Path- Gi/liver/pancreas/biliary System

Front 1

What is the name of the test that uses the identification of inclusion-bearing cells or polyakrons, in smears of blister fluid for diagnosis of HSV infection?

Back 1

The name of this test is called the Tzank test.

Front 2

In what type of patient do we see Hairy Leukoplakia almost exclusively? What causes this disease?

Back 2

We see this disease almost exclusively in patients infected with HIV. The Epstein Barr Virus infection of the oral epithelial cells causes this disease.

Front 3

Define Leukoplakia.

Back 3

This is a white lesion of the oral cavity that cannot be scrapped off and cannot be attributed to any other disease.

Front 4

What is practice is Leukoplakia most commonly associated with? Which virus? What can these lesions progress too?

Back 4

It is most commonly associated with using tobacco; It is being found to also be associated with HPV; 3-25% of cases progress to transformed squamous cell carcinoma.

Front 5

What is are the most common types of cancer to arise in the oral cavity?

Back 5

Squamous Cell Carcinomas

Front 6

What are the three most common sites of origin for oral cavity carcinomas?

Back 6

The vermillion border of the lateral margins of the lower lip, the floor of the mouth, the lateral borders of the mobile toungue

Front 7

What is the most common lesion to salivary glands? What mechanism of this? What are the most common causes?

Back 7

The most common lesion is usually Mucocele and this is most often cause by blockage or rupture of a salivary gland duct, with consequent leakage of saliva into surrounding tissues. The most common cause of this is usually injury to the lower lip, and viral infection with the Mumps.

Front 8

Which is more ominous, a neoplasm in the submaxillary glands or the parotids?

Back 8

A neoplasm in the sbmaxillary gland is more ominous than a neoplasm in the parotids.

Front 9

Which Leukoplakia has the most likelihood of transforming?

Back 9

Erythroplakia

Front 10

Where does oral HSV take up residency in its latent state?

Back 10

In the trigeminal ganglia.

Front 11

What is sialadenitis and what is the most common cause? What is the syndrome associated with this?

Back 11

Sialadenitis arises from a decrease in production of saliva with subsequent inlammation. The most common cause of chronic sialadenitis is Autoimmune sialadenitis. Sjogren syndrome associated with xerostoma and keratoconjunctivitis sicca. Mikulicz syndrome is associated wtih salivary and lacrimal gland inflammatory enlargement along with xerostoma. sometimes called )

Front 12

Describe the most malignant tumor of the salivary glands.

Back 12

The most malignant tumor of the salivary glands is Mucoepidermoid carcinoma, which occurs mainly in the Parotid glands.

Front 13

Malignancy of which salivary gland is more common, parotid or submandibular?

Back 13

Malignancy of the submandibular gland is more common than malignancy of the parotid.

Front 14

What tumor accounts for the majority (90%) of the benign tumors of the salivary glands(locally infiltrative)? Where does it occur? What types of cells make up the tumor?

Back 14

Pleomorphic adenoma that occurs in the Parotid Glands makes up the majority of benign tumors of the salivary glands. This is a tumor consisting of heterogeneic epithelial elements of myoepithelial derivation (myxoid stroma).

Front 15

What benign tumor found in the Parotid gland is thought to arise from heterotopic salivary tissue trapped within a regional lymph node during emryogenesis?

Back 15

Warthin Tumor, which is a small, well encapsulated tumor that often reveals mucin-containing, cleft-like cystic space inside.

Front 16

What is the significance of the Canals of Hering in the Liver?

Back 16

The Canals of Hering constitute a reserve compartment of progenitor cells for hepatocytes and bile duct cells.

Front 17

What are the major syndromes associated with liver disease?

Back 17

The major syndromes associated with liver disease are Hepatic Failure, Cirrhosis, Portal Hypertension, and Cholestasis.

Front 18

Define what percentage of hepatic function must be lost before hepatic failure ensues?

Back 18

80-90% of hepatic function must be lost before hepatic failure ensues.

Front 19

What two physiological conditions are important in the genesis of Hepatic Encephalopathy? What is the mechanism of this disease?

Back 19

1) Severe loss of hepatocellular function
2) Shunting of the blood from portal to systemic circulation around the chronically diseased liver

***The net result is exposure of the brain to an altered metabolic milieu. In the acute setting elevations in blood ammonia promote brain edema and impair neurological function. In the chronic setting, deranged neurotransmission arises from alterations in amino acid metabolism in the brain.

Front 20

What are the 5 major causes of Cirrhosis?

Back 20

Alcohol abuse, Chronic infection (Hep B and C), Autoimmune hepatitis, Biliary disease, and Iron overload (hemochromatosis).

Front 21

What is the definition of Cirrhosis?

Back 21

A diffuse process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.

Front 22

What are the three main characteristics of Cirrhosis?

Back 22

1) Bridging fibrous septa
2) Parenchymal nodules
3) Disruption of the entire liver architrecture (focal injury with scarring does not constitute cirrhosis).

Front 23

Which cells are responsible for the major source of excess collagen in cirrhosis? What is the main fibrotic agent associated with these cells?

Back 23

The major source of excess collagen in cirrhosis are the Perisinusoidal Stellate Cells. Transforming Growth Factor Beta is the main fibrotic agent for these cells.

Front 24

Describe the three most common complications and ultimate mechanisms of death in most individuals with cirrhosis.

Back 24

1) Progressive liver failure and decreased function
2) Complication related to portal hypertneison
3) Development of hepatocellular carcinoma

Front 25

Explain the mechanism of Portal Hypertension as attributed to the intrahepatic cause of cirrhosis (which is the most common cause of portal hypertension)

Back 25

Portal hypertension in cirrhosis results from increased resistance to portal flow at the level of the sinusoids and compression of central veins by perivenular fibrosis and expanded parenchymal nodules.

Front 26

What are the 4 major clinical consequences of Portal hypertension?

Back 26

Ascites, Formation of portosystemic venous shunts, Congestive splenomegaly, and Hepatic Encepalopathy

Front 27

What is the definition of Ascites?

Back 27

Ascites refers to the collection of fluid in the peritoneal cavity

Front 28

The pathogenesis of Ascites generally involves one or more of what 3 mechanisms?

Back 28

Sinusoidal Hypertension, Leakage of hepatic lymph, Renal retention of sodium and water

Front 29

What clinical manifestations represent Portosystemic shunts?

Back 29

Hemorrhoids, Esophageal Varicies (fatal in ~50% presentations), Capute medusa (abdominal wall collaterals that appear as dilated subcutaneous veins extending outward from the umbilicus)

Front 30

Describe the two main functions of bile.

Back 30

The first function of bile is the primary pathway for the elimination of bilirubin, excess cholesterol, and xenobiotics that are insufficiently water soluble to be excreted in the urine. The second function of bile is to secrete bile salts and phospholipid molecules to promote emulsification of dietary fat in the lumen of the gut.

Front 31

What level must the serum bilirubin reach in order to see jaundice and icterus in the adult? What are normal levels of serum bilirubin?

Back 31

Jaundice and icterus occur when serum bilirubin levels reach above 2.0 mg/dL. In the normal adult these levels are <1.2 mg/dL

Front 32

What is Cholestasis?

Back 32

Cholestasis is defined as system retention of not only bilirubin, but also other solutes eliminated in bile (particularly bile salts and cholesterol)

Front 33

What are the sources that bilirubin normally comes from?

Back 33

Normal bilirubin production is derived primarily from the breakdown of senescent RBCs with the remainder derived from the turnover of hepatic hemoproteins and from premature destruction of newly formed erythrocytes in the bone marrow.

Front 34

Describe the Extrahepatic production/processing of bilirubin from a heme molecule to entering the liver.

Back 34

These conversions take place extrahepatically in the cells of the mononuclear phagocyte system:
Heme --(heme oxygenase)--> Biliverdin --(biliverdin reductase)--> Bilirubin (binds to serum albumin while making its way to the liver)

Front 35

Describe the Hepatocelluar processing of bilirubin.

Back 35

Hepatocellular processing of bilirubin involves 1) Carrier mediated uptake at the sinusoidal membrane 2) Cytosolic protein binding and delivery to the ER 3) Conjugation with one or two molecules of glucuronic acid by bilirubin uridine diphosphate-glucuronosyltransferase
4) Excretion of the water-soluble, nontoxic bilirubin glucuronides into bile

Front 36

Describe the fate of the conjugated bilirubin that is released into the bile.

Back 36

Most bilirubin gulcuronides are deconjugated by gut bacteria and degraded to colorless urobilinogens. Urobilinogens and the residue of intact pigment are largely excreted into the feces. Approx 20% are reabsorbed in the illeum and colon, returned to the liver and promptly re.-excreted in the bile

Front 37

When does jaundice occur? Which mechanisms are involved? Which mechanisms produce unconguated vs. conjugated hyperbilirubinemia?

Back 37

Jaundice occurs when the equilibrium between bilirubin production and clearance is disturbed by one or more of the following mechanisms: 1) Excessive bilirubin production 2) Reduced hepatic uptake 3) Impaired conjugation 4) Decreased hepatocellular excretion 5) Impaired bile flow (both intra and extra-hepatic); The first three produce UN-conj. Hyperbili vs. the last two producing CONj. Hyperbili

Front 38

Explain why the physiological presence of neonatal jaundice.

Back 38

Because the hepatic machinery for conjugating and excreting bilirubin does not full mature until about 2 weeks of age almost every newborn developes transient, mild unconjugated hyperbilirubinemia.

Front 39

How much of the cardiac output does the liver receive?

Back 39

About 25% of the cardiac output

Front 40

How much of the blood that the liver receives comes from the Portal vein and how much come from the Hepatic artery?

Back 40

~70% comes from the Portal vein and about ~30% come from the Hepatic artery.

Front 41

What are some descriptions of the main Hepatocellular changes that we see associated with liver injury?

Back 41

Acidophilic bodies (apoptotic bodies), Ballooning degeneration, Mallory Bodies, Ground glass hepatocytes, Atrophy, Fat

Front 42

Describe what process is taking place in the pathological ballooning degeneration of the liver.

Back 42

Large vacuoles form inside cells and the organelles get pushed towards one side of the cells. Ballooning degeneration of hepatocytes, is a form of liver parenchymal cell death. It is generally regarded to be a form of apoptosis, and is a descriptor used in the context of inflamed fatty liver.

Front 43

Describe what process is taking place when we see Councilman bodies or Acidophil bodies in the liver.

Back 43

When we see Councilman bodies or Acidophil bodies in the liver this is a sign of apoptosis.

Front 44

Describe what process is taking place when we see Mallory bodies in the liver.

Back 44

Mallory bodies are most common in alcoholic hepatitis and alcoholic cirrhosis. They are a recognized feature of Wilson's disease, primary biliary cirrhosis, non-alcoholic cirrhosis, hepatocellular carcinoma and morbid obesity, among other conditions. Mallory bodies have a characteristic "twisted-rope" appearance.

Front 45

What are some molecules associated with storage diseases seen in the liver?

Back 45

Alpha-1 Antitrypsin, Lipid (fat) accumulation, Mucopolysaccharides, and Glycogen

Front 46

What are some pigments/syndrome associated with accumulation diseases seen in the liver?

Back 46

Hemochromatosis (iron), Hemosiderin, Dubin-Johnson syndrome (bilirubin), Lipofuscin, Bile, Wilson's Disease (copper)

Front 47

Describe the pattern of injury observed with Acute Hepatitis.

Back 47

Acute hepatitis is associated with spotty injury in the parenchyma.

Front 48

Describe the pattern of injury observed with Chronic Hepatitis.

Back 48

Chronic hepatitis is associated with portal and periportal injury.

Front 49

Describe the pattern of injury observed that Severe Acute and Chronic Hepatitis share in common.

Back 49

Confluent necrosis (sub-massive or massive)

Front 50

What is the definition of Acute Hepatitis and what types of things cause it?

Back 50

Acute Hepatitis is defined as necroinflammatory liver disease of less than 6 months duration. It can be caused by viral infection, alcohol, drugs, and other toxins.

Front 51

What is the definition of Chronic Hepatitis and what types of things cause it?

Back 51

Diffuse necroinflammatory and fibrosing liver disease of more than 6 months' duration. Viral hepatitis B, C, D, Autoimmune hepatitis, drug induced hepatitis, ethanol induced hepatitis, and other cryptogenic causes can be at the root of Chronic hepatitis

Front 52

How does one make the diagnosis of Nonalcoholic Fatty Liver Disease NAFLD or NASH?

Back 52

There is a negative alcohol history and the presence of a fatty liver; Liver biopsy is the gold standard, along with radiological imaging such as sonography, and CT/MRI

Front 53

What are the Hepatocellular, Inflammatory, and Fibrotic changes seen in NASH?

Back 53

Ballooning, Apoptosis/necrosis, Mallory's hyaline, Neutrophil polymorphs, lymphoctes, macrophages, Perisinusoidal fibrosis, and Pericellular fibrosis

Front 54

Name the nine regions of the abdominal area on the patient from right to left, top to bottom.

Back 54

Right Hypochondriac, Epigastric, Left Hypochondriac, Right Lumbar, Umbilical, Left Lumbar, Right Iliac, Hypogastric, Left Iliac

Front 55

What is a Mallory-Weiss tear? What is it from and what does it produce?

Back 55

Mallory-Weiss syndrome refers to bleeding from tears (a Mallory-Weiss tear) in the mucosa at the junction of the stomach and esophagus, usually caused by severe retching, coughing, or vomiting.

Front 56

Why would a full rupture of the esophagus cause someone to increase their breathing and present with no bowel sounds and distention?

Back 56

The air that would normally travel down the esophagus now enters the abdominal cavity disrupts the viscera. With air in the belly it is harder for the diaphragm to move, so to compensate the patient tends to breath a little bit faster and presents as bloated.

Front 57

What does Murphy's march to McBurney's point associated with rebound tenderness describe?

Back 57

This describes classic appendicitis that begins with periumbilical pain and in a very short time moves down and localizes to the right lower quadrant where the appendix is.

Front 58

With abdominal discomfort and pain, what does pain with movement often indicate? (patient hurts even with bumping into the bed)

Back 58

This abdominal pain with movement can likely indicate a peritonitis.

Front 59

What are some classic signs and symptoms of the pain experienced and associated with Gallbladder disease?

Back 59

Pain should get worse after meals (fatty meals in particular). Gallbladder disease (specifically biliary colic) tends to radiate around to the back, and sometimes up to the shoulder.

Front 60

If the cystic duct (which attaches the gallbladder to the common bile duct) becomes blocked will we see jaundice?

Back 60

No, there will be cholecystitis, but there should be no jaundice.

Front 61

Describe the difference in the size of a liver associated with cirrhosis vs. an acute or sub-acute problem.

