NURSING CARE OF CLIENTS WITH PROBLEMS ON IMMUNE RESPONSE

Inflammatory Disorders

A. Gastrointestinal Disorders

INFLAMMATORY BOWEL DISEASE (IBD)

• A group of chronic disorders:
o Crohn's disease (i.e., regional enteritis)
o Ulcerative colitis

• This results in the inflammation or ulceration of the bowel

• Exact cause is still unknown but researchers theorize that environmental triggers (e.g., exposure to air pollutants),
food, tobacco, and viral illnesses in people genetically predisposed to developing an IBD can trigger the cell-
mediated immune response that results in the inflammatory changes that characterize IBDs

CROHN'S DISEASE AND ULCERATIVE COLITIS

Crohn's Disease Ulcerative Colitis

Course Prolonged, variable Exacerbations, remissions

Pathology

• Early Transmural thickening Mucosal ulceration

• Late Deep, penetrating granulomas Minute, mucosal ulcerations

Clinical manifestations

• Location Ileum, ascending colon (usually) Rectum, descending colon

• Bleeding Usually not, but if it occurs, it tends to be mild Common-severe

• Perianal Common Rare-mild

involvement

• Fistulas Common Rare

• Diarrhea Less severe Severe

• Abdominal Common Rare

mass

Diagnostic Study Findings

• Barium studies Regional, discontinuous skip lesions Diffuse involvement

Narrowing of the colon No narrowing of colon

Thickening of bowel wall No mucosal edema

Mucosal edema Stenosis rare

Stenosis, fistulas Shortening of colon

• Sigmoidoscopy May be unremarkable unless accompanied by Abnormal inflamed mucosa

perianal fistulas

• Colonoscopy Distinct ulcerations separated by relatively Friable mucosa with pseudopolyps or ulcers in
normal mucosa in ascending colon descending colon

Therapeutic Management
 Corticosteroids, aminosalicylates (sulfasalazine Corticosteroids, aminosalicylates
[Azulfidine]) (sulfasalazine) useful in preventing recurrence

Immunomodulators (e.g. azathioprine [Imuran]) Immunomodulators (e.g. azathioprine

or monoclonal antibodies (e.g. infliximab [Imuran]) or monoclonal antibodies (e.g.
[Remicade], adalimumab [Humira]) may be tried infliximab [Remicade], adalimumab [Humira])
if refractory to corticosteroids and may be tried if refractory to corticosteroids
aminosalicylates and aminosalicylates

Antibiotics Bulk hydrophilic agents

Parenteral nutrition Antibiotics

Partial or complete colectomy, with ileostomy or Protocolectomy, with leostomy

anastomosis

Rectum can be preserved in some patients Rectum can be preserved in only a few
patients "cured" by colectomy

Recurrence is common

Systemic Complications

Small bowel obstruction Toxic megacolon

Right-sided hydronephrosis Perforation

Nephrolithiasis Hemorrhage

Colon cancer Colon cancer

Cholelithiasis Pyelonephritis

Arthritis Nephrolithiasis

Uveitis Cholangiocarcinoma

Erythema nodosum Arthritis

Uveitis

Erythema nodosum

CROHN'S DISEASE (REGIONAL ENTERITIS)

• A subacute and chronic inflammation of the GI tract wall that extends through all layers (i.e., transmural lesion)
• Histopathologic changes can occur anywhere in the GI tract but it commonly occurs in the distal ileum in the
ascending colon
• Characterized by periods of remission and exacerbation
• Crypt inflammation and abscesses →> develop into small, focal
ulcers → deepen into longitudinal and transverse ulcers which are
separated by edematous patches → cobblestone appearance;
inflammation extends into the peritoneum → formation of fistulas,
fissures, and abscesses → interference of intestinal peristalsis because
of a constricted lumen → crampy abdominal pain/tenderness/spasm;
advanced disease, bowel wall thickens and becomes fibrotic (tissue
doesn’t function normally) → narrowed intestinal lumen; diseased
bowel loops sometimes adhere to other loops surrounding them
• Regional enteritis/Skip lesions: diseased bowel segments are sharply demarcated by adjoining areas of normal
bowel tissue
• Clinical Manifestations/Symptoms:
o RLQ pain and diarrhea unrelieved by defecation
o Crampy abdominal pain after meals
o Anorexia, weight loss, malnutrition as a result the patients tends to limit food intake to prevent further
abdominal pain
o Nutritional deficiencies (i.e., anemia)
o Chronic diarrhea
o Fever and leukocytosis (if the inflamed intestine may perforate which leads to intra-abdominal and anal
abscesses)
o Steatorrhea (excessive fat in feces)
• Assessment and Diagnostic Findings:
o Barium Study of the Upper GI Tract: String sign of the terminal ileum
(a traditional conclusive diagnostic test)
o Improved diagnostic exams - CT scan and MRI: highlights bowel wall
thickening and mesenteric edema, also highlights obstructions,
abscesses, and fistulae
o Thus, CT scan is more sensitive in diagnosing Crohn's disease than
Barium Studies
o CBC: assess for hematocrit and hemoglobin levels (may be decreased),
WBC count (may be elevated), erythrocyte sedimentation rate (may
be elevated)
o Albumin and protein levels may be decreased, indicating malnutrition
• Complications:
o Intestinal obstruction
o Stricture formation
o Perianal disease
o Fluid and electrolyte imbalances
o Malnutrition from malabsorption
o Fistula and abscess formation
• Enterocutaneous fistula
▪ Abnormal opening between the small bowel and skin
▪ Most common type of small bowel fistula caused by
Crohn's disease
o Colon cancer

