Republic of the Philippines

Bulacan State University

City of Malolos, Bulacan

COLLEGE OF NURSING
Medical-Surgical Nursing
ANATOMY OF THE ACCESSORY DIGESTIVE ORGANS
(HEPATO-BILIARY & PANCREATIC SYSTEM)

I. Major Functions of the Liver (largest gland in the family of visceral organs) (organ responsible
for detoxification of blood before returning in the cardiac circulation)
1. Carbohydrate metabolism
-generation of energy from glucose sources, for the liver, one of the glucose sources ae
the glycogens (glycogenolysis) (building up glycogen from the glucose sources)
- Polymerizes glucose to glycogen; breaks down glycogen to glucose; converts
noncarbohydrates to glucose
2. Lipid metabolism
- Oxidizes fatty acids; synthesizes lipoproteins, phospholipids and cholesterol;
converts portion of carbohydrate and protein molecule into fats (if need ng body ng
fats, liver will play a major role; no cells in the body would be regenerating cells in
the body without presence of lipid. Without liver, no cells in body would be
regenerating; no cell walls, no cell membranes which are highly made of
phospolipids
3. Protein metabolism
-from the protein compounds, liver is responsible from breaking down these protein
compounds into building blocks such as amino acids, forming urea…etc. Without ability
of your liver to metabolize and to produce and excrete waste products from protein

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 metabolism such as ammonia, it would be detrimental in the body because ammonia
couldn’t be long staying in the bloodstream because it could be neurotoxin for the body
- Deaminates amino acids; forms urea; synthesizes plasma proteins; converts certain
amino acids to other amino acids
4. Storage
- Stores glycogen, iron, and vitamins A,D, and B12 (B complex)
5. Blood filtering
- Removes damaged red blood cells and foreign substances by phagocytosis (made
possible by Kuppfer cells) Kuppfer cells are specialized form of WBCs particularly
macrophages responsible for phagocytosis process. Phagocytosis when wbcs
engulfed bacterias other foreign substances that should be disposed of the
bloodstream because they shouldn’t be thre.
6. Detoxification
- Removes toxins from blood
7. Secretion
- Bile: function to emulsify fatty globules (Aids in the digestion process for the fats in
to simpler component into fatty acids. (bile doesn’t come from gallbladder, because
it only stores the bile)
8. Bilirubin Metabolism
-Bilirubin is pigment derived from hemoglobin breakdown (RBC BREAKDOWN) caused
by Kuppfer cells (one of the many components of bile). Without your liver, your
bilirubin would be very harmful or dangerous for your body to keep on harboring. It
would be very irritating not only to the skin but also to the liver kaya dapat hindi siya
long staying and needs to be removed by the body.

9. Blood Clotting Functions

-Synthesizes prothrombin, fibrinogen, and clotting factors I, II VII, IX, and X. (very
important component of blood responsible when we would be encountering wounds or
injury or overall healing process of our body. Blood coagulation
- for clotting cascade . blood coagulation
II. Function of the Gallbladder
- Stores bile between meals, reabsorbs water to concentrate bile and contracts to
release bile into the small intestine (helps us release more bile into the duodenum)
III. Function of the Pancreas (secretion for digestive juices or enzymes)
1. Enzyme Secretion
a. Pancreatic amylase – breaks down starch and glycogen into disaccharides
b. Pancreatic lipase – breaks down fats into fatty acids and glycerol
c. Proteolytic enzyme (trypsin (responsible for protein metabolism), chemotrypsin,
carboxypeptidase) – breaks down proteins or partially digested proteins into
peptides
d. Nucleases – breaks down nucleic acids into nucleotides

