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125 Cards in this Set
- Front
- Back
Renal mass
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Is there a significant cystic component, or is it predominantly solid?
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Predominantly solid
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Is there macroscopic fat (i.e. NOT just suppressing on out of phase imaging)
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yes, there is macroscopic fat
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AML
2 Things to do: 1) Measure it -- if larger than 4CM, needs to be embolized to prevent hemorrhage 2) Look for other evidence or stigmata for TS, especially if patient is young and has multiple bilateral AMLs |
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No, there is no macroscopic fat
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RCCA until proven otherwise
Imaging findings (i.e. infiltrating bean or renal coll system tumor suggesting TCCA) or clinical history (i.e. young male with sickle cell suggesting Renal medullary CA) may suggest another diagnosis, BUT REGARDLESS there is no way to exclude malignancy, and they all come out. |
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Significant cystic component
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Bosniak classification
Group them mentally into BENIGN and SUSPICIOUS categories. |
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Benign features
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= B1 and B2 classifications
NO FURTHER EVALUATION REQUIRED |
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Bosniak 1
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TOTALLY SIMPLE CYST
-imperceptible or very thin wall -no Ca -no septations -no nothing |
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Bosniak 2
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- Thin septation (may have PERCEIVED enhancement, since thin enhancement in these really cant be determined definitively)
- Fine calcified rim or septation |
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Bosniak III
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Thick or irregular or enhancing wall or septation
Chunky calcification |
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What then is IIf?
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Characteristics between a pure II and a definite III. Instead of ripping it out, follow-up imaging is preferred since only a small proportion of these (maybe 10-20%) will turn out to be malignant
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Bosniak IIf
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NO MEASURABLY OR DEFINITELY ENHANCING COMPONENTS
3 characteristics: 1) Minimal SMOOTH thickening of wall or septations 2) Increased # of thin septations 3) Hyperdense cysts larger than 3CM |
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What is Bosniak IV
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Cystic RCCAs. These are actually primarily solid tumors which have a cystic component, unlike the others which are truly cystic lesions.
What differentiates these from the IIIs is that the soft tissue mass is more extensive, not just related to the cyst. |
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Stage I RCCA
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Confined to renal capsule
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Stage II RCCA
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Penetrates renal capsule, but confined to Gerota's fascia.
Can involve ipsilateral adrenal gland. |
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Stage IIIa RCCA
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Renal vein involvement (may extend into IVC)
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Stage IIIb
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Local nodal involvement
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Stage IIIc
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Both vascular and local nodal involvement
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Stage IVa
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Distant nodal involvement
Invasion of adjacent organs |
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Stage IVb
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Distant mets
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RCCA with mass in ipsilateral renal vein
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Must determine whether this is extension of tumor or just bland thrombus due to hypercoagulability
Decide with doppler ultrasound or enhanced MRI with subtraction. Difference is potentially very significant both in regards to treatment and prognosis. |
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Cystic RCCA
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PAPILLARY RCCA
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RCCA with mass in ipsilateral renal vein
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Must determine whether this is extension of tumor or just bland thrombus due to hypercoagulability
Decide with doppler ultrasound or enhanced MRI with subtraction. Difference is potentially very significant both in regards to treatment and prognosis. |
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DDx for solid renal mass
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ANY patient:
RCCA TCCA Lymphoma Mets Patients with specific history Sickle cell -- Renal medullary CA VHL -- MULTIPLE RCCAs |
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DDx for solid renal mass
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ANY patient:
RCCA TCCA Lymphoma Mets Patients with specific history Sickle cell -- Renal medullary CA VHL -- MULTIPLE RCCAs |
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RCCA with mass in ipsilateral renal vein
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Must determine whether this is extension of tumor or just bland thrombus due to hypercoagulability
Decide with doppler ultrasound or enhanced MRI with subtraction. Difference is potentially very significant both in regards to treatment and prognosis. |
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Cystic RCCA
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PAPILLARY RCCA
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DDx for solid renal mass
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ANY patient:
RCCA TCCA Lymphoma Mets Patients with specific history Sickle cell -- Renal medullary CA VHL -- MULTIPLE RCCAs |
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DDx multiple bilateral renal masses
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1) METS
