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MHD2 > Block 7 (GI) - L7 to L8 > Flashcards

Block 7 (GI) - L7 to L8 Flashcards

1
Q

Oxygenated blood is supplied to the liver via the ___.

A

Hepatic artery only

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2
Q

Describe the hepatic circulation.

A

The heart pumps oxygenated blood through the hepatic artery to the liver. In addition, the splenic vein and superior mesenteric vein combine to form the hepatic portal vein, which goes to the liver. Blood is drained to the hepatic veins and to IVC.

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3
Q

What is a lobule?

A

Hexagonal building block of the liver parenchyma with a portal tract at each apex

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4
Q

What makes up the portal tract?

A

Hepatic artery, portal vein, bile duct

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5
Q

Blood flows ___ the central vein; bile flows ___ the central vein.

A

Toward; away from

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6
Q

___ are arranged in linear cords from the periphery to the central vein.

A

Hepatocytes

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7
Q

What are periportal hepatocytes?

A

First to receive blood and to regenerate, last to undergo necrosis

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8
Q

What are centrilobular hepatocytes?

A

Most susceptible to ischemic insults

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9
Q

What are sinusoids?

A

Capillary network through the liver that converts nutrient rich portal venous and highly-oxygenated arterial blood past the hepatocytes

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10
Q

What are Kupffer cells?

A

Macrophage cells of the liver

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11
Q

Describe the endothelium of the liver.

A

Fenestrated to allow passage of nutrients and lipids from portal blood to the hepatocyte

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12
Q

What is the Space of Disse and what does it contained?

A

Loosely arranged ECM containing stellate cells, NK cells, and T/B cells.

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13
Q

How is the surface area increased in hepatocytes?

A

Microvilli

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14
Q

What are 2 of the metabolic functions of hepatocytes?

A

Glucose and lipid metabolism

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15
Q

What are 2 proteins synthesized in the liver?

A

Albumin and coagulation factors (except 8)

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16
Q

What 5 things are stored in the liver?

A

Glycogen, triglycerides, iron, copper, lipid soluble vitamins

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17
Q

What are 3 of the catabolic functions of the hepatocytes?

A
  1. Converting ammonia to urea
  2. Catabolizing certain proteins and hormones
  3. Detoxifying drugs and chemicals
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18
Q

What is one excretory function of the liver?

A

Bile excretion

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19
Q

What is hepatic encephalopathy and what does it require?

A

Reversible neuropsychiatric abnormalities seen in patients with liver failure; requires the presence of portal HTN

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20
Q

How does hepatic encephalopathy develop?

A

Normally, the liver clears portal vein ammonia, converting it to glutamine and urea, but it remains in the blood, where it becomes neurotoxic at elevated concentrations

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21
Q

How are liver injury tests classified by type?

A
  1. Hepatocellular (ALT/AST elevation)

2. Cholestatic (Alk Phos/T.bili elevation)

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22
Q

How are liver injury tests classified by duration?

A
  1. Acute: abrupt onset, <6 months but usually <1 month

2. Chronic >6 months

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23
Q

How are liver injury tests classified by magnitude?

A
  1. Mild (AST/ALT elevations <200)
  2. Moderate (200-600)
  3. Severe (>600)
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24
Q

Which serum transaminase is more specific for hepatocyte damage?

A

ALT (alanine aminotransferase)

AST (aspartate) can be found in parts of the body

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25
Q

What are causes of markedly elevated aminotransferase levels (>1,000 U/L)?

A
  1. Drug/toxin-induced injury (tylenol, NOT alcohol alone)
  2. Acute viral hepatitis
  3. Shock liver
  4. Autoimmune hepatitis
  5. Common bile duct stone
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26
Q

What is cholestasis?

A

Any condition in which substances normally excreted into the bile are retained

Decrease in bile flow due to impaired secretion/formation by hepatocytes OR to obstruction of bile flow through intra- or extra-hepatic ducts

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27
Q

How does cholestasis appear histologically?

