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Archive for the ‘Favorites @ Louisville’ Category

Favorites @ Louisville

Posted by oralboards on April 19, 2009

Brief Guide to the American Board of Radiology Oral Examination

100 Days of Solitudeby Henry Shih, based on his 1996 experience

  • Started studying the day after Presidents’ Day in February for a total of about 15 weeks or 100 days
  • Practiced taking cases in many noon conferences and about 60 review sessions
  • Read Fundamentals of Diagnostic Radiology by Brant & Helm
  • Read Primer of Diagnostic Imaging by Weissleder & Wittenberg
  • Attended UCLA general review course
  • Studied every current ACR teaching file cases on either film or LD
  • Studied the old ACR teaching file cases for Bone and GI
  • Read ACR Syllabi in GU, Mammo, Nucs
  • Read Essentials of Nuclear Medicine Imaging by Mettler & Guiberteau (Recommend studying newly published ACR teaching file on CD-ROM instead)



There are no direct flights to Louisville.  Airlines serving Louisville and LAX are Delta, NW, and United.  I looked on the web for morning flights from LAX that allowed me to arrive in Louisville even if there is a missed connection.  Airfare was only $200.


Many UCLA people have stayed at the Seelbach Hotel (800-333-3399) in downtown because using the VA ID, a government rate, back in 1996, was only $67 including tax.  It is a nice old style hotel and less populated with nervous radiology residents than the official Executive hotels.  The Seelbach has a van that will pick you up from the airport, and will take you and your baggage to the Executive West the next day.  There are a few restaurants in the downtown area; just ask the doorman.  My Favorite Muffin is a good breakfast place.  I had a hard time deciding whether to eat lunch.  Weighting the risk of vomiting on my examiners versus collapsing on their bed from hypoglycemia, I opted for a small sandwich and a non-carbonated beverage.

Day of Reckoning

Historically, UCLA and west coast candidates are given afternoon sessions to help with jet lag.  I arrived at the Executive West an hour earlier than the appointed time and immediately ran into many familiar faces from UCLA, AFIP and earlier life.  There is the inevitable small talk, and attempted words of reassurance from UCLA faculty members.  The air is thick and my fight or flight reflex engaged.  There is a large unattended storage room for you to leave your coat and baggage.


On the elevator, an examiner (wearing the tell-tale name card) next to me told me in a stern voice to “calm down.”  This sent my pulse higher than the Sears tower.  When I arrived at the orientation suite listed on the admission ticket, the room was already filled with many frightened faces.  I signed in and was then handed my “dance ticket” listing no less than five of the biggest names in Radiology, including Bassett.  Bob Campbell, a RSNA Gold Medalist himself, gave the introductory explanation.  This only took 15 minutes, then some official looking person walked in and spoke into Bob Campbell’s right ear.  Next thing I heard, he was announcing “Dr. Shih, the problem with one of your examiner will be corrected.”  Everyone stared at me for the longest 15 minutes of my life waiting for the first session to start.  By now, I have spent my adrenaline reserve and my heart is in asystole.

Torture Chambers

Neuro on LD

Dr. Lukin, an upper middle-age gentleman from the Midwest, welcomed me to the first session at the door, and explained to me that this section is given on LD, and each case only has selected images on the LD.  Then he transitioned with “let’s start with something not too hard” which is surely a kiss of death.


1)       This “average difficulty case” was an MRI L-Spine.  Axial images showed laminectomy defects and soft tissue materials.  Lukin confirmed the back surgery.  I asked for Gado images, and with those, diagnosed Failed Back and finally felt that I might just survive the day and pass the darn exam.

2)       I don’t quite remember the imaging modality on the “tumor” cases.  There was a cystic suprasellar mass for which I applied a few of the SATCHMO differential as best I could remember, throwing in a few cystic sellar differentials since I was asked if I’m confident about suprasellar versus sellar location.  I came to conclude craniopharyngioma, but hedged plenty.

3)       The other “tumor” case was an enhancing intraventricular mass in an adult.  Again, I gave a few differentials based on location, but did receive a snicker for offering choroid plexus pappiloma.

4)       The case that seemed to have turned the tide in my favor was a single CT slice from the level of the ventricular atria showing multiple small enhancing masses.  I noted that a few of the masses seem to protrude into the ventricle, and before I could make the mistake of saying intraventricular extension, Lukin interjected with a questions about the precise location of these juxtaventricular masses.  I took the hint and went down the path of subependymal nodule.  The case became clearly tuberous sclerosis for me and I was able to mention a few key concepts like “foramen of Monro” and “malignant degeneration into giant cell astrocytoma” for which I was rewarded psychologically by the appropriate images in sequence supporting my diagnosis.  I can tell Lukin wrote “7” something on the scorecard.

5)       He gave me an MR orbit case and I discussed optic neuritis versus meningioma versus glioma.  He had me explain how I would distinguish those entities.

6)       There was a CT of infarcts in a weird distribution in one hemisphere.  I speculated on vasculitis and asked for MR but was given a lateral view cerebral angiogram.  After a millisecond of panic, I calmed down and methodically explained how I look at an angiogram by pointing out simple things like the Sylvian triangle.  By this approach, I came to the realization that the ICA was cutoff!  So I mentioned Moya-Moya.  Lukin was pleased, and asked me what is Moya-Moya.  I said “a puff of smoke, in Japanese” then explained how it is sort of an ideopathic vasculitis (justifying my earlier suspicion).  I imagine him writing “72” on the scorecard.  But who knows.

7)       Another case of infarct was, I believe, a classic right MCA infarct.  Don’t remember details.

CV on LD

Dr. Elliott has a big reputation for being of the old school and tough.  Also, he is an authority on cardiac imaging of the cath variety.  Recalling the tales Dr. Hathout told me of his session with Larry Elliott, I was petrified.  Upon meeting, I tried to kiss ass by saying “What an honor to meet a giant of radiology …” but he was gruff and said “let’s get started.”  He sat me down in front of the monitor, and he sat next to me, elbow to elbow.  I felt very uncomfortable.  The image quality sucked, especially for trying to decide pulmonary blood flow on congenital heart cases.  Larry Elliott even conceded that twice when I said the PBF was such and he said “I see why you might say that because you really can’t see the pulmonary vascularity on this monitor, so let me just tell you what the vascularity should be.”  That helped.  In fact, he turned out to be a very nice examiner, guiding me through some of the cases by asking very specific questions the answers of which helped to discriminate between differentials.


1)       I got three congenital heart CXR cases.  There was a straight forward ASD where he asked me which chambers were enlarged before asking for the diagnosis.

2)       Another is a huge heart on CXR.  This was mitral regurgitation which I figured out based on chambers.  On the cine, aortic insufficiency was also obvious.  He asked for a unifying diagnosis, and I told him rheumatic heart disease.  He was pleased.

3)       The other is a boot shaped heart and a right arch on CXR.  I decided to start from the right arch and arrived at tetralogy.  He then asked me about the branching patterns on a right arch.  I immediately told him aberrant left subclavian and mirror image branching.  But he said there is a third pattern especially in tetralogy.  I couldn’t think of any, but speculated out loud on possibilities.  He got angry and said, “Don’t guess; either you know it, or you don’t.”  I turned white and meekly admitted that I did not know.  He said in all his years of examining, only two residents have ever answer that question correctly.  Again, I immediately thought of Gasser Hathout, and stopped feeling inadequate.  [Gasser still knows the answer to this question – ask him.]

4)       LV pseudoaneurysm case just like the one described by Mike Noronha on his recall notes.

5)       The cardiac MR case I got was lipoma.  Thanks to Stan Liu’s recall notes, I nailed the case.

6)       The body angio case was cecal bleed.  Elliott asked about management options, but he was clearly not very interested in body angio, or intervention.

7)       A simple right groin AVF case, and discussion on management options.

8)       Aortic dissection case.  Several classic pimp questions like classification.

Nucs on LD

Dr. Eggli is an non-descript examiner, I think from Penn State.


1)       Large cold thyroid nodule should have been a straight forward case affording me a chance to do the I-123 v. Tc-99m song and dance.  But I almost tripped myself up and had to recover quickly.  Eggli was laughing at me. 

2)       Classic pneumocystis pneumonia on a Gallium.  I asked for immune status history and then committed to PCP, gave no differential.  He asked what about KS and I explained why not.

3)       HIDA with no GB filling at an hour.  I explained that at this point there are several options.  He asked me which option I like, and I said morphine.  He then showed the post-morphine images.  The GB filled.

4)       Captopril renal case.  Straight forward discussion on the mechanism of ACE-challenge.

5)       Bone case was a pediatric tibial plateau fracture.

6)       Cardiac case was an RVG.  I pointed out the wall motion abnormality and said it can be confirmed by amplitude and phase images.  He asked what were those and I dazzled him with my erudition on the mathematics of harmonic analysis.

7)       The obligatory VQ.  Mine was a COPD pattern which gave me the opportunity to point out the few remaining differences between the modified-modified PIOPED and the revised Biello criteria.

US on LD

Dr. Kazam had a strange demeanor and a foreign accent that made the situation that much more Kafka-esque.  He told me he could see the findings just well as I, so did not want me to describe the findings, but wanted the one or two diagnosis.  I said what about a third; he remained steadfast, one or two only.  The LD cases are shown as real-time, but the image quality sucked.  Many of the studies are done on older machines, with very poor resolution.  I could not make out major landmarks on several cases and kept on asking Kazam to re-run the cineloop.  He would get annoyed if I asked for a third look.  I had a terrible experience and am too shell-shocked to remember any detail.


1)       Prenatal anterior abdominal wall defect case.  I knew I was in the gastroschisis v. omphalocele game, but could not pick out the findings necessary for the discrimination.  So I just talked about what features could be used.  He wanted me to commit to one, but I just could not.

2)       Ovarian mass with Doppler.  Some discussion on the value of Doppler.  I couldn’t remember the RI threshold, and personally felt Doppler to be worthless.  But I did not reveal either.

3)       Some renal case, also had Doppler, but my PTSD prevents me from a total recall.

4)       Portal vein thrombosis.  This one I got easily.  Hope it made up for the deficit on my score card.

5)       Renal stone.  Simple enough.

6)       Hyperechoic mass in the liver.  I offered hemangioma.  He asked what else.  I said I thought he only wanted the one or two diagnosis.  He did not smile.  I’m now convinced I would fail.

7)       Oligohydramnios.  I regurgitated the DRIPP differential but was chastised for including too many.

Peds on LD

Dr. Ralph Lachman was very nice.  But I was afraid he was going to show me syndrome after syndrome from his book.  In fact, he did not until the very end.


1)       My battered child case started off as a head CT showing SAH.  Once I clued in that SAH should raise suspicion of child abuse, I was inundated in rapid order with many classic films of fractures in varying stages of healing.  As each image came up, I would say the key finding, and he moved on.

2)       Congenital lobar emphysema

3)       Bilateral Wilms tumor.  Was not asked about staging.

4)       Lead poisoning case started off from a bone film.  Once I clued in, I was able to manage.  If you want to see the film for this case, check out ACR Bone LD image #534.

5)       Ureterocele.  Obviously, we talked about the Weigert-Meyer rule.

6)       My notes scribbled on  the back of my boarding pass for the flight back seems to say a case of typhlitis.  But I can’t remember a thing about it.  Did I seriously overcall an appy?  Zero recall.

7)       Double aortic arch MR case.  Thought I was back with Larry Elliot.

8)       Some fibula lesion.  I recall mumbling EG but I still don’t know what it was.

9)       He gave me a history of a child whose parents are concerned about growth delay.  AP pelvis seemed like Champaign pelvis.  I asked if the child was really short for his family and was told that actually, the parents were both about 4 ft. tall.  I took that as the signal that this is my dwarf case.  I then asked for more films and was shown a whole bunch.  As each came up, I mentioned the key findings that went with Achondroplasia, and concluded that the family members are familial achondroplastic dwarves.  Lachman was pleased, and asked me if I should ever have trouble with a syndrome case in my future practice, is there a reference source or book I could use to help me figure things out.  I said, “Yes, most definitely, your book.”  Ralph was beaming!  And I was sure I passed peds, possibly garnering a 72.

Breast on composite film

I had been told that Larry Bassett would not be my examiner, but did not know who the replacement killer would be.  When I walked in, I was pleased to see Valerie Jackson.  She explained how Larry didn’t check his “dance card” until around 1 PM and realized that there was a problem.  She volunteered to substitute for him, and hope I was not too perturbed.  I was only too happy to have an examiner I know to be a nice person.  However, I was concerned that my lack-luster performance would reflect poorly on the UCLA training program, and on Larry.  Mammo cases flew by very quickly, and many are so similar, I can only say that I was shown mostly classic cases and was always asked to come down to a final ACR classification and recommendation.  There were unequivocal fibroadenoma, hamartoma, sclerosing adenosis and simple cysts.  After about 15 minutes, Valerie asked me if I’d mind her switching from the official ABR exam cases to her own teaching file.  I knew I had passed, and so cheerfully agreed.  She then showed me lots more cases, but I was relaxed and so time passed quickly.  Out at first bell.

Bone on film

Having free time from getting out at first bell is not necessarily good because it only gave me the opportunity to focus on my fear and panic.  Despite good performance on mammo, I walked into Bone an emotional wreck to face Dr. R. Daffner.  He proved to have a poker face and the change from nice smiling Valerie Jackson disturbed me.


1)       MR case was pretty easy.  Just a straight forward ACL tear.  Was asked about Segond fracture.

2)       Arthritis case was classic Gout.  No problemo.

3)       Soft tissue calcification.  I asked and was given a history of trauma.  So, I went with myositis ossificans and was asked about management.  I may have messed up by not insisting on follow-up radiographs or order CT.  Other people later reminded me about the infamous MO versus Parosteal sarcoma trap.

4)       Sclerotic pedicle on L-spine.  Said osteoid osteoma, but forgot to mention contralateral pars defect.

5)       Large bubbly lesion in ankle.  I only offered ABC and GCT.  Should have used the “ICE BAGS” differential, and calcaneus simple cyst would have also been nice.  Probably was ABC.

6)       Aggressive lesion on tibia.  Mentioned Ewing, infection, EG, osteogenic sarcoma, but could not commit.  Afterwards, I thought it was Ewing

7)       Multiple lytic lesions in a child.  Mentioned EG and infection, but forgot to mention HPT, enchondroma, or FD.  Probably was EG.

8)       Trauma case was lateral view C-spine.  Thought I saw a unilateral jumped facet, but couldn’t really find the facet or lamina fracture.

Chest on film

Dr. Carl Ravin’s reputation amongst Duke residents scared me.  But he turned out to be a very nice examiner often giving me encouragement.


1)       Right paratracheal mass and left scapula destruction on CXR.  He then showed me the CT but was impressed that I picked up the scapula destruction on CXR.  Cancer.

2)       Classic LUL collapse CXR.  I immediately called it.  Again, he seemed impressed.

3)       Bronchial fracture.  Cool case.  I actually enjoyed this case.

4)       Bibasilar interstitial pattern CXR.  We discussed differentials of interstitial disease, and narrowed the field based on the lower lobe predominance distribution.

5)       Then there was an air space pattern CXR.  I methodically went through the possibilities using the water, pus, blood, and cell approach.  Ravin seemed to liked that.

6)       Lymphangitic spread carcinomatosis.  Absent breast shadow helped me to nail this case.

7)       Sequestration?  I’m not sure.

