NRS - MEDICAL SURGICAL NURSING II (LEC)

Hepatobiliary and Pancreatic Disorders (PLM-CN BATCH 2020) NRS 3217-9

OUTLINE o increased bilirubin production/ accelerated

Care of the Client with VI. Hepatitis breakdown of hemoglobin.
Hepatobiliary and Pancreatic A. Viral Hepatitis o we are talking about blood here.
Disorder B. Toxic Hepatitis o massive blood destructions (hemolysis).
I. Jaundice o Too much blood, cannot be metabolized by the body
A. Etiology VII. Cholelithiasis/Cholecystitis (too much work for the liver)
B. Pathophysiology A. Definition of Terms o
C. Clinical Manifestations B. Cause b. Hepatic/ hepatocellular Jaundice
D. Diagnostics C. Prediposing Factors o Too much blood formation in the body
E. Management D. Theories
E. Assessment c. Post-hepatic
II. Liver Cirrhosis F. Management 1. Occlusion of gallstones- CBD or CD
A. Types 2. Inflammatory process
3. Tumor
B. Assessment VIII. Pancreatitis
4. Pressure from an enlarged organ
C. Management A. Cause
5. Intrahepatic/ Extrahepatic obstruction
B. Assessment
III. Ascites C. Manifestations o That is what happened in pre-hepatic, in the bilirubin
A. Assessment D. Management secretion, the hemoglobin mabrebreakdown niya.
B. Management o Remember the parts, we have the
Reticuloendothelial System which is very responsible
IV. Esophageal Varices in breaking it down. Into your liver meron ka niyan
A. Assessment which actually serves as your Kupffer cells that will
break down your hemoglobin into heme and globin.
V. Hepatic Encephalopathy
PATHOPHYSIOLOGY

GI CONTINUATION: CARE OF THE CLIENT

WITH HEPATOBILIARY AND PANCREATIC
DISORDER
JAUNDICE
o Per se is not really a disorder but a manifestation of
a certain pathologic condition that happens in your
body.
o Yellow discoloration of the skin that includes your
sclera, and mucous membrane due to the increase in
the level of bilirubin.
→ Also called “icterus”
o (kaya makikita niyo sa mga discussion ay tinatawag
na icteric phase- ibig sabihin nandiyan na yung
paninilaw. May mga pre-icteric and post-icteric
phases kayong makikita sa mga stages of
your problem).
o Main problem is: Bilirubin metabolism. So
nagkaroon kayo ng disruptions on the bilirubin
metabolism. Yung normal breakdown of RBC. Yung
hemoglobin niyo yung nag-release ng bilirubin.
o Bilirubin is transported to the liver and conjugated.
o Conjugated bilirubin- is the one that is excreted into
the bile and the one that can be eliminated into the
feces.
o Whenever you have disruptions of bilirubin
metabolism it leads to jaundice.
→ Yellow pigmentation of the sclerae, skin and deeper tissues due to
excessive accumulation of the bile pigments in the blood.
→ Bilirubin is deposited in the skin and excreted in the urine when
present in the blood in excessive amounts.

ETIOLOGY
THREE KNOWN REASONS WHY YOU DEVELOP JAUNDICE:
1. Location
o kung saan nangyayari/ origin of the problem.
a. Pre-hepatic Jaundice

