Module 4 : Metabolic Disease Flashcards

1
Q

what is a metabolic disease

A
  • an abnormality that occurs globally and affects severe organs
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2
Q

what is hepatocellular disease and why does it occur

A
  • dysfunction of hepatocytes

- normal liver tissue is replaced with fat or fibrosis

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3
Q

is hepatocellular disease focal or diffuse

A
  • usually diffuse process
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4
Q

what lab tests will be abnormal with hepatocellular disease

A
  • LFTs
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5
Q

what physical aspect of the liver is usually affected by hepatocellular disease

A
  • the liver size
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6
Q

what are two types of hepatocellular disease

A
  • fatty infiltration

- cirrhosis

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7
Q

what is fatty infiltration

focal or diffuse?

A
  • accumulation triglycerides (fat) in hepatocytes
    + precursor to significant chronic disease
  • not always uniform throughout the liver
    diffuse or focal
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8
Q

what is another name for fatty infiltration

A
  • steatosis
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9
Q

what is steatosis

A
  • fat accumulation within hepatocytes
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10
Q

is fatty infiltration developmental or acquired, reversible or permanent?

A
  • aquired
  • reversible
    + life style change required
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11
Q

2 most common causes of fatty infiltration

A
  • alcohol abuse

- obesity

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12
Q

what 4 things do we look for when assessing for fatty infiltration

A
  • echogenicity changes
  • echo texture changes
  • attenuation characteristics
  • ability to visualize vessels (paucity)
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13
Q

what 3 machine factors are important to consider when assessing fatty infiltration

A
  • gains
  • TGC
  • focus
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14
Q

sonographic appearance of mild (grade 1) fatty infiltration

A
  • slight increase in liver echogenicity

- diaphragm and vessels clearly defined

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15
Q

sonographic appearance of moderate (grade 2) fatty infiltration

A
  • increase in liver echogenicity

- vessels and diaphragm not sharply

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16
Q

sonographic appearance of severe(grade 3) fatty infiltration

A
  • liver echogenicity is increased markedly

- extremely difficulty to define diaphragm and vessel walls

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17
Q

what are the two types of focal fatty changes

A
  • focal fatty infiltration

- focal fatty sparring

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18
Q

what is focal fatty infiltration

A
  • focal areas of increased echogenicity
    + fatty deposits
  • mostly normal liver parenchyma
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19
Q

what is focal fatty sparring

A
  • majority of liver parenchyma has experienced fatty infiltration
  • focal hypo echoic areas (normal liver tissue)
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20
Q

what are 4 similarities between fatty sparring and fatty infiltration

A
  • both commonly involve the periportal area of the medial LL (segment 4)
  • no mass effect
  • rapid change with time
  • map like boundaries (LINEAR vs round)
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21
Q

what 3 lab values could be elevated with fatty infiltration

A
  • ALT
  • AST
  • if related to alcohol abuse then GGT
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22
Q

what is cirrhosis and what does it result in

A
  • a diffuse process that destroys the liver cells

- resulting in fibrosis with nodule changes

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23
Q

what are the underlying causes of cirrhosis

A
  • alcohol abuse
  • chronic viral hepatitis
  • primary sclerosing cholangitis
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24
Q

what is the most common underlying cause of cirrhosis

A
  • alcohol abuse
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25
Q

what is the progressive change that occurs in liver cells with cirrhosis

A
  • cell death» fibrosis» regeneration
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26
Q

is cirrhosis reversible

A
  • no
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27
Q

what are the two types of nodular change

A
  • micronodular

- macro nodular

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28
Q

what causes micro nodular cirrhotic change

A
  • alcohol consumption
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29
Q

what causes macro nodular cirrhotic change

A
  • chronic viral hepatits
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30
Q

what is the sonographic appearance of acute cirrhosis

A
  • same as severe fatty infiltration
  • enlarged liver
  • textural changes
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31
Q

what is the sonographic appearance of chronic cirrhosis

A
  • small liver (CL/RL >0.65)
  • course echo texture
  • nodular surface
  • paucity of vessels
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32
Q

what does paucity mean

A
  • poor ability to see vessels
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33
Q

