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231 Cards in this Set
- Front
- Back
How is the alveolar surface optimized for gas exchange
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short transit distance between aveloar surface and blood supply and large surface area
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What happesn to air as it enters the nose and mouth
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they increase the temp of air and humidy the air for the internal environemnt
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Is the nose more important for increase temp and humidity
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YES
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What are the defense of the airways
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filtration
mucus reflexes |
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How is filtration a defense
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hair in the nose remove large particles
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What are components of mucus
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glycoproteins
proteins ions water mucociliary escaltor |
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What do glycoproteins do
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give mucus gel-like properties
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Mucus is 99% water, loss of water makes
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mucus really thick
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What does mucociliary escaltor do
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trapped partcles in mucus are removed by coordinated beeating of cilila--to swallow or cough up
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What are the 2 reflex defense mechanisms
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afferent nerves
efferenet nerves |
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What do the AFFERENT nerves contain
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c-fibers and irritant receptors stimulates by dust and citirc acid
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What are afferent nerves lead to
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cough
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What do efferent nerves contain
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parasymaptehtic
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What eo EFFERENT nerves lead to
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reflex broncocontristion
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What is benefit of reflex bronconstriction
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reduces penetration by irriation, b/c broncoconstriction increase speed though airways
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What does inspiration involve
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contraction of diaphragm adn external intercostal muscles
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What does expriation nromally involve
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passive
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Only ACTIVE expiration inovles
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contraction of internal intercostal muscles and abd ucles--which are always active in people with airway obstruction
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Lung volumes and capacticites are measured by
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spirometry
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What is tidal vlumes
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volume of air inhaled and exhaled with each breath
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What is rediual volume
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volume of air remaining in lugns after forced expiration
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Is there sympatethic to airway smooth muscle
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NO
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Spirometry is seen in clinical office what are other measures of pulmonary function
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peak flow measurements
forced expiraotry flow airways resitance and dynamic lung compliance |
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What is simiples measure of expiratory flow
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peak flow measurement
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Peak flow measumrents may be used for self-evlauation , and measures
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maximal flow rate of expiraotrion
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Forced expiratory flow measruemtns involed the use of
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a spirometer
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What does Forced expriaotry flow measure
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FEV1--and FVC
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What is FEV1
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forced expitoary volume in one sec
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What is FVC
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forced vital cpacity
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FEV1/FVC is a use measure of pumonary function, normal is 80%, what is indicative of obsturction
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50%
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Airways resistance and dynamic lung complaices is VERY INVASIVE, and involes
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use of whole body pletyhsmograph
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What does airways resistnace and dynamic lung complice measure
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CENTRAL airway cailber and PERIPHAEAL airway caliber
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Increase airway resistance (central airway caliber), and decrease dynamic lung complicaed (peripheral airway caliber)
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broncoconstriction of central and peripheral airways
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Pulmonary circulation beings when it leaves
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the right heart via the pulmonary artery
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The pulmonary atery branches to form
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dense capillart network around the alveoli,
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After they form a dense capillary network around the alveoli, they coalesces to form
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pulmonary veins that drain to the left via the pulmonary vein
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Deoxygened blood enters the pulmonary circulation and oxgenated blood is returned to
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the left heart
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Pulomonary ciruclation is a LOW pressure, LOW resistance vascular beed
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YES
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What happens to pulomary circulation with poorly ventilated alveoli
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Decreased O2 tension, and aterial constriction, and redistruction of blood to well ventilated area of the lung
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B2 agoinsts can dilate blood vessels and mess up
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ventilation perufsion matchign
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Aerosol is a presurized dosage form containing one or MORE activate ingredients which upon acutation emit
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a fine dispersion of liquid, and or solid materials in a gaseous medium
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What are uses of aerosols besides inhalation therapy (broncodilatoros)
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dermatological (local anesthetics), space sprays, surface sprays,
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Is mantipulating particle size is important
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YES
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What are the MAIN particle properties
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inerital impaction
sedimentation diffusion |
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Inertial impaction is affect is by mass and inital velocity, and affets the tendcy of dropled to move
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in a STRAIGHT direction, increasing mass increases straight direction, and increase inertial impaction
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Sedimentation follow Stoke lase of diameter and dnesity, and movement of droplets under
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GRAVITY
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What affects diffusion of particles
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droplet diameter
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Decrease droplet diameter
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INCREASES diffusional depoistion
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What are 2 ways you can effect aerosol particle movement
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1. inspiration volume
2. inhalation flow rate |
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What is the benefit of increase inspiration volume (breath in more deeply)
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increase penetration of particle into airwats
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What is disadvantage of increase inhalation flow rate (fast inhalation)
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Increase particle velocity, and increase inertial impaction
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Why is a fast inhaltion BAD for MDI
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want to breah in slowed dont want particle impacting with BACK of mouth
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Large paticles will tend to move in a stight driection will have
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inetial impaction on tissue
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What do smaller paricles do
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will tend to follow airflow
