the duodenum
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what does the neuronal input do with slow waves?
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does not change frequency but rather changes magnitude
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what part of the stomach is involved with receptive relaxation and what initiates this?
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the orad part of the stomach relaxes to accept food from primary paristaltic movements
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what part of the stomach is involved in mixing of chyme?
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caudad
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how long does it take to empty the stomach and how much chyme is release per peristaltic wave?
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3 hours to empty with 1% being released on every wave
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increased or deceased gastric emptying?
increased volume |
increased
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increased of deceased gastric emptying?
lipids in duodenum |
decreased
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increased of deceased gastric emptying?
increased fluidity of chyme |
increased
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increased of deceased gastric emptying?
hypertonic or hypotonic chyme |
decreased
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increased of deceased gastric emptying?
chyme below pH of 2 |
decreased
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increased of deceased gastric emptying?
sympathetics |
decreased
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increased of deceased gastric emptying?
parasympathetics |
increased
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what is the most potent inhibitor of gastric emptying?
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lipids in duodenum
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what clears the stomach of any residual chyme about every 90 minutes? what causes this to happen?
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migrating myoelectric complexes, caused be release of motilin from M cells
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what is the most prevalent movement of the intestine and what function does it serve?
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segmentation mixes chyme with digestive enzymes
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how long does it take for chyme to move through that small intestine?
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3-5 hours
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where does segmentation occur in the large intestine?
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the cecum and proximal colon
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how long does it take fecal material to pass through the colon?
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16-24 hours
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what is the purpose of gastrocolic and duodenocolic reflexes?
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clear the bowels of residual fecal matter to make way for a large meal
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the urge to defecate (rectosphincteric reflex) occurs when the rectum fills to what capacity?
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25%
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Explain the process be which saliva is formed?
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Acinar cells create ultrafiltrate from interstitial fluid which is then tweaked by the ductal cells as it progresses to the mouth
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describe what is removed and what is added to saliva by ductal cells?
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net addition of K+ and HCO3-
net loss of Na+ |
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what is the highest flow rate for saliva? slowest?
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4ml/min, 1ml/min
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describe the concentrations of K+, Na+, and Cl- in saliva during high flow? low flow?
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high flow = increased Na+ and Cl- and decreased K+
low flow = increased K+ and decreased Na+ and Cl- |
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what are the antibacterials found in the saliva?
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IgA and lysozyme
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what is unique about the control of salivary excretion?
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it is only under neuronal control and unlike the rest of the GI has no hormonal input
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what is the main neuronal control of salivation? (parasympathetics or sympathetics)
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parasympathetics
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what happens to the HCO3- that is formed in parietal cells after H+ production?
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it is secreted into the blood and carried to the pancreas where is will be reintroduced to the GI (alkaline tide in blood flow from stomach)
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describe the function of the parietal cells (what do they put where)
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take H+ from the breakdown of H2O and secrete it into stomach along with Cl- from the blood
Secrete bicarb into the blood along with Na+ |
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what are the 3 agents which stimulate gastric acid secretion?
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1. acetylcholine
2. gastrin 3. histamine |
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what are the 2 agents which retard gastric acid secretion?
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1. somatostatin
2. prostaglandins |
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what receptors does acetylcholine bind to on parietal cells after its release from parasympathetic neurons?
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M3
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what is the action of ACTH on gastric parietal cells?
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increase action of proton pump
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what cells produce gastrin?
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G cells
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what receptor does gastrin bind to on parietal cells?
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CCK receptor
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what is the action of gastrin on parietal cells
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stimulated proton pump
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what cells produce the histamine which acts on parietal cells?
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enterochromaffin-like cells in gastric mucosa
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the drugs that end in "-tidine" such as famotidine, cimetidine, and ranitidine have what mechanism of action?
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inhibit histamine binding at H2 receptor on gastric parietal cells
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what cells produce somatostatin?
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D cell
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what is the mechanism of action of somatostatin in reducing gastric acid secretion in gastric parietal cells?
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antagonizes the actions of histamine
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what effect do prostaglandins have on gastric parietal cells?
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the antagonize the stimulator effects of histamine
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what are the four gastric secretions?
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1. pepsinogen
2. intrinsic factor 3. gastric lipase 4. mucus |
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what cells produce pepsinogen and where are they located?
