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70 Cards in this Set
- Front
- Back
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Lung volumes cannot be measured with spirometry
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Anything with RV in it
TLC FRC RV |
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Measuring dead space
Alveolar ventilation |
Anatomic - volume of conducting airways (150mL)
Physiologic - can be more in pathology Vd = Vt x (PA CO2 - PE CO2) / PA CO2 Or Tidal volume times arterial blood CO2 minus expired air PCO2 Alveolar ventilation = (Vt - Vd) x breaths/min |
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FEV1
FEV1/FVC ratio |
FEV1 - forced expiration amount in first second at max expiration. Norm is 80%
FEV1/FVC is decreased (more FEV1 loss) in OBSTRUCTIVE lung conditions (COPD, Asthma, bronchiectasis, emphysema, bronchitis), Increased or normal in RESTRICTIVE (fibrosis, autoimmune, poor breathing muscles/structure, sarcoid) b/c lower lung volume overall too |
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Inspiration and expiration muscles
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Inspiration - DIAPHRAGM, external intercostals and accessory in exercise of disease (COPD)
Expiration - internal intercostals or abdominals during exercise or disease (asthma), usually passive due to diaphragm relax |
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Compliance of system
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C=V/P; measure distensibility (volume change per given pressure change). Highest in middle, lowest at extremes
At rest Chest wall wants to move out (negative pressure) and lung wants to collapse (positive pressure) both greater compliance than sum. Create negative intrapleural pressure. Sum is at 0 airway pressure and constitutes FRC Emphysema - greater lung compliance, less collapse, FRC shift right (more; barrel chest) Fibrosis - less lung compliance, more collapse, FRC shift left |
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Pneumothorax physiology
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Air into intrapleural space disrupts negative intrapleural pressure (chest wall and lung balance) so lung collapses and chest springs out
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Surface tension in alveoli
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P = 2T/r
Tendency to collapse is balanced by higher tension (surfactant) and radius Small alveoli - lower radius, easy to collapse (atelectasis) so need more tension (SURFACTANT) Large alveoli - high radius, hard to collapse |
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Airflow and Resistance
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Q = pressure difference/airway resistance
High resistance, low flow High pressure difference, high flow Resistance varies on length of airway (longer = more) and radius^4 (halving radius = 16x more resistance) and density (low density helium has lower resistance) Highest resistance in MEDIUM bronchi b/c smallest are in parallel (1/R = 1/R1 + 1/R2 .....) PNS - increase resistance via constriction SNS - decrease (B2 agonist) |
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Breathing Cycle
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Inspiration - Alveolar pressure below zero (back to zero at end of inspiration); intrapleural even more negative (elastic recoil of lung builds); air pulled in
Expiration - alveolar pressure rises above zero, intrapleural returns to -3 (due to recoil) and air forced out |
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"Pursed lips" breathing
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B/c alveolar pressure actually becomes positive in expiration some collapse
Pursed breathing keeps open so some COPD pts do this |
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Pink Puffers vs Blue Bloaters
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Pink Puffer - emphysema mostly, mild hypoxemia, normocapnia and maintained alveolar ventilation
Blue bloater - bronchitis mostly, severe hypoxemia, cyanosis b/c don't maintain ventilation, hypercapnia. RV failure and edema |
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Perfusion vs Diffusion limited exchange
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Perfusion - exchange fast, get more in system with cardiac output up. O2, CO2, N2O
Diffusion - NOT fully equalized by end of capillary, cannot increase with more CO. O2 in strenuous exercise, fibrosis (greater thickness), emphysema (less area), CO |
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O2 content of blood
HgB sat curve |
O2 content = (O2 binding capacity x % sat) + dissolved O2
Dissolved is PP x Solubility PO2 of 100 = 100% Hgb sat PO2 of 40 = 75% Hgb sat Curve is sigmoid b/c each one bound increases affinity Right shift - Higher P50, lower affinity - exercise, acidic, 2,3BPG, temperature, CO2 Left shift - Lower P50, higher affinity - CO, HgbF, opposite of above Relaxed Hgb form has higher affinity for O2 than taut form. |
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Aa gradient, Alveolar gas eq.
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Alveolar gas eq - PAo2 = PIo2 - (PAco2/R); R=0.8 normally.
