GI Section III: Diffuse Liver Processes Flashcards

1
Q

How to Call Fatty Liver on CT?

A
  1. < 40 HU on NECT
  2. < 100 HU on PVP
  3. < 25 HU less than the spleen
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2
Q

How to Call Fatty Liver on US?

A

Brighter than the kidney

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3
Q

How to Call Fatty Liver on MRI?

A

Two standard deviation difference between in and out of phase imagin

Out-of-phase SIGNAL DROP

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4
Q

What does signal drop out assume on MRI?

A

there is more water than fat in the liver

the degree of signal loss is maximum when the fat infiltration is 50% (exactly 1:1 signal loss)

When the percentage of fat grows larger than 50% you will actually see a less significant signal loss on out of phase imaging, relative to that maximum 50%.

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5
Q

What causes signal drop?

A

McDonalds, Burger King, and Taco Bell.

Additional causes include:
chemotherapv (breast cancer)
steroids
cystic fibrosis.

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6
Q

Iron overload

A

Hemochromatosis

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7
Q

You can show hemochromatosis is three main ways:

A
  1. The liver and spleen being T1 and T2 dark.
  2. T2 only: absent spleen (chronic hemolytic anemia = multiple blood transfusions = hemochromatosis = splenectomy), liver is darker (low signal) than muscle)
    * On T2 a normal liver should always have a signal higher than muscle
  3. Low signal on in phase, and high signal on out of phase. (“Iron on In-phase”)
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8
Q

FAT vs IRON in IP - OOP MRI

A

FAT - Signal Drop on OOP

IRON - Signal drop in IP

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9
Q
A

A. Hereditary hemochromatosis - Low signal Liver / Normal spleen

B. Prolonged treatment with phlebotomies: Normal Signal liver

C. Secondary hemochromatosis: Low signal on Liver and spleen

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10
Q

Hemocrhomatosis

Liver + Pancreas

A

Primary hemochromatosis

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11
Q

Hemochromatosis

Liver + spleen

A

Secondary hemochromatosis

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12
Q

Hemochromatosis

Genetic - increased absorption

A

Primary hemochromatosis

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13
Q

Hemochromatosis

Acquired - chronic illness, and multiple transfusions

A

Secondary hemochromatosis

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14
Q

How does the body react in secondary hemochromatosis?

A

result of either chronic inflammation or multiple transfusions.

body reacts by trying the “Eat the Iron,” with the reticuloendothelial system

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15
Q

Hypercoaguable patient (pregnant or idiopathic - mc example) = Hepatic vein thrombosis

A

Budd Chiary Syndrome

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16
Q

Budd-Chiary syndrome

A
  1. Obstruction - hepatic venous outflow
  2. Intrahepatic and systemic collateral veins
  3. Large regenerative (hyperplastic) nodules in a dysmorphic liver
  4. LArge caudate lobe (massive) - spared from separate drainage into IVC)
17
Q

Early and delayed phases of liver enhancement

A

Budd-Chiari Syndrome

“flip-flop pattern

AP: Central enhancement Peripheral minumal
PVP: Central washout (Low attenuation) and high peripherally

18
Q

Who gets a “Nutmeg Liver”

A
  • Budd Chiari
  • Hepatic Veno-occlusive disease
  • Right Heart Failure (Hepatic Congestion)
  • Constrictive Pericarditis
19
Q

“nutmeg” with an inhomogeneous mottled appearance, and delayed enhancement of the periphery of the liver.

A

Budd-Chiari Syndrome

20
Q
A

Regenerative (hyperplasic) nodules in Budd Chiari

High T1 low/iso T2

21
Q

Budd-Chiarri vs HCC nodules

A

Big (>10cm) and small (<4cm) nodules in Budd chiarri = benign

Budd Chiari = T2 Dark
HCC = T2 bright

22
Q

Acute vs Chronic Budd-Chiari syndrome

A

Acute = rapid onset ascites

Chronic = fibrosis of the intrahepati veins due to infplammateion

23
Q

Who gets massive caudate lobe hypertrophy?

A

Budd-Chiari
Primary Sclerosing Cholangitis
Primary Biliary Cirrhosis

24
Q

Budd Chiari that occurs from occlusion of the small hepatic venules (Instead of hepatic venous outflow)

A

Hepatic Veno-occlusive Disease

25
Q

Hepatic Veno-occlusive Disease waveforms

A

Nomal Hepatic veins
Normal IVC
Abnormal Portal waveforms (Slow, reversed, to-and-fro)

26
Q

Passive hepatic congestion is caused by

A

stasis of blood within the liver due to compromise of hepatic drainage

27
Q

common complication of congesfive heart
failure and constrictive pericarditis

A

Passive congestion

28
Q

Result of elevated CVP transmitted from the right atrium to the hepatic veins

A

Passive congestion

29
Q

Passive congestion findings:

A

Refluxed contrast into the hepatic veins
Increased portal venous pulsatility
Nutmeg liver