ULCERATIVE COLITIS
• Chronic ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum
• Characterized by unpredictable periods of remission and exacerbation with bouts of abdominal cramps and
bloody or purulent diarrhea
• Inflammatory changes begin in the rectum and progress proximally through the colon (LLQ)

• Multiple ulcerations, diffuse inflammations,

desquamation/shedding at the superficial mucosa of the colon
→ bleeding
• Mucosa becomes edematous and inflamed → muscular
hypertrophy and fat deposits → the bowel narrows, shortens,
and thickens
• Since the inflammatory process affects the inner lining of the
colon only, abscesses, fistulas, obstruction, and fissures are
rare

• Clinical Manifestations/Symptoms:
o Diarrhea with mucus/pus/blood
o LLQ abdominal pain
o Intermittent tenesmus (cramping rectal pain)
o Passage of 6 or more liquid stools each day
o Hypoalbuminemia
o Electrolyte imbalances
o Anemia

• Assessment and Diagnostic Findings:

o Abdominal x-ray
• to determine the cause of symptoms
o Colonoscopy
• Definitive test
• To distinguish ulcerative colitis from other diseases of the
colon with similar symptoms
• May reveal friable, inflamed mucosa with exudate and
ulcerations
 o Colon biopsy
• To determine histologic characteristics of the colonic tissue and extent of disease
o CT scan/MRI/Ultrasound studies
• Identify abscesses and perirectal involvement
o Fecal Occult Blood Test
o Stool exam for parasites or microbes
o CBC: low hematocrit, low hemoglobin, elevated WBC
o Albumin level: low (indicating malabsorptive disorders)
o C-reactive protein: elevated
• Complications:
o Toxic megacolon
• Inflammatory process extends into the muscular layer of the colon,
inhibiting its ability to contract and resulting in colonic distention
• Symptoms: fever, abdominal pain and distention, vomiting, fatigue
• Subtotal colectomy: if bowel perforation has not occurred, otherwise,
colectomy is indicated (removal of colon)
• Surgery becomes necessary to relieve the effects of the disease and treat
these serious complications

• Medical Management (for Inflammatory Bowel Diseases: Crohn's Disease and

Ulcerative Colitis)
o Nutritional therapy
• Oral fluids
• Low-residue, high protein, high calorie diet with supplemental
vitamin therapy and iron replacement
• IV therapy for fluid and electrolyte imbalances
• Cold foods (can cause cramping) and smoking are avoided since both
increase intestinal motility

o Pharmacologic therapy
• Sedatives
• Antidiarrheals and antiperistaltic medications (Loperamide) - to rest the inflamed bowel
• Aminosalicylates
▪ Sulfasalazine (Azulfidine)
• Sulfa-free aminosalicylates
▪ Mesalamine (Asacol, Pentasa)
• Antibiotics
▪ Metronidazole (Flagyl)
• Corticosteroids - taken orally, intravenously, or rectally (Prednisone)
• Immunomodulators - to alter immune response
▪ Azathioprine (Imuran)
▪ Mercaptopurine (6-MP)
▪ Methotrexate (MTX)
▪ Cyclosporine (Neoral)
• Monoclonal antibodies
▪ Infliximab (Remicade)
▪ Adalimumab (Humira)
▪ Certolizumab pegol (Cimzia)
▪ Natalizumab (Tysabri)

• Surgical Management:
o Indications for surgery from ULCERATIVE COLITIS:
• Presence of colon cancer
• Colonic dysplasia/polyps
• Megacolon
• Severe, intractable bleeding
• Colon perforation
o Indications for surgery from CROHN'S DISEASE:
• Recurrent partial intestinal obstructions
• Complete intestinal obstructions
• Intractable fistulas/abscesses
 o Total colectomy with ileostomy
• Total removal of the colon with an ileostomy created in the
abdomen
• Drainage is liquid to unformed and occurs at frequent intervals

o Restorative proctocolectomy with ileal pouch anal anastomosis

• Proctocolectomy - removal of the rectum and colon

• Surgical procedure of choice in cases where the rectum can be
preserved because it eliminates the need for a permanent
ileostomy
• It establishes an ileal reservoir that functions as a “new”
rectum, and anal sphincter control of elimination is retained.