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CARE OF THE CLIENTS WITH HEPATO-BILIARY AND PANCREATIC DISORDERS

I. Assessment of the Liver Function

A. Health History
1. Previous exposure to hepatotoxic substances (e.g. industrial chemicals)
2. History of alcohol and drug use (e.g. acetaminophen, ketoconazole, valproic acid)
acetaldehyde, (if pt will be long engagement in it, it would be injurious for the liver)
3. Sedentary Lifestyles (e.g. unsafe sex (hepatitis), foreign travel (more of practices
that could damage the liver, preparation of foods, meals, snacks that we order
would not be safe for us to eat because there are diseases that could be get from
fecal oral route, alcohol abuse)
4. Familial liver disorders (e.g. hemochromatosis (iron related disorder, Wilson’s
disease build up of copper in the blood)
B. Physical Assessment
1. Inspection
- Pallor, jaundice, edema, skin excoriation, petechiae (pinakamaliit) next size is
purpura or ecchymosis (pinakamalaki), gynecomastia (Abnormal enlargemet of
breast), asterixis (flapping movement of upper xtremity particularly hands,
excessive ammonia in blood that irritates the brain tissues ), slurred speech
(Aphraxia is when patient suffering from inability to execute certain activities that
he or she is familiar doing in the past), impaired neurologic status (if there are brain
tissue irritation when there is liver dysfunction)
2. Palpation and Percussion
- The examiner places one hand under the right lower rib cage and presses
downward with light pressure with the other hand.
Walang auscultation dahil wala naman yung beating or pumping
C. Diagnostic Tests
1. Bilirubin Metabolism (Pigment Studies)
a. Total serum bilirubin
- ↑ hepatocellular damage
- Normal results : 0.1 – 1mg/dl; 1.5 mg/dl and above result to jaundice
- Regardless of conjugated and unconjugated. When we observe high level of it, it
would suggest hepatocellular damage. We examine blood here dahil serum means
blood or plasma. Hepatocellular are hepatocytes basic units of liver. If meron
damage sa liver, hindi mamemetabolize ng liver kaya magaccumulate lang yun kaya
tataas level.

- Bilirubin actually came from RBC destruction or hemolysis. With this, not only the
RBC or cell itself will be destructed but also the substances inside the RBC
particularly the hemoglobin. It is a combination of two globules particularly the
heme and the globin. Heme is a pigment carrying component of the hemoglobin.
Globin is the protein carrier. Heme would have two products from its breakdown.
First is iron, and a free bilirubin or unconjugated bilirubin (lipid-soluble). Unless this
free bilirubin would be binding to another substance that would make it conjugated

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 or water soluble that’s a further process. Globin would only go in the amino acid
pool that will either be excreted from the body. We would be focusing in bilirubin.
- Once we derived free bilirubin from RBC destruction, we get an unconjugated
bilirubin. This bilirubin is important to be combined with bile. Bile is very
encompassing when it comes to contents. Its so important that it contains lots of
nutrients, bile salts like bilirubin. (It produces color of stool urine). It would never be
able to combine with bile unless it will be added to a glucuronic acid. Glucoronic
acid would be found in the liver gland. Once your unconjugated bilirubin would be
transported in liver tissue, it would meet glucuronic acid. The combi would produce
conjugated bilirubin. Then it would combine with the bile which we find in the liver.
It will be free or welcome to the duodenum. Di siya makakarating sa duodenum ng
hindi siya conjugated meaning water-soluble kasi yun lang winewelcome ni
duodenum mga water-soluble digestive juices. Now it will become urobilinogen, the
it will join the necessary digestive process the net effect will become urobilin in
urine that gives colon to urine and stercobilin in feces that gives color to feces.
b. Conjugated / direct bilirubin
- ↑ biliary obstruction (happen exactly at the liver organ itself kapag meron
inflammation infection si liver baka di makalabas si bile from inside hence we call it
biliary obstruction. Hindi naman kay liver lang, minsan naoobstruct ang bile right at
the duct system that connects liver to duodenum. Bilirubin wouldn’t reach
duodenum kaya rereturn sa bloodstream, they would be found elevated in level.
c. Unconjugated / indirect bilirubin
- ↑hemolysis of RBC (hepatocellular damage)
d. Urine bilirubin (foam test)
- ↑ conjugated bilirubin in urine – hepatocellular / obstructive biliary disease
- Unconjugated bilirubin is not excreted in urine because it is not water – soluble
e. Urine urobilinogen
- ↓ obstructive biliary disease
- ↑ hepatocellular damage
- Normal result : 0.2 – 1.2 units
f. Fecal urobilinogen (Stercobilin)
- ↑ hemolysis of RBCs
- Absence : obstructive biliary disease

2. Protein Metabolism
a. Total serum protein
↓ hepatocellular damage
b. Immunoglobulins
(Antibodies)
- IgA, IgG - ↑ in liver cirrhosis
- IgG - ↑ chronic active hepatitis; biliary cirrhosis
- IgM - ↑ hepatitis A
c. BUN
-urea or byproducts of protein metabolism