Used to differentiate hypoxemia causes = difference in alveolar P02 and arterial PO2. Normally <10mmHg. ELEVATED when cannot diffuse adequately - R to L shunt, Fibrosis, V/Q defect NORMAL in hypoventilation and high altitude b/c diffuses just fine |
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CO2 transport in blood
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CA converts to H+ and HCO3. HCO3 exchanged for Cl-; H+ binds deoxyhemoglobin to buffer acidification
Little bound to N-terminus (not heme) of Hgb Even less dissolved as CO2 |
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Pulmonary circuit and V/Q
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Pressures AND resistance much lower (so flow about same)
V and Q both higher at base but Q biggest ranges. Apex - HIGH V/Q (best exchange); Base - LOW V/Q (best flow; respond best to 100% oxygen) Zone 1 - alveolar pressure > arterial > venous - can get zero Q Zone 2 - arterial > alveolar > venous - Alveolar to venous difference dominates flow Zone 3 - arterial > venous > alveolar - arterial to venous dominates flow PTE - infinite V/Q, dead space, alveolar gases = inspired Obstruction - 0 V/Q, capillary blood = venous blood |
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Breathing control centers
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DRG - medulla - inspiration. Input from X and IX via peripheral chemoreceptors and mechanoreceptors. Output via phrenic
VRG - medulla - expiration, ONLY in exercise or active process Apneustic center - pons, inspiration gasps Pneumotaxic center - pons, inhibits inspiratoin Cortex - voluntary control Peripheral receptors (carotid and aortic body) - respond to CO2 and pH and O2 (<60mmHg) Central - respond to pH via CO2 diffusion |
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Misc receptors for breathing
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Lung stretch - decrease frequency of breath if stretched
Irritant - between epithelial cells, stimulated by noxious J receptors - in alveolar walls by capillaries, engorgement (Left CHF) and cause rapid shallow breath Joint and muscle - movement = anticipatory breaths for exercise |
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Changes in exercise
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O2 consumption, CO2 production and ventilation all rise. Blood flow rises. V/Q becomes more even
Arterial O2 and CO2 are same; Venous CO2 rises Arterial pH should be same, drops in strenuous |
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Adaptation to high altitude
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Low Po2 inhaled, activates chemoreceptors, hyperventilation, respiratory alkalosis (treat with acetazolamide), HCO3- wasting in kidney (enhanced by acetazolamide)
Hypoxemia stimulates EPO and 2,3DPG production (right shift), pulmonary vasoconstriction too Can get Right side hypertrophy from higher resistance and pressure |
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Pneumocytes
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Pseudostratified ciliated columnar to respiratory bronchioles. Goblet cells till bronchi
Type I, Type II (surfactant, cuboidal, clustered), Clara (nonciliated, surfactant, degrade toxin, reserve) |
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Lung Anatomy Relevant
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3 lobes right, 2 left
Pulmonary artery to bronchus. Right anterior, left superior (RALS) Aspiration - Right lower lobe because bronchus vertical and wider Psudostratified ciliated columnar epithelium with goblet cells making mucus to terminal bronchiles. Ciliated last. Diaphragm - T8 (IVC), T 10 (esophagus, vagus), T12 (aorta, thoracic duct, azygous vein) |
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Methemoglobin, treatment
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Oxidized Fe3+ Hgb, cannot carry O2, higher affinity for CN-
Treat with methylene blue |
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CN- poisoning treatment
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nitrites to oxidize Hgb to Methemoglobin (binds up to lessen cytochrome oxidase damage),
Thiosulfate to form thiocyanate for renal excretion |
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Pulm HTN: Primary, Secondary
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Normal is 10-14mmHg, HTN is >25 or >35 in exercise
Primary - BMPR2 gene mutation - normally inhibits smooth muscle proliferation Secondary - COPD, mitral stenosis, thromboemboli, autoimmune disease, left to right shunt (endothelial injury from stress), sleep apnea, high altitude CHRONIC Leads to respiratory distress, cyanosis, RVH and death from decomp cor pulmonale |
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Emboli types
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FAT BAT
Fat Amniotic fluid Thromboemboli Bacteria Air (nitrogen) Tumor Helical CT to image. 95% are from deep leg thromboemboli. May have lines of Zahn |
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DVT Predisposal and signs
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Predisposal in Virchow's Triad (Stasis, hypercoagulability, endothelial damage)
Dorsiflexion of foot, tender calf, dyspnea, chest pain, tachypnea Treat with heparin |
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Obstructive Lung diseases
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Chronic Bronchitis (Blue Bloater) - Hypertrophy of bronchioles mucus glands, need productive cough for >3 months for >2 years. Wheeze, crackle, cyanosis, dyspnea. Reid index of mucous glands to thickness of wall down to cartilage (not including)
Emphysema - pink puffer, barrel chest, less recoil, more compliance. Due to high elastase Asthma - Hyperresponsiveness and smooth muscle hypertrophy and Curschmann's spirals (epithelium from mucus plug) and Charcot-Leydin crystals (epithelium from mucus plug). Methacholine challenge to find. Triggers. Bronchiectasis - necrotizing chronic infection of bronchi, dilation and recurrent infections. Smoking, Kartagener's. Aspergillis predilection |
