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21 Cards in this Set

  • Front
  • Back
Upper 16 branches are in the conducting zone; no exchange of gas between atmosphere and blood

Last 7 branching points = gas exchange
Nasal Receptor Activation
via trigeminal nerves; results in sneezing
Nasopharyngeal receptors
via glossopharyngeal nerves; results in aspiration or sniff reflex
Laryngeal and tracheal receptors
via vagus nerves; results in coughing
Nucleus ambiguus; cough center in brain in medulla; found approximately in same area as respiratory center/cardiovascular control center
Sympathetic nerve NT
NE
B/C = bronchioconstriction
B/D = bronchiodilation
Efferent Nerves, Transmitters, and REceptors
ACE Inhibitors and Cough
Cough side effect; accumulation of bradykinin and prostaglandins sensitize cough receptors

Best action for ACE inhibitor cough is to discontinue tx and replace it with an angiotensin-II receptor antagonist
Mechanics of Cough
Rapid air inspiration; epiglottis closes tightly; abs/intracostal muscles contract to increase lung pressure; epiglottis opens suddenly and air is expelled at a velocity of up to 100 MPH

Usually stimulated by signals sent to cough center (medulla/nucleus ambiguus) via vagus nerve
Sneeze
Same mechanism as cough except during sneeze, uvula is depressed so air is expelled through the nose
where are cough receptors highest in density
branch points in the tracheobronchial tree and mucosa of the larynx; these are sites where particles are most likely to be deposited
what happens when macrophages can't digest a particle
they release proteases that will productive an activation of lung fibroblasts and attract leukocytes that results in permanent lung damage if it occurs over a long period of time
Hypoxic Pulmonary Vasoconstriction
Region of lung underperfused will not receive blood vessels (since no gas exchange would take place); the response is due to a local effect of hypoxia on the vessel itself and not central occur (likely due to P02 of the alveolas gas and NOT pulmonary arterial blood that determines this response)
Hypoxic Pulmonary Vasoconstriction at high altitudes
the pulmonary vasoconstriction is throughout the lungs and results in increased pulmonary artery pressure; causes a thickening of the right ventricle wall; can cause pulmonary edema and individuals may develop chronic mountain sickness if an individual is not taken to lower elevations
Compare the location of the cough center in the brain to the centers that help regulate respiration and the cardiovascular center.
Same area; gives us an indication of how important the cough center was as our brain was developing; cough must be crucial for our long term existence
Explain why pharmacological companies have attempted to develop “inhalers” that produce particles in the size range of 1-3 mm?
Inhalers with smaller particles can deliver drug to lower regions of the respiratory tree; although often the problem is upper airway constriction so it sometimes doesn't matter; still the companies are seeking to improve drug delivery to respiratory system
Explain the potential problem that can develop if a person with asthma is give an beta-blocker to treat CHF.
B-blockers are useful for tx htn and CHF; however the circulating epinephrine is important in keeping airways dilated; if a B blocker is given to a pt with asthma or propensity towards developing asthma airway constriction may develop and asthma symptoms may occur
Why are atropine like drugs useful in treating patients with asthma?
Parasympathetic nerves release ACh; blocking Ach prevents constriction of airways

Atropine = muscarinic antagonist
Why do people at high altitude develop a thickened right ventricular wall?
Hypoxic regions of lung have decreased perfusion; this is normally to keep blood from going to region sof lung that are not well ventilated; at high altitude the entire lung is not well ventilated because of decreased alveolar P02 and entire lung becomes constricted; increases pulmonary artery pressure which over time will lead to a thickening of right ventricle wall as the heart tries to push against this increased pulmonary resistance
Why is the central respiratory center depressed when a person travels to high altitude?
At high altitude = hyperventilation; blow off C02 = decreased C02 levels depress respiratory center; however the need for oxygen overcomes this and an individual will continue to hyperventilate
How many branches occur in the airways of the lungs before oxygen can be exchanged with the blood?
Upper 16 = dead space of alveoli = conducting = can't exchange gas

Lower 7 branching points are capable of exchanging gases