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- ↓ severe hepatocellular diseases → obstruction of portal venous flow (portal veins

ay nasa liver, dun lang sila nakikita)
d. Blood ammonia levels (byproducts of protein metabolism)
- ↑ severe hepatocellular damage
- Normal result: 75 ʮg / dl

3. Fat Metabolism
a. Serum Total Cholesterol and Cholesterol Esters
- ↓ hepatocellular damage
- ↑ biliary obstruction
- Normal result: 140 – 220 mg/dl
b. Serum phospholipids
- ↓ hepatocellular damage
- ↑ biliary obstruction
- Normal result: 150 – 250 mg/dl

4. Pro Time; PTT; APTT

- ↑ hepatocellular damage (long clotting time)

5. Serum Enzymes : ↑ hepatocellular damage (Can be found in the blood)

a. AST (Aspartate aminotrasferase/ SGOT
b. ALT (alanine aminotransferase/ SGPT (most specific indicator of liver function)
(n kapag tumataas, it suggests impending liver disease
c. LDH (lactic dehydrogenase)
d. GGT (gamma glumatamile transferase)
- ↑ in alcohol-induced liver cirrhosis
e. Serum alkaline phosphatase
- Slight to moderate elevation: hepatocellular damage
- Severe elevation: obstructive biliary disease

6. Ultrasound of the liver

- Nursing Responsibility:
i. NPO 8-12 hours (the meals can cause
interference)
ii. Laxative the night before the
procedure
iii. Adequate hydration (would aid in
accurate visualization of liver tissue)

7. Liver Biopsy
- Removal of small small amount of liver tissue, usually through needle
aspiration.(sometimes, the excision may be performed when undergoing open
surgery na kapag meron access to handle the liver in actual then right away excision

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 should be done and undergo biopsy) – simple aspiration of liver tissue is
performed.
- Nursing Responsibility (Preop):
i. Secure written consent (Due to invasive procedure)
ii. NPO 2-4 hours
iii. Vitamin K injection (puncturing liver can cause profuse bleeding because its
highly vascularized organ)
iv. iv. Monitor Pro Time ; initial VS
v. Position in the left side because liver is underneath right upper quadrant. or
supine position with pillow under the right shoulder (for full access of liver
tissue of patient)
vi. Instruct to exhale deeply; hold breath 5-10 seconds during needle insertion to
prevent trauma to diaphragm –
Nursing Responsibility (Postop):
i. Turn to right side for 4hours to apply pressure and prevent
bleeding (we want to prevent bleeding) (We put pressure on the injection
or extraction site) (higa lang sa affected side ay kapag liver biopsy,
pneumonectomy (lung surgery because we want to allow unaffected side
to expand fully), and bone marrow aspiration (we want to prevent
bleeding or profuse bleeding)
ii. Bed rest for 24 hours
iii. Monitor VS every 30 minutes – every hour for the first 24 hours
(because profuse bleeding can alter the vital signs)

8. Paracentesis (remove excess

fluid in peritoneal cavity)
- Nursing Responsibility (Preop):
i. Secure written
consent
ii. Check initial VS iii. Ask to
empty bladder to prevent
puncture (nagpupuncture
right beneath the umbilicus)
iv. Check serum protein
studies
v. Place in sitting/upright
position
- Nursing Responsibility (Postop):
i. Assess VS ii. Assess urine
output iii. Rigidity of abdomen (s/sx of bleeding; peritonitis)
iv. Signs and symptoms of hypovolemic
shock (kapag masyado naubos fluid
sa tao, baka magkahypovolemic
shock)

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9. Endoscopic Retrograde Cholangiopancreatography (ERCP) (cholangio is the duct

system that connects gallbladder, liver and pancreas to duodenum) (pancreato is
pancreas and pancreatic duct)

- Direct visualization with radiographic examination of the liver, gallbladder and the
pancreas. Contrast medium is introduced via the endoscope, as x-rays are taken
simultaneously.
Nursing Responsibility (Preop):
i. Secure written consent ii.
NPO 10-12 hours
ii. Check for allergy to iodine /
seafoods
iv. Take initial VS
v. AtSO4; Valium – as ordered (To relax
patient and depressed gag reflex) vi.
Local anesthetic spray into the throat
vii. Place in left side to facilitate introduction of endoscope tubing)
- Nursing Responsibility (Postop):
i. NPO until gag reflex returns ii.
Turn to side to prevent aspiration iii.
Monitor VS
iv. Monitor signs and symptoms of sepsis, perforation, pancreatitis

