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Liver Flashcards

1
Q

The caudate and quadrate lobes are found within the posterior surface of the (right/left) lobe

A

The caudate and quadrate lobes are found within the posterior surface of the right lobe

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2
Q

The caudate and quadrate lobes are separated by the _

A

The caudate and quadrate lobes are separated by the porta hepatis which contains the vasculature
* The portal triad enters at the porta hepatis

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3
Q

25% of the liver’s blood supply comes from the _

A

25% of the liver’s blood supply comes from the proper hepatic artery
* Carries oxygenated blood to the liver

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4
Q

75% of the liver’s blood supply comes from the _

A

75% of the liver’s blood supply comes from the portal vein
* Carries blood from the GIT to the liver to be filtered

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5
Q

Blood leaving the liver drains through the _

A

Blood leaving the liver drains through the hepatic vein –> IVC

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6
Q

The hepatic lobule is _ shaped

A

The hepatic lobule is hexagonally shaped

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7
Q

Four regions of the hepatic lobule on histology include _ , _ , _ , _

A

Four regions of the hepatic lobule on histology include portal triad –> zone 1 –> zone 2 –> zone 3 –> central vein

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8
Q

The portal triad includes _ , _ and _

A

The portal triad includes portal vein, hepatic artery, bile duct

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9
Q

Portal traid –> zone 1 –> zone 2 –> zone 3 –> ??

A

Portal traid –> zone 1 –> zone 2 –> zone 3 –> central vein

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10
Q

Viral hepatitis mostly affects zone _

A

Viral hepatitis mostly affects zone 1

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11
Q

Ischemia is most common in zone _

A

Ischemia is most common in zone 3

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12
Q

Ingested toxins most affect zone _

A

Ingested toxins most affect zone 1

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13
Q

Yellow fever mostly affects zone _

A

Yellow fever mostly affects zone 2

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14
Q

CYP450 is most concentrated in zone _

A

CYP450 is most concentrated in zone 3

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15
Q

Metabolic toxins and alcoholic hepatitis mostly affect zone _

A

Metabolic toxins and alcoholic hepatitis mostly affect zone 3
* This is where CYP450 is most concentrated

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16
Q

We have specialized calls called _ located in the space of disse between sinusoids and hepatocytes

A

We have specialized calls called stellate cells (ito cells) located in the space of disse between sinusoids and hepatocytes

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17
Q

Stellate cells are normally quiescent and function to store _

A

Stellate cells are normally quiescent and function to store vitamin A

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18
Q

When activated, stellate cells mediate _ and _

A

When activated, stellate cells mediate liver repair and fibrosis

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19
Q

_ are specialized macrophages found in the sinusoids of the liver

A

Kupffer cells are specialized macrophages found in the sinusoids of the liver

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20
Q

AST is a liver enzyme that stands for _

A

AST is a liver enzyme that stands for aspartate aminotransferase

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21
Q

ALT is a liver enzyme that stands for _

A

ALT is a liver enzyme that stands for alanine aminotransferase

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22
Q

The ratio of _ is classically elevated in alcoholic liver disease

A

The ratio of AST/ALT is classically elevated in alcoholic liver disease

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23
Q

If AST/ALT is elevated in non-alcoholic liver disease, it is suggestive of _

A

If AST/ALT is elevated in non-alcoholic liver disease, it is suggestive of advanced cirrhosis/fibrosis

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24
Q

Super high aminotransferases signals _

A

Super high aminotransferases signals drug-induced liver disease, ischemic, viral, autoimmune hepatitis

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25
Q

Cholestasis, infiltrative disorders, or bone diseases may cause increased _ levels

A

Cholestasis, infiltrative disorders, or bone diseases may cause increased alkaline phosphatase (ALP) levels

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26
Q

GGT stands for _ ; it can be elevated in liver or biliary disease

A

GGT stands for gamma-glutamyl transpeptidase ; it can be elevated in liver or biliary disease

