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Pathology II > Exam 2 - Liver And Pancreas > Flashcards

Exam 2 - Liver And Pancreas Flashcards

1
Q

Increased levels of bilirubin cause

A

Jaundice (icterus)

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2
Q

Serum bilirubin levels are abnormal when they exceed _____ however skin discoloration is not apparent until _____

A

Excess serum bilirubin level: 1.2 mg/dl

Skin discoloration: 2-3 mg/dl

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3
Q

How much bilirubin is formed daily?

A

250-350 mg

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4
Q

Within the hepatocyte, billirubin is…

A
  1. Conjugated with glucuronide to form billirubine diglucuronide secreted in bile
  2. This post-hepatic or conjugated billirubin is water-soluble and enters urine when serum levels are atypically high
  3. Billirubin in bile reaches intestines and is acted upon by bacteria to form stercobilin, a pigment of stool
  4. Portions of urobilin are absorped by intestines and after reaching circulation, some of this appears as urinary urobilin (urobilinogen)
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5
Q

Indirect vs direct bilirubin

A

Indirect: unconjugated, prehepatic
Direct: conjugated, posthepatic

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6
Q

Is prehepatic or posthepatic bilirubin insoluble in water?

A

Prehepatic bilirubin = unconjugated

Note: Posthepatic / conjugated bilirubin is water soluble and so it DOES appear in urine.

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7
Q

Obstructive jaundice (cholestasis) is caused by what?

A

Biliary obstruction

So bile “spills over” into tissue. Components are absorbed by circulation. Accumulated bilirubin is predominantly conjugated.

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8
Q

Jaundice associated with liver damage or dysfunction is often known as

A

Hepatic (hepatomegaly-cellular) jaundice

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9
Q

Causes of Hepatic (hepatomegaly-cellular) jaundice include

A

Cirrhosis, hepatitis, liver infarcts, toxic injury and defects in assimilation, conjugation and transport of bilirubin into bile

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10
Q

Atypically high conjugated bilirubin leads to a type of jaundice called

A

Choluric jaundice

Diffuses freely into blood and tissue fluids

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11
Q

Why are newborns often jaundice?

A

The hepatic mechanisms for conjugating and excreting often do not mature until about 2 weeks of age.

Mild unconjugated hyperbilirubinemia is frequent in young infarcts, especially premature and underweight.

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12
Q

Kernicterus

A

Infantile severe unconjugated hyperbilirubinemia with brain damage

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13
Q

What kind of bilirubin DOES enter the urine

A

Conjugated bilirubin

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14
Q

Acholuric jaundice

A

Unconjugated bilirubin that does not enter urine

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15
Q

3 Stages of cirrhosis

A

1- Fatty liver stage (fatty metamorphosis)
2- Alcoholic hepatitis
3- Cirrhosis (fibrosis) “end stage”

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16
Q

Mallory bodies are seen in which stage of liver disease

A

Alcoholic hepatitis

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17
Q

Biliary cirrhosis

A

Most damage occurs in periportal areas that surround bile ducts

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18
Q

“Pigment” cirrhosis is associated with

A

Hemachromatosis “bronze diabetes”

Accumulated iron and injury to hepatocytes and hepatic scarring

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19
Q

Hemosiderin

A

Insoluble aggregates consisting of degraded ferritin

Deposits are common in macrophages of the liver, spleen and marrow and hepatocytes

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20
Q

Systemic iron overload

A

Deposits accumulate and damage parenchymal tissues.

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21
Q

Causes of systemic iron overload:

A

Unregulated intestinal absorption, hemolytic anemia, multiple transfusions

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22
Q

Hemochromatosis “bronze diabetes” triad

A

Cirrhosis
Pancreatic fibrosis
Bronzed skin

(Also causes atypical arthritis)

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23
Q

What is the primary reason for hemochromatosis

A

Defect in chromosome 6 that affects regulation of intestinal absorption of iron

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24
Q

Secondary hemochromatosis may result from

A

Chronic hemolytic disorders and/or multiple transfusions

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25
Q

What is characterized by increased tissue iron generally limited to the macrophages with little effect on parenchyma

