Gastroenterology Flashcards

1
Q

Intussusception

How do you Dx - ileoileal intussusception?

A

Ileoileal intussusception is best demonstrated by abdominal ultrasonography

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2
Q

Intussusception

What are risk factors for - ileoileal intussusception?

A

Risk factors after bowel surgery and Henoch-Schönlein purpura

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3
Q

Intussusception

How do you Rx - ileoileal intussusception?

A

Rx - ileoileal intussusception Reduction by instillation of contrast agents, saline, or air might not be possible. If manual operative reduction is impossible or the bowel is not viable, resection of the intussusception is necessary, with end-to-end anastomosis

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4
Q

Liver transplantation

What are the diseases for which liver transplantation is indicated?

A

Diseases indicating liver transplantation

  1. Liver structure: a. Obstructive biliary tract disease: b. Intrahepatic cholestasis: c. Primary liver tumors:
  2. Metabolic disorders:
  3. Hepatitis: a.Acute hepatitis: b.Chronic hepatitis:
  4. Other: a. Miscellaneous: b. Emerging indications:
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5
Q

Intussusception

What is the success rate of hydrostatic reduction?

A

80-95% in patients with ileocolic intussusception (Nelsons)

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6
Q

Intussusception

What is the bowel perforation rate in hydrostatic reductions?

A

0.5-2.5%

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7
Q

Intussusception

What is the bowel perforation rate in air reductions?

A

0.1-0.2%.

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8
Q

Intussusception

What are the indications for Surgical reduction of intussusception?

A

a) refractory shock,
b) suspected bowel necrosis or perforation,
c) peritonitis
d) multiple recurrences (suspected lead point)

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9
Q

Intussusception

What are the contraindications to using air enema?

A

a) prolonged intussusception with signs of shock
b) peritoneal irritation,
c) intestinal perforation or pneumatosis intestinalis

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10
Q

Intussusception

What are the indications for Surgery for intussusception?

A

●Unstable patient – In this case, initiate resuscitation, consult surgeon, and stabilize the patient before proceeding to the operating room.

●Peritonitis or intestinal perforation.

●Nonoperative reduction is completely unsuccessful. If the reduction attempt was partially successful, it may be repeated.

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11
Q

Intussusception

How frequently does Spontaneous reduction of intussusception occur?

A

4-10% of patients

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12
Q

Intussusception

What is the prognosis for intussusception?

A

Untreated intussusception in infants is usually fatal

Most infants recover if reduced in the 1st 24 hr (mortality rate higher > 24 hrs)

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13
Q

Intussusception

What is the recurrence rate after reduction (air/hydrostatic) of intussusception?

A

10%

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14
Q

Intussusception

What is the recurrence rate after surgical reduction of intussusception?

A

2-5% Most recurrences occur within 72 hr of reduction. Corticosteroids may reduce the frequency of recurrent intussusception.

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15
Q

A1AT

What causes α1-Antitrypsin deficiency?

A

Mutation in the SERPINA1 gene and it is an autosomal recessive disorder.

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16
Q

A1AT

What is the role for α1-Antitrypsin?,

A

It is a protease inhibitor synthesized by the liver Protects lung alveolar tissues from destruction by neutrophil elastase

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17
Q

A1AT

What are the important alleles of the protease inhibitor?

A

The most common allele of the protease inhibitor (Pi) system is M, and the normal phenotype is PiMM. The Z allele predisposes to clinical deficiency; patients with liver disease are usually PiZZ homozygotes and have serum α1-antitrypsin levels <2 mg/mL (∼10-20% of normal). The incidence of the PiZZ genotype in the white population is estimated at 1 in 2,000-4,000 live births.

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18
Q

A1AT

What is the importance of Compound heterozygotes of the protease inhibitor?

A

PiZ-, PiSZ, PiZI are not a cause of liver disease alone but can act as modifier genes, increasing the risk of progression in other liver disease such as nonalcoholic fatty liver disease and hepatitis C.

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19
Q

A1AT

How do you Dx A1AT?

A
  1. Serum immunoassay measures low levels of α1-AT; normal serum levels are 150-350 mg/dL. PiZZ homozygotes and have A1AT levels <2 mg/mL (∼10-20% of normal)…or < 2g/L
  2. Serum electrophoresis reveals the phenotype (PiZZ), and genotype is determined by polymerase chain reaction.
  3. Radiology: a. CXR: In the rare patient with lung disease in adolescence, CXR reveals overinflation with depressed diaphragms. b. Chest CT can show more hyperexpansion in the lower lung zones, with occasional bronchiectasis; CT densitometry can be a sensitive method to follow changes in lung disease.
  4. Lung function testing is usually normal in children, but it can show airflow obstruction and increased lung volumes, particularly in adolescents who smoke
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20
Q

Malabsorption

What stool tests do you order in child with suspected malabsorbtion?

