9.6, 9.7 Pulm HTN, RDS Flashcards
Pulm HTN
-what would you see if you took autopsy
- atherosclerosis of pulm trunk
- smooth m hypertrophy in pulm arteries
- plexiform lesions (capillary tufts) in longstanding disease
secondary pulm HTN:
main causes (know all 3)
- hypoxemia in lung disease (COPD, interstitial disease)
- increase blood volume in pulmonary circulation (eg congential Eisenmengers, L sided heart failure)
- recurrent pulm embolism (thickens vascular walls)
What complications can happen when giving supplemental O2 to newborn with Neonatal Resp distress syndrome?
Free radical damage:
- blindness
- lung dysplasia
ARDS
-clinical presentation
- hypoxemia, cyanosis, resp distress.
1. thickened diffusion (hyaline membrane)
2. collapsed alveoli (hyaline membrane) - ‘white out’ on CXR
ARDS
-what lung disease complicates ARDS recovery?
- interstitial fibrosis.
- this damages type II pneumocytes, which are the stem cells. So regeneration of damaged pneumocytes is impaired.
what is major component of surfactant?
lecithin (aka phosphatidylcholine)
Pulm HTN
-definition
>25mm Hg in pulmonary circuit
normal is 10mm Hg
Neonatal Resp distress syndrome
-complications at birth (3)
- hypoxemia at birth: prevent closure of PDA
- necrotizing enterocolitis (low O2 to gut at birth)
- Blindness, lung dysplasia–Free radical damage from supplemental O2 tx at birth
surfactant production, fetal:
- what week starts
- what week is adequate level reached
- begins 28 weeks
- finishes 34 weeks
ARDS
-mech of disease
- damage to alveolar-capililary interfaces causes leakage of protein-rich fluid into alveoli. this forms a hyaline membrane in alveolar wall.
- caused by activated neutrophils, which induce protease and free radical damage of pneumocytes (Type I and II)
Pulm HTN:
3 highest yield points, according to Pathoma
- BMPR2 inactivating mutations, cause vascular smooth m proliferation in primary pulm HTN
- Plexiform lesions (tufts of capillaries) in Pulm HTN
- atherosclerosis of pulm artery
Neonatal Resp distress syndrome
-causes (3)
- premature (
- C-section. Steroids from stress required for surfactant production. Normal birth induces steroid production, but C section does not.
- Maternal diabetes. Insulin decreases surfactant production, and fetus makes lots of insulin to mom’s sugar
Maternal diabetes:
what to worry about in newborn?
- neonatal resp distress syndrome
- lack of surfactant production b/c insulin inhibits its production. fetus’s pancreas is making insulin to mom’s high sugar
primary Pulm HTN:
- mech
- classic population
- young women
- etiology unknown, some genetic forms caused by BMPR2 inactivating mutations–cause vascular smooth m proliferation
Neonatal Resp distress syndrome
-appearance on CXR
-diffuse granular appearance (‘ground glass’ appearance)
ARDS
-tx
- tx underlying cause
- use PEEP (positive end-expiratory pressure) ventilation to keep alveoli open at end of expiration (prevent them from collapsing, which takes a lot of energy to reopen)
ARDS
-what do you see on CXR
“white-out” on CXR
C-section delivery:
-what happens to baby’s lungs?
- Neonatal Resp distress syndrome, possible
- lack of surfactant production b/c its production is induced by the stress of vaginal birth
Type II pneumocytes
-2 important functions
- stem cells
- produce surfactant
Young, health woman with exertional dyspnea:
-suspect what
primary Pulm HTN.
-etiology unknown, some inherited forms caused by BMPR2 inactivating mutations. cause proliferation of vascular smooth m
fetus: what to measure if surfactant production is adequate?
- measure L:S ratio (lecithin: sphingomyelin) in amniotic fluid
- Lecithin (phosphatidylcholine) is main component of surfactant and will increase over time, while sphingomyelin remains constant
- L:S ratio >2 is adequate surfactant
ARDS
-causes
- too many to list. Remember it results in activated neutrophils, which induce protease and free radical damage of type I, II pneumocytes.
- sepsis, infection, shock, trauma, aspiration, pancreatitis, DIC, HSR, drugs