GI on film

Dr. Harell is an older private practitioner from New Orleans.


1)       The dreaded SB case gave me much trouble.  I could not see the abnormality but Harell was very patient and steered me to recognized some kinking and angulation.  After several minutes of struggle, I finally started generating good differentials.  He kept on saying what else to each of my suggestions until I finally ran out of ideas and said radiation enteritis.  He stopped pushing me so I asked if the patient had XRT.  He confirmed that.  I’m not sure if I got 69 or 70 on this case.

2)       Smooth mass lesions in esophagus.  Probably a leiomyoma or lipoma.

3)       Lead pipe colon.  This was easy.

4)       ERCP case turned out to be Mirizzi syndrome.  Harell was impressed and asked me what is Mirizzi syndrome, even as he put up the CT.

5)       I think my UGI case was just gastritis.

6)       Liver case was FNH on CT.  Discussions centered on the central scar.

GU on film

As I entered the last torture chamber, I am on a high knowing that the ordeal would soon be over.  I am looking forward to a stiff drink of Kentucky bourbon as I shook hand with Dr. Stephen Amis.


1)       The first case was a delayed nephrogram.  I thought this was going to be the famous contrast reaction case and jumped all over it.  I was so jumpy Dr. Amis had to tell me to calm down, get a hold of myself, and think slower.  I followed his advice and regained some composure.  I was then able to generate the differentials for delayed nephrogram but was not shown any more films.  Interestingly, Steve To was given the same case by Amis, but the diagnosis was contrast reaction.

2)       Stricture in the bulbous urethra.

3)       RCC with hemorrhage.

4)       Duplicated collecting system with obstruction at UPJ.  Wasn’t sure what the case is really about.

5)       I scored on an excellent discussion about the work-up of adrenal mass, especially the use of chemical shift MR images.  Amis was very impressed.

6)       Prostate cancer.

7)       Medullary nephrocalcinosis.  Straight forward differential did the job.


Common Interventional Radiology Topics and Questions at the Radiology Oral Board Exam


Common Interventional Radiology Topics and Questions at the Radiology Oral Board Exam include: nephrostomy tube placement, biliary drainage and cholangiography, abscess drainage, cholecystostomy tube placement, lung biopsy, gastrostomy tube placement, treatment of pancreatic pseudocysts, treatment of liver cysts (sclerotherapy), treatment of esophageal carcinoma with stents, sclerosing cholangitis, treatment of pericardial effusion, treatment of a patient with fractured ureteral stents, and management of a patient with a chest tube in the wrong position.

Biliary Obstruction and Drainage


The radiology candidate at the oral board examination should be able to discuss imaging findings of biliary obstruction on conventional percutaneous and tube cholangiography as well as MR cholangiopancreatography (MRCP), CT and ultrasound. The differential diagnoses such as sclerosing cholangitis, biliary stricture, cholangiocarcinoma, metastases, and pancreatic carcinoma will likely be discussed. The procedure for performing transhepatic cholangiography and drainage are a frequent part of this discussion. Be sure to remember to mention antibiotic therapy before the procedure to minimize the risk of sepsis.

Lung Biopsy


At the radiology oral board examination you will be highly likely to have a case which will revolve around the discussion of lung biopsy. The context of the discussion may revolve around solitary or multiple pulmonary nodules. The differential diagnosis may be discussed. Remember to exclude a pulmonary AVM before you decide to proceed with a biopsy. (Safety of the patient is most important.) Be prepared to discuss the lung biopsy procedure as well as risks (complications).

Nephrostomy Tube Placement


Nephrostomy tube placement is a frequent topic at the radiology oral board examination. Hydronephrosis is very common in Louisville. Be prepared to discuss the etiologies of hydronephrosis including: stones, strictures, and neoplasms. You will likely be asked to briefly explain the procedure as well as percutaneous nephrostomy indications and complications.Antibiotic prophylaxis is controversial, but should definitely be used for stones or suspected infection. When in doubt give the antibiotics (safety is always the best approach in Louisville).  

Abscess Drainage


Abscess drainage is another frequent topic at the radiology board examination. Be prepared to discuss the potential source of the abscess and potential drainage routes (including transvaginal and transrectal drainage approaches). Potential sites most commonly discussed are: peri-appendix (right lower quadrant), liver, and spleen. Be prepared to discuss potential complications and reasons for choosing specific drainage approach. Would you use CT, ultrasound, or fluoroscopy? Think about safety issues including radiation exposure to pediatric and female patients. Verbalize your safety concerns. Remember the antibiotics to prevent sepsis.

Percutaneous Cholecystostomy Tube Placement


The placement of a percutaneous cholecystostomy tube is a potential topic in Louisville. You may be shown nuclear medicine, ultrasound, or CT images of a patient with acute cholecystitis (usually acalculous cholecystitis). The case will probably be framed in light of a severely ill patient in the intensive care unit who is too ill for surgery. What can you do to help? Be prepared to discuss the cholecystostomy tube procedure and possible complications. Remember to give antibiotics pre-procedurally.

Treatment of Esophageal Cancer


Treatment of Esophageal carcinoma with esophageal stent placement has been a topic on the radiology oral board. This question is not likely to come up as often as the previously mentioned topics. However, you should be prepared to briefly discuss this as a treatment option if the case warrants.

Pericardial Effusion Treatment


You may see a case of pericardial effusion on CT. If the patient is symptomatic, treatment with catheter drainage could be discussed. Again, this topic is less likely than some of the earlier topics, but you should be able to discuss catheter drainage of a pericardial effusion if the case warrants it.

Treatment of Fractured Ureteral Stents


You may see fractured ureteral stents on a case at the oral board exam. If you recognize this on a KUB or CT, you will want to be able to discuss percutaneous snare retrieval of the catheter fragments and placement of a new double j stent.

Chest Tube Management


You may encounter a case of an incorrectly placed chest tube for pneumothorax or empyema. You should be able to discuss etiologies of the underlying problem, techniques of chest tube placement, repositioning options, and possible complications.

Gastrostomy Tube Placement


You should be able to discuss how to place a gastrostomy tube.

Pancreatic Pseudocyst Treatment


Be prepared to discuss the role of percutaneous aspiration and/or drainage of a pancreatic pseudocyst. Know the technique, timing considerations, and potential complications.

Treatment of Hepatic and Renal Cysts


Symptomatic hepatic or renal cysts can be treated with sclerotherapy. I would know the various materials that can be used and the technique. If you choose to use alcohol to ablate the cyst, be sure to mention sedation for the patient.

Treatment of a Bile Duct Injury


You may see images of a bile leak or bile duct stricture related to a laparoscopic cholecystectomy. Be prepared to discuss this type of case. You may not be told the etiology of the problem. You should be able to discuss drainage of the biloma and possible drainage catheter placement for diversion of a leak. Most leaks respond to drainage of the biloma and time for the leak to seal. Stricture may be treated with balloon dilatation and catheter drainage.

Boards 2000:

Briefly: If you have any question


I passed outright. Overall, it wasn’t as bad as I thought it would be. To put it to the point: “Study until you puke” puts it quite nicely into the right setting. (Quote from one attending who shall remain anonymous.) One textbook a week. One disk a week depending on number of cases. Disks first slowly, read every word. Second time fast. Try for all discs once by MOB time, then focus on weak spots. 4 weeks for general review and cool off period (nerves) was very helpful.

Casebooks are good – Nice change from the computer; also just looking at textbooks (pictures only)



The best are slide reviews, since they resemble the boards and everybody can see. You can get through 20 cases in 1-2 hours, sometimes more depending on general speed of the group.

Practice speaking, stick to the same routine for every film – it will save you.

Don’t waste time trying to figure out the age: newborn, young skeletally immature/mature; young adult/ elderly will do. If the age is important, they will let you know the age if it is important.



I stayed in the Executive West; for the full experience. Order room service for breakfast. Shower before breakfast, since it will be late and 0700 is early. (Breakfast served at 0630- arriving at my door at 0645). Go out to dinner the night before- everybody in the hotel (and across the street) seems to be an examiner or examinee.


The examiners are generally nice, don’t want to harm you – rather help you.


Yes you may answer questions wrong. Don’t keep score from one to the next session. Remind yourself actively not to do that. Don’t get scared by famous names, they all have been there.


If someone asks what do need to do from here, and then they ask again would you follow this patient, think again. A follow up study usually doesn’t hurt. It might be a hint, that the initial answer was not quite right.


The doors are open and other people are walking into and out of the room.


General introduction: Good Morning, I am Joe / Jane Doe. Handshake; hand over computer stripe.

 “I am XYZ; how are you?

My answer: I am still alive, have a pulse and breathe.

General response was a smile and something like “you will be ok.”

Sit down. Then” This is Ultrasound / or VIR section?”

Ending a case:

After describing the type of study, findings, differential and presumed diagnosis there are several options:


My favorite:

I would recommend a follow-up/biopsy/surgery/ additional imaging/other diagnostic test and call the referring physician and discuss the case.


Not as good:

This is all I can say about this case at this point.


Stop speaking after: My most likely diagnosis is Coarctation.


Worst choice: keep talking.







Ultrasound – Dr. Fagan

First session: My mouth was dry. Could hardly talk.  I hated the movies.


RUQ anatomy

graft stenosis with wave form

post transplant liver with flowing particles, but not color??? Weird looking. No clue, Said possible Budd Chiary

Ovarian cysts with abnormal thickened wall ? CA discussion about follow-up vs. surgery

Diaphragmatic hernia in utero with questions of post delivery problems (pulmonary hypoplasia)

Cystic hygroma what would you do? Talk to the patient and physician

Retroperitoneal LN (weird movie with nodules flying by the aorta on transverse imaging)



Pediatrics Dr. Poznanski

Still dry mouth, little better. Convinced I had failed this section.


Subdural hematoma

Epidermoid on plainfilm pelvis

Rickets femur

Plainfilms nonweightbeiring: ?fracture/leucemia/ JRA/ bilateral pain 2 years old

? Gastric filling defect, empty stomach on follow-up film; no clue mumbled about extrinsic compression, mass would do CT/US.

Hyperlucent left lung DD Aspiration, FB, no ptx, lobar emphysema, (no signs for scimitar, mass) he kept asking anything else, I said more but not what he wanted.

CRX with? bone finding- no clue


Mammography – Dr.Helvie

A Walk.

Sat down and grabbed the magnifying glass. Realized, that you can’t hang the films with one hand very well. So I put it back down.  I looked at all the images, with and without glass and said there are 1/2/3/… lesions I am worried about. I would spot/mag the US, place BB. Do 90degree lat. for calcs…., then biopsy stereotactic for calcs, or US guided, excisional for radial scar….; Then BIRADS code.

Few questions asked.

Spiculated mass

Spiculated mass / radial scar

Cyst on one side, spicualted mass on the other side; do spot compression, us

FA one side, two axillary spiculated LN axilla other side

Palp mass in fatty fibroglandular tissue on bad mammogram, repeat study with Marker and small pedicles shows nice spiculated mass.

Branching calcifications what to do with LCIS on stereotactic bx, then do excisional bx

What to do with atypical ductal hyperplasia on stereotactic bx – excisional bx

Cyst with bad US



BONE – Dr.Daffner


Enchondromatosis with degeneration into chondrosarc

Bucket handle mcl tear with double PCL sign

Hand with erosions, ray thickening psoriasis, reiters

Hemangioma/pagets of C7 with h/o trauma; close to “The Pagets vs. Prostate Ca trap” Dr.Leffler

Posterior right hip dislocation

Left sacral insufficiency fracture


Pulmonary – Dr.Curry

No high res.


Multiple miliary nodules

Right apical pancoast tumor

Cardiac enlargement with mass: met breast ca

bronchogenic cyst

Narrow anterior thorax: pectus deformity?

Anterior mediastinal mass: thymic cyst


GI – Dr.Scholz

ERCP pancreas divisum

ERCP bil dil panc head mass

hepatic abscess

Meckels tic

Linitis plastica

Panc tail mass





GU – Dr.Dunnick

Cysts in kidneys and pancreas ADPCK

Unicornuate uterus on pelvic MRI

Cervical mass on pelvic MRI

Us with duplex collecting system and renal cell ca

Adenoma with mult masses? Pheo – ass c men syndromes (Mentioning MEN opened the Candorras box (Greek Goddess; box filled with snakes))

Ureteral pseudodiverticulosis,  ? Of follow-up/malignant potential

Unsure unop bowel, other; no clue



Neuro – Dr.Deck


Arachnoid cyst

Meningeal enhancement

Chondrosarc of sella

CT with bleed MCA trifurcation aneurysm

Hemangioblastoma/ pilocyst. Astrocytoma brainstem

Periventricular heterotopia

Left parietal T2/Flair Incr signal in 35-yr. old aerobic female: carotid dissection



VIR – Dr.Barth

No doses, no injection rates.


Aortic rupture

Ergot intox: vasospasm

Thoracic outlet syndrome

Renal artery stenosis

Duodenal ulcer bleed

SMA occlusion

Perc cholangiogram with obstruction internal stent


NUCS – Dr.Perez


Strange section. Started out 3 times with the wrong study, was then corrected and went on. In the end he said after the second bell: I now have to end the exam – and I was convinced I had fail the section outright.

No doses. No QA.


Thyroid scan: deQuervains

Octreotide with pheo/paraganglioma; planar and spect

VQ scan: contaminated vial, multiple spots on lung on perfusion scan

Biliary atresia/neonatal hepatitis

RAS vs. high-grade obstruction on captopril renal scan

Muga scan cardiomyopathy; decrease in EF

Bonescan with rib fractures vs. mets. H/h breast ca 10 years ago. Clue: activity in left cerebral hemisphere c/w prior stroke. (Jack: You are the man!)






First of all he asked no quality control questions.  He wanted me to give him the name of each study, what isotope was used and how much.  Showed me about ten cases.


1)      Thallium SPECT of the heart with reversible defect in the septal region and                                                       nonreversible defects in the inferior/apical region—ques: what vessel supplies this area?

2)      A octreotide scan with activity in the liver and the pancreas—ques: what is the agent, where does it localize, what is MEN1 syndrome consist of? 

3)      Renal scan with immediate uptake and poor excretion.—ques what other isotopes could be used for this study? 

4)      Bone scan of a hip prosthesis with activity at acetabulum and along the shaft.  History of placement 6months before. 

5)      V\Q scan with patchy perfusion (multiple large defects) and >50% area of air trapping on the wash out portion of the ventilation images indicating COPD.—I said that it was indeterminate due to the fact that >50% of the lung was involved with COPD.  He asked me where I got the info (its in an article that Guiberteau gave us) 





Very nice examiner.  Showed me about ten cases all of which were real time, some with still images.


1)      Hydrocephalus in fetus with lemon head sign—No ques after I told him nml size of ventricles and the differential diagnosis.

2)      Dilated lateral ventricles with no dilatation of third ventricle.  No ques after I said Aqeductal stenosis 

3)      Fetus with mild hydronephrosis and a large cystic structure in the middle of the abdomen connected by a thin anechioc line to smaller cystic structure in the pelvis.  No ques after I put post urethral valves in the diff 

4)      Fetus with large cystic structures behind neck—Cystic Hygroma in Turners syndrome 

5)      Heterogeneous mass in the right adenexa with low res. flow on color Doppler—I asked if positive preg, he answered yes I said ectopic—ques what is significance of low res flow on Doppler? 

