Neonatal, developmental, vascular lung disease Flashcards

1
Q

Describe how the design of the lung works to protect the organism from airborne toxins while still performing gas exchange

A

Upper airway filter that filters out particles over 10 microns in diameter.
Tracheobronchial mucociliary apparatus filters out particles that are over 5 microns
Intraalveolar phagocytic system traps other particles.

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2
Q

Normal histology of a bronchi from outter to inner

A

Pseudo-stratified ciliated columnar epithelium, thin Basement membrane, subepithelial layer, cartillaginous ring. (I think Heron says its a little more complicated. Check out his first pwrpt).

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3
Q

Right mainstream bronchus is more vertical than the left?

A

True…creates a greater risk for aspiration on the right

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4
Q

“Fetuses breathe with their placentas, newborns breathe with their lungs” What is the significance of this?

A

If a fetus has a lung problem we dont know it until its a newborn

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5
Q

Name two developmental anomalies involving the lung

A
  • Pulmonary agenesis or hypoplasia

- Tracheobronchial anomalies

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6
Q

What is pulmonary agenesis or hypoplasia

A

multiple malformation syndromes such as a diaphragmatic hernia

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7
Q

Tracheobronchial anomalies

A

…see slide

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8
Q

Congenital emphysema?

What lobes does it tend to effect?

A

Accounts for half of congenital lung lesions in infancy. Tends to effect upper left lobe (50%) and right middle lobe (24%). Air traps due to a cartilage deficiency in bronchial tree

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9
Q

Congenital cyst?

When is it found?

A

Mucus filled bronchial epithelium cells….not found until 14-30 yrs of age. May occur anywhere in the lungs

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10
Q

Explain pulmonary sequestrations

A

It is pulmonary tissue that is within (intrlobar) or outside of (extralobar) normal lung. It does not connect to the tracheobronchial tree.

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11
Q

Intralobar sequestration usually present as

A

recurrent infection

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12
Q

Extralobar sequestration usually associated with

A

I dont know but they are usually recognized in kids as mass lesions

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13
Q

3 types of neonatal aspiration syndromes

A

Inhalation of amniotic fluid/MECONIUM in utero due to fetal distress…most likely to see this
Inhalation of bloody amniotic fluid peripartum
Inhalation of gastric contents postpartum

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14
Q

Hyaline membrane disease

A

Pulmonary edema, membrane formation, resorptive atelactisis, bronchiolar epithelium necrosis.
More common in males, prematures, twins, mild maternal diabetes, C-section, colder weather.
Due to the physiochemical shock of lung expansion

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15
Q

What is atelectasis

A

collapsing of a lung or incomplete lung expansion at birth

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16
Q

Three types of atelactasis

A

1) Resorption- intrabronchial obstruction in this one- it is reversible
2. ) compression- compression from outside- reversible
3. ) Contraction- Caused by parenchymal scarring, this is not reversible

17
Q

Which type of atelectasis is not reversibel

A

Contraction- caused by parenchymal scarring

18
Q

What is pulmonary edema

A

Intraalveolar pooling of proteinaceous fluid due to hemodynamic causes or microvascular injury.

19
Q

Two categories of pulmonary edema causes

A

hemodynamic and microvascular

20
Q

Hemodynamic causes of pulm edema are

A

increased hydrostatic pressure in the vasculature or decreased oncotic pressure

21
Q

Increased hydrostatic pressure can be caused from>

A

Left sided heart failure. Mitral valve stenosis, volume overload, pulmonary vein obstruction

22
Q

Decrease oncotic pressure causes

A

hypoalbuminemia, nephrotic syndrome, liver disease

23
Q

Microovascular causes of pulm edema are

A

infectious gasses, irritant gasses, toxic drugs, sepsis, radiation

24
Q

Proinflammatory cytokines

A

IL-1, IL-8, TNF….released by macrophages during acute lung injury and ARDS

25
Q

What factors do neutrophils release in the alveolar space and what do these things do>

A

Leukotrienes, oxidants, proteases, Platelett Activating Factor
These contribute to local tissue damage, accumulation of fluid, surfactant inactivation and hyaline membrane formation.

26
Q

What does MIF do?

A

MIF (macrophage inhibiting factor) sustains the local proinflammatory response.

27
Q

TGF-Beta and PDGF stimulate what

A

Fibroblast growth and collagen deposition associated with healing

28
Q

Two Pulmonary hemorrhagic syndromes

A

Goodpasture’s and Granulomatosis with polyangiitis

29
Q

Goodpastures syndrome triad is

A

Glomerulonephritis, lung hemorrhage, and antibodies to the alpha 3 chan of type IV collagen

30
Q

Typica goodpasture’s patient

A

Youbg adult male…20-30 yo

Left untreated….renal failure

31
Q

Granulomatosis with Polyangiitis affects?

A

Lungs and upper resp tract, potentially the kidney

32
Q

G w/ P is characterized by

A

necrotizing vasculitis and granulomas

33
Q

G w/ P most commonly affects

A

middle aged men

34
Q

Look for what with G w/ P

A

ELevated serum C-ANCA corresponding to ant PR# proteinase antibodies

35
Q

What the hell are ANCAs

A

Anti- neutrophil cytoplasmic antibodies are a family of autoantibodies that react with myeloid specific proteins found in white blood cells

36
Q

What is the most common tracheoesophageal fistulae?

A

One in which the trachea communicates with the distal portion of an esophagus that was atretic at the top.

37
Q

Common causes of ARDS

A

Burns, Near drowning, mechanical trauma

Smoke or irritant gasses