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Clinical Medication: HEENT > Pediatric Pathology, Disorders and Illnesses > Flashcards

Pediatric Pathology, Disorders and Illnesses Flashcards

1
Q

• What is the definition of Microcephaly?

A

• >2 standard deviations below the mean for the age/sex

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2
Q

• What can cause Microcephaly?

A

• Can occur d/t chromosomal abnormalities, infections, metabolic disorders and or neurologic insult

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3
Q

• How do you diagnose Microcephaly?

A

• CT/MRI may aid in dx

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4
Q

• What is the treatment of Microcephaly?

A

• Treatment is supportive and or aimed at underlying etiology

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5
Q

o Macrocephaly:

A

• Head circumference>2 standard deviations above the mean for age/sex

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6
Q

• What is the cause of Macrocephaly?

A
  • Rapid head growth suggest increased ICP (mist likely caused by ICP, extra axial fluid collection or neoplasms)
  • Normal growth rate a/w Microcephaly can be d/t familial Macrocephaly or true megalocephaly (nerurofibromatosis)
  • Preterm infants can have Microcephaly d/t “catch up growth”
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7
Q

• How do you dx Microcephaly?

A

• CT/MRI study of choice to t/o structural causes.

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8
Q

• What is Plagiocephaly?

A

• Asymmetry of the cranial vaults

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9
Q

• What is Brachycephaly?

A

• Asymmetry of the cranial vaults

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10
Q

• What is the most common cuase of Brachycephaly?

A
  • Supine sleeping position
  • May also occur d/t pathology including trticollis or lack of stimulation
  • May occur d/t Craniosynostosis
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11
Q

• Dx and Treatment of Brachycephaly

A

• Rarely requires skill film or consult

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12
Q

• What has led to earlier detection of hearing defects?

A

• Universal screening

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13
Q

• Hearing loss in children can significantly impair what?

A

• A Childs ability to communicate and will delay academic, social and emotional development.

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14
Q

• Pts with + hearing screen should what?

A
  • Be referred for further audiologic evaluation

* Early intervention is critical

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15
Q

• What is the most common cause of hearing loss in children?

A

• Conductive hearing loss

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16
Q

• What pathology would suggest the need for assessment of conductive hearing loss?

A

• Recurrent otitis media or middle ear effusion lasting > 3 mo should have hearing and language skills assessment

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17
Q

• Treatment of conductive hearing loss?

A

• Middle ear fluid can be treated with placement of Tympanostomy tubes

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18
Q

• Causes of sensorineural hearing loss?

A
  • May be congenital or acquired
  • Risk factors for neonatal hearing loss include positive family hx, low birth weight, low apgar scores, craniofacial abnormalities, hypoxia, in-utero infections, hyperbilirubinemia requiring exchange transfusion, mechanical ventilation >5 dayls
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19
Q

• How is sensorineural hearing loss treated?

A

• With amplification

o Cochlear implantation may be option for pts with severe defects

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20
Q

o Foreign Body in the Ear Canal

• How do dx a FB?

A

• Visualization

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21
Q

how do you remove a FB in the ear?

A
  • Most Fb can safely be removed by PCP utilizing techniques including irrigation of instrumentation under direct visualization
  • If concern regarding removal refer to ENT
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22
Q

• What FB od the ear MUST be refereed to ENT?

A
  • Button Batteries
  • Penetrating FB
  • Fb associated with injury/ trauma
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23
Q

• How will a FB in the nasal cavity present?

A

• Often asymptomatic but may be a/w mucopurulent nasal draining, foul odor, epistaxis, nasal obstruction, mouth breathing

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24
Q

• How do you Dx a fb in nasal cavity?

A
  • Typically based on visual inspection

* If unable to visualize may require fiber optic endoscopy

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25
Q

• What FB of the nose would require Xray?

A

• Button Battery or magnets

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26
Q

• Treatment of FB in nasal cavity?

A

• Majority are removed without referral
o Techniques for removal include positive pressure techniques or direct instrumentation
o Button batteries and paired disc magnets can cause serious damage to nasal structures and should be removed urgently

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27
Q

• What are complications of FB in the nasal Cavity?

