Pathology of the Liver, Gall Bladder, and Pancreas Flashcards
1
Q
Anatomy of the Liver
1. ——— gm (approximately 2.5% of body weight)
A
1400 to 1600
2
Q
Anatomy of the Liver
2. ——– supply-portal vein (60-70%) and —– artery (30-40%).
A
Dual blood
hepatic
3
Q
Anatomy of the Liver
3. Zonation in liver parenchyma-
A
note gradient of activity of many hepatic enzymes, usually see a lobular architecture.
4
Q
Anatomy of the Liver
- Major diseases of the liver are:
A
viral hepatitis, alcoholic liver disease, nonalcoholic liver disease (fatty liver, etc.), hepatocellular carcinoma (HCC)
5
Q
Anatomy of the Liver
- Hepatic injury-
A
see hepatocyte degeneration or accumulation of toxic products, necrosis and apoptosis of hepatocytes, inflammation (may facilitate or impede healing), regeneration and fibrosis.
6
Q
Liver B. Physiological Functions
1. Maintains
A
metabolic homeostasis-processes amino acids, carbohydrates, lipids, vitamins
7
Q
Liver B. Physiological Functions
- Synthesizes
A
serum proteins
8
Q
Liver B. Physiological Functions
- Primary site for
A
detoxification of xenobiotics and waste products
9
Q
Liver B. Physiological Functions
- Enormous functional
A
reserve and regenerative capacity can mask early hepatic injury
10
Q
C. Cirrhosis
1. Among top 10 most common
A
causes of death in the U.S and the primary route for liver-related deaths.
11
Q
Cirrhosis
- Etiologies include:
A
Alcohol (EtOH) abuse (toxicity, nutritional deprivation), viral hepatitis, non-EtOH steatohepatitis, biliary disease, obesity, DM, medications, iron overload.
12
Q
Cirrhosis
o Iron overload can lead to
A
hepatocyte death and inflammation.
13
Q
Cirrhosis
- Morphologic changes are:
A
1) bridging fibrous septa, 2) parenchymal nodules, 3) changes in architecture, with parenchymal injury and scarring as the end result.
14
Q
Cirrhosis
A fibrotic liver has a markedly
A
compromised blood supply and decreased function.
15
Q
Cirrhosis
Complications include
A
reduced liver function, portal hypertension and increased risk for hepatocellular Ca
16
Q
Cirrhosis
. Clinical manifestations:
A
o Nonspecific symptoms e.g. weight loss, weakness. Reserve may mask symptoms.
o Liver failure
o Portal hypertension
17
Q
D. Portal hypertension
1. Increased pressure of
A
portal blood flow can occur: prehepatic (obstructive thrombi), intrahepatic (cirrhosis), and post hepatic (right sided heart failure).
18
Q
- Consequences of portal hypertension:
A
1) ascites (excess fluid in peritoneal cavity-fluid is generally serous in nature), 2) esophageal varices, 3) splenomegaly, 4) hepatic encephalopathy, 5) hypogonadism.
19
Q
Jaundice and cholestasis
- Excess
A
bilirubin. 2.0 mg/dl
• Unconjugated: Insoluble, toxic
• Conjugated: Soluble, nontoxic
20
Q
Jaundice and cholestasis;
2. Causes of jaundice:
A
hemolytic anemias (#1), bilirubin overproduction, hepatitis, obstruction of bile flow.
21
Q
Jaundice and cholestasis;
- Function of hepatic bile:
A
1) emulsification of fats with bile salts, 2) elimination of bilirubin, excess cholesterol, xenobiotics, etc.
22
Q
Jaundice and cholestasis; symptoms
A
- Yellow color of skin (classically, jaundice) and sclera (classically, icterus).
23
Q
F. Infectious Disorders of the Liver.
. Viral hepatitis-systemic viral infections can involve
A
liver e.g. Epstein Barr Virus (EBV), Cytomegalovirus (CMV), yellow fever, rubella, herpesviruses.
