GIT Flashcards
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?
Triple therapy: PPI + amoxicillin + clarithromycin for 10–14 days.
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?
Telescoping of one segment of bowel into another causing obstruction and ischemia.
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?
Parental reassurance, soothing techniques, trial of hypoallergenic formula if needed.
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?
Disimpaction (oral PEG or enemas), maintenance therapy (laxatives), behavioral interventions.
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?
Normal growth, no weight loss, pain unrelated to meals or bowel movements, normal physical exam.
226
What is irritable bowel syndrome (IBS)?
Chronic abdominal pain/discomfort associated with altered bowel habits (diarrhea and/or constipation).
227
What are the subtypes of IBS?
IBS with constipation (IBS-C), IBS with diarrhea (IBS-D), mixed IBS (IBS-M).
228
What is the Rome IV criteria for diagnosing IBS?
Abdominal pain ≥4 days/month associated with defecation changes or altered stool form/frequency.
229
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.
231
What are symptoms of functional dyspepsia?
Postprandial fullness, early satiety, epigastric pain or burning.
232
What is cyclic vomiting syndrome (CVS)?
Recurrent stereotypical episodes of intense vomiting separated by symptom-free periods.
233
What are features of cyclic vomiting syndrome?
Sudden onset vomiting lasting hours to days, often predictable pattern.
234
What are possible triggers for CVS episodes?
Infections, stress, excitement, certain foods (e.g., chocolate, cheese).
235
What is the management of CVS?
Supportive care, antiemetics, migraine prophylaxis (e.g., cyproheptadine, propranolol).
236
What is rumination syndrome?
Repetitive, effortless regurgitation and rechewing of food without nausea or retching.
237
What are features of rumination syndrome?
Occurs during or after meals, disappears during sleep, absence of weight loss.
238
What is aerophagia?
Excessive air swallowing leading to abdominal distension and belching.
239
What are features of aerophagia?
Abdominal bloating, belching, audible air movement in esophagus.
240
What is abdominal migraine?
Migraine variant presenting with episodic abdominal pain, nausea, and vomiting in children.
241
What is malabsorption?
Impaired nutrient digestion or absorption in the gastrointestinal tract.
242
What are common causes of malabsorption in children?
Celiac disease, cystic fibrosis, lactose intolerance, short bowel syndrome, infections.
243
What are clinical features of malabsorption?
Chronic diarrhea, steatorrhea, weight loss, growth failure, vitamin deficiencies.
244
What laboratory tests are used to evaluate malabsorption?
Stool fat analysis, fecal elastase, serum albumin, iron studies, vitamin levels.
245
What is celiac disease?
An autoimmune disorder triggered by gluten ingestion causing small intestinal mucosal damage.
246
What triggers celiac disease?
Ingestion of gluten (wheat, barley, rye) in genetically predisposed individuals (HLA-DQ2/DQ8).
247
What are classical features of celiac disease?
Chronic diarrhea, failure to thrive, abdominal distension, irritability.
248
What are atypical features of celiac disease?
Iron deficiency anemia, short stature, delayed puberty, dental enamel defects.
249
What serologic tests are used for celiac disease?
Anti-tissue transglutaminase (tTG) IgA, total IgA; anti-endomysial antibody (EMA).
250
What is the role of small bowel biopsy in celiac disease?
Confirms diagnosis showing villous atrophy, crypt hyperplasia, intraepithelial lymphocytes.
251
What is the treatment for celiac disease?
Strict lifelong gluten-free diet.
252
What is lactose intolerance?
Deficiency of lactase enzyme leading to carbohydrate malabsorption.
253
What are symptoms of lactose intolerance?
Bloating, diarrhea, abdominal cramps, flatulence after lactose ingestion.
254
How is lactose intolerance diagnosed?
Hydrogen breath test, lactose elimination trial.
255
What is the management of lactose intolerance?
Lactose-free diet, lactase enzyme supplements as needed.
256
What is cow’s milk protein allergy (CMPA)?
Immune-mediated reaction to proteins in cow's milk.
257
What are types of CMPA?
IgE-mediated (immediate) and non-IgE-mediated (delayed) types.
258
What are symptoms of CMPA?
Vomiting, diarrhea, blood in stool, eczema, wheezing.
259
How is CMPA diagnosed?
Clinical history, elimination diet, specific IgE testing, food challenge.
260
What is the treatment for CMPA?
Avoidance of cow's milk proteins; use of extensively hydrolyzed or amino acid formulas.
261
What is short bowel syndrome (SBS)?
Condition resulting from significant resection of small intestine causing malabsorption.
262
What are consequences of SBS?
