GIT Flashcards
(348 cards)
1
Q
What is esophageal atresia (EA)?
A
A congenital obstruction of the esophagus, often with a fistula to the trachea.
2
Q
What is the most common type of tracheoesophageal fistula (TEF)?
A
EA with distal TEF (Gross Type C).
3
Q
What are clinical features of EA with TEF?
A
Excessive salivation, choking, cyanosis, abdominal distension with feeding.
4
Q
What is the initial diagnostic step in suspected EA?
A
Attempt to pass nasogastric tube — fails to pass into stomach.
5
Q
What radiographic finding suggests EA with distal TEF?
A
Nasogastric tube coiled in upper esophageal pouch on x-ray.
6
Q
What is the VACTERL association?
A
Association of anomalies: Vertebral, Anal, Cardiac, TEF, Renal, Limb.
7
Q
How is EA with TEF managed?
A
Stabilize, avoid bag-mask ventilation, surgical correction.
8
Q
What is congenital diaphragmatic hernia (CDH)?
A
Failure of diaphragm formation allowing herniation of abdominal contents into thorax.
9
Q
What are clinical signs of CDH in newborns?
A
Respiratory distress, scaphoid abdomen, decreased breath sounds on left.
10
Q
What imaging confirms diagnosis of CDH?
A
Chest x-ray shows bowel loops in thorax and mediastinal shift.
11
Q
What is the most common site of CDH?
A
Left posterolateral (Bochdalek hernia).
12
Q
What is the initial management in CDH?
A
Stabilize with intubation, NG decompression, surgical repair after pulmonary optimization.
13
Q
What is intestinal malrotation?
A
Abnormal rotation/fixation of midgut during fetal life.
14
Q
What is midgut volvulus?
A
Twisting of bowel around mesenteric base leading to obstruction and ischemia.
15
Q
How does midgut volvulus present?
A
Bilious vomiting, abdominal distension, shock.
16
Q
What imaging study is diagnostic in volvulus?
A
Upper GI contrast study.
17
Q
What is the ‘corkscrew’ appearance on UGI contrast study?
A
Characteristic finding in midgut volvulus.
18
Q
What is the Ladd procedure?
A
Surgical correction for malrotation; includes widening mesenteric base.
19
Q
What is duodenal atresia?
A
Complete obstruction of the duodenal lumen due to failure of recanalization.
20
Q
What are clinical signs of duodenal atresia?
A
Bilious vomiting within first 24–48 hours of life, no abdominal distension.
21
Q
What is the ‘double bubble’ sign?
A
X-ray sign with gas in stomach and proximal duodenum only.
22
Q
Which syndromes are associated with duodenal atresia?
A
Down syndrome, cardiac anomalies, annular pancreas.
23
Q
What is jejunal/ileal atresia?
A
Congenital blockage of jejunum or ileum, often with multiple atretic segments.
24
Q
What causes jejunoileal atresia?
A
Intrauterine vascular accidents.
25
What are signs of distal intestinal atresia?
Abdominal distension, bilious vomiting, delayed meconium passage.
26
What is anal atresia (imperforate anus)?
Absence of normal anal opening with possible recto-urethral or recto-vaginal fistula.
27
What is the initial management in imperforate anus?
NG decompression, IV fluids, evaluation of associated anomalies.
28
What imaging is used to evaluate level of imperforate anus?
Cross-table lateral pelvic x-ray or prone invertogram.
29
What are associated anomalies in imperforate anus?
VACTERL, genitourinary anomalies, spinal dysraphism.
30
What is meconium ileus and which condition is it associated with?
Obstruction due to thick meconium; strongly associated with cystic fibrosis.
31
What is gastroesophageal reflux (GER) in infants?
Physiologic passage of gastric contents into esophagus; common and self-limited.
32
How does GER differ from GERD in pediatrics?
GERD implies reflux with troublesome symptoms or complications like failure to thrive or esophagitis.
33
What are common signs of GERD in infants?
Regurgitation, irritability, arching, apnea, poor weight gain.
34
What symptoms suggest GERD in older children?
Heartburn, chest pain, epigastric pain, vomiting, chronic cough.
35
What complications may arise from GERD?
Esophagitis, stricture, Barrett’s esophagus, respiratory symptoms.
36
What conservative measures help manage infantile GER?
Upright positioning, smaller frequent feeds, burping, thickened feeds.
37
What is the role of thickened feeds in GER?
Increases feed viscosity and reduces reflux episodes.
38
What pharmacologic options are used in pediatric GERD?
H2 blockers, PPIs (e.g., omeprazole), prokinetics (rarely used).
39
What are indications for fundoplication in pediatric GERD?
Refractory GERD, life-threatening aspiration, failed medical therapy.
40
What is eosinophilic esophagitis (EoE)?
Chronic immune-mediated esophageal disease with eosinophilic infiltration.
41
What are symptoms of EoE in children?
Dysphagia, food impaction, vomiting, feeding refusal.
42
What diagnostic findings confirm EoE?
Endoscopy shows trachealization; biopsy shows >15 eosinophils/HPF.
43
What is the first-line treatment of EoE?
Dietary elimination, swallowed topical corticosteroids (fluticasone, budesonide).
44
What is congenital esophageal stenosis?
Congenital narrowing of the esophagus due to fibrous ring, cartilage, or tracheobronchial remnants.
45
How does esophageal stenosis present?
Vomiting, dysphagia, feeding difficulties, aspiration.
46
What imaging helps diagnose esophageal stenosis?
Barium swallow shows fixed narrowing; endoscopy confirms.
47
What is esophageal achalasia?
Motility disorder with failure of LES relaxation and absent peristalsis.
48
How does pediatric achalasia present?
