liver pathology : diffuse abnormalities Flashcards

1
Q

____ is due to congestive heart failure. Due to cardiac
insufficiency, blood backs up into liver. This could
be due to Rt. heart failure or Lt. heart failure.

clinical signs are : Hepatomegaly, there may be ascites

A

Passive Congestion

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2
Q

describe passive congestion sonographically?

what about the labs?

A

Acutely the liver is usually large and hypoechoic due to the increase in blood volume within the organ. The liver is congested with a fluid, blood, making it enlarges and more hypoechoic in appearance.

• Dilated IVC, HV’s, PV, Mesenteric and Splenic vein. Loss of diameter changes in these venous systems.

• Prominent walls of the PV will give a “Starry Sky” appearance. In chronic passive congestion the liver will become more fibrotic and the echogenicity
will increase. AJR:178, Jan. ‘02

Labs • Could be normal to slightly elevated

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3
Q

describe passive congestion doppler waveform

which is normal, which is passive congestion?

A

– Doppler will show less triphasic HV flow & a loss of phasicity. • Note the this type of waveform is not “Pathognomonic” for passive hepatic congestion.

“Pathognomonic” = Characteristic or symptomatic of a particular disease or condition. • Other diffuse liver conditions can cause a waveform like this

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4
Q

___ is viral. Other: Alcohol, medicines, chemicals, genetic problems, metabolic disorders, immune related injuries. Obesity can be a cause of liver damage which can lead to inflammation. These are non-infectious causes.

A

hepatitis

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5
Q

what is described?

A

viral hepatitis

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6
Q

____ is caused by blood exposure, Blood exposure, transfusions before screening, tattoos, piercing, multiple sex partners, needle sticks injuries. No cure, TX
only option. > 20% of cases the mode of transmission is not identified.

• Asymptomatic or flu like illness lasting a few days, without jaundice.

how long can it go undetected?

is it contagious?

what does it progress into?

A

hepatitis c

It goes undetected for years. 50-60% of patients develop chronic Hep. C disease, most of these remain contagious for life. Many pt. who have chronic Hep. C disease develop aggressive hepatitis with gradual progression to cirrhosis (permanent scarring) and liver failure.

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7
Q

___ is – Asymptomatic in some individuals.
– Jaundice, loss of appetite, N/V, fatigue, Hepatomegaly and tender, pruritus “PROO-RITIS” (severe itching) caused from too much biliary salts within the subcutaneous tissues.

A

Hepatitis

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8
Q

what labs are associated w/ hepatitis

A

– Markedly elevated AST, ALT
– Serum Bili minimally elevated
– Serum Albumin, PT usually are normal particularly in HAV/HBV.
– Late in HCV when cirrhosis has occurred, i.e. liver functions are diminished.
– Albumin will be decreased, (hypoalbuminemia).
– Clotting factors diminish, clotting times will be elevated.

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9
Q

describe how hepatitis is going to look acutely or chronically.

A

In the acute phase you
may or may not find these appearances.

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10
Q

what do you see?

A

acute vs chronic

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11
Q

___ is – A chronic disease of the liver characterized by the replacement of normal tissue with fibrous tissue and the loss of functional liver cells. It is a progressive DZ with Liver failure and Portal HTN coming at the end stage.

• Etiologies – Multiple causes; Alcohol abuse, Biliary (primary and secondary), Post necrosis (post hepatitis), metabolic (glycogen storage Dz.), and Unknown.

A

Cirrhosis

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12
Q

describe the 4 types of cirrhosis

A

• Alcohol (ETOH)
– Chronic ETOH, common abbreviation on req.’s, intake in toxic to hepatocytes. Fat accumulation and inflammation, damage the architecture of
the hepatocyte by necrosis and fibrosis.

• Biliary
– Primary, Lobular ducts become inflamed and scarred. Very small, very proximal ducts are affected.
– Secondary, bile ducts become inflamed and scarred proximal to an obstruction

• Post necrosis
– Necrotic tissue is replaced with fibrous, nodular scar tissue.

