< GASTROINTESTINAL NURSING

< IAGNOSTIC TESTS: PATIENT PREPARATION /CARE

FecaI Studies to detect blood, fat and infectious organisms
Collect stool in a clean and dry container.
Don't use stool that has been in contact with toilet bowl water and urine
For fat or infectious organisms, collect 3 separate specimen and label day 1, 2, 3
ematoIogic Studies
Hgb, hct, WBC
SeroIogic tests Carcinoembryonic antigen (CEA)
Hepatitis and associated antigens
Radiography- abdominal X-Ray, also called
fIat pIate of the abdomen- helps detect tumors, abnormal gas collections, stones and other abdominal disorders.
X- ray appears black, fat looks gray and bones look white
Nsg. Care- no special pre and post test care
UItrasonography- this techniques uses a
focused beam high frequency sound waves to create echoes
Upper GI Series (UGIS) or Barium SwaIIow-
Flouroscopic examination of the upper G tract to determine structural problems and gastric emptying time. Client must swallow barium
sulfate or other contrast medium, sequential films taken as it moves through the system.
Nsg care pre test
a. Keep patient NPO pmn or 6-8 hrs pre test
b. Explain that the barium will taste chalky
Nsg care post test
AINISTER LAXATIVES TO ENANCE ELIINATION OF BARIU
Lower GI Series (LGIS) or Barium Enema-
Barium is instilled in the colon by enema, client retains the contrast medium while x- rays are taken to identify structural abnormalities of
the colon
Nsg. Care- pre test
a. Keep patient NPO pmn
b. Give enema in the morning of test
c. Administer laxative or suppository
d. Explain that cramping may occur during procedure
Post test- administer Iaxatives and fIuid to assist in expeIIing the barium
< Endoscopy (Esophagogastroduodenoscopy)
Direct visualization of the esophagus, stomach and duodenum by insertion of a lighted fluoroscope to observe strictures, ulcerations,
inflammations and tumors
Nsg care pre test- NPO 6-8 hrs
Explain that local anaesthesia will be used to ease discomfort and that speaking during the procedure is not allowed
< Colonoscopy
Visualization of the large intestines and may include biopsy and removal of foreign substances
Nsg Care pre test-
NPO for 8 hrs
Administer laxatives for 1-3 days
Explain that an instrument is inserted in the rectum
< Sigmoidoscopy
Visualization of the sigmoid colon
Nsg care pre test-
1. Offer a light supper and light breakfast
2. Do bowel prep
3. Explain to client that the sensation of urge of discomfort and abdominal cramping might be experienced
Post test- assess for bIeeding and perforation
< Gastric analysis
nsertion of NGT to examine gastric content for acidity and volume
Nsg care pre test
1. Keep patient NPO 6-8 hrs pre test
2. Advise cIient about smoking, anti choIinergic and uIcer medications for 24 hrs prior the test
< Esophageal manometry
Measures the intraluminal pressure of the esophagus
Also evaluates the quality of the esophageal peristaltic actions
Patient swallows manometric catheter containing transducer
< nterpretations
Normal LES pressure- 15-25 mmHg
ncompetent sphincter 0-5mmHg
GERD, hiatal hernia, esophagitis
High Esophageal LES pressure- up to 50mmHg
Hypertensive sphincter- achalasia. Esophageal spasm, diverticula and CA
< Oral Cholecystogram
njection of radiopaque dye and x-ray examination to visualize the gallbladder
Nsg care pre test-
1. Offer a low fat meal in the evening before the test
2. Check for iodine sensitivity and administer dye tablets as ordered
Nsg care post test
Observe for side effects of the dye tablets like nausea, vomiting and diarrhea
< Liver Biopsy
nvasive procedure where a specially designed needle is inserted into the liver to remove a small piece of tissue for study
Nsg Care Pre test
Keep NPO 6-8 hrs
nstruct the patient to hold breath during biopsy

Nsg Care post test-
Assess vital signs every hour for 8-12 hours
Place patient on right side for few hrs, with a pillow against the abdomen to provide pressure on the liver
Observe puncture site for hemorrhage
Assess for compIications Iike pneumothorax

Nursing Procedures for GastrointestinaI System
< Total Parenteral Nutrition
< t is indicated in clients who need extensive nutritional support over an extended period like major G.. Diseases, severe
malnutrition and cancer. The primary purpose is to provide glucose .
< The usual site is subclavian
vein. The clavicle provides
good support to catheter
< Nursing Responsibilities
Trendelenburg position during insertion
Administer at room temperature
Consume TPN formula within 24 hours
Monitor urine and blood glucose levels
Prevent infection of the catheter
< Gastric and ntestinal Decompression
Removal of fluid and gas to prevent gastric and intestinal distention
< Miller abbott tube

