Chapter 9 Gastrointestinal Function - PowerPoint Presentation

Slide1

Chapter 9

Gastrointestinal Function

Slide2

Gastrointestinal System

Consumes, digests,

and

eliminates

food

Includes

Upper Division:

oral cavity, pharynx, esophagus, and stomach

Lower Division:

small

intestine,

large

intestine,

and anus

Hepatobiliary

System:

liver, gallbladder, and pancreas

Slide3

Gastrointestinal System

Four layers: mucosa,

submucosa

, muscle, and

serosa

P

eritoneum – large

serous membrane that lines the abdominal

cavity

Parietal

peritoneum

– outer layer

Visceral

peritoneum

– inner layer

P

eritoneal cavity – space between the two layers

Slide4

Gastrointestinal System

Mesentery – double-layer peritoneum containing blood vessels and nerves that supplies the intestinal wall

Slide5

Upper GI TractFood enters through the mouth to begin digestion chemical and mechanical digestion

Swallowing is coordinated by the swallowing center in the medulla and

cranial nerves V, IX, X, and XII

Slide6

Liver

Main functions

Metabolize carbohydrates, protein, and fats

Synthesize glucose,

protein,

cholesterol, triglycerides, and clotting factors

Store

glucose, fats,

and micronutrients

and

release

when

needed

Detoxify blood of potentially harmful

chemicals

Maintain intravascular fluid

volume

Metabolize medications to prepare them for excretion

Produce bile

Inactivate and prepare hormones for excretion

Remove damaged or old erythrocytes

to

recycle iron and protein

Serve as a blood

reservoir

Convert fatty acids to

ketones

Slide7

GallbladderStores bile produced by the liver

Slide8

PancreasExocrine functions: produces

enzymes,

electrolytes,

and water necessary for digestion

Endocrine function: produces

hormones

to

help regulate blood

glucose

Slide9

Lower GI TractContinues digestion

Absorbs nutrients and water

Slide10

Changes Associated with Aging

Atrophic gastritis

Achlorhydria

B

12

deficiency

Decreased digestion

Liver experiences reduced

blood flow, delayed drug clearance,

and diminished regeneration capacity

Changes

in

lactose, calcium, and iron metabolism

and absorption

Decreased peristalsis

Slide11

Understanding Gastrointestinal Conditions

Altered Nutrition

Impaired Elimination

Slide12

Cleft Lip and Palate

C

ommon congenital

defects of the mouth and face that are apparent at birth

and vary in severity

Usually

develop in the 2nd or 3rd  month of gestation and are

multifactoral

in

origin

Associated

with genetic mutations, drugs, toxins, viruses, vitamin deficiencies, and cigarette

smoking

Most frequent in

American

Indians, Hispanics,

and

Asians while African Americans

are the least likely to have

Males

are twice as likely as females to have a cleft

lip

Females are

twice as likely as males to have a cleft

palate

Slide13

Cleft Lip and Palate Can affect the one’s appearance and may lead to problems with feeding, speech, ear infections, and hearing problems

May occur separately or together

Cleft

lip may

be

unilaterally or bilaterally

and results

from failure of the maxillary processes and nasal elevations or upper lip to fuse during

development

Cleft

palate results from failure of the hard and soft palate to fuse in development, creating an opening between the oral and nasal cavity.

Teeth

and nose malformations

may also

be

present

Slide14

Cleft Lip and Palate Diagnosis:

history, physical examination, and prenatal

ultrasound

Treatment: temporary

measures (e.g., special nipples or dental

appliances), surgical repair, cosmetic

plastic

surgery, speech

therapy,

orthodontist consultation, and multidisciplinary case management

Slide15

Pyloric Stenosis

N

arrowing

and obstruction of the pyloric sphincter

.

The pyloric

sphincter muscle fibers become thick and stiff, making it difficult for the stomach to empty food into the small

intestines

May

be present at birth or develop later in

life

The

exact cause of pyloric

stenosis

is unknown, but genetics is thought to play a

role

Most

common in Caucasians and

males

Slide16

Pyloric Stenosis

Manifestations

appear within several weeks after

birth and include: a

hard mass in the

abdomen, regurgitation, projectile vomiting, wavelike

stomach

contractions, small and

infrequent

stools, failure

to gain

weight, dehydration, and irritability

Diagnosis:

history, physical examination, abdominal ultrasound, barium X-ray, and blood chemistry

Treatment: surgical

repair called

pyloromyotomy

or balloon dilatation

Slide17

DysphagiaD

ifficulty swallowing

Causes: congenital

atresia

, esophageal

stenosis

or

stricture, esophageal

diverticula

, tumors, stroke, cerebral damage,

achalasia

, Parkinson’s disease, Alzheimer’s disease, and muscular

dystrophy

Slide18

Dysphagia

Manifestations: a sensation of food being stuck in the throat, choking, coughing, “pocketing” food in the cheeks, difficulty forming a food bolus, delayed swallowing, and

odynophagia

Diagnosis: history, physical examination, barium swallow, chest and neck X-ray, esophageal pH measurement, esophageal

manometry

, and esophagogastroduodenoscopy

Treatment: specific for the causative condition but usually include speech therapy

Slide19

Vomiting

Involuntary or voluntary forceful ejection of

chyme

from the stomach up through the esophagus and out the mouth

Causes: protection, reverse peristalsis, increased intracranial pressure, and severe pain

Controlled by the medulla coordinates

.

