ESOPHAGEAL

DISORDERS
GASTRO
ESOPHAGEAL
REFLUX DISEASE
Backflow of gastric or duodenal contents
into the esophagus
r/t inappropriate relaxation of the
stomach and duodenum.
Aka Acid Reflux or GERD.

GASTROESOPHAGEAL REFLUX
Presence of hiatal hernia
Physical and environmental stress factors
Dietary factors
Elevated intra abdominal pressure

CAUSATIVE FACTORS
Pyrosis
Dyspepsia
Regurgitation
Dysphagia
Odynophagia
Hypersalivation
Flatulence

CLINICAL MANIFESTATIONS
Endoscopy
Barrium Swallow
12-36 hours esophageal secretion pH
monitoring
Bernstein test

DIAGNOSTIC PROCEDURES
Low fat-high fiber diet
Avoid caffeine, tobacco and carbonated
beverages
Avoid eating 2 hrs. before bedtime
Maintain N body wt.
Elevate HOB 6-8 inches esp. after meals
Avoid constrictive clothing
Avoid activities that involve straining, heavy
lifting or working in a bent position
Never sleep flat on bed

NURSING MANAGEMENT
Antacids
Histamin or H2 beta-blockers
Prokinetic agents

MEDICATIONS
ESOPHAGEAL
ACHALASIA
Failureof the lower esophageal muscles
and sphincter to relax during swallowing

ESOPHAGEAL ACHALASIA
Idiopathic. Maybe r/t neuromuscular
defect of inner circular muscle layer of the
esophagus

ETIOLOGY
Dysphagia
Regurgitation
Feeling of food sticking the LE
Pyrosis

CLINICAL MANIFESTATION
Barium swallow
CT scan of esophagus
Endoscopy as confirmed by manometry in
w/c the esophageal pressure is measured

DIAGNOSTIC EXAMS
Esophageal dilation using polyurethane
balloon (Bougie Tx)
Esophagomyotomy
Injection of Botox to inhibit contractions
Eat slowly and drink plenty of fluids

MANAGEMENT
CONGENITAL
ABNORMALITIES of
the ESOPHAGUS
ESOPHAGEAL ATRESIA – esophagus is
interrupted ending in a blind pouch

ESOPHAGEAL STENOSIS – constriction

at one point or another

TRACHEOESOPHAGIAL FISTULAS –
abnormal sinus connection between the
esophagus and trachea
I or A – upper & lower segment is blind or
close. No connection to trachea
II or B – upper segment opens to trachea.
Blind lower segment
III or C – upper segment is blind. Lower
segment opens to trachea
IV or D – both segments open into the
trachea
V or E – no atrasia but w/ fistula. “H” type
VI or F – 2/3 stenosis down the
esophagus. No atrasia, no fistula
TYPES OF ATRESIA
When esophagus and trachea fail to
separate normally during the embryonic
stage
Idiopathic
Common in babies with chromosomal
abnormalities

ETIOLOGY
Constant Drooling
Cyanosis
Collic
Choking and Coughing
Catheter can’t pass

CLINICAL MANIFESTATIONS
Position NB head and chest elevated 20-30°
Reg. suctioning
Assist in Bougie Tx
Put NB in incubator w/ high humidity
Admin. O2 as necessary
Give antibiotics as ordered
Give IV or hyperalimentation
Observe VS and NVS
◦ Respi. Patterns
◦ Amt. of secretions
◦ Abdominal distention
◦ Skin color
Oralhygiene
Continous oral stimulation
Encourage parental participation in care

NURSING RESPONSIBILITIES
Observe for stricture at the anastomosis
site
Maintain airway patency
Maintain adequate nutrition
◦ Commence feeding 6-14 days post-op
◦ Low residue diet
◦ Slow feeding in upright position
◦ Enough swallowing time

NURSING RESPONSIBILITIES
HIATAL HERNIA
A part of the stomach protrudes thru the
diaphragm and into the chest

HIATAL HERNIA
Idiopathic,maybe r/t weakening of
supporting tissue

Increased age (60 and above)

Obesity
Smoking

ETIOLOGY and RISK FACTORS

SLIDING – gastroesophageal junction
and part of the stomach protrude into the
chest. Usually requires no Tx.

ROLLING or PARAESOPHAGEAL –
Gastro esophageal junction stays where it
belongs but part of the stomach passes or
bulges into the chest beside the
esophagus. Requires surgery.