TRANSCRIBED BY: Groups 1 and 2

Ganito na brebreakdown sa loob ng katawan niyo ang inyong mga
bilirubin excretions supposed to be.
o ‘Yung hemoglobin mag brebreakdown, you RES
(very specialized cells which contain your Kupffer
cells if it's in the liver). Certainly marami ‘yan sa loob
ng katawan natin, hindi lang limited into your liver
o Pag nag breakdown ang hemoglobin into two form (1)
heme & (2) Globin, sa heme mag brebreakdown into
two that is the Porphyrin and Fe (Iron)
o Your Porphyrin that is your pre-bilirubin, ‘yung Iron
mo maiistore back siya into the liver. Gagamitin ulit
‘yan ng katawan mo, the Ferritin, para makapag buo
ulit ng panibagong hemoglobin formations
o In the pre-bilirubin, that is unconjugated or indirect -
that will bind or attach to the albumin or other proteins
you have in your system. Into your hepatocytes
excretions, your extra bilirubin in the blood which is sabi
natin conjugated kasi lahat yan dadaan sa liver. So the
hepatocytes which is extracting the bilirubin in the blood
those are conjugated with Glucuronic Acid which will
become direct bilirubin and that will be excreted into the
bile, dadaan sa bile caniculi the into the canaliculi then
into the bile duct. From bile duct to the hepatic duct to
common bile duct - that is the circulation over to your
hepatic system.
o From the bile canaliculi to your cystic duct which is
going to your gallbladder, the secretions of the bile
into the duodenum in a form of cholecystokinin every
time you eat certain fatty foods.
o The actions of intestinal bacteria, kaya important ito
kasi eto yung nag coconvert ng bilirubin into
urobilinogen. When it is already converted into
urobilinogen, some will be reabsorbed in the
intestinal mucosa and go back to the portal blood
back to the liver. Pag nasa liver na pwede ulit itapon
ni liver, the urobilinogen will be removed by the
hepatocytes or mag-eenter ulit sa systemic
circulations when that urobilinogen enters the
systemic circulations, the blood dadaaan ulit sa
kidney which will be filtered again then eexcrete na
siya into urine. That is why your urine is color
yellow.
o Once it has been excreted in the intestine,
maeexcrete mo naman into through your feces that is
why you called that stercobilin pag nasa poop na.
That is why the color of your poop is golden brown.
o Bottomline: babalik ito sa liver, yung urobilinogen
removed by the hepatocytes excreted into the bile
once again kasi mag-eenter ulit siya sa entero
hepatic system. IT IS A CYCLE!
o Kung overwhelming ang katawan mo sa dami ng bile
formations or bilirubin na ginawa ng katawan mo,
hindi niya ma-eeliminate or excrete.
o Sa Chole, may 5Fs: Female, Fertility, Fair
complexions, Fats
o If you have so many rbc breakdown, the body is being
overwhelmed for hemoglobin breakdown. So, hindi
kakayanin ng liver so, some of them will be stored into
your skin particularly the bile salt.
B. Hepatic Jaundice
o Hepatic or hepatocellular jaundice - impaired liver.
o Yung liver uptake mo with the conjugated or the
excretions of the bilirubin is the major problem kapag
meron kang liver diseases such as Hepatitis,
Cirrhosis, etc.
C. Post-Hepatic
o Here we’re talking about the bile flow. Sa bile flow
may problema doon, pagkalabas sa liver (basta
outside the liver) madedrain yung bile into the bile
duct. When it is into the bile duct including the
common bile duct, that is your obstructive jaundice.
o Post-hepatic Jaundice = Obstructive Jaundice
(SAME)
o You do not have problem with the liver per se but
into the duct of the liver. Wala na (yung problem)
sa loob ng liver. Nasa mga biliary tree, sa mga
common bile duct, sa mga duct palabas ng liver,
nandoon na yung problem.
o Ito yung kadalasang problema ng mga taong
mayroong gallbladder stone, yung mga may
cholelithiasis, cholecystitis whenever they have
accumulations of stone formations in their
gallbladder.
o Whenever you have stone formations in chole (where bile is
stored), so everytime na kailangan ng katawan mo, mayroong kang
reservoir para sa pangangailangan ng katawan mo.
o Example: Kumain si Kobe ng sangkatutak na taba ng
baboy. Hindi agad makakapagcreate ng bile yung
liver para madigest yung fats. Hindi madadigest yung
fats without the bile. Kaya ang punta ng bile is into
the intestine. If wala kang bile formations or hindi
nakakarating yung bile sa intestine, ma-iipon and
marereabsorb sa dugo then it will be reabsorbed back
into the bloodstream so that’s why overwhelming ulit
siya sa katawan mo. Hindi siya nakakaya ng liver mo
i-filter para kuhanin. So, maninilaw ka ulit because it
will be restored into the skin (the bile salt). When it
can't be in your blood, your blood will actually restore
where it can store it because the moment the bile acid
or bile formations increase, it becomes acidic in
nature, so your blood doesn't want that. Your blood is
vulnerable to acid, so your blood is damaged again;
therefore, you have many massive destructions of
hemoglobin again. It's another form of jaundice, so
it's like a double whammy.
o The gallbladder is a reservoir; every time you need bile, it draws
from the reservoir and has rhythmic contractions. You already have
a stone formation over your bile because the concentrations of your
bile increased too much for so many reasons, even your diet. You
didn't eat, you fasted for quite a period of time, or sometimes you
did TPN. Due to the absence of food in the duodenum, the
pancreatic enzyme activities decrease, and the secretions of
lipases, secretin, and cholecystokinin all decrease, so the
stimulation of the bile secretions in your gallbladder also
decreases.
o For example, if you're fasting, your TPN is too high,
or you're undernourished, it will prolong the
sequestration of bile salt into your bile; in other words,
the bile becomes supersaturated. The bile is made up
of cholesterol and salt, and when the bile is
supersaturated, the ratio of those will increase, and
that particular alterations will become concentrated,
which is why you form stone formations there. When
it forms a stone, it crystallizes inside, so it has rough
edges. Again, it has continuous rhythmic
contractions, more likely when you are still eating and
eating fatty materials, the contractility measures that
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 happen in your gallbladder are higher because that's
the normal response of your body. When it contracts,
they traumatize the lining of the gallbladder, so there
is pain, and for those who have chole, their stomachs
hurt because of this. Possibility: When the stone is
masyadong magaan because cholelithiasis is still
small, it can come with it. Pag sumama yan, it goes
from the gallbladder into the common bile duct. In the
common bile duct, it's only small; therefore, you may
have obstructions, so it can't flow.
o This is your gallbladder, so it goes into the common
bile duct before it goes to the biliary tree. When it
becomes obstructed there, there is no flow of the bile,
so it will be reabsorbed back because lahat ng
ginagawa ng liver ng mga bagong bile di na mastore
kasi puno na, so it will be reabsorbed into the
bloodstream. Remember, you have so many hepatic
pains in your liver.
o Common reason why you develop post-hepatic
jaundice
1. Occlusion of a gallstone - CBD or CD
2. Inflammatory process
o Pancreatitis - The pancreas is inflamed, so it
compresses the common bile duct that’s why you are
having obstructions.
3. Tumor
o when you have a pancreatic head mass, you have a
tumor in your pancreas.
4. Pressure from enlarged organ
5. Intrahepatic/Extrahepatic Obstruction
o Physiologic jaundice is common to newborns
because a child's body adjusts, so some children turn
yellow, but it should be ruled out that it is actually
physiologic. What we do is expose them to the
fluorescent light to correct their jaundice and protect
the baby's eyes because of the possibility of
blindness due to overexposure to the fluorescent
light. Technically, newborns can't see much during
the early months of their lives. We should cover their
eyes with a lampen while we expose them to the sun
because we don't want them to look at the sky. There
is a strain that happens in their eyes, but they don't
feel much yet because they are still babies. Their
senses are not yet fully developed, but the damage
that will occur to their eyes is the same. Whenever
you have a physiologic or pathologic jaundice patient,
we expose them to the fluorescent light, and you have
to be very sure that the eye is covered with the gauze
pad, layer after layer of gauze pad, and then we will
put micropore in their eyes and anchor it on their head
so that hindi sila masyadong masilaw or they just
closed their eyes during that time.
CLINICAL MANIFESTATIONS OF JAUNDICE
o Yellowish or yellowing of the skin, sclera and mucous
membrane
