Gastroenterology

Question 1

What are the 6 steps in digestion?

Answer 1

See picture1. Ingestion2. Mechanical digestion3. Propulsion4. Chemical digestion5. Absorption6. Defecation

Question 2

Layers (Tunics) of GI Wall4

Answer 2

1. Mucosa2. Submucosa3. Circular and Longitudinal Smooth Muscle4. Serosa

Question 3

Mucosa1. What does this layer face?2. Made of? Specialized for?3. Blood supply?Submucosa4. What does it consist of? 4Circular and Longitudinal Smooth Muscle5. Function?Serosa6. Faces what?

Answer 3

Mucosa1. Innermost layer (faces lumen)2. Layer of epithelial cells specialized for absorption and secretion3. Highly vascularizedSubmucosa4. Consists of collagen, elastin, glands, and blood vesselsCircular and Longitudinal Smooth Muscle5. Provides motility for GI tractSerosa6. Faces the blood

Question 4

What enzymes break down food in the mouth?2

Answer 4

1. lingual amylase carb. (step 1)2. lingual lipaselipid (step 1)

Question 5

1. ____muscles and 2.___cranial nerves (600 times/daily)3. What doesthe esophageal phase of swallowing begin with?4.Composition of Saliva→ Secreted by ______ and _______cells5. What is saliva composed of? 6

Answer 5

1.262. 53.-Begins with crico-pharyngeal relaxation-Involuntary4.serous and mucous5.a) 97–99.5% water, slightly acidicb) lytes—Na+, K+, Cl–, PO4 2–, HCO3–c) Salivary amylase and lingual lipased) Mucine) Metabolic wastes—urea and uric acidf) Lysozyme, IgA and a cyanide compound protect against microorganisms

Question 6

1. Salivary glands produce how much saliva a day?2. Functions of saliva? 4

Answer 6

1. Salivary glands produce 1 L/day of saliva-Each gland delivers saliva to mouth through a ductFunctions of saliva1. Initial digestion of starches and lipids by salivary enzymes2. Dilution and buffering of ingested foods3. Lubrication of ingested food to aid its movement4. Many more functions

Question 7

Secretions are produced by what? 4What do secretions add to the lumen of GI tract? 4

Answer 7

Secretions produced by1. Salivary glands (saliva)2. Gastric mucosal cells (gastric secretion)3. Pancreatic exocrine cells (pancreatic secretion)4.Liver (bile)Addition of GI tract:1. fluids,2. enzymes,3.electrolytes4. mucus

Question 8

Function:1. Stomach?2. Small intestine?3. Large intestine?

Answer 8

1. Stomach: digestion and break down of food to smaller, absorb-able particles.2. Small intestine: absorption of nutrients3. Large intestine: absorption of water

Question 9

1. What is the stomach specialized for?2. Holds how much?3.Gastric juice converts food into semiliquid called what?4. 4 parts of the stomach?

Answer 9

1. Specialized for accumulation of food2. Capable of considerable expansion (can hold 2-3L)3. Gastric juice converts food into semiliquid called chyme4. 4 Parts-Cardia-Fundus-Body-Pylorus

Question 10

Functions of Stomach6

Answer 10

1. Short-term storage reservoir2. Absorption, digestion and secretion3. Chemical and enzymatic digestion is initiated, particularly of proteins4. Liquefaction of food→ chyme5. Slowly released into the small intestine for further processing6. The stomach uses pepsin and peptidase (enzymes) to break down proteins

Question 11

Why is the acidic anvironment of the stomach important?

Answer 11

The acid provides good environment for the enzymes to work in.

Question 12

What are theThree Phases of Digestion?

Answer 12

1. Cephalic Phase 2. Gastric Phase3. Intestinal Phase

Question 13

1. Cephalic Phase: What structures are involved? 4 2. Gastric Phase: What substances are involved? 23. Intestinal Phase: What hormone is involved?

Answer 13

Cephalic Phase :1. Cortex,2. amygdala3. hypothalamus4. vagus nerve Gastric Phase:1. hydrochloric acid2. pepsinIntestinal Phase:1. enterogastrone Hormones secreted in duodenum and lower GI tract.

Question 14

1. During cephalic and gastric phases, stimulation by vagal nerve fibers causes release of what?2. Acidic chyme entering duodenum causes the enteroendocrine cells to release what?3. Whereas fatty, protein rich chyme induces release of what?4. Where do these two enzymes go next?

Answer 14

1. pancreatic juice and weak contractions of the gallbladder2. secretin3. cholecystokinin4. Blood stream

Question 15

1. Upon reaching the pancreas, cholecystokinin induces the secretion of what?2. Secretin causes copious secretion of what?

Answer 15

1. enzyme-rich pancreatitis juice2. bicarbonate-rich pancreatic juice

Question 16

1.Gastric mucosal cells secrete what?2. What two substances initiate protein digestion?3. What is required for absorption of Vit B12?4. Body of the stomach conatins what kind of glands?5. Atrum of the stomach conatins what kind of glands?6. What protects gastric mucosa from HCL?

Answer 16

1. gastric juice2. HCl and pepsinogen initiate protein digestion3. Intrinsic factor required for absorption of vitamin B12 4. Body of stomach contains oxyntic glands 5.Antrum of stomach contains pyloric glands 6.Mucus protects gastric mucosa from HCl

Question 17

1.What are the two types of cells in the body of the stomach?2. What are the two types of cells in the antrum of the stomach?

Answer 17

1. Parietal cells and Chief cells2. G cells and Mucous neck cells

Question 18

1. What do parietal cells secrete? 22. What do chief cells secrete? 13. G cells secrete what? 14. What do mucous neck cells secrete? 3

Answer 18

1. Parietal cells → HCl and Intrinsic Factor2. Chief cells → Pepsinogen3. G cells → Gastrin into the circulation4. Mucous neck cells → Mucus, HCO3-, and Pepsinogen

Question 19

1.Gastrin:Secreted by G cells in stomach in response to what?2.Stimuli includes what? 33. Gastrin promotes what kind of secretion?4. Stimulates the growth of what?5. What is its secretion inhibited by?

Answer 19

1.eating2.-proteins,-distention of stomach-vagal stimulation3. Promotes H+ secretion by gastric parietal cells4. Stimulates growth of gastric mucosa5. Low pH in the stomach

Question 20

Other Functions of GASTRIN HORMONE:4

Answer 20

1. Pepsinogen release2. Increase stomach motility3. Relax pyloric sphincter4. Contract LES

Question 21

Regulation of HCl SecretionWhat three hormones are involved in this?

Answer 21

1. ACh2. Histamine3. Gastrin

Question 22

1. ACh is realeased from?2. Binds to receptors where?3. Produces what by parietal cells?4. Whatblocks muscarinic receptors on parietal cells?

Answer 22

1. Released from vagus nerve2. Binds to receptors on parietal cells3. Produces H+ secretion by parietal cells4.Atropine blocks muscarinic receptors on parietal cells

Question 23

1. Histamines released from mastlike cells where?2. Binds to what on parietal cells?3. Produces what by parietal cells?4. What block H2 receptors?

Answer 23

1. Released from mastlike cells in gastric mucosa2. Binds to H2 receptors on parietal cells3. Produces H+ secretion by parietal cells4. Cimetidine blocks H2 receptors

Question 24

Gastrin1. Released into circulation by what of stomach antrum?2. Binds to receptors of what cells?3. Stimulates what?

Answer 24

1. Released into circulation by G cells of stomach antrum2. Binds to receptors on parietal cells3. Stimulates H+ secretion

Question 25

What are the two general processes that cause peptic ulcers?

Answer 25

Increased damageImpaired host defenses

Question 26

What things could cause increased damage in the stomach causing a peptic ulcer? 8 What things could cause impaired defenses in the stomach that lead to peptic ulcers? 3

Answer 26

See picture

Question 27

What is segmentation contractions?2

Answer 27

1. Circular muscle contracts sending chyme in both  directions2. Intestine then relaxes allowing chyme to merge back together

Question 28

What is peristalic contractions? 2

Answer 28

1. Longitudinal muscle contracts propeling chyme along small intestine2. Simultaneously, portion of intestine caudad to bolus relaxes

Question 29

1. What are the enzymes (2) in the salivary glands and what are their targets (2)?2. What are the enzymes (2) in the stomach and what are their targets (2)?3. What are the enzymes (5) in the Pancreas and what are their targets (5)?4. What are the enzymes (3) in the intestine and what are their targets (3)?

Answer 29

See picture

Question 30

Autonomic Nervous System has an extrinsic and an intrinsic component1. Extrinsic controls what? 22. What is the intrinsic also called?3. Contained where?4. Communicates with what?

Answer 30

1. Extrinsic-Sympathetic and-Parasympathetic innervation of GI tractIntrinsic2. Called Enteric Nervous System3. Contained within wall of GI tract4. Communicates with Extrinsic component

Question 31

1. The nervous system of the GI tract regulates what? 32. Parasympathetic nerve supply comes from where and provides motor innervation to what?3. Sympathetic nerve supply comes from the cervical and thoracic sympathetic chain and regulates what? 4

Answer 31

1. Regulates-glandular secretion,-blood vessel caliber, and the-activity of striated and smooth muscle. 2. Parasympathetic nerve supply comes from the-nucleus ambiguus and dorsal motor nucleus of the vagus nerve***** and-provides motor innervation to the esophageal muscular coat and secretomotor innervation to the glands.3.  regulates-blood vessel constriction,-esophageal sphincters contractions,-relaxation of the muscular wall, and-increases in glandular and peristaltic activity

Question 32

Intrinsic InnervationCan direct all functions of GI in absence of extrinsic innervation1. Which functions of the GI system does it control? 32. Where does it recieve input from? 23. Sends information directly where? 3

Answer 32

1. Controls-contractile,-secretory, and-endocrine functions of GI tract2. Receives input from-Parasympathetic and sympathetic nervous systems-Mechanoreceptors and chemoreceptors in mucosa3. Sends information directly to-smooth muscle,-secretory, and-endocrine cells

Question 33

1. Gastric mucosa has numerous openings called what?2. What empties into these?3. 4 functionally different cell types compose glands?

Answer 33

1. Gastric pits2. Gastric glands3. -Mucous cells-Chief cells-Parietal cells-Enteroendocrine cells

Question 34

What is the primary site fo digestion and absorption of nutrients?What empties into the the duodenum? 2

Answer 34

small intestineBile duct and pancreatic duct

Question 35

1. Function of the hepatic portal vein?2. Describe its high blood flow?

Answer 35

Receives major blood supply from hepatic portal vein1. Brings venous blood rich in nutrients from digestive tract2. High blood flow - 1350 ml/min to liver sinusoids (1050 ml from the portal vein, 300 ml from hepatic artery) = functional and nutritive blood circulation

Question 36

Describe the vascular resistance in the liver?Describe how this changes with cirrhosis?

Answer 36

1. low vascular resistance (small difference between pressures in the portal vein and hepatic vein) -2. in case of cirrhosis, the vascular resistance increases, blood flow decreases (portal hypertension……………ascites)

Question 37

1. Hepatocytes are in contact with blood in structures called _________within the  liver.2. These function like ______ ________.   -Arranged to form functional units (lobules)

Answer 37

1. sinusoids2. blood capillaries

Question 38

Overview Of HepaticFunction10

Answer 38

1. Carbohydrate metabolism.2. Lipid metabolism.3. Protein metabolism.4. Removal of drugs and hormones.5. Excretion/secretion of bilirubin.6. Synthesis of bile salts.7. Storage of some compounds.8. Phagocytosis.9. Aids in the synthesis of active vitamin D.10. Urea formation from ammonium

Question 39

Steps in food digestion1- Carbohydrates? 22- Proteins? 23- Lipids? 2

Answer 39

1- Carbohydrates       ---> disaccharides        ---> monosaccharides2- Proteins                 --->   peptides                ---> amino acids3- Lipids                    --->   diglycerides            ---> monoglycerides and fatty acids

Question 40

Absorption of carbohydrates1. In what form are they absorbed?2. The monomers are carried by transporter molecules across the epithelial cells and into the what?

Answer 40

1. Monosaccharides (mostly glucose) are absorbed2. blood capillary present in the villus → portal vein → liver

Question 41

Overview of digestion of Lipids

Answer 41

See picture

Question 42

Fat metabolism1. _________of fatty acids to supply energy for other body function2. Synthesis of large quantities of what? 33. Inactivation of ______and their excretion from the body

Answer 42

1. Oxidation2. -cholesterol (80% of cholesterol synthesized in the liver is converted into bile salts),-phospholipids-most lipoproteins3. steroids

Question 43

1. What is Ammonia detoxification disorder and failure of urea formation. Ammonia comes from? 32. Hyperammonemia = ?

Answer 43

1. ammonia comes-from bacterial degradation of nitrogen substances in intestines,-from intestinal mucosa during glutamine degradation,  -from degradation of amino acids in kidneys and muscles2. Hepatic encephalopathy = toxic effect of ammonia in the brain

Question 44

Hyperammonemia = Hepatic encephalopathy = toxic effect of ammonia in the brain. What signs and symptoms will you have?2

Answer 44

1. Mental changes (disorientation, sleeping disorders, chaotic speech, personality changes)2. Motor changes (increased in muscle reactivity, hyperreflexia, tremor)

Question 45

Endogenous causes of hepatic coma and death? 2Exogenous? 1

Answer 45

Hepatic coma to death1. Endogenous =-viral hepatitis and-poisoning (hepatic cell disintegration)2. Exogenous = final status of chronic cirrhosis (ammonia and other toxic substances bypass the liver through the extrahepatic anastomoses)

Question 46

1. What is bile necessary for?2. What is it a mixture of? 33. What do bile salts do?

Answer 46

1. Necessary for digestion and absorption of lipids in small intestine2. Mixture of-bile salts,-bile pigments, and-cholesterol3. Bile salts emulsify lipids to prepare them for digestion

Question 47

Bile Secretion and Recycling1. Produced and secreted where?2. Stored where?3. Ejected into the small intestine when what happens?4. After lipids absorbed, bile salts are re-circulated to liver via what?5. Extraction of bile salts from the portal blood by what?

Answer 47

1. Produced and secreted by liver2. Stored in gallbladder3. Ejected into small intestine when gallbladder contracts4. After lipids absorbed, bile salts are re-circulated to liver via enterohepatic circulation5. Extraction of bile salts from the portal blood by hepatocytes

Question 48

After lipids absorbed, bile salts are re-circulated to liver via enterohepatic circulation1. Absorption of from where to where?2. Delivery back to?

Answer 48

1. Absorption of bile salts from ileum into portal circulation2. Delivery back to liver

Question 49

Formation Of Bilirubin1. Formed from?2. Hb is phagocytosed by what?3. Iron released is bound to what and transported in the blood?4. The remainder of the heme group is converted to ________, which is rapidly reduced to_______.5. What does it then attach to? 

Answer 49

1. hemoglobin2.  tissue macrophages (spleen)3. transferrin4. biliverdin, bilirubin5. albumin

Question 50

Secretion of bilirubin into bile by the liver is a classic example of what?

Answer 50

waste and toxic elimination by the liver

Question 51

Processing of bilirubin by hepatocytes1. Albumin is removed as unconjugated bilirubin passes through the what?2. Bilirubin is conjugated with ____________(80%), ________(10%) or a variety of other substances (10%)Secretion of Conjugated Bilirubin Into Bile1. Conjugated bilirubin has a _______ solubility?2. Hepatocytes actively transport conjugated bilirubin into the what?3. Conjugated bilirubin then enters duodenum through the what?

Answer 51

1. hepatocyte membrane.2. glucoronic acid, sulphate 1. higher2. bile canaliculi3. sphincter of Oddi

Question 52

Role of Small Intestine In Bile Metabolism1. Bile and bile salts increase growth of what?2. In return, intestinal bacteria metabolise conjugated bile to what?3. Urobilirubin = _______soluble = what happens because of this?Fates of reabsorbed Urobilirubin4. 95% of reabsorbed urobilirubin is what?5. 5% is what?6. Small part excreted where?

Answer 52

1. intestinal bacteria2. urobilirubin (urobilinogen)3. highly, reabsorbed back into blood4. excreted again by liver into bile5. excreted into urine6. Small part excreted into feces (gives it the characteristic colour)

Question 53

Bile1. Secreted by cells of the liver into the _________, which drains into the __________.2. Between meals the duodenal orifice (sphincter of Oddi) is _______and bile flows into the gallbladder, where it is stored (how much?).3. The bile is concentrated in the_________?4. Oddi _____within 30 minutes of food intake, the presence of aminoacids and fatty acids in duodenum activates __________, which causes gallbladder contractions and excretion of bile5, Production……____________ ml of bile daily

Answer 53

1. bile duct, duodenum2. closed, 50 – 80 ml3. gallbladder4. opens, cholecystokinin5. 500-1000

Question 54

Composition of bile2 Remaining smaller components of bile?7

Answer 54

1. Water = 97 %2. Bile salts (0.7%) = primary bile acids are transported to the bile as sodium and potassium salts 1. Bile pigment = glucuronides bilirubin and biliverdin (golden-yellow color of bile)2. Cholesterol = increased in patients with obstructive jaundice3. Inorganic salts4. Fatty acids5. Lecithin  = the main phospholipid of bile6. Fat7. Alkaline phosphatase

Question 55

Two bile salts that make up bile?

Answer 55

1. Cholic acid (converted by colon bacteria to Deoxycholic acid)2. Chenodeoxycholic acid (converted by colon bacteria to Lithocholic acid) 

Question 56

Jaundice1. Detectable when the total plasma bilirubin > __mg/dl2. Causes? 5

Answer 56

1. 22. -excess production of bilirubin (hemolytic anemia)-decreased uptake of bilirubin into hepatic cells-disturbed intracellular protein binding or conjugation-disturbed secretion of conjugated bilirubin into the bile canaliculi-intrahepatic or extrahepatic bile duct obstruction

Question 57

Obstructive Jaundice1. Bile is obstructed from flowing where?2. Occurs if what blocks the duct? 23. Conjugated bilirubin builds up in the biliary duct and what increases?4. How is conjugated bili returned to the blood?5. So what is a good diagnostic test for obstructive jaundice?6. What will unconjugated levels of bili be in obstructive?

Answer 57

1. biliary duct2. gall stones, tumors3. pressure within the biliary duct increases4. -rupture of the bile caniliculi -via lyphmphatic drainage by the liver5. conjugated bili6. normal or low

Question 58

Formation and secretion of bile1. Detoxification of various substances - such as? 32. Synthesis of plasma proteins - ? 43. Coagulation –? 14. Blood reservoir – ?15. Immunity in the form of what?6. Vitamins - metabolism and storage of vitamins ? 37. Relation to blood formation - ? 3

Answer 58

1. -Metabolic products of intestinal microbes,-Exogenous toxins (medicaments, alcohol, poisons),-Hormones (thyroxine, estrogen, cortisol, aldosterone)2. -Acute-phase proteins,-Albumin,-Clotting factors,-Steroid-binding and other hormone-binding proteins3. synthesis of coagulation factors4. filtration, storage of blood (up to1L)5. Kupfer cells/macrophages6. A, D, B127. -storage of vitamin B12,-metabolism of iron and its storage as ferritin,-production of erythropoietin

Question 59

1. Gallbladder attached where?2. Stores how much bile?3. Ducts of the gallbladder? 3

Answer 59

1. Attached to surface of the liver2. Blind pouch that stores bile (50ml)3. Ducts-Hepatic Duct-Cystic Duct-Common Bile Duct

Question 60

Cirrhosis leads to 1._________which can obstruct Blood and Bile flow. Obstruction of hepatic venous blood flow can increase pressures within other veins leading to other circulatory diseases such as what? 2

Answer 60

1. Scar tissue2. varices & ascites

Question 61

Pancreatic Duct1. Main duct (Wirsung) runs the entire length of________?2. Joins CBD at the what?3. _______mm in diameter, drains up to 20 secondary branches4. Ductal pressure is ________mm Hg (vs. 7 – 17 in CBD) thus preventing reflux and damage5. Lesser duct (________) drains superior portion of head and empties separately into 2nd portion of duodenum

Answer 61

1. pancreas2. ampulla of Vater3. 2 – 44. 15 – 305. Santorini

Question 62

Innervation of the Pancreas1. Sympathetic fibers from the ?2. Parasympathetic fibers from the?3. Parasympathetic fibers stimulate both ______ and ______secretion4. Sympathetic fibers have _______effect5. Rich _______ sensory fiber network6.  What (2) blockade interrupt  somatic fibers (pancreatic pain)?

Answer 62

1. splanchnic nerves2. vagus3. exocrine and endocrine4. inhibitory5. afferent6. Ganglionectomy or celiac ganglion

Question 63

1. Exocrine—Acinar Cells do what?2. Endocrine—Islets of Langerhans have four major cell types. What are they? 

Answer 63

Exocrine—Acinar Cells1. Secretes essential digestive enzymes through pancreatic duct into duodenumEndocrine—Islets of Langerhans                 Four major cell types1. Alpha (A) cells secrete glucagon2. Beta (B) cells secrete insulin3. Delta (D) cells secrete somatostatin4. F cells secrete pancreatic polypeptide--These Secretes insulin and glucagon into blood stream

Question 64

Physiology – Exocrine Pancreas1. _________ml pancreatic fluid secreted per day2. Alkaline pH results from what?3. Centroacinar cells and ductular epithelium secrete what? and how much?4. Fluid (pH from 7.6 to 9.0) acts as a vehicle to carry inactive proteolytic enzymes to the what?5. Enzymes digest what? 3

Answer 64

1. 500 to 8002. secreted bicarbonate which neutralizes gastric acid and regulate the pH of the intestine3. 20 mmol of bicarbonate per liter in the basal state4. duodenal lumen5. carbohydrates, proteins, and fats

Question 65

Bicarbonate Secretion1. Major stimulants? 42. Major inhibitors? 43. Secretin - released from the duodenal mucosa in response to a duodenal luminal pH less than? 

Answer 65

1. Major stimulants-Secretin,-Cholecystokinin,-Gastrin,-Acetylcholine2. Major inhibitors-Atropine,-Somatostatin,-Pancreatic polypeptide and-Glucagon 3. 3 

Question 66

Amylase1. only digestive enzyme secreted by the pancreas in an ______form?2. functions optimally at a pH of___?3. hydrolyzes starch and glycogen to what? 4Lipase4. function optimally at a pH of_____?5. emulsify and hydrolyze fat in the presence of _______?

Answer 66

1. Active2. 73. -glucose,-maltose,-maltotriose, and-dextrins4. 7 to 95. Bile salts

Question 67

1. Insulin is synthesized where?2. ___% of the islet cell mass must be surgically removed before diabetes becomes clinically apparent

Answer 67

1. Synthesized in the B cells of the islets of Langerhans2. 80%

Question 68

Regulation of Pancreatic Secretion1. Acinar cells (enzymatic secretion). _______ is most important stimulant? 

Answer 68

1. CCK 

Question 69

1. Secretion of CCK in presence of what (2)in intestinal lumen?2. Ductal cells (aqueous secretion of ________)3. Secretin (from __cells of duodenum) is major stimulant4. Secreted in response to ___in intestine

Answer 69

1. amino acids and fatty acids2. HCO3-3. S4. H+

Question 70

Duodenum 1. ___ portions2. Sphincter of Oddi __cm from pylorus3. Posterior ulcers _____? 4. Anterior ulcers______?5. Hugs ______of pancreas6. _______portion most vulnerable to traumatic rupture

Answer 70

1. 42. 73. erode4. perforate5. head 6. Third

Question 71

GI Peptides1. Includes what kind of substances? 32. Regulate functions of GI tract. Such as? 4

Answer 71

1. Includes-hormones,-neurocrines, and-paracrines2. Regulate functions of GI tract-Contraction and relaxation of smooth muscle wall and sphincters-Secretion of enzymes for digestion-Secretion of fluid and electrolytes-Regulate secretion of other GI peptides

Question 72

Hormones and Paracrines that act in digestion

Answer 72

See picture

Question 73

Small intestine Digestion via________ must precede absorption Causes of Malabsorption of Nutrients 2

Answer 73

hydrolysis1. Anything that interferes with delivery of bile or pancreatic juice2. Damaged intestinal mucosa (e.g., bacterial infection)

Question 74

Functions of Small intestine1. Electrolyte Absorption 62. Water absorption 3 

Answer 74

Electrolyte Absorption1. Mostly along the length of small intestine2. Iron and calcium are absorbed in duodenum3. Na+ is coupled with absorption of glucose and amino acids4. Ionic iron is stored in mucosal cells with ferritin5. K+ diffuses in response to osmotic gradients6. Ca2+ absorption is regulated by vitamin D and parathyroid hormone (PTH) Water Absorption1. 95% is absorbed in the small intestine by osmosis2. Net osmosis occurs whenever a concentration gradient is established by active transport of solutes3. Water uptake is coupled with solute uptake

Question 75

Small Intesine:1. Intestinal lining increases what?2. What are Villi?3. What are Microvilli? 2

Answer 75

1. absorptive surface area2. Finger-like projections of the mucosa3. -Tiny projections on luminal membrane of each intestinal cell-Give the apical region striated appearance called brush border

Question 76

Describe and explain the steps in Carbohydrate Digestion Describe and explain the steps in Protein Digestion

Answer 76

See picture

Question 77

Describe the digestion of Fat Describe the digestion of Nucleic Acids

Answer 77

See picture

Question 78

Where does the small intestine empty into the large intestine?

Answer 78

Ileocecal valve

Question 79

Functions of the large intestine3

Answer 79

1. Reabsorb water and compact material into feces 2. Absorb vitamins produced by bacteria   3. Store fecal matter prior to defecation

Question 80

The physiology of different colon regions1. The ascending colon is specialized for what?2. The transverse colon is specialized for what? 23.  The descending colon is a conduit between the what?

Answer 80

1. processing chyme delivered from the terminal ileum2. the storage and dehydration of feces and is the primary site for the removal of water and electrolytes and the storage of feces3. transverse and sigmoid colon

Question 81

The physiology of the rectosigmoid region, anal canal, and pelvic floor musculature is what?

Answer 81

maintains fecal continenceThe sigmoid and rectum are reservoirs with a capacity of up to 500mL

Question 82

Motility in the Large Intestine1. The proximal half of the colon is concerned with _________and the distal half with_______?2. The transit of small labeled markers through the large intestine occurs in ______hrsMovements of the colon2. Mixing movements?4. Propulsive movements?

Answer 82

1. absorption, storage2. 36-483. (Haustrations)4. (Mass Movements)

Question 83

Mixing movements (Haustrations)1. Ring-like contractions (about 2.5 cm) of the circular muscle divide the colon into pockets called______?2. Net forward propulsion occurs when what?

Answer 83

1. haustra2. sequential migration of haustra occurs along the length of the bowel

Question 84

Propulsive movements (Mass Movements)1. The motor events in the ________ and ___________colon?2. May be triggered by the increased delivery of _____ ______into ascending colon following a meal (_______ reflex)3. Irritants, e.g., castor oil, threatening agents such as parasites and enterotoxins can initiate what?4. Starts in the ______of transverse colon and is preceded by ________ of the circular muscle and the downstream disappearance of haustral contractions  

Answer 84

1. transverse and descending2. ileal chyme, gastrocolic3. mass movement4. middle, relaxation

Question 85

Reabsorption in the large intestine includes: 5 

Answer 85

1. Water2. Vitamins – K, biotin, and B53. Organic wastes – urobilinogens and sterobilinogens4. Bile salts5. Toxins

Question 86

1. Villi in the large instestine?2. Mucosa contains numerous tubular glands called______?3. Responsible for what?

Answer 86

1. NO2. crypts3. mucus secretion

Question 87

Rectum1. Terminates where?2. How long?3. Used for?

Answer 87

1. Terminates at the anal canal2. 15 cm3. STORAGE

Question 88

What does feces contain?6

Answer 88

Contain1. water,2. dietary fiber,3. inorganic salts,4. dead cells,5. bacteria, and6. anything the body cannot or will not absorb.

Question 89

Water‑ all but about 100 ‑200ml reabsorbed, about 500ml residue enters LI/day, thus about _____ml vol leaves as feces

Answer 89

150

Question 90

Sensory innervation and continence1. What in the rectum detect distention and supply the ENS?2. The anal canal in the region of the skin is innervated by what nerves that transmit signals to CNS?3. This region has sensory receptors of what? 34. Contraction of  what (2) blocks the passage of feces and maintains continence?

Answer 90

1. Mechanoreceptors2. somatosensory3. pain, temperature and touch4. internal anal sphincter and puborectalis muscle

Question 91

Anus1. Rectum fills with feces increasing what?2. Contractions of what (2) create intra-abdominal pressure which increases intra-rectal pressure?3. ________ relaxes4. Feces to enter the______?5. _________waves push the feces out of the rectum.6. Relaxation of the what (2) allows the feces to exit from the anus?  7. What pull the anus up over the exiting feces (physiologic valve)?

Answer 91

1. pressure2. abdominal and pelvic floor muscles3. Sphincters4. canal.5. Peristaltic6. internal and external anal sphincters7. Levatori ani muscles

Question 92

What are the advanatages of abdominal xrays?5

Answer 92

1. Plain abdominal x-rays are readily available2. Often used for urgent investigation3. Does show gas in abnormal places or abnormal amounts4. Can show stones and metallic foreign bodies well---Kidney and gall bladder stones5. Solid organs can be seen but not well 

Question 93

What kind of xrays may you need for abdominal views?2What do you get better imaging with?2

Answer 93

May need upright and lateral decubitus films as well as flat plates Better imaging with CT or ultrasound

Question 94

Abdominal xrayIndications 5Not indicated for 3

Answer 94

Indications 1. Suspected bowel obstruction/Perforation2. Suspected intussusception3. Foreign bodies4. Suspected abdominal mass5. Blunt abdominal traumaNot indicated1. Vague central abdominal pain2. Gastroenteritis3. Haematemesis

Question 95

InterpretationDetermine ownership, adequacy, and technical quality of the filmTHEN?3

Answer 95

1. Gases2. Abdominal findings3. Solid organs (liver, kidneys, spleen, psoas muscles, bladder) 

Question 96

What are we looking for with gases in general?

Answer 96

Normal and abnormal gas distribution

Question 97

What are we looking for with gas in the small bowel?(normal findings 4)

Answer 97

1. Intraluminal gas usually minimal2. Centrally located3. Numerous tight loops of small diameter (2.5-3.5cm)4. Valvulae conniventes (Stack of coins)

Question 98

What are we looking for with gases in the large bowel?(normal findings 3)

Answer 98

1. Mixture of gas and feces2. Loops are larger in diameter (3-5cm)3. Haustra

Question 99

What are abnormal findings in gas patterns?5

Answer 99

1. Dilated loops2. Air-fluid levels on erect film3. Intramural gas4. Intraperitoneal gas5. Extraperitoneal gas

Question 100

1. What is the large area in the RUQ of the xray?2. Its bulk prevents what in this area?

Answer 100

1. liver2. any bowel occupying this area

Question 101

What is the soft tissue in the LUQ, size of a fist?

Answer 101

spleenCan be seen, obscured, or not at all

Question 102

Kidney shape?Which is higher than the other?What size?

Answer 102

Bean shapedLeft higher than rightAbout 3 vertebrae in size

Question 103

Explain where you will find the psoas muscles on the xray?

Answer 103

Forms straight lines extending inferolaterally from lumbar spine to lesser trochanter of femur

Question 104

Bladder appears how on the xray?

Answer 104

If full appears as soft tissue density in pelvis

Question 105

Normal Gas Pattern

Answer 105

See picture

Question 106

What is these xrays showing?What symtpoms does he have from this pathology? 3

Answer 106

SMALL BOWEL OBSTRUCTION TWO PATIENTS WITH1. ABDOMINAL DISTENSION,  2. CRAMPY MID-ABDOMINAL PAIN 3. VOMITING

Question 107

What are these two xrays showing?What symptoms come with this pathology? 3

Answer 107

LARGE BOWEL OBSTRUCTION TWO PATIENTS WITH1. ABDOMINAL DISTENSION.2. LOWER ABDOMINAL PAIN, AND3. CONSTIPATION

Question 108

What are these two xrays showing?Often occurs when?

Answer 108

IleusAfter surgery

Question 109

What are these xrays showing?

Answer 109

Constipation (full of stuff/stool)

Question 110

What are these xrays showing1?2?

Answer 110

 1. Calcified gallbladder2. Kidney stones

Question 111

Abdominal organs

Question 112

Find the Foreign Body!

Question 113

1. Upper GI series aka?2. Uses what tools?3. What are the two types?4. What does it look at? 3 

Answer 113

1. Also called a barium swallow2. Uses plain film x-ray and fluoroscopy3. 2 types-Standard barium upper GI series-Double-contrast upper GI series4. Looks at the-esophagus,-stomach, and-duodenum

Question 114

Indications for an Upper GI series?4

Answer 114

Indications1. Dysphagia2. GERD3. Assessment of hiatal hernia4. Strictures

Question 115

Upper GI series contraindications?4Risk? 1 

Answer 115

Contraindications1. Intestinal obstruction2. Esophageal perforation or rupture is suspected3. Pregnant women4. Individuals with poor swallowing reflexRisk1. Constipation

Question 116

Small Bowel Follow ThroughIndications3

Answer 116

1. Chrohn’s2. Tumors3. Unexplained abdominal pain

Question 117

1. Lower GI studies aka?2. What does it evaluate?3. What kinds? 24. Indications? 25. Risks? 2

Answer 117

1. Also called Barium Enema2. Evaluates the colon3.-Barium enema-Air-contrast (double-contrast) enema4. Indications-Colon cancer (apple core lesion)-Diagnose/monitor UC or Crohn’s disease5. Risk-Pregnant women-Colon perforation

Question 118

Lower GI series

Question 119

What is a sensitive method to diagnosis abdominal disease?

Answer 119

CT

Question 120

CT: Frequently used to do what?(In the picture what does the 3rd pic show?)

Answer 120

stage and follow cancer(Abdominal aneurysm)

Question 121

Indications for abdominal CT? 3

Answer 121

1. Patients with jaundice2. Pancreatic disease3. Hepatic metastases

Question 122

Abdominal CT1. Shows abdominal wall – localizes_______?2. What may be used to augment the scan?3. Downsides? 2

Answer 122

1. Hernias2. Dilute contrast3. Expensive, high doses of radiation

Question 123

What is this CT showing?

Answer 123

Gallstone pancreatitis

Question 124

HEPATOBILIARY SCINTIGRAPHY aka?

Answer 124

(HIDA SCAN/Cholescintigraphy) 

Question 125

HEPATOBILIARY SCINTIGRAPHY (HIDA SCAN/Cholescintigraphy)1. used for what?2. How does it work?3. Indications? 3

Answer 125

1. Used in diagnosis of problems with the liver, gallbladder, or bile ducts2. Radio-isotope is taken up in the liver and secreted into the bile3. Indications-Cholecystitis-Bile duct obstruction-Assessment for liver transplant

Question 126

Label the following letters?

Answer 126

A: liver parenchymaB: gallbladderC: small bowelD: common bile ductE: intrahepatic bile duct

Question 127

Nuclear Imaging of the Gall Bladder

Question 128

ABDOMINAL ULTRASONOGRAPHY1. How does it work?2. what is it also known as?3. Can be combined with what to visualize hollow structures?

Answer 128

1. Sound waves to visualize internal organs thru abdominal wall2. Known as transabdominal ultrasound3. Can be combined with endoscopy, visualize structures in hollow organs*

Question 129

Abdominal US: Advantages? 5

Answer 129

Can be performed1. quickly at bedside;2. no radiation;3. inexpensive4. Imaging occurs real time without need for sedation5. Influence of movements can be assessed quickly

Question 130

1. Disadvantages of Ab US? 32. Preferred imaging for what?3. Useful in evaluation of what patient?4. What does FAST mean?-What does it show?5. What provides more definitive information? 2

Answer 130

1.-Hampered by fat and air-operator dependent;  -limited sensitivity**2. Preferred imaging for right upper quadrant pain3. unstable trauma patient4. Focused Assessment with Sonography for Trauma-shows intraperitoneal fluid and also hemopericardium5. Abdominal and chest CT provides more definitive information 

Question 131

ABDOMINAL ULTRASOUNDS-Needs skilled technician and able interpreter

Question 132

1. Endoscopy aka?2. Can visualize what area?3. Advantages? 24. Most pts have what afterwords?

Answer 132

1. EGD – esophagogastroduodenoscopy2. Can visualize the esophagus to the duodenum--High-definition white light endoscope3.-Minimally invasive with quick recovery-Usually done under conscious or moderate sedation4. Most patients have a sore throat afterwards

Question 133

Endoscopy?Indications? 4Contraindications? 3

Answer 133

Indications1. Signs and symptoms of upper GI disease2. Surveillance for upper GI cancer in high-risk settings3. Biopsy4. Therapeutic intervention    Contraindications1. Possible perforation2. Medically unstable/unwilling patients3. anticoagulation             

Question 134

Capsule Endoscopy Indications? 4Contraindications? 2

Answer 134

Indications1. Obscure gastrointestinal bleeding2. Inflammatory bowel disease3. Small bowel polyps and tumors4. Celiac diseaseContraindications1. Swallowing d/o2. Small bowel obstruction/stenosis 

Question 135

Why do we use capsule endoscopy?

Answer 135

Patient swallows pill containing a cameraParts of small bowel not reachable by other endoscopy

Question 136

FLEXIBLE SIGMOIDOSCOPYPros? 4Cons? 3

Answer 136

Pros1. May be done in office2. Inexpensive, cost-effective3. Reduces deaths from rectal cancer4. Easier bowel preparation, rarely needs sedation Cons1. Detects only half of polyps2. Misses 40-50% of cancers located beyond the view of the sigmoidoscope3. Often limited by discomfort, poor bowel preparation

Question 137

FLEXIBLE SIGMOIDOSCOPYIndications? 4Contraindications? 3

Answer 137

Indications1. Screening test2. Blood in stool3. Evaluation of colon4. Medical management of colitisContraindications1. Bowel perforation2. Acute diverticulitis3. Active peritonitis

Question 138

1. Colonoscopy visualizes what? 32. White kind of light?3. Requires what?

Answer 138

1. Visualization of-rectum,-colon-distal ileum2. High definition white light colonoscope3. Requires bowel prep

Question 139

Uses, complications similar to upper GI endoscopyComplications rare in diagnostic colonoscopy But can be what? 2 

Answer 139

Can have-bleeding,-perforation with polypectomy

Question 140

ColonoscopyIndications: 3Contraindications: 4

Answer 140

Indications1. Screening2. Evaluation3. Follow-up colorectal cancerContraindications1. PregnancyRelative contra:2. Colonic perforation3. Toxic megacolon4. IBD with ulceration

Question 141

ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP) is what?

Answer 141

Technique that uses combination of luminal endoscopy and fluoroscopic imaging to diagnose and treat conditions associated with the pancreatobiliary system

Question 142

ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP)Indications?2

Answer 142

Biliary diseasePancreatic disease

Question 143

ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP)What reasons would we use this for biliary diseases? 3

Answer 143

1. Assessment and treatment of biliary obstruction secondary to choledocholithiasis2. Treatment of choledocholithiasis during cholecystectomy after intraoperative cholangiography3. Assessment and treatment of bile duct strictures

Question 144

ERCPWhat reasons would we use this for pancreatic disease? 2

Answer 144

1. Assess and treat acute pancreatitis, strictures, pancreatic duct stones2. Treatment of pseudocyst and malignancies

Question 145

ERCP Contraindications? 3

Answer 145

1. Refusal2. Unstable cardiopulmonary, neurologic, or cardiovascular status3. Existing bowel perforation 

Question 146

Strucutures of the Abdomen

Question 147

What is the esophagus?

Answer 147

Muscular tube that conveys food from pharynx to stomach

Question 148

Muscle layers of the esophagus? 2What is it missing?Food passes through quickly because of what?

Answer 148

1. Inner circular muscle2. Outer longitudinal muscle No serosa peristalsis

Question 149

Which part of the muscle is contracting during swallowing and which is relaxaing?

Answer 149

1. Circular muscle contraction after the bolus2. Circular muscle relaxation before the bolus

Question 150

What are the two types of movement in the esophagus and describe them?

Question 151

Dysphagia common etiologies1. Originating in the lumen? 12. Originating in the wall? 3 main ones, 3 more rare3. Originating outside the wall? 1 main, 3 more rare4. Neuromuscular disorders? 1 main, 1 more rare

Answer 151

1. ^ In the lumen-Tumor2. ^ In the wall-Achalasia*-Tumor of the esophagus*-GERD*-Plummer Vinson syndrome- iron deficiency anemia-Scleroderma- replaced with collagen tissue that has no contractibility-Chagas’ disease- infectious.3. ^ Outside the wall-Pressure of enlarged lymph nodes*-Thoracic aortic aneurysm-Bronchial carcinoma-Retrosternal Goiter 4. ^ Neuromuscular disorders-Myesthenia gravis-Stroke* 

Question 152

1. UES moves how?2. LES moves how?3. Longitudinal and circular muscle moves how?

Answer 152

1. UES….closes and relaxes2. LES….base line tone. Mostly stays shut3. Longitudinal and circular muscle…peristalsis

Question 153

Normal phases of swallowing1. The voluntary part of swallowing consists of what?2. Involuntary swallowing consists of what? 3

Answer 153

Voluntary1. Oropharyngeal phase – bolus is voluntarily moved into the pharynxInvoluntary1. UES relaxation2. peristalsis (aboral movement)3. LES relaxation

Question 154

Between swallows:1. UES prevents what? 22. LES prevents what? 1  

Answer 154

1. -prevents air entering the esophagus during inspiration and-prevents esophagopharyngeal reflux2. gastroesophageal reflux 

Question 155

Esophageal disorders6

Answer 155

1. Motility2. Anatomic & Structural3. Reflux4. Infectious5. Neoplastic6. Miscellaneous (Perforation, Burns, Bleeding)

Question 156

What kind of epithethium makes up the esophagus?

Answer 156

squamous

Question 157

Oropharyngeal dysphagia (transfer dysphagia)1. Patients complain of what?2. What may cause symtpoms?