2) Lymphoma/Leukemia -- NON-Hodgkins 3) Multiple RCCAs (VHL) 4) TB |
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Patterns of renal lymphoma
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4
Perinephric encasement from retroperitoneum -- VERY SPECIFIC but uncommon appearance Multiple bilateral masses Diffuse enlargement SINGLE RENAL MASS -- mimics RCCA |
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Solitary renal mass and small hypodense lesion of spleen
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Think LYMPHOMA
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Clue that its lymphoma
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Since exceedingly rare to have primary renal lymphoma, will have other evidence of lymphoma elsewhere
--RP lymph nodes --Hilar enlargement --Neck nodes enlarged etc |
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TS transmission
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AD but up to 50% new mutations
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Prognosis of TS
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POOR
75% mortality by age 20! |
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% patients with AML who have TS
% patients with TS who have AML |
20%
80% |
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Only time solid renal mass does not come out
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1) Patient has history of lymphoma and single renal mass -- this is one of two cases that you would biopsy to see if RCCA or lymphoma, because lymphoma treated with chemo
2) Can do same thing if patient has a primary malignancy, or may just take it out assuming its a RCCA. If it is RCCA, that is actually better for the patient as its better to have two different malignancies in remission than one same malignancy that is metastatic. Whether biopsied or not, something HAS to be done in order to get the information needed. |
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Renal mass and surrounding perinephric soft tissue density
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2 Possibilities
Give contrast to determine whether surrounding soft tissue density is FLUID or SOLID If fluid, it is high density fluid, probably blood. Mass is probably AML. DO FAT SAT TO CONFIRM MACROSCOPIC FAT. RISK OF PAGE KIDNEY. If peripheral lesion is enhancing and solid, likely retroperitoneal lymphoma with renal invasion |
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Angiogram with AML
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May not see entire mass as blush. WHAT YOU SEE ARE THE FOCAL ANEURYSMS WITHIN THE AML.
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Treatment of bleeding AML
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COIL THE ANEURYSMS
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Patients at increased risk for RCCA
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Prior history of RCCA
VHL Renal cystic disease of dialysis |
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What is not associated with increased risk of RCCA
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Autosomal dominant PCKD; but it is harder to diagnose by imaging
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Most common adrenal masses
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Nonfunctional adenoma
METS That is why we are always trying to differentiate between these two |
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Adrenal cysts common or uncommon
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RARE, just like thymic cysts
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Macroscopic fat in adrenal
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Myelolipoma. No DDx
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What can myelolipomas be associated with?
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congenital adrenal hyperplasia
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HU for adenoma
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under 10
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Evaluation of adrenal mass in patient with known malignancy
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1) Noncontrast CT shows adrenal mass with HU 10 or lower. Enhances post contrast (rules out cyst) -- Evaluation complete, lesion is adenoma
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Mass is greater than 10 HU on precontrast CT
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DDx at this point is
1) Lipid poor adenoma 2) Metastasis MRI is not useful for evaluation of lipid poor adenomas, since they tend not to suppress on out of phase images. Thus, the next step in evaluation is the contrast enhanced CT with washout imaging. The reason this works is that ADENOMAS HAVE RAPID WASHOUT Only 2 values are required at this point: The precontrast doesn't matter anymore. It was above 10, so we don't care about it. All we care about now is how the lesion is washing out, so all we need is: Post-contrast (portal phase) 15 minute delay |
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What next
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The portal phase image is considered the peak, and we calculate what percent WASHOUT occurs at 15 minutes. We are interested in the percentage DROP in HU during this interval.
portal - delay / portal So, if precon was 42, postcon 150, and 15 min delay 45, then you calculate the percent washout as: 150 - 45 / 150 = 105/150 = 0.7 or think of it as total amount of washout (in HU) / original HU Simple calculation |
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What next
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If percent washout is 0.6 or GREATER, it is a lipid poor adenoma.
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What if percent washout is 0.52?
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Can consider going to MRI
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What is criteria for adenoma on MRI?
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20% or greater loss in signal between in and out of phase sequences
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Why does chemical shift occur?
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Not all protons are the same. Like we learned in organic chemistry, a proton spins at a rate largely dependent on the ambient magnetic environment, but also slightly dependent on its own LOCAL environment. For water, the proton sitting there attached to a single oxygen molecule with just one other proton attached to it has a different home environment than the proton attached to a carbon of a hydrocarbon (lipid), which itself is then attached to other protons and at least one other carbon attached to more protons.
