Digestive MUSTAFA Ppt

8/8/2019 Digestive MUSTAFA Ppt

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MUSTAFA SHOULI

RN,BSN,MPHS

IBN SINA COLLEGE

PALESTINEMEDICAL SURGICAL NURSING

DEPARTMENT

MIDWIFERY STUDENTS


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Assessment of Digestive and Gastrointestinal

Function(p1121)Learning Objectives

On completion of this chapter, the learner will be able to:

Describe the structure and function of the organs of the

gastrointestinal (GI) tract

Describe the mechanical and chemical processesinvolved in digesting and absorbing foods and eliminatingwaste products.

Use assessment parameters appropriate for determiningthe status of GI function.

Describe the appropriate preparation, teaching, andfollow-up care for patients who are undergoing diagnostic

testing of the GI tract.


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Anatomic and Physiologic

Overview The gastrointestinal (GI) tract is a 23- to

26-foot-long pathway that extends from

the mouth to the esophagus, stomach,small and large intestines, and rectum, to

the terminal structure, the anus (Fig. 34-1)


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The esophagus is located in the

mediastinum

in the thoracic cavity, anterior to the

spine and posterior to the trachea and

heart.


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The stomach can be divided into

four anatomic regions:


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The common bile duct, which allowsfor the passage of both bile and

pancreatic secretions, empties into the

duodenum at the ampulla of Vater.


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The large intestine consists of :

1-ascending segment on the right sideof the abdomen.

2- a transverse segment that extends

from right to left in the upper abdomen.

3- a descending segment on the left

side of the

abdomen.


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FUNCTION OF THE DIGESTIVE

SYSTEM

1 The break down of food particles into

Digestion.the molecular form for

2 The absorption into the bloodstreamthe small molecules produced by

digestion.

3 The elimination undigested and

unabsorbed foodstuffs and Other waste

products from the body.


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Go to p1123

Chewing and swallowing Gastric function

Small intestine function

Colonic function and waste products ofdigestion


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The stomach can produce about 2.4 L per

day of these gastric secretions.

Intrinsic factor is also secreted by the gastricmucosa.

In the absence of intrinsic factor, vitamin B12

cannot be absorbed and pernicious anemia

results .

Intestinal secretions total approximately:

1) 1 L/day of pancreatic juice.

2) 0.5 L/day of bile.3) 3 L/day of secretions from the glands of

the small intestine.


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Absorption is the primary function of the

small intestine.

Absorption begins in the jejunum

Absorption of different nutrients takes place

at different locations in the small intestine.

(Give examples). The brown color of the feces results from

the breakdown of bile by the intestinal

bacteria.

Chemicals formed by intestinal bacteria

(especially indole and skatole) are

responsible in large part for the fecal odor.


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The internal sphincter iscontrolled by the autonomic

nervous system.

the external sphincter is

under the conscious control

of the cerebral cortex


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Assessment

HEALTH HISTORY AND CLINICALMANIFESTATIONS:

complete history

any previous GI disease .

past and current medication .

Information pertaining to medications

is of particular interest, Why?a dietary history.


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tobacco and alcohol

changes in appetite

stool characteristics

questions about psychosocial,

spiritual, or cultural factors that may beaffecting the patient.


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Assess Clinical Manifestations

Pain


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Indigestion (Dyspepsia)

Intestinal Gas(2 types).

Nausea and Vomiting

Change in Bowel Habits andStool Characteristics


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PHYSICAL ASSESSMENT

includes assessment of the mouth,abdomen, and rectum.

The patient lies supine with kneesflexed slightly auscultation, palpation,and percussion of the abdomen. (Fig.34-4).

The nurse performs inspection firstThe nurse performs auscultation before

percussion and palpation. Why?


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It is important to documentthe frequency of the sounds

The final part of the

examination is inspection ofthe anal and perineal area


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Diagnostic Evaluation

Blood tests are ordered initially

a) Common blood tests include complete

blood count (CBC).

b) PT, PTT

c) Amylase, Lipase.

d) carcino embryonic antigen (CEA).

e) liver function tests.f) serum cholesterol, and triglycerides.


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STOOL TESTS

ABDOMINAL ULTRASONOGRAPHY


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Imaging studies include:

1- x- ray and contrast studies2- computed tomography (CT) scans

3- magnetic resonance imaging (MRI)

4- scintigraphy (radionuclide imaging).


