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GI Exam 3 > Pathology > Flashcards

Pathology Flashcards

1
Q

Inflammatory Bowel Disease

A

chronic, relapsing inflammation resulting from inappropriate mucosal immune activation

  • classified into ulcerative colitis and Crohn’s disease
  • etiology not completely understood
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2
Q

Ulcerative Colitis

A

inflammatory changes involve mucosa and superficial submucosa

  • disease limited to colon, begins in rectum, continuous (always involves rectum) –> L sided disease
  • HALLMARK -> crypt abscess with neutrophils
  • loss of haustra –> lead pipe on x-ray
  • risk of toxic megacolon -> based on extent involved and duration of disease
  • pANCA (+)
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3
Q

Crohn’s Disease

A

inflammatory changes are transmural (full-thickness with knife like fissures)

  • disease can affect any area of GI tract, non-continuous -> R sided disease
  • Cobblestone mucosa, creeping fat, strictures (string-sign on x-ray), fistulas
  • risk of malabsorption with nutritional deficiencies
  • ASCA (+)
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4
Q

Diversion Colitis

A

colitis developing in blind distal segment of colon which is excluded from fecal stream following surgery

  • cause –> thought to be deficiency of SCFA
  • mucosal erythema, friability, nodularity with ulcers
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5
Q

Microscopic colitis

A

2 entities -> lymphocytic colitis and collagenous colitis

  • chronic watery diarrhea (no blood) and a normal colonoscopic exam
  • can be treated with glucocorticoids
  • crypt architecture is intact –> KEY
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6
Q

Long-term complication of both UC and CD

A

development of intestinal adenocarcinoma

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7
Q

Lymphocytic colitis

A

increased lamina propria chronic inflammation with increased intraepithelial lymphocytes and surface epithelial damage

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8
Q

Collagenous colitis

A

similar features as lymphocytic along with a band a subepithelial collagen

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9
Q

Radiation enterocolitis

A

complication of radiation therapy

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10
Q

Neonatal necrotizing enterocolitis

A

first week of premature infants life -> small and large bowel exhibit transmural necrosis -> bacterial overgrowth -> air bubbles

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11
Q

Drug-Induced enterocolitis

A

NSAID enteropathy -> use of NSAIDs can result in gastric, duodenal ulcerations -> can also occur in jejunum, ileum, colon –> can look like crohn’s disease

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12
Q

Graft vs Host disease

A

donor lymphocytes attack the host colon

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13
Q

Irritable Bowel Syndrome (IBS)

A

chronic, relapsing, abdominal pain or discomfort, bloating, changes in bowel habits
- endoscopic and colonoscopic exam is normal
MANY FACTORS
1. increased/decreased colon contractions/transit rates
2. Excess bile acid synthesis or malabsorption
3. Disturbance in enteric nervous system
4. Immune activation or shift in gut microbiome

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14
Q

ROME diagnostic criteria for IBS

A

recurrent ab pain or discomfort for 3 days per month with 2 of following:

  1. Improved with defecation
  2. Onset associated with change in frequency of stool
  3. Onset associated with change in form of stool
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15
Q

Sigmoid diverticulitis

A

formation of multiple diverticulae –> usually sigmoid
- if they become inflamed -> diverticulitis
results from elevated intra-luminal pressure in sigmoid colon –> outpouchings of mucosa and formation of the diverticulae (false)
- can cause lower GI bleed and diverticulitis

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16
Q

Solitary Rectal Ulcer Syndrome

A

malfunction of puborectalis muscle -> leading to excessive straining with defecation–> rectal mucosal prolapse -> ulcerate -> form polypoid mass -> may think it is adenocarcinoma

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17
Q

Non-neoplastic intestinal polyps

A

Inflammatory
Hamartomatous
Hyperplastic

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18
Q

Neoplastic intestinal polyps

A

Adenoma

Sessile serrated adenoma

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19
Q

Inflammatory polyp

A

results from inflammatory, non-neoplastic process

  • associated with solitary rectal ulcer, ulcerative colitis, Crohn’s
  • can occur ANYWHERE in GI tract
  • can be inflammatory pseudopolyps
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20
Q