Answer 157

1. patients complain of difficulty swallowing2. tracheal aspiration may cause symptoms

Question 158

What are some pharyngoesophageal neuromusclar disorders?8

Answer 158

1. stroke2. Parkinson’s3. poliomyelitis4. ALS5. multiple sclerosis6. diabetes7. myasthenia gravis8. dermatomyositis and polymyositis

Question 159

Upper esophageal sphincter dysfunction/HTN aka?

Answer 159

cricopharyngeal

Question 160

What is a achalasia?

Answer 160

Incomplete relaxation of lower sphincter during swallowing leading to functional obstruction and proximal dilatation  (failure to relax)

Question 161

Achalasia:1. PP: 3 contributing factors?2. What structures are usually dimished or absent?3. Histology findings?4. Hypotheses for etiologies? 25. 5% develop what?

Answer 161

1.-Aperistalsis,-incomplete relaxation,-increased resting tone2. Ganglion cells of the myenteric plexus are diminished or absent3. Histology: Inflammation in the area of M. plexus4. Hypotheses: autoimmune, viral infections5. 5% develop squamous cell carcinoma

Question 162

Clincial picture of Achalasia:History? 5 

Answer 162

1. Dysphagia (most common)2. Regurgitation3. Chest pain4. Heartburn5. Weight loss 

Question 163

Achalasia: 1. 25-50% report episodes of what?2. 80-90% experience spontaneous what?3. some patients may present with signs or symptoms of what? 

Answer 163

1. retrosternal chest pain2. regurgitation.3. pneumonia

Question 164

Lab studies for Achalasia? 1Imaging studies? 3 (and what will the findings be?)The radiologic examination of choice in the diagnosis of achalasia is what?

Answer 164

Lab Studies1. Laboratory studies are noncontributory. Imaging Studies1. UGI: Bird’s Beak.2. EGD: Normal or dilated esophagus.3. Manometry Test of Choice: a barium swallow study performed under fluoroscopic guidance.

Question 165

Normal esophageal mucosa appears what color?

Answer 165

white to tan

Question 166

What is esophageal manometry used to assess? 2

Answer 166

Used to assess LES pressure & peristalsis

Question 167

1. The goal of therapy for achalasia is to do what?2. What are our two types of treatment?

Answer 167

1. relieve symptoms by eliminating the outflow resistance caused by the hypertensive and nonrelaxing LES.2. -Medical Management-Surgical Management

Question 168

Diffuse Esophageal Spasm (DES) Characteristics5

Answer 168

1. Chest pain2. Intermittent dysphagia3. Segmental non-peristaltic contractions4. Corkscrew esophagus5. Muscular hypertrophy

Question 169

What is a nutcracker esophagus characterized by?

Answer 169

High pressure peristaltic contractions(Nutcracker esophagus, or Hypertensive peristalsis, is a disorder of the movement of the esophagus characterized by contractions in the smooth muscle of the esophagus in a normal sequence but at an excessive amplitude or duration.)

Question 170

What is esophageal atresia?

Answer 170

congenital abnormality in which the mid-portion of the esophagus is absent

Question 171

What is a TE fistula?What are the etiologies depending on age? 2

Answer 171

A tracheoesophageal fistula is an abnormal connection (fistula) between the esophagus and the trachea.TEF is a common congenital abnormality, but when occurring late in life is usually the sequela of surgical procedures such as a laryngectomy.

Question 172

What will show that the tube has not reached the abdomen suggesting either atresia or a fistula?

Answer 172

A plain radiograph will confirm the tube has not reached the stomach

Question 173

Absence of gas in the abdomen suggests that the patient has either what or what?

Answer 173

1. atresia without a fistula or2. atresia with a proximal fistula only

Question 174

Gastroesophageal reflux (GERD) is defined as what?

Answer 174

Mucosal damage produced by the abnormal reflux of gastric contents into the esophagus

Question 175

PP of GERD?

Answer 175

-Primary barrier to gastroesophageal reflux is the lower esophageal sphincter-LES normally works in conjunction with the diaphragm-If barrier disrupted, acid goes from stomach to esophagus**

Question 176

WHat are the four major physiological mechanisms that protect against esophageal acid injury?

Question 177

Classic GERD symptoms2

Answer 177

1. Heartburn (pyrosis): substernal burning discomfort2. Regurgitation: bitter, acidic fluid in the mouth  when lying down or bending over

Question 178

Extraesophageal Manifestations of GERDPulmonary? 4ENT? 9Other? 2

Answer 178

Pulmonary    1. Asthma2. Aspiration pneumonia3. Chronic bronchitis4. Pulmonary fibrosisENT1. Hoarseness2. Laryngitis3. Pharyngitis4. Chronic cough5. Globus sensation6. Dysphonia7. Sinusitis8. Subglottic stenosis9. Laryngeal cancerOther1. Chest pain2. Dental erosion 

Question 179

Potential oral and laryngopharyngeal signs associated with GERD?7

Answer 179

1. Edema and hyperemia of larynx2. Vocal cord erythema, polyps, granulomas, ulcers3. Hyperemia and lymphoid hyperplasia of posterior pharynx4. Interarytenyoid changes5. Dental erosion6. Subglottic stenosis7. Laryngeal cancer

Question 180

GERD etiology?6

Answer 180

Could be a combination of these1. Hiatal hernia2. Incompetent LES3. Decreased esophagus clearance4. Decreased gastric emptying5. Medications6. Anything that results in esophageal irritation and inflammation

Question 181

1. What is a hiatal hernia?2. Types? 2 

Answer 181

1. Herniation of portion of stomach adjacent to the esophagus through an opening in the diaphragm2. Types-Sliding-Paraesophageal/rolling

Question 182

1. A hiatal hernia is stomach which has slipped above the what?2. The opening in the diaphragm which allows this to happen is called the what?3. Hiatal hernias are common, most are harmless, but they may promote what?

Answer 182

1. Diaphragm2. Hiatus3. reflux

Question 183

Hiatal hernia:1. Food lodges in pouch and causes what? 32. What structure is often incompetant?3. Other contributing factors? 3

Answer 183

1. -Inflammation of mucosa,-reflux of food up to esophagus,-dysphagia2. Often incompetent gastro-esophageal sphincter3. Contributing factors-Shortening of esophagus-Weakness of diaphragm-Increased abdominal pressure (pregnancy)

Question 184

Etiology of Hiatial Hernia? 4

Answer 184

1. Structural changes2. Obesity3. Pregnancy4. Heavy lifting

Question 185

Complications of a hiatal hernia? 7(most common)

Answer 185

1. GERD**2. Hemorrhage3. Stenosis of esophagus4, Ulcerations5. Strangulation of hernia6. Regurgitation7. Increased risk for respiratory disease

Question 186

Clincial manifestations of hiatial hernia?5

Answer 186

1. May be asymptomatic2. Heartburn3. Dysphagia4. Reflux with lying down5. Pain, burning when bending over

Question 187

Treatment goals of GERD?3

Answer 187

1. Eliminate symptoms2. Manage or prevent complications3. Maintain remission

Question 188

GERD lifestyle modifications?9

Answer 188

1. Avoid large meals2. Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate, onions, garlic, peppermint3. Decrease fat intake4. Avoid lying down within 3-4 hours after a meal5. Elevate head of bed 4-8 inches6. Avoid meds that may potentiate GERD (alpha agonists, theophylline, sedatives, NSAIDS)7. Avoid clothing that is tight around the waist8. Lose weight9. Stop smoking

Question 189

GERD: What is appropraite for inital therapy?

Answer 189

AntacidsOver the counter acid suppressants and antacids appropriate initial therapyApprox 1/3 of patients with heartburn-related symptoms use at least twice weekly

Question 190

Acid suppression therapy for GERD2

Answer 190

1. H2-Receptor Antagonists (H2RAs)2. Proton Pump Inhibitors (PPIs) 

Question 191

What are the medications available in the following categories:1. H2-Receptor Antagonists (H2RAs) 42. Proton Pump Inhibitors (PPIs) 5

Answer 191

1. -Cimetidine (Tagamet®)-Ranitidine (Zantac®)-Famotidine (Pepcid®)-Nizatidine (Axid®)2. -Omeprazole (Prilosec®)-Lansoprazole (Prevacid®)-Rabeprazole (Aciphex®)-Pantoprazole (Protonix®)-Esomeprazole (Nexium)

Question 192

Antireflux surgery accomplishes what?5

Answer 192

1. Reduce hiatal hernia2. Repair diaphragm3. Strengthen GE junction4. Strengthen antireflux barrier via gastric wrap5. 75-90% effective at alleviating symptoms of heartburn and regurgitation

Question 193

What are the four principles of Anti-refulx surgery?

Question 194

Postsurgery (studies)1. 10% have what?2. 2-3% have what?3. 7-10% have what?4. Within 3-5 years 52% of patients are what?

Answer 194

1. solid food dysphagia2. permanent symptoms3. gas, bloating, diarrhea, nausea, early satiety4. back on antireflux medications

Question 195

Complications of GERD(This is where we come in….don’t let patients get to this stage!)3

Answer 195

1. Erosive esophagitis2. Stricture3. Barrett’s esophagus

Question 196

GERD  Complications: Erosive esophagitis1. Responsible for _____% of GERD symptoms2. Severity of symptoms often ________severity of erosive esophagitis

Answer 196

1. 40-602. fail to match

Question 197

GERD complications: Esophageal stricture1. Result of healing of what?2. May need what?

Answer 197

1. erosive esophagitis2. Dilation

Question 198

GERD complications: Barrett's Esophagus1. PP? 22. This specialized intestinal metaplasia can progress to what? 2

Answer 198

1. -Acid damages lining of esophagus and causes chronic esophagitis-Damaged area heals in a metaplastic process and abnormal columnar cells replace squamous cells2. -dysplasia and-adenocarcinoma

Question 199

When to perform diagnostic tests?5

Answer 199

1. Uncertain diagnosis2. Atypical symptoms3. Symptoms associated with complications4. Inadequate response to therapy5. Recurrent symptoms

Question 200

Diagnostic tests for GERD? 4

Answer 200

1. Barium swallow2. Endoscopy3. Ambulatory pH monitoring4. Esophageal manometry

Question 201

What is the most useful first diagnostic test for patients with dysplagia?

Answer 201

Barium swallow

Question 202

What could a barium swallow show us?

Answer 202

1. Stricture (location, length)2. Mass (location, length)3. Bird’s beak4. Hiatal hernia (size, type)

Question 203

1. What study will help us quantify reflux in the proximal/distal esophagus?2. What does it measure?

Answer 203

1. Ambulatory 24 hour pH monitoring2. % time pH less than 4

Question 204

Esophageal manometry has a limited role in GERD but what may it help you with?3

Answer 204

1. Assess LES pressure, location and relaxation2. Assist placement of 24 hr. pH catheter3. Assess peristalsis prior to antireflux surgery

Question 205

Infection-induced esophagitis:1. More common in pts with what?2. Fungal origins?3. Viral origins? 2

Answer 205

1. More common in patients with impaired immunity2. Fungal : Candida3. Viruses: Herpes and Cytomegalovirus

Question 206

1. How do we diagnosis eosinphilic esophagitis?2. What is it associated with?3. Treatment? 

Answer 206

1. Esophageal biopsies:  Many intraepithelial eosinophils (80/high power field)2. Associated with food allergies 3. Treatment:    -Oral steroid (Fluticasone) therapy-220 mcg two puffs a day

Question 207

Etiologies of esophageal bleeding?2

Answer 207

1. Mallory-Weiss Tear2. Esophageal varicies

Question 208

1. What is a mallory-weiss tear caused by?2. Where does the tear occur?

Answer 208

1. Caused by severe retching and vomiting2. Tear occurs at the junction of the esophagus and stomach

Question 209

Esophageal varicies1. Usually secondary to what?2. Anything that increase pressure can cause what? (example)

Answer 209

1. cirrhosis of the liver2. can start massive bleed (coughing)

Question 210

Esophageal lacerations (mallory-weiss syndrome)1. ___________ tears at the gastroesophageal junction2. Clinical setting where this often happens?3. Tear may be how deep? 24. Clinical picture: symptoms? 35. _______________is found in 75% of patients6. Most often bleeding stops w/o intervention, but life-threatening____________ may occur.

Answer 210

1. Longitudinal2. chronic alcoholics after a bout of severe vomiting3. superficial or deep affecting all layers4. -Pain,-bleeding,-superimposed infection5. Hiatal hernia6. hematemesis

Question 211

What are esophageal varices?

Answer 211

Tortuous dilated veins in the submucosa of distal esophagus

Question 212

Esophageal varices1. Etiology?2. Asymptomatic until when?3. What percent subsides spontaeously?4. What percent die during the first episode?5. Rebleeding occurs in what percent within one year?

Answer 212

1. Etiology: portal hypertension secondary to liver cirrhosis2. Asymptomatic until they rupture leading to massive hemorrhage3. 50% subsides spontaneously4. 20-30% die during the first episode5. Rebleeding occurs in 70% of cases within one year

Question 213

What are esophageal diverticula?What is the most common of the esophageal diverticula?

Answer 213

Saclike outpouching of one or more layers of the esophagus Zenker’s diverticulum

Question 214

Zenker's diverticulum1. Where is it located?2. Sympotms? 5

Answer 214

1. Located above the upper esophageal sphincter2. Symptoms-Dysphagia-Weight loss-Regurgitation-Chronic cough-Aspiration

Question 215

1. What is an epiphrenic diverticulum?2. Arises from where?

Answer 215

1. Pulsion diverticulum    (arrow) that probably   related to incoordination of esophageal peristalsis    and relaxation of the   lower  esophageal   sphincter2. Arises in the distal esophagus, just above diaphragm

Question 216

Treatment for esophageal diverticulum?3

Answer 216

1. Clients learn to empty esophagus by applying pressure2. Limit foods (blenderize)3. Endoscopic Surgery

Question 217

Scleroderma1. What is it?2. What is the motility pattern in the esophagus with this?3. What happens to the GE junction?4. GE reflux can cause what?

Answer 217

1. Chronic hardening and tightening of the skin and connective tissues.2. -Proximal 1/3 striated muscle = normal peristalsis-Distal 2/3 smooth muscle = impaired motility3. Patulous GE junction4. GE reflux can cause distal stricture

Question 218

Esophoageal perforation1. whats the number one cause?2. Boerhaave syndrome caused by? 2

Answer 218

1. Iatrogenic 75%-endoscopy #1 cause2. Boerhaave syndrome 10-15%-ETOH-emesis

Question 219

Esophageal perforation:1. Very lethal: what two things lead to shock?2. What other things will this cause? 2

Answer 219

1. -Necrotizing mediastinitis and-polymicrobial infection lead to shock2.-Pleural/peritoneal space- rapidly progressive infection/shock-Empyema

Question 220

What is the definition of constipation?2

Answer 220

1. Passage of stool infrequently or with difficulty.2. Stool frequency of less than three per week.

Question 221

Characteristics passing the stool in constipation?3

Answer 221

1. Straining2. Hard Stool3. Incomplete evacuation

Question 222

1. What is the most common etiology of constipation?2. What leads to this? 3

Answer 222

1. Lifestyle2. -Inadequate fiber in diet-Inadequate hydration-Inactivity

Question 223

Fiber promotes what?3

Answer 223

1. normal transit time, 2. frequent stools, 3. lower use of laxatives.

Question 224

Medications that cause constipation?9

Answer 224

1. Opiates/narcotics2. Antidepressants3. Calcium channel blockers4. Antipsychotic5. Antiparkinsonian agents6. Anticholinergics7. Calcium, iron supplements8. Antispasmodics9. Antacids (calcium and aluminum)

Question 225

Structural Abnormalities that could lead to constipation5

Answer 225

1. Carcinoma2. Ischemia3. Volvulus4. Megacolon5. Anorectal disorders

Question 226

Anorectal disorders that lead to consitpation? 3

Answer 226

1. Prolapse2. Rectocele3. Pelvic floor dysfunction

Question 227

Metabolic causes of constipation? 7

Answer 227

1. Hypokalemia2. Hypomagnesemia3. Hypothyroidism****4. Hyperparathyroidism5. Porphyria genetic hemoglobin disorder6. Addison’s disease7. Hypercalcemia

Question 228

Neurologic causes of constipation? 7

Answer 228

1. Parkinson’s2. Multiple Sclerosis3. Automonic neuropathy4. Hirschprung disease5. Chagas disease6. Spinal cord lesions7. Cerebrovascular disease

Question 229

Systemic causes of constipation? 4

Answer 229

1. Amyloidosis2. Scleroderma3. Polymyositis4. Pregnancy

Question 230

Surgical causes of constipation? 4Psychiatric causes of constipation? 2

Answer 230

Surgical1. Abdominal2. Pelvic3. Colonic4. AnorectalPsychiatric:1. Depression2. Eating disorders

Question 231

Examination of constipation?3

Answer 231

1. Full history2. Full physical exam3. DRE - Stool for occult blood

Question 232

In patients less than 50y/o with no alarm symptoms, may start what?

Answer 232

empiric therapy

Question 233

Further treatment should be performed on patients with any of the following:6

Answer 233

1. Over age 502. Severe constipation3. Signs of an organic disorder4. Hematochezia5. Weight loss6. Positive FOBT

Question 234

Consitipation evaluation?4

Answer 234

1. KUB (abdominal xray), 2. Barium enema or 3. colonoscopy4. Blood Tests5. Colonic Transit Study

Question 235

What blood tests would you do to work up constipation?6

Answer 235

1. Glucose2. CBC --anemia detect colorectal neoplasm3. Thyroid***4. Calcium5. Magnesium6. Phosphorous

Question 236

Colonic transit study is used for what?

Answer 236

To observe transit time in patients with refractory constipation not responding to conservative measures.

Question 237

Management first and foremost for constipation is what?

Answer 237

prevention

Question 238

Patient education for constipation3

Answer 238

1. Exercise:key stimulus to colon peristalsis and defecation encourage and enable patient to be mobile, or be in upright position.2. Fluid intake: constipated stools are low in water content.3. Fiber intake: acute constipation low on fiber diet, chronic constipation responds poorly to fiber.

Question 239

Treatment types of constipation? 4

Answer 239

1. Stool softeners (surfactants)2. Laxatives3. Opiod-receptor antagonists4. Digitial disimpaction

Question 240

What are the types of laxatives? 3

Answer 240

1. Bulk2. Osmotic 3. Stimulant laxatives

Question 241

What are the stool softener medications?2

Answer 241

1. Colace (docusate sodium)2. Docusate calcium

Question 242

What are the drugs in the following categories:1. Bulk 42. Osmotic 53. Stimulant laxatives 24. Opioid-receptor antagonist 1

Answer 242

1. Bulk laxatives-Psyllium-Methylcellulose-Fibercon (polycarbophil)-Benefiber (wheat dextran)2. Osmotics-Lactulose-Sorbitol-Polyethylene glycol-Magnesium Citrate-Magnesium Sulfate (caution in renal impairment)3. Stimulant laxatives-Bisacodyl-Senna4. Methylnaltrexone

Question 243

Opioid-receptor antagonist(Methylnaltrexone) is approved for who?2What does it not affect?

Answer 243

Approved for 1. palliative care pts, 2. pts on chronic opiod tx, doesn’t effect central analgesia

Question 244

What is the definition of diarrhea?2

Answer 244

1. increase in daily stool weight above 200-300g/24hrs2. Clinically: increase in stool liquidity and/or frequency

Question 245

1. In developed countriesNormal stool weight of an adult human is less than _____ g/d2. Stool water accounts for ___ to __ % of weight 3. Normal bowel frequency ranges from what to what?4. Greater then __ x a day is considered abnormal

Answer 245

1. 2002. 60, 853. three times a week to three times a day4. 3

Question 246

Diarrhea PP. Describe the following reasons that contribute to constipation:1. Osmotic?2. Secretory?3. Motility?

Answer 246

1. non-absorbable substance draws out excess water into the intestines & increases stool weight and volume2. mucosal secretion of fluid & electrolytes secondary to bacterial enterotoxins, neoplasms or exotoxins3. food is not mixed properly, digestion is impaired and motility is increased; secondary to resection of the small intestine, surgical bypass of an area of intestine or diabetic neuropathy

Question 247

1. What is acute diahhrea?2. Persistant?3. Chronic?

Answer 247

1. Acute — ≤14 days in duration2. Persistent diarrhea — more than 14 days in duration3. Chronic — more than 30 days in duration

Question 248

1. Clinical Manifestations of diarrhea: 32. Acute diarrhea is usually due to what?

Answer 248

1. -Fever-Cramping pain-If severe, can get dehydrated, especially in children or elderly2. Acute usually due to infections with viruses and bacteria and are self-limited

Question 249

What is chronic diarrhea usually secondary to? 3

Answer 249

Chronic usually secondary to 1. irritable bowel syndrome (IBS), 2. inflammatory bowel disease, or 3. malabsorption syndromes

Question 250

Acute Infectious Diarrhea1. Viral causes? 42. Bacterial? 53. Protozoa? 4

Answer 250

1. Viral-Norovirus-Rotavirus-Adenoviruses-Astrovirus2. Bacterial-Salmonella-Campylobacter- Guiene Barre-Shigella-enterotoxigenic E. coli, -C. difficile 3. Protozoa-Cryptosporidium- most common parasitic cause of acute foodborne diarrhea in the US-Giardia-Cyclospora-entamoeba(wet mount for protozoa)

Question 251

Acute Diarrhea noninfectious etiologies? 3

Answer 251

1. Drugs2. food allergies3. disease states such as thyrotoxicosis and the carcinoid syndrome.

Question 252

Acute diarrhea: Indications for diagnostic evaluation?9

Answer 252

1. Profuse watery diarrhea with signs of hypovolemia2. Passage of many small volume stools containing blood and mucus3. Bloody diarrhea4. Temperature ≥38.5ºC (101.3ºF)5. Passage of ≥6 unformed stools per 24 hours or a duration of illness >48 hours6. Severe abdominal pain7. Hospitalized patients or recent use of antibiotics8. Diarrhea in the elderly (≥70 years of age) or the immunocompromised9. Systemic illness with diarrhea, especially in pregnant women (in which case listeriosis should be suspected)

Question 253

Chronic Diarrhea etiology?7

Answer 253

1. Medications2. Osmotic 3. Secretory4. Inflammatory5. Malabsorptive6. Motility Disorders7. Chronic Infections

Question 254

Osmotic diarrhea1. Clues to diagnosis? 22. Causes of this? 3

Answer 254

1. CLUES: -Stool volume decreases with fasting-increased stool osmotic gap 2. -Medications: -Disaccharidase deficiency: lactose intolerance -Factitious diarrhea

Question 255

1. Meds that cause osmotic diarrhea?2. Who often has Disaccharidase deficiency?3. Factitious diarrhea from?

Answer 255

1. Meds-antacids, -lactulose, -sorbitol 2. Lactose intolerance3. magnesium (antacids, laxatives)

Question 256

Secretory diarrhea 1. Clues?2. Causes? 5

Answer 256

1. CLUES: -Large volume (> 1 L/d)-little change with fasting; -normal stool osmotic gap 2. -Hormonally mediated: -Factitious diarrhea -Villous adenoma-Bile salt malabsorption -Medications

Question 257

1. Hormone mediated secretory diarrhea can be caused by? 32. Factitious secretory diarrhea can be caused by? 43. Why does Villous adenoma cause constipation?4. What bile salt malabsorption problems cause secretory diarrhea? 3

Answer 257

1. -carcinoid, -medullary carcinoma of thyroid (calcitonin), -Zollinger-Ellison syndrome (gastrin) 2. -(laxative abuse); -phenolphthalein, -cascara, -senna 3. Secretes K+ rich fluid 4. -ileal resection; -Crohn ileitis; -postcholecystectomy

Question 258

Peritoneal signs are what?

Answer 258

rebound sign for distention is an example

Question 259

Inflammatory conditions that cause chronic diarrhea:1. Clues? 32. Causes? 3

Answer 259

1. CLUES: -Fever, -hematochezia, -abdominal pain2. -Inflammatory Bowel Disease: -Malignancy: -Radiation enteritis

Question 260

1. What are the inflammatory bowel diseases that cause chronic diarrhea? 22. Malignancies that can cause inflammatory chronic diarrhea? 2

Answer 260

1. -Ulcerative colitis-Crohn’s disease 2. -lymphoma, -adenocarcinoma (with obstruction and pseudodiarrhea)

Question 261

Malabsoprtion syndromes that cause chronic diarrhea:1. Clues? 33. Causes? 4

Answer 261

1. CLUES: -Weight loss, -abnormal laboratory values-fecal fat > 10 g/24h 2. -Small bowel mucosal disorders-Lymphatic obstruction-Pancreatic disease-Bacterial overgrowth

Question 262

Malabsoprtion syndromes that cause chronic diarrhea:1. Small bowel disorder causes? 72. Lymphatic obstruction? 63. Pancreatic disease? 24. Bacterial overgrowth? 4

Answer 262

1. -celiac sprue, -tropical sprue, -Whipple disease, -eosinophilic-gastroenteritis, -small bowel resection (short bowel syndrome), -Crohn’s disease 2. -lymphoma, -carcinoid, -infectious (tuberculosis, MAI), -Kaposi sarcoma, -sarcoidosis, -retroperitoneal fibrosis 3. -chronic pancreatitis, -pancreatic carcinoma 4. -motility disorders (diabetes, vagotomy), -scleroderma, -fistulas, -small intestinal diverticula

Question 263

Motility disorders causing chronic diarrhea:1. Clues? 22. Causes? 3

Answer 263

1. CLUES: -Systemic disease or -prior abdominal surgery2. -Postsurgical-Systemic disorders-Irritable bowel syndrome

Question 264

Motility disorders causing chronic diarrhea:1. Postsurgical causes?32. Systemic causes?3

Answer 264

1. -vagotomy, -partial gastrectomy, -blind loop with bacterial overgrowth 2. -scleroderma, -diabetes mellitus,-hyperthyroidism

Question 265

The diarrhea workup: History?4

Answer 265

1. Travel, 2. longevity of symptoms, 3. family history, 4. food intake and relationship to onset.

Question 266

The diarrhea workup: Fecal analysis?6

Answer 266

1. Fecal leukocytes (invasive infection)2. Fecal Occult blood3. Fecal Fats4. Enteric Pathogen cultures5. Clostridium difficile (C. diff) toxin6. Ova & Parasites

Question 267

1. What does fecal leuks indicate?2. When do you find this? 2

Answer 267

1. Presence indicated bowel mucosal inflammation, 2. which occurs in -Invasive bacterial enteritis-Ulcerative colitis.

Question 268

Fecal Occult Blood1. Immunochemical tests for fecal blood(FIT or iFOBT) for hemoglobin are more specific than guaiac tests because why?2. HemoccultWhat do we need to do to make results significant?

Answer 268

1. they respond only to human globin and do not detect upper gastrointestinal bleeding2. + result obtained on multiple specimens performed on excessive days

Question 269

Stool for culture and sensitivity?3

Answer 269

1. Enterococcus2. E-coli3. Clostridium

Question 270

Stool for ova and parasite?3What do you want to treat all these with?

Answer 270

1. Salmonella2. Shigella3. GiardiaCipro

Question 271

C-diff Toxin Assay: How does C-Diff cause diarrhea?

Answer 271

C-diff multiplies and releases toxin that causes necrosis of the colonic epithelium which causes the diarrhea.

Question 272

Fecal fat- Quantitative stool fat4

Answer 272

1. Confirms steatorrhea2. Sprue3. Crohn’s4. Whipples Dz

Question 273

1. Colonoscopy with mucosal biopsy to exclude what? 32. Upper Endoscopy when what is suspected such as celiac sprue or whipple disease?

Answer 273

1. -IBD, -Microscopic Colitis-Colonic Neoplasia2. small intestine disorder

Question 274

Further studies for diarrhea?1

Answer 274

24 hour stool collection

Question 275

Treatment of diarrhea5

Answer 275

1. Fluid replacement2. Antibiotic therapy3. Bismuth subsalicylate (Pepto-Bismol, OTC)‏4. Opiate antidiarrheal agents 5. Cholestyramine (Questran)‏

Question 276

What diseases do we make sure to give antibiotics to for diarrhea?5

Answer 276

1. shigellosis, 2. traveler's diarrhea, 3. pseudomembranous enterocolitis, 4. cholera, and 5. parasitic diseases

Question 277

What are the Opiate antidiarrheal agents?2Used to treat what?

Answer 277

1. Diphenoxylate (Lomotil) and 2. Loperamide (Immodium)‏Mild to moderate secretory diarrhea

Question 278

Cholestyramine (Questran)‏ is used to treat diarrhea caused by what?

Answer 278

diarrhea caused by ileal bile salt malabsorption

Question 279

Whats the difference between IBS and IBD?

Answer 279

IBS- no constitutional symptomsconstipation and diarrheaIBD- ulcerative colitis and chrohns-blood -mucus-constitutional syndromes-abdominal pain-weight loss

Question 280

1. Anemia?2. Albumenia?3. SED rate?

Answer 280

1. blood loss- colon cancer2. malabsoprtion syndrome3. cancer or inflammatory disease

Question 281

Homemade fluid replacement for diarrhea patient?4

Answer 281

1. Half tsp of salt2. 1 tsp baking soda3. 8 tsp of sugar4. 8 oz of OJ diluted in a liter of water

Question 282

RBCs—anemia from GI disease could be?2

Answer 282

1. Multifactorial—depends on etiology of liver disease2. Liver disease due to alcoholism:

Question 283

Liver disease due to alcoholism?3

Answer 283

1. GI blood loss2. Nutritional deficiency—B12 and folate (macrocystic anemia)3. Alcohol as a direct toxin

Question 284

WBCs—neutropenia1. Why does this happen?2.

Answer 284

1. Sequestering of WBCs in the spleen because of portal hypertension 2. Results in the patient being ?

Question 285

(Etiology of portal HTN: ?

Answer 285

cirrhosis of the liver)

Question 286

Platelets—thrombocytopeniawhy does this happen?

Answer 286

Sequestering in the spleen secondary to portal hypertension

Question 287

Liver Function Tests7

Answer 287

1. ALT2. AST3. Alkaline Phosphatase4. GGT5. 5’-Nucleotidase6. Bilirubin7. Ammonia

Question 288

Applications of LFTs?4

Answer 288

1. Provide a noninvasive method to screen for the presence of liver disease2. Used to measure the efficacy of treatments for liver disease3. Used to monitor progression of liver disease4. Can reflect the severity of liver disease, particularly in patients who have cirrhosis

Question 289

Assess liver function not destruction or failure? 2

Answer 289

Albumin and PT

Question 290

Cons of LFTs3

Answer 290

1. Most do not accurately reflect how well the liver is functioning2. Abnormal values CAN be caused by diseases unrelated to the liver3. The tests may be normal in patient’s who have advanced liver disease

Question 291

Tests that reflect injury to hepatocytes?(whats normal?)2

Answer 291

Serum aminotransferases:1. Alanine aminotransferase (ALT)* 2. Aspartate aminotransferase (AST) (Normal

Question 292

1. ALT and AST is normally located where?2. When are they released intot he blood stream?

Answer 292

1. Enzymes are normally intracellular:2. Released into the blood stream when hepatocytes are injured---Damage or destruction of tissues or changes in cell membrane permeability permit leakage

Question 293

AST is also produced in what type of cells?7

Answer 293

1. cardiac muscle, 2. skeletal muslce, 3. kidneys 4. the brain 5. pancreas 6. lungs and 7. erythrocytes

Question 294

Extent of ____________ correlates poorly w/ the rise of aminotransferases?Highest elevations seen in what diseases? 3

Answer 294

liver necrosis1. viral hepatitis, 2. ischemic hepatitis, 3. toxicity

Question 295

Rapid decline in aminotransferases usually a sign of ________ but may reflect what?

Answer 295

1. recovery2. massive destruction of viable hepatocytes signaling acute liver failure

Question 296

1. What does alkaline phosphatase refer to?2. Found where?3. Sources? 34. In bone it is involved in what?5. MAJOR value of elevated serum alkaline phosphatase in diagnosis of liver disease is recognition of what?

Answer 296

1. Refers to a group of enzymes that catalyze the hydrolysis of organic phosphate esters at an alkaline pH2. Found in many areas of the body it’s precise function is not known3. Sources: -liver, -bone, & -sometimes the intestinal tract4. In bone the enzyme is involved in calcification5. MAJOR value of elevated serum alkaline phosphatase in diagnosis of liver disease is recognition of cholestatic disease!

Question 297

5`-nucleotidase:1. Found where? 62. In the liver where is it located?3. An increase in a non-pregnant patient with an increase in AP suggests the increase in AP is from where?4. Elevations in 5’-nucleotidase are seen in the same types of ________________ associated w/ an increase in APHOWEVER sometimes the two are discordant and cannot be totally reliable

Answer 297

1. Found in the -liver, -intestine, -brain, -heart, -blood vessels, & -endocrine pancreas2. In the liver subcellular location in hepatocytes3. liver4. hepatobiliary disease

Question 298

Gamma-glutamyl Transpeptidase (GGT):1. PLays an important role in what?2. Elevated serum activity is found in diseases of the what? 33. Major clinical value is for what?4. In what else do we see this in?

Answer 298

1. Plays a role in amino acid transport2. Elevated serum activity is found in diseases of the -liver, -biliary tract-pancreas corresponding to increases in AP3. Major clinical value is for conferring organ specificity to an elevated AP level4. Also see early peaks in acute liver toxicity such as after an alcohol binge

Question 299

1. Bilirubin the 80% the product of what?2. Other 20% of the time?

Answer 299

1. Bilirubin is the product of heme metabolism (80%)2. The other 20% is from other heme proteins

Question 300

Elevated bilirubin is due to:4

Answer 300

1. Overproduction of bilirubin2. Impaired uptake of bilirubin3. Impaired conjugation or excretion of bilirubin4. Backward leaking from damaged hepatocytes or bile ducts

Question 301

Conjugated bilirubin:1. Relates only to what kind of disease?2. What can it not differentiate though?

Answer 301

1. relates to only hepatobiliary disease2. It does not differentiate it from obstructive vs. hepatocellular damage

Question 302

Why does unconjugated bilirubin not get filtered by the kidneys?

Answer 302

adheres tightly to albumin

Question 303

Increased levels of unconjugated bilirubin levels are caused by what 2? (not caused by?)

Answer 303

1. from increased production 2. or decreased excretion usually not from hepatobiliary disease

Question 304

UA—urobilinogen: is positive when direct bilirubin is what?

Answer 304

excreted via the kidneys

Question 305

See slide 15

Answer 305

see slide 15

Question 306

See slide 16

Answer 306

See slide 16

Question 307

Ammonia1. What is Hepatic encephalopathy?2. Increased concentrations of what play a role in this?3. What is one part of treatment because of this?

Answer 307

1. Reversible impairment of neuropsychiatric function associated w/ impaired hepatic function2. Increased ammonia concentrations play a role3. One part of treatment is to decrease the ammonia levels

Question 308

Cycle of increased ammonia:3 steps of normal ammonia clearance?4 What happens when there is advanced liver failure?

Answer 308

1. Produced by the catabolism of colonic bacteria in the GI tract2. Enters the circulation via the portal vein3. The intact liver clears the ammonia from the circulation4. When there is advanced liver disease the liver cannot clear the ammonia

Question 309

Obtaining an ammonia level:1. Whats the most accurate way?2. Many factors can result in inaccurate results? 33. Following the ammonia level is necessary why?

Answer 309

1. Drawing an arterial ammonia level is the most accurate method to determine a level2. Many factors can result in inaccurate results:-Fist clenching-Use of a tourniquet-Whether the sample was put on ice or not 3. to know if treatment aimed at helping the liver is successful in lowering the ammonia level

Question 310

Biosynthetic Functionwhat two tests?

Answer 310

AlbuminPT

Question 311

1. Liver is the major site where what is synthesized?2. What is the most important serum plasma protein?3. This serum level reflects what? 34. Hypoalbuminemia can reflect other disorders such as?3

Answer 311

1. Liver is the major site where serum proteins are synthesized2. Albumin is the most important serum plasma protein3. The serum level reflects the:-Rate of synthesis-Rate of degradation-Volume of distribution4. Hypoalbuminemia can reflect other disorders:-Systemic inflammation-Malnutrition-When present with chronic liver disease it reflects the severity of the liver disease

Question 312

When albumin goes down how does this affect PT?

Answer 312

up

Question 313

Clotting factors—PT 1. The liver is the site of synthesis for the what?2. How does severe liver disease affect this?3. Instead of measuring the individual clotting factors the what is measured?4. What else is also measured?

Answer 313

1. 11 blood coagulation proteins2. clotting factor deficiency occurs3. PT4. INR

Question 314

Pancreatic Enzymestests? 2

Answer 314

AmylaseLipase

Question 315

Amylase & Lipase1. Both secreted by what?2. How are they affected by acute pancreatitis? 23. The level of elevation DOES NOT correlate with the level of what?It is important to correlate elevations of these enzymes with the history and clinical exam of the patient as well as with other studies

Answer 315

1. pancreas2. -Both can rise in acute pancreatitis—lipase remains elevated longer so is thought to be more accurate-Both may be in the normal range in acute pancreatitis3. damage to the pancreas

Question 316

Amylase:1. Main source in humans is what? 22. It is also secreted by what? 23. It rises early in what disease and is the first to drop?4. Function?

Answer 316

1. Main source in humans is -pancreas and -salivary glands2. It is also secreted by the -kidneys and the -reticuloendothelial system3. It rises early in pancreatitis and is the first to drop4. Function of amylase is to cleave starch into smaller polysaccharides

Question 317

Lipase1. Activity of all lipases is inhibited by what?2. Activity of the lipase in the pancreas depends on what?3. It remains elevated longer in ____________ so sometimes it alone is tested for?4. Function?

Answer 317

1. bile acids2. co-lipase and prevents the bile salts from degrading it3. pancreatitis 4. Function of lipase is to hydrolyze triglycerides into glycerol and free fatty acids

Question 318

Can't give what kind of vanco to clear C. Diff?

Answer 318

IV

Question 319

Stool examination includes:5

Answer 319

1. Microscopic exam:2. Stool culture3. Ova and Parasites (O & P) X 34. Clostridium difficile toxin5. Testing for occult blood in the stool

Question 320

What are the componenets of the microscopic stool analysis?4

Answer 320

1. RBCs2. Epithelial cells3. WBCs4. Fat globules

Question 321

Stool Analysis—General 4Microscopic General? 3

Answer 321

1. Bulk2. Color3. pH4. OsmolalityMicroscopic:+ RBCs—+ epithelial cells—+ WBCs—

Question 322

1. What would RBCs in the stool suggest? 32. What would epithelial cells in the stool suggest? 3. WBCs? 2

Answer 322

1. -cancer, -infection, -IBS2. irritated GI tract3. -infection, -IBS

Question 323

1. Fecal fat is detected by what?2. Increased amounts can indicate what?

Answer 323

1. detected with Sudan stain2. increased amounts can indicate malabsorption or pancreatitis

Question 324

Normal analysis microscopic:1. RBCs?2. Epithelial cells?3. Neutral fat globules?

Answer 324

1. RBCs--------------------------------none2. Epithelial cells---------------present3. Neutral fat globules---------0-2+

Question 325

What are Charcot-Leyden crystals----sometimes found in ?

Answer 325

parasitic infections (especially amebiasis)

Question 326

Color1. What is the normal color?2. If its clay color?3. Tarry?4. Red?5. Black?

Answer 326

1. Normal-----------------brown2. Clay color-------------biliary obstruction3. Tarry----------------- > 100 mL blood upper GI tract4. Red--------blood in large intestine, or undigested beets or tomatoes5. Black----------------------Blood

Question 327

What is infectious diarrhea defined as?

Answer 327

Acute diarrhea due to viruses & bacteria is self-limited & when evaluation fails to ID a pathogen noninfectious etiologies need to be considered

Question 328

For infectious diarrhea what would we see?

Answer 328

FECAL ANALYSIS--+for occult blood and WBCs support bacterial etiology

Question 329

Infectious diarrhea etiologies?3

Answer 329

Etiologies:1. Viruses most common cause2. Bacteria usually show signs of fever3. Parasites when persistent diarrhea or travel to endemic area or exposure

Question 330

When would we obtian stool cultures for infectious diarrhea?5

Answer 330

1. Immunocompromised patients2. Patients w/ comorbidities—increased risk for complications3. Patients w/ inflammatory bowel disease4. Patients w/ severe inflammatory diarrhea (including bloody diarrhea)5. Routine stool cultures test for: Shigella, Salmonella, Campylobacter**

Question 331

C difficile Colitis often develops with what kind of pts?2

Answer 331

1. Develops in patients treated w/ antibiotics or hospitalized patients2. Now also becoming more common in peds and geriatric pts.

Question 332

C Diff: Can test stool directly for what?

Answer 332

Can test stool directly for toxins A & B using ELISA which is found in 95% of patients w/ infected stoolSensitivity of test is 72-84%

Question 333

C diff aka?Treatment? 2

Answer 333

as—pseudomembranous colitisTreatment: 1. Metronidazole (Flagyl)2. Oral vancomycin

Question 334

When to send a stool samples for O & P:4

Answer 334

1. Persistent diarrhea (associated w/ Giardia, cryptosporidium and Entamoeba hystolytica)2. Persistent diarrhea following travel to countries w/ endemic parasites such as Russia, Nepal, or mountainous regions (even our Rocky mountains!)3. Persistent diarrhea w/ exposure to infants in daycare centers (associated w/ giardia & cryptosporidium)4. Bloody diarrhea w/ few or no fecal leukocytes

Question 335

Ova and Parasites.Specimens sent on consecutive days: How should we manage that? 2

Answer 335

1. Separated by at least 24 hrs for O & P examinations2. Parasite excretion is intermittent in contrast to bacterial pathogens

Question 336

H pylori Tests4

Answer 336

1. Endoscopic Biopsy:2. Serologic tests for IgG AB**3. Antigen in stool detects active infection & if negative confirms eradication**4. Urease breath tests:

Question 337

Endoscopic Biopsy: H. PyloriWhat two things are we testing during this?

Answer 337

1. Kit for rapid urease test—urease converts urea in kit to ammonia changing pH changes color2. Culture—can be used to determine antibiotic resistance

Question 338

Urease breath tests: H pylori1. What is this test based on?2. Process?3. What can the test determine?

