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GEE

it’s

GI:

A Med-Surg Review of the GI

System

Laura Habighorst BSN RN CAPA CGRN

August 26, 2015

Objectives

Identify the organs of the GI System

Identify the accessory organs associated with the GI System

Identify the functions of those organs

Describe pathophysiology associated with the GI System

Develop nursing actions for the various pathologies discussed

ASSESSMENT

Four components and must be done in order

INSPECTION

Cullen’s sign: bruising around umbilicus

indicates intrabdominal bleeding

Grey-Turner’s sign: bruising of the lower

abdomen and flank indicates retroperitoneal

bleeding

ASSESSMENT

AUSCULTATION

Listen each quadrant 2-5 minutes

Bowel sounds are absent if not heard for 5 minutes

PERCUSSION

Tympany: heard over stomach and intestines

Dullness: presence of fluids or masses

PALPATION

Light palpation (one handed) of all four quadrants

Rebound tenderness indicates peritoneal irritation

The GI System

Mouth

Esophagus

Stomach

Small Intestine

Large Intestine

Rectum

Anus

Accessory organs: Gallbladder, biliary tract,

pancreas, and liver

Function of the GI System

Supply nutrients to body cells

Ingestion Digestion Absorption

Mechanical/chemical Movement of

breakdown of nutrients nutrients into

bloodstream

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The Mouth The Mouth

Salivary glands of the mouth secrete saliva and mucus

Humans produce 1-2 liters of saliva per day

Enzymes: Amylase breaks down large carbohydrates

primarily starches

Antibacterial prevent infection of the

mouth

Swallowing begins and is an “all or none reflex involving

over 25 muscles”

ESOPHAGUS ESOPHAGUS

23-25 cm in length and 2-3 cm in diameter

Swallowing reflex is initiated in the medulla

Muscles in esophagus are longitudinal and

circumferential and it is through peristalsis food

moves from mouth to stomach. Movement from

pharynx to stomach is 3-5 cm per second.

Pathophysiology of the

Esophagus Disorders of the esophagus include :

Gastroesophageal reflux disease (GERD)

Esophageal varices Barretts esophagus

Tumors Fistulas

Diverticula Inflammatory disease

Esophageal rings or webs

Foreign body obstruction

Mallory-Weiss tears

Motility disorders

GERD

GERD is the “abnormal reflux of gastric contents into the

esophagus.”

Causes: hiatal hernia, decreased lower esophageal sphincter

pressures, gastroparesis, smoking, and pregnancy

Common symptoms include epigastric pain (dyspepsia),

heartburn, regurgitation, difficulty swallowing (dysphagia),

and may also include asthma as a result of chronic aspiration

pneumonia or esophageal bleeding as a result of esophagitis.

25-35% of US population has GERD

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GERD continued

Diagnosis made by: patient history, EGD,

barium swallow, esophageal manometry,

pH studies.

Objectives for treatment include: relief of

symptoms, healing of damaged mucosa, and

prevention of complications.

GERD continued

Therapies include:

Pharmacologic - H2 Histamine blockers such as Tagamet or

Zantac; PPI (proton pump inhibitors) such as Prilosec,

Aciphex, Prevacid; antacids; Reglan or Urecholine (promote

gastric emptying and increase LES tone)

Patient education – small meals; avoid caffeine, mints, fats;

avoid lying down after meals; elevate head of bed to 40°; take

medications on a regular basis and as prescribed

Surgery - fundoplication

Esophageal Varices

Engorged vessels in the submucosa of the esophagus and may

be caused by portal hypertension as a result of chronic

hepatitis; alcoholic cirrhosis; portal vein thrombosis; or

congenital anomalies such as biliary atresia

Diagnosis made most often as an upper GI bleed (12% of all

upper GI Bleeds) and subsequent EGD

Treatment may include band ligation, use of sclerosing agents

such as sodium morrhuate, use of vasopressin; and

tamponade of the vessels (rare and dangerous)

Esophageal Varices

Esophageal Obstruction

Caused by achalasia ( peristalsis is absent with

increased LES pressures and incomplete

esophageal relaxation), stricture, tumor,

bacterial/viral infections , foreign body, or

anomaly

Occurs 1 in 100000 Americans most often between

the ages of 20 and 60.

