 Can everybody see my screen. Yes, sir. Okay, so thank you so much for the introduction and thank you for the opportunity to present. I wish I had looked at the agenda prior to accepting this talk because it's impossible to follow speakers like Dushan Bahar, Antonio and Kilarame but nonetheless, and especially cover the breadth of abdominal imaging in a case based review. And I'm going to give it a shot. I was able to collect a bunch of cases that I think are a mix of day to day things that we see on a common basis. And also some rare cases that I think, particularly that mimic lesions and stuff like that that I think might be helpful for the audience. So, without further ado, I have no financial disclosures and I want to thank some folks who were very kind enough to share their cases with me, including Dr. And rather should I bang bang Lee Dr. Ryan Chung from Mass General and Guilherme from UW here. So first case, you know, not a very complex case, just simple. And again, just because of the format I think I'm going to not go into questions but just sort of walk everyone through it and if we have time we can have questions at the end so on the top. On the left you can see a haste image where you can see a fat fatty lesion. And then on the post fat saturated images you can see T1 post fat saturated images you can see that the lesion has dropped the fat signal that you would expect with macroscopic fat in and out of phase not so much of signal drop but very little enhancement as well. So containing exophiric lesion arising from the left kidney, demonstrating some heterogeneous enhancement. It's a renal angiomyelopoma most common benign renal and neoplas contains vascular smooth muscle and fat elements, and can spontaneously hemorrhage due to pseudo aneurysm formation, because of its rich blood supply. So this increases with increase in size, and hence, they usually recommendation is to embolize them if they start to grow beyond four centimeters. They usually sporadic 80% of the cases, 20% of the cases are usually associated with the phycomatosis, most commonly being to bislerosis. Moving on to the next case. So here we roll with the prosthetic cardiac valve. If you look at the T2 image you're nothing's very remarkable as any stock of normality that you see but if you look closely I think you'll be able to appreciate the bilateral symmetrical renal cortical high point density on both T2, on the T2 sequences here. And here's the cortical renal cortex that is markedly T2 high point tense. And this can be seen in the setting of renal hemosetrosis, not a very sort of a diagnosis that really helps at clinicians because they usually know the history. In this case, this was a case of a patient who had a cardiac valve prosthetic mechanical cardiac valve which can also cause this and it's essentially hemosetron depositing along the cortex that causes that appearance on T2 and T1 sequences as well. And it's also very common, as you would expect with hemolytic anemias and paroxysmal and octal hemoglobinuria. And here's a marked example of the same case, you can see that the CT you really do not appreciate any changes, but on the MRI you can see the marked T2 high point density of the renal cortex. Next case, this is a 22 year old male presenting with dysuria PSA levels were mildly elevated but not significantly. And as you can see on the images here on the axial T2 and chronal T2 images there's a heterogeneous mass arising from the left side of the prostate here, and you can see that it's sort of infiltrating into the adjacent structures. It demonstrates marked diffusion restriction as you can see with DWI and ADC on the images here. And on post contrast images there's heterogeneous enhancement. You can also see on these images sort of diffusion restricting multiple pelvic lymph nodes as well that show enhancement. So this was, so you know I'll just pause real quick here just give you guys a quick second to think about it is this a prostate lymphoma and a 22 year old prostate rhabdomyosarcoma, prostate adenocarcinoma non-musinus, prostate adenocarcinoma non-musinus or a prostate leomyosarcoma. So this was a prostate rhabdomyosarcoma alveoliotype and it is a malignancy arising from mesenchymal cells. The epidemiology is most common prostate tumor in the first two decades of life. It's rare in adults once the mesenchymal cells have evolved and the embryonal subtype more common better prognosis, whereas the alveolar subtype is the less common and the worst prognosis. The presentation is usually urinary retention dysuria in which in this patient, the patient did present with dysuria, abdominal and pelvic pain or prostate enlargement. Imaging features, which we saw in this case, a large infiltrative tumor with central necrosis sometimes which we didn't really appreciate in this case, but does demonstrate