2 Flashcards
What is fluorosis?
Mottled enamel with white patches to brown discoloration and hypoplasia; from high fluoride content of drinking water, swallowed toothpaste, inappropriate fluoride treatment.
What are the causes of delayed eruption of primary teeth?
Hypopituitarism, hypothyroidism, trisomy 21, rickets.
What is the inheritance pattern of cleft lip and palate?
Multifactorial inheritance; also autosomal dominant in families (cleft palate). Highest among Asians, lowest among Africans. Special nipple needed for feeding. Increased risk of otitis media, hearing loss, speech problems.
What is the most common cause of diarrhea in infancy?
Rotavirus
What are the common causes of bloody diarrhea?
Campylobacter, amoeba (E. histolytica) Shigella, E. Coli, salmonella
What are the causes of acute diarrhea in infants?
Gastroenteritis, systemic infection, antibiotics.
What are the causes of chronic diarrhea?
Postinfectious, lactase deficiency, milk or soy intolerance, chronic diarrhea of infancy, celiac disease, cystic fibrosis.
What are the causes of acute diarrhea in children?
Gastroenteritis or food poisoning, systemic infection, postinfectious lactase deficiency, irritable bowel syndrome, celiac disease; lactose intolerance, giardiasis, inflammatory bowel disease.
What are the causes of acute diarrhea in adolescents?
Gastroenteritis, food poisoning, systemic infection, irritable bowel syndrome, inflammatory bowel disease, lactose intolerance, Giardiasis, laxative abuse. Major transmission is fecal, oral or by ingestion of food or water.
What are the bacterial (inflammatory) causes of acute diarrhea?
Campylobacter, Enteroinvasive E. coli, Salmonella, Shigella, Yersinia, Clostridium difficile, E. coli O157:H7.
What are the viral causes of acute diarrhea?
Rotavirus, enteric adenovirus, astrovirus, calicivirus, Norwalk agent.
What are the parasitic causes of acute diarrhea?
Giardia lamblia (most common), E. histolytica, Strongyloides, Balantidium coli, Cryptosporidium parvum, Trichuris trichiura
What is the management of acute diarrhea?
Assess hydration and replace fluid and electrolytes. In severe, bloody diarrhea, determine etiology and provide specific therapy.
What labs are used to evaluate acute diarrhea?
Stool exam for mucus, blood, leukocytes indicate colitis. Stool cultures done if blood, leukocytes, hemolytic uremic syndrome, immunosuppression. C difficile toxin if recent antibiotics. Ovum/parasites. Immunoassays for viruses.
What is the clinical presentation of chronic nonspecific diarrhea?
Weight, height, and nutritional status is normal, and there is no fat in stool. Caused by excessive intake of fruit juice, carbonated fluids, and low fat intake.
What is the laboratory evaluation of chronic diarrhea?
Stool pH, reducing substances, fat, blood, leukocytes, culture, C. difficile toxin, ova, parasites. CBC, differential, ESR, electrolytes, glucose, BUN, cr. Sweat test, 72–hour fecal fat, breath hydrogen. Endoscopy, colonoscopy, biopsy. Gastrin, secretin.
What situations are associated with Enteropathogenic E. coli?
Nurseries, daycare. Supportive care is usually sufficient; in severe cases, neomycin or colistin.
What type of diarrhea is caused by Enterotoxigenic E. coli?
Traveler’s diarrhea. Usually supportive care is sufficient; trimethoprim–sulfamethoxazole in severe cases.
What type of diarrhea is caused by Enterohemorrhagic E. coli?
Hemorrhagic colitis, hemolytic uremic syndrome. Antimicrobial therapy is contraindicated in suspected cases because of increased risk of hemolytic uremic syndrome. Supportive care only.
What are the risk factors for Salmonella gastroenteritis?
Infected animals (cattle, tortoises, snakes) and contaminated eggs, milk, poultry. Treatment indicated only for patients who are less than 3 months of age, toxic, disseminated disease, or S. typhi.
What is the mode of transmission for Shigella?
Person–to–person spread, contaminated food. Treatment is trimethoprim/sulfamethoxazole.
What is the mode of transmission for Campylobacter gastroenteritis?
Person–to–person spread, contaminated food.
What is the treatment of severe Campylobacter gastroenteritis?
