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457 Cards in this Set
- Front
- Back
what is the function of the conchae in the lateral wall
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increase surface area and create turbulent airflow to maximize warming and filtering of entering air
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What type of epithelium is the respiratory epithelium
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pseudostratified columnar epithelium
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what is the mucociliary escalator
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moves mucus from nasal cavity towards the oropharynx and from the lower respiratory towards the pharynx
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what are the purpose of swell organs in the nasal mucosa
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large venous sinuses of the mucosa over the concha form erectile tissue that affects passage of air through the nasal cavity
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the hard palate is made of 2 types of epithelium, one type on the upper surface and one on the lower surface. Describe the different types
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upper surface- respiratory epithelium (pseudostratified columnar )
lower surface- stratified squamous |
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what is the composition of the soft palate
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muscle, aponeurosis, and mucous membrane
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what are the 5 muscles of the soft palate
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1. musculus uvulae
2. palatoglossus 3. levator veli palatini 4. tensor veli palatini |
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which 3 muscles act to lift the pharynx during swallowing
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1. stylopharyngeus
2. palatophrayngeus 3. salpingopharyngeus |
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which nerve innervates the cricothyroid. What is the embyonic origins
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CN X- superior branch of the vagus
Muscles of mesoderm from arch 4 are pharyngeal constrictors, cricothyroid, levator veli palatinini Arteries from mesoderm of Arch 4- Arch of the aorta, R. subclavian, sprouts of pulmonaries Arch 4 Pouch endoderm--> superior parathyroids Connective tissue from neural crest of Arch 4- thyroid cartilage |
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which nerve innervates the intrinsic larynx. What are the embyonic origins
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Recurrent laryngeal nerve of the Vagus
Muscles of mesoderm from arch 4 are all the laryngeal constrictors, NOT THE cricothyroid, Arteries from mesoderm of Arch 4- ductus arteriosus, definitive pulmonary arteries Connective tissue from neural crest of Arch 4- cricoid cartilage |
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which type of epithelium is on the following structures
nasopharynx a. respiratory epithelium- cilicated pseudostratified b. stratified squamous non-ketatinized c. stratified squamous ketatinized |
a. respiratory epithelium- cilicated pseudostratified
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which type of epithelium is on the following structures
oropharynx a. respiratory epithelium- cilicated pseudostratified b. stratified squamous non-ketatinized c. stratified squamous ketatinized |
b. stratified squamous non-ketatinized
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which type of epithelium is on the following structures
larynx a. respiratory epithelium- cilicated pseudostratified b. stratified squamous non-ketatinized c. stratified squamous ketatinized |
b. stratified squamous non-ketatinized
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Name the action:
Must close the oropharyngeal isthmus Palatoglossus and palatopharyngeus depress palate and move arches towards midline Palatoglossus also raises back of tongue a. normal breathing b. Breathing with food or liquid in oral cavity c. Swallowing |
b. Breathing with food or liquid in oral cavity
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Name the action
Must close the pharyngeal isthmus and open the oropharyngeal isthmus Tensor palatini makes soft palate firm Levator palatini raises palate above the horizontal Larynx elevated to push epiglottis against root of tongue, closing inlet a. normal breathing b. Breathing with food or liquid in oral cavity c. Swallowing |
c. Swallowing
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t/f Trachea and bronchi have complete cartilaginous rings to prevent the trachea from collapsing during absence of air and for protection
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false- incomplete C shaped rings to prevent collapse and for protection
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Oblique fissure separates which lobes
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Oblique fissure separates superior and inferior lobes
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Horizontal fissure defines which lobe
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Horizontal fissure defines middle lobe of right lung
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List the components of the conducting zone of the respiratory tree
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1. nose
2. pharynx 3. trachea- cartilage 4. bronchi- cartilage 5. bronchioles 6. terminal bronchioles |
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which components of the conducting zone of the respiratory tree have cartilage
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3. trachea- cartilage
4. bronchi- cartilage |
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what is the function of the conducting zone of the respiratory tree
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brings air in and out, warms, humidifies, and filters the air
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t/f wall of the conducting zone contain skeletal muscle
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false- contain smooth muscle
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List the components of the respiratory zone of the respiratory tree
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1. respiratory bronchioles
2. alveolar ducts 3. alveoli |
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what is the function of the respiratory zone of the respiratory tree
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respiration, gas exchange
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t/f Conducting bronchioles have cartilage and glands
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false- Conducting bronchioles (no cartilage or glands) —›
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name the portion of the respiratory tract
typical respiratory epithelium with lots of mixed glands hyaline cartilage rings a. trachea b. bronchial tree c. bronchioles d. alveoli |
a. trachea
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name the portion of the lower respiratory tract
decrease in cartilage increase in smooth muscle and elastic fibers decreased cell height and number of glands |
b. bronchial tree
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name the portion of the lower respiratory tract
no cartilage or glands a. trachea b. bronchial tree c. bronchioles d. alveoli |
c. bronchioles
d. alveoli |
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Name the portion of the bronchioles
pseudostratified columnar epithelium –› ciliated simple columnar with goblet cells a. conducting bronchioles b. terminal bronchioles c. respiratory bronchioles d. alveolar ducts |
a. conducting bronchioles
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Name the portion of the bronchioles
ciliated cuboidal cells with Clara cells (secretory) a. conducting bronchioles b. terminal bronchioles c. respiratory bronchioles d. alveolar ducts |
b. terminal bronchioles
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Name the portion of the bronchioles
simple non-ciliated cuboidal cells and Clara cells; alveoli open from one side a. conducting bronchioles b. terminal bronchioles c. respiratory bronchioles d. alveolar ducts |
c. respiratory bronchioles
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Name the portion of the bronchioles
no smooth muscle; alveoli open from all sides a. conducting bronchioles b. terminal bronchioles c. respiratory bronchioles d. alveolar ducts |
d. alveolar ducts
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what makes up the air-blood barrier
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Type I cell - basal lamina - capillary endothelium - rbc membrane
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Eupnea is Normal quiet breathing at rest. What is the normal number of breaths per minute
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8-16 breaths per minute
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Fill in the blank:
to low PaCO2 results in respiratory ( acidosis/ alkalosis) whereas too high of a PaCO2 results in respiratory (acidosis/alkalosis) |
to low PaCO2 results
in respiratory ALKALOSIS, whereas too high of a PaCO2 results in respiratory ACIDOSIS |
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too low PIO (e.g., at high altitude) and thus PaO results in which condition (hyperoxemia/ hypoxemia)
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hypoxemia
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t/f Composition of air changes as the altitude increases.
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false- Composition of air remains the same regardless of the altitude.
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t/f Partial pressure of inspired O2 decreases with increasing altitude.
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true- Fractional concentration of O2 remains at
0.21 regardless of altitude. Percentage of O2 saturation of arterial blood, however, decreases with increasing altitude. |
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what is Dalton's Partial Pressure equation
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Pgas X = Fgas X • PB
Dalton's Law of partial pressures. In a gas mixture, each specific gas will exert a pressure as if it alone occupied the entire volume. The pressure exerted by the gas is proportional to its own concentration. To calculate the partial pressure of a dry gas |
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what does Boyle’s Law state
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At constant temperature, the volume of a given quantity of gas varies inversely with the
pressure to which that gas is exposed chnique for pressure breathing is not unlike that used for intermittent positive pressure breathing in the clinic for providing intermittent mechanical ventilation for purposes of augBoyle’s Law predicts that as pressure decreases (with increasing altitude) the volume of gas in sealed cavities in the body will increase. |
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what is Decompression sickness
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mostly nitrogen bubbles when breathing
air) can develop in the body of a diver, aviator or caisson worker whenever they are exposed to a rapid reduction in barometric pressure (decompression). |
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list names the layers of structures
that present a resistance to the diffusion of O2 as it passes from the alveolar gas into the RBC traveling through a pulmonary capillary. |
1. fluid layer lining the alveolus (surfactant)
2. alveolar epithelium 3. interstitium 4. capillary endothelium 5. plasma 6. RBC membrane 7. RBC intracellular fluid |
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Definition
Increased respiratory rate greater than 18 breaths / minute |
Tachypnea
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Definition
Increased ventilation that meets metabolic needs |
Hyperpnea
Increased respiratory rate (i.e. tachypnea) and/or overly deep breaths e.g. during exercise |
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Definition:
Increased ventilation that exceeds metabolic needs |
Hyperventilate-Increased respiratory rate (i.e. tachypnea) and/or overly deep breaths
e.g. during anxiety attack |
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Definition:
Decreased respiratory rate less than 10 breaths / minute |
Bradypnea
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Defintion
Cessation of breathing |
Apnea
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Definition
Labored breathing |
Dyspnea
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what contributes mostly to the elasticity in the thorax
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Elastic due mainly to the joints of the ribs
Causes thoracic cavity to expand (opposes recoil of the lungs) |
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List the muscle of normal respiration
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1. diaphragm
2. external intercostals |
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Which muscles are used during forced inspiration
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1. diaphragm
2. external intercostal 3. Pectoralis minor 4. Sternocleidomastoid 5. Scalenes |
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which muscles are used during forces expiration
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1. Internal intercostals
2. Obliques 3. Rectus abdominis |
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which pleura Lines thoracic cavity and is attached to the diaphragm
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parietal pleura
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which pleura Covers lungs
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visceral pleura
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what is the pleura space
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Fluid-filled potential space between the pleural layers
Pressure in the space is less than pressure in the lungs (discussed later) Due to recoil of lung and expansion of thorax Allows lung to remain inflated |
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in which zone is the Mucociliary escalator present
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conducting zone
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what is the effect of sympathetics on the smooth muscles of pulmonary tree? Which receptors are used to achieve this goal
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Sympathetics relax pulmonary smooth muscle (dilate bronchioles)
Via β2 adrenergic receptors |
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what is the effect of parasympathetics on the smooth muscles of pulmonary tree? Which receptors are used to achieve this goal
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contract pulmonary smooth muscle (constrict bronchioles)
Via acetylcholine receptors (muscarinic receptors |
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Describe the mucociliary escalator
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Goblet cells produce mucus which traps fine particulates (including pathogens)
Ciliated epithelial cells “beat” to propel particulates trapped in mucus to the pharynx |
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what is the Anatomical dead space in the lungs? what is the volume of this space
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Conducting zone volume
Rule of thumb: volume in ml is equal to weight in pounds e.g. 200 pound person has a 200 ml anatomical dead space |
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what is Alveolar dead space? what is the volume in a normal health adult?
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Alveoli that do not participate in gas exchange
Due to lack of blood supply or damage to alveoli Zero in normal, healthy individuals |
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what is the Physiological dead space?
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Combination of anatomical and alveolar dead spaces
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Name the volume:
approximately 500 ml Volume of air inspired or expired during normal, quiet breathing |
tidal volume
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Name the volume
approximately 3,000 to 3,300ml Maximum amount of air that can be inspired at end of a normal inspiration |
Inspiratory reserve volume (IRV)
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Name the volume
– approximately 1,000 to 1,200ml Maximum amount of air that can be expired at end of a normal expiration |
Expiratory reserve volume (ERV)
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Name the volume of air
cannot be measured with a spirometer (~ 1,200ml) Volume of air remaining in the lungs after a forced expiration |
Residual volume (RV
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name the capacity
– approximately 2,200 to 2,400ml Volume of air remaining in the lungs after a normal expiration |
Functional residual capacity (FRC)
FRC = ERV + RV |
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name the capacity
– approximately 4,500 to 5,000ml Volume of air forcefully expired from lungs after a maximal inspiration |
Vital capacity (VC)
VC = VT + IRV + ERV or VC = TLC – RV |
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name the capacity
approximately 5,700 to 6,200ml Volume of air in the lungs after a maximal inspiration |
Total lung capacity (TLC)
TLC = VT + IRV + ERV + RV |
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Name the unit of rate for air flow
Volume of air forcefully expired after a maximal inspiration? What is the normal amount |
Normal FVC ≈ 5,000 ml
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Name the unit of rate for air flow
Volume forcefully expired in the first second? What is the normal value |
Normal FEV1 ≈ 3,500 to 4,000 ml
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Name the unit of rate for air flow
Volume forcefully expired in three seconds? What is the normal amount of air? |
Nearly the entire vital capacity (i.e. ~ 95% of)
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what is the formula for Helium Dilution Method to Measure FRC
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(C1) (V1) = C2 (V1 + V2)
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what is the formula for Boyle's Law? What does it state?
