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Gen path 3 > liver gall bladder pancreas > Flashcards

liver gall bladder pancreas Flashcards

1
Q

duel blood supply to then liver what is it

A 
portal vein (60-70%)
hepatic artery
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2
Q

major diseases of the liver (4)

A

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

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3
Q

The enormous functional reserve in the liver masks _____

A

early changes

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4
Q

It represents the primary route for liver-related deaths.

A

Cirrhosis

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5
Q

etiology of cirrhosis

A

Alcohol (EtOH) abuse, viral hepatitis, non-EtOH steatohepatitis, biliary disease, iron overload.

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6
Q

cirrhosis liver morphological features

A

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

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7
Q

A fibrotic liver has a markedly compromised ______ and decreased _______

A

blood supply and decreased function.

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8
Q

3 types of portal hypertension

A
  1. prehepatic (obstructive thrombi),
  2. intrahepatic (cirrhosis), and
  3. post hepatic (right sided heart failure).
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9
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.

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10
Q

what is Jaundice (clinically)

A

Yellow color of skin (jaundice) and sclera (icterus).

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11
Q

causes of jaundice

A

bilirubin overproduction, hepatitis, obstruction of bile flow.

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12
Q

Function of hepatic bile

A

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

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13
Q

Viral hepatitis causes (viruses)

A

Epstein Barr Virus (EBV), Cytomegalovirus (CMV), yellow fever, rubella, herpesviruses.

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14
Q

Generally use “hepatitis” for

A

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

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15
Q

T/F Hepatitis A is a benign, self-limiting disease.

A

TRUE

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16
Q

Possible results of Hepatitis B infection:

A

1) acute hepatitis with recovery and clearance, 2) nonprogressive chronic hepatitis, 3) progressive disease ending in cirrhosis, 4) asymptomatic carrier state.

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17
Q

Hepatitis B induced liver disease is an important precursor for ____

A

HCC.

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18
Q

what determines the outcome of Hep B infection

A

immune response

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19
Q

Hepatocyte damage-likely reflects what

A

CD8+ cytotoxic T cell damage to Hepatitis B infected hepatocytes.

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20
Q

what occurs more in Hep C than Hep B?

A

chronic disease and cirrhosis (20-30%)

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21
Q

what % of people develop cirrhosis that have chronic Hep C disease over 5 to 20 years

A

80%. Definite risk factor for hepatocellular carcinoma.

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22
Q

Hep D occurs as a ______

A

co-infection, needs Hep B. Coninfection presents like Hepatitis B-usually transient and self-limited.

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23
Q

Hepatitis E

A

enterically transmitted, water-borne infection-high mortality rate in pregnant women. Not associated with chronic liver disease.

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24
Q

T/F Hepatitis G hepatotropic

A

false, it is not. and it does not increase liver enzymes

Replicates in bone marrow and spleen.

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25
Q

Autoimmune hepatitis is a _____,_____ hepatitis variant with an unknown etiology.

A

chronic, progressive.

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26
Q

Always include _________ in the differential diagnosis of liver disease.

A

exposure to a drug or toxicant

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27
Q

Alcoholic liver disease

A

1) hepatic steatosis,
2) EtOH hepatitis,
3) cirrhosis (only develops in a minority of patients).

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28
Q

Fatty liver from EtOH

A

little fibrosis at onset, increased deposition with EtOH consumption. Fatty change is reversible if discontinue EtOH consumption.

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29
Q

Fatty liver from EtOH distinguishing histo features

A

mallory bodies- clumps of cytokeratins-eosinophilic.

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30
Q

T/F ? Only develop cirrhosis in a small fraction of alcoholics.

A

TRUE

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31
Q

most common metabolic liver disease`

A

non-EtOH fatty liver disease

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32
Q

other conditions that cause metabolic liver disease

A

other conditions include hemochromatosis, Wilson disease, and alpha 1 anti-trypsin deficiency.

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33
Q

primary cause liver disease in US.

A

Non EtOH fatty liver disease (NAFLD)

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34
Q

Nonalcoholic steatohepatitis (NASH).

A

Patients develop hepatocyte injury, and 10-20% progress to cirrhosis (seen primarily in obese patients). mainly in fat people

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35
Q

Hemochromatosis

A

excessive accumulation of body iron. Most is deposited in liver and pancreas. Hereditary.

