The pancreas is one of the most important organs in the

body, especially when it comes to the breakdown of

dietary fats and lipids. It is known as one of the body’s
main source of lipases (enzymes that break down fat
into simpler molecules) which is why it can have such
dire consequences when infected. Because the pancreas
is so vital to something as important as fat digestion, it
comes as no surprise how it can be affected by a myriad
of pathologic events.

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Most often when people think of a pancreatic infection,
they think of something like acute pancreatitis. Acute
pancreatitis is a disease of the pancreas involving
swelling as well as necrosis, and it happens to be the
most common gastrointestinal disease leading to acute
hospitalization.3 The disease itself is becoming more
commonly seen in today’s society, and cases have only
seen an increase within the last two decades. 7
 
Looking at the pancreas specifically, one might wonder
how the organ keeps itself from getting digested on an
everyday basis. To keep autodigestion from occurring in
a healthy pancreas, the body has multiple mechanisms
in place. These protective mechanisms are maintained
intracellularly due to the presence of a mucous film for
added protection around the duct epithelium, through
the use of zymogens (inactive precursors) which do not
become activated until a specific set of criteria are met,
and through a system of enzyme inhibitors circulating
throughout the bloodstream in case pancreatic juices
happen to escape.1 Although these methods are all
equally important to ensure pancreatic enzymes are
maintained, one of the most significant protective
mechanisms involved is the use of a one-way
permeability system to ensure the enzymes, once they
are cleaved and activated, cannot return to the
pancreatic cells from which they came.1   

Having all these protective systems in place, it would

seem as if there were no possible way of causing
damage to the pancreas nor to the areas around it.
Seeing as how pancreatitis exists, however, shows
evidence these systems can and will be avoided
depending on the pathology being looked at. Whenever
these digestive enzymes leak out and cause
autodigestion to surrounding cells, this usually points to
a breakdown of the protective mechanisms listed above.
Most often, the cause of acute pancreatitis is due to
damage of the pancreatic ducts leading to changes in
the vasculature permeability.6 In a healthy pancreas, the
ducts are only permeable to contents of a certain size,
but when alcohol or some other damaging agent comes
into play, the cells of the pancreatic duct experience
increased permeability allowing enzymes and other
similarly sized molecules to leak out into the
surrounding interstitial space. This may be one of the
reasons why heavy alcohol consumption is seen as one
of the causes for acute pancreatitis- because it can
change the permeability of the ducts in such a drastic
way.

Once the permeability of the ducts has been altered and

the enzymes have leaked out into the extracellular
space, many damaging events take place. As mentioned
earlier, pancreatic enzymes are created and stored in the
pancreas as inactive zymogens before being sent out to
the duodenum of the small intestine where a majority of
the body’s digestion takes place. Once in the small
intestine, the zymogens undergo a conformational
change as a result of the physiological aspects of the
duodenum and become activated. If these zymogens
leak out into the interstitial space separate from the
small intestine though (such as in acute pancreatitis),
they become activated simply due to the physiological
conditions maintained within that particular space. As it
turns out, the proteolytic zymogens and other enzymes
residing in the pancreatic juice are extremely easy to
activate, especially in patients with pancreatitis who have
an overactive amount of proteolytic activity.4  This
increased activity only leads to a greater amount of
inflammation and damage, so unless scientists find more
efficient ways to inactivate leaked zymogens, the break-
down of cellular components at and near the pancreas
will only continue.

Whenever patients are suffering from acute pancreatitis,

one of two things can happen. The patient can either be
labeled as having edematous interstitial pancreatitis or,
in more severe cases, as having necrotizing
pancreatitis.2 In most cases when the pancreatitis is on
the milder side (as is the case with edematous interstitial
pancreatitis) it is able to resolve within a few months of
treatment. If a patient has a more intense form of the
disease, however, then a fatal outcome including
multiple organ failures can result. On a positive note,
only about 20% of patients suffering from pancreatitis
will have it progress to the more aggressive form3 with
the remaining 80% having a rapid improvement within
days of receiving treatment.2

Referring to the unlucky few who have their pancreatitis

progress to the necrotizing form, the pancreatitis
becomes a lot more difficult to treat. When someone is
suffering from necrotizing pancreatitis, a complicated
course follows along with the release of multiple toxic,
septic, and vasoactive agents from the infected
pancreatic gland.2 This release of agents leads to many
drastic effects and can even cause injury to systems
separate from the digestive system such as the
cardiovascular and renal systems.
Not only does pancreatitis damage other systems, but
the fat storage cells surrounding the pancreatic area as
well. When acute pancreatitis reaches its necrotizing
form, it is often referred to by physicians as
peripancreatic fat necrosis,3 and the reason for this may
be because of the fat necrosis that occurs in the area
surrounding the pancreas once pancreatic lipases are
released. These lipid digesting enzymes, once activated,
will break down any kind of triglyceride storing cell it
comes into contact with- most notably the adipocytes
residing in adipose tissue. After these cells have been
destroyed, the dead cells will accumulate and cause
further damage to the area as fat necrosis begins to
occur, and as fat necrosis continues to worsen in the
pancreatic area, infected patients become increasingly at
risk for persistent systemic inflammatory response
syndrome and, in some cases, organ failure.3

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 One specific way fat necrosis associated with acute
pancreatitis can be characterized is if there are any ghost
cells present. Ghost cells are simply cells damaged by
pancreatic enzymes and can be viewed microscopically
after taking a sample from the patient.8 Along with the
presence of ghost cells, an increase in calcium and free
floating fatty acid molecules to the affected area are
excellent indicators for fat necrosis as well, which is why
doctors often look for these before diagnosing someone
with pancreatitis. The reason this is such a great
indicator is because once cells lose their membrane
integrity due to the presence of digestive enzymes, their
intracellular storages of calcium and fatty acids get
released and may even combine to form basophilic
calcium deposits- yet another characteristic of acute
pancreatitis. This means evidence for pancreatitis cannot
just be diagnosed through the presence of ghost cells,
but through histological stains as well.

