Clinical 2 Flashcards

Question 1

Q

A question on most useful method for assessing a right to left shunt and briefly describe how you would do it.

Answer

A

 IV microsphere injection, typically MAA
 Use geometric means of ant and post
 % right to left shunt = (total body count – total lung count) / total body count x 100%
 Normal <10%

Question 2

Q

List 3 ways of calculating a right to left shunt

Answer

A

 Use geometric means of ant and post

 % right to left shunt ~ (total body count – total lung count) / total body count x 100%
 % right to left shunt ~ 2(kidneys + brain) / (2(kidneys + brain) + lung) x100%
 % right to left shunt ~ 4kidneys / (4kidneys + lung) x 100%
 Normal <10%

Question 3

Q

Schematic of nasolacrimal system - label anatomy

Answer

A

 1 - lacrimal gland drain via lacrimal ducts
 2 – superior & inferior puncta/ampulla
 3 - superior and inferior canaliculus -> common canaliculus
 4 - lacrimal sac
 5 - nasolacrimal duct opens into inferior nasal meatus via valve of Hasner

Question 4

Q

Most common indication for salivary gland study. 3 most common causes of this problem.

Answer

A

Xerostomia
o Radiotherapy/radioiodine therapy
o Medications (antimuscarinic)
o Sjogren’s syndrome

Question 5

Q

Assessing a mass with salivary gland study. Name 3 causes of a “hot” mass and 3 causes of a “cold” mass.

Answer

A

 Hot:
o Warthin’s tumor
o pleomorphic adenoma
o Oxyphilic adenoma (oncocytoma)

 Cold
o Cyst
o Abscess
o Primary salivary gland tumour (adenoid cystic, mucoepidermoid)

Question 6

Q

Most common cause of hot spot on salivary imaging.

Answer

A

Warthin’s tumour

Question 7

Q

List the dosage, mechanism of action & when the following medications might be used in nuclear medicine: Phenobarbital, Heparin, Cimetidine, Morphine

Answer

A

 Phenobarbital
o pretreatment prior to hepatobiliary imaging in neonate
o 5mg/kg/day in 2 divided doses for 5 to 7 days.
o It is a potent inducer of the liver microsomal enzyme system

 Heparin (SNM procedure guideline)
o provocation in GI bleed study
o 6000 U IV loading dose, then 1000 U IV / hr
o anticoagulation by inactivating thrombin and activated factor X

 Cimetidine
o pretreatment in Meckel’s scan (Tc-99m pert)
o adult: 300mg po QID x 2 days
o IV 300mg in 100ml D5W over 20minutes 1 hour before exam
o peds: 20mg/kg/day x 2 days

 Ranitidine
o IV 1 mg/kg (max 50mg) x1 over 20min 1 hour prior) OR
o PO 2 mg/kg dose po for children & 150 mg/dose for adults
o H2 receptor blocker increases uptake of Tc-99m pertechnetate by inhibiting its release from gastric mucosa

 Pentagastrin:
o Increases gastric mucosa uptake of pertechnetate but also stimulates pertechnetate secretion and GI motility.
o H2 blockers antagonize pentagastrin
o Dose: 6 ug/kg SC 15-20 minutes prior to injecting Tc-99m pertechnetate

 Morphine
o used to decrease time required to confirm acute cholecystitis
o 0.04 mg/kg (max 2-3mg) given 3 minutes, after 1 hour if GB not seen and 1) no evidence of CBD obstruction 2) sufficient activity within liver to allow for subsequent imaging
o produce up to 10x increase in resting pressure of CBD by causing contraction of sphincter of Oddi. This increases flow into GB unless cystic duct is obstructed

Question 8

Q

Effects of certain drugs on the appearance of scans. Matching question. Drugs: Melphalan, corticosteroids, nicotinic acid, estrogen, atropine. Effects: Decreased uptake on HIDA, decreased MDP uptake, increased MDP uptake, slowed GB ejection, increased Ga uptake in the breast

Answer

A

o Melphalan increases MDP uptake (↑ lung uptake on Ga-67)
o Corticosteroids decrease MDP uptake
o Nicotinic acid decreases hepatic uptake and bile excretion on HIDA
o Estrogen alters the biodistribution of gallium-67 with uptake in breast
o Atropine decreases GB emptying (↓ pertechnetate uptake in salivary glands & stomach)
o Progesterone decreases GB emptying on HIDA

PLUS TABLE PAGE 226

Question 9

Q

critical organ of pertechnetate and effective dose /mCi/MBq

Answer

A

 Critical organ is the stomach wall for the resting population, and the thyroid for the active population (package insert)

 Effective dose is 0.011 mSv/MBq

Question 10

Q

Five methods of marking and an example of each.

Answer

A

 Flood source behind patient: Co-57 sheet source
 Tracing body outline: Tc-99m in syringe tip point source
 Static anatomical marker: Co-57 sealed point source
 Distance/length calibration: lead ruler +/- Co-57 sheet source
 Post-acquisition image labeling: “right” or “left” markers

Question 11

Q

Name three collateral networks that form as a result of superior vena cava thrombosis.

Answer

A

 Azygos-hemiazygos
 Mediastinal venous plexus
 Internal thoracic veins to superior/inferior epigastric veins

Question 12

Q

List 5 common indications for myocardial stress perfusion imaging

Answer

A

Diagnose CAD in symptomatic patients with intermediate pre-test probability, or asymptomatic high risk.
Risk stratify patients with chronic stable CAD
Risk stratify patients with ACS (acute coronary syndrome) within 4 days
Risk stratify patients post MI within 6 weeks or before discharge
Assess pre-op for non-cardiac surgery in patient with high risk factors or known CAD.
Evaluate efficacy of therapy (CABG after 5 years, PCI after 2 years)

Question 13

Q

Explain right dominance.

Answer

A

 PDA supplied by RCA rather than left circumflex (85%)
 7% left dominant
 8% co-dominant

Question 14

Q

Describe preferred method of performing same day rest/stress myocardial perfusion studies with Tc-99m MIBI. Justify your answer.

Answer

A

Rest first: use 10 mCi of Tc-99m MIBI IV, wait 60 minutes then image.

Stress: wait 2-4 hours after rest portion. Stress the patient. One minute prior to peak exercise, inject
30 mCi of Tc-99m MIBI. Wait 15-30 minutes then image.
1. Higher blood flow with stress and greater activity with 2nd injection drowns out the rest injection background.
1. 60 minute delay after rest allows liver to wash out

Question 15

Q

What’s the myocardial wall motion abnormality in patients with LBBB. Explain your finding briefly:

Answer

A

 Secondary to delayed activation of septal wall due to aberrant conduction of depolarization wave (lateral wall ->apex->septal wall) bypassing dysfunctional bundle of His

 Delayed asynchronous systolic septal contraction with paradoxical motion of septum toward RV during LV systole

Question 16

Q

A table comparing Tl-201, Tc-MIBI and Tc Tetrofosmin for mechanism of uptake, time to image and reversibility

Answer

A

TI201: 
Time to image = 20 min and 4 hours
Uptake = Na/K+ channels, passive diffusion
reversibility = Viable
Localizes to cytoplasm
85% first pass extraction
Renal clearance
2-4 mCi
Redistribution

MIBI:
Time to image = 60/30 min post rest/stress
Uptake = passive diffusion with mitochondrial adhesion 2
Reversability = ischemia
Localizes to mitochondira
Minimal myocardial clearance
Hepatobiliary clearance
10-30 mCi
60-65% first pass
Trace redistribution

tetrafosmin:
Same
50-54% first pass

Question 17

Q

Ask about artifact of cardiac imaging with noncircular acquisition.

Answer

A

 Regional non-uniformity, as well as distortion of shape on reconstructed images, due to varying spatial resolution secondary to varying distance to activity source
 Constitutes 180-degree diametrical defects

Question 18

Q

List 3 ways you might determine if a defect on SPECT is due to artifact

Answer

A

o Attenuation artifacts (AC, look at the raw images-breast/diaphragm, do prone imaging-diaphragm)

o Motion artifacts (look at the raw images, look at the sonogram)

o Processing artifacts (look at the attenuation maps)

Question 19

Q

What do you analyze the cine data for in MPI?

Answer

A

o artifact
o motion
o attenuation
o gating (flicker artifact)
o subdiaphragmatic activity (scatter &amp; volume averaging, side lobe)
o abnormal extracardiac activity

Question 20

Q

Name 3 methods most commonly used for detection of patient movement during a myocardial SPECT study. Name a disadvantage of each method. Which method is best and why?

Answer

A

Visually inspect the rotating raw images – disadv: time consuming
Summed image – Disadv: difficult to detect lateral motion
Inspect the sinogram – horizontal motion, Disadv : gradual, continuous motion is usually not apparent.
Inspect the Linogram – for vertical motion. Diadv : limited to vertical motion only
Best: raw images – can detect all types of motion

Question 21

Q

Give 2 reasons why movement artifacts are generally less apparent on Tl-201 images than Tc-99m-sestamibi images.

Answer

A

Images with Tl-201 are usually done with higher sensitivity/lower resolution collimator (low counts)
More smoothing is required, cut-off frequency of smoothing filter is lower.

Question 22

Q

What is the J-point? The ST80? How is ST depression measured?

Answer

A

J-point: junction of the QRS complex and ST segment; normally near the isoelectric line
 ST80: is the point that is 80 ms from the J-point (2 small squares)
 Positive stress test: is the J-point and ST80 depression of >= 1mm

Question 23

Q

Give 5 causes of ST depression not due to ischemia

Answer

A

LVH
cardiomyopathy
Biochemical: hypokalemia, hypocalcemia,
LBBB
MVP (mitral valve prolapse)

Question 24

Q

ECG parameters for AV block and QRS complex widening

Answer

A

 AV block: P-R interval >0.20 sec (5 small squares)

 QRS complex widening: >0.12 sec (3 small squares)

Question 25

Q

What are the end points for an exercise stress test?

Answer

A

Moderate-to-severe angina pectoris.
Marked dyspnea or fatigue.
Ataxia, dizziness, or near-syncope.
Signs of poor perfusion (cyanosis and pallor).
Patient’s request to terminate the test.
Excessive ST-segment depression (>2 mm).
ST elevation (>1 mm) in leads without diagnostic Q waves (except for leads V1 or aVR).
Sustained supraventricular or ventricular tachycardia.
Development of LBBB or intraventricular conduction delay that cannot be distinguished from ventricular tachycardia.
Drop in systolic blood pressure of >10 mm Hg from baseline, despite an increase in workload, when accompanied by other evidence of ischemia.
Hypertensive response (systolic blood pressure >250 mm Hg and/or diastolic pressure >115 mm Hg).
Technical difficulties in monitoring

Question 26

Q

Define typical angina, atypical angina and non cardiac chest pain

Answer

A

Criteria:
o retrosternal/left-sided chest pain radiating to jaw, neck or arm
o brought on by exercise or emotional stress
o relieved by rest or nitroglycerine

 typical: 3 criteria from above
 atypical: 2
 non-cardiac: 1

Question 27

Q

What is the likelihood of significant CAD in a 50 yo male with (1) typical angina, (2) atypical angina, (3) noncardiac chest pain?

Answer

A

Pre-test probabilities:
o Typical: high
o Atypical: intermediate
o Noncardiac: intermediate

Question 28

Q

Advantages of exercise test of pharm exercise.

Answer

A

 Exercise advantages:
o Reproduce patient symptoms
o Assess exercise capacity (HR, BP changes), independent prognostic factors

 Pharmacologic advantages:
o If have contraindications to exercise
o If unable to exercise

Question 29

Q

4 absolute/relative contraindications for EST.

Answer

A

Absolute:
o Unstable angina with recent (<48h) angina or CHF
o Documented acute MI within 2-4d of testing
o Uncontrolled systemic (>220 mmHg SBP, >120 mmHg DBP) or pulmonary hypertension
o Untreated life-threatening arrhythmias
o Uncompensated CHF
o Advanced AV block (without pacemaker)
o Acute myocarditis
o Acute pericarditis
o Severe mitral or aortic stenosis
o Severe obstructive cardiomyopathy
o Acute systemic illness

 Relative:
o Neurologic disease
o Orthopedic disease
o Arthritic disease
o Severe pulmonary disease
o Peripheral vascular disease
o Severe deconditioning
o Inability to comprehend the exercise protocol

Question 30

Q

Classes of medications that interfere with EST, mechanism. (Two drugs that interfere with exercise MPI)

Answer

A

For exercise MPI:
o CCB and beta blockers by preventing adequate heart rate response and achieving heart rate target
o Nitrates and dipyridamole being vasodilators (limiting ischemic response)

 For EST
o CCB and beta blockers by preventing adequate heart rate response and achieving heart rate target
o Digoxin, estrogen cause ST depression (for EST alone)

Question 31

Q

In treadmill stress test why each stage is 3 minutes?

Answer

A

 To allow for stabilization of HR and BP

Question 32

Q

Define double product.

Answer

A

 Double product = peak HR x peak systolic BP
 It correlates well with peak myocardial oxygen demand during exercise test.
 It should be greater than 20,000 – 25K or at least double from the patients resting value for sufficiency of exercise test.

Question 33

Q

4 types of cardiac stress that can be used in Nuclear Medicine besides treadmill test and dipyridamole

Answer

A

Exercise – seated bicycle, lying bicycle
Adenosine
Regadenoson (A2A receptor agonist)
Dobutamine
Cold pressor test (put hand in icy water bath for 3 minutes)
Isometric hand grip exercises (hand grip machine)

Question 34

Q

Mechanism of Persantine action:

Answer

A

 Dipyridamole:
o Indirectly augments effect of adenosine by:
– inhibiting adenosine reuptake by cell membrane transporters (mostly RBC)
– inhibiting breakdown by adenosine deaminase

 Adenosine:
o Produces coronary vasodilatation as A2A & A2B receptor agonist (cAMP-mediated)
o Non-selective and causes undesirable side effects by binding to other adenosine receptors (A1/A3)

 Dobutamine:
o Synthetic sympathomimetic catecholamine with inotropic and chronotropic effects on the myocardium (β1, weak β2 and α1)
o ↑ myocardial O2 demand by increasing HR, BP & contractility

Question 35

Q

Two clinical signs of persantine effect:

Answer

A

Hypotension and ↑ HR.

S/E of dipyridamole are flushing, headache, chest pain, hypotension and dizziness

Question 36

Q

What are the 2 cardiovascular effects from persantine (not the clinical signs which was question right after)

Answer

A

↑HR ~ 10/min from the baseline

* ↓ BP ~ 10 mm Hg from the baseline

Question 37

Q

What is the half-life of adenosine?

Answer

A

2-10 sec (<10s ASNC)

Question 38

Q

Half-lives of adenosine and dipyridamole

Answer

A

 Adenosine 2 – 10 seconds
 Dipyridamole – 30 – 45 minutes
 Dobutamine 2 minutes
 Regadenoson initial phase 2-4 min, second phase 30 min, final phase 2 hours

Question 39

Q

5 contraindications to dipyridamole

Answer

A

Absolute contraindication:
o history of severe bronchospasm
o 2nd or 3rd degree AV block without pacemaker or sick sinus syndrome
o hypotension - SBP < 90 mm Hg
o recent use of dipyridamole or dipy-containing medication (Aggrenox)
o methylxanthines within the last 12 hours before exam
o known hypersensitivity / allergy
o acute MI within preceding 48 hr / unstable angina

Relative contraindication:
o profound sinus bradycardia (HR < 40 bpm)

Question 40

Q

Describe protocols of stress study with adenosine including dose and the time of tracer injection

Answer

A

Describe protocols of stress study with adenosine including dose and the time of tracer injection

Question 41

Q

Huge table wanting 5 pharmacologic agents used for stress MPI, listing name, half life of pharmacologic action, one advantage and one disadvantage

Answer

A

Adenosine:
MOA = Nonselective A2A receptor agonist with A1 and A3 as well, causing vasodilation, non-specific also affects 1/2 life <10s.

Dose = 140 mcg/kg/min over 6 minutes

S/E = Minor S/E in 80% (flushing, dizziness, dyspnea, chest pain, headache), conduction abnormalities 30%, 1st degree heart block 8%, second-degree 4%, total 1%. Side effects subside within several minutes

Adv/Dis = 1.Short half-life S/E resolve by stopping infusion as opposed to persantine which requires aminophylline, + those in cell below/1.S/E more common than in persantine + those below

Persanatine
MOA = Prevents reuptake of intracellular adenosine, prevents inactivation of adenosine by adenosine deaminase in RBCs, lung and myocardial tissue, adenosine accumulation results in maximal coronary vasodilation, reversed by aminophylline. 1/2-life 30-45 minutes, sx last for approximately 25 minutes.

Dose = (142 mcg/kg/min) over 4 minutes

S/E = 50% side effects (flushing, dyspnea, chest pain, headache, dizziness and hypotension), less frequent than adenosine of last for much longer time.

Adv/ = 1.Intense coronary vasodilation, 2.Easy, safe, Few side effects, 3.Achieve increased coronary flow in patients who cannot adequate or maximal treadmill response/

Dis = Absence of diagnostic information associated with exercise, 2.Induces flow disparity, not ischemia, 3.Cannot correlate symptoms with myocardial perfusion, 4.May detect stenosis of 30-50% of doubtful clinical significance, 5. Gives only a Yes/No answer (does the patient have CAD?),

Dobutamine
MOA = Direct β1, β2 agonist with chronotropic, iontropic and increased contractility, 1/2-life 2 minutes

Dose = 5-10 mcg/kg/min,which is increased at 3-minute intervals to 20, 30, and 40 mcg/kg/min. Can augment with atropine 0.25-0.5 mg IVq2min to 2 mg

S/E = 75% side effects (palpitations, chest pain, headache, flushing and dizziness), significant arrhythmias including supraventricular or ventricular tachyarrhythmias (10%). Ischemic ST depression (1/3). Severe side effects require short-acting beta blocker infusion (esmolol 0.5 mg / kilogram over 1 minute)

Adv: 1.Can be performed on those patients with inability to stress and those who have severe asthma, 2.Short half life

Disadv: 1.Difficult protocol, 2.Often patients do not reach target with dobutamine alone and atropine is required, 3.S/E very common

Atropine:

1/2-life of 2-3 hours

0.25-0.5 mg IV, q2min to a max of 2 mg.

SOB, palpitation, headache, anxiety, nausea, dyspnea

Only used in conjunction with Dobutamine

Rogadenoson

Low affinity receptor agonist of A2A, low if any A2B and A3. Max 1-4 minutes, 1/2-life 3 phases; phase 1, 2-3 minutes, phase 2, 30 minutes which is when sx resolve, phase 3, 2 hours

5 ml, 0.4 mg in 10 s

Most common flushing, headache, dyspnea; most common chest pain, dizziness, nausea, abdominal pain. Conduction abnormalities 26%,1st degree heart block 3%, 2nd degree 0.1%. Most side effects last 15 minutes with headache 30 minutes.

1.Simple protocol, bolus injection, 2. More specific MOA, S/E less common than either above/1.S/E more perisistent, up to 20 minutes aminophylline required, 2.No exercise, 3.Cost

Question 42

Q

Questions on the mechanism of uptake of caffeine, the peak time of caffeine concentration in blood, what the effect of caffeine is on diapridimole, and what drugs increase the half time of caffeine in the blood stream.

Answer

A

 Mechanism: competitive inhibition adenosine receptor
 Peak time: 1h
 T1/2: 6h
 Medications that increase t1/2: liver disease, pregnancy, OCP’s, and cimetidine
 Vasodilatation impaired as low as 0.6 mg/L

Question 43

Q

Classes of medications that interfere with MPI, causes

Answer

A

 Aminophylline or other methylxanthine-containing medications
o Methylxanthines (aminophylline and caffeine) antagonize dipyridamole and adenosine
 Vasodilators
o Nitrates and persantine
 Controversial, may reduce sensitivity
o Beta-blockers and CCB

Question 44

Q

Describe coronary steal syndrome. Next part was – name two causes of coronary steal syndrome and describe one cause.

Answer

A

 more significant dilation of normal arteries results in a further disparity of flow between normal and stenotic vessels (less response of diseased vessel to vasodilator)
 May cause ischemia.
 Pharmacologic stress - vasodilation
 Hypotension
 Any agent that causes a primary (Adenosine, Regadenoson) or secondary (Persantine) coronary vasodilatation can cause coronary steal.

Question 45

Q

Describe the dobutamine protocol with atropine. What are the effects of dobutamine on blood pressure and heart rate?

Answer

A

 Patient prep
o Stop β blockers, CCBs and nitrates 24h
o Fast >4h (2h for ASNC)
o Connect EKG, check resting 12-lead

 Escalating dose
o 5 ug/kg/min x 3 min iv (start with 5-10 ug/kg/min), then 20, 30, 40
o 10 ug/kg/min x 3 min iv
o 20 ug/kg/min x 3 min iv
o 30 ug/kg/min x 3 min iv
o 40 ug/kg/min x 3 min iv
o Inject at target HR (85% max age predicted HR) & continue dobutamine for 2 minutes
o If submaximal HR at maximum dose of dobutamine, augment with atropine 0.25-0.5 mg (ASNC; 0.5-1mg for other guidelines) IV q 2 min to a max dose of 2mg

 ↑ HR & BP increase (chronotropic & inotropic)

Question 46

Q

What are the indications for persantine versus dobutamine versus exercice in MPI

Answer

A

• Persantine :
o Cannot exercise
o LBBB, WPW
o Pacemaker (with LBBB configuration always on)
o Risk stratification 2-4 days post MI

 Dobutamine
o Unable to exercise and have contraindications to adenosine (severe reactive airway disease)
o Can do with AV block

Question 47

Q

4 contraindications for atropine

Answer

A

 Glaucoma, prostatic hypertrophy/obstructive uropathy, acute MI (potentiate arrhythmias), tachyarrythmias

Question 48

Q

What do you do if during a persantine or dobutamine MPI, the patient develops ST depressions?

Answer

A

Persantine: wait 2 to 3 minutes post injection of MIBI and inject aminophyline IV and use nitro as required. Monitor EKG for improvement.

• Dobutamine: try to continue dobutamine perfusion for 2 to 3 minutes post injection of tracer
• Terminate Dobutamine Test if :
o Max predicted HR achieved
o Severe chest pain, side effects
o ST depression ≥ 2mm
o ST elevation ≥ 1mm with no Q wave
o Significant arrhythmias
o BP ≥ 240/120 mm Hg
o Systolic BP drop ≥ 40 mm Hg

Question 49

Q

What do you do if during a dipyridamole stress test a patient develops rapid atrial fibrillation > 160bpm?

Answer

A

Contact cardiology right away to come see the patient
Stop dipyridamole
Give amino 125 mg IV
Get vitals, ECG, O2
Give diltiazem 20mg IV over 2 min

Question 50

Q

What is the steal phenomenon? Give 2 examples of steal phenomena and mechanism of one.

Answer

A

Steal phenomenon occurs when you get ↓ blood flow distal to a stenosis during vasodilation and re-direction to a vessel capable of vasodilation.

Coronary artery steal following administration of persantine.

Cerebrovascular steal following administration of diamox
Mechanism: healthy vessels dilate while diseased vessels are unable to, hence the blood follows the path of least resistance. The flow through the healthy vessels increases, while the flow through diseased vessels decreases (steal).

Question 51

Q

Next question was on the AHA, ABNM or American Board of Nuclear Cardiology position paper on attenuation correction. What other three procedures should be performed on the acquisition data?

Answer

A

motion correction
 scatter correction
 resolution recovery (to correct for depth-dependent spatial resolution)

Question 52

Q

EKG shows LBBB. What stress protocols do you use? What artifacts are associated with exercise stress protocol and why?

Answer

A

 LBBB:
o QRS >0.12s
o Monophasic R waves in V1-V6, with inverted T-wave

 Stress: vasodilator
 Artifacts with exercise: ↓septal perfusion on MPI
 Causes
o Impaired early diastolic flow in LAD due to asynchronous and delayed systolic septal contraction
o Tachycardia also ↓ diastolic filling time post-exercise/dobutamine stress, causing reversible anteroseptal perfusion defect

Question 53

Q

Causes of fixed defects on 20 minute/4 hour thallium.

