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
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 (+)
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 (+)
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
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
6
Q
Long-term complication of both UC and CD
A
development of intestinal adenocarcinoma
7
Q
Lymphocytic colitis
A
increased lamina propria chronic inflammation with increased intraepithelial lymphocytes and surface epithelial damage
8
Q
Collagenous colitis
A
similar features as lymphocytic along with a band a subepithelial collagen
9
Q
Radiation enterocolitis
A
complication of radiation therapy
10
Q
Neonatal necrotizing enterocolitis
A
first week of premature infants life -> small and large bowel exhibit transmural necrosis -> bacterial overgrowth -> air bubbles
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
12
Q
Graft vs Host disease
A
donor lymphocytes attack the host colon
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
14
Q
ROME diagnostic criteria for IBS
A
recurrent ab pain or discomfort for 3 days per month with 2 of following:
- Improved with defecation
- Onset associated with change in frequency of stool
- Onset associated with change in form of stool
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
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
17
Q
Non-neoplastic intestinal polyps
A
Inflammatory
Hamartomatous
Hyperplastic
18
Q
Neoplastic intestinal polyps
A
Adenoma
Sessile serrated adenoma
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
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
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
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
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
24
Q
Sessile serrated adenoma
A
Sessile polyps resembling hyperplastic polyps -> precursor to adenocarcinoma
- lac adenomatous epithelium -> R colon
- crypt dilation
25
Serrated adenoma
exhibits serration along with uniform, eosinophilic dysplastic epithelium
26
Familial Adenomatosis Polyposis
autosomal dominance inheritance
- mutations in APC tumor suppressor gene (double-hit)
- develop large number (1000s) of polyps in colon
27
Gardner's Syndrome
in addition to FAP, patients develop desmoid tumors, osteomas, epidermal cysts, and thyroid tumors
28
Turcot Syndrome
coexistence of hereditary CRC and CNS tumors
29
Hereditary Non-polyposis Colorectal Cancer
Lynch Syndrome --> caused by mutations in genes that encode enzymatic MMR proteins
- need the 2nd hit (LOH)
30
Colorectal Adenocarcinoma
```
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
```
31
APC/beta-catenin pathway
mutation in APC (tumor suppressor gene) --> 2nd hit of APC/beta-catenin --> K-RAS mutation --> p53 --> tumors
- often left-sided tumors
32
MMR pathway
mutation in MMR --> 2nd hit in MMR gene --> microsatellite instability --> accumulated mutations --> tumors
- often right-sided tumors
33
Iron-deficiency anemia in older man/woman?
CRC until proven otherwise!!!!
34
What does staging indicate?
the extent of the disease!!!!!
35
K-Ras mutation
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
36
Proto-onco gene
genes that regulate cell cycle --> when mutated they become onco-genes that are unregulated cell cycle genes
37
Cologuard
Stool DNA test that detects abberant methylation of 2 promoter genes as well as K-Ras mutations
38
Small bowel carcinoma
much less common that CRC
- 50% occur in duodenum and around ampulla of vater
Risks:
- FAP, Crohn's, celiac disease
39
Gastrointestinal Stromal Tumors (GIST)
gain of function mutation in KIT (tyrosine kinase receptor)
40
Acute Appendicitis
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
41
Complications of Appendicitis
perforation -->
| periappendiceal abscess, pyelophlebitis, portal venous thrombosis, liver abscess, bacteremia, sepsis, death
42
Appendiceal neuroendocrine tumor
most common tumor of appendix
- typically small --> non-functioning
- large --> functioning
43
Pseudomyxoma peritonei
gross descriptive term for presence of abundance mucinous material on peritoneal surfaces
44
Anal hemorrhoids
result from ectasia of rectal venous plexus --> persitently elevated venous pressure (straining at stool)
External --> below pectinate line
Internal --> above pectiante line
45
Anal fissure
linear separation of tissue of anal canal extending through mucosa
46
Anal fistula
fistula tract may lead to skin, end blindly in peritoneal tissue
47
Rectal prolapse
intussusception of rectum through anus --> due to weak rectal support
48
Anal intraepithelial neoplasia (AIN)
various degress of pre-malignant squamous dysplasia of anal canal --> associated with HPV infections
49
Anal carcinoma
RARE
| - most are squamous cell type --> associated with HPV
50
Jaundice
yellow discoloration of skin --> retention of bilirubin (2-3 mg/dL)
51
Icterus
yellow discoloration of sclera --> retention of bilirubin
52
Bilirubin metabolism
Reticuloendothelial cells convert heme to bilirubin --> transported to liver complexed with albumin --> conjugated with glucuronic acid in liver cells --> conjugated bilirubin excreted in bile
53
Unconjugated bilirubin
bilirubin complexed with albumin --> water insoluble
| - toxic to tissues --> not excreted in urine