• Metabolic
– Morphologic (deals with the form and structure, NOT function) changes occur, such as inflammation and scarring related to the cause. EXAMPLE;
glycogen storage disease (large amounts of glycogen are deposited into the hepatocytes, thus causing damage to the liver which can result in cirrhosis.
Hemochromatosis: Large amounts of Iron accumulate in the liver and/or other organs.

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13
Q

what clinical signs are associated w/ cirrhosis

A

– Jaundice
– Ascites
– GI bleeding – Secondary to PV HTN
– Decreased alertness
– Spider angiomas of the face
– Palmer Erythema – Redding of the palms
– Light colored stools
– Nausea
– Anorexia - Loss of appetite
– Abd. pain

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14
Q

which labs are abnormal if a pt has cirrhosis?

A

– Abnormal LFT’s
– Abnormal albumin
– Abnormal coagulation

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15
Q

describe what cirrhosis looks like on us?

A
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16
Q

what is volume redistribution?

course echotexture?

nodular surface?

Nodules regenerative and dysplastic:?

A

Early stages – Liver generally enlarges, Late or advanced stages – Liver generally is small, with relative enlargement of the Lt. and caudate lobe, in comparison with the Rt.

This is a subjective finding and can be made worse with an inappropriate gain or TGC settings.

Irregularity of the liver surface, this correlates to regenerating nodules and fibrosis. Is easier to see when ascites is present.

Regenerating nodules represent regenerating hepatocytes surrounded by a fibrotic septa. There appearance is similar to the architecture of the normal liver. US and CT have a limited ability in there detection. MRI is more sensitive then both US and CT at detecting RN. DYPLASTIC nodules are considered pre malignant. There are hyperplastic nodules and are lager then RN.

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17
Q

___ is Fibrosis with in the hepatocytes is affecting the flow of blood through the liver. The flow of blood slows to < 16 cm/s2. The volume of blood will remain the same. There is still the same amount of blood going to the liver. The pressure within the PV and tributaries increases as a result of the liver not allowing blood to flow freely through it. The pressure causes the diameters of the PV and
tributaries to enlarge. > 13mm in diameter is abnormal in UIHC Radiology. The spleen will enlarge, WHY?, and Ascites will develop.

A

Portal Hypertension:

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18
Q

this Sonographic Appearance describes ______:
– Depends on Acute or Chronic
– Hepatomegaly or small atrophic liver
– Increased attenuation
– Nodularity seen, particularly on the surface; nodules are easier seen when ascites is present
– Possible ascites
– Decreased visualization of vascularity
– Generally more echogenic than kidney

A

cirrhosis

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19
Q

what does the gross appearance of cirrhosis look like?

A

Many regenerative nodules

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20
Q

____ is An accumulation of lipids in the hepatocytes. (AKA steatosis) Due to injury which affects the function of the liver or systemic diseases like DM, ETOH, obesity, malnourishment, steroids. it is acquired and reversible.

  • Why Obesity?
  • WHY Malnourishment? .
  • A Fatty liver
  • Steroids
A

Fatty infiltration - Steatosis

  • Why Obesity? because excess glycogen is being stored in liver.
  • WHY Malnourishment? Liver is storing much fat to prevent starvation.

• A Fatty liver is a non specific sign. It can be the result of several problems.

• Steroids – Not necessarily abuse like weightlifters, but also pt. with CF, and other conditions where
steroids are used.

• It is acquired and it is reversible.

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21
Q

what are these • Clinical Signs associated with?
– Asymptomatic
– Depends on Etiology
– Hepatomegaly- maybe
– Pain – maybe

labs are variable » Depends of severity
» LFT’s can increase

A

Fatty infiltration

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22
Q

what types of diffuse fatty inflitration of the liver are there?

what about focal?