A

Hemosiderosis

Versus hemochromatosis which is asssociated with damaging parenchymal tissue deposits

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26
Q

Treatment (2) of hemochromatosis

A

Phlebotomy

Dietary restriction of iron

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27
Q

Hepatolenticular degeneration

A

Wilson’s disease

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28
Q

What condition is associated with disturbances in regulation of copper transport and excretion into bile

A

Wilson’s disease

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29
Q

In Wilson’s disease, copper accumulates in (4)

A

Liver, brain, eyes, kidneys

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30
Q

In Wilson’s disease, copper is deposited where in the eye and what is this called

A

Cornea-sclera junction; Kaiser Fleischer ring

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31
Q

Cholelithiasis (lith = stone)

A

Gall stones

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32
Q

4F risks of cholelithiasis

A

Female
Fat
Forty (older than)
Fertile

(And the 5th is Flatulence)

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33
Q

What are contributing factors of abnormal bile?

A

Hypercholesterolemia
Inadequate levels of bile acids
Hemolytic disease with hyperbilirubinemia

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34
Q

How does Hypercholesterolemia contribute to abnormal bile?

A

Causes chemical injury to gall bladder mucosa

Cholesterol absorbed by gall bladder diminishes motility of musculature and gives rise to “sluggish” gall bladder

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35
Q

Nucleation is promoted by increased

A

Mucin

36
Q

Kidney stones vs Gall stones

A

Kidney stones = calcium

Gall stones = cholesterol

37
Q

What are cholesterol stones

A

When the stone deposit is made up of 50% or more cholesterol

38
Q

Pure stones

A

10% of all stones. Cholesterol (large, oval, small) and pigmented

39
Q

How common are “Mixed” and “combined” stones?

A

80-90%

40
Q

Cholecystitis

A

Inflammation of gall bladder

41
Q

Majority of Cholecystitis is associated with

A

cholelithiasis (gall stones) 80-90% of the time

42
Q

What contributes to chemical injury to bladder mucosa?

A

Hyperconcentrated bile

43
Q

What enteric organisms are a concern with bacterial infection

A

E.coli and other organisms may enter gall bladder

44
Q

What is the role in pathogenesis of pancreatic reflux?

A

Uncertain. When it occurs, mixing of the pancreatic secretions with bile may contribute to mucosal injury by activation of pancreatic enzymes.

45
Q

When is bacteria present, in acute or chronic cholecystitis?

A

Acute cholecystitis (80% of the time vs 30% of the time with chronic)

46
Q

Presentation/symptoms of acute cholecystitis

A

Enlarged, edematous and hyperemia (red)

Steady, progressive right upper quadrant or epigastric pain and tenderness with fever, leukocytosis and nausea

47
Q

Morphology of chronic cholecystitis

A

Gall bladder is often fibrotic and reduced in size.

48
Q

In some chronic cholecystitis cases the gall bladder may be distended (_______)

A

Mucocele, “hydrops”

49
Q

In chronic cholecystitis, calcified gallbladders is known as

A

“Porcelain gall bladder”

50
Q

Symptoms of chronic cholecystitis

A

Right epigastric pain, nausea, intolerance of fatty foods

51
Q

What is a first sign of liver tumor

A

Hepatomegaly

52
Q

Most common cause for enlarged liver

A

Fatty liver caused by poor diet, obesity, alcohol, OTC meds (because liver processes)

53
Q

Causes of hepatocarcinoma

A
  • Hepatitis B (HPB)
  • Aflatoxin (peanuts)
  • Cirrhosis
54
Q

Primary malignant tumors of the liver 93)

A

1- Hepatocarcinoma
2- Cholangiocarcinoma (of bile ducts)
3- Hemangiosarcoma (vascular)

55
Q

Crohn’s, cystic fibrosis, (some) parasites, exposure to chemical agents can all lead to what primary malignant liver tumor

A

Cholangiocarcinoma (of bile ducts)

56
Q

Gall bladder causes how many deaths per year?

A

5,000

57
Q

What are symptoms of malignant gall bladder tumors?

A

Resembles cholecystitis and cholelithiasis: not much happens.

