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148 Cards in this Set
- Front
- Back
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What is the disease process of someone who has an extended expiratory phase?
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Obstructive lung disease
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A tall, think male teenager has an abrupt-onset dyspnea and left-sided chest pain. There is hyperresonant percussion on the affected side. Breath sounds are diminished.
What is the diagnosis? |
Spontaneous pneumothorax.
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A young man is concerned about his wife's inability to conceive and her recurrent URIs. She has dextrocardia.
What protein is deficient? |
Dynein
Kartagener's |
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What are the cells of the lungs?
Where do you find them? |
Pseudocolumnar cilliated cells extend to the resp bronchioles
goblet cells extend only to the terminal bronchioles Type I alveolar cells 97% Type II alveolar cells 3%- secrete surfactant. Type II in lung damage. |
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What can you measure in the amniotic fluid to make sure the lung is fully developed?
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lecithin to sphingomyelin ration > 2.0
mature levels of surfactant |
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breakdown the bronchopulmonary segments
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Each segment has 3ry (segmental) bronchus and 2 arteries (bronhical and pulmonary) in the center
Veins and lymphatics drain along borders. Arteries run with Airways |
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what is the relationship between the pulmonary artery and the to the bronchus at each hilus?
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RALS
Right Anterior Left Superior |
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What structures perforate the diaphragm? And at what level?
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I 8 10 EGGs AT 12
T8- IVC T10- esophagus, vagus T12: aorta, thoracid duct, azygous vein (red, white, blue) |
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What are the muscles of respiration? Normal breathing and excercise?
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Normal
Insp- diaphragm Exp- passive Exercise Insp- external intercostals, scalene muscles, sternomastoids Exp- rectus abdominis, internal and external obliques, transversus abdominis, internal intercostals. |
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Define the following:
Tidal volume Inspiratory reserve volume Expiratory Reserve volume Residual volume Functional Residual Capacity Inspiratory capacity Vital capacity Total Lung Capacity Forced expiratory Volume Dead space (anatomic and physiologic) |
TV- volume inspired and expired on a NORMAL breath
IRV- volume that can be inspired over and above the tidal volume ERV- volume that can be expired after the tidal volume Residual Volume- what's left after maximum expiration (not measurable by spirometry) FRC- ERV + RV Inspiratory Capacity- TV + IRV Vital Capacity- From max out to max in. Total Lung Capacity- Everything FEV1- The amount that can be expired in the first second of a max expiration (normally 80%) Dead space Anatomic- teh volume of the conducting airways (150ml) Physiologic- the volume of lung that does not participate in gas exchange |
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When is FEV1 increased? Decreased?
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increased- obstruction
FEV reduced more than FVC (FEV/FVC is decreased) decreased- restrictive FEV and FVC are reduced (FEV/FVC is normal or increased) |
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How is dead space calculated?
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Vd=Vt x (Paco2 - Peco2)/Paco2
Dead space increases with V/Q defects |
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How do you calculate the Ventilation Rate?
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Minute ventilation= Tv x B/min
Alveiolar ventilation = Tv-Vd x B/m |
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Breakdown compliacne
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It is the distensibility of lungs and chest wall; the change in volume given the change in pressue
inverse to elastance Surfactant increases compliance (slope of pressure volume curve) |
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When does compliance change?
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emphysema- lung compliance is increase, tendency for collapse is decreased.
Higher FRC- barrel chest Fibrosis- lung compliance is decreased, lower FRC |
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What is Laplace's law on the pressure in the alveolus?
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P=2T/r
large alveoli- have low collapsing pressures. small alveoli- have high collapsing pressures (no surfactant=atelectasis |
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What is primatly phospholipid of surfactant?
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dipalmitoyl phosphatidylcholine (DPPC)
fetus- no surfactant until week 24 or as late as wk. 35 |
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What is the major site of airway resistance?
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medium-sized bronchi
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What is the relationship between lung volume and resistance?
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High- decreased resistance
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Why do people with COPD use pursed lips?
