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Flashcards in Gastroenterology Deck (123)
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1
Q

What are essential nutrients?

A

Cannot be synthesized by the body and must be derived from the diet

2
Q

What are the macronutrients?

A

Supply energy and essential nutrients needed for growth, development, disease prevention, and activity

  • Carbohydrates
  • Proteins
  • Fats
  • Minerals
3
Q

Carbohydrates make up approximately __% of the typical diet

A

50%

4
Q

How many essential amino acids are there?

A

9

5
Q

What are micronutrients?

A
  • Water-soluble vitamins
  • Fat soluble vitamins (ADEK)
  • Essential trace minerals (iron, iodine, fluoride, zinc, selenium, and copper)
6
Q

What is the most common ernergy depletion state?

A

Marasmus - characterized by near starvation from protein and nonprotein deficiencies

7
Q

What is Kwashiorkor?

A

Protein deficient state characterized by generalized edema, abdominal distension, changes in skin pigmentation, and thin, sparse hair

8
Q

What is malabsorption?

A

Inadequate absorption of nutrients - most often characterized by diarrhea, abdominal distension and impaired growth

9
Q

How does malabsorption of carbohydrates lead to diminished absorption of nutrients?

A

Undigested sugars are osmotically active and draw water into the intestinal lumen, causing increased stool volume, increased peristaltic activity, and decreased transit time

10
Q

In carbohydrate malabsorption the resulting stool is watery and ______

A

acidic

11
Q

What is a clinitest?

A

Detects unabsorbed sugars as reducing substances; test for carbohydrate malabsorption

12
Q

What are some causes of carbohydrate malabsorption?

A
  • Congenital enzyme deficiency (Lactase deficiency)
  • Mucosal atrophy
13
Q

What breaks down dietary proteins into amino acids or oligopeptides?

A

Pepsinogen and pancreatic proteases in the proximal small intestine

14
Q

What are some causes of protein malabsorption?

A
  • Congenital enterokinase deficiency
  • Protein-losing enteropathies (transudation of protein from inflamed intestinal mucosa)
  • Inflammatory disorders (Chron’s, colitis)
15
Q

Levels of _______can be used to document enteric protein losses

A

Fecal α1-antitrypsin levels

16
Q

Fats are ________ in water and must be incorporated into ______ ______ _______ to be absorbed

A

insoluble; bile salt micelles

17
Q

What results from decreased lipase activity?

A

Steatorrhea

Decreased absorption of fat soluble vitamins

18
Q

What are some causes of fat malabsorption?

A
  • Exocrine pancreatic insufficiency
  • Intestinal mucosal atrophy
  • Bile acid deficiency
  • Abetalipoproteinemia
19
Q

What stool studies should be done to determine fat malabsorption?

A

Stool studies for fat, carbohydrates, pH, reducing substances, and α1-antitrypsin

20
Q

Infection with _____ ______ can cause chronic fat malabsorption and can be diagnosed by stool studies

A

Giardia Lamblia

21
Q

What are the symptoms of protein intolerance?

A

Diarrhea, vomitting, and colicky abdominal pain after exposure to dietary protein

22
Q

Protein intolerance occurs in up to __% of children

A

8%

23
Q

Describe Enteropathy vs. Enterocolitis in protein intolerance

A

Enteropathy: Progressive onset of diarrhea, vomiting, irritability, and abdominal pain; chronic blood loss in stool may lead to anemia, and protein loss may cause edema and FTT

Enterocolitis: Acute diarrhea, rectal bleeding, mucus in stool, abdominal distension , and irritability (may also cause edema and FTT)

24
Q

What is the management of protein intolerance?

A

Withdrawal and avoidance of suspected dietary protein; most protein intolerance is transitory

25
Q

What is celiac disease?

A

Autoimmune disorder of the proximal small intestine characterized by intolerance to gluten, which results in mucosal damage

26
Q

Celiac disease generally presents between __ _____ and __ _____ of age when gluten is introduced into the diet

A

between 6 months and 2 years of age

27
Q
A
28
Q

What are the primary symptoms of celiac disease?

