10. Liver Flashcards

1
Q

The liver is a bilobed organ that is richly vascularized with two main supply vessels. What are they and what is the difference between the two?

A

The hepatic artery carries blood from the aorta to the liver, whereas the portal vein carries blood containing the digested nutrients from the entire gastrointestinal tract, and also from the spleen and pancreas to the liver.

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2
Q

What is the microscopic unit of the liver?

A

Lobule

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3
Q

What does the lobule consist of (3 parts)? What are their functions?

A
  1. Hepatocytes - main liver cell, nutrient storage/release, bile production/secretion, plasma protein synthesis, cholesterol synthesis, carbohydrate synthesis, detoxification
  2. Sinusoids - blood spaces lined with endothelial cells and Kupffer cells (macrophages) that surround hepatocytes. Serves as a location for mixing of the oxygen-rich blood from the hepatic artery and the nutrient-rich blood from the portal vein.
  3. Bile canaliculi - small channels between hepatocytes that carry bile formed from hepatocytes to bile ducts
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4
Q

What are the 6 functions of the liver? (hepatocytes)

A
  1. Bile production/secretion
  2. Plasma protein synthesis
  3. Cholesterol synthesis
  4. Carbohydrate synthesis
  5. Nutrient storage/release
  6. Detoxification
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5
Q

What is bile composed of? (4 contents)

A
  1. HCO3- (Bicarbonate)
  2. Bile salts or acids
  3. Bile pigments
  4. Cholesterol
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6
Q

Bile is formed by ________, excreted into the ___________, and stored in the ________, where it is concentrated and acidified.

A

Bile is formed by hepatocytes, excreted into the bile canaliculi, and stored in the gallbladder, where it is concentrated and acidified.

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7
Q

What are the two main functions of bile?

A
  1. To carry away waste

2. Aid in digestion of fats in duodenum

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8
Q

Bile is discharged into the _________, via ____________, from the __________ to aid in the digestion of fats.

A

Bile is discharged into the duodenum (small intestine), via bile duct, from the gall bladder to aid in the digestion of fats.

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9
Q

What is a major bile pigment?

A

Bilirubin

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10
Q

How is bilirubin formed?

A

Formed from the breakdown of hemoglobin when RBCs are phagocytized

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11
Q

Hemoglobin is broken down into 4 parts when RBCs are phagocytized, what are they and which are reused or excreted?

A
  1. Globin (reused)
  2. Iron (reused)
  3. Porphyrin (excreted)
  4. Biliverdin (excreted, is reduced to bilirubin, macrophages break down senescent (old) erythrocytes and break the heme down into biliverdin, in which biliverdin normally rapidly reduces to free bilirubin)
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12
Q

Where is unconjugated bilirubin?

A

Seen when reticuloendothelial cells (phagocytes) breakdown hemoglobin (primarily in the spleen). Macrophages break down senescent (old) erythrocytes and break the heme down into biliverdin, in which biliverdin normally rapidly reduces to free bilirubin.

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13
Q

Where is unconjugated bilirubin-albumin complex seen?

A

Bilirubin is produced from metabolism of heme (primarily in the spleen), and is transported to the liver bound to albumin. Bilirubin moves into the bloodstream in combination with albumin.

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14
Q

What is another name for unconjugated bilirubin? Is it water soluble or unsoluble?

A

Indirect bilirubin. It is unsoluble. Unconjugated bilirubin is called indirect because it has to be solubilized first.

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15
Q

What is another name for conjugated bilirubin? Is it water-soluble or unsoluble?

A

Direct bilirubin. It is water-soluble. Conjugated bilirubin also is called direct bilirubin because it reacts directly with the reagent.

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16
Q

Where is conjugated bilirubin?

A

In the liver, bilirubin is conjugated (esterfied)

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17
Q

The liver is the only organ with the capacity to …..

A

Rid body of heme waste

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18
Q

___________ goes out via the ___________, and into the gut (small intestine) where it is eventually broken down by gut bacteria to form _____________

A

Conjugated bilirubin goes out via the bile canaliculi, and into the gut (small intestine) where it is eventually broken down to form urobilinogen

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19
Q

Most urobilinogen is excreted in the _______, some is transported back to the ________, and very little is excreted in the ________.

A

Most urobilinogen is excreted in the feces, some is transported back to the liver (to form bile), and very little is excreted in the urine.

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20
Q

What is jaundice and what is it a result from?

A

Jaundice is yellow discoloration of skin, eyes, and mucous membranes. Results from abnormal bilirubin metabolism or retention of bilirubin

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21
Q

Jaundice can be classified based on site of disorder. What can cause pre-hepatic jaundice and what is the result of it?

A

Prehepatic: problems occur before liver
1. Hemolytic anemia or ineffective erythropoiesis in newborns and people, results in increase in unconjugated serum bilirubin. Liver can only process a limited amount at a time, bilirubin overflows into bodily tissues

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22
Q

Jaundice can be classified based on site of disorder. What can cause hepatic jaundice and what is the result of it?