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What is drug hygroscopicity
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airways 99.5% humidity, the particles will increase in size as they adsorb water and move through airways
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What does breath-holding relates to
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sedimentaion and diffusion
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What does breath holding do
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provides time for drug to deposit on airway wall and diffuse
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What is the main componetn for larger patricles
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inerial impaction
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What is the main compoenet for smaller particles
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diffusion
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Different sized particles depoist at differnt site of the repiratory tree
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YES
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Particles >10 ug deposit
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oral pharangeal regions (in mouth or back of throat
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What to particles 3-10 get
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tracheal or bronchail tre
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Paricles size of 3-10 is important for treating
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bronchoconstriction of asthma
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Particles size <3ug leads to
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ends in periperhal airways which leads to SEs
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Characteristics of aerosols
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polydisperse and particle size is log-normally distributed
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What is polydisperse
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aersol with range of particle sizes
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Aerosols that have paricle size that is log-normally distributed have a standard devations that
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gives an idea of spread of particle sizes
DO NOT WANT large SD |
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Is there mucus in the aveolus
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NO
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The central airways are the trachea and broncial trees, and DRUG dissolves in
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mucus layer
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In the central airways the drug dissolves in mucus layer then removed by
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mucociliary escalter,
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Some drug is removed by mucociliary escalter it
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pass through the epithelium and is subject to metabolism,
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After passing though the epithelium and being subject to metabolism is it then removed by
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submucsal blood vessels, and remaining reaches smooth mucsle
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What is the target in central airways
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smooth muscle
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In the Avelovous the drug initally dissolves in the
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surfactant layer
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What size drug is needed for Alveous for systemic delivery
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<1 ug
|
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In the avelous the drug dissolves in the surfactant layer and is removed by
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macrophages
|
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After some drug is removed by macrophates it pass though
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epithelium and is removed by Lumathic vessels in the intersitatal space
|
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After pass though the epithelium and being removed by lumhatic vessels, it is
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mestabolized by enodthelium, and reaches target cells
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What is the target cell in teh alveolus
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blood for systemic use
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What are factors affect rate of absroption
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PCL MT
Paraceullar aqueosu pores carrier mediated transport lipid solubility moculear weight transcytosis |
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Decreasing MW and its affets on absroption
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increases
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Increasing the partition coefficent does what
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more lipophilic, and crosses membrane better and increases absorption
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What is an example of carrier-mediated transport
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cromolyn
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What do paraceullar aqueous pores do
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permit hydrophilic drug passage
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What does transcytosis permits
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protein passage thorugh vesicle transport process
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Metered dose inhalers comprise solutions of drugs in a sealed container containuing
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liquidfied gas propellant under pressure
|
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What are the types of propellants
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CFCs
Non-CFCs (HFA) non-lqiuidred compressed gases |
|
What is CFCs
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chlorofluorocarbons (CFCs)
AKA Freon 12 |
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CFCs are being phased out becuase of the effects on ozone layers
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YES
|
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What are non-CFC gases
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HFA (hydrofluoroalkane)
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HFAs are not as cold,and should be watched in indivduals with what allerhy
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corn allergy problems
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What are non-liquifed compresses gases
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carbon dioxide, nitrogen nitROUS oxide
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In metered dose inhalers how can DRUG be assoicated with propellant
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1. Dissolved in propellant
2. Suspended in propellant 3. Dissoved in aqueous solution |
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If the drug is suspended in propellat such as micronized powders, what is included so particles do not stick together
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surfactant
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Drugs suspend in propellant shold be skaen prior to use
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YES
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If the drug is dissolved in aqueous solution, the aqueous solution floats on
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TOP of the propellant
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When you depress the acutator, propellant vapor pressure forces solution into the dip tube thotouh the valve mechanism and out the nozzle
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YES
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Increasing vaptor pressure
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increase force of ejeciton
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If you decrease orifice diameter you decrease
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particle size
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Do MDI only relase a qunatal dose of drug compared to aerosol
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YES
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There are 8 steps to using an inhaler what is 1st step
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Remove the cap and hold inhaler upright
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What is step 2
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Shake the inhaler
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What is step 3
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Tilt the head back slightly and breathe out
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What is step 4
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Open mouth with inhaler 1-2 inches away
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What is Step 5
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Press down on inhaler to release medication
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What is step 6
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Breathe is slowly for 3-5 sec
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What is step 7
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Hold breath for 10 sec and allow medicines to reach deply into lungs
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Step 8
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Reated puffs as directed waiting one minute betweeen pufss may permit second puff to penetrate the lungs better
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Most inhaled drugs without a spacer majority does not deposit in the lungs SE's include
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ORAL--candiasis
GI- by swallowing |
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What are 3 types of spacers
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1. reservior bag
2. tube spacer 3. aerochamber |
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Why do spacer devices increase lung deposition?