Slide20

VomitingInvoluntary vomiting sequence:

A deep breath is taken.

The glottis closes and the soft palate rises.

Respirations cease to minimize the risk of aspiration.

The

gastroesophageal

sphincter relaxes.

Abdominal muscles contract, squeezing the stomach against the diaphragm and forcing the

chyme

upward into the esophagus.

Reverse peristaltic waves eject

chyme

out of the mouth

Slide21

Vomiting

May be preceded by nausea or retching

Recurrent vomiting can be exhausting and lead to fluid, electrolyte, and pH imbalances

Aspiration can cause serious damage and inflammation and can

occur when supine, unconscious, or the vomiting

or cough reflex

is suppressed

Hematemesis – blood in the vomitus

Has

a

characteristic “coffee grounds” appearance resulting from

protein in the blood being partially

digested

Blood is

irritating to the

gastric mucosa

Can occur from any conditions that causes

upper GI

bleeding

Slide22

Vomiting

Yellow or green colored

vomitus

Usually indicates the presence of bile

Can occur as a result of a GI tract obstruction

A deep brown colored

vomitus

May indicate content from the lower intestine

Frequently results from intestinal obstruction

Undigested food

vomitus

Caused by conditions that impair gastric emptying

Diagnosis: history, physical examination, and blood chemistry

Treatment: antiemetic medications, oral or intravenous fluid replacement, correct electrolyte imbalance, and restore acid-base balance

 

Slide23

Hiatal Hernia

A stomach section protrudes upward through an opening in the diaphragm toward the lung

Causes: weakening of the diaphragm muscle, frequently resulting from increased

intrathoracic

pressure or increased intra-abdominal pressure; trauma; and congenital defects

Risk factors: advancing age and smoking

Vary in severity depending on size

Slide24

Hiatal Hernia

Manifestations

Include: indigestion, heartburn, frequent belching, nausea, chest pain, strictures,

dysphagia

, and soft upper abdominal mass (protruding stomach pouch)

Worsen with recumbent positioning, eating (especially after large meals), bending over, and coughing

Slide25

Hiatal Hernia

Diagnosis: history, physical examination, barium swallow, upper GI tract X-rays, and esophagogastroduodenoscopy

Treatment: eating small frequent meals (six small meals a day), avoiding alcohol, assuming a high Fowler’s position after meals, ceasing smoking, reducing stress (stress increases gastrointestinal ischemia), antacids, acid-reducing agents , mucosal barrier agents, and surgical repair

Slide26

Gastroesophageal Reflux Disease

Chyme

periodically backs up from the stomach into the esophagus

Bile can also back up into the esophagus

These gastric secretions irritates the esophageal mucosa

Causes: certain food (e.g., chocolate, caffeine, carbonated beverages, citrus fruit, tomatoes, spicy or fatty foods, and peppermint), alcohol consumption, smoking,

hiatal

hernia, obesity, pregnancy, certain medications (e.g., corticosteroids, beta blockers, calcium channel blockers, and

anticholinergics

),

nasogastric

intubation, and delayed gastric emptying

Slide27

Gastroesophageal Reflux Disease

Manifestations: heartburn,

epigastric

pain (usually after a meal or when recombinant),

dysphagia

, dry cough, laryngitis,

pharyngitis

, regurgitation of food, and sensation of a lump in the throat

Often confused with angina and may warrant ruling out cardiac disease

Complications:

esophagitis

, strictures, ulcerations, esophageal cancer, and chronic pulmonary disease

Slide28

Gastroesophageal Reflux Disease

Diagnosis: history, physical examination, barium swallow, esophagogastroduodenoscopy, esophageal pH monitoring, and esophagus

manometry

Treatment: avoid triggers, avoid clothing that is restrictive around the waist, small frequent meals, high Fowler’s positioning 2–3 hours after meals, weight loss, stress reduction, elevate the head of the bed approximately 6 inches, antacids, acid-reducing agents, mucosal barrier agents, herbal therapies (e.g., licorice, slippery elm, and chamomile), and surgery

Slide29

Gastritis

Inflammation of the stomach’s mucosal lining

Acute gastritis

Can be a mild, transient irritation, or it can be a severe ulceration with hemorrhage

Usually develops suddenly and is likely to be accompanied by nausea and

epigastric

pain

Chronic gastritis

Develops gradually

May be asymptomatic, but usually accompanied by a dull

epigastric

pain and a sensation of fullness after minimal intake

Slide30

Gastritis

Gastroenteritis

Inflammation of the stomach and intestines usually because of an infection or allergic reaction

Helicobacter pylori

Most common cause of chronic gastritis

E

rode the stomach’s protective mucosal barrier

Genetic vulnerability and lifestyle behaviors (e.g., smoking, and stress ) may increase the susceptibility

Other causes: organisms transmitted through food and water contamination, long-term use of

nonsteroidal

anti-inflammatory drugs, excessive alcohol use, severe stress, autoimmune conditions, and other chronic diseases

Slide31

Gastritis

Complications of chronic gastritis: peptic ulcers, gastric cancer, and hemorrhage

Manifestations

Include: indigestion, heartburn,

epigastric

pain, abdominal cramping, nausea, vomiting, anorexia, fever, and malaise

Hematemesis

and dark, tarry stools can indicate ulceration and bleeding

Slide32

Gastritis

Diagnosis: history, physical examination, upper GI tract X-ray, esophagogastroduodenoscopy, serum