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Fluoroscopic examination


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Lower Gastrointestinal Tract

Study


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When barium is instilled rectally to

visualize the lower GI

tract, theprocedure is called a barium enema.

The purpose of a barium enema is to

detect the presence of polyps, tumors,

and other lesions of the large intestineand to demonstrate any abnormal

anatomy or malfunction of the bowel.


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Computed Tomography


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Magnetic Resonance Imaging


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ENDOSCOPIC PROCEDURES

Fibroscopy/esophagogastroduodenoscopy

(EGD).

Anoscopy

Proctoscopy

Sigmoidoscopy

Colonoscopy

Small-bowel enteroscopyEndoscopy through ostomy.


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esophagogastroduodenoscopy

(EGD)


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Endoscopic retrograde

Cholangiopancreatography

(ERCP)uses the endoscope in combination

with radiographic techniques to view

the ductal structures of the biliary tract.ERCP is helpful in evaluating jaundice,

pancreatitis, pancreatic tumors,

common duct stones, and biliary tractdisease.


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LAPAROSCOPY

(PERITONEOSCOPY)P1139

Laparoscopy can be used for the

diagnosis of GI disease.

This procedure is performed through asmall incision in the abdominal wall.

Go to Video Downloading.


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Abnormalities of the Lips

Actinic cheilitis


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)Herpes simplex (coldsore or2

fever blister)


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3- Chancre


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GASTROESOPHAGEAL REFLUX

DISEASE

Definition: (GERD)

gastroesophageal reflux (backflow of gastric

or duodenal contents into the esophagus).

Excessive reflux may occur because of an

incompetent lower esophageal sphincter,

pyloric stenosis, or a motility disorder.

The incidence of refux seems to increasewith aging.


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Clinical Manifestations

1- pyrosis (burning sensation in theesophagus).

2- dyspepsia (indigestion).

3- regurgitation.4- dysphagia or odynophagia (difficulty

swallowing, pain on swallowing).

5- hypersalivation.

6- and esophagitis. The symptoms may mimic those of a heart

attack.


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Assessment and Diagnostic

Findings

Endoscopy

barium swallow

(To evaluate damage to the esophagealmucosa).


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Management

Management begins with teaching the

patient to avoid .

medications such as antiacids orhistamine receptor blockers.

Proton pump inhibitors (medications

that decrease the release of gastric

acid, such as lansoprazole [Prevacid]

or rabeprazole [Aciphex]) may be used.


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If medical management is unsuccessful,surgical intervention may be necessary.

Surgical management involves afundoplication

(wrapping of a portion of the gastric fundusaround the sphincter area of the esophagus).

Fundoplication may be performed bylaparoscopy.

In a fundoplication, the gastric fundus (upperpart) of the stomach is wrapped, or plicated,around the lower end of the esophagus andstitched in place, reinforcing the closingfunction of the lower esophageal sphincter:


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fundoplication


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Gastritis

(inflammation of the gastric or stomach

mucosa).

Gastritis may be acute, lasting severalhours to a few days, or chronic,

resulting from repeated exposure to

irritating agents or recurring episodes

of acute gastritis.


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6) A more severe form of acute gastritis

is caused by the ingestion of strong

acid or alkali, which may cause themucosa to become gangrenous or to

perforate.

Scarring can occur, resulting in pyloricobstruction.

Gastritis also may be the first sign of

an acute systemic infection.


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Chronic gastritis

Causes:

1) by either benign or malignant ulcers of thestomach

2) or by the bacteria Helicobacter pylori.

3) associated with autoimmune diseases suchas pernicious anemia.

4) dietary factors such as caffeine; the use

of medications, especially NSAIDs; alcohol;

smoking.5) or reflux of intestinal contents into the

stomach.


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Pathophysiology

the gastric mucous membrane becomes

edematous and hyperemic (congested with

fluid and blood) and undergoes superficial

erosion (Fig. 37-1). It secretes a scanty amount of gastric juice,

containing very little acid but much mucus.

Superficial ulceration may occur and can

lead to hemorrhage. (Look Photo)


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The patient with acute gastritis

abdominal discomfort.

headache, lassitude, nausea, anorexia,vomiting, and hiccupping.