Answer

A

 On a rest-redistribution study, a fixed defect could represent infarction or ischemia
 Two further tests
o Stress MPI should be performed: either exercise or pharmacologic, with Tc-99m-MIBI, Rb-82, or another perfusion tracer
o Re-injection
o FDG viability

Question 54

Q

What is the function of prone imaging in MPI, how does it work, why isn’t it done all the time?

Answer

A

 Prone imaging improves the specificity for inferior wall ischemia by minimizing diaphragmatic attenuation.
 This approach can limit throughput and efficiency and can create FP anterior, anteroseptal and lateral wall defects.

Question 55

Q

list 4 techniques or reading methods to deal with breast attenuation artifact

Answer

A

 1.Breast binding (Practical nuclear medicine, pg.164)
 2.Attenuation correction, assess the rotating raw planar projection images to confirm
 3.NH3 PET, less likely to suffer from attenuation artefact (works for obese people)
 4.Ensure that breasts are in the same position on both sets of images and if they are a fixed anterior wall defect with no other defects are likely to be secondary to breast attenuation especially in females
 5.Assess for normal regional wall motion.

Question 56

Q

Suspecting a breast attenuation artifact in anterolateral wall, what would you do to confirm?

Answer

A

Inspect raw images
Breast-up imaging
Assess wall motion post-stress and at rest
SPECT-CT with CT attenuation correction
Consider prone imaging

Question 57

Q

Next question was a table asking to fill in the blanks for the appearance on a rubidium and FDG PET study for the following: ischemia, stun myocardium, hibernating myocardium and infarct.

Answer

A

 ischemia - increased FDG, reversible rubidium
 hibernating - increased FDG, fixed rubidium
 infarct - decreased FDG, fixed rubidium

Question 58

Q

Describe 2 clinical situations when stunning may occur.

Answer

A

Post PTCA or thrombolysis for acute MI
Post cardioplegic arrest during open heart surgery
Unstable angina
After exercise induced ischemia

Question 59

Q

Define hibernating myocardium. Define Stunned myocardium. In which clinical situation is detection of hibernating myocardium important? Why?

Answer

A

Stunned myocardium – reversible myocardial contractile dysfunction, in the presence of myocardial blood flow that was recently impaired but has normalized.
After attacks of unstable angina
After Exercise induced ischemia
Post PTCA or thrombolysis for acute MI
Post cardioplegic arrest during open heart surgery
Hibernating myocardium – impaired LV contractility as a result of reduced resting coronary blood flow (flow-contraction match).
Theory: hibernation results from repetitive stunning.
Repetitive stunning → ↓ coronary flow reserve → ↓ resting blood flow.
Myocytes become partially de-differentiated: loss of myofibrils, ↑ glycogen

Question 60

Q

Mechanisms for wall motion abnormalities in stunned myocardium?

Answer

A

 Abnormal energy utilization by myofibrils
 Production of cytotoxic oxygen free radicals
 Altered calcium flux
 Accumulation of neutrophils in previously ischemic tissue

Question 61

Q

What’s the normal lung/heart ratio for 201Tl and SestaMIBI, respectively?

Answer

A

 0.5 and 0.45.

Question 62

Q

Questions on 20 segment vs. 17 segment model, which is better?

Answer

A

 20 segment model has 2 segments in apex and 6 in distal segments
 17 segment model has 1 segment in apex, 4 periapical segments and 6 in distal segments
 20 segment model over-represents the apex and distal myocardium (giving it 40% of myocardial area), while the 17-model is more representative of true geometry of the LV.

Question 63

Q

Define SDS, SSS, SRS and gradation and indicate what they measure. How many segments are in the widely accepted polar model?

Answer

A

Post stress and rest perfusion images are scored using a 17 or 20 segment, 5-point model (0= normal; 1= mildly reduced uptake; 2= moderately reduced uptake; 3= severely reduced uptake; 4=absent uptake) compared to sex matched normal database

summed stress score (SSS) combines extent and severity of perfusion abnormalities into a single measure and it has been shown to provide risk stratification

Question 64

Q

Exact recall question: Define Sum stress score, Sum difference score and their significance. What is Transient ischemic dilatation and its significance?

Answer

A

 SSS: summed stress score, sum of all parametric stress scores from the 17 segment polar map.
o Good predictor of annual MI risk

 SRS: summed rest score, sum of all parametric rest scores from the 17 segment polar map.

 SDS: summed difference score, calculated by SSS – SRS. Best indicator of future risk of non-fatal MI.

 TID: Transient ischemic LV cavity dilation – apparent larger LV cavity volume at stress compared to rest.
o Abnormal TID > 1.22 for men, > 1.3 for women.
o Mechanism is subendocardial ischemia more often than actual dilation.
o Powerful predictor of high-risk CAD and multivessel disease.
o TID thresholds are actually depend on whether dual isotope or single isotope, and are probably also different for PET

Answer 65

A

 TID ratio > 1.22 (dual isotope exercise)
 LHR > 0.5 (MIBI)
 EF decreases by 10% on the post stress study
 SSS > 13
 ESV >70 ml
 TID, ↑LHR, >2 vessels affected, EF<30%, SSS>12.

Answer 66

A

 TID ratio > 1.22 (dual isotope exercise)
 LHR > 0.5 (MIBI)
 EF decreases by 10% on the post stress study
 SSS > 13
 ESV >70 ml
 multivessel distribution
 Abnormal resting LVEF
 Transient ↑ RV uptake post-stress

Answer 67

A

 low risk definition:
o SSS 4-8
o small perfusion defect (1 segment LV)

 The subsequent rate of re-infarction/death in this group was 1.8% and coronary revascularization did not improve outcome in this group compared to medical therapy.

 Low risk <1%, medium risk 1-3%, high risk >3%. Low risk is 1% because this is the mortality rate from angioplasty.

Answer 68

A

 Normal / near normal (SSS < 4), < 1% cardiac event 1st year
 Mildly abnormal (SSS 4-8) suggests low risk
 Prognostic: 0.8% cardiac death; 2.5% for MI in 1st year
 Moderately abnormal (SSS 9-13) suggests moderate risk
 Prognostic: 2.3% cardiac death & 2.9% for MI in 1st year
 Severely abnormal (SSS >13) suggests high risk
 Prognostic: 2.9% cardiac death & 4.2% for MI in 1st year

Answer 69

A

 LVEF < 35-40%, and decrease in EF post-stress >10%
 SSS > 13 / SDS > 7-8
 LV volume – ESV > 70ml
 elevated TID
 Elevated lung heart ratio
 number of reversible defects (multi-vessel disease)
 size & severity of reversible defects (amount of ischemic myocardium)
 extent of fixed defects (amount of infracted myocardium)
 Reversible defects in the left main coronary artery territory

Answer 70

A

Patients with moderate to severe ischemia involving more than 10% of the myocardium have been shown to have an increased survival benefit from revascularization compared to medical therapy alone

Answer 71

A

Patients with adequate exercise stress and a normal perfusion exam have an overall annualized cardiac event (MI or cardiac death) rate of less than 0.5-2% per year. However, even if the perfusion scan is normal, it has been demonstrated that the cardiac death or non-fatal infarction rate is higher:
o previously document coronary artery disease (2% / year)
o pharmacologic stress (2% / year)
o diabetes mellitus (2-3 % / year)
o male gender
o increasing age

Answer 72

A

 AM’s list:
o Normal variant (diaphragmatic, breast or pacemaker attenuation)
o Mitral valve prolapse
o Valvular heart disease (aortic stenosis, aortic regurgitation)
o LBBB
o Idiopathic subaortic stenosis
o Hypertensive myocardial hypertrophy
o Cardiac contusion
o Infiltrating myocardial disease
o Cardiomyopathy (dilated &amp; hypertrophic cardiomyopathy)
o Bland-White-Garland (LCA from PA)
o Coronary spasm
o Myocardial bridge
o Myocarditis

Answer 73

A

False negative FOR EXERCISE (NOT MPI)
o Unable to reach target heart rate/submaximal effort
o Single ECG monitoring(will miss the inferior wall)
o Physical training lead to decreased ECG changes even at maximal stress
o B-blocker therapy(insufficient heart rate response, less ECG changes)
o Calcium channel blockers
o Nitrates (fewer ischemic changes)
o Resting ST depression
o RBBB

Answer 74

A

o Beta blocker/CCB
o “Balanced” ischemia and left main stenosis
o Insufficient luminal obstruction
o Inadequate stress
o Poor technique
 Infiltrated dose
 Inadequate dose
 Delay in imaging at stress (allowing redistribution)
o Adjacent activity
 Liver
 Breast low angle scatter

Answer 75

A

 Cardiac cause
o left sided heart failure
o pulmonic valve stenosis

 Pulmonary parenchymal disease

 Pulmonary vascular disease
o PE
o primary pulmonary hypertension

Answer 76

A

 Cor pulmonale
 L-R shunt
 RV infarct
 Congestive cardiomyopathy
 Pulmonic valve stenosis

Answer 77

A

 MIBI: 65%
 201Tl: 85%
 82Rb: 50-70% (rest), 25-40% (high flow rate)
 13NH3: 83% (1 ml/g/min), 69% (3 ml/g /min)

Answer 78

A

 Rubidium-82
o generator produced (Strontium-82 (T1/2=25.5 days) – EC -> Rb-82)
o T1/2 75 s
o Positron range 5.5 mm
o potassium analog, need active Na/K-ATPase pump for intracellular transport
o least accurate because of poor extraction at high flow rates and relatively worse spatial resolution

 N-13 ammonia
o Cyclotron produced
o T1/2 10 mins
o Positron range 0.4 mm
o Extraction is non-linear at high flow states (under-estimate flow)

 O-15 water
o Cyclotron produced
o T1/2 2 mins
o Positron range 1.1 mm
o theoretically superior to N-13 ammonia because freely diffusible with virtually complete myocardial extraction that’s independent of flow rate and myocardial metabolic state.

Answer 79

A

 Mechanisms:
o Blood flow
o Passive diffusion (NH3)
o Active transport (NH4+) by Na/K ATPase pump
o Trapping by incorporation into glutamate glutamine by glutamine synthase
 Rate limiting step
o At high flow rates, metabolic trapping is rate limiting step

Answer 80

A

 Half life-FDG (110 minutes)>13N (10 minutes)>82Rb (75s)
 Soft tissue range-Rb-82 (14 mm)
 Myocardial extraction-13N ammonia

Answer 81

A

o Freely diffusible perfusion tracer
o 95% extraction by myocardium (maintained at very high flow rates)
o Not affected by metabolic factors
o Simple blood flow estimation using 1-compartment model

Answer 82

A

 Reconstructed dynamic PET data analyzed to sample RV and LV blood pool as well as LV myocardium to derive the blood pool and tissue time activity curves

 Time activity curve in each voxel modeled as a combination of 3 contributions: compartment analysis, which for N-13 ammonia is with a previously validated 3-compartment model, and contributions from RV and LV blood pools

 Kinetic analysis performed, with parametric mapping of the LV myocardium into a 17-segment polar map

Answer 83

A

 14N(p,α) 11CO2, which can be reduced to 11CO
 Used to label blood pool and subtract from 15O-H2O cardiac perfusion study
 Critical organ: lung

Answer 84

A

With exercise stress - there is a 4% annual event rate. Repeat testing in 1 year.
With pharm stress – there is a 10% annual event rate (7%)

Answer 85

A

This patient is at high risk of MI during the surgery.
Patient will need further characterization of coronary anatomy by coronary angiography.
The stenosis will then need to be repaired either by stenting or CABG

Answer 86

A

In patients with stable coronary artery disease, there is no improvement in non-fatal MI or survival between patients who were treated with optimal medical therapy (including lifestyle modification) and patients who were treated with PCI.
Ref: COURAGE Trial, NEJM 2007.

Answer 87

A

Non-occlusive thrombus forming on a pre-existing atherosclerotic plaque (due to ruptured fibrous cap)

Prinzmetal angina - coronary artery spasm – due to cocaine, cold weather, emotional stress, nicotine.

Mechanical obstruction without thrombus (restenosis of stent, progressive atherosclerosis)

Arterial infection or inflammation (vasculitis)

Answer 88

A

CAD, MI
Hypertension, LVH
Aortic valve disease
Cardiomyopathy, myocarditis
Post-cardiac surgery
Pacemaker (LBBB configuration)

• Motion Abnormalities :
o Asynchronous and delayed systolic septal contraction
o paradoxical motion of septum toward the RV during LV systole.

Answer 89

A

A) Among patients having reversible thallium perfusion defects, those with overt angina have a higher risk of complications (unstable angina, infarction, death) than those without angina.
(TRUE)

B) In the follow-up of patients with acute myocardial infarction, antimyosin antibody studies
become negative before those done with Tc-99m Pyrophosphate. (FALSE)

C) Rubidium-82 emission tomography/dipyridamole perfusion imaging is more sensitive than
Thallium-201 dipyridamole perfusion imaging for detection of cardiac ischemia. (TRUE)

D) Right ventricular ejection fraction obtained by the first pass technique is typically greater
than that obtained by the equilibrium blood pool technique. (TRUE)

E) Glucose metabolism studies with F-18 deoxyglucose (FDG) in patients under fasting
conditions, suggest that glucose utilization in viable ischemic myocardium cannot be
suppressed to the same extent as in normal myocardium. (TRUE)

F) An important limitation in the detection of viable ischemic myocardium with FDG in fasting
patients is that fasting does not consistently suppress glucose utilization in normal
myocardium resulting in interpretable images in only 50% of cases. (TRUE)

G) In diabetic patients, insulin administration to control plasma-glucose levels does not
improve the diagnostic quality of imaging with FDG. (FALSE)

H) Regarding diastolic function, the PFR normalized for EDV decreases with increasing
age. (TRUE)

I) The PFR normalized for EDV decreases with decreasing heart rate. (TRUE)

J) The TPFR decreases with increasing heart rate. (TRUE)

Answer 90

A

Inferior defect - (I)
Anterior defect - (I)
Lateral defect - (III)
Septal defect - (III)
Small high septal defect - (II)
Small inferior defect - (II)
No artifact

Answer 91

A

50%.
RV infarction results in increased incidence of CHF and PE.
Volume loading may be necessary to maintain cardiac output.

Answer 92

A

insulin drives Tl-201 into myocardial cells, which causes defects that would normally redistribute by 4 hours to appear non-reversible.

Gastric distension can elevate the diaphragm accentuating attenuation artifacts.

Answer 93

A

LV dysfunction during exercise due to coronary or non-coronary disease.
Mitral stenosis or regurgitation
LV hypertrophy with decreased compliance
Poor exercise level
Smoking

Answer 94

A

Flow

viability

Answer 95

A

SEE NOTES PG 262

Answer 96

A

Tc-MIBI stress and rest protocol – assess relative perfusion
Thallium stress and rest protocol – assess relative perfusion
Tc-RBC – blood pool imaging

Answer 97

A

o Quantifying parameters of ventricular function (e.g., ejection fraction, wall motion, ventricular volume, cardiac output, diastolic function)

o Detecting the presence, location, and extent of coronary artery disease

o Assessing whether congestive heart failure is due to ischemic or nonischemic causes

o Evaluating and monitoring potential cardiotoxic effects of cancer chemotherapy

Answer 98

A

Amplitude = (max counts – min counts) per pixel.

Phase = Fourier Transfer applied to each pixel, Each pixel’s cosine curve is characterized by amplitude and relationship to time of onset of cardiac cycle (R Wave). Cardiac cycle is mapped over 360°.

Answer 99

A

Fewer counts in the last bin due to R-R beat variation.

Answer 100

A

Cardiac cycle is arbitrarily divided into a fixed number of frames (usually 16-32) and the data from each cycle are divided up and stored in individual frame memory bins

Forward gating – assign frame 1 to R-wave.

Reverse gating - Last frame is assigned to end on the R wave: end-diastolic portion of the TAC is protected

Answer 101

A

SEE NOTES PAGE 264

Answer 102

A

List mode collection:
Beat preceding PVC = R; PVC = R; beat following PVC = Accept

Post-beat filtration:
Beat preceding PVC = A; PVC = R; following PVC = A

Dynamic beat filtering:
Same as list mode

Answer 103

A

 MUGA
o Based on planar count data: fewer assumptions need to be made about cardiac volumes to calculate an LVEF
o Also higher temporal resolution gating (16 bins/cardiac cycle)

 Gated SPECT MPI
o Requires algorithms to detect endocardial surfaces and valve plane estimated based on flat surface at base of heart

 MUGA > perfusion SPECT > angiography

Answer 104

A

 small volume of left ventricle
 incorrect contour of LV
 any high-flow state
      o anemia
      o sepsis
      o hyperthyroid
 hypertrophic cardiomyopathy

Answer 105

A

 No special patient preparation is necessary
 administer labeled autologous RBC with 15-30 mCi activity
 LEAP or high-resolution parallel hole collimator
 64 x 64 matrix – pixel depth = 4096 bits
 appropriate ECG gating, selection of beat acceptance window
 minimum 16 frames / R-R interval, up to 32-64 for assessment of diastolic function
 Typically 200,000 to 250,000 counts per frame should be acquired for a rest study to be statistically reliable for evaluation of wall motion.
 LAO, anterior and lateral views

Answer 106

A

 Isovolumetric relaxation phase – closure of AV to opening of MV
 Early rapid filling phase: atrial blood fills ventricles rapidly after MV opening (60-80% of normal diastolic flow)
 Slow/passive filling (Diastasis): slow filling from peripheral veins/lungs(equilibration of pressure between LA & LV, < 5% blood flow)
 Atrial kick/contraction: filling from atrial kick (normal 10-20%, may be up to 25-30% in LVH)

Answer 107

A

 Normal aging
 HTN
 LVH due to aortic stenosis
 Coronary artery disease
 CHF
 restrictive cardiomyopathy (infiltrative diseases – amyloidosis, sarcoidosis, hemochromatosis)
 mitral stenosis
 Medications: e.g., doxorubicin

Answer 108

A

 PFR: peak filling rate: normal >2.5 EDV cnts/s
 tPFR: time to peak filling: normal <180 ms
 AFR: atrial filling rate: normal 1.0 EDV counts/s
 PFR/AFR ratio: assess early rapid filling vs. late (Atrial) filling of LV. Normal ratio >2.5
 Filling fraction: % of filling that has occurred at 1/3, ½ and 2/3 diastole

Answer 109

A

 Ischemia
 Hypertension
 Viral
 Alcoholic
 Drug-induced (Adriamycin)
 Stress cardiomyopathy (Takotsubo)
 Infiltrative: amyloidosis, sarcoidosis

Answer 110

A

 Acute:
o Appears after an infusion of doxorubicin, seen between 4 & 24 hours, with significant recovery by 72 hours

 Chronic:
o Dose dependent and less reversibility
o the incidence increases beyond a cumulative dose of 400 mg/m2

Pre-treatment LVEF stopping criteria
 > 50% EF falls > 10% to a value below 50%
 < 50% EF falls > 10% OR below 30%
 < 30% DO NOT start therapy

Answer 111

A

List mode:
o digitized X and Y signals are time stamped as they are received in sequence and they are stored as individual events in the order they occur.
o After completion of data acquisition, the data can be sorted to form images in a variety of ways to suit a specific need (data manipulation by changing matrix size, time of acquisition per frame, rejection of bad gated data)

Advantages: wide flexibility, allows retrospective framing of data
 Data can be sorted after acquisition to form images in a variety of ways to suit a specific need
 Physiologic markers, eg start of cardiac cycle in a gated study, can be incorporated and bad signals from arrhythmic cycles can be discarded

o Disadvantage:
 Larger memory requirement
 Longer processing time
 Unavailability of images during or immediately after study completion

Frame mode:
o a matrix is chosen to approximates the entire area of the detector so a position (X,Y) in the detector corresponds to a pixel position in the matrix
o digitized signals (X,Y) are stored in the corresponding (X,Y) position in the matrix and subsequent signals are added
o Advantage: provides instant images for storage and display
o Must specify time of data collection per frame or total counts. Acquisition continues until a preselected time or total count is reached.

Answer 112

A

 Dodge-Sandler method: analogue method for manual edge detection and tracing for calculating areas and deriving %stenosis from coronary angiography
 Gaussian fitting (quantitative gated SPECT analysis): method to locate the mid-myocardial surface by fitting the count profiles from the perfusion data to asymmetric Gaussian curves
 Laplace operator: second derivative zero-crossing analytical method for edge detection

Answer 113

A

 pericardial effusion and or hemopericardium
 breast tissue or breast prosthesis attenuation artifact
 epicardial/pericardial fat pads
 mediastinal infiltrate
 pneumomediastinum
 mediastinal fibrosis

Answer 114

A

 Baseline exam before initiation chemotherapy or prior to 100 mg/m2; follow-up 3 weeks after last dose, before next planned treatment

 Baseline LVEF >=50%; second study after 240-300 mg/m2; repeat exam after 400 mg/m2 with known heart disease, hypertension, radiation exposure, ECG findings, or cyclophosphamide therapy; or repeat after 450 mg/m2 without risk factors

 Baseline 30-50%: repeat study before each dose

Answer 115

A

 Constrictive pericarditis (occasionally)
 Mitral regurgitation
 Medications: CCBs

Answer 116

A

 Technical
 Myocardial infarction with viable stunned myocardium
 Hypertension
 Hypertrophic cardiomyopathy
 Coronary artery spasm

 Resting reverse redistribution with thallium-201 uptake is caused by the increased washout of thallium-201 uptake in reperfused myocardium, such as stunned myocardium
 In these myocardial segments, interstitial edema after injury also is responsible for increased thallium-201 influx and early washout, resulting in reverse redistribution

Answer 117

A

 Rest-redistribution: image @10 min (Rest), 3-4h (redistribution)
 Stress-redistribution: image @10 min (post-stress), 3-4h (redistribution)
 Stress-late redistribution: image @10 min (post-stress), 24h (late redistribution)
 Stress-redistribution-reinjection: image @10min (post-stress), 2-3h (redistribution), then reinject 1 mCi 201Tl, then image 30 min later (reinjection)

Answer 118

A

extensive coronary artery disease
Infiltrated dose
Imaged too soon
Insufficient effort

Answer 119

A

Anterolateral base of heart -> spread to apex
 MIBG uptake: anterior, anterolateral and septal regions
o Only recover 25% of normal innervation
o With ↑ time after transplantation, MIBG heart-to-mediastinum uptake ratio ↑

Answer 120

A

 free fatty acids

 variable - depends on insulin levels; if not diabetic then ~ 70 %

Answer 121

A

 Oral glucose loading – for non-diabetic patients
 Hyperinsulinemic euglycemic clamping - simultaneous infusion of glucose and insulin to achieve perfect metabolic regulation
 Administration of nicotinic acid derivatives - inhibits peripheral lipolysis and thereby reduces circulating free fatty acids

TI201 more sensitive; Dobutamine echo more specific
201Tl vs. dobutamine echo vs FDG
Rest-redistrib TI-201 Sn = 85%; Sp = 60
FDG Sn = 92; Sp = 60
Dobutamine echo Sn = 80; Sp = 80

Answer 122

A

 hyperinsulinemic, euglycemic clamp (insulin 100 mU/kg/hr; glucose/K+ solution)

 oral glucose loading (50 - 100 g, sliding scale insulin if diabetic)

 nicotinic acid derivatives (Acipimox 250mg 2 hrs prior to FDG)

Answer 123

A

Recent MI (there is variable metabolism with a return to oxidative metabolism even in patients receiving clamping for prep)
Artifact (always a good answer)
LBBB (the cause is not totally clear however one group noted normal 11C-acetate metabolism, therefore this implies shift to oxidative metabolism, even though the patients in the above study were prepped with clamping)

o 4. Multivessel disease/ischemic cardiomyopathy (variable metabolic patterns again are the anticipated cause)

o 5. Diabetes (heterogenous uptake can often be seen in diabetics, likely due to insulin insensitivity)

Significance:
o The reverse mismatch pattern is seen almost as commonly as the “classic” pattern, and it seems to indicate viable, but jeopardiazed myocardium.