H. pylori

antibodies levels,

H. pylori

breath test, and stool analysis (

H. pylori

and occult blood)

Treatment:

Acute is often self-limiting and resolves within 3 days

Treatment strategies for acute vary depending on the underlying etiology (e.g. antibiotics)

Treatment strategies for chronic include etiology specific interventions, antacids, acid-reducing agents, and mucosal barrier agents

Other strategies include those for GERD

Slide33

Peptic Ulcer Disease

Lesions affecting the lining of the stomach or duodenum

Risk factors; being male, advancing age,

nonsteroidal

anti-inflammatory drug use,

H. pylori

infections, and certain gastric tumors, and those for GERD (e.g., smoking and alcohol use)

Vary in severity from superficial erosions to complete penetration through the GI tract wall

Develops because of an imbalance between destructive forces and protective mechanisms

Slide34

Peptic Ulcer Disease

Duodenal ulcers

Most commonly associated with excessive acid or

H. pylori

infections

Typically present with

epigastric

pain that is relieved in the presence of food

Gastric ulcers

Less frequent but more deadly

Typically are associated with malignancy and

nonsteroidal

anti-inflammatory drugs

Pain typically worsens with eating

Slide35

Peptic Ulcer Disease

Stress ulcers

Develops because of a major physiological stressor on the body due to local tissue ischemia, tissue acidosis, bile salts entering the stomach, and decreased GI motility

Curling’s ulcers – stress ulcers associated with burns

Cushing’s ulcers – stress ulcers associated with head injuries

Most frequently develop in the stomach, and multiple ulcers can form within hours of the precipitating event

Often hemorrhage is the first indicator because of the rapid development and being masked by the primary problem

Slide36

Peptic Ulcer Disease

Complications: GI hemorrhage, obstruction, perforation, and peritonitis

Manifestations:

epigastric

or abdominal pain, abdominal cramping, heartburn, indigestion, nausea, and vomiting

Slide37

Peptic Ulcer Disease

Diagnosis: history, physical examination, upper GI tract X-ray, esophagogastroduodenoscopy, serum

H. pylori

antibodies levels,

H. pylori

breath test, and stool analysis (

H. pylori

and occult blood)

Treatment

Include those for gastritis

Surgical repair may also be necessary for perforated or bleeding ulcers

Prevention is crucial and may include prophylactic medications (e.g., acid-reducing agents) to persons at risk

Slide38

Cholelithiasis

Gallstones

A common condition that affects both genders and all ethnic groups relatively equally

Risk factors: advancing age

Calculi vary in size and shape

Cholecystitis

–inflammation or infection in the biliary system caused by calculi

Vary in severity depending on size

May obstruct bile flow and cause gallbladder rupture, fistula formation, gangrene, hepatitis, pancreatitis, and carcinoma

Slide39

Cholelithiasis

Manifestations:

biliary

colic, abdominal distension, nausea, vomiting, jaundice, fever, and

leukocytosis

Diagnosis: history, physical examination, abdominal X-ray, gallbladder ultrasound, and laparoscopy

Treatment: low-fat diet, medications to dissolve the calculi (e.g., bile acids), antibiotic therapy,

nasogastric

tube with intermittent suction, lithotripsy,

choledochostomy

(surgery to create an opening for drainage), and laparoscopic removal of calculi or gallbladder

Slide40

Hepatitis

Inflammation of the liver

Causes: infections (usually viral), alcohol, medications (e.g., acetaminophen [Tylenol],

antiseizure

agents, and antibiotics), or autoimmune disease

Can be acute, chronic, or

fulminant

Can be active or

nonactive

Slide41

Hepatitis

Nonviral

Usually recover

May develop liver failure, liver cancer, or cirrhosis

Not contagious

Viral hepatitis

Contagious

Usually recover in time with no residual damage

Advancing age and

comorbidity

increase the likelihood that liver failure, liver cancer, or cirrhosis will develop

Can result in hepatic cell destruction, necrosis, autolysis, hyperplasia, and scarring

Slide42

Types of Viral Hepatitis

A

B

C

D

E

Sources

Feces

Blood/blood-derived

body fluids

Blood/blood-derived

body fluids

Blood/blood-derived

body fluids

Feces

Route of Transmission

Fecal-oral

Percutaneous

Permucosal

Percutaneous

Permucosal

Percutaneous

Permucosal

Fecal-oral

Chronic Infection

No

Yes

Yes

Yes

No

Prevention

Pre/Post-exposure immunization

Pre/Post-exposure immunization

Blood

donor screening; risk behavior modification

Pre/Post-exposure immunization;

risk behavior modification

Ensure safe drinking

water

Slide43

Hepatitis

Acute hepatitis

Has three phases – an asymptomatic incubation phase and three symptomatic phases

Chronic hepatitis

Characterized by continued hepatic disease lasting longer than 6 months

Symptom severity and disease progression varies depending on degree of liver damage

Can quickly deteriorate with declining liver integrity

Fulminant

hepatitis

An uncommon, rapidly progressing form that can quickly lead to liver failure, hepatic encephalopathy, or death within 3 weeks

Slide44

Hepatitis

Diagnosis: history, physical examination, serum hepatitis profile, liver enzyme panel, clotting studies, liver biopsy, and abdominal ultrasound