Self–limiting; erythromycin speeds recovery and reduces carrier state; recommended for severe disease or with dysentery.
What is the mode of transmission for Yersinia enterocolitica?
Pets, contaminated food. Causes arthritis, rash.
What is the treatment of Yersinia gastroenteritis?
No antibiotic therapy unless severe; aminoglycosides plus a third–generation cephalosporin for infants
What is the risk factor for Clostridium difficile?
History of antibiotic use. Treatment of pseudomembranous colitis is metronidazole or oral vancomycin and discontinuation of other antibiotics.
What is the time of onset of Staphylococcus aureus gastroenteritis?
Food poisoning with onset within 12 h of ingestion. Supportive care. Antibiotics are usually not indicated.
What are the signs of Entamoeba histolytica infection?
Acute bloody diarrhea. Treatment is metronidazole.
What are signs of Giardia infection?
Anorexia, nausea, abdominal distension, watery diarrhea, weight loss. Cysts ingested from contact with infected individual or from contaminated food or water.
What is the treatment of giardiasis?
Metronidazole, furazolidone.
What is the presentation of Cryptosporidium diarrhea?
Mild diarrhea in immunocompromised infants; severe diarrhea in AIDS patients.
What is the treatment of Cryptosporidium diarrhea in AIDS patients?
Raising the CD4 count to normal is the best treatment. Rifabutin may be effective.
What is the initial laboratory evaluation for fat malabsorption?
Sudan red stain for fat. Confirm with 72–h fat. Steatorrhea is most common with pancreatic insufficiency. Sweat chloride. Serum trypsinogen is useful screen for cystic fibrosis. Screen for CHO malabsorption by measuring reducing substances (Clinitest).
What is the hydrogen breath test?
Breath hydrogen test after a known CHO load, the collected breath hydrogen is analyzed, and malabsorption of the specific CHO is identified. Screen: stool alpha1antitrypsin is a screening test for intestinal protein leakage.
What is the differential diagnosis of fat malabsorption?
Giardiasis is the only infection causing chronic malabsorption. HIV or T– or B–cell defects. Small–bowel disease: gluten enteropathy, abetalipoproteinemia. Pancreatic insufficiency: fat malabsorption (cystic fibrosis).
What foods cause celiac disease?
Gluten, rye, wheat, barley. Celiac disease appears at 6 months to 2 years of age, and gluten intolerance is permanent.
What is the clinical presentation of celiac disease?
Diarrhea, failure to thrive, growth retardation, vomiting. Anorexia, ataxia.
What is the presentation of Shwachman–Diamond syndrome?
Pancreatic insufficiency, neutropenia, fat malabsorption.
What is intestinal lymphangiectasia?
Leakage of lymph fluid into bowel lumen, steatorrhea, protein–losing enteropathy.
What is the presentation of disaccharidase deficiency?
Osmotic diarrhea, acidic stools.
What is the presentation of abetalipoproteinemia?
Severe fat malabsorption from birth, acanthocytes, absent plasma cholesterol, triglycerides.
What laboratory tests are diagnostic of celiac sprue?
Antiendomysial and antigliadin antibodies; histologic confirmation is mandatory.
What is the treatment of celiac sprue?
Strict gluten–free diet. Rye, wheat, barley.
What is tracheoesophageal fistula (TEF)?
Most common anatomy is upper esophagus ends in blind pouch and TEF is connected to distal esophagus. H–type is diagnosed later in life with chronic respiratory problems. Half with associated anomalies, such as the VACTERL.
What is the clinical presentation of tracheoesophageal fistula in the neonate?
Frothing, bubbling, cough, cyanosis, respiratory distress with feedings; immediate regurgitation and aspiration with first feed.
How is tracheoesophageal fistula diagnosed?
Inability to pass nasogastric or orogastric tube. X–ray shows tube coiled and an air–distended stomach. Esophagram with contrast media (or bronchoscopy or endoscopy with methylene blue).
What is the VACTERL association?
Nonrandom association of birth defects: Vertebral anomalies. Anal atresia. Cardiac defect. Tracheoesophageal fistula. Renal anomalies. Limb abnormalities.
4–month–old with apnea for 20 min after feeds. Spitting up since birth. Fifth percentile for weight. What is the diagnosis?