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expire more slowly-> prevent airway collapse
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What's the difference between "pink puffers" and "blue bloaters"
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Pink puffers- 1ry emphysema- mild hypoxemia, normocapnia (alveolar ventilation maintained)
Blue bloaters- severe hypoxemia w/ cyanosis, hypercapnia (not maintained alveolar ventilation) |
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What is the respiratory response to high altitude?
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1. Acute increase in ventilation
2. Chronic increase in ventilation 3. Increase in epo-> increased Hct and Hb (chronic hypoxia) 4. Increase 2,3DPG- binds to hemoglobin to release more O2 5. Increase in mitochondria 6. Increased renal excretion of bicarb (augment by acetazolamide) compensates for resp alkalosis 7. Chronic hypoxic pulm vasoconstriction results in RVH |
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What are some products of the lung?
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Prostaglandins
Histamine ACE- AI->AII; inactivates bradykinin Kallikrein- activates bradykinin |
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What is methemoglobin?
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Hb with Fe3+ instead of Fe2+. Does not bind O2
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What is the difference between adult and fetal hemoglobin?
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Fetal- left-shift- binds O2 better. binds DPG less.
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What causes the O2-heme dissociation curve to right-shift?
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Decreased O2 affinity
P50 increased Increase in everything but pH CADET face right CO2 Acid/Altitude DPG Exercise Temp Increased Pco2/decreased pH- Exercise- decreased pH-> increased O2 delivery. Increased T Increased H High altitude, increased DPG |
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What causes the O2-heme curve to left-shift?
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Increased affinity
decreased P50 Caused by decrease in everything but pH Decreased Pco2 Increased pH decreased Temp Decreased DPG HbF CO poisoning |
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What is the difference between perfusion limited and diffusion limeted ventilation?
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Perfusion- (normal)- Gas equilibrates early along the length of capillary. More blood for more diffusion
Diffusion- Blood moves too fast- exercise, emphysema, fibrosis |
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How is CO2 handled in the blood?
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90% bicarb
5% bound to hemoglobin 5% dissolved |
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WHat is the haldane effect?
the bohr effect? |
Haldane- Ox of heme promotes CO2 dissociation. In lungs
Bohr- increase of H shifts curve to right, unloads O2. In peripheral tissue. |
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Compare Zones 1, 2, 3 of the lung
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1- low flow; PA>Pa>Pv (compressed capillaries in hemorrage(decreased Pa) or PPV (increased PA)) High V/Q
2- medium flow; Pa>PA>Pv 3- high flow; Pa>Pv>PA; lower V/Q |
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What is the best V/Q? What happens in Exercise?
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1 is the best.
In excercise, increased Cardiac Ouput-> apex capillary dilation-> closer to 1. |
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How does allergic rhinitis come about?
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IgE-type I immune. Mucosal and submucosal mast cells.
Eos. |
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What are the major causes of Acute Rhinitis?
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Adenovirus- runny nose, sneeze, congestion
Allergic Rhinitis Bacterial- Sterp, Staph, Haemophilus |
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What is sinusitis?
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inflam o fthe paranasal sinuses- extension of nasal or dental infection.
Obstructed drainage. Acumulation of mucoid secretions or exudate |
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Epiglottitis:
Why is it risky? What is the most common cause? |
can kill kids
H. flu |
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What is croup?
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laryngotracheobronchitis
viral harsh cough and stridor |
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What tumors can arise in teh nose and nasal sinuses?
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Nasopharyngeal carcinoma
Asia and East Africa- EBV Squamous cell- most frequent Adenocarcinoma- 5% Plasmacytoma |
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What are the tumors of the Larynx?
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Singer's nodule- benign polyp- localized to true vocal cords
Laryngeal papilloma- benign neoplasm on the true vocal cords. Kids can have mult lesions caused by HPV Squamous Cell- most common malignant tumor. Men>40; smoke and alcohol- presents with persistant hoarseness Glottic carcinoma- true vocal cords- good prognosis. Supraglottic adn subglottic carcinoma- less common, worse prognosis |
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What is the difference between Extrinsic and Intrinsic Bronchial asthma?
