Respiratory Flashcards
type I pneumocytes
97% of aveoli surface, just thin and don’t do shit
type II pneumocytes
screte surfactant, cuboidal, differentiate into type I cells, they proliferated in response to injury
what in amniotic fluid indicates fetal lung maturity
lecithin:sphingomyelin ratio >2
of lobes of each lung
left has 2
right jhas 3
which lung more commonly gets inhaled foreign body
right
aspirate peanut while standing, where does it go?
lower portion of right inferior lung
aspirate peanut while lying (supine), where dose it go?
superior portion of right inferior lobe
location of pulmanary arteries in relation to hilum of bronchus?
RALS: Right Anterior Left Superior
perforates diaphram at T8
IVC
perforates diaphragm at T10
esophagus and vagus
perforates diaphragm at T12
aorta, thoracic duct, azygos vein
diaphragm pain refers to?
C3, 4, 5 shoulder and trapzius
muscles used during maximal inspiration?
external intercostals, scalene muscles, sternocleidomastoids
muscles used during maximal expiration
rectus abdominis, internal/external obliques , transversus abdominus, internal intercostals
functional vs anatomical dead space
functional is aveoli not being perfused (apex of lung), anatomical is conducting system
hemoglobin two states
tense: low affinity for oxygen (periphery)
relaxed: high affinity for oxygen
conditions which favor taut form of Hb?
high: Cl, H, CO2, 2,3-BPG and temp (shifts curve right)
how to treat cyanide poisoning?
Nitrates oxidize hemoglobin to methemoglobin which favors binding cyanide. then treat with thiosulfate to form thiocyanate to excrete
what is methemoglobin and how to treat methemoglobin?
methemoglobin is oxidized hemoglobin that favor cyanide. give methylene blue
what creates methemoglobin?
nitrates
histology of conducting zone vs respiratory zone (respiratory bronchioles and aveoli)
conducting zone is pseudostrat columnar ciliated
respiratory bronchioles are cuboidal
aveoli are simple squams
(no cilia cause macrophages clear)
oxygen binding curve after carbon monoxide
left shift cause CO binds waaaaaay stronger
hemoglobin vs myoglobin multimer state?
4 vs 1
effects of CO2 and O2 on pulmanary circulation
opposite of the rest of the body. hypoxia = vasoconstriction
is normal gas exchange diffusion or perfusion limited?
perfusion
cor pulmonale
enlargment of right heart due to increased pulmanary circulation resistance
normal pulm artery pressure?
10-14
gene responsible for primary pulmonary hypertension (and defect?)
BMPR2 w/ inactivating mutation
ventilation and perfusion are greatest where?
base of lung
Haldane effect
oxygenated hb dump H which causes biocarb to become CO2 at lungs (opposite of bohr effect/shift)
virchows triad of DVT risk factors
Stasis, hyper coagulability, endothelial damage
dorsiflexion of foot elicits calf pain
sign for a deep vein thrombosis
heparin vs warfarin for DVT treatment
Heparin is acute prevention and treatment. warfarin is for chronic prevention of recurrance
sudden onsent dyspneia, chest pain, tachypnea
Pulm embolism
high altitutde compensation mechanisms
acute: increase ventilation
chronic: high epo to increase hct, high 2,3-BPG, high bicarb excretion
types of pulmonary emboli
FAT BAT: Fat, Air, Bactera, Amniotic, Tumor
Fat emboli etiology and triad
long bone fractures/liposuction
triad: hypoxemia, neurological abnormalities, and petechial rash
how to distinguish between post and premortum emboli via histology?
pink = plates (pre) red = RBCs (post)