These differences in home environment make for very small differences in spin frequency. The difference in spin frequency is dependent on the overall spin frequency (which is much faster) which is itself dependent on the ambient field strength. At 1.5 T, the spin frequency difference occurs at such a rate that the two spins are exactly in phase every 4.4 ms. That means that halfway between these intervals, the spins are exactly out of phase. So, you have your RF pulse, and that sets all the spins exactly in phase. Then you set your TE to 4.4 milliseconds, and get images with fat and water in phase. Then you do the RF pulse again, but this time you set your TE to 2.2 milliseconds. Now fat and water will be exactly out of phase. Thus, if there are 1000 water protons and 1000 fat protons in the same voxel, (and nothing else) there will be signal void. The proportion of signal dropout in each voxel is related to closeness in number of fat protons to number of water protons. |
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T1WI adenoma
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Short TR
Short TE |
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T2WI adenoma
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Long TR
Long TE |
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PDWI adenoma
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Long TR
Short TE |
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Practically, how do you decide if its an adenoma or not on MRI?
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Look at adrenal on in-phase image, and compare its intensity to EITHER SPLEEN OR SKELETAL MUSCLE. You use these as a reference because they have NO FAT in them, and will not change on opposed phase images. DO NOT use liver, because it frequently is fatty infiltrated.
Then look at the out of phase images, and check to see if there is signal dropout RELATIVE TO SPLEEN OR SKELETAL MUSCLE versus its appearance on the in phase images. |
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Size of adenomas
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Should be LESS THAN 4 CM
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Adrenal adenoma on T2 WI
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Usually Dark
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Adrenal mass bright on T2WI
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CLASSIC APPEARANCE OF PHEO
Howerver, most pheos are not light bulb bright on T2, just mildly bright. Another characteristic is LATE ENHANCEMENT, just the opposite of an adenoma. -- Why late enhancement? They tend to have few feeding vessels and a large extracellular space, so it takes a long time for the contrast to diffuse in. |
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PHEOCHROMOCYTOMA
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10% RULE
10% BILATERAL 10% MALIGNANT 10% EXTRAADRENAL |
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Adrenal mass, when should you think of pheo
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ANY ADRENAL MASS IN PATIENT WITH HYPERTENSION. Of course the HTN may be unrelated, but you MUST RULE IT OUT.
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Big mass adjacent to kidney
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ADRENAL CARCINOMA, especially if there is associated central necrosis or hemorrhage
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How big are adrenal carcinomas usually
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90% are over 6 cm, so if you see a 3 cm adrenal mass, its probably not and adrenal CA, and definitely not in Louisville
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What do adrenal CAs commonly do?
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Invade IVC
Invade spleen and kidneys Mets to liver |
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DDx for solid adrenal mass that is not an adenoma or a myelolipoma
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Met
HEMORRHAGE (pseudocyst) Pheo Adrenocortical CA Lymphoma |
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What would hemorrhagic adrenal pseudocyst probably look like on boards?
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Bright on T1, so you ask for fat suppressed image. Doesn't suppress. You ask for in/out of phase. Doesn't fall out. So its not fat making the signal high on T1, what else could it be? Proteinaceous cyst? Melanoma met? Probably not. MUCH MORE LIKELY HEMORRHAGE.
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Renal pathology, not a tumor
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There are 3 things to evaluate:
Morphology/position of the kidneys --look for congenital (pelvic) or acquired (cysts) abnormalities Ureters and renal vasculature --Look for disease but also look for anatomical variants Parenchyma --Striated nephrogram --Prolonged nephrogram etc |
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DDx when empty renal fossa
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Ectopic kidney (pelvic, crossed fused) -- Look for the normally inserting ureter in crossed fused
Renal agenesis or MCDK that totally regressed |
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Complication of all ectopic kidneys
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ALL prone to reflux
ALL prone to stone formation |
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Nerka podkowiasta powikłania, asocjacje
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Increased risk for traumatic injury
Increased risk for Wilms Increased risk for UPJ obstruction Associated with VATER Associated with Turner's |
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Congenital renal lesion
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ASK TO SEE UTERUS TO DIAGNOSE ASSOCIATED MULLERIAN DUCT ABN
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Bicornuate uterus
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ASK TO SEE KIDNEYS TO DIAGNOSE ASSOCIATED RENAL ABNL
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Unilateral large kidney
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Infiltrating tumor
OBSTRUCTION RVT PYELO CYSTIC RENAL DISEASE Contralateral absence of kidney Klippel-Trenaunay |
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Klippel-Trenaunay
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Hemangiomas and hemihypertophy
So one kidney is bigger. On that same side, proliferation of fat and muscular enlargement |
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Bilateral renal enlargement
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Cystic renal disease
Deposition diseases like amyloid Leukemia (less commonly lymphoma for this appearance) Lupus -- think of Charlie's wife HIV NEPHROPATHY SINUS LIPOMATOSIS -- The parenchyma is not enlarged, but the kidney is because of fatty proliferation in the renal sinus Edema |
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HIV nephropathy
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Rapid onset of elevated creatinine progressing to renal failure
2 phases In the acute phase, both kidneys become edematous, so large and hypodense on CT (non-con, since in renal failure) Then they shrivel down to atrophic kidneys in the chronic phase. |
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Kidney expansion of renal sinus with fat
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Renal sinus lipomatosis
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Renal sinus lipomatosis
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Proliferation of renal sinus fatty tissues due to chronic irritation
History of chronic infections, chronic hydronephrosis, persistent renal calculi. Can result in renal parenchymal atrophy in late stages, and can cause pain due to capsular expansion necessitating nephrectomy for palliation. |
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Simple renal cysts
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Can be symptomatic when large, and can rupture from trauma.