< Enemas
< Cleansing enema- stimulates peristalsis by irritating the colon and rectum by distending the intestine with fluid
< 500-1000 ml of fluid
< Carminative enema- to expel flatus
< 60-180 ml of fluid
< Retention enema- introduces oil in the rectum and sigmoid colon and is being retained for 1-3 hrs to soften the feces
< Return flow enema-/colonic irrigation
< Used to expel flatus
< Used 100-200 ml of fluid and is introduced in and out of the large intestines for 5 times
< Non retention enema
Tap water- 500-1000ml
Soap suds- 20 ml of castile soap in 500-1000ml of water
Fleet enema-90-20ml
Height of solution 18 inches above the rectum
ORAL ISORERS
cheiIitis
< Causes= exposure to sun, radiation
< May lead to squamous cell carcinoma
< Assessment findings- scaling. Fissuring, painful crusting and it usually involves the lower lip
< Treatment management- protect lips using lip ointment or balm, electro or cryo surgery to reduce inflammation
CheiIosis or AnguIar Stomatitis
Causes
Mechanical trauma of poorly fitting dentures
Overclosure of the mouth
Poor oral hygiene
stress
Assessment findings softening of the skin at the angles of the mouth, followed by fissuring or cracking
Often leading to secondary infection like moniliasis and bacteria
Treatment/management
Oral hygiene, good nutrition, soft bland diet, antibiotics
erpes simpIex
< clinical signs - Cold Sores, herpes labialis, blister, fever
< opportunistic infection common in immuno-supressed patients
< recurrent- which appears to lie dormant after primary herpes infection
< lesions are contagious
< coated tongue -> foul breath

< clinical signs - Cold Sores, herpes labialis, blister, fever
< opportunistic infection common in immuno-supressed patients
< recurrent- which appears to lie dormant after primary herpes infection
< lesions are contagious
< coated tongue -> foul breath
< Conservative management focus in relief of symptoms
< pain may be treated with analgesics
< Acyclovir (drug of choice], healing is 10-14 days
< Apply cold soaks to the lips for 20 minutes
< Refrain from direct contact or kissing
< Avoidance of spicy foods
Chancre sore
< Hard papule as a primary lesion of syphilis
< Very contagious
< Reddened circumscribed lesion that ulcerates and become crusted
< Antibiotics, analgesics, cold compress to relieve pain
IeukopIakia
< Painless white thickened patches adherent to mucous membrane
< Appearance is likened to a dry, white paint
< Common to smokers
< May progress to Ca see doctor if persists for 2 wks
< Management
< Avoid tobacco , biopsy if the lesion is more than 2 weeks
CANIIASIS
O Monilial thrush
O Caused by Candida Albicans yeast like fungus
O common in immuno-suppressed pts
O mmuno suppressed decrease levels of normal flora> leads to overgrowth of rest normal flora
O common in intubated patients
O White patches on tongue, palate and mucosa
O Lesions difficult to remove referred to as milk curds
APTOUS STOATITIS
O Canker sores
O Shallow ulcers with white or yellow centre
O With red border
O Starts with burning, tingling, sensation and slight swelling
O Pain last 4-7 days and heals without a scar
O Cause unknown- related to stress, trauma, food drug allergy, vit deficiency, endocrine imbalances
anagement
< Oral hygiene
< Soft, bland diet
< Topical antibiotics and steroids
VINCENT'S ANGINA
< Trench mouth/Necrotizing gingivitis
< Sudden onset of painful superficial bleeding, gingival ulcers covered with grey white membrane
< Ulcers become punched out lesions after a slight pressure or irritation
< Malaise, fever, excessive salivation, bad breath, pain while talking or eating
< Removal of devitalized tissue using an ultrasonic scaler
< Antibiotics, analgesic
< Hourly mouth rinses(equal amount of water and hydrogen peroxide)
< Soft, non irritating diet

EsophageaI isorders
GER
< Management
< PP, ANTACDS, H2BLOCKERS
< AVOD DRUGS THAT DECREASE THE LES, ex. Anticholinergics, xanthine derivatives, diazepam and calcium channel
blockers
< Small, frequent feedings avoid eating before sleeping
< High fowlers position or upright up to 2 hrs after eating
< Lose weight if obese
< Elevate head of the bed8-12 inches
< No constrictive clothing
< No heavy lifting or exercise after eating
< Avoid alcohol and tobacco
< Drink adequate fluid to enhance passage
< Surgery - NSSENS FUNDOPLCATON, hill repair, angel chick


AchaIasia-progressive increasing dysphagia
< Cause- unknown
< ncreased basal tone of LES and fails to relax
< Resulting to impaired propulsion and accumulation of food
< Bougienage- temporary relief (balloon tamponade)
< Surgery- ESOPHAGOMYOTOMY
iataI or diaphragmatic hernia
< Sliding hernia- upper stomach and parasesophageal junction are displaced upward the thorax
< ROLLING ERNIA/paraesophageaI hernia
< Gastroesophageal junction stays below the diaphragm but all parts of the stomach pushes through into the thorax