rapid growth. T1 iso intense, T2 hypo intense and markedly diffusion districting lesion with heterogeneous enhancement. Differential diagnosis, some of the options did talk about a prostate lymphoma, but a prostate lymphoma is usually T2 hypo intense, usually homogenous signal and enhancement and not infiltrative like it was in this case. A prostate adenocarcinoma would usually be seen in older patients, elevated PSA, and they have two types, non-musinus and musinus. And then obviously a prostate lyoma, myosarcoma, most common prostate sarcoma in adults. Moving on to the next case. This is my personal favorite. This is a 59-year-old man with a history of T1 urethral carcinoma of the bladder status post-induction BCG treatment presenting for prostate MRI for elevated PSA of 3.27. And as you see on the images here, you can see a T2 hypo intense lesion in the left anterior peripheral zone at the level of the apex that demonstrates marked diffusion restriction and peripheral enhancement. If you were to apply pirates as we heard Antonio talk about in his talk, this would qualify for a pirate's five lesion for all purposes would be marked for guided biopsy. But this on biopsy actually turned out to be a focal non-necrotizing canal matis inflammation consistent with non-specific canal matis prostatitis. And given the history that we had that the patient had PT1 urethral carcinoma of the bladder and had induction BCG treatment that could be suggested. But for all purposes, clinical purposes, rising PSA pirates five, that lesion doesn't need to be biopsy. But this is just the lesion that I think especially in the setting of recent BCG treatment, I think we can keep in mind. The key points being that it's clinically significant prostate cancer and canal matis prostatitis are indistinguishable on imaging. Both demonstrate marked diffusion restriction, most often in the peripheral zone. And in the event of a pirate's five lesion with negative biopsy for malignancy, you can then actually suggest this being a canal matis prostatitis if it's a non-diagnostic biopsy or a negative biopsy to prevent unnecessary additional biopsies. Scenarios in which it may be helpful to offer differential particularly like in this case we saw T2 hyper intense lesion, but usually for pirate's five lesions you should have T2 hyper intensity that is characteristic of prostate cancer. So when you see a T2 hyper intense lesion that's markedly diffusion restricting. Then you can suggest it but then again for all purposes of reporting it it still qualifies as a prostate as a pirate's five lesion. And then post contrast rem enhancement again if you look at this lesion sort of focal early enhancement instead of the focal early enhancement you have the rem enhancement of the lesion. So just if you correlate with the T2's here and sort of hallucinate it's obviously we don't have the luxury of scrolling through that there was sort of peripheral rem enhancement in this case. And the relevant technical history is I think the most important in this case. And I think having seen multiple of these types of cases whenever I see prior BC treatment while reporting prostate MRI and sort of cautious and just sort of take a second look. And the other indication other clinical history that is relevant is obviously infectious tuberculosis and I approach a neck inclusion post radiotherapy. Moving on to the next case. So these are multiple cases of adrenal lesions and if you look at these lesions. The middle case on your left is actually a right adrenal lesion sort of T2 hyper intense the middle case is a T2 iso intense lesion. And then on the right is sort of a mixed hyper intense and hyper intense lesion heterogeneous. So I think I just wanted to use all three cases an example to suggest that, you know, when you're looking at these adrenal lesions and particularly if you promise a few chromosomes, you can have sort of variability to intensity for the lesions. And the typical imaging findings on CT would be unenhanced lesion on unenhanced CT you would have a lesion that's greater than 10 Houndsville units. That's not an adenoma on portal venous phase you would get sort of 110 to 120 Houndsville units, and they can show wash out I think that's important to remember a lot of sort of I think there's increasing data to suggest historically we would, if these should wash out and be as unqualified as adenomas, we would leave it at that but I think there is enough data to suggest that then does clinical correlation is still required because a lot of them of your chromosomes can show or show. And the cystic change and like necrosis occurs in 20 to 97% patients, and this is based on CT literature, and they can also be hemorrhage but on MRI, when you look at the literature the cystic chain slash necrosis obviously MRI being better at evaluating that