Answer 124

A

 Palmitate:
o Assess viability through fatty acid metabolism
o Uptake decreased in ischemic myocardium (myocardium shifts to glucose)

 Acetate:
o Direct substrate for TCA cycle by conversion to acetyl-CoA by acetyl-CoA synthetase
o Preferred as uptake not affected by plasma substrate concentration

Answer 125

A

F-18 FDG (glucose metabolism)
o Glucose metabolism by the heart is dependent on both dietary state and the level of ischemia.
o Glucose or FDG uptake is promoted by elevated glucose/ insulin levels.
o Ischemic, but viable myocardium uses glucose in preference to other substrates.
o Hibernating myocardium will show FDG-avidity.
o Scar tissue will not be metabolically active and will not show FDG-avidity.
o Uptake can be used to distinguish viable myocardium from non-viable (scarred) myocardium.

C-11 Acetate or C-11 Palmitate
 substrate for tricarboxylic acid (TCA) cycle and assesses cellular oxidative metabolism, essential for viable cells.
 C-11 acetate is NOT affected by plasma substrate concentration like C-11 palmitate. (C-11 acetate preferred; best for regional metabolic activity)
 infarct – decreased uptake and delayed clearance

Answer 126

A

 201Tl: cell viability, cell membrane activity, blood flow
 99mTc-sestamibi: nitrate enhancement
 18F-FDG: glucose metabolism
 11C-acetate: reflects overall regional myocardial oxidative metabolism (oxygen consumption)
 11C-palmitate
 18F-FMISO: hypoxia imaging

Answer 127

A

First-Pass Cardiac Imaging
o Caculating left and right ventricular ejection fractions
o Assessing wall motion abnormalities
o Quantifying left-to-right cardiac shunts
o Measuring cardiac output and absolute ventricular chamber volumes

Myocardial Infarction Imaging
o Diagnosing and assessing the location and extent of acutely infarcted myocardium

Right-to-Left Shunt Evaluation
o Detecting and quantifying right-to-left shunts using radiolabeled particles

Answer 128

A

 Not accurate

 To save:
o Deconvolution
o Equilibrium L-R shunt quantitation based on RV and LV stroke volumes
o Repeat with double the dose

Answer 129

A

γ-variate method (preferred) - the right lung TAC is fitted with a gamma variate function, which has a rapid upslope and exponential decay.
o Shunt component area = pulmonary - systemic blood flow.
o Size of shunt is determined by Qp/Qs = A1 / (A1 – A2) = 1 / 1 – K (shunt % = K)
o mild shunt Qp/Qs = 1.2-2.0, moderate 2.0-3.0, large >3.0
o Can detect shunts reliably down to Qp/Qs of 1.2. Surgery warranted if > 2.0

Area Ratio method – a 1st order exponential curve is fitted to the right lung TAC curve.
o A – area under the curve from Cmax to 0.01Cmax
o B – area under the remainder of the curve, but above A
o The Ratio B/A closely approximates Qp/Qs.

C2/C1 method – using the right lung TAC, calculate :
o recirculation peak counts (C2) over initial peak counts (C1).
o C2/C1 > 0.45 = shunt.
o Problem – can’t do a proper quantification of the size of the shunt

Answer 130

A

Normal value is between 1 and 1.2.

Qp/Qs is accurate between 1.0 and 3.0.

Answer 131

A

Mechanism: Pyrophosphate binds to mitochondrial calcium complexes and proteins in necrotic myocardium.
o Some residual blood flow necessary to deliver tracer to necrotic tissue (uptake highest peripherally)

Best time to inject: 15-20 mCi 24-72 hrs post infarct & image 1-2 hrs post injection (ANT, LAO, L LAT)
o First becomes positive 10-12 hours post infarct, highest sensitivity at 24-72 hours
o Maximal uptake at 48-72 hours with persistent abnormality seen up to 7 days out (normalizes by 2 weeks)

biventricular sign:
o intense biventricular uptake seen in amyloidosis

Myocardial uptake is non-specific:
o Acute MI
o Unstable angina
o Valvular calcification (very focal)
o Resuscitation / cardioversion
o Myocarditis / pericarditis
o Amyloid heart
o cardiomyopathy

Answer 132

A

Amyloidosis
sarcoidosis
Myocarditis
Radiation
Cardiotoxic drugs (doxorubicin)
Following cardioversion
Delayed renal clearance
unstable angina

Answer 133

A

 binds to heavy chain of cardiac myosin, exposed with disruption of cell membrane after infarction

Answer 134

A

 (Hypocalcemia)
 Rheumatoid factor
 Lithium or thiazide diuretics
 Tertiary hyperparathyroidism

Answer 135

A

Adenomas - 85 - 90%
Hyperplasia - 10 - 15%
Carcinoma - < 1%

Answer 136

A

 small scar
 faster recovery time
 less complications, smaller risk of hypoparathyroidism
 shorter operation time, less anaesthesia required, less expensive
 higher success rate

Answer 137

A

 false positive: thyroid adenoma, thyroid or lymph node malignancy, contamination
o AM has motion as most common

 false negative: rapid washout (assess 15 minute image), too small, no significant uptake (only 85% sensitive)

Answer 138

A

Add TcO4 or 123I scan (dual isotope study), and for TcO4 scan give perchlorate to wash out the gland. Suppress the thyroid gland with synthroid, before imaging with Tc-sestamibi. Use pinhole imaging or SPECT-CT

Answer 139

A

 renal failure

Answer 140

A

 subtraction technique with TcO4 (more likely to rule out false positive images)
 Pinhole images
 SPECT +/- CT

Answer 141

A

 20 % anterior mediastinum (lower parathyroid glands derived from 3rd branchial cleft, same as thymus) - Thyrothymic tract is the most common
 5-10 % posterior mediastinum
 5 % intrathyroid
 1 % carotid sheath

Answer 142

A

 F-18 FDG: conflicting results, Neumann found success that has not been replicated.
 F-18 DOPA – not useful
 C-11 methionine (best) – possibly better than sestamibi

Answer 143

A

Asymptomatic:
o serum Ca2+ 1.0 mg/dL above upper limits of normal
o 24 hour urine Ca2+ >= 400mg
o ↓ creatine clearance > 30%
o BMD T-score < -2.5 at any site
o age < 50 years old

 Symptomatic:
o Signs of calcium imbalance: nephrolithiasis, nephrocalcinosis, renal dysfunction, osteopenia with fracture, osteitis fibrosa cystica (brown tumor), any altered neurologic function

Answer 144

A

1. Thyroid binding globulin (75%)
o Increased binding:
 Estrogen (pregnancy, OCP)
 Infectious hepatitis
 Biliary cirrhosis
 Genetic determination

o Decreased binding:
 Androgens and anabolic steroids
 Large doses of glucocorticoids
 Nephrotic syndrome
 Major systemic nonthyroidal illness
 Active acromegaly
 Chronic liver disease
 Drugs – Dilantin, tegretol
 Genetic determination

Transthyretin (10-15%)
Albumin (5-15%)

Answer 145

A

 6.7 days

Answer 146

A

 sub-acute thyroiditis, iodine load i.e. iodinated contrast, exogenous thyroid hormone, struma ovarii or choriocarcinoma.

Answer 147

A

 Organification defect, peripheral resistance to thyroid hormone, PTU, recovery phase of sub-acute thyroiditis, iodine deficiency.

Answer 148

A

 If hypothyroid: iodine deficiency, dyshormonogenesis

 If thyrotoxic: TSH producing adenoma

Answer 149

A

 Lithium inhibits release of newly formed thyroid hormone, via not well characterized mechanisms (at supratherapeutic doses can inhibit Tg iodination and coupling reactions)

Answer 150

A

 Iodine load causes paradoxical blocking of iodine incorporation into thyroid hormone and transient hypothyroid state. Iodination of fatty acids blocking the action of NADP oxidase is the main mechanism.

 Protective mechanism

Answer 151

A

 Iodine load causes increased uptake and transient hyperthyroid state, usually in context of iodine deficient goiter

Answer 152

A

 Wolff-Chaikoff effect – a protective mechanism in which there is decreased formation and release of thyroid hormone in the presence of an excess of iodine

 Plummer’s Disease = toxic multinodular goiter

 Dyshormonogenesis results from a deficiency or absence of one or more of the enzymes involved in thyroid hormone synthesis or secretion. The most common is peroxidase deficiency which results in failure of organification of iodide to iodine. The perchlorate washout test will be positive.

 Pendred’s syndrome (AR) – peroxidase deficiency (hypothyroidism + goiter) + sensorineural hearing loss

 Marine-Lenhart syndrome – coexistence of TSH dependent nodule and Grave’s disease (cold on scan due to suppression)

Answer 153

A

3 clinical findings concerning for thyroid cancer:

Male sex, 2×
Age under 20 and over 60
History of radiation therapy
Family history
Lymph node enlargement
Suspicious US characteristics

Answer 154

A

Benign (80%)
o Simple cyst
o Adenomatous hyperplasia/colloid cyst/non-functioning follicular adenoma
o Focal hemorrhage
o Inflammatory
o Parathyroid adenoma

Malignant (20%)
o Thyroid carcinoma
o Parathyroid adenoma/carcinoma
o Thyroid lymphoma

Answer 155

A

i-131
Principle photopeak - 364 keV
Dose (uptake) - 5-10 uCi
Dose to thyroid assuming 25% uptake - 1330 mRad/uCi

I-123
Photopeak - 159 keV
Dose (uptake) - 50 to 200 uCi
Dose to thyroid - 12 mRad/uCi

Answer 156

A

 More ideal gamma emission for detection by NaI(Tl) scintillation crystal (159 keV vs. 364 keV)
 Shorter half life (13.3h vs. 8d)
 No beta emission to contribute to dose
 Less thyroid stunning

Answer 157

A

 Leakage
Thyroiditis

 Iodine excess
Jod-basedow effect
Iodinated contrast
Amiodarone

 Endogenous thyroid
Struma ovarii
Follicular thyroid CA with functional mets

 Exogeneous thyroid
Facticious

Answer 158

A

Hyperthyroid with increased RAI:

Graves
Large autonomously functioning nodule
Hashitoxicosis
Toxic MNG
TSH producing adenoma

Hyperthyroid with Normal RAI:

Toxic MNG
PTU, Tapazol
Graves with rapid turnover

Hyperthyroid with decreased RAI

Thyroiditis (subacute, silent, post-partum)
Expanded iodine pool
Facticious
Struma ovarii

Answer 159

A

Euthyroid with increased RAI

Rebound after T4 or antithyroid drug withdrawal
Subacute thyroiditis: recovery
Hashimotos, early phase

Euthyroid with normal RAI
1. Normal

Euthyroid with decreased RAI

Hashimotos
iodine pool (contrast dye for CT)

Answer 160

A

Hypothyroid with increased RAI

Recovery phase of subacute thyroiditis
Hashmotos
Iodine deficient goitre

Hypothyroid with normal RAI

Subaute thyroiditis early recovery
Hashimoto’s

Hypothyroid with decreased RAI

Hypothyroidism (1 or 2)
Hashimoto’s
Burnt out Graves

Answer 161

A

 Determine presence/absence of thyroid tissue
 Determine cause of hypothyroidism
 To start synthroid as soon as possible

Answer 162

A

Trapping (Na/I symporter)
Transport
Organification (Thyroid peroxidase)
Oxidation - Iodinating-tyrosine residues on thyroglobulin form iodotyrosines (MIT and DIT) stored in colloid
Micropinocytosis-vesicles containing colloid fuse with lysosomes to produce phagolysosomes
Proteolysis-produces iodothyronines that dffuse into the cytoplasm
Release (Secretion).

TSH affects TrICEPS=trapping (increases NIS synthesis), transport, iodination (increased TPO, its incorporation into apical membrane, Tgb, and generation of H2O2) coupling (increases TPO), endocytosis (micropinocytosis by activating cAMP), proteolysis?, secretion?.

 Lithium: Primarily inhibits release, this occurs by potentiating the iodine induced block of bonding and release by↑ intrathyroidal iodine content, but more likely by inhibiting cAMP mediated translocation of thyroid hormone

 Propranolol: mild ↓ peripheral T4 to T3 conversion, also reduces peripheral tissue response to T4 and T3

 Amiodarone: Major effects are due to its resemblance to thyroid hormone, causing inhibtion of type I and II deiodinase ↓ peripheral T4 to T3 conversion resulting in a decreased level of T3, may also decrease thyroid hormone entry into the tissues and binding of hormones to the receptor.

 PTU: Affects thyroid peroxidase therefore decreases oxidation/iodination/coupling, Non-conpetitive inhibitor for T4 to T3 conversion

 Methimazole: Affects thyroid peroxidase therefore decreases oxidation/iodination/coupling

Answer 163

A

 To demonstrate dissociation of trapping and organification functions in the thyroid in the setting of dyshormonogenesis/organification defect

 Protocol
o Tracer dose of radioiodine
o % uptake measured at 1-4 hours
o 1g KClO4 given orally (109 mg/kg)
o % uptake measured at 30-60 after

 Positive result
o Washout >10% suggests organification defect

Answer 164

A

 Ectopic thyroid can be lingual, substernal, pelvic/ovarian (struma ovarii); prevalence is 1/100000, 90% of ectopic thyroid tissue is lingual.

Answer 165

A

Regional nodal mets (75%) more common in children
Extrathyroidal extension (15% in adults) more common in children at presentation
Lung mets (5-20%, 10-20% have distal mets overall)
Metastases doe not indicate as poor a prognosis (mortality rate 15% at 15 years in children, 75% in adults)

Prognosis:
1. Adult; 93-97% 25 year survival in patients with complete resection and no metastases. 10-year overall survival rate 93% papillary, 85% follicular, 75% medullary, 14% undifferentiated.
o Children overall 95% 15-20 year survival. Pediatric papillary cancer does carry a much better prognosis than adult

Answer 166

A

 Pentagastrin stimulated plasma calcitonin (rises more with well-differentiated form) (0.5 μg/kg slow IV)

 CEA and histamine (rise with more aggressive undifferentiated form)

Answer 167

A

 All patients with MTC or other MEN II malignancies as well as consideration for family members of these patients, new evidence from BCCA appears to confirm the utility of this.

Answer 168

A

 MTC represents 10% of all thyroid carcinomas
 20-25% familial (autosomal dominant trait)
 Arises from para-follicular C-cells
 associated with MEN syndromes IIA and IIB
 MTCs express & release calcitonin and CEA (biomarkers)

Answer 169

A

 MEN I, II, III
 Zollinger-Ellison
 Von Hippel-Lindau
 NF1
 Tuberous sclerosis

Answer 170

A

 Zona glomerulosa

Answer 171

A

 Confirm non-pregnancy
 Block thyroid with SSKI (1 drop tid 2d before and continue 7d post-injection)
 Dexamethasone (1mg po qid7 days before and continue 5 days post-injection

Answer 172

A

 The dexamethasone suppression exam is indicated for the evaluation of primary aldosteronism or hyperandrogenism. Suppression helps to improve specificity of NP-59 exam because neither suppresses pituitary ACTH secretion and adrenal glands can be visualized normally, making detection of lesion more difficult.
 Dose: dexamethasone 1mg q6f for 7 days prior and continued through the exam.

Answer 173

A

Patterns of uptake:

unilateral uptake – functional adenoma suppressing contralateral gland.
bilat asymmetric uptake – bilateral nodular hyperplasia
bilat nonvisualization – glucocorticoid secreting carcinoma, severe hypercholesterolemia (false +)
bilat symmetric uptake – Cushings disease (pituitary), ectopic ACTH syndrome

Answer 174

A

 History to rule out medication known to alter adrenal uptake of NP-59 (spironolactone; is an aldosterone receptor inhibitor, increases aldo production, ketoconazole; decreases cortisol biosynthesis, medications that increase plasma renin; diuretics, OCP, ACEI) and whether excessive hypercholesterolemia is present (may decrease NP-59 uptake)
 SSKI 1 drop tid 1-2 days before and continue 7 days after to block thyroid uptake of radioiodide
 dexamethasone 4mg po od (divided dose) for 7 days before and continue through exam
 NP-59 dose - 1mCi/1.73m2 IV by slow infusion
 Image on days 3, 4 and 5 (Breakthrough visualization of the normal adrenal glands can be expected after 5 days)
 Diagnostic criteria:
o unilateral early uptake – functional adenoma
o bilateral early uptake (often asymmetric) – adrenal hyperplasia
o bilateral late uptake – non-diagnostic
o bilateral absent uptake – adrenal carcinoma / drug therapy

Answer 175

A

 No bowel activity

Answer 176

A

Phenobarbital 5mg/kg/day po in 2 divided doses for 5-7 days prior to the study may increase diagnostic accuracy

Dose of tracer: 200 uCi/kg (Requisites P181), 1 – 5 mCi (SNM/Auntminnie)

Imaging protocol:
o patient supine
o 128x128 matrix
o Large FOV gamma camera, LEAP or LEHR collimator
o Continuous dynamic acquisition in Anterior or LAO (1 frame/min), for 60 minutes

o At the completion of the 60 min dynamic study determine if additional images need to be acquired at 4 hours and 24 hours post tracer administration

Answer 177

A

 Kasai procedure (portoenterostomy) is performed initially to re-establish bile flow in biliary atresia. The fibrous remnant of the bile duct is transected at the portal vein bifurcation, flush with liver. A conduit of small bowel is constructed and anastomosed around the cut surface of the fibrous tissue.

 Phenobarbital pretreatment: (5mg/kg/day po in 2 divided doses) is instituted for 5 to 7 days to enhance biliary excretion of IDA. It is a potent inducer of the liver microsomal enzyme system, increases bilirubin conjugation, and provides better excretion of the IDA compound for earlier identification of a patent biliary tree

Answer 178

A

 CCK, somatostatin, atropine, prostigmine, secretin, bethanacol, erythromycin

Answer 179

A

 atropine or other anticholinergic
 morphine
 inhibitory hormone such as somatostatin
 loperamide
 CCB nifedipine
 progesterone

Answer 180

A

 0.02 μg/kg either over 3 minutes or 30 minutes

Answer 181

A

 relax LES
 increase pyloric tone
 decrease gastric motility
 increase pancreatic secretions
 increase gall bladder contraction
 increase small bowel motility
 increase bile production

(essentially promoting emptying of duodenum in preparation of next bolus)

Answer 182

A

 non-visualization of bowel activity
 allergy
 CNS and respiratory depression
 true rim sign (sign of gangrenous gallbladder and possible rupture)
 pancreatitis

Answer 183

A

 0.04 mg / kg IV over 2 minutes

Answer 184

A

 delayed liver-to-bowel transit time
 delayed gall bladder filling
 diminished response to CCK

Answer 185

A

 Calculous and acalculous biliary disease
o Chronic acalculous cholecystitis
o Cystic duct syndrome
o Sphincter of Oddi spasm

 Medications
o Morphpine
o Atropine
o CCBs

 Diseases with poor GB contraction
     o Diabetes
     o Sickle cell disease
     o Irritable bowel syndrome
     o Truncal vagotomy
     o Pancreatic insufficiency

Answer 186

A

 Main:
o Severe intercurrent illness
o Fasting
o Hyperalimentation

 Other:
o Recent meal <4-6h
o Prolonged fasting >20-24h
o Prior cholecystectomy
o Acute pancreatitis
o CCK just before exam

Answer 187

A

 Incomplete cystic duct obstruction
 Acalculous cholecystitis
 Accessory cystic duct
 Duodenal diverticulum stimulating GB activity

Answer 188

A

 Acute CBD obstruction (choledocholithiasis)
 Acute pancreatitis
 Carcinoma
 Infection
 Cholestasis

Answer 189

A

a) LS/SC scan = focal defect
b) HIDA = usually no uptake; definitely no excretion
c) gallium = similar or just above normal liver
d) Tc-RBCs = similar or just above normal liver

Answer 190

A

a) LS/SC scan = normal > cold > hot
b) HIDA = delayed washout
c) gallium = similar or just above normal liver
d) Tc-RBCs = similar or just above normal liver

Answer 191

A

a) LS/SC scan = focal defect
b) HIDA = focal defect
c) gallium = focal defect
d) Tc-RBCs = hypoperfused but hot spot on delayed images

Answer 192

A

a) LS/SC scan = focal defect on delayed; +/- hyperemia early
b) HIDA = cold initially; late uptake without washout on 2-4 hr images
c) gallium = uptake in most
d) Tc-RBCs = normal

Answer 193

A

a) LS/SC scan = Normal
b) HIDA = Normal
c) gallium = Normal
d) Tc-RBCs = Normal

Answer 194

A

a) LS/SC scan = normal or cold, liver looks heterogenous
b) HIDA = normal
c) gallium = normal; remainder of liver may be decreased
d) Tc-RBCs = normal

Answer 195

A

 nutcracker (multiple uncoordinated contractions)
 delayed esophageal emptying
 normal LES function

Answer 196

A

 achalasia - poor esophageal transit through all segments OR hold up distal segment only, aperistalsis of the esophagus with flat pattern in all segments and very prolonged retention in the distal esophagus.

 scleroderma - severely prolonged esophageal transit, >50% retention at 10 minutes.

 diffuse esophageal spasm - uncoordinated motions, multiple high amplitude nonpropulsive contractions, multiple uncoordinated peaks, normal LES.

Answer 197

A

 Arithmetic, Geometric, LAO positioning

Answer 198

A

 lag phase / trituration = time required for transfer of solid food from fundus to antrum and for grinding of food into smaller particles for passage into duodenum. Little or no gastric emptying occurs in this phase.

 Emptying phase – linear rate of emptying once food particle is small enough to pass into duodenum.

Answer 199

A

OR i.e. pyloroplasty, gastrectomy, vagotomy
Medications; erythromycin, cisapride, synthroid, metoclopromide, domperidone,
Illness - hyperthyroidism, ZES, gastritis, malabsorption,
Diabetic subjects without autonomic neuropathy.

Answer 200

A

 increased:
o erythromycin
o thyroxine

 delayed:
o nicotine
o gastrin (not true, this increases emptying)
o CCK
o Secretin
o progesterone
o glucagon
o somatostatin

Answer 201

A

duodenal ulcer
Zollinger-Ellison
Hyperthyroidism
Post-op (pyloroplasty, hemigastrectomy, vagotomy),
diabetes

Answer 202

A

 Causes of rapid gastric emptying
o Postsurgical; antrectomy, gastrectomy, vagotomy
o Hormonal; ZES, carcinoid
o Duodenal ulcer disease
o Medications (above)

Answer 203

A

 reflux “milk study” – NPO 4 hours, 0.2 – 1 mCi Tc-99m SC in milk, 10-15 cc/kg, primarily used to assess GERD and esophageal/gastric transit. Dynamic (15s for 1 hour) & delayed views (5 minute at 3 hours) over the chest and abdomen for aspiration. Reflux within 5 minutes of formula is not significant.

 salivagram – NPO 4 hours, 1cc of 0.5 mCi Tc-99m SC placed on dorsal surface of the tongue, dynamic images for 30-60 minutes. Look for tracheobronchial activity. Most sensitive

Answer 204

A

 Cyst
 Abscess
 Hematoma
 Laceration
 Benign and malignant tumors
 Dilated bile ducts

Answer 205

A

 Focal nodular hyperplasia
 Budd-Chiari syndrome (relative to adjacent tissue)
 Cirrhosis (regenerating nodule) (relative to adjacent tissue)
 SVC syndrome (arm injection)
 IVC obstruction (leg injection)

Answer 206

A

 FP - HCC, angiosarcoma, metastases (carcinoid and colon)

 FN - size < 1.5 cm; near vascular structure, thrombosed

Answer 207

A

 1.Cell and humoral mediated immune response
 2.Storage of platelets
 3.Mechanical filtration of RBCs
 4.Phagocytosis of encapsulated microorganisms
 5.Extrmedullary hematopoiesis.

Answer 208

A

 Budd-Chiari syndrome (hepatic vein thrombosis) has relatively more uptake in the caudate lobe than rest of liver. The impaired venous drainage of liver results in poor hepatic function, but the caudate lobe retains good function because it has direct venous drainage to IVC.