o Dark urine - due to the excretions of bilirubin that are excreted in
the urine but not excreted into the feces because the bile does not
reach the intestines. Therefore, you have pale or clay-colored
stools. Urine is foamy and very yellow, up to the point of becoming
tea-colored urine due to the increase in bilirubin excretions into
your urine, but it is not in your intestine.
o Fatigue
o Malaise
o Pruritus (itchiness) - when the bile salt is stored underneath your
skin because your body stores it there, it itches.
o Abdominal pain and discomfort
o Nausea and vomiting
Common Causes: (bumalik na naman pi siya sa causes medj magulo siya hng)
Pre-hepatic jaundice
o hemolytic anemia; increased breakdown of RBCs whenever you
have sickle cell disease or if you have an inherited disorder of
abnormality in bilirubin metabolism or Gilbert's syndrome.
o If you have G6PD, you have a lack of certain proteins in your body
that protect your blood. Your blood becomes vulnerable to other
substances that are actually present in your body, including the
milk that children drink – common pediatric disorder.
o It is a genetic anomaly; both parents actually carry this particular
gene, which is why it manifests in newborns because this is a
recessive gene. Supposedly, if those genes are recessive, they
won't manifest; they can’t be seen in a person, but the recessive
one becomes dominant or seen when both parents have that
particular gene or carry that gene together, so there will be
manifestations of that. No matter what they eat or what medicine
they take, their RBCs are destroyed and they have massive
destruction of red blood cells, so they will also have jaundice, and
if they have too much, they have anemia.
Hepatic
o viral hepatitis, alcohol liver disease, drug-induced liver injury, and
the most common, liver cirrhosis. Liver cirrhosis can also be
caused by fatty liver diseases.
Post Hepatic
Biliary obstructions
1. Occlusion of gallstones - CBD or CD
2. Inflammatory process
3. Tumor
o Nagkaroon ka ng mga biliary strictures,sumikip kasi dumaan
yung stone dati doon na medyo naka-pass through siya pero
nasugat so nagkaroon ng formation ng scar kaya nagkaroon
ng stricture
4. Pressure from enlarged organ
6. intrahepatic/ extrahepatic obstructions
o Choledocholithiasis or obstructions of the common bile duct,
congenital anomaly, biliary atresia. Yan yung mga congenital
absence or obstructions of the bile duct. Pag pinanganak ka meron
ka na niyan.
DIAGNOSTICS
o Very important ang history and physical examination.
o You have your serum bilirubin, total bilirubin, direct
bilirubin (conjugated), and indirect bilirubin
(unconjugated).
o You also have your liver function test (ALP, AST,
Alkaline phosphatase, albumin, PT, PTP, INR) and
we also do viral hepatitis serology (if applicable),
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 yung mga pangtest sa h-bug (di ko sure, pero ayan
lumabas sa google) sa hepatitis para malaman if it is
viral. Pero normally, eto yung mga common
diagnostic laboratory examinations na ginagawa
1. TB, B1, B2
2. ↑ urine urobilinogen
3. ↓ Fecal urobilinogen
4. ↑ ALP
5. Unusually low serum cholesterol level
6. ↑ Serum bile salts
7. Prolonged protime
o Imaging tests: ultrasound, CT scan, MRI (lahat ng imaging
pwede.)
o Liver biopsy (if indicated)
o is another form of diagnostic procedure
o to assess the liver tissue
o to determine the cause of the problem.
MEDICAL MANAGEMENT
1. Resolution of underlying cause
→ Supportive care
o Treat the underlying cause
o If viral type, medical management is antiviral therapy
or we do certain supportive care for the liver disease.
o Lifestyle modifications.
o Symptom management and supportive care ,
o pharmacologic interventions.
- Symptom like prutitus, we do as supportive.
- Medications to relieve the symptom.
- Vomiting, we give medications
o . Increasing fluid intake, soothing bath, and providing
a cold environment to our pt.
2. Dissolution therapy/ surgical removal of obstruction
• CBDE (choledochostomy)
- Differentiates between choledocholithiasis and
tumor
o Choledochostomy or common bile duct
exploration, kadasalan yung mga nagkaroon nito
yung mga Choledocholithiasis, cholecystitis, etc.
once they perform certain operations, yung
choledochostomy, open kapag meron kang problema
sa common bile duct, kapag need iexplore yung
common bile duct.
o Laparoscopic cholecystectomy (simple chole)
walang paninilaw, walang evidence that there is an
obstruction into the biliary tree, common bile duct.
Pwede yung laparoscopic chole, 4 na butas sa tyan.
When you have affectations sa common bile duct,
nabarahan, na-dislodge dun yung stone so they are
going to do open cholecystectomy with common bile
duct exploration (CBDE), so makikita sa doctor’s
order, CBDE and IOC (Intraoperative
cholangiogram), habang nakabukas ang patient,
bladder is removed and bile duct is explored, dahil
there are times na hindi ito makikita sa exploration
because masyadong gelatinous yung structure ng
common bile duct so we need to use x-ray, tatawag
for portable x-ray papasok sa OR, then mag-undergo
na ng x-ray si patient. It was discussed before na ang
x-ray technicians ay part din ng non sterile team in
the surgery, there are times that we need them, na
we conduct using x-ray during a surgery, ayan yung
IOC.
o In IOC, may ipinapasok na dye, so habang ine-x ray
si patient dapat yung dye magtutuloy-tuloy lang, so
kung sa isang part nag-obstruct siya, makikita natin
na nandyan ang obstruction, ayan ang i-
mamanipulate through surgical procedure, with your
choledochostomy.
o Cholecystitis with choledochostomy, ang
nangyayari sa patient, if there are obstructions in the
common bile duct, so we’re going to do exploration,
hinahanap natin kung saan yung obstruction.
Syempre, yung tumor, we differentiate the
manifestations and symptoms between
choledocholithiasis and tumor, so when there is
tumor, we won’t be doing surgery agad-agad, dapat
makita ng doctor if resectable yung area, kasi there
are moments na patient is in the OR bubuksan kahit
‘di masyadong nagawa mga diagnostic procedures,
ang dictum din naman is to open, if it is not resectable
then we close it na (close-open-close), bubuksan
titignan, masyadong malaki ang tumor naka-adhere
sa nearby structures, kung saan ‘di pwedeng i-resect
nor tanggalin, because the patient will die in the
operating table.
→ (+) pancreatic head carcinoma
● Palliative anastomosis of GB duodenum
o If there are things that we can do, which is the
palliative anastomosis of the gallbladder to the
duodenum, by passing your common bile duct, (refer
to the pic below this) bina-bypass na natin yung bile
duct so gagawa tayo ng panibago para ilagay na into
the duodenum, ‘di na siya mapupunta saan, ‘di na siya
dadaan sa bile duct, kasi obstructed siya, so for example
you have pancreatic tumor, sobrang laki na, palliative na
lang just to relieve the symptoms, commonly based on
exp, whenever you have head mass, kapag ganyan ang
nangyari diyan ang tumor or cancer, usually patient is
good for 3-6 months, swerte na kung umabot ng 6
months upon diagnosing. Sobrang bilis ang pag-spread
ng tumor, and deterioration ng patient kapag pancreas,
because pancreas has a lot of functions, including the
secretions of glucagon and insulin (very important
hormones in the body).
NURSING MANAGEMENT
1. Control pruritus
o maintain the skin integrity. When itchy, kamot nang
kamot na naglelead sa nagsusugat.
o Cool bath (do not use hot bath) every time na we’re
taking a bath with warm water, nag-tatowel right away
because makati ang balat, so kapag mainit
nagkakaroon ng pruritus sa balat,
o we can give certain medications like phenobarbitals,
antihistamine, and cholestyramine resin
exchange in renal failure - one of the methods of
addressing the hyperkalemia into patients with renal
failure
o paiinomin sa patient then the bile salts into the
intenstine will be excreted because there will be
exchange
o kapag nasa intestine na yung gamot, lahat ng mga
bile salt hahatakin palabas kasi rich ng blood vessels
ang intestine so lahat ng mga bile salts mag bibind sa
cholestyramine resin at mailalabas siya sa
pamamagitan ng pag dumi
o Hindi siya mag-aaccumulate sa loob ng katawan
2. Offer emotional support
o Remember!! Walang taong gustong naninilaw
o Problem with body image and self-esteem
disturbance related to skin and sclera color can arise.
o WHAT TO DO? Advise the patient to use sunglasses
when going out so hindi pansin yung yellowish eyes.
o Use also skin moisturizer.
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Question:
Is it possible that the patient will be impaired in absorbing fat soluble
vitamins?
Answer:
Definitely. If you do not have bile, your body does not have the capacity
to digest the fats and those fat solube vitamins will be needing fats. So
kung walang ma-digest na fats yung katawan mo, hindi rin madidigest
