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MOD 4 - VOMITING Flashcards

1
Q

•Coordinated reflex process via the medullary vomiting center

A

Vomiting

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2
Q

Where is the vomiting center located?

A

Medullary

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3
Q

What are the events during vomiting?

A
  • Salivation and involuntary retching
  • Violent descent of the diaphragm
  • Constriction of abdominal muscles
  • Relaxation of the gastric cardia
  • Gastric contents actively forced up the esophagus
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4
Q

Is Vomiting Physiologic behavior in children?

A

YES

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5
Q

What are the possible causes oif vomiting?

A
  • GI disease
    Systemic disturbances
    Intracranial pathology
    Inborn errors of metabolism
    Non-GI infections
    Systemic poisoning
    Eating disorders
    Pregnancy
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6
Q

What is the pathophysio of vomiting?

A
  • Protective reflex
  • Removes toxic substances fr the body
  • Removes pressure in hollow organs distended by distal obstruction
  • May be accompanied by nausea & retching
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7
Q

________ – unpleasant, vague epigastric sensation

A

Nausea

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8
Q

What happens in nausea?

A

DECREASE

  • gastric tone,
  • secretions,
  • contractions,
  • mucosal blood flow.

• **INCREASE **

  • salivation,
  • sweating,
  • pupil diameter,
  • HR.
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9
Q

____________- – strong involuntary effort to vomit with spasmodic contraction of the diaphragm, relaxation of lower esophageal sphincter

A

Retching

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10
Q

What happens in retching?

A

•gastric material moved into esophagus but not expelled from the mouth.

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11
Q

Regurgitation – Gastroesophageal reflux due to lower esophageal sphincter dysfunction and reverse propulsion of stomach contents by somatic muscle contraction.

A

Regurgitation

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12
Q

________– regurgitation also occurs but the ruminated material is reswallowed (rather than ejected from the mouth).

A

Rumination

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13
Q

What stimulates the vomiting center?

A
  1. GI receptors
  2. chemoreceptor trigger zone
  3. vestibular center
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14
Q

When the vomiting center has been stimulated, what nerves are affected?

A
  1. phrenic nerve
  2. Vagus nerve
  3. Spinal nerve
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15
Q

The pherenic nerve affects what organ?

A

diaphragm

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16
Q

The vagus nerve affects which organs?

A
  1. esophagus
  2. stomach
  3. duodenum
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17
Q

Spinal nerves affect what?

A

Abdominal Rectus intercostals

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18
Q

What to ask in history in vomiting?

A
  • WHEN
  • TIMING
  • WHAT
  • COLOR
  • AMOUNT
  • ACUTE OR CHRONIC SYMPTOMS
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19
Q

Associated symptoms:

A

Abdominal pain/irritability in infants
•Nausea
•Headache
•Bowel disturbance
•Pyrexia
•Respiratory symptoms
•Neurological symptoms
•Anorexia, weight loss

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20
Q

Differential Diagnosis of Vomiting by Anatomic Locus of Stimulus

A
  1. Stimulation of supramedullary receptors
  2. Stimulation of chemoreceptor trigger zone
  3. Stimulation of peripheral receptors and/or obstruction of the GIT
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21
Q

Stimulation of supramedullary receptors

A
  • psychogenic vomiting
  • •Increased intracerebral pressure: subdural effusion, cerebral edema, hydrocephalus, meningitis, encephalitis
  • •Vascular: migraine, severe hypertension
  • •Seizures
  • •Vestibular disease,“motion sickness”
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22
Q

Stimulation of chemoreceptor trigger zone

A
  • Drugs: opiates, ipecac, digoxin, anticonvulsants
  • Toxins
  • Metabolic products: ketones, ammonia, lactic acid, aminoacids, urea
  • Dopamine neurotransmitters
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23
Q

Stimulation of peripheral receptors and/or obstruction of the GIT

A
  • Pharyngeal: gag reflex:
  • Esophageal:
  • Gastric
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24
Q

Stimulation of peripheral receptors and/or obstruction of the GIT
•Pharyngeal: gag reflex:

A

sinusitis secretions, post tussive, self induced, rumination

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25
Q
  • Stimulation of peripheral receptors and/or obstruction of the GIT
  • Esophageal:

What are the functional causes?