A

Bile within the hepatocytes and canalictular spaces; often with associated cell injury

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28
Q

What are 4 markers of cholestasis?

A
  1. Alkaline phosphatase
  2. Gamma glutamyl transferase (GGT)
  3. 5’-nucleotidase
  4. Bilirubin
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29
Q

Where is alkaline phosphatase located in the liver?

A

Microvilli of the bile canaliculus

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30
Q

What happens to alkaline phosphatase in cholestasis?

A

Increases (sensitive indicator of obstructive and space-occupying lesions of the liver)

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31
Q

What induces gamma glutamyl transferase (GGT)?

A

Alcohol and medication

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32
Q

What causes bilirubin to increase?

A

With extensive biliary obstruction or diffuse hepatic cell disruption as a result of cholestasis

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33
Q

What are liver function tests and what do they reflect?

A

Albumin, PT/INR, serum bilirbuin

The liver’s synthetic or excretory capactiy

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34
Q

What is the most abundant blood protein?

A

Albumin

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35
Q

What happens to albumin in acute and chronic liver disease?

A
  1. Preserved in acute liver disease

2. Low due to cirrhosis in the setting of chronic liver disease

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36
Q

What does PT/INR indicate regarding the liver?

A

Clotting factors that are synthesized by the liver in a vitamin-K dependent fashion; helpful in the diagnosis of hepatic dysfunction

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37
Q

What does serum bilirubin reflect?

A

The ability of the hepatocyte to secrete bilirubin into the bile canaliculus; can be elevated in hepatocellular injury or cholestatic injury

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38
Q

In both hepatocellular and cholestatic injury, the ___ fraction predominates.

A

Direct (conjugated)

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39
Q

What are the three broad forms of hepatic dysfunction?

A
  1. Acute hepatitis
  2. Acute liver failure (fulminant liver failure)
  3. Chronic hepatitis
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40
Q

What is acute liver injury?

A

Hepatic dysfunction without encephalopathy

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41
Q

What are 5 pathologic findings seen in acute hepatitis?

A
  1. Ballooning degeneration
  2. Apoptosis
  3. Necrosis
  4. Inflammation
  5. Cholestasis
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42
Q

What is ballooning degeneration and what is it associated with?

A

Swollen liver cells with lots of debris int he cytoplasm

NASH, alcohol, acute hepatitis

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43
Q

What is acute liver failure?

A

Sudden loss of hepatic function in a person without evidence of preexisting liver disease

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44
Q

What is the clinical definition of acute liver failure?

A

Coagulopathy (INR >1.5) and any degree of hepatic encephalopathy both occurring within 24 weeks of the first onset of symptoms in patients without underlying liver disease

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45
Q

What are exceptions to the definition of acute liver failure?

A

Wilson’s disease, vertically-acquired HBV, and autoimmune hepatitis

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46
Q

What are causes of acute liver failure?

A
  1. Hepatitis A or B
  2. Drugs and chemical toxicity
  3. Autoimmune hepatitis
  4. Wilson’s disease
  5. Budd-Chiari
  6. Rare (ischemia, malignancy)
  7. Unknown (15%)
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47
Q

What is seen on histology in acute liver failure?

A

Massive hepatic necrosis

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48
Q

What are causes of chronic hepatitis?

A
  1. Hepatitis B, C, or D
  2. Autoimmune hepatitis
  3. Drugs
  4. Wilson’s disease
  5. Alpha-1 antitrypsin deficiency
  6. Hemochromatosis
  7. NASH
  8. Alcohol
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49
Q

What is seen on histology in chronic hepatitis?

A

Lack of balloon cells and fibrosis

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50
Q

What role do stellate cells play in chronic hepatitis?

A

Deposit collagen, leading to fibrosis

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51
Q

How is chronic hepatitis characterized?

A
  1. Grade (how bad the inflammation is)

2. Stage (how much fibrosis there is)

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52
Q

What are the 4 stages of fibrosis in chronic hepatitis?