D. Clinical Manifestations of Hepatic Dysfunction

1. Jaundice (icterus)
a. Resulting from increased bilirubin concentration in the blood
b. Types:
i. Hemolytic jaundice (results
from increased destruction of

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 RBCS which hinder liver to
excrete excessive bilirubin in
the blood
iii. Hepatocellular
jaundice- caused by
inability of the damaged
liver cells to clear
normal amount of
bilirubin from the blood.
iv. Obstructive Jaundice
-caused by intrahepatic meaning
the problem is within the liver
itself. Extrahepatic obstruction
or outside the liver of the bile
duct which lead to systemic
reabsorption of bile
iv. Hereditary
hyperbilirubinemia – increased
serum biliburin levels due to
several inherited liver disorders
(E.g. Gilbert’s syndrome, Rotor’s
syndrome)
2. Portal Hypertension
a. Obstructed blood flow through the damaged liver results in increased pressure
throughout the portal venous system. Consequences include ascites and
esophageal varices. (obstruction in the portal veins that would be found in the
liver.) (Before the blood would return to the heart, specifically at the right side
of the heart when it must travel through the IVC, lahat ng dugon a makakabalik
sa puso must travel first through the liver) and you will travel freely inside the
liver if you have intact portal veins.

2.1 Ascites –abnormal fluid accumulation in the peritoneal cavity

Real culprit is portal hypertension and when your liver is not accommodating the
blood that must be returning to the heart what will be the effect? Certainly the
blood would go back to its origin dahil di makadaan kay liver. Closest origin would
be the splanchnic blood vessels these portains to blood vessels surround the
intestines. If very minimal or no blood would go through your liver, walang
ipupump yung heart hence there would be low circulating arterial blood volume.
Then yung body natin magcocompensate, it would initiate RAAS and ADH. (RAAS is
a regulatory or compensatory mech that would be activated if our body is suffering
from hypovolemia. Kapag ang body nauubusan ng dugo, gagawa ang katawan ng
body to compensate. Number 1 is to release renin. Renin will activate liver to
secrete angiotensin 1. However, it wouldn’t be a potent vasoconstrictor. Kailangan
niya maging malakas na vasoconstrictor to counteract the problem above which is

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massive vasodilation. Need magvasoconstrict dahil nauubos ang blood volume so

need pataasin ang pressure. Tataas lamang ito kapag nagnanarrow ang blood
vessels. RAAS would also intensify or increase the Na reabsorption of the body. The
more we conserve Na, the more we conserve water na need dahil nga meron
decreasing blood volume. Mangyayari lamang ito kung angiotensin one ay
magcoconvert sa more potent which is the angiotensin II na magkakaron body
natin to have a massive vasoconstriction. Likewise it would promote Na
reabsorption. We save body from decreasing blood volume because blood is highl
composed of water at the same time ADH production which is a hormone that
would come from hypothalamus and would be stored by the posterior pituitary
gland. Kapag marami yan, there would be an antidiuresis. You conserve water
hence increase blood volume. Hindi to normal dahil hypervolemia ay nasa
periotoneal spaces. Kaya ang body natin receives fake signal. Nagmukhang
naghyhypovolemia si patientna kanyang mga fluids ay nagcoconcentrate in one
compartment not normally filled with fluids.
2.2 Esophageal Varices

Collaborative Management
1. Dietary Modifications
- Strict sodium restriction (to conserve water through aldosterone hormone
produced by adrenals)
2. Diuretics
- E.g. Spironolactone (Aldactone) (potassium sparing diuretics) (The pt in the
beginning conserves Na, if we conserve sodium, we will be excreting potassium)
(Kapag naubos si K, delikado dahil baka magkahypokalemia without enough level of
potassium the cardiac level would suffer, furosemide (Lasix) (loop diuretic or
excrete both sodium and potassium because in the long run baka masobrahan din
sa potassium na delikado rin. Kaya dapat continuous tapon ng tubig sa pt thru
diuretics. So dapat matapon yung sodium, itapon na rin si potassium para balance
3. Bed rest
4. Paracentesis
5. Transjugular Intrahepatic Portosystemic Shunt (TIPS) (bypass for liver
circulation)
- Method of treating ascites in which a cannula is threaded into the portal vein by the
transjugular route. Treatment of choice for refractive ascites (repetitive ascite
(kapag di makatravel ng ays para makabalik kay IVC yung dugo, lagyan ng shunt).