24
Q
F. Infectious Disorders of the Liver.
- Generally use “hepatitis” for
A
hepatotropic viruses e.g. A, B, C, D, E and G
25
F. Infectious Disorders of the Liver.
3. Hepatitis A is a
benign, self-limiting disease. HAV viremia is transient-rarely screen donor blood for HAV.
• Fecal-oral route of transmission, seen with overcrowding/unsanitary conditions. Ingestion of contaminated water and food
• Incubation 2-6 weeks
• NO carrier state. No chronic disease
26
F. Infectious Disorders of the Liver.
Possible results of Hepatitis B infection:
a. acute hepatitis with recovery and clearance (Self-limited in 90% cases)
b. nonprogressive chronic hepatitis
c. progressive disease ending in cirrhosis
d. asymptomatic carrier state. Hepatitis B induced liver disease is an important precursor for hepatocellular carcinoma.
27
F. Infectious Disorders of the Liver.
Hepatitis B
* DNA virus
* Parenteral contact/sexual spread
* Incubation 4-26 weeks
28
F. Infectious Disorders of the Liver.
Hep b
• Host immune response determines the
ultimate outcome. Hepatocyte damage-likely reflects CD8+ cytotoxic T cell damage to Hepatitis B infected hepatocytes. Optimal outcome is to obtain viral clearance without a lot of collateral damage to liver tissues.
29
```
F. Infectious Disorders of the Liver.
Hep B
• Serology:
• Vaccine:
• Increased risk of
```
Remains in blood
95 % protective Ab response
hepatocellular response
30
F. Infectious Disorders of the Liver.
5. Hepatitis C is a major cause of liver disease worldwide. Unlike Hepatitis B, with Hepatitis C infection the
progression to chronic disease occurs in the majority of patients and cirrhosis develops in 20-30% of infected individuals.
31
F. Infectious Disorders of the Liver.
5. Hepatitis C
With Hepatitis C, note persistent
infection, chronic hepatitis.
32
F. Infectious Disorders of the Liver.
5. Hepatitis C
* RNA virus
* Parenteral contact/sexual spread
* Incubation 7-8 weeks, acute phase is asymptomatic
* No vaccine because of genomic instability
* Cirrhosis occurs in approximately 80-85%, and may develop 5 to 20 years later.
* Risk factor for hepatocellular carcinoma.
33
F. Infectious Disorders of the Liver.
5. Hepatitis C
• Most frequent viral infection associated with
the need for liver transplantation. Previously treated with interferon and ribavirin. Treatment with protease and nucleoside inhibitors now considered curative.
34
F. Infectious Disorders of the Liver.
5. Hepatitis C
o Combination drugs:
Harvoni (2014, sofosbuvir & ledipasvir). 12 week course, several others since 2014; often given with ribavirin
35
F. Infectious Disorders of the Liver.
5. Hepatitis C
o Curative in
most patients. Side effects fatigue and headache.
36
F. Infectious Disorders of the Liver.
5. Hepatitis C
o Drugs are Very
expensive (Harvoni $95K, Mavyret [2017] 12 weeks $40K)
37
F. Infectious Disorders of the Liver.
7. Hepatitis D (requires presence of
Hepatitis B for infection) occurs as a co-infection. Co-infection presents like Hepatitis B-usually transient and self-limited.
38
F. Infectious Disorders of the Liver.
| 8. Hepatitis E (similar to A) is an
enterically transmitted, water-borne infection-high mortality rate in pregnant women.
39
Hep E is Not associated with
chronic liver disease.
40
9. Hepatitis G (some similarity to C but is not hepatotropic) infection does not
increase liver enzymes such as serum aminotransferases.
41
Hep G Replicates in
bone marrow and spleen.
42
10. Autoimmune hepatitis is a
chronic, progressive, hepatitis variant with an unknown etiology.
43
Autoimmune hep
| Pathology is associated with
T-cell mediated autoimmunity.
44
F. Drug, Toxin, Alcohol associated liver disease.
1. Drug and toxic injury may be
predictable (intrinsic) or unpredictable (idiosyncratic). Generally adults affected more frequently than pediatric patients, females more than males.