Back 61

In cirrhosis, the liver will become small and scarred. In an acute or sub-acute problem the liver will become large and inflamed.

Front 62

When you hear about pain in the LUQ what should you think of?

Back 62

Think of problems with the spleen, the stomach, and the first part of the duodenum.

Front 63

When you hear about pain in the Epigastric region what should you think of?

Back 63

Think of the stomach, duodenum, and pancreas.

Front 64

When you hear about pain in the RUQ region what should you think of?

Back 64

Think of the the liver edge and the Gallbladder.

Front 65

When you hear about pain in the RLQ region what should you think of? (Men vs. Women?)

Back 65

In men we think almost exclusively of appendicitis, or hernias if it is a little lower. In women we will think of these things , but also ovarian cysts, tubo-ovarian abscess, ectopic pregnancy.

Front 66

When you hear about pain in the LLQ region what should you think of? (Men vs. Women?)

Back 66

In men we think sigmoid, or diverticular disease. In women we will think of these things , but also ovarian cysts, tubo-ovarian abscess, ectopic pregnancy.

Front 67

What is the most common diagnostic sign of someone with Right-sided colon cancer?

Back 67

Anemia

Front 68

Where does most diverticulitis present?

Back 68

Most diverticulitis presents with left-sided symptoms.

Front 69

What does UPT stand for?

Back 69

Urine pregnancy test

Front 70

With appendicitis does the pain start in the area of the appendix of somewhere else? Is there nausea and vomiting at the onset of pain or after?

Back 70

There is a characteristic pain associated with appendicitis that starts in the periumbilical region and moves down and localizes in the RLQ. Nausea and vomiting usually starts after the onset of pain, not concomitant.

Front 71

Provide a description of the nature of colon cancer. Does it have a quick onset or are there progressive symptoms?

Back 71

The nature of colon cancer is a slow, progressive obstruction to bowel movements, changes in the caliber of stool, and worsening constipation of a long period of time.

Front 72

What is a progression that must be treated surgically with diverticulitis?

Back 72

When a diverticula becomes an abscess.

Front 73

What is the disease mechanism in biliary colic? Is it more of a chronic or acute disease?

Back 73

Contraction of the sphincter of Oddi down against gallstones or biliary sludge generally causes the pain and problems associated with biliary colic. This is more of a chronic disease that commonly has many recurrent episodes.

Front 74

Describe what causes Acute Cholecystitis and how it is treated.

Back 74

Acute cholicystitis is an infection or inflammation in the cystic duct usually caused by a blocked stone, which is generally treated with antibiotics followed by cholecystectomy.

Front 75

Where is biliary colic pain classically represented?

Back 75

BIliary colic pain is classically represented in the RUQ, but may also be felt in the epigastric region, or LUQ.

Front 76

Explain what Murphy's sign is, when it is seen and what it is used for.

Back 76

Classically Murphy's sign is tested for during an abdominal examination; it is performed by asking the patient to breathe out and then gently placing the hand below the costal margin on the right side at the mid-clavicular line (the approx. location of the gallbladder). The patient is then instructed to inspire. Normally, during inspiration, the abdominal contents are pushed downward as the diaphragm moves down (and lungs expand). If the patient stops breathing in b/c the gallbladder is tender and, in moving downward, comes in contact with the examiner's fingers, the test is considered positive.

Front 77

Who are the patients that fall into the "F" category Gallbladder disease?

Back 77

Forties, Fertile, Fat, Female

Front 78

Why do livers get tender? Is this an acute or chronic association?

Back 78

Tender livers are those that are inflammed and are being stretched acutely. The capsule, where the nerve endings are, is being stretched. Those livers that have chronic hepatomegaly, are not tender because they have been stretched over time and are able to adapt.

Front 79

What are two serum tests that we perform that are very sensitive markers of hepatic function?

Back 79

Serum Albumin and Prothrombin time. This indicates whether or not the liver's ability to make albumin protein or clotting factors is still intact.

Front 80

Why does someone who has pancreatitis or pancreatic cancer feel better sitting up rather than lying down? Where is pancreatic pain most often felt?

Back 80

Because there is less traction on the pancreas in the upright position. Pancreatic pain is most often associated with the back.

Front 81

What are the three main causes of pancreatitis?

Back 81

Alcoholic (40%), Idiopathic (40%), Biliary disease (20%)

Front 82

When we see tarry black stool we know that this indicates an upper GI bleed, but at least how far up is it?

Back 82

It is proximal, in the GI tract, to the Ligament of Treitz, which is a suspensory muscle of the duodenum. We know this because the black tarry substance is formed from blood-acid interaction (acid hematin, which can sometimes have a laxative effect and cause a patient diarrhea)

Front 83

If someone presents with a GI bleed after having chronic pain or having been in an accident with no GI problems, but other associated pains, what should you think of and why?

Back 83

You should think of the pain medication that they might be using because they could be overdosing on NSAIDs, which would cause erosive gastritis and bleeding.

Front 84

How can clots formed due to atrial fibrillation cause problems in the GI tract?

Back 84

They can lead to embolic infarction of portions of the GI tract.

Front 85

Do you see fever and leukocytosis in Appendicitis? If so when?

Back 85

There is often no fever or leukocytosis present in Appendicitis early on. This is not a feature that is generally seen until much later.

Front 86

What is the modalitly of choice for diagnosing acute appendicitis? For which patients is ultrasound particularly useful in diagnosing acute appendicitis? What is the overall accuracy associated in diagnosing acute appendicitis?

Back 86

High resolution CT is the modality of choice. Ultrasound is particularly useful in diagnosing appendicitis in pregnant patients, who we want to limit exposure of radiation to. The accuracy of ultrasonographic studies is 90-94% in diagnosing acute appendicitis.

Front 87

Specific types of liver injury determine particular patterns of enzyme changes. Which enzymes are located in the cytoplasm of hepatocytes?

Back 87

ALT, AST, and LDH

Front 88

Specific types of liver injury determine particular patterns of enzyme changes. Which enzymes are located in the Mitochondria of hepatocytes?

Back 88

Mitochondrial isoenzyme of AST

Front 89

Specific types of liver injury determine particular patterns of enzyme changes. Which enzymes are located in the Canalicular cells of the liver (released in obstructive processes)?

Back 89

ALP, GGT

Front 90

What is the best test available for picking up liver injury?

Back 90

ALT(SGPT), because it is the most specific for the liver

Front 91

What does a high AST:ALT ratio indicate?

Back 91

1) Alchohol injury; usually 2:1 AST:ALT
2) When a chronic hepatitis elevates to a cirrhotic stage

Front 92

What are all the enzymes that we measure levels of to identify hepatocellular injury?

Back 92

ALT, AST, LDH

Front 93

What are some processes that damage hepatocytes and can elevate levels of ALT, AST, and LDH?

Back 93

Viruses, Drugs, Toxins, Alcohol, NASH, Shock, passive congestion, biliary obstruction, metabolic disorders

Front 94

What liver marker ratio helps differentiate alcoholic from Non-alcoholic steatohepatitis?

Back 94

A raised ALT over AST in the presence of fatty liver disease helps diagnose Non-alcoholic steatohepatitis over alcoholic steatohepatits

Front 95

What are the enzymes increased in diseases of Cholestasis?

Back 95

Alkaline phosphatase (AP), gamma-Glutamyltransferase (GGT); others include leucine aminopeptidase and 5'-nucleotidase

Front 96

Which liver enzyme is more prevalent when the cytochrome P-450 system is induced (e.g. use of alcohol, phenobarbital, rifampin)?

Back 96

GGT (Gamma-Glutamyl Transferase)

Front 97

What does Prothrombin Time (PT) assess in patients with liver disease?

Back 97

It helps to make an assessment of how intact their liver function is. Prolonged PT can indicate functional impairment, and in cirrhosis, prolonged PT does not correct with intramuscular vitamin K

Front 98

Is albumin or prealbumin better for assessing acute loss of liver synthetic function and why?

Back 98

prealbumin is better for assessing acute loss of liver synthetic function because it has a shorter half life

Front 99

What is the MELD score? Why is it used? What parameters does it take into account?

Back 99

The MELD score is the Model for End stage Liver Disease, which is used to evaluate priority for liver transplantation. The parameters it takes into account are Bilirubin, Creatinine, and INR(standardized PT).

Front 100

What does a MELD score of less than 15 indicate?

Back 100

This indicates that a person has a better chance of living one year without a transplant, than with a transplant.

Front 101

What does a MELD score of more than 17 indicate?

Back 101

This indicates that a person has a better chance of living one year with a transplant rather than without.

Front 102

What is the enzyme responsible for conjugating bilirubin in the liver?

Back 102

UDP-glucuronyl transferase

Front 103

What does it mean if there is an absence urobilinogen in the urine? Why?

Back 103

It means there is a complete obstruction of the common bile duct because normally urobilinogen, which is a flora metabolite of bilrubin, is reabsorbed in the bowel and excreted in the urine. If it isn't in the urine, then it wasn't in the intestine and the only way it could have gotten there was through the common bile duct. So it must have been obstructed.

Front 104

If someone is Jaundice, but there is an absence of bilirubin in their urine, what might that indicate about the cause of their jaundice? Why?

Back 104

It might indicate that there is a process leading to a backup of unconjugated bilirubin in the body, because unconjugated bilirubin cannot be excreted in the urine.

Front 105

What type of pathologies tend to fall in to the category of presenting with Unconjugated Hyperbilirubinemia?

Back 105

Increased production of bilirubin (e.g. hemolysis), impaired uptake by the liver, defective conjugation of bilirubin by the liver

Front 106

What type of pathologies tend to fall in to the category of presenting with Mixed Hyperbilirubinemia?

Back 106

Viral or alcoholic hepatitis

Front 107

What type of pathologies tend to fall in to the category of presenting with Conjugated Hyperbilirubinemia?

Back 107

Intra- or extrahepatic obstruction to bile flow

Front 108

When you hear that there is a rise in Antimitochondrial Antibody what do you think?

Back 108

Primary Biliary Cirrhosis (PBC)

Front 109

What is the diagnosis if you have a patient the looks like they have Primary Biliary Cirrhosis, but their antimitochondrial antibody is negative?

Back 109

This person would have Primary Sclerosing Cholangitis and would most likely be p-ANCA positive

Front 110

Describe the type of Autoantibodies that might be present in a case of Autoimmune hepatitis.

Back 110

Anti-smooth muscle, anti-liver/kidney microsome, and other antinuclear antibodies

Front 111

What is the primary test used to rule out Hepatitis A virus infection? Does this virus lead to a chronic or acute infection?

Back 111

The test is for HAV-Ab (IgM). This virus leads to an acute, self-limiting infection.

Front 112

Describe what causes the most injury to host liver cells during an infection with HBV?

Back 112

The mechanism that is responsible for the most damage is the virus expressing viral antigenic proteins on the host cells it infects, and the host immune system coming to attack those infected cells.

Front 113

What are Dane particles associated with?

Back 113

HBV

Front 114

Which antibody marker helps you distinguish between acute and chronic infection with HBV.

Back 114

The Anti-HBc antibody helps you distinguish. The IgM subtype indicates an acute infection. The IgG subtype indicates chronic infection.

Front 115

How do you distinguish a person who has a naturally acquired HBV infection and someone who has been vaccinated?

Back 115

When someone has been vaccinated, the only antigen they are exposed to is surface antigen. Thus, the only antibody marker they have is Anti-HBs. Whereas someone who has had a naturally acquired infection will have antibodies to all three antigens: HBs, HBc, HBe.

Front 116

Does HCV present with a more chronic or acute infection?

Back 116

HCV causes the body to mount a less vigorous immune response and so it persists with a more chronic infection.

Front 117

What is the primary indication for liver transplantation in the U.S.?

Back 117

HCV infection

Front 118

What is the confirmatory test for a person with positive HCV-Ab? What else can confirm infection?

Back 118

An HCV RIBA (recombinant immunoassay). An HCV RNA test can also confirm infection.

Front 119

Name some of the causes of Non-viral chronic hepatitis.

Back 119

Autoimmune, alcoholic, non-alcoholic, WIlson's disease, Alpha1-antitrypsin Storage disease, Hemochromatosis, Drug-induced

Front 120

Classify the stages of Chronic hepatitis.

Back 120

Stage:
0-No fibrosis
1-Periportal fibrosis (portal tract expansion)
2-Septal fibrosis (periportal, portal/portal)
3-Bridging fibrosis/ architectural distortion
4-Cirrhosis

Front 121

Describe the natural history of autoimmune hepatitis. Does it occur more often in men or women? At what age group is it usually seen? Are the signs and symptoms usually harsh or less severe?

Back 121

Autoimmune hepatitis has a 70-90% Female predominance. There is a bimodal distribution of age presentation and the signs and symptoms generally fluctuate, with many cases including jaundice, but more mild disease.

Front 122

What are the main clinical associations with NAFLD?

Back 122

Obesity, increased calorie intake and a sedentary lifestyle

Front 123

What percentage of obese individuals have Fatty liver?

Back 123

70-80%

Front 124

What percentage of heavy drinkers develop Fatty liver?

Back 124

90-100%

Front 125

What 3 specific signs can tip you off to a diagnosis of Wilson's Disease in a young person?

Back 125

Hemolytic anemia, liver failure, and low Alkaline Phosphatase.

Front 126

What mode of inheritance is associated with Wilson's disease and what is the mechanism of the genetic defect?

Back 126

Wilson's disease is inherited in an autosomal recessive manner. The genetic defect incurred is a metabolic defect that leads to reduced copper excretion in the bile. Thus, accumulation of toxic levels of copper in the liver, brain, eye and other organs results from spillage of nonceruloplasmin bound copper into the circulation.

Front 127

Describe the specific gene defect found in Wilson's disease and what type of normal protein it usually encodes?

Back 127

The specific gene defect in Wilson's disease occurs in the ATP7B gene. There are many mutations present and no one mutation predominates. The gene normally encodes a Copper binding membrane bound ATPase.

Front 128

Describe some of the characteristic histological features of Wilson's disease.

Back 128

Some of the more characteristic features include vacuolated hepatocyte nuclei, macrovesicular steatosis, and Mallory bodies.

Front 129

What is the mode of inheritance for Alpha1-Antitrypsin Storage disease? On which chromosome does the gene defect take place? What is the most common mutation, and what is one of the more serious mutations?

Back 129

A1AT storage disease is inherited in an autosomal recessive manner. The gene that encodes A1AT is found on chromosome 14. The most common mutation seen is PiMM (90%), and one of the more serious mutations leading to <10% production of the normal level of A1AT is the PiZZ mutation.

Front 130

What causes the actual pathology in A1AT Storage Disease?