• Continent ileostomy
▪ Creation of a continent ileal reservoir (i.e., Kock pouch) by diverting a
portion of the distal ileum to the abdominal wall and creating a stoma
▪ This procedure eliminates the need for an external fecal collection bag

• Nursing Management of a Patient with Chronic Inflammatory Bowel Disease

o Assessment
• Obtain health history
• Assess for pain, presence of diarrhea, fecal urgency, straining at stool (tenesmus), nausea, anorexia,
weight loss, family history of IBD, patterns of bowel elimination, allergies
• Monitor I&O
• Obtain daily weights
• Assess for skin turgor
• Maintain normal elimination patterns
o Nursing Diagnoses
• Diarrhea related to the inflammatory process
• Acute pain related to increased peristalsis and GI inflammation
• Deficient fluid volume related to anorexia, nausea, and diarrhea
• Imbalanced nutrition: less than body requirements related to dietary restrictions, nausea, and
malabsorption
• Activity intolerance related to generalized weakness
• Anxiety related to impending surgery
• Ineffective coping related to repeated episodes of diarrhea
• Risk for impaired skin integrity related to malnutrition and diarrhea
• Deficient knowledge related to the concern of the process and management of the disease
o Planning and Goals
• Attainment of normal bowel elimination patterns
• Relief of abdominal pain and cramping
• Prevention of fluid volume deficit
• Maintenance of optimal nutrition and weight
• Avoidance of fatigue
• Reduction of anxiety
• Promotion of effective coping
• Absence of skin breakdown
• Increased knowledge about the disease process and self-health management
• Avoidance of complications
 o Nursing Interventions
• Administer antidiarrheal (loperamide) medications as prescribed
• Administer pain medications as prescribed
• Change into a comfortable position, apply heat (as prescribed), divert activities, and prevent fatigue
• Encourage oral fluid intake
• Regulate IVF at prescribed rate
• Maintain optimal nutrition
• Promote rest
• Reduce anxiety
• Enhance coping measures
• Prevent skin breakdown
• Monitor and manage potential complications
• Promote home, community-based, and transitional care
• Evaluate the patient's response to the interventions

APPENDICITIS

• Inflammation of the appendix

• The appendix fills with by-products of digestion and empties regularly into
the cecum. Since the appendix empties inefficiently and its lumen is small,
the appendix is prone to obstruction and is vulnerable to infection

• Causes:
o Being kinked
o Being occluded with fecalith (hardened mass of stool)
o Lymphoid hyperplasia (secondary to inflammation or infection)
o Foreign bodies (e.g. fruit seeds) or tumors
o Causes of appendicitis→appendix becomes ischemic →bacterial overgrowth
→gangrene or perforation → peritonitis

• Clinical Manifestations/Symptoms:
o Vague periumbilical pain that progresses to RLQ pain
o Nausea
o Anorexia
o Low-grade fever
o (+) McBurney point tenderness
o (+) Rovsing sign - palpation of the LLQ causes pain at the RLQ
o Rebound tenderness (intensification of pain when pressure is released)
o Ruptured appendix = pain is consistent with peritonitis, abdominal distention develops as a result of
paralytic ileus
• Assessment and Diagnostic Findings:
o CBC: elevated WBC and neutrophils
o C-reactive protein levels are elevated
o CT Scan: RLQ density or localized distention of the bowel; enlargement of the appendix by at least 6 mm is
suggestive of appendicitis
• Complications:
o Gangrene/perforation of the appendix resulting in peritonitis, abscess
formation, or portal pylephlebitis (septic thrombosis of the portal vein
caused by vegetative emboli that arise from the septic intestines)
o Perforation generally occurs within 6 to 24 hours after the onset of pain
and leads to peritonitis

• Medical/Surgical Management:
o For fluid and electrolyte imbalance,
dehydration, sepsis: IV fluids and antibiotics
o Once appendicitis is diagnosed, immediate surgery is indicated
o Surgery: Appendectomy (surgical removal of the appendix) to decrease the risk
of perforation
o Laparoscopic Appendectomy (faster recovery, small incisions)
o For complicated appendicitis (e.g., with gangrene or perforation), the patient is
typically treated with a 3- to 5- day course of antibiotics postoperatively
• Nursing Management:
o Relieve pain
o Prevent fluid volume deficit
o Reduce anxiety
o Prevent or treat surgical site infection
o Prevent atelectasis
• Incentive spirometry
o Maintain skin integrity
o Attaining optimal nutrition
o For post-appendectomy surgery:
• Place in high fowler position
▪ Rationale: This reduces the tension on the incision and abdominal organs, helping to reduce
pain. It also promotes thoracic expansion, diminishing the work of breathing, and decreasing the
likelihood of atelectasis
• Educate on the use of an incentive spirometer
• Give analgesics as prescribed
• Regulate IV at prescribed rate
• Auscultate for the return of bowel sounds and passing of flatus (5-30 clicks/min)
▪ Rationale: To determine if intestinal peristalsis has started after the operation. Also, this may
signal that the patient may start on oral fluids/foods.
• Encourage ambulation
▪ Rationale: to reduce the risk of atelectasis and venous thromboemboli formation
• Encourage patient to perform proper incision care, monitor for any post-op complications, and
instruct to avoid heavy lifting

PERITONITIS

• Inflammation of the peritoneum (the serous membrane lining the abdominal

cavity and covering the viscera)
• Most common bacteria: Klebsiella, Proteus, Pseudomonas, Streptococcus

• Caused by:
o External sources (e.g. abdominal surgery, trauma - gunshot/stab wound)
o Medical procedures such as peritoneal dialysis
o Pancreatitis – if infections spreads outside the pancreas
o Diverticulitis – infection of small, bulging pouches in the digestive tract
(diverticulosis); if one pouch ruptures, there is a spillage of the intestinal waste into
the abdominal cavity