A

Hepatic: problem occurs in liver
1. Liver cirrhosis, inflammation and damage caused by bacterial infection, drugs, toxins, viral infections (hepatitis), alcoholic liver disease, hepatocellular carcinoma, results in an increase in unconjugated and conjugated bilirubin in the blood

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23
Q

Jaundice can be classified based on site of disorder. What can cause post-hepatic jaundice and what is the result of it?

A

Post-hepatic: problem occur after liver
1. Obstruction of biliary drainage (flow of bile into the gut), either by gallstones or tumor at bile duct, pancreatic cancer or cysts, results in an increase in conjugated bilirubin in the blood

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24
Q

Why/when is stool white?

A

Stool gets its normal brownish color from bile, which is excreted into the small intestine during the digestive process. If the liver doesn’t produce bile (hepatic jaundice) or if bile is obstructed from leaving the liver (post-hepatic jaundice), stool will be light colored or white

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25
Q

How are hepatocytes involved in cholesterol synthesis?

A

The liver breaks down fatty acids to form triglycerides, phospholipids, or cholesterol. Cholesterol needed as precursor to steroid hormones such as estrogen, progesterone, and vitamin D

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26
Q

How are hepatocytes involved in carbohydrate synthesis?

A

Liver maintains stable glucose concentrations by storing glucose as glycogen and degrading glycogen to form glucose

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27
Q

How are hepatocytes involved in plasma protein synthesis?

A

The liver makes albumin, alpha and beta globins, and clotting factors

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28
Q

How are hepatocytes involved in nutrient storage/release?

A

Hepatocytes absorb and store excess nutrients in the blood, nutrients released when levels are low

  1. Glucose (glycogen)
  2. Iron
  3. Retinol (Vitamin A)
  4. Calciferol (Vitamin D)
  5. And more…
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29
Q

How are hepatocytes involved in detoxification?

A

Hepatocytes have the ability to prevent toxic and harmful substances from reaching systemic circulation by binding or chemical modification to inactivitate it.

30
Q

What are the 4 important liver enzymes?

A
31
Q

Which liver enzymes are elevated in hepatic injury? Which one out of the two is more specific for liver injury?

A

Alanine aminotransferase (ALT) and Aspartate aminotransferase (AST). ALT has greater specificity for liver injury.

32
Q

Which liver enzymes are elevated in cholestatic injury?

A

Alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT)

33
Q

What does cholestatic injury mean?

A

Any condition in which the flow of bile from the liver stops or slows

34
Q

What does an elevation in liver enzymes indicate?

A

Liver cells may be damaged or inflamed or that the gallbladder and the bile ducts might be obstructed. Damage causes leaking elevated quantities into the blood stream

35
Q

What ratio of AST to ALT is indicative of alcoholic liver disease

A

AST > ALT 2:1 - 3:1, AST > 300: alcohol

36
Q

ALT > or < AST in fatty liver disease?

A

ALT > AST in fatty liver disease

37
Q

ALT > AST by 1000x is indicative of what?

A

Acute viral hepatitis, ischemic hepatitis, toxins, autoimmune hepatitis, Wilson’s disease

38
Q

Where is ALP found besides the liver and when is it elevated in what kind of liver injury?

A

ALP also found in bones and placenta. Found in hepatocytes that line bile canaliculi. Level is raised in biliary obstruction (causes stretch of the bile canaliculi.

39
Q

Which enzyme can be used in conjunction with ALP and why?

A

GGT, because it is also found in bile canaliculi, so if ALP activity is of hepatic origin, both GGT and ALP will be elevated. If elevated ALP is from the bone, GGT will be normal

40
Q

Why is GGT considered non-specific for biliary obstruction?

A

Because it can be raised by many drugs especially alcohol

41
Q

What is the serum bilirubin level of jaundice patients?

A

Serum bilirubin level > 2.5 mg/dL

42
Q

What does it mean if a patient is vomiting green?

A

Bowel Obstruction below the level of the Ampulla of Vater

43
Q

What specimen is needed for bilirubin analysis?

A

Serum (preferred) or plasma, fasting sample (preferred), hemolyzed should be avoided. Sensitive to light so it should be protected.

44
Q

What is urobilinogen?

A

A colorless end product of bilirubin metabolism formed in the small intestine, when conjugated bilirubin from the liver gets excreted to the small intestine.

45
Q

Increased levels of urobilinogen in urine found in what conditions?

A

Hemolytic disease and defective liver cell function

46
Q

Absence of urobilinogen in urine and stool found in what condition?

A

Complete biliary obstruction (colorless stool)

47
Q

What quantitative method is used to detect urobilinogen? What is the principle?

A

Ehrlich’s reagent, containing p-dimethylaminobenzaldehyde (DMAB), that acts as an indicator of urobilinogen by forming a red color

48
Q

Is prothrombin time/INR increased or decreased in liver disease and why?