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DDx multiple renal cysts
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Autosomal dominant -- Larger cysts. Some hyperdense due to hemorrhage. How frequently should you follow them for development of RCCA? -- NOT AT ALL. NO INCREASED RISK.
Autosomal recessive -- in older children/adults who have less aggressive forms and survive, see more organized appearance of smaller cysts than you do in ADPCKD. Also see splenomegaly. All have some degree of hepatic insufficiency. Acquired renal cystic disease -- LOOKS JUST LIKE Autosomal dominant PCKD. BUT if patient is on dialysis, and did not have cystic disease PRIOR to being put on dialysis, then this is the answer. |
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Autosomal dominant PCKD
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MUST SCREEN THEM FOR BERRY ANEURYSMS
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Lots of cysts, patient on dialysis
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DID PATIENT HAVE CYSTIC DISEASE BEFORE DIALYSIS??? (i.e. is ADPCKD the cause of the renal failure)
No? Then its acquired renal cystic disease of dialysis. INCREASED RISK FOR RCCA |
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Acquired renal cystic disease treatment
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1) Screening for RCCA if short life expectancy
2) Bilateral nephrectomy -- not done as frequently anymore Now . . . 3) Put in transplant kidney -- risk returns to near baseline |
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Renal cyst with focal calcification at the dependent aspect
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FLIP THE PATIENT OVER AND RE-SCAN
If the calcification moves, the patient does not have a cyst. The patient probably has a calyceal diverticulum. CONFIRM BY GIVING CONTRAST and looking on delayed images for contrast eventually entering the diverticulum. |
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Calyceal diverticulum
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Sequela of prior infection or papillary necrosis
STONE FACTORY due to stasis |
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Lots of calcifications contained in a structure on plain film
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IN RUQ -- Gallstones
IN LUQ -- THINK CALYCEAL DIVERTICULUM WITH LOTS OF STONES |
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IVP with calyces pointing down
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DDX = DUPLICATED COLLECTING SYSTEM (drooping lily) vs. HYPERMOBILE KIDNEY (renal ptosis)
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Differentiate renal ptosis from duplicated collecting system
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In duplicated collecting system, the lower pole moitey is compressed inferiorly by the dilated obstructed upper pole moiety. But since the kidney is split into 2 moieties, the lower pole moiety will have fewer calyces than a normal kidney will.
Hypermobile kidney is just a normal kidney that is not as well attached as a normal one. YOU CAN NOT USE DILATION OF THE CALYCES AS EVIDENCE FOR REFLUX INTO A LOWER POLE MOIETY OF A DUPLICATED COLLECTING SYSTEM BECAUSE THE HYPERMOBILE PTOTIC KIDNEY GETS UPJ OBSTRUCTION DUE TO KINKING, IN FACT THAT IS WHY THEY PRESENT IN THE FIRST PLACE |
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How many calyces is normal?