Some patients, however, have no

symptoms.


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The patient with chronic gastritis

Anorexia.

heartburn after eating.

Belching.

a sour taste in the mouth.

or nausea and vomiting.

Patients with chronic gastritis fromvitamin deficiency usually have

evidence of malabsorption of vitaminB12 caused by antibodies againstintrinsic factor.


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Diagnostic Findings:

Endoscopy.

upper GI radiographic studies.

histologic examination of a tissue

specimen obtained by biopsy.

H. pyloriinclude serologic testing for

antibodies against the H. pyloriantigen.


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Medical Management

The gastric mucosa is capable of repairing

itself after a bout of gastritis.

(As a rule, the patient recovers in about 1

day, although the appetite may bediminished for an additional 2 or 3 days).

Acute gastritis is also managed by

instructing the patient to refrain from alcohol

and food until symptoms subside.


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After the patient can take nourishment by

mouth, a nonirritating diet is recommended.

If the symptoms persist,fluids may need tobe administered parenterally.

If bleeding is present, management is similar

to the procedures used for upper GI tract

hemorrhage.

If gastritis is caused by ingestion of strong

acids or alkalis, treatment consists of

diluting and neutralizing the offending agent.

To neutralize acids, common antacids (eg,

aluminum hydroxide) are used.


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to neutralize an alkali, diluted lemon juice ordiluted vinegar is used.

If corrosion is extensive or severe, emeticsand lavage are avoided because of thedanger of perforation and damage to theesophagus.

Therapy is supportive and may includenasogastric (NG) intubation, analgesicagents and sedatives, antacids, andintravenous (IV) fluids.

Fiberoptic endoscopy may be necessary.

In extreme cases, emergency surgery may berequired to remove gangrenous or perforatedtissue.


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Gastrojejunostomy or gastric resection may benecessary to treat pyloric obstruction, a

narrowing of the pyloric orifice. Chronic gastritis is managed by modifying

the patients diet, promoting rest, reducingstress, and initiating pharmacotherapy.

H. pylorimay be treated with antibiotics (eg,tetracycline or amoxicillin, combined withclarithromycin) and a proton pump inhibitor(eg, lansoprazole [Prevacid]), and possiblybismuth salts (Pepto-Bismol) (Table 37-1).

Research is being conducted to develop avaccine against H. pylori.


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antrectomy: removal of the pyloric

(antrum) portion of the stomach with

anastomosis

(surgical connection) to the duodenum

A t t i th ti i l l f


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An antrectomy is the resection, or surgical removal, of apart of the stomach known as the antrum. The antrum isthe lower third of the stomach that lies between the body

of the stomach and the pyloric canal, which empties intothe first part of the small intestine. It is also known as theantrum pyloricum or the gastric antrum. Because anantrectomy is the removal of a portion of the stomach, itis sometimes called a partial or subtotal gastrectomy.

Purpose An antrectomy may be performed to treat several

different disorders that affect the digestive system:

Peptic ulcer disease (PUD). An antrectomy may be doneto treat complications from ulcers that have not

responded to medical treatment.


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(gastroduodenostomy or Billroth I)


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anastomosis to the jejunum

(gastrojejunostomyor Billroth II)


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dumping syndrome:

physiologic response to rapid emptying

of gastric contents into the jejunum,

manifested by nausea, weakness,

sweating, palpitations, syncope, and

possibly diarrhea; occurs in patients

who have had partial gastrectomy andgastrojejunostomy.

NURSING PROCESS


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NURSING PROCESS:

THE PATIENT WITH GASTRITIS Anxiety related to treatment.

Imbalanced nutrition, less than bodyrequirements, related to inadequate intake ofnutrients

Risk for imbalanced fluid volume related toinsufficient fluid intake and excessive fluidloss subsequent to vomiting.

Deficient knowledge about dietary

management and disease process. Acute pain related to irritated stomach

mucosa


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Gastric and Duodenal Ulcers

A peptic ulcer:

is an excavation (hollowed-outarea) that forms in the mucosal wall of the

stomach. in the pylorus (opening between stomach

and duodenum).

in the duodenum (first part of small

intestine),or in the esophagus. A peptic ulcer is frequently referred to as a

gastric, duodenal, or esophageal ulcer.


