Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

@xirurgi_2025 - 329 - файл

.pdf

Скачиваний:

Добавлен:

28.08.2026

Размер:

56 Мб

Скачать

☆

<<< < Предыдущая 1 2 34 / 504 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 > Следующая >>>

(b)

(a)

Pancreatic nerve plexuses (cross-sectional diagram)

Extrapancreatic nerve plexuses

Duodenum PL ph II

PL sma: Superior mesenteric arterial

SMA

Downloaded from https://onlinelibrary.wiley.com/doi/ by Universität Bern, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

https://t.me/medicina_free

PL ph I

Aorta

Histology andUltrastructure 15

SMA

Pancreas

Right kidney

Duodenum

Figure2.9 Nerves (yellow) serving the pancreas. The cross- sectional image (a) emphasizes the location of the celiac ganglia of the

autonomic system lateral to the aorta while (b) emphasizes the rich nerve plexus that connects these ganglia to the pancreas. SMA, superior mesenteric artery; PL, plexus. Source: Classification of Pancreatic Carcinoma, 2003[7]. Reproduced with permission of the Japan Pancreas Society.

Celiac ganglion

Inferior vena cava

Right celiac ganglion

Left kidney

PL ph I

PL ph II

Uncinate process

PL sma

PL ce

Left celiac ganglion

PL ph I: Pancreatic head plexus I

plexus

PL hdl: Plexus within the hepato duodenal ligament

PL ce: Celiac plexus

PL ph II: Pancreatic head plexus II

PL cha: Common hepatic artery plexus

PL sp: Splenic plexus

homogeneous densities. These are nascent zymogen granules (also termed immature zymogen granules or condensing vacuoles) and they progressively lose membrane as contents condense to become mature zymogen granules.

The apical cytoplasm near the acinar lumen is occupied by variable numbers of mature zymogen granules. These are usually spherical (appearing round in crosssection) with a single bilayer membrane surrounding homogeneous dense content (see Figs 2.12, 2.13, 2.18, and2.22). Fusion of the membranes of zymogen granules and adjacent lumenal cell membrane is observed prior to secretion of the zymogen into the lumen. See Longnecker[1] for additional electron micrographs that illustrate acinar cell ultrastructure.

Acinar cell cytoplasm may contain fat or autophagic vacuoles (sometimes called residual bodies) that are walled- off areas of damaged cytoplasm (Fig.2.12).

Duct System

The components of the duct system are the main pancreatic duct (duct of Wirsung); its major branches, called interlobular ducts, that drain into the main duct throughout the pancreas as depicted in Fig.2.2; smaller intralobular ducts; and ductules that link acinar tubules to the smallest intralobular ducts. The small intralobular ducts and ductules are ordinarily seen only at the level of light and electron microscopy. The accessory duct (duct of Santorini; Fig. 2.2) that connects the main duct to the duodenum at the minor papilla in some humans (Fig.2.3) is of variable importance and is similar in structure to the main duct, although typically it is slightly smaller.

Enzymes from acinar cells are released into a bicarbonate- rich solution that is secreted by the centroacinar and ductal cells and flows from the acini and

https://t.me/medicina_free

Figure2.10 Pancreatic lobular tissue with acinar cells, small duct,

ductule, and small islet. This H&Eof acini and acinar tubules cut in crossAsmall intralobular duct (a) is shown image right and at its upper end it gives rise to a ductule (b) with virtually no connective tissue evident in its wall. Liquid content of the duct and ductule is homogeneous and pink (eosinophilic). Large, clear spaces are fat cells (c). A small vein (d) and artery (e) are at image right above center. A small islet is near the lower image right corner. Source: Hruban RH, Pitman MB, Klimstra DS. Tumors of the pancreas. AFIP Atlas of Tumor Pathology, 4th series, fascicle 6. Washington, DC: American Registry of Pathology; 2007. Reproduced with permission.

stained section is largely composed

section or tangentially.