Retention polyps

A

Hamartomatous polyp –> disordered collection of normal tissue

  • Sporadic -> no increased risk for malignancy
  • Polyposis syndrome -> increased risk for adenocarcinoma of GI tract
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21
Q

Peutz-Jeghers polyps

A

Hamartomatous polyps -> Peutz-Jeghers syndrome

  • multiple P-J polyps and mucocutaneous hyperpigmentation
  • loss of function mutation in STK11
  • at risk for GI adenocarcinoma as well as other malignancies
  • aborizing smooth muscle pattern -> pedunculated
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22
Q

Hyperplastic Polyps

A

occurs in colon, most common type of adult polyp in colon

  • small, found on left and especially in rectum
  • proliferative polyp without malignant potential
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23
Q

Adenoma

A

neoplastic polyp characterized by dysplastic glandular proliferation

  • can occur anywhere in colon, but in small bowel occur in duodenum
  • can progress to adenocarcinoma –> needs to be removed
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24
Q

Sessile serrated adenoma

A

Sessile polyps resembling hyperplastic polyps -> precursor to adenocarcinoma

  • lac adenomatous epithelium -> R colon
  • crypt dilation
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25
Q

Serrated adenoma

A

exhibits serration along with uniform, eosinophilic dysplastic epithelium

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26
Q

Familial Adenomatosis Polyposis

A

autosomal dominance inheritance

  • mutations in APC tumor suppressor gene (double-hit)
  • develop large number (1000s) of polyps in colon
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27
Q

Gardner’s Syndrome

A

in addition to FAP, patients develop desmoid tumors, osteomas, epidermal cysts, and thyroid tumors

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28
Q

Turcot Syndrome

A

coexistence of hereditary CRC and CNS tumors

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29
Q

Hereditary Non-polyposis Colorectal Cancer

A

Lynch Syndrome –> caused by mutations in genes that encode enzymatic MMR proteins
- need the 2nd hit (LOH)

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30
Q

Colorectal Adenocarcinoma

A 
most common malignancy of GI tract
Risk Factors:
1. Bad diet, cigs, obesity, alcohol, inactivity
2. family history of CRC
3. IBD
*aspirin/NSAIDs may be protective
Most arise from adenomatous polyps and they contain one of the two main genetic pathways:
1. APC/beta-catenin
2. MMR with microsatellite instability
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31
Q

APC/beta-catenin pathway

A

mutation in APC (tumor suppressor gene) –> 2nd hit of APC/beta-catenin –> K-RAS mutation –> p53 –> tumors
- often left-sided tumors

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32
Q

MMR pathway

A

mutation in MMR –> 2nd hit in MMR gene –> microsatellite instability –> accumulated mutations –> tumors
- often right-sided tumors

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33
Q

Iron-deficiency anemia in older man/woman?

A

CRC until proven otherwise!!!!

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34
Q

What does staging indicate?

A

the extent of the disease!!!!!

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35
Q

K-Ras mutation

A

Wild-type mutation means the receptor is working and the anti-body treatment will work
Mutant K-Ras means the receptor is no longer controlling the intracellular pathway and the anti-body treatment will be ineffective

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36
Q

Proto-onco gene

A

genes that regulate cell cycle –> when mutated they become onco-genes that are unregulated cell cycle genes

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37
Q

Cologuard

A

Stool DNA test that detects abberant methylation of 2 promoter genes as well as K-Ras mutations

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38
Q

Small bowel carcinoma

A

much less common that CRC
- 50% occur in duodenum and around ampulla of vater
Risks:
- FAP, Crohn’s, celiac disease

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39
Q

Gastrointestinal Stromal Tumors (GIST)

A

gain of function mutation in KIT (tyrosine kinase receptor)

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40
Q

Acute Appendicitis

A

acute inflammation involving at least muscularis propria
- results from increased intraluminal pressure that compromises venous outflow
- ischemic injury and stasis of luminal contents –> bacterial overgrowth –> acute inflammatory response
McBurney’s point
N/V follow development of pain

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41
Q

Complications of Appendicitis

A

perforation –>

periappendiceal abscess, pyelophlebitis, portal venous thrombosis, liver abscess, bacteremia, sepsis, death

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42
Q

Appendiceal neuroendocrine tumor

A

most common tumor of appendix

  • typically small –> non-functioning
  • large –> functioning
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43
Q