SLIING/ROLLING ERNIA
< Management
< PP, ANTACDS, H2BLOCKERS
< Surgery- Nissen Fundoplication, Hill repair
ESOPAGEAL IVERTICULA
< Sac like outpouchings in one or more layers of the esophagus
< Food can be trapped in the diverticulum and can be later regurgitated
< Hypopharynx or Zenker's- most common
< Midpoint- caused by scar adhesion, chronic irritation
< Epiphrenic
Signs and symptoms-
Halitosis, dysphagia, regurgitation, aspiration, fullness in the neck, sour taste in the mouth
< Diagnosis
< Barium swallow
< ENOSCOPY IS CONTRAINICATE BECAUSE IT AY PERFORATE TE IVERTICULU
< Surgery- diverticulum is excised and esophageal mucosa is anastomosed
GASTRIC ISORERS
< PEPTC ULCER DSEASE
< t is circumscribed break in the mucosa occurring in the duodenum, stomach and less common in esophagus and jejunum
< Thought to be caused by H. Pylori usually due by eating raw or improperly cooked food
< Hydrochloric acid and pepsin serve as aggressors to G mucosa
< Contributing factors
< Altered gastric acid levels
< Smoking and alcohol use- nicotine stimulates increased HCL secretion and vasoconstriction
< Caffeine- increased HCL secretion and vasoconstriction resulting to decreased blood flow to the G mucosa that causes
decreased mucous secretion
< NSADS, Aspirin
< Genetic predisposition
< Medications- antacids, PP, ANTBOTCS TO TREAT H.PYLOR
< Surgeries- antrectomy BLROTH 1 and BLROTH
< vagotomy , pyloroplasty
Post op compIications
< Hemorrhage
< Pyloric stenosis
< Pernicious anemia- Vit B 12 deficiency
< Perforation
< Dumping syndrome- rapid emptying of hyperosmolar fluid into the jejunum. Rapid emptying causes fluid shift from
bloodstream into the jejunum resulting to decreased blood volume
< Dumping Syndrome

INTESTINAL ISORERS
< APPENDCTS
< Pathophysiology
nflammation accompanies the ulceration and temporarily obstruct the appendix
Obstruction if present is usually caused by stool accumulation around the vegetable fibers(fecalith)
< The abdominal pain usually occurs suddenly, often causing a person to wake up at night
< begins near the periumbilical area and then descends to right lower quadrant
< gets worse in a matter of hours
< gets worse when moving around, taking deep breaths, coughing, or sneezing
Assessment
< Vague epigastric pain sometimes described as cramping, then localized at the right lower abdominal area
< N/V
< Low grade fever
< Either diarrhea or constipation
< Elevated WBC
< n case of RUPTURE, spasm will occur followed by a BREF CESSATON of abdominal pain
< DX- X-ray with radiographic contrasts
< Special Abdominal Examinations
Guarding. Guarding occurs when a person subconsciously tenses the abdominal muscles during an examination.
< Rebound tenderness. applying hand pressure to a patient's abdomen and then letting go.
< NTENSFCATON OF PAN WHEN PRESSURE S RELEASED
< Rovsing's sign. applying hand pressure to the lower left side of the abdomen. Pain felt on the lower right side of the
abdomen upon the release of pressure on the left side
< Psoas sign.
< applying resistance to the right knee as the patient tries to lift the right thigh while lying down.
< Alternately do it on the left side increased abdominal pain on either maneouver means irritation of the psoas muscle by the
inflamed appendix
< Obturator sign.
< Flex the patient's right thigh at the hip, when the knee bent, rotate the leg internally at the hip. This maneuver stretches the
obturator muscle. Right hypogastric pain means positive obturator sign
< When the appendix is inflamed, tenderness can be noted in the RLQ at the c Burney's point
anagement
< Place patient on NPO, Start VF
< Do not give pain medications
< Place ice pack for 20 minutes
< Place on right side lying or low fowlers position to relieve pain
< No hot water compresses/applications
< Avoid enemas/ suppositories
< Monitor for changes in pain level
< Monitor for changes in temperature
PERITONITIS
< Most common complication of ruptured appendix
< Localized or generalized inflammation of part or all the parietal and visceral surfaces of the abdominal cavity
< t caused by a leakage of contents from abdominal organs to abdominal cavity usually as a result of inflammation, infection,
ischemia, trauma
< ntestinal motility gradually decreases that will result to paralytic ileus
< Assessment Findings
< Severe abdominal pain, rebound tenderness, muscle rigidity (boardlike) because of the reflex muscle guarding, absent
bowel sounds, abdominal distention
< Anorexia, n/v
< Shallow respirations- the patient is trying to avoid pain caused by body movement
< Patient lies still because any movement aggravates the pain
< Decreased urinary output, weak rapid pulse and elevated temperature
< Diagnostic tests will reveal elevated WBC, HCT ( if there is hemoconcentration) decreased electrolytes
< management
< NPO with fluid replacement
< Assess respiratory status and provide O2 supplementation, Assess characteristic of pain
< Monitor and maintain F&E balance, monitor for signs of septic shock
< Administer analgesics and antibiotics as ordered
< Sx- Laparotomy- opening made through the abdominal wall into the peitoneal cavity
< Bowel resection depending on the cause
IVERTICULAR ISEASES
< Diverticulum- saclike herniation of the lining of the bowel that extends through a defect in the muscle coat of the large intestine
< t may occur anywhere but most common site is sigmoid colon
< Diverticulosis if there are multiple diverticula without inflammation or symptoms
< Diverticulitis- when becomes infected and inflamed that impedes drainage and leads to perforation and abscess formation
< ncidence- more common in men, 45 years and above and obese
< Risk factors- chronic constipation due to low fiber diet
Pathophysiology
< Atrophy or weakness of the bowel muscle
< Mucosal and submucosal layer of the colon herniate through muscular wall because of high intraluminal pressure, decreased
muscle strength in the colon caused by hardened fecal mass secondary to low fiber diet
< Signs and symptoms
< Mild episodic dull, steady left quadrant or mid abdominal pain
< Rectal bleeding in 15% of patients- anemia
< n mild diverticulosis- bowel irregularity, nausea, vomiting, bloating and abdominal distention
< Diverticulitis- LLQ pain, narrow stool, leukocytosis, fever, weakness and may lead to septicemia
Urinary frequency if the site is proximal to the bladder
< Diagnostic exams
< Radiographic studies- narrowing of the colon and thickened mucus layers
< Sigmoidoscopy, colonoscopy, barium enema, CT scan
Management
< Diverticulosis- high fiber diet
< BULK FORMNG LAXATVE- METAMUCL, drink at least 8 glasses of water
< Diverticulitis- NPO,VF, broad spectrum antibiotic, corticosteroids, anti spasmodics, NGT suctioning to rest the bowel
< Meperidine or demerol for pain
< Avoid morphine because it can increase intraluminal pressure in the colon, exacerbating symptoms
Avoid activities that increase intra abdominal pressure
Reduce weight if obese
Surgery is done if complication develops like hemorrhage, obstruction, abcesses and perforation
Total colectomy, ileorectal/ileoanal anastomosis (entire coIon is removed and the end of the smaII intestine is joined to the
rectum or anus)