Figure2.12 Acinar cells with RER, mature, and immature

zymogen granules. Two centroacinar cells are near the center. Theacinar cell at 3 o’clock, image right, is binucleate. Numerous mitochondria are present in the acinar cells. There are several electrontwo have been extruded into theinterstitial space at the top of the image and others are being extruded into the acinar lumen near the center of the image. These pathways for clearing the cell of autophagic vacuoles and residual bodies have been documented in an animal model (rat) of acute pancreatitis[14]. Source: Micrograph contributed by James Jamieson.

dense residual bodies in the acinar cells. It appears that

Figure2.11 Pancreatic tissue with acinar, centroacinar, and ductal

cells. The acinar cells are easily identified because of the darkly stained zymogen granules (ZG) and are larger than centroacinar and ductal cells. The basal portion (B) of the acinar cells lies next to the interstitial space that contains vessels (V), nerves, and connective tissue. Nuclei (N) with nucleoli (n) are in the basal portion of the acinar cells. The Golgi (G) lies at the junction of the basal (B) and apical (A) portions of the cell that borders the lumen (L) of the acinus. Centroacinar cells (CAC) have pale cytoplasm with no secretory granules. A small ductule (D) extends from image right to below center. Mitochondria (m) are identified at the top of the field. This is a 1 μm thick section of plastic embedded tissue prepared for electron microscopy that was stained with toluidine blue. Source: Micrograph contributed by James Jamieson.

Figure2.13 Apical portions of several acinar cells border two

luminal spaces, lower image right and upper image left. A centroacinar cell with numerous mitochondria borders the lumen, lower image right. Microvilli protrude into the lumens from the luminal aspect of the acinar and centroacinar cells. Zymogen granules are prominent in all acinar cells. Source: Micrograph contributed by James Jamieson.

(a) (b)

(c)

(d)

https://t.me/medicina_free

Histology andUltrastructure 17

Figure2.14 Serial cross- sections of main pancreatic duct (a) (H&E stain) stained to demonstrate collagen (b) (trichrome stain),

myofibroblasts (c) (immunoperoxidase stain to demonstrate smooth muscle actin, a marker for myofibroblasts), and smooth muscle (d) (immunoperoxidase stain to demonstrate desmin, a marker for smooth muscle). The lining epithelium has been lost, probably reflecting preoperative ERCP and stenting of the pancreatic duct. The patient underwent a Whipple procedure because of chronic pancreatitis. There are many myofibroblasts and fewer smooth muscle cells in the wall of the main duct. Source: Micrographs contributed by Arief A. Suriawinata.

acinar tubules into the ductules that join to form the intralobular ducts, then into the interlobular ducts and main duct, and finally into the duodenum at the major or minor papillae. Ducts are illustrated in Figs 2.10, 2.11,

2.14, 2.15, and2.16. The integrity of the duct system is of key importance in

preventing entry of the exocrine enzymes into the interstitial space, where they may be activated and cause tissue damage manifested as pancreatitis. As ductules anastomose to form intralobular ducts, the duct walls begin to develop a connective tissue wall (Fig.2.10) that becomes progressively thicker as the smaller ducts join to form larger ducts and the main pancreatic duct. The main and interlobular ducts have thick, dense, collagenous walls that contain myofibroblasts and smooth muscle cells (Fig.2.14). The connective tissue component of the duct wall becomes progressively thinner and contains fewer myofibroblasts and smooth muscle cells as the

ducts branch and become narrower in the lobules (Fig.2.15). The smallest intralobular ducts lack smooth muscle cells. Intercellular tight junctions, also called zonula occludens, between duct cells, centroacinar cells, and acinar cells play a major role in preventing leakage of the duct system. Kern provided excellent images and discussion of these tight junctions[15].

The lumen of the duct system is normally lined by a single layer of cuboidal epithelial cells that have a single nucleus and a smaller amount of cytoplasm than acinar cells (Figs2.10, 2.15, and2.16). The cytoplasm is pale pink and homogeneous in H&E

- stained sections. The duct lumen may contain homogeneous material reflecting the protein content of the secretions (Figs 2.10 and 2.16). Sometimes epithelial cells may be shed into the lumen.

