Peds GI.txt

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Peds GI.txt
2013-10-06 15:02:36
Peds GI

Peds GI
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  1. Leading cause of diarrhea
  2. Clinical manifestations of Rotavirus
    vomiting followed by onset of watery stools, fever; mild to severe symptoms
  3. Clinical manifestations of salmonella
    N/V, colicky ADB pain, bloody diarrhea, fever, mild to severe symptoms, headache, drowsiness, confusion, seizures
  4. Most serious complications of diarrhea
    dehydration, acidosis and shock due to severe dehydration
  5. What foods should be avoided with diarrhea
    no rectal temps, no fruit juices, no caffeine or carbonated drinks, no brat diet
  6. Patho of Hirschsprung
    absence of ganglion cells in the affected areas of the intestine resulting in a loss of rectosphincteric reflex and abnormal microenvironment of the cells of the affected intestine
  7. What does Hirsch look like
  8. Signs of Hirsch in newborn
    feeding intolerance with bilious vomiting, distended ABD, delay in passage of meconium
  9. Signs of Hirsch in infancy
    growth failure, constipation, ABD distention, diarrhea and vomiting, fever, explosive watery diarrhea
  10. Signs of Hirsch in childhood
    constipation, ribbonlike foul smelling stools, ABD distention, visible peristalisis, easily palpable fecal mass, undernourished and anemic appearance
  11. Therapeutic mgmt. of Hirsch
    surgery after pt has stabilized; pull through procedure
  12. Chronic problems of Hirsch
    constipation and fecal incontinence
  13. Nursing considerations in Hirsch
    help parents adjust to congenital defect in child, foster bonding, prepare for surgery, assist in colostomy care
  14. Most serious complication of Hirsch
  15. What to monitor for in preop Hirsh
    signs of shock, vitals, fluid and electrolyte replacements, fever, ABD distention, vomiting, cyanosis, dyspnea; measure ABD circumference at umbilicus or widest part of ABD
  16. Colostomy is
  17. Patho of GER
    inappropriate relaxation of lower esophageal sphincter; factors that increase ABD pressure (coughing, sneezing, scoliosis and overeating)
  18. How to diagnosis GER
    24 hour intraesophageal pH monitoring, upper GI series helps show anatomic abnormalities, endoscopy with biopsy
  19. Clinical manifestations of GER
    vomiting (may be forceful), excessive crying, irritability, respiratory problems, weight loss; in children-heartburn, ABD pain, chest pain, cough, dysphagia, nocturnal asthma, recurrent pneumonia
  20. Complications of GER
    esophagitis, esophageal stricture, laryngitis, recurrent pneumonia, anemia, barrett esophagus
  21. Mgmt of GER
    avoid certain foods, lifestyle modifications (wt control, smaller more frequent meals), feedings in infants (thickened feedings is 1tsp to 1T of rice cereal per ounce of formula, upright positioning)
  22. Nursing care of GER
    identifying children with symptoms, educating parents, caring for child with surgical interventions
  23. Meckel definition
    a fibrous band connecting the small intestine to the umbilicus; most common congenital malformation of GI tract; often exists without symptoms
  24. Meckel patho
    bleeding, obstruction or inflammation; gastric mucosa
  25. Diagnosis of Meckel
    history, physical exam and radiographic studies; meckel scan used most often, but less reliable in the presence of bleeding
  26. Clinical manifestations of Meckel
    painless rectal bleeding, ADB pain or signs of obstruction, currant jelly stools, sometimes severe anemia, shock, hypotension, caused by peptic ulceration/perforation
  27. Mgmt of Meckel
    surgical removal of diverticulum, might need blood replacement, IV fluids, O2 if severe hemorrhage
  28. Nursing care of Meckel
    frequent monitoring of vitals including BP, bed rest, recording the amount of blood in stools
  29. Post op Meckel
    IV fluids and NG tube for decompression and evacuation of gastric secretions, onset of illness is usually sudden
  30. Peptic Ulcer disease etiology
    increased familial incidence and in type O people; h pylori weakens gastric mucosal barrier and allows acid to damage mucosa; acquired by fecal oral route
  31. DX of peptic ulcer
    epigastric pain, nocturnal pain, oral regurg, heartburn, weight loss, hematemesis and melena; may have causative substances like NSAIDS, corticosteroids, alcohol and tobacco; labs of CBC, stool analysis, LFTs, lactose breath test, upper GI
  32. Therapeutic mgmt. of Peptic ulcer
    relieve discomfort, promote healing, prevent complications, prevent recurrence
  33. Meds for peptic ulcer
    antacids, h2 receptors (zantac, Pepcid), PPI (omeprazole), mucosal protective (sucralfate and bismuth)
  34. What med is used to prevent fever in pts with peptic ulcer disease
    acetaminophen (NOT NSAIDS or aspirin)
  35. Critically ill kids should receive
    H2 blockers to prevent stress ulcers
  36. Cleft lip
    failure of maxillary and median nasal processes to fuse; defect in cell migration
  37. Cleft palate
    midline fissure of the palate that results from failure of the two palatal processes to fuse
  38. Cause of CP and CL
    genetic and environmental (alcohol, smoking, anticonvulsants, steroids and retanoids) and folate deficiency
  39. Feeding effect of CP
    unable to create suction
  40. Cleft lip repair usually occurs
    2-3 months of age; rule of “10s”-10 pounds, 10 wks old, HgB 10
  41. Cleft palate usually occurs
    6-12 months
  42. Feeding with cleft lip
    ok to breastfeed as boob conforms to cleft lip, bottle with wide base of nipple; feed kid upright
  43. Post op care
    protect operative site, may need to apply petroleum jelly; avoid objects in the mouth
  44. Nursing dx for cleft lip
    altered nutrition, pain, altered parenting, risk for trauma
  45. Hyper Pyloric stenosis
    causes projectile nonbilious vomiting, dehydration, metabolic acidosis and growth failure, genetic predisposition
  46. Hyper PS
    occurs when the circumferential muscle of the pyloric spincter becomes thickened resulting in elongation and narrowing of the pyloric channel; produces obstruction and compensatory dilation, hypertrophy and hyperperistalsis of the stomach
  47. Hypertrophied pylorus may be palpable as an
    olivelike mass in upper ABD; not congenital
  48. DX of Hyper PS
    vomiting 30-60 minutes after feeding and becomes projectile as obstruction progresses, nonbilious consisting of stale milk; may become dehydrated and appear malnourished if early DX is not established; chronicly hungry, distended ABD; peristalsis waves move left to right
  49. If stomach decompression is used
    nurse makes sure it’s patent
  50. Celiac characteristics
    fatty, foul, frothy and bulky stools; general malnutrition; ABD distention and vitamin deficiencies
  51. Rehydration
    75-90 nEq/L of Na; 40-50 ml/kg over 4 hours; don’t exceed 150 ml/kg/day; 5-10 ml every 2-3 minutes