Answer 209

A

 Prevalence in population is stated to be about 2%, actually ranges from 0.2-4%
 Complications in 5% with an anomaly
 Based on rate of hemorrhage, about 32% with ectopic gastric mucosa

 3 complications
o Bowel obstruction (including intussusception)
o Hemorrhage
o Diverticulitis
o Umbilical fistula

Answer 210

A

Cimetidine:
o H2-receptor antagonist inhibits secretion of Tc-99m pertechnetate from gastric mucosa without impairing uptake
o 300 mg qid x 2 days for adults; 20 mg/kg/day po x 2 days prior to the study for peds
o OR 300 mg in 100ml D5W iv over 20 min with imaging starting 1 hr later

Ranitidine:
 Ranitidine works the same way as cimetidine & may be substituted
o 1 mg/kg iv for infants, children & adults up to a max of 50 mg infused over 20 min & imaging starting 1 hour later OR 2 mg/kg dose po for children & 150 mg/dose for adults

Glucagon:
o Decreases peristalsis but also decreases TcO4- uptake.
o Used in conjunction with pentagastrin
o Dose: 50 ug/kg iv 10 min after the Tc-99m pertechnetate

Pentagastrin:
o Increases gastric mucosa Tc-99m pertechnetate uptake but also increases its secretion and intestinal motility, potentially reducing ectopic site activity.
o H2 blockers antagonize pentagastrin; therefore, do NOT use
o Dose: 6 ug/kg SC 15-20 minutes prior to injecting Tc-99m pertechnetate
o Used in conjunction with glucagon

Perchlorate:
o Perchlorate should NOT be given prior to the exam as it will decrease gastric uptake of the tracer -> false negative study. Similarly atropine can cause false negative results. WHY???

 Protocol:
o 99mTcO4: 10mCi adult; 200 uCi/kg children IV
o LEAP, 128x128 matrix
o 20% window @ 140 keV
o Have patient fast for 4 hours prior to study
o No barium study or perchlorate prior to study
o Image for 30-60 min immediately after injection
 Medications:
o Cimetidine: 20 mg/kg/d for 2 days (adults 300 mg po qid x2d)
o Glucagon: 50 mcg/kg IV 10 min before study
o Pentagastrin: 6 mcg/kg sc 5-15 min before study

Answer 211

A

 Protocol:
o 99mTcO4: 10mCi adult; 200 uCi/kg children IV
o LEAP, 128x128 matrix
o 20% window @ 140 keV
o Have patient fast for 4 hours prior to study
o No barium study or perchlorate prior to study
o Image for 30-60 min immediately after injection

Answer 212

A

 vascular tumor
 aneurysm
 abscess
 inflammatory bowel disease
 contamination

Answer 213

A

FP:
o Any cause of focal hyperemia: Hemangioma (usually multiple), AVM, Vascular tumor
o Duplication cyst containing gastric mucosa
o Intussusception
o Inflammation: Appendicitis/Abscess/IBD
o Renal pelvis or collecting system activity
o Uterine Blush: Menstruating females

False negative
o Small amount of ectopic gastric mucosa - < 2cm^2
o Uptake in Meckel’s diverticulum obscured by overlying activity (urine, bladder)
o Uptake obscured by barium from prior study
o Technical problem
 Drugs – perchlorate

Answer 214

A

Most of the Tc-99m label would have decayed by 4 x T1/2 or 24 hours, so it is ok to do the Meckel’s scan, but it may be prudent to do a quick static image to see how much residual activity is left from the GI bleed study.

Answer 215

A

Glucagon

Heparin (If surgeon OK)

Answer 216

A

 Vascular neoplasm
 Splenosis
 Varices
 Vascular grafts
 Bladder/penile activity
 Inflammation

Answer 217

A

 Cylindrical balloon filled with Tc-99m solution in water, and placed in rectum/anal canal
 Image at rest, during sphincteric squeeze, and during a Valsalva maneuver, decubitus, sitting and standing

Answer 218

A

LEHR
Parallel hole
128x128

Answer 219

A

MAG3 10mCi (peds 0.1 mCi/ kg, min dose 0.5 mCi)
o Protein binding: mean 81% (66-90%)
o 98% secreted in PCT, 2% filtered
o extraction fraction: 40-50%

DTPA 10-20 mCi (peds 0.1 mCi/kg, min dose 0.5 mCi)
o Protein binding: 5-10%
o 100% filtered
o extraction: 20%

DMSA 5mCi (peds 0.05 mCi/ kg, min dose 0.3 mCi)
o Protein binding: ~ 90%
o 40-50% cortical accumulation, remaining for 24 hours
o Extraction fraction: 4-5% per pass
o Urine excretion: 4-8% 1st hour, 30% 14 hours

I-131 OIH 100-300 uCi (peds 3 uCi/kg, min 25uCi)
o Protein binding: 70%, 5% diffuse into RBC
o 80% tubular secretion, 20% glomerular filtration
o extraction fraction: 70 – 90%

Glucoheptonate 15mCi (peds 0.1 mCi/ kg, minimum dose 0.5 mCi)
o BOTH glomerular filtration (80-90%)/tubular secretion (10-20%) -> cortical uptake
o Protein binding: 7%
o 10-20% retained in renal tubular cells, rest excreted
o Extraction fraction: 20%

Answer 220

A

 ACE inhibitors inhibit angiotensin converting enzyme, which converts angiotensin I to angiotensin II

 Alternate to captopril (Requisites)
o Enalaprilat 40 μg/kg IV up to 2.5 mg over 3-5 minutes

Answer 221

A

hypotension, dehydration, Ca2+ channel blocker, obstruction

Answer 222

A

SNM guidelines: 7 ml/kg po >30-60 min prior to study

Answer 223

A

o Change of renogram grade
o [20 minute / maximum uptake] ratio change by >= 15% (cortical retention)
o Relative renal function change >= 10%
o Tmax increase by >= 2 min or 40% compared with baseline

Answer 224

A

o abrupt or severe HTN (diastolic BP > 120 mm Hg)
o HTN resistant to medical therapy
o HTN with onset in patients < 30 yo or > 55 yo
o abdominal or flank bruits
o unexplained azotemia
o worsening renal function during ACE inhibitor therapy

Answer 225

A

Hydration prior to the study:
 10 ml/kg water 30-60min before the study OR
 10 ml/kg half NS iv x 1 hour (500 ml max)

D/C certain medications before the study:
o ACE inhibitors (3 days short acting [captopril], 5-7 days longer acting agents)
o Angiotensin receptor blockers (3 days)
o Consider stopping calcium channel blockers & diuretics

o Make sure the patient has an iv before the study (many drop their blood pressure)
o Obtain a baseline pulse & blood pressure. Do not proceed with the study if an adult has a resting systolic pressure less than 140 mm Hg

should not be permitted to leave the department unless their blood pressure is at least 70% of baseline and they are asymptomatic.
o NPO for 4 hours prior to the study (otherwise food can compete with captopril absorption).

Choice of ACEI
o Captopril (25-50 mg crushed) po 1 hour prior to start of exam. Dose in children is 1 mg/kg up to 50 mg [Requisite: 0.5mg/kg up to 25]
 Monitor BP q 15min
o Enalapril 40 ug/kg (max 2.5mg) slow (over 5 min) IV infusion 10 – 15 minutes prior to start of exam.
 Monitor BP q 5 min
 Advantage – not affected by variable rate of GI absorption
 Disadvantage – longer duration of action

Answer 226

A

Lasix – 1mg /kg, maximum 20mg in children

Captopril – in children is 1 mg/kg up to 50 mg

Dehydration or poor renal function can affect collecting system clearance.

Answer 227

A

 Theory is that angiotensin I actually has other effects, such as bradykinins, which can independently increase efferent arteriole tone, separate from angiotensin-receptor stimulation by angiotensin II

Answer 228

A

1 mg/kg to a maximum of 20 mg in children (AM) or 40 mg (SNM) IV.

Answer 229

A

F0, F-15, F+20

Answer 230

A

 Diuretic clearance T1/2
 < 10 min = no obstruction
 < 10 < T1/2 < 20 min = indeterminate
 >20 min = obstruction

Answer 231

A

 Extraction fraction
 Mean transit time
 Vascular transit time
 Time to 20% extraction fraction

Answer 232

A

Gold standard

o Whitaker test; >22 cm of H2O at a flow rate of 10 ml/min.

Answer 233

A

 Dehydration
 IV infiltration
 Poor renal function
 Extremely dilated renal pelvis
 Full or non-compliant bladder
 Reflux

Answer 234

A

Gross ureteric dilatation/obstruction can cause missing of distal obstruction

 Low anatomical detail unable to detect mild vesicoureteric reflux

Answer 235

A

 UPJ obstruction
 UVJ obstruction
 Bladder outlet obstruction
 Vesicoureteric reflux
 Any obstructive lesion in collecting system
o Renal calculi
o tumor
o Fungal ball
o Blood
o Pus
 megaureter
 postural stasis

Answer 236

A

o response to diuretics
      hydration status
      diuretic dose (1mg/kg up to 40 mg)
      renal immaturity
      degree of renal insufficiency

o volume of dilated collecting system
o background activity or prolonged cortical retention distorts true activity in the collecting system

o functional obstruction
 distended bladder
 postural stasis

Answer 237

A

o Improper hydration
o Low diuretic dose
o Renal immaturity
o Renal insufficiency
o Prolonged cortical retention
o Massive renal pelvis
o Background activity
o Distended bladder
o Postural stasis

Answer 238

A

 UPJ obstruction (most common)
 VUR
 Posterior urethral valves
 Prune belly syndrome
 Duplex kidney

Answer 239

A

 Time to peak (Tmax), can be useful in assessing RAS post-captopril, increase of >2 minutes or increase of more than 40% indicates RVH, although not a high risk finding. Normal <5 minutes.

 20 min / max count ratio was found by some groups to be useful in assessing RVH but others reported it did not improve accuracy. In fact 15% increase was noted in a significant number of people who did not have RVH.

 ½ time to washout, normal is <10 minutes, 10-20 is nondiagnostic and >20 minutes is indicative of obstruction during Lasix renography.

Answer 240

A

 Deconvolution of the renogram curves allows the response of the kidneys to an ideal injection to be determined. As a result, improved inter- and intra-patient comparisons can be obtained.
 R(t) = I(t) * H(t)
o R(t) = real response of kidney to non-ideal input
o I(t) = ideal injection input
o H(t) = impulse response of kidney
 Real renal curve is considered a convolution of the Impulse input I(t) and the Impulse response H(t).

 To solve for H(t),
     o R(t) = background corrected renogram curve
     o I(t) = vascular region of interest, eg over heart

Answer 241

A

 1st day
o Hyperacute rejection
o RVT

 1st week
o ATN
o Hematoma
o Urinoma

 2nd week
o Acute rejection

 1 month
o Lymphocele

 6 months
     o Chronic rejection
     o Drug toxicity
     o Renal artery stenosis
     o Ureteral obstruction

Answer 242

A

 Post-partum hemorrhage (abruptio placenta)- 50% of cases 
 Bacterial sepsis 
 Shock 
 Myocardial Infarction 
 Burns 
 Severe dehydration (children) 
 Hyperacute transplant rejection

Answer 243

A

 equal, >90% for each

Answer 244

A

 No, can’t differentiate scar from acute pyelo

Answer 245

A

DMSA
o Advantages
 Good renal parenchymal images with minimal
interference from renal pelvis activity
 Lower dose to achieve the same cortical uptake
(40% retention vs. 10-20%)
 Lower gonadal dose
 Better target to background
o Disadvantages
 Uptake decreased in renal tubular acidosis,
Fanconi’s syndrome with nephrotoxic drugs

Glucoheptonate
o Advantages
 also allows for dynamic assessment of flow and
function
o Disadvantages
 unwanted collecting system activity may interfere
with renal parenchymal evaluation
 hepatic, gb, bowel activity can make assessment
difficult

Answer 246

A

Acute pyelonephritis (3 patterns)
o focal defect without loss of renal contour
o multiple focal defects
o diffuse involvement with reduced uptake and often
enlargement due to edema

Chronic scarring:
o Focal retraction of cortex with loss of renal contour
o Atrophy of one or both kidneys

Serial follow-up in 3-6 months shows persistence if scarring

Answer 247

A

pyelonephritis
o inflammation & edema compromise renal micro-circulation, causing ischemia
o later micro abscesses and necrosis

 Because there is more renal cortex in the upper and lower pole compared with the midpole

 Also, renal scarring due to VUR, VUR is more common in compound pyramids than in simple pyramids which are more common in the polar regions

 Compound calyces at polar regions are more prone to intratubular reflux, hence more susceptible to infection and scarring.

Answer 248

A

The HVT of 140 keV is 4.6 cm, the 12 cm right kidney is therefore only getting credit for about half of the photons it should in comparison to the left, if you double the relative amount (a 2:1 ratio turns into a 2:2 ratio), the differential function is symmetric

Answer 249

A

Intravaginal torsion (common)
o bell clapper deformity: tunica vaginalis completely surrounds testis

 Extravaginal torsion (rare)
o newborns
o testis and tunica vaginalis twist at external ring

 Blood supply:
o Testis: testicular (majority), cremasteric, and deferential arteries.
o Scrotum: branches of the pudendal artery, external to spermatic cord, so not affected by torsion

 Tc-99m pertechnetate 15 mCi IV (minimum dose 5 mCi)

 SSKI given immediately before exam to block thyroid uptake

 Flow images followed immediately by static and pinhole images
 Early:
o Blood flow – normal, decreased or absent
o Static image – decreased uptake, no halo

 Mid phase:
o Flow – increased to dartos
o Static – mildly increased halo, decreased central activity

 Late:
o Flow – marked increased to dartos
o Static – increased halo, absent central activity

Testicular survival:
Nearly 100% within 6 hours
55-85% 6 – 12 hours
10% after 24 hours

Answer 250

A

The clinical indications for radionuclide cystography include:
o Follow-up exam for patients with known reflux.
o Initial screening test for reflux in girls with UTI’s.
o Screening of asymptomatic siblings.
o Serial evaluation of children with neuropathic bladders who are at increased risk for reflux to develop.
o Assess of the results of antireflux surgery

Answer 251

A

 Probably more sensitive (0.2 ml reflux at a distance of 2 cm from the bladder)
 Ability to continuously monitor
 Irrelevancy of overlying bowel contents
 Lower gonadal dose (by 100x) than standard VCUG

Answer 252

A

 Protein that binds to a particle and induces phagocytosis by macrophages and neutrophil

Answer 253

A

Oxine - reacts with plasma proteins (transferrin, increased liver activity), therefore plasma must be removed before reaction

Tropolone - does not bind to transferrin; therefore, can label in plasma (Requisites) and still have high binding;
- tropolone is less efficient and causes impairment of neutrophil chemotaxis

Answer 254

A

In-111 oxyquinoline (oxine)
o cyclotron produced
o pure gamma emitter – 173 + 247 keV
o T1/2 67 hours
o Decays by EC to stable Cd-111

 In-111 oxine (0.5 mCi) is highly lipophilic and diffuses across leukocyte membrane. Once inside In-111 binds to intracellular proteins and oxine diffuses out

 Disadvantages:
o In-111 oxine not specific and will label other cells present
o In presence of proteins, eg transferrin, In-111 oxine will preferentially label
o need good vascular access (at least 19G), volume of blood (15ml), adequate leukocyte count (4000 cells / ml)
o high splenic dose in infant
o not useful if suspected infection doesn’t generate significant leukocyte response – chronic, fungal, or parasitic

Potential negative effect
o Neutrophils: (not proven)
o WBCs may not maintain adequate function after they have been removed from plasma for labeling
o potential effect on leukocyte migration and chemotaxis

Properties of ideal carrier molecule
o would specifically only label neutrophils – allows in vivo labeling after a single intravenous injection
o delivery into cell would be permanent – label would not dissociate or diffuse out of cell
o if label is released by cell, it would not label other cells
o carrier molecule would not affect cell viability or function

Answer 255

A

 18F-FDG
 64Cu
 111In-oxine
 111In-tropolone
 99mTc-HMPAO

Answer 256

A

In111-Oxine:

43 ml blood + 7 ml ACD or heparin
Sediment ~60 min
Centrifuge
Suspend pellet in saline, save plasma
label with ~ 1 mCi In111-oxine
Wash
Inject 500 uCi

99mTc-HMPAO (exametazime)
o Separated leukocytes suspended in plasma/ACD mixture
o Freshly formulated 99mTc-HMPAO added to cell
o Incubated for 15 min at room temperature
o Washed with plasma
o Suspended in plasma for injection
o Labeling yield 50-60%

Answer 257

A

111In
o no biliary excretion
o no significant renal excretion
o free In binds to transferrin and localizes to liver / marrow
o epithelial sloughing

99mTc
o some biliary excretion and GI activity after 1 hour, some concentration in GB
o significant renal excretion
o free TcO4 in prep localizes to stomach

Answer 258

A

o Tc-99m label allows higher dose, improves visualization of small part anatomy
o Tc-99m shorter T1/2, limits delayed imaging
o Tc-99m HMPAO normal distribution: bowel, urinary tract, GB
o faster uptake of Tc-99m HMPAO at sites of infection, allows earlier imaging
o lower absorbed dose more suitable for pediatric patients

o Lung activity is the result of cellular activation from in vitro cell manipulation. Lung & blood pool activity should not been seen by 18-24 hours

Differences in biodistribution:
With 99m-Tc-WBC
o Renal activity
o Bladder activity
o Gallbladder activity
o Bowel excretion

Answer 259

A

Well established:
 Gallium-67
 In-111 WBC
 Tc-99m HMPAO WBC

Not well established: 
 F-18 FDG
 99mTc-ciprofloxacin (infecton)
 99mTc-nanocolloids
 radiolabelled polyclonal IgG
 radiolabelled monoclonal antigranulocyte antibodies

Answer 260

A

 vascular tumor
 inflammatory bowel disease
 splenosis / ectopic spleen
 marrow distribution
 hematoma/GIB
 bowel activity
 tubes/lines/recent OR

Answer 261

A

C2010-16: 4 non-infectious causes of uptake on In-111 WBC scan in the abdomen
 GI bleed
 IBD
 NG tube, G tube, ostomy
 Surgical incision
 Swallowed activity from sinustitis or pulmonary infecttion
 Hematoma
 Infarct
 Accessory spleen

Answer 262

A

 spine infection
o large % of spinal osteomyelitis produce a cold lesion
o marrow in spine may mask abnormality

 infection in liver / spleen
o normal WBC activity may obscure infection

 antibiotic usage
o potential effect on leukocyte migration or chemotaxis

 chronic infection
o lymphocyte mediated infection (granulomatous process)

Answer 263

A

 There is no definite evidence that Abx decrease the sensitivity of a WBC scan. This is a theoretical concern, study showed that sensitivity on Abx for OM 90%, off Abx 92% (AM). Also the effect of Abx therapy on the labelled leukocyte behaviour is negligible

Factors which may reduce the sensitivity of 111In WBC imaging include:
o Neutropenic patient
o Adjacent soft tissue infection or septic joint
o Liver/Spleen activity may obscure site of infection
o Inadequate blood withdrawn for labeling (esp. children)
o Marrow hyperplasia (Sickle cell, Thalassemia): May have asymmetries which can mimic osteomyelitis
o Uptake in inguinal/iliac reactive adenopathy

Antibiotic therapy, Steroids, Hyperglycemia, Uremia, and Hyperalimentation have not been shown to reduce the sensitivity of 111In WBC imaging.

Answer 264

A

 Both In-111 WBC or Tc-99m HMPAO-labeled WBC can be used.

 111In WBC: early imaging (1-2 hours) is required as labeled cells sloughed from sites of active inflammation can be carried distally causing the appearance of pan-colitis or multiple sites of bowel inflammation.

 Tc-99m-HMPAO labeled WBC’: images should be acquired at 1 hour post-injection as later images (after 3 hours) may demonstrate non-specific bowel activity due to biliary excretion of secondary hydrophilic complexes

Answer 265

A

 Combined In-111/Tc-99m WBC and Tc-99m sulfur colloid marrow scan

 FP
o up to 50% of neuropathic joints have hematopoietically active marrow and may show WBC accumulation in the absence of infection
o WBC accumulation in adjacent soft tissue ulcer
o fracture

 Lesions that mimic osteomyelitis on 3PBS (Requisite P157)
o active OA
o gout
o fracture
o healing osteonecrosis
o Charcot’s joint
o recent surgery

Answer 266

A

Common:

Acute osteomyelitis
Radiation therapy
Metastases
Orthopedic prosthesis

Uncommon:

AVN
Treated osteomyelitis
Post laminectomy
Paget’s

 Early imaging at 4 hours may miss two-thirds of the lesions detected on later images.

 Occasionally significant blood pool activity remains- this may indicate that a large number of erythrocytes / platelets have also been labeled (proper label requires 1) gravity sedimentation + centrifugation)

Answer 267

A

 Documented fevers > 38.3°C for > 3 weeks

 Source of fever not known either 3 days of hospital investigation or 3 outpatient visits

Answer 268

A

 Scintigraphy has lowest specificity (84.5%), with MRI second lowest (92.8%)

 No significant differences in sensitivity (MR highest at 93%, lowest is CT at 84.3%)

 CT significantly less sensitive and specific compared with scintigraphy and MRI

 However, meta-analysis showed no significant differences in diagnostic accuracy overall

Answer 269

A

 Non-specific vascular
o Increased blood flow
o Increased capillary permeability

 Physicochemical environment
o Low pH promotes dissociation of Ga-transferrin complex

 Gallium is an iron analog & binds to
o transferrin (in plasma) – lowest affinity
o lactoferrin (in tissue, on leukocytes)
o ferritin (plasma & tissue)
o siderophore (protein released by microorganism) binds to iron/gallium
o phagocytosis of protein-iron complexes by macrophages

 Receptor-mediated
o Ga will bind to transferrin receptor on B cells

Answer 270

A

 recent chemotherapy, blood transfusion, hemochromatosis

 non-specific: increased permeability, increased interstitial fluid volume, increased osteoblast activity, increased vascularity.

 specific: PMNs incorporate Ga-lactoferrin intracytoplasmic, Beta-lymphocytes have lactoferrin binding sites, Macrophages engulf gallium protein complexes, bacterial siderophores.

Answer 271

A

o causes of iron overload (saturation of transferrin binding sites)
 iron dextran
 multiple transfusions
 hemolytic anemia
o gadolinium
o chemotherapy

 Competition for binding to transferrin causes gallium to behave more like calcium analog and bind to bone.

Answer 272

A

 Iron overload (iron supplementation, haemolytic anemia, multiple transfusions) saturates the Fe binding sites on transferrin, causing Ga to act more like Ca, therefore increased uptake in bone), gadolinium (similar mechanism), chemotherapy (causes increased lung uptake), antibiotics (increased colon and kidney uptake), estrogens (increased breast uptake)

 Hepatic cirrhosis

Answer 273

A

Altered biodistribution, with:
 Decreased hepatic uptake
 Increased bone uptake

Answer 274

A

 Correlates well with severity of disease determined by BAL or Bx.
 Diagnose sites of extrapulmonary disease.
 Assess for those with inactive or fibrotic disease that are unlikely to respond to tx
 Assess for response to therapy.

Answer 275

A

Pulmonary uptake grading by intensity relative to liver:
o 0 = uptake comparable to background
o 1 <
o 2 =
o 3 > liver

Answer 276

A

 Diagnosing disc space infection and vertebral osteomyelitis
 Evaluation and follow-up of active lymphocytic or granulomatous inflammatory process (sarcoidosis, tuberculosis)
 Chronic infection
 Fever of unknown origin
 Detection of pulmonary and mediastinal infection in immunocompromised patient
 Diagnosis and follow-up medical treatment of retroperitoneal fibrosis
 Evaluation and follow-up of drug-induced pulmonary toxicity (e.g., bleomycin, amiodarone)

Answer 277

A

• Ga-67 citrate has been used both in experimental animal systems of acute interstitial nephritis and clinically

Answer 278

A

4 causes for panda sign:

uveoparotid fever, 80% of patients with stage I disease, lymphoma, sjrogrens, HIV.

