Metabolic Diseases Flashcards

1
Q

What is hepatocellular disease?

A

A diffuse dysfunction of the hepatocytes where normal liver tissue is replaced with fat or fibrosis and the liver size is often affected.

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2
Q

What lab values would you expect to affected by hepatocellular disease?

A

LFT’s

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3
Q

What is another name for fatty infiltration?

A

Steatosis

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4
Q

What is fatty infiltration?

A

Accumulation of triglycerides (fat) within hepatocytes

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5
Q

What are the 2 most common causes of fatty infiltration?

A

Alcohol abuse and obesity

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6
Q

What is fatty infiltration a precursor to?

A

Significant chronic disease (Cirrhosis)

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7
Q

What four things should be looked for when evaluating the liver for fatty infiltration?

A
  • Echogenicity changes
  • Echotexture changes
  • Attenuation characteristics
  • Ability to visualize vessels
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8
Q

What is the sonographic appearance of fatty infiltration?(3)

A
  • Difficult penetration
  • Paucity of vessels
  • Echogenicity change
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9
Q

What is the prognosis of fatty infiltration and the prognosis of focal fatty changes?

A

Infiltration - Can be reversed by fixing lifestyle habits

Fatty changes - Can resolve rapidly (as fast as 6 days)

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10
Q

Describe the sonographic characteristics of MILD fatty infiltration: (2)

A
  • Slight increase in liver echogenicity

- Diaphragm and vessels clearly defined

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11
Q

Describe the sonographic characteristics of MODERATE fatty infiltration: (2)

A
  • Increase in liver echogenicity

- Vessels and diaphragm not sharply defined

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12
Q

Describe the sonographic characteristics of SEVERE fatty infiltration: (2)

A
  • Liver echogenicity increased markedly

- Extremely difficult to define diaphragm and vessel walls

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13
Q

What are two types of focal fatty change?

A

Infiltration and sparing

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14
Q

Describe the sonographic characteristics of focal fatty infiltration:

A

Focal areas of increased echogenicity and mostly normal liver parnechyma

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15
Q

Describe the sonographic characteristics of focal fatty sparing:

A

Majority of liver parenchyma has fatty infiltration, focal hypoechoic areas (normal liver tissue)

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16
Q

What lab values could potentially be elevated with fatty infiltration?

A

ALT, AST, possibly GGT

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17
Q

What is cirrhosis?

A

A diffuse process that destroys the liver cells and results in fibrosis of liver parenchyma with nodular changes

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18
Q

What is the most common cause of cirrhosis and what are the other underlying?

A

Most common = Alcohol abuse

Other:

  • Chronic viral hepatitis
  • Primary sclerosing cholangitits
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19
Q

What are the three stages of progressive change in cirrhosis?

A

Cell death, fibrosis, and regeneration (of fibrotic tissue)

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20
Q

Is cirrhosis reversible?

A

No, it’s irreversible

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21
Q

What are the two types of nodular change with cirrhosis?

A

Micro nodular and macro nodular

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22
Q

What would micro nodular cirrhosis likely be due to?

A

Alcohol consumption

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23
Q

What would macro nodular cirrhosis likely be due to?

A

Chronic viral hepatitis

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24
Q

How does acute cirrhosis appear?

A

Same as severe fatty infiltration

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25
Q

How does chronic cirrhosis appear? (4)

A
  • Small liver (CL/RL >.65)
  • Coarse echotexture
  • Nodular surface
  • Paucity of vessels
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26
Q

Why does cirrhosis have the potential to progress to end stage liver failure?

A

Blockage of vessels within the liver leads to portal hypertension

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27
Q

What do lab values depend on when assessing cirrhosis?

A

The stage of the disease

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28
Q

What lab values would you see increased in a patient with cirrhosis?

A

AST, ALT, LDH, ALK PHOS, conjugated bilirubin, GGT

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29
Q

What lab values would you see decreased in a patient with cirrhosis?

A

Serum albumin

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30
Q

Which other organ can be affected by liver cirrhosis?

A

Spleen

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31
Q

What is the classical presentation of cirrhosis?

A

Hepatomegaly, jaundice, and ascites

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32
Q

What is glycogen storage disease also known as?

A

GSD and Von Gierke’s disease

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33
Q

What kind of disorder is glycogen storage disease?