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chief cells from the body of the stomach
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what cells release intrinsic factor, where are they located, and what is the purpose of intrinsic factor?
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parietal cells, located in body (upper portion), and intrinsic factor is needed for absorption of vitamin B12
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at what pH is pepsinogen activated?
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pH 3 or below
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what are the three phases of gastric acid secretion? what happens in each?
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1. cephalic (higher CNS input) - parasympathetics and gastrin cause increase in gastric motility and acid secretions (histamine also involved in acid) = 30% of acid
2. gastric - mechanoreceptor stimulate parasympathetic release of gastrin, histamine, and gastric acid - 60% of acid 3. intestinal - either increases parasympathetic acid secretion (pH of chyme in duodenum >3) or inhibits (pH < 2 or contains lots of lipids) |
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what is the reflex that stops gastric emptying when the duodenum is being over filled?
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enterogastric reflex
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where is the most common place for ulcers to form in the GI? What is the cause of these ulcers?
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duodenum, stomach emptying too fast
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describe the production of pancreatic secretions?
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exact same as parietal cell secretions except in opposite direction (acid tide in blood from pancreas)
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what enzyme activates trypsinogen?
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enterokinase
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where is enterokinase located in the bowels?
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the striated border (some say brush border) of the proximal small intestine
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the names of the phases of pancreatic excretion are the same as that of gastric secretion, which is responsible for the highest pancreatic output?
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intestinal phase stimulates 80% of the pancreatic secretions
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what are the hormones that are involved with pancreatic secretions during the intestinal phase?
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1. CCK
2. secretin |
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what cells produce CCK?
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I cells
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what makes up bile?
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bile acids, cholesterol, phospholipids, bilirubin, ions, and water
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conjugation is the act of adding ___ or ____ to bile acids making the amphipathic?
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glycine or taurine
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how much cholesterol is produced by the liver and what is its function in bile?
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1 gram per day and its helps to form micelles around large lipids to aid in absorption
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what is responsible for the release of bile into the duodenum?
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CCK
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where are bile salts reabsorbed?
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the ileum
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describe how fat gets into circulation from the gut?
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gets absorbed into villi -> lacteals -> lymphatic system -> venous blood
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what are the 3 monosaccharides the body absorbs?
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1. glucose
2. fructose 3. galactose |
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what transporter facilitates the absorption of glucose into intestinal epithelial cells?
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SGLT 1
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what transporter facilitates the absorption of galactose into intestinal epithelial cells?
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SGLT 1
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what transporter facilitates the absorption of fructose into intestinal epithelial cells?
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GLUT 5
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which transporter facilitates the excretion of glucose, fructose, and galactose from intestinal epithelial cells into the blood stream?
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GLUT 2
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what are the 3 types proteins that are absorbed? (referring to size)
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1. amino acids
2. dipeptides 3. tripeptides |
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most of the proteins absorbed from the gut are in which twp forms?
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dipeptides and and tripeptides
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amino acids are absorbed into intestinal epithelial cells how?
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cotransporter which utilizes Na+ gradient into the cell
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dipeptides and tripeptides are absorbed into intestinal epithelial cells how?
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cotransporter which utilizesH+ gradient into the cell
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why are infections easily spread from the esophagus to the mediastinum?
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the esophagus lacks serosa
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what is most common cause of esophageal stenosis?
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acquired type after inflammation or trauma
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what is the triad of plummer-vinson syndrome?
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1. upper esophageal web
2. Fe deficiency anemia 3. glossitis |
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a female age 43 presents with Fe deficiency anemia and glossitis. what additional complication could explain her recent difficulty swallowing and what is the name of this syndrome?
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an upper esophageal web, plummer-vinson syndrome
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what additional complication are individuals (usually woman >40) at greater risk for?
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squamous carcinomas in the oral cavity
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what is the most common esophageal diverticulum?
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zenker's diverticulum
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where do diverticuli form in elderly people with muscle weakening in the esophagus? (this is called a zenker's diverticulum)
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just above the UES
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what is the cause of a traction diverticulum and where is it most likely to occur?
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in the mid esophageal area due to post-inflammatory fibrosis
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regurgitation of large volumes of fluid that occurs when sleeping or laying supine for prolonged periods is likely cause be what?
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Epiphrenic diverticulum causing insufficiency of the LES
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what is achalasia of the esophagus?
