College of Nursing

Santiago City

CHOLEDECTAL CANCER STAGE 3

In partial fulfillments of the requirements in

Nursing Leadership and Management (RLE)

NC 129A

Presented to the Faculty of

College of Nursing

Submitted by:
Donglon, Princess
Gonzaga, April Rose P.

Clinical Instructor:
NAME NI SIR -

Bachelor of Science in Nursing

2nd Semester, 2025-2026
PAST HEALTH HISTORY
The patient has a history of Hypertension (HTN) and Type 2 Diabetes Mellitus (T2DM).
Further details regarding the onset and management of these conditions were not
obtained.

PRESENT HEALTH HISTORY

In March 2025, the patient was diagnosed with a cyst in her colon. She underwent
surgery at SIMC (name of hospital) during the same month. Following the operation,
she received six cycles of intravenous chemotherapy. However, the chemotherapy
medication caused side effects, particularly diarrhea, which led her to discontinue the
treatment before completing the full course.

One week prior to admission, the patient experienced body weakness. Three days
before admission, she developed dizziness associated with nausea and vomiting. Her
highest recorded blood pressure during this time was 140/90 mmHg. On the day of
admission, she had multiple episodes of diarrhea, approximately 10 to 20 times, which
prompted her to seek medical care.

SOCIAL HISTORY

The patient is a 74-year-old housewife who has spent most of her life at home, caring
for her family and managing household chores. She has a simple daily routine, mostly
revolving around cooking, cleaning, and looking after her grandchildren. Due to her
lifestyle, she engaged in minimal physical activity and often spent long hours indoors.
She maintained close ties with her neighbors and relatives, frequently visiting or
chatting with them after dinner, sometimes sharing food during gatherings. She was not
a smoker but was often exposed to secondhand smoke from her neighbors and
relatives who smoked nearby.

In terms of diet, the patient was accustomed to eating fried and oily foods such as fried
fish, pork, chicken, and eggs, which were easy and convenient to prepare. On days
when the family felt tired or undecided about meals, they would often rely on fried foods
or processed items like canned sardines, corned beef, or instant noodles. Fresh fruits
and vegetables were eaten less frequently compared to meat and oily dishes. She
occasionally drank soft drinks with meals, especially during family occasions. Eating
patterns were often irregular, and she sometimes rested or lay down shortly after meals.
 FAMILY HISTORY

FEMALE
DECEASED

MALE CANCER

PATIENT
DM

HYPERTENSION

INTERPRETATION:

The patient is the youngest among three siblings, having two older brothers. Both of her parents are deceased and
had a history of hypertension. Her eldest brother was diagnosed with Type 2 Diabetes Mellitus and eventually
passed away due to old age. The second brother is living with hypertension. The patient, being the youngest, is
currently diagnosed with cancer, Type 2 Diabetes Mellitus, and hypertension.
PATIENTS PROFILE

Name: PATIENT P
Age: 74 years old
Sex: Female
Civil Status: Married
Birthdate: March 03,1951
Nationality: Filipino
Religion: Roman Catholic
Address: Santiago City
Occupation: Housewife
Weight: 60kg
Height: 5’2
BMI: 24.3 kg/m²
Chief Complaint: Body weakness, Dizziness, Vomiting, Diarrhea
Admitting Diagnosis: Choledectal Cancer Stage 3
Admission Date & Time: September 01, 2025 – 7:40 PM

Admitting physician: Dr. K. Co

Attending Physician: Dr. K. Co

 Overview of the Disease

Definition
Choledochal cancer, also called cholangiocarcinoma, is a rare malignancy that forms in
the slender tubes (bile ducts) that carry the digestive fluid bile. Bile ducts connect your
liver to your gallbladder and to your small intestine.
Cholangiocarcinoma, also known as bile duct cancer, occurs mostly in people older
than age 50, though it can occur at any age. It is an aggressive cancer, which means it
spreads fast. Most people receive a cholangiocarcinoma diagnosis after it’s already
spread outside of their bile ducts. At this point, bile duct cancer is difficult to treat, and
the prognosis (chance of recovery) is usually poor.
Types
 Intrahepatic cholangiocarcinoma is bile duct cancer inside your liver.
 Perihilar (hilar) cholangiocarcinoma is bile duct cancer in your hilum. The
hilum is the area just outside your liver where the smaller bile ducts from inside
your liver merge to form a larger duct called the common hepatic duct. It’s the
most common form of cholangiocarcinoma. Another name for perihilar
cholangiocarcinoma is a Klatskin tumor.
 Distal cholangiocarcinoma is bile duct cancer that starts outside your liver, in
the ducts closer to your small intestine.