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27
Q

Gamma-glutamyl transpeptidase (GGT) is associated with _

A

Gamma-glutamyl transpeptidase (GGT) is associated with alcohol use

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28
Q

Name some hepatic lab values that may be abnormal in liver disease

A
  1. Bilirubin: increased in biliary and liver disease, hemolysis
  2. Albumin low in advanced liver disease
  3. Clotting factors low in advanced liver disease
  4. Thrombopoietin low in advanced liver disease; thrombocytopenia
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29
Q

Two reasons why platelets are low in liver disease (2):

A

Two reasons why platelets are low in liver disease (2):
1. Thrombopoietin is made by the liver; decreased production of platelets
2. Sequestration by liver and spleen

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30
Q

(3) stages of alcoholic hepatitis

A

(3) stages of alcoholic hepatitis:
1. Hepatic steatosis
2. Alcoholic hepatitis
3. Alcoholic cirrhosis

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31
Q

Hepatic steatosis can be characterized by (reversible/irreversible) (micro/macro) vesicular fatty changes in the liver

A

Hepatic steatosis can be characterized by reversible, macrovesicular fatty changes in the liver

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32
Q

Explain how alcohol damages the liver over time, causing hepatic steatosis

A

Alcohol –> alcohol dehydrogenase –> acetaldehyde –> NADH production –> decreased free fatty oxidation –> lipid accumulation

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33
Q

Acetaldehyde (produced by alcohol dehydrogenase) generates NADH which (increases/decreases) free fatty oxidation

A

Acetaldehyde (produced by alcohol dehydrogenase) generates NADH which decreases free fatty oxidation –> lipid accumulation –> fatty liver

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34
Q

Alcoholic hepatitis can be diagnosed via _ findings

A

Alcoholic hepatitis can be diagnosed via:
* AST/ALT > 2
* Low albumin
* Leukocytosis
* High GGT
* High ALP

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35
Q

Alcoholic hepatitis has what effect on bilirubin?

A

Alcoholic hepatitis causes a mixed hyperbilirubinemia
* Increased unconjugated and conjugated bilirubin

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36
Q

Alcoholic hepatitis may present with _ on physical exam

A

Alcoholic hepatitis may present with:
* Painful hepatomegaly
* Jaundice
* Ascites
* Anorexia

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37
Q

Alcohol ingestion that leads to alcoholic hepatitis may cause the release of inflammatory markers like _

A

Alcohol ingestion that leads to alcoholic hepatitis may cause the release of inflammatory markers like cytokine IL-8 –> recruits neutrophils

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38
Q

Alcoholic hepatitis is associated with intracytoplasmic keratin deposits called _

A

Alcoholic hepatitis is associated with intracytoplasmic keratin deposits called Mallory bodies

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39
Q

Fibrosis and steatosis associated with alcoholic hepatitis begins in zone _

A

Fibrosis and steatosis associated with alcoholic hepatitis begins in zone 3 (centrilobular)

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40
Q

_ is the irreversible progression of alcoholic hepatitis

A

Alcoholic cirrhosis is the irreversible progression of alcoholic hepatitis

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41
Q

Alcoholic cirrhosis can be characterized by _ on histology

A

Alcoholic cirrhosis can be characterized by sclerosis around central veins and regenerative nodules surrounded by fibrosison histology

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42
Q

The consequence of fibrosis in alcoholic cirrhosis is the formation of _ and _

A

The consequence of fibrosis in alcoholic cirrhosis is the formation of portal hypertension and shunts
* Varices

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43
Q

Cirrhosis can also lead to (increase/decrease) in ammonia metabolism

A

Cirrhosis can also lead to decreased ammonia metabolism
* Ammonia build up –> encephalopathy

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44
Q

Alcoholic hepatitis is associated with _ anemia

A

Alcoholic hepatitis is associated with macrocytic anemia
* Deficiency of B1, B9, B12 associated with excessive alcohol use

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45
Q

Non-alcoholic hepatic steatosis is most commonly caused by _

A

Non-alcoholic hepatic steatosis is most commonly caused by obesity, metabolic syndromes
* Fat accumulates in the liver –> can progress to cirrhosis

