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Neo boards > Respiratory Disease > Flashcards

Respiratory Disease Flashcards

1
Q

Pleural fluid > 1000 cells, >80% lymphocytes, TG > 100s.

A

Chylothorax

R>L
FA, TG and protein LOSS
Risk infection - also lose immunoglobulins

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2
Q

Transudative vs exudative

A

Transudative -pH>7.4, wbc< 1000, LDH <200

Exudative pH < 7.4, wbc > 1000, LDH > 200

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3
Q

Describe congenital pulmonary lymphangiectasia

  • when does lymphatic system develop
  • genetic associations (primary CPL)
  • secondary CPL exs

Mgmt, Prognosis

A

Devp - starst 6 wks, usually complete by 20 wks

Genetics - Associated with Noonan’s, Ehlers-Danlos, Ullrich-Turner, Down’s syndrome

Secondary - TAPVR, HLH with restricted septum

Supportive care, poor prognosis, later dx has a better prognosis

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4
Q

Review stages of lung devp and congenital lung abnormalities – 2 mistakes!

A

cong lobar emph - LUL #1, increased risk CHD, disruption of brochopulm devp (cartilageous defect?)

CPAM - branchingabnormalitof lung at differentairway levels; imbalance cell proliferation and celldeath; cystic and adenomatous overgrowth, 5 types, #1 70%
0,2 with anomalies - poor prognosis, 3 vey large

bronchogenic cyst - anomalousbudding of foregut, mostly posterior trachea, sx dep on size, location

Cong pulm lymph - M>F increased risk pleural effusions, often need bx to dx, hyperinflated lungs, poor prognosis if severe

BPD - nonfunctioning lungtissue

bronchogenic cyst - embryonic stage

cong lobar emphysema - pseudoglandular stage

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5
Q
A
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6
Q
A
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7
Q

Types 0 to 4 CPAM
- most common
- most severe / bad prognosis
- most associated with other anomalies

A
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8
Q

intralobar vs extralobar BPS

A
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9
Q

congenital pneumonia
- organisms by when it presents - perinatal, early (1 wk) or late (after 1 week)

A
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10
Q
A
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11
Q

Choanal atresia

  • R vs L
  • Unilateral vs bilateral
  • Bony vs mixed
  • How often associated with other anomalies
A
  • Right
  • FEMALES > males
  • 70% mixed
  • 50% other anomalies
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12
Q

Phrenic nerve injury

  • which cranial nerves
  • causes of injury
  • sx
A

C3 - C5
75% from associated injuries – neck hyperextension
innervates diaphragm - resp distress
could - rare - assocaited with spinal cord injury (VASCULAR or bony injury or fracture)

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13
Q

Pneumothorax

  • when does it resolve
A

1 to 2 days

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14
Q

Pneumomediastinum

  • XR finding
  • causes
A
  • sail sign / angel wings
  • can be associated with pharyngeal perf (see air around mediastinum, air around airway)
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15
Q

Chylothorax

-what causes
- MOST COMMON PLEURAL EFFUSION IN NEONATES

  • M vs F
  • analysis of pleural fluid
  • primary vs secondary (%)
  • examples of primary
A

primary -
— congenital chylothorax eg trisomy 21, noonan, turner’s
— congenital pulm lymphangiectasia - abnormally wide or dilated lymphatics, can compress airway

M&raquo_space; F

Fluid: lymph predominance > 80%, TG >100, LDH elevated

Can give MCT, fat free diet (MCT absorbed into vasculature not lymphatics)

Most are secondary / acquired

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16
Q

Congenital lobar emphysema

  • pathophysiology
  • primary area of lung
A

1 LUL

defective bronchial cartilage –> overexpansion of 1+ pulmonary LOBES which can compress others / airtrap

Non functional lobe

pseudoglandular stage?

about 1/4 present at birth

17
Q

CDH

  • most common location
  • when dx (when develop)
  • what LHR is poor prognosis; what LHR may be associated with high survival
  • what O:E poor survival
A

1 - posterolateral

can dx around 24 weeks although develops around 16 wks (pseudoglandular stage)

LHR > 1.3 to 1.4 - good prognosis
LHR < 1 - poor

O:E < 25% - poor survival

18
Q

NEHI

A

CXR hyperexpansion and increased ground glass

ILD

initially asx, then sx within 1st 3 months

disorder of poorly understood or unknown etiology

19
Q

Pulmonary interstitial glycogenesis

A

Hypoxemic at birth, mild symptoms

may respond to steroids

disorder of poorly understood / unknown etiology

20
Q

Pulmonary hemorrhage

A
  • due to acute increase in capillary hydrostatic pressure — can result from L to R shunt from PDA OR vasoconstriction after perinatal depression or ACUTE pressures changes after surfactant
  • capillary vessels break down and “leak” fluid

Mgmt - increase PEEP (distend against blood, decrease PBF), check coags

21
Q

CPAM

A

see by 18 weeks

tend to grow by 28 weeks

22
Q

Alveolar capillary dysplasia

A

LARGE pulm veins next to bronchovascs thick alveolar septa, capillary not close to alveoli

PPHN presentation at term, resp failure within 48 hours.

HUGE air leak risk

acinar dysplasia

80% associated with other anomalies

23
Q

Cystic fibrosis

A

increase IRT

pancreatic insufficiency, FTT, fat malabsorption, mec ileus, bilateral agenesis vas deferencs, obstructive lung disease

24
Q

VV vs VA ECMO

  • achievable PaO2
  • high or low perfusion state required
  • maintains pulm blood flow
  • caridac support
  • which lower risk of arterial emboli
A

VV
- lower achievable PaO2
- as maintains PBF
- no cardiac support
- requires higher perfusion rates
- lower risk of arterial emboli

VA - higher achievable PaO2
- bypasses pulm circulation
- cardiac support
- requires lower perfusion rates

25
Q

Acinar dysplasia

A

complete absence of alveolar development, ONLY airway structures

Largely in FEMALES

Term infant, severe PPHN, severe resp failure in 48 hours (like ACD)

26
Q
A

Neo boards (14 decks)

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