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71 Cards in this Set
- Front
- Back
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Pleurisy
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inflammation of the plueral sac
dry cough, frictional rub, pain viral infect, pneu, TB, cancer |
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Pleural Effusion
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excess fluid
balance between hydro/oncotic |
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chylothorax
hemothorax pyothorax hydrothorax |
fatty lymph fluid
blood pus-cellular debris serous fluid |
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Dyspnea
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shortness of breath
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Transudates
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Heart failure, edema systemic factors Pale yellow & CLEAR- decreased protein content
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Exudates
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lung cancer, TB, Pneumonia
Local factors- pale yellow & cloudy; increased protein conten |
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Conducting zone
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first 16 branches
anatomic dead space warm, humidify, filter |
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Respiratory Zone
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branches 17-23
gas exchange region |
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SNS adrenergic
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B2 neurons, relaxation = epi, isoproterenol, albuterol
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PNS cholinergic
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muscarinic receptors
muscarine, carbachol constriction |
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Pores of Kohn
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in walls of adjacent alveoli, allows airflow between adjacent alveoli- collateral ventilation
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Type I cells
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squamous alveolar cells
wall/lining cells |
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Type II cells
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granular alveolar cells
sufactant producing |
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Sol Layer
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thin allows cilia to beat- CFTR channels- less fluid, cilia cant beat, increase infections
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Gel Layer
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sticky environment removes particles from airway- goblet cells- macromolecules, glycoproteins, electrolytes, h20
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Ciliary Dyskinesia
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recessive disorder- defect in gene encoding for dynein- bad cilia
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Vt (tidal volume)
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includes the gas in alveoli (gas Xchange) and dead space in ariway
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Cannot be measured by spirometry
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TLC, RV, FRC
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VC
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increases with gender, body size, conditioning.
decrease with age |
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FRC
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Measured by Helium dilution
Body plethysmograph |
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Obstructive Lung Disease
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increased RV/TLC ratio
barrel chest, emphysema Increased RV Decreased FEV/FVC |
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Restrictive lung disease
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Increased RV/TLC ratio
fibrosis, lung volumed decreased (TLC), increased FEV/FVC |
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Physiologic Dead Space
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Total LV not in gas exchange
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Transmural Pressure Gradient
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intra-alveolar> intrapleural P
lung is always stretched |
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Compliance
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more elastic, less compliant
high compliance = easier to inflate lung = less elastic tissue *measured in expiration* |
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Pneumothorax
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air in space- atm P = lung P
lungs collapse and chest wall springs out ( no negative IPP) |
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Emphysema
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obstructive- loss of Elastic fiber
(proteases/elastases) increased compliance with increased slope |
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Fibrosis
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restrictive- stiffening of lung tissue- decreased compliance associated with decreased slope
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CO2 Diffusion
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20x faster than O2
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DL
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diffusion capacity of the lung
increases with exercise, decreases with disease |
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methemoglobin
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Fe3+
Does not bind O2, cyanotic treat with METHylene blue caused by low metheme reductase, nitrates/sulfates |
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HbF
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2a 2 delta chains higher affinity for O2
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Hemoglobin S
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Valine not glutamic acid B chain
sickle cell anemia- less affin |
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Right Shift
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CO2, acid/altitude, 23DPG, exercise, temperature
* decreased affinity |
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Left Shift
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Increased affinity
fetal hemoglobin |
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hypoxic vasoconstriction
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inhibition of NO in endothelial cells therefore no cGMP produced
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Global hypoxic vasoconstriction
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Increased Resistance = increased arterial pressure= hypertrophy of RV
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Thromboxane A2
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cyclooxygenase
vasoconstriction |
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Prostacyclin
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cyclooxygenase
vasodilation |
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leukotrienes
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lipoxygenase
vasoconstriction |
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R-L shunts
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hypoxemia
can not be corrected by high O2 tetrology of fallot |
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L-R shunts
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do not cause hypoxemia
Patent DA increased PO2 in R heart |
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V/Q
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= 0.8
O2= 100; CO2= 40 |
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Medulla respiratory center
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inspiratory = dorsal- always
expiratory = ventral- exercise (nucleus ambiguus etc) |
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Pneumotaxic Center
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turns off inspiration
limits tidal volume (respiratory rate secondarily) |
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Nucleus ambiguus
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inspiratory and expiratory innervates laryngeal/pharyngeals
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Nucleus retroambiguous
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Inspiratory neurons- ext.intercos
expiratory neurons internal ints & abdominal muscles |
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Nucleus retrofacialis
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inhibit inspiratory cells in DRG
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Apneusis
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an abnormal breathing pattern: prolonged inspiratory gasps followed by brief expiratory
lower pons- ketamine |
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hyperventilation
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decrease PCO2 = increase pH
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Hypoventilation
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increase PCO2 decrease PO2
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RAS
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shifted R/tuned off with sleep, drugs, etoh- decreased RR
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Peripheral Chemoreceptors
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detect drop in PO2
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Central chemorecptors
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chages in PCO2
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decreased arterial Ph
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Mediated ONLY by chemoreceptors in the carotid not aortic bodies
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Lung stretch receptors
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mechanorecptors- decrease RR with distension of the lungs Hering-Breuer reflex- prevent over inflation of lungs
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Joint/muscle receptors
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mechanoreceptors increased RR in response to limb movement
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Irritant receptors
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dust/pollen constriction of sm muscle and increase RR
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Juxtacapillary or J receptors
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alveolar walls (near capiliary)
engorgement of blood = increased RR |
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Brief apnea
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1/3 of people
short >10s no change on PCO2/PO2 |
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Central Sleep Apnea
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↓ ventilatory drive to the respiratory motor neurons
no breathing efforts made- flat Plural pressure curve |
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Obstructive sleep apnea
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upper airway closes in inspiration- self awakening hypoxia/hypercammpnia
common- obesity- high PP curve |
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most significant modification to high altitude?
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hyperventilation
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Polycythemia
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increase in RBC
advantage- more O2 carrying disadvantage- high viscosity (increased resistance to BF) |
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2,3 DPG
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decreased affinity for O2 = right shift. adv- more unloading
disadv- harder to load up in lung |
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gland/wall ratio
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normal 0.4
bronchitis- 0.7 |
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Pink Puffers
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Type A
mild hypoxemia, normal PCO2 recent SOB, wt loss, no cyan, barrel chest |
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Blue Bloaters
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Type B; chronic cough, sputum, rales, JVD, edema, cyanosis, SOB, hypoxemia, hypercamp
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COPD asthma
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Increased R
Tx: B-a agonists, Corticostero, Antileukotrienes, Dilate airways ↓ inflammation |
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sarcoidosis
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restrictive- multi organ
fibrotic alveoli, granulomas tiss decreased LV, compliance, VC |
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Scoliosis
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cant take deep breath- shallow/rapid; all lung vol decreased; hypoxemia, hard work to breath-
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