Pseudomyxoma peritonei

A

gross descriptive term for presence of abundance mucinous material on peritoneal surfaces

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44
Q

Anal hemorrhoids

A

result from ectasia of rectal venous plexus –> persitently elevated venous pressure (straining at stool)
External –> below pectinate line
Internal –> above pectiante line

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45
Q

Anal fissure

A

linear separation of tissue of anal canal extending through mucosa

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46
Q

Anal fistula

A

fistula tract may lead to skin, end blindly in peritoneal tissue

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47
Q

Rectal prolapse

A

intussusception of rectum through anus –> due to weak rectal support

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48
Q

Anal intraepithelial neoplasia (AIN)

A

various degress of pre-malignant squamous dysplasia of anal canal –> associated with HPV infections

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49
Q

Anal carcinoma

A

RARE

- most are squamous cell type –> associated with HPV

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50
Q

Jaundice

A

yellow discoloration of skin –> retention of bilirubin (2-3 mg/dL)

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51
Q

Icterus

A

yellow discoloration of sclera –> retention of bilirubin

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52
Q

Bilirubin metabolism

A

Reticuloendothelial cells convert heme to bilirubin –> transported to liver complexed with albumin –> conjugated with glucuronic acid in liver cells –> conjugated bilirubin excreted in bile

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53
Q

Unconjugated bilirubin

A

bilirubin complexed with albumin –> water insoluble

- toxic to tissues –> not excreted in urine

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54
Q

Conjugated bilirubin

A

not bound to albumin –> water soluble

- not toxic to tissues –> excreted in urine

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55
Q

Unconjugated hyperbilirubinemia

A

conjugated fraction <20%

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56
Q

Conjugated hyperbilirubinemia

A

conjugated fraction >50%

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57
Q

Neonatal jaundice

A

primarily caused by normal neonatal alterations in bilirubin metabolism including increased bilirubin production, decreased clearance, increased enterohepatic circulation
- if it gets too much –> CNS toxic effects

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58
Q

Gilbert’s Syndrome

A

autosomal recessive inheritance
- decreased glucuronyltransferase activity –> increased unconjugated bilirubin
benign

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59
Q

Intrahepatic Cholestasis

A

bile within hepatocytes, canalicular bile stasis

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60
Q

Extrahepatic cholestasis

A

canalicular bile stasis, bile lakes, bile within distended bile ducts –> promote development of ascending cholangitis

61
Q

Chronic Passive Congestion

A

CPC –> centrilobular congestion

62
Q

Centrilobular hemorrhagic necrosis

A

centrilobular congestion with necrosis

63
Q

Cardiac sclerosis

A

fibrosing reaction following longstanding CPC or centrilobular necrosis
- caused by RHF, hepatic vein thrombosis, LHF, shock

64
Q

Liver infarcts

A

RARE –> secondary to double blood supply

65
Q

Hepatic vein thrombosis –> Budd-Chiari syndrome

A

thrombosis of 2 or more hepatic vein branches (outflow problem)
CLASSIC TRIAD –> hepatomegaly, ascites, ab pain
- can have thrombosis of IVC
- diagnosis confirmed by imaging

66
Q

Sinusoidal obstruction syndrome

A

presence of obstruction (nonthrombotic) in patients exposed to radiation (iatrogenic)

  • marked narrowing and obliteration of central vein lumens
  • painful hepatomegaly, weight gain, increased serum bilirubin
67
Q

Portal Vein Thrombosis

A

INFLOW OBSTRUCTION
Extrahepatic cause -> intra-abdominal sepsis, inherited/acquired hypercoaguable disorder, trauma, pancreatitis
Intrahepatic cause -> cirrhosis, invasion or portal vein by cancer

68
Q

Peliosis hepatitis

A

RARE -> primary hepatic sinusoidal dilatation with rupture

- use of anabolic steroids, AIDS, malignancy

69
Q

Hepatitis A virus

A

SS RNA virus

  • infects liver cells –> injury due to immune response (CD8 Tcells) –> lysis of cells
  • viremia is transient –> shed in feces (fecal-oral)
  • majority of infections are subclinical (0.1% acute liver failure)
  • does not cause chronic hepatitis
  • IgM HAV antibody shows first –> then IgG HAV antibody (protective immunity)
70
Q