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Extrinsic- immune- type I with IgE bound to mast cells; begins in childhood.
Intrinsic- asthma associated with chronic bronchitis and cold/exercise induced asthma. Adult life, no Hx of allergy |
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What are the pathologic findings in Bronchial asthma?
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Bronchial smooth muscle hypertrophy
Hyperplasia of bronchial submucosal glands and goblet cells Thickening of basement membrane prolif of eos Airways plugged by viscid mucus Curschmann spirals, eos, and Charcot-Leyden crystals (Eos derive) |
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What are the clinical correlations with asthma?
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dyspnea, wheezing
cough, tachypnea hypoxemia, pulsus paradoxus |
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What are the complications of Asthma?
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superimposed infection, chronic bronchitis, pulm emphysema
status asthmaticus- prolonged bout of asthma that lasts for days |
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What are some triggers for asthma?
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viral URIs
allergens stress |
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Chronic Bronchitis:
what is the clinical definition? What are the risk factors? What are the pathologic changes? What is a major complication? What are the clinical findings? |
productive cugh for 3 months over 2 years.
Cigarrettes, pollution, infection, genetic factors Hyperplasia of mucus-secreting submucosal glands Cor pulmonale wheezing, crackles, cyanosis blue bloater |
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What are the following:
Centrilobular emphysema Panacinar emphysema Paraseptal empysema Irregular emphysema |
centrilobular- dilation of brioncioles
Panacinar- dilation of the acinus- alveoli, alevolar ducts, resp bronchioles, terminal bronchioles. Deficiency of alpha antitrypsin. Paraseptal- dilation of the distal acinus- alveoli, some duct. localizes to pleura and interlobar septa. Subpleural bullae or blebs Irregular- irregular involvement of the acinus w/ scarring w/in the wall sof enlarged spaces. |
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Emphysema:
definition Pathologic change Clinical Sx |
Dilation of air spaces w/ destruction of alveolar walls.
increased anteroposterior diameter of chest; increaced TVC hypoxia, cyanosis, resp acidosis dyspnea, decreased breath soudns, tachy pink puffer |
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What are the posulated causes of emphysema?
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elastase action on the alveolar walls. usually neutralized by antitrypsin
Cigarettes- attract neutrophils and macros and their elastase; inactivates alpha1 Hereditary alpha1 deficiency- panacinar; chromosome 14. piZ allele-> Hepatic cytoplasmic droplets-> liver damage piZZ-> cirrhosis and emphysema |
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Bronchiectasis:
Definition what is a risk? What part of the lung is affected? What are the Sx |
abnl permanent bronchial dilation from chronic infection w/ inflamm and necrosis
predisposed by obstruction, sinusitis (postnasal drip), Cystic Fibrosis, rarely- Kartagener syndrome lower lobes copious purulent sputum, hemoptysis, pulm infections that can cause abscess |
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What is Kartagener syndrome
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defect in cilia from a dynein arm defect. Infertility, bronchiectasis, sinusitis. W/ situs inversus no motility in resp, auditory, sperm ciliea
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What is ARDS?
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Diffuse alveolar damage. increase in alveolar capillary permeability; leakage of protein-rich fluid into alveoli.
intra-alveolar hyaline membrane- fibrin and debris bad gas exchange |
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What can cause ARDS?
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toxic agents
shock sepsis trauma uremia aspiration of gastric contents acute pancreatitis inhalation of chemical irritants- chlorine, o2, OD of heroin; bleomycin |
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What are the pathogenic factors that influence ARDS?
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1. neutrophils release toxic substances to alveolar wall
2. activation of the coag cascade. microemboli O2 toxicity mediated by the formation of o2 free radicals |
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What are the predisposing factors for neonatal respiratory distress syndrome?
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prematurity
maternal DM caesarean Most common cause of resp failure. Most common cause of death in premature infants |
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What are the path findings in NRDS?
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heavy lungs with areas of atelectasis alternating with dilated
small pulm vessels are engorged. intra-laveolar hyaline membranes. |
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What are the complications of NRDS
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Bronchopulmonary dysplasia- From O2 and mechanical ventilation
Patent Ductus from hypoxia Intraventricular brain hemorrhage Necrotizing enterocolitis- inflamm of intestines |
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What is Anthracosis?