ALABSORPTION SYNROE
< nability of the digestive system to absorb one or more of the major nutrients, minerals and nutrients
< nterruptions of the complex digestive process may occur anywhere but the most common site is small intestine.
CeIiac or non tropicaI sprue- accumulation of amino acid glutamine which is toxic to intestinal mucosal cells
ntolerance to gluten an protein component of
Barley Rye Oats Wheat (BROW)
TropicaI sprue- associated with folic acid deficiency
Lactose intoIerance- absence or deficiency in lactase required for the digestion of lactose
< Signs and symptoms
< Foul smelling, bulky diarrhea with increased fat content- steatorrhea
< Malnutrition- weight loss, anemia, easy brusing, osteoporosis

IRRITABLE BOWEL SYNROE
used to describe a functional G.. disorder characterized by a combination of chronic and recurrent intestinal symptoms not explained
by structural and biochemical abnormalities
< More common in women
< Exact cause remains unknown but can be linked to STRESS
< Pathophysiology
< BS results from a functional G.. disorder of intestinal motility
< May be a result of diverticular disease, ingestion of irritants, abuse of laxatives, food poisoning and colon cancer
< Change may be from neuroendocrine dysregulation, infection or irritation or metabolic disturbance that affects the peristaltic
waves of the intestines
< Signs and symptoms
< Alternate diarrhea or constipation or combination of both
< Abdominal pain and bloating
< Diagnostic exams- stool exam, Barium enema, colonoscopy, x-ray
InfIammatory BoweI iseases
Causes unknown
Can affect the entire G tract
< Chronic relapsing disease that may develop discontinuously in any segment of the alimentary canal
< nflammation extends through all the layers of the intestinal wall and may involve lymph nodes
< Regional enteritis- when it affects small intestines
< Crohn's disease of the colon or granulomatous colitis- colon
< Pathophysiology
Lymph nodes enlarge and lymph flow in submucosa is blocked edema, ulcerations (skipping lesions) fissures, granulomas,
abcesses development of oval elevated patches of closely pacled lymph follicles(peyer's patch) on the small intestine
Fibrosis occurs that causes thickening and shortening of the bowel resulting to stenosis and narrowing of the lumen loops adhere to
other diseased or normal loops that will eventually become thicker and shorter
< Cobblestone appearance in Crohn's disease
< Signs and symptoms
RLQ Abdominal pain
Chronic diarrhea from bile salts malabsorption
and bacterial growth
Stool- soft semi fluid consistency, fat malabsorption(steatorrhea) may be bloody
Malaise and weight loss, fever
< Complications
Severe diarrhea and corrosion of perianal area can cause fistula(most common complication)
ntestinal obstruction
Nutrient deficiency VT B12, fluid imbalance
UIcerative CoIitis
Causes Unknown
< Signs and Symptoms
Abdominal Cramping, Nausea, Vomiting, Diarrhea
Fever or Weight Loss
< Treatment
Follow general treatment guidelines.
An inflammatory disease that spans the entire length of the colon. t starts from the rectum spreads upward to involve the sigmoid and
descending colon
Etiology is unknown but may be related to immune response in the G tract
genetics
< Pathophysiology
Starts from the rectum and lower colon proximally affecting the mucosa to submucosal layer mucosa develops diffuse ulceration with
hemorrhage, congestion and edema inflammation causes pinpoint mucosal bleeding and suppurate(crypt abcesses) becomes
necrotic and denuded areas as a result of inflammatory process, tongue like projections that resembles into polyps repeated
episodes will result to thickening of the bowel and loss of the haustral folds
< Signs and symptoms
recurrent bloody diarrhea with pus and mucus with tenesmus- 20x/day
LLQ colicky pain
N/V, Anemia, Fever
iagnostic exams
< FOBT
< Small bowel x-ray- ulceration, stiffening, irregular mucosa
< Barium enema- strictures, narrowing
< Biopsy- granulomas
< Decreased hemoglobin, K, Ca, Mg, Elevated WBC
Treatment
Corticosteroids to reduce inflammation
Sulfasalazine- has anti inflammatory and antimicrobial properties
Anti diarrheals like diphenoxylate
ron supplements
Anti spasmodics