• Categories:
o Primary/Spontaneous bacterial peritonitis - bacterial infection of ascitic
fluid; commonly in adults with liver failure
o Secondary peritonitis - perforation/rupture of abdominal organs with
spillage that affects the serous peritoneum
• Common causes:
▪ Perforated appendix
▪ Perforated peptic ulcer
▪ Perforated sigmoid colon caused by severe diverticulitis
▪ Volvulus of the colon
▪ Strangulation of the small intestine
o Tertiary peritonitis - occurs as a result of a suprainfection in a patient who
is immunocompromised
• Example: Tuberculous peritonitis
• Pathophysiology: inflammation, infection, ischemia, trauma, or tumor perforation → leakage of contents from
abdominal organs to abdominal cavity →the normally sterile abdominal cavity gets infected with foreign
substances (bacteria, gastric acid, partially digested food) →bacterial proliferation →infectious process →tissue
edema and fluid exudation →fluid in peritoneal cavity becomes turbid with increasing amounts of protein, WBCs
cellular debris, and blood →immediate response of the intestinal tract is hypermotility →this is soon followed by
paralytic ileus with an accumulation of air and fluid in the bowel
• Clinical Manifestations/Symptoms:
o Symptoms depend on the location and extent of inflammation
o Constant abdominal pain which is more intense over the site of the pathological process (site of maximal
peritoneal irritation)
o Abdomen becomes extremely tender and distended; muscles become rigid
o Board-like abdomen
o Rebound tenderness
o Anorexia, nausea, vomiting - caused by decreased/diminished peristalsis
o Fever
o Tachycardia
o Without swift and decisive intervention, clinical manifestations will mirror those of sepsis and septic shock
• Assessment and Diagnostic Findings:
o CBC - elevated WBC for infection, hemoglobin and hematocrit levels may be, low if blood loos has occurred
o Serum electrolyte studies - may reveal altered levels of potassium, sodium, and chloride
o Abdominal x-ray: may show fluid and air levels as well as distended bowel loops
o Abdominal ultrasound: may reveal abscesses and fluid collections
o CT scan: may show abscess formation
o Peritoneal aspiration, culture and sensitivity studies of the aspirated fluid may reveal infection and identify
the causative organisms
o MRI: may be used to diagnose intra-abdominal abscesses
• Medical Management:
o Major focus of medical management: fluid, colloid, and electrolyte replacement
o Analgesic agents
o Antiemetic agents
o Intestinal intubation and suction - to relieve abdominal distention and promote intestinal function
o Oxygen therapy - as fluid in the abdominal cavity can cause pressure that restricts expansion of the lungs
o Antibiotic therapy
o Surgical treatment for secondary peritonitis: excision, resection with or without anastomosis, repair,
drainage, fecal diversion (for extensive sepsis)
o Ultrasound-guided and CT-guided peritoneal drainage/aspiration of abdominal and extraperitoneal
abscesses
• Nursing Management:
o Increase fluid and food intake gradually as prescribed
o Must prepare for emergency surgery in case of a
worsening clinical condition
o Monitor for signs of improving peritonitis:
• Decrease in temperature and pulse rate
• Softening of the abdomen
• Return of peristaltic sounds
• Passing of flatus
• Bowel movement/s
o Administer medications as prescribed

PANCREATITIS

• Inflammation of pancreas and can be classified as acute (a medical emergency)

or chronic (often goes undetected because the classic clinical and diagnostic
findings are not always present in the early stages of the disease
• Pancreatitis is commonly described as autodigestion of the pancreas
• Pancreatic duct becomes temporarily obstructed → hypersecretion of
exocrine enzymes of the pancreas → enzymes enter bile duct -> enzymes are
activated with bile→back-up/reflux into the pancreatic duct → pancreatitis
• Caused by smoking and alcohol abuse (alcohol has a direct toxic effect on the
pancreatic cells)
• Acute pancreatitis:
o Interstitial edematous pancreatitis
• Affects majority of the patients
• Considered the milder form
• Characterized by a lack of pancreatic or peripancreatic
parenchymal necrosis with diffuse enlargement of the
gland due to inflammatory edema
• Edema and inflammation is confined to the pancreas
o Necrotizing pancreatitis
• Presence of tissue necrosis in either the pancreatic
parenchyma or in the tissue surrounding the gland
• Characterized by a more widespread and complete enzymatic
digestion of the gland
• Enzymes damage the local blood vessels, thus, bleeding and
thrombosis can occur

• Chronic pancreatitis
o Inflammatory disorder characterized by a progressive destruction of the
pancreas
o Pancreatic cells are replaced with fibrous tissue due to repeated attacks
of pancreatitis