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1. Timing for breathing is not as crictial
2. Decrease inertial impaction (pt can inhlae more slowly 3. Particles getting smaller as propellant evaporates |
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The main advantae of spacers is INCREASE pulmoanry deposition which restuls in
|
better therapuetic effects
|
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Spaces also DECREASE oropharygneal depostion which results in
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Decrease SEs
|
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DPI (DRY powder inhalers) are micronized powers what size
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<5u--good for central air ways (trachea and bronchial tree)
|
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DPI require a divice that breaks the capsule open, why must you breath in faster in DPI
|
inspiraotry flow dispereses the powder for inhaltion
|
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DPI are more stable b/c they are powders NOT liquids, making formulations easier
|
YES
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Do DPI have more DRUG than a MDI paricle?
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DPI particle have 5x more drug
|
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Why do DPI have a decrease risk of microbial growth
|
NO WATER
|
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DPI have no issue with ozone destruction
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YES
|
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What are disadvantages of DPIs
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cumbersome equipments
particles >5u cause coughing |
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Nebulizers are solutions of drug that are place in the nevulizer reserviors what are 2 types
|
1. JET or air driven
2. Ultrasonic |
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What is the JET nebulizer
|
high velocity gas propels liquid against a baffle to make aersol
|
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What is Ultrasonic nebulizer MOA
|
piezoeletci membrane--aerosol
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How are nebulizers dosed
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based on time
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What are advantages of nebulizers
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timing of inhlation is NOT critical, and insipriaotry volume is NOT criciation
|
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Pts with decrease insprioatry capacity can still use nebulizers
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YES
|
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Nebulizers are also easier to formulate and can deliver larger doses than inhalers
|
YES
|
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Wht are disadvantages of nebulizers
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specialized and expensive equipments, can destory proteins, varability in performance
|
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What nebulizer has short-life span
|
ultrasonic beblizer
|
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Do nebulizers reserviors need to be clearned regularly
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YES
|
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Do inhaled drugs have a fast onset, as fast as
|
IV
|
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What are advantages of inhaled drugs
|
By-pass first pass metabolism
fast onset drug delier to site of action (pulmomnary Few barriers to drug absroption into systemic |
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Do nebulizers reserviors need to be clearned regularly
|
YES
|
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What are disadvantages of Inhaled drugs
|
low efficeincy of delivery--a lot of drug is waster
patietn compliance (timing inhlation, convience) pulmonary toxicity |
|
What are the upper airways
|
nose-pharyn
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What are the central ariways
|
trachea and bronchial tree
|
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What are the peripheral airways
|
alveoli (pulmonary)
|
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What are 2 purposes for drug delivery to upper airways
|
1. local effect
2. systemic effects |
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What are example of local effects to upper airways
|
vasconstriction (decongestants) and anti-allergy
|