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Boyle’s Law: the product of pressure and volume is constant for a confined gas
P1V1 = P2V2 |
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Definition:
measure of how volume changes as a result of a pressure change ( delta Volume/ delta Pressure) a. Compliance b. Air Flow c. Pressure d. Resistance |
Compliance
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what is the normal compliance volume in the lungs
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Normal value of the lung is 0.13 liters / cm H2O
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what is Hysteresis
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a pathway, process or property in one direction differs from the pathway, process or property in the reverse direction
like the lung compliance curves |
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At what point in the graph, is Recoil of lung and expanding force of chest wall equal each other
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When lung volume is at FRC
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At what point in the graph is Recoil of lung is decreased while expanding force of chest wall is increased
Lung and chest wall want to expand |
When lung volume is less than FRC
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when on the graph is Recoil of lung is increased while expanding force of chest wall is decreased
Lung and chest wall want to collapse |
When lung volume is greater than FRC
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why is normal lung compliance is dependent on surfactant
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Surfactant reduces surface tension (T)
Pressure (P) to keep alveoli inflated (i.e. collapsing pressure) is therefore very low Allows alveoli to more easily remain inflated |
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describe the pathogenesis of infant respiratory distress syndrome
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Lungs without surfactant
Surface tension is now very high Collapsing pressures are now high, especially in smaller alveoli due to smaller radii (r) Alveoli tend to collapse (type of atelectasis), especially smaller alveoli Pressure gradients also produced from smaller alveoli to larger alveoli Smaller alveoli collapse into larger alveoli |
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how is Air Flow, Pressure and Resistance related
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Airflow= P1-P2/ R
R= 8vl/ Π r4 P1 = pressure at point 1 (e.g. of the alveoli) P2pressure at point 2 (e.g. of the air we breathe) ν = viscosity (e.g. of inspired air) l = length R= radius (e.g. of airways) |
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what is the effects of sympathetics on the airway and resistance
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Sympathetics dilate airways (decreases resistance)
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what is the effects of parasympathetics on the airway and resistance
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Parasympathetics constrict bronchioles airways (increases resistance)
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what is the effect of High lung volume on resistance
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High lung volume (decreases resistance)
High lung volumes are associated with greater radial traction i.e. airways are pulled open by interstitium Increases radius and therefore decreases resistance |
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what is the effect of low lung volume on resistance
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Low lung volume (increases resistance)
Low lung volumes are associated with less radial traction i.e. airways not pulled open by interstitium Decreases radius, even to the point of collapse |
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Minute ventilation (VE) – volume of air moved into the airways per minute
what is the equation for minute ventilation |
VE = (VT) x (Respiratory Rate)
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Alveolar ventilation (VA) – volume of air moved into the alveoli per minute
what is the equation for alveolar ventilation |
VA = (VT – VD) x Respiratory rate
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ventilation requires pressure gradients. how are pressure gradients
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Pressure gradients created by changes in volumes (Ideal Gas Law)
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t/f Pleural pressure (Ppl), Pressure in the pleural cavity is always less than Palv. Why
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true-Aids in keeping the alveoli inflated
Produced by tendency of lungs to recoil and chest wall to expand |
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t/f Transpulmonary pressure (Ptp) needs to be negative to keep the alveoli and airways inflated
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false- Transpulmonary pressure (Ptp) needs to be positive to keep the alveoli and airways inflated
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Describe the changes to the lungs during inspiration
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1. Contraction of respiratory muscles- Causes thoracic cavity to expand and thus pulls on the lungs via pleural membrane
Recoil of lungs is now increased- Ppl decreases toward -8 cm H2O, causing alveoli to inflate Increases alveolar volume- Palv decreases toward -1 cm H2O (less than PB now) Air rushes into lung down pressure gradient- Causes Palv to increase toward zero |
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Describe what happens during expiration
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Relaxation of respiratory muscles
Decreases thoracic cavity volume toward resting (end of expiration) level-Recoil of lung decreases toward resting levels- Ppl increases toward -5 cm H2O- Decreases alveolar volume toward resting levels Palv increases above PB toward +1 cm H2O- Greater than zero due to greater air volume Air rushes out of lung down pressure gradient- Causes Palv to decrease toward zero |
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Describe the basis for how a pneumothorax develops
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Presence of air in the pleural cavity leading to an increase in Ppl
Ppl is no longer less than Palv Causes the lung to collapse |
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Describe the basis for how a pneumothorax develops
|
Presence of air in the pleural cavity leading to an increase in Ppl
Ppl is no longer less than Palv Causes the lung to collapse |
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Describe the basis for how a pneumothorax develops
|
Presence of air in the pleural cavity leading to an increase in Ppl
Ppl is no longer less than Palv Causes the lung to collapse |
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what is the difference between PaO2 and SaO2
|
PaO2 = measures oxygen in the blood (80-100)
SaO2 = measures tissue perfusion (pulse ox >95%) |
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What type of pnuemothroax? What causes this type of pneumo
|
Simple pneumothorax means that air is allowed to enter and exit the pleural cavity
Causes equilibration of either Palv and Ppl or PB (and in essence, Palv) and Ppl Ppl = Palv or PB = Ppl this pic. pneumo from broken rib |
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what type of pneumothorax? what causes this ?
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Tension pneumo
Air enters but does not exit the pleural cavity (air is trapped) Causes a large increase in Ppl (Ppl > Palv) Mediastinal structures are pushed to the opposite side of the thoracic cavity Compresses the “unaffected” lung, the heart, and the great vessels Unaffected lung is now “affected” Decreases cardiac output |
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which respiratory center ( dorsal or ventral) respiratory group?
Most active during inspiration Some neurons also active during expiration Primarily drive the diaphragm |
dorsal respiratory group
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which respiratory center ( dorsal or ventral) respiratory group?
Active during inspiration and expiration Also contains pacemaker neurons (pre-Bötzinger complex) Primarily drive the intercostals |
ventral respiratory group
|
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which center is responsible for the following in breathing ( apneustic or pneumotaxic- pontine) respiratory group
Not vital to the generation of respiratory rhythm Helps regulate duration of inspiration Causes longer inspiratory bursts Causes long, deep inspiration |
apneustic respiratory group
|
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which center is responsible for the following in breathing ( apneustic or pneumotaxic- pontine) respiratory group
Not vital to the generation of respiratory rhythm Helps regulate duration of inspiration Causes shorter inspiratory bursts Causes short, shallow inspiration |
pneumotaxic- pontine respiratory group
|
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Which portion of the breathing center is described by the following
voluntary aspect of breathing Breathing is involuntary but can be voluntarily overridden e.g. breath-holding or voluntarily hyperventilating a. cerebrum b. hypothalamus c. chemoreceptors d. diaphragm |
cerebrum
|
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which portion of the controlling of breathing does the following?
emotional aspect of breathing e.g. increases respiratory rate during stress or excitement |
hypothalamus
|
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name the breathing control mechanism for the followig
Neurons in multiple areas of the medulla and pons Play the biggest role in the regulation of breathing Monitor the level of PCO2 / pH in arterial blood a. cerebrum b. hypothalamus c. central chemoreceptors d. lung stretch receptors |
c. central chemoreceptors
|
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name the breathing mechanism responsible for the following
Carotid body (glomus cells) in the the wall of carotid arteries Monitor the level of PO2 (and to a lesser extent PCO2 / pH), in arterial blood Oxygen stimulates breathing in extreme instances (PaO2 < 60 mm Hg) a. cerebrum b. hypothalamus c. peripheral chemoreceptors d. lung stretch receptors |
c. peripheral chemoreceptors
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which breathing mechanism Sends inhibitory impulse to brainstem when lungs are over-inflated
|
lung stretch receptors
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according to Fick's Law:
Diffusion of gas across membrane is directly proportional to: |
VX = (D) (A) (P1 – P2) / ∆x
Diffusion coefficient (D) Surface area (A) Pressure gradient (P1 – P2) |
|
according to Fick's Law:
Diffusion of gas across membrane is inversly proportional to: |
Membrane thickness (∆x)
|
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what is the Physiologic shunt
|
about 2% of cardiac output bypasses alveoli
Bronchial veins drain directly into pulmonary veins Thebesian veins drain directly into left ventricle and left atrium |
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how is Physiological Dead Space Volume (VD) estimated
|
VD = VT X [(PaCO2 – PECO2)/ PaCO2 ]
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how is Alveolar Ventilation Equation calculated
|
VA = ( VCO2 x K)/ PACO2
K = constant (863 mm Hg) PACO2 = alveolar PCO2 VCO2 = rate of CO2 production |
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how is Oxygen is transported in blood
|
1. Dissolved
2. Hemoglobin |
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how is Carbon dioxide is transported in blood
|
1. Dissolved
2. Hemoglobin 3. Bicarbonate |
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definition:
percent of Hb fully saturated with oxygen a. SaO2 b. O2 capacity c. O2 content |
a. SaO2
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|
definition:
greatest amount of O2 (in ml) that can be carried in 100 ml of blood a. SaO2 b. O2 capacity c. O2 content |
b. O2 capacity
|
|
definition:
amount of O2 that is carried in 100 ml of blood a. SaO2 b. O2 capacity c. O2 content |
c. O2 content
|
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When each gram of Hb is fully saturated, it carries ___ ml of oxygen
|
~ 1.36 ml of O2
|
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how how much O2 is extracted from blood by tissues
|
approximately 5 vol % (20 vol % – 15 vol %) is extracted from blood by tissues
, 25% of O2 is extracted from the blood by the tissues |
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which shift Indicates a decrease in the affinity of Hb for O2
|
Right shift- Hb releases O2 more readily
|
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which shift Indicates an increase in the affinity of Hb for O2
|
left shift- Hb binds O2 more tightly
|
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which factors cause a right shift in the O2 – Hb binding curve
|
↓ pH
↑ PCO2 ↑ temperature BPG HBS |
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which factors cause a left shift in the O2 – Hb binding curve
|
Increase the Affinity of Hb for O2
↑ pH ↓ PCO2 ↓ temperature HbF Methemoglobin CO |
|
what is the double whammy of carbon monoxide poisoning
|
CO displaces oxygen from hemoglobin
Hb has 250 times greater affinity for CO Whatever oxygen is bound, is tightly bound CO increases affinity of Hb for oxygen Left shift All of the above occurs while PO2 is unchanged |
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what is the Haldane effect
|
As more oxygen is bound to Hb, more CO2 will be released from Hb
Haldane effect (effect of oxygen on CO2 binding to Hb) e.g. as occurs at the lungs |
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how is CO2 transported at the tissue
|
CO2 (produced during cellular respiration) enters red blood cell
CO2 hydrated (aided by carbonic anhydrase) CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3- Accumulation of HCO3- causes diffusion to plasma HCO3- exchanges for Cl- (chloride shift) Hemoglobin aids in buffering the H+ also (Hb-H) |
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how is CO2 transported in the lungs
|
CO2 diffuses from red blood cells to alveoli
Causes HCO3- to combine with H+ to form more CO2 HCO3- + H+ ↔ H2CO3 ↔ CO2 + H2O Decrease in HCO3- causes diffusion from plasma Cl- exchanges for HCO3- (chloride shift) Hemoglobin releases H+ |
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what is the difference between Diffusion-limited gas exchange and Perfusion-limited gas exchange
|
Diffusion-limited gas exchange: the total amount of gas transported
across the alveolar-capillary barrier is limited by the diffusion process As long as the partial pressure gradient is maintained, diffusion will continue along the length of the capillary Perfusion-limited gas exchange: the total amount of gas transported across the alveolar-capillary barrier is limited by blood flow through the pulmonary capillary The partial pressure gradient is not maintained and the only way to increase the amount of gas transported is by increasing blood flow |