STAGES
Staging looks at the size of the tumor, where it is, and if it has spread to other organs.
The staging system for cholangiocarcinoma is called the “TNM system.” The staging
has three parts:
 T-describes the size/location/extent of the "primary" tumor in the bile duct. The
size of your tumor seen on imaging tests and what is found after surgery.
 N-describes if the cancer has spread to the lymph nodes. Surgery to test if your
lymph nodes have cancer cells.
 M-describes if the cancer has spread to other organs (called metastases). Any
evidence of spread to other organs (metastasis).

 Intrahepatic Bile Duct Cancer Staging

 Stage 0
o Tis: The cancer is only in the mucosa (the inner layer of cells in the bile
duct). It hasn't started growing into the deeper layers.
o N0: It has not spread to nearby lymph nodes.
 o M0: It has not spread to distant sites.
 Stage IA
o T1a: The tumor is no more than 5 cm (about 2 inches) across and has not
invaded nearby blood vessels.
o N0: It has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IB
o T1b: The tumor is more than 5 cm (about 2 inches) across but has not
invaded nearby blood vessels.
o N0: The cancer has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage II
o T2: The tumor has grown into nearby blood vessels, OR there are 2 or
more tumors, which may or may not have grown into nearby blood
vessels.
o N0: The cancer has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IIIA
o T3: The cancer has grown through the visceral peritoneum (the outer
lining of organs in the abdomen).
o N0: The cancer has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IIIB
o T4: The cancer has grown directly into nearby structures outside of the
liver.
o N0: The cancer has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
o OR Any T, N1, M0: The cancer is any size and might or might not be
growing outside the bile duct, and has spread to nearby lymph nodes. It
has not spread to distant sites.
 Stage IV
o Any T: The cancer is any size and may or may not be growing outside the
bile duct.
o Any N: It may or may not have spread to nearby lymph nodes.
o M1: It has spread to distant organs such as the bones or lungs.

 Perihilar (Hilar) Bile Duct Cancer Staging

 Stage 0
o Tis: The cancer is only in the mucosa (the innermost layer of cells in the
bile duct). It hasn't started growing into the deeper layers.
o N0: It has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage I
o T1: The cancer has grown into deeper layers of the bile duct wall, such as
the muscle layer or fibrous tissue layer.
 o N0: It has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage II
o T2a: The tumor has grown through the bile duct wall and into the nearby
fatty tissue.
o T2b: The tumor has grown into the nearby liver tissue.
o N0: The cancer has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IIIA
o T3: The cancer is growing into branches of the main blood vessels of the
liver (the portal vein and/or the hepatic artery) on one side (left or right).
o N0: The cancer has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IIIB
o T4: The cancer is growing into the main blood vessels of the liver (the
portal vein and/or the common hepatic artery) or into branches of these
vessels on both sides (left and right), OR the cancer is growing into other
bile ducts on one side and a main blood vessel on the other side.
o N0: The cancer has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IIIC
o Any T: The cancer is any size and may or may not be growing outside the
bile duct or into nearby blood vessels.
o N1: It has spread to 1 to 3 nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IVA
o Any T: The cancer is any size and may or may not be growing outside the
bile duct or into nearby blood vessels.
o N2: It has spread to 4 or more nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IVB
o Any T: The cancer is any size and may or may not be growing outside the
bile duct or into nearby blood vessels.
o Any N: It may or may not have spread to nearby lymph nodes.
o M1: It has spread to distant organs such as the bones, lungs, or distant
parts of the liver.

