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Abdo review > Liver normal and diffuse, metabolic, infections > Flashcards

Liver normal and diffuse, metabolic, infections Flashcards

1
Q

functions of the liver?

A
  • produces most proteins
  • Metabolizes or breaks down nutrients for food to produce energy when needed
  • prevents shortages of nutrients by storing certain vitamins, minerals, sugar
  • Produces bile
  • produces most substances that regulate blood clotting
  • immune function
  • removes potentially toxic byproducts of certain medications
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2
Q

what is a hepatocyte?

A
  • triad of a bile duct, portal vein, and hepatic artery throughout the liver parenchyma
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3
Q

where is bile produced within?

A
  • produced within the cell
  • bile enters the bile duct to be transpoted to the GB
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4
Q

hepatic artery supplies?

A

oxygenated blood

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5
Q

portal vein supplies?

A

WBC and returns flow to the liver from the intestines for cleansing

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6
Q

the central vein function?

A

drains old blood back to the hepatic veins

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7
Q

what is the hepatic artery?

A
  • branch of the celiac axis
  • supplies the liver cells with oxygenated blood
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8
Q

what is the main portal vein?

A
  • formed by the confluence of the SMV and splenic vein
  • supples liver with lympocytes and RBC’s from the spleen and blood from the intesttimes that needs to be purifies by the liver
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9
Q

HV function?

A
  • drains deoxygenated blood from the liver into the IVC and returns it to the cardiopulmonary system for rejuvenation
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10
Q

Which structure separates the medial and lateral left lobe?

A

Left intersegmental fissure

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11
Q

Which structures lie within the left intersegmental fissure?

  • cranially
  • middle
  • caudally
A

Cranially-LHV
Middle-Ascending LPV
Caudally-ligamentum teres

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12
Q

The hepatic veins are visualized when scanning which portion of the liver?

A

superior

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13
Q

What does the MHV separate?

A

Anterior RL and medial LL

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14
Q

What borders on each side of the RHV?

A

Anterior and posterior RL

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15
Q

What is the name of the capsule surrounding the liver?

A

glisson’s capsule

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16
Q

Why is there a bare area on the liver?

A

lacks peritoneum

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17
Q

right lobe normal measurement?

A

13-17 cm

  • abnormal >14 cm (compare with rt kidney)
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18
Q

hapatopetal flow of the liver?

A

portal venous flow

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19
Q

hepatofugal flow of the liver?

A

hepatic veins

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20
Q

MPV should not exceed what AP diameter?

A

13mm

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21
Q

list 4 normal variants?

A

Diaphragmatic Slips
Reidels lobe
Papillary Process Caudate
Long left lobe

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22
Q

Normal Variants- Diaphragmatic Slips is a cause of?

A
  • cause of pseusomass on liver
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23
Q

Diaphragmatic Slips are associated with?

A

diaphragmatic muscle bundles that attach the central tendon tot he thoracic cage

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24
Q
A

Diaphragmatic Slip

  • apperance changes with respiration
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25
Q
A

papillary process of caudate

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26
Q

Situs inversus totalis?

A

liver is found in the LT hypochondruim

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27
Q

Alpha-fetoprotein (AFP)?

  • what is it?
  • what is it a marker for?
A
  • Not seen under normal circumstances
  • A protein normally synthesized by the liver, yolk sac and GI tract of the fetus
  • A nonspecific marker for malignancy
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28
Q

Alkaline Phosphatase(ALP)?

  • what is it?
  • where is it excreted
  • marked elevation is associated with?
A
  • enzyme produced primarily by liver, bone, and placenta
  • excreted through bile ducts
  • marked elevation is associated with obstructive jaundice
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29
Q

what is Alanine aminotransferase-ALT?

A
  • enzyme found in high concentration in the liver and lower concentrations in the heart, muscle, and kidneys
  • remains elevated longer than AST
  • used to assess jaundice
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30
Q

Alanine aminotransferase-ALT elevation is associated with?

A
  • cirrhosis
  • hepatitis
  • biliary obstruction
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31
Q

Alanine aminotransferase-ALT mild elevation associated with?

A

liver metastases

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32
Q

Aspartate aminotransferase-AST?