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46
Q

Non-alcoholic hepatic steatosis is associated with an increased _ ratio

A

Non-alcoholic hepatic steatosis is associated with an increased ALT/AST
* Reverse of alcoholic hepatitis

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47
Q

Non-alcoholic hepatic steatosis can be characterized by _ on histology

A

Non-alcoholic hepatic steatosis can be characterized by fatty infiltration of hepatocytes –> cellular ballooning –> necrosis

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48
Q

Non-alcoholic hepatic steatosis is associated with:

A

Non-alcoholic hepatic steatosis is associated with:
* Native americans
* Obesity
* Diabetes

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49
Q

We can manage non-alcoholic hepatic steatosis with drugs like _ or _

A

We can manage non-alcoholic hepatic steatosis with drugs like metformin or TZDs

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50
Q
A

Alcoholic cirrhosis
* Blue fibrosis
* Nodular liver

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51
Q
A

Alcoholic hepatitis
* Mallory bodies

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52
Q

Etiology for cirrhosis includes:

A

Etiology for cirrhosis includes:
* Alcohol use disorder
* Non-alcohol steatohepatitis
* Viral hepatitis
* Autoimmune
* Genetic disorders
* Medications

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53
Q

Cirrhosis results from chronic inflammation that activate _ cells

A

Cirrhosis results from chronic inflammation that activate stellate (Ito) cells in the hepatic sinusoids

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54
Q

The central mediator of fibrogenesis in liver cirrhosis is _

A

The central mediator of fibrogenesis in liver cirrhosis is TGF-beta –> fibrosis, nodular scarring

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55
Q

How does cirrhosis lead to portal hypertension?

A

Fibrosis disrupts normal hepatic architecture –> vasculature is disrupted –> portal hypertension –> varices

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56
Q

Cirrhosis can cause _ which manifests as ascites and edema

A

Cirrhosis can cause hypoalbuminemia which manifests as ascites and edema

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57
Q

How does cirrhosis cause splenomegaly?

A

Cirrhosis –> portal hypertension –> splenomegaly –> splenic sequestration of plateletes –> thrombocytopenia –> increased bleeding time

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58
Q

Cirrhosis is associated with decreased clotting factors and decreased TPO production which manifests as _

A

Cirrhosis is associated with decreased clotting factors and decreased TPO production which manifests as coagulopathies, increased PT, increased INR

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59
Q

Clotting factor _ is a good measure of liver function since it has a short half life

A

Factor VII is a good measure of liver function since it has a short half life

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60
Q

Cirrhosis may present with hypokalemia due to _

A

Cirrhosis may present with hypokalemia due to impaired aldosterone metabolism

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61
Q

Cirrhosis may present with hyponatremia (despite high aldosterone) due to _

A

Cirrhosis may present with hyponatremia (despite high aldosterone) due to decreased intravascular volume –> triggering ADH secretion

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62
Q

Cirrhosis can impair normal biochemical processes that occur in the liver such as _

A

Cirrhosis can impair normal biochemical processes that occur in the liver such as gluconeogenesis, glycogenolysis –> hypoglycemia

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63
Q

Spider angiomas and palmar erythema are dermatologic manifestations of _ that is caused by cirrhosis

A

Spider angiomas and palmar erythema are dermatologic manifestations of decreased estrogen metabolism that is caused by cirrhosis

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64
Q

Gynecomastia can be caused by cirrhosis; how?

A

Low androstenedione, low estrogen metabolism –> high serum estrogen –> increases sex hormone binding globulin –> decrease in free testosterone –> gynecomastia, ED, amenorrhea

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65
Q

Stellate cells largely respond to the release of _ during chronic inflammation

A

Stellate cells largely respond to the release of TGF-beta during chronic inflammation

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66
Q

Cirrhosis may present with general symptoms like:

A

Cirrhosis may present with general symptoms like:
* Fatigue
* Nausea
* Vomiting
* Abdominal pain
* Anorexia
* Jaundice

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67
Q

Signs of portal hypertension and hypoalbuminemia in cirrhosis include:

A

Signs of portal hypertension and hypoalbuminemia in cirrhosis include:
* Ascites
* Edema
* Varices

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68
Q

Which type of varices are most prone to rupture? (esophageal/ umbilical/ gastric/ anorectal)

A

Which type of varices are most prone to rupture? Esophageal

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69
Q

_ is a halitosis unique to cirrhosis

A

Fetor hepaticus is a halitosis unique to cirrhosis

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70
Q

An individual with cirrhosis may have stinky breath that smells like _

A

An individual with cirrhosis may have stinky breath that smells like sulfur
* Due to the build up of sulfur containing compounds

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71
Q

Cirrhosis and ascites can progress to ?