 Distal Bile Duct Cancer Staging

 Stage 0
o Tis: The cancer is only in the mucosa (the innermost layer of cells in the
bile duct). It hasn't started growing into the deeper layers.
o N0: It has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage I
 o T1: The cancer has grown less than 5 mm (about 1/5 of an inch) into the
bile duct wall.
o N0: It has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IIA
o T2: The cancer has grown between 5 mm (about 1/5 of an inch) and 12
mm (about ½ inch) into the bile duct wall.
o N0: It has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
o OR T1, N1, M0: The cancer has grown less than 5 mm into the bile duct
wall and has spread to 1 to 3 nearby lymph nodes. It has not spread to
distant sites.
 Stage IIB
o T3: The cancer has grown more than 12 mm into the bile duct wall.
o N0: It has not spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
o OR T2 or T3, N1, M0: The cancer has grown 5 mm or more into the bile
duct wall and has spread to 1 to 3 nearby lymph nodes. It has not spread
to distant sites.
 Stage IIIA
o T1, T2, or T3: The cancer has grown to any depth into the bile duct wall.
o N2: Spread to 4 or more nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IIIB
o T4: The cancer is growing into nearby blood vessels (the celiac artery or
its branches, the superior mesenteric artery, and/or the common hepatic
artery).
o Any N: The cancer may or may not have spread to nearby lymph nodes.
o M0: It has not spread to distant sites.
 Stage IV
o Any T: The cancer has grown to any depth within the bile duct wall and
may or may not be growing into nearby blood vessels.
o Any N: It may or may not have spread to nearby lymph nodes.
o M1: It has spread to distant organs such as the liver, lungs, or peritoneum
(inner lining of the abdomen).

SYMPTOMS

 Early Stage (localized tumor, no major spread yet)

 Mild abdominal discomfort → Tumor starts pressing on bile ducts or nearby

tissue.
 Fatigue → Body uses more energy fighting the cancer, and bile flow disruption
affects metabolism.
 Occasional jaundice (yellowing of eyes/skin) → Tumor partially blocks bile flow,
causing bilirubin buildup.
 Progressing Stage (tumor growing, bile duct more blocked, some spread
possible)

 Persistent jaundice → Tumor more firmly blocks bile ducts → continuous

bilirubin buildup.
 Dark urine → Excess bilirubin filtered by kidneys instead of going to intestines.
 Pale stools → Lack of bile reaching intestines, so stool loses its normal brown
color.
 Itching (pruritus) → Bile salts deposited in the skin due to poor drainage.
 Abdominal pain → Tumor invades liver tissue or presses nerves and nearby
structures.

 Advanced Stage (large tumor, spread to vessels, lymph nodes, or distant

organs)

 Severe weight loss → Cancer increases energy use and reduces appetite;
malabsorption from blocked bile.
 Loss of appetite (anorexia) → Buildup of toxins in blood and systemic effects of
cancer reduce hunger.
 Hepatomegaly (enlarged liver) → Tumor spreads inside the liver or causes
congestion.
 Ascites (fluid in abdomen) → Blocked veins/lymphatic drainage + liver
dysfunction leads to fluid leakage.
 Generalized weakness → Combination of malnutrition, anemia, and cancer-
related fatigue.

CAUSES
The exact cause is not always clear, but it can develop due to chronic inflammation or
conditions that damage the bile ducts (e.g., primary sclerosing cholangitis, choledochal
cysts, chronic bile duct infections, or gallstones). These conditions promote abnormal
cellular changes leading to cancer formation.