A

reflux, achalasia, dysmotility;

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26
Q

Stimulation of peripheral receptors and/or obstruction of the GIT

Esophageal:

structural

A

stricture, ring, atresia

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27
Q

Differential Diagnosis of Vomiting by Age

Newborn

A
  • Congenital obstructive gastrointestinal malformations
  • •Inborn errors of metabolism
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28
Q

Differential Diagnosis of Vomiting by Age

Infant

A
  • Acquired or mild obstructive lesions
    •Metabolic diseases
    •Nutrient intolerances
    •Functional disorders: Gastroesophageal reflux
    •Psychosocial disorders: rumination, child abuse
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29
Q

Newborn

Infectious

A

Sepsis, meningitis, UTI, thrush

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30
Q

Etiologies of Vomiting

Anatomic

A
  • Atresia and webs,
  • malrotation,
  • stenosis,
  • meconium ileus,
  • Hirschsprung’s disease
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31
Q

Etiologies of Vomiting

Infant

Infectious

A

Pneumonia, otitis media, thrush

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32
Q

Etiologies of Vomiting

Infant

Anatomic

A

Pyloric stenosis, intussuscep-tion, Hirschsprung’s disease

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33
Q

Etiologies of Vomiting

Child

Infectious

A

Gastro-enteritis

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34
Q

Etiologies of Vomiting

Anatomic

Child

A

Bezoars, chronic granulo-matous disease

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35
Q

Etiologies of Vomiting

Adolescent

Infectious

A

Gastro- enteritis, URI

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36
Q

Etiologies of Vomiting

Adolescent

Anatomic

A

PUD, superior mesenteric syndrome

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37
Q

Etiologies of Vomiting

Newborn

Gastro-intestinal

A
  • Reflux,
  • overfeeding,
  • gastric outlet obstruction,
  • volvulus
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38
Q

Etiologies of Vomiting

Newborn

Neurologic

A

Subdural hematoma, hydroce-phalus

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39
Q

Etiologies of Vomiting

Infant

Gastro-intestinal

A

Reflux, gastritis, milk intolerance

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40
Q

Etiologies of Vomiting

Infant

Neurologic

A

Subdural hematoma

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41
Q

Etiologies of Vomiting

Child

Gastro-intestinal

A

Appendicitis, pancreatic, hepatitis, other food intolerance

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42
Q

Etiologies of Vomiting

Child

Gastro-intestinal

A
  • Appendicitis,
  • pancreatic,
  • hepatitis, other food intolerance
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43
Q

Etiologies of Vomiting

Child

Neurologic

A
  • Neoplasia,
  • migraine,
  • Reye syndrome,
  • motion sickness,
  • hypertension
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44
Q

Etiologies of Vomiting

Adolescent

Gastro-intestinal

A

Achalasia,

hepatitis

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45
Q

Etiologies of Vomiting

Adolescent

Gastro-intestinal

A
  • Achalasia,
  • hepatitis
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46
Q

Etiologies of Vomiting

Adolescent

Neurologic

A
  • Neoplasia,
  • migraine
  • , motion sickness,
  • hypertension
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47
Q

Temporal Association of Chronic and Recurrent Vomiting

Time of day: early am

Other clues:

  • Headache,
  • papilledema
  • sinus tenderness
  • amenorrhea
A
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48
Q

Temporal Association: During/after meals:anytime

Other clues:

  • Epigastric pain
  • Heartburn
A

PUD
Reflux

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49
Q

Temporal Association of Chronic and Recurrent Vomiting

Temporal Association:

  • cow/soy milk
  • Gluten

Other clues:

  • Failure to thrive
A

Intolerance
Glutensensitive
Enteropathy

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50
Q

Temporal Association of Chronic and Recurrent Vomiting

Temporal Association:

  • Egg,wheat,cheese,
  • fish,nuts,strawberry

Other clues:

  • Hx of asthma, hives, ↑eos
  • Family hx
A

Allergies,

eosinophilic gastro enteropathy

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51
Q

Temporal Association of Chronic and Recurrent Vomiting

Temporal Association:

  • After fasting: Food vomited

Other clues:

  • Distention &
  • Tympany
A

Gastric stasis/ obstruction

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52
Q

Temporal Association of Chronic and Recurrent Vomiting

Temporal Association:

  • After fasting:Food not vomited
A

Metabolic dis

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53
Q

Temporal Association :