6)      Same as above with a neg. preg. test.—ques how can you tell diff between B9 ovarian tumor and malignant tumor.





1)      Neonatal chest at birth with hyperinflation and streaky parenchymal disease.  I gave a differential then he showed me a follow up the next day that showed almost complete opacification of the lungs bilaterally.

2)      Obstructed Kidney with enlargement 

3)      Multiple dilated loops of bowel in neonate 





1)      Spiculated mass in one breast.  After discussion of degree of malignancy (highly suspicious) no other ques.

2)      Multiple small heterogeneous calcs in one quadrant of the breast. 

3)      Multiple heterogeneous calcs in linear pattern leading from the middle of the breast to the edge of the pectoralis muscle.  Ques: what would you do in this case (what type of biopsy, and would the breast need to be removed or would you do lumpectomy. I said remove if it involves the pectoralis mm 

4)      Bilateral spiculated masses 

5)      Two palpable masses in a heterogeneously dense glandular breast with no definite abnormalities on the original two views.  I told her I would do tangential views next after marking the masses with nipple markers.  She then gave me a mag tangential view with no evident mass in area of marker but deep in the breast there were heterogeneous calcs.  I said I would biopsy the calcs, she said you could not see them when core biopsy attempted.  Then told me that they did fine needle aspiration on the palpable masses and got positive results thus leading to a complete mastectomy. 





1)      Multiple lytic lesions in the calcaneous, tibia, fib, with a well marginated flamed sped lytic area in the distal tibia

2)      Lytic lesions with irregular sclerotic margins in the humerus and the radius. 

3)      All the DIP destroyed with sausage like soft tissue swelling around the involved joints in both hands.  Differential Dx = Reiters, Psioriatic, Erosive Osteoarthritis

4)      Unilateral SI joint destruction, I said infection or Rheumatoid, he asked what organism, specifically what fungal organism

5)      Pagets disease with films of the pelvis and the skull.

6)      MRI of the knee with disruption of the lateral collateral ligament complex. Quest: what ligaments make up the lateral collateral ligament complex






1)    Apical mixed lung disease

2)      Multiple large pulmonary nodules in the lungs bilaterally with varying sizes.  Quest: what is your differential

3)      RUL collapse





1)      CT of Menetraires disease with history of diarrhea, hypoproteinemia.  Then he gave me the UGI study which showed the char. Changes in the body with sparing of the antrum.

2)      Multiple plaques in the large bowel with the history of antibiotic treatment.—Pseudomembranous colitis was all I said before he pulled it

3)      Hiatal hernia with stenosis in the distal esophagus.

4)      Multiple dilated loops of small bowel with grossly enlarged cecum in the RUQ.  I said cecal Basqual, he asked me if it could be cecal volvulus—I said yes ALWAYS SAY YES TO A YES OR NO QUESTION UNLESS YOUR SURE OF THE ANSWER BECAUSE 75% OF THE TIME YES IS THE RIGHT ANSWER





1)      Duplicated collecting system on one side with large ureterocele and obstruction of the upper pole.

2)      ARPCKD

3)      ADPCKD

4)      Well marginated multicystic mass in a portion of the kidney that otherwise was unremarkable in an adult.  I said Multilocular nephroma Vs Cystic renal cell.

5)      US of a large adrenal mass that spread posteriorly behind the kidney (my last case)





1)      Bilateral low density confluent areas that involve the gray and white matter in both frontal lobes in a non arterial distribution in an adult patient with history of headache then coma, on the contrast scans there was gyriform enhancement.  I said meningitis with venous infarction.

2)      Multiple white matter lesions that show variable enhancement with contrast.  I said MS.

3)      Multiple subependymal nodules with large enhancing mass in the subependymal location of the R frontal horn.—I said Tuberous sclerosis.

4)      Large cystic mass with enhancing nodule in the cerebellum of an adult.—I said hemangioblastoma.

5)      Discitis with prevertebral and spinal extension in a child.




1)      AVM with contrast flowing up the aorta and IVC simultaneously in a man post surgery two months before with progressive weakness.

2)      Mitral valve stenosis on a plain film of the chest

3)      Mitral insufficiency on a plain film of the chest

4)      Angiogram with hemmeroidal venous bleeding

5)      Angiogram of a renal mass with neovascularization in a young female—I said angiomyolipoma.

6)      Pseudoaneurysm of the LV apex in a man S/P MI.  First he gave me a plain film that looked almost normal except for slight contour abn of LV.  Then gave me a MRI and asked me the arterial distribution involved and whether or not its a pseudo or real aneurysm

7)    Coronary angiogram of the RCA with lots of questions about branches that come off, what orientation was the radiograph taken in (LAO,RAO, etc..)


JUNE 1, 1998



I found the experience of studying with someone for the examination to be very useful.  Many things you won=t know whomever your are studying with will.  They can confirm your knowledge and just overall it helps.  I think it vastly broadens your knowledge base.  What we did for the Boards, you=ll get your acceptance to the Boards and the dates several months prior.  I stayed at the Hampton Inn which is very close to the Executive West where the Boards are done.  The number of the Hampton Inn in Louisville is (502)366-8100.  This turned out to be ideal.  It=s away from all of the people that are stressing during the Boards.  It=s a lot nicer hotel to begin with.  There=s a pool out back.  We actually came in one day early just because the flights were a lot less expensive if we went on Saturday.  Our test was on Monday.  We flew in on Saturday night.  On Sunday, we just sat by the pool and read and kind of just took it easy.  Then we didn=t have to worry about late plane flights the night before the Boards.  You had a day to kind of relax.  Its=s just normal middle America hotel stuff.  The pool is fine, the rooms were good.  So it wasn=t bad sitting there for a day and you had a chance to kind of casually look over anything you wanted to bring.  That=s another thing, looking over stuff, I=m not sure how helpful it is.  It probably just helps you in that you are more relaxed.  You know you think uh you may see something in the last day of studying and it=s on the Boards.  This probably isn=t true but I think it just helps kind of ease you up about it.  Then from the hotel in the morning, they have shuttle service or you can walk.  It=s less than a block.  It=s several hundred yards.  It=s an easy walk to the hotel, the Executive West.  You go into a room at 7 in the morning.  Now I think it=s best to get there on time because it=s only a half hour wait.  The guy who will explain the Boards to you doesn=t scare you.  He actually just tells you, you know this is just like sitting down reviewing cases.  It=s fairly straightforward and gives short lists of differentials.  That=s essentially a synopsis of what he says.  Then they give you a list of all your examiners, the times and the rooms and what the exam is about.  And then they just let you go to the exam rooms.  This was at 7:30 and so the following is just the experience with the examiners.






My first examiner which was relieved of was Vascular Interventional Dr. Kerland.  He started asking me without showing me a case how we work up suspected pulmonary emboli.  I said we get a VQ scan. However, many times the Medicine people won=t adhere to it strictly and so the next step is either a CT scan or a pulmonary angiogram.  Then he asked me how would you do a pulmonary angiogram and I explained usually through the right venous approach and went on to explain the procedure and then he showed me a case of a definite easily identified pulmonary emboli in the right pulmonary artery.  The second case was a case where he put up a film and there was a right subclavian occlusion on a patient who was 80 years old.  I asked if there was an example of the left subclavian and he showed the left subclavian was occluded.  Thanks to Dr. Glanz this was identifiable as a giant cell arteritis and he took the film down.  (One thing I would do prior to the Boards and even the written boards is pay attention, I mean not just all the attendings, but Sid seems to have a pulse on whatever is going on with the Boards.  Both Sid and Manny[Hon] were great with the angio and the interventional and everything Sid says in Cardiac comes up at some point in either one of the tests.  So I believe that=s the reason why Sid keeps going over the stuff a thousand times.)  Next I was shown an angiogram where the distal abdominal aorta was occluded.  I said this is compatible with Reyes syndrome.  He asked me to mention both collaterals.  I said the ileal lumbars.  You can get it from the hemmorhoidals and medial lateral sacrals and he was fine with this and took the film down.  Then there was an occlusion of the left brachycephalic vein and asked me to identify it which I did.   Then he asked me what would I do and I said I______ thrombolytic therapy.  That was it and he took the film down.  He then showed me a case of a 36 year old male with a stab wound in his left arm.  The injection was into the subclavian artery at the region of the axillary artery.  There was a venous fistula going back to the heart and I said this is an AV fistula.  Then he asked me what I would do and said that it=s in a good location and the neck is fairly wide.  I probably would do surgery but at some institutions they could put a coil in the lesion and he seemed satisfied with this answer.  Next he showed me a pseudoartery injection which demonstrated kind of a spider-webbed appearance to the interhepatic arteries which I described.  Then he asked me what could cause this and I said it appears like a case of Budd Chiari.  However, cirrhosis or possible hepatic mass may show similar appearance, although less likely.  Then he showed me the same case with injection into the SMA with delayed images showing the portagram and there was no flow into the interhepatic portal system.   So I said this is likely but Chiari demonstrated hepato____al

flow.  Mike Hayt later told me that he could see partial view of the IVC in this case which then indicated that it was likely a mesocaval shunt which I did not pick up.  The final case I had was a case of a lower GI bleed.  The examiner showed SMA injection which demonstrated blood in the extravasation in the region of the cecum.  He then questioned me about what could cause this lesion and I explained that it was likely diverticula which are more likely to bleed on the right or possibly angio dysplasia or tumor.  He seemed satisfied and let me go at the time the first bell range.  An additional note and I wanted to state this earlier in this dictation that I felt that all of the examiners were very friendly and pleasant.  You=ll note that some of the examiners don=t talk much.  They sit down.  They=re always writing notes or I guess your scores down but they were all very friendly and I didn=t see anyone that was unfriendly. 






My examiner was Dr. Baxter in Nuclear Medicine.  He seemed very friendly.  He began by showing me a ventilation study on a patient with acute shortness of breath.  The ventilation study was clear.  Then he showed me a perfusion study and there was a large defect in the left lower lobe of the lung.  There was some delay but I did ask for a chest study which showed a right pleural effusion which could be seen on the perfusion study.  I said that this looked like one segment that may represent two segments as it looked big but I couldn=t definitely separate the two segments so that this was either intermediate or high probability.  He seemed satisfied with this and asked me what I would do next and what I would tell the surgeons and I said that it was likely pulmonary emboli especially given all of the findings and that an angiogram or anticoagulation could be given at this point and he was satisfied with this answer.  Next there was a full body bone scan in a child with significant increase of foci of activity in the right metaphyseal region of the femur.  I asked the patient=s age and he said it was 11.  I gave the differential of osteosarcoma first, then a Ewing=s sarcoma based on age and he asked if there is anything else and I said yes that there are lesions in the liver and the spine compatible with metastatic disease and he took down the film.  Next he showed me an MIBG scan and asked me what agent was associated with and I said I-131 and then I proceeded to demonstrate the lesions throughout.  There was one main lesion near the iliac bifurcation and multiple lesions in the liver and I said this is compatible with a pheo vs other neuro endocrine tumors and he took the film down.  The next case was a large defect in the right lobe of the thyroid.  I gave him the differential but emphasized thyroid cancer and he said what would you do next and I said well this patient should have a biopsy.  He was satisfied with this.  Then I was shown a cardiac study.  He asked the agents I would use.  I explained thallium and sestimedi and he seemed fine with this and then continued to ask me what I thought the case was.  On the stress images, there was decreased uptake in the inferior wall and on the rest of the images this filled in so I said ischemia which he appeared happy with and then asked what agent I would give to the patient if he had a left bundle branch block and I said dipyramidol or adenosine as these are vasodilators and don=t stress the heart as much as other agents.  The next case which was a testicular scan with a hot left testicle.  I asked him which side was tender.  He said that the left side was tender and I gave him the differential of epididymal orchitis.  That was the end of the Nuclear section.






I then went on to Ultrasound with Dr. Woodward.  The initial case was a GYN ultrasound which demonstrated a mass between the uterus and the bladder.  It was isoechoic to the surrounding tissue and I suggested that it was likely a subcirrhosal myoma which she was happy with and moved on.  The next case was right upper quadrant ultrasound with large region posterior acoustic shadowing compatible with gallstone about the size of my head and gallbladder wall thickening.  I said cholelithiasis with cholecystitis.  She asked what I would do and I said I would check the rest of the gallbladder or the bile ducts to see if there were any residual stones and she showed me the next case.  It was OB ultrasound through the cranium which demonstrated cystic appearing brain with no definite parenchyma.  There was, however, a thin septum going between the cranium compatible with a falx.  I gave the differential of hydrocephalus vs hydrencephaly.  I continued to say the hydrocephalus.  However, you usually see a parenchymal mantle surrounding or adjacent to the calvarium which I did say and my main diagnosis was hydramencephaly.  We moved on then to a case of mild hydronephrosis and a small cystic dilatation of the posterior aspect of the bladder.  I gave the differential or ureterocele hydronephrosis.  I told her I=d like to see the bladder again.  On a repeat view of the bladder, I didn=t see any indication for duplicating cyst and so I thought this was just a primary ureterocele.  The next case was an OB ultrasound which demonstrated double bubble sign in the abdomen.  I gave the differential for duodenal before the double bubble such as duodenal atresia, stenosis, _______ in the pancreas and she finally stopped me and said what would you do next.  I said I would probably do amniocentesis to evaluate for trisomy 21 or Down=s syndrome and she seemed fine with this.  The last case that I was shown was a groin ultrasound Doppler image.  Initially, it appeared that there was to and fro flow within the aneurysm and so I said it was a pseudoaneurysm and she asked me what the spectral reading would look like and I said during systolic flow there would be flow into the aneurysm and during diastolic flow the aneurysm decompresses back to the artery and you have reversal of flow.  However, after the test, I thought about the Doppler spectral tracing and it appeared to me that it may have just been forward flow indicating an AV fistula in the groin.  So beware of that one very possibly.  I was let out before the bell and I felt OK about that section. 





The next was Pediatrics with Dr. Rumack. Initially I was shown a lytic expansile distal femoral lesion.  I gave the differential of aneurysmal bone cysts and possibly EEG less likely NE met and I kind of continued down the differential of expansile lesions in children and she stopped me and said well if it=s an aneurysmal bone cyst how could you confirm this.  I said MR where you could see fluid levels and she went on to the next case.  I was given a frontal view of the chest in a child with left upper lobe density.  I asked how old was the child and she replied newborn.  I said do you have any follow up films and she proceeded to show me a film four days later with clearing and mediastinal shift to the right.  I gave the diagnosis of congenital lobar emphysema.  The next case was a neonatal chest which demonstrated ground glass appearance to the lungs diffusely bilaterally.  The second film was the patient=s five days out who had similar appearance yet slightly nodular.  I gave the differential of island membrane disease in RDS vs possible neonatal pneumonia.  She asked me which neonatal pneumonias are possible and I gave her strep B, possible e.coli and comidian pneumonia. She felt fine with this and went to the next case of a small bowel series in a patient.  There was narrowing of the mid small bowel and distal ileum.  I gave the differential of Crohn=s, lymphoma, lymphangiectasis, HAP.  She seemed fine with this and went to the next case which was a plain film of the pelvis.  Given the pelvic films on children, I always think of three things and choose this to evaluate for septic hips, capital femoral epiphysis, and avascular necrosis.  So looking at the film, there was widening of the joint space on the right and I said that I wouldn=t worry about septic arthritis.  She asked me what to do next and I said that given the clinical history I would tap the patient.  She proceeded to show me an MRI with effusion and so I said septic arthritis and the next film was shown which was a thin vertebral body in a child compatible with the vertebral plana.  When asked what else could it be I said possibly EG lymphoma can give this finding.  One case I had difficulty with was a case where there was lobulation to the kidney in ultrasound.  The parenchyma did not appear to be enlarged and, therefore, I thought it just may be fetal lobulation but I couldn=t rule nephroblastomatosis.  The last case was a case of a patient who presented with shortness of breath – a 10 year old.  She asked me what could cause this and I said well congenital heart defects and then she asked me to explain which one.  I asked if the patient was cyanotic and she said yes.  I said the tetralogy of Fallot can present at 10 years.  Actually this is the last case – a case where I was shown dilated on the frontal film dilatation of the main pulmonary artery segment.  Then she showed me a lateral which the technique you could see the esophagus and the trachea well aerated.  In between them, there is a round nodule.  I said this likely represents a pulmonary sling and she said goo and let me out.  