A
  1. Portal
  2. Periportal
  3. Bridging
  4. Cirrhosis
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53
Q

What is cirrhosis?

A

A diffuse process characterized by fibrosis and a conversion of normal architecture into structurally abnormal nodules

54
Q

What is the most common route to hepatic failure?

A

Cirrhosis

55
Q

What are causes of cirrhosis?

A
  1. Alcoholic liver disease
  2. Viral hepatitis
  3. NASH
  4. Biliary disease
  5. Primary hemochromatosis
  6. Wilson’s disease
  7. Alpha-1 antitrypsin deficiency
  8. Cryptogenic
  9. Metabolic disorders
  10. Drug reactions
56
Q

What are the clinical symptoms of cirrhosis?

A

Typically asymptomatic

Anorexia, loss of muscle mass, weakness, fatigue

57
Q

What are the advanced symptoms associated with cirrhosis?

A
  1. Lower extremity edema
  2. Abdominal distension (ascites)
  3. GI bleeding
  4. Hepatic encephalopathy
  5. Muscle wasting and loss of muscle mass
  6. Muscle cramping
  7. Gynecomastia
58
Q

What is portal hypertension?

A

Increase in the blood pressure within a system of veins called the portal venous system; blood cannot flow through the liver and high pressure develops

59
Q

How does cirrhosis lead to portal hypertension?

A
  1. Increased vascular resistance due to distorted vascular architecture and increased vascular tone (myofibroblasts contract around hepatic sinusoids, increased production of vasodilators, reduced release of vasodilators)
  2. Increased portal inflow due to splanchnic vasodilation (increased NO production) and angiogenesis
60
Q

Portal hypertension leads to the development of ___.

A

Intra- and extra-hepatic venous collaterals, including esophageal varices

61
Q

What are complications of cirrhosis?

A

Related to portal HTN and hepatic dysfunction: ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome

Unrelated to portal HTN: hepatocellular carcinoma

62
Q

What is the most reliable indicator of liver function?

A

PT/INR

63
Q

In addition to acute and chronic hepatotropic viruses (A-E), what are other causes of viral hepatitis?

A

Infectious mononucleosis (EBV), CMV, and adenovirus and herpes virus in immunosuppressed patients

64
Q

How is Hepatitis A transmitted?

A

Fecal-oral/poor hygiene

65
Q

Discuss the clinical presentation of Hepatitis A.

A

Incubation period: 3-6 weeks
Symptoms: mild or asymptomatic (severity increases with age/underlying chronic liver disease)

NO chronic state

66
Q

True or false - 50% of people over 50 show previous exposure to Hepatitis A.

A

True

67
Q

How is Hepatitis B transmitted?

A

Perinatal (SE Asia, Sub-Saharan Africa)

Sexual (primary mode in US)

68
Q

What type of virus is Hepatitis B (DNA vs. RNA)?

A

DNA

69
Q

Discuss the clinical presentation of Hepatitis B.

A

Incubation period: 4-26 weeks

Symptoms: acute or chronic hepatitis

70
Q

Hepatitis B involves an increased risk of ___.

A

Hepatocellular cancer

71
Q

Describe the levels of various antibodies in acute infection with Hepatitis B.

A
  1. HBsAg - increases, peaks, and decreases from 4-24 weeks
  2. Anti-HB - increases beginning around week 24
  3. IgM Anti-HBc - increases around week 6 and stays high
72
Q

Discuss progression of HBV to chronic infection and list the 4 stages.

A
  1. Immune tolerant
  2. Immune clearance
  3. Inactive carrier phase
  4. Reactivation

ALT increases and HBV DNA decreases (both cycle) during the immune clearance phase

73
Q

Discuss the presence/absence of HBsAG, anti-HBc, and anti-HBs when a person is susceptible.

A

All negative

74
Q

Discuss the presence/absence of HBsAG, anti-HBc, and anti-HBs when a person is immune due to natural infection.