54
Conjugated bilirubin
not bound to albumin --> water soluble
| - not toxic to tissues --> excreted in urine
55
Unconjugated hyperbilirubinemia
conjugated fraction <20%
56
Conjugated hyperbilirubinemia
conjugated fraction >50%
57
Neonatal jaundice
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
58
Gilbert's Syndrome
autosomal recessive inheritance
- decreased glucuronyltransferase activity --> increased unconjugated bilirubin
benign
59
Intrahepatic Cholestasis
bile within hepatocytes, canalicular bile stasis
60
Extrahepatic cholestasis
canalicular bile stasis, bile lakes, bile within distended bile ducts --> promote development of ascending cholangitis
61
Chronic Passive Congestion
CPC --> centrilobular congestion
62
Centrilobular hemorrhagic necrosis
centrilobular congestion with necrosis
63
Cardiac sclerosis
fibrosing reaction following longstanding CPC or centrilobular necrosis
- caused by RHF, hepatic vein thrombosis, LHF, shock
64
Liver infarcts
RARE --> secondary to double blood supply
65
Hepatic vein thrombosis --> Budd-Chiari syndrome
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
Sinusoidal obstruction syndrome
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
Portal Vein Thrombosis
INFLOW OBSTRUCTION
Extrahepatic cause -> intra-abdominal sepsis, inherited/acquired hypercoaguable disorder, trauma, pancreatitis
Intrahepatic cause -> cirrhosis, invasion or portal vein by cancer
68
Peliosis hepatitis
RARE -> primary hepatic sinusoidal dilatation with rupture
| - use of anabolic steroids, AIDS, malignancy
69
Hepatitis A virus
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
Hepatitis B virus
- 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
Carrier state of Hep B virus
persistent HBV infection without significant ongoing disease
| - typically occurs as result of exposure at childbirth
72
HBV Serologies
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
Diagnosis of acute HBV
made with clinical features and positive HBsAg or IgM anti-HBc
74
HDV
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
HDV Serologies
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
Hepatitis C Virus
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
HCV Antibodies
anti-HCV develop around 10 weeks --> does not confer immunity because of high mutation rate
- active infection confirmed by PCR measuring viral load
78
Things screened for on blood donors
```
HBsAg
anti-HBc
HBV DNA
anti-HCV
HCV RNA
```
79
Hepatitis E virus
ss RNA virus --> fecal-oral
- does not cause chronic hepatitis (vowels = A, E)
- diagnosis established by anti-IgM HEV and HEV RNA
80
Clinical syndromes of acute viral hepatitis
Incubation --> variable
Preicteric prodrome --> non-specific constitutional symptoms, elevated ALT and AST
Icteric phase --> jaundice not always present, conjugated hyperbilirubinemia, dark urine
81
Pathology of acute viral hepatitis
LOBULAR HEPATITIS --> diffuse liver cell degeneration, focal hepatocellular necrosis and apoptosis
- Kupffer cell hyperplasia
82
Clinical syndromes of chronic viral hepatitis
>6 months (consonants --> B, D, C)
| - periportal hepatitis with bridging necrosis and progressive fibrosis
83
Massive hepatic necrosis
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
Perinatal HBV
infants born to mothers (+) for HBsAg and HBeAg --> become chronic HBV carriers
85
Autoimmune Hepatitis
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
Acute Hepatitis Panel
IgM anti-HAV
HBsAg
IgM anti-HBc
Anti-HCV
87
Chronic Hepatitis Panel
HBsAg
Anti-HBs
Anti-HBc
Anti-HCV
88
Cirrhosis
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
Complications of cirrhosis
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
Hepatic failure
Acute -> associated with encephalopathy and coagulopathy (ABSENCE of pre-existing liver disease)
Chronic --> chronic liver disease associated with cirrhosis
91
Portal HTN
EVA-SHE
posthepatic, intrahepatic, or prehepatic causes
- Ascites, portosystemic shunts (esophageal varices), splenomegaly, hepatic encephalopathy
92
Alcoholic Liver Disease
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
Major causes of death in ALD
```
hepatic encephalopathy
massive hemorrhage (esophageal varices)
infection -> secondary to ascites
hepatorenal syndrome
hepatocellular carcinoma
```
94
Non-alcoholic fatty liver disease
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
Primary Biliary Cirrhosis
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
Stages of PBC
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
Secondary Biliary Cirrhosis
cirrhosis secondary to any disorder causing prolonged extrahepatic bile duct obstruction
98
Primary Sclerosing Cholangitis
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
Hemochromatosis
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
Hereditary Hemochromatosis
autosomal recessive disorder --> excessive absorption
- decreased hepcidin which regulated iron absorption
- adult form = HFE (chromo 6)
- low penetrance
101
Secondary Hemochromatosis
parenteral iron overload (transfusion), ineffective erythropoiesis, increased oral intake
102
Hemochromatosis pathology
hemosiderin deposition in tissues and organs
| - liver, pancreas, heart, skin, endocrine, joints
103
Best screening test for hemochomatosis?