Dysphagia, weight loss, regurgitation, aspiration pneumonia.
49
What radiologic findings suggest achalasia?
Bird-beak narrowing of distal esophagus on barium swallow.
50
What is the gold standard for diagnosing achalasia?
Esophageal manometry (gold standard).
51
What are treatment options for achalasia in children?
Heller myotomy, pneumatic dilation, botulinum toxin (temporary).
52
What is caustic esophageal injury?
Esophageal damage after ingestion of corrosive agents (alkali or acid).
53
What are phases of caustic injury and their complications?
Phase 1 (acute inflammation), Phase 2 (ulceration), Phase 3 (fibrosis, stricture).
54
How is caustic ingestion initially managed?
Avoid vomiting induction; NPO, endoscopy within 24–48h if indicated.
55
What is esophageal web?
Thin membranous narrowing, often in upper esophagus.
56
What is Plummer-Vinson syndrome?
Esophageal web + iron deficiency anemia + dysphagia.
57
What is Schatzki ring?
Distal esophageal mucosal ring causing intermittent dysphagia.
58
What is esophageal duplication cyst?
Congenital cyst adjacent to esophagus; may compress airway or esophagus.
59
What are complications of esophageal foreign bodies?
Perforation, mediastinitis, stricture, aspiration, pressure necrosis.
60
When is endoscopic removal of esophageal foreign body indicated?
If sharp object, disk battery, symptoms present, or >24 hours in esophagus.
61
What is hypertrophic pyloric stenosis (HPS)?
Hypertrophy and hyperplasia of pyloric muscle causing gastric outlet obstruction.
62
What are clinical features of HPS?
Projectile non-bilious vomiting, palpable 'olive', visible gastric peristalsis.
63
What is the typical age of presentation for HPS?
Typically between 2–8 weeks of age.
64
What electrolyte abnormalities are seen in HPS?
Hypochloremic, hypokalemic metabolic alkalosis.
65
What imaging confirms diagnosis of HPS?
Abdominal ultrasound (first-line).
66
What is the characteristic ultrasound finding in HPS?
Pyloric muscle thickness >3 mm and length >14–16 mm.
67
What is the treatment for HPS?
Correct electrolytes and dehydration, then surgical pyloromyotomy (Ramstedt).
68
What is congenital gastric outlet obstruction besides HPS?
Congenital antral diaphragm, duodenal web, annular pancreas.
69
What is peptic ulcer disease (PUD)?
Mucosal erosion in the stomach or duodenum caused by acid-peptic injury.
70
What are causes of primary and secondary PUD in children?
Primary: idiopathic or H. pylori; Secondary: NSAIDs, stress, systemic illness.
71
What are symptoms of PUD in children?
Epigastric pain, vomiting, hematemesis, melena.
72
What are complications of untreated PUD?
Bleeding, perforation, gastric outlet obstruction.
73
What is the gold standard for diagnosing PUD?
Upper GI endoscopy with biopsy.
74
What is the role of H. pylori in pediatric ulcers?
Most duodenal ulcers in children are H. pylori-associated.
75
What is the treatment for H. pylori infection?
First-Line Therapy (10-14 Days)
1. Amoxicillin-Based Triple Therapy
PPI (e.g., omeprazole, lansoprazole) twice daily
Amoxicillin 50 mg/kg/day (max 1000 mg twice daily)
Clarithromycin 15 mg/kg/day (max 500 mg twice daily)
2. Bismuth Quadruple Therapy
PPI twice daily
Bismuth subsalicylate 8-12 mg/kg/day in 4 divided doses
Metronidazole 20-30 mg/kg/day in 3-4 divided doses (max 500 mg three times daily)
Tetracycline (if >8 years old) 25-50 mg/kg/day in 4 divided doses
Second-Line (Rescue) Therapy
Levofloxacin triple therapy (if not previously used) or rifabutin-based therapy in resistant cases.
Follow-Up
Confirm eradication 4-6 weeks post-therapy using a urea breath test or stool antigen test (avoid serology).
76
What is acute gastritis?
Inflammation of gastric mucosa, often reversible.
77
What are causes of acute gastritis in children?
H. pylori, NSAIDs, infections (CMV, HSV), chemical injury.
78
What are features of chronic gastritis?
Chronic mucosal inflammation; may lead to atrophy and metaplasia.
79
What is Menetrier disease?
Protein-losing hypertrophic gastropathy with enlarged rugal folds; rare in children.
80
What is Zollinger-Ellison syndrome?
Gastrin-secreting tumor (gastrinoma) causing refractory ulcers.
81
How does Zollinger-Ellison syndrome present?
Multiple peptic ulcers, diarrhea, weight loss, refractory to standard therapy.
82
What lab test is used to diagnose Zollinger-Ellison syndrome?
Elevated fasting serum gastrin level (>1000 pg/mL) and secretin stimulation test.
83
What is stress ulcer prophylaxis and when is it indicated in pediatrics?
Critically ill children (mechanical ventilation, coagulopathy, burns, head trauma).
84
What is gastric volvulus?
Abnormal rotation and fixation of the stomach causing volvulus.
85
What are symptoms of gastric volvulus?
Severe epigastric pain, vomiting, difficulty passing NG tube.
86
What is the ‘Borchardt triad’?
Borchardt triad: unproductive retching, epigastric distension, inability to pass NG tube.
87
What imaging is used to diagnose gastric volvulus?
Upper GI contrast study or CT scan.
88
What is congenital duodenal web?
Incomplete diaphragm in duodenum causing partial obstruction.
89
What are clinical signs of duodenal web?
Bilious vomiting, intermittent feeding intolerance, failure to thrive.
90
How is duodenal web managed?
