Nukes Flashcards
knee jerk for ocreotide scan
hot spleen & kidneys
I-123 vs I-131
- 1-123 lower E (159 keV)–> higher dose –> 24 hr imaging. 1/2 life 13 hrs. no b-emisison. Cardiac & adr act MC.
- I-131 high E (~364)–> crummier images. 1/2 life 8d. b-emission
Tc WBC vs In WBC
- both spleen > liver
- Tc-renal & GI. In does NOT. Higher count –> cleaner
- WBC- lung (<24 hrs)–> GI.
Tracer localization via chemisorption
- Tc-99 Medronate (MDP)
- binds HYDROXYAPATITE
Tracer localization via facilitated diffusion
F-18 FDG
Tracer localization via passive diffusion
T-99 sestamibi, tetrofosmin, HMPAO, ECD.
Tracer localization via secretion
-T-99 IDA, pertechniate
I-123, 131, T99 pertechnetate- mech of transport
I-analog transported via Na/I symported NIS.
K analogues
Thallium, Rb (transplant via Na/K ATP pump)
T-99 sestamibi-how is it transported
lipophilic cation with affinity to negatively charged mitochondria
ECD vs HMPAO
ECD faster clearance from blood pool
preparation bone scan
15-25mCi tracer
img at 2-4 hr (let ST clear)
MDP uptake dep on…
1) OB act (1˚at cortex)
2) blood flow
3) vitD
normal MDP uptake/localization
- bone
- kid, bladder
- breasts,
- ST
ways of getting free Tc
1) no enough Sn
2) air (oxide)
3) H2O–> clumping
Where is free Tc
- stomach
- thyroid
- salivary glad
making a good bone scan in setting of poor renal function
1) oral hydration 2-6 hrs before
2) 4th phase (24 hr delay)-problem=T99 half life is 6hrs
when does “flare phenomenon” occur. Why. How you know it’s flare?
2wk-3 mo
- bone healing
- xray: more sclerotis, start improving at 3 mo
persistent visualization skull sutures on bone scan
renal osteodystrophy
focal breast uptake on bone scan
-cancer
renal cortex hotter than adj lumbar spine on bone scan
hemochromatosis
diffuse renal uptake on bone scan
crx, urinary obstr
Liver uptake on bone scan
1) Al3+ contamination
2) hepatoma, mets
3) amyloidosis
4) liver necrosis
spleen uptake on bone scan
-autoinfarcted spleen
+ scattered hot & cold areas from mult bone infarcts
lung uptake on bone scan
- hetrotopic Ca (dystrophic or mets)-classically OS
- fibrothorax
- 1˚ lung tumor
- radiation change
- sarcoid, berrylliosis
- wegener’s
- alveolar microlithiasis
muscle uptake on bone scan
rhabomyolysis
diffusely decreased skel uptake on bone scan
1) Free Tc
2) bisphos
arterial intravasation on bone scan
arterial–> distal
causes insufficiency sacral fractures
- OP
- radiation
when should bone scan be performed to evaluate for fracture in elderly?
1 wk
AVN dx tests
MRi–> bone scan (if CI or need to image mult bones at once)
Donut sign-AVN femoral head
-hot on outside, cool in inside
AVN appearance on bone scan
dep on timing
- early=normal or cold (via interrupted bs)
- later-hot (at time that radiographs are becoming sclerotic)
hypertrophic osteoarthropathy affects what pt of bone
periosteum
donut sign-tumors
cystic (GCT, ABC, telangiectasia OS)
benign HOT bone lesions
- abc, gct
- oo, ob
- FD
use of PSA in predicting bone mets
<10 ng/ml nearly excludes
>100 highly predictive
MC loc for single metastatic lesion
spine
Mets on a bone scan
1) rarely single (15-20%)
2) super scan
3) MULT, randomly distributed into diff sites
how many dying prostate cancer pts have mets?
85%
which nuc medicine scan is bone uptake always abN
MIBG, 1-131, ocreotide
where does breast bone met usually go
spine
what pt of skeleton does lung cancer met to?
appendicular
which scan is most sup at detecting NB bone met?