Nutrient deficiencies, dehydration, diarrhea, failure to thrive.
263
What is tropical sprue?
Chronic diarrheal illness due to small intestinal infection (possibly bacterial) in tropical regions.
264
How does tropical sprue present?
Watery diarrhea, weight loss, megaloblastic anemia; history of residence in endemic areas.
265
What is Whipple’s disease?
Rare systemic infection by Tropheryma whipplei causing malabsorption and arthropathy.
266
What is protein-losing enteropathy?
Loss of serum proteins into the GI tract leading to hypoalbuminemia.
267
What are causes of protein-losing enteropathy?
Congenital lymphangiectasia, IBD, intestinal lymphoma, infections.
268
What is abetalipoproteinemia?
Rare inherited disorder with absence of apolipoprotein B leading to fat malabsorption.
269
What is the characteristic finding in abetalipoproteinemia?
Acanthocytosis (spur cells) on blood smear, fat-soluble vitamin deficiency.
270
What is the treatment for abetalipoproteinemia?
High-dose fat-soluble vitamins, low-fat diet supplemented with medium-chain triglycerides.
271
What are common causes of infectious diarrhea in children?
Viruses (rotavirus, norovirus), bacteria (Salmonella, Shigella, E. coli), parasites (Giardia, Entamoeba).
272
What viruses are commonly responsible for viral gastroenteritis?
Rotavirus, norovirus, adenovirus, astrovirus.
273
What bacteria are associated with bacterial gastroenteritis?
Salmonella, Shigella, Campylobacter, pathogenic E. coli, Yersinia.
274
What parasites cause infectious diarrhea in children?
Giardia lamblia, Entamoeba histolytica, Cryptosporidium.
275
What are signs of severe dehydration in pediatric diarrhea?
Sunken eyes, lethargy, poor skin turgor, prolonged capillary refill, tachycardia.
276
What is the first-line management of acute gastroenteritis?
Rehydration (oral or IV), continued feeding, zinc supplementation.
277
What is the role of oral rehydration therapy (ORT)?
Restores fluid and electrolyte balance safely and effectively in most children with mild-moderate dehydration.
278
When are IV fluids indicated in gastroenteritis?
Severe dehydration, shock, inability to tolerate oral fluids.
279
What are red flags indicating serious bacterial infection in gastroenteritis?
High fever, bloody stools, toxic appearance, severe abdominal pain.
280
When should antibiotics be used in diarrhea?
Confirmed or strongly suspected invasive bacterial diarrhea (e.g., Shigella, cholera, typhoid).
281
What is the causative agent of cholera?
Vibrio cholerae.
282
What is the clinical presentation of cholera?
Profuse 'rice water' stools, vomiting, severe dehydration.
283
What is the treatment for cholera?
Aggressive rehydration, antibiotics (azithromycin or doxycycline).
284
What is typhoid fever?
Systemic bacterial infection caused by Salmonella Typhi.
285
What organism causes typhoid fever?
Salmonella enterica serovar Typhi.
286
What are clinical features of typhoid fever?
Prolonged fever, abdominal pain, rose spots rash, hepatosplenomegaly, constipation or diarrhea.
287
What is the diagnosis of typhoid fever?
Blood culture (gold standard), Widal test (limited utility).
288
What is the treatment of typhoid fever?
Antibiotics: ceftriaxone, azithromycin, or fluoroquinolones (based on sensitivity).
289
What are complications of untreated typhoid fever?
Intestinal perforation, hemorrhage, encephalopathy.
290
What is amebiasis?
Infection by Entamoeba histolytica causing colitis or liver abscess.
291
What are clinical manifestations of amebiasis?
Bloody diarrhea, abdominal pain, fever; liver abscess with right upper quadrant pain.
292
How is amebiasis diagnosed?
Stool microscopy, antigen detection, PCR, serology for liver abscess.
293
What is the treatment of amebiasis?
Metronidazole followed by a luminal agent (paromomycin).
294
What is giardiasis?
Infection by Giardia lamblia causing small intestinal malabsorption.
295
What are symptoms of giardiasis?
Chronic diarrhea, steatorrhea, weight loss, bloating.
296
How is giardiasis diagnosed?
Stool antigen test, stool microscopy, PCR.
297
What is tropical sprue?
Chronic diarrheal syndrome endemic to tropical regions associated with small bowel injury.
298
What infections can cause tropical sprue?
Possible bacterial overgrowth (Enterobacteriaceae, Hemophilus).
299
What is ascariasis?
Infection with Ascaris lumbricoides (intestinal roundworm).
300
What are complications of heavy ascariasis infection?
Intestinal obstruction, biliary obstruction, pancreatitis, malnutrition.