Gastroesophageal reflux disease.
What is gastroesophageal reflux disease?
Insufficient lower esophageal sphincter tone. Symptoms during first few months of life; resolves by 12–24 months of age; chronic in older children.
What is the clinical presentation of gastroesophageal reflux disease in infants?
Postprandial regurgitation. Arching, irritability, feeding aversion, failure to thrive. Obstructive apnea, stridor, cough, wheezing.
How is gastroesophageal reflux disease diagnosed in children?
Esophageal pH monitoring is best test. Endoscopy shows erosive esophagitis. Radionucleotide scintigraphy (Tc) to document aspiration.
What is the treatment of gastroesophageal reflux disease?
Normalize feeding technique, appropriate volume, thicken feeds, upright positioning. H2 antagonist (ranitidine, cimetidine) have best safety. Proton pump inhibitors (omeprazole, lansoprazole, pantoprazole). Fundoplication.
What is the differential diagnosis of gastroesophageal reflux disease?
Milk or food allergy, pyloric stenosis, intestinal obstruction, infection, tracheoesophageal fistula, inborn errors of metabolism, increased intracranial pressure.
What is the role of prokinetic agents in the treatment of GERD in children?
Prokinetic agents (metoclopramide, bethanechol, erythromycin) have no efficacy in the treatment of GERD in children.
3–week–old boy with nonbilious projectile vomiting. Small, olive–sized mass in the abdomen. What is the diagnosis?
Pyloric stenosis.
What is the clinical presentation of pyloric stenosis?
Nonbilious, projectile vomiting. More common in Northern European ancestry, first–born males; associated with tracheoesophageal fistula. Infant has an insatiable hunger and desires to feed. Presents 1 wk to 5 mths.
What is the presentation of pyloric stenosis?
Mild–to–moderate dehydration, hypochloremic, hypokalemic metabolic alkalosis. Firm, movable, 2–cm, olive–shaped, hard mass in midepigastrium.
How is pyloric stenosis diagnosed?
Best test is ultrasound (target–like appearance).
What is the treatment of pyloric stenosis?
Rehydration, correction of electrolyte abnormalities. Pylorotomy.
What is the presentation of duodenal atresia?
Newborn with bilious vomiting with every feed. Double bubble on abdominal film.
What disorders are associated with duodenal atresia?
Half are born premature, down syndrome. Other anomalies include malrotation, esophageal atresia, congenital heart defects, anorectal malformation, renal anomalies
What is the clinical presentation of duodenal atresia?
Bilious vomiting (obstruction distal to ampulla) without abdominal distention on the first day of life. Prenatal polyhydramnios. Jaundice.
How is duodenal atresia diagnosed?
X–ray shows double bubble with no distal bowel gas. X–ray spine for anomalies; ultrasound for other anomalies.
What is the treatment of duodenal atresia?
Nasogastric decompression, intravenous fluids, duodenoduodenostomy
What is malrotation?
Incomplete rotation of intestine during fetal development. Superior mesenteric artery acts as axis for rotation. Ladd bands may extend from cecum to right upper quadrant to produce duodenal obstruction.
What is the clinical presentation of malrotation?
Acute or chronic obstruction in the first year of life. Bilious emesis, recurrent abdominal pain with vomiting.
How is malrotation of the bowel diagnosed?
Barium enema shows malposition of cecum. Upper gastrointestinal series will show malposition of ligament of Treitz. Ultrasound shows inversion; duodenal obstruction with thickened bowel loops to right of spine.
What is the presentation of jejunal or ileal atresia?
Presents on the first day of life with bile–stained emesis with abdominal distention. (duodenal atresia does not cause abdominal distention.) Plain films show air–fluid levels.
What complication can result if treatment of volvulus is delayed?
Short bowel syndrome.
2–year–old boy with painless rectal bleeding. What is the diagnosis?
Meckel diverticulum.
What is Meckel diverticulum?
Remnant of embryonic yolk sac; lining of the diverticulum is similar to stomach. Most frequent congenital gastrointestinal anomaly.
What is the clinical presentation of Meckel diverticulum?
Acid–secreting mucosa in diverticulum causes intermittent painless rectal bleeding and anemia. Blood loss self–limited. Bowel obstruction (lead point for intussusception) or diverticulitis. May be mistaken for appendicitis.