Back 130

The genetic defect causes the liver to produce abnormal forms of A1AT. These abnormal forms of A1AT accumulate within the endoplasmic reticulum of hepatocytes, and due to defects in degradation, the proteins remain in the ER and lead to disease

Front 131

There is variable presentation of A1AT deficiency, but regardless of when clinical symptoms begin to present themselves (as a neonate or in adulthood) what is the ultimate treatment?

Back 131

Liver transplant.

Front 132

What are the two main organs affected in A1AT? What are the two disease manifestations that occur in those organs?

Back 132

The liver and lungs are mainly affected. Both cirrhosis and/or emphysema can be observed.

Front 133

Describe the main mechanism of pathology in hemachromatosis. What is the genetic defect associated with this disease and what is the mode of inheritance?

Back 133

The mechanism of pathology in hemochromatosis is an accumulation of body iron that gets deposited in the liver, pancreas, myocardium, pituitary, adrenal, thyroid, parathyroid glands, joints, and skin. The genetic defect is transmitted via autosomal recessive inheritance. The defect results in increased intestinal absorption of iron and comes from a specific mutation in the HFE gene on chromosome 6p. The most common mutation is C282Y

Front 134

Who dose hemochromatosis affect more often, men or women? When does this disease typically manifest? What ethnic group stands out with this disease?

Back 134

This disease more commonly affects men than women, and typically occurs after the 4th decade of life. People of Northern European descent and some people from areas of sub-Saharan Africa have a stronger prevelance of carriers in their communities.

Front 135

Describe the classic triad associated with hemochromatosis. Do you see this early on or late in the disease course?

Back 135

This triad develops late in the course of the disease and is characterized by cirrhosis, skin pigmentation, and diabetes ("bronze diabetes").

Front 136

Compare and contrast the etiology and effects of hemochromatosis and hemosiderosis.

Back 136

Hemochromatosis is largely a genetic disorder and the iron overload is generally contained within the hepatocytes. In hemosiderosis people drink a lot (e.g. fortified wine) end up retaining iron in the hepatic reticulocytes secondary to liver injury from drinking. Another tool is the hepatic iron index is used to biopsy and measure hepatic iron levels and correct for age b/c hemochromatosis take years to collect, whereas hemosiderosis does not.

Front 137

What is the treatment once the diagnosis of hemochromatosis is made and why are women less susceptible that men?

Back 137

The treatment is to phlebotomize the patient to remove iron from their body. Women are less susceptible because they have spontaneous iron loss with their monthly cycle and through child birth.

Front 138

Name the spectrum of diseases that can be caused by drug induced liver toxicity.

Back 138

Acute hepatitis, chronic hepatitis, Cholestatic hepatitis, and Granulomatous hepatitis

Front 139

What are two syndromes caused by hereditary defect that lead to unconjugated hyperbilirubinemia (i.e. there is an actual problem with the conjugation of the bilirubin and there is an accumulation in the liver)?

Back 139

Crigler-Najjar (intra hepatic cholestasis), Gilbert's (lipofuscin pigement)

Front 140

What are two syndromes caused by hereditary defect that lead to conjugated hyperbilirubinemia (i.e. there is conjugation of the bilirubin, but there is a problem in excretion of the bile)?

Back 140

Dubin-Johnson (coarse pigment), Rotor's (no pigment)

Front 141

With Progressive Familial Intrahepatic cholestasis what is causing the pathology, how is this syndrome inherited, what happens to the liver?

Back 141

Here the pathology is being caused by abnormal bile salt excretion. The genetic transmission is passed on in a autosomal recessive manner. The liver undergoes changes due to cholestasis that include ductular proliferation and fibrosis.

Front 142

What are the main biliary tract diseases that we have learned about?

Back 142

Primary biliary cirrhosis, Primary sclerosing cholangitis, and Secondary biliary cirrhosis

Front 143

In cholestatic disorders what is the chemistry profile lab tests? Does AP or ALT/AST predominate with elevated levels?

Back 143

The AP predominates.

Front 144

What is the principle method by which the body gets rid of cholesterol? If there is an elevation with of cholesterol and hepatomegaly what type of disease might be taking place?

Back 144

The body gets rid of cholesterol primary through bile excretion. If a patient has high cholesterol counts in the presence of other liver abnormalities you should consider a disease of cholestasis that may account for the increased levels of cholesterol.

Front 145

What is characteristically seen with regard to autoantibodies and immunoglobulin levels in patients with Primary Biliary Cirrhosis (PBC)?

Back 145

Typical auto antibodies that are seen in this disease are Anti-Mitochondrial Antibodies. In overall immunoglobulin levels IgM is observed to be markedly raised.

Front 146

When you encounter a patient with cholestasis, what does knowing that there is no bile duct dilation make you think? What is there was bile duct dilation?

Back 146

Knowing that there is no dilation makes you steer away from a diagnosis of obstruction leading to cholestasis. If there were dilation then you should look into checking for gallstones.

Front 147

Why do patients with long standing cholestasis disease often present with bone density problems? How do you Tx this?

Back 147

This is because bile is responsible for helping absorb fat and fat soluble vitamins, such as Vit D, which help bone formation and maintenance. You can Tx this with ursodiol (bile salt), multivitamins, calcium, and alendronate

Front 148

Who gets Primary Biliary Cirrhosis (PBC) most often and what are key features associated with this disease?

Back 148

This is normally a disease of middle-aged women, and is usually associated with the key features of AMAs, elevated IgM levels, and is associated with other autoimmune diseases.

Front 149

What are some key histologic features that are seen with Primary Biliary Cholestasis (PBC)? (think fibrosis, bile ducts, and metal deposits)

Back 149

A "jigsaw" pattern of fibrosis, bile duct proliferation & ductopenia, and periportal copper deposits. There is granulomatous destruction of intrahepatic bile ducts, portal inflammation, and portal fibrosis leading to cirrhosis

Front 150

Describe the staging for PBC.

Back 150

I- Florid duct lesion
II- Ductular proliferation
III- Scarring
IV- Cirrhosis

Front 151

Who more commonly gets Primary Sclerosing Cholangitis (PSC), men or women?

Back 151

Men are more prone to getting PSC

Front 152

What are some key features of Primary Sclerosing Cholangitis (PSC)?

Back 152

Pruritus (itching), ulcerative colitis (inflammatory bowel disease) often is associated (~70%), diffuse abnormalities of the biliary system upon imaging with ERCP (Endoscopic retrograde cholangiopancreatography), onion skinning and sclerosing cholangitis of the bile ducts. There are often repeated episodes of fever, jaundice, and abdominal pain. There may also be a recurrent bacteremia.

Front 153

What is the diagnostic test for cholangitis?

Back 153

Endoscopic retrograde cholangiopancreatography (ERCP)

Front 154

What are some of the histologic features associated with Primary Sclerosing Cholangitis (PSC)?

Back 154

Inflammation, obliterative fibrosis, segmental dilatation/constricture of the intrahepatic and extrahepatic bile ducts

Front 155

Compare and contrast PSC and PBC.

Back 155

PSC- occurs in men with mean age of ~40; associated with IBD abnormal extrahepatic bile ducts, fibro-obliterative cholangitis, neg AMA.

PBC- occurs in women with mean age of ~50; associated with Sicca syndrome (dryness), Arthritis, Thyroid disease; extrahepatic ducts are always normal; Granulomatous cholangitis; pos AMA

Front 156

What is a cause of secondary PSC that may be hard to distinguish from primary PSC?

Back 156

Malignancy

Front 157

What is the most common disorder of Cholestasis in infants? What is the mechanism of this disease? What is the treatment?

Back 157

Extrahepatic Biliary Atresia. This is a complete obstruction of bile flow due to destruction or absence of part or all the extrahepatic bile duct. The Tx is Kasai surgery.

Front 158

What are the early symptoms of a baby with Extrahepatic Biliary Atresia? What are some of the late symptoms? What other malformations may be present?

Back 158

With early symptoms, the baby will have light colored stools and be jaundiced. They will likely have an enlarged liver and by the time they are diagnosed there may already be cirrhosis present. Included in the late symptoms may be malnutrition, portal hypertension, variceal bleeding, and liver failure. There may be the presence of other malformations such as polysplenia, cardiovascular defects, and situs inversus.

Front 159

Describe the pathology observed in Polycystic Liver Disease. What is an associated disease? Does it occur more commonly in men or women?

Back 159

Present in this disease in the liver are multiple cystic lesions (benign) lined by cuboidal or flattened biliary epithelium. There is no communication with the biliary tree. It occurs more commonly in women. This disease is associated with Autosomal Dominant Polycystic Kidney Disease. (ADPKD)

Front 160

Describe the pathology in Congenital Hepatic fibrosis. What other organ disease is of concern? What two other diseases are commonly associated?

Back 160

The pathology of this disease consists of portal areas being enlarged and fibrotic with small irregularly shaped bile ducts which communicate with the biliary tree. Renal disease is of great concern. Two other diseases that are associated with Congenital Liver Fibrosis are Caroli Disease and Autosomal Recessive Polyscystic Kidney disease (ARPKD)

Front 161

In the pathology of Chronic Hepatitis what are meant by Grading and Staging of the hepatitis?

Back 161

Grading is measuring the level of necrosis. Staging is measuring the level of Fibrosis.

Front 162

Define the level of Necrosis, Inflammation, Fibrosis, and changes in Architecture found in Mild Hepatitis.

Back 162

Necrosis: focal
Inflammation: focal
Fibrosis: focal
Architecture: preserved

Front 163

Define the level of Necrosis, Inflammation, Fibrosis, and changes in Architecture found in Moderate Hepatitis.

Back 163

Necrosis: periportal
Inflammation: periportal
Fibrosis: progressive
Architecture: preserved

Front 164

Define the level of Necrosis, Inflammation, Fibrosis, and changes in Architecture found in Severe Hepatitis.

Back 164

Necrosis: peripoprtal + lobular
Inflammation: lobular
Fibrosis: marked
Architecture: distorted

Front 165

How do you classify Acute Viral Hepatitis? What do you see on the histology?

Back 165

Here you have hepatitis lasting <6months. Histology will show lobular and portal inflammation/necrosis.

Front 166

How do you classify Chronic Viral Hepatitis? What do you see on the histology?

Back 166

Here you have hepatitis lasting >6months. Histology will show inflammation/necrosis that is more portal with some spilling over into the parenchyma (vs. acute hepatitis with lobular and portal inflammation and necrosis) and fibrosis that leads to cirrhosis.

Front 167

What is Hepatorenal failure? What is its etiology?

Back 167

It is a life-threatening medical condition that consists of rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure. Deteriorating liver function is believed to cause changes in the circulation that supplies the intestines, altering blood flow and blood vessel tone in the kidneys. The renal failure of HRS is a consequence of a lack of blood flow, rather than direct damage to the kidney.

Front 168

What is an important indicator of severe liver disease and failure with respect to serum glucose levels?

Back 168

Patients will become hypoglycemic when suffering liver failure because their bodies will consume the glucose that is already in there blood and not be able to undergo glycogenolysis or gluconeogenesis because the liver is failing. This hypoglycemia adds to the life-threatening nature of this situation.

Front 169

Is the natural history of Hep A infection chronic or acute? How is it transmitted? What type of virus is it? Is it associated with hepatocellular carcinoma?

Back 169

Hepatitis A is most often an acute, benign, self-limiting disease. It is transmitted via the fecal oral route with a very transient viremia. The Hep A virus is a ssRNA virus and is not associated with hepatocelluar carcinoma.

Front 170

What is the HBc-Ab (core antibody) useful for?

Back 170

The HBc-Ab is useful for diagnosing acute infection (IgM) and chronic infection (IgG)

Front 171

Explain the significance of the presence of HBeAg (Hep B envelope protein antigen) in a patient's serum?

Back 171

This indicates an active, replicating, viral infection. An individual is very infectious during this stage.

Front 172

If you know that someone is a carrier of Hep B, what class of medication should you be sure not to give them (i.e. what class of medication is Hep B permissive)?

Back 172

You should not give them steroids or chemotherapy if it can be at all avoided. These therapies permit the replication of Hep B, due to a suppression of immune function.

Front 173

What is the most common (50%) form of transmission of Hep B in the U.S.?

Back 173

Sexual transmission (50%)

Front 174

What must be present to see an infection with Hep D in an individual? What kinds of pathology are associated with Hep D?

Back 174

There must also be concomitant infection with Hep B. Acute pathology seen with Hep D includes microvascular steatosis, while chronic pathology show more severe activity and HDAg in nuclei of hepatocytes.

Front 175

Where in the world are HBsAg carriers more likely to be found with HDV-Ab?

Back 175

Africa, Middle East, Southern Italy

Front 176

What is the main route of transmission for HCV? What type of infection does it most commonly produce? How do you treat HCV infection?

Back 176

Blood-borne transmission. It most commonly produces a chronic infection. The common treatment for HCV infection type 1a is pegylated interferon alfa-2b + ribavirin.

Front 177

What are some of the classic histological features associated with Hepatitis C?

Back 177

Portal follicular lymphoid aggregate, bile duct injury, and steatosis.

Front 178

What liver disease can very easily be confused with liver transplant rejection based on histological findings? What are the easily confused findings?

Back 178

Hep C can very easily be confused with liver transplant rejection because both conditions show bile duct injury, which appear similar.

Front 179

What percentage of people chronically infected with Hep C go on to develop cirrhosis?

Back 179

20-50%

Front 180

What is the #1 reason for liver transplantation in the U.S.?

Back 180

Hep C infection.

Front 181

What percentage of people with acute Hep C infection go on to develop a chronic infection?

Back 181

70-85%

Front 182

In addition to antibody testing with Hep C, what other tests are performed? Why?

Back 182

In addition to antibody testing with Hep C, there is also genotype testing that is done. This is because different genotypes respond to differently to treatment.

Front 183

Explain the differences with success of treatment between Hep C Genotypes 1, 2, & 3.

Back 183

Type 1 is the most common in the U.S. and this generally responds poorly to treatment with interferon. Types 2 & 3 account for about 25% of the infections in North America and respond relatively well to treatment. About 75-80% of patients are with Types 2 & 3 are cured with in 24 weeks of treament.

Front 184

How do you determine if someone has been cured of HCV after a course of treatment?

Back 184

A negative HCV RNA 6 months after completing therapy = sustained virologic response (SVR) and indicates cure in >99% of cases

Front 185

What are 3 examples of Non-hepatotropic viruses that can cause hepatitis? In what types of settings are these infections observed to cause hepatitis?

Back 185

Herpes Simplex Virus (Pregnant women & immunosupressed patients), Cytomegalovirus (Liver transplant recipient), Epstein-Barr Virus (In patients with infectious mononucleosis)

Front 186

What is the most common cause of acute liver failure in the U.S.?

Back 186

Acetominophen toxicity.