45
F. Drug, Toxin, Alcohol associated liver disease.
2. Predictable hepatic injury with established
liver toxins such as acetaminophen, carbon tetrachloride, EtOH.
46
F. Drug, Toxin, Alcohol associated liver disease.
3. Always include exposure to a
drug or toxicant in the differential diagnosis of liver disease.
47
F. Drug, Toxin, Alcohol associated liver disease.
4. Alcoholic liver disease
o 3 overlapping forms:
1) hepatic steatosis, 2) EtOH hepatitis, 3) cirrhosis (only develops in a minority of patients).
o 60 % of chronic liver disease associated with overuse of alcohol
o 40-50 % of deaths due to cirrhosis
48
F. Drug, Toxin, Alcohol associated liver disease.
5. Fatty liver from
EtOH-little fibrosis at onset, increased deposition with EtOH consumption.
49
F. Drug, Toxin, Alcohol associated liver disease.
Fatty liver form:
Fatty change is
reversible if discontinue EtOH consumption.
50
F. Drug, Toxin, Alcohol associated liver disease.
Fatty liver form:
Mallory or Mallory-Denk bodies:
clumps of cytokeratins, eosinophilic cytoplasmic inclusions.
51
F. Drug, Toxin, Alcohol associated liver disease.
| 6. Final stage of cirrhosis
-the liver resembles from both macro and micro cirrhosis developing from hepatitis.
52
F. Drug, Toxin, Alcohol associated liver disease.
7. EtOH liver disease is a
chronic disorder, steatosis, hepatitis, progressive fibrosis, cirrhosis, marked perturbations of vascular perfusion. Only develop cirrhosis in a small fraction of alcoholics.
53
G. Metabolic liver disease
1. Most common is
non-EtOH fatty liver disease; other conditions include hemochromatosis, Wilson disease, and alpha 1 anti-trypsin deficiency.
54
G. Metabolic liver disease
2. Non EtOH fatty liver disease (NAFLD)-primary cause liver disease in US. NAFLD can arise
with or without nonspecific inflammation.
55
G. Metabolic liver disease
3. Nonalcoholic steatohepatitis (NASH). Patients develop
hepatocyte injury, and 10-20% progress to cirrhosis (seen primarily in obese patients).
56
G. Metabolic liver disease
NASH:
• Approximately------ obese persons have some form of fatty liver disease
• Liver biopsy necessary to -----
70%
establish the diagnosis, note increased liver enzymes in 90% of affected patients.
57
G. Metabolic liver disease
| Hemochromatosis. Excessive accumulation of
body iron. Most is deposited in liver, pancreas and heart.
58
G. Metabolic liver disease
Hemochromatosis:
4 hereditary forms
(autosomal recessive, chromosome 6) and acquired form with excess iron intake.
59
G. Metabolic liver disease
Hemochromatosis:
• Liver features:
Micronodular cirrhosis with hemosiderin, Hepatosplenomegaly, diabetes mellitus, skin pigmentation
60
G. Metabolic liver disease
Hemochromatosis:
• Lifetime accumulation of Fe-
symptoms generally slow onset and notice around 5th or 6th decade of life.
61
G. Metabolic liver disease
Hemochromatosis:
• Males to females:
5 to 7:1
62
G. Metabolic liver disease
Hemochromatosis:
• Associated with
abnormal regulation of intestinal absorption of Fe
| •
63
G. Metabolic liver disease
Hemochromatosis:
Clinical and microscopic features of hereditary hemochromatosis:
increased in males, hepatomegaly, abdominal pain, increased skin pigmentation (especially after UV light), deranged glucose metabolism, cardiac arrhythmias, atypical arthritis.
64
G. Metabolic liver disease
Hemochromatosis:
Classic triad:
cirrhosis with hepatomegaly, diabetes mellitus, and skin pigmentation.
65
G. Metabolic liver disease
Hemochromatosis:
• Diagnosis obtained by assessing
serum Fe.