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Inhalation of carbon- no harm; carbon macros-> black patches
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What is coal miner's silicosis?
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inhalation of coal- carbon and silica.
Coal macules around bronchioless no disability fibrotic nodules with necrotic black fluid bronchiectasis, pulm htn |
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What is silicosis?
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inhalation of silica dust.
miners, glass, stone cutters damage to macrophages-> inflam silicotic nodules silicotuberculosis. |
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what is the Rx for NRDS?
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steroids for mom during pregs
surgactant for infant |
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What is another name for surfactant?
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dipolmitoyl phophatidylcholine
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What is asbestosis?
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Diffuse interstitial fibrosis from asbestos fibers.
increased risk of mesothelioma adn bronchogenic carcinoma Long latency Ferruginous bodies in long Ivory-white pleural plaques |
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Who are at risk for abestosis?
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shipbuilders and plumbers
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What happens when asbestosis and smoking are combined?
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increased risk of bronchogenic cancer.
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What fibers stane with Prussian blue?
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asbestis
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Sacroidosis:
What is the characteristic path findings? What group is most at risk? When does the disease occur? |
Noncaseating granulomas- multiple organ systems
African Americans Teenage or young adults. |
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What are the common path changes in sarcoid?
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interstitial lung disease
enlarged hilar lymph nodes anterior uveitis erythema nodosum of the skin polyarthritis |
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What are the immune effects of sarcoid?
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reduced sensitivity of skin test antigens
poly clonal hyperglobulinemia |
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What are the clinical abnlties in sarcoid?
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Chest x-ray
1- bilat hilar lymphadenopathy 2- interstitial lung disease- defuse reticular densities Labs 1- hypercalcemia 2- hyper gammaglobulinemia 3. increased serum ACE Dx- biopsy |
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What is idiopathic pulmonary fibrosis?
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chronic inflamm and fibrosis of the alveolar wall
begins with alveolitis- progresses to fibrosis, ends in a distorted fibrotic lung filled with cystic spaces (honeycomb lung death in 5 years. |
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Eosinophilic granuloma?
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localized proliferation of histiocytic cells like the langerhans cells- Birbeck granules.
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What is 2ry pulm hypertenstion
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from increased pulm blood flow- l->r shunt.
increased resistance w/in pulm circulation embolism or vasoconstriction from hypoxia |
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What are some causes of pulm edema?
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Increased hydrostatic pressure- LV failure or mitral stenosis
Increased alveolar capillary permeaility- inflamm alveolar reactions, ihalation of irritant gases,pneumonia, shock, sepsis, pancreatitis, uremia or OD Miscellaneous- Rapid ascent to high altitude. |
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Lobar pneumonia:
most common cause what is it characterized by? |
S. pneumoniae
intra-alveolar exudate-> consolidation may involve whole lung |
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Bronchopneumonia:
most common cause characteristics |
S. aureus, h.flu, klebsiella, s. pyogenes
Acute inflamm infiltrates from bronchioles into adjacent alveoli; patchy distribution involving >1 lobe |
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Interstitial pneumonia:
cause characteristics |
RSV, adenoviruses, M. pneumonia, legionella, chlamydia
Diffuse patchy inflamm localized to interstitial areas at alveolar walls distribution >1 lobe |
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Break down the pneumonia caused by S. pneumoniae
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elderly or debilitated
those with cardiopulmonary disease malnourished can cause empyema |
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Break down the pneumonia caused by S. aureus
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superinfection on fluo or viral
IV drug users hospitalized, elderly, chronic lung disease Can cause focal inflam exudates or abscess empyema or other infectious complications bacterial endocarditis brain and kidney abscesses |
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Break down the pneumonia caused by S. pyogenes
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complication of flu or measles
abscess |
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Klebsiella pneumonaie
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Debilitated hospitalized patients and diabetic or alcoholic
High mortality in elderly Alveolar wall damage-> necrosis. sometimes with abscess formation |
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Break down the pneumonia caused by H. flu
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kids and infants
debilitaated adults COPD Can cause meningitis and epiglottitis in kids |
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Break down the pneumonia caused by Legionella
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infection from inhalation of air-conditioning aerosol
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what's special about measles and pneumonia?