A

Cirrhosis and ascites can progress to fever, abdominal pain, ileus, encephalopathy

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72
Q

_ occurs when the free fluid associated with cirrhosis (ascites) becomes infected

A

Spontaneous bacterial peritonitis occurs when the free fluid associated with cirrhosis (ascites) becomes infected

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73
Q

The most common bacteria responsible for spontaneous bacterial peritonitis are _ , _ , _

A

The most common bacteria responsible for spontaneous bacterial peritonitis are E.coli , Klebsiella , Streptococcus

74
Q

Spontaneous bacterial peritonitis is diagnosed via paracentesis of ascitic fluid which reveals an absolute neutrophil count > _

A

Spontaneous bacterial peritonitis is diagnosed via paracentesis of ascitic fluid which reveals an absolute neutrophil count > 250

75
Q

We treat spontaneous bacterial peritonitis with _

A

We treat spontaneous bacterial peritonitis with third gen cephalosporin (ceftriaxone, cefotaxime)

76
Q

Hepatic encephalopathy is caused by _

A

Hepatic encephalopathy is caused by increased ammonia build up; decreased ammonia metabolism
* Result of portal hypertension, portosystemic shunts

77
Q

A patient with asterixis (flapping tremor), confusion, disorientation, drowsiness and history of cirrhosis should be concerning for _

A

A patient with asterixis (flapping tremor), confusion, disorientation, drowsiness and history of cirrhosis should be concerning for hepatic encephalopathy

78
Q

Hepatic encephalopathy can be treated with a drug that increases NH4+ generation like _

A

Hepatic encephalopathy can be treated with a drug that increases NH4+ generation like lactulose

79
Q

_ and _ are two drugs that may be indicated in encephalopathy to decrease the NH3 produced by gut bacteria

A

Rifaximin and neomycin are two drugs that may be indicated in encephalopathy to decrease the NH3 produced by gut bacteria

80
Q

A patient with alcohol use disorder and confusion, ophthalmoplegia (paralysis of extraocular muscles), ataxia may have _

A

A patient with alcohol use disorder and confusion, ophthalmoplegia (paralysis of extraocular muscles), ataxia may have Wernicke’s encephalopathy (thiamine deficiency)

81
Q

Wernicke’s encephalopathy may progress to Wernicke-Korsakoff syndrome which presents with _

A

Wernicke’s encephalopathy may progress to Wernicke-Korsakoff syndrome which presents with confabulation, memory loss, personality change

82
Q

Explain the pathogenesis of hepatorenal syndrome

A

Liver failure –> increase in NO –> splanchnic vasodilation –> decrease in systemic BP –> renal hypoperfusion –> increased RAAS –> High RAAS with impaired aldosterone metabolism –> Hepatorenal syndrome
* Can see progressive loss of RBF, renal failure

83
Q
A
84
Q

(3) Mechanisms in which EtOH damages the liver

A

(3) Mechanisms in which EtOH damages the liver
1. Hepatic fat; normally NAD helps to oxidize fat but it is also used to oxidize alcohol; all of the NAD gets consumed trying to metabolize the alcohol
2. Direct hepatotoxicity: acetaldehyde
3. Hepatic inflammation: IL-7, IL-8, TNFa

85
Q

Normally the liver will metabolize fat and cholesterol and transport them out of the liver into the circulation as _

A

Normally the liver will metabolize fat and cholesterol and transport them out of the liver into the circulation as VLDL
* So a healthy liver only has a small amoutn of fat within the liver