A
  • Diarrhea
  • Vomiting
  • Bloating
  • Anorexia (and sometimes FTT)
29
Q

What is involved in the evaluation of celiac disease?

A
  • Small bowel biopsy (gold standard) demonstrates short, flat villi, deep crypts, and vacuolated epithelium
  • Resolution of symptoms when gluten is removed from the diet
  • Serum IgA-endomysial and serum tissue transglutaminase antibody testing
30
Q

What is the management of Celiac disease?

A
  • Strict gluten-free diet for life results in complete reversal of intestinal damage
  • Corticosteroids are used for severe diarrhea
  • Dietary changes in children often yield a rapid response, but noncompliance in adolescents is common
31
Q

What can lead to short bowel syndrome?

A
  • Congenital lesions of the gut (gastroschisis, volvulus)
  • Infants who had undergone intestinal surgery for necrotizing enterocolitis
  • Chron’s disease, tumors, and radiation enteritis
32
Q

After gut resection, _____ and _____ malabsorption are common

A

carbohydrate and fat

33
Q

Distal small bowel resection limits ________ and _____ absorption

A

Vitamin B12 and Bile acid

34
Q

What are the clinical features of short gut syndrome?

A

Diarrhea, malabsorption, and FTT

35
Q

What is the management for short bowel syndrome?

A
  • Total parenteral nutrition
  • Early enteral feedings to ensure adaptive growth of remaining bowel
  • Small bowel transplantation is reserved for patients with coexisting liver disease
36
Q

What are complications of short bowel syndrome?

A
  • TPN cholestasis
  • Intestinal bacterial overgrowth
  • Nutritional deficiencies
  • Poor bone mineralilzation
  • Renal stones
37
Q

What is GERD?

A

A pathologic state associated with GI or pulmonary symptoms and sequelae

38
Q

What is the predominant cause of GERD during childhood?

A

Inappropriate transient lower esophageal sphincter relaxation (TLESR)

39
Q

How to infants present with GERD? (what presentation is most common)

A
  • Emesis is the most comomn presentation (but not always present)
  • Sandifer syndrome - torticollis with arching of the back caused by painful esophagitis
  • Feeding refursal with irritability or constant hunger
40
Q

How do older children present with GERD?

A
  • Symptoms of esophagitis, including midepigastric pain (heartburn)
  • Nausea, hoarseness, halitosis, and wheezing
41
Q

How does GERD contribute to upper and lower airway disease?

A

Acidic reflux induces bronchopulmonary constriction that can also lead to frank aspiration or microaspiration

42
Q

What are some GI sequelae of GERD?

A
  • FTT
  • Esophageal strictures
  • Barret’s esophagus
43
Q

Infants who remain symptomatic past _____ of age are unlikely to have spontaneous resolution of GERD

A

1 year

44
Q

What can be used to diagnose GERD?

A
  • Barium upper GI study (poor test for diagnosis of GERD)
  • Scintigraphy to measure rate of gastric emptying
  • pH probe measurement is the gold standard for diagnosis
45
Q

What is done in GERD with suspected aspiration?

A

Bronchoscopy with alveolar lavage

46
Q

What constitutes conservative management of GERD?

A
  • Positioning in an upright or sitting position
  • Dietary recommendations include small frequent meals and thickening of feeds
  • Acid inhibition with antacids, H2 blockers and PPI
47
Q

What is the most commonly used motility agent for GERD?

A

Metoclopramide

48
Q

What surgical procedures are used to treat GERD (patients who fail conservative and medical treatment)

A
  • Nissen fundoplication
  • Gastric antroplasty
  • Gastrostomy tube often accompanies Nissen fundoplication in infants
49
Q

What intestinal anatomic obstructions result in vomiting?

A
  • Hypertrophic Pyloric Stenosis
  • Malrotation and midgut volvulus
  • Atresias
  • Intussusception
  • Hirschsprung’s disease
50
Q

What is Pyloric stenosis?

A

Thickening of the circular pylorus muscle results in gastric outlet obstruction with projectile vomiting

51
Q

Who is more likely to have pyloric stenosis?

A

Caucasians and first born male children

52
Q

What are the clinical features of hypertrophic pyloric stenosis?