Ductal epithelium may undergo squamous metaplasia or mucinous metaplasia. In the latter process, the ducts are lined by tall columnar cells with abundant pale apical

Anatomy, Histology, andFine Structure ofthe Pancreas

(a) (b)

(c)

https://t.me/medicina_free

Figure2.15 Serial cross- sections of a small intralobular duct surrounded by acinar tissue from the same patient as in Fig.2.14. (a) H&E

stain. Note the origin of a ductule branching into acinar tissue at 7 o’clock. (b) Trichrome stain with blue- staining collagen. There is fibrosis around acinar lobules (upper image left). (c) Immunoperoxidase stain with antibody to smooth muscle actin (SMA) to demonstrate the abundant myofibroblasts. (d) Immunoperoxidase stain with antibody to desmin to demonstrate smooth muscle cells. There is little staining. Source: Micrographs contributed by Arief A. Suriawinata.

(d)

cytoplasm that contains mucin. This type of change is characteristic of low- grade pancreatic intraepithelial neoplasia (PanIN) lesions and is possibly an early step in the development of PanIN.

At the ultrastructural level, duct cells have a simple

structure compared with acinar cells. RER is sparse but

mitochondria are numerous, and there are no secretory granules. The luminal surface gives rise to numerous microvilli, similar in appearance to those arising from acinar cells (Fig. 2.13). Ductal cells have single cilia, although they are difficult to detect without special tissue preparation and labeling[16].

Figure2.16 Pancreas ductule (top center) branches (upper image

https://t.me/medicina_free

right) to reach several acini or acinar tubules (upper image right and near the center). Blue zymogen granules are conspicuous in the acinar cells and the liquid content of the ductule is also dark blue. Ductal and centroacinar cells have pale cytoplasm. The presence of numerous round empty capillaries (arrows) in the interstitial spaces indicates that the pancreas was perfused with fixative. Toluidine blue stain, 1 Source: Micrograph contributed by James Jamieson.

μm thick plastic embedded tissue.

Endocrine Pancreas 19

Figure2.17 Pancreatic stellate cell (PSC) from a patient with

acutepancreatitis. The PSC is near a macrophage (Ma), image right, and an acinar cell (Ac), image left. Fat droplets (F) and RER are conspicuous in the PSC cytoplasm below the nucleus (N). Original magnification 6000×. Source: Bachem etal. 1998[17].

Interstitial Tissue

The interstitium contains capillaries, arteries, veins, lymphatics, nerve fibers, fat cells, and stellate cells. The stellate cells are undifferentiated connective tissue cells with characteristic structure (Figs2.17 and2.18) that are activated by inflammation to form fibroblasts and contribute to fibrosis associated with chronic pancreatitis and some neoplasms[17] (see Chapter10).

Endocrine Pancreas

The pancreatic islets (islets of Langerhans) collectively comprise the endocrine pancreas that synthesizes and secretes insulin, glucagon, pancreatic polypeptide, and somatostatin. Most islets are too small to be seen by gross examination, hence they were not depicted in Figs2.1 to 2.7. Islets vary greatly in size and ~70% are in the size range 50–250 μm in diameter in humans, with an average in the range 100–150 μm [18]. Small islets are dispersed throughout the acinar lobules (Fig. 2.19) and most larger islets lie along the main and interlobular ducts of the pancreas. Most islets are spherical or ellipsoid, but they can be irregular in shape— sometimes reflecting the presence of an adjacent structure, often a duct, or limitation by a tissue plane. Several reports provide support for the presence of a higher population

Figure2.18 A pancreatic stellate cell (PSC) in situ is surrounded

by multiple acinar cells containing zymogen granules. Extensions of PSC cytoplasm between acinar cells are conspicuous, upper image right and lower image left. The dark, irregular cytoplasmic inclusions at the origin of the latter interstitial extension may represent lipid droplets— a characteristic of PSC. Source: Contributed by the Pancreatic Research Group, UNSW, Australia, with special thanks to Dr. Murray Killingsworth.

Anatomy, Histology, andFine Structure ofthe Pancreas

(b)(a)

https://t.me/medicina_free

Figure2.19 Pancreatic lobules with acinar cells and four islets at

12, 3, 6–7, and 9 o’clock. The islets are paler than the surrounding acinar tissue. The upper and lower islets are small and the lateral islets are medium size. H&E stain.

density of islets in the tail of the pancreas than in the head and body[5,19], although another study found no difference[20]. In adult humans, the number of islets is estimated to be 5 × 105–106 [21], whereas there are far fewer in smaller animals [22]. Islets comprise 1–2% of the pancreas in adults of most mammalian species. In addition to the islets, isolated islet cells may be found dispersed in the acinar lobules or in association with ducts.