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which gas is used to demonstrate diffusion-limited gas exchange
|
Carbon monoxide (CO) is a gas used to demonstrate diffusion-limited gas exchange
|
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which gas is used to demonstrate perfusion-limited gas exchange
|
Nitrous oxide (N2O) is a gas used to demonstrate perfusion-limited gas exchange
Perfusion-limited gas exchange also occurs with O2 transport during normal conditions |
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what is the difference is diffusion vs perfusion in the upper, middle and lower lobes of the lung
|
|
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what is the effect of obstructive pulmonary disease on
1. ventilation 2. airway flow 3. TLC, FRC, RV |
Caused by airway obstruction
Decrease in ventilation Decreases PaO2 (hypoxemia) Increases PaCO2 (hypercapnia) Impaired gas exchange can occur, Hypoxemia Hypercapnia Changes in air flow FEV1 is reduced due to obstruction FEV1 / FVC is greatly reduced Hyperinflation of the lungs Development of barrel chest in later stages |
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name the obstructive disease
Loss of elastic fibers of airways and/or alveoli via proteases (especially elastase) Loss of elastic recoil and thus an increase in lung compliance |
Emphysema
|
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in emphysema- which cells released Proteases and what is the effect of proteases
|
mainly by neutrophils and macrophages in response to inflammation
|
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In which obstructive disease ( emphysema, bronchitis or asthma) does the following occur
Airways more prone to collapse (especially during forced expiration) Breathe through pursed lips Increases pressure within airways to keep them from collapsing |
emphysema
|
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what are 2 causes of emphysema
|
1. Cigarette smoke increases release of proteases
2. AAT normally inhibits proteases from breaking down elastic fibers |
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name the obstructive disease
Increased daily mucus production for at least 3 months in 2 or more consecutive years |
Chronic Bronchitis
|
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name the obstructive disease:
Hyperplasia and hypertrophy of goblet cells of the submucosa and thickening of mucosa No damage to pulmonary capillary bed (therefore, perfusion is fine) |
Chronic Bronchitis
|
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name the obstructive disorder
1. Airway inflammation 2. Bronchoconstriction 3. Airway hyper-responsiveness |
asthma
|
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which type of pulmonary disorder this the following
FEV1 is reduced However, FEV1 / FVC is normal or increased FVC reduced relative to FEV1 |
Restrictive Pulmonary Disease
|
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name the following restrictive lung disease
Inflammation to bronchioles and / or alveoli and / or pulmonary capillaries Causes scarring and fibrosis Lung becomes “stiff” (decrease in lung compliance |
Interstitial Lung Disease (ILD)
|
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Restrictive pulmonary disease can involve disease that affect the respiratory muscles. name 4 disease that would cause the following symptoms
|
Amyotrophic lateral sclerosis / Lou Gehrig’s Disease
Guillain Barré Myasthenia gravis Muscular dystrophy |
|
name the restrictive lung disease
Immature respiratory system fails to produce surfactant Decrease in lung compliance- Surface tension is now very high Collapsing pressures are now high, especially in smaller alveoli - Atelectasis of alveoli (especially smaller alveoli) |
Infant Respiratory Distress Syndrome (IRDS)
|
|
list 4 Adaptation to High Altitude / Hypoxemia
|
1. Hyperventilation
2. Polycythemia 3. Increase in 2,3-biphosphoglycerate (BPG) 4. Pulmonary Vasoconstriction |
|
when will hyperventilation occur
|
Will not occur unless PaO2 is less than 60 mm Hg
Stimulates peripheral chemoreceptors- Causes an increased level of expired CO2 (initial response) Decrease in PaCO2 with a subsequent increase in arterial pH- Respiratory alkalosis Inhibits central chemoreceptors Decrease in ventilatory output |
|
what are the Compensatory mechanism in response to respiratory alkalosis
|
Kidneys secrete (and thus excrete) HCO3-
pH returned to normal values (PaO2 is still low however) Hyperventilation is allowed to resume |
|
t/f Hypoxemia causes the stimulation of erythropoietin release from kidneys
|
true
|
|
Acute Mountain Sickness (AMS) can be prevented with which drug and why
|
Prevention with acetazolamide (Diamox)
Increases HCO3- excretion by the kidneys Creates mild compensatory metabolic acidosis Counteracts initial respiratory alkalosis |
|
why is Nifedipine used in High Altitude Pulmonary Edema (HAPE)
|
Calcium channel blocker normally used to treat hypertension
Used to decrease increased pressure of pulmonary vasculature |
|
why is Dexamethasone used in High Altitude Cerebral Edema (HACE)
|
Very powerful glucocorticoid
Used to decrease inflammation |
|
what are 6 benefits of hyperbaric oxygen therapy
|
1. Greatly increases oxygen concentration in all body tissues
2. Stimulates angiogenesis to locations with reduced circulation 3. Improves blood flow to areas with arterial blockage 4. Stimulates an adaptive increase in superoxide dismutase 5. Powerful endogenous antioxidant 6. Aids the treatment of infection by enhancing neutrophil action |
|
Markus- PFT demo
Define the lung volume volume of gas added to and then removed from the lungs with each breath |
tidal volume (VT)
|
|
maximum volume of gas inhaled at the end of a spontaneous inspiration. It represents the lung’s reserve for increasing VT
|
inspiratory reserve volume (IRV)
|
|
maximum volume of gas expired at the end of a normal spontaneous expiration
|
expiratory reserve volume (ERV)
|
|
volume of gas left in the lungs at the end of a maximal expiration. It represents the minimum volume of gas that the lungs contain if both the lungs and thorax are intact;
|
residual volume (RV
|
|
t/f residual volume RV can be measured by spirometry
|
RV cannot be measured via spirometry. In order to determine RV we must employ indirect methods
|
|
what is the normal FEV1/FVC Ratio
|
>70% of FVC
|
|
what is the normal FEV3 / FVC ration
|
>95% of FVC
|
|
what is the FEV1/FVC Ratio in Obstructive airway disease
|
less than 70%
|
|
FVC ( Forced Vital Capacity) is a ( Volume or Flow) test
|
FVC ( Forced Vital Capacity)
a VOLUME test |
|
FEV1 – (Forced Expiratory Volume in 1 second) is a ( Volume or Flow test
|
FEV1 – (Forced Expiratory Volume in 1 second)
a FLOW test |
|
Describe the flow rates in obstructive vs restrictive
FEV1 FVC FEV1/FVC FRC RV TLC compliance PaO2 PaCO2 |
OBSTRUCTIVE
FEV1-significantly ↓ FVC- ↓ FEV1/FVC- less than 80% FRC- ↑ RV- ↑ TLC ↑ hyperinflation compliance- ↑ loss of recoil PaO2- ↓ PaCO2 - ↑ decrease pulmonary diffusing capacity ( DL ) loss of peripheral vascular elements on CXR due to loss of tissue RESTRICTIVE FEV1- ↓ FVC- ↓ FEV1/FVC- greater than 80% FRC- ↓ RV- ↓ TLC ↓ compliance- ↓ PaO2- ↓ PaCO2 - ↑ |
|
In asthma, maximum expiratory flows are ( increased or reduced) as measured by FEV1.
Moreover, TLC and FRC are ( increased or decreased) during episode |
In asthma, maximum expiratory flows are REDUCED as measured by FEV1.
Moreover, TLC and FRC are INCREASED during episode |
|
t/f weight is a factor in Normal Spirometric Values
|
false- only a factor is severely obese
factors are age height sex race |
|
Reduced FEV1 indicates a flow abnormality of (obstruction or restriction)
|
obstruction
|
|
Reduced FVC indicates a volume abnormality of (obstruction or restriction)
|
restriction
|
|
Obstruction or Restriction
present when FEV1/FVC ratio is < 70% |
Obstruction
|
|
Obstruction or Restriction
(often) present when FEV1/FVC ratio is > 80% (But may be normal) |
Restriction
|
|
t/f in restrictive lung diseases volumes are increased, but flow rates are normal or increased
|
false- Volumes are DECREASED, but flow rates are normal or increased
|
|
restrictive lung disease can be due to: Parenchyma, chest wall , diaphragm
Parenchymal diseases have numerous etiologies, and are referred to as interstitial lung diseases (ILD) what are the common features of ILD (3) |
1. decreased lung compliance
2. decreased lung volumes 3. diffusion (DL) at the alveolar-capillary membrane is impaired (or decreased DLco)* |
|
In obstructive lung disease is the airway narrowing during ( inspiration or expiration)
|
KNOW!!
during EXPIRATION obstructs or limits outflow of air from lungs Both flow rates and volumes are affected |
|
List 4 Mechanisms of Obstruction in Disease
|
1. Chronic Bronchitis - blue bloaters
2. Emphysema - pink puffers 3. Asthma 4. Bronchiectasis |
|
name the obstructive disease and the findings
spasmodic contraction of smooth muscle in the bronchi |
asthma
cough, wheezing, dyspnea, tachypnea, hypoxemia, pulsus paradoxus, mucus plugging reversible bronchoconstriction from hyperresponsiveness |
|
name the obstructive disease and the findings
an inflammatory condition of the bronchi, which results in the excessive production of mucus |
Chronic Bronchitis - blue bloaters
productive cough for more than 3 consecutive months in 2 years. disease of small airway |
|
name the obstructive disease and the findings
enlargement of air spaces and loss of lung recoil resulting destruction of lung alveolar wall |
Emphysema - pink puffers
increase elastase activity, increase lung compliance due to loss of elastic fibers. pts exhale through pursed lips to increase airway pressure and prevent airway collapse during exhalation centriacinar- from smoking panacinar-alpha 1 antiprotease deficiency or liver cirrhosis paraseptal-from bullae which can rupture and cause spontaneous pneumothorax, in you healthy males |
|
t/f In asthma both inflow and outflow limited due to bronchoconstriction throughout respiration, but the pattern on PFTs is that of obstruction
|
true -
|
|
name the obstructive disease
Epithelial cells exhibit abnormal Cl- transport resulting in viscous mucus in the airways with impaired mucociliary clearance; recurring respiratory infections destroy the cellular constituents of the airways resulting in irreversible obstruction to airflow |
cystic fibrosis
|
|
emphysema, anemia*, restrictive diseases, pneumonectomy, pulmonary hypertension*, and recurrent pulmonary emboli*
will have (low or high) Diffusion Test (DLCO) |
low
|
|
The amount of gas in the lungs depends on which 2 factors
|
1. activity of the respiratory muscles
2. mechanics of the Lung Chest wall system (L-CW) |
|
which 2 methods can be used to measure FRC
|
Helium dilution
Body plethysmograph *FRC = ERV + RV |
|
RV (increases or decreases) with obstructive lung disease and (increases or decreases) with restrictive lung diseases
|
RV INCREASES with obstructive lung disease and DECREASES with restrictive lung diseases
|
|
Anesthetic Lecture: Koerker
Preanesthetic Medications include which groups of med |
1. Sedatives
2. Analgesics 3. anticholinergic muscarinic blockers (atropine) to dry secretions & reduce reflexes |
|
list the Stages of Anesthesia
|
1 analgesia
2. excitement 3. surgical anesthesia 4. medullary depression |
|
what leads to the Neuropharmacological Basis for Stages of Anesthesia
|
- due to differential sensitivity of specific neurons or neuronal pathways to the anesthetics
|
|
What causes Stage I (Analgesia) in the Stages of Anesthesia
|
an interruption of sensory transmission in the spinothalamic tract, including nociceptive (painful) stimuli. This interruption occurs because the cells in the substantia gelatinosa in the dorsal horn of the spinal cord are very sensitive to a relatively low concentration of anesthetic in the central nervous system.
|
|
what causes Stage II (Excitement), seen only with diethyl ether,
|
resulted in irregular respiration, coughing, dilated pupils, and marked eye movements. Due in part to irritation of respiratory mucosa and release of catecholamines. Occurs with higher, disinhibitory concentrations of anesthetic, resulting in blockade of many small inhibitory neurons such as Golgi type II cells. A paradoxical facilitation of excitatory neurotransmitters also occurs
|
|
what causes Stage III (Surgical Anesthesia)
|
progressive depression of ascending pathways in the reticular activating system. In addition, the suppression of spinal reflex activity contributes to the muscle relaxation that is produced by some agents in this stage of anesthesia
|
|
what causes Stage IV (Medullary Depression)
|
observed only at toxic doses of anesthetic when cardiorespiratory collapse occurs. Fortunately, neurons in the respiratory and vasomotor centers of medulla are relatively insensitive to the effects of the general anesthetics. It is speculated that regional variations in anesthetic actions may correspond to regional variations in subtypes of the GABAA receptor.
|
|
name the stage in the anesthetic pathway
Minimal CNS depression Some amnesia along with analgesia Respiration and pupils normal No eye movement or loss of reflexes a. analgesia b. excitement c. surgical anesthetic d. medullary depression |
analgesia
|
|
name the stage in the anesthetic pathway
Sensory transmission of nociceptive (painful) stimuli in spinothalamic tract are interrupted due to depression of substantia gelatinosa in dorsal horn of spinal cord a. analgesia b. excitement c. surgical anesthetic d. medullary depression |
analgesia
|
|
name the stage in the anesthetic pathway
Due to inhibition of inhibitory neurons (e.g. Golgi type II cells) & release & paradoxical facilitation of catecholamines a. analgesia b. excitement c. surgical anesthetic d. medullary depression |
excitement
|
|
name the stage in the anesthetic pathway
Respiration – very irregular, coughing Pupils dilated Eye movements marked Loss of eyelid (blink) reflex a. analgesia b. excitement c. surgical anesthetic d. medullary depression |
excitement
|
|
name the stage in the anesthetic pathway
Respiration normal and regular Pupils normal Diminishing eye movements to fixed stare Loss of swallowing, conjunctival and pharyngeal reflexes a. analgesia b. excitement c. surgical anesthetic d. medullary depression |
c. surgical anesthetic
|
|
name the stage of anesthesia
Depth of expiration decreases Pupils dilate and won’t respond to light Loss of carinal reflex Can rapidly progress to Stage IV unless action is taken to decrease depth of anesthesia & stress |
stage 3: surgical anesthesia
|
|
name the stage of anesthesia
Cardio-respiratory collapse due to depression of respiratory and vasomotor centers of medulla. Fortunately, neurons are relatively insensitive to depressant effects of GA. |
stage 4: medullary depression
|
|
name the stage of anesthesia
Fixed, dilated pupils = signs of pending coma or death |
stage 4: medullary depression
|
|
what is the Induction Phase of anesthesia
|
Time to reach plane 3 of stage III. The shorter, the better.