Symptoms include dysphagia, painful swallowing,

substernal chest pain, bad breath, weight loss and

malnutrition

Esophageal Obstruction

Treatment includes removal of foreign objects or foodstuffs;

dilation of esophagus; esophageal stents; use of smooth

muscle relaxants such as nitrates and calcium-channel

blockers

Education for patients: frequent dilation may be required;

potential for surgery; sleep with HOB ^; semi-soft bland

diet; “if nifedipine (Procardia, Adalat) is prescribed

instruct to take with water and to avoid consuming

grapefruit because of food-drug interactions”; if stents are

required this is life-long.

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Mallory-Weiss Tears

Esophageal tear occurring most often at the

esophagogastric junction. Occurs in 8% of all

upper GI bleeds.

Causes – prolonged forceful vomiting, dry heaves,

alcohol, aspirin use

Diagnosed by EGD

Treatment includes cautery of bleeding area, liquid

or soft diet, avoidance of sharp foods, use of

medications such as Carafate to heal and protect

the esophagus

Barrett’s Esophagus

Normal esophageal tissue is replaced by epithelial tissue

typically of the fundus of the stomach and occurs as a

result of esophageal reflux. 20% of patients with reflux

will go on to develop Barretts.

Diagnosis is made by EGD and biopsy

Treatment centers on prevention of high-grade dysplasia

through the use of PPIs and esophageal dilatation.

Definitive treatment of high-grade dysplasia is offered

with HALO™ ablation therapy. Without treatment

adenocarcinoma of the esophagus is 30-50 times greater.

Barrett’s Esophagus Inflammatory Disease

Variety of disease processes can cause inflammation

of the esophagus: candida (yeast), herpes simplex

virus, cytomegalovirus (CMV), HIV, eosinophilic

esophagitis (immune mediated reaction

characterized by excessive histamine production)

Diagnosed by EGD, biopsy, and or tissue brushings

Treatment may include nystatin, viscous lidocaine,

histamine 2 blockers, sucralfate, or steroids

Eosinophilic Esophagitis Esophageal Candidiasis

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Stomach Stomach

Comprised of 3 parts: fundus, body, and the antrum but

includes the lower esophageal sphincter (between the

esophagus and stomach) and the pyloric sphincter

(between the stomach and small intestine)

Two functions: mixing and grinding of food through

peristalsis and the controlled emptying of the gastric

contents (CHYME) into the duodenum.

Stomach

Secretes the following : hydrochloric acid ,

pepsinogen, intrinsic factor (essential for

absorption of B12), mucus, gastrin,

serotonin, somatostatin, glucagon, and

bicarbonate.

Normal secretions occur at a rate of 0.5

ml/min; with a full stomach 3ml/min

Secretes a total of 1500-3000 ml of gastric

Pathophysiology of the

Stomach Disorders of the stomach include:

Peptic ulcer disease

Gastritis

Cancer

Hiatal hernia

Gastric outlet obstruction

Gastric motor disorders

Bezoars

Peptic Ulcer Disease

An upset in the balance of factors protecting

the stomach mucosa and those factors that

may cause disease.

Risk factors include: increased hydrochloric

acid production, chronic aspirin and NSAID

use, alcohol, cigarette smoking, family

history of gastric ulcers, and presence of

H.Pylori (a bacterial inflammation of the

stomach)

PUD continued

Stress Ulcers are a subset of Peptic Ulcer Disease

Causes: “severe trauma, burns, multisystem trauma, intense

hypotensive events, cardiac arrest, lengthy cranial surgery,

or massive infection” all of which may cause a decrease in

blood flow r/t shunting to vital organs resulting in

ischemia to gastric mucosa.

Bleeding may occur as late as three weeks post incident and

studies indicate “nearly 100%” of patients with the above

factors will present with stress ulcers. While only 5% may

actually bleed of those that do the mortality rate is

approximately 50%.