  • other precipitants
  • Cough
  • Infections

Other clues

  • Respiratory disease
A

Post-tussive
Recurrent gastroenteritis

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54
Q

Temporal Association :

  • Vestibular stimulation

Other clues:

  • Nystagmus
    Vertigo
A

Motion sickness
Menetrier’s dis

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55
Q

Temporal Association: Hyperhydration

Other clues: Resolves with normal hydration

A

Ureteropelvic jxn obstruction

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56
Q

Temporal Association:

  • Menses

Other clues:

  • Relief with NSAIDs
A

Dysmenorrhea assoc vomiting

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57
Q

Temporal Association:

  • Medications/toxins

Other clues:

  • Opiate withdrawal
A

Medication side effect
Steroid withdrawal
Poisoning
Ipecac abuse in anorexia nervosa

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58
Q

Temporal Association:

  • Episodic/cyclic
A

Metabolic inborn errors
Malrotation/volvulus

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59
Q

Clues to the Dx & Localization of the Cause of Emesis

Assoc sx
Local abdom pain

Epigastric

A

Diagnosis to consider

PUD, reflux, pancreatitis

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60
Q

Clues to the Dx & Localization of the Cause of Emesis

Assoc sx
Local abdom pain

Periumbilical

A

Small int. obstruction; non-specific

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61
Q

Clues to the Dx & Localization of the Cause of Emesis

Assoc sx

Pelvic

A

Cystitis, PID, ovarian torsion

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62
Q

Clues to the Dx & Localization of the Cause of Emesis

Assoc sx
Local abdom pain

LUQ

A
  • Pneumonia,PUD,
  • pancreatitis, splenic torsion,
  • L pyelonephritis
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63
Q

Clues to the Dx & Localization of the Cause of Emesis

RLQ

A

Appendicitis, R tuboovarian disease

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64
Q

Clues to the Dx & Localization of the Cause of Emesis

LLQ

A

L tuboovarian disease, sigmoid disease

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65
Q

Clues to the Dx & Localization of the Cause of Emesis

Right flank

A
  • Ureteropelvic jxn/obstruction/infection,
  • biliary obstruction,
  • adrenal hemorrhage
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66
Q

Clues to the Dx & Localization of the Cause of Emesis

A

Ureteropelvic jxn/obstruction/infection

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67
Q

Clues to the Dx & Localization of the Cause of Emesis

Assoc sx

Headache
Vomiting

A

↑ICP,sinusitis,migraine

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68
Q
A
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69
Q

Clues to the Dx & Localization of the Cause of Emesis

Chest pain dysphagia

Esophagitis, achalasia, pneumonia

A

Clues to the Dx & Localization of the Cause of Emesis

Chest pain dysphagia

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70
Q

Clues to the Dx & Localization of the Cause of Emesis

Diarrhea
Vomiting

A

Partial intestinal obstruction, poisoning, infectious enteritis, inborn errors metab

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71
Q

Clues to the Dx & Localization of the Cause of Emesis

Vertigo,visual changes, seizures, full fontanel

A
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72
Q

Metabolic disease, CNS disease, hepatic failure

A
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73
Q

Clues to the Dx & Localization of the Cause of Emesis

Vertigo,visual changes, seizures, full fontanel

A

Metabolic disease, CNS disease, hepatic failure

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74
Q

Clues to the Dx & Localization of the Cause of Emesis

Respiratory sx

A

Pneumonia, otitis ,
aspiration of vomitus

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75
Q

Clues to the Dx & Localization of the Cause of Emesis

Urinary sx

A

Pyelonephritis, hydronephrosis, calculi, renal hypertension, cholestasis

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76
Q

Clues to the Dx & Localization of the Cause of Emesis

Gynecologic sx menstrual irreg vaginal discharge

A

Pregnancy, PID, endometriosis

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77
Q

Physical Examination
•A complete PE is essential:

vomiting can be a manifestation of diseases involving multiple systems of the body

A
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78
Q

BP/VS derangements – determine urgency of the situation

A
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79
Q

RR – ______________ slow prolonged respiratory phase: respiratory compensation for metabolic acidosis

A

Kussmaul breathing –

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80
Q

Funduscopy– absence of venous pulsations or sharp optic disc margins: brain tumor________________