How is Meckel diverticulum diagnosed?
Meckel radionuclide scan (Tc–99m pertechnetate). Treatment is excision.
12–month–old child with cramping, colicky abdominal pain for 12 hours. Vomiting, fever. Bloody stool with mucus; tender abdomen. Leukocytosis. What is the diagnosis?
Intussusception
What is intussusception?
Telescoping bowel; ileal–colic. Presents at 3 mths to 6 yrs following an adenovirus or rotavirus infection, URI, otitis media. Associated HSP. Occur with a leading point (Meckel, polyp, neurofibroma, hemangioma, malignancy).
What is the clinical presentation of intussusception?
Sudden, severe, paroxysmal, colicky abdominal pain; straining with legs flexed. Lethargy, shock, fever. Vomiting, decreased stooling; bloody stool. Mucosal necrosis causes black currant jelly stool. Tender sausage mass RUQ.
How is intussusception diagnosed?
Plain film may show a density; free air indicates perforation; contrast shows coiled–spring sign. Air enema is diagnostic and curative. Ultrasound also sensitive.
17–year–old girl with chronic, cramping abdominal pain, chronic diarrhea. Occasional blood in stools. Fever, wrist pain. Anemia, elevated sedimentation rate. What is the diagnosis?
Inflammatory bowel disease.
What is the clinical presentation of Crohn disease?
Fever, arthritis, weight loss, malaise, growth retardation; abdominal pain; bloody diarrhea. Perianal disease (abscesses and fistulas). Can occur anywhere in gastrointestinal tract. More extraintestinal manifestations than UC.
What are the diagnostic findings in Crohn disease?
ESR. Abdominal films show partial small bowel obstruction. String sign on upper GI (narrowed tract). Skip lesions are normal areas between affected areas. Cobblestoning of mucosa. Fistulas on contrast studies. Colonoscopy and biopsy.
What is the treatment for Crohn disease?
Steroids, aminosalicylates. Azathioprine and metronidazole for fistulas. Immune suppression (anti–TNF agents including infliximab), antibiotics, hyperalimentation, surgical resection.
What are the complications of Crohn disease?
Remissions and exacerbations. Gastrointestinal obstruction. Malabsorption, anemia, weight loss, and growth failure.
What is the clinical presentation of ulcerative colitis?
Only the colon. Bloody diarrhea with mucus, abdominal pain, tenesmus. Fever, anemia, hypoalbuminemia. Leukocytosis, tachycardia. Diagnosis of exclusion. Symptoms present for at least 3–4 weeks. Endoscopy with biopsy.
What is the treatment for ulcerative colitis?
Aminosalicylates, sulfasalazine, steroids (oral or enemas), anti–TNF agents (infliximab), total colectomy for failure of medical treatment is curative.
What are the complications of ulcerative colitis?
Higher risk of colon cancer; toxic megacolon with perforation.
What is the treatment of functional constipation?
Relief of impaction with enemas, then stool softeners (mineral oil, lactulose, polyethylene glycol; no stimulant medications).
What is Hirschsprung disease?
Absent ganglion cells in colon wall beginning at internal anal sphincter and extending proximally. Most common cause of bowel obstruction in neonates. Symptoms at birth. Suspected in full–term infant with a delayed meconium (>48 h).
How is Hirschsprung disease diagnosed?
Rectal manometry, then rectal suction biopsy.
What is the treatment for Hirschsprung disease?
Temporary colostomy and definitive correction at 6–12 months.
What is the epidemiology of pediatric urinary tract infection?
Boys have UTI most often in first yr. UTI is more common in boys than in girls until after second yr; girls have first UTI by 5 (peak in infancy and toilet–training). Colonic bacteria (mostly E. coli, then Klebsiella, Proteus; some S. saprophyticus).
What are the signs of cystitis?
Dysuria, urgency, frequency, suprapubic pain, incontinence; no fever.
What are the signs of pyelonephritis?
Abdominal or flank pain, fever, malaise, nausea, vomiting, diarrhea; nonspecific in infants.
What are the risk factors for pyelonephritis?
In females causes include wiping, sexual activity, pregnancy. Males: uncircumcised. Males and females: Vesicoureteral reflux, toilet–training, constipation, anatomic abnormalities.