86
Q

Abnormal or excessive fat accumulation in the liver is called _

A

Abnormal or excessive fat accumulation in the liver is called steatosis

87
Q

Gross pathology and PE of a steatotic liver may reveal _

A

Gross pathology and PE of a steatotic liver may reveal hepatomegaly
* However, it is clinically asymptomatic

88
Q

The two major causes of steatosis are _ and _

A

The two major causes of steatosis are alcohol associated liver disease and metabolic dysfunction- associated steatotic liver disease (MASLD)

89
Q

Which processes are reversible? Steatosis –> steatohepatitis –> fibrosis

A

Steatosis: reversible
Steatohepatitis: maybe reversible
Fibrosis: irreversible

90
Q
A

Alcohol related steatohepatitis showing mallory bodies and neutrophilic inflammation

91
Q

The most important management for alcohol-related hepatitis is _

A

The most important management for alcohol-related hepatitis is alcohol cessation

92
Q

When liver disease progresses to cirrhosis we see (enlargement/shrinking) of the liver

A

When liver disease progresses to cirrhosis we see shrinking of the liver from the fibrosis
* Remaining healthy hepatocytes try to proliferate via “regenerative nodules”

93
Q
A
94
Q
A

Cirrhosis: shows bridging fibrosis + regenerative nodule formation

95
Q

Although alcoholic cirrhosis will have mixed bilirubinemia, more of it will be (conjugated/unconjugated)

A

Although alcoholic cirrhosis will have mixed bilirubinemia, more of it will be unconjugated

96
Q

Name some of the physical exam findings associated with cirrhosis

A
97
Q

Portal hypertension can lead to _

A

Portal hypertension can lead to…
* Esophageal varices
* Rectal varices
* Caput medusae
* Splenomegaly

98
Q

Variceal bleeding can be life-threatening (50% mortality); we treat esophageal varices with _

A

Variceal bleeding can be life-threatening (50% mortality); we treat esophageal varices with urgent EGD with banding

99
Q

Hepatic encephalopathy is caused by an increase in ammonia and _

A

Hepatic encephalopathy is caused by an increase in ammonia and glutamine
* Ammonia crosses BBB and causes glutamate –> glutamine

100
Q

We screen patients with cirrhosis for _ cancer

A

We screen patients with cirrhosis for hepatocellular cancer (HCC)

101
Q

Viral hepatitis involves _ mediated hepatocyte apoptosis

A

Viral hepatitis involves CD8+ T-cell mediated hepatocyte apoptosis
* Leads to inflammation of the lobules and portal tracts

102
Q

The first zone affected by viral hepatitis is the _ zone

A

The first zone affected by viral hepatitis is the periportal, zone 1

103
Q

Viral hepatitis causes elevation in liver enzymes: _ > _

A

Viral hepatitis causes elevation in liver enzymes: ALT > AST

104
Q

The prodrome of viral hepatitis manifests as:

A

The prodrome of viral hepatitis manifests as:
* Fever
* Anorexia
* Nausea
* Vomiting

105
Q

Later manifestations of viral hepatitis include:

A

Later manifestations of viral hepatitis include:
* Jaundice
* Pruritis
* Pale stool
* Dark urine

106
Q

Viral hepatitis is associated with an increase in _ bilirubin

A

Viral hepatitis is associated with an increase in conjugated and unconjugated bilirubin

107
Q

Causes of viral hepatitis:

A

Causes of viral hepatitis:
* Hepatitis A-E
* EBV, CMV, yellow fever

108
Q

Hepatitis A is a (ss/ds) (DNA/RNA) virus in the _ family

A

Hepatitis A is a ss RNA picornavirus

109
Q

Hepatitis B is a (ss/ds) (DNA/RNA) virus in the _ family

A

Hepatitis B is a ds DNA hepadnavirus

110
Q

Hepatitis C is a (ss/ds) (DNA/RNA) virus in the _ family

A

Hepatitis C is a ss RNA flavivirus

111
Q

Hepatitis D is a (ss/ds) (DNA/RNA) virus in the _ family

A

Hepatitis D is a ss RNA deltavirus

112
Q

Hepatitis E is a (ss/ds) (DNA/RNA) virus in the _ family

A

Hepatitis E is a ss RNA hepevirus

113
Q

All hepatitis viruses (A-E) are ss-RNA viruses except for _

A

All hepatitis viruses (A-E) are ss-RNA viruses except for Hepatitis B
* Hep B is a ds DNA hepadnavirus