RISK FACTORS

 Structural abnormalities where the bile duct and pancreatic duct meet
This condition causes chronic irritation of the bile duct lining. Over time, repeated
injury and repair of the cells may result in abnormal growth and cancer.
 Bile duct stones or choledochal cyst disease (bile duct cysts)
The presence of stones or cysts leads to blockage of bile flow, which results in
long-term inflammation and scarring. Continuous cellular repair in this setting
increases the chance of mutations that develop into cancer.
 Clonorchiasis (Chinese liver fluke infection)
The parasite damages the bile duct lining and triggers ongoing inflammation. The
toxins it produces can alter DNA, which may cause malignant transformation.
 Chronic ulcerative colitis
This condition increases the likelihood of developing primary sclerosing
cholangitis, which causes bile duct inflammation. Persistent injury and scarring
create a background for cancer to form.
 Cirrhosis of the liver
Cirrhosis leads to scar tissue formation that changes bile flow and cell structure.
The environment of chronic damage and regeneration promotes cancer
development.
 Hepatitis B or Hepatitis C
These viral infections damage liver cells and bile ducts over time, leading to
cirrhosis and genetic changes. These alterations increase the risk of cancer.
 Human immunodeficiency virus (HIV)
HIV weakens the immune system, making it difficult to clear infections. Chronic
inflammation and poor immune surveillance increase the likelihood of abnormal
cell growth and cancer.
 Inflammatory bowel disease (IBD)
IBD is linked with bile duct inflammation, particularly through primary sclerosing
cholangitis. Long-term scarring and irritation of the ducts may progress to cancer.
 Metabolic dysfunction–associated steatotic liver disease (MASLD/NAFLD)
Fat accumulation in the liver causes chronic liver injury and can progress to
cirrhosis. Repeated cellular damage increases the chance of malignant change.
 Primary sclerosing cholangitis (PSC)
PSC is one of the strongest risk factors for cholangiocarcinoma. It causes long-
standing bile duct scarring and blockage, which promotes cancer through
continuous inflammation and abnormal healing.
 Alcohol use disorder
Alcohol damages liver cells and contributes to cirrhosis. Continuous regeneration
of injured cells increases cancer risk.
 Diabetes
Diabetes alters metabolism, placing stress on the liver. The resulting chronic
inflammation and fibrosis may promote cancer formation.
 Obesity
Obesity promotes fat accumulation in the liver, which often leads to cirrhosis.
Persistent DNA damage in bile duct cells can lead to cancer.
 Smoking
Chemicals in tobacco act as carcinogens that damage DNA in the bile ducts and
liver. With time, these mutations may develop into cancer.
 Exposure to toxins (chemicals in rubber plants or automotive factories)
Chronic exposure to harmful chemicals may damage DNA. The gradual buildup
of mutations increases the risk of cancer.
DIAGNOSTICS

 Liver function tests (LFTs)

A venous blood sample is obtained to assess serum levels of bilirubin, alkaline
phosphatase, AST, and ALT. Elevated levels indicate hepatocellular dysfunction or
cholestasis. Obstructive patterns, such as markedly elevated alkaline phosphatase and
bilirubin, may suggest bile duct obstruction secondary to cholangiocarcinoma.
 Tumor marker tests
Serum or urine is analyzed for tumor markers, particularly carbohydrate antigen 19-9
(CA 19-9) and carcinoembryonic antigen (CEA). Elevated CA 19-9 and/or CEA levels
are nonspecific but may support the suspicion of bile duct malignancy, especially when
correlated with imaging findings.
 Imaging tests
o Abdominal ultrasound is the initial modality to detect biliary dilatation or
intraductal masses.
o Computed tomography (CT) scan provides cross-sectional imaging to evaluate
the primary lesion, extent of invasion, and possible metastasis.
o Magnetic resonance imaging (MRI) with MRCP offers detailed visualization
of the biliary tree, delineating strictures, masses, and ductal involvement.
 Endoscopic tests
Performed under sedation. An endoscope, a flexible fiberoptic tube, is introduced orally
and advanced to the duodenum.

o Endoscopic ultrasound (EUS): High-frequency sound waves provide detailed

images of the bile ducts, pancreas, and surrounding vasculature. EUS-guided fine-
needle aspiration (FNA) may be used for cytology.
o Endoscopic retrograde cholangiopancreatography (ERCP): Contrast dye is
injected directly into the bile ducts via a catheter introduced through the
endoscope. Fluoroscopy is then performed to evaluate strictures or blockages.
Therapeutic interventions such as stent placement or biopsy of suspicious lesions
may also be performed during ERCP.