A

HBsAg: negative
anti-HBc: positive
anti-HBs: positive

75
Q

Discuss the presence/absence of HBsAG, anti-HBc, and anti-HBs when a person is immune due to hepatitis B vaccination.

A

HBsAg: negative
anti-HBc: negative
anti-HBs: positive

76
Q

Discuss the presence/absence of HBsAG, anti-HBc, and anti-HBs when a person is acutely infected.

A

HBsAg: positive
anti-HBc: positive
IgM anti-Hbc: positive
anti-HBs: negative

77
Q

Discuss the presence/absence of HBsAG, anti-HBc, and anti-HBs when a person is chronically infected.

A

HBsAg: positive
anti-HBc: positive
IgM anti-Hbc: negative
anti-HBs: negative

78
Q

What is a classic histologic finding of HBV?

A

Ground glass hepatocytes (fuzzy/hazy)

79
Q

What type of virus is Hepatitis C (DNA vs. RNA)?

A

Single-stranded RNA virus

80
Q

Discuss the clinical presentation of Hepatitis C.

A

Incubation period: 2-26 weeks

Symptom: most people have chronic infection

81
Q

Hepatitis C involves an increased risk of ___.

A

Hepatocellular cancer

82
Q

How is Hepatitis C transmitted?

A

Injection drug use (most commonly)

83
Q

What histologic finding is seen in viral Hepatitis C?

A

Portal inflammation

84
Q

What is necessary for Hepatitis D to survive?

A

HBsAg of HBV, which is needed to encapsulate it (either co-infection or super-infection)

85
Q

Discuss the clinical presentation of Hepatitis D.

A

Incubation period: 4-24 weeks

86
Q

Hepatitis C involves an increased risk of ___.

A

Hepatocellular cancer

87
Q

Discuss the difference between a co-infection and super-infection of HBV and HDV.

A

In co-infection, 90% recover with immunity, 3-4% get fulminant hepatitis, rarely progresses to chronic hepatitis. Blood contains IgM anti HDAg, HBSAg, and anti-HBcIgM

In super-infection, 80% progress to chronic hpeatitis, 10-15% have acute/severe disease, and 7-10% have fulminant hepatitis. In addition, there is no IgM antiHBcAg

88
Q

How is Hepatitis E transmitted?

A

Fecal-oral/contaminated water, animal reservoirs (zoonotic disease)

89
Q

Discuss the clinical presentation of Hepatitis E.

A

Incubation period: 6 weeks

No carrier state

90
Q

Who is more likely to develop Hepatitis E?

A

Pregnant women and elderly

91
Q

Which viruses are most likely to cause acute asymptomatic infection with recovery?

A

A and B

92
Q

Which viruses are most likely to cause acute symptomatic infection with recovery?

A

A, B, C (rare), D, E

93
Q

Which viruses are most likely to cause chronic hepatitis?

A

B and C

94
Q

Which viruses are most likely to cause fulminant hepatitis?

A

A (rare), B, E (rare)

95
Q

What drug tends to cause cholestasis?

A

Anabolic steroids

96
Q

What drugs tend to cause microvesicular steatosis?

A

Valproic acid, tetracycline, aspirin, NSAID’s

97
Q

What drugs tend to cause centrilobular necrosis?

A

Acetaminophen, isoniazid, ketoconazole, hydralazine

98
Q

What drugs tend to cause granulomas?

A

Allopurinol, sulfonamide, carbamazepine, diltiazem

99
Q

What is the leading cause of acute liver failure in the US and Europe?

A

Acetaminophen-related liver injury

100
Q

How does acetaminophen-related liver injury present?

A

History, very high aminotransferase levels (>3500 IU/mL), low t.bilirubin

101
Q

Why does acetaminophen become toxic at high doses?

A

Enzyme converting it to non-toxic moieties is used up, and it is converted to NAPQI

102
Q

How is acetaminophen overdose treated?

A

NAC

103
Q

Autoimmune hepatitis affects ___ more than ___ (gender).

A

Females > males

104
Q

What are some aspects of autoimmune hepatitis?