A
  • Most serious complications r/t button batteries including septal perforation with saddle nose deformity, nasal metal stenosis, inferior tubinate necrosis, and collages of the alar cartilage
  • Instrumentation during removal may cause trauma to the nasal cavity
  • Chronic FB may predispose to infection (sinusitis)
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28
Q

o Foreign Body in the Eye

• What will a fb in the eye present with?

A

• Photophobia, tearing and redness

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29
Q

• Where might the FB be?

A

• May be present on the surface of the cornea or on the bulbar or palpebral conjunctiva

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30
Q

• How do you Identify the FB/Dx of the eye

A

• With a slit lamp (may need to every the lid)

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31
Q

• If you can visualize the FB how should you remove it

A

• IF visualized, attempt at removal may be performed with irrigation or swab, DO NOT patch an eye with a FB

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32
Q

• What is a nasolacrimal duct obstuction?

A

• Obstruction in any part of the drainage system

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33
Q

• What will a nasolacrimal duct obstruction present with?

A

• Tearing and mucoid d/c from affected eye, erythemia of one or both lids, and or conjunctivitis

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34
Q

• what is the treatment for a nasolacrimal duct obsruction?

A
  • Majority clear spontaneously by 1 year of age
  • Massage over gland
  • Treat infection with topical ABX PRN
  • Surgical probing can be perfomed if persists to 6-12 mo of age.
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35
Q

• What causes pediatric cataract?

A

• May occur as isolated defects or maybe a/w other ocular disorders or systemic diease

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36
Q

• What is the clinical presentation of Pediatric Cataract?

A
  • Lukocoria
  • Poor fixation
  • Strabismus or nystagmus
  • May be unilateral or bilateral
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37
Q

• How do you Dx Pediatric cataract?

A

• Lab evaluation for infectious and metabolic cause

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38
Q

• How do you treat Pediatric cataract?

A
  • Early dx and tx to prevent deprivation amblyopia
  • May require removal
  • Visual rehab
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39
Q

• What is the cause of Infantile Glaucoma?

A

• Congenital or acquired

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40
Q

• Clinical presentation of infantile Glaucoma?

A
  • Unilateral or bilateral
  • Open or closed
  • GLOBE ENLARGMENT!
  • Treating, photophobia, blepharospasm may occur
  • Corneal clouding, optic n cupping may be noted on exam
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41
Q

• Treatment for infantile Glaucoma?

A
  • Refer to Ophthalmologist
  • Often requires surgical intervention
  • Prognosis of vision is poor.
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42
Q

• What is a corneal Abrasion?

A

• Any defect on the surgace of the cornea (transparent tissue covering the iris)

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43
Q

• What causes a corneal Abrasion?

A

• Can be traumatic, related to a FB, Contact lens or spontaneous

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44
Q

• How do pts present with corneal abrasions?

A
  • Similarly regardless of etiology
  • EXCRUCIATING eye pain and inability to open his/her eye d/t FB sensation
  • Children typically present with a less specific history but may present with photophobia, tearing, redness, +/- a hx that is suggestive of a mechanism of injury
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45
Q

• What is the PE for a corneal abrasions?

A

• Need to r/o Penetrating trauma
• Test visual acuity (may or may not be altered depending on location of lesion) may be difficult in children
• Diffuse corneal edema/ haziness may be present
o Localized changes, consider corneal infiltrate and refer to Ophthalmology
• Penlight and fundoscopic exam should be performed
• Fluorescein staining after penlight and fundoscopic exam

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46
Q

• What is the tx of a corneal abrasions?

A
  • Majority heal within 24-72 H
  • Avoid rubbing eye
  • Topical ABX for 3-5 days (Ointment over drops- better tolerated)
  • Pressure patches are of NO PROVEN BENEFIT and poorly tolerated in children
  • Analgesia such as acetaminophen or ibuprofen may be helpful
  • Healing occurs at night so sleep aid such as a sedating antihistamine may be helpful
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47
Q

• What is Strabismus?

A

• Anomaly of ocular alignment ( commonly known as “ cross eyes”)

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48
Q

• Why does Strabismus occur?

A

• Extraoccular muscles do not work together resulting in one eye looking at an objest and the other eye looking in another direction

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49
Q

• Is it common for Strabismus to occur in one eye or both?

A

• Can occur in one or both eyes and can occur vertically or horizontally

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50
Q

• How does one get Strabismus?

