pulmonary anatomy + physiology Flashcards
most common type of tracheoesophageal anomaly
esophageal atresia with distal tracheoesophageal fistula
“gastric bubble” on CXR
NG tube stuck in blind pouch of esophagus
esophageal atresia with distal tracheoesophageal fistula
ciliated columnar epithelium
trachea
tracheal epithelium of smokers
metaplasia: columnar cells → squamous epithelium (no cilia - can’t mobilize sputum - get chronic bronchititis)
opposite of distal esophagus metaplasia in BE: squamous → columnar with goblet cells
nonfunctional cilia in: respiratory tract sinuses eustachian tubes fallopian tubes flagella of sperm chronic infections infertility hearing loss
Kartagener syndrome: primary ciliary dyskinesia
defective dynein arm (need for moving along microtubule)→ nonfunctional cilia
Kartagener syndrome: primary ciliary dyskinesia
associated with situs inversus reversal of circulatory system + viscera (50%)
Kartagener syndrome: primary ciliary dyskinesia
divides thorax from abdominal cavity
diaphragm
4 embryological structures that form the diaphgragm
septum transversum
pleuroperitoneal membranes
dorsal mesentary of esophagus
abdominal wall
congenital defect in pleuroperitoneal membrane → abdominal contents in pleural cavity → lung hypoplasia
usually occur on left side
associated with polyhydramnios
congenital diaphragmatic hernia
flattened abdomen
cyanosis
inability to breath
congenital diaphragmatic hernia
innervated by phrenic nerve (C3 C4 C5)
diaphragm
C3 C4 C5 keeps diaphragm alive
neck or shoulder pain can suggest
irritated diaphragm (affecting phrenic nerves): referred pain due to:
gallbladder disease
splenic rupture
structures that perforate the diaphgragm:
T8
T10
T12
I 8 10 EGGS AAT 12
T8: IVC
T10: esophagus, vagus
T12: aorta, azygous vein, thoracic duct
cells that line alveoli
responsible for gas exchange
pneumocytes
simple squamous epithelial cells
>97% alveolar surface
GAS EXCHANGE
susceptible to toxic insults (can’t replicate)
type I pneumocyte
larger
cuboidal
located at alvelar septal junction
cover 3% alveolar surface
secrete SURFACTANT: dipalmitoyl phosphatidylcholine
REPLICATE after lung damage: precursor to type I and type II cells
type II pneumocyte
↓ alveolar surface tension → more compliant (stay open)→ prevent atelectasis (alveolar collapse)
surfactant
sample of amniotic fluid of premature baby
lecithin:sphingomyelin ratio >2.0 suggests
fetal lung maturity (type II pneumocytes are making enough surfactant)
to enhance fetal lung maturity, give mom
corticosteroids: matures type II pneumocytes
DOC for altitude sickness
acetazolamide
rapid ascent to high altitude
begins few hours to 2 days after ascent
headache
fatigue
acute cerebral edema due to hypoxia-induced vasodDILATION
acute pulmonary edema: hypoxia causes vasoCONSTRICTION (↑ cap pressure → transudate of fluid into lungs)
acute mountain sickness
visual black out occurs at what + G force
4-6 G
force pulling blood into abdomen + legs
insufficient blood return to heart
insufficient pumping of blood to brain
G force achieved during spacecraft liftoff
8-9 G
need to be in semi reclined position on take-off
occurs when diver breathing compressed air for hour at 120 feet (extreme depths for too long)
nitrogen dissolves into neural membrane →↓ neuronal excitability → diver becomes jovial/careless → drowsy →
loss of strength + coordination
nitrogen narcosis (not decompression sickness)
at depth: high pressure → nitrogen gas dissolves into blood
surfacing: ↓ pressure → nitrogen escapes solution → formation of bubbles that can occlude vessels
decompression sickness (bends or Caisson Disease)
joint/muscle pain in arms + legs
neuro sx: dizzy, paralysis, syncope
“the chokes”: air bubbles occlude lung capillaries → SOB, pulmonary edema, death
decompression sickness
prevention of decompression sickness
surface slowly
allow nitrogen to be eliminated through lungs by expiration
treatment of decompression sickness
hyperbaric O2 therapy (high pressure room):
convert nitrogen from gaseous state to dissolved state so it can be exhaled by lungs
use of hyperbaric O2 therapy
decompression sickness
arterial gas emboli
CO monoxide poisoning
gas gangrene due to clostridium perfringens (anerobe) or osteomyelitis: increase O2 to part of area
