GI Disorders Flashcards
2-5 yo patient, with early morning onset of vomiting attacks >4x in an hour for several hours, preceded by nausea, pallor, noise and light hypersensitivity, lethargy and headache. Attacks have occured more than 5 times in the past 6 mos, precipitated by infection, psychological or physical stress. Careful investigation in the past months ruled out any other cause of vomiting. Px appears well and asymptomatic in between attacks.
What is the probable diagnosis? What is the treatment for this condition?
cyclic vomiting
- Rome III criteria for fcnl GI disorders (FGID) (both must be present)
1. 2 or more periods of intense nausea and unremitting vomiting or retching lasting hours to days
2. return to usual state of health lasting weeks to months
Consensus definition:
• At least 5 attacks in any interval, or a minimum of 3 attacks during a 6-month period
• Episodic attacks of intense nausea and vomiting lasting 1hr to 10 days and occurring at least 1wk apart
• Stereotypical pattern and symptoms in the individual patient
• Vomiting during attacks occurs ≥4 times/hr for ≥1hr
• Return to baseline health between episodes
• Not attributed to another disorder
- tx: hydration and antiemetics, address complications of vomiting
A highly coordinated reflex process that may be preceded by increased salivation and begins with involuntary retching.
vomiting
- process is coordinated in the medullary vomiting center
What is the definition of acute and chronic diarrhea?
Acute: sudden onset of excessively loose stools of >10 ml/kg/day in infants or >200 g/day in older children, which lasts < 14 days
Chronic: >14 days
- Disorders that interfere with absorption in the small bowel tend to produce voluminous diarrhea, whereas disorders compromising colonic absorption produce lower-volume diarrhea
What are the more probable causes of true constipation in infancy?
Hirschsprung disease
intestinal pseudo-obstruction
hypothyroidism
Two types of nerve fibers transmit painful stimuli in the abdomen. Which pain fibers mediate the following:
- sharp, localized pain
- poorly localized, dull pain
- in skin and muscle - A fibers
2. from viscera, peritoneum, and muscle - C fibers
Acute epigastric and left upper quadrant pain radiating to the back, characterized as constant, sharp, and boring, accompanied by nausea, emesis, tenderness
probable diagnosis?
acute pancreatitis
Acute or gradual periumbilical to lower abdominal pain referred to the back, colicky in character (alternating cramping and painless periods), associated with distention, obstipation, emesis, and increased bowel sounds.
Probable diagnosis?
intestinal obstruction
Acute, sharp and steady periumbilical abdominal pain which localizes to lower right quadrant with generalized peritonitis, which may radiate to back or pelvis, accompanied by anorexia, nausea, emesis, local tenderness, and fever if with peritonitis.
probable diagnosis?
acute appendicitis
Acute periumbilical to lower abdominal pain, characterized as cramping with painless periods, associated with hematochezia, knees usually in pulled-up position
intussusception
Acute and sudden unilateral back pain with referral to the groin, characterized as sharp, intermittent and cramping, associated with hematuria
Probable diagnosis?
urolithiasis
Acute dull to sharp back pain with referral to the bladder associated with fever, CVA tenderness, dysuria and urinary frequency
probable diagnosis?
urinary tract infection
Red or maroon blood in stools, signifies either a distal bleeding site or massive hemorrhage above the distal ileum
a. hematemesis
b. hematochezia
c. melena
b. hematochezia
Moderate to mild bleeding from sites above the distal ileum or major hemorrhages in the duodenum and above tend to cause blackened stools of tarry consistency
a. hematemesis
b. hematochezia
c. melena
c. melena
What is the most common cause of bleeding in the GI tract?