Several of the images of islets are from sections that have been immunostained using antibodies to specific islet peptide hormones to demonstrate various islet cell types, including β cells (insulin), α cells (glucagon), δ cells (somatostatin) (Fig. 2.20), and pancreatic polypeptide (PP) (Fig. 2.21). In the portion of the pancreas derived from the dorsal pancreatic anlage, the majority of islet cells are β cells (75–80%), followed by α cells (about 15%), δ cells (about 5%), and very few PP cells. Most PP cells are in the portion of the pancreas derived from the ventral

(c)

Figure2.20 Serial sections of a human islet immunostained using antibodies to insulin (a), glucagon (b), and somatostatin (c). The

presence of the hormones is indicated by brown staining. The predominance of insulin- secreting β cells is obvious. In (b) and (c), the location of α cells and δ cells is primarily at the border of groups of β cells. Source: Photos provided by Arief A. Suriawinata.

Figure2.21 Mouse islet stained to demonstrate pancreatic

https://t.me/medicina_free

polypeptide (red) and insulin (green). Immunofluorescence using antibodies to insulin and neuropeptide Y (NPY) that crosswith PP. Source: Micrograph contributed by Susan Bonner- Weir.

Figure2.22 Mouse islet with β- cell cytoplasm containing insulin

granules (image left), a δ cell with nucleus and less dense secretory granules (right of center), and αglucagon granules (upper image right corner) and at the bottom margin near the center. In murine species, β- cell granules have a wide halo surrounding the dense core. Acinar cell cytoplasm with zymogen granules, RER, and mitochondria is present (lower image right). Source: Micrograph contributed by Fred Gorelick.

cell cytoplasm with

reacts

pancreatic anlage, namely the uncinate process that is reported to comprise about 10% of the pancreas[23,24]. In the uncinate process, islets contain few α cells and many more PP cells. Stefan etal. presented data from a study of 13nondiabetic human pancreases, showing that the PP cells comprise 54.3–93.7% of the volume of islets in the uncinate region, displacing most α cells and some

Acknowledgments 21

Figure2.23 Human islet from transplant isolation with α, β, and δ

cells labeled. The α- cell granules are typically slightly larger than β- cell granules; δ- cell granules are typically less densely stained

than the granules in α and β cells. The cytoplasm of several islet cells contains lipid— most notably in the central β cell where lipid bodies lie at 4 and 11–12 o’clock around the nucleus. Source: Micrograph contributed by Susan Bonner- Weir.

β cells [24]. They provided data that indicated that PP cells were the second most prevalent endocrine cell type overall in the pancreases of their 13 subjects.

At the ultrastructural level, islet cells contain numerous mitochondria, a modest amount of RER, and small secretory granules (islet hormones). The granules vary in size and density with cell type and hormone and show some variation between species (Figs2.22 and2.23).

Capillaries in the islets connect with capillaries serving the adjacent acinar cells before draining into veins. These proximal acinar cells are exposed to higher concentrations of islet hormones than the majority acinar cells that are more distant from islets. The proximal acinar cells sometimes are larger and contain more zymogen than more distant acinar cells, and they form a halo around the islets. This unique feature of islet–acinar blood supply has been referred to as an insulo- acinar portal system[25].

Acknowledgments

The authors thank Fred Gorelick who contributed as a coauthor of this chapter in the previous edition of this book and Dale Bockman for reviewing the section that reflects his work on microanatomy of the acinar lobules. Figures 2.2, 2.3, 2.7, 2.8, 2.9, 2.11, 2.16, 2.20, and 2.23 have been published previously online in a Pancreapedia chapter on anatomy and histology of the pancreas [1]. The authors thank the contributors of many of the images as listed in the captions.

