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pathophysiology 4802 > Disorders of the Liver (Final Exam) > Flashcards

Disorders of the Liver (Final Exam) Flashcards

1
Q

what are some of the functions of the liver

A
  • detoxify certain substances
  • secrete bile
  • important role in metabolism of all three kinds of foods (proteins, fats and carbs)
  • store several substances (glucose, iron, vitamin A, B12 and D)
  • produces plasma proteins
  • serves as a site of hematopoiesis during fetal development
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2
Q

what are the two main disorders of the liver

A
  1. Jaundice
  2. Hepatitis (viral hepatitis)
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3
Q

this is a yellow or greenish pigmentation of the skin caused by hyper-bilirubinemia (plasma bilirubin concentrations above 2.5 to 3.0 mg/dL)

A

jaundice

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4
Q

explain the metabolism of Bilirubin

A
  • see slide 7 in lecture *
    spleen and liver:
    RBC gets destroyed -> hemoglobin -> heme + globin (globin goes to amino acid pool) -> heme gets broken down into iron + biliverdin (iron goes to iron pool) -> biliverdin gets broken down into unconjugated bilirubin which is lipid soluble ->

plasma:
unconjugated bilirubin + albumin (this combinations makes bilirubin soluble in blood) ->

liver:
unconjugated bilirubin + glucuronic acid (conjugated bilirubin is water soluble)

bile channels:
conjugated bilirubin is excreted with bile

intestine:
conjugated bilirubin stools -> urobilinogen (by bacterial activity in the intestine)

liver and kidney:
urobilinogen gets excreted with urine or faces

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5
Q

what are the 3 types of jaundice

A
  1. hemolytic/pre-hepatic
  2. obstructive/post-hepatic
  3. hepatocellular/hepatic
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6
Q

explain the hepatobiliary mechanism of Intrahepatic Obstructive Jaundice

A

hepatocellular damage or obstruction of the bile canaliculi -> liver is unable to conjugate and excrete bilirubin -> conjugated and unconjugated hyperbilirubinemia -> bilirubin deposition in tissues (Jaundice)

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7
Q

explain the hepatobilliary mechanism of extraheptaic obstructive jaundice

A

bile duct obstruction (cholestasis) = this can cause light coloured stools -> conjugated bilirubin accumulates in the liver and enters the bloodstream -> conjugated hyperbilirubinemia -> increased excretion of bilirubin in urine OR bilirubin deposition in tissues (Jaundice)

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8
Q

explain the hematologic mechanisms of jaundice

A

excessive lysis of RBCs -> hepatocytes cannot conjugate and excrete bilirubin as rapidly as its formed so bilirubin enters the bloodstream -> unconjugated hyperbilirubinemia -> bilirubin deposited in tissues (Jaundice)

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9
Q

what are some clinical manifestations of jaundice

A
  • darkened urine
  • light stools
  • yellow discolouration of the sclera of the eye
  • yellow pigmentation of the skin
  • pruritus
  • kernicterus (brain damage caused by too much bilirubin in babies blood)
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10
Q

this is defined as inflammation of the liver

A

hepatitis

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11
Q

this subtype of hepatitis is usually caused by autoimmune disorders, reactions to drugs, toxins and infectious disorders including viruses

A

acute hepatitis

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12
Q

this subtype of hepatitis has symptoms that persist for more than 6 months. (viruses, alcoholism, drug toxicity and autoimmune disorders)

A

chronic hepatitis

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13
Q

____ hepatitis is sometimes associated with cholestatic hepatitis

A

acute

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14
Q

_____ hepatitis is associated with massive necrosis and has a high mortality rate

A

fulminant

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15
Q

this type of chronic hepatitis leads to cirrhosis

A

continuing necrosis

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16
Q

this type of chronic hepatitis does not normally lead to cirrhosis

A

carrier state

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17
Q

this is a relatively common systemic disease that affects primarily the liver. it is caused by five strains of viruses & there are two mechanisms for hepatocyte injury

A

viral hepatitis

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18
Q

this phase of viral hepatitis usually lasts 3-4 days and symptoms are present

A

prodromal phase

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19
Q

this phase of viral hepatitis lasts about 1-4 weeks. threshold bilirubin is 2.6 mg/dL

A

icteric phase

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20
Q

this phase of viral hepatitis includes the disappearance of symptoms. some liver dysfunction may persist

A

convalescent phase

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21
Q

is HAV a DNA or RNA virus

A

RNA

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22
Q

does HAV have antigens or antibodies present

A

antigen (anti-HAV)

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23
Q

what is the incubation period of HAV

A

~30 days therefore onset can be abrupt

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24
Q

what is the route of transmission of HAV

A
  • fecal-oral
  • parenteral
  • sexual
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25
Q

true or false: HAV has a known carrier state

A

false

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26
Q

how can HAV infection be prevented

A

HAV vaccine and hygiene

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27
Q

true or false: HAV leads to chronic hepatitis

A

false

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28
Q

what is the typical severity of HAV

A

mild

29
Q

how is HAV diagnosed?

