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303 MEDIMAGE > 6. Contrast media I: general imaging and CT > Flashcards

6. Contrast media I: general imaging and CT Flashcards

1
Q

what does the contrast media do

A

changes density of structures in the body and improves visualisation

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2
Q

what will an ideal contrast agent do

A

provide opacification without altering physiology

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3
Q

what is the atomic number level of positive contrast media

A

high atomic number

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4
Q

what is the atomic number level of negative contrast media

A

low atomic number

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5
Q

what does positive contrast media do to the opacity

A

increases opacity

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6
Q

what does negative contrast media do to the opacity

A

decreases opacity

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7
Q

what are 2 examples of positive contrast media

A

iodine and barium

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8
Q

what are 2 examples of negative contrast media

A

air or CO2

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9
Q

what are the soluble and insoluble positive contrast media

A

iodinated CM = soluble

barium sulphate = insoluble

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10
Q

what is the functional group of all iodinated contrast media - ie what are they all derived from

A

derived from tri-iodinated benzene rings

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11
Q

what are 3 reasons that iodine is used

A

high atomic number for radiopacity

can form soluble compound with low toxicity

suitable for injection into human body

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12
Q

what are the 5 key properties of iodinated CM

A 
iodine conc
osmolality
ionicity
chemical structure
viscosity
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13
Q

what does iodine concentration affect for iodinated CM

A

affects the degree of contrast

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14
Q

the higher the conc of iodine what effect does this have for iodinated CM

what is the pro and con

A 
pro = better opacification
con = higher risk of adverse reactions
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15
Q

higher conc of iodine means what for the osmolality and viscosity

A

higher for both

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16
Q

what does the choice of iodine conc depend on - 2 things

A

patient and type of exam

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17
Q

can ionic agents contain different ratio of iodinated compounds

A

yes

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18
Q

what is osmolality

A

measure of solute particles

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19
Q

what is osmolality expressed as

A

milliosmoles per Kg of water

osm/kg or mOsm/kg

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20
Q

in normal water how does water diffuse

A

in both directions so 0 net movement and volume remains constant

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21
Q

what will a CM administration to water do

A

create a conc difference

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22
Q

what is responsible for the flow of fluids to maintain balance

A

osmotic pressure

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23
Q

what are osmolality and osmolarity measures of

A

solute particles

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24
Q

what is the osmolarity

A

osmalal conc expressed as milliosmoles per L of soln

Osm/L or mOsm/L

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25
Q

what is osmolality based on

A

number of solutes based on weight

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26
Q

what is osmolarity based on

A

number of solutes based on volume

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27
Q

osmolarity is dependent on what

why

A

temperature as body volume is dependent temp

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28
Q

is osmolality dependent on temperature

why

A

no as it is based on mass

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29
Q

what is a osmole

A

one osmole is one gram of molecular weight of osmotically active solute

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30
Q

what is the tonicity related to

A

the impact of the osmolality of a soln on the surrounding cells

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31
Q

what is the osmolality of a isotonic soln relative to blood

what impact does this have on surrounding cells

A

similar

no impact on surrounding cells

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32
Q

what is the osmolality of a hypertonic soln relative to blood

what impact does this have on surrounding cells

A

higher than blood

water is drawn out of the cells

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33
Q

what is the osmolality of a hypotonic soln relative to blood

what impact does this have on surrounding cells

A

lower than blood

water is taken into cells

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34
Q

what are the 3 groups of osmolality CM can be classified into

A

high, low and iso-osmolar

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35
Q

what is the mOsm/kg of high osmolar CM

A

> 1400mOsm/kg

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36
Q

what is the mOsm/kg of low osmolar CM

A

780-800mOsm/kg

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37
Q

what is the mOsm/kg of iso-osmolar CM

A

290mOsm/kg

similar to plasma

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38
Q

most ICM are what osmolar

A

hyperosmolar

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39
Q

high osmolality have what effects on reactions

A

high reactions

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40
Q

what kind of osmolality of CM has better tolerance

A

closer the osmolality of CM to body fluid

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41
Q

tolerability and safety improves with ___/___-osmolar agents

A

low/iso-osmolar

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42
Q

what will hyperosmolar iodinated CM do to the water movement in the body

A

Iodinated CM are hyperosmolar in relation to blood so administration will cause movement of water into vascular compartment so water is pulled from tissues into vasculature leading to expansion of blood volume

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43
Q

what are the vascular effects of injection of hyperosmolar ICM in terms of plasma osmolality and water movement

A

increases plasma osmolality and water moves out from cells and extracellular spaces

fluid from cells in interstitial space to move into vascular lumen and dilutes the osmotically active particles