How is pyelonephritis diagnosed?
Urine culture. If toilet–trained, obtain a midstream collection; otherwise, supra–pubic tap or catheterization. Culture is positive if >100,000 colonies/mL (single pathogen) or if symptomatic with >10,000 colonies/mL.
What is the treatment for pediatric pyelonephritis?
Intravenous antibiotic treatment and total of 14 days of oral antibiotics. Start with intravenous ceftriaxone or ampicillin plus gentamicin.
What is the follow–up evaluation after a pediatric urinary tract infection?
Urine culture 1 week after stopping antibiotics to confirm sterility; periodic reassessment for next 1–2 years. Obtain ultrasound with febrile UTI for anatomy, abscess, hydronephrosis.
What are the indications for a voiding cystourethrogram (VCUG) in children who have had a urinary tract infection?
All males, all females 5 years old with second UTI.
What is vesicoureteral reflux?
Backflow of urine bladder to kidney. Submucosal tunnel between mucosa and detrusor is short. Pyelonephritis, scarring nephropathy may cause HTN, proteinuria, renal insufficiency end–stage renal disease, impaired renal growth.
How is vesicoureteral reflux diagnosed?
VCUG for diagnosis and grading. Grade I or II resolves. Grade III–IV resolves by age 6–7 years; grade V rarely resolves.
What is the treatment for vesicoureteral reflux?
Continuous prophylaxis with sulfamethoxazole/trimethoprim, trimethoprim alone, or nitrofurantoin in 1/4 to 1/3 dose.
What is the clinical presentation of obstructive uropathy?
Hydronephrosis, upper abdominal or flank pain. Pyelonephritis, UTI. Weak urinary stream.
What are the most common causes of an abdominal mass in a newborn?
Palpable abdominal mass in a newborn is most commonly caused by hydronephrosis or polycystic kidney disease.
What is the presentation of obstructive uropathy?
Walnut–shaped mass (bladder) above pubic symphysis. Caused by posterior urethral valves. Infection, sepsis. Obtain VCUG in congenital hydronephrosis and ureteral dilatation to detect posterior valves. CT for suspected ureteral calculi.
What are the causes of obstructive uropathy?
Ureteropelvic junction obstruction most common. Ureterocele is cystic dilatation with obstruction from a pinpoint ureteral orifice is the most common cause of severe obstructive uropathy, mostly boys. Ectopic ureter may cause obstruction.
What is the presentation of uterocele?
End–stage renal disease; male with a palpable, distended bladder and weak urinary stream.
How is obstructive uropathy diagnosed?
Voiding cystourethrogram.
What is the treatment for obstructive uropathy?
Decompress the bladder with a catheter. Antibiotics. Transurethral ablation or vesicostomy.
7–year–old boy with Coca–Cola–colored urine, edema, blood pressure of 185/100 mm Hg, sore throat 2 weeks before. What is the diagnosis?
Acute poststreptococcal glomerulonephritis.
What is poststreptococcal glomerulonephritis?
Follows infection with group A beta–hemolytic strep of throat or skin. Diffuse mesangial cell proliferation with an increase in mesangial matrix; lumpy–bumpy deposits of immunoglobulin, complement on glomerular basement membrane.
What is the clinical presentation of post streptococcal glomerulonephritis?
Patients are 5–12 years old (typical age for strep throat). Occurs 1–2 weeks after strep pharyngitis or 3–6 weeks after impetigo. Asymptomatic microscopic hematuria to acute renal failure.
What is the triad of post streptococcal glomerulonephritis?
Edema, hypertension, hematuria (classic triad). There is also malaise, lethargy, fever, abdominal or flank pain
How is post streptococcal glomerulonephritis diagnosed?
Urinalysis shows RBCs, RBC casts, protein, polymorphonuclear cells. Positive throat culture or increasing antibody titer to streptococcal antigens; best test is the anti–DNase antigen (streptozyme test).
What is the treatment for post–streptococcal glomerulonephritis?
Antibiotics for 10 days (penicillin). Sodium restriction, diuresis. Control hypertension with calcium channel blocker, vasodilator, or angiotensin converting enzyme inhibitor. Complete recovery in 95%.
What is IgA nephropathy (Berger disease)?
