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86 Cards in this Set
- Front
- Back
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gas exchange area of human placenta
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~ 5 meters squared
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oxygenated blood from placenta reaches fetus via what?
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umbilical vein
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compare efficiency of gas exchange in human placenta vs. lung
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PLACENTA IS LESS EFFICIENT
10-20x more O2 exchanged in lung per mass VO2 of placenta is significant (consumes 20-50%) Placenta is a much larger functional shunt (20-35% shunt, vs. 2% shunt in lung) |
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Factors that determine placental gas exchange
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*PaO2 of the uterine artery and umbilical artery (GRADIENT)
*UTERINE BLOOD FLOW and HGB levels *RELATIVE AFFINITIES of MATERNAL and FETAL HGB |
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what factors promote O2 transfer from maternal to fetal HGB
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1) Difference in relative amounts of HGB
2) difference in relative affinities of HGB 3) Double BOHR effect (co2 exchange accounts for 8% of O2 exchange) 4) Double Haldane Effect (effect of O2 exchange on CO2 exchange) 5)small amt of CO causes big change in fetal O2 |
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fetal PaO2
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20-30 mmHg
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02 consumption of fetus relative to adult (per unit weight)
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O2 consumption of fuetus is 2x that of an adult
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oxygen reserve of fetus is enough for how long?
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1-2 minutes
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Fetal Adaptations to hypoxic environment
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1) Fetal Hgb (beta chains vs. alpha, higher affinity Hgb)
2) Fetal and Maternal O2 content (fetal [Hgb] increases while maternal O2 capacity decreases during gestation) 3) Fetal Blood Flow distribution (highest PaO2 goes to vital tissues) |
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at term what percentage of Hgb is fetal Hgb?
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~85%
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contrast fetal Hgb to adult Hgb
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fetal Hgb has >> O2 affinity
-oxyhemoglobin curve shifted left -P50 for fetal Hgb is lower (20) than for adult Hgb (26) -fetal Hgb does not bind 2,3, DPG as well as adult Hgb -for any given sat. PaO2 << that of adult Hgb |
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what happens to fetal [Hgb] during gestation
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increases to ~14 (versus adult 12)
to ~85% of total Hgb decrease Hgb saturation in fetus |
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what percentage of combined CO goes to fetal lungs?
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~5-8%
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why does such a small % of combined caridac output go to fetal lungs?
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1) High PVR (pulmonary vascular resistance)
2) flow to lungs not needed for gas exchange, some needed for growth and development |
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placental blood flow is influenced by what?
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pulmonary blood flow
-as Pulmonary BF decreases -placental BF increases |
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blood with the highest O2 concentration flows from the placenta to where?
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placenta-->
Umbilical vein ---> Ductus Venosus --> IVC |
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mixing and streaming of blood in the heart is decreased by what structure?
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Foramen Ovale
distributes high [O2] blood from RA to LA so that it can go directly to the brain and heart |
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3 big fetal adaptations to hypoxic enviro
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specialized Hgb
increased red cell mass specialized distribution of Cardiac output |
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despite a low PaO2 and an Hgb sat 25% lower than the adult, the Oxygen content of fetal blood is great than or equal to that of
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the moterh
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what accompanies and develops with airways in the fetus?
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arteries
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what type of branching pattern is complete by 16 weeks gestation
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pre-acinar (pre-respiratory) branching pattern
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when do intra-acinar arteries develop?
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later (after 16 weeks) and continue to form after birth
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what prevents bloodflow through fetal lungs?
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high pulmonary vascular resistance
ductus arteriosus allows circulation to bypass lungs |
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Placenta --> ??? --> FO --> Left Heart --> ???
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Ductus Venosus
Body/ Placenta |
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what factors affect PVR (pulmonary vascular resistance)
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Morphology (vessls themselves)
Relative hypoxia and acidosis otehr factors |
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factors promoting vasoconstriction (increasing PVR)
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-physical (lung fluid)
-decreased O2 and pH -leukotrienes -TxA2 |
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factors promoting vasodilation (decreasing PVR)
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-NO
-increasing O2 and pH -PGI2 |
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Major dilator of the ductus arteriosus
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PGE2
-produced in placental, cleared in fetal lung |
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Major constrictor of the ductus arteriosus
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ET-1
(formation increased by increasing PO2) |
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what is responsible for closing the ductus after birth
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apparently O2
associated with increase in intracellular Ca2+ and depolarization of SM cell membranes probably involves changing balance of constrictor and dilator factors +PO2 leads to + ET-1 ET-1 overcomes dilating effects of PGE2 and NO May be assisted by decrease in vascular pressure |
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Stage I of pulmonary vascular changes at birth
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rapid adaptation (24 hours)
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Stage II of pulmonary vasculature changes following birth
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structural stabilization (3 months)
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Stage III of pulmonary vasculature changes following birth
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GROWTH
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transitional circulation
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placenta removed
FO and DA still open PVR decreasing once FO and DA clos PVR is low |
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main changes in Pulmonary vasculature post-birth
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decreased PVR (mechanical and O2)
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main changes in circulation following birth
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closure of foramina
-ductus arteriosus -foramen ovale -ductus venosus |
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what establishes continuous breathing?