• Clinical Manifestations:
o Severe abdominal pain (caused by the irritation and edema of the inflamed pancreas)
o Abdominal distention
o Poorly defined, palpable abdominal mass
o Decreased peristalsis
o Vomiting that fails to relieve the pain or nausea
o Abdominal guarding
o Rigid/boardlike abdomen - usually a threatening sign indicating peritonitis
o Ecchymosis in the flank or around the umbilicus
o Nausea/vomiting
o Fever
o Jaundice
o Mental confusion
o Agitation
o Hypotension
o Tachycardia
o Cyanosis
• Assessment and Diagnostic Findings:
o Serum amylase and serum lipase - used in making the diagnosis of acute pancreatitis; usually elevated
within 24 hours of the onset of symptoms; serum amylase usually returns to normal within 2-3 days but
serum lipase levels may remain elevated for a longer period
o Urine amylase levels - elevated
o CBC: elevated WBC
o Hypocalcemia which correlates with the severity of pancreatitis
o Ultrasound studies/contrast-enhanced CT scans, MRI: used to identify an increase in the diameter of the
pancreas and to detect pancreatic cysts, abscesses, or pseudocysts
o Chronic pancreatitis: ERCP - the most useful study in the diagnosis of chronic pancreatitis because it
provides details about the anatomy of the pancreas and the pancreatic and biliary ducts
• Medical Management:
o NPO - to inhibit stimulation of the pancreas and its secretion of enzymes
o Parenteral nutrition for severe acute pancreatitis, and for those who are unable to tolerate enteral nutrition
o Nasogastric suction - to relieve nausea and vomiting, decrease painful abdominal distention, and paralytic
ileus
o H2 antagonists: cimetidine (Tagamet), ranitidine (Zantac)
• To decrease pancreatic activity by inhibiting secretion of gastric acid
o Proton pump inhibitors: pantoprazole (Protonix)
• For those who cannot tolerate or improve with H2 antagonists
o Analgesics:
• Opioids: morphine, fentanyl (Sublimaze), hydromorphone (Dilaudid)
o Antibiotics - if infection is present
o Aggressive respiratory care because of the high risk of elevation of the diaphragm, effusion, and atelectasis
o Placement of biliary drains (for external drainage)
 o Surgery: resect or debride an infected, necrotic pancreas
o Surgical management for chronic pancreatitis:
• Pancreaticojejunostomy (aka Roux-en-Y)
▪ Side-to-side anastomosis of the pancreatic duct to the
jejunum
• Pancreaticoduodenectomy (aka Whipple resection)
▪ Removal of the head of the pancreas, duodenum,
gallbladder, and bile duct

• Nursing Management:
o Relieve pain and discomfort
• Assess for pain
• Administer analgesics (opioids) as prescribed
• Nonpharmacologic pain relief interventions such as proper positioning, music, distraction, and guided
imagery
• NPO temporarily to decrease secretion of secretin (this is a gastrointestinal hormone that stimulates
the secretion of pancreatic fluids)
• Nasogastric suction to relieve nausea/vomiting, treat abdominal distention, or paralytic ileus
• Provide frequent oral hygiene
• During the acute phase, maintain on bed rest to decrease metabolic rate and reduce secretion of
pancreatic and gastric enzymes
o Improving breathing pattern
• Semi-fowler's position to increase respiratory expansion
• Frequent position changes to prevent atelectasis and pooling of secretions
• Encourage use of incentive spirometry, DBE, and coughing
o Improving nutritional status
• Monitor serum glucose levels every 4-6 hours or as prescribed
• Administer enteral or parenteral nutrition
• Diet: high carbohydrate, low protein, low fat
o Maintaining skin integrity
• Because of poor nutritional status, enforced bed rest, and restlessness, the patient is at risk for skin
breakdown
• For post-op patients, check incision sites and monitor for presence of infection; also do appropriate
wound care
o Monitoring and managing potential complications
• Monitor skin turgor and moistness of mucous membranes
• Weigh daily
• Monitor I&O
• Measure abdominal girth if ascites is suspected
• Monitor for presence of fluid and electrolyte imbalances (due to nausea&vomiting (hypokalemia),
movement of vascular compartment to the peritoneal cavity, diaphoresis, fever, and use of gastric
suction
o Promoting home, community-based, and transitional care
• Educating patients about self-care
• Continuing and transitional care

CHOLECYSTITIS
• Inflammation of the gallbladder
• Calculous cholesystitis
o A gallstone obstructs bile outflow → bile remaining on the gallbladder initiates a chemical reaction →
autolysis and edema →blood vessels of gallbladder are compressed →compromised blood supply →
gangrene of the gallbladder
• Acalculous cholecystitis
o Acute gallbladder inflammation in the absence of obstruction by gallstones
o May be caused by alterations in fluids and electrolytes, alterations in regional blood flow in the visceral
circulation, bile stasis (lack of gallbladder contraction), and increased bile viscosity
 CHOLELITHIASIS

• Calculi, or gallstones, usually form in the gallbladder from the solid

constituents of bile
• Two major types of gallstones:
o Pigment stones
• Form when unconjugated pigments in the bile precipitate to form
stones
• Cannot be dissolved and must be removed surgically
o Cholesterol stones
• Bile is supersaturated with cholesterol →
cholesterol-saturated bile predisposes to the
formation of gallstones → act as an irritant that
produces inflammatory changes in the mucosa of
the gallbladder

• Risk Factors:
o 5Fs:
• Fat
• Female
• Forty
• Fair
• Fertile
o Cystic fibrosis
o Diabetes
o Frequent changes in weight
o Obesity
o Ileal resection or disease
• Clinical Manifestations/Symptoms:
o Biliary colic with excruciating upper right abdominal pain that radiates to the back or right shoulder
o Nausea and vomiting after a heavy meal
o Restlessness due to pain
o Fever (if with cholecystitis)
o Jaundice - bile, which is no longer carried to the duodenum, is absorbed by the blood and gives the skin and
mucous membranes a yellow color
o Acholic/clay-colored stool - since the feces are no longer colored with bile pigments
o Dark color urine - due to excretion of bile pigments by the kidneys
o Fat-soluble vitamin deficiency (i.e., bleeding caused by vitamin K deficiency since vitamin K is necessary for
blood clotting)
• Assessment and Diagnostic Findings:

Studies Diagnostic Uses

Magnetic resonance cholangiopancreatography Visualizes the biliary tree and capable of detecting biliary
(MRCP) tract obstrution

Cholecystogram, cholangiogram Visualize gallbladder and bile duct

Celiac axis arteriography Visualize liver and pancreas

Laparoscopy Visualize anterior surface of liver, gallbladder, and

mesentery through a trocar

Ultrasonography Show size of abdominal organs and presence of masses

NPO post-midnight, 6-8hrs before

Helical computed tomography and magnetic Detect neoplasms; diagnose cysts, pseudocysts, abscess,
resonance imaging and hematomas; determine severity of pancreatitis based
on the presence of necrosis and/or peripancreatic fluid
collections

Endoscopic retrograde cholangiopancreatography Visualize biliary structures and pancreas via endoscopy

Endoscopic ultrasound Identify small tumors and facilitate fine-needle aspiration

biopsy of tumors or lymph nodes for diagnosis
Serum alkaline phosphatase In absence of bone disease, to measure biliary tract
obstruction

Gamma-glutamyl, gamma-glutamyl transpeptidase, Markers for biliary stasis; also elevated in alcohol abuse
lactate dehydrogenase

Cholesterol levels Elevated in biliary obstruction; decreased in parenchymal

liver disease

o Abdominal x-ray
o Ultrasonography
• Diagnostic procedure of choice because it is rapid and accurate
• Procedure is more accurate if the patient fasts overnight so that the gallbladder is distended
o Radionuclide imaging or Cholescintigraphy
• A radioactive agent is administered through IV which is taken up by the hepatocytes and excreted
rapidly through the biliary tract
• Biliary tract is scanned and images of the gallbladder and biliary tract are obtained
o Oral cholecystography
• Patient takes iodine-containing tablets by mouth for one/two nights in a row → iodine is absorbed from
the intestine into the bloodstream →removed from the blood by the liver →excreted by the liver into
the bile →iodine, together with the bile, is highly concentrated in the gallbladder
o Endoscopic retrograde cholangiopancreatography (ERCP)
• A fiberoptic endoscope is inserted through the esophagus to the descending duodenum
o Percutaneous transhepatic cholangiography
• Injection of dye directly into the biliary tract

• Medical Management:
o Ursodeoxycholic acid UDCA (Ursofalk) - acts by inhibiting
synthesis and secretion of cholesterol, thereby desaturating
bile; this medication can reduce the size of existing stones,
dissolve small stones, and prevent new stones from forming
o Stone removal by instrumentation
o Intracorporeal lithotripsy
• Stones are fragmented by laser
pulse technology under
fluoroscopic guidance with the use
of devices that can distinguish
between stones and tissue.
• Electrohydraulic lithotripsy uses
a probe with two electrodes that deliver electric sparks in rapid pulses, creating
expansion of the liquid environment surrounding the gallstones. This results in
pressure waves that cause stones to fragment
o Extracorporeal shock wave lithotripsy (ESWL)
• Uses repeated shockwaves directed at the gallstones to fragment the stones

• Surgical Management:
o Laparoscopic cholecystectomy
• Removal of gallbladder through a small incision
through the umbilicus
• Standard of therapy for symptomatic gallstones
• Patient is often discharged from the hospital on the
same day of surgery or within 1-2 days
o Cholecystectomy
• Gallbladder is removed through a large abdominal
incision (usually right subcostal)
 o Choledochostomy
• Reserved for a patient with acute cholecystitis who may be too
ill to undergo a surgical procedure
• Incision is made at the common duct, usually for removal of
stones. After the stones have been evacuated, a tube is
usually inserted into the duct for drainage of bile until edema
subsides
• Laparoscopic cholecystectomy is planned for a future date after
acute inflammation has resolved
o Percutaneous cholecystostomy
• Fine needle is inserted through the abdominal wall and liver edge
into the gallbladder under guidance of ultrasound or computed
tomography (CT). Bile is aspirated to ensure adequate
placement of needle, and a catheter is inserted into the
gallbladder to decompress the biliary tract

• Nursing Management:
o Nursing Management Planning and goals:
• Pain relief
• Adequate ventilation
• Intact skin and improved biliary drainage
• Optimal nutritional intake
• Absence of complications
• Understanding of self-care routines
o Pre-op teachings: avoid smoking, avoid blood thinners (aspirin, NSAIDS, herbal remedies)
o Post-op diet: soft, low-fat diet once bowel sounds return, and advance to full, low-fat, high carbohydrate
and protein diet once fully recovered (Fat restriction usually is lifted in 4-6 weeks when the biliary ducts
dilate to accommodate the volume of bile once held by the gallbladder and when the ampulla of Vater again
functions effectively.)
o Relieve pain by administering analgesics
o Encourage DBE and cough every hour to prevent atelectasis
o Instruct on the use of incentive spirometry
o Encourage to do early ambulation to prevent venous complications (i.e., venous thromboembolism
formation)
o Keep dressings clean, dry, and intact
o Do wound care as directed
o Monitor for signs and symptoms of infection
o Monitor and manage potential complications
B. Reproductive System

