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Pathology for Health Professionals > Ch.11 The Liver and Biliary System > Flashcards

Ch.11 The Liver and Biliary System Flashcards

1
Q

Anatomy of Nomal Liver

A
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2
Q

The point in which the bile duct exits the liver

A

The hilium is where the liver receives its dual blood supply:

Arterial blood through hepatic artery

and Venous blood through hepatic portal vein

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3
Q

Major functions of the liver

A

Excretory (bile)

Metabolic (processing for food components, intermediary metablolism of carbohydrates, fats, and proteins)

Storage (carbohydrates and lipids)

Synthetic (Synthesis of all plasma proteins except for immunoglobulins, albumin is the most copious plasma protein)

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4
Q

Bile is produced by ___ and secreted into the ___

A

Liver, intestine

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5
Q

Obstruction of the bile duct causes

A

jaundice

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6
Q

Obstruction of the portal blood flow causes

A

Formation of ascites

Spenomegaly

*occurs in portal HTN

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7
Q

In order to bypass a block in portal flow, the body

A

The body develops anastomosis between portal and systemic venour circulation

Most important in the lower esophagus, hemorrhoidal plexus, and periumbilical area of anterior abdominal wall

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8
Q

Where can the liver be palpated?

A

The liver moves down with each inspiration, and can be be palpated undernear the right costal margin

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9
Q

What externally covers the normal liver?

A

Glissons capsule - contains nerves

-Distension of this capsule, due to tumors or chronic passive congestion, can cause pain

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10
Q

What is the role of the liver with bilirubin?

A

The Liver is essential to the uptake, processing, and excretion of bilirubin released from aged red blood cells

Bilirubin that is released from RBC is taken up by the liver and excreted in bile

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11
Q

How do liver diseases affect plasma proteins?

A

The liver is a major soure of plasma proteins (except immuniglobulins

Liver diseases result in hypoproteinemia

Lack of albumin results in decreased oncotic pressure, and therefore edema

Decreased production of coagulation factors result in bleeding

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12
Q

Enzymes which are released during liver injury

A

AST

ALT

Alkaline phosphatase is used in detecting bile duct obstruction

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13
Q

Why is the liver a common site for metastases?

A

The liver is more often the site for metastatic cancer than primary liver cell tumors because the liver recieves blood from two sources an thus serves as a major blood thoroughfare

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14
Q

What is jaundice?

A

clinical condition characterized by yellow discoloration of skin or mucosa caused by hyperbilirubinemia

>1.2mg/dl

Jaundice becomes apparent >3mg/dl

Jaundice is symptom or sign, not a disease entitiy

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15
Q

How is bilirubin formed and how is it used?

A

Senecent RBC’s are taken up by the phagocytotic cells of the spleen and the Kuppfer cells of the liver

Within these cells, the hemoglobin is degrated to heme and globin

The heme loses the iron and is transformed into yellow pigment bilirubin

Bilirubin is released into blood and binds with albumin

This nconjugated bilirubin is not water soluble, but is taken up by the liver cells and conjugated with glucuronide

Bilirubin bound to glucuronide becomes water soluble, and is excreted in bile and into the intestine, where it participates in the digestion of fats

Bilirubin that is not used up in the intestine is converted by bacteria into urobilinogen and is reabsorbed

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16
Q

How is hyperbilirubinemia classified?

A

Unconjugated, Conjugated, Mixed

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17
Q

Unconjugated Hyperbilirubinemia

A
  • Prehepatic
  • Mostly caused by excessive bilirubin formation, secondary to hemolysis.

Gilberts disease is another example

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18
Q

Most common cause of hemolysis worldwide

A

Malaria

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19
Q

Conjugated Hyperbilirubinemia

A

Reflects disturbances in the excretion of bilirubin that has been conjucated to glucuronide in the liver cells.

Typically occurs as a result of obstruction of bile flow, usually at level of common bile duct

Gallstones and tumors can be a cause of obstruction

Bile can not reach intestine, so stools are clay colored. Stools are called acholic and associated with steatorrhea

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20
Q

Mixed conjugated and non-conjugated hyperbilirubinemia is marked by___

occurs in____

A

liver cell necrosis and destruction of liver parenchyma

Occurs in viral or drug induced hepatitis, metabolic liver diseases, alcoholic hepatitis and cirrhosis

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21
Q

Where is jaundice best seen?