A

Prothrombin time is commonly increased in liver disease due to decreased protein synthesis. Prothrombin time measures Vitamin K dependent clotting factors. The liver is involved in activating Vitamin K, so if there is liver damage, these clotting factors (protein) cannot be produced in the liver (measuring synthetic ability of liver)

49
Q

What should you do to make sure that increased PT/INR time is actually due to liver disease?

A

Give patient consumable Vitamin K. If giving Vitamin K has no effect on the prolonged INR, then the patient has impaired synthetic function of liver. If giving Vitamin K decreases INR time, then the patient has a problem activating Vitamin K or has a deficiency of Vitamin K

50
Q

Is serum albumin increased or decreased in liver disease and why?

A

Decreased level caused by decreased protein synthesis. Liver failure, cannot produce albumin.

51
Q

Why is it important to check urine for albumin when correlating decreased serum albumin with liver disease/failure?

A

In liver failure, hepatic synthetic ability (protein synthesis of albumin) is decreased, so there is low serum albumin. However, there is also low serum albumin in nephrotic syndrome, so always check urine for albumin. If there is high albumin in urine too, then its nephrotic syndrome. If not, then it is impaired hepatic synthetic ability.

52
Q

Which two tests are used to measure hepatic synthetic ability?

A

Measuring prothrombin (PT)/INR time and serum albumin

53
Q

What levels of ethanol (ETOH) is seen in steatosis (fatty liver), hepatitis, and cirrhosis?

A

Steatosis 90-100%, hepatitis 10-35%, cirrhosis 8-20%

54
Q

What components are indicative of alcoholic liver disease?

A
  1. AST > ALT
  2. 2:1 - 3:1 ratio (AST:ALT)
  3. AST > 300
  4. Elevated ETOH
  5. Elevated GGT
55
Q

What is cirrhosis?

A

Condition in which scar tissue replaces healthy liver tissue and blocks blood flow and prevents proper functioning

56
Q

Cirrhosis is commonly caused by

A

Leading cause is alcohol abuse. Also can be due to hepatitis C infection.

Smaller causes: chronic hep B and D, autoimmune disorders, inherited

57
Q

90-95% of hepatic malignancies are ___________. There are two types of tumors, _________ and __________.

A

Metastatic (not originating in liver cells).

There are two types of tumors, benign (hepatocellular adenoma) and malignant (hepatocellular carcinoma)

58
Q

Reye’s syndrome is often preceded by what?

A

Often preceded by viral syndrome such as varicella (chickenpox), gastroenteritis, or upper respiratory tract infection (influenza).

59
Q

Reye’s syndrome is often associated with ingestion of what medication during viral syndrome?

A

Associated with ingestion of aspirin during viral syndrome

60
Q

Acute illness of Reye’s syndrome is characterized by (5):

A
  • Fatty changes of the liver
  • Acute swelling of the brain (cerebral edema), encephalopathy
  • Persistent vomiting
  • Unusually high amounts of ammonia in the blood (hyperammonemia)
  • Neurologic impairment
61
Q

What are 3 genetic liver diseases?

A
  1. Hemochromatosis
  2. Alpha-1 Antitrypsin deficiency
  3. Wilsons Disease
62
Q

What causes hemochromatosis? What is the result?

A

Iron overload is usually caused by an inherited condition called hemochromatosis. Increased Fe absorption from the gut, depositied in tissues causing cirrhosis and functional failure

63
Q

What causes alpha-1 antitrypsin deficiency? What is the result?

A

Decreased level or deficiency of alpha-1 antitrypsin (that protects lungs) in the blood. People with alpha-1 antitrypsin deficiency are able to produce this protein in liver; however, unable to enter bloodstream and accumulates in liver. Resulting in cirrhosis, severe liver damage and scarring.

64
Q

What causes Wilson’s disease? What is the result?

A

Accumulation of copper in tissues and organs. Ceruloplasmin, a protein that carries copper in the bloodstream. People with Wilson’s disease often have low ceruloplasmin levels, but not always. Can be due to failure of biliary excretion. Results in cirrhosis of liver, liver failure, neurological problems

65
Q

If HBsAg is positive, and Anti-HBs, Anti-HBc IgM, and Anti-HBc IgG is negative, what is the interpretation?

A

Early acute HBV infection

66
Q

If HBsAg and Anti-HBc IgM are positive and Anti-HBs and Anti-HBc IgG are negative, what is the interpretation?

A

Acute HBV infection

67
Q

If HBsAg and Anti-HBc IgG are positive and Anti-HBs and Anti-HBc IgM are negative, what is the interpretation?

A

Chronic HBV infection

68
Q

If Anti-HBs is positive and HBsAg, Anti-HBc IgM, and Anti-HBc IgG are negative, what is the interpretation?

A

Not infected, prior vaccination for HBV

69
Q

If Anti-HBs and Anti-HBc IgG are positive, and HBsAg and Anti-HBc IgM are negative, what is the interpretation?

A

Resolved acute HBV infection

70
Q

What is present in Hepatitis B vaccine and what does that result in for vaccinated patients?

A

HbsAg which helps form Anti-HbsAg (antibody against Hepatitis B surface antigen)