Answer 338

1. Based upon the hydrolysis of urea by H. pylori to CO2 & ammonia2. A labelled carbon isotope is given by mouth—H. pylori liberates CO2 can then be detected in breath samples3. Test can determine if infection is active or if Rx has been successful

Question 339

Carcinoembryonic Antigen (CEA)‏1. Is a marker for what?2. Who else is this elevated in? 4

Answer 339

1. Marker for colon cancer2. Also elevated in >30% of patients w/ -breast, -lung, -liver and -pancreas adenocarcinomas

Question 340

Carcinoembryonic Antigen (CEA)‏Use?2(what are we NOT using this for?)

Answer 340

1. Monitoring for persistent, metastatic or recurrent adenocarcinoma of colon after surgery2. Determination of prognosis for patients w/ colon cancerNOT useful for local recurrence or screening because of low sensitivity and specificity

Question 341

Celiac Disease (CD) is what?

Answer 341

an immune disorder that is triggered by an environmental agent (the gliadin component in gluten) in genetically predisposed individuals

Question 342

Describe the pathway for wheat digestion

Question 343

Serologic studies are used to follow the course of the disease: 2

Answer 343

1. IgA antibodies to gliadin2. IgA antibodies to endomysium

Question 344

WHat are IgA antibodies to endomysium?

Answer 344

A structure of the smooth muscle connective tissue-Its presence is nearly pathognomonic for CD

Question 345

Gliadin receptors on intestinal epithelial cells may mediate what?

Answer 345

transport of gliadin peptides into the lamina propria where T cell activation occurs—this may someday lead to drug therapy for CD

Question 346

Which is a normal small intestine and which as celiac?

Question 347

Describe the PP of Celiac Disease

Question 348

CD Classic Clinical manifestations4

Answer 348

1. Diarrhea w/ bulking, foul-smelling, floating stools due to steatorrhea (malabsorption)2. Weight loss3. Vitamin deficiencies—B vitamins, iron, copper, zinc, vitamins A, D, E, & magnesium4. On small bowel biopsy—villlous atrophy

Question 349

Atypical Manifestations of CD?4

Answer 349

1. Minor GI symptoms2. Can have anemia, osteoporosis, arthritis3. Increased LFTs, neurological symptoms, or infertility4. Most show severe mucosal damage & possess the CD antibody pattern

Question 350

1. Silent CD is recognized how? 2. Often have changes in what?3. How do they usually present?

Answer 350

1. Recognized incidentally based upon screening for antibodies 2. Often have some changes in mucosa of the small bowel 3. They DO NOT show clinical symptoms but may complain of fatigue

Question 351

Several studies have shown that patients with CD have a slight increased of malignancies: such as? 6(but what is there a decrease in?) 

Answer 351

1. Non-Hodgkin’s lymphoma2. Small intestinal adenocarcinoma3. Hepatocellular carcinoma4. GI cancer5. Lymphoproliferative disease6. Hodgkin lymphoma Studies also showed a DECREASED risk of breast cancer!

Question 352

Associated Conditions with CD?9

Answer 352

1. Dermatitia herpetiformis (autoimmune rash)2. Type I DM3. Down syndrome4. Liver disease5. Autoimmune thyroid disease6. GERD7. Inflammatory bowel disease8. Menstrual and reproductive issues in women9. Infertility in men

Question 353

What is this a picture of?

Answer 353

Dermatitis herpitiformis 

Question 354

Baseline Serology--Diagnosis1. What should we begin with?2. What are these?3. Used in what ages?

Answer 354

1. Begin w/ IgA anti-tissue transglutaminase (TTG):2. Auto-antibodies against the bodies on tranglutiminases***3. Used for anyone over the age of 2Single preferred test for detection of CD!

Question 355

If High probability of disease & if IgA based serology is negative: What tests should we do? 2

Answer 355

1. Test Total IgA or2. IgG-deaminated gliadin peptides (DGP)

Question 356

1. Patients w/ POSITIVE serology should undergo what?2. from where? 2 

Answer 356

1. small bowel biopsy2. -1-2 biopsies from the duodenal bulb-At least 4 from the 2nd and 3rd portion of the duodenum

Question 357

1. Patients on a gluten free diet who have NEGATIVE serology's—should have what done?2. What is this used to determine?3. If negative?

Answer 357

1. HLA/DQ1/DQ8 testing:2. Determine if the patient is genetically susceptible to the disease3. If negative CD is ruled out

Question 358

If the serology is positive but the small bowel biopsy is negative the patient can be managed how?

Answer 358

high gluten diet and be re-biopsied after 6-12 wks.

Question 359

1. Individuals w/ low pretest probability (purely Chinese, Japanese and Sub-Saharan African descent): recommend what kind of testing?2. Why?3. Downside?

Answer 359

1, recommend—IgA endomysial antibody test:2, It has higher specificity3. It is more costly

Question 360

Some people are “sensitive” to gluten without having CD. How do they present?

Answer 360

They get diarrhea, feel “ILL” and bloated and find if they eliminate gluten from their diet they feel better

Question 361

Treatment—6 key elements 

Answer 361

1. Consultation w/ a skilled dietitian2. Education about the disease3. Lifelong adherence to a gluten free diet4. Identification and treatment of nutritional deficiencies5. Access to an advocacy group6. Continuous ongoing follow-up by a multidisciplinary team

Question 362

General Rules for Gluten Free7

Answer 362

1. Foods containing wheat, rye and barley AVOID2. Soybean or tapioca flours, rice, corn, buckwheat and potatoes are safe3. READ labels4. Distilled alcohol, vinegar, and wine are gluten free5. Beers, ales, lagers, and malt vinegars should be avoided because they are often made w/ gluten grains6. Dairy products may not be well tolerated initially since many patients w/ CD can have secondary lactose intolerance—initially dairy should be avoided7. Oats should be introduced into the diet w/ caution

Question 363

Lactose IntoleranceSymptoms: (due to low levels of lactase in small bowel)3

Answer 363

1. Diarrhea2. Abdominal pain3. Flatulence

Question 364

What causes lactose intolerance symptoms?

Answer 364

Unabsorbed lactose in the large intestine 

Question 365

Developmental lactase deficiency:1. Results from what?2. Infants born at _____ weeks gestation have reduced lactase activity

Answer 365

1. Results from low lactase levels as a result of prematurity2. 28-32

Question 366

Congenital lactase deficiency:1. Inherited how?2. What is the PP? 

Answer 366

1. Rare autosomal recessive disorder2. Absence of any lactase activity in the small intestine 

Question 367

Secondary lactase malabsorption:1. Bacterial overgrowth or stasis may be associated w/ what?2. Seem w/ any mucosal injury to the small bowel such as what? 3

Answer 367

1. increased fermentation of dietary lactose in the small bowel2. -gastroenteritis,-CD,-IBD [especially 

Question 368

Clinical Manifestations of lactose intolerance?5

Answer 368

1. Abdominal pain—crampy, usually periumbilical and lower quadrants 2. Bloating 3. Flatulence 4. Diarrhea 5. Vomiting—in adolescents 

Question 369

Diagnosis for lactose intolerance? 2

Answer 369

1. Lactose tolerance test:2. Lactose breath hydrogen test:

Question 370

Describe the lactose tolerance test:1. Process? 22. Positive result is?3. Downside?

Answer 370

1.-50g test dose given in adults-Blood glucose levels drawn at—0, 60 and 120 minutes2. An increase in blood glucose by less than 20 mg/dL plus symptoms is diagnostic3. Cumbersome and time-consuming

Question 371

Describe the Lactose breath hydrogen test:1. Process? 22. what is a positive result?

Answer 371

1.-Oral lactose given in fasting state [2 gm/kg—max 25 mg]-Breath hydrogen levels measured at baseline and 30 min intervals for 3 hrs. after lactose ingestion2. Values over 20 ppm diagnostic

Question 372

Treatment for lactose intolerance?4 

Answer 372

1. Dietary restriction of lactose intake:-Read labels-Usually some lactose containing foods [cheese] can be tolerated 2. Substitution of alternative sources to maintain energy and protein intake 3. Administration of commercially available enzyme substrate** 4. Maintenance of calcium and Vit D intake

Question 373

1. What is ileus?2. Etiologies? 7

Answer 373

1. Definition: temporary absence of the normal contractile movements to the intestinal wall 2. Etiologies:-Postoperative—especially abdominal when the intestine’s have been manipulated-Drugs:  opioids and anticholinergics-Hypothyroidism-Electrolyte disorders—hypokalemia, hypercalciemia-Intestinal peritonitis-Kidney failure-Pancreatitis

Question 374

Clinical Manifestations of ileus?5

Answer 374

1. Bloating 2. N/V 3. Crampy abdominal pain—pain precedes vomiting when associated with acute surgical etiology 4. Severe constipation 5. Loss of appetite

Question 375

Ileus DDx?4

Answer 375

1. Adynamic [Paralytic] Ileus 2. Intestinal obstruction 3. Acute abdomen 4. Post-op adhesive disease

Question 376

How do we diagnosis ileus?4

Answer 376

1. X-rays 2. Lytes 3. CBC 4. CMP including magnesium

Question 377

Treatment for ileus?4

Answer 377

1. NPO advancing to clear liquids as tolerated 2. IV fluids to maintain hydration and correct electrolyte abnormalities 3. Stop drugs that make the ileus worse 4. Occasionally NG tube

Question 378

Anal Fissures definition?

Answer 378

Painful linear tear or crack in the distal anal canal

Question 379

Etiologies 3Most common area of injury?

Answer 379

Usually from trauma to anal canal1. Defecation2. Straining3. ConstipationMost commonly occur in the 12 or 6 O’clock area

Question 380

Clinical presentation of anal fissures?2

Answer 380

1. c/o severe tearing pain during defecation2. Mild associated hematochezia--Blood on stool or toilet paper

Question 381

Anal FissureWhat confirms the Dx?

Answer 381

PE:Confirmed by visual inspection of the anus

Question 382

On PE what would we find for acute anal fissures?Chronic?

Answer 382

1. Acute: look like cracks in the epithelium2. Chronic: fibrosis and development of a skin tag

Question 383

First line treatment for anal fissure? 3Seond line treatment? 1SE? 6

Answer 383

1. First-line-Fiber supplements, -stool softeners-sitz baths2. Second-line-0.4% nitroglycerin ointment-Bid for 6-8 weeks3. SE-Headaches and dizziness-Botulinum toxin (Botox)-Inject into internal anal sphincter-Last about 3 months-Internal anal sphincterotomy-Risk is minor fecal incontinence

Question 384

Perianal abscess1. PP?2. Appears as what?3. Most common type?

Answer 384

1. Anal glands at the base of the rectum become infected 2. Appears as a boil-like swelling near the anus3. Most common type is perianal abscess

Question 385

Perianal abscess1. Causes? 32. Risk factors? 3

Answer 385

1. Causes-Anal fissure/fistulas-hemorrhoids-Blocked anal glands2. Risk factors-Colitis-Inflammatory bowel disease-DM2

Question 386

Perianal abcess Clinical presentation4Deeper abscesses present how?3

Answer 386

1. Constant pain, throbbing and worse when sitting2. Swelling and redness around the anus3. Discharge of pus from around the anus4. Painful bowel movements1. Fever2. Chills3. malaise

Question 387

Perianal abscess1. Lab studies?2. Treatment? 4

Answer 387

1. Laboratory studiesWound cultures when I&D doneTreatment1. I&D2. Packing and return in 24 hours3. Sitz baths tid and after bowel movements4. f/u in 2-3 weeks for wound evaluation and inspection for possible fistula formation

Question 388

1. Anal fistula aka?2. Usually results from what?3. Etiology? 3

Answer 388

1. Also known as fistula-in-ano2. Usually results from previous or current anal abscess3. Etiology-Anorectal abscess-Crohn’s -Radiation proctitis

Question 389

Anal Fistula Clinical presentation 3PE2

Answer 389

Clinical presentation1. History of drained abscess2, Anorectal pain3. Purulent drainage and irritation from the skinPE1. Identification of the external opening that drains pus, blood or stool2. DRE may express pus or stool from the opening

Question 390

Treatment of anal fistula?1Complex fistulas?2

Answer 390

Treatment1. FistulotomyComplex fistulas1. Fibrin glue2. Fistula plug

Question 391

Pruritus Ani1. What is this?2. Characterized by what?

Answer 391

1. Perianal itching or discomfort2. An itch-scratch-itch cycle--Skin becomes excoriated and secondary infections

Question 392

Causes of Pruritis Ani?6

Answer 392

1. Idiopathic2. Hygiene related3. Fistulas/fissures4. Fecal incontinence5. Parasites6. Lichens sclerosis

Question 393

Prutitis PE?4

Answer 393

1. Inspection of the area may reveal anal excoriations and erythema2. Hygiene issues3. Chronic issues show thickened or leathery skin4. Anoscopy

Question 394

Pruritis treatment and prevention6

Answer 394

1. Treat underlying cause2. Avoid spicy and acidic foods3. After BM clean with unscented wipes4. Place gauze or cotton ball next to anal opening5. Talcum powder6. Use zinc oxide or hydrocortisone ointment

Question 395

1. Rectal Prolapse aka?2. What is it?3. Common in who? 3

Answer 395

1. Also called Rectal Procidentia2. Painless protrusion of the rectum through the anus3. -Common in older adults with long history of constipation and weak pelvic floor muscles-More common in women over age 50-Can also occur in infants

Question 396

Rectal Prolapse symptoms?3

Answer 396

Symptoms1. Feeling a bulge or appearance of reddish-colored mass that extends outside the anus2. Pain in the anus or rectum 3. Leakage of blood or stool

Question 397

Causes of rectal prolapse? 4

Answer 397

Causes1. Chronic constipation or diarrhea2. Straining during BM3. Weakness of the anal sphincter4. Damage to nerves

Question 398

Diagnosis of rectal prolapse? 5

Answer 398

Diagnosis1. Anal EMG2. Anal manometry3. Anal ultrasound4. Colonoscopy5. proctosigmoidoscopy

Question 399

Rectal prolapse Treatment? 2

Answer 399

1. Treat first at home with stool softeners and pushing the fallen tissue back up into the anus by hand2. Surgery

Question 400

Rectal prolapse surgeries? 2Recovery consists of? 2

Answer 400

1. Surgery-Abdominal repair-Rectal (perineal) repair2. Recovery-3-5 hospital stay-Complete recovery in 3 months

Question 401

1. What is a Pilonidal Cyst?2. Usually happens how?3. Occurs in who?4. Risk factors?

Answer 401

1. Cyst near the natal cleft of the buttocks that often contains hair or skin debris2. Usually happens when hair punctures the skin and becomes embedded3. Occurs in hairy young men4. Sitting for long periods of time can be a risk

Question 402

Pilonidal cyst1. Clinical presentation? 32. Risk factors? 3

Answer 402

Clinical presentation1. Pain2. Erythema and swelling of the skin3. Drainage of foul smelling pus or blood from the opening of the skinRisk factors1. Obesity2. Prolonged sitting3. Local trauma/irritation

Question 403

Pilonidal cystTreatment and prevention 3

Answer 403

1. I & D cyst first--May need to leave open or pack to heal2. If reoccurs will need surgical cyst removal3. Antibiotics

Question 404

1. Usually in the setting of what?2. What kind of antibiotics for Pilonidal cyst? 2

Answer 404

1. Usually in setting of cellulitis2. First generation cephalosporin (cefazolin) plus metronidazole (Flagyl)

Question 405

1. What are hemorrhoids?2. Arise from where?3. What are the two different kinds?

Answer 405

1. Are dilated veins of the hemorrhiodal plexus in the lower rectum- Normal vascular structures in the anal canal2. Arise from a channel of arteriovenous connective tissue that drains into the superior and inferior hemorrhoidal veins3. -External hemorrhoids -Internal hemorrhoids

Question 406

Classification of Hemorrhoids?Describe grades I-IV?

Answer 406

Classification1. Grade IHemorrhoids that do not prolapse2. Grade IIHemorrhoids prolapse on defecation and reduce spontaneously3. Grade IIIHemorrhoids prolapse on defecation and must be reduced manually4. Grade IVHemorrhoids are prolapsed and cannot be reduced manually

Question 407

Hemorrhoids causes?4

Answer 407

1. Pregnancy2. Frequent heavy lifting3. Repeated straining during defecation4. Constipation

Question 408

Clinical presentation1. Most often they present how? 22. External hemorrhoids may become thrombosed-Whats it look like?-Complications? 2-Usually resolves when?-Swelling lasts how long?-Can have what symptom around the anus?

Answer 408

1. -Often asymptomatic or -may simply protrude2. -Painful and purplish swelling-Rarely ulcerate and cause minor bleeding-Usually resolves in 2-3 days-Swelling last a few weeks-Can have itchiness around the anus

Question 409

1. Internal hemorrhoids manifest how?2. 3 main symptoms?

Answer 409

1. with bleeding after defecation2. -On stool or TP-Mucous and fecal incontinence-Itchiness

Question 410

What are Strangulated hemorrhoids?

Answer 410

strangulated hemorrhoid an internal hemorrhoid that has prolapsed sufficiently and for a long enough time for its blood supply to become occluded by the constricting action of the anal sphincter.

Question 411

Diagnosis of hemorrhoids? 2

Answer 411

1. Anoscopy2. Sometimes sigmoidoscopy or colonoscopy

Question 412

Treatment of hemorrhoids1. First line 32. Second line?3. Third line?

Answer 412

1. Symptomatic treatment is usually all that is needed-Stool softeners/Fiber-Sitz baths after BM -Anesthetic ointments2. Second-line would be banding if conservative treatment is unsuccessful3. Third-line would be surgical

Question 413

1. Hernia definition?2. They are usually harmless but what can cause serious complications?3. When does it become a medical and surgical emergency?

Answer 413

1. A protrusion, bulge, or projection of an organ or part of an organ through the body wall that normally contains it2. Hernias by themselves usually are harmless, but nearly all have potential risk of having their blood supply cut off (becoming strangulated)3. If the blood supply is cut off at the hernia opening in the abdominal wall

Question 414

Types of hernias?6

Answer 414

1. Inguinal2. Umbilical3. Incisional /Ventral4. Epigastric5. Femoral6. Spigelian

Question 415

What are the following found:1. Inguinal2. Umbilical3. Incisional /Ventral4. Epigastric5. Femoral

Answer 415

1. Inguinal-Direct- near the opening of the inguinal canal-Indirect- At the opening of the inguinal canal2. Umbilical- at the navel3. Incisional /Ventral- at the site of a previous surgery4. Epigastric- upper abdomen at the midline5. Femoral- Occur in the femoral canal

Question 416

What is the most common type of hernia in adults?

Answer 416

Inguinal hernia

Question 417

Inguinal hernia1. What is it?2. Risk factors? 3

Answer 417

Weak area occurs in the inguinal canal where the spermatic cord or round ligament exits the abdomenRisk factors1. History of hernia or repair 2. Chronic cough or constipation3. Abdominal wall injurysmoking

Question 418

Whats the most common type of inguinal hernia?

Answer 418

indirect

Question 419

Indirect inguinal hernias1. Hernia protrudes where?2. Hernia sac is located where?3. Sometimes it can protrude into where?4. More common in who?

Answer 419

1. Hernia protrudes through the internal inguinal ring2. Hernia sac is located lateral to the inferior epigastric artery3. Sometimes the hernia will protrude into the scrotum4. Can occur at any age, but becomes more common as people age

Question 420

Direct Inguinal1. Protrudes where?2. It is a result of what?3. Rarely protrudes where?4. Almost exclusively occurs in what people?

Answer 420

1. Protrude medial to the inferior epigastric vessels within the Hesselbach’s triangle 2. Result of a weakness in the floor of the inguinal canal3. Rarely protrude into the scrotum4. Almost always occur in older individuals as their abdominal walls weaken with age and stretching

Question 421

What are the boundaries of Hesselbach triangle:1. Laterally?2. Medially?3. Inferiorly?

Answer 421

1. inferior epigastric artery2. lateral border or restus abdominis3. Base/Inguinal ligament

Question 422

1. Where is a femoral hernia located?2. More common in what gender?3. Least common type of groin hernia but has a high chance of what?

Answer 422

1. Hernia located inferior to the inguinal ligament and protrudes through the femoral ring2. More common in women3. strangulation

Question 423

Inguinal hernias clinical presentation?3

Answer 423

1. Painless bulge in the groin or scrotum2. Groin discomfort of pain3. Swelling or tugging in the groin

Question 424

When would you be concerned that the hernia has strangulated?2

Answer 424

1. Sudden pain, 2. N/V

Question 425

PE inguinal hernia:1. Most common finding is what?2. Exam best done when?

Answer 425

1. Bulge in groin2. Exam best done with patient standing and asking them to cough or Valsalva

Question 426

On PE what signs would tell us its a strangulated inguinal hernia?4

Answer 426

1. Irreducible2. Painful to palpation3. N/V4. Patient may appear ill with or without fever

Question 427

Inguinal herniadiagnosis?3

Answer 427

1. Usually done with history and exam2. Not apparent, then initial study is groin ultrasound3. CT/MRI

Question 428

Treatment inguinal 1. nonsurgical? 22. Surgical? 2

Answer 428

Non-surgical1. Watchful waiting2. TRUSSSurgical1. Open repair2. Laparoscopic repair

Question 429

1. Umbilical hernia is what?2. More common in what population?

Answer 429

1. An outward bulging of the lining of the abdomen or abdominal organs around the belly button2. More common in infants

Question 430

Causes of umbilical hernia?

Answer 430

Muscle through which the umbilical cord passes doesn’t close completely after birth

Question 431

Umbilical hernia:1. Clinical presentation?2. Only infants?3. Adults? 2

Answer 431

1. A soft swelling or bulge near the umbilicus2. In infantsMore noticeable when baby cries, coughs or strains3. Adults-May cause abdominal discomfort-Bulging with straining or coughing

Question 432

Umbilical hernia causes?4Treatment?

Answer 432

1. Obesity2. Multiple pregnancies3. Fluid in abdominal cavity (ascites)4. Previous abdominal surgerySurgery+/- mesh

Question 433

1. What is a incisional/ventral hernia?2. Describe reoccurrence after repair?3. What has shown to help with this?

Answer 433

1. Abdominal surgery causes a flaw in the abdominal wall that must heal on its own--This flaw can create an area of weakness where a hernia may develop2. After surgical repair they have a high reoccurrence rate (20-45%)3. Use of mesh has helpedIatrogenic

Question 434

1. What is an epigastric hernia?2. What age group?3. What may cause discomfort with this?4. Risks for this are what? 2

Answer 434

1. A type of hernia that develops in the epigastrium between the breast bone and belly button2. Usually appear in adults3. May trap fat and other tissues which cause discomfort4. Risk are -obesity and -pregnancy

Question 435

1. What is a spigelian hernia?2. Presentation? 63. Diagnosed how?4. Treated how?Rare

Answer 435

1. Hernia through the spigelian fascia2. -Often no notable swelling-Risk of strangulation is high due to small size-Most occur on right side-intermittent mass, -localized pain, or -N/V3. Diagnosed made with ultrasound4. Surgery is the treatment of choice

Question 436

Acute abdominal pain:Which populations pose the most diagnostic challenge?3

Answer 436

1. The elderly, 2. immunocompromised and 3. women of childbearing age pose special diagnostic challenges

Question 437

Acute abdomenDDx: Immediate life threatening conditions?8

Answer 437

1. AAA2. Mesenteric ischemia3. Perforation of GI tract4. Acute bowel obstruction5. Volvulus6. Ectopic pregnancy7. MI8. Splenic rupture

Question 438

Pathophysiology of visceral pain:1. Where is it coming from?2. Innervated by what?3. Responds to sensations of what? 24. Describe the pain.

Answer 438

1. From abdominal viscera2. Innervated by autonomic nerve fibers3. Respond to sensations of -distention and -muscular contraction4. Pain is typically vague, dull and nauseating

Question 439

Pathophysiology of Somatic pain:1. Where is it coming from?2. Innervated by what?3. Responds to sensations of what? 34. Describe the pain.

Answer 439

1. From parietal peritoneum2. Innervated by somatic nerves3. Respond to -irritation from infection, -chemical and -inflammatory process4. Pain is sharp and well localized

Question 440

Pathophysiology of referred pain:1. Pain is percieved where?2. Results from what?

Answer 440

1. Pain perceived distant from its source2. Results from convergence of nerve fibers at the spinal cord

Question 441

Pathophysiology of peritonitis:1. Caused by what?2. What are the most serious cases that cause this?3. Causes fluid shift into the peritoneal cavity and bowel, leads to what? 2

Answer 441

1. Inflammation of the peritoneal cavity2. Most serious cause is perforation of GI tract (Blood) 3. -severe dehydration and -electrolyte problems

Question 442

Most common extrauterine cause for abdominal surgery in pregnant women?

Answer 442

Appendicitis

Question 443

Appendicitis1. First symptoms? 32. Leads to?3. What kind presents with urinary symtpoms and diarrhea?

Answer 443

1. -Anorexia and -vague periumbilical discomfort that -develops into RLQ pain2. N/V generally not first symptoms3. Pelvic appendix can present with urinary symptoms and diarrhea

Question 444

Biliary disease:\Clinical presentation?4

Answer 444

1. Acute cholecystitis complain of RUQ or epigastrium pain2. Pain may radiate to right shoulder or back3. N/V and anorexia4. Murphy’s sign may be present

Question 445

Biliary disease:Progress seriously to what?

Answer 445

Progression of septic shock can occur

Question 446

Pancreatitis:Clinical presentation?4

Answer 446

1. Pain is steady in upper abdomen2. Band-like radiation to the back is common3. Pain often reaches maximum intensity within 10-20 minutes of onset4. N/V common

Question 447

Diverticular disease:1. Most common complaint?2. Other symptoms? 2

Answer 447

1. LLQ pain most common complaint2. -N/V and +/- change in bowel habits

Question 448

Peptic ulcer disease1. Symptoms? 32. Complications? 2

Answer 448

1. -Epigastric pain, -indigestion-reflux symptoms 2. Complications-Bleeding-perforation

Question 449

Incarcerated hernia1. What is the most common?2. Cause what kind of symptoms and should be managed how?

Answer 449

1. Inguinal are most common with mild lower abdominal discomfort exacerbated by straining2. Incarcerated hernias cause severe pain and require immediate surgical consultation

Question 450

Complications of Inflammatory bowel disease?6

Answer 450

1. pain, 2. bleeding, 3. perforation, 4. bowel obstruction, 5. fistula and abscess formation6. toxic megacolon

Question 451

Irritable bowel syndrome1. Symptoms need to last how long for diagnosis?2. presentation?

Answer 451

1. Symptoms need to persist for 3 months over a one year period2. Abdominal pain associated with change in stool frequency or consistency

Question 452

Features of high risk abdominal pain:1. History? 72. Pain characteristic? 43. Exam findings? 3

Answer 452

1.-Age over 65-Immunocomprimised-Alcoholism-Cardiovascular dz-Major comorbidities-Prior sugery or recent GI instrumentation-Early pregnancy2. -Sudden onset-Maximal at onset-Pain then subsequent vomiting-Constant pain of less than two days duration3. -Tense or rigid abdomen-Involuntary guarding-Signs of shock

Question 453

Important History for acute abdomen pain?6

Answer 453

1. Age2. Sex3. PMHX & SHX4. Meds5. Characterize pain as precisely as possible6. Women of childbearing age pregnancy status must be determined

Question 454

See slide 99

Answer 454

See slide 99

Question 455

PE for acute abdomen pain?7

Answer 455

1. General appearance is important2. Begin with inspection and auscultation3. Followed by palpation and percussion4. Rectal and pelvic exam5. Palpation begins away from area of greatest pain6. Look for guarding, rigidity and rebound7. Surgical scars should be palpated

Question 456

Red flags on physical exam?4

Answer 456

Red flags1. Severe pain2. Signs of shock3. Signs of peritonitis4. Abdominal distention

Question 457

Acute abdominal pain testing?5

Answer 457

1. Urine pregnancy test for all women of childbearing ageException2. Serum lipase and amylase strongly suggest diagnosis of acute pancreatitis3. Plain x-rays4. US5. CTCBC, chemistries, UA are of little value

Question 458

What are plain xrays good for in abdominal pain assessment?3

Answer 458

Helpful for 1. bowel obstruction, 2. bowel perforation, 3. radiopaque foreign body

Question 459

What are US good for in abdominal pain assessment?4

Answer 459

1. Biliary tract disease2. Ectopic pregnancy3. Appendicitis in children4. AAA

Question 460

What are CT good for in abdominal pain assessment?

Answer 460

Study of choice in evaluation of undifferentiated abdominal painCT with oral and IV contrast is diagnostic in about 95% of patients with significant abdominal pain

Question 461

What are the four important key points for acute abdominal pain?4

Answer 461

1. Look for life-threatening causes first2. Rule out pregnancy in women of childbearing age3. Seek signs of peritonitis, shock, and obstruction4. Blood test are of minimal value except specific labs

Question 462

Risk factors for colorectal cancer?6

Answer 462

1. Age > 502. History of adenomatous polyps3. Personal history of inflammatory bowel disease4. Family history5. African-American or Eastern European Jews6. Type 2 DM

Question 463

Adenomatous polyps (adenomas) increase colon cancer risk1. What characteristics of these make the risk greater? 22. What kind of polyps do not increase risk?

Answer 463

1. Large in size or multiple polyps increase risk2. Hyperplastic polyps do not increase risk

Question 464

Lifestyle related factors:1. What kind of diet would put you at risk for colon cancer? 22. What other lifestyle factors would contribute to this? 4

Answer 464

1. High in -red meat (beef, pork, lamb) and processed meats-Low fruit and vegetable consumption2. -Physical inactivity-Obesity-Smoking-Heavy alcohol useSounds like typical American diet and lifestyle

Question 465

How does having a first degree relative with colorectal cancer increase your risk of cancer?

Answer 465

First degree relative with colorectal cancer doubles risk-Even higher risk if that person was 45 years or younger at diagnosis-Family members with adenomatous polyps also increases risk

Question 466

What are inherited syndromes that would increase your risk of colon cancer?4

Answer 466

1. Familial Adenomatous Polyposis (FAP)-1% of all colorectal cancers2. Hereditary non-polyposis colon cancer (HNPCC)-2-4% of all colorectal cancers3. Turcot syndrome4. Peutz-Jeghers syndrome

Question 467

Even after adjusting for obesity what disease increases risk of colon cancer and also has a less favorable outcome if they are diagnosed?

Answer 467

Type 2 Diabetes

Question 468

Previous treatments for other cancers also increase risk. Specially what two?

Answer 468

Testicular cancerProstate cancer

Question 469

Colorectal Cancer Screening Tests6

Answer 469

1. Flexible sigmoidoscopy2. Colonoscopy3. Double-contrast barium enema4. Virtual colonoscopy5. Fecal Occult Blood Test (FOBT)…stool guaiac test6. Fecal Immunochemical Test (iFOBT or FIT)

Question 470

What does guaiac detect in the stool?

Answer 470

Guaiac detects heme in stool

Question 471

Advantages of Fecal Immunochemical Test (iFOBT or FIT)?4

Answer 471

1. More accurate measurement 2. Less false positives3. No need to avoid meat and vitamin C4. Uses antibodies to detect HB in stool

Question 472

Flexible Sigmoidoscopy1. Advatnages? 32. Done every how many years?3. Views how much of the colon?4. Disadvantages? 35. Small risk of what? 3

Answer 472

1. -Fairly quick and safe-Sedation usually not used-Does not require a specialist to perform2. Done every 5 years3. Views only about a third of the colon4. -Can miss small polyps-Can’t remove all polyps-Will need a colonoscopy if abnormal5. Small risk of -bleeding, -infection or -bowel tear

Question 473

What is the preferred method of colon cancer screening?

Answer 473

colonoscopy

Question 474

Colonoscopy1. Advantages? 22. Done every how many years?3. Disadvantages? 34. Small risk of what? 3

Answer 474

1. -Can usually view the entire colon-Can biopsy and remove polyps2. Done every 10 years3. -Can miss small polyps-Full bowel prep needed-Sedation is needed4. Small risk of -bleeding, -bowel tears or infection-Expensive

Question 475

Double Contrast Barium Enema1. Advantages? 32. Done every how many years?3. Disadvantges? 5

Answer 475

1. -Can usually view the entire colon-Relatively safe-No sedation needed2. Done every 5 years3. -Can miss small polyps-Full bowel prep needed-Some false positive test results-Can’t remove polyps during testing-Colonoscopy will be needed if abnormal

Question 476

Double Contrast Barium Enema1. Test has largely been replaced by what?2. Use has also declined with the increasing use of what? 2

Answer 476

1. colonscopy2. endoscopic and CT procedures

Question 477

Virtual Colonoscopy1. Advanatges? 32. Done every how many years?3. Disadvantages? 4

Answer 477

1. -Fairly quick and safe-Can usually view the entire colon-No sedation needed2. Done every 5 years3. -Full bowel prep needed-Can miss small polyps-Some false positive test results-Colonoscopy will be needed if abnormal

Question 478

Virtual Colonoscopy1. aka?2. What is given first in the process?3. What kind of imaging is done and how?

Answer 478

1. Also known as CT colonography2. Air enema is given3. CT scan of the colon done X 2 (supine and prone positions)

Question 479

Fecal Occult Blood Test (FOBT)1. Advantages? 42. Disadvantages? 33. Should be done how often?4. Process? 2

Answer 479

1. -No direct risk to the colon-No bowel prep needed-Sampling done at home-Inexpensive2. -May produce false positive test results-May have pre-test dietary restrictions-Colonoscopy will be done if abnormal3. Should be done yearly4. -Need 3 different stool samples-Patient drops off or mails in cards

Question 480

FOBT1. Avoid _______ for 7 days prior to testing2. why?3. Avoid WHAT for 3 days prior to testing?4. why?5. Avoid _________ for 3 days prior to testing6. WHy?

Answer 480

1. NSAIDs2. Can cause false positives3. vitamin C in excess of 250mg daily (supplements or foods) 4. False positives5. red meats6. False positives

Question 481

Fecal Immunochemical Test (FIT) or iFOBT: Difference between this and the FOBT?9

Answer 481

1. No pre-test dietary or medication restrictions2. More accurate measurement 3. Less false positives4. No need to avoid meat and vitamin C5. Uses antibodies to detect HB in stool6. Only need one day’s sample7. Automated vs manual system8. Closed system, less risk of exposure9. Better patient compliance

Question 482

American Cancer Society Guidelines for Colon Cancer Screening

Answer 482

Beginning at age 50 (to age 75-85) men and women at average risk should be screened with:Colonoscopy every 10 years

Question 483

If colonoscopy refused or contraindicated pick one of the following:3If all imaging tests refused or contraindicated then what? 2

Answer 483

1. Flexible sigmoidoscopy every 5 years2. Double contrast barium enema every 5 years3. Virtual colonoscopy every 5 years1. FOBT yearly on 3 stool samples2. Or FIT x 1 yearly

Question 484

Exceptions to the guidelines4

Answer 484

1. African-Americans 2. If at high risk for colon cancer the guidelines are more aggressive3. Familial adenomatous polyposis (FAP) –4. Hereditary nonpolyposis colon cancer (HNPCC)

Question 485

1. African american should begin screening when?2. Familial adenomatous polyposis (FAP) – yearly flexible sigmoidoscopy beginning at age _____ years. If genetic testing is positive consider ________.3. Hereditary nonpolyposis colon cancer (HNPCC) – colonoscopy every _____ years beginning at age _____ years or ____ years before the youngest case in the immediate family

Answer 485

1. should begin screening at age 452. 10-12, colectomy3. 1-2, 20-25, 10

Question 486

If at high risk for colon cancer the guidelines are more aggressivesuch as?3

Answer 486

1. If 1st degree family member with colon cancer need colonoscopy 10 years prior to the relative’s age at diagnosis2. Inflammatory bowel disease (UC and Crohn’s) – colonoscopy every 1-2 years3. Personal history of adenomatous polyps or colon cancer – colonoscopy 1 yr post resection then every 3-5 yrs

Question 487

Risk factors for HCC(Hepatocellular carcinoma)4

Answer 487

1. Hepatitis B viral (HBV) infection2. Chronic hepatitis C virus (HCV) infection3. Hereditary hemochromatosis4. Cirrhosis of almost any cause80% of cases are due to underlying Chronic Hepatitis B or C

Question 488

Further risk factors for HCC5

Answer 488

1. Nonalcoholic fatty liver disease2. Diabetes mellitus3. Chronic alcohol abuse4. Chronic tobacco abuse5. Alpha-1 antitrypsin deficiency

Question 489

HCC Screening needed for…. 8

Answer 489

1. All patients with cirrhosis regardless of etiology2. Chronic Hepatitis B infection +3. Asian (men > 40, women > 50)4. African and African-Americans5. Family history of HCC6. Caucasians with Chronic Hepatitis B +7. Active inflammation and high viral load for several years8. Start men > 40, women > 50

Question 490

What Screening tests are recommended for HCC?2

Answer 490

1. Liver ultrasound-Every 6 months2. If abnormalities found on liver ultrasound patient will need further workup

Question 491

Hepatitis __ infection highly associated with development of hepatocellular carcinoma

Answer 491

B

Question 492

Esophageal cancer risk factors6

Answer 492

1. Age > 552. Men are 3x more likely than women to develop 3. ETOH abuse4. Tobacco use5. Obesity6. Diet

Question 493

What kind of diet would increase risk for esophageal cancer?2

Answer 493

1. High in processed meats2. Low in fruits and vegetables

Question 494

Medical conditions associated with esophageal cancers6

Answer 494

1. HPV infection2. GERD3. Barrett’s esophagus (Caused by GERD)4. Achalasia (Narrowing of distal esophagus)5. Tylosis (Esophageal papillomas)6. Plummer-Vinson syndrome (Esophageal webs)

Question 495

Those with conditions that increase their risk need periodic endoscopies. Such as? 3

Answer 495

1. Barrett’s, 2. achalasia, 3. Plummer-Vinson syndrome

Question 496

Increasing dietary fiber can be beneficial for treatment of:4

Answer 496

1. Hemorrhoids2. Constipation3. Diarrhea4. Diverticulosis

Question 497

What are the two types of fiber?

Answer 497

1. Soluable2. Insoluable

Question 498

Describe soluable fiber?Which foods?

Answer 498

1. Dissolves in water2. oatmeal, oat cereal, lentils, apples, oranges, pears, oat bran, strawberries, nuts, flaxseeds, beans, dried peas, blueberries, psyllium, cucumbers, celery, and carrots.

Question 499

Describe insoluable fiber?Which foods?

Answer 499

1. Nondigestible2. whole wheat, whole grains, wheat bran, corn bran, seeds, nuts, barley, couscous, brown rice, bulgur, zucchini, celery, broccoli, cabbage, onions, tomatoes, carrots, cucumbers, green beans, dark leafy vegetables, raisins, grapes, fruit, and root vegetable skins

Question 500

Fiber treats both diarrhea and constipation1. Insoluable fiber helps with what?2. Soluable fiber helps with what?

Answer 500

1. Insoluble fiber helps pull water from the colon** making the stool softer and easier to pass and helps treat constipation2. Soluble fiber helps to absorb water in the colon and can bulk up the stool** to treat chronic diarrhea

Question 501

Chronic constipation can lead to:3

Answer 501

1. Hemorrhoids2. Anal fissures3. Possibly the development of diverticulosis

Question 502

Dietary fiber recommendations1. women?2. men?

Answer 502

1. Women - 25 grams per day2. Men - 38 grams per day

Question 503

Diverticulosis1. Starting at age 40, incidence increases about every ___ years2. About half of people between the ages of ________ have diverticular disease 3. Almost everyone over ___ has itHigh fiber diet helps to prevent constipation which can lead to worsening diverticular disease and diverticulitis

Answer 503

1. 102. 60 and 803. 80

Question 504

GERD risk factors7

Answer 504

1. Eating large meals or laying down right after a meal2. Obesity3. Foods: citrus, tomato, chocolate, mint, garlic, onions, spicy or fatty foods4. Drinks: ETOH, carbonated drinks, coffee, tea5. Smoking6. Pregnancy7. Hiatal hernia

Question 505

Meds that can worsen GERD7

Answer 505

1. NSAIDs2. Beta-blockers3. Calcium channel blockers4. Bronchodilators5. Dopamine active drugs (treatment of Parkinson’s)6. TCAs7. Some muscle relaxants

Question 506

Dietary and lifestyle counseling to reduce GERD symptoms8

Answer 506

1. Maintain a healthy weight2. Avoid tight fitting clothes3. Avoid known trigger foods-Encourage a food and symptom journal for 7-14 days-Usual culprits are ETOH and coffee4. Eat smaller meals5. Wait 3 hours after eating to lay down6. Elevate the head of the bed 6-9 inches7. Don’t smoke or chew tobacco8. Decrease stress and anxiety through exercise or other relaxation techniques

Question 507

Antacids used for the treatment of what?

Answer 507

ulcers

Question 508

What meds are antacids? 3

Answer 508

1. Aluminum salts2. Magnesium hydroxide3. Calcium carbonate

Question 509

MOA: Antacids1. In general how do they work?2. How do they do this? 4

Answer 509

1. In general work by neutralizing gastric acid2. -Protect gastric mucosa against acute chemical injury-Bind bile acids and inhibit peptic activity-Promote angiogenesis in injured mucosa-Heavy metals suppress H. pylori

Question 510

1. What substances are in magnesium salts?2. Brand names? 53. Common side effects? 54. Caution with what?

Answer 510

1. Magnesium hydroxide/aluminum hydroxide2. Brand names-Maalox, -Alamag, -Mag-Al, -Mag-Al Ultimate, -Mylanta 3. Common side effects:-Diarrhea, -constipation, -abd cramps, -N/V-Hypermagnesemia4. Caution with renal insufficiency

Question 511

Aluminum salts1. Caution with what?2. Can block the intestinal absorption of what?3. Brand names? 2

Answer 511

1. Caution in renal insufficiency2. Can block the intestinal absorption of phosphate3. -Acid gone-Gaviscon

Question 512

Calcium carbonate1. Brand names? 62. Indications? 23. Most common side effects? 64. Separate from other meds by what?