A
  • Vomiting of nonbilious, milky fluid starts during the second or third week of life
  • Projectile vomiting
  • Irritable but hungry
  • Jaundice (5% of patients)
  • Dehydration
53
Q

What is seen on physical exam of a patient with pyloric stenosis?

A

Hypertrophied pylorus muscle may be palpable (olive)

Abdominal peristaltic waves may be visible after feeding

54
Q

What is the metabolic finding in hypertrophic pyloric stenosis?

A

Hypochloremic, hypokalemic, metabolic alkalosis

55
Q

What are the diagnostic studies for pyloric stenosis?

A
  • Ultrasound is the diagnostic method of choice
  • UGI may demonstrate an elongated narrow pyloric channel
56
Q

What is the management for hypertrophic pyloric stenosis?

A
  • Electrolyte abnormalities and dehydrate corrected first
  • Surgical correction with parital pyloromyotomy
57
Q

What is malrotation?

A

Anatomic abnormality of intestinal rotation that allows the mdigut to twist around the superior mesenteric vessels

58
Q

How does malrotation occur?

A

The intestines normally return to the abdomen throught the umbilical cord during the 10th week of gestation and undergo counterclockwise rotation about the axis of the SMA

Malrotation occurs when the normal bowel rotation is interrupted

59
Q

Lack of fixation of the small bowel in malrotation results in _______ ______ that can compress the duodenum, causing mechanical obstruction

A

Peritoneal bands (Ladd’s bands)

60
Q

What are the clinical features of malrotation?

A
  • Bilious vomiting and sudden onset of abdominal pain in an otherwise healthy infant
  • Anorexia, distension, and blood tinged stools
61
Q

What is done to evaluation malrotation?

A
  • Abdominal radiographs
  • Upper intestinal contrast inmaging (diagnostic tool of choice)
  • Lower intestinal contrast studies
62
Q

What is the management of malrotaion/volvulus?

A
  • Volvulus is a surgical emergency requiring immediate exploration
  • Fluid resuscitation, nasogastric suctioning, and broad spectrum parenteral antibiotics should be administered
  • TPN may be required if a large segment of bowel is resected
63
Q

What is duodenal atresia?

A

Congenital obstruction of the duodenum caused by failure of the lumen to recanalize at 8-10 weeks gestation

64
Q

One fourth of cases of duodenal atresia occur in patients with _______ ______

A

Down Syndrome

65
Q

What are the clinical features of duodenal atresia?

A
  • Gastric dilation with polyhydramnios
  • Scaphoid abdomen with epigastric distension
  • Duodenal stenosis may present with emesis, weight loss, and FTT
  • Other congenital defect
66
Q

What is used to evaluate duodenal atresia?

A
  • Abdominal radiography shows air in the stomach and proximal duodenum creating a double bubble sign
  • Intestinal contrast studies
67
Q

What is the management of duodenal atresia?

A
  • Nasogastric decompression, hydration, and correctionof electrolyte abnormalities
  • Atresia is surgically corrected by duodenoduodenostomy
  • Exploration for malrotation and other luminal obstructions is also performed at the time of surgical correction
68
Q

What is jejunoileal atresia?

A

The congenital obstruction of the jejunum or ileum is caused by a mesenteric vascular accident during fetal life

69
Q

What clincal features are seen with jejunoileal atresia?

A

Bilious emesis and abdominal distension occur within the first few days of life

70
Q

What can be seen with imaging in jejunoilial atresia?

A

Abdominal radiographs reveal air-fluid levels, and contrast studies reveal atresia

71
Q

What is the management for jejunoilial atresia?

A

Patients should receive nasogastric suctioning and fluid resuscitation before surgical resection and anastomosis of the atretic segment of small bowel

72
Q

What is intussusception?

A

Intussusception in the telescoping or invagination of a more proximal portion of intestine into a more distal portion

73
Q

Where is the most common location for intussusception?

A

Ileocolic intussusception is the most common location

74
Q

What can serve as a lead point for intussusception?

A
  • Meckel’s diverticulum
  • Polyp
  • Intestinal duplicatoin
  • Peyer’s patch
  • Lymphoma
75
Q

What are the clinical features of intussusception?