A

Autosomal recessive

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34
Q

What is glycogen storage disease?

A

Enzyme deficiency causing excess glycogen deposits in hepatocytes

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35
Q

What is GSD associated with?

A

Benign adenomas and HCC

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36
Q

Is ascites a metabolic condition?

A

No, but occurs along with most of them

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37
Q

What is ascites?

A

Accumulation of free serous fluid in the peritoneal cavity

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38
Q

What are the two kinds of ascites?

A

Transudate and exudate

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39
Q

What is transudate ascites?

A

Contains little protein or cells and suggests a non-inflammatory process

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40
Q

In what two situations would you see transudate ascites?

A

Cirrhosis and CHF

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41
Q

What is exudate ascites?

A

High protein content of blood, pus, and chylous, and suggests an inflammatory or malignant cause

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42
Q

What would be the sonographic difference between transudate and exudate ascites?

A

Exudate ascites will have internal echoes and loculations

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43
Q

Free fluid in the peritoneal cavity may be what two things?

A

Free or loculated

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44
Q

What is the sonographic confirmation of free fluid?

A

Changes with patient position and conforms to surrounding organs

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45
Q

What is the sonographic confirmation of loculated fluid?

A

No change with patient movement and rounded margins

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46
Q

What are the three most dependent spaces in the peritoneal cavity?

A

Morrison’s pouch, posterior cul-de-sac, and pericolic gutters

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47
Q

What is biliary sludge also known as?

A

Biliary sand and microlithiasis

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48
Q

What is biliary sludge?

A

Mixture of particulate matter and bile

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49
Q

Biliary sludge is a potential precursor to what?

A

Gallbladder disease

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50
Q

What are four causes of bile stasis?

A

Prolonged fasting, rapid weight loss, TPN, and extrahepatic biliary obstruction

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51
Q

What are tumefactive sludge balls?

A

Sludge that mimics polypoid tumors

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52
Q

How can you differentiate between tumefactive sludge balls and polypoid tumors?

A

Assess vascularity, mobility, and GB wall thickness

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53
Q

What is hepatization in terms of biliary sludge?

A

When sludge has the same echogenicity as the liver

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54
Q

What is empyema?

A

Presence of pus in bile

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55
Q

What is hemobilia?

A

Presence of blood in bile

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56
Q

How does Milk of Calcium appear in the gallbladder?

A

Highly echogenic with posterior shadowing, mobile, fluid-fluid level, stretches like fluid unlike a stone

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57
Q

What is the most common disease of the gallbladder?

A

Cholelithiasis

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58
Q

What are three factors that affect gallstone formation?

A

Abnormal bile composition, stasis of bile, and infection

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59
Q

What is the most common composition of gallbladder stones?

A

Cholesterol

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60
Q

What are the risk factors of cholelithiasis?

A

Female, fat, fertile, forty, family history

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61
Q

What can false shadowing in the gallbladder be caused by?

A

Valves of Heister, fat of porta hepatis, duodenal gas

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62
Q

How can you differentiate between between false shadowing and true shadowing?

A

Whether its dirty or not

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63
Q

Gallbladder stones less than what measurment will not shadow?

A

<5mm

64
Q

What is the WES sign?

A

Wall, echo, shadow

65
Q

What lab values would you expect to see altered with cholelithiasis?

A

AST, ALT, ALP, and bilirubin

66
Q

Whats the most common complication of gallstones?

A

Biliary colic

67
Q

What causes ducts to dilate?

A

Obstruction, loss of duct wall elasticity, amupullary dysfunction

68
Q

Which is more serious, painless or painful jaundice?

A

Painless

69
Q

What does painless jaundice suggest?

A

Neoplastic conditions, choledochal cysts

70
Q

What is choledocholiathiasis?

A

Stones in the biliary tree

71
Q

What is the most common cause of choledocholiathiasis?

A

Stones pass from gallbaldder to ducts (secondary)

72
Q

What are primary causes of choledocholiathiasis?

A

Inflammation, infection, Caroli’s disease, prior surgery

73
Q

Where is the most common location for stones in the biliary tree?

A

Distal CBD

74
Q

What lab values would you expect to see increased with choledocholiathiasis?