2.2 Esophageal varices – dilated, tortuous, bleeding prone esophageal veins

(pakibasa)

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 Diagnostic Tests
1. Endoscopy
2. Barium swallow, UTZ, CT and
angiography
Collaborative Management
1. Note for signs of hypovolemic
shock
2. Blood transfusion
3. Sengstaken – Blakemore tube
(Balloon tamponade)
4. Avoid ASA
5. Administer either vasopressin
drugs combined with Nitrates or
administer Somatostatin

II. Management of the Client with Hepatic Disorders

A. Hepatic Encephalopathy and Coma
- A life threatening complication of liver disease, occurs with profound liver failure
and may result from the accumulation of ammonia and other toxic metabolites in
the blood. (unsuccessful recovery from previous liver disorder)
Signs and Symptoms
1. Mental changes 2. Motor disturbances
- Drowsiness - Asterixis
- Disorientation - Apraxia (speech defect or motor disturbance)
- Mood swings - Hyperactive DTR (deep tendon reflexes)
- Stuporous (looking weak) - Flaccidity (lack of muscle tone)
- Insomnia - Coma (brain could not stand neurotoxins)
o -fetor hepaticus (fecal like breath odor)
- Incoherence
These damaged hepatocytes would experience failure in detoxifying and conversion of ammonia to
urea. Your ammonia, instead of being excreted in the form of urine, it would go back in the
bloodstream. E ammonia should’nt be long staying in the blood because ammonia can travel along
the brain vasculature and it would be very harmful because its considered a neurotoxin or capable
of irritating brain tissues leads to inflammation that we call encephalopathy. Brain disorder brought
by liver disorder. Mental changes and motor disturbances appear.
Diagnostic Test
1. EEG – generalized slowed movement of brain waves.
Medical Management
1. Pharmacologic Treatment
a. Lactulose – to reduce serum ammonia levels which is the main culprit of disorder
b. IV administration of glucose – eg D50:50 (We give glucose concentrated soln to
prevent metabolizing protein sources like glycogen. Dahil the more na
nagmemetabolize ang body ng protein, the more lang siya magpproduce ng

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ammonia. Para maprevent to, tayo na magbigay ng glucose. (50 percent glucose in
a 50ml soln)
c. Vitamin administration and electrolyte administration
Nursing Management
1. Maintain a safe environment (because of motor disturbances that would put the pt for
injury possibilities)
2. Monitor mental status by keeping a daily record of handwriting and arithmetic
3. Monitor serum ammonia level daily
4. Protein intake is moderately restricted

B. Hepatitis
- Any acute inflammatory disease of the liver. It can be caused by viruses, bacteria or
toxic injury to the liver.
B.1 Toxic Hepatitis (non-communicable hepatitis)– this can be caused by drugs, alcohol,
industrial toxins and plant poisons
Signs and Symptoms
Anorexia
- Nausea and vomiting
- Lethargy
- Icterus
- Hepatomegaly
- Hepatic tenderness
Collaborative Management
1. Identify the cause and eliminate it.
2. Gastric lavage and cleansing of the bowel to remove hepatotoxins as indicated
3. Educate the need for well – balanced diet that is protective to the liver
4. Minimal or no alcohol
5. Maintain normal fluid and electrolyte balance
6. Promote well – balanced diet
7. Promote rest.

B.2 Viral Hepatitis (communicable)

Comparison of Major Forms of Viral Hepatitis

Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E

Previous Infectious Serum Non – A, non – Delta Hepatitis

names hepatitis hepatitis B hepatitis
Causes Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
virus (HAV) virus (HBV) virus (HCV) virus (HDV) virus (HEV)