66
Hemochromatosis:
| • Treatment:
Phlebotomy, Fe chelators
67
G. Metabolic liver disease
1. Wilson’s disease. Results from a failure to
incorporate copper (Cu) into ceruloplasmin-consequently get accumulation of toxic Cu levels in liver, brain and eye.
68
G. Metabolic liver disease
Wilson's disease
• Usually presents between
6 to 40 years of age.
| • Autosomal recessive
69
G. Metabolic liver disease
Wilson's disease
• Morphology:
Acute/chronic, steatosis, necrosis, cirrhosis
70
G. Metabolic liver disease
Wilson's disease
• Presentation:
acute or chronic liver disease. May present with tremor or behavioral changes.
71
G. Metabolic liver disease
Wilson's disease
• Screening test-
NOT serum (as levels may actually be low), instead use Cu levels in urine (good for screening) or Cu levels in liver (definitive diagnosis).
72
G. Metabolic liver disease
Wilson's disease
• Chelation:
D-Penicillamine
73
G. Metabolic liver disease
| 6. Alpha1-antitrypsin deficiency. Develop
pulmonary emphysema from protein degrading enzymes. Also develop liver disease, formation of Mallory bodies and PAS positive granules within hepatocytes.
74
H. Intrahepatic Biliary Tract Disease, which includes
secondary biliary cirrhosis, primary biliary cirrhosis, primary sclerosing cholangitis.
75
Intrahepatic Biliary Tract Disease
1. Secondary biliary cirrhosis-
results from obstruction extrahepatic duct
76
Intrahepatic Biliary Tract Disease
1. Secondary biliary cirrhosis-
a. Biliary tree obstruction-
the primary cause is cholelithiasis (gall stones), then malignancies of biliary tree or head of pancreas.
77
Intrahepatic Biliary Tract Disease
1. Secondary biliary cirrhosis-
b. Develop secondary inflammation-
then fibrosis, hepatic scarring.
78
Intrahepatic Biliary Tract Disease
2. Primary biliary cirrhosis (PBS)
a. Inflammatory autoimmune disease-affects
intrahepatic bile ducts.
79
Intrahepatic Biliary Tract Disease
2. Primary biliary cirrhosis (PBS)
b. Primary feature-
nonsuppurative inflammatory destruction of medium sized intrahepatic ducts-also get portal inflammation, scarring and eventually cirrhosis.
80
Intrahepatic Biliary Tract Disease
2. Primary biliary cirrhosis (PBS)
c. Thought to be an
autoimmune etiology.
81
Intrahepatic Biliary Tract Disease
3. Primary sclerosing cholangitis (PSC)
a. Fibrosing cholangitis of bile ducts-
develop luminal obliteration
| b. Liver eventually develops
82
Intrahepatic Biliary Tract Disease
| 3. Primary sclerosing cholangitis (PSC)
biliary cirrhosis
83
Intrahepatic Biliary Tract Disease
3. Primary sclerosing cholangitis (PSC)
c. NOTE: same common
endpoint i.e. biliary cirrhosis as primary and secondary biliary cirrhosis
84
Intrahepatic Biliary Tract Disease
3. Primary sclerosing cholangitis (PSC)
d. Note an increase in
chronic pancreatitis and hepatocellular carcinoma (HCC) in PCS patients
85
I. Liver Nodules and Tumors
Nodular hyperplasia-
single or multiple nodules may develop
86
I. Liver Nodules and Tumors
Nodular hyperplasia-
a. In a non-cirrhotic liver
“focal nodular hyperplasia” or “nodular regenerative hyperplasia”
87
I. Liver Nodules and Tumors
Nodular hyperplasia-
b. Common factor-
focal or diffuse alteration in hepatic blood supply, resulting in obliteration of the portal veins and a compensatory increase in arterial supply
88
I. Liver Nodules and Tumors
| Benign liver neoplasms.
b. Cavernous hemangioma
| c. Hepatic adenoma
89
I. Liver Nodules and Tumors
Benign liver neoplasms.
c. Hepatic adenoma
-increase in young women using oral contraceptives
90
I. Liver Nodules and Tumors
Benign liver neoplasms.
d. Concerns with these:
1) mimic HCC, 2) subcapsular hemorrhage-from a rupture and bleed, 3) may transform to HCC.
