GIT Flashcards

1
Q
  1. What is intestinal duplication and how does it present?
A

Duplication: Cystic/communicating GI segments
- Presents with mass, pain, bleeding or obstruction

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2
Q
  1. What are congenital anomalies of the GI tract in neonates?
A

Anomalies: Duodenal atresia, annular pancreas, malrotation, omphalocele, gastroschisis
- Often present with bilious vomiting

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3
Q
  1. What are the common causes of constipation in children?
A

Causes: Functional constipation, low-fiber diet, inadequate fluid intake, withholding behavior, hypothyroidism, Hirschsprung disease

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4
Q
  1. What are the red flags in a child presenting with constipation?
A

Red flags: Delayed meconium (>48h), poor growth, abdominal distension, severe pain, neurologic signs, anal abnormalities

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5
Q
  1. What is Hirschsprung disease and how does it present?
A

Hirschsprung: Absence of enteric ganglia → failure to pass meconium, chronic constipation, abdominal distension

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6
Q
  1. How is Hirschsprung disease diagnosed?
A

Diagnosis: Contrast enema, anorectal manometry, confirm with rectal suction biopsy (no ganglion cells)

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7
Q
  1. What is the treatment of Hirschsprung disease?
A

Treatment: Surgical resection of aganglionic segment (pull-through procedure)

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8
Q
  1. What are the features of pediatric pseudo-obstruction syndromes?
A

Features: Recurrent vomiting, bloating, feeding intolerance, failure to thrive
- Diagnosis: Manometry, imaging
- Often genetic or neuromuscular

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9
Q
  1. What are the complications of short bowel syndrome?
A

Complications: Malnutrition, dehydration, electrolyte imbalance, liver disease from TPN, bacterial overgrowth

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10
Q
  1. What are the features and diagnosis of celiac disease?
A

Features: Chronic diarrhea, failure to thrive, abdominal distension, irritability
- Diagnosis: Anti-tTG IgA, total IgA, confirm with duodenal biopsy

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11
Q
  1. What are the extraintestinal manifestations of celiac disease?
A

Manifestations: Iron-deficiency anemia, delayed puberty, dermatitis herpetiformis, short stature, dental enamel defects

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12
Q
  1. What is the treatment of celiac disease?
A

Treatment: Lifelong gluten-free diet (no wheat, barley, rye)

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13
Q
  1. What are the nutritional deficiencies seen in celiac disease?
A

Deficiencies: Iron, folate, calcium, vitamin D, vitamin A, zinc, B12 (if extensive)

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14
Q
  1. What are the causes and types of protein-losing enteropathy?
A

Causes: Intestinal lymphangiectasia, IBD, infections, cardiac failure
- Types: Mucosal, lymphatic, inflammatory

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15
Q
  1. What is short bowel syndrome and its common causes?
A

Short bowel syndrome: Malabsorption due to significant resection of small intestine
- Causes: NEC, volvulus, atresia, gastroschisis

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16
Q
  1. What are the causes of malabsorption in children?
A

Causes: Celiac disease, CF, short bowel syndrome, lactose intolerance, giardiasis, cow’s milk protein allergy

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17
Q
  1. What are the causes of chronic bloody diarrhea in children?
A

Causes: IBD (UC, Crohn), infections (Amoeba, Shigella), polyps, food protein-induced colitis

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18
Q
  1. How is short bowel syndrome managed in children?
A

Management: Parenteral nutrition initially, enteral feeding advancement, micronutrient support, intestinal rehabilitation

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19
Q
  1. What is the definition and evaluation of chronic diarrhea in children?
A

Chronic diarrhea: >2 weeks duration
- Evaluation: History, stool studies, growth, labs (CBC, ESR, IgA, tissue transglutaminase), imaging if needed

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20
Q
  1. What are the causes of acute diarrhea in children?
A

Causes: Viral (rotavirus, norovirus), bacterial (Shigella, Salmonella, Campylobacter, E. coli), parasites (Giardia, Entamoeba)

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21
Q
  1. When are antibiotics indicated in pediatric acute diarrhea?
A

Indications: Dysentery, suspected cholera, immunocompromised, prolonged fever or systemic toxicity