Anatomy, Histology, andFine Structure ofthe Pancreas

https://t.me/medicina_free

References

Several of the references are chapters in Go VLW, DiMagno EP, Gardner JD et al., eds. The Pancreas: Biology, Pathobiology, and Disease, 2nd edn. NewYork: Raven Press, 1993. These may be downloaded at https:// journals.lww.com/pancreasjournal/Pages/the- pancreas_ bio_pathobio_disease.aspx

1 Longnecker DS. Anatomy and histology of the pancreas.

Pancreapedia: Exocrine Pancreas Knowledge Base. Miami: American Pancreatic Association, 2014. DOI: 10.3998/ panc.2014.3; https://www.pancreapedia.org/reviews/ anatomy- and- histology- of- pancreas (accessed November 30, 2021).

2 Hruban RH, Pitman MB, Klimstra DS. Tumors of the

pancreas. AFIP Atlas of Tumor Pathology, 4th series, fascicle

6. Washington, DC: American Registry of Pathology, 2007.

3 Bockman DE. Anatomy of the pancreas. In: Go VLW,

DiMagno EP, Gardner JD etal., eds. The Pancreas: Biology, Pathobiology, and Disease, 2nd edn. NewYork: Raven Press, 1993: 1–8.

4 Hellman B. Actual distribution of the number and volume

of the islets of Langerhans in different size classes in non

- diabetic humans of varying ages. Nature

1959;184(Suppl 19):1498–1499.

5 Wittingen J, Frey CF. Islet concentration in the head, body,

tail and uncinate process of the pancreas. Ann Surg 1974;179(4):412–414.

6 Kamisawa T, Amemiya K, Tu Y etal. Clinical significance

of a long common channel. Pancreatology 2002;2:122–128.

7 Japan Pancreas Society. Classification of Pancreatic

Carcinoma, 2nd Engl. edn. Tokyo: Kanehara, 2003: 57.

8 Bockman DE, Boydston WR, Parsa I. Architecture of

human pancreas: implications for early changes in pancreatic disease. Gastroenterology 1983;85:55–61.

9 Bockman DE. Cells of origin of pancreatic cancer:

experimental animal tumors related to human pancreas. Cancer 1981;47:1528–1534.

10 Bockman DE. Morphology of the exocrine pancreas related

to pancreatitis. Microsc Res Tech 1997;37:509–519.

11 Bockman DE. Toward understanding pancreatic disease:

from architecture to cell signaling. Pancreas 1995;11:324–329.

12 Morgan RG, Schaeffer BK, Longnecker DS. Size and

number of nuclei differ in normal and neoplastic acinar cells from rat pancreas. Pancreas 1986;1(1):37–43.

13 Oates PS, Morgan RG. Changes in pancreatic acinar cell

nuclear number and DNA content during aging in the rat. Am J Anat 1986;77(4):547–554.

14 Longnecker DS. Fate of autophagic vacuoles in acinar cells

during pancreatitis. Pancreas 2019;48(9):E71–E75.

15 Kern HF. Fine structure of the human exocrine pancreas.

In: Go VLW, DiMagno EP, Gardner JD etal., eds. The Pancreas: Biology, Pathobiology, and Disease, 2nd edn. NewYork: Raven Press, 1993: 9–19.

16 Aughsteen A. The ultrastructure of primary cilia in the

endocrine and excretory duct cells of the pancreas of mice and rats. Eur J Morphol 2001;9(5):277–283.

17 Bachem MG, Schneider E, Gross H etal. Identification,

culture, and characterization of pancreatic stellate cells in rats and humans. Gastroenterology 1998;115(2):421–432.

18 Hellman B. The frequency distribution of the number and

volume of the islets of Langerhans in man. Acta Soc Med Upsal 1959;64:432–460.

19 Rahier J, Guiot Y, Goebbels RM, Sempoux C, Henquin JC.

Pancreatic beta

- cell mass in European subjects with type

2 diabetes. Diabetes Obes Metab 2008;10(Suppl 4):32–42.

20 Yoon KH, Ko SH, Cho JH etal. Selective beta- cell loss and

alpha

- cell expansion in patients with type 2 diabetes mellitus in Korea. J Clin Endocrinol Metab 2003;88(5):2300–2308.

21 Korc M. Normal function of the endocrine pancreas. In:

Go VLW, DiMagno EP, Gardner JD etal., eds. The Pancreas: Biology, Pathobiology, and Disease, 2nd edn. NewYork: Raven Press, 1993: 751–758.

