small, and increased

lots of diapers

gluconeogenesis

the formation of glycogen

circular

longitudinal

sphincter

digestion

large intestine:

completes process

absorbs water and sodium

mechanisms of absorption:

(four types)

passive diffusion

carrier mediated diffusion

active absorption

energy-driven transport and engulfment

history

ask about:

recent changes in appetite

changes in fluid intake/thirst

food intolerances

belching

vomiting

heartburn

flatulence

feeding or eating routine/ritual

SPITTING UP OR REGURGITATION WITH MEALS

cleft lip and palate

can occur:

cleft lip and palate

union of upper lip is complete by:

cleft lip and palate

treatment:

cleft lip and palate

#1 goal during treatment:

cleft lip and palate

children prone to:

recurrent otitis

hearing loss

or speech delay

observe bonding patterns

colic

feeding disorder

abdominal pain outbursts

colic

may be related to:

colic

patho:

colic

enzyme quantity:

colic

usually worse:

colic

s/s

infant cries loudly and constantly for several hours

abdomen distended, tense

draws legs up toward abdomen

clenched fists

colic

begins at what age?

colic

lasts for how long?

failure to thrive

failure to thrive

two types:

failure to thrive

organic:

physical causes:

cystic fibrosis

celiac disease

system failures

failure to thrive

nonorganic:

psychosocial factors

bonding attachment disorders

NEGLECT!

failure to thrive

diet:

failure to thrive

children need:

failure to thrive

indicators:

cachexia

and generalized weakness

avoidance of eye contact

sleep disturbances

failure to thrive

diagnosis:

physical and medical work up to r/o organic causes

bowel and muscle biopsies

failure to thrive

intussusception:

intussusception

s/s

sudden, acute pain, "currant jelly" stools

sausage shaped mass RUQ

intussusception

most common site:

ileocecal valve

RUQ

intussusception

diagnosis:

barium enema (may correct problem)

intussusception

treatment:

intussusception

4- 10% will have what outcome within 36 hours?

pyloric stenosis

pyloric stenosis

more common in:

males 5x more common than girls

full term infants rather than preterm infants

pyloric stenosis

can start with:

pyloric stenosis

s/s

progressive, projectile, non-bilious vomiting

moveable, palpable, olive shaped mass in RUQ

visible deep peristalic waves

irritability

HUNGER

crying

sunken fontanels

dehydration

pyloric stenosis

diagnostics:

abdominal ultrasound

upper GI

labs

pyloric stenosis

treatment:

NG tube

surgery

IV fluids

pyloric stenosis

management:

maintain NG patency

small frequent feedings

IV hydration

VS

incisional site care

Omphalocele

defintion:

intra-abdominal contents herniate through

umbilical cord

Omphalocele

patho:

gastroschisis

assessment:

true of false

gastroschisis may be noted on prenatal ultrasound

gastroschisis

immediately:

gastroschisis

monitor for:

circulatory compromise

NG compression

observe for possible ileus

congenital diaphramatic hernia

is a failure of what type of tissues?

pleuroperitoneal tissues

failure to properly develop and form diaphram

congenital diaphramatic hernia

what is the effect on the lungs?

lung growth may cease

decreased breathing by pulmonary hypoplasia and compression of the lungs, airways and vessels

congenital diaphramatic hernia

assessment:

depends on severity of lesion

dimisnished/absent breath sounds

bowel sounds heard in chest

cardiac sounds on RIGHT side of chest

congenital diaphramatic hernia

s/s

dyspnea

cyanosis

nasal flaring

tachypnea

retractions

sunken abdomen

congenital diaphramatic hernia

Pre-op:

elevate HOB on affected side

maintain: NG patency, monitor IV fluids, mechanical ventilation

congenital diaphramatic hernia

Post-op:

wound care- prevent infection

monitor for respiratory distress, position in semi-fowlers on affected side

promote nutrition when feedings resume

Biliary Atresia

Biliary Atresia

progressive inflammatory process:

Biliary Atresia

obstruction of normal flow of the bile duct out of the liver causes:

Biliary Atresia

caused by:

teratinogen

originates PRENATAL period

may be viruses, toxins, or chemicals

Biliary Atresia

s/s:

inflammation

edema

permanent injury

Biliary Atresia

liver becomes:

Biliary Atresia

if not treated:

Biliary Atresia

at birth the infant appears:

Biliary Atresia

the bilirubin levels:

Biliary Atresia

jaundice begins:

Biliary Atresia

s/s:

acholic stools: putty like, clay colored

hepatomegaly

abdominal distention

FTT

malnutrition

intense itching

tea colored urine

Biliary Atresia

diagnostic:

Biliary Atresia

ultrasound reveals:

Biliary Atresia

non surgical treatment:

TPN or lipids

monitor weight

vitamins

monitor stool

pattern

tepid baths

nutrional support

emotional supprt

Biliary Atresia

Education:

meticulous skin care

home medication regimen

s/s of liver failure

available support groups

MEDICATIONS TO PREVENT REJECTION

Esophageal Atresia

malformation from:

failure of esophagus to develop as a continuous tube

foregut fails to seperate into 2 distinct tubes

Esophageal Atresia

the esophagus:

Esophageal Atresia

tracheoesophageal fistula:

esophageal pouch connected to trachea bya fistula

* aspiration risks*

Esophageal Atresia

associated with:

GI anomalies(imperforate anus)

Malformation of:

cardiac

urinary

musculoskeleton

Esophageal Atresia

s/s:

excessive salivation

drooling

cyanosis

coughing and choking with feeding

fluid return via nose

aspiration

Esophageal Atresia

diagnostic:

inability to pass NG tube into stomach

x-ray shows blind pouch

Esophageal Atresia

Rx:

surgical emergency!

Esophageal Atresia

surgical repair prognosis:

Esophageal Atresia

surgical repair may involve:

biliary atresia

surgical treatment:

Hirschsprung's Disease

(congenital Aganglionic megacolon)

Hirschsprung's Disease

two types:

acute

chronic

Hirschsprung's Disease is a congenital __________

_____________ disease

Hirschsprung's Disease

mechanism:

lack of innervation to colon

preventing peristalis and results in mechanical obstruction

Hirschsprung's Disease

more common in:

Hirschsprung's Disease

s/s of newborn:

failure to pass mechonium stools

abdominal distention

bile stained emesis

reluctant to take fluids

Hirschsprung's Disease

s/s for infants:

FTT

constipation

vomiting

episodic diarrhea

Hirschsprung's Disease

s/s for toddlers:

chronic constipation

foul smelling stools

visible peristalsis

palpable fecal mass

anemia

hypoproteinemia

abdominal distention

Hirschsprung's Disease

diagnosis:

rectal exam

rectal biopsy

barium studies

Hirschsprung's Disease

Rx:

Hirschsprung's Disease

surgical Rx:

removal of aganglionic bowel segment and

temporary colostomy

later surgery- colostomy take down

reanastomosis the bowel and colostomy closed

Hirschsprung's Disease

pre-op:

antibiotics

colostomy education to family

Hirschsprung's Disease

post-op:

assess stoma for: color, bleeding, breakdown of surrounding skin

NPO

pain management

fluid management I&O's

Hirschsprung's Disease

post-op keep child NPO until:

Gastroesophageal Reflux

(GERD)

regurgitation of gastric contents into esophagus

Gastroesophageal Reflux

(GERD)

cause:

incompetence of lower esophageal sphincter

reflux(backward flow) damages esophagus

Gastroesophageal Reflux

(GERD)

typically is self limiting by age:

Gastroesophageal Reflux

(GERD)

rate increases with:

Gastroesophageal Reflux

(GERD)

Gastroesophageal Reflux

(GERD)

complications occur most in who:

males 3x more than females

*complications pathological

Gastroesophageal Reflux

(GERD)

when complications occur they are:

Gastroesophageal Reflux

(GERD)

treatment depends on:

Gastroesophageal Reflux

(GERD)

Rx for MILD refulx:

Gastroesophageal Reflux

(GERD)

Rx for severe reflux:

surgical treatment (nissen fundoplication)

small frequent feedings, medications

Gastroesophageal Reflux

(GERD)

medications:

antacids

histamine blockers (ranitidine, cimetidine)

prilosec

encourage the use of tylenol (not advil or motrin)

Appendicitis

Appendicitis

causes:

maybe caused by fecalith (hardend feces)

obstructing the lumen of cecum

parasites

stenosis

Appendicitis

more common in:

Appendicitis

assessment:

generalized abdominal pain

progressively worsening in RLQ at Mcburney's point

Appendicitis

s/s:

nausea

vomiting

fever

chills

guarding

rigidity

rebound tenderness

diarrhea

constipation

Appendicitis

WBC count:

elevated

(15-20,000 cells/mm3)

Appendicitis

diagnostic:

x-ray or abdominal ultrasound

*reveals enlarged appendix*

Appendicitis

Rx:

surgery

*appendectomy*

Appendicitis

Pre-op:

NPO

IV

assess bowel sounds

do NOT stimulate peristalsis (rupture)

Appendicitis

palpating the abdomen:

may cause rupture

NEVER palpate their abdomens

Appendicitis

post-op:

IV- electrolytes, antibiotics

Appendicitis

rupture:

slows recovery!