Front 187

What are the principle causes of Acute Liver Failure from Viruses?

Back 187

Type A, B, C, D, F & Herpes simplex virus

Front 188

What are the principle causes of Acute Liver Failure from Drug-related liver injury?

Back 188

Acetominophen, idiosyncratic drug reactions (INH, NSAIDs, PTU)

Front 189

What are the principle causes of Acute Liver Failure from Toxic Liver Injury?

Back 189

CCl4, Amanita phalloides (mushroom), phosphorus

Front 190

What are the principle causes of Acute Liver Failure from Vascular etiologies?

Back 190

Ischemia, venoocclusive, heat stroke, malignant infiltration

Front 191

What are the principle causes of Acute Liver Failure from genetic and conditional etiologies?

Back 191

Wilson's disease, acute fatty liver of pregnancy

Front 192

Explain the time frame that HbA1c gives a window into for monitoring average blood glucose levels.

Back 192

The life span of a RBC in circulation is about 120 days. Therefore, looking at glycosylated hemoglobin from the non-enzymatic attachment of glucose the Hb protein gives us an idea of average glucose blood levels over the past 4 months (120 days).

Front 193

What is a key feature of Islet cell adenomas? How do they affect blood glucose levels?

Back 193

These tumors are generally about 1cm big and can increase the amount of insulin secreted. This can lead to hypoglycemia and its associated symptoms.

Front 194

What happens to Islet Cells in the pancreas of a person with cystic fibrosis?

Back 194

They generally disappear over time.

Front 195

What types of retinal lesions are typical in diabetic patients?

Back 195

Retinopathy, cataracts, glaucoma

Front 196

What are some of the effects on the newborn of a mother who has Maternal Diabetes?

Back 196

Maternal diabetes can result in Hyperplasia of the fetal islet cells because of the maternal hyperglycemic environment. This can occur if gestational diabetes is present or if the mother has had diabetes mellitus prior to pregnancy. After birth hyperplastic islet cells continue to overfunction, resulting in neonatal hypoglycemia. Infants of diabetic mothers tend to exhibit macrosomia due to growth promoting effects of increased insulin levels.

Front 197

What is a congenital condition that affects the lungs that commonly is associated with fibrosis and fatty infiltration of the pancreas?

Back 197

Cystic fibrosis.

Front 198

A patient's insulin levels are high, but upon serum analysis has no detectable C-peptide (the test used to detect endogenous insulin). Why? What condition does this person have?

Back 198

This person has Type I Diabetes Mellitus. There body lacks the ability to produce insulin so their insulin associated C-peptide is absent as would be expected. The reason they still have insulin present is because they have administered it exogenously.

Front 199

Which form of diabetes is associated with a Hyperosmolar crisis that can lead to coma?

Back 199

Type II Diabetes Mellitus

Front 200

Where do most peudocysts occurring from chronic pancreatitis occur in the organ of the pancreas?

Back 200

Most of pseudocysts occur in the body and tail of the pancreas, and not the head.

Front 201

What is the main mechanism responsible for atherosclerotic injury in diabetic patients?

Back 201

Nonenzymatic glycosylation of collagen accelerates the development of atheroscleorsis, because it eventually leads to the formation of irreversible Advanced Glycosylation End-products (AGEs), which accumulate of a period over time. Such changes aid in trapping LDL and accelerate lipid deposition.

Front 202

What mechanism is responsible for the retinopathy, neuropathy, and cataracts seen in diabetic patients?

Back 202

Intracellular sorbitol accumulation with subsequent osmotic cell injury.

Front 203

Describe the etiology of Zollinger Ellison Syndrome.

Back 203

Zollinger-Ellison syndrome occurs when islet cell adenomas of the pancreas secrete excess gastrin. This secretino leads to intractable peptic ulcer disease with multiple duodenal or gastric ulcerations

Front 204

Describe some of the neuroendocrine problems that can result and may be associated with Islet Cell Adenomas of the pancreas.

Back 204

These types of tumors may over-secrete a variety of hormones. Insulinomas may produce hypoglycemia. Glucagonomas and somatostatinomas may produce a syndrome characterized by mild diabetes mellitus. VIPomas may be associated with marked watery diarrhea, hypokalemia, and achlorhydria.

Front 205

Which type of diabetes mellitus is associated with certain alleles of MHC class II molecules?

Back 205

Type I

Front 206

Which type of diabetes mellitus is associated with autoantibodies against islet cells?

Back 206

Type I

Front 207

When you see a myocardial infarction in a premenopausal woman what should you think of?

Back 207

A predisposing condition; one example is diabetes mellitus

Front 208

When someone incurs an attack of acute pancreatitis, what is a common possible complication that you should think about?

Back 208

Pseudocyst formation. During acute pancreatitis, the extent of necrosis may be so severe that a liquefied area becomes surrounded by granulation tissue, forming a cystic mass. Because there is no epithelial lining in the cyst, however, this is better referred to as a pseudo cyst.

Front 209

Which patients are more likely to develop ketoacidosis: Type I or Type II diabetics? Why?

Back 209

Type I diabetics are more likely to develop ketoacidosis because the diminished insulin levels associated with Type I diabetes permit a rise in serum glucagon levels. This results in catabolism of adipose tissue. The released fatty acids can then become oxidized to form ketone bodies and produce kenoturia and possibly ketoacidosis.

Front 210

Why are patients with Type II diabetes less likely to develop ketonuria and ketoacidosis?

Back 210

This is because while patients with Type II diabetes mellitus can have mild to moderately decreased insulin levels, there is still sufficient insulin to prevent the release of glucagon and fat breakdown to fatty acids, which (in the Type I diabetic) would normally be responsible for the ketonuria and ketoacidosis.

Front 211

What are the alleles of MHC-class II molecules that are most strongly associated with Type I diabetes mellitus?

Back 211

The presence of HLA-DQA1 and HLA-DQB1 alleles of the MHC class II region has the strongest linkage to Type I diabetes mellitus. Autoantibodies to islet cell antigens such as Glutamic Acid Decarboxylase are present years before overt clinical diabetes develops. Similarly, an insulinitis cause by T-cell infiltration occurs prior to the onset of symptoms or very early in the course of Type I diabetes mellitus.

Front 212

What nephropathies are commonly seen in diabetic patients?

Back 212

Changes involving the glomeruli in diabetic patients most often include Diffuse glomerulosclerosis and Nodular Glomerulosclerosis.

Front 213

What retinopathies are commonly seen as a back ground in patients with diabetes mellitus? What is a sign of more ominous proliferative retinopathy?

Back 213

Hard exudates and cotton-wool spots are part of background retinopathy. Progressive retinopathy is associated with neovascularization.

Front 214

What progressive vascular changes in the kidney are associated with diabetes mellitus?

Back 214

Large-artery atherosclerosis and hyaline arteriolosclerosis.

Front 215

When are Polycystic changes most likely to show up in a patient with diabetes?

Back 215

Polycystic changes are most likely to appear in diabetic patients who have received long-term hemodialysis.

Front 216

What is the most common cause of death in diabetic patients?

Back 216

Ischemic heart disease.

Front 217

Do nerve cells require insulin for glucose uptake? What happens to excess intracelluar glucose that is taken up by nerve cells? What enzyme is responsible for converting excess glucose to problematic sugars? What are those problematic sugars?

Back 217

Nerve cells do not require insulin for glucose uptake. In the presence of hyperglycemia, excess glucose diffuses into the nerve cell cytoplasm and accumulates. This excess glucose is metabolized by intracellular aldose reductase enzyme to sorbitol and then to fructose. These increase intracellular osmolarity and free water influx, injuring the cell.

Front 218

What is the etiology of Galactosemia and its effects on the liver?

Back 218

Galactosemia is an inborn error of metabolism in which deficiency of galactose-1-phosphtate uridylyl transferase damages cells of the kidney, liver, and brain; there is hepatomegaly, splenomegaly, hypoglycemia and eventual cirrhosis.

Front 219

What does an AST elevated higher than an ALT indicate? What chronic habit/condition is this often associated with?

Back 219

An elevated AST over and ALT is indicative of hepatocelluar injury associated with chronic alcoholism.

Front 220

What is a Prussian blue stain used to observe? What is a hereditary condition in which extra iron absorption can lead to liver cirrhosis?

Back 220

Iron deposition; Hemochromatosis.

Front 221

Explain which organs Hemochromatosis affects. How do we visualize iron deposition in tissue? High serum levels of what molecule indicate an increase in iron absorption?

Back 221

Hemochromatosis is a genetic, autosomal recessive condition in which iron overload occurs because of excessive absorbtion of dietary iron. Iron is deposited in many tissues including the heart, pancreas, and liver, which leads to heart failure, diabetes, and cirrhosis. We visualiize iron deposition in tissue by using the Prussian Blue stain. We look for high levels of serum Ferritin as an indicator for an increase in body iron.

Front 222

Describe some of the histological changes seen in chronic hepatitis.

Back 222

Chronic hepatitis is characterized by necrosis of hepatocytes at the interface between portal tracts and the liver lobule. This eventually leads to bridging necrosis and, finally, to cirrhosis without portal bridging fibrosis and nodular regeneration.

Front 223

What is a common progression from a benign to malignant lesion that is commonly seen in the colon?

Back 223

Adenoma progressing to a colon carcinoma.

Front 224

What genetic mutation is Hereditary Nonpoylposis Colon Carcinoma (HNPCC) syndrome associated with?

Back 224

HNPCC is associated with inherited mutations in DNA mismatch-repair genes

Front 225

What form of cancer is the liver fluke Clonorchis sinensis associated with?

Back 225

Clonorchis sinensis predisposes one to bile duct carcinoma.

Front 226

In a patient with amebiasis affecting the liver, what sort of symptoms are most likely to be associated?

Back 226

There is most likely going to be presentation of diarrhea along with blood and mucus.

Front 227

Which hepatitis virus is most associated with IDU (injection drug usage)?

Back 227

HBV

Front 228

What serum marker is indicative of hepatocellular carcinoma?

Back 228

Alpha-fetoprotein

Front 229

What are the normal serum levels of the hepatic enzymes ALT, AST, AlkPhos, and GGT?

Back 229

ALT: 8-20 U/L
AST: 8-20 U/L
AlkPhos: 20-70 U/L
GGT: Men(0-65 U/L), Women (0-45 U/L)

Front 230

What kind of necrotic changes in the liver are seen with right-sided heart failure? Is the necrosis centrilobular, periportal, or both?

Back 230

The hepatocellular necrosis associated with right sided heart failure is centrilobular.

Front 231

What are two characteristic features of Sclerosing Cholangitis? What associated pathology occurs in the colon?

Back 231

Inflammation and obliterative fibrosis of the bile ducts. Ulcerative colitis is commonly seen in patients with sclerosing cholangitis.

Front 232

What denotes a chronic carrier state for HBV? How do the majority of persons with a chronic carrier state acquire the infection? What percentage of adult HBV infections yield the chronic carrier state?

Back 232

Persistance of HBs-Ag in the serum for 6 months or more after initial detection, especially in the absence of symptoms. The majority of chronic carriers were infected via vertical transmission from their mothers in utero or at birth. Only 1% to 10% of adult HBV infections yield the chronic carrier state.

Front 233

When staining the liver what is the Periodic Acid Schiff (PAS) stain most often used for? Which genotype of this disease will develop significant liver disease? What problems associated with other organ systems can develop?

Back 233

PAS positive globules seen in the liver are characteristic of alpha-1-antitrypsin (AAT) deficiency. Approximately 10% of persons with the homozygous deficiency, PiZZ phenotype, of ATT deficiency will develop significant liver disease. including neonatal hepatitis and progressive cirrhosis. Deficiency of ATT also allows unchecked action of elastases in the lung, which destroys the elastic tissue and causes emphysema.

Front 234

What is the classical triad of Budd-Chiari syndrome? What is the classic triad that presents with it?

Back 234

Budd-Chiari syndrome is the clinical picture caused by occlusion of the hepatic veins. It presents with the classical triad of abdominal pain, ascites and hepatomegaly. Examples of occlusion include thrombosis of hepatic veins. The syndrome can be fulminant, acute, chronic, or asymptomatic. It is more common in females. Some (10-20%) also have obstruction of the portal vein.

Front 235

What is the single most important predictor of whether a patient with viral hepatitis will develop chronic liver disease that progresses to cirrhosis?

Back 235

The single most important predictor is the type of virus they are infected with. The most likely infection to lead to chronic liver disease and cirrhosis is infection with HCV.

Front 236

Name some risk factors for developing biliary bile pigment stones that are supersaturated with cholesterol.

Back 236

Risk factors for biliary bile pigment stones that are supersaturated with cholesterol include Native American descent, female sex, obesity, and increasing age. These factors cause secretion of bile that is super saturated in cholesterol.

Front 237

Provide a brief description of what would be seen in the liver associated with Primary Biliary Sclerosis.

Back 237

Liver is diffusely nodular and intensely green with small, uniform nodules and microscopically shows prominent bile stasis and fibrous bridging between portal areas.

Front 238

Provide a brief description of what would be seen in the liver associated with Acute Fulminant Hepatitis.

Back 238

Liver is shrunken with a wrinkled capsular surface and microscopically shows massive irregular areas of necrosis without an obvious pattern.

Front 239

Provide a brief description of what would be seen in the liver associated with Alpha-1 Antitrypsin deficiency.

Back 239

Liver is diffusely nodular with small, uniform nodules and microscopically shows diffuse fibrosis encirclling regenerative nodules; liver contains PAS-positive, globular cytoplasmic inclusions.

Front 240

Provide a brief description of what would be seen in the liver associated with Alcohol Abuse.

Back 240

Portal fibrosis with nodular hepatocyte regeneration and steatosis are typical features of chronic alcohol abuse.

Front 241

What is the etiology behind Spider telangectasias (angiomas), testicular atrophy, and gynecomastia in a patient with a failing liver?

Back 241

These symptoms are all due to hyperestrogenism resulting from the failing liver being unable to metabolize estrogen properly.

Front 242

What type of hyperbilirubinemia does not tend to lead to kernickterus in newborns?

Back 242

Conjugated hyprebilirubinemia.

Front 243

What are typical causes of Ascending Cholangitis?

Back 243

E. coli or Klebsiella infection. This also presents acutely with fever, chills, and abdominal pain.

Front 244

Describe the bilirubin and AP levels associated with Sclerosing Cholangitis.

Back 244

The bilirubin concentration is often increased as is the alkaline phosphatase level.

Front 245

Explain why there are pigment stones, decreased urobilinogen in the urine, increased fecal bile acids, and macrocytic anemia associated with Crohn disease.

Back 245

Decreased urinary urobilinogen, and increased fecal bile acids indicate decreased reabsorption in the ileum, which reduces enterohepatic circulation and favors the formation of pigment stones. Crohn disease often involves the terminal ileum and this also disturbs absorption of vitamin B12 complexed with intrinsic factor, leading to macrocytic anemia.