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22
Q
  1. What is the presentation of galactosemia and how is it diagnosed?
A

Presentation: Jaundice, vomiting, hepatomegaly, hypoglycemia, sepsis (E. coli)
- Diagnosis: Non-glucose reducing substances in urine, GALT enzyme assay

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23
Q
  1. What are the causes of chronic non-bloody diarrhea?
A

Causes: Toddler’s diarrhea, lactose intolerance, IBS, post-infectious, excessive fruit juice, CF

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24
Q
  1. What is the management of acute diarrhea with some dehydration?
A

Management: ORS 75 mEq/L Na+ per WHO plan B
- 75 mL/kg over 4 hours, continue feeding and breastfeeding

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25
Q
  1. What are the red flag signs in a child with chronic abdominal pain?
A

Red flags: Weight loss, nocturnal pain, GI bleeding, delayed puberty, persistent vomiting, fever, family history of IBD

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26
Q
  1. What are the common functional gastrointestinal disorders in children?
A

Functional disorders: Functional abdominal pain, IBS, functional constipation, functional dyspepsia, abdominal migraine

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27
Q
  1. What is irritable bowel syndrome (IBS) and how does it present in children?
A

IBS: Recurrent abdominal pain with change in stool frequency/form and relief with defecation

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28
Q
  1. How is functional abdominal pain diagnosed and managed?
A

Diagnosis: Rome IV criteria
- Management: Reassurance, dietary fiber, gut-directed CBT, antispasmodics if needed

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29
Q
  1. What are common pediatric feeding disorders and their causes?
A

Feeding disorders: Oral aversion, food refusal, sensory issues
- Causes: Prematurity, GERD, developmental delay

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30
Q
  1. How is functional constipation diagnosed in children?
A

Diagnosis: Based on Rome IV criteria and absence of red flags
- Most cases are functional

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31
Q
  1. What is the Rome IV criteria for functional constipation?
A

Rome IV: 2+ features for ≥1 month: <2 stools/week, fecal incontinence, retentive posturing, hard stools, large stools, stool impaction

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32
Q
  1. What is the initial management of functional constipation?
A

Initial: Education, dietary fiber, oral laxatives (PEG), stool softeners, toilet training

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33
Q
  1. What is the management of variceal bleeding in pediatric portal hypertension?
A

Management: Resuscitation, endoscopy for band ligation or sclerotherapy, octreotide, beta-blockers for prophylaxis

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34
Q
  1. What are the causes of rectal bleeding in children?
A

Causes: Anal fissure (most common), polyps, infections, IBD, Meckel’s diverticulum, intussusception

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35
Q
  1. What is Meckel’s diverticulum and how does it present in children?
A

Meckel’s: Remnant of vitelline duct
- Painless rectal bleeding, intussusception, obstruction, mimics appendicitis

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36
Q
  1. How is Meckel’s diverticulum diagnosed?
A

Diagnosis: Technetium-99m pertechnetate scan (Meckel’s scan)

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37
Q
  1. What are the common causes of lower GI bleeding in infants vs older children?
A

Infants: Anal fissure, cow’s milk protein allergy, polyps
- Older: IBD, infection, juvenile polyps, Meckel’s

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38
Q
  1. What are the causes of upper GI bleeding in children?
A

Upper GI bleed: Esophagitis, gastritis, peptic ulcer, varices, Mallory-Weiss tear, foreign body, coagulopathy

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39
Q
  1. What is hereditary fructose intolerance and its clinical features?
A

Features: Vomiting, hypoglycemia, hepatomegaly after fructose intake
- Avoid fructose, sucrose, sorbitol

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40
Q
  1. How is GSD diagnosed in children?
A

Diagnosis: Clinical features, glucose response to fasting, enzyme assay, genetic testing, liver biopsy if needed

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41
Q
  1. How is SBP treated in children?
A

Treatment: IV cefotaxime or ceftriaxone
- Albumin may be added to prevent renal dysfunction

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42
Q
  1. What is spontaneous bacterial peritonitis (SBP) and how is it diagnosed?
A

SBP: Infection of ascitic fluid without secondary source
- Diagnosed when PMNs >250/mm³ or positive culture