My next examiner was Dr. Patterson.  To begin the breast was the only exam that was shown on plain film.  They handed you the films and you put them up on the light box.  It was easy to put up, it wasn=t like there was any confusion as to which way they go.  It was very straightforward.  There were four films on one large radiographic image.  Without going into each individual study, overall they showed the typical breast lesions.  Only one was hard to identify which were dense breasts kind of tough to find lesion.  Dr. Patterson asked me what I would do next.  I said a compression view.  It looked almost the same.  Then I said I would do an ultrasound and it was a large cyst.  Then she continued on showing me a very obvious spiculated lesion, obvious microcalcifications and other easily identifiable masses.  Most of these I said, some I said, if I was unclear I would ask for spot images, but then I said it likely represented carcinoma and I would have these biopsied.  The ones that were definitely carcinoma I said I would localize and then it=s a surgical case.  And she agreed.  There were several round densities identified which could have been fibroadenomas but initially she said that she had no priors and no history on the patient so if you=re given this condition I would say to stay conservative and biopsy and he may be able to follow up for three months but I think she appeared to be happy when I said I would biopsy these lesions.  One case I was given of multiple low density lesions throughout the breast and I said galactoceles or oil cysts and she took the film down.  I was also shown several large benign calcifications and she asked me if they were malignant and they were obviously just large involuting fibroadenomas______________ calcifications.  The only difficult case that I encountered was significant asymmetry to the breast tissue where the right breast was very dense and I said that this may represent either mastitis or inflammatory carcinoma.  She then asked me what I would do next and I said a skin punch biopsy and she seemed satisfied with this and let me go early. 






Next was Dr. Sanders with Bones. Initially he showed me a case of clavicular reabsorption and then showed me a lateral chest film which demonstrated rugger jersey spine which was compatible with hypoparathyroidism.  Then I was shown a case of sclerosis of the anterior osteal reaction of the distal tibia in a child.  I said that this may represent Cafe=s disease but I could not exclude osteomyelitis.  Then he pointed out that there was a linear density surrounded by a lucency in the mid tibia.  Given this he said it is likely a Brody=s abscess with a sequestrum.  He then asked me what an indilucum was and I said it is the area that surrounds the sequestrum and he was satisfied with this.  He said what=s the problem with the Brody=s abscess and I said down the road a sinus tract can form and possibly squamous carcinoma and he went to the next case.  There was a hand case which showed in the distal and proximal interphalangeal joints erosive changes with s_____al appearance compatible with osteoarthritis.  I asked the patient=s age and he said 80 so I said it=s just osteoarthritis and not inflammatory osteoarthritis.  He then gave me history of patient with leg pain who was a jogger and asked me what I would consider is the differential. I replied stress fractures or shin splints.  He then proceeded to show me a study of a transverse linear line with surrounding sclerosis in the femur and I said it was a stress fracture and he proceeded to the next case.  The next case was angulation of the medial tibial plateau medial and inferior with slight erosive changes.  He asked me what disease could this be.  I said it could be infectious or given the angulation of the bone it could be Blount=s disease and he was pretty happy that I knew Blount=s and I went onto the next case.  Then he said that he would buy me dinner in five years if I got the next case which was an unusual appearance to the humeral head which I had never seen and I gave a differential of infectious trauma.  He didn=t buy this and said I need to be more specific and so I made up something which was incorrect and he said you don=t have to worry I don=t eat much, but I wasn=t sure of this because he is a very large man.  So now I=m waiting on his call.  The last case he showed me was several small stout appearing lesions in the distal phalanges.  Dr. Katz and Dr. Losada showed similar cases of this and I said this is compatible with sarcoid.  Then he showed me a chest film with hilar adenopathy and increased interstitial markings and again reminded me that I had to buy him lunch in five years and dismissed me.  





The next section I felt was the hardest.  It was the Cardiopulmonary section with Dr. Ganther.  The reason I felt it was difficult was when we=re doing board review or when we=re in conference here we know that we=re looking at cardiology vs chest.  But many of the chest findings such as some of the infiltrates, pulmonary edema can be secondary to the congenital heart problems.  So your differential gets significantly, at least mine gets significantly, longer.  The first case was a cavitary lesion in the right upper lobe with lung destruction.  I said well it looks like it=s possibly TB at which time I was stopped and she said does TB cavitate.  I replied yes and the examiner asked whether this would be primary or reactivated TB.  I replied reactivation and she went on to the next case.  I really can=t remember which the examiner was.  The next case was a case where the heart was shifted to the left. There was kind of a bulging appearance of the atrium which was compatible with partial absence of the pericardium.  Unfortunately, I didn=t know this until about four cases away and I mentioned it and the examiner looked at me what are you talking about so I just casually went on to the next case which was increased vascularity at which time in a frontal film I asked for a lateral.  The left atrium was small and I said this likely is SD or partial anomalous venous return and then the case was changed to a frontal view of the chest with diffuse kind of nodular patchy infiltrates.  I gave a differential of the pneumonias, possible metastatic disease and named off multiple possible metastatic etiologies.  Then the examiner said well what if this patient was from here.  I replied is this technically in the Ohio River Valley and she said yes.  I said histioplasmosis and I think there were several other cases which I could not recall but this turned out to be the toughest case and the case I struggled through most trying to differential between lung findings. 





Next was the GI section with Dr. Smith.  The first case was the dreaded small bowel study.  Within the small bowel there were thickened loops, a string sign in one image, and I felt this was likely Crohn=s and he asked what to do next and I said a CT scan.  Given the CT scan, the bowel loops were thickened.  There was a large abscess so I said it was abscess likely related to a fistula – an infectious abscess – and went on to the next case.  The next case was a single contrast esophagram with a filling defect at the GE junction.  The filling defect appeared to be linear in shape and I said that this could be a carcinoma or a varices and I cannot exclude Barrett=s esophagus and then went to the next case.  The next case was an ERCP with a significantly dilated pancreatic duct and dilated pancreatic radicles.  I asked history and the examiner said that the patient had colon carcinoma.  Then I said well I can see the entire duct to the duodenum.  There is no obstruction and I don=t have any reasons that colon carcinoma would give dilated pancreatic ducts so I think this is chronic cholecystitis.  The examiner seemed happy with this and went to the next case which was again an ERCP.  The interhepatic ductal branches were narrowing with some areas of dilatation compatible with sclerosing cholangitis.  I asked for history and the examiner said yes the patient had ulcerated colitis and we went to the next case.  I was then shown mets in the liver, a large invading mass into the spleen and a large mass above the spleen.  I located it to the stomach and said stomach carcinoma with invasion of the spleen and liver mets and she seemed fine with this and went to the next case.    The next case was a CT scan through the abdomen with oral and intravenous contrast.  I looked over the entire scan at every organ and saw absolutely nothing.  The examiner let me struggle for a while and then said well what=s missing.  Then I looked again and noticed that the patient had absolutely no pancreas.  I asked her clinical history and they gave me longstanding illness but I said likely cystic fibrosis and that was the end of this section. 





The next section was GU with Dr. Siegel.  The initial case was CT scan through the abdomen and it showed a large calcified renal mass so I gave the differential 1, 2, 3 on the list for renal cell carcinoma and then he showed me the next case.  The second case was an excretory urogram which showed hydroureteronephrosis with kind of a tapered obstruction just at the sacral region on the right.  I said that this could be transitional cell carcinoma or obstruction from fungus bowel or a stone or blood clot and he asked if there was anything else and I said the stricture was fairly long for a megaloureteral but you know it=s also consideration.  Then he said is there anything else you=d like to do and I said at this point due to the location I=d like to see a CT scan and he showed me a CT scan and there was a large psoas abscess in this region; and then I equated it towards the hydroureteronephrosis.  The third case was enlargement of the prostate on CT with kind of a lobular appearance into the bladder.  I mentioned that a benign prostatic hypertrophy generally wouldn=t give you this nodular appearance.  Although this is an anterior position, my first consideration would be prostate cancer followed by benign prostatic hypertrophy and I would biopsy this lesion.  The next case was CT scan through the kidney with fat density in the lesion and I said this is compatible with angiopmyolipoma and suggested the other possibilities such as a lipoma in the kidney and very less likely renal cell with fat entrapment from the sinuses but I doubt this and felt it was a benign lesion.  The following case was through the adrenal glands and there was a low attenuated adrenal lesion shown.  I said it was likely a myolipoma and to further delineate could do in and out of phase MR imaging.  He then asked what components were involved and I said ______genous elements plus the fatty elements.   The next case was a case with fracture of the inferior pubic rami.  I said that this may represent ureteral trauma and I would do a retrograde urethrogram.  Then he proceeded to show me film from a retrograde urethrogram demonstrating a type II urethral tear and asked whether I would do a cystogram.  I replied that the only type of cystogram you could perform was a pubic cystogram and that I would not catheter into the urethra.   The last case I was shown was a 78 year old male CT scan through the mid abdomen.  The examination demonstrated perinephric edema.  The kidney was small in size.  The ureter was not significantly dilated.  Given this finding I suggest the possibility of pyelonephritis vs possible obstruction at the UPJ.  However, I did not see any stone or mass within the ureter.  With this I was dismissed.





The last section was Neuro from Dr. Deck.  I believe he=s at Cornell.  The initial case shown was T1 and T2-weighted MR images through the brain.  Demonstrated are low signal within a large mass in the left parietotemporal region as well as multiple small foci throughout the brain and in the cerebellum of both high and low signal.  Initially, I stalled on the case by describing the findings and then gave the differential of metastatic disease or possibly multiple cavernous hemangiomas.  Then he asked me what was the low signal surrounding the masses and I said that it was the blooming artifact from the paramagnetic effect and he further asked me look give this to you.  This can be seen both in melanoma and cavernous angiomas.  I asked whether the patient had any clinical history of melanoma and he said the patient did have a lesion on his back and we went to the next case.  The second case was a sagittal T2-weighted MR through the cervical spine which demonstrated both the inferior end plate C2 and the superior end plate of C3 were high in signal and there is abnormal signal in the disc.  Posteriorly with slight impression on the anterior aspect of the cervical cord was a heterogeneous elliptical mass with signal intensity which was adjacent or arising from the disc space.  Given these findings I said that cervical discitis with an epidural abscess was most likely the consideration and he went to the next case.  The third case was a CT scan through the brain which demonstrated several low attenuated regions which I felt were fairly hard to locate initially.  After explaining this finding, he asked me the next thing that I would do and I explained that I would given the patient contrast.   The areas of low signal demonstrated ring-enhancement.  With this I mentioned the differential of tumor, infection.  With these findings I would less likely include demyelinating diseases.  Asked what my leading differential was, I in turn asked him if the patient was HIV positive.  He replied yes.  With this, I said either lymphoma or toxoplasmosis, possibly cystosarcosis and TB.  He then asked how could you differentiate lymphoma from toxo and I said Indium labeled scan.  He said that this would not clearly identify it and that PET imaging would be better for further evaluation. He then asked me to describe PET imaging and I said we don=t do it at our institution; however, I know that you use FDG.  Although I=m not sure if this is correct, I said that I think that the lymphoma would updated the FDG.  Next there was a young male with an anterior frontal mass.  It was extra-axial.  I gave the differential of a cineo neuroblastoma vs mucocele.  He then asked for an exam with contrast.  The mass demonstrated no contrast enhancement; therefore, I suggested mucocele was the most likely diagnosis.  The next case was an intraventricular mass seen on MR T1 and T2-weighted images that when given contrast demonstrated significant enhancement.  I gave a differential of choriplexus, papilloma, carcinoma, ependymoma  and meningioma.  After mentioning meningioma, he said well if it was meningioma what artery would feed it.  I said since it was near the atria of the ventricles, I thought it was the posterior choroidal artery.  He then proceeded to show me an internal carotid artery injection which demonstrated a feeding vessels from the anterior choroidal artery but he seemed OK with this and went to the next case which was a CT scan through the posterior fossa in an 88 year old female.  The scan demonstrated a high attenuation in the fourth ventricle which was compatible with hemorrhage.  He then asked what I would do next and I said a vertebral artery injection.  Then he showed me a vertebral artery injection and there was an aneurysm of the left posterior inferior cerebellar artery.  The last case I was given, and I=m note sure I think this was a neuro but it could have been in bone, I was shown the entire lumbar vertebral bodies were very sclerotic and had a destructive appearance to them.  They seemed to be slightly enlarged, although it was difficult to tell on this single image.  He asked for a differential and I said with this density it could be Paget=s ascending upwards, it could be metastatic disease.  He then asked what else could it be and I said well it could also be neuropathic spine and he said that was in fact what it was and I was dismissed early. 


So, overall impression of the boards was that first of all the attendings here show cases that are similar and basically identical to the cases you=ll see on the boards and the board reviews with all of the attendings were excellent.  Just additionally, Dr. Gold gave a review, since he is a board examiner, that was identical to the boards.  He would show four films quickly and take them down even in mid sentence which happened to me several times during the boards.  Dr. Fruauff=s examinations were overall the hardest but there were many cases that he showed especially in the ultrasound section that were given to me on the boards.  Overall all of the attendings= board reviews demonstrated multiple cases that were on the boards and I feel that the discussion that the attendings required was also very similar. 


JUNE 1, 1998




1.         A double bubble sign of duodenal atresia or stenosis

2.         A 1.2 cm empty gestational sac within the uterus

3.         Viable ectopic pregnancy with a thickened echogenic endometrial stripe

4.         Either a severe hydrocephalus vs hydranencephaly.  A falx was present

and the thalami were not fused.