Diagnosis is 1% for 5 year survival

58
Q

Pancreatitis: what is it and what are some causes of it

A

Inflammation of pancreas

Caused by infection, trauma, ischemia, drugs, hyperthermia, secretory obstruction, etc

59
Q

Acute pancreatitis is associated with

A

Enzyme activation within pancreas that contributes to “auto digestion”

60
Q

What are symptoms of acute pancreatitis

A

Sudden pain “acute abdomen”

It’s the reason for about 1/500 emergency room admissions

61
Q

Mild acute pancreatitis vs severe acute hemorrhagic pancreatitis

A

Mild: self-limiting
Severe: extensive damage and possible death

62
Q

Severe pancreatitis is also called

A

Acute hemorrhagic pancreatitis

63
Q

Pathogenesis of severe (acute hemorrhagic) pancreatitis

A

Normally, pancreatic enzymes are activated in the gut and do not injure the pancreas. In acute pancreatitis, activation of trypsin may be a key step since it has the capacity to activate other enzymes (elastases, collagenases, phospholipidase, etc.) and the kinin system within the pancreas.

64
Q

Causes of severe acute pancreatitis

A

Chronic biliary disease and chronic alcohol abuse

65
Q

Symptoms of severe acute pancreatitis

A

Sudden, intense, CONSTANT pain

66
Q

Sudden, intense, constant pain that refers to upper back and usually follows meal or alcohol ingestion

A

Severe (acute hemorrhagic) pancreatitis

67
Q

What is more common: chronic or acute pancreatitis

A

Chronic

68
Q

What kind of pancreatitis occurs after multiple episodes that contribute to fibrosis, parenchymal atrophy and ultimately, pancreatic failuter

A

Chronic (relapsing) pancreatitis

69
Q

Pancreatic carcinoma symptoms

A

Vague and mild early on.

70
Q

What cell type is pancreatic carcinoma

A

Duct cell

71
Q

Risk factors of pancreatic carcinoma

A

Smoking, diet, chemicals, more frequent in African-Americans and diabetics

72
Q

When pancreatic carcinoma is located in pancreatic head, obstructive jaundice is likely. This may be associated with

A

Courvoisier’s “sign”

73
Q

About 10% of obstructive jaundice is likely exhibit increased tendency for spontaneous (migratory) thrombosis which is associated with

A

Trousseau’s sign

74
Q

What are two islet cell tumors?

A

1 - Beta cell tumors (insulinomas)

2 - Gastrin-producing tumors (gastrinomas)

75
Q

What kind of islet cell tumor might cause hypoglycemia

A

Beta cell tumor

76
Q

What kind of islet cell tumor includes a classic “triad” and is the second most common form of islet tumor?

A

Gastrin-producing tumors

77
Q

What is the classic “triad” of gastrin-producing tumors and what is it known as

A

Zollinger Ellison syndrome
1 - gastrin producing islet cell tumor
2 - gastric hyperaciditiy
3 - intractable multiple peptic ulcers (stomach, duodenum, esophagus, jejunum)

78
Q

Type I IDDM

A

Insulin dependent diabetes mellitus “juvenile onset”

79
Q

Type II NIDDM

A

Non-insulin independent diabetes myelitis “adult onset”

80
Q

Secondary contributing factors to diabetes mellitus

A

Inflammatory, surgical, neoplasticism or other conditions that damage islet tissue.

Dysfunction of pituitary or suprarenal glands, certain drugs, etc.

81
Q

When do chronic lesions appear in Type I and Type II Diabetes?

A

10-15 years

82
Q

Glomerular sclerosis

A

Nephropathy

83
Q

DM causes ___% legal blindness in US

A

15%

84
Q

What is a common lesion of the eyes that is associated with disease of retinal vessels with exudation, fibroproliferative responses, microaneurysms, hemorrhages

A

Retinopathy

85
Q

DM is most common metabolic cause for

A

Peripheral neuropathy

86
Q

Is Peripheral neuropathy unilateralal or bilateral

A

Bilateral. Because its systemic disease

87
Q

Type I diabetes and the 3 Ps

A

Polyuria
Polydipsia
Polyphagia

Pathology II (7 decks)

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