|
|
how can the induction phase of anesthesia be shortened
|
Induction is shortened by hyperventilating (with ventilation-limited (diffusion-) GAs (eg. halothane with high B/G part. coef.), decreasing cardiac output (allows pp to ), in children (high resp. rate)or patients in shock ( CO & vent. ppalv,) or with thyrotoxicosis (high resp. rate).
|
|
t/f Agents that are very soluble in the blood (e.g., nitrous oxide) show rapid induction and recovery.
|
false- Agents that are POORLY soluble in the blood (e.g., nitrous oxide) show rapid induction and recovery.
|
|
t/f . Agents that are poorly soluble in the blood (e.g., halothane) have prolonged induction and recovery
|
false- . Agents that are HIGHLY soluble in the blood (e.g., halothane) have prolonged induction and recovery
|
|
The more soluble an anesthetic is in the blood, the ( lower or higher) will be the coefficient, and the longer will be the induction and recovery periods
|
The MORE soluble an anesthetic is in the blood, the HIGHER will be the coefficient, and the LONGER will be the induction and recovery periods
|
|
what is the Maintenance phase of anesthesia
|
period where the administration of the anesthetic agent is kept at the right level to accommodate the surgical procedure
|
|
what is the Recovery phase of anesthesia
|
reverse of induction (there is a decreasing concentration
of the anesthetic agent) |
|
The more soluble an agent is in blood, the (shorter or longer) the time required for equilibrium to be established between the pulmonary phase and the circulatory phase
|
The MORE soluble an agent is in blood, the LONGER the time required for equilibrium to be established between the pulmonary phase and the circulatory phase
|
|
Describe the following as either Ventilation (diffusion) -limited anesthetics or Perfusion-limited anesthetics and give examples
Have slow, rate limiting equilibration of alveolar with inspired partial pressures. Results in slow induction and slow recovery. Can speed up induction by increasing rate of rise of alveolar partial pressures |
Ventilation (diffusion) -limited anesthetics (e.g. diethyl ether, enflurane, isoflurane, halothane)
|
|
Describe the following as either Ventilation (diffusion) -limited anesthetics or Perfusion-limited anesthetics and give examples
Induction and recovery occur quickly. Agents that are less soluble in blood, induce anesthesia faster |
Perfusion-limited anesthetics (e.g. nitrous oxide, desflurane, sevoflurane)
|
|
75% of cardiac output/min. goes to organs representing 10% of body mass. list the organs
|
brain, liver, kidneys, heart, lungs
|
|
Potency of general anesthetic is directly related to which component of the general anesthetic
|
Potency of GA is directly related to its lipid solubility.
More potent GAs require lower concentrations to produce anesthesia |
|
t/f MAC is directly related to anesthetic potency
|
false- MAC is INVERSLEY related to anesthetic potency
The higher the potency, the lower the MAC) |
|
what is Minimum alveolar concentration, MAC
|
is an attempt to determine the true potency of an anesthetic agent.
The MAC is the percent alveolar concentration at one atmosphere pressure at which 50% of patients will not respond to a skin incision, i.e., ED50 |
|
what is the major route of elimination for a general anesthetic
|
exhalation
Exhalation of GA with low blood:gas partition coefficients (e.g. nitrous oxide or desflurane) is so rapid, back diffusion from blood to alveoli, displaces air from alveoli, leading to diffusion hypoxia. Prevent by ventilating with O2 after terminating GA |
|
match the blood gas coefficient with its respective anesthetic
halothane or nitrous oxide 0.47 or 2.30 |
halothane = 2.30 MAC=.75 long onset and slow recovery
nitrous oxide= 0.47 MAC >100 rapid onset and recovery |
|
t/f GAs excite excitable tissue.
|
false- GAs DEPRESS excitable tissue.
|
|
t/f GAs depress frequency of EEG.
|
true
|
|
t/f GAs increase metabolic rate of brain.
|
false- GAs decrease metabolic rate of brain.
|
|
what is the Effects of general anesthesia on Respiratory System (4)
|
1. Tonic stimulation by reticular activating system to respiratory center is lost. Therefore, respiratory center loses its drive to increase ventilation during hypoxia.
2. Respiratory Center is depressed.Sensitivity to changes in CO2 is reduced. Consequently, partial pressure of CO2 in arterial blood increases. 3. Amplitude of respiration is depressed resulting in decreased tidal volume 4. Mucociliary function in airways is depressed leading to pooling of mucus, atelectasis, and respiratory infections |
|
t/f GAs cause CV changes by depressing the integrative functions of the CNS
|
true
|
|
is the heart itself is directly affected by anesthetic agents.
|
Yes, The heart itself is directly affected by anesthetic agents. Anesthetics may effect the CVS by acting on the central nervous system, acting on the heart muscle itself, on cardiovascular smooth muscle and/or on other aspects of the vascular system
|
|
t/f Halogenated GAs sensitize the myocardium to cardiac arrhythmias, especially in presence of elevated levels of catecholamines.
|
true called catecholamine sensitization
|
|
which catecholamines sensitize the myocardium to anesthetic effects
|
epinephrine or norepinephrine. Halogenated anesthetic agents are most likely to produce this sensitization.
|
|
what are the Effects of general anesthetics on the Renal System
|
1. decrease urinary output due to:
2. Decreased BP 3. Vasoconstriction within kidney 4. Central stimulation of anti-diuretic hormone Halogen radical metabolites of some GAs may be directly nephrotoxic (e.g. Sevoflurane) |
|
what are the Effects of general anesthetics on the liver function
|
All inhalation GAs decrease hepatic blood flow by 15-45%
|
|
what is the effect of Halogenated hydrocarbon GAs on the uterine smooth muscle
|
Halogenated hydrocarbon GAs RELAX the uterine smooth muscle
|
|
what is the most commonly used anesthetic for children in U.S. because of low incidence of adverse effects
|
Halothane (Fluothane®)
|
|
which anesthetic can be Secondary Rx for status asthmaticus
|
Halothane (Fluothane®)
|
|
what is the risk of using Halothane (Fluothane®) during delivery of a baby
|
Causes uterine relaxation which is helpful in manipulating and positioning fetus for delivery BUT may lead to INCREASE blood loss after caesarean section or therapeutic abortion
|
|
what are Halothane's adverse effects (5)
|
1. Respiratory Depression
2. Profound myocardial depression 3. Poor analgesia 4. Hepatotoxicity 5. malignant hyperthermia |
|
what is the inheritance patter of Malignant Hyperthermia and the genetic defect behind the condition
|
autosomal dominant characteristic linked to chromosome 19 which effects ryanodine receptor in sarcoplasmic reticulum Ca++ channel.
Halothane incriminated more than other GAs |
|
what are the warning signs of Malignant Hyperthermia
|
1. Myopathy or neuropathy
2, Muscle spasms and pain 3.Elevated serum creatinine phosphokinase |
|
what is the Prodromal sign of malignant hyperthermia
|
Prodromal sign = muscle hypertonus in masseter muscle in response to succinylcholine
|
|
what is the population that malignant hyperthermia is usually seen
|
Risk absent < 3 yo, peak at 20 yo
Predominantly in muscular males |
|
what is the treatment for malignant hyperthermia (5)
|
1. Quickly cool body
2. Use sodium bicarbonate to correct acidosis 3. Administer O2 3. Correct hyperkalemia with insulin and glucose 3. Specific antidote = procaine or procainamide 4. iv mannitol is used to clear myoglobin from kidneys. 5. Dantrolene, a central acting muscle relaxant that blocks calcium release from sarcoplasmic reticulum, is used to relieve muscle hypertonus |
|
Isoflurane is pre-eminent GA for adults in U.S. even though costs 25X more than halothane.
Isoflurane is :Non-flammable Better muscle relaxant than enflurane Less respiratory depression than enflurane Less depression of cardiac output (CO) than enflurane or halothane what is the major adverse effect of using Isoflurane |
May cause coronary steal and worsen angina in patients with ischemic heart disease
|
|
which anesthetic has Closest to ideal inhalation anesthetic and why
|
Sevoflurane (Ultane®)
Pleasant odor provides useful alternative to halothane in children Popular for outpatient anesthesia due to rapid smooth induction and rapid recovery Does not produce tachycardia-Therefore, preferable in patients with myocardial ischemia Most effective bronchodilator among inhalation GAs |
|
why are Barbiturates Contraindicated in patients with acute intermittent porphyria
|
1. Induces hepatic ALA synthase
2. Effects liver microsomes 3. Aggravates porphyria |
|
Elder Microbiology
what is the infection that is the leading cause of death world wide |
acute LRTI
|
|
what is the leading cause of community acquired pneumonia, follwed by #2 and #3
|
the most common cause of CAP,
#2 Haemophilus influenzae #3 atypicals, Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella |
|
which drug is recommended in as an antibiotics for community acquired pneumonia in a pt who was previously healthy with no use no use of antibiotics in the past 3 months
|
macrolide (MACE)
|
|
which drugs are recommended in as an antibiotics for community acquired pneumonia in a pt who has comorbities such as CHF, diabetes, renal dysfunction, alcholism or use use of antibiotics in the past 3 months
|
give respiratory fluoroquinolones
or beta-lactam + macrolide |
|
what are the major criteria for community acquired pneumonia
|
invasive mechanical ventilation
septic shock with the need for vasopressors |
|
what are 4 minor criteria for community acquired pneumonia
|
respiratory rate >30
PaO2/FiO2 <250 multi-lobar infiltrates confusion/disorientation |
|
if Pseudomona Aeroginosa is suspected in community acquired pneumonia what is the treatment
|
beta-lactams (pippercillin+tazobactam, cefepime)
or beta-lactam + aminoglycosie +azithromycin or eta-lactam + aminoglycosie +fluoroquinolone |
|
t/f most Hospital Acquired Pneumonia is from staff not washing their hands
|
false- 80%-90% are ventilator related
|
|
what are the risk factors for multi-drug resistance in ventilator acquired pneumonia
|
1. previous antimicrobial therapy
2. currently hospital stay or ICU 3. high frequency of mutli-drug resistance in community 4. risk factors for hospital acquired pneumonia |
|
what is the antibiotic of choice for a pt with hospital acquired pneumonia with Step pneumo or H. Influenza with early onset and no previous illness or antimicrobial use and not know to be MDR
|
Ceftrioxone
|
|
definition
refers to pneumonia that occurs prior to hospitalization with specific risk factors immunosuppression recent hospitalization residence in a nursing facility need for dialysis |
Healthcare Associated Pneumonia
|
|
Amphotericin B- is lipophilic
binds to ergosterol/cholesterol What are the adverse effects of Ampho B |
nephrotoxicity
hypokalemia hypomagnesaemia anemia renal tubular acidosis |
|
Ampho B, is useful for treating which life-threatening, progressive fungal infections
|
aspergillosis
cryptococcus histoplasmosis |
|
which azole has >90 oral bioavailability and is renally excreted
|
Fluconazole
|
|
t/f Fluconazole covers all fungus
|
false- does NOT cover Aspergillus
|
|
Which 2 azoles coverall the major fungi such as Aspergillus ,Histoplasma , Coccidioides , Blastomyces and Sporothrix
|
Itraconazole and Voriconazole
|
|
what are the AEs of VORICONAZOLE
|
alterations in visual perception ~30%
blurring, color discrimination, photophobia if Rx > 28 d, then must test visual acuity, visual fields, and color perception pregnancy category D |
|
list the Echinocandins
|
anidulofungin
caspofungin micafungin |
|
what is the mechanism of action for Echinocandins
|
cell wall inhibitor
1,3--D glucan cell wall target absent from mammalian cells |
|
what is the treatment for Aspergillus
|
lipid ampho-B itraconazole
caspofungin posaconazole voriconazole |
|
what is the treatment for Histoplasmosis
|
itraconazole lipid ampho-B
|
|
what is the treatment for Blastomycosis
|
itraconazole lipid ampho-B
|
|
what is the treatment for Crytpococcosis
|
fluconazole lipid ampho-B
|
|
what is the treatment for coccidioidomycosis
|
fluconazole lipid ampho-B
posaconazole |
|
what is the treatment for mould or Fusarium
|
voriconazole lipid ampho-B
|
|
what are the first line of drugs for Tb
|
RIPES
rifampin (RIF) isoniazid (INH) pyrazinamide (PZA) ethambutol (ETH) streptomycin |
|
what is the mechanism of action for isoniazid (INH) and how is it metabolized
|
disrupts cell wall formation by inhibition of mycolic acids, bactericidal, active against intracellular and extracellular organisms
penetrates into phagocytes hepatic metabolism, rate of metabolism is genetically determined |
|
what is the mechanism of action of rifampin
|
inhibits RNA synthesis by binding to DNA-dependent RNA polymerase
|
|
what are the AE of ethambutol
|
optic neuritis-
loss of visual acuity red-green color blindness |
|
which aminoglycoside is used in the treatment of Tb and what is its mechanism of action
|
streptomycin
inhibits protein synthesis at the 30s subunit |
|
what other conditions (other than Tb) can streptomycin be used for
|
tuberculosis
plague tularemia |
|
what are the AEs of streptomycin
|
Aminoglycosides:
nephrotoxicity ototoxicity neuromuscular blockade |
|
which drug is used for the following and what is its mechanism of action
Herpes simplex (HSV) pneumonia Herpes varicella-zoster (HVZ) pneumonia |
acyclovir-inhibits DNA synthesis
irreversibly binds to DNA complex terminating replication |
|
which drug is used for the following and what is its mechanism of action
Respiratory Syncytial Virus (RSV) default setting for other respiratory viruses measles pneumonitis hantavirus pulmonary syndrome SARS |
ribivarin-by inhibits
viral mRNA, viral RNA dependent RNA polymerase and interferes with guanine triphosphate synthesi |
|
which drug is used for Influenza A as a treatment and prophylaxis. what is its mechanism of action
|
amantidine and ramantadine- inhibit viral mRNA disrupting RNA synthesis
|
|
which influenza A and B drug is inhaled and which one is oral. ( zanamivir and oseltamivir)
what is their mechanism of action |
zanamivir is inhaled- no systemic absorption
renal excretion. AE bronchospasm and cough oseltamivir is PO- good oral absorption and activated in liver, also renal excreted both are neuramidase inhibitors |
|
Name the virus:
Nonenveloped, ss (+) RNA, preferes to grow at 33C, Binds to ICAM-1 on nasal epithelium to trigger cytokines and inflammatory process, peaks in fall and and spring. most common cause of common cold a. Rhinovirus b. Coronavirus c.Adenovirus d. Coxsackie A virus |
Rhinovirus
|
|
Name the virus:
enveloped, ss (+) RNA, preferes to grow at 33C, replicates in ciliated epithelium o trigger cytokines and inflammatory process, peaks in winter and and spring. Second most common cause of common cold a. Rhinovirus b. Coronavirus c.Adenovirus d. Coxsackie A virus |
Coronavirus
|
|
Name the virus:
nonenveloped, ss (+) RNA, Bind to ICAM-1, early replicaiton in lymphoid tissue . Lytic virus antibody formation most important protective response against reinfection. prevalent in summer and also causes Herpangina a. Rhinovirus b. Coronavirus c.Adenovirus d. Coxsackie A virus |
d. Coxsackie A virus
also causes Hand-foot-and-mouth disease |
|
Name the virus:
nonenveloped, ds (+) DNA, preferes to grow at 33C, • Lytic virus – results in cell death, causes pharyngitis, acute respiratory disease in military recruits a. Rhinovirus b. Coronavirus c.Adenovirus d. Coxsackie A virus |
Adenovirus
|
|
what is the most probably source of this pulmonary thomboembolus and what are the risk factors for developing this thromboembolus
|
Majority (95%) originate in the femoral vein
Stasis of blood flow (e.g., prolonged bed rest), hypercoagulable states |
|
what determines the pulmonary vessels that are occuluded
|
Size of the embolus determines pulmonary vessel that is occluded.
