Gi Flash Cards

Front 1

What is danger of long standing GERD?

Back 1

epithelium of distal ESO may undergo metaplastic change to a columnar epithelium initially resembling gastric cardia mucosa and then intestinal mucosa with goblet cells (intestinal metaplasia) known as Barrett ESO

Front 2

What % pts w/ Barreett Esophagus develop invasive adenocarcinoma?

Back 2

10%

Front 3

What % pts w/ initestinal metaplasia in cardia of stomach develop carcinoma?

Back 3

None, normal rate

Front 4

What are the m.c agents of infectious esophagitis?

Back 4

Candida, herpes simplex, and cytomegalovirus are common agents.

Front 5

What does viral agents do different than bacterial agents for infectious esophagitis?

Back 5

Viruses tend to cause small elevated lesions of mucosal surface with central ulcerations that are painful and may produce significant bleeding.

Front 6

What are predisposing factors for chronic esophagitis?

Back 6

reflux, uremia, alcohol abuse, smoking. Most are idiopathic.

Front 7

Who tends to get esophageal malignancy? Problem w/ dx?

Back 7

Tends to arise in men older than 50. There is insidence onset that leads to delay in dx. There is gradual onset of weight loss and malnutrition.

Front 8

What is m.c. type of esophageal malignancy?

Back 8

SCC, it arises in mid-ESO, and m.c. in blacks. Predisposing factors include chronic EtOH and tobacco use and function abnormalities of ESO

Front 9

What are gross presentations of esophageal malignancy?

Back 9

Presents as either a polypoid fungating mass protruding into lumen (60%), a necrotic ulcerative lesion that may erode through the esophageal wall and into surrounding structures (25%), or a diffuse infiltration into the wall causing rigidity and lumenal narrowing (15%).

Front 10

Where does esophageal malignancy spread to?

Back 10

Metastatases to liver, lung, and bone

Front 11

Who gets adenocarcinoma of esophagus?

Back 11

20% of total, m.c. in whites and mainly men.

Front 12

Where does adenocarcinoma arise and from what?

Back 12

arise from submucosal mucous glands or a preexisting Barrett ESO, they are more frequently seen in distal ESO.

Front 13

Describe process of normal swallowing.

Back 13

palate protects nasopharynx, relaxation of UES, glottis closes airway, beginning of pharyngeal peristalsis

Front 14

Describe pressure of following: UES, intraesophageal, LES, and Intragastric

Back 14

UES = 100 mmHg; Intraesophageal = -5 mmHg; LES = 20 mmHg; Intrgastric = +5 mmHg

Front 15

What initiates primary and secondary peristalsis of esophagus?

Back 15

Primary is swallowing and if there is incomplete clearence or reflux then secondary occurs.

Front 16

What hormones affect LES?

Back 16

Gastrin, motillin, progesterone, and estrogen

Front 17

What agents can be used to increase LES?

Back 17

Cholinergic agonist, anticholinesterase (Endrophonium), Metaclopramide, Domperidone, and Cisapride

Front 18

What agents are known to decrease LES?

Back 18

Progesterone, Estrogen, Anticholinergics, foods (fatty foods, peppermint, smoking, chocolate, and EtOH), and drugs (Ca++ blockers, nitrates, and anti-anginal agents).

Front 19

When is oropharyngeal seen and what can result?

Back 19

Oropharyngeal seen w/ strokes, CN illness (polio), MG, dermatomyositis, obstruction to flow may result in Zenker diverticulum.

Front 20

How does myasthenia Gravis affect the esophagus? Tx?

Back 20

Causes weak pharyngeal muscles including UES. Causes aspiration and poor bolus transportation. Tx w/ endrophonium to increase ACh.

Front 21

What disease does the UES become non-comopliant?

Back 21

Sarcoidosis

Front 22

How does scleroderma affect esophagus?

Back 22

More the distal esophagus and LES affected. So muscles can't accommodate bolus. Prone to GERD

Front 23

What esophageal dysfunction has normal peristalsis?

Back 23

Nutcracker but it is very hypertensive and long duration. Abnormally appears to be in afferent limb.

Front 24

What is source for hydrochloric acid?

Back 24

Parietal Cells

Front 25

What is source for pepsin?

Back 25

Chief Cell secretes pepsinogen which is cleaved by trypsin

Front 26

What stims gastrin production?

Back 26

ACh (vagal stimulation), gastrin (antral pyloric glands due to local stim and vagal stim), and histamine (H2 receptors).

Front 27

What is the protection mech of epithelium in stomach?

Back 27

The presence of mucosal barrier formed by tight junctions and surface insoluble mucus and epi cells secrete HCO3 and PG

Front 28

Give order of layers in intestine

Back 28

L. propria-> thin muscularis mucosa -> submucosa (vessels, nerves, lymphatics) -> thick muscularis propria -> serosa and subserosal

Front 29

How does esophagus differ in its layers?

Back 29

ESO does not have a true serosal surface but is instead in direct continuity with the surrounding thoracic viscera.

Front 30

Describe the histo of the colon

Back 30

colonic crypts that serve to absorb water. It has a more flattened luminal surface.

Front 31

Describe the histo of the small intestine

Back 31

villous projections, which serve to increase absorptive area. Villi varies according to area of small bowel. Longest in jejunem then ileum.

Front 32

What is the m.c. developmen disorder of esophagus, its associations, and signs?

Back 32

Esophageal Atresia. A/w/ vertebral defects, cardio malformations, or other GI abnormal. Maternal polyhydramnios is early clue. After birth kid will exhibit excessive drooling and will regurgitate after feeding. Gaseous distension of stomach and pneumonia also occur.

Front 33

At what location does esophageal atresia most often occur?

Back 33

near tracheal bifurcation

Front 34

Describe esophageal webs

Back 34

Redundant mucosal folds that occur in upper ESO of middle-aged or elderly women

Front 35

What are signs of Plummer-Vinson?

Back 35

severe Fe def anemia and atrophic glossitis occuring w/ esophageal webs

Front 36

Describe esophageal rings (location, who, a/w/, represent)

Back 36

in lower ESO at squamocolumnar junction (Schatzki rings), and may become symptomatic in young adults. A/w/ hiatal hernias and represent hypertrophied SM and fibrous tissue.

Front 37

What is the m.c. collagen vascular disease to affect esophagus? Consequences?

Back 37

Scleroderma, where distal end is replaced by fibrous tissue. There is loss of peristalsis and chronic reflux of gastric secretions which may cause stenosis.

Front 38

The functional obstruction of distal esophagus is what? Consequences?

Back 38

Achalasia is failure of LES to relax. Seen in young adults. Leads to increase intralumenal pressures, and progressive esophageal dilation.

Front 39

What are clinical signs of achalasia?

Back 39

progressive dysphagia, eventual regurg of food, and sometimes pneumonia. This chronic inflammation can lead to esophageal carcinoma.

Front 40

Describe pulsion diverticulum

Back 40

abnormal outpouches of esophageal mucosa and submucosa through weak areas in the muscle wall related to ↑ intralumenal pressures

Front 41

Describe traction diverticulum

Back 41

eversions of all layers resulting from healing of inflammatory processes external to ESO . Usually occur at or below tracheal bifurcation and are often a/w/ tuberculous scarring of hilar LN.

Front 42

What is the m.c. Pulsion diverticulum? Location? Signs?

Back 42

Zenker diverticulum develops on posterior wall of ESO prox to the cricopharyngeal muscle. Due to ↑ peristalsis needed to push food through an incompletely relaxed UES. Symptoms are bad breath and lump in throat. Less commonly, pulsion diverticula develops proximal to LES.

Front 43

What type of hiatal hernia is accentuated by swallowing?

Back 43

SLIDING HERNIA (80-90%) - from a scarred or congenitally shortened ESO pulls cardia of stomach upward. Pts most likely to develop GERD.

Front 44

What type of hiatal hernia is accentuated by increase intraabdominal pressure? Danger?

Back 44

PARAESOPHAGEAL (ROLLING) HERNIA (10-20%) - A defect in the esophageal hiatus allows a portion of stomach to protrude and lie alongside ESO to form an intrathoracic sac which may become strangled and infarcted.

Front 45

What changes about blood flow in esophageal varices?

Back 45

Portal HTN diverts normal portal venous flow into azygous system via left gastric veins and esophageal veins.

Front 46

What is signs of esophageal varies?

Back 46

asymptomatic until rupture occurs with ensuing hematemesis (frequently massive). 50% Mortality

Front 47

Describe Mallory-Weiss Syndrome

Back 47

Linear, longitudinal lacerations of the mucosa and submucosa occurring along the lesser curvature of the proximal gastric cardia or distal ESO.

Front 48

Who tends to get Mallory-Weiss syndrome? Pgx?

Back 48

Most frequently seen in chronic alcoholics. Commonly seen after prolonged vomiting. Has a much better pgx than ruptured varices, and there is less of a tendency for recurrence.

Front 49

What is esophagitis main sign?

Back 49

odynophagia

Front 50

Describe histo changes of GERD.

Back 50

o Intraepithelial inflammatory infiltrates (eosinophils +/- neutrophils), basal zone hyperplasia, and extensions of lamina propria into the higher layer of the epidermis closer to the lumen are characteristic.

Front 51

What are some potential irriants of Esophagus?

Back 51

acid, pepsin, and bile salts are potential irritants. OJ, coffee, and tomato juice can cause too.

Front 52

What is essential to clearence of stomach acid?

Back 52

Must have contractions and salivary HCO3.

Front 53

What is tx for GERD?

Back 53

H2 blockers and PPI (omeprazole)

Front 54

The embryonic foregut develops into what? And their function?

Back 54

esophagus, stomach, and proximal duodenum. Performs gross digestion.

Front 55

The embryonic hindgut develops into what? And their function?

Back 55

lower GI and performs water and electrolyte reclamation activites. Acts as a storage vessel.

Front 56

What is the myenteric plexus located in layers?

Back 56

between inner circular and outer longitudinal layers of muscularis propria

Front 57

What is responsible for the myoelectric activity of intestines?

Back 57

interstitial cells of Cajal, which are the origin of slow waves, which are the basic myo-electrical rhythm of the stomach and small bowel activity

Front 58

What causes peristalsis in intestines?

Back 58

Myogenic slow waves are rhythmic oscillations in membrane potential of myocytes. These waves don’t produce muscular contractions by themselves, only when ENS causes full depolarization does the electric rhythm produce spikes that sit on top of slow waves. Slow waves just set the stage for peristalsis

Front 59

What is MMC function, duration, and onset time?

Back 59

3-4 hours after meal, GI wants to sweep out any leftover indigestible stuff and prevent bacterial overgrowth, so it goes into an MMC pattern. MMC last about 1.5-2 hrs

Front 60

Describe different phases of MMC?

Back 60

"Phase I – last 45-60 mins, almost no contractile activity, only slow waves present, no spikes; Phase II – for 30-45 mins, up to ½ of slow waves are a/w/ depolarization and contractions are created; Phase III – at end of 1.5 hrs, there is short period of intense contraction, that is a/w/ spikes. This is the real MMC activity that actually sweeps everything out.

Front 61

What does the fed state look like?

Back 61

Just like the phase II of fasting state

Front 62

What is the main function of the fundus of stomach?

Back 62

Acts as storage reservoir and it needs to be able to accommodate varying volumes of liquids and solids, and also needs to keep the prep chamber of distal stomach primed by maintaining slight pressure.

Front 63

What causes loss of compliance of fundus?

Back 63

Vagotomy or proximal gastric resection causes a loss of receptive relaxation

Front 64

What is the main function of the antrum of stomach?

Back 64

the prep chamber, it beats up the food into pulp and knocks down into nice digestion particles

Front 65

What happens to food particles that will don't break down, are they left?

Back 65

Indigestibles cannot be broken down by prep chamber are left in stomach until MMC comes along after 4 hrs and cleans them out

Front 66

What are the pace maker cells of the stomach located and their rate?

Back 66

Slow waves are regulated by pacemaker cells located high up on the gastric body, generated by ENS, they generate 3 waves/min activity

Front 67

What stim contractions in stomach and what suppresses contractions?

Back 67

ACh lower the threshold and promotes contraction. NE suppresses contractions.

Front 68

What is the limiting factor for rate of stomach emptying?

Back 68

Size of particles

Front 69

If vagometry is performed, what changes?

Back 69

If vagometry is performed, phasae III of MMC will not happen, and the indigestible left after 3-4 hr fed state will not be moved

Front 70

Which empties quicker: small or large volume of fluids?

Back 70

Large volumes, due to gastric distention

Front 71

Which empties quicker: hypo, iso, or hyperosmotic fluids?

Back 71

Isotonic, other must undergo some work

Front 72

What is constant in delivery to duodenum?

Back 72

Calorie delivery rate at 10Kcal/5 min

Front 73

What are some causes of failure of driving force w/ normal slow waves?

Back 73

Decreased electromechanical coupling, muscle loss, ENS damage, and loss of entrinsic innervations usually due to vagotomy

Front 74

What can cause decreased electromechanical coupling?

Back 74

Anticholinergics, vagometry, or catecholamines

Front 75

What is tx for ENS damage?

Back 75

Bethanecol

Front 76

What causes obstruction of flow at pyloris?

Back 76

Peptic ulcer (m.c.), hypertrophic pyloric stenosis, or diabetic pylorospasm

Front 77

What causes increase pyloric competence?

Back 77

CCK, secretin, and intra-duodenal HCl. Some gastric ulcer pts seem to have pyloric sphincters that are less competent and less responsive to these hormones than normals.

Front 78

What is the only prokinetic drug available for use?

Back 78

Metaclopramide, causes ACh release that stims M2

Front 79

What is the main cause of cirrhosis of liver?

Back 79

Viral hepatitis and EtOH

Front 80

What factor define decompensated cirrhosis?

Back 80

Ascites, portal-systemic encephalopathy, esophageal varices, and Hepatocellular carcinoma

Front 81

What is the definition of portal HTN?

Back 81

Free Portal Vein pressure > 10 mmHg and wedge pressure no more than 5 mmHg greater than IVC pressure

Front 82

What are causes of ascitis?

Back 82

Organ failure including liver, malignancy, or increase peritoneal fluid production.

Front 83

What are the signs of hepatic encephalopathy?

Back 83

Asterixis and abnormal EEG. This is a reversible neuropsychiatic condition

Front 84

What is pathogenesis for hepatic encephalopathy?

Back 84

Ammonea, GABA, and tryptophan

Front 85

In patients with hepatic encephalopathy, do you withhold protein in diet?

Back 85

No, it was them worse

Front 86

What are the RF for hepatocellular carcinoma?

Back 86

HCV (25x), HBV(200x), Hemochromatosis (400x) and HBV pts who smoke or drank daily greatly increase their risk

Front 87

What do you use to screen for HCC?

Back 87

Pts w/ cirrhosis test for AFP and US every 6 months

Front 88

What is the most common reason for FDA to pull drug?

Back 88

liver toxicity

Front 89

What are some common drugs that cause hepatotoxicity?