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Mode of Fecal – oral Blood borne or Infected blood Same as HBV Fecal – oral
Transmission route (would be body fluids; transfusion; route
eating food perinatal (ast parenteral drug
handled birth) (Semen abuse (neede-
unsanitarily vagina stick);
with person secretions) contaminated
who have hepa water; direct
A) (street contact (sexual
foods) intercourse)
Incubation 15 – 50 days 45 – 160 days 14 – 150 days 21 – 140 days 15 – 65 days
period
Signs and May occur with May occur Similar to HBV; Similar to HBV Similar to HAV;
symptoms or without without less severe and very severe in
symptoms; symptoms; anicteric (not pregnant
flulike illness may develop icteric) women
Preicteric arthralgia (joint
phase: pain) or rash
Headache,
malaise,
fatigue,
anorexia, fever
Icteric Phase:
Dark urine,
jaundice of
sclera and skin,
tender liver

Preicteric Phase: athralgia, tenderness in RUQ, weaknesses, weight loss, hepatomegaly,

lymphadenopathy (swelling of lymph nodes)
(Ang mga hepatitis po ba ay gumagaling pa? who among them would be treatable and
who among them would never give u hope)
Prevention
1. General preventive measures:
- Handwashing by all persons
- Feces, urine, blood and other body fluids are considered potentially infectious and
should be disposed properly.
- Contaminated needles and other equipment that come in contact with infected
blood and body fluids, disposable and non-disposable needles, syringes and other
equipment used in patient care must be handled with great care; discarded in
appropriate containers
- Practice “Universal Precautions” in all clients
- Do not recap needles
- Proper sterilization of equipment used in clients

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2. Preventive measures used with persons with known hepatitis:

- For clients with known hepatitis A, enteric precautions should be implemented as it
is fecal-oral disease transmission
- For clients with hepatitis B, Hepatitis C and delta hepatitis, blood and body fluid
precautions should be observed
- Instruct client with viral hepatitis not to donate blood esp in hepa C infection
- Advise client with Hepatitis B, C and D not to have intimate sexual contact during
the period of infection
Collaborative Management
1. Promotion of rest to relieve fatigue
2. Increase fluid intake up to 3000ml/day
3. Well – balanced diet – fruit juices and carbonated beverages; fats may need to be
restricted; alcoholic beverages should be avoided
4. Monitor Pro Time and assessing for bleeding tendencies
5. Avoid and prevent any means of trauma
6. Administer vitamin K as ordered
7. Provide comfort measures

C. Liver Cirrhosis
- A chronic disease characterized by replacement of normal liver tissue with diffuse
fibrosis that disrupts the structure and function of the liver
Types
1. Laennec’s Cirrhosis
- Scar tissue of the liver caused by chronic alcoholism
2. Postnecrotic Cirrhosis
- A late result of previous acute viral hepatitis (kind of secondary liver disease)
3. Biliary Cirrhosis
- It results from chronic biliary obstruction and infection (cholangitis) (inflammation of
bile duct system)
4. Cardiac Cirrhosis
- Resulting from RSCHF (right-sided congested heart failure)
Signs and Symptoms
- Anorexia, weakness and weight loss – due to liver’s inability to metabolize nutrients
and store fat-soluble vitamins
- Fever – tissue injury
- Jaundice, pruritus, tea-colored urine – due to high serum bilirubin
- Bleeding tendencies – inability of liver to store vit. K thereby unable to synthesize
clotting factors
- Immunocompromised – due to low kuppfer cells (macrophages that help us get rid
of many infections): high phagocytosis
Portal hypertension (hepatomegaly, splenomegaly, spider angioma/telangiectasia
or protrusion of blood vessels to underlying skins, palmar erythema)