A

• Congenital or acquired

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51
Q

• Does Strabismus occur all of the time?

A

• It can be consistent or intermittent

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52
Q

• What will patients with Strabismus c/o?

A

• Patients may c/o depth perception loss, diplopia, uncoordination eye movement and/or vision loss.

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53
Q

• What are the PE findings of Strabismus?

A
  • Examine for head tolt ( torticollos)
  • Assess cisual acuity
  • Assess visual function, papillary reactivity, eyelid position and extraocular movements
  • Assess the corneal light reflex
  • Perfom cover test (cover/uncover)
  • Perfom the Bruckner red reflex exam
  • Cycloplegic regraction
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54
Q

• What is the treatment of strabismus?

A
  • Treat the underlying etiology if present
  • Refer to ophthalmology
  • Correct refractive error
  • Patching of the better eye may be helpful to focus the weaker eye to work harder
  • Surgical correction may be needed
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55
Q

• What are some possible complications of Strabismus?

A
  • Amblyopia
  • Diplopia
  • Secondary contracture of extra ocular muscles
  • Adverse psychosocial and vocational consequences
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56
Q

• Is oral Candidiasis common in infants?

A

• Yes it is common in infants

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57
Q

• What is the clinical presentation of oral Candidiasis ?

A
  • Creamy white lesions on the buccal, gingical or lingual mucosa
  • May be painful
  • Can vary in number
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58
Q

• What is the treatment of oral Candidiasis ?

A

• Oral nystatin suspension

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59
Q

• Who is Umbilical hernias common in?

A

• More common in full term, AA infants

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60
Q

• What is the cause of Umbilical hernias ?

A

• Defects in the abdominal wall

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61
Q

• When do the marjority of Umbilical hernias disappear?

A

• By one year of age and nearly all disaperar by 5 years of age

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62
Q

• When should Umbilical hernias be treated surgically?

A

• Persisting after age 4 should be treated surgically.

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63
Q

• What is intussuseption?

A

• Part of the intestine slides into another part of the intestine ( “telescopes”)

64
Q

• Where can intussuseption occur?

A

• In either the small or large intestine

65
Q

• What does intussuseption do to the passage of food?

A

• Prevents food or fluid from passing through

66
Q

• Intussuseption often resuts in?

A

• Assiciated ischemia

67
Q

• Intussuseption is the most common cause of?

A

• Intestinal obstuction in children

68
Q

• What is the cause of intussuseption?

A 
•	Majority of causes in children, have no identifiable cuase
•	Triggers can include
o	Viral infection 
o	Bacterial Enteritis 
o	Intestinal Growth
69
Q

• What children are at increased risk of intussuseption?

A
  • Most commonly occur in children <2 years
  • More common in boys
  • Congenital malrotation of the intestines
  • Prior hx of intussuseption
70
Q

• What is the clinical presentation of intussusception?

A
  • Sudden onset of severe intermittent, crampy, progressive abdominal pain
  • Current jelly stool
  • Abdominal lump may be felt in the right side of the abdomin (“sausage shaped abdoiminal mass”)
  • Abdominal distention
  • Vomiting/dehydration/lethargy
  • Diarrhea
  • Fevere
71
Q

• How do you diagnose Intussuscetion?

A
  • For patients with classic clinical presentation, may proceed directly to non- operative reduction, which can be diagnostic and therapeutic
  • For unclear diagnostic cases, abdominal US or AXR may be helpful
  • CT may be utilized in certain cases
72
Q

• What will intussusception look like on X ray?

A

• Bulls eye

73
Q

• What is the treatment of Intussusception

A
  • Supportive care with IVF and NG tube prior to reduction

* Non operative reduction is successful in 80-95% of patients with ileocolic intussusception

74
Q

• When is reduction of intussusception felt to be successful?

A

• If there is free flow of constrast or air into the small bowel or there is relief of symptoms and disappearance of abdominal mass

75
Q

• When may surgery be required for the treatment of intussusception?

A

• Should be the first line treatment for patients with evidence of perforation or who appear acuterly ill

76
Q

• What is pyloric stenosis?

A

• Hypertorophy of the pylorus which prevents the stomach from emptying into the small intestine

77
Q

• What is the etiology of pyloric stenosis?