ang fat soluble vitamins. Lahat ng fats na kinakain mo, mai-tatae mo
lang. Makikita mo sa poop ng mga patients na pale colored stool at
lumulutang kasi punong-puno ng fats, hindi na-absorb sa loob ng
katawan. Very important ang fats in fat soluble vitamins absorbtions at
sa paggawa ng katawan ng hormones such as bile. If you do not have
that, gaya nga ng sabi ko sa diagnostic, yung bleeding, INR, protile very
important yan kasi vitamin k is very important for clotting factor. Kapag
walang fats, walang absorbtions or metabolism ng fats syempre wala
ring absorption, mailalabas lang sa katawan. So hindi natin ma-uutilize
yung mga fat soluble vitamins including vitamin K. Kung wala kang
vitamin K, kaya yung mga pasyenteng merong jaundince prone sila sa
bleeding depending sa particular area kung bat sila nagkaroon ng
jaundince pero kung yan ay obstructive jaundice at nagkaroon na ng
abnormality into their clotting factor, they are prone to bleeding.
Question:
Is it possible that jaundice can cause brain damage?
Answer:
Yes, its possible. It can cause damage into the brain stem pero in a long
run. Usually kasi ang jaundince ay hindi naman talaga siya masama pero
kapag sobra at umabot na hanggang sa loob ng brain (kernicterus: will
cause damage into the brain if not being adressed)
Later on sa liver cirrhosis andito talaga yung damage. Pag mga
obstructions lang, kasi you have to address the issue. Kapag marami
kang blood distruptions, i-address ang blood distruptions. I-ayos yung
anemia. Kung merong obstructions, you remove the obstructions. Ang
problema kapag ang liver ang nagka-problema ito ang mahirap i-
address. So kapag masyado nang maraming bile at nakapasok na sa
BBB, that we call kernicterus, the damage into the brain stem will occur.
If you have so many indirect bilirubin level (greater than 20-25
mg/dL), that will cause kernicterus; will cause brain stem
damage *JAUNDICE SHOULD BE MANAGED IN THE
HOSPITAL*
Question:
In differentiating the type of jaundice, are all diagnostics test should be
implemented?
Answer:
In bilirubin test, it may not be accurate to differentiate what type of
jaundice the client manifest; so several diagnostics must be done if you
are not certain. Cross out the manifestations na present sa isang type at
wala sa iba (example: may pain = obstructive type of jaundice).
History taking and physical examinations is very important in order
to know what type of laboratory or diagnostics imaging needed to
perform to the patient. As laboratory result will increase in general; the
diagnostics imaging will determine the exact etiology (example: maga
ang liver, may cirrosis o obstruction– the diagnostic imaging will show),
thus making it possible to differentiate what type of jaundice that client
have.
In hemolytic, may unexplained anemia, bagsak na bagsak ang
hemoglobin count. Means may massive destruction of blood.
(DIFFERENTIAL DIAGNOSIS)
History taking and physical examinations is more important than
diagnostics; u do not treat laboratory, u treat px based on s/sx and
physical examinations. U do not treat laboratory alone as there is a
possibility that it is incorrect– unlike the data gathered in history taking
and physical examinations, hindi maaaring magkamali. Dapat may
congruency ng data.
Question:
In regards with (hindi ko maintindihan yung word, halp), flushing of
gallstones is one of the management– hindi po mas malaki ang chance
for obstruction?
Answer:
U first need to do history taking, physical examinations and
then do diagnostic imaging para makita gaano kalaki ang
stone formation; some medication can dissolve if the stones
are not that big in size
Walang literature na makakapagsabi na hindi sya
madidislodge or ma-oobstruct into the common bile duct.
It’s much better to remove the gallbladder to prevent complications. Also,
pagna-remove na sya, wala ng area to concentrate for the formation of
stones. Therefore, surgical removal is better as compared to flashing,
medications, etch.
Question: Kapag nagka-jaundice po ba makikita kaagad ang paninilaw
sa buong katawan ng patient? Or some parts of the body muna?
Answer: No! Some parts of the body muna usually the sclera. Pagnag-
aassess ka ng mata ng pasyente, tinitignan mo ung sclera since dito
unang nagmamanifest ung discoloration. Pre-icteric phase muna, means
wala pang paninilaw. Ang paninilaw ay magsisimula sa sa ilalim ng mata,
wala pa sa katawan.
Question: Paglumala na po ung jaundice, doon pa lang po ba makikita
sa buong katawan?
Answer: Yes. Since sobrang dami na sya sa loob ng katawan, hindi na
sya mahohold ng katawan, kaya magsstore na sya sa balat. That’s why
nagmamanifest na ung jaundice sa balat
Question: Sa mata po ba unang nag-aappear ang jaundice?
Answer: That’s commonly appear in the sclera. Pag sa mga medyo
morena or black, hindi naten commonly makikita ung discoloration due
to their color of skin. Kaya sa mga black people, yung palad den ung
tinitignan naten. But usually, sclera is the first manifestation. Tignan mo
yung ilalim ng mata dahil dyan una nagmamanifest ung discoloration.
Question: Pag may jaundice po ba na may related sa anemia, mas
napapataas ba neto ung risks for liver disease since na-ooverwhelmed
ung liver dahil sa dami ng mga RBC na nade-destroy?
Answer: If the liver has already an existing condition, syempre
napapalala. Kumbaga, binibigyan mo siya ng trabaho instead na
napapahinga na sana siya. In a normal circumstance, the liver has an
excellent capability to regenerate. If the individual has severe anemia,
the doctor must find the cause of anemia. Whole body CT scan and bone
marrow aspiration para makita nila kasi may pathology kung bakit
nagkaroon ng severe anemia. That’s what we call the hemolytic type of
Jaundice. Maraming nadedestroy na RBC sa katawan niya, hindi
kinakaya ng katawan nya na iexcrete agad agad. Dapat hanapin ang
dahilan kung bakit nagkaroon ng anemia. Hindi pwedeng sasalinan ka
lang ng dugo then after that, you’re okay na. Kailangan hanapin yung
pathological reason, the origin of the problem why you developed that
LIVER CIRRHOSIS
→ Liver cell necrosis occurs and destroys the liver cells and is replaced
by scar tissue.
TYPES
→ Laennec
→ Post-necrotic
→ Biliary
→ Cardiac necrosis
o Dahil pumangit yung circulations mo. Puso mo yung
may problema, hindi nasupplyan nang maigi yung
liver mo that’s why nagkaroon ka ng necrosis
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 EARLY ASSESSMENTS → Pt is already immunocompromised
→ Fatigue → We cannot give antibiotic
→ Anorexia o Liver cannot handle it already; will lead to toxic levels
→ Dyspepsia in the body
→ Flatus
o Utot nang utot Avoid Sedatives
→ Nausea and vomiting → We must check the level of sensorium of the pt
→ Diarrhea o Minsan nawawalan tayo ng choice but to give
→ Constipation sedatives most specially if the pt is nasa hepatic
→ Dull abdominal ache encephalopathy stage – nagwawala si pt
o Parang masakit ang tiyan na ‘di maintindihan
although tolerable ang pain Avoid Aspirin
→ May problem na sa bleeding
LATE ASSESSMENTS
→ Lethargy Eliminate Alcohol
o Because ang katawan ay nalalason ng ammonia → Most especially of pt has liver cirrhosis due to alcoholism
levels o Pt is alcoholic, hindi na nila kayang tanggalin sa
→ Mental changes sistema nila
→ Asterixis → If in the hospital, it is easy to eliminate
→ Hepatomegaly
→ Jaundice ASCITES
→ Spider angiomas o Common complication of a person with liver cirrhosis
o Pwede sa mukha at sa tiyan. Yung mga blood o Not a disorder but another consequence of a disorder
vessels nagiging masiyadong prominent. → Accumulation of serous fluid in the peritoneal cavity
→ Coagulation problem ● It increases as the pressure in the liver increase
o Kaya kapag may liver cirrhosis, madalas hindi nag- → Due to liver damage, there is a production of hypoalbuminemia
iinjection. o Low albumin in blood → increase portal venous
o If multiple administration of drugs is pressure → leads to portal hypertension
required/necessary, utilize IV para meron tayong one
area kung saan ilalagay ang gamot. If hindi talaga → Portal hypertension – characterized by increased blood pressure
maiwasan, like when you need to administer Vitamin K within the portal venous system
via IV, you need to press it for 5 full minutes because ● Occur as a result of obstruction or increase in resistance
they are prone to bleeding. in blood flow within the portal venous system
→ Portal hpn ● Resistance in blood flow due to many pathological
→ Esophageal varices reasons:
→ Increase ammonia o Liver cirrhosis
o That’s why nagkakaroon ng lethargy leading to coma. o Portal vein thrombosis (blockage)
→ Coma o Hepatic vein obstructions
o For patients with liver cirrhosis, possibility of o Congenital anomalies – biliary atresia (bile ducts are
coagulopathy and bleeding tendencies are very high. scarred and blocked)