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PUD continued

Symptoms of PUD may include: epigastric pain, burning,

belching, “pain-food-relief” cycle, or “food-pain” cycle when

erosion occurs.

Medical treatment includes: In the absence of H. Pylori-PPIs, H2

blockers, Carafate, antacids (taken 1 and 3 hours after meals

and at bedtime) , clipping for bleeding, or surgery

In the presence of H. Pylori treatment includes a PPI, a single

or combination of antibiotics, and an antifungal.

Gastric Ulcer

Complications of PUD

TYPE

Hemorrhage – 15% of all ulcer

patients, hematemesis and/or

black stools

Perforation – 5-7% occurrence;

ulcer has eroded through stomach

wall and has spilled into the

peritoneum

Penetration – ulcer has eroded into

another organ

Obstruction – Pylorus becomes

edematous and does not allow

chyme to pass

TREATMENT

Control bleeding, fluid and

electrolyte replacement; in

presence of perforation or

penetration – antibiotics and

surgery; in presence of

obstruction any of the above

and NG tube decompression

as well as correction of any

metabolic acidosis

PUD continued

Nursing interventions : patient education

regarding medications and importance of

adhering to dosing schedules; elimination of

coffee, caffeine, spicy foods, carbonation,

alcohol, chocolate and any other food that

has caused pain and discomfort; small

meals; smoking cessation; avoidance of

aspirin and NSAIDS (if aspirin use is

necessary then enteric coated is best)

Gastritis

Inflammation of the gastric mucosa most

often caused by an irritant such as gastric

acid, bile reflux, medications, or toxins.

Maybe chronic or acute in nature

Treatment is to discover the pathology and

correct with PPIs, and/or antibiotics

Gastritis

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Cancer

Tends to be hereditary in nature occurring more often in

individuals with type A blood, blacks, men, and northern

United States population.

Incidence increases with “age, and those who eat foods high

in starch, nitrates, pickled vegetables, and salted fish and

meat.” A history of gastric ulcers, previous gastric

surgery, and adenomatous polyps also increase the risk of

gastric cancer - 97% of gastric cancer is adenomatous.

Develop primarily in the antrum or along the lesser curvature

of the stomach.

Cancer continued

Signs and symptoms: “epigastric discomfort,

vomiting , unexplained weight loss, early satiety,

anorexia, anemia, abdominal or epigastric mass,

gastric outlet obstruction, ascites, enlarged lymph

nodes in the supraclavicular areas”

Definitive diagnosis is made by EGD or EUS with

biopsy

5 year survival rate is 95% when caught early or is

superficial in nature (not extending beyond the

submucosa of the stomach)

Cancer continued

In US as compared to other countries with gastric screening

programs, gastric cancer is unfortunately discovered most

often in advanced stages and prognosis for 5 year survival

rate is approximately 5%.

Surgery is treatment of choice with partial or total

gastrectomy required as well as chemotherapy and/or

radiation.

Nursing interventions include emotional support, provision of

adequate nutrition, and good pain control

Hiatal Hernia

Occurs when part of the stomach protrudes through

the diaphragm and into the thoracic cavity. Most

are “sliding” hernias, that is a portion of the

stomach slides up above the level of the

diaphragm.

Common in older people and women

Complications include reflux with esophagitis,

heartburn, acid regurgitation, and dysphagia.

Treatment is surgical - fundoplication.

Gastric Outlet Obstruction

“Obstruction of the pyloric sphincter at the outlet of

the stomach blocks the flow of gastric contents

into the duodenum”

Symptoms include vomiting partially digested food,

gastric pain especially with eating, satiety relieved

by vomiting, metabolic alkalosis as a result of

frequent vomiting

Treatment includes restoration of fluid and

electrolytes, decompression of the stomach,

pyloric dilatation, and surgery if necessary

Gastric Motor Disorders

Most common is “Dumping Syndrome” following

gastrectomy, Roux-en-Y for weight loss, Billroth II or

gastrojejunostomy.

Occurs as a result of rapid food transition through the

stomach remnant and the “rapid introduction of

hyperosmolar solutions into the jejunum and the release of

hormones and vasoactive intestinal polypeptides into the

bloodstream.”