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The nasal passages have a large SURFACE area and are richly
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vasculatirzed with fenestrated capillaries
|
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Where does the ciliated epthelium lie in the nose
|
posterior region
|
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Air flow in the nose has increase trousoity, which means
|
increase turbulent air flow,
|
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WHat is benefit of increase tubulent air flow
|
increase dopsittion of particles in nasal cabity and it is richly vascultized with blood so better absorbed, and how it warms the air
|
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Drug delvier to the airways is paricle size-dependent, and what is the IDEAL sizes for upper airways (nose)
|
drops/sprays >10
LARGER particles are better |
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What are drug factors that affect intranasal BIOAVAILABILITY
|
applied drug volume/conc
distibution in nasal cavity density/viscosity of drug soultion |
|
The amount of drug absorbed is realted to
|
the area of contact
|
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What passage way in the nasal vacity is clearned more slowly
|
anterior passage b/c no cilia and smaller SA compared to posterior
|
|
What has better CSF access
|
olfactory eptheium
|
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What does desntiy and viscosity of drug solution determine
|
ease of mucociliary clearance (more viscous less easily cleared)
|
|
What are nasal absoprtion mechansisms
|
1. diffusion
2. aqueous pores 3. active/selective transport 4. olfactory nerve uptake |
|
What is absobed by diffusion
|
lipophilic agents
|
|
What are absrobed by aqueous pores
|
hydrophilic agents
|
|
What is absorbed by active/selective transport
|
insulin/propranolol
|
|
What is absrobd by olfactory nerve uptaken
|
drugs by transcytosis
|
|
Is there mucociliary transport in the nose
|
YES
|
|
Particles in the nose are trapped in muchs and the cilia transport mucto to
|
nasopharxyn--DOWN to the throat
|
|
How do drugs enter the CNS though the nose
|
oflactory nerve uptake
|
|
Enzymes present in the nasal epthelium can degrade drugs, and can disease also modulate drug absoprtion
|
YES
|
|
What are advatnages of intranasal
|
convients, good access to circulation, better acess to CNS, rapid onset and avoiuds 1st pass metabolism
|
|
What are disadvantages of intranasal
|
irritaion
|
|
What is Rhinitis in general
|
inflammation of nasal mucous membranes
|
|
What are characteristic of rhinitis
|
nasal congestion/ watery rhinohhea, itching of nose, eyes pharynx, and palate, sneezing, and can be assoicated with allergic conuctivits
|
|
Rhinitis can be classified as
|
allergic
and non-allergic |
|
Allergic rhinitis may be classified as
|
seasonl
perennial (thoughout the year 70%) |
|
What are complications of rhinitis
|
sleep distubances, loss smell, tast epistaxis, asthma risk factor
|
|
What mediates allergic rhinits
|
IgE mediation
|
|
What are common allergens
outdoor indoor |
outdoor allergens: ragweed, grass, tree pollen
indoor: dutst mite, animal dander, mold spores |
|
Allergic rhinitis affects 10-20% of the popualtion most common chronic conditon in
|
<18 yo (12-15)
|
|
Does Allergic rhinits incidence decrease with age
|
YES
|
|
Allergic rhinits has a strong genetic component--one atopic paret, what is risk, vs 2 atopic parents
|
one atopic--30%
two atopic 70% |
|
Allergic rhinitis is IgE mediation and comprise 2 parts
|
1. immediate allergic response
2. late phase response in only 10-30% of pts |
|
When does the late response occur (if it happens at all)
|
4-8 hours after immediate response
|
|
What is PRIMARY mediator of ALLERGIC RHINITIS
|
HISTAMINE
|
|
Mast cells are under epithelium, and antigen binds to IgE, and what happens
|
cross-linking of IgE and increases Ca+ influx into the mast cell, and the mast cell contents are released
|
|
What are components from mast cells that are IMMEDIATELY released
|
chymase
leukotrienes PAF bradykinin histamine |
|
What does chymase cause
|
rhinorrhea
|
|
What do luekotirenes, PAF, and brady kinin and histamine cause
|
congestion
|
|
Bradykinin and histamine also do what
|
C-fiber activation, which activates CNS, leading to snezzing and inctcing and parasymahtetic drive
|
|
Histamine and bradkininae and increase parasymahtetic drive, which can cause
|
rhiinorrhea and congestion
|
|
The Late response is driven by mast cells that release
|
chemotatic factors, and adhesion moleculs
|
|
What do the chemotatic and adhesion molecules do