114
Q

Hepatitis _ and _ viruses have no envelope so therefore can be consumed

A

Hepatitis A and E viruses have no envelope so therefore can be consumed

115
Q

Hepatitis A is transmitted via fecal-oral exposure from _

A

Hepatitis A is transmitted via fecal-oral exposure from contaminated shellfish
* Causes a self-limited infection with a short incubation period

116
Q

Hepatitis A is characterized by _ on histology

A

Hepatitis A is characterized by councilman bodies on histology
* Eosinophilic globule of apoptotic hepatocytes

117
Q

Hepatitis B is transmitted via _

A

Hepatitis B is transmitted via blood, unprotected sex, during birth

118
Q

Hepatitis _ and _ commonly lead to chronic hepatitis and increase the risk for hepatocellular carcinoma

A

Hepatitis B and C commonly lead to chronic hepatitis and increase the risk for hepatocellular carcinoma

119
Q

Hepatitis B can cause HCC via cirrhosis or via a direct pathway; explain

A

Hep-B DNA integrates into hepatocytes –> suppression of p53 –> HCC

120
Q

Hepatitis B has a _ appearance on liver biopsy

A

Hepatitis B has a “ground glass” eosinophilic appearance on liver biopsy

121
Q

Hep B can be treated with _ , _ , _

A

Hep B can be treated with Interferon alpha , lamivudine , tenofovir

122
Q

Hepatitis C is transmitted via _

A

Hepatitis C is transmitted via blood- transfusions, IV drug use

123
Q

Hepatitis C is characterized by _ and _ on liver biopsy

A

Hepatitis C is characterized by macrovesicular steatosis and lymphoid aggregates on liver biopsy

124
Q

Treatments for Hep C include:

A

Treatments for Hep C include:
* Ribavirin
* Simeprevir
* Sofosbuvir
* Interferon alpha

125
Q

Hepatitis D requires the presence of _ to replicate

A

Hepatitis D requires the presence of hepatitis B to replicate

126
Q

A co-infection in the context of Hepatitis D is when _

A

A co-infection in the context of Hepatitis D is when the patient simultaneously acquires hep B and D

126
Q

Hepatitis E is commonly transmitted via _

A

Hepatitis E is commonly transmitted via contaminated water

126
Q

A super-infection in the context of hepatitis D is when _

A

A super-infection in the context of hepatitis D is when patient with chronic hep B acquires hepatitis D –> rapid progression of cirrhosis
* This is worse than a co-infection

127
Q

_ hepatitis can cause acute icteric hepatitis but is rarely chronic

A

Hepatitis E can cause acute icteric hepatitis but is rarely chronic

128
Q

_ is a parasitic liver disease that is caused by the ingestion of eggs in dog stool that causes RUQ pain, N/V, hepatomegaly; can cause anaphylaxis, fever, eosiniphilia if the cysts rupture

A

Echinococcus granulosus is a parasitic liver disease that is caused by the ingestion of eggs in dog stool that causes RUQ pain, N/V, hepatomegaly; can cause anaphylaxis, fever, eosiniphilia if the cysts rupture

129
Q

Entamoeba histolytica is a parasitic liver disease that is transmitted via _

A

Entamoeba histolytica is a parasitic liver disease that is transmitted via cysts in contaminated water
* Trophs invade gut wall and migrate to the liver

130
Q

Parasite that causes hydatid liver cysts with eggshell calcifications and internal septations:

A

Parasite that causes hydatid liver cysts with eggshell calcifications and internal septations: echinococcus granulosus

131
Q

Bloody diarrhea, flask shaped ulcers in colon, hepatic abscesses with anchovy past exudate

A

Bloody diarrhea, flask shaped ulcers in colon, hepatic abscesses with anchovy past exudate: entamoeba histolytica