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12 - 14
So count em; if too few its duplicated collecting system |
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VCUG performed, and demonstrates reflux into a BLIND ENDING URETER
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Most commonly due to MCDK which has regressed
Also ectopic insertion of ureter, with subsequent hydronephrosis and eventual regression of that kidney, or you may just be seeing the obstructed moiety's ureter, and the other one is not refluxing. Prior nephrectomy (for RCCA or trauma, NOT for TCC because the entire ureter is resected in those cases due to likelihood of occult neoplasm in the remaining ureter). And finally, what you are seeing may just be a ureteral diverticulum, and not the real ureter leading to the kidney. |
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Given CT or US of kidney through midpole and no sinus fat
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FACELESS KIDNEY
If normal anatomy otherwise -- duplicated collecting system If medullary pyramids disorganized, think MASS |
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Dilated calyces
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LOOK AT RENAL PELVIS
If renal pelvis is distended, its probably obstruction or reflux. If renal pelvis is not distended, think congenital megacalyces (megacalicosis). To confirm its megacalicosis, all you have to do is COUNT THE CALYCES. There are TOO MANY with congenital megacalyces. |
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Congenital megacalyces (megacalicosis)
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Associated with 3 things:
Congenital megaureter Ureterocele Contralateral UPJ obstruction |
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Dilated ureter
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May be CONGENITAL MEGAURETER
Associated with prune belly? Check in peds section |
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UPJ obstruction causes
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Usually idiopathic, due to muscular dysfunction in ureter
Crossing vessel -- accessory renal artery. Mass Circumcaval ureter Retroperitoneal fibrosis |
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UPJ obs treatment
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Urologist goes in with a scope, and uses a balloon with a cutting edge to incise the UPJ (endopyelotomy), almost like a myotomy for pyloric stenosis, but from the inside
BUT IF THE CAUSE IS A CROSSING VESSEL, THE PROCEDURE WILL NOT WORK AND THE PATIENT MAY BLEED HEAVILY AND/OR LOSE PART OF THE KIDNEY Therefore, secondary causes of UPJ obstruction must be sought in all cases, to include MRA or CTA to exclude such pathology and eliminate incidence of such catastrophes. |
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When suspect crossing vessel
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ADULT WITH UPJ obs
50% of them are caused by crossing vessel, versus only 10% in peds |
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IVP or urogram or VCUG with proximal right ureter coursing medial to lateral margin of vertebral bodies.
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Circumcaval ureter
DDx: could be due to retroperitoneal fibrosis or mass. USE CT or CTA or MRA to confirm. |
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Lots of filling defects in upper urinary tract
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1) Must always consider multifocal TCC
2) If history of infection: Pyelouretritis cystica 3) Malakoplakia -- Malka (benign) 4) Leukoplakia -- PREMALIGNANT. More common in bladder. 5) Chronic renal vein thrombosis -- with formation of lots of collateral veins causing little vascular impressions |
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Most important prognostic factor in bladder CA
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Depth of invasion
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Advanced TCC?
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Invade deeply into muscularis propria. 50% have occult metd.
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Most common GYN malig
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endometrial,
ovarian,then cervical |
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Stage I cervical
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confined to cervix
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Stage II
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IIb or not tIIb
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Bilateral adrenal masses
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Adenomas
Mets Hemorrhage Pheos |
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Bladder filling defect
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Neoplasm
Calculus Blood clot Fungus ball (same for anywhere in collecting system) |
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DDx for TOA
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Ovarian neoplasm, but different presentation
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Tx of TOA
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ABX. Only drain complex cases that dont resolve
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Calcification in scrotum outside of testis
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Scrotal pearl
łagodna zmiana zw. z hydrocele w wyniku skrętu przyczepku jądra |
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Large intratesticular calc
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BURNED OUT SEMINOMA
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Cause of striated nephrogram
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Pyelo- interstitial edeme causes urinary stasis in tubules, which do not opacify
Ureteral obstruction Contusion can look like it |
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Dilated renal pelvis
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Could be obstructed, but more commonly due to paralysis by bacteria
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Bladder calculus
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Is it midline. If off midline, think displacement of stone by mass or enlarged prostate
Bladder tic with stone ureterocele with stone |
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Lots of small dots in proximal part of fallopian tube on HSG. = ampullary part
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Salpingitis isthmica nodosa (SIN)
Tuberculosis of the fallopian tube Tubal adenomyosis |
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Contraind to HSG
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Menstrual bleeding
Acute PID Recent D and C -- 4 days Pregnancy |
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DDx hypointense nodule in peripheral zone on T2WI
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CA
BPH nodule Prostatitis Hemorrhage post biopsy |
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Normal peripheral zone
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HYPERINTENSE ON T2
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Ovarian malignancy
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Size greater than 6 cm
Solid component Mural nodules Internal papillary projections Thickened septations Lymphadenopathy ASCITES |
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Most common adrenal cyst
Next most common |
Endothelial cyst
Lymphangioma |
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Calcified cystic structure
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ADRENAL CYSTS COMMONLY CALCIFY
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Mural enhancement in what appears to be adrenal cyst
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Thats OK. Allowed to enhance, like pseudocyst.
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Calcified renal mass
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REGADLESS OF PATTERN OF CALCIFICATION, any renal mass with calcification is RCCA until proven otherwise
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Complete DDx of bladder mass
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CA
Calculus Blood clot ureterocele Less likely: Fungus ball, focal cystitis |
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Percent bladder tumor TCC
Percent SCC Rest |
90%
5% 2% adeno CA |
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Testicular microlithiasis
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Associated with testicular neoplasm, cryptorchidism, testicular atrophy, infertility
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