A

Mild: minimal diffuse increase in echogenicity; normal
visualization of the diaphragm and intrahepatic blood vessels

» Moderated: moderate increase in echogenicity, slightly impaired visualization diaphragm and intrahepatic blood vessels

» Severe: Marked increase in liver echogenicity, poor penetration of the posterior segment of the rt. liver lobe and poor or nonvisualization of hepatic vessels and diaphragm

Focal: Fatty deposits typically in the periportal area of the medial segment of the Lt. lobe. The will be no mass effect, even though it will look like a mass there will no mass effect. Blood vessels will not be pushed aside.

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23
Q

can you tell which of these fatty infiltration livers are mild and moderate?

A

a, b, c are mild d is moderate

the below is severe

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24
Q

Focal fatty infiltration and focal fatty sparring OFTEN mimic _______.

Focal Fatty infiltration are areas of increased echogenicity

Notice there is no mass effect to surrounding tissue

A

neoplasms

25
Q

what is this?

A

focal fatty sparring

26
Q

what’s happening here?

A

Same pt. from prior slide. 4 ½ yrs. later

fatty sparring resolution

27
Q

what 3 types of etiology for protal hypertension?

A

Prehepatic

» PV Thrombosis, Splenic V thrombosis, Cavernous transformation…

– Intrahepatic

» Presinusoidal: chronic HBV, chronic HCV,
hemochromatosis, polycystic liver dz….
» Hepatic: acute viral, acute etoh, acute fatty liver of
pregnancy…
» Postsinusoidal: Venous-occlusive dz. central veins
are scarred…

– Extrahepatic
» Budd-Chiari, heart diseases, valve diseases…

28
Q

what collaterals are there w/ portal hypertension?

A
29
Q

what is happneing w/ the portal hypertensive patient?

A

Cavernous transformation
– Cavernous transformation of the portal vein is defined as
the formation of venous channels within or around a
previously thrombosed portal vein.

30
Q

what labs are associated w/ portal hypertension?

PV diameter?

flow?

any other us findings?

A

– None specific to PV. HTN.
– Cirrhosis labs

– Large PV diameter, >13mm
– Slow flow < 16cm/s2
– Patent Umbilical Vein
– Patent Coronary or Lt. gastric vein
– Flow direction reversals and discrepancies.
– Splenomegaly
– Splenic Varices
– Periportal Varices
– Prominent HA flow – To make up for the lack of PV flow
– Hepatopedal vs. Hepatofugal: Toward the liver and Away from the
liver

31
Q

what could be happening here. portal hypertension

A


Reverse flow in the lt. gastric vein (coronary v.)

Flow should be from the lt. gastric vein into the MPV. Color Doppler shows the reversal.

32
Q

what could be happening here? portal hypertension

A

Reversal of flow in the Splenic V

33
Q

what treatment is available for portal hypertension?

A

Surgical shunt to decrease PV pressure: Not done much anymore.

Mesocaval Shunt, Portocaval Shunt, Splenorenal Shunt

Interventional Radiology: Much easier on patient with great results.

TIPS – Transjugular Intrahepatic Portosystemic Shunt

34
Q

what is this?

A

portal hypertension

35
Q

what is this? how can you tell?

A

portal hypertension

36
Q

what do these illustrate?

A

portacaval shunt, splenorenal shunt; treatment for PHN

37
Q

how does TIPS work? what is it for?

A

Transjugular Intrahepatic Portosystemic Shunt

38
Q

____ is the Occlusion of the hepatic veins with or without occlusion of the IVC. Characterized by massive ascites hepatomegaly and abdominal pain. Relatively rare. Poor prognosis

its etiology is –
Idiopathic, Hypercoagulable states, Chronic Leukemia, trauma, tumor extension from HCC or Renal Cell, Pregnancy, congenital abnormalities such as obstructing membranes within the IVC.

A


Budd-Chiari syndrome

39
Q

what clinical signs are associated with •
Budd-Chiari syndrome

labs?

ddx?

A


Sudden onset of ascites, RUQ pain.

The classic patient in North America is a young female was is taking BCP who presents with acute onset of ascites, RUQ pain, hepatomegaly.