91
I. Liver Nodules and Tumors
Benign liver neoplasms.
e. Are associated with
hormonal stimulation
92
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
a. Cholangiocarcinoma (CCA)
* Cancer of biliary tree-most are adenoCAs
* Very desmoplastic tumor-tumors are firm and gritty
* Can get collision tumor with HCC
* Asymptomatic until late stage
* Generally fatal within 6 months
93
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
b. Hepatoblastoma
• Most common liver tumor in
young pediatric patients
• Epithelioid type
• Mixed epithelial-mesenchymal
94
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
b. Hepatoblastoma
• Treatment-
chemotherapy then surgical resection
| • Is rapidly fatal (within months) if not treated
95
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
c. Hepatocellular adenoma
* Benign
* Association with oral contraceptives, if discontinued, may regress
* Presentation
* Acute abdomen
* Intra-abdominal bleed
* Histology: bland hepatocytes and no bile ducts
96
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
Hepatocellular Carcinoma
• Worldwide-
3rd most common cause of cancer deaths; 3:1 males
97
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
• Etiologic factors-
cirrhosis (90%), due to chronic viral infection (HBV, HCV) or chronic alcoholism, NASH (nonalcoholic steatohepatitis), food contaminants (primarily aflatoxins).
98
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
• All HCC variants-
strong propensity for vascular invasion
99
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
• Fibrolamellar variant
```
o Young males and females (20-40 yo)
o Distinct from HCC
o No known risk factors
o “Scirrhous tumor”
o Patients generally do NOT have underlying liver disease-better prognosis.
```
100
I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver
• Fibrolamellar variant
o Treatment:
Surgery
| o Better prognosis (32 % 5 yr survival)
101
a. Metastatic spread to liver
| • Liver and lungs-
primary soft tissue sites for metastases to occur. Metastatic tumors are more common than primary tumors
102
a. Metastatic spread to liver
• Most common primary cancers are
colon, breast, lung and pancreas
103
a. Metastatic spread to liver
• Liver weight may exceed
several kilograms. Often multiple nodules
104
a. Metastatic spread to liver
• Often only sign is hepatomegaly-
liver has tremendous functional reserve
105
II. Biliary Tract Pathology:
A. Cholelithiasis (gall stones)
1. 10-20% of adults. Increased risk with increasing age and obesity, Caucasian women over men (2:1), cholesterol (80 %) and pigment/bilirubin stones (20 %).
106
II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
• Cholesterol cholelithiasis (mostly radiolucent) vs
bilirubin cholelithiasis (mostly radiopaque)
107
II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
• Pigment stones →
Hemolysis, GI disorders, Biliary infections
108
II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
2. Increased with
estrogen (pregnancy and oral contraceptives)
109
II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
3. Increased with
gall bladder stasis
110
II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
4. Hereditary
contribution
111
II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
5. 80% of patients with stones remain
asymptomatic
112
II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
6. If symptomatic, develop
colicky biliary pain, inflammation, may eventually note perforation, obstruction of gall bladder or erode into ileum with GI obstruction.
113
B. Cholecystitis
| 1. May be
acute or chronic, 4th – 6th decades, F > M
114
B. Cholecystitis
2. Almost always occurs in
association with gallstones
115
B. Cholecystitis
3. Note
upper right quadrant pain, may note low level fever, anorexia, tachycardia, nausea, vomiting. Acute symptoms-can arise very abruptly.
116
B. Cholecystitis
| 4. Chronic-
not as dramatic a presentation. Note recurrent bouts of colicky epigastric or right quadrant pain.
117
B. Cholecystitis
| • Vague symptoms,
Stones (90 %), Fibrosis & Inflammation
118
Cancer of the gallbladder - Adenocarcinomas
| 1. Increased frequency in
women in their seventh decade of life.