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pregressive aperistalsis with incomplete relaxation of of the LES or increased resting tone of the LES - leads to dysphagia + nocturnal regurgitation of food
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what is the serious concern with achalasia? (esophagus)
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5% develope squamous cell carcinoma
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describe the gross appearence of a person with achalasia?
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progressive dilation of the esophagus proximal to a denervated segment
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what is a pouch of stomach extending > 2 cm above the diaphragmatic hiatus into the thorax called?
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hiatal hernia
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most hiatal hernias are this type?
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sliding
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what is the second most common hiatal hernia?
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paraesophageal
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describe the changes in the squamous epithelium of the esophagus with reflux esophagitis?
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Barretts metaplasia = change from regular squamous to a glandular type mucosa
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describe changes to the basal zone of the epithelium in the esophagus with reflux esophagitis?
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2x thicker and hyperplastic
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what type of patient is most liekl to have infectious esophagitis?
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immunocompromised
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what are the top 3 most common infections in infectious esophagitis?
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1. candida
2. herpes simplex 3. CMV |
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what neoplasm is likely to occur in 10-15% of people with BE?
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adenocarcinoma 40x higher prevalence than normal population
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what is the prognosis for someone with BE + high grade dysplasia?
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it will progress to invasive adenocarcinoma within 5 years in 30-60%
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what is the origin of most of the benign neoplasms of the esophagus?
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mesenchymal - leiomyomas, lipomas, hemangiomas, neurofribromas
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what are the 2 types of benign neoplasms in the esophagus?
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1. fibrovascular polyp
2. squamous papilloma |
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where will most of the fibrovascular polyps be found and what is the presenting sign?
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most found in upper 1/3 of esophagus (the one where patients can pop it out of their mouth to show you) with dysphagia being the presenting complaint
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what is the molecular mutation associated with BE?
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point mutation in p53
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what is the main risk factor for adenocarcinoma of the esophagus and also for BE?
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chronic reflux esophagitis
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95% of adenocarcinomas occur in what section of the esophagus?
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lower 1/3
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which has a worse prognosis? Esophageal SCC or adenocarcinoma?
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SCC
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plummer-vinson syndrome is more likely to lead to which malignant esophageal neoplasm?
SCC or adenocarcinoma |
SCC
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which gastric cell produces these substances?
mucus and carbonic anhydrase |
surface (foveolar) cell
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which gastric cell produces these substances?
mucus and pepsinogen |
mucus neck cell
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which gastric cell produces these substances?
HCl, intrinsic factor, and carbonic anhydrase |
parietal cells
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which gastric cell produces these substances?
pepsinogen and carbonic anhydrase |
chief cells
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which gastric cell produces these substances?
Lots of different hormones |
endocrine cells
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infant has vomiting third week post-birth and a palpable mass in the distal stomach. whats going on?
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pyloric stenosis
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pyloric stenosis would more likely be seen in a male or female?
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male
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what is the hallmark sign of acute gastritis?
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neutrophils invading foveolar pit epithelium with variable epithelial damage (mucosa is still intact however so this is NOT and ulcer)
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what is the definition of an ulcer?
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loss of mucosa down to the submucosa
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in the stomach where is the most common ulcer site?
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the antrum
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why do all ulcers need to be biopsied?
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gross appearance cannot differentiate them from cancers
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what are the two factors that are needed to form an ulcer?
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acid and pepsin
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why do chronic NSAIDs cause gastric ulcers?
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prostaglandins are inhibited
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25% of deaths from peptic ulcers are caused by?
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hemorrhage
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65% of deaths caused by PUD are the result of?
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perforation
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where does the chronic gastritis due to HP normally occure?
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antrum, but in few cases can be a difuse atrophic gastritis
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what causes pernicious anemia with autoimmune chronic gastritis?
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anti-parietal cell and anti-intrinsic factor Abs are formed -> decrease in intrinsic factor -> pernicious anemia
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gram staining of HP will show?
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gram negative rod
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what is the most frequent precursor to an adenocarcinoma of the esophagus?
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CG with intestinal metaplasia
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when the gross appearance of the stomach reveals enlarged rugau due to epithelial hyperplasia what is this called?
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hypertrophic gastropathy
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what are the 3 types of chronic gastric?