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43
Q
  1. What is eosinophilic esophagitis (EoE) and how does it present in children?
A

EoE: Chronic immune-mediated esophageal inflammation
- Symptoms: Dysphagia, food impaction, GERD-like symptoms, feeding difficulties

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44
Q
  1. What is the approach to evaluating a child with FTT?
A

Approach: Detailed history, growth chart review, diet assessment, labs (CBC, ESR, LFTs), stool studies, screen for celiac/CF

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45
Q
  1. What are the gastrointestinal causes of FTT?
A

GI causes: GERD, celiac, CF, food allergies, IBD, short bowel, pyloric stenosis

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46
Q
  1. What are the features of Alagille syndrome?
A

Alagille: Genetic syndrome (JAG1/NOTCH2 mutation)
- Cholestasis, butterfly vertebrae, posterior embryotoxon, cardiac defects, facial features

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47
Q
  1. How is eosinophilic esophagitis diagnosed?
A

Diagnosis: Endoscopy with esophageal biopsy showing >15 eosinophils/HPF, after excluding other causes

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48
Q
  1. What are the common causes of hepatomegaly in children?
A

Causes: Infections (CMV, EBV), storage diseases, malignancy, CHF, hemolysis, hepatitis

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49
Q
  1. What are the causes and diagnosis of Helicobacter pylori infection in pediatrics?
A

H. pylori: Diagnosed via endoscopic biopsy (gold standard), or urea breath test/stool antigen
- Test-and-treat only in symptomatic cases with confirmed diagnosis

50
Q
  1. What is distal intestinal obstruction syndrome (DIOS) in cystic fibrosis?
A

DIOS: CF complication with thick intestinal secretions → RLQ pain, obstruction
- X-ray: Fecal loading
- Treat with hydration, laxatives

51
Q
  1. What is the treatment for eosinophilic esophagitis in pediatrics?
A

Treatment: Dietary elimination (6-food), topical steroids (swallowed fluticasone/budesonide), PPI trial

52
Q
  1. What is the definition and causes of failure to thrive (FTT)?
A

FTT: Weight <3rd percentile or crossing 2 major percentile lines
- Causes: Inadequate intake, malabsorption, chronic illness

53
Q
  1. What are the indications for upper endoscopy in pediatric patients?
A

Indications: Persistent upper GI symptoms, unexplained anemia, bleeding, suspected celiac/IBD, biopsy for H. pylori

54
Q
  1. What are the clinical features of intussusception in children?
A

Features: Colicky abdominal pain, vomiting, red currant jelly stools, sausage-shaped mass, lethargy

55
Q
  1. What are the features of GSD type III (Cori disease)?
A

GSD III: Hepatomegaly, mild hypoglycemia, elevated CK, cardiomyopathy, muscle involvement

56
Q
  1. What is food protein-induced enterocolitis syndrome (FPIES)?
A

FPIES: Non-IgE food allergy causing profuse vomiting, diarrhea, lethargy
- Triggers: Milk, soy, rice
- Managed by avoidance, supportive care

57
Q
  1. What is pyloric stenosis and how does it present?
A

Pyloric stenosis: Hypertrophy of pyloric muscle → non-bilious projectile vomiting at 2–8 weeks of age, hungry after feeds, weight loss

58
Q
  1. What are the diagnostic features of pyloric stenosis on ultrasound?
A

Ultrasound: Muscle thickness >3 mm, pyloric length >14–16 mm, target sign

59
Q
  1. What is the electrolyte abnormality seen in pyloric stenosis?
A

Electrolytes: Hypochloremic, hypokalemic metabolic alkalosis

60
Q
  1. What is the management of pyloric stenosis?
A

Management: Correct dehydration/electrolytes → pyloromyotomy (Ramstedt procedure)

61
Q
  1. How is dehydration assessed clinically in pediatric patients?
A

Assessment: Based on weight loss, general appearance, skin turgor, mucous membranes, sunken eyes/fontanelle, capillary refill

62
Q
  1. How is intussusception diagnosed and treated?
A

Diagnosis: Ultrasound shows target sign
- Treatment: Air/contrast enema reduction, surgery if unsuccessful or signs of perforation

