Sbm Respiration: Copd And Neonatal Respiration

Front 1

These are some maternal causes of acute perinatal asphyxia

Back 1

Chronic HTN, pregnancy-induced HTN (PIH--pre-eclampsia), renal disease, heart disease, uterine abnormalities, fever, placental abruption

Front 2

Placental abruption

Back 2

Separation of placenta from the uterine lining, occurs in 1% of pregnancies, 20-40% fetal mortality rate

Front 3

These are some fetal causes of acute perinatal asphyxia

Back 3

Arrhythmias, hydrops fetalis (edema of any cause), polyhydramnios (too much amnionic fluid), infection

Front 4

These are some iatrogenic causes of acute perinatal asphyxia

Back 4

Regional anesthetic hypoperfusion, uncorrected supine positioning, beta blockade

Front 5

This is the way blood redistributes in acute perinatal asphyxia

Back 5

Flow to vital organs (brain, heart, adrenals) maintained or increased; flow to placenta maintained unless cord obstruction; decreased flow to liver, kidneys, GI tract, skin

Front 6

These are the four specific findings of failure/delay in decreasing PVR at birth

Back 6

Tachypnea--pulmonary
Scaphoid abdomen--diaphragmatic hernia
Heart murmer--congenital heart disease
Abnormal CXR--RDS, pneumonia, venous congestion

Front 7

These are possible causes of failure or delay in PVR reduction in newborns

Back 7

Decreased size of lung vascular bed (eg, diaphragmatic hernia), pulmonary vascular constriction (RDS, PFC, premature ductal closure), obstruction (polycythemia), pulmonary venous HTN (incl. surgical emergency: PV, LA or mitral obstruction; or LV problems causing backup of blood into lungs)

Front 8

Causes of patent ductus arteriosus

Back 8

Premature birth--the DA is less sensitive to the constrictive effects of O2, and there is incomplete development of the muscles in the premature infant, ie, less contractile ability

Front 9

Diagnosis of PDA

Back 9

Worsening apea
Failure to wean
Heart murmur
Widened pulse pressure
Full or "bounding" pulse
"Hyperactive precordium

Front 10

Treatment of PDA

Back 10

PG synthetase inhibitors (Indomethacin) or surgery; prevention by maternal steroid administration

Front 11

Definition of COPD

Back 11

* partially reversible
* abnormal inflammatory response (PMN's, macrophages)
* significant systemic consequences
* 1 in 5 smokers (thus there is some genetic component)

Front 12

Diagnosis of chronic bronchitis

Back 12

Clinical diagnosis: productive cough on most days for a min of 3 mos/yr for at least 2 successive yrs

Front 13

Diagnosis of emphysema

Back 13

Pathological diagnosis: abnormal enlargement of airspaces distal to terminal bronchiole, accompanied by destruction of their wall, and w/o fibrosis

Front 14

This is the mechanism responsible for the increase in residual volume (RV) in all obstructive lung diseases.

Back 14

Air trapping

Front 15

Features of chronic bronchitis

Back 15

1. Hypersecretion of mucus (goblet cell hyperplasia, mucous gland hyperplasia)
2. Small airway alteration (mucus plugging, macs. + inflam. cells,submucosal FIBROSIS)
3. Secondary infections (common b/c of epithelial alterations METAPLASIA)
4. Bronchospam of smooth muscle lining airway (asthamatic component of COPD)

Front 16

Features of emphysema

Back 16

1. Shiny balloon-like appearance (lungs lose elastic recoil)
2. Destruction of tissue by ELASTASE released by neutrophils and macs.
3. Imbalance of anti-elastases (eg, alpha 1 anti-trypsin, A1AT)

Front 17

FRC is normal in this COPD

Back 17

Chronic bronchitis

Front 18

FRC is changed in this COPD

Back 18

Emphysema. It is larger because there is less elastic recoil of the lung to resist the outward force of the chest wall

Front 19

DLCO is changed in this COPD

Back 19

It is decreased in emphysema because alveoli are destroyed

Front 20

RV is changed in this COPD

Back 20

All obstructive lung diseases, due to air trapping.

Front 21

T/F: 10% of patients with severe chronic bronchitis are lifelong non-smokers

Back 21

True.

Front 22

A1AT

Back 22

Protective anti-protease, produced in liver.

Front 23

T/F: Patients with bronchitis can suffer from overlapping asthma symptoms, and some asthma patients can suffer bronchitis flare ups.

Back 23

True.

Front 24

An imbalance in these cells are thought to be involved in extrinsic (allergic) asthma

Back 24

Types I and II helper T cells. More type II at work in asthma

Front 25

These cells induce bronchial allergic inflammation

Back 25

Type II helper T cells stimulate B cells to produce IgE

Front 26

Features of asthma

Back 26

1. Thick mucus plugs
2. Eosinophils
3. Thickened epithelial BMs
4. Submucosal edema and inflammation
5. Hypertrophied smooth muscle
6. Hypertrophied submucosal glands

Front 27

Features of bronchiectasis

Back 27

Irreversible abnormal dilatation of airways, usually secondary to chronic infections.

Front 28

Non-COPD causes of bronchiectasis

Back 28

Repeat infections, aspergillus colonization, primary cilia disorders, cystic fibrosis.