Answer 512

1. Brand names-Tums, -Maalox regular chewable, -Calci-chew, -Rolaids, -Chooz, -Alka-Mints2. Indications: -Acid indigestion, -heartburn3. Most common side effects: -constipation, -bloating, -gas, -N/V, -abdominal pain, -xerostomia4. Separate from other meds by 2 hours

Question 513

H2 Blockers indications3

Answer 513

1. Treatment and maintenance therapy of peptic ulcer disease2. Treatment of GERD3. Management of dyspepsia

Question 514

1. MOA of H2 blockers?2. When should we take these?

Answer 514

1. Inhibit acid secretion by blocking histamine H2 receptors on the parietal cell2. Generally dosed to take 30-60 min prior to a meal (if using for acid suppression with meals)

Question 515

H2 blocker side effects?2

Answer 515

1. Rare, severe adverse events, such as renal and hepatic toxicity2. Myelosuppression

Question 516

H2 blocker SE: Myelosuppressio. What will you see on the CBC?4

Answer 516

1. Thrombocytopenia2. Neutropenia3. Anemia4. Pancytopenia

Question 517

Rare CNS side effects with H2 blockers?Rare cardiac side effects?

Answer 517

Can cause confusion, restlessness, somnolence, agitation, headaches, and dizziness and, with prolonged therapy, hallucinations, focal twitching, seizures, unresponsiveness, and apnea (primarily in the elderly with concomitant renal and/or hepatic failure)Sinus bradycardia, hypotension, AV block, prolongation of the QT interval, and sinus and cardiac arrest have occurred with the rapid infusion

Question 518

Cimetidine has some unique side effects such as?5

Answer 518

1. Can rarely cause gynecomastia and impotence2. Polymyositis3. Interstitial nephritis4. Cleared through the P450 system so has multiple drug interactions5. Giving rapidly IV can cause cardiac arrhythmias and hypotension

Question 519

Absorption and distributionof H2 blockers:1. How well is it absorbed?2. Peak serum concentrations occur when?3. Absorption is reduced by 10-20% if taken with what?

Answer 519

1. Well absorbed after oral dosing2. Peak serum concentrations occur within one to three hours3. antacids

Question 520

What are the H2 blockers?4

Answer 520

1. Cimetidine (Tagamet)2. Ranitidine (Zantac)3. Famotidine (Pepcid)4. Nizatidine (Axid)

Question 521

What are the Proton pump inhibitors?6

Answer 521

1. Omeprazole (Prilosec, Zegrid)2. Lansoprazole (Prevacid)3. Pantoprazole (Protonix)4. Esomeprazole (Nexium)5. Dexlansoprazole (Kapidex)6. Rabeprazole (AcipHex)

Question 522

PPI: Indications?5

Answer 522

Treatment of all acid-related disorders1. peptic ulcer disease2. gastroesophageal reflux disease3. Zollinger-Ellison syndrome4. Treating and preventing nonsteroidal anti-inflammatory drug (NSAID)-associated gastroduodenal mucosal injury5. Eradication of Helicobacter pylori infection

Question 523

PPIs MOA

Answer 523

Block acid secretionirreversibly binds to and inhibits the hydrogen-potassium ATPase pump on the parietal cell membrane

Question 524

PPIs MOA1. What need to be active for PPIs to work so don’t give other antisecretory meds at the same time?2. The amount of H-K-ATPase present in the parietal cell is greatest after when? 3. PPIs should be administered when?

Answer 524

1. Parietal cells2. a prolonged fast3. before the first meal of the day

Question 525

PPIs: 1. Onset of action?2. Peak concentration?

Answer 525

1. About 1 hour2. Peak concentration in about 2 hours

Question 526

PPI’s side effects3

Answer 526

1. Diarrhea2. Headache3. Plus flatulence with Protonix

Question 527

Drug interactions1. Which PPI has the lowest drug interaction?2. Which drugs are metabolized largely via CYP2C19, and the potential for interactions thus appears to be the greatest among the PPIs?

Answer 527

1. Pantoprazole (Protonix) 2. -Omeprazole (Prilosec, Zegrid) -Esomeprazole (Nexium)

Question 528

What is the omeprazole?

Answer 528

Significant interaction between omeprazole and clopidogrel (black box warning)

Question 529

Long term administration of PPIs may increase the incidence of what? 3

Answer 529

1. Infections2. Fractures3. Malabsorption issues

Question 530

PPIs1. Which infections does it increase incidence of?2. Which fracturs?3. What kind of Malabsorption issues? 3

Answer 530

1. Infections-C. difficile-pneumonia2. Fractures-Hip, -wrist, -spine3. Malabsorption of-B12 (check levels)-Magnesium (check levels esp. with diuretics and digoxin administration)-Iron

Question 531

PPI administration:1. Take when?2. What if twice daily dosing is needed?

Answer 531

1. Take 30-60 min before first meal of the day2. If twice daily dosing is needed then take second dose 30-60 min prior to the last meal of the day

Question 532

Sulcralfate (Carafate)1. What substances are in this drug?2. Prevents what?3. Heals what?

Answer 532

1. Sucrose octasulfate-aluminum hydroxide2. Prevents chemical induced mucosal damage3. Heals chronic ulcers

Question 533

1. Sulcralfate (Carafate) MOA?2. Binds to the ulcer base best at a pH below ___ so should be administered 30-60 min prior to meals

Answer 533

1. Stimulates angiogenesis and formation of granulation tissue likely due to growth factor binding2. 3.5

Question 534

Sulcralfate (Carafate) Cautions?2

Answer 534

1. Due to the combination with aluminum hydroxide do not administer with aluminum containing antacids in patients with renal failure2. Do not administer with citrate containing compounds – increases aluminum absorption by 50X in normal renal function

Question 535

1. Bismuth suppresses what?2. However, not helpful in the treatment of what?

Answer 535

1. Suppresses H. pylori infection2. Not helpful in treatment of non H pylori induced ulcers

Question 536

Bismuth MOA?4

Answer 536

1. Inhibition of peptic activity but not pepsin secretion2. May bind to ulcer craters3. Recruits macrophages to the edge of the ulcer crater to promote healing4. May increase mucosal prostaglandin production and mucus bicarbonate secretion

Question 537

Misoprostol (Cytotec)1. INdicated for what?2. Preg cat?3. What class of drug?4. MOA? 2NOT A FIRST LINE THERAPY

Answer 537

1. Indicated for the prevention and treatment of NSAID induced ulcers2. Pregnancy category X3. Prostaglandin E1 analog4. Enhances mucosal defenses and promote ulcer healingNot a first line therapy

Question 538

Black box warning for misoprostol

Answer 538

[U.S. Boxed Warning]: Use of misoprostol during pregnancy may cause abortion, birth defects, or premature birth. It is not to be used to reduce NSAID-induced ulcers in a woman of childbearing potential unless she is capable of complying with effective contraceptive measures and is at high risk of developing gastric ulcers and/or their complications.

Question 539

WHat drug is the Prokinetic?

Answer 539

Metaclopramide

Question 540

Metaclopramide (Reglan)1. First line therapy for what?2. MOA?

Answer 540

1. First line therapy for gastroparesis for no longer than 12 weeks unless benefits outweigh risks2. Improves gastric emptying by increasing gastric antral contractions and decreasing postprandial fundus relaxation

Question 541

Metaclopramide3 different drug classes it falls under. What are they?

Answer 541

1. Dopamine receptor antagonist2. 5-HT4 agonist3. Weak 5-HT3 receptor antagonist

Question 542

Metaclopramide (Reglan)7

Answer 542

1. Anxiety2. Restlessness3. Depression4. Hyperprolactinemia5. QT prolongation Extrapyramidal side effects6. Dystonia7. Tardive dyskinesia

Question 543

Dangerous drug interactions to avoid with metoclopramide5

Answer 543

1. Antispsychotics2. Droperidol (Inapsine)3. Promethazine (Phenergan)4. Tetrabenazine (Xenzine)-Huntington’s chorea5. Trimetazidine (Vastarel MR)-Antianginal

Question 544

More drug interactions to avoid with metoclopramide?4

Answer 544

1. SSRIs2. TCAs3. Atovaquone (Mepron)-Antimalarial 4. Metyrosine (Demser)-Tx symptoms of pheochromocytoma

Question 545

Antiemetics4

Answer 545

1. Anticholinergics2. Antihistamines3. Dopamine receptor antagonistsPhenothiazinesBenzamides4. Serotonin antagonists

Question 546

WHat are the Dopamine receptor antagonists? 2

Answer 546

1. Phenothiazines2. Benzamides

Question 547

Neurotransmitter receptor sites involved in the vomiting reflex?5

Answer 547

1. M1 – muscarinic2. D2 – dopamine3. H1 – histamine4. 5-hydroxytryptamine (HT)-3--serotonin5. Neurokinin 1 (NK1) receptor--substance P

Question 548

Anticholinergic agents1. Acts on what receptors?2. Main drug in this category?3. Predominantly used for what?4. Administered how?5. SE? 3

Answer 548

1. M1 – muscarinic receptor2. Scopolamine is the main drug in this category3. Predominantly used as prophylaxis against motion sickness4. Delivered transdermally, 1.5 mg every 72 hours5. Side effects include -dry mouth, -drowsiness-vision disturbance

Question 549

Antihistamines:1. MOA? 2. Primary use is for?3. What are the drugs?4. Common side effect?

Answer 549

1. H1 blockers2. Primary use is for motion sickness3. -Diphenhydramine (Benadryl)-Cylizine (Cyclivert)-Dimenhydrinate (Dramamine)-Meclizine (Dramamine-Less Drowsy)4. Sedation is a common side effect along with anticholinergic effects

Question 550

Dopamine Receptor Antagonists1. What are the phenothiazines?2 2. What are the benzamides? 2

Answer 550

1. Phenothiazines-Prochlorperazine (Compazine)-Promethazine (Phenergan)2. Benzamides-Metachlopramide (Reglan)-Trimethobenzamide (Tigan)

Question 551

Phenothiazines1. Work on what receptor sites? 32. Commonly used as what line of agent?3. Administration? 3

Answer 551

1. Have antagonistic properties at D2, H1 and M1 sites2. Commonly used as first line agents3. Oral, rectal or IV

Question 552

Main adverse effects of the phenothiazines5

Answer 552

1. Extrapyramidal reactions such as dystonia--Compazine has higher incidence of EPS than Phenergan2. Tardive dyskinesia with prolonged use3. Acute dystonia can be treated with diphenhydramine 25 to 50 mg IV or IM4. Hypotension can also occur, particularly in the elderly or with intravenous infusion5. Sedation, drowsiness, anticholinergic effects (dry mouth, urinary retention, blurred vision)

Question 553

Precautions with phenothiazines?4

Answer 553

Use with caution in 1. elderly, 2. with other CNS depressants, 3. poorly controlled seizures,4. severe liver dysfunction

Question 554

Benzamides:Metachlopramide (Reglan)1. MOA at low doses?2. MOA at high doses?3. How does it act on gastric smooth muscle? Neuromuscular junction?

Answer 554

Metachlopramide (Reglan)1. Central and peripheral dopamine D2 antagonism at low doses2. Weak 5-HT3 blockade at the higher doses3. Stimulates cholinergic receptors on gastric smooth muscle cells and enhances acetylcholine release at the neuromuscular junction

Question 555

Benzamides:Trimethobenzamide (Tigan)1. Mechanism of action is unclear but works centrally in the area of the what?2. Is generally considered the most potent antiemetic that does not have effects on the serotonergic, dopaminergic, or histaminergic systems, so it has a lower likelihood of causing what?

Answer 555

1. medulla oblongata2. undesired side effects

Question 556

Serotonin 5-HT3 Antagonists1. Potent antiemetic properties mediated mainly through what?

Answer 556

central 5-HT3-receptor blockade in vomiting center AND chemoreceptor trigger zone blockade of 5-HT3 receptors

Question 557

Serotonin 5-HT3 Antagonists Clinical Uses3

Answer 557

1. Great for postoperative and chemotherapy induced nausea and vomiting2. Can be used for most cases of nausea and vomiting except not great for nausea secondary to vestibular system etiology (vertigo)--Usually effective as single agents

Question 558

5-HT3 Receptor Antagonists1. Most common adverse effects include?2. Examples? 4

Answer 558

1. -Headache, -dizziness, and -constipation2.-Ondansetron (Zofran) **Most popular-Granisetron (Kytril)-Dolasetron (Anzemet)-Palonosetron (Aloxi)

Question 559

1. Most commonly used 5HT-3 Receptor Antagonist is what?2. Approved use for who? 23. Preg cat?4. Drug interactions? 3

Answer 559

2. Odansetron (Zofran)Approved for use in children and adultsPregnancy cat BDrug interactions: -caution for serotonin syndrome, -QT prolongation, -monitor liver function tests if prolonged use

Question 560

What are the ways to administer zofran?4

Answer 560

1. Solution (Zofran Injection)40 mg/20 mL (20 mL): $256.402. Tablet, orally-disintegrating (Ondansetron Oral)4 mg (30): $668.788 mg (30): $1113.953. Tablet, orally-disintegrating (Zofran ODT Oral)4 mg (30): $752.178 mg (30): $1252.864. Tablets (Ondansetron HCl Oral)4 mg (30): $735.058 mg (30): $1217.42

Question 561

Differential diagnosis of nausea/vomiting6

Answer 561

1. Medications, toxicities2. Infections (GI, ear)3. Gut disorders4. CNS causes5. Endocrine6. Misc.-Post operative, cardiac, radiation, etc.

Question 562

Nausea and vomiting associated with chemotherapy is treated differently (_____________ is a helpful adjunct)

Answer 562

Dexamethasone

Question 563

Antibiotics for Treatment of Infectious Diarrhea: Empiric Antibiotic Therapy? 2

Answer 563

1. Oral Fluoroquinolone: -Ciprofloxacin 500 mg PO twice daily, -Norfloxacin 400 mg PO twice daily, or -Levofloxacin 500 mg PO once daily (all for 3-5 days)2. Oral Macrolides: -Azithromycin 500 mg PO once daily for 3 days or -Erythromycin 500 mg PO twice daily for 5 days (especially if fluoroquinolone resistance is suspected)

Question 564

When would you reccommend pharmacologic therapy for the symptomatic treatment of diarrhea? 2What would we use?

Answer 564

1. NO fever2. NO blood in stoolThen can use an antimotility agent to decrease the number of stools per day

Question 565

1. Bismuth subsalicylate (Pepto-Bismol) can be used for treatemant of what?2. Considered what kind of drug?3. MOA?

Answer 565

1. traveler’s diarrhea2. Considered an absorbant3. MOA: may exert its antidiarrheal action not only by stimulating absorption of fluid and electrolytes across the intestinal wall but also, when hydrolyzed to salicylic acid, by inhibiting synthesis of a prostaglandin responsible for intestinal inflammation and hypermotility.

Question 566

Bismuth subsalicylate (Pepto-Bismol)1.SE? 22. Cautions? 23. Contraindications? 2

Answer 566

1. Side effects-Dark stools, -black tongue2. Cautions-Do not take with other ASA components-Can potentiate anticoagulants 3. Contraindications-ASA allergy-Infants and children

Question 567

Symptomatic treatment of diarrhea: What meds? 3

Answer 567

1. Loperamide (Imodium)2. Diphenoxylate/atropine (Lomotil)3. Cholestyramine

Question 568

Loperamide (Imodium)1. Acts directly on what?2. Which results in what? 5

Answer 568

1. MOA: acts directly on circular and longitudinal intestinal muscles, through the opioid receptor2. -Inhibits peristalsis and prolongs transit time-Reduces fecal volume, increases viscosity-Diminishes fluid and electrolyte loss-Demonstrates antisecretory activity-Increases tone on the anal sphincter

Question 569

Loperamide (Imodium)1. Preg cat?2. How and when to administer?3. How long should you take it?4. Avoid is what?

Answer 569

1. Pregnancy category COTC2. 4 mg initially then 2 mg after each stool3. Don’t use longer than a few days, if needed longer – reevaluate patient4. Avoid if enteroinvasive organism is suspected

Question 570

Loperamide (Imodium)SE? 6

Answer 570

1. Abdominal pain2. Abdominal distention3. Constipation4. Dry mouth5. Nausea6. Dizziness, drowsiness

Question 571

Dipenoxylate/atropine (Lomotil)1. MOA?2. This results in? 3

Answer 571

1. MOA: Opiod antagonist and anticholinergic2. -Inhibits peristalsis and slows intestinal motility-Inhibits GI propulsion-Prolongs the movement of fluid and electrolytes through the bowel

Question 572

Dipenoxylate/atropine (Lomotil)1. Preg cat?2. How and when to administer?3. Maintance dose?4. Avoid if what?

Answer 572

1. Pregnancy Cat C- Prescription2. 2 tablets QID until diarrhea is controlled3. Maintenance is 2 tabs per day4. Avoid if enteroinvasive organism is suspected

Question 573

Dipenoxylate/atropine (Lomotil)SE7

Answer 573

1. Paralytic ileus, toxic megacolon2. Drowsiness, dizziness3. Euphoria4. Tachycardia5. Pruritis, urticaria6. Respiratory depression7. Anticholinergic effects

Question 574

Cholestyramine (Questran)1. Preg cat?2. Useful for what? 23. How to administer?

Answer 574

1. Cholestyramine (Questran) Preg. Cat C2. -Bile acid-binding agent used for hyperlipidemia-Useful for the treatment of chronic diarrhea post cholecystectomy3. 1 pack or scoop mixed with fluids or food BID

Question 575

Cholestyramine (Questran)SE 6

Answer 575

1. Constipation2. Abdominal pain and bloating3. Vomiting4. Excessive flatulence, diarrhea5. Weight loss6. Decreases absorption of warfarin, thyroid hormones, digoxin and thiazide diuretics. These drugs should be administered 1 hour before or 4-6 hours after the administration of cholestyramine.

Question 576

Laxative step therapy?3

Answer 576

1. First line-Bulk forming or surfactant agents2. Second line-Saline or hyperosmotic laxatives3. Third line-Stimulant laxatives

Question 577

First line pharmacotherapy for the treatment of constipation3

Answer 577

1. Bulk forming agents-Psyllium (Metamucil)2. Ducosate derivatives-Ducosate sodium (Colace)3. Glycerin-Suppository – most often used for infants

Question 578

OTC bulk forming laxatives4(which is preferred?)Not for pts with what?

Answer 578

1. Metamucil (psyllium) -preferred agent as it is the most physiologic2. Fibercon (Polycarbophil)3. Citrucel (methylcellulose)4. Benefiber (wheat dextrin)Powder and chewablesNot for patients with Celiac

Question 579

Bulk forming agents:1. Not absorbed how?2. MOA? 3

Answer 579

1. Not systemically absorbed2. -Bind to the fecal contents and pull water into the stool-Softens and lubricates the stool-Increased water in the stool makes it swell and increase in size – stimulates movement of the intestines

Question 580

Bulk forming agents:1. Onset of action?2. Take with what?

Answer 580

1. Onset of action 12-24 hours but may take up to 3 days for the full effect2. Take with at least 8 ounces of water

Question 581

Bulk forming agents:SE?4(most common side affect)

Answer 581

1. Most common side effect is flatulence2. Bloating3. Abdominal cramping4. Excessive use can cause nausea and vomiting

Question 582

Contraindications for bulk forming agents? 4Caution in who?

Answer 582

1. Esophageal strictures2. GI ulcerations3. Strictures anywhere along the GI tract4. Celiac patients need a specific gluten free formulationCAUTION in DM: some contain up to 20 g carbohydrates per servingMetamucil has a sugar free formula

Question 583

Drug interactions with bulk forming agents?

Answer 583

Fibercon can decrease absorption of tetracycline and quinolones

Question 584

Ducosate derivatives1. What kind of laxative?2. MOA? 23. Two types?

Answer 584

1. Surfactant laxatives2. -Reduces the surface tension of the liquid contents of the bowel-Commonly referred to as “stool softeners”3. -Ducosate sodium (Colace) 50-500mg/dayUsual dose 100 mg qday to bid-Ducosate calcium (Surfak)

Question 585

Surfactant laxatives1. Use for what kind of pts?2. What kind of treatment?3. absorption?4. Combining with what helps promote defecation?

Answer 585

1. Use for patients who should not strain with bowel movements and for those on narcotics2. Only prevent constipation – don’t treat3. No systemic absorption4. Combining with fiber based laxatives helps promote defecation

Question 586

Surfactant laxativesSE?3

Answer 586

1. Most common SE is stomach upset2. Mild abdominal cramping3. DiarrheaOverall – very well tolerated

Question 587

Second line therapyfor constipation? 4

Answer 587

1. Phillips Milk of Magnesia2. Magnesium sulfate (Epsom salt)3. Lactulose4. Sorbitol

Question 588

Magnesium hydroxide (Milk of magnesia)1. Is what kind of laxative?2. MOA? 23. Used for what?4. What is a concern for excessive use?5. Avoid in who?6. SE? 2

Answer 588

1. Saline laxative2. -Draws water into the bowel through osmosis-Increases intraluminal pressure & motility3. Used for more rapid onset of action4. Dehydration is a concern if excessive use5. Avoid if renal dysfunction and elderly6. SE: GI upset, diarrhea

Question 589

Lactulose (Kristalose) or sorbitol1. When do we use it?2. What kind of laxative?3. Use with caution in who?

Answer 589

1. Use if failed bulk forming agents, and failure of magnesium hydroxide (MOM)2. Hyperosmotic laxatives3. Use with caution in diabeticsSolution contains galactose and lactose

Question 590

Lactulose (Kristalose) and sorbitol 1. MOA?2. Can be given how?3. SE? 3

Answer 590

1. - Metabolized to solutes and increase osmotic pressure by drawing in fluid from less concentrated areas- Increased pressure stimulates intestinal motility2. Can be given PO or as an enema3. SE: GI upset, diarrhea, flatulence

Question 591

Third line therapy5

Answer 591

1. Stimulant laxatives2. Mineral oil3. Sodium biphosphates4. Magnesium citrate5. Castor oil

Question 592

WHat are the stimulant lax? 2

Answer 592

1. Senna (Senokot)2. Bisacodyl (Dulcolax)

Question 593

Stimulant laxatives1. For what kind of use?2. MOA? 23. Onset of action? 2

Answer 593

1. Not for long term use2. -Increase peristalsis through direct effects on the smooth muscle of the intestines-Promote fluid accumulation in the colon and small intestine3. Onset of action15 min – 2 hrs PR6-10 hrs PO

Question 594

Stimulant laxatives1. SE? 22. Complications? 13. Contraindications? 2

Answer 594

1. SE: -N/V, -abdominal cramping2. Rectal fissures and hemorrhoids can be exacerbated3. Contraindications: -surgical abdomen, -fecal impaction

Question 595

Sodium phosphate1. Can be administered how?2. Can cause what problem?3. Used as bowel prep for?4. MOA?

Answer 595

1. -Fleet enema -Fleet Phospho-soda2. Can cause electrolyte disturbances3. Can be used as bowel prep for endoscopy procedures4. Osmotic effect in the small intestine by drawing water into the lumen of the gut, producing distention and promoting peristalsis and evacuation of the bowel

Question 596

Sodium phosphate BBW?

Answer 596

Oral (BB warning for nephrotoxicity)

Question 597

Magnesium citrate (Citroma)1. Describe its onset?2. Used for what?

Answer 597

1. Rapid onset of action2. Can be used for bowel prep for endoscopy procedures

Question 598

Polyethylene glycol electrolyte solution (Golytely)1. What kind of laxative?2. Used for?3. SE? 7

Answer 598

1. Powerful osmotic laxative2. Used for bowel prep for endoscopic procedures3. Side effects-Sleep disorder, -rigors, -malaise-Increased thirst, -abdominal distention and pain-Anorectal pain, -bloating, nausea

Question 599

Dyspepsia features? 8Common complaint with disorders of the?

Answer 599

Features1. Indigestion, 2. chronic/recurrent pain in upper abdomen, 3. upper abdominal fullness, 4. early satiety, 5. bloating, 6. belching, 7. nausea,8. heartburnCommon complaint with disorders of the stomach

Question 600

What is gastritis?What are the two kinds of gastritis?

Answer 600

inflammatory changes in the gastric mucosa1. Erosive and hemorrhagic gastritis2. Nonerosive, nonspecific gastritis

Question 601

What causes the following:1. Erosive and hemorrhagic gastritis? 32. Nonerosive, nonspecific gastritis? 3

Answer 601

1. -Stress, -NSAID and -Alcoholic gastritis2. -H. pylori, -pernicious anemia, -eosinophilic gastritis

Question 602

Most common causes of erosive and hemorrhagic gastritis4

Answer 602

1. Stress (from a medical or surgical illness)2. NSAIDs3. Alcohol4. Portal hypertension

Question 603

Most cases of gastritis are asymptomatic but may have what?5

Answer 603

1. Anorexia2. Epigastric pain3. Nausea4. Vomiting5. Upper GI bleeding

Question 604

Upper GI Bleeding from erosive gastritis1. If due to erosive gastritis it is probably what?2. Usually does not lead to what?3. What may be noted?4. What might you find on nasogastric suction?

Answer 604

1. If due to erosive gastritis it is usually superficial2. Usually does not lead to hemodynamically significant bleeding3. Melena (dark sticky feces containing partially digested blood) may be noted4. Coffee ground emesisBlood noted in nasogastric suction

Question 605

Work up for Upper GI Bleeding from erosive gastritis?3

Answer 605

1. CBC, 2. serum iron3. Upper endoscopy

Question 606

Stress Gastritis1. IN critically ill patients how soon may this occur?2. Major risk factors for stress induced ulcers?7

Answer 606

1. In critically ill patients may occur within 72 hours of admissionAt highest risk for bleeding due to stress induced ulcers:1. Coagulopathy2. INR > 1.5 and platelets less than 50K3. Need for mechanical ventilation > 48 h4. Trauma, burns, shock5. Sepsis, Liver failure, kidney disease6. Multi-organ failure7. CNS injury

Question 607

Stress Gastritis1. Best treatment is what?2. What can decrease the risk?3. Prophylaxis should be routinely given to all critically ill patients. What would we do for this? 2

Answer 607

1. prevention2. enteral nutrition3.- IV or oral proton pump inhibitors (omeprazole, esomeprazole, lansoprazole, pantoprazole) are best- IV or oral H2 blockers (cimetidine, famotidine, ranitidine) help but are not as good as PPIs

Question 608

Treatment for GI bleeding secondary to stress induced gastritis3

Answer 608

1. IV PPI bolus followed by continuous infusion2. Sucralfate suspension given orally3. Endoscopy to look for treatable causes

Question 609

1. Which NSAIDs have a much lower incidence of significant ulcer formation?`

Answer 609

1. COX-2 inhibitors

Question 610

But COX-2 inhibitors have 2X the risk of what compared to nonselective NSAIDS?

Answer 610

CV complications

Question 611

How does the degree of symptoms does correlate with degree of mucosal abnormalities?

Answer 611

it does not

Question 612

Red flagsfor NSAID gastritis6

Answer 612

1. Severe pain2. Weight loss3. Vomiting4. GI bleeding5. AnemiaRefer for upper endoscopy

Question 613

NSAID gastritisTreatment?1. 1. If no red flag symptoms… treatment consists of what?2. Trial of what for 2-4 weeks?3. If no improvement?

Answer 613

1. discontinuation of NSAIDs if possible2. Trial of PPI for 2-4 weeks-Can use H2 blockers but not as effective3. If no improvement in 2 weeks refer for endoscopy

Question 614

Pathophysiology of ETOH gastritis2

Answer 614

1. Alcohol disrupts the mucosal barrier2. Alcohol and aspirin together increase the permeability of the gastric mucosal barrier and cellular damage occur

Question 615

Alcoholic Gastritis1. Caused by?2. Symptoms? 43. Treatment? 3

Answer 615

1. Excessive alcohol consumption2. Symptoms: -dyspepsia, -nausea, -emesis, -minor hematemesisTreatment -H2 blockers or PPIs-And sucralfate 2-4 weeks-And decrease ETOH consumption

Question 616

1. Portal hypertensive gastropathyleads to what?2. Can cause chronic what?3. Treatment with what to lower pressures?4. IF this fails?

Answer 616

1. Portal hypertension leads to congestion of gastric vessels.2. Can cause chronic GI bleeding3. Treatment with propranolol or nadolol to lower the portal pressures4. If failure of medical therapy may need a portal decompression procedure

Question 617

Nonerosive, nonspecific gastritis3

Answer 617

1. H. pylori2. Pernicious anemia3. Eosinophilic gastritis

Question 618

Helicobacter pylori1. What kind of bacteria?2. Lives where in the GI tract?3. What is its normal function?4. Pathologically what can it cause?

Answer 618

1. Spiral gram negative rod2. Lives beneath the gastric mucous layer next to the gastric epithelial cells3. Secrete urease and enables them to produce ammonia to buffer the acid4. Causes gastric mucosal inflammation

Question 619

H. pylori1. Spread how?2. Increase risk of what from infection?3. If untreated it can lead to what?

Answer 619

1. Fecal-oral spread2. Increases risk of gastric cancer3. If untreated leads to lifelong infections

Question 620

Risk factors for H. pylori2

Answer 620

1. Correlates inversely with socioeconomic status2. Contaminated water supply

Question 621

H. pylori clinical presentation?2

Answer 621

1. most are asymptomatic and suffer no complications2. Others may have an alteration in acid production and increased gastrin

Question 622

H pylori: Others may have an alteration in acid production and increased gastrin. Over time this may cause?

Answer 622

Over time may cause cellular changes and lead to duodenal or gastric ulcers, gastric cancer and low grade B cell gastric lymphoma

Question 623

Testing for H. pylori

Answer 623

1. Serology2. Urea breath test3. Stool antigen testing4. Endoscopic biopsy

Question 624

H. pylori1. What kind of serology?2. Disadvantage of this?3. Breath test is the test for?4. Must be off of what for the breath test? 25. Stool antigen test is for what?

Answer 624

1. IgG antibody testing2. Can’t distinguish between active vs. inactive infection3. Tests for active infection4. Off abx for 4 weeks, PPIs for 2 weeks5. Tests for active infectionSensitivity 94%, Specificity 86%

Question 625

Treatment for H pylori gastritis2

Answer 625

Eradication therapy2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)

Question 626

1. What is Pernicious anemia gastritis?2. What areas of the stomach are most affected? 23. Gastric gland and mucosal atrophy causes what?4. May be associated with what?3

Answer 626

1. Autoimmune gastritis---Autoantibodies to gastric gland parietal cells and intrisic factor2. Body and fundus of stomach mostly affected3. loss of acid production4. -Hashimoto thyroiditis, -Addison disease, -Graves disease

Question 627

1. Eosinophilic gastritis is what?2. What organ is most commonly affected?3. Symptoms may include what?4. Associated with a history of what?5. Diagnosis?6. Treatment? 2

Answer 627

1. Infiltration of eosinophils into GI tissue2. Stomach is the area most common affected3. Symptoms may include: -abdominal pain, -nausea, -vomiting, -early satiety-diarrhea 4. Associated with a history of -allergies, -asthma, -atopy5. Diagnosis: biopsy6. Treatment: -elimination diet. -May need steroids

Question 628

1. What is peptic ulcer disease?2. Can be caused by what? 23. Size and extends through where?4. 5x more likely where in the intestine?5. Gastric ulcers are most common where?

Answer 628

1. Break in the gastric or duodenal mucosa2. Can be caused by too much acid or pepsin3. > 5 mm in diameter and extend through the muscularis mucosae--Lifetime prevalence 10%4. 5X more common in the duodenum5. Gastric ulcers most common in the antrum

Question 629

1. Duodenal ulcers….. most common ages are ______?2. Gastric ulcers most common _____ years3. Most common in who? 2

Answer 629

1. 30-552. 55-703. smokers and NSAID users

Question 630

Etiology of PUD3(two most common)

Answer 630

1. NSAIDs2. Chronic H. pylori infection3.

Question 631

Clinical presentation of PUD8

Answer 631

1. Dyspepsia2. Pain in the epigastric area3. Gnawing, dull, aching, “hunger like”4. Pain may be relieved with food or antacids and return 2-4 hours later5. Sometimes have nocturnal pain6. Periodicity 7. Nausea and anorexia may occur with gastric ulcers8. Less likely to have symptoms other than GI bleeding in NSAID induced cases

Question 632

PE for PUD?3

Answer 632

1. Often normal2. May have some epigastric tenderness to deep palpation3. FOBT or FIT may be positive in 1/3 of patients

Question 633

Work Upfor PUD?5 (whats the test of choice?)

Answer 633

1. CBC, 2. FOBT/FIT3. Upper endoscopy is the test of choice4. Abdominal CT needed if ulcer perforation is suspected5. Biopsy samples are tested for H pylori infection and evaluated for malignancyBarium upper GI series is not as sensitive or specific for the detection of ulcers or GI malignancies

Question 634

If ulcer diagnosed without endoscopy then test for H pylori with what? 2

Answer 634

1. a fecal antigen test or 2. urea breath test

Question 635

For fecal antigen testing or urea breath test:1. Stop PPIs for ____ days prior to testing, otherwise false negatives2. Serologic testing for H pylori….appropriate where the prevalence is > ___%....neg confirms absence of infection. 3. Can test _______ for years after eradication of infection 4. Stool antigen tests…appropriate where the prevalence ___%....+ ________ highly predictive for active infection

Answer 635

1. 7-142. 30%3. positive4. less than 30%, stool test

Question 636

Treatment for PUD5

Answer 636

1. Proton pump inhibitors2. H2 blockersSecond line agents to enhance mucosal defenses3. Bismuth4. Misoprostol (Cytotec)….prostaglandin e1 analog5. antacids

Question 637

1. PUD preferred treatment?2. duodenal3. gastric4. Advantages over H2 blockers?

Answer 637

1. Preferred treatment2. Heal 90% of _________ ulcers in 4 weeks3. Heal 90% of ______ ulcers in 8 weeks4. Provide faster symptom relief and promote faster ulcer healing compared to H2 blockers

Question 638

1. H2 blockers MOA?2. Administer when?3. Heal 85-90% of duodenal ulcers at_ weeks4. Heal 85-90% of gastric ulcers at __ weeks5. What should we avoid?

Answer 638

1. Inhibit nocturnal acid secretion but do not work as well against meal stimulated acid secretion2. Administer at bedtime3. 64. 85. Avoid cimetidine due to drug interactions

Question 639

H pylori eradication1. Combination therapy?2. 50% of strains resistant to what?3. 13% of strains resistant to what?

Answer 639

1. 2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)2. metronidazole3. clarithromycinEradication rates 93% with quadruple therapy70% with triple therapy

Question 640

Medical treatment of PUD1. How does smoking affect ulcers?2. ETOH? Encourage a balanced diet

Answer 640

1. Smoking decreases ulcer healing rates and increases recurrence rates2. Moderate ETOH is ok

Question 641

H pylori associated ulcersGoals of therapy?3

Answer 641

1. Relive symptoms2. Promote ulcer healing3. Eradicate infection

Question 642

Treatment after Triple or Quadruple therapy depends on ulcer severity:1. Small ulcer?2. Large or complicated ulcer? 2

Answer 642

1. Small ulcer (less than 1 cm) no further treatment2. -continue PPI for up to 6 weeks post completion- If eradicated most patients don’t need further acid suppression therapy

Question 643

Retesting for H pylori2With what tests? 3

Answer 643

1. > 4 weeks post antibiotic therapy and2. > 2 weeks post discontinuation of PPI1. Urea breath test, 2. fecal antigen3. endoscopy with biopsy

Question 644

Medical treatment of NSAID induced ulcers2

Answer 644

1. Stop offending agent whenever possible2. H2 blockers or PPIs80% of ulcers heal at 8 weeks even if they continue to take NSAIDs

Question 645

Prevention after NSAID ulcer healing3

Answer 645

1. Long term PPI therapy if NSAIDs must be continued2. Prescribe NSAIDs at the lowest dose and shortest duration possible3. Use cox-2 inhibitor instead of a nonselective NSAID if no significant CV risks identified

Question 646

Risk factors for NSAID ulcer related complications6

Answer 646

1. > 60 y/o2. History of PUD or complications3. Aspirin or other antiplatelet therapy4. Anticoagulation therapy5. Oral glucocorticoid use6. Serious underlying medical illness

Question 647

1. What is Zollinger-Ellison Syndrome (Gastrinoma)?2. What does it cause?

Answer 647

1. Gastrin secreting gut neuroendocrine tumor2. Causes hypergastrinemia from increase acid secretion

Question 648

Zollinger-Ellison Syndrome (Gastrinoma)Sites of primary tumors? 4

Answer 648

1. Pancreas 25%2. Duodenal wall 45%3. Lymph nodes 5-15%4. Unknown location

Question 649

Whats the gastrinoma triangle?

Answer 649

Gastrinoma triangle: bounded by the porta hepatis, the neck of the pancreas and the 2nd/3rd portion of the duodenum

Question 650

How many of the Zollinger-Ellison Syndrome are malignant?

Answer 650

2/3 are malignantMost are resectable25% of patients have small nonresectable gastrinomas associated with MEN 1

Question 651

Clinical presentationof Zollinger-Ellison Syndrome (Gastrinoma)?5

Answer 651

1. Dyspepsia2. 90% have peptic ulcers3. Ulcers usually located in the duodenum4. No isolated gastric ulcers5. Diarrhea, steatorrhea, weight loss if pancreas affected

Question 652

Screeningfor Zollinger-Ellison Syndrome (Gastrinoma): When should we check fasting gastrin levels?8

Answer 652

1. Refractory duodenal ulcers2. Large ulcers > 2 cm3. Ulcers distal to the duodenal bulb4. Multiple duodenal ulcers5. Frequent recurrent ulcers6. Ulcers associated with diarrhea7. Ulcers + hypercalcemia8. If ulcers + negative for NSAID use + negative for H pylori

Question 653

Imaging for Zollinger-Ellison Syndrome (Gastrinoma)?3

Answer 653

1. CT and MRI to evaluate for hepatic metastases and primary lesions2. Nuclear med study : SPECT Somatostatin receptor scintigraphy (SRS)3. Endoscopic ultrasound if SRS is negative

Question 654

What is the best imaging test to find gastrinoma tumors? why?

Answer 654

Nuclear med study : SPECT Somatostatin receptor scintigraphy (SRS)Gastrinomas have somatostatin receptors that take up the radiolabled somatostatin80% sensitivity…. the best imaging study to find the tumors

Question 655

Treatment of gastrinomas:1. Malignant? 12. Localized disease? 1

Answer 655

1. Metastatic disease-PPIs to decrease acid hypersecretion-Biggest predictor of survival is degree of hepatic metastasis10 year survival is 30%2. Localized disease-Resection before hepatic metastasis is the only cure15 year survival 95%

Question 656

What is gastroparesis?

Answer 656

Delayed gastric emptying in the absence of a mechanical obstruction

Question 657

Gastroparesis is usually secondary to what?3

Answer 657

1. Diabetes2. Post surgical3. Idiopathic….Most common – about ½ of all cases

Question 658

Other etiologies of gastroparesis?4

Answer 658

1. Viral2. Medications3. Neurologic disease4. AutoimmuneOther

Question 659

Diabetic gastroparesis1. MOre common in what type?2. Chronic hyperglycemia can lead to what?3. What is abnormal? 2

Answer 659

1. Type 1 > Type 211-18% of diabetics2. Chronic hyperglycemia can lead to neuropathy3. Autonomic dysfunction and abnormal intrinsic nervous system

Question 660

Viral gastroparesis1. How does it present?2. Two examples?3. Symptoms usually improve with in how long?4. Which viruses may lead to severe long term symptoms? 3

Answer 660

1. Sudden onset of symptoms post a viral prodrome2. Norwalk and Rotavirus3. Symptoms usually improve within a year4. Cytomegalovirus, Epstein-Barr virus and varicella-zoster virus may lead to severe long term symptoms

Question 661

Several medications can delay gastric emptying11

Answer 661

1 Oxycodone (narcotic)2. Clonidine (alpha-2 adrenergic agonist)3. TCAs4. Calcium channel blockers5. Dopamine agonists6. Muscarinic cholinergic receptor antagonists-Scopolamine, atropine8. Ocreotide (used to treat acromegaly and also diarrhea associated with certain tumors)9. Phenothiazines--Antipsychotics, antiemetics10. Cyclosporine11. GLP-1 agonists and amylin analogues--Byetta, Victoza

Question 662

Postsurgical gastroparesis6 causes (one most common)

Answer 662

1. Injury to the vagus nerve2. Gastrectomy3. Fundoplication (surgery for intractable reflux) --*most common cause4. Lung or heart transplantation5. Variceal sclerotherapy6. Botulinum toxin injection

Question 663

Neurologic diseasethat could cause gastroparesis?

Answer 663

1. Loss of extrinsic neural control…examples:-Multiple sclerosis, -brainstem stroke or -tumor, -diabetic or amyloid neuropathy2. Myenteric plexus-AIDS, -diabetes, -Parkinson’s

Question 664

Autoimmune causes of gastroparesis?

Answer 664

Idiopathic or part of a paraneoplastic syndrome (small cell lung cancer)

Question 665

Other causes of gastroparesis?2

Answer 665

1. Mesenteric ischemia2. Scleroderma (infiltration of the muscular layer of the stomach)

Question 666

Gastroparesis…Symptoms5

Answer 666

1. Nausea2. Vomiting3. Early satiety4. Bloating5. Upper abdominal pain

Question 667

Gastroparesis PE?3

Answer 667

1. Epigastric tenderness but no guarding or rigidity2. May note abdominal distention3. Look for signs of the underlying disorder

Question 668

What would cause skin taut over the hands and chest, telangiectasias?What would cause signs of autonomic dysfunction (orthostatic hypotension, lack of pupillary response to light with delayed response to accommodation)?

Answer 668

1. Schleroderma2. Diabetes

Question 669

Workup for gastroparesis?3

Answer 669

1. Upper endoscopy2. CT enterography or MRI to rule out mechanical obstruction3. Assessment of gastric motility with scintigraphic gastric emptying

Question 670

Describe scintigraphic gastric emptying?