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1. hypertrophic-hypersecretory = hyperplasia of chief and parietal cells with increased acid production and ulceration
2. Menetrier's disease = idiopathic hyperplasia of foveolar mucus cells leading to excess mucu production, diarrhea, abdominal pain, protein loosing enteropathy occurs 3. Zollinger-Ellison syndrome = gastrin-producing tumor of pancreas or duodenum leading to chronic peptic ulcers |
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describe the histologic appearance of Menetrier's disease?
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hyperplasia and cycstic dilation of foveolar pits - lined with mucin-secreting columnar epithelium even in the pits of the stomach rugue + cystic changes in mucosa
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what are the 3 tumor-like leasions of the stomach?
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1. hyperplastic polyp
2. fundic gland polyp 3. inflammatory fibrous polyp (Vanek Polyp) |
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what is the most common tumor-like lesion of the stomach?
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hyperplastic polyp
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a hyperplasia and cystic dilation of body-type glands lined by parietal and chief cells resulting in many smooth bumps in stomach mucosa is?
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fundic gland polyp
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which gastric precursor lesion is present in 5% of those with gastric polyploid lesion and has a high risk of coexistent adenocarcinoma?
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adenoma
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what is central to the development of adenocarcinoma, although it is not entirely certain why?
|
H. pylori
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what is the mutation that all gastrointestinal stromal tumors will express?
|
c-KIT = tyrosine kinase receptor mutation (CD117)
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what is the profound finding in MALT lymphoma of the stomach?
|
80% are found to have H pylori infections and 50% are found to have regression of ONLY antibiotic therapy
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MALT tumors which are resistant to antibiotics in the stomach likely have which mutation?
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trisomy 3 or t(11,18) producing a fusion protein inhibiting apoptosis
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what is "piecemeal" necrosis in the liver?
|
degeneration of hepatocytes around portal tracts
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what type of liver injury results in centrilobular necrosis?
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ischemia
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what type of injury to the liver results in focal necrosis?
|
viral hepatitis - will see lymphocytes mixed in with scattered necrotic cells
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what are the 3 pathological criteria to make the diagnosis of cirrhosis?
|
1. diffusely disrupted architecture
2. bridging fibrosis (stage 4) 3. formation of neonodules of hepatocytes indicating regeneration |
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what are the top 4 causes of cirrhosis? (KNOW THESE COLD)
|
1. 65% alcoholic liver disease
2. 10% chronic viral hepatitis 3. Biliary tract disease 4. Hemochromatosis (primary) |
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what are the 2 important rare causes of cirrhosis we need to be familiar with?
|
Wilson's disease and Alpha-1-antitrypsin deficiency
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if a patient has ascites and there are many RBC's in the fluid, what do you have to assume until proven otherwise?
|
malignant neoplasm
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what are the acute causes of hepatitis that do not present with necrosis?
|
1. Reye's syndrome
2. acute fatty liver of pregnancy -both of these only have microcytic fatty changes |
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describe some male specific findings in liver failure and why they occur?
|
gynecomastia and testicular atrophy result from impaired estrogen metabolism by failing liver
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what is the likely cause of hepatic encephalopathy?
|
liver failure results in build up of ammonia in the blood which impairs neurons and promotes brain edema
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T or F, when conjugated bilirubin builds up in the brain of infants it can cause neurologic symptoms and is termed kernicterus?
|
F - its unconjugated that is harmful to cells and is insoluble in blood
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a build up of conjugated bilirubin in the blood is indicative of what pathology?
|
bile-duct obstruction leading to an intra/extra hepatic block - conjugation process still happens because liver cells are still functional
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a build up of unconjugated bilirubin in the blood is indicative of what pathology?
|
muscle breakdown or some source of haemolysis causing excess release of hemoglobin/myoglobin into the blood supply
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a build up of unconjugated and conjugated bilirubin in the blood is indicative of what pathology?
|
liver cell damage that impairs normal conjugation and may result in intrahepatic block
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describe the pathogenesis of crigler-najjar syndrome and its two types?
|
Genetic loss (Type 1 - deadly in infants) or deficiency (type 2) of UGT1A1 which is necessary for bilirubin conjugation
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what is the pathogenesis of Gilbert's syndrome?
|
same as crigler-najjar syndrome type 2 - a deficiency in UGT1A1
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what is the pathogenesis of dubin-johnson syndrome?
|
defect in canalicular membrane carrier defect impairing excretion of pigments needed for bilirubin conjugation - leads to pigment accumulations in liver cells
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elevated serum alkaline phosphatase is indicative of what?
|
injured bile duct epithelial cells - cholestasis
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what is the pathogenesis of Gilbert's syndrome?
|
same as crigler-najjar syndrome type 2 - a deficiency in UGT1A1
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what is the pathogenesis of dubin-johnson syndrome?