Large emboli occlude the major vessels (saddle embolus) Small emboli occlude medium-sized and small pulmonary arteries. |
|
Chapter 8 notes and TL #1
Cancers of the lung, head and neck present with which symptoms |
Present with dyspnea, weight loss, abnormal weakness or neurologic
symptoms coupled with abnormal mass, adenopathy , percussion or lung sounds helps to differentiate between neoplastic tumors and other disease |
|
t/f Lung cancer is the Leading cause of cancer death, and the leading cause of cancer death in women since 1987
|
trud
|
|
what are the risk factors for lung cancer
|
Smoking
• Obstructive lung disease – Worse spirometry = greater risk • Passive smoke • 1st degree relative with lung cancer • Pulmonary Fibrosis → linked to “scar carcinoma” • Air pollutants • Radon • Other: asbestos, arsenic, nickel, hydrocarbons, radiation |
|
Asbestos causes mesothelioma . Is there an increased risk of mesothelioma with asbestos/smoking combination
|
No increased risk
|
|
rank the lung cancers in order from most frequent to least frequent
|
most frequent-
– Adenocarcinoma (30%) peripheral- early mets, Hypertrophy Pul Osteo, DIC – Squamous cell carcinoma (25%+)-central. obstruction, cavitation, late mets, superior sulcuc, hypercalcemia, clubbing Small cell carcinoma (25%)- early mets, SIADH, Eaton Lambert Large cell carcinoma (15%)- peripheral . early mets, clubbing – Bronchioalveloar (5%) - bronchorrhea- non-smokers' lung cancer • Other (endocrine and pleural derivatives) Rare. – Carcinoid – Mesothelioma |
|
where is adenocarcinoma usually located in the lung
|
periphery
|
|
why is the considered non-smokers lung
|
Women frequently affected
• Peripheral (75%) • Aggressive metastases – Well-differentiated – Alveolar bronchial and lymphatic spread – mistaken for “the unresolving pneumonia” • Most present as SOLITARY PULMONARY NODULE • Sputum cytology, low yield without cough/hemoptysis • Clubbing/hypertrophic pulmonary osteoarthropathy more common than in squamous cell carcinoma • Chemo- and radiation therapy response poor |
|
which lung cancer has the best prognosis. how does this cancer present. In what patient population is this found
|
multifocal bronchoalveolar
1 yr survival >80% after resection • DIFFUSE form survival is poor: median < 6 mos • Bronchorrhea (copious sputum production) present in 20% • Most likely form to find in NON-SMOKER |
|
Is squamos cell carcinoma (central of peripheral) .
Is there an association with smoking list 5 characteristics |
strong association with smoking
prevalence =25%+ Obstruction Cavitation Late metastases Superior sulcus Hypercalcemia Clubbing |
|
where is large cell carcinoma located (central or peripheral) which other lung cancer is located peripherally
what other conditions are associated with this type of CA what is the treatment |
peripheral- along with adenocarcinoma
Aggressive metastases • Clubbing and pulmonary osteoarthropathy common (but <adenocarcinoma) • Growth more rapid than adenocarcinoma • Treatment by surgery |
|
where is small cell carcinoma usually located (central or peripheral)- what other CA also located here
list the defining features is this associated with smoking what other conditions are associated with small lung CA what is the treatment |
central- also squamous
80% hilar/perihilar location • Smokers & titanium miners • Non-surgical treatment only • Paraneoplastic Syndromes are prominent, including • -SIADH - ACTH production - Lambert-Eaton (Myasthenic) Syndrom |
|
what other conditions are associated SVC syndrome
|
SPHERE of complications in lung Ca
SVC syndrome Pancost tumor Horner's (PAM) Endocrine problems Recurrent laryngeal Effusions (pleural and pericardial) |
|
“PARANEOPLASTIC” SYNDROMES include
SIADH- what is this |
SIADH- small cell (ADH excess leads to water retention which leads to hyponatremia)
|
|
what other paraneoplastic syndromes are seen with lung cancer
|
Increased ACTH- Small cell, Bronchial carcinoid- (hypokalemia, muscle weakness)
• Hypercalcemia- Squamous cell, carcinoid • Calcitonin- (hypocalcemia) small cell, adenocarcinoma • Gynecomastia-(Increased FSH)-large cell, adenocarcinoma |
|
what is the TNM system of staging cancers
|
TNM SYSTEM (Tumor, lymph Nodes, Metastases
|
|
TL #2 ARDS
Define ARDS by 4 clinical criteria: 3 positive features and one exclusion criterion. |
1. new bilateral infiltrates and Severe respiratory distress (without CHR)and 1 or more risk factors
(including infection, aspiration, pancreatitis, and trauma) 2.Impaired arterial oxygenation (hypoxemia) 3. Bilateral pulmonary infiltrates on chest radiograph 4. No clinical evidence of elevated left atrial pressure (or pulmonary artery occlusion pressure of < 18mmHg) |
|
what is the he cardinal feature of ARDS, and what causes it
|
refractory hypoxemia, caused by protein rich alveolar edema after damage to the integrity of the lungs capillary-alveolar barrier
|
|
what is the effect of Widespread alveolar flooding in ARDS (3)
Describe the effect on compliance, V/Q, and shunting |
1. impairs alveolar
ventilation, 2. excludes oxygen, 3. inactivates surfactant; this, in turn, decreases lung compliance, increases dispersion of ventilation and perfusion, and produces INTRApulmonary shunt. |
|
how can an intrapulmonary shunt be found
|
when hypoxemia does not
improve despite oxygen administration hypoxemia in ARDS does respond to positive end-expiratory pressure, |
|
what are the most common causes of ARDS
|
1. sever infection( sepsis, pneumonia)
aspiration, trauma, pancreatitis, several blood transfusions, smoke or toxic gas inhalation, and certain types of drug toxicity |
|
Define acute lung injury (ALI) and ARDS by ratios of pulmonary gas exchange.
|
ALI- A PaO2-FiO2 of 300 or less. (ALI- hypoxemia + pulmonary infiltrates WITHOUT elevated left atrial pressures) decreased lung compliance
ARDS- PaO2-FiO2 of 200 or less regardless of the amount to fPEEP needed to support oxygenstion |
|
Describe 3 aspects of pathophysiology in ARDS, regardless of cause: cell types damaged, histopathologic features in acute phase, and effect on PaO.
|
Acute exudative phase
1. damage involves both the endothelial and epithelial surface and disrupts the lung's barrier function--> flooding alveolar spaces with fluid--> inactivating surfactant--> inflammation--> severe gas Xchange abnormalities and loss of lung compliance =bilateral infiltrates findings- 1. diffuse alveolar damage, including capillary injury, and areas of exposed alveolar epithelial basement membrane 2. alveolar spaces are lined with hyaline membranes and are filled with protein-rich edema fluid and inflammatory cells. The interstitial spaces, alveolar ducts, small vessels,and capillaries also contain macrophages, neutrophils, and RBCs Decrease in PaO2 as there is an increase in lung water and pulmonary artery pressure |
|
Identify 4 cell types that are activated and 3 biochemical sequthe development of edema and hyaline membranes in ARDS.
|
1.a. endothelial activation, and adhesion molecule expression
b. fibroblast activation c. neutrophil activation and migration d. alveolar macrophage activation 2. a. activation of coagulation, b. inhibition of fibrinolysis c. inactivation of surfactant d. hyaline membrane deposit |
|
Describe pathophysiologic sequelae when the acute (exudative) phase of ARDS
progresses to the fibrosis (proliferative) phase. |
progress to a fibrosis with persistent hypoxemia, increased dead space pulmonary hypertension, and further loss of lung compliance.
CT may show often shows diffuse interstitial thickening and blebs or honeycombing. Pathologic examination of the lung shows fibrosis with collagen deposition, acute and chronic inflammation, and incomplete resolution of edema |
|
Explain how the immune response to sepsis produces inflammation in ARDS.
|
Activation of innate responses generates the inflammatory mediators of ARDS.