Answer 670

Nuclear medicine studyOvernight fastEat a breakfast of eggs and toast sprinkled with a dash of isotopeImaging at timed intervals up to 4 hours to determine degree of gastric emptying

Question 671

Further work up to help determine the etiologyof gastroparesis?7

Answer 671

1. Hemoglobin2. fasting plasma glucose3. serum total protein4. albumin5. TSH6. ANA7. HbA1C in patients with DM to assess glucose control

Question 672

Treatment of gastroparesis5

Answer 672

1. Dietary modifications2. Hydration3. Vitamin supplementation may be needed4. Optimize glycemic control5. Prokinetics (enhance GI motility)

Question 673

Dietary modifications for gastroparesis?6

Answer 673

1. Small frequent meals 4-5 times daily2. Low fatAvoid3. Insoluble fiber4. ETOH5. Carbonated drinks6. Tobacco

Question 674

What are prokinetics?2 meds

Answer 674

1. Metaclopramide (Reglan)2. Macrolide antibiotics

Question 675

MOA of erythromycin?

Answer 675

1. Induces gastric contraction and stimulates fundic contractilityLiquid formulation 40-250mg TIDUse no longer than 4 weeks at a time otherwise efficacy decreases

Question 676

Refractory cases of gastroparesis warrant what?

Answer 676

Surgical treatmentGastrostomy tube for decompression and jejunostomy for feeding

Question 677

The pancreas is an endocrine gland producing: 3

Answer 677

1. Insulin2. Glucagon3. somatostatin

Question 678

Also functions as an exocrine gland secreting what? It secretes approximately ____ liters of enzyme-rich fluid every day for the digestion of fats, starch, and protein.

Answer 678

digestive enzymes via a duct. 1.5

Question 679

1. Secretin- released from the duodenal mucosa in response to what?2. What does it stimulates? 2

Answer 679

1. the presence of acid in the duodenum.2. stimulates the release of-bicarbonate-water.

Question 680

1. Cholecystokinin (CCK)- released from SI endocrine cells in response to what?2. acts directly and through vagal afferents to stimulate pancreatic acinar cells to release what?

Answer 680

1. the entry of fats and proteins into the proximal intestine. 2. digestive proenzymes.

Question 681

Acute pancreatitis is an acute inflammatory process of the pancreas. Etiologies? 5

Answer 681

1. Mechanical2. Toxic3. Trauma4. Metabolic5. Infection

Question 682

Acute Pancreatitis:1. Gallstones are more common in who?2. Alcohol are more common in who?

Answer 682

1. Gallstones more common cause in women2. Alcohol more common cause in men

Question 683

If 2nd attack and not one of main 2 causes then look for the less common causes such as? 6

Answer 683

1. hypercalcemia2. hyperlipidemias3. biliary sludge4. drugs5. cancer6. missed stone in duct,

Question 684

Acute onset clinical manifestations? 5What can this progress to? 2

Answer 684

1. persistent, severe epigastric pain2. or RUQ pain may be steady or colicky3. N/ V4. 50% experience band like radiation of pain to back;5. some may get relief w/ bending forward or sitting up.  1. Dyspnea2. Shock/Coma

Question 685

Acute pancreatitis5-10% of patients may have painless disease and have what?

Answer 685

Unexplained hypotension

Question 686

Physical exam of acute pancreatitis? 5

Answer 686

1. Fever, tachycardia, (hypotension if severe)2. Epigastric/RUQ tenderness3. Shallow respirations- pain with deep breaths4. Possible dyspnea if pleural effusion5. Epigastric mass if pseudocyst or tumor.  In 3% of pts, ecchymotic discoloration may be observed in the periumbilical region (Cullen’s sign) or along the flank (Grey-Turner's sign).

Question 687

1. ecchymotic discoloration may be observed in the periumbilical region. What sign is this? 2. Along the flank. What sign is this?

Answer 687

1. Cullen's sign2. Grey-Turner's sign

Question 688

Lab Tests for Acute Pancreatitis?3

Answer 688

1. Serum Amylase2. Serum Lipase3. C reactive protein

Question 689

Serum amylase1. Rises how?2. Elevated for how many days?Serum Lipase1. Describe sensitivity and specificity compare to amylase2. Describe its elevation and how long it lasts?3. If ____x nl think pancreatitis.

Answer 689

Serum amylase:1. rises quickly (6 to 12 hrs)2. elevated for 3-5 days Serum lipase:1. sensitivity 82-100%, more specific than amylase2. elevations occur earlier and last longer3. If 3-4x nl think pancreatitis.

Question 690

C reactive protein levels1. Levels at what and how long after presentation can predict a more severe course? 2. So what do we use this to differentiate?

Answer 690

C-reactive protein:1. levels above 150 mg/dL at 48 hrs after pt presents can predict more severe course.2. Used to differentiate severe from mild disease 

Question 691

Imaging for Pancreatitis?5

Answer 691

Abdominal plain filmCXRUSCT scanMRI

Question 692

1. What does abdominal plain film help us with on pancreatitis? 22. What percent of pts with pancreatitis have abnormal findings on CXR?3. What are these? 3

Answer 692

1. -helps to exclude other causes of abdominal pain-may have localized ileus 2ndry to inflammation2. CXR: 1/3 of pts w/ pancreatitis have abnormal findings:3.-Elevation of hemidiaphragm-Pleural effusions            -Pulmonary infiltrates

Question 693

What is the most important test for diagnosis acute pancreatitis & intraabdominal complications and assessment of severity?

Answer 693

CT scan

Question 694

Pancreatitis1. What would the US show? 

Question 695

MRI for pancreatitis1. Describe its sensitivty compared to CT?2. Advantages? 3

Answer 695

1. Higher sensitivity for the diagnosis of early acute pancreatitis than CT scan.2.-Lack of nephrotoxicity-Ability of MRI to better detect fluid collections, necrosis, hemorrhage and pseudocyst-MRCP better shows the pancreatic and bile ducts

Question 696

What does this CT show?

Answer 696

pancreatitis

Question 697

Treatment of pancreatitis?7

Answer 697

1. Admit to hospital with acute pancreatitis2. NPO3. IV hydration with crystalloids to keep UO>30ml/hr (lactated ringers except in hypercalcemia)4. Pain control (morphine, fentanyl, ketorolac)5. Ondansetron (zofran), or Promethazine (Phenergan) prn nausea6. +/- antibiotics,7. +/- surgery (cholecystectomy, necrosectomy- severe dz) 

Question 698

What labs would we do for Pancreatitis?6

Answer 698

Labs:1. CBC,2. lipase,3. amylase,4. CMP,5. bilirubin,6. C-reactive protein in 48 hrs,

Question 699

Severe pancreatitis1. Complications with what can develop? 42. Treatment? 3

Answer 699

1. Complications w/-pulmonary,-renal,-circulatory-hepatobiliary dysfx can occur 2.-ICU monitoring and supplemental O2-Prevent infection w/ broad spectrum antibiotics-Nutrition preferably enteral- Tube feeding

Question 700

Risk Factors for Disease Severity5

Answer 700

1. Age > 55 yrs2. Obesity—BMI > 30 kg/m23. Organ failure at admission4. Pleural effusion or pulmonary infiltrate5. Elevated C-reactive protein

Question 701

What is Chronic Pancreatitis? 

Answer 701

Progressive inflammatory changes result in permanent structural damage to the pancreas, leading to impairment of exocrine & endocrine function

Question 702

Etiologies of chronic pancreatitis?5

Answer 702

1. Alcohol abuse (75%)2. Genetic: cystic fibrosis, hereditary pancreatitis3. Ductal obstruction: trauma, pseudocysts, stones, tumors4. Systemic: SLE, hypertriglyceridemia5. idiopathic

Question 703

Acute vs. Chronic1. Acute is usually _________?2. Reccurrent acute leads to what?3. Symtpoms of chronic?4. Serum Amylase and Lipase in Chronic?

Answer 703

1. Acute is usually nonprogressive2. Recurrent episodes of acute lead to chronic over time 3. Chronic may be asymptomatic over long periods of time4. Serum amylase and lipase concentrations tend to be normal in chronic 

Question 704

1. Cardinal feature of Chronic pancreatitis?2. Other clinical manifestations of chronic pancreatitis? 3

Answer 704

1. Chronic abdominal pain—cardinal feature although 20% may have little to no pain2. -Pancreatic insufficiency-Fat malabsorption-Pancreatic diabetes

Question 705

Describe why the following happen:1. Pancreatic insufficiency?2. Fat malabsorption?3. Pancreatic diabetes?

Answer 705

1. Pancreatic insufficiency—exocrine dysfunction cannot digest complex foods or absorb digestive breakdown products, wt. loss: 90% of pancreatic function has to be lost for this to occur2. Fat malabsorption (steatorrhea)--lipolytic activity decreases faster then proteolysis: malabsorption of fat sol-uble vitamins (A, D, E, K)3. Pancreatic diabetes —DM late in course of disease, seen pts w/ calcifying disease.

Question 706

Chronic Pancreatitis1. Why are amylase and lipase usually normal?2. What is the diagnostic gold standard test?3. What test is performed at specialized centers?

Answer 706

1. amylase and lipase usually normal because pancreas fibrotic resulting in decreased abundance of these enzymes within the pancreas2. Steatorrhea: 72-hour quantitative fecal fat determination is the gold standard, excretion > 7g fat day; pts w/ steatorrhea usually > 10g q day 3. Direct pancreatic function tests: performed via specialized centers

Question 707

 Chronic Pancreatitis Imaging?3

Answer 707

1. Calcifications on plain films2. CT/MRI/US3. ERCP 

Question 708

Chronic Pancreatitis1. CT/MRI/US may show what? 32. ERCP can reveal what?

Answer 708

1. CT/MRI/USmay show-ductal dilatation,-enlargement of pancreas,-pseudocysts2. ERCP-can reveal changes in the ducts 

Question 709

What does this CT show?3

Answer 709

1. Inflammatory mass at head of pancreas2. Calcifications3. Low attenuation areas of necrosis

Question 710

Treatment of Chronic Pancreatitis4

Answer 710

1. Establish Dx2. Pain management and control N/V3. Diet4. Surgery

Question 711

Whats on our differential for chronic pancreatitis?4

Answer 711

1. PUD,2. biliary obstruction,3. pancreatic cancer,4. pancreatic duct strictures or stones

Question 712

How would we manage pain management and control N/V?3

Answer 712

1. NSAIDs,  2. low dose amitriptyline,3. opiates

Question 713

Diet changes for chronic pancreatitis?4

Answer 713

1. cessation of alcohol and smoking;2. small low fat meals3. with pancreatic enzyme supplements and4. acid suppression (H2 blockers or PPIs) to reduce inactivation of enzymes from gastric acid

Question 714

1. Who is surgery for in pts with pancreatitis?2. What kinds? 3

Answer 714

1. for those who fail medical therapy, for pain relief—2.-decompression of main pancreatic duct/psuedocyst,-resection of part of the pancreas,-denervation procedures

Question 715

1. Why does pancreatic cancer have a poor diagnosis?2. Risk factors? 43. 85% of all pancreatic cancers are what?

Answer 715

1. Poor prognosis because of late presentation2. Risk factors:-chronic pancreatitis-smoking-obesity-male gender3. Ductal adenocarcinoma85% of all pancreatic cancers

Question 716

Clinical features of pancreatic cancer? 3(most common?***)

Answer 716

1. +/- pain,2. weight loss,3. jaundice.Painless jaundice w/  wt. loss***

Question 717

Tumors in body or tail present w/ what? 2Tumors of the head present w/ what? 3

Answer 717

1. Pain and weight loss2. weight loss, steatorrhea, jaundice

Question 718

PE of pancreatic cancer will show what?3

Answer 718

1. abdominal mass/ascites 20%  pts,2. L supraclavicular node (Virchow's node)3. palpable periumbilical mass (Sister Mary Joseph’s node)

Question 719

Workup for chronic pancreatitis:1. Imaging? What would it show? 32. Labs? What would they show? 33. Serum tumor marker? 1

Answer 719

1. Imaging: US/CT shows pancreatic mass, dilated bile ducts, liver mets Labs: LFT’s show elevated bilirubin, alk phos, aminotransferases normal or slightly elevated Serum tumor maker:CA 19-9 closely related to tumor size

Question 720

1. CA 19-9 can be elevated also in who?2. Serial monitoring can assess what?

Answer 720

1. Can be elevated  in pts w/ benign pancreaticobiliary disorders2. Serial monitoring can assess the response to treatment 

Question 721

Diagnosis of Pancreatic cancer?

Answer 721

FNA, via ERCP, or during surgery

Question 722

Treatment of Pancreatic Cancer5

Answer 722

1. surgical resection is preferred tx****2. +/- radiation therapy or  chemotherapy3. Usually unresectable if involves vascular structures4. endoscopic stent insertion or palliative surgery5. Pain control and pancreatic enzyme replacement

Question 723

1. Treatment of stage I and II pancreatic cancer? and Prognosis?2. Treatment for stage III? and prognoiss?3. Stage IV prognosis?

Answer 723

1. Resectable disease (stage I, II): 15-20% of pts have resectable disease at time of dx, median survival rate 15-20 mos, 5-year survival rate is 20%.2. Unresectable locally advanced (stage III): 30% present in stage III, chemotherapy with or w/o radiation gives modest improvement in survival and palliation.3. Mets (stage IV): 50% have limited survival of 3-6 months.

Question 724

Imflammatory bowel disease: Ulcerative colitis and Crohn's dzDescribe what each causes?UC- 1C- 3

Answer 724

Ulcerative only is muscosa and occasionally submucosa (all throughout)Crohns is tranmural (skip lesions)

Question 725

Etiologic theories of IBD?9

Answer 725

Most common in 2nd & 3rd decades, but can affect any age.Males = females.

Question 726

Pathophysiology of IBD?4

Answer 726

Pathophysiology–Defect in the function of the intestinal lumen–Breakdown of the defense barrier of the gut–Exposure of mucosa to microorganisms or their products–Results in chronic inflammatory process mediated by T cells.

Question 727

Systemic complications of IBD related to imflammatory activity:1. Oral? 12. Eye? 23. Cutaneous? 24. Cardiac? 15. Muskuloskeletal? 1 

Answer 727

HLA B28 presentation

Question 728

Systemic complications of IBD related to small bowel pathophysiology:1. Gallbladder? 12. Intestinal? 13. Renal? 4

Question 729

1. What is Ulcerative Colitis?2. Always includes what? Spreads where?3. What kind of inflammation does it cause with distal colitis? 24. –Extensive colitis aka?

Answer 729

1. uInvolves the mucosal surface of colon with the formation of crypt abscesses.2. Always includes the rectum, spreads proximally3.-Proctitis-Proctosigmoiditis4. Pancolitis

Question 730

Is uniformly continuous, NO SKIP LESIONS1. 50% is where?2. 30% is where?3. 20% is where?WHY WOULD WE DO A colonscopy and not a sigmoidoscopy?

Answer 730

1. –50% rectosigmoid (Proctosigmoiditis)2. –30% to splenic flexure (Left sided colitis)3. –20% extend proximally (Pancolitis)THey are at much higher risk for cancer

Question 731

What are the two pictures showing?

Answer 731

ALWAYS HAVE TO BE THINKING ABOUT COLON CANCER

Question 732

Ulcerative Colitis Clinical Course?4

Answer 732

1. –Flare-ups and remissions.2. –More common in nonsmokers.3. –Disease severity may be lower in active smokers and may worsen in patients who stop smoking.4. –Higher risk for development of cancer. 

Question 733

1. Onset of flares occasionally appears to coincide with what?2. What is the development of cancer in UC related to? 2

Answer 733

1. Onset occasionally appears to coincide with smoking cessation 2.-related to extent and duration of disease and-age at diagnosis

Question 734

Signs and symptoms:–Mild to moderate disease3(hallmark sign)

Answer 734

1. Bloody diarrhea  (hallmark)***2. Lower abdominal cramps–Relieved with defecation3. Fecal urgency

Question 735

Signs and symptoms of severe disease UC?7

Answer 735

–Severe disease:1. Rectal bleeding2. Left lower quadrant cramps3. Severe diarrhea4. Fever (high grade fever would be perforation)5. Anemia (blood loss- iron deficiency)6. Hypoalbuminemia7. Hypovolemia

Question 736

Ulcerative Colitis: Systemic associations?5

Answer 736

–Peripheral arthritis–Central (axial) arthritis–Erythema nodosum (raised rash on the skin that isnt itchy)–Uveitis–Sclerosing cholangitis  

Question 737

What is sclerosing cholangitis?treatment?

Answer 737

Sclerosing cholangitis:  disease of bile ducts that causes inflammation and obstruction,80% of these patients have UC,Treatment: liver transplant.

Question 738

UC labs?4

Answer 738

1. CBC2. Sed rate and CRP3. CMP4. –Perinuclear antineutrophil cytoplasmic antibodies (pANCA) - a lot of people don't have this but still have the disease.

Question 739

Ulcerative Colitis:1. What would the CBC show us? 22. Sed rate and CRP?3. CMP? 3

Answer 739

1. CBC-anemia is common due to multiple factors-leukocytosis2. Sed rate and CRP-elevated sedimentation rate & C-RP reflect acute phase (only elevated while having symptoms)3. CMP-electrolyte disturbances-decreased serum albumin-prolonged clotting time

Question 740

UCDescribe the following for mild, moderate and severe UC–Stools: ?–Pulse: ?–Hematocrit :?–Weight loss: ?–Temperature: ?–ESR: ?–Albumin : ?

Answer 740

Mild–Stools: less than 4/day–Pulse: less than 90–Hematocrit :normal–Weight loss: none–Temperature: normal–ESR: less than 20–Albumin : normal Moderate–Stools: 4-6/day–Pulse: 90-100–Hematocrit : 30-40–Weight loss: 1-10%–Temperature: 99-100–ESR: 20-30–Albumin : 3-3.5 Severe–Stools: >6/day (mostly bloody)–Pulse: >100–Hematocrit : less than 30–Weight loss: >10%–Temperature: >100–ESR: >30–Albumin : less than 3

Question 741

What is an ulcerative colitis diagnosis based on?3

Answer 741

Diagnosis is usually based on1. clinical presentation,2. sigmoidoscopic demonstration of inflammation and3. the exclusion of bacterial and parasitic infection. 

Question 742

What 4 things would give us our diagnosis of UC?(dignosis is best made at?)

Answer 742

1. –Bloody diarrhea (differentiates from Crohn’s)2. –Plain abdominal xrays3. –Sigmoidoscopy4. –CT Scan – (complications) –diagnosis is best made at Sigmoidoscopy. 

Question 743

Ulcerative ColitisDDx?7

Answer 743

–Infectious colitis–CMV colitis–Rectal carcinoma–Crohn’s disease–GI Bleed–Mesenteric Ischemia–Diverticulitis 

Question 744

Ulcerative ColitisIntestinal complications?6

Answer 744

–Bleeding–Toxic megacolon–Perforation–Benign stricture–Malignant stricture–Colorectal cancer

Question 745

Ulcerative colitis treatment?6

Answer 745

–Reduce dietary fiber during an exacerbation.–Prescribe folic acid supplements with Sulfasalazine.–Oral iron may be needed with rectal bleeding and documented iron deficiency anemia.–Frequent follow-up and close monitoring.–Short course of Loperamide for troublesome diarrhea.--Periodic colonoscopy and biopsy in patients with pancolitis lasting more than 8 years

Question 746

Mild to Moderate UC Disease medical treatment? 4

Answer 746

1. –Sulfasalzine (suicidal thoughts and severe depression in males)2. –Olsalazine (non sulfa)3. –Mesalamine4. –May have to add prednisoneTaper to lowest therapeutic dose needed

Question 747

UC uModerate to Severe Disease treatment? 3

Answer 747

–Sulfasalazine–Olsalazine–PrednisoneMay need to consider immunosuppresive therapy for patients who need constant high doses of steroids

Question 748

If the UC is limited to the rectosigmoid what can we do?4

Answer 748

1. Proctocolitis (limited to rectosigmoid)2. Sulfasalazine3. Oral or topical (enema, suppository)4. Hydrocortisone (Enema, Suppositories, Foam)

Question 749

Ulcerative colitis indications for surgery?7

Question 750

Ulcerative colitis surgical options?3

Question 751

What is Crohns Dz?

Answer 751

Transmural involvement with formation of fistulas, narrowing of lumen, obstruction. 

Question 752

CrohnsCan involve any segment of the G.I. tract.List them from most common to least common 5

Answer 752

–Ileocolitis = 45%–Ileitis = 28%–Colitis = 15%–Gastroduodenitis = 7%–Jejunoileitis = 5%

Question 753

What does crohns usually spare?

Answer 753

Rectal sparing

Question 754

How does cigarette smoking relate to  crohns?3

Answer 754

Cigarette smoking is strongly** associated with the1. development of Crohn’s Disease,2. resistance to medical therapy and3. early disease relapse.

Question 755

Crohn’s Disease Clinical Manifestations?8

Answer 755

1. –Presentation depends upon site and severity.2. –Insidious onset usually.3. –Intermittent bouts of low-grade fever, diarrhea and RLQ pain (but all over the place depending on where it can be)4. –Postprandial pain common.5. –RLQ mass6. –Perianal disease (abscess, fistula)7.  Often nocturnal B.M.’s, night sweats, weight loss.8. Skin lesions, primarily erythema nodosum, may precede intestinal symptoms.

Question 756

Patients are often chronically ill with what?\2

Answer 756

–Patients are often chronically ill:1. Weight loss2. pallor 

Question 757

Children & Adolescents: presentation often insidious with what? 4

Answer 757

1. weight loss,2. failure to grow or develop 2° sex characteristics,3. arthritis, or4. fever of unknown origin. 

Question 758

Distinguishing features of Crohns dz of the colon?10

Question 759

On PE what will Crohns show?4

Answer 759

–abdominal distention–abnormal bowel sounds–tenderness in area of involvement–perianal region problems

Question 760

What kind of perianal problems will show on Crohns pts?4

Answer 760

1. Abscess2. Fistula3. skin tag4. anal stricture

Question 761

Labs for Crohns?4

Answer 761

1. CBC2. Sed rate and CRP3. CMP4. ASCA

Question 762

What will the following show on a crohns pt:1. CBC? 22. ESR and CRP? 13. CMP? 34. ASCA? 1

Answer 762

1. CBC-anemia is common due to multiple factors (with diff and also B12 and folate)-leukocytosis2. Sed rate and CRP-elevated sedimentation rate & C-RP reflect acute phase3. CMP-electrolyte disturbances-decreased serum albumin-prolonged clotting time.4. ASCA-serum anti-saccharomyces cerevisiae antibody (ASCA) highly specific, but sensitivity = 30%

Question 763

What kind of imaging is best for Crohns dz and why?

Answer 763

–Barium contrast studies most commonly used for upper & lower G.I tract.ubetter for finding complications…. strictures & fistulas.

Question 764

What will we often see on imaging for crohns dz? 5(two most common?)

Answer 764

1. “cobble stoning”,2. “skip lesions”,3. pseudodiverticula,4. dilated bowel,5. fistulas communicating to adjacent bowel/mesentery/bladder/vagina

Question 765

What other procedure would we do for crohns and why?

Answer 765

–Histology:  from endoscopic biopsy

Question 766

Crohns Dz approach to differential diagnosis? 9

Question 767

What are the two pictures showing with Crohns Dz?

Answer 767

1. Ileitis2. String sign

Question 768

Intestinal complications of CrohnsFistulaWhat are the different kinds?5

Question 769

Describe a typical hemorrhoid tag compared to a Crohns one?

Question 770

Treatment of Crohns Dz?5

Answer 770

1. 5-Aminosalicylic Acid Agents controversial2. Antibiotics3. Corticosteroids4. Anti-TNF therapy5. Immunomodulating drugs

Question 771

What are the three meds in –5-Aminosalicylic Acid Agents controversial?

Answer 771

1. Sulfasazine2. Mesalamine3. Pentasa

Question 772

What are the immunomodulating drugs? 3

Answer 772

1. Azathioprine2. Mercaptopurine3. Methotrexate

Question 773

–Anti-TNF therapy drug?

Answer 773

uInfliximab (Remicade)

Question 774

Older terms describing IBS?4

Answer 774

–Spastic colon–Spastic colitis–Mucous colitis–Functional bowel disease 

Question 775

What is the definition of IBS?

Answer 775

A functional gastrointestinal disorder that  is a variable combination of chronic or recurrent gastrointestinal symptoms not explained by structural or biochemical abnormalities (NCCP,  NUD, IBS)

Question 776

Characteristic symptoms of IBS8 (these are diagnostic)

Answer 776

Continuous or recurrent symptoms for at least 3months of:1. abdominal pain or discomfort 2. pain relieved by defecation3. pain with a change in frequency or form of stoolsand a varying pattern of defecation with 3 or more of the following:4. Altered stool frequency5. Altered stool form6. Altered stool passage (straining, urgency, incomplete evacuation/ sensation of rectal fullness)7. Abdominal distension and bloating8. Passage of mucus

Question 777

Associated symptoms of IBS in order of prevalence?7

Answer 777

Fatigue  96%Back ache  75%Early satiety  73%Nausea   62%Headache   61%Irritable bladder  56%Functional dyspepsia  51%

Question 778

Describe the Rome II criteria for IBS?4

Answer 778

–.  Rome II Criteria:  (most commonly used)1. Abdominal discomfort/pain with 2 of the following 3 features for at least 12 weeks, not necessarily consecutive, for the past 12 months:2. Relief with defecation.3. Onset associated with change in stool frequency.4. Onset associated with change in stool formation

Question 779

Describe the manning criteria for IBS?6

Answer 779

Manning Criteria:1. Pain relieved by defecation.2. More frequent stools associated with pain onset.3. Looser stools assoc with onset of pain.4. Abdominal distention.5. Passage of mucus.6. Feeling of incomplete evacuation.

Question 780

DDX for IBS:Dietary factors? 5Malabsorption? 3Infection? 3Misc? 3Psychologic? 3Inflammatory Bowel? 4

Question 781

Patient assessment: History for IBS?8

Answer 781

1. dietary habits (sorbitol sweetener, caffeine, cruciferous vegetables) carb malabsoption2. travel history3. medication use4. recent gastro-enteritis or food-born illness5. lactose intolerance6. gender, age7. family history8. night time defecation

Question 782

PE for IBS?

Answer 782

Complete physicalA full physical examination is necessary to exclude organic diseasePatient will not usually have abdominal guarding (should have guarding considering the pain the patient is having)

Question 783

Labs for IBS?8

Answer 783

Labs:1. CBC2. ESR3. serum electrolytes4. liver enzymes5. stool occult blood X 36. stool cultures X 37. stool O & P8. urinalysis

Question 784

Imaging for IBS?4

Answer 784

Imaging:–flex sigmoidoscopy–upper GI series with small bowel follow through–plain abdominal radiograph–air contrast barium enema

Question 785

Warning Signs & Red Flags for IBS?8

Answer 785

–Any abnormality on physical exam–Anemia–Clinical or biochemical evidence of malnutrition–Family history of GI cancer, inflammatory bowel disease, or sprue–Fever–Hematochezia–Nocturnal symptoms–Onset of symptoms after age 50

Question 786

Alarm symptoms for IBS?6

Answer 786

1. Constant abdominal pain2. Constant diarrhea3. Constant abdominal distension4. Nocturnal disturbance5. Passage of blood with stool6. Weight loss

Question 787

How do we make a positive diagnosis without costing the patient tons of money?

Answer 787

–Use Rome and Manning Guidelines

Question 788

–American College of GastroenterologistsPatients without alarm features. How should we procede?

Answer 788

–Flex sig, barium enema, colonoscopy, FOBT, stool for O & P or culture or thyroid tests cannot be recommended.

Question 789

Management of IBS?4

Answer 789

1. Make a positive dx2. Consider patients agenda3. Make a management classification4. Plan a management strategy

Question 790

Make a positive Dx:1. Usually possible from hx alone.  What will the hx describe? 32. –In younger patients, a normal what (2) may help to reassure patient.3. In patients >45 with long history and no recent change,  what might help reassure the pt? 2

Answer 790

1. Usually possible from history alone-symptoms usually begin in the late teens to twenties-Pain is intermittent and crampy-Pain does not occur at night or interfere with sleep2. ESR and Hgb3. –a sigmoidoscopy and/or barium enema may help to reassure.

Question 791

Consider patients agenda: What questions should we ask?

Answer 791

A full psychological, social and family history inquiry             is necessary.-Try to get an answer to the question”              “Why has this patient presented at this time”?

Question 792

Make a management classification:–To which category does this patient belong? 5

Answer 792

1. Bloating and pain predominant2. Constipation predominant3. Diarrhea predominant4, Anxiety associated5. Depression associated 

Question 793

Plan a management strategy–Establish a therapeutic provider-patient relationship.1. Focus should be on?2. Who should be responsible for treatment decisions?3. Demonstrate a commitment to what?

Answer 793

1. Focus should be on symptom relief and in addressing the patient’s concern.2. Shift responsibility for treatment decisions to the patient by providing therapeutic options3, Demonstrate a commitment to the patient well being rather than to the treatment of the disease

Question 794

IBS patient education? 5

Answer 794

Patient education1. Validates the patient’s illness and sets the basis for therapeutic interventions.2. Set realistic goals rather than cure3. Teach symptoms monitoring4. Reassure the benign nature of IBS5. Address psychosocial issues

Question 795

The liver produces 1.______ml of bile each day which either drains directly into 2.where or is temporarily stored 3.where?4. The gallbladder then releases bile into duodenum under stimulation of hormone what?

Answer 795

1. 500-15002. the duodenum via the common bile duct3. in the gallbladder via the cystic duct.4. cholecystokinin (CCK).

Question 796

1. CCK released after food is ingested causes what?2. Bile is used to do what?

Answer 796

1. Spincter of Oddi to contract and relax which sends a bolus of bile into duodenum2. emulsify fats and assist with the excretion of cholesterol

Question 797

Biliary Tract Disorders8

Answer 797

1. Cholelithiasis2. Choledocholithiasis3. Acute cholecystitis4. Cholangitis5. Primary sclerosing cholangitis6. Primary biliary cirrhosis7. Carcinoma of the biliary tract8. Hyperbilirubinemia

Question 798

1. What is colelithiasis?2. Supersaturation of bile with cholesterol and GB hypomotility leads to what?

Answer 798

1. the formation of gallstones (choleliths) which are solid concretions of varying quantities of cholesterol, ca+, and bilirubin… which usually form in the GB, but may form in the bile ducts (choledocholithiasis). 2. the formation of cholesterol stones.

Question 799

What are the types of gallstones?2

Answer 799

1. Cholesterol stones 90%2. Pigmented (10%)

Question 800

What are the pigmented types of gallstones? 2

Answer 800

1. Black stones (contain Ca bilirubinate, associated with cirrhosis and hemolysis)2. Brown stones (a/w biliary tract stasis & infection)

Question 801

Risk factor for gallstones?4

Answer 801

1. Fat2. Fertile3. Female4. Forty

Question 802

CHOLELITHIASIS: Symptoms and Signs1. Most common presentation?2. The cardinal symptom?3. Describe this?4. Pain may be brought on by what?If uncomplicated may have normal PE and normal labs

Answer 802

1. Most patients with stones are asymptomatic, however, approximately 20% will become symptomatic during up to 15 years of follow-up2. The cardinal symptom of gallstones is biliary colic; 3. steady RUQ pain radiates to back and right shoulder, may be accompanied by nausea. 4. Pain may be brought on after ingestion of fatty foods.

Question 803

How do you differentiate a gall stone from a polyp?

Answer 803

There is a shadow cast by the stone and no shadow with the polyp

Question 804

CHOLELITHIASIS Treatment1. 60-80% treated how?2. Symptomatic?3. Consider prophylactic cholecystectomy for who? 5

Answer 804

1. asymptomatic/observation2. cholecystectomy3. -Diabetics (Not routinely recommended)-Porcelain gallbladder ( blue discoloration and brittle consistency)-Sickle cell disease-Hereditary spherocytosis (Not routinely indicated in patients w/o gallstones)-Gastric bypass surgery (usually recommended)

Question 805

What is porcelain gallbladder due to?

Answer 805

due to calcification from excessive gallstones

Question 806

Gallstone complications?6

Answer 806

1. Gallstone ileus2. Gallstone pancreatitis3. Acute cholecystitis\4. Choledocholithiasis5. Cholangitis6. Bile Duct injuries

Question 807

What is gallstone ileus?

Answer 807

stone erodes through GB wall and develops a cholecystoenteric fistula leading to obstruction of narrowest segment of bowel causing ileus

Question 808

Acute cholecystitis: 10-20% of pts w/ symptomatic gallstonesWhat can this cause? 4

Answer 808

1. GB gangrene 2. GB perforation3. GB empyema (pus in the GB)4. Emphysematous cholecystitis

Question 809

What would be precipating factor to cause Emphysematous cholecystitis?4

Answer 809

1. GB vascular compromise, 2. stones, 3. impaired immune system, 4. infection w/gas-forming organisms - clostridium, E. coli, Klebsiella

Question 810

PROTECTIVE FACTORSfor gallstones?(whats the big one?)

Answer 810

1. Statins***2. Ascorbic acid 3. Coffee- caffeinated 4. Vegetable protein

Question 811

Choledocholithiasis1. What is this?2. If symptomatic how does the pt usually present? 23. What labs will be elevated? 24. What also may be elevated? 2

Answer 811

1. The presence of gallstones within the common bile duct-May be asymptomatic in up to 30% of pts.2. If symptomatic typically present with -RUQ or epigastric pain, & -nausea and vomiting.3. -LFT’s (ALT-alanine aminotransferase, -AST-aspartate aminotransferase) are elevated, 4. -bilirubin-alkaline phosphatase may be elevated.

Question 812

Complicated choledocholithiasiscan lead to?3

Answer 812

Complicated choledocholithiasis1. acute cholangitis, 2. acute pancreatitis, 3. hepatic abscesses

Question 813

Choledocholithiasis: imaging5(imaging of choice/first choice?)

Answer 813

1. Transabdominal ultrasound2. Abdominal CT3. Endoscopic retrograde cholangiography (ERCP)4. Intraoperative cholangiography or ultrasonography5. Magnetic resonance cholangiopancreatography (MRCP)

Question 814

Endoscopic Retrograde Cholangiopancreatography (ERCP) is the gold standard for what?2

Answer 814

Gold standard for diagnosis of 1. CBD stones, and 2. sphincter of Oddi dysfunction

Question 815

Endoscopic Retrograde Cholangiopancreatography (ERCP)Advanatages? 3Disadvantages?4

Answer 815

1. Therapeutic option when CBD stone identified2. Stone retrieval and 3. sphincterotomyDisadvantageComplications: 1. pancreatitis, 2. cholangitis, 3. perforation of duodenum or bile duct, 4. bleeding

Question 816

Magnetic resonance cholangiopancreatography (MRCP)Advantages? 3Indications?

Answer 816

1. Detects choledocholithiasis, neoplasms, strictures, biliary dilations2. Sensitivity of 81-100%, specificity of 92-100% of choledocholithiasis3. Minimally invasive- avoid invasive procedure in 50% of patientsIf cholangitis not severe, and risk of ERCP high, MRCP useful

Question 817

Magnetic resonance cholangiopancreatography (MRCP)1. Disadvantages? 32. Contraindications? 3

Answer 817

1. cannot -sample bile, -test cytology, -remove stone2. Contraindications: -pacemaker, -implants, -prosthetic valves

Question 818

Treatment for choledocholithiasis?How do we accomplish this? 3

Answer 818

REMOVE THE STONE1. ERCP2. Lithotripsy3. Laparoscopic CBD exploration

Question 819

Acute cholecystitis1. Symptoms? 32. What is this associated with?3. Usually caused by?

Answer 819

1. A syndrome of - RUQ pain, - fever, and - leukocytosis 2. associated with gallbladder inflammation 3. usually caused by cystic duct obstruction.

Question 820

Acute cholecystitis1. 90% caused by what?2. 10% caused by what? 2

Answer 820

1. impacted gallstone2. -bile stasis or -acalculus cholecystitis

Question 821

Acute cholecystitis caused by bile stasis or acalculus cholecystitis happens in what pts?Prognosis?

Answer 821

occurs in critically ill patients.associated with high morbidity and mortality

Question 822

Acute cholecystitisHistory and Physical?9

Answer 822

1. RUQ or epigastric pain 2. may have radiation to right shoulder, 3. often occurs after fatty meal.4. anorexia, 5. nausea and vomiting,6. fever7. Murphy's sign8. Palpable enlarged GB in 30% of pts9. Jaundice in about 10%

Question 823

What is the murphy sign?

Answer 823

(+) Murphy’s sign1. Have patient breathe out2. Examiner places hand below costal margin at RUQ3. Have patient breathe in, if tender, then+ Murphy’s sign

Question 824

Acute cholecystitisLabs? 3Imaging? 2

Answer 824

1. LFTs and bilirubin elevated2. CBC- leukocytosis with left shift 3. C-reactive protein elevated >3 mg/dl1. Ultrasound2. Radionuclide scans (HIDA scan)

Question 825

What will the imaging for Acute cholecystitis show:1. US? 42. Radionuclide scans (HIDA scan)? 1

Answer 825

1. -stones or sludge, -pericholecystic fluid, -distended GB, -thickened GB wall2. failure of GB filling.

Question 826

1. The imaging modality of choice for the gallbladder is what?2. Why? 33. 95% sensitivity for detection of cholelithiasis. Diagnosis based on what?4. >90% sensitivity for detection of acute cholecystitis. Diagnosis based on what? 35. What is this limited by? 2

Answer 826

1. ultrasound.2. It is -fast, real-time, -non-invasive, and -does not utilize ionizing radiation. 3. visualization of a mobile, hyperechoic, intraluminal mass with acoustic shadowing.4. -presence of cholelithiasis, gallbladder wall thickening, -pericholecystic fluid, -and a sonographic Murphy sign.5. Limited by -skill of operator, and -patient’s body habitus.

Question 827

Cholescintigraphy (HIDA scan)Indications?2

Answer 827

1. Functional assessment of the hepatobiliary system2. Integrity of the hepatobiliary tree

Question 828

Cholescintigraphy (HIDA scan)Integrity of the hepatobiliary tree-What are we evaluating? 5

Answer 828

1. Evaluation of suspected acute cholecystitis2. Evaluation of suspected chronic biliary tract disorders3. Evaluation of common bile duct obstruction4. Detection of bile extravasation5. Evaluation of congenital abnormalities of the biliary tree

Question 829

What is Cholescintigraphy (HIDA scan)?

Answer 829

Nuclear medicine exam uses a technetium labeled hepatic iminodiacetic acid (HIDA), which is injected IV and is taken up by hepatocytes and excreted into bile.

Question 830

1. What is a normal HIDA?2. What does slow uptake mean?3. Filling of GB/CBD w/delayed or absent filling of intestine indicates?4. Non-visualization of GB with filling of the CBD and duodenum indicates?5. also can give cholecystokinin to calculate what? and reproduce what?

Answer 830

1. Uptake by liver, GB, CBD, duodenum within 1hr…..normal2.hepatic parenchymal disease 3. obstruction of ampulla 4. cystic duct obstruction and 5. also can give cholecystokinin to calculate GB ejection fraction & can reproduce symptoms

Question 831

Requirements for HIDA Scan1. Patient preparation?2. What may cause a false positive? 2

Answer 831

1. fasted for 2-4 hours2. -Fasted for > 24 hrs -TPN

Question 832

Additional information you need on the Hx before a HIDA scan?5

Answer 832

1. History of previous surgeries, especially biliary and gastrointestinal2. Time of most recent meal3. Current medications esp. opioid compounds-Delaying the study for 4 hours after the last dose4. Bilirubin and liver enzyme levels5. Results of ultrasound

Question 833

Treatment for cholecystitis4

Answer 833

1. Admit to hospital- supportive care, NPO, IV fluids, analgesia, close monitoring of vitals and urinary output2. Antibiotics3. Early laparoscopic cholecystectomy preferred treatment… eventually will need surgery!*****4. Emergency surgery for advanced disease or sepsis

Question 834

Cholecystitis antibiotics?3

Answer 834

1. ciprofloxacin or levofloxacin 2. +Flagyl, or 3. cefuroxime (Ceftin)

Question 835

If fail medical management and poor surgical candidate…. then what do we do? 2

Answer 835

percutaneous cholecystostomy tube + antibiotics

Question 836

Cholecystitis complications?8What are red flags to look for? 4

Answer 836

1. Emphysematous cholecystitis2. Gangrenous cholecystitis3. Pericholecystic abscess formation4. Sepsis5. Peritonitis6. Ascending cholangitis7. Cholecystoenteric fistula8. Perforation Elderly, diabetic, & recurrent cholecystitis10% present with complicationsLook for: -fever + shaking chills, -high WBC, -increased abdominal pain, -persistent symptoms.

Question 837

Chronic Cholecystitis1. Occurs when?2. Usually due to what?3. Symptoms from what?4. Mild histologic inflammation can lead to what? 5

Answer 837

1. Occurs after repeated episodes of mild attacks 2. Usually due to presence of stones3. Symptoms from transient obstruction of cystic duct by gallstones4. Mild histologic inflammation can lead to -shrinking, -scarring,-thickened walls, -mucosal atrophy and -fibrosis of GB wall.

Question 838

Chronic Cholecystitis1. How does pain present?2. Usually precipated by what?3. May have what symptoms? 24. Usually what symptoms do we not have? 25. Can you palpate the GB?6. Trigger?7. Episodes variable intervals: example?

Answer 838

1. Pain: RUQ pain that comes and goes, may be referred to right shoulder or right scapula, subsides in 30 minutes. 2. Usually precipitated by a fatty meal3. May have nausea, vomiting4. Usually no fever, WBC normal5.Gallbladder not palpable6. Trigger: ingestion of fatty foods7. Episodes variable intervals: days to years

Question 839

1. Treatmentfor chronic Cholecystitis?2. Look for concomitant what?3. Prevents future complications by what? 3

Answer 839

1. Cholecystectomy by laparotomy or laparoscopy***2. choledocholithiasis3. Prevents future complications: -acute cholecystitis, -choledocholithiasis, -cholangitis

Question 840

1. What is porcelain gallbladder?2. Thought to be an uncommon manifestation of what?3. Patients with porcelain gallbladder are usually _________?4. the condition is usually found how?