A

Both conjugated and unconjugated bilirubin bind to connective tissue to stain it yellow

Best seen on the sclera which is normally white

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22
Q

Jaundice is usually accompanied by

A

itching

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23
Q

What is the relationship of bilirubin (unconjugated an conjugated) to urine?

A

Unconjugated: not water soluble, bound to albumin, not excreted in urine, therefore urine in hemolytic jaundice, urine is normal color.

Conjugated: Water soluble and excreted in urine. Appears brown and foamy. Brown urine may be the first sign of viral hepatitis.

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24
Q

Most common form of viral hepatitis in the USA

A

Hepatitis C

Incidence of hep A and B significantly reduced in USA due to vaccination

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25
Q

Hepatitis A

(type of virus, transmission, source, location, symptoms, prognosis)

A
  • Nonencapsulated RNA virus
  • Transmitted fecal-oral route
  • Sources of virus are sewage, contaminated food/drinks
  • Most prevalent in children of underdeveloped countries
  • Symptoms start after a short incubation period of 15-50 days
  • Mild enteric fever, vomiting, loss of appetite, jaundice
  • Recovery within days
  • Good prognosis, does not advance to cirrhosis or chronic hepatitis
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26
Q

Hepatitis B and HBsAG

A
  • Encapsulated DNA virus
  • HBsAG is circulated in blood early, and can be detected within 1 week after onset of infection
  • HBsAG dissapears after convalescent period, which is marked by the appearance of antibody to HBsAG
  • HBsAG persists in circulation only when patients develop chronic hepatitis. These patients can not produce anti-HB’s, and can not clear the virus from the body
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27
Q

Hepatitis B and HBeAG

A
  • HBeAG appeats in acute infection, but dissapears before HBsAG
  • Found it patients with chronic hepatitis
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28
Q

Symptoms of HBV

A

Appear 40-180 days after infection

  • in preicteric phase, there is weakness, nausea and vomiting. Mild enlargement and tenderness of the liver.
  • Some patients develop measles like skin rash
  • darkening of urine (bilirubin)
  • Jaundice is found in less than 30%, found 2-3 months after exposure and associated with worsening symptoms and lab finding
  • HBV produces clinically recognisable symptoms in 1/3 of people
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29
Q

Jaundice and HBV

A
  • Found in less than 30% of infected patients
  • Found 2 months after exposure
  • Associated with worsening symptoms and lab findings (AST, ALT)
  • Jaundice persists for several weeks and in most patients resolves spontaneously
  • More profound the jaundice, more likely the disease will enter an uneventful period of recovery
  • Mild jaundice may herald a protracted course of disease and transition to chronic hepatitis
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30
Q

Symptomatic and Asymptomatic HBV

A

Symptomatic: Produces symptomatic in 1/3. Chronic hepatitis develops in less than 10% of those with clinically evident infection

Asymptomatic: Remaining 2/3 of people have sublinical disease, which is recognised only as the appearance of antibodies to HBs and HBc

  • 90% of patients recover completely
  • Chronic hepatitis in less than 10%
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31
Q

Chronic Hepatitis from HBV: Subclinical

A

-Subclinical:

in 25% of cases

  • HBsAG seen in serum
  • Mild portal tract inflammation on liver biopsy is only sign, and these people are chronic asymptomatic carriers.
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32
Q

Chronic Active Hepatitis from HBV

A

Develops in 25% of those with serologic evidence of chronic hepatitis, more serious, and may lead to cirrhosis or hepatocellular carcinoma

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33
Q

Hepatitis C

(dx., aquired through)

A
  • RNA virus
  • Antibodies used for dx.
  • Infection aquired through IVDU (50%), multiple sex partners (35%), surgery (15%), or needle sticks (10%)
  • 30% of people do not know how they were infected
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34
Q

Clinical Presentation of HCV

A
  • indistinguishable from HBV, but less severe
  • mild abormalities in lab results
  • 80% will progress to chronic hepatitis
  • 20% cirrhosis
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35
Q

What is the portal triad?

