Exam 2 Flashcards
lamberts canals
terminal and respiratory airways to alveoli
allows 1 alveolus to help open another
volatile vs. fixed acids
volatile: from CO2, can be eliminated by respiration (12,000-20,000 mEq/day)
fixed: from protein catabolism, eliminated by kidneys (50-100 mEq/day)
basal cells
adult stem cells of respiratory epithelium; at the base of epithelium above the basement membrane
AMP Kinase
activated with AMP:ATP ratio is low (ATP used up) that activates PGC-1alpha to go to nucleus for mitochondrial biogenesis and energy production
how is the epithelium in the larynx
false vocal cords: typical respiratory epithelium
true vocal cords: squamous epithelium
body’s 3 methods of preserving pH
- extracellular and intracellular buffering (sponge) - immediate
- respiratory adjustments - few seconds
- renal adjustments - hours to days
where are intrapleural pressures less negative? what are the implications of this?
the dependent portion of the lung
means that in the apex of the lung there is higher transpulmonary pressure/are already distended and less compliant
pink puffer
emphysema
pneumotaxic center
(pons) can inhibit inspiration
cromolyn sodium
asthma treatment
targets mast cells
mesothelioma
malignant tumor of the pleura assoc. with asbestos exposure
where is the central chemoreceptor located and what does it sense
brainstem (ventral surface of medulla), senses changes in CSF pH when CO2 diffuses out of cerebral capillaries
what is wedge a surrogate marker of?
left arterial pressure
fowler method
anatomic dead space
breathing in 100% O2 and wait to detect nitrogen
haldane effect
when Hb is bound to less O2 it has more affinity for CO2
H dissoc. from Hb shifts equilibrium to CO2 formation so it can leave the RBC
what is the A-a gradient?
by the time blood exits to the left heart there is a gradient between O2 in the alveolus and O2 in arterial system that creates the venous admixture (due to intrapulmonary and anatomical shunts)
irritant receptors
located between airway epithelial cells, rsponse is to constrict (from noxious gases, cigarette smoke, inhaled dust/cold air
J receptors
juxtacapillary receptors
located in alveolar walls close to capillaries, activated by engorgement of pulm caps and inc. in interstitial lung volume. result in increased breathing rate
what is the optimal position of a swan ganz catheter
zone 3 because Pa>Pv>PA
expiratory time constant
describes lung emptying
Exp TC = C x R
(in emphysema higher because higher compliance and increased resistance)
glutaminase
stimulated by low pH to make glutamate –> alpha KG –> bicarb (reabsorbed) and also make NH4 which becomes NH3 (diffuses out) and H pumped out to excrete NH4
cortex controls
voluntary ventilation (hyper/hypoventilation)
what happens to fixed acid?
100% gets excreted!
40% excreted as titratable acid and is excreted with urinary buffers
60% excreted as NH4+
pleurisy
inflammation of the pleura, secondary infection and exudate cause restriction of lung movement
Dalton’s law
Px=(PB-PH2O) x F
ventral respiratory group
(medulla) assoc with expiration
seromucous glands found in
extrapulmonary bronchi
main immune cells activated in asthma
eosinophils and mast cells
mast cells = bronchoconstriction
dendritic cells = release TH2 which causes B cell and Ab production which makes more mast cells and eosinophils that lead to inflammation
chloride shift
trade bicarb for chloride in RBC to continue driving reaction forward
why is nitrogen washout used?
to assess anatomic dead space - underestimate lung volumes in COPD, use C1V1=C2V2
where are peripheral chemoreceptors? what do they repsond to?
carotid and aortic bodies
respond to dec. PO2, inc. PCO2, dec. pH
inflammatory cell population differences between COPD and bronchial asthma
COPD: neutrophila, macrophages, CD8 T lymphocytes, eosinophils (exacerbations)
Asthma: eosinophils, mast cells, CD4 T lymphocytes, macrophages and neutrophils
alpha 1 antitrypsin deficiency
increases neutrophil elastase with no antiprotease activtity
impaction occurs in the
nasopharynx (largest particles)
what does macrophage recruitment in COPD do?
Th1 and Tc1 cells –> alveolar wall destruction
neutrophils (proteases like n elastase and MMP9) –> destruction and mucous hypersecretion
monocytes
normal arterial plasma H
40 nM (means pH = 7.4)