Surgical excision of the web (duodenotomy and web resection).
91
What is Hirschsprung disease (HD)?
Congenital absence of ganglion cells in the distal intestine leading to functional obstruction.
92
What is the pathophysiology of HD?
Failure of neural crest cell migration leading to lack of enteric nervous system in segments of colon.
93
What are clinical features of neonatal Hirschsprung disease?
Failure to pass meconium within 48 hours, abdominal distension, bilious vomiting.
94
How does Hirschsprung disease present in older infants and children?
Chronic constipation, abdominal distension, poor weight gain, enterocolitis episodes.
95
What is the gold standard for diagnosing Hirschsprung disease?
Rectal suction biopsy showing absence of ganglion cells.
96
What imaging finding suggests Hirschsprung disease?
Contrast enema showing transition zone between narrow aganglionic and dilated proximal bowel.
97
What is the treatment for Hirschsprung disease?
Surgical resection of aganglionic segment and pull-through procedure.
98
What is enterocolitis in Hirschsprung disease?
Severe, life-threatening infection characterized by fever, abdominal distension, diarrhea, sepsis.
99
What is meconium plug syndrome?
Functional colonic obstruction due to thick meconium plugs in newborns.
100
How is meconium plug syndrome managed?
Rectal stimulation, saline enema, supportive care.
101
What is small bowel obstruction (SBO)?
Partial or complete blockage of the small intestine.
102
What are causes of SBO in children?
Postoperative adhesions, hernias, intussusception, Meckel’s diverticulum, volvulus.
103
What are clinical features of small bowel obstruction?
Vomiting (bilious if proximal), abdominal distension, constipation, dehydration.
104
What imaging study helps diagnose SBO?
Abdominal x-ray, contrast studies (upper GI series, small bowel follow-through).
105
What is intussusception?
Intussusception is the telescoping of a proximal segment of the intestine (intussusceptum) into a distal segment (intussuscipiens).
106
What is the most common site for intussusception?
Ileocecal region (ileocolic intussusception).
107
What are classic symptoms of intussusception?
Colicky abdominal pain, vomiting, 'currant jelly' stools, palpable sausage-shaped mass.
108
What is the ‘target sign’ on ultrasound?
Characteristic appearance of intussusception on ultrasound.
109
How is intussusception treated?
Air or contrast enema reduction (therapeutic and diagnostic).
110
What are contraindications to non-surgical reduction of intussusception?
Peritonitis, bowel perforation, hemodynamic instability.
111
What is inflammatory bowel disease (IBD)?
Chronic inflammatory disease of GI tract causing ulceration and tissue injury.
112
What are the types of pediatric IBD?
Crohn’s disease and ulcerative colitis.
113
What are key features distinguishing Crohn’s disease from ulcerative colitis?
Crohn’s: transmural, skip lesions, any GI tract; UC: mucosal, continuous, colon-only.
114
What is the role of fecal calprotectin in IBD diagnosis?
Elevated in intestinal inflammation; useful non-invasive marker.
115
What is the role of endoscopy in IBD diagnosis?
Colonoscopy with biopsy is definitive for diagnosis and classification.
116
What is medical treatment for pediatric IBD?
Corticosteroids, immunomodulators (azathioprine), biologics (anti-TNF agents), 5-ASA drugs.
117
What is short bowel syndrome?
Malabsorption syndrome after extensive resection of small intestine.
118
What are causes of short bowel syndrome?
Necrotizing enterocolitis, midgut volvulus, intestinal atresia, trauma, Crohn’s resections.
119
What is the primary nutritional concern in short bowel syndrome?
Malabsorption of fluids, electrolytes, vitamins, and energy substrates.
120
What is necrotizing enterocolitis (NEC)?
Serious inflammatory condition mainly in premature infants causing intestinal necrosis.
121
What are signs of liver disease in children?
Jaundice, hepatomegaly, splenomegaly, ascites, pruritus, failure to thrive.
122
What is neonatal cholestasis?
Direct (conjugated) hyperbilirubinemia in neonates persisting beyond 2 weeks of age.
123
What are causes of neonatal cholestasis?
Biliary atresia, neonatal hepatitis, infections, metabolic disorders, Alagille syndrome.
124
What is biliary atresia?
Fibro-obliterative disorder of extrahepatic bile ducts causing obstruction.
125
What are clinical features of biliary atresia?
Persistent jaundice, acholic (pale) stools, dark urine, hepatomegaly.
126
What investigation is used first for suspected biliary atresia?
Abdominal ultrasound to assess gallbladder and biliary tree.
127
What is the gold standard for diagnosing biliary atresia?
Intraoperative cholangiography or liver biopsy.
128
What is the treatment for biliary atresia?
Kasai portoenterostomy, followed by liver transplant if needed.
129
What is the Kasai procedure?
Surgical connection of the liver hilum to the intestine to allow bile drainage.
130
What are long-term outcomes after Kasai procedure?
Better outcomes if performed early (<60 days); many still eventually require transplant.
131
What is neonatal hepatitis?
Inflammatory liver disease causing cholestasis in neonates; can mimic biliary atresia.
132
What are infectious causes of neonatal hepatitis?
CMV, HSV, rubella, hepatitis B, hepatitis C.
133
What are metabolic causes of neonatal hepatitis?
Galactosemia, tyrosinemia, Niemann-Pick, A1ATD.
134
What is Alagille syndrome?
Genetic disorder causing bile duct paucity and multisystem involvement.
135
What are features of Alagille syndrome?
Cholestasis, butterfly vertebrae, peripheral pulmonary stenosis, renal anomalies, peculiar facies.
136
What is alpha-1 antitrypsin deficiency (A1ATD)?