63
Q
  1. What are the signs of moderate and severe dehydration in children?
A

Moderate: Restless, thirsty, dry mouth, decreased tears, skin recoil <2 sec
- Severe: Lethargy, sunken eyes, skin recoil >2 sec, weak pulse

64
Q
  1. What is the WHO classification of dehydration?
A

WHO: No dehydration, some dehydration, severe dehydration
- Based on clinical signs

65
Q
  1. What are the clinical features of GSD type I (Von Gierke disease)?
A

GSD I: Hepatomegaly, doll face, fasting hypoglycemia, lactic acidosis, hyperuricemia, hyperlipidemia

66
Q
  1. What is juvenile polyp and how is it managed?
A

Juvenile polyp: Painless rectal bleeding in young children
- Diagnosed by colonoscopy, treated with polypectomy

67
Q
  1. How is cow’s milk protein allergy diagnosed and managed?
A

Diagnosis: Symptom response to elimination diet and oral challenge
- Management: Eliminate cow’s milk protein for 6–12 months

68
Q
  1. What are the clinical features and management of peptic ulcer disease in children?
A

Peptic ulcers: Epigastric pain, vomiting, GI bleed
- Causes: H. pylori, NSAIDs, stress ulcers
- Treat with PPI ± antibiotics

69
Q
  1. What are the clinical features of inflammatory bowel disease (IBD) in children?
A

IBD: Chronic diarrhea (± blood), weight loss, abdominal pain, growth failure, fatigue, perianal disease (Crohn)

70
Q
  1. What investigations are used to diagnose IBD in pediatric patients?
A

Investigations: CBC, ESR/CRP, stool calprotectin, endoscopy + biopsy, imaging (MRE, barium studies)

71
Q
  1. What is the role of fecal calprotectin in pediatric GI disease?
A

Fecal calprotectin: Marker of intestinal inflammation
- Elevated in IBD, normal in functional GI disorders

72
Q
  1. What is the difference between Crohn’s disease and ulcerative colitis?
A

Crohn’s: Transmural, skip lesions, terminal ileum, perianal disease
- UC: Continuous, limited to colon, rectal involvement

73
Q
  1. What are the complications of Crohn’s disease in pediatrics?
A

Complications: Fistulas, strictures, growth failure, abscess, B12 deficiency, osteoporosis

74
Q
  1. What is the treatment approach for IBD in children?
A

Treatment: 5-ASA, corticosteroids, immunomodulators (azathioprine), biologics (infliximab), nutritional therapy (EEN)

75
Q
  1. What are the common causes of acute liver failure in pediatrics?
A

Causes: Viral hepatitis (A, B, E), drug toxicity (acetaminophen), metabolic diseases, autoimmune hepatitis, Wilson’s disease

76
Q
  1. What are the indications for liver transplantation in children?
A

Indications: Fulminant hepatic failure, end-stage liver disease, metabolic liver disease not responsive to medical therapy

77
Q
  1. What is the management approach to pediatric acute liver failure?
A

Management: ICU care, correct coagulopathy, treat cause, monitor ICP
- Consider transplant early if worsening

78
Q
  1. What is TPN-associated cholestasis and who is at risk?
A

Seen in long-term TPN-dependent infants (e.g., short gut)
- Risk: Prematurity, sepsis, lack of enteral feeds

79
Q
  1. What are the long-term complications of pediatric liver cirrhosis?
A

Complications: Variceal bleeding, encephalopathy, growth retardation, vitamin deficiencies, HCC

80
Q
  1. What is the role of surveillance in pediatric patients with chronic hepatitis or cirrhosis?
A

Surveillance: Periodic ultrasound and AFP for HCC, endoscopy for varices, LFTs, nutritional monitoring

81
Q
  1. What are the clinical signs of acute liver failure in children?
A

Signs: Jaundice, coagulopathy, encephalopathy, hepatomegaly, ascites
- Rapid progression

82
Q
  1. What are the nutritional considerations in children with chronic liver disease?
A

Nutrition: High-calorie, high-protein diet with vitamin supplementation (A, D, E, K), MCT oils if cholestasis