Answer 279

A

Chronic infection (osteomyelitis) (conventional nuclear medicine is better, no mention of FDG in Ell and Gambhir), B/D

Vasculitis - A based on better spatial resolution.

Vascular grafts A.

IBD - B

Infected hardware imaging (arthropathy with prosthetic infection) - B I think, FDG too non-specific (Ell and Gambhir, FDG is always less specific than WBC imaging pg. 688), but there is a crappy study in JNM that said it was good so they could be referring to that, who knows.

Answer 280

A

Bronchogenic CA PET+, Gallium+

Sarcoidosis (active) PET+, Gallium+

BAC - PET variable,

Answer 281

A

FDG uptake in sarcoidosis is nonspecific in both intensity and pattern, but typically shows uptake in intrathoracic lymphadenopathy (lambda sign – paratracheal + bilateral hilar), +/- lung parenchyma, cervical/abdominal lymphadenopathy, +/- spleen

Answer 282

A

Immune-mediated:
 Takayasu arteritis
 Giant cell arteritis
 Polyarteritis nodosa
 Behcet disease

Infectious:
 Neiserria (gonorrhea)
 TB
 Rickettsia

Answer 283

A

 Prosthetic joint infection (Sn 82%, Sp 87%,

Answer 284

A

The bone matrix has two main components :
o Organic matrix
o Inorganic salts – hydroxyapatite

 There are two main categories of bone :
o Spongy bone (trabecular bone, cancellous bone)
o Compact bone (cortical bone)

Answer 285

A

About 50% of the compound will be affixed to bone by 2-4 hours after injection. Maximal skeletal uptake occurs at 5 hours.
o rate of blood flow
o rate of bone formation – osteoblastic activity
o interruption of sympathetic supply
o extraction efficiency

Answer 286

A

o radiochemical impurity
o radionuclidic impurity
o chemical impurity
o insufficient uptake time
o patient motion during scan
o large amount of interstitial injection
o urine contamination
o grossly distended bladder obscures pelvis

Medications:
o ↓ bone uptake: corticosteroids, phospho-soda
o ↑ renal uptake: chemotherapy, iron, dextrose

Answer 287

A

Amphojel (Aluminum Hydroxide used to treat reflux) - forms colloids and liver is visualized
Iron overload - ↓ Tc-MDP uptake in bone
Bisphosphonates - ↓ Tc-MDP uptake in bone
Steroids - ↓ Tc-MDP uptake in bone
Melphalan - ↑ Tc-MDP uptake in bones (only agent ↑ MDP uptake)

Answer 288

A

24 hr delayed imaging
Diabetics, arterial insufficiency (PVD), old age, osteoporosis.
C2003-

Answer 289

A

 Freiberg’s infraction: metatarsal (usually 2nd)
 Kienbock’s disease: lunate
 Kohler: navicular
 Osgood-Schlatter’s disease: anterior tibial tubercle

Answer 290

A

Complications: (Primer)
o malignant degeneration (<=1%) – osteosarcoma most common (decreased activity compared to adjacent bone)
o pathological fracture
o secondary OA
o bone deformity, nerve compression
o if severe, high output heart failure

Answer 291

A

The most commonly involved bones:
o vertebral bodies (30-75%)
o skull (25-65%)
o pelvis (30-75%),
o proximal long bones (25-30%)

Answer 292

A

Three phases:
o lytic phase – increased uptake
o mixed phase – increased uptake
o sclerotic phase – mild to normal uptake

Answer 293

A

Hot calvarium, hot mandible, hot sternum, hot ant ribs, peri-articular accentuation, uniform skeletal uptake

Answer 294

A

 P - pancreatitis, pregnancy
 L - Legg-Calves Perthes, lupus
 A - alcohol, atherosclerosis
 S - steroids
 T - trauma
 I - idiopathic (SONK, LCP, Freiberg etc), infection
 C - caisson disease, collagen vascular disease
 R - radiation, rheumatoid arthritis
 A - amyloid
 G - Gaucher disease
 S - sickle cell disease

Answer 295

A

 Most common drugs
o Bisphosphonates
o Denosumab
o Bevacizumab, sunitib

Risk factors
o High dose IV bisphosphonate therapy
o Myeloma, breast, prostate
o Dental procedures: tooth extraction, dental implants,
o Co-existent cytotoxic drugs and glucocorticoid

 Osteonecrosis of the jaw is associated with high dose, IV bisphosphonates used in treatment bone metastases, for bone pain, pathologic fracture, limited mobility, malignant hypercalcemia and spinal cord compression. This has been found with the new generation bisphosphonates including zoledronate and palmidronate being the most common offenders, non-nitrogen containing BP (etidronate) have not yet been implicated in a single case.
 Mandible:Maxilla, 2:1.
 Osteonecrosis of the jaw is associated with high dose, IV bisphosphonates used in treatment bone metastases, for bone pain, pathologic fracture, limited mobility, malignant hypercalcemia and spinal cord compression. This has been found with the new generation bisphosphonates including zoledronate and palmidronate being the most common offenders, non-nitrogen containing BP (etidronate) have not yet been implicated in a single case.
 Mandible:Maxilla, 2:1.
 Three phase bone scan findings included increased perfusion in 9/12, increased blood pool in 10/12, and increased uptake in mandible in 9, maxilla in 2 and both in 4/12.

Answer 296

A

 Peripheral increased uptake in crescentic pattern in the tibial plateau as well as focal posterior femoral condylar uptake
 Other elements:
o medial collateral ligament, ACL
o tibial plateau fracture

Answer 297

A

 About 80% of bone scans will show increased activity at a site of fracture by 24 hours, and 95% by 72 hours, although older (> 65-75) and debilitated patients may not show activity for several days to a week. For this case, image in 3 days and if negative and continued clinical suspicion repeat in 7 days.

Answer 298

A

 stress fracture - normal bone, overuse
 insufficiency fracture - normal use, abnormal bone
 pathologic fracture - weakened bone due to focal pathology, normal use

Answer 299

A

 What is it: herniation of synovium into the anterior superior femoral neck through a cortical defect.
o Associated with femoroacetabular impingement
 How patients present: usually asymptomatic, larger ones present with hip pain (in runners)
 Bone scan findings: usually negative (any reference other than AM), can see focal uptake along the upper portion of the femoral neck (AM).

 Name 2 lesions with similar bone scan findings: 1.tension stress fracture is often seen, but more lateral towards the greater trochanter (elderly at risk for fracture),

compression type stress fracture is usually along the inferior aspect (young adults, more stable, treat conservatively),
Bone island, also usually asymptomatic and negative on bone scan, Journal of Nuclear Medicine Vol. 43 No. 4 484-486, showed that bone island and herniation pit were the most common causes of asymptomatic femoral neck uptake.

Answer 300

A

 ACL injury
 it would help confirm the diagnosis because the findings suggest “kissing contusions” due to valgus stress, commonly associated with ACL disruption
 Tibial tuberosity:
o Osgood-Schlatter
o Bone scan: anterolateral uptake

Answer 301

A

Upper extremity
 Subacromial
 Subcoracoid
 Ulnolunate (ulnar impingement syndrome)
 Dorsal wrist impingement (radiocarpal)

Lower extremity

 Femoroacetabular
 Anterior ankle impingement
 Anterolateral ankle impingement (soft tissue)
 Anteromedial ankle impingement
 Os trigonum (posterior impingement syndrome)

Answer 302

A

Technical/methodological:
o Blood flow and pool phases
o Delayed imaging at 24 hours
o SPECT/CT

Answer 303

A

 Children under 18 months - Epiphyseal and joint involvement due to the presence of trans-physeal vessels
 Older children - metaphysis of long bones where turbulent, slow flow is felt to favor bacterial deposition
 Adult (if hematogenous spread): vertebral bodies most common because of red marrow with abundant vascular supply

 Most common organism:
o Overall – S. aureus
o Neonates – group B streptococcus
o Sickle cell anemia – S. aureus, Salmonella

Answer 304

A

 Bone and gallium, and MRI have similar sensitivity for osteomyelitis
 MRI: assess spinal canal, soft tissue/epidural abscess
 Gallium: metallic hardware, followup with treatment

Tc99mdp Sn 95% Sp 90, improve with gallium and spect

Gallium - Sn 85, Sp 77, improve with bone scan

In111 - Sn 35%, Sp 98%, improve with SC bone marrow subtraction

Answer 305

A

 Pain
 Fever
 Neuropathy
 ↓ ROM
 Irritibility in young children
 Local muscle spasms

Answer 306

A

 Involucrum: layer of new bone growth outside existing bone seen in pyogenic osteomyelitis
 Brodie’s abscess: intraosseous abscess in cortex, metaphysis, becomes walled off by reactive bone
 Cloaca: allow pus and sequestra to drain along sinus tracts to the skin
 a) detached necrotic bone b) thickened periosteum overlying

Answer 307

A

 Salmonella 1st

 S. aureus 2nd.

Answer 308

A

 Diaphysis, most common in femur, tibia, and humerus

Answer 309

A

 Subperiosteal/intramedullary pus/edema and vasospasm can cause vasoocclusion than can lead to absent hyperemia.

 Pediatric:
o Ischemia from thrombosis
o Regional vascular tamponade from edema, abscess, joint effusion, subperiosteal extension of fluid

Answer 310

A

 1.Ankylosing spondylitis
 2.Reiters disease
 3.Enteropathic arthropathy
 4.psoriatic
 5.undifferentiated

Answer 311

A

 Acute; 0 – 20 weeks - increased all phases
o Pain, swelling, stiffness of involved joint
 Dystrophic; 20-60 weeks - blood flow and pool may normalize; delay remain increased, particularly periarticular
o Changes in skin/nails, muscle wasting, osteopenia
 Atrophic 60 weeks + - all 3 phases may be normal or diminished; delayed phase may remain increased (variable, 30% ↓, , ↑)
o Joint ankylosis (from synovial proliferation)
 NOTE: all 3 phases may be decreased acutely in children`

Answer 312

A

CRPS I - (RSDS)

Initiating noxious event or cause of immobilizaiton
Continuing pain, alloldyneia ,hyperalgesia
Edema, changes in skin blood flow

CRPS II (casualgia)

Continuing pain, allodynia, or hyperalgesia after a nerve injury, not necessarily in distrubution of nerve
Edema, changes in skin blood flow

Answer 313

A

 Infection
 Prosthesis loosening
 Fracture
 Dislocation/subluxation
 Small particle disease/ inflammation associated with the THA
 Heterotopic ossification
 Trochanteric or iliopsoas bursitis

Answer 314

A

1. Direct extension (eg. chest wall in breast/lung ca)
1. Hematogenous seeding of bone marrow
1. Batson’s vertebral venous plexus – valveless, low pressure venous system that communicates with pelvis/abdo/chest. Connects to intercostals, lungs, kidneys.

o Metastases can go from pelvis to skull and bypass IVC, portal venous system.
o Can also get retrograde flow into this system due to ↑intraabdominal pressure from coughing.
• 4. Bone metastases from lymphatic drainage are very uncommon.

Answer 315

A

Primary tumor < 4 cm - F
Asymptomatic patient F/U - F
Assess response to therapy - T
Large mass with nodules - T
Small completely excised nodule - F
Pt with bone pain - T

Answer 316

A

 Confirm flare response
o Repeat bone scan in 6 months (Seminars 2009)
o Follow blood tests: bone specific ALP, urine hydroxyproline, N-terminal telopeptide

Answer 317

A

Scintigraphic flare on bone scan is seen after chemo (2 weeks – 3 months), has to do with bone healing, and has good prognosis (i.e. bone scan looks worse but only because the bone has begun healing itself).

Clinical flare (= PET flare) – is seen only with hormone therapy for breast cancer (tamoxifen) – there is objective clinical worsening of symptoms but 80% will respond to therapy or continued treatment. This can be seen as increased uptake on PET lasting a few days after hormone therapy is given.

Answer 318

A

Prevalence of skeletal metastasis correlates with increased PSA level. Bone scan should be limited to PSA greater than 10 ng/mL, high gleason scores, locally advanced disease, elevated alk phos or bone sx.

 Assuming the use of F-18 FDG PET, then it has limited role, but F-18 PET is a different story: F-18 is more sensitive than bone scan for the detection of bone metastases (sensitivity 81% vs 70%, better than that on a per lesion basis)

Answer 319

A

o Without bone mets: median PSA 12 ng/ml
o With bone mets: median PSA 59 ng/ml
o <10 ng/ml NPV of 96%
o >100 ng/ml PPV 50%

Answer 320

A

Patient on hormone therapy with anti-androgens.

Answer 321

A

 StatDX:
o Osteoid osteoma: 10-25y
o Osteosarcoma: 75% <20y (peaks in adolescence)
o Ewings: 5-20y (peaks in adolescence)
o Osteochondroma: 1st 3 decades (peak 10-15y)
o Non-ossifying fibroma: childhood and adolescence
o Chondrosarcoma: peak, 5-7th decade

Answer 322

A

 Most common presentations:
o pain
o local soft tissue swelling
o 70% neurologic abnormalities
o fever
 Clinical presentation; Pain with mass, limp, swelling, path frature rare (except telangiectatic) as is systemic sx (unlike ES)
 Most common site of metastases is around the knees (1.distal femoral, 2.proximal tibia) followed by humerus (3.proximal humerus), 4.flat bones are more aggressive.

Answer 323

A

 Most common age range: most common malignant bone tumor of children and young adult. Rare in <5y, 2-3/1000000 in 5-9, 8-9/1000000 in 10-20 when the incidence is highest.
 Most common sites – name 3: 50% around the knee, 1.Distal femoral metaphysis > 2.Proximal tibial metaphysis > 3.Proximal humerus (15%)&raquo_space; 4.Flat bones
 Most common sites of metastasis: AM says lung and bones; Dahnert says Lung, lymph nodes, liver and brain with bones uncommon. Emedicine says lungs and other sites are unusual.
 Clinical presentation: most often pain with a mass, limp and swelling. Path fracture unusual except in telangiectatic, systemic sx rare. (emedicine)

Answer 324

A

 LCH sensitivity ~85% (radiographs preferred)

 Ewing sarcoma lung metastases: low sensitivity

Answer 325

A

 Most lesions are osteolytic, and photopenic on bone scintigraphy
 Also marrow-based lesions
o 18F-FDG
o 99mTc-sestamibi

Answer 326

A

Why is skeletal survey in radiology better than bone scan for multiple myeloma?
 See above, most lesions are osteolytic, and appear photopenic on bone scintigraphy
 Also marrow-based lesions
 Skeletal survey detects lytic lesions with >30% trabecular loss

Answer 327

A

 POEMS syndrome osteosclerotic or osteolytic lesions
o http://biomed.papers.upol.cz/pdfs/bio/2012/01/08.pdf
o http://www.ncbi.nlm.nih.gov/pubmed/9442145
 Complications
o Osteoblastic lesions with multiple myeloma is from pathologic fractures
o Osteomyelitis, sinusitis or mastoiditis due to increased disposition from steroids
 Plasmacytoma
 Osteolytic lesions of multiple myeloma do not incite much reactive bone formation

o Primarily marrow involvement
o Aggressive, no chance for osteoblastic repair

Answer 328

A

 6-12h post-injection

Answer 329

A

 Osteomalacia = normal volume of bone with diminished mineralization of the organic matrix, associated with vitamin D deficiency

Findings:
 Metabolic bone disease:
o generalized increased uptake with increased bone to soft tissue ratio
o increased uptake in axial skeleton
o increased uptake in periarticular areas
o increased uptake in long bones
o increased uptake in calvaria
o increased uptake in mandible
o increased uptake in costochondral junctions (beading)
o increased uptake in sternum (tie sternum)
o Faint or absent renal uptake

 Specific to osteomalacia:
o focal increase uptake due to pseudofractures

 Depends on the metabolic bone disease;
o Hyperparathyroidism; Primary-usually normal, generalized increased uptake in the axial skel, long bones, mandible, hands, sternum, brown tumors late in disease, CF, metastatic calcification.
o Secondary-Usually abnormal, Low renal uptake, generalized increased uptake skeleton, brown tumors less often.
o Osteomalacia-Generalized increased uptake, looser zones, pseudofractures.

Answer 330

A

 Calciphylaxis is a small vessel vasculopathy with vascular calcification, fibrosis, and thrombosis. It results in ischemia and necrosis of skin, subcutaneous fat, visceral organs and skeletal muscle. It is usually seen in patients with ESRD.

Answer 331

A

 Increased regional vascularity/ vessel permeability/ inflammation
 MDP may complex with dextran or iron at the site of injection (paper from 1976)
o Proposed mechanism is iron-mediated dissociation of Tc-99m diphosphonate complex and subsequent formation of Tc-99m iron complexes (transchelation)
o Increased calcium content of tissue following the injection

Answer 332

A

 Pre-renal
o Poor hydration with delayed excretion of the tracer
 deposition
o Iron overload (eg. multiple transfusions)
o Amyloidosis
 Drugs (probably due to interstitial nephritis)
o Chemotherapy
o antibiotics
 Nephrocalcinosis / metastatic calcification
 pyelonephritis
 ATN (early stage)
 Glomerulonephritis
 Thalassemia major
 Sickle cell – due to abnormally renal concentrating ability due to medullary ischemia
 Vascular
o Renal vein thrombosis
o Renal artery stenosis

Answer 333

A

Patient factors
o 1:Dehydration/renal failure
 Excess serum aluminum (e.g., renal failure)
CHF
o Hemochromatosis
o Metastatic calcification

Technical factors
o 2:Insufficient uptake time
o 3:Radiochemical impurity
 Free pertechnetate
 Excess aluminum ion in radiopharmaceutical
 Excessive colloid formation
o Interstitial injection
o Off-peak

Drugs
o 4:Meperidine
o Iron dextran
o Bisphosphonates

Answer 334

A

 Long-standing congestive heart failure
 Myocardial infarction
 Pericarditis
 Amyloidosis
 Unstable angina
 Post-resuscitation or cardioversion

Answer 335

A

 Deltoid insertion
 Bilateral rotator cuff injury/calcification
 Enthesopathy

Answer 336

A

 HO findings on bone scan reversible in 1-6 month

Answer 337

A

 Knee: microfractures, interruption of blood supply

 Hip: unknown, fat emboli?, interruption of blood supply

Answer 338

A

Infection/inflammation: periostitis (eg. syphilis)
Trauma: stress changes
Metabolic: HO, hypervitaminosis A, skeletal fluorosis, thyroid acropachy, renal osteodystrophy
Congenital: Caffey disease (infantile cortical hyperostosis)
Misc: venous insufficiency

Answer 339

A

I – 0%
II – 3%
III – 7%
IV – 47%

Answer 340

A

Metastatic calcification
Diffuse metastases (especially osteosarcoma)
Pleural effusions (especially malignant), pleural metastases
Post-radiation changes
Primary lung ca
Alveolar proteinosis, alveolar microlithiasis

Answer 341

A

Multiple myeloma (age > 40)
metastases
Eosinophilic granuloma (age < 30)
bone cyst
prior craniotomy
metal plate, attenuation artifacts

Answer 342

A

Iron overload
Amyloidosis
Metastases (lymphoma, colorectal ca)
Aluminum (external or internal)
TcO2 colloid impurity
Recent sulfur colloid scan

Answer 343

A

Neuroblastoma
Metastases
Infarct
Granuloma
hemorrhage

Answer 344

A

Very common, 10% of autopsy series. Incidence increases with age.
50% are located in the vertebrae, 20% in the skull.
If < 3cm, bone scan is normal in almost all cases, if > 3cm, can be ↑↓→.

Answer 345

A

Preop injection with radiotracer, to localize the osteoma with an intra-operative probe.
Intraoperative gamma camera imaging, with portable camera

Answer 346

A

Proximal femur, tibia (70%)
Spine – posterior elements (15%)
carpal/tarsal bones (8%)

Answer 347

A

giant cell tumor – moderate-intense ↑
osteopoikilosis - N
fibrous dysplasia – moderate-intense ↑
vertebral hemangioma – N or ↓
unicameral bone cyst – N or mildly ↑
sphenoid wing meningioma – moderate-intense

Answer 348

A

(RAS)
Calyceal diverticulum
Duplicated renal collecting system
Renal mass
Obstruction
Renal vein thrombosis
Radiation nephritis

Answer 349

A

Golf → hook of hamate
Ballet → metatarsal (calcaneus)
Backpacking → clavicle
Sky diving → tibia (calcaneus)
Forced march → metatarsal
Deep sea diving → femoral head
Long distance running → femoral neck
Pneumatic drilling → metacarpals
Gymnast → vertebra

Answer 350

A

 Cortical uptake (tram track sign) in long bones
 Spares periarticular regions (lack of periosteum)
 Clubbing: uptake in distal phalanges of hands and feet (due to hyperemia in nail beds – mechanism unknown

Answer 351

A

polycythemia rubra vera – peripheral marrow expansion
myelofibrosis – massive splenomegaly, moderate hepatomegaly, ↓central marrow, ↑↑ peripheral expansion
aplastic anemia – decreased marrow uptake
multiple myeloma – peripheral expansion, focal defects
external radiation – local sharply demarcated defects
hemochromatosis – absent marrow uptake (normal in primary)

Answer 352

A

a) 14 yo boy with painful scoliosis and a small focus of intense uptake in lamina of L2 on bone
scan - osteoid osteoma
b) 56 yo woman with lower spinal fusion and normal ESR with linear increased bone uptake
just above the fusion – degenerative disc disease above the rigid segment.
c) 66 yo man with lytic lesion of clavicle on x-ray and reduced bone uptake – myeloma
d) 12 yo girl with salmonella osteomyelitis and soft tissue MDP uptake in LUQ – sickle cell
e) 8 yo girl with multiple bone lesions in metaphyses of long bones on x-ray and bone scan and a
soft tissue mass with MDP uptake displacing the right kidney downward – neuroblastoma.
f) 70 yo man with Pagets of left innominate bone with diffuse increased activity on bone scan
except for a photopenic center – sarcomatous degeneration.
6 yo boy with absent activity in antero-lateral portion of left capital femoral epiphysis – Legge-Calve-Perthes Disease.
38 yo man with increased MDP uptake in right femoral head and normal X-rays – idiopathic AVN.
4 month old baby with multiple foci of increased uptake in ribs on both sides near the spine – child abuse.
72 yo woman with dementia and Stage II breast ca with focal bone uptake in right superior and inferior pubic rami and right side of sacrum, with generalized osteopenia on X-rays – insufficiency fractures.
40 yo diabetic with a rocker bottom foot swelling and warmth but no ulceration and intense MDP uptake in midfoot – Charcot joint.