132
Q

The liver fluke _ is called the chinese liver fluke; it is transmitted via _

A

The liver fluke Clonorchis sinensis is called the chinese liver fluke; it is transmitted via ingestion of undercooked fish
* Causes cholangitis, biliary fivrosis, pigmented gallstones, risk of cholangiocarcinoma

133
Q

The most common primary liver cancer is _

A

The most common primary liver cancer is hepatocellular carcinoma
* Spreads hematogenously

134
Q

The risk for hepatocellular carcinoma increases from _ or _

A

The risk for hepatocellular carcinoma increases from cirrhosis or genetic disorders (hemochromatosis, wilsons, A1AT)

135
Q

Hepatocellular carcinoma presentation:

A

Hepatocellular carcinoma presentation:
* Jaundice
* Hepatomegaly
* Ascites
* Anorexia
* Polycythemia
* Hypercholesterolemia
* Hypercalcemia
* Hypoglycemia

136
Q

HCC can cause thrombosis or compression of the hepatic veins which leads to centrilobular congestion and necrosis called _ syndrome

A

HCC can cause thrombosis or compression of the hepatic veins which leads to centrilobular congestion and necrosis called Budd Chiari syndrome

137
Q

Budd-Chiari syndrome will show _ liver on pathology

A

Budd-Chiari syndrome will show nutmeg liver on pathology
* Mottled appearance of the liver as a result of hepatic venous congestion

138
Q

HCC is associated with an increase in _ liver protein

A

HCC is associated with an increase in alpha fetoprotein

139
Q

MRI with contrast shows _ with HCC

A

MRI will show central vein congestion (contrast can’t move through)

140
Q

Wilson’s disease is a _ disorder that can lead to liver damage/cirrhosis

A

Wilson’s disease is a copper transport disorder that can lead to liver damage/cirrhosis

141
Q

Wilson’s disease is a (AD/AR) mutation in _

A

Wilson’s disease is an autosomal recessive mutation in ATP7B

142
Q

In Wilson’s disease, there is a mutation in ATP7B, a gene that codes for the _

A

In Wilson’s disease, there is a mutation in ATP7B, a gene that codes for the copper transport ATPase

143
Q

Wilson’s disease involves a decrease in copper transport into the _ and _

A

Wilson’s disease involves a decrease in copper transport into the bile and apocerulopasmin

144
Q

Wilson’s disease causes (high/low) serum ceruloplasmin and (high/low) urinary copper

A

Wilson’s disease causes low ceruloplasmin and high urinary copper

145
Q

Wilson’s disease can cause copper accumulation in the _ , _ , _

A

Wilson’s disease can cause copper accumulation in the basal ganglia , cornea , kidney
* Copper can cause free radical damage to the tissues
* Dystonia, tremor, dementia, hemolytic anemia, renal damage

146
Q

The corneal deposition of copper results in _ finding on slit lamp examination

A

The corneal deposition of copper results in Kayser-Fleischer rings finding on slit lamp examination

147
Q

We can treat wilson’s disease with _ and _

A

We can treat wilson’s disease with penicillamine, zinc and trientine
* Liver failure can require transplant

148
Q

Hemochromatosis is an (AD/AR) mutation in the _ gene

A

Hemochromatosis is an autosomal recessive mutation in the HFE gene (chromosome 6)

149
Q

Hemochromatosis is most commonly caused by a single point mutation in _

A

Hemochromatosis is most commonly caused by a single point mutation in C282Y

150
Q

Hemochromatosis is associated with HLA _

A

Hemochromatosis is associated with HLA-A3

151
Q

Hemochromatosis is caused by abnormal iron sensing from a defective _ receptor or _ gene

A

Hemochromatosis is caused by abnormal iron sensing from a defective transferrin receptor or hepcidin gene
* Leads to increased intestinal iron absorption

152
Q

Secondary hemochromatosis can be acquired from _

A

Secondary hemochromatosis can be acquired from repeat blood transfusions

153
Q

What happens to the following in hemochromatosis:
Ferritin
Iron
TIBC
Transferrin saturation

