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Gen Path Final > Pathology of the Liver, Gall Bladder, and Pancreas > Flashcards

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

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2
Q

Anatomy of the Liver

2. ——– supply-portal vein (60-70%) and —– artery (30-40%).

A

Dual blood

hepatic

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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.

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4
Q

Anatomy of the Liver

  1. Major diseases of the liver are:
A

viral hepatitis, alcoholic liver disease, nonalcoholic liver disease (fatty liver, etc.), hepatocellular carcinoma (HCC)

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5
Q

Anatomy of the Liver

  1. 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.

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6
Q

Liver B. Physiological Functions

1. Maintains

A

metabolic homeostasis-processes amino acids, carbohydrates, lipids, vitamins

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7
Q

Liver B. Physiological Functions

  1. Synthesizes
A

serum proteins

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8
Q

Liver B. Physiological Functions

  1. Primary site for
A

detoxification of xenobiotics and waste products

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9
Q

Liver B. Physiological Functions

  1. Enormous functional
A

reserve and regenerative capacity can mask early hepatic injury

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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.

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11
Q

Cirrhosis

  1. Etiologies include:
A

Alcohol (EtOH) abuse (toxicity, nutritional deprivation), viral hepatitis, non-EtOH steatohepatitis, biliary disease, obesity, DM, medications, iron overload.

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12
Q

Cirrhosis

o Iron overload can lead to

A

hepatocyte death and inflammation.

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13
Q

Cirrhosis

  1. Morphologic changes are:
A

1) bridging fibrous septa, 2) parenchymal nodules, 3) changes in architecture, with parenchymal injury and scarring as the end result.

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14
Q

Cirrhosis

A fibrotic liver has a markedly

A

compromised blood supply and decreased function.

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15
Q

Cirrhosis

Complications include

A

reduced liver function, portal hypertension and increased risk for hepatocellular Ca

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16
Q

Cirrhosis

. Clinical manifestations:

A

o Nonspecific symptoms e.g. weight loss, weakness. Reserve may mask symptoms.
o Liver failure
o Portal hypertension

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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).

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18
Q
  1. 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.

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19
Q

Jaundice and cholestasis

  1. Excess
A

bilirubin. 2.0 mg/dl
• Unconjugated: Insoluble, toxic
• Conjugated: Soluble, nontoxic

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20
Q

Jaundice and cholestasis;

2. Causes of jaundice:

A

hemolytic anemias (#1), bilirubin overproduction, hepatitis, obstruction of bile flow.

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21
Q

Jaundice and cholestasis;

  1. Function of hepatic bile:
A

1) emulsification of fats with bile salts, 2) elimination of bilirubin, excess cholesterol, xenobiotics, etc.

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22
Q

Jaundice and cholestasis; symptoms

A
  1. Yellow color of skin (classically, jaundice) and sclera (classically, icterus).
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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.

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24
Q

F. Infectious Disorders of the Liver.

  1. Generally use “hepatitis” for
A

hepatotropic viruses e.g. A, B, C, D, E and G

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25
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis A is a
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

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26
Q

F. Infectious Disorders of the Liver.

Possible results of Hepatitis B infection:

A

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.

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27
Q

F. Infectious Disorders of the Liver.

Hepatitis B

A
  • DNA virus
  • Parenteral contact/sexual spread
  • Incubation 4-26 weeks
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28
Q

F. Infectious Disorders of the Liver.
Hep b
• Host immune response determines the

A

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.

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29
Q 
F.  Infectious Disorders of the Liver.
Hep B
•	Serology: 
•	Vaccine: 
•	Increased risk of
A

Remains in blood

95 % protective Ab response

hepatocellular response

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30
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis C is a major cause of liver disease worldwide. Unlike Hepatitis B, with Hepatitis C infection the
A

progression to chronic disease occurs in the majority of patients and cirrhosis develops in 20-30% of infected individuals.

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31
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis C

With Hepatitis C, note persistent

A

infection, chronic hepatitis.

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32
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis C
A
  • 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.
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33
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis C

• Most frequent viral infection associated with

A

the need for liver transplantation. Previously treated with interferon and ribavirin. Treatment with protease and nucleoside inhibitors now considered curative.

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34
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis C

o Combination drugs:

A

Harvoni (2014, sofosbuvir & ledipasvir). 12 week course, several others since 2014; often given with ribavirin

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35
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis C

o Curative in

A

most patients. Side effects fatigue and headache.

