Respiratory Flashcards
Which airways have cartilage and which airways do not?
large airways- cartilage
small airways- non-cartilage
What decreases and increases surface tension in lungs?
decreased- saline filled lungs
increased - surfactant deficiency
Flow limitation
point where any increase in effort makes no increase in flow because airway can collapse
Pcritical is a marker of
tendency of airways to collapse
Three Factors that contribute to maximum flow rate
decreased Elastic recoil
Increase in Pcritical
Increase in R upstream
decreased expiratory flow rates seen in (3)
1- increased airway resistance
2- decreased elastic recoil
3- decrease in lung volume
RV is increased most in
obstructive airway disease (air trapping)
5 general categories of restrictive lung disease
neuromuscular disease chest wall problems pleural disease loss of lung interstitial lung disease
Efferent impulses in respiratory control from Cranial nerves
9,10,11,12
Length tension, a short muscle is a
weak muscle
energy consumption is via 2 factors in muscles
tension produced by muscle
velocity of shortening in muscle
two reasons resp muscles require more energy
- asked to do more
- at a mechanical disadvantage
Centriacinar Emph
enlarged resp bronchioles and normal distal ascini
panacinar emph
resp–>distal ascini all affected
Paraseptal emph
distal ascinus only
associated with bullae and pneumothroax
charcot-leyden crystals
degranulated eosinophil membranes found in asthma
curschmann spirals
whorls of shed epithelium in asthma
acute vs late phase asthma
acute- mast cell mediated
late phase- leukocyte mediated, tissue destruction
3 types of medications for COPD
B-agonists, Anticholinergic, Methylxanthines
when are glucocorticoids appropriate for COPD patients?
<50% FEV1 and freq exaccerbations
airway remodeling
increase in ECM
pulmonary arterial hypertension
pH when fundamental abnormality arises in pulmonary vasculature
2 ways that pulmonary arterioles dilate
passive- thin-walled and contain little muscle (so due to CO2)
active- release of EDRF/NO
ihibitors vs constrictors in PVR
inhibitors- prostacyclin, NO
vasoconstriction- thrmboxane A2, endothelin-1, 5HT
Pressure left atrium best estimated by
pulmonary wedge pressure
pulmonary artery pressure equation
Ppa= (CO x PVR) + PLa
two types of granulomatous ILD
sarcoidosis
hypersensitivity pneumonia
smoking related ILD
respiratory bronchiolitis ILD
desquamative interstitial pneumonia
first thing that happens in ILD
type 2 pneumocyte hyperplasia
3 ways lung can get fibrotic
fibroblast can get activated –>interstitum thicker
epithelial gets injured–>fibrin leaks out and fibroblasts pass through
granulomas
caplan syndrome
rheumatoid arthritis + pneumoconiosis
2 forms silicosis
crystalline- most fibrogenic, 100x smaller than sand
amorphous (talc)-more clearance, less firbogenic
two fiber types in asbestosis
serpentine-curly and flexibile- more widely used in industry
amphibole- straight and rigid- more pathogenic
smoking + asbestos
55 fold increase in lung cancer–>synergistic!
three examples of hypersensitivity pneumonitis
1) farmers lungs
2) pigeon breeders lungs
3) humidifier lung
patient profile of sarcoidosis
cytokines- IL2
CD4+ lymphs
activated macrophages
class II HLA expression
why does ILD have decreased compliance and diffusion impairment?