what does chronic cirrhosis eventually lead to

A
  • portal hypertension&raquo_space; end stage liver failure
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34
Q

what associated abnormality is commonly seen with cirrhosis

A
  • ascites quite common
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35
Q

what do the lab value levels for cirrhosis depend on

A
  • stage of disease
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36
Q

which 6 lab values will be increased with cirrhosis

A
  • AST
  • ALT
  • LDH
  • ALP
  • bilirubin (conjugated)
  • GGT
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37
Q

what lab value will be decreased with cirrhosis

A
  • serum albumin
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38
Q

what other organ is affected by liver cirrhosis and why

A
  • the spleen due to portal hypertension
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39
Q

what are the 3 classic clinical presentation of patients with cirrhosis

A
  • hepatomegaly
  • jaundice
  • ascites
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40
Q

what are three less common clinical presentations of cirrhosis

A
  • diarrhea
  • feeling of fullness
  • weight loss
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41
Q

what is glycogen storage disease and what causes it

A
  • autosomal recessive disorder

- excess glycogen deposits in the hepatocytes

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42
Q

what is another name for glycogen storage disease

A
  • GSD

- Von Gierkes disease

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43
Q

what 2 other abnormalities is GSD associated with

A
  • benign adenomas and HCC
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44
Q

does GSD begin in adults ?

A
  • no begins neonatally
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45
Q

how is GSD managed

A
  • controlled and monitored diet
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46
Q

sonographic appearance of GSD

A
  • diffuse fatty infiltration (cannot differentiate between causes)
  • adenomas = solid masses with variable echogenicity
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47
Q

what is the only metabolic disease of the peritoneum

A
  • ascites
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48
Q

what is ascites

A
  • accumulation of serous fluid in the peritoneal cavity
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49
Q

what are the two types of fluid in ascites

A
  • transudate

- exudate

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50
Q

what is transudate fluid

A
  • contains little protein or cells

- suggests a non inflammatory response

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51
Q

two non inflammatory responses causing ascites

A
  • cirrhosis

- CHF

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52
Q

sonographic appearance of transudate ascites

A
  • anechoic fluid
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53
Q

what is exudate fluid

A
  • high protein content
  • blood, pus, chylous
  • suggests an inflammatory or malignant cause
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54
Q

what is chylous

A
  • milky fluid with a high fat content

- usually from lymphatic system

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55
Q

sonographic appearance of exudate ascites

A
  • internal echoes
  • echogenic
  • locations
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56
Q

characteristics of free fluid in peritoneum

A
  • changes with patient position

- conforms to surrounding organs

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57
Q

characteristics of loculated fluid in peritoneum

A
  • no change with movement
  • rounded margins
  • mass effect
  • walled off
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58
Q

what are the three most dependant spaces in the peritoneal cavity

A
  • Morrisons pouch (rt kidney and liver)
  • pouch of Douglas (uterus and rectum)
  • parabolic gutters
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59
Q

what is biliary sludge and what is it a precursor to

A
  • a mixture of particulate matter and bile

- precursor to biliary disease

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60
Q

2 other names for biliary sludge

A
  • biliary sand

- microlithiasis

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61
Q

symptoms of biliary sand

A
  • asymptomatic

- biliary colic and infmallation of GB and panc

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62
Q

can biliary sludge resolve on its own

A
  • yes
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63
Q

what is the most likely cause of biliary sand

A
  • bile stasis
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64
Q

what are 4 causes of bile stasis

A
  • prolonged fasting
  • rapid weight loss
  • TPN (total parenteral nutrition IV food)
  • extra hepatic biliary obstruction
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65
Q

what is the sonographic appearance of biliary sand

A
  • no shadowing
  • homogeneous low level echoes
  • layers in the dependant portion of the gallbladder
    + fluid-fluid levels
  • moves with change in patient position
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66
Q

what are tumefactive sludge/ sludge balls

A
  • sludge that mimic polypoid tumors

- to differentiate look at vascularity, mobility, and GB wall thickness

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67
Q

what is hepatization

A
  • when sludge has sam echogenicity of liver

- camouflages the GB

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68
Q

what is pseudo sludge

A
  • imaging artifact
  • caused by excessive gains, slice thickness or side lobe artifact
  • idependent of gravity
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69
Q