A

hepatic artery, portal vein, bile duct

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36
Q

Liver histology

A
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37
Q

Bilirubin Metabolism

A
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38
Q

Lab Evaluation of bilirubin

A

Total: All forms

Direct: Conjugated

Indirect: Unconjugated

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39
Q

Tests to evaluate liver function

A

Albumin: Decrease with injury (liver is only source)

  • Albumin is critical to oncotic pressure. Half life for albumin is 20 days. Helpful in chronic, not acute liver disease.

Prothrombin time: Increase with injury (lack of vit k).

  • Liver is major source of clotting factors, activation depends on vitamin K (all but factor 5)
  • In acute, is a sign of significant liver injury, marker of severity
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40
Q
A
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41
Q

Tests to detect inflammation (liver) or hepatitis

A

AST (can be associated with other organ damange)

ALT (more specific to liver)

AST/ALT ratio: alcohol, malnutrition, cirrhosis

Lactate Dehydrogenase (LDH)- not used often

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42
Q

Lab evaluation of liver disease: tests to detect cholestasis

A
  • Bilirubin: conjugated, unconjucated
  • Alkaline Phosphatase: injury to hepatocyte canalicular membrane induces synthesis and release
  • Gama-glutamyl transferase (GGT): Injury to hepatocyte canilcular membrane or stimulation of microsomal enzymes induce synthesis and release

*GGT and Alk Phosphatase can be elevated in other organs

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43
Q

Signs and Symptoms of liver disease:

Chronic and Acute (table)

A
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44
Q

Recognition of liver disease

A
45
Q

Recognition of liver disease: labs

A
46
Q

Jaundice:

Refers to, due to, means

A
47
Q

Causes of unconjugated hyperbilirubinemia

A
48
Q

Causes of conjugated hyperbilirubinemai

A
49
Q

Causes of Jaundice in adults

A
50
Q

Congenital causes of jaundice

A
51
Q

Obstructive causes of jaundice

A
52
Q

Parenchymal causes of jaundice

A
53
Q

Hepatitis VS. Obstruction:

liver tests: table

A
54
Q

Major Patterns of acute liver injury

A
55
Q

Viral Hepatitis symptoms

A
56
Q

Pathology of Acute Viral Hepatitis

A
57
Q

Acute Viral Hepatitis:

what do you see in the labs?

A
58
Q

Acute Ischemic or Toxic drug hepatitis: What do you see in the labs?

A
59
Q

Drug Induced Liver Injury

A
60
Q

Alcoholic Hepatitis

A
61
Q

Fatty Liver under the microscope

A
62
Q

Lab test markers of Severe Hepatitis

A
63
Q

Cholestasis: Large duct obstruction

causes

A
64
Q

Complete Obstruction; Cholestasis

what do the labs do?

A
65
Q

If uptake of liver cells is blocked or can not take place because of liver insufficiency, then what will happen to metabolites?

A
  • then the substances persist and may have adverse effects on other tissues
    ex. ammonia and hepatic encephalopathy
66
Q

Are liver cells mitotic?

A

Yes, liver cells are faculative mitotic - meaning they can regenerate

67
Q

Jaundice is classified as

A

prehepatic

Hepatic

Post-Hepatic

68
Q

Unconjugated bilirubin is bound to ____. Meaning it….

A

-unconjugated bilirubin is bound to albumin

does not cross blood brain barrier, and does not enter cerebrospinal fluid

-does not filter into urine

69
Q

How is conjugated bilirubin excreted?

A

-in urine, makes brown and foamy

70
Q

How do you determine the cause of jaundice?

A
  • conjugated or unconjugated bilirubin
  • signs of liver injury
  • is there obstruction of bile ducts?
71
Q

Viral Hepatitis

A
  • clinical syndrome of varying severity
  • caused by hepatotropic viruses: hepatitis A, B, C, D, E
  • Is most prevalent liver disease in the world
  • often no symptoms
  • Hep C most common in usa
72
Q

Hepatitis A

A
  • RNA virus
  • spread through fecal-oral route (sewage, contaminated food, shellfish)
  • symptoms: short incubation period 15-50 days
  • short lived fever, loss of appetite, and jaundice
  • recovery occurs within days, without complications
  • transition to chronic hepatits or cirrosis never occurs
  • favorable prognosis
73
Q