A

brain tumor

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81
Q

Abdominal

scars

A

obstruction from adhesions

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82
Q

•Abdominal exam
visible distention –

A

ascites due to intraluminal distention from intestinal obstruction/ileus

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83
Q

Physical Examination

_____________ – ↑in gastroenteritis/bowel

A

bowel sounds

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84
Q

Physical Examination

bowel sounds – ↑

A

in gastroenteritis/bowel obstruction;

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85
Q

bowel sounds: ↓or absent –

A

ileus/peritonitis

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86
Q

localized sharp pain –______________, requires immediate attention

A

inflammation of peritoneum

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87
Q

Physical Examination

Rectal exam - should be performed

_________ – generally object to exam – explain then proceed gently but firmly

A

12-24mos

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88
Q

Physical Examination

___________________– respond much as adults if their sensitivity and privacy are respected.

A

older children/adolescents

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89
Q

Physical Examination
How will you do the Rectal exam?

A

Recumbent position, lying on left side, flex hips and knees maximally (prevents gluteal contraction)
Do not hurry the examination (spasm of the external anal sphincter)

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90
Q

Pelvic masses/tenderness –

A

appendicitis, ovarian torsion, PID

91
Q

Well appearing infants/children with typical regurgitant reflux –

A

no need for lab evaluation

92
Q

GI Obstruction

• : drooling of oropharyngeal secretions/contents

A

Esophageal Lesions

93
Q
  • Esophageal atresia
  • at birth: intolerance of initial feeding
  • Prenatal hx: polyhydramnios
  • Assoc with other anomalies – VACTERL (vertebral, anorectal, cardiac, tracheoesophageal, renal, radial, limb)
  • Dx: plain films demonstrate coiled feeding tube in the upper esophageal pouch
  • Tx: surgical
A

•Esophageal atresia

94
Q

What is the prenatal history of Esophageal atresia

A

polyhydramnios

95
Q

What are the associated anomalies of Esophageal atresia?

A

VACTERL

vertebral, anorectal, cardiac, tracheoesophageal, renal, radial, limb

96
Q

What is demonstrated in the plain film of esophageal atresia?

A

plain films demonstrate coiled feeding tube in the upper esophageal pouch

97
Q

Esophageal atresia

98
Q

Hypertrophy of the muscular layers of the pylorus resulting in a functional gastric outlet obstruction.

A

Pyloric Stenosis

99
Q

Most common intestinal obstruction in infancy

A

Pyloric Stenosis

100
Q

What is the epidemiology of pyloric stenosis?

A

2-4 per 1000 live births
•4:1 (male:female)
•30% first born males
•7% incidence in children of affected parents

101
Q

Pyloric Stenosis

What type of vomiting?

A

Non-bilious projectile vomiting at 2-3 wks of age: lethargy, dehydration, poor wt gain, metabolic alkalosis, jaundice

102
Q

palpable “olive” in the epigastrium(RUQ) – hypertrophic pyloric mm (felt best after feeding)

A

Pyloric Stenosis

103
Q

In plain film contrast study, what is the appearance of Pyloric Stenosis?

A

gastric distention

104
Q

What is the appearance of Pyloric stenosis in UTZ?

A

“string sign” ultrasonography

105
Q

What is the treatment of Pyloric Stenosis?

A

Tx: correct fluid, acid-base imbalance, electrolyte losses, Surgery:pyloromyotomy (splitting of antro- pyloric mass longitudinally leaving the mucosal layer intact)

107
Q

In Intestinal Obstruction must identify if it is what?

A

Simple vs. Strangulating

108
Q

What are the classic symptoms of Intestinal Obstruction?

A

nausea, vomiting, abdominal distention, obstipation

109
Q

What are the sympstoms of intestinal obstruction if it is high?

A

(duodenum, proximal jejunum):

vomiting-bilious, non-feculent, acute onset, with crampy intermitent pain relieved by vomiting and minimal distention

110
Q

What are the symptoms in low obstruction?

A

Low obstruction:(distal):

feculent, less acute, more distention, diffuse pain over entire abdomen

**” **Malamang sa may colon na so kaya FECULENT tapos more distented kasi may laman”

111
Q

What are the clinical manifestation of

Duodenal Atresia/stenosis/web

A

bilious vomiting without abdominal distention on the 1st day of life
•Hx: polyhydramnios
•Jaundice in 1/3 of patients

112
Q

How to diagnose Duodenal atresia/ stenosis/ web in plain film?

A

Double bubble sign on upright film; absent gas in distal bowel

113
Q

What imaging study to use to confirm duodenal atresia/ stenosis/ web vs volvulus and malrotation?