Symptoms include weakness, dizziness, tachycardia with a

pounding pulse, diaphoresis, flushing, abdominal cramps,

and diarrhea within 15-120 minutes of eating

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Gastric Motility Disorders

“Dumping Syndrome” continued:

Nutritional education is important for these patients in order

to slow down the gastric emptying rate.

High fat and high protein diet

Low carbohydrates

Fluids before and after meals not during the meal.

Medications such as Reglan have NOT been shown to be

effective.

Bezoars

THE HUMAN HAIRBALL

Compositions of foreign materials found in

the stomach that may cause gastric outlet

obstruction and abdominal pain. Composed

of vegetable or plant material or hair.

Treatment is EGD with removal of the matter.

Bezoar

Note the ruler in the right lower corner!

Small Intestine

Small Intestine Length: 23 feet Diameter: 1.5 inches

The mucosa of the small intestine is covered in villi and

microvilli. These increase the absorptive area of the small

intestine by 600 fold.

Receives 8 liters of fluid/day but passes 500-1000ml to the large

intestine

Comprised of the duodenum, the jejunum, and the ileum

The jejunum and the ileum are the principle sites for absorption

of nutrients. All nutrients are absorbed upon reaching

ileocecal valve and the majority of water absorption takes

place in the ileum as well.

Small Intestine continued

Duodenum: iron and calcium absorption

Jejunum: absorption of fats, proteins, and

carbohydrates

Ileum: absorption of vitamin B12 and bile

acids

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Small Intestine Pathology

Disease processes include: duodenal ulcers,

parasitic infestations, bacterial and viral

infections, Crohn’s disease, Meckel’s

diverticulum, vitamin B12 deficiency, small

bowel tumors

Malabsorption syndromes include: celiac

disease, Whipple’s disease, short bowel

syndrome, lactose intolerance

Infectious and Parasitic Disease

Nursing assessment is helpful in diagnosis: symptom pattern

and types of stools, exposure to affected individuals,

contaminated food or water, foreign travel.

Treatment may include fluid and volume replacement r/t large

amounts of watery diarrhea and diets should remain

unchanged. Antidiarrheals should not be used as they may

prolong the infection. When the source is identified,

antibiotics or antifungals may be prescribed.

Round Worms in Small Intestine Meckel’s Diverticulum

A congenital anomaly outpouching of the ileum which

contains normal tissues as well as gastric and pancreatic

tissue. These abnormal tissues for the ileum secrete acid

and pepsin and can cause ulcerations of the ileum.

Symptoms include: abdominal pain, bilious vomiting, and

“red currant jelly” like stools.

Diagnosed by Meckel’s scan – a radiology contrast study

Treatment is surgical removal of the diverticulum or resection

of the ileum

Meckel’s Diverticulum Celiac Disease or Celiac Sprue

Defined as poor food absorption and an intolerance to glutens

(wheat, oats, rye, barley, and by-products)

Causes: combination of environment and genetic

predisposition. Most common in females, familial history,

and those of northwestern European ancestry.

Symptoms: recurrent attacks of diarrhea, vomiting,

steatorrhea, abdominal distension, flatulence, cramps,

weakness, and anorexia. Muscle wasting and growth

failure in children and adolescents.

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Celiac continued

Diagnosis is made by EGD and biopsy.

Treatment is lifelong elimination of gluten containing foods.

Patient education includes identification of foods that contain

wheat fillers, ie. hotdogs, ice cream, candies. In some severe

cases of Celiac disease, a lactose free diet may need to be

added until exacerbation of Celiac is over.

www.GlutenFreeDietFoods.com

Complications may include osteoporosis, anemia, predisposition

to small bowel lymphoma, esophageal and gastric cancers

Large Intestine

Large Intestine/Colon

5-6 feet in length; and 2.5 inches in diameter

Consists of the cecum, appendix, ascending colon, hepatic

flexure, transverse colon, splenic flexure, descending

colon, sigmoid colon, rectum, and anus.

Functions in reabsorption of water and as a “reservoir for

fecal contents…and contains bacteria that synthesize

vitamins and breakdown cellulose.”