Hepatitis B virus

A
  • infects liver cells –> injury due to immune response (CD8 Tcells) –> lysis of cells
  • virus present in blood and body fluids (transmitted parenterally, sex, perinatal)
  • majority are asymptomatic, 30% develop acute hepatitis
  • can develop chronic hepatitis –> may resolve, may progress to cirrhosis, may develop carrier state
71
Q

Carrier state of Hep B virus

A

persistent HBV infection without significant ongoing disease

- typically occurs as result of exposure at childbirth

72
Q

HBV Serologies

A

HBsAg –> indicates ongoing HBV infection (acute/chronic)
HBeAg and HBV DNA –> active viral replication
IgM anti-HBc –> detected at onset –> replaced by IgG anti-HBc
IgG anti-HBc –> indicates past exposure
Anti-HBs –> indicates recovery and immunity from HBV
Anti-Hbe –> indicates infection is resolving

73
Q

Diagnosis of acute HBV

A

made with clinical features and positive HBsAg or IgM anti-HBc

74
Q

HDV

A

defective ss RNA virus –> ONLY IN PRESENCE OF HBV –> must be encapsulated by HBsAg
- can infect individual with chronic infection or co-infection
- HDV infection superimposed on existing HBV infection is worse (SUPERINFECTION)
- combined infection worse than just HBV infection
IV DRUG USERS

75
Q

HDV Serologies

A

IgM anti-HDV –> acute or recent HDV infection
IgG anti-HDV –> indicates previous infection with HDV
Anti-HDV –> measures both IgG and IgM
HDAg and HDV RNA –> active viral replication and ongoing infection
Coinfection = IgM anti-HBc (+) –> active or recent HBV
Superinfection = IgM anti-HBc (-) –> chronic HBV

76
Q

Hepatitis C Virus

A

ss RNA virus –> spread parenterally, sexually

  • acute liver failure is RARE
  • chronic HCV infection = 50% chronic liver disease
  • many genotypes and subtypes –> treatment/prognosis
  • HIGH MUTATION RATE –> no vaccine
77
Q

HCV Antibodies

A

anti-HCV develop around 10 weeks –> does not confer immunity because of high mutation rate
- active infection confirmed by PCR measuring viral load

78
Q

Things screened for on blood donors

A 
HBsAg
anti-HBc
HBV DNA
anti-HCV
HCV RNA
79
Q

Hepatitis E virus

A

ss RNA virus –> fecal-oral

  • does not cause chronic hepatitis (vowels = A, E)
  • diagnosis established by anti-IgM HEV and HEV RNA
80
Q

Clinical syndromes of acute viral hepatitis

A

Incubation –> variable
Preicteric prodrome –> non-specific constitutional symptoms, elevated ALT and AST
Icteric phase –> jaundice not always present, conjugated hyperbilirubinemia, dark urine

81
Q

Pathology of acute viral hepatitis

A

LOBULAR HEPATITIS –> diffuse liver cell degeneration, focal hepatocellular necrosis and apoptosis
- Kupffer cell hyperplasia

82
Q

Clinical syndromes of chronic viral hepatitis

A

> 6 months (consonants –> B, D, C)

- periportal hepatitis with bridging necrosis and progressive fibrosis

83
Q

Massive hepatic necrosis

A

caused by a variety of agents
- typically suffer from acute liver failure –> if survive –> reticulin framework is intact and architecture can be regenerated
FOCAL RANDOM –> (inflammatory) viral, autoimmune
ZONAL –> (non-inflammatory) drugs, ischemia

84
Q

Perinatal HBV

A

infants born to mothers (+) for HBsAg and HBeAg –> become chronic HBV carriers

85
Q

Autoimmune Hepatitis

A

liver injury due to T-cell mediated autoimmune pathogenesis (increased plasma cells)
Type 1 –> anti-nuclear antibodies, anti-smooth muscle actin, anti-soluble liver antigen/liver-pancreas
- middle age (HLA-DR3)
Type 2 –> anti-liver/kidney microsome-1, anti-liver cytosol antigen antibodies
- kids
DIAGNOSIS OF EXCLUSION