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36
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis C

o Drugs are Very

A

expensive (Harvoni $95K, Mavyret [2017] 12 weeks $40K)

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37
Q

F. Infectious Disorders of the Liver.

  1. Hepatitis D (requires presence of
A

Hepatitis B for infection) occurs as a co-infection. Co-infection presents like Hepatitis B-usually transient and self-limited.

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38
Q

F. Infectious Disorders of the Liver.

8. Hepatitis E (similar to A) is an

A

enterically transmitted, water-borne infection-high mortality rate in pregnant women.

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39
Q

Hep E is Not associated with

A

chronic liver disease.

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40
Q
  1. Hepatitis G (some similarity to C but is not hepatotropic) infection does not
A

increase liver enzymes such as serum aminotransferases.

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41
Q

Hep G Replicates in

A

bone marrow and spleen.

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42
Q
  1. Autoimmune hepatitis is a
A

chronic, progressive, hepatitis variant with an unknown etiology.

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43
Q

Autoimmune hep

Pathology is associated with

A

T-cell mediated autoimmunity.

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44
Q

F. Drug, Toxin, Alcohol associated liver disease.

  1. Drug and toxic injury may be
A

predictable (intrinsic) or unpredictable (idiosyncratic). Generally adults affected more frequently than pediatric patients, females more than males.

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45
Q

F. Drug, Toxin, Alcohol associated liver disease.

  1. Predictable hepatic injury with established
A

liver toxins such as acetaminophen, carbon tetrachloride, EtOH.

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46
Q

F. Drug, Toxin, Alcohol associated liver disease.

  1. Always include exposure to a
A

drug or toxicant in the differential diagnosis of liver disease.

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47
Q

F. Drug, Toxin, Alcohol associated liver disease.

  1. Alcoholic liver disease
    o 3 overlapping forms:
A

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

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48
Q

F. Drug, Toxin, Alcohol associated liver disease.

  1. Fatty liver from
A

EtOH-little fibrosis at onset, increased deposition with EtOH consumption.

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49
Q

F. Drug, Toxin, Alcohol associated liver disease.
Fatty liver form:
Fatty change is

A

reversible if discontinue EtOH consumption.

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50
Q

F. Drug, Toxin, Alcohol associated liver disease.

Fatty liver form:
Mallory or Mallory-Denk bodies:

A

clumps of cytokeratins, eosinophilic cytoplasmic inclusions.

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51
Q

F. Drug, Toxin, Alcohol associated liver disease.

6. Final stage of cirrhosis

A

-the liver resembles from both macro and micro cirrhosis developing from hepatitis.

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52
Q

F. Drug, Toxin, Alcohol associated liver disease.

  1. EtOH liver disease is a
A

chronic disorder, steatosis, hepatitis, progressive fibrosis, cirrhosis, marked perturbations of vascular perfusion. Only develop cirrhosis in a small fraction of alcoholics.

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53
Q

G. Metabolic liver disease

  1. Most common is
A

non-EtOH fatty liver disease; other conditions include hemochromatosis, Wilson disease, and alpha 1 anti-trypsin deficiency.

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54
Q

G. Metabolic liver disease

  1. Non EtOH fatty liver disease (NAFLD)-primary cause liver disease in US. NAFLD can arise
A

with or without nonspecific inflammation.

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55
Q

G. Metabolic liver disease

  1. Nonalcoholic steatohepatitis (NASH). Patients develop
A

hepatocyte injury, and 10-20% progress to cirrhosis (seen primarily in obese patients).

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56
Q

G. Metabolic liver disease
NASH:
• Approximately—— obese persons have some form of fatty liver disease
• Liver biopsy necessary to —–

A

70%

establish the diagnosis, note increased liver enzymes in 90% of affected patients.

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57
Q

G. Metabolic liver disease

Hemochromatosis. Excessive accumulation of

A

body iron. Most is deposited in liver, pancreas and heart.

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58
Q

G. Metabolic liver disease

Hemochromatosis:
4 hereditary forms

A

(autosomal recessive, chromosome 6) and acquired form with excess iron intake.

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59
Q

G. Metabolic liver disease
Hemochromatosis:
• Liver features:

A

Micronodular cirrhosis with hemosiderin, Hepatosplenomegaly, diabetes mellitus, skin pigmentation

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60
Q

G. Metabolic liver disease
Hemochromatosis:
• Lifetime accumulation of Fe-

A

symptoms generally slow onset and notice around 5th or 6th decade of life.