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44
Q

what are the vascular effects of injection of hyperosmolar ICM in terms of haematocrit and plasma volume

A

decrease in both

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45
Q

why does the plasma volume decrease after injection of hyperosmolar ICM

A

due to rapid clearance of ICM and diuretic effect of hyperosmolality on the kidney

Urine becomes hyperosmolar when CM is excreted into it so Promote production of urine = diuretic effect

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46
Q

what does hemodilution do to blood electrolytes

A

transient decrease in blood electrolytes

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47
Q

what are the 4 vascular effects of ICM

A

haemodilution
increase in blood viscosity
peripheral arterial vasodilation
vasodilation

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48
Q

what does peripheral arterial vasodilation from ICM lead to

A

transient hypotension

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49
Q

what does vasodilation from ICM lead to in terms of intravascular volume and CO

A

increase in both

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50
Q

how can IV injection of hyperosmolar fluids temp disrupt the BBB

A

impair the BBB impermeability

transient reversible opening of intracellular junctions

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51
Q

how much damage to the endothelial cells does low osmolality CM cause compared to HOCM

A

less damage

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52
Q

how does HOCM damage endothelial cells

A

water loss = shrinkage and damage

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53
Q

what aspect of ICM interaction with BBB can explain some adverse clinical symptoms

A

direct contact with CM and areas that lack BBB

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54
Q

what are 6 effects of hyperosmolality

A 
sensation of heat/discomfort
endothelium damage
BBB damage
renal damage
thrombosis and thrombophlebitis
disturbance of electrolyte balance in small children
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55
Q

how does hypo osmolality lead to thrombosis and thrombophlebitis

A

Hypoosmolality CM can lead to hypo tension and hyper viscosity of blood which can predispose patients to thrombosis and thrombophlebitis

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56
Q

how does hypo osmolality lead to renal damage

A

Osmotic shift between intra and extravascular compartments can lead to renal damage

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57
Q

how does hypo osmolality lead to vasovagal reaction

A

If the hypo osmolar CM is injected into carotid arteries can result in intra arterial osmotic pressure changes that can stimulate receptors involved in vascular homeostasis such as baroreceptors and chemoreceptors and these can lead to a vasovagal reaction resulting in hypotension and bradycardia

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58
Q

what is ionicity about

A

molecules break up or dissociate into positive cations and negative anions (charged)

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59
Q

what osmolality are ionic CM

A

higher osmolality

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60
Q

what osmolality are non ionic CM

A

lower osmolality

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61
Q

do ionic or non ionic CM dissociate

A

ionic = yes dissociate in soln

non ionic = no its soluble but remain as one particle in soln

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62
Q

what is the pro and con of meglumine salts compared to sodium salts

A

meglumine has better solubility but has higher viscosity

63
Q

what is the difference between a monomer and a dimer

A

monomer is one benzene ring

dimer is 2 benzene rings

64
Q

what is the ratio equation for iodinated CM

A

ratio = number of iodine atoms/number of particles

65
Q

what is ratio 1.5 media like in terms of structure and dissociation

A

ionic monomer dissociates to form cation and anion

66
Q

what is ratio 3 media like in terms of structure and dissociation

2 options

A

ionic dimer dissociates to form cation and anion

non ionic monomer

67
Q

what is ratio 6 media like in terms of structure and dissociation

A

non ionic dimer

68
Q

what is viscosity

A

measure of fluidity of a soln

69
Q

what is the unit for viscosity

A

milipascal second (mPa.s)

70
Q

what does high viscosity mean in terms of contrast

A

thicker contrast

71
Q

what can thicker high viscosity contrast do to the body and what does it mean for the delivery of the CM (3 things)

A

cause friction and resistance when it travels through the body

more pressure needed to deliver CM
injection can cause discomfort
lower rate of flow so needs longer infusion times

72
Q

what viscosity allows the use of rapid bolus

A

low viscosity

73
Q

how does increasing iodine conc influence the viscosity

A

increases viscosity

74
Q

how does the size of the molecule influence the viscosity

A

larger molecules have higher viscosity

75
Q

how does the temperature influence the viscosity

A

increase temp means lower viscosity

76
Q

what are 2 advantages of using intra arterial CM delivery for digital subtraction angiography

A

allows a lower total dose of CM = less haemodilation

advantageous for patients with poor CO

77
Q

why does using intra arterial CM delivery for digital subtraction angiography allow for lwoer total dose

A

due to difference of distribution of CM when injected into arteries and veins

78
Q

what does the amount of CM depend on for enteral administration

A

size of patient and site of examination

79
Q

what is an advantage of using enteral administration

A

poor absorption in GI tract so less toxic effects

80
Q

what is intra thecal CM delivery used for

A

looking at spinal canal - myelographic exam

81
Q

what type of contrast media can result in serious adverse reactions if given intra thecally for a myelographic exam