A
  1. Can present as acute or chronic hepatitis
  2. Elevated LFTs
  3. Positive auto-antibodies like ANA
  4. Negative viral markers
  5. Other autoimmune processes may be present
105
Q

How is autoimmune hepatitis treated?

A

Steroids

106
Q

What is a classic histologic finding of autoimmune hepatitis?

A

Plasma cell infiltration (fried egg cell)

107
Q

What are the three presentations of alcoholic liver disease?

A
  1. Hepatic steatosis
  2. Alcoholic hepatitis
  3. Alcoholic cirrhosis
108
Q

What causes hepatic steatosis?

A

Short-term ingestion of 80 grams of alcohol; it is reversible

109
Q

What is alcoholic hepatitis?

A

Acute onset of symptomatic hepatitis after a recent period of heavy alcohol consumption

110
Q

How is alcoholic hepatitis treated?

A

Alcohol avoidance and supportive care

111
Q

Describe the classic histologic appearance of alcoholic hepatitis.

A

Fatty liver with inflammation and hepatocellular injury; mallory hyaline often associated with neutrophils; pericellular fibrosis (chicken wire)

112
Q

What is histologically identical to alcohol-induced liver disease?

A

Non-alcoholic fatty liver disease (NAFLD)

113
Q

What is a risk factor for NAFLD?

A

Obesity and metabolic syndrome

114
Q

What is the most common cause of abnormal LFT’s in the US?

A

NAFLD

115
Q

What is macrovesicular steatosis?

A

Accumulation of fat droplets in hepatocytes

116
Q

Compare NASH and simple steatosis.

A

Both have elevated transaminases and may be asymptomatic. Simple steatosis is benign. NASH progresses to cirrhosis 20-30% of the time and is associated with cardiovascular disease and metabolic syndrome (may also have fatigue and RUQ discomfort)

117
Q

What is hemochromatosis?

A

Disease of iron overload leading to iron deposition in parenchymal tissues (most commonly the liver)

118
Q

What is the inheritance pattern of hereditary hemochromatosis? What is the most common mutation?

A

Homozygous recessive

HFE gene mutation

119
Q

What can cause secondary hemochromatosis?

A

Excessive transfusions or hemolysis

120
Q

How is hemochromatosis treated?

A

Phlebotomy or chelation

121
Q

How is hemochromatosis diagnosed?

A
  1. Elevated serum iron
  2. Elevated ferritin (often >1,000) with transferrin saturation at 95%
  3. Genetic testing
  4. Liver biopsy
122
Q

What is Wilson’s disease?

A

Accumulation of copper in the liver and brain

123
Q

What causes Wilson’s disease?

A

Autosomal recessive mutation in ATP7B gene (responsible for linking copper to ceruloplasmin for release into the blood; copper is stuck in the liver)

124
Q

What are the symptoms of Wilson’s disease?

A
  1. Presents between 6-20 y/o
  2. Neuropsychiatric (psychosis, Parkinson-like tremors, depression)
  3. Kayser Fleischer rings (copper ring in eye)
  4. Liver failure
125
Q

How is Wilson’s disease treated?

A

Copper chelation

126
Q

How is Wilson’s disease diagnosed?

A
  1. Low ceruloplasmin (non-copper-bound ceruloplasmin is rapidly degraded in blood stream)
  2. Increased urinary copper
  3. Liver biopsy
  4. Kayser Fleischer rings
127
Q

What causes alpha-1 anti-trypsin deficiency?

A

Defective production of A1At in the liver due to errors in coding sequence which prevent its export from the heaptocyte (leads to cell death, inflammation, fibrosis, and icrrhosis)

128
Q

What type of genetic disorder is A1AT deficiency?

A

Autosomal recessive (PiZZ)

129
Q

A1AT deficiency is associated with early-onset ___.

A

COPD

130
Q

What histologic finding is seen in A1AT deficiency?

A

Positive PAS stain in liver (excess alpha-1 globules)

MHD2 (34 decks)

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