1. Innate immunity provides the first-line host defense against pathogens-identifies certain patterns of cell activation; so only needs, a few patterns to recognize a lot of different microbes and endogenous ligands (such as fibronectin and hyaluronic acid) Such as:highly conserved lipid A portion of lipopolysaccharide, or direct CD14-recognizing and -binding lipopolysaccharide or toll-like receptor 4 (TLR4) which recognize about 10 patterns and then activates proinflammatory transcription factors (NFkB) or MHCII on macrophages |
|
Describe how changes in the VA/Q ratio contribute to hypoxemia and shunt.
|
areas of high VA/Q ratio cause inefficient ventilation (VA/Q � is infinity is dead space
and areas of low VA/Q ratio cause hypoxemia (VA/Q �0 is is 0 is a shunt) because of perfusion of poorly or nonventilated alveoli In ARDS, gas exchange is affected by increases in the dispersion of both alveolar ventilation and cardiac output because bronchial and vascular functions are altered by disease-related factors, such as the effects of inflammatory mediators on airway and vascular smooth-muscle tone. Beause CO2 exchange is determined by alveolar ventilation reas of high VA/Q ratio and dead space in ARDS increase the ventilation required to keep the arterial PCO2 level constant. As lung compliance decreases, the work to expand the lungs to maintain the arterial PCO2 level must alsothe lungs to maintain the arterial PCO2 level must also increase. Hypoxemia produced by alveolar edema is most important to gas exchange in the acute phase. Pulmonary edema causes hypoxemia by creating areas of low VA/Q ratio and shunt; the latter cannot be overcome by oxygen administration because of the absence of alveolar ventilation |
|
Identify two physiologic parameters that regulate fluid exchange between capillaries and interstitial spaces and 3 aspects of “safety factor” that prevent pulmonary edema.
|
Capillary fluid filtration is determined by the hydrostatic and osmotic pressure gradients across the capillary wall, as described by the Starling equation: simplified net (hydrostatic) filtration pressure- net osmotic (oncotic) pressure
Safety Factor- change in absorption forces caused by increased filtration pressure, capacity of the interstitial space to absorb fluid, and capacity of the lung’s lymphatic system to transport fluid out of the lung. These mechanisms maintain dry alveoli even when microvascular capllary pressure is moderately elevated, such as during exercise, hypoxia, or with compensated mitral stenosis. Normal is 21 mm Hg for the healthy lung |
|
Explain how “safety factor” is compromised to make protein-rich edema in alveoli.
|
As capillary pressure increases, the edema factor is introduced
First, filtration pressure increases and diluted fluid from the capillaries enters the interstitial space. The dilution decreases interstitial osmotic pressure, which increases the absorption force opposing the hydrostatic pressure. Second, as the interstitial pressure increases, interstitial fluid enters the perivascular space where lymphatic channels arise. The perivascular space swells, causing perivascular cuffing and interstitial edema without affecting gas exchange. The third component of the safety factor is the actual removal of interstitial fluid by the lymphatic system, which has at least an order of magnitude of reserve flow capacity The interstitial fluid pressure exceeds the safety factor when interstitial volume increases by about 40%, and alveolar flooding will begin. The barrier collapses suddenly and plasma proteins of all sizes pass through. Protein rich edema impairs gas exchange by excluding oxygen and inactivating surfactant, |
|
Describe the pathophysiologic consequences of alveolar flooding in ARDS.
|
Protein rich edema impairs gas exchange by excluding oxygen and inactivating surfactant
In ARDS, permeability edema occurs because capillary conductance increases( this regulates the lymphatic flow) and the reflection coefficient decreases (the interstitial osmotic pressure becomes higher around leaky capillaries. This shifts the pressure–fluid curve of the lung to the left because the net absorption force in the Starling equation is minimized by capillary leakiness. ARDS, the edema safety the edema safety factor decreases by about half, and flooding develops at lower capillary pressures. Pulmonary edema may actually contribute to the pathogenesis of ARDS |
|
Explain the roles of endothelial activation and epithelial damage in ARDS, and the mechanisms involved in epithelial repair.
|
that pulmonary endothelial cells are activated in ARDS because pulmonary vascular endothelial integrity is often preserved microscopically even at sites of leukocyte accumulation
Endothelial activation-new protein was synthesized in response to endothelial cell activation. endothelial cell activation participates and partly drives the neutrophil inflammatory response that contributes to edema formation and fibrosis- also expression of adhesion and signaling molecules, which facilitate leukocyte adherence, coagulation is activated, tissue factor is produced, and fibrinolysis is inhibited; the resulting procoagulant environment and therefore pro-inflammatory After an acute lung injury, the alveolar epithelium seems to resist more injury than the adjacent endothelium. Repair requires II alveolar epithelial cells, which are progenitors of the type I and type II. Type II cells are more robust than type I cells, Optimal repair requires an intact basement membrane and provisional fibrin matrix to provide a platform for cell adhesion, spreading, and migration. |
|
Describe two physiologic benefits and two potential risks of using PEEP.
|
Positive end-expiratory pressure improves oxygenation in ARDS by stabilizing damaged alveoli and improving areas of low VA/Q ratio and shunt . PEEP may also prevent further injury from repeatedly opening and closing alveoli. However, risks include oxygen toxicity, lung overdistention, and destructive cycles of alveolar opening and closure. increasing in lung water, lung stretch
|
|
Identify two goals of using lung-protective mechanical ventilation to treat ARDS.
|
, ventilation with lower tidal volumes and lower peak airway pressures (
|
|
Identify two major mechanisms that serve to classify causes of pulmonary edema.
|
1. HEMODYNAMIC EDEMA
2. EDEMA DUE TO MICROVASCULAR INJURY (ALVEOLAR INJURY) |
|
Name 3 causes of increased hydrostatic pressure, 3 disorders causing
hypoalbuminemia, and 7 causes of microvascular injury. |
Increased hydrostatic pressure (increased pulmonary venous pressure)
1. Left-sided heart failure 2.Volume overload 3. Pulmonary vein obstruction decreased oncotic pressure 1. Hypoalbuminemia 2. Nephrotic syndrome 3. Liver disease 4. Protein-losing enteropathies EDEMA DUE TO MICROVASCULAR INJURY (ALVEOLAR INJURY) Infections: pneumonia, septicemia, Inhaled gases: oxygen, smoke, Liquid aspiration: gastric contents, near-drowning, Drugs and chemicals: chemotherapeutic agents (bleomycin), other medications (amphotericin B), heroin, kerosene, paraquat Shock, trauma, Radiation Transfusion |
|
Compare histologic features of exudative vs. proliferative vs. fibrotic stages of
diffuse alveolar damage |
In the acute stage, the lungs are heavy, firm, red, and boggy, havecongestion, interstitial and intra-alveolar edema, inflammation, fibrin deposition, and diffuse alveolar damage. alveolar walls become lined with waxy hyaline membranes like hyaline membrane disease of neonates. Alveolar hyaline membranes consist of fibrin-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells. In the organizing stage, type II pneumocytes undergo proliferation, and there is a granulation tissue response in the alveolar walls and in the alveolar spaces. In most cases the granulation tissue resolves, leaving minimal functional impairment. Sometimes, however, fibrotic thickening of the alveolar septa ensues, caused by proliferation of interstitial cells and deposition of collagen. Fatal cases have superimposed bronchopneumonia.
|
|
Describe how nuclear factor-κβ, IL-8, neutrophils, and dysregulated coagulation
|
Although the cellular and molecular basis of acute lung injury and ARDS remains an area of active investigation, it appears that in ARDS, lung injury is caused by an imbalance of pro-inflammatory and anti-inflammatory mediators.[4] The most proximate signals leading to uncontrolled activation of the acute inflammatory response are not yet understood. However, nuclear factor κB (NF-κB), a transcription factor whose activation itself is tightly regulated under normal conditions, has emerged as a likely candidate shifting the balance in favor of a pro-inflammatory state. As early as 30 minutes after an acute insult, there is increased synthesis of interleukin-8 (IL-8), a potent neutrophil chemotactic and activating agent, by pulmonary macrophages. Release of this and similar compounds, such as IL-1 and tumor necrosis factor (TNF), leads to endothelial activation, and pulmonary microvascular sequestration and activation of neutrophils. Neutrophils are thought to have an important role in the pathogenesis of ARDS
|
|
. Identify two conditions responsible for most deaths in patients with ALI/ARDS.
|
The majority of deaths are attributable to sepsis or multi-organ failure and, in some cases, direct lung injury.[6]
|
|
Describe how three cell types contribute to resolution of diffuse alveolar damage.
|
Pro-inflammatory cytokines such as interleukin 8 (IL-8), interleukin 1 (IL-1), and tumor necrosis factor (TNF) (released by macrophages), cause neutrophils to adhere to pulmonary capillaries and extravasate into the alveolar space, where they undergo activation. Activated neutrophils release leukotrienes, oxidants, proteases, and platelet-activating factor (PAF), which contribute to local tissue damage, accumulation of edema fluid in the airspaces, surfactant inactivation, and hyaline membrane formation. Macrophage migration inhibitory factor (MIF) released into the local milieu sustains the ongoing pro-inflammatory response. Subsequently, the release of macrophage-derived fibrogenic cytokines such as transforming growth factor β (TGF-β) and platelet-derived growth factor (PDGF) stimulate fibroblast growth and collagen deposition associated with the healing phase of injury
|
|
Compare definitions of diffuse alveolar damage/ALI vs. acute interstitial pneumonia
|
Acute interstitial pneumonia is a clinicopathologic term that is used to describe widespread ALI associated with a rapidly progressive clinical course that is of unknownetiology (sometimes referred to as idiopathic ALI-DAD
|
|
Identify two permanent pathophysiologic sequelae of DAD in the fibrotic stage.
|
death or chronic interstitial disease may develop
|
|
Markus: Vascular Disorder
Define pulmonary HTN |
Sustained mean pulmonary artery pressure exceeds 25 mmHg at rest or 30 mmHg with exercise
|
|
what is the normal pulmonary pressure
|
15mm Hg
|
|
why can Sickle cell anemia be a trigger for elevated pulmonary arterial pressure
|
free hemoglobin scavenges nitric oxide, endothelin rises, and vessels constrict
|
|
define Cor pulmonale
|
right heart failure due to pulmonary HTN
|
|
what are the early vs late effects of pulmonary HTN
|
Transient or early hypoxemia or volume overload causes transient pulmonary hypertension; in hypoxemia through reflexive vasoconstriction. This process is reversible.
After repetitive triggers however, there is intimal and medial wall thickening and eventually fibrosis with a permanent elevation in pulmonary pressures. |
|
name 5 findings on physical exam of a pt with pulmonary HTN
|
Increased intensity of the pulmonic component of the second heart sound
Diastolic murmur of pulmonary regurgitation Left parasternal lift Jugular venous distension Hepatomegaly, ascites, peripheral edema |
|
Idiopathic (sporadic) PH carries a poor prognosis, what medications should patients be put on for life
|
All should receive lifelong anticoagulation due to high incidence of pulmonary thrombosis and thromboembolism due to stasis of blood and sedentary lifestyle
|
|
List 3 FDA approved treatments for idiopahtic PH
|
Calcium channel blockers,
prostacyclin analogues, endothelin-receptor antagonists |
|
list the risk factors for developing a Pulmonary embolism
|
Immobilization
CHF Surgery within last three months History of previous thromboembolism Malignancy Pregnancy Lifestyle factors- smoking Medications (estrogen, progesterone, raloxifene) Hypercoagulable state (ProteinC, S, or antithrombin II deficiency, Lupus) |
|
what are the classic presentations of pt with a major Saddle embolus?
|
With inability to empty the RV, there is decreased cardiac output and systemic hypotension.
classic impending dome |
|
what is the classic finding on an EKG of a pt with pulmonary embolism
|
This is the typical right heart strain pattern – S1, Q3, T3.
|
|
what would the blood gases be of this pt
|
With embolism there may be reduced arterial pO2 and usually reduced pCO2 as well.
|
|
what is the D-dimer level in this pt
|
D-dimer- degredation product of cross-linked fibrin. Indicates fresh clot. If high, somewhat non-specific (especially post-op). If LOW, pulmonary embolus or DVT very UNLIKELY
|
|
how can this CXR help you differentiate between PE and Infacrction
|
Embolism
Normal Decreased vascular markings Elevated hemi-diaphragm Infarction Wedge-shaped densities Pleural based density “Hampton’s hump” Pleural effusion |
|
describe the presentation of a pt with Alveolar Hemorrhage
|
Pink frothy sputum
Blood-tinged sputum Frank hemoptysis Common causes include CHF and acute bronchitis or pneumonia |
|
list 3 causes of alveolar hemorhage
|
Systemic vasculitis – Wegener’s
Collagen vascular disease - SLE Goodpastures’s |
|
Cystic Fibrosis lecture
t/f CF is AD |
false- AR
|
|
describe the CF gene defect
|
The gene affected in CF encodes for the protein cystic fibrosis transmembrane conductance regulator (CFTR). CFTR facilitates the chloride transport of electrolytes across cell membranes in the epithelial lining of the ducts of exocrine glands, including sweat and mucus-producing glands. long (q) arm of chromosome 7. The most common mutation in caucasians (approx. 70%) is a deletion of phenylalanine at base pair 508 on the CFTR gene.
|
|
Describe a Class I - Defective protein production of CFTR
|
Class I - Defective protein production — This defect is usually caused by nonsense, frameshift, or splice-site mutations, leading to premature termination of the mRNA and complete absence of CFTR protein.
|
|
Describe a Class II - Defective protein processing of CFTR
|
Class II - Defective protein processing — With class II defects, the mutations in the CFTR sequence prevent the protein from trafficking to the correct cellular location. The most common CFTR mutation, delta F508 (deletion of a single phenylalanine residue in the first NBF), belongs to this category.
|
|
describe a Class III - Defective regulation in CFTR
|
Class III - Defective regulation — These mutations lead to diminished channel activity in response to ATP. Many involve alterations of the NBF regions, NBO1 and NBO2, which may retain varying degrees of sensitivity to nucleotide binding.