< Nursing interventions
1. Provide appropriate nutrition while reducing bowel motility
a. Provide TPN
b. HGH CHON, CALORC DET
c. Low residue diet(low fiber, no milk products
d. Omit gas producing foods
e. Weigh patient daily
f. Monitor and record stool characteristics
< Surgeries repair bowel perforation, fistula and intestinal obstruction
Crohn's- colectomy with ileostomy
Ulcerative colitis- performed when patient has massive dilatation of the colon (toxic megacolon), does not respond to drugs or the
symptoms are unbearable
Proctocolectomy with ileostomy, pouch ileostomy
< KOCK POUCH
< ntestinal obstructions
< nterference with the normal peristaltic movement of intestinal contents due to the neurogenic or mechanical impairment
< Types of intestinal obstructions
1. mechanical- physical blockage of the passage of intestinal contents with the subsequent distention by fluid and gas caused by
adhesion, hernias, volvulus, intussusception, BD, foreign bodies, strictures, fecal impaction
Post-op adhesion- after abdominal surgery, when some area of the abdomen may not completely healed and loops of the intestine
become adherent and may cause kinking of an intestinal loop-3
rd
-4
th
day post-op
ntussusception- condition in which one part of the intestines slips into another part located below (telescoping)
Volvulus- life threatening obstruction in which the bowel is twisted upon itself and the intestinal lumen is obstructed. The accumulation
of gas and fluid in the trapped bowel leads to necrosis, perforation and necrosis
2. Paralytic ileus- neurogenic/adynamic ileus- obstruction results from neurogenic or muscular impairment of the peristalsis which
results to inability to propel the contents along the bowel in the interference of the blood supply to the intestine resulting to dcreased or
absence of peristalsis
Causes abdominal surgery, peritonitis, shock, burn, toxic conditions
3. Vascular obstruction- interference with the blood supply to a portion of the intestines resulting in ischemia or gangrene of the bowel
Causes embolus, atherosclerosis
The major effects of intestinal obstructions are abdominal distention, loss of F&E , strangulation, gangrenous changes and ultimately
perforation of the bowel
< Signs and symptoms
1. Small intestines- non fecal vomiting, colicky intermittent abdominal pain
2. Large intestines- cramp like abdominal pain, occasional fecal type vomitus, unanble to pass flatus or stool
3. Abdominal distention- rigidity, high pitched bowel sound above the level of obstruction, decreased or absent bowel sound
distal the obstruction
x exams
< Flat plate xray of abdomen- presence of gas and fluid
< ncreased hct- dehydration
< Decreased serum Na, K, Cl- may indicate small bowel obstruction
< anagement
1. Decompression
2. Monitor F&E balance
3. NPO with VF replacement
4. Fowler's position to alleviate pressure in the diaphragm and encourage nasal breathing to minimize swallowing of air and
further abdominal distention
5. Measure abdominal girth and assess signs of peritonitis
Surgery- incision of the cause to relieve obstruction and remove ischemic bowel to reestablish bowel patency (bowel resection and
colostomy)
ERNIAS
Abnormal protrusion of an organ or structure, fissure, part of an organ from its normal cavity through an abnormal opening/weakened
area/congenital/acquired weakness of abdominal musculature
< Types of hernias
1. reducible- can be manually placed back into the abdominal cavity
2. rreducible/incarcerated- cannot be manually reduced and which the intestinal flow may be obstructed completely
3. Strangulated- not only are the contents irreducible but the blood and intestinal flow through the intestine in the hernia is
stopped completely
4. nguinal hernia
a. direct- passes through the posterior inguinal wall. More common in males and harder to repair than indirect hernia. Believed to
be hereditary
b. ndirect- most common type of hernia. Due to the weakness of the abdominal wall where the spermatic cord in men and round
ligament in women, through this opening, the hernia extends down the inguinal canal into the scrotum or the labia
5. Umbilical hernia- most found in children but also common in obese women as the protrusion in the umbilicus. Result of the failure of
the umbilical orifice to close.
6. Ventral or incisional hernis- occurs at the site of previous surgical incision in which the drainage is necessary resulting to inadequate
healing. Weakened by infection, a slight bulge will result to a definite hernial sac
7. Femoral hernia- appears below the poupart's ligament below the groin as a round bulge. More common in women due to the
changes in pregnancy
< Signs and symptoms
1. vomiting, protrusion of involved area (more obvious when coughing or straining or lifting) and discomfort at the site of protrusion
2. Crampy abdominal pain and abdominal distention if it is strangulated with a bowel obstruction
< Management
1. Manual reduction- use of truss
2. Bowel surgery if strangulated
3. Herniorrhaphy- surgical repair of the hernia by suturing the defect
Postpone the operation if the patient has cough or colds
Post op- elevate the scrotum by a rolled towel and ice pack for 20 minutes to relieve swelling and pain
Use of jock strap for support and comfort
Splint the incision when coughing
Report any drainage from incision
Diet modification- high fiber diet
Limit activities for 7 days and no heavy lifting for 6 weeks