|
attach eosinoprhil and neutrophils---which continue the inflammatory response
|
|
What is diagnosis of rhinitis dependent
|
skin testing
|
|
Main non-pharm treat of rhinitis
|
avoidance of antigen
|
|
What is the OTC treatment of allergic rhinits
|
antihistamines (hitsmiane is the primray mediator of allergic rhinits
|
|
Are all symtpoms of allergic rhinits relived by anti-histamines
|
NO congestion still present slightly
|
|
Are antihistamines more effective in preventing then reversing
|
YES
|
|
What 2 classes of antihistamines
|
1. sedating
2. non-sedating H1 antagoinsts |
|
What CLASS of antihistamines are least sedating of sedating antihistamines
|
alkylamines
|
|
What are the alkylamines
|
ABCD T
acrivastine bromphenirmaine chlopheniramine dexchrlpheiramine triporlidine |
|
What are the ethanolamines
|
diphenhydramine
clemastine |
|
What are th phenothiazines
|
promethazine
|
|
What are the piperazines
|
hydroxyzine
|
|
What are the piperidines
|
azatadine
|
|
What are phthalazinones
|
azelastine
|
|
What antihistmaines posses antimuscarinic activity
|
sedating--antimuscarinic does contribue to therapuetic effects
|
|
What contributes to the sedation of sedating antihistamines
|
lipohilic readily penetrate the CNS,
|
|
Can tolerance occur with sedating antihistmaines, how do acheive
|
start at low subtheraptic doses and gradulally increase dose over 2 weeks
|
|
What is the intranasal antihisaminte
|
azelastine--phthalazinones
|
|
What are the NON-sedating antihistamines
|
fexofenadine, loratidine, desloratidne, cetirizine
|
|
Non-sedating anti-histamines may work by inhibtion of medator release from mast cells,a nd inhibition of eosinphil chemotaxis
|
YES
|
|
Do non-sedating antihistamines penetirate the CNS
|
no--so not sedating (cetrizine may be mildy sedaitng
|
|
Loratidine has a long duration of aciton
|
once a day dosign
|
|
Non-sedating no more efficcious, and should only be reserved for pts who
|
have sedative effect or atropine like side effects
|
|
What are the number 1 treatment for allergic rhinits
|
cotricosterios
|
|
Whata are the corticosteriods
|
beclomethasone, budesonide, dexamethsone, lfuticasone, memetasone, triamcinolone
|
|
What are corticosteriods MOA
|
ihbition of early and late phase responses
|
|
What are corticosteriods number 1 for allergic rhinits
|
control all symtpoms of allergic rhinits
|
|
When do effects of corticosteriods begin
|
1-2 days can start in 8 hrs
|
|
Corticosteriods are most effective when used prophylaticaly (ie seasonal should begin)
|
2-3 weeks prior to season
|
|
What are SEs of corticosteriods
|
local irriation, sitings, n cataracts
|
|
30% of intranasal coticosteriods enters nose, the rest is
|
swallowed by gut (70%) and majority the undering 1st pas metabolism
|
|
What are the chromones
|
cromolyn
|
|
What is cromolyn MOA
|
mast cell stablizer
|
|
How is cromolyn used
|
prophylactically, start 2-3 weeks prior to allergy season
|
|
Cromolyn has relative poor eficacy
|
YES
|
|
What are leukotriene receptor antagoinsts
|
montelukast, and zariflukast
|
|
MOA of luekotirene receptor antagoisnts
|
inbhit the effect os luekotrines C4, D4 and E4
|
|
What is result of inhibiting leukotriens C4, D4, E4
|
decreased rhinorrhea, and congestion
---similar to non-sedating antihistamines |
|
What are you anticholinergics
|
ipratropium bromide
|
|
What is the largest effect of ipratroium bromide
|
largest effect on RHINORRHEA
|
|
What are decongestants
|
pheylephine, psudoehpredine, naphazoline, oxymetzoline, xylometzoline, tetrahydrzoline
|
|
What is MOA of decongestants
|
actvate alpha aderenceptors in nasal mucosal vessels causing vasoconstrction
|
|
Vasoconstriction of nasal mucsoal vessels results in
|
decreasing blood volume and edema, and nasal congesiton
|
|
Why do decongestnat have limited role in LONGTERM treatment of allergic rhintis
|
rebound congestion, and persistent vasoconstrtion and decrease supply of nutrient to nasal mucose and cause damage
|
|
What are SEs of decongestants
|
local irriation, stiging, can cause sympathomimietic side effects, increase BP, BPH, PVD
|
|
What is rule of immunotherapy
|
uses a series of sc ijectiosn to desenstive pateints to an antigen
|
|
How long does immunotherapy take
|
takes several motnhs after treatment is started
|
|
What are Anti-IgE antibodies
|
omalizumab
|
|
What is MOA of Omalizumab
|
antigcody against IGE-prevent IgE from binding to mast cell so improve nasal symtoms with alelrgic rhintis
|
|
What is Non-allergic rhinits
|
nasal bosturction WITHOUT rhinorrhea
|
|
What can be causes of non-allergic rhinits
|
bacterial/viral infection/ drugs or pregancy
|