A
  • Sudden onset of crampy or colicky abdominal pain
  • Vomiting and lethargy are common
  • Currant jelly stool
  • Sausage shaped mass may be palpated in the abdominal right upper quadrant
76
Q

How is intussusception evaluated?

A
  • Initial management should include fluid resuscitation
  • Radiographs are of limited usefulness
  • Abdominal ultrasound may be diagnostic tool, but air or contrast enema remains the gold standard
77
Q

What is the management for intussusception?

A
  • Contrast enemas with air or hydrostatic pressure successfully reduce intussusception in 80-90% of cases
  • Operative reduction if contrast enema fails
78
Q

Review of systems for acute abdominal pain should focus on…

A

Associated symptoms of fever, vomiting, diarrhea, constipation, anorexia, dysuria, or worsening pain with eating

79
Q

In abdominal exam for acute abdomen, how does intestinal obstruction present?

A
  • High-pitched bowel sounds
  • Abdominal distension
  • Tenderness
  • Visible peristalsis
80
Q

How does peritonitis present on abdominal examination?

A
  • Diminished or absent bowel sounds
  • Abdominal wall rigidity
  • Involuntary guarding
  • Rebound tenderness
81
Q

What is the most common pediatric emergency operation?

A

Appendectomy

82
Q

What causes appendicitis?

A

The lumen of the appendix is obstructed by either a fecalith or by lymphoid tissue causing appendiceal distension and ischemia

83
Q

Distension in appendicitis produces visceral pain referred to the _____ dermatome or ________ region

A

T10; periumbilical

84
Q

What are the symptoms of appendicitis?

A
  • Periumbilical pain
  • Vomiting
  • Within hours, the pain localizes to the right lower quadrant
  • Fever and anorexia
85
Q

What are the physical exam findings for appendicitis?

A
  • Tenderness to palpation at McBurney’s point
  • Voluntary guarding
  • Rebound tenderness
86
Q

How is appendicitis diagnosed?

A

Abdominal ultrasound or CT often aids in diagnosis

Can be diagnosed clinically

87
Q

What is the management for appendicitis?

A
  • Fluid resuscitation
  • perioperative antibiotics
  • Appendectomy
  • Drainage if perforated appendicitis
88
Q

What is acute pancreatitis?

A

Acute inflammatory process oft he pancreas that may involve peripancreatic tissues and other organ systems

89
Q

Pancreatitis is _______ in children

A

uncommon

90
Q

What is the pathophysiology of acute pancreatitis?

A

An initial insult (obstruction or infection) causes premature activation of pancreatic proenzymes and autodigestion of pancreatic cells

91
Q

What are the possible causes of acute pancreatitis? Which is most common?

A
  • Trauma (most common)
  • Infections
  • Drugs/toxins
  • Congenital anomalies
  • Obstruction
92
Q

What is the second most common cause of pancreatitis during childhood?

A

Idiopathic

93
Q

What are some clinical features of acute pancreatitis?

A
  • Abominal pain in the periumbilical or epigastric area
  • Fever, anorexia, nausea, vomiting
94
Q

What are Gray-Turner sign and Cullen sign in the context of acute pancreatitis?

A

Physical exam findings

  • Gray-Turner sign - bluish discoloration of the flanks
  • Cullen sign - bluish discoloration of the periumbilical area
95
Q

What labs are important to obtain in cases of acute pancreatitis?

A

Serum amylase levels rise within hours of pain onset and remain elevated for 4-5 days

Serum lipase level elevation is more specific for acute pancreatitis and remains elevated longer

96
Q

What is the most common method used for diagnosing and monitoring acute pancreatitis?

A

Abdominal US (Abdominal CT is useful in diagnosing complications such as pseudocyst, abscess, or necrosis)

97
Q

How is acute pancreatitis managed?

A
  • Supportive care (bed rest, hydration, electrolyte correction)
  • TPN
  • Antibiotics (for acute necrotizing pancreatitis)
  • Surgery (to remove necrotic tissue)
98
Q

What is a pseudocyst?

