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102 Cards in this Set
- Front
- Back
airways --
cartilage is present only in the _ |
trachea
bronchi |
|
respiratory zone includes what components _
and participates in gas exchange |
respiratory bronchioles
alveolar ducts alveoli |
|
goblet cells extend only to the _
|
bronchi
|
|
pseudostratified ciliated columnar cells extend to _
|
respiratory bronchioles
|
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type _ cells secrete pulmonary surfactant
|
II
|
|
pulmonary surfactant is named
|
dipalmitoyl phosphatidylcholine
|
|
histological classification, cell types:
type I cells are _ type II cells are _ |
squamous
cuboidal |
|
~ lab test
_ indicates fetal lung maturity |
lecithin-to-sphingomyelin ratio of > 2.0
in amniotic fluid |
|
type II cells functions
|
secrete surfactant
precursors to type I and type II proliferate during lung damage |
|
clara cells functions
|
secrete component of surfactant
degrade toxins act as reserve cells |
|
clara cells description
|
nonciliated
columnar with secretory granules |
|
clara cells functions
|
secrete component of surfactant
degrade toxins act as reserve cells |
|
lung endothelium is of what type?
|
"continuous endothelium" with tight junctions
|
|
anatomical / physical description of a bronchopulmonary segment
|
in the center:
3^ segmental bronchus 2 arteries (bronchial and pulmonary) along the borders: veins and lymphatics |
|
if you aspirate a peanut--where will it go?
|
if you're upright:
--> lower portion of right inferior lobe if you're supine: --> superior portion of right inferior lobe |
|
relationship of
pulmonary artery to the bronchus at each lung hilus |
RALS
right anterior left superior |
|
the horizontal fissure of the right lung is at the level of
|
4th rib
|
|
big structures that perforate the diaphragm are where?
|
I ate
ten eggs at twelve IVC -- T8 esophagus -- T10 aorta -- T12 |
|
_ runs with the esophagus through the diaphragm
|
2 trunks of vagus
|
|
_ runs with the aorta through the diaphragm
|
thoracic duct
azygous vein |
|
muscles of inspiration during exercise
|
external intercostals
scalene muscles sternomastoids |
|
muscles of expiration during exercise
|
rectus abdominis
obliques transversus abdominis internal intercostals |
|
re: breathing during exercise
internal intercostals --> external intercostals --> |
expiration
inspiration |
|
_ surfactant is deficient in neonatal respiratory distress syndrome
|
dipalmitoyl phosphatidylcholine (lecithin)
|
|
collapsing pressure equation
|
P = 2 (surface tension) / radius
|
|
important lung products (5)
|
surfactant
prostaglandins histamine ACE kallikrein |
|
histamine effect on the lung
|
bronchoconstriction
|
|
(2) in the lung affect bradykinin
|
ACE inactivattes bradykinin
(ACE inhibitors ^ bradykinin) kallikrein activates bradykinin |
|
ACE inhibitors --> re: bradykinin
|
^ bradykinin
|
|
kallikrein in the lung -->
|
activates bradykinin
|
|
lung volumes
4 ways to add up to the full lung |
TLC =
VC + RV = IRV + TV + ERV + RV = IC + FRC = |
|
bohr equation to determine physiologic dead space
Vd = |
Vt x (PaCO2 - PeCO2)/PaCO2
Vd = physiologic dead space Vt = tidal volume PaCO2 = arterial PCO2 (i.e. all the CO2 that's produced) PeCO2 = expired air PCO2 i.e. all the CO2 that we're rid of |
|
_ is the largest contributor of functional dead space
|
alveoli in apex of healthy lung
|
|
_ pressure is 0 at what lung volume?
|
airway and alveolar
functional residual capacity |
|
what are (3) lung pressures
at FRC? |
airway and alveolar pressures are 0
intrapleural pressure is negative |
|
compliance is decreased in (3)
|
pulmonary fibrosis
insufficient surfactant pulmonary edema |
|
how does pulmonary edema affect compliance
|
decreases it
|
|
_ form of hemoglobin has _ times as much afffinity for O2 than the _ form of hemoglobin does
|
R (relaxed)
300x T (taut) |
|
_ chemical changes favor _ form of hemoglobin
to increase oxygen unloading in the tissues |
^ Cl-
H+ CO2 2,3-BPG temperature favor the T (taut) form |
|
why does fetal hemoglobin have higher affinity for O2?
|
fetal Hb has lower affinity for 2,3-BPG
(2,3-BPG causes oxygen unloading) |
|
hemoglobin modifications include (2)
|
methemoglobin
carboxyhemoglobin |
|
methemoglobin is (2)
|
oxidized form of Hb (Fe +++)
has ^ affinity for CN- |
|
to treat cyanide poisoning
|
use nitrates to oxidize hemoglobin to methemoglobin
which binds cyanide allowing cytochrome oxidase to function ----------------------- use thiosulfate to bind this cyanide forming thiocyanate, which is renally excreted |
|
methemoglobinemia can be treated with
|
methylene blue
|
|
carboxyhemoglobin is
|
hemoglobin bound to CO in place of O2
|
|
carboxyhemoglobin
how does it behave differently? (2) |
left shift --
v oxygen unloading in tisssues |
|
Hb curve diagram:
things that make it shift left (5) |
v metabolism
v PCO2 v temperature v H+ v 2,3-BPG |
|
high altitude causes _ shift in hemoglobin curve
|
right shift
|
|
what effect does BPG have on hemoglobin
|
right shifts it
|
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what substances in the lung are perfusion-limited?
|
O2 (in normal health)
CO2 N2O |
|
what substances in the lung are diffusion limited?
|
O2 (emphasema, fibrosis)
CO |
|
diffusion equation for a gas in the lung. volume of gas that diffuses...