Hepatitis B

A
  • DNA virus
  • symptoms occur 40-180 days after
  • exposure to blood, blood products, or sexual contact
  • Pre-icteric features: weakness, n&v, enlargement of liver, some have measles like rash
  • dianostic: darkening of urine d/t bilirubin
  • Jaudince is found in 30% of patients - usually associated with worsening clinical and labs (bilirunin, AST, ALT)
  • HBV produces clinical symptoms in 1/3, rest of 2/3 have subclinical disease, and recognisible due to antibodies to HBs and HBc
  • 90% of patients recover completely
74
Q

Hepatitis C

A

RNA virus

  • transmitted by infected needles during IVDU (50%)
  • sexual partners (35%)
  • surgery (15%)
  • accidental needlestick (10%)
  • 30% of people dont know where they got it

Clinical presentation: simliar to HBV, but less severe

  • progress to chronic hepatitis in 80%
  • 20% will develop cirrhosis
75
Q

Hepatits D

A

RNA virus that requires HBV for replication

may occur concurrently with HBV or as superinfection following HBV

76
Q

Hepatits E

A

RNA virus

fecal-oral route

waterborn epidemics

resembles HAV

77
Q

Pathology of Hepatitis

A

hepatotropic and invade liver cells, damaging and disrupting normal functions while promoting cell death by apoptosis

morphologic changes

  • reversible hepatocellular changes
  • irreversible hepatocellular changes
  • inflammatory infiltrates
  • regeneration of hepatocytes
78
Q

Chronic Hepatitis Classification

A

mild: mild inflammation limited to portal tracts, limited intralobular infiltration
moderate: portal tract inflammation is accompanied by spilling of inflammatory cells across limiting plate, and all the way into the lobule
severe: disruption of lobular architecture, secondary to aggresive inflammation and fibrosis that accompanies liver cell death. Bridging fibrosis can lead to cirrhosis

79
Q

What is Cirrhosis?

A

Chronic liver disease characterized by loss of structure and function

synonym for end-stage liver disease.

-irreversible and incurable - except for transplatiation

characterised by fibrosis and regenerative liver cell nodules that replace normal parenchyma

80
Q

Etiology of Cirrhosis

A
  • Alcohol, hepatitis virus most common (65%)
  • estimated that steatohepatitis will become more prominent
  • etiology in 20% can not be established
81
Q

Pathogenesis of Cirrhosis

A

Exact is unknown, however main include

  1. Necrosis of liver cells
  2. Repair by fibrosis
  3. Regeneration of liver cells with formation of nodules
82
Q

Two basic patterns of cirrhosis

A

portal cirrhosis and billiary cirrhosis

83
Q

Compliations of cirrhosis (illustration)

A
84
Q

Consequences of portal HTN

A

ascites

splenomegaly

anastomoses between portal and systemic circulation

85
Q

What is ascites?

A

Fluid accumilation in the abdominal cavity

results from portal HTN and hypoproteinemia

  • backpressures in the portal vein result in transudation of fluid from the serosal surfaces of the intestines, peritoneal surfaces lining the abdominal cavity
  • reduced oncotic pressure in the plasma from hypoalbinemia, causes fluids into abdominal cavity
  • results in hypovolemia which triggers aldosterone from renal cortex- NA and H20 retention = affects kidneys- they stop producing urine and thus hepatorenal syndrome

Ascites is resistant to tx., and draining will have no effect

86
Q

What is splenomegaly?

A
  • enlarges 3-6x its size
  • enalged spleen destroys RBC=anemia, leukopenia, thrombocytopenia
87
Q

What is anastomosis in cirrhosis?

A

caused by shunting between portal and systemic circulation

most important are the lower esophagus - which undergo dilation and develop varicies

metabolic consequences: encephalopathy (neurotoxins and ammonia- not processed in liver)

88
Q

what are esophageal varicies?

A

dilated veins in lower esophagus. prone to bleeding

may result in hematoemesis or melena

89
Q

Most common cause of death in patients with cirrhosis

A

hemmorhage

90
Q

What is hepatic encephalopathy?