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defect in canalicular membrane carrier defect impairing excretion of pigments needed for bilirubin conjugation - leads to pigment accumulations in liver cells
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elevated serum alkaline phosphatase is indicative of what?
|
injured bile duct epithelial cells - cholestasis
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which HV has dsDNA?
|
HBV
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how is HAV spread?
|
fecal-orally
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how is HEV spread?
|
water-borne (eating raw oysters)
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which HV's have long incubation periods?
|
HBV and HVC
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which HV has no carrier state?
|
HAV
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which HV is most likely to result in chronic hepatitis?
|
HCV (>50%) followed by HBV (5-10%)
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which two HV's can lead to hepatocellular carcinoma?
|
HBV and HCV
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how is the diagnosis of HAV made?
|
presence of IgM-antiHAV
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how is the diagnosis of acute HBV diagnosed?
|
HBsAg + IGM-antiHBc
|
|
|
what indicates recovery from HBV?
|
No HBsAg + IgG antiHBs
|
|
|
what is the best way to pick up HCV?
|
PCR for RNA
|
|
|
what defines recovery from HCV?
|
complete and lasting loss of HCV rna in PCR assay
|
|
|
what are the criteria for diagnosing chronic hepatitis and which is the most important?
|
1. lasting > 6 months (+serological evidence is most important factor in determining prognosis)
2. biopsy proving inflammatory process (lymphocytic infiltrates + ballooning necrosis) |
|
|
what is the most common cause of fulminant hepatic failure?
|
drugs are the cause in 52% of cases
|
|
|
chronic hepatitis with no evidence of infection is likely what etiology?
|
autoimmune
|
|
|
describe the serological findings in autoimmune hepatitis?
|
1. ANA
2. anti-smooth muscle antibodies 3. anti-microsomal antibodies 4. NEGATIVE for anti-mitochondrial antibodies |
|
|
what is treatment for autoimmune hepatitis?
|
immunosuppresion
|
|
|
what is the most sensitive test for recent alcohol abuse?
|
GGT
|
|
|
males or females mainly effected by hereditary HC?
|
males 7:1, but has low penetrance
|
|
|
what is the protein that is mutated to cause hereditary HC?
|
HFE protein stops crypt cells from taking up iron from the blood thus faking a iron deficiency and causing crypt cells to increase iron uptake in villus cells -> iron overload
|
|
|
what is the net accumulation of iron each year with HHC and what amount do patients reach when they become symptomatic?
|
.5-1 gm/year and become symptomatic after 20gm have been built up
|
|
|
what is the average age range for manifestation of HHC?
|
5th-6th decade
|
|
|
ATP7B on chromosome 13 is mutated in this disease?
|
Wilson's disease
|
|
|
what causes the copper build up in Wilson's disease?
|
defective biliary excretion of copper
|
|
|
what is the normal age of onset for Wilson's?
|
>6 because it takes time to saturate the copper carrying capacity of ceruplasmin
|
|
|
what is the most common presentation of a person with Wilson's?
|
acute/chronic liver disease
|
|
|
what is the treatment of Wilson's?
|
copper chelation therapy
|
|
|
what is the most commonly diagnosed genetic liver disease in children?
|
Alpha-1-antitrypsin deficiency
|
|
|
what is the cancer risk seen with alpha-1-antitrypsin deficiency?
|
2-3% progress to hepatocellular carcinoma
|
|
|
what is the strongest prognostic indicator in primary biliary cirrhosis?
|
the degree of fibrosis
|
|
|
what is the diagnostic test of choice with primary sclerosing cholangitis?
|
cholangiogram
|
|
|
which liver enzymes will be significantly raised with primary sclerosing cholangitis?
|
alkaline phosphatase and GGT
|
|
|
a woman with long term use of oral contraceptives is more at risk for this liver disease than others?
|
peliosis hepatis - cause by increased estrogen exposure or anabolic steroids
characterized by primary diffuse dilation of sinusoids forming cystic areas filled with blood |
|
|
what is Budd-Chiari syndrome?