MIBI
what pt of bone does NB met to?
metaphysis
what pt of skeleton does osteopokilosis spare?
spine & skull
next step: equivocal lesion on bone scan
plain film- no corresponding lesion=more concerning –> MRI
radiation change on bone scan
- acute (2-3 mo)-warm
- late (~6 mo)-cold. Persistent.
trickery re: bone scan and no kidneys
horseshoe
ways of showing FD on bone scan
- hot mandible
- leg that looks like pagets
superscan causes
1) diffuse mets-breast & prostate
2) metabolic-hyperPTH, renal osteodystrophy, Pagets, thyrotoxicosis
cold lesions on bone scan
1) late radiation change
2) early AVN
3) infarct (very early or late)
4) anaplastic/lytic tumor (renal, thyroid, NB, myeloma)
5) artifact-prosthesis, PM, etc
6) hemangioma-vairable
7) bone cyst (w/o fx)
8) mature HO
utility of bone scan re: heterotypic ossification
- serial exams to detect if process is active-resect once mature (cold)
- *still active=higher rate recurrence
F18-NA PET vs T99-MDP
F18-Na-cleaner, shorter exam time, more expensive. critical orgn=bladder
-MDP: bone (critical) & kidney, fuzzy
F18-NA vs FDG PET
will look similar in pts w/ GCSF or EPO (diffuse bmarrow) but brain uptake on FDG
when would you use Tc99 HMPAO instead of In-WBC for infection? Why not use it all the time?
Uses:
1) kids (lower absorbed dose & shorter imaging)
2) small pts-T99 does better in hands, feet
Not all the time:
1) .T99 shorter half life
2) GI and gb act obscures act in those areas
In-WBC-which cells are labeled?
90% NP (lymphocytes tend to be killed by radiation)
In-WBC critical orgn
spleen
what happens if In-labeled cells fragment?
indium binds transferrin-see liver and bmarrow uptake
How is MAA prepared?
denaturation of human serum albumin
-give via IV
MAA biologic half life
4 hrs
xenon 133 vs Tc99DTPA: gas vs aerosol
x=gas
DTPA=aerosol
Xenon 133: KeV, half life and bio halflife, critical orgn
- 81 KeV
- 5.2 d
- 30 s
- trachea
3 phases of xenon 133 administration
1) wash in (single max inspiration and breath hold)
2) equilibrium (breathing room air and xenon mix)
3) washout (Breathing normal air)
DTPA administration
- requires more pt cooperation (breath through mouth guard w/ nose clamp for several mins)
- must do this part before MAA?
quantification studies
- before lung resection/tx
- must use Xe + Tc MAA bc Xe won’t interfere w/ Tc
significance of tracer in brain during v/q scan
shunt
MAA particle size and #
- 10-100 micrometers
- 500K
when do you reduce particle amount and why?
- risk a functional PE
- anyone with fewer capillaries (don’t want to block more than 0.1% of caps, ie: children, 1 lung)- 10-50K in neonates
- R–>L shunt (don’t want to block caps in brain). 100K
- pulm HTN
- pregnant
- this does not reduce dose-normal dose of Tc added to fewer particles
clumped MAA moa, app
blood in syringe
multiple scattered focal hot spots
persistent pulmonary activity during xenon washout
air trapping (COPD)
accumulation Xe over RUQ
fatty liver
clumping Tc-99m DTPA
mouth, central airways, stomach (from swallowing)
what if tracer is in thyroid or stomach on VQ scan?
1) free Tc
2) R to L shunt
what do you need to call R to L shunt?
tracer in brain
if you suspect a R–>L shunt, how do you alter scan?
decreased particles
unilateral perfusion defect of whole lungg, no ventilation defect
CT or MR
Ddx= mass (MC), fibrosing mediastinitis, central PE
Gallium vs Indium WBC?
- gallium can bind to NP mets after cells are dead (helpful particularly in chronic inf)
- spine-gallium
- abd/pelvis-I-WBC
Gallium-67: production, half life, decay, emitting gamma photopeaks, when do you scan, critical orgn, normal localization?