Large Intestine/Colon

Pathophysiology includes the following:

polyps, angiodysplasia, diverticular disease,

irritable bowel syndrome, colitis

(inflammatory bowel disease), cancer,

tumors, obstructions, anorectal disorders,

and parasitic disease.

POLYPS

Tissue mass that is attached to the colon wall, asymptomatic

in nature, diagnosed by colonoscopy or air-contrast barium

enema

Two Types

Pedunculated Sessile

Has a stem Broad flat base

Removed during colonoscopy and repeat colonoscopy

dependent upon pathology and family history (1-5 years)

Polyps

Pedunculated

Sessile

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Colon Cancer

Number One preventable cancer when colonoscopy is

performed according to standards endorsed by the

American Cancer Society and the American Society of

Gastroenterologists.

Age 50 or 10 years prior to the diagnosing age of a first

degree relative with history of colon cancer.

Repeat colonoscopy every 1-5 years dependent upon type of

polyps discovered.

Requires surgery when mass too big for removal

endoscopically, maybe resection with or without ostomy.

Colon Cancer

DIVERTICULAR DISEASE

Outpouchings or herniation of the colon wall

Diverticulitis is the inflammation of diverticulum

Affects 33-50% of all adults over age 50 and 50% of all

adults over age 80.

Contributing factors: “hypertrophy of the circular muscle of

the colon wall, increased intracolonic pressure, age-related

atrophy or weakness in bowel wall, chronic constipation

and straining, irregular uncoordinated bowel contractions,

lack of dietary fiber, and obesity”

Diverticular disease

Typically asymptomatic unless diverticulitis occurs.

Common symptoms of diverticulitis: fever, abdominal pain,

nausea/vomiting, constipation, left lower quadrant

tenderness

Complications: rupture of diverticulum with localized or

generalized peritonitis, abscess formation, edema, fistula

formation, erosion of underlying artery or vein, fibrosis

and narrowing.

Treatment: Mild – high fiber diet bulk forming laxatives;

Acute – bedrest, antibiotics, analgesics, and possibly

surgery

Diverticulum Irritable Bowel Syndrome

Most common GI disorder in the US; ranking a close second

to the common cold as a cause of work absenteeism.

Symptoms: abdominal distention, pain, constipation and/or

diarrhea. Anatomical abnormalities and other illnesses

have been ruled out. Symptoms may vary and have been

associated with emotional stress.

Treatment: Emotional support, high fiber diet,

anticholinergic agents

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Inflammatory Bowel Disease

Includes the following diagnoses: colitis,

Crohn’s disease, and ulcerative colitis. May

be caused as a result of altered immune

response or genetic.

Diagnosis made by colonoscopy or EGD

when involving the small intestine.

Inflammatory Bowel Disease

Ulcerative Colitis

• Affects 10 in 100000 people of all

races, gender, and society

• Affects left colon, starting in the

rectum and moves up

• Shallow ulcerations

• Bloody diarrhea or fatty stools

and may occur hourly

• Complications : megacolon,

bleeding, absorpton problems,

malignancy

Crohn’s disease

• Occurs between ages 15-30;

most common in Caucasions

and Jewish descent

• Can occur anywhere in the

GI tract primarily right

colon

• “Cobblestone effect”

• Abdominal pain, weight

loss, may have fatty stools

• Complications: fistulas,

stricture, malabsorption

Inflammatory Bowel Disease

Ulcerative Colitis

• Treatment: Bowel rest,

aminosalicylates and

corticosteroids; surgery

Crohn’s Disease

• Treatment: Bowel rest;

aminosalicylates,

corticosteroids, immuno-

suppressants, biologics;

surgery. Care is considered

palliative

Inflammatory Bowel Disease

Patient Education

Diet: high protein, high carbohydrate, low residue, low

roughage, low fat. Starchy foods enhance bowel transition

times. Corn, celery, cabbage, coconut increase risk of

blockage; radishes, spicy foods, onions, asparagus increase

odor of flatus. Enteral feedings may be required.