|
hepatic vein outflow obstructionby a thrombus or other obstruction (cancer, pregnancy)
|
|
|
nearly all primary malignant liver cancers are this type?
|
hepatocellular carcinoma
|
|
|
what is the serum finding with HCC?
|
alpha-fetal protein is elevated
|
|
|
what is the neoplasm seen in females, mostly during reproductive years?
|
liver cell adenoma
|
|
|
describe the gross appearance of a liver cell adenoma?
|
well circumscribed , encapsulated mass with NO central scaring
|
|
|
how can you differentiate liver cell adenoma from normal hepatic tissue?
|
there are no portal tracts of central veins which there remains well-differentiated hepatocytes
|
|
|
what is most commonly found benign neoplasm?
|
hemangioma - LEAVE IT ALONE
|
|
|
what is the difference in appearance between focal nodular hyperplasia and liver cell adenoma?
|
both are composed of hyperplastic well-differentiated hepatocytes, but the focal nodular has a central scarring
|
|
|
what is screening test of choice for gallstones?
|
ultrasound
|
|
|
neonatal jaundice is a warning sign for what situation?
|
extrahepatic biliary atresia
|
|
|
why must extrahepatic biliary atresia be repidly diagnosed?
|
can lead to biliary cirrhosis if not fixed soon
|
|
|
what increases risk of calcium/bilirubin gall stones?
|
any disorder which increases the amount of unconjugated bilirubin in bile
|
|
|
what is the treatment of choice for gall stones?
|
removal of the gall bladder
|
|
|
what change in the gallbladder indicates chronic cholecystitis?
|
thickening of bladder wall due to fibromuscular hyperplasia
|
|
|
what is porcelain gallbladder?
|
chronic inflammatory state in which bladder wall mucosa is eroded leaving a leather fibrous surface
|
|
|
what is cholesterolosis of the gallbladder?
|
diffuse linear yellow streaks in the mucosa consisting of lipid filled "foamy" macrophages forming polyploid structures
|
|
|
describe the frequency of neoplasms in the gallbladder?
|
very infrequent, but when present are more likely to be malignant
|
|
|
what is present in almost all cases of carcinoma of the gallbladder?
|
gallstones
|
|
|
90% of bladder carcinomas are this type?
|
invasive adenocarcinomas
|
|
|
what is over all survival rate of gallbladder cancer?
|
5-10% in 5 years
|
|
|
where is the most common site of carcinoma in bile ducts?
|
ampulla of vater
|
|
|
what is the clinical presentation of a person with a bile duct carcinoma?
|
obstructive jaundice
|
|
|
what is the surgical procedure for resection of a bile duct cancer involving the ampullary?
|
whipple's procedure
|
|
|
what is pancreas divisum?
|
pancrease drains into minor papilla which is not big enough to handle all the secretions - can result in segmental pancreatitis with need of surgical intervention to open up the minor papilla more
|
|
|
double bubble sign is seen with what condition?
|
annular pancreas
|
|
|
if a person has hypotension and discrete mid-upper back pain and is an alcoholic, what is the most likely problem?
|
pancreatitis
|
|
|
large increases in which two serum markers are indicative of pancreatitis?
|
amylase and lipase
|
|
|
while the initiating cause is can be different, where do all causes of pancreatitis converge and what is the result of this convergence?
|
they all end up causing acinar cell injury causing the release and activation of digestive enzymes
|
|
|
what causes the hemorrhage seen in pancreatitis?
|
release of elastase which chew up vessel walls - this is why you can get hypotension with pancreatitis
|
|
|
steatorrhia + onset of diabetes in a patient a history of alcoholism is likely to be?
|
chronic pancreatitis
|
|
|
why do calcium salts build up in the pancreas causing calcifications in chronic pancreatitis?
|
the protein lithostathine is hyposecreted and its main function is to inihibit calcium build up in the pancreas
|
|
|
what is the most common cyst found in the pancreas?
|
psuedocysts - collection of normal pancreatic tissue that
|
|
|
if you saw a cystic looking pancreatic lesion that upon microscopic observation lacked an epithelial covering what is it?
|
pseudocyst
|
|
|
most of the neoplasms in the pancreas are malignant or benign?
|
malignant
|
|
|
what is the most common malignant neoplasm of the pancreas?