Labs
Non specific
variable

DX (differential diagnosis)
Portal HTN

40
Q

___ is a –
A disorder of carbohydrate metabolism. Abnormally large amounts of glycogen are stored in the liver and kidney’s. There are 6 categories, type 1 is most common.

it is aka ________

its etiology is • Genetic, autosomal recessive. There are enzymatic deficiencies which allow amounts of glycogen to be deposited with in the hepatocytes of the liver and the proximal convoluted tubules of the kidney. Usually manifests itself in the neonatal period. Can be managed with dietary modifications and supportive therapy. Patients are currently surviving into childhood and young adulthood.

A

Glycogen Storage Disease

Von Gierke’s disease

41
Q

what does glycogen storage dx lead to?

labs?

A

Leads to developmental and growth problems.

Unstable blood sugars

42
Q

what will glycogen storage dx look like?

A


Sonographic appearance

Type 1 GSD will look like diffuse fatty infiltration of the liver. They are associated with adenomas and less frequently HCC.

Echogenic liver, increased attenuation.

43
Q

___ is an An abnormal accumulation of serous – yellowish fluid resembling serum - (what is left after the cells are removed from whole blood) fluid in the abdominal cavity.

its –
Etiology
Heart failure
Portal HTN
Liver Damage
Hypoalbuminemia
Malignancies
Others

A

ascites

44
Q

what types of ascites are there?

A

Transudative:
Clear fluid
Cirrhosis
CHF
Nephrotic syndrome
Chylous ascites – Lymph fluid, emulsified fat – milky fluid

Exudative:
Cellular or debritic fluid
Inflammatory – TB, Pyogenic
Malignant – Peritoneal tumor, especially the ovary
Bloody – Traumatic, post operative, ruptured ectopic, leaking aneurysm

45
Q

what scaning techniques can be employed when looking for ascites?

A


Look in the dependent portions of the body. When the pt. is supine, LUQ perisplenic, RUQ perihepatic. Look in both Long and Trans.

Check pericolic gutters along the flanks and LLQ, RLQ. It is important to show relational anatomy so the Radiologist or the next sonographer can tell where you took the image at.

Posterior to the bladder

46
Q

How can air/gas get into the PV? what is this known as?

how can it be detected?

A

Portal Venous Air

necrotic bowel
ulcerative colitis
intra abdominal abscess
small bowel obstruction
gastric ulcer

Abdominal x-ray, CT, US

47
Q

what does this look like?

A

Portal Venous Air


PV air is typically disbursed more peripherally in the liver. Air within the biliary tree is typically located more centrally within the liver.

48
Q

what is this?

A

portal venous air

49
Q

When assessing the liver parenchyma with ultrasound the size, configuration homogeneity and
_____ are included.

A

___contour

50
Q

Are the following liver diseases focal or diffuse?

chronic hepatitis

fatty infiltration

echinococcal cyst

passive congestion

A

diffuse

diffuse

focal

diffuse

51
Q

Foie gras is a meal made with the fatty infiltrated liver of what animal? Just put the animals name, don’t put an “a” in front.

A

duck

52
Q

Fatty liver is an example of a diffuse liver disease that can be reversible. t/f

A

t

53
Q

In focal sparing, the hypoechoic region is actually normal liver parenchyma in an otherwise fatty liver. t/f

A

t

54
Q

Excluding viral causes, which of the following are know causes for hepatitis?

a) drug toxicity
b) alcohol
c) being dehydrated
d) infections elsewhere in the body, such as infectious mononucleosis.

A

a, b, d

55
Q

It only takes a ____ amount of inflammation to impair hepatocyte function.

A

mild

56
Q

Ethanol (ETOH) abuse is a common cause for fatty liver particularly here in the USA. Nutritional deprivation is also a cause but it is not common here in the USA. t/f

A

t

57
Q

Portal vein hypertension occurs in the early stages of cirrhosis. t/f

A

f

58
Q

The common term for inspissated bile is?

A

sludge