119
Cancer of the gallbladder - Adenocarcinomas
| 2. Whites >
Blacks
120
Cancer of the gallbladder - Adenocarcinomas
| 3. 5th among
GI malignancies
121
Cancer of the gallbladder - Adenocarcinomas
| 4. Mean five year survival is
5%
122
Cancer of the gallbladder - Adenocarcinomas
| 5. Risk factors include
gallstones (95 % associated with stones) or infectious agents within the gallbladder (chronic inflammatory states)
123
Pancreatic anatomy
| 1. Distinct
exocrine and endocrine functions
124
Pancreatic anatomy
2. Endocrine →
regulates glucose homeostasis via insulin & glucagon.
125
Pancreatic anatomy
| Exocrine → arise from
acinar cells that produce enzymes (released primarily as proenzymes) used in digestion.
126
Pancreatic anatomy;
| a. Most significant pathology of the exocrine pancreas-
associated with cystic fibrosis, congenital anomalies, acute and chronic pancreatitis, pseudocysts and neoplasms.
127
b. Acute Pancreatitis
| • Reversible parenchymal injury associated with
inflammation,
• 80% of cases related to biliary tract disease or alcoholism; infections e.g. mumps, trauma, metabolic diseases (e.g. hypercalcemic states), medications (e.g. estrogens, chemotherapy), idiopathic.
128
Acute pancreatitis;
| • Release of
lipases, inflammation, proteolysis. Necrosis of vessels with hemorrhage. Fat necrosis.
129
Acute pancreatitis;
| • Symptoms are
ABDOMINAL PAIN. This is the cardinal manifestation. “upper back intense pain”.
130
Full blown acute pancreatitis is a
medical emergency due to the potential to release toxic enzymes.
131
Acute pancreatitis;
| • Elevated
enzymes (Amylase, Lipase), Organ failure, Abscess, Mortality (8 %)
132
1. Chronic pancreatitis
| • Develop irreversible
destruction exocrine pancreas, with ensuing fibrosis and eventual destruction of the endocrine parenchyma.
133
1. Chronic pancreatitis
| • Etiology unclear:
Alcoholism, biliary disease, hypercalcemia, hyperlipidemia, oxidative stress, idiopathic? genetic?
134
1. Chronic pancreatitis
| • Morphology:
Reduced acini, chronic inflammation, fibrosis, obstruction ducts, spare islets
135
1. Chronic pancreatitis
| • Symptoms range from
severe abdominal pain to silent (only detected once the patient develops diabetes mellitus).
136
1. Chronic pancreatitis
| • Diagnosis-
requires a high degree of suspicion-may have already destroyed acinar cells, so may not see an increase in serum amylase.
137
B. Pancreatic Neoplasms
cystic;
e.g.
serous cystadenomas, females over males, 2:1, usually seventh decade
138
B. Pancreatic Neoplasms
cystic;
• Close to ------- mucinous cystic neoplasms arise in -------. Can be associated with --------.
95% of
women
invasive cancer
139
B. Pancreatic Neoplasms
cystic;
• Intraductal papillary mucinous neoplasms increased
Fourth leading cause of
males over females
140
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
Fourth leading cause of
cancer death in the US (lung, colon, breast, pancreas)
141
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
• Precursor lesion is
PanINS (pancreatic intraepithelial neoplasias)
142
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
• Primarily a disease of the
elderly, 80% of the cases between 60-80 years
143
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
• Environmental influence-
primarily cigarette smoking (Doubles risk)
| •
144
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
Also increased risk with
diabetes mellitus & chronic pancreatitis
145
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
• New onset diabetes mellitus in older patient-
raises concern re: Pancreatic Cancer
146
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
• Often remain
silent until invade into adjacent structures. Pain is usually the first sign, but typically too late.
147
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
Obstructive jaundice is associated with
tumors at the pancreatic head.
148
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
• Trousseau sign:
Migratory thrombophlebitis-formation of platelet aggregation factors and procoagulants from tumor or its necrotic products.
149
2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
• Clinical course is very
brief and very aggressive. Rapidly fatal. Most patients die within 6 months.