Answer 840

1. Extensive calcium encrustation of the gallbladder wall has been given the term "porcelain gallbladder“ to emphasize the blue discoloration and brittle consistency of the gallbladder wall at surgery2. chronic cholecystitis3. asymptomatic4. incidentally on plain abdominal radiographs, sonograms, or CT

Question 841

1. An uncommon condition; however important to recognize the imaging characteristics because of the risk of what in porcelain gallbladder?

Answer 841

1. GB adenocarcinoma Surgery should not be delayed even if the patient is asymptomatic, because of the association of porcelain gallbladder with carcinoma, although the reported incidence of is highly variable (5-60%).

Question 842

1. Acute cholangitis (inflammation or infection of the bile duct system) is caused primarily by what?2. The organisms typically ascend from where?3. The most important predisposing factor for acute cholangitis is what?

Answer 842

1. Bacterial infection2. Duodenum3. biliary obstruction and stasis secondary to biliary calculi (CBD stone) or benign stricture

Question 843

Cholangitis1. What is Charcots triad? 2. Can start mild then quickly progress to severe and include what? 23. In severe cases, bacteremia and sepsis may lead to what? 2

Answer 843

1. Charcot’s Triad (50-70%)-RUQ pain-Jaundice-Fever and chills2. sepsis, and shock3. -hypotension and -altered mental status (Reynolds' pentad).

Question 844

Septic Cholangitis: 50% mortality rate, usually life threatening sepsis. Describe this?

Answer 844

this is a bacterial infection superimposed on an obstruction of the biliary tree most commonly from a gallstone, but it may be associated with neoplasm or stricture

Question 845

CholangitisLabs will show? 6Imaging? 2

Answer 845

1. leukocytosis, 2. elevated LFTs, 3. elevated CRP, 4. blood cultures usually gram-neg but may be gram-positive or anaerobes, 5. ABGs in severe cases will be metabolic acidosis, 6. may be in renal failure with elevated BUN and creatinine1. Ultrasound2. ERCP

Question 846

What will the following show:1. Ultrasound2. ERCP

Answer 846

1. Ultrasound: dilated bile duct, CBD stones2. ERCP: bile duct stone or obstruction or stricture, also is therapeutic as it can extract stone

Question 847

Cholangitis treatment?4

Answer 847

1. Hospitalize, treat infection with IV antibiotics2. Remove stones (ERCP)3. Blood cultures should be performed in all patients in whom cholangitis is suspected4. Biliary drainage (on elective basis)

Question 848

1. Primary Sclerosing cholangitisis what?2. What develops? 23. Progressive destruction of bile ducts may progress to what?4. Common in what population?5. Closely associated with what?6. Increased risk for what? 4

Answer 848

1. A chronic inflammatory cholestatic disease; characterized by diffuse inflammation of biliary tract2. Fibrosis and strictures develop3. -cirrhosis, -end-stage liver disease4. More common in men, age 20-405. Closely associated with ulcerative colitis6. Increased risk for -cholangiocarcinoma, -gallbladder CA, -colon CA-in patients with cirrhosis, hepatocellular carcinoma.

Question 849

Presentation of PSC6Late presentation will develop symptoms of what? 2What labs will be elevated? 2

Answer 849

1. Progressive, obstructive jaundice2. Malaise, fatigue, 4. pruritus, 5. anorexia, 6. dyspepsia1. cirrhosis2. portal hypertension1. Elevated Alk Phos (3-10x normal), 2. ALT, AST(2-3x normal)

Question 850

Diagnosis of PSC1. Difficult diagnosis to make, but is demonstrated by characteristic what?2. What is found in 70%, A number of other autoantibodies may also be present, but of uncertain clinical significance?3. What may be an alternative to ERCP will see multifocal stricturing and dilation of bile ducts as well, but less invasive?

Answer 850

1. multifocal stricturing and dilation of intrahepatic and/or extrahepatic bile ducts on ERCP. 2. ANCA (anti-neutrophil cytoplasmic antibodits)3. MRCP (magnetic resonance cholangiopancreatography)

Question 851

Treatment of PSC2

Answer 851

1. Balloon dilation or stenting can improve clinical, biochemical and cholangiographic appearances(can delay transplantation)2. only liver transplantation shown to improve survivalImmunosuppressive and anti-inflammatory agents and direct injection of steroids into biliary tree ineffective!

Question 852

Primary Biliary Cirrhosis (PBC)1. Is what?2. Peak incidence?3. Portal inflammation and autoimmune destruction of what?4. Leads to what? 25. 90-95% test positive for what?

Answer 852

1. Slowly progressive autoimmune liver disease2. 90% femalesPeak incidence in 40’s3. intrahepatic bile ducts4. Leads to cirrhosis and liver failure5. antimitochondrial antibody (AMA)

Question 853

Clinical features of PBC1. 50% present how?2. Most common symptoms? 23. Skin hyperpigmentation due to what?4. Rheumatic symptoms, musculoskeletal complaints, frequently due to what?5. What other diseases are associated? 46. Leads to what? 2

Answer 853

1. ~50% asymptomatic at diagnosis 2. Fatigue and pruritus most common symptoms~20%3. melanin deposition4. an inflammatory arthropathy5. -Hyperlipidemia, -hypothyroidism, -osteopenia, -autoimmune diseases6. Portal hypertension, liver failure

Question 854

Physical examination in PBC1-3What are late manifestations of disease and imply cirrhosis?4-8

Answer 854

1. Dry hyperpigmented skin, excoriations2. Xanthelasmas (yellow plaques near the inner canthus of the eyelid) 3. Hepatomegaly ~70%4. Jaundice, 5. spider nevi, 6. temporal and proximal limb muscle wasting, 7. ascites, and 8. edema

Question 855

Diagnosis of PBCNeed 2 of 3 criteria

Answer 855

1. Positive AMA (antimitochondrial Ab) 2. Abnormal LFT3. Compatible biopsy shows destruction of interlobular bile ducts

Question 856

PBC which LFT levels are usually high?2

Answer 856

1. typically alk phos2. GGTP very high

Question 857

Treatment: PBC

Answer 857

Ursodeoxycholic acid

Question 858

Treatment:-Ursodeoxycholic acid (UDCA (ursodiol))What does it do? 3Who does it not work in?

Answer 858

1. Reduces bilirubin, LFTs, cholesterol and IgM2. Delays fibrosis and varices3. Reduced risk of need for liver transplantation and death over 4 years Does not work in advanced disease

Question 859

Treatment: PBC Other drugs?3If they have end stage liver disease?

Answer 859

Other Drugs: if there is significant inflammatory component1. Colchicine2. Methotrexate3. BudesonideTransplant

Question 860

Carcinoma of the Biliary Tract:Cholangiocarcinoma (CA of bile ducts)1. What is dangerous about this cancer?2. Known risk factors?4

Answer 860

1. is often in an advanced stage by the time symptoms develop, which may limit treatment options2. Known risk factors for cholangiocarcinoma include-Primary sclerosing cholangitis -Congenital liver malformations -Infection with parasitic liver flukes and -Exposure to Thorotrast (thorium dioxide) which is a chemical formerly used in medical imaging

Question 861

Diagnostic TestingCholangiocarcinoma4

Answer 861

1. Ultrasound2. CT Scan3. MRI4. Cholangiography via ERCP

Question 862

Cholangiocarcinoma1. Both ultrasound & CT can detect what? 22. CT adds the ability to detect what?3. MRI has also been used to determine what?4. Cholangiography allows for what?

Answer 862

1. -actual tumor and the extent to which it has spread. -Dilatation of the gallbladder or bile ducts can be seen. 2. enlarged lymph nodes throughout the abdominal cavity3. the involvement of bile ducts and blood vessels.4. access to the biliary tree in cases where ERCP has been unsuccessful

Question 863

Carcinoma of the Biliary TractTreatment:1. The majority of cases of cholangiocarcinoma present as what?2. Due to what?3. So how are these pts treated? 2

Answer 863

1. inoperable disease2. due to it’s advanced stage in which case patients are generally 3. treated with -palliative chemotherapy, -with or without radiotherapy

Question 864

Cholangiocarcinoma is considered to be an incurable and rapidly lethal disease unless what?

Answer 864

all of its tumors can be fully resected.Patients may receive adjunctive chemotherapy or radiation therapy after surgery to improve the chances of cure

Question 865

Carcinoma of the Biliary Tract1. What offers the only potential chance of cure in cholangiocarcinoma?2. For non-resectable cases, the 5-year survival rate is __% where the disease is inoperable because of what?3. Overall median duration of survival is what in inoperable, untreated, otherwise healthy patients with tumors involving the liver by way of the intrahepatic bile ducts and hepatic portal vein?

Answer 865

1. Surgical resection2. 0, distal lymph nodes metastases3. less than 6 months

Question 866

Gallbladder cancer (GBC) is an uncommon. Prognosis?High incidence where?How are the majority of these found?

Answer 866

highly fatal malignancyHigh incidence in South America (Chile) maybe due to high prevalence of gallstones and/or salmonella infectionThe majority are found incidentally in patients undergoing exploration for cholelithiasis

Question 867

Gallbladder cancer (GBC) risk factors?7(most important?)

Answer 867

1. Gallstones2. Gallbladder Polyps3. Chronic Salmonella infection4. Abnormal pancreaticobiliary duct junction5. Porcelain gallbladder*****6. Diabetes7. Obesity

Question 868

Presentation/Diagnostic Imaging of gallbladder cancer3 ways?

Answer 868

Presentation is non-specific, usually incidental finding on imaging or intraoperatively.Three Presentations:1. GB CA discovered during or after lap/open cholecystectomy for assumed benign disease2. GB CA suspected after diagnostic evaluation and found on imaging3. GB CA in advanced stage at presentation

Question 869

Histology / Pathology of gallbladder cancer4

Answer 869

1. Adenocarcinoma 80-90%2. Small cell neuroendocrine tumors 7%3. Adenosquamous or squamous cell carcinoma 6%4. Lymphoma, Sarcoma 5%

Question 870

Surgical Managementof GB cancer?4 kinds

Answer 870

Only 10-30% resectable @ time of diagnosis1. Simple cholecystectomy2. Radical cholecystectomy3. Radical cholecystectomy with anatomic liver resection4. Radical cholecystectomy with Whipple procedure…. (pancreaticoduodenectomy)

Question 871

Tumors of the Ampulla of Vater (aka the hepatopancreatic duct….union of the pancreatic duct and the common bile duct)1. The average age at diagnosis of ampullary carcinomas is what?2. What are the most common malignant tumors of the ampulla of Vater? 2

Answer 871

1. 60 to 70 years old 2. Adenomas and adenocarcinomas most common

Question 872

Cancer of the what occurs more commonly near the ampulla than at any other site in the small intestine?

Answer 872

intestinal mucosa

Question 873

Clinical Features of Tumors of the Ampulla of Vater1. Presents most commonly with what?2. Other symptoms?43. 1/3 of patients have what?4. Other tests results?

Answer 873

1. Present most commonly with obstructive jaundice (80%)2. -Weight loss, -anorexia,-fatigue, -abdominal pain, 3. Occult gastrointestinal bleeding is common (one third of patients)4. Positive fecal occult blood test result

Question 874

Imaging for ampulla of vater tumors?4

Answer 874

1. US or CT… CT more sensitive, but US more readily available 2. ERCP3. EUS (endoscopic ultrasound)4. MRCP

Question 875

1. Treatment of ampulla of vater tumors?2. Survival in patients with unresectable ampullary adenocarcinoma is what?3. The overall 5-year survival rate for patients with resected ampullary cancer ranges from what to what?

Answer 875

1. Surgery: Whipple operation is considered the standard approach for ampullary cancer2. 5 to 9 months3. 25% to 55%

Question 876

1. Bilirubin is a yellow pigment formed by breakdown of what?2. Unconjugated bilirubin transported to liver Bound to _______ because _______ in water3. Transported into _________ & conjugated4. Conjugated with what? Secreted into bile5. In ileum & colon… converted to ___________?10-20% reabsorbed into portal circulation and re-excreted into bile or into urine by kidneys

Answer 876

1. heme present in hemoglobin2. albumin, insoluble3. hepatocyte4. With glucuronic acid → now water soluble5. urobilinogen

Question 877

Causes of HyperbilirubinemiaIncreased production of bilirubin: Hemolytic disease causes?6

Answer 877

1. Isoimmune-mediated hemolysis (ABO or Rh(D) incompatibility). 2. Hereditary spherocytosis, elliptocytosis 3. Erythrocyte enzymatic defects (G6PD) deficiency, pyruvate kinase deficiency, and congenital erythropoietic porphyria. 4. Sepsis5. Polycythemia6. Sequestration of blood within a closed space, which occurs in cephalohematoma.

Question 878

The most common hereditary cause of increased bilirubin (5-10% of the population)?

Answer 878

GILBERTS SYNDROME

Question 879

Causes of Hyperbilirubinemia: Decreased clearance of bilirubin? 1

Answer 879

Inherited defects in the UGT1A1 gene, which catalyzes the conjugation of bilirubin with glucuronic acid, decrease bilirubin conjugation. This reduces hepatic bilirubin clearance and increases total bilirubin levels. ( aka Gilbert's Syndrome).GILBERTS SYNDROME

Question 880

1. What does gilbert syndrome produce?2. What may appear under conditions of exertion, stress, fasting and infections, but otherwise patients are usually asymptomatic?

Answer 880

1. Produces an elevated level of unconjugated bilirubin in the bloodstream, but normally causes no serious consequences2. Mild jaundice

Question 881

What is gilbert syndrome caused by?

Answer 881

Caused by a 70-80% reduction in the glucuronidation (the addition of glucoronic acid to a substrate) activity of the UGT1A1 enzymeThis enzyme is also responsible for some of the liver’s ability to detoxify certain drugs

Question 882

What will lab work show for gilbert's syndrome?3

Answer 882

Lab work will show predominantly 1. elevated unconjugated bilirubin (indirect) bilirubin, 2. while conjugated (direct) bilirubin is usually WNL and 3. all other LFTs will be normal

Question 883

Gilbert syndrome treatement?

Answer 883

-No specific therapy is required for patients with Gilbert syndrome. -The most important aspect of care is recognition of the disorder and its benign nature. -Its mode of inheritance should also be discussed to prevent unnecessary testing in family members.

Question 884

Indications for Bariatric surgery?3

Answer 884

1. BMI ≥ 40 kg/m2 without comorbidities2. BMI 35-39.9 kg/m2 with comorbidity3. BMI 30-34.9 kg/m2 (w/specific comorbodities)

Question 885

BMI 35-39.9 kg/m2 with comorbidity which comorbities? 13

Answer 885

1. Type 2 DM 2. OSA3. HTN4. Hyperlipidemia5. Obesity-hypoventilation syndrome (OHS)6. Pickwickian syndrome (OSA+OHS)7. Nonalcoholic steatohepatitis (NASH)8. Pseudotumor cerebri9. GERD10. Venous stasis disease11. Severe urinary incontinence12. Debilitation arthritis13. Impaired quality of life

Question 886

BMI 30-34.9 kg/m2 with what comorbidites? 2

Answer 886

1. Uncontrollable Type 2 DM2. Metabolic syndrome Lack of evidence to support long term benefit in this group

Question 887

Contraindications to bariatric surgery? 10

Answer 887

1. History of bulimia2. Age > 65 or less than 183. For lipid or glycemic control4. For CV risk reduction5. Untreated major depression or psychosis6. Binge-eating disorders7. Current drug or alcohol abuse8. Severe cardiac disease with prohibitive anesthetic risks9. Severe coagulopathy10. Inability to comply with requirements including (life-long nutritional supplements) & dietary changes**

Question 888

Preoperative assessment includes what? 3

Answer 888

1. Psychological2. Medical3. Anesthetic risk

Question 889

Preoperative assessment requires a team approach Who? 5

Answer 889

1. Nutritionist2. Medical bariatric specialist3. Psychologist/Psychiatrist4. Clinical nurse specialist5. Surgeon

Question 890

Goals of the psychologic assessment 4

Answer 890

1. Is the patient able and willing to make the necessary changes?2. Identification of mental disorders3. Social history in regards to previous weight loss attempts, physical activity, substance abuse, compulsive eating4. Does the patient have the cognitive ability to do this and the support to carry it through?

Question 891

Components of the psychological assessment 4

Answer 891

1. Behavioral2. Cognitive/emotional3. Current life situation4. Expectations

Question 892

Medical assessmentincludes? 2

Answer 892

Complete history and physical exam

Question 893

Mechanisms of weight loss with surgery 3

Answer 893

RestrictionMalabsorptionBoth

Question 894

Restrictive surgeries do what? What are the three general processes?

Answer 894

Limit caloric intake by reducing the stomach's capacity:1. Resection2. Bypass3. Creation of a proximal gastric outlet

Question 895

Specific Restrictive surgeries? 3

Answer 895

1. Vertical banded gastroplasty2. Laparoscopic adjustable gastric banding3. Sleeve gastrectomy

Question 896

Malabsorptive surgeries do what? How is this accomplished? 2

Answer 896

Decrease the effectiveness of nutrient absorption by shortening the length of the functional small intestine: 1. bypass of the small bowel absorptive surface area2. diversion of the biliopancreatic secretions that facilitate absorption

Question 897

Malabsorption surgeries 2

Answer 897

1. Jejunoileal bypass2. Duodenal switch operation

Question 898

Combination restrictive/malabsorptive surgeries 3

Answer 898

1. Roux-en-Y gastric bypass (RYGB)2. Biliopancreatic diversion3. Biliopancreatic diversion with duodenal switch

Question 899

3 Most common bariatric surgeries

Answer 899

1. Roux-en-Y gastric bypass (47%)2. Sleeve gastrectomy (28%)3. Laparoscopic adjustable gastric band (18%)

Question 900

Roux-en Y gastric bypass (RYGB)Most commonly performed bariatric surgery in the US47% of weight loss surgeries done in 2011Describe this?

Question 901

RYGB surgery1. Gastric pouch is how big?2. Gastric pouch attached to a section of small bowel ______cm in length (gastrojejunostomy)3. Cut ends of the _____________and the __________are then connected 75 to 150 cm distal from the gastrojejunostomy

Answer 901

1. Gastric pouch less than 30 ml 2.  75-150 cm in length (gastrojejunostomy) 3. biliopancreatic limb, the Roux limb 

Question 902

RYGBMajor digestion and absorption of nutrients occurs where?

Answer 902

in the common channel where pancreatic enzymes and bile mix

Question 903

Weight loss mechanism1. What part of restrictive?2. What contributes to the malabsorption part?3. What suppressses the appetite?4. What two substances are increased post bypass? and what will this promote?

Answer 903

1. Small pouch is restrictive2. There is malabsorption because of the “removed” small bowel3. Ghrelin inhibition (suppresses appetite)4. GLP-1 and CCK increased post bypass (may promote an anorectic state)

Question 904

Gastrojejunostomy can result in ____________with high sugar mealsDescribe this?

Answer 904

1. Dumping syndrome2. lightheadedness, nausea, diaphoresis and/or abdominal pain, and diarrhea

Question 905

Expected weight loss with RYGB 

Answer 905

Up to 70% of extra weight in 2 years

Question 906

Describe the Sleeve gastrectomy? Second most common weight loss surgery performed worldwide28% of all procedures in 2011

Question 907

Sleeve Gastrectomy1. Most of the what is removed?2. Advantages? 23. New stomach is resistant to what?4. Contains a few _______producing cells

Answer 907

1. Most of the greater curvature of the stomach is removed2. Safer and technically less difficult to perform than RYGB3. New stomach is resistant to stretching without the fundus4. ghrelin 

Question 908

Weight loss mechanism: for sleeve gastrectomy?4

Answer 908

1. Restrictive2. Alterations in gastric motility3. Decreased ghrelin levels4. Increased GLP-1 and PYY (promote less hunger)

Question 909

Expected weight loss with sleeve gastrectomy?

Answer 909

60% of excess weight lost in 2 years

Question 910

Laparoscopic adjustable gastric band surgeryDescribe this?18% of bariatric surgeries done in 2011

Question 911

1. What is the lap band and where is it placed?2. How does it work?3. Goal of band adjustments? 2

Answer 911

1. Soft silicone ring connected to an infusion port placed in the subcutaneous tissue2. Ring is inflated with saline to cause variable degrees of restriction3. Goal of band adjustments-Allow a cup of dried food-Satiety for at least 1.5 to 2 hrs after a meal.

Question 912

1. Lowest mortality rate among bariatric pts? 

Answer 912

1. Lap band

Question 913

Weight loss mechanism for Lap Band?

Answer 913

Purely restrictive

Question 914

Expected weight loss for lap band?

Answer 914

50-60% of excess weight lost at 2 years

Question 915

Expected short term weight loss following bariatric surgery for:Gastric bipass?Gastric band?Sleeve gastrectomy?

Question 916

Post surgical diet?

Answer 916

Usually have a liquid diet that progresses to soft then full diet over a period of weeks to months

Question 917

1. When should we monitor weight and blood pressure?2. Watch for what? especially if the pt is vomiting?3. How often should they F/U? 3

Answer 917

1, Monitor at every follow up visit2. Watch for hypotension (especially if persistent vomiting)3. Check BP and weight every 4-6 weeks for the first 6 months-Then at 9 and 12 months post surgery-Then annually

Question 918

Macronutrient needs? 3 Which surgery does not cause significant macronutrient deficiencies?

Answer 918

1, Protein**,2. carbohydrates and3. fats  RYGB

Question 919

1. Lap band common deficiency?2. Sleeve geastrectomy common deficiency?3. RYGB? 7 (but how many vit? 6)

Answer 919

1. Lap BandFolate deficiency 2. Sleeve gastrectomyB12 3. RYGB1. Vit A, D, E, K, B1 (thiamine), B122. Iron,3. Copper,4. Zinc5. Folic acid,6. Biotin,7. Selenium

Question 920

Routine labs at 3, 6, 12 months then annually10

Answer 920

1. CBC2. CMP3. Iron studies, ferritin4. B125. Lipids6. 25 OH-Vit D, PTH*7. Thiamine8. Folate9. Zinc10. Copper

Question 921

Medication management post surgery1. Change meds from delayed release to immediate release. How?2. How should we manage glycemic control?3. How should we manage antireflux symptoms?

Answer 921

1. Crush or liquid formulation2. In general should DC oral antidiabetic meds and use insulin therapy for glycemic control3. Usually can DC antireflux meds except after sleeve gastrectomy reflux symptoms increase

Question 922

Medication management post surgery1. What kind of pills may be less effective?2. In general avoid_____?

Answer 922

1. OCP2. NSAIDs

Question 923

In general avoid NSAIDs:1. Especially in who?2. Why?

Answer 923

1. Especially in patients who have had a Roux-en-Y2. They have very little stomach area and are a set up for ulcers!

Question 924

Factors that affect glycemic control post surgery1. How many calories a day for the first month?2. Average weight loss in the first month?

Answer 924

1. 400-800 kcal diet/day for the first month2. Average weight loss in first month is 20-40 pounds 

Question 925

Further improvement in glycemic control post RYGB1. Improvement in DM control happens regardless of what? 2. DM remission can occur in the first monthBut in 1/3 of patients recurs when? 3. Exposure of distal jejunum to the undigested nutrients. This causes increased what? 3

Answer 925

1. the amount of weight loss2. 5 years3. -peptid YY,-GLP-1-GIP

Question 926

Late complications (post 30 days)4

Answer 926

1. Cholelithiasis2. Nutritional deficiencies3. Neurologic complications4. Psychological complications

Question 927

Complications of RYGB11

Answer 927

1. Gastric remnant distention2. Stomal stenosis3. Internal hernias4. Short  bowel syndrome5. Dumping syndrome6. Metabolic/nutritional derangements7. Renal failure8. Post-op hypoglycemia9. Change in bowel habits10. Failure to lose weight and weight regain11. Ventral incisional hernias** 

Question 928

Which complication would present with these symptoms?Upper abdominal painHiccupsLUQ tympany to percussionShoulder painAbdominal distentionTachycardiaShortness of breathLarge gastric bubble on Xray

Answer 928

Gastric remnant distention 

Question 929

Gastric remnant distention is what? 2Treatment?

Answer 929

1. Gastric pouch severe distention secondary to mechanical obstruction or paralytic ileus2. Progressive distention and rupture 3. Treatment – emergent surgery MAY BE FATAL

Question 930

Stomal stenosispresents how?6

Answer 930

1. Several weeks post op2. Nausea3. Vomiting4. Dysphagia5. GE reflux6. Inability to tolerate oral intake 

Question 931

Stomal stenosis1. is what?3. Workup? 24. Tratment?

Answer 931

1. Narrowing at the anastomosis (pouch to Roux limb) 2. Work up: endoscopy or UGI series 3. Treatment: endoscopic balloon dilation

Question 932

Marginal ulcers1. Occur near where?2. What is it? 23. Causes? 5

Answer 932

1. Occur near the gastrojejunostomy2. -Acid injury to the jejunum or-associated with gastrogastric fistula3. Causes:-Poor tissue perfusion-Excess acid-NSAIDs-H. pylori*-Smoking

Question 933

Marginal ulcers1. symptoms? 42. diagnosis and3. treatment? 5 

Answer 933

1. Symptoms:-Nausea,-pain,-bleeding and/or-perforation2. Diagnosis:Upper endoscopy3. Treatment:-Acid suppression-Sucralfate-DC NSAIDs-DC smoking-Test and treat H. pylori

Question 934

Acute cholecystitis/cholelithiasissigns and symptoms?7

Answer 934

1. RUQ pain2. R shoulder pain or pain in the R upper back3. Nausea and vomiting4. Fever5. Pain may worsen with deep inspiration6. Pain may last longer then 6 hr and start post eating7. Tender RUQ on exam

Question 935

Acute cholecystitis/cholelithiasis1. Can be prevented by what?2. Dx?3. Tx?

Answer 935

1. Can be prevented by post operative ursodiol2. DX:  ultrasound3. TX:  surgical removal of the gallbladder 

Question 936

What is this?Patient presented with abd pain post gastric bypass 

Question 937

1. Short bowel syndrome results in what?2. In severe cases it may require what?

Answer 937

1. Results in severe micro and macronutrient deficiencies 2. In severe cases may require intestinal transplantation

Question 938

Early dumping syndrome presents how?4What percent of pts develop this?What causes it?

Answer 938

15 min after eating development of1. colicky abdominal pain,2. diarrhea,3. nausea and4. tachycardia Up to 50% of patients develop either early or late dumping syndrome Prominent post ingestion of simple carbohydrates

Question 939

Late dumping syndrome1. How long after meal?2. Symptoms? 4

Answer 939

1. 2-3 hours after a meal2.-Dizziness,-fatigue-Diaphoresis-weakness

Question 940

What complication would this patient have?Blackouts and Seizures

Answer 940

Severe hypoglycemia 

Question 941

Severe hypoglycemia1. May be secondary to what?22. What may resolve these symptoms?

Answer 941

1.-May be secondary to insulinoma-May be secondary to islet cell hypertrophy 2. Slowing food transit time may resolve the symptoms

Question 942

Change in bowel habits1. Whats common in RYGB?2. Whats common in gastric banding?

Answer 942

1. Diarrhea or loose stools common post RYGB2. Constipation common post gastric banding

Question 943

Pt complains “I’m not losing weight” or “I’m gaining weight”what could this be?4

Answer 943

1. Maladaptive eating patterns 2. Gastrogastric fistula 3. Gradual enlargement of the gastric pouch 4. Dilation of the gastrojejunal anastomosis

Question 944

Complications from gastric banding8

Answer 944

1. Pouch dilation2. Stomal obstruction3. Band slippage, infection or erosion4. Incisional hernias5. Port-tubing disconnections6. Port infections7. Esophagitis8. Esophageal dilation

Question 945

What would these symptoms indicate?Persistent nausea, vomiting and inability to tolerate secretions or oral intake?

Answer 945

Stomal obstruction 

Question 946

Stomal onstruction1. Can occur when?2. Mayb be secondary to what?23. Dx?4. Tx?

Answer 946

1. Can be acute (shortly following surgery)2. May be secondary to-edema or-due to the band being too tight3. DX:  UGI4. TX:  NG tube to decompress until edema subsides or surgery for band revision

Question 947

Band erosionwill cause what kind of sympotms?5

Answer 947

1. Infection2. Failure of weight loss3. Nausea and vomiting4. Epigastric pain5. Hematemesis

Question 948

Band erosion1. Occurs at a mean of how many months?2. Dx?3. Tx?

Answer 948

1. Occurs at a mean of 22 months 2. DX:  endoscopy 3. TX:  surgical removal

Question 949

Most common sleeve gastrectomy complications4

Answer 949

1. GERD2. Bleeding3. Stenosis of the stoma4. Leaks 

Question 950

What is the most serious complication of SG?

Answer 950

gastric leaksOccur in up to 5.3% of patients

Question 951

Gastric Leaks usually due to local factors that impede healing?

Answer 951

1. Inadequate blood supply at the staple line2. Gastric-wall heat ischemia3. There can be high intragastric pressure

Question 952

What is the differentiation point for the upper and lower GI bleeding?

Answer 952

Ligament of Trietz (LoT) is at the duodenojejunal junction-Upper GI bleedFrom a source above the LoT-Lower GI bleedFrom a source below the LoT

Question 953

Presentation of Upper GI bleeding4

Answer 953

1. Hematemesis2. Blood or coffee grounds detected during nasogastric lavage3. Melena4. BUN to serum creatinine ratio greater than 30

Question 954

Presentation of Lower GI bleeding3

Answer 954

1. Blood clots in the stool2. Red blood that is mixed with solid brown stool3. Dripping of blood into the toilet after a bowel movement

Question 955

1. Hematemesis will look like what?2. Melena can occur with just how much blood loss in the upper GI tract?3. Hematochezia is what color?4. Hematochezia is generally caused by what but can also be caused by?

Answer 955

1. Red or brown flakes like coffee grounds2. 50-100 mL of blood3. Red or maroon colored stool4. Generally from a lower GI source but can occur with a loss of more than 1000 mL of blood in the upper GI tract

Question 956

What causes coffee-ground emesis?

Answer 956

Blood sitting in the stomach acid causes the iron to oxidize resulting in the appearance of coffee ground like flakes

Question 957

Describe the following for Upper GI bleeds and also for Lower GI bleeds:1. Severity?2. Site?3. Presentation? Upper- 3 Lower -14. Nasogastric lavage?5. Bowel sounds?6. BUN:Creat ratio?

Answer 957

Upper GI Bleed(2/3 of cases of GIB)1. More likely to have significant bleeding2. Above the Ligament of Trietz3. -Hematemesis, -melena,-Hematochezia with massive UGI of > 1000 mL4. Blood5. Hyperactive6. > 30:1Lower GI Bleed1. Less likely to present with shock or require transfusion2. Below the Ligament of Trietz3. Hematochezia4. Clear fluid5. Normal6. Normal

Question 958

Review: Where does BUN come from?5 steps

Answer 958

1. When protein is used for energy the carbon is cleaved from the amino acid and leaves behind a Nitrogren. 2. The N takes up 3 H+ to form NH3+ which is ammonia.3. The ammonia (NH3+) is then processed through the liver to become urea. 4. When the urea enters the blood stream it is called the blood urea nitrogren.5. The blood urea nitrogren is then excreted by the kidney

Question 959

BUN increases when protein is broken down and more ammonia formsExamples? 6

Answer 959

1. Burns2. Tetracycline3 Steroids4. Fever5. Catabolic state6. Upper GI bleeding

Question 960

How does Upper GI bleeding cause increased BUN?

Answer 960

(breakdown of the hemoglobin protein by the stomach acid, enzymes)

Question 961

Etiology of Upper GI bleeds?(in order of prevelance)8

Answer 961

1. Peptic ulcer dz 50%2. Portal HTN 20%3. Mallory-Weiss Tear 10%4. Vascular anomalies 7%5. Others 6%6. Erosive Gastritis 5%7. Erosive esophagitis 1%8. Gastric neoplams 1%

Question 962

1. Portal HTN is most commonly caused by?2. Results in formation of what? 3

Answer 962

1. Most common cause is cirrhosis2. Results in formation of -esophageal, -gastric and -duodenal varices that can rupture

Question 963

1. What is a mallory weiss tear?2. Most often caused by?3. Other causes? 6

Answer 963

1. Laceration of the gastroesophageal junction2. Often report a history of retching which may be due to heavy drinking3. -Seizure, -childbirth, -coughing, -straining, -defecation, -weight lifting

Question 964

Vascular anomalies that cause UGI bleeding?2

Answer 964

1. Angiodysplasia2. Telangectasias

Question 965

1. Angiodysplasia are what?2. Telangectasias associated with what?

Answer 965

1. Small AV malformations2. Associated with connective tissue disease like CREST syndrome and HHT

Question 966

1. Erosive gastritis is usually described as what kind of bleeding?2. Erosive esophagitis secondary to what?

Answer 966

1. Usually superficial bleeding that does not lead to acute significant blood loss2. Secondary to chronic reflux

Question 967

“Other” causes of UGI5

Answer 967

1. Aortoenteric fistula2. Hepatic tumor3. Angioma4. Penetrating trauma5. Pancreatic malignancy

Question 968

Other causes of UGI: Aortoenteric fistula. What is it?

Answer 968

Complication post abdominal aortic aneurysm (initial presentation or post graft placement)

Question 969

Etiology of LGI bleeding1. If age younger than 50? 32. If age older than 50? 4

Answer 969

1. Age 50-Diverticulosis-Agioectasias-Malignancy-Ischemia

Question 970

Etiology of Lower GI bleedingDiverticulosis:1. Causes what % of LGIs?2. What increases the risk of bleeding with diverticulosis? 23. Presents how?

Answer 970

1. Causes 50% of LGIs2. ASA and NSAIDs3. Acute, painless, large volume maroon or bright red hematochezia

Question 971

Etiology of Lower GI bleeding:Angioectasias1. Presents how?2. Most common in what ages?

Answer 971

1. Painless bleeding in the upper or lower GI tract2. Most common in > 70 years

Question 972

Anorectal disease causes of LGI? 2What will it look like?

Answer 972

1. Hemorrhoids and fissures2. Bright red blood noted on toilet paper, blood streaked stool or blood dripping into toilet

Question 973

Ischemic colitis1. Most often in pts with what?2. Can be a complication of what?3. When would it be seen in younger pts?

Answer 973

1. Most often older patients with atherosclerotic disease2. Can be a complication of aortic surgery3. Can be seen in younger patients post long distance running

Question 974

When would Radiation induced proctitis present?

Answer 974

Months to years post pelvic radiation

Question 975

Initial management of bleeds3

Answer 975

1. Stabilization2. Blood replacement3. GI consult for Upper or lower endoscopy

Question 976

Assess the degree of bleeding from SBP and HR1. Severe?2. Moderate?3. Minor bleeding?

Answer 976

1. Severe bleedingSBP less than 100 mmHgHR > 1002. Moderate bleedingSBP > 100 mmHgHR > 1003. Minor bleedingNormal HR and BP

Question 977

Labs for bleeding?4

Answer 977

1. CBC--May take 24 hours to reflect the degree of blood loss2. PT/INR3. CMP4. Blood type and screening

Question 978

Stabilization of bleeding?4

Answer 978

1. 2 large bore IV’s2. NS or Lactated Ringer solution3. Nasogastric tube +/-4. IV proton pump inhibitor for UGI

Question 979

Why would we consider a nasogastric tube?

Answer 979

Can lavage with saline and aspirate contents looking for blood to confirm upper source

Question 980

If due to varices from portal HTN then can give what?2

Answer 980

IV octreotide or somatostatin to reduce splanchnic blood flow and portal pressures

Question 981

Transfusion1. Usually target is to maintain Hgb of what?2. How much should Hgb go up per each unit transfused?3. Give one unit of FFP for each _______ of packed red blood cells4. Transfuse platelets if

Answer 981

1. 7-10 g/dL2. 1 g/dL for each unit transfused3. 5 units 4. 1.86. DDAVP

Question 982

Endoscopy1. Unless very unstable usually prefer to do a what?2. Upper endoscopy, can help enhance stomach emptying by the administration of what?3. Endoscopy can be both...?

Answer 982

1. bowel prep if colonoscopy is needed2. IV erythromycin3. diagnostic as well as therapeutic

Question 983

What kind of therapeutic measures can we take with endoscopy? 2

Answer 983

1. Sclerosis or banding of varices2. Cautery of bleeding vessels

Question 984

Treatment:Depending on the underlying cause of the GI bleeding? 3

Answer 984

1. May require surgical repair2. Intra-arterial embolization (done percutaneously)3. Decompression of the portal vein with a shunt placement if varices are not manageable

Question 985

1. If abdominal pain and periotoneal signs consider there is a what?2. If may take the HCT __ hrs or more to reflect the current state of blood volume, so act clinically

Answer 985

1. Bowel of esophageal perforation2. 24

Question 986

The higher the BUN:creat ratio the more likely the bleeding is from what?

Answer 986

upper GI source

Question 987

1. Acute blood loss anemia?2. Chronic?

Answer 987

1. Normocytic/ Just low2. Microcytic

Question 988

Liver Function testsEnzyme tests? 3Synthetic Function? 2Other? 1

Answer 988

Enzyme tests:1. Aminotransferases—ALT & AST2. Alkaline phosphatase—AP3. Gamma glutamyl transpeptidase—GGTSynthetic function:1. Serum albumin2. PT—prothrombin timeOther1. Bilirubin

Question 989

History, History, Historyfor Liver problems?8

Answer 989

1. Exposure to chemicals, meds, herbs2. Accompanying symptoms3. Parenteral exposure4. IV and intranasal drug use5. Tattoos and piercings6. Sexual activity7. Travel and exposure history8. Alcohol history

Question 990

Physical Examfor liver problems?6

Answer 990

1. Cachexia suggests malnutrishment - drinking or drug use 2. Stigmata of longstanding liver disease3. Signs of alcoholic liver disease4. Enlarged left supraclavicular node- Cancer5. JVP suggests RHF secondary to portal HTN6. Right pleural effusion in  the absence of advanced ascites can be seen in cirrhosis

Question 991

Autoimmune Hepatitis1. Two types?2. Characterized by what? 2

Answer 991

1. -Type 1 (Classic): occurs in women of all age groups-Type 2 (ALKM-1): occurs in girls and young women2. Characterized by-circulating autoantibodies (not thought to be part of the pathophysiology)-High levels of serum globulin concentrations

Question 992

Histopathology Autoimmune Hepatitis 

Question 993

Clinical Manifestations of Autoimmune Hepititis? 3Labs? 2

Answer 993

Clinical Manifestations1. Asymptomatic2. Subclinical and those presenting w/ advanced cirrhosis3. Fulminant hepatitisLabs:1. Presence of serological markers2. Generally aminotransferases more elevated than bilirubin and AP

Question 994

Extrahepatic Manifestations of autoimmune anemia?6

Answer 994

1. Hemolytic anemia2. Thyroiditis3. Celiac sprue4. ITP5. Type I DM6. Ulcerative colitisALL of these tend to be AUTOIMMUNE 

Question 995

1. Treatment of Autoimmune Hepatitis?2. Acute risks and complications with steriods? 53. Long term risks? 64. 2nd line?

Answer 995

1. Corticosteriods for sympatomatic disease2.-HTN-high blood sugar,-psychosis,-insomnia-gastric irritation2. -Clouding of the lens in one or both eyes (cataracts)-High blood sugar, which can trigger or worsen diabetes-Increased risk of infections-Thinning bones (osteoporosis) and fractures-Suppressed adrenal gland hormone production-Thin skin, bruising and slower wound healing3. Azathioprine a 2nd line agent

Question 996

1. Hemachromatosis is what?2. What gene? 

Answer 996

1. Genetic disease due to autosomal recessive 2. Identified gene HFE Most common single gene disorder:10% Caucasians heterotozygous0.5% Caucasians homozygousVery rare in other populations

Question 997

Hemochromatosis--Pathophysiology1. Gene defect results in what?2. What does this cause?3. Eventual fibrosis & organ failure leads to what? 4

Answer 997

1. Gene defect results in increased iron absorption in the intestinal tract from the diet2. Iron overload in the body3. -Cirrhosis-Cardiomyopathy-Diabetes-Hypogonadism

Question 998

Iron Overload1. Normal iron content in the body?2. Normally iron storage is controlled so there is no what?3. Accumulation of _______ mg/yr. of iron occurs in hemochromatosis4. Symptoms usually occur when? 25. Females have delayed symptoms because of what? 2

Answer 998

1.  3-4 mg /day2. no excess accumulation3. 500-1000 mg/yr. 4.-around age 40-when iron stores reach 15-40 g!5.-menstruation-breast feeding 

Question 999

Hemochromatosis Clinicical Manifestations are influenced by?6

Answer 999

1. Age2. Sex3. Alcohol use4. Dietary iron5. Menstruation & breast feeding6. Unknown factors

Question 1000

1. Hemochromatosis is accelerated by what? 22. Classic presentation? 

Answer 1000

1. -Alcohol abuse &-hepatitis C accelerate the process2. Classic presentation:-cutaneous hyperpigmentation w/ diabetes & cirrhosis

Question 1001

Reversible Manifestations of hemachromatosis?1. CV? 22. Liver? 33. Skin? 24. Infections? 3

Answer 1001

1. CV:                               -Cardiomyopathy                        -conduction disturbances               2. Liver:                                -abdominal pain                        -elevated LFTs-hepatomegaly3. Skin:-bronzing (melanin deposition)- grayness (iron deposition)4. Infections:-Vibrio vulnificus-Listeria monocytogenes-Pastcuerlla pseudotubercullosis       

Question 1002

Irreversible Manifestations  of Hemacromatosis1. Liver? 22. Anterior pituitary gland?3. Pancreas?4. Thyroid?5. Genitalia?6. Joints?