Genetic disorder leading to defective alpha-1 antitrypsin protein accumulation in liver.
137
How does A1ATD present in children?
Neonatal hepatitis, prolonged jaundice, later risk of liver cirrhosis.
138
What is the definitive diagnosis of A1ATD?
Low serum A1AT level with PiZZ phenotype on phenotyping/genotyping.
139
What is progressive familial intrahepatic cholestasis (PFIC)?
Inherited defects in bile acid transport proteins leading to severe cholestasis.
140
What are features of PFIC?
Severe itching, growth failure, progressive liver dysfunction.
141
What is physiologic jaundice?
Transient unconjugated hyperbilirubinemia due to immature hepatic conjugation; resolves by 2–3 weeks.
142
How is breast milk jaundice different from breast feeding jaundice?
Breast milk jaundice persists longer (>1 week); breast feeding jaundice occurs early due to poor intake.
143
What is acute viral hepatitis?
Liver inflammation due to viral infection causing jaundice, anorexia, vomiting, fever.
144
What are common viruses causing pediatric hepatitis?
Hepatitis A, B, C, Epstein-Barr virus (EBV), cytomegalovirus (CMV).
145
What are signs of fulminant hepatic failure in children?
Coagulopathy unresponsive to vitamin K, encephalopathy, hypoglycemia.
146
What is autoimmune hepatitis?
Chronic immune-mediated liver disease leading to hepatitis and fibrosis.
147
What are autoantibodies associated with autoimmune hepatitis?
ANA, anti-smooth muscle antibody (SMA), anti-LKM1 (liver-kidney microsomal antibody).
148
How is autoimmune hepatitis treated?
Immunosuppressive therapy (steroids, azathioprine).
149
What is Wilson disease?
Autosomal recessive disorder of copper metabolism leading to accumulation in liver, brain, and other tissues.
150
How is Wilson disease diagnosed in children?
Low ceruloplasmin, elevated urinary copper, Kayser-Fleischer rings on slit-lamp exam, liver biopsy copper quantification.
151
What is cystic fibrosis (CF)?
An autosomal recessive disorder caused by CFTR gene mutations affecting multiple organs.
152
How does CF affect the pancreas?
Thickened secretions obstruct pancreatic ducts causing damage and fibrosis.
153
What are pancreatic manifestations of CF?
Exocrine pancreatic insufficiency, recurrent pancreatitis, diabetes mellitus.
154
What is newborn screening for CF based on?
Measurement of immunoreactive trypsinogen (IRT) levels in blood spots.
155
What is the confirmatory diagnostic test for CF?
Sweat chloride test (>60 mmol/L is diagnostic).
156
What is pancreatic insufficiency?
Failure of the pancreas to produce enough digestive enzymes.
157
What are symptoms of pancreatic insufficiency in CF?
Steatorrhea, failure to thrive, fat-soluble vitamin deficiencies.
158
How is pancreatic insufficiency managed in CF?
Pancreatic enzyme replacement therapy (PERT) with meals and fat-soluble vitamin supplementation.
159
What is acute pancreatitis?
Acute inflammation of the pancreas causing abdominal pain and elevated enzymes.
160
What are common causes of acute pancreatitis in children?
Idiopathic, trauma, medications, infections, gallstones, metabolic diseases.
161
What are clinical features of acute pancreatitis?
Severe epigastric pain radiating to back, nausea, vomiting, abdominal tenderness.
162
What lab findings are diagnostic of pancreatitis?
Elevated serum amylase and lipase (>3× normal).
163
What imaging is used in suspected pancreatitis?
Ultrasound (initial), CT abdomen (if severe or complicated).
164
What is the treatment of mild acute pancreatitis?
Supportive care: bowel rest, IV fluids, analgesia, gradual refeeding.
165
What are complications of severe acute pancreatitis?
Necrosis, pseudocyst formation, infection, systemic inflammatory response syndrome (SIRS).
166
What is chronic pancreatitis?
Progressive pancreatic destruction leading to fibrosis and calcifications.
167
What are causes of chronic pancreatitis in children?
Genetic mutations (PRSS1, SPINK1), CF, autoimmune diseases.
168
What are features of chronic pancreatitis?
Chronic epigastric pain, exocrine insufficiency, diabetes mellitus.
169
What are pancreatic pseudocysts?
Encapsulated collections of pancreatic fluid after pancreatitis.
170
What is the management of pancreatic pseudocysts?
Observation if asymptomatic; drainage if large, infected, or symptomatic.
171
What is Shwachman-Diamond syndrome (SDS)?
A rare AR disorder with pancreatic insufficiency, neutropenia, skeletal abnormalities.
172
What are features of Shwachman-Diamond syndrome?
Neutropenia, exocrine pancreatic insufficiency, short stature, metaphyseal dysplasia.
173
What is hereditary pancreatitis?
Autosomal dominant disorder causing recurrent acute and chronic pancreatitis.
174
Which gene mutations are associated with hereditary pancreatitis?
PRSS1, SPINK1, CFTR gene mutations.
175
What is exocrine pancreatic insufficiency (EPI)?
Severe reduction of pancreatic enzyme secretion leading to malabsorption.
176
How is EPI diagnosed?
Low fecal elastase, clinical features of steatorrhea and malnutrition.
177
What is the role of fecal elastase testing?
Measures pancreatic elastase-1; low levels suggest EPI.
178
What is the function of pancreatic enzymes?
Digest proteins, fats, and carbohydrates for absorption in small intestine.
179
What are indications for pancreatic enzyme replacement therapy (PERT)?
CF, Shwachman-Diamond syndrome, chronic pancreatitis, pancreatic resection.