61
Q

G. Metabolic liver disease
Hemochromatosis:
• Males to females:

62
Q

G. Metabolic liver disease

Hemochromatosis:

• Associated with

A

abnormal regulation of intestinal absorption of Fe

•

63
Q

G. Metabolic liver disease

Hemochromatosis:

Clinical and microscopic features of hereditary hemochromatosis:

A

increased in males, hepatomegaly, abdominal pain, increased skin pigmentation (especially after UV light), deranged glucose metabolism, cardiac arrhythmias, atypical arthritis.

64
Q

G. Metabolic liver disease

Hemochromatosis:

Classic triad:

A

cirrhosis with hepatomegaly, diabetes mellitus, and skin pigmentation.

65
Q

G. Metabolic liver disease

Hemochromatosis:

• Diagnosis obtained by assessing

66
Q

Hemochromatosis:

• Treatment:

A

Phlebotomy, Fe chelators

67
Q

G. Metabolic liver disease

  1. Wilson’s disease. Results from a failure to
A

incorporate copper (Cu) into ceruloplasmin-consequently get accumulation of toxic Cu levels in liver, brain and eye.

68
Q

G. Metabolic liver disease
Wilson’s disease
• Usually presents between

A

6 to 40 years of age.

• Autosomal recessive

69
Q

G. Metabolic liver disease
Wilson’s disease

• Morphology:

A

Acute/chronic, steatosis, necrosis, cirrhosis

70
Q

G. Metabolic liver disease
Wilson’s disease

• Presentation:

A

acute or chronic liver disease. May present with tremor or behavioral changes.

71
Q

G. Metabolic liver disease
Wilson’s disease

• Screening test-

A

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
Q

G. Metabolic liver disease
Wilson’s disease

• Chelation:

A

D-Penicillamine

73
Q

G. Metabolic liver disease

6. Alpha1-antitrypsin deficiency. Develop

A

pulmonary emphysema from protein degrading enzymes. Also develop liver disease, formation of Mallory bodies and PAS positive granules within hepatocytes.

74
Q

H. Intrahepatic Biliary Tract Disease, which includes

A

secondary biliary cirrhosis, primary biliary cirrhosis, primary sclerosing cholangitis.

75
Q

Intrahepatic Biliary Tract Disease

  1. Secondary biliary cirrhosis-
A

results from obstruction extrahepatic duct

76
Q

Intrahepatic Biliary Tract Disease

  1. Secondary biliary cirrhosis-
    a. Biliary tree obstruction-
A

the primary cause is cholelithiasis (gall stones), then malignancies of biliary tree or head of pancreas.

77
Q

Intrahepatic Biliary Tract Disease
1. Secondary biliary cirrhosis-

b. Develop secondary inflammation-

A

then fibrosis, hepatic scarring.

78
Q

Intrahepatic Biliary Tract Disease

  1. Primary biliary cirrhosis (PBS)
    a. Inflammatory autoimmune disease-affects
A

intrahepatic bile ducts.

79
Q

Intrahepatic Biliary Tract Disease

  1. Primary biliary cirrhosis (PBS)
    b. Primary feature-
A

nonsuppurative inflammatory destruction of medium sized intrahepatic ducts-also get portal inflammation, scarring and eventually cirrhosis.

80
Q

Intrahepatic Biliary Tract Disease

  1. Primary biliary cirrhosis (PBS)
    c. Thought to be an
A

autoimmune etiology.

81
Q

Intrahepatic Biliary Tract Disease

  1. Primary sclerosing cholangitis (PSC)
    a. Fibrosing cholangitis of bile ducts-
A

develop luminal obliteration

b. Liver eventually develops

82
Q

Intrahepatic Biliary Tract Disease

3. Primary sclerosing cholangitis (PSC)

A

biliary cirrhosis

83
Q

Intrahepatic Biliary Tract Disease
3. Primary sclerosing cholangitis (PSC)

c. NOTE: same common

A

endpoint i.e. biliary cirrhosis as primary and secondary biliary cirrhosis

84
Q

Intrahepatic Biliary Tract Disease
3. Primary sclerosing cholangitis (PSC)

d. Note an increase in

A

chronic pancreatitis and hepatocellular carcinoma (HCC) in PCS patients

85
Q

I. Liver Nodules and Tumors

Nodular hyperplasia-

A

single or multiple nodules may develop

86
Q

I. Liver Nodules and Tumors
Nodular hyperplasia-
a. In a non-cirrhotic liver

A

“focal nodular hyperplasia” or “nodular regenerative hyperplasia”

87
Q

I. Liver Nodules and Tumors
Nodular hyperplasia-
b. Common factor-

A

focal or diffuse alteration in hepatic blood supply, resulting in obliteration of the portal veins and a compensatory increase in arterial supply

88
Q

I. Liver Nodules and Tumors

Benign liver neoplasms.