< ntussusception
< Volvulus
< Adhesions
ERNIAS
< Abdominal truss
< Umbilical hernia
AnorectaI isorders
< emorrhoids
< Pathophysiology
Mass of swollen veins in anus or rectum
diopathic
< Signs and Symptoms
Limited bright red bleeding and painful stools
Consider lower G bleeding
RectaI Fissure
< Ulceration or tear of the lining of the anal canal usually on the posterior wall
< Acute fissures occur as a result of excessive stretching and possibly from the passage of hard stool through the area
< Management
< Keep the stool soft by using Metamucil, mineral oil or Colace as prescribed
< Clean the area after defecation
< Hot sitz bath to aid healing and relieve pain
< Suppositories with local anesthesia
RectaI abcess
< With Most abcesses starts as cryptitis with the formation of cysts that extends though the tubular ducts into the submucosal
space
< May also originate from the abrasions of local tissues with the entry of virulent organisms
< MANAGEMENT- draining the abcess
RectaI FistuIa
< A sinus tract that develops between two body cavities or between a body cavity and external environment
< A chronic condition where a rectal fistula develops a tract that leads from the anal canal to the skin outside the anus .
< Management- Surgery is the only cure leaving it open to heal by granulation
CoIon Cancer
< Usually caused by adenocarcinomas
< Most tumors are found in rectal area, sigmoid and descending colons
< Risk factors
< Family hx of colon cancer, familial polyposis
< Age greater than 40
< Hx of BD
< High fat, low residue, high refined foods
< Living in industrialized, urban societies
Signs and symptoms
< Ascending colon (right)- occult blood in stool, anemia, anorexia and weight loss
< Abdominal pain above umbilicus, palpable mass in the area
< Distal colon and rectal area
< Hematochezia, change in bm, pencil or ribbon shaped stool, tenesmus, pain below the umbilicus
uke's cIassification of coIon CA
< STAGE A- confined to bowel mucosa- 80-90%, 5 year survival rate
< STAGE B- invades muscle wall of the colon
< STAGE C- lymph node involvement
< STAGE D- metastasis , less than 5%- 5 year survival rate
< Surgeries
< Hemicolectomy for ascending and transverse colon
< APR or Mile's Surgery
For recto sigmoid cancer- this surgery involves 2 incisions to remove the sigmoid, perineal incision to remove the rectum
< T-binder to secure perineal dressing
< Requires permanent colostomy
< Pre op
< Bowel prep by administering oral cathartics, antibiotics like neomycin or sulfonamides 24 hrs pre op
< Low residue diet for 3-5 days, clear liquid 24 hrs pre op
< Administration of bowel enema
< Correction of anemia
< Post op
Kinds of colostomies
Ascending colostomy- stoma is on the right side
Fecal drainage is watery
< Transverse or double barrelled colostomy-
< Two stomas- right side or proximal stoma drains semi formed stool
< Left side or distal stoma drains mucus
< Descending or sigmoid colostomy
< Stoma is on the left side of the abdomen
< Fecal drainage is well formed
COLOSTOMY STES
< Monitor the stoma- it must be red and moist
< Report immediately if it turns dusky or dark
< t should protrude - inch over the abdomen
< Monitor colostomy output and care for the incision site
< Patient may remain in gastric suction for several days until peristalsis returns
< Flatus and fecal drainage usually begins 3-7 days
< Empty the pouch when 1/3 to full of stool to prevent leakage
< Use skin barrier like karaya powder
CoIostomy irrigation
< t is being done to promote peristalsis initially then to promote evacuation of feces on a regular interval
< rrigating solution should be 12-18 inches above the stoma using 500-1000ml NSS OR warm tap water
< Lubricate catheter before inserting it 2-4 inches without force and allow it 5-10 minutes while massaging abdomen gently for
better cleansing
< Foods that reduce odor- yogurt, parsley, green beets
< Foods that form foul odor- dairy products, fish, cabbage, celery, cauliflower, nuts, highly seasoned foods
< Place deodorant tablet or mouthwash or charcoal in the pouch
< Rinse pouch in weak vinegar solution
< A colostomy pouch is normally emptied one or more times daily.
< The pouch itself usually needs to be
changed every four to six days
< The stoma and surrounding skin need to
be kept clean and sanitary
< Colostomy pouches may be either open ended or closed.
Open-ended pouches require a clamp for closure. They can be drained simply and reused after they are emptied.
< Closed pouches are sealed at the
bottom and are usually used by patients who irrigate their colostomies or who have a regular bowel elimination pattern
Functions of the Iiver
Glucose metabolism
Ammonia conversion
Protein metabolism
Synthesizes almost all plasma proteins except gamma globulin
Needs Vit K in synthesis of prothrombin and some clotting factors
Amino acids are building blocks for protein synthesis
Fat metabolism
Vitamin and ron storage
Vitamin A, B and D
Vitamin B complex vitamins
ron
Drug metabolism
May affect activity of the medication
may need conjugation with some compounds to become more soluble.
*Liver function is compIex and any dysfunction affects aII systems of functioning in the body
* It is considered a chemicaI factory where it manufactures, stores, synthesize, stores substances needed in metaboIism
Liver disorders
ResuIt of viraI infection
Exposure to toxic substances
BiIiary Obstruction
Assessment