A

presence of anti-HAV
- immune globulin M or G
(serologic test is highly reliable)

30
Q

the peak of which of the following curves present acute symptoms along with jaundice and an increase in ALT
- HAV in stools
- IgM anti-HAV
- IgG anti-HAV

A

IgM anti-HAV

31
Q

the peak of which of the following curves occurs in the convalescence and recovery period?
- HAV in stools
- IgM anti-HAV
- IgG anti-HAV

A

IgG anti-HAV

32
Q

the peak of which of the following curves occurs FIRST (within incubation period of ~ 30 days)
- HAV in stools
- IgM anti-HAV
- IgG anti-HAV

A

HAV in stools

33
Q

how does HAV infection develop (pathogenesis)?

A

hepatocyte injury due to direct killing and cellular immune responses (T cells, NK cells and cytokines)

34
Q

is HAV a DNA or RNA virus

A

DNA

35
Q

does HBV have antigens or antibodies present

A

antibodies (HBsAg)

36
Q

what is the route of transmission of HBV

A

parenteral and sexual

37
Q

what is the incubation period of HBV

A

60 - 180 days thus onset is insidious

38
Q

true or false: HBV has a known carrier state

A

true

39
Q

what is the typical severity of HBV

A

can be severe and chronic

40
Q

how does HBV infection develop (pathogenesis)

A

hepatocyte injury caused by cellular immune responses to viral replication and inflammation resulting in cellular necrosis

41
Q

what does it mean if HBsAb is positive?

A

have immunity from vaccine

42
Q

what does it mean if HBcAb is positive?

A

had previous infection

43
Q

what does it mean if HBsAg is present?

A

have the infection

44
Q

does IgM represent an acute or chronic infection

A

acute

45
Q

what does it mean if HBeAb is positive

A

body has high immunity against the virus q

46
Q

what does it mean if HBeAg is positive

A

infectious

47
Q

in both HAV and HBV infections, which phase (prodromal/preicteric, icteric or convalescence phase) does AST, which is an indicator for hepatocellular damage and necrosis, peak?

A

icteric phase

48
Q

Is HCV a RNA or DNA virus

A

RNA

49
Q

does HCV have antibodies or antigens present

A

Anti-HCV

50
Q

how is HCV transmitted

A

parenteral and sexually

51
Q

what is the incubation period of HCV

A

35-60 days

52
Q

is the onset of HCV acute or insidious

A

insidious

53
Q

true or false: HCV has a known carrier state

A

true

54
Q

what is the type of severity of HCV

A

mild

55
Q

how can HCV be prevented

A

hydride and blood screening

56
Q

what does a serology test show that would be indicative of a HCV diagnoses

A
  • antibodies for HCV
  • HCV in serum
57
Q

which of the following curves peak first at ~4-5 weeks
- Anti-HCV
- HCV RNA
- ALT

A

HCV RNA

58
Q

which of the following curves peak after HCV RNA
- Anti-HCV
- HCV RNA
- ALT

A

ALT

59
Q

which of the following curves peak last at ~24 weeks and then the curves begins to plateau for years
- Anti-HCV
- HCV RNA
- ALT

A

Anti-HCV

60
Q

how does HCV develop (pathogenesis)

A

hepatocyte injury caused by immune response, inflammation and fibrosis leading to cirrhosis

61
Q

this type of viral hepatitis is caused by a defective RNA virus and it can cause acute and chronic hepatitis

A

hepatitis D

62
Q

what does a serology test show that would be indicative of a HDV diagnosis

A
  • anti-HDV IgM and IgG ELISA
63
Q

how can HDV be prevented

A
  • safe sexual practices
  • screening of blood products
  • avoidance of IV use
  • vaccination with HBV vaccine
64
Q

this is an RNA virus that is spread via the fecal-oral route, especially through contaminated water. parenteral transmission may occur

A

hepatits E

65
Q

this type of hepatitis is one of the most common causes of acute hepatitis in developing countries. cases in developed countries are usually related to recent travel

A

hepatitis E

66
Q

this incubation period for this type of hepatitis is 2 to 9 weeks. symptom development is similar to that of HAV and usually lasts 2 weeks. fulminant hepatic failure may occur, esp in pregnant women

A

hepatitis E

67
Q

this represents the irreversible end stage of many different hepatic injuries, including severe acute hepatitis, chronic hepatitis, the metal storage diseases, alcoholism and toxic hepatitis

A

cirrhosis

68
Q

how may cirrhosis cause ascites (buildup of fluid in the spaces of the abdomen)

A

cirrhosis -> increased resistance to portal flow -> portal hypertension -> splanchnic vasodilation ->

  1. increase in splanchnic capillary pressure -> lymph formation that exceeds lymph return -> ascites
  2. arterial underselling -> activation of vasoconstrictor and antinatriuretic factors -> sodium and water retention -> ascites
69
Q

what are some clinical manifestations of cirhhosis

A
  • anorexia
  • weight loss could be masked by ascites
  • weakness
  • diarrhea or constipation
  • jaundice
  • pain
  • bleeding
  • thrombocytopenia
  • palmar erythema

pathophysiology 4802 (16 decks)

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