what is empyema

A
  • presence of pus in bile
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70
Q

what is hemobilia

A
  • presence of blood in bile

- usually due to liver biopsy and percutaneous biliary procedures

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71
Q

what is milk of calcium / limey bile

A
  • rare
  • separate category from biliary sludge
  • GB becomes filled with semi solid substance (calcium carbonate)
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72
Q

sonographic appearance of milk of calcium / limey bile

A
  • highly echogenic with posterior shadowing
  • changes with patient position
  • forms calcium/bile fluid level
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73
Q

what is cholelithiasis / gallstones

A
  • most common disease of the gallbladder
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74
Q

what 3 factors affect gallstone formation

A
  • abnormal bile composition
  • stasis of bile
  • infection
75
Q

3 different compositions of stone

A
  • cholesterol (most common)
  • bilirubin (pigment stone)
  • calcium
76
Q

what are the 5 F risk factors with gallstone

A
  • female
  • forty
  • fatty
  • fertile
  • family history
77
Q

what is the clinical presentation of gallstones

A
  • asymptomatic
  • RUQ pain (after meals) radiates to back
  • nausea and vomitting
  • belching
78
Q

sonographic appearance of gallstones

A
  • echogenic focus
  • posterior shadowing
  • MOBILITY
  • may float in the bile
79
Q

what size should stones being to shadow in GB

A
  • > 5mm
80
Q

what is the WES sonographic sign

A
  • Wall > Echo > Shadow

- seen when gallbladder is filled with multiple stones or one large stone

81
Q

what lab values will be altered with GB stones

A
  • AST
  • ALT
  • ALP
  • BILIRUBIN
82
Q

what 3 things in the gallbladder also cause shadowing

A
  • valves of heister
  • fat of portahepatis
  • duodenal gas
83
Q

5 complications of gall stones

A
  • biliary colic (MOST COMMON)
  • obstruction of cystic duct or CBD
    + leads to GB hydrops
  • bacterial infection
  • cholecystitis
  • ascending cholangitis
84
Q

what 3 questions should an US investigation of biliary obstruction try to answer

A
  • are the bile ducts or GB dilated
  • if yes, to what extent
  • if no , what is the cause
85
Q

what are the 3 causes of biliary dilation

A
  • obstruction (MOST COMMON)
    + stone, tumor
  • loss of duct wall elasticity
  • ampulla of vater dysfunction
86
Q

is biliary dilation intra or extrahepatic

A

both

87
Q

2 clinical presentation of biliary obstruction

A
  • painless jaundice

- painful jaundice

88
Q

what is painless jaundice indicative of

A
  • neoplastic conditions (panc head)

- choledochal cysts

89
Q

what is painful jaundice idicitve of

A
  • acute obstruction

- infection of biliary tree

90
Q

4 signs and symptoms of biliary obstruction

A
  • jaundice
  • clay coloured stools
  • abnormal LFTs
  • pain, nausea
91
Q

what is choledochallithiasis (intra or extra hepatic)

A
  • stones in biliary tree
92
Q

what is the secondary causes to biliary stones

A
  • stones pass from gallbladder to ducts

+ MOST COMMON

93
Q

what are the 4 primary causes to biliary stones

A
  • inflammation
  • infection
  • carolis disease
  • prior surgery
94
Q

what is the most common location for stones in biliary tree

A
  • distal CBD at ampulla of vater
    + difficult to visualize due to bowel gas
    + look for hyperchoic foci with shadowing
    + false positives = air, surgical clips, edge artifact
95
Q