- cyclotron via bombardment of Zn68 –> complexed with citric acid –> gallium citrate
- HL 78 hr
- electron capture
- 93 KeV (40%), 184 (20%), 300 (17%), 393 (5%)
- colon
- liver (highest), MARROW (and cortex), spleen, salivary/lacrimal glands, breasts, GP/thymus (kids)
- kid/bladder <24 hr (faintly up to 72 hr)
- <24 hr faint lung, >24 hr faint bowel
when is gallium uptake + in chest?
-infection
-sarcoid-active disease, guide bx/lavage graded ag bg lung
-CHF
-atelectasis
-ARDS
-idiopathic pulmonary fibrosis-monitor resp to rx
-immsupp: PCP, bacterial PNA. (-) for kaposi and ?lymphoma
-early drug run-bleomycin, amdiodarone)
-
lambda sign
1-2-3 (bilateral hila, R paratracheal LN)
panda sign
NP, parotid, lacrimal
*sarcoid, sjogrens, treated lymphoma
FDG-PET pleural talc
+ via granulomatous rxn
doses MAA, Xe and DTPA
- 3-5 mi
- 10-20
- 30
segmental defect size
- small <25%
- moderate 25-75%
- large: >75%
high probability PE (97%, PPV 88%)
- mismatched segmental defects. No associated radiographic abN (excludes clinical mimics).
- 2+ L
- 2 L & 2 mod
- 4 mod
intermediate probability (20-85%)
- 1L mismatch
- 1-4 M
- triple match LOWER lung
low probability (5-19%; NPV 84%)
- 1 L or M matched
- UPPER/MID lung triple match
very low probability (2-5%)
- 3- sm perfusion defects
- non segmental lesions-CMG, diaph elevation, aortic aneurism, pl eff, hila, PM artifact, fissure, bullae
- fissure/stripe sign-thin line MAA uptake btw perfusion defect and adjacent pleural surface representing intervening perfused lung
CTA vs VQ scan radiation doses to maternal breast and fetus
- CTA: breast 10-70mGy (ACR rec 3mGy/br). Fetal dose 0.1-0.66mGy
- VQ: breast <0.31 mGy, fetus 0.1-0.37
changes to routine VQ scan in the pregnant pt
-perfusion only
-adm 1/2 standard dose
~100K particles
what are the functions of the kidney?
80% secretion
20% filtration
Tracers used in renal scintigraphy
- DTPA- Filtration. GFR (small portion protein bound, not filtered–> slightly underestimation)
- MAG3-Secretion (ERPF)
- DMSA-binds prox tub cortex-ass cortical integrity
- GH (glucoheptonate)-structural (binds to cortex) or functional (filtered)
- critical orgn= bladder (exc dmsa-kid)
how is renal scintigraphy performed and phases
- pst (ant if tx or horseshoe)
- 3 phases-blood flow (~20s), cortical, clearance
symmetrically decreased flow to kidneys
technical error (poor bolus)
asymmetrically decreased flow to kidneys
- renal a/v thrombosis
- acute rejection
- acute pyelo
- chronic high grade obstruction
asymmetrically increased renal flow
renal artery aneurysm
kidney pathology in which flow is normal
- vasomotor nephropathy- imm after sx, should recover 1st 2 weeks
- ATN-~wks-mo’s
- interstitial nephritis
- cyclosporin tox
how is cortical function/phase of renal scan assessed?
- 1 min (really drinking up that contrast)
- steep slope :)
- draw area of interest and background area of interest-correct for background. Can be screwed up if obtained over liver or spleen
how is clearance/excretory function/phase of renal scan assessed?