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giant cell pneumonia
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What is the pneumonia caused by Coxiella burnetii?
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Q fever
cattle, sheep or unpasteurized milk |
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What are the common hospital aquired pneumonias?
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Klebsiella, Pseudomonas, E. coli
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What bacteria cause lung abscesses?
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staph
pseudomonas klebsiella proteus |
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What is Pancoast's tumor?
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Carcinoma that occurs in the apex of the lung.
Cervical sympathetic plexus- Horner's (ptosis, miosis, anhidrosis) |
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Squamous cell carcinoma
Where is it found in the lung? What are the characteristics? What is the clinical presentation? |
Central
hilar mass and frequently results in cavitation smoking can have PTH and HyperCa Presents as cough, hemoptysis, bronchial obstruction, wheezing, coin lesion |
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Small Cell Cancer:
Where is it found? What are the characteristics? What is the clinical presentation? |
Central
Undiffed tumor; aggressive carcinoma. Hard to cure by surg. Usually mets at Dx. with ectopic production of corticotrophin or ADH Can cause lambert eaton syndrome Presents as cough, hemoptysis, bronchial obstruction, wheezing, coin lesion |
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Lung Adenocarcinoma
where is it found in the lung? What are the characteristics? |
Peripheral- most common
Develops on site of prior pulm inflammation less linked to smoking |
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Bronchioloalveolar cancer
Where is it found in the lung? What are the characteristics? |
Peripheral- not related to smoking
columnar->cuboidal cells that line the alveolar walls. can have multiple densities |
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Large Cell Carcinoma
Where is it located? What are teh characteristics? |
Peripheral
Has both squamous and adenocarcinoma cells. |
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Carcinoid tumor
Where is it located? What are the characteristics? |
major bronchi
Low malignancy, spreads by direct extension, may result in carcinoid syndrome -flushing, diarrhea, wheezing, salivation |
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Metastatic carcinoma
What organs mets to the lung? |
Very common
From Brain bone liver |
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What are the major complications of lung cancer?
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SPHERE
Superior vena cava syndrome Pancoast Tumor Horner's syndrome Endocrine- paraneoplastic Recurrant Laryngeal symps- hoarseness Effusions- pleural or pericardial |
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What is the role of LTB4?
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neutrophil chemotactic agent
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What is the role of LTC4, D4, E4?
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broncho constriction, vasoconstriction, contraction of smooth muscle and increased vasc permeability
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What is the role of PGI2?
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inhibs platelet aggregation and promotes vasodilation
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What is the role of Zafirlukast?
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blocks the actionof leukotrienes
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what is the role of montelukast?
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blocks the action of leukotrienes
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What is the role of Phospholipase A2?
What blocks this enzyme? |
converts lipid to arachanodinic acid
Corticosteroids block it. |
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What is the role of lipoxygenase?
what blocks this enzyme? |
converts Arachandonic Acid to Hydroperoxides for Leuko synth
Zileuton |
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What is the role of Zileuton?
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blocks Lipoxygenase from forming hydroperoxides to form leukotrienes
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What is the role of cyclo-oxygenase?
What blocks it? |
turns Arachodonic Acid into endoperoxides which become Prostacyclin, prostaglandins, adn thromboxane
NSAIDS Acetominophen and COX-2s block |
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What is the role of PGE,F?
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Increase uterine tone,
decrease vascular tone decrease bronchial tone |
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What is the role of thromboxane?
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increase platelet aggregation
increase vasc tone increase bronchial tone |
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What is the difference between 1st and 2nd generation H1 blockers?
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2nd generation are not as sedating
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What are the clinical uses for 1st generation H1 blockers?
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allergy
motion sickness sleep aid |
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What are the SEs of 1st and 2nd generation H1 blockers?