|
|
how does a dysfunctional CFTR protein increase the risk of infections in pt with CF
|
defective cellular transport of chloride and sodium across epithelial cell membranes. Sweat becomes abnormally salty and mucus in the respiratory tract, GI tract, or reproductive tract is abnormally viscous. Mutant CFTR aggravates the development of pulmonary infection by promoting initial bacterial adhesion by upregulating epithelial cell adhesion molecules for bacteria and by decreasing the production of innate host defense molecules, such as nitric oxide.
|
|
what types of infections are pt with CF more likely to have
|
H. influenza
Staph aureus MRSA Pseudomonas aeruginosa Burkholderia cepaciae Aspergillus fumigatus |
|
what is the pathogenesis of this CF pts symtoms
|
brochioectasis- Bronchial mucous plugging causes partial and complete blockages of airways. The lung develops areas of atalectasis and other areas of air trapping. Blockages also facilitate inflammation. Pathogens (bacteria and fungi) may become trapped and colonize the airways. Smoldering infection aggravates inflammation. Eventually, bronchi become bronchiectatic: they become dilated and lose adequate cartilaginous supports. Bronchiectasis further impairs mucous clearance from the respiratory tract
|
|
what are the 3 physicial signs associated with this CF pts condition
|
Bronchiectasis is associated with productive cough, clubbing, and the development of “barrel chest”.
|
|
what would be an indication that a newborn has CF
|
Meconium ileus occurs when the meconium is abnormally thick and obstructs the GI tract.
|
|
what is meconium
|
Meconium is the 1st bowel movement that a newborn passes. It consists of bile salts, bile acids and debris shed from the intestinal epithelial lining during embryonic life.
|
|
describe the systemic effects and complications of CF
|
Unlike endocrine glands (which release secretions into the bloodstream), exocrine glands release secretions through ducts. The highest concentrations of CFTR are in the submucosal exocrine glands in the airways, pancreas, salivary glands, sweat glands, intestines, and reproductive tract
|
|
in newborn screening, what test is done to look for CF
|
Immunoreactive trypsinogen (IRT) from heel blood spot
Elevated IRT leads to 2nd tier of testing Positive screen (IRT and 2nd tier) then sweat test |
|
describe the pancreatic problems in pt with CF
|
thick secretions produced within the pancreas partially or completely block the ducts leading to the small bowel. Duct obstruction prevents pancreatic enzymes from entering the intestine. The result is incomplete digestions of fats and proteins as well as poor absorption of fat soluble nutrients (vitamins).
|
|
what conditions are associated with pancreatic insufficiency in pts with CF
|
Failure to thrive
Steatorrhea Weight loss fat soluable vitamin deficiency Abdominal pain Bloating, distension, excessive flatus Meconium ileus Distal intestinal obstruction syndrome Rectal prolapse |
|
describe the unique lesions of the liver in pt with CF
|
Focal biliary cirrhosis is characterized by concretions of eosinophilic material plugging the bile ductules, biliary proliferation, inflammatory reaction, and absence of marked bile stasis in the surrounding liver parenchyma.
|
|
what is The most common long term antibiotic therapy for pt with CF
|
The most common long term antibiotic therapy are inhaled antibiotics (tobramycin is most common, though others are near the market, such as aztreonam)
|
|
which The mucus thinning agents are used in pts with CF
|
The mucus thinning agents used are DNAse (Pulmozyme) and inhaled 7% saline (which hydrates CF mucus and promotes cough).
|
|
what immunizations are given to pt with CF
|
Immunizations mean influenza and pneumoccocus, predominately. Palimizumab (a passive immunization against RSV virus) is often provided to CF infants.
|
|
Which drugs are used for the common bacterial infections in pt with CF
|
|
|
what are the signs and symptoms of respiratory distress in newborns
|
tachypnea, grunting, flaring, retractions, hypoxemia, cyanosis
|
|
what is the difference between newborn respiratory distress and respiratory distress syndrome
|
Respiratory Distress Syndrome in Newborns
Term generally reserved for respiratory distress associated with prematurity, and surfactant deficiency or surfactant abnormalities. |
|
how does a newborn present with respiratory distress syndrome
|
Acute illness characterized by increased RR, grunting, retractions, dyspnea that develop in the first hours after birth.
|
|
what are the risk factors for hyaline membrane disease
|
IRDS-
Pre-term labor Premature rupture of amniotic membrane Placental insufficiency Chorioamnionitis Cesearan section delivery Infant of diabetic mother |
|
what is the treatment of an newborn with IRDS
|
Exogenous surfactant
Antenatal corticosteroid administration Supplemental Oxygen Mechanical ventilation CPAP, Positive pressure controlled ventilation Diuretics |
|
what is Bronchopulmonary Dysplasia
|
A chronic lung disease of infancy associated mostly with prematurity.
BPD appears to be the final common pathway of lung injury. Premature lungs + O2 toxicity + ventilator baro-trauma + inflammatory response leads to BPD. |
|
Describe the pathology of this infant that died of Bronchopulmonary Dysplasia
|
BPD is disruption of lung development. Decreased septation and alveolar hypoplasia lead to fewer and larger alveoli. Reduced microvascular development also may occur.
|
|
describe the pathophysiology that leads to bronchopulomonary dysplasia
|
BPD is associated with increased airway resistance, decreased lung compliance, increased airway reactivity, and increased airway obstruction.
injury to the pulmonary circulation can lead to pulmonary hypertension and cor pulmonale, which substantially contribute to the morbidity and mortality associated with severe BPD. |
|
what is the treatment for BPD
|
Support good growth
Support ventilation and oxygenation Bronchodilators Diuretics Systemic corticosteroid |
|
describe the FRC in a pt with IRDS or BPD
|
.His functional residual capacity (FRC) is low at 56% predicted (which is expected in RDS and advanced BPD).
|
|
an infant with brochopulmonary dysplasia will have a curve that looks more like (emphysema or fibrosis) Why
|
the fibrotic lung is stiff with low compliance and the emphysematous lung is more complaint.
In emphysema, lung compliance decreases with increasing volume. Therefore as the lung increases in size, more pressure must be applied to get the same increase in volume. |
|
Describe the Lung interstitium
|
encompasses the space between alveolar epithelium and capillary endothelium. It includes the blood vessels, connective tissues surrounding the blood vessels, lymphatics and terminal airways.
|
|
list 7 Systemic Rheumatoid Disorders associated with interstitial lung disease
|
RA, SLE, scleroderma, ankylosing spondylitis, mixed connective tissue disease, polymyositis/dermatomyositis, Sjogrens
|
|
list 6 environment-occupations associated ILD
|
Organic-Hypersensitivity pneumonitis, Famer's lung
Inorganic- Silicosis, Asbestosis, Beryliosis, Coal Worker's pneumonicosis |
|
which alveolar filling disorder is associated with ILD
|
Goodpasture's
|
|
IDL is associated with which two vasculitis disorders
|
Wegner's and Churg-Strauss
|
|
ILD is associated with which 5 inherited disorders
|
Familial idopathic pulmonary fibrosis, Neimann-Pick, Gaucher, Neurofibromatosis, Tuberous Sclerosis
|
|
DDx
Tachypnea, Crackles at both lung bases, Signs of right sided heart failure , Hilar or mediastinal adenopathy |
Sarcoidosis
Silicosis (egg shell calcification) Lymphocytic interstitial pneumonia Amyloidosis Gaucher’s disease |
|
DDx:
Tachypnea, Crackles at both lung bases, Signs of right sided heart failure , Upper lobe involvement |
Ankylosing spondylitis
Berylliosis Histiocytosis X Silicosis Chronic hypersensitivity pneumonitis |
|
In addition to Tachypnea, Crackles at both lung bases, Signs of right sided heart failure . What is highly suggested sign of Idiopathic Pulmonary Fibrosis(Cryptogenic Fibrosing Alveolitis)
|
clubbing
Dyspnea insidious in onset, at least for 2-3 years |
|
what is Caplans’s Syndrome
|
Described in coal workers with rheumatoid arthritis.
Presence of rounded densities in these patients which undergo cavitation. |
|
why would ACE levels be elevated in a pt with Sarcoidosis? In what other conditions is ACE elevated?
|
ACE-converts angiotensin I to angiotensin II, usually produced by capillary endothelial cells, also produced by alveolar macrophages.
elevated in 60% of patients with active dis. Also elevated in cases of silicosis, asbestos exposure, Gauchers dis, leprosy, coccidiodomycosis, miliary TB, IBD |
|
In a pt with Silicosis, describe the pt population and CXR,
|
Silicosis-Inhalation of free crystalline silica dust
Foundry worker, sandblaster, tunneling, pottery making Cxray with upper lobe nodules with egg shell calcifications of hilar nodes. |
|
t/f pt with silicosis are at high risk for Tb
|
true- Patients at high risk for typical as well as atypical Mycobacterial infections
|
|
what occupations expose a person to asbestos
|
Shipyard workers, pipefitters, welders, sheet metal workers, workers involved in automotive repair esp. brake lining work.
|
|
Coal Worker Pneumoconiosis is associated with inhalation of coal, where are the nodules usually located on CXR
|
Simple CWP: nodules which are less then 1 cm in size with predilection for upper lobes.
Complicated CWP: presence of density of more then 1cm in size |
|
what is the most common fungi affecting people with Hypersensitivity Pneumonitis?
what is hypersensitivity pneumonitis |
Actinomycetes
Secondary to inhalation of organic dust derived from animal dander and proteins or saprophytic fungi contaminating water reservoir, dairy products, wood bark and animal droppings. |
|
why is Chronic eosinophilic pneumonias confused with Tb? what is the treatment
|
Usually presents with chronic sxs of cough, night sweats and wt. Loss
Cxray shows infiltrates in lung periphery Blood eosinophilia is absent Treatment is steroids |
|
in general, what is the Ddx for an ear infection, and treatment
|
ear- viral, strep pneumo, antihistamines and decongestants
|
|
in general, what is the Ddx for an nose infection, and treatment
|
nose-bacterial- H. flu, antibiotics
|
|
in general, what is the Ddx for an throat infection, and treatment
|
throat-allergic- M. catarrhalis, steroids, nasal spray
|
|
how will this pt present?
which pathogens are associatd and what drugs are used? |
with itching or pain in the ear canal, Sometimes discharge
Usually painful to touch the ear lobe or lie on that ear at night Topical drops directed at usual pathogens: Strep, Staph, fungus, Pseudomonas Possibly use wick |
|
how will this pt present?
which pathogens are associatd and what drugs are used? |
Swimmers ear- with itching or pain in the ear canal, Sometimes discharge
Usually painful to touch the ear lobe or lie on that ear at night Topical drops directed at usual pathogens: Strep, Staph, fungus, Pseudomonas Possibly use wick |
|
what 3 signs or symptoms must the pt have?
what are the usual pathogens? what are the usual treatments? |
acute otitis media- Acute 1.onset of signs and symptoms
2.Presence of middle ear effusion: bulging, decreased movement of TM, air/fluid levels 3.Middle ear inflammation: redness of TM or otalgia Strep. Pneumoniae, Hemophilus Influenza, and Moraxella Catarrhalis and pain control. Usual treatment is with antibiotics for 10 days. |
|
what symptoms are associated with this condition?
|
AOM-Fever, ear pain (is not worsened by moving the earlobe), decreased hearing, vertigo
Current or recent setting of “a cold” In babies, sometimes pulling at ears or irritability: won’t drink or lie down |
|
what is the drug of choice for this condition? what is an option for those that don't respond to the typical treatment early on?
|
Amoxicillin at a dose of 80-90 mg/kg given twice a day is the drug of choice followed by
Augmentin for early non-responders(Amoxicillin/clavulanate ) |
|
this Characteristic bluish tint to the inferior turbinate is classic in which condition?
What is the treatment |
allergic rhinitis
The mainstays of treatment are anti-histamines [Antihistamines: Loratadine (Claritin) Cetirizine (Zyrtec) ] and nasal steroid sprays-Flonase, Nasacort |
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The common cold, viral rhinitis, is associated with which 3 symptoms and what medication are prescribed?