Front 246

In what setting do most gallbladder cancers occur?

Back 246

Most gallbladder cancers occur in cholelithiasis.

Front 247

What are three characteristic signs of Primary Biliary Cirrhosis.

Back 247

The presence of obstructive jaundice, granulomatous destruction of bile ducts, and elevated titers of antimitochondrial antibodies is characteristic of Primary Biliary Cirrhosis.

Front 248

What is Piece-meal necrosis commonly associated with?

Back 248

Chronic HBV or HCV infection.

Front 249

What is a common etiologic agent leading to Concentric bile duct fibrosis?

Back 249

Primary Sclerosing Cholangitis.

Front 250

What is Wilson's disease and which organs does it affect? How is the gene associated with Wilson's disease responsible for the pathophisology it creates? What is Ceruloplasmin and how are its levels affected in this disease?

Back 250

Wilson's disease is an inherited disorder in which toxic levels of copper accumulate in tissues, particularly the brain, eye, and liver. The gene for Wilson disease encodes a copper-transporting ATPase in the hepatocytes. With the gene copper cannot be secreted into the plasma. Ceruloplasmin is an Alpha2-globulin that carries copper in the plasma. Because copper cannot be secreted into the plasma ceruloplasmin levels are low.

Front 251

Explain how each of these can lead to liver pathologies:
1) Aspergillus Flavus
2) Raw Oyster
3) Aspirin
4) Nitrites
5) Acetomenaphin

Back 251

1) Aspergillus Flavus- aflatoxin is a hepatotoxin that can be carcinogenic leading to hepatocellular carcinoma

2) Raw Oysters- oysters can concentrate HAV from seawater contaminated with sewage

3) Aspirin- associated with Reye's syndrome, which results in extensive microvesicular steatosis

4) Nitrites- have been causally linked with cancers in the upper G.I. tract

5) Acetomenaphin- large amounts lead to hepatocellular necrosis

Front 252

What structures are the main structural targets in Primary Sclerosing Cholangitis? What is a characteristic description and a characteristic lesion associated with PSC?

Back 252

The main targets in PSC are intrahepatic bile ducts. There is a characteristic description of these bile ducts to have undergone "onion skinning", and PSC is often associated with Ulcerative Colitis.

Front 253

What antibodies are associated with Autoimmune Hepatitis? What other autoimmune-associated factor is elevated? How is it treated?

Back 253

ANA and Anti-smooth muscle antibodies are elevated in association with Autoimmune hepatitis. Rheumatoid factor is also often present. Patients generally respond well to glucocorticoid therapy.

Front 254

What is causing the damage during an HBV infection? How does the answer to the previous question explain why vertical transmission leads to a HBV carrier state 90% of the time? What is the increased risk of hepatocellular carcinoma in the carrier state?

Back 254

In immunocompeten persons, HBV induces T-cell response specific for HBs-Ag that causes apoptosis of liver cells. In the neonatal setting the immune system is not fully developed, hence hepatitis does not occur. The carrier state increases the risk for hepatocellular carcinoma 200X.

Front 255

Explain the etiology of Gilbert syndrome. How prevalent is this syndrome? When do people notice tend to notice the symptoms associated with this syndrome?

Back 255

Gilbert's syndrome results from decreased levels of uridine diphosphate glucuronosyltransferase (UGT). Up to 7% of persons in the general population may have decreased levels of this enzyme, and the condition is never diagnosed. Stress may cause transient unconjugated hyperbilirubinemia to a point that scleral icterus is detectable, when the serum bilirubin reaches about 2-2.5 mg/dL.

Front 256

What is the genetic defect associated with Hereditary Hemochromatosis? What is the etiology of this disease? What are some signs and symptoms?

Back 256

This disease results from a mutation in the HFE gene that encodes for an HLA class I-like molecue that binds Beta 2-microglobulin. HFE is expressed on the basolateral surface of the small intestinal crypt epithelial cells, where it is complexed with transferrin receptor and senses the levels of plasma transferrin. Through this sensing, HFE regulates the levels of several proteins such as DMT-1 that are involved in iron absorption. Mutant HFE fails to do this job allowing excessive Fe absorption and accumulation in the liver and other organs.

Front 257

Primary Biliary Cirrhosis (PBC) is an uncommon autoimmune disorder that causes progressive intrahepatic bile duct destruction. What are some symptoms indicative of obstructive jaundice resulting from bile duct destruction? What are the autoimmune antibodies associated with PBC?

Back 257

Pruritus, Conjugated hyperbilirubinemia, and increased AlkPhos levels are indicative of the obstructive jaundice resulting from the bile duct destruction associated with PBC. In PBC Antimitochondrial antibodies are often found to be present.

Front 258

What are the three possible outcomes when HDV infection is superimposed on chronic HBV?

Back 258

1) Mild HBV hepatitis may be converted to fulminant disease
2) Acute hepatitis may occur in an asymptomatic HBV carrier
3) Chronic progressive disease may develop culminating in cirrhosis

Front 259

What type of tissue does the esophagus not have?

Back 259

The esophagus does not have a serosa

Front 260

What is disorder is the most common cause of esophagitis? Describe what permits this disorder to occur.

Back 260

Gastro Esophageal Reflux Disease (GERD). Transient relaxation of the Lower Esophageal Sphincter (LES) allowing the reflux of acid and bile into the distal esophagus along with ineffective esophageal clearance of reflux material helps to create this problem.

Front 261

What are some of the risk factors associated with GERD?

Back 261

The risk factors associated with GERD include Smoking, Alcohol, Caffeine, Fatty foods, chocolate, and Hiatal hernia

Front 262

What are the histological findings associated with Reflux esophagitis? Describe the inflammatory cells that are found to be associated with this disease.

Back 262

With Reflux esophagitis you will see Basal Cell Hyperplasia and Elongation of the dermal papillae. Eosinophils and lymphocytes will generally be found in the epithelial layer

Front 263

What is Barrett's Esophagus? What part of the esophagus does it occur in? What other disease is it commonly associated with? Describe the process of Barrett's formation.

Back 263

Barrett's esophagus is an Adenocarcinoma. It is commonly associated with GERD and thus is most lilkely to develop in the distal esophagus. Glandular metaplasia occurs due to acid injury and gastric type columnar cells and small intestinal type cells (goblet cells) form to protect the tissue from acid exposure. In the process adenocarcinoma can arise from the metaplasia.

Front 264

What are the histological features that are found in Barrett's Esophagus? What are some of the complications that can be associated with this disease?

Back 264

Dysplasia (malignant transformation) of the newly formed columnar cells and goblet cells from Barrett's is usually associated with mucin depletion and cytoplasmic basophilia. A complication that can occur other than malignancy is ulceration with stricture formation (most common)

Front 265

What is the most important source of protection in the esophagus with regard to acid? Where does this protection come from?

Back 265

The most important source of protection come from bicarbonate that is found in the saliva.

Front 266

What are the 3 most common causes of Infectious Esophagitis? What is the state of the immune system in most patients suffering from infectious esophagitis?

Back 266

The 3 most common agents that cause infectious esophagitis in order of prevalence are Candida, CMV, and Herpes Simplex. The patient who comes in with infectious esophagitis is most usually immunocompromised, commonly AIDs related.

Front 267

What are some physical agents that are responsible for esophagitis?

Back 267

Acid and alkali agents, pill induced, and radiation.

Front 268

Is you suspect eosinophilic esophagitis what portion of the esophagus do you biopsy?

Back 268

You biopsy all along the length of the esophagus because it can occur across the entire span versus esopagitis from GERD, which mostly effects the distal esophagus.

Front 269

How do strictures form in response to GERD?

Back 269

When inflammation penetrates deep to the muscularis this can result in fibrosis and scarring, which can narrow the lumen of the esophagus.

Front 270

How often is Barrett's esophagus found in patients with GERD?

Back 270

8-20% of patients have Barrett's esophagus.

Front 271

Name some of the malignant tumors that can arise in the esophagus.

Back 271

Leiomyosarcoma, Melanoma, Lymphoma, Metastatic tumors, rare sarcomas.

Front 272

Explain the etiology of esophageal varices. What are the most common complications associated with this? When does it contribute to mortality?

Back 272

Portal hypertension causes the dilation of the Left Gastric vein and backup to the anastomoses with the esophageal veins. Rupture with massive hematemesis can be a complication of this condition. This is the most common cause of death associated with cirrhosis of the liver.

Front 273

What is Boerhaave's Syndrome? What most often causes it? Describe its most common complication and characteristic sounds associated with it.

Back 273

Boerhaave's syndrome is a rupture of the distal esophagus. Endoscopy is the cause in ~75% of cases, others can be retching and bulemia. Pneumodediastinum is commonly associated with this, where air dissects into the subcutaneous tissue and produces a crunching sound on examination. Pleural effusions containing, food, acid, and amylase can occur as well.

Front 274

Describe Achalasia? What does it affect and why? Name the most common acquired cause of achalasia.

Back 274

Achalasia is the most common neuromuscular disorder of the esophagus. It occurs when there are absent ganglion cells in the myenteric plexus. This causes a decrease in proximal smooth muscle contraction and a loss of vasointestinal peptide (VIP), which normally relaxes LES. Thus, you see dilation of the esophagus proximal to the LES with absent peristalsis. Chagas disease produces the most common acquired form of this as there is destruction of ganglion cells by leishmanial forms. Scleroderma (CREST syndrome) can also cause achalasia.

Front 275

What are the #1 risk factors associated with developing squamous cell carcinoma of the Esophagus? Where are the locations that it occurs most? Clinical findings?

Back 275

Smoking and alcohol abuse. It most commonly occurs in the middle 1/3, with controversy over the lower and upper 1/3 of the esophagus. Clinical findings include Dysphagia for solids, and weight loss.

Front 276

Where does adenocarcinoma most commonly occur in the esophagus?

Back 276

The lower 1/3.

Front 277

What percent of duodenal ulcers can be correlated with H. pylori infection?

Back 277

~80%

Front 278

What are some of the the endogenous Gastric molecules and organisms that can potentially cause tissue insult?

Back 278

Pepsin, HCl, Bile acids, H.pylori

Front 279

What are some of the endogenous Gastric defenses against endogenous molecules and organisms causing harm?

Back 279

The mucosal barrier, mucus, blood flow, endogenous prostaglandins, bicarbonate, and cell restitution.

Front 280

When you hear about a Duodenal Ulcer what cause should you assume until proven otherwise? If it is not the most likely cause, what other causes could it be?

Back 280

H.pylori is the most common cause of duodenal ulcers by far. If H.pylori is not the cause it could be due to NSAIDs (altered prostaglandin balance), Zolling-Ellison Syndrome (Gastrin secreting tumor), Smoking (increased acid output), Stress??

Front 281

What are the associated causes of Acute Gastritis? (Erosive)(More sever symptoms, but self limiting) Is scar formation an issue in this condition?

Back 281

Hemorragic (erosive)
-Trauma, Shock, etc.
-Drug induced (EtOH, NSAID, Cortisone, Chemo)

H.Pylori related

Scars do not form in acute gastritis. Scars are associated with chronic gastritis.

Front 282

What are the associated causes of Chronic Gastritis? (Less severe symptoms, but more persistent)

Back 282

H.pylori associated
-Atrophic or non-atrophic

Autoimmune gastritis

Front 283

What are the associated causes of Special forms of Gastritis?

Back 283

Reactive (reflux), Granulomatous (Crohn's Sarcoidosis), Eosinophilic (allergic), Collagenous, Lymphocytic, Non HP infectious gastritis

Front 284

What percentage of patients with Chronic Gastritis suffer from autoimmune gastritis? Which antibodies are most likely present?

Back 284

<10% of Chronic gastritis cases are due to autoimmune gastritis. Antibodies to parietal cells and intrinsic factor are most likely present.

Front 285

Where is Non-atrophic Gastritis focused in the stomach?

Back 285

Non-atrophic gastritis is focused in the antrum.

Front 286

What portion of the stomach is likely to be involved in Atrophic Chronic Gastritis?

Back 286

Atrophic Chronic Gastritis is more likely to involve multifocal inflammation, even leading to a pan-gastritis and metaplasia.

Front 287

What parts of the stomach are more likely to be involved in Autoimmune Chronic Gastritis?

Back 287

The Fundus and the Body.

Front 288

What would the biopsy of Chronic Gastritis due to H.pylori infection show with regard to inflammatory cells and tissue size and morphology?

Back 288

Biopsy of tissue from chronic gastritis due to H.pylori infection would show Lymphoplasmacytic infiltrate, Neutrophilic infiltrate, Regenerative changes, Intestinal metaplasia, and Atrophy.

Front 289

Why type of cancer are patients with Chronic Gastritis due to H.pylori infection at risk for?

Back 289

Lymphomas (induced Maltomas) because they can disturb the lymphoid tissue in the submucosa in the G.I tract.

Front 290

Describe the progression (in 3 steps) from HP Gastritis or Autoimmune Gastritis to Carcinoid tumor.

Back 290

HP/AI Gastritis --} Gastric Atrophy --} Endocrine Cell Hyperplasia --} Carcinoid Tumor

Front 291

Describe the progression (in 3 steps) from HP Gastritis or Autoimmune Gastritis to Carcinoma.

Back 291

HP/AI Gastritis --} Gastric Atrophy --} Intestinal Metaplasia --} Carcinoma

Front 292

Define what an Ulcer in the G.I. tract is.

Back 292

This is a breach in the mucosa of the G.I. tract that extends through the muscularis mucosae into the mucosa or deeper.

Front 293

What are some of the possible locations for Chronic Peptic Ulcers to take place?

Back 293

The duodenum and the stomach account for ~98%; other locations include Gastroenterostomy stroma, Meckel's diverticulum, atypical locations due to Zollinger-Ellison syndrome.

Front 294

What percentage of Gastric Ulcers are due to H.pylori infection?

Back 294

~75%

Front 295

Which wall of the stomach are ulcers more likely to develop on?

Back 295

They are more likely to develop on the lesser curvature of the stomach.

Front 296

What are the most common complications associated with Peptic ulcer disease?

Back 296

Bleeding (25% of deaths), Perforation (75% of deaths), Obstruction (due to scarring), Intractable pain.

Front 297

The osmolarity of the stool is normally similar to the osmolarity of what bodily fluid?

Back 297

Stool has a similar osmolarity to plasma.

Front 298

What are the clinical definitions of Exogenous causes of secretory diarrhea?

Back 298

The exogenous causes of secretory diarrhea include laxatives or bacterial toxins (e.g. Cholera or E.coli)

Front 299

What are the clinical definitions of Endogenous causes of secretory diarrhea?

