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GI Nelson > Liver 1 (not including viral hepatitis) > Flashcards

Liver 1 (not including viral hepatitis) Flashcards

1
Q

What is jaundice?

A

Retention of bilirubin –> yellow discoloration

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2
Q

What is icterus?

A

Basically jaundice of the sclera

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3
Q

What is cholestasis?

A

Impaired bile secretion

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4
Q

How is bilirubin made?

A

Reticuloendothelial cells convert heme –> bilirubin

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5
Q

Where does the heme that becomes bilirubin come from?

A

85% from breakdown of senescent RBCs

15% from hepatic heme or marrow RBC precursors

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6
Q

What happens to the bilirubin after it is formed from heme?

A

Bilirubin is complexed to albumin and transported to the liver

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7
Q

What form is the bilirubin in when it is being transported to the liver?

A

Unconjugated (Indirect)

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8
Q

What happens to bilirubin in the liver?

A

Bilirubin is conjugated with glucuronic acid in liver cells

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9
Q

What distinguishes unconjugated bilirubin from conjugated bilirubin?

A

Unconjugated: water INsoluble, TOXIC to tissues, NOT secreted in urine

Conjugated: water SOLUBLE, NOT toxic to tissues, SECRETED in urine

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10
Q

Although conjugated bilirubin can be excreted in urine, what is it usually excreted in?

A

Bile…poop

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11
Q

What causes unconjugated hyperbilirubinemia?

A

Increased bilirubin production
Impaired hepatic bilirubin uptake
Impaired bilirubin conjugation

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12
Q

What causes conjugated hyperbilirubinemia?

A 
Extrahepatic cholestasis (biliary obstruction)
Intrahepatic cholestasis
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13
Q

What are some potential causes of neonatal unconjugated hyperbilirubinemia?

A

Normal neonatal alterations in bilirubin metabolism (increased production, decreased clearance, increased enterohepatic circulation)

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14
Q

What are some possible conditions that could manifest as neonatal unconjugated hyperbilirubinemia?

A

Immune-mediated hemolysis
Inherited RBC membrane/enzyme defects
Sepsis
Inherited defects in UGT1A1 activity (Crigler-Najjar or Gilbert’s syndrome)

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15
Q

What can be affected by neonatal unconjugated hyperbilirubinemia?

A

Neuro system:

Bilirubin Induced Neurologic Dysfunction (BIND)

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16
Q

What is one method of treating neonatal unconjugated hyperbilirubinemia?

A

Phototherapy…converts bilirubin to water soluble isomers

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17
Q

What is Gilbert’s syndrome?

A

A benign autosomal recessive mutation that decreases glucuronyltransferase activity (UGT1A1 30% of normal)

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18
Q

What is the effect of Gilbert’s syndrome?

A

Increased unconjugated bilirubin (

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19
Q

What is seen with hepatocellular cholestasis?

A

Bile within hepatocytes
Canalicular bile stasis
Feathery degeneration of hepatocytes

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20
Q

What is seen with canalicular cholestasis?

A 
Bile within hepatocytes
Canalicular bile stasis
Feathery degeneration of hepatocytes
Bile lakes
Bile within distended bile ducts
Portal tract edema
Bile duct proliferation within portal tracts
21
Q

What is chronic passive congestion?

A

Centrilobular congestion

22
Q

What causes chronic passive congestion?

A

Right or left sided heart failure
Hepatic vein thrombosis
Shock (congestion + hypoperfusion –> centrilobular necrosis)

23
Q

What is centrilobular hemorrhagic necrosis?

A

Centrilobular congestion with centrilobular necrosis

24
Q

What is seen with centrilobular hemorrhagic necrosis?

A

Nutmeg liver

Sparing of periportal areas

25
Q

What causes centrilobular hemorrhagic necrosis?

A

Right or left sided heart failure
Hepatic vein thrombosis
Shock (congestion + hypoperfusion –> centrilobular necrosis)

26
Q

What is cardiac sclerosis?