MANAGEMENT OF LIVER CIRRHOSIS → Portal venous system – responsible for carrying blood from
Rest digestive organ, including the liver
→ Do not stress the pt
● Give a long resting period ASSESSMENT FINDINGS:
● Rest is necessary, but still address the circulation → Abdominal distention
→ Peripheral edema
Diet → Shortness of Breath (SOB)
→ Early Stage
● Check for the quality of Liver MANAGEMENT:
● If not too compromised, we can still give high protein diet → Administer diuretics as ordered
o High caloric, high carbohydrate, LOW FAT; LOW ● Initial administration
SALT (usual in late stage) o Potassium (K) sparing
o Kailangan pa magtrabaho ni liver para ● Later administration
makapagmetabolize ng fats o Loop diuretics – potassium wasting diuretics
● Protein on early stage, in the premise of we wanted to o Hindi pwedeng puro potassium sparing, that will
have tissue repair create danger
o Magbuild uli o Body does not want potassium just sitting on blood →
→ Late Stage will cause accumulation kaya magbibigay tayo ng
● NO high protein potassium wasting para mailabas
o Protein = CHO(N) → product – Nitrogen → converted → Measure abdominal girth
to ammonia → Promote skin integrity
● Protein in late stage → Surgery
o Body cannot metabolize more protein → Monitor weight, I & O, abdominal girth
o Excess protein will be converted into TOO MUCH → Diet restriction
ammonia → Administer albumin / IV as ordered
Skin Care ● To compensate hypoalbuminuria
● To hold oncotic pressure and eliminate occurrences of
Avoid Trauma / Injury edema.
→ Avoid injection or any other form of trauma to pt with liver problem o Oncotic pressure is poor, fluids cannot be held inside
the cell, leading to edema
Prevent Infections → Assist in paracentesis
6
 ● Ideal procedure is ultrasound guided. Some physicians no
longer use ultrasound, prefers blind approach
● Maintain homeostasis.
o Px’s body got used to having fluid accumulation,
abrubt evacuation of fluid could disrupt homeostasis.
Monitor VS while the procedure is done.
o Taper off fluid removal until totally drained.
o If px experience VS depression, paracentesis is
discontinued.
● Avoid unecessary punctures on visible blood vessels, it
can rupture easily causing massive bleeding.
● IV tubings are placed to drain fluid through IV needles.
● Fluid is analyzed for pathological analysis.
● Empty IV bolltes are used to collect and measure fluid
output.
o Ascites – pag ginalaw, magkakaroon ng wave form
ESOPHAGEAL VARICES
→ Dilated tortuous vein in the submucosa of the lower esophagus
caused by portal hypertension and associated with cirrhosis
o If pressure is too high, the esophageal vein will
protrude.
o One of the reasons why patients with liver cirrhosis
die.
ASSESSMENT
→ Bleeding
→ Hypotension
→ Neck vein
→ Distention
→ Hematemesis
→ Strain with coughing and vomiting
AVOID THE FOLLOWING TO PREVENT RUPTURE OF VARICES
→ Shouting, yelling, screaming
→ Straining at stool
→ Bending and stooping
→ Lifting heavy objects
→ Hot, spicy foods
HEPATIC ENCEPHALOPATHY
→ Restrict protein in the diet
→ Laxative
→ NeomycinSO4
→ Tap water on NSS enema
o When patients develop hepatic encephalopathy, they
are not in the right track of their mind. Therefore,
there are higher chances of aspiration in patients.
o Duphalac, known as your lactulose is prescribed to
patients who have liver cirrhosis. This reduces
ammonia inside the body of the patient most
especially if their liver has inability to detoxify
ammonia.
o Lactulose acidifies intestines, breaking down bacteria
converting ammonia inside the body.
o How to dilute the lactulose is included in the
supplemental reading given by sir.
HEPATITIS
→ Acute inflammatory disease of the liver
→ Can be caused by virus, bacteria or any toxin
→
TYPES
TOXIC HEPATITIS
- Could be a bacteria or toxin
VIRAL HEPATITIS
- virus
● Hepatitis A
● Hepatitis B
● Hepatitis C
● Hepatitis D
● Hepatitis E
VIRAL HEPATITIS
→ Comparison of major forms of Viral Hepatitis (Please see Page 12
for the table)
→
GENERAL CONSIDERATION
→ Hand washing by all person
→ Feces, urine, blood and other body fluid precaution
→ Contaminated needles and other instruments that came in contact
with infected body fluids should be handled with great care and
properly discarded
→ Practice “Universal Precaution" in all clients
o we have to put in context that all clients are
INFECTIOUS including HIV
o kailangan mag ingat sa lahat ng body secretions
(saliva, sweat, or etc.) consider it as infectious
o everytime we encounter needle puncturing, we have
to report it to INFECTION CONTROL
DEPARTMENT because they will conduct
investigations
o Incidental report kasi kung mangangailangan ka ng
hemoglobulin transfusion or infusions dapat magawa
within 24 hrs post puncturing
o Napuncture ka na may HIV, there are ways to prevent
acquiring HIV within 24 hrs post puncturing dapat
irefer ka na to evaluate and monitor for 3-6 months
o Usually the effectivity rate is 98% (di ka mahahawa)
→ Do not recap needies
o Kung magrerecap, dapat scoop method, hindi
hahawakan yung takip iiscoop niyo lang and then
ididiin niyo lang sa kama
o - Hardest scoop method (usually cause
needle puncturing in the hospital) is INSULIN
SYRINGE dahil sobrang nipis siya tapos ibang klase
yung takip niya
o Do not put syringe in the tray while holding the tray.
Syringe may be displaced while walking and hand
may be punctured.
o Hold the syringe at the edge of the tray so it won’t be
displaced.
o If possible, dispose whole plunger and needle to
avoid getting more risk for needle puncture.
→ Proper sterilization of equipments
o There are items that are only soaked in Cidex solution
and not put in autoclave (cause damage) ex. Scissors
o Some hospitas use the same Cidex solution for a
month, but ideally, it should be replaced daily after
soaking equipment
o When preparing surgical materials, from Cidex
Solution > wash again in Normal Saline Solution
(NSS) > sterile table in operating room
o Still need to wash in NSS because you need to wash
out the chemical. Then change NSS every shift or
every patient
NURSING MANAGEMENT
• Preventive precautions
o Hepatitis A and E= enteric precautions (oro-fecal
transmission)
o Proper handwashing when changing patient
7
 o Usually, patient with hepatitis A and E are not allowed → 5 mil. ‘u’ daily or 10 mmil. ‘u’ 3x a week for 4-6 mos. IV
to be food handler to avoid transmission when hands → Results in remission of disease (1/3 of cases)
are not washed. (Orofecal Transmission) → Has significant SE
o Not sexually transmitted if there is no foreplay or anal ● Fever
rimming. Otherwise, it is not sexually transmitted ● Chills
o Hepatitis B, C, and D – body fluid precaution must be ● Anorexia
considered ● Nausea
▪ Advise client not to donate blood and ● Myalgia
practice safe sex ● Fatigue
→ Late SE – more serious:
HEPATITIS A ● Alopecia
Supportive ● BM suppression
o We have a phase called Pre-enteric or Prodromal o Bone marrow suppression makes individuals more
phase which usually lasts for a week susceptible to infections
▪ Wala pang paninilaw o Advised to do reverse isolation while on the
▪ Usually happens upon obtaining the virus medication
▪ Patient experiences fevel, chills, N/V, ● Thyroid suppression
anorexia ● Bacterial infections
o Enteric phase
▪ Where jaundice usually starts HEPATITIS C
▪ Starts within 2 weeks → NO benefit from REST, DIET, or VITAMINS
▪ Lasts for about 4-6 weeks
▪ Progression of several symptoms Pharmacologic Therapy
▪ Assessment is vital → Combination Therapy (Antivirals)
o Post-enteric phase ● treatment of choice
▪ Disappearance of jaundice ● Produces complete remission in some patients
▪ Hepa A and E – lasts for several weeks to ● Examples:
4 months o Interferon (Intron-A)
▪ Hepa B and D – lasts longer o Ribavirin (Rebetol) – use with caution for wome of
→ Bed rest with gradual and progressive ambulation childbearing age
→ Adequate diet and nutrition o Pegylated Interferon (Pegasys) – given once a
● Small frequent feedings (4-6 times daily) week
● IVF w/ glucose ● SE:
● High in CHO and calories, moderate CHON, and small o Hemolytic anemia – most frequent SE
amount of fats o If severe, D/C treatment
● Diets rich in vitamin K HEPATITIS D
o Will depend upon MD
o Carbonated and alcoholic beverages are not allowed → Similar to other forms of hepatitis (B & C)
o Fat restrictions are necessary → Interferon use for Hepa D is still under investigation
→ Increased OFI (Oral Fluid Intake) o This type of hepatitis is chronic, patients usually die
● Even before icteric phase, some patients recover their within 6 months.
appetite
o 3000 mL / 3L per day HEPATITIS E
o Do I/O and weight monitoring → Same with Hepa A
o Patients with hepatitis have the potential to develop o Give sweets to client since liver cells are rich in
liver cirrhosis and ascites mitochondria, which needs a great supply or glucose
→ Bleeding problems to function.
o Bleeding problems must also be monitored such as → Immunoglobulin use is still under investigation
PT, HGB, HCT
o Avoid parenteral injections – but if it is highly TOXIC HEPATITIS
necessary, you must apply pressure on the site of ETIOLOGY
injection for 5 minutes or more → Drugs
o Monitor urine, stool, and skin for presence of
→ Alcohol
petechiae
→ Industrial toxin
▪ Pag urine namumula = bleeding
▪ Pag stool may melena or hematochezia = → Poisonous chemicals
bleeding o E.g. newly bought clothes that have not yet been
▪ Petechiae = bleeding washed
o Administer Vitamin K as ordered by MD
o IV glucose PRN ASSESSMENT
▪ Pag bumagsak lang ang blood glucose ni pt → Anorexia
▪ Do not do this if otherwise → N/V
→ Relief or pruritus → Lethargy
→ Frequent soothing baths → Icterus
o Provide comfortable and cool environment → Hepatomegaly