86
Q

Acute Hepatitis Panel

A

IgM anti-HAV
HBsAg
IgM anti-HBc
Anti-HCV

87
Q

Chronic Hepatitis Panel

A

HBsAg
Anti-HBs
Anti-HBc
Anti-HCV

88
Q

Cirrhosis

A

caused by various etiologies

  • WIDELY distributed interconnecting fibrous scars with NODULAR parenchymal regeneration
  • stellate cells proliferate and become activated into fibrogenic myofibroblasts
  • possibly reversible (controversial)
89
Q

Complications of cirrhosis

A
  1. hepatic failure –> fibrosis destroys and impairs normal vascular interconnections –> decreased perfusion
  2. Portal HTN –> increased resistance to portal blood flow as result of fibrosis of sinusoids and central veins
  3. Hepatocellular carcinoma
90
Q

Hepatic failure

A

Acute -> associated with encephalopathy and coagulopathy (ABSENCE of pre-existing liver disease)
Chronic –> chronic liver disease associated with cirrhosis

91
Q

Portal HTN

A

EVA-SHE
posthepatic, intrahepatic, or prehepatic causes
- Ascites, portosystemic shunts (esophageal varices), splenomegaly, hepatic encephalopathy

92
Q

Alcoholic Liver Disease

A

ethanol (acetaldehyde) is hepatotoxin
Early –> alcoholic steatosis (fatty liver) - reversible, swollen fatty liver
Middle –> steatohepatitis (liver cell injury, mallory bodies, neutrophilic inflammation)
Late –> steatofibrosis (perivenular and pericellular fibrosis) -> shrunken, non-fatty liver

93
Q

Major causes of death in ALD

A 
hepatic encephalopathy
massive hemorrhage (esophageal varices)
infection -> secondary to ascites
hepatorenal syndrome
hepatocellular carcinoma
94
Q

Non-alcoholic fatty liver disease

A

pathology is similat to ALD without consumption of alcohol

  • seen with metabolic syndrome, obesity, type 2 diabetes, dyslipidemia, insulin resistance (steatosis)
  • often indolent disease but can lead to cirrhosis
95
Q

Primary Biliary Cirrhosis

A

autoimmune cholangiopathy with progressive inflammatory destruction of small and medium INTRAHEPATIC ducts (extrahepatic ducts spared)

  • middle-aged females
  • associated with anti-mitochondrial antibodies
  • can get AMA negative PBC
  • insidious onset and pruritis -> increased risk for HCC
  • elevated alkaline phosphatase and GGT
96
Q

Stages of PBC

A

Stage 1 -> lymphocytic/granulomatous cholangitis (florid duct lesion) –> loss of intrahepatic bile ducts
Stage 2 -> periportal hepatitis and periportal fibrosis
Stage 3 -> bridging necrosis and fibrosis
Stage 4 -> cirrhosis

97
Q

Secondary Biliary Cirrhosis

A

cirrhosis secondary to any disorder causing prolonged extrahepatic bile duct obstruction

98
Q

Primary Sclerosing Cholangitis

A

autoimmune cholangiopathy with progressive, random, fibroinflammatory obliteration of extra and intrahepatic bile ducts

  • p-ANCA (+) and associated with UC
  • elevated alkaline phosphatase and GGT
  • cholangiography demonstrates strictures and dilations of ducts (beaded)
99
Q

Hemochromatosis

A

disorder of excessive iron absorption resulting in accumulation of iron in tissues –> organ injury
- inhertied -> hereditary
- acquired -> transfusions
CLASSIC TRIAD -> cirrhosis, diabetes, skin pigmentation

100
Q

Hereditary Hemochromatosis

A

autosomal recessive disorder –> excessive absorption

  • decreased hepcidin which regulated iron absorption
  • adult form = HFE (chromo 6)
  • low penetrance
101
Q

Secondary Hemochromatosis

A

parenteral iron overload (transfusion), ineffective erythropoiesis, increased oral intake

102
Q

Hemochromatosis pathology

A

hemosiderin deposition in tissues and organs

- liver, pancreas, heart, skin, endocrine, joints

103
Q

Best screening test for hemochomatosis?