Back 89

Isoniazid, estrogen, ketoconazole, phenytoin, amoxicillin, nitrofurantoin, and dicloxacillin

Front 90

CYP450 is key NZM for what phase of metabolism?

Back 90

One

Front 91

What drugs have short latency and relatively constant hepatotoxicity?

Back 91

Acetaminophen, Cyclophosphamide, busulfan, carbon tetracholide, alfatoxins, and ethanol

Front 92

What triggers tend to have short latency and is person specific for hepatotoxicity?

Back 92

Idiosyncratic like allergies.

Front 93

If pt has elevated bilirubin and no change in ALT or AST, what do they have?

Back 93

99% chance pt has drug rxn

Front 94

What is role of liver biopsy?

Back 94

Often for excluding hepatobiliary disorders. Use if pt is not improving after removing agent.

Front 95

What is the leading cause of acute liver failure in US?

Back 95

Acetaminophen, just a single dose can cause liver necrosis.

Front 96

What is the antidote for acetaminophen?

Back 96

N-acetyl Cystine

Front 97

What does biopsy of acetaminophen toxicity look like?

Back 97

Centrizonal necrosis – appears as ischemic liver

Front 98

Is tylenol safe for pt w/ liver failure?

Back 98

Yes, tylenol can be taken in low doses

Front 99

Describe the phases of acetaminophen hepatotoxicity.

Back 99

"1st phase 12-24 hrs – anorexia, N/V; 2nd phase 24 hrs – symptom free but liver fnct test will be way off; 3rd phase 48-72 hrs – signs of liver failure

Front 100

What is histo changes of pyloric stenosis?

Back 100

Hypertrophy of circular muscle of gastric pylorus (perhaps due to muscular hypersensitivity and spasm) produces a stenosis that may be aggravated by subsequent inflammation and edema of submucosa

Front 101

What is signs of pyloric stenosis?

Back 101

Projectile vomiting characteristically begins around 2-4 weeks of life

Front 102

When does gastric rupture occur?

Back 102

Usually due to trauma to a previously distended stomach and is rapidly followed by shock and death. Stomach content have spread into peritoneal cavity

Front 103

What occurs when we think about eating?

Back 103

Cephalic phase - vagal mediated direct to innervations of parietal cells and G cells.

Front 104

What occurs when the stomach is distented?

Back 104

Gatric Phase

Front 105

What mediated the intestinal phase?

Back 105

Hormones

Front 106

What is contained in the fundus and body of stomach?

Back 106

contains parietal cells (H+), G-cells (gastrin), enterochromaffin cells (histamine), and D-cells (somatostatin).

Front 107

What is contained in the antrum of the stomach?

Back 107

contains ghrelin cells (Ghrelin-satiety stim) and G-cells (gastrin)

Front 108

What are the main stimulants of parietal cell acid secretion?

Back 108

Gastrin, Histamine, and ACh

Front 109

How does gastrin stim acid secretion?

Back 109

stim parietal cells directly and stim enterochromaffin-like cells to release histamine.

Front 110

What stims gastrin producton?

Back 110

Vagal nervous, Proteins and AA stim G-cells to release gastrin.

Front 111

What releases histamine for digestion in stomach?

Back 111

enterochromaffin-like cells

Front 112

What releases ACh for digestion in stomach?

Back 112

ACh from enteric nervous system that is released from vagal stimulation

Front 113

How long does it take after a meal to reach peak acid secretion levels?

Back 113

90 minutes

Front 114

When during eating does the stomach pH become highest, what level, and how long until returns to normal?

Back 114

The highest pH reached is about 4, at about 1/2 hour after eating, and returns to pH of 2 in about 90 minutes.

Front 115

Describe the process of acid secretion by the parietal cells.

Back 115

H/K ATPase is main mechanism for acid secretion, (H+) is pumped out in exchange for K+ ion and Cl- ion is released to maintain charge so HCl is released.

Front 116

How do proton pump inhibitors work? Requirements?

Back 116

PPIs are taken up into parietal cells and bind covalently to cysteine 813 (in presence of H+) of H/K ATPase and inhibit the fnct of the pump. Must have active acid secretion to work

Front 117

What is the mucosal defense of stomach dependent on?

Back 117

Compromise in blood flow will impair mucosal defense

Front 118

What can increase pts RF for developing peptic ulcer disease?

Back 118

Taking NSAIDs, low dose aspirin, EtOH, anticoagulants, and anti-platelet meds

Front 119

What are complications of PUD?

Back 119

bleeding, penetration, perforation (emergency), and gastric outlet obstruction (pt vomits a lot of food)

Front 120

What is your differential diagnosis for suspected uncomplicated ulcer?

Back 120

Nonulcer dyspepsia, GERD, biliary colic, pancreatitis, angina pectoris, gastric cancer

Front 121

What is your differential diagnosis for bleeding ulcer?

Back 121

Varices, Mallory-Weiss, esophagitis, vascular lesion

Front 122

What is your differential diagnosis for perforated ulcer?

Back 122

Appendicitis, pancreatitis, cholecystitis, spontaneous bacterial peritonitis, bowel ischemia or infarction, diverticulitis

Front 123

What is your differential diagnosis for penetrating ulcer?

Back 123

Pancreatitis, muscle strain, herniated vertebral disk, ureteral stone

Front 124

What is your differential diagnosis for fistulizing ulcer?

Back 124

Gallstones, GI malignancy, Crohn's disease, intra-abdominal abscess

Front 125

What is the sign of H. pylori colonization?

Back 125

Biopsy of antrum is placed in agar w/ urea. If pH change occurs then pts is colonized. It is urease positive and causes PUD, gastric ulcers, and duodenal ulcers.

Front 126

How does H. pylori induce ulcer formation?

Back 126

It has several virulence factors including Cag A. It secretes various mediators that diffuse into underlying mucosa that initiates an inflammatory response. It is a/w/ decrease in D cell responsive for inhibitory effect of acid secretion. It causes chronic active gastritis.

Front 127

Can H. pylori solely cause PUD?

Back 127

No, it takes multiple factors

Front 128

How do you treat H. pylori colonization?

Back 128

2 antibiotics and an antisecretory drug (omeprazole)

Front 129

Which ulcers are a/w/ malignant transformation?

Back 129

Gastric have a risk whereas duodenal is almost never.

Front 130

What is the m.c.c. of ulcers?

Back 130

NSAIDs, they cause a decrease in PG synthesis at mucosal layer

Front 131

PGs normally effect mucosal levels how?

Back 131

They increase bicarb and mucus secretion. They also increase blood flow.

Front 132

NSAIDs cause what kind of ulcers? H. pylori?

Back 132

NSAIDs are mainly Gastric whereas, H. pylori causes Duodenal ulcers.

Front 133

What causes acute gastritis?

Back 133

It is a/w/ variety of predisposing factors (aspirin, toxins) which can alter mucosal blood flow causing ischemia, or interfere w/ protective mucoid barrier that prevents acid digestion of the gastric mucosa.

Front 134

Describe histo of acute superficial gastritis.

Back 134

localized hyperemia, edema, and mild neutrophilic inflammatory infiltrates of the lamina propria and surface epithelium

Front 135

Describe histo of acute hemorrhagic gastritis.

Back 135

focal hemorrhage and superficial sloughing of mucosa

Front 136

Describe histo of acute hemorrhagic erosive gastritis.

Back 136

diffuse hemorrhage and erosion of the mucosa

Front 137

An acute peptic ulceration is also known as a what?

Back 137

stress ulcer

Front 138

Describe an acute peptic ulceration.

Back 138

An exaggeration of AEG in which the mucosal erosion penetrates the muscularis mucosa. Tend to arise initially in prox stomach but, depending on severity, multiple ulcers may involve entire gastric mucosa and occasionally duodenum. Usually they are small, circular ulcers with a reddish-brown base rarely extending deeper than submucosa.

Front 139

What is acute peptic ulceration a/w/?

Back 139

steroid therapy, aspirin abuse, and smoking

Front 140

Are acid levels changed for ulcers to occur?

Back 140

No, acid must be present for ulcer to form but not increased above normal except w/ Cushing ulcers b/c high vagal stimulation.

Front 141

Once stressor of peptic ulcer is removed, what occurs w/ ulcer?

Back 141

They usually heal w/out sequelae once stress has been removed and do not progress to chronic peptic ulcers.

Front 142

What are the histologic changes of chronic superficial gastritis?

Back 142

Localized or diffuse superficial lymphocytic and plasmacytic infiltrates of lamina propria. The glandular compartment is usually unaffected.

Front 143

What are the histologic changes of chronic atrophic gastritis?

Back 143

Has a heavier and deeper inflammatory infiltrates with thinning of the mucosa, atrophy of the glands, and surface epithelial atypia

Front 144

What are the histologic changes of gastric atrophy?

Back 144

flattening or loss of normal rugal folds; lymphocytic, plasmacytic, and occasionally eosinophilic infiltrates; marked glandular atrophy; and replacement of the surface or pit epithelium by gastric goblet cells and intestinal epithelium (intestinal metaplasia) which frequently show atypical or dysplastic changes.

Front 145

What is the major clinical significance of chronic gastritis?

Back 145

Serious disorders like pernicious anemia and gastric carcinoma

Front 146

Chronic fundal gastritis is due to what?

Back 146

Results from autoimmune destruction of gastric parietal cells and is therefore most prominent in fundus and body. These pts produce ABs directed against IF, IF-Vit B12 complexes, and gastric parietal cells.

Front 147

What can pernicious anemia lead to?

Back 147

An increase risk of gastric carcinoma

Front 148

What is chronic antral gastritis a/w?

Back 148

H pylori infections, seen most prominently in prox antral region

Front 149

What stomach hormone levels are altered w/ H. pylori infection?

Back 149

promote gastrin secretion perhaps by inhibiting the secretion of somatostatin.

Front 150

What % pts w/ duodenal or gastric ulcers have concomitant H. pylori infection? What % develop ulcers?

Back 150

> 90% of pts w/ duodenal ulcers and 75% of pts w/ gastric ulcers also have concomitant H. pylori infection but only ~15% of infected pts ever develop ulcers.

Front 151

What is the mech of ulceration for duodenal ulcers?

Back 151

Mechanism of ulceration relates to delivery of ↑ acid-pepsin secretion to duodenum rather than altered mucosal resistance although both mechanisms may play a role

Front 152

Who is at increase frequent risk for duodenal ulcers?

Back 152

↑ in frequency in patients with a genetic predisposition (type O blood, non-secretors of blood group antigens into body fluids, MEN I), those who smoke, and those who have concurrent COPD, hepatic cirrhosis, rheumatoid arthritis, or hyperparathyroidism

Front 153

What is the mech of ulceration for gastric ulcers?

Back 153

Mechanism of ulceration relates to function of altered mucosal resistance. Almost all gastric ulcer pts have preexisting or concurrent chronic gastritis and are normal or hyposecretors of acid-pepsin

Front 154

Who is at increase risk for gastric ulcer?

Back 154

↑ incidence in pts who have type A blood, who smoke and/or drink, abuse aspirin, or have COPD. There is less evidence of a genetic predisposition than with duodenal ulcer pts.

Front 155

Describe the location of duodenal and gastric ulcers. Which order do you see them occur?

Back 155

Duodenal ulcers most often occur on anterior wall of 1st portion while gastric ulcers are usually found in antrum with slightly greater predilection for lesser curvature. If duodenal and gastric ulcers are both present (10% pts), duodenal is the first to appear.

Front 156

Describe the morphology of ulcers

Back 156

A crater appears punched-out with a straight wall perpendicular to base of ulcer which usually lies within the submucosa or muscularis propria. The crater base is usually grossly free of exudate and, over time, scarring creates mucosal folds that radiate outward from the central crater.

Front 157

When do duodenal ulcer cause burning epigastric pain? Relieving factors?

Back 157

classically begins within a few hours after eating and is relieved by antacids, milk, or food which tends to neutralize the excess acid

Front 158

When do gastric ulcers cause burning peigastric pain? Other signs?

Back 158

food may be irritating and induce vomiting which is more likely to lead to anorexia. Referred pain may be present in thorax, back, or upper abdomen

Front 159

What are complications of ulcers?

Back 159

Complications include bleeding (30%-pts, 25%-deaths), perforation (5%-pts, 65%-deaths), or pyloric obstruction due to scarring.

Front 160

What disorder is seen in middle aged men who present w/ epigastric pain and have blood and protein loss? There is also enlarged rugae.

Back 160

Menetrier disease has rugae enlargement seen in the fundus or antrum. This disorder is recognized as a potentially pre-malignant condition and should be endoscopy periodically.

Front 161

What is the Histo of Menetrier disease?

Back 161

there is hyperplasia mucus-producing cells and gastric pits with variable atrophy of underlying gastric glands which may cause low acid secretion.

Front 162

What disease has enlarged rugae of fundal w/ sparing of antrum? Pt suffer from chronic peptic ulcer disease.

Back 162

Hypersecretory gastropathy, there is enlargement of gastric glands secondary to parietal and chief cell hyperplasia

Front 163

What disease is associated w/ gastrinoma and has enlarged rugae?

Back 163

Zollinger-Ellison syndrome has parietal cell hyperplasia is secondary to gastrin stim from an associated gastrinoma.

Front 164

What is the locations of gastric carcinomas?

Back 164

most often found in the distal antral and pyloric regions, but there has been ↑ frequency of proximal tumors

Front 165

What are some drugs that are a/w/ gastric carcinoma?

Back 165

nitrites and nitrosamines

Front 166

What disease is a/w/ signet ring carcinoma?

Back 166

Gastric mucus producing cells tend to be less cohesive and diffusely infiltrating eliciting a striking desmoplastic stromal response or sometimes producing abundant mucin

Front 167

What are some of the physiological forms of gastric carcinomas?

Back 167

may grow into the gastric lumen as fungating or polypoid masses, extend diffusely into the gastric wall creating ill-defined mural thickening (linitis plastica), or create ulcerative lesions with indurated, heaped up margins and a shaggy, necrotic base.

Front 168

What are the poor pgx factors of gastric cancers?

Back 168

advanced stage of the disease and a proximal location in the stomach

Front 169

What occurs w/ linitis plastica?

Back 169

Lose of peristalsis, seen w/ gastric carcinoma

Front 170

What are the m.c. atresias?

Back 170

Rectal then small bowel

Front 171

What causes small bowel atresia? Signs?

Back 171

Intauterine vascular insult. Clinically manifested by early and persistent vomiting of bile-stained material.

Front 172

What is hirschsprung disease a/w/?

Back 172

Strong male preference. It is a/w/ Down syndrome or other cong abnormalities.

Front 173

What causes hirschsprung disease?

Back 173

Due to failure of neural crest cells to migrate to and populate the Meissner (submucosal) and Auerbach (myenteric) plexuses in distal colon. Anorectal junction is always involved and lack of ganglion cells extends variably prox but normally limited to rectum and sigmoid. A lack of peristalsis creates a functional obstruction and results in dilatation of colon prox to the aganglionic segment.