|
ductal adenocarcinoma
|
|
|
what are the two types of benign neoplasms of the pancreas that we studied?
|
1. serous cystadenoma
2. mucinous cystadenoma |
|
|
what is the large tumor found in the pancreas of young women that has uniform solid sheets or papillae of cells - has malignant potential?
|
solid pseudopapillary neoplasm
|
|
|
what are the genetic alterations that are present in most of pancreatic ductal carcinomas?
|
K-ras and P16 CDKN2A
|
|
|
nearly all pancreatic carcinomas are this type?
|
ductal cell
|
|
|
what are the 2 definite risk factors for pancreatic carcinoma?
|
smoking and chronic pancreatitis
|
|
|
most pancreatic cancer occurs in what age group?
|
elderly > 65
|
|
|
painless jaundice + weight loss is always ____ until proven otherwise?
|
pancreatic CA (likely to be ductal cell in origin)
|
|
|
what is the 5 year survival from pancreatic cancer?
|
REALLY bad 2-4% although whipple procedure can increase survival in stage 1 up 50% at 3 years
|
|
|
what is the required small intestinal length to live?
|
200 cm
|
|
|
what key function does the gut maintain that allows for exchange of fluids and nutrients across the intestinal epithelium?
|
maintains contents osm at blood osm
|
|
|
where does absorption of fats occur?
|
in the jejunum and duodenum (95%)
|
|
|
what are the most common vitamin deficiencies?
|
A and D
|
|
|
what part of the small intestine is Ca+ absorbed? what about Mg+?
|
proximal, distal
|
|
|
what is the most important factor in vit A absorption?
|
presence of adequate amounts of bile
|
|
|
if vit A is low what should be used to replace it?
|
beta carotene
|
|
|
what part of the bowel is thiamine absorbed in?
|
proximal small bowel
|
|
|
why do our bodies need thiamine?
|
required for normal neuronal, cardiovascular, gastrointestinal, and musculoskeletal activity
|
|
|
patient presenting with nerve palsies/motor neuropathies + rapid weight loss may have what as the underlying etiology? (think atypical stocking and glove neuropathy
|
thiamine deficiency
|
|
|
what defines obesity?
|
a BMI greater than or equal to 30
|
|
|
what is the cutoff for eligibility for bariatric surgical intervention?
|
BMI equal to or greater than 35 with comorbidities or a BMI >40
|
|
|
what is the diet post-bariatric surgery like?
|
clear liquids only with no sugar, carbonation, or caffeine - slowly progress to teaspoon size meals with high protein MAKE SURE to stay hydrated
|
|
|
what kidney manifestation will be present with fat malabsorption?
|
renal oxalate stones - fat doesn't get absorbed in small intestine and Ca+ binds to it so less can bind oxalate - excess fat also changes the absorption properties of the colon causing oxalate absorption to increase
|
|
|
what is hirschsprung disease?
|
absence of auerbach and meissner plexi leading to proximal dilation due to a distal constricted aganglionic segment of the intestine
|
|
|
what is the most common mutation involved in hirschsprung disease?
|
RET mutation
|
|
|
exploding crypts is indicative of this disease state?
|
pseudomembranous enterocolitis
|
|
|
what is the offending antibiotic in a lot of C. diff cases?
|
clindamycin
|
|
|
what does C. diff cause?
|
psuedomembranous enterocolitis
|
|
|
dermatitis herpetiformis + villous atrophy + crypt hpyerplasia +lymphocytic infiltrates =?
|
celiac sprue
|
|
|
what are the 2 antibodies that are likely to be seen in celiac sprue?
|
1. anti-endomysial
2. anti-gliadin |
|
|
who is most likely to get whipple's disease?
|
men in their 30's and 40's
|
|
|
histological evaluation of a patients intestinal walls reveals a shaggy mucosa with lots of foamy, bacteria filled macrocytes below the mucosa, what is this?
|
Whipple's disease
|
|
|
what are the two main types of idiopathic IBD?
|
1. UC
2. Crohn's |
|
|
HLA-DR1 is associated with what IBD?
|
Crohn's
|
|
|
HLA-DR2 is associated with which IBD?
|
UC
|
|
|
HLA-B27 is associated with which IBD?
|
ankylosing spondylitis
|
|
|
pANCA is more likely to be seen with which IBD?