HEPATITIS B MANAGEMENT
→ Supportive → Patient education
→ → Rest
ALPHA INTERFERON → Maintain FEB
→ Retroviral agent → Promote a well-balanced diet
→ Best treatment modality for Hepa B o For the liver to recuperate.
8
→ Identify toxic agents and eliminate it
→ Gastric lavage
o Such as when client ingests chemicals or excessive
medication (e.g. paracetamol) which are toxic to the
liver.
▪ Paracetamol – Oral is 500 mg
• Yung 200 mg will go through the
Hepatic first-pass; it will get
metabolized. Thus, the remaining
300 mg will remain bioavailable
inside the body.
▪ Paracetamol – IV is 300 mg
o May also give fluimucil (?) which is rich in glutathione.
CHOLELITHIASIS/CHOLECYSTITIS
→ Cholelithiasis is stone formation in the gall bladder.
o Surgery management
▪ Simple surgery
▪ Laparoscopic surgery
• Maraming complications like
bumubuka yung tahi.
▪ Open cholycystectomy.
• Mabilis lang ang procedure;
within the day dapat ay tumatayo
na ang patient
o When cholecystectomy is performed, removed na
ang gall bladder.
▪ The reservoir for the bile is also gone.
▪ Based on the books, kapag kumain ang
isang tao ng puro fats, hindi agad
makakapag produce ang liver ng bile.
• Initially, pwedeng ma-experience
ni patient ang nasusuka; may iba
rin na naiisip pa lang nila na
kumain ng taba ay nasusuka na
agad sila which is called Fat
Intolerance.
• However, nasasanay din naman
si patient – kakayanin or
matotolerate na rin ng katawan.
• Pero mayroon din namang
patients na natotolerate agad at
hindi nasusuka.
▪ General anesthesia ang commonly
ginagamit at hindi spinal anesthesia so
nakakatayo naman agad.
• Kapag hindi nakatatayo agad,
check the BP. Kapag
bumabagsak or tumataas ang
BP, bed rest muna si patient.
→ Cholecystitis is inflammation of the gall bladder.
o Could be with the presence of a stone or infection.
▪ Di porket may cholecystitis ay may stone na
agad, there is a possibility na infection has
developed lang.
▪ Cholecystitis is usually flushed to remove
the infected bile na nakastore.
DEFINITION OF TERMS
Micelles
→ Ultra microscopic units of protoplasm
Nidus
→ a cluster, nestlike structure; focus/ origin of infection or pathology
Beta Glucuronidase
→ Enzyme secreted by certain bacterias (E-Coli, Bacteroides,
Clostridium) which de-conjugates bile salts and promotes
precipitation of Ca salts
Deoxycholic Acid
→ A crystalline acid found in the bile; ↑ in amount facilitates
precipitation of crystals
Bilirubinate
→ A polymer/ salt of bilirubin
Mucin
→ A glycoprotein found in mucus. It is present in bile and saliva. It is
formed from mucigen and in water forms a slimy solution.
Lecithin
→ A fatty substance of the group called phospholipins, found in blood,
bile, brain, nerves and animal tissues and yielding stearic acid,
glycerol, phosphoric acid and choline on hydrolysis. In the bile, it
maintains cholesterol in suspension together with bile acids (salt) to
prevent its precipitation.
Stearate
→ An ester or salt of stearic acid. In the bile, it may combine with
Calcium to form Ca stearate stone
Palmitate
→ An ester or salt of palmitic acid derived from fat of both animal and
vegetable origin. In the bile, it may combine with Calcium to form Ca
palmitate stone
Esterification
→ Process by which an organic acid is combined with alcohol. Water
is eliminated in this reaction giving rise to an compound known as
ester.
Acetyl-Coenzyme A Acetyl transferase
→ 3-Hydroxy 3-Methyl 3-Glutaryl (HMG) Co-enzyme Reductase →
rate controlling enzyme that produces cholesterol
Cholate
→ Primary bile salts which are preferentially partial to cholesterol
Chenodeoxycholate
→ Primary bile salts which maintain cholesterol in suspension
preventing its precipitation
Nucleation
→ Formation of a nucleus or center which is either a salt (i.e.
Cholesterol salt) or ester of nucleic acid
Biliary Sludge
→ Precipitate of microcrystals consisting of Ca bilirubinate and
cholesterol microcrystals occurring in bile with high mucous (mucin-
glycoprotein content) which may contain “microliths” that develops
during gallbladder stasis
Microlith
→ A very tiny calculus/ stone
Lithogenic bile
→ A solution of bile wherein the ration between bile salts, cholesterol
and phospholipids favors cholesterol precipitation
Phospholipase A
→ An enzyme which promotes liberation of stearic acid and palmitic
acid in the bile
Arachidonic Acid
→ An essential fatty acid (phospholipids) which stimulates mucus
glycoprotein synthesis by Gallbladder mucosa
Murphy’s sign
→ Inspiratory arrest following deep palpation in the Right subcostal
area; (+) guarding secondary to pain
CAUSE
→ Unknown
9
 → Low fat diet
PREDISPOSING FACTORS (5Fs) o Since fat intolerance can occur
→ Female → Bile salts – both given after meals
→ Forty ● Medicines that can be given to exchange the bile and
→ Fertile excrete it through the feces to prevent accumulation into
→ Fat the body
o Initial fat intolerance, later on ay natotolerate naman ● Also used to avoid too much concentrations of bile and to
o There are patients na kahit kakatapos lang ng prevent stone formations
operation ay hindi nagkakaroon ng fat intolerance o Chenodeoxycholic acid – used therapeutically to
o Nakakatayo na ang pt. after operation since general dissolve cholesterol gallstones. (Betheseda, 2016)
anesthesia ang common na gamit at hindi spinal o Ursodioxycholic acid – works by reducing the amount
anes. Unless may problem with the pt’s BP (need na of cholesterol released by your liver and by slowly
bed rest si pt.) dispersing the cholesterol, which breaks up the
o Advice the pt. to stand once the pt. can tolerate stones. (Stewart, 2022).
→ Fair complexion
CHOLYSYSTECTOMY
THEORIES → Indicated when medications cannot control gallstone formations
→ Includes: → Preop care:
● Metabolic factors ● IVF to replace loss in vomiting and avoid F&E imbalance
● Biliary stasis ● DBCT (Deep breathing and coughing technique)
● Inflammation o DBE 5-10 times every 1-2 hours
→ No exact cause for the development of gallbladder stones ● Vit K. injection
→ Composition of gallbladder stones: (CCPBB) → Postop care:
● Cholesterol ● Low or semi-fowler’s position
● Calcium ● NGT for decompression
● Protein ● DBCT
● Bile salts ● Diet
● Bilirubin ● Ambulation after 24h post op
→ If there is stasis or concentrations of the CCPBB, (body keeps on o Ambulation within 24 hours is important, especially
producing cholesterol, increased protein and calcium intake), there with abdominal surgeries because of the possibility of
will be compositions of gallstones post-op adhesions.
o Magdedeposit yan sa loob at lalaki siya nang lalaki o Adhesions – “nagdikit-dikit” ang bituka ng pasyente
o May mga gallstones na isa lang pero malaki at dahil hindi nagambulate, possibility of another
mayroon ding multiple surgery (adhesiolysis) a year after the procedure to
address obstructions due to adhesions.
ASSESSMENT o Prevent complications from poor ciculation (MI,
→ Decreased fat emulsification – bile cannot flow accordingly to the stroke, pulmonary embolism)
intestine, which results to the following: o Once anesthesia wears off, allow patient to sit in a
● Fat intolerance high-fowler’s sitting position and dangle the feet
● Anorexia o Progressive movements are required to avoid
● Nausea and vomiting orthostatic hypotension (higa → sitting position in
● Flatulence high-fowler’s → dangling the feet over the bed →
● Steatorrhea – presence of fats in feces standing up bedside while having support with IV pole
→ Inflammation → roam around if the patient can tolerate
● Causes pain – expected in the right upper quadrant of the o Give pain reliever if patient does not want to ambulate
abdomen (RUQ) due to pain, binder/pillow if the patient ay natatakot
o In management of pain, we do NOT give MORPHINE na baka mabuka ang tahi
● Fever – also expected to have leukocytosis o State the consequences (complications) that may
→ Decreased bile flow in colon arise when patient does not want to ambulate
● Causes acholic stool (light, pale, clay-colored stool) – ● T tube if with CBD exploration
happens when there is decreased bile flow and when o Drains excess bile and blood kaya need ang strict
there is a poor absorption of fat-soluble vitamins, including monitoring of I&O
vitamin K o Malaki ang hiwa, buong tiyan may hiwa
o It is important to monitor for bleeding parameters if pt. o Has a T shape inside and a drainage bottle that
is subjected to surgery to be addressed prior surgery comes with it. The bottle can be Jackson-Pratt or a
by giving supplemental vitamin K for better simple bedside bottle
absorption o Bottle should be elevated to the incision site and
→ Increased serum bilirubin should be lowered as to use the law of gravity to drain
● Jaundice excess bile. The bile should not be spilled inside the
● Pruritus body especially in the abdomen, as it acts like acid
● Tea-colored urine and would melt anything that it comes in contact with.
→ Infection – due to cholecystitis and pancreatitis o I&O is important as it indicates when it is necessary
→ for the drainange to be removed. Ex. <50 cc x 3 days
MANAGEMENT is an indication that the drainage should be removed.
→ Relieve the pain Drainage is also considered as foreign, and should
● Positioning is very important not stay long inside the body. It would also prevent
● Provide hot compress to relieve pain and decrease spasm total would closure and healing (for other secretions,
of the sphincter of Oddi but for bile , it should not be removed even if it is less
● Meperidine HCL (Demerol) than 50 cc)
o We do NOT give MORPHINE because morphine can
increase spasms of the sphincter of Oddi = lalong
sasakit