Erosive damage to the mucosa
- variceal bleeding secondary to portal hypertension occurs often enough to require consideration
What are the specific diagnostic modalities utilized in the following cases:
a. UGIB
b. LGIB
c. small intestines
d. occult blood in stool
e. brisk intestinal bleeding of unknown location
a. UGIB - esophagogastroduodenoscooy (EGD)
b. LGIB - colonoscopy
c. small intestines - capsule endoscopy
d. occult blood in stool - guaiac test
e. unknown location of bleed - RBC scan
Prolonged elevation of the serum levels of conjugated bilirubin beyond the 1st 14 days of life
neonatal cholestasis
- Jaundice that appears after 2wk of age, progresses after this time, or does not resolve at this time should be evaluated and a conjugated bilirubin level determined
- mechanical obstruction of bile flow or functional impairment of hepatic excretory function and bile secretion
Idiopathic familial intrahepatic cholestasis associated with lymphedema of the lower extremities
Aagenaes syndrome
- relationship between liver disease and lymphedema is not understood
- Affected patients usually present with episodic cholestasis
Rare autosomal recessive genetic disorder marked by progressive degeneration of the liver and kidneys
Zellweger (cerebrohepatorenal) syndrome
- Affected infants have severe, generalized hypotonia and markedly impaired neurologic function with psychomotor retardation.
- fatal in 6-12 mos
the most common syndrome with intrahepatic bile duct paucity, marked reduction in the number of interlobular bile ducts in the portal triads, with normal-sized branches of portal vein and hepatic arteriole
Alagille syndrome (arteriohepatic dysplasia)
The most common form of biliary atresia, accounting for ∼85% of the cases
obliteration of the entire extrahepatic biliary tree at or above the porta hepatis
Ultrasonographic triangular cord (TC) sign, which represents a cone-shaped fibrotic mass cranial to the bifurcation of the portal vein, may be seen in patients with this condition
biliary atresia
The most valuable procedure in the evaluation of neonatal hepatobiliary diseases and provides the most reliable discriminatory evidence
Percutaneous liver biopsy
- Biliary atresia is characterized by bile ductular proliferation, the presence of bile plugs, and portal or perilobular edema and fibrosis, with the basic hepatic lobular architecture intact.
- In neonatal hepatitis, there is severe, diffuse hepatocellular disease, with distortion of lobular architecture, marked infiltration with inflammatory cells, and focal hepatocellular necrosis; the bile ductules show little alteration
What is the underlying mechanism in diarrhea caused by the ff agents: cholera toxin, ETEC, carcinoid, C. difficile
a. mucosal invasion
b. decreased surface area
c. decreased motility
d. increased motility
e. osmotic
f. secretory
f. secretory
- increased secretion, decreased absorption
- watery and large volume
- PERSISTS with fasting
What is the underlying mechanism in diarrhea caused by the ff agents: Salmonella, Shigella, amebiasis, Yersinia
a. mucosal invasion
b. decreased surface area
c. decreased motility
d. increased motility
e. osmotic
f. secretory
a. mucosal invasion
- organisms cause inflammation, decreases colonic reabsorption, increases motility
What is the underlying mechanism in diarrhea caused by the ff agents: lactase deficiency, lactulose, laxative overdose
a. mucosal invasion
b. decreased surface area
c. decreased motility
d. increased motility
e. osmotic
f. secretory
e. osmotic
- due to maldigestion, usually low in volume
- STOPS with fasting
What is the underlying mechanism in diarrhea caused by the ff agents: short bowel, celiac disease, rotavirus
a. mucosal invasion
b. decreased surface area
c. decreased motility
d. increased motility
e. osmotic
f. secretory
b.decreased surface area
- decreased functional capacity
- watery
What is the underlying mechanism in diarrhea caused by the ff agents: irritable bowel syndrome, thyrotoxicosis
a. mucosal invasion
b. decreased surface area
c. decreased motility
d. increased motility
e. osmotic
f. secretory
d. increased motility
- decreased transit time
- loose to normal stools
Among disk button batteries, coins, or small plastic toys, which should be removed expediently because they can induce mucosal injury in as little as 1hr of contact time and involve all esophageal layers within 4hr?
disk button batteries
- Asymptomatic blunt objects and coins lodged in the esophagus can be observed for up to 24hr in anticipation of passage into the stomach
Between acidic and alkali caustic ingestions, which is ingested in greater volume because it is tasteless and not bitter?
liquid alkali substances produce severe, deep liquefaction necrosis; drain decloggers are most common, and because they are tasteless, more is ingested
alkali - liquefaction necrosis
acid - coagulation necrosis
What is the recommended acute treatment for caustic ingestion?
a. dilution by milk or water
b. neutralization
c. induced emesis
d. gastric lavage
a. dilution with milk or water
- all other choices are contraindicated
What is the most common type of esophageal atresia?
type A: the upper esophagus ends in a blind pouch and the TEF is connected to the distal esophagus
- Esophageal atresia (EA) is the most common congenital anomaly of the esophagus; of these, >90% have an associated tracheoesophageal fistula (TEF).