83
Q
  1. What is the management approach to neonatal cholestasis?
A

Neonatal cholestasis: Rule out biliary atresia urgently
- Labs: LFTs, US, TORCH, metabolic screen
- Early referral for HIDA scan, possible surgery

84
Q
  1. What is the treatment for biliary atresia and its long-term prognosis?
A

Treatment: Kasai portoenterostomy
- Many require liver transplant later due to progressive liver damage

85
Q
  1. What is the diagnostic approach to autoimmune hepatitis?
A

Approach: Elevated AST/ALT, hypergammaglobulinemia (IgG), positive autoantibodies, biopsy showing interface hepatitis

86
Q
  1. What is the treatment of autoimmune hepatitis in children?
A

Treatment: Prednisolone ± azathioprine for induction and maintenance
- Long-term monitoring required

87
Q
  1. What are the types and clinical features of viral hepatitis in children?
A

Types: HAV (acute, self-limited), HBV (chronic risk if neonatal), HCV (chronic, asymptomatic), HEV (rare)
- Features: Jaundice, hepatomegaly, malaise, nausea

88
Q
  1. What are the causes of conjugated hyperbilirubinemia in neonates?
A

Causes: Biliary atresia, neonatal hepatitis, infections (TORCH), metabolic diseases (galactosemia, tyrosinemia), genetic syndromes

89
Q
  1. How is hepatitis A virus (HAV) diagnosed and prevented?
A

Diagnosis: Anti-HAV IgM in serum
- Prevention: Vaccination (from 1 year), good hygiene

90
Q
  1. What are the complications of hepatitis B virus (HBV) in children?
A

Complications: Chronic hepatitis, cirrhosis, hepatocellular carcinoma, especially with perinatal infection

91
Q
  1. What are the causes and types of autoimmune hepatitis in children?
A

Types: AIH-1 (ANA, SMA), AIH-2 (anti-LKM1)
- Causes: Idiopathic, viral trigger, genetic predisposition

92
Q
  1. What are the types of glycogen storage diseases (GSDs) with liver involvement?
A

GSDs with liver involvement: Type I (Von Gierke), III (Cori), VI, IX
- Cause hepatomegaly and hypoglycemia

93
Q
  1. How is chronic hepatitis B diagnosed and managed in pediatrics?
A

Diagnosis: HBsAg >6 months, HBeAg/anti-HBe, HBV DNA
- Treatment: Antivirals (e.g., entecavir, tenofovir) if active disease

94
Q
  1. What is the role of hepatitis B vaccination in prevention?
A

Vaccination: Highly effective
- Given at birth, 6 weeks, 10 weeks, 14 weeks (EPI schedule) with booster if needed

95
Q
  1. How is hepatitis C diagnosed and treated in children?
A

Diagnosis: Anti-HCV antibodies, HCV RNA PCR
- Treatment: Direct-acting antivirals (DAAs) for children >3 years

96
Q
  1. What are the common metabolic liver diseases in children?
A

Metabolic liver diseases: Galactosemia, hereditary fructose intolerance, tyrosinemia, alpha-1 antitrypsin deficiency, glycogen storage diseases

97
Q
  1. How is neonatal hepatitis differentiated from biliary atresia?
A

Biliary atresia: Firm liver, persistently pale stools, elevated GGT, triangular cord sign on US
- Confirm with intraoperative cholangiogram

98
Q
  1. What are the clinical features of neonatal hepatitis?
A

Neonatal hepatitis: Prolonged jaundice, hepatomegaly, acholic stools, elevated transaminases

99
Q
  1. What is biliary atresia and why is early diagnosis important?
A

Biliary atresia: Progressive fibrosing obliteration of bile ducts
- Early diagnosis is critical as surgery before 8 weeks improves outcomes

100
Q
  1. What are the clinical features of Wilson’s disease in children?
A

Features: Hepatomegaly, jaundice, neurological signs, behavioral change, Kayser-Fleischer rings, low ceruloplasmin

101
Q
  1. How is alpha-1 antitrypsin deficiency diagnosed?
A

Diagnosis: Low serum AAT level, phenotype/genotype testing
- Liver biopsy may show PAS-positive globules