A
  • Unknown but may have a genetic componet
  • Macrolide use in late preg
  • Oral Erythromycin in the 1st 2 weeks of child life
78
Q

• What sex is more likely to have pyloric stenosis?

A

• Males more than females

79
Q

• What born child is most likely to have pyloric stenosis?

A

• More common in 1st born child

80
Q

• When do symptoms typically develop?

A

• B/w 3 and 5 weeks of age and rarely present after 12 weeks of age

81
Q

• What is the clinical presentation of pyloric stenosis?

A

• Vomiting is typically initial symptom
o Usually occur after every feeding or intermittently
o Usually between 3-6 weeks of age
o Projectile
• Persistent hunger (sick children not hungry)
• Persistent hunder
• Peristaltic waves may be noted after feeding but prior to vomiting
• Constipation can develop
• Can develop significant dehydration
• Can suffer weight loss or failure to gain weight

82
Q

• What will the Physical exam findings of pyloric stenosis show?

A
  • Dehydration
  • Abdominal distention
  • Olive shaped mass may be palpated over the gastric region
83
Q

• How do you dx pyloric stenosis?

A
  • BMP may reveal electrolyte disturbances
  • Abdominal US imaging of choice
  • Barium x-ray
84
Q

• What is the treatment of pyloric stenosis?

A

• Rehydration
• Surgical repair
• Endoscopic balloon dilation
o Not as effective as surgical repair but can be considered in infants when risk of general anesthesia is high

85
Q

o Gastroesophageal reflux
• This is common in infants
• how does Gastroesophageal reflux commonly present?

A

• Postprandial regurgitation that can range from effortless to forceful

86
Q

• How is Gastroesophageal reflux dx?

A

• Clincial dx

87
Q

• What is the tx of Gastroesophageal reflux

A
  • Resolves spontaneously in majority of infants by 12 mo
  • Small feeding
  • Thicken formula with rice cereal
  • H2 blockers and PPIs do not reduce reflux by may reduce associated pain if present
88
Q

• What is Gastroesophageal reflux Disease termed in older children when reflux causes persistent symptoms?

A

• GERD

89
Q

• Older children with Gastroesophageal reflux disease c/o?

A

• Adult like symptoms of regurgitation into the mouth, heartburn and dysphagia

90
Q

• What is the treatment of Gastroesophageal reflux diease?

A

• Trial of acid suppressing medications may be both diagnostic and theraputic.

91
Q

• What is neonatal acne?

A
  • Acne that develops on a newborns skin

* Characterized by small red bumps or pustules on a babys cheeks, nose and forehead

92
Q

• When does neonatal acne develop?

A

• Within in 2-4 weeks of birth and resolves spontaneously

93
Q

• What is the treatment for neonatal acne?

A

• No specific treatment

94
Q

• What is Seborrheic Dermatitis?

A
  • Common inflammatory skin conduction that causes flaky, white to yellowish scales to form on the scalp
  • Termed “cradle cap” when affects the scalp og an infant
95
Q

• What is the treatment of seborrheic dermatitis?

A
  • Emollients and frequent shampooing to soften and removes scales
  • If conservative measures fail, can use topical low potency corticosteroids or ketconazole shampoo or cream.
96
Q

• What is diaper dermatitis?

A
  • Erythemia that is sharply defined and has assoc. satellite lesions
  • Pustules, vesicles, papules or scales may occur
97
Q

• What is the cause of diaper dermatitis?

A

• Candida species

98
Q

• How do you dx diaper dermatitis?

A

• Can be confirmed with demonstration of yeast on wet mount if needed

99
Q

• What is the treatment of diaper dermatitis?

A
  • Cream or lotion containing nystatin, amphotericin B, or an imidazole
  • Skin Care
100
Q

• What is asthma?

A

• Chronic inflammatory disorder characterized by episodes of inflammation and small airway narrowing in response to triggers

101
Q

• What are common triggers for asthma?

A

• Animal, dust, weather changes, chemicals in the air or in food, exercise, mold, pollen, respiratory infections, stress, and tobacco smoke

102
Q

• Asthma may appear at any age, however 80-90% of children with asthma have symptoms when?

A

• 4-5 years old

103
Q

• what are common disorders that are associated with asthma?

A
  • Atopy/eczema starting in the early months of life
  • Frequent lower respiratory symptoms in the 1st year of life
  • Wheezing that is initated by a variety of triggers
  • Family Hx of asthma
104
Q

• What is the clinical presentation of Asthma?