A

Fibrosing reaction following long standing CPC and/or centrilobular necrosis
Centrilobular fibrosis

27
Q

What causes cardiac sclerosis?

A

Right or left sided heart failure
Hepatic vein thrombosis
Shock (congestion + hypoperfusion –> centrilobular necrosis)

28
Q

What causes a hepatic infarct?

A

Double blood supply…seen with arterial occlusion d/t vasculitis, embolism, or tumor

29
Q

What is Budd-Chiari syndrome?

A

Thrombosis of 2 or more hepatic vein branches

30
Q

What microscopic (smaller) things are seen with Budd-Chiari syndrome?

A

Centrilobular hemorrhagic necrosis

Cardiac sclerosis

31
Q

What are the gross findings of Budd-Chiari syndrome?

A

Hepatomegaly
Ascites
Abdominal pain

32
Q

What causes Budd-Chiari syndrome?

A

Conditions that make blood clots more common (there are a lot of them)

33
Q

What is sinusoidal obstruction syndrome?

A

Presence of obstructive, non-thrombotic lesions of the small (central) hepatic veins

34
Q

Who is most likely to have sinusoidal obstruction syndrome?

A

Patients exposed to radiation and/or hepatotoxins

35
Q

What is seen microscopically (smaller) with sinusoidal obstruction syndrome?

A

Subendothelial swelling/fibrosis –> narrowing/obliteration of central vein lumens

36
Q

What are some signs of acute sinusoidal obstruction syndrome? What is it associated with?

A

Hepatomegaly
Sudden weight gain
Increased serum bilirubin

Allogeneic bone marrow transplant or chemo patients

37
Q

What are the signs to chronic sinusoidal obstruction? What is it associated with?

A

Chronic sinusoidal obstruction presents similar to Budd-Chiari syndrome

Chronic sinusoidal obstruction is associated with toxic side effects of pyrrolizidine alkaloids (certain herbal teas)

38
Q

What is seen with portal vein thrombosis?

A

Portal hypertension

NOT ascites

39
Q

What causes portal vein thrombosis?

A

Extrahepatic causes: intra-abdominal sepsis, inherited or acquired hypercoagulable disorders, trauma, or pancreatitis/pancreatic cancer

Intrahepatic causes: cirrhosis, invasion of portal vein by hepatocellular carcinoma

40
Q

What is peliosis hepatitis?

A

Primary hepatic sinusoidal dilation with sinusoidal rupture…results in the formation of blood filled spaces

41
Q

What are the symptoms of peliosis hepatitis?

A

Usually asymptomatic

Rarely, intra-abdominal hemorrhage or hepatic failure

42
Q

What causes peliosis hepatitis?

A

Anabolic steroids, oral contraceptives, or danazol
AIDS associated hepatic infection by bartonella henselae
Nearby malignancy or tumor

43
Q

What causes acute massive hepatic necrosis?

A 
Acute viral hepatitis
Toxin induced hepatitis (tylenol OD)
Vascular liver disease
Autoimmune hepatitis
Wilson's disease
44
Q

Why isn’t cirrhosis commonly seen with massive hepatic necrosis?

A

There isn’t usually fibrosis, so the liver is able to regenerate

45
Q

What is autoimmune hepatitis?

A

T-cell mediated autoimmune disease

More common in females

46
Q

What markers are seen in autoimmune hepatitis?

A

Type 1: ANA, anti-smooth muscle (SMA), anti-actin (AAA), anti-soluble liver antigen/liver-pancreas antibodies (anti-SLA/LP)

Type 2: anti-liver/kidney microsome (ALKM-1), antibodies to a liver cytosol antigen (ALC-1 or LC1)

47
Q

What is seen on a biopsy of autoimmune hepatitis?

A

Increased number of plasma cells in the inflammatory infiltrate

48
Q

What is used to treat autoimmune hepatitis?

A

Steroids

GI Nelson (11 decks)

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