Newborn was noted to be frothing and bubbling at the mouth and nose after birth as well as episodes of coughing, cyanosis, and respiratory distress. Feeding exacerbates these symptoms, causes regurgitation, and can precipitate aspiration. At the NICU,there was an inability to pass a nasogastric or orogastric tube.
What is your probable diagnosis?
EA with TEF
(esophageal atresia with tracheoesophageal fistula)
- H type fistula (TEF without EA) is usually later in life with chronic respiratory problems, including refractory bronchospasm and recurrent pneumonias
What is the underlying mechanism in diarrhea caused by the ff agents: pseudoobstruction, blind loop
a. mucosal invasion
b. decreased surface area
c. decreased motility
d. increased motility
e. osmotic
f. secretory
c. decreased motility
- defect in neuromuscular unit
- bacterial overgrowth
What is the management of patients with suspected biliary atresia?
All patients with suspected biliary atresia should undergo exploratory laparotomy and direct cholangiography to determine the presence and site of obstruction
For patients in whom no correctable lesion is found, the hepatoportoenterostomy (Kasai) procedure should be performed
- *transection of the porta hepatis with anastomosis of bowel to the proximal surface of the transection might allow bile drainage
- *success rate of Kasai is greater (90%) if performed before 8wks of life
- *short-term benefit - decompression and drainage sufficient to forestall onset of cirrhosis, until liver transplant can be done
To prevent malnutrition, patients with persistent cholestasis may benefit from replacement of dietary formula and supplements containing
a. long chain triglycerides
b. medium chain triglycerides
b. medium chain triglycerides
- Decreased delivery of bile acids to the proximal intestine leads to inadequate digestion and absorption of dietary long-chain triglycerides and fat-soluble vitamins.
- Malnutrition may result from malabsorption of dietary long-chain triglycerides. Replace with dietary formula or supplements containing medium-chain triglycerides
What are the concomitant clinical impairments to be expected in a patient with persistent cholestasis?
fat soluble vitamin malabsorption (vit A,D,E,K)
micronutrient deficiency (Ca, phosphate, Zn)
deficiency of water soluble vitamins
Retention of biliary constituents such as cholesterol (itch or xanthomas)
Progressive liver disease; portal hypertension (variceal bleeding, ascites, hypersplenism)
End stage liver disease
What is the most common cause of cholestasis with onset after the neonatal period?
acute viral hepatitis or exposure to hepatotoxic drugs
Identify which serologic marker for HBV infection is being described:
the first serologic marker of infection to appear and is found in almost all infected persons; its rise closely coincides with the onset of symptoms
HBsAg
Identify which serologic marker for HBV infection is being described:
During recovery from acute infection, because HBsAg levels fall before symptoms wane, this might be the only marker of acute infection; rises early after the infection and remains positive for many months, a valuable serologic marker of acute HBV infection
anti-HBc IgM
- remains positive for many months before being replaced by anti-HBc IgG, which then persists for years
Identify which serologic marker for HBV infection is being described:
marks serologic recovery and protection
anti-HBs
Identify which serologic marker for HBV infection is being described:
the only marker present in persons immunized with hepatitis B vaccine
anti-HBs
Identify which serologic marker for HBV infection is being described:
detected in persons with resolved infection (2)
anti-HBs and anti-HBc
Identify which serologic marker for HBV infection is being described:
present in active acute or chronic infection and is a marker of infectivity
HBeAg
Identify which serologic marker for HBV infection is being described:
marks improvement and is a goal of therapy in chronically infected patients
anti-HBe
If treatment for HBV infection is largely supportive, what would be the goals of treatment?
goal of treatment is to reduce viral replication as defined by
- undetectable HBV DNA in the serum
- development of anti-HBe
The most likely hepatotropic virus to cause chronic infection
Hepatitis C virus (C=chronic)
What is the initial symptom of pyloric stenosis?
nonbilious vomiting
- vomiting may or may not be projectile initially but is usually progressive, occurring immediately after a feeding
- starts after 3wk of age
- As vomiting continues, a progressive loss of fluid, hydrogen ion, and chloride leads to hypochloremic metabolic alkalosis
What is the most common clinical association of pyloric stenosis?