5.         Pseudoaneurysm with color Doppler. How would you treat this?

6.         Renal sonogram with mild hydronephrosis and a stone measuring approximately

3 to 4 mm

7.         Sonogram of the liver which was echogenic with a focal area of normal echogenicity

(focal fatty sparring)

8.         Ectopic ureterocele with hydronephrosis.

9.         Intrauterine gestation with oligohydramnios, hydrops and a cervical hygroma





1.         Chest x-ray in a three day old which showed a left-sided infiltrate which cleared

(congenital lobar emphysema)

2.         Coarctation in a one year old chest x-ray and sagittal MRI

3.         Infiltrate in a newborn, B-strep pneumonia (not meconium, nor RDS)

4.         Choledochocele (sono and nuclear medicine study)

5.         Chest x-ray which showed predominantly upper lobe interstitial infiltrates with

lytic rib lesion (EG)

6.         Plain film showing sacral and lumbar vertebral abnormalities with sagittal MRI

(showing sacral agenesis and claudal regression)





1.         Multiple well-defined masses in both breasts.  How to work these up.

2.         Dermal calcifications

3.         Fibroadenolipoma

4.         Two areas of microcalcifications

5.         How do you do a localization in your hospital?

6.         A single well-defined mass which on sonography was shown to be a cyst – patient had      nipple discharge

7.         Multiple dense microcalcifications seen localized to one quadrant

8.         Multiple bilateral thin-walled lucent lesions (galactoceles vs oil cysts)






1.         Irregular femur with periosteal reaction and erosions within the medullary cavity


(chronic osteomyelitis)

2.         Distal femur – lytic Paget=s disease (what are the stages)

3.         Hands – inflammatory osteoarthritis

4.         Periarticular osteopenia (RSD)

5.         MRI of the knee with bucket-handle tear and torn ACL (?segond fx)

6.         Lytic expansile lesion in the distal fibula with MRI aneurysmal bone cyst vs

telangiatatic osteosarcoma

7.         Hands with acrooseolysis and other well-defined lesions with subsequent chest

x-ray (sarcoid)

8.         DISH with sclerotic mets upper lumbar spine





1.         Chest x-ray and CT scan right upper lobe atelectasis with mass (cancer staging)

2.         Chest x-ray with rib notching and subtle figure 3 (coarctation)

3.         Multiple peripheral cavitary lesions, one with a possible fungus ball

(aspergilloma ? septic emboli)

4.         Partial absence of the pericardium

5.         Pneumothorax on supine film (deep sulcus sign)

6.         Interstitial edema (possible mitral stenosis)

7.         Corrected transposition





1.         Small bowel series with skipped lesions with mass effect (Crohn=s disease with

psoas abscess)

2.         ERCP with sclerosing cholangitis

3.         Thin section CT with dilatation of the biliary radicles and soft tissue mass at the

ampulla (cholangiocarcinoma)

4.         CT scan showing inflammatory changes in the mesentery and small lymph nodes

(enteritis-mesenteric adenitis)

5.         Multiple large soft tissue masses on CT scan lymphoma vs mesothelioma

6.         CT with pancreatic atrophy in a CF patient





1.         IVP horseshoe kidney with ureteritis cystica

2.         Left lower pole eggshell type calcifications associated with a mass.  Follow up CT.

RCC (How would you treat the patient?)

3.         IVP with irregular soft tissue mass in renal pelvis which on CT is attached to the

wall (TCC vs fungus ball)

4.         Ultrasound and CT of nephroblastomatosis

5.         Renal cortical necrosis – s/p trauma

6.         CT scan which shows aortic and cable perirenal mass and follow up sonogram showing     testicular tumor

7.         Nuclear scan showing increased flow to symptomatic testicle (epididymal orchitis)

8.         Pelvic fractures and cystogram (How do you do a cystogram?)





1.         Signal on T2-weighted imaging in the cerebellum and occluded left vertebral artery

(posterior fossa infarcts)

2.         Multiple foci – one with hemorrhage (hemorrhagic metastases)

3.         Cavernous sinus aneurysm (CT, MR and DSA) – how would you treat this

4.         CT with fourth ventricular blood (follow up angio PICA aneurysm)

5.         CT with temporal lobe subdural hemorrhage extending to the parietal region

(spontaneous possible mass)

6.         Global infarct

7.         Sagittal MR cervical spine with epidural and retropharyngeal abscess (and possible


8.         Frontal sinus mucocele





1.         Bilateral subclavian artery stenosis and occlusion (giant cell-Takayasu)

2.         Cecal bleed status post polypectomy (petressin infusion and embolization)

3.         Pulmonary angiogram (How do you work up in your institution? How to treat?

Indication for IVC filter)

4.         Distal aorta occlusion with collateralization (How to treat?)

5.         Descending aorta pseudoaneurysm

6.         Thoracic outlet obstruction – would you stent

7.         AV fistula with psueodaneurysm (How to treat?)

8.         S/P trauma with small pelvic bleed





1.         SPECT cardiac with reversible defect

2.         Bone scan of a 9 year old with very hot knee (Ewing=s vs osteosarcoma), poor

images ?wrong collimator

3.         VQ scan with PE and pneumonia

4.         HIDA scan with gallbladder leak – possible biloma (increased liver activity s/additional     injection

5.         Splenosis using damaged red blood scan

6.         Cysternography for CSF leak (How do you do it?) (Indium DTPA)

             I-125 thyroid w/ large cold defect, adenoma w/hemorrhage, cyst, parathyroid adneoma,   etc.


June 1, 1998


There are a few myths about the oral boards which I=d like to dispel.  These are the following:


Myth #1: Study.  Absolutely unnecessary.


Myth #2: Go to a board review course.  This too is unnecessary. 


Myth #3: Attend board review.  This is unnecessary.


Myth #4: Attend conference.


Myth #5: Sleep the night before the examination.


Myth #6: Never listen to a guy who gives information as myths.



Stan and I had the examination on the same day at 7:00 AM on a Monday morning.  We left, however, on Saturday afternoon and flew through St. Louis to Louisville because it was cheaper.  This turned out to be a good idea because it gave us an extra day to be at Louisville and we rested that day and studied by the pool.  Additionally, we stayed at the Hampton Inn rather than at the Executive West.  The Hampton Inn was a much nicer hotel.  It was new, clean and did not smell.  Also, we didn=t want to be around the other examinees who were taking the exam.  However, out hotel was filled with other examinees.  I also recommend another hotel which is about five minutes= walk from the Executive West and that=s the Best Western.  That is even a newer hotel and fewer people know about it.  Both of those hotels will send jitneys to the airport to pick you up.  Also, I recommend requesting a room facing away from the airport because some people hear the airplanes all night long.  The nearest restaurant to eat in there is at the Executive West.  However, you can also eat at the bowling alley.  Stan and I walked through the bowling alley which was filled with a bunch of smoking rednecks.  Checking out of the Hampton Inn was quite convenient.  In fact, they gave you an express check out and slipped it underneath your door so you didn=t even have to talk to the receptionist when you checked out.  However, I gave my bags to the front desk to hold while I took the exam.  For breakfast, I ate two doughnuts, had orange juice and tea with sugar.  I wanted to have a lot of sugar on board in order to take the exam.  I recommend the glazed doughnuts. 


Stan and I walked over to the Executive West for the examination at 7:00 AM.  As we entered the hotel we were overwhelmed with a musty odor, and then we ran into Dr. Beuchert.  The three of us went to our separate rooms to which we were assigned.  The first room you go to is an orientation room where approximately 30 to 40 candidates were seated and the spokesperson hands out slips and tells you where to go and what to do.  He tried to put us at ease by telling us jokes about a bunch of losers.  My slip said that I should go to GU first.




I was examined by Dr. Hattery.  He seemed pleasant and tried to reassure me.  Of course, what does he show me on the first case?  He showed me a case of ureteritis cystica on an excretory urogram.  This examination also showed papillary necrosis as well as a mass within the renal pelvis that was quite large and multilobulated.  He asked if I could put it together and I really couldn=t.  The next case was a case of an aortic dissection and bilateral renal ischemia.  The next case was a calcified renal mass on plain film.  I then asked for a CT.  It showed a calcified renal mass which was heterogeneous.  I said renal cell carcinoma and a bunch of other things that didn=t fit.  He finally said what do you think this is?  I told him renal cell carcinoma.  The next case was hydronephrosis of the right kidney on an excretory urogram.  The right ureter was dilated up to the mid right ureter.  I then asked for a CT and he showed a large right psoas abscess and I said this could be the cause of the hydronephrosis.  The next case was a renal stone on a non-contrast CT.  I had trouble following the ureter.  I told him I want to put a cursor on the ureter and follow it up and down sequentially on the monitor.  He asked me to explain it further.  I did and eventually just told him that I think this is kidney stone.  I got a history of right flank pain.  I got another case of bilateral papillary necrosis, on an excretory urogram.  My last case was a bleeding angiomyolipoma.  I also included oncocytoma and renal cell carcinoma for the differential with bracketing masses.  This was on a CT.






I was examined by Dr. Kido.  This dude is from the Mallinckrodt, not particularly personable.  I thought I was going to do well on this section.  The first case I was shown was a 39-year-old white male I was told.  The MR showed multiple areas of hemorrhage.  I first gave a differential of multiple cavernous angiomas and said, however, this is more common in an Hispanic male.  I mentioned amyloid angiopathy but expected this in an older patient also in high distribution.  He then told me that the patient had melanoma of the skin.  I said of course this could represent melanoma mets and he took the case down.  The next case was a T1 on a 19 or 27-year-old male.  The first image was a T1 sagittal of the cervical spine which showed unusual bones and perhaps an osteophyte.  The second image was T2-weighted sagittal of the spine which showed increased signal in the cord.  For some reason, I got the idea in my head that this was cord contusion.  He then showed me a parasagittal T2-weighted image and I didn=t say anything.  I then said I think this might represent cord contusion.  Did the patient have a history of trauma?  He said yes and I said I think this is cord contusion.  I also said there may be a fracture here and I would like to correlate this with plain films and/or CT.  He then took the film down.  The next case he showed was a parapharyngeal mass on the right which was iso on T1 and bright on T2.  I asked for a contrast enhanced image and he said that he didn=t have any.  He then told me that the history was a 17-year old female who had recent tonsillar surgery but they didn=t find anything and that there is no evidence of abscess.  So I was thinking that this might represent a paraganglioma although I didn=t say it because they didn=t provide the contrast enhanced images.  I therefore looked more closely and saw that this mass arose from the parotid and I said I think this is a parotid mass and he took the film down.  My last case was a mass within the cavernous sinus shown on a CT.  I didn=t give a differential.  I asked for an MR.  He showed me an MR and it showed flow void and some pulsation artifact, so I thought this might represent a CC fistula or cavernous sinus aneurysm.  I tried to evaluate the superior ophthalmic vein but it wasn=t on the film.  I said it might represent a CC fistula or cavernous sinus aneurysm and then asked for an angio.  I was shown two images of an aneurysm and asked for delayed images.  He said he didn=t have any.  So I told him I think this is an aneurysm and he took the film down.  And that was it.  He let me out early after only four cases. 





The examiner was Dr. Mewissen.  I suggest you bring your Preparation H in case you have him as an examiner because you=ll need it.  He seemed pleasant enough when he greeted me and got down to business.  The first case I was shown was a mycotic aneurysm of the descending thoracic aorta.  He asked me to tell him about mycotic aneurysms.  I told him they usually occur on the undersurface of the aortic arch.  He then took the film down.  The next case was clogged axillary and brachiocephalic vein. He asked me what causes this. I said thoracic outlet syndrome.  Anything else?  He mentioned something about repetitive chronic use syndromes.  And I said AOh, yeah, I think pitchers get this@.  And he said ARight@.  And he asked me how to treat it and I said UK.  And he said how would you approach it.  Would you go through the groin or the arm.  I said groin if I could get a coaxial cable through the entire clot.  He then asked me contraindications to UK and I gave it to me.  The answers that is.  He then showed me a large PE on a pulmonary angiogram.  He asked what we do for this in our institution.  I said heparin.  However, at some institutions I know they give UK.   The next case he gave me a history of the patient s/p polypectomy and I saw bleeding in the colon.  He asked how to treat this.  I said I would give pitressin.  He asked the contraindications to pitressin.  At first I remembered hypertension and I couldn=t remember anything else.  He said how about if the patient had CHF.  And I said oh yes if there is coronary artery ischemia.  He then showed me a patient with pelvic fractures in bilateral internal iliac artery hemorrhage.  He asked how I would treat this. I said I would embolize.  He said which one first and I said the bigger one.  He then asked me the branches of the SMA and I named them.  The next case he showed me was an aortogram where I could seen the left kidney, left renal artery, right renal artery, but not the right kidney.  I told him I think this might represent renal vein thrombosis and he took the film down.  He then showed me a case of celiac injection with delayed images and an SMA injection with delayed images showing a large spleen and small liver.  I said this likely represents cirrhosis and portal hypertension and I then noticed a clip in the upper right abdomen and he pointed to a structure. He said what=s this.  I said the IVC which was opacified.  He said what do you think the patient has and I said a mesocaval shunt.  He then asked if we do TIPS at our institution and I said very few.  He then showed me a case of a catheter going in from the SVC through to the right ventricle and going out the left side of the heart.  He said how did it get there.  At first I thought it was in the pulmonary artery and then he showed me a second case where they advanced it further and apparently it went through an ASD and closed a pulmonary infarction which he said I was correct.  The last case he showed me was a frontal view of the thorax with an aberrant right subclavian and which he helped me decipher. I asked to see a lateral. He said he didn=t have one.  He then said there is little diverticulum here.  What=s the name and I said diverticulum of the cumeral.  The second bell rang and I was out.  This was the only session where I did not get out after the first bell.  I had the feeling while taking the exam that he was toying with me. 




The examiner was Dr. Davis.  He seemed like a pretty nice guy but he asked lots of questions.  The first thing he showed me was a high prob VQ scan.  He then asked me what are ventilation agents.  How do you know which one is which?  I gave ___________Technetium, krypton and xenon and told him how you know the difference.  He then showed me a MIBG study which showed mets everywhere and I said this is probably a neuro endocrine tumor such as a pheo.  He said how often does pheo have mets and I said well I=ve never seen it so I think it=s very rare.  But he seemed happy.   The next case was a thyroid scan.  I said I don=t see salivary glands.  He said what type of study do you think it is?  I said an iodine study and he was happy with that and I noticed a large photopenic defect in the right lobe of the thyroid.  I gave catch lamp differential.  He asked what I would do next.  I said I=d put a marker on it and reimage.  He said images in the probable mass.  Then what would you do?  I said I would biopsy it.  He came back with papillary follicular carcinoma.  He said what would you do?  I said I=d tell them to remove the gland surgically.  He then said then what would you do?  I said I would then bring the patient back in about six weeks and reimage them with I-131 looking for recurrent tumor, recurrent gland or metastatic disease.  He said how much would I give of I-131.  I said 3 to 5 millicures.  He then said the patient now comes back with metastatic disease.  How would you treat it?  I said if there was widespread metastatic disease, I would give 200 millicures of I-131 and if it was confined to  the tumor bed, I would give 100 millicures.  He seemed satisfied with that.  The next case he showed me was a bone scan with metastatic osteosarcoma.  The next case was cysternagram where I believe they showed epistaxis.  He also asked why else would we do the exam and I said to differentiate between a communicating and non-communicating hydrocephalus.  He then asked me how to differentiate between the two and I kind of fuddled my way through it.  He showed me another case where there was increased uptake in the right pedicle of L5.  I told him I=d like to do a SPECT and I did and again there was uptake there.  He said what is this from? And I said probably spondylysis on one side and compensatory stress on the other.  This also could represent a fracture of the pedicle.  He then showed me a thallium cardiac study which showed ischemic lesion at the base and he said what vessel is this from.  I said probably the RCA.  He then asked if the patient is a quadriplegic what would you use to stimulate the heart.  I said dipyromil or idenasene.  He said what is the mechanism of action of dypyramile and I told him idenasene diamenase inhibitor.  He asked if the patient started to crap out on dypryramile what can you give him and I told aminophylline.  He seemed happy with that.  I was then shown a superscan and asked the difference between metastatic.  How to differentiate between metastatic disease and metabolic disease.  I was shown lymphoscintigraphy with a _______ node.  He asked if we do this for other things at our institution besides melanoma.  I said no.  Even though we do.  I was shown a testicular scan and I asked him which side the pain was on.  He said you=ll tell me.  It looked like there was increased activity on the left and I said epididymal orchitis and then he went through and asked me questions about torsion and this torsion.  The last case I saw was a bialoma on HIDA scan.  I told him that I clearly don=t see the gallbladder.  However, there is quite a bit of small bowel activity.  I=d like to give this patient water.  He told me the patient was given water and it didn=t wash away.  He said what do you think.  I said bialoma.  He asked me to point to where.  Then he finished and let me out at the first bell. 