deposition of collagen
thickening of interstitum
ILD breath patterns
rapid and shallow
treatments in IPF
Pirenidone-inhibits TGFB1- slows progression IPF
Nitendanib- inhibits multiple tyrosine kinases and a variety of growth factor receptors–>slows decline in lung function
inertial impaction increases with
large particle size
high inspiratory flow rates
tortuous pathways
interceptors
sedimentation increases with
lower airflow
smaller airway lumen
optimal particle size
three variations of disease in mucociliary disease
cystic fibrosis: sol phase
chronic bronchitis: gel phase
kartagener syndrome: cilia
varenicline
smoking pharmaceutic–partial agonist of A4B2 nicotinic acetylcholine receptor which may play a role in addiction
pleurodesis
process or intervention where inject something or do something to pleural surface to make it inflamed and when body has inflammation, responds by forming adhesions
opiate antidote
naloxone
central alveolar hypoventlation
due to altered function of brainstem resp neurons, resulting in hypoventilation
Obestiy-Hypoventilation/Pickwickian Syndrome
R heart failure due to plum vasoconstriction from hypoxemia
no hypercapnia in
asthma
where is periodic breathing seen
bilateral cerebral dysfunction
congestive heart failure
hypoxia
paraneoplastic syndrome
signs and symptoms caused by factors produced by cancer cells that act a distance from both primary cancer site and its metastases
ectopic ACTH secretion
small cell lung carcinoma with poor prognosis
inappropriate secretion of ADH
small cell lung carcinoma that does not effect prognosis
pancoast tumor
tumor at lung apex where pleural reflex is
horner’s syndrome
pancoast syndrome
recurrent laryngeal nerve–>hoarseness
squamous cell carcinoma
central lesion, may cavitate
adenocarcinoma
peripheral lesion
Erlotinib
EGFR-TK1 tyrosine kinase inhibitor
Class 1 mutation
defective protein product
class 2 mutation
defective protein processing
class III
defective protein regulation- diminished ATP binding and hydrolysis
class IV
defective protein conductance- defective chloride conductance or channel gating
class V
promoter or splicing abnormality-reduced number of CFTR transcripts due to promoter or splicing abnormality
class VI
accelerated turnover-accelerated turnover from cell surface
fetal vasoconstriction
physical lung fluid
dec O2 and pH
leukotrienes
thrmboxane A2
fetal vasodilation
NO
increase O2 and pH
PGI2 prostacyclin
major constrictor ductus arteriosus
ET1
major dilator ductus arteriosus
PGE2
4 things that cause DA constriction
increase PaO2
decrease PVR from O2–>decrease in BP in DA
decrease PGE2 (loss of placenta and increased PG removal from lung)
decrease in PGE2 receptors in DA wall
indomethacin
prostaglandin synthetase inhibitors
complications-renal failure, GI perforations, necrotizing enter colitis
what age are alveoli close enough to caps to transmit o2?
24 weeks
bronchial tree developed by
16th week of intrauterine life
alveoli continue to grow
through life
preacinar blood vessels follow
airways
intra-acinar vessels
follow alveoli
aberrant subclavian artery only compresses
esophagus
anomalous innominate artery only compresses
trachea
extrathoracic obstruction produces
inspiratory stridor
intrathoracic obstruction
exp wheeze
single point of obstruction
one wheeze
mutiple pts of obstruction
lots of little wheezes
in situ means
hasn’t invaded through the basement membrane yet
cytokeratin
intermediate filament in the cytoplasm of epithelial cells
vimentin
intermediate filament in the cytoplasm of tissue derived from mesoderm
TTF1
nuclear transcription factor expressed in lung epithelium and thyroid epithelium
synaptophysin
neuroendocrine marker
Met vs Primary
Met has sharp demarcation of metastasis
carcinoid tumor
ribbons of cells
positive synaptophysin stain
small cell carcinoma
virchow’s triad
endothelial injury
abnormal blood flow
hypercoag
saddle embolus
thromboembolus that lodges at bifurcation of right and left plum arteries
associated with sudden death
pulmonary infarcts early
deep red color
ischemic necrosis
diffuse RBC
exudate
infarcts greater than 48 hrs
RBC lysis
hemosiderin laden
macrophages
lung appears paler
days
fibrosis (from margins inward)
gray-white color
compliance
deltaV/deltaP
Pmax=
Pelastic-Pcrit/R upstream
Pcrit=
> 0 tendency to collapse
<0 tendency to stay rigid
Pcrit=Pcollapse-Ppleural
PIO2
(Pb-47)(.21)
sol phase
water and solute that lines resp tract
gel phase
glyoprotiens
pleurodesis
chemical irritant put to increase inflammation and remove what is bothering
zone 1 conditions
Palv>Ppa>Ppv
no cap perfusion; in normal conditions no zone 1
zone 2 conditions
Ppa>Palv>Ppv
driving pressure is difference between Ppa and Palv
as you move down the lung, driving pressure and blood flow increases
zone 3
Ppa>Ppv>Palv
traditional flow relationship
pvr=
ppa-pla/co
usually < 2
hemoglobin does not affect
po2 or O2sat
oxygen content but not saturation shift based on
polycythemia vs anemia
extrathoracic obstruction causes
collapse on inspiration (decrease flow on inspiration)
intrathoracic obstruction causes
a collapse on expiration (decrease flow on expiration)