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Peptic ulcers are more likely to be in

the duodenum than in the stomach (As

a rule they occur alone, but they mayoccur in multiples).

Table 37-2 compares the features of

gastric and duodenal ulcers. Peptic ulcer disease occurs with the

greatest frequency in people between

the ages of 40 and 60 years.


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The ingestion of milk and caffeinated

beverages, smoking, and alcohol also may

increase HCl secretion. Familial tendency may be a significant

predisposing factor.

A further genetic link is noted in the finding

that people with blood type O are more

susceptible to peptic ulcers than are those

with blood type A, B, or AB.

There also is an association betweenduodenal ulcers and chronic pulmonary

disease or chronic renal disease.

Oth di i f t i t d


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Other predisposing factors associatedwith peptic ulcer include chronic use of

NSAIDs, alcohol ingestion, andexcessive smoking.

Rarely, ulcers are caused by excessiveamounts of the hormone gastrin,

produced by tumors. This Zollinger-Ellison syndrome (ZES)

consists of severe peptic ulcers,extreme gastric hyperacidity, andgastrin secreting benign or malignanttumors of the pancreas.

St l hi h li i ll


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Stress ulcers, which are clinicallydifferent from peptic ulcers, are

ulcerations in the mucosa that canoccur in the gastroduodenal area.

Stress ulcers may occur in patientswho are exposed to stressful

conditions. Esophageal ulcers

occur as a result of the backward flow

ofHCl from the stomach into theesophagus (gastroesophageal re.uxdisease [GERD]).


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Table 37-2 Comparing Duodenal and

Gastric Ulcers

Pathophysiology


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Pathophysiology

Peptic ulcers occur mainly in thegastroduodenal mucosa because this tissuecannot withstand the digestive action ofgastric acid (HCl) and pepsin.

The erosion is caused by the increasedconcentration or activity of acid-pepsin, orby decreased resistance of the mucosa.

A damaged mucosa cannot secrete enoughmucus to act as a barrier against HCl.

The use of NSAIDs inhibits the secretion ofmucus that protects the mucosa.


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Patients with duodenal ulcer diseasesecrete more acid than normal,

whereas patients with gastric ulcertend to secrete normal or decreasedlevels of acid.

ZES is suspected when a patient hasseveral peptic ulcers or an ulcer that isresistant to standard medical therapy.

It is identified by the following findings:

hypersecretion of gastric juice,duodenal ulcers, and gastrinomas (isletcell tumors) in the pancreas.


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Stress ulcer

is the term given to the

acute mucosal ulceration of the

duodenal or gastric area that occurs

after physiologically stressful events,

such as burns, shock, severe sepsis,and multiple organ traumas.

Usually, it is preceded by shock; this

leads to decreased gastric mucosalblood flow and to reflux of duodenal

contents into the stomach.


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In addition, large quantities of pepsin

are released.

The combination of ischemia, acid, and

pepsin creates an ideal climate for

ulceration.

Stress ulcers should be distinguishedfrom Cushings ulcers


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1)pain or a burning sensation in the

midepigastrium or in the back.

2) pyrosis (heartburn)

3)vomiting.

4) constipation or diarrhea.

5) bleeding.



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Findings A physical examination may reveal pain, epigastric

tenderness, or abdominal distention.

A barium study of the upper GI tract may show anulcer.

Endoscopy is the preferred diagnostic procedurebecause it allows direct visualization of inflammatorychanges, ulcers, and lesions.

Through endoscopy, a biopsy of the gastric mucosaand of any suspicious lesions can be obtained.

Endoscopy may reveal lesions that are not evident

on x-ray because of their size or location. Stools may be tested periodically until they are

negative for occult blood.


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Gastric secretory studies are of value

in diagnosing achlorhydria and ZES.

H. pyloriinfection may be determined

by biopsy and histology with culture.

There is also a breath test that detects

H. pylori, as well as a serologic test forantibodies to the H. pyloriantigen.

Pain that is relieved by ingesting food

or antacids and absence of pain onarising are also highly suggestive of an

ulcer


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Medical Management

Once the diagnosis is established, thepatient is informed that the problem can becontrolled.

Recurrence may develop.

peptic ulcers treated with antibiotics toeradicate H. pylorihave a lower recurrencerate than those not treated with antibiotics.