A

do contrast studies

114
Q
A

Duodenal Atresia/stenosis/web

115
Q
A

Duodenal Atresia/stenosis/web

116
Q

Duodenal Atresia/stenosis/web
•Treatment

A
  • Nasogastric/orogastric decompression
  • IV fluid replacement
  • 2D echocargrogram and radiology of chest and spine (assoc. anomalies)
  • Surgical repair: duodenoduodenostomy
117
Q

Intestinal Obstruction

A

Jejunal atresia, Ileal atresia, Ileal stenosis

118
Q

Jejunal atresia, Ileal atresia, Ileal stenosis present with___________________

A

bilious vomiting, more abdominal distention

119
Q

How Jejunal atresia, Ilal atresia, Ileal stenosis may be diagnosed prenatally by

A

ultrasonography

120
Q

In intestinal obstruction, polyhydramnios occurs in _________

121
Q

Intestinal Obstruction
•Jejunal atresia, Ileal atresia, Ileal stenosis associated with:

A

Associated with LBW, multiple births, maternal cocaine and cigarette smoking

122
Q

What is the treatment for intestinal obstruction?

A
  • Treatment of small bowel obstruction
  • Resection of dilated proximal gut then end to end anastomosis
123
Q
  • Twisting of the bowel loop on the mesentery
  • Can be extremely hazardous when luminal obstruction is closed at both ends – leading to sepsis and ischemia of small intestine
A

Malrotation/Volvulus

124
Q

Why is malrotation/ volvulus extremely hazardous when luminal obstruction is closed at both ends

A

leading to sepsis and ischemia of small intestine

125
Q

What is the manifestation of malrotation/ vulvulus in the 1st year of life?

A

Clinical manifestations: (1st yr of life) bilious emesis, s/sx of acute obstruction

126
Q

What is the manifestation of malrotation/ vulvulus in the

older infants/children of life?

A

recurrent colic, recurrent vomiting and abdom pain

127
Q

What is the finding of Malrotation/ Volvulus in the UTZ?

A

Ultrasonography – inversion of superior mesenteric artery and vein location

128
Q

What is the finding of malrotation/ Volvulus in abdominal plain film?

A

Abdominal plain film – double bubble sign/corkscrew pattern

129
Q

What is the finding in Barium enema of Malrotation/ volvulus?

A

Abdominal plain film – double bubble sign/corkscrew pattern

130
Q

What is the diagnosis in Upper GI series of Malrotation/ Volvulus?

A

Upper GI series – malposition of the ligament of Treitz

131
Q

What is the treatment of Malrotation/ Volvulus

A

Surgical Intervention

132
Q
A

Malrotation/Volvulus

133
Q

________________ of proximal intestine into the distal intestine - luminal obstruction and mesenteric vascular compromise.

A

Telescoping

134
Q

Intussusception

Pathology – usually__________

135
Q

____________– upper bowel segment that invaginates into the lower segment (includes its mesentery)

A

Intussusceptum

136
Q

__________ – the lower bowel segment that receives the intussusceptum

A

Intussuscipiens

137
Q

What is the pathophysio of the presentation of symptoms of Intussusception?

A

Mesenteric constriction obstructs venous return, intussusceptum engorges – edema, bleeding from the mucosa: bloody stools

138
Q

What are the clinical manifestation of Intussusception?

A

Clinical manifestations:
•Sudden onset of severe paroxysmal colicky pain that recurs at frequent intervals, straining effort, flexed knees, loud cries, shock-like state

•Vomiting becoming bilious, currant jelly stools (mucosal hemorrhage)
•Tender sausage shaped mass in abdomen

139
Q

Coiled spring sign

A

Intussusception

141
Q

GI Dysmotility

A

Ileus

Gastroesophageal Reflux

142
Q

Failure of intestinal peristalsis without evidence of mechanical obstruction

143
Q

_________________
•effortless regurgitation:

most common cause of vomiting in infants

A

Gastroesophageal Reflux

144
Q

What is Ileus?

A

•Lack of normal gut motility

145
Q

What are the clinical manifestation of Ileus?

A

Clinical manifestations:
•Emesis with increasing abdominal pain as distention progresses
•Decreasing bowel sounds with increasing abdominal distention

” Malamang decrease bowel sound kasi nga walang motility diba diba ;)”

146
Q

What are the causes of ileu?

