Infant Disorders Flashcards
What is a cleft lip? what does it look like?
Can vary from an indentation to a fissure
May be unilateral or bilateral gap in upper lip extending to the nose
Incidence of cleft lip
1 in 700 live births
Etiology of cleft lip
teratogens (any factors that effect development of fetus)
i.e smoking, viral infections, folic acid deficiency
(CL) What is the issue during development?
When is the critical period?
maxillary and ansal str do not fuse (wk 5-8 critical period)
What other defect commonly comes along with cleft lift
Cleft palate
Tell me all about cleft palate
including incidence, etiologic, critical period, tx
Incomplete fusion of palatine strs (wk 9-12) (bone str of skull- hard palate) Strong link to smoking in pregnancy ~ 1 in 2000 births Malformed nasal strs? Sx required
What is pyloric stenosis?
Muscle hypertrophy at pylorus (distal end of stomach) leading to constriction
When does pyloric stenosis begin?
2-8 weeks after births
not congenital, but a functional problem
Who more likely to develop pyloric stenosis? incidence?
~1 in 1000 births
4:1 Male to Female
Etiology of pyloric stenosis
Idiopathic
Linked to hypergastrinemia, PGE (local hormone) & erythromycin exposure (medication side effects)
Path leading to MNFTS of Pyloric stenosis
Hypertrophy -> constriction -> inflm -> obstr
Inflm is what causes obstr
MNFTS- Projectile vomiting, dehydration, malnourishment
Dx and Tx of pyloric stenosis
Hx and Px
US ( and palpation to suggest it)
Tx involves Sx
What is gastroesophageal reflux and what is it’s incidence in infants?
Gastric reflux via distal esophageal sphincter r/t incomplete closure
Common GI problem (~50% incidence)
(0-3 months common)
Etiology of gastroesophageal reflux
Neuromuscular - it is a functional problem, not str or congenital
Path and Complications of gastroesophageal reflux
Gastric contents -> esop -> esophagitis?
Growth problems?
how is gastroesophageal reflux treated?
Mostly self limiting (~1yr) (But requires attention)
Symptomatic tx (antacid, PPI, H2RA) Positioning Modify feeding Modify Feed (small thick meals) Fundoplication ? (limited use, fortifying sphincter)
What is Hirschsprung Disease? Incidence?
Disorder sometimes called megacolon often developing in infancy related to inadequate stimulation of peristalsis in colon.
~ 1 in 5000 births
Etiology of Hirschsprung Disease?
•RET gene mutation, CHr 10
Codes for Proteins are involved in cell signaling for formation of tissue
Disorder is r/t neural tissue in the colon (neural innervation of muscle required for peristalsis)
Patho of Hirschsprung Disease
Tx?
Areas of colon lack PS ganglia -> no peristalsis (localized) -> accum of contents -> colon distention -> abdm distention.
Perf possible and peritonitis
What is Intussusception?
Intestine invaginates into adjoining section
Where is Intussusception like to occur?
Mostly at ileocecal valve (r/t smaller vessel pushing into larger diameter vessel)
Incidence of Intussusception
1-4 in 1000 birth
Describe the Patho and potential complications of Intussusception
invagination -> obstr -> inflm -> edema -> ischemia
necrosis, perf and peritonitis possible
Tx of Intussusception
Hydrostatic reduction
Water-soluble contrast medium and air pressure
Some require Sx