Front 174

Where do pulsion diverticula tend to occur at?

Back 174

tend to occur along mesenteric border (where mesenteric vessels and nerves enter) w/ protrusion of mucosa and submucosa through muscularis propria.

Front 175

What can result from pulsion diverticula?

Back 175

Rarely, may result in bacterial overgrowth and B12 deficiency, bleeding, or perforation

Front 176

What does a merkel diverticulum arise from?

Back 176

anomaly arises from persistence of proximal portion of the omphalomesenteric (vitelline) duct which links midgut to yolk sac.

Front 177

Where do meckel diverticulum tend to occur at?

Back 177

Variable in size, they are located along antimesenteric border of ileum usually w/in 30 cm. of ileocecal valve.

Front 178

What can result from meckel diverticulum?

Back 178

about ½ contain heterotopic gastric mucosa and may develop peptic ulceration and bleeding leading to iron deficiency anemia. Scarring from repeated subclinical inflammation may lead to bowel obstruction. Rarely, they may perforate.

Front 179

What causes diverticular disease of colon?

Back 179

weakness of bowel CT either through disease processes or by normal aging, ↑ intralumenal pressures created by alteration of stool (low residue-low fiber diets), or is an intrinsic defect of colonic muscular coat.

Front 180

What is the histological changes seen w/ diverticular disease? Where does herniation occur at?

Back 180

there is hypertrophy of muscular layers (prediverticular disease) w/ subsequent herniation of mucosa and submucosa through colon wall (diverticulosis) at points of weakness between mesenteric and antimesenteric taenia where the vessels penetrate circular muscle

Front 181

What part of colon do almost all herniations occur?

Back 181

95% occur in sigmoid colon, but they may involve the entire length of colon

Front 182

What are the signs of diverticulosis?

Back 182

Most patients are asymptomatic, but if symptoms occur, onset is insidious w/ intermittent or continuous lower abdominal discomfort, constipation, and distension. Progression of the disease results in worsening constipation, abdominal cramps, and bleeding. A mass may be palpable in LLQ.

Front 183

What is danger of diverticulosis?

Back 183

diverticulitis may follow perforation or fecal impaction w/in a diverticulum and infrequently may result in pericolic abscesses, peritonitis, or sinus/fistula tracts.

Front 184

What can chronic diverticulitis lead to?

Back 184

fibrous thickening of wall and ↓ lumenal diameter which may simulate malignancy.

Front 185

What is the danger of abnormal rotation of pancreatic bud?

Back 185

The ventral pancreatic bud may circle the duodenum before fusing w/ dorsal bud, thereby obstructing of duodenum

Front 186

What can cause abdominal hernia?

Back 186

They occur in areas of weakness or defect in abdominal wall. They are particularly prone to do so during periods of increased intraabdominal pressure

Front 187

What is danger of abdominal hernias? Process?

Back 187

If venous drainage of the bowel is compromised, ensuing venous stasis and edema traps the bowel within hernia sac (incarceration) and may ultimately result in ischemic necrosis (strangulation) and possible perforation.

Front 188

What causes fibrous adhesions?

Back 188

Due to Peritonitis from any cause (bacterial, surgical, etc.)

Front 189

Describe process of intussusception.

Back 189

When a portion of bowel (intussusceptum) becomes telescoped into a more distal portion (intussuscipiens). As the prox portion is being propelled further distally, its attached mesentery is being pulled along also and may lead to vascular compromise and infarction.

Front 190

Who tends to get intussesception and where?

Back 190

Usually occurs in children and involves the telescoping of the terminal ileum into the cecum.

Front 191

What causes intussesception in children at terminal ileum into cecum?

Back 191

Hyperplasia of Peyer patches is the most frequent cause in children.

Front 192

How do adults tend to get intussesception?

Back 192

it is often associated with polyps or tumors which get caught up in peristaltic action

Front 193

What disease is char by asymptomatic brown-black discoloration of the colon mucosal surface?

Back 193

Melanosis coli, due to accumulation of brown-black pigment within macrophages of lamina propria

Front 194

Melanosis coli is a/w/ what?

Back 194

Chronic anthracene laxative abuse

Front 195

What causes the brown black pigment seen in melanosis coli?

Back 195

Pigment apparently results from apoptosis of colonic epithelial cells, which are then digested by macrophages in lamina propria, with indigestible cell fragments becoming the pigment.

Front 196

In transmural infarction, consequences depend on what?

Back 196

"consequences of vascular compromise depends on degree, rate of

Front 197

What is responsible for majority transmural infarcts? What reduces its incidence rate?

Back 197

Interruption of arterial flow is responsible for 60% of TBIs although the numerous anastomoses between branches of celiac, superior mesenteric, and inferior mesenteric arteries reduces overall incidence.

Front 198

How does colon tend to get TBIs?

Back 198

colon infarcts are most commonly due to hypovolemia/hypotension. The colon has another vascular supply from the posterior wall.

Front 199

Venous obstructions are usually due to what?

Back 199

due to thrombus formation secondary to trauma, intraperitoneal infection, polycythemia, or external compression

Front 200

Which type of infarct tends to be blurred?

Back 200

Venous

Front 201

Which type of infarct tends to have distinct borders?

Back 201

Arterial

Front 202

Vascular occulsion leads to what histo change?

Back 202

will result in patchy or confluent hemorrhagic infarction of bowel which is first manifest by congestion and hemorrhage of mucosal, submucosal, and subserosal tissue. Edematous thickening of the bowel wall, sloughing of the mucosal surface, and inflammatory infiltrates follow.

Front 203

How long post-infarct before fibrinous exudate appears? Secondary complications?

Back 203

Fibrinous or fibrinopurulent exudate appears on the serosal surfaces within 24 hours and, w/out surgical intervention, secondary bacterial contamination, peritonitis, and perforation will occur.

Front 204

What is signs of TBI?

Back 204

develop abrupt onset of severe abdominal pain w/ N, V, possible bloody diarrhea, and ensuing shock. Bowel sounds are ↓ and, w/ onset of peritonitis, a rigid abdomen develops.

Front 205

Without treatment what will occur in TBI pts?

Back 205

W/out intervention, sepsis, shock, blood loss, or perforation will culminate in death w/in 48 hours

Front 206

Where in colon do you see TBIs?

Back 206

seen in the "watershed" areas (splenic flexure and mid-rectum).

Front 207

What is acute hemorrhagic enteropathy due to?

Back 207

tissue hypoperfusion secondary to shock, cardiac failure, infections, vasoconstrictive drugs, etc

Front 208

What is affected in acute hemorrhagic enteropathy?

Back 208

of ischemic necrosis of mucosa and submucosa (mucosal infarction) and muscularis propria (mural infarction) with sparing of serosa

Front 209

What is the difference between acute hemorrhagic enteropathy and TBI?

Back 209

Acute hemorrhagic enteropathy has sparing of the serosa and subserosal tissue and a patchy multifocal nature.

Front 210

Describe volvulus and where it occurs at.

Back 210

Twisting of bowel on itself resulting in obstruction, vascular compromise, and infarction. This occurs most often in small bowel due to its ↑ mobility.

Front 211

What is a major cause of lower GI bleeding and anemia in elderly population?

Back 211

Angiodysplasia - has telangiectasiain superficial lamina propria of cecum. They are asymptomatic until they rupture, which causes limited hemorrhage

Front 212

Who gets hemorrhoids?

Back 212

Usually pts over 30 y.o. unless thet are prego.

Front 213

What causes hemorrhoid formation?

Back 213

Persistently elevated venous pressure in hemorrhoidal plexuses (chronic constipation, prego, portal HTN, etc) causes variceal dilatation of veins

Front 214

What covers external hemorrhoids? Internal hemorrhoids?

Back 214

anal squamous epithelium (external hemorrhoids) rectal epithelium (internal hemorrhoids)

Front 215

What are complications of hemorrhoids?

Back 215

Thrombosis, superficial ulceration, fissure formation, and hemorrhagic infarction

Front 216

What is big sign of hemorrhoids?

Back 216

Hematochezia, bright red blood in stool is sign of lower GI bleed.

Front 217

Where does majority of absorption occur in GI tract? Exceptions?

Back 217

. Most absorption occurs in the duodenum and jejunum except for vitamin B12 and bile salts which are absorbed in the ileum.

Front 218

Describe daily absorption of GI tract if pts has intake of 10L/day

Back 218

6 L will be absorbed by jejunum, 2.5 L absorbed by terminal ileum, and 1.5 L makes it to colon. Remember colon max capacity is 3-4 L/day.

Front 219

Describe how small bowel absorption can affect absorption in GI tract.

Back 219

only 3 L will be absorbed by jejunum, still 2.5 L absorbed by ileum, and now 5.5 L reaches colon, more than its capacity -> diarrhea

Front 220

Who has high lactase def rates?

Back 220

75% of AA, Asians, Native Americans, are intolerant

Front 221

Where normally is lactose absorbed? Products?

Back 221

normally broken down by NZM in small intestine on brush border into galactose and glucose, which are then absorbed by body and utilized

Front 222

If pt has lactase def, what changes about lactose metabolism?

Back 222

lactose enters colon where it is broken down by bacteria into short chain FAs, water and carbon dioxide. This causes substantial increase in motility b/c SCFA stim both fluid secretion and contractility of the gut, bad, bad!

Front 223

What other changes occur w/ LD?

Back 223

Normally, fluid increases in duodenum and jejunum cause increase net absorption in ileum but w/ LD this fluid accumulates and goes to colon.

Front 224

What is the asociated w/ osmo of stool water?

Back 224

Anything that increases the osmolality of stool water, increases output of stool in linear fashion.

Front 225

What is easy way to tell if pt has malabsorption?

Back 225

If pt is having solid stool then not present. Steatorrhea is the hallmark of malabsorption syndrome

Front 226

What is changed in stool if FA are present in stool?

Back 226

The oxylate goes up if you have FAs that bind up calcium. Calcium normally binds to oxylate and takes it out of stool. If FFA’s are present in high amounts, they bind calcium in oxylate’s place.

Front 227

Describe classical test to measure carb absorption in small intestine

Back 227

D-xylose, historic interest test, is non-metabolized pentose sugar. You give 25 g in water to fasting patient and normally > 4 grams (25%) is secreted in urine 5hr collection. This is used to evaluate the absorptive capacity of the gut for carbohydrate.

Front 228

What should small bowel biopsy look like?

Back 228

look at crypts to villous height ratio, normally 4:1

Front 229

Celiac disease is a hypersensitivity to what?

Back 229

hypersensitivity to gliadin (glycoprotein of gluten found in wheat, oats, barley, and rye products) which induces, usually beginning in childhood, ↑ levels of IgA and IgM antibodies in intestinal mucosa

Front 230

What histo changes occur w/ celciac disease?

Back 230

accelerated sloughing of jejunal epithelium (worse in upper jejunum and decreasing distally) leading to severe atrophy of jejunal villi (↓ absorptive SA), ↑ depth of intervillous crypts due to epithelial hyperplasia (an attempt to repopulate surface epithelium), and ↑ chronic inflammatory cell infiltration of lamina propria.

Front 231

What is presenting complaint of celiac disease?

Back 231

Diarrhea is usually but they can come w/ unexplained anemia

Front 232

How do you tx celiac disease?

Back 232

Elimination of wheat, oats, barley, and rye products from diet will restore normal physiologic function and, in most cases, will restore normal histology of jejunum

Front 233

Celiac disease raises risk of what?

Back 233

there is an ↑ incidence of subsequent small bowel lymphomas and, to a lesser extent, adenocarcinomas

Front 234

How is tropical sprue differ from celiac disease?

Back 234

the histologic changes tend to involve the small bowel uniformly or be more severe in the distal bowe

Front 235

How is tropical sprue characterized?

Back 235

steatorrhea and folate deficiency anemia. The histology varies from no mucosal abnormality to changes resembling celiac disease

Front 236

How is tropical sprue tx?

Back 236

cured by broad-spectrum antibiotic therapy and folic acid supplementation.

Front 237

Describe the typical onset of tropical sprue?

Back 237

Seen in pts that have vacation in foreign land and were fine during trip but 2 weeks post they developed malabsorption.

Front 238

Who gets whipple's disease and how does it present?

Back 238

Having a strong predilection for males, the disorder usually presents in middle age as severe malabsorption (steatorrhea, abdominal cramps, fever, and emaciation), but alternatively it may also present with migratory polyarthralgia, CNS symptoms, lymphadenopathy, etc.

Front 239

What is the causative organism for whipple's disease?

Back 239

Causative organism (Tropheryma whippelii). EM reveals rod-shaped bacilli within lysosomes of macrophages and along the brush border of (and occasionally within) epithelial cells

Front 240

What is the characteristic feature of whipple's disease?

Back 240

Characteristic feature is presence of macrophages filled with PAS-positive, diastase-resistant granules (the bacilli-bearing lysosomes) which are found most commonly in lamina propria of small bowel but which may be seen in LNs, synovial tissue, etc.

Front 241

What is genetic linkage of abetalipoproteinemina and signs?

Back 241

AR inborn error of metabolism manifested in infancy by diarrhea, steatorrhea, and failure to thrive.

Front 242

What is abnormal in abetalipo…?

Back 242

Pts are unable to synthesize apoprotein B utilized of chylomicrons, VLDL, and LDL and are therefore unable to transport lipids in the circulation

Front 243

What are histo signs of abetalipoproteinemia?

Back 243

There is an accumulation of fat in villous tips b/c they lack apo B so they can’t repackage triglycerides

Front 244

What is genetic linkage of agammaglobulinemia?

Back 244

X-linked

Front 245

What is histo signs of agammaglobulinemia?

Back 245

In mucosa there is no villi. There are few crypts left, but it is a flat surface. There is increase in inflammatory cells, but no plasma or mast cells. Pt generally has malabsorption b/c they have lost SA.

Front 246

What disease is char by high number of red staining cells in small bowel biopsy? Other signs?

Back 246

Eosinophilic gastroenteritis (> 20 per HPF) can cause malabsorption leading to abdominal pain and diarrhea.

Front 247

What disease has large accumulation of fats in lacteals, creating club shaped villous structures?

Back 247

Lympangectasia has white spots caused by lymphatics being blocked, perhaps by tumor, due to disruption by surgery, or due to idiopathic causes.

Front 248

What presents w/ severe diarrhea with cyst present in stool?

Back 248

Giardiasis, which is endemic in St. Petersburg and Mexico City, does not begin to experience signs until post 2 weeks.

Front 249

What histo changes are present in Giardiasis?

Back 249

There is cyst seen in lower 1/3 villous structure, which produce malabsorption and diarrhea even though villous structure is intact

Front 250

If you lose 100 cm of distal end of ileum, what changes occur?

Back 250

Like w/ Crohn’s disease you tend to malabsorb bile acids, thus they are delivered into colon and this produces diarrhea from effect of bile acids on colic mucosa.

Front 251

What mimic ileoresection of last 100 cm?

Back 251

Gallbladder removal surgery

Front 252

If you lose more than 100 cm of distal end of ileum, what changes occur?

Back 252

You begin to malabsorb FAs b/c you lose amount of bile acids that are needed to produce critical micellar concentrations

Front 253

How many death occur every year due to diarrhea and who is at highest risk?

Back 253

5 million per year and 80% are less than 1 y.o.

Front 254

What are some causes of secretory diarrhea?

Back 254

Due to toxins produced by Cholera. Can be due to bisacodyl, aloe, lasix, thiazides, asthma medication, metformin for diabetes, colchicines used for gout, ace inhibitors, and H2 blockers too. Rarely Zollinger-Ellison syndrome can produce hormone causing secretory.

Front 255

What are some causes of osmotic diarrhea?

Back 255

Due to undigested carbs as seen w/ LD and milk of magnesia. Also overgrowth of bacteria, abetalipoproteinemia, pancreatic disease, sprue, giardiasis. Can be drug induced w/ Cholestyramine, miralex, lactulose, and laxative abuse.

Front 256

What is the sodium levels and osmotic gap for secretory diarrhea?

Back 256

Stool Na > 90 and osmotic gap < 50

Front 257

What is the sodium levels and osmotic gap for osmotic diarrhea?

Back 257

Stool Na < 60 and osmotic gap > 100

Front 258

What type of diarrhea will cause on despite fasting?

Back 258

Secretory

Front 259

What are the main causes of acute diarrhea?

Back 259

Typically infectious, seen in pts who have eaten unusual foods that contain spices, pts w/ AIDS, or IV drug abusers, and daycares and initutions are suspect for infectious diarrhea

Front 260

What are some of the major causes of travelers diarrhea?

Back 260

Traveler’s diarrhea: 40% is enterotoxigenic E. coli; rotavirus and Norwalk virus is seen in cruise ships

Front 261

What is the major source of food poisoning?

Back 261

Food poisoning is usually due to Staph Aureus, which pt ingest a performed toxin and generally vomiting is more of a compenent than diarrhea.

Front 262

What are the danger signs of acute diarrhea?

Back 262

High fever (>38.5 C), systemic illness, cramping abdominal pains, dysentery, dehydration, and prolonged course.

Front 263

How to you tx acute diarrhea w/ and w/out danger signs?

Back 263

W/out danger signs just give fluids containing salt, sugar, and cooling fluids. Void mile products b/c LD. Most improve w/in 72 hrs. If w/ danger signs, you should give IV fluids along w/ antibiotics if serious.

Front 264

What antibiotics are used to tx acute diarrhea w/ danger signs?

Back 264

Tx w/ quinolones first, sulfa-tremethoprim second, metronidazole for anaerobic and protozoans. Macrolides and rifaximin are 3rd and 4th line drugs.

Front 265

What is major source of diarhhea in ICU?

Back 265

Drugs, mainly the delivery vehicle.\

Front 266

How long does diarrhea have to be present before it becomes chronic?

Back 266

3 weeks

Front 267

What chronic disease can lead to steatorrhea?

Back 267

Chronic pancreatitis

Front 268

Nocturnal bowel movements are a/w/ what?

Back 268

IBD

Front 269

With chronic disease, what lab tests should be conducted?

Back 269

CBC, metabolic profile, prothrombin time (Vit K absorption), B12 and folate absorption, iron studies, cholesterol, and carotene. If first tests were negative: Schilling tests, breath hydrogen methane, and thyroid studies (hypothyroidism)

Front 270

What are some major causes of chronic diarrhea?

Back 270

Watery diarrhea (m.c.), carbohydrate malabsorption, bile acid diarrhea, IBD, food allergies, microscopic colitis, hormonal tumors, factitious, diabetic, alcoholic, and congenital secretory diarrhea (C.F.)

Front 271

What is the time honered tx for chronic diarrhea?

Back 271

bismuth b/c only heavy metal tx on market, toxic chemical only in lose doses, useful in both chronic and acute diarrhea, toxic to most bacteria and parasites, and subsalicylate moiety inhibits net secretion of fluids into gut

Front 272

What tx is good for chronic diarrhea but dangerous for acute diarrhea?

Back 272

Opiates, lomeramide

Front 273

What tx is used to absorb toxins, seen w/ chronic diarrhea?

Back 273

Kaopectate

Front 274

What tx is used to absorb to bile?

Back 274

Cholestyramine

Front 275

What tx is used in AIDS dairrhea w/ unknown source?

Back 275

Octreotide

Front 276

What tx is used for diarrhea in DM pts?

Back 276

Clonidine

Front 277

Describe appendix

Back 277

The organ is lymphoid w/ many lymphoid follicles and mucus cells. . It receives blood and nerve from mesoappendix.

Front 278

What causes appendicitis?

Back 278

Acute Appendicitis felt to come from obstruction of lumen of appendix due to pinworm, fecoliths, secretions, or lymphoid hyperplasia. Bacterial infection is usually secondary.

Front 279

What results in gangrenous necrosis of appendicitis?

Back 279

Suppurative necrosis of the mucosa and muscularis further compromises the vascular supply resulting in gangrenous necrosis and predisposing to frank rupture.

Front 280

What is initial signs of appendicitis?

Back 280

Clinically characterized by diffuse abdominal discomfort eventually localizing to the RLQ (McBurney point) accompanied by N/V, anorexia, and diarrhea/constipation.

Front 281

What are histo signs of acute appendicitis?

Back 281

slough of mucosa and lymphocytic infiltrate

Front 282

What are most of the antigens in lumen seen w/ IBD?

Back 282

Most are microbial origin

Front 283

Does CD or UC have highest genetic linkage?

Back 283

CD, first degree have 10-15x RF

Front 284

What is indeterminate colitis?

Back 284

In cases where there is histo features of UC and CD.

Front 285

What is histo signs of CD?

Back 285

Segmental involvment (sharp demarcation), transmural thickening and fibrosis w/ narrowing lumen, and non-caseaating granulomatous formation (pathomemonic)

Front 286

What is potenial span of CD? M.C. area?

Back 286

May involve any portion of GI tract, terminal ileum and cecum have highest incidence

Front 287

What genetic change has been a/w/ CD? What is its fnct?

Back 287

NOD2 gene on chromo 16 is only 1 of a number of gene loci that have been implicated in CD. NOD2 gene encodes protein a/w/ innate immune system, it is expressed in paneth cells. If mutated then may confer reduced ability to kill gut bacteria. Highest risk is in Jews.

Front 288

What % of CD can mimic UC?

Back 288

20% of CD cases affect large intestine only (Crohn's colitis)

Front 289

What are hallmarks of CD?

Back 289

Segmental involvement, transmural thickening and fibrosis, cobblestone mucosa, creeping fat, and non-caseating granuloma

Front 290

What cytokines are elevated in CD?

Back 290

 Many Th1 cytokines, including TNF-a, IL-2, and INFy

Front 291

What must be ruled out w/ non-caseating granulomas?

Back 291

Must rule out TB

Front 292

Describe the clincal course for CD.

Back 292

Characterized by: inflammatory, fistulizing, fibrostenotic/structuring. It has a high rate of relapse.

Front 293

What is presenting signs of CD?

Back 293

Presents as intermittent bouts of fever, RLQ abdominal pain, and diarrhea. As the disease progresses, the intervals between attacks become shorter and the symptoms become more pronounced leading to N/V, anorexia, weight loss, slow blood loss, and electrolyte imbalance.

Front 294

What are complications of CD?

Back 294

bowel obstruction secondary to fibrous strictures (especially of terminal ileum), adhesions, fistula formation, peritoneal abscess, hemorrhage, and malabsorption of protein, vitamin B12, folic acid, and iron.

Front 295

What must CD pts be screen for routinely?

Back 295

Adenocarcinoma of colon (5-6%), must screen for 8 years

Front 296

What are the extraintestinal manifestations of CD?

Back 296

Uveitis, photophobia, episcleritis, ankylosing spondylitis or sacrolitis, erythema nodosum, pyoderma gangrenosum, DVT, Autoimmune hemolytic anemia, osteoporosis

Front 297

Which extraintestinal manifestations run parallel to activity of CD?

Back 297

includes disorders of skin, eyes, joints, and mouth.

Front 298

What are secondary complications bowel disease? Is it m.c. in CD or UC?

Back 298

This includes kidney stones, obstructive uropathy, malabsorption, and gallstones. These occur in pts w/ CD rather than UC.

Front 299

What are some nonspecific complications of bowel disease?

Back 299

osteoporosis, hepatic diseases, and amyloidosis

Front 300

What type of peripheral arthropathy parallels underlying bowel disease? A/W?

Back 300

Type I (<5 joints and usually big joints). It is a/w/ ↑ incidence of erythema nodosum and uveitis

Front 301

What type of peripheral arthropathy is independent of underlying bowel disease? A/W?

Back 301

Type 2 peripheral arthropathy (<5 joints and more small joints), last for about 3 yrs. There is increase RF for uveitis.

Front 302

How does axial arthritis diifer from peripheral arthritis with IBD?

Back 302

Axial arthropathy is less frequent than peripheral and is INDEPENDENT of bowel disease acitivity. Medical surgery of underlying IBD dose not alter the progressive nature of axial arthropathy.

Front 303

Most ankylosing spondylitis are positive for what?

Back 303

HLA-B27

Front 304

What are the symptoms of AS early on?

Back 304

severe onset back pain at young age, usually a/w/ morning stiffness or exacerbated by periods of rest.

Front 305

What are some absolute reasons for pts w/ CD to have surgery?

Back 305

free perforation, massive hemorrhage, cancer or dysplasia, chronic high grade obstruction

Front 306

What are some relative reasons for pts w/ CD to have surgery?

Back 306

intractability, complex fistulae and abscesses, perianal complications, and growth retardation

Front 307

What drugs are used to induction of remission in CD?

Back 307

For remission induction: aminosalicylates, antibiotics, immunomodulators, defined diets

Front 308

What drugs are used to maintenance of remission in CD?

Back 308

For remission maintenance: immunomodulators, aminosalicylates, and antibiotics

Front 309

What is used for mild-moderate CD?

Back 309

5-ASA

Front 310

What is used for severe flares of CD?

Back 310

Corticosteroids

Front 311

What drugs are used for steroid refractory CD?

Back 311

Azathioprine and 6-MP

Front 312

What decreases the RF for UC?

Back 312

Smoking and early age appendectomy

Front 313

What if UC limited to rectum?

Back 313

Proctitis

Front 314

What if UC involvement of rectosigmoid colon?

Back 314

Proctosigmoiditis

Front 315

What if UC involvement of entire colon?

Back 315

Pancolitis

Front 316

What are the major morphology factors of UC?

Back 316

Always begins in rectum. Early lesions begin as small mucosal hemorrhages and crypt abcesses. Inflammatory pseudopolyps appear too.

Front 317

What accounts for the high incidence of malignance seen w/ UC?

Back 317

epithelium of ulcer margins may undergo metaplastic and dysplastic changes

Front 318

How often are fistulas seen in UC and where at?

Back 318

They can occur but are less frequent than in CD and usually is confined to perianal regions.

Front 319

Describe the histo changes of UC.

Back 319

Mucosa shows extensive ulceration and diffuse thickening w/ inflammatory infiltrate. Ulcerate underline surrounding mucosa lacks depth and avoids muscularis properia.

Front 320

What are the classic symptoms of UC?

Back 320

bloody diarrhea, tenesmus, and fecal urgency

Front 321

What does UC initially manifest as?

Back 321

most often in early adulthood (20-40 years) as abdominal pain, cramps, and bloody diarrhea often subsequent to emotional stress.

Front 322

The risk of malignant transformation is dependent on what?

Back 322

Dependent on duration of disease, the age of onset, the chronicity, and extent of spread.

Front 323

What drugs are used for remission induction of UC?

Back 323

Remission induction: aminosalicylates, corticosteroids, 6-MP, and cyclosporine

Front 324

What drugs are used for remission maintenance of UC?

Back 324

Remission maintenance: aminosalicylates, 6-MP

Front 325

What are some absolute reasons to have surgery for UC pts?

Back 325

exsanguinating hemorrhage, perforation, cancer or dysplasia, unresponsive acute disease

Front 326

What are some relative reasons for pts w/ UC to have surgery?

Back 326

chronic intractability, steroid dependency, growth retardation, and systemic complications

Front 327

What organsim causes pseudomembranous Colitis?

Back 327

C difficile secretes toxins that are toxic to epithelium of GI tract. It refers to presence of membrane-like inflammatory exudate consisting of mucin, neutrophils, and fibrin, which is patchily distributed over the mucosal surface of the colon or, to a lesser extent, small bowel

Front 328

What condition allows C difficile infection?

Back 328

The usage of some antibiotics (clindamycin and ampicillin) rids natural bacterial presence in area.

Front 329

Describe process of pseudomembranous formation.

Back 329

The bacterial exotoxins bind to the colonic epithelial cells causing hypersecretion and inducing a suppurative inflammation with focal mucosal necrosis. This initially occurs within the crypts and spews an inflammatory coagulum onto the surface of the bowel which may coalesce into large patches forming a pseudomembrane.

Front 330

Child has a smooth, unfissured, pedunclated mass found in his colon, what is it?

Back 330

Juvenile Retention Polyp, seen in 4-5 y.o. mainly at the rectum. There can be several present at once.

Front 331

Describe the histo of JRP

Back 331

Microscopically, there are dilated, cystic spaces lined by normal colonic epithelium w/in an expanded lamina propria containing a mild acute and chronic inflammatory infiltrate. Malignant transformation is extremely rare.

Front 332

What disease has the classic melanin pigmentation on buccal mucosa? Genetics?

Back 332

Peutz-Jeghers syndrome is an AD disease first manifested in adolescence and young adults by polyposis of entire GI tract (w/ predilection for jejunum, ileum, and stomach) in a/w/ melanin pigmentation of buccal mucosa, lips, and digits.

Front 333

What is the histo of Peutz-Jeghers polyp?

Back 333

Short peduniculated stalk. Core is from smooth muscle of muscularis mucosa w/ convoluted epithelium covering. Little or no atypia.

Front 334

The atypia and mitosis maybe assoc with what other neoplasms?

Back 334

other visceral neoplasms (pancreas, breast, ovary, and lung).

Front 335

What are the m.c. polyp seen in adults?

Back 335

Hyperplastic polyps, seen mainly in rectosigmoid area

Front 336

Descsribe histo of hyperplastic polyps.

Back 336

Result from a loss of normal growth restraint, there is cellular crowding, hyperchromatism and ↑ mitotic activity in the proliferative zone at base of crypts but nuclei retain their basal position within the cell. There is lengthen¬ing of crypts and as cells migrate toward surface, crypt lumen acquires a serrated or "saw-tooth" appearance. A similar proliferative stimulus acts on fibroblasts to produce a thickened collagen layer beneath the surface epithelium. These changes produce small (< 0.5 cm.), pink-tan, sessile mucosal nodules that are frequently multiple.

Front 337

What differentiates hyperplastic from adenocarcinoma?

Back 337

There is increase in sub-epithelial collagen formation which differentiates it from adenocarinoma.

Front 338

Where do half of adenomatous polyps arise?

Back 338

Rectosigmoid area

Front 339

Describe histo of tubular adenoma

Back 339

Typically, they begin as sessile polyps but as they enlarge, they become pedunculated with a tan, spherical, irregularly-fissured head measuring < 2 cm diameter, occasionally larger. Stalk usually consists of a fibrovascular core made up of submucosal tissue which is covered by normal mucosa. W/in the head, tubular spaces are lined by pseudostratified epithelium which has lost normal diff and shows varying degrees of cellular dysplasia and mitotic activity.

Front 340

What % of tubular adenoma can be villous?

Back 340

Up to 25%

Front 341

What signifies malignant transformation of tubular adenoma?

Back 341

As size of polyp increases (usually due to increase in villous component), cellular dysplasia tends to become more severe and elongated tortuous tubules form cribriform histologic pattern with little intervening lamina propria.

Front 342

When does the malignancy of tubular adenoma become significant?

Back 342

When the malignant cells invade the muscularis mucosa where they may be borne off to distant sites by the submucosal lymphatics. Malignant transformation is most likely to occur in areas showing a villous architecture.

Front 343

Describe the morphology of villous adenoma

Back 343

usually large (> 2 cm), solitary, firm, gray-tan, sessile lesions that occur most frequently in the rectosigmoid area.

Front 344

What do villous adenoma's look like histologically?

Back 344

more than 50% of lesion reveals long, slender, villous, "finger-like" projections having a scant fibrovascular core and lined by pseudostratified epithelium with varying degrees of cellular dysplasia.

Front 345

If you find a villous adenoma, what should be considered? Factors?

Back 345

30-50% have undergone malignant transformation at time of dx and, of these, about half will have invaded through the muscularis mucosa. The larger the tumor, the greater the chance of invasive carcinoma.

Front 346

What are clinical signs of villous adenoma?

Back 346

May be asymptomatic but more often produce rectal bleeding and/or copious mucoid diarrhea with resultant loss of protein, fluid, and electrolytes (particularly K+).

Front 347

What is difference between tubulovillous and tubular adenoma?

Back 347

Tubular adenoma can have up to 25% villous component whereas, tubulovillous adenoma can have up to half villous. Remember that the malignant potential is proportional to the degree of villous component.

Front 348

What is genetics of familial polyposis coli?

Back 348

AD, a mutation of the APC (adenomatous polyposis coli) gene located at C-5q

Front 349

Describe onset of familial polyposis coli.

Back 349

Appearance during the teenage years of thousands of neoplastic polyps (tubular adenomas) of mainly colon. Unless the colon is resected, carcinoma invariably develops by the age of 40 years.

Front 350

What must be done w/ familial polyposis coli?

Back 350

Must remove colon due to carcinoma.RF

Front 351

What disease is classified by polyposis of colon, small bowel, and stomach? Genetics?

Back 351

Gardner's syndrome, AD

Front 352

What is Gardner's Syndrome a/w/?

Back 352

a/w/ benign lesions of skin (epidermoid cysts), soft tissue (fibroma, lipoma), and/or bone (osteomas). There is inevitable development of colon carcinoma.

Front 353

What disease is char by colonic polyposis in a/w/ malignancies of CNS?

Back 353

Turcot syndrome is a/w/ CNS tumors including medulloblastoma, glioblastoma, ependymoma and there is a high risk of developing colon cancer

Front 354

What tumor is solid and when in small intestine appears as dumbell shaped?

Back 354

Leiomyoma, from smooth muscle

Front 355

What are the m.c. malignant tumors of small bowel?

Back 355

Carcinoid tumors and lymphoma

Front 356

Describe primary small bowel adenocarcinomas

Back 356

Rare, they usually arise in the ileum and produce a constricting mass but rarely cause symptoms until late in the course of the disease. They spread to involve regional lymph nodes, liver, lungs, and other viscera.

Front 357

Why do small bowel adenocarcinomas present late in disease stage?

Back 357

Carcinomas of small intestine are slow constricting pattern lesions. They form inter-luminal ring pattern. Late signs only b/c only liquids in small intestine

Front 358

What carcinoma presents with jaundice?

Back 358

Carcinomas that involve the ampulla of Vater. Should see dilation of both common bile duct and systemic jaundice signs.

Front 359

Who tends to get colorectal malignancies in USA?

Back 359

About 5% of population will get it, with most appearing over 50 y.o.

Front 360

Where in colon do you find most malignant lesions?

Back 360

About half are in rectal-sigmoid and about 40% are seenon cecum and ascending colon.

Front 361

What type of diet has been a/w/ colorectal cancer?

Back 361

High calorie diet rich in red meat and low in fiber. Red meats increase bile acid secretion, therefore it is concentrated within bowel. The bile acid become secondary acids that may be directly toxic to mucosa or potentiate action of various carcinogens.

Front 362

How does fiber help reduce colorectal cancer risk?

Back 362

↑ fiber intake may be beneficial since fiber may bind to potential carcinogens and lower their concentration. It also increases the stool bulk thereby speeding the transit time through the bowel.

Front 363

Describe the genetic alterations in the progression of colorectal cancer.

Back 363

Normal goes APC gene mutation -> Proliferation goes K-ras mutation -> Intermediate adenoma goes DCC gene loss (18q LOH) -> Late adenoma goes p53 mutation (17p LOH) -> carcinoma -> metastasis

Front 364

What would a left sided colon carcinoma appear as?

Back 364

These tumors begin as small plaques which tend to remain superficial, but over the course of 1-2 years completely encircle the lumen.

Front 365

How do left sided colon carcinoma spread?

Back 365

Tumor then begins to invade deeper into wall of colon and as it compromises blood supply, ulceration of central portions occur. It may spread by direct extension into surrounding fat or metastasize to regional LNs.

Front 366

Where does left side carcinoma metastasis?

Back 366

primarily to the liver, but lung, bone marrow, brain, and other visceral metastases can also occur

Front 367

What would a right sided colon carcinoma appear as?

Back 367

tumors also begin as mucosal indurations but tend to develop into a fungating mass lesion that protrudes into the lumen

Front 368

How do right sided colon carcinoma spread?

Back 368

o They eventually may spread to mesentery by direct extension or metastasize to regional LNs and other viscera.

Front 369

What side of colon cancer would you see obstructive symptoms?

Back 369

Left

Front 370

How would pts w/ right side colon cancer present?

Back 370

pts often have occult blood in stool and present with symptoms (weakness, malaise, etc) related to a microcytic, hypochromic (iron deficiency) anemia and weight loss.

Front 371

How sensitive is Guaiac test for colon cancer?

Back 371

It is positive in less than half of the cases of asymptomatic colorectal carcinoma.

Front 372

What marker in serum is seen w/ colon cancer? How does this correlate w/ disese?

Back 372

Elevated levels of carcinoembryonic antigen (CEA) in the serum is usually only seen in advanced carcinoma (Stage B2 or greater) and is not appropriate as an early screening mechanism

Front 373

What is CEA good for in colon cancer?

Back 373

It and is not appropriate as an early screening mechanism b/c must be at stage 2 or higher. It may, however, be valuable in following the course of the disease and detecting the presence of metastases or recurrences.

Front 374

Give stage of modified dukes classification and 5yr SR for following: Limited to mucosa or submucosa

Back 374

Stage A - 95% 5yr SR

Front 375

Give stage of modified dukes classification and 5yr SR for following: Extension into but not through the muscularis propria. Negative lymph nodes.

Back 375

Stage B1 - 85% 5yr SR

Front 376

Give stage of modified dukes classification and 5yr SR for following: Extension through wall. Negative lymph nodes.

Back 376

"Stage B2 - 70% 5yr SR

Front 377

Regional lymph node involvement."

Back 377

Stage C1 - 50% 5yr SR

Front 378

Regional lymph node involvement."

Back 378

Stage C2 - 35% 5yr SR

Front 379

Give stage of modified dukes classification and 5yr SR for following: Distant metastases

Back 379

Stage D - <10% 5yr SR

Front 380

Describe a non-neoplast mucocele and what it can lead to?

Back 380

Local obstruction of lumenal drainage of appendix or hyperplasia of mucosa with excessive mucus production may lead to a distended appendix

Front 381

What malignant neoplasm is char by excessive production of mucin and will seed the peritoneal cavity?

Back 381

APPENDICEAL MUCINOUS CYSTADENOCARCINOMA

Front 382

If pseudomyxoma peritonei occurs in males think what?

Back 382

appendical malignancy

Front 383

If pseudomyxoma peritonei occurs in females think what?

Back 383

ovarian malignancy

Front 384

What is the most frequent cause of mucoid filled cystic dilated appendix?

Back 384

APPENDICEAL MUCINOUS CYSTADENOMA

Front 385

What is the difference between Appendiceal mucinous cystadenoma and cystadenocarcinoma?

Back 385

The cystadenoma does not seed the peritoneal cavity nor produce pseudomyxoma peritonei

Front 386

What is char by spindle cell neoplasm of GI tract?

Back 386

GI stromal tumors, majority arise from SM and may be malignant or benign in natural.

Front 387

How do tumor of anal canal present?

Back 387

often present with bleeding, pain, and presence of a mass in anal canal

Front 388

What are the predisposing factors for anal cancer?

Back 388

chronic irritation, viral infections

Front 389

How are anal cancers divided?

Back 389

They are divided into keratinizing and nonkeratinizing squamous cell carcinomas, although their microscopic patterns may be varied (cloacogenic carcinoma, mucoepidermoid carcinoma, transitional carcinoma, basaloid carcinoma, etc)

Front 390

How is anal cancer tx?

Back 390

treated with a combination of radiation therapy and chemotherapy

Front 391

What does the liver and gallbladder develop from?

Back 391

From a diverticulum which arises from ventral foregut

Front 392

What % does the liver receive blood from portal vein?

Back 392

75% portal vein and 25% hepatic artery

Front 393

What are the anastomoses between portal and systemic venous circulations?

Back 393

gastric and esophageal veins; para-umbilical veins; hemorrhoidal veins; and retroperitoneal veins.

Front 394

Describe the histology of hepatic lobules.

Back 394

classic hexagonal hepatic lobule is centered around central vein with chords of hepatocytes radiating out toward portal tracts that contain branches of hepatic artery and portal vein and bile ducts

Front 395

What is the limiting plate?

Back 395

hepatocytes surrounding portal tracts

Front 396

Describe the hepatic acinus

Back 396

functional hepatic acinus is centered around portal tract (zone 1) and delimited by central veins (zone 3)

Front 397

What is the best perfused and worst perfused area in liver?

Back 397

The best perfused area is the periportal region (zone 1) and the worst is the centrilobular region (zone 3)

Front 398

Where does majority of bilirubin derive from?

Back 398

3/4 comes from breakdown of RBCs in reticuloendothelial system where heme pigment is converted to biliverdin, then to bilirubin

Front 399

What is danger of hyper-unconjugated bilirubin?

Back 399

It may become more than capacity of albumin (>20 mg/dL), thus it may cross the BBB and cause kernicterus

Front 400

What are the signs of kernicterus and where does the bilirubin localize to cause this?

Back 400

Kernicterus will result in brain damage and can cause death. Bilirubin localizes to the basal ganglia and cerebral cortex.

Front 401

How is conjugated bilirubin created and where?

Back 401

Bilirubin dissociates from albumin at liver CM and enters hepatocyte where, in ER, it is made water soluble by conjugation to glucuronic acid through NZM glucuronyl (UDP) transferase. When present in blood, conjugated bilirubin is only loosely bound to albumin and excreted in urine. The hepatocyte excretes conjugated bilirubin into bile canaliculi by rate-limiting mechanism.

Front 402

Describe process of discharge of bile into duodenum

Back 402

Upon appropriate stimulus, such as ingestion of a fatty meal, the sphincter of Oddi at ampulla of Vater relaxes, and gallbladder contracts to discharge bile into the duodenum.

Front 403

Describe the processes of bile in the bowels.

Back 403

Diglucuronide is split and the bilirubin is converted by small bowel bacteria to urobilinogen (UBG). Some of the UBG reabsorbed into the portal circulation and some passes into general circulation to be later excreted by the kidneys. The UBG left in the stool is oxidized to urobilin which is partially reason for normal brown shit color

Front 404

What form of bilirubin is reabsorbed in terminal ileum?

Back 404

urobilinogen (UBG)

Front 405

What is the dominant form of bilirubin in the blood?

Back 405

95% in serum is unconjugated

Front 406

How can you measure serum bilirubin levels?

Back 406

Van den Bergh rxn. Bilirubin reacts w/ diazo reagent causing breakdown of tetrapyyrole of two azopyyrole. Indirect form reacts slowly w/ diazo reagent, whereas direct reacts quickly.

Front 407

What levels of bilirubin must be present to see jaundice?

Back 407

1.8 - 3 mg/dL

Front 408

What are the most frequent causes of juandice?

Back 408

hepatitis, cirrhosis, extrahepatic biliary obstruction and drug-induced cholestasis

Front 409

Describe signs of hemolytic anemia

Back 409

↑ levels of unconjugated bilirubin and mild jaundice. Serum bilirubin levels rarely >5 mg/dl b/c liver is capable of conjugating and excreting most overload.

Front 410

Describe process of hepatice cell uptake of unconjugated bilirubin

Back 410

unconjugated bilirubin separates from albumin prior to being taken up. Inside cell, bilirubin is picked up by acceptor proteins and ultimately transported to ER to be conjugated.

Front 411

What drug is a major source of interference in uptake of unconjugated blirubin?

Back 411

Rifampin

Front 412

Why do some newborns have jaundice? Tx?

Back 412

Due to immaturity of the hepatic conjugating system. Jaundice results from more unconjugated bilirubin. Phototherapy can breakdown bilirubin to smaller, more polar, less toxic derivatives which are excreted in bile or urine.

Front 413

How can breast feeding create jaundice?

Back 413

It may be related to glucuronidases present in breast milk which allows ↑ intestinal absorption of Adecongugated bilirubin. There may also be some depression of UDP transferase activity.

Front 414

What is the genetics and NZMatic changes of Gilbert Syndrome?

Back 414

AD disease, these pts have ↓ UDP-transferase activity, 30% of normal

Front 415

What are the signs of Gilbert syndrome?

Back 415

Labs show high uncongjugated and low conjugated bilirubin levels. Usually detected only as an incidental lab finding (usually < 3 mg/dl.) or when an unrelated event transiently elevates bilirubin levels further, producing jaundice.

Front 416

What disease is noted for taking no UDP-transferase? Genetics? Problems?

Back 416

Crigler-Najjar syndrome type I, AR. ↓ bilirubin conjugation and kernicterus invariably develops with pts ultimately dying of CNS problems.

Front 417

What disease is noted for having low levels of UDP-transferase? Genetics? Problems?

Back 417

Crigler-Najjar syndrome type II, AD. There is normal conjugation bilirubin concentrations and is not fatal.

Front 418

What disease involving hyperbilirubinemia in newborns will respond to Phenobarbital?

Back 418

Physiological Jaundice, Breast milk Jaundice, CN type II. Only CN type I will not respond.

Front 419

What results in cholestasis?

Back 419

Interference with excretion of conjugated bilirubin may occur anywhere between liver cell and ampulla of Vater

Front 420

How do you tx extrahepatic and intrahepatic jaundice?

Back 420

Extrahepatic by surgery and intrahepatic by drugs

Front 421

What are some signs of intrahepatic causing jaundice?

Back 421

↑ levels of transaminases and LDH, and also may result in ↓ prothrombin levels with consequent prolonged PT

Front 422

What disease appears in adults as mild conjugated bilirubinemia and accumulation of dark pigment in hepatocytes?

Back 422

Dubin-Johnson syndrome, the problem is due to excretion of conjugated bilirubin

Front 423

What are some drugs that can cause jaundice?

Back 423

Estrogen, OC, anabolic steroids

Front 424

What is some extrahepatic causes of jaundice?

Back 424

result from narrowing or obstruction of biliary tract or ampulla of Vater.

Front 425

Blockage of the hepatic duct can be due to what?

Back 425

sclerosing cholangitis, cholangiocarcinoma

Front 426

Blockage of the common bile duct can be due to what?

Back 426

pancreatic carcinoma, post-op stricture, and choledocholithiasis

Front 427

Blockage of the ampulla of vater can be due to what?

Back 427

ampullary carcinoma

Front 428

How does extrahepatic obstruction effect liver architecture?

Back 428

Bile backs up into intrahepatic ducts and induces proliferation of portal tract bile ducts which also become twisted and tortuous. Acute inflammatory cells may be present in the portal areas indicating infection proximal to obstruction. Ultimately canaliculi rupture to produce "bile lakes" containing dead bile-stained hepatocytes.

Front 429

How is the stool changed in obstructive jaundice?

Back 429

Stools lose their normal color to become clay-colored (acholic stools). Lack of bile in the gut also causes ↓d absorption of fats and fat-soluble vitamins causing a temporary malabsorption syndrome to develop.

Front 430

What are some other blood changes seen w/ chronic obstructive jaundice?

Back 430

The accumulation of bile acids in the blood causes pruritus. Plasma cholesterol levels also increase due to both ↑ hepatic synthesis and ↓d excretion.

Front 431

How is obstructive jaundice induced hypercholesterolemia manifested early and late?

Back 431

Early by xanthelasma at inner canthus of eyes and spreading laterally. Later tuberous xanthomas may develop on extensor surfaces, in pressure areas, and in scars. Discoloration of the nails by bile pigment and clubbing of the digits may also occur.

Front 432

What are expected lab signs of cholestasis only?

Back 432

↑serum APase, normal or prolonged PT (extrinsic pathway), and normal albumin

Front 433

What are expected lab signs of Hepatocellular Necrosis?

Back 433

↑ALT and APase(?), normal or prolonged PT, and decreased albumin

Front 434

Quickly name causes of unconjugated hyperbillrubinemia.

Back 434

↑ bilirubin production, Fasting, Gilbert syndrome, CN syndrome, erythrocytes abnormalities, hematoma breakdown

Front 435

Quickly name causes of conjugated hyperbillrubinemia.

Back 435

Intrahepatic disorder, Dubin-Johnson syndrome, Rotor syndrome, Pncreatic and Biliary pathology, Viral hepatitis, EtOHism, cirrhosis, sepsis, choledocholithiasis

Front 436

What is the main cause of jaundice in infants?

Back 436

Most is physiologic

Front 437

What is the main cause of jaundice in adolescents?

Back 437

1/2 gilbert’s syndrome (indirect hyperbilirubinemia) and next is viral hepatitis

Front 438

What is the main cause of jaundice in young adults?

Back 438

most is viral hepatitis, EtOHism, autoimmune in females, and biliary tract

Front 439

What is the main cause of jaundice in elderly?

Back 439

50% malignancy, also toxicity from drugs, stones….

Front 440

Describe the pattern of injury - cholestatis

Back 440

drugs that interfere with the excretion of conjugated bilirubin and other organic anions from the hepatocytes. Microscopically, intracytoplasmic bile pigment is present within swollen hepatocytes and Kupffer cells, and small bile plugs are seen in the canaliculi

Front 441

Describe the pattern of injury - cholestatis and focal necrosis

Back 441

in addition to cholestatic changes, there may be focal necrosis of the hepatocytes with a scant mononuclear infiltrate. Adjacent portal triads may contain lymphocytes or eosinophils.

Front 442

Name drugs that cause necrosis of liver

Back 442

Certain drugs (halothane, isoniazid, etc) may produce either zonal or massive necrosis of the liver. This may be followed by fibrosis/cirrhosis.

Front 443

Name drugs that can cause neoplasia in liver

Back 443

oral contraceptives, anabolic steroids

Front 444

What histo changes occur w/ acute congstion of liver?

Back 444

Enlarge liver engorged w/ blood. Central veins of lobules are dilated and appear dark purple-red. If sever sinusoids may rupture and produce central hemorrhagic necrosis.

Front 445

What lab values are expected w/ acute liver congestion?

Back 445

LDH become elevated almost immediately and ALT may become slightly elevated

Front 446

If you see hemorrhage around central vein think what?

Back 446

acute congestion

Front 447

What is major sign of chronic congestion?

Back 447

Nutmeg liver due to congested central portions of lobule becoming depressed. There is irregular dilation of sinusoids progressing toward periphery of lobule.

Front 448

Long standing pressure within liver lead to what?

Back 448

Cause atrophy or necrosis of adjacent liver cells and then fibrosis of necrotic areas may lead to cardiac sclerosis. Fibrosis produces shrunken liver w/ fine granular pigskin surface.

Front 449

What type of infarct results in pale possible hemorrhagic area?

Back 449

Arterial infarction

Front 450

What type of infacrt results in purplish discoloration of parenchyma?

Back 450

Venous infarction

Front 451

Where are arterial occlusions most dangerous?

Back 451

When it occurs distal to Gastroduodenal artery

Front 452

What are possible causes of venous infarction?

Back 452

Regional infections, thrombus from portal vein, hypercoagulable states, or external compression

Front 453

What area is most effected by systemic hypotension?

Back 453

Centilobular area (zone 3) regions

Front 454

What is seen in pregos that develop sudden acute painful enlargement of liver along w/ subc veins of abdomen?

Back 454

Budd-Chiari results from thrombosis of major hepatic veins or IVC. Sudden occlusion causes an acute painful enlargement of the liver. Severe, intractable ascites develops and patients usually die in hepatic failure. If the obstruction develops insidiously, liver enlargement is gradual and less painful, but ascites develops nonetheless.

Front 455

What histo changes occur w/ Budd-Chiari syndrome?

Back 455

Blockage of outflow of blood results in sinusoidal congestion. Central veins become thickened, sometimes with atrophy of the adjacent hepatocytes and delicate fibrosis in the central regions of the liver lobules. Should see centrilobular necrosis and hemorrhage.

Front 456

What is a serios complication in BM transplant pts who have had radiation and/or chemotherapy?

Back 456

Veno-occlusive disease

Front 457

What histo changes seen w/ Veno-occlusive disease?

Back 457

toxic damage to small branches of the hepatic veins with subendothelial edema obstructing blood flow and leading to central vein congestion and necrosis of adjacent hepatocytes.

Front 458

What are signs of portal vein thrombosis?

Back 458

The liver is not enlarged or tender but portal HTN will occur and result in congestive splenomegaly and circulatory diversion through systemic venous anastomoses especially retroperitoneal and esophageal veins.

Front 459

What is the principal cause of death for pts w/ cirrhosis?

Back 459

The principle cause of death in about 1/2 of pts w/ cirrhosis is bleeding from ruptured esophageal varices.

Front 460

What % pts w/ cirrhosis develop hemorrhoidal?

Back 460

50%

Front 461

What can develop from hypersplenism?

Back 461

anemia, leukopenia, and thrombocytopenia and, especially if combined with abnormalities of clotting factors, the patient may develop a hemorrhagic diathesis.

Front 462

What drives ascites?

Back 462

↑ sinusoidal pressures drive the venous fluid across the discontinuous endothelial lining of the sinusoids and into the hepatic lymphatics where it ultimately weeps in large quantities from the surface of the liver into the peritoneal cavity.

Front 463

What effects does ascitis have on rest of body and its response?

Back 463

Sequestration of fluid in the peritoneal cavity reduces renal blood flow which stimulates renin activity to retain sodium and water thereby entering into a vicious cycle. Liters of ascitic fluid may accumulate and produce discomfort due to distension of the abdomen.

Front 464

What effect does removal of ascitis cause?

Back 464

Drainage of such fluid produces considerable loss of protein and electrolytes. Removal of ascitic fluid is often followed by prompt reaccumulation since the rate of exchange of the peritoneal fluid with the plasma is as high as 80% per hour. Red cells and neutrophils are normally not present in ascitic fluid, although mesothelial cells and a few lymphocytes may be present normally.

Front 465

If you see RBC in ascitis fluid, what would you assume? Neutrophils?

Back 465

The presence of red cells in ascitic fluid may indicate possible involvement of the peritoneal surfaces by malignancies. The presence of large numbers of neutrophils probably indicates peritoneal irritation, most likely peritonitis.

Front 466

What is a bacteria infection of bile ducts called?

Back 466

Cholangitis, it begins as complication of obstruction of common bile duct by gallstones or carcinoma at head of pancrease.

Front 467

What are clinical signs of cholangitis?

Back 467

High fever and large tender liver, signs similar to acute cholecystitis.

Front 468

What is histo change of cholangitis?

Back 468

There is necrosis and biliary stasis. It is centered around bile ducts, where neutrophilic infiltrates.

Front 469

What is the causative organism of liver abscess?

Back 469

E. coli or other intestinal organisms, streptococcus or staphylococcus, septic emboli or bacteria from bacterial endocarditis.

Front 470

How do most asbcess appear in liver?

Back 470

Usually small and widely distributed thoughout liver

Front 471

What is the m.c.c. of jaundice? Histo changes?

Back 471

Viral hepatitis, Swollen hepatocytes and infiltrates around central vein

Front 472

What hep virus is spread by close contact?

Back 472

Hep A

Front 473

What is the first serum sign of Hep A?

Back 473

Spike in ALT that last around month, then rise of HAV-IgM antibodies

Front 474

What is Hep A clinical outcome of kid under 6 y.o. verses an 18 y.o.?

Back 474

If kid < 6 y.o. then 90% have asymptomatic course whereas, 75% of pts > 14 y.o. develop liver disease or failure

Front 475

What are signs of Hep A?

Back 475

Flu-like symptoms, some become icteric w/ jaundice, malaise and loss of appetite, mild N/V, and elevated ALT and AST.

Front 476

What present as flu like w/ itching and elevated Apase, that last few weeks?

Back 476

Cholestatic Hep A

Front 477

Describe Fulminant Hep A failure

Back 477

seen in .5% pts, mostly older, and consist of acute Hep A plus encephalopathy, a/w/ cerebral edema, ↑ PT and has high mortality rate.

Front 478

Who should receive Hep A vaccine?

Back 478

Give to high risk pts: travels to endemic areas, man-on-man, IV drug user, persons w/ chronic liver disease, and high risk communities (native Americans, school kids, and Alaskan natives)

Front 479

When should pt receive Hep A vaccine?

Back 479

"Pre-exposure – give few days before leaving; Post-exposure – given w/in 14 days;

Front 480

What Hep virus is ds DNA?

Back 480

Hep B

Front 481

What is E antigen of Hep B dependent on?

Back 481

Core antigen gene has pre-core area (pre-C) that some pts have virus w/ a mutation here that prevents E antigen from being made

Front 482

How is Hep B spread and where is it prevelent?

Back 482

Very common with mother-child transmission at birth, common in Asia. Also can be by IV drug use, transfusion, occupational exposure, household contacts, perinatal, and sexual (m.c.)

Front 483

Who is most likely to develop chronic Hep B?

Back 483

The younger the pt the more likely

Front 484

Pts w/ chronic HBV infection are at increased risk to develop what?

Back 484

cirrhosis and hepatocellular carcinoma (HCC)

Front 485

What is major antigens seen w/ HBV?

Back 485

HBsAg, HBcAg (core antigen), and HBeAg

Front 486

What is sign of actively replicating chronic HBV?

Back 486

HBeAg(+)> 6 months, serum HBV DNA (>million copies/mL), persistent elevated ALT, and liver biopsy (HAI>4)

Front 487

If pt is HBeAg(-), what does that mean?

Back 487

They are inactive carriers or have mutation that leads to no production of E antigen and are really Hep B cases.

Front 488

What are predictors of HBeAg clearance?

Back 488

Older age and elevated ALT

Front 489

What are signs of inactive carriers of HBV?

Back 489

HBsAG will be present > 6 months after infection, they will be HBeAg(-) but will have anti-HBeAg antibodies. Usually will be <100,000 HBV-DNA, normal liver NZMs.

Front 490

How do you tx inactive carrier?

Back 490

They require no tx but must be followed since they can revert to disease state. If they lose HBsAg then no need to follow.

Front 491

What is important to monitor in pts w/ HBV?

Back 491

Watch for encephalopathy, PT (sign of acute liver injury)

Front 492

What is goals of tx for HBV?

Back 492

sustained suppression of HBV replication, measured by HBV DNA present in blood; remission of liver NZMs; no HCC or cirrhosis

Front 493

What is potential drugs for HBV?

Back 493

Interferon alpha, Lamivudine, Adefovir, and Dipivoxil

Front 494

What type of drug is Lamivudine and what is its efficacy?

Back 494

Nucleoside analog, low AE. 15% chance of seroconversion, the higher pts ALT at beginning of tx more likely to seroconvert.

Front 495

What drug is used if HBV is resistent to Lamivudine? AE?

Back 495

Adefovir and dipivoxil, nucleoside analog, has no recorded resistent after one year. It has dose dependent nephrotoxicity. It has less of an impact on HBV DNA levels then Lamivudine.

Front 496

What is contained in Hep B vaccine?

Back 496

HBsAg, should have >10 IU/L antibodies to be protected

Front 497

How do you protect newborns from Hep B virus?

Back 497

Give vaccine and HBV immune globulins. Must give another IG at 1 and 6 months.

Front 498

What is biggest sign that mother-child Hep-B transmission will occur?

Back 498

If she is HBeAg(+), 90% chance. If just HBsAg(+) then just 10% chance

Front 499

What is the m.c.c. of liver disease in US?

Back 499

Hep C

Front 500

How is Hep C primarily spread?

Back 500

Blood-Blood transmission, mainly via IV drug users (60%) and sexual contact (18%).

Front 501

What are signs of Hep C?

Back 501

Acutely pt will have mid flu-like sympoms. But 20 yrs post-infection, they will have cirrhosis and other complants.

Front 502

What % pts w/ HBC will develop cirrhosis?

Back 502

20%

Front 503

If pt clears virus when does this occur?

Back 503

First six months

Front 504

What factor are a/w/ fibrosis?

Back 504

Duration of infection, EtOHism, older than 40 y.o. at time of infection, and being male

Front 505

What stage of fibrosis in chronic HCV is mild disease w/ increased collagen limited to portal area?

Back 505

Stage 1 - portal

Front 506

What stage of fibrosis in chronic HCV is fibrosis extending out of portal areas but do not interconnect?

Back 506

Stage 2 - periportal

Front 507

What stage of fibrosis in chronic HCV is bridging fibrosis from one portal area to another?

Back 507

Stage 3 - septa formation

Front 508

What stage of fibrosis in chronic HCV is sepa forming network of interconnecting bands surrounding nodules of liver cells?

Back 508

Stage 4 - cirrhosis, at this point the original arch of liver has been transformed

Front 509

What can accelerate HCV progression to cirrhosis?

Back 509

Co-infection w/ HIV

Front 510

In what pts should be checked for HCV antibody?

Back 510

pts w/ RF for HCV, have elevated ALT, cryoglobulinemia, or porphyria cutanea tarda

Front 511

If pt has HCV antibody what should you check next?

Back 511

Check HCV RNA level and genotype. Consider liver biopsy

Front 512

What is the m.c. genotype of US?

Back 512

Type #1

Front 513

What is the easiest and hardest HCV to tx?

Back 513

The easiest is #2. The hardest is #1 and #4.

Front 514

What is aims of tx for HCV?

Back 514

Mainly eradicate virus. But also prevent progression to cirrhosis, reduce HCC incidence, reduce need for transplant, and enhance survivial.

Front 515

What are signs of early virological response?

Back 515

decrease in HCV RNA by >2logs after 12 weeks of therapy. If there is a response you continue tx

Front 516

What is end of treatment response?

Back 516

HCV RNA <50 IU/mL at end of tx

Front 517

What is sustained virological response?

Back 517

HCV RNA < 50 IU/mL 6 months after completing tx. If SVR occurs then usually not get virus back.

Front 518

What is best tx for HCV?

Back 518

PEGINF/Ribavirin: 55% reached SVR

Front 519

What is AE of INF?

Back 519

INF AE: flu-like symptoms, injection site rxn, myalgia, arthralgia, N/V, anorexia, weight loss, depression, BM suppression, thyroid dysfnct, exacerbation of underlying immune disease

Front 520

What is AE of Ribavirin?

Back 520

Ribavirin AE: teratogenic, hemolytic anemia, skin rash, cough, and insomnia

Front 521

What are hematologic effects of HCV?

Back 521

essential mixed cryroglobulinemia, NHL

Front 522

What are renal effects of HCV?

Back 522

membranoproliferative glomerulonephritis, membranous nephropathy

Front 523

What are derm effects of HCV?

Back 523

poprphyria cutanea tarda, leukocyte vasculitis, lichen planus

Front 524

What are autoimmune effects of HCV?

Back 524

DM, idiopathic thrombocytopenic purpura

Front 525

What % of pts w/ essential mixed crytoglobulinemia have HCV-RNA?

Back 525

> 90 %

Front 526

What is the smallest Hepatitis virus and what is it dependent on?

Back 526

HDV is smallest virus and is a defective virus. It is dependent on HBsAG to replicate. It has only one protein, a core protein known as delta antigen.

Front 527

If pt has both HBV and HDV RNA present, what do you assume?

Back 527

They experienced coinfection, and would have had two separate ALT peaks. This condition will result in more serious disease w/ higher chance of liver failure.

Front 528

If pt has rapidly developing cirrhosis, w/ fulminant hepatic failure, and pt is positive for HBV and HCV?

Back 528

They experienced superinfection, where pt was chronic carrier of HBV and was infected by HDV. This conditon can cause increased incidence of fulminant, life-threatening hepatitis, chronic hepatitis, and liver failure.

Front 529

If prego goes to 3rd world country and then develops hepatitis, what type does she have?

Back 529

Hep E, found in water supplies in tropical and 3rd world countries.

Front 530

Prego's w/ Hep E have greater risk of developing what?

Back 530

Fulminant clinical course

Front 531

What does HEV resemble?

Back 531

HAV w/ the only exception being high mortality in prego's

Front 532

What are histo signs of Hepatitis?

Back 532

During prodromal period injured cells swell and cytoplasm appears vacuolated (ballooning degeneration). Hepatocytes may undergo apoptosis leaving behind Councilman bodies. Hepatocellular necrosis may be extensive forming bridging necrosis. Kupffer cells become more prominent. Infiltrate can be seen in portal areas and areas of necrosis. There maybe evidence of regeneration by binucleated cells. Droplets of bile pigment can be seen in Kupffer cells and inspissated w/in canaliculi. There cna be lobular disarray as well.

Front 533

Dx of chronic hepatitis consist of what?

Back 533

indication of the severity of the inflammatory response (grading), the degree of fibrosis (staging) and, if possible, a statement as to the likely etiology

Front 534

What type of Hep is most likely to result in chronic Hepatitis?

Back 534

Hep C

Front 535

What are clinical signs of chronic hepatitis?

Back 535

Low grade lesions present as a vague recurrent symptoms of malaise, weakness, loss of appetite, RUQ discomfort and occasionally mild jaundice in about 1/2 of pts. The others remain asymptomatic.

Front 536

What is liver histo changes seen w/ chronic hepatitis?

Back 536

Liver histology reveals mononuclear inflammation (lymphocytes, macrophages, and plasma cells) spilling out of the portal areas with piecemeal necrosis (destruction of the limiting plates) and, in severe cases, bridging necrosis with extensive fibrosis and cirrhosis.

Front 537

What is causes nodules seen w/ cirrhosis?

Back 537

If total lobule and its reticulin framework are destroyed, adjacent liver cells may proliferate producing nodules of hepatic cells which lack normal canalicular and sinusoidal relationships. Such cells can function in normal metabolic activities of liver but cannot normally excrete bile.

Front 538

What is the m.c. form of cirrhosis in US?

Back 538

Laennec's Cirrhosis, due to EtoHism

Front 539

Ingested of ethanol results in what changes to liver over time?

Back 539

"↑ transport of fat from periphery of body to liver; reduced FA oxidation in liver; ↑ synthesis of triglycerides; mobilization of lipids as lipoprotein is impaired

Front 540

What are some early histo signs of laennec's cirrhosis?

Back 540

Hepatic cells may be swollen with some bile stasis apparent in bile canaliculi and in hepatocytes. Frequently, Mallory bodies are present w/in cytoplasm of scattered liver cells many of which are necrotic and surrounded by neutrophils.

Front 541

What are some late histo signs of laennec's cirrhosis?

Back 541

Active fibroblastic proliferation produces progressive fibrosis w/in lobule. Gradually, liver size ↓ (<1.2 kg) and demonstrates micronodular cirrhosis w/ yellow-orange color. As liver shrinks, fat tends to disappear and liver becomes progressively darker brown.

Front 542

What are clincal signs of liver cirrhosis?

Back 542

non-specific symptoms of weight loss, anorexia, nausea, vomiting and vague GI complaints occur.

Front 543

If small liver has variable sized regenerative nodules interspersed among depressed scars, what is disease?

Back 543

Postnecrotic cirrhosis, seen after episode of viral hepatitis or drug or chemical toxicity which resulted in acute hepatocellular necrosis.

Front 544

What is histo change of postnecrotic cirrhosis?

Back 544

irregular coarse scarring with only occasional scattered bile ducts and blood vessels in the scars. Occasional areas of persistent normal liver parenchyma may be present between scars, but most areas are regeneration of liver cells in large disorganized masses. Prominent bile stasis is usually present in regenerative nodules.

Front 545

What type of cirrhosis is HCC most frequently a/w/?

Back 545

HCC

Front 546

What are key factors of dx primary biliary cirrhosis?

Back 546

Antimitochondrial IgM antibodies(90% pts), elevated serum cholesterol levels, and skin xanthomas. Splene is often enlarged due to portal HTN.

Front 547

What are early histo changes seen w/ primary biliary cirrhosis?

Back 547

Septal and larger interlobular bile ducts are damaged and surrounded by a dense infiltrate of lymphocytes, histiocytes, plasma cells, and occasionally eosinophils. Poorly defined granulomas may be present. Limiting plate is intact.

Front 548

What are late histo changes seen w/ primary biliary cirrhosis?

Back 548

As disease progresses, there is ductular proliferation, fibrosis, and acute and chronic inflammation with granulomas becoming less frequent. Later inflammation subsides and acellular fibrous septa extend from portal tracts into and around lobules. Regenerative nodules develop and cholestasis may become severe.

Front 549

How does primary biliary cirrhosis initally present?

Back 549

Starts most frequently as pruritus w/out jaundice. Jaundice may develop w/in 6-24 months. Pts feel well and have a good appetite in spite of jaundice. Liver is usually enlarged and firm, and spleen palpable. Duodenal ulcers and hemorrhage are common. Portal HTN, w/ bleeding esophageal varices is frequent, but usually a late development.

Front 550

What is histo signs seen w/ secondary biliary cirrhosis?

Back 550

Bile statis develops into plugged bile duct. Bile lakes occur when bile ducts rupture. You often see coiled bile ducts too.

Front 551

What occurs in pts w/ hemochromatosis or hemosiderosis?

Back 551

Pigmentary cirrhosis occurs, the excessive iron is stored in liver and other parts. Thus liver assumes a depper brown color and grossly, similar to Laennec's cirrhosis.

Front 552

Other than pigmentary cirrhosis, what other manifestations can occur w/ hemochromatosis?

Back 552

They can develop DM w/ pigment of pancrease and dark skin due to melanin production. The melanin is result of failure of feedback to shut off pituitary MSH production.

Front 553

What is Wilson's disease a result from?

Back 553

Genetic (AR) error in coding ceruloplasmin, a copper binding protein.

Front 554

What is presentation of Wilson's disease?

Back 554

Usually young adults w/ bird like faces,tremor, behaving oddly and Kayser-Fleisher rings.

Front 555

Where is copper deposited in Wilson's disease?

Back 555

Liver, basal ganglia, cerebral cortex, kidney, and cornea. Wherever copper is deposited, damage to tissues occurs.

Front 556

What do lab test for Wilson's disease show?

Back 556

low serum copper levels, low serum ceruloplasmin levels and ↑ excretion of copper in the urine.

Front 557

What is used to tx Wilson's disease?

Back 557

Penicillamine

Front 558

What would liver biopsy in Wilson's disease show? Stain?

Back 558

Early disease, hepatocellular necrosis accomp by formation of hyaline acidophilic inclusions, Mallory bodies. Rotamine is the stain.

Front 559

If liber biopsy shows piecemeal necrosis of the limiting plate and the scarring tends to be irregular, what disease is present?

Back 559

Alpha-1-Antitrypsin deficiency, AR

Front 560

What is the characterist feature of A-1-Antitrypsin deficiency?

Back 560

round, PAS(+), diastase-resistant bodies w/in cytoplasm of hepatocytes. This represents IC accumulation of alpha-1-antitrypsin

Front 561

What are some causes of hepatic cysts?

Back 561

They can be inherited (polycystic) or acquired (simple)

Front 562

Describe nodular hyperplasia of liver

Back 562

M.C. women and has been a/w/ OC. Large mass w/ central scarring

Front 563

What is the m.c. benign tumor of liver?

Back 563

Cavernous Hemangioma, arise from blood vessels that aregenerally <1 cm and subcapsular

Front 564

Describe histo of hemangioma in liver

Back 564

some show large endothelial lined vascular spaces filled with red cells while others may have become sclerosed by fibrous replacement. Gross they look spongy

Front 565

What is the pattern called of a diffuse angiomatoid lesion throughout liver?

Back 565

Peliosis Hepatis

Front 566

What type of liver tumor is a/w/ CHF? Describe

Back 566

Hemangioendothelioma, well-encapsulated, benign but potentially malignant tumor that usually is found in infant girls and may present as jaundice and hepatomegaly. CHF may occur b/c of AV shunts that form the tumor.

Front 567

Describe the histo of hemangioendothelioma.

Back 567

an orderly proliferation of the small blood vessels, occasionally with an aggressive pattern of darker pleomorphic endothelial cells, is seen.

Front 568

What tumor of liver has spindle shaped endoothelial cells? Describe

Back 568

Angiosarcoma, pleomorphic endothelial cells w/ large hyperchromatic nuclei, giant cells in frequent mitosis and irregular vascular channels.

Front 569

What are known risk factors for angiosarcoma development in liver?

Back 569

vinyl chloride and thorotrast exposure

Front 570

Describe histo of bile duct adenoma.

Back 570

These are usually small encapsulated, spherical, yellow-white nodules ranging < 1 cm in diameter. Microscopically, multiple small acini lined by epithelium and are surrounded by fibrous stroma.

Front 571

What tumor arises from bile duct epithelium to form acini structures lined by mucous secreting cells?

Back 571

Cholangiocarcinoma, abundant fibrosis creates a sclerotic pattern.

Front 572

How do you differentiate Cholangiocarcinoma from HCC?

Back 572

In contrast to hepatocellular carcinoma, cholangiocarcinoma is not a/w/ cirrhosis, AFP is not elevated, and it does not produce bile although bile may be detected in tumor mass when it cannot drain adequately into the external biliary tract. It tends to metastasize earlier and more widely than HCC

Front 573

Who is at an increased risk for developing choangiocarcinoma?

Back 573

Pts w/ thorotrast exposure, hemochromatosis, polycystic disease, or liver flukes

Front 574

What liver tumor consist of primative cells?

Back 574

Hepatoblastoma, a tumor seen mainly before 2 y.o. Fetal and embryonal type hepatocytes may be seen with primitive spindle cells, osteoid tissue, cartilaginous tissue and muscle cell elements.

Front 575

What liver tumor is seen in young women on OC and may hemorrhage into peritoneum during prego?

Back 575

Liver adenoma

Front 576

Describe histo of liver adenoma

Back 576

they are composed of well-diff liver cells w/ sinusoids and plates but lack normal lobular structure or bile ducts. When subcapsular, they may hemorrhage into peritoneum especially during pregnancy. There is no portal tracts present.

Front 577

What are RF for HCC?

Back 577

HBV, HCV, chemicals (vinyl chloride, thorotrast, aflatoxin), liver cirrhosis

Front 578

What is presentation of liver cirrhosis?

Back 578

hepatomegaly, abdominal pain, and abdominal mass. About 15% of pts are jaundiced and 10% are febrile.

Front 579

If pt has cirrhosis what are major signs of HCC development?

Back 579

cirrhotic patients who suddenly develop an enlarged liver, ascites, or deteriorating hepatic function.

Front 580

What extrahepatic changes can occur for pts with HCC?

Back 580

Polycythemia (erythropoietin), hypercalcemia (PTH), hyperlipemia or hypoglycemia

Front 581

How does HCC like to spread?

Back 581

have a propensity to invade hepatic veins and spread hematogenously primarily to lungs. It may also produce a Budd-Chiari syndrome from hepatic vein obstruction. Occasionally, they even extend directly from the hepatic vein into the right side of the heart via IVC.

Front 582

Describe histo of HCC.

Back 582

The cells resemble hepatocytes but may have ↑ cytoplasmic basophilia. In well differentiated tumors, cells tend to form cords, sometimes separated by sinusoids, or pseudoacinar/microacinar structures and may elaborate bile. Others, however, are composed of anaplastic giant cells with abundant cytoplasm and multiple nuclei, frequently in mitosis. Usually, very little fibrous stroma is present in hepatocellular carcinoma.

Front 583

Where do most malignant tumor found in liver originate from?

Back 583

Colon but can be pancreas, lung, breast, and kidney.

Front 584

When is it safe to assume you are dealing w/ a primary tumor of the liver?

Back 584

If pt has cirrhosis

Front 585

What population has a very high rate of gallstone formation? RF?

Back 585

Native Americans and Hispanics. Age is RF

Front 586

What type of gall stones are radio-opaque? Describe their contents, associations, and location.

Back 586

Black pigment stones. They contain bilirubin polymer and calcium salts. They occur in gall bladder and bile duct and are a/w/ hemolysis or cirrhosis. Usually several 100's to 1000's present.

Front 587

What gall stone is a/w/ cholesterol metabolism issues? Describe contents, associations, and location.

Back 587

Cholesterol stones are made up of mainly cholesterol and are radio-lucent. They form in gall bladder and rarely form in common bile duct. They are a/w/ problems in cholesterol metabolism, resulting in excess amounts of cholesterol excreted in bile (rapid weight loss, estrogens, obesity, ethnic differences in cholesterol metabolism).

Front 588

What type of gall stones is seen with infection of bile duct? Describe contents, associations, and location.

Back 588

Brown pigment stones, they contain calcium bilirubin and soaps. They are soft/greasy and radio-lucent, frequently form in the common bile duct, and are a/w/ biliary infection, inflammation, and infestation (such as in Southeast Asia).

Front 589

How do microorganisms cause brown pigment stones?

Back 589

Microorganisms produce glucuronidase that will remove glucuronide from bilirubin, rendering it insoluble and also produce phospholipase, which acts to release free FAs from lecithin into bile which then precipitate as calcium soaps.

Front 590

What increaes risk of developing gall stones?

Back 590

Gall stones are more likely to occur with gallbladder stasis, which can be due to fasting, pregnancy (high estrogen and progesterone), vagotomy, spinal cord injury, diabetes (peripheral neuropathy), obesity, and somatostatin therapy.

Front 591

What presents as postprandial by 1/2 hour, RUQ epigastric steadypain that radiates to right scapula for around 2 hrs? Cause?

Back 591

Biliary Colic, b. Stone impacted in gallbladder neck or cystic duct as bile trying to pass to digest fatty meal. If stone falls back into gallbladder then pain subsides. If it stay stuck then can lead to acute cholocystitis

Front 592

What presents as fever, RUQ pain, and Jaundice?

Back 592

Acute Cholangitis presents as Charcot triad, usually due to GS(-) rod

Front 593

What presents as fever, RUQ pain, jaundice, hypotension, and confusion?

Back 593

Acute Cholangitis but presenting with Reynold's pentad, worse pgx

Front 594

What is the term for blockage of bile duct w/ stone?

Back 594

Choledocholithiasis. Tx w/ usually w/ ERCP w/ sphincterotomy and stone extraction

Front 595

What is term for gallbladder ischemia? Danger? Tx?

Back 595

Acalculous Cholecystitis which is seen in old ill men, can lead to perfusion. TX w/ percutaneous cholecysostomy tube until pt can be stabilized for cholocystectomy.

Front 596

What does pt who has chonic biliary pain w/ no gallstones on US have?

Back 596

They have gallbladder dyskinesia. Tx w/ IV cholecystokinin (stims GB contaction)

Front 597

Who gets gall bladder cancer?

Back 597

Older women, strong a/w/ gallstones. Poot pgxdue due to locally invasive and incurable.

Front 598

What is used to disolve stones in pts who are unfit for surgery? What are requirements?

Back 598

Ursodeoxycholic acid (URSO) or chenodeoxycholic acid. Patient must have a patent cystic duct, and adequate gall bladder emptying based on an oral cholecystogram.

Front 599

What is main cause of acute cholecystitis?

Back 599

Due to obstruction of cystic duct. Less than 10% is due to severe illness, trauma, statis of gall bladder. Acalculous cholecystitis has a high risk of perforation (70%).

Front 600

What unique signs of acute cholecystitis?

Back 600

Murphy's sign, pt will avoid taking a full breath when pressure is applied to RUQ. There is also fever, leukocytosis, and occasional jaundice.

Front 601

What are US signs of acute cholecystitis?

Back 601

thickened gall bladder wall, possibly a gall stone, pericholecystic fluid, an ultrasonographic Murphy’s sign and air in the gallbladder wall

Front 602

If you infect pt w/ radionucleotide scanning agent and the gallbladder filling is absent, why?

Back 602

indicates cystic duct obstruction. The test has a 95% sensitivity.

Front 603

Describe cholangiocarcinoma: source, RF, location, and tx

Back 603

A. Cancer of intra or extra hepatic biliary epithelium, RF of choledochal cyst, C. 2/3 situated at bifurcation of hepatic duct into the R/L main hepatic ducts (Klatskin’s tumor), and tx w/ : resection, liver transplant, palliation of jaundice w/ stints placed at RCP, chemoradiation, photodynamic tx w/ photosensitizing agent and laser directed into duct

Front 604

Primary sclerosing cholangitis leads to what? What is high correlated with this?

Back 604

It leads to hepatic fibrosis and cirrhosis over time. 70% will have IBD due to anti-P-ANCA, ASMA, and ANA antibodies. They have H. High rate of metabolic bone disease, osteopenia and osteoporosis. They can develop dominant biliary strictures. There is increases risk of developing cholangiocarcinoma 15 fold and high rate of colon cancer.

Front 605

What is the m.c. disorder of pancreas?

Back 605

acute and chronic pancreatitis and adenocarcinoma of the pancreas

Front 606

What are the m.c.c. of acute pancreatitis in US?

Back 606

chronic alcohol use and gallstones

Front 607

What present w/ epigastric pain, which radiates to mid back?

Back 607

acute pancreatitis

Front 608

What does severe pancreatitis present as?

Back 608

fever, hypotension, severe electrolyte disorders, and other organ failure including renal failure, respiratory failure, and a sepsis shock-like syndrome

Front 609

What is an area of pancreatic juice in nonepithelialized wall? When does it occu?

Back 609

pseudocyst, generally requires 4-6 weeks to develop after an attack of acute pancreatis.

Front 610

How do pancreatic abscess form?

Back 610

abscess is circumscribed region of pus that is usually due to infection of pre-existing pseudocyst.

Front 611

What is used to tx pancreatitis?

Back 611

o Initially rest the GI tract by making pt NPO, aggressive IV hydration b/c of often extensive 3rd-spacing of fluid into retroperitoneum, correction of any electrolyte abnormalities and analgesia. o In pts w/ severe disease broad-spectrum antibiotics particularly fluoroquinolones are often prescribed prophylactically to prevent infection in retroperitoneum, namely infected pancreatic necrosis.

Front 612

What is used to tx pts that have unrelenting acute pancreatitis related to gallstones?

Back 612

ERCP has been shown to reduce morbidity. This can shorten biliary sepsis.

Front 613

What is the major cause of chronic pancreatitis?

Back 613

vast majority due to EtOH use. Gallstones ARE NOT a cause.

Front 614

What are the main features of chronic pancreatitis?

Back 614

chronic abdominal pain (epigastric pain radiating to the back), steatorrhea primarily due to exocrine insufficiency of lipase, and DM

Front 615

What x-ray finding is consistent w/ chronic pancreatitis?

Back 615

calcification throughout the parenchyma

Front 616

What test is most sensitive for dx chronic pancreatitis?

Back 616

ERCP and endoscopic US are the most sensitive

Front 617

What is the most sensitive functional assay for determining chronic pancreatitis?

Back 617

Secretin stim test, where patient is given an injection of secretin and output of HCO3- by the pancreas is assayed and quantitated.

Front 618

What is tx for pt w/ pancreatic duct markedly dilated in the body and tail?

Back 618

Peustow procedure or pancreaticojejunostomy

Front 619

What is tx for pt w/ marked imflammatory changes in the head of the pancreas and minimal ductal dilation?

Back 619

pancreaticoduodenectomy

Front 620

What RF for developing pancreatic adenocarcinoma?

Back 620

Older age, being male, smoking, high-fat diet, and exposure to petroleum products and aromatic compounds.

Front 621

Where do majority of tumors of pancreas arise at?

Back 621

70% arise in the head, these pts present w/ obstructive jaundice. These patients also frequently present with weight loss anorexia and typically a dull mild discomfort in the upper abdomen. Painless jaundice is a classic description of pancreatic adenocarcinoma of the head.

Front 622

If pt presents w/ abdominal pain and weight loss but no jaundice?

Back 622

adenocarcinoma of body and tail of pancreas

Front 623

What is the two critical factors in determining the stage of pancreatic canceres?

Back 623

the presence or absence of distant medistatic disease and the presence or absence of invasion of the major vascular structures in the peripancreatic bed

Front 624

What potential sources of vascular supply for pancreatic cancers?

Back 624

portal vein, superior mesenteric vein, the superior mesenteric artery and the celiac artery

Front 625

What is the procedure of choice for palliation?

Back 625

percutaneous placement of a biliary stent or endoscopy placement of a biliary stent to relieve obstructive jaundice

Front 626

What type of chemo is used for tx advanced metastatic disease?

Back 626

five-fluorouracil based therapy or gemcitabine

Front 627

What are some histo signs of pancreatic carcinoma?

Back 627

Most of the glands are well-diff. They like to invade the perineural space.

Front 628

Where are inactive form of digestive NZMs stored? What stim there release? What stim mucin and bicarb production?

Back 628

In zymogen granules of acinar cells, and when stim by cholecystokinin, they release into acinar lumen. They are carried to duodenum by series of ductules and ducts lined by columnar cells that secretin mucin and bicarbonate in response to another hormone, secretin.

Front 629

What duct joins to empty into the duodenum at ampulla of Vater?

Back 629

The duct of Wirsung (ventral duct) and common bile duct.

Front 630

What can occur if ventral buds rotate improperly?

Back 630

an annular pancreas develops which may predispose to duodenal obstruction, especially in children

Front 631

Where does the body of the pancrease set?

Back 631

Body sets retroperitoneum

Front 632

What is dx for acute abdominal pain and elevation of serum amylase and lipase?

Back 632

Acute Pancreatitis

Front 633

How do gallstones cause acute pancreatitis?

Back 633

When a gallstone obstructs the ampulla it causes bile to flow into pancreatic duct and produces symptoms of pancreatitis. Gallstones w/ wider cystic duct size, multiple stones, and smaller stones are at higher risk due to greater chance of mobilization from the gallbladder.

Front 634

Men w/ acute pancreatitis present how?

Back 634

often present due to complications of EtOH and at younger age (39).

Front 635

Women w/ acute pancreatitis present how?

Back 635

Women often present due to gallstones and at older age (69).

Front 636

What is need for dx acute pancreatitis?

Back 636

bile stones in gallbladder or common bile duct on US. 3x increase in ALT at presentation is 95% positive predictive value.

Front 637

What drugs can induce pancreatitis?

Back 637

asparaginase, azathioprine, 6-MP, Valproate, Pentamidine. There effects are not dose dependent.

Front 638

How can lipid levels cause pancreatitis?

Back 638

Hypertriglyceridemia – rare cause, serum triglycerides usually > 1000 mg/dL. Can be drug induced w/ EtOH, estrogens, isotretinoin, and HIV protease inhibitors

Front 639

What is a potential pitfall of ERCP?

Back 639

Can cause pancreatitis, seen in young females w/ anatomically normal ducts, abdominal pain, and anicteric. Prevention includes avoid ERCP, gabexate and somatostatin infusion to decrease the risk, and pancreatic duct stenting.

Front 640

What lab signs show pancreatitis?

Back 640

elevated WBC, amylase, and lipase

Front 641

What NZM is most specific more acute pancreatitis?

Back 641

Elevated serum amylase occurs also w/ intestinal obstruction, ischemia, or perforation. Also w/ chronic renal disease pts. Lipase is a more specific for pancreatitis!

Front 642

What is timing for increased NZMs seen w/ acute pancreatitis?

Back 642

Serum amylase levels rise w/in first 24 hours and serum lipase follows suit 2-3 days later. Both are relatively short-lived (2-4 days) in the serum but can also be found in the urine.

Front 643

What are danger signs of pancreatitis?

Back 643

Danger signs: encephalopathy, hypoxemia, tachycardia, hypotension, decreased urine output

Front 644

What are ways to determine pancreatitis pgx?

Back 644

Ranson's Criteria (mortality increases w/ >3), Hematocrit (to determine fluid resuscitation), and CT scan(use if fluid collection or high Ranson or APACHE score). 90% pts w/ acute pancreatitis do not need CT scan.

Front 645

Pts w/ chronic pancreatitis may develop pain, why is that?

Back 645

pain is due to pseudocyst development and obstruction of ducts, neural inflammation, and duodenal and common duct obstruction due to fibrosis in the head of the gland causing strictures.

Front 646

If pt w/ pancreatitis develops DM, where in there disease process are they?

Back 646

DM develops late in pancreatitis

Front 647

What is the most and least sensitive test for dx pancreatitis?

Back 647

Endoscopic US is the most sensitive test.
Abdominal X-ray is the least sensitive

Front 648

What is clear sign of pancreatic adenocarcinoma?

Back 648

Double duct sign is when both common bile and pancreatic ducts dilate. A person w/ jaundice and dilated ducts has 99.9% of having pancreatic cancer in head of pancreas. Seen in alcoholics and hereditary cases.

Front 649

What is a premalignant cyst in pancreas?

Back 649

Mucinous cystadenoma

Front 650

What is a inflammatory cyst in pancreas?

Back 650

Pseudocyst

Front 651

What do cystadenomas of pancreas arise from?

Back 651

Ductal Epithelium

Front 652

What do cystadenomas groosly look like? Location?

Back 652

Usually solitary and multilocular with a tendency to occur more frequently in tail.

Front 653

How is severity of acute pancreatis determined?

Back 653

"Random's criteria: * 5 parameters at time of admission: (>55 yo, WBC >16,000, glucose > 200, LDH > 250, AST > 250)
* 6 clinical predictors after 48 hrs (hematocrit ↓ > 10, BUN ↑ > 5, Ca++ < 8 mg/dL, arterial O2 content < 60 mmHg, a base deficit > 4 mEq/L, and fluid sequestration > 6 L.
* In general, > 3 of these criteria is consistent with severe pancreatitis.
"