Treatment

Vaccinations are cornerstone of prevention – available for hepatitis A and B

Prevention also includes limiting exposure to the virus

No method of destroying the virus

Hepatitis A and E usually resolve with no treatment

Other types of viral hepatitis can be treated with interferon injections and antiviral medications

Additional strategies: rest, adequate nutrition, increased hydration,

paracentesis

, and liver transplant

Slide45

Cirrhosis

Chronic, progressive, irreversible, diffuse damage to the liver resulting in decreased liver function

Causes: hepatitis and all those factors that can lead to hepatitis

Chronic alcohol abuse is the most frequent cause of cirrhosis in the United States

Hepatitis is the most common etiology in developing countries

Leads to fibrosis, nodule formation, impaired blood flow, and bile obstruction that can result in liver failure

May take up to 40 years to develop

Can develop even with the removal of the underlying cause

Slide46

Cirrhosis Manifestations

Portal hypertension

Varicosities in the esophagus and abdomen

Enlargement of nearby organs

Bleeding, either slow or severe, particularly in the esophagus

Ascites

Changes in clotting factors

Muscle wasting

Hyperlipidemia

Hyperglycemia or hypoglycemia

Bile accumulation in the liver causes inflammation and necrosis

Jaundice

Intolerance to fat and fat-soluble vitamin deficiency

Clay-colored stools

Dark urine

Intense itching

Excessive estrogen leads to female characteristics in men and irregular menstruation in women

Numerous toxins and waste products accumulate

Neurologic impairment

Ulcers and GI bleeding

Encephalopathy

Spontaneous bacterial peritonitis

Slide47

Cirrhosis

Diagnosis: history, physical examination, liver biopsy, abdominal X-ray, liver enzyme panel, esophagogastroduodenoscopy, clotting studies, and stools examination (for occult blood)

Treatment:

Complex and vary depending on the underlying cause

Hepatitis-related cirrhosis will be treated with antiviral agents and interferon

Avoid alcohol, drugs, and

hepatotoxic

medications

Nutritional imbalances (usually treated with total

parenteral

nutrition [TPN]) and metabolic dysfunction are corrected

Bile acid-binding agents can aid bile excretion

Slide48

Cirrhosis

Treatment continued

Portal hypertension is treated with a surgically implanted shunt

Fluid restriction, a low-sodium diet, diuretics,

paracentesis

, and shunts may be used to treat

ascites

Esophageal

varices

are treated with endoscopic bands, shunts, or

sclerose

procedures

Antacids and acid-reducing agents

Encephalopathy is treated by eliminating the source of protein breakdown

Lactulose

can promote ammonia excretion in the stools

Antibiotics can be given to suppress intestinal flora and decrease endogenous ammonia production

Liver transplant

Slide49

Pancreatitis

Inflammation of the pancreas

Can be acute or chronic

Causes:

cholelithiasis

, alcohol abuse ,

biliary

dysfunction,

hepatotoxic

drugs, metabolic disorders , trauma, renal failure, endocrine disorders, pancreatic tumors, and penetrating peptic ulcer

Pancreatic injury causes pancreatic enzymes to leak into the pancreatic tissue and initiate

autodigestion

resulting in edema, vascular damage, hemorrhage, and necrosis

Pancreatic tissue is replaced by fibrosis, which causes exocrine and endocrine changes and dysfunction of the islets of

Langerhans

Slide50

Pancreatitis

Acute pancreatitis

Considered a medical emergency

Mortality increases with advancing age and

comorbidity

Complications: acute respiratory distress syndrome, diabetes mellitus, infection, shock, disseminated intravascular coagulation, renal failure, malnutrition, pancreatic cancer,

pseudocyst

, and abscess

Slide51

Pancreatitis

Manifestations of acute pancreatitis are usually sudden and severe:

Upper abdominal pain that radiates to the back, worsens after eating, and is somewhat relieved by leaning forward or pulling the knees toward the chest

Nausea and vomiting

Mild jaundice

Low-grade fever

Blood pressure and pulse changes

Slide52

Pancreatitis

Manifestations of chronic pancreatitis tend to be insidious:

Upper abdominal pain

Indigestion

Losing weight without trying

Steatorrhea

Constipation

Flatulence

Slide53

Pancreatitis

Diagnosis: history, physical examination, serum amylase and lipase levels, serum calcium levels, complete blood count, liver enzymes panel, serum

bilirubin

level, arterial blood gases, stool analysis (lipid and

trypsin

levels), abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging,  abdominal ultrasound, and endoscopic

retrograde cholangiopancreatography

Slide54

Pancreatitis

Treatment:

Close monitoring and aggressive management

Resting the pancreas by not eating, administering intravenous nutrition, and gradually advancing diet from clear liquids as tolerated to low fat

Pancreatic enzyme supplements when diet is resumed

Maintaining hydration status with intravenous fluids

Nasogastric

tube with intermittent suction

Antiemetic agents

Slide55

Pancreatitis

Treatment continued:

Pain management

Antacids and acid-reducing agents

Anticholinergic

agents

Antibiotic therapy

Insulin

Identifying and treating complications early  

Slide56

Diarrhea

Change in bowel pattern characterized by an increased frequency, amount, and water content of the stool