 Percutaneous transhepatic cholangiography (PTC)

Indicated in patients who are not candidates for ERCP. Under local anesthesia and imaging
guidance, a needle is advanced percutaneously into a peripheral intrahepatic bile duct.
Contrast dye is injected to outline the biliary tree, and fluoroscopy is performed to identify
strictures, obstructions, or masses. A drainage catheter may be inserted for biliary
decompression in cases of obstruction.

 Biopsy (Definitive diagnosis)

Histopathologic confirmation is obtained through biopsy. This may be performed during
ERCP (endoscopic biopsy or brush cytology of bile duct strictures). Biopsy establishes the
presence of malignant cholangiocytes and is the gold standard for confirming
cholangiocarcinoma.
TREATMENT

 Surgery
Surgical resection is the only potential curative treatment, but it depends on tumor location,
extent, and patient condition. The goal is complete removal with negative margins. If
unresectable, palliative stent placement maintains bile duct patency. Selected centers may
consider liver transplantation combined with chemotherapy/radiation for intrahepatic cases.
 Radiation Therapy
Uses high-energy beams (external or brachytherapy) to destroy cancer cells. It can be
neoadjuvant (shrink tumor before surgery), adjuvant (reduce recurrence after surgery), or
palliative (when surgery is not possible). Brachytherapy is significant after stenting to
prevent tumor regrowth but carries risks like cholangitis and strictures.
 Chemotherapy
Systemic drugs (e.g., gemcitabine, cisplatin, 5-FU) are used to control disease progression,
prolong survival, and provide palliation. Regional techniques like HAI and TACE deliver
higher drug concentration to the tumor while minimizing systemic toxicity.
 Targeted Therapy
Targeted therapy medications attack certain genes and proteins found on cancer
cells. Your tumor may be tested for certain genetic markers. These medications can
be used to treat cancer cells with certain markers: pemigatinib, infigratinib,
futibatinib, larotrectinib, entrectinib, repotrectinib, selpercatinib, pralsetinib,
dabrafenib, trametinib, zanidatamab, adagrasib, and ivosidenib. These medications
stop the cancer from growing and spreading, and limits the effects on healthy cells.
 Immunotherapy
Checkpoint inhibitors (e.g., pembrolizumab, durvalumab) enhance immune recognition and
destruction of tumor cells. They are valuable in advanced or refractory disease and are often
combined with other treatments.
 Palliative Treatments
For unresectable disease, interventions focus on symptom relief and quality of life.
 Stenting or biliary bypass: relieve obstruction, prevent jaundice and pruritus.
 Catheter drainage: allows external bile diversion when internal drainage is not possible.
 Ablation and photodynamic therapy (PDT): locally destroy tumor tissue, reduce
obstruction, and enhance stent function.

Prevention

 Managing chronic liver diseases – Effective treatment of hepatitis B and C, and controlling
cirrhosis, reduces long-term inflammation and malignant transformation of hepatobiliary tissue.

 Avoiding exposure to liver flukes and toxins – Preventing parasitic infections (e.g.,
Clonorchis sinensis) and minimizing occupational or chemical toxin exposure lowers bile duct
irritation and mutation risk.
 Regular monitoring of high-risk individuals – Patients with primary sclerosing cholangitis
(PSC), choledochal cysts, or chronic biliary diseases benefit from routine imaging and tumor
marker surveillance for early detection.

 Limiting alcohol intake – Reduces progression to cirrhosis and subsequent risk of bile duct
cancer.

 Maintaining a healthy body weight – Prevents metabolic dysfunction-associated steatotic

liver disease, which can lead to chronic liver injury and increase cancer risk.

 Smoking cessation – Eliminates carcinogen exposure that accelerates DNA damage and
cholangiocarcinoma development.