Back 299

The ednogenous causes of secretory diarrhea include hormones or bile salts (e.g. VIP, gastrin, calcitonin, prostaglandins)

Front 300

What are some examples of invasive infectious organisms that cause diarrhea? Which are the subset that produce toxins?

Back 300

Salmonella (invasive, but only causes watery diarrhea), Shigella, Invasive E.coli, C.difficile (these others can cause bloody diarrhea)

***Shigella, Invasive E.coli, and C.difficile produce toxins

Front 301

What are some examples of non-invasive infectious organisms that cause diarrhea? Which are the subset that produce toxins?

Back 301

Viruses, Cryptosporidium, Girardia, V. cholerae, Enterotoxigenic E.coli, and Bacillus cereus

***V.cholera, Enterotocigenic E.coli and Bacillus cereus produce toxins

Front 302

Where do the Enterotoxic Organism toxins (e.g. V.cholera, Bacillus cereus, Staph aureus-preformed toxin, Enterotocigenic E.coli, Yersinia, Aeromonas) that cause diarrhea usually found? What kind of diarrhea is it and are inflammatory cells usually present?

Back 302

The toxins from these organisms primary affect small bowel secretion. Watery diarrhea with cramps ensues and, rarely, PMNs are found.

Front 303

Crohn's inflammatory bowel disease can be confused with inflammatory bowel disease of the terminal small intestine by infection from what organsim?

Back 303

Yersinia enterocolitica.

Front 304

Where do the Invasive Organisms (e.g. Shigella, Salmonella, Campylobacter, C.diff., Yersinia, Vibrio parahemolyticus, Enteroinvasive E.coli, Entamoeba histolytica) that cause diarrhea generally invade? Are there inflammatory cells present? What kind of diarrhea is it? Are there systemic symptoms?

Back 304

These organisms usually invade the Colon. All but Salmonella (watery diarrhea) produce a bloody form of diarrhea. Fecal PMN's (can be a diagostic feature) are prominent, but systemic symptoms are unusual.

Front 305

What are two invasive organisms that cause bloody diarrhea and cause fever, that were are likely to see in the hospital? Are these cytotoxic?

Back 305

Shigella and C. difficile. Yes, these are both cytotoxic.

Front 306

Which organisms have been shown to infect AIDs patients and cause Tenesmus?

Back 306

Gonorrhea, HSV, and CMV.

Front 307

What are the two forms of inflammatory bowel disease that we know of?

Back 307

Crohn's disease and Ulcerative Colitis.

Front 308

What section of the small intestine does Giardia mainly affect?

Back 308

The upper portion of the small intestine.

Front 309

What is the most common viral etiology of viral diarrhea in children?

Back 309

Rotavirus.

Front 310

What is the most common viral etiology of viral diarrhea in adults?

Back 310

Norwalk virus.

Front 311

What is the most common viral etiology of viral diarrhea in young children?

Back 311

Adenovirus.

Front 312

Compare and contrast the histological findings and testing of the ulcers found in Colitis due to CMV or HSV infection.

Back 312

CMV: causes large ulcers, inclusion bodies, biopsy in the center of ulcer, likes to infect endothelium

HSV: causes small ulcers, biopsy in the periphery of the ulcer, likes to infect squamous epithelium

Front 313

What part of the GI tract does CMV infect? How does the infection proceed in immunocompetent patients? Which can acquire this infection from reactivation of CMV infection? What do the symptoms include?

Back 313

CMV infection affects the entire GI tract. In immunocompetent patients the infection is selflimited. AIDs, transplant, and steroid immunosuppressed patients can all be subject to reactivation of CMV infection. Symptoms include severe diarrhea, multiple bleeding ulcers, and perforation of ulcers.

Front 314

What are the causes of Acute Colitis?

Back 314

Infectous (E.coli, Shigella) and Drug induced

Front 315

What are the causes of Chronic Colitis?

Back 315

Inflammatory bowel disease, Diversion colitis/Pouchitis, Lymphocytic/Collagenous, Radiation

Front 316

Which type of inflammatory cells can be normally found in the epithelium of the colon? Which are abnormal?

Back 316

Lymphocytes can be found in the colonic epithelium normally, but neutrophils seen in the epithelium is always a sign of an abnormal process.

Front 317

When comparing Chronic vs. Acute Colitis there may or may not be a difference in the amount of inflammatory cells that you see, but what is a key feature of Chronic Colitis that would be distinguished from acute?

Back 317

In Chronic Colitis there is Architectural distortion of the colonic tissue and possibly fibrosis.

Front 318

What type of metaplasia takes place with Chronic Colitis?

Back 318

You see the increased formation of Paneth Cells (cells that have increased amounts of lysozyme and zinc) in response to long-standing microbial assault. You also may see Psuedopyloric cells.

Front 319

Does intestinal resection cure Crohn's disease?

Back 319

Crohn's has a strong capacity to recur even following bowel resection.

Front 320

What are the two age peaks that we see Crohn's disease occurring at?

Back 320

We see the development of Crohn's in the teens to 20's and a 2nd peak in the 50-60's.

Front 321

Is Crohn's disease more common in whites or non-whites? Jews or non-jews?

Back 321

Crohn's is more commonly seen in whites, and in Jews.

Front 322

Which parts of the GI tract does Crohn's affect most commonly?

Back 322

Crohn's can affect any part of the GI tract from mouth to anus the most common involvement is:

Distal ileum + proximal colon (40%)
Small intestine only (30%)
Colon only (25%)
Gastroduodenal, Jejunal, Perianal (5%)

Front 323

What section of the GI tract is spared in Crohn's disease?

Back 323

In Crohn's disease the entire GI tract can be involved, but usually the rectum is spared (for unknown reasons).

Front 324

Describe the morphology of the tissue associated with Crohn's disease. Which layers of tissue of the GI tract are affected? Are there areas where Crohn's skips its inflammation? Are the crypts affected? Do Granulomas form? Is there fibrosis?

Back 324

With Crohn's disease there are many morphological abnormalities of note. The tissues invovled show a transmural inflammation with area that are inflamed and areas that are characteristically skipped. The mucosa shows crypt distortion and possibly metaplasia and abscess formation. There are non-caseating Granulomas that are formed along with a lympoplasmacytic infiltration that is seen. Fissures and fistulas can form along with submucosal fibrosis, and Neuronal hyperplasia is observed.

Front 325

What are some of the complications associated with Crohn's disease?

Back 325

Intestinal obstruction, Internal fistula, Perianal Disease, Arthritis, Calcium Oxalate renal calculi, Malabsorption due to bile salt deficiency, Macrocytic anemia due to B12 deficiency.

Front 326

In Ulcerative Colitis where does disease usually start? How does it progress/is it limited in its progression? Does it skip areas of tissue? What depth of tissue is involved (is it transmural)?

Back 326

Ulcerative Colitis usually starts in the rectum (but not the anus) and progresses backward up the GI tract in the colon, however, it usually does not progress out of the colon (there still is the possibility of backwash ileitis). Left colon involement (20-30%), Pancolitis (20%). The inflammation tends to be diffuse and does not create skip lesions as are seen in Crohn's disease. The inflammation is usually confined to mucosal and submucosal depths and does not produce the transmural lesions seen in Crohn's disease.

Front 327

What are some of the Gross and Microscopic features seen in Crohn's disease?

Back 327

Gross: Thick bowel wall and narrow lumen (leads to obstruction), Apthous ulcers (early sign), Skip lesions, strictures, fistulas, deep linear ulcers with cobblestone pattern, Fat creeping around serosa

Microscopic: Non-caseating granulomas (60%), lymphoid aggregates, dysplasia or cancer less likely

Front 328

What are some of the Gross and Microscopic features seen in Ulcerative Colitis?

Back 328

Gross: Inflammatory Pseudopolyps, areas of friable, bloody, residual mucosa, Ulceration and hemorrhage

Microscopic: Ulcers and crypt abscesses containing neutrophils, Dysplasia or cancer may be present

Front 329

What are the complications associated with Ulcerative Colitis?

Back 329

Toxic Megacolon, Primary Sclerosing Cholangitis (fibrosing around the common bile duct leading to jaundice), ADENOCARCINOMA (greatest risks are pancolitis, early onset, and duration >10 years)

Front 330

What are the clinical findings/presentation commonly associated with Crohn's disease?

Back 330

Recurrent right lower quadrant colicky pain (obstruction) with diahrrea. Bleeding occurs only with colon or anal involvement (fistulas)

Front 331

What are the clinical findings/presentation commonly associated with Ulcerative Colitis?

Back 331

Recurrent left sided abdominal cramping with bloody diarrhea and mucus.

Front 332

What are some examples of malabsorbtion diseases caused by defects in absorption of the intestinal cell mucosa?

Back 332

Lactose intolerance and Abetalipoproteinemia

Front 333

Explain the etiology of Lactose intolerance? What are the symptoms associated with it and why do they occur? Which is worse, the inherited form or the acquired form? What is a test that is used to diagnose this?

Back 333

Lactose intolerance is caused by a deficiency of disaccharidase (lactase enzyme). Symptoms involve, flatulence, GI discomfort, and Osmotic diarrhea. The omotically active sugars draw H2O out in to the lumen of the small bowel and cause the diarrhea. The acquired form is of greater consequence because in infants it produces milk intolerance, leading to diarrhea, weight loss, and failure to thrive. Diagnosis is readily made by measurement of breath H+ level, which reflects bacterial overgrowth in the presence of intraluminal carbohydrate.

Front 334

What is the etiology of Abetalipoproteinemia? Describe some of the associated symptoms. What are some characteristic cells associated with this disease that are seen on a smear?

Back 334

Abetalipoproteinemia makes the mucosal epithelial cell unable to export lipid due to a deficiency of Apolopoprotein B. This proteinis required for assembly of dietary lipids into chylomicrons, which are then secreted into intestinal lymphatics. This deficiency causes diarrhea and steatorrhea in infancy and significant failure to thrive. There are systemic lipid membrane abnormalities as well which give rise to Burr cell transformation of erythrocytes can Acanthocytosis.

Front 335

Explain the etiology of Celiac disease. Describe the histological findings you would expect to see in someone with Celiac disease.

Back 335

Celiac disease is caused by an immunological sensitivity to Gliadin, a component of Gluten which is found in wheat. The small intestinal mucosa, when exposed to gluten accumulates intraepithelial CD8+ T cells and large numbers of lamina propria CD4+ T cells that are sensitized to Gliadin. The effect of this immune response can result in total flattening of mucosal villi and thus the LOSS OF SURFACE AREA.

Front 336

What is the frequency of Celiac disease? What portion of the small intestine does it usually affect? What other disease can it put you at risk for?

Back 336

The frequency is thought to be 1:300. It usually affects the proximal, more than the distal small intestines. There is about a two-fold increase in the rate of malignant disease with lymphomas and esp. T-cell lymphomas being disproportionately represented.

Front 337

Which other malabsorption disease does Tropical Sprue resemble? Describe the tissue changes associated. What is thought to be the cause?

Back 337

Tropical sprue resembles Celiac disease in symptomology, but occurs almost exclusively in persons living in or visiting the tropics. In contrast to Celiac disease with Tropical Sprue, injury is seen at all levels of the small intestine as opposed to primarily the proximal portions. An infectious process is strongly implicated in the development of this disease.

Front 338

Malabsorption indicates a disturbance in at least one of which three digestive functions?

Back 338

Intraluminal Digestion, Mucosal Absorption, or Nutrient Delivery.

Front 339

What is the most common presentation of a malabsorption disease? What is the hallmark of the disease?

Back 339

The most common presentation is a chronic diarrhea and the hallmark of malabsorption syndromes is steatorrhea.

Front 340

Describe some of the typical features of malabsorption due to Defective Intraluminal Digestion. Explain some of the etiologies that can produce these features.

Back 340

Typical features of defective intraluminal digestion are an Osmotic Diarrhea from undigested nutrients and Steatorrhea. The most common cause of these symptoms is Pancreatic Insufficiency associated with chronic alcoholism and Crohn Disease, but other causes of Defective Intraluminal Digestion include inadequate solubilization of fat by bile, intestinal bacerial overgrowth, cholestatic liver disease, and intestinal resection surgeries.

Front 341

Describe the etiology of Whipple disease. What is the organsim that causes it? What systems does it affect?

Back 341

Whipple disease is a rare systemic infection that may involve any organ in the body, but primarily affects the intestine, CNS, and joints. The organism is Tropheryma whippelii and the infection generally occurs in males in the fourth to fifth decade of life. Whipple disease causes a malabsorptive syndrome occasionally accompanied by lymphadenopathy, hyperpigmentation, polyarthritis, and CNS complaints.

Front 342

Malabsorption indicates a disturbance in at least one of which three digestive functions?

Back 342

Intraluminal Digestion, Mucosal Absorption, or Nutrient Delivery.

Front 343

What is the most common presentation of a malabsorption disease? What is the hallmark of the disease?

Back 343

The most common presentation is a chronic diarrhea and the hallmark of malabsorption syndromes is steatorrhea.

Front 344

Describe some of the typical features of malabsorption due to Defective Intraluminal Digestion. Explain some of the etiologies that can produce these features.

Back 344

Typical features of defective intraluminal digestion are an Osmotic Diarrhea from undigested nutrients and Steatorrhea. The most common cause of these symptoms is Pancreatic Insufficiency associated with chronic alcoholism and Crohn Disease, but other causes of Defective Intraluminal Digestion include inadequate solubilization of fat by bile, intestinal bacerial overgrowth, cholestatic liver disease, and intestinal resection surgeries.

Front 345

Name some conditions that are examples of malabsorption due to Defective Intraluminal Digestion.

Back 345

Pancreatic insufficiency (pancreatitis, cystic fibrosis), Zollinger-Ellison syndrome, Ileal dysfunction/resection, Cessation of Bile flow

Front 346

Name some conditions that are examples of malabsorption due to Primary mucosal cell abnormalities.

Back 346

Disaccharidase deficiency (lactose intolerance), Bacterial Overgrowth, with damage to the brushborder. Abetalipoporteinemia, Bile acid malabsorption

Front 347

Name some conditions that are examples of malabsorption due to Reduced Surface Area of the small intestine.

Back 347

Celiac Sprue and Crohn's Disease

Front 348

Name some conditions that are examples of malabsorption due to Lymphatic Obstruction.

Back 348

Lymphoma and Tuberculosis.

Front 349

Name some conditions that are examples of malabsorption due to Infection.

Back 349

Acute infectious enteritis, Parasitic infestation, Tropical sprue, Whipple's disease.

Front 350

Name some conditions that are examples of malabsorption due to Iatrogenic causes.

Back 350

Gastrectomy, Short-gut syndrome, Distal ileal bypass/resection

Front 351

What type of organisms generally cause what we call Pyogenic liver abscess? These abscesses usually form on the background of what type of disease? Which age group does this usually happen in?