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36
Q

Hemochromatosis speed of progression

A

accumulation of iron over 5 or 6 decades

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37
Q

liver features of hemochromatosis

A

1) micronodular cirrhosis, 2) diabetes mellitus, 3) skin pigmentation

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38
Q

hemochromatosis more in males or females?

A

males

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39
Q

what is associated with abnormal regulation of intestinal absorption of Fe

A

Hemochromatosis

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40
Q

how is a diagnosis of hemochromatosis obtained

A

by assessing serum Fe.

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41
Q

Classic triad of hereditary hemochromatosis

A

cirrhosis with hepatomegaly, diabetes mellitus, and skin pigmentation.

42
Q

Hemosiderosis is an ______ disease.

A

acquired. (nonhereditary)

43
Q

causes of hemosiderosis

A

Causes include: ineffective erythropoiesis and myelodysplastic syndromes. Note increased absorption of Fe. Also, high number of transfusions can get Fe overload.

44
Q

high number of transfusions a person can get _______

A

hemosiderosis

45
Q

Wilson disease results from…….what does this lead to….

A

a failure to incorporate copper (Cu) into ceruloplasmin

consequently get accumulation of toxic Cu levels in liver, brain and eye.

46
Q

what happens to the liver in wilsons disease

A

acute or chronic liver disease

47
Q

how do you test for wilsons disease

A

use Cu levels in urine (good for screening) or Cu levels in liver (definitive diagnosis).

48
Q

alpha1-antitrypsin deficiency

A

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

49
Q

3 Intrahepatic Biliary Tract Disease

A

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

50
Q

Secondary biliary cirrhosis is a problem with which duct?

A

extrahepatic duct

51
Q

primary cause of Secondary biliary cirrhosis

A

gall stones, obstruct. then malignancies of biliary tree

52
Q

what develops from the obstruction

A

inflammation, then fibrosis, then scarring

53
Q

Primary biliary cirrhosis (PBS) is a problem in which duct and is what kind of diseas

A

intrahepatic

autoimmune inflammatory

54
Q

PBS main feature

A

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

is an autoimmune disease of the liver.[1][2] It is marked by slow progressive destruction of the small bile ducts of the liver, with the intralobular ducts (Canals of Hering) affected early in the disease.[3] When these ducts are damaged, bile and other toxins build up in the liver (cholestasis) and over time damages the liver tissue in combination with ongoing immune related damage. This can lead to scarring, fibrosis and cirrhosis.

55
Q

Primary sclerosing cholangitis (PSC)

A

Fibrosing cholangitis of bile ducts-develop luminal obliteration
b. Liver eventually develops biliary cirrhosis

is a disease of the bile ducts that causes inflammation and subsequent obstruction of bile ducts both inside and outside of the liver. The inflammation impedes the flow of bile to the gut, which can ultimately lead to cirrhosis of the liver, liver failure, and liver cancer. The underlying cause of the inflammation is believed to be autoimmunity;[1] and more than 80% of those with PSC have ulcerative colitis.[2] The definitive treatment is a liver transplant.

56
Q

Note an increase in _______ and _______ in PCS patients

A 
chronic pancreatitis
hepatocellular carcinoma (HCC)
57
Q

what is same common endpoint for PBS, PSC and secondary biliary cirrhosis

A

biliary cirrhosis

58
Q

Nodular hyperplasia of liver

A

-single or multiple nodules may develop
Common factor-focal or diffuse alteration in hepatic blood supply, resulting in obliteration of the portal veins and a compensatory increase in arterial supply
-non-cirrhotic liver

59
Q

obliteration of the _______ in nodular hyperplasia

A

portal veins

60
Q

Benign liver neoplasms

A

a. Cavernous hemangioma

b. Hepatic adenoma-increase in young women using oral contraceptives

61
Q

Malignant Tumors of the Liver

A

a. Hepatoblastoma
b. Hepatocellular Carcinoma
c. Cholangiocarcinoma (CCA)
d. Metastatic spread to liver

62
Q

most common liver tumor in young pediatric patients

A

a. Hepatoblastoma

63
Q

Hepatoblastoma

A

1) Epitheliod type
2) Mixed epithelial-mesenchymal
3) Treatment-chemotherapy then surgical resection
4) Is rapidly fatal (within months) if not treated

64
Q

Hepatocellular Carcinoma

A

1) Worldwide-third most common cause of cancer deaths
2) Etiologic factors-chronic viral infection (HBV, HCV), chronic alcoholism, NASH (nonalcohol steatohepatitis), food contaminants (primarily aflatoxins).
3) All HCC variants-strong propensity for vascular invasion
4) **Fibrolamellar variant-young males and females (20-40 yo), Patients generally do NOT have underlying liver disease-better prognosis.