A

b. Cavernous hemangioma

c. Hepatic adenoma

89
Q

I. Liver Nodules and Tumors
Benign liver neoplasms.
c. Hepatic adenoma

A

-increase in young women using oral contraceptives

90
Q

I. Liver Nodules and Tumors
Benign liver neoplasms.

d. Concerns with these:

A

1) mimic HCC, 2) subcapsular hemorrhage-from a rupture and bleed, 3) may transform to HCC.

91
Q

I. Liver Nodules and Tumors
Benign liver neoplasms.
e. Are associated with

A

hormonal stimulation

92
Q

I. Liver Nodules and Tumors

  1. Malignant Tumors of the Liver
    a. Cholangiocarcinoma (CCA)
A
  • 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
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

b. Hepatoblastoma
• Most common liver tumor in

A

young pediatric patients
• Epithelioid type
• Mixed epithelial-mesenchymal

94
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

b. Hepatoblastoma

• Treatment-

A

chemotherapy then surgical resection

• Is rapidly fatal (within months) if not treated

95
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

c. Hepatocellular adenoma

A
  • Benign
  • Association with oral contraceptives, if discontinued, may regress
  • Presentation
  • Acute abdomen
  • Intra-abdominal bleed
  • Histology: bland hepatocytes and no bile ducts
96
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

Hepatocellular Carcinoma
• Worldwide-

A

3rd most common cause of cancer deaths; 3:1 males

97
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

• Etiologic factors-

A

cirrhosis (90%), due to chronic viral infection (HBV, HCV) or chronic alcoholism, NASH (nonalcoholic steatohepatitis), food contaminants (primarily aflatoxins).

98
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

• All HCC variants-

A

strong propensity for vascular invasion

99
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

• Fibrolamellar variant

A 
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
Q

I. Liver Nodules and Tumors
2. Malignant Tumors of the Liver

• Fibrolamellar variant

o Treatment:

A

Surgery

o Better prognosis (32 % 5 yr survival)

101
Q

a. Metastatic spread to liver

• Liver and lungs-

A

primary soft tissue sites for metastases to occur. Metastatic tumors are more common than primary tumors

102
Q

a. Metastatic spread to liver

• Most common primary cancers are

A

colon, breast, lung and pancreas

103
Q

a. Metastatic spread to liver

• Liver weight may exceed

A

several kilograms. Often multiple nodules

104
Q

a. Metastatic spread to liver

• Often only sign is hepatomegaly-

A

liver has tremendous functional reserve

105
Q

II. Biliary Tract Pathology:

A. Cholelithiasis (gall stones)

A
  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
Q

II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)

• Cholesterol cholelithiasis (mostly radiolucent) vs

A

bilirubin cholelithiasis (mostly radiopaque)

107
Q

II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
• Pigment stones →

A

Hemolysis, GI disorders, Biliary infections

108
Q

II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)

  1. Increased with
A

estrogen (pregnancy and oral contraceptives)

109
Q

II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)

  1. Increased with
A

gall bladder stasis

110
Q

II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)
4. Hereditary

A

contribution

111
Q

II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)

  1. 80% of patients with stones remain
A

asymptomatic

112
Q

II. Biliary Tract Pathology
A. Cholelithiasis (gall stones)

  1. If symptomatic, develop
A

colicky biliary pain, inflammation, may eventually note perforation, obstruction of gall bladder or erode into ileum with GI obstruction.

113
Q

B. Cholecystitis

1. May be

A

acute or chronic, 4th – 6th decades, F > M

114
Q

B. Cholecystitis

  1. Almost always occurs in
A

association with gallstones

115
Q

B. Cholecystitis

  1. Note
A

upper right quadrant pain, may note low level fever, anorexia, tachycardia, nausea, vomiting. Acute symptoms-can arise very abruptly.

116
Q

B. Cholecystitis

4. Chronic-

A

not as dramatic a presentation. Note recurrent bouts of colicky epigastric or right quadrant pain.