The goals are to eradicate H. pyloriand to

manage gastric acidity. Methods used include medications,

lifestyle changes, and surgical intervention.


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B) STRESS REDUCTION AND REST


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B) STRESSREDUCTION AND REST

C) SMOKING CESSATION

D) DIETARYMODIFICATION

E) SURGICAL MANAGEMENT

surgery is usually recommended

for patients with intractable ulcers (those that fail toheal after 12 to 16 weeks of medical treatment).

life-threatening hemorrhage,perforation, orobstruction, and for those with ZES not respondingto medications

(Surgical procedures include vagotomy, with orwithout pyloroplasty, and the Billroth I and Billroth II

procedures (Table 37-3; see also the section ongastric surgery later in this chapter).


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Patients who need ulcer surgery may

have had a long illness. They may be

discouraged and have had

interruptions in their work role and

pressures in their family life.

THE PATIENT WITH ULCER


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THE PATIENT WITH ULCER

DISEASE

NURSING DIAGNOSES Acute pain related to the effect of gastric acid

secretion on damaged tissue

Anxiety related to coping with an acutedisease

Imbalanced nutrition related to changes in

diet

Deficient knowledge about prevention of

symptoms and management of the condition

Abnormalities of Fecal


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Abnormalities of Fecal

Elimination Changes in patterns of fecal elimination are

symptoms of functional disorders or disease of theGI tract.

The most common changes seen are constipation,

diarrhea, and fecal incontinence. The nurse should be aware of the possible causes

and therapeutic management of these problems andof nursing management techniques.

Education is important for patients with these

abnormalities.


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CONSTIPATION

Constipation is a term used to describe

an abnormal infrequency or irregularity

of defecation, abnormal hardening of

stools that makes their passagedifficult and sometimes painful, a

decrease in stool volume, or retention

of stool in the rectum for a prolongedperiod.

Constipation can be caused by :


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Constipation can be caused by :

1- certain medications (ie,tranquilizers,anticholinergics,

antidepressants, antihypertensives, opioids,antacids with aluminum, and iron).

2- rectal or anal disorders (eg, hemorrhoids,fissures).

3- obstruction (eg, cancer of the bowel).4- metabolic, neurologic, and neuromuscularconditions (eg, diabetes mellitus,Hirschsprungs disease, Parkinsonsdisease, multiple sclerosis).

5- endocrine disorders (eg, hypothyroidism,pheochromocytoma).


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M l d l i i


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Many people develop constipation

because they do not take the time to

defecate or they ignore the urge todefecate.

In the United States, constipation is

also a result of dietary habits (ie, lowconsumption of fiber and inadequate

fluid intake), lack of regular exercise,

and a stress-filled life.


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Any of the causative factors previously


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Any of the causative factors previously

identified can interfere with any of

these three processes.Go to page 201


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Findings

patients history.

physical examination.

barium enema or sigmoidoscopy.

stool testing for occult blood. Anorectal manometry (ie, pressure studies)

may be performed to determine malfunctionof the muscle and sphincter.

Defecography and bowel transit studies canalso

assist in the diagnosis.


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M di l M t


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Medical Management

Treatment is aimed at the underlyingcause of constipation and includeseducation, bowel habit training,

increased fiber and fluid intake, andjudicious use of laxatives.

Management may also includediscontinuing laxative abuse.

Routine exercise to strengthenabdominal muscles is encouraged.


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DIARRHEA


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DIARRHEA

Diarrhea is increased frequency of

bowel movements (more than three per

day), increased amount of stool (more

than 200 g per day), and alteredconsistency (ie, looseness) of stool.

It is usually associated with urgency,

perianal discomfort, incontinence, or acombination of these factors.

P th h i l


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Pathophysiology

Types of diarrhea include secretory,

osmotic, and mixed diarrhea.

Secretory diarrhea is usually high-

volume diarrhea and is caused by

increased production and secretion of

water and electrolytes by the intestinal

mucosa into the intestinal lumen.


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Osmotic diarrhea occurs when water is

pulled into the intestines by theosmotic pressure of unabsorbed

particles, slowing the reabsorption of

water.

Mixed diarrhea is caused by increased

peristalsis (usually from IBD) and a

combination of increased secretion and

decreased absorption in the bowel.


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