A
  1. history and physical examination.
  2. stool a.Infection: cultures and antibody tests for parasites, stool microscopy for ova and parasites such as Giardia, and b. inflammatory disorders: stool occult blood and leukocytes to exclude c. carbohydrate malabsorption: pH and reducing substances for, and d. Fat: quantitative stool fat examination e. protein malabsorption: α1-antitrypsin f. exocrine pancreatic insufficiency: Fecal stool elastase-1 can determine
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21
Q

Malabsorption

What blood tests do you order in child with suspected malabsorbtion?

A
  1. CBC + smear for microcytic anemia, lymphopenia (lymphangiectasia), neutropenia (Shwachman syndrome), and acanthocytosis (abetalipoproteinemia) is useful.
  2. If celiac disease is suspected, serum immunoglobulin (Ig) A and tissue transglutaminase (TG2) antibody levels should be determined
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22
Q

Malabsorption

What are the causes of low albumin in blood?

A
  • Nephrotic syndrome
  • Liver disease
  • protein-losing enteropathy
  • inadequate protein intake
  • extensive skin disorder
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23
Q

Malabsorption

What stool tests do you order in child with suspected malabsorbtion?

A

Measurement of stool α1-antitrypsin - screening test for protein-losing enteropathy (it is resistant to digestion in the (GI) tract). …Excessive α1-antitrypsin excretion in the stool should prompt further investigations to identify the specific cause of gut or stomach (Menetrier disease) protein loss.

24
Q

Alagille

What are the most common ocular abnormalities in patients with Alagille Syndrome?

A
  • posterior embryotoxon (95%)
  • iris abnormalities (45%),
  • diffuse fundus hypopigmentation (57%)
  • speckling of the retinal pigment epithelium (33%)
  • optic disc anomalies (76%)
25
Q

GERD

How do you Dx typical GERD?

A

thorough history and physical examination suffice to reach the diagnosis. Hx identifies +vs for GERD, its Cplxns and the -vs The Hx may use by questionnaires – Infant-IGERQ

26
Q

GERD

Red flag Symptoms?

A
  • bilious emesis,
  • frequent projectile emesis,
  • gastrointestinal bleeding, l
  • ethargy,
  • organomegaly,
  • abdominal distension,
  • micro- or macrocephaly,
  • hepatosplenomegaly,
  • failure to thrive,
  • diarrhea,
  • fever,
  • bulging fontanelle, and
  • seizures.
27
Q

GERD

What are the important differential diagnoses to consider in GERD?

A
  • milk and other food allergies,
  • eosinophilic esophagitis,
  • pyloric stenosis,
  • intestinal obstruction (especially malrotation with intermittent volvulus),
  • nonesophageal inflammatory diseases,
  • infections,
  • inborn errors of metabolism,
  • hydronephrosis,
  • increased intracranial pressure,
  • rumination, and
  • bulimia.
28
Q

GERD

What are the indications for esophageal pH monitoring?

A
  • assessing efficacy of acid suppression during treatment,
  • evaluating apneic episodes with a CXR and perhaps
  • impedance evaluating atypical GERD presentations - chronic cough, stridor, and asthma.
29
Q

GERD

What are the limitations of the pH monitoring?

A
  • Normal values of distal esophageal acid exposure (pH < 4) are generally established as <5-8% of the total monitored time
  • These quantitative normals are insufficient to establish or disprove a diagnosis of pathologic GERD.
30
Q

GERD

How do Dual pH probes work?

A

Dual pH probes, adding a proximal esophageal probe to the standard distal one, are used in the diagnosis of extraesophageal GERD, identifying upper esophageal acid exposure times of 1% of the total time as threshold values for abnormality

31
Q

GERD

When is barium indicated?

A

Hx of vomiting and dysphagia to evaluate for achalasia, esophageal strictures and stenosis, hiatal hernia gastric outlet or intestinal obstruction

32
Q

GERD

What are the indications for endoscopy in GERD?

A

allows diagnosis of erosive esophagitis and complications such as strictures or Barrett esophagus; esophageal biopsies can eliminate allergic and infectious causes. used therapeutically to dilate reflux-induced strictures

33
Q

GERD

Infantile reflux

A
  • regurgitation (especially postprandially),
  • signs of esophagitis (irritability, arching, choking, gagging, feeding aversion)
  • resulting failure to thrive;
34
Q

GERD

Progx:

A

symptoms resolve spontaneously in the majority of infants by 12-24 mo.

35
Q

GERD

Older children

A
  • regurgitation during the preschool years; this complaint diminishes somewhat as children age
  • abdominal and chest pain in later childhood and adolescence.
  • Occasional children present with food refusal or neck contortions (arching, turning of head) designated Sandifer syndrome.