22 Longnecker DS, Wilson GL. Pancreas. In: Haschek- Hock

WM, Rousseaux CG, eds. Handbook of Toxicologic Pathology. San Diego: Academic Press, 1991: 253–278.

23 Rahier J, Wallon J, Loozen S, Lefevre A, Gepts W, Haot J.

The pancreatic polypeptide cells in the human pancreas: the effects of age and diabetes. J Clin Endocrinol Metab 1983;56(3):441–444.

24 Stefan Y, Orci L, Malaisse- Lagae F, Perrelet A, Patel Y,

Unger RH. Quantitation of endocrine cell content in the pancreas of nondiabetic and diabetic humans. Diabetes 1982;31:694–700.

25 Lifson N, Kramlinger KG, Mayrand RR, Lender EJ. Blood

flow to the rabbit pancreas with special reference to the islets of Langerhans. Gastroenterology 1980;79(3):466–473.

https://t.me/medicina_free

Congenital andInherited Anomalies ofthe Pancreas

Heiko Witt1 and Martin Zenker

Pediatric Nutritional Medicine and Else Kröner Fresenius Center for Nutritional Medicine (EKFZ), Technical University of Munich (TUM), Freising,

Germany

Institute of Human Genetics, Otto- von- Guericke- University Magdeburg, Magdeburg, Germany

Introduction

Most congenital anomalies of the pancreas are attributable to disturbances in the three critical developmental steps: tissue differentiation, rotation, and fusion. Differentiation and rotation defects are usually rare, while defective fusion is common but mostly asymptomatic.

Primary Malformations

Pancreatic Agenesis

Complete (aplasia) or incomplete (hypoplasia) agenesis of the pancreas are very rare developmental disorders that can occur isolated or in combination with other defects such as polysplenia syndrome, congenital heart defects, or cerebellar agenesis. Their exact incidence is unknown. Partial agenesis is more common and is known as congenital short pancreas.

The clinical presentation is dependent on the degree of agenesis. Aplasia manifests clinically with neonatal diabetes mellitus, exocrine pancreatic insufficiency, and severe intrauterine growth retardation [1]. The lastappears to relate to the fact that insulin is a major intrauterine growth factor. Complete agenesis is incompatible with life, whereas the clinical presentation of hypoplasia varies from an asymptomatic course to endocrine and exocrine pancreatic insufficiency; pancreatitis may be an associated presentation. Pancreatic agenesis can be monogenic and half of the patients have heterozygous GAT A 6 mutations [2]. The pancreatic phenotype ranges from aplasia to hypoplasia and most patients have cardiac malformations. Other features include gallbladder agenesis,

mentioned

biliary atresia, developmental delay, transient hypothyroidism, pituitary agenesis, and intestinal abnormalities. GATA6 mutations have also been detected in a few patients with adult-

onset diabetes with subclinical or no

exocrine insufficiency[3].

In isolated families with autosomal recessive inheritance, defects in other genes have been described including pancreatic transcription factors PDX1 (also known as insulin promoter factor 1, IPF1) and PTF1A [4,5]. Pancreatic agenesis appears to be isolated in PDX1 mutated patients. Interestingly, heterozygotes are predisposed to maturity- onset diabetes of the young (MODY4); some patients show only subclinical or no exocrine insufficiency [4]. PTF1A plays a pivotal role in mammalian pancreatic development. PTF1A coding mutations cause pancreatic and cerebellar agenesis, whereas mutations in a PTF1A downstream enhancer cause isolated pancreatic agenesis[5,6]. Pancreatic agenesis associated with holoprosencephaly can be caused by defects in CNOT1[7].

In mice, a lack of hepatocyte nuclear factor- 1- beta (Hnf1b) leads to pancreas agenesis[8]. In humans, heterozygous HNF1B mutations are associated with renal cysts and diabetes syndrome. Some of these patients show pancreatic atrophy/hypoplasia and exocrine insufficiency[9].

Partial agenesis of the pancreas mostly affects the dorsal part [10]. With this entity only a pancreatic head is seen on imaging. Dorsal pancreatic agenesis may be isolated or associated with polysplenia syndrome and can be accompanied by diabetes and pancreatitis[11]. It has been observed in patients with PDX1- MODY. Since most of the islet cells are located in the absent distal pancreas, the risk of diabetes mellitus is increased[12].