10
 PANCREATITIS → Patient shall be kept in Semi-Fowler’s position – to promote comfort
→ Acute inflammation of the pancreas → Antimcrobials and Calcium Supplements
→ Can be acute or chronic o Antimcrobials are given as necessary.
→ Unknown etiology o Calcium supplements are given since patients are
hypocalcemic. But remember that, absorption of
CAUSE calcium will not happen if there is Vitamin D
→ Alcohol deficiency. So, usually, if calcium supplements are
→ Biliary obstruction given, Vitamin D is also given.
→ Intesitinal diseases → Insulin administration to manage hyperglycemia.
o Remember that if a patient has pancreatitis, the islets
ASSESSMENT of Langerhans has incapacity to produce hormones
→ Pain that form insulin.
● Incapacitataing pain
o Brought about by the release of chemical mediators
which can lead to neurogenic shock.
o Hemorrhage can cause hypovolemic shock.
o If there is a peritoneal spill, the patient can experience
peritonitis which can lead to respiratory distress.
o Peritonitis can also cause septic shock, that is why
pancreatitis has high mortality rate.
→ Anorexia, N/V
→ Steatorrhea
→ Jaundice
→ Hypocalcemia
→ Fever
→ Severe dehydration with loss
→ Hyperglycemia
→ Severe amylase, serum lipase, urine lipase is elevated