A
  • Exam will be nl if exacterbation is not present
  • Cough ( may be productive or non productive
  • Dyspnea
  • Wheezing/prolonged expiratory phase
  • Signs of distress can include intercostal retractions, cyanosis, letharagy, tachycardia, diaphoresis
105
Q

• How do you Dx Athma?

A
  • Spirometry reveals reversible airflow obstruction
  • Impulse oscillometry is an alternative to spirometry in young children if available
  • If younger children, diagnosis may be made with a trail of asthma medications
  • Ancillary studies can include broncho provocation testing, CXR, allergy testing, barium swallow (R/O GERD) swear chloride test (r/ocystic fibrosis)
  • Peak flow measurements not as specific for diagnosis
106
Q

• what is the treatment of Asthma?

A

• Check peak flow readins every morning to determine what zone pt is in
o 80-100% green
o 50-80% yellow
o 50% red
• Identify triggers and avoid if possible
• Develop an asthma action plan
o Include what medications to take when stable
o Indentify specific triggers and ways to avoid them
o Identify how to recognize worsening of symptoms and what to do in these situations
• Education is vital

107
Q

• What are rescue medications?

A
  • Short acting bronchodilators
  • Oral steroids
  • Oxygen
108
Q

• What are preventative medication?

A
  • Inhaled steroids
  • Long acting beta agonist
  • Leukotriene inhibitors
  • Omalizumab
  • Cromolyn sodium
109
Q

• What are the compilations of asthma?

A
  • Decreased exercise capacity
  • Insomnia due to nighttime symptoms
  • Persistent cough
  • Permanent pulmonary damage
  • Respiratory failure
110
Q

• What is cystic fibrosis?

A

• Genetic disorder resulting in abnormally thick, sticky mucus that builds up in the lungs, digestive tract and other areas of the body

111
Q

• When is cystic fibrosis usually dx?

A

• By 2 years of age

112
Q

• What are the infantile/newborn symptoms of cystic fibrosis?

A
  • No bowl movement in the 1st 24-48 hours of life, delayed growth, poor weight gain, and salty tasting skin
  • GI symptoms can include severe constipation, bloating, abdominal distention, nausea, anorexia, pale or clay colored stools, weight loss
  • Respiratory symptoms can include coughing, fatigue, nasal congestion, recurrent infections, digital clubbing
113
Q

• How do you dx Cystic Fribrosis?

A
  • Sweat chloride test is the standard dx test

* Immunoreactive trypsinogen (IRT) is a standard newborn screening test for cystic fibrosis

114
Q

• What is the treatment of Cystic Fibrosis?

A
  • Antibiotics to treat infections
  • Bronchodilators may be needed
  • DNAse enzyme therapy may help to thin mucus and make it easier to cough up sputum
  • high concentrations of salt solutions
  • Immunization
  • High Calorie, high protein diets.
  • Increased fluid
  • Pancreatic enzymes to aid in digestion
  • Vitamin supplementation
  • Bowel regimen to treat constipation
115
Q

• What is the prognosis of Cystic Fibrosis?

A
  • Generally do well in childhood
  • pulmonary Disease progresses with age
  • Average life span is appx 27 years
116
Q

• What are some complications of CF?

A
  • Gi disorders
  • Chronic resp infections
  • DM
  • Infertility
  • Liver disease, pancreatits
117
Q

• What makes children more prone to FB aspiration?

A

• Smaller diameter of the airway in young children makes them more prone to airway obstruction

118
Q

• What are commonly aspirated objects?

A

• Nuts, seeds, popcorn, food particles, hardware and pieces of toys (Toy balloons are the object most commonly involved in fatal aspirations

119
Q

• Where do most Aspirated FB usually go?

A

• Bronchi

120
Q

• What is the clinical presentation of Fb aspiration?

A

• Presentation can vary from mild to severe and is usually sudden in onset.
o May present with severe resp distress, cyanosis and altered mental status
o May present with generalized or localized wheezing, regional variation in aeration, non specific cough , hoarseness

121
Q

• What is the classic triad of FB aspiration

A
  • Wheezing
  • Coughing
  • Diminished breath sounds
122
Q

• How is FB dx?