what lab values will be abnormal with biliary obstruction

A
  • ALP
  • AST
  • ALT
  • bilirubin
96
Q

what is treatment of biliary obstruction

A
  • ERCP spincterotomy
  • ERCP extraction
  • stenting
97
Q

what is ERCP

A
  • endoscopic retrograde cholangiopacreatography

+ put endoscopic through esophagus into duodenum to open up ampulla of vater

98
Q

definition of urolithiasis

A
  • stones in urinary system
99
Q

definition of nephrolithiasis

A
  • stones in the renal collection system
100
Q

defintion of nephrocalcinosis

A
  • calcifications in the renal parenchyma
101
Q

is nephrolithiasis common or uncommon

A
  • very common

- caucasian males

102
Q

does it increase or decrease with age

A
  • increase with age
103
Q

what are 4 underlying risk factors for getting nephrolithiasis

A
  • hereditary
  • limited water intake
  • high animal protein diet
  • urinary stasis
104
Q

can stones move through the collecting system

A
  • yes

- can lodge in the natural narrowing of the ureter

105
Q

what are the three natural narrowings of the ureter

A
  • just past UPJ (ureteropelvic junction)
  • at the iliac vessels
  • at the UVJ (most common) (ureterovesicular junction)
106
Q

what must the size of stone be in order to be able to pass

A

< 5mm

107
Q

clinical presentation of nephrolithiasis

A
  • asymptomatic
  • hematuria (microscopic or gross)
  • flank pain
108
Q

what is the sonographic appearance of kidney stones

A
  • echogenic focus
  • posterior shadowing
  • twinkle artifact
109
Q

what 5 things should you asses for the rad

A
  • number
  • size
  • location
  • complications
110
Q

what is stag horn calculi

A
  • calcification filling the collecting system

+ an entire major or minor calyc

111
Q

what are 5 things that can cause false positives

A
  • intrarenal gas
  • renal artery calcification
  • calcified sloughed papilla
  • calcified tumors
  • ureteric jet
112
Q

what are 3 other imaging modalities that can detect urolithiasis

A
  • x ray
  • tomography
  • CT
113
Q

characteristics of stones in ureter

A
  • location creates imaging problems
  • stones lode at narrowest point
  • look for dilated tubes
  • identify echogenic foci with shadowing at distal end
114
Q

characteristics of bladder calculi

A
  • usually single
  • asymptomatic
  • may migrate from kidney or be result of urinary stasis (neurogenic bladder or BPH)
  • patient may present with hematuria and pain
  • check for mobility to dependant portion of bladder
115
Q

what is hydronephrosis

A
  • dilated renal vessels
  • due to obstructive or non obstructive causes
  • may lead to renal atrophy
116
Q

obstructive causes of hydronephrosis

A
  • intrinsic (stone/mass) or extrinsic (mass/aneurysm) obstruction to flow
  • can be diagnosed on ultrasound
117
Q

non obstructive causes of hydronephrosis

A
  • reflux
  • infection
  • polyuria (to much urine production=diabtetes mellitus)
118
Q

three classifications of hydronephrosis

A
  • grade 1 = mild
  • grade 2 = moderate
  • grade 3 = severe
119
Q

grade 1 / mild hydro

A
  • slight separation of renal collecting system

+ 2mm seperation

120
Q

grade 2 / moderate hydro

A
  • anechoic separation of entire central renal sinus
  • pelvis and calyces are dilated
  • clubbed calyces
121
Q

grade 3 / severe hydro

A
  • thinning renal cortex
  • extensive enlargement of renal sinus and calyces
  • loss of individual calyx definition
122
Q

what should we do when we see hydronephrosis

A
  • look for cause of hydro
123
Q

what 4 things could cause false positives for hydro

A
  • over distended bladder
  • extra renal pelvis
  • multiple paraplevic cysts
  • AV malformation
124
Q

what assessment should you always do when you see hydro

A
  • POST VOID
125
Q

what is another name for renal parenchymal calcium deposits

A
  • nephrocalcinosis
126
Q

can renal parenchymal calcium deposits be bilateral or unilateral, cortical or medullary

A
  • yes they can be both
127
Q

what are 3 things renal parenchymal calcium deposits caused by

A
  • ischemia
  • necrosis
  • hypercalcemic states
128
Q

what other disease is hard to differentiate between renal parenchymal calcium deposits