Back 351

Bacteria. They usually contribute to liver abscess formation on the background of Biliary Disease. Thus, liver abscesses usually form in middle aged persons because this is the same population that has the most common incidence of biliary disease.

Front 352

Which organism specifically is referred to when talking about Amoebic abscesses?

Back 352

E.histolytica

Front 353

What is the most common source of transmission for bacterial liver abscesses?

Back 353

The most common source comes from the Biliary tree. The inciting even is usually Acute Cholecystitis, and it produces multiple abscesses.

Front 354

Do people with pyogenic liver abscesses usually come in displaying many key diagnostic feature?

Back 354

No, only ~50-60% come in with any RUQ pain, they may have a low grade fever, only10-25% may have Jaundice, there may be a mild elevation in AST/ALT, and a mild leukocytosis. Pyogenic liver abcesses may have a chronic or insidious presentation, and the signs and symptoms may be very non-specific without imaging.

Front 355

Name some of the low infectious inocculum pathogen pathogens that cause infectious diarrhea.

Back 355

Shigella, Campylobacter jejuni, C.diff, G.lambia, Cryptosporidium, Rotaviruses

Front 356

What is an indirect method of checking for Fecal leukocytes if you suspect and invasive GI process? What type of patients may give you a false positive?

Back 356

Detecting Fecal lactoferrin. Breast feeding infants may give a false positive.

Front 357

How do you I.D. Shigella and Salmonella from a fecal sample? Which media do you use and what are the characteristic results that you see?

Back 357

You use MacConkey agar and these two bacteria will create colonies that are white because they do not ferment lactose.

Front 358

What are some complications that may be seen with Shigella infection?

Back 358

Ractive arthritis, Reiter's syndrome, rectal prolapse, HUS (hemolytic uremic syndrome)

Front 359

What type of reservoirs usually carry salmonella?

Back 359

Animal reservoirs.

Front 360

Describe two complications of Salmonella infections?

Back 360

Meningitis (almost exclusively in newborns) and Osteomyelitis (classically associated with Sickle Cell Disease).

Front 361

Describe the mode of transmission for Campylobacter jejunii. Who most commonly gets infected? Is this an invasive or non-invasive infection?

Back 361

The mode of transmission for Campylobacter is fecal-oral and is common in children less than 1 year and animal vectors are common such as cats and chickens, esp young animals. Campylobacter produces an invasive infection the invades the mucosa superficially and produces watery diarrhea or dysentery and occasionally bloody stools without diarrhea.

Front 362

Campylobacter infection is associated with non-suppurative complicaitons. Describe some of those complcations.

Back 362

The non-suppurative complications associated with Campylobacter infection are Guillan-Barre Syndrome, Reactive Arthritis, and Erythema Nodosum.

Front 363

Where is the entero-pathogen Yersinia enterocolitica most often found? How is this bug transmitted? Name its most common animal reservoirs.

Back 363

This bacteria is mostly found in colder climates with winter seasonality. Transmission usually occurs through a foodborne mechanism associated with poorly cooked pork products (e.g. Chitterlings- classic example) and unpasteurized milk. Animal reservoirs include rodents, birds, and swine.

Front 364

Describe some of the most common complications of Yersinia enterocolitica infection.

Back 364

Some of the more common complications of Yersiia enterocolitica infection include Bacteremia with Hepatic and Splenic abscess formation esp in the setting of predisposing conditions (e.g. excessive iron storage), Mesenteric adenitis (classic), Pseudoappendicitis, E. nodosum, and E. multiforme.

Front 365

Name some of the signs, symptoms and conditions caused by Yersinia pseudotuberculosis.

Back 365

Fever, Scarletinaform rash, abdominal pain with appendicitis or ileitis, pleural and joint effusions- mimicking Kawasaki syndrome.

Front 366

When attempting to diagnose C.difficile disease what type of test do you use to test the fecal material and what are you detecting?

Back 366

You use an ELISA test that is trying to detect the TOXIN produce by C.difficile.

Front 367

What are the Toxins that C.difficile produces?

Back 367

The two Toxins are C.difficile Toxin A and B.

Front 368

How do you treat C.difficle infection?

Back 368

You treat C.difficile with Metronidazole because it is an Anaerobic organism.

Front 369

What is the only real indication for ORAL Vancomycin?

Back 369

C.difficile gut infection.

Front 370

What kind of diarrhea does C.perfringens produce? What symptoms are uncommon with this that helps you distinguish it from Shigellosis or Salmonellosis? What similar pathogenic mechanism does it share with Staph aureus?

Back 370

C.perfringens produces a watery diarreah. Fever and vomiting are uncommon, which helps distinguish C.perfringens infection from Shigellosis and Salmonellosis. C.perfringens makes a preformed toxin just like Staph aureus hence incubation period before the onset of symptoms is usually rapid.

Front 371

What is the only protozoan known to ingest RBCs?

Back 371

Entamoeba histolytica.

Front 372

Describe the main reservoir for Entamoeba histolytica. What is the spectrum of disease that it causes? How is this bug transmitted? If one gets liver abscessed with this infection are they more likely to be male or female?

Back 372

The main reservoir for Entamoeba histolitica is Humans and the spectrum of disease that it causes ranges from asymptomatic to acute colitis to liver abscesses. This bug is transmitted via fecal-oral transmission and is most sever at extremes of age and in pregnancy. Liver abscesses occur 90% in males.

Front 373

What are some organisms that are responsible for the production of Secretory Diarrhea?

Back 373

V.cholerae (cholera toxin), ETEC (Labile and Stable Toxin), Rotavirus.

Front 374

Explain the mechanism that leads to the production of infectious Secretory Diarrhea.

Back 374

Secretory diarrhea is most often produced by enterotoxins that stimulate active secretion of Na+ and Cl- into the intestinal lumen, resulting in water loss into the gut to balance the osmotic load.

Front 375

Explain the mechanism that leads to the production of infectious Osmotic Diarrhea.

Back 375

Osmotic diarrhea is most often produced by organisms that damage the brush border mictovilli, resulting in focal loss of disaccharidases and carbohydrate malabsorption.

Front 376

What are the two most common organisms causing Dysentery?

Back 376

Campylobacter and Shigella

Front 377

What are two organisms associated with infection of the GI tract that can lead to sever submucosal inflammation and cause Rectal Prolapse?

Back 377

Shigella and Whipworm

Front 378

What are the main problems associated with stool culture?

Back 378

Separation of pathogens from normal flora, Time factor, Limited number of pathogens are easily detectable, Requires a extra equipment that most labs may not have, Delay in plating of specimens

Front 379

What are the two medications that are used in most instances of infections with invasive pathogen that cause diarrhea?

Back 379

Ciprofloxacin and Metronidazole.

Front 380

Why is Glucose such an important molecule in Oral Rehydration Therapy?

Back 380

It is important because it is required for co-transport of the Na+ into the cell.

Front 381

What percent infection by Entamoeba histolitica actually results in Amebic Liver Abscess? What is the classical description of what the abscesses look like? Are the purulent? Where are the amoebas found in the abscess?

Back 381

~1%. The classical description is of the non-purulent abscess filled with cellular debris that looks like anchovy paste. Here the parasites are found only in the periphery of the abscess chewing their way out.

Front 382

Is there presence of Eosinophilia with amoebic abscess?

Back 382

No, eosinophilia is typically absent.

Front 383

What is the medication of choice in treating Amoebic abscess in the liver?

Back 383

Metronidazole

Front 384

Describe some common abscess-like liver lesions that can get confused for actual liver abscesses.

Back 384

Adenoma or other malignancy, Hydatid cyst, Tuberculous abscess, Liver flukes

Front 385

What are Fascioloa hepatica and what type of problems do they cause? Describe the type of immune response they elicit.

Back 385

These are liver flukes (worms) that migrate through the abdominal cavity and liver. They cause Febrile Fasciolitic Eosinophilic Syndrome, which consists of tender hepatomegaly, fever, and eosinophilia. If the worms invade the biliary tract they can cause biliary obstruction.

Front 386

Describe the predisposing conditions that have the potential to lead to Acalculous cholecystitis. How do they do this?

Back 386

Trauma, burns, sepsis, HIV infection, immunosuppression, diabetes, nonbiliary surgery, and childbirth. Some of these conditions predispose to ischemia in the gallbladder wall or stasis of bile (or both) resulting in concentration of bile salts and leading to inflammation and necrosis of the gallbladder wall.

Front 387

Where does Cholangitis specifically refer to having inflammation?

Back 387

Cholangitis refers to inflammation or infection of the common bile duct.

Front 388

What are the typical enteric pathogens that cause biliary tract disease?

Back 388

E.coli, Klebsiella, Enterobacter

Front 389

What are the anaerobic organisms that can be recovered from a patient with biliary tract disease?

Back 389

Bacteroides, Fusobacterium, and Clostridia.

Front 390

Which organ gives a positive Murphy's sign?

Back 390

The Gallbladder.

Front 391

What techniques do you use to diagnose inflammatory diseases of the Gallbladder?

Back 391

Ultrasound, HIDA scan, ERCP (for cholangitis), CT (less sensitive/specific), MRI (may have use)

Front 392

What is AIDs cholangiopathy and what are its etiologies? How is this diagnosed?

Back 392

This is stenosis of the distal common bile duct and irregularities of the intrahepatic and extrahepatic bile ducts. The causes can include Cryptosporidium, Microsporidium, CMV, Mycobacterium avium, Direct HIV infection, and drugs. ERCP is used for diagnosis.

Front 393

What is Hepatic Schistosomiasis? Describe the main complications and pathogenesis of Hepatic Schistosomiasis.

Back 393

Hepatic Schistosomiasis is caused by infection of the liver with S.mansoni, or S.japonicum. Although liver function is spared, these cause liver disease by causing periportal fibrosis and disease due to portal hypertension. From the portal hypertension, ruptured esophageal varices is the most common cause of death.

Front 394

What organisms are most commonly responsible for causing spontaneous bacterial peritonitis?

Back 394

E.coli, Klebsiella, and Enterobacteriaceae

Front 395

What class of drugs are the 1st drugs of choice when treating Spontaneous Bacterial Peritonitis?

Back 395

Third generation cephalosporiins are the drugs of first choice. Cefotaxime and Ceftriaxone are very effective in managing SBP.

Front 396

What type of foods is Yersinia eneterolitica usually found in? Where can infection commonly spread to?

Back 396

It is most often found in contaminated milk or pork products. After infection of the gut it may disseminate to produce lymphadenitis and further extraintestinal infection.

Front 397

What type of stain is used to visualiize H.pylori?

Back 397

Silver stain.

Front 398

Name some gastric disorders that H.pylori is associated with.

Back 398

Chronic gastritis with erythema and thickened rugal folds, peptic ulcers, adenocarcinoma.

Front 399

What is Vacuolating cytotoxin and which organism produces it?

Back 399

Vacuolating cytotoxin (VacA) is one of several toxic substances produced by H.pylori and its expression is controlled by another gene encoding cytotoxin-associated antigen (CagA).

Front 400

What organism that invades the GI tract is responsible for producing Cysteine proteinases?

Back 400

Entamoebo hystolytica.

Front 401

Which strain of E.coli is responsible for producing Heat Stable (ST) and Heat Labile (LT) toxin? What type of diarrhea does it cause?

Back 401

ETEC- causes watery (traveler's diarrhea)

Front 402

Which form of E.coli produces Verocytotoxin? What other syndrome is this strain associated with?

Back 402

EHEC-(O157:H7); produces bloody diarrhea and Hemolytic Uremic Syndrome (HUS).

Front 403

Can invasive infections that cause bloody diarrhea cause watery diarrhea too?

Back 403

Yes, even the invasive causes of infectious diarrhea typically begin with a mild, watery diarrhea - i.e. you don’t necessarily have fever and bloody diarrhea right off the bat.

Front 404

What is the most common cause of Traveler's Diarrhea is the duration of stay is short (a couple of days)?

Back 404

Staph, B.cereus, C.perfringens, ETEC

Front 405

What is the most common cause of Traveler's Diarrhea is the duration of stay is extended (days-weeks)?

Back 405

Salmonella, Giardia, Amoeba, Cyclospora, Cryptosporidium, Tropical Sprue, Brainerd

Front 406

What is the most common cause of Traveler's Diarrhea is the duration of stay is longer (more than a couple of days)?

Back 406

ETEC, Campylobacter, Salmonella, Vibrio spp.

Front 407

What does Listeria Gram stain? What type of hemolysis does it produce? What kind of motility does it display?

Back 407

Listeria is a Gram positive rod (may be Gram variable) that produces Beta hemolysis and exhibits a "tumbling" motility.

Front 408

How does infection occur?

Back 408

It is felt that infection usually occurs after ingestion of contaminated foods such as raw meats, vegetables, soft cheeses, deli meats, and deli foods.

Front 409

What tropisms does Listeria more commonly have? What is a virulence factor that it produces that allows it to escape macrophage phagolysosomes?

Back 409

Its is usually Neurotropic and placenta-tropic. It produces Listeriolysin O which allows it to escape macrophage killing.

Front 410

The unexpected isolation of diptheroids from blood or CSF cultures should alert you to the possibility of what uncommon infection?

Back 410

Listeria infection.

Front 411

Describe the 3 forms of CNS Listeriosis that are seen.

Back 411

1) Meningitis (most common form for Listeria, and most lethal of all meningitis)
2) Cerebritis
3) Abscess

Front 412

Can invasive infections that cause bloody diarrhea cause watery diarrhea too?

Back 412

Yes, even the invasive causes of infectious diarrhea typically begin with a mild, watery diarrhea - i.e. you don’t necessarily have fever and bloody diarrhea right off the bat.

Front 413

What is the most common cause of Traveler's Diarrhea is the duration of stay is short (a couple of days)?

Back 413

Staph, B.cereus, C.perfringens, ETEC

Front 414

What is the most common cause of Traveler's Diarrhea is the duration of stay is extended (days-weeks)?

Back 414

Salmonella, Giardia, Amoeba, Cyclospora, Cryptosporidium, Tropical Sprue, Brainerd

Front 415

What is the most common cause of Traveler's Diarrhea is the duration of stay is longer (more than a couple of days)?

Back 415

ETEC, Campylobacter, Salmonella, Vibrio spp.

Front 416

What does Listeria Gram stain? What type of hemolysis does it produce? What kind of motility does it display?

Back 416

Listeria is a Gram positive rod (may be Gram variable) that produces Beta hemolysis and exhibits a "tumbling" motility.

Front 417

How does infection occur?

Back 417

It is felt that infection usually occurs after ingestion of contaminated foods such as raw meats, vegetables, soft cheeses, deli meats, and deli foods.