180
What vitamins require pancreatic enzyme function for absorption?
Vitamins A, D, E, and K (fat-soluble vitamins).
181
What are causes of upper GI bleeding in children?
Esophagitis, gastritis, esophageal varices, peptic ulcer disease, Mallory-Weiss tear.
182
What are causes of lower GI bleeding in children?
Anal fissures, polyps, Meckel’s diverticulum, IBD, infectious colitis, HSP vasculitis.
183
What are signs of significant GI bleeding in children?
Hypotension, tachycardia, pallor, delayed capillary refill, altered consciousness.
184
What are the initial steps in management of GI bleeding?
ABC approach: airway, breathing, circulation; establish IV access; fluid resuscitation; labs.
185
What is the role of nasogastric (NG) tube in GI bleeding evaluation?
Detects blood in stomach, helps localize bleeding source.
186
What is hematemesis?
Vomiting fresh blood or coffee-ground material.
187
What is melena?
Black, tarry, foul-smelling stools from digested blood.
188
What is hematochezia?
Passage of bright red blood per rectum.
189
What does coffee ground emesis indicate?
Suggests upper GI bleeding with slower bleeding or partial digestion.
190
What are causes of esophageal bleeding?
Esophageal varices, esophagitis, Mallory-Weiss tear.
191
What are causes of gastric bleeding?
Gastritis, gastric ulcer, gastric varices, portal hypertensive gastropathy.
192
What are causes of small intestinal bleeding?
Meckel’s diverticulum, vascular malformations, Crohn’s disease.
193
What are causes of colonic bleeding?
Juvenile polyps, IBD, infectious colitis, intussusception, angiodysplasia.
194
What are Meckel’s diverticulum and its relevance to GI bleeding?
Congenital anomaly containing ectopic gastric mucosa that can ulcerate and bleed.
195
What test diagnoses Meckel’s diverticulum?
Technetium-99m pertechnetate (Meckel) scan.
196
What is juvenile polyp?
Benign hamartomatous polyp, typically solitary, in rectosigmoid colon.
197
How do juvenile polyps present?
Painless rectal bleeding, usually small-volume; sometimes prolapse through anus.
198
What is Peutz-Jeghers syndrome?
Autosomal dominant syndrome with multiple hamartomatous polyps and mucocutaneous pigmentation.
199
What are clinical features of Peutz-Jeghers syndrome?
Melanotic spots on lips, oral mucosa, hands, feet; risk of small bowel obstruction and malignancy.
200
What is familial adenomatous polyposis (FAP)?
Inherited disorder with hundreds to thousands of adenomatous polyps in colon; high cancer risk.
201
When does screening for FAP begin?
At age 10–12 years with colonoscopy and genetic testing if positive family history.
202
What are angiodysplasias?
Dilated blood vessels in GI tract wall causing intermittent bleeding.
203
What is the role of endoscopy in GI bleeding?
Visualization of mucosa to identify, diagnose, and sometimes treat bleeding lesions.
204
What is the role of technetium-99m RBC scan?
Detects active bleeding by labeling RBCs and tracking their extravasation.
205
What laboratory tests are important in GI bleeding evaluation?
CBC, coagulation profile, type and crossmatch, electrolytes, liver function tests.
206
What is Henoch-Schönlein purpura (HSP) gastrointestinal involvement?
GI bleeding secondary to small vessel vasculitis causing submucosal hemorrhage and ulceration.
207
What is intussusception-related bleeding?
Currant jelly stool from ischemic mucosa in telescoped bowel.
208
What is cow’s milk protein allergy and how does it cause GI bleeding?
Allergic proctocolitis causing rectal bleeding in otherwise healthy young infants.
209
What are varices and how are they treated in GI bleeding?
Dilated submucosal veins prone to rupture, associated with portal hypertension.
210
What medications are used to control variceal bleeding?
Octreotide infusion, beta-blockers, endoscopic band ligation.
211
What are functional GI disorders (FGIDs)?
Disorders characterized by chronic/recurrent GI symptoms without structural or biochemical abnormalities.
212
What are common FGIDs in infancy?
Infantile regurgitation, infantile colic, functional diarrhea, functional constipation.
213
What are common FGIDs in childhood and adolescence?
Functional abdominal pain, IBS, functional dyspepsia, aerophagia, cyclic vomiting syndrome.
214
What is infantile colic?
Self-limited disorder with excessive crying in otherwise healthy infants.
215
What are features of infantile colic?
Paroxysmal crying, facial grimacing, pulling up legs, inconsolability.
216
What is the rule of 3s for infantile colic?
Crying >3 hours/day, >3 days/week, for >3 weeks.
217
What is the management of infantile colic?
**Onset: Peaks at 6 weeks, resolves by 3–4 months**
1. **Reassurance**
Benign, self-limited
Support parents; screen for maternal stress or depression
2. **Feeding Review**
Ensure proper technique
For formula-fed: consider trial of hydrolyzed formula if CMPA suspected
3. **Soothing Measures**
Swaddling, rocking, white noise, pacifier
4. **Maternal Diet (if breastfeeding)**
Trial dairy-free diet if allergy suspected
5. **Probiotics**
Lactobacillus reuteri may help in breastfed infants
6. **Avoid Harmful Medications**
Simethicone is safe but of limited benefit
Avoid dicyclomine – serious side effects
7. **Rule Out Red Flags**
Vomiting, poor weight gain, fever, blood in stool → assess for organic causes
218
What is functional constipation?
Chronic constipation without identifiable organic cause.
219
What are clinical features of functional constipation?
Infrequent stools, hard painful stools, withholding behaviors, large diameter stools.
220
What is the Rome IV criteria for diagnosing functional constipation?