Epidemiology
Cholangiocarcinomas comprise about 3% of gastrointestinal malignancies, are the second
most common primary liver tumors, and account for approximately 10% to 15% of all
hepatobiliary malignancies.[13] The incidence of intrahepatic cholangiocarcinoma has been
rising, possibly due to improved diagnostic and classification techniques, while the incidence of
extrahepatic lesions has been falling in recent years. The incidence of cholangiocarcinoma varies
markedly according to the geographic area; the incidence rates are up to 50-fold higher in parts
of Thailand than in the United States. The incidence of cholangiocarcinoma increases with age,
is slightly more common in men, and is most commonly diagnosed between the ages of 50 and
70 years.[14][15]
Perihilar cholangiocarcinoma is the most commonly encountered subtype, accounting for
approximately 50% of cases. Distal (40%) and intrahepatic cholangiocarcinoma (10%) are less
common.[1]

Statistics:
The number of Acute Gastroenteritis cases in the Philippines amounted to
approximately 60.6 thousand in 2020, reflecting a decline from the previous year's total.
The number of Acute Gastroenteritis cases in the country had fluctuated in the past
years.

References:
[Link]
cholangiocarcinoma
[Link]
cholangiocarcinoma-bile-duct-cancer-staging-and-treatment

[Link]
NURSING CARE PLAN
ASSESSMENT DIAGNOSIS PLANNING INTERVENTIONS RATIONALE EVALUATION
Subjective: Imbalanced Within 30 - 1 hour Offer small, To encourage After an hour of
Patient nutrition: less of nursing frequent feedings intake despite nursing
verbalized, “Wala than body intervention, the poor appetite intervention, the
po akong ganang requirements patient will Provide bland, patient was able
kumain.” related to express easily digestible To avoid to take small,
decreased willingness to try foods gastrointestinal frequent feedings
and expressed
Objective: appetite small, tolerated irritation
willingness to eat
Patient ate only a secondary to meals.
and tried bland,
small portion of acute Monitor food and To determine tolerated food.
meals, looks gastroenteritis as fluid intake adequacy of
weak, BMI = 17.3 evidenced by nutrition GOAL MET
(underweight). reduced oral Encourage fluid-
intake and rich foods (soups, To maintain
underweight BMI. oral rehydration hydration and
solution) calorie support.
ASSESSMENT DIAGNOSIS PLANNING INTERVENTIONS RATIONALE EVALUATION
Subjective: Activity Within an hour of Encourage rest Adequate rest After 1 hour of
Patient verbalized Intolerance nursing periods and allows the body to nursing
feeling weak and related to intervention, the conserve energy restore strength intervention, the
tired. weakness patient will and reduces patient reported
secondary to verbalize fatigue. slight relief of
Objective: decreased food decreased fatigue Assist with basic fatigue after rest
(+) lethargic, and fluid intake as after rest. needs. Providing but still required
evidenced by assistance assistance in
prefers to lie patient minimizes sitting up and
down, verbalization of physical strain performing self-
feeling weak and Encourage the and conserves care.
unable to tired, observed patient to attempt limited energy.
participate lethargy, light activity such
actively in preference to lie as sitting up in Gradual activity
activities. down, and bed with helps improve
inability to assistance circulation,
participate prevents
actively in deconditioning,
activities. and enhances
stamina.
DRUG NAME CLASSIFICATIO MECHANISM INDICATION SIDE EFFECTS NURSING
N OF ACTION RESPONSIBILITY

GENERIC Pharmacologic Omeprazole To reduce stomach  Headache BEFORE:

NAME: Class: interferes with acid production.  Nausea and  Check
OMEPRAZOL Proton Pump gastric acid vomiting, doctors
E Inhibitor secretion by  Flatulence order
inhibiting the  Dizziness  Explain to
DOSAGE Therapeutic hydrogen- the patient
40 mg Class: potassium- about the
Anti -Ulcer agent adenosine importance
FREQUENCY triphosphatas and
e (H+K+- CONTRAINDICATIO ADVERSE EFFECT purpose of
OD ATPase) N the drug
enzyme  Check IV
Hypersensitivity to  Psychic
ROUTE: system, or patency
omeprazole, other disturbance
IV proton pump, DURING:
proton pump  Peripheral
in gastric  Administer
inhibitors, or their edema
parietal cells. the right
components.  Neuropathy
Normally, the drug , time
 agranulocytosi
proton pump and
s allergic
uses energy dosage
reaction
from the  Administer
 hyponatremia,
hydrolysis of slow IV
photosensitivit
adenosine push
y
triphosphate AFTER:
 abdominal
to drive  Monitor for
pain
hydrogen effectivenes
 diarrhea.
(H+) and s
chloride (Cl-)  Watch for
out of parietal adverse
cells and into reaction
the stomach  Document
lumen in
exchange for
potassium (K*),
which acid
(HC1).
Omeprazole
irreversibly
blocks the
exchange of
intracellular H+
DRUG NAME CLASSIFICATIO MECHANIS INDICATION SIDE EFFECTS NURSING
N M OF RESPONSIBILITY
ACTION