A

marked by clouded mentation and neuro symptoms

“Cerebral dysfunction is thought to be caused by ammonia and putative neurotoxins absorbed from the intestine. Because the shunts allow the enteric venous blood to bypass the liver, neurotoxic substances are not detoxified and therefore act directly on susceptible cells in the brain. The diseased brain shows edema and altered astrocytes but no other morphologic changes that would explain the patho-genesis of neurologic symptoms. Hepatic coma is associated with a high mortality rate, and the patient’s life can be saved only by emergency liver transplantation”

91
Q

Associated findings with cirrhosis

A

Liver cell injury and death:

  • ALT and AST levels are the best markers of liver cell injury. Acute liver injury is characterized by an elevation of these liver enzymes in serum, but as the acute injury ceases, the levels of ALT and AST may revert to normal.
  • In end-stage liver disease, often there is no ongoing liver cell death. ALT and AST concentration in the blood may be only mildly elevated.
  • Loss of liver cell function. Decreased production of albumin leads to hypoalbuminemia, which contributes to the formation of ascites and edema. Do not forget that albumin is the most abundant plasma protein and the most important oncotic component of the blood, keeping the fluid in circulation and preventing edema formation. Decreased synthesis of coagulation proteins results in a bleeding tendency. Defective excretion of bilirubin may result in jaundice, which is usually mild.
  • Portal hypertension. The principal consequences of portal hypertension are ascites, splenomegaly, and anastomosesbetween the portal and systemic circulation. Spleno-megaly results in the pooling of platelets, leading to thrombocytopenia and bleeding tendency. The bleed-ing from ruptured esophageal varices leads to an accumulation of blood in the stomach and the intestines, where it serves as a major source of ammonia. Ammonia is degraded from blood protein and absorbed in the intestines, and thus contributes to hepatic encephalopathy.
92
Q

Chonic alcohol abuse can cause (3)

A

Fatty liver

alcoholic steatohepatitis

cirrhosis

93
Q

Effects of alcohol on the body

A

Alcohol is an important source of calories (7 calories per gram) and has complex metabolic and poten-tially toxic effects on many cells in the body.

Alcohol affects the liver, inhibiting some enzymes and stimulating others

It also alters the fluidity and function of cell membranes, as well as the intracellular transport of organelles and metabolites.

Because of increased fatty acid synthesis, decreased fatty acid oxidation, and decreased export of fats in the form of lipoproteins, alcohol invariably produces fatty changes in liver cells in a dose-dependent manner.

The liver becomes enlarged but without any metabolic consequences or symptoms.

These changes are completely reversible, disappearing after the patient stops drinking.A small number of patients with alcoholic fatty liver (10% to 15%) develop signs of alcoholic hepatitis. These signs usually include fever, leukocytosis, abdominal pain, and jaundice.

Histologic examination of the liver shows fatty change of hepatocytes and focal necrosis of liver cells associated with leukocytic infiltrates and bile stasis. The cytoplasm of hepatocytes often contains eosinophilic aggre-gates of intermediate cytoskeletal filaments, which form so-called Mallory-Denk bodies (Figure 11-13). Special stains show pericellular fibrosis, especially around the central venule”

94
Q

Most serious consequence of alcohol abuse

A

Cirrhosis

95
Q

Hereditary diseases of the liver

A

Gilberts disease: benign recurrent jaundice with unconjugated bilirubin

Hemochromatosis: excessive accumliation of iron in many organs, cirrhosis

Wilsons Disease: excessive accumilation of copper (liver, eye, CNS), cirrhosis

Alpha1-antitrypsin deficiency: accumulation of AAT, cirrhosis

96
Q

α1-antitrypsin deficiency

A

“α1-antitrypsin deficiency (α1-AT) is an autosomal reces-sive disorder that is related to the presence of the PiZ allele of the gene that encodes for α1-AT.

this mutation in the Pi gene is found in about 5% of the population, and in homozygous PiZ mutants it may cause emphysema and cirrhosis of the liver.

α1-AT is synthesized in the liver; in PiZ homozygotes it accumulates in the form of cytoplasmic globules inside the liver cells

The exact mechanism of liver cell injury is unknown.A significant number of affected persons develop child-hood cholestasis and chronic hepatitis, which progress to cirrhosis in about 20% of affected individuals.