Results because of increased fluid secretion, decreased fluid absorption, or an alteration in GI peristalsis

Acute diarrhea

Often caused by viral or bacterial infections or certain medications (e.g., antibiotics, antacids, and laxatives)

Usually self-limiting, depending on the cause

Chronic diarrhea

Last longer than 4 weeks

Causes: inflammatory bowel diseases,

malabsorption

syndromes, endocrine disorders, chemotherapy, and radiation

Slide57

Diarrhea Manifestations

Originating in the small intestine

Stools are large, loose, and provoked by eating

Usually accompanied by pain in the right lower quadrant

Originating in the large intestine

Stools are small and frequent

Frequently accompanied by pain and cramping in the left lower quadrant

Acute diarrhea is generally infectious and accompanied by cramping, fever, chills, nausea, and vomiting

Blood (may be frank, occult, or

melena

), pus, or mucus may be present

Bowel sounds may be hyperactive

Fluid, electrolyte, and pH imbalances

Slide58

Diarrhea

Diagnosis: history (including usual bowel pattern and completion of the Bristol Stool chart), physical examination, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, arterial blood gases, and abdominal ultrasound

Slide59

Diarrhea Treatment

Fasting for acute diarrhea with infectious origins

Antidiarrheal

agents may or may not be used

Antibiotics may be necessary

Anticholinergics

Antispasmodic agents

When oral intake is recommended, a clear liquid diet is usually ordered until the diarrhea subsides

Then the diet is advanced to a regular diet as tolerated

Dietary fiber can be used to manage chronic diarrhea

Maintaining hydration status and correcting electrolyte and pH imbalances

Meticulous skin care in cases of bowel incontinence

Slide60

Constipation

Change in bowel pattern characterized by infrequent passage of stool in reference to the individual’s typical bowel pattern

Stool remains in the large intestine longer than usual, increasing the amount of water removed

Causes: low-fiber diet, inadequate physical activity, insufficient fluid intake, delaying the urge to defecate, laxative abuse, stress, travel, bowel diseases, certain medications, mental health problems, neurologic diseases, and colon cancer

Common in children who are toilet training

Slide61

Constipation

Manifestations: pain during the passage of a bowel movement, inability to pass stool after straining or pushing for more than 10 minutes, no bowel movements for more than 3 days, and hypoactive bowel sounds

Complications: anal bleeding, anal fissure to develop, pH disturbances, hemorrhoids, diverticulitis, impaction, intestinal obstruction, and fistulas

Slide62

Constipation

Diagnosis: history (including usual bowel pattern and completion of the Bristol Stool chart), physical examination (may include a digital examination), abdominal X-ray, upper GI series, barium swallow, colonoscopy, and

proctosigmoidoscopy

Treatment: increasing dietary fiber with concomitant increase in hydration, increasing physical activity, defecating when initial urge is sensed, taking stool softeners, limiting use of laxatives and enemas, and digitally removing impaction

Slide63

Intestinal Obstruction

Blockage of intestinal contents in the small intestine or large intestine.

Causes

Mechanical obstructions: foreign bodies, tumors, adhesions, hernias,

intussusception

,

volvulus

, strictures,

Crohn’s

disease, diverticulitis,

Hirschsprung’s

disease, and fecal impaction

Functional obstructions (also called paralytic ileuses): neurologic impairment; intra-abdominal surgery complications; chemical, electrolyte, and mineral disturbances; intra-abdominal infections; abdominal blood supply impairment; renal and lung disease; and certain medications (e.g. narcotics)

Slide64

Intestinal Obstruction

Can develop suddenly or gradually and can be partial or complete

Chyme

and gas accumulate at the site of the blockage

Saliva, gastric juices, bile, and pancreatic secretions begin to collect as the blockage lingers

Serum electrolytes and protein increases, causing abdominal distension and pain

Intestinal blood flow can become impaired, leading to strangulation and necrosis

Intestinal contents can seep into the abdomen as the pressure increases

Complications: perforation, pH imbalances, fluid disturbances, shock, and death

Slide65

Intestinal Obstruction

Manifestations: abdominal distension, abdominal cramping, colicky pain, nausea, vomiting, constipation, diarrhea,

borborygmi

, intestinal rushes, decreased or absent bowel sounds, restlessness, diaphoresis, tachycardia progressing to weakness, confusion, and shock

Diagnosis: history (including usual bowel pattern), physical examination, blood chemistry, arterial blood gases, complete blood gases, abdominal computed tomography,  abdominal X-ray, abdominal ultrasound,

sigmoidoscopy

, and colonoscopy

Slide66

Intestinal Obstruction

Treatment:

Strategies depend on the underlying causes

Correcting fluid, electrolyte, and pH imbalances

Nasogastric

tube with intermittent suctioning

Fasting and total parental nutrition until bowel function is restored

Ambulation

Laxatives should be avoided in most cases until the obstruction is resolved

Surgery

Slide67

Appendicitis

Inflammation of the vermiform appendix

Most often caused by an infection

Triggers local tissue edema, which obstructs the small structure

Fluid builds inside the appendix, and microorganisms proliferate

The appendix fills with purulent

exudate

and area blood vessels becomes compressed

Ischemia and necrosis develop

The pressure inside the appendix escalates, forcing bacteria and toxins out to surrounding structures