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 - Ascites- due to fluid shifting caused by portal hypertension, hypoalbuminemia, and
hyperaldosteronism which are both related to RAAS activation
- Esophageal varices – blood circumvents into collateral circulation (esophageal vein
is close to portal veins that if the liver wont accommodate expected amt of blood
for return in right side of heart, babalik din yan sa origin and another close origin of
the blood that must go thru liver is esophageal veins. So fragile thin and prone to
overdistention which re esophageal varcies
- Internal hemorrhoids, leg varicosities, dependent edema – due to venous stasis
abnormal venous return
- Males (↑estrogen): gynecomastia, ↓libido, impotence, fall of body hair, atrophy of
testicles (dapat testosterone ang tumataas sa kanila)
- Females (↑androgen): hirsutism, acne, deepening of voice
- Asterixis due to high ammonia levels
- Hepatic encephalopathy due to high ammonia levels
- Fetor hepaticus
Diagnostic Test
1. Enzyme tests – serum alkaline phosphatase, AST, ALT (most specific indicator for liver
damage) and GGT levels increase; serum cholinesterase decrease
2. Bilirubin test – increase result
3. Prothrombin Time – prolonged
4. CT scan and MRI
5. Liver Biopsy -confirmatory for malignancy
Collaborative Management 1. Provide rest periods
2. Diet:
Early stage: ↑caloric, ↑CHO, ↑CHON liver damage, ↓Fats liver responsible for fat
metabolism without the help of this we need to lower fat in diet
Late stage: ↑caloric, ↑CHO, ↓CHON (more protein, more ammonia), ↓Fats
3. Skin care for pruritus
4. Avoid trauma / injury / infection immunosuppressed si pt
5. Ascites management
- Monitor weight (indicator of fluid status and nutritional status), I & O, abdominal
girth
- Restrict sodium & fluid intake (more sodium, more fluid)
- Administer diuretics as ordered: Spironolactone then Furosemide (the client
experiences hypokalemia due to hyperaldosteronism… then hyperkalemia will
occue due to prolonged use of spironolactone)
- Administer albumin / IV as ordered
- Assist in paracentesis
6. Esophageal varices management
- Avoid the following to prevent rupture of the varices: shouting, straining at stool,
bending, hot & spicy foods, lifting heavy objects - If bleeding occurs:
i. Place the client in semi-Fowler’s to prevent aspiration ii.
Suction the mouth

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iii. Administer IVFs, blood transfusion, plasma expanders as ordered

iv. Administer vasopressin (Antidiuretic drug to promote
vasoconstriction of sphlancnic arterial bed) as ordered v. Gastric
lavage as ordered (so that the pt would not swallow blood or travel in
entire bowel system)
vi. Sclerotherapy – an injection of sclerosing agent (a soln which aim
to harden the site of bleeding, stop or hinder the bleeding) into the
bleeding varices through an endoscope
vii. Balloon tamponade (Sengstaken – Blakemore tube)
7. Management to decrease ammonia formation
- Restrict protein in the diet
- Duphalac (Lactulose) – To lower pH in colon, and reduce formation of alkaline
ammonia; increases peristalsis thereby excretion of ammonia via feces.
- Neomycin sulfate – To reduce colonic bacteria which are responsible for ammonia
formation
- Tap water or NSS enema to remove digested blood from the colon since the pt can
have swallowed the bleeding from varices-
-Avoid sedatives . These are hapatotoxic

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 - Avoid ASA . This can cause further bleeding
- Eliminate alcohol because they can aggravate or worsen the cirrhosis

III. Management of the Clients with Gallbladder Dysfunction

A. Cholelithiasis / Cholecystitis
Cholelithiasis – stone formation in the gallbladder (cholecyst or gallbladdedand
lithiasis stone formation) lit- stone
Cholecystitis – inflammation of the gallbladder
Choledocholithiasis- presence of gallstone in the common bile duct
Choledocho is the bile duct (Stone may be dislodged from the gallbladder inside into
the tubing of common bile duct. If that would be lodging the flow of bile from the
gallbladder, liver, pancreas to duodenum)
Predisposing Factors: 5F’s
1. F – emale (anatomically having a lot of fatty depositions)
2. F – at (obese) (gallstones related to fatty acid deposition)
3. F – air (caucasian) (anatomically predisposition)
4. F – orty and above (related to lifestyle)
5. F – ertile (multigravida; use of contraceptive pills)
Signs and Symptoms
- Fat intolerance (there would be no bile to be transported into the duodenum and
will do fat digestion) - alcoholic stool
- anorexia and weight loss - jaundice
- flatulence - pruritus
- steatorrhea - tea-colored urine
- pain (RUQ) location of gallbladder - gaseous eructation
or stagnation of bile no more reaching duodenum. Babalik sa bloodstream. Magkakalow
fat emulsification. Magkakaoverdistention sa organs like gallbladder kaya
magkakainflammation.
Diagnostic Test
1. Abdominal x-ray – could help but not sufficient
2. Ultrasonography
3. Cholescintigraphy
4. Cholecystography
5. Endoscopic Retrograde Cholangiography (ERCP)
Collaborative Management
1. Pharmacologic treatment
a. Meperidine HCl, drug of choice not Morphine SO4 causes spasm of the sphincter of
Oddi (prevent reflu from bile from duodenum to duct system
2. Low fat diet
3. Bile salts. Chenodeoxycholic acid; ursodioxycholic acid (UDCA) pc
4. Surgery – Cholecystectomy Preop Care:
- IVF to replace fluid and electrolyte losses due to vomiting
- DBCT exercises to prevent respiratory complications