 Another more obvious yet vague component of

identifying pancreatic fat necrosis is the presence of
inflammation. One would expect the inflammation to be
a result of inflammatory infiltration but seeing as how
there is an absence of infiltrate in the area7 of an
infected patient, a more likely cause for this could be the
presence of all the necrotic cells in the area. One other
possible cause for the inflammation of these cells is
STING signaling. STING signaling, when studied in
patients with acute pancreatitis, has been found to
promote inflammation of the cells, at least at the
experimental level.Researchers were able to find how
STING (a transmembrane protein found in macrophages)
causes inflammation in pancreatic cells after sensing
acinar cell death in the area.9 This seems to act as a
safety mechanism to keep inflammation from occurring
before acinar cell death has been detected. If the
macrophages could promote inflammation whenever
they wanted, many harmful effects could arise.

 Although most people can be treated for acute

pancreatitis within a matter of months, scientists are still
looking for ways to treat the more advanced form of the
disease within a shorter period. Currently, researchers
are working on discovering new strategies to overcome
this disease, some of which involve nutritional
intervention due to its possibility of maintaining gut
barrier functionality.5 Researchers are consistently trying
to discover therapeutic agents that will allow for the
maintenance of the small intestine barrier due to how
necessary it is for everyday function and in keeping
intestinal bacteria from spreading. If the gut barrier is
unable to be sustained, further damage will result as well
as the progression of the disease overall.

  Noting how acute pancreatitis and its progression can

be the result of multiple etiological factors, it can be said
further research needs to be done both on stopping it
from spreading and in preventing it from occurring in
the first place. Albeit some forms of treatment have
been discovered, scientists have yet to find an agent that
targets acute pancreatitis specifically, which may be a
reason as to why it is such a common gastrointestinal
disorder. It should be of utmost importance to discover
an overall cure for the disease seeing as how so many
people are affected by it, and until specific treatment
can be found, people are only going to continue to
suffer.

References Cited:

 Becker, V. “Acute Pancreatitis: A Brief Introduction

of the Pathology.” Acute Pancreatitis, 1987, pp. 3–6.,
doi:10.1007/978-3-642-83027-3_1.
 Beger, H. G., et al. “Prognostic Criteria in Necrotizing
Pancreatitis.” Acute Pancreatitis, 1987, pp. 198–200.,
doi:10.1007/978-3-642-83027-3_26.
 Bouwense SAW, Gooszen HG, van Santvoort HC,
Besselink MGH, Chapter 91 – Acute Pancreatitis,
Editor(s): Charles J. Yeo, Shackelford’s Surgery of the
Alimentary Tract, 2 Volume Set (Eighth Edition),
Content Repository Only!, 2019, 1076-1084, ISBN
9780323402323, https://doi.org/10.1016/B978-0-
323-40232-3.00091-1.
 Figarella, C., et al. “Enzyme Activation and
Liberation: Intracellular/Extracellular Events.” Acute
Pancreatitis, 1987, pp. 53–60., doi:10.1007/978-3-
642-83027-3_8.
 Li-Long Pan, Jiahong Li, Muhammad Shamoon,
Madhav Bhatia, Jia Sun. Corrigendum: Recent
Advances on Nutrition in Treatment of Acute
 Pancreatitis. Frontiers in Immunology, Vol 9 (2018).
2018. doi:10.3389/fimmu.2018.00849/full.
 Reber, H. A. “Changes in Duct and Vascular
Permeability: The Key to the Development of Acute
Pancreatitis.” SpringerLink, Springer, Berlin,
Heidelberg, 1 Jan. 1987,
link.springer.com/chapter/10.1007/978-3-642-
83027-3_7.
 Sepúlveda EVF, Guerrero-Lozano R, Acute
pancreatitis and recurrent acute pancreatitis: an
exploration of clinical and etiologic factors and
outcomes, Jornal de Pediatria, 2018, ISSN 0021-
7557, https://doi.org/10.1016/j.jped.2018.06.011.
 Smith J, Arnoletti J, Varadarajulu S, Morgan D, Post-
pancreatitis Fat Necrosis Mimicking Carcinomatosis,
Radiology Case Reports, Volume 3, Issue 2, 2008,
192, ISSN 1930-0433,
https://doi.org/10.2484/rcr.v3i2.192.
 Zhao Q, Wei Y, Pandol SJ, Li L, Habtezion A. Original
Research: STING Signaling Promotes Inflammation
in Experimental Acute Pancreatitis. Gastroenterology.
2018;154:1822-1835.e2.
doi:10.1053/j.gastro.2018.01.065.