Hyperbilirubinemia
- also known as icteropyloric syndrome
- Unconjugated hyperbilirubinemia is more common
- usually resolves with surgical correction
Patient presents with nonbilious vomiting, usually postprandial, nonprojectile, but progressive. Vomiting started at 3 wks of age. Parents noted an abdominal mass which, upon palpation by the pediatrician, was firm, movable, ∼2cm in length, olive shaped, hard, best palpated from the left side, and located above and to the right of the umbilicus in the mid-epigastrium beneath the liver’s edge.
What will you recommend as ancillary procedure to confirm the diagnosis?
- This is a classic description of hypertrophic pyloric stenosis.
- Ultrasound examination confirms the diagnosis in the majority of cases. Criteria for diagnosis include pyloric thickness 3-4mm, an overall pyloric length 15-19mm, and pyloric diameter of 10-14mm
On barium contrast studies, what are the classic signs noted in pyloric stenosis?
- elongated pyloric channel (string sign)
- bulge of the pyloric muscle into the antrum (shoulder sign)
- parallel streaks of barium seen in the narrowed channel (“double tract sign”)
What metabolic disturbance is expected in children with pyloric stenosis?
hypochloremic metabolic alkalosis
-chronic vomiting will induce loss of fluid, H+, and chloride
What is the surgical procedure of choice in correcting pyloric stenosis?
surgical procedure of choice is pyloromyotomy
What should be first suspected in an infant or child presents with painless rectal bleeding?
Meckel diverticulum
- because Meckel dicerticulum accounts for 50% of all lower GI bleeds in children <2 y/o
What is the most sensitive diagnostic procedure that could confirm a diagnosis of Meckel diverticulum?
Meckel radionuclide scan, which is performed after intravenous infusion of technetium-99m pertechnetate
- treatment is surgical excision
Deep mucosal lesions that disrupt the muscularis mucosa of the gastric or duodenal wall are called
peptic ulcers
Where is the most common location of gastric ulcers and duodenal ulcers?
Gastric ulcers are generally located on the lesser curvature of the stomach, and 90% of duodenal ulcers are found in the duodenal bulb
primary peptic ulcers - chronic, duodenal. (p-d imagine an inverted p in d of ‘duodenal’), associated with H. pylori
secondary peptic ulcers - acute, often gastric (S-gaStric)
What are the secretagogues that promote gastric acid production?
acetylcholine, histamine and gastrin
Ach - vagus nerve
histamine - enterochromaffin cells
gastrin - G cells of the antrum
prostaglandins - enhance protective mucin production, decrease gastric acid secretion
The classic symptom of peptic ulceration, epigastric pain alleviated by the ingestion of food, is present only in a minority of children. What are the common symptoms in the ff age groups?
- newborn
- infants and younger children
- older children
- school-aged children and adolescents
- newborn - gastric perforation
- infants and younger children - feeding difficulty, vomiting, crying episodes, hematemesis, or melena
- older children - Dyspepsia, epigastric abdominal pain or fullness
- school aged children and adolescents - epigastric pain and nausea
- Hematemesis or melena is reported in up to half of the patients with peptic ulcer disease.
What is the recommended regimen for H. pylori eradication?
amoxicillin 14d + clarithromycin 14d + PPI 1 mo
amoxicillin + metronidazole + PPI
clarithromycin + metronidazole + PPI
- The first-line drugs for the treatment of gastritis and peptic ulcer disease in children are H2 receptor antagonists and PPIs
- Antibiotics + PPI must be used for the treatment of H. pylori-associated ulcers
- Triple therapy yields a higher cure rate than dual therapy
A rare syndrome characterized by refractory, severe peptic ulcer disease caused by gastric hypersecretion due to the autonomous secretion of gastrin by a neuroendocrine tumor, a gastrinoma
Zollinger-Ellison Syndrome
- common in patients with multiple endocrine neoplasia (MEN1) and rare with neurofibromatosis and tuberous sclerosis
- diagnosis is suspected by the presence of recurrent, multiple, or atypically located ulcers