is 30 to 52% and as I showed in the three cases here, the T2 hyper intense signal is variable, and you can have, ranging from 35 to 65% cases depending on the literature you see. And here's a nice examples of basically cystic changes here within the lesion. And also, another case that where you see the cystic changes here. This is another example where you see the cystic change in the central of the lesion it's a right adrenal lesion as you can see and sort of T2 heterogeneous lesion focal areas of necrosis in the center. And then another case of a 40 year old female with incidental findings of a left and a right adrenal lesion as you can see the left adrenal lesion has marked central necrosis on post contrast images that way you can appreciate it. Both in this case both are marked T2 hyper intense lesions. The T2 chromositomas, they are tumor arising from chromophilic cells of the adrenal medulla. They, the extra adrenal fibrochromis, the tumors are known as paragangliomas. The presentation is usually episodic or proxysmal symptoms. The cases, if you may, then you have few chromositomas is usually presents with headaches, hypertension, palpitation, sweating, tremor, arrhythmia and pain. The classic fried, which is 90% specific but an uncommon presentation is headache palpitations and sweating. The atypical features being labile hypertension, myocardial infarction and stroke. And like I mentioned earlier it's important to be cautious when reporting adenomas, adrenal adenomas as there's increasingly more literature saying reported that you do need to clinically rule out some of these to be few chromositomas with 24 are you re-infractionated net and effort in levels. The demographics females more common than males middle-aged adults sporadic, usually sporadic in the middle-aged adults and hereditary in some young adults and they're obviously as everybody, everybody knows they're associated with several fake chromatosis that are being the most common in this group. On imaging, I think we went over most of those in a number of cases but you cannot reliably distinguish from other adrenal lesions and you need that lab and histology as I stressed earlier. All have metastatic potential based on presence of the chromophilic cells and tissues that don't normally have them and cannot reliably distinguish on path. So on CTMR, we went over the features that on portal venous phase you can have even greater than 120 household units and may have washed out with heterogeneous enhancement. Nukea medicine or MIBG scans are very specific but more so the dota-tate scans and they bind to the SSTR which is found in neuroendocrine tumors. I'll skip the slide for sake of time so moving on to the next case. This is again one of the run-of-the-mill cases, right adrenal lesion again just sort of going over a lot of adrenal cases here, a fatty lesion in the right adrenal gland that you can see on both axial and non-coronal images. And on the axial in phase and axial out of phase MRI, you can see there's not significant signal drop and this is sort of representing macroscopic fat in this case. And as you can see on the fat side you can because of the of it being macroscopic fat you can see the signal drop and on post-contrast images you do not really see a lot of enhancement there. Here's a companion case of the left adrenal gland, again a fat-containing lesion in the left adrenal gland over here. So adrenal myeloepomas benign tumors of mature adiapocytes and hematopoietic cells, they contain variable amounts of fat and soft tissues on imaging, occasionally contain calcifications. And they can be T1 hyper intense and they suppress fat on the fat side of sequences with soft tissue components that enhance and loss of signal at the fat water interfaces on the in and out of phase imaging. Next case again another one that could qualify as one of my favorites but a very nice diagnosis that you can make once you've seen one of these. And usually at least add to the differential. So here's a pre-sacral lesion on the sagittal CTs as you can see on the axial CTs and on the haze sequences you can see that there is sort of a fat signal intensity lesion with some of which suppresses fat on the T1 pre-fat sequence here. And on the post contrast you can see that there is heterogeneous enhancement of the lesion. I'll give everybody a second to just think of what differential they can think of and just moving on to the next slide. So this is a nice case of a pre-sacral extra adrenal myeloepoma just to be in sync with the previous case that we saw. You can have extra adrenal myeloepoma like POMAS account for 50% in the pre-sacral area when they're extra adrenal 50% of the time they are pre-sacral and they're usually seen in early females. They are asymptomatic occasionally symptomatic from mass effect on adjacent organs and imaging