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Abrupt onset with fever, chills or body aches
Gets better in 7-14 days w/o treatment Can suggest- Decongestants and fever relievers.The best decongestant is pseudoephedrine HCL (Sudafed) |
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what are the signs and symptmos of sinusitis?
which organisms are usually at fault. how is this different from viral rhinitis? name 4 finding on physical exam what is the treatment |
1. Headache: facial, frontal, or between eyes , Congestion
Sometimes fever, 2. S. pneumoniae, H. flu, M. catarrhalis 3. No rhinorrhea 4. red turbinates with pus emanating, May see PND in throat, Swelling/Tenderness to palpation of sinuses Transillumination:opacification 5.Antibiotics: Amoxicillin, TMP/SMX for 7-14 days, Recurrent sinusitis: consider anaerobes Clindamycin |
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what is the treatment
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Topical anti-fungal: nystatin “Swish and Swallow”, Mycostatin troches, Diflucan pills
Rinse mouth after inhaled steroid MDI use |
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what is the treatment
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Fever Blisters”
Treat with acyclovir, famciclovir, valacyclovir pills |
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t/f Pharyngitis (Sore Throat)Etiology is usually bacterial
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false- usually viral
Rhinoviruses, Adenoviruses, Influenza A+B, Respiratory Syncytial Virus (RSV), Parainfluenza Also seen with Epstein-Barr, CMV, Measles |
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Streptococcal Pharyngitis
how will this patient present what is the treatment |
Prominent dysphagia, fever, “Hot potato” voice, huge Tonsils & exudate,Petechiae on palate, no cough or No cough/rhinorrhea, HA or stomach ache
Penicillin is drug of choice Erythromycin for PCN allergic pts |
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croup-
list the 3 classic findings what is treatment |
Laryngotracheitis is the inflammation of the larynx and trachea.
classic triad of inspiratory stridor, a harsh barking cough, and hoarseness Since it is a viral illness, if there is no respiratory distress, simply waiting it out is enough treatment or cool mist vaporizers , Severe cases may need evaluation for respiratory distress and treatment for wheezing and edema of airway, Oral steroids |
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Epiglottis
what are the physical exam findings? which pathogens are usually associated? what is treatment |
Anxious appearance, Prominent drooling, Child prefers sitting up, leaning forward, chin hyper-extended
Inspiratory stridor, retractions, fatigue and cyanosis are late findings Caused by H. flu or strep Treat with IV cephalosporins Treat household and daycare contacts with oral Rifampin |
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t/f Humans and animals are the only known reservoir for tuberculosis
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false -only humans
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how is Tb transmitter
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Transmission - airborne droplet nuclei
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what are the symptoms of Tb
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Productive cough
Fever and night sweats Weight loss Hemoptysis (late symptom) Chest pain Anorexia Fatigue |
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t/f lower lobe involvement is most common in Tb
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false- Upper lobe involvement is most common
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what is Miliary TB
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numerous small nodular lesions (resembling millet seeds)
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Decribe the what a Ghon complex is and how it is formed as shown on CXR
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The Ghon's complex is a combination of the Ghon's focus (arrow, area of initial infection in the lung) and a lymphatic lesion. Approximately two to three weeks after the Ghon's focus has developed, the area undergoes necrosis. Free bacilli, or bacilli within macrophages, drain from the area into the affected lungs' lymph nodes. Typically these areas heal with calcification visible on chest X-ray.
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Describe the organism in the picture, the stain used and if what are the tuberculin skin test 5mm diameter cut offs,
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Positive Acid-Fast B smear, numerous red organisms present.
1.Close contacts to persons with newly diagnosed tuberculosis 2) HIV positive 3) Organ transplant 4) Corticosteroids (>15 mg per day prednisone or equivalent for > 1 month) 5) Patients with fibrotic lesions on chest x-ray (not granulomas) |
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what are the 10mm cut offs for this disease
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Recent converter - at least 10 mm increase in skin test in past 2 years
-Weight loss > 10% of ideal body weight -Children < 4 years old -Residents and employees from health care, homeless, or long-term care facilities -Recent immigrant (past 5 years) from a high-prevalence country |
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what are the 10mm cut offs for this disease
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Recent converter - at least 10 mm increase in skin test in past 2 years
-Weight loss > 10% of ideal body weight -Children < 4 years old -Residents and employees from health care, homeless, or long-term care facilities -Recent immigrant (past 5 years) from a high-prevalence country |
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what is the TST cut off for 15mm
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No risk factors for TB
Not always treated Usually seen in an individual being hired to a position in high risk setting |
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what are the complications that could be associated with Tb. What is noted on this pt
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Aspergilloma: “crescent sign” on this CXR
Hemoptysis Broncholithiasis Fibrothorax Carcinoma (controversial) |
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if a pregnant pt present with this stain. Which of the first line drugs will not be used and why
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streptomycin, bc aminoglycosides are teratogenic
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which drugs are used for a Mycobacterium avium Complex and for how long
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Primary drugs
Rifabutin Azithromycin Quinolones Ethambutol Streptomycin Therapy requires 3 or more drugs for 12-18 months |
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what is this organism and what is its route of dissemination once inside the body
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Histoplasmosis
Hematogenous dissemination occurs occurs in Ohio River valley |
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name the organism and what will CXR show. Describe physical exam
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Chest x-ray: hilar/mediastinal lymph nodes, patchy infiltrates
Rheumatologic manifestations Erythema nodosum-tender, red nodules under the skin most common on the shins |
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name the organism inside this cell and how is the diagnosis made
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histoplasmosis inside macrophage
Antigen Tests Urine positive in 90 % of patients with disseminated disease Sensitivity lower in serum than urine, the highest yield achieved by testing both |
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what is the treatment for this organism
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histoplasmosis- Antifungal choices
Amphotericin B Itraconazole Corticosteroids Acute infection with severe hypoxia Granulomatous mediastinitis |
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in what areas is this organism located
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histoplasmosis in ohio river valley
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what kind of conditions can this organism cause if left untreated
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, chronic skin ulcer due to Blastomycosis
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where is this organism found
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Blastomyces dermatitidis, a dimorphic fungus.
Blastomyces is endemic to the Mississippi and Ohio river valleys and the vicinity of the Great Lakes. |
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what is this organism and in what area is it located
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Coccidioidomycosis-also known as "California disease, "Desert rheumatism,"San Joaquin valley fever," and "Valley fever"
Arizona, California, Nevada, New Mexico, Texas, Utah and northwestern Mexico.[3] |
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in what pt population is this more likely.
what symptoms will the pt experience how will this look on CXR what it the treatment |
Pre-existing pulmonary cavities (COPD, prior TB)
Minimally invasive Hemoptysis: invasion of blood vessels Asymptomatic crescent-nodule on chest x-ray CT: rim of air around mass Tx: resection, itraconazole |
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t/f humans are the only reservoir
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true- bordetella pertussis- whooping cough
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describe the Catarrhal phase of bordetella pertussis
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. Rhinorrhea, lacrimation, low-grade fever, sneezing, and mild cough are characteristic. Patients can develop a leukocytosis > 50,000 cells/mm3, with a relative lymphocytosis.
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describe the Paroxysmal phase of bordetella pertussis
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Lasts 1-6 weeks
Paroxyms of coughing (up to 30/day) Coughing followed by “whoop” or gasp Post-tussive emesis Cough may be productive |
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describe the Convalescent phase of bordetella pertussis
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Lasts 2-3 weeks
Paroxysms are less common Coughing decreases |
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what is the gold standard for testing for this organisms
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Culture from nasopharynx is the gold standard for pertussis
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what is the drug of choice and duration for this organism
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. Erythromycin is the antibiotic of choice, standard treatment course is 14 days. for bordetella pertussis
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Markus- Pneumonia
"Pneumonia" is a term used to indicate inflammation of the which part of the lung: |
e inflammation of the distal lung:
1. terminal airways, 2. alveolar sacs and 3. interstitium. |
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list the 4 routes that Infectious agents gain entry to the lower respiratory tract through
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1. microaspiration of oropharyngeal secretions: pneumococcus, anaerobes
2. inhalation of airborne material: TB, Legionella, viral 3. metastatic seeding of the lung from blood: S. aureus 4. direct extension: amoebic liver abscess |
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describe the Pathophysiology of Pneumonia
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The invading organism causes symptoms, in part, by provoking an inflammatory
response in the lungs The capillaries become leaky, and protein-rich fluid seeps into the alveoli. This results in a less functional area for oxygen-carbon dioxide exchange. |
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describe the result of Mucus plugs decrease the efficiency of gas exchange in the lung during pneumonia
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The alveoli fill further with fluid and debris from the large number of white blood
cells being produced to fight the infection. The patient becomes relatively oxygen deprived, while retaining carbon dioxide. The patient breathes faster and faster, in an effort to bring in more oxygen and blow off more carbon dioxide. |
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describe Consolidation in pneumonia
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Consolidation, a feature of bacterial pneumonias, occurs when the alveoli, become
solid, due to quantities of fluid and debris. Red (early) hepatization Grey (late) hepatization |
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what is the most important causes of death in patients with acute pneumococcal pneumonia
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Respiratory Failure
but pneumonia also causes: Ventilatory failure Hypoxemic respiratory failure |
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what causes the Ventilatory Failure in pneumonia
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Caused by mechanical changes in the lungs resulting from pneumonia.Inflammatory exudate fills alveoli at slightly less than their normal functional residual
capacity (FRC) Resulting volume loss at FRC roughly proportional to the extent of the pulmonary infiltrate. Consolidated air space does not inflate easily at higher transpulmonary pressures so there is a Loss of volume: 1. reduces total lung compliance 2. increases the work of breathing. |
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what causes the Hypoxemic Respiratory Failure in pneumonia. what is the effect of the result of hypoxemic respiratory failure
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Arterial Hypoxemia early in acute pneumococcal pneumonia due to:
Persistence of pulmonary artery blood flow to consolidated lung Resulting in an intrapulmonary shunt |
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t/f the Nasopharynx defense against pathogens includes:
Nasal hair, turbinates, IgG secretion, and Mucociliary apparatus |
false- IgA and
Nasal hair, turbinates, Mucociliary apparatus |
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is a CXR necessary for diagnosis of pneumonia?
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yes-CXR: ESSENTIAL for diagnosis
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when should a pt be considered to have Community Acquired Pneumonia (CAP)
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CAP should be considered when a patient presents with 2 or more of the following
symptoms: fever; chills; new-onset cough; change in sputum color or increase in the volume if there is a chronic cough; chest discomfort; or dyspnea. |
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in which areas can pneumonia be caused by Hanta virus
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Hanta virus pneumonia occurs at higher rates in the “four corner area” in the US (CO, UT, NM, NE)
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t/f serum cultures are the most specific diagnostic test for the causative agent
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false- Blood cultures are the most specific diagnostic test for the causative agent
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Name the organism involved in this pneumonia:
Alcoholics Lobar CXR “currant Jelly” sputum PMNs -Encapsulated gnr |
Klebsiella
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Name the organism involved in this pneumonia
Often elderly Lobar CXR “rusty” colored sputum GP Diplococci “lancets” |
Streptococcus pneumonia
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Name the organism involved in this pneumonia
Younger Interstitial CXR Scant Pmn, No organisms on gram stain |
mycoplasma pneumonia
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Name the organism involved in this pneumonia
COPD Smoker Lobar CXR Purulent - (“safety pins”) bipolar staining |
H. influenza
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Name the organism involved in this pneumonia
Alcoholic, Mental Status decreases Multi- Lobar CXR (Lower) Foul sputum Mixed Organisms and Pmns |
Aspirate- of anaerobes
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Name the organism involved in this pneumonia
Prior Influenza Lobar CXR Cavitary Bloody sputum Gpc in Clusters Pmns |
staphylococcus pneumonia
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Definition:
represents an adaptation to the development of host antibodies. (antigenic drift or antigenic shift) |
antigenic drift
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Definition:
occurs as soon as a type A influenza virus with a completely novel hemagglutinin or neuraminidase formation moves into humans from other host species. |
antigenic shift
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what is the function of Hemagglutinin in influenza
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Hemagglutinin derives its name from its activity. The virus the ability to agglutinate, red blood cells. functions in the binding of the virus to cells, via the recognition of sialic acid.
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what is the function of Neuraminidase in influenza
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Neuraminidase ( acetyl-neuraminyl hydrolase). The enzyme removes residues called N-Acetyl-neuraminic acid from chains of sugars and from other glycoproteins.
allows the virus to both pass out of the human epithelial cells in which it is replicating, and enter new cells to initiate a new round of viral replication. |
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in diaganosing influenza, what is the gold standard
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Viral culture: “gold standard”
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Air Pollutants:
what are the 5 main air pollutants |
Carbon Monoxide (52 %)
Sulfur Dioxide (14 %) Nitrogen Oxides (14 %) Ozone (14 %) Particulate matter (4 %) |
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list 4 major sources of air pollutants
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1. Combustion of fossil fuels (motor vehicles)
2. Coal fired power plant emissions 3. Waste incinerators 4. Atmospheric reactions |
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what are the major indoor pollutants
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Tobacco smoke
Gas and wood stoves Furnaces Construction materials Furniture Radon Allergens |
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list 2 Reducing type of pollution
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SO2 and smoke from incomplete combustion of coal)
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list 3 oxidizing type pollution
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Oxidizing or photochemical type (nitrogen oxides, hydrocarbons, and ozone
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