The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Fourth Edition. Edited by Hans G. Beger, Markus W. Büchler, RalphH. Hruban, Julia Mayerle, John P. Neoptolemos, Tooru Shimosegawa, Andrew L. Warshaw, David C. Whitcomb, and Yupei Zhao. © 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd. Companion website: www.wiley.com/go/beger/thepancreas4e

Congenital andInherited Anomalies ofthe Pancreas

https://t.me/medicina_free

Ectopic Pancreas

In ectopic pancreas, also designated as heterotopic, aberrant or accessory pancreas, normally developed pancreatic tissue is anatomically separate from the gland and lacks ductal or vascular continuity. It can be found in various locations and can be made up of any cell found in the pancreas. Autopsy studies indicate that ectopic pancreas is quite common (0.5–15%), but its clinical manifestation is very rare[13]. In most cases, ectopic tissue is discovered in the submucosa of the stomach (particularly along the greater curvature of the antrum) and the duodenum (Fig. 3.1) as an incidental finding during endoscopy, where it appears as a 0.3–3 cm nodule. Other locations include the jejunum, ileum, a Meckel diverticulum, liver, spleen, biliary tract, mesentery, or umbilicus[12]. Although ectopic pancreas is primarily located in the submucosa, in some cases it is found in the muscularis or serosa.

The mechanisms leading to ectopic pancreas remain elusive. Misplacement of pancreatic cells into the developing gastrointestinal system, pancreatic metaplasia of other endodermal areas during embryogenesis, and an inaccurate differentiation of pluripotent endodermal stem cells are discussed.

Although ectopic pancreatic tissue can undergo

similar changes as the orthotopic pancreas, particularly cystic degeneration, ectopic pancreatitis, and even pancreatic cancer formation, in most cases ectopic pancreas remains asymptomatic. If patients with ectopic pancreas become symptomatic, this may be due to the mass effect, which can cause either obstruction of the intestinal passage (mainly in the prepyloric localization)[14] or bowel intussusception, gastrointestinal hemorrhage secondary to mucosal ulcerations close to the pancreatic tissue[15], pain secondary to pancreatitis, and exceptional malignant transformation[16].

Diagnosis is made endoscopically or radiographically in antral localization. In other localizations, diagnosis is made at the time of surgery. The definite diagnosis relies on histology. The treatment is either surgical or endoscopic.

Annular Pancreas

In annular pancreas, the duodenum is completely, or rarer partly, surrounded by a ring- like band of pancreatic tissue. Early autopsy and surgical series reported an incidence of 3in 20,000 but the increased use of imaging has raised the incidence to approximately 1in 1,000.

Figure3.1 Ectopic pancreas under endoscopic vision and during endoscopic snare dissection (top images) and histologically (bottom

panels, right cytokeratin staining). Note the complete absence of endocrine cells on histology, which corresponds to a type II ectopic pancreas according to Heinrich (1909). Source: Courtesy of M. Androshchuk and G. Lorenz, Greifswald.

<<< < Предыдущая 1 2 34 / 504 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 > Следующая >>>

Соседние файлы в папке @xirurgi_2025

#
28.08.202658 Мб0@xirurgi_2025 - 319 - файл.pdf
#
28.08.202657 Мб0@xirurgi_2025 - 322 - файл.pdf
#
28.08.202657 Мб0@xirurgi_2025 - 324 - файл.pdf
#
28.08.202657 Мб0@xirurgi_2025 - 326 - файл.pdf
#
28.08.202657 Мб0@xirurgi_2025 - 328 - файл.pdf
#
28.08.202656 Мб0@xirurgi_2025 - 329 - файл.pdf
#
28.08.202656 Мб0@xirurgi_2025 - 330 - файл.pdf
#
29.08.202656 Мб0@xirurgi_2025 - 331 - файл.pdf
#
29.08.202656 Мб0@xirurgi_2025 - 332 - файл.pdf
#
29.08.202656 Мб0@xirurgi_2025 - 334 - файл.pdf
#
29.08.202655 Мб0@xirurgi_2025 - 335 - файл.pdf