A

fasting transferrin saturation

104
Q

Treatment of hemochromatosis

A

chelation or phlebotomy

- increased risk for HCC, cardiac disease, liver failure

105
Q

Wilson’s disease

A

VERY heterogeneous presentations

  • autosomal recessive disorder of copper metabolism –> accumulation of toxic levels of copper (liver, eye, brain)
  • mutations in ATP7B –> impaired secretion of copper as ceruloplasmin
  • copper accumulates and ‘spills’ over into blood –> toxic
  • 40% patients present with neuropsychiatric symptoms (CNS toxicity)
  • Kayser-Fleischer rings
106
Q

Alpha-1-Antitrypsin deficiency

A

co-dominant autosomal disorder –> abnormally low levels of alpha-1-antitrypsin (protease inhibitor)
- without it, you get protease damage (emphysema)
- liver disease is related to accumulation of A1AT in hepatocytes –> null-null don’t get liver disease
Diagnostic test = A1AT level and phenotype

107
Q

Drug-related liver injury

A

Direct hepatotoxicity –> toxic to liver is predictable and dose-dependent
Unpredictable hepatotoxicity –> produce liver injury in unpredictable manner, not all exposed develop injury

108
Q

Reye’s Syndrome

A

acute postviral illness characterized by liver injury and encephalopathy due to aspirin administration
- microvesicular steatosis (mitochondrial injury)

109
Q

Neonatal cholestasis

A

prolonged conjugated hyperbilirubinemia

  • Biliary atresia –> complete/partial obstruction of lumen
  • Neonatal hepatitis
110
Q

Liver Function Tests

A
  1. Hepatocellular damage –> AST and ALT
  2. Cholestasis –> Alkaline phosphatase, GGT (injury to bile duct epithelium)
  3. Hepatic synthesis –> Albumin, PTT, clotting factors
  4. determine specific etiology
111
Q

Aspartate aminotransferase

A

indication of hepatocellular damage –> not specific for liver, found in heart, muscle, brain, and kidney
- 80% found in mitochondria –> damage by ethanol

112
Q

Alanine aminotransferase

A

indication of hepatocellular damage –> specific for liver

113
Q

Alkaline Phosphatase

A

indication of bile duct damage/obstruction –> increase is usually due to bone or liver disease
- measure GGT to be sure

114
Q

Liver Test Etiologies

A

Viral hepatitis –> serology/nuclear testing
Autoimmune hepatitis –> ANA, aSMA
Wilson’s –> ceruloplasmin
A1AT –> A1AT, phenotype
Hemochromatosis –> Fe, TIBC, transferrin saturation, genetics
PBC –> anti-mitochondrial antibodies

115
Q

Liver Biopsy findings

A

Ground glass appearance –> chronic HBV
Plasma cells –> autoimmune hepatitis, PBC
Lymphocytic/granulomatous cholangitis –> PBC
Fibrous obliterative cholagnitis –> PSC
Periportal hepatitis w/ mild steatosis –> chronic HCV
Globular hepatocyte inclusion –> A1AT deficiency

116
Q

Preeclampsia

A 
maternal HTN, proteinuria, peripheral edema, coag abnormalities
HELLP syndrome
Hemolysis
Elevated Liver enzymes
Low Platelets
117
Q

Acute fatty liver of pregnancy

A

acute onset of liver dysfunction

  • severe cases can result in acute hepatic failure
  • microvesicular steatosis
118
Q

Intrahepatic cholestasis of pregnancy

A

mild increase in serum conjugated bilirubin

119
Q

Hemangioma

A

most common benign neoplasm of liver

- discrete lesions of red-blue hemorrhagic nodules composed of dilated endothelial lined blood filled channels

120
Q

Cysts

A

composed of atrophic biliary epithelium, detached from biliary tree

121
Q

Simple Cysts

A

single, small cluster not associated with another condition

122
Q

Polcystic liver disease

A

multiple cysts –> associated with PCKD

123
Q

Choledocal cyst

A

congenital dilatation of common bile duct

124
Q

Caroli’s disease

A

congenital disorders resulting in intrahepatic biliary dilatations
- suffer from bouts of cholangitis

125
Q

Congenital hepatic fibrosis

A

non-cirrhotic fibrotic liver disease of children (autosomal recessive)