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 - Vitamin K injection, especially if the prothrombin time is prolonged
- Postop Care: (general anesthesia)
- Semi – Fowler’s position to promote lung expansion (Dapat magsubside yung
anesthesia effect)
- NGT to prevent gastric distention (decompress stomach)
- DBCT to prevent atelectasis
- Low fat diet for 2-3 months - Ambulation after 24h postop -
- T-tube care: (gallbladder removal)
i. Inserted for bile drainage
ii. Drainage is brownish red for the first 24h;this is due to combination of blood
and bile
iii. 300 – 500ml of bile drainage for the 1st 24h but if beyond that, report to the
physician
iv. Drainage bottle should be placed in bed at the level of incision; not too low
because too much pull of gravity would drain all bile.- this is to drain the
excess bile not all of the bile

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IV. Care of the Clients with Pancreatic Disorder
A. Pancreatitis
- Inflammation of the pancreas, classified either acute or
chronic - Either acute or chronic
Acute pancreatitis- a disease ranging from a mild, self- limited
disorder to a severe, rapidly fatal disease that does not respond to
any treatment. It usually occurs within 6 months
Chronic Pancreatitis- a progressive, functional, and repetitive
disorder of the pancreas and associated glands; occurs more than 6
mos
Causes
1. Alcoholism
2. Drugs (Antihypertensives, diuretics, antibiotics, immunosuppressive, oral
contraceptives)
3. Biliary obstruction – related to bile reflux
4. Intestinal diseases – related to duodenal or small intestinal obstructions
5. autoimmunity
Signs and Symptoms
- Pain (LUQ); may start at the epigastrium, radiate to the back, flanks and
substernal area
- Anorexia
- Fever
- Nausea and vomiting
- Severe dehydration
- Weight loss

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 - Steatorrhea (prob with the lipase)
- ↑ serum amylase
- ↑urine lipase
- Hypocalcemia- calcium binds with undigested fats and it is lost in steatorrhea
- Hyperglycemia – damage of Langerhans’ islets cause low insulin production
- Jaundice
- Post – hemorrhagic necrosis
- Cullen’s sign – purplish discoloration of the periumbilical area
- Grey – turner’s sign - purplish discoloration of the flanks
With all causes, they can damage pancreatic cells, initiate inflammatory process, then edema due
to unresolved inflammary process, it would obstruct the outfow of pancreatic enzymes that must
reach the duodenum. If they wouldn’t be reaching the duodenum, they would accumulate in
pancreatic islet or cells and would be harmful for pancreas because they supposed to digest the
foods that we have eaten. The chyme that would come from the stomach. They would digest the
pancreas itself instead (Autodigestion of pancreas)
Diagnostic Test
1. Serum amylase and lipase – increasing in level within 24 hrs
2. X-ray, ultrasound, CT scan -image how does pancreas, condition of pancreas
3. Hct and hgb – to monitor bleeding tendencies
4. ERCP -endoscopic retrograde – visualize duct system and pancreas
Collaborative Management
1. Pharmacologic Treatment
a. Meperidine HCl (Demerol) opioid. Avoid morphine SO4 as it causes spasm of the
pancreas and sphincter of Oddi mas lalo magsstay mga substances and autodigest
it
b. Antimicrobials – to control infection
c. Ca supplement (Ca Gluconate) – to manage hypocalcemia
d. Vit D – to promote absorption of calcium
e. Insulin (e.g. Humulin R) – to manage hyperglycemia
2. Diet – NPO during acute phase; then bland or low fat diet (kung bigyan pagkain yung
pt, maano ng pancreas na meron siya dapat meron idigest, kaya it would secrete
enzyme. Kaso di makareach ng duodenum si enzyme) (gano po kadalasan
magtransform from npo to bland or low fat)
3. TPN – to provide nutritional supplement
4. IVF therapy (e.g. Plasma Expander) (hypovolemia)
5. NGT – to remove gastrin from the stomach and secretin from the duodenum. This
prevents further stimulation of the pancreas which is to produce to much pancreatic
enzyme.
6. Eliminate alcohol

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