A

hyperosmolar ionic contrast

82
Q

why does patient movement need to be limited in intra thecal myelographic exam

A

to prevent mixing of CM with CSF

83
Q

intrathecal injections are absorbed from where to where

how does this impact the way its excreted

A

from CSF to blood stream

excreted in same way as IV CM

84
Q

why is active manipulation required for direct CM injections in arthrography

A

to disperse the CM throughout the joint space

85
Q

how is contrast injection different from IV injection

A

contrast is not rapidly cleared by kidneys as it is absorbed slowly back by kidneys

86
Q

what is the difference between hepatobiliary CM and ECF CM

A

low water solubility than ECf CM and higher plasma protein binding

87
Q

where does the hepatobiliary CM distribute to in hepatocytes

A

ECF and intracellularly

88
Q

what is the 2 ways of excreting hepatobiliary CM and which is the main method

A

biliary = main

renal

89
Q

how does the hepatobiliary CM differ from ECF CM in terms of PK variability

what are the 2 reasons for this

A

PK varies more for hepatobiliary CM

plasma protein binding and hepatobiliary CM is cleared by biliary system so is dependent on liver blood flow

90
Q

what is the PK of ICM distribution in terms of plasma protein binding level and what kind of ICM they are

A

are ECF ICM and is very low in PPbinding

91
Q

what does poor lipid solubility for ICM mean for its distribution

A

limited distribution to intracellular compartments

92
Q

why does ICM’s poor lipid solubility cause it to have limited distribution to intracellular compartments

3 things

A

poor permeability across all membranes

BBB tight endothelial junctions prevent distribution into normal CNS

pathological tissues may be more permeable

93
Q

what 2 factors influence the intensity and timing of the contrast enhancement

A

rate and extent of the distribution of CM

94
Q

ICM is primarily eliminated by what

A

the kidneys

95
Q

does ICM undergo metabolism

A

not really, its negligible

96
Q

with normal renal function how fast is ICM excreted

A

all of ICM dose is excreted within 24hrs

97
Q

what is the elimination half life in normal renal function for ICM

what about renal impairment

A

1.5-2h

renal impairment = prolonged and can take up to several days

98
Q

what might be observed in renal impairment for the routes of elimination

A

increased elimination via hepatic biliary duct

99
Q

in renal impairment excretion of ICM what might you see in the image that is different from normal renal function excretion

A

Much lower opacification in kidney as more will be eliminated by biliary and Gi tract so those areas are more

100
Q

what is the 2 compartment model of ICM excretion

A

IV injection into vascular compartment/plasma has quick exchange with extravascular compartment

it also has slow excretion into urine

see 2 distinct phases in conc time profile

101
Q

what is the eGFR

A

used to identify severely impaired renal function

102
Q

what are the 3 categories of ICM adverse reactions

A

acute vs delayed
idiosyncratic vs chemotoxic
renal vs non renal

103
Q

when do ICM acute adverse reactions occur

A

<1hr of contrast media administration

104
Q

what is idiosyncratic adverse reactions

A

method not well understood but its not dose related so increasing conc will not affect it

105
Q

what is chemo toxic adverse reaction

A

related to CM dose and result from CM disrupting homeostasis

106
Q

what are 3 patient related risk factors for acute reactions

A

hx of reaction to ICM
asthma
hypersensitivity

107
Q

what are 2 contrast medium related risk factors for acute reactions

A

osmolality and iconicity

108
Q

which types of CM increase risk of acute adverse reactions in terms of osmolality and iconicity

A

HOCM>LOCM & IOCM

ionic > non ionic CM

109
Q

when do delayed adverse reactions occur

A

1h to 1wk after contrast media administration

110
Q

what are 2 risk factors for delayed adverse reactions

A

previous late reaction to CM

IL2 treatment

111
Q

what is contrast induced encephalopathy

A

acute and reversible neurological deficit

112
Q

what are 3 symptoms of CIE

A

transient cortical blindness
transient global amnesia
epilepsy

113
Q

what kinds of CM have higher incidence of CIE

A

high osmolality > LOCM

114
Q

what is the pathogenesis of CIE

A

BBB suspected involved

high conc of CM can increase BBB permeability causing osmotic pressure changes leading to cerebral edema

115
Q

how do HOCM affect CIE

A

hyperosmolality can cause hemodynamic changes which can aggravate cerebral vasospasm