Answer 353

A

L-amino acid transporter (presynaptic)
 F18-DOPA

D1 receptors
 C11-NNC112

D2 receptors (post-synaptic)
 123I iodobenzamide (IBZM) (striatum)
 123I-IBF
 11C N-methylspiperone (striatum)

D2 & D3 receptors
 123I epidepride
 123I iodobenzamide (IBZM)

Dopamine Transporter (DAT), presynamptic
 123I b-CIT
 123I FP-CIT (Ioflupane = DaTscan)
 11C CFT 18F CFT

Answer 354

A

DAT (SNM)
o To confirm diagnosis in setting of tremor: essential tremor vs. presynaptic Parkinsonian syndromes (Parkinson’s disease, multiple system atrophy, progressive supranuclear palsy)
o Early diagnosis
o Differentiation of presynaptic Parkinsonian syndromes from parkinsonism without presynaptic dopaminergic
o Differentiation of dementia with Lewy bodies from Alzheimer’s disease

D2 (EANM)
o Differential diagnosis of parkinsonian syndromes
o Asessment extent of D2 receptor blockade during treatment with D2 antagonists
o Huntington’s disease
o Wilson’s disease
o Pituitary adenoma

Answer 355

A

 Cocaine, amphetamines, methylphenidate
 Ephedrine, phentermine
 Bupropion
 Fentanyl
 Anesthetics (ketamine, phencyclidine, isoflurane)

Answer 356

A

 Thyroid blockade: 100 mg I
 5 mCi slow IV (20s)
o Don’t need dim or quiet environment
 Imaging:
o 3-6 h
o 159 keV photopeak +/- 10%
o FOV brain
o SPECT smallest rotational radius (11-15 cm), 3°, 30-40s/position
o 128x128 matrix
o >1.5 million counts

Answer 357

A

Perfusion
Decreased temporal/parietal association cortex, posterior cingulate/precuneus Preserved sensorimotor cortex, basal ganglia, visual cortex, brainstem, cerebellum

Glucose metabolism
18F FDG: decreased parietotemporal, posterior cingulate, medial temporal; proresses to prefrontal; preserved sensorimotor cortex, midbrain, pons, thalamus, cerebellum

β amyloid plaque
11C PiB 18F florbetapir (Amyvid)

β amyloid plaque & neurofibrillary tangles
18F FDDNP

Answer 358

A

 Selectively binds to only amyloid
 High affinity for amyloid (Kd ∼ 1 nM)
 Crosses the blood–brain barrier well at early times after injection (≥0.4%ID/g in rat brain or ≥4%ID/g in mouse brain; may be expressed as a species-independent value where 0.10 (%ID/g) × kg = 100(% ID/g)×g = 1 SUV unit)
 Rapid brain clearance of compound not bound to targeted amyloid (clearance t1/2 ≤ 30 minutes in rodents)
 No radiolabeled metabolites in brain
 Works well in transgenic mice models of AD

Answer 359

A

 Something tryptophan (probably alpha-[11C]methyl-L-tryptophan, probably 5-HT receptors, that is why it was developed, but nothing definite, along with 18F-FCWAY, 18F-MPPF)

 C-11 carfentanil (opiate)

 C-11/F-18 flumazenil - GABAA
o GABA is the primary inhibitory neurotransmitter and implicated in seizure

 FCWAY
o Agonist of 5HT1a
o (Serotonin is now thought to be implicated in seizure cessation)

 [11C]methyl-L-tryptophan (AMT)
o Increased uptake in epileptogenic tubers in Tuberous Sclerosis. AMT images serotonin synthesis.

 11C-diprenorphine-Non subtype selective Opioid receptor imaging

 C-11 carfentanil (opioids implicated in sz cessasion)
o Mu-Opioid selective receptor imaging agent.

Answer 360

A

F-18 DOPA evaluates dopamine synthesis

 I-123 B-CIT evaluates dopamine transporter .
 In someone with Parkinson’s, what does I-123 B-CIT scan show and if symptoms more severe on one side?
 Cocaine analog which has decreased striatal uptake in Parkinsons. Substantial striatal specificity. If unilateral severity, decreased contralateral tracer uptake. Predominantly decreased in the putamen.

Answer 361

A

What are Lewy bodies made of? What diseases are they found in?
 Eosinophilic cytoplasmic inclusion: aggregations of α-synuclein, neurofilaments and other proteins
 Diseases:
o Parkinson: substantia nigra, hippocampus, amygdala, cingulate gyrus, other regions
o Lewy body dementia
o Multiple system atrophy
o Down syndrome

Answer 362

A

tremor, rigidity and bradykinesia along with response to L-dopa.

Answer 363

A

 Frontal: personality
 Parietal: language
 Temporal: memory

Answer 364

A

Huntingtons - ↓ caudate and lentiform nuclei
Parkinsons - similar to AD, with involvement of visual cortex.
Alzheimers - ↓ bilateral posterior temporal and parietal regions, extending medially into posterior cingulate gyrus. Initially asymmetric but then bilateral.
multi-infarct dementia - single infarct dementia usually in left hippocampus, multi-infarct shows many infarcts that can be anywhere.

Answer 365

A

Schizophrenia

Answer 366

A

 Hypofrontality

 Reversal with therapy

Answer 367

A

What pattern of perfusion abnormality is seen with ADHD?
 Hypoperfusion: caudate + central frontal lobes
 Hyperperfusion: occipital lobes
 Reversal with therapy

Answer 368

A

 Bipolar: frontal/global hypometabolism, temporal lobe asymmetries

 Unipolar: global/caudate nucleus hypometabolism (lateral frontal, left>right)

Answer 369

A

 Anterior-posterior commissure line is the line passing through superior edge of anterior commissure and inferior edge of the posterior commissure

 Anterior commissure = white matter that connects cerebral hemispheres

Answer 370

A

 Penumbra

Answer 371

A

 FDG-PET/CT

 Tl-201

Answer 372

A

 Interictal SPECT – 40-66 %, incorrect localization in 7%
 Post-ictal-75%, incorrect localization in 2%
 ictal 80 - 90 %, up to 95%
 interictal PET 79%
 Specificity 100% is there is interictal hypoperfusion and ictal hyperperfusion in the same location.

Answer 373

A

 neurofibrillary tangles, amyloid plaques
 biparietal-temporal earliest involved, posterior cingulate is also involved early
 FDG, ECD, HMPAO; true but others include, 18F-FDDNP (imaging plaques and tangles), 18F-PIB (plaques), 18F-MPPF is a selective 5-HT1A imaging agent, decreased in Alzheimer’s disease.

Answer 374

A

o “earliest MR changes occur in the posterior cingulate, the entorhinal cortex and the hippocampus” – medial temporal lobe (hippocampus)

o 2 pathologic findings:
 amyloid plaque
 neurofibrillary tangles
 progressive lossof cortical neurons

o SPECT pooled data: sensitivity: 81%, specificity: 70%

o PET FDG imaging has been shown to have a sensitivity of 92-96%, specificity of 63-89%

o F-18 FDDNP targets amyloid plaques / neurofibrillary tangles in AD patients
o 18F-florbetapir (Amyvid)
o C-11 Pittsburgh Compound-B (PIB) targets beta amyloid plaque
o False positive studies in normal aging.

Answer 375

A

o AKA frontotemporal dementia
o Changes in personality, language and behaviour; memory dysfunction late
 Attention deficits
 Impaired executive function

 FDG-PET
o Hypometabolism: frontal and anterior temporal lobes (vs. biparietotemporal, posterior cingulate and precuneus for Alzheimer’s)
o Hypometabolism in the frontal and anterior temporal lobes

Answer 376

A

 Tauopathy vs. non-tauopathy

o Non-tauopathy: ubiquitin positive neuronal inclusions

Answer 377

A

 Luxury perfusion = CBF exceeds metabolic demands. Relative hyperemia where blood flow exceeds metabolic requirements through tissue acidosis, usually >72 hours but has been seen as early as 24 hours.

 Misery perfusion = ↑ O2 extraction fraction (OEF) in ischemic brain due to ↓ cerebral blood flow. Regional CBF is inadequate to supply the metabolic demand, disproportionate decrease in CBF compared to CRMO2 and CRMG. 80% in 12 hours.

Answer 378

A

 Cerebral metabolic rate of oxygen consumption
 Measured by 15O-O2
 Normal rCMO2 = 3 ml/100g/min
 rCMRO2 is calculated from measurements of CBF, CBV, and OEF
 CMRO2 = CBF (15O-H2O) x OEF (15O-O2)

Answer 379

A

Reflow hyperemia (luxury perfusion)
o Occurs 3-7d after stroke, or when the affected vessel is recanalized
o Relative blood flow exceeds metabolic demands of the area affected by stroke (‘decoupling’)
 However, absolute blood flow rate is still

Answer 380

A

 11C-MET ([11C]methyl-L-methionine)
 18F-FET (O-(2-18F-fluoroethyl)-L-tyrosine)
o High grade glioma: early peak 10-15 min
o Low grade glioma: delayed, steadily increasing uptake
 123IMT (L-3[123I]iodo-α-methyl tyrosine)
 FET & IMT differentiate post-therapy changes from recurrent tumour (Sn, Sp 90%)

Answer 381

A

 Good for high grade, poor for low grade

 Ki-67

Answer 382

A

 HMPAO is lipophilic and crosses the intact blood brain barrier by passive diffusion. It has a 1st pass extraction of about 80%. Peak activity occurs within 1-2 mins after injection and 4% of dose remains in brain. Then there is rapid washout over 10-15 minutes of about 15% of the brain activity. The remaining activity is then fixed by conversion to hydrophilic compound by glutathione. Activity persists for up to 24 hours.

 Things to watch out for:
o need to have high radiochemical purity (>85%) because only a small portion crosses the BBB
o Use fresh generator eluate (<2 hr old)
o generator should have been eluted in previous 24 hours
o must be used within 30 minutes of its preparation because rapid decomposition into hydrophilic form
o stabilize with methylene blue + phosphate buffer, or cobalt chloride, shelf life 4 hr
o mixing with blood in syringe will cause poor quality image (lipophilic HMPAO enter RBC)

Dose for both agents: 15-30 mCi

 ECD – similar to HMPAO, but lower 1st pass extraction (60-70%), higher brain-to-background ratio (lack of back diffusion across BBB due to conversion to a charged hydrophilic compound and faster blood clearance). Peak activity is 1-2 min post injection and 5-6% is retained. Clearance from brain parenchyma is slow (6% / hr).
o stable in vitro – good for 4 – 6 hours after reconstitution
o better image quality vs HMPAO
 faster background clearance
 higher grey-to-white matter ratio (4:1 vs 2-3:1)

Answer 383

A

 There are two stereoisomers: d,l-HMPAO, not meso-HMPAO, has much higher uptake (R and meso)
 It is a lipophilic compound that diffuses into the brain by crossing the BBB. It is converted to a secondary complex that is hydrophilic and trapped in brain. It is oxidized by glutathione to a hydrophilic product.

 If not stabilized with methylene blue or CoCl, 30 minutes after reconstitution, otherwise 4 hours
 I would say no as ECD is stable invitro, and the imaging characteristics are better (increased percent uptake), although the prep takes longer, not sure what they are getting at.

Answer 384

A

o Meso-HMPAO highest uptake in cerebellum, and lowest in brainstem
o D,l-HMPAO more uniform in uptake

 T/F HMPAO is best for seizure imaging
o True
o Tc-HMPAO has higher first pass extraction which becomes significant at high flow rates (e.g., during an ictal episode)

o HMPAO ictal SPECT = ECD ictal SPECT for TLE
o HMPAO ictal SPECT superior to ECD ictal SPECT in localizing the epileptogenic zone in neocortical epilepsy

 T/F Injection affects distribution
o Yes: inject after QC check, but not earlier than 10 min for HMPAO, not later than 30 min for unstabilized HMPAO, 4h for stabilized HMPAO, and 6h for ECD
 Mechanism of uptake in one line
o Initially lipophilic, and becomes hydrophilic after crossing blood brain barrier, and therefore is trapped within cells
 ECD also has backdiffusion, but has more linear relationship between uptake and rCBF

Answer 385

A

 Exists in l,l-ECD, d,d-ECD and mesoisomers (Saha)
 Both l,l and d,d diffuse into the brain, but only l,l-ECD is metabolized by an enzymatic process to a polar species that is trapped in the brain
 ECD initially lipophilic, and can cross BBB
 Intracellular ECD cleaved by esterases, becomes hydrophilic

Answer 386

A

 Assuming HMPAO vs ECD, ECD has more rapid soft tissue clearance (see 2006 Q24)
 French answer:
 HMPAO: 12% in blood at 1hr
 ECD: < 10% in blood at 5min

Answer 387

A

Hydrophilic agents
Tc-DTPA, Tc-GH
20 mCi of Tc-DTPA
Image: statics @5min
Rapid
Can be quickly repeated
Cannot visualize brain parenchyma
May get sagittal sinus activity from external carotid circulation

Lipophilic agents
Tc-HMPAO, Tc-ECD
20 mCi of Tc-HMPAO
Image: statics @20 min
Not affected by metabolic disturbances or hypothermia
SPECT
Low labeling efficiency of Tc-HMPAO can mimic cortical uptake

Answer 388

A

 Generic
o Availability
o Ideal photon energy
o No particulate radiation
o Reasonable cost
o Target to background ratio
o Dose
o Half life
o Clearance time to imaging time
o Should not alter physiologic process

 Specifics
o Linear relationship between perfusion and uptake
o Fixed uptake
o Crosses BBB (lipophilicity)

Answer 389

A

Prerequisities:
o Clinical/neuroimaging evidence of acute CNS catastrophe
o Exclusion of complicating medical condition
o No drug intoxication or poisoning
o Core temperature >= 32°C

 Three cardinal findings
o Coma/unresponsiveness
o Absence of brainstem reflexes
o Apnea

Answer 390

A

 0-3 mos: perfusion in frontal lobe remains low, ↑ sensorimotor cortex, thalamus, brainstem, cerebellar vermis
 3 mos: increase in parietal, temporal, occipital
 6 mos: increase in lateral frontal
 8 mos: increase in medial frontal cortex
 1 yo: overall pattern of perfusion similar to that of a young adult
 Adult: Visual cortex, basal ganglia and cerebellum most intense. Otherwise symmetric cortical uptake

Answer 391

A

 1-2 years

Answer 392

A

indications:
o Carotid stenosis, TIA, cerebrovascular disease, vascular cause of dementia, diabetes
o Post SAH to determine risk of vasospasm-induced cerebral infarction
o assess AVM-induced cerebral hypotension
o previous extracranial-intracranial bypass
o pre-op assessment of need for selective carotid shunting during carotid endarterectomy

 Adult dose: 1g IV push, can use children formulas (or 14 mg/kg)

 Mechanisms of action:
o 1. carbonic anhydrase inhibitor – causes ↓pH and ↑CO2, leading to vasodilation
o 2. Direct effect on smooth muscle cells of cerebral blood vessels causing vasodilation
• ↓flow but normal response to diamox = normal cerebrovascular reserve

Answer 393

A

There is cerebellar normalization post diamox in a majority of patients.

Those with crossed cerebellar diaschisis at baseline showed significantly augmented perfusion after Diamox administration in the affected thalamus and cerebellum compared with that in the contralateral unaffected areas.

Answer 394

A

 Clinically patients with Lewy body disease often have:
o Fluctuating dementia (100%)
o Parkinsonian motor features (80%)
o Visual hallucinations (60%)
 Typical SPECT perfusion pattern:
o Pattern similar to Alzheimer disease (decreased perfusion to the temporoparietal cortex) but tends to have decreased perfusion to the occipital & sometimes frontal lobes

Answer 395

A

 Hypercapnic challenge
o Patient inhales 5% CO2 (20% O2, 75% N2)

 Diamox (acetazolamide) challenge study
o Acetazolamide inhibits carbonic anhydrase, causing /\ CO2 and \/ pH, also has direct effect on smooth muscle of vessels, causing vasodilation
o Protocol
 Most common is 2 day study with Diamox challenge portion performed first
 Give 1g Diamox by slow IV push (14 mg/kg in pediatrics)
 Wait 15 min, then administer Tc-ECD or Tc-HMPAO
 Image at 90 min
 Rest study done the following day
o Contraindication
 Sulfa allergy
 Avoid within 3 days of acute stroke

 Adenosine study
o Use same adenosine dose as cardiac studies (0.14 mg/kg/min for 6 min)

Answer 396

A

Alzheimers
Parkinsons
Lewy Body disease
Multi-infarct dementia
Herpes Encephalitis
Carbon monoxide poisoning

Answer 397

A

 Interictal PET: reflects not only ictal onset site, but areas of ictal spread and postictal depression
o Area of hypometabolism cannot be used to refine surgical borders
o May help with general localization and guiding placement of intracranial electrodes
 Ictal SPECT: localize epileptogenic focus during ictal state

Answer 398

A

 Irreversible cerebral infarction: CBF <7-12 ml/100g/min (ischemic core)
 Abnormally functioning but viable: CBF <20 ml/100g/min (penumbra)
o O2 extraction >1.3 ml/100g/min
 Mildly hypoperfused, normally functioning: CBF >20-22 ml/100g/min (oligemia)
 Normal: 50-55 ml/100g/min
 Misery perfusion:
o Brain distal to vascular occlusion remains viable, with preserved CMRO2, through compensatory increase in OEF
 Luxury perfusion:
o Current definition: decreased OEF in the face of normal, increased or decreased blood flow
o Infarcted brain demonstrating relative or absolute increase in rCBF with low OEF secondary to delayed reperfusion

Answer 399

A

 HMPAO and 133Xe more reliably demonstrate reperfusion hyperemia during subacute period
o Stroke could be masked by relative hyperemia appearing as normal perfusion
 ECD and IMP demonstrate normal to decreased uptake

Answer 400

A

 Images effect of vasospasm on tissue perfusion, not vasospasm itself
 Therapy:
o Hyperdynamic hypertension
o Hypervolemia
o Hemodilution
o CCB (nimodipine)
o Intracisternal tissue plasminogen activator

Answer 401

A

 A type of remote metabolic effect
 Involves cerebellar hemisphere contralateral to stroke
o Affects CMRO2, CBF, and CMRglc
 Likely results from injury to glutamatergic crossed corticopontocerebellar descending pathway

Answer 402

A

 AIDS dementia complex
 Cocaine polysubstance drug abuse
 Lyme disease
 Chronic fatigue syndrome

Answer 403

A

 Lumbar puncture below conus medullaris (below L2/L3), into thecal (subarachnoid) space
 Or cervical spine (C1-2)
 lumbar spine, subarachnoid space

Answer 404

A

 Spinal CSF leak can be seen as early as 30 min post-injection
 Base of skull CSF leak can be seen as early as 60 min post-injection

 111In-DTPA, allows longer delayed imaging (routinely delays up to 48h, although can do 72h)
 Images:
o 30 min, 1h, 3h and delays at 24-48h

 Minimum time to visualize leak: 2h
o Pledget counts after 24h (>1.5-3:1)
o Measure β2 transferrin in nasal secretion

Answer 405

A

Symptoms:
o Positional headache (relieved when supine)

Causes:
o Spontaneous leak
o Iatrogenic leak
 LP
 Surgery
o Trauma

Test
o CSF leak study with Tc-99m-DTPA (1 mCi) or In-111 DTPA (0.5 mCi) administered intrathecally
o Can do nasal pledgets: ratio to plasma >1.5-3.0:1 = leak
o Early visualization of kidneys

Therapy
o Blood patch

Answer 406

A

2-6 pledgets are inserted into the nose and ears by ENT specialists.
22G LP into subarachnoid space (L2-L5) injection of 0.5 mCi 111In-DTPA in 5mL dextrose 10% in water.
Patient is placed in Trendelenburg to pool tracer into the basal cisterns.
At 1-2hr image to see if tracer is in basal cisterns.
If yes, patient sits head forward, camera pressed laterally against the side of the head, if otorrhea is suspected, obtain posterior views.
At 4 hr, remove pledges, count activity in well counter.
Also take a blood sample and count in well counter.
pledget : plasma > 1.3 is positive (for blood > 1.5 is positive) for CSF leak.

Answer 407

A

 Check fluid pH, electrolyte balance, osmolarity – nerve function is very sensitive to these
o ↓ calcium ions causes a tetany
o Low pH causes dilatation of pial blood vessels
o Aseptic meningitis has been reported related to the chemical amount of albumin
 LAL testing is preferred to the traditional rabbit pyrogen test, because of its increased sensitivity for pyrogens (intrathecal route is more damaging)

Answer 408

A

 Most common site: Ventricular portion of catheter (Henkin)
 Normal time for abdominal activity ~15-20 min
 In-111-DTPA, Tc-DTPA 0.5-1 mCi

 Tc99m DTPA 1mCi in a small volume (1ml)
 Most common site of obstruction: distal catheter
 Time for appearance in the abdomen – fast within 15-20 minutes

Answer 409

A

 1. Patient preparation: check for papilledema (↑ICP), INR/PT/PTT and platelets
o Test intrathecal injection by LAL test (14 EU/V limit)

 2. Standard lumbar punture is done with 22g needle, into L2-L5, or C1-C2 in the subarachnoid space. CSF pressure is measured
o Aspirate 2ml of CSF, some is sent for biochem, some used to flush after dose is given.

 3. 0.5 mCi of 111In DTPA is injected into lumbar subarachnoid space.
o can be given with equal volume of 10% dextrose to speed up ascent
 4. Image initially at 15-30 min to show ascent of tracer
 5. Delayed images at 1h, 4h, 24 and 48hr after injection.
o Do anterior, posterior and lateral projections.

Answer 410

A

Non-communicating: intraventricular obstruction
o 1°: obstruction of aqueduct of Sylvius, Dandy-Walker syndrome (atresia of 4th ventricular outlet)
o 2°: hemorrhage, benign and malignant tumors, colloid cysts

Communicating: extraventricular obstruction
o Due to damaged arachnoid granulations and basilar cisterns, or thrombosis in venous drainage
o 1°: Arnold-Chiari malformation – cerebellum protrudes into spinal cord
o 2°: previous SAH, meningitis, leptomeningeal carcinomatosis; meningeal infiltration by lymphoma, leukemia, sarcoid

Answer 411

A

a) communicating hydrocephalus – ventricular reflux (transient or permanent), delayed or absent flow
over convexities.
b) noncommunicating hydrocephalus – no ventricular reflux, normal or delayed flow over convexities
c) cerebral atrophy – no ventricular reflux, delayed flow over convexities

Answer 412

A

 Mental status changes
 Incontinence
 Ataxia
 Also: hydrocephalus, normal CSF pressures

Answer 413

A

brain, nasopharynx, larynx, salivary, thyroid, mediastinum, heart, liver, spleen, kidneys, bowel, bladder

Answer 414

A

 Main route of excretion of FDG? Urinary
 Percentage is excreted by that route? 50% of the dose is present in the urine at 2h
 What could explain the long component of the effective half-life? Physical t1/2 of 18F

Answer 415

A

 Due to smooth muscle activity associated with peristalsis, bacterial uptake, gastrointestinal lymphoid tissue, and metabolically active mucosa

Answer 416

A

 Bowel smooth muscle contraction
 Glandular secretions
 Gut-associated lymphoid tissue
 Mucosal metabolic activity
 Intraluminal, related to bidirectional glucose transporters in intestinal membrane
 Colonic bacteria

Answer 417

A

 On FDG PET/CT, unilateral vocal cord paresis appears as asymmetric increased FDG uptake in the normal vocal cord contralateral to the side of nerve injury.

Answer 418

A

 Upregulated GLUT-1
 upregulated hexokinase
 downregulated G-D-P.

Also:
 Enhanced rate of glucose metabolism due to increased number of cell surface glucose transporter proteins
(primarily Glut-1 (insulin independent) and Glut-3 that are hypoxia responsive) and increased intracellular
enzyme levels of hexokinase and phosphofructokinase which promote glycolysis as well as decreased levels of
glc-6-phosphatase.
 Integrity of the vascular network that is necessary for supply of nutrients to the cell . With an intact vascular
supply,

Increased cell proliferation in tumors (assessed by the mitotic rate) also results in increased glucose utilization

Tumor hypoxia will also increase FDG uptake through hypoxia-inducible factor-1-alfa that up-regulates Glut-1
receptors

Answer 419

A

 Infection
 Inflammation
 Malignancy

Answer 420

A

 Administering insulin at the same time as FDG should be avoided because it tends to increase accumulation in
skeletal muscle and thus less FDG is available for accumulation in tumors. Also, perhaps more importantly, Glut-
1 is the most important transporter for the uptake of FDG in tumor cells and it is insulin independent.