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Drugs implicated in restrictive lung disease
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Bleomycin
Busulfan Amiodarone |
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Pmeumoconioses, Coal, Silica, Asbestosis, Berylliosis
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Coal - upper lobe, cor pulmonale and arthritis, macrophages with dust
Silicosis - foundries, sandblasting, mines, upper lobes, Eggshell calcifications, birefringent particles surrounded by dense collagen. Hilar adenopathy Asbestosis - shipbuilding, roofing, plumbing, ivory white pleural plaques. Bronchogenic cancer and mesothelioma, lower lobes. May see dumbell fusiform golden rods in machrophages Berylliosis - noncaseating epitheloid granulomas after exposure. |
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Risk of supplemental O2 in neonatal respiratory distress syndrome
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retinopathy of prematurity
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ARDS cause
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trauma, sepsis, shock, aspiration, uremia, pancreatitis, amniotic fluid
Diffuse damage, exudate into alveoli, hyaline membrane formation. Less diffusion, hypoxemia. Initially due to PMNs releasing toxic things to alveolar wall and ROS formation |
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Tension vs Spontaneous pneumothorax
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From blebbing at apex
Tension - cannot get out - trachea away from lesion Spontaneous - toward lesion |
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Lung cancer types
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Small cell - undifferentiated, central - aggressive. ACTH or ADH, can cause Lambert-Eaton (Abx to Ca++ channels), Small blue cells, inoperable
Adenocarcinoma - peripheral, NOT SMOKING RELATED, Broncial and Brochiolalveolar (grows along airway) Squamous Cell Carcinoma - central. SMOKING. PTHrP producers Large cell - Peripheral, aggressive, undifferentiated, giant cells with leukocyte fragments Carcinoid - Serotonin syndrome, may deposit stuff on right heart valves, tricuspid insufficiency Mesothelioma - asbesos, psammoma bodies |
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Complications of Lung cancer
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SPHERE
Superior vena cava syndrome Pancoast tumor - apex and can get to cervical SNS plexus for below Horner's Sydnrome - ptosis, miosis, anhydrosis Endocrine (Paraneoplastic) Recurrent laryngeal hoarseness Effusions (pleural or pericardial) |
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Pneumonia types and organisms
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Lobar - Pneumococcus, Klebsiella - consolidation and intra-alveolar exudate
Bronchopneumonia - S. aureus, H. flu, Klebsiella, S. pyogenes - patchy inflammation with PMNs Interstitial (atypical) - Viruses, mycoplasma, Legionella, Chlamydia - patchy and localized to interstitium at alveolar walls. >1 lobes, Indolent |
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Abscess formers
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S. aureus
Anaerobes - Bacteroides, Fusobacterium, Peptostreptococcus (aspiration usually) |
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Types of Pleural effusions
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Transudate - low protein, due to CHF (hydrostatic), nephrotic (oncotic), or cirrhosis (oncotic)
Exudate - high protein, malignancy, pneumonia, collagen disease, trauma, drain to prevent infection Lymphatic - milky with TGs. Chylothorax |
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Diphenhydramine, dimenhydrinate, chlorpheniramine
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H1 1st gen blockers - used for allergy, motion sickness, sleep aid
ASE: CNS sedation, antimuscuarinic and anti alpha-adrenergic |
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Loratadine, Fexofenadine, desloratadine, cetirizine
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H1 2nd gen blockers - used for allergy
MUCH LESS cross CNS so less sedating |
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Isoproterenol
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Non specific B agonist
Relaxes bronchial muscle via B2 ASE: tachycardia via B1 |
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Albuterol
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B2 agonist
Used for acute exacerbation |
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Salmeterol
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Long acting B2 agonist
ASE: tremor and arrythmia |
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Theophylline
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Phosphodiesterase inhibitor, more cAMP, leading to bronchodilation
Narrow window (cardio and nephro tox). Blocks adenosine |
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Ipratropium
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Competitive muscarinic receptor blocker
Prevents bronchoconstriction COPD |
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Cromolyn
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Prevents mast cell mediator release, PROPHYLAXIS for asthma, NOT during attack
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Steroids
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Beclomethasone, prednisone
Inhibit cytokines by activating NF-kB. Less TNFa produced, less bronchial hyperreactivity |
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Zileuton
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5-lipoxygenase path inhibitory by blocking arachidonic acid to leukotriences
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Zafirlukast, montelukast
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Blocks leukotriene receptors. Good for aspirin induce asthma
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Guaifenesin
