Respiratory Flashcards
Lg airways have (2)?
Lg and sm airways to term bronchioles have?
- Cartilage and goblet cells
- pseudostratified ciliated columnar cells; SmM in airway walls
Cells of conducting zone?
Cells of resp zone?
Clara cells are?
- Pseudostratified ciliated columnar cells
- Cuboidal cells in resp bronchioles (type II pneumocytes) and simple sq cells (type I pneumocytes) in alv
- nonciliated columnar cells w/ secretory granules
Collapsing P of alv?
- Incr’d T? incr’d r?
P = 2T/r
- incr’d T -> incr’d collapsing P
- incr’d r -> decr’d collapsing P (as w/ insp)
Surfactant prod begins when? Mature levels when?
Begins at 26wks
Mature levels at 35wks
Where is the PA in relation to the bronchus at ea lung hilus?
RALS:
R ant, L sup
R PA is ant to the R bronchus; L PA is sup to the L bronchus
R lung fissures?
L lung fissures?
R: Horiz fissue in front sep’ing Upper from Middle loves; Oblique fissure on side/bottom sep’ing Middle from Lower lobes
L: Oblique fissure sep’ing Upper and Inf lobes
What struc’s go thr diaphragm? At what levels?
T8 - IVC
T10 - eso (and 2 trunks of vagus)
T12 - Ao (and thoracic duct, azygous v.) (red, white and blue)
Diaphragm:
- innervated by?
- pain from it is referred to where?
C3,4,5 keep the diaphragm alive!
Shoulder (C5) and Trapezius ridge (C3,4)
Dead space of lung =
vol of inspired air that doesn’t participate in gas exchange
Vd = TV x [(PaCO2 - PeCO2)/PaCO2]
aka total vol breathed in x frxn of air NOT expired
At FRC: P’s of airway, alv and intrapleura are?
Airway and alv are 0, intrapleural space is (-) to prevent pneumothorax
Methemoglobin =
- trtmt of methemoglobinemia?
- nitrates -> poisoning, how?
Ox’d Hb (Fe3+) that doesn’t bind O2 -> binds CN
- methylene blue + VitC (reducing agent to make Fe2+ again)
- ox’ing Fe2+ to 3+
Cyanide poisoning -> trtmt?
- Nitrates: oxidize Hgb to Fe3+ to bind CN (so doesn’t hurt cytochrome oxidase func)
- Thiosulfate: bind CN on methemoglobin -> thiocyanate -> renal excretion
Diff btwn myoglobin and Hgb?
Myoglobin in monomeric -> no sigmoid binding curve (looks like sidewards upsidedown L)
1* pulm HTN due to?
Mutation in BMPR2 gene -> incr’d vasc SmM prolif, usu in yg F
Plexiform lesion =
- see in?
tuft of cap’s together
- severe LT pulm HTN
PVR =
[P(PA) - P(LA)] / CO
- where P(LA) = PCWP
Alv gas equ, PAO2 =
PAO2 = PIO2 - PaCO2/R
= 150 - PaCO2/0.8
Haldane effect w/ CO2 in lungs?
- what happens in the tissues to make CO2 bind RBCs?
Oxygenation of Hb promotes dissociation of H+ from Hb -> CO2 is made, and thus released from RBCs
- incr’d H+ from tissue metab -> shifts curve to right (Bohr effect) -> unloading O2 so H+ can bind Hb (CO2 is carried as bicarb in the bl)
Virchow’s triad =
stasis
hypercoag
endo damage
Sign of DVT on PE?
Homans’ sign = dorsiflexion of foot -> calf pain
Fat emboli are assoc’d w/?
3 presenting sx?
- fx of long bones, lipo
- hypoxemia, neuro abnl’ities, petechial rash
How to tell if thrombus was made before or after death?
Lines of Zahn = alt’ing layers of plts mixed w/ fibrin (lighter) and RBCs (darker); made from thrombus being at site of rapid bl flow
-> thus was pre-mortum (thrombus also will be attached to wall)
COPD = chronic bronchitis or emphysema
What is the difference in mech btwn these two?
- Chronic bronchitis is dz of sm vessels, high mucus production (Reid index >50)
- Emphysema is enlargement of air spaces from destruc of alv walls -> incr’d compliance and decr’d elastic recoil so sm airways collapse on exhale
Panacinar emphysema is usu where in lungs? Where is centriacinar?
Pan - LLs (a1AT defic)
Centri - ULs (smoke rises)