GENERIC Paracetamol Use to treat mild to  Headache BEFORE:

NAME: Pharmacologic relieves pain moderate pain  Dizziness  Check
PARACETAMO Class: and reduces  Dyspepsia doctors
L fever by (indigestion) order
Analgesic inhibiting  Diarrhea  Review
BRAND NAME: central  Abdominal patients
Therapeutic prostaglandi pain history
Class: n synthesis  Upper  Prepare
DOSAGE and acting respiratory drug using
600mg Antypyretic
on the tract infection correct
hypothalami  Peripheral dilution and
FREQUENCY c heat- edema follow
q6 regulating reconstitutio
center. CONTRAINDICATIO ADVERSE EFFECT n
ROUTE: N guidelines
IV  Explain to
 Hypersensitivit  Cardiovascula
the patient
y to celecoxib, r: Increased about the
sulfonamides, risk of importance
aspirin, or myocardial and
other NSAIDs infarction, purpose of
stroke, the drug
hypertension,  Check IV
 History of heart failure patency
asthma, DURING:
urticaria, or  Administer
allergic-type  Gastrointestin
the right
reactions after al: GI
 aspirin or bleeding,
NSAID use ulceration,
perforation
 Renal: Acute
 Active GI renal failure,
bleeding or decreased
peptic ulcer kidney
disease function
 Hepatic:
Hepatitis,
 Severe hepatic elevated liver
impairment enzymes, liver
failure (rare)
 Dermatologic:
Rash, pruritus, drug , time
Stevens– and dosage
Johnson  Administer
syndrome slow IV push
(SJS), toxic AFTER:
epidermal  Monitor for
necrolysis effectiveness
(TEN)  Watch for
 Allergic: adverse
Anaphylaxis, reaction
angioedema,  Document
bronchospasm
DRUG CLASSIFICATION MECHANISM INDICATION SIDE EFFECTS NURSING
NAME OF ACTION RESPONSIBILITY

Generic Therapeutic: . Inhibits  Headache BEFORE:

Name: histamine Inhibits histamine  Dizziness • Check doctors
Ranitidine Therapeutic class: action at action at histamine H2-  Fatigue order for
Histamine H2- histamine H2-  Constipation ranitidine
receptor receptors of gastric
or diarrhea • Assess
receptors of parietal cells.
Brand antagonist.  Nausea, patient for any
gastric Therapeutic Effect: vomiting, or
name: medical history
parietal cells. Inhibits gastric acid abdominal
Zantac and allergies to
CLINICAL: Therapeutic secretion. discomfort ranitidine.
Effect: Inhibits
Dosage: GI agent. Reduces • Inform the
gastric acid patient about
1 amp secretion. gastric volume, the purpose
hydrogen ion of ranitidine, its
Reduces
concentration potential
gastric benefits, and
volume, possible side
Route: hydrogen ion effects.
concentration
IV
CONTRAINDICATION ADVERSE DURING:
EFFECT • Ensure that the
Frequency: dosage and
Q8 hypersensitivity to Cardiac arrythmias route match the
ranitidine physician's
-use cautiously with - dizziness
impaired renal or
hepatic function - fatigue
- gynecomastia
- headache
- mild and transient
diarrhea

order.