Answer 1002

1. Liver: : cirrhosis, hepatocellular CA ** 2. Anterior pituitary gland: gonadotropin insufficiency leading? 3. Pancreas: diabetes mellitus (30-60%) 4. Thyroid: hypothyroidism 5. Genitalia: primary hypogonadism 6. Joints: pseudogout 

Question 1003

Diagnosis of HemochromatosisCombination of?3

Answer 1003

1. Clinical2. Laboratory3. Pathologic

Question 1004

Diagnosis of Hemochromatosis1. Laboratory? 22. Gold Standard?

Answer 1004

1. -Elevated serum transferrin saturation > 45%**-Elevated serum ferritin2. -Confirmation = ‘Gold Standard’ = liver biopsy (also defines extent of disease)

Question 1005

Treatment of Hemacromatosis1. Education for evidence of iron overload/complications? 42. Mainstay of treatment?

Answer 1005

1. Education for evidence of iron overload/complications:-Avoid red meat, iron supplements-Avoid alcohol-Avoid handling or eating raw seafood (increased risk of infections)-Receive vaccinations for hepatitis A & B 2. Mainstay of treatment--Phlebotomy

Question 1006

Hemacromatosis Phlebotomy1. Removal of 500 ml of blood removes ______mg Iron2. Do weekly until iron depletion:Hgb = ?Ferritan ?Transferritin saturation ?3. Maintenance:  ?

Answer 1006

1. 2502. Do weekly until iron depletion:Hgb = 10 – 12  gm/dLFerritan < 50Transferritin saturation < 50%3. Maintenance:  phlebotomy every 2-4 months

Question 1007

Hemacromatosis Genetic Testing1. Screen who? 2. Likely to uncover who? 3. Screening test cost: ?

Answer 1007

1. Screen 1st degree relatives  unless under 18 YO 2. Likely to uncover homozygotes who are asymptomatic 3. Screening test cost: $200; done on whole blood sample

Question 1008

Wilson’s Disease1. aka?2. Inheritated how?3. Affects what kind of metabolism?4. Organ damage due to what?5. Easily treated if what?

Answer 1008

1. a.k.a. “hepatolenticular degeneration”2. Autosomal recessive3. Affects copper metabolism4. Organ damage due to copper build up in the liver and brain5. Easily treated if diagnosed early-Difficult to diagnose!!!

Question 1009

Pathogenesis of Wilson’s Disease2

Answer 1009

Pathogenesis:1. The abnormal gene ATP7B affects the carrier protein of copper which is primarily in hepatocytes2. It also impairs the excretion of copper via bile

Question 1010

Wilson's Disease Clinical manifesations?1. Presents when?2. What kind of symptoms? 3

Answer 1010

Presentation varies widely and is often non-specific 1. Generally presents between the 1st and 3rd decade:2.-Liver disease (usually presenting sx in    young children)-Neurologic symptoms-Psychiatric symptoms

Question 1011

Wilson's diseaseDx? 3Tx? 1Prognosis? 

Answer 1011

DIAGNOSIS:1. Ceruoplasmin level2. 24-hour urine for copper excretion3. Look for Kayser-Fleischer rings in eyes Tx:1. Once diagnosed chelation therapy w/ D-penicillamine is the treatment of choice (lifelong) PROGNOSIS:Universally fatal if untreated 

Question 1012

Alcoholic liver dz: three stages?

Answer 1012

Three stages:1. Fatty liver (steatosis)2. Alcoholic hepatitis3. Alcoholic fibrosis and cirrhosis

Question 1013

Fatty Liver1. Most patients present how?2. Can occur how soon after a large alcohol binge & if continues to drink can progress? 3. May have tender what? 4. What is mildly elevated? 5. Can also occur in what other populations? 2

Answer 1013

1. Most patients asymptomatic2. Can occur within hours of a large alcohol binge & if continues to drink can progress3. May have tender hepatomegaly4. Transaminases mildly elevated5. Can also occur in obese individuals and pregnancy

Question 1014

Alcoholic Hepatitis1. Range of presentation?2. Symptoms? 8

Answer 1014

1. Asymptomatic to extremely ill 2.-Anorexia,-N/V,-weight loss,-abdominal pain,-poor nutritional status-HSM-Jaundice-Fever is common

Question 1015

Physical Exam for alcoholic hepatitis?7

Answer 1015

1. Spider angiomas2. Palmar erythema3. Gynecomastia4. Parotid enlargement5. Testicular atrophy6. Ascites7. Encephalopathy 

Question 1016

Lab findings for alcoholic hepatitis?8

Answer 1016

1. Leukocytosis w/ left shift (in severe disease)2. Anemia (Macrocytic- B12*** or GI blood loss/microcytic)3. Transaminases elevated: AST: ALT ratio usually greater than 2:0 (ratio rarely seen in other forms of liver disease)4 Increased AP (> 3x normal)5. Hyperbilirubinemia (60-90%)6. Hypoalbunemia (severe disease)7. Coagulopathy (severe disease)8. Elevated ammonia level (severe disease)

Question 1017

Complications of Alcoholic LD6

Answer 1017

1. Alcoholic fatty liver is reversible2. Alcoholic hepatitis—usually is reversible, but may run a fulminant course progressing to fibrosis and death3. Long standing alcoholic liver disease can lead to cirrhosisOthers:   4. GI bleeds5. esophageal varices6. gastritis/PUD

Question 1018

What are these?

Answer 1018

Mallory Bodies

Question 1019

1. Treatment of Alcoholic LD? 22. Supportive therapy? 5

Answer 1019

1.-CESSATION of ALCOHOL!-Liver transplant in appropriate patients 2. Supportive treatment:-Nutrition- Folic Acid & Vitamin B12-Fluids-R/O other causes for fever, liver disease such as Hep C, Hemochromatosis, neoplasm-Glucocorticosteroids for severe hepatitis

Question 1020

Toxic Hepatitis: Factors influencing toxicity?8

Answer 1020

1. Excessive intake2. Excessive cytochrome P450 activity3. Decrease metabolism pathways in liver4. Depletion of glutathione stores5. Concomitant us of alcohol or other drugs6. Comorbid illness7. Advancing age8. Nutritional status

Question 1021

What is the most common cause of liver failure in the US?

Answer 1021

Toxic HeptitisDrug-induced liver injury (DILI):

Question 1022

DILI: What kind of liver injury could it cause?3Least likely to cause?

Answer 1022

May be1. cholestasis,2. cytotoxic or3. mixed, less likely steatosis

Question 1023

Toxic Hepatitis: Most common drugs implicated in DILI in U.S.? 2

Answer 1023

AcetaminophenAntibiotics 

Question 1024

Treatment for acetaminophen overdose: 3

Answer 1024

1. Acetaminophen level2. Activated charcoal if ingested within 2-3 hours3. N-acetylcysteine for severe overdose 

Question 1025

Chronic Acetaminophen Intoxication1. Signs and symptoms are nonspecific and often confused with what?2. Patients who are at greater risk for developing hepatotoxicity:? 4

Answer 1025

1. Signs and Sx are nonspecific: confused w/ viral diagnosis2. -Ingestion of > 7.5 to 10 g over 24 hours-Ingestion of less than 4g w/ increased susceptibility-Liver tenderness, jaundice or ill-appearing-Supratherapeutic acetaminophen concentrations (> 20 mcg/mL)

Question 1026

Treatment Chronic Acetaminophen Toxicity: Treatment w/ NAC recommended for? 4

Answer 1026

1. All patients w/ liver tenderness &2. Elevated aminotransferases &3. Serum acetaminophen concentrations  >10 mcg/mL4. If serum acetaminophen concentrations are potentially toxic by the nomogram

Question 1027

Viral Hepatitis’sWhat are the types?6

Answer 1027

A, B, C, D, E, & GHepatitis A (HAV)Hepatitis B (HBV)Hepatitis C (HCV)Hepatitis D (HDV)Hepatitis E (HEV)Hepatitis G (HGV)GB virus type C (GBV-C)

Question 1028

General PresentationPrimarily seen w/ HAV, HBV, HCV, HEV: Many cases can be asymptomatic especially in children1. Usually prodrome after exposure: this consists of what? 5

Answer 1028

1. Malaise and fatigue2. Anorexia, N/V3. Myalgia's4. Pale stools, dark urine (urobiligen- direct being excreted in the urine and not in the stool like usual)5. Jaundice

Question 1029

General Signs on Exam of viral hep?3

Answer 1029

1. Jaundice2. RUQ pain3. +/- Hepatomegaly

Question 1030

Labs for viral hep?6

Answer 1030

1. Transaminases elevated, usually in thousands w/ ALT > AST2. Hyperbilirubinemia3. Bilrubinuria4. Alkaline phosphatase mildly elevated5. WBC normal to low6. May have prolonged PT

Question 1031

Acute Viral Hepatitis Management5

Answer 1031

1. Supportive care***2. Manage symptomsNo other liver toxins:3. Acetaminophen4. Alcohol5. Avoid exposure to other hepatitis viruses

Question 1032

How is HAV different from the other Hep viruses?

Answer 1032

NO Chronic infection

Question 1033

HAV Routes of Transmission1. Which one predominates?2. Close personal contact such as? 33. Contaminated what?4. Exposure to?Maternal-fetal transmission has NOT been reported

Answer 1033

1. Fecal-oral route predominates2. Close personal contact -household contact,-sex contact,-day care centers)3. Contaminated food/water4. Blood exposure

Question 1034

Hepatitis A Vaccinatioin1. What kind of vaccine?2. SE? 43. Regimen? 

Answer 1034

1. Inactivated vaccine (Part of childhood vaccinations since 2006)2. SE:-fever,-injection site reactions,-rash,-HA3. Regimen: two doses 6-12 months apart 

Question 1035

Hepatitis A Vaccinatioin: CDC recommendations5

Answer 1035

1. Persons w/ clotting factor disorders or chronic liver dz2. Men who have sex with men3. Users of illegal drugs4. Those traveling to countries w/ high or intermediate levels5. Any person wishing to obtain immunity

Question 1036

1. Postexposure Prophylaxis HAV treatment?2. Situations? 6 

Answer 1036

1. Hep A vaccine or IG 2. Situations:-Close personal contact-Sexual contact-Sharing IV drug apparatus-Child care centers—depends on number of cases-Food handler caseSchools, hospitals, other work settings

Question 1037

HBV Modes of Transmission 

Answer 1037

1. Sexual contact2. Perinatal3. 

Question 1038

1. What is the major mode of transmission in developed countries?2. Major mode in underdeveloped countries?

Answer 1038

1. Sexual contact2. Perinatal. Most infections occur at or near birth

Question 1039

1. How is HBV transmitted horizontally?2. How long can HBV last outside the body?3. How can HBV be spread percutaneously? 3

Question 1040

HBV prevention?Post exposure prophylaxis? 2

Answer 1040

1. Hepatitis vaccine 2. Post-exposure prophylaxis:-Give first dose of vaccine-Administer HBIG at same time—different site than vaccine

Question 1041

Hep B clinical outcomes of accute infection4

Question 1042

Chronic HBV Infection1. Most patients present how?2. Other presentations? 4

Answer 1042

1. Many patients asymptomatic2. Others:-Nonspecific symptoms-Exacerbations similar to the acute infection-Cirrhosis-Hepatic cell carcinoma (HCC)

Question 1043

Extrahepatic Manifestations1. 10-20% of these are due to what?2. What are they?  5

Answer 1043

1. 10-20% due to circulating immune complexes:2.-Fever-Rash-Arthralgias, arthritis-Polyarteritis nodosa-Glomerular disease

Question 1044

HBV Serology5

Answer 1044

1. Hepatitis B surface antigen (HbsAg)2. Hepatitis B core antigen (HbcAg)3. Anti-HBsAg4. Hepatitis B e antigen (HbeAg)5. HBV DNA assays

Question 1045

Hepatitis B surface antigen (HbsAg)1. Appears when?2. Resolved infection becomes undetectable in how many months?3. What makes it a chronic infection?

Answer 1045

Hepatitis B surface antigen (HbsAg):1. Appears prior to onset of symptoms2. 4-6 months3. Persistence past 6 m = chronic infection 

Question 1046

Hepatitis B core antigen (HbcAg)1. Intracellular antigen in what?2. Presence of Anti-HBc of IgM class indicates what?

Answer 1046

1. affected hepatocytes2. acute infection

Question 1047

Anti-HBsAg1. Follows the disappearance of what?2. Usually persists for how long?3. When coexists with HBsAg these persons are regarded as what?4. Presence of anti-HBs only, indicates what?

Answer 1047

1. Follows the disappearance of HBsAg2. Usually persists for life3. When coexists with HBsAg these persons are regarded as carriers of HBV**4. Presence of anti-HBs only, indicates immunity by vaccination

Question 1048

Hepatitis B e antigen (HbeAg):1. What is it?2. Marker of what? 3. HBeAg to anti-HBe occurs early in patients w/ what?4. Seroconversion is delayed for years in patients w/ what?5. when they do seroconvert usually means what?

Answer 1048

1. Secretory protein2. replication and infectivity3. acute infection4. chronic HBV,5. remission of their disease

Question 1049

HBV DNA assays:1. USed for what?2. Recovery from HBV associated w/ what?3. Major role is in patients with HBV to monitor for what?

Question 1050

Treatment for Chronic HBV Infection1. What is the agent of choice?2. Patients who show evidence of virus replication are candidates for therapy. Who are these patients? 33. Patients who have decompensated cirrhosis or are carriers should be managed how?

Answer 1050

1. Interferon or peginterferon is the agent of choice2. Patients who show evidence of virus replication are candidates for therapy:-HBeAg positive patients  -High serum HBV DNA levels  -Active liver disease (chronic hepatitis on liver biopsy) or elevated LFTs3. SHOULD NOT receive treatments

Question 1051

Side Effects of Peginterferon7

Answer 1051

1. Flu-like symptoms2. Immunosuppression3. Abdominal pain, N/V, dry mouth4. Hair loss5. Blurred vision6. Depression7. Anemia

Question 1052

Other Meds for Treating Hep B1. Hep B easily becomes resistant so often what has to be used?2. Treatment is for how long? 3. What are the meds? 4 The meds are complicated and have multiple side effects so I would defer to a specialist

Answer 1052

1.  a combo2. Treatment is for months3. Meds:    -Lamivudine (Epivir)    -Adefovir (Hepsera)    -Entecavir (Baraclude)    -Telbivudine (Tyzeka)

Question 1053

A patient presents with these lab serology's:HBeAg +HBsAg +IgM anti-HBc + What does this patient have?

Answer 1053

Acute Hep B infection

Question 1054

A patient presents with the following lab results:HBsAg + (> 6 months)HBV DNA +ALT and AST moderately elevated ALT > AST What does this patient have?

Answer 1054

Chronic Hep B

Question 1055

Transmission of HCV9(most common)

Answer 1055

1. **IVDU/having sex with IVDU2. Having been in jail more than 3 days3. Religious scarification4. Blood transfusion—since routine testing risk very low****5. Having been struck or cut w/ bloody object6. Pierced ears or body parts7. Immunoglobulin injection8. Perinatal transmission can occur9. Solid organ transplant

Question 1056

Who Should be Screened for HCV?7

Answer 1056

1. Ever injected illegal drugs2. Received clotting factors made before 19873. Received blood/organs before July 19924. Were ever on chronic hemodialysis5. Have evidence of liver disease (increased ALT)6. Are infected w/ HIV7. Healthcare workers after needle stick/mucosal exposure to HCV + bloodChildren born to HCV + mothers

Question 1057

Chronic HCV Infection1. What percent of patients remain HCV RNA positive?2. What percent of patietns have persistently elevated liver enzymes3. Most common presentation/symptom?4. HCV accounts for what percent of HCC cases in the US?

Answer 1057

1. 80-100%2. 60-80%3. Symptoms: most common complaint is fatigue;symptoms are rarely incapacitating, but may lead to a decrease in quality of life4. HCV accounts for 1/3 of HCC cases in the U.S.!!!

Question 1058

Diagnosis of HCV1. HCV RNA rises within what time frame following exposure?2. Anti-HCV is positive within what tie frame after exposure?3. Why is it difficult to distinguish acute from chronic HCV?

Answer 1058

1. 8 days to 8 weeks2. 12 weeks3. both HCV RNA and anti-HCV are present in both

Question 1059

Management of Chronic HCV4

Answer 1059

1. Assess for severity of disease 2. Treat as indicated 3. Counsel to reduce further harm to liver- No tylenol 4. If not already done vaccinate against ?? Vaccinate Hep B or A

Question 1060

Patient Selection for Therapy for Chronic HCVPatient evaluation for therapy? 4

Answer 1060

1. Liver biopsy—almost all patients undergo this2. Test for HIV3. Evaluation for other types of liver disease4. Continued IVDU or alcohol abuse

Question 1061

Treatment for Chronic HCV Infection1. Combination of antivirals? 32. How do we assess treatment response? 2

Answer 1061

Combination of antivirals:1. Peginterferon2. Ribavirin3. Protease inhibitors Assessing treatment response:1. HCV RNA negativity2. Sustained response HCV RNA negativity 6 months after treatment is stopped

Question 1062

Side Effects of Peginterferon/Ribavirin7

Answer 1062

1. Bone marrow suppression2. Myalgia's, HAs, low grade fevers—common 1st 48 hours after infusion3. Neuropsychiatric symptoms (irritability)—must screen for?4. Non-productive cough and dyspsnea5. Ocular: ischemic retinopathy, retinal hemmorrhage—evaluate by ophthalmologist6. Thyroid dysfunction—monitor7. Rash, hair loss, hearing loss, insomnia

Question 1063

Protease Inhibitors: Can be used to treat Hep C1. What med is this?2. Side effects?

Answer 1063

-Harvoni is a tablet of 2 protease inhibitors that is showing promise—VERY expensive-Many side effects including death!

Question 1064

Liver Transplant for HCV Patients1. Describe what would happen in a liver transplant with an HCV patient?2. What meds may prolong survival?3. What other strategies may prolong survival? 2

Answer 1064

1. A non-infected liver transplanted into an HCV infected patient becomes infected and decreases survival 2. Treatment w/ peginterferon + ribavirin may prolong survival 3. Using a younger liver or a liver that is already HCV infected also seems to help

Question 1065

HDV1. Requires what for replcation?2. Why?3. Describe its structure?

Answer 1065

1. Requires HBV for replication2. HBsAg coat3. Single stranded RNA rod-like structure 

Question 1066

HDV1. What activates replication of the HDV RNA in hepatocyte?2. What directs packaging HD virion into HBsAg?3. What envelope provided by HBV?

Answer 1066

1. Small HDAg2. Large HDAg3. Lipoprotein 

Question 1067

HDV Genotypes1. What type is most common in the western world?2. Compare its prognosis with acute HBV?3. Describe its progression?

Answer 1067

1. Western world**2. Increased risk of fulminant course when compared to acute HBV3. Progression toward cirrhosis rapid

Question 1068

Genotype II for HDV is found where?Genotype III?

Answer 1068

Genotype II: far East Genotype III: Venezuela, Columbia, Brazil, Peruvian and Amazon bases

Question 1069

Transmission of HDV? 4Other info:10% of HBV patients have HDVHDV may be cytotoxic

Answer 1069

1. Parenteral 2. Close personal contact 3. Multiple transfusions 4. Contaminated dialysis equipment 

Question 1070

Clinical Features of HDV1. Coinfection with HBV? 22. Superinfection on top of chronic HBV? 2

Answer 1070

Coinfection w/ HBV:1. Severe acute disease B + D; usually self-limited (direct cytopathic damage)2. Low risk of chronic infection Superinfection on top of chronic HBV:1. Usually develop chronic HDV infection, HBV suppressed2. High risk of severe, progressive chronic liver disease (immune damage)

Question 1071

1. HDV Prevention & Treatment?2. HBV-HDV Coinfection?3. Chronic HDV?

Answer 1071

1. Hep B vaccine2. HBV-HDV Coinfection:Pre- or post-exposure prophylaxis to prevent HBV infection 3. Chronic HDV treated w/ peginterferon 

Question 1072

HEV1. What kind of virus?2. Transmitted how?3. Usually have a hx of what?4. Infects in what forms?

Answer 1072

1. RNA virus 2. Enterically transmitted, waterborne virus 3. U.S. cases usually have travel history to HEV-endemic area 4. NO chronic form

Question 1073

HEV Transmission1. Spread by what most commonly?2. What transmission is uncommon?3. Can also be transmitted by what other things? 2 

Answer 1073

1. Spread by fecally contaminated water 2. Person-person transmission uncommon 3.-Can be transmitted by blood transfusion in endemic areas-CAN BE transmitted from mother to newborn

Question 1074

HGV = GB virus type C (GBV-C)3 different agents isolated: A, B, C—C is identical to HGV1. How is it spread?2. Evidence suggests it doesnt cause what?3. How does it affect HIV pts?

Answer 1074

1. Flavivirus, can be spread through contaminated blood and sexual contact2. Evidence suggests doesn't cause hepatitis in humans3. Protective effect on patients coinfected w/ HIV

Question 1075

Acute Hepatitis Complications3

Answer 1075

1. Cholestatic hepatitis 2. Raging fulminant hepatitis 3. Chronic hepatitis

Question 1076

Chronic Hepatitis: Liver BiopsyWhat do we do before treatment?Typical presentation? 4

Answer 1076

1. Disease staging before treatment Typical progression:1. Chronic inflammation in portal areas2. Necrosis/inflammation (moderate activity)3. Fibrosis (Marked activity)4. Cirrhosis (non-reversible)

Question 1077

Cirrhosis 

Answer 1077

Definition: development of fibrosis of liver with formation of regenerative nodules; results in impairment of synthetic, metabolic and hemodynamic functions of the liver.

Question 1078

Diagnosing Cirrhosis1. Imaging studies such as what can suggest dx? 32. What is the gold standard?3. Determine underlying etiology using Hx & labs? 3

Answer 1078

1. US, CT, MRI2.Biopsy is gold standard**3. Determine underlying etiology using Hx & labs:-Chronic hepatitis-Alcoholic hepatitis-Wilson's disease

Question 1079

Etiologies1. What causes account for 1/2 of transplant pts? 22. Other etiologies? 6

Answer 1079

1. Alcohol and Chronic HCV in U.S. account for ½ of transplant patients 2.-10-15% cryptogenic—diagnosis of exclusion-Primary biliary cirrhosis (PBC)-Chronic HBV-Wilson's disease-Hemochromatosis-Nonalcoholic steatohepatitis

Question 1080

Pathophysiology1. Cirrhosis is a process of what of the liver?2. Normally the extracellular matrix has different types of what that are in balance? 23. As chronic insult to the liver persists over years the collagen production in the liver does what?4. The ECM becomes what and the normal functions of the liver are compromised?5. The change in the ECM affects hepatic what cells?6. Early fibrotic changes are ________,  as progression occurs the changes become_________?

Answer 1080

1. scarring2. ollagen and glycoproteins3. increases 4-10 fold4. stiffer5. stellate cells6. reversible, irreversible

Question 1081

Laboratory Abnormalities in Cirrhosis6

Answer 1081

1. Aminotransferases2. Alkaline phosphatase3. Bilirubin4. Albumin5. Prothrombin time6. Serum sodium 

Question 1082

Lab Abnormalities in CirrhosisHow will the following be affected?1. Aminotransferases?2. Alkaline phosphatase?3. Bilirubin?4. Albumin?5. Prothrombin time?6. Serum sodium? 2 

Answer 1082

1. Aminotransferases: AST/ALT--moderately elevated2. Alkaline phosphatase: Elevated, but < 2-3 x normal3. Bilirubin: levels rise as cirrhosis progresses4. Albumin: levels fall as cirrhosis worsens5. Prothrombin time: increases as ability of cirrhotic liver to synthesize clotting factors diminishes6. Serum sodium: Hyponatremia seen w/ ascites and High levels of ADH (Why?)

Question 1083

Higher levels of Alkaline phosphatase would lead us to suspect what?2

Answer 1083

primary sclerosing cholangitis or PBS

Question 1084

Cirrhosis Hematologic lab abnormalities 3

Answer 1084

1. Thrombocytopenia2. Leukopenia3. Anemia

Question 1085

What is the first hematologic change to occur in cirrhosis and why? 

Answer 1085

Thrombocytopenia: usually the first; secondary to portal hypertension and attendant congestive splenomegaly

Question 1086

1. Leukopenia occurs in cirrhosis why?2. What is anemia from in cirrhosis? 5

Answer 1086

1. Leukopenia: hypersplenism w/ margination2. Anemia:-Acute/chronic GI blood loss-Folate deficiency (Occurs early in malnutrition, B12 deficiency occurs quite late)-Hypersplenism-Bone marrow suppression-Anemia of chronic disease (inflammation)

Question 1087

What is portal HTN? What does it result in? 5

Answer 1087

Increased blood pressure in the portal vein due to increased resistance to the blood passing through the vessels in the liver Results in:Alternate “routes”:1. Esophageal varices2. Enlarged abdominal wall vessels(caput medusa)3. Hemorrhoids4. Splenomegaly5. Ascites (protein rich fluid)

Question 1088

Managing Portal Hypertension4

Answer 1088

1. Temporary measures: remove ascitic fluid 2. Portal shunts 3. Treat liver disease 4. Liver transplant

Question 1089

Hepatic Encephalopathy (HE)1. Spectrum of potentially reversible neuropsychiatric abnormalities: 32. Syndrome observed in patients with cirrhosis-Whats a prerequisite for this?-Can occur in what kind of patients that dont have cirrhosis?

Answer 1089

Spectrum of potentially reversible neuropsychiatric abnormalities:-Cognitive abilities-Psychiatric state-Motor impairment, including focal neurologic findings 2. Syndrome observed in patients with cirrhosis:-Prerequisite is a diversion of portal blood to the systemic circulation-Can occur in patient’s without cirrhosis who have surgically created portosystemic shunts

Question 1090

Hepatic Encephalopathy (HE): What other causes need to be ruled out before diagnosis?7

Answer 1090

Other precipitating causes need to be ruled out:1. Hypovolemia2. GI bleed3. Hypokalemia/metabolic alkalosis4. Hypoxia5. Sedatives or tranquilizers6. Hypoglycemia7. Infection (including SBP)Rarely hepatoma or vascular occlusion

Question 1091

Diagnosing Hepatic encephalopathy: What two staging techniques are used for this?2

Answer 1091

1. West-Haven Classification system grades HE stages 0-42. Glasgow Coma Scale may be used in severe HE 

Question 1092

Describe Stages 0-4 for the West-Haven Criteria for HE?

Question 1093

Tests for diagnosing HE?4

Answer 1093

1. Ammonia and manganese are neurotoxins that precipitates HE2. Serial ammonia levels are inferior to clinical assessment in gauging improvement or deterioration in patient who is being treated for HE3. EEG findings are not specific to HE, but if seizure activity needs to ruled out an EEG may be helpful4. CT and MRI are helpful in ruling intracranial lesions

Question 1094

Treating HE:1. What is the first thing we need to do in treatment?2. How much should we give?3. SE? 34. Another option?5. What other correction do we need to make if present?

Answer 1094

1. Need to lower ammonia levels: Lactulose:2. Give enough so that the patient has 3-4 soft stools a day3. SE: abdominal cramping, bloating, flatulence4. Enemas5. hypokalemia

Question 1095

Differential Diagnosis for HE?6

Answer 1095

1. Intracranial Lesions (?)2. Infections (?)3. Metabolic encephalopathy4. Toxic encephalopathy5. Organic brain syndrome6. Postseizure encephaolpathy

Question 1096

Treatment of HESteps 6

Answer 1096

1. Determine the stage of HE2. Exclude nonhepatic causes of altered mental function3. For overt HE lactulose may suffice4. Low protein diet may be helpful5. Rifampin orally effects the metabolic function of the gut microbiota and is as effective as lactulose with less SE’s6. For more severe HE the patient may be at risk of aspiration and may need to intubated 

Question 1097

LactuloseSE? 2Severe SE? 2

Answer 1097

Overdosage:1. severe diarrhea,2. eletrolyte abnormalitiesSevere SE:1. ileus2. hypovolemiato the point of worsening HE 

Question 1098

Ischemic Bowel Disease1. Changes how with age?2. Mortality?3. Patterns? 4

Answer 1098

1. Increases with age2. High mortality, 50~90%3. Patterns: -small and/or large bowel -diffuse or localized-segmental or focal-superficial or transmural

Question 1099

4 Major causes of Acute Mesenteric Ischemia

Answer 1099

1. SMA embolism—50%2. SMA thrombosis—15-25%3. Nonocclusive ischemia—20-30%4. Mesenteric venous thrombosis—5%

Question 1100

1. SMA thrombosis is often imposed on what?2. Also occurs with what? 2

Answer 1100

1. Often superimposed on patients w/ progressive atherosclerotic disease2. Also occurs w/ trauma or infection

Question 1101

Acute mesenteric ischemia1. Occlusive causes? 32. Non-occlusive causes? 1

Answer 1101

1. Occlusive-Mesenteric arterial embolism-Mesenteric arterial thrombosis-Mesenteric venous thrombosis2. Non-Occlusive-Hypoperfusion

Question 1102

Circulation to the intestines1. Primarly through what? 22. Requires how much of our cardiac output?

Answer 1102

1. Primarily SMA and IMA-Lots of collateral circulation2. Requires 10-35% of the cardiac output

Question 1103

Regulation of intestinal circulation: In what ways?5

Answer 1103

1. Perfusion pressure2. Neural and hormonal mechanisms3. Sympathetic nervous system, 4. Renin angiotensin system, 5. vasopressin from the pituitary

Question 1104

What does vasopression do for the intestinal vasculature?2

Answer 1104

Vasopressin 1. Causes mesenteric (arterial) vasoconstriction and venous dilation2. Reduces portal venous pressure in patients bleeding from portal hypertension

Question 1105

Acute mesenteric ischemia: Hallmarks of clinical presentation3

Answer 1105

1. Severe cramping abdominal pain, 2. out of proportion of physical findings, 3. poorly localized

Question 1106

Acute mesenteric ischemia: Clincial presentation1. Abdominal exam?2. Occult blood sample?3. As bowel ischemia worsens what will happen? 4

Answer 1106

1. Abdominal exam may be normal initially2. Occult blood in stool3. As bowel ischemia worsens-Abdominal distention-Absent bowel sounds-Peritoneal signs-+/- feculant odor to the breath

Question 1107

Risk factors associated with acute mesenteric arterial embolism11

Answer 1107

1. Advanced age2. Coronary artery disease3. Cardiac valvular disease4. History of dysrhythmias**Atrial fibrillation5. Post-myocardial infarction mural thrombi6. History of thromboembolic disease 7. Aortic surgery8. Aortography9. Coronary angiography10. Aortic dissection11. CHF

Question 1108

Mesenteric arterial embolism1. What demographic affected mostly?2. What artery does it involve and affects what structure?3. Where?

Answer 1108

1. Median age: 70, 2/3 are woman2. Superior Mesenteric Artery often involved and affects the jejunum3. 6-8 cm beyond the arterial origin, near middle colic artery

Question 1109

Mesenteric arterial embolism1. Comes from where?2. What also occurs to promote the embolism?3. Clinical presentation? 44. Prognosis compared to SMA thrombosis?

Answer 1109

1. Thrombus from L atrium, L ventricle or cardiac valves:--Over 20% of cases have emboli multiple2. Arteriolar vasoconstriction also occurs 3. -Sudden onset of severe pain, that is out of proportion to the physical findings 75%-Nausea, vomiting, -frequent bowel movement-Occult blood in stool 25%4. More favorable prognosis than SMA thrombosis

Question 1110

Mesenteric arterial thrombosis usual suspects4

Answer 1110

1. Atherosclerotic disease2. Trauma3. Infection4. Does not appear to be associated with a coagulopathy

Question 1111

Mesenteric arterial thrombosis1. Hx of?2. Usual site of blockage is what? 23. Prognosis?4. When do symptoms develop?

Answer 1111

1. Usually can elicit a history of chronic mesenteric ischemia2. Usual site of blockage is the -origin of the SMA or -celiac axis3. Less favorable prognosis4. Symptoms do not develop until significant blockage (collateral circulation) which can complicate revascularization

Question 1112

Mesenteric venous thrombosis1. In what population of ppl?2. Onset?3. Thrombosis of superior mesenteric vein or?4. 30% of the cases involve thrombosis of what?

Answer 1112

1. Younger population 48~60 y/oPrimary 20%Secondary 80%2. Onset can be acute or develop over the course of a few weeks3. Thrombosis of superior mesenteric vein or- intestinal strangulation from hernia or volvulus4. thrombosis of the portal vein

Question 1113

Mesenteric venous thrombosis:Longer symptoms presentation5Sympotom onset?

Answer 1113

1. Pain diffuse and nonspecific initially, but later becomes constant2. Anorexia 53-54% 3. vomiting 41-77%4. diarrhea 36%, constipation 13-34% 5. hematemesis 9-42%More insidious onset of symptoms

Question 1114

Mesenteric venous thrombosisrisk factors?9

Answer 1114

1. Hypercoagulable state (up to 75% have a hypercoagulable disorder)2. Portal hypertension3. Abdominal infections4. Blunt abdominal trauma5. Pancreatitis6. Splenectomy7. Malignancy in portal region8. Personal or family history of DVT or PE9. Dehydration

Question 1115

Intestinal ischemia in mesenteric venous thrombosis pathophysiology6 steps to the end result?

Answer 1115

1. Decreased mesenteric venous blood flow2. Results in bowel wall edema (tons of this!!! this is how you know its venous and not arterial)3. Fluid efflux into the bowel lumen4. Results in systemic hypotension & an increase in blood viscosity5. This results in diminished arterial flow6. Leading to submucosal hemorrhage & bowel infarction

Question 1116

1. Nonocclusive mesenteric ischemia is a result of what?2. Risk factor?3. Often the pt has what? 2

Answer 1116

1. Result of splanchnic hypoperfusion & vasoconstriction2. Risk factor—atherosclerotic disease3. Often the patient has a -life-threatening illness/-is being treated e.g. CHF, MI, sepsis etc.

Question 1117

Nonocclusive mesenteric ischemia: Pathogenesis1. In general?2. How does this happen? 2

Answer 1117

1. mesenteric vasospasm2. -Homeostatic mechanism maintains cardiac and cerebral blood flow-Vasopressin & angiotensin involved

Question 1118

Nonocclusive mesenteric ischemia1. Mortality?2. Severity and location of pain may be different than occlusive mesenteric ischemia. Presentation? 4

Answer 1118

1. high mortality -up to 70%2. -Progressive abdominal pain, -bloating, -N/V, -mental status changesUp to 25% of patients do not have abdominal pain

Question 1119

What if the ischemia is in the colon?1. 90% of pts are of what age?2. How do patients appear?3. Presentation? 44. Dx?

Answer 1119

1. 90 percent of patients over age 60 years 2. -Acute precipitating cause is rare -Patients do not appear severely ill 3. -Mild abdominal pain, -tenderness present -Rectal bleeding, -bloody diarrhea typical4. Colonoscopy is procedure of choice

Question 1120

Summary of the etiology of acute mesenteric ischemia 1. Aterial emboli? 22. Arterial thrombosis? 13. Venus thrombosis? 24. Nonocclusive mesenteric flow? 1

Answer 1120

1. Arterial emboli: -Atrial fibrillation, -MI2. Arterial thrombosis: -Atherosclerotic disease3. Venous thrombosis: -Underlying disorder in coagulation (hypercoagulable), -neoplasm4. Nonocculsive mesenteric ischemia: -Low flow states

Question 1121

Acute mesenteric ischemia workup?2

Answer 1121

1. Lab2. Imaging

Question 1122

Which labs for Acute mesenteric ischemia ?5

Answer 1122

1. ↑WBCs with predominance of immature cells2. ↑HCT (hemoconcentration)3. ↑Amylase (50%), ↑phosphate (80%)4. ↑Serum lactate--77-100% sensitivity/42% specificity5. Metabolic acidosis

Question 1123

Which imaging tests for Acute mesenteric ischemia?2

Answer 1123

1. Plain abdominal x-rays2. CT scan of the abdomen

Question 1124

Any patient with 1._____________ and 2._____________ has intestinal ischemia until proven otherwise

Answer 1124

1. abdominal pain2. metabolic acidosis

Question 1125

Imaging – Plain X-rays will show?6

Answer 1125

1. Pneumatosis intestinalis2. Portal venous gas 3. Thickened bowel wall with thumb-printing4. Air fluid levels5. Dilated bowel loops6. Gasless abdomen

Question 1126

In cases of surgically proven acute mesenteric ischemia:what will you find on the XRAY? 5

Answer 1126

1. Air fluid levels 67%, 2. Dilated bowel loops 18%, 3. Gasless abdomen 10%, 4. Pneumatosis 2%, 5. Portal venous gas 2%

Question 1127

1. What is Pneumatosis intestinalis?2. Suggestive of what?

Answer 1127

1. Gas cysts in the bowel wall (It is not gas in the bowel lumen)2. Suggestive of necrotizing enterocolitis

Question 1128

1. Portal venous gas is what?2. A variety of causes such as what? 2

Answer 1128

1. Accumulation of gas in the portal vein and it’s branches2. A variety of causes such as -ischemic bowel, -intra-abdominal sepsis

Question 1129

What are the first step in evaluation of the acute abdomen?

Answer 1129

Upright and supine plain abdominal x-rays

Question 1130

What will you see on xrays that are suggestive of bowel ischemia?5

Answer 1130

1. Free air, 2. obstruction,3. ileus, 4. intussusception, 5. volvulusMesenteric ischemia is difficult to diagnose on plain films alone

Question 1131

What is the next step if the dx is not made on plain films?

Answer 1131

CT

Question 1132

CT is the preferred imaging study: appearance will vary based on what?7

Answer 1132

1. Cause2. Severity3. Localization4. Extent and distribution5. Presence and degree of submucosal or intramural hemorrhage, 6. superimposed bowel wall infection, or 7. bowel wall perforation

Question 1133

1. CT with or without contrast?2. What about if ordering a CT angiogram?

Answer 1133

1. Oral and IV contrastOral contrast necessary for evaluation of the mucosal thickening of the bowel wall2. If just ordering a CT angiogram (CTA) may not want to have oral contrast because it can obscure the view of the mesenteric vessels

Question 1134

CT findings5

Answer 1134

1. Bowel wall thickening2. Bowel dilation (can be assoc. with wall thinning)3. Fat stranding and ascites4. Varying degrees of attenuation-High attenuation (white)-Low attenuation (black)5. Pneumatosis and portomesenteric gas

Question 1135

What is the most common finding in ischemic colitis, colonic infarction, and venous occlusion?

Answer 1135

Bowel wall thickening

Question 1136

Contrast-enhanced transverse CT scan shows several infarcted small-bowel loops (arrows), which manifest with dilatation and air-fluid levels but no wall thickening, due to what?

Answer 1136

transmural small-bowel necrosis

Question 1137

What is a good study for evaluation of suspected intestinal ischemia but don’t do if planning on percutaneous angiography too (excessive contrast with 2 studies)?

Answer 1137

CT angiography

Question 1138

What test is better at diagnosing venous occlusions?

Answer 1138

MR angiography

Question 1139

May need mesenteric percutaneous arteriography. When? 2

Answer 1139

1. If the diagnosis is in doubt after non-invasive radiologic evaluation2. If diagnosis is fairly certain and need consideration for percutaneous treatment or for surgical planning

Question 1140

mesenteric percutaneous arteriography cannot be used for what?

Answer 1140

Can’t be used for venous occlusions

Question 1141

Treatment of acute mesenteric ischemia?9

Answer 1141

1. Hemodynamic monitoring and support (Correct hypotension, hypovolemia)2. Correction of metabolic acidosis3. Broad spectrum antibiotics4. NG tube for gastric decompression5. Vasopressors that have less effect on mesenteric perfusion: 6. Anticoagulation unless actively bleeding7. Correction of arrhythmias8. Then imaging9. At angiography can give papaverine directly to relieve mesenteric vasoconstriction10. If peritoneal signs, may proceed directly to the OR for surgical repair

Question 1142

Which vasopressors would you use in treatment?3

Answer 1142

1. dobutamine, 2. low dose dopamine, 3. milrinone

Question 1143

How should imaging proceed?

Answer 1143

-May start with plain films or CT, but if strong clinical suspicion should proceed DIRECTLY to angiography

Question 1144

If you have peritoneal signs proceed directly to what?

Answer 1144

may proceed directly to the OR for surgical repair

Question 1145

At angiography can give what to relieve vasoconstriction?

Answer 1145

papaverine

Question 1146

1. Gold standard diagnostic study for acute arterial ischemia?2. What is MAE?3. MAT?4. MVT?

Answer 1146

1. Mesenteric Angiography/Treatment2. MAE: Surgery & embolectomy; or local infusion of thrombolytic therapy3. MAT: Surgery w/ thrombectomy + revascularization or heparinization 4. MVT: heparinization + resection of infarcted bowel

Question 1147

Nonocclusive mesenteric ischemia: treatment?4

Answer 1147

1. Papaverine infusion during angiography2. Reverse underlying conditions3. Repeat angiography can be done in 24 hrs4. Surgical exploration reserved for patients with peritoneal signs

Question 1148

Overview of the care of these patients 6

Answer 1148

1. Cardiac monitor, 2. venous access, 3. oxygen4. May require fluid resuscitation5. Broad-spectrum antibiotics6. Surgery

Question 1149

Chronic mesenteric ischemia1. Presentation? 22. Secondary to what?3. Strongly associated with what?

Answer 1149

1. -Intestinal angina-Episodic or constant intestinal hypoperfusion2. Secondary to atherosclerosis3. Strongly associated with meals

Question 1150

Esophageal Tumors1. Benign?2. Malignant?

Answer 1150

1. BenignLeiomyoma2. MalignantEsophageal carcinoma

Question 1151

Esophageal carcinomasSquamous cell carcinoma1. More prevalent where?2. Risk factors? 5

Answer 1151

1. More prevalent worldwide2. Risk factors: -long-standing esophagitis, -achalasia, -smoking, -alcohol, -diet

Question 1152

Esophageal carcinomasAdenocarcinoma1. More common where?2. Occurs in what disease?3. What part of the esophagus?

