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# Congenital ltuahiolies
☐ pulmonary hypoplasia
Affects development^ of^
teeth lungs
It's caused^ by
abnormalities like
① Diaphragmatic hernia -
congenital ② oligohydramneas which campuses
- lungs & itcan be fatal . Foregut cyst^
Arising from^ abnormal
detaihmenb
of primitive^ foregut ④ hilum^ 1hr9Idle^ mediastinum
Pulmonary sequestration Aosta. § e-^ Abnormal blood^ supply from Discrete (^) / (^) Separate area^ in^ tiny tissue
F-
Exkalobar Tutralobar
- (^) text. to (^) lung • we Ethan teeny
- (^) Mars (^) tension ◦ (^) in older child
- (^) Due (^) to Recurrent BRONCHIECTASIS
'
- (^) Tracheal htsaondu.at (^) Anomalies ☐ (^) Atresia → stenosis
Jeaeheo esophageal fistula E) Vascular Anomalies 0 Congenital pulmonary^ airway malformed
congenital
takas aueuiufleunmofr≥ Emphysema
(^) ATELECTASIE [
COLLAPSE] → (^) hreowpkte expansion (^) of (^) lungs i neonatal atelectasis^ I collapse of previously (^) inflated lungs ① Resorption Atelectasis
obstruct
by mucus^ plugs
/excessive
& deueeatw Air (^) is (^) iresorbed from that^ obstructed distal abvolt i
③ Contention^ atelectasis^
occurring when whole^ pulmonary or pleural fibrosis^ peanuts^ full leung expansion
- PULMONARY EDEMA → Excessive^ interstitial^ fluid accumulate in (^) alveoli Due to ← Hemodynamic
Microvascular
disturbances (^) trying
- Increased^
hydrostaticpressure a)^
das culler endo-
- t.US^ →^ CCF^221 £^ edit^ £!
- hydrostatic^ pressure^ greater^ thulium t damage , at basal^
region of
laurel '
- Produces reason
take (^) live exudate^ leaking
into interstitial
Alveolar
capillary are +^ engaged Intra -^ alveolar^ taausduale that
appears
as - granular pale^
pork
Alveolar microbemassages
to failure nhemosoedoedeutaden macrophages } (^) Mb
ACUTE^ LUNG^ INJURY &^ ACUTE
RESPIRATORY DISTRESS SYNDROME
hung ihfwy
CALI] ÷ onset of hypoxemia Bilateral
pulmonary
edema ais^ absence of cardiac failure him> Non - cardiogenic pulmonary edema
- (^) Severe manifested (^) of His →^ gives acute respiratory distress (^) syndrome CAROB
- Accumulate^ of intra- alveolar fluid 2 hyaline fermata
→ Endothelial activated
injury ie.^142 steps matte (^) capillaries leaky t Allowing accumulate
of fluid^
I necrosis of (^) type
(^) pneumonitis
leads to surfactant abnormalities + compromising GAG (^) EXCHANGE ⊕ ↓ Protein crick edema fluid
cetlbaig Hyaline whom Lorene HALLMARK (^) ⑨ ALI/ ARDS ↓ a) Resolution of injury → Macrophages
alveolar
depose
Release
fibro
③ (^) genie
Pt&F
② cytokines egi. TGF-^ P transforming
BiowᵗFadoiB
All ① +②^ +^
Fibroblast
growth
collagen deposit leading fibrosis^ of^
Alveolar Wall.
* Pniuuocyte Pastorate^ is^
done by
tmewmeeeyle II^ tnunuaeyle
I curvingweeds
- endothelial (^) → proliferates to cuwiwjureds form healthy endothelium torsion are not distributed^ rather those are^ constricted (^) in spot like manner (^) CEla which (^) are
→ stiff
→
poorly
arcaded
It (^) has Horst^ prognosis in^ chronic alcoholic (^) & In saryokers .
- (^) Histological (^) Findings ☐ (^) hyaline membrane^ @^ alveolar (^) really
- Edema &cultured^ neutrophils +^ Macrophages
Necrosis
→ Hyaline (^) Deposit
a-satiate^ Manifest
Dyspnea 2J Jadvyphlll
- (^) Resp. Failure V. Hypoxemia ↑
cyuosis ↑
Sepsis
② Hutto^
organ
fail ③ (^) Severe thug ihyhiry.