This was given by Dr. White.  My first case was a mass between the uterus and bladder.  I gave a differential but favored myoma.  The next case was double bubble on OB sono.  At first I came up with choledochocele duplication cyst, pancreatic pseudocyst or meconium pseudocyst.  Then she said double bubble and I said of course it would be duodenal stenosis.  She what is this associated with?  I told her Downs and I also checked for cardiac abnormalities.  The next case was a case of fetal hydrops where at first I saw echogenic mass adjacent to the heart.  I started giving a differential for that and she said look again and I noticed that there were bilateral pleural effusions and the lungs were unexpanded.  She said look in the region of the neck.  I didn=t notice a cystic hygroma so I told her the patient I think has hydrops and Turner syndrome.  She asked what about Turner syndrome gives hydrops.  I said I don=t know perhaps chromosomal abnormalities.  The next case was a clear case of ectopic pregnancy, a viable one, with a beating heart.  The next case was someone status post groin on a cardiac cath which showed an AVM vs pseudoaneurysm.  She asked how I can differentiate the two and I told her use spectral Doppler.  She said what on spectral Doppler and I mentioned spectral broadening and arterialization of the venous white form with an AVM.  The next case was a testicular sono which showed some increased flow and an epididymal cyst.  I said I see increased flow on this one side and I=d like to compare it to the other.  And if there is increased flow I would think it was epidydmal or c___rs.  The next case was a case of focal fatty sparring in the liver.  She asked how could I prove this?  I told her I would do in and out phase MR imaging.  She said really?  And then I thought she didn=t understand what that was.  So I told her we could also do CT and she said OK and that was the end of this section.  I got out after the first bell. 





This was given by Dr. Smith.  I was shown a case of neonatal pneumonia and asked to name the bugs found in neonatal pneumonia.  I was told the kid had murmur and had decreased vascularity.  I said tricuspid atresia.  He said do you really tricuspid atresia in a child who was like 8 years old and I said no just _________ and he left me alone.  The next case was nephroblastomatosis shown on ultrasound.  He said how would you further evaluate this? And I said CT, show me that and I thought it was nephroblastomatosis.  The next case was a case of Crohn=s and abscess in an 8 year old seen on a small bowel series.  The next case was 3 year old with a septic hip.  That=s all I remember.   





The next section was Breast with Dr. Jackson.  She was rather abrupt.  I nailed every case in Breast.  I was shown a case of spiculated mass with microcalcification.  I gave her a differential and told her I would biopsy.  She asked how and I said either open or stereotactic.  The next case was a mass in the breast.  They did an ultrasound and it was a clear cyst.  She said what would I do next?  I said if the patient demands that it be removed or if it was painful I=d aspirate it or I would do nothing.  The next case was multiple bilateral oil cysts vs fat necrosis in a 78 year old.  The next case was fibroadenoma.  The next case DCIS.  The last case that I can remember were multiple bilateral masses in the breasts.  I favored metastatic disease but also included focal carcinoma and told her I would biopsy and search for mets.  Oh, and I had one more case where she said there was redness and thickening to the skin.  She showed me mammograms and one of the breasts was much denser.  I said this could be mastitis or inflammatory carcinoma and less likely symmetric CHF.  I favored inflammatory carcinoma or mastitis and recommended a skin biopsy. 





The next section was Bone.  The first case I was shown was a Brody=s abscess with sequestrum and gave a differential.  I was then showed an MR and asked what was pathognomonic on this and I didn=t know.  I was then showed an expansile lytic lesion in the fibula.  I gave an exhaustive differential.  He asked how I could narrow it and I said do an MR; if I saw fluid levels and I gave a smaller differential.  He said the kid had trauma 2 months ago I told him that I think that is an ABC.  The next case was a case of Paget=s in the distal femur.  He said how can I prove that it=s Paget=s and I said I would get urinary serum alkaline and phosphates and urinary hydroxy prolium levels.  The next case was a medial meniscus tear and ACL tear.  He asked if I could put this together and I said I=m afraid to give you a name for this to be wrong.  The next case was septic right hip, narrow joint space on the right.  I asked for an MR and it showed fluid on the T2 weighted images and I told him that I would tap this kid immediately.  The next case was a case of erosive osteoarthritis.  The differential was erosive osteoarthritis vs psoriatic.  I told him I favored erosive osteoarthritis and he took the film down.  The next case was a clear case of renal osteodystrophy and he showed me erosions of the ends of the clavicles, all the hand findings you see in osteodystrophy and a rugger jersey spine.  The next case was posterior hip dislocation with fragments.  The next case was a stress fracture of the tibia.  The last case, I believe, was a cortical desmoid of the tibia in a child.






The next examiner was Dr. Lipton.  This is under the cardiopulmonary section. If you can ever request an examiner, you would want this guy >cause I did well but he helped lead me to the answers and he told me if I was right which is very good.  He is very sympathetic and he tried to teach me during the exam and of course I forgot everything he said.  My first case was a case of CHF.  He asked for causes.  I gave a few and I mentioned renal failure.  He said this patient in effect did have renal failure.  Then he asked me do you see any lines out peripherally.  I said yes Kerley B lines.  Then he told me that he worked with Dr. Kerley and I acted interested.  The next case was pulmonary edema.  I mentioned that and he said well this could also represent contusion and I agreed.  The next case was a case of cavitary TB in the right upper lobe.  He asked me if this is found anterior or posterior.  I said I didn=t know.  He said usually posterior.  I said next case was a cardiac case and I said murmur and it may be a teeny bit increase in vascularity.  I said ASD or PADA.  He said which one and I said I=m not sure.  He said well you can tell if it is PDA if the aorta was enlarged.  The next case which I got immediately was partial absence of the pericardium.  He loved this and he told me I was right.  He said what=s the best view to show this.  I said I don=t know and he told me but I don=t remember his answer.  The next case was a case of histoplasmosis.  Another case was a case of endobronchial tumor with right upper lobe atelectasis and metastatic disease to the spine.  Another case was aspergillosis and the halo sign. 





The last professor was Dr. Lamki of GI.  The first case was an esophagram.  It showed a mass at the GE junction.  I mentioned Barrett=s could favor carcinoma.  I told him I would perform endoscopy and biopsy.  The next case was multiple nodules in the small bowel in a ratty-looking bowel.  She then showed me a CT after giving no differential for nodules.  I told her I think this is Crohn=s.  The next case was a big mass up in the colon with mets.  I was worried about stomach colon cancer and it looked like there was pelvic masses and it could have been Krukenberg tumors and mets but I wasn=t sure.  The next case was annular constricting mass in the ascending colon.  I said adenocarcinoma vs lymphoma. The next case was a case of sclerosing angiitis on ERCP.  The next case was a huge dilated pancreatic duct, which may be due to chronic pancreatitis.  The last case was a case of someone who had recurrent pulmonary infections and there was an absent pancreas so I said cystic fibrosis.  Dr. Lamki said well that=s it and she said why do you want more and I said no. 



And that was the end of my exam.



Oral Boards 2000


I have to say that boards was a surreal experience. After the anticipation of the exam, I couldn’t believe it was show time.  It was really wild pulling up to the Executive West in the cab, but I was ready to get it over with.  I got into Louisville Saturday morning. I stayed at the Hyatt, which was nice, and far enough away from the Executive West  to relax. I tested on Sunday afternoon and flew out right afterwards.


The lobby of the hotel was full of stressed out candidates. One half hour before the exam starts, you meet in a room for your orientation and to get your routing slip.  I shared mine with other people around me and I looked at theirs.  I knew my bone examiner from medical school, but he examined me anyways.  After we had the rules of the game explained, I talked  to  a few people,  got a sip of water and we were off. Cases below are not remembered in order- except for the first cases, which I could seem to recall ok. It’s hard to remember them all; here is the best I could do:


Cardio-Pulmonary- Dr Baron- a nice older gentleman who was helpful and tried to put me at ease.

  1. First case was a CXR with increased reticular-nodular pattern.  Examiner said the patient had a history of weight loss. It looked kind of granular and I thought it was PCP, then  I noticed a mass in the retrocardiac region. Called it lymphangitic spread from a primary lung CA and I was done with my first case.
  2. CXR with a huge (5cm) pulmonary nodule. I mentioned benign and malignant things. He showed me the same film and said that this was taken 2 yrs earlier. I said I thought it was benign, we could do a CT looking for calcs. CT, no calcs. I said I still thought it was benign- plasma cell granuloma or post infectious mass (cocci/TB). He asked me what to do. I said we could biopsy it, but I thought we should leave it alone, given its stability- gulp!
  3. CXR with prominent rounded density adjacent to aortic knob- probable aortic aneurysm.
  4. CXR with subtle increased soft tissue in R paratracheal region. He gave me an unenhanced CT and I said that  I couldn’t see the finding on the CT. He said, “I don’t like this case” and we moved on.
  5. CXR big pulmonary arteries, bilaterally. Talked about PAH
  6. CXR with R sided cardiac apex, L sided stomach. I said situs ambiguus and mentioned polysplenia/asplenia. He said the patient didn’t have polysplenia and asked how we determined situs. I mentioned bronchial anatomy.
  7. CXR with curvilinear calcifications overlying the heart. They didn’t quite conform to the pericardium or a particular chamber. Had a hard time deciding exactly where they were and discussed the possibilities. He told me the patient had ascites and I decided they were pericardial calcs from uremia?
  8. CXR he said the patient had halitosis. I was looking for an esophageal diverticulum, thought I saw something. He moved on to the barium swallow (by accident) which showed a Zenkers. He said “well, that shows you what you didn’t see, initially”.  I chuckled and we moved on.
  9. CXR with RUL collapse, I mentioned an endobronchial lesion or adenopathy compressing  the R bronchus. CT showed mass/nodes narrowing the bronchus.


I finished my first section and was thrilled. I thought this isn’t going to be so bad- especially since I was dreading chest. But …….


GI-Dr Scott- a younger guy (mid–late 40s) who wasn’t volunteering any information.

  1. First case was a barium esophagram- two views. Varicoid mass of distal esophagus. I thought it was varicoid variant of squamous cell, less likely varices. He asked me what else-darn! I couldn’t think of anything and he said “what do you know about Barrets?” I mentioned that there are usually associated strictures and he asked if I saw anything else. I pointed at a subtle stricture and we moved on.
  2. SBFT, no history.  I was having a hard time with the findings, decided that I didn’t see normal jejunal fold pattern in the upper abdomen and thought maybe it was sprue. He asked how the patient would present- I said diarrhea from malabsorption. He asked about treatment and I said dietary restriction of gluten. He asked me the other type of sprue and I blanked. He said, “this is nontropical” I caught on
  3. Another SBFT- darn.  I thought the folds looked a little thick (not really, but it was the only thing I could find to talk about). After I said that, he told me the patient was a young F with hematuria- I said some vasculitis with hemorrhage and renal disease. Who knows? But we moved on.
  4. DCBE with multiple varioloform (target) lesions in the colon. Hard to see on full image- once I mentioned it, he gave me a close up. There was also a stricture of small bowel- Crohns
  5. DCBE with irregularity to posterior and anterior wall of rectum in an older (post menopausal) F. I said primary adenoCA, vs extension from ovarian tumor. Direct viz/bx
  6. CECT of the liver. Enhancing liver mass – aorta was still bright. I said FNH, adenoma. He asked about nuclear medicine imaging and how that would help. I mentioned SC. He then showed me a sulfur colloid scan with homogeneous uptake- I said FNH.


GU- Dr Dyer– middle aged guy, asked a lot of questions.

  1. First case, US kidneys, medullary nephrocalcinosis- gave HPth, MSK , RTA as ddx- nice start
  2. CT at level of bladder. Fluid filled mass with gas within it, adjacent to sigmoid filled with diverticuli. Was adjacent to (on top of bladder). I said diverticular abscess and he reminded me that it was the GU section-oops!! I wasn’t coming up with anything and he told me the patient had urine coming from his umbilicus- infected urachal cyst. He asked the management- should be resected because of  possibility of malignant change
  3. CT kidneys, cysts bilaterally- ADPKD but early on in the disease (less severe) a little harder to recognize. Solid mass- renal cell. I was asked about staging.
  4. CT- angiomyolipomas of kidneys with hemorrhage on one side- asked size at which they should be taken out and risk of bleeding. Image had HU of –54 printed on screen.
  5. MRI- septate uterus. When I asked, he told me the patient had one cervix Talked about the difference between bicornuate and septate. He asked why it was important to know the difference. Management- I think a septum can be resected?
  6. CT of abdomen with bulky retroperitoneal adenopathy in a young male. I said lymphoma v testicular CA. He showed me an US of testicular microlithiasis- a mass was shadowed out by a cluster of calcifications.
  7. IVP with distal ureteral sticture in young female. I said endometriosis and he showed me an MRI to confirm it.
  8. MRI with fluid signal mass surrounding the urethra in a female- “periurethral cysts” I said. He asked if there was a name for it. I made something up and he laughed, saying “that’s creative”. I laughed and said I didn’t know. I guess it was a urethral diverticulum.
  9. CT bilateral pyelonephritis with renal abscess.
  10. CT- retrocaval ureter- easy to see with contrast in ureter. Talked about embyrology of it.

***  Somewhere along the line I was shown a dense nephrogram and had to discuss how to treat a contrast reaction.


Neuro- Dr Cinnamon– young guy wearing a yarmulke.Very  helpful. I think  it was his first time testing.

  1. CT with mass in interhemispheric fissure- couldn’t see frontal horns of vents at all. So I didn’t know if it was intraventricular or not. Showed me sag MRI pre and post. Meningioma. Hard first case for me
  2. MRI multiple sequences showing enhancing basilar meninges. I mentioned carcinomatosis, TB and sarcoid. He gave clinical scenarios for each and  I changed the differential accordingly (i.e. young black female with abnormal CXR v patient with known primary CA)
  3. CT with low density in midline- hard a hard time placing it- just superior to pineal. Looked like CSF density- MRI- T1 showed me a lipoma of CC with partial agenesis.
  4. Sag MRI with large flow void- vein of galen aneurysm. He showed me an angio and asked me why it only was only partially filling. Thrombus?
  5. Sag MRI- posterior fossa mass in an adult. I said met/hemangioblastoma. He said there was another lesion in spine- I said hemangioblastoma and mentioned the association with VHL. He asked me why the patient was hypertensive. I didn’t know. He said “We aren’t supposed to teach, but it is because they secrete erythropoietin”. I thanked him and we moved on to the next case.
  6. Axial brain- bright T2 signal, low T1 in cortex frontal region- looked like an infarct but I was told that the patient had a gradual change in sx- nothing acute that sounded like stroke. No volume loss, no mass. We moved on- I couldn’t figure it out. I said a lot of what it wasn’t.
  7. CT fluid filled elongated mass in submandibular region- ranula, less likely a  branchial cleft cyst, TGD
  8. CT mass in lacrimal gland. I mentioned lymphoma/pseudotumor, infection. But he didn’t like that. He asked me what if it was a parotid gland- I went through some tumors. I don’t think I gave him the answer he wanted, but he moved on.
  9. Pineal mass in a kid with calcification on CT- I said pinealcytoma and germ cell tumor, I said pineoblastoma would be less likely  because calcs were intact. He wanted something else, but I didn’t know what else to say. He said what if it was an adult?
  10. Sag MRI- I don’t remember what I saw, but the first thing I mentioned was an aneurysm, he showed me an angiogram (vertebrobasilar) and asked me which vessel the aneurysm was coming from-PCOM.