A
  • enzyme present in many kinds of tissue that is released then cells are injured or damaged
  • levels proportional to amount of damage and the time between cell injury and testing
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33
Q

Aspartate aminotransferase-AST us used to diagnose?

A
  • liver disease before jaundice occurs
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34
Q

Aspartate aminotransferase-AST elevation is associated with? (3)

A
  • cirrhosis
  • hepatitis
  • mononucleosis
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35
Q

prothrombin time- normal clotting time?

A

10-15 secs

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36
Q

what is prothrombin time?

A
  • enzyme produced by liver
  • producation depends on the amount of vitamin k
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37
Q

elevation of prothrombin time is associated with?

A
  • cirrhosis
  • malignancy
  • malabsorption of vitamin K
  • clotting failure
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38
Q

prothrombin time decreases with?

A
  • subacute or acute cholecystitis
  • internal biliary fistula
  • carcinoma of GB
  • biliary duct injury
  • prolonged extrahepatic biliary obstruction
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39
Q

what are leukocytosis?

A
  • WBC count above the normal range
  • sign of inflammatory or infection response
  • includes parasitic infections
  • not a disease but a lab finsing
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40
Q

what is serum albumin?

A
  • decrease suggests a decrease in protein synthesis
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41
Q

what is bilirubin?

A
  • A product from the breakdown of hemoglobin in old red blood cells
  • A disruption in the process may cause abnormal levels
  • Leakage into tissues gives the skin a yellow appearance
  • Reflects the balance between production and excretion of bile
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42
Q

elevation of direct or conjugated bilirubin is associated with?

A
  • obstruction
  • hepatitis
  • cirrhosis
  • liver meastases
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43
Q

elevation of indirect or unconjugated bilirubin is associated with?

A
  • nonobstructive conditions (steatosis)
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44
Q

indication for liver exam? (6)

A

abnormal LFT’s
hepatocellular disease
biliary disease
abdominal /postprandial pain
palpable liver or spleen
pancreatitis

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45
Q

whats included in the medial segment of the liver?

A
  • segment 4a and 4b
  • includes quadrate lobe
  • left portal vein is the anatomical landmark dividing 4a and 4b
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46
Q

what is the round ligament?

A
  • remnant of umbilical vein
    = inferior landmark that divides the inferior lateral segment from inferior medial segment
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47
Q

where is the gallbladder fossa located?

A
  • inferiorly and is the anatomical landmark separating the segment 4b from segment 5
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48
Q

what is hepatocellular disease?

A
  • liver cells (hepatocytes) are the immediate problem
  • usually treated medically with supportive measures and drugs
49
Q

what is obstructive disorders?

A
  • bile excretion is blocked
  • usually treated surgically
50
Q

what is diffuse disease?

A
  • affects the hepatocytes and interferes with liver function
  • measured through a series of liver function tests
51
Q

hepatic enzyme levels are elevated with?

A

cell necrosis

52
Q

4 disorders of metabolism?

A
  • steatosis (fatty liver)
  • glycogen storage disease- neonatal
  • cirrhosis- chronic liver disease
  • NASH- non-alcoholic steatohepatitis
53
Q

what is Steatosis-Fatty Liver?

A
  • an acquired reversible disorder of metabolism
54
Q

causes of Steatosis-Fatty Liver?

A
  • obesity (M/C)
  • excessive alcohol
  • severe hepatitis
  • hyperlipidemia
55
Q

Steatosis-Fatty Liver correction?

A
  • correction of the primary abnormality will usually reverse the process
56
Q

Steatosis-Fatty Liver is a precursor for?

A

significant chronic disease

57
Q

Steatosis-Fatty Liver may lead to?

A

HCC

58
Q

Steatosis-Fatty Liver deposits?

A

may be focal or diffuse

59
Q
A

steatosis

60
Q

mild Characterization of Steatosis?

A
  • minimal diffuse increase in hepatic echogenicity
61
Q

moderate Characterization of Steatosis?

A
  • moderate diffuse increase in hepatic echogenicity
  • slightly impaired visualization of intrahepatic vessels and diaphragm
62
Q

severe Characterization of Steatosis?