A

A complication of acute pancreatitis in which a collection of fluid rich in pancreatic enzymes arises from pancreatic tissue

99
Q

What is cholecystitis?

A

Inflammation of the gallbladder with transmural edema that may be associated with gallstones

100
Q

What predisposing conditions increase the risk of cholecystitis in children?

A
  • Sickle cell disease
  • Cystic fibrosis
  • Prolonged TPN therapy
101
Q

What causes acute acalculous cholecystitis?

A

Usualy caused by infection

Also may be seen after abdominal trauma, burns, or vasculitis

102
Q

What are the clinical findings in cholecystitis?

What is Murphy’s sign?

A
  • Abdominal pain is initially diffuse but eventually worsens and localizes to the right upper quadrant
  • Fever, anorexia, and vomiting are common
  • Jaundice may be a late finding
  • Murphy’s sign: palpation of the right upper quadrant during inspiration elicits intense pain and causes the patient to stop inspiratory effort
103
Q

Diagnosis of cholecystitis is confirmed by…

A

Abdominal US

104
Q

What is the managment for cholecystitis?

A
  • Fluid resuscitation
  • Parenteral antibiotics
  • Analgesia
  • Cholecystectomy if the disease progresses
105
Q

What is the definition of chronic abdominal pain?

A

Abdominal pain that occurs each month for at least 3 consecutive months

106
Q

What are the two types of Chronic abdominal pain (CAP) and which is more common in females?

A
  • Organic
  • Nonorganic (functional) - more commonly in females
107
Q

What are some causes of organic CAP?

A
  • Constipation
  • Peptic ulcer disease
  • Carbohydrate intolerance
  • IBD
  • Pancreatitis
  • Parasitic infection
  • GU disorder (pyelonephritis)
  • Congenital abnormalities of GI tract
108
Q

What is important to understand about Non-organic CAP?

A

The patient senses real pain, even in the absence of an underlying organic cause

109
Q

What type of pain represents classic funcitonal abdominal pain?

A

Periumbilical pain

110
Q

Chronic infraumbilical pain is the childhood equivalent of _______ _______ _____ in adults

A

irritable bowel syndrome

111
Q

What past medical history can increase risk for CAP?

  • Maternal:
  • Child:
A
  • Maternal: pregnancy problems, intrapartum problems (labor difficulty, C-section)
  • Child: Neonatal problems (colic), childhood problems (enuresis, nightmares)
112
Q

What are some psychosocial risk factors for chronic abdominal pain?

A
  • Personality (timid, nervous, anxious)
  • Birth order (first-born and last-born)
  • Life stressors
  • Extreme methods of discipline
113
Q

What type of laboratory evaluations are important for CAP?

A
  • CBC, electrolytes, liver function, stool screening, ESR
  • Screening for H. Pylori should only be done in children with symptoms of dyspepsia
  • Lactose breath hydrogen testing to rule out lactose intolerance
114
Q

For patients with non-orgaic CAP, prognosis is _____

____% of patients have complete symptom resolution during childhood

A

poor; 50%

115
Q

What is encopresis?

A

Developmentally inappropriate release of stool unrelated to organic etiology

116
Q

Encopresis is almost always associated with severe ________

A

constipation

117
Q

Frequncy of stooling averages __/day during the first week of life

A

4x

118
Q

What is functional fecal retention (FFR)?

A

The most common form of constipation during childhood (results from innapropriate constriction of the external sphincter)

119
Q

Functional fecal retention (FFR) is a ________ pattern of stool withholding

A

behavioral

120
Q

What is the most comomn cause of organic constipation?

A

Hirschsprung’s disease

121
Q

What are some H&P findings that suggest an organic cause of encorporesis rather than FFR?

A
  • Delayed meconium passage (>48 hours after birth)
  • Onset of constipation during infancy
  • H/o pelvic surgery
  • Encopresis before 3 years of age
  • Inability to toilet train
122
Q

Mild episodic constipation can be addressed by ensuring the diet contains adequate _______ _______

A

soluble fibers

123
Q

How is FFR managed?

A
  • Stool evacuation
  • Maintenance therapy (mineral oil to soften and lubricate the stool)
  • Education (most important intervention)