A
  • medullary sponge kidneys
129
Q

sonographic appearance of renal parenchymal calcium deposits

A
  • increased cortical echogenicity
  • echogenic pyramids or wall of pyramids
  • possible shadowing
130
Q

characteristics of Anderson-Carr kidney

A
  • theory of stone progression
  • high concentration of calcium in fluid (early development of stone)
  • results in deposits of calcium in margins of the medulla
131
Q

sonographic appearance of Anderson-Carr kidney

A
  • non shadowing echogenic rims of renal pyramids
132
Q

what is medical renal disease

A
  • disease affecting renal parenchyma diffusely and bilaterally (always both)
    + cortex
    + medulla
  • broad term used to describe renal disorders
  • describes poorly functioning but unobstructed kidneys
  • can lead to renal failure
133
Q

what is needed to identify cause of medical renal disease

A
  • renal biopsy
134
Q

what is the treatment of medical renal disease

A
  • initially treatable by medication rather than surgery
135
Q

5 areas to evaluate sonographically with medical renal disease

A
  • renal size and contour
  • cortical echogenicity
  • CM junction distinction
  • renal pyramids
  • renal sinus
136
Q

what lab value will be increased with medical renal disease and why

A
  • creatinine
  • sent for US as initial screening
  • purpose of US is to check for a mechanical obstruction.. if there is no obstruction this indicates a renal parenchymal abnormality
137
Q

sonographic appearance of medical renal disease

A
  • depending on underlying cause

- acute and chronic

138
Q

acute medical renal disease sonographic appearance

A
  • diffuse increase in cortical echogenicity
  • prominent CM junction
    + exception = if the pyramids are affected then CM junction will not be defined
  • enlarged kidneys
  • KIDNEYS MAY APPEAR NORMAL
139
Q

chronic stage medical renal disease sonographic appearance

A
  • small

- echogenic

140
Q

5 causes of medical renal disease

A
  • acute tubular necrosis
  • acute cortical necrosis
  • acute glomerulonephritis
  • amyloidosis
  • diabetes mellitus
141
Q

what is the most common cause of acute reversible renal failure

A
  • acute tubular necrosis
142
Q

what is acute tubular necrosis

A
  • deposits of debris in the renal collecting tubules
  • can have hematuria
  • can be result of toxic or ischemic insults
    + chemotherapy, antibiotics, antifreeze
143
Q

ultrasound appearance of acute tubular necrosis

A
  • kidneys most often appear normal but may be bilaterally enlarged
  • echogenic pyramids
  • RI > 0.75 (abnormal resistance to flow)
144
Q

what is acute cortical necrosis

A
  • rare cause of acute renal failure
  • ischemic encores of the cortex with sparing of the pyramids
  • due to sepsis, burns, severe dehydration PIH (pregnancy induced hypertension)
145
Q

ultrasound appearance of acute cortical necrosis

A
  • initially normal size, hypo echoic cortex and loss of CM junction
  • over time kidneys atrophy and cortex calcifies
146
Q

what is acute glomerulnephritis

A
  • autoimmune reaction
  • patient presentation
    + hematuria, hypertension, azotemia
147
Q

ultrasound appearance of acute glomerulonephritis in early stage

A
  • may be normal or enlarged
  • cortex may be normal , echogenic, or hypo echoic
  • EXTREMELY VARIABLE
148
Q

ultrasound appearance of acute glomerulonephritis in lateraled stage

A
  • small

- echogenic kidneys

149
Q

what is amyloidosis

A
  • systemic metabolic disorder resulting in amyloid (protein) deposits in the kidney
  • patient presents with proteinuria
150
Q

ultrasound appearance of amyloidosis

A
  • variable appearance

+ large, normal, or small kidney size = hypo or hyper

151
Q

diabetes mellitus

A
  • MOST COMMON CAUSE OF CHRONIC RENAL FAILURE
  • initially kidneys will be enlarged
  • end stage = small echogenic, loss of CMJ
152
Q

what is renal failure

A
  • inability of kidneys to remove metabolites from blood
153
Q

what does renal failure result

A
  • azotemia (uremia)
154
Q

what is azotemia

A
  • overload of urea and nitrogenous wastes in the blood
155
Q

three different causes of renal failure

A
  • pre renal
  • renal
  • post renal
156
Q

pre renal causes of renal failure

A
  • sepsis

- renal artery stenosis

157
Q

renal cause of renal failure

A
  • parenchymal disease
158
Q

post renal cause of renal failure

A
  • obstruction of collecting system
    + complete obstruction = irreversible damage in 3 weeks
    + incomplete obstruction = irreversible damage in 3 months
159
Q

acute stage of renal failure

A
  • reversible

- medical renal disease (renal parenchymal disease)