Answer 1152

Adenocarcinoma1. More common in USA2. Occurs in Barrett’s esophagus3. More in distal 1/3

Question 1153

Cancer of the EsophagusSymptoms? 7

Answer 1153

1. Progressive dysphagia2. Odynophagia3. Regurgitation4. Heartburn5. Anorexia6. Vomiting7. Weight loss

Question 1154

Diagnosis of esophageal cancer?4

Answer 1154

1. UGI/barium swallow2. Endoscopic ultrasound3. EGD…tissue is the issue4. CT for staging and r/o mets

Question 1155

Treatment for esophageal cancer?3

Answer 1155

1. Chemo (preop and post-op protocols)2. Radiation (post-op)3. Surgery (best cure)Combined Modality Treatment leads to the best outcome

Question 1156

Benign stomach tumors?1. Polyps?2. Tumors? 2

Answer 1156

1. Polyps-Hyperplastic2. Tumors-Leiomyomas (smooth muscle)-Lipomas

Question 1157

Malignant stomach cancers1. Tumors? 4

Answer 1157

1. Carcinoma (epithelial cell origin)2. Lymphoma (lymphatic system)3. Sarcoma (connective tissue tumor)4. Carcinoid (serotonin secreting)

Question 1158

Gastric Polyps: Neoplastic polyps?1. Types? 22. Macroscopic appearance more often where?3. What do they look like? 44. Treatment?

Answer 1158

1. -Tubular-Villous (often larger …> 2cm and malignant)2. More often in antrum3. -Pedunculated with malignant potential-Solitary, -large-ulcerated4. Treatment-Endoscopic removal if no malignancy identified… the periodic surveillance

Question 1159

Gastric Leiomyoma: Pathology?1. Arise from where?2. What is it difficult to distinguish from?3. More benign or malignant?4. Differentiatied how?5. What do they look like?

Answer 1159

1. Arise from smooth muscle of the GI tract2. Difficult to distinguish from Gastrointestinal stromal tumor3 75% benign4Differentiation only on mitotic index5. Large protruding lesions with central ulcer

Question 1160

1. Gastric Leiomyomausually present how?2. Treatment?

Answer 1160

1. Usually presents with bleeding if at all2. Treatment is local excision with 2 – 3cm margin

Question 1161

Adenocarcinoma of the Stomach1. What bug is associated with this and why?2. Also related to what? 4

Answer 1161

1. HP associated due to chronic atrophic gastritis2. Also related to-Low dietary intake vegetables and fruit-High dietary intake of starches-More common in males ( 3 : 1 )-Increased incidence with pernicious anemia and blood group A

Question 1162

Adenocarcinoma of the StomachHistological typing? 4

Answer 1162

1. Ulcerated carcinoma (25%)2. Polipoid carcinoma (25%)3. Superficial spreading carcinomas (15%)4. Linitis plastica (aka Brinton’s disease or leather bottle stomach) (10%)

Question 1163

1. Ulcerated carcinoma (25%) looks like what?-Usually through what layers of the stomach?2. Polipoid carcinoma (25%) look likw what?-Metastasis?3. Superficial spreading carcinomas (15%) are confined to where?-Prognosis?4. Linitis plastica (aka Brinton’s disease or leather bottle stomach) (10%) involves what layers of the stomach and what is the prognosis?-what kind of appearance on XRAY?

Answer 1163

1. Deep penetrated ulcer with shallow edges-Usually through all layers of the stomach2. Intraluminal tumors, large in size-Late metastasis3. Confinement to mucosa and sub-mucosa-Metastasis 30% at time of diagnosis (Best prognosis)4. involves all layers of stomach(poor prognosis)-“leather-bottle” appearance on X-ray

Question 1164

1. Adenocarcinoma of the Stomachsigns and symptoms? 32. At late stages? 3

Answer 1164

1. -Vague discomfort difficult to distinguish from dyspepsia-Anorexia-Pronounced weight loss2. At late stage-Epigastric mass-Hematemesis usually coffee ground -Metastasis...Virchow’s node (L supraclavicular)

Question 1165

What kind of anorexia is specific to adenocarcinoma?

Answer 1165

Meat aversion

Question 1166

Spread of Gastric Carcinoma4

Answer 1166

1. Local infiltration (through wall of stomach to peritoneum, pancreas etc)2. Lymphatic – local and regional lymph nodes3. Blood – liver, lungs4. Transcoelomic (across peritoneal cavity).

Question 1167

Transcoelomic (across peritoneal cavity) often involves what?

Answer 1167

1. Often involves ovaries (esp. signet ring cancer) – Krukenberg tumour (ovarian tumor that metastasized from a primary site…colon or stomach

Question 1168

Diagnosis of Gastric Cancer5

Answer 1168

1. Anemia in 40%2. Elevated CEA in 65%3. UGI4. Endoscopy…..tissue is the issue5. CT scans for metastatic work up

Question 1169

Adenocarcinoma of the Stomach1. Whats the only cure?2. Prognosis? 23. What offers little benefot for treatment?

Answer 1169

1. Surgical resection only cure2. -Prognosis overall…. 12% 5 year survival-90% for stage I disease3. Radiation and chemo offer little benefit

Question 1170

Adenocarcinoma of the Stomach1. What often makes surgery futile?2. Palliation controversial for what? 2

Answer 1170

1. Late presentation makes surgery often futile 2. -Hemorrhage-Gastric outlet obstruction

Question 1171

Less Common Gastric Neoplasms3

Answer 1171

1. Lymphoma2. Gastrointestinal stromal tumour (GIST)3. Neuroendocrine (carcinoid) tumours

Question 1172

Gastric Lymphoma1. Whats the lymphoma called?2. treatment?

Answer 1172

1. (MALT…mucosa associated lymphoid tissue)2. Treatment….sensitive to radiation

Question 1173

1. Gastrointestinal Stromal Tumors (GIST)?2. most common site?

Answer 1173

1. Mesenchymal neoplasms2. Stomach most common site

Question 1174

Neuroendocrine Tumors1. What are the tumors of resident neuroendocrine cells in gastric glands?

Answer 1174

carcinoids

Question 1175

Gastric SarcomaIncludes a variety of tumors such as? 3

Answer 1175

1. Leiomyosarcoma2. Leiomyoblastoma3. GIST

Question 1176

Pathophysiology of Pancreatic Cancer1. Arises from where?2. Tumor usually discovered when?3. Describe its progression?4. Whats the most common site for it on the pancreas?

Answer 1176

1. Usually arises from epithelial cells of the pancreatic ducts2. Tumor typcially discovered in late stages so has spread throughout pancreas3. Rapid growing with spread to surrounding tissue4. Most common site is head of pancreas

Question 1177

Signs and Symptoms of pancreatic cancer10

Answer 1177

1. Vague, dull, abdominal pain2. “Painless jaundice”3. Weigh loss, weakness4. Anorexia, nausea, vomiting5. Glucose intolerance6. Flatulence7. GI bleeding8. Ascites9. Leg/calf pain10. Jaundice (if head of pancreas involved)-Clay colored stools-Dark urine

Question 1178

Diagnostics of pancreatic cancer?4

Answer 1178

1. No specific blood tests to diagnose2. Elevated amylase, lipase, alkaline phosphatase, bilirubin, CEA (carcinoembryonic antigen) C19-93. CT, Ultrasonography4. ERCP – most definitive diagnostic test

Question 1179

Clinical Management of pancreatic cancer?5

Answer 1179

1. Goal is to prevent spread of tumor2. Chemotherapy or radiation3. Pain control (opioids)4. Distal resection5. Whipple procedure

Question 1180

1. What is the whipple procedure?2. Used for what only?

Answer 1180

1. Radical pancreaticoduodenectomy-Excision or all or part of the pancreas together with the duodenum and usually the distal stomach2. Used for cancer of the pancreas head only

Question 1181

1. What is Zollinger-Ellison Syndrome?2. What is hypergastrinemia and what does it lead to?

Answer 1181

1. “Islet cell” tumor of the pancreas [or of the duodenum] →Gastrinoma2. Hypergastrinemia (excess levels of serum gastrin) →Gastric acid hypersecretion

Question 1182

Zollinger-Ellison Syndrome:1. Gastric acid hypersecretion leads to what? 3

Answer 1182

1. Consequences of acid hypersecretion:2. PUD, GERD [ with or without complications]3. Diarrhea, malabsorption*******

Question 1183

Symptoms in patients with the Zollinger-Ellison syndrome: Presentation from most common to least common?5

Answer 1183

1. Pain and diarrhea 50-60%2. Pain without diarrhea 25%3. Diarrhea without pain 20%4. Heartburn ± dysphagia 30%5. Multiple Endocrine Neoplasia-1 features 20-25%

Question 1184

Diagnosis of ZE Syndrome 2

Answer 1184

Begins with clinical suspicion Fasting serum gastrin measurement-high sensitivity (> 95%)-poor specificity, even at high levels

Question 1185

1. Management of ZE syndrome?2. Prognosis?3. Tumor search is used for what and what do we use?4. Tumor search and possible resection for cure is only prudent for patients who are what?

Answer 1185

1. Acid control (PPIs) takes precedence over tumor search2. Prognosis is excellent in patients w/o metastatic disease3. Tumor search is designed to find tumor and to stage its/their extent…CT Scan4. surgical candidates

Question 1186

1. What is the most common form of liver cancer and it comes from the main type of liver cell, the hepatocyte?2. Cholangiocarcinoma starts where and is carried where?

Answer 1186

1. Hepatocellular carcinoma2. starts in the small bile ducts that carry bile to the gallbladder.

Question 1187

Liver Cancer…..causes?4

Answer 1187

1. Chronic infection with hepatitis B (HBV) and hepatitis C (HCV)2. Cirrhosis (scar tissues in liver) due to alcohol, hepatitis3. Tobacco use.4. Aflatoxins from a fungus that can contaminate peanuts, wheat, soybeans, groundnuts, corn, and rice.

Question 1188

Can cancer of the liver be prevented?1. Hep B is found where?2. It can be transmitted through what?

Answer 1188

1. Hepatitis B transmission:Hepatitis B is found in body fluids including blood, saliva, semen, mucus, vaginal fluid, and breast milk.2. It can be transmitted through sexual activity, sharing injecting equipment, toothbrushes, or razors.It can be transmitted from mother to child at birth.

Question 1189

WAYS TO REDUCE HEPATITIS B TRANSMISSION:?4

Answer 1189

1. Wash hands after touching blood or body fluids.2. Avoid sharing personal hygiene items that may come into contact with body fluids.3. Cover all cuts and open sores with bandage.4. Practice safe sex.

Question 1190

Preventing liver cancer2

Answer 1190

1. Hepatitis B vaccinationFor all children.For adults at high risk.2. Avoid alcohol abuse.

Question 1191

1. Hep C is generally transmitted how?2. Different ways?5

Answer 1191

1. Hepatitis C is transmitted by blood to blood contact only.2. -Transmission can occur through sharing of needles, unsterile tattooing, body piercing.-Sharing razor blades and toothbrushes.-Certain sexual activities.-Mother to baby.-No vaccine

Question 1192

Symptoms of liver carcinoma4

Answer 1192

1. Loss of appetite and weight2. Jaundice 3. Swelling of the abdomen4. Pain in the abdomen.

Question 1193

Liver Cancer….diagnosisLabs?3

Answer 1193

1. LFTs2. AFP (alpha fetoprotein) blood test (tumor marker to help detect and diagnose cancers of the liver, testicles and ovaries.)3. Blood tests for Hepatitis B and C.

Question 1194

Imaging and procedures for Liver Cancer?5

Answer 1194

1. Ultrasound of the liver.2. CT scan or MRI scan of liver.3. Biopsy4. Angiogram of the liver.5. Laparoscopy.

Question 1195

Liver Cancer Staging:Describe stages I-IV?

Answer 1195

Stage I – Single small tumor less than 2 cm.Stage II – Single large tumor or many small tumors confined to one lobe of the liver.Stage III – Many large tumors confined to one lobe of the liver or cancer spread to lymph nodesStage IV – Cancer spread to both lobes of the liver.

Question 1196

Liver Cancer Treatment: Surgery4

Answer 1196

SURGERY:-Curative intent in Stages I, II-Liver wedge resection-Liver lobectomy-Liver transplantation

Question 1197

Liver Cancer Treatment: Chemotherapy1. Drugs are given how? 2

Answer 1197

1. Drugs given by hepatic artery infusion.2. Drugs given by chemo embolization.

Question 1198

Liver Cancer….survival rates1. Survival rates at 5 years?-Early localized?-All stages combined?

Answer 1198

Early localized cancer – 30-40%All stages combined – 10%

Question 1199

Small Bowel Cancers (RARE)Name the top 4 types in order of prevelance?

Answer 1199

1. 30-50% are adenocarcinomas***2. 25-30% are carcinoids3. 15-20% are lymphomas4. 10-20% are gastrointestinal stromal tumors

Question 1200

Risk Factors for Small Bowel Adenocarcinoma8

Answer 1200

1. Pre-existing adenoma, either single or multiple2. Crohn’s 3. Celiac disease 4. IgA deficiency5. Alcohol abuse6. Neurofibromatosis7. Urinary diversion procedures8. Red meat

Question 1201

Clinical Presentation of Small Bowel CA6

Answer 1201

1. Abdominal pain2. Nausea and vomiting3. Bleeding/Anemia4. Weight loss5. Gastric outlet obstruction6. Diarrhea

Question 1202

Diagnosis of Small Bowel Malignancies4

Answer 1202

1. UGI/SBFT2. Single contrast flouroscopy-Mass -Mucosal defect3. CT scan as well4. Capsule endosocopy

Question 1203

Prognosis and treatmentof small bowel CA

Answer 1203

Pretty good with surgery

Question 1204

Colorectal Cancer screenning1. The vast amjority of colorectal cancers arise from where?2. The polyps grow from small to larger polyps ultimately accumulating what?3. Current thought is that this progression probably takes at least how long in most people?

Answer 1204

1. adenomatous polyps.2. accumulating increasing dysplastic characteristics. --Dysplasia means neoplastic (tumor like) changes. 3. 10 years in most people.

Question 1205

Adenoma Carcinoma Sequence1. Some cancers unfortunately also arise from flat adenomas (i.e. they are not polypoid). The two main types of colorectal polyps are either what two things? 2. What is required for diagnosis?3. Two-thirds of polyps are what?

Answer 1205

1. adenomas or hyperplastic polyps. These lesions cannot be distinguished reliably on gross appearance; 2. biopsy is required for diagnosis.3. adenomas

Question 1206

Adenoma Carcinoma Sequence1. The ______ the polyp, the more likely is progression to cancer. 2. Hyperplastic polyps account for most of the remaining polyps and are mainly ______. They are generally thought not to progress to cancer, although some may.

Answer 1206

1. larger2. distal

Question 1207

Why is this important?1. If you remove the polyps when they are smaller, they cannot do what?2. Colonoscopy drastically decreases the risk of colorectal cancer (well over ___%).

Answer 1207

1. grow into cancer. 2. 90

Question 1208

Screening tests for colon cancer?

Answer 1208

1. Fecal occult blood tests (FOBT & FIT). 2. Flexible sigmoidoscopy. 3. Colonoscopy.

Question 1209

Flexible sigmoidoscpoy1. This test involves which part of the colon?2. This has largely been replaced by what?

Answer 1209

1. This test involves inspecting only the last third of the colon.2. This has largely been replaced by complete colonoscopy.

Question 1210

Why colonoscopy has become the screening test of choice 4

Answer 1210

1. It looks at the entire colon.2. If a polyp is found, it can be removed through the scope and sent to pathology to determine the type of polyp and to rule out cancer.3. Other abnormalities of the colon can be identified. 4. When polyps are removed, they cannot grow into cancer.

Question 1211

1. Describe colon cancer histology?2. Usually begins as a what?

Answer 1211

1. A disease in which normal cells in the lining of the colon or rectum begin to change, grow without control, and no longer die2. noncancerous polyp

Question 1212

Risk Factors for Colorectal Cancer7

Answer 1212

1. Polyps (a noncancerous or precancerous growth associated with aging)2. Age3. Inflammatory bowel disease (IBD)4. Diet high in saturated fats, such as red meat5. Personal or family history of cancer6. Obesity7. Smoking

Question 1213

1. Hereditary Colorectal Cancer Syndromes: HNPCC aka?2. The risk of colorectal cancer in families with HNPCC is _______, which is several times the risk of the general population 3. People with HNPCC are diagnosed with colorectal cancer at an average age of ___?

Answer 1213

1. Lynch syndrome2. 70% to 90%3. 45

Question 1214

Hereditary Colorectal Cancer Syndromes: FAP 1. People with FAP typically develop how many colon polyps (small growths)?2. the polyps are initially what, but there is nearly a 100% chance that the polyps will develop into cancer if left untreated3. Colorectal cancer usually occurs by age __ in people with FAP

Answer 1214

1. hundreds to thousands 2. benign (noncancerous)3. 40

Question 1215

Symptoms of colon cancer?3

Answer 1215

1. A change in bowel habits: diarrhea, constipation, or a feeling that the bowel does not empty completely2. Bright red or dark blood in the stool3. Abdominal discomfort

Question 1216

How is Colorectal Cancer Evaluated?1. Diagnosis is confirmed with?2. Stage of disease is confirmed by what? 4

Answer 1216

1. a biopsy2. -pathologists and imaging tests, -(CT) scans….nodes and liver, lung involvement-Endoscopic ultrasound and -magnetic resonance imaging (MRI) may also be used to stage rectal cancer

Question 1217

Cancer Treatment: -Foundation of curative therapy?

Answer 1217

Surgery:-The tumor, along with the adjacent healthy colon or rectum and lymph nodes, is typically removed to offer the best chance for cureMay also use chemo and or radiation

Question 1218

New Therapies: Antiangiogenesis Therapy1. How is this done?2. Given along side what?

Answer 1218

1. “Starves” the tumor by disrupting its blood supply2. This therapy is given along with chemotherapyBevacizumab (Avastin) was approved by the U.S. Food and Drug Administration (FDA) in 2004 for the treatment of stage IV colorectal cancer

Question 1219

Staging is described by the TNM system describe this?

Answer 1219

the size (the depth of penetration of the Tumor into the wall of the bowel), whether cancer has spread to nearby lymph Nodes, and whether the cancer has Metastasized

Question 1220

Stage I Colorectal CancerDescribe stage I?Treatment?

Answer 1220

The cancer has grown through the mucosa and invaded the muscularis (muscular coat)Treatment is surgery to remove the tumor and some surrounding lymph nodes

Question 1221

Stage II Colorectal CancerDescribe?Treatment?

Answer 1221

The cancer has grown beyond the muscularis of the colon or rectum but has not spread to the lymph nodesStage II colon cancer is treated with surgery and, in some cases, chemotherapy after surgery

Question 1222

Describe Stage III ?Treatment?

Answer 1222

The cancer has spread to the regional lymph nodes (lymph nodes near the colon and rectum)Stage III colon cancer is treated with surgery and chemotherapy

Question 1223

Describe stage IV and treatment?

Answer 1223

The cancer has spread outside of the colon or rectum to other areas of the bodyStage IV cancer is treated with chemotherapy. Surgery to remove the colon or rectal tumor may or may not be done

Question 1224

Follow-Up Carefor colon cancer?3

Answer 1224

1. Serial carcinoembryonic antigen (CEA) measurements are recommended2. Colonoscopy one year after resection of colorectal cancer3. Surveillance colonoscopy every three to five years to identify new polyps and/or cancers

Question 1225

Colon vs. Rectal5

Answer 1225

1. Rectal better prognosis2. Rx not beneficial for colon3. DRE/Hemoccult4. CEA5. Surgery

Question 1226

Anal Cancer1. Most common kind?2. Symtpoms? 23. Risk associations? 24. Treatment? 35. Survival?

Answer 1226

1. SCC2. -Bowel changes-Bleeding3. -HPV association (major cause)-smokers/HIV4. Treatment….often effective/cured--Surgery, Radiation, Chemo5. Survival….better than CRC5 year 65.7% overall...for localized dz with early dx 80%

Question 1227

Treatment of Ulcerative Colitis and Crohn’s Disease5 drugs

Answer 1227

1. Aminosalicylates2. Corticosteroids3. Antibiotics4. Immunosuppresive agents5. Biological Agents

Question 1228

Drugs that are used for treatment are based on?4

Answer 1228

1. Severity of disease2. Ulcerative colitis3. Crohn’s disease location of lesions4. Exacerbation vs. maintenance therapy

Question 1229

Drugs used for treatment of inflammatory bowel disease1. Aminosalicylates -used how? 22. Corticosteroids-Used how?-Should not be used for what?

Answer 1229

1. -Mild to moderate UC and CD exacerbations-Maintenance of remission2. -Treatment of UC and CD acute exacerbations-Should not be used chronically to maintain remission

Question 1230

Drugs used for treatment of inflammatory bowel disease1. Antibiotics-Used for?2. Immunosuppresive agents-Used for?

Answer 1230

1. Acute exacerbations and maintenance of remission2. To maintain remission

Question 1231

Drugs used for treatment of inflammatory bowel disease1. IV cyclosporine used for?2. Immune modifiers used for?

Answer 1231

1. Severe active steroid refractory UC2. Maintain remission in steroid refractory UC and CD

Question 1232

Treatment Options for Crohn’s and Ulcerative Colitis:Describe treatment of Distal UC1. Mild 2. Moderate3. Severe4. Remission

Answer 1232

Severity of Disease Distal UC1. MildOral/rectal aminosalicylate or rectal corticosteroid 2. ModerateOral Aminosalicylate and oral/rectal steroids and/or immunosuppressive 3. SevereIV corticosteroids with/without IV cyclosporine 4. RemissionOral/rectal aminosalicylate with/without oral immunosuppressive

Question 1233

Treatment Options for Crohn’s and Ulcerative Colitis:Describe treatment of Extensive UC?1. Mild 2. Moderate3. Severe4. Remission

Answer 1233

Extensive UC1. Mild- Oral Aminosalicylate 2. Moderate- Oral Aminosalicylate and oral steroids and/or immunosuppressive 3. Severe- IV corticosteroids with/without IV cyclosporine4. Remission- Oral/rectal aminosalicylate with/without oral immunosuppressive

Question 1234

Treatment Options for Crohn’s and Ulcerative Colitis:Describe treatment of CD?1. Mild 2. Moderate3. Severe4. Remission

Answer 1234

CD1. MIld- Oral Aminosalicylate with/without antibiotics 2. Moderate- Oral Aminosalicylate and oral steroid and/or immunosuppressive 3. Severe- IV corticosteroids with/without IV cyclosporine 4. Remission- Oral Aminosalicylate with/without oral immunosuppressive

Question 1235

What are the Aminosalicylates?4

Answer 1235

1. Sulfasalazine (Azulfidine)2. Mesalamine (Asacol, Pentasa)3. Olsalazine (Dipentum)4. Basalazide (Colazal)

Question 1236

Aminosalicylates clinical uses2

Answer 1236

1. Induce and maintain remission in UC2. Efficacy in Crohn’s is not well established, but often used as 1st line tx of Crohn’s involving the colon or distal ileum.

Question 1237

Aminosalicylates forms of administration?3

Answer 1237

1. PO2. Enema3. Suppository

Question 1238

Aminosalicylates: Sulfasalazine (Asulfidine)1. Preg cat?2. Converted to what in the proximal colon?3. Take how many times daily?4. Contraindication?

Answer 1238

1. Pregnancy cat. B (Sulfapyridine-mesalamine compound)2. Converted to mesalamine in the proximal colon3. Tablets administered 4 times daily4. Contraindicated in sulfa allergy

Question 1239

Aminosalicylates: Mesalamine (Asacol, Pentasa) 1. Preg cat?2. Poorly absorbed in the GI tract so works primarily like a topical agent with what kind of effects?3. Describe the four ways of administration?

Answer 1239

1. B2. limited systemic SE and drug interactions3. -Oral tablets (Asacol) released in the distal ileum and colon-Oral capsules (Pentasa) released in the proximal small intestine and throughout the colon-EnemaCan reach distal and sigmoid colon, administered at bedtimeRectal suppositories-Primarily used for UC proctitis

Question 1240

Aminosalicylates: Basalazide (Colazal)1. Preg cat?2. Converted to mesalanine where?Olsalazine (Dipentum)1. Preg cat?2. Converted to mesalanine where?These 2 drugs are not used as much as the others due to the increased cost but no added efficacyBoth are poorly absorbed in the GI tract so work primarily like a topical agent with limited systemic SE and drug interactions

Answer 1240

Basalazide (Colazal) 1. Pregnancy cat. B2. Converted to mesalamine in the proximal colonOlsalazine (Dipentum) 1. Pregnancy cat. C2. Converted to mesalamine in the proximal colon

Question 1241

MOA Aminosalicylates3

Answer 1241

1. Blocks prostaglandin production2. Perhaps interferes with production of inflammatory cytokines3. May inhibit natural killer cells, lymphocytes and macrophagesExact mechanism unknown

Question 1242

Contraindications to Aminosalicylates3

Answer 1242

1. Aspirin or other salicylate allergy2. Glucose-6-phosphate dehydrogenase deficiency3. Sulfasalazine is contraindicated with a history of sulfa allergy

Question 1243

Dosing of Aminosalicylates?1. What must we dose at?2. SE increase with what?

Answer 1243

1. Must be used at max doses for maximum therapeutic benefit2. Side effects increase as the dose increases-Dosing varies from once daily to four times daily depending on the formulation

Question 1244

Side effects of sulfasalazine 5Severe rxns? 5What do we need to supplement with?

Answer 1244

1. Worst side effect profile of all the aminosalicylates2. Nausea, Vomiting3. Photosensitivity, oligospermia4. Skin discoloration5. Decreased folate levels Severe: 1. Steven-Johnson syndrome, 2. crystalluria, 3. pancreatitis, 4. hepatitis, 5. bone marrow suppressionNeed to take a folic acid supplement

Question 1245

What do we need to monitor with Sulfasalazine and how often? 2Periodically what else? 2

Answer 1245

1. CBC with differential,2. LFTs prior to therapy then every other week for 3 months, then every month for 3 months, then quarterlyPeriodic renal and LFTs

Question 1246

Side effects of mesalamine & it’s compoundsMesalamine 4Olsalazine 1Balsalazide 1Rarely these can be associated with what?

Answer 1246

Mesalamine1. Headache, 2. malaise, 3. abdominal pain and 4. diarrheaOlsalazine1. Similar to mesalamine but has more severe secretory diarrheaBalsalazideSimilar to mesalamine1. If capsules opened and sprinkled in food may cause staining of the teethRarely can be associated with renal impairment

Question 1247

Mesalamine No specific recommendations on how frequent to monitor these labs-Which ones? 3

Answer 1247

1. Renal function prior to and during therapy2. CBC3. Hepatic function

Question 1248

Corticosteroids1. Used for what?2. Short term side effects? 63. Long term side effects? 5

Answer 1248

1. Used for acute exacerbationsNot used for maintaining remission2. Short term side effects-Increased glucose levels, -increased appetite,- insominia, anxiety,- tremors, -increased fluid retention, -increased blood pressureLong term side effects-Decreased bone mineral density, -fat redistribution, -ulcers from decreased prostaglandin production, -hypertriglyceridemia, -hirsutism

Question 1249

Prednisone (Deltasone) and Prednisolone (Prelone) are most commonly used oral medications1. Initial dose? then what?2. IV formulas? 2

Answer 1249

1. 40-60mg/d initiallyTaper with patients response2. IV – Hydrocortisone (Solu-Cortef) and Methylprednisolone (Solumedrol)

Question 1250

1. Budesonide (Entocort) is what?-It is used how for treatment?

Answer 1250

Budesonide (Entocort)1. Controlled release with limited systemic absorption-Has been used as the treatment of choice in patients with mild to moderate CD in combo with 5-ASA or as mono therapy

Question 1251

What are the topical steriods?3What is this used to treat?

Answer 1251

1. Cortenema, 2. Cortifoam, 3. Anusol-HC suppositories-Hydrocortisone enemas, foam or suppositories1. For IBD involving the rectum/sigmoid colonSometimes referred to as topical

Question 1252

Antibiotics are generally used for the treatment of what?

Answer 1252

1. Used generally for treatment of Crohn’s disease that does not respond to 5-ASAs after 3-4 weeks or if the patient is intolerant to 5-ASAsEfficacy in Ulcerative colitis has not been established

Question 1253

What antibiotics are used in the treatment of Crohn's?2

Answer 1253

1. Cipro2. Metronidazole (Flagyl)

Question 1254

1. Why do we use cipro for crohns?2. May take up to how long for remission?

Answer 1254

1. May have some immunosuppressive properties2. May take up to 6 weeks for remission

Question 1255

1. HOw should we administer Flagyl?2. May have what kind of properties?3. May take how long to respond to therapy?4. Duration of therapy may be up to how long?

Answer 1255

1. Start at a higher dose and decrease after response is noted2. Likely also has some immunosuppressive properties3. May take 1-2 months for response to therapy4. Duration of therapy may be up to 12 months

Question 1256

What are the Immune modifiers?4

Answer 1256

1. Azathioprine2. 6-mercaptopurine3. Methotrexate4. Infliximab

Question 1257

Clinical use of Azathioprine and 6-mercaptopurine1. Uses?2. Specific diseases?3. ______months of treatment induces remission in 50-60% of patients with active disease?4. _____% maintain remission?5. Use may allow you to do what?

Answer 1257

1. Induction and maintenance of remission2. UC and Crohn’s3. 3-6 months4. 80% maintain remission5. Use may allow reduction of steroid therapy

Question 1258

Immune Modifiers1. Is an active metabolite of what?2. Describe its half life?3. Prolonged kinetics results in a what?4. Preg cat?

Answer 1258

1. Active metabolite of azathioprine2. Short half life but active metabolite with long half life of 3-13 days3. Prolonged kinetics results in a median delay of 17 weeks before onset of therapeutic benefit from oral medication.4. Preg Cat. D (although recent publications suggest it may be continued safely during pregnancy)

Question 1259

Azathioprine and 6-mercaptopurine MOA2

Answer 1259

1. Inhibition of purine neucleotide metabolism and DNA synthesis and repair, resulting in inhibition of cell division and proliferation.2. May decrease proliferation of immune cells leading to lower autoimmune activity

Question 1260

Azathioprine and 6-mercaptopurine side effects8Monitor what? 2

Answer 1260

1. Side effects are mostly dose related2. Nausea, vomiting, diarrhea3. Fever, rash4.Pancreatitis5. Bone marrow suppression (leukopenia)6. Hepatic toxicity7. Arthralgias, malaise8. Drug toxicity with use of concurrent use of AllopurinolMonitoring: Routine 1. CBC and 2. liver function tests

Question 1261

Azathioprine and 6-mercaptopurine1. COntraindicated in who?2. Decrease dose for CrCl of what?

Answer 1261

1. Contraindicated in pregnancy or active liver disease2. Decrease dose for CrCl less than 50

Question 1262

Methotrexateclinical uses? 2Can be given how? 3

Answer 1262

Clinical Use:1. Induction and maintenance of remission in patients with Crohn’s disease2. Effects in UC are uncertainCan be given PO, SQ or IM

Question 1263

MethotrexateMOA?2

Answer 1263

1. Inhibits metabolism of folic acid--Shares structural homology with interleukin-1, thus interferes with its inflammatory actions2. May stimulate apoptosis and death of activated T lymphocytes

Question 1264

Methotrexate1. Preg cat?2. Adjust dose for who?3. Contraindicated in who? 2

Answer 1264

1. Preg Cat. X 2. Adjust dose for altered renal clearance3. Contraindicated in -pregnancy and -active liver disease

Question 1265

Methotrexate SE?9

Answer 1265

1. Alopecia2. Muscositis3. Bone marrow depression – higher dosage4. Megaloblastic anemia – higher dosage5. Cirrhosis and liver fibrosis6. Pneumonitis7. Folic acid deficiency8. Rash9. Nausea and diarrhea

Question 1266

Cyclosporine1. Used for what?2. Improvement should be seen in who?3. Duration of therapy?4. Given how?5. SE? 3

Answer 1266

1. Used for the acute treatment of severe, steroid refractory exacerbations of UC in hospitalized patients2. Improvement should be seen in 2-3 days3. Duration of therapy 7-10 days4. Given IV5. Side effects-Nephrotoxicity, -hypomagnesemia,- hypertension

Question 1267

Anti-tumor necrosis factor agentsTNF Inhibitors1. Leads to symptomatic improvement in 2/3 of patients with what kind of dz?2. Leads to disease remission in 1/3 of patients with what kind of dz?3. Used when pts arent responding to what? 3

Answer 1267

1. moderately severe or fistulizing Crohn’s2. moderately severe or fistulizing Crohn’s3. Used when patients are not responding to -steroids, -6-mercaptopurine or -methotrexate

Question 1268

TNF inhibitors approved for use in severe refractory CD. What are the drugs? 3

Answer 1268

1. Infliximab (Remicade)2. Adalimumab (Humira)3 .Certolizumab Pegol (Cimzia)

Question 1269

Infliximab (Remicade)is also indicated in what?

Answer 1269

Also indicated for maintaining remission in CD and treating UC

Question 1270

Anti-tumor necrosis factor agentsTNF InhibitorsInfliximab (Remicade) 1. Preg cat?2. Administered how?3. Describe the dosing? 2

Answer 1270

1. Preg. Cat B2. Administered via IV infusion3. Given 5mg/kg dose intially, at two weeks and at 6 weeks.Then maintenance every 6-12 weeks

Question 1271

Anti-tumor necrosis factor agentsTNF InhibitorsInfliximab (Remicade) MOA?3

Answer 1271

1. Dysregulation of the TH1 T cell response present in IBD.2. Antibody to human TNF-alpha3. Neutralizes membrane bound TNF

Question 1272

Anti-tumor necrosis factor agentsTNF InhibitorsSE?4

Answer 1272

Infusion reaction (>10% of patients)>10% of patients1. Fever, chills2. Pruritis, urticaria3. Chest pain, dyspnea4. Hemodynamic instabilityProphylactic Tylenol and Benadryl

Question 1273

Anti-tumor necrosis factor agentsTNF Inhibitors: 1. Infusion reaction more common with which infusions?2. Prophylactic treatment? 2

Answer 1273

1. Infusion reaction more common with 2nd and subsequent infusions other than the 1st.2. Prophylactic Tylenol and Benadryl

Question 1274

Anti-tumor necrosis factor agents-TNF Inhibitors: Delayed infusion reaction: (5 % of patients)? 4-occurs how soon after treatment?- Treat with?

Answer 1274

1. Myalgia, arthralgia2. Fever3. Rash, urticaria4. Facial, hand and lip edema1. Occurs 1-2 weeks after infusion1. Treat with antihistamines or corticosteroids

Question 1275

Anti-tumor necrosis factor agentsTNF Inhibitors1. BBW?2. What do we need to test for?

Answer 1275

1. Side effects: Black box warningReactivation of latent TB2. All patients must have PPD prior to useProphylactic therapy for those with + PPD’s

Question 1276

1. Start with an what for most cases except severe?2. Choose the formula for delivery based on the extent of what?3. Use of combo oral and rectal 5-ASA have better efficacy when?4. Move onto what if no response in 3-4 weeks or 5. start with _______ if more severe cases?6. Antibiotics are beneficial in what only and can be used 2nd line after failure of 5-ASA.

Answer 1276

1. aminosalicylate like mesalamine2. GI tissue involved3. better efficacy than either agent alone. Use together4. corticosteroids5. steroids, (rectal steroids very effective in UC)6. CD

Question 1277

Pharmacologic therapy for IBS7

Answer 1277

1. Antispasmodic agents2. Antidiarrheal agents3. Anticonstipation agents4. Psychotropic agents5. Serotonin receptor agonists and antagonists6. Nonabsorbable antibiotics7. Probiotics

Question 1278

IBS PharmacotherapyBased on predominant complaintConstipation?5

Answer 1278

Constipation1. Increase fluids, fiber2. TCAs or SSRIs3. Peppermint oil4. Osmotic laxatives5. Lubiprostone

Question 1279

IBS PharmacotherapyBased on predominant complaintPain?4

Answer 1279

Pain 1. Antispasmodics (Anticholinergics)2. TCA’s (Tricyclic antidepressants) (low dose)3. SSRI (Selective serotonin reuptake inhibitors) 4. Peppermint oil

Question 1280

IBS PharmacotherapyBased on predominant complaintDiarrhea?6

Answer 1280

1. Fiber (sometimes controversial in the symptomatic treatment of IBS)2. Loperamide3. Cholestramine4. TCA’s5. Lotronex6. SSRI’s

Question 1281

Antispasmodics2Work primarily through what receptors?

Answer 1281

1. Anticholinergics2. Belladonna alkaloids-Work primarily thru cholinergic receptors-Provide relief through antispasmotic action

Question 1282

Antisposmodics1. What are the anticholinergics? 22. What are the Belladonna alkaloids? 2Preg cat?

Answer 1282

Anticholinergics1. Hyoscyamine (Levbid, Levsin SL)2. Dicyclomine (Bentyl)Belladonna alkaloids1. Donnatol2. Clidinium (Librax)C

Question 1283

MOA of Antispasmodics2

Answer 1283

1. Block action of acetylcholine at parasympathetic sites in secretory glands, smooth muscle and CNS2. Inhibit muscarinic cholinergic receptors in the enteric plexus and on smooth musclePlain and simple, these reduce contraction of the bowel

Question 1284

Pharmacotherapy of antispasmotics1. What kind of SE?2. Caution in what pts? 43. Contraindications? 8

Answer 1284

1. Watch for anticholinergic side effects2. Caution in the -elderly, -BPH, -HTN, -hyperthyroidism3. Contraindications:-Peptic ulcer-Arrhythmias-Congestive heart failure -Severe ulcerative colitis where bowel movements have stopped-Glaucoma -Myasthenia gravis , COPD-Infants less than 6 months of age -Nursing Mothers

Question 1285

1st and 2nd line antispasmodics1. Used for treatment of what? 32. First line agent?3. Second line agent?4. Can be used how?

Answer 1285

1. Treatment of -postprandial abdominal pain, -gas, bloating, -fecal urgency2. Dicyclomine (Bentyl) 1st line agentShort half life = less cholinergic side effects3. Hyoscyamine Sulfate (Levbid, Levsin SL) 2nd line agent Longer half lifeSublingual, oral, or oral sustained release (Q 12 hours)4. Can be used on a prn basis and with anticipation of stressors

Question 1286

Antispasmodics summary1. Causes relaxation of what?2. MOA?3. Most commonly used types? 24. SE?

Answer 1286

1. Smooth muscle relaxation of the GI tract2. MOA: Block acetylcholine at muscarinic cholinergic receptors3. Most commonly used: Bentyl and Levbid4. Anticholinergic side effects

Question 1287

Anticonstipation agents3

Answer 1287

1. Miralax (polyethylene glycol)-Osmotic laxative2. Increased intestinal chloride and fluid secretion-Lubiprostone (Amitiza)-Linaclotide (Linzess)

Question 1288

Chloride Channel Activator: Lubiprostone (Amitiza)1. MOA?2. Approved only for who?3. Use only when?4. SE?45. Long term use?

Answer 1288

1. MOA: Locally acting calcium channel activator that increases intestinal fluid secretion2. Approved only for women with constipation dominant IBS3. Use only if persistent constipation after trial of other treatments4. SE: -most common nausea, -diarrhea, -abdominal pain, -abdominal distention5. Long term safety has not been established

Question 1289

Linaclotide (Linzess)1. MOA?2. Interactions? 3. Administration?

Answer 1289

1. MOA: Binds to GC-C receptor on luminal surface of the intestinal epithelium ultimated affects the chloride and bicarbonate levels in the intestine and increases intestinal fluid and causes accellerated intestinal transit.2. Interactions: none3. Admininstration: once daily in the AM after eating

Question 1290

Psychotropic agents used in IBS1. TCAs? 32. SSRI? 5

Answer 1290

1. TCA’s-Amitryptyline (Elavil)-Desipramine (Norpramin)-Imipramine (Tofranil)2. SSRI-Escitalopram (Lexapro)-Citalopram (Celexa) -Sertraline (Zoloft)-Paroxetine (Paxil)-Fluoxetine (Prozac)

Question 1291

Tricyclic Antidepressants (TCA’s)MOA 3Preg cat?

Answer 1291

1. Visceral analgesic effect by increasing pain threshold in the gut2. Prolongs oral-cecal transit time3. Increases global well beingCat C

Question 1292

What are the TCAs?3

Answer 1292

1. Imipramine (Tofranil) Preg. Cat C2. Amitriptyline (Elavil) Preg. Cat C3. Desipramine (Norpramin) Preg.

Question 1293

TCA contraindications?3

Answer 1293

Contraindications:1. Narrow angle glaucoma2. Recent MI3. MAOI’s or Fluoxetine (Prozac) in patients who took them in the previous 2 weeks

Question 1294

SSRIs may help with what?

Answer 1294

May lead to improvement in overall sense of well being but have little impact on abdominal pain or bowel symptoms.

Question 1295

Alosetron (Lotronex) is what kind of drug?

Answer 1295

5-HT3 receptor inhibitor

Question 1296

Alosetron (Lotronex): Contraindications: Hx of… ?7

Answer 1296

1. chronic/severe constipation or sequelae from thereof2. Ileus, obstruction, stricture, toxic megacolon3. GI perforation, adhesions4. Ischemic colitis, impaired intestinal circulation5. Crohn’s or UC6. Diverticulitis/diverticulosis7. Hx of thrombophlebitis/hypercoagulable state

Question 1297

1. Alosetron (Lotronex)who is this indicated for?2. Why was it initially pulled from the market?

Answer 1297

1. Indicated only for women with severe diarrhea-predominant IBS who have not responded adequately to conventional therapy. 2. because of serious life-threatening, gastrointestinal side effects including ischemic colitis and serious complications of constipation

Question 1298

Before receiving the initial prescription for LOTRONEX what must happen? 2

Answer 1298

1. the patient must read and sign the Patient-Physician Agreement for Alosetron 2. Prescribers need to enroll in the Prometheus Prescribing Program for alosetron

Question 1299

1. Nonabsorbable antibioticsused for what?2. What is the antibiotic in this category?

Answer 1299

1. Refractory symptoms, esp. bloating2. Rifaximin (Xifaxan)Not FDA approved

Question 1300

What probiotic has been used for IBS?

Answer 1300

Bifodobacterium infantis has shown modest improvement in symptoms in small studies