Health history
Exposure of patient to hepatotoxics or infection
Occupation, social activities family lifestyle/background and
Travel history
Hx of Alcohol or drug abuse/medications
Past medical history

Diagnostics
Liver function tests
serum enzyme activity
serum concentration of proteins
* serum aminotransferases- denotes injury to liver cells, and hepatitis
ALT, AST, GGT most common
C T Scan, MR
Ultrasonography, Liver biopsy
PhysicaI assessment
Pallor
Jaundice (skin, mucosa, sclera)
Muscle atrophy ( extremities)
Skin excoriations, itching, ecchymosis, palamar erythema, spider angiomas
Male patient assessed for testicle atrophy
Mental clarity (recall, memory
Neurologic (tremor, slurred speech, asterixis)
Hepatic dysfunction
Maybe acute or chronic, chronic more common (cirrhosis 40% related to alcohol)
Disease process leading to hepatocellular dysfunction may be caused by infectious agents, medications, metabolic disorders
etc. most common to tissue damage is malnutrition especially related to alcoholism
Parenchymal cells protective response is replacing glycogen with lipids resulting to fatty infiltration
Resulting into shrunken, fibrotic liver if not necrosis.
signs and symptoms
Jaundice = bilirubin concentration in the blood
Portal hypertension, ascites, and Varices due to circulatory changes w/in the diseased liver
Nutritional difficiencies due to inability of the liver cells to metabolize
Hepatis encepalopathy - ammonia
EPATITIS
nflammation > Liver damage
Caused by infection, drugs, alcohol
Chronic, Acute
epatitis A (infectious hepatitis)
Most common
Fecal oral route
Contaminated food, water
Oral anal sexual practices
S/s low grade fever, nausea, fatigue, hepatomegaly
Tx rest, ^ CHO diet