116
Q

what is contrast induced acute kidney injury

A

abrupt decline in renal function

117
Q

what is the serum creatine level change associated with CI-AKI

A

relative increase of serum creatinine >25% from baseline or rise in serum creatinine within 3 days of exposure to CM

118
Q

what are the 4 things that ICM can affect that lead to adverse reactions

A

cytotoxicity and oxidative stress
hyperosmolality
viscosity
RBC deformity

119
Q

how does ICM induced cytotoxicity and oxidative stress cause injury

2 ways

A

tubular epithelial cells undergo tubular dysfunction

endothelial cells can undergo dysfunction and vasoconstriction

120
Q

how does ICM induced hyperosmolality cause injury

A

intra renal hemodynamic changes

121
Q

how does ICM induced viscosity cause injury

A

intra renal hemodynamic changes

122
Q

what is the final result of all factors of ICM induced acute kidney injury

A

hypoxia, ischemia, tubular necrosis

123
Q

what are 5 CI-AKI risk factors related to patients

A 
preexisting renal dysfunction 
increased age
diabetes mellitus
dehydration
poor renal perfusion
124
Q

is metformin nephrotoxic

A

no

125
Q

are there direct drug drug interactions between metformin and ICM

A

no

126
Q

what % of metformin is excreted unchanged in 24hrs and in form are they excreted

A

90% excreted renally and unchanged form

127
Q

what 3 factors increasing and decreasing can increase the risk of lactic acidosis

A

factors that decrease metformin excretion
factors decreasing metabolism of lactate
factors increasing blood lactate levels

128
Q

what should patients with low eGFR or with AKI do with metformin before procedure

and when should metformin be restarted

A

stop taking metformin for 48hrs

restarted if renal function has returned to normal

129
Q

what are 4 CI-AKI CM related risk factors

A

high osmolality
high viscosity
high injection volume
multiple injections within 3 days

130
Q

what can ICM do to clotting time

A

prolong clotting time

131
Q

does ionic or non ionic agents interact with drugs and can precipitate

A

ionic agent can precipitate but not an issue with non ionic

132
Q

what is extravasation

A

accidental release of injected soln from vein into surrounding tissues

133
Q

what is air embolism

A

blood vessel blockage due to air bubbles in the circulatory system

134
Q

what are 3 patient related risk factors for extravasation

A

inability to communicate
fragile or damage veins
obesity

135
Q

what are 3 CM related risk factors for extravasation

A

high osmolar contrast media
high viscosity contrast media
injecting large volume

136
Q

what are technique related risk factors for extravasation

A

power injector

lower limbs and small distal veins

137
Q

what can IV administration of CM do in pregnancy

A

ICM can cross the placenta and enter foetal circulation

138
Q

why is osmolality of CM in pediatrics important

A

as they are more susceptible to fluid shift
lower tolerance for intravascular osmotic loads

injection of hyperosmolar agents can lead to blood volume expansion and there if there is a large fluid shift then it may lead to cardiac fail and pulmonary edema

139
Q

why is viscosity of CM in pediatrics important

A

small gauge angiocatheters in very small blood vessels and there is risk of blood vessel injry

140
Q

what are 3 things that we need to keep in mind when using CM for the pediatric population

A

small volumes of CM used
injection site monitored for extravasation
slower injection rate to prolong intravascular acquisition

141
Q

what are 4 medical considerations for ICM

A

thyroid disease
myasthenia gravis
phaeochromocytoma
sickle cells disease

142
Q

why is thyroid disease a medical considerations for ICM

A

increases risk of developing thyrotoxicosis

143
Q

why is myasthenia gravis a medical considerations for ICM

A

breathing difficulty may worsen with ICM

144
Q

why is phaeochromocytoma a medical considerations for ICM

A

injection of ICM into adrenal or renal arteries/veins may precipitate a hypertensive crisis

145
Q

why is sickle cell disease a medical considerations for ICM

A

high osmolality may induce osmotic shrinkage of RBC and may exacerbate sickle cells

146
Q

what is the use of barium sulfate

A

imaging procedures of the GI tract

147
Q

what is a non iodinated CM

A

barium sulfate

148
Q

what is the route of administration for barium sulfate

A

only oral or rectal routes

149
Q

what is oral admin of barium sulfate used to visualise

A

oesophagus and stomach or small intestine

150
Q

what is rectal admin of barium sulfate used to visualise

A

rectum and colon

151
Q

is bariums sulfate absorbed in the normal GI tract

A

not absorbed

152
Q

is bariums sulfate distributed widely in the body or is it limited to one area

A

limited to GI lumen

153
Q

is bariums sulfate metabolised

A

no

154
Q

how is bariums sulfate excreted

A

excreted unchanged in faeces

303 MEDIMAGE (14 decks)

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