A
  • marked increase in echogenicity
  • poot penetration of posterior liver
  • poor or no visualization of hepatic vessels and diaphragm
  • hepatomegaly
63
Q
A

steatosis

64
Q

Other Sonographic Appearances of Fatty Liver (3)

A
  1. focal fatty infiltration
  2. fatty sparing
  3. focal fat
65
Q

what is focal infiltration?

A
  • regions of increased echogenicity are present within a background of normal liver
  • can mimic a mass
66
Q
A

focal fatty infiltration

67
Q

what is focal fat? where is the preferred site for focal fat?

A
  • hyperechoic- no mass effect
  • preferred site is anterior to portal vein at porta hepatis
68
Q

what is NASH?

A
  • nonalcoholic steatohepatitis
  • “silent” liver disease
69
Q

NASH u/s features?

A
  • resembles alcoholic liver disease
  • occurs in people who drink little or no alcohol

major features:

  • fat in the liver
  • inflammation
  • damage
70
Q

NASH can lead to?

A

cirrhosis

71
Q

NASH is commonly related to?

A

obesity

72
Q

NASH S/S? (3)

A
  • fatigue
  • weight loss
  • weakness may begin once disease is advanced or cirrhosis is present
73
Q

NASH lab values?

A

increased LFT’s

74
Q

NASH diagnosed by?

A

biopsy

75
Q

NASH treatment?

A
  • reduce weight
  • eat well
  • phusical activity
  • avoid alcohol and unnecessary medication
  • liver transplant may be necessary if cirrhosis ensues
76
Q

NASH on u/s?

A
  • dense fatty infiltation
  • cirrhosis
77
Q

what is glycogen storage disease?

A

• Inherited disease - occurs in neonatal period

78
Q

Glycogen storage disease characterized by?

A
  • abnormal storage and accumulation of glycogen in the tissues (especially liver and kidneys)
79
Q

Glycogen storage disease may develop?

A
  • benign adenomas
  • HCC
80
Q

Glycogen storage disease appearance?

A
  • indistinguishable from diffuse fatty infiltration
  • (different age group)
81
Q

Six categories of glycogen storage disease based on clinical symptoms and specific enzymatic defects?

A
  • most common is type 1 or von gierke disease
  • abnormally large amounts of glycogen are deposited in the liver and kidneys
82
Q
A

glycogen storage disease

83
Q

what is viral hepatitis?

A
  • inflammation of liver
  • common disease that occurs worldwide
  • 6 distinct hepatitis- A through E and G
  • may be fatal if not treated
84
Q

viral hepatis may lead to? (3)

A
  • portal hypertension
  • cirrhosis
  • HCC
85
Q

Hepatitis A?

A
  • HAV
  • worldwide
  • spreads fecal-oral route
  • endemis in developing countries- affects the young
  • acute infection
  • death from acute liver failure
86
Q

Hepatitis B?

A
  • HBV
  • Worldwide
  • transmitted parenterally (not oral)
  • blood transfusions, needle punctures, sexual contact, and at birth
  • predominate in asia, aferica, and Greenland
87
Q

hepatitis D?

A
  • dependent on hep B for infectivity
  • geographically the same as hep B
  • uncommon in north America
  • IV drug use
88
Q

s/s of viral hepatitis? (8)

A
  • fatigue
  • headache
  • anorexia
  • fever
  • abdo pain
  • nausea
  • vomiting
  • jaundice
89
Q

acute hepatitis?

A
  • recovery within 4 months
  • liver parenchyma more hyopechoic leading to appearance of bring periportal walls
  • starry night sign
90
Q
A

acute hepatitis

91
Q

chronic hepatitis?

A
  • exists when clinical or biochemical evidence of hepatic inflammation extends beyond 6 months
92
Q

chronic hepatitis causes (4)?

A
  • viral
  • metabolic
  • autoimmune
  • drug-induced
93
Q

s/s chronic hepatitis?

A
  • nausea
  • anorexia
  • weight less
  • tremors
  • jaundice
  • dark urine
  • fatigue
  • varicosities
94
Q

chronic active hepatitis usually progresses to?

A
  • cirrhosis
  • liver failure
95
Q

chronic hepatitis u/s?

A
  • liver parenchyma is coarse with decreased brightness of the portal triads
  • does not increase in size
  • fibrosis may be seen which may produce “soft shadowing” posteriorly
96
Q
A

chronic hepatitis

97
Q

what is cirrhosis?