Vascular interventional-Dr. Becker- kind of gruff- not very helpful at all.

  1. CXR- widened mediastinum. I said do a CT first. Then angio if hematoma. He showed me an arch and great vessels with transection of the inominate a. Asked me management and I said surgery
  2. Popliteal artery with abrupt truncation- no collaterals. I said it looked embolic. He asked me what to do, I said thombolysis if <3mos. He asked me what to use. I said TPA- no dose asked. He showed me the angio post lysis and it had an underlying stenosis. He asked me if I still thought it was embolic and I said that no, it was likely thrombotic, given the underlying stenosis and we could plasty.
  3. Run off with disease of anterior tibial artery. We talked about angioplasty and he asked me patency rate.
  4. Abdominal angiogram- celiac with no vessels over the liver. I said replaced R hepatic and he showed me the SMA injection.
  5. AP pelvis showed bullet fragment in thigh. I was told that this was the only place the pt was shot. Then I was shown an AP chest. Bullet fragment overlying heart. Embolized fragment into RV- retrieved with loop snare.
  6. Cavagram with clot extending into cava from L common iliac v. Talked about placing a filter using IJ approach. I questioned if there was enough room infrarenal-looked like clot extended pretty high. Next film with filter showed it at the level of the R renal vein ostium.
  7. Cholangiogram with dilated CBD, intrahepatic ducts and pancreatic duct- ampullary mass. He asked if there was some specific tumor this might be if the patient was HIV +.  I didn’t know.
  8. Plain film with staghorn calculus filling upper pole of kidney. He asked me about ESWL and percutaneous lithotripsy, which calyces I should enter (anterior or posterior) Ugh- like I have ever seen one of these cases before?
  9. Percutaneous cholangiogram with a stent in place. He asked me how to do all that and then he told me the patient came back with UGI bleed. I said to do a celiac injection and it showed a pseudoaneurysm of a hepatic branch with the drain passing right through it. I said to coil it and he showed me a post coil image.


Nuclear Medicine-Dr Staab- a nicer older man, helpful and not many questions.

  1. First case-sestamibi parathyroid adenoma. He asked for a differential and the sensitivity of the study.
  2. Myocardial scintigraphy- I thought there was some ischemia on one axis but couldn’t confirm it. He showed me a wall motion study (cine) and said “maybe this will help”  EF was 35%. Went back to SPECT images and I saw that there was LV dilation. I said dilated cardiomyopathy and let the ischemia go.
  3. Gallium scan- young male. Bilateral inguinal adenopathy and some activity in the chest. I said lymphoma. He said what else. I said melanoma and we moved on.
  4. FDG in a patient with history of  gastric CA–looking for recurrence. I saw some activity in the region of the stomach and some activity in the region of the  L kidney. Couldn’t tell if the activity was in the kidney or not. Hard decision. He asked if FDG was excreted by kidneys- there was activity in bladder.
  5. SPECT images of the brain, HMPAO? In a 10yr female with some motor dysfunction. Told me the MRI was normal. Decreased activity in L temporal and frontal region.  Maybe it was for seizures, but that wasn’t the history. Had a hard time with that one.
  6. Whole body bone scan- photopenic defect in R femoral head. After I noticed that, he said “What do you think of the images” I said there was poor target to background and that either the camera was off peak or something was wrong with the tag. He said what can you do? I said talk to the tech and re-peak the camera. He showed me the images after the camera was re-peaked- looked much better.
  7. Three phase bone scan of feet- increased 3 phase with periarticular activity in a few joints and diffusely throughout foot- RSD. I talked about why it wasn’t fx or infection. Examine pt, etc…
  8. CXR in a patient with known lung CA, mass on film. VQ scan because of suspected PE. Matched defect in region of CA and mismatch in same lung but different lobe, acute PE.
  9. Lasix renogram in a kid- images didn’t look too bad. Time activity curves were a little slow to take up DTPA and excretion was a little slow, but not obstructed on either side.


Ultrasound-Dr Kane– middle aged guy. Pretty nice. Not too many questions.  I had a couple of cine loops. Just asked him to run them again, no problem. They are pretty slow and show you trans and long.

  1. Cine loop of anencephaly. Asked about increased risk with future pregnancies
  2. Bilateral ovarian dermoids- cyst with mural nodule on one side, homogeneous low level echoes on the other. He asked me what to do next, I said CT. He said  I must come from an institution where there is no managed care. I wanted to say something but bit my tongue.  He asked me if we needed the CT and I said probably not.
  3. Testicular microlithiasis (again)
  4. Endovaginal  cine loop in pt who was recently s/p D&C. Uterus showed multiple anechoic areas in myometrium that with flow were highly vascular. I asked if HCG was positive and was told yes- gestational trophoblastic disease, I thought it looked invasive-looked like it was in myometrium.
  5. Hypoechoic mass in liver (transplant patient)-I didn’t see the portal vein coming in, instead I saw lots of collaterals- looked like cavernous transformation/thrombosis. I talked about infarct of the liver but mentioned that it was rare.
  6. Bilateral carotids- oh NO!! Grey scale images first- showed severe narrowing of one side, better on the other. Then wave forms and velocities. The worse grey scale had a lower velocity- more severe, heading towards complete stenosis (string sign). Velocities were in meters/sec and I had to convert.
  7. Cine loop- prenatal US with septated mass behind head. Also thick skin around head and neck-hydrops with cystic hygroma
  8. Cine loop showing a dilated CBD and pancreatic head mass.


Pediatrics – Dr Genieser– by far my hardest examiner. An older woman who gave me and Josh our hardest section.

  1. First case- sagittal MRI brain. I was a little shocked to get this as my first case and it took me a while to figure it out. Young boy with visual problems.- sellar mass. CT with calcs- craniopharyngioma. She asked me if the calcs helped, I said yes.
  2. Lucent metaphyseal lines bilateral- leukemia
  3. IVP with small irregular bladder. I thought it was post void but she said it didn’t change. Then she showed me a VCUG and bladder still looked small and irregular. I mentioned TB and then she said pt was immunocompromised and had hematuria- hemorrhagic cystitis?
  4. UGI with markedly thickened folds in fundus- leukemia/lymphoma, even mentioned Menetriers. She didn’t respond at all, let me think a little longer and finally moved on.
  5. CXR older kid with a murmur. Prominent aortic knob- I said coarctation or bicuspid valve- saw that the asc aorta was also tortuous as she was moving to the next case.
  6. AP pelvis with funky looking hips- small epiphyses, widened metaphyses. Similar looking  around knee at prox tibia- this was a hard one- ? epiphyseal dysplasia. I flailed with this one for a while.
  7. Neonate with small chest, pneumopericardium, small lungs. I mentioned Potter’s facies and oligo because of the small chest and she showed me an US of the adrenal glands which were huge. Kidneys weren’t on the image. Potter’s syndrome.
  8. CXR with multiple, big cystic lucencies in chest. She showed me a film from a few weeks prior that had a single cavity with a big air fluid level. I said abscess and pneumatocele formation, less likely CCAM.

Breast- Dr Paredes (she has written a book, so I recognized her name)- pretty cool. I asked for old films on the first case and she said to assume that all the cases were screening exams and no old films were available. She wanted BIRADS on all cases.

  1. Spiculated mass-  she gave me my spots that I asked for. BR 5- bx. She asked if we did stereo and if the lesion was amenable.
  2. Calcifications on MLO, couldn’t see  them on CC. I asked for spot mags and she asked me specifically what views. I said mag MLO, ML and mag ML. They were milk of calcium on mags. She asked me where the calcs were on the CC, given the motion from the MLO to the ML.
  3. Palpable mass, didn’t see it on MMG. I said to get an US. There was something subtle there. I said to biopsy it- either in US or mentioned that our surgeons would do it if it was too hard for us to see.
  4. Large well circumscribed mass- and a second mass. The larger one was a cyst the other one had to be biopsied.
  5. Two spiculated masses, one looked like a radial scar. The other one was harder to make out. I said to go to excision for the radial scar and take the other one out while they were there. I don’t remember if it was this case or a different one with multiple lesions, but she asked me about contraindications to breast conservative therapy. (inability to get to XRT, multicentric dz, poor cosmetic result, prior XRT)
  6. Extracapsular rupture on MLO and suspicious calcs on same view. She asked what  if they came back ADH. I said go to excision. She asked what % will come back DCIS on excision.  Ummmmm?
  7. Well circumscribed mass, on two views- solid on US. Looked like fibroadenoma. I said still needed to be biopsied if no old films.
  8. Large portion of breast with malignant calcs. I said we could bracket the area for needle loc or stereo the most suspicious group.


Musculoskeletal- Dr Edgar Colon Negron– It was great that I already knew him, from rotating at WRAMC. He was very helpful when I had trouble and totally laid back. We chatted when it was all over.

  1. Moth eaten appearance to proximal humerus of a kid- looked like a Ewings. Gave small round blue cell tumor differential. He was happy with that.
  2. Routine ankle views- rounded lucency in distal metaphysis of tibia. CT showed central punctate calcific density- Brodie’s abscess with sequestrum?
  3. Unicameral bone cyst in humerus of a child with pathologic fx and fallen fragment
  4. Sag MRI of knee- ruptured patellar tendon
  5. AP pelvis- partially collapsed femoral head. AVN- MRI showed it was bilateral.
  6. AP knee- sclerotic area in prox tibial metaphysis with lucency just distally. It looked funny. He said the guy was a runner- healing stress fx.
  7. Frontal L shoulder- head looked partially collapsed- maybe sclerotic. Mentioned AVN and sickle cell
  8. AP both feet. Sclerotic first digits bilaterally with erosions of MT heads- Psoriasis
  9. Lateral C spine- jumped facets- I said I thought it was bilateral. He asked how I could tell. There was a significant degree of anterolisthesis, so I favored bilat.
  10. AP chest- resorbed distal clavicles in a kid and something with the cervical vertebrae. He was trying to help me but I wasn’t making the findings so we moved on. Thank goodness!!
  11. AP wrist- sclerotic, irregular metaphysis of distal radius, resorption distal phalanges- Rickets. Asked for possible etiologies. He helped me with this one.
  12. AP and lat spine with flowing syndesmophytes  and fracture through ankylosed vertebrae- Ank Spon
  13. Single view of pevis- subcapital femur fx- subtle disruption of trabeculae
  14. Lat L spine with well defined area of sclerosis abutting end plate- discogenic sclerosis. But at the same level, there was a well defined lucency with part of the endplate eroded- didn’t know what to do with that.

Oral Exam 95                                                                                      Bob Tambeaux

“What rough beast, it’s hour come ’round at last, slouches toward Louisville to be grilled?”

                                                                 (appologies to W.B. Yeats)


Hurt me. 

It feels like I spent my entire fourth year studying for boards, and I still didn’t feel that well pre-

pared.  Most helpful for writtens were old questions and ACR syllabi.  Physics was painful, as I am a physics cretin.  I think a review course like the one given by Loyola might have been helpful, but I ended up doing okay anyway.  Take your exam at Rochester, which is a very pleasant setting with minimal weirdness.  The room is spacious, compared to what I hear about Chicago.  You have plenty of time to finish physics, but the diagnostic portion (day 2) crowds 500 questions into about four hours, and some people didn’t finish.  Do not say the F-word around the nuns.   I did (it was an accident).


          For orals, I spent a lot of time memorizing differentials I had spent the previous three years avoiding.  Wolfgang Amadeus Dahnert is indispensible.  I barely used the Duke book at all.  There is a new primer out of Mass General (look in the “Snobbery” section of your local bookstore) which had a few decent pearls, but in general, it was not as useful for me.  Again, the ACR syllabi were great.  You MUST do the ACR videodiscs and film files.  I don’t know how you can get through without this.  You WILL see these cases in Louisville (the jewel of the Ohio River valley).  If nothing else, going over cases helps you practice your differentials.  It worked best when I did this with other people, as we could pimp each other with impunity.      

          I am not an encyclopedic reader, and was not very good at reading texts cover-to-cover.  I used most books as references for specific situations, and therefore reviewing teaching cases made a gooding starting point  for an overall subject review.  (Did that make sense?  Oh, shut up and get me a Prozac).


          In Louisville, I stayed across the street from the Mother Ship at the Executive Inn (owned by the same people).  The psychosis level was supposed th be lower there, but there seemed to be just as many examinees flipping flash cards by the pool.  Flying out of Chicago was $230 cheaper than leaving from Madison and only slightly less convenient, and if you’re strapped for cash, I might advise this. 


          The evening before the exam, I went jogging at the state fairgrounds, which are right across the street.  This seemed to help reduce my SVT to a mere 200 BPM, but in the 93 degree heat, I was still sweating when I went down to dinner two hours later.  There is no place to eat except in the hotel, and immediately after I sat down, the place was infested with board examiners.  I felt like a gopher that had tunneled into  pen full of boa constrictors.  I had A beer just before I went to bed,  and felt  rather relaxed, but I did not sleep.  Not a wink.  Louisville is a hub for Federal Express, and at  midnight, jet after jet began coming in directly over my bed (I think they  were practicing touch-down landings on the pool).  At  four-thirty, they all took off again.  Bring your ground-to-air missiles (the airlines will require you to check these as baggage).


          In the morning, I put on my suit and my new lucky tie and went across the street to the  Executive West (part of the Temple of Doom hotel network).  They send you to an assigned room where you sit with approximately 30 other hyperventilating people.  Jen and Lisa were in the same group.  A kindly old radiologist came in and gave us an introductory talk which ran right up to the 7:30 starting time, so there was no time to review the small stack of flash cards I had in my pocket.  We were then dispatched to our individual Kamikaze missions. 


1.  PEDIATRICS, Dr Boechat

          The examiner was very nice, but did not offer much feedback.

          The first case was a preemie with hyperexpanded cystic lungs.  I said BPD and couldn’t give a differential because that’s what it was, though I did babble a little about why it wasn’t one of the other cystic lesions. 

          She showed me wide, ragged epiphyses, and I said rickets, though I mentioned hypophosphatasia and scurvy in the diff.  Then she had me tell her about all the causes of rickets and cut me off when it got to be ad nauseum. 

          She showed me a KUB of a three year-old with constipation who was FOS.  I asked for a BE, and there was an obvious transition zone near the rectosigmoid junction.  I said Hirschprungs, and talked about it for a minute or so.  She asked about other forms of colonic obstruction, and we went down the yellow (brown?) brick road of meconium plug, hypoplastic left colon etc., and why they weren’t applicable in a  three year-old.

          The next case was a Wilm’s with invasion of the renal vein and IVC.  No questions on staging.