102
Q
  1. How is Wilson’s disease diagnosed?
A

Diagnosis: Low ceruloplasmin, ↑24hr urinary copper, KF rings on slit-lamp, liver biopsy with copper quantification

103
Q
  1. What is the treatment for Wilson’s disease in pediatrics?
A

Treatment: Chelators (penicillamine), zinc (blocks absorption), liver transplant in advanced disease

104
Q
  1. What is alpha-1 antitrypsin deficiency and its hepatic presentation in children?
A

AAT deficiency: Genetic disorder (PiZZ phenotype)
- Hepatic presentation: Neonatal cholestasis, elevated LFTs, cirrhosis in older children

105
Q
  1. How is hereditary tyrosinemia type 1 diagnosed and treated?
A

Diagnosis: Succinylacetone in urine, liver dysfunction, confirm by FAH gene mutation
- Treat with NTBC and dietary tyrosine restriction

106
Q
  1. What are the causes and clinical features of acute pancreatitis in children?
A

Causes: Trauma, gallstones, infections, drugs (valproate, steroids), metabolic (hypertriglyceridemia), genetic
- Features: Abdominal pain, vomiting, ↑amylase/lipase

107
Q
  1. What is chronic pancreatitis in children and its common causes?
A

Chronic: Recurrent inflammation → fibrosis and pancreatic insufficiency
- Causes: Genetic (PRSS1, CF), autoimmune, idiopathic

108
Q
  1. How is pediatric pancreatitis diagnosed and managed?
A

Diagnosis: Abdominal pain + elevated enzymes + imaging (US or CT/MRI)
- Management: Supportive care (fluids, pain control, nutrition)

109
Q
  1. What are the clinical features of portal hypertension?
A

Features: Splenomegaly, ascites, GI bleeding (varices), growth failure, thrombocytopenia

110
Q
  1. What is the diagnostic approach to ascites in pediatric patients?
A

Approach: Clinical exam + ultrasound
- Diagnostic paracentesis: SAAG, cell count, culture, albumin/protein

111
Q
  1. What are the causes and types of portal hypertension in children?
A

Causes: Intrahepatic (cirrhosis, Wilson), prehepatic (portal vein thrombosis), posthepatic (Budd-Chiari)
- Types: Pre-, intra-, post-hepatic

112
Q
  1. What are the causes of ascites in children?
A

Causes: Cirrhosis, nephrotic syndrome, heart failure, infections (TB, SBP), malignancy, Budd-Chiari syndrome

113
Q
  1. What are the management strategies for cyclic vomiting syndrome?
A

Management: Supportive care, antiemetics during episodes, prophylaxis with amitriptyline, propranolol, cyproheptadine

114
Q
  1. What is cyclic vomiting syndrome and how is it diagnosed?
A

Cyclic vomiting syndrome: Recurrent, stereotyped episodes of intense vomiting with symptom-free intervals

115
Q
  1. What is the management approach for GERD in pediatrics?
A

Management: Parental reassurance, thickened feeds, positioning, trial of acid suppression (H2 blocker/PPI), surgery if severe

116
Q
  1. What are the complications of untreated GERD in children?
A

Complications: Esophagitis, failure to thrive, strictures, Barrett’s esophagus, aspiration pneumonia

117
Q
  1. How is GERD differentiated from physiological GER in infants?
A

GERD: Causes irritability, poor weight gain, feeding refusal, apnea
- GER is physiological and self-resolving

118
Q
  1. What are the causes and features of gastroesophageal reflux (GER) in infants?
A

GER: Common and self-limited in infants
- Features: Effortless regurgitation, normal growth, peaks at 4 months

119
Q
  1. How can you differentiate between bilious and non-bilious vomiting in neonates?
A

Bilious: Suggests obstruction distal to ampulla of Vater (e.g., malrotation/volvulus)
- Non-bilious: More proximal causes (e.g., pyloric stenosis)

120
Q
  1. What are the common causes of vomiting in infants?
A

Common causes: Gastroesophageal reflux, pyloric stenosis, milk protein allergy, infections, increased ICP, intestinal obstruction