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Expectorant, no effect on cough reflex
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N-acetylcysteine
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Mucolytic
Removes plugs in CF pts, also acetaminophen overdose reversal by providing more substrate for GSH |
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Bosentan
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Competitively antagonist of endothelin 1 receptors
Reduces pulm. HTN |
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Dextromethorphan
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Antagonist of NMDA receptors
Suppresses cough reflex Some opioid effect in excess (naloxone for OD), mild abuse |
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Pseudophedrine, phenylephrine
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SNS alpha agonist
Nasal decongestion, reduces hyperemia, edema, opens eustachian tubes Pseudophedrine is CNS stimulant and can cause HTN or anxiety |
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Methacholine
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Muscarinic agonist
Used in challenge test for asthma diagnosis |
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Shunt effect
L to R R to L |
R to L - due to obstruction of bronchi, poor ventilation, fibrosis, less gas exchange, capillary blood closer to venous blood
L to R - ASD, VSD, heart defects, tetrology of Fallot. Pulmonary vein blood more oxygenated BUT causes Pulm. HTN and CHF |
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Centrilobular emphysema vs Panlobular emphysema vs Distal acinar emphysema
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Centrilobular - mid and upper lung, due to smoking and elastase from neutrophils
Panlobular - all over lungs, lack of a1 antitrypsin, no block on elastase Distal acinar - Localized in upper lung lobe, fibrosis and scare, prone to pneumothorax with minor trauma |
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Pulmonary alveolar proteinosis
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Autoantibodies to GM-CSF
Do not clear surfactant in lungs. Chunks of gelatinous sputum, dullness in lung fields, BIL diffuse opacities. Many lamellar bodies |
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Asthma types
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Atopic - mast cell and eosinophil accumulation in lung
Nonatopic - no family history, no eosinophilia, normal IgE. Just bronchial hyperresponsiveness to inflammation. Get after infection or due to environment Allergic Asthma - IL-4, IL-5 secretion, More eosinophils, higher IgE |
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Atalectasis Types
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Resorption - due to mucuous or mucopurulent plug obstruction
Compression/Relaxation - air or fluid accumulation in pleural cavity (pneumothorax, effusion, hemothorax) Microatelectasis - post op in diffuse alveolar damage, surfactant loss in new born. Smallest alveoli Contraction atelectasis - fibrous tissue surrounds lung |
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Most common CFTR mutation
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delta508, 3 nucleotide deletion - abnormal postranslational processing leads to degradation
Others include absence (Ashkenazi), defective ATP binding, impaired conductance and less receptors |
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Most common S. aureus reservoir
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Anterior nares
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Vocal cord epithelium
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Stratified squamous epithelium
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TB Drugs
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RIPE
1) Isoniazide - inh. mycolic acid synthesis, can cause B6 def (neuropathy) or liver tox. Resistance when less bacterial catalase-peroxidase (needed to activate) 2) Rifampin - inh. DNA dep RNA pol., hepatotoxicity and RED body fluids 3) Ethambutol - inh. arabinosyl transferase (carbohydrate polymerization) for mycolic all. Optic neuropathy and color blindness 4) Pyrazinamide - Lowers pH via acidification (pyrazinamidase in mycobacterium) |
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Legionalle pneumophilia presentation and culture
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Grows in H20
Fever, confusion, diarrhea, many neutrophils and no organism on stain Grow: Complex media PLUS CYSTEINE |
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Cold agglutins means
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Mycoplasma pneumoniae - transient anemia due to mimicry to RBCs
EBV Hematologic malignancy |
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Pulmonary Blastomycosis vs Histoplasmosis vs Coccioidies
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Blastomycosis - Great lakes, Ohio river valley, asymptomatic to flu-like with granulomas in immunocompetent. Broad based buds in double wall
Histoplasmosis - Bat or bird droppings, Mississippi Valley, Several spherules inside of a macrophage Coccioides - Arizona, West, San Juacin Valley. Several spherules inside a capsule |
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Dx of cryptococcus neoformans
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Lung disease and meningitis in immunocompromised
Red mucarmine stain to see |
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TB course
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Week 1 - mycobacterium enters macrophages, secretes sulfatide virulence factor to allow proliferation. Lysis and reinfection
Week 2-4 - T cell response revs up. IFN secretion, epitheloid transformation of macrophages and granuloma formation |
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Mycoplasma pneumonia presentation
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Walking pneumonia
Dry, chronic nagging cough, low grade fever, malaise X-ray looks much worse than clinical picture; needs cholesterol to grow |