65
Q

Hepatocellular Carcinoma bold words

A

Fibrolamellar variant-young males and females (20-40 yo), Patients generally do NOT have underlying liver disease-better prognosis.

66
Q

Cancer of biliary tree-most are adenoCAs

A

Cholangiocarcinoma (CCA)

67
Q

Cholangiocarcinoma (CCA)

A

2) Very desmoplastic tumor-tumors are firm and gritty
3) Can get collision tumor with HCC
4) Generally fatal within 6 months

68
Q

primary soft tissue sites for metatases to occur

A

1) Liver and lungs

69
Q

2) Most common primary cancers

A

are colon, breast, lung and pancreas

70
Q

usually the only sign in a cancerous liver

A

hepatomegaly-liver has tremendous functional reserve

71
Q

Cholelithiasis are what?

A

gall stones

72
Q

increase in what things causes gall stones

A

age
caucasian females
obesity

73
Q

Cholelithiasis (gall stones)

A
  1. Increased with estrogen (pregnancy and oral contraceptives)
  2. Increased with gall bladder stasis
  3. Hereditary contribution
  4. 70-80% of patients with stones remain asymptomatic, if symptomatic, develop colicky biliary pain, may eventually note perforation, obstruction of gall bladder or erode into ileum and develop GI obstruction.
74
Q

what Almost always occurs in association with gallstones

A

Cholecytitis

75
Q

Cholecytitis can be _____ or _____

A

acute or chronic

76
Q

Cholecytitis symptoms

A

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

77
Q

chronic cholecytitis

A

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

78
Q

Cancer of the gallbladder

A
  1. Increased frequency in women in their seventh decade (i.e. in their 60s) of life.
  2. Mean five year survival is 5-12%
  3. Risk factors include gallstones or infectious agents within the gallbladder (chronic inflammatory states)
79
Q

gallstones or infectious agents within the gallbladder are risk factors for what

A

cancer of the gallbladder

80
Q

pancreas has distinct _____ and _____ functions

A

Distinct exocrine and endocrine functions

81
Q

exocrine pancreas cells and function

A

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

82
Q

Most significant pathology of the exocrine

A

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

83
Q

Pancreatitis reversible or irreversible

A

reversible

84
Q

Pancreatitis

A

reversible parenchymal injury associated with inflammation, causes include obstructions, infections e.g. mumps, trauma, metabolic diseases, medications e.g. estrogens.

85
Q

Pancreatitis may symptom

A

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

86
Q

Full blown acute pancreatitis is a medical emergency due to the potential to…

A

to release toxic enzymes.

87
Q

Chronic pancreatitis

A

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

88
Q

symptoms of chronic pancreatitis

A

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

89
Q

Diagnosis of chronic pancreatitis requires a high degree of _____

A

suspicion-may have already destroyed acinar cells, so may not see an increase in serum amylase.

90
Q

Pancreatic Neoplasms

A
  1. cystic

2. Pancreatic Cancers “infiltrating ductal carcinomas of the pancreas”

91
Q

cystic pancreatic neoplasms

A

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

a. Close to 95% of mucinous cystic neoplasms arise in women. Can be associated with invasive cancer.
b. Intraductal papillary mucinous neoplasms increased males over females.

92
Q

Precursor lesion of pancreatic cancer is what

A

PanINS (pancreatic intraepithelial neoplasias)

93
Q

pancreatic cancer Primarily a disease of the ______

A

elderly

94
Q

pancreatic cancer Environmental influence

A

primarily cigarette smoking

95
Q

New onset _______ in older patient-raises concern re: Pancreatic Cancer

A

diabetes mellitus

96
Q

______` is usually the first sign, by then it’s already too late

A

Pain

97
Q

pancreatic cancer Often remain ______ until invade into adjacent structures.

A

silent

98
Q

_________ is associated with tumors at the pancreatic head.

A

Obstructive jaundice

99
Q

Trousseau sign

A

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

100
Q

pancreatic cancer clinical course and fatality.

A

Clinical course is very brief and very aggressive. Rapidly fatal.

Gen path 3 (6 decks)

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