A
  • Rigid Bronchoscopy is gold standard (dx and tx)
  • CXR
  • CT or MRI
123
Q

• Tx of FB aspiration?

A
  • Initially presentation with life threatening airway obstruction, attempt dislodgement utilization back blows with chest compression in infants and Heimlich maneuver in older children
  • If unsuccessful, attempt intubation until bronchoscpy can be performed
124
Q

o Atrial Septal defect

• What is an atrial septal defect?

A
  • Congenital defect in which there is a hole between the left and right atria
  • Allows oxygenatied blood to flow from the left atrium to the right atrium which can lead to right heart strain and ultimately right sided heart failures, pulm HTN or CVA
125
Q

• Are Atrial Septal defects usually problematic?

A

• Typically asymptomatic until adulthood

126
Q

• What is the clinical presenation of a atrial spetal defect?

A
  • Many infants are asymptomatic
  • Many are dx after incidental note of heart murmur on PE
  • May experience mild cyanosis due to transient right to left shunting across the ASD in the neonatal period
  • If ASD is large: Infants may present with heart failure, recurrent resp infections or failure to thrive
127
Q

• What are the PE findings of Atrial septal defects?

A
  • Wide fixed split S2
  • Several types of murmurs can be heard- characteristic murmur is a midsystolic pulmonary flow or ejection murmur
  • Findings of pulmonary HTN may be noted
128
Q

• How do you Dx Atrial septal defects?

A

• EKG:
o Prolonged sinus node recovery time
o PR interval may be prolonged
o Arrhythmias common after the 3rd decade of life
o Right ventricular conduction delay
• CXR- cardiomegaly and increased pulmonary vascular later on in disease course
• ECHO is imaging of choice for dx!

129
Q

• what is the treatment of atrial sepral defects?

A

• Monitor:
o Children should be folled by ped cardiologist of ASD is clinically significant
o Many close spontaneously
• Repair indicated if large left to right shunt that results in symptoms or with significant right heart enlargment
o SXR with a patch
o Transcatheter closure can proved a less invasive treatment option for smaller defects.

130
Q

• Ventricular Septal Defects

A

o A congenital opening or hole that allows communication between the right and left ventricles
o Most common congenital heart lesion
o Can occur in isolation or in association with other congenital defects
o Progression depends on size and location

131
Q

• What is the clinical presentation of ventricular Septal Defects?

A

o Generally dx in the neonatal periods but presentations can vary significantly depending on the size and location of the defect and the ability of the left ventricles to maintain systemic output
o Small defects often asymptomatic (detected after murmur auscultated on exam)
o Moderate to large defects often become symptomatic in 1st week of life
• Mild tachycardia and tachypena

132
Q

• what are the PE findings of ventricular Septal Defects?

A

o Murmur may be heard as early as 4-10 days of life or may be delayed until several weeks of age
o A thrill may be palpated
o Apical pulse may be prominent due to vigorous LV contraction
o Cardiac apex may be displaced laterally as heart enlarges
o Systolic and diastolic murmur can be heard and can vary based on the size and location of the defect
o S2 can vary but is difficult to assess d/t murmur
o Arterial pulses can be diminished as LV failure occurs

133
Q

• How do you dx ventricular septal defects?

A

o EKG
• RVH, LVH, and or right BBB
o CXR
• Can reveal increased pulmonary vascular markings, RV and LV enlargment
o Echo useful to identify size and location of the defect

134
Q

• What is the treatment of ventricular Septal Defects?

A

o monitor
o initate medical therapy as needed
o SXR repair should be made by:
• 6 mo of age if Pulm vascular resistance is elevated
• By 1 year if pulm vascular resistance is normal but there is a significant left to right shunt
o Children >2 years old who do not experience spontaneous closer need to monitored and evaluated periodically

135
Q

• Complications of ventricular Septal Defects?