Meds: Must take meds as directed to prevent flares and heal

Emotional support paramount with Crohn’s

Pancreas

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Pancreas

Located behind the stomach and has 3 parts – head, body, and

tail

Functions: Endocrine – production of glucagon (alpha cells);

insulin (beta cells); somatosin (delta cells) – all of which

regulate blood sugars

Exocrine – produces enzymes that aid in

digestion – amylase, lipase, protease

Pathophysiology consists of pancreatitis, Zollinger-Ellison

Syndrome, malignant and benign tumors, and cystic

fibrosis

Acute Pancreatitis

• “Autodigestion of pancreas due to inappropriate activation

of pancreatic enzymes” causing a severe inflammation of

the pancreas

• Causes: ETOH, biliary disease, mumps, scarlet fever and

endocrine disorders

• S&S: Acutely ill with severe pain, guarding, rigidity of

abdomen, hypotension, respiratory distress, shock. Labs:

Increased amylase. Physical exam: Turner’s or Cullen’s

sign

Acute Pancreatitis

• Interventions: hemodynamic monitoring, antibiotics, pain

management, body positioning – sidelying, knees flexed,

HOB up. Patients hemodynamic status may change rapidly

with acute pancreatitis due to peripheral vascular collapse

and acute respiratory distress from fluid shifts.

• Treatment: Remove potential causes necrotic pancreatic

tissue, gallstones (cholecystectomy, ERCP), or repair

problems within biliary system with stents

• Prognosis: May never experience another episode.

Instruct patient to monitor ETOH and dietary intake

Chronic Pancreatitis

• “Continuous progressive and irreversible

destruction of cells with replacement with fibrotic

tissue.”

• Periods of remission and exacerbation

• Causes: Similar to acute; however, 80% have

history of ETOH abuse

• S&S: Similar to acute but may be less severe;

intense unrelenting pain; hypocalcemia; symptoms

of malabsorption (fatty stools, weight loss);

diabetes mellitus

Chronic Pancreatitis

• Interventions: Low fat, high carbohydrate, high protein

diet – allows pancreatic rest; encourage use of enzymatic

supplements appropriately after every snack and meal;

assess stools for fats; provide ETOH/drug abuse therapy;

provide effective pain management (meperidine preferred,

morphine may cause spasms of Sphinctor of Oddi); assess

for abscesses (elevated temp or change in pain); assess for

S&S of diabetes mellitus (polyuria, polydipsia,

polyphagia)

• Prognosis: Continual problem especially with continued

ETOH/drug use

Biliary System

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Biliary System

• Composed of the gallbladder and biliary duct; located

upper right quadrant of the abdomen

• “Main function is to store and concentrate bile, 600mls of

bile produced daily. Bile contains bile salts which are

needed for fat emulsion and digestion”

• Pathophysiology: cholecystitis, cholelithiasis, cholangitis,

cancer, congenital anamolies, sphincter of Oddi (regulates

flow of bile and pancreatic juices into the small

bowel)disease

Cholecystitis and cholelithiasis

• Inflammation of the gallbladder, typically caused by the

presence of stones or malfunctioning gall bladder

• Two types of stones – cholesterol and pigment

• Occurs in 10% of the US population. Fifth leading cause

of hospitalization. More common in postmenopausal,

postpartum women.

• S&S: Biliary colic pain that radiates to right shoulder,

RUQ tenderness and rigidity, N&V and indigestion

especially after fatty meals, fever, increased WBC,

jaundice with bile duct obstruction; HOWEVER, can be

asymptomatic

Gallstones

Cholecystitis and cholelithiasis • Treatment: pain management, fluid and electrolyte

maintenance, surgical (cholecystectomy, open or laparoscopic)

vs. endoscopic intervention (ERCP – endoscopic retrograde

cholangiopancreatography) vs. shock therapy (ESWL – extra

corporal shock-wave lithotripsy)

• Care after surgical procedure includes good respiratory care,

ie. incentive spirotomy; pain control including opioids and

NSAIDS; fat soluble vitamins

• Dietary instruction should include slow reintroduction of fatty

foods.