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the first breath and expulsion of fetal lung fluid
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2 clinical problems associated with failure of transition
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PFC (persistance of fetal circulation, or delay in normal decrease in PVR)
PDA (patent ductus arteriosus) |
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what can cause persistance of fetal circulation?
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-asphyxia around time of birth
-undergrowth of pulmonary vasculature -chronic intrauterine hypoxia -idiopathic PFC |
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asphyxia
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failure of gas exchange (decreased PaO2 and increased PaCO2)
fetus: placental failure newborn: pulmonary failure |
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redistribution of blood flow during asphyxia
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-BF to lung remains decreaed or decreases
-flow to vital organs is maintained or increased -in fetus, blood flow to placenta is maintained unless there is cord obstruction -blood flow to liver, kidneys, GI tract, and skin decreases |
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PFC causes profound hypoxia caused be a decrease in pulmonary blood flow:
characterized by... |
cyanosis/pallor
low O2 saturation or PaO2 in room air variable increases in PaO2 when breathing 100% oxygen (hyperoxia test) |
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clinical presentation of PFC
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tachypnea, scaphoid abdomen, heart murmur, abnormal chest x-ray
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clinical classification of PFC
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-decreased size of pulmonary vascular bed
-functional obstruction -pulmonary vascular constriction -pulmonary venous hypertension |
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causes of decreased size of pulmonary vascular bed
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congenital pulmonary hypoplasia
secondary pulmonary hypoplasia (diaphragmatic hernia, oligohydramnios, absent fetal breathing, congenital chylo or hydro-thorax) |
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an example of a functional obstruction leading to PFC
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POLYCYTHEMIA (too many RBCs) with increased viscosity, decreases pulmonary blood flow (often due to placental transfusion, high altitude birth)
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examples of pulmonary vascular constriction (that can result in PFC)
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perinatal asphyxia
pulmonary parenchymal disease (RDS, pneumonia) transient Persistence of Fetal Circulation syndrome (PFC) |
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Pulmonary Venous hypertension can be caused by:
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OBSTRUCTION: pulmonary venous, left atrial or mitral obstruction
LV FAILURE secondary to congential heart disease Transient LV dysfunction |
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severe, non-responsive hypoxia and a chest xray that looks like HMD, severe pneumonia or pulmonary venous congestion strongly suggests:
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PULMONARY VENOUS OUTFLOW OBSTRUCTION
only chance of survival = URGENT SURGERY |
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how does one differentiate non-cardiac hypoxia from cyanotic congenital heart disease
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HYPEROXIA TEST:
measure PaO2 in 100% oxygen if you get PaO2 > 150mmHg probably not congenital heart disease |
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what does meconium staining reveal about hypoxia?
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hypoxia increases peristalsis, meconium can be swallowed by hypoxemic fetus
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rule of thumb regarding suspected congenital heart disease
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a very low PaO2 from the moment of birth that doesn't increase substantiall with 100% oxygen and positive pressure ventilation is cardiac disease until proven otherwise by echo- TGA, TAVR, Truncus arteriosis, Tricuspid atresia, Tetralogy of Fallot (the 5 Ts)
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most infants with pulmonary causes of PFC respond to 100% oxygen +/- positive pressure ventilation early in their course with...
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a substantial increase in PaO2 (> ~150 torr)
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Conventional Tx for diaphragmatic hernia
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-gentle ventilation (to establish risk)
-low risk: surgery after delay -high risk: early ECMO --> surgical repair |
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Experimental Tx for Diaphragmatic hernia
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fetoscopic temporary tracheal occulsion (effort to expand lungs)
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Tx for Left Atrial Obstruction
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create shunt ax atria
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general Tx for PFC
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CONSERVATIVE VENTILATION
HYPERVENTILATION (reduces PVR by decreasing PaCO2 and increasing pH) NO inhalation (reduces PVR by direct effect) Experimental pulmonary vasodilators ECMO |
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what leads to PDA in premature infants?