A 
o	Endocarditits
o	Aortic regurgitation 
o	Subaortic stenosis 
o	RV outflow obstruction 
o	Left ventricle to right atrial shunting
136
Q
  • Tetralogy of Fallot

* Classic form includes 4 defects

A

o ventricular Septal Defects
o Pulmonary artery stenosis
o Overriding aorta that is shifted over the right ventricle and ventricular Septal Defect
o Right ventricular hypertrophy/ right ventricular outflow obstruction

137
Q

• Tetralogy of Fallot is the d/t

A

o Certain Chromosome disorders

138
Q

• What is the clinical presentation of Tetralogy of Fallot

A 
o	Degree of symptoms dependent upon the severity of right ventricular outflow obstruction 
o	Cyanosis
o	Digital clubbing
o	Difficulty feeding
o	Irritability / prolonged crying
o	Fatigue
o	Fainting
o	Failure to gain weight
o	Poor development
o	Tet spells ( intermittent hyppercyanotic spells)
139
Q

• What are the PE findings of Tetralogy of Fallot ?

A

o Crescendo- decrescendo harsh systolic ejection murmur

o Single S2

140
Q

• How do you dx Tetralogy of Fallot

A 
o	CBC may reveal erythrocytosis
o	Pulse ox= hypoxia
o	CXR boot shaped heart (RVH)
o	EKG 
o	Echo
141
Q

• What is the treatment of Tetrology of fallot?

A

o SXR within 1st year of life
o Medical treatment in severe pts with symptoms while they await treatment:
• IV prostaglandins, Dig, Diuretic therapy

142
Q

• What is PAD?

A

o Ductus arteriosus is a vascular connection used in fetal circulation to divert blood from the fetal lungs
o From the pulmonary artery to the left atrium

143
Q

• When does the Ductus arteriosis typically close?

A

o 2-3 days after birth

o if the Ductus arteriosis does not close by 2-3 days it is then termed PAD

144
Q

• Who is PAD likely to occur in?

A

o Females, Premature infants, infants with neonatal respiratory distress syndrome, infants with congenital heart defects, infants born to mothers who had rubella during their pregnancy and in certain genetic disorders such as downs syndrome.

145
Q

• What is the clinical presenation of PAD?

A

o May be asymptomatic
o Some infants will have symptoms including tachypnea, poor feeding habits, tachycardia, deyspnea, and diaphoresis with feeding, fatigue and poor growth.

146
Q

• What are the PE findings of PDA?

A

o Continuous flow murmur

o In larger defects, the pMI may be displaced laterally due to left ventricular hypertroph and a thrill may be palpated

147
Q

• How do you dx PDA?

A

o Echo

148
Q

• What is the treatment of PAD?

A

o The goal of Tx is close the PAD
• Can be monitored clinically or closed via a trans catheter approach or open heart
o NSAIDS may be helpful in these situations to help close PDA

149
Q

• What is aortic Coarctation?

A

o Discrete narrowing of the thoracic aorta

150
Q

• Where does the aortic coarctation commonly occur?

A

o Near the ductus arteriosis

151
Q

• What is the etiology of Aortic coarctation?

A

o Unknown, but appears to be an increased risk associated with bicuspid aortic vavle, patent ductus ateriosus, aortic hypoplasia, VSD, aortic valve stenosis, mitral valve disorder and certain genetic conditions such as turners syndrome

152
Q

• What is the clinical presentation of aortic coarctation?

A

o Neonate: Asymptomatic especially if PDA is patent- if severe coarction heart failure and or shock may be present
o Older infants : Majority are asymptomatic
• If symptomatic, can experience evectional chest pain, cold extremities, and claudicating with Physical activity
o In undiagnosed adults, the classic presenting symptom is HTN, Claudicating

153
Q

• What are the PE findings of aortic coarctation?

A

o Elevated systolic BP in the upper extremities when compared to the lower extremities
o Weak or delated pulse in the lower extremities (Brachial Femoral Delay)
o Cardiac exam may be normal
o Murmur may be auscultated due to presence of associated cardiac defects

154
Q

• How do you dx aortic coarcations?

A

o CXR- enlarged heart or aortic narrowing
o EKG ventricular hypertrophy
o Echo can detect location and severity of aortic coarctation as well as associated cardiac defects

155
Q

• What is the treatment of Aortic Coarctation?

A

o Medications do not repair the coarctation but may be helpful for symptomatic control while awaiting surgical repair
• Infants can be given Prostaglandin E which can help to keep the ductus arteriosus open
o Angioplasty and stenting
o SXR
• Resection/patch/bypass

156
Q

• Abnormal developmental primitive reflexes

o Absence at age when they should normally be present

A

• Suggests underlying neurologic disorders

Clinical Medication: HEENT (39 decks)

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