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Sedation
antimuscarinic anti-alpha-adrenergic |
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What are the 1st generation H1 blockers?
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Diphenhydramine
Dimenhydrinate Chlorpheniramine |
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What are the 2nd generation H1 blockers?
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Loratadine
fexofenadine desloratadine |
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What is Isoproterenol?
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Non-specific B-agonist
relaxes bronchial smooth muscle Adverse effects-tachy |
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What is Salmeterol?
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long-acting B2 agonist
used for prophylaxis Adverse effects are tremor and arrhythmia |
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What is the mechanism of action of theophylline?
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inhibs phosphodiesterase->decrease in cAMP hydrolysis-> bronchodilation
Cardiotox and neurotox |
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What are the SEs of theophylline?
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cardiotox and neurotox
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What is the mechanism of action of Ipratropium?
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competative block of muscarinic receptors, prevents bronchoconstriction
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What is cromolyn?
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prevents release of mast cell mediators- prophylaxis of asthma.
Not good for acute |
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What is the role of corticosteroids in asthma?
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inhibit the synth of cytokines.
inactivate NF-kB- transcription factor for TNF-a. 1st line |
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What is the mechanism of action of Zileuton?
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blocks 5-lipoxygenase
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what is the mechanism of action of Zafirlukast and montelukast?
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block leukotriene receptors
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What is the role of leukotrienes in asthma?
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they are part of late response inflamm-> bronchial hyperreactivity
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What is the role of histamine in asthma?
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triggers the early response in asthma
bronchoconstriction |
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What is the histologic presentation of an emphysematous lung?
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destruction of the alveolar walls and associated capillary beds
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What is a saddle embolus?
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embolus from the legs that blocks the biforcation of the pulmonary trunk blocking all pulmonary circulation
non-cardiac cause of sudden death |
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What can cause asthma by an enhanced sensitivity to vagal stimulation?
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viral URI
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A hemoglobin drop would lead to what change in the blood?
a. arterial O2 content b. arterial O2 sat c. arterial pO2 d. CO e. HR f. SV |
arterial O2 content
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What would cause hemosiderin-laden macrophages?
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pulm edema
from injestion of RBCs |
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What is the characteristic path of pulm edema?
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proteinaceous granular precipitate
hemosiderin-laden macrophages engorged alveolar capillaries |
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What is the path of pneumocystis?
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hat-shaped, silver-staining cysts
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What is the path of Candida?
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hyphae and spores
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What is the path of pulm infarction?
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ischemic necrosis of alveoli
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What would cause a wedge shaped opacity on x-ray?
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pulm infarction
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What is the histologic presentation of pneumocystic carinii?
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cup shaped, crushed tennis ball
silver staining and frothy exudate |
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What is the histologic presentation of Cryptococcus?
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encapsulated yeast- india ink
Broad-slimy capsule |
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What is the histologic presentation of histoplasma?
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silver staining
but mainly seen in the cytoplasm of histiocytes thin cell wall, no true capsule |
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What is the histologic presentation of Coccidiodes?
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non-budding spherule
filled with endospores |
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What is the histologic presentation of paracoccidiodes?
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yeast with multiple budding
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When is one exposed to beryllium?
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mining and fabrication
looks like sarcoid |
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What exposure leads to byssinosis?
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cotton
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What is the mechanism of N-Acetylcysteine?
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splits the disulfide linkages in mucus.
Mucolytic for CF |
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What is Dextromethropan?
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cough suppressant
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What is Ipratropium?
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antiCholinergic
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what is pentamidine?
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antiprotozoal for pneumocystis carinii
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What are Charcot-Layden crystals? Curshman spirals?
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rhomboid crystals of asthma
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What are some peripheral causes of hypoventilation?
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pickwickian
suffocation submersion skeletal abnlties trauma phrenic nerve paralysis polio tetanus |
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What is the relationship between lung volume and radial traction?
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when volume decreases, traction increases
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What is the Reid index?
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for bronchitis
gland depth to bronchial wall thickness |
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What B-blockers can be given in an ephysema pt?
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metoprolol
atenolol |