126
Q

Focal Nodular Hyperplasia

A

well-demarcated lesion composed of proliferation of all liver parenchymal elements
- hyperplastic response to localized vascular occlusive event
central fibrous scar with STELLATE CONFIGURATION

127
Q

Nodular Regenerative Hyperplasia

A

diffuse nonfibrosing nodular hyperplasia of liver

- compression of liver can result in portal HTN

128
Q

Hepatocellular Adenoma

A

well-circumscribed benign neoplasm composed of well-differentiated hepatocytes
- young women on oral contraceptives

129
Q

Bile Duct Hamartoma

A

von Meyenberg Complex

  • grossly –> single or multiple small white nodules (looks like metastatic carcionma)
  • disordered collection of ectatic bile ducts in fibrous stroma
130
Q

Bile Duct Adenoma

A

usually solitary, benign proliferation of bile ducts

- NEED BIOPSY

131
Q

Metastatic tumors of liver

A

MORE COMMON THAN PRIMARY TUMORS

  • usually multiple tumors from lung, GI, breast, and pancreas
  • usually liver function is fine!
132
Q

Hepatocellular Carcinoma

A

Solitary large mass or multiple nodules
aggressive tumor, range of microscopic appearances
chronic liver diseases most common setting for HCC
- hepatotrophic viruses
- hepatocarcinogens (aflatoxins)
- cirrhosis

133
Q

Fibrolamellar variant of HCC

A

polygonal oncocytic tumor cells in nests and cords separated by lamellar fibrous stroma

134
Q

Cholangiocarcinoma

A

carcinoma arising from intrahepatic or extrahepatic bile ducts –> adenocarcinomas
- associated with chronic cholangitis, infections, PSC, and other inflammatory conditions of liver

135
Q

Mixed hepatocholangiocarcinoma

A

HCC with ductular proliferation

136
Q

Angiosarcoma

A

malignancy of endothelial cells –> anastamosing vascular channels lined by malignant cells showing endothelial differentiation
- Risks –> thorostat, vinyl chloride, arsenic
aggressive malignancy

137
Q

Cholelithiasis

A

gallstones

  • any supersaturation of bile by cholesterol –> lithogenic
  • any increase in unconjugated bilirubin –> lithogenic
138
Q

Types of Gallstones

A

Cholesterol –> 90%
Pigment –> 10% (bilirubin plus calcium)
Most could be classified as mixed
Best way to visualize = ultrasound

139
Q

Conditions associated with increased biliary cholesterol

A 
Age
Obese/metabolic syndrome
Female
Rapid weight loss
Drugs
Gallbladder stasis
4 F's = female, fat, forty, fertile
140
Q

Acute Calculous Cholecystitis

A

due to obstruction of cystic duct by gallstone

- irritation, inflammation, distention, increased pressure, compromised blood flow

141
Q

Acute Acalculous Cholecystitis

A

due to ischemia of gallbladder –> very sick individuals

142
Q

Chronic Colecystitis

A

always associated with cholelithiasis

  • chronic lymphocytic inflammation and fibrosis
  • ‘porcelain’ gallbladder
143
Q

Cholesterolosis

A

subepithelial accumulation of lipid-laden macrophages

- excessive accumulation of cholesterol from supersaturated bile

144
Q

Cholesterol polyp

A

yellow, small polyps associated with cholesterolosis

145
Q

Hydrops of gallbladder

A

total obstruction of cystic duct –> trapped bile –> resorbed –> atrophic walls of gallbladder

146
Q

Adenoma of gallbladder

A

hardly every discovered, asymptomatic

147
Q

Adenomyoma

A

located in fundus –> gallbladder diverticulae with focal muscular hypertrophy of gallbladder wall

148
Q

Carcinoma of gallbladder

A

old age –> associated with cholelithiasis

  • irritative trauma or chronic inflammation
  • most are adenocarcinomas
149
Q

Extrahepatic cholangiocarcinoma

A

uncommon –> almost all adenocarcinomas
Klatskin tumor –> cholangiocarcinoma arising at confluence of R/L hepatic ducts at liver hilus
Also at ampulla of Vater –> periampullary carcinoma
- increased alkaline phosphatase and GGT

GI Exam 3 (10 decks)

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