At least 2 of the following for ≥1 month: ≤2 defecations/week, painful/hard stools, large stools, retentive posturing.
221
What are red flags in constipation suggesting organic disease?
Delayed passage of meconium, bloody stools, severe abdominal distension, abnormal neurologic exam.
222
What is the initial management of functional constipation?
**✅ 1. Education & Reassurance**
Explain it's common and treatable
Normalize the condition to reduce fear
**✅ 2. Disimpaction (if needed)**
Oral polyethylene glycol (PEG) is first-line
Alternatives: high-dose lactulose, rectal enema
**✅ 3. Maintenance Therapy*
Daily PEG or lactulose at lower dose
Continue for at least 2–3 months
✅ 4. Dietary & Lifestyle Changes
Increase fiber and fluids
Encourage regular toilet sitting after meals
223
What medications are used to treat constipation in children?
Polyethylene glycol (PEG), lactulose, mineral oil, senna (stimulant laxative).
224
What is functional abdominal pain (FAP)?
Chronic recurrent abdominal pain without identifiable organic cause.
225
What are features suggesting FAP rather than organic disease?
**✅ 1. Education & Reassurance**
Explain it's common and treatable
Normalize the condition to reduce fear
**✅ 2. Disimpaction (if needed)**
Oral polyethylene glycol (PEG) is first-line
Alternatives: high-dose lactulose, rectal enema
**✅ 3. Maintenance Therapy**
Daily PEG or lactulose at lower dose
Continue for at least 2–3 months
**✅ 4. Dietary & Lifestyle Changes**
Increase fiber and fluids
Encourage regular toilet sitting after meals
226
What is irritable bowel syndrome (IBS)?
Chronic abdominal pain/discomfort associated with altered bowel habits (diarrhea and/or constipation).
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What are the subtypes of IBS?
IBS with constipation (IBS-C), IBS with diarrhea (IBS-D), mixed IBS (IBS-M).
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What is the Rome IV criteria for diagnosing IBS?
Abdominal pain ≥4 days/month associated with defecation changes or altered stool form/frequency.
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What role does psychosocial stress play in IBS?
Psychological factors can exacerbate IBS symptoms; stress management is important.
230
What is functional dyspepsia?
Epigastric discomfort not explained by structural abnormalities; meal-related or independent.
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What are symptoms of functional dyspepsia?
Postprandial fullness, early satiety, epigastric pain or burning.
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What is cyclic vomiting syndrome (CVS)?
Recurrent stereotypical episodes of intense vomiting separated by symptom-free periods.
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What are features of cyclic vomiting syndrome?
Sudden onset vomiting lasting hours to days, often predictable pattern.
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What are possible triggers for CVS episodes?
Infections, stress, excitement, certain foods (e.g., chocolate, cheese).
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What is the management of CVS?
Supportive care, antiemetics, migraine prophylaxis (e.g., cyproheptadine, propranolol).
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What is rumination syndrome?
Repetitive, effortless regurgitation and rechewing of food without nausea or retching.
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What are features of rumination syndrome?
Occurs during or after meals, disappears during sleep, absence of weight loss.
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What is aerophagia?
Excessive air swallowing leading to abdominal distension and belching.
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What are features of aerophagia?
Abdominal bloating, belching, audible air movement in esophagus.
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What is abdominal migraine?
Migraine variant presenting with episodic abdominal pain, nausea, and vomiting in children.
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What is malabsorption?
Impaired nutrient digestion or absorption in the gastrointestinal tract.
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What are common causes of malabsorption in children?
Celiac disease, cystic fibrosis, lactose intolerance, short bowel syndrome, infections.
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What are clinical features of malabsorption?
Chronic diarrhea, steatorrhea, weight loss, growth failure, vitamin deficiencies.
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What laboratory tests are used to evaluate malabsorption?
Stool fat analysis, fecal elastase, serum albumin, iron studies, vitamin levels.
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What is lactose intolerance?
Deficiency of lactase enzyme leading to carbohydrate malabsorption.
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What are symptoms of lactose intolerance?
Bloating, diarrhea, abdominal cramps, flatulence after lactose ingestion.
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How is lactose intolerance diagnosed?
✅ 1. Clinical trial – Symptoms improve with lactose-free diet
✅ 2. Hydrogen breath test – ↑ hydrogen after lactose = positive
✅ 3. Stool test (infants) – Acidic pH + reducing substances
✅ 4. Lactose tolerance test – Low rise in blood glucose after lactose
✅ 5. Biopsy – Rare; shows low lactase levels
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What is the management of lactose intolerance?
Lactose-free diet, lactase enzyme supplements as needed.
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What is cow’s milk protein allergy (CMPA)?
Immune-mediated reaction to proteins in cow's milk.
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What are types of CMPA?
IgE-mediated (immediate) and non-IgE-mediated (delayed) types.
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What are symptoms of CMPA?
Vomiting, diarrhea, blood in stool, eczema, wheezing.
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How is CMPA diagnosed?
Clinical history, elimination diet, specific IgE testing, food challenge.
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What is the treatment for CMPA?
Avoidance of cow's milk proteins; use of extensively hydrolyzed or amino acid formulas.
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What is short bowel syndrome (SBS)?
Condition resulting from significant resection of small intestine causing malabsorption.
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What are consequences of SBS?
Nutrient deficiencies, dehydration, diarrhea, failure to thrive.
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What is tropical sprue?
Chronic diarrheal illness due to small intestinal infection (possibly bacterial) in tropical regions.
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How does tropical sprue present?
Watery diarrhea, weight loss, megaloblastic anemia; history of residence in endemic areas.
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What is Whipple’s disease?
Rare systemic infection by Tropheryma whipplei causing malabsorption and arthropathy.