Vgas = |
A deltaP Dk / T
area pressure difference diffusion constant / thickness |
|
the physics reason for
v diffusion in emphysema |
decreased area
|
|
the physics reason for
v diffusion in pulmonary fibrosis |
increased thickness
|
|
normal pulmonary artery pressure
|
10-14 mmHg
|
|
pulmonary hypertension definition
|
=> 25 mmHg
or > 35 mmHg during exercise |
|
pulmonary hypertension results in (3)
|
atherosclerosis
medial hypertrophy intimal fibrosis |
|
1^ pulmonary hypertension is due to _
|
inactivating mutation in the
BMPR2 gene |
|
the BMPR2 gene
function |
inhibit vascular smooth muscle proliferation
|
|
prognosis for 1^ pulmonary hypertension
|
poor prognosis
|
|
gene that's mutated in 1^ pulmonary htn
|
BMPR2
|
|
causes of 2^ pulmonary hypertension
|
COPD
mitral stenosis autoimmune disease left-to-right shunt sleep apnea living at high altitude |
|
disease course of pulmonary hypertension
|
severe respiratory distress-->
cyanosis and RVH--> death from decompensated cor pulmonale |
|
how does COPD cause pulmonary htn?
|
destruction of lung parenchyma
|
|
how does mitral stenosis cause pulmonary htn?
|
^ resistance --> ^ pressure
|
|
how do recurrent thromboemboli cause pulmonary htn?
|
v cross-sectional area of pulmonary vascular bed
|
|
how does autoimmune disease cause pulmonary htn?
|
inflammation-->
intimal fibrosis--> medial hypertrophy |
|
how does L-->R shunt cause pulmonary htn?
|
^ shear stress -->
endothelial injury |
|
how does living at high altitude cause pulmonary htn?
|
hypoxic vasoconstriction
|
|
two equations for pulmonary vascular resistance
|
(Ppulm artery - P left atrium)
/ CO R = 8 eta length / pi r^4 |
|
O2 content of blood =
|
(O2 binding capacity) x
(% saturation) + dissolved O2 |
|
normally 1g Hb can bind
how much O2 |
1.34 mL O2
|
|
cyanosis results when
(Hb lab value) |
deoxygenated Hb > 5 g/dL
|
|
O2 binding capacity =
|
20.1 mL O2/dL
|
|
blood oxygen values
_ decreases with lung disease _ decreases as Hb falls |
arterial PO2
O2 content |
|
oxygen delivery to tissues =
|
CO x oxygen content
|
|
alveolar gas equation
|
PA O2 =
PI O2 - (Pa CO2/R) ----------------------- alveolar O2 = O2 in inspired air - arterial CO2 / R R = CO2 produced/O2 consumed |
|
respiratory quotient R in the alveolar gas equation
|
CO2 produced/O2 consumed
|
|
A-a gradient is
|
PA O2 - Pa O2
10-15 mmHg |
|
^ A-a gradient may occur in _
causes include |
hypoxemia
shunting V/Q mismatch fibrosis |
|
3 forms of oxygen deprivation
(table) |
hypoxemia: v PaO2
hypoxia: v O2 delivery to tissue ischemia: loss of blood flow |
|
causes of hypoxemia
|
normal A-a gradient
--high altitude --hypoventilation ^ A-a gradient --V/Q mismatch --diffusion limitation --right to left shunt |
|
hypoxemia means
|
v PaO2
|
|
hypoxia means
|
v O2 delivery to tissue
|
|
ischemia means
|
loss of blood flow
|
|
two hypoxemias that have a normal A-a gradient
|
high altitude
hypoventilation |
|
3 hypoxemias that have an
^ A-a gradient |
V/Q mismatch
diffusion limitation right-to-left shunt |
|
5 causes of hypoxia
|
v CO
hypoxemia anemia cyanide poisoning CO poisoning |
|
V/Q ratio at
apex base |
3 (wasted ventilation)
0.6 (wasted perfusion) |
|
V/Q at the base of the lung
|
V/Q = 0.6
both are greater at the base than at the apex, however |
|
exercise effects on V/Q ratio
|
vasodilation of apical capillaries-->
V/Q ratio that approaches 1 |
|
V/Q --> 0 means
|
airway obstruction (shunt)
|
|
in _, 100% oxygen does not improve _
|
shunt
PO2 |
|
V/Q --> infinity means
|
blood flow obstruction (physiologic dead space)
|
|
pressures in zones of the lung
1 2 3 |
PA > Pa > Pv
Pa > PA > Pv Pa > Pv > PA |
|
in the apex,
_ pressure is greater than another, therefore |
PA > Pa > Pv
high alveolar pressure compresses capillaries |
|
if carbon dioxide is bound to hemoglobin, it's called _
|
carbaminohemoglobin
|
|
Haldane effect
|
in lungs, oxygenation of Hb -->
dissociation of H+ from Hb--> shifts equilibrium toward CO2 formation--> CO2 is released from RBC |
|
Bohr effect
|
in peripheral tissue
^ H+ from metabolism --> curve to shift toward right--> unloading of O2 |
|
which "effect" is operative in the lung, which is operative in the tissues, and what's the basic result in each?
|
lungs: Haldane effect.
unloading CO2 tissue: Bohr effect unloading O2 |
|
respiratory system response to high altitude (7)
|
acute ^ in ventilation
chronic ^ in ventilation ^erythropoetin (chronic hypoxia ^ 2,3 BPG ^ mitochondria ^ renal excretion of bicarbonate chronic hypoxic pulmonary vasoconstriction --> RVH |
|
respiratory system response to exercise:
blood pressures of various molecules etc. |
no change:
--PaO2 --PaCO2 ^ in venous CO2 content |