*infection present*

Irritable Bowel Syndrome:

key points

diarrhea and constipation

food intolerances common

Ulcerative Colitis:

key points

limited to colon and rectum

bloody diarrhea

abdominal pain

Chron's disease:

key points

involves any part of the GI system

INFLAMMATION

ulceration -bleeding -edema

narrowed bowel

inflexible scar tissue

Necrotizing eterocolitis:

key points

primarily premature infants

usually first 2 weeks of life

Irritable bowel syndrome

Ulcerative colitis

Chron's disease

Necrotizing enterocolitis

Ulcerative colitis AND Chron's

origin:

Ulcerative colitis AND Chron's

develops at age:

15-25

Ulcerative colitis AND Chron's

Cause:

Ulcerative colitis AND Chron's

marked by:

Ulcerative colitis AND Chron's

medications:

corticosteriods

immunosuppressantsw

antidiarrheals

sulfasazine

folic acid supplements

metronidazole (flagyl)

antispasmotic agents

cyclosporin

Ulcerative colitis AND Chron's

encourage:

Ulcerative colitis AND Chron's

nutrition:

involve child in meal planning

INCREASED:

calories

carbs

protein

DECREASE fiber

*frequent small feedings*

NG feedings, TPN/lipids

Ulcerative colitis AND Chron's

NG feedings:

Ulcerative colitis AND Chron's

surgery:

gluten insensitive eropathy

*Chronic malabsorption*

chronic inability to tolerate gluten

Celiac disease:

nutrition:

LIFELONG management of gluten free diet

Celiac disease

more common:

within families

*it IS your mothers fault*

Hepatitis

type of disease:

Hepatitis

definition:

inflammation of liver, viral infection

*wide range of severity*

Hepatitis

types:

Oral/fecal route

*contagious*

blood borne

parenteral route

*sexual Activity*

body fluids

IV drug use

frequent transfusions

*most common CHRONIC Hepatitis*

percutaneous route in people infected with Hep B

*must be already infected with type B*

transmitted enterically

*contaminated water*

Hepatitis

Two types:

Hepatitis

children < 5 are usually:

asymptomatic with Hep A

*highly contagious*

Hepatitis

Anicteric:

(absence of jaundice)

lasts 5 days

Hepatitis

symptomatic:

ancinteric (absence of jaundice) 5-7 days

anorexia

RUQ pain

fever

malaise

hepatosplenomegaly

Icteric: (jaundice) lasting up to 4 weeks

uticaria

darking urine

light colored stools

*child feels temporarily better as jaundice appears*

Hepatitis

child temporarily feels better as:

Acute Fulminating Hepatitis

total destruction of hepatic paraenchyma

*bleeding problems*

hepatic encephalopathy

Acute Fulminating Hepatitis

associated:

Acites

acute liver failure

Acute Fulminating Hepatitis

can lead to death within:

Acute Fulminating Hepatitis

positive history of:

Acute Fulminating Hepatitis

percutaneous exposure to:

Acute Fulminating Hepatitis

at risk for:

Acute Fulminating Hepatitis

diagnositcs:

elevated liver function tests (SGOT, SGPT)

antigen indentification markers ( IgM anti-HAV)

positive liver biopsy

Hepatitis

nursing interventions

supportive Rx

symptomatic Rx

Provide homeostasis, nutrition, and hydration support

Hepatitis

fulminating cases treatment:

Hepatitis A & B

education:

disinfection of dirty diaper changing area

hand washing

universal precautions

vaccinations for hep A & B

Dehydration

deficit from which fluid volume:

Dehydration

loss of fluid containing what?

Dehydration

main cause:

Dehydration

accompanies:

Dehydration

types:

acute/chronic

inflammatory/non inflammatory

Dehydration

major concerns:

electrolyte imbalance

hypovolemic shock

& death

*esp. in ped pt's*

Dehydration

assessment:

Dehydration

Green bilious vomiting indicates:

vomiting

curdled content, mucous indicates:

vomiting

Coffee grounds colored may indicate:

vomiting

accomanying fever may indicate:

how much of the bodies fluid is made up of

intracellular fluid?

Exchange of fluid across the membranes:

younger children have more fluid:

intracellular K:

r/t

muscle function

Intracellular K

decreased levels cause:

flaccid skeletal muscles

GI cramping

Cardiac arrythmias

Diarrhea

common in:

increased motility and rapid emptying

*decreased electrolytes*

Diarrhea

what two electrolytes are affected the most?

Diarrhea

causes:

colon disease

infection

stress

food intolerance

medications

surgery

Diarrhea

which types of infectious agents:

viral

bacterial

parasitic

Acid/Base Balance determines:

Acid/Base Balance

balance maintained through:

Acid/Base Balance

Acidosis determined by:

# of H ions in fluid

*increase=acidosis*

Acid/Base Balance

lungs compensate with:

increased rate and depth of respirations

<CO2

Acid/Base Balance

kidney's compensate with:

Acid/Base Balance

Alkalosis is a shift of:

Acid/Base Balance

body :

Acid/Base Balance

highest priority for assesment in pediatrics:

Acid/Base Balance

assess:

amount

color

consistency

timing of stools and emesis

history

Acid/Base Balance

monitor:

daily weights

I&O's

abdominal cramping

diarrhea

nursing interventions

s/s of dehydration

oral or IV rehydration

reduce fever

maintain skin integrity- manage diaper rash

universal precautions