features like we went over in this case. Just to stress that if there is a question of a differential diagnosis, a lot of time the sulphur colloid scan can help differentiate from other differentials just because of the presence of reticulo endothelial elements, the lesion will demonstrate sulphur colloid uptake. And differential diagnosis in this case is a lipoma, liposarcoma, pterotoma, and lipomatosis, as you would expect all fat containing lesions in the differential diagnosis. Moving on to the next case. So this is a 40 year old male who had a prior left nephrectomy as you can see. Over here you don't really appreciate the left kidney. The right adrenal gland demonstrates on the inner and outer phase you can see signal dropout consistent with an adenoma. But then moving on two years later in 2012, you can see that between 2010 and 2012 this patient has now developed an area of sort of hyper intense signal on the in phase and a hyper intense signal. On the outer phase sequence that on post contrast images, you can see there's some heterogeneous arterial enhancement that kind of persist from the post portal venous and delayed phases. I'll just pause real quick there if anybody has any thoughts for the differential diagnosis. And just again, so this case, the same patient, as you can see on the T one three, there's a high point intense lesion here on the T one freeze in the pancreas that enhances our T really on enhances our T really and sort of persist on the portal venous and delays phase imaging. And this turned out to be a case of RCC meths based on the history that I've provided earlier, the patient have had a left left nephrectomy for clear cell. Renal cell carcinoma. And this is a very, very nice example of a renal collision tumor. So at renal collision tumors, they can coexist to adjust in histologically distinct tumors, and they can be two benign tumors to malignant tumors or one of each. So the most common being an adenoma and a myelolipoma additional cases you can get an adenoma and a metastasis as in this case that we saw in patients with lung breast and melanoma. And including RCC, which it was in this case, imaging features, you can see the change in characteristics of the previously seen benign lesion, particularly in patients with non malignancy. And yeah, so moving on to the next case. 58 year old female with right up a quarter of pain and weight loss. You can see a heterogeneous mass in the liver. And if you sort of follow it, you can see that it is sort of particularly located in a segmental area of the liver. And if you can hallucinate somewhat of a tubular appearance and the MRI again shows mild T2 hypentensity, heterogeneous enhancement, you can see central areas that do not enhance sort of almost if I can sell it to your biliary kind of pattern here. And this is, this was a nice case of hepatic fasciola or kind of liver flu that has two hosts and eventually make it makes its way into the bile ducts. And I did have another companion case with this that unfortunately could not pull up the images but I think, you know, once you see a couple of these cases, which I happen to come across, I think, you know, you, it sort of always stands out when you see it again. Moving on to the next case. I just wanted to very quickly just before I go on to some of the atypical tumors of the liver, just for completion sake just highlight a laryx 5 lesion which is my definition, a definite at CC. So you have here at T2 mildly hyper intense lesion that on free contrast you can kind of see here, and then on enhances arterially and you have a wash out. You can see the capsule very clearly so a laryx 5 lesion by definition definite at CC. Moving on to the next case. And this just keeping that in perspective. Guillermo was kind enough to share this very nice case with me. This is the heterogeneous mass and the MRI here you can see that there's capsule of retraction. There is peripheral enhancement and gradual centripetal enhancement in this in this case. And if I asked anybody a differential here I think Colandia carcinoma would be your top of the differential, which this was in this case, but just to add to it. This lower slice CT from the same case. And you can see a utterly really enhancing lesion with wash out. So this on biopsy was actually a. And you can call it what you may, but essentially it is the Colandia carcinoma and it's CC on histology or crane simultaneously and they develop this informatically and when advanced present with right up according to pain weight loss and obstructive there's 2010 Wichita classification sort of differentiates into two types classical and the stem cell features, but one of the key features I think that should make you point towards them as Mark diffusion description and the two components if you can deal with it like we could in this case it