Cross-sectional imaging often reveals unexpected pancreatic cystic lesions, it is a frequent clinical problem, Should we observe or remove it? What's the diagnosis? Is our patient in danger of malignancy?
Don’t miss this @aegastro @my_ueg #EducAEG #UEGambassador twitter thread

Importance of Pancreatic Cystic Neoplasms (PCN):
Most are asymptomatic at diagnosis, frequency increases with age
Symptoms: acute pancreatitis (Wirsung obstructed by the cyst or mucus), pain, obstructive chronic pancreatitis, jaundice
> symptoms, >malignancy risk!
Classification of PCN:
Mucinous: intraductal papillary mucinous neop. and mucinous cystic neop.
Nonmucinous: serous cystic neoplasm, solid pseudopapillary neoplasm and cystic neuroendocrine tumours
Endoderm- derived columnar epithelium is characteristic for mucinous lesions
👇
Intraductal papillary mucinous neoplasms (IPMN)
Characterized by papillary proliferation+mucus production. It may involve Wirsung (becomes dilated) and/or branch ducts (cysts connected to the ductal system). It may evolve to pancreatic cancer particularly if Wirsung is involved
IPMN subtypes :
Intestinal: main duct, head, 40%->coloid/tubular adenoca
Pancreatobiliary: main duct,head, 68%->tubular adenoca
Oncocytic: rare, nodules,50%-> coloid/tubular adenoca
Gastric: most frequent, branch-type, uncinate, 10%->tubular adenoca
https://t.co/CyvfrBGrXZ
IPMN: risk factors for malignancy
Main duct involvement (60% in resected specimens vs 10 to 30% in resected side branch IPMNs), specially>1cm
Contrast-enhanced mural nodules
Size>3-4cm
Symptoms
Pts at risk of PDAC even in other regions of the gland without involvement
👇👇👇
Intraductal papillary mucinous neoplasms -> management: follow these guidelines:
European guidelines 2018 @Gut_BMJ @chiaro_del @MarcBesselink https://t.co/x8waod12xr
Fukuoka 2017 @pancreatology@SalviaRobi https://t.co/PaEYljt5N9
Mucinous Cystic Neoplasms (MCN)
Characterized by mucinous epithelium and ovarian-type stroma, in body/tail
It is described as macrocystic, septated cyst with small number of cavities, it may have eccentric calcifications, no connection to ductal system
95% women, 5-7th decades
MCN:
>risk malignancy:
≥5cm
Nodules/mass
Thickened/irregular Wall
Calcifications
Management of MCN according to the European guidelines: a conservative approach is recommended for asymptomatic MCN measuring <40 mm without an enhancing nodule
https://t.co/x8waod12xr
@chiaro_del @MarcBesselink @Gut_BMJ
Serous cystic neoplasm (SCN). Cuboidal epithelium without dysplasia
70% women, 5-7th decades, NON-MUCINOUS solitary lesion
Classic SCN is microcystic (multiple small cysts, honeycomb-like) but can be macrocystic or solid. A central scar or calcification can be present
SCN management: remove only if symptoms, for example this case from @Dhgua, the patient had jaundice due to a a massive SCN, a Whipple procedure was performed
Cystic neuroendocrine tumor
It is a pancreatic NET with a central cystic changes. Solitary lesion, 5-6th decades, frequently with wall contrast enhancement, 10% malignant potential
Cystic neuroendocrine tumor management: asymptomatic and <2 cm you may follow the patient https://t.co/8EhhAet35T
It seems that these cystic NET are less aggressive than solid NET
Finally,solid pseudopapillary neoplasm
They have malignant potential(15%), >risk if >5 cm
Young women=90% (2-3rd decades),body/tail.Solid and cystic solitary masses, calcifications,often with intracystic bleeding.They can spread to the peritoneum or distant organs like the liver
This twitter thread was based on:
https://t.co/dAuGI0qzLK
https://t.co/x8waod12xr
https://t.co/Ywp7zQF2wE
And Pancreatic cystic neoplasms, several articles from @UpToDate Editors: JR Saltzman S Grover Authors: Asif Khalid, MDKevin McGrath, MD https://t.co/nYN3MKTnl8
If you liked this twitter thread, please retweet the first tweet and follow me! #PancreasTwitter

I hope you enjoyed it, it took me a lot of effort to do this! 😅
@drdalbir @BilalMohammadMD @KralJan @drkeithsiau @MZorniak @DCharabaty @RashidLui @SunilAminMD @SanchezLunaMD @stevenbollipo @Samir_Grover @RishadJkhan @drmoutaz @RodriguezParra_

More from Health

1/16
Why do B12 and folate deficiencies lead to HUGE red blood cells?

And, if the issue is DNA synthesis, why are red blood cells (which don't have DNA) the key cell line affected?

For answers, we'll have to go back a few billion years.


2/
RNA came first. Then, ~3-4 billion years ago, DNA emerged.

Among their differences:
🔹RNA contains uracil
🔹DNA contains thymine

But why does DNA contains thymine (T) instead of uracil (U)?

https://t.co/XlxT6cLLXg


3/
🔑Cytosine (C) can undergo spontaneous deamination to uracil (U).

In the RNA world, this meant that U could appear intensionally or unintentionally. This is clearly problematic. How can you repair RNA when you can't tell if something is an error?

https://t.co/bIZGviHBUc


4/
DNA's use of T instead of U means that spontaneous C → U deamination can be corrected without worry that an intentional U is being removed.

DNA requires greater stability than RNA so the transition to a thymine-based structure was beneficial.

https://t.co/bIZGviHBUc


5/
Let's return to megaloblastic anemia secondary to B12 or folate deficiency.

When either is severely deficient deoxythymidine monophosphate (dTMP*) production is hindered. With less dTMP, DNA synthesis is abnormal.

[*Note: thymine is the base in dTMP]

https://t.co/AnDUtKkbZh

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