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What is protein-losing enteropathy?
Loss of serum proteins into the GI tract leading to hypoalbuminemia.
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What are causes of protein-losing enteropathy?
Congenital lymphangiectasia, IBD, intestinal lymphoma, infections.
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What is abetalipoproteinemia?
Rare inherited disorder with absence of apolipoprotein B leading to fat malabsorption.
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What is the characteristic finding in abetalipoproteinemia?
Acanthocytosis (spur cells) on blood smear, fat-soluble vitamin deficiency.
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What is the treatment for abetalipoproteinemia?
High-dose fat-soluble vitamins, low-fat diet supplemented with medium-chain triglycerides.
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What are common causes of infectious diarrhea in children?
Viruses (rotavirus, norovirus), bacteria (Salmonella, Shigella, E. coli), parasites (Giardia, Entamoeba).
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What viruses are commonly responsible for viral gastroenteritis?
Rotavirus, norovirus, adenovirus, astrovirus.
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What bacteria are associated with bacterial gastroenteritis?
Salmonella, Shigella, Campylobacter, pathogenic E. coli, Yersinia.
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What parasites cause infectious diarrhea in children?
Giardia lamblia, Entamoeba histolytica, Cryptosporidium.
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What are signs of severe dehydration in pediatric diarrhea?
Sunken eyes, lethargy, poor skin turgor, prolonged capillary refill, tachycardia.
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What is the first-line management of acute gastroenteritis?
Rehydration (oral or IV), continued feeding, zinc supplementation.
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What is the role of oral rehydration therapy (ORT)?
Restores fluid and electrolyte balance safely and effectively in most children with mild-moderate dehydration.
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When are IV fluids indicated in gastroenteritis?
Severe dehydration, shock, inability to tolerate oral fluids.
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What are red flags indicating serious bacterial infection in gastroenteritis?
High fever, bloody stools, toxic appearance, severe abdominal pain.
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When should antibiotics be used in diarrhea?
Confirmed or strongly suspected invasive bacterial diarrhea (e.g., Shigella, cholera, typhoid).
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What is the causative agent of cholera?
Vibrio cholerae.
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What is the clinical presentation of cholera?
Profuse 'rice water' stools, vomiting, severe dehydration.
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What is the treatment for cholera?
Aggressive rehydration, antibiotics (azithromycin or doxycycline).
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What is typhoid fever?
Systemic bacterial infection caused by Salmonella Typhi.
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What organism causes typhoid fever?
Salmonella enterica serovar Typhi.
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What are clinical features of typhoid fever?
Prolonged fever, abdominal pain, rose spots rash, hepatosplenomegaly, constipation or diarrhea.
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What is the diagnosis of typhoid fever?
Blood culture (gold standard), Widal test (limited utility).
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What is the treatment of typhoid fever?
Antibiotics: ceftriaxone, azithromycin, or fluoroquinolones (based on sensitivity).
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What are complications of untreated typhoid fever?
Intestinal perforation, hemorrhage, encephalopathy.
283
What is amebiasis?
Infection by Entamoeba histolytica causing colitis or liver abscess.
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What are clinical manifestations of amebiasis?
Bloody diarrhea, abdominal pain, fever; liver abscess with right upper quadrant pain.
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How is amebiasis diagnosed?
Stool microscopy, antigen detection, PCR, serology for liver abscess.
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What is the treatment of amebiasis?
Metronidazole followed by a luminal agent (paromomycin).
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What is giardiasis?
Infection by Giardia lamblia causing small intestinal malabsorption.
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What are symptoms of giardiasis?
Chronic diarrhea, steatorrhea, weight loss, bloating.
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How is giardiasis diagnosed?
Stool antigen test, stool microscopy, PCR.
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What is tropical sprue?
Chronic diarrheal syndrome endemic to tropical regions associated with small bowel injury.
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What infections can cause tropical sprue?
Possible bacterial overgrowth (Enterobacteriaceae, Hemophilus).
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What is ascariasis?
Infection with Ascaris lumbricoides (intestinal roundworm).
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What are complications of heavy ascariasis infection?
Intestinal obstruction, biliary obstruction, pancreatitis, malnutrition.
294
What is celiac disease?
An autoimmune disorder triggered by gluten in genetically susceptible individuals, causing small intestinal mucosal damage (villous atrophy).
295
What are Cause & Genetics of celiac disease?
Trigger: Gluten (wheat, barley, rye). Genetics: HLA-DQ2 (95%) or HLA-DQ8 (5%).
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What are Classical Symptoms of celiac disease?
Chronic diarrhea, abdominal distension, failure to thrive, irritability, muscle wasting.
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What are Atypical / Extraintestinal Features of celiac disease?
Short stature, iron-deficiency anemia, delayed puberty, dental enamel defects, dermatitis herpetiformis.
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What is Screening of celiac disease?
First-line: IgA anti-tTG. Check total IgA. If IgA deficient → IgG DGP (deamidated gliadin peptide antibodies)
.
299
What is Confirmatory Diagnosis of celiac disease?
Duodenal biopsy: villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes. ESPGHAN: biopsy may be skipped if tTG >10x + EMA + HLA positive.
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What is Treatment of celiac disease?
Strict lifelong gluten-free diet. Avoid wheat, barley, rye. Monitor nutrition and growth.
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How is Monitoring of celiac disease?
Track symptom resolution, anti-tTG IgA titers, growth parameters, iron, calcium, vitamin D.
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What Complications of celiac disease?
Growth failure, osteopenia/osteoporosis, delayed puberty, infertility, enteropathy-associated T-cell lymphoma.
303
What Classical Type of celiac disease?