|
UC
|
|
|
Anti-saccharomyces cerevisiae is more likely to be seen with which cause of IBD?
|
Crohns
|
|
|
this type of colitis is associated with granuloma formation?
|
Crohn's disease
|
|
|
where can Crohn's disease be found in the GI?
|
all throughout from mouth to anus
|
|
|
describe the appearance of of intestines affected by Crohns?
|
skip patterns of thickened rubbery walls and narrowed lumen - can have fistula formation if serositis develops and adhesion's between organs and intestines form
|
|
|
describe the 3 most frequent involved areas of the GI for Crohns?
|
1. small intestine only 1/3
2. large intestine only 1/3 3. both 1/3 |
|
|
is toxic megacolin more associated with UC or crohns?
|
UC
|
|
|
describe the pattern of disease for UC?
|
"backwash" = spreading from anus up the bowel in a contiguous pattern
|
|
|
describe the appearance of the serosa of UC?
|
intact with atrophic smooth patches with regular wall thickness, but contraction of the bowels (the are shorter)
|
|
|
crypt abcesses and mucin depletion are characteristic of UC or Crohns?
|
Crohns
|
|
|
musclaris mucosae hypertrophy + crypt distortion and shortening + paneth cells in colin and distal small intestine =?
|
UC
|
|
|
right to left spread indicates UC or Crohn's?
|
Crohn's
|
|
|
transmural inflammation is seen with UC or Crohn's?
|
Crohn's
|
|
|
which has a greater risk for cancer, Crohns or UC?
|
UC
|
|
|
where is the most common site for low flow ischemic colitis?
|
the watershed zone at the junction between superior and inferior mesenteric arteries (the upper flexion of the large intestine on the left side)
|
|
|
20% of lower GI bleeds result from this disorder causing tortuous submucosal vessels in the cecum and right colon?
|
Angiodysplasia
|
|
|
how is angiodysplasia diagnosed?
|
radiological studies
|
|
|
describe the location and conditions that allow for diverticular disease (acquired form) to occur?
|
in the lower colon (sigmoid) where pressure during defecation is highest - occurs along weakened taeniae coli
|
|
|
what is important about the finding of intussusception?
|
often associated with a tumor in adults
|
|
|
what is the disorder characterized by hamartomatous polyps throughout the GI tract consisting of all layers of the bowel and causing mucosal hyperpigmentation?
|
Peutz-Jeghers
|
|
|
which colonic tumor has an arborizing pattern which a muscularis core?
|
PJ polyp
|
|
|
odd hyperpigmentation around the mouth during adolescence is characteristic of?
|
Peutz-Jeghers syndrome
|
|
|
Expansion of the lamina propria by cystic glands is characteristic of this colonic polyp type?
|
Juvenile Polyposis
|
|
|
Familial adenomatous polyposis has a germline mutation of what protein?
|
APC of 5q21 resulting in inhibition of apoptosis and increased cell proliferation
|
|
|
MSH2 and MLH1 are important germline mutations which cause of colon cancer?
|
HNPCC
|
|
|
what is a diagnostic feature of HNPCC?
|
microsatellite instability
|
|
|
almost all cancers in the colon are this type?
|
adenocarcinoma
|
|
|
list the likely sites from highest to lowest for colonic adenocarcinoma
|
ascending>sigmoid>tranverse
|
|
|
A Fe+ deficiency in older males indicates what?
|
must suspect GI carcinoma until proven otherwise
|
|
|
do mucin producing tumors have better or worse prognosis?
|
worse
|
|
|
what can look very much like a GI adenocarcinoma but isnt?
|
endometriosis
|
|
|
list the locations in descending order of prevalence for carcinoid tumors of the GI?
|
appendix>ileum>rectum>stomach>colon
|
|
|
give an example of a GI carcinoid tumor?
|
One would be Zollinger-Ellison syndrome - gastrin secreting carcinoid tumor
|
|
|
if carcinoid syndrome is present with a GI carcinoid tumor, what do you know about staging?
|
it is T4 because mets have to reach liver to produce carcinoid syndrome
|
|
|
Where are the locations that GI lymphomas are located, list in descending order of prevalence?
|
stomach>SI>proximal colon
|
|
|
of the GI mesenchymal tumors, which one has a definitive cytologic test?
|
gastrointestinal stromal tumor (GIST) has c-kit (CD117) mutation - mostly seen in stomach
|