A

peritonitis, intestinal ischemia, sepsis
drugs - narcotics,atropine, laxatives
electrolyte disturbances - ↓K,↑Ca
endocrinopathies – hyperthyroidism

147
Q

What is found in the plain abdominal radiographs in ILEUS?

A

multiple air-fluid levels throughout the abdomen

Slow movement of contrast material through patent lumen

148
Q

What is the treatment for ILEUS?

A

Treatment:
•correction of underlying provocative abnormalities, NGT decompression until peristalsis begins

•Prokinetic agents: metoclopramide

149
Q
150
Q

Retrograde movement of gastric contents across the lower esophageal sphincter into the esophagus

A

Gastroesophageal Reflux

151
Q

What is the sequelae of GERD?

A

Pathologic
•Frequent or persistent episodes leading to esophagitis, esophageal symptoms, respiratory sequelae

152
Q

What is the pathophysiology of GERD?

A

•Antireflux barrier:

  • •Lower Esophageal Sphincter
  • •Diaphragm (crura) at the Gastroesoph jxn
  • •Esophagogastric Junction - valve

•Primary mechanism of reflux

  • •Transient Lower Esophageal Sphincter relaxation
  • •Aggravating factors: straining, increased movement, obesity, large volume meals, hyperosmolar meals, coughing, increased respiratory effort
153
Q

Gastroesophageal Reflux
•Pathophysiology
•Antireflux barrier:

A
  • •Lower Esophageal Sphincter
    •Diaphragm (crura) at the Gastroesoph jxn
    •Esophagogastric Junction - valve
154
Q

Gastroesophageal Reflux

Primary mechanism of reflux

A
  • Transient Lower Esophageal Sphincter relaxation
  • •Aggravating factors: straining, increased movement, obesity, large volume meals, hyperosmolar meals, coughing, increased respiratory effort
155
Q

Gastroesophageal Reflux

Infant reflux:

peaks at?

156
Q

Gastroesophageal Reflux
•Epidemiology and Natural History
•Infant reflux: resolves by

157
Q

Gastroesophageal Reflux

Epidemiology and Natural History

Infant reflux

A

completely gone by 24 mos.

158
Q

Gastroesophageal Reflux

•Epidemiology and Natural History

Older children: ________________

A

chronic waxing and waning, resolve in 50%

159
Q

Is genetic predisposition is likely in GERD?

160
Q

What are the Clinica of l Manifestation of GERD in infants?

A

Clinical Manifestations
•Infantile reflux: postprandial regurgitation, esophagitis, failure to thrive
•Airway manifestations
•Sx resolve by 12-24 mos.

161
Q

What are the clinical manifestation of GERD in older children?

A

Older children: regurgitation starting in pre-school years, abdominal/chest pain;

Sandifer syndrome: neck contortions
Airway manifestations: asthma, laryngitis, sinusitis

162
Q

What is the managment of GERD?

A

Management
•Conservative; lifestyle changes
•Dietary measures

  • •Normalization of feeding techniques, volumes and frequency
  • •Thickening of formula:
  • 1tbsp rice cereal/ oz. formula
  • •Hypoallergenic diet
  • •Avoidance of reflux-inducing food/drinks
  • Weight reduction for obese
  • Elimination of smoke exposure
163
Q

What are the positioning maneuvers in the management of GERD in infants?

A

•Infants:supine position during sleep;

prone and upright carried position when awake

164
Q

What are the positioning maneuvers in the management of GERD in Children?

A

Children:left side position and head elevation during sleep

165
Q

What are the pharmacotherapy in the mgt of GERD?

A

Pharmacotherapy
•Antacids, H2 receptor antagonists, PPI, Prokinetic agents

166
Q

Most common intestinal condition in neonates

A

Necrotizing Enterocolitis (NEC)

167
Q

What is the frequently affecting area in NEC?

A

terminal ileum and proximal ascending colon

168
Q

What is the pathogenesis of NEC?

A

Pathogenesis:

  • gut hypoxia/ischemia,
  • abnormal intestinal flora,
  • intestinal immaturity,
  • excessive inflammation, genetic
169
Q

NEC usually affects:

A

Usually affects prematures/10% - term babies

170
Q

What is the clinical presentation of NEC?