A
  • chronic degenerative disease of the liver
  • lobes covered with fibrous tissue
  • parenchyma degenerates
  • lobules are infiltrated with fat
98
Q

essential feature of cirrhosis?

A
  • simultaneous parenchymal necrosis
  • regeneration
  • diffuse fibrosis resulting in disorganization of lobular architecture
99
Q
A

cirrhosis

100
Q

cirrhosis causes?

A
  • most common cause of micronodular form- alcohol consumption
  • most frequent cause of macronodular form- chronic viral hepatitis

most common cause/etiology of portal hypertension

101
Q

etiologies of cirrhosis?

A
  • biliary cirrhosis
  • wilsons disease
  • primary sclerosing cholangitis
  • hemochromatosis
102
Q

cirrhosis clinical presentation?

A
  • hepatomegly
  • jaundice
  • ascites
103
Q

cirrhosis on u/s? (5)

A
  • Volume redistribution
  • coarse echotexture
  • nodular surface
  • nodules: regenerative and dysplastic
  • portal hypertension: ascites, spenomegly, varices
104
Q

cirrhosis early stages on u/s?

A
  • enlarged liver
  • may be difficult to distinguish from fatty liver
  • look for irregular contour
105
Q

advanced stages of cirrhosis?

A
  • liver is often small- shrinking
  • ascites
106
Q

nodular surface- cirrhosis?

A
  • irregularity of liver surface
  • due to presence of regenerating nodules and fibrosis
  • ascites helps outline edges
  • linear probe delineates contour well
107
Q

regenerating nodules- cirrhosis?

A
  • hepatocytes surrounded by fibrotic septae
  • may be isoechoic or hypoechoic with a thin echogenic border
108
Q

dysplastic nodules- cirrhosis?

A
  • adenomatous hyperplastic nodules
  • >10mm- considered premalignant
  • well-differentiated hepatocytes, portal venous blood supply, atypical or malignant cells
109
Q
A

HCC

110
Q

Doppler Characteristics of Cirrhosis?

A
  • The hepatic vein velocity waveform reflects the hemodynamics of the right atrium.
  • This triphasic pattern has two large antegrade diastolic and systolic waves and a small retrograde wave that corresponds to the atrial kick (from the heart).
  • Hepatic veins easily receive the transfer of flow via the collaterals from the portal veins in a normal liver.
111
Q
A

doppler characteristics of cirrhosis: hepatic venous flow

112
Q

what is hepatic failure?

A
  • inability of the liver to perform its normal synthetic and metabolic function as part of normal physiology
  • 2 forms are recognised- acute and chronic
113
Q

acute liver failure?

A
  • the rapid development of hepatocellular dysfunction, specifically coagulopathy and mental status changes in a patient without known prior liver disease
114
Q

chronic liver failure usually occurs in?

A

cirrhosis

115
Q

chronic liver failure causes?

A
  • excessive alcohol intake
  • hep B or C
  • autoimmune, hereditary and metabolic causes- iron or copper overload
  • steatohepatitis or non-alcoholic fatty liver disease
  • ascites occurs secondary to liver cell failure
  • worsening jaundice
  • coagulopathy
  • hepatic encephalopathy
  • drug toxicity
  • death occurs if loss of hepatic parenchyma by necrosis is >40%
116
Q

what is coagulopathy?

A
  • AKA clotting and bleeding disorder
  • bloods ability to clot is impaired
  • may occur spontaneously or following a medical condition
117
Q

what is hepatic encephalopathy?

A
  • brought on by disorders that affect liver
  • AKA portosystemic encephalopathy or hepatic coma
  • patient exhibits confusion, altered level of consciousness, coma
  • result of liver failure
118
Q

what is drug toxicity?

A
  • drugs account for 20-40% of hepatic failure
  • alcoholics are susceptible
  • outcome is liver transplant or death
119
Q

what is hemochromatosis?

A
  • rare disease of iron metabolism characterized by iron deposits through the body
  • may lead to cirrhosis and portal hypertension

u/s features:

  • hepatomegaly
  • cirrhotic changes
  • increased echogenicity may be seen uniformly throughout hepatic parenchyma

Abdo review (11 decks)

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