Gross hematuria in association with upper respiratory infection or gastrointestinal infection. Mild proteinuria, hypertension, normal C3. Most common chronic glomerular disease. Treatment is blood pressure control.
8–year–old with deafness. Family history of renal disease in male relatives. Microscopic hematuria. What is the diagnosis?
Alport Syndrome.
What is Alport syndrome?
Hereditary nephritis (X–linked dominant); renal biopsy foam cells. Hematuria 1–2 days after upper respiratory infection. Hearing deficits (bilateral sensorineural, never congenital); females have subclinical hearing loss. Extrusion of lens.
What is benign familial hematuria?
Autosomal dominant mutation in type IV collagen. Diffuse thinning of glomerular basement membrane. Prognosis is excellent without treatment.
What is the most common cause of nephrotic syndrome in adults?
Membranous glomerulopathy.
What is the most common cause of chronic glomerulonephritis in older children and young adults?
Membranoproliferative glomerulonephritis.
What is Henoch–Schönlein Purpura?
Small vessel vasculitis, which presents with purpuric rash, joint pain, abdominal pain. Resolves spontaneously. Treatment is nonsteroidal antiinflammatory medications, steroids.
What is hemolytic uremic syndrome?
Most common cause of ARF in children. Microangiopathic hemolytic anemia, thrombocytopenia, uremia; caused by E. coli 0157:H7 (shiga toxin). Undercooked meat, unpasteurized milk; spinach. Also Shigella, Salmonella, Campylobacter, viruses.
What is the pathophysiology of hemolytic uremic syndrome?
Subendothelial and mesangial deposits cause vascular occlusion, glomerular sclerosis, cortical necrosis. Capillary and arteriolar endothelial injury, localized clotting; prothrombotic state.
What is the clinical presentation of hemolytic uremic syndrome?
Child less than 4 years old with bloody diarrhea. 5–10 days after infection. There is sudden pallor, irritability, weakness, oliguria; mild renal insufficiency to acute renal failure.
What are the laboratory findings in hemolytic uremic syndrome?
Hemoglobin 5–9 mg/dL, helmet cells, burr cells, fragmented cells, moderate reticulocytosis; Coombs negative, low–grade, microscopic hematuria and proteinuria.
What is the treatment for hemolytic uremic syndrome?
Treat hypertension; dialysis. No antibiotics. Plasmapheresis or fresh frozen plasma.
What is autosomal–recessive type (infantile) polycystic kidney disease?
Enlarged kidneys with many cysts. Interstitial fibrosis and tubular atrophy causes renal failure. Liver disease with bile duct proliferation; hepatic fibrosis.
What is the clinical presentation of autosomal recessive polycystic kidney disease?
Bilateral flank masses in neonate or early infancy. Potter sequence may occur. Hypertension, oliguria, acute renal failure, liver disease in newborn period.
How is autosomal recessive polycystic kidney disease diagnosed?
Bilateral flank masses in infant with pulmonary hypoplasia. Oliguria and hypertension in newborn. Ultrasound is diagnostic.
What is the prognosis for autosomal recessive polycystic kidney disease?
80% 10–year survival, end–stage renal failure. Treatment is dialysis and transplant.
What is autosomal–dominant (adult) polycystic kidney disease?
Most common hereditary kidney disease. Both kidneys enlarged with cysts in fourth to fifth decade; ultrasound shows bilateral macrocysts in liver, pancreas, spleen, ovaries; intracranial (Berry) aneurysms; mitral valve prolapse.
How is autosomal–dominant polycystic kidney disease diagnosed?
Enlarged kidneys with bilateral macrocysts on ultrasound with affected first–degree relative.
What is the treatment for autosomal–dominant polycystic kidney disease?
Control of blood pressure.
What conditions are associated with transient proteinuria?
Fever, exercise, dehydration, cold exposure, congestive heart failure, seizures, stress. Orthostatic proteinuria is the most common persistent proteinuria in school–aged children.
What conditions are associated with fixed proteinuria?
Glomerular or tubular disorders; suspect a glomerular disorder in any patient with proteinuria of more than 1 g/24 hours or with proteinuria and hypertension, hematuria, or renal dysfunction.
5–year–old with periorbital edema, proteinuria, hyperlipidemia, hypoalbuminuria. What is the diagnosis?
Nephrotic syndrome.