AFTER:
• Observe
the patient for
any delayed or
ongoing adverse
effects And
improvements in
their condition.
DRUG CLASSIFICATIO MECHANISM INDICATION SIDE EFFECTS NURSING
NAME N OF ACTION RESPONSIBILIT
Y

GENERIC Pharmacologic Blocks the  Relief of  Dry mouth BEFORE:

NAME: Class: action of smooth muscle  Blurred vision  Check
HNBB Anticholinergic acetylcholine spasms in GI  Drowsiness doctors
(Hyoscine-N- at tract  Constipation order
butylbromide Therapeutic parasympatheti  Preoperative  Urinary  Explain to
) Class: c sites in medication to retention the patient
Antispasmodic smooth reduce salivary  Flushing about the
DOSAGE: muscle, and respiratory  Dilated pupils importance
1 amp secretory secretions and
glands, and the purpose of
FREQUENC central nervous CONTRAINDICATIO ADVERSE EFFECT the drug
Y system; N  Check Iv
now(As relaxes smooth patency
 Hypersensitivit  Severe allergic
needed) muscles of the DURING:
GI tract and y to hyoscine reactions  Administer
ROUTE: urinary tract, or other (anaphylaxis) the right
IV and in motion belladonna  Hallucinations,
drug , time
sickness, alkaloids confusion and
 Narrow-angle (especially in
inhibits signals dosage
to the vomiting glaucoma elderly)  Administer
 Myasthenia  Heat stroke due
center slow IV
gravis to decreased push
 Severe sweating AFTER:
ulcerative  Tachyarrhythmi
 Monitor for
colitis or toxic as effectivene
megacolon  Paralytic ileus
ss
 Obstructive
 Watch for
uropathy or GI adverse
obstruction reaction
  Paralytic ileus
 Unstable
cardiovascular
conditions with  Document
tachycardia

DRUG NAME CLASSIFICATIO MECHANIS INDICATION SIDE EFFECTS NURSING

N M OF RESPONSIBILITY
ACTION

GENERIC Pharmacologic Inhibits To prevent  Rash BEFORE:

NAME: class: Second- synthesis of postoperative  Difficulty of  Check
CEFUROXIM generation bacterial cell infection. Breathing doctors
E cephalosporin wall, causing  Fatigue order
cell death.  Nausea  Review
 Vomiting patients
DOSAGE: Therapeutic  Diarrhea history
750mg class:  Prepare drug
Antibacterial / CONTRAINDICATIO ADVERSE EFFECT using correct
FREQUENCY Antibiotic N dilution and
TID(Three follow
times a day) Contraindicated with CNS:headaches, reconstitutio
allergy to dizziness, lethargy, n guidelines
cephalosporin. paresthesias  Explain to
ROUTE: GI: nausea, the patient
IV vomiting, diarrhea, about the
anorexia, abdominal importance
pain, flatulence, and purpose
pseudomembranou of the drug
s colitis,  Check IV
hepatotoxicity patency
GU: nephrotoxicity
hematologic, bone
marrow depression
(decreased WBC,
platelets, Hct)
Hypersensitivity:
ranging from rash to
fever to
anaphylaxis; serum
sickness reaction
Local: pain,
abscess at injection
site, phlebitis, DURING:
inflammation at IV
site
Other:  Administer the
superinfections, right drug
Disulfiram-like  Administer at
reaction with the right time
alcohol and right
dosage
 PATHOPHYSIOLOGY

PREDISPOSING FACTOR PRESIPITATING FACTOR

 Age  Contaminated food
 Poor sanitation  Contaminated water

Ingestion of contaminated foods

PATIENT BASE
Entry of large amount of pathogen in GIT
BOOK BASE
Exposure of pathogens to gastric
acaid

Circulation of Increase intraluminal Increase activity Increase consumption

toxins in the body pressure of of organisms to of nutrients by
intestines digestive food pathogens

Recognition
of toxins in Perforating Compression Production of Cellular deprivation
the body of intestinal of nerve gas by of nutrients
lining endings product

Cellular starvation
Rapture of Excess gas
Pain formation
capillaries

Bleeding Melena Flatulence Hunger Weakness

Histamine Prostaglandin Release of pyrogen

release

Parasitic movement Irritation of

hypothalamus
Abdominal pain
Alteration of
Increase frequency of defecation thermoregulation

Decrease water absorption Fluid loss

Fever
Watery stool
Dehydration

Decrease Thirst
urine output Poor skin Sunken Dry mucosal
turgor eyeball membrane