• Complications: cirrhosis, pancreatitis, rupture

LIVER Liver

• Largest internal organ and has the ability to regenerate

because of its vascularity

• Function includes: “metabolism and storage of fats,

carbohydrates, proteins, and vitamins; metabolism of

steroids; synthesis of albumin, globulin, prothrombin, and

fibrinogen; detoxification of the blood; excretion of

bilirubin; manufactures bile at a rate of 500-1000ml/24

hours.

• Pathophysiology: Hepatitis, liver failure, cirrhosis, tumors,

Wilson’s disease

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Hepatitis

Inflammation of the liver typically caused by a virus (one of

six different viruses) alcohol or drug induced

Six Viruses of Hepatitis

Hep A: spread through fecal/oral route

Hep B: spread via body fluids – IV drug use, dialysis, sex

Hep C: Posttransfusion or hemophiliacs

Hep D: replicates in the presence of Hep B

Hep E: water-bourne, mostly in underdeveloped countries

Hep G: transmitted parenterally and sexually

Hepatitis and Incidence

50000-60000 cases yearly in the US.

Hep A accounts for 40% of hepatitis worldwide

4 million Americans are infected with Hep C

Higher incidence in health care workers, IV drug users

Hepatitis

Four stages of symptoms

• Prodomal – “lasts 7-10 days, vague symptoms, of malaise,

headache, anorexia, low-grade fever, sometimes RUQ

pain, no jaundice”

• Icteric – “acute phase,” jaundice, lasts 4-6 weeks, minimal

discomfort with liver enlargement and tenderness

• Post-icteric – convalescent lasts 2-4 months

• Recovery – 6-12 months of liver rest

Hepatitis Treatment includes a variety of immuneglobulins dependent upon

virus; however, Hep C, E, and G do not have vaccines. The

CDC recommends all individuals be vaccinated for Hep B.

Nursing care includes dietary instruction (high calories with high

protein and carbs, low fat, and Vitamin B and K supplements;

abstain from ETOH/drugs; enforce and encourage complete

rest; maintain universal precautions; monitor liver enzymes for

liver failure (AST, ALT, bilirubin); instruct patient not to

donate blood, compliance with treatment plan essential to

avoid relapse

AND EVERYTHING ELSE! Obesity and Bariatrics

Body Mass Indexing

(based on height to weight computation)

Overweight: 25-29.9

Obese: greater than 30

Morbidly Obese: greater than 40

65% of Americans over 20 years of age are overweight

Second leading cause of preventable death

Complications: cardiopulmonary, muscular, GI, endocrine

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Obesity

Treatment include DIET, medications (appetite suppressant,

nutrient absorption blocking, UCG) and surgery

Types of surgery include: Lap Band, Roux-en-Y, J-Loop,

Sleeve

Nursing care: Head of bed elevated, use of lifts for moving

and bariatric furnitures, DVT prophylaxis, and dietary

instruction and reinforcement paramount – small frequent

meals, high protein, low carbohydrates and roughage.

Avoid drinking and eating at the sametime.

Bariatrics

Gastric banding Roux-en-Y

Bariatrics

Sleeve

Obesity

Complications include anastomatic leaks, ulcers, dumping

syndrome, malnutrition, vitamin deficiencies, anemia,

psychosocial

Leaks require further surgery and may require resection, roux-en-

y, or gastrectomy depending upon the site

Ulcers can occur in an area of the stomach that has decreased

blood supply after roux-en-y.

Obesity and Bariatrics

Complications, continued

Dumping syndrome: Occurs as a result of rapid

transit of food into the stomach and intestine

Nutritional deficiencies: Requires B-12 injection

due to inability to absorb B-12 in the

diminished gut.

Psychological support: “I am the same person

THANK YOU

GOOD LUCK

TO

EACH OF

YOU!

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BIBLIOGRAPHY

• Core Curriculum for Medical-Surgical

Nursing 4th Edition. 2009. Academy of

Medical-Surgical Nurses.

• Gastroenterology Nursing: A Core

Curriculum, 4th Edition. 2008. Society of

Gastroenterology Nurses and Associates