Pathology Liver And Gi Medical School

Front 1

palmer erythema, spider angiomatas, and gynecomatastia

Back 1

cirrhosis

-all caused by hyperestrinism

Front 2

soft, yellow, greasy liver

Back 2

fatty liver hepatic steatosis

Front 3

astrerixis

Back 3

Hepatic (portosystemic) encephalopathy

-flapping tremor and neurologic sign, caused by nitrogenous metabolites which can not be detoxified by the damaged liver

Front 4

most common primary malignacy of the liver

Back 4

hepatocellular carcinoma

-often associated with Hep B infection

Front 5

inc in AFP(a-fetoprotien)

Back 5

Hepatocellular carcinoma

-also present in yolk sac tumors

Front 6

triad of cirrhosis, skin pigmentation, and diabetes mellitus

"bronze diabetes)

Back 6

Idiopathic hemochromotosis

-primary defect in iron absorption leading to a net accumulation

Front 7

macronodular pattern on liver surface

Back 7

posthepatic (postnecrotice, macronodular) cirrhosis

Front 8

middle-aged femail with prutitus, jaundice, xanthomas, and antimitochondrial antibodies

Back 8

primary billiary cirrhosis

-histologically characterized by granulomatous destuction of intrahepatic bile ducts

Front 9

billary tract disease, commonly seen in association with ulcerative colitis

Back 9

primary sclerosing cholangitis

-histologically characterized by onion-skin fibrosis of bile ducts

Front 10

councilman bodies

Back 10

viral hepatitis

-apoptotic hepatocytes

Front 11

hepatolenticular degeneration causing extrapyramidal motor signs

Back 11

Wilson disease

-copper deposits in the liver, corniea of the eye (Kayser-Fleischer rings), and putamen and lenticular nucleai of the basal ganglia

Front 12

sudden right upper quadrant or epigastric pain with nausea, vomitting and leukocytosis

Back 12

acute calculous cholecystitis

Front 13

micronoducles on the liver surface in early stages

Back 13

alcoholic cirrohsis

Front 14

mallory bodies, neutrophilic infitrate, and hepatocyte swelling andnecrosis

Back 14

alcoholic hepititis

->Mallory bodies associated ith accumulation of cytokeratin intermediate filaments in heptocytes

Front 15

most common liver disese in US?

Back 15

alcoholic liver disease

Front 16

fatal thrombbotic occulustion of the hepatic vein associated with poly cythemia vera and other hypercoagulable states

Back 16

Budd-Chiari syndrome

Front 17

obstructive jaundice with palpable enlarged gallbalder

Back 17

carcinoma of the head of the pancrease or carcinoma of the extrabiliay ducts and ampula of Vater

Courvoisler law obstructive jaundice with palpable gallblader indicates probable tumor

-jaundice iwth nonpalpable gallblader indicates probable gallstones

Front 18

obese multiparous women with fat intolerance

4 F's: female, fat, fertile, forty

supersaturation of bile with cholesterol due to:
1. inc hepatocyte cholesterol secretion
2. dec bile salt / lecithin

Back 18

cholelithiasis (gallstones)

Front 19

grossly distended abdomen, esophageal, varicies, caput meducsae, and hemorrhoids

Back 19

cirrhosis, caused by portal hypertenstion and active portocaval anastomoses

Front 20

low mag trichrom stain

Back 20

clinically the patient may have hepatice failure

Front 21

most likely eteology or cause for pathologic change shown in this liver biopsy

Back 21

hemochromatosis

-inherited disease characterized by inc intestinal Fe uptake, result in systemic overload and eventually cellular toxicity and death

Front 22

most likely clinicopathologic syndrome corresponding to changes in liver biopsy

Back 22

cholestasis

-bile secretory impairment or failure, resulting in hepatocellular and serum accumulation of bile constituents and prominent elevation of alkaline phospatase and other enzymes derived from heptocyte canalicular membrane

Front 23

which of the following is false for this liver biopsy from an alcholic abuser?

a. histologic change reversible
b. liver enlarged
c. pt consumes 10 - 20 gm alcohol per day for 2 - 3 weeks
d. serum alkaline phosphatatse may be elevated
e. pt hepatic illness is most likely clinically mild

Back 23

which of the following is false for this liver biopsy from an alcholic abuser?

c. pt consumes 10 - 20 gm alcohol per day for 2 - 3 weeks

pt must drink 80 gm/day to acheive reversible injury (steatosis)

one beer = 10 gm EtOH

Front 24

< 3 mo
encephalopathy
hypoglycemia
bleeding
renal failure

elevated ast/alt

Back 24

acute hepatic failure

Front 25

-have sx for years
-portal htn (acities & angiomata)
-encephalopathy
-may or may not have hypoglycemia
-bleeding
-renal failure

mildly elevated ast/alt and T. Bili

Back 25

chronic hepatic failure

Front 26

portal htn (ascities & angiomata)

synthetic derangements (dec albumin, inc PT, hypogonadism, wasting)

possible encphalopathy

Back 26

cirrhosis with probable chronic hepatic failure

Front 27

what liver disease causes the liver to dec in size due to shrinkage from collagenous scares?