Front 418

What tropisms does Listeria more commonly have? What is a virulence factor that it produces that allows it to escape macrophage phagolysosomes?

Back 418

Its is usually Neurotropic and placenta-tropic. It produces Listeriolysin O which allows it to escape macrophage killing.

Front 419

The unexpected isolation of diptheroids from blood or CSF cultures should alert you to the possibility of what uncommon infection?

Back 419

Listeria infection.

Front 420

Describe the 3 forms of CNS Listeriosis that are seen.

Back 420

1) Meningitis (most common form for Listeria, and most lethal of all meningitis)
2) Cerebritis
3) Abscess

Front 421

When you think of Actinomycosis what processes and features do you think of?

Back 421

Sulfur granules, Gram + filamentous organism that creates inflammatory masses with draining sinuses; it is involved in cervicofacial, abdominal, pelvic, or thoracic processes

Front 422

How is staging of the tumors of the GI tract made?

Back 422

It is determined by which layers of the GI wall have been invaded.

Front 423

What are the two most common tumors of the Esophagus?

Back 423

Squamous cell carcinoma and Adenocarcinoma

Front 424

What is the morphology of the majority of esophageal carcinomas?

Back 424

Polypoid exophytic

Front 425

Who get esophageal cancer more, men or women? What is the average age of onset?

Back 425

Men. The average age of onset is about 45yrs.

Front 426

Where do Squamous cell carcinomas and Adenocarcinomas occur in the esophagus respectively?

Back 426

Squamous cell carcinomas tend to occur in the upper 2/3 of the esophagus. The Adenocarcinoma tends to occur in the lower 1/3.

Front 427

Name the most common sites of metastasis for Esophageal Carcinoma.

Back 427

Liver and lung.

Front 428

What disease has a strong causal relation to Esophageal adenocarcinoma? What condition is considered to be a prelesion?

Back 428

GERD; Barret's esophagus

Front 429

What is the single most important prognosticator in Esophageal carcinoma? What two features determine the staging?

Back 429

Staging of the cancer is the single most important factor. Staging is determined based on the depth of invasion into the GI wall and the nodal and distant metastases involved.

Front 430

What is the most common Esophageal tumor world wide?

Back 430

Squamous cell carcinoma.

Front 431

What are some of the Bengin Neoplasms found in the esophagus?

Back 431

Leiomyomas, squamous papillomas, fibrovascualr polyps, fibroma, lipomas, hemangiomas, inflammatory pseudotumors

Front 432

What are the two biggest risk factors associated with Squamous cell carcinoma of the esophagus? What is the prognosis in the U.S.?

Back 432

Smoking and alcohol. The prognosis in the U.S. is not good.

Front 433

What disorder of the Lower Esophageal Sphincter increases ones chance for Squamous cell carcinoma?

Back 433

Achalasia

Front 434

What is the most common malignant tumor of the stomach?

Back 434

Carcinoma

Front 435

What are the #1 and #2 location for Adenocarcinoma in the stomach?

Back 435

1) Antrum and Pylorus

2) Lesser Curvature

Front 436

What are the two types of Gastric Adenocarcinoma?

Back 436

Intestinal type and Diffuse types

Front 437

Compare the Intestinal Type vs. the Diffuse Type of Gastric Adenocarcinoma.

Back 437

Intestinal- older patients, associated atrophic chronic gastritis (H.pylori) and intestinal metaplasia, more common in men, expansile growth

Diffuse- younger patients, poorly differentiated to Signet ring cell, infiltrative growth

Front 438

Is it common to find malignant tumors in the Small Intestine? If there are tumors, what type could arise?

Back 438

No, this is rare. Adenocarcinomas, carcinoids, lymphomas, sarcomas

Front 439

What type of benign neoplasms do we find in the Small Intestine?

Back 439

Adenomas and leiomyomas.

Front 440

What is the a main difference in the morphology of the tumors found in the Right colon vs. the Left colon?

Back 440

Tumors of the Right colon tend to be more polypoid fungating masses, whereas the tumors of the Left colon tend to be more annular, 'napkin ring' lesions.

Front 441

What is the main theory behind how an adenoma becomes a Carcinoma?

Back 441

The multi-hit theory.

Front 442

What is the definition of Irritable Bowel Syndrome?

Back 442

IBS is a chronic, episodic medical condition characterized by abdominal pain or discomfort associated with alterations in bowel function.

Front 443

Is IBS more prevalent in males ore females?

Back 443

Females

Front 444

A prolonged (what) is seen in IBS?

Back 444

A prolonged gastro-colic refelx.

Front 445

IBS is thought to be partially due to a defect in what? A hypersensitivity to what, is also thought to play a role?

Back 445

A defect in gastric motility; a hypersensitivity to pain in the gut.

Front 446

What is a particular neurotransmitter that increases motility and sensitivity of the gut?

Back 446

Serotonin.

Front 447

Where is serotonin most found in the body and what type of cells release it there?

Back 447

95% of the serotonin in the body is found in the gut and it is released by enterochromaffin cells.

Front 448

What is Acute Abdomen?

Back 448

Acute abdomen is any sudden spontaneous disorder where the main manifestation is in the abdominal area for which urgent or emergent operation may be required. This is frequently characterized by a progressive underlying pathologic disorder where undue delay in Dx and treatment affects outcome in an adverse manner.

Front 449

What type of nerve fibers are the hollow viscus and capsules of solid organs primarily innervated by? What elicits pain in these fibers?

Back 449

These tissues are primarily innervated by afferent C fibers of the sympathetic and parasympathetic nervous system. Pain is most often elicited by distension, deep seated contraction, inflammation, or ischemia.

Front 450

Poorly localized tenderness without guarding in the abdomen is usually indicative of a surgical or non-surgical problem?

Back 450

Non-surgical.

Front 451

What is Murphy's sign?

Back 451

A distended gallbladder.

Front 452

About how long after birth should a baby have passed their first stool?

Back 452

98% of babies have passed their first stool at 48 hours.

Front 453

If a baby has not passed its first stool within 48hrs of birth what disease processes might you consider?

Back 453

Hirschsprung's disease or Cystic Fibrosis.

Front 454

Explain what Meconium Aspiration Syndrome is and what causes it.

Back 454

Meconium Aspiration Syndrome is when meconium is expelled early into the amniotic fluid and the baby swallows it. This happens when the baby is hypoxic.

Front 455

What congenital chromosomal disorder is Hirschsprung's associated with?

Back 455

Trisomy 21

Front 456

What two GI abnormalities are associated with Trisomy 21?

Back 456

Duodenal atresia and Hirschsprung's disease

Front 457

Necrotizing Enterocolitis (NEC) is a disease that is seen in premature babies due to what? Is it more common no the right side or the left side?

Back 457

The problem is related to ischemia due to immature nervous systems. NEC is more common on the right side.

Front 458

What part of the small intestine does the D-xylose absorption test, test the function?

Back 458

This tests for Jejunal function.

Front 459

What test is for evaluating the function of the Terminal Illeum? What vitamin does it test for?

Back 459

The Schilling test. It tests for B12 absorption.

Front 460

What diseases are common causes of fat malabsorption?

Back 460

Pancreatic or Biliary tract diseases.

Front 461

Homozygous loss of which genes can give rise to Right colon and Endometrial cancer? What do these genes code for?

Back 461

hMSH2 or hMLH1. These genes code for DNA mismatch repair genes.

Front 462

Which gene pathway is associated Familial Adenomatous Polyposis Syndrome?

Back 462

The APC-Beta-Catenin Pathway

Front 463

What is the association of duodenal ulcers with H.pylori? Is H.pylori found in the duodenum?

Back 463

Virtually all duodenal ulcers are associated with H.pylori. H.pylori is not found in the duodenum, but in the antrum and pylorus of the stomach.

Front 464

Fibrosis with stenosis of the esophagus is a component of what two diseases?

Back 464

GERD and Scleroderma

Front 465

What are the most likely infections involving the esophagus in AIDS patients?

Back 465

Herpes simplex and Candida.

Front 466

What type of gastric adenocarcinoma does Linitis Plastica occur in? What is the morphology of the cells?

Back 466

This occurs in Diffuse adenocarcinoma of the stomach. The cells look like signet ring cells.

Front 467

What are two possible complications associated with Meckel diverticulum?

Back 467

Etopic Gastric and Ectopic Pancreatic tissue.

Front 468

In Achalasia which nerve plexus is usually absent from the body of the esophagus? Risk of which cancer is associated with long-term Achalasia?

Back 468

The myenteric plexus is usually abscent. There is an increased risk of Squamous cell carcinoma

Front 469

Reflux esophagitis is associated with what type of hernia?

Back 469

Hiatal hernia.

Front 470

What is the most common cause of Ischemic Colitis?

Back 470

Sever atherosclerotic disease involving the mesenteric vessels.

Front 471

Is Necrotizing Enterocolitis associated with full term or premature infants? What does is result from?

Back 471

Premature infants. It is believed to result from the immaturity of the immune system of the gut and is often precipitated by oral feeding. The necrotic bowel can perforate and lead to sepsis, or shock.

Front 472

What vesicular dermatologic lesion is associated with Celiac Sprue?

Back 472

Dermatitis herpatiformis.

Front 473

Meckel's diverticulum is an embryological reminant of what duct? What complication of this condition can lead to intestinal ulceration?

Back 473

The Omphalomesenteric duct. Ectopic gastric tissue associated with Meckel diverticulum can lead to intestinal ulceration.

Front 474

What age patient population are Angiodisplasias most commonly seen in?

Back 474

Older populations, usually over 70.

Front 475

What is the genetic mutation linked with Crohn disease?

Back 475

NOD2

Front 476

If you see mucocutaneous pigmentation associated with poylps, what do you think?

Back 476

Puetz-Jehgers polyps.

Front 477

What is the most common organism cultured in Spontaneous Bacterial Peritonitis.

Back 477

E.coli

Front 478

What extraintestinal conditions is Ulceratvie Colitis associated with? what are the immune cells most responsible for causing damage? Autooantibodies against what molecule are present (although they do not play a role in pathogenesis)?

Back 478

Polyarthritis, ankylosing spondylitis, and sclerosing colangitis. CD4+ T-cells present in the lesion secrete damaging substances. Anti-tropomyosin antibodies.

Front 479

Mutations in the NOD2 gene are linked to what disease?

Back 479

Crohn disease

Front 480

What are stress ulcers due to severe burn injury called? Describe the morphology of these ulcers.

Back 480

Curling ulcers. These ulcers are small (<1cm) and shallow never penetrating the muscularis propria, but they can bleed profusely. Similar lesions occur after traumatic or surgical injury to the nervous system.

Front 481

Hypoperfusion and hypotension associated with congestive heart failure can cause what acute bowel problem?

Back 481

Ischemic colitis.

Front 482

What are some microscopic findings that you might find in a patient with Crohn disease?

Back 482

Microscopic examination would reveal ulcerated areas with patchy acute and chronic inflammatory infiltrate, crypt abscesses, and noncaseating granulomas.

Front 483

What is Toxic Megacolon associated with?

Back 483

Toxic Megacolon is a rare condition that is associated with inflammatory bowel disease.

Front 484

What are three GI cancers that are associated with AIDS patients?

Back 484

Kaposi's sarcoma (can occur anywhere), Non-Hodgkin lymphoma (can occur anywhere), Anorectal Squamous cell carcinoma.

Front 485

What are the three most common causes of acute bowel obstruction?

Back 485

Adhesions, hernias, and metastases.

Front 486

What is the most common congenital disorder of the oral cavity?

Back 486

Cleft lip.

Front 487

What are two pre-AIDS defining lesions that occur in the mouth? Describe what causes them.

Back 487

Oral Hairy Leukaplakia (EBV), Oral Thrush (Candida)

Front 488

Melanin pigmentation in the oral cavity most commonly occurs from what?

Back 488

Addison's disease or Puetz Jeghers syndrome

Front 489

What is the most common benign tumor in the oral cavity?

Back 489

Squamous papilloma

Front 490

What is the most common site of squamous cell carcinoma in the mouth?

Back 490

The Lower lip

Front 491

What is the most common site of basal cell carcinoma in the oral cavity?

Back 491

The Upper Lip

Front 492

What is the most common tumor of the major and minor salivary glands?

Back 492

Pleomorphic adenoma

Front 493

What salivary gland tumor is due to heterotopic salivary gland tissue trapped in a lymph node?

Back 493

Warthin's tumor.

Front 494

What is the most common malignant salivary gland tumor?

Back 494

Mucoepidermoid carcinoma.

Front 495

What is VATER syndrome and what are the clinical finding that make it up?

Back 495

A package of congenital anomalies. Vertebral abnormalities, Anal atresia, TE fistula, Renal disease and absent radius.

Front 496

What is the most common type of Hiatal Hernia?

Back 496

The sliding type.

Front 497

Describe the most common cause of death associated with cirrhosis.

Back 497

Esophageal varicies.

Front 498

Describe Boerhavve's syndrome. What is the most common cause?

Back 498

Boerhavve's syndrome is a rupture of the distal esophagus. The most common cause is endoscopy.

Front 499

Name the most common benign tumor of the Esophagus.

Back 499

Leiomyoma.

Front 500

Describe the most common cause of hematemesis and melena.

Back 500

Peptic Ulcer Disease.

Front 501

When does congenital pyloric stenosis take place? Is it present from birth?

Back 501

Congenital pyloric stenosis is not present from birth, but occurs over the ensuing 2-4 weeks.

Front 502

Describe the most common complications of Chronic atrophic gastritis of the body and fundus.

Back 502

Achlorydria due to loss of negative feedback), Macrocytic anemia due to vitamin B12 deficiency, Increased risk of adenocarcinoma

Front 503

What is the most common cause of atrophic gastritis of the pylorus and antrum?

Back 503

H.pylori

Front 504

What are the two diseases most commonly associated with H.pylori? How is it transmitted?

Back 504

Chronic gastritis and PUD. It is transmitted via the fecal oral route.

Front 505

Describe the diseases associated with H.pylori.

Back 505

Duodenal and gastric ulcers, Type B antal chronic gastritis, Gastric Carcinoma, Low-grade B-cell malignant lymphoma

Front 506

What morphologic and clinical features are associated with Menetrier's disease?

Back 506

Giant rugal folds due to hyperplasia of mucus secreting cells, hypoproteinemia (protein-losing enteropathy), atrophy of parietal cells (achlorydria), increased risk for adenocarcinoma.

Front 507

Which three types of malabsorption can give you anemia?

Back 507

Iron, Folate and B12 malabsorption.

Front 508

What is hematochezia and what are the conditions most associated with it?

Back 508

Hematochezia is massive loss of whole blood per rectum. The most common causes of this are sigmoid diverticulosis or angiodysplasia.