Radrev multisystem calcium

Question 1

What is the mechanism whereby Crohn’s disease makes calcium stones in the kidney? What type of stones

Answer 1

Crohn’s disease is associated with calcium oxalate stones. Oxalate normally binds with calcium in the bowel lumen to be excreted in the stool. With fat malabsorption, such as with Crohn’s disease, calcium in the bowel binds to fat more than it binds to oxalate. Oxalate is then reabsorbed at higher than normal levels and is renally excreted. These can then form calcium oxalate stones.

Question 2

How does bile contribute to this phenomenon of calcium oxalate stone formation in Crohn’s disease?

Answer 2

Sick/absent ileum –> no bile resorption –> not enough recycled bile to help with fat reabsorption –> calcium binds fat instead of oxalate —> oxalate instead of being pooped out is reabsorbed –> goes to kidneys –> binds to calcium in kidneys –> STONES Bile, which helps with fat absorption, is normally excreted into the small bowel to promote fat absorption and the bile is then reabsorbed in the ileum as part of the enterohepatic circulation of bile salts. In patients with Crohn’s disease that have ileal dysfunction and in patients who have had ileal resection, the bile is not reabsorbed, there is a paucity of bile to help with fat absorption, calcium binds to fat instead of oxalate, oxalate is then absorbed and renally excreted, and can form calcium oxalate stones

Question 3

Bonus question: Struvite stones classically form secondary to which bacteria?

Answer 3

Struvite stones are classic on board exams and you need to know that they have ammonium that results from urease in the setting of proteous and/or klebsiella.

Question 4

What are top differential considerations for a spiculated mesenteric mass that is calcified?

Answer 4

Think desmoid tumor, carcinoid, and sclerosing mesenteritis (aka retractile mesenteritis). Carcinoid is most common about the terminal ileum and pancreas and is arterially enhancing. Retractile mesenteritis has a classic “misty” attenuation. Note that all of these have various imaging manifestations but one way they can present is with a spiculated, calcified, mesenteric mass.

Question 5

A pathologist is examining core biopsy specimens from a stereotactic biopsy of calcifications, thought to possibly be related to milk of calcium. The pathologist does not see any calcifications in the biopsy specimen under standard microscopy. What could the pathologist consider adding in order to potentially reveal calcifications that are present but not seen on standard microscopy?

Answer 5

POLARIZED LIGHT The pathologist could evaluate the biopsy specimens with polarized light which may show calcium oxalate which can be seen with benign milk of calcium. Calcium oxalate is seen under polarized light microscopy whereas calcium phosphate is the more common type of calcification seen on standard microscopy and is stained purple with H & E staining. Calcium oxalate is more likely to be benign whereas calcium phosphate can be benign or malignant.

Question 6

Besides the breast can you think of another organ that can show milk of calcium on x-rays?

Answer 6

First, I think of renal cysts in which calcium can precipitate. Renal milk of calcium can also be seen in calyceal diverticula. The appear layering on layering on an erect film and rounded on a supine film (change configuration as also seen in mammography). You also can have milk of calcium in other places like the gallbladder (but that is less likely to be tested on a radiology board exam.)

Question 7

What are Randall’s plaques?

Answer 7

These are subendothelial deposits of calcium carbonate or calcium phosphate within the loops of Henle within the kidney. These appear hyperdense on an abdominal CT but are not renal stones. Key is that these are abutted by 50% or greater renal parenchyma—they are intimately associated with the renal papilla and renal parenchyma. These are often thought to denote an increased risk of stone formation

Question 8

What is a key sequence that is necessary on a triple phase CT to differentiate contrast from calcium on CT angiography, such as for endoleak evaluation?

Answer 8

Precontrast imaging is key on a triple phase CT to differentiate between calcium and contrast. If the hyperdensity seen on later phase images is also present on precontrast images then it is calcium. If the hyperdensity seen on later phase images is not present on precontrast images this is presumed to represent contrast, such as in an endoleak.

Question 9

What are differential considerations for renal medullary nephrocalcinosis?