Complications: abscesses, peritonitis, gangrene, and death

Slide68

Appendicitis Manifestations

Vary from asymptomatic to sudden and severe

Sharp abdominal pain develops, gradually intensifies (over about 12–18 hours), and becomes localized to the lower right quadrant of the abdomen (

McBurney

point)

Pain may occur anywhere in abdomen

Pain will temporarily subside if the appendix ruptures, and then the pain will return and escalate

Nausea, vomiting, and bowel pattern changes

Indications of inflammation and infection (e.g., fever, chills, and

leukocytosis

)

Indications of peritonitis (e.g., abdominal rigidity, tachycardia, and hypotension)

Slide69

Appendicitis

Urgent diagnosis and treatment is crucial

Diagnosis: history, physical examination, complete blood count, abdominal ultrasound, abdominal X-ray, abdominal computed tomography,  and laparoscopy

Treatment:

Surgery, either laparoscopic or open, and may include extensive irrigation

Drainage tubes

Long-term antibiotic therapy

Analgesics

Avoid activities that increase intra-abdominal pressure (e.g., straining and coughing)

Slide70

Peritonitis

Inflammation of the peritoneum

Causes: chemical irritation (e.g., ruptured gallbladder or spleen) or direct organism invasion (e.g., appendicitis and peritoneal dialysis)

Several protective mechanisms are activated

A thick, sticky

exudate

that bonds nearby structures and temporarily seals them off

Abscesses may form in an attempt to wall off the infections

Peristalsis may slow down in a response to the inflammation, decreasing the spread of toxins and bacteria

Slide71

Peritonitis Manifestations

Usually sudden and severe

Classical manifestation = abdominal rigidity

Abdominal tenderness and pain

Large volumes of fluid leak into the peritoneal cavity

Nausea and vomiting

Decreased peristalsis

Intestinal obstruction

Indicators of infection (e.g., fever, malaise, and

leukocytosis

)

Indications of sepsis and shock (e.g., tachycardia, hypotension, restlessness, and diaphoresis)

Slide72

Peritonitis

Diagnosis: history, physical examination, complete blood count, abdominal X-ray, abdominal ultrasound, abdominal computed tomography,

paracentesis

with peritoneal fluid analysis, and

laparotomy

Treatment: surgical repair, long-term antibiotic therapy, correcting fluid and electrolyte imbalances,

nasogastric

tube insertion with intermittent suction, and total parental nutrition

Slide73

Celiac disease

Also known as celiac

sprue

Inherited, autoimmune,

malabsorption

disorder

Primarily a childhood disease, but it can develop at any age

The exact cause is unclear

Most common in Caucasians and females

Tropical

sprue

is a related disorder that occurs in tropical regions and is thought to be caused by a bacterial, viral, parasitic, or amoebic infection

Can be resolved with antibiotic therapy

Slide74

Celiac disease

Results from a defect in the intestinal enzymes that prevent further digestion of

gliadin

(a product of gluten digestion)

Gluten is an ingredient of grains

Intestinal

villi

atrophy and flatten, resulting in decreased enzyme production and less nutrient absorption

Complications: anemia,

arthralgia

,

myalgia

, done disease, dental enamel defects and discoloration, intestinal cancers, depression, growth and development delays in children, hair loss, hypoglycemia, mouth ulcers, increased bleeding tendencies, neurologic disorders, skin disorders, vitamin or mineral deficiency, and endocrine disorders

Slide75

Celiac disease

Manifestations

In infants, generally appear as cereals are added to their diet (usually around 4–6 months of age)

Include: abdominal pain, abdominal distension, bloating, gas, indigestion, constipation, diarrhea, changes in appetite, lactose intolerance, nausea, vomiting,

steatorrhea

, unexplained weight loss, irritability, lethargy, malaise, and behavioral changes.

Slide76

Celiac disease

Diagnosis: history, physical examination, duodenal biopsy, and celiac blood panel (includes immunoglobulin A antibody-

endomysium

antibodies, immunoglobulin A

antigliadin

antibodies,

deaminated

gliadin

peptide antibody, immunoglobulin A

antitissue

transglutaminase

, lactose tolerance test, and D-

xylose

test)

Treatment: gluten-free diet, periodic monitoring for cancer development, and long-term support

Slide77

Inflammatory Bowel Disease

Chronic inflammation of the GI tract, usually the intestines

Chiefly seen in women, Caucasians, persons of Jewish descent, and smokers

Includes

Crohn’s

disease and ulcerative colitis

Characterized by periods of exacerbations and remissions

Thought to be caused by a genetically associated autoimmune state that has been activated by an infection

Immune cells located in the intestinal mucosa are stimulated to release inflammatory mediators that alter the function and neural activity of the

secretory

and smooth muscle cells

Fluid, electrolyte, and pH imbalances develop

Can be painful, debilitating, and life threatening

Slide78

Crohn’s Disease

Insidious, slow-developing, progressive condition

Often develops in adolescence

Characterized by patchy areas of inflammation involving the full thickness of the intestinal wall and ulcerations (skip lesions)

Form fissures divided by nodules, giving the intestinal wall a cobblestone appearance

The entire wall becomes thick and rigid, and the intestinal lumen becomes narrowed and potentially obstructed

Granulomas

develop on the intestinal wall and nearby lymph nodes

The damaged intestinal wall losses the ability to digest and absorb

The inflammation also stimulates intestinal motility, decreasing digestion and absorption