PELVIC INFLAMMATION DISORDER

- Inflammatory condition of the pelvic cavity that may begin with cervicitis and may involve the uterus, fallopian
tubes, ovaries, pelvic peritoneum or pelvic vascular system.
- Increases the risk for ectopic pregnancy, infertility, recurrent pelvic pain, tubo-ovarian abscess.
Causes:
- Gonnorheal and chlamydial organism (Common)
- CMV
- Bacteria, viruses, fungus or parasite
Pathophysiology
- Pathogenesis- unknown
- Presumed that organisms enter Vagina→ Cervical canal→endocervix→uterus
- After childbirth or abortion- pathogen spreads through tissues by lymphatics and blood vessels
- Pregnancy- increased blood supply needed by placenta increases the risk for infection
- Gonorrheal infection- pass through cervical canal and into uterus, where the environment (especially during
menstruation) allows to multiple and spread
- Commonly caused by sexual transmission
- Can also occur with invasive procedures (Hysterectory, Emdometrial biopsy, Surgical abortion, Insertion of IUD)
Risk factors:
- Early age at first intercourse
- Multiple sex partners
- Frequent intercourse
- Intercourse without condoms
- Sex with a partner with STD
- History of STDs or previous pelvic infection
Clinical Manifestations:
- malodorous purulent vaginal discharge - Fever
- Dyspareunia -dysuria and dyschezia
- Lower abdominal pelvic pain - General malaise
- Tenderness that occurs after menses - h/a
- Anorexia - n/v
- intense tenderness upon palpation of -leukocytosis
uterus or movement of cervix (pelvic exam)
Medical Management:
- Antibiotic
- IV therapy
- NGT and suction (abdominal distention or ileus)
- Careful monitoring of v/s
- Treatment of sexual partner
Nursing Management:
- Provide physical and emotional support
- Instruct to increase fiber diet and EOF
- Position to semi-Fowlers position
- Monitor vital signs and vaginal discharges
- Analgesics prescribed for pain relief
- Heat compress to abdomen
- Dispose properly the used perineal pads and discarded soiled pads
- Hand washing before and after contact with patient
 SIMPLE VAGINITS
- inflammation of the vagina
- cause vulvovaginal symptoms (itching, irritation, burning, and abnormal discharge)
- Urethritis may accompany vaginitis
- Symptoms may be aggravated by voiding and defecation
Risk Factors:
- Premenarche
- Pregnancy Risk Factors for Vulvovaginal Infections
- Perimenopause/Menopause
- Poor personal hygiene
- Tight undergarments
- Synthetic clothing
- Frequent douching
- Allergies
- Use of oral contraceptives
- Use of broad-spectrum antibiotics
- Diabetes mellitus
- Low estrogen levels
- Intercourse with infected partner
- Oral–genital contact (yeast can inhabit the mouth and intestinal tract)
- HIV infection
3 common types:
1. Bacterial Vaginosis
2. Candidiasis
3. Trichomoniasis

1. Bacterial Vaginosis
-caused by an overgrowth of anaerobic bacteria and Gardnerella vaginalis
- is not usually considered a serious condition, although associated with premature labor, premature rupture of
membranes, endometritis, and recurrent urinary tract infection.

Risk factors:
-douching after menses
-smoking
-multiple sex partner
-other sexually transmitted diseases (STDs)

Clinical Manifestations:
-More than half of patients with bacterial vaginosis do not notice any
symptoms.
-vaginal discharges: gray to yellowish white, fish like odor (noticeable after sexual
intercourse/ during menstruation)

Medical Management:
-Metronidazole (Flagyl)
-vaginal gel
- Clindamycin (Cleocin) vaginal cream or ovules (oval suppositories)
-Treatment of patients’ partners does not seem to be effective, but use of condoms
may be helpful.

2. Vulvovaginal Candidiasis
-is a fungal or yeast infection caused by strains of Candida
-many women are asymptomatic

Clinical Manifestations:
-vaginal discharges: watery or thick, white cottage cheese like appearance
: It causes pruritus and subsequent irritation

Symptoms:
-more severe before menstruation
-less responsive to ttt during pregnancy
 Diagnosis:
-wet mount preparation
-gram staining

Medical Management:
-Goal: eliminate symptoms
-Antifungal medications:
CREAM: miconazole (Monistat), nystatin (Mycostatin),
clotrimazole (Gyne-Lotrimin), and terconazole (Terazol)
ORAL: fluconazole (Diflucan)
-treatment of sex partners is not necessary

3. Trichomoniasis vaginalis
-is a flagellated protozoan
-sexually transmitted vaginitis that is often called
“trich”
-Trich may be transmitted by an asymptomatic
carrier

Clinical Manifestations:
-vaginal discharge: thin (sometimes frothy),
yellow to yellow-green, malodorous
-Vulvovaginal burning and itching

Diagnosis:
-culture
-testing of trichomonal discharge demonstrates a pH greater than 4.5
- Inspection with a speculum: reveals vaginal and cervical erythema (redness)
: multiple small petechiae (“strawberry spots”).