160
Q

sonographic appearance of acute stage renal failure

A
  • most often normal
  • may be enlarged or hypo echoic
  • check for hydronephrosis, obstruction
  • check echogenicity of parenchyma (usually increased)
161
Q

chronic stage of renal failure

A
  • irreversible

- most common cause is diabetes mellitus

162
Q

sonographic appearance of renal failure

A
  • small kidney

- echoegenic cortex

163
Q

what lab values increased

A
  • serum creatinine (most common and most important)
  • BUN
  • Uric acid
  • RBC/WBC in urine
  • protein uria
164
Q

treatment for renal failure

A
  • dialysis or renal transplant
165
Q

what is dialysis

A
  • removes waste from blood

- “artificial kidney”

166
Q

what is a renal transplant

A
  • usually on R sides of pelvis and document nature kidney too
167
Q

3 causes of hyperadrenalism

A
  • cushings syndrome
  • conns disease
  • MEN (multiple endocrine neoplasia)
168
Q

what is cuchsings syndrome a result of

A
  • excess secretion of cortisol
169
Q

what are 4 causes of bushings syndrome

A
  • adrenal hyperplasia
  • adrenal adenoma
  • adrenal carcinoma
  • exogenous corticosteroid administration
170
Q

clinical presentation - of cushings syndrome

A
  • moon face
  • buffalo hump (upper neck/lower back)
  • truncal obesity (eggs on legs)
  • hirsutism
  • amenorrhea
  • hypertension
171
Q

what is the different between cushings syndrome and cuttings disease

A
  • syndrome = due to adrenal abnormality

- disease = due to pituitary adenoma producing too much cortisol

172
Q

what causes conns disease

A
  • excess aldosterone secretion
173
Q

what 3 things causes an excess of aldosterone

A
  • ADENOMA (aldosteronoma)
  • hyperplasia
  • carcinoma (uncommon)
174
Q

clinical presentation of Conns disease

A
  • hypernatremia = increased sodium in blood
  • hypokalemia = decreased potassium
  • hypertension
  • muscle cramps
  • altered renal function
175
Q

sonographic appearance of Conns disease

A
  • small
  • solid
  • round mass
  • hypo echoic
176
Q

MEN (multiple endocrine neoplasia)

A
  • 3 types
  • tumors develop in several endocrine glands
    + adrenal
    + panc
    + pituitary
    + parathyroid gland
  • excessive hormones produced
  • benign or malignant
177
Q

MEN type 2

A
  • autosomal dominant
  • pheochromocytomas in adrenal (usally benign but with MEN its malignant)
  • typically bilateral
  • malignant
178
Q

what is hypoadrenalism

A
  • due to primary disorders of the adrenal cortex or disorders of the hypothalamus or pituitary
  • may cause adrenal atrophy
179
Q

two types of hypoadrenalism

A
  • Addisons disease

- Waterhouse-friderichsen syndrome

180
Q

2 types of Addisons disease

A
  • autoimmune (80%)

- TB (20%)

181
Q

what is Addisons disease

A
  • chronic

- primary hypoadrenalism

182
Q

autoimmune Addisons disease

A
  • females

- not typically identified on ultrasound

183
Q

TB Addisons disease

A
  • males
  • enlarged, firm, nodular adrenals
  • hyperpigmentation
  • low blood pressure, muscle weakness, fatigue
  • 90% of gland is nonfunctioning
184
Q

what is Waterhouse-friderichsen syndrome

A
  • acute hypoadrenalism
  • secondary to hemorrhage, infection
  • massive destruction of adrenals
  • glucocorticoid therapy necessary