within the same lesion. Moving on to the next case. So pseudo lesions of the liver I just wanted to talk about this real quick for the next two cases. And so lesions mistaken for primary hepatic tumors or meds are most often due to hemodynamic alterations without going into details I think just to highlight that the portal in obstruction can sometimes cause increased arterial flow and kind of can cause a pseudo lesion but on conversely you have third flow areas within the lesion that is actually flow coming in from adjacent veins and anastomers with the portal in branches that can sort of cause these to the lesion so just a diagrammatic representation that as we all know, these are very common areas that are called blood of Fossa, but essentially highlighting that these are aberrant veins or parts of normal veins that are independently draining into the portal venous system and causing lesion and so here you can sort of see a lesion along the called blood of Fossa that in this case was called a LR5 lesion, but I think ended up being called that twice and both the times actually the biopsy showed that this was just stear hepatitis with cirrhosis and no evidence of Casinoma and again called LR5 lesion and biopsy again showed that this was not a Casinoma. Moving on to the next case in the in the scheme of lesions in the liver that are atypical. So on the ultrasound you can see a hyperquake mass with peripheral flow within the lesion. And then when on the MR, you can see a heterogeneous mass here on T2 with sort of heterogeneous enhancement again doesn't really fit the bill of a typical liver lesion and in this case this was biopsy then this was a hepatic plasma Cytoma and without going into details just again one of those rare diagnosis that I think one should just keep in mind, given that when it doesn't really fit the bill, these eventually need to go to biopsy I don't think you can make out these lesions prospectively on imaging, but one of the differentials in the rare lesions. And on the same bread, here's a well encapsulated lesion no significant arterial enhancement over here, as you can see, and sort of heterogeneous enhancement within the lesion with some edema and man mark diffusion this friction. So this is again another of those lesions that are atypical in the liver, but one to keep in mind and it is a inflammatory pseudo tumor, and rare benign hepatic lesions, not only theology but definitive diagnosis always requires a biopsy, but plasma Cytomas and pseudo tumors I just wanted to highlight in addition to the third space flow of the liver, just to keep in mind when you're sort of chasing it CCs and obviously it's helpful to see that the liver is not and then last case, just keeping in mind time. This is a CT from 10 years ago, and there's as you can see along the right paracolic out of there's a heterogeneous enhancing soft tissue lesion, and on the sort of anterior the rectum you can also see a lesion. I do not want to provide the history in this case that which will clearly give it away, but four years later after the CT you can see sort of anterior to the rectum you can see enlarged mass if you may knowing that in hindsight, and that shows T2 hypotensity and T1 hypotensity. Oops. And now if I can sell it to you this is that same lesion that has now grown and similar images of T2 images of the lesion here in the right paracolic data and then on post contrast enhancement you can see it with homogenous enhancement and on the chronal images you can see the same lesion. And if I can sell it to you again this is the same lesion that has now grown. Just pause the real quick two seconds just let people think of what this possibly could be. And this is a nice case of peritoneal leomyomatosis. They are basically Lyoma is dropped within the peritoneal cavity during uterine surgery mostly myomectomies and sometimes hysterectomy and C section. But this is essentially smooth muscle metatlasia in peritoneal lining stimulated by hormones and the epidemiology is females of reproductive age as you would expect. And you can see circumscribed round lobulate in masses with a tenure signal that would be typical for a uterine Lyoma and they can grow just similar to them, like in this case. And the differential diagnosis obviously if you were worried about malignancy would be peritoneal carcinomatosis. And here's just a companion case in a 45 year old female with right upper quadrant pain, who had a history of hysterectomy you can see sort of along the liver margin, a heterogeneous mass and along the margin of the stomach so quite a few dropped. Leomyomas in this case that were both consistent with peritoneal Lyoma myomatosis. With that, I would like to thank you for your time. And I hope these cases were helpful. Thank you so much. I think they were wonderful cases. I don't have any questions.