A

ALP, AST, ALT, bilirubin

75
Q

What is urolithisasis?

A

Stones in the urinary system

76
Q

What is nephrolithiasis?

A

Stones in the renal collecting system

77
Q

What is nephrocalcinosis?

A

Calcifications in the renal parenchyma

78
Q

What are the underlying risk factors of nephrolithiasis?

A

Hereditary, limited water intake, high animal protein diet, urinary stasis

79
Q

What are the three natural narrowings of the ureter?

A

UPJ, iliacs, and UVJ

80
Q

80% of stones get lodged where?

A

UVJ

81
Q

Stones of what measurement can be passed?

A

<5mm

82
Q

Hematuria can be what two things?

A

Microscopic or gross (Frank)

83
Q

What is a possible sign and symptom of kidney stones?

A

Nausea and vomiting

84
Q

What are complications of nephrolithiasis?

A

Hydronephrosis, absent jets

85
Q

Tiny stones can be difficult to identify, what can you look for?

A

Twinkling artifact

86
Q

What is staghorn calculi?

A

Calcifications filling the collecting systemq

87
Q

What are false positives of nephrolithiasis?

A

Intrarenal gas, renal artery calcifications, calcified sloughed papilla, calcified tumors, ureteric stent

88
Q

What are 3 other imaging modalities that can detect urolithiasis?

A

X-ray, tomography, CT

89
Q

Bladder calculi are usually what?

A

Single

90
Q

What should you check for with bladder calculi?

A

Mobility

91
Q

Hydronephrosis can be due to what two causes?

A

Obstructive or non-obstructive

92
Q

What is obstructed flow broken down into?

A

Intrinsic and extrinsic

93
Q

What are examples of non-obstructive hydronephrosis?

A

Reflux, infection, polyuria

94
Q

What could hydronephrosis lead to?

A

Renal atrophy

95
Q

What is Grade 1 Mild hydro?

A

Slight separation of renal collecting system

96
Q

What is Grade 2 Moderate hydro?

A

Separation of entire central renal sinus including dilated pelvis and calyces

97
Q

What is Grade 3 Severe hydro?

A

Thin renal cortex, extensive enlargement of renal sinus and calyces, loss of calyx definition

98
Q

What are false positives of hydro?

A

Over distended bladder, extra-renal pelvis, multiple parapelvic cysts, AV malformation

99
Q

What are renal parenchymal calcium deposits referred to as?

A

Nephrocalcinosis

100
Q

Renal parenchymal calcium deposits are bilateral and what?

A

Diffuse

101
Q

What can renal parenchymal calcium deposits be caused by?

A

Ischemia, necrosis, or hypercalcemic states

102
Q

What is a DDx of renal parenchymal calcium deposits?

A

Medullary sponge kidney

103
Q

What is the sonographic appearance of renal parenchymal calcium deposits?

A

Increased cortical echogenicity with echogenic pyramids or wall of pyramids

104
Q

What is thought to be a possible precursor to development of renal stones?

A

Anderson-Carr Kidney

105
Q

What is Anderson-Carr kidney?

A

High concentration of calcium in fluid around tubules

106
Q

High concentration of calcium in the fluid around the tubules of Anderson-Carr kidney results in what?

A

Deposits of calcium in the margins of the medulla

107
Q

What is the sonographic appearance of Anderson-Carr kidney?

A

Non-shadowing echogenic rims of renal pyramids

108
Q

What is medical renal disease?

A

Disease affecting renal parenchyma diffusively and bilaterally

109
Q

What does medical renal disease describe?

A

Poorly functioning but unobstructed kidneys

110
Q

What is the sonographic appearance of acute medical renal disease?

A

Increase in cortex echogenicity, prominent CM junction, enlarged kidneys

111
Q

When would the CM junction not be defined with acute medical renal disease?

A

If the pyramids are affected

112
Q

What is the sonographic appearance of chronic medical renal disease?

A

Small, echogenic kidneys

113
Q

What are the causes of medical renal disease?

A

Acute tubular necrosis, acute cortical necrosis, acute glomerulonephritis, amyloidosis, diabetes mellitus

114
Q

What is the most common cause of acute reversible renal failure?

A

Acute tubular necrosis

115
Q

Acute tubular necrosis can be the result of what?