Answer 9

HAMHOP H=hyperparathyroidism A=acidosis (Renal tubular acidosis TYPE 1) M=medullary sponge kidney H=hypercalcemia/hypercalciuria (sarcoid, milk-alkali syndrome, hypervitaminosis D) O=oxalosis (Crohn’s disease, ileal surgical resection) P=papillary necrosis Remember a unilateral calcified kidney think TB as nephrocalcinosis would be expected to be bilateral

Question 10

Bonus: What is a reasonable differential for renal papillary necrosis?

Answer 10

NSAID N=NSAIDs S=sickle cell disease A=acetaminophen I=infection (TB, pyelonephritis) D=diabetes/dehydration

Question 11

appearance of calcifications associated with papillary necrosis

Answer 11

The calcifications with renal papillary necrosis may be curvilinear or ring-shaped (arc of calcs around the papillary tips), or triangular in appearance (more extensive calcification of the papilla). Detached triangular calcs should make you consider sloughed papilla in the setting of renal papillary necrosis.

Question 12

What are characteristic imaging findings of medullary sponge kidney?

Answer 12

Pyramid like calcifications of the renal medulla on a noncontrast CT that develop a paintbrush like appearance on delayed post-contrast images. These patients are often asymptomatic but they can present with intermittent flank pain and/or UTI’s due to ureteral obstruction by small calculi in dilated renal tubules. The medullary pyramids would also look echogenic on ultrasound.

Question 13

In hepatic echinococcal disease what is the significance of complete rim calcifications of the hydatid cysts?

Answer 13

With hepatic echinococcal disease you often get a “cyst within a cyst” or large cyst with multiple daughter cyst appearance. You can also have the “water lily sign” which is the ruptured cyst envelope floating within the fluid filled cystic space. The cysts often get peripheral calcifications and if the peripheral calcification is complete so you have complete rim calcification that often denotes inactive hydatid disease. On a plain film you can see large curvilinear or rounded calcification(s) that should make you consider hepatic hydatid disease. Random fact is that hydatid disease is endemic in countries with lots of sheep.

Question 14

What is the main difference in internal calcifications between an immature and mature teratoma?

Answer 14

Calcifications in an immature teratoma are often irregular and amorphous. Calcifications in a mature teratoma are coarser and tooth-like. Both mature and immature teratoma have macroscopic fat which are smaller and more scattered in an immature teratoma and larger collections of fat are often seen in a mature teratoma.

Question 15

If you have a renal cyst with a few thin septa under 1 cm in thickness with thin calcifications, internal blood products or protein, and the cyst is less than 3 cm in size what Bosniak classification is this?

Answer 15

Bosniak II (benign, minimally complex)

Question 16

If you have a renal cyst with the above features but the septa contain thick calcifications, septa are increased in number, and cyst is larger than 3 cm what Bosniak classification is this?

Answer 16

Bosniak IIF (minimally complex, warrants follow-up, often in 6 months). F=follow-up. Tip with Bosniak is a 1 is a simple cyst, 2 is benign with no follow-up, 2F is most likely benign but needs follow-up, 3 starts to have thickened walls and mural nodules, 4 has an overt mass associated with the cyst. Bosniak 3 and 4 need an MRI and urology consultation. Treatment is often with something like radiofrequency ablation for a Bosniak 3 and partial/total nephrectomy for a Bosniak 4 lesion.

Question 17

What percentage of pheochromocytomas are calcified?

Answer 17

Remember 10%. With pheochromocytomas there are lots of 10% associations to include 10% bilateral, 10% extra-adrenal, 10% malignant, 10% pediatric, 10% clinically silent, 10% autosomal dominant, 10% are calcified. Pheochromocytoma—rule of 10s. If they ask you a pheochromocytoma asking about the percentage likelihood of an association, 10% is statistically likely to be the answer.

Question 18

what percent of meningiomas are calcified

Answer 18

25%

Question 19

How can calcifications help differentiate the true from the false lumen in the setting of aortic dissection?

Answer 19

The true lumen has calcifications around the lumen. This makes sense because we know on CT scans that calcifications, when present, are seen circumferentially in the wall of the aortic lumen. The false lumen opens up in the potential space in the aortic wall, not within the existing lumen with atherosclerotic calcifications.