GI symptoms predominate (diarrhea, FTT). Seen in infants and toddlers.
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What Atypical Type of celiac disease?
Extraintestinal signs dominate (anemia, short stature). Common in older children.
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What Silent Type of celiac disease?
No symptoms. Positive serology and abnormal biopsy. Found via screening.
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What Potential Type of celiac disease?
Positive antibodies but normal biopsy. No treatment unless symptoms develop. Monitor regularly.
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What Refractory Type of celiac disease?
Persistent symptoms despite >12 months of gluten-free diet. Rule out poor compliance or other pathology. Rare in children.
308
What Latent Type of celiac disease?
Normal biopsy currently but genetically predisposed (HLA-DQ2/8). May develop disease later.
309
Which regions of the GI tract are involved in Crohn’s disease vs Ulcerative Colitis?
CD: Any part of GI tract (mouth to anus), often terminal ileum; UC: Limited to colon and rectum.
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Describe the pattern of inflammation in CD and UC.
CD: Transmural, segmental (skip lesions); UC: Mucosal, continuous from rectum proximally.
311
Which pediatric IBD is more associated with perianal disease?
Crohn’s disease—fissures, fistulas, abscesses, skin tags.
312
Which disease is more likely to present with bloody diarrhea in pediatrics?
Ulcerative colitis.
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What is the typical age of presentation in pediatric Crohn’s vs UC?
CD: Often 10–20 years; UC: Slightly older, 11–20 years.
314
What are common constitutional symptoms in CD but less so in UC?
Weight loss, fatigue, and growth failure are more prominent in CD.
315
Which IBD subtype is more associated with upper GI symptoms like mouth ulcers or esophageal involvement?
Crohn’s disease.
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What is the typical histologic hallmark of Crohn’s disease?
Non-caseating granulomas (found in ~30%).
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Describe the endoscopic findings typical of UC.
Continuous mucosal erythema, granularity, friability, pseudopolyps, loss of vascular markings.
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What are the classic endoscopic findings in CD?
Cobblestoning, deep linear ulcers, skip lesions, aphthous ulcers.
319
Which IBD subtype shows “lead pipe” colon on barium enema?
Ulcerative colitis—due to loss of haustra.
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What are common complications of Crohn’s disease not typically seen in UC?
Fistulae, strictures, abscesses, and bowel obstruction.
321
Which IBD subtype is curable by total colectomy?
Ulcerative colitis.
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Which subtype carries a higher risk of colorectal carcinoma?
UC (especially pancolitis >10 years); CD risk increases with colonic involvement.
323
Which nutritional deficiencies are more common in CD?
Iron, B12, folate, fat-soluble vitamins (A, D, E, K), zinc.
324
Which serologic marker is more specific for Crohn’s disease?
Anti-Saccharomyces cerevisiae antibodies (ASCA).
325
Which serologic marker is more associated with UC?
Perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA).
326
What is the preferred imaging for small bowel evaluation in CD?
MR enterography.
327
What is the mainstay for inducing remission in mild UC?
Oral or rectal 5-ASA (5-Aminosalicylic Acid) (mesalamine).
328
What is first-line treatment for moderate-severe pediatric CD?
Corticosteroids + immunomodulators or biologics (e.g., infliximab).
329
What is the recommended treatment for perianal fistulizing Crohn’s disease?
Biologics (anti-TNF agents like infliximab or adalimumab).
330
Which subtype has a higher incidence of extraintestinal manifestations (EIMs)?
Both can have EIMs, but PSC is more associated with UC; growth failure more with CD.
331
Which IBD subtype is associated with primary sclerosing cholangitis (PSC)?
Ulcerative colitis.
332
What is the typical growth pattern in pediatric UC vs CD?
CD: Growth failure common; UC: Growth typically preserved unless severe disease.
333
What role does exclusive enteral nutrition (EEN) play in pediatric CD?
EEN is effective for induction of remission in mild-moderate CD.
334
Can EEN be used in UC?
No clear benefit; it’s specific to Crohn’s disease.
335
How does the response to corticosteroids differ between CD and UC?
Both respond, but UC may be more corticosteroid-sensitive initially.
336
Which IBD subtype is more likely to present with nocturnal diarrhea?
Ulcerative colitis.
337
What is the relapse pattern in CD vs UC?
CD: Relapsing-remitting with complications; UC: Relapse with mucosal symptoms.
338
What is the most common presenting symptom in pediatric CD?
Abdominal pain, often in RLQ.
339
What is the most common presenting symptom in pediatric UC?
Bloody diarrhea and urgency.
340
How does fecal calprotectin help in pediatric IBD?
Elevated in both UC and CD; useful for screening and monitoring inflammation.
341
When is colonoscopy indicated in suspected pediatric IBD?
To confirm diagnosis, evaluate extent, and obtain biopsies.
342
Which IBD subtype is associated with granulomatous appendicitis?
Crohn’s disease.
343
What imaging findings suggest CD over UC in pediatric patients?
Bowel wall thickening, comb sign, mesenteric fat creeping, strictures.
344
Which IBD subtype is more often associated with iron deficiency anemia in children?
Both can cause it, but more severe and chronic in Crohn’s due to malabsorption and bleeding.
345
What is the best predictor of long-term growth in pediatric IBD?
Disease control, especially in Crohn’s.
346
What is the long-term effect of IBD on puberty in pediatric patients?
Delayed puberty, especially in Crohn’s.
347
What is the risk of surgical recurrence after bowel resection in CD vsUC?
CD: High risk of recurrence; UC: Colectomy is usually curative
348
How does psychosocial impact differ in pediatric CD and UC?
CD tends to have greater impact due to more systemic illness, growth issues, and surgery risk.