A

Toxic or ischemic insults

116
Q

What is the sonographic appearance of acute tubular necrosis?

A

Bilaterally enlarged with echogenic pyramids and an RI >0.75

117
Q

What is a considered to be a rare cause of medical renal failure?

A

Acute cortical necrosis

118
Q

What is acute cortical necrosis?

A

Ischemic necrosis of the cortex with sparing of the pyramids

119
Q

How would acute cortical necrosis appear on ultrasound?

A

Initially normal, more hypoechoic cortex with loss of CM junction. Kidneys become atrophied over time and cortex calcifies

120
Q

What is an an autoimmune reaction that causes medical renal disease?

A

Acute glomerulonephritis

121
Q

What are the three patient presentations of someone with acute glomerulonephritis?

A

Hematuria, hypertension, azotemia

122
Q

Describe the sonographic appearance of acute glomerulonephritis

A

Early stages are variable. Later stages show small, echogenic kidneys

123
Q

What is amyloidosis?

A

Systemic metabolic disorder resulting in amyloid deposits in the kidneys

124
Q

How does amyloidosis occur sonographically?

A

Variable (large, normal, small, hypo or hyper)

125
Q

What is the most common cause of chronic renal failure?

A

Diabetes mellitus

126
Q

Explain the sonographic appearance of diabetes mellitus:

A

Enlarged kidneys initially, end stage shows small, echogenic kidneys with loss of CMJ

127
Q

What is renal failure?

A

Inability of kidneys to remove metabolites from blood?

128
Q

What does renal failure result in?

A

Azotemia

129
Q

What is azotemia?

A

Overload of urea and nitrogenous wastes in the blood

130
Q

What 3 things does renal failure cause?

A

Pre-renal, renal, and post-renal

131
Q

What is pre-renal failure?

A

Sepsis, renal artery stenosis

132
Q

What is renal failure characterized by?

A

Parenchyma disease

133
Q

What is post-renal failure?

A

Obstruction of collecting system

134
Q

The obstruction of the collecting system in post-renal failure is further categorized into what?

A

Complete and incomplete obstruction/

135
Q

What is complete obstruction in post-renal failure?

A

Irreversible damage in 3 weeks

136
Q

What is incomplete obstruction in post-renal failure?

A

Irreversible damage in 3 months

137
Q

Which stage of renal failure is reversible? Irreversible?

A

Acute stage is reversible, chronic stage is irreversable

138
Q

What is the sonographic appearance of acute renal failure?

A

Possibly enlarged, hypoechoic kidneys

139
Q

What is the sonographic appearance of chronic renal failure?

A

Small kidneys with an echogenic cortex

140
Q

What is the most common cause of chronic renal failure?

A

Diabetes mellitus

141
Q

What lab value is most commonly increased with renal failure?

A

Serum creatinine

142
Q

What are examples of hyperadrenalism?

A

Cushing’s syndrome, Conn’s disease, and MEN

143
Q

What is Cushing’s syndrome?

A

Result of excess secretion of cortisol

144
Q

What is the clinical presentation of someone with Cushing’s syndrome?

A

Moon face, buffalo hump, truncal obesity, hirsutism, amenorrhea, and hypertension

145
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A

The disease is due to a pituitary adenoma

146
Q

What is Conn’s disease?

A

Excess aldosterone secretion

147
Q

What is the most common cause of Conn’s disease?

A

An aldosteronoma

148
Q

What is the clinical presentation of someone with Conn’s disease?

A

Hypernatremia, hypokalemia, hypertension, muscle cramps, and altered renal function

149
Q

What is MEN?

A

Where tumors develop in several endocrine glands

150
Q

Which type of MEN is malignant?

A

Type 2

151
Q

What is hypoadrenalism due to?

A

Primary disorders of the adrenal cortex or disorders of the hypothalamus or pituitary

152
Q

What are examples of hypoadrenalism?

A

Addison’s disease and Waterhouse-Friderichsen

153
Q

What are the two different causes of Addison’s disease? Which is more common?

A

Autoimmune and tuberculosis. Autoimmune at 80%

154
Q

Waterhouse-Frederichsen syndrome is an example of what kind of hypoadrenalism?

A

Acute

155
Q

What does Waterhouse-Frederichsen syndrome result in?

A

Massive destruction of adrenals