          The next case was most disturbing, and woke me from a sound sleep two days later.  It was a normal chest.  No rib fractures, normal lungs, no cuffing, no nodes.  I flailed for a while, then she took the case.  One of my cohorts called me after he got home, and was very upset because he felt he’d missed an epiglottitis, which sounds like a capital punishment-type offense.  At 4:00 AM I awoke remembering this ‘normal’ chest and realized I hadn’t looked at the trach!  Somebody shoot me. 

          The last case showed paddle ribs, beaked vertabrae, normal interpedicular distances.  I said mucopolysacharidosis, and she asked me a few questions about the types, then the room spat me into the hall. 

          I wasn’t shown a child abuse, and I looked for one.


2.  MAMMO, Dr. Dempsey.

          Very friendly little Southern gentlman who offered me water, the use of his bathroom, lifesavers, mints, use of his condo in Florida, the keys to his Lexus, a seven-course meal, his VISA card number to call a local escort service.  Okay, okay, not the last stuff. 

          The first case showed a large ugly mass about 3 cm in one breast, but had suspicious microcalcifs in the other.  I said Bx both. 

          The next case showed a very dense breast with a subtle area of architectural distortion.  I asked for a compressed view, which showed a stellate lesion.  Off to the sturgeon!

          Another case was status-post Bx of the right breast.  There was soft tissue density in the biopsy site along with benign calcifications, so I said I would want to be certain the scar was shrinking in size rather than enlarging.  He said it was okay, so I started looking at the other side and inventing abnormalities (barking up the wrong breast, if you will).   He finally said, “what about the calcifications?”  Oh, those are dermal. 

          I was shown multiple rounded densities bilaterally on an initial screen, which I tossed into follow-up.

          Another case showed a lesion which was smooth-bordered on two sides, but the remainder of the borders weren’t seen even on mag.  I recommended an ultrasound, which showed it to be solid.  Pop that puppy outa there!

          The last case was a round fat containing lesion which I said was  a fibroadenolipoma, but which had a lot of dense material within it.  He asked what I’d do,  and I said these were usually considered benign, but that the differential included liposarc, and that I was a little bothered by the density.  He asked me again what I’d do, and I said Bx even though it would likely be benign.

          The chimes went off and I boogied.


3.  BONE, Dr. Freiberger.

          Kind, elderly gentleman , who did not offer me treats or money.

          The first case was a CXR which showed a big heart and infarcts in the humeri.  The lateral showed H-shaped vertebrae.  Sickle cell.

          Another case showed a knee with big osteophytes, normal mineralization, narrowing of the medial joint space, and a couple of calcified loose bodies.  No condrocalcinosis.  I said DJD, but he didn’t seem to like that.  I couldn’t come up with much else.

          I was shown an MR of a knee with a PHMMT.

          The next case was a lucent lesion in both the femur and tibia of a kid.  No periostitis, fracture, matrix, or destruction.  I ended up running a gamut that seemed appropriate for a kid, but he did not seem completely satisfied with this. 

          MR of a shoulder.  The subacromial space was gone, there was spurring at the AC, the belly of the supraspinatus was retracted, and I couldn’t find the tendon.  Cuff tear. 

          I felt I was stumbling through this one.  However, I looked back at the examiner at one point late in the exam, and my scores were in plain view in his lap.  I was passing every case, but I deferred any questions that would have ascertained whether Dr. F. had actually been listening to me.


4.  CHEST, Dr. Brown.

          Younger examiner who was rather neutral.  She did “point the way” once or twice.

          One case showed multiple tiny nodules without adenopathy.  Ran the gamut of miliary diseases, and concluded it was probably TB.

          The next case showed a lobulated mass in the RML with air-fluid levels, decreased volume in the right lung, and a prominent scoliosis.  I started thinking congenital and mentioned sequestration and CAM.  Then she said the patient wheezed.  This is the weirdest ABPA I’d ever seen.  We talked about the pathogenesis of ABPA, and diagnosis.

          Mass  splaying the carina.  Gave DDx of bronchogenic cyst, less likely duplication of esophagus, adenopathy, primary tumor.  Recommended CT.  No CT was supplied, but examiner asked questions about bronchogenic cysts.

          I was shown a cavitary lesion in superior segment of LLL.  Gave the full differential, soft-peddling lesions that would usually be multiple.

          Three fuzzy lesions in a twenty  year-old female, one of which may have had a little cavitation.  Gave a multiple nodule diff, and included Cocci because the film was from the southwest.  The examiner then asked, “What if the patient has a fever but is otherwise asyptomatic?”  I flopped like a doomed lake trout for a minute or so, then ejected.


5.  GI, Dr. Smith.

          Jocular, middle-aged woman who laughed and cussed during the exam.  I thought at one point she would offer me a beer.

          The first case was multiple umbilicated lesions in the body and fundus of the stomach, with one in the distal esophagus.  I mentioned mets first (melanoma foremost) then lyphoma, less

likely apthous ulcers, blah blah blah.  She told me at the end that the clinicians had neglected to inform me that the patient had melanoma.  Jen Wong described the same case to me and said that his examiner had told him it was gastritis.

          KUB of a young male with seminoma on chemo.  The small bowel was okay, but the colon showed thumbprinting in the cecum.  I mentioned typhylitis and pseudomembranous colitis, and soft-peddled the other causes.  She showed me a CT with ascities and PMC.  Then she asked about cause and treatment. 

          Next was a SBFT with floculation, a transcient intussussception, and decreased folds in the proximal SB.  Sprue.  I was asked about diagnosis and complications.  Also asked other causes of transient intussussception, and mention scleroderma.

          I got a distended colon next with normal folds.  Mentioned distal obstrution, ileus (had to give causes).  Subsequent BE showed sigmoid tumor.

          The last case showed a somewhat low-density mass with septations in the pancreatic head of a young woman.   Mentioned the cystadenomas (but usually a bit older), the said if it was a black woman it might be a… a…a… at which point Dr. Smith pointed at me and laughed and said “Brain  block!  Brain block!”  Then she told me the answer.


6.  GU, Dr. Korobkin.

          Congenial, but quiet man who offered guidance a couple of times.

          The first case showed irregularities of the papillae, and I jumped on papillary necrosis.  He asked for causes, and I gave him the postcard gamut, leaving out cirrhosis.  Then he said look again.  It was a medullary sponge kidney.  Later during the exam, I found my scores again sitting under my nose, and that I had flunked this case, probably due to my haste.

          The next case showed a 1 cm mass in the right ureter and a Bergman goblet sign.  I said tumor.  He asked about types, and what other filling defects of the ureters I could describe.

          Grade 3 urethral tear on a retrograde with a pubic diastasis.  He asked about types.  Also asked clinical findings (blood at meatus, high-ridin’ prostate, pardner), and what shouldn’t be done (Foley placement).  Then he showed me the Foley placed by the ER doc that had turned this into a complete tear.

          KUB showing large but smooth left kidney and several calcified cysts on right without a clear right renal outline.   Mentioned MCDK in adult with compensatory hyprtrophy on left.

          Left renal mass with the remainder of the left kidney showing wedge-shaped defects.  No evidence of renal vein invasion.  Mentioned tumor, but I couldn’t figure out the wedged defects.  Likewise, vascular insults like emboli didn’t fit because the other kidney was normal.  I thought maybe this was pyelo with an intrarenal abscess.

          Last, he showed me a left adrenal mass with HU’s of 10 in a patient with a primary lung carcinoma and asked me how I coulnd’t be sure it  wasn’t a met without Bx.

          I was not shown a contrast reaction.


Now  began the descent into videodisc hell.


7.  NEURO, Dr, Deck.

          Rather harsh guy.  But could have been worse (see Cardiovasc.)

          The first case was a kid (age 7) with a mass in the nasal cavity on plain film.  Said I was worried about a rhabdo, then gave a diff that included lymphoma, antrochoanal polyp, blah blah.  Mentioned that if the kid was older, would include juvenile angiofibroma.  CT showed the mass extending through the sphenopalatine foramen.  He asked what next, and I said angio? hoping I would not be slain and left for the coyotes.  The angio showed a juvenile angiofibroma.

          Next case was a head ultrasound of a TERM infant.  I couldn’t see vents, and there was a lot of hyperechoic material centrally.  I said it might be blood, but that it didn’t fit with the kid being term.  A follow-up showed what looked like periventricular leukomalacia.  I flailed, but he refused to euthanize me.  He asked if this could represent  perinatal asphyxia.   Uhhhhh, I guess so.

          Posterior fossa mass lesion.  Contrast MR showed obvious meningioma hanging off the tent, with a dural tail.  Barfed up everything I knew about meningiomas.  He then asked what else this could be?  Uhhhhhhh.     Could this be a hemangiopericytoma?  Uhhhhhhh, I dunno.

          Next was a peds spine MR in a kid with lower extremity weakness.  I saw the syrinx, but almost missed the tethered cord and diastem until he was ready to beat me over the head with them.

          Head CT of  wino with decreased mental status.  There was subfalcian herniation, and I said isodense subdural, and recommended contrast to make the pial vessels light up.  Ding-ding-ding-ding.

          Destructive lesion of the clivus, and I ran the list of nasties.  He asked lots of questions about chordomas.

          Escaped with my life.


          At this point, I passed my mammo exam room, where Dr. Dempsey was offering an examinee lottery tickets and his daughter’s hand in marraige.



          Lectured at San Diego review course, where he seemed rather congenial.  However, on this occasion, he was a true appendage.

          The videodisc images were horrible.  The first case showed a big heart (I think).  Probably LV enlargement.  When I showed the least hesitation, Dr. Green grew irritable and demanded an immediate answer.  I flailed with MR and AoR, and he cut to the next case.

          Density in region of azygous vein on CXR.  I said nodes, volume overload, azygous continuation of the IVC.  CT confirmed it as azygous continuation.  Was going to mention polysplenia, but he zipped to subdiphragmatic cuts before I could, which confirmed it.  He asked me polysplenia/asplenia questions which I thought I fielded okay,  but he frowned at my answers.  He asked how I could have gotten the whole case off the plain film.  I mentioned fissures and bronchi, and he still frowned.  Then I noticed the right sided stomach bubble.  As if I could see it on the freakin’ thirteen inch low-res screen.

          Another big heart.  So?  Then the lateral show three prosthetic valves you couldn’t see at all on the PA.  He asked for a cause, and I say rheumatic heart disease.

          MR of a low signal mass on the tricuspid.  I make the finding easily enough, and mention vegitations in an IV drug abuser.  I also mention intracardiac tumors, and don’t handle the subsequent questions well, chumming the waters.  He smells blood and closes for the kill.

          MR of a kid with wheezing.  There’ s a pulmonary sling,  and he asks all the questions which I thought I handled well, but with which he is displeased. 

          Plain film of LV calcification (again, barely discernable on the intercoursing video monitor).  I say LV aneurysm, which seems to urinate him off.  He thrashes me with several questions to which I say “Uhhhhh, I dunno,” then shows me an MR which shows a paper-thin septum and mural thrombus.  Then he asks me how to protocol a cardiac MR, including sequences so that he can hear me say , “Uhhhhhhh, I dunno” just one more time.

          Clotted anterior tibial artery.  He asks me thrombolysis questions, to which I actually know the answer.  It’s more than he can bear! 

          The chimes rescue me.


9.  NUKES, Dr. Eggli

          Nice, youngish guy, but my hydraulics are out, I’m fighting the controls, we’re in a tailspin, people!

          First case is a big, cold thyroid nodule.  Leads to a discussion of thyroid cancer, tumor types, incidence in single and multiple cold nodules, incidence status-post irradiation.  He asks about I-123 scanning, to which I back out, saying I’ve never used it.

          The next case shows this big, blurry blob with a hot spot in the middle. I don’t know what I’m looking at until I back up and realize it’s a liver from a hepatobiliary scan.  There’s no tracer in the bowel, and I recommend delayed scanning or CCK, if you’re certain the patients not obstructed.  Delayed scan shows tracer in the bowel.  After sincalide, there was a .38% ejection fraction.  I stated this was consistent with chronic cholecystitis.  I was asked normal ejection fractions, and other means of augmenting a scan.  He may have also asked me the tracer dose.

          Testicular scan with a hot right scrotum on flow and delayeds.  Mentioned infections, then backed off and came down hard on varicoceole. 

          VQ scan with two segmental defects.  It’s high probability.  Then I get grilled on PIOPED and the need for a CXR.  I don’t handle this very well. 

          Thallium scan with  huge fixed anterolateral defect.  However, a repeat scan after angioplasty shows most of the defect fills in.  He asks what could have helped, and he’s happy when I say reinjection. 

          Three phase bone scan showing hot-hot-hot throughout entire midfoot.  I list the gamut, and settle heaviest on RSD.  He asks RSD questions with which I sorta kinda do okay.

          No QC questions, only minimal dose and imaging qustions. 

          The bell tolls.


10.  ULTRASOUND, Dr. Abu Yousef

          Somewhat aloof, but not overtly hostile.

          Every single case is REAL TIME!  And they last for all of FIVE SECONDS!  I started getting chest pain. 

          I wasn’t certain what organ I was looking at.  Liver?  No, kidney.  Yeah, that’s it.  With a big honkin’ mass in the upper pole.  I did the big honkin’ mass differential. 

          Again, location was the issue on case 2.  It was a linear transducer, and finally I guessed I was looking at something tubular.  APPENDIX!  OH, HAPPY DAY!  But there was no rock, no surrounding fluid, and maybe just a little debris in the lumen.  And I couldn’t remember the size criteria for appendicitis.  When I asked for a repeat, I was told “but you’ve seen it twice already.”  

          Next, I was shown a testicle (I hope) with a heterogeneous mass.  I said tumor (embyonal or teratoma but not seminoma), maybe abscess.  He asked how doppler might help and I did my patented trout flop.

          Then I was shown a fetal study which started with something cystic in the belly and ended with a hydronephrotic kidney.   Posterior urethral valves, which was pretty clear by the second viewing. 

          Next was the embryo with a membrane floating in the breeze.  I mention subchorionic hemorrhage.  He starts asking me about chorioamniotic separation.  But this thing is wrinkled and ugly.  Then he says  “Is the embryo normal?”  On the final leisurely 1.6 second scan I determine that I can’t see a heartbeat, and he asks me ultrasound criteria for heartbeat, yolk sac, etc. 

          Fetal US showing choroid plexus cysts.  I tell him it may be normal, but there is an association with Trisomy 18.  Then he shows me the belly at the level of the cord insertion.  I’m looking for an omphaloceole or renal funk, and don’t look much at the cord because it’s not in CROSS-SECTION when he says “What about the cord?  How many vessels?”  I tell him there’s only two, but it’s a  LONGITUDINAL cut!!!  I eat crow (tastes just like chicken) and say I would do an amnio. 

          The last case was representative of this section as a whole.  A liver with diffuse low echogenicity lesions with echogenic centers.  Were they actually cystic?  Who the hell could tell?  They were on the screen just long enogh to blink.   I gave a long and undistinguished differential that went from Caroli’s to candida to mets.

          At this point, the chimes sounded and the room barfed me into the hall.



          The whole process flies by.  Each section seemed to end very quickly, and I was over half done before I realized it.   My initial impression was that the first six sections went pretty well, and that the last four were iffy.  I fully expected to condition something, and as the days went on, I felt there was a decent chance of having flunked the exam outright.  I was very pleasantly surprised   by the outcome.   Receiving the results quickly probably saved me from slashing my wrists or voting Republican.

Chest Review (#1 – 76)

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