- reach half peak counts ~7-10 mins
- quantify retention via 20/3 or 20/peak ratio
20/3 or 20/peak ratio
peak count at 20 mins vs peak count at 3 (Normal <0.8)
-peak count at 20 vs peak count (N 0.3)
what to do in setting of suspected obstruction. how does this differ from standard renal scintigraphy scan?
lasix renogram
- wait 30 mins after clearance phase. If act still in collecting system-give lasix
- MAG3 > DTPA (better in pts w/ poor renal function)
lasix renogram exam interpretation-no obs, indeterminate, obstructed
- no obstruction-clears w/o lasix
- no obs-50%+ w/i 10 mins after lasix
- indeterminate: w/o 50% 10-20 mins
- obstructed-w/o >20 mins
MCC indeterminate lasix renogram
-dilated pelvis (reservoir effect)
false positive “obstruction” on lasix renogram
- poor response to lasix-bad renal function or dyhydration
- reservoir effect-v dilated renal pelvis (MC)
- back pressure-full bl, neurogenic bladder (resolve w/ foley)
DTPA vs MAG3 renal fx
- DTPA-GFR, ie: decreased uptake and flow (loss of perfusion pressure)
- MAG3- secretion tracer (retention)
2 ways of performing ACE-i renogram
1) standard dynamic study –> ace-i
2) 1/2 dose baseline study –> full dose
(+) ACE-i renogram
->10% worsening
ACE-i renogram study preparation
- stop ACE-i (3-5 d if captopril), CCB
- NPO 6 hr (for PE ace-i)
- maintain IV access in case of hypoTN
how would a suspected fluid collection app on renal scintigraphy
photopenic (exc urinoma only on DELAYED phase)
renal scintigraphy chronic kidney transplant rejection
-no uptake
renal scintigraphy vascular complication (thromb) s/p kid tx
-no flow or function
indications for structural renal scintigraphy
acute pyelo- (-) uptake)
- scarring/mass- (-) uptake, scarring decr volume
- coumn of bertin vs mass-mass=cold
testicular scintigraphy
blood flow study
- torsion vs other cause of pain
- Na99m-TcO4
- tape penis up out of way
- normal= symmetric flow
- acute torsion=nubin sgx (focal decrease)
- delayed torsion-halo of increased activity w/ central photopenis
- abscess-same as delayed
- acute epididymitis-(+)
trapping vs organification of iodine analogues
- “trapping”-analog transported into glad. I-123, I-131, Tc-99
- organification-oxidized by thyroid peroxidase, bound to tyrosyl moiety. Tc-99 does not do this
- only 1-5% Tc-99 taken up by thyroid==> background levels higher
when would you choose Tc-99 over I-analogue?
if pt had recent I blocker (ex: I contrast)
when can you resume breastfeeding?: Tc-99, I-123, I-131, fdg 18
- Tc-99: 12-24 hrs
- I-123: 2-3 d
- I-131: nxt pregn
- fdg 18-8 hrs
how much I analogue do you give for uptake test? When do you image?
- 5 microCi 131
- 10-20 microCi 123
image at 4-6 hr and 24 hr
normal values I uptake. How do you correct for background?
4-6 hr: 5-15%
24 hr: 10-35%
correct background prior to 24 hr (use neck counts - thigh counts)
factors that affect I-uptake test
1) renal function- (+) stable I pool –> (-) numbers
2) dietary I-variable and controversial
3) meds-Thyroid blockser, nitrates, IV contrast, amiodarone
Causes of increased I uptakes
- graves
- early Hashimoto
- rebound after abrupt withdrawal of antithyroid mx
- dietary I deficiency
Decreased I uptakes
- hypoth
- renal fx
- mx (Th blockers, nitrates, IV contrast, amiodarone
- deiatry iodine overload
which meds decrease I uptake test?
- Thyroid blockers
- nitrates
- IV contrast
- amiodarone
MCC hyperTh
graves 75%!
nukes findings Graves
-diffuse homog uptakes
*24 hr may be lower/N than 6 hr via rapid TH production
+pyramidal lobe (45%)
Plummer dx
Multinodular toxic goiter
-wt loss, anxiety, niosmina, tachycardia
nukes findings multi nodular toxic goiter
-heterogenous, moderately elevated uptake
-
toxic vs non toxic MN goiter
- toxic=hot nodules, cold background
- non toxic= moderate/warm nodules, normal background
toxic MN goiter vs graves
- toxic MN goiter=medium high uptakes (<50%)
- graves= high uptake (>50%)
MCC goitrous hypothyroidism in US
-hashimotos