A

What happens to the following in hemochromatosis:
High Ferritin
High Iron
Low TIBC
High Transferrin saturation

154
Q

Iron deposits in _ tissues in hemochromatosis, causing free radical damage

A

Iron deposits in liver, skin, heart, pancreas, joints in hemochromatosis, causing free radical damage

155
Q

The “classic triad” of hemochromatosis is:

A

The “classic triad” of hemochromatosis is:
1. Diabetes
2. Cirrhosis
3. Bronze skin

156
Q

Hemochromatosis often presents after age _ in men and _ in women

A

Hemochromatosis often presents after age 40 in men and 50-60 in women

157
Q

Other manifestations of hemochromatosis include:

A

Other manifestations of hemochromatosis include:
* Cardiomyopathy
* Arthropathy
* Gonadal dysfunction
* Malabsorption and steatorrhea (pancreatic deposition)
* Increased risk for HCC

158
Q
A

Steatosis: deposition of fat within the hepatocyte cytoplasm

159
Q
A

Steatohepatitis: steatosis + inflammation and hepatocellular injury

160
Q

Fibrosis and cirrhosis

A
161
Q

The most common cause of hemochromatosis is a _ point mutation in the HFE gene which causes defective _

A

The most common cause of hemochromatosis is a C282Y point mutation in the HFE gene which causes defective hepcidin

162
Q

Treatment for hemochromatosis includes _

A

Treatment for hemochromatosis includes therapeutic phlebotomy to lower iron stores
* Can use chelating agents

163
Q
A

Hemochromatosis: periportal hepatocytes with yellow-brown pigment

164
Q
A

Hemochromatosis

165
Q

ATP7B gene encodes _

A

ATP7B gene encodes transporter in hepatocytes that allows copper excretion in bile and copper incorporation into ceruloplasmin

166
Q

Wilson’s disease most commonly presents around _ age

A

Wilson’s disease most commonly presents around age 20s-30s
* Or may present in childhood with liver/neuro sx
* Or not until adulthood as hepatitis, cirrhosis, liver failure

167
Q

A heme extra-hepatic manifestation of wilson’s disease is _

A

A heme extra-hepatic manifestation of wilson’s disease is hemolytic anemia
* Copper is damaging to RBC membranes

168
Q

Wilson’s disease can present with neurological sx such as:

A

Wilson’s disease can present with neurological sx such as:
* Dystonia
* Parkinson like syndrome
* Memory changes
* Behavior changes
* Dementia

169
Q

Wilson’s disease can cause _ syndrome (excess excretion of glucose, bicarb, potassium in the urine)

A

Wilson’s disease can cause fanconi syndrome (excess excretion of glucose, bicarb, potassium in the urine)
* Malabsorption in the proximal tubule

170
Q

A medication that can be used in Wilson’s disease to prevent copper absorption is _

A

A medication that can be used in Wilson’s disease to prevent copper absorption is zinc

171
Q
A
172
Q

What are three contributing factors to neonatal jaundice?

A
  1. Transiently low UDPGT activity
  2. Fetal RBCs have shorter lifespan, high turnover
  3. Newborn gut is sterile so less conversion to urobilinogen
173
Q
A
174
Q
A
175
Q
A
176
Q

SAAG stands for _

A

SAAG stands for serum to ascites albumin gradient

177
Q

We have suspicion for portal hypertension/ cirrhosis when the SAAG is _

A

We have suspicion for portal hypertension/ cirrhosis when the SAAG > 1.1

178
Q

We expect greater albumin in the _ than the _ in the case of portal hypertension

A

We expect greater albumin in the serum than the ascites in the case of portal hypertension
* Hence the high SAAG (serum to albumin ratio)

179
Q

A high SAAG tells us that the fluid in the ascites is _

A

A high SAAG tells us that the fluid in the ascites is low in albumin and essentially just hepatic lymph from hepatic sinusoids

180
Q

Ascites is likely from an extra-hepatic cause if SAAG is _

A

Ascites is likely from an extra-hepatic cause if SAAG is < 1.1

GI (13 decks)

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