α1-AT defi-ciency is one of the most common causes of childhood cirrhosis. The disease may be latent until puberty or adult-hood, when it usually presents with clinical signs of cirrhosis that may give rise to liver cancer”

97
Q

Immune Disorder of the liver (3)

A

Autoimmune hepatitis: occurs in young women;associated with other immune diseases (antibodies in serum, ANA, ASM)

Primary biliary cirrhosis: occurs in middle-aged women; chronic jaundice, hypercholesterolemia, (antibodies: AMA)

Primary sclerosing cholangitis: occurs in men less than 40 years old, associated with ulcerative cholitis (no specific antibodies)

98
Q

Chronic biliary cirrhosis

A

disease of uknown etiology

characterized by the destruction of intrahepatic bile ducts and progression to cirrhosis

“non-supurulative destructive cholangitis”resembles t-cell mediated destruction of bile ducts associated with liver teansplant

-females more than males

99
Q

ALT patterns in acute hepatitis

A
100
Q

Drug induced

A
101
Q

Predictable drug related injury

A
102
Q

What are gallstones?

Where are they common (geography)?

Risk with age and gender

A

concretions composed of chemicals normally formed in bile.

They are extremely common, and in the United States more than half a million people undergo biliary surgery for gallstones each year.

An estimated 20% of people older than 65 years have gall-stones.

Women are especially at risk; the incidence of gallstones is three times higher in women than in men.

Because of a metabolic deficiency, Native Americans, such as Pima Indians, are at an extremely high risk for develop-ing gallstones. Indeed, 75% of the women in this population develop gallstones by the age of 25 years.

The incidence of gallstones is higher in whites than in blacks, which further underscores the genetic predisposition for this disease”

103
Q

Pathogenesis of gallstones

A

There are two types of gallstones: cholesterol stones and pigmentary stones.

More than 75% of the gallstones that develop in patients in the United States are cholesterol stones; the remainder are either brown or black pigmentary stones.

Each of these stones is formed as a result of a distinct mechanism, although it is not uncommon to have mixed stones, which shows that these pathogenetic mechanisms may be interrelated”

104
Q

What are cholesterol stones?

A

Cholesterol stones are formed in bile that is supersaturated with cholesterol and contain decreased amounts of bile acids and lecithin.

Bile acids and lecithin are secreted together by the liver cells, but independently of cholesterol.

In the gallbladder these substances form water-soluble micelles with cholesterol. These micelles form only if the three substances are present in appropriate concentrations. If the normal ratio of bile components is altered, the bile becomes lithogenic (i.e., capable of stone formation). This occurs typically in obese persons who excrete large amounts of cholesterol in the bile but also may occur in patients with certain metabolic disorders, such as diabetes.

Pregnancy, estrogen therapy, use of oral con-traceptives, and certain drugs used in the treatment of hypercholesterolemia (e.g., clofibrate) also promote choles-terol excretion in the bile. Such bile is prone to accelerated nucleation of cholesterol crystals, which is most apparent during the concentration of bile in the gallbladder.

The slower bile flow that occurs with age also predisposes such individuals to gallstone formation. It is thus understandable that most cholesterol gallstones are located in the gallblad-der and that the typical risk factors include the so-called four Fs: female, older than forty, fertile, and fat”

105
Q

What are pigmentary stones?

A

Pigmentary stones are composed of calcium bilirubinate and are either black or brown. The black stones, which are most common in Western countries, form in the gallbladders of patients with chronic hemolytic anemia (e.g., sickle cell anemia) and those with cirrhosis.

In such patients the stones form presumably because of supersaturation of bile with bilirubin.

Brown stones are often laminated and consist of alternating layers of calcium bilirubinate and cholesterol admixed with calcium. These stones occur more commonly in individuals living in the Far East than in those from the West and are often associated with biliary infections or infestations with liver flukes, such as Clonorchis sinensis. Brown stones are most often located in the extrahepatic bile ducts and tend to recur after removal”

106
Q

Complications of gallstones

A
107
Q

Most common benign tumor of the liver

A

hemangiomas

108
Q

What is hepatocellular carcinoma?

A

-highly malignant tumor composed of liver cells

Male to female 4:1

originate in cirrhotic livers

they produce a-fetoprotein in 50%, level can be used for dx.

symptoms are non-specific: weight loss, loss of appetite

may block hepatic vein and cause thrombosis and impede outflow of venous blood from liver

poor prognosis less than 5%

Pathology for Health Professionals (14 decks)

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