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-ductus less sensitive to constricting effects of O2
-ductus more sensitive to dilating effects of PGE2 and NO -incomplete muscle development (less contractile capacity) |
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clinical presentation of PDA
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premature infant
respiratory distress syndrome (increasing compliance) failure to improve |
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physical exam findings of PDA
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wide pulse pressure (BPs-BPd)
full/bounding peripheral pulses hyperactive precordium heart murmur |
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Tx of PDA
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-administration of steroids to mom reduces incidence of PDA
-INDOMETHACIN (prostaglandin synthetase inhibitors, inhibits production of PGE) -Surgery |
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complications of INDOMETHACIN (prostaglandin synthetase inhibitor used to treat PDA)
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renal failure
GI perforations |
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formation of proximal airways happens when?
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embryonic period
wks 3-8 |
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3 weeks:
26 days: 28 days: 33 days: 41 days: 52 days: |
3 weeks: median pharyngeal groove, laryngotracheal sulcus, caudal end of which is the respiratory primordium
26 days: ventral outpouching from foregut: respiratory bud 28 days: R&L MAINSTEM BRONCHI 33 days: LOBAR BUDS 41 days: SEGMENTAL BUDS (completion of proximal airway dvpt) 52 days: pleural cavity separate from peritoneal cavity |
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pseudoglandular phase
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8-16 wks
formation of conducting airways bronchial tree arborizes (16-25 generations, final = terminal bronchioles) advancing airways with COLUMNAR EPITHELIUM surrounded by mesenchyme |
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canalicular phase
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16-24 weeks
Formation of Acini budding and branching of terminal bronchioles to form respiratory bronchioles differentiation of respiratory epithelium, thinning into Type I pneumocytes and appearance of type II pneumocytes capillary proliferation and closer proximity to air spaces |
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Acini
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respiratory units distal to terminal bronchioles
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when do pneumocytes form/appear?
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Type I form by thinning of respiratory epi
and Type II appear in CANALICULAR phase of development (16-24 weeks) |
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what is limiting factor of survival in extremely premature infants
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at the end of the canalicular phase (24 wks) there are only respiratory bronchioles and no true saccules or air exchange spaces
(even if there is surfactant sufficiency there still is no gas exchange area) |
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saccular phase
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24 weeks to term
formation of gas exchange sites ~3 generations of respiratory bronchioles 1 generation transitional duct 3 generations of saccules (last = terminal saccule) decreased thickness of interstitial tissue is marked close spatial relationship bt caps and epithelial layer develops epithelium differentiates fully into Type I and II pneumocyte |
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alveolar phase
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post natal: birth- 8 years
at birth there are few true alveoli increase air phase surface area (increase in capillaries) saccules and transitory ducts become alveolar sacs and ducts ~300 million alveoli |
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postnatal phase
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growth pahse
> 8 years furthing thinning of interstitium |
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cells of endodermal origin
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those associated with conducting airways
alveolar cells: - Type I Pneumocyte (simple, covers 96% of surface) -Type II Pneumocyte (surfactant secreting) |
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cells of mesodermal origin
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SM cells (surround conducting airways, pulmonary arteries and arterioles)
Vascular endothelium Fibroblasts Capillary pericytes Other |
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Cells of ECTODERMAL origin
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pulmonary innervation
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Free cells
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lymphocytes, plasma cells, macrophages, mast cells, granulocytes
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factors affecting structural development
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1) intrauterine environment
2) fetal breathing 3) corticosteroids |
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Function of Surfactant
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Lower surface tension on dynamic compression
re-spread after dynamic compression past monolayer collapse adsorb well from subphase to interface |
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composition of surfactant
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phospholipid composition ? %
pulmonary surfactant proteins ? |
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factors affecting development of SURFACTANT
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fetal sex, race
fetal stress, asphyxia, maternal diabetes glucocorticoids beta-adrenergic stimulation thyroid hormones |
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composition of extracellular matrix
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collagen
elastin other |
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pulmonary mechanics at the onset of breathing
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a) conversion from fluid to air-filled lungs
B) decreased PVR, chnage in circulation |
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examples of Pulmonary hypoplasia
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renal agenesis
diaphragmatic hernia second trimester prolonged rupture of membranes |
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RSD (surfactant deficiency)
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prematurity
infants of diabetic mothers |
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transitional problems
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transient tachypnea
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bronchopulmonary dysplasia often results
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due to iatrogenic disease (ventilation causes more severe damage)
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