Slide79

Crohn’s Disease

Complications: malnutrition, anemia (especially iron deficiency), fistulas, adhesions, abscesses, intestinal obstruction, perforation, anal fissure, delayed growth and development as well as fluid, electrolyte, and pH imbalances

Manifestations: abdominal cramping and pain (typically in the right lower quadrant), diarrhea,

steatorrhea

, constipation, palpable abdominal mass,

melena

, anorexia, weight loss, and indications of inflammation (e.g., fever, fatigue,

arthralgia

, and malaise)

Slide80

Crohn’s Disease

Diagnosis: history, physical examination, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, barium studies (swallow and enema),

sigmoidoscopy

, colonoscopy, and biopsy

Treatment: low-residue, high-calorie, high-protein diet; oral nutritional supplements; multivitamin supplements; total parental nutrition;

antidiarrheal

agents;

aminosalicylates

(5-ASAs);

glucocorticoids

; immune modulators; biologic agents; analgesics; antibiotics; surgical intestine resection; stress management; and support

Slide81

Ulcerative Colitis

Progressive condition of the rectum and colon mucosa

Usually develops in the 2nd or 3rd decade of life

Inflammation causes epithelium loss, surface erosion, and ulceration that begins in the rectum and extends to the entire colon

Rarely affects the small intestine

The mucosa becomes inflamed, edematous, and frail

Necrosis of the epithelial tissue can result in abscesses

Granulation tissue forms that is fragile and bleeds easily

The ulcers combine, creating large areas of stripped mucosa that results in an adequate surface area for absorption

Slide82

Ulcerative Colitis

Complications: malnutrition, anemia, hemorrhage, perforation, strictures, fistulas,

pseudopolyps

, toxic

megacolon

, colorectal carcinoma, liver disease as well as fluid, electrolyte, and pH imbalances

Manifestations: diarrhea (usually frequent [as many as 20 daily], watery stools with blood and mucus),

tenesmus

,

proctitis

, abdominal cramping, nausea, vomiting, weight loss, and indications of inflammation (e.g., fever, fatigue,

arthralgia

, and malaise)

Slide83

Ulcerative Colitis

Diagnosis: history, physical examination, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, barium enema, colonoscopy, and biopsy

Treatment: high-fiber, high-calorie, high-protein diet; oral nutritional supplements; multivitamin supplements; total parental nutrition;

antidiarrheal

agents; antispasmodics;

anticholinergics

;

aminosalicylates

(5-ASAs);

glucocorticoids

; immune modulators; biologic agents; analgesics; antibiotics; surgical intervention (e.g.,

ileostomy

or colostomy); stress management; and support

Slide84

Irritable Bowel Syndrome

Chronic,

noninflammatory

, GI condition characterized by exacerbations associated with stress

Includes alterations in bowel pattern and abdominal pain not explained by structural or biochemical abnormalities

Less serious than IBD and does not cause permanent intestinal damage

More common in women

Thought to be triggered by stress, food (e.g., chocolate, alcohol, dairy products, carbonated beverages, vegetables, and fruits), hormone changes (e.g., menstruation), and GI infections

Thought to be an intensified response to stimuli with increased intestinal motility and contractions – may have a low tolerance for stretching and pain in the intestinal smooth muscle

Slide85

Irritable Bowel Syndrome

Complications: hemorrhoids, nutritional deficits, social issues, and sexual discomfort

Manifestations:

Stress and mood disorders often worsen symptoms

Abdominal distension, fullness, flatus, and bloating

Intermittent abdominal pain exacerbated by eating and relieved by defecation

Chronic and frequent constipation or diarrhea, usually accompanied by pain

Nonbloody

stool that may contain mucus

Bowel urgency

Intolerance to certain foods (usually gas forming foods and those containing

sorbitol

, lactose, and gluten)

Emotional distress

Anorexia

Slide86

Irritable Bowel Syndrome

Diagnosis: history (including bowel pattern and Rome III criteria), stool analysis (including cultures and occult blood), celiac blood panel, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance,  barium studies (swallow and enema),

sigmoidoscopy

, colonoscopy, and biopsy

Treatment:

antidiarrheal

agents, laxatives, antispasmodics, antidepressants, avoid triggers, maintain adequate fiber intake, stress management, and support  

Slide87

Diverticular Disease

Conditions related to the development of diverticula, outwardly bulging pouches of the intestinal wall that occur when mucosa sections or large intestine

submucosa

layers herniate through a weakened muscular layer

May be congenital or acquired

Thought to be caused by a low-fiber diet and poor bowel habits that results in chronic constipation

The muscular wall can become weakened from the prolonged effort of moving hard stools

More common in developed countries where processed foods and low-fiber diets are typical

Slide88

Diverticular Disease

Diverticulosis

Asymptomatic

diverticular

disease

Usually there are multiple

diverticula

present

Diverticulitis

Diverticula

have become inflamed, usually because of retained fecal matter

Can result in potentially fatal obstructions, infection, abscess, perforation, peritonitis, hemorrhage, and shock

Often asymptomatic until the condition becomes serious

Slide89

Diverticular Disease

Manifestations: abdominal cramping followed by passing a large quantity of frank blood, low-grade fever, abdominal tenderness (usually left lower quadrant), abdominal distension, constipation,

obstipation

, nausea, vomiting, palpable abdominal mass, and

leukocytosis

Slide90

Diverticular Disease

Diagnosis: history, physical examination, stool analysis (including that for occult blood), abdominal computed tomography, abdominal magnetic resonance imaging,  colonoscopy, barium enema, and biopsy