The respiratory presentations are also age dependent:

36
Q

GERD

GERD in infants can manifest with the following respiratory Sx

A
  • obstructive apnea or as stridor or lower airway disease in which reflux complicates primary airway disease such as laryngomalacia or bronchopulmonary dysplasia.
  • Otitis media, sinusitis, lymphoid hyperplasia, hoarseness, vocal cord nodules, and laryngeal edema have all been associated with GERD.
37
Q

GERD

Airway manifestations in older children are more commonly related to

A

asthma or to otolaryngologic disease such as laryngitis or sinusitis. Despite the high prevalence of GERD symptoms in asthmatic children, data showing direction of causality are conflicting.

38
Q

Alagilles

What are the features of Alagilles Syndrome?

A

triangular facies, frontal bossing

Eyes: posterior embryotoxin

Cholestatic neonatal jaundice butterfly vtb, heart murmur

39
Q

Abdominal Pain

What is the most likely cause of childhood functional abdominal pain?

A

Visceral hypersensitivity and motility disturbances (decreased)

40
Q

FB esophagus

What are the risk factors for foreign-body ingestions?

A

80% in children between 6 mo and 3 yr of age.

Older children - developmental delays + psychiatric disorders

41
Q

FB esophagus

What are the risks of foreign-body in esophagus ?

A

perforation and sepsis.

42
Q

FB esophagus

What are the items of foreign-body in esophagus ?

A

Coins and small toy items commonly Food impactions – - eosinophilic esophagitis, -repair of esophageal atresia and Nissen fundoplication.

43
Q

FB esophagus

Where are foreign-bodies in esophagus located?

A
  • most - cricopharyngeus (upper esophageal sphincter),
  • aortic arch - just superior to the diaphragm at the gastroesophageal junction (lower esophageal sphincter)
44
Q

FB esophagus

How do you Inv for FB in esophagus?

A

-AP Xray neck, chest, and abdomen + Lat views of the neck and chest

45
Q

FB esophagus

What is the picture of coins in esophagus on AP and Lat Xrays?

A

The flat surface of a coin in the esophagus AP edge on the lateral view

46
Q

FB esophagus

What is the picture of coins in trachea on AP and Lat Xrays?

A

The edge of a coin in the trachea on AP The flat surface edge on the lateral view

47
Q

FB esophagus

How are different Esophageal FB managed?

A
  1. Sharp FB’s, disk button batteries, FB’s with Resp Sx’s -urgent removal. Button (disk) batteries, in particular, must be expediently removed because they can induce mucosal injury in as little as 1 hr of contact time and involve all esophageal layers within 4 hr
  2. Asymptomatic blunt objects and coins can be observed for up to 24 hr in anticipation of passage into the stomach.
  3. Meat impactions with no problems in handling secretions, can be observed for up to 12 hrs
48
Q

FB esophagus

How do you manage an emergency with coin ingestion in esophagus?

A
  • assess risk for airway compromise
  • chest CT scan and surgical consultation in cases of suspected airway perforation
49
Q

Lactose intolerance

What causes Secondary lactose intolerance?

A

follows small bowel mucosal damage (celiac disease, rotavirus infection) and is usually transient, improving with mucosal healing.

50
Q

Lactose intolerance

How do you Dx Lactase deficiency?

A

-H2-breath test -measurement of lactase activity in mucosal tissue retrieved by small bowel biopsy. N.B. Diagnostic testing is not mandatory, and often simple dietary changes that reduce or eliminate lactose from the diet relieve symptoms.

51
Q

Lactose intolerance

How do you rx Secondary lactose intolerance?

A
  • milk-free diet. A lactose-free formula (based on either soy or cow’s milk) can be used in infants.
  • In older children, low-lactose milk can be consumed.
  • Addition of lactase to dairy products usually abbreviates the symptoms.
  • Live-culture yogurt contains bacteria that produce lactase enzymes and is therefore tolerated in most patients with lactase deficiency.
  • Hard cheeses have a small amount of lactose and are generally well tolerated.
52
Q

Constipation

How do you define constipation?

A
  1. Constipation is defined as a delay or difficulty in defecation present for 2 wk or longer and significant enough to cause distress to the patient.
  2. Another approach to the definition is the Rome Criteria
53
Q

Constipation

What are the triggers for constipation?

A
  1. change from human milk to cow’s milk, secondary to the change in the protein and carbohydrate ratio or an allergy to cow’s milk.
  2. In toddlers- early toilet training that can initiate stool retention.
  3. In older children, retentive constipation when stooling is inconvenient such as school.
54
Q

Constipation

What is the Chronic Constipation: Rome III Criteria for infants and toddlers?

A
55
Q

Constipation

What is the Chronic Constipation: Rome III Criteria for children of developmental age 4-18?

A
56
Q

Constipation

What tests, in addition to those ruling out Hirschsprung disease, are commonly considered for refractory cases of constipation?

A
  • BLOOD: serum calcium, thyroid-stimulating hormone, lead, and

celiac disease panel.

  • A sweat test might be considered.
  • MRI spine to rule out spina bifida occulta or tethered cord
  • Anorectal manometry can help diagnose a motility disorder.