Answer 421

A

 Insulin increases skeletal muscle and cardiac uptake through upregulation of GLUT4 transporter expression
 Decreased hepatic uptake a secondary sign

Answer 422

A

 1.Brain
 2.Lymphoid tissue (waldeyers ring)
 3.Salivary glands (parotid)
 4.Brown fat
 5.Skeletal muscle
 6.Soft palate
 7.Thyroid

Answer 423

A

o Cerebral cortex (brain is 6% of total dose)
o Tonsils
o Salivary glands (variable but typically low grade)
o Muscles:
 Any skeletal muscles: strap muscles, sternocleidomastoid
 Tongue
 Larynx (vocal cords with phonation)
o Brown fat
o Bone marrow (low grade)
o Thyroid (Hashimoto's, Graves)
o Lymph nodes
o Degenerative disc disease

Answer 424

A

 Brown fat
 Neck muscles
 Reactive lymphadenopathy
 Vascular uptake (atheroma, thrombus)

Answer 425

A

 Most common H&N cancer = squamous cell carcinoma

 To minimize frequency of false positive:
o post biopsy – 5 – 7 days
o post chemotherapy – at least 3 weeks
o post surgery – 6 weeks
o post RT – 8 – 12 weeks

 False positive:
o inflammatory/infectious lymph nodes
o asymmetric lymphoid tissue
o brown fat
o salivary gland activity

Answer 426

A

 Greater sensitivity for poorly differentiated thyroid cancer, anaplastic, medullary, Hurthle cell
 One day imaging procedure
 Do not absolutely need thyroid stimulation (Sn improved with thyrogen)
 Non-iodine avid lesions and bone mets
 Thyroglobulin positive, iodine negative

Answer 427

A

 Patients with elevated thyroglobulin levels but negative I-131 scans may have de-differentiated thyroid tumor. Less differentiated tumors will generally be FDG PET positive and I-131 negative, likely related to a decrease in sodium-iodide symporter expression and an increase GLUT-1 expression.
 So FDG-PET can be used for the evaluation of recurrent or metastatic thyroid cancer that is non-iodine avid

Answer 428

A

 Normal structures
o Salivary
o Thymus
o Brown fat
o Bowel
o Renal collecting system/bladder
o Gonadal

 Granulomatous disease
o Sarcoidosis
o TB

 Infection
o Sinusitis
o Esophagitis
o Pulmonary
o Lymphadenitis

 Other malignancies
o Esophageal CA
o Breast CA
o Lung CA

Answer 429

A

Stage 1; 1 lymph node group or extranodal site

Stage 2; 2 lymph node groups or extranodal site and associated nodes on the same side of the diaphragm.

Stage 3; 2 lymph node groups or extranodal site and lymph node group on opposite sides of the diaphragm.

Stage 4; Diffuse disease.

A-no B symptoms
B-B symptoms present
E-extension of disese from nodes into adjacent tissue

Answer 430

A

Patient factors
o Hyperinsulinemia (exogenous, endogenous)
o Hyperglycemia

Lesion factors
o Low metabolic activity
      Bronchioloalveolar CA
      Carcinoid
o Low cellularity
o Low GLUT-1 expression
o Glucose-6-phophatase

Technical factors
o Too little
o Too short uptake period
o Too small lesion
o High background (low CNR)

Answer 431

A

 FDG imaging has also been shown to be less sensitive for the detection of mucinous carcinoma (sensitivity 58% compared to 92% for non-mucinous lesions), possibly due to relative hypocellularity

o colon-mucinous adenocarcinoma
o ovary-mucinous cystadenocarcinoma
o stomach-mucinous gastric carcinoma
o pancreas-MCN
o Breast-mucinous carcinoma
o Appendix-mucinous cystadenocarcinoma

Answer 432

A

They tend to be paucicellular and low-grade (AM). The amount of uptake in a mucinous carcinoma is dependant on the cellularity and the amount of mucin.

Answer 433

A

T1a/b
a is < 2cm, b is 2-3 cm, surrounded by lung or visceral pleura. no bronchoscopic evidence of invasion more proximal than lobar bronchus (not in mainstem bronchus)

T2a/b
a is > 3-5 cm, b is 5-7 cm in largest dimension or
invades visceral pleura
involves mainstem bronchus, but > 2cm from carina
atelectasis / post-obstructive pneumonitis extending to hila but does NOT involve entire lung

T3
>7 cm or tumor any size invading – chest wall (incl superior sulcus), diaphragm, phrenic nerve, mediastinal pleura, parietal pericardium
Tumor in mainstem bronchus, < 2cm from carina (not involving carina)
Atelectasis / post-obstructive pneumonitis involving entire lung

T4
Tumor any size invading -mediastinum, heart, great vessels, trachea, esophagus, vertebral body, carina
Malignant pleural or pericardial effusion
Satellite lung nodules in ipsilateral lung

Regional LN
N0 - No involvement
N1 - Ipsilateral peribronchial, intrapulmonary or hilar
N2 - Ipsilateral mediastinal / subcarinal
N3 - Contralateral mediastinal, hilar
Ipsilateral or contralateral scalene or supraclavicular

M1a/b
a is separate tumor nodule in a contralateral lobe or tumor with pleural nodules or malignant pleural/pericardial effusion.
b is distant mets
Different cell type = synchronous primary – STAGE SEPARATELY

Answer 434

A

SEE PAGE 379

Stage 3B = non-resectable
= any N3 OR T4 + N2/N3

Answer 435

A

T2 – tumor 3-7cm, can involve the main bronchus, invades visceral pleura

N2 – ipsilateral mediastinal or subcarinal nodes

M0 – no distant metastases

Answer 436

A

 >7 cm or direct invasion of: parietal pleura, chest wall, diaphragm, phrenic nerve, mediastinal pleura, parietal
pericardium; or,
 Tumour in main bronchus <2 cm distal to the carina, but not involving carina; or,
 Associated atelectasis or obstructive pneumonitis of entire lung; or,
 Separate tumour nodule(s) in the same lobe

Answer 437

A

T1/T1 N2

T3/N1

T4/N0N1

Answer 438

A

 BOOP = bronchiolitis obliterans organizing pneumonia =
 COP = cryptogenic organizing pneumonia
 BOOP = organizing pneumonia with granulation tissue in lumen of small airways
 FDG-PET may be falsely positive in BOOP for malignancy

Answer 439

A

 Technical
o thrombus

 Normal structures
o Atherosclerosis
o Thymus

 Altered normal structures
o Round atelectasis

 Benign neoplasm
o Hamartoma

 Inflammatory
o Sarcoidosis
o Wegener’s
o Amyloidosis
o Esophagitis
o Talc pleurodesis

 Infectious
o Pneumonia
o Abscess
o Empyema
o TB granuloma

Answer 440

A

Hepatomas have a relatively low density of Glut-1 receptors and high levels of Glc-6-phosphatase

 Varying degrees of glucose transporter and hexokinase II expression, and effect of P-glycoprotein as efflux pump for FDG

Answer 441

A

 PSA nonspecific marker used in screening for and follow-up of prostate cancer
 Assess response of therapies - anti-androgen or chemotherapy
 To find source of rising PSA not identifiable with conventional imaging
 Also useful in assessing patients with aggressive or hormone refractory disease

Answer 442

A

 PET has no role in T or N staging, only good for M staging.
 Tc-MDP bone scan is more sensitive for bone mets in prostate cancer, than FDG PET.
 11C-acetate, 11C-choline, 18F-choline, 11C-methionine, 18F-FDHT

Answer 443

A

 small malignant lesions
 metastases from non FDG avid tumors
 presence of necrosis

Answer 444

A

Cancer type   Sensitivity  Specificity
Overall 93%  96%
Head and neck 90% 95%
Lung
91%
96%
Breast
97%
95%
Digestive system
92%
97%

Answer 445

A

 Overall sensitivity 89%, specificity 89%

 Where performed for differentiating PTLD from other diseases, sensitivity 90%, specificity 85%

Answer 446

A

 About 50% of clear cell RCC are positive on FDG-PET
 FDG-PET useful in staging for detection of metastases
 FDG-PET can predict and monitor response to therapy with tyrosine kinase inhibitors
 FLT may be useful in monitoring response to treatment

Answer 447

A

Neuroendocrine tumour -
G1 (carcinoid) < 2 mitoses/HPF, Ki67 inex <=2
G2 2-20, 3-20

Neuroendocrine carcinoma
G3 >20; >20

Mixed adenoneuroendocrine carcinoma

Hyperplastic and preneoplastic lesion

Answer 448

A

 Pituitary, thyroid, liver, spleen, kidney and bladder; variable gut and gallbladder

Answer 449

A

 Normal distribution: pituitary gland (faint), thyroid (faint), liver, gallbladder, spleen, kidneys, urinary bladder, +/- bowel, +/- breast

 Carcinoid syndrome – serotonin hypersecretion by metastatic carcinoid in liver produces flushing, diarrhea, bronchoconstriction and right sided valvular heart disease.

 Surgery:
o Cytoreductive surgery, radiofrequency ablation (RFA), chemoembolization, liver transplantation
 Medical therapy:
o Somatostatin analogues, interferon alfa, radionuclide therapy (I-131 MIBG, In-111 / Y-90 DOTA-octreotide, Lu-177 octreotate)

Answer 450

A

obtain whole body images
differentiate between neuroendocrine pancreatic tumor and adenocarcinoma
better sensitivity for carcinoid tumors
effective in assessing response to octreotide therapy

Answer 451

A

 Accessory spleen
 Surgical wounds, stomies, drains
 Parapelvic renal cyst
 Granulomatous disease (Crohn’s)
 Physiologic bowel uptake
 Swallowed activity (URTI)

Answer 452

A

 Types: 5

 Octreoscan: SST2>5>3

Answer 453

A

 Originally I-123 label for Octreotide
 Subsequently In-111-DTPA labeled pentetreotide
 Modifications of the octreotide octapeptide at positions 3 and 8 can result in increased somatostatin receptor affinity: DOTA-NOC, DOTA-TOC, DOTA-TATE

Answer 454

A

 pheo - MIBG
 carcinoid - octreo
 neuroblastoma - MIBG
 paraganglioma – Octreotide (superior to MIBG-AM)

Answer 455

A

 1.Can visualize uptake in buttock granulomas due to chronic administration
 2.Reduced spleen, thyroid, pituitary (uptake to these due to receptor binding)
 3.Reduced uptake tumors (due to receptor binding)stopped for 24-72 hours
 4.May in fact have improved tumor-to-background ratio however (one paper)
 5.Increased blood pool

Answer 456

A

 Bone scan has significantly lower specificity and sensitivity, and higher rate of FN vs somatostatin receptor scintigraphy (SRS) for detection of bone metastases in patients with gastrinoma.
 MRI and SRS are both more sensitive, but given the ability to provide whole body images with SRS, it is preferred.

Answer 457

A

 Carcinoid - 111In-Octreotide
 MTC - 111In-Octreotide
 Paraganglioma - 111In-Octreotide
 Pheochromocytoma - 131I MIBG or 123I MIBG 90%, (Octreotide 85%, Both 95% sensitivity)
 Neuroblastoma - 131I MIBG or 123I MIBG

Answer 458

A

Carcinoid (sen 71-100%) > Gastrinoma (60-93%) > VIPoma (86-88%) > non-functional islet cell tumor (80%) > glucagonoma (73%) > > insulinoma (30-40%)

Answer 459

A

 The sensitivity of Octreotide for the detection of MTC is variable (41-71%) and may be related to loss of somatostatin receptors as the tumor becomes less differentiated.
 MTC arises from para-follicular C-cells that secrete calcitonin.
 25% MTC is familial, associated with MEN 2A/2B.
 Mutation in RET proto-oncogene on chromosome 10

Answer 460

A

 4 sites of normal uptake
o Pituitary faint, thyroid faint, liver, spleen, bowel (variable degree), kidneys, bladder (both gall and urinary), breast uptake in 15%.
 why sensitivity for MTC is lower than other neuroendocrine tumors
o Loss of SSR during dedifferentiation. A high calcitonin:CEA ratio increases likelihood for positive scan.
 3 sites of most common metastasis for MTC
o Local lymph nodes commonly (50%), liver, lung, bone, brain.

Answer 461

A

 Injection: 120 MBq + furosemide
 Maximum tumour activity: 70 ± 20 min
 Start PET/CT acquisition at 45-90 min

Answer 462

A

 NF1
 VHL (10-20%)
 MEN IIA (50%)
 MEN IIB (90%)
 Carney’s syndrome/triad
o GIST, pulmonary chrondromas, extra-adrenal paragangliomas

Answer 463

A

Adrenal medulla, liver, spleen, urinary bladder, colon (15-20%), salivary glands, heart/myocardium, lung, thyroid, uterine, neck muscle, brown fat

Answer 464

A

 Uptake 1: active transport, Na dependent, high affinity, low capacity, saturability, temperature dependence
o Predominates at low MIBG levels

 Uptake 2: passive diffusion, low affinity, high capacity, nonsaturability, no Na/energy/temperature dependence
o Predominanates at high MIBG levels

 Localized in Pre-synaptic storage granules of adrenergic tissue of neural crest origin through an energy mediated type I uptake mechanism (noradrenaline re-uptake mechanism) and minimal passive diffusion.

Answer 465

A

 Lugols or SSKI (100 mg Iodine equivalent, 130 mg KI. Lugols 8 mg/drop, SSKI 30 mg/drop;

I always say SSKI 1 drop tid administered one day previous, on the day of imaging and for the following 2 days (package insert) or 4 days (according to auntminnie)

Answer 466

A

 A slow IV infusion of MIBG (0.5-1 mCi of I-131 MIBG or 3-10 mCi of I-123 MIBG, adjusted for body size in children) is administered over 2 – 3 minutes. To limit the side sympathetic side effects from the medication.

Answer 467

A

 inhibit catecholamine uptake
o cocaine, TCA

 inhibit active transport into storage vesicle
o reserpine

 deplete storage granules
o amphetamine, pseudoephedrine

 calcium mediated
o CCB

 BP meds that interfere:
o Combined alpha/beta blocker (labetalol)

Answer 468

A

 Can interfere; Labetolol-α and β-antagonist, CCB, nonselective α-antagonist (phenylbenzamine)
 Alpha-blocker; Terazosin- selective α1-antagonist, Metoprolol-β-blocker, Diuretics

Answer 469

A

pheochromocytoma
neuroblastoma
paraganglioma
carcinoid
(MTC)

Answer 470

A

Detection, localization, staging and follow-up of neuroendocrine tumours and their metastases:
o Pheochromocytomas
o Neuroblastomas
o Ganglioneuroblastomas
o Ganglioneuromas
o Paragangliomas
o Carcinoid tumours
o Medullary thyroid carcinoma
o Merkel cell tumour
o MEN2 syndrome

 Study of tumour uptake and residence time to decide and plan treatment

 Evaluation of tumour response to therapy

 Confirmation of suspected tumours derived from neuroendocrine tissue

Answer 471

A

 Stage I: Confined to the organ of origin with complete gross surgical excision
 Stage IIA: Localized tumor with incomplete gross excision
 Stage IIB: Localized tumor with complete or incomplete gross excision. Tumor extends into adjacent structures, but does NOT cross midline. Ipsilateral regional lymph nodes positive for tumor, but contralateral nodes are negative.
 Stage III: Unresectable tumor which crosses midline; or unilateral tumor with contralateral regional lymph node involvement
 Stage IV: Distant metastases
 Stage IVs: Localized primary lesion (1, 2A/2B) that does NOT cross midline, with metastases to liver, skin, and/or bone marrow (but NOT cortical bone) in infants < 1 year of age. Stage IVS disease is associated with very good survival following chemotherapy and radiation.

Answer 472

A

Neuroblastoma is the most common extracranial solid tumor in children, and the most common neoplasm in infants

Answer 473

A

 More specific tumor agent; gallium is taken up by inflammation as well.
 Can image earlier than with gallium
 Gives positive results with KS, low grade NHL
 Not affected by steroids, chemotherapy or radiation while Gallium can be

 Radiation therapy and chemotherapy do not immediately inhibit Tl uptake (do for Ga)
 Tl better for bone and soft tissue tumours than both Tc-99m MDP and Ga-67 (uptake determined by factors related primarily to tumor response to therapy)

Answer 474

A

 1st lymph node in a LN basin to receive drainage from an anatomically defined area.
 Various definitions in literature and SNM/EANM guidelines; best is probably:
o Any lymph node that receives direct lymphatic drainage from the tumour

Answer 475

A

SC, Antimony colloid, HSA

Answer 476

A

Breast
Melanona
Vulvar
Cervical
SCC head and heck
Penile
Testicular

Answer 477

A

Tumor devoid of normal lymphatic tissue so slow drainage of tracer
Dense tumor causing leakage of tracer
possible seeding from tumor tract
Scatter or shine through in the retained activity may interfere with imaging and intra-op gamma probe

Answer 478

A

 Superficial (intradermal, subdermal, perareolar, retroareolar) and deep (peritumoral, intratumoral)

Answer 479

A

 11C-choline, 18F-choline, 11C-acetate, 18F-FDHT, 18F-fluoride,

Answer 480

A

 Oxidative Metabolism:
o 11C-acetate: oxidation in TCA cycle to CO2 and H2O

 Androgen receptor:
o 18F-FDHT (fluoro-5α-dihydrotestosterone): analogue of dihydrotestosterone, ligand for androgen receptor

Nucleotide uptake:
o 18F-FLT (3’-deoxy-3’-fluorothymidine): nucleotide analogue retained in proliferating cells after phosphorylation by thymidine kinase 1 (TK1);

Membrane synthesis:
o 11C/18F-choline: membrane synthesis (phosphoryl-11C-choline incorporated membrane phospholipids

Protein synthesis - C11-methionine

Bone metabolism
o 18F-NaF: OH- analogue, incorporates in calcium hydroxyapatite mineral of bone

Answer 481

A

 Assessment
o Direct probe measurement
o 18F-MIS
o 18F-EF-5
o 18F-FETNIM
o 18F-FAZA
o 62/64Cu-ATSM

 Therapy
o Hyperbaric oxygen
o Radiosensitizers (mimic action of oxygen)
o Cytotoxins (reduced to cytotoxic species in presence of hypoxia)
o Boost RT dose with intensity-modulated radiation therapy

Answer 482

A

 Choline is a phospholipid precursor which shows progressive uptake over time in brain tumors with negligible normal brain uptake, and a high tumor-to-background ratio
 Uptake is not related to blood flow
 Higher uptake with high grade brain tumors
 Indirect measure of tumor cell proliferation

Answer 483

A

 Distinguishes focal vs. diffuse forms

 Focal form can be cured by resection

Answer 484

A

Basal ganglia, GB, kidneys, urinary tract, liver, low level GI tract, epiphyseal plates of long bones

Answer 485

A

1.Can give a standard dose
 2.Weight based dosing
 3.Dosimetry

Answer 486

A

 The mainstays of radiologic pediatric sedation are choral hydrate and phenobarbital.
 < 18 months
o Chloral hydrate 50-70mg/kg po max 100 mg/kg
o Contra: hypersensitivity, hepatic or renal impairment; gastritis or ulcers; severe cardiac disease
 >18 months
o Pentobarbital sodium iv (Nembutal) 2-6 mg/kg with versed iv 0.1mg/kg up to 2.5mg
o Contra: hypersensitivity, porphyria, marked hepatic impairment; dyspnea or airway obstruction

Answer 487

A

 Cross-linked fibrin degradation product from plasmin metabolism.

Answer 488

A

 Prot C & S deficiency, Factor V Leiden deficiency, lupus anticoagulant, hyperhomocyteinemia

Answer 489

A

 immobilization
o prolonged bed rest
o obesity

 hypercoagulable state
o pregnancy
o OCP
o Cancer
o Smoking
o Hypercoagulability disorders
 Antiphospholipid antibody syndrome
 Protein C/S/Antithrombin deficiency
 Factor V Leiden mutation
 Hyperhomocysteinemia
 Thrombocytosis
 Polycythemia vera

 epithelial injury
o surgery
o trauma
o venous catheters
 age > 60 years
 previous DVT/PE

Answer 490

A

 Asymptomatic
 Dyspnea
 Pleuritic chest pain
 Hemoptysis

Answer 491

A

 The typically quoted number is 60,000 to ensure sufficient counts to limit statistical noise, but with new equipment some references say 100,000 counts is required. I am sticking with 60,000.

Answer 492

A

 Typically 200,000-700,000
 In what circumstances should you decreased the particle number
o Pulmonary hypertension
o R to L shunting
o Infants and children
o Can reduce to 100,000-200,000

Answer 493

A

 In adult lungs, there are approx 200 – 300 million precapillary arterioles.
 The # of alveoli & pulmonary arterioles do not reach adult levels until 8 years.
 MAA’s biological T1/2 is 2 – 10.8 hours, effective T1/2 1.5 – 3.8 hours.
 Clots have a biologic T1/2 of 3 – 5.5 days or longer.
 In normal subjects, 60-70% of pulmonary circulation must be occluded before changes in lung hemodynamics are noted.

Answer 494

A

 Occlusion of ~0.1% pre-capillary arterioles

 No hemodynamically significant effects until 40-80% occlusion

Answer 495

A

Glenn shunt can direct flow only to right lung or can be bi-directional.
First, you must reduce the # of Tc-MAA particles to 100,000.
To get a good assessment of perfusion (or if quantification is desired), inject in the arm and take pictures. Then inject in the foot and get pictures.
In a unidirectional shunt, the arm injection will result in right lung visualization, and the foot injection will result in left lung visualization.

Answer 496

A

o Particle and Vascular factors.
 particle size
 shape of particle
 orientation of particle
 rigidity of particle
 size of vessel lumen
 blood flow or lack thereof
 vascular anatomy

Answer 497

A

 MAA goes to pre-capillary pulmonary arterioles

o occlude ~ 0.1% of pre-capillary arterioles

Answer 498

A

o Simmer phase: load crucible with Tc-99m pertechnetate and evaporate to dryness
o Burn phase: heat crucible under pure argon atmosphere

 Unbound soluble Tc-99m, which run with pertechnetate on TLC (~5%) (Pertechnegas, in the setting oxygen in the system?)

Answer 499

A

o Behaves as true gas, allowing nanosized particles to penetrate deep into alveoli
o Remain bound to lining of alveoli, resulting in stable image
 Less central airways deposition
 Ability to perform ventilation SPECT
o Little degradation or translocation across pulmonary alveolar bed

Answer 500

A

 Alternative diagnosis
 Fewer indeterminant results
 More available
 More specific
 Prognosis, signs of right heart strain are evident
 Better in patients with COPD/abnormal chest xrays

Answer 501

A

 PIOPED II since these were directly compared.

 Sensitivity for high prob V/Q 77%, CT 84%. NPV for negative VQ 98%, CT 98% (probably overestimated because of the large number of outpatients unlike PIOPED I).

 Senstivity for SPECT is typically quoted at approx. 90%, no good studies though.

Answer 502

A

 CT breast dose&raquo_space; V/Q

Fetal dose:
o Higher with V/Q
o Higher with lung perfusion only in 1st and 2nd trimester
o Comparable in 3rd trimester

Effective female dose is greater for CT
o Yes: 0.9 mSv lung scintigraphy; 7.3 mSv CT

V/Q preferred over CT for pregnancy

Answer 503

A

 renal failure
 contrast allergy
 unable to attain venous access
 claustrophobia
 Unable to breath-hold
 Radiation dose concerns (e.g., pregnancy)

Answer 504

A

o tomographic sections – avoid missing small perfusion mismatches
o higher image contrast
o higher sensitivity
o higher specificity
o higher accuracy
o can correlate with CT if available

Answer 505

A

 High Probability (≥80% PE):
o ≥2 large mismatched segmental perfusion defects or the arithmetic equivalent in moderate or large and moderate defects

 Intermediate Probability (20-80% likelihood for):
o 0.5-1.5 large equivalent mismatched perfusion
o Solitary moderate or large segmental triple-match in the lower lung zone.
o Difficult to categorize as high or low.
o Multiple opacities with associated perfusion defects.

 Low Probability (10-19% likelihood for PE [12,19]):
o a single large or moderate matched V/Q defect
o > 3 small segmental perfusion mismatches
o Probable PE mimic-absent perfusion to entire lung, lobe
o pleural effusion < 1/3 pleural cavity
o heterogenous perfusion

Very Low Probability (< 10%)
o non-segmental mismatch
o perfusion defect < radiographic abnormality
o >= 2 matched defect with normal CXR
o 1 – 3 small segmental perfusion defects
o solitary triple match in mid to upper lung zone
o stripe sign
o pleural effusion >= 1/3 pleural cavity

Answer 506

A

o Better specificity (directly visualize the clot)
o Better availability
o Ability to provide an alternate diagnosis
o Low number of indeterminate studies compared to at least planar V/Q.
o Prognosis-evidence of right heart strain is a predictor of poor outcome, V/Q with>50% of lung perfusion defect is also a predictor of poor outcome.
o Evaluation of COPD patients (especially with DTPA, not so with technegas or Kr)
o Evaluation of PE in a patient with abnormal CXR.