A
  • •Feed intolerance
  • •Bilious vomiting & aspirates
  • •Abdominal distension
  • •Bloody stools
  • •Abdominal wall tenderness/edema/discoloration
  • •Decreased bowel sounds
  • •Systemic disturbances
171
Q

In NEC, what can be found in abdomina x-ray?

A
  • abnormal gas pattern,
  • dilated/thickened bowel loops
  • pneumatosis intestinalis-pathognomonic
  • bowel perforation – intraperitoneal air (lat decubitus)
172
Q

What is phatognomonic for NEC?

A

pneumatosis intestinalis-pathognomonic

173
Q

What is the mgt for NEC?

A

Management:

  • supportive tx – bowel rest, TPN, gastric decompression with NGT, broad spectrum Abs, surgery if with evidence of perforation/intestinal necrosis
174
Q

What is the mortality rate for NEC?

A

10-50% mortality

highest for LBW/premature

175
Q

NEC outcome for 50% survivors:

A

50% survivors – complications:

int strictures,

short bowel syndrome

177
Q

IgE or non-IgE mediated/ seen in 15% of infants

A

Cow Milk Protein Allergy

178
Q

What is the presentation of Cow Milk Protein Allergy?

A

GI symptoms: non-IgE mediated
•Vomiting
•Diarrhea
•Constipation
•Frank or occult blood in stools
•Slow weight gain

**Note: **

Other sx suggestive of CMPA:
•Chronic cough, rhinitis, wheezing
•Atopic dermatitis, urticaria, angioedema, anaphylaxis

179
Q

How to diagnose CMPA?

A

Skin prick and allergen-specific IgE testing is unhelpful

180
Q

What is the gold standard (even for mother) for CMPA?

A

Elimination diet

181
Q

Formula fed infants:

A

extensively hydrolysed formula for at least 2-4wks

182
Q

_____________: for those not improving or those with severe sx

A

Amino acid formula

183
Q

not recommended (not nutritionally suitable)

A

Sheep, goat, soy or rice milk

184
Q

In CMPA, If improved with elimination diet?

A

continue until 9-12 mos of age

Then gradually reintroduce milk-containing foods

185
Q

CMPA: If sx return

A

If sx return, restart milk-free diet for another 3 mos, reattempt challenge later

186
Q

Good prognosis, CMPA resolves in majority by 5 yrs of age

187
Q

Metabolic Disorders

A
  • Inborn Errors of Metabolism
  • Congenital Adrenal Hyperplasia
  • •Diabetic Ketoacidosis
188
Q

Present with a variety of s/sx

  • •Poor feeding, persistent vomiting, lethargy, seizure unresponsive to glucose or calcium
  • •Metabolic acidosis, failure to thrive, developmental delays
  • •blood or urinary levels of particular metabolite (amino a,organic a, ammonia)
  • •Peculiar odors and physical changes
A

Inborn Errors of Metabolism

189
Q

What is the reason for Congenital Adrenal Hyperplasia?

A

Due to 21-hydroxylase deficiency

190
Q

When do symptoms manifest in Congenital Adrenal hyperplasia?

A

(1st 2wks of life)

191
Q

What are the clinical manifestation of Congenital Adrenal Hyperplasia?

A
  • •Deficiency of aldosterone and cholesterol (Salt-losing)
  • •Hypoglycemia, hyponatremia, hyperkalemia, progressive wt loss, anorexia, vomiting, dehydration, hypotension, weakness
  • •Female masculinization of external genitalia
192
Q

•End result of metabolic abnormalities due to severe insulin deficiency or insulin ineffectiveness

A

Diabetic Ketoacidosis

193
Q

Accumulation of ketoacids:

A
  • •Inappropriate polyuria in a dehydrated child with poor weight gain or flu-like sx
  • •Abdom discomfort, nausea, vomiting,dehydration, weakness, kussmaull respiration, acetone breath
194
Q

vomiting assoc with diarrhea: Rotavirus, food poisoning
•PUD, mesenteric adenitis(l.n. inflamm)
•Appendicitis, GI perforation, peritonitis
•Inflammatory bowel disorders
•Allergic enteropathy

A

GI Inflammation

195
Q

when is the highest incidence of ACute appendicitis?

196
Q

What is the incidence of Acute appendicitis?

A

19-28 children/10000 children under 14 yrs of age

197
Q

What is the classic presentation of ACute appendicitis?

