cdunbar4's version from 2016-09-16 16:31



Question Answer
allergic rhinitisrxn of nasal mucosa to a specific allergen
cystic fibrosisautosomal recessive; altered function of exocrine glands involving lungs, pancreas, & sweat glands
apneasuspension of breath
emphysemaabn permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls
deviated septumdeflection of normally straight nasal septum
O2 toxicityinability to expire oxygen out of lungs; respiratory acidosis
epistaxis & causes ofnosebleed; trauma, foreign bodies, corticosteroids, nasal spray, street drugs, allergic rhinitis, tumors, anatomic malformation
pursed-lip breathingexhalation via mouth w lips pursed together to slowly expel air; COPD, asthma; strategy to slow expiration & ↓ dyspnea
status asthmaticusone asthma attack after another; serious condition
nasal polypsbenign mucous membrane massess that form slowly in response to repeated inflammation of the sinus or nasal mucosa
obstructive sleep apneapartial or complete upper airway obstruction during sleep
rhinoplastysurgical reconstruction of the nose
tracheostomythe stoma that results from the tracheotomy
tracheotomyprovides airway for an intubated pt who needs prolonged mechanical ventilation & helps to remove lower secretions for pts who can't clear them.
adventitious soundsabnormal sounds
chemoreceptor; where are they located?receptor that responds to change in the chem composition (PaCO2 & pH) of the fluid around it; located in medulla
compliance"distendability" is a measure of the ease of expansion of air The elasticity of the lungs and elastic recoil of chest wall.
crackleslong, discontinuous, low-pitched sounds caused by air passing intermittently occluded by mucous, unstable bronchial wall or fold of mucosa. (straw bubbling water)



Question Answer
dyspneadifficulty breathing
elastic recoil tendency of lungs to relax after being stretched or expanded (passive expiration); exacerbations of asthma, COPD can cause expirations to become active
fremitusvibration of chest wall produced by vocalization
mechanical receptors(juxtacapillary & irritant receptors)located in lungs, upper airways, chest wall & diaphragm; stimulated by variety (irritants, muscle stretching & alveolar wall distortion
pleural friction rubcreaking or grating sound from roughened or inflamed pleural surfaces; heard both insp./exp.
rhonchi; conditions heard in?rumbling, snoring or rattling sounds d/t obs. of large airways; heard on expiration; COPD, CF, pneumonia, bronchiectasis
surfactanta lipoprotein that lowers the surface tension in alveoli. ↓ amt of pressure needed to inflate alveoli & decreases tendency of alveoli to collapse
tidal volume (Vt)the amount of air inhaled or exhaled during normal breathing; ↓ Vt can mean restrictive disease & may require further tsets, like PFT & chest xrays.
ventilationexchange of oxygen and carbon dioxide into and out of ciruclation
wheezesmusical sounds that are audible to pt. & nurse. Indication of some degree of airway obstruction: asthma, foreign body aspiration & emphysema
bronchitisinflammation bronchi
atelectasiscollapsed lung
bronchiectasisthickening of bronchial walls d/t inflammation, scarring, damage
chlyothoraxpresence of lymphatic fluid in pleural space
community acquired pneumonia"CAP" lower resp. tract infection w onset in community or w/in 1st 2 days in hospitalization
cor pulmonalehypertrophy of the right ventricle of the heart (w or w/o R sided heart failure), caused by pulmonary hypertension
empyemacollection of pus, esp. in pleural cavity
flail chestasymmetrical rising and fall of chest wall usually d/t broken ribs on one side.
hemothoraxcollapsed lung filled with blood
absorption atelectasisNorm. Nitrogen is not absorbed into bs (this prevents collapse). When high concentrations of O2 are given, nitrogen is washed out of alveoli & replaced w O2. If obstruction occurs, O2 is absorbed into bs & alveoli collapse.
asthmachronic inflammatory disorder of the airways
chest physiotherapy"CPT" breathing improved by indirect removal of mucous from airways
chronic bronchitisproductive cough for 3 months in each of the 2 consecutive years
COPDpreventable & treatable disease state characterized by chronic airflow limitation that is not fully reversible. Airflow limiation is usu progressive & associated w abn inflmmatory response of lungs to noxious particles or gases. Cigarette smoking #1 cause
thoracentesispleural fluid aspiration. Used to obtain a sample of pleural fluid for analysis, relieve lung compression and sometimes to obtain a lung tissue biopsy



Question Answer
Classes of drugs used for airway mgmt. in bronchial asthma & chronic bronchitisxanthines & adrenergics (to dilate); corticosteroids to reduce inflammation; antihistamines, antitussives & expectorants to suppress coughing & mobilize secretions; antimicrobials; leukotrine modifiers
Ventilationinspiration and expiration of air in and out of lungs because intrathoracic pressure changes in r/t pressure at airway opening
conditions which compliance is decreasedpulmonary edema, ARDS, pneumonia
conditions that make lung tissue less elastic or distensiblepulmonary fibrosis, sarcoidosis
conditions that increase compliance in lungswhenever there is destruction of alveolar walls and loss of tissue elasticity (COPD)
PFTs measurelung volumes and airflow. Results are used to diagnose pulmonary disease progression, evaluate disability & evaluate response to bronchodilators

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