TYPES OF HIATAL HERNIA

Pyrosis
Chest pain
Belching
Dysphagia

CLINICAL MANIFESTATIONS
Avoid coffee and smoking
Avoid large meals and citrus fruits
Avoid eating 2-3 hours before bedtime
Avoid tight clothing
Raise HOB 4-6 cm.
Lose weight

NURSING INTERVENTIONS
Unconsciousswallowing of air
Consumption of gas-producing foods or
drinks
GERD

COMMON CAUSES
Upper G.I series
EGD

DIAGNOSTIC STUDIES
ESOPHAGEAL
DIVERTICULUM
Out-pouching of the esophageal mucosa
that creates a blind pouch in w/c foods
and liquids are trapped.
Common in pharyngoesophageal junction
Results from weakening of the muscular
layer of the esophagus

ESOPHAGEAL DIVERTICULUM
Achalasia
Dysphagia
Halitosis
Feelings of pressure or fullness in the
throat
Regurgitation
Nocturnal cough

CLINICAL MANIFESTATIONS
Proper positioning
Diet modification (small servings, semi
liquid)
Freq. oral hygiene w/ mouthwash
Elevate HOB
Esophagomyotomy

NURSING MANAGEMENT
THE END…
 DISTURBANCES in
ACCESSORY ORGANS
LIVER
A systemic viral infection in w/c necrosis
and inflammation of liver cells produce a
characteristic and clusters of clinical,
chemical and cellular changes
Inflammation of the liver
Most common cause is acute viral
infection

HEPATITIS
HEPATITIS A and E
Same characteristics; Same MOT

HEPATITIS B, C and D
Same characteristics

TYPES of HEPATITIS
Drugs
Alcohol
Chemicals
Autoimmune Liver Diseases

OTHER POSSIBLE CAUSES

Cytomegalovirus
Epstein-Barr Virus
Herpes Virus
Rubella Virus
Coxsackle Virus

COMMON VIRAL CAUSES

TYPES OF HEPATITIS
Caused by Hepa A Virus/RNA Virus
MOT: Fecal-oral
Occurs in small outbreaks
Rarely, if ever, transmitted by blood
transfusion but can also be transmitted thru
sex
Incubation period: 15-50 days
Infective days: 30 days (average)
Duration: 4 to 8 weeks
Aka INFECTIOUS HEPATITIS

HEPATITIS A
Anicteric (in some cases)
Jaundice
Dark Colored Urine
Anorexia
Indigestion
Nausea
Flatulence
Heart Burn

CLINICAL MANIFESTATIONS
StoolAnalysis
RESULT = (+) Antigen A
Should be done 10 days before and 2
weeks after Sx appears)

VACCINE
Havrix
Vagta

DIAGNOSTIC TESTS
Caused by Hepa B Virus/DNA Virus
More infectious than HIV
MOT: Percutaneous or permucosal
exposure to infectious blood, blood
products or other body fluids
Incubation Period: 1-6 months
Highest prevalence is in South East Asia
May also be sexually transmitted
Aka Serum Hepatitis

HEPATITIS B
@ GREAT RISK @ GREATER RISK
Surgeons Staff and Pt. at
Clinical Lab workers Hemodialysis
Dentist Oncology Units
Nurses Sexually Active
Respiratory Promiscuous
Therapist individuals
Drug Users

PEOPLE @ RISK
Caused by Hepa C Virus/DNA Virus
MOT: Percutaneous
Incubation Period: 15-160 days
DOC: (Anti-viral Agents effective in
improvement and Tx of relapses)
◦ INTRON-A
◦ REBETOL
Aka Non-A and Non-B Hepatitis

HEPATITIS C
Injecting Drugs
Transfusion of infected blood products
Hemodialysis
High-Risk Sexual Behavior
Organ transplants
Exposure to blood and blood products by
health care workers

MAJOR RISK FACTORS

Caused by Hepa D Virus/ Defective single
stranded RNA virus
Incubation Period: 21-140 days

HEPATITIS D
Caused by Hepa E Virus
Incubation Period: 15-65 days
MOT: Fecal-Oral
Drinking contaminated H2O

HEPATITIS E
Caused by Hepa G Virus/RNA Virus
Found in some blood donors
MOT: Blood transfusion
Often coexists with other types of
Hepatitis

HEPATITIS G
Liver damage r/t lysis of infected
hepatocytes due to cytotoic cytokines
Hepatocyte damage = hepatic cell
necrosis
Proliferation and enlargement of Kupffer
cells
Inflammation of periportal areas, resulting
to bile flow interruption
Hepatomegaly

PATHOPHYSIOLOGY
Rash
Angioedema
Arthritis
Fever
Body Malaise

SYSTEMIC EFFECTS
PREICTERIC PHASE (1 to 21 days)
Precedes Jaundice
Period of maximal infectivity of Hepa A
Anorexia
Nausea
Abd’l discomfort
Vomiting
Constipation
Body Malaise
Headache
Low-grade fever
Arthralgia
Skin Rashes

CLINICAL MANIFESTATIONS
ICTERIC PHASE POSTICTERIC
2-4 weeks PHASE
Characterized by Begins as jaundice
jaundice disappears
Pruritus Malaise
Easy Fatigability
Lasts weeks to
months

CLINICAL MANIFESTATIONS
Hepatic Failure
Chronic Hepatitis
Cirrhosis
Hepatocellular Carcinoma (Common in
Hepa B)

COMPLICATIONS
Transaminase
Alkaline
phosphatase
Serum proteins
Serum billirubin

DX STUDIES
No spec. tx for acute viral hepa
Most pt can be managed at home
Hepa Virus can be killed by chlorox

COLLABORATIVE CARE
Antiemetics
Diphenhydramine
Chloral Hydrate

SUPPORTIVE DRUG THERAPY

CHRONIC HEPA B
Lamivudine (Epivir)
Alpha Interferon
Adefovir dipivoxil

HEPA C
Alpha-interferon
Ribavirin (Rebetol)