Treatment: high-fiber diet, omitting foods with seeds or popcorn, decreased food intake when active bleeding is present, adequate hydration, proper bowel habits (e.g., defecating when urge is sensed and not straining), stool softeners, antibiotics, analgesics, colon resection, and blood transfusions

Slide91

Oral Cancer

Most are

squamous

cell carcinomas of the tongue and mouth floor

Risk factors: smoked and smokeless tobacco, alcohol consumption, viral infections (especially the human

papillomavirus

),

immunodeficiencies

, inadequate nutrition, poor dental hygiene, chronic irritation, and exposure to ultraviolet light

Most common and most deadly in men, especially African Americans

Very treatable if caught early, but most cases are advanced upon diagnosis

Slide92

Oral Cancer

Usually appears initially as a painless, whitish thickening that develops into a nodule or an ulcerative lesion that persists, does not heal, and bleeds easily

Multiple lesions may be present

Additional manifestations: a lump, thickening, or soreness in the mouth, throat, or tongue as well as difficulty chewing or swallowing

Often metastasizes to neck lymph nodes and esophagus

Treatment: surgery, radiation, and speech therapy

Slide93

Esophageal Cancer

Usually a

squamous

cell carcinoma in the distal esophagus

Most common in men

Associated with chronic irritation

Tumors grow the circumference of the esophagus creating a stricture, or they can grow out into the lumen of the esophagus, creating an obstruction

Complications: esophageal obstruction, respiratory compromise, and esophageal bleeding

Usually asymptomatic early, delaying treatment

Manifestations:

dysphagia

, chest pain, weight loss, and

hematemesis

Treatment: surgery, chemotherapy, radiation, and speech therapy

Slide94

Gastric Cancer

Occurs in several forms, but

adenocarcinoma

(an ulcerative lesion) is the most frequent type

Incidence and mortality rates have declined in the US, but remains extremely prevalent worldwide, especially in Japan

Strongly associated with increased intake of salted, cured, pickled, preserved, and smoked foods

Other risk factors: low-fiber diet, constipation, family history,

H. pylori

infections, smoking, pernicious anemia, chronic atrophic gastritis, and gastric polyps

Slide95

Gastric Cancer

Asymptomatic early stages, delaying diagnosis and treatment

Manifestations: abdominal pain, abdominal fullness,

epigastric

discomfort, palpable abdominal mass, dark stools,

melena

,

dysphagia

that worsens over time, excessive belching, anorexia, nausea, vomiting,

hematemesis

, premature abdominal fullness after meals, unintentional weight loss, weakness, and fatigue

Treatment:

gastrectomy

, chemotherapy, radiation, and nutritional support

Slide96

Liver Cancer

Most commonly occurs as a secondary tumor that has metastasized from the breast, lung, or from other GI structures

Primary tumors are rare in the US, but common worldwide

Causes of primary tumors: chronic cirrhosis and hepatitis

Manifestations

Similar to those of other liver diseases

Include: anorexia, fever, jaundice, nausea, vomiting, abdominal pain (usually in the upper right quadrant),

hepatomegaly

,

splenomegaly

, portal hypertension, edema, third spacing,

ascites

,

paraneoplastic

syndrome, diaphoresis, and weight loss

Slide97

Liver Cancer

Treatment

Varies depending on the primary site and progression of the cancer

Chemotherapy

Surgically removal

Liver transplant

Cryoablation

Radiofrequency ablation

Pure alcohol can be injections into the tumor

Slide98

Pancreatic Cancer

Aggressive malignancy that can quickly metastasize

Usually adenocarcinoma

Most frequently in men and African Americans

Risk factors: family history, obesity, chronic pancreatitis, long-standing diabetes mellitus, cirrhosis, alcohol abuse, and tobacco use

Often asymptomatic until well advanced and has metastasized

Manifestations: progressive upper abdominal pain that may radiate to the back, jaundice, dark urine, clay-colored stools, indigestion, anorexia, weight loss, depression, malnutrition, hyperglycemia, and increased clotting tendencies

Treatment: surgical tumor removal, chemotherapy, radiation, and surgery or endoscopy repair of any

biliary

blockages

Slide99

Colorectal Cancer

Most often develops from an

adenomatous

polyp

Very common and fatal in the US and worldwide

Incidence and mortality highest among men and African Americans

Associated with excessive intake of fat, calories, red meat, processed meat, and alcohol as well as decreased fiber intake

Other risk factors: family history, advancing age, obesity, tobacco use, physical inactivity, and inflammatory bowel disease

Slide100

Colorectal Cancer

Often asymptomatic until well advanced

Manifestations: lower abdominal pain and tenderness, blood in the stool (occult or frank), diarrhea, constipation, intestinal obstruction, narrow stools, unexplained anemia (usually iron deficiency), and unintentional weight loss

Routine screening can improve prognosis, including:

High-sensitivity fecal occult blood test every year

Flexible

sigmoidoscopy

every 5 years

Colonoscopy every 10 years

Treatment: colonoscopy removal, chemotherapy, surgical resection, colostomy, lifestyle changes (e.g., diet and physical activity), and follow-up screenings