MANIFESTATIONS
→ Abdominal tenderness and distention
→ Pain
o Abrupt pain in the left lower quadrant – more
prominent in this area since pancreas is in this
location)
o Pain description: Burning, stabbing, pressing pain
o Pain can also be felt in epigastric area, radiate to
different body parts such as the shoulders, substernal
area, back, and plank area.
→
→ Cullen’s Signs
o Signs of hemorrhage
o Defined as the bluish, purplish discoloration in the
periumbilical area accompanied by tachycardia,
hypotension, fever, and some develop jaundice

→ Grey Turner’s Signs

o Discoloration in the plank area – bruises in the plank
area due to hemorrhagic activity

MANAGEMENT
→ Assess abdominal, cardiac, and respiratory status of the patient.
→ Relieve pain: Meperidine HCL as ordered.
o Demerol can also be prescribed
o Morphine is not prescribed
→ Assess for fluid and electrolyte balance
→ Monitor vital signs and I/O.
→ Secure laboratory studies.
o Some patients need central venous pressure (CVP)
monitoring and/or urine and stool monitoring as well
as blood sugar monitoring (since pancreas is the one
that is affected, thus abnormalities in blood sugar are
expected).
→ TPN for nutritional support.
o Because we need the patient to be put in NPO to rest
the pancreas and for management of nausea and
vomiting.
→ NGT
o To decompress and remove gastrin and secretion
from intestines to give rest to pancreas – since if
gastrin is present, the pancreas will continue to
produce lipase.
11
 NRS - MEDICAL SURGICAL NURSING II (LEC)
Hepatobiliary and Pancreatic Disorders (PLM-CN BATCH 2020) NRS 3217-9

Table: COMPARISON OF MAJOR FORMS OF VIRAL HEPATITIS

HEPATITIS A HEPATITIS B HEPATITIS C HEPATITIS D HEPATITIS E
Previous Infectious Hepatitis Serum Hepatitis Non-A, non-B
Names
Epidemiology
Cause: HAV HBV HCV HDV HEV
Incidence: Epidemic in areas of poor sanitation Worldwide; especially in drug Post-transfusion Found in conjunction Same with Hepa A
Common in fall and winter addicts and clients exposed to Those working around blood and with Hepa B
blood and blood products. blood products
Occurs all year Occurs all year
Mode of Fecal-oral Parenterally Parenterally; Same as HBV; Fecal-oral route
Transmission Poor sanitation Sexual contact with infected Transfusion of blood and blood HBsAg needed for Person-to-person
Person to person contact persons; carriers products replication contact possible
Waterborne; foodborne Perinatal transmission Contaminated drug Pattern similar to HBV (low risk)
Airborne if copious secretions Fecal-oral route paraphernalia Co-infects with Hepa B;
Transmission possible with oral-anal Sexual contact close personal contact
contact during sex
Incubation 15-50 days 28-160 days 15-160 days 21-140 days 15-65 days
Period
Risk factors Close personal contact Health care workers in contact w/ Same as for HB Same as for Hepa B Handling feces
Handling feces contaminated wastes blood and blood products contaminated wastes
Hemodialysis and post transfusion
clients
Homosexually active males and drug
users
Immunity Average 30 days Average 70-80 days Average 50 days Average 35 days Average 42 days
2nd attack indicates weak immunity
or infection w/ another agents
Nature of May occur w/ or w/o symptoms May occur w/o symptoms Smilar to Hepa B Similar to Hepa B Similar to Hepa A
Illness Flu-like symptoms Arthralgias, rash Less severe; anicteric Very severe in
Pre-icteric phase: pregnant women
HA, malaise, anorexia, fever, fatigue
Post-icteric phase:
Dark urine, icteric sclerae, jaundice,
tender liver
Diagnostic IgM (+) acute infection (+) HbcAg, HBsAg, HBeAg Not identified HD Ag (+) HE Ag (+)
tests IgG (+) post infection
Vaccine HAV vaccines HBV Vaccine None None None
Havrix, Vagta Recombivax HB
Severity Usually not fatal; More serious; may be fatal Not Known Increase mortality w/ Not fatal
Hepa B
Outcome Mild w/ recovery Maybe severe Frequent occurrence of chronic Similar to Hepa B Mild with recovery
Mortality rate: < 1% Mortality rate: 1-10% Carrier state and chronic liver Greater likelihood of Mortality rate <1%
NO carrier state Carrier state possible disease carrier state No carrier state
No  risk of chronic hepatitis, cirrhosis,  risk of chronic hepatitis, cirrhosis,  risk of, Hepatic CA No  risk of active No  risk of chronic
Hepatic CA Hepatic CA hepatitis, cirrhosis, hepatitis, cirrhosis,
Hepatic CA

TRANSCRIBED BY: Groups 1 and 2

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