Medical Management:
- Metronidazole or Tinidazole (Tindamax) -Most effective treatment.
-Tinidazole is not considered safe in pregnancy.

VULVITIS
- Inflammation of the vulva
- May occur with other disorders (diabetes, dermatologic problems or poor hygiene)
- May affect: women between 18-25 years old
- Pathophysiology is unknown

Risk factors:
-Prepubescent girls
-Postmenopausal women

Symptoms:
-burning

-stinging
-irritation
-stabbing pain
-swelling

Medical Management:
-Antifungal and antibiotic
-Cortisone cream- steroids
-Do not over clean the affected area
 TOXIC SHOCK SYNDROME

-is an infection that usually is caused by Staphylococcus aureus organisms.

-possible cause: insertion of tampons

Clinical Manifestations:
(3 symptoms must be present for diagnosis.)
• Temperature greater than 102° F (38.9° C)
• Vomiting and diarrhea
• A macular (sunburn-like) rash that desquamates on palms and
soles 1 to 2 weeks after illness
• Severe hypotension (systolic pressure less than 90 mm Hg)
• Shock, leading to poor organ perfusion
• Impaired renal function with elevated blood urea nitrogen or
creatinine at least twice the upper limit of normal
• Severe muscle pain or creatine phosphokinase at least twice
the upper limit of normal
• Hyperemia of mucous membrane
• Impaired liver function with increased total bilirubin and increased serum glutamate oxaloacetate transaminase
(aspartate aminotransferase) at twice the upper limit of normal
• Decreased platelet count
• Central nervous system symptoms of disorientation, confusion, severe headache

Medical Management:
-remove tampon particles (Iodine douches, penicillinase resistant antibiotics)
*recurrence may happen if organism is not completely eliminated from the body.
-IV therapy
-vasopressors (dopamine(Intropin))
-Osmotic therapy

BENIGN PROSTATIC HYPERPLASIA

- Enlargement or hypertrophy of the prostate gland.

- Prostate gland enlarges, extending upward into the bladder and
obstructing the outflow of urine.
- Most common disease in aging men.
- Occurs in mean older than 40 years of age

Pathophysiology
- The cause is not well understood, but evidence suggest hormonal
involvement (high estrogen level and Dihydrotestosterone DHT
level) a metabolite of testosterone.

Risk factors:
- Smoking
- Heavy alcohol consumption
- Obesity
- HPN
- Heart disease
- Diabetes
- Western diet (high animal fat and protein and refines carbs, low in fiber)

Clinical Manifestations:
- Prostate: large, rubbery and nontender
- Hesitancy in starting urination, urinary frequency, urgency, nocturia, abdominal straining
- Dec. in volume and force of urination, interruption of urinary stream, dribbling Incomplete bladder emptying,
Acute urinary retention (>60ml ), and recurrent UTIs
- Fatigue, anorexia nausea and vomiting, and pelvic discomfort are also reported, and ultimately azotemia, and
renal failure

Assessment:
-Physical examination, including digital rectal examination (DRE), and health history
-Urinalysis to screen for hematuria and UTI
-Prostate specific antigen (PSA) level is obtained if the patient has at least 10-year life expectancy and for whom
knowledge of the presence of prostate cancer would change management
-Urinary flow-rate recording and the measurement of postvoid residual (PVR) urine.
-Urodynamic studies, urothrocystoscopy, and UTZ
-Complete blood studies including clotting studies

Medical Management:
- Goals: improve quality of life, improve urine flow, relieve obstruction, prevent disease progression, minimize
complications.
- Urinary catheter- if patient unable to void
- Pharmacologic ttt
o Alpha adrenergic blockers –relaxes the smooth muscle of the bladder neck and prostate. (improve urine
flow and relieves symptoms of BPH)
Ex. alfuzosin (Uroxatral), terazosin (Hytrin), doxazosin (Cardura), talmusolin
o 5-alpha-reductase inhibitors- prevent conversion of testosterone to DHT and decrease prostate size
Ex. finasteride (Proscar), dutasteride (Avodart)
o Use of phytotherepeutic agents and other dietary supplements are not recommended, although they
are commonly used.
Ex. Serenoa repens, Pygeum africanum

- Minimally invasive procedures

o Transurethral microwave heat treatment (TUMT)
– involves application of heat to prostatic tissue
o Transurethral needle ablation (TUNA) – uses low level radiofrequencies delivered by thin needles
placed in prostate gland to produce heat that destroys prostate tissue
o Prostatic stents – for patients with urinary retention and with poor surgical risks

- Surgery
o Surgical resection of prostate gland
o Transurethral resection of the prostate (TURP)
– benchmark for surgical ttt of BPH
-removal of the inner portion of the prostate through an endoscope inserted through the urethra.
o Transurethral incision of the prostate (TUIP)
-use to treat smaller prostates
-cuts are made in prostate and prostate capsule to reduce constriction of urethra and decrease
resistance to flow of urine out of the bladder
-can be performed on an outpatient basis
-lower complications
o Prostatectomy
-Laparoscopic Radical Prostatectomy – laparoscope is inserted to remove prostate gland.
-Robotic Assisted Laparoscopic Radical Prostatectomy – uses computer console and da Vinci robot to
replicate the movement of surgeon’s hand.