117
Q

B. Cholecystitis

• Vague symptoms,

A

Stones (90 %), Fibrosis & Inflammation

118
Q

Cancer of the gallbladder - Adenocarcinomas

1. Increased frequency in

A

women in their seventh decade of life.

119
Q

Cancer of the gallbladder - Adenocarcinomas

2. Whites >

120
Q

Cancer of the gallbladder - Adenocarcinomas

3. 5th among

A

GI malignancies

121
Q

Cancer of the gallbladder - Adenocarcinomas

4. Mean five year survival is

122
Q

Cancer of the gallbladder - Adenocarcinomas

5. Risk factors include

A

gallstones (95 % associated with stones) or infectious agents within the gallbladder (chronic inflammatory states)

123
Q

Pancreatic anatomy

1. Distinct

A

exocrine and endocrine functions

124
Q

Pancreatic anatomy

  1. Endocrine →
A

regulates glucose homeostasis via insulin & glucagon.

125
Q

Pancreatic anatomy

Exocrine → arise from

A

acinar cells that produce enzymes (released primarily as proenzymes) used in digestion.

126
Q

Pancreatic anatomy;

a. Most significant pathology of the exocrine pancreas-

A

associated with cystic fibrosis, congenital anomalies, acute and chronic pancreatitis, pseudocysts and neoplasms.

127
Q

b. Acute Pancreatitis

• Reversible parenchymal injury associated with

A

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
Q

Acute pancreatitis;

• Release of

A

lipases, inflammation, proteolysis. Necrosis of vessels with hemorrhage. Fat necrosis.

129
Q

Acute pancreatitis;

• Symptoms are

A

ABDOMINAL PAIN. This is the cardinal manifestation. “upper back intense pain”.

130
Q

Full blown acute pancreatitis is a

A

medical emergency due to the potential to release toxic enzymes.

131
Q

Acute pancreatitis;

• Elevated

A

enzymes (Amylase, Lipase), Organ failure, Abscess, Mortality (8 %)

132
Q
  1. Chronic pancreatitis

• Develop irreversible

A

destruction exocrine pancreas, with ensuing fibrosis and eventual destruction of the endocrine parenchyma.

133
Q
  1. Chronic pancreatitis

• Etiology unclear:

A

Alcoholism, biliary disease, hypercalcemia, hyperlipidemia, oxidative stress, idiopathic? genetic?

134
Q
  1. Chronic pancreatitis

• Morphology:

A

Reduced acini, chronic inflammation, fibrosis, obstruction ducts, spare islets

135
Q
  1. Chronic pancreatitis

• Symptoms range from

A

severe abdominal pain to silent (only detected once the patient develops diabetes mellitus).

136
Q
  1. Chronic pancreatitis

• Diagnosis-

A

requires a high degree of suspicion-may have already destroyed acinar cells, so may not see an increase in serum amylase.

137
Q

B. Pancreatic Neoplasms
cystic;
e.g.

A

serous cystadenomas, females over males, 2:1, usually seventh decade

138
Q

B. Pancreatic Neoplasms
cystic;
• Close to ——- mucinous cystic neoplasms arise in ——-. Can be associated with ——–.

A

95% of

women

invasive cancer

139
Q

B. Pancreatic Neoplasms
cystic;
• Intraductal papillary mucinous neoplasms increased

Fourth leading cause of

A

males over females

140
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”
    Fourth leading cause of
A

cancer death in the US (lung, colon, breast, pancreas)

141
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

• Precursor lesion is

A

PanINS (pancreatic intraepithelial neoplasias)

142
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

• Primarily a disease of the

A

elderly, 80% of the cases between 60-80 years

143
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

• Environmental influence-

A

primarily cigarette smoking (Doubles risk)

•

144
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

Also increased risk with

A

diabetes mellitus & chronic pancreatitis

145
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

• New onset diabetes mellitus in older patient-

A

raises concern re: Pancreatic Cancer

146
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

• Often remain

A

silent until invade into adjacent structures. Pain is usually the first sign, but typically too late.

147
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

Obstructive jaundice is associated with

A

tumors at the pancreatic head.

148
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

• Trousseau sign:

A

Migratory thrombophlebitis-formation of platelet aggregation factors and procoagulants from tumor or its necrotic products.

149
Q
  1. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

• Clinical course is very

A

brief and very aggressive. Rapidly fatal. Most patients die within 6 months.

Gen Path Final (18 decks)

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