DRUG THERAPY
No specific diet
High Carbs and Protein
Low-fat
Adequate calories

NUTRITION THERAPY
IV Drug and Alcohol abuse
Wt. Loss
Dark Urine
Fatigue
RUQ Pain

NURSING ASSESSMENT
Health Promotion
HEPA A
Vaccine
Good Hygiene
HEPA B and C
Screen blood, organ and tissue donors
Infection control precaution
Modif. Of high-risk behavior

NURSING MANAGEMENT
LIVER CIRRHOSIS
NORMAL LIVER
CIRRHOTIC LIVER
A chronic progressive disease of the liver
characterized by diffused damage to cells
with fibrosis and nodular regeneration
Repeated destruction of hepatic cells
results in the formation of scar tissues
"cirrhosis" derives from Greek kirrhos,
meaning "tawny" (the orange-yellow colour
of the diseased liver).
Cirrhosis is generally irreversible once it
occurs, and treatment generally focuses on
preventing progression and complications.
LIVER CIRRHOSIS
LAENNER’S PORTAL CIRRHOSIS
Scar tissue characteristically surrounds
the portal areas due to chronic alcoholism
and is the most common type of cirrhosis
Usually caused by Excessive
Alcohol/Alcoholism and Nutritional
Imbalance

MAJOR TYPES of CIRRHOSIS

POST NECROTIC CIRRHOSIS
In w/c there are broad bands of scar
tissue as late result of a previous acute
viral hepatitis.
most massive loss of liver cells, wit
irregular patterns of regenerating cells

MAJOR TYPES of CIRRHOSIS

BILLIARY CIRRHOSIS
bile flow decreased with concurrent cell damage
to hepatocytes around the bile ductules
Primary Cause:
◦ Chronic stasis of the bile in intrahepatic ducts
◦ autoimmune process implicated
Secondary Cause:
◦ Obstruction of bile ducts outside the liver

MAJOR TYPES of CIRRHOSIS

CARDIAC CIRRHOSIS
Chronic liver disease associated with RHF.
Causes:
◦ Atrioventricular valve dse
◦ Prolonged constructive peritonitis
◦ Decompensated cor pulmonale

MAJOR TYPES of CIRRHOSIS

Alcoholism Hepatotoxic Drugs
 CHON (Acetaminophen,
Exposure to Oncologic drugs,
Chemicals Contrast mediums)
Exposure to Metabolic and

infectious inherited disorders

schistosomiasis Excess deposits of
Chronic viral Hepa iron in the liver
Autoimmune
chronic active hepa

ETIOLOGY
5 CLASSICAL
Fector Hepaticus
Spider Telangiectasia/Telangiectasis
Caput Medusae
Ascites
Jaundice

CLINICAL MANIFESTATIONS
ASCITES
ASCITES
CAPUT MEDUSAE
Chronic Dyspepsia
Constipation and Diarrhea
Chronic wt. loss
Splenomegaly
Hematemesis
Melena
Edema
Bleeding
Anemia
Deterioration of Mental Fxn. (Hepatic
Encepalopathy)
OTHER SIGNS and SYMPTOMS
LFT
Direct Billirubin
Inderect Billirubin
Urine Billirubin
Fecal Billirubin
CHON Studies
SGOT
SGPT

LABORATORY EVALUATIONS
Abd’l X-ray
Abdominal Series
Liver Biopsy
Examination of the Liver
Liver Scan
Celiac Axis Arteriography
EEG
Peritoneoscopy
Measurment of Portal Pressure
MRI

DIAGNOSTIC EVALUATIONS
DietModification
Diuretics
Bedrest
Paracentesis
Shunting

MEDICAL MANAGEMENT
Observe for objective signs of Dse.
Observe pt’s mental status
Observe for bleeding
Provide skin care and keep nails trimmed
Maintain in semi-fowler’s position
Monitor I/O, abdominal girth and daily wt.
Assist with paracentesis
Instruct on Diet: Low CHON,Na and Fats,
Inc. Carbs.

NURSING INTERVENTIONS
PANCREATITIS
Inflammation of the Pancreas caused by
pancreatic enzymes, primarily trypsin
Inflammation w/ or w/o edema of the
pancreatic tissues, abscess formation,
hemorrhage or necrosis depending on the
severity of the disease and the cause

PANCREATITIS
Alcoholism
BiliaryDisease
Infections
Hyperparathyroidism
Hypertriglyceridemia
Hypercalcemia
Peptic Ulcer Disease
Cystic Fibrosis
Vascular Disease
Multiple Drugs

CAUSES
Be alert for hyperglycemic states
Monitor VS
Administer analgesics as ordered
Maintain NPO during acute stage
Semi-fowler’s;encourage deep breathing and
coughing
Closely monitor IV feedings until Oral feedings is
tolerated
Diet modificatin; Low-fat, Avoid gas-forming foods
Encourage lifestyle w. emotional stability, rest and
follow-up care
Teach about preventing recurrence and control of
symptoms
NURSING INTERVENTIONS
THE END... 