Question 20

Bonus question: What are other ways to tell the true from the false lumen in aortic dissection?

Answer 20

The false lumen is usually larger than the true lumen, enhances later than the true lumen. Thrombosis is more common in the false rather than the true lumen. The true lumen more often contains the celiac, superior mesenteric artery and right renal artery. Two facts to definitely know: 1. The left renal artery usually arises from the false lumen. 2. If you are unsure which is the true or false lumen, the larger of the two lumen is more likely to be the false lumen.

Question 21

What is the significance of atherosclerosis calcifications of the ascending aorta?

Answer 21

Atherosclerosis typically spares the ascending aorta so if you see atherosclerotic calcifications of the ascending aorta, consider a non-atherosclerotic process such as Takayasu and Syphilis.

Question 22

What are differential considerations for urinary bladder wall and/or urinary lumen calcifications?

Answer 22

Top differential considerations include bladder calculi, schistosomiasis and tuberculosis. Less common entities include things like amyloidosis and alkaptonuria.

Question 23

What cancer is associated with urinary bladder schistosomiasis?

Answer 23

Squamous cell carcinoma of the urinary bladder

Question 24

What stage of neurocysticercosis is calcified?

Answer 24

Stage 4 nodular calcified neurocysticercosis. This is the quiescent stage with a calcified remnant of the prior viable parasite.

Question 25

Bonus: What is the most symptomatic stage of neurocysticercosis?

Answer 25

Stage 2: colloidal vesicular stage which is the stage at which the parasite dies, the cyst membrane becomes leaky, and there is prominent edema and enhancement.

Question 26

What is the significance of calcifications in neurotoxoplasmosis?

Answer 26

Calcifications denote non-active treated lesions.

Question 27

Bonus: In the setting of uncertainty regarding toxoplasmosis vs CNS lymphoma, thallium uptake supports which entity?

Answer 27

Thallium uptake would typically be seen with primary CNS lymphoma with no uptake in neurotoxoplasmosis.

Question 28

What are characteristic imaging features of Fahr syndrome?

Answer 28

The primary imaging feature of Fahr syndrome is extensive and symmetric calcifications of the basal ganglia and thalami and calcifications can also be seen elsewhere in the white matter. Some say Fahr disease is related to the genetic form of the disease and Fahr syndrome is the secondary form of the disease which can be due to things like parathyroid hormone dysregulation, infections like HIV, and carbon monoxide poisoning.

Question 29

What is a description of the calcifications in the brain associated with Sturge Weber Syndrome?

Answer 29

Buzzword is tram-track calcifications with gyriform cortical and subcortical parenchymal calcifications. Associated features include the classic facial port wine stain in a V1 ophthalmic division of the trigeminal nerve distribution. Childhood seizures are common.

Question 30

What are some intracranial lesions that frequently calcify in tuberous sclerosis?

Answer 30

Cortical and subcortical tubers and subependymal hamartomas are common lesions in tuberous sclerosis that commonly calcify. Note that calcification of these lesions typically starts in childhood with the cortical and subcortical tubers often showing calcification by age 2.

Question 31

Answer 31

Hydatid cyst lung

Question 32

Answer 32

hydatid cyst liver

The cysts often get peripheral calcifications and if the peripheral calcification is complete so you have complete rim calcification that often denotes inactive hydatid disease. On a plain film you can see large curvilinear or rounded calcification(s) that should make you consider hepatic hydatid disease.

Question 33

asymptomatic patient. incidental finding.

Answer 33

Randall’s plaques

These are subendothelial deposits of calcium carbonate or calcium phosphate within the loops of Henle within the kidney. These appear hyperdense on an abdominal CT but are not renal stones. Key is that these are abutted by 50% or greater renal parenchyma—they are intimately associated with the renal papilla and renal parenchyma. These are often thought to denote an increased risk of stone formation.

Question 34

Answer 34

medullary sponge kidney

associations:

• Ehlers-Danlos syndrome
• congenital hemihypertrophy / Beckwith-Wiedemann syndrome (rare)
• Caroli disease