A

Classic presentation:

  • •anorexia, abdom pain migrating to Rt Iliac fossa
  • •vomiting, pyrexia, diarrhea, constipation, dysuria
  • •Tenderness with rigidity at McBurney’s point
  • •Generalized tenderness with guarding (peritonitis)
198
Q

MGT for ACUTE APPENDICITIS?

A

Appendectomy

199
Q

Hepatitis in children – vomiting with fatigue, fever, headache, sore throat, cough
•Biliary colic and cholecystitis
•Pancreatitis

A

Hepatobiliary disease

200
Q

Rare in childhood but should be a differential for abdom pain and vomiting.

A

Pancreatitis

201
Q

What are the causes of Pancreatitis?

A
  • •trauma 30%
  • •Congenital abnormalities
  • •Metabolic: cystic fibrosis/ hypertriglyceridemia
  • •Infection: e.a. mumps
  • •Drugs and toxins (immunosuppressants, Na valproate)
202
Q

87% of the presentation of Pancreatitis is?

A

Abdominal pain

203
Q

64% of the presentation of Pancreatitis is?

204
Q

Diagnosis:Pancreatitis

A
  • elevated wbc, se amylase, hyperglycemia
  • UTZ : enlarged, edematous pancreas
205
Q

What is the mgt for pancreatitis?

A

Management:

  • •Fluid resuscitation
  • •Adequate nutrition
  • •Analgesia
  • •Surgery for congenital abnormalities or complications (pseudocyst)
206
Q

What is the prognosis of pancreatitis?

A

Prognosis : good, most recover quickly

207
Q

Urologic Disorders

A
  • Pyelonephritis, renal colic due to stones
  • Ureteropelvic junction obstruction: during increased fluid intake with hydronephrosis – pain and vomiting
  • Testicular torsion
208
Q

Obstetric/Gynecologic Disorders

A

Dysmenorrhea, endometriosis
•PID
•Ovarian torsion
•Pregnancy/Hyperemesis gravidarum

209
Q

Obstetric/Gynecologic Disorders

A
  • Dysmenorrhea, endometriosis
  • •PID
  • •Ovarian torsion
  • •Pregnancy/Hyperemesis gravidarum
210
Q

Respiratory disorders

A

Sinusitis, pharyngitis, otitis
•Pneumonia

211
Q

CNS Disorders

•↑ICPtumors – projectile but without retching

212
Q

Vestibular disorders –

A

motion sickness: nausea, nystagmus, vertigo

213
Q

Condition characterized by discrete recurrent episodes of vomiting with periods of wellness in between

A

Cyclic Vomiting Syndrome

214
Q

When does Cyclic Vomiting Syndrome begins?

A

Occurs at any age but begins between 3-7 yrs

215
Q

How to diagose Cyclic Vomiting Syndrome?

A

Diagnosis: by exclusion

  • •at least five episodes, or a minimum of three over a 6-month period
  • •episodic attacks of intense nausea and vomiting lasting hours to days, occurring at least 1 week apart
  • •stereotypical pattern and symptoms in the individual patient
  • •vomiting during episodes occurs at least four times an hour for at least 1 h
  • •a return to baseline health during episodes
  • •not attributed to another disorder.
216
Q

What is the Cyclic Vomiting syndrome presenetation?

A
  • Vomiting, nausea, abdominal pain, pallor
  • •Triggers: infection, emotion, foods ( cheese, chocolate)
  • •Linked to migraine headaches (family hx in 80%)
  • •May respond to anti-migraine medications
217
Q

What is the treatment for Cyclic Vomiting Syndrome?

A

Treatment
•Supportive
•Admission for IV fluids/anti-emetics
•Avoid triggers
•Pizotifen – for children with frequent episodes

218
Q

Psychological Disorders

A

no organic cause determined, chronic, associated with stress/ meals, can be suppressed by distracting the patient

219
Q

– food is regurgitated, mouthed or chewed and reswallowed – voluntarily and pleasurably

A

Rumination

220
Q

Eating Disorders

A

Anorexia nervosa

•Bulimea nervosa

221
Q

Intense preoccupation with weight with behaviors aimed at a relentless pursuit of thinness(emaciated)

A

•Anorexia nervosa

222
Q

•Bulimea nervosa

A

Longterm dietary restraint interrupted by episodes of reactive hyperphagia and compensatory behavior: vomiting and laxative abuse (binge-purge behavior)

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