fasting transferrin saturation
104
Treatment of hemochromatosis
chelation or phlebotomy
| - increased risk for HCC, cardiac disease, liver failure
105
Wilson's disease
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
Alpha-1-Antitrypsin deficiency
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
Drug-related liver injury
Direct hepatotoxicity --> toxic to liver is predictable and dose-dependent
Unpredictable hepatotoxicity --> produce liver injury in unpredictable manner, not all exposed develop injury
108
Reye's Syndrome
acute postviral illness characterized by liver injury and encephalopathy due to aspirin administration
- microvesicular steatosis (mitochondrial injury)
109
Neonatal cholestasis
prolonged conjugated hyperbilirubinemia
- Biliary atresia --> complete/partial obstruction of lumen
- Neonatal hepatitis
110
Liver Function Tests
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
Aspartate aminotransferase
indication of hepatocellular damage --> not specific for liver, found in heart, muscle, brain, and kidney
- 80% found in mitochondria --> damage by ethanol
112
Alanine aminotransferase
indication of hepatocellular damage --> specific for liver
113
Alkaline Phosphatase
indication of bile duct damage/obstruction --> increase is usually due to bone or liver disease
- measure GGT to be sure
114
Liver Test Etiologies
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
Liver Biopsy findings
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
Preeclampsia
```
maternal HTN, proteinuria, peripheral edema, coag abnormalities
HELLP syndrome
Hemolysis
Elevated Liver enzymes
Low Platelets
```
117
Acute fatty liver of pregnancy
acute onset of liver dysfunction
- severe cases can result in acute hepatic failure
- microvesicular steatosis
118
Intrahepatic cholestasis of pregnancy
mild increase in serum conjugated bilirubin
119
Hemangioma
most common benign neoplasm of liver
| - discrete lesions of red-blue hemorrhagic nodules composed of dilated endothelial lined blood filled channels
120
Cysts
composed of atrophic biliary epithelium, detached from biliary tree
121
Simple Cysts
single, small cluster not associated with another condition
122
Polcystic liver disease
multiple cysts --> associated with PCKD
123
Choledocal cyst
congenital dilatation of common bile duct
124
Caroli's disease
congenital disorders resulting in intrahepatic biliary dilatations
- suffer from bouts of cholangitis
125
Congenital hepatic fibrosis
non-cirrhotic fibrotic liver disease of children (autosomal recessive)
126
Focal Nodular Hyperplasia
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
Nodular Regenerative Hyperplasia
diffuse nonfibrosing nodular hyperplasia of liver
| - compression of liver can result in portal HTN
128
Hepatocellular Adenoma
well-circumscribed benign neoplasm composed of well-differentiated hepatocytes
- young women on oral contraceptives
129
Bile Duct Hamartoma
von Meyenberg Complex
- grossly --> single or multiple small white nodules (looks like metastatic carcionma)
- disordered collection of ectatic bile ducts in fibrous stroma
130
Bile Duct Adenoma
usually solitary, benign proliferation of bile ducts
| - NEED BIOPSY
131
Metastatic tumors of liver
MORE COMMON THAN PRIMARY TUMORS
- usually multiple tumors from lung, GI, breast, and pancreas
- usually liver function is fine!
132
Hepatocellular Carcinoma
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
Fibrolamellar variant of HCC
polygonal oncocytic tumor cells in nests and cords separated by lamellar fibrous stroma
134
Cholangiocarcinoma
carcinoma arising from intrahepatic or extrahepatic bile ducts --> adenocarcinomas
- associated with chronic cholangitis, infections, PSC, and other inflammatory conditions of liver
135
Mixed hepatocholangiocarcinoma
HCC with ductular proliferation
136
Angiosarcoma
malignancy of endothelial cells --> anastamosing vascular channels lined by malignant cells showing endothelial differentiation
- Risks --> thorostat, vinyl chloride, arsenic
aggressive malignancy
137
Cholelithiasis
gallstones
- any supersaturation of bile by cholesterol --> lithogenic
- any increase in unconjugated bilirubin --> lithogenic
138
Types of Gallstones
Cholesterol --> 90%
Pigment --> 10% (bilirubin plus calcium)
Most could be classified as mixed
Best way to visualize = ultrasound
139
Conditions associated with increased biliary cholesterol
```
Age
Obese/metabolic syndrome
Female
Rapid weight loss
Drugs
Gallbladder stasis
4 F's = female, fat, forty, fertile
```
140
Acute Calculous Cholecystitis
due to obstruction of cystic duct by gallstone
| - irritation, inflammation, distention, increased pressure, compromised blood flow
141
Acute Acalculous Cholecystitis
due to ischemia of gallbladder --> very sick individuals
142
Chronic Colecystitis
always associated with cholelithiasis
- chronic lymphocytic inflammation and fibrosis
- 'porcelain' gallbladder
143
Cholesterolosis
subepithelial accumulation of lipid-laden macrophages
| - excessive accumulation of cholesterol from supersaturated bile
144
Cholesterol polyp
yellow, small polyps associated with cholesterolosis
145
Hydrops of gallbladder
total obstruction of cystic duct --> trapped bile --> resorbed --> atrophic walls of gallbladder
146
Adenoma of gallbladder
hardly every discovered, asymptomatic
147
Adenomyoma
located in fundus --> gallbladder diverticulae with focal muscular hypertrophy of gallbladder wall
148
Carcinoma of gallbladder
old age --> associated with cholelithiasis
- irritative trauma or chronic inflammation
- most are adenocarcinomas
149
Extrahepatic cholangiocarcinoma
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