EP B (serum hepatitis)
DNA virus, contaminated blood,
Semen saliva
Tendency to go chronic > cirrhotic > Ca
s/s jaundice, hepatomegaly, pale stools, lethargy, nausea
Tx rest, nutrition, no alcohol
ep C
Extra hepatic disease
Transfer from mother to baby
V drug use, multiple blood transfusion
Tendency to go Chronic > CA
ep
V drug use
Transmission parenteral co infects with HVB to replicate
ep E
Water borne
Fecal oral
Resemble HVA
No chronicity
rug Induced epatitis
Adverse reaction to drugs > damage of hepatocytes
Fulminant Hepatic Failure
Massive liver death following acute hepatitis
Confusion, ascites, coagulation problem, shrinking of liver
Mx liver transplant
CIRROSIS
extensive scarring - caused by irreversible reaction to inflammation
Degeneration > destruction of hepatocytes
tissue becomes nodular > blocks bile ducts and blood flow.
Flow alteration caused by compression and proliferation of fibrous tissue
Types:
Alcoholic scar tissue surrounding the portal areas. Caused by alcoholism (most common type of cirrhosis)
Post necrotic caused by previous bouts of acute viral hepatitis. Broad bands of scar tissue
Biliary Cirrhosis scarring occurs around bile ducts .. May be caused by chronic biliary obstruction or biliary infection
Medical management
Antacids, H2 R antagonist minimize gastric distress
spironolactone ascites
sylimarin anti oxydant- improve liver function
Nursing
Rest reduce demands on the liver > increase blood supply. May resume after nutritional status improves
Hi protein diet ?? High CHO, restricted sodium
Skin care no soap, no tapes..lotion
Risk of injury
CompIications (Iiver disease)
anifestations
Portal Hypertension
Ascites
Esophageal/Gastric Varices
Hepatic Encephalopathy
hemorrhoids
Jaundice
Hi bilirubin concentration in the blood
Obstructive Jaundice- caused by an occlusion in the bile duct with stones, inflammation, tumor, pressure from another organ.
Portal hypertension
ascites
ncreased girth
ncreased weight
Striae , distended veins
fluid electrolyte imbalance
Presence of fluid wave
edicaI management
Dietary modification ( sodium restriction)
Use of diuretics
Bed rest
Paracentesis
PVS
Nursing management
Teaching patient self care
Diet (low sodium)
Abstinence from alcohol
Medications (diuretics)
Weights and girth assessments
Skin care, Bed rest
EsophageaI varices
Medical
ScIerotherapy injecting an sclerosing agent to promote thrombosis and eventual sclerosis via endoscopy
Esophageal Banding
Bleeding varices balloon tamponade
epatic encephaIopathy (PSE)
Life threatening complication of liver failure associated with accumulation of ammonia and other toxic metabolites in the blood
Onset is insidious and subtle
asterixis (flapping tremor) liver flap
Fetur hepaticus sweet, slightly fecal odor
acetone breath
anagement:
Medical eliminating precipitating cause (lactulose ) via NGT or rectal
- V glucose , antibiotics
Nursing- monitor mental status
& O, watch out for dehydration
Vital signs
low protein diet

GaII BIadder
Pear shaped sac like located in a depression in the posterior surface of the liver
3-4 in. long (7.5-10cm)
Can hold 30 50 mls of bile
Connects to the CBD thru the cystic duct
functions
A storage reservoir for bile
Bile enters the Gall Bladder in between meals when the sphincter of Oddi is closed
PeopIe at Risk (4 Fs)
Female
Fat
Forty and above
Fertile

Clinical Manifestations
Presence of murphy's sign
Pain and biliary colic
Jaundice and pruritus
Changes in urine and stool color
Vitamin deficiency due to interference of absorption of fat soluble vitamins A,D.E.K
ChoIecystitis
Pathophysiology
nflammation of the Gallbladder
Cholelithiasis
W Bacterial infection
Acalculus Cholecystitis
W Burns, sepsis, diabetes
W Multiple organ failure
Gall Stones
Pigment stones
Cholesterol stones
Management
ESWL
ERCP with Basketting
Cholecystectomy
CBDE with T-Tube
LAP CHOLE
T-tube
Pancreas
Has exocrine as well as endocrine functions
Acinar cells -exocrine portion of the organ.(99%)
secrete pancreatic juice consisting of digestive enzymes, sodium bicarbonate and water
The remaining 1% make up the endocrine portion
cell clusters are called "slets of Langerhands composed of alpha, beta, and delta cells.
beta cells - secreting insulin
Alpha cells - glucagon,
Delta cell - somatostatin,
Neural and hormonal stimulation of pancreatic juice secretion
Pancreatitis
Signs & Symptoms
Mild Pancreatitis
W Epigastric Pain, Abdominal Distention, Nausea/Vomiting
W Elevated Amylase and Lipase Levels
Severe Pancreatitis
W Refractory Hypotensive Shock and Blood Loss
W Respiratory Failure
Common causes:
Alcohol abuse, gallstone
Assessment
LUQ Pain- starts with midepigastrium with radiation to the back, flanks and substernal area
Nausea and vomiting
Severe dehydration
Steatorrhea due to excretion of undigested fats
Elevated serum amylase and lipase
Hypocalcemia- Ca binds with undigested fats and it is lost in steatorrhea
Hyperglycemia
Post hemorrhagic necrosis- purplish discoloration- cullen's sign-{ periumbilical area} and turner's sign {flanks}
anagement
Relieve pain
NPO during acute phase, then bland low fat diet
Antimicrobials to prevent infections, PP, H2Blockers, antacids
Ca supplement
nsulin
Eliminate alcohol
pancrelipase (Creon-10, Pancreatin,Pancrease, Viokase)
Pancreatic enzyme replacement
Treatment of malabsorption
Often used with cystic fibrosis patients
Can be taken before or with meals