Answer 507

A

When thoracic CT indicated on clinical grounds (abnormal CXR, dissection?)

Complex cases, abnormal CXR

Acute presentation adn hemodynamic instability

Answer 508

A

Normla or near normal CXR

Renal dysnfunction

Contrast allergy

All cases of follow-up

Pregnancy (due to high number of technically inadequate studies)

Answer 509

A

 PE
 Bronchogenic carcinoma
 Extrinsic compression of PA &amp; PA
 Congenital HD
 Unilateral PA agenesis

Answer 510

A

 Reverse mismatch = area of perfused but non-ventilated lung, indicates physiologic R -> L shunt. It is due to failure of reflex hypoxic vasoconstriction.
 4 Causes
o 1.partial obstruction not allowing the reflex vasoconstriction
o 2.chronic lung disease with decreased pulmonary vascular reserve therefore redistribution not possible.
o 3.metabolic alkalosis
o 4.chronic pulmonary hypertension, lead to intimal hyperplasia and inability to vasocontrict.

Answer 511

A

Diagnose PE:
o 2 or more large segmental equivalent mismatches (prev CP disease)
o 1 or more large segmental equivalent mismatches (no prev CP disease)
o triple match lower lobes

Exclude PE:
o stripe sign
o normal
o nonsegmental
o Reverse mismatch
o i.e., all the very low criteria

Answer 512

A

 FEV1 > 0.8 L needed to survive
 Want to remove entire right lung due to tumor
 Calculate % uptake in left lung x FEV1 – if > 0.8 L do the surgery

i.e. Pulmonary quantification calculation, right lung 45%, left 55%, VEMS 1,5L, proximal right tumor

Post right pneumonectomy – 1.5L x 55% = 825ml > 800ml FEV1, so won’t be ventilator dependent

Answer 513

A

99mTc labeled synthetic peptide that binds to the glycoprotein IIb/IIIa receptors on the surface of activated platelets

Answer 514

A

Tc-apcitide (Acutect)
Tc-MAA
Tc-99m-anti-D-dimer
111In-platelets
123I-fibrinogen
123I-fibrin

Answer 515

A

Tc-Apcitide
Sn 90%
Sp 85%

TcMAA
Sn 100%
Sp 75%

Doppler US
Sn 90%
Sp 98%

Impedance Plethysmography
Sn 80%
Sp 90%

Answer 516

A

 Contraindications
o Life expectancy < 3 months
o High risk of pathologic fracture or cord compression
o Neutrophils < 1.5 x 109/L
o Platelets < 60 x 109/L
o Hemoglobin < 90 g/L
o Pregnancy
o Acute or chronic renal failure; GFR < 30 mL/min
o Bone pain that does not match bone metastases as seen on Tc-MDP bone scan.

 Exam done before
o Bone scan, looking for osteoblastic mets with increased uptake corresponding to painful sites. Within 4 weeks before treatment

Answer 517

A

 Major hematologic toxicities include: pancytopenia and bone marrow suppression
 Hematologic Toxicity peaks: 4-5 weeks post therapy

o Patients should be told that 60–80% of patients benefit from 89 Sr, 153 Sm-lexidronam or 186 Re-etidronate therapy.
o Patients should be warned of the risk of temporary increase in bone pain (pain flare).

o The patient should be told that pain reduction is unlikely within the first week, more probable in the second week and could occur as late as 4 weeks or longer after injection, particularly for long-lived isotopes. Patients should continue prescribed analgesics until bone pain decreases and receive advice regarding subsequent analgesic dose reduction where appropriate.

o Patients should also be informed on the duration of the analgesic effect, generally of 2–6 months and that retreatment is possible.
o The patient should understand that 89 Sr, 153 Sm-lexidronam or 186 Re-etidronate are palliative treatments especially designed for treating bone pain and are unlikely to cure metastatic cancer

Answer 518

A

 89SrCl; 50 days, Beta, 1.46 MeV
 32P PO4-; 14.6 days, Beta, 1.71 MeV
 153Sm EDTMP; 46 hours, Beta, 0.64, 0.71, 0.81 MeV
 186Re HEDP; 89 hours, Beta, 1.08 and 0.97 MeV

Answer 519

A

 Subdivide myelosuppression into
o drop in WBC, starts in 3-4 weeks Henkin P1606
o drop in platelets, starts in 12-16 weeks Requisite P297

 According to Ell and Gambhir
o 1.Myelosuppression is usually mild <2%, usually thrombocytopenia
o I would add pain flare 48-72 hours to the answer.

Answer 520

A

 Na-P32 orthophosphate.

 85% accumulates in hydroxyapetite and emit β-particles (Eβave= 694 keV) that damage precursor cells in marrow.

Also

Cells take up the 32P, and beta emission cause DNA damage,
32P is incorporated into the DNA and after decay 32S remains, causing problems with replication.

Answer 521

A

 32P - orthophosphate

 32P - colloidal chromic phosphate suspension

Answer 522

A

 Collidal chromic phosphate, used for serosal implants.

Answer 523

A

 Dose of 32P: 111-148 MBq. (3-4 mCi)
 If first treatment unsuccessful: 25% higher at 3 months.
 If recurrence: Last effective treatment

Answer 524

A

 Myeloproliferative disease (polycythemia vera and essential thrombocytosis)
o IV or oral, 74-111 MBq/m2 BSA (maximum 185 MBq) or 3.7 MBq/kg (maximum 260 MBq)
o Increased risk of acute leukemia (2-15% at 10y)
 Metastatic bone pain palliation
o 185-370 MBq IV or 370-444 MBq po

Answer 525

A

What’s the long term side effect of 32P therapy?

Answer 526

A

Note – “A” criteria:
o A1 – Raised RBC mass (25% above mean normal predicted value)
o A2 – Absence of secondary polycythemia
o A3 – Palpable splenomegaly
o A4 – Clonality marker (abnormal marrow karyotype)

 “B” criteria:
o B1 – Thrombocytosis (platelet count > 400 x 109/L)
o B2 – Neutrophil leukocytosis (neutrophil count > 10 x 109/L)
o B3 – Splenomegaly on US/ isotope scan
o B4 – Characteristic BFU-E growth or reduced serum erythropoietin

Answer 527

A

 90Y silicate/citrate colloid
 186Re sulfide colloid
 169Er citrate colloid

Answer 528

A

 Three properties;
o 1.Size (non-degradable particles showed decreasing leakage with increasing size)
o 2.Biodegradability (independent of size)
o 2.Stability of the label

Answer 529

A

 Absolute:
o pregnancy
o breastfeeding
o cellulitis
o septic arthritis
o ruptured popliteal cyst (knee)
o massive hemarthrosis
o joint instability (intra-articular fracture)

 Relative:
o age < 20
o evidence of significant cartilage loss
o joint instability with bone destruction

Answer 530

A

Previous attempt a intraarticular glucocorticoid injection without affec
Regular analgesics 3
Pain severe enough to limit normal activity.

Answer 531

A

 2-6 weeks

Answer 532

A

 Most retained in joint and taken up by synovial cell by phagocytosis, but some leak into lymphatics into regional lymph nodes and ultimately to liver.

Answer 533

A

 what happens to tracer once injected
o within the first hour it is distributed throughout the joint with the majority sequestered in the synovial membrane taken up by the synovial macrophages. Some leaks into the lymphatics, into the regional lymph nodes and into the liver depending on the size of the particles.

o Acute; 1.Erythema or skin necrosis, especially if there is leakage, 2.Temporary increase in synovitis and pain is common before improvement at 1 mos., 3.Other complications of any puncture including infection, haemorrhage, etc., 4.Risk of DVT since immobilization for 48 hours is required.
o Chronic; 1.Hyaline cartilage breakdown, little mitotic activity of chondrocytes, however there has been some evidence of ultrastructural change and metabolic effects in dogs and humans, the long term effects are unknown 2.Hematologic malignancy, following knee injection of 90Y colloid, regional lymph node dose is estimated at 100 Gy, although there is no definite evidence for malignancy, only theoretic.

Answer 534

A

 Chimeric antibodies are hybrid monoclonal antibodies that are part human and part mouse. They are formed by coupling the smaller variable region of a murine antibody to the larger constant region of a human monoclonal antibody.
 Advantages:
o They are considerably less immunogenic than murine antibodies
o Therefore, they are more slowly cleared from the circulation and can result in higher circulating levels immunoradiotherapy antibodies
o They can also have more effective tumor targeting ability and the human constant region may stimulate a more potent immune effector response (antibody mediated cell cytotoxicity and complement-dependent cytotoxicity)
o They are less likely to produce a systemic allergic type of reaction (anaphylaxis)

Answer 535

A

 Advantages of Fab vs whole antibody:
o less immunogenic so less likely to get HAMA
 re-treatment more effective (no formation of antibody/HAMA complexes which are quickly removed by RES)
o smaller so better tissue penetration
o rapid blood clearance -> better tumor-to-background ratio
 shorter t1/2 in serum

 Disadvantages:
o short tumor residence time (fast washout)
o excessive radiation dose to kidneys/bladder
 Whole antibody
o Longer serum t1/2
o Cleared by RES (liver, spleen)

Answer 536

A

 HAMA may cause release of previously bound radionuclides into the circulation and non-specific radiation exposure.
 HAMA may reduce tumor targeting because antibody/HAMA complexes are cleared by RES
 The HAMA response may result in an allergic type of reaction to the murine monoclonal antibodies that may range from a mild form, like a rash, to a more extreme life-threatening response such as renal failure or anaphylaxis.

Answer 537

A

 The agent is administered on an outpatient basis as the radiation exposure risk to family members is in the range of background radiation.
 The primary route of elimination is via the urine (about 7% eliminated over the first 7 days). For the first 7 days following treatment, patients should wash their hands thoroughly after using the toilet, avoid the transfer of bodily fluids, clean up after spilled urine, and dispose of any materials that are contaminated with bodily fluids.

Answer 538

A

 Indication: Recurrent or refractory low-grade follicular or transformed B cell NHL
 90Y anti-CD20 murine IgG (ibritumomab)
 Dosing scheme: Day 1 give cold Rituximab 250 mg / m2 followed 4 hours later by 111In Zevalin 5mCi over 2 min. Image at 48-72 hours to assess the biodistribution (blood pool activity remaining is a good sign. Lung greater than liver on anterior views or Kidney greater than liver posterior views is bad, as is excessive BM uptake which indicates HAMA.
 Day 7, 8, or 9 cold Rituximab 250 mg / m2 followed within 4 hours by 0.3 - 0.4 mCi / kg 90Y Zevalin over 10 min (0.3 mg/kg is plt <150-100, 0.4 mg/kg if >150)

Answer 539

A

 Indications: for the treatment of relapsed or refractory low-grade, follicular, or CD20 (+) transformed B-cell non-Hodgkins lymphoma

 Zevalin should not be administered to patients who have:
o ≥ 25% bone marrow involvement (bone marrow biopsy ideally within 6 weeks of tx)
o Platelets < 100,000 cells/mm3 (100 x 10^9 / L)
o ANC (absolute neutrophil count) < 1500 cells/mm3 (1.5 x 10^9 / L)
o Patient with impaired bone marrow reserve:
 Prior myeloablative therapies with bone marrow transplant or peripheral stem cell rescue
 Hypocellular bone marrow (≤15% cellularity)
 History of failed stem cell collection
 History of external beam radiation to more than 25% of the active bone marrow
o History of Type I hypersensitivity to murine proteins or to any component of the product including rituximab, yttrium chloride and indium chloride
o abnormal bio-distribution
o pregnancy
o poor compliance
o No prior history of radioimmunotherapy (relative)

Answer 540

A

 Zevalin (Ibritumomab tiuxetan)
o In-111 for imaging and Y-90 for therapy

Bexxar (tositumomab)
o I-131
 Indications: both are murine monoclonal antibodies for the treatment of relapsed or refractory low-grade, follicular, or CD20 (+) transformed B-cell non-Hodgkins lymphoma

Answer 541

A

 Bexxar (Tositumomab) & Zevalin (Ibritumomab Tiuxetan) & Rituximab all target CD20 antigen on B lymphocytes

Answer 542

A

 Bulky disease
 poor tumor vascularity
 development of immune response to radiolabeled antibody (HAMA)
 No pretreatment
 Abnormal biodistribution, high lung/renal uptake
 Transformed disease
 Intermediate histology

Answer 543

A

 Zevalin: 11 mm
 Bexxar: 2.5 mm
 Lymphocide (90Y or 67Cu-epratuzumab) (targets Cd22 on B cells): 2 mm 67Cu
 177Lu-Prostascint: 1.6 mm
 131I-anti-CEA: 2.5 mm

Answer 544

A

6 months

100 mCi I-131 are administered for remnant ablation. How do you counsel the man regarding fertility? Why?
 Males: do not conceive 6-12 months after (EANM)
o Risk of permanent sterility with 100 mCi is negligible
o Takes 2-4 months for germ cell mutation rate to decrease

 Females
o Risk of permanent sterility with 100 mCi is negligible
o Wait 1 year before conception, to allow repeat therapy if required

Answer 545

A

 Permanent sterility:
o 6 Gy, single dose OR
o 2.5 – 3 Gy, fractionated over 2 -4 weeks

 So
o 0.2 Gy: reduced fertility
o 1 Gy: temporary sterility
o 6 Gy: permanent sterility

Answer 546

A

 >0.15 Gy results in oligospermia and decreased fertility
 >0.50 Gy results in temporary azospermia and temporary infertility; <1Gy < 1year, 2 Gy 2-3 years
 6 Gy (or 2-3 Gy is fractionated) results in permanent sterility.
 LD50/60 4-6 Gy
 Hematopoietic syndrome 2.5-5 Gy in Hall, 1-10 Gy in most other references.

Answer 547

A

 Spermatogonial stem cells most radiosensitive
 Mature spermatozoa are the most radioresistant
 Temporary sterility can be caused by 0.15 Gy and permanent sterility by 6 Gy
 Wait 2-4 mo for germ cell mutation rate to decrease

Answer 548

A

 Ablation: 30-100mCi I-131 (100 mCi most commonly used)
 Regional adenopathy: 150 – 175 mCi
 Lung metastasis: 175 – 200 mCi
 Skeletal Metastasis: 200 mCi
 NB – CCI uses much lower dose
 Acute Side Effects:
o Sialoadenitis/ xerostomia (most frequent adverse events from high dose therapy)
o Altered taste,
o Sore throat/ neck pain/ dysphagia
o GI symptoms (nausea & vomiting – seen in < 1% of cases)
o Minimal bone marrow suppression (Transient pancytopenia)
o Radiation thyroiditis; thyroid storm

Alkso:
 30 – 100 mCi according to American Thyroid Association guidelines
o Empiric dosing for ablation: 50 mCi (now 30 mCi @Cross Cancer Institute)
o Dose for lymph node metastasis: 50 mCi (CCI)
o Dose for bone metastasis: 150 mCi (CCI)
o Dose for palliation of bone mets: 300 mCi (CCI)

Answer 549

A

 Reasons for remnant ablation:
o Eradicate all thyroid cells to
o reduce risk of local / distant recurrence
o prolong survival
o easier follow-up with thyroglobulin and I-131 scans
o subsequent RAI therapy more effective
 tumor less avid for RAI vs normal thyroid tissue
 TSH lower with residual normal thyroid tissue present
 30 – 100 mCi according to American Thyroid Association guidelines
o Empiric dosing for ablation: 50 mCi (now 30 mCi @Cross Cancer Institute)
o Dose for lymph node metastasis: 50 mCi (CCI)
o Dose for bone metastasis: 150 mCi (CCI)
o Dose for palliation of bone mets: 300 mCi (CCI)

Answer 550

A

capsular invasion.
• Then asked for dose limit for bone marrow –< 2 Gy
• Target dose to thyroid
• Dosimetry based on desired delivered dose to tumor (eg. 300 Gy to deliver to tumor)
 If lung uptake, dose limits:
o WB retention @48 <120 mCi, or <80 mCi if +lung mets
o Blood (bone marrow) <2Gy
o If dosimetry not available, 200 mCi will give 5% of patients a blood dose of >=2Gy

Answer 551

A

 Dose= (Thyroid mass[gms] x 80-200 uCi/gm)/ Percent uptake
 fixed standard dose (8 – 12 mCi for Graves)
 Quimby-Marinelli formula based on dosimetry (Radiation dose (cGy) = administered 131I activity (μCi) × % uptake (24 h) × 90/thyroid weight (g) × 100)

Answer 552

A

 Radioiodine therapy of hyperthyroidism (5 side effects)
 Transient side effects: nausea, thyroid/ neck pain, dysphagia, abnormal taste, sialadenitis
 Exacerbation of thyrotoxicosis
 Three difference treatment strategies:
 Surgery – classical approach, may be done in pregnant women
 Medical – PTU or methimazole
 Radioactive iodine
 Ophthalmopathy may not improve or in fact be exacerbated. Systemic steroids may be indicated. If patients ophthalmopathy is progressive and symptomatic, treat with steroids and early institution of thyroid replacement, if stable, follow closely.

Answer 553

A

 Side effects:
o Thyroid storm
o Sialoadenitis
o Exacerbation of ophthalmopathy
o Hypothyroidism (long term)
 Prophylatic prednisone 0.5 mg/kg 1 month after I-131 therapy, then taper over 3 months
 Dose = (Thyroid mass[gms] x 80-200 uCi/gm)/ 24hr % uptake

 % Uptake= [(net neck counts - net thigh counts)x 100] / (net standard counts)
 Dose = (Thyroid mass[gms] x 80-200 uCi/gm)/ 24hr % uptake
 Dose can either be empirical or calculated as above.

Answer 554

A

First of all, pretreatment assessment;
 -Assess for risk factors; 1.smoking, 2.pre-existing, (4% vs. 23%), 3.Elevated TRAb, 4. Active disease, 5. Severe hyperthyroidism etc

EANM guidelines
o Assessment by ophthalmologist to establish clinical disease activity
o Smokers: advise smoking cessation
o For active ophthalmopathy, treat with steroids (prednisone 0.2-0.5 mg/kg/d, 1-3 days after iodine treatment, continue for 1 month, taper for 2 months)
o Start thyroxine as soon as TSH rises after ablation, as elevated TSH can worsen ophthalmopathy

Answer 555

A

 Acute
o Transient swelling (1 week) and dyspnea
o Salivary gland discomfort
o Transient rise in FT4 and FT3 7-10d post-therapy
o Exacerbation of heart arrhythmias and heart failure if poorly controlled before therapy
o Thyroid storm
 Treat with IV ATDs, corticosteroids and β-blockers

 Hypothyroidism
o Higher incidence in Graves’ than toxic goitre
o Rate in solitary hyperfunctioning nodules
o LT4 for patients with elevated TSH after 131I therapy and with subclinical hypothyroidism

 Ophthalmopathy
o Greater risk of appearance or worsening of ophthalmopathy in Graves’ vs. antithyroid treatment
o Especially in smokers: suggest quitting
o Prednisone helps to prevent exacerbation
o Elevated TSH may worsen ophthalmopathy

 Autoimmune thyroiditis
o 1% of patients following radioiodine therapy of goitre/autonomous nodules
o Risk up to 10% with pre-existing thyroid peroxidase or Tg antibodies

 Radiation-induced cancers
o Small excess reported (1.09 [1.03-1.16]) but biased by increased surveillance, changes in reporting and higher proportion of smokers

 Considering proptosis:
o If active and moderate to severe ophthalmopathy, treat with methimazole
o If mild active ophthalmopathy and smoker or other risk factors, treat with steroids
o If mild active ophthalmopathy, radioiodine w/o steroids
o Suggest smokers quit
o Prednisone to prevent exacerbation
o Follow closely for hypothyroidism (start Synthroid to avoid elevated TSH)

Answer 556

A

 High pre-therapy TSH receptor antibody (aka TRAb, TSI)
 High pre-therapy serum T3 level
 Active ophthalmopathy
 Smoking
 Post-therapy hypothyroidism

Answer 557

A

 Typical Iodine turnover rate is 1%/day
 Half-life of T4 in the body, 6.7 days.

 Graves’
o anti TSH receptor antibodies - stimulate TSH receptors
o therapy options: PTU or methimazole, surgery, 131I
o 131I

 standard 8-12 mCi dose
 alternative formula dose (mCi) = (weight in g x 100 μCi/g) / 24h uptake

 dosimetry based; in dose elevating studies, it has been found that 270 Gy is required, Dose in Gy=(90×Oral dose in μCi×Thyroid uptake)/(mass of thyroid in grams) assuming an effective half-life of 6 days of 131I.
 Assess patient 6 weeks post Sx (diagnostic testing is actually done 9 months after therapy)

 Want TSH < 0.2 mU / ml (not really; 1.0-0.5 in low risk of recurrence, 0.1-0.5 intermediate risk, <0.1 in high risk patients, according to the ATA guidelines, CCI handout says 0.2)

 For 131I therapy want TSH > 30mU / mL
 RDA = 150 μg / day; normal daily intake = 150 - 500 μg
o low iodine diet < 50 μg / day
o should be on 2 weeks prior to therapy

 Thyroid cancer post-op
o 6-8 weeks

Answer 558

A

 30 mCi I-131
 Synthroid
 Surgery

Answer 559

A

 seafood
 dairy
 No processed or organ meats, no egg yolks
 Fats (only vegetable oils) no butter, lard, shortening, cream cheese.
 Liquids-no filtered water (BRITA), herbal teas, red or orange soft drinks, alcohol
 iodine-containing vitamins
 some breads, no dry or instant cereal, no enriched/instant pasta, rice or potato mixes
 Snacks, nothing with salt in it.
 iodized salt
 red food dye

Answer 560

A

 Rare (0.34%)
 usually occurs 3-15 days post therapy
 oxygen, ventilatory support, IV fluids (aggressive fluid replacement)
 acetaminophen (no aspirin as it decreases TBG and increases free T3T4), ice packs, cooling blankets for hyperthermia
 B-blockers (symptoms and decreased peripheral conversion)
 iodine load 3-4 days after treatment to decrease release, but wait one hour after Methimazole administration (lithium if there is an iodine allergy)
 anti-thyroid meds - thionamides (PTU, methimazole) for 6-12 weeks before treatment to deplete stores, stop 2-3 days before and restart after for 3-4 days

Answer 561

A

 Symptoms
o Fever, sweating, resp distress, seizures, tachycardia

 Support vital functions
o Adequate O2 (may need to intubate)
o Large bore IVs
o NG tube
o Consider admitting to ICU

 Anti-thyroid medication: PTU 200-400 mg po q4-8h
o decrease peripheral conversion of T4 to T3
o causes rapid reduction in circulating hormone level
o available as PO only so may need to use NG tube
o consider giving lithium
o (methimazole)

 Wait 1h after PTU before giving iodine (SSKI): 5 drops q6h po
o Wait to shut down organification
o Prevents release of more T3 and T4 from the thyroid gland, without the iodine being used to make more hormone

 Give β blockers
o Propranolol 1mg/min IV as needed to get symptoms under control, then 80 mg po q4h
o But use with caution in patients with CHF

 May need to give steroids (depleted in thyroid storm)
o Dexamethasone 2 mg po/iv q6h
o decrease peripheral conversion of T4 to T3

 Treat hyperthermia with ice packs, fans, cooling blankets and Tylenol (not aspirin, as can increase circulating thyroid hormone levels)

Answer 562

A

Sour candy is given to prevent sialoadenitis (or reduce severity).
Give 24hr after I-131 dose, because at that time, blood levels of I-131 are decreasing while salivary gland levels of I-131 are high.
If you give it earlier, it will actually draw I-131 from the blood into salivary glands, causing or worsening sialoadenitis.

Answer 563

A

 absolute contraindications:
o significant hepatopulmonary shunting (>30 Gy to the lungs)
o Flow to the GI tract that cannot be corrected with catheter techniques.
 Others:
o limited hepatic reserve
o irreversibly elevated bilirubin levels
o compromised portal vein (PVT)
o prior radiation therapy involving the liver
o Indication
o Unresectable primary or secondary hepatic lesions with liver dominant tumor burden and a life expectancy >3 mos.