Back 27

cirrhotic liver (typically but not always)

Front 28

what hepatic syndrome has alkaline phosphatase ice 3 to 10 times the normal?

Back 28

cholestasis

Front 29

< 3 mo
encephalopathy
hypoglycemia
bleeding
renal failure

elevated ast/alt

Back 29

acute hepatic failure

Front 30

-have sx for years
-portal htn (acities & angiomata)
-encephalopathy
-may or may not have hypoglycemia
-bleeding
-renal failure

mildly elevated ast/alt and T. Bili

Back 30

chronic hepatic failure

Front 31

portal htn (ascities & angiomata)

synthetic derangements (dec albumin, inc PT, hypogonadism, wasting)

possible encphalopathy

Back 31

cirrhosis with probable chronic hepatic failure

Front 32

what liver disease causes the liver to dec in size due to shrinkage from collagenous scares?

Back 32

cirrhotic liver (typically but not always)

Front 33

what hepatic syndrome has alkaline phosphatase inc 3 to 10 times the normal?

Back 33

cholestasis

Front 34

what is this hepatic syndrome?

Back 34

Fatty change, asymptomatic or mild hepatocellular
injury/cholestasis syndrome

Front 35

hepatic syndrome?

Back 35

Fatty change, asymptomatic or mild hepatocellular
injury/cholestasis syndrome

Front 36

hepatic syndrome?

Back 36

Cirrhosis, there are regenerative nodules
surrounded by “bands” of collagen

Front 37

hepatic syndrome?

Back 37

Cirrhosis, there are regenerative nodules
surrounded by “bands” of collagen

Front 38

hepatic syndrome?

Back 38

Alcoholic hepatitis (PMN's, Mallory hyaline, lobular disarray, steatosis, fibrosis syndrome), causes an acute cholestatic or hepatocellular injury syndrome

Front 39

hepatic syndrome?

Back 39

Alcoholic hepatitis (PMN's, Mallory hyaline, lobular disarray, steatosis, fibrosis syndrome), causes an acute cholestatic or hepatocellular injury syndrome

Front 40

which of the following 3 hepatic syndromes is least likely to cause hepatomegaly?

a. cholestasis syndrome
b. cirrhosis
c. alcholic hepititis

Back 40

b. cirrhosis

Cirrhosis. Fatty change and alcoholic hepatitis increase liver size by virtue of intracellular accumulation and ↑ cellularity, respectively. Cirrhotic livers are typically (but
not always) decreased in size due to shrinkage from collagenous scars.

Front 41

– ↑↑↑ alk phos with pruritus (deposition of bile acids
in skin)

– xanthomas ( ↓ cholesterol excretion)

Back 41

cholestasis

Front 42

inc ast/alt

Back 42

heptocellular injury

Front 43

elevated transaminase and alk phos

Back 43

heptocellular carcinoma

Front 44

anti-mitochondrial antibody (AMA) is a confirmatory test for what hepatic syndrome?

Back 44

primary billary cirrohsis (PBC)

Front 45

is copper elevated in cholestasis / duct obstruction?

Back 45

Hepatic copper is ↑ in any cause of cholestasis/duct obstruction due to impaired
excretion into bile.

Front 46

why is copper elevated in Wilson's disease?

Back 46

an inability to export copper from hepatocytes.

Front 47

hepatice syndrome?

Back 47

Adenocarcinoma (cholangiocarcinoma), with obvious glandular
differentiation.

Front 48

hepatic syndrome?

Back 48

Adenocarcinoma
(cholangiocarcinoma), with obvious glandular
differentiation.

Front 49

hepatic syndrome?

Back 49

Hepatoblastoma, with “embryonal” appearance and “mesenchymal” differentiation. (Recall-this is a pediatric neoplasm.)

Front 50

hepatic syndrome?

Back 50

Hepatoblastoma, with “embryonal” appearance and “mesenchymal” differentiation. (Recall-this is a pediatric neoplasm.)

Front 51

hepatic syndrome?

Back 51

Hepatoblastoma, with “embryonal” appearance and “mesenchymal” differentiation. (Recall-this is a pediatric neoplasm.)

Front 52

hepatic syndrome?

Back 52

Hepatocellular carcinoma (HCC) in which tumor cells resemble hepatocytes (cord-like growth+resemblance to hepatocytes).

Note: HCC is associated with cirrhosis (of virtually any etiology) as well as HBV infection.

Front 53

hepatic syndrome?

Back 53

Hepatocellular carcinoma (HCC) in which tumor cells resemble hepatocytes (cord-like
growth+resemblance to hepatocytes).

Note: HCC is associated with cirrhosis (of virtually any etiology) as well as HBV infection.

Front 54

hepatic syndrome?

Back 54

vascular invasion by the tumor, which is very typical of HCC. If this were extensive, it may have caused hepatic vein thrombosis, which presents with a syndrome of rapidly developing/worsening portal hypertension ( ↑ ascites, variceal bleeding) with tender hepatomegaly.

Front 55

hepatic syndrome?

Back 55

shows Primary Biliary Cirrhosis (PBC)
def: chronic, progressive, AUTOIMMUNE destruction of the medium sized intra-hepatic bile ducts, characterized by presence of anti-mitochondrial antibodies (AMA)

pathology: “florid duct lesion” (mononuclear infiltration/granulomatous
inflammation of bile duct epithelium)

Front 56

hepatic syndrome?

Back 56

Primary Sclerosing Cholangitis (PSC) - idiopathic fibrosis and obliterative inflammation with segmental dilation of intra and/or extrahepatic bile ducts, often associated with UC

pathology: periductal concentric fibrosis

Front 57

hepatice syndrome

Back 57

Primary sclerosing cholangitis (PSC) - indiopathic obliterative inflammation and fibrosis of intra and/or extrahepatic bile ducts

Pathology: periductal concentric fibrosis often with chronic inflammation

Front 58

hepatic syndrome?

Back 58

Chronic active hepatitis, with periportal mononuclear infiltrates
and focal “piecemeal” necrosis of hepatocytes near the limiting
plate. (Causes a chronic hepatocellular injury syndrome.)

Front 59

hepatic injury?

Back 59

Chronic active hepatitis, with periportal mononuclear infiltrates and focal “piecemeal” necrosis of hepatocytes near the limiting plate. (Causes a chronic hepatocellular injury syndrome.)

Front 60

hepatic syndrome?

Back 60

Acute viral hepatitis, with “ballooning”, lobular “disarray” and
hyperplasia of Kupffer cells.(Causes an acute hepatocellular injury syndrome.)

Front 61

hepatice injury?

Back 61

Acute viral hepatitis, with “ballooning”, lobular “disarray” and
hyperplasia of Kupffer cells.(Causes an acute hepatocellular injury syndrome.)

Front 62

hepatic syndrome?

Back 62

Massive necrosis, with hepatocyte “dropout”, minimal
inflammation and little regeneration.

Front 63

hepatic syndrome?

Back 63

Massive necrosis, with hepatocyte “dropout”, minimal
inflammation and little regeneration.

Front 64

hepatic syndrome?

Back 64

Fibrosis with ↑↑↑ iron compatible with hemochromatosis. This
disease causes gradual hepatic damage + damage to heart, endocrine glands, pancreas.

Front 65

hepatic syndrome?

Back 65

Fibrosis with ↑↑↑ iron compatible with hemochromatosis. This
disease causes gradual hepatic damage + damage to heart, endocrine glands, pancreas.

Front 66

when does the liver size inc?

Back 66

with alcholic or viral hepatitis

Front 67

whendoes the liver size dec?

Back 67

during fulminant hepititis / massive necrosis, which is characterized by shrinkage due to extensive cell loss

Front 68

describe?

Back 68

• Normal esophagus is lined by smooth mucosa that is nearly white or pink-gray
• longitudinal esophageal mucosal folds are pliable
• the gastric mucosa is pink, darker than the esophagus, moist, and glistening
• the junction of esophagus and stomach (squamocolumnar junction), or ‘Z’ line may be slightly irregular\

DIAGNOSIS
• normal gastroesophageal junction

Front 69

describe

Back 69

• Normal esophagus is lined by smooth mucosa that is nearly white or pink-gray
• extending proximally from GEJ are red patches and streaks
• areas of friability and bleeding are also present

• DIAGNOSIS
• esophagitis, consistent with acid reflux

Front 70

describe?

Back 70

• The gastric mucosa erythematous (red) and ‘blotchy’
• numerous small superficial erosions are apparent
• note the small, smooth-bordered, benign ulcer

DIAGNOSIS
• gastritis
• benign ulcer

Front 71

describe?

Back 71

• Normal esophagus is lined by smooth mucosa that is nearly white or pink gray
• extending proximally from the GEJ are red patches and streaks
• the Z line is irregular, with tongues of columnar appearing mucosa extending proximally
• islands of squamous-appearing mucosa are present within the tongues of columnar-appearing mucosa

DIAGNOSIS
• Barrett’s esophagus (requires biopsy information)

Front 72

describe?

Back 72

• This slide shows active esophagitis.
• The squamous mucosa and subepithelial tissue is infiltrated by eosinophils and neutrophils .
• The presence of eosinophils is consistent with (but not diagnostic of) reflux esophagitis .
• In response to the inflammation, the epithelium is reactive, as evidenced by the basal zone hyperplasia.

Front 73

describe?

Back 73

• These slides are an example of Helicobacter pylori-associated gastritis.
• The typical morphology includes plasma cells within the superficial lamina propria, and active inflammation of the pits (pit abscesses).
• The inset is a silver strain (Warthin-Starry) that shows the curved bacilli. They do not invade, but are
trapped within the surface mucous and attached to the apical surface of the foveolar cells.

Front 74

describe?

Back 74

• Mucosa is erythematous and hyperemic
• erosions and ulcerations are present
• pseudomembranes may be present
• the mucosal vascular pattern is not apparent
• linear ulcers may be present
• disease is continuous from the rectum, but may stop abruptly

DIAGNOSIS
• suggestive of ulcerative colitis (history and biopsy will be helpful in evaluation)

Front 75

describe

Back 75

• This slides shows chronic active colitis.
• The active neutrophils component
• The glands are branched and irregularly spaced.
• Paneth cells are present in this sigmoid biopsy(metaplasia).
• This histology is typical of inflammatory bowel disease(IBD) and could represent either ulcerative colitis or Crohn’s disease. In the absence of granulomata, these entities can be indistinguishable on biopsy.
• Therapy for IBD includes sulfasalazine, steroids, and other immunosuppressive agents.

Front 76

describe?

Back 76

• The biopsy shows crypts atrophy (loss) (mucosal atrophy)
• The presence of mucosal atrophy, crypt distortion, and epithelial metaplasia (Paneth cells in the left colon) is diagnostic of chronic colitis.
• There are few neutrophils infiltrating the epithelium (inactive colitis)
• There is no dysplasia. (this is the part of the diagnosis in which you were most interested )

DIAGNOSIS
• chronic inactive colitis
• no dysplasia

Front 77

describe?

Back 77

• This is an example of juvenile polyp.
• These are often present in younger patients (hence the name) and commonly present with rectal bleeding.
• Grossly these polyps are typically smooth and glistening.
• Microscopically, cystically-dilated non-neoplastic glands are present within the inflammatory stroma.
• The disorganized appearance of the glands as well as disorganized strands of smooth muscle within the
lamina propria have led some to conclude that these are hamartomatous polyps.
• 85%-90% are solitary, and these are NOT associated with increased risk of cancer. Polypectomy is the only therapy necessary.
• For a patient with numerous polyps and uncontrollable bleeding, colectomy may be necessary. An elevated cancer risk in these patients also leads to some advise colectomy.
• juvenile polyposis coli is an autosomal dominant inherited disease

Front 78

describe

Back 78

• This is adenoma.
• The cells are by Definition, dysplastic, with nuclear elongation pseudostratification.
• Dysplastic morphology = neoplastic biology.
• While not malignant, adenomas do have malignant potential and are considered premalignant.
• Classification as a patient who ‘makes adenomas’ puts his patient in a higher risk category and requires more
frequent colonoscopic surveillance with polypectomy.
• Aggressive removal of adenomas at surveillance colonoscopy reduces the incidence of colon cancer.
• For young patients with hundreds of adenomas ,the diagnosis is familial adenomatous polyposis, an autosomal dominant inherited disease. Colectomy prior to the development of cancer is the therapy of choice.

Front 79

describe

Back 79

• This is hyperplastic polyp.
• Grossly these are typically small (<5mm) lesions most common the left colon.
• Histologically the cells are not cytologically dysplastic, and, due to crowding, develop pseudopapillary
infoldings with characteristic ‘sawtooth’ or ‘serrated’ shape.
• At present these polyps have no clinical significance (unless mistaken for adenomas).

Front 80

describe

Back 80

• This is an adenoma with intramucosal carcinoma in the stalk.
• The transformation to high grade dysplasia and intramucosal carcinoma is apparent as the cells become
more crowded, and form cribriform and sheetlike structures.
• Intramucosal carcinoma is present at the stalk margin, thus, this polyp deserves a surgical segmental resection in case it represents the surface of a deeply invasive carcinoma.
• If the intramucosal carcinoma were only present at the surface of the polyp, well away from the margin, Polypectomy would be definitive therapy. No further therapy would be necessary in that case, as resected
• intramucosal carcinomas have a <1% chance of metastasizing (due to the absence of lymphatics in the lamina propria of the colon).

Front 81

describe

Back 81

see above

Front 82

describe?

Back 82

see above

Front 83

describe?

Back 83

see above

Front 84

describe

Back 84

see above

Front 85

describe

Back 85

see above

Front 86

2 critical factors for diverticulosis?

Back 86

1. higher intraluminal than intra-abdominal pressure

2. weak point in bowel wall, through which mucosa can herniate

Front 87

when does diverticulosis becomes diverticulitis?

Back 87

1. acute inflammation of one or more diverticula

2. can be due to neck obstruction as with appendicitis

3. can result in serositis and rupture and perforation - weakened wall, little m. propria

Front 88

hallmark of hepatocellular carcinoma

Back 88

elevated aminotransferase (transaminases)

Front 89

problem is largely of "Nitrogenous" origin with some correlation with hyperammonemia

Back 89

hepatic encephalopathy manifested by mental status disturbances, hyperreflexia, eeg changes and asterixis (flapping tremor)

Front 90

-jaundice (bilirubin)
-xanthomas (from cholesterol)
-pruritus (bile acids)

Back 90

signs and sx of Cholestasis

Front 91

what systemic disease can present with:
1. constipation
2. peptic ulser disease due to hypergastrinemia
3. Multiple endocrine neoplasia synderome: develop diarrhea due to secreatagogue - producing tumor
4. pancretitis

Back 91

hyperparathyroidism, also see inc Ca and with MEN see zolinger-ellison syn and VIPoma

Front 92

systemic condition associated with:
-GERD
-hemorrhoids
-gallstones
-n/v

Back 92

pregnancy

Front 93

what aspect of gi tract in HIV pt effect with:
1. candida
2. cmv
3. herpes simplex

Back 93

esophagus

Front 94

what aspect of gi tract in HIV pt effect with:
1. mycobacterium avium complex (MAC)
2. TB
3. cryptosporidium

Back 94

small intestine

Front 95

what drug toxicity is idiosyncratic and unpredictable?

Back 95

acetaminophine

Front 96

autosomal recessive inheritance, associated with HLA-A3 haplotype

inc intestinal iron uptake resulting in systemic overload and eventually cellular toxicty and death

Back 96

primary hemochromatosis

gold standard dx test - liver biopsy

Front 97

gingival hyperplasia, gingivitis, hemorrhage, petechia and ulceration of mucosa all relate to what disease?

Back 97

leukemia

Front 98

what disease is associated with these oral manifestations?

Back 98

leukemia

Front 99

what is this?

Back 99

lichen planus - lower risk associated with malignancy, autoimmune, has branching features,looks like moss on a tree

Front 100

what pt population is most likely to have this?

Back 100

this is Moniliasis, also known as candidosis or thrush which is seen in pt whor are immunocompromised such as in cancer, tb, hiv, diabetes, etc

Front 101

what is the cause of this?

Back 101

fluorosis

Front 102

what pt population should this be avoided in?

Back 102

this is tetracycline staining which should not be given to pregnant women or young children as antibiotic tx

Front 103

what is this and what disease first orally manifests in this way?

Back 103

hairy leukoplakia is white in color and can NOT be scraped off and frequently the first sign of hiv infection

Front 104

what is this and what is it a sign of?

Back 104

this is erythroleukoplakia a pre-malignant lesion

Front 105

major salivary gland tumors are

Back 105

most often found in parotid glands

Front 106

what lab finding is most associated with portal htn?

Back 106

serum-ascites albumin gradient

Front 107

achalasia
diffuse esophageal spasm (DES)
nutcracker esophagus
scleroderma
dm, aging

what type of dysphagia do all of these have in common?

Back 107

esophageal motor dysphagia
-difficulty with peristalsis, smooth muscle spasm, les fxn

also called TRANSPORT dysphagia

Front 108

-cva
-polyositis
-MG
-circophyryngeal achalsia
-zenker's (pharyngoesophageal) diverticulum

what type of dysphagia do all of these have in common?

Back 108

Oropharyngeal dysphagia - difficulties with swallowing mechanism

also refered to as TRANSFER dysphagia

Front 109

what condition has less incompetence (always open) and aperistalsis in distal 1/2 of esophagus?

Back 109

scleroderma bc smooth mucle inflitrated and atrophy from collagen deposition

Front 110

what condition presents as dyspagia and chest pain made worse by emotional distress and by drinking hot fluids

Back 110

diffuse esophageal spasms (DES)

Front 111

failure if LES to fully relax after swallowing

loss of autonomic (auerbach's) ganglia in the body of the esophagus and lower esophaeal sphincter area resulting in esopheageal dilation

Back 111

achalasia

this is a type of esophageal motor dysphagia often called transport dysphagia

Front 112

what type of acute pancretitis has the highest mortality

Back 112

severe or necrotizing acute pancretitis

Front 113

what can cause all of the following:
-gastric cancer of body and antrum (distal stomach)
-gastric ulcer
-duodenal ulcer
-gastric lymphoma

Back 113

h. pylori

Front 114

what three conditions would fasting have little or no effect on diarrhea?

Back 114

1. cholera - exogenous luminal stimuli from bacteria toxin

2. VIPoma - endogenous humoral peptide from tumor enters blood and stimulates enterocytes to secrete

3. celiac sprue - intrinsic crypt hyperplasia results in increased secretion

Front 115

UES myotomy (incision of sphincter muscle) or Botulinum toxin (Botox) is used for the treatment of what disease type?

Back 115

oropharyngeal dysphagia

Front 116

the following are used to dx what condition?

1. serology - measuring antibodies
2. rapid urease test (CLO-test) on biopsy
3.C13 or C14 - urea breath test
4. stool test

Back 116

gastritis due to h pylori

Front 117

what condition is dx with the following tests?

1. serology: anti-parietal cell antibodies, anti-IF antibodies
2. serum gastrin levels very high due to loss of neg feedback to antral G-cells
3. EGD and biopsy - see mucosal atrophy
4. schilling test - measuring vit B12 absorption

Back 117

autoimmune gastritis

Front 118

type of colon cancer?

sx:
-crampy abdominal pain
-constipation
-streaks of blood mixed wit stool

Back 118

sigmoid colon cancer

Front 119

how is Zollinger -Ellison syndrome (gastrinoma) dx?

Back 119

fasting serum gastrin levels - usually elevated also see antral G-cell hyperplasia and achlorhydria

secretin stimulation test - in gastromia pt see inc in gastrin levels

Front 120

what do the following cause?

1. steatorrhea
2. colon
3. bile salt malabsorption
4. fatty acid malabsorption

Back 120

hyperoxaluria - excess urniary oxalate, bc calicum usually binds to oxalate but with fatty acid malabsorption the fatty acids bind to the calcium leaving the oxalate to be absorbed in the colon

Front 121

rod shaped bacilli which infiltrate the lamina propria of the small bowel mucosa by destending PAS positive macrophages and villous blunding (proximal small bowel > ileum)

Back 121

Whipples's diseae due to tropheryma whippelii

Front 122

all of the following are associated with:

1. appendiceal carcinoid tumor
2. increased serum serotonin
3. metastitic disease
4. diarrhea

Back 122

carcinoid syndrome

Front 123

what colon related disease risk of cancer is directly related to extent, duration of disease and age of sx onset?

Back 123

ulcerative colilits

Front 124

idiopathic fibrosis and obliterative inflamation with segmental dilation of intra and/or extrahepatic bile ducts, often associated with IBD (70% have UC)

Back 124

primary sclerosing cholangitis (PSC)

Front 125

what IBD has the discriminating feature of deep fissues / linear ulcerations?

Back 125

Crohn's disease

Front 126

what disease is characterized by:
-hypercalmeia
-hemorrhage
-abdominal pain
-fat accumulation in acinar cells
-respiratory distress

Back 126

acute pancreatitis

Front 127

all of the following are predisposed to form ___?____

1. chronic hemolysis
2. inc chenodeoxycholic acid secretion
3. DM
4. dec bile salt enterohepatic circulation

Back 127

gallstones

Front 128

Fe deficient anemia
glossitis
cheilosis

are a tetrad of sx for what syndrome?

Back 128

Plummer-Vinson Syndrome

-associated with inc risk of upper esophageal squamous cell carcinoma

Front 129

webs in the distal esophagus at or just above the gastroesophageal jxn associated with hiatal hernia

Back 129

schatzki rings

Front 130

protien folds incorrectly and is retained in the RER accumulating within the heptocytes appearing as cytoplasmic globules which statin with PAS stain

Back 130

alpha - 1 antitrypsin deficiency

-combined progressive injury of hepatic / pulmonary tissue injury due to inheritance of mutated protease inhibitor (Pi) which is normally synthesized in the liver

Front 131

what structural disorder is associated with the following:

1. cardiac malformations
2. esophageal atresia
3. upper esophagus ends in a blind pouch
4. associated with aspiration

Back 131

congenital trachoeo-esophageal fistula

Front 132

adenoma (gland-forming carcinoma) derived from intrahepatic bile ducts

-no bile production
-intense desmoplastic (fibroblastic )rxn to tumor cells

Back 132

cholangiocarcinoma

Front 133

hemorragic/necrosis surrounded by granulation tissue and fibrosis

-also lack true epithelial lining

Back 133

pancreatic pseudocyst

Front 134

disease with polyps that do not have malignant potential but pt has inc risk of carcinoma at other sites including breast, pancrease, lung, gynecologic

Back 134

peutz-jeghers polyposis

Front 135

polyps disease that is hereditary and has an increase risk of colon cancer

Back 135

juvenile polyposis - a polyposis syndrome, autosomal dominant inheritance

DO NOT confuse this with Juvenile polyps (hamartomatous polyps) which have not increased risk of carcinomas

Front 136

colon cancer with germline defect in DNA mismatch repair gene, results in replication errors positive phenotype, microsatellite instability and inc DNA mutation rate

Back 136

hereditary nonpolyposis colon cancer

Front 137

virus not associated with chronic carrier condition

Back 137

HEV

Front 138

Interferon (IFN) in combo with rebaverin can be used to treat which hepitits virus

Back 138

HBV

Front 139

acute hepatitis presents significant greate danger for pregnant women

Back 139

HCV

Front 140

pathology with the following sx?

-severe Malase
-jaundice
-enlarged liver
-aminotransferase elevated 15x

Back 140

mononuclear inflitrates limited portal triad

Front 141

collagen synthesis
macrovascular steatosis
hypertrophy of ser
cell swelling

Back 141

effects of alcohol on hepatocytes

Front 142

cell death and mononuclear infiltrate focal and tend to center on portal triad, occuring near the limiting plate (piecemeal necrosis)

Back 142

chronic hepitits

Front 143

associated with "foamy degeneration": accumulation of cholestrol and other lipids in some hepatocytes adn sinusoidal cells gives a bubbly or foamy apprearence

Back 143

hepatocellular injury in cholestasis

Front 144

where is conjugated bilirubin normally secreted

Back 144

bilirubin is normally secreted into the space of Disse

Front 145

associated with portal granulomas (granulomatous bile duct destruction)

Back 145

primary biliary cirrhosis

Front 146

fibrosis in sinusoids close to central vein

Back 146

alcoholic liver disease

Front 147

regenerative nodules throughout the liver, alteration of hepatic architecture by fibrosis

Back 147

cirrhosis

Front 148

-pruritis, fatigue, jaudice
-elevated alk phos
-liver biopsy reveals centrilobular bile canalicular pluging with normal triads
-associated with UC

Back 148

primary sclerosing cholangitis

Front 149

present as submucosal polyps

Back 149

carcinoids

Front 150

altered luminal phase absorption fxn

Back 150

cystic fibrosis

Front 151

frequent site of obstruction 2nd to intra-abdominal adhestion or hernia

Back 151

jejunum / ileum

Front 152

-crampy abdominal pain
-weight loss
-bloody diarrhea

Back 152

UC

Front 153

-abdominal pain often in LRQ
-bloody diarrhea
-sometimes see gallstones or calcium oxalate kidney stones

Back 153

CD

Front 154

IBD that does not involve the jejunum

Back 154

UC

Front 155

gut vascular disorder?

syndrome associated with wt loss, abdominal pain, diarrhea

Back 155

chronic intestinal ischemia

Front 156

-seizure
-cerebral edema
-renal failure

what liver disease/ syndrome is associated with the above sx?

Back 156

acute hepatic failure

Front 157

presents with bergan's traid of acute abdominal pain, spontaneous GI emptying, history of cardiac disease

Back 157

mesenteric arterial emboli

SMA most common site for emboli

Front 158

due to low flow condition and may be managed medically

Back 158

nonocculusive mesenteric ischemia

Front 159

most pt lack predisposing condition, high rate of re-thrombosis

Back 159

mesenteric venous thrombosis

Front 160

sudden onset of abdominal pain, sugical findings inlcude necrosis of the small bowel and right and transverse colon

Back 160

mesenteric arterial thrombosis

Front 161

seen in association with low cardiac output states, heart failure and dialysis

Back 161

nonocculusive mesenteric ischemia

Front 162

most frequent site of obstruction due to volvulus

Back 162

colon

Front 163

a risk factor for severe acute hep A infection

Back 163

hep C

Front 164

complication of gastroparesis, a motor disturbance seen in DM pt

Back 164

bezoar - concentrations of vegetable matter that build up in the stomach, often becoming symptomatic

Front 165

NSAIDS, slow release potassium cholride tablets and doxycycline can all cause

Back 165

intestinal ulcers

Front 166

what gi disease is associated with renal failure

Back 166

angiodysplasias

Front 167

what gi condition is associated with dermatomyositis?

Back 167

transfer dysphagia

-skeletal muscle diseases frequently give rise to significant chewing and swallowing problems

Front 168

best way to determine pancreatic necrosisas as a result of acute pancretitis

Back 168

abdominal ct scan with IV contrast

Front 169

steatorrhea
recurrent abdominal pain
vit b12 deficiency
DM

Back 169

chonic pancretitis

Front 170

drug used for prophylaxis of ulcers to prevent complications of excessive NSAID use for inflammatory arthritis

Back 170

misoprostol - a prostaglandin analogue

Front 171

pseudomemebranous colitis is most closely associated with what?

Back 171

antibiotic use

Front 172

what conditions have a serum-ascites albumin gradient of less than 1.1 g/dl

Back 172

cirrhosis
chf
constrictive pericarditis
hepatiac vein thrombosis

Front 173

what is used to improve portalsysttemic encephalopathy?

Back 173

lactulose
neomycin
laxatives
antibiotics

Front 174

-hypoalbuminemia
-inc hepatic lymph prod and flow
-renal Na retention
-splanchnic and systemic arterail vasodilation
-inc sinusoidal hydrostatic pressure

Back 174

formation of ascities in cirrhosis

Front 175

-jaundice
-itching
-caricoma of the head of the pancrease

what necessary tx would this pt need

Back 175

intramuscular injection of vit k to correct patient ptt time

Front 176

tonic contraction of rectosigmoidal area and absence of normal peristaltic contraction causing functional obstruction and dilation proximal to obstucted segment

Back 176

hirschsprung disease - congenital defect in migration of ganglion cells of neural crest- dervived

Front 177

A 45 year old male presents to the emergency room complaining of abdominal pain and lack of appetite. He has past medical history significant for diabetes mellitus, hypertension and gastroparesis. On EKG evaluation, he is noted to have prolonged QT interval which converts to a fatal arrhythmia. Which one of the following is linked to his current EKG findings?


a. Cisapride
b. Erythromycin
c. Domperidone
d. Metoclopramide

Back 177

A 45 year old male presents to the emergency room complaining of abdominal pain and lack of appetite. He has past medical history significant for diabetes mellitus, hypertension and gastroparesis. On EKG evaluation, he is noted to have prolonged QT interval which converts to a fatal arrhythmia. Which one of the following is linked to his current EKG findings?


a. Cisapride - correct answer. the major reason this drug was pulled from the market was secondary to this fact.
b. Erythromycin - incorrect. known to effect QT interval, should be monitored for prolongation
c. Domperidone - incorrect. no known issues with prolonged QT interval or fatal arrhythmia
d. Metoclopramide - incorrect. no known issues with prolonged QT interval or fatal arrhythmia

Front 178

Which one of the following is the best first line treatment option for mild to moderate colitis?


a. Surgical excision
b. 5-ASA
c. Azathioprine
d. Metoclopramide

Back 178

Which one of the following is the best first line treatment option for mild to moderate colitis?


a. Surgical excision - incorrect. would be considered second-line unless the patient had severe toxic mega colon and/or fistula formation
b. 5-ASA - correct answer; considered as first line therapy in mild to moderate colitis
c. Azathioprine - incorrect